Prognosis.

Any functional derangement will tend to improve for up to two years after surgery. Failure of the track to heal may result from residual infection, which may require examination under anesthesia; excess granulation tissue, which may need to be cauterized with silver nitrate or curetted; or ingrowth of hair resulting from lack of shaving. Crohn’s disease should also be excluded. The two crucial outcomes of fistula surgery are anal sphincter function and recurrence of the fistula. Of those in whom the sphincter had been preserved, 83 per cent had full continence whereas only 32 per cent of those who had undergone sphincter division were fully continent, and some of these needed a subsequent sphincter repair.

UNIT: COLOPROCTOLOGY

Theme: SACROCOCCYGEAL PILONIDAL SINUS (DISEASE)

KEY QUESTIONS FOR HOMEWORK:

1. Definition, location and aetiology.

2. Pathology.

3. Clinical features.

4. Differential diagnosis.

5. Treatment.

6. Recurrent pilonidal sinus.

1. Definition, location and aetiology.

Pilonidal sinus (Latin: pilus = hair, nidus = nest) is an acquired disease due to obstruction of hair follicles in the natal cleft, often associated with ingrowth of hair. Subcutaneous hair acts as a foreign body, initiating a reaction which is often complicated by varying degrees of infection. By reason of the shearing action of the buttocks or by sitting on a hard seat, and especially by vibration of a vehicle, loose hair travels down the intergluteal furrow, to penetrate the skin or the open mouth of a sudoriferous gland, such glands being more active in early manhood. It is not yet clear whether the initial entry of hairs through the skin is a primary event, or follows the softening of the skin due to pustular or other forms of dermatitis. Once a sinus has formed, intermittent negative pressure of the area may suck other loose hairs into the pit. Now is also proved congenital origin of the pilonidal sinus. The sinus is pit lined with epithelium and sometimes containing hair. It is centrally placed in area of the the intergluteal furrow and 4 to 8 cm cephalad to the anus. When the pilosebaceous follicle has been obstructed a cavity lined with granulation tissue forms, with the subsequent development of secondary tracks; these may rupture lateral to the midline creating secondary openings. Pilonidal disease affects young adults after puberty and is unusual after the age of 40. Males with this condition outnumber females by 4 to 1. The condition rarely occurs in blonds; many of the patients are exceptionally hairy and are usually obese. Patients have often poor personal hygiene. The epidemic of pilonidal disease is seen in American military personnel during the Second World War among jeep riders that it became known as «jeep drivers’ disease».

2. Pathology. The sinus extends into the sub­cutaneous planes as an infected track. Branching side channels are not infrequent. A stratified squamous epithelial lining, of varying degrees of integrity, is found in about half the cases. Hair shafts are found either lying loose in the sinus, embedded in granula­tion tissue, or deep in mature scar tissue in three-quarters of the cases. Foreign-body giant cells are common.

3. Clinical features.

There is a chronic or recurring sinus in the midline about the level of the first piece of the coccyx. Typically, a tuft of hairs projects from its mouth. The discharge from the sinus or sinuses is often bloodstained, contains foul sebum, and some­times hairs. The primary sinus may have one, or as many as six openings, all of which are strictly in the midline between the level of the sacrococcygeal joint and the tip of the coccyx. Secondary openings may be present on either side of the midline, often far out on to the buttocks or in the perineum. As has been indicated already, symptoms usually commence during the third decade; patients present­ing later in life nearly always give a history dating back to this period.

Clinical features of the pilonidal abscess.

In all cases, it is important to establish whether there is a history of previous episodes of the pilonidal abscess and how these were treated. Often there is a history of repeated abscesses in the region that have discharged spontaneously or have been incised. Pain is a prominent initial feature of the pilonidal abscess, followed by local signs of inflammation. In the case of a abscess, there is a localized, fluctuant, red, hot, and tender swelling placed in area of the the intergluteal furrow and 4 to 8 cm cephalad to the anus.

4. Differential diagnosis.

The sinus is not necessarily pilonidal. It could be a sinus connected with a postanal dermoid or a sinus resulting from a persistent caudal remnant of the original neural canal. The latter occurs in the sacral rather than the coccygeal region, and is definitely connected with the spinal theca. On this account, meningitis from an extradural abscess may occur in a child. Unlike a fistula in ano, the sinus passes upwards and forwards towards the sacrum. It does not reach bone, but ends blindly near the bone.

5. Treatment.

The patient is placed on the operating table, for preference in the «jack-knife» position. Methylene blue is injected into the sinus to colour all the tracks, the nozzle of the syringe being pressed against the opening to obtain some pressure. Excise all the tracks, as stained by blue dye and using sutures.The wound is closed with three or four deeply placed mattress sutures or Donati’s sutures, which are introduced about 1 cm away from the skin edges, and pass right through the fat to the level of the sacral fascia. The sutures are removed after 1 week. If the wound becomes obviously infected during this period, the sutures are removed earlier. Immediately after operation, the patient should avoid sitting on the wound. Preventing further ingrowth of hair whilst the wound remains immature is important, and the patient is advised to keep the area scrupulously clean and free of hair by the use of depilating agents or by shaving.

Treatment of an acute exacerbation (abscess). It is advisable to administer a perioperative bolus of a broad spectrum antibiotic, active against aerobic and anaerobic bacteria. A abscess should be treated in a timely fashion by incision and drainage. The abscess should be opened through a comparatively small incision. Drainage of the abscess under general or local anaesthetic rapidly relieves pain.

6. Recurrent pilonidal sinus. Three possibilities account for this disappointment:

1. a diverticulum of the main channel has been overlooked at the primary operation;

2. new hairs enter the skin or the scar;

3. when the natal fold is deformed by scarring, the least trauma causes tearing of the scar, and the resulting crevice becomes contaminated with coliform and cutaneous bacteria.

TESTS

1. Commonest type of anorectal

abscess is -

1. Ischiorectal

2. Submucous

3. Pelvirectal

4. Perianal

2. Deep type of anorectal

abscess is -

1. Ischiorectal

2. Submucous

3. Pelvirectal

4. Perianal

3. Superficial types of anorectal

abscesses are -

1. Ischiorectal

2. Submucous

3. Pelvirectal

4. Perianal

4. Anorectal abscesses is caused by -

1. Nonspecific infection of cryptoglandular origin

2. Specific infection

3. Viral infection

4. Pseudomonas

5. The treatment of choice in fistula in

anus -

1. Anal dilatation

2. Fissurotomy

3. Fistulectomy

4. Fistulotomy

6. The most common complication of pilonidal sinus (disease) is –

1. Bleeding

2. Perforation

3. Abscess

4. Stricture formation

7. Five-day self subsiding pain is diagnostic of -

1. Anal fissure

2. Fistula-in-ano

3. Thrombosed external hemorrhoids

4. Thrombosed internal hemorrhoids

8. The treatment of choice in pilonidal sinus (disease) without complications is –

1. Incision and drainage

2. Excision

3. Medical therapy

9. The treatment of choice in pilonidal abscess is –

1. Incision and drainage

2. Excision

3. Medical therapy

10. The treatment of choice in anorectal abscess is –

1. Incision and drainage

2. Excision

3. Medical therapy

ANSWERS

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

CANCER OF THE COLON AND RECTUM. PRECANCER (polyps, familial adenomatous polyposis, inflammatory diseases – ulcerative colitis, colonic Cron’s disease)

Составитель доц. Ю.И.Ломаченко

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

UNIT: COLOPROCTOLOGY

Theme: COLORECTAL CANCER

Basic information

1. Most colorectal cancers develop as a result of a stepwise progression from normal mucosa to adenomatous polyp into invasive cancer.

2. A polyp is an elevation above the mucosal surface. The majority of colorectal polyps are adenomas with malignant potential. Adenomatous colon polyps are premalignant, but only those with a villous component (50%-60% of all polyps) have a markedly increased tendency to become malignant.

Polyps must be removed endosco-pically for histological examination: when an infiltrating cancer is revealed, colon resection should be performed. Villous adenomas of the large bowel require total resection of the wall.

3. Most polyps are asymptomatic and find by chance on X-ray or on colonoscopy when patients are investigated for abdominal pain, intestinal malfunction, haemorrho-idal bleeding or some other causes.

4. The incidence of colorectal cancer is low in Africa and Asia and this

Раздел: КОЛОПРОКТОЛОГИЯ

Тема: колоректальный рак Цели изучения

Студент должен знать:

1. Большая часть колоректальных раков развивается путем образо-вания аденоматозных полипов из клеток слизистой оболочки с их трансформацией в инвазивный рак.

2. Полип представляет собой обра-зование, возвышающееся над поверхностью слизистой оболочки. Аденоматозные полипы являются предраком, ворсинчатые полипы из их числа (50-60% всех полипов) наиболее часто подвергаются озлокачествлению.

Полипы должны быть подверг-нуты гистологическому исследова-нию после эндоскопического уда-ления: в случае выявления рака пациент нуждается в резекции толстой кишки. Ворсинчатые аденомы требуют полнослойной резекции стенки кишки.

3. Полипы чаще клинически себя не проявляют и обнаруживаются случайно при рентгенологическом или эндоскопическом обследова-нии больных с болями в животе, дисфункцией толстой кишки, геморроидальным кровотечением или по другим причинам.

4. Болезнь является редкой в Африке и Азии, и эта особенность, вероят-

feature is thought to be largely environmental rather than racial. In the developed countries the inci-dence is rather high. In countries at low or intermediate risk, colorectal cancer is increasing.

5. There is a certain correlation between the consumption of meat and animal fats and colorectal cancer development.

6. In the colon certain bacteria convert bile acids into potential carcinogens.

7. The risk of colorectal cancer may be closely related to a positive family history. There is a 1.7 times increased lifetime risk of colorectal cancer if one first-degree relative is affected, but rises progressively with the number of affected family members. Patients with family polyposis almost invariably develop colorectal cancer at an more early age. Family polyposis requires total colectomy. The risk of colorectal cancer in patients with symptomatic ulcerative colitis may be 20%-25% in long-term cases (over 10 years).

8. About 90% of colorectal cancers occur in individuals who do not have a strong family history.

9. Any intestinal malfunction or rectal bleeding must be investigated, particularly in elderly people.

но, определяется окружающей средой, а не расовыми факторами. В развитых странах - высокие показатели заболеваемости. Часто-та колоректального рака увеличи-вается в странах с низким и средним уровнями заболеваемости.

5. Имеется зависимость заболевания колоректальным раком от употреб-ления мяса и животного жира.

6. В толстой кишке некоторые бакте-рии преобразовывают желчные кислоты в канцерогены.

7. Риск заболевания колоректальным раком может быть связан с наслед-ственной предрасположенностью. Вероятность развития рака увели-чивается в 1,7 раза, если болел один из близких родственников, и прогрессивно повышается с увели-чением больных раком в семье. У пациентов с семейным полипо-зом почти всегда развивается рак толстой кишки в более раннем возрасте. Семейный полипоз требует выполнения операции в объеме тотальной колэктомии. Риск заболевания колоректальным раком у больных с неспецифичес-ким язвенным колитом составляет 20-25% при анамнезе заболевания более 10 лет.

8. Приблизительно в 90% случаев ко-лоректального рака нет указаний на это заболевание у близких родственников больного.

9. Любое нарушения функции толс-той кишки или выделение крови из прямой кишки - показание к обсле-дованию, особенно у пожилых.

10. Faecal occult blood tests must use for mass screening for colorectal cancer.

11. Rectal cancer can be palpated by the digital rectal examination.

12. Colonoscopy is used to confirm tumor lesions and to obtain specimens for histological examination. Fifty percent of colo-rectal cancers are located within the reach of the proctosigmoidoscope (rectoromanoscope – RRS).

13. Abdominal and rectal ultrasound is performed prior to surgery to evaluate of the primary tumor size, its local and secondary (metastatic) spread.

14. Computed tomography (CT) and magnetic resonance imaging (MRI) are useful to evaluate hepatic metastases.

15. The primary tumor can be removed surgically in over 90% of cases. As a rule surgery is a method of choice and provides cure in a large percentage of cases. The segment of bowel with tumor is resected together with the lymph nodes draining it.

16. Preoperative radiation therapy is performed in large rectal cancers. Radiation therapy can decrease local recurrence and prolong survival period. Postoperative chemotherapy

10. Тесты на скрытую кровь в кале необходимо применять в скри-нинге колоректального рака.

11. Рак прямой кишки можно выявить при пальцевом исследо-вании прямой кишки.

12. Колоноскопия используется для подтверждения опухолевого по-ражения и взятия материала на гистологическое исследование. Метод проктосигмоскопии (рек-тороманоскопии – RRS) позво-ляет выявить 50% колоректаль-ных раков.

13. УЗИ брюшной полости и УЗИ ректальным датчиком произво-дятся до операции для оценки размера первичной опухоли, ее местного распространения и метастазирования.

14. Компьтерная томография и ЯМР полезны для подтверждения или исключения метастазов в печени.

15. Первичная опухоль может быть удалена хирургическим путем более чем в 90% случаев. Как правило, операция – первичный метод лечения в большинстве случаев колоректального рака. Пораженный отдел кишечника удаляется в едином блоке с регионарными лимфатическими узлами.

16. Показанием к предоперационной лучевой терапии являются боль-шие размеры опухоли прямой кишки. Лучевая терапия может предупредить развитие местного

is a consideration in patients with invasive tumors and those with metastases in lymph nodes.

17. Squamous cancers (syn. – cloaco-genic, epidermoid tumors) of the anus are treated successfully with radiotherapy (usually combined with chemotherapy).

18.Although the causes and patho-genesis of the tumors are similar throughout the large bowel, significant differences in the use of diagnostic and therapeutic methods differentiate colon and rectal tumors.

Practical skills:

1. history-taking procedure;

2. examination of the abdomen (inspection, palpation, percussion, auscultation);

3. interpretation of the history and results of examination using obtained knowledge of anatomy, physiology and pathology;

4. making diagnosis on the basis of laboratory tests and other investi-gations;

5. digital examination of the rectum;

6. to choose proper method of treatment and necessary variety of an operation.

рецидива опухоли и продлить жизнь пациента. Проведение послеоперационной химиотера-пии рассматривается у пациентов с агрессивными опухолями и метастазами в лимфоузлах.

17.Анальный плоскоклеточный рак хорошо лечится методом лучевой терапии (обычно в комбинации с химиотерапией).

18.Хотя причины и патогенез рако-вых опухолей толстой кишки являются сходными, важные раз-личия в применении диагности-ческих и лечебных методов требуют разграничения опухолей ободочной и прямой кишок.

Студент должен овладеть:

1. процессом опроса пациента о его жалобах и развитии заболевания.

2. обследованием живота (осмотр, пальпация, перкуссия, аускульта-ция).

3. интерпретацией данных анамнеза и обследования, основываясь на знаниях анатомии, физиологии и патологии.

4. диагностической гипотезой, кото-рая будет подтверждаться соот-ветствующими лабораторными и другими исследованиями.

5. пальцевым обследованием пря-мой кишки

6. знаниями, которые позволят избрать метод лечения и необхо-димый объем операции.

QUESTIONS TO ASSESS BASIC LEVEL OF KNOWLEDGE:

1. Anatomy of the large bowel (large intestine).

2. Blood supply to the large bowel.

3. Function (physiology) of the large bowel.

4. Macroscopical and microscopical forms of colorectal cancer.

BRIEF INFORMATION TO ANSWER THE QUESTIONS :

1. The large bowel extends from the ileocecal valve to the anus and is divided into five main segments. From proximal to distal these segments are: caecum with the vermiform (wormlike) appendix, ascending (right) colon, transverse colon, descending (left) colon, sigmoid colon and rectum. The hepatic flexure separates the ascending and the transverse colon and the splenic flexure separates transverse colon from the descending colon. Although the average total length of the large bowel is relatively constant (135 to 150 cm), the length of its anatomic divisions varies from person to person.

The large bowel contains the same circular muscular layer underneath the serosa as does the small intestine, but its outer longitudinal muscle layer is quite distinct. This outer longitudinal muscular coat consists of three separate longitudinal strips – the taeniae coli – which give the colon its characteristic appearance. At the level of the rectosigmoid junction, the taeniae generally coalesce and provide a complete longitudinal muscular coat for

ВОПРОСЫ ПО ИСХОДНОМУ УРОВНЮ ЗНАНИЙ:

1. Анатомия толстой кишки.

2. Кровоснабжение толстой кишки.

3. Функции толстой кишки.

4. Макро- и микроскопические фор-мы колоректального рака.

КРАТКИЕ ОТВЕТЫ НА ВОПРОСЫ ПО ИСХОДНОМУ УРОВНЮ ЗНАНИЙ:

1. Толстая кишка простирается от илеоцекального клапана до заднего прохода и подразделяется на пять основных отделов: слепая кишка с червеобразным отростком, восходя-щая ободочная, поперечно-ободочная нисходящая ободочная, сигмовидная кишка и прямая кишки. Печеночный изгиб отделяет восходящую и поперечно-ободочную кишки, селезе-ночный изгиб – поперечно-ободоч-ную и нисходящую ободочную киш-ки. Хотя средняя длина толстой кишки относительно постоянна (135–150 cm), длина его анатомических отделов может варьировать.

Толстая кишка содержит такой же циркулярный мышечный слой под серозной оболочкой, как тонкая кишка, но его внешний продольный мышечный слой весьма отличается. Он сконцентрирован в три отдельные продольные "полосы" – taeniae coli –что придает толстой кишке характер-ный вид. На уровне ректосигмоид-ного перехода, taeniae вообще соеди-няются и обеспечивают полный продольный мышечный слой для

the rectum. The state of contraction coli is what determines the typical configu-ration of the large bowel with successive sacculations, or protrusions, namely, haustra. On radiographs their appearance is quite characteristic. It allows a distinction of a normal large bowel from an abnormal large or small bowel. The third characteristic feature of the large bowel is the appendices epiploicae, which are extensions of peritoneal fat that hang off the antimesenteric side of the large bowel. The other characteristic features to the large bowel are the differences in diameter of the right and left colon, much higher location of the splenic flexure compared with the hepatic flexure, and the extraperitoneal nature of the pelvic rectum.

The rectum has an ill-defined ana-tomical beginning, the rectosigmoid junction lies opposite the sacral pro-montory. From the site the rectum follows the curve of the sacrum to end at the anorectal junction. At this point, the puborectalis muscle encircles the pos-terior and lateral area of the anorec-tal junction, creating the anorectal angle (normally 120°).

The rectum has three lateral curva-tures: the upper and lower are convex to the right, and the middle convex to the left (Houston's semicircular folds). That part of the rectum that lies below the middle valve has a much wider diame-ter and is known as the ampulla of the rectum. The adult rectum is approxima-tely 18-20 cm in length. The rectum is separated by Denonvilliers' fascia - from the prostate, and Waldeyer's fascia from the coccyx and last two sacral vertebrae. These fascial layers are surgi-

прямой кишки. Их сокращение опре-деляет типичную конфигурацию колон с последовательным мешко-видными расширениями (гаустрами). Их вид на рентгенограммах весьма характерен и позволяет различать нормальную толстую кишку от кишки с патологическими изменени-ями и тонкой кишки. Третье большое уникальное отличие заключается в наличии epiploicae (жировые привес-ки), которые состоят из жировой ткани и свисают с противобрыжееч-ной стороны толстой кишки. Другими характерными особеннос-тями толстой кишки являются различие в диаметре правой и левой половин толстой кишки, более высо-кое расположение селезеночного изгиба по сравнению с печеночным, экстраперитонеальное расположение тазового отдела прямой кишки.

Прямая кишка имеет условное анатомическое начало, ректосигмоид ный переход находится напротив промонториума. Отсюда прямая кишка повторяет искривления крест-ца, заканчиваться аноректальным пе-реходом. В этом месте, m.puborecta-lis, окружая сзади и сбоку область аноректального перехода, создает аноректальный угол (обычно 120°).

Прямая кишка имеет три боковых искривления: верхнее и более низ-кое – направо, среднее – налево (полукруглые складки Гаустона). Та часть прямой кишки, которая нахо-дится ниже средней складки, имеет наиболее широкий диаметр и назы-вается ампулой. Длина прямой киш-ки – приблизительно 18-20 см. Она отделена фасцией Денонвиллье от простаты и фасцией Валдейера – от

cally important as they act as a barrier to malignant penetration.

2. The cecum, ascending colon, hepatic flexure and proximal portion of the transverse colon receive arterial blood from the superior mesenteric artery.

The inferior mesenteric artery supplies blood to the distal transverse colon, splenic flexure, descending colon, and sigmoid via the left colic artery and branches of the sigmoid and superior rectal vessels. As the main vessels course through the mesentery toward the bowel wall, they bifurcate and form arcades at 1 to 2 cm from the mesenteric border. The arcades form a continuous chain of communicating vessels (the marginal artery of Drummond). Anastomosis between the superior and inferior mesenteric vessels is known as the anastomosis of Riolan (the arc of Riolan). The superior rectal artery is the direct continuation of the inferior mesenteric artery and is the main arterial supply of the rectum. A rich network of vessels that originate in both the middle and the inferior rectal arteries also supplies the rectum. The middle rectal artery arises on each side from the internal iliac artery and passes to the rectum in the lateral ligaments. The interior rectal artery arises on each side from the internal pudendal artery.

3. The main function of the colon is the absorption of water and electrolytes.

Approximately 2 L of fluid passes

копчика и последних двух крестцо-вых позвонков. Эти фасциальные слои имеют хирургическое значение, поскольку они препятствуют рас-пространению опухоли.

2. Слепая, восходящая ободочная кишка, область печеночного изгиба, и проксимальный отдел поперечно-ободочной кишки получают артери-альную кровь из верхней брыжееч-ной артерии.

Нижняя брыжеечная артерия кро-воснабжает дистальный отдел попе-речно-ободочной кишки, область селезеночного изгиба, нисходящую ободочную и сигмовидную кишки посредством левой толстокишечной, сигмовидных и верхней прямокишеч-ной артерий. В брыжейке магист-ральные сосуды раздваиваются и формируют аркады, которые образу-ют цепь сообщающихся сосудов (ар-терия Drummond). Анастомоз между верхней и нижней брыжеечными артериями известен как анастомоз Riolan (дуга Риолана). Верхняя пря-мокишечная артерия – прямое про-должение нижней брыжеечной арте-рии и главный источник артери-ального кровоснабжения прямой кишки. Богатой сетью сосудов, обра-зованных средней и нижней прямо-кишечными артериями, также обес-печивается кровоснабжение прямой кишки. Средние прямокишечные ар-терии отходят от внутренних под-вздошных артерий и проходят к киш-ке в боковых связках, нижние прямо-кишечные – от внутренних половых артерий.

3. Главная функция ободочной кишки – всасывание воды и электро-литов. Приблизительно 2 л жидкости

through the ileocaecal valve dayly. The absorption of fluid and electrolytes takes place mainly in the right side of the colon. And only about 150 mL of fluid is passed in the faeces.

The function of the rectum and anus in defaecation is complex. The rectum is usually empty. The entry of faeces from the colon produces relaxation of the internal sphincter and the puborectal muscle. This decreases the acute angle between the rectum and the anal canal. When the rectum contains approxima-tely 100 mL of faeces the urge to defecate is experienced. The rectum is emptied by relaxation of the external anal sphincter (under voluntary control) and an increase in intraabdominal pressure.

4. Microscopically, large bowel tumors are usually adenocarcinomas. Tumors of the anal canal are mostly of the squamous type. Macroscopically, the tumour may be one of five forms: annular, polypoid (cauliflower), diffusely infiltrating (tubular), ulcerative and colloid (mucocele). Cauliflower type is the least malignant form. The annular variety tends to give rise to obstructive symptoms whereas other forms commonly demonstrate bleeding.

проходит каждый день через илеоце-кальный клапан. Всасывание жидкос-ти и электролитов происходит глав-ным образом в правой половине обо-дочной кишки, и только приблизи-тельно 150 мл выделяется с калом.

Функция прямой кишки и заднего прохода в дефекации является слож-ной. Прямая кишка обычно пуста; при поступлении кала из ободочной кишки происходит расслабление внутреннего сфинктера и пуборек-тальной мышцы. Это уменьшает ост-рый угол между основной осью пря-мой кишки и осью анального канала. Когда прямая кишка содержит при-близительно 100 мл кала, появляет-ся позыв на дефекацию. Прямая киш-ка освобождается при расслаблении наружного анального сфинктера (процесс управляем человеком) и увеличении внутрибрюшного дав-ления.

4. Микроскопически раки толстой кишки – обычно аденокарциномы, раки анального канала имеют глав-ным образом форму плоскоклеточ-ного рака. Макроскопически опухоль может иметь одну из пяти форм: стенозирующую, экзофитную (поли-повидную), инфильтративную, язвен-ную и слизистую (коллоидную). Экзофитный тип опухоли – наименее злокачественная форма. Стенозиру-ющие формы вызывают кишечную непроходимость, тогда как другие обычно проявляют себя кровотече-нием.

KEY QUESTIONS FOR HOMEWORK:

1. Diseases of the large bowel having malignant potential.

2. Clinical classifications of colon and rectal tumors.

3. Metastatic spread of colorectal cancer.

4. Clinical features of colorectal cancer.

5. Diagnostic procedures (investiga-tions).

6. Screening of colorectal cancer.

7. Surgical management. Types of surgical treatment.

8. Rehabilitation.

9. Follow-up.

BRIEF INFORMATION TO ANSWER THE QUESTIONS :

1. Diseases of the large bowel, which have malignant potential:

• polyps of the large bowel;

• nonspecific inflammatory bowel disease.

Polyps of the large bowel (classification of polyps – see Table 1)

Adenomatous polyps and family adenomatous polyposis have signifi­cant malignant potential. Family adenoma-tous polyposis inevitably leads to cancer development. The risk of malignancy in an adenoma depends on the size of tumor. Peutz-Jeghers polyps and Juvenile polyps have minimal malignant potential.

ВОПРОСЫ ДЛЯ САМОПОДГОТОВКИ

1. Предопухолевая патология толс-той кишки.

2. Клинические классификации коло-ректального рака.

3. Метастазирование колоректаль-ного рака.

4. Клинические проявления.

5. Диагностические мероприятия.

6. Скрининг коллоректального рака.

7. Варианты хирургического лечения.

8. Реабилитация.

9. Отдаленные результаты.

КРАТКИЕ ОТВЕТЫ НА КЛЮЧЕВЫЕ ВОПРОСЫ

1. Предопухолевая патология толс-той кишки.

• полипы толстой кишки;

• неспецифические воспалительные заболевания толстой кишки.

Полипы толстой кишки (классифика-ция полипов – см. табл. 1).

Аденоматозные полипы и семейный аденоматозный (диффузный) поли-поз отличаются наиболее вероятным риском малигнизации. Семейный аденоматозный (диффузный) поли-поз является облигатным предраком. Риск малигнизации в аденоме повышается с увеличением размера опухоли. Малигнизация полипов не характерна для полипоза Пейтц-Егерса (Джегерса) и ювенильного полипоза.

Table 1

Classification of large bowel polyps

Классификация полипов толстой кишки

Nonspecific inflammatory bowel diseases.

Two major forms of nonspecific inflammatory bowel diseases are recognized: Crohn's disease and ulcerative colitis. Crohn's disease affects any part of the GI tract. Ulcerative colitis affects only the large bowel. In 10% of clinical colitis cases Crohn's disease and ulcerative colitis cannot be differentiated. Some experts consider these conditions represent two types of the same disease.

Crohn's disease can involve one small area. There also may bee multiple spread with relatively normal areas between them (so called «skip lesions»). The whole colon can also be effected (total colitis).

Ulcerative colitis can affect the rectum alone (proctitis). It can extend proximally to involve the sigmoid and descending colon («left-sided colitis»), or may involve the whole colon («total colitis»).

The incidence of carcinoma is 3‑5% in both conditions. Carcinoma is unlikely to develop in Crohn's disease. Risk of carcinoma development does not depend on the duration of treatment. In ulcerative colitis the risk of colon carcinoma is higher in a patient with 10 year-old total colitis. Ulcerative colitis is the nonobligative precancer.

Неспецифические воспалительные заболевания толстой кишки.

Основными формами неспецифичес-ких воспалительных заболеваний толстой кишки признаны: болезнь Крона, которая может поражать любую часть желудочно-кишечного тракта, и неспецифический язвенный колит, который считается самостоя-тельным заболеванием толстой кишки. В 10% клинических наблю-дений невозможно различить язвен-ный колит от болезни Крона толстой кишки. Не исключается, что эти забо-левания представляют две разновид-ности одной и той же болезни.

В болезнь Крона может вовле-каться часть кишки или обширные области с наличием неизмененных отделов между пораженными участ-ками («скачущий характер пораже-ния»). Болезнь Крона может пора-жать всю толстую кишку.

В язвенный колит может быть вовлечена прямая кишка (проктит), патологический процесс может рас-пространяться проксимально с вовле-чением сигмовидной и нисходящей ободочной кишок («левосторонний колит») или поражать всю толстую кишку («тотальный» колит).

Вероятность развития рака увеличена при обоих патологических состояниях (3-5%). Развитие рака при болезни Крона маловероятно и не зависит от лечения. Риск рака у пациентов с язвенным колитом выше после 10 лет консервативного лече-ния по сравнению с частотой его выявления в общей популяции насе-ления. Неспецифический язвенный колит является факультативным предраком.

2. Different approaches to classification of colon and rectum tumors.

Table 2

2. Клинические классификации для опухолей ободочной и прямой кишок.

* ESMO - Европейское общество медицинской онкологии (ЕвМО).

Classification of colon and rectum cancer spread (TNM-classification):

T – Primary Tumor

T_x – Primary tumor cannot be assessed.

T₀ – No evidence of primary tumor.

T_is – Carcinoma in situ (tumor invades only mucosa or malignanc polyps).

T₁ – Tumor invades submucosa.

T₂ – Tumor invades muscular layer of the intestinal wall.

T₃ – Tumor invades through muscular layer of the intestinal wall into subserosa or into nonperitoneali-zed pericolic or perirectal tissues.

T₄ – Tumor perforates visceral peritoneum or directly invades other organs or structures.

Note: Direct invasion in T4 includes invasion into other segments of the colorectum through serosa, e.g. invasion of caecum carcinoma into the sigmoid colon.

N – Regional Lymph Nodes

N_x – Regional lymph nodes cannot be assessed.

N₀ – No regional lymph node metastasis.

N₁ – Metastasis in 1-3 pericolic or perirectal lymph nodes.

N₂ – Metastasis in 4 or more pericolic or perirectal lymph nodes.

N₃ – Metastasis in any lymph node localed along major blood vessels.

Классификация распространения рака толстой кишки по системе TNM:

Т – первичная опухоль

Т_х – Недостаточно данных для оценки первичной опухоли.

Т₀ – Первичная опухоль не опреде-ляется.

Т_is – Инвазия только слизистой обо-лочки, до базальной мембраны (малигнизированный полип).

Т₁ – Опухоль распространяется на подслизистой слой стенки кишки.

Т₂ – Опухоль распространяется на мышечный слой стенки кишки.

Т₃ – Опухоль распространяется на субсерозу и ткани, прилежащие к неперитонизированным участкам ободочной и прямой кишок.

Т₄ – Опухоль прорастает висцераль-ную брюшину или непосредст-венно распространяется на сосед-ние органы и структуры.

Примечание: Прямая инвазия при Т₄ включает распространение на другие сегменты толстой кишки путем прорастания серозы, например, инвазия опухоли сле-пой кишки в сигмовидную.

N – регионарные лимфоузлы

N_х – Недостаточно данных для оцен-ки регионарных лимфоузлов.

N₀ – Нет метастатического пораже-ния регионарных лимфоузлов.

N₁ – Метастазы в 1-3 околокишечных лимфатических узлах.

N₂ – Метастазы в 4 и более околоки-шечных лимфатических узлах.

N₃ – Метастазы в лимфатических уз-лах, расположенных вдоль любо-го из магистральных сосудов.

M – Distant metastasis

M_x – Distant metastasis cannot be assessed.

M₀ – No distant metastasis.

M₁ – Distant metastasis.

Duke’s staging

A – The growth is within the intestinal wall. Favourable prognosis.

B – The growth is extended to the extracolic or extrarectal tissues, but no metastasis to the regional lymph nodes. Relatively favourable prognosis.

C – There are secondary deposits in the regional lymph nodes. These are subdivided into C₁, in which the local pericolic or pararectal lymph nodes alone are involved, and C₂, in which the nodes accompanying the supplying blood vessels are implicated up to the point of division. Cases of hematogenous metastases or metastases in regional lymph nodes are not taken into account. Poor prognosis.

Stage D (it was not described by Duke) signifies the residual disease following surgery or the presence of widespread metastases, mainly hepatic.

Other staging systems have been developed (e.g. Astler-Coller, ESMO) to improve prognostic accuracy.

The TNM clas­sification is now recognised internationally as the optimal classification of staging.

M – Отдаленные метастазы

М_х – Недостаточно данных для опре-деления отдаленных метастазов

М₀ – нет отдалённых метастазов;

M₁ – имеются отдалённые метастазы.

Классификация Dukes

A – Опухолевый рост ограничен стенкой толстой кишки. Прогноз считается благоприятным.

B – Опухоль распространяется за пределы кишки при отсутствии метастазов в региональных лимфо-узлах. Прогноз считается относи-тельно благоприятным.

C – Имеются метастазы в региональ-ных лимфоузлах (C₁ – единичные метастазы в региональных лимфо-узлах, C₂ – метастазы по ходу магистральных сосудов, крово-снабжающих пораженный отдел кишечника, от уровня их отхож-дения). Исключаются случаи с гематогенными метастазами и метастазами в отдаленных лимфа-тических узлах. Прогноз считается неблагоприятным.

Часто выделяется стадия D (не счита-ется предложением Dukes). Эта ста-дия обозначает наличие нерадикаль-но удаленной опухоли или отдален-ных метастазов, обычно – в печени.

Для более точного прoгнозиро-вания предложены модификации клинических классификаций (напри-мер: Astler-Coller, ЕвМО).

TNM-классификация является международной и общепризнанной.

Early colorectal cancer.

Early colorectal cancer is carcinoma that invades as far as the submucosa. Patients having this type of cancer demonstrate a five-year survival rate about 90%.

3. Metastatic spread of colorectal cancer.

Colorectal cancer spreads directly into the adjacent organs and struc­tures. Metastatic spread occurs by both the lymph and blood streams; most colon cancers metastasize to the retroperitoneal periaortic nodes following the mesenteric vessels. Anal carcinomas spread more commonly to the groin nodes, rather than retroperitoneally. Distant spread by blood stream affects, in particular, the liver, as well as the lungs and bone. Rectal cancers (below the peritoneal reflection) tend to spread laterally into the pelvic tissues and then directly to the lungs. Anal carcinoma may extend directly into the sphincters, perianal tissues, vagina, or prostate, and it tends to metastasize to lymph nodes behind the rectum and in the groins.

4. Clinical manifestations.

Alteration in bowel habit, with or without abdominal pain, is a common symptom of left-sided colonic lesions. Rectum and sigmoid carcinomas usually discharge blood mixed in with the stool. Sigmoid lesions more commonly cause obstructive symptoms.

Ранний колоректальный рак.

К раннему колоректальному раку относят опухоли, распространяю-щиеся не глубже подслизистого слоя. Пятилетняя выживаемость пациентов с эти видом рака составляет почти 90%.

3. Метастазирование колоректаль-ного рака.

Колоректальный рак распространяет-ся непосредственно в окружающие органы и структуры. Метастазирова-ние происходит гематогенным и лим-фогенным путями; раковые опухоли ободочной кишки главным образом метастазируют в забрюшинные пара-аортальные лимфоузлы по ходу мезентериальных сосудов. Анальные раки метастазируют как правило в паховые, с меньшей вероятностью – в забрюшинные лимфоузлы. Отда-ленное метастазирование происходит гематогенно наиболее часто в печень, а также в легкие и кости. Раки пря-мой кишки склонны распространять-ся на окружающие ткани и органы малого таза, а затем гематогенно метастазируют прямо в легкие. Анальный рак может распростра-няться на близрасположенный сфинктер, перианальные ткани, вла-галище или простату, что сопровож-дается метастазированием в позади-прямокишечные и паховые лимфо-узлы.

4. Клинические проявления.

Изменение функции толстой кишки, с или без абдоминальной боли, является распространенным симпто-мом поражения ее левых отделов. Раки прямой и сигмовидной кишок обычно проявляются кровотечением, кровь смешивается с калом. Рак сиг-

Rectal cancers cause obvious bleeding with defecation and a feeling of incomplete evacuation when the tumor becomes larger. Symptoms of the anal carcinoma (bleeding, pain and a mass) are often mistakenly attributed to hemorrhoids. Carcinoma of the caecum may become large and be asymptomatic. It can present simply as an iron-deficiency anemia or anemia with unknown etiology. Elderly people are often admitted to the hospital with intestinal obstruction.

5. Diagnostic procedures (investiga-tions).

Diagnostic procedures include:

1. in order to exclude or confirm local spread (for evaluation of tumor size and local spread):

• digital examination;

• proctosigmoidoscopy (colonoscopy);

• rectal ultrasound;

• CT- or MRI-scanning;

• barium enemas (Double-contrast barium enema);

• urography;

• cystoscopy;

2. biopsy of the tumor provides proof of cancer development;

3. additional investigations to detect metastases (for evaluation of meta-stases size and secondary spread):

• chest and bone X-rays;

• liver scanning (abdominal ultrasound and CT or MRI);

4. other diagnostic procedures:

• laboratory studies (blood count and routine biochemistry);

мовидной кишки часто сопровожда-ется развитием признаков кишечной непроходимости. Раки прямой кишки кровоточат при дефекации и могут вызывать чувство неполного опорож-нения прямой кишки, когда опухоль становится большой. Симптомы анального рака (кровотечение, боль, узловое образование) часто ошибоч-но объясняются геморроем. Рак сле-пой кишки даже при больших размерах опухоли могут протекать бессимптомно. При этом может выявляться железодефицитная или необъяснимая анемия. Пациенты пожилого возраста часто поступают с симптомами кишечной непроходи-мости.

5. Диагностические исследования.

1. Чтобы исключать или подтвердить местное распространение (для оценки размера опухоли и местного распространения): пальцевое иссле-дование прямой кишки; проктосиг-москопия (колоноскопия); эндорек-тальное ультразвуковое исследова-ние; компьютерное и ЯМР-сканиро-вание; ирригография (в том числе – по методике двойного контрастиро-вания); урография; цистоскопия.

2. Биопсия доказывает наличие рака.

3. Дополнительние исследования, с целью обнаружить метастазы (для оценки размера метастазов и распространенности метастазирова-ния): рентгенологическое обследо-вание грудной клетки и костей; сканирование печени (УЗИ брюшной полости, КТ или ЯМРТ);

4. Другие диагностические проце-дуры:

• лабораторные исследования (анализ крови и обычная биохимия);

• carcinoembryonic antigen (CEA) is often elevated in colorectal cancer. It is use for early diagnosis. It can also be used to detect recurrence.

• fecal occult blood tests for mass screening. But they are of no value in hospital practice.

6. Screening of the colorectal cancer.

Fecal occult blood test is used for screen­ing and is being applied widely. Patients with positive tests are studied further with sigmoidoscopy, barium enemas, and colonoscopy. Annual occult blood stool testing is aimed at both detection of earlier stage cancers and improved long-term survival. Screening sigmoidoscopies are recommended every 4-5 years. Any screening strategy utilizing sigmoido-scopy also requires a colonoscopy to follow any positive sigmoidoscopy to look for synchronous lesions in the more proximal colon. In the lack of screening programs, the existence of colon and rectal cancer must be suspected because of the history. Changes in bowel habits, blood in stools, tenesmus, mucoid discharge, anemia with unknown etiology, and weight loss are suggestive symptoms.

• определение уровня карцино-эмбрионального антигена (CEA) – часто повышается при колоректаль-ном раке. Не доказано значение этого исследования для установления ран-него диагноза рака, но имеет значе-ние в выявлении рецидивов заболева-ния прежде, чем появятся клиничес-кие симптомы. В этом случае повтор-ные операции имеют больше шансов на успех.

• Анализ кала на скрытую кровь – используется для скрининга рака, но не имеют значения для выбора методов лечения.

6.Скрининг колоректального рака.

Анализ кала на скрытую кровь разра-ботан и широко используется для скрининга колоректального рака. Пациенты с положительным тестом подлежат дальнейшему обследова-нию методами сигмоскопии, колоно-скопии или ирригографии. Ежегод-ное исследования кала на скрытую кровь позволяет выявить опухоли на более ранних стадиях развития, что улучшает результаты лечения. Сиг-москопию с целью скрининга реко-мендуется выполнять каждые 4-5 лет. Любой скрининг, предусматриваю-щий сигмоскопию, при выявлении опухоли требует последующего выполнения колоноскопии, чтобы исключить синхронные опухоли в вышележащих отделах ободочной кишки. В отсутствии программ скри-нинга, рак толстой кишки должен быть заподозрен по анамнестическим данным. Нарушения функций киш-ки, кровь в кале, тенезмы, слизистые выделения, необъясненная анемия и потеря веса – симптомы, позволяю-щие заподозрить рак.

7.Types of surgical treatment.

Radical operations are designed to remove the primary tumor and its draining local lymph nodes. The extent of resection is determined by the location of the tumor, its blood supply and draining lymphatic vessels, and the lack of direct extension into adja­cent organs. Manipulation of the tumor should be careful because tumor cells easily dissiminate and reimplant within the peritoneal cavity. There is some evidence that early division of major blood vessels supplying the involved colon can slightly improve the number of successful operations.

Cancer of the caecum or ascending colon. Cancer of the caecum or ascending colon is treated when resectable by right hemicolectomy. Anastomosis is performed between the terminal ileum and the transverse colon.

Cancer of the hepatic flexure.

When the hepatic flexure is involved, the resection must be extended correspondingly (an extended right hemicolectomy). Anastomosis is performed between the terminal ileum and the proximal left colon.

Cancer of the transverse colon.

When there is no obstruction, excision of the transverse colon together with the transverse mesocolon and the greater omentum, followed by end-to-end anastomosis, can be used. An alternative is an extended right hemicolectomy.

7. Варианты хирургического лече-ния. Операции предусматривают удаление первичной опухоли с зоной регионарных лимфатических узлов. Протяженность резекции кишки зависит от местоположения опухоли, особенностей кровоснабжения и лимфооттока, наличия распростране-ния опухоли на соседние органы. При возможности необходимо избе-гать лишних манипуляций с опухо-лью, поскольку опухолевые клетки, как известно, легко диссеминируют и имплантируются в пределах брюш-ной полости. Доказано, что изначаль-ная обработка сосудов, участвующих в кровоснабжении отдела кишки, пораженного опухолью, улучшает результаты лечения.

Рак слепой и восходящей ободоч-ной кишки. Радикальной операцией является правосторонняя гемикол-эктомия. Анастомоз после резекции накладывается между подвздошной и поперечноободочной кишками.

Рак области печеночного изгиба ободочной кишки. При локализации опухоли в области печеночного изгиба границы резекции ободочной кишки расширяются (расширенная правосторонняя гемиколэктомия). Анастомоз после резекции наклады-вается между подвздошной кишкой и проксимальными отделами левой половины ободочной кишки.

Рак поперечноободочной кишки. При отсутствии непроходимости выполняется резекция поперечнообо-дочной кишки вместе с ее брыжей-кой и большим сальником. Альтерна-тивной операцией является расши-ренная правосторонняя гемикол-эктомия.

Cancer of the splenic flexure or descending colon.

Left hemicolectomy is the procedure of choice for descending colon tumors. Anastomosis is performed between the transverse and sigmoid colon. When the splenic flexure is involved, the resection must be extended correspondingly (an extended left hemicolectomy). Anastomosis is performed between the distal right and sigmoid colon. Sometimes removal of the colon up to the ileum (the subtotal colectomy), with an ileorectal anastomosis, is preferable.

Cancer of the sigmoid colon.

Sigmoidectomy is oncologically adequate for tumours of the sigmoid colon.

Subtotal colectomy.

Subtotal colectomy is indicated for multiple primary tumors. Subtotal colectomy is sometimes termed as total colectomy. Subtotal colectomy involves removal of the colon from the cecum to the peritoneal reflection, with an ileorectal anastomosis. Due to loss of the absorptive capacity of the colon, this procedure results in a high postoperative stool frequency.

Cancer of the rectum.

The choice of surgery is determined by the distance of the tumor from the

Рак области селезеночного изгиба и нисходящего отдела ободочной кишки. Левосторонняя гемиколэкто-мия является операцией выбора при раке нисходящего отдела ободочной кишки. Анастомоз после резекции кишки накладывается между попе-речноободочной и сигмовидной киш-ками. При локализации опухоли в области селезеночного изгиба грани-цы резекции ободочной кишки рас-ширяются (расширенная левосторон-няя гемиколэктомия). Анастомоз после резекции накладывается между дистальными отделами правой поло-вины ободочной и сигмовидной киш-ками. Иногда предпочтительным является удаление ободочной кишки до уровня терминального отдела подвздошной кишки с наложением илеоректального анастомоза (субто-тальная колэктомия).

Рак сигмовидной кишки. Резекция сигмовидной кишки при ее опухоле-вом поражении является адекватной операцией с точки зрения онкологи-ческих принципов.

Субтотальная колэктомия. Суб-тотальная колэктомия показана при наличии множественных первичных опухолей. Субтотальная колэктомия (иногда упоминается как тотальная колэктомия) предусматривает удале-ние всей ободочной кишки с после-дующим наложением илеоректоана-стомоза. Из-за потери абсорбционной способности в связи с удалением ободочной кишки, после этой операции отмечается учащение количества актов дефекации.

Рак прямой кишки. Выбор спосо-ба операции во многом определяется

dentate line. A important general principle is that the ends of the colon and rectum to be anastomosed after resection should have a good blood supply and be seen to bleed arterial blood. Ischemia is the main cause of anastomotic failure and subsequent leakage.

Basic types of operations:

1) anterior resection (lesions located 5 to 6 cm above the dentate line). Stapling instruments, first developed in Russia, are now widely used to perform anastomoses.

High anterior resection of the rectum is a colorectal resection with anastomosis of the sigmoid colon to intraperitoneal rectum.

Low anterior resection of the rectum is a colorectal resection with anastomosis of the sigmoid colon to extraperitoneal rectum.

Low anterior resection of the rectum with coloanal anastomosis is a colorectal resection with anastomosis of the colon to the anal canal circumferen-tially.

2) abdominoperineal resection (lesi-ons located 5 to 6 cm to the dentate line).

Complete removal of the rectum and anus, by concomitant dissection through the abdomen and perineum, with permanent closure of the perineal rafe and creation of an end colostomy is called the Quenu’s and Miles’ opera-tion. The abdominal portion of the procedure reaches the level of the levator ani muscles, with removal of the

расстоянием края опухоли от зуб-чатой линии. Важным общим прин-ципом наложения межкишечного анастомоза по типу «конец в конец» является хорошее кровоснабжение, как замечено с краев разреза при этом выделяется алая (артериальная) кровь. Ишемия – основная причина несостоятельности швов анастомоза.

Основные типы операций:

1. передняя резекция (нижний край опухоли располагается выше 5-6 см от зубчатой линии). Для наложения межкишечных анастомозов сейчас широко применяются сшивающие аппараты, первоначально разрабо-танные в России.

Высокая передняя резекция прямой кишки – резекция с анастомозом сигмовидной кишки и интраперито-неальной части прямой кишки.

Низкая передняя резекция прямой кишки – резекция с анастомозом сигмовидной кишки и экстраперито-неальной части прямой кишки.

Низкая передняя резекция прямой кишки с колоанальным анастомо- зом – резекция с анастомозом ободочной и прямой кишок по окружности в анальном канале.

2. брюшно-промежностная экстирпа-ция (нижний край опухоли распола-гается на расстоянии 5-6 см от зубчатой линии).

Полное удаление прямой кишки и ануса из брюшного и промежност-ного доступа с закрытием промеж-ностной раны и наложением коло-стомы называется операцией Кеню-Майлса. Абдоминальный этап опера-ции предусматривает достижение уровня мышцы, поднимающей зад-ний проход, путем диссекции вдоль

entire mesorectum and dissection to and along the parietal endopelvic fascia. The perineal portion of the operation removes the anorectal junction and distal rectum, as well as the anal sphincter mechanism.

3) sphincter-sparing procedures.

Although the Quenu’s and Miles’ operation (abdominoperineal resection) is the gold standard for the treatment of distal rectal cancers. Patients with local disease may be adequately treated with sphincter-sparing procedures. To reach adequate continence after resection of the rectum, both sphincter muscles – the puborectalis and the levator ani – must be preserved, as well as the sympathetic and parasympathetic innervation of these muscles, which derives from the sacral plexus.

4) Hartmann's operation.

Hartmann's operation is an anterior resection of the rectum without anastomosis. The proximal bowel end is brought out as a left iliac fossa colostomy and the rectal stump is oversewn. The operation is usually performed as a palliative procedure or sometimes as a procedure for acute cases (acute malignant colonic obstruct-tion, peritonitis from perforation of rectal cancer or bleeding, a much more advanced tumor).

Now it is possible to perform a high anterior resection, hemicolectomy and other operations laparo-scopically.

пристеночной внутритазовой фасции. Промежностный этап операции пре-дусматривает удаление зоны анорек-тального перехода, дистальных отде-лов прямой кишки и мышц анального сфинктера.

3. сфинктер-сохраняющие операции.

Хотя операция Кеню-Майлса являет-ся золотым стандартом для лечения раковых опухолей дистального отдела прямой кишки, пациентов с местно нераспространенными раками можно лечить с применением сфинктер-сохраняющей операции. Чтобы сфинктер оставался функцио-нально состоятельным после резек-ции прямой кишки, должны быть сохранены обе мышцы сфинктерного аппарата – пуборектальная и подни-мающая задний проход, а также симпатическая и парасимпатическая иннервация этих мышц, исходящая из сакрального сплетения.

4) Операция Гартмана, в сущности, является передней резекцией прямой кишки, но без наложения межкишеч-ного анастомоза. Проксимальный отдел кишки выводится в левой подвздошной области с формирова-нием колостомы, а культя прямой кишки ушивается. Операция обычно выполняется как паллиативная или иногда – в неотложных случаях (острая опухолевая толстокишечная непроходимость, перитонит с перфо-рацией рака прямой кишки или кровотечение, местнораспространен-ная опухоль).

В настоящее время возможно вы-полнение высокой передней резек-ции прямой кишки, гемиколэкто-мии и других операций лапаро-скопическим методом.

Colostomy.

Colostomy is an artificial opening made in the large bowel to divert faeces to the exterior, where it can be collected in an external appliance. A wide range of disposable adhesive bags are available now. Depending on the purpose for which the diversion has been necessary, colostomy may be temporary or permanent.

When the obstructing tumors present in the left colon or rectum, a single stage operation is seldom performed. If a resection can be carried out, an end proximal colostomy should be done. Otherwise, a proximal defunctioning colostomy alone is done. The defunctioning colostomy can be carried out in the sigmoid colon or transverse colon. A proximal colostomy must be performed in these cases as a first stage, with resection of the tumor deferred until proper conditions can be secured. The site of the colon or rectum obstruction and the general condition of the patient determine whether a colostomy is indicated.

Solitary liver metastasis.

The presence of a solitary liver metastasis does not necessarily rule out the feasibility of a radical excision. Many instances have been reported where a presumed solitary liver metastasis has been resected either at the time of excision of the large bowel or subsequently with long-term survival being achieved.

Колостомия. Колостома – искус-ственно наложенный свищ на один из отделов толстой кишки. Выделяю-щийся кал может быть собран в кало-приемник. В настоящее время досту-пен широкий выбор одноразовых фиксирующихся калоприемников. В зависимости от цели, для которой было предпринято оперативное вме-шательство, колостома бывает вре-менной или постоянной.

Когда опухоль, обтурирующая просвет кишки, располагается в ле-вой половине ободочной или прямой кишках, операция редко выполнима в один этап. Если может быть выпол-нена резекция, то должна быть нало-жена концевая колостома на приво-дящий отдел кишки. В других слу-чаях проксимально должна быть наложена декомпрессивная колосто-ма. Она может быть сформирована на сигмовидной или поперечноободоч-ной кишках. В этих случаях колосто-ма на приводящий отдел кишки должна быть наложена как первый этап, резекция по поводу опухоли откладывается, пока не будет долж-ных условий для ее выполнения. Локализация кишечной непроходи-мости в толстой кишке и общее состояние пациента определяют, показана ли колостомия.

Солитарные метастазы в печени. Наличие солитарного метастаза в печени не исключает его радикального удаления. Имеется много сообщений об удалении солитарных метастазов в печени либо во время резекции толстой кишки или в последующем с достижением хороших отдаленных результатов лечения.

8.Rehabilitation.

A good rehabilitation program benefits the colostomy patients in returning to normal life. Special programs have been developed in which patients are instructed in the use of irrigation in order to limit discharge to a once-per-day occurrence. Patients must been trained to manage a variety of problems related to the colostomy (odor, leakage, equipment, sexual readjustment, etc.).

9. Follow-up.

The incidence of subse­quent (metachronous) polyps and/or cancer is high, approaching a total of 15%-20% after 15-20 years. These should be diagnosed and treated early. Since patients who have had one colorectal cancer are at much higher risk than other patients, periodic colonoscopy is appropriate. If careful examination of the entire large bowel was not done either preoperatively or at the time of surgery, early follow-up (within 3-4 months) is important because of the high risk of synchronous polyps or carcinomas. Then colonoscopies should be perfopmed periodicaly (every 6-12 months during 5 years, then every 2-3 years). Follow-up for the possibility of recurrences is also very important because some recurrences have a significant chance of being cured:

1) anastomotic recurrences;

8. Реабилитация.

Хорошая программа реабилита-ции помогает возвратиться колосто-мированным пациентам к нормаль-ной жизни. Разработаны специаль-ные программы, в которых пациенты проинструктированы в использова-нии ирригации для того, чтобы ки-шечник опорожнялся один раз в день. Пациенты должны быть обу-чены решению различных проблем, связанных с колостомой (запах, исте-чение жидкого кала, специальные приспособления, вопросы сексуаль-ных отношений и т.д.).

9.Отдаленные результаты.

Выявление последующих (метахрон-ных) полипов и/или рака является частым, приближается к 15-20% после 15-20 лет. Они должны быть диагностированы и своевременно подвергнуты лечению. Поскольку больные, лечившиеся по поводу колоректального рака, имеют более высокий риск повторного заболева-ния, чем другие пациенты, им необ-ходимо периодически выполнять колоноскопию. Если тщательного обследования всей толстой кишки не проведено до или во время операции, важно продолжить обследование (в первые 3-4 месяца) из-за высокого риска синхронных полипов или рака. Затем колоноскопии должны выпол-няться периодически (каждые 6-12 месяцев в течение 5 лет, потом каждые 2-3 года). Продолжение наблюдения за больными также очень важно в связи с возможностью рецидивов рака, некоторые из которых могут быть подвергнуты лечению:

1) рецидивы в области анастомоза;

2) pelvic recurrences that are not fixed to the lateral pelvic walls;

3) apparently single metastases in the liver or (less often) in the lung after a fairly long disease-free interval (1-2 years or more)

2) рецидивы в полости малого таза, не фиксированные к его боковым стенкам;

3) явно одиночные метастазы в печени или (менее часто) в легком после довольно длительного безреци-дивного периода (1-2 года или больше).

TESTS

1. The superior rectal artery arises from the -

a) Superior mesenteric artery

b) Inferior mesenteric artery

c) Internal illiac artery

d) Internal pudendal artery

2. Middle rectal artery is branch of......... artery :

a) Internal iliac

b) Internal pudendal

c) External iliac

d) Femoral

3. Fascia of Denonvilliers -

a) Membranous layer of fascia of the thigh

b) Perirenal fascia

c) Fascia between the rectal ampulla and the prostate and the seminal vesicles

d) Posterior layer of perirenal fascia

4. Muscle which is primarily responsible for rectal continence -

a) Ext. sphincter

b) Int. sphincter

c) Puborectalis

d) Sacrococcygeous

5. Internal sphincter of rectum is formed by -

a) Levator ani

b) Puborectalis

c) Longitudinal muscle fibres condensation

d) Circular muscles fibres condensation

6. Ulcerative colitis almost always involves the ... -

a) Caecum

b) Sigmoid

c) Right colon

d) Rectum

7. Predisposing factors for colonic carcinomas - a) Familial polyposis

b) Gardener's syndrome

c) Juvenile polyp

d) Chronic ulcerative colitis

8. Tenesmus occurs in lesions of - a) ileum

b) Right side of colon

c) Descending colon

d) Sigmoid colon

9. Sulfonamide useful in treating ulcerative colitis is -

a) Sulfadiazine

b) Sulfasalazine

c) Sulfamethoxazole

d) Sulfadimidine

10. Highest risk for malignancy in colon is for -

a) Gardners syndrome

b) Ulcerative colitis

c) Crohn’s disease

d) Familial polyposis

11. Which is true of Ulcerative colitis -

a) Sting sign of kantor positive

b) Skin lesions are seen

c) Rectum is always invlolved

d) Fistulas are common

12. Which is not true of arthritis associated with inflammatory bowel disease -

a) Migratory arthritis

b) Knee joint most common

c) Deformities are common

d) Correlates to severity of colitis

13. Prophylactic polypectomy is done in -

a) Peutz Jegher’s syndrome

b) Gardner's syndrome

c) Familial polyposis

d) None of the above

14. The incidence of carcinoma of the caecum in relation to colonic adenocarcinoma is -

a) 2%

b) 4.5%

c) 20%

d) 44'%

e) 62%

15. The appearance of anastamotic leakage following a low colonic anastomosis most often mainfests -

a) 1-4 days

b) 5-10 days

c) 11-15 days

d) 16-20 days

e) None of the above

16. The most likely cause for suture leak after colon resection and anastomosis for cancer sigmoid is -

a) Subclinical malnutrition

b) Infection of anastomotic site

c) Mechanical disruption due to colonic pressure and contractility

d) Ischemia

17. The adenomatous polyps of large bowel are most often situated in -

a) Ascending colon

b) Transverse colon

c) Descending colon

d) Sigmoid colon

18. Which of the following is not a precancerous condition of colon -

a) Irritable bowel syndrome

b) Ulcerative colitis

c) Familial polyposis

d) All

19. Toxic megacolon is a complication of -

a) Ulcerative colitis

b) Crohn's

c) Aganglionic megacolon

d) Ischemic colitis

20. False regarding involvement in Crohn’s disease -

a) Anorectal area

b) Rectum

c) Small intestine with Rt. colon

d) Large intestine alone without involvement of small intestine

21. Most precancerous condition for carcinoma colon is -

a) Familial polyposis

b) hamartomatous polyps

c) Juvenile polyps

d) Hyperplastic polyps

22. Duke's stage C2 refers to carci-noma –

a) Bladder penetrating the extravesical fat

b) Bladder with metastasis to internal iliac lymph nodes

c) With histological features of 75% anaplastic cells

d) Rectum with metastasis to inferior mesentric lymph nodes

23. Carcinoma of the colon is associated with all of the following except -

a) Low residue diet

b) Vegetarian diet

c) Ulcerative colitis

d) Familial polyposis

24. Best investigation for carcinoma colon -

a) Barium enema

b) Colonic biopsy

c) Clinical examination

d) Colonoscopy

25. Regarding incidence of carcinoma colon in ulcerative colitis which is true -

a) Arise from pseudopolyps

b) Increased incidence if age of onset of ulcerative colitis early

c) Always associated with extraintestinal manifestation

d) Increased incidence with increase in age

26. The best investigation for colorectal carcinoma -

a) Exfoliative cytology

b) Air contrast barium enema

c) Ultrasound

d) Colonoscopy and biopsy

27. In ulcerative colitis, the inflammatory process is usually confined to -

a) Mucosa alone

b) Mucosa and submucosa

c) Mucosa, submucosa and muscularis

d) Mucosa submucosa, muscularis and serosa

28. The polyp with least malignant potential -

a) Hyperplastic polyp

b) Pseudo adenoma

c) Vilious adenoma

d) Tubular adenoma

29. On colonoscopy which of the following is highly malignant -

a) Single pedunculated polyp

b) Multiple flat polyps about hundreds

c) Multiple pedunculated polyps

d) Solitary flat polyp

30. Carcinoma of the right colon usually present with -

a) Perforation

b) Massive bleeding

c) Large bowel obstruction

d) Alteration of bowel habits

31. Management of carcinoma descending colon in a 75 year old male is -

a) Total colectomy

b) Left hemicolectomy

c) Defunctional colostomy

d) Harmann’s procedure

32. True about carcinoma colon is -

a) Left side present with anemia

b) Solitary liver metastasis is not a contraindication to surgery

c) Most common site is ascending colon

d) Right side are usually stenosing variety

33. Which of the following is true about carcinoma colon -

a) Lesion on the left side of the colon presents with features of anemia

b) Solitary metastasis in liver is not a contraindication for surgery

c) Mucinous carcinoma has a good prognosis

d) Duke's A stage should receive adjuvant chemotherapy

34. The following regarding colostomy are true except –

a) A colostomy is an artificial opening made in large bowel to divert the faces to the exterior

b) Temporary colostomy is established to defunction an anastomosis

c) Permanent colostomy is formed after the resection of rectum by the abdominoperineal technique

d) Double barreled colostomy is commonly done nowadays

e) Colostomy hernia is a common complication

35. Best investigation of acute mecha-nical intestinal obstruction is -

a) X-Ray abdomen

b) Barium enema

c) Proctosigmoidoscopy

d) Flatus tube

36. Acute mechanical large bowel obstruction should be operated early because -

a) Electrolyte imbalance due to third space loss

b) Septicemia from absorption of bowel contents

c) Early gangrene and perforation

d) Respiratory embarrassment to massive abdominal distension

37. Acute mechanical large bowel obstruction should be operated early because of the risk of -

a) Respiratory embarrassment due to abdominal distension

b) Electrolyte imbalance from vomiting

c) Septicemia from bowel contents

d) Closed-loop obstruction and caecal perforation

38. Treatment of choice of acute obstruction due to left sided colonic carcinoma in a 70 year old male is -

a) Left sided colectomy

b) Total colectomy

c) Hartman’s procedure

d) Defunctioning colostomy

39. Best way to diagnose lower intestinal obstruction -

a) Pain abdomen

b) Abdominal distension

c) Profuse vomiting

d) Multiple air gas shadows on X-ray

40. Prognosis for carcinoma rectum is best assessed by

a) Site of tumour

b) Histological grading

c) Size of tumours

d) Duration of the symptoms

41. Earliest symptoms of carcinoma rectum-

a) Pain

b) Alteration of bowel habits

c) Bleeding PR

d) Tenesmus

42. Villous polyp of rectum manifest -

a) Bleeding PR

b) Mucus diarrhoea with hypokalemia

c) Prolapse rectum

d) Obstruction

43. Anterior resection is contra indicated in the following-

a) Age more than 60 years)

b) Undifferentiated carcinoma

c) Melanin in liver

d) Cancer is less than 5 cm from anorectal margin

44. In Duke's classification of cancer rectum, B2 denotes-

a) Growth extends to perirectal fat

b) Regional nodes involved

c) Limited to thickness of bowel wall

d) Hepatic metastasis

45. Distal clearance in surgery for carcinoma rectum is-

a) 2 cm

b) 5 cm

c) 10 cm

d) 8cm

46. Best procedure in mid rectal carcinoma is -

a) Abdominoperineal resection

b) Anterior resection

c) Perineal loop

d) Transverse colostomy

47. The best surgical management for villous adenoma of the rectum is –

a) Local resection of lesion

b) Repeated sigmoidoscopy

c) Abdominoperineal resection

d) Electrolyte infusion and chemotherapy

48. Treatment of carcinoma rectum 5 cm from anal verge without nodal  metastasis is -

a) Abdominoperineal resection

b) Radiotherapy

c) Endoscopic resection

d)Chemotherapy

49. Rectal polyps usually present with -

a) Obstruction

b) Perforation

c) Bleeding

d) Malignant change

50. In carcinoma of anus distal margin of clearance of anal canal of at least .............

a) 2 cm

b) 5 cm

c) 4 cm

d) 7 cm

51. Cancer of the anus is commonly -

a) Adenocarcinoma

b) Squamous carcinoma

c) Melanoma

d) Sarcoma

52. Below the pectineal line the lymphatic spread is to .....nodes-

a) Superficial inguinal

b) Internal iliac

c) External iliac

d) Para aortic

53. Commonest cause of bleeding PR in a male between 20-40 yrs is -

a) Carcinoma rectum

b) Internal haemorrhoids

c) Fissure in anus

d) Rectal polyp

54. Commonest cause of bleeding PR in India -

a) Cancer rectum

b) Internal haemorrhoids

c) Rectal polyps

d) Fissure-in-ano

55. The most common cause of painless bleeding PR in a man is -

a) Fissure-in-ano

b) Diverticulosis

c) Piles

d) None

56. Ideal treatment for squamous cell carcinoma of Anal canal is –

a) Pelvic exentration

b) Chemotherapy and radiotherapy

c) Chemotherapy alone

d) Abdominoperineal resection

57. In anal carcinoma the treatment of choice is -

a) Radio+ Chemo

b) APR + Radiation c) Only radio

d) Radio+Chemo followed by APR

58. Commonest site for carcinoid tumour is -

a) ileum

b) Appendix

c) Rectum

d) Colon

59. Raised level of Carcino-embryonic antigen is seen in –

a) Carcinoma colon

b) Carcinoma breast c) Carcinoma lung d) Carcinoma ovary

60. The commonest cancer of adult man in India is -

a) Carcinoma lung

b) Carcinoma colon

c) Carcinoma stomach

d) Aerodigestive carcinoma

61. Gasless abdomen in X-ray is a sign of -

a) Acute pancreatitis

b) Necrotising enterocolitis

c) Ulcerative colitis

d) Intussusception

62. Which tumour is treated by hormones –

a) Carcinoma prostrate b) Carcinoma bladder

c) Carcinoma colon

d) Carcinoma pancreas

63. Ca-125 is a tumor marker for - a) Cervix b) Ovary

c) Colon

d) Breast

Answers

Test	Answer
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63	b a c c d d a,b,d d b d c d d None b d d a a b a d b b b,d d b a b b d b b d a c d c d b c b b,d c a b a a c a b a b b c b b a a,b,c d c a b

References

Church J., Lowry A., Simmang C. Practice parameters for the identification and testing of patients at risk for dominantly inherited colorectal cancer - supporting documentation // Diseases of the Colon and Rectum. – 2001. – Vol.44. – No.10, October.

Manual of Clinical Oncology / Edited by D.K.Hossfeld (Chairman), C.D.Sherman, R.R.Love, F.X.Bosch. – Fifth Edition. – P. 228-252.

New trends in coloproctology / Edited by J.A.Reis Neto. – 2000. – P.337-454.

Oxford Textbook of Surgery. - http://med-lib.ru/english/index.shtml

Shankar A., Taylor I. Colorectal cancer // Surgical Treatment: Evidence-Based and Problem-Oriented / Edited by René G. Holzheimer, John A. Mannick. – Part IV. Colon.

Short Practice of Surgery / Edited by R.C.G.Russell, Norman S. Williams, Christopher J.K. Bulstrode. – 24 th Edition. – Chapter 68, chapter 71. – P. 1153-85, 1219-41.

Tjandra J.J., Kilkenny J.W., Buie W.D. et al. Practice Parameters for the Management of Rectal Cancer (Revised) // Diseases of the Colon and Rectum. – 2005. – Vol.48. – No.3, March.- P.411-423.

Ривкин В.Л., Бронштейн А.С., Файн С.Н. Руководство по колопроктологии. – М.: изд-во «Медпрактика», 2001. – Ч.4. – С.195-277.

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

ACUTE INTESTINAL OBSTRUCTION (classification, clinical features, surgical tactics).

METHODS OF INTESTINAL DECOMPRESSION, ENTERAL LAVAGE.

Составитель асс. О.Г.Шахбазян

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

The student should know:

• The modern theory, etiology and a pathogenesis of acute intestinal obstruction (AIO);

• Classification AIO;

• The pathoanatomical characteristic of various kinds of intestinal obstruction and complications;

• Clinic and features of current of dynamic, mechanical and mixed forms AIO;

• Stages of development AIO;

• Value of tool methods in diagnostics AIO (radiological, US-researches, videolaparoscopies)

• Surgical tactics at various kinds AIO;

• Preoperative preparation of patients;

• Volume of operations at not complicated and complicated forms AIO, sequence of surgical manipulations and algorithm of the decision of problems at operative intervention;

• Conducting the postoperative period, diagnostics and treatment of early and late postoperative complications, prophylaxis and their treatment;

• Mistakes in treatment of intestinal obstruction (diagnostic, medical tactical, technical, organizational) and conducting the medical documentation. The reasons of diagnostic mistakes and ways of their prevention;

• Qualitative and quantity indicators of treatment AIO: a place in emergency surgical pathology, character of complications, lethality, questions of medical labour examination;

• Ways of decrease in lethality at AIO. Value of early diagnostics and duly hospitalization of patients in surgical department.

-Definition

-Classification

-Etiology

-Clinical manifestations. Signs and symptoms.

-Diagnostics. Differential diagnostics

-Treatment: therapy and surgery

Definition.

Impairment of bowel content passage through the intestine can be defined as intestinal obstruction

Classification.

There are different types of intestinal obstruction:

• acute;

• subacute.

• Chronic.

Acute intestinal obstruction can also be classified according to morpho-functional impairments into:

Dynamic.

1. Spastic

2. Paralytic (e.g. mesenteric vascular occlusion)

Mechanical.

According to the mechanism of its development intestinal obstruction can be classified into:

• strangulation intestinal obstruction (incarceration, volvulus (torsion), formation of nodules)

• obturation intestinal obstruction (cancer, a foreign body, a gallbladder or fecal calculas, fetobezoar, a mass of ascarids);

• mixed (intussusception, adhesive).

According to the level of obstruction it can be classified into:

• high (small bowel);

• low (large bowel).

Etiology

Etiology of intestinal obstruction is due to a number of factors.

Mechanical obstruction develops due to anatomical factors having hereditary or acquired nature.

Predisposing factors;

• dolichosigma;

• cecum mobile;

• peritoneal additional folds;

Acquired factors are more common than hereditary.

Acquired factors:

• adhesion;

• dolichosigma in elderly people;

• external and internal hernia.

- intestinal and other abdominal tumors

The nature of presentation will also be influenced by whether the presentation is:

• acute;

• chronic;

• subacute.

Acute obstruction usually occurs in small bowel obstruction with sudden onset of severe colicky central abdominal pain, dis­tension, and early vomiting and constipation.

Chronic obstruction is usually seen in large bowel obstruction with lower abdominal colic and absolute constipation, followed by distension.

Subacute obstruction implies an incomplete obstruction.

Presentation will be further influenced by whether the obstruc­tion is:

• simple - where the blood supply is intact;

• strangulating/strangulated - where there is direct interfer­ence to blood flow, usually by hernial rings or intraperitoneal adhesions.

Clinical manifestations.

Small bowel obstruction

GENERAL CONSIDERATIONS

Presentation

Whatever its site and cause, small bowel obstruction leads to rapid accumulation of fluid and gas in the lumen proximal to the site of obstruction. This event is the result both of swallowed air and of intestinal fluid excretion. Peristalsis causes distension in the distal obstructed segment first, with gradual proximal accumulation of air and intestinal fluid. With so-called high obstruction, in areas such as the proximal jejunum, vomiting may supervene early, relieving the distension. When obstruction is distal, vomiting may not occur until late in the course of the disease.

In typical cases of acute obstruction there is initial active peristaltic activity proximal to the site. Most patients complain of crampy pain. Within a few hours this activity declines, and oedema and increasing distension mark the end of peristaltic activity; there may be no cramps or only occasional cramps. Persistent, steady pain usually indicates ischaemia or perforation. A change in the characteristics of small bowel contents is also characteristic of the later stages of obstruction. Bacterial overgrowth and stagnation make the fluid feculent, with an increase in opacity and a foul odour. Appearance of fluid of this type in the vomitus or from a nasogastric tube confirms the diagnosis of obstruction.

Obtaining a detailed history and performing a thorough examination will provide a diagnosis of underlying cause in more than three-quarters of cases. It is especially important to identify abdominal wall hernias, which frequently strangulate when surgery is delayed.

Laboratory tests are of little value beyond helping to rule out other causes of abdominal pain. The exception to this rule is the plain radiograph of the abdomen, which is especially helpful in confirming the clinical impression of obstruction, and can also, when interpreted by an experienced clinician, add additional useful information as to completeness, site, and aetiology of obstruction. Upright films may show air in the biliary or portal system and beneath the diaphragm; these are important observations with respect to timing of surgery.

Etiology

A list of the causes of intestinal obstruction is long, even if those normally only encountered during infancy and childhood are excluded. In geographic areas where life expectancy is long and surgical care readily available, at least half of the cases are the result of adhesions, usually postoperative. Hernias, whether of the abdominal wall or internal organs, are the second leading cause. Other important general causes are primary and metastatic tumours, local inflammatory processes such as appendicitis or diverticulitis of the colon, and various strictures, such as those seen in Crohn's disease. The causes and their relative incidence vary widely with geographic region.

The mechanism of the obstruction is more important than the specific aetiology, since this factor bears on the likelihood of bowel compromise. There are four general mechanisms: most dangerous are, first, volvulus with torsion and, second, incarceration in a confined space. Although volvulus can be the result of a failure of fixation of all or the distal part of the small bowel it is more commonly the result of twisting around a fixed point, as from an adhesion or tumour nodule. This event can rapidly lead to vascular compromise and infarction.

Incarceration in a fixed space is usually due to an abdominal wall hernia. Intra-abdominal defects and traps, congenital or acquired, are also sites of potential incarceration. Once entrapped, impaired venous return and torsion may rapidly lead to infarction of the segment.

Obturation of a segment of bowel, usually narrowed by a pathological process such as fibrosis or tumour growth, is the third mechanism. Such obstruction may be intermittent because of the repeated gradual passage of a bolus of intestinal contents through the stricture. A large bezoar or gallstone may obstruct a normal segment of bowel, usually the distal ileum, by this mechanism. Vascular compromise is unlikely in obturation obstruction.

The last mechanism is intussusception. In adults, it is almost always due to an intramural or mucosal lesion. It does not usually lead to ischaemia and infarction.

Non-operative measures

As a rule, mechanical small bowel obstruction is an urgent indication for surgical intervention. This practice reflects the risks of strangulation and perforation, the fact that persistence of obstruction will eventually require an operation in many cases, and the likelihood of recurrence even with spontaneous resolution.

Preoperative assessment of fluid status with rapid replacement of deficits is important. A patient whose obstruction has been identified many hours from its onset, when there has been vomiting or sequestration of large amounts of fluid in the lumen, intestinal wall and peritoneal cavity, may require administration of several litres of fluid. In these cases, restoration of an adequate urine output serves as a useful general index of adequate replacement. In older patients, especially those with a history of cardiac disease, central venous or pulmonary artery pressure monitoring may be needed. Concurrent, sometimes exacerbated, medical problems such as diabetes mellitus and cardiac impairment must be considered and managed separately.

Nasogastric suction relieves distension from air swallowing and reduces fluid passage into the small bowel; it should be instituted early in management. The use of long intestinal tubes has less justification. They do not pass readily, do not empty the stomach, and delay more definitive management. Generally, they have no useful role in the management of acute obstruction. Although exceptions may be cited, an efficiently functioning nasogastric tube is clearly preferable in most cases.

Surgical intervention

Though sometimes easy, operative intervention may be complex. The procedure requires the management of the segment of intestine at the site of obstruction, the distended proximal bowel and the underlying cause of obstruction.

If the patient has had a previous surgical incision which, with enlargement, will afford a portal for complete abdominal exploration, it should be used. This approach allows repair of all associated hernias and easy access to the most frequent site of obstruction by adhesions, which is the incision itself. It is usually wise to enter the abdomen through an extension into normal tissues to avoid injury to adherent loops.

In patients with late obstruction and in the elderly, the distended segments should be handled with care as they may easily be torn. The object is to find the junction of dilated and collapsed bowel. Though it may be preferable to follow collapsed loops proximally, this is not usually possible.

Decompression of dilated loops may be desirable to facilitate an anastomosis or closure of the abdominal wound. Closed methods of accomplishing this goal include the milking of contents back into the stomach with aspiration through a nasogastric tube. This method is usually possible without excessive trauma to the bowel only in young children. Alternatively, a long tube may be advanced from the stomach by digital manipulation into the distended loops. Finally, a sump suction device may be passed directly into the distended loops through an enterotomy controlled with a ‘purse string’ suture. Even with careful attention to prevention of local soilage, direct aspiration of enteric contents is associated with an increase in postoperative wound sepsis. Unless clearly needed, the best policy often is to omit decompression altogether.

When indicated, a simple resection of small bowel and direct anastomosis, even when the proximal bowel is distended, is safe enough. Sometimes, as with carcinomatosis or extensive pelvic adhesions, a side-to-side bypass is the better choice. Parenteral administration of antibiotics, begun preoperatively, decreases the incidence of septic complications when resection or bypass is performed.

The determination of the viability of a segment of intestine is a common problem. Generally, the opinion of an experienced surgeon after 10 to 20 min of observation suffices. To prevent early perforation or late strictures, a resection is the best choice when doubt exists. Although fluorescein injections with illumination of the surface with a Wood's lamp and detection of surface flow by Doppler devices provide scientific approaches to the diagnosis, they are neither necessary nor commonly available at the moment they are needed.

When obstruction is due to adhesions the question of whether all or only the offending adhesions should be released is unresolved. Generally, adhesions can be expected to recur when there has been any trauma to serosal surfaces. Thus, as a rule it is probably wise to divide only those adhesions involving the bowel at the site of obstruction and those that prevent restoration of the proximal and distal segments to their normal place of residence in the abdominal cavity.

Reduction of abdominal wall hernias before operation is desirable when easily accomplished. An exception is a hernia in the inguinal or femoral area; prompt operation is required. The surgeon may prefer to be able to examine the incarcerated segment of bowel through the herniorrhaphy incision before it is dropped back in. Another exception is the presence of local signs of inflammation that may indicate strangulation or perforation.

Prevention

Any laparotomy should be performed with operative measures that minimize adhesion formation, decreasing the incidence of small bowel obstruction. All reasonable steps to minimize serosal trauma should be utilized, including gentle handling and packing of intestine and avoiding the unnecessary introduction of foreign material into the peritoneal cavity. Sutures and ties involving the serosa cause small areas of tissue ischaemia and necrosis which can cause adhesions. Serosal defects should not be repaired if the underlying muscularis and submucosa are intact.

The second preventive measure, of course, is the repair of abdominal wall hernias. Any inguinal hernia that is symptomatic or is the site of occasional temporary bowel incarceration should be repaired, as should all incisional hernias.

COMPLEX PROBLEMS

Postoperative obstruction

Mechanical small bowel obstruction can complicate the postoperative course after any operative entry into the peritoneal cavity. The diagnosis is obscured by ileus and the symptoms and signs that are a usual accompaniments of a laparotomy incision.

Normally, paralysis of peristaltic function resolves within 72 h after a laparotomy involving handling of the intestine. There is then an absence of distension, and the patient reports a return of appetite along with expulsion of flatus and faeces. In cases of obstruction, normal peristaltic function may never return, or may do so only to be interrupted by an episode of obstruction. The superimposition of the signs and symptoms of obstruction on those of convalescence after laparotomy makes the diagnosis elusive.

Most cases are the result of adhesions and involve the ileum. Although the extent of adherence of peritoneal surfaces to each other is variable, the time course usually is not. By 72 h after laparotomy, extensive soft adhesions will have formed. These seem most extensive at about 10 days to 2 weeks, by which time they become dense and vascular. A gradual process of resolution then occurs; this may go on for many years, accounting for appearance of obstruction at remote times. This process of adhesion formation in some cases is abnormally vigorous and may then reflect peritoneal reaction to foreign material introduced during the operation. Sterile peritonitis can be an important contributor to a course of delayed resumption of intestinal function without actual mechanical obstruction. Obstruction by adhesions in the early period is usually the result of kinking and tensions on adherent loops of intestine rather than of obturation. The presence of a stoma or intestinal tube may contribute to these mechanical problems by offering a fixed cicatricial point. Other causes of obstruction include internal hernias and peritoneal defects after partial dehiscence of the deep layer of a wound or the peritoneal floor. An abscess involving adjacent segments of intestine can cause obstruction or can lead to localized ileus.

The clinical problem is to distinguish between cases of mechanical obstruction and those that reflect ileus prolonged by a sterile peritonitis or other factors, such as chronic narcotic use. Fortunately, except when there is a peritoneal defect, strangulation of an obstruction is rare in a postoperative patient. Careful repeated observation of the patient is paramount. Radiography offers the next best help: plain films show gas throughout the small and large bowel in most cases of ileus. In difficult cases, the use of barium will sometimes provide important information

Careful replacement of fluid and electrolytes is needed, and nutritional support may facilitate overall recovery. It is generally believed that nasogastric decompression is essential and that decompression through a long tube may be helpful; passage of such tubes is most likely to succeed in those patients with mechanical obstruction. The usefulness of long tubes in the overall management of patients is estimated to be high by some surgeons, but many do not find them useful.

The timing of surgical intervention is difficult. Although it is important to relieve mechanical obstruction promptly, operations on patients with profound ileus and in those with extensive nonobstructing adhesions are fruitless and delay recovery. No simple rule can be offered. Generally, complete obstruction, evidence of sepsis, and an unacceptably prolonged course dictate an exploratory operation. An unacceptably long course is the least useful indication.

Recurrent obstruction

The risk of strangulation and the likelihood of early recurrence usually dictate prompt operation at the first episode of obstruction. An operation for obstruction due to adhesions carries a higher likelihood of recurrence than a laparotomy for other indications. This is of the order of 20 per cent. When obstruction recurs, the possibility of a cause other than adhesions is lower, and there is perhaps more justification for a non-operative management, in the form of decompression with a nasogastric tube and careful parenteral replacement of lost fluids and electrolytes.

During any period of observation, there will be continued concern about the possibility of bowel compromise. The nature of pain is the best indicator of this complication. Plain and contrast studies are helpful in ruling out complete obstruction, which also serves as an indication for surgical relief. If the obstruction resolves, there is generally no reason for a laparotomy in the patient with recurrent obstruction due to adhesions.

There is no good way to prevent the recurrence of adhesions. Some authorities have suggested that plication of the wall or mesentery of the small bowel to form a ladderlike configuration may be helpful: there is no good evidence for the efficacy of these measures, and few surgeons use them. An in-lying long enteric tube may also produce a configuration of loops less prone to obstruction from adhesions. Such tubes should be left in place for at least 2 weeks, but their efficacy has not been clearly established.

Radiation enteritis

Injuries to the small intestine may follow radiation to any part of the abdominal cavity: many result from therapy for pelvic tumours. Although these injuries may lead to perforation with abscess formation of fistulae, the most common complication is intestinal obstruction.

During the actual course of radiation treatment, damage to the mucosa may lead to ulceration and oedema. Delayed damage to small blood vessels causes more serious complications such as progressive arteritis and eventual thrombosis. Infarction and perforation may ensue, but the more frequent result is the induction of dense adhesions containing collateral vessels, and the occurrence of fibrous strictures. Serosal surfaces of injured intestinal segments acquire a characteristic thickened, scarred, hypervascular appearance.

The cause of acute complete obstruction can only be established at the time of operation. Segments of intestine with a grossly abnormal appearance may not heal; when used for anastomosis, there is a high incidence of failure. A segment with a nearly normal appearance and satisfactory bleeding on transection can be used confidently. Microscopic examination adds little to the surgeon's impression in selecting bowel for anastomosis. Resection is the preferred management. If dissection of radiation-damaged loops of bowel out of the pelvis offers an unacceptable risk, a bypass may be selected. It is better to transect the bowel above the obstruction for an end-to-side anastomosis than to perform a side-to-side bypass in continuity.

A trial of non-surgical management is reasonable when a prior history or contrast study has established the diagnosis of radiation enteritis and obstruction is not complete. Some episodes due to obturation or oedema will resolve and may not recur. Parenteral nutrition may aid the process of resolution.

Metastatic malignant tumours

Peritoneal seeding sometimes leads to multiple narrowed segments and consequent obturation obstruction; this may occur in the absence of other terminal manifestations of the tumour. Strangulation is rare, since the loops are relatively fixed. Retroperitoneal or mesenteric deposits may contribute to the impaired motility.

Patients tend to have intermittent episodes of obturation obstruction. A minimal residue diet may reduce symptoms and acute obstruction usually clears on nasogastric suction. In patients with a relatively good prognosis, there may be a role for surgical intervention for bypass or even resection of obstructed sites. Careful evaluation with contrast studies allows selection of the smallest feasible procedure, to be performed through a limited field. Wide exploration of the abdomen is likely to be both unnecessary and counterproductive.

Superior mesenteric artery syndrome

Obstruction of the distal duodenum due to its compression between the artery and posterior structures, either the aorta or vertebral bodies, has been termed the superior mesenteric artery syndrome. Findings on plain film and contrast studies are dilatation of the stomach and duodenum with a termination by obstruction with a linear configuration at the level of the artery.

The syndrome may follow weight loss, immobilization in bed, and various operative procedures, but it also may occur spontaneously. It is seldom seen in obese patients. There appears to be a component of impaired motility in some patients and abnormalities of fixation of the ligament of Treitz have also been cited. The onset is often insidious with the gradual appearance of nausea and vomiting.

Though conservative measures should first be tried, the majority of patients eventually require surgical relief. Simple gastrojejunostomy does not relieve symptoms. Various measures can be used to adjust the position and fixation of the duodenum and proximal jejunum. Duodenojejunostomy performed through the mesocolon in a side-to-side fashion is most likely to succeed. The jejunum just beyond the ligament of Treitz should been employed in the anastomosis.

Obstruction of the colon

Obstruction of the colon as a separate clinical entity is singled out for discussion for two reasons. Firstly, it brings its own serious complications (the most dramatic being perforation), which are not directly related to the underlying cause. Secondly, it introduces special elements that influence the timing and limit the selection of procedures in managing the actual cause of obstruction.

GENERAL CONSIDERATIONS

Obstruction of the intestine at any level leads to progressive distension of the proximal bowel with fluid and gas. In the small intestine, distension may result in early vomiting if the site is proximal or in the sequestration of large amounts of fluid if it is more distal. Neither distension nor sequestration is an important elements in the presentation and course of obstruction of the colon.

The obstructed colon has less peristaltic activity, and dilatation tends to cause fewer and less severe cramps than small bowel obstruction. In the majority of patients the ileocaecal valve prevents decompression of the colon into the small intestine. This situation results in closed loop obstruction, which is especially hazardous because it can result in massive dilatation of a segment of the colon without the signs and symptoms usually associated with intestinal obstruction. Secondary dilatation of the small intestine with its consequences may follow, but it is slow to develop and is usually unimportant.

Colon obstruction presents as an emergency, especially because of the associated complication of perforation. Even when intraluminal pressure is constant, the tension on a segment of colon wall increases with an increase in diameter; the relatively larger diameter and thinner wall of the caecum and ascending colon make these the most frequent sites of perforation. In the final stages before perforation there is an embarrassment of circulation, which can also contribute to rupture of the wall. The site of perforation may be in a more distal segment of the colon, usually just proximal to an obstructing lesion such as a carcinoma.

During barium studies under the fluoroscope the normal ascending colon dilates readily up to only about 9 cm in diameter. In chronic obstruction, much larger degrees of distension may nevertheless be quite harmless. Still, when plain radiographs show distension of the ascending colon beyond 10 cm, the possibility of rupture must be considered as imminent. If the capacity of the right colon is exceeded, the serosa between the taeniae splits, perforations, usually punctuate, appear in the mucosa, and patches of haemorrhage and even infarction are also commonly observed. Perforations of this type initially lead to progressive contamination of the peritoneal cavity, but may not actually decompress the obstructed colon.

The clinical course of colon obstruction is often quite insidious. Up to 80 per cent of cases are caused by a carcinoma. Many of these patients will have experienced prior episodes of partial obstruction and may not be aware that complete obstruction has developed until 2 or 3 days have passed. Although lower abdominal cramps are usually reported, these may be mild. Cessation of the passage of stool or gas is the most frequent complaint, and an observant patient will also report abdominal distension. Physical examination shows a quiet abdomen with obvious tympany and distension, sometimes most pronounced over the ascending colon. There may be tenderness over compromised bowel, the caecum or the area proximal to a tumour. Rectal examination may disclose a low rectal tumour as the cause of obstruction. More commonly, the rectum feels capacious and empty. In the presence of a tumour or compromised bowel, there may be traces of blood. The physical examination should include a careful search for abdominal wall hernias, especially in any old surgical incisions.

Plain radiographs of the abdomen are usually helpful in colon obstruction. They may confirm or support the diagnosis and point to the site and aetiology; they can also suggest the presence of perforation by showing free air and can demonstrate a dangerously distended right colon. If an expeditious barium study is obtained, it will help identify the actual site and nature of obstruction. The barium enema examination should be done without preparation and care must be taken not to push barium above the obstruction.

In practice, it is difficult to assess the likelihood of colon perforation. When obstruction is partial, sequential evaluation of symptoms and the presence and degree of tenderness over the right colon can suggest impending perforation. If obstruction is complete, and especially if decompression into the small intestine is absent, urgent surgical exploration with decompression is the first consideration.

CAUSES OF COLON OBSTRUCTION

Carcinoma

In the more economically developed areas of the world, carcinoma is by far the most frequent cause of colon obstruction. Carcinomas of the left colon are the most likely to lead to obstruction, although those in other areas also cause obstruction, the least frequent being those of the rectum. Most patients in whom the obstruction involves the distal colon have a presentation that includes an initial period of symptoms of partial obstruction. Final obstruction reflects obturation of the narrow residual channel by faecal material. Obstruction in the right or transverse colon is more likely to occur without preceding symptoms, perhaps because of the liquid nature of the stool.

The prognosis of treated obstructing carcinomas is not very different from that of non-obstructing lesions of similar location and extent. Prognosis may be estimated by use of the Dukes' or other classification. The early operative risk is much higher in these patients especially with respect to perforation.

Diverticulitis

Complete acute colon obstruction is rarely caused by diverticular disease, although it sometimes occurs due to obturation of a strictured oedematous segment. Incomplete obstruction is more usual, and there may be associated partial or complete obstruction of an adherent loop of small intestine.

Differentiation between a carcinoma and diverticular disease of the sigmoid may be very difficult and can lead to an incomplete or delayed resection in a patient incorrectly diagnosed as having diverticulitis.

Volvulus

Volvulus of either the ileum, caecum and right colon or of the sigmoid colon almost always leads to acute obstruction. The twist of 180° or more around the mesenteric axis imparts a similar twist in the longitudinal axis; this is the immediate cause of obstruction. Because vascular compromise may result, there is a danger of perforation in neglected cases. Expert interpretation of the plain radiograph will usually establish the diagnosis. Contrast enemas may be needed when there is considerable dilatation of the proximal colon or small intestine. Volvulus of the right colon generally reflects a failure of fixation of the colon. Sigmoid volvulus is probably an acquired abnormality but is usually observed in patients with an elongated colon. Spontaneous reduction of all forms of volvulus will often occur, relieving obstruction; recurrence is the rule.

Other causes

Only a few cases of colon obstruction are due to causes other than cancer diverticulitis, and volvulus. The uncommon causes include incarceration in hernias, strictures such as those that follow vascular compromise, metastatic malignant tumours, especially those of pelvic origin, radiation strictures, and various inflammatory conditions. Adhesions, although a common cause of small bowel obstruction, are a rare cause of colon obstruction.

MANAGEMENT

General principles

Management should be directed at relief of obstruction before perforation occurs. Secondary objectives include treatment of the underlying cause and restoration of the continuity of the colon with the smallest number of operations in the shortest time feasible. Choices between the various surgical alternatives reflect the urgency of the situation, the condition of the patient, the state of the bowel to be used for anastomosis, and the potential for cure of a malignancy. Impending or actual rupture of the right colon is another major modifying factor. As with anastomosis in elective resections, tension, impaired circulation, and local contamination may all dictate a staged procedure. An anastomosis between distended ileum and normal colon is usually safe: one between distended and normal colon much less so.

Carcinoma of the colon

In the treatment of obstructing tumours in the caecum, ascending or right transverse colon, a right colectomy extended across to the transverse colon as needed is the usual procedure. Even if the colon is distended, an adequate dissection for cure is feasible, and an anastomosis of the ileum to normal and usually empty collapsed distal colon is safe. If the caecum is perforated or when other factors make the risk exceptionally high, a resection with ileostomy carries less immediate risk, although a second stage is required for reanastomosis.

If the obstructing lesion is in the region of the splenic flexure and down to the mid-sigmoid colon, a right colectomy with extension to include the lesion (a subtotal colectomy) with ileocolonic anastomosis may still be selected. In the young and healthy patient seen by an experienced surgeon subtotal colectomy is an acceptably low risk and troublesome diarrhoea afterward is the exception. A segmental resection with direct anastomosis using distended and unprepped proximal bowel carries a high risk. The safe procedure is to perform a resection with an end colostomy and with reanastomosis as a second stage. A proximal transverse colostomy or a caecectomy and ileostomy for caecal perforation with staged later section may be dictated by the general or local operating conditions. Recent reports suggest that antegrade intraoperative irrigation may be used in selected cases to establish safe conditions for a direct anastomosis.

When a tumour is present in the distal sigmoid colon or upper rectum, a single stage operation is seldom feasible. If a satisfactory dissection can be carried out under the operating conditions, a resection with an end proximal colostomy should be done. Otherwise, a proximal defunctioning colostomy alone is done. If the defunctioning colostomy can be carried out in the sigmoid colon rather than in the transverse colon, a single subsequent operation may be possible: many surgeons consider it unsafe to have two separate colon suture lines because of an increased risk of postoperative leakage. A prior colostomy remote from the operative anastomoses makes a third stage necessary.

When the obstructing tumour is at or below the peritoneal reflection, fortunately an unusual site for obstruction, a two- or three-stage operation is generally the best choice because a satisfactory dissection for the resection of a malignant tumour is often neither feasible nor safe under these conditions. If hepatic or other unresectable metastases are present, however, a Hartmann procedure (resection of the tumour with closure of the rectum and an end sigmoid colostomy) is a good single stage choice. Alternatively, a proximal transverse colostomy must be performed as a first stage, with resection of the tumour deferred until proper conditions can be secured.

In the presence of colonic obstruction there is always a risk when the caecum is not directly examined: severe damage to the wall caused by distension can result in perforation occurring even after distal decompression. Most operations should therefore include visualization of the caecum. Some minor transmural injuries can be managed by imbrication or by the placement of a caecostomy tube. Right colectomy is necessary with more advanced injuries or perforation. The site of colon obstruction and its management and the general condition of the patient determine whether an ileostomy or an ileocolonic anastomosis is indicated.

Diverticulitis

Complete obstruction from diverticulitis is, in fact, rare. In most cases, obstruction is incomplete, and an element of inflammation and oedema will respond to antibiotics and to ‘putting the colon at rest’. When non-surgical treatments fail, a primary resection can almost always be performed safely. An extensive dissection of mesenteric nodes is not necessary.

Conditions for a primary unprotected colonic or colorectal anastomosis often cannot be met. A safe colon anastomosis is one that can be left in a clean, normal field: there must be no gross faecal contamination, nor any exudate and purulent material from an abscess. Most cases of obstructive diverticulitis are best managed by primary resection and end colostomy. Continuity is restored at a second operation several weeks later. When there is a large abscess or the local inflammatory reaction precludes a safe dissection, a defunctioning transverse colostomy with drainage of the abscess as a first stage may be the only safe alternative. Another alternative in selected patients is percutaneous drainage of the abscess, with later resection if obstruction resolves.

Volvulus

Obstruction due to volvulus of the ileocaecal area requires prompt diagnosis and management in order to avoid the otherwise common complication of perforation. The diagnosis can be made on plain radiograph, but a contrast study is usually obtained. Once the diagnosis is established, an urgent laparotomy is needed. Although colonoscopic decompression or reduction by a column of barium may be feasible, the possibility of mural compromise and the likelihood of recurrence make resection with primary anastomosis the favoured management in almost all cases. In the presence of perforation with extensive peritoneal contamination or when other factors dictate a more expeditious procedure, resection with ileostomy and later reanastomosis may be the best choice.

When the caecum is intact and undamaged, caecopexy offers an alternative to resection. A long segment of the ascending colon should be secured to the left abdominal wall by raising a peritoneal flap and forming a retroperitoneal track for the colon, fixing the cut edge of the peritoneum to the anterior aspect of the colon with multiple sutures.

The management of sigmoid volvulus is in some ways quite different from that of a caecal volvulus. Perforation is rare and decompression through a rigid sigmoidoscope, perhaps by inserting a well lubricated tube through the lumen, is easily accomplished in most patients. The tube can be left in place. In chronically debilitated patients, simple decompression by this technique, when needed, may be the best choice.

If decompression is successful and definitive treatment is selected, the procedure would be an elective sigmoid resection after routine bowel preparation. An unprotected primary resection and anastomosis can usually be undertaken safely. Fixation of the sigmoid colon without resection is usually not successful because of marked redundancy and the adjacent location of the colon segments in the proximal and distal ends of the volvulus.

When decompression fails or when there is evidence of infarction or perforation, management is difficult. Reduction of the loop at operation can result in perforation and massive faecal contamination of the peritoneal cavity. If a tube is placed in the rectum before surgery, it can sometimes be manipulated into the loop by the surgeon for decompression. Primary anastomosis is seldom feasible after emergency resection. Most surgeons perform an end sigmoid colostomy with staged restoration of colon continuity. An alternative in the absence of perforation or of bowel infarction would be intraoperative decompression with the rectal tube, followed by an elective resection after proper preparation of the colon and patient.

Volvulus of the transverse colon is rare, and principles of management are the same as for caecal volvulus.

Miscellaneous causes

Numerous other anatomical and pathological causes of acute colon obstruction are encountered. Although certain principles for their management can be re-emphasized, the surgeon is left to analyse and resolve each as an individual problem. Whatever the primary site of obstruction, the possibility of caecal perforation should be considered; failure to visualize the caecum always carry a risk. Healing of any anastomosis is uncertain when it cannot be placed in a normal, uncontaminated area of the peritoneal cavity. Even a diverting proximal colostomy will not ensure healing of a questionable anastomosis. The additive risks of staged operations favour a one-stage procedure, but only under near optimal conditions of anastomosis. Finally, bypassing an obstructed segment of colon does not always preclude the risk of subsequent perforation, especially when an ileocolonic bypass is used.

The task for independent work.

1. Prophylaxis of an adhesive desease of a belly cavity.

2. Laparoscopy in diagnostics and treatment of adhesive intestinal impassability.

3. Enterosorbtion - mechanisms of medical action.

TESTS

1. Acute intestinal obstruction can also be classified according to morpho-functional impairments into:

1)

2)

2. According to the mechanism of its development intestinal obstruction can be classified into:

1)

2)

3)

3. According to the level of obstruction it can be classified into:

1)

2)

4. Cardinal features of obstruction:

1)

2)

3)

4)

5. Clinical features of strangulation:

1)

2)

3)

6. Principles of treatment of intestinal obstruction:

1)

2)

3)

7. The causes of obstruction may be organic:

1)

2)

3)

8. The causes of intraperitoneal adhesions:

1)

2)

3)

4)

5)

6)

9. The following are potential sites of internal herniation:

1)

2)

3)

4)

5)

6)

7)

8)

10. Definition of volvulus.

Answers

1. Acute intestinal obstruction can also be classified according to morpho-functional impairments into:

1) Dynamic;

-Spastic:

-Paralytic (e.g. mesenteric vascular occlusion)

2) Mechanical.

2. According to the mechanism of its development intestinal obstruction can be classified into:

1) strangulation intestinal obstruction (incarceration, volvulus (torsion), formation of nodules)

2) obturation intestinal obstruction (cancer, a foreign body, a gallbladder or fecal calculas, fetobezoar, a mass of ascarids);

3) mixed (intussusception, adhesive).

3. According to the level of obstruction it can be classified into:

1) high (small bowel);

2) low (large bowel).

4. Cardinal features of obstruction:

1) Abdominal pain

2) Distension

3) Vomiting

4) Absolute constipation

5. Clinical features of strangulation:

1) Constant pain

2) Tenderness with rigidity

3) Shock

6. Principles of treatment of intestinal obstruction:

1) Gastrointestinal drainage

2) Fluid and electrolyte replacement

3) Relief of obstruction

7. The causes of obstruction may be organic:

1) intramural - faecal impaction;

2) mural - colorectal cancer, diverticulitis, strictures (Crohn's disease, ischaemia), anastomotic stenosis;

3)extramural - adhesion (small bowel only), metastatic deposits, endometriosis

8. The causes of intraperitoneal adhesions:

1) Ischaemic areas (sites of anastomoses, reperitonealisation of raw areas, trauma, vascular occlusion)

2) Foreign material (talc, starch, gauze, silk)

3) Infection (peritonitis, tuberculosis)

4) Inflammatory conditions (Crohn's disease)

5) Radiation enteritis

6) Drugs (Practolol)

9. The following are potential sites of internal herniation:

1) the foramen of Winslow;

2) a hole in the mesentery;

3) a hole in the transverse mesocolon;

4) defects in the broad ligament;

5) congenital or acquired diaphragmatic hernia;

6) duodenal retroperitoneal fossae - left paraduodenal and right duodenojejunal;

7) caecal/appendiceal retroperitoneal fossae - superior, inferior and retrocaecal;

8) intersigmoid fossa.

10. Definition of volvulus:

A volvulus is a twisting or axial rotation of a portion of bowel about its mesentery.

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

PERITONITIS (classification, clinical features, surgical tactics). INDICATIONS FOR METHODS PERITONEAL LAVAGE. INDICATIONS FOR PROGRAMMED RELAPAROTOMY. LAPAROSTOMY.

Составитель доц. Н.П.Снытко

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

THE PERITONEUM

The peritoneum is conveniently divided into two parts: the visceral surrounding the viscera and the parietal lining the rest of the cavity. The parietal portion is richly supplied with nerves and, when irritated, produces severe pain accurately localised to the affected area. The visceral peritoneum, on the other hand, is poorly supplied with nerves, and pain arising therefrom is vague and badly localised.

Surgical physiology. The peritoneal cavity is the largest cavity in the body, the surface area of its lining membrane being nearly equal to that of the skin. This veil-like, serous membrane is composed of flattened polyhedral cells, one layer thick, resting upon a thin layer of fibroelastic tissue, the two layers constituting the peritoneum. Beneath the peritoneum, supported by a small amount of areolar tissue, lies a network of lymphatics and rich plexuses of capillaries, from which all absorption and exudation must occur. In health, only sufficient peritoneal fluid, which is a pale yellow, somewhat viscid fluid containing lymphocytes and polymorphs, is secreted to ensure that the more mobile viscera glide easily. The specific gravity of the intra-abdominal contents is approximately 1-000. Mobile, gas-filled structures float upwards under the influence of posture, as does free air ('gas') in the peritoneal space.

In the erect position, when free fluid is present in the peritoneal cavity, pressure is reduced in the upper abdomen compared with the lower abdomen. When air is introduced it rises, allowing all the abdominal contents to sink.

Under the influence of decreased intra-abdominal pressure occasioned by the upward movement of the diaphragm during expiration, aided by capillary attraction, intraperitoneal fluids travel continuously in an upward direction to the subphrenic region where experimental evidence shows that fine coloured particulate matter and bacteria are absorbed rapidly into the peritoneal lymphatic network. In a matter of minutes, these coloured particles reach the lymph vessels above the diaphragm. This upward movement of intra-abdominal fluids is responsible for the subphrenic distribution of many intra-abdominal purulent collections.

When there is outpouring of large amounts of peritoneal fluid, e.g. when the contents of the stomach or duodenum escape into the peritoneal cavity through a perforation, such excess of free fluid within the peritoneal cavity unobstructed by adhesions runs downwards, largely directed by the normal peritoneal attachments.

When parietal peritoneal defects are created, healing occurs not from the edges, but by metamorphosis of mesenchymal cells in situ. Large defects heal as rapidly as small defects.

The peritoneal membrane can absorb and secrete large volume of fluid under osmotic principles: this ability to act like a semipermeable membrane is made use of by the process of peritoneal dialysis in the treatment of renal failure.

ACUTE PERITONITIS

Nearly all varieties of peritonitis are due to an invasion of the peritoneal cavity by bacteria. To such an extent is this true that when the term peritonitis is used without qualification, bacterial peritonitis is implied. Most cases of bacterial peritonitis are polymicrobial and usually both aerobic and anaerobic organisms are present. The exception is primary peritonitis (‘spontaneous' peritonitis) in which a pure infection with streptococcal, pneumococcal, or haemophilus organisms is seen.

Bacteriology

Bacteria from the alimentary canal. Usually the infection is caused by two or more strains. The commonest invaders are Escherichia coli, aerobic and anaerobic streptococci, and the Bacteroides. Less frequently Clostridium welchii is found; still less frequently staphylococci or Klebsiella pneumoniae (Friedlander's bacillus). Many of the strains of E. coli, Bacteroides, and Cl. welchii produce toxins that cause severe illness or death when they invade a large absorptive area (endotoxin shock).

The Bacteroides. Only recently has the frequency and importance of the presence of Bacteroides in the causation of peritonitis been realised. These Gram-negative, nonsporing organisms, though predominant in the lower intestine, often escape detection because they are strictly anaerobic, and slow to grow on culture media unless there is an adequate carbon dioxide tension in the anaerobic apparatus (Gillespie). In many laboratories, the culture is discarded if there is no growth in 48 hours. These organisms are resistant to penicillin and streptomycin but sensitive to metronidazole, clindamycin and lincomycin and the new cephalosporin compounds.

Since the widespread use of metronidazole (Flagyl), Bacteroides infections have diminished greatly.

Bacteria NOT from the alimentary canal. Examples are peritonitis due to the gonococcus, beta-haemolytic streptococcus, pneumococcus, and Mycobacterium tuberculosis. Since the advent of antibiotics, haemolytic streptococcal peritonitis has lost many of its dreaded lethal properties. In young girls and women, pelvic infection via the Fallopian tubes is responsible for a high proportion of 'nonalimentary' infections, e.g. gonococcus and streptococcus, but Bacteroides is also found normally in the female genital tract.

Paths of bacterial invasion of peritoneal space

1.Direct infection

- via perforation of some part of the gastrointestinal canal;

- through a penetrating wound of the abdominal wall;

- operative, e.g. drains, dialysis tubes, foreign material.

2.Local extension

- from an inflamed organ, e.g. appendicitis, cholecystitis;

- migration through gut wall, e.g. strangulated hernia;

- from or via the Fallopian tubes.

3.Blood-stream

- Part of general septicaemia.

Even an initially 'sterile' peritonitis (e.g. one due to intraperitoneal rupture of the bladder or a haemoperitoneum) so on becomes infected by transmigration of organisms from the bowel, and it is not long (often a matter of hours) before such a situation becomes a peritonitis in the usual meaning of the term. Most duodenal perforations are initially sterile for up to several hours, and many gastric perforations are also sterile at first; intestinal perforations are usually infected from the beginning. The proportion of anaerobic to aerobic organisms increases with the passage of time. Mortality reflects:

• the degree and duration of peritoneal contamination;

• the age of the patient;

• the general health of the patient;

• the nature of the underlying cause.

Natural factors that favour localisation of peritonitis

These factors are anatomical, pathological and surgical.

Anatomical. Excluding the subphrenic spaces, the greater sac of the peritoneum is divided into the pelvis, and the peritoneal cavity proper. The latter is redivided into a supracolic and an infracolic compartment by the transverse colon and transverse mesocolon, which deter the spread of infection from one to the other. When the supracolic compartment overflows, as is often the case when a gastric ulcer perforates, it does so over the colon into the infracolic compartment, or, by way of the right paracolic gutter to the right iliac fossa, and thence to the pelvis. Posture can assist in directing collections into the pelvis, as in the Sherren regime for perforated appendicitis.

Pathological. The clinical course is largely governed by the manner in which adhesions form around the affected organ. Inflamed peritoneum loses its glistening appearance and becomes reddened and velvety. Flakes of fibrin appear and cause coils of intestine to become adherent to one another and to the parietes. There is an outpouring of serous fluid rich in leucocytes and antibodies that soon becomes turbid; if localisation occurs, the turbid fluid becomes frank pus. Peristalsis is retarded in affected coils, and this helps in preventing distribution of the infection. The greater omentum, by enveloping and becoming adherent to inflamed structures, often forms a substantial barrier to the spread of infection.

Surgical. Drains are frequently used postoperatively to assist localisation (and exit) of intra-abdominal collections: their value is disputed, and certain types of drain, e.g. red rubber, are known to be both a cause of increased peritoneal exudate and a route for bacterial invasion.

Natural factors that tend to cause diffusion of peritonitis

There are several natural factors promoting diffusion:

• a prime factor in the spread of peritonitis is whether it develops rapidly or slowly. If an inflamed appendix or other hollow viscus perforates early on before protective mechanisms have mobilised, there is a free gush of intestinal contents into the peritoneal cavity, which spreads over a large area almost instantaneously (Fig. 1). Perforation proximal to an obstruction, or from sudden anastomotic separation, is associated with severe generalised peritonitis and a high mortality.

• the ingestion of food, or even water, by stimulating peristaltic action, hinders localisation. Violent peristalsis occasioned by the administration of apurgative or an enema, promotes a widespread distribution of an infection that might otherwise have remained localised;

• when the virulence of the infecting organism is so great as to render control of the infection difficult or impossible;

• in children, the omentum is small;

• injudicious and rough handling of localised collections, e.g. appendix mass or pericolic abscess;

• deficient natural resistance ('immune deficiency'): this can result from drugs (e.g. steroids), disease (e.g. AIDS) or infancy and old age.

Fig. 1 Sudden perforation, especially if engendered by purgation,

often results in an immediate, widespread bacterial peritonitis.

Clinical features

Localised peritonitis is bound up intimately with the causative lesion, and the initial symptoms and signs are those of that lesion. When the peritoneum becomes inflamed the temperature, and especially the pulse rate, rise. The pain increases and usually there is associated vomiting. The most important sign is guarding and rigidity of the abdominal wall over the area of the abdomen which is involved, with a positive 'release' sign. If inflammation arises under the diaphragm, shoulder tip ('phrenic') pain may be felt. In cases of pelvic peritonitis arising from an inflamed appendix in the pelvic position or from salpingitis, the abdominal signs are often slight, deep tenderness of one or both lower quadrants alone being present, but a rectal or vaginal examination reveals tenderness, often exquisite, of the pelvic peritoneum. With appropriate treatment, localised peritonitis usually resolves. In about 20 per cent of cases an abscess follows. Infrequently, localised peritonitis becomes diffuse. Conversely, in favourable circumstances diffuse peritonitis can become localised, most frequently in the pelvis or at multiple sites within the abdominal cavity. A large collection of bile localised to the subhepatic space can remain dangerously 'silent' until a late stage.

Diffuse (syn. generalised) peritonitis.

Initial phase. There is severe pain which is made worse by moving or breathing. It is first experienced at the site of the original lesion, and spreads outwards from this point. Vomiting may occur. The patient usually lies still. Tenderness and rigidity on palpation are typically found when the peritonitis affects the anterior abdominal wall. Abdominal tenderness and rigidity are diminished or absent if the anterior wall is unaffected as in pelvic peritonitis or, rarely, peritonitis in the lesser sac. Patients with pelvic peritonitis may complain of urinary symptoms; they are tender on rectal or vaginal examination. Infrequent bowel sounds may still be heard for a short time, but they cease with the onset of paralytic ileus. The pulse rises progressively but if the peritoneum is deluged with irritant fluid there is a sudden rise. The temperature changes are variable and can be subnormal.

Intermediate phase. Peritonitis may resolve, so that the pulse slows, the pain and tenderness diminish leaving a silent, soft abdomen. (These are features that can easily mislead the observer.) The condition may localise, producing one or more abscesses, will overlying swelling and tenderness.

Terminal phase. If resolution or localisation have no occurred, the abdomen remains silent, and increasingly distends. Circulatory failure ensues, with cold, clammy extremities, sunken eyes, dry tongue, thready (irregular) pulse, drawn and anxious face (Hippocratic facies. Fig. 2). The patient finally lapses into unconsciousness. With early diagnosis and adequate treatment, this condition is rarely seen in moden surgical practice.

Diagnostic aids. Investigations will not save the need for careful confirmation of the history and physical signs, which are tendeness, guarding and rigidity with a distending silent abdomen. It unwise to rely slavishly on any single symptom or sign; not one incontrovertible.

A battery of investigations may elucidate a doubtful diagnosis. More often, they only confuse it. Peritonitis usually produces leucocytosis, often delayed for many hours.

Peritoneal diagnostic aspiration may be helpful but is usual unnecessary. After infiltrating the skin of the abdomen with local anaesthetic, fine-needle aspiration of each quadrant of the abdominal cavity is made. Bile-stained fluid indicates perforated peptic ulcer, the presence of pus indicates bacterial peritonitis; blood is aspirated in a high proportion of patients with intraperitoneal bleeding. When aspiration fails, the introduction of a small quantity of sterile physiological saline, followed after a few minutes by repeat aspiration, may produce fluid of diagnostic value.

A radiograph of the abdomen may reveal free air, or confirm the presence of dilated gas-filled loops of bowel with multiple fluid levels. If the patient is too ill for an 'erect' film to demonstrate free air collecting under the diaphragm, a lateral decubitus film is just as useful, showing gas beneath the abdominal wall.

Serum amylase estimation may uphold the diagnosis of pancreatitis, provided it is remembered that raised values are frequently found following other abdominal catastrophes, and operations, e.g. perforated duodenal ulcer.

Ultrasonography is a most valuable investigation for demonstrating the presence of intraperitoneal collections of fluid or pus. It can be combined with guided aspiration of any demonstrated collection.

An isotope scan is valuable in cases of serious difficulty.

Treatment

It cannot be stressed too strongly that in any case of doubt, early surgical intervention is to be preferred to a 'wait and see' policy; for greater numbers of patients die from delay than from an 'unnecessary' laparotomy. This rule is particularly true for postoperative peritonitis.

Treatment consists of three parts:

• general care of the patient;

• neutralisation of the local source;

• peritoneal lavage.

General care of the patient.

Intravenous fluids. These patients are often hypovolaemic and have electrolyte disturbances. The plasma volume must be restored and the plasma electrolyte concentrations corrected. The use of a central venous line is imperative for monitoring accurate fluid replacement. Plasma protein depletion may need correction – inflamed peritoneum leaks protein calamitously and continuously. If the patient's recovery is delayed for more than 7-10 days, intravenous feeding ('hyperalimentation') is required.

A nasogastric tube is passed into the stomach, which is aspirated. Intermittent aspiration is maintained until paralytic ileus resulting from peritonitis has resolved. Measured volumes of water are allowed by mouth when only small amounts are being aspirated. If the abdomen is soft and not tender, and bowel sounds return, oral feeding may be progressively introduced. It is important not to prolong the ileus by missing this stage.

Antibiotics. Administration of antibiotics prevents the multiplication of bacteria, and the release of endotoxins. As the infection is usually a mixed one, initially parenteral broad-spectrum antibiotics active against aerobic and anaerobic organisms and metronidazole may be given.

A fluid balance chart must be started at once so that daily output by gastric aspiration and urine are known, and losses from the lungs, skin, and in faeces are estimated, so that the intake requirements can be calculated and seen to have been administered.

Throughout recovery, haematocrit and serum electrolyte values and the blood urea must be checked frequently.

Analgesia. The patient, nursed in the sitting-up position, must be relieved of pain before and after operation. Once the diagnosis has been made, morphine may be given, and small doses continued for 48 hours. Freedom from pain allows early mobilisation and adequate physiotherapy in the postoperative period, to prevent atalectasis, deep-vein thrombosis and pulmonary embolism.

Oxygen. Especially if septic shock is present, special measures may be needed for cardiac, pulmonary and renal support. Administration of oxygen postoperatively can help to prevent and mitigate the effects of septic shock, especially adult respiratory distress syndrome (ARDS). If oligaemia persists despite adequate fluid replacement, both dopamine and diuretics may be needed.

Neutralisation of local source. If the cause is amenable to surgery, such as in perforated appendicitis, diverticulitis, peptic ulcer, gangrenous cholecystitis, or rarely in perforation of the small bowel, operation must be carried out as soon as the patient is fit for anaesthesia. This is usually within a few hours. In peritonitis due to pancreatitis, salpingitis, or in cases of primary peritonitis of streptococcal or pneumococcal origin, conservative treatment is the procedure of choice (if the diagnosis can be made with certainty).

Peritoneal lavage. In surgery for general peritonitis it is essential that after the cause has been dealt with, the whole peritoneal cavity should be explored with the sucker and mopped dry, if necessary until all seropurulent exudate is emoved. The use of a large volume of antibiotic saturated saline (1-2 litres) has been shown to be very effective for 'cleaning' the peritoneum.

Prognosis

With modern treatment diffuse peritonitis carries a mortality of about 10 per cent. The lethal factors are:

• bacterial toxaemia;

• paralytic ileus;

• bronchopneumonia;

• electrolyte imbalance;

• renal failure;

• undrained collections;

• bone-marrow suppression;

• 'multisystem breakdown'.

Post-operative peritonitis has a mortality of at least 50 per cent. Faecal peritonitis has a mortality of 75 per cent. Peritonitis associated with appendicitis, perforated peptic ulcer or bile-leakage are much less dangerous (mortality less than 10 per cent).

Complications of peritonitis

All the complications of a severe bacterial infection are possible, but the special complications of peritonitis are as follows.

Acute intestinal obstruction due to peritoneal adhesions. This usually gives central colicky abdominal pain with radiological evidence of gas and fluid levels confined to the upper portion of the small intestine. It is more common with localised peritonitis. It is essential to distinguish this from paralytic ileus.

Paralytic ileus. There is usually little pain and gasfilled loops with fluid levels are seen distributed throughout the small and large intestines on the radiograph. In intestinal obstruction, bowel sounds are increased. In paralytic ileus bowel sounds are reduced or absent.

Residual abscesses. Abscess formation following local or diffuse peritonitis usually occupies one of the situations shown in Fig,2, The symptoms and signs of a purulent collection may be very vague and consist of nothing more than lassitude, anorexia, and failure to thrive; pyrexia (often low-grade), tachycardia, leukocytosis, and localised tenderness are also common. Later on a palpable mass may develop. When palpable, an intraperitoneal abscess should be monitored marking out its limitations on the abdominal wall, meticulous daily examination.

Fig.2 Common situations for residual abscesses: (1) subphrenic(2) paracolic; (3) right iliac fossa(4) elvic.

In the majority of cases with the aid of antibiotic treatment, the mass becomes smaller and smaller, and finally is impalpable. In others, the abscess fails to resolve, or becomes large in which event it must be opened. In many situations, by waiting a few days, the abscess becomes adherent to the abdominal wall, so that it can be drained without opening the general peritoneal cavity. For deeper-situated residual collections, percutaneous placement of drainage tubes under fluoroscopic or ultrasonographic control can be very effective. Open drainage of an intraperitoneal collection should carried out by cautious blunt finger exploration to minimise the risk of an intestinal fistula.

PELVIC ABSCESS

The pelvis is the commonest site of an intraperitoneal abscess, because the vermiform appendix is often pelvic in position and also the Fallopian tubes are frequent loci of infection. A pelvic abscess can also occur as a sequel to any case of diffuse peritonitis and is a common sequel of anastomotic leakage following large bowel and rectal surgery. Pus can accumulate in this area without serious constitutional disturbance, and unless the patient is examined carefully from day to day, such abscesses may attain considerable proportions before being recognised. The most characteristic symptoms of a pelvic abscess are diarrhoea and the passage of mucus in the stools. It is no exaggeration to say that the passage of mucus occurring for the first time in a patient who has, or is recovering from, peritonitis, is pathognomonic of pelvic abscess. Rectal examination reveals a bulging of the anterior rectal wall which, when the abscess is ripe, becomes softly cystic. Left to nature, a proportion of abscesses burst into the rectum, after which the patient nearly always recovers rapidly. If this possible happy termination does not readily occur, the abscess should be drained deliberately. In women, vaginal drainage through the posterior fornix is often chosen. In other cases, where the abscess is definitely pointing into the rectum, rectal drainage (Fig.3) is employed. If any uncertainty exists as to the presence of pus, either an ultrasound examination aspirating needle introduced into the collection through the rectal wall or through the abdominal wall (after emptying the bladder by a catheter) will settle the question. Laparotomy is almost never necessary.

Provided the abscess is shut off from the general peritoneal cavity, a point which can be ascertained undeniably when the abdomen has been opened, rectal drainage of a pelvic abscess is far preferable to suprapubic drainage, which breaks down nature's barriers and exposes the general peritoneal cavity to the dangers of spreading infection.

Fig.3 Opening a pelvic abscess into the rectum.

SUBPHRENIC ABSCESS

Anatomy. The complicated arrangement of the peritoneum results in the formation of four intraperitoneal and three extraperitoneal subphrenic spaces in which pus may collect. Three of these spaces are on either side of the body, and one approximately in the midline

(Figs 4 and 5).

Left superior (anterior) intraperitoneal ('left subphrenic'), bounded above by the diaphragm, behind by the left triangular ligament and left lobe of the liver, the gastrohepatic omentum and anterior surface of the stomach. To the right is the falciform ligament, and to the left the spleen, gastrosplenic omentum, and diaphragm. The common cause of an abscess here is following operations on the stornach, the tail of the pancreas, the spleen or the splenic flexure of the colon or in diverticulitis.

Left inferior (posterior) intraperitoneal ('left subhepatic') is another name for the ‘lesser' sac. The commonest type of suppuration here is the pancreatic pseudocyst. In practice, perforated gastric ulcer rarely causes a collection here, because the potential space is obliterated by adhesions.

Right superior (anterior) intraperitoneal ('right subphrenic'), which lies between the right lobe of the liver and the diaphragm. It is limited posteriorly by the anterior layer of the coronary and the right triangular ligaments, and to the left by the falciform ligament.

Common causes here are perforating cholecystitis, a perforated duodenal ulcer, a duodenal cap 'blow out' and appendicitis.

Right inferior (posterior) intraperitoneal ('right subhepatic') lies transversely beneath the right lobe of the liver in Rutherford Morison's pouch. It is bounded on the right by the right lobe of the liver and the diaphragm. To the left is situated the foramen of Winslow, and below this lies the duodenum. In front are the liver and gallbladder, and behind, the upper part of the right kidney and diaphragm. The space is bounded above by the liver, and below by the transverse colon and hepatic flexure. It is the deepest space of the four and the commonest site of a subphrenic abscess which usually arises from appendicitis, cholecystitis, a perforated duodenal ulcer or following upper abdominal surgery.

Extraperitoneal. There are three of these:

• Right and left extraperitoneal which are terms given to perinephric abscesses.

• Midline extraperitoneal which is another name for the 'bare' area of the liver which may develop an abscess in amoebic hepatitis (the commonest cause) or it may be a pyogenic liver abscess.

Fig. 4. Intraperitoneal subphrenic abscesses on transverse

section. (1) the left superior space; (2) left inferior space (lesser sac);

(3) right superior space which becomes shut oft by adhesions from (4)

right inferior space.

Fig. 5. Intraperitoneal subphrenic abscesses on sagittal section.

(1) left superior erior) abscess (left subphrenic'); (2) left inferior

(posterior) abscess (left subhepatic'); (3) right superior (anterior)

abscess ('right subphrenic'); (4) right inferior (posterior) abscess ('right

subhepatic').

Clinical features. The symptoms and signs of subphrenic infection are frequently unspecific, and it is well to remember the aphorism, 'Pus somewhere, pus nowhere else, pus under diaphragm'.

Symptoms. A common history is that when some infective focus in the abdominal cavity has been dealt with, the condition of the patient improves temporarily, but after an interval of a few days or weeks, symptoms of toxaemia reappear. The condition of the patient steadily, and often rapidly, deteriorates.

Sweating, wasting, and anorexia are present. There is sometimes epigastric fullness and pain, or pain in the shoulder on the affected side, owing to irritation of sensory fibres in the phrenic nerve, referred along the

descending branches of the cervical plexus. Persistent hiccup may be a presenting symptom.

Signs. A swinging pyrexia is usually present, unless antibiotics or drugs (steroids) have interfered. If the abscess is anterior, abdominal examination will reveal some tenderness, rigidity, or even a palpable swelling.

Sometimes the liver is displaced downwards, but more often it is fixed by adhesions. Examination of the chest is important, and in the majority of cases collapse of the lung or evidence of basal effusion or empyema is to be found.

Accessory investigations.

Blood count. A relative and absolute leucocytosis is usual.

A plain radiograph sometimes demonstrates the presence of gas (Fig.6) or a pleuralffusion. On screening, the diaphragm is often seen to be elevated (so-called 'tented' diaphragm) and its movements impaired.

Ultrasonography and CT, NMR and scinti-scanning have proved strongly contributory to diagnosis (Fig. 9).

Differential diagnosis. Pylephlebitis, tropical abscess, pulmonary collapse, and empyema give rise to most of the diagnostic difficulties.

Treatment. The clinical course of suspected cases is watched, and blood and radiological examinations are made at suitable intervals. If suppuration seems probable, intervention is indicated. If skilled help is available it is frequently possible to insert a percutaneous drainage tube 'blindly' under combined ultrasonic and fluoroscopic control. The same tube can be used to instil antibiotic solutions into the abscess cavity. To pass an aspirating needle at the bedside through the pleura and diaphragm invites catastrophic spread of the infection into the pleural cavity.

If a swelling can be detected in the subcostal region or in the loin, an incision is made over the site of maximum tenderness, or over any area where oedema or redness is discovered. The parietes usually form part of the abscess wall, so that contamination of the general peritoneal cavity is unlikely.

If no swelling is apparent, the subphrenic spaces should be explored either by an anterior subcostal approach or from behind after removal of the outer part of the 12th rib according to the position of abscess as indicated on a lateral radiograph (see above). With the posterior approach the pleura must not be opened, and after the fibres of the diaphragm have been separated a finger is inserted beneath the diaphragm so as to explore the adjacent area. Thus both approaches must be extraserous to avoid dissemination of pus into the peritoneal or pleural cavities (Barnard).

When the cavity is reached, all the fibrinous loculi must be broken down with the finger and one or two drains or drainage tubes must be fully inserted. Drains are withdrawn gradually during the next 10 days and the closure of the cavity checked by radiological sinograms (as also after percutaneous drainage).

SPECIAL FORMS OF PERITONITIS

Postoperative peritonitis. The patient is ill, with raised pulse and peripheral circulatory failure. Following an anastomotic dehiscence, the general condition of a patient is far more grave than if the patient had suffered leakage from a perforated peptic ulcer with no preceding operation. Local symptoms and signs are less definite, particularly if steroids are being given,

Abdominal pain may not be prominent, tenderness may be masked by the presence of a recent wound.The patient's deterioration may be wrongly attributed to cardiopuirnonary collapse, which is usually concomitant.

Peritonitis follows abdominal operations more frequently than is realised. The principles of treatment do not differ from those of peritonitis of other origin. Antibiotic therapy alone is inadequate; no antibiotic can stay the onslaught of bacterial peritonitis due to leakage from a suture line, which must be dealt with surgically.

In patients under treatment with steroids. Pain is frequently slight or absent. Physical signs are similarly vague and misleading.

In children. The diagnosis is in some ways more difficult, in other ways more easy, than in adults. If a history can be taken it is plain and unembroidered. Any physical signs elicited, by a gentle, patient, and sympathetic examiner are meaningful. The 'assistance' of an overanxious mother can be a serious impediment: conversely, the opinion of an experienced nurse can be fundamental in making the diagnosis.

In senile patients. These can be as fractious as, children and unable to give a reliable history. Abdominal tenderness is usually well localised, but guarding and rigidity are less marked because the abdominal muscles are thin and weak.

Bile peritonitis. Unless there is reason to suspect that bile duct was damaged, it is improbable that bile has a cause of peritonitis will be thought of until the

• following biliary surgery, e.g. damage to the common bile duct, slipping of a ligature on the cystic duct, leakage from a divided accessory bile duct in the gallbladder bed or dislodgement of a T-tube drain in the early postoperative phase;

• instrumental perforation at endoscopic retrograde cholangiopancreatography or placement of a bile-duct stent;

• following perforation or gangrene of the gallbladder or leakage from a choledochus cyst;

• following gastroduodenal surgery, e.g. duodenal cap 'blow out' or leakage from a suture line.

Unless the bile has extravasated slowly, when the collection becomes shut off from the general peritoneal cavity, there are signs of diffuse peritonitis with a degree of shock. After a few hours a tinge of jaundice is not unusual. Local drainage, and when necessary suprapubic peritoneal drainage, is imperative, and if performed early enough, these measures will save the patient's life. When bile is seen issuing from a perforation of some part of the biliary tree, a drainage tube should be passed through the opening and secured there. Infected bile is more lethal than sterile bile. The gallbladder, if present, hould be drained. A 'blown' duodenal stump must be drained as it is too oedematous to repair, but sometimes it can be covered

by a jejunal patch. If the patient is jaundiced the surgeon must ensure that the abdomen is not closed until any possible cause of obstruction to a major bile duct has been either excluded or relieved.

Meconium peritonitis. Meconium is a sterile mixture of epithelial cells, mucin, salts, fats, and bile, and is formed when the fetus commences to swallow amniotic fluid. By the third month of intrauterine life, the upper third of the small intestine has become filled with meconium; by the fourth month, the accumulation has reached the ileocaecal valve; during the remainder of intrauterine life the colon becomes increasingly filled.

Meconium peritonitis is an aseptic peritonitis which develops late in intrauterine life or during, or just after, delivery. Meconium enters the peritoneal cavity through an intestinal perforation, and in over 50 per cent of cases the perforation is the result of some form of neonatal intestinal obstruction; in the remainder no cause for the perforation is discernible. When meconium, which is sterile, enters the peritoneal cavity an exudate is secreted that organises rapidly; matting of intestinal loops occurs, and in many cases in a matter of weeks the extruded meconium becomes calcified.

Meconium remains sterile until about 3 hours after birth; thereafter, unless the perforation has become sealed, sterile meconium peritonitis gives place to acute bacterial peritonitis which, unless treated promptly, is rapidly fatal.

Clinical features. Meconium peritonitis should always be considered when a baby is born with a tense abdomen. There is vomiting, and failure to discharge meconium. The differential diagnosis between neonatal intestinal obstruction and peritonitis is, in many cases, virtually impossible; indeed, in half the cases both are present. Free fluid in the peritoneal cavity is often sufficient to give a fluid thrill. In many cases, there are exocrine secretory deficiencies elsewhere, e.g. lungs, pancreas, salivary glands (syn. 'mucoviscidosis'). Bronchial obstruction by mucus plugs can be an immediate cause of fatal pneumonia. In some cases the mother may have been identified as having the abnormal genes responsible for the condition.

Radiography. Free air in the peritoneal cavity, an abundant quantity of abdominal fluid, fluid levels, calcification (often most distinct on the surface of the liver or the spleen, and most readily seen in a lateral view) are characteristic findings, all of which are unlikely to be present in every case. Meconium peritonitis has been diagnosed by radiography of the fetus in utero 2days before birth.

Treatment. The prognosis is bad, but recovery has followed prompt operation in some cases. The greatest

chance of survival is in those patients who have an intestinal perforation but no intestinal obstruction, in which case closing the perforation and draining the peritoneal cavity is all-sufficient, and can be performed expeditiously. Intestinal lavage can prevent reformation of meconium bolus' obstruction, and supplements of pancreatic exocrine enzymes may be necessary until adult life. If there is an associated pulmonary problem, the condition requires special treatment (e.g. 02, bronchial lavage, nebulisers and long-term use of antibiotics).

Pneumococcal peritonitis. There are two forms of this disease: (1) primary, and (2) secondary to pneumonia.

Primary pneumococcal peritonitis is much the more common. The patient is often an undernourished girl between 3 and 6 years of age, and it is probable that the infection sometimes occurs via the vagina and Fallopian tubes, for pneumococci have been cultured from patients' vaginas. At other times, and always in males, the infection is blood-borne from the upper respiratory tract or the middle ear. After the age of 10 years, pneumococcal peritonitis is most unusual. Children with nephritis are more liable to this condition than others. During the past 30 years, the incidence of pneumococcal peritonitis has declined greatly and the condition is now rare. Perhaps this is on account of the greater cleanliness and higher standard of living of what were the poorer classes, as well as early use of antibiotics to treat infections.

Clinical features. The onset is sudden, and the earliest symptom is pain localised to the lower half of the abdomen. The temperature is raised to 39.8°C or more, and there is usually frequent vomiting. After 24 to 48 hours profuse diarrhoea, occasionally bloodstained, is characteristic. There is usually increased frequency of micturition. The last two symptoms are due to severe pelvic peritonitis. Herpes on the lip or nostril is often present. In acute forms of the disease, even in cases where there is no involvement of a lung, there is a tinge of cyanosis of the lips and cheeks, and movement of the alae nasi is often discernible. On examination rigidity is usually bilateral, but is less than in most cases of acute appendicitis with peritonitis.

Differential diagnosis. A leucocytosis of 30 OOO/mm3 (30 x 10"/l) or more with approximately 90 per cent polymorphs speaks more for pneumococcal peritonitis than appendicitis. Even so, it is often impossible, especially in males, to exclude perforated appendicitis. The other condition which is extremely difficult to differentiate from primary peritonitis in its early stage is pneumonia. An unduly high respiratory rate and the absence of abdominal rigidity are the most important signs supporting the diagnosis of pneumonia, which is usually clarified by a radiograph of the thorax.

Treatment. Early operation is always required. After correcting dehydration and electrolyte imbalance, a short paramedian incision is made over the right rectus abdominis. The peritoneum is incised. Should the exudate be odourless and sticky, the diagnosis of pneumococcal peritonitis is practically certain, but it is desirable to perform a routine laparotomy to exclude other lesions. Assuming that no other cause for the peritonitis is discovered, some of the exudate is removed with a syringe, and sent to the laboratory for culture and sensitivity tests. Thorough peritoneal lavage is carried out and the incision closed. The patient is returned to bed and antibiotic and fluid replacement therapy continued. Gastrointestinal suction drainage is essential. Recovery is usual.

Primary streptotoccal peritonitis of infants and children is rather more frequent than the foregoing but still uncommon. When a streptococcus is the infecting organism, the peritoneal exudate is thin, slightly cloudy, and contains flecks of fibrin. From the standpoints of clinical aspects and treatment, streptococcal peritonitis in infants and children does not differ from those detailed in the account of pneumococcal peritonitis (see above), but the mortality is higher. An intravaginal foreign body (e.g. a toy) should always be looked for in female patients.

Idiopathic streptococcal and staphylococcal peritonitis in adults is fortunately rare, for, before the antibiotic era, it was nearly always fatal, and the mortality is still very high. Rightly, in early cases the abdomen is opened, usually on a diagnosis of acute appendicitis. In streptococcal peritonitis the peritoneal exudate is odourless, thin, contains small flecks of fibrin, and may be bloodstained. In these circumstances pus is removed by suction, the abdomen closed with suprapubic drainage, and the measures detailed in the conservative treatment of peritonitis carried out. The use of intravaginal tampons has led to an increased incidence of Staph. aureus infections: these can be associated with 'toxic shock syndrome' and disseminated intravascular coagulopathy.

Peritonitis following abortion/parturition. The abortionist has usually pushed an instrument through the uterine vault and streptococcal peritonitis follows. When peritonitis follows puerperal infection, it is a notifiable disease. It is more common after first deliveries. Rigidity is seldom much in evidence; this, in part, is due to the stretched condition of the abdominal musculature. The lochia may be offensive but not necessarily so. Diarrhoea is common.

Treatment. Provided the infection is limited strictly to the pelvis, the correct treatment is rest for the alimentary canal, intravenous fluids, the required antibiotic, and attention to electrolyte balance. Posterior colpotomy may be necessary if a pelvic abscess forms. If the peritonitis is generalised, the patient is usually extremely ill and drainage is advisable. This is best carried out by making a small suprapubic incision under local anaesthesia and inserting a drain. This can be done with the patient in bed, if necessary. In the preantibiotic era, the mortality of general peritonitis following parturition or abortion was at least 50 per cent; with antibiotic therapy and timely operation, the mortality has fallen to less than 10 per cent (Brews).

Periodic peritonitis is characterised by abdominal pain and tenderness, mild pyrexia, polymorphonuclear leucocytosis and, occasionally, pain in the thorax and joints. The duration of an attack is 24 to 72 hours, when it is followed by complete remission, but exacerbations recur at regular intervals. Most of the patients have undergone appendicectomy in childhood. The disease, often familial, is limited principally to Arabs, Armenians, and Jews; other peoples occasionally are affected. At laparotomy, which may be necessary to exclude other causes, the peritoneum - particularly in the vicinity of the spleen and the gallbladder - is inflamed. There is no evidence that the interior of these organs is abnormal.

Differential diagnosis. Patients with abdominal epilepsy do not have positive physical signs of pyrexia, and their attacks are usually controlled by anticonvulsive medication. The aetiology of periodic peritonitis is unknown, and no form of treatment has been found to be of the slightest avail. Usually, children are affected, but it is not rare for the disease to make its first appearance in early adult life, when females out- number males by two to one. Exceptionally, the disease becomes manifest in patients over 40 years of age.

TUBERCULOUS PERITONITIS

Acute tuberculous peritonitis. Tuberculous peritonitis sometimes has an onset that resembles so closely acute peritonitis that the abdomen is opened. Straw-coloured fluid escapes, and tubercles are seen scattered over the peritoneum and greater omentum. Early tubercles are greyish and translucent. They soon undergo caseation, and appear white or yellow, and are then less difficult to distinguish from carcinoma. Tubercles occasionally simulate fat necroses or the nodules of peritoneal carcinomatosis. On opening the abdomen and finding tuberculous peritonitis, the fluid is evacuated, some being retained for bacteriological study. A portion of the diseased omentum is removed for histological confirmation of the diagnosis, and the wound closed without drainage. At other times, although acute abdominal symptoms arise, the presence of ascites makes the diagnosis of acute tuberculous peritonitis reasonably evident.

Chronic tuberculous peritonitis. Although the incidence of turberculous peritonitis has declined in Britain, in many parts of the world where measures for eradicating tuberculosis (especially the disease in cows) are enforced less strictly, the condition still occurs.

Presentation. Abdominal pain is present in 90 per cent, fever in 60 per cent, loss of weight in 60 per cent, ascites in 60 per cent, night sweats in 37 per cent, and abdominal mass in 26 per cent.

Origin of the infection

Infection originates from:

• tuberculous mesenteric lymph nodes;

• tuberculosis of the ileocaecal region;

• a tuberculous pyosalpinx;

• blood-borne infection from pulmonary tuberculosis, usually the 'miliary' but occasionally the 'cavitating' form.

There are four varieties of tuberculous peritonitis: ascetic, encysted, fibrous and purulent.

Ascitic form. The peritoneum is studded with tubercles, and the peritoneal cavity becomes filled with pale, straw-coloured fluid. The onset is insidious. There is loss of energy, facial pallor, and some loss of weight. The patient is usually brought for advice because of enlargement of the abdomen. Pain is often completely absent; in other cases there is considerable abdominal discomfort which may be associated with constipation or diarrhoea. On inspection, dilated veins can be seen coursing beneath the skin of the abdominal wall. Shifting dullness can be elicited readily. In the male child, congenital hydroceles sometimes appear, due to the patent processi vaginales becoming filled with ascitic fluid from the peritoneal cavity. Because of the increased intra-abdominal pressure, an umbilical hernia commonly occurs. On abdominal palpation, a transverse solid mass can often be detected. This is rolled-up greater omentum infiltrated with tubercles.

Diagnosis is seldom difficult, except when it occurs in an acute form or when it first appears in an adult, in which case it has to be differentiated from other forms of ascites, especially from malignant secondary deposits. A positive Mantoux test in a child with ascites strongly suggests, and a negative test is good evidence against, tuberculosis. In adults this test is of negligible value. The diagnosis of tuberculous peritonitis having been made, it is always important to look for tuberculous disease elsewhere, and in this respect the possibility of tuberculous salpingitis in females should be remembered. A chest radiograph should always be taken before a laparotomy is performed.

The fluid is pale yellow, usually clear, and rich in lymphocytes.

The specific gravity is comparatively high, often 1.020 or over. Even after centrifugation, rarely can M. tuberculosis be found, but presence can be demonstrated by culture and confirmed by guineapig inoculation.

Treatment. If the general condition is good, the patient can return home and, if an adult, to light work, before the course of chemotherapy has been completed.

Encysted (syn. loculated) form is similar to the above, but one part of the abdominal cavity alone is involved. This produces a localized intra-abdominal swelling which gives rise to difficulty in diagnosis.

In a female above the age of puberty, when the swelling is in the pelvis, an ovarian cyst will probably be diagnosed. In the case of a child, it is sometimes difficult to distinguish the swelling from a mesenteric cyst. For these reasons laparotomy is often performed, and if an encapsulated collection of fluid is found, it is evacuated and the abdomen is closed. The general treatment already detailed is required, but the response to this treatment is more rapid. Late intestinal obstruction is a possible complication.

Fibrous (syn. plastic) form is characterised by the production of widespread adhesions, which cause coils of intestine, especially the ileum, to become matted together and distended. These distended coils act as a 'blind loop' and give rise to steatorrhoea, wasting and attacks of abdominal pain. On examination, the adherent intestine with omentum attached, together with the thickened mesentery, may give rise to a palpable swelling or swellings. The first intimation t of the disease may be subacute or acute intestinal obstruction. Sometimes the cause of the obstruction can be remedied easily by the division of bands. Lateral anastomosis between an obviously dilated loop and a collapsed loop of small intestine should not be done, as the 'blind loop' syndrome is a certain outcome. If the adhesions are accompanied by fibrous strictures of the ileum as well, it is best to excise the affected bowel, provided not too much of the small intestine needs to be sacrificed. If adhesions only are present, a plication may be performed. Chemotherapy after adequate surgery will rapidly cure the condition.

Purulent form is rare. When it occurs, usually it is secondary to tuberculous salpingitis. Amidst a mass of adherent intestine and omentum, tuberculous pus is present. Sizeable cold abscesses are wont to form, and point on the surface, commonly near the umbilicus, or burst into the bowel. In addition to prolonged general treatment, operative treatment may be necessary for the evacuation of cold abscesses and possibly for intestinal obstruction. If the patient survives long enough to overcome the infection, it may be possible to close a faecal fistula, which otherwise usually persists because of obstruction distal to it. Closure must therefore be combined with some form of anastomosis between the segment of intestine above the fistula and an unobstructed area below. The prognosis of this variety of tuberculous peritonitis is relatively poor.

SCLEROSING PERITONITIS

Practolol, a b-adrenergic blocking agent used in the treatment of cardiovascular disorders, has been found to be associated with the late development of a sclerosing condition in the peritoneum, which may cause intestinal obstruction. At laparotomy, the condition resembles plastic tuberculous peritonitis. It may be confused with mesothelioma or carcinoid syndrome. Lysis of the adhesions is indicated. The condition may cause recurrent obstruction. Since the development of better drugs, this condition is no longer seen.

PERITONEAL BANDS AND ADHESIONS

Congenital bands and membranes occur in the peritoneum as described in textbooks of anatomy. None of them causes intestinal obstruction except an obliterated vitellointestinal duct.

Talc granuloma. Talc (silicate of magnesium) should never be used as a lubricant for rubber gloves for it is a cause of peritoneal adhesions and granulomas in the Fallopian tubes. Potassium bitartrate, which is completely soluble, is free from these serious objections.

TESTS

1. Commonest site of an intraperitoneal absecess is-

a) Subphrenic

b) Paracolic

c) Paraappendix

d) Pelvic

2. Treatment of pouch of Douglas abscess is -

a) Laparotomy

b) Posterior colpotomy

c) Antibiotics

d) Extraperitoneal drainage

3. Early surgery is indicated in -

a) Amoebiasis peritonitis

b) Biliary

c) Typhoid peritonitis

d) All

4. Most common site for intra abdominal abscess following laparotomy is -

a) Subhepatic

b) Subphrenic

c) Pelvic

d) Paracolic

5. Most common cause of generalised peritonitis in a 40 year old adult male is -

a) Enteric perforation

b) Ruptured liver abscess

c) Duodenal Ulcer perforation

d) Perforated Ca stomach

6. Correct about subphrenic abscess is

a) Rarely chest symptoms

b) Toxaemia

c) Rarelly toxaemia

d) No sign and symptoms

7. Odourless peritoneal fluid is noticed in -

a) Perforated petic ulcer

b) Perforated ileum

c) Perforated appendix

8. Best investigation for air in peritoneal cavity is -

a) USG

b) Laparotomy

c) Laparoscopy

d) X-ray abdomen-erect view

e) CT scan

9. Colpotomy is done to treat -

a) Ischeorectal abscess

b) Pelvic abscess

c) Appendicular abscess

d) Perianal abscess

10. Least irritant fluid to peritoneum -

a) Blood

b) Urine

c) Bile

d) Pancreatic fluid

e) Pus

11. The commonest organism seen in peritonitis is -

a) Escherichia coli

b) Clostridium welchii

c) Staphylococci

d) Klebsiella

12. Clinical sign of peritonitis is –

a) Coffee-grounds vomit

b) Sense of fullness in the abdomen

c) Abdominal pain

d) Melena

13. Symptom of peritonitis is –

a) Frog abdomen

b) Board-like abdomen

c) Soft abdomen

d) Abdominal murmur

14. Rebound tenderness symptom is –

a) Symptom of reflex constipation

b) Only abdominal painfulness

c) Guarding of abdominal muscles

d) Shchotkin-Blumberg symptom

15. Sign of peritonitis in its later stage isn’t –

a) Hypoproteinemia

b) Secondary constipation

c) Septic shock (SIRS)

d) Increase of intestinal peristalsis

16. What of investigations is particularly important for the proper diagnostics of peritonitis before the operation?

a) Physical examination

b) USG

c) Laboratory investigations

d) X-ray abdomen-erect view

17. What are functions of the peritoneum? (To answer in writing)

a)

b)

c)

d)

e)

18. What are causes of a peritoneal inflammatory exudate? (To answer in writing)

a)

b)

c)

d)

e)

19. What are paths to peritoneal infection? (To answer in writing. To write examples.)

a)

b)

c)

d)

e)

Answers

17. What are functions of the peritoneum? (To answer in writing)

a) Pain perception (parietal peritoneum)

b) Visceral lubrication

c) Fluid and particulate absorbtion

d) Inflammatory and immune responses

e) Fibrinolytic activity

18. What are causes of a peritoneal inflammatory exudate? (To answer in writing)

a) Bacterial infection, e.g. appendicitis, tuberculosis

b) Chemical injury, e.g. bile peritonitis

c) Ischaemic injury, e.g. strangulated bowel, vascular occlusion

d) Direct trauma, e.g. operation

e) Allergic reaction, e.g. starch peritonitis

19. What are paths to peritoneal infection? (To answer in writing. To write examples.)

a) Gastrointestinal perforation (for example perforated ulcer, diverticular perforation)

b) Exogenous contamination (for example drains, open surgery, trauma)

c) Transmural bacterial translocation, no perforation (for example inflammatory bowel disease, appendicitis, ischaemic bowel)

d) Female genital tract infection (for example pelvic inflammatory disease)

e) Haematogenous spred (rare, for example septicaemia)

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

WOUNDS AND SURGICAL INFECTION IN WOUNDS. ULCERS OF THE LEG (classification, management), PRESSURE SORES (decubitus ulcers) AND ISCHAEMIC ULCERS (classification, prevention, treatment)

Составитель ассистент О.Г.Шахбазян

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

Motivation.

Annually in the country than 12 million patients with bruises, wounds, crises of bones of the top and bottom extremities is registered more, that very often leads to development of purulent processes. In the general structure of surgical diseases the surgical infection is observed at 35-45 % of patients and proceeds in the form of sharp and chronic illnesses or a suppuration of posttraumatic and postoperative wounds (A.M. Svetuhin, UL. Amiraslanov, 2003).

The problem of a surgical infection remains to one of actual in modern surgery. It is connected both with high frequency of case rate, and with essential material inputs that translates this problem from the category medical in the category social and economic, i.e. the state problems. The problem has got the special importance in connection with growth of number of technogenic and natural accidents, military conflicts and acts of terrorism.

Owing to the big social and economic importance of their decision it is necessary to carry questions of an intrahospital infection which development essentially increases lethality, to number of priority questions terms of stay of patients in a hospital and demands significant additional charges on treatment. Today an intrahospital infection transfer from 12 up to 22 % of patients, lethality among which exceeds 25 %.

The retrospective analysis of the reasons of development of heavy purulent complications at 15000 patients translated from various hospitals on treatment in specialized branch of purulent surgery of Institute of surgery of a name of A.V.Vishnevskogo of Russian Academy of Medical Science (Moscow), has revealed in many cases unjustified use of antibiotics (benzilpenicillin, semisyntetic penicillins, cefalosporins and aminoglicozids I-II generations), ineffective now, and the out-of-date preparations for local treatment of wounds (a hypertonic solution of chloride of sodium, ointment Vishnevskovo, ichtiol ointments, streptocid, tetraciklin, phurocillin, hentamicin ointments on a fatty basis). As a result the due antibacterial effect is not provided, and at local treatment of wounds also is not reached necessary anesthetizing, osmotic and antiedematic effects. As show numerous researches, the structure of originators of purulent complications of wounds (the significant share is necessary on anaerobs and fungi) has changed also.

Formation of stability of microorganisms to "old" preparations dictates necessity of introduction of new groups of medical products with a wide spectrum of activity (not only concerning aerobs, but also anaerobs) and their applications in strict conformity with a phase of wounds process.

The purposes of studying.

The student should be able :

• To estimate complaints of the patient, revealing data for the complicated current wound process (strengthening be ill, occurrence of attributes of an inflammation, development of the general reaction of an organism in the form of a fever, rises in temperature of a body, etc.);

• In detail to collect the anamnesis of disease, paying special attention On aetiological and the pathogenetic moments of formation of a wound, background conditions (stress, an alcoholic, medicamental, narcotic intoxication, violent actions, etc.);

• To reveal in the anamnesis the diseases influencing on reparativ process and the immune status of the patient;

• To estimate a way of life and working conditions, to establish their possible value in development of a pathology;

• To make external survey and to interpret the received data (character of damage of tissues, the sizes of a wound, number of damages, their localization, presence of inflammatory changes, danger of development of a bleeding, a condition regional lymphatic noduls);

• To estimate the general condition of the patient, a degree of an intoxication of an organism, character and volume of lesion (depth of a wound, the attitude the wound channel to cavities of a body, presence of damages of bones and internal organs, presence of inflammatory changes in depth of a wound);

• To interpret results of bacteriological research (to detail a microbic landscape of a wound to estimate its microbic obsemenation, sensitivity of microflora antibiotics);

• To estimate dynamics of current wound process;

• To carry out a fence of a material from a wound for microbiological research;

• Independently to tie up patients with purulent wounds, to make necrectomia;

• To appoint antibacterial, immuncorrectial, dezintoxication treatment, physiotherapeutic methods of treatment.

The student should know:

• Wound process is a complex of local and general reactions of the organism developing in reply to damage of tissues and introduction of an infection;

• The so-called "critical" level is necessary for development of an infection in a wound bacteriemic obsemenation, corresponding concentration of microorganisms - 105-106 microbic bodies on 1 gram of a tissue (in the certain conditions the "critical" level can be and lower);

• The surgical infection has features of clinical displays depending on the originator or associations of microorganisms in a wound that defines strictly an individual approach in treatment on a background of a recognition of uniform principles of treatment of purulent wounds;

• The mephitic gangrene is the heaviest kind of a surgical infection;

• Treatment of purulent wounds provides carrying out of the multidirected medical influence which is carried out according to a phase of wound process;

• Principles of active surgical treatment of purulent wounds include a complex of the actions directed on the maximal reduction of terms of current of all phases of wound process with the purpose of its limiting approach not complicated current;

• Microbiological researches of contents from a wound is obligatory and provides direct microscopy a material, bacterial inculatiuon and definition of sensitivity of microflora to antibiotics;

• Results of microbiological research allow to corection spent treatment of a purulent wound;

• Modern preparations for local treatment of wounds possess the combined medical action (antimicrobic, anesthetizing, osmotic, antiedematic, wound healing, necrolitic), and application wound coverings, owing to their structure, promote least traumatic and to painless carrying out of bandagings;

• Any change of a bandage should occur in sterile conditions;

• The doctor who is carrying out bandaging, should take special measures for own protection against an infection - from latex, protection gloves are necessary for eyes, and also a mask on a mouth and a nose;

• Accurately imposed bandage, being visible end of processing of a wound, creates feeling at the patient, that it qualitatively treat and serve.

Basic knowledge.

1. Patophisiology of wound process.

Lectures on pathological physiology.

2. The Doctrine about an inflammation.

Lectures on pathological physiology.

3. Morphology of wound process.

Lectures on pathological anatomy.

4. Microbiology of wounds.

Lectures on microbiology.

5. Aseptics and antiseptics.

Lectures on the general surgery.

6. Kinds of healing of wounds.

Lectures on the general surgery.

6. Primary and secondary surgical treatments of wounds.

Lectures on the general surgery, traumatology.

7. Methods drenaging of wounds.

Lectures on the general surgery.

8. Bandaging.

Lectures on the general surgery.

9. The Surgical infection.

Lectures on the general surgery.

Questions for self-preparation:

On basic knowledge;

1. Attributes of an inflammation.

2. The Pathogenesis of wound process.

3. The Histogenesis of wound process.

4. The Microbiological characteristic of wounds.

5. Kinds of healing of wounds.

6. Primary and secondary surgical treatments of wounds.

7. Kinds of a surgical infection.

8. Methods drenaging of wounds.

9. Principles of imposing of bandages.

On a new theme:

1. Concept about a wound, classification of wounds.

2. Phases of current of wound process.

3. Characteristic of a purulent wound.

4. General principles of treatment of wounds.

5. Treatment of wounds depending on a stage of wound process.

6. Principles of active surgical treatment of purulent wounds.

7. Suturation on a purulent wound.

8. Rules of a fence of a material from a wound for microbiological research.

9. " Physical methods of influence " on wound process.

10. The Mephitic gangrene.

11. Practical carrying out of change of a bandage.

The maintenance of employment.

1. Wounds - mechanical damage of a tissue with infringement of their integrity.

Classification of wounds.

1. 1. By the form the wound agent

Bullet

Fragmental

From influence of a blast wave

From a secondary splinter

From a cold steel

From the casual reasons (trauma)

Surgical

2. On character of damage of tissues

Dot

Fragmentary

Crushed

Contused

Incised

Chopped

Chipped

Sawed

Bitten

Scalped

3. On extent and the attitude To cavities of a body

Blind

The Tangent

Through

Not Getting

Getting into a cavity

4. On number of damages At one wounded

Single

Plural

Combined

5. By the form damaged tissues- With damage:

Soft parts

Bones and joints

Nerves

Large arteries and veins

Internal organs

6. To an anatomic attribute

Heads

Necks

Breasts

The Stomach

The Basin

Extremities

7. On microbic obsemenation

Is bacteriemic-polluted

Aseptic

Fresh wounds till the moment of a full covering their granulations are capable to soak up toxins, bacteria, products of disintegration of tissues. The wounds covered by granulations, practically do not possess soaking up ability.

Theoretical researches show, that the major factor in development of an infection are the structure and a functional condition of tissues of a wound. Presence at a wound of the closed cavities, the alien bodies which have become lifeless, the tissues deprived blood supply promotes development of a wound fever. Development of pathogenic microflora in a wound and resorption products of disintegration of impractical tissues stimulations of blood cells and promote a connecting tissue, lead to allocation citokins and other mediators of an inflammation with a wide spectrum of biological action (system changes of a metabolism, immunity, a condition of a vascular wall, hemopoesis, functions of regulitary systems).

A.M. Svetukhin and J.L.Amiraslanov (2003) specify, that there are no qualitative distinctions during of wound process depending on aetiologycal factors. Proceeding from it, the concept of unity of a pathogenesis wound process irrespective of an origin, the sizes, localization and character of a wound is developed.

2. Phases of current wound process.

Current wound process can be divided into three basic phases:

I - a phase of an inflammation

• The period of vascular changes;

• The period of clarification from necrosis tissues;

II - a phase of neogenesis and development granulation tissues;

III - a phase of scar reorganization and cuticularizations.

3. The characteristic of a purulent wound.

It is proved, that for development of an infection in a wound presence of 105-106 microbic bodies on 1 gram of a tissue is necessary. It is a so-called "critical" level bacteriemic obsemenation. But the "critical" level can be and low. So, for development of an infection at presence of blood, alien bodies, ligature in a wound there are enough 104 (10000) microbic bodies; at setting ligature in a zone the ligatur ischemia of tissues - has enough 103 (1000) microbic bodies on 1 gram of a tissue. The combination of damage of tissues to a shock reduces threshold value of microbic number up to 103 (1000) in 1 г tissues, and with radiating lesions - up to 102 (100).

Wound ekssudat from a purulent wound it is rich with fiber, consists of cellular elements, basically - neutrophil leukocytes, a plenty of bacteria, the rests of the destroyed cells and a mix transsudat with fibrin.

A plenty of the microorganisms, the expressed degeneration neutrophil leukocytes, phagocytozis in pus specify presence of plasmocytes, decrease in quantity of one-nuclear leukocytes and absence adverse current of healing of a wound.

Development of inflammatory reaction depends on a degree of resistibility of tissues, reactance of an organism and virulently of infections.

According to recommendations the CART, all most often meeting bacteriemic patogens are divided on levels prerogative:

I. Patogens a high level prerogative:

A piogenic streptococcus;

A golden staphilococcus.

II. Patogens an average level prerogative:

Enterobacterias;

Pseudomonads and other not fermenting Gram-negative bacteria;

klostridias

bacteroids and others anaerobs;

Streptococcuses (other kinds).

III. Patogens a low level prerogative:

Bacillus anthracis;

Mycobacterium tuberculosis, Mulcerans, etc.;

Pasteurella multocida.

Originators of virus infections unlike fungi and bacteria very seldom are producers purulent ekssudat.

4. The general principles of treatment of wounds.

• Surgical methods: a surgical treatment of a wound, disclosing congeries, necrectomia, performance decompression cuts, suturation, dermal plastic (the artificial skin, the split moved rag, a walking stalk on Filatov, autodermoplastic completlayer rag, free autodermoplastic slightlayer rag on Tirsh).

• Local treatment of a wound with application of various kinds of drenaging, bandages and medicinal preparations.

• Physiotherapeutic treatment: laser therapy, a magnetotherapy, UHV, UVI, the operated abacterial environment, etc.

• The General treatment: antibacterial therapy; correction of infringements of functions of organs and systems, metabolic frustration; detoxication therapy; Increase of nonspecific resistency of an organism and immunocorrection therapy; stimulation reparativ processes.

5. The medical program depending on a stage wound process.

The phase of an inflammation (ekssudation) is characterized plentiful wound separated, expressed by peryfocal inflammatory reaction of soft parts and bacteriemic obsemenation the wounds, therefore applied medical preparations should possess high osmotic activity to provide intensive outflow ekssudat from depth of a wound in a bandage, should render antibacterial influence on contagiums, cause tearing away and fusion necrosis tissues. With this purpose antiseptic bandages (moist desiccation with chemical preparations and antiseptics, water-soluble ointments), during vascular changes - drenaging and hydrophil bandages (hypertonic, absorbing and adsorbing), during clarification from necros tissues - necrolitic means (proteplitic enzymes, hydrogel bandages) are applied; For stimulation of tearing away necrosis tissues - ointments on the water-soluble basis, possessing high osmotic activity (levomecol, levosin, dioxicol, etc.).

Considering the high cost price wound sorbtion coverings (hydrophil bandages), in a daily medical practice with success it is possible to use children's pampers or hygienic linings.

During clarification of a wound from necrosis tissues ointments for enzymatic clarifications of wounds which worthy representative is ointment «Irucsol», containing enzymes from Clostridium hystolyticum and broad-spectrum antibiotic «Chloramfenicol» (levomicetyn) are applied.

At presence perifocal dermatitis around of a wound it is expedient to impose zincoxid ointment (paste Lassara).

To all patients for 10-14 days recommend semi bed rest. The basic components of therapy are broad-spectrum antibiotics Ftorchinolon (maxaquin, tarivid, ciproby, cyfran, etc.) or Cefalosporin (dardum, duracef, cephzol, mandol, cefamezin, etc.) of some, entered parenteral (it is less preferable - peroral). Considering frequent associations of pathogenic microorganisms with bacteroid and fungoid flora, antibacterial therapy in some cases is expedient for strengthening, having included in it antifungoid preparations (diflucan, nizoral, orungal, etc.) and derivatives nitroimidazol (flagil, metronidozol, trichopol ,tinidazol, etc.).

The active inflammation and the expressed painful syndrome define expediency of system application of nonspecific antiinflammation means, such as dyclofenac (voltaren, ortophen), cetoprophen, oruvel, etc.

System and local hemoreological infringements follows correction by infusions antiagregants (reopolyglucin in a combination with pentoxiphillin).

Sensitization of an organism as a result of massive resorbtion structures with antigenic activity (fragments of fibers of microorganisms, products of degradation of soft parts, etc.), synthesis of a plenty of mediators of an inflammation (hystamin, serotonin, etc.) are absolute indications to carrying out desensitization therapies (Dimedrolum, suprastyn, diazolin, claritin, cetotyfen, etc.).

The basic preparations for treatment of wounds in 1-st phase wound process:

Ointments on a water-soluble basis: ( levomecol, levosin, dioxicol, dioxidin 5 % ointment, ointment of 10 % mafenid acetate, sulfamecol, furagel, ointment of 0,5 % chinifuril, iodopiron 1 % ointment, iodmetrixelen, streptonitol, nitacid, ointment miramistin 0,5 %, ointment lavendula, ointment lipacantin, methylurocil ointment with miramistin.

Sorbents and hydrogels: gelevin, celosorb, immosgent, carbonet, Multidex Gel, AcryDerm, Carrasin Hydrogel, Hydrosorb, Elasto-Gel, Purilon.

Enzymes: chimopsin, callagenasa the crab, caripasim, terrilitin (proteasa), protogentin (sipralin, lizoamidasa), enzim content dressing means (teralgim, immosgent), trypsin + urea, trypsin +chlorgecsidin, profezim, sipralin, lysosorb, collavin.

Solutions of antiseptic tanks: a solution iodopyroni, 02 % a solution furagini kalii, suliodopyroni, 15 % a solution dimefosfoni, 30 %-solution ПЭГ-400, 0,01 % solution miramistini.

Aerosols: nitazol, dioxizol, gentazol.

Wound bandages: «TenderVet», «Sorbalgon».

The phase of a reparation(neogenesis, formation and maturing granulation tissues) is characterized by clarification wound surfaces, occurrence of granulations, стиханием perifocal inflammations and reduction of ekssudation. The Primary goal of treatment becomes stimulation of growth and maturing of a connecting tissue alongside with suppression of microbes remaining in a small amount or their again appeared hospital shtamms. Such stimulators of neogenesis, as vinilin, vulnuzan, polymerol, and also antiseptic bandages with fat-soluble ointments and hydrophyl bandages (polyuretan and ot.) are widely applied.

System therapy correction, appointing antioxidants (aevit, tocopherol, etc.) and antihypoxants - deproteinic derivatives of blood cows (actovegin, solcoseril). For acceleration of growth of a connecting tissue it is expedient to appoint curiozin. It represents association hyaluronic acids and zinc. The hyaluronic acid increases activity phagocytozis in granulocyts, makes active phybroblasts and endoteliocyts, promotes their migration and prolipheration increases prolipherativ activity of cells of an epithelium, creating favorable conditions for remodelation connective tissue matrix. Zinc, possessing antimicrobic action, makes active a lot of the enzymes participating in neogenesis.

Very well itself have recommended biodegrading wound coverings (it is scarlet-levin, альгипор, альгимаф, гешиспон, свидерм, etc.).

The basic preparations for treatment of wounds in 2-nd phase wound process:

Ointments on an adjustable osmotic basis: methyldioxylin, sulfargin, fuzidini 2 % gel, lyncomicini 2 % ointment.

Polymeric coverings: combutec-2, digispon, algipor, algimaf, algicol, algico-АКF, kolahit, kolahit-F, sisorb, hydrosorb.

Hydrocolloids: galagran, galakton, hydrocoll.

Oils: meliacyl, oil of sea-buckthorn berries, oil of a dogrose.

Aerosols: dioxyplast, dioxyzol.

In a phase of the cuticularization, described the beginning of a cuticularization and maturing connective tissue of scar (scar formations and reorganization), among means of local influence optimum is application polymeric wound coverings which essentially accelerate process of a cuticularization, and also silicon semipermeable bandages.

Polymeric wound coverings can be subdivided conditionally (one bandage can be multi-purpose) on absorbing, protective, isolating, atraumatic and biodegrading. Sorbtion ability of coverings (the degree and speed of linkage ekssudat wounds) depends on the size of times of coverings.

6. Principles of active surgical treatment of purulent wounds (A.M.Svetukhin, J.L.Amiraslanov, 2003).

• Wide section and disclosing of the purulent center. Already at this stage of treatment (the purulent surgery and traumatology) should contain elements of plastic surgery. At performance of cuts of tissues and a choice of access to the purulent center it is necessary to expect an opportunity of formation of the future blood suppling rags from the sites of a body next to a wound.

• Excision all impractical and doubtful soft parts impregnated by pus within the limits of healthy tissues (in one or several stages). Removal of all osteal sequesters and necrosis bones shplins. Performance of a regional, trailer or segmentary resection of the amazed site of a bone also within the limits of healthy tissues.

• Removal the immerse metal clamps which are not carrying out the applicability, and vascular prostheses.

• Application of additional physical methods of processing of a wound.

• Use during a surgical treatment of elements of plastic or reconstructive operations with the purpose of restoration or closing of the important anatomic formations.

• The external osteosynthesis of long bones (under indications), provides an opportunity dynamic distraction-compressions manipulations.

7. Suturation on a purulent wound.

The primarily-delayed seam - apply in 5-6 days after a surgical treatment, before occurrence in a wound of granulations (is more exact within the first 5-6 days).

Early secondary seam - impose on the wound covered by granulations with mobile edges before development in it a cicatricial tissue. An early secondary seam impose within 2-nd week after a surgical treatment.

Late secondary seam - impose on granulating wound in which the cicatricial tissue has already developed. Closing of a wound probably in these cases only after preliminary cicatricial excision of tissue. Operation is made on 3-4 week after wound and later.

Indispensable condition for suturation on a purulent wound is maintenance of sufficient outflow wound separated, that is reached active drenaging, and the rational antibacterial therapy directed on destruction of a microflora which has remained in a wound.

8. Rules of a fence of a material from a wound for microbiological research.

After careful processing a surgery field the surgeon defines a place where pus accumulates, are located necrosis tissues, gas (crepitating is allocated or other attributes of an infection are observed. The particles of the amazed tissues intended for laboratory research, place in a sterile gauze and then in sterile capacity. Pus or another exudates should be accurately collected and placed in a sterile test tube. If it is possible, it is not necessary to use a wadded tampon. Exudates it is necessary to select a sterile syringe with a needle. If the wadded tampon is used, it is necessary to select as much as possible exuded and to place all tampon in capacity for sending in laboratory.

9. " physical methods of influence " on wound process.

1). The methods based on use of mechanical fluctuations:

• Processing of a liquid by a pulsing jet,

• Processing by low-frequency ultrasound.

2). The methods based on change of external pressure of the air environment:

• Vacuum processing and vacuum therapy,

• The operated abacterial environment,

• Hyperbaric oxygenation.

3). The methods based on change of temperature:

•cryotherapy.

4). The methods based on use of an electric current:

• Direct currents of a low pressure (an electrophoresis, an electrical stimulation),

• The modulated currents (electrical stimulation).

5). The methods based on use of a magnetic field:

• Low-frequency magnetotherapy,

• Influence of a constant magnetic field.

6). Use of electromagnetic fluctuations of an optical range:

•laser radiation:

High-energy,

Low intensity,

•ultraviolet radiation.

7). The combined methods of influence.

Application of plasma streams. Influence of high-temperature streams of plasma on a wound surface allows to execute an adequate surgical treatment of a wound without blood and precisely. Advantage of a method besides is aseptic and a noninvasive section of tissues, that at a surgical infection has important value.

Ozonotherapy. Local ozonotherapy in the form of the ozonized solutions with concentration of ozone of 15 mkg/ml leads to decrease microbic obsemenation the purulent center, to increase of sensitivity of microflora to antibacterial preparations, stimulates reparaiv processes in a wound. System ozonotherapy renders antiinflammatory, detoxication, antihypoxy action and normalizes metabolic processes in an organism.

Use oxide nitrogen. Opening endogenous oxide nitrogen (NO) which is produced by cells by means of NO-syntez and carries out functions of a universal regulator-messenger, was large event of biology and medicine. In experiment the role endogenous NO in oxygenations of tissues and its deficiency in purulent wounds is established. Combination application of surgical treatment is purulent-necrosis lesions of soft parts and a complex of factors of physical influence (US, ozone and to NO-therapy) promotes acceleration of clarification of a wound from microflora and necros weights, to easing and disappearance of inflammatory displays and microcirculation infringements, activization to macrophageal reaction and prolypheration of fybroblasts, to growth a granulation tissue and a regional cuticularization.

10. A mephitic gangrene.

Anaerobs make overwhelming majority of normal microflora of the person. They live: in a mouth (in gingival pockets the flora on 99 % consists from anaerobs), in a stomach (at hypo-and anacids conditions the microbic landscape of a stomach comes nearer to intestinal), in a thin gut (anaerobs contain in smaller quantity, than aerobs), in a thick gut (the basic place of dwelling anaerobs). On etiology anaerobs are subdivided on clostridial (forming disputes), nonclostridial (not forming disputes), bacteroids, peptstreptoccocs, fuzobacterial.

One of the general symptoms of a mephitic gangrene is absence of microflora in crops at standard ways of their allocation (without application anaerostats). As microbiological identification anaerob microflora demands the special equipment and long time, great value methods get the express train-diagnostics, allowing to confirm the diagnosis within an hour:

- Microscopy of fixed smear, painted on Gram;

- Urgent biopsy the amazed tissues (are characteristic expressed focus of hypostasis tissues, necrosis basic layer focus of epidermis, hypodermic cellulitis, fascias, miolysis and destruction muscular fibres, perivascular hemorrhages, etc.)

- gas-liquid chromatography (flying fat acids-acetic, oil, isooil, kapron are defined, phenol and its derivatives produced on Wednesday of growth or in pathologically changed tissues anaerobs during a metabolism).

According to gas-liquid chromatographies and weights-spectrometry it is possible to identify not only asporogenic anaerobs, but also clostridial microflora (originators of a gas gangrene), for which presence 10-oxyacid is characteristic.

Without dependence from localization of the center anaerob process has a number of the general and characteristic attributes:

• The Unpleasant putrefactive smell ekssudat.

• Putrefactive character of lesion.

• Dirty poor ekssudat.

• Gas-plant (bubbles gas from a wound, crepiting hypodermic , gas above a level of pus in a cavity of an abscess).

• Affinity of a wound to places of natural dwelling anaerobs.

From the anaerob processes which are taking place in surgical clinic, it is necessary to note the special form - epifascialis creeping phlegmon of a forward abdominal wall which develops as complication after operations (more often after appendectomia at gangren-perphorativ appendicites).

Anaerob clostridial infection - the acut infectious disease caused by penetration into a wound and duplication in it forming disputes anaerobs of a sort clostridis (Clostridium perfringens, Clostridium oedematiens, Clostridium septicum, Clostridium hystolyticum). Disease develops in the first 3 days after wound, less often - later some hours or week is more often, is observed at gunshot wounds, in surgical branches - after ablation of the bottom extremities in occasion of an atherosclerotic gangrene and even after appendectomia, etc. the Probability of occurrence of a mephitic gangrene acutly raises at presence in wounds of alien bodies, crises of bones and the damaged large arteries as in such wounds it is a lot of ischemic, necrosis tissues, deep, badly aerated pockets.

Anaerobs clostridium allocate a number of the strongest eczotoxins (neuro-, necro-, enterotoxins, hemolyzin) and enzymes (gialuronidase, neuraminidase, fibrinolisine, a collagenase and elastase, lecytinase, etc.) which cause a hypostasis of tissues, acut permeability of vessels and hemolyzis, necrosis and fusion of tissues, a heavy intoxication of an organism with damage of internal organs.

Patients first of all feel holding apart pain in a wound, the hypostasis of tissues around of it quickly accrues. On a skin there are the centers of cyanotic painting extending quite often on significant distance from a wound in a proximal direction, and the bubbles filled muddy by hemorragial contents. Palpation at tissues around of a wound it is defined crepitation.

Simultaneously with local displays deep general frustration are marked: weakness, depression (less often - excitation and euphoria), rise in temperature of a body up to the febril figures, acutly expressed tachycardia and increase of breath, pallor or yellowness of the skin, a progressing anemia and an intoxication, at lesion of a liver - yellowness of sclers.

At roentgenography of the amazed extremity gas in tissues is found out. Diagnostics of a mephitic gangrene is based basically on clinical data. Medical tactics is under construction also in a clinical picture of disease.

At a mephitic gangrene prevail necros changes in tissues and practically are absent inflammatory and prolypheration.

Anaerob nonclostridial infection (a putrefactive infection) is caused anaerobs, not forming dispute: B. coli, B. putrificus, Proteus, bacteroides (Bacteroides fragilis, Bacteroides melanogenicus), Fusobacterium, etc., it is frequent in a combination with staphilococcuses and streptococcuses.

On local changes of tissues and the general reaction of an organism the putrefactive infection is close to anaerob clostridial infection. Prevalence processes of necrosis above processes of an inflammation is characteristic.

Clinically local process in soft parts usually proceeds in the form of nonclostridial phlegmons, destroying hypodermic fatty cellulitis, fasces (fasciitis), muscles (miozitis).

The general condition of the patient is accompanied expressed toxemia, quickly leads to a is bacteriemic-toxic shock with a frequent lethal outcome.

The putrefactive infection is more often observed at heavy infected lacerate-contusion wounds or at the open crises with extensive destruction of soft parts and pollution of a wound.

The surgical intervention at anaerob clostridial and nonclostridial infections consists in a wide section and full excision become lifeless tissues, first of all muscles. A wound after processing plentifully wash out solutions of oxidizers (peroxide of hydrogen, a solution KMnO4, the ozonized solutions, hypochlorir sodium), make additional «lampas» cuts in a zone of pathological changes outside a wound, « lampas » cuts overstep the bounds of edge of the center of an inflammation, in addition excision of necroses, a wound do not sew up and not tamponade, provide in subsequent their aeration. After operation use hyperbaric oxygenation.

Antibioticotherapia of mephitic gangrenes.

For empirical application at mephitic gangrenes it is recommended clyndomycin (delacil). But considering, that the majority of such infections mixed, therapy is usually spent by several preparations, for example: clyndomycin with aminoglycozids. Many stamms of aerobs suppresses riphampin, lyncomycin. On Gram-positive and Gram-negative anaerob coccuses well operates benzilpeniccils. However to it quite often there is an intolerance. Its substitute is erythromycin, but it badly acts Bacteroides fragilis and fuzobacterias. Concerning anaerob coccuses and sticks the antibiotic fortum (it is combined with minoglycozids), cefobid (cefalosporins) is effective.

The special place among the preparations applied to influence on anaerobic microflora, borrows metronidazole - metabolic poison for many strict anaerobs. On Gram-positive forms of bacteria metronidazole operates much more poorly, than on Gram-negative, therefore its application in these cases is not justified. Relatives on action to metronidazole have appeared others imidazols - niridazol (more actively metronidazole), ornidazol, tynidazol.

Solution dioxydin (up to 120 ml in/in 1 % is applied to adults) also, and also carbenicillin (12-16 g/day in the adult).

11. Practical carrying out of change of a bandage.

Any change of a bandage should occur in sterile conditions. Always it is necessary to use so-called « non-touch technique » (a contactless technique). To a wound or a bandage it is not supposed touches without gloves. The doctor doing bandaging, should take special measures for own protection against an infection: from latex, protection gloves are necessary for eyes, and also a mask on a mouth and a nose. The patient it is necessary to arrange conveniently, and the area of a wound should be well accessible. The good source of illumination is necessary.

If the bandage is not removed, it cannot be torn off. A bandage moisten with aseptic solution (peroxide of hydrogen, solution Ringer) while it will not come unstuck.

At the infected wounds the area of a wound is cleared in a direction outside inside, disinfectants are if necessary used. Necroses in a wound it is possible to remove mechanical by by means of a scalpel, scissors or curette (the preference should be given a scalpel, removal by scissors or curette entails risk compression of tissues and repeated trauma).

Are effective enough for clearing a wound of washing aseptic solution from a syringe at easy pressure of the piston. At deep wounds washing is spent by means of bulbous-end, grooved probe or through short cateter. The liquid should be collected by means of a napkin in a tray.

Granulation tissue sensitively reacts to external influences and damaging factors. Granulation tissue constant maintenance of a wound in a damp condition and protection from trauma in the best way promotes formation at change of bandages. Excessive granulations usually leaves by means of a cauterizing pencil.

If edges of a wound show propensity to a cuticularization and kinking inside carrying out of a surgical treatment of edges of a wound is shown.

Well developing epithelium does not demand other leaving except for maintenance in a damp condition and protection from trauma change of bandages.

The surgeon should provide, that chosen the wound bandage optimum approached to a surface of a wound - wound secret can be absorbed only under condition of good contact between a bandage and a wound. Unreliably fixed bandages at movement can cause irritation of a wound and slow down its healing.

The scheme of inspection of the patient.

At revealing complaints at the patient to reveal data of the complicated current wound process (attributes of an inflammation, rise in temperature of a body, etc.).

The anamnesis of disease to collect in detail, paying special attention On etiological and the pathogenetic moments of formation of a wound, background conditions (stress, an alcoholic, medicamental, narcotic intoxication, violent actions, etc.).

In the remote anamnesis to reveal the transferred diseases or the available sufferings influencing on reparativ process and the immune status, to establish possible value in development of a pathology of a way of life and working conditions of the patient.

To make external survey and to interpret the received data (character of damage of tissues, the sizes of a wound, number of damages, their localization, presence of inflammatory changes, danger of development of a bleeding, a condition regionar lymphatic nodules).

To estimate the general condition of the patient, a degree of an intoxication of an organism, to specify character and volume of lesion (depth of a wound, the attitude wound channel to cavities of a body, presence of damages of bones and internal organs, presence of inflammatory changes in depth of a wound).

To carry out a fence of a material from a wound for microbiological research or to interpret already available results (a microbic landscape of a wound, a degree microbic obsemenation, sensitivity of microflora antibiotics).

To tie up the patient, if necessary to make necrectomia, washing of a wound, drenaging, physiotherapeutic treatment.

At repeated bandaging to estimate dynamics of current wound process.

To appoint antibacterial, immunocorrectial, dezintoxication treatment, physiotherapeutic methods of treatment.

TESTS

1. Primary closure of incised wounds must be done within ...........

a) 2hrs

b) 4hrs

c) 6hrs

d) 12hrs

e) 16hrs

2. The tensile strength of wound reaches that of normal tissue by-

a) 6 weeks

b) 2 months

c) 4 months

d) 6 months

3. The worst position for scars is

a) Back

b) Shoulder

c) Sternum

d) Abdomen

4. The best scars are seen in

a) Infants

b) Children

c) Adults

d) Very old people

5. Patient has lacerated untidy wound of the leg and attended the casualty after 2 hours. His wound should be -

a) Sutured immediately

b) Debrided and sutured immediately

c) Debrided and sutured secondarily

d) Cleaned and dressed

6. Lacerated wound looks like an incised wound in the

a) Scrotum

b) Scalp

c) Abdomen

d) Thigh

7. Following are required for wound healing

a) Zinc

b) Copper

c) Vitamin C

d) Calcium

8. Wound healing is worst at -

a) Sternum

b) Anterior neck

c) Eyelid

d) Lips

9. When is the maximum collagen content of wound tissue -

a) Between 3rd to 5th day

b) Between 6th to 17th day

c) Between 17th to 21st day

d) None of the above

10. If rupture marks are to be avoided, skin sutures should be removed by -

a) 72 hours

b) 1 week

c) 2 weeks

d) 3 weeks

11. What is true about keloids -

a) It appears immediately after surgery

b) It appears a few days after surgery

c) It is limited in its distribution

d) It is common in old people

12. Keloid is best treated by -

a) Intrakeloidal injection of triamcinolone

b) Wide excision and grafting

c) Wide excision and suturing

d) Deep X-ray therapy

13. A patient with grossly contaminated wound presents 12 hours after an accident. His wound should be managed by -

a) Thorough cleaning and primary repair

b) Thorough cleaning with debridement of all dead and devitalised tissue without primary closure

c) Primary closure over a drain

d) Covering the defect with split skin graft after cleaning

14. Delayed wound healing is seen in all except -

a) Malignancy

b) Hypertension

c) Diabetes

d) Infection

15. Keloid scars is made up of -

a) Dense collagen

b) Loose fibrous tissue

c) Granulamatous tissue

d) Loose areolar tissue

16. Highest concentration of hydroxy proline is seen in -

a) Elastin

b) Collagen

c) Fibrous tissue

d) Gelatin

17. The following statement about keloid is true -

a) They do not extend into normal skin

b) Local recurrence is common after excision

c) They often undergo malignant change

d) They are more common in whites than in blacks

18. Fibroblast in healing wound derived from -

a) Local mesenchyme

b) Epithelium

c) Endothelial

d) Vascular fibrosis

19. In the healing of a clean wound the maximum immediate strength of the wound is reached by -

a) 2 - 3 days

b) 4-7 days

c) 10- 12

d) 13- 18 days

20. The normal tensile strength of tissue at the site of wound is gained after --

a) One week of wound healing

b) Two weeks of wound healing

c) Two months of wound healing

d) Two years of wound healing

21. Management of an open wound seen 12 hrs. after the injury-

a) Suturing

b) Debridement and suture

c) Secondary suturing

d) Heal by granulation

22. Degloving injury is -

a) Surgeon made wound

b) Lacerated wound

c) Blunt injury

d) Avulsion injury

e) Abrasive wound

23. The best cure rate in keloids is achieved by -

a) Superficial X - ray therapy

b) Intralesional injection of triamcinolone

c) Shaving

d) Excision and radiotherapy

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

SURGICAL DISEASES AND DIABETES. PROBLEMS OF THE INFECTION IN DIABETES (IN DIABETIC PATIENTS). THE DIABETIC FOOT

Составитель асс. О.Г.Шахбазян

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

The purpose of employment.

Mastering by students of special knowledge and purchase of practical skills on diagnostics and treatment of such complication of diabetes mellitis (SD), as « a syndrome of diabetic foot » (DF), leading development ulcer-necrosis and infectious process, and in the further - a gangrene of foot.

The student should know:

1. Urgency of a studied problem and patophiziologi mecanizms developments micro-and macroangiopathy at DF.

2. Role not fermental autooxidation glycolysis and oxidizing stress in development of aggregation trombocitis, increase of permeability of a vascular wall, decrease antiagregations functions of an endothelium and induce is permanent existing trombodangerous.

3. The classification of syndrome DF accepted on 1-st International symposium on diabetic foot (the Netherlands, 1991), and recommended by domestic experts.

4. Degrees of ischemic damages of the bottom extremities according to the classification offered W. Wagner in 1979.

5. Features of purulently-necrosis process at diabetic foot.

6. Clinical and special methods of research in diagnostics of syndrome DF.

7. Methods of conservative treatment diabetic angiopathy.

8. Choice of medicamental preparations and their combinations depending on a stage of an ischemia, weight of trophic infringements, the mechanism of action of a preparation, a kind and weight of an accompanying pathology.

9. Role prostoglandin and its derivatives (vasoprestan, etc.), preparations glicozaminoglicans (sulphodexid, etc.) and enzim therapy (vobenzim, flogenzim) in correction of infringements of a blood flow and treatment of purulent complications.

10. Feature of a surgical treatment of the purulent center and ablations at diabetic foot.

The student should be able:

1. To diagnose various clinical forms DF.

2. To estimate a degree of lesion by purulently-necrosis process of feet.

3. To interpret on doppler-and angiograms of infringement of an arterial circulation of the bottom extremities.

4. To define a pulsation of arteries on a femoralis, a poplitea and vessels of foot.

5. To estimate on roentgenograms attributes osteopathy and deformations of foot.

6. To tie up patients with purulent-necrosis processes of foot and after ablations.

7. To prepare for a set of surgical toolkit for a resection of a segment of foot and ablations of an extremity at a level of a hip and a shin.

The maintenance of studied disease.

Urgency of a problem

Diabetes mellitis (SD) now is the widespread disease. In economically developed countries meets at 2-6 % of adult population. According to the CART (1999г.), now diabetes mellitis 120 million person suffers. In Russia the number of patients with SD comes nearer to 8 million person.

Patients with SD in 2-3 times have ischemic heart disease, a blindness - in 10, and a gangrene of the bottom extremities - in 20 times more often, than at persons without SD is more often. Lethality at patients of elderly and senile age at purulent-necrosis complications and a gangrene of extremities at SD reaches 20 %. For development of the uniform approach to diagnostics and treatment of patients with SD characteristic for a diabetes neuropathy, angiopathy and osteopathy in 1987г. Under the decision of research group the CART has been offered the term « diabetic foot » and it is recommended to consider it as a potential infectious problem.

Pathogenesis diabetic angiopathy

«Diabetic angiopathy» - the term entered H. Burger in 1954г., includes various on character morphofunctionals multiorgan lesions of vessels at patients SD. Thus lesion arteriols, venuls and capillaries H. Burger has named diabetic microangiopathy . While atherosclerotic lesion of average and large vessels carry to diabetic microangiopathy.

In norm there are two ways of oxidation of glucose:

• the glycolitic way of oxidation to cycle of Crebs demands presence of enough of insulin;

• At deficiency of insulin joins a sorbitology way.

At surplus of glucose in blood and insufficiency of insulin in tissues and vessels collects sorbitol and fructose which lead angiopathy by infringement of osmotic balance in walls of capillaries and to a thickening basic membranes.

Development diabetic angiopathy influences not only duration of disease SD, but also its weight. The basic changes thus occur in to a basic membrane of capillaries in which collect mucopolisacarids, fructose, sorbitol, glucoproteids, lipids, various albuminous substances. A basic membrane thickening in 2-5, and sometimes at 8-10 time.

Besides at microangiopathis occurs prolipheration and a thickening of cytoplasm of cells of an endothelium arteriols and fine arteries, that appreciably complicates transcapillar exchange. The thickening of basic membranes of capillaries and an endothelium breaks a selective filtration of biological liquids and exchange diffusion that interferes with removal of products of an exchange, maintenance of tissues with nutrients and oxygen. The thickening basic membrane also complicates migration of leukocytes and phagocytes in paravasalis space, reducing resistibility of tissues to an infection. Infringement of vascular permeability and change of microcirculation in turn promotes an output of plasma in soft parts, than presence at patients with diabetic angiopathy a subfascial hypostasis speaks. All these circumstances promote occurrence of various degrees of an ischemia and a diabetic gangrene.

For diabetic lesions of arteries it is characteristic segmentary and circular mediocalcinosis (arteriosclerosis of Menkeberg). As a result calcification vascular wall becomes rigids, loses ability to reduction and dilitation, that sharply reduces adaptable opportunities of vascular system of extremities, and lesion of fine intramuscular arteries interferes with development collateral circulations.

A number of authors consider, that microangiopathy is not complication, and enters into clinical syndrome SD. Thus some authors consider as the basic or initial form of display of disease neuropathy which in turn leads to development microangiopathy. At the same time W. Kane (1990г.) considers, that neuropathy at a diabetes is consequence of an ischemia of a nerve, т. е. Result of lesion vasa nervorum. In its opinion, lesion of fine vessels (capillaries, vasa vasorum, vasa nervorum) is characteristic and patognomatic for a diabetes. Lesion of independent nerves in turn leads to infringement of function of vessels. Degenerate changes in peripheral nerves owing to what there can come full loss of painful sensitivity stop and a shin in parallel develop.

Classification

The most widespread classification diabetic microangiopathy is classification W. Wagner (1979) on which distinguish 6 degrees of ischemic lesion of the bottom extremities:

Degree 0 - without visual changes of integuments;

Degree 1 - the superficial ulcerations which are not extending on all derms, without attributes of an inflammation;

Degree 2 - deeper ulcerations grasping adjoining sinews or an osteal tissue;

The degree 3 – ulcer and necrosis process, is accompanied by connection of an infection with development of a hypostasis, hypertherms, occurrence of abscesses, phlegmons, contact osteomyelitis;

Degree 4 - a gangrene of one finger and more or a gangrene distal department of foot;

Degree 5 - a gangrene of a greater part of foot or all foot.

For the characteristic diabetic microangiopathy the majority of surgeons classification of Fonten-Pokrovsky adhere.

Methods of diagnostics

Methods of inspection of patients with diabetic angiopathy can be divided into following groups:

1. Clinical;

2. Special;

-Reflecting macro-and microcirculation of an extremity;

-Studying a condition of various parts of a homeostasis: a metabolism, endotoxigions, immunoreactions, a hemostasis, central hemodinamic, etc.

Clinical methods

Clinical methods of diagnostics are of great importance at specification of the diagnosis diabetic angiopathy.

So, well collected and correctly estimated anamnesis enables not only correctly to formulate the primary diagnosis, but also to define character of current of disease.

Frequency of exacerbations and remissions allows to make a full picture of disease as a whole, to predict its current and consequently and to plan subsequent tactics of treatment.

At survey of the patient the doctor should pay attention to the following moments:

• Condition of a skin (thickness, color, presence of ulcers, scars, attritions, corns);

• Deformation of fingers and feet;

• Hypostasis;

• Condition of nails (hyperceratousis);

• Pulsation of arteries;

• Capillary blood flow;

• Blood supply veins;

• Scalp;

• Muscle tone;

• Sensitivity;

• Presence be ill in rest and at walking;

• Dermal temperature.

Thus both extremities should be surveyed in the comparative plan.

Special methods of research

At presence diabetic angioneuropathy patients should be directed on more profound clinical and tool inspection including:

1. Research of vibrating sensitivity a tuning fork or biotenzimetr.

2. Research of tactile temperature sensitivity.

3. Estimation of a dermal blood flow - laser research of a dermal blood flow,

a capillaroscopy, polarygraphy, transcutaneus definition of a pressure of oxygen.

4. Ultrasonic dopplerographia with definition of ankle-humeral index and linear speed of a blood flow.

5. Duplex scanning of arteries.

6. Rentgenography of bones of foot for osteopatology and deformations.

7. Angiographia.

Features of purulently-necrosis process

At diabetic foot

1. Acute decrease the in the general both local immunoactivity and resistibility to an infection because of reduction of transport O₂, leukocytes and phagocytes and paravasalis space through thickening basic membrane.

2. Because of presence diabetic neuropathy and decrease in a threshold of painful sensitivity a trauma of patients do not pay to infectious process of attention that promotes fast distribution of purulently-necrosis process.

3. Purulently- necrosis process usually begins in the field of heads deformed metatarsus bones with frequent development of osteomyelitis and pathological crises.

4. The damp component of an inflammation because of interstitial hypostasis as a result of a thrombosis of lymphatic and venous vessels and infringement of an adequate drainage of tissues (microlimphatic and venous trombosis) prevails.

5. Propensity to fast generalization of purulent process on tendinous and to interfascial spaces at a constant skin.

6. Mediocalcinosis of Menkenberg and hyalinosis of arteries leads them rigidity, to decrease in an extensibility and reduction collateral overflow and decompensation blood supplies of tissues.

7. Expressed endotoxigy with fast development of multiorgan insufficiency.

8. Frequent development of a sepsis.

9. Fast decompensation SD with development of a metabolic acidosis, ketosis, and their difficult correction without liquidation the centers of necrosis.

10. Heavy infringement of an albuminous, fatty and electrolytic exchange.

11. Prevalence anaerobic and the mixed flora in the center of an inflammation.

12. Presence of hypercoagulation and the raised aggregation and adhesion of uniform elements of blood.

13. Fast approach of an anemia and hypoproteinemia.

Principles of treatment it is purulent-necrosis complications of diabetic foot

1. Urgent hospitalization in angiological department or department « diabetic foot ».

2. Insulin therapy (insulin before full healing wounds and ulcers).

3. Surgical treatment - wide necrectomia within the limits of healthy tissues.

4. Antibioticotherapia (it is better long intraarterial continuous) in view of sensitivity dosages, nefropatology.

5. At indications extracorporalis detoxication (hemosorbtion, a plasmapheresis, enterosorbtion).

6. Introduction of the preparations improving microcirculation (anticoagulants, antiagregants, antioxidants).

7. Immunostimulation (Т-activin, licopid, leycinpheron, an antibody, pentoglobin, immunal, etc.).

8. Sindromic therapy (correction AAS (acid alkaline status); the broken functions of organs and systems; a metabolism).

9. Local treatment.

10. After decrease inflammatory process it is necessary to solve the problem improvements of a circulation in stop and shins.

(Items 2, 3, 4, 5, should be realized after hospitalization in parallel with inspection of the patient).

Treatment purulently-necrosis complications at diabetic macroangiopathy can be divided into three stages.

1-st stage:

1. Liquidation of an acuteness of purulently-necrosis process:

• Opening and drenaging phlegmons;

• Wide necrectomia;

• Translation of a damp gangrene in dry;

• Achievement of a precise demarcation shaft.

2. Struggle with endotoxigions.

3. Normalization of carbohydrate, albuminous, fatty and HYDRO-ELECTROLYTIC exchanges.

4. Restoration of the immune status.

5. Improvement of microcirculation.

2-nd stage: restoration or improvement of a circulation.

3-rd stage: closing of defect of tissues after necrectomia and restoration of functions of an extremity.

Conservative treatment diabetic macroangiopathy

Long-term supervision show, that the basis of treatment of diseases of vessels is made with complex therapy which should be rational and individual.

We emphasize a word "rational" as, unfortunately, in most cases in out-patient departments reception and treatment of this category of patients are carried out by surgeons of the general structure, thus the opportunity of casual selection of medical products as the market is more and more sated various is great, including effective enough and is very frequent inefficient preparations. Treatment should be directed on removal of a spasm and a pain, improvement collateralis circulations, microcirculation, reological properties of blood with the purpose of translation of disease from a heavy stage to easier. Prophylaxis of the further developments (stabilization) overcooling, nervous stresses, infringement of a diet spend by influence on the general condition of the patient, its activation protective and compensatory mechanisms with obligatory elimination of such factors, as smoking.

Diet and mode

At treatment of a diabetes basic value equally important four moments - a feed, physical activity have, medicines and self-checking. Its health depends on a level of consciousness of patient SD. Very important that each patient competently concerned to the illness and observed a special diet, works, rest, etc.

Medicamental therapy

The choice of this or that preparation and their combinations depends on a stage of an ischemia, weight of trophic infringements, the mechanism of action of a preparation, compatibility, changes in a homeostasis, a kind and weight of an accompanying pathology, etc. is the Most frequent at treatment diabetic micro-and macroangiopathy use following groups of the preparations united on the mechanism of action:

1. Spasmolitics (papaverini, drotoverina hydrochloride, tolperison).

2. The preparations, improving fabric a metabolism (solcoseril, actovegin).

3. Hypolipidemic preparations.

4. Angioprotectors (pentoxiphillini, hynko biloba, alprotastil, vazoprostan).

5. Dezagregants (Acidum acetylsalicylicum, thyclopediny, sulodexid).

6. Reological preparations (reopoliglyukin).

7. Antioxidants (vitamin E, Acidum ascorbinicum, mexidol).

8. Immunostimulators (immunophan, polioxidony, Т-activin).

9. Anticoagulants (phraxipariny, enoxapariny, varpharin, etc.).

10. The preparations improving venous and lymphatic outflow (calcium debosilat, escusan, troxerutin, diosminy).

Alongside with medicinal therapy at not complicated diabetic angiopathy appoint following actions.

1. Physiotherapy

As indications to purpose of physiotherapeutic procedures at diabetic macroangiopathy initial stages of disease serve in a phase decrease inflammatory process and a stage of remission of pathological process.

Pulse currents, magnetotherapy, laser therapy, diadinamic currents which appoint to lumbar area and on a course of a neurovascular bunch on a hip and a shin are most effective.

2. Sanatorium treatment

At initial stages of disease, when there is no trophic infringements and exacerbations, alongside with a physiotherapy sanatorium treatment is recommended.

Sanatorium treatment has double medical effect - owing to change of a habitual mode, a climate, a conditions of life and as a result applications of balneological procedures.

From balneological procedures are most effective rodonic, hydrosulphuric, narzans, iodbromic baths.

The resorts located in an average strip of Russia and on Caucasus (Pyatigorsk, Mineral Waters, Kislovodsk, etc.) are recommended.

Local treatment

At purulently-necrosis processes the actions directed on improvement of the general condition of the patient, restriction of necrosis, improvement of a circulation, removal of the become lifeless tissues, prophylaxis and treatment of an ascending infection are spent. At a damp gangrene with the purpose of its translation in dry appoint antibiotics, diuretics, UFО. Necrosis fingers close the gauze napkin impregnated of 3-5 % by iod tincture, 5-10 % a solution manganous K, camphor spirit, xeroforms, tincture of a calendula, 70 % spirit a solution.

At quickly progressing damp gangrene with its transition to a back surface of foot or a shin, especially at the expressed intoxication, it is necessary to execute ablations at a level of a hip or the top third of shin for rescue of a life of the patient.

At patients with a dry gangrene the basic actions are directed on mummification of tissues, thus application of damp bandages and ointments is inadmissible. To the amazed site access of air should be provided. Some times in day the area of necrosis is processed 70 % spirit by a solution, 3-5% iod tincture, tincture of diamond greens, tincture of a calendula. Fast mummification and demarcation comes at processing a place of necrosis 5-10 % a solution KMnO4 At favorable current it is necessary to aspire to independent tearing away mummificatioms site or spend bloodless necrectomia on a line of demarcation.

At necroses and ulcers before clarification purulently-necroses tissues spend bandagings 1-2 times to day with use of a fabric sorbent "MISS-TH", etc. After removal necroses tissues of a wound wash out 3 % a solution of peroxide of hydrogen, solutions phuracillini, hypoclorit sodium, and impose bandages with proteolitics enzymes (tripsyn, chymotripsyn, rhybonucleaza, dezoxyrhybonucleaza , etc.) with water-soluble ointment, curiozins, etc.

Application for bandagings sorbents and various napkins with immobilizing enzymes, antiseptics and biostimulators allows to reach following results:

1. To lead dehydrotation tissues in a zone of purulently-necroses process at the first stage of wounds process

2. To create local high concentration antiseptics.

3. To reach atravmatic bandagings.

4. To reduce time of bandaging and to facilitate work of medical staff.

5. To exclude a hotbed effect under a napkin as a result of good air permeability.

6. To accelerate terms of treatment and transition in a phase dehydrotation.

During bandagings at good blood supply it is recommended to irradiate a wound erythema doses of ultra-violet beams. At occurrence of granulations for acceleration of clarification of bandaging spend with iruxol ointment, juice calanhoe, solkoseril jelly, ektericids, ointment of a calendula, vulnuzan, 40 % ointment of Acidum salicylicum, ointment levomecol, etc. After clarification of a wound (ulcer) and at good granulations of bandaging spend in day with use of 10 % methyluracil ointments, sperm ointment, solkoseril ointments, vinilin, ointment with heparin (hepatrombin, etc.).

The success of treatment of trophic infringements can be reached only under condition of improvement of a circulation in an extremity.

Prophylaxis of complications of diabetic foot

1. Indemnification SD - the first necessary condition of prevention of lesion of the bottom extremities.

2. For the most effective treatment of lesions of foot early revealing the patients having raised risk of development of a syndrome of diabetic foot is necessary. The risk raises with the years and duration of illness.

3. The patients having especially high risk, should be examined by the expert for acceptance of urgent measures.

4. Adequate training of patients considerably reduces frequency of ablations of the bottom extremities.

5. Survey of legs of patient SD with the purpose of revealing of a mycosis is necessary for spending dermatology not less often than 1 time to a year.

As at far come stages of disease diabetic polyneuropathy is irreversible without special prophylaxis it is necessary to collide with relapse of a syndrome of the neuropathy-infected foot. Basically this prophylaxis consists in an explanation of patients, in what consequences results infringement of painful and temperature sensitivity. Patients should examine daily the legs, paying attention on damage of integrity of a skin and attributes of an inflammation (reddening, hyperemia, puffiness). Nails on legs should be shortened so that they could not grow (to not cut, and accurately to file a file). Callouses need to be processed cautiously pumice. Even the smallest scratchs need to be processed antiseptics. At presence of intermanual mycosises it is necessary to spend antymycos treatment.

The ILLUSTRATIONS:

Tables and figures, slides, videofilms, angiograms, dopplerograms.

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

SURGICAL SEPSIS. SEPTIC MANIFESTATION (MULTIPLE ORGAN DISFUNCTION SYNDROME – MODS). SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)

Составитель асс. О.Г.Шахбазян

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

The student should be able:

• To estimate complaints of the patient, bringing to a focus to a fever, a fever, dryness in a mouth, the general weakness, infringement of a dream, a short wind, vomiting;

• In the anamnesis of disease special attention to turn on presence of the purulent center and zones of aggressive manipulations (a purulent wound; bacteriemic lesion of internal organs, bones, joints; a puncture and catheterizations of vessels; quinsy; purulent diseases of integuments and hypoderms; a thrombophlebitis);

• In the anamnesis of a life to reveal the burdening factors promoting development of a sepsis: treatment of immunosuppressive preparations, diseases of blood, diabetes mellitis, a cirrhosis of a liver, collagenose, a radial illness, a HIV - an infection, is purulent-infectious lesions of urinogenital ways, a gastrointestinal tract, bilious channels, respiratory ways;

• At survey to pay attention to a condition of integuments and mucous: petexis, attributes of exicosis, pallor, cyanosis, hot or cold;

• At physical research to estimate a condition of primary purulent process: color and viability of granulations, character and quantity purulent separated, presence purulent not drenaging centers, presence regional lymphangitis, lymphadenitis and thrombophlebitis. At localization of purulent process in a belly cavity to reveal symptoms of functional infringement of a gastrointestinal tract and a peritonitis: meteorism, oppression or absence peristaltic, a pressure of muscles of an abdominal wall, positive symptom Shetkin-Blumberg;

• To mark infringements of a mental condition (from anxiety up to delirium and coma), cardiovascular system (a tachycardia, a hypotonia, hipoxigen changes of an electrocardiogram, increase CVP; infringements of microcirculation); to reveal pulmonary complications (a pneumonia, a pleurisy, attributes of a "shock" lung, sharp respiratory « distress syndrome »); lesion of a liver (yellow sclera’s and integuments, increase in an organ), kidneys (oligury, change of color of urine), spleens (increase);

• Correctly to interpret data of a laboratory blood analysis, bringing to a focus on leucocytes and shift leukocyte formulas to the left, electrolytic balance, a condition of an oxygen mode and AAC blood, a level of bilirubin, fiber, a fibrinogen, sugar, urea, creations, to estimate of enzimemia (LDG, ALT, nuclear heating plant, alkaline phosphatesis), parameters of a coagulogram (attributes of development of the DIC-SYNDROME), daily allowances quantity of urine and changes in urine (proteinuria, microhemouria);

• To estimate data of tool diagnostics:

• Roentgenographies of a belly cavity and thorax, radiopaque methods of research;

• Ultrasonic scanning and computer tomography of the pathological center;

• Endoscopic methods (a laparoscopy, FEGDS);

• To spend differential diagnostics: with purulent-resorb fever, a heart attack of a myocardium, aseptic pancreonecrosis, a thromboembolism of a pulmonary artery, a thrombosis mesenteric vessels, a poisoning, diabetic coma;

• To carry out bandagings, to open the purulent centers, to make laparocentes, punctures of a pleural cavity and joints at their purulent lesions, to spend active drenaging a purulent cavities.

Summary of the maintenance of employment.

The urgency of a problem of a sepsis and toxic-septic shock is caused by that for last 50 years lethality at this heavy pathology has decreased only on 20 %, and to the beginning of XXI century on the average makes about 40 %. Specification of concept of "sepsis", as syndrome of the system inflammatory answer arising in conditions of massive receipt of an infection and their toxins from the purulent center in a blood flow and leading development of infectious multiorgan insufficiency. Clinical attributes of system inflammatory reaction are simple. They include: a body temperature more 38⁰С or less 36⁰С, a tachycardia more than 90 impacts in a minute, tachypnoe more than 20 in a minute or Pa _СО2 less 32 mm Hg, leukocytes more than 12000 or less than 4000, or more than 10 % of unripe forms of leukocytes. Diagnostic information these attributes it is rather great and at presence of the center of an infection these symptoms should guard, as the sepsis is the phasic process leading development of a polysystem inconsistency and deep hemodynamic infringements , hypoxigen, a metabolism. It is necessary to note, that the sepsis is a dynamic pathological process which initial displays can quickly pass in a fatal stage of multiorgan insufficiency and an irreversible toxics-septic shock. It is necessary to pay attention to ways of penetration of an infection to a vascular channel and the reasons of development septic endotoxicosis. To note features of current of a toxics -septic shock at Gram-negative microflora, a mephitic gangrene and a staphylococcal bacteriemia. To disassemble mechanisms of formation the factor of necrosis tumors, proinflammatory cytokines, endogenous toxins and to emphasize their role in development of set of the pathological reactions defining weight endtoxics. To pay attention on pat morphology aspects septic endtoxics.

Clinical picture of a sepsis - a basis of its diagnostics. The major method of acknowledgement of the diagnosis at a sepsis is the microbiological blood analysis, separated of wounds, the purulent center, and as urine, separated of belly and chest cavity. Thus essential value has not only identification of the found out microorganisms, but also their degree , and also sensitivity antibacterial preparations.

Features of a clinical picture, as a rule, depend on extensiveness and character of the primary purulent center. Now clinical and laboratory attributes of the system inflammatory answer, a sepsis, a heavy sepsis and a toxic-septic shock are precisely formulated. It is necessary to note value of modern methods of tool diagnostics (ultrasonic scanning, a computer tomography) in revealing the primary center and an establishment of indications to volume and character of operative intervention, for revealing of the primary purulent center important for successful treatment of a sepsis of any genesis. Special value has it for a surgical intervention as successful operative sanitation of the center is impossible without the topic diagnosis. Special attention to turn on the abdominal sepsis complicating current of various intrabelly inflammatory and destructive processes. The abdominal sepsis represents most a challenge as in the diagnostic and medical plan, and economically. In structure of an abdominal sepsis the priority place is borrowed with a peritonitis and pyoinflammatory complications of a destructive pancreatitis. It is necessary to note a role of gastrointestinal decompression, enterosorbtion and intestinal oxygenations in knocking over of «an intestinal intoxication» and in struggle against a multiorgan inconsistency at an abdominal sepsis.

Intestinal insufficiency - the major component of a vicious circle at a sepsis as translocation of bacteria and their toxins from intestines in a belly cavity and in portal system supports inflammatory reaction, aggravating infringement of a metabolism. Thus infringements practically all functions of a gastrointestinal tract - barrier, metabolic, immunoprotection and endocrinic are observed. Conservative treatment of a surgical sepsis includes: the directed antibioticotherapia, correction electrolytic balance, AAC, hemoreologycal, and also an oxygen mode of blood with use of methods of an oxygenotherapy and AVP, hyperbaric oxygenation; intravenous infusions of glucose, albuminous preparations, blood; a hormonetherapy, application antihistamine preparations and vitamins, cardiotropic medicines and hepoprotectors. It is necessary to bring to a focus to value and features of an immunotherapy of a sepsis. To note the role recombinant interleycine - 2 (roncoleycin), antibodies, and others imunomodulation preparations in treatment of a sepsis and septic endotoxicosis. To disassemble indications to carrying out extracorporeal methods hemocorrection: a hemodialysis, hemofiltration, hem and lymphosorbtion, plazmopheresis, ultrafiltrations and extracorporal membranic oxygenations. To note expediency of a combination of various methods detoxication with UFO blood, etc. methods of quantum therapy.

Tasks for independent work

1. Efferent therapy in complex treatment of edotoxicosis.

2. Immunotherapy of a sepsis.

3. Role of the primary purulent center in development of a sepsis.

1. Radical surgical treatment of the purulent centers at sick of a sepsis.

TESTS

1. The local signs of septic wounds are as follows:

1. Copious purulent exudate.

2. Scanty purulent exudate.

3. Marked local hyperaemia.

4. Dirty-grey wound tissues.

5. Pronounced local oedema.

Choose the right combination of answers:

A. 1,3, 5. B. 4, 5. С. 2, 4, 5. D. 2, 4. E. 2, 5.

2. The common clinical signs of sepsis are as follows:

1. Fever.

2. Dizziness.

3. Adynamia.

4. Bradycardia.

5. Rigors.

6. Profuse perspiration.

Choose the right combination of answers:

A. 4, 5. B. 2, 4, 5. С. 2, 3,5. D. 1,2, 3. E. 1,3,5, 6.

3. The typical signs of sepsis are as follows:

1. Fever.

2. Rigors.

3. Primary focus.

4. Bacteraemia.

5. Jaundice.

Choose the right combination of answers:

A. 1,2, 3. B. 2, 4, 5. С. 1,4, 5. D. 3, 4, 5. E. 2, 3,4,5.

4. The septic fever may be of the following types:

1. Remittent.

2. Hectic.

3. Intermittent.

4. Inaccurate.

5. Continual.

Choose the right combination of answers:

A. 1, 2, 3, 5. B. 3, 4, 5. С. 1, 2, 4. D. 1, 3, 5. E. 1,2, 3,4, 5.

5. Suppurative absorption fever is characterized by the fol­lowing signs:

1. Extensive primary purulent focus.

2. Evident in all types of the inflammation.

3. Specific causative agent.

4. Rapid exhaustion of patient.

5. Resolution with elimination of the purulent focus.

Choose the right combination of answers:

A. 1, 2, 3. B. 1, 3, 5. С. 3, 4, 5. D. 1, 3, 4. E. 1,2,4,5.

6. The major signs of bacterial toxic shock are as follows:

1. Fever.

2. Bradycardia.

3. Rigors.

7. What methods of treatment would you apply for intoxi­cation:

1. Blood transfusion.

2. Detoxication.

3. Complete bed rest.

4. Antibacterial therapy.

5. Immunotherapy.

Choose the right combination of answers:

A. 1, 2, 3, 4. B. 2, 3, 4, 5. С. 3, 4, 5. D. 4, 5. E. 1,2,3,4,5.

8. The initial therapy of primary focus in sepsis may be as follows:

1. Surgical debridement of the wound.

2. Proteolytic enzymes.

Answers

1 - C, 2 - E, 3 - A, 4 - D, 5 - E, 6 - A, 7 - E, 8 - A.

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

VARICOSE VEINS IN THE LOWER LIMB. CHRONIC LYMPHOVENOUS FAILURE. THROMBOPHLEBITIS (classification, clinic, diagnostics, treatment)

Составитель: доцент Ю.И.Ломаченко

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

Definitions.

Thrombophlebitis is inflammation and clotting in a vein.

Deep vein thrombosis is blood clotting in the deep veins.

Classification and Etiology

Thrombosis may affect superficial veins (superficial thrombophlebitis) or deep veins (deep vein thrombosis). Prolonged venous thrombosis may lead to chronic venous in­sufficiency, in which there is edema, pain, stasis pigmentation, stasis dermatitis, and stasis ulceration. Thrombosis is virtually always accompanied by phlebitis, thus the terms thrombosis and thrombophlebitis are used interchangeably. Thrombosis may oc­cur on the basis of coagulation abnormalities that may be familial or related to an under­lying malignancy.

Iliofemoral thrombophlebitis refers to extensive thrombosis of the involved extremity that has developed a milky white color. Phlegmasia cerulea dolens indicates a massive ve­nous thrombosis, in which the leg is often blue. It often leads to venous gangrene and death due to underlying disease (eg, widespread malignancy).

Other eponyms describe thromboses in specific anatomic areas: pelvic vein, mesenteric vein, portai vein, renal vein, and jugular-mesenteric vein thromboses.

Endothelial injury can expose collagen, causing platelet aggregation and tissue throm-boplastin release that, when stasis or hypercoagulability is present, trigger the coagula­tion mechanism. Many factors may contribute to venous thrombosis: injury to the endo-thelium of the vein, eg, from indwelling catheters, injection of irritating substances, thromboangiitis obliterans, and septic phlebitis; hypercoaguiability associated with ma­lignant tumors, blood dyscrasias, oral contraceptives, and idiopathic thrombophlebitis; and stasis in postoperative and postpartum states, varicose thrombophlebitis, and the thrombophlebitis that complicates prolonged bed rest of any chronic illness, heart fail­ure, stroke, and trauma. Prolonged immobilization with the legs dependent while travel­ing (especially on long flights) is a risk factor, even in normal persons. Strenuous exer­cise of muscles in the affected extremity (eg, arm) is also a risk factor.

Septic phlebitis is possible whenever a septic process is present in the extremity distal to or at the ievel of the venous obstruction. Septic thrombi may form separately from the in­fectious focus or may occur in contiguity with the inflammatory area as part of a cellulitis.

Pathophysiology

Most venous thrombi begin in the valve cusps of deep calf veins. Tissue thromboplastin is released, forming thrombin and fibrin that trap RBCs and propagate proximally as a red or fibrin thrombus, which is the predominant morphologic venous lesion (the white or platelet thrombus is the principal component of most arterial lesions). Anticoagulant drugs (eg, heparin, the coumarin compounds) can prevent thrombi from forming or extending. Anti-platelet drugs, despite intensive study, have not proved effective for prevention.

Symptoms and Signs

Symptoms of acute thrombophlebitis arise over hours to 1 or 2 days. The disease is usually self-limited and lasts 1 to 2 wk, after which the acute process subsides and pain­ful symptoms disappear.

In superficial thrombophlebitis, a thrombosed superficial vein can be palpated as a Hnear, indurated cord; it may be associated with variable inflammation manifested by pain, tenderness, erythema, and warmth and may need to be differentiated from acute secondary lymphedema with infection. Palpation of a superficial cord in the leg reflects occlusion of a superficial vein; it is seldom due to deep vein thrombosis.

Deep vein thrombosis (DVT) may be asymptomatic or may manifest over the involved area as combinations of tenderness, pain, edema, warmth, skin discoloration, and prominent superficial veins. DVT involving the popliteal, femoral, and iliac segments may be tender, with a hard cord palpable over the involved vein in the femoral triangle in the groin, medial thigh, or popliteal space. With iliofemoral venous thrombosis, dilated superficial collateral veins usually appear over the leg, thigh, and hip areas and lower abdomen.

Because at least three main veins drain the lower leg, thrombosis in one does not ob­struct venous return, and there is no swelling, cyanosis of the skin, or dilated superficial vein. The patient complains of soreness or of pain on standing and walking that is usu­ally relieved by rest with the leg elevated. On examination, deep calf tenderness can be elicited, but the pain of DVT is often difficult to differentiate from muscle pain. Pain from muscular causes will be absent or minimal on dorsiflexion of the ankle with the knee flexed but maximal on dorsiflexion of the ankle with the knee extended or during straight-leg raising (Homans' sign); thus, this test is unreliable for DVT. Loss of periph­eral arterial pulses occasionally accompanies massive DVT, but venous thrombosis can also be secondary to acute arterial occlusion.

Chronic venous insufficiency in the leg after DVT manifests as edema and dilated su­perficial veins. The patient may complain of fullness, aching, or tiredness in the leg or may have no discomfort. Symptoms occur during standing or walking and are relieved by rest and elevation. There is no tenderness over the deep veins to indicate an acute thrombophlebitis, but a history of DVT should be elicited. Stasis syndrome occurs if edema is not controlled by an elastic support. With time, skin pigmentation appears on the medial and sometimes the lateral aspect of the ankle and lower leg. Further complica­tions include stasis dermatitis and stasis uiceration in these areas. Patients with chronic venous insufficiency may develop varicose veins, which are secondary to DVT, are often mild, and function as collateral vessels. They should not be excised unless severe.

Diagnosis

Superficial thrombophlebitis is diagnosed by the symptoms and by finding a swollen, tender, superficial venous cord on examination.

Physical examination usually can differentiate acute arteria! from deep venous obstruc­tion. In > 50% of cases, acute DVT cannot be diagnosed by clinical findings alone; Homans' sign should not be relied on for the diagnosis, and edema may be due to other causes. Specific limb findings (eg, edema, dilated superficial veins), evidence of pulmo­nary embolism, and the overall clinical setting, including risk factors, permit the physi­cian to estimate the likelihood of DVT. The diagnosis can be confirmed by noninvasive testing or by venography if necessary. Duplex ultrasonography is diagnostic in most cases in which thrombus involves the iliac, femoral, or popliteal veins. If the diagnosis is in doubt, a venogram should be obtained. Pulmonary embolism can be sought with lung scan or pulmonary arteriogram. If overlooked, DVT may lead to death from pulmonary embolism, but use of anticoagulants without having demonstrated an intravascular thrombus on ultrasonography, venography, or lung scan risks serious hemorrhage.

Plethysmography, as with ultrasonography, can be used with acceptable accuracy to diagnose thrombotic obstruction of major proximai veins of the extremities or chronic venous insufficiency. It cannot detect DVT of the calf. Plethysmography is noninvasive and relatively inexpensive, requires minimal patient cooperation, and can be performed well by a trained technician. It is frequently used with duplex ultrasonography, and this combination enhances the accuracy of diagnosis. Patients may be treated if the results of either test are positive. If the results are negative and DVT is still suspected, veno­graphy should be done.

Prognosis

DVT is usually benign but can cause lethal pulmonary emboli or chronic venous insuffi­ciency. Superficial thrombophlebitis alone, even when recurrent, causes neither of these serious complications, although nonlethal pulmonary emboli rarely originate in superfi­cial veins.

Although superficial thrombophlebitis and DVT are more common in patients with can­cer, the mechanism is obscure. Most clinically recognized episodes of DVT are not as­sociated with cancer. However, when malignancy is the only risk factor in a patient with superficial thrombophlebitis or DVT, the malignant process is almost invariably ad­vanced.

Treatment

Superficial thrombophlebitis requires no specific therapy other than relief of dis­comfort. Warm compresses over involved veins and NSAIDs are helpful. Hospi-talization is unnecessary, and antibiotics are not needed.

For DVT, the objectives of therapy are to prevent pulmonary embolism and chronic ve­nous insufficiency. When acute DVT is diagnosed, the patient may be hospitalized ini­tially. However, because of advances in heparin therapy, selected patients with DVT can be treated at home, reducing or eliminating hospitalization. The foot of the bed is elevated 6 in, and the patient heparinized; in either setting, bathroom or commode privi­leges can then be permitted. Drugs such as phenylbutazone or corticosteroids are not indicated routinely, and antibiotics should be used only for a specific infection. Warm moist packs are comforting but optional in patients without arterial insufficiency.

Low inol wt heparin is followed soon by oral warfarin, with the dosage adjusted to achieve an INR between 2 and 3. Duration of anticoagulant therapy depends on the pa­tient. A single episode of thrombophlebitis subsiding clinically in 3 to 6 days in a young, active patient free of risk factors may require only 2 mo of therapy, but a patient with a demonstrable pulmonary embolus and persistent risk factors may require 6 mo of ther­apy. After >= 2 episodes of DVT, oral anticoagulant prophylaxis should be continued indefinitely. The value of antithrombotic drugs (eg, snake venoms, platelet antiaggre-gates, thrombolytic compounds) has not been established.

Thrombolytic therapy: Thrombolytic therapy using tissue plasminogen activator or urokinase in tandem with anticoagulants is effective for acute DVT of the popliteal and more proximal veins. The best results occur when the DVT has been present for < 48 to 72 hr. Complete or partial dissolution of thrombi usually occurs within 24 to 48 h. Suc­cessful treatment restores venous anatomy and thus may prevent valvular damage and resulting chronic venous insufficiency. Before thrombolytic therapy is used, the diagno­sis must be confirmed by venography. The contraindications and adverse effects, espe­cially bleeding, and the details of treatment and monitoring must be understood.

When edema subsides, the patient should be measured for a firm below-knee elastic stocking (providing 30 to 40 mm Hg pressure) to control the edema that will occur with ambulation. The stocking should be worn while the patient is ambulatory to prevent the postphlebitic sequelae of chronic venous insufficiency: edema, pain, stasis pigmenta­tion, and subsequent stasis dermatitis and stasis uiceration. When these complications occur, treatment with an Unna's paste boot or bed rest with elevation and compression dressings will heal most ulcers. Antibiotics are usually indicated only when the ulcer is surrounded by severe acute cellulitis. Wet NaCI dressings may help to loosen superfi­cial exudate and slough. Large refractory or recurrent ulcers may have to be excised, the incompetent perforating veins ligated, and the area covered with a split-thickness skin graft.

TESTS

1. The complications of lower limb thrombophlebitis are commonly due to:

1. Superficial vein thrombosis.

2. Superficial vein dilatation.

3. Femoral artery thrombosis.

4. Lower limb deep vein thrombosis.

Choose the right combination of answers:

A. 1,2. B. 2. С. 3,4. D. 4.

2. Thrombophlebitis is seen in -

a) Carcinoma ovary

b) Carcinoma breast

c) Carcinoma testes

d) Carcinoma stomach

3. Treatment of post thrombophlebitis involves the follow­ing methods:

1. Anticoagulants.

2. Antibiotics.

3. Bypass of the occluded vessel.

4. Insertion of a probe into the affected vessel's lu­men.

5. Ligation and removal of the affected vein.

Choose the right combination of answers:

A. 1,2, 3. B. 1,4. С. 1,3, 5. D. 2, 5. E. 1, 2.

4. To assess the potency of venous valves, the following methods are used:

1. Trials by fingers and tourniquets signal.

2. Rheovasography.

3. Doppler ultrasonography.

4. Infrared thermography.

5. Contrast phlebography.

Choose the right combination of answers:

A. 1,2, 3. B. 1, 3, 5. С. 1,2, 3,4, 5. D. 2, 3, 4. E. 2, 3, 4, 5.

5. The causes of acute vein insufficiency are as fol­lows:

1. Vein thrombosis.

2. Deep vein thrombophlebitis.

3. Obesity.

4. Varicose veins.

5. Traumatic venous injury.

Choose the right combination of answers:

A. 1, 3, 5. B. 1, 2, 4, 5. С. 2, 3, 4. D. 2, 3, 5. E. 1,2,5.

6. Preventive measures in post surgery deep vein throm­bophlebitis include the following:

1. Antibacterial therapy.

2. Lower limbs bandaging pre- and postoperatively.

3. Prolonged postoperative bed rest.

4. Prevention of prolonged immobilization after sur­gery.

5. Intake of vasodilators.

Choose the right combination of answers:

A. 1,2. B. 4, 5. С. 2, 3,5. D. 2, 4. E. 1,3, 5.

7. The signs characteristic of acute deep vein thrombosis are as follows:

1. Acute local pain (in the affected limb).

2. Cutaneous pallor or cyanosis.

3. Fever.

4. Hyperaemia.

5. Pronounced swelling of the limbs.

Choose the right combination of answers:

A. 1,4. B. 1,2, 5. С. 1,3, 5. D. 2, 4. E. 3, 5.

8.Migrating thrombophlebitis is associated with cancer of-

a) Liver

b) Lung

c) Kidney

d) Pancreas

9. The most common vein to get thrombosed is the

a) Long saphenous

b) Short saphenous

c) Both

d) Posterior tibial

Answers

1 – D

2 – A,B,D

3 – A

4 – B

5 – B

6 – D

7 – B

8 – B, D

9 – D

References

Gostischev V. K. General surgery / The manual. – M.: GEOTAR-MED, 2003. – Charter XI. – P.150-191.

Moukonin A.A., Golub A.V. Venous and lymphatic disorders: Textbook for foreign students. – Smolensk: Smolensk State Medical Academy, General Surgery Department. – 2005. – 5p.

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

CHRONIC ARTERIAL OCCLUSIVE DISEASES IN THE LOWER LIMB – AORTOILIAC DISEASE, DISEASE OF THE FEMORAL AND DISTAL ARTERIES (classic buerger disease, thromboangiitis obliterans). GANGRENE OF THE LOWER LIMB.

Составитель асс. А.А.Безалтынных

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

Basic information

Necrosis is the death of tissues of part or a whole organ of the living body.

Causes of necrosis are as follows:

• physical;

• high or low temperatures;

• radiation or electrical energy;

• chemicals;

• Mechanical;

• pressure on or crushing of tissues.

These types of injury directly lead to necrosis of tissues. Local circulatory disorders (e.g. thrombosis, embolism or vascular occlusion) often result in indirect necrosis. The condition is accompanied by abnormal innervation when the nerves are damaged (e.g. leprosy, syringomyelia).

Necrosis can be:

• coagulative, or dry (burns, dry gangrene);

• colliquative, or wet (alkaline burns, wet gangrene).

The signs of necrosis become obvious within 4 to 6 hours after tissue death. The necrotic tissue undergoes rejection and, if located on the surface of an organ, an ulcer develops. Extensive necrosis with widespread tissue decay results in systemic absorption of toxic products, which, in turn, leads to intoxication.

GANGRENE

Necrosis due to primary blood circulatory disorders is referred to as gangrene.

Causes:

• extensive crushing;

• severe pressure on tissues;

• vascular injuries;

• organ compression (e.g. POP bandage);

• volvulus with compression of the vessels;

• leaving the tourniquet on a limb for a long time;

• vascular thrombosis and embolism;

• obliterating endarteritis;

• obliterating arteriosclerosis.

Most commonly acute and chronic arterial occlusion lead to gangrene.

Dry gangrene is caused by fast dehydration of the necrotic tissues without bacterial contamination.

This results in tissue mummification. In wet gangrene, colliquative tissue necrosis occurs, which is usually complicated by an ichorous infection, with subsequent disintegration of the devitalised tissue and severe intoxication. The tissue debris is dirty-green or black in colour and smells very offensive.

Gangrene resulting from acute ischaemia of an organ is accompanied by severe ischaemic pain that is normally felt below the level of vascular occlusion. The colour of the limb changes very fast from pale to marble-bluish; it becomes cold and skin sensations disappear.

In dry gangrene, the gradual drying up of the necrotic area is followed by a clear-cut demarcation between the intact and necrotic areas. The skin becomes black, which is accompanied by minimum, if at all, intoxication. In wet gangrene the patient's condition is generally severe from the very onset (fever, tachycardia, chills, thirst, and dehydration) because of absorption of ichorous tissue disintegration products into circulation.

Over the areas of necrosis (often in the foot and the lower third of the leg) the skin becomes bluish with dark-red patches and haemorrhagic blisters. The extremity is oedematous, enlarged, and dirty-greyish tissues with offensive odour are visible (see fig. 126, colour inset).

Once the signs of necrosis appear, the limb is to be immobilised and an aseptic dressing applied.

Types of surgical treatment.

The treatment of necrosis depends on its cause. The common strategy of the management of all types of necrosis is the removal of the necrotic tissue, or necrectomy.

Necrectomy requires that several parallel incisions be done in the necrotic area without anaesthesia and an antiseptic dressing be applied. This contributes to the removal of the degenerated necrotic tissues and, therefore, reduces the intoxication of the body.

Necrectomy can be performed with a scalpel or scissors (mechanical necrectomy), proteolytic enzymes (chemical necrectomy), physical factors -ultrasound or laser rays (physical necrectomy).

It is advisable:

• in progressive wet gangrene, to undertake above-knee amputation (without waiting for tissue demarcation) without delay;

• in dry gangrene, to first allow the demarcation line appear and then amputate the limb above it within the intact area.

ARTERIAL OCCLUSION (ACUTE AND CHRONIC ARTERIAL INSUFFICIENCY)

Examining the patient with arterial diseases the surgeon has to consider a number of peculiarities:

1. The examination must occur in a warm room;

2. It is required that the symmetrical sites of the j limbs be inspected.

Skin color is compared on both limbs. Pale or violet-bluish discoloration acquired on moving the limb from the horizontal position to the vertical one strongly suggests deficient circulation. The skin is usually dry and scaly, and the nails are deformed, thickened and brittle; a loss of hair and muscle atrophy may also be observed.

The feeling of the arteries shows a weak or absent pulse. On the lower limb the pulse is to be felt on the femoral artery (below the middle of the Poupart's ligament), popliteal artery (in the popliteal fossa with the leg Hexed in the knee joint and the muscles maximally relaxed), dorsalis pedis artery (between the first and second metatarsal bones) and tibialis posterior artery (behind the medial malleolus). Pulsation on the upper limb will be evaluated on the subclavian, humeral and radial arteries.

Diagnostic procedures (investigations).

To assess the severity of arterial circulatory disorder special tests are performed.

Oppel test. Have the patient lie supine with his/her leg raised at an angle of 45°. The appearance of paleness on the sole (the plantar ischaemic sign) serves as the evidence of arterial circulation insufficiency.

Samuel's test. Have the patient lie in the position as described above and do 20 to 30 flexions in the ankle joint. The appearance of paleness on the sole is also a sign of arterial circulation insufficiency.

Moshkovich's test. Have the patient lie supine raise his/her leg and apply a tourniquet for 5 minutes. The period needed for the skin to regain hyperaemia following the removal of the tourniquet is normally 5 to 30 seconds whereas that in arterial occlusion is as long as 3 to 5 minutes.

The above-mentioned tests can only be diagnostic at initial, or compensated, stages of the disease. If intermittent claudication appears, the diagnosis is easy to make (the sub- and decompensation stages of circulatory failures).

Special methods are used to assess the severity of circulatory disorders, monitor pathologic progression and the efficacy of therapy. These are primarily as follows:

1. Thermometry, the technique of measuring skin temperature at symmetrical limb areas using an electric thermometer. A reduction in temperature by 0,5— 0,7°C strongly suggests deficiency in the blood flow.

2. Oscillograph, recording oscillations produced by changes in electrical potentials caused by vibrations of an artery. A decrease in vibration amplitude indicates deficient circulation.

3. Impedance rheovasography, the technique to register the resistance produced by pulsating limb arteries as a result of their filling. In health, the rheographical index is as high as 0.8-1.0; its reduction being evident of deficiency in the arterial circulation.

4. Doppler ultrasound, the method of listening to the arterial blood flow with the velocity detector (Doppler probe) to recognize arterial occlusion or stenosis.

5. Capillaroscopy, microscopical examination of the capillary vessels of the skin or nail beds. In occlusive arterial diseases the capillaries become convoluted, winding and constricted.

6. Arteriography, the visualisation of arteries by means of X-rays after injection of radio-opaque material. In obliterating atherosclerosis, the vessels with the «eaten up» internal contours, as well as areas of the constricted, or occluded, lumen are seen. In endarteritis, the arterial lumina are markedly narrowed, often over wide areas. Thrombosis/thromboembolism cause obstruction of the artery,

ACUTE ARTERIAL OCCLUSION

Suits from the sudden arrest of the blood flow in an artery and is the commonest cause of gangrene.

The factors that contribute to arterial occlusion include trauma, the excessive pressure from a tourniquet, intra-operative ligation of the artery, thromboembolism (i.e. the obstruction of a vessel, mainly by thrombus and occasionally by air, fat).

Arterial embolism results in ischaemia of the limb, the severity of which depends on the size of the thrombosed vessel, the level of obstruction, the capacity of the collateral circulation as well as the duration of the problem (the time lag between the moment of occlusion and the reporting time).

In thromboembolism of a major artery, the sign of acute organ ischaemia (e.g. the limb) is observed. Thromboembolism causes the following pathogenic changes:

• obstruction of a main vessel;

• acute distension of the vessel above the area of obstruction;

• reflex spasm of all the arterial network of the limb — the obstructed vessel, its branches and collaterals beneath the area of obstruction;

• formation of a sequel thrombus beneath the area of obstruction because of a decrease in blood flow and defects of blood coagulation and anticoagulation systems.

To verify the diagnosis and identify of the level of occlusion special investigations are applied: cutaneous thermometry, oscillograph, rheography and angiography.

According to V. Saveliev, the clinical course of thromboembolism of the major vessels divides into three stages:

• stage 1 - ischaemia causing functional disorders. This lasts a tew first hours. The clinical picture includes (I) acute pain in the limb affected, pale and cool skin, absent pulse on the peripheral arteries. It is noteworthy that pain and touch senses usually remain intact, active joint motions are slightly limited. The restoration of blood supply to the limb at this stage leads to a full functional recovery;

• stage 2 — structural changes — includes such signs as absent pain and touch sensations, markedly limited active and passive joint movements, muscular oedema and contractures, bluish discolouration of the skin. This stage lasts for 12 to 24 hours. The restoration of blood supply within the above-mentioned period, can save the limb although its functions are, as a rule, either partially or fully lost;

• stage 3 — necrosis — is characterised by the development of gangrene. It follows within 24 to 48 hours after embolisation. At this stage, due to gangrene virtually all forms of sense and movement will be lost, while resume of the blood flow in the vessel can occasionally reduce the level of the demarcation line, hence the level of amputation.

The staging of ischaemia helps choose the therapeutic modality:

• stages I and 2 require radical treatment - restoration of the arterys patency (i.e. restoration of the blood flow);

• stage 3 precludes the aforementioned therapy as the necrosis of an extremity is a life-threatening condition and thus calls for urgent options, of these the amputation of the limb affected being the mainstay.

The clinical features of the disease, leg pain particularly, may readily be identified the moment embolisation has occurred. The severe ischaemic pain, which results not only from occlusion but also from the reflex spasm of collateral vessels, is of sudden onset and of persistent duration. Occasionally, it can produce shock. The pain is mostly often located at the distal parts of the limb; it sometimes appears at the area of occlusion and spreads distally later on. Alternatively, the patient may present with numbness sensation, paraesthesia (tingling), while coolness to touch and pain come on thereafter. This suggests that the incomplete occlusion of the artery by an embolus precedes the complete one due to secondary thrombosis that causes limb ischaemia.

The incidence of the subacute course of thromboembolism of a major artery is as high as ten percent.

The patients with arterial thromboembolism are usually those with serious cardiac disease, which accounts for the severity of their condition.

Physical examination yields helpful clinical signs as follows:

1. Vital signs:

• increased pulse rate;

• low blood pressure (a sign of impending shock);

• labial and mucosal cyanosis;

• fast breathing.

2. Skin:

• a change in the skin colour, which becomes cyanotic, pale or even white with bluish patches («the marble skin») that resemble those of the cadaver:

• coolness to touch is more pronounced at the peripheral areas; skin temperature is reduced by 2-3 °C as compared to that of the intact side;

• both pain and touch sensations checked with a needle are diminished. The inability of the patient with their eyes closed to distinguish between being pricked by a sharp object and touched by a blunt one indicates the loss of both pain and touch sensations. This suggests irreversible damage to the tissues as the circulation in the limb fails to maintain the viability of tissues.

3. Pulses:

• absent lower limb pulse is a typical sign.

4. Neurologic signs. It should be emphasized that neurological signs

(numbness sensation and paraesthesia with subsequent loss of all kinds of sensation) become visible very fast. The pain can shortly be followed by motor deficit of various degrees (finger and toe paralyses).

The combination of pulselessness with paresthesias, acute pain, pallor and palsy are therefore diagnostic of acute arterial ischaemia.

If measures are not taken to restore circulation, the signs of acute ischaemia progress and gangrene, which is usually dry ensues.

Treatment. The first aid in arterial thromboembolism includes:

• analgesia and cardiac medications;

• transport immobilisation of the limb either by a standard or an improvised splint;

• application of ice packs to the affected limb;

• immediate transportation of the patient to the surgical unit.

The management of the patient with arterial thromboembolism must be individualised depending on the location of the embolus; the stage of disease and its duration.

The preoperative treatment should start with conservative measures. Failure of ischaemia to subside and (hat of pain to relieve and touch sensations to recover within 2 hours of the therapy is an indication for surgery.

The conservative treatment is applicable:

• at the initial stages of the disease (i.e. within 6 hours from its onset of disease);

• in critically-ill patients;

• in embolism of small arteries (i.e. those of the foreleg and forearm);

• in obscure clinical picture;

• as a method additional to surgery. Jt involves the following:

1. Anticoagulation therapy (heparin, indirect anticoagulants) and fibrinolytic agents (streptokinase, streptodecase, urokinase) to prevent formation of clots and lyse the the preformed ones;

2. Antispasmodic therapy to eliminate the vascular spasm (vasodilators, novocain block, papaverin, carbacholin);

3. Improvement of collateral circulation (Bernard's current; vacuum apparatus applied to the limb).

Surgical treatment simplies radical operations (i.e. embolectomy arterioplasty and vascular shunting) to restore the patency of arteries, whereas alliative ones are performed to improve the collate -"al circulation without restoring the patency of the ain vessel (e.g. sympathectomy). The gangrenesnt limb is subject to amputation.

CHRONIC ARTERIAL OCCLUSION

Chronic arterial occlusion is a condition caused (he gradual narrowing of an artery with the re-ant ischaemia of the limb.

Causes of chronic ischaemia of the limb include following:

Thromboangiitis obliterans (Indarterilis Buerger's disease) and Raynaud's disease. Thromboangiitis is the inflammation of the entire wall and connective tissue surrounding medium - sized arteries and views especially of the legs of young and middle-aged men.

Raynaud's disease has a vasospastic origin and affects mainly the upper limbs.

Obliterating artheriosclerosis that results from artheriosclerotic narrowing and occlusion of the vascular lumina.

It is chronic arterial insufficiency that underlies each of these diseases and produces the ischaemic syndrome. The diagnosis is based on the degree of the arterial insufficiency and its progression rate.

History:

• pain (it is usually the earliest complaint);

• intermittent claudication: severe pain in the legs, tension and weakness on walking which makes the patient stop. The symptoms increase as walking proceeds until further progress is impossible (being the chief but late symptom, it indicates pronounced disorder in the limb circulation, even though most patients associate it with the beginning of their disease).

The severity of the syndrome correlates directly with the degree of ischaemia:

• degree I (the pain follows the walking of 500 m);

• degree II (the pain is evident on walking 200 m);

• degree III (the pain appears after walking 20-30 m or at rest);

• degree IV (the signs indicative of necrosis, or gangrene).

The clinical stages of chronic arterial insufficiency are as follows:

Stage I, or compensation History:

• fatigability, a feeling of pressure and pain in the gastrocnemii muscles on walking;

• coolness in the feet, intermittent claudication on walking 200-500 m, numbness and tingling sensation at the finger and toe tips, muscular weakness;

• past medical history indicative of heavy tobacco smoking, long exposure to cold and frequent stress.

Physical examination of the limbs:

• minimum physical signs: hair loss, skin pallor, coolness to touch mostly confined to the fingers and toes, diminished peripheral pulses, «white patches» on pressing the feet.

Stage II, or subcompensation, is characterised by transient ischaemia History:

• a feeling of cold fingers and toes; intermittent claudication more pronounced than at stage I;

• transient ischaemia (subsides on resting);

• effectiveness of conservative therapy. Physical examination:

• pallor and coolness of the foot skin. Stage III, or decompensation History:

• severe pain at the fingers or toes, sole, dorsum of the foot and occasionally in the leg, both on walking and at rest, presumably nocturnal, which makes the patient sit up in bed with their legs on the floor and therefore interferes with their night sleep.

Physical examination:

• dry and pale skin with bluish patches of ulceration (i.e. foci of necrosis) and oedema on one of the toes and fingers;

• thickened and brittle nails;

• muscle atrophy;

• absent arterial pulse on the feet.

Stage IV, or gangrene History:

• persistent and unbearable pain. Physical examination:

• marked oedema and cyanosis with bluish black discolouration of the whole foot;

• wrinkling of the skin (which suggests dry gangrene);

• superimposed infection (which leads wet gangrene).

OBLITERATING ARTERIOSCLEROSIS

Obliterating arteriosclerosis, which is a local pre­sentation of generalised atherosclerosis, often produces chronic deficiency of arterial blood supply to the lower limbs and is manifested by ischaemia of the anatomic sites. The major arteries - bifurcation of the aorta, and iliac, femoral and the popliteal arteries - are most commonly involved. In contrast, the upper limb vessels may hardly ever be affected.

History:

The risk factors include the following:

• age over 50 years;

• heavy tobacco smoking;

• coronary heart disease (e.g. myocardial infarction);

• cerebrovascular disease;

• hypertension;

• metabolic disorders (e.g. diabetes mellitus, hypercholesterolemia, vitamin deficiency);

• history of long exposures of the feet to cold;

• stress.

Clinical picture:

• patients tend to look old for their age;

• femoral pulses are often absent;

• the areas of necrosis on the foot may not be present.

Diagnostic studies:

• angiography shows jagged and defective arterial walls with proximal occlusion of the arteries.

• X-ray films help detect calcifications of the vessels.

Treatment:

• vasodilating agents;

• anticoagulant therapy (indicated in thrombosis),

• health resort therapy.

Occlusion of main artery is an indication for reconstructive surgical procedures (e.g. bypass graft) while gangrene invariably requires amputation of the limb affected.

ENDARTERITIS OBLITERANS

The disease starts with the involvement of the small vessels of the lower limbs; occasionally, those of the upper limbs may also be affected.

History

The risk factors are usually as follows:

• age under 40 years;

• frequent psychological stress;

• heavy tobacco smoking;

• rarely, history of

• coronary heart disease;

• cerebrovascular disease;

• hypertension;

• diabetes mellitus;

• history of long exposures of the feet to cold frostbites.

Clinical picture:

Pulsation in the foot, and rarely thigh, is reduced or absent. In spite of the pressure of pulsation on one of the arteries of the foot or the popliteal pulse, necrosis appears over the toes.

Diagnostic studies:

• angiogram demonstrates smooth vascular walls and narrowing of the peripheral arteries.

In thromboangiitis obliterans, apart from the characteristic features of endarteritis, there is evidence of phlebitis or thrombophlebitis. The progression of the disease may often lead to wet gangrene.

Treatment:

• analgesics;

• nonsteroidal anti-inflammatory drugs;

• antihistamines;

• vasodilating agents, including those that payse transmission across the synapses;

• female sex hormone therapy (synoestrol, folliculin); physiotherapy (ultra-high frequency current; Of the surgical methods, operations on the sym-Bernard's current; electrophoresis with drug pathetic nervous system are commonly performed preparations); (lumbar, thoracic and periarterial sympathectomy).

• health resort therapy. Amputation takes priority in gangrene.

KEY QUESTIONS FOR HOMEWORK:

1. The complications of lower limb thrombophlebitis are commonly due to:

1. Superficial vein thrombosis.

2. Superficial vein dilatation.

3. Femoral artery thrombosis.

4. Lower limb deep vein thrombosis.

Choose the right combination of answers:

A. 1,2 B. 2 C. 3,4 D. 4

2. The typical signs of obliterating endarteritis are as follows:

1. Creeping sensation.

2. Chilly sensation in the feet.

3. Local hair falling.

4. Intermittent claudication.

5. Thickening nails.

Choose the right combination of answers:

A. 1,2 B. 3,4,5 C. 1,3 D. 2,4 E. 1,2,3,4,5

3. The characteristic signs of lower limb arterial thromboembolism are as follows:

1. Slowly progressing pain.

2. Sudden acute pain.

3. Bluish discolouration of the skin.

4. Skin pallor

5. The limbs' coolness to touch.

Choose the right combination of answers:

A. 1,2,3 B. 2,3,4 C. 4,5 D. 2,4,5

4.The causes of lymphatic circulatory disturbance are as follows:

1. Lymphatic vessel hypoplasia.

2. Erysipelas.

3. Chronic lymphadenopathy (tuberculosis, syphilis).

4. Vascular constriction by tumours or scars.

5. Atherosclerosis obliterans.

Choose the right combination of answers:

A. 1,2 B. 1,2,3,4 C. 2,3,4,5 D. 3,4,5 E. 1,3,4

5. Treatment of post thrombophlebitis involves the following methods:

1. Anticoagulants.

2. Antibiotics.

3. Bypass of the occluded vessel.

4. Insertion of a probe into the affected vessel's lumen.

5. Ligation and removal of the affected vein.

Choose the right combination of answers:

A. 1,2,3 B. 1,4 C. 1,3,5 D. 2,5 E. 1,2

6. To assess the potency of venous valves, the following methods are used:

1. Trials by fingers and tourniquets signal.

2. Rheovasography.

3. Doppler ultrasonography.

4. Infrared thermography.

5. Contrast phlebography.

Choose the right combination of answers:

A. 1,2,3 B. 1,3,5 C. 1,2,3,4,5 D. 2,3,4. E. 2,3,4,5.

7. The causes of pulmonary embolism are as follows:

1. Obliterating thrombosis of superficial veins.

2. Thrombus of the femoral artery.

3. Floating thrombus of the vena cava.

4. Diffuse thrombus of the skin and femoral veins.

5. Thrombus of the sapheno-femoral anastomosis.

Choose the right combination of answers:

A. 1,2,5 B. 2, 3,4 C. 2,3 D. 3,4,5 E. 3,4

8.The agents for pathogenic treatment of obliterating endarteritis are as follows:

1. Desensitizors.

2. Corticosteroids.

3. Vasodilators.

4. Platelet aggregation inhibitors.

5. Antibiotics.

Choose the right combination of answers:

A. 1,2,3 B. 2, 3,4 C. 2,4 D. 1,3, 4 E. 2,3

9.The risk groups of obliterating endarteritis are as follows:

1. Children.

2. 20-40 year-old men.

3. 50-60 year-old women.

4. Smokers.

5. Patients after frostbite.

Choose the right combination of answers:

A. 1,5. B. 1,2,3. C. 2,3,5.D. 2,4,5. E. 2,4.

10. The causes of acute vein insufficiency are as follows:

1. Vein thrombosis.

2. Deep vein thrombophlebitis.

3. Obesity.

4. Varicose veins.

5. Traumatic venous injury.

Choose the right combination of answers:

A. 1,3,5. B. 1,2,4,5. C. 2,3, 4. E. 1,2,5.

11.Preventive measures in post surgery deep vein thrombophlebitis include the following:

1. Antibacterial therapy.

2. Lower limbs bandaging pre- and postoperatively.

3. Prolonged postoperative bed rest.

4. Prevention of prolonged immobilization after surgery.

5. Intake of vasodilators.

Choose the right combination of answers:

A. 1,2. B. 4, 5. C. 2,3,5. D. 2.4. E. 1,3, 5.

12.The signs characteristic of acute deep vein thrombosis are as follows:

1. Acute local pain (in the affected limb).

2. Cutaneous pallor or cyanosis.

3. Fever.

4. Hyperaemia.

1. Pronounced swelling of the limbs. Choose the right combination of answers:

A. 1,4. B. 1,2,5. C. 1,3,5. D. 2,4. E. 3,5.

13.The causes of gangrene are as follows:

1. Major vessel embolism.

2. Arterial injuries.

3. Arterial thrombosis.

4. Frostbite.

5. Bum.

Choose the right combination of answers:

A. 1,2. B. 1,3,4. C. 2,4,5. D. 1,2,3,4,5.

14.Common causes and risk factors of moist gangrene are as follows:

1. Acute circulatory defect in the limbs.

2. Obesity.

3. Putrid wound infection.

4. Defective perfusion of the viscera (the bowel, lungs).

5. Obliterating endarteritis.

Choose the right combination of answers:

A.1,2,3,5. B.1,3,4,5. C. 1,2,3,4. D. 1,2,4,5. E. 1,2,3,4,5.

15.Dry gangrene is characterized by:

1. Inclination to putrid infection.

2. Demarcation line.

3. Pronounced intoxication.

4. Absence of intoxication.

5. Mummification of necrotic tissues.

Choose the right combination of answers:

A. 1,2. B. 2, 3. C. 1,3. D. 1,4. E. 2, 4, 5.

16.The clinical signs of limb moist gangrene are as follows:

1. Oedema and local skin discolouration.

2. Intoxication.

3. Delimitation of necrotic areas.

4. Offensive smell.

5. Absence of the demarcation line.

Choose the right combination of answers:

A.1.2. B.1,3,4, 5. C.2,4. D.1,2,4, 5. E.2, 3.

17.The appropriate treatment of limb moist gangrene with severe intoxication and fever may be as follows:

1. Necrectomy.

2. Limb bandaging with antiseptics.

3. Intra-arterial injection of antibiotics.

4. Local hyperbaric oxygenation.

5. Amputation of the affected limb.

Choose the right combination of answers:

A. 1,2. B. 2,3. C. 1,2,3,4. D. 3,4. E. 5.

18.The appropriate surgery for varicose ulcers may be as follows:

1. Ulcer dissection.

2. Autodermic plastics.

3. Secondary suturing.

4. Pathogenic treatment.

1. Grafting of the ulcer surface with jump graft.

Choose the right combination of answers:

A. 1,2. B. 3,4. C. 2,4,5. D. 2, 3. E. 1,2,4,5.

19.The causes of varicose ulcers are as follows:

1. Venous circulatory defect.

2. Arterial circulatory defect.

3. Lymph circulatory defect.

4. Spinal or neural.

5. Diabetes mellitus.

Choose the right combination of answers:

A.1,2,3. B.2,3,4. C.1,2,3,4. D.1.2,3,5. E. 1.

FURTHER READING

1. Oxford Textbook of Surgery. - http://med-lib.ru/english/index.shtml

2. Short Practice of Surgery / Edited by R.C.G.Russell, Norman S. Williams, Christopher J.K. Bulstrode. – 24 th Edition. – Chapter 68, chapter 71. – P. 1153-85, 1219-41.

3. Bell, P.R.F., Jamieson, C.W. and Ruckley, C.V. The Surgical Management of Vascular disease, W.B. Saunders, London, 1992.

4. Galland, R.B. and Clyne, C.A.C. Clinical problems in vascular surgery, Edward Arnold, London.

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

INFLAMMATARY DISEASES OF THE SKIN AND SUBCUTANEOUS (erysipelas, cellulites, abscess, furuncles and furunculosis, carbuncle)

Составитель: доцент Ю.И.Ломаченко

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

ERYSIPELAS

A superficial cellulites with marked lymphatic vessel involvement caused by group A (or rarely group С or G) -hemolytic streptococci.

An interdigital fungal infection of the foot may provide a nudes for infection. The legs are the most frequent anatomic location.

Symptoms, Signs, and Diagnosis

The lesion is well demarcated, shiny, red, edematous, indurated, and tender, vesicles and bullae sometimes develop. The face (often bilaterally), arms, and legs are the most common sites, although not in that order. Patches of peripheral redness and regional lymphadenopathy occasionally occur. High fever, chills, and malaise are common. Erysipelas may be recurrent and may result in chronic lymphedema.

The characteristic appearance suggests the diagnosis. The causative organism is difficult to culture from the lesion but may occasionally be cultured from blood. Staining bacteria by direct immunofluorescence may also identify the causative organism, but the diagnosis is usually based on clinical morphology. Erysipelas of the face must be differentiated from herpes zoster, angioneurotic edema, and contact dermatitis; erysipelas of the arm or hand, from the rare erysipeloid.

Treatment

Penicillin V or macrolide antibiotics (erythromycin) should be given for >= 2 wk. In acute cases, penicillin G should be given parenteraly and than should be replaced by oral therapy after 36 to 48 h. Local discomfort may be relieved by cold packs and analgesics. A fungal nidus may require long-term antifungal therapy (itraconazole or terbinafine) to prevent recurrence.

CELLULITIS

Diffuse, spreading, acute inflammation within solid tissues, characterized by hyperemia, WBC infiltration, and edema without cellular necrosis or suppuration.

Etiology

Streptococcus pyogenes (group A-hemolytic streptococcus) is the most common cause of superficial cellulitis; diffuse infection occurs because streptokinase, DNase, and hyaluronidase - enzymes produced by the organism - break down cellular components that otherwise would contain and localize the inflammation. Group В, С, D, or G -hemolytic streptococci are less common causes. Staphylococcus aureus occasionally produces a superficial cellulitis typically less extensive than that of streptococcal origin and usually only in association with an open wound or cutaneous abscess. Superficial cellulitis caused by other organisms, primarily aerobic gram-negative bacilli, occurs rarely (generally in special circumstances). With granulocytopenia, diabetic foot ulcers, or severe tissue ischemia, aerobic gram-negative bacilli may be responsible.

Cellulitis occurring after animal bites may be caused by unusual bacteria from dogs and cats. Immersion injuries in fresh water may result in cellulitis caused by Aeromonas hydrophila in warm salt water, Vibrio vulnificus may cause cellulitis.

Symptoms and Signs

Infection is most common in the lower extremities. A cutaneous abnormality (e.g., skin trauma, ulceration, tinea pedis, dermatitis) often precedes the infection; areas of lymphedema or other edema seem especially susceptible. Scars from saphenous vein removal for cardiac or vascular surgery are common sites for recurrent cellulitis, especially if tinea pedis is present. Frequently, however, no predisposing condition or site of entry is evident. The major findings are local erythema and tenderness, frequently with lymphangitis and regional lymphadenopathy. The skin is hot, red, and edematous, often with an infiltrated surface resembling the skin of an orange. The borders are usually indistinct, except in erysipelas, a type of cellulitis in which the raised margins are sharply demarcated. Petechiae are common, large areas of ecchymosis, rare. Vesicles and bullae may develop and rupture, occasionally with necrosis of the involved skin. Systemic manifestations (fever, chills, tachycardia, headache, hypotension, delirium) may precede the cutaneous findings by several hours, but many patients do not appear ill. Leukocytosis is common but not constant.

Diagnosis

The diagnosis usually depends on the clinical findings. Unless pus has formed or an open wound is present, the responsible organism often is difficult to isolate, even on aspiration or skin biopsy. Blood cultures are occasionally positive. Serologic tests, especially measurement of rising titers of anti-DNase B, confirm a streptocqecal cause but are usually unnecessary.

Although cellulitis and deep vein thrombosis usually are easily differentiated clinically, many physicians confuse these entities when edema occurs in the lower extremities.

Course and Prognosis

Local abscesses form occasionally, requiring incision and drainage. Serious but rare complications include severe necrotizing subcutaneous infection and bacterernia with metastatic foci of infection. Even without antibiotics, most cases of superficial cellulitis resolve spontaneously; however, recurrences in the same area are common,

sometimes causing serious damage to the lymphatics, chronic lymphatic obstruction, marked edema, and, rarely, elephantiasis. With antibiotics, such complications are uncommon. Symptoms and signs of superficial cellulitis usually resolve after a few days of antibiotic therapy.

Treatment

For streptococcal cellulitis, penicillin is the drug of choice. For severe infections, which require hospitalization, parenteral introduction of drug is indicated. In penicillin-allergic patients, macrolides are effective for mild infections, and lincosamides (parenteral clindamycin) for severe infections. For penicillin-allergic patients or those with suspected methicillin-resistant S. aureus infection, vancomycin is the drug of choice. When pus or an open wound is present, results of a Gram stain should dictate antibiotic choice. Immobilization and elevation of the affected area help reduce edema, and cool, wet dressings relieve local discomfort.

ABSCESS (BOIL)

This is a localized accumulation of pus in different tissues or organs resulting from suppu­rative tissue disintegration and cavity formation un­like an empyema, which involves the accumulation of pus into natural body cavities and cavities of hol­low organs.

The agents of infection are normally staphylococci in the form of a monoculture or in association with other microbes – E. Coli, proteus, streptococ­cus, bacterioides etc.

The infectious agents normally enter the organ­ism from outside (exogenic infections), but can also invade the body from within (endogenic) – as for instance, when the organisms enter from neighbor­ing or distant organs, metastatic abscesses in cases of sepsis. Abscesses can result from the injection into tissues of concentrated solutions of drugs – 25% solutions of magnesium sulphate, 24% solutions of cordiamin, 50% solutions of analgin etc. The devel­opment of suppurative inflammation leads to tissue disintegration and sometimes necrosis with rejection of the dead tissues – sequestration. Sequestra can subsequently dissolve when acted upon by enzymes. The form of the abscess cavity can be a simple one or complex with several pockets. The abscess wall is initially covered with purulent fibrinous deposits and fragments of necrotic tissues. Then an inflammation zone develops at the periphery leading to the for­mation of the pyogenic membrane made up of con­nective tissue.

An abscess that has resulted from a suppurative or aseptic inflammation can have different out­comes: spontaneous opening (burst) outside (abscess of the subcutaneous fatty layer, abscess of the mus­cles, mastitis, paraproctitis etc.), burst opening of an abscess into a closed cavity (abdominal, pleura, in a joint space etc.). An abscess can also open into a hollow cavity that has a connection to the outside (the intestinal lumen, the urinary bladder etc.). Un­der favourable conditions an abscess cavity decreases in size after the pus has evacuated, collapses and heals up by scarring; when evacuation is not com­plete the process can develop into a chronic one with formation of a fistula at the site where it burst.

Superficially located abscesses are marked by redness, swelling, pain, local rise in temperature, functional disorders and sometimes fluctuations can be elicited. The sites of infection may vary in size. The characteristics of the pus contained in an ab­scess cavity (consistency, colour and odour) depend on the type of causative agent involved: foul-smell­ing odour, dirty grey colour of pus is characteristic of ichorous strains; thick yellowish green pus – for staphylococcus; a bluish-green colour and sweetish smell – pseudomonas bacilli etc.

General clinical features of an abscess are: a rise in body temperature from subfebrile to high, gener­al malaise, weakness, loss of appetite and headache. The peripheral blood picture shows leucocytosis with neutrophilia and a shift of the leukocyte count to the left. ESR is raised.

Signs of intoxication that occur in cases of seri­ous abscesses can result from the absorption of tox­ic products from the focus of infection (suppurative resorptive fever), as well as from the development of sepsis.

An abscess has to be differentiated from haematoma, cysts and tumor degenerations. Diagnostic puncture can play a very important role here: when pus is obtained in this procedure it not only helps to establish the diagnosis in unclear cases but also can be sent for bacteriologic analysis – to isolate the agent and to determine its sensitivity to antibiotics.

The presence of gas – producing bacterial strains lead to the accumulation of gas in the abscess cavi­ty, so-called gaseous abscess. Percussion over such an abscess gives a tympanic sound; X-ray films show the presence of gas bubbles with horizontal fluid lev­els beneath them (it is often observed in abscesses caused by agents of ichorous infections).

Treatment of an abscess is by incision, evacua­tion and drainage of the abscess cavity. Cold tuber­culous abscesses are not to be incised since there is always the danger of causing superinfections by sup­purative strains. Small abscesses with well-formed capsules have to be removed in whole without first opening them.

An abscess has to be incised using the shortest: surgical approach based on the anatomic and topo­graphic peculiarities of the organ. Not infrequently an abscess is opened along a needle: the abscess is initially punctured with a needle, then the incision is made along the needle into the abscess cavity. The incision has to be made as much as possible towards the lower poles in order to create better conditions for drainage.

In order to reduce contamination of the sur­rounding tissues during the process of incision, the surgical field is well isolated by gauze or napkins and after a small incision into the cavity an electric suc­tion machine is used to evacuate the pus. After the pus has been suctioned, the incision is increased, the cavity is explored by using the finger, breaking in the process the lacunae, and tissue sequestra are removed. All manipulations should be done careful­ly, so as not to destroy the pyogenic membrane. The abscess cavity is washed with an antiseptic solution, and then drained with one or several plastic or PVC tubes, or gauze swabs soaked with some proteolytic enzymes and antiseptics are packed into the cavity for drainage purposes. If drainage through the main incision is not adequate, another one is made on the opposite side – counter-aperture. Treatment of ab­scesses after incision and drainage is identical to that for treating infected wounds.

General therapeutic measures include body for­tifying therapies, blood and plasma transfusions, and prescription of antibiotics taking into consideration the sensitivity results of the microbiologic analysis, specific therapeutic modalities (immunization with staphylococcal anatoxin, specific anatoxin etc.).

FURUNCLES

Acute, tender, perifollicular inflammatory nodules resulting from infection by staphylococci.

The condition often occurs in healthy young persons. Clustered cases may occur among teenagers living in crowded quarters with relatively poor hygiene or among contacts of patients infected with virulent strains.

Symptoms and Signs

Furuncles occur most frequently on the neck, breasts, face, and buttocks but are most painful when on skin closely attached to underlying structures (e.g., on the nose, ear, or fingers). The initial nodule becomes a 5- to 30-mm pustule that discharges a core of necrotic tissue and sanguineous pus. Furuncles may recur. Material for culture should be obtained from patients with single furuncles on the nose or central face, from patients with multiple furuncles, and from immunosuppressed patients.

Treatment

Treatment is incision and drainage or application of liquid soap containing either chlorhexidine gluconate with isopropyl alcohol or 2 to 3% chloroxylenol, which may be prophylactic but is not therapeutic. A single furuncle is treated with intermittent hot compresses to allow the lesion to point and drain spontaneously. A patient with a furuncle in the nose or central facial area and patients with multiple furuncles should be treated with systemic antibiotics. Usually a penicillinase-resistant penicillin (amoxicillin/clavulanic acid) or cephalosporins (cephalexin) are required. For recurrent furuncles, oral antibiotic therapy continuously for 1 to 2 months may be advisable. Patients with recurrent furunculosis should be evaluated for predisposing factors, including obesity, diabetes, occupational or industrial exposure to inciting factors, and nasal carriage of S. aureus.

CARBUNCLES

A cluster of furuncles with subcutaneous spread ofstaphylococcal infection, resulting in deep suppuration, often extensive local sloughing, slow healing, and a large scar.

Carbuncles occur most frequently in males and most commonly on the nape of the neck. Although carbuncles occur in healthy persons, diabetes mellitus, debilitating diseases, and old age are predisposing factors. Carbuncles develop more slowly than single furuncles and may be accompanied by fever and prostration. Treatment is the same as for clusters of furuncles.

TESTS

1. Therapeutic measures in furuncles are as follows:

1. Cleansing the surrounding skin with ethyl alcohol.

2. Pressing necrotic masses out and bandaging with 70% alcohol.

3. Injection of penicillin and novocain around the affected area.

4. Administration of oral sulphonamides.

5. Local ultraviolet irradiation.

Choose the right combination of answers:

A. 1,3,4,5. B. 1,2. С. 1,2,4,5. D. 3, 5. 3,4,5. E. 1, 2.

2. The therapies of erythaematous erysipeloid localized in the shin are as follows:

1. Moist bandaging with furacillin.

2. Antibiotics IM.

3. Desensitization (dimedrol, calcium chloride).

4. Local ultraviolet irradiation.

5. Warm bath with the potassium permanganate.

Choose the right combination of answers:

A. 1, 2, 3. B. 2, 3, 4. С. 2, 3, 5. D. 1, 2, 3, 5. E. 1,2,3,4,5.

3. The clinical signs characteristic of carbuncle are as fol­lows:

1. Tender infiltrate.

2. Non-tender infiltrate.

3. Skin necrosis and pus pustules.

4. Necrosis with small haemorrhagic blisters.

5. Regional lymphadenopathy.

Choose the right combination of answers:

A. 1,3, 5. B. 2, 3, 5. С. 2, 4, 5. D. 1,3, 4. E. 1,4, 5.

4. The clinical stages of erysipelas are as follows:

1. Erythaematous.

2. Bullous.

3. Phlegmonous.

4. Suppurative.

5. Necrotic.

Choose the right combination of answers:

A. 1,2, 3,4. B. 2, 3,4, 5. С. 1, 2, 3, 5. D. 1, 3, 4, 5. E. 1,2, 3,4, 5.

5. Phlegmon of soft tissues in the stage of softening re­quires one of the following:

A. Local application of cold.

B. Extensive incision and drainage.

C. Puncture with subsequent bacteriologic culturing. D.Warm compression.

E. Injection of novocain and antibiotics.

Choose the correct answer.

6. A boil is due to staphylococcal infection of -

a) Hair follicle

b) Sweat gland

c) Subcutaneous tissue

d) Epidermis

7. A carbuncle is treated by -

a) Incision and drainage

b) Cruciate incision and deroofing

c) Antibiotics alone

d) Wide excision

8. Cellulitis is infection of -

a) Hair follicles

b) Subcutaneous spaces

c) Nail bed

d) Any of the above

9. Treatment of spreading streptococcocal cellulitis is-

a) Erythromycin

b) Penicillin

c) Tetracycline

d) Chloramphenicol

10. Following is true about erysipelas except –

a) Streptococcal infection

b) Contagious and infectious

c) Margins are raised

d) Common in tropics

11. Erysipelas is caused by -

a) Staph aureus

b) Staph albus

c) Strep pyogenes

d) Hemophilus

12. Commonest cause of cellulitis is

a) Staphylococcus

b) Streptococcus

c) E. coli

d) Hemophilus

13. Which is not true of carbuncle -

a) Infective gangrene of subcutaneous tissue

b) Caused by staphylococcus

c) Diabetics are more prone

d) Caused by streptococcus

e) Pencillin and excision of necrotic tissue treatment of choice

ANSWERS:

1 - A

2 - B

3 - A

4 - C

5 -B

6 - A

7 - A, D

8 - B

9 - B

10 - B, D

11 - C

12 - B

13 - B

References

Gostischev V. K. General surgery / The manual. – M.: GEOTAR-MED, 2003. – Charter XI. – P.150-191.

Moukonin A.A., Golub A.V. Soft tissue infection: Textbook for foreign students. – Smolensk: Smolensk State Medical Academy, General Surgery Department. – 2005. – 9p.

ГОУ ВПО «Смоленская государственная медицинская академия

Федерального агентства по здравоохранению и социальному развитию»

МЕТОДИЧЕСКИЕ УКАЗАНИЯ ДЛЯ СТУДЕНТОВ

ПО ДИСЦИПЛИНЕ хирургические болезни

INFLAMMATORY DISEASES OF FINGERS. ACUTE AND CHRONIC OSTEOMYELITIS (classification, clinical features, diagnostics, treatment)

Составитель: доцент Ю.И.Ломаченко

Методические указания утверждены на методическом совещании кафедры госпитальной хирургии (протокол № 2 от 6 октября 2008 г.)

Зав. кафедрой______________(проф. С.А.Касумьян)

2008 г.

Paronychia

Infection of the area of the lateral nail fold typically is due to superficial trauma (e.g., hangnails, nail biting, manicuring, dishwashing). Paronychia in children often is the result of finger sucking. Although typically starting as a cellulitis, progression to abscess formation is not uncommon. Infection that spreads to the proximal nail edge is termed an eponychia.

Felon

The distal palmar phalanx is compartmentalized by tangentially oriented fibrous septa. These septa result in a closed compartment at the distal phalanx, which helps prevent the proximal spread of infection. Infection typically is due to direct inoculation of bacteria by penetrating trauma but may be caused by hematogenous spread and by local spread from an untreated paronychia.

Infection results in edema and increased pressure within the closed compartment. This, in turn, can impair venous outflow and lead to a local compartment syndrome and myonecrosis. Invasion of the bone leads to osteomyelitis.

Infectious tenosynovitis

Tendon sheathis consist of a visceral layer adherent to the tendon and a parietal layer. Notably, the flexor tendon sheath of the thumb is continuous with the radial bursae, while the flexor tendon sheath of the fifth digit is continuous with the ulnar bursae. In 80% of individuals, communication exists between the radial and ulnar bursae. The tenosynovial coverings of the second, third, and fourth digits do not communicate with either the radial or ulnar bursae in most individuals. Infection within a tendon sheath, as in other infections of the hand, usually is the result of direct inoculation of bacteria from penetrating trauma.

A common cause of penetrating trauma occurs when one person strikes another in the mouth, resulting in a fight bite. With the hand clenched in a fist, laceration of the skin on the dorsum of the hand by a tooth may involve the tendon sheath or tendon, surrounding soft tissue, and underlying bone.

Infection also can occur by hematogenous spread, with Neisseria gonorrhoeae the offending agent in many cases. Infection typically follows the course of the tendon sheath, which results in spread of infection into the radial or ulnar bursae, depending on the primary tendon sheath involved. Elevated pressure within the tendon sheath due to infection may impair nutrient flow to the tendon. Tendon necrosis and/or impaired function are disastrous sequelae of untreated elevated tendon sheath pressure.

Deep fascial space infection

The deep fascial spaces of the hand are potential spaces and consist of the dorsal subaponeurotic space, subfascial web space, midpalmar space, and thenar space. The dorsal subaponeurotic space lies dorsal to the extensor tendons of the hand. The subfascial web space is contiguous with the dorsal subcutaneous space of the digits. The midpalmar space is demarcated by the palmar interosseous muscles dorsally and the flexor tendons of the third, fourth, and fifth digits ventrally. Lastly, the thenar space consists of the area between the adductor pollicis muscle dorsally and the flexor tendon of the second digit ventrally.

These compartments are susceptible to infection by direct penetrating trauma, spread from a neighboring compartment, or hematogenous seeding. Due to the dorsal location of the hand lymphatics, erythema and swelling commonly appear over the dorsum of the hand, even when the injury is of palmar origin.

Mortality/Morbidity: Infections of the hand (especially dominant hand infections) can be devastating and frequently require admission for antibiotic therapy and/or surgical intervention.

History:

• Paronychia

1. Recent trauma to lateral nail fold

2. History of nail biting, manicuring, or dishwashing

3. In children, history of finger sucking

4. Erythema and pain in early stages, followed by frank abscess formation with increased pain

5. May relate history of spontaneous drainage of pus

   • Felon

1. Recent trauma to finger pad

2. Pain, typically throbbing in nature

3. Swelling, pressure, and erythema

4. Presence and/or progression from paronychia

   • Infectious tenosynovitis

     1. Recent penetrating trauma to hand

     2. Gonococcal infection, particularly disseminated infection

     3. Pain, especially with passive extension of finger

     4. Edema of entire finger

     5. Variable history of fever

        • Deep fascial space infection

          1. Recent penetrating trauma to hand

          2. Recent or untreated tenosynovitis

          3. Palmar blister (may result in subfascial web space abscess)

          4. Pain and edema of hand

          5. Pain with movement of fingers

          6. Variable history of fever

Physical:

• Paronychia

  1. Edema, erythema, and pain along lateral edge of nail fold

  2. May have extension to proximal nail edge (eponychium)

  3. Frank abscess formation possible

     • Felon

       1. Painful, tense, and erythematous finger pad

       2. Pointing of abscess possibly present

       3. Signs typically limited to area distal to the distal interphalangeal joint due to

       4. anatomic constraints

       5. Evidence of penetrating trauma

• Infectious tenosynovitis

  1. The 4 cardinal signs, include the following:

     • Tenderness along the course of the flexor tendon

     • Symmetric edema of involved finger

     • Pain on passive extension (believed by some authors to be the most important sign)

     • Flexed resting posture of finger

  2. All 4 signs possibly not present early in the course of infection

  3. May have associated lymphangitis, lymphadenopathy, and fever

• Deep fascial space infections:

All possibly presenting with lymphangitis (identified dorsally), lymphadenopathy, and fever

Dorsal subaponeurotic abscesses: Result in swelling and pain on the dorsum of the hand and pain with passive movement of the extensor tendons (difficult to distinguish from dorsal subcutaneous infection)

Subfascial web space infections: Present with pain and swelling on the dorsum and palmar surfaces of the hand (because the subfascial space is contiguous with the dorsal subcutaneous space, tracking of infection from the former to the latter results in a collar button abscess named for its hourglass shape)

Midpalmar space infections: Present with pain, swelling, loss of palmar concavity, pain with movement of the third and fourth digits, and dorsal swelling secondary to the tracking of infection dorsally along the lymphatics

Thenar space infections: Result in marked swelling of the thumb-index web space, flexed and abducted resting posture of the thumb, and pain with passive adduction

Causes:

• Paronychia

  • Staphylococcus aureus and Streptococcus species are most common in acute cases.

  • Atypical mycobacteria and fungi may be offending agents in chronic cases and in patients who are immunocompromised.

  • Anaerobes may be involved in the pediatric population due to finger sucking.

• Felon: S. aureus is the most common causative organism, but gram-negative organisms have been identified.

• Infectious tenosynovitis

  • S. aureus and Streptococcus species commonly are isolated; however, some authors feel that N. gonorrhoeae should be considered a possible pathogen until excluded by culture data.

  • Eikenella corrodens is observed in infections caused by human bites.

  • Pasteurella muttocida and Capnocytophaga infections caused by cat and dog bites can progress rapidly to septic shock and death.

    • Deep fascial space infections

• S. aureus and Streptococcus species are isolated most commonly.

• Organisms mentioned for infectious tenosynovitis also apply to deep space infections. This may be the result of local spread from infected neighboring tendon sheaths.

Lab Studies:

Paronychia and felons: These often require no laboratory tests since the diagnosis is made clinically.

Infectious tenosynovitis and/or deep fascial space infections

• As the infected spaces are drained and d6brided in the operating room, preoperative lab tests often are requested by the hand surgeons, but the diagnosis is made clinically.

• Cultures are obtained in the operating room.

Imaging Studies:

X-rays

• Since trauma often is a contributing factor in most hand infections, plain films are useful in excluding fractures and retained foreign bodies, if radiopaque.

• Х-rays help identify subcutaneous or subfascial gas formation, if present.

• X-rays may indicate osteomyelitis.

Emergency Department Care:

Paronychia

1. If no frank abscess or fluctaance is noted along the lateral nail edge, frequent hot soaks and a short course of antibiotics may result in resolution of the infection. If pus is present, perform incision of the area.

   • Perform a digital nerve block using lidocaine without epinephrine.

   • Using a scalpel blade or an needle, elevate the lateral nail fold at the site of the abscess to allow for drainage of pus.

   • As with any abscess, incision and drainage is the cornerstone of therapy for felons. A small wick is left in the incision to allow for continued drainage.

   • If pus has tracked beneath the nail, remove an adjacent longitudinal section of the nail to promote drainage.

   • Removal of the entire nail plate typically is not indicated unless the subungual abscess results in a floating nail.

2. After drainage and wick placement, dress the finger appropriately.

3. Update tetanus booster status as needed.

Felon

1. If frank abscess formation is present or the finger pad is tense, incision and drainage is indicated.

   • Incision and drainage is similar to that for a paronychia. This should not be undertaken lightly, since improper placement of the incision can lead to scarring, sensory loss, unnecessary pain, instability of the finger pad, and spread of infection into the adjacent tendon sheath.

   • Although many approaches have been described, such as the fish-mouth or hockey stick incisions, most authors recommend a digital nerve block as initial treatment followed by a longitudinal incision over the area of greatest fluctuance.

   • To avoid penetration of the tendon sheath, the incision should not extend to the distal interphalangeal crease.

   • Using a hemostat, bluntly dissect the wound to promote drainage.

   • Irrigate the cavity copiously and loosely pack with a gauze wick.

2. After irrigation and loose packing of the wound, apply a dry gauze dressing and overlying splint.

3. Update tetanus booster status as needed.

Infectious tenosynovitis and/or deep fascial space infections: ED care consists of making the correct diagnosis, providing pain relief, initiating antibiotic therapy, elevating and immobilizing the hand, and promptly consulting an experienced hand surgeon for definitive treatment. Experienced surgeons in the operating room should perform the incision and drainage.

Consultations:

Prompt consultation with an experienced hand surgeon is indicated for patients with evidence of infectious tenosynovitis, deep fascial space infections, or osteomyelitis.

Pharmacotherapy:

Antibiotics

The goals of therapy are to eradicate the infection and prevent complications. Antibacterial therapy must cover all likely pathogens in the context of the clinical setting. First-generation cephalosporins, lincosamides, combinations of aminopeniciliins with beta-lactamase inhibitor are considered. Vancomicin - potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or for those who have infections with resistant staphylococci (MRSA),

Antitoxin (toxoid) is used to induce and boost active immunity.

Tetanus toxoid - Used to induce active immunity against tetanus in selected patients. Immunizing agents of choice for most adults and children >7 у are tetanus and diphtheria toxoids. Necessary to administer booster doses to maintain tetanus immunity throughout life.

Do not use toxoid to treat actual tetanus infections or for immediate prophylaxis of unimmunized individuals (use instead tetanus antitoxin, preferably human tetanus immune globulin)!

Further Inpatient Care:

• Patients with evidence of infectious tenosynovitis or deep fascial space infections require inpatient treatment consisting of parenteral antibiotics and definitive incision and drainage by an experienced hand surgeon.

• Inpatient splinting and occupational therapy for range of motion is essential to preserve function.

Further Outpatient Care:

• Paronychia

  • Instruct the patient to soak the affected finger 3-5 times per day in warm water.

  • If a wick was placed, the patient usually can remove it easily after 24 hours if it has not fallen out already.

  • Schedule follow-up care with the primary care doctor or at the ED for 48 hours after initial incision.

  • Antibiotics, if prescribed, should be continued for 3-5 days.

    • Felon

      • Reevaluate the wound 48 hours after initial incision.

      • At this time, remove the packing and irrigate the wound.

      • If continued drainage is present, loosely repack the wound and schedule another follow-up appointment in 24 hours.

      • If no further drainage is present, repacking is unnecessary.

      • Instruct the patient to keep the wound clean by washing it twice daily with warm, soapy water followed by a clean gauze dressing.

      • Continue antibiotics for 5-7 days.

Complications:

• Paronychia

  1. Subungual abscess

  2. Osteomyelitis of the distal phalanx

  3. Development of a felon

  4. Chronic infection

• Paronychia

1. Most resolve in 2-4 days.

2. Chronic infections are likely fungal infections.

   • Felon

1. Osteomyelitis of the distal phalanx

2. Skin pulp necrosis

3. Sinus tract formation

4. Septic joint

5. Tenosynovitis

6. Inappropriate incision and drainage technique, resulting in sensory loss, tendon injury, spread of infection, or instability of the finger pad

• Infectious tenosynovitis

  1. Tendon destruction

  2. Functional disability

  3. Extension of infection to deep fascial space

• Deep fascial space infection

1. Functional disability

2. Tendon destruction

3. Sepsis

4. Hand loss

Prognosis:

• Paronychia

  • Most resolve in 2-4 days.

  • Chronic infections are likely fungal infections.

    • Felon: The prognosis is good, with healing in 1-2 weeks.

    • Infectious tenosynovitis and/or deep fascial space infection: These have a fair prognosis, depending on the extent of tissue destruction, bony involvement, preexisting vascular insufficiency, and systemic complications (e.g., bacteremia, sepsis).

OSTEOMYELITIS

SHORT-CUT of pathogenesis of hematogenous osteomyelitis

In classical hematogenous osteomyelitis of childhood, organisms in bloodstream gain access to bone by way of the nutrient artery and pass through branches of this vessel to the metaphysis;

- terminal vessels enter small, bone-lined channels on metaphyseal side of the epiphyseal plate;

- these channels have a blind end, and each terminates in the last hypertrophic cartilage cell of epiphyseal plate;

- on reaching the end of the tunnel, capillary inside this channel must turn 180 deg and exit through the same passage by which it entered;

- it is in this area of sluggish circulation, in tunnels whose walls are essentially impermeable, that bacteria lodge and hematogenous osteomyelitis begins;

- once the process starts, thrombosis of small terminal vessel and exudate seal the entrance to channel;

- in depths of this bone tunnel the organisms begin to proliferate.unimpeded by the host defenses that are unable to reach them;

- after the infection is established in one channel, it extends into metaphysis and involves other channels;

- hordes of PMNs are mobilized in metaphysis, and cellular destruction occurs at a rapid rate;

- in adolescents, infection usually begins in metaphysis because of tendency for sluggish & turbulent blood flow in capillary-sinusoid loops adjacent to growth plate & absent or nonfunctioning phagocytes;

- bacteria that localize to this area proliferate and easily obstruct blood flow, resulting in infarction and creation of environment conducive to further bacterial proliferation;

- pus in the metaphysial area expands under pressure and travels up the marrow cavity or passes out of the cortex through the many small metaphyseal openings;

- in certain areas such as the hip, where epiphyseal plate is situated w/in joint capsule, early joint involvement by infection is common;

- at knee, the joint is usually spared, and infections beginning in the distal femoral or proximal tibial metaphysis usually spread along shaft of the bone moving away from the joint;

- stripping of the periosteum from the shaft by pus stimulates intense osteoblastic response;

- new immature bone is formed as response to periostea) stripping, and, in severe cases, the entire shaft may be encased in a sheath of new bone referred to as an involucrum;

- where a major portion of the shaft has been deprived of blood supply, resulting sequestrum lies within the involucrum;

- openings in the involucrum, called cloacae, may permit escape of pus from bone may be fulminant, w/ overwhelming sepsis & death;

- septicemia can cause bacterial seeding to other bones, leading to multiple sites of osteomyelitis;

- if disease is treated early w/ appropriate antibiotics, septicemia is controlled, and there may be only limited bone damage.

Osteomyelitis is a difficult-to-treat infection of bone and bone marrow, it is progressive and results in inflammatory destruction of the bone, bone necrosis, and new bone formation. Bacterial osteomyelitis causes substantial morbidity worldwide, despite continued progress toward understanding its pathophysiology and optimal management.

The approach to osteomyelitis depends upon the route by which bacteria gained access to bone, bacterial virulence, local and systemic host immune factors, and patient age. While imaging studies and nonspecific blood tests may suggest the diagnosis, an invasive technique is generally required to identify the causative pathogens. Antibacterial regimen selection has been largely guided by knowledge of the relative activities and pharmacokinetics of individual drugs, supported by data from animal models.

Definitive therapy often requires a combined medical and surgical approach. Newer microvascular and distraction osteogenesis techniques and the use of laser Doppler allow more complete surgical resection of infected material while maintaining function. Despite recent advances, aggressive medical and surgical therapy fails in many patients with osteomyelitis. More accurate diagnostic methods, better ways to assess and monitor the effectiveness of therapy, and novel approaches to eradicate sequestered bacteria are needed.

History of the Procedure: Osteomyelitis has been well known since antiquity.

Problem: Osteomyelitis results in inflammatory destruction of the bone, bone necrosis, and new bone formation. Three major categories of osteomyelitis exist, based upon pathogenic mechanisms of infection, as follows:

• Osteomyelitis following hematogenous spread of infection

• Osteomyelitis secondary to a contiguous focus of infection

• Osteomyelitis associated with vascular insufficiency

Three different subtypes of osteomyelitis are known: acute osteomyelitis, subacute osteomyelitis, and chronic osteomyelitis.

Frequency: The overall prevalence of acute osteomyelitis is 2 cases per 10,000 children. Neonatal prevalence is approximately 1 case per 1000 children. The annual incidence in patients with sickle cell anemia is approximately 0.36%.

The prevalence of osteomyelitis after foot puncture may be as high as 16% (30-40% in patients with diabetes).

Excluding the axial skeleton, lower extremity osteomyelitis accounts for 90% of osteomyelitis cases and is much more common than upper extremity osteomyelitis, which accounts for 10% of extremity cases.

The most common bones involved in osteomyelitis in descending order are as follows:

• Tibia (50%)

• Femur (30%)

• Fibula (12%)

• Humerus (3%)

• Ulna (3%)

• Radius (2%)

The prevalence of chronic osteomyelitis is 2 cases per 10,000 people.

Most studies support the idea that incidence is similar in developed countries. In

developing countries, incidence is higher due to higher incidence of puncture wounds, contaminated injuries, and less wound care.

Epidemiology of vertebral osteomyelitis

It is primarily a disease of adults; the majority of patients are older than 50 years. As a general rule, the incidence increases progressively with each successive decade of life. Men are affected approximately twice as often as women in most case series; the reason for this male predominance is not clearly understood.

It is difficult to obtain reliable information of the overall incidence of vertebral osteomyelitis. However, most authorities believe that the overall incidence of vertebral osteomyelitis has steadily increased in recent years for 3 primary reasons: increasing rates of nosocomial bacteremia due to intravascular devices and other forms of instrumentation, increasing age of the population, and increasing injection drug use.

Etiology: While normal bone is resistant to infection, a number of conditions can

predispose one to development of osteomyelitis, including the following:

1. Large inoculation of an organism

2. Trauma leading to bone damage or infarction.

3. Presence of a foreign body

4. Illnesses compromising host defense

A single pathogenic organism is almost always recovered from the bone. The most common bone isolates are Staphylococcus species, the most common gram-negative organism is Pseudomonas aeruginosa, and the most common anaerobe is Peptostreptococcus species. However, in immunocompromised patients, other organisms, including fungi and mycobacteria, also must be considered. Commonly isolated organisms in osteomyelitis can be summarized as follows:

• Hematogenous osteomyelitis (monomicrobial infection)

  • Infants (<1 y)

    • Group В Streptococcus

    • Staphylococcus aureus

    • Escherichia coli

• Children (aged 1-16 у)

  • S. aureus

  • Streptococcus pyogenes

  • Haemophilus influenzas

    • Adults (> 16 у)

      • S. aureus

      • Coagulase-negative Staphylococcus species

      • Gram-negative bacilli

      • Paeruginosa

      • Serratia marcescens

        • Contiguous focus osteomyelitis (polymicrobial infection)

          • S. aureus

          • Coagulase-negative Staphylococcus species

          • Spyogenes

          • Enterococcus species

          • Gram-negative bacilli

          • Anaerobes

            • Diabetic foot osteomyelitis (polymicrobial Infection)

              • S. aureus

              • Streptococcus species

              • Enterococcus species

              • Proteus mirabilis

              • Р.aeruginosa

              • Anaerobes

Pathophysiology: The pathogenesis of osteomyelitis is multifactorial and poorly understood. Some important factors include the following:

1. Virulence determinants of the organisms

2. Underlying disease and the immune status of the host

3. Type and location of the bone

It is clear that bacterial cells adhere to nucleated cells, platelets, and a variety of components of the extracellular bone matrix collagen and noncollagenous proteins.

Cellular and molecular pathogenesis

Cellular and molecular techniques provide new methods for determining the relative importance of the many potential virulence factors by facilitating study of the interaction between the host immune response and potential bacterial virulence factors. As an example, S aureus, which is an important cause of both hematogenous and contiguous focus osteomyelitis, produces a large number of extracellular and cell-associated factors that may contribute to virulence, including the following:

• Bacterial adherence: Bacteria adhere to bone by expressing receptors for the components of bone matrix including fibronectin, laminin, collagen, and bone sialoglycoprotein. Adherence appears to play a central role in the early stages of S. aureus-induced osteomyelitis or arthritis. Expression of adhesins permits attachment of the pathogen to cartilage and synovial membrane. Strains positive for collagen adhesin are also associated with the production of high levels of immunoglobulin G(IgG) and interleukin (IL)-6. Bone infection has been speculated to possibly be prevented by an adhesin-derived vaccine.

• Proteolytic activity: Potential proteolytic activity present in normal joints is inhibited in the absence of infection. However, this protective effect may be lost with infection. In an in vitro model of adult chondrocytes inoculated with S. aureus, for example, overall protein synthesis was reduced by 84%, with an increase in the release of collagenase and gelatinase.

• Resistance to host defense mechanisms: The ability of microorganisms to resist host defense mechanisms at both the cellular and matrix levels presents difficulties in the treatment of osteomyelitis. S aureus can survive intracellularly in cultured osteoblasts. Furthermore, the presence of arachidonic acid metabolites such as prostaglandin E2, which is a strong osteoclast agonist, decreases the bacterial inoculum needed to produce infection. Once the microorganisms adhere to bone, they express phenotypic changes that make them resistant to antimicrobial treatment.

• S. aureus organisms express a 42-kd protein, protein A, which is bound covalently to the outer peptidoglycan layer of their cell walls. Protein A binds to the Fc portion of IgG on polymorphonuclear leukocytes, interfering with opsonization and phagocytosis of S aureus. This interference has been demonstrated in vitro and in animal models of subcutaneous abscess and peritonitis.

• S. aureus also secretes 2 toxins, exotoxin and toxic shock syndrome toxin (TSST)-1, which exert a profound effect on the immune system when administered parenterally. The toxins act as superantigens and suppress plasma cell differentiation. They also stimulate production of cytokines, such as IL-1, interferon-gamma, and tumor necrosis factor (TNF)-a. Animals infected with strains of S aureus isogenic for TSST-1 developed frequent and severe arthritis. Staphylococcal enterotoxin and TSST-1 subvert the cellular and humoral immune system, which may determine whether a local infection is eliminated or develops into osteomyelitis or septic arthritis.

• Nitric oxide: The increased turnover of bone in osteomyelitis suggests that the balance between bone formation and resorption is altered, an effect that may be mediated by nitric oxide. Greatly increased levels of nitric oxide and bone resorption have been recorded in the septic skeleton. This response may be driven by the increased levels of cytokines, enterotoxin, and TSST-1, which may stimulate nitric oxide production by endothelial, macrophage, and mesenchymal cells such as osteoblasts. Thus, while low concentrations of nitric oxide are typically thought to inhibit osteoclastic bone resorption, this response may be lost when cytokine and nitric oxide levels increase greatly in skeletal inflammatory disease. Adjunctive local treatment of osteomyelitis with nitric oxide synthetase inhibitors could be beneficial.

Routes of infection

As noted above, osteomyelitis develops via 3 major routes: hematogenous, contiguous focus spread, and vascular insufficiency.

• Hematogenous osteomyelitis: Hematogenous osteomyelitis is predominantly encountered in children; 85% of patients with hematogenous osteomyelitis are younger than 17 years, accounting for 20% percent of the total cases of osteomyelitis. In one study of 659 cases of S aureus osteomyelitis occurring in Denmark from 1959-1988, the number of hematogenous osteomyelitis cases declined, especially in children, and cases of vertebral osteomyelitis, more common in adults, increased. In children, the bone infection usually affects the long bones, while in adults, the lesion is usually located in the thoracic or lumbar vertebrae.

• Contiguous focus osteomyelitis without generalized vascular insufficiency: Osteomyelitis secondary to contiguous foci of infection accounts for at least one half of all cases and has increased in incidence. The organisms may be directly inoculated into the bone at the time of trauma, spread by nosocomial contamination during perioperative or intraoperative procedures, or extend from an adjacent soft tissue infection.

• Contiguous focus osteomyelitis with generalized vascular insufficiency: The primary cause of vascular insufficiency in patients with osteomyelitis is diabetes mellitus. The small bones of the feet, talus, calcaneus and distal fibula, and tibia are commonly involved. The patients in this group are aged 35-70 years. The infection frequently is initiated by a portal of entry for organisms, such as infected nail beds, cellulitis, or atrophic skin ulceration.

Diminished arterial blood supply has traditionally been considered to be the major predisposing factor for contiguous focus osteomyelitis with generalized vascular insufficiency in patients with diabetic foot. However, neuropathy now appears to be an equally important factor. Identifiable neuropathy as a complication of diabetes mellitus is present in approximately 80% of patients with foot disease. Neuropathy can cause foot ulceration through 3 main mechanisms, as follows:

• Decreased sensation leads to mechanical or thermal injuries in the unaware patient that can develop into skin ulcerations.

• Motor neuropathy affecting the intrinsic muscles of the foot predisposes affected persons to gait disturbances and foot deformities, such as hammertoe - and clawtoe deformity and Charcot foot. These anatomic alterations can lead to a maldistribution of weight and elevated focal pressure over the bony prominences. Subsequently, the increase in pressure where the foot contacts the ground or rubs against shoes can lead to skin ulceration.

• Autonomic neuropathy interferes with sweating; the resultant dry, cracked skin allows entry of microorganisms into the soft tissue.

A higher rate of nasal and skin colonization with S aureus, defects in host immunity, and impaired wound healing are all important factors in diabetic foot infection. Superficial fungal skin infections, which are common in patients with diabetes, also can facilitate bacterial entry through macerated or broken skin. Pathological differences based on age

Basic differences exist in the pathology of osteomyelitis in infants, children, and adults. In infants, small capillaries cross the epiphyseal growth plate and permit extension of infection into the epiphysis and joint space. This is a newly well-understood condition referred to as septic osteomyelitis in infants. The cortical bone of neonates and infants is thin and loose, consisting predominantly of woven bone, which permits escape of the pressure caused by infection but promotes rapid spread of the infection directly into the subperiosteal region. A large sequestrum is not produced because extensive infarction of the cortex does not occur; however, a large subperiosteal abscess can form. In children older than 1 year, infection presumably starts in the metaphyseal sinusoidal veins and is contained by the growth plate. The joint is spared unless the metaphysis is intracapsular. The infection spreads laterally where it breaks through the cortex and lifts the loose periosteum to form a subperiosteal abscess.

In adults, the growth plate has resorbed, and the infection may again extend to the joint spaces, as in infants. In addition, the periosteum is firmly attached to the underlying bone; as a result, subperiosteal abscess formation and intense periosteal proliferation are observed less frequently. The infection can erode through the periosteum, forming a draining sinus tract.

STAGING

Cierny-Mader classification

The Cierny-Mader system is a good model for the diagnosis and treatment of long bone osteomyelitis, since it permits stratification of infection and the development of comprehensive treatment guidelines for each stage.

The Cierny-Mader classification is based upon the anatomy of the bone infection and the physiology of the host. The stages are dynamic and may be altered by therapy outcome or change in host status. The classification is determined by the condition of the disease process itself, regardless of its etiology, region, or chronicity. The anatomic types of osteomyelitis are medullary, superficial, localized, and diffuse.

Stage 1, or medullary osteomyelitis, denotes infection confined to the intramedullary surfaces of the bone. Hematogenous osteomyelitis and infected intramedullary rods are examples of this anatomic type.

Stage 2, or superficial osteomyelitis, is a true contiguous focus infection of bone; it occurs when an exposed infected necrotic surface of bone lies at the base of a soft tissue wound.

Stage 3, or localized osteomyelitis, usually is characterized by a full-thickness cortical sequestration that can be removed surgically without compromising bony stability.

Stage 4 or diffuse osteomyelitis is a through-and-through process that usually requires an intercalary resection of the bone to arrest the disease process. Diffuse osteomyelitis includes those infections with a loss of bony stability either before or after debridement surgery.

CLINICAL PICTURE

Clinical: The clinical presentation and location of osteomyelitis differ in infants, children, and adults. In infants, medullary infection may spread to the epiphysis and joint surfaces through capillaries that cross the growth plate. In contrast, in children older than 1 year, the growth plate is avascular and infection is confined to the metaphysis and diaphysis. The joint is spared unless the metaphysis is intracapsular. Thus, cortical perforation at the proximal radius, humerus, or femur enables the infection to migrate to the elbow, shoulder, or hip joint, respectively, regardless of the age of the patient.

Hematogenous osteomyelitis

In hematogenous osteomyelitis, local symptoms referable to bones are more frequently absent in neonates than in children. In adults, soft tissue findings may be more prominent than bony involvement.

In infants, local findings that may lead the clinician to suspect osteomyelitis are usually absent in neonates. When they develop, local findings can include decreased motion of a limb and edema (pseudoparalysis) and joint effusion adjacent to the bone infection (present in 60-70% of cases).

Systemic symptoms are frequently present in S. aureus osteomyelitis but may be absent when other pathogens are involved.

Children with hematogenous osteomyelitis, in contrast with neonates, typically have the following systemic symptoms:

• Abrupt fever

• Irritability

• Lethargy

• Refusal to use the affected limb

• Local signs of inflammation present for 3 weeks or less

While this is the classic presentation, signs of systemic toxicity other than minimal temperature elevation are absent in 50% of children with osteomyelitis.

In adults, acute clinical presentations of fever, chills, swelling, and erythema over the involved bones are usually seen in acute hematogenous osteomyelitis.

Vertebral osteomyelitis is usually hematogenous in origin but may be secondary to trauma. A preceding history of urinary tract infection or injection drug use often is present. Other sources of infection include skin and soft tissue, respiratory tract, infected intravascular device site, endocarditis, dental infection, or unknown sources.

The patient usually presents with vague symptoms and signs consisting of dull, constant back pain and spasm of the paravertebral muscles. Localized pain and tenderness of the involved bone segments is present in at least 90 percent of cases. The pain is usually insidious and slowly progresses over 3 weeks to 3 months.

Contiguous focus osteomyelitis without vascular compromise

Common predisposing factors for contiguous focus osteomyelitis include surgical reduction and internal fixation of a fracture, open fractures, and chronic soft tissue infections. This form of osteomyelitis is biphasic in its age distribution. The infection occurs in younger persons secondary to trauma and related surgery and in older adults from decubitus ulcers.

The infection usually manifests within 1 month after inoculation of the organisms from trauma, surgery, or a soft tissue infection. Affected patients typically present with low-grade fever, pain, and drainage. Loss of bone stability, bone necrosis, and soft tissue damage frequently occur, making this form of osteomyelitis difficult to treat.

Contiguous focus osteomyelitis with vascular compromise

Osteomyelitis in patients with vascular compromise, who are often diabetic, can be difficult to diagnose. Patients can present with an apparently localized process including an ingrown toenail, a perforating foot ulcer, cellulitis, or a deep space infection. Concurrent peripheral neuropathy often alters the patient's perception of pain. Fever and systemic toxicity are frequently absent.

Physical examination commonly reveals diminished dorsal pedis and posterior tibia pulses, poor capillary refill, and decreased sensation.

Chronic osteomyelitis

The hallmark of chronic osteomyelitis is the presence of dead bone (the sequestrum). Involucrum (reactive bony encasement of the sequestrum), local bone loss, persistent drainage, and/or sinus tracts are other common features of chronic disease.

The patient with chronic osteomyelitis commonly presents with chronic pain and sinus formation with purulent drainage. Fever is usually low grade or absent. The chronic infection usually does not progress or does so slowly. If a sinus tract becomes obstructed, the patient can present with a localized abscess and/or soft tissue infection.

Prospects of halting the infection are reduced when the integrity of surrounding soft tissue is poor or the bone is unstable due to an infected nonunion or an adjacent septic joint. Squamous cell carcinoma at the site of tissue drainage and amyloidosis are rare complications of chronic osteomyelitis.

INDICATIONS for surgical intervention

Successful management of osteomyelitis requires aggressive pursuit of the diagnosis and early antimicrobial and surgical therapy. If acute osteomyelitis is not treated optimally, the risk is high of developing chronic osteomyelitis, which is significantly less amenable to treatment.

Staging and classification systems may be used in determining appropriate treatment for osteomyelitis.

Surgical intervention is indicated in the following situations:

• The patient has not responded to specific antimicrobial therapy within 48 hours.

• Evidence exists of a persistent soft tissue abscess.

• Concomitant joint infection is suspected or diagnosed.

In adults with hematogenous osteomyelitis, a thorough intramedullary reaming and unroofing is usually performed with or without bone grafting. Soft tissues are reapproximated, and the limb is protected by external means (brace or cast) until the structural integrity of the bone is reestablished by normal remodeling.

Contraindications: Contraindications to debridement of infected bone are limited and include the following:

• In acute osteomyelitis in infants, the infection usually responds well to medical therapy alone. Surgery should be reserved for nonresponsive cases.

• Suspicion of malignancy or presence of secondary bone infection with malignancy should not be treated with debridement alone. Tumor workup and biopsy should be performed first. If infection cannot be eradicated or tumor is not resectable, amputation is indicated.

• Massive debridement is not recommended in the presence of sickle cell disease; usually a mixture of infection and avascular necrosis is present that may improve after good reperfusion. Massive debridement may produce very large defects that may not be easily amenable to reconstruction surgeries.

• The use of a tourniquet is not recommended by many authors due to the acute bacteremic phase after the tourniquet is released and toxemia.

• Local anesthesia is generally ineffective and should be avoided due to the change in the local PH of the tissue that prevents the metabolism of the local anesthetics to the active ingredients.

The general condition of the patient should not be considered a contraindication to urgent surgery. Delaying surgery may lead to further deterioration.

CLINICAL RECOGNIZING

Lab Studies:

• Routine laboratory test findings are usually nonspecific. These include CBC, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), renal and hepatic profile, and bone profile.

  • Complete blood count: Leukocytosis is common in acute osteomyelitis but not in chronic osteomyelitis.

  • Erythrocyte sedimentation rate

    • The ESR is usually elevated but may be in the reference range. In a patient with a high ESR initially, monitoring the ESR may be useful in detecting a relapse. In patients with a foot ulcer and diabetes mellitus, an ESR greater than 100 mm/h is highly specific but insensitive for a diagnosis of osteomyelitis.

    • Although ESR is associated with low sensitivity and specificity, it is widely employed. In the patient without a prior history of osteomyelitis, the ESR is most helpful when infection is unlikely. For example, in patients with low-back pain but without historical clues to suggest vertebral osteomyelitis (eg, recent urinary tract infection), a normal ESR is a reassuring finding. Conversely, an elevated ESR suggests the need for further evaluation.

      • C-reactive protein

        • CRP, like ESR, is an acute-phase reactant. Although said to be more specific for infection than ESR, it is also relatively insensitive and nonspecific.

        • The primary difference between these tests is that the CRP has a shorter half-life than the ESR. Measuring in vitro clumping of venous leukocytes (leukergy) may more closely correlate with severity of infection than the ESR.

          • Renal and hepatic profile: Whether leukergy, which reflects altered surface expression of leukocyte adhesion molecules, will be useful for managing osteomyelitis is not known. This test is not routinely available.

• Efforts have been made to develop serologic assays to diagnose osteomyelitis caused by S aureus. Patients with osteomyelitis mount a vigorous antibody response, but the utility of detecting antibodies to cell wall components such as peptidoglycan or teichoic acid has been limited by the presence of such antibodies in uninfected, healthy persons. In a preliminary study, serum antibodies to S aureus exoproteins differentiated 3 cases of S aureus osteomyelitis from 4 cases caused by other organisms. Another limitation of serology is that it is unlikely to be developed for nonstaphylococcal disease. However, highly specific assays for staphylococcal osteomyelitis would be very useful. At present, serology cannot be recommended clinically, and such tests are available only for research purposes.

• Blood culture results are positive in 50% percent of cases of acute osteomyelitis. A positive blood culture result in a patient with radiological findings consistent with osteomyelitis obviates the need for biopsy to obtain the specific microbiologic diagnosis.

Imaging Studies:

• Plain films: Plain radiographs are relatively inexpensive, may be used to make the diagnosis, help in interpreting and choosing other studies, and allow one to exclude other conditions (eg, gas in the soft tissues). In uncomplicated acute infection, the triad of soft tissue swelling, bone destruction, and periosteal reaction is fairly specific for osteomyelitis and is sufficient to warrant a course of therapy (empiric until the microbiologic diagnosis has been established).

  • Plain films are generally insensitive for the diagnosis of acute osteomyelitis. This is in part due to the 2-3 weeks required for bone changes to be evident on plain films, although changes may be seen at this time on the other imaging modalities. Furthermore, in complicated situations, bone changes may not be distinguishable from those due to another process, such as a Charcot joint, fractures, or cancer. Thus, the diagnosis of acute osteomyelitis cannot be excluded if the plain film findings are negative. Further testing should be performed because early therapy is essential to reduce the formation of necrotic bone and the development of chronic osteomyelitis.

  • The primary findings are different in chronic osteomyelitis, which is characterized by bone sclerosis, periosteal new bone formation, and sequestra. It is difficult to distinguish active from inactive infection.

• CT scan: This modality is used to evaluate an area in which focal findings are

present on examination and plain films findings are negative. The CT scan (with

and without contrast) is very accurate for detecting cortical destruction,

intraosseous gas, periosteal reaction, and soft tissue extension.

• MRI: This study is an alternative to CT scan and is especially useful in evaluating a patient for osteomyelitis in the vertebrae and in the infected foot. In vertebral osteomyelitis, findings on T1-weighted images include decreased signal intensity in the disk and adjacent vertebral bodies and loss of endplate definition. Findings on T2-weighted images include increased signal intensity in the disk and adjacent vertebral bodies. With gadolinium, there is enhancement of the disk, adjacent vertebral bodies, and involved paraspinal and epidural soft tissue.

  • MRI provides useful anatomic detail in planning for surgical debridement, since it may show abscesses that need drainage, and can reduce the risk of operating on bland cellulitis. MRI also can be used to delineate soft tissue/epidural involvement and spinal cord impingement that cannot be seen on nuclear medicine images.

  • When evaluating the foot for osteomyelitis, MRI is as specific or more specific and more sensitive than technetium bone scan. In one series in which bone biopsy was used as the criterion standard, the sensitivity was 72% for MRI, 68% for bone scan, and 45% for indium white blood cell scan.

  • MRI cannot be used in patients with certain metal implants. In addition, false-positive results can occur with bone infarct or fracture or in healed osteomyelitis. Differentiating cancer from osteomyelitis may be difficult with MRI.

  • MRI for diabetic foot ulcers

    • The diagnosis of osteomyelitis in diabetic foot ulcers is often missed because of 2 major factors, most cases occur in ulcers not exposing bone and most have no evidence of inflammation on physical examination. In comparison, osteomyelitis was present in all patients in whom bone was exposed in one series.

    • MRI is the imaging procedure of choice for osteomyelitis in diabetic foot ulcers, being more accurate than the other modalities (95% versus 50-70% for plain films, bone scan, and indium scan in one series). Two clinical factors also may be useful in these patients, probing the ulcer and ulcer size.

• Ultrasonography: Ultrasound findings consistent with osteomyelitis include fluid collection adjacent to the bone without intervening soft tissue, elevation of the periosteum by more than 2 mm, and thickening of the periosteum. Ultrasound also may improve the yield from fine needle biopsies.

• Scintigraphy: Multiple different nuclear medicine imaging procedures are available to evaluate for osteomyelitis, including bone scan, indium-labeled leukocyte scan, and bone marrow scan.

  • Three-phase bone scan

• The 3-phase bone scan uses technetium Tc 99m bound to phosphorus as the tracer, which accumulates in areas of increased osteoblast activity (reactive new bone formation and increased blood flow). The images obtained are immediate (flow), 15 minute (blood pooling), and 4 hour (bone imaging). The scan findings are different in cellulitis and osteomyelitis. Cellulitis results in increased activity in the first 2 phases and normal or diffusely increased activity in the third phase. In comparison, osteomyelitis results in intense uptake in all 3 phases.

• The 3-phase technetium bone scan is the test of choice in evaluating for acute osteomyelitis if the plain film findings are normal. In this situation, it has an estimated sensitivity and specificity of almost 95% and findings generally are positive in 2-3 days of infection. However, any process that results in increased bone turnover appears as a hot spot that is indistinguishable from osteomyelitis. These false-positive findings can occur with posttraumatic injury, following surgery, diabetic feet, septic arthritis, noninfectious inflammatory bone disease, cancer, healed osteomyelitis, and Paget disease.

• Indium-labeled leukocyte scan: Indium-labeled leukocyte scanning uses white blood cells labeled with radioactive indium as the tracer. It accumulates at sites of inflammation or infection and in the bone marrow. It is not specific for bone. Since it accumulates in marrow, it is less sensitive for imaging those areas with red marrow (eg, the axial skeleton). The indium scan also can be used for the diagnosis of osteomyelitis at sites of fracture nonunion. Two prospective studies found a sensitivity and specificity of 91% and 97%, respectively, in this setting. Indium scans have better sensitivity and specificity than bone scans in diabetic feet, but the specificity is poor, especially in the hindfoot.

• Bone marrow scan: The bone marrow scan uses technetium Tc 99m-labeled sulfur colloid as the tracer. It is taken up by the reticuloendothelial system, including the bone marrow, spleen, and liver. It allows one to image the marrow instead of the bone. Its main use is in conjunction with the indium-tagged white blood cell scan to evaluate for suspected osteomyelitis in the axial skeleton, where the presence of marrow decreases the accuracy of the indium scan.

• Gallium citrate scanning: Gallium citrate scanning uses radioactive gallium citrate as the tracer. It acts as an analog of calcium and iron and attaches to transferrin to accumulate at sites of inflammation. Gallium imaging is the most sensitive and specific radionuclide scanning technique for vertebral osteomyelitis. A typical positive test result reveals intense uptake in 2 adjacent vertebrae with loss of the intervening disk space. In one study of 41 patients with suspected vertebral osteomyelitis, increased gallium uptake was detected in all of the 39 patients with biopsy-proven osteomyelitis.

• Dual tracer scans: Dual tracer examinations combine an inflammation imaging tracer (indium or gallium) with an "anatomic" tracer (either technetium bone scan or technetium sulfur colloid marrow scan), with images being collected either sequentially or simultaneously. Sequential studies combine the sensitivity of the bone scan (if findings are negative, no further imaging is done) with the specificity of the indium scan. Simultaneous studies combine the sensitivity and specificity of the indium scan and the bone scan to provide the anatomic detail needed to localize the infection to bone or soft tissue.

• Other: Radiolabeled antigranulocyte antibodies are being investigated in an

• attempt to find a more accurate tracer for localizing infection.

Other Tests:

• Extended field of view ultrasound in musculoskeletal disorders: With the advent of high-resolution linear array transducers (7.5 MHz and 10 MHz), interest in musculoskeletal ultrasonography has continued to develop. Ultrasonography has been applied in the evaluation of infectious processes such as osteomyelitis, cellulitis, and subcutaneous abscesses. Extended field of view ultrasonography combines the convenience of a real-time scanner with the spatial advantages of a static B-mode scanner. Detailed examination of surfaces of cortical bone and cartilage has application in the evaluation of rheumatologic diseases for periarticular erosions, trauma for radiographically occult fractures, congenital hip dysplasia, and early osteomyelitis.

Diagnostic Procedures:

• Bone biopsy: The criterion standard for the diagnosis of osteomyelitis is open bone biopsy with histopathologic examination and cultures. Histopathologic features indicating osteomyelitis include necrotic bone with extensive resorption adjacent to an inflammatory exudate. Needle biopsy is commonly used to obtain bone for histopathologic analysis. However, the incidence of sampling error is not negligible, with the sensitivity and specificity of this technique being 87% and 93%, respectively. Sensitivity of needle biopsy is particularly low in the postoperative or posttrauma patient.

• If the clinical suspicion is strong and blood culture results and the needle biopsy findings are negative, the needle biopsy should be repeated or an open biopsy should be performed. In patients with compromised vasculature, a bone sample can be obtained at debridement for the histopathologic diagnosis of osteomyelitis.

• Accurate cultures can be obtained only if the bone biopsy is performed through uninvolved tissue. In addition, cultures of the sinus tract are useful if S aureus and possibly Salmonella species are cultured. The presence of other common organisms does not predict those that will be found on bone biopsy.

  • Probing a diabetic foot ulcer

    • In a recent report, the detection of bone when probing a diabetic foot ulcer with a sterile probe was highly accurate in ruling in osteomyelitis. Seventy-five patients with 76 ulcers were studied, with the criterion standard for the diagnosis of osteomyelitis being histopathologic examination of bone resected at debridement. Contiguous osteomyelitis was present in 50 of the 76 ulcers. Of these, bone was palpable by probe in 33. The sensitivity and specificity were 66% and 85%, respectively, giving a positive predictive value of 89% and a negative predictive value of 56% in this population. These patients had a very high rate of osteomyelitis (61%); thus, the high positive predictive value is not likely to be applicable to ulcers with a lower risk of complicating osteomyelitis.

    • The size of a diabetic foot ulcer also may be helpful. In one series, osteomyelitis was present in 94% of ulcers greater than 2 cm2 in area. Thus, in a diabetic patient with a foot ulcer, either probing of bone or ulcer area above 2 cm2 is associated with about a 90% chance of having underlying osteomyelitis. Further noninvasive testing is unlikely to improve the accuracy of diagnosis.

Histologic Findings: Acute osteomyelitis presents as a suppurative infection with acute inflammatory cells, accompanied by edema, vascular congestion, and small vessel thrombosis. In early acute disease, the vascular supply to the bone is compromised by infection extending into the surrounding soft tissue. When both the medullary and periosteal blood supplies are compromised, large areas of dead bone (sequestra) may be formed. Within this necrotic and ischemic tissue, the bacteria can be difficult to eradicate even after an intense host response, antibiotic therapy, or both.

Pathologic features of chronic osteomyelitis include necrotic bone, the formation of new bone, and polymorphonuclear leukocyte exudation joined by large numbers of lymphocytes, histiocytes, and occasional plasma cells.

Host defense and mesenchymal cells, mainly the polymorphonuclear leukocytes, macrophages, and the osteoclasts, release proteolytic enzymes that break down organic elements in the dead bone. Because of lost blood supply, dead bone appears whiter than living bone. Cancellous bone is absorbed rapidly and may be completely sequestrated or destroyed in 2-3 weeks, but necrotic cortex may require 2 weeks to 6 months for separation. After complete separation, the dead bone is slowly eroded by granulation tissue and absorbed.

New bone formation is another characteristic feature of osteomyelitis. New bone forms from the surviving fragments of periosteum, endosteum, and the cortex in the region of the infection and is produced by a vascular reaction to the infection. New bone may be formed along the intact periosteal and endosteal surfaces and also may arise when the periosteum forms an encasing sheath of live bone (involucrum) surrounding the dead bone. Involucrum is irregular and is often perforated by openings through which pus may track into the surrounding soft tissues and eventually to the skin surfaces through a sinus tract. The involucrum can gradually inaease in density and thickness to form part or all of a new shaft.

New bone increases in amount and density for weeks or months according to the size of the bone and the extent and duration of infection. Endosteal new bone may proliferate and obstruct the medullary canal. After host defense, removal or surgical removal of the sequestrum, the body, especially in children, may fill the remaining cavity with new bone. However, in adults, the cavity may persist or the space may be filled with fibrous tissue. The surviving bone in the osteomyelitis field usually becomes osteoporotic during the active period of infection. Osteoporosis is the result of the inflammatory reaction and disuse atrophy. After the infection subsides, bone density increases partially from reuse. It may be difficult to distinguish between the old living bone and the newly formed bone as time passes. All traces of osteomyelitis can disappear in children and, to a lesser extent, in adults.

TREATMENT

Medical therapy: A single pathogenic organism is almost always recovered from the bone. The most common bone isolates are staphylococci, the most common gram-negative organism is P aeruginosa, and the most common anaerobe is Peptostreptococcus species. However, in immunocompromised patients, other organisms must also be considered, including fungi and mycobacteria.

Hematogenous osteomyelitis in children usually can be treated with antibiotic therapy alone. However, it is vital to identify a pathogen in order to select the optimal antibiotic therapy. Mismanagement with inappropriate antibiotic(s) encourages disease extension, necrosis, and sequestra formation. A bone biopsy for culture is necessary unless the patient has positive blood cultures along with radiographic findings consistent with osteomyelitis. After cultures are obtained, empiric antibiotics should be selected to cover the most probable pathogens.

Once the etiologic organism is identified, the antibiotic regimen should be modified, if needed, based upon susceptibility patterns. The patient should be treated for 4-6 weeks with appropriate antimicrobial therapy, dating from the initiation of therapy or following the last major debridement surgery. If the initial medical management fails and the patient is clinically compromised by a recurrent infection, medullary and/or soft tissue debridement is necessary in conjunction with another 4- to 6-week course of antibiotics. Oral antibiotics can be used in pediatric hematogenous osteomyelitis. However, the child should receive 7-14 days of IV antibiotics or continue to receive IV antibiotics until systemic improvement occurs prior to changing to an oral regimen. The latest reports suggest the use of IV antibiotics for 3-4 days; this usually is enough for the systemic manifestations to improve. In order to undergo oral therapy, the patient must be compliant and have close outpatient follow-up care. Absorption and activity of the orally administered antibiotic should be monitored using serum cida! levels. High doses of the quinolone class of antibiotics can cause articular cartilage damage in young animals, generating some concern about the long-term use of these agents in infants and children. Thus, under most circumstances, children with osteomyelitis should not be treated with a quinolone.

Surgical therapy: Surgical management of contiguous focus osteomyelitis can be very challenging. The principles of treating any infection are equally applicable to the treatment of infection in bone. These include adequate drainage, extensive debridement of all necrotic tissue, obliteration of dead spaces, stabilization, adequate soft tissue coverage, and restoration of an effective blood supply.

The number and nature of the required surgical procedures increases with the severity of the infection, which can be divided into 4 categories, as follows:

Category 1 - Removal of necrotic tissue by extensive debridement

Category 2 - Dead space obliteration with flaps, antibiotic beads, and bone grafts

Category 3 - Provision of soft tissue coverage of the bone

Category 4 - Stabilization of bone by external or open reduction and internal fixation

Category 1

Debridement surgery is the foundation of osteomyelitis treatment. It is the most commonly performed procedure and may need to be repeated multiple times. The goal of debridement is to reach healthy, viable tissue, but even when all necrotic tissue has been adequately debrided, the remaining bed of tissue must be considered contaminated with the responsible organism. Debridement should be direct, atraumatic and executed with reconstruction in mind. All dead or ischemic hard and soft tissue is excised unless a noncurative procedure has been chosen. Surgical excision of bone is carried down to uniform haversian or cancellous bleeding, known as the paprika sign.

Category 2

Adequate debridement may leave a large bony defect (dead space). Appropriate management of dead space created by debridement surgery is mandatory in order to arrest the disease and to maintain the integrity of the skeletal part. The goal of dead space management is to replace dead bone and scar tissue with durable vascularized tissue. Local tissue flaps or free flaps may be used to fill dead space. An alternative technique is to place cancellous bone grafts beneath local or transferred tissues where structural augmentation is necessary. Careful preoperative planning is critical for conservation of the patient's limited cancellous bone reserves. Open cancellous grafts without soft tissue coverage are useful when a free tissue transfer is not a treatment option and local tissue flaps are inadequate.

Complete primary or delayed primary wound closure should be performed whenever possible. Suction irrigation systems are not recommended because of the high incidence of associated nosocomial infections and the unreliability of the apparatus. Healing by secondary intent is also discouraged since the scar tissue that fills the defect may later become avascular. Antibiotic-impregnated acrylic beads can be used to sterilize and temporarily maintain dead space. The beads are usually removed within 2-4 weeks and replaced with a cancelious bone graft. The most commonly used antibiotics in beads are vancomycin, tobramycin and gentamicin. Local delivery of antibiotics (amikacin, clindamycin) into dead space also can be achieved with an implantable pump.

Category 3

Adequate coverage of the bone by soft tissue is necessary to arrest osteomyelitis. Most soft tissue defects are closed primarily, but small soft tissue defects may be covered with a split thickness skin graft. In the presence of a large soft tissue defect or an inadequate soft tissue envelope, local muscle flaps and free vascularized muscle flaps may be placed in a 1- or 2-stage procedure.

Local and free muscle flaps, when combined with antibiotics and surgical debridement of all nonviable osseous and soft tissue for chronic osteomyelitis, have a success rate ranging from 65% to 100%. Local muscle flaps and free vascularized muscle transfers improve the local environment by supplying blood vessels, which are critical for host defense, antibiotic delivery, and osseous and soft tissue healing.

Category 4

If movement is present at the site of infection, measures must be taken to achieve permanent stability of the skeletal unit. Stability can be achieved with plates, screws, rods, and/or an external fixator. One type of external fixation allows bone reconstruction of segmental defects and difficult infected nonunions. The Ilizarov external fixation method uses the theory of distraction histogenesis, in which bone is fractured in the metaphyseal region and slowly lengthened. The growth of new bone in the metaphyseal region pushes a segment of healthy bone into the defect left by surgery. The Ilizarov technique is used for difficult cases of osteomyelitis when stabilization and bone lengthening are necessary. It also can be used to compress nonunions and correct malunions, and in a small group of patients for reconstruction of difficult deformities that result from osteomyelitis. However, this technique is labor intensive and requires an extended period of treatment, averaging 9 months in the device. The Ilizarov pins usually become infected, and the device is painful. Infected pseudoarthrosis with segmental osseous defects can be treated by debridement and microvascular bone transfers. Vascularized bone transfer is also useful for the treatment of infected segmental osseous defects of long bones that are more than 3 cm in length. Vascularized bone transfers can be placed after 1 month without clinical evidence of infection.

Loss of bone stability, bone necrosis, and soft tissue damage frequently occur in contiguous focus osteomyelitis. Surgical debridement of infected bone and soft tissue provides specimens for culture and hastens eradication of the infection. Other steps in the surgical management of contiguous focus osteomyelitis should be tailored to the specific anatomy of the bone infection. When osteomyelitis is characterized by a full thickness, cortical sequestration, patients usually can be treated with removal of the dead infected bone (bone saucerization). Bone grafting may be necessary to augment structural support. These patients may require external fixation for structural support while the bone graft incorporates. Complex reconstruction of both bone and soft tissue is frequently necessary. In some cases, osteomyelitis progresses to an infection involving the entire diameter of the bone. These patients often require an intercalary resection of the bone in order to arrest the disease process. Since this advanced stage of osteomyelitis involves an entire through-and-through section of bone, a loss of bony stability occurs either before or after debridement surgery. As a result, treatment often must be directed toward establishing structural stability and obliterating debridement gaps by means of cancellous bone grafts or the Ilizarov technique. Vascularized bone grafting is the other possible treatment modality.

Preoperative details: In addition to routine preoperative preparations, supportive therapy is needed; infants and children must be well hydrated and fever must be controlled before the patient undergoes general anesthesia. Patients who are medically compromised should be stabilized and supported. Diabetes should be controlled as much as possible, but this should not delay drainage because the presence of infection makes the blood sugar level refractory and difficult to control. Most of the systemic manifestations of osteomyelitis improve dramatically after drainage and debridement.

Intraoperative details: Position the patient in the most accessible position to drain the infected areas. Prepare all containers and swabs, and prepare the requests before scrubbing. Prepare containers for tissue cultures. Prepare for Gram stain, aerobic culture and sensitivity, anaerobic culture and sensitivity, fungal culture and sensitivity. (Acid-fast bacillus [AFB] stain and culture and sensitivity are recommended.) Incision should be generous for ease of access to the infected bone. Decompression may release intrameduilary or subperiosteal pus. All necrotic soft tissue, bone, and devitalized tissue must be removed. Infected loculations must be broken and thorough washing with as much as 2-4 L of isotonic sodium chloride solution is essential.

Complete debridement of all the devitalized bone and soft tissue, regardless of the size of the wound created, is essential for cure. Immobilization of the bone by cast or external fixations is a must.

Revascularization procedures are the best means of fighting recurrent infection; those involving local pedicle muscle flaps and myocutaneous flaps are now the ones most frequently used to fill the space created by surgery. Local muscle flaps are limited by the availability of adjacent muscle but are very useful because the vascular supply is kept intact. Myocutaneous flaps have the advantage of providing vascular supply to both the muscle and the overlying skin. Increasingly, microsurgically transplanted muscle flaps (ie, free-flaps) are being used in areas such as the distal tibia where no appropriate muscle exists.

Complex orthopedic techniques are necessary to repair very large bone defects that would otherwise be considered untreatable except by amputation. In the Ilizarov technique, the resection of diseased tissue and bone creates a gap partially filled by a weli-vascularized bone segment. Transfer of the bone graft leads to progressive local generation of new bone.

Postoperative details: Dramatic improvement is the usual course after debridement, but patients require attention to prevent complications related to their original medical conditions, such as diabetes and heart failure. IV fluids, IV antibiotics, and suitable analgesics are required for the first few days after surgery. Intensive care unit (ICU) admission for respiratory support and blood gases and renal function monitoring should be considered for patients who have septicemia.

The wound should be dressed daily, and early sitting and mobilization (affected limb must be immobilized) should be encouraged.

If no Improvement occurs within 48 hours, a second look debridement and dressing under general anesthesia is indicated.

Follow-up care: The patient must be compliant with care and have close outpatient follow-up. The first visit is usually a week after discharge and consists of a general examination for evaluation of improvement. Local examination and documentation of pain, wound condition, tenderness, swelling, and discharges from wounds should be made in all visits, Repeat CBC, CRP, ESR, and plain radiographs to evaluate the progression and behavior of the infection.

The cast should be removed when infection is eradicated, which is usually determined by good reduction in the level of CRP, ESR, or both. The shoulder, elbow, and wrist should not be immobilized more than 3, 4, and 5 weeks, respectively.

Physiotherapy is an essential part of follow-up care; isometric exercises should be started early, and once the cast is removed, active and passive range of motion exercises are suggested.

CHRONIC OSTEOMYELITIS

Chronic osteomyelitis is prolonged inflammation of bone marrow, almost invariably due to infection.

This was once the almost inevitable outcome of acute haematogenous osteomyelitis; today, antibiotics will normally prevent this progression and now the most common causes of chronic osteomyelitis are open fractures and surgery.

Causative organisms

Chronic osteomyelitis is always a mixed infection. The common organisms include:

• Staphylococcus aureus

• Escherichia coti

• Streptococcus pyogenes

• Proteus spp.

• Pseudomonas spp.

In the presence of a foreign implant, a common opportunist is Staphylococcus epidermidis.

Pathology

The infection may remain focussed in a discrete region, or more commonly spread along the shaft of a long bone.

Necrotic bone is found in cavities - sequestrum - containing pus and walled of with vascular tissue and sclerotic new bone - involucrum.

The sequestrum acts as a haven for bacteria, permitting continued infection until the bone is passed through a draining sinus or removed surgically.

The infection may follow a relapsing and remitting course; the sinuses may close off for weeks or months, only to reopen as pus reaccumulates.

The sclerotic involucrum is more brittle than normal bone and is liable to pathological fractures.

Clinical features

The patient will have a history of osteomyelitis, and will present with:

• recurrent pain, pyrexia, redness and swelling

• reopening of the sinus

The overlying tissues are often thickened and puckered where they are tethered to the bone.

Any discharge is foul and seropurulent. There may be excoriation of surrounding skin.

Diagnostic imaging

Plain radiographs show bone resorption at the site of infection with thickening and sclerosis of surrounding bone. The thickened bone may resemble a bone tumour. Sequestrae are necrotic and appear abnormally radio-dense. A sino-gram may help estimate the extent of the abscess.

Radioisotope scans using 99m-Tc diphosphonates show increased uptake at the sites of osteomyelitis. Indium- labelled leukocytes are more specific for infection.

CT and MRI are essential for surgical planning as they allow visualisation of the extent of infection and tissue destruction.

Investigations

During a flare-up of chronic osteomyelitis the ESR and white blood cell count may be elevated.

Discharging pus should be cultured to determine the organisms and their sensitivity.

Treatment

There are three principles of treatment:

• antibiotic therapy

• local treatment of the sinus

• surgery

Surgery should be postponed until there are significant symptoms combined with clear evidence of a sequestrum.

Sulphan blue is injected preoperatively; this stains all vital tissue green, leaving dead tissue unstained. Under antibiotic cover, the surgeon removes all dead i.e. unstained -tissues and bone.

There are several strategies to prevent reinfection and promote healing:

• double lumen tubes are left in the lumen and antibiotic solution is introduced and aspirated 4 hourly; this is continued until the aspirate is sterile (3-6 weeks) and then the tube is gradually removed

• the cavity may be packed with gentamicin beads

• the cavity may be packed with multiple small bone grafts

• a muscle flap with an intact blood supply may be laid into the cavity

Antibiotic therapy

Chronic osteomyelitis is rarely cured by antibiotic therapy alone. Their role is twofold:

• to prevent the spread of infection to healthy bone

• to control acute flares of infection

Sensitivity determination of the pathogens is essential. It is also important that the drugs are non-toxic with long term use and that they penetrate bone well. Good examples are clindamycin and cephalosporins.

Local treatment

The discharging sinus may be painless and only require simple dressing.

Excoriation can be prevented with colostomy paste.

An acute abscess may be treated temporarily by incision and drainage.

Complications

• septicaemia / pyaemia

• septic arthritis

• direct spread of infection

• deformity or alteration in growth rate due to damage to the growth plate

• amyloidosis

PRIMARY-CHRONIC OSTEOMYELITIS

1. Chronic Sclerosing Osteomyelitis:

• chronic sclerosing osteomyelitis (of Garre) has dense sclerotic

• appearance and often no associated lucency on radiographs;

• lesion usually involves the entire circumference of the bone and is much more widespread than a stress fracture;

• thinner linear sclerotic appearance of a stress fracture should be characteristic enough to distinguish the two lesions;

• serial radiographs generally show little or no change within a short time in sclerosing osteomyelitis;

• typical stress fracture, however, has a rapidly evolving course over several weeks;

2. Brodie's abscess

• A Brodie's abscess is a localised pyogenic abscess cavity arising in the metaphysis of one or more long bones - in particular the tibia and the femur.

• This condition develops insidiously, often with no prior symptoms.

• The abscess cavity is lined with granulation tissue and there is a surrounding reactive bone sclerosis.

• In established infection treatment involves excision and sequestrectomy

TESTS

1. Felon in the form of cuff-link is as follows:

A. Thecal with spreading of process to the hand.

B. Subcutaneous with spread of in the epidermis.

С Paronychia.

D. Osteal felon with spread of process to the joint.

E. Aritcular felon.

Choose the correct answer.

2. The types of early felon that require puncturing both for diagnosis and treatment are as follows:

A. Cutaneous.

B. Subcutaneous.

C. Tenosynovitis.

D. Paronychia.

E. Osteal.

Choose the correct answer.

3. The risk of suppurative spreading onto the forearm is high in the following felons:

1. The I finger.

2. The II finger.

3. The III finger.

4. The intravenous finger.

5. The V finger.

Choose the right combination of answers:

A. 1,3. B. 2, 3, 4. С. 1,5. D. 2, 5. E. 1, 2, 3, 4, 5.

4. Subungual felon requires the following surgeries:

1. Oval incision by Klapp.

2. Perforation of the nail.

3. Semi-oval incisions.

4. Resection of the nail bed.

5. Removal of the nail plate.

Choose the right combination of answers:

A. 1,4, 5. B. 2, 3,4. С. 2, 4, 5. D. 3, 4, 5. E. 1, 3, 5.

5. The clinical signs of paronychia are as follows:

1. Swelling of the cutaneous margin.

2. «Floating» nails.

3. Secretion of pus from under the cutaneous margin.

4. Suppurative fistula.

5. Extensive contracture of finger.

Choose the right combination of answers:

A. 1,2, 3. B. 1,3. С. 3,4, 5. D. 2, 4. E. 1,3,4.

6. The local signs of tenosynovitis are as follows:

1. Throbbing pain.

2. Swelling of the entire finger.

3. The finger is extensively straightened out.

4. Fixation of the finger.

5. Painful sensation along the tendon on palpation with a probe.

Choose the right combination of answers:

A. 1, 2. B. 1, 2, 3. С. 1, 3, 4. D. 1, 3, 4, 5. E. 1,2,4,5.