Хирургические болезни. Практикум = Surgical diseases. Practice book. Учебное пособие

−the age from 4 to 6 years or over 55–60 years;

−muscular hypotrophy due to the lack of exercise, hypodynamia, obesity or prolonged starvation;

−general dysplastic constitution;

contributing factors are subdivided into 2 groups:

−pathological and physiological ones weakening the abdominal wall and its muscular-aponeurotic frame (contribute to the development of hernias due to weakness). They include:

obesity;

pregnancy;

multiple injuries and childbirth;

age involution of tissues;

chronic diseases leading to rapid and severe weight loss, disappearance of intermuscular tissue and muscle atrophy;

−diseases and conditions accompanied by increased intrauterine pressure:

chronic diseases of the lungs and bronchi;

diseases accompanied by constipation or difficulty urinating;

hemorrhoids or varicose veins;

physical exercises.

Clinical picture. An uncomplicated (reducible) hernia is clinically characterized by:

•the appearance of a pain syndrome in a specific anatomical area of the body, which increases with the tension of the abdominal muscles, coughing or changes in the body position. In case of large hernias due to the involvement of several loops of the intestine in the hernial sac and the tension of the intestinal mesentery the pain syndrome is revealed not only at the point of the hernial defect, but also all over the abdominal wall;

•a “hernial” swelling of a solid elastic, homogeneous structure, round in shape, completely reducible into the free abdominal cavity in a horizontal position (for reducible or free hernias) spontaneously or by applying hand pressure. Repeated straining or cough causes its repeated appearance. After correction of the hernial swelling a defect in the muscular-aponeurotic layer is revealed, or a hernial opening (hernial orifice) of rounded shape and variable in size. The diameter of the hernial orifice is estimated by the number of fingers it lets pass: 1–2 fingers correspond to about 1.5–3 cm, while a handful (fist) passing corresponds to about 10–20 cm or more;

•a positive symptom of a “cough impulse” felt on the finger inserted into the hernial canal (after the swelling has been reduced), the patient in the vertical position.

Treatment. Surgical principles for the treatment of abdominal hernias include:

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•dissection of the outer hernial membranes (skin, subcutaneous tissue, external fascia);

•isolation and treatment of the hernial sac (opening, separation of contents – in the presence of adhesions, stitching at the cervix, ligation and excising);

•various types of plastic surgery of the hernial orifice (abdominal wall) called hernioplasty;

•suturing of external hernial membranes.

Autoplastics with the patient’s own local tissues (or nonfree) is used while conducting hernioplasty. It includes the following types:

•fascial;

•aponeurotic;

•muscular-aponeurotic;

•muscular.

In fascial-muscular-aponeurotic auto-hernioplasty, several techniques are possible:

•direct connection of previously mobilized edges;

•creation of a duplicate from the tissues sutured above the area of the hernial orifice;

•use of free (or displaced on a flat base) muscular aponeurotic flaps. The disadvantage of these types of hernioplasty is the impossibility of

using local tissues due to their pathological changes (atrophy); the appearance of tension in case of herniated defects of large sizes.

The advantage of hernioplasty with local tissues is the histological homogeneity of the tissues sutured together along the line of their direct contact (in the presence of mobility and displacement ability of the aponeurotic edges of the muscles along the perimeter after their preliminary mobilization).

Free autoplasty is carried out by suturing proper tissues taken at a distance from the primary hernial defect.

Homoplasty (or alloplasty), i.e. the plastics of the hernial orifice by applying cadaveric cryopreserved tissues (most often pericardium, dura mater, peritoneum).

Video-laparoscopic technique opened new perspectives in the surgical treatment of hernia, which enabled the surgeons to avoid many shortcomings characteristic of conventional surgical techniques. In the course of its development in the 90s of the twentieth century a number of successful attempts were made to combine transabdominal and posterior preperitoneal access to the posterior wall of the inguinal canal using less traumatic videoendoscopic techniques.

In 1979 American surgeons (R. Ger) were the first to perform hernioplasty by closing the internal inguinal ring with an overlay of brackets by an endostapler, which was used in the abdominal cavity under the control of a laparoscope.

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Subsequently, laparoscopic hernioplasty was proposed for the treatment of inguinal hernia (L. Schultz, USA). According to this technique the hernial bag was transferred to the abdominal cavity after dissection of the parietal peritoneum over the defect area of the abdominal wall. Two flaps / sheets of synthetic material were used for hernioplasty, one of which, of a smaller size, was placed in the inguinal canal in the form of a “plug”, the other covered the defect of the abdominal wall on the side of the abdominal cavity.

N. Reich, based on L. Schults method, suggested using the portion of the peritoneum from the area of the hernia orifice instead of the second synthetic flap to strengthen the posterior abdominal wall in case of indirect inguinal hernias.

J. Corbitt combined these two techniques, as a result both synthetic meshes were covered on top with peritoneum after high ligation of the inverted hernial sac and its resection.

With accumulated joint experience most surgeons switched to full preperitoneal access or to the pre-peritoneal prosthetic placement in case of transabdominal access with mandatory fixation of the mesh. The use of mesh prosthesis of sufficient size for simultaneous covering of the places with possible direct and indirect inguinal hernia has become common.

P. Fidzgibbons made a major contribution to the development of endovideosurgical hernioplasty. He is the founder of the method of preperitoneal placement of mesh prosthesis with transabdominal access, i.e. true laparoscopic hernioplasty, which has now become widespread.

In most clinics, this method is currently the main laposcopic intervention for inguinal intersections due to the following advantages:

•low invasiveness and nontension technology of operation;

•low incidence of relapses and complications; reduced risk of damage to the spermatic cord;

•the possibility to perform hernioplasty on both sides simultaneously without additional access;

•minimal pain after surgery and the possibility of early activation of patients;

•the possibility to perform simultaneous operations on the abdominal organs;

•reduction of hospital stay and general disability period. The possibility of outpatient management of patients.

Later, the technique, applied by the American surgeon J. McKerman, became widespread, which consists in placing the polypropylene meshpreperitoneally with the use of extraperitoneal access.

Its main advantage is the absence of complications associated with entry into the abdominal cavity and the possibility of manipulation under local anesthesia – L.W. Popp, E.H. Phillips, R.B. Brown.

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At the same time, this method has several drawbacks: it is more technically complicated due to the narrow working space and the need to install trocars in one line. In addition, it is labor and time consuming.

Xenoplasty – plastic by foreign, mainly synthetic endoprostheses, having different configurations (flat and three-dimensional nets, plugs, patches) or materials based on polypropylene, dacron (mercilene, polytetrafluoroethylene (PTFE)), etc.

Complications. Complications of abdominal hernias include:

•coprostasis, i.e. obstruction of the intestinal loop inside the hernial sac with fecal masses. Most often it develops in the elderly in the distal portions of the colon containing dense fecal masses. In contrast to strangulation, coprostasis is characterized by gradual onset, sometimes – by the presence of a pasty palpable swelling in the hernial orifice;

•hernial sac inflammation is a hernial complication caused by inflammation of the hernial sac from the outside (from the skin due to bandage associated injury) or from the peritoneum (spreads from the side of the inner organs inside the hernial sac and is a complication of a variety of processes, e.g. destructive appendicitis, inflamed Meckel’s diverticulum, postpartum salpingitis);

•strangulation (herniae incarceratae).

12.2. STRANGULATED HERNIA

Strangulated hernia (SH) is a pathological condition caused by a sudden (less often gradual) sharp compression of the contents in the hernial orifice accompanied by impairment of blood circulation and subsequent necrosis.

Strangulation is the most frequent and dangerous complication observed in 8–20% of patients with anterior abdominal wall hernias (AAWH). Among emergency surgical diseases, SH ranks 4th after acute appendicitis, cholecystitis and pancreatitis. SH associated mortality rate increases with age and makes up 4–5% at the age of 50–59 years, 15–16% at the age of 60–69 years and more than 25% in patients older than 78– 79 years.

The incidence of strangulations depends on the location and type of hernia and is found:

•with inguinal hernias – in 40–45% of cases;

•with postoperative hernias – in 15–25% of cases;

•with femoral hernias – in 15–20% of cases;

•with midline hernias – in 3–5% of cases.

Etiology. Factors contributing to the strangulation include:

•weight lifting;

•overeating;

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•constipation;

•intake of laxatives;

•severe coughing;

•abrupt physical exertion;

•act of defecation;

•difficulty urinating associated with a sharp increase in intraabdominal pressure.

Clinical picture. The clinical features of strangulated hernias include:

•severe pain after physical exertion (which may develop into pain shock);

•localization of the pain syndrome at the points of primary strangulation with irradiation into the epigastric area (due to the involvement of the nerve plexuses of the mesentery). Further on, as necrosis of the strangulated organ progresses and intramural intestinal nerve plexuses die, the intensity of the pain syndrome decreases;

•irreparability of a previously freely reparable hernia;

•tension and tenderness of the hernial protrusion on palpation;

•negative symptom of a “cough impulse”.

Treatment. The main method of management of strangulated hernia is emergency surgery.

The specific techniques used in the surgical treatment of AH with strangulation include:

•dissection of external hernial membranes (skin, subcutaneous tissue);

•opening the hernial sac with mandatory isolation of the contents from the subcutaneous tissue and surrounding tissues;

•fixation of the injured organ in the wound followed by dissection of the restraining ring (hernial orifice);

•evaluation of the viability of the impaired organ (gut). For this purpose, 100–150 ml of 0.25% novocaine solution is injected into the mesentery of the strangulated loop; thereafter the loop is wrapped in sheets moistened in warm physiological solution for 10–15 minutes.

The viability of the intestinal loop is assessed on the basis of the following criteria:

•color (in the viable loop, the color is restored from cyanotic red to pink, the gloss of the visceral peritoneum being preserved);

•presence of peristalsis (turgor and peristaltic ability are preserved in the viable organ);

•presence of pulsation of the mesentery artery (absence of pulse and other criteria indicates irreversible changes in the strangulated organ).

If the organ is confirmed viable, the loop is inserted into the abdominal cavity; in case of the loop’s nonviability resection must be carried out, stepping not less than 30–40 cm in the afferent direction and 15–20 cm in the efferent direction from the strangulation furrow with the subsequent formation of entero-enteroanastomosis.

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Chapter 13

ACUTE INTESTINAL OBSTRUCTION

13.1. ACUTE INTESTINAL OBSTRUCTION

Acute intestinal obstruction (AIO) (IBC 10: K56.5) (ileus) – comes from the Greek word and means “blockage as a result of inversion of the intestine”. Based on current concepts ileus is a pathological syndrome complex characterized by acute blockage of passage of intestinal contents in the natural direction and accompanied by severe disorders of homeostasis and all kinds of metabolism.

Among emergency surgical diseases AIO accounts for 1.2–4.8% or 5 new cases per year per 100,000 adults. Mortality depends on the cause, stage and degree of severity of the syndrome disorders and makes up from 4 to 25% for nontumoros AIO and from 10 to 39% and higher for tumoral AIO.

Classification. AIO differs according to:

•the mechanism of occurrence:

dynamic (functional):

−paralytic (intestinal paresis);

−spastic;

•mechanical:

strangulated (volvulus, nodulation, strangulated hernia);

obturated. It includes three forms of obturation:

−intra-organic (foreign bodies, closed-loop obstruction, constricted hernia);

−extra-organic (retroperitoneal tumors, retroperitoneal infiltrates, cysts, adhesions, arteriomesenteric obstruction);

−intramural (tumors, polyps, cicatricial strictures);

mixed (characterized by a combination of strangulation and obturation). It includes invagination and adhesive intestinal obstruction;

•anatomical localization:

small intestinal (high and low);

large intestinal (right or left parts);

•pathogenesis (stages of development):

acute impairment of the intestinal passage (the first 12–16 hours) – the stage of initial disorders;

acute disorders of intestinal microcirculation and intoxication (16– 36 hours) – the intermediate stage;

development of peritonitis (> 36 hours) – the late stage;

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•clinical course:

acute;

−chronic;

−recurrent;

the disturbances of intestinal passage:

−complete (with obturation of the lumen more than 50%);

−partial;

•origin:

congenital;

acquired.

13.2. MECHANICAL ACUTE INTESTINAL

OBSTRUCTION

Etiology. Predisposing factors of mechanical obstruction can be:

•congenital:

Ledd’s syndrome (or incomplete intrauterine turn of the intestine) and / or rotational anomalies (volvulus);

congenital dolichosigmoid, it is a congenital lengthening of the sigmoid and its mesentery;

the presence of additional ligaments, pockets, folds of the peritoneum (e.g., a common mesentery for the iliac and cecum);

•acquired, associated with:

adhesive process (in the form of adhesions or bands in the abdominal cavity);

age-related relaxation of the sigmoid;

inflammatory infiltrates in the abdominal cavity;

foreign bodies (including phyto-bezoars of the gastrointestinal tract);

development of cholecysto-intestinal fistula (including Mirrizi syndrome);

large (multi-chambered) hernias of the anterior abdominal wall;

tumors (malignant and benign) of large sizes;

coprostasis;

stenosis of the gastrointestinal tract at different levels.

The triggers of AIO that contribute to a sharp change in the motor function of the digestive tract (most often hypermotility) and are directly related to abnormalities in diet include:

•increased food intake after prolonged starvation;

•rough food or excessive consumption of fruit and vegetables;

•prolonged medication (especially against the background of prolonged starvation).

Pathogenesis. Pathogenesis of AIO depends on its type and includes a number of consecutive stages.

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In case of the obturated form of AIO the feeding of the intestinal walls does not change significantly in the initial stage. Then, as the adducting part of the intestine above the obstacle becomes overfilled, its wall becomes sufficiently distended (distensio). The muscular layer of the intestine, which functions only in case of peristalsis wave aimed at overcoming the obstacle, becomes hypertrophic and thickened. Venous congestion and stasis contribute to edema of this part of the intestine visually giving it a “cyanotic character”. Due to overfilling with the contents and gas, the pressure in the lumen of the adducting intestine begins to exceed the venous pressure and after reaching 100 mm of water column (after 24 hours from the beginning of the process) leads to ischemic damage in the intestinal wall and the transition to the stage of acute disorders in intestinal microcirculation. The thickened intestinal wall, due to the disturbances in the muscle layer, loses its ability of peristaltic movements. The abducting segment of the intestine below the obstacle does not relatively change and is in a collapsed state.

In case of the strangulated form of AIO, circulatory disturbances in the intestinal loop occur much earlier and are clearly marked, which is identical to changes in the intestine in case of a strangulated hernia. Hypertrophy and expansion of the walls of the adducting segment of the intestine do not develop due to the short-term course of the process and the severity of rapidly developing necrobiotic changes (within 2–4 hours).

In the future the course of both types of AIO is accompanied by the same type of functional and structural damage:

•development of thrombocyte aggregation with the deposition of fibrin in the blood vessels of the microvasculature of the intestinal mucosa;

•progression of local circulatory ischemia and venous stasis;

•disruption of the integrity of the endothelial barrier for macromolecules, water and electrolytes;

•functional loss of the epithelial barrier of the intestinal mucosa (primarily for macromolecules) due to its absorption capacity.

Clinical picture. Clinical manifestations of mechanical AIO depend on its type, level of localization, stage of the process.

In the obstructive form of IO, the clinical manifestations are characterized by painful attacks of cramping character due to the spasm of the adducting loop followed by periods of improvement (relief). The pain syndrome has a permanent localization, lasts for a short time and is accompanied by a visible increase in peristalsis (in patients without marked subcutaneous fatty tissue). A characteristic feature of peristalsis is the propagation

of consecutive peristaltic waves in just one direction (to the obstacle) where they stop. When the attack of cramping pain stops, a painless period follows. Over time attacks of pain become more frequent and painless periods are shorter. Then, as the changes in the intestinal wall increase, beginning with the second stage of the AIO, the intensity of the pain syn-

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drome becomes less and decreases within 2–3 days up to its complete absence (due to the destruction of the intestinal wall). In the future the renewal of the pain syndrome is associated with widespread peritonitis.

The strangulated form of AIO is manifested by intense acute pains and causes the patient to scream or get a temporary forced and sometimes even immobile position to relieve pain (the stage of “ileus screaming”). In this case, the pain syndrome usually has a constantly increasing character, and in particularly severe cases leads to the development of pain shock (15– 17% of observations).

Vomiting in the first period of AIO development may occur once or twice, has a reflex character and gives temporary relief. Then, as the process progresses, it becomes permanent. In the third period of AIO due to overfilling of the adducting loops and proximal parts of the gastrointestinal tract, vomiting acquires a “fecal” stagnation character. The time of its occurrence depends on the level of the obstacle (the higher it is, the sooner it appears).

The retention of the passage of flatus and defecation are detected even in the early stages of low small intestinal and high colonic obstruction. If an obstacle is high, due to medical measures, a short-term nonprofuse passage of flatus and defecation from the distal intestinal parts below the obstacle are possible. The invagination form of AIO is characterized by bloody discharge from the rectum. In a number of cases in the early period of colonic AIO, the appearance of a frequent reflexive loose stool is possible.

Diagnosis. For diagnosis of AIO the following methods are applied:

•plain radiography of the abdominal cavity which makes it possible to detect early radiographic signs (within 2–3 hours after the occurrence of clinical symptoms) which become more informative after another 3–5 hours. They include:

pneumatosis of separate intestinal loops (Stirlin’s symptom);

presence of Clauber bowls representing horizontal levels of liquid with gas (darker) bubbles above them, in shape resembling overturned bowls. More often they are detected already within 1–2 hours in strangulated and within 5–6 hours in obturated forms of AIO;

presence of intestinal arches;

a symptom of a “stretched spring” due to edematous circular (or “kerkring”) intestinal folds – Casey’s symptom or a “fish skeleton” that occurs in case of severe AIO;

pendular movements of the liquid due to its transfusion from one intestinal loop to another – above the obstacle level;

a “stop” symptom arising at the site of obstruction, after introducing barium sulfate suspension (BaSO4) – Schwartz’s symptom;

•dynamic radiography with passage control of barium sulphate (about 200 ml). The first image is taken within 3–4 hours after the radiopaque mass intake. The latter, in the absence of intestinal motility disturbances, should

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