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26
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Treatment
¾
Control of diabetes using insulin.
¾
Antibiotics.
¾
Nutritional supplements.
¾
Regular cleaning, debridement, dressing.
¾
Once granulates, the ulcer is covered with skin graft or flap.
¾
Revascularisation procedure is done by endarterectomy
or thrombectomy or balloon angioplasty or arterial bypass
graft. But if distal vessels are involved then success rate
is less.
¾
Toe/foot/leg amputation.
¾
Microcellular rubber (MCR) shoes to prevent injuries;
SRB's Manual of Surgery
care of foot.
It is polymicrobial symbiotic infection by microaerophilic
streptococci and Staphylococcus aureus. Neither organism
is capable of causing such typical lesion independently.
It begins in the wound margin, spreading more in the subcu-
taneous area, often involving extensively.
It can often take long time to develop; but may be rapidly
spreading ulcer with destruction and deep burrowing of the
subcutaneous tissues with excruciating pain. There is small
vessel thrombosis with endarteritis and necrosis of the
subcutaneous tissue.
Outer red area with abundant granulation tissue, middle dusky
purple and inner gangrenous with central granulation tissue
are often typical.
Spreading painful ulcer with discharge is obvious and
toxaemia is not uncommon.
Management
¾
Initial evaluation, blood sugar estimation, often critical
care, antibiotics.
¾
Fluid management, blood transfusion, renal and pulmonary system care.
¾
Adequate debridement with wound excision is essential.
¾
Later once ulcer granulates split skin grafting is done.
Microcellular rubber (MCR) chappal is used in patients
with diabetic neuropathy involving foot.
It is commonly seen in postoperative wounds in the
abdomen and chest wall like empyema drainage, lung
abscess or after surgery for peritonitis. It is common in
thorax and abdomen but occasionally can occur in limbs.
In the limbs it can be de novo associated with ulcerative
colitis or in a pre-existing venous ulcer. It is common in old
age and immunosuppressed individuals and after surgery
for infected cases.
It is cutaneous tuberculosis which occurs in young age group.
Commonly seen on face, hand and forearm; starts as typical
apple-jelly nodule with congestion of skin around. Eventually
a superficial ulcer with undermined edge is formed.
Glass slide pressed firmly on the diseased area to eliminate
the surrounding hyperaemia causes clinically obvious apple-
jelly appearance.
The ulcer is active with destruction occurs at the periphery
and healing taking place at the centre.
Often lesion extends into nose and oral cavity involving the
mucosa.
Meleney’s ulcer.
Typical lupus vulgaris
(Courtesy: Professor Sukumar Maiti, Kolkatta).
Due to lymphatic obstruction facial oedema can occur.
Long-standing lupus vulgaris can turn into squamous cell
carcinoma.
Investigation: ESR, discharge study, biopsy, chest X-ray.
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Treatment:
¾
Antituberculous drugs.
¾
If complete healing does not occur, then excision and
skin grafting is required.
It is due to Mycobacterium tuberculosis. It is usually due
to cold abscess later forming ulcer in the neck, chest wall,
axilla and groin. It can also be primary tuberculosis of the
skin (commonly in face). Ulcer can be single or multiple; oval
or rounded; with undermined edge (due to progression of
disease outwards underneath and healing inwards by skin),
painless with caseating material on the floor. Ulcer is usually
not deep. Regional lymph nodes may be enlarged matted,
firm, and nontender.
Note: Tuberculous ulcer is usually painless except in the tongue.
Management: Discharge study for epithelioid cells (modified
histiocytes), AFB; edge biopsy, antituberculous drugs.
(Pierre Bazin, 1850, Paris)
It is localised area of fat necrosis with chronic ischaemia of
ankle skin affecting exclusively adolescent girls. It may be
due to tuberculosis. It is observed in girls with more/thick
subcutaneous fat around ankle.
Bluish pink leg which becomes bluish mottling in extreme cold
season. On warming, skin turns bright red and painful which is
typical due to hyperaemia. In these patients perforating arteries
perfusing the skin around the ankle are small/poor/not existing
causing ischaemia of skin around ankle which becomes hyperaesthetic and sensitive for temperature alteration.
Symmetrical, purple nodules develop in ankles and lower
leg which later break down forming multiple, small, painful,
superficial ulcers often with ankle oedema and pigment scars.
Treatment is antitubercular drugs and lumbar sympathectomy.
It is endemic in monsoon hit humid tropics with repeated
epidemics but sporadic in subtropics. Trauma or insect bite
leads into infection exclusively in the lower part of the leg
and foot.
It is an acute ulcerative lesion of the skin observed in tropical
regions like Africa, India and South America. It is associated
with lower socioeconomic group, anaemia, and malnutrition
and vitamin deficiency.
It is commonly caused by Fusobacterium fusiformis
(Vincent’s organisms) and Borrelia vincentii.
There are abrasions, redness, papule and pustule formation,
acute regional lymphadenitis and severe pain.
Pustule bursts in 3 days along with necrobiosis and
phagedena causing a spreading painful ulcer with an undermined edge, brownish floor and serosanguineous discharge.
Spreading stops in few weeks with ulcer persisting for many
months to years. Eventually a chronic, large nonhealing/
callous ulcer forms with persistent pain, profuse serosanguineous discharge, extremely unpleasant odour, long existing
firmly adherent slough in the floor without any obvious
constitutional symptoms. During healing it causes a slight
pigmented, parchment like round scar.
Often destruction is progressive without cessation
(phagedena) to extend into entire soft tissues of foot and leg
inviting amputation. Phagedena (Greek—to eat) is also seen
in chancroid and cancrum oris. Phagedena is destruction
without proliferation.
Occasionally squamous cell carcinoma can develop in it.
Improvement in nutrition, penicillin, metronida-
zole, Eusol dressing, skin grafting at a later date.
It is common around ankle (gaiter’s zone) due to ambula-
tory chronic venous hypertension. It is due to varicose veins
(long saphenous vein/short saphenous vein/perforators) or
post-phlebitic limb.
Post-phlebitic limb consists of veins that is been partially
recanalised following deep venous thrombosis which
causes increased venous pressure around ankle through
perforators.
Varicose veins are common in females. 50% of venous
ulcers are due to varicose veins; 50% are due to postphlebitic limb (previous DVT). Pain, discomfort, pigmentation, dermatitis, lipodermatosclerosis, ulceration, periostitis,
ankle joint ankylosis, talipes equinovarus deformity and
Marjolin’s ulcer are the problems of varicose veins and
later of venous ulcer.
Ulcer is initially painful; but once chronicity develops it
becomes painless. Ulcer is often vertically oval; commonly
located on the medial side; occasionally on lateral side; often
on both sides of the ankle; but never above the middle third
of the leg. Floor is covered with pale or often without any
granulation tissue. When well-granulated, edge is sloping.
Induration and tenderness is seen often at the base of an ulcer.
Venous ulcer is vertically oval with sloping edge and will not
penetrate deep fascia.
Inguinal lymph nodes (vertical group) are often enlarged.
Ulcer often attains very large size which is nonhealing, indolent and callous.
Ulcer heals on rest and treatment; but reforms again. Scar-
ring is common due to repeated healing and recurrent ulcer
formation. This unstable scar of long duration may lead into
squamous cell carcinoma (Marjolin’s ulcer).
27
CHAPTER 1B General Surgery: Ulcer
A man without purpose is like a ship without rudder.
28
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: Venous Doppler, regular dressing, skin
grafting, specific treatment for varicose veins.
litic osteitis with ‘ivory’ sequestrum, coppery red skin rash,
moth-eaten alopecia are other features of secondary syphilis.
In tertiary/late stage syphilis gummatous ulcer develops.
It is deep, punched out, painless, nontender ulcer with wash
leather slough in the floor, with ‘silvery tissue paper’ like
scar around and occurs over the subcutaneous bones like
tibia, sternum, skull, palate or other area. It also can occur
over the tongue, anterior aspect of the scrotum. It is due to
delayed hypersensitivity reaction with endarteritis obliterans
and vasculitis. Perforation of nasal septum/palate can occur.
Clutton’s joint and Sabre tibia are often seen. Lymph nodes are
SRB's Manual of Surgery
not affected in tertiary syphilis. Neurosyphilis (tabes dorsalis),
aneurysm of arch of aorta are other features of tertiary syphilis.
Tabes dorsalis presenting as generalized paralysis of insane
is often called as late tertiary or quaternary syphilis.
Long quiescent asymptomatic period from secondary to
Venous ulcer around ankle with skin changes over
surrounding area. It is the most common site of venous ulcer.
tertiary is called as latent syphilis.
Secondary syphilitic stage shows plenty of circulating
Treponema spirochaetes in blood where as in tertiary stage
Nowadays it is a rare entity. It is caused by Treponema
pallidum bacterium. It is a sexually transmitted disease. It
is named as ‘Syphilis’ after a shepherd named Syphilus who
acquired the disease as was written in a poem by Francastorius of Verona. Many clinical lesions are observed in different
stages of syphilis.
John Hunter inoculated himself with syphilis organism to
study the clinical features and effects. After 24 years of
inoculation, he died from rupture of syphilitic aortic aneurysm
spirochaetes are less or absent.
Early syphilis lasts for 2 years and the patient is infective
during this period. Primary syphilis occurs within 4 weeks;
secondary in 12 weeks; latent lasts from 2 years to life time.
Investigations: VDRL, Kahn test; Treponema pallidum
haemagglutination test (TPHA); Treponema pallidum immobilisation test (TPIT).
Treatment: Penicillin (drug of choice); doxycycline (100
mg 3 times a day for 15 days); erythromycin; trtracycline;
cephalosporins. Jarisch-Herxheimer reaction is commonly
seen after penicillin therapy.
at the age of 65.
Genital chancre (Hard chancre, Hunterian chancre) is pain-
less, hard, button like, indurated, nonbleeding ulcer; usually
seen in corona or frenum of penis, often on lips, breasts and
anal region; appears 4 weeks after initial infection in first
stage of the disease (primary syphilis). Shotty, painless,
firm, discrete groin lymph nodes may get enlarged along with
genital chancre. Suppuration in these nodes will not occur.
Extragenital chancres in lips and breasts show enlarged neck/
axillary nodes which are inflamed, painful and also often may
be matted.
During second stage (secondary syphilis) white, thickened
mucous patches appear commonly in the mouth like small,
These multiple irregular genital ulcers appear 3 days after
infection with Haemophillus ducreyi as a venereal disease.
They are acute painful, tender, nonindurated ulcers. Floor
shows yellowish slough with purulent discharge. Edge is
oedematous and inflamed. Acute regional lymphadenitis
with suppuration presenting as tender, soft or firm swelling
is common. Such soft fluctuant inguinal swelling is termed
as bubo.
Treatment is by drugs like co-trimoxazole, erythromycin,
ciprofloxacillin, ceftriaxone; aspiration of bubo.
circular, superficial snail track ulcers. Also there appears
raised, flat, hypertrophied, and warty like epithelium at
mucocutaneous junctions (mouth, genitalia) called as condy-
loma lata. Generalised, shotty, hard, discrete, painless lymph
nodes are palpable, epitrochlear and suboccipital nodes
in particular are enlarged. Epitrochlear nodes are felt 1–2
cm above the medial epicondyle (It is also enlarged in nonHodgkin’s lymphoma/NHL). Iritis, arthritis, hepatitis (massive
liver in syphilis is called as hepar lobatum), meninigitis, syphi-
It is due to lymphogranuloma inguinale, a venereal spreading
organism (LGV, Chlamydia type L1, 2, 3).
In LGV, lesion of primary genital stage is small, painless and
commonly unnoticed.
Lesion of secondary stage develops in 2 weeks. In males
inguinal lymph nodes; in females intrapelvic and pararectal
nodes are involved. Suppuration of inguinal nodes eventually
occurs leading into discharging sinuses. Frei intradermal test
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becomes positive in 6 weeks and remains positive for life time.
In tertiary stage, eye, joint, meninges may get involved after
many years. Repeated chronic inflammation, lymphatic
blockage, scarring can cause rectal stricture and vulval
elephantiasis (esthiomene) in females.
Treatment is tetracycline for 3 weeks.
Ulcers can occur, in various parts like over shin, legs, feet, face,
chest wall, in various diseases like anaemia, polycythaemia,
sickle cell disease, hereditary spherocytosis, leukaemia, vasculitis, autoimmune diseases like rheumatoid arthritis, Paget’s
disease of bone (deep, nonmobile, fixed to bone; common in
tibia), ulcerative colitis, etc.
Treponema pertenue causing Yaws (Frambesia) can have
multiple painless ulcers in leg and feet due to walking with
bare foot (organism enters through abrasion) which heals
spontaneously leaving a tissue paper like scar.
Poor hygiene and dressings can cause multiple, small, red
often scabbed Staphylococcus aureus ulcers on the skin
over the leg and feet which is often recurrent and disturbing.
Buruli ulcer: It is chronic ulcer caused by Mycobacterium
ulcerans (acid-fast bacillus). Initially it forms a subcutaneous
nodule later forming non-caseous necrosis showing slow
healing with severe scarring.
Veld sore: It is cutaneous diphtheria through the skin causing
vesicles with a straw coloured fluid; once vesicles rupture
chronic tender shallow ulcers will form.
Delhi boil (Oriental sore): Here Leishmania tropica infection
causes indurated papule on the face and exposed body parts
causing indolent chronic ulcer which heals producing an ugly
pigmented scar.
29
CHAPTER 1B General Surgery: Ulcer
When you cease to dream, you cease to live.
C. Sinus and Fistula
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C hapter Outline
·
Sinus
·
Fistula
·
Median Mental Sinus
SINUS
It is a blind track lined by granulation tissue leading from an
epithelial surface into the surrounding tissues.
Sinus means “hollow” or “a bay” (Latin).
A B
Figs. 1.73A and B: (A) Sinus; (B) Fistula.
Causes of Sinus
1. Congenital: Preauricular sinus.
Acquired: Actinomycosis, tuberculosis, pilonidal sinus,
2.
chronic osteomyelitis, median mental sinus.
·
Sequestrum
·
Preauricular Sinus
Causes Fistula
1. Congenital: Branchial fistula; Tracheo-oesophageal fistula;
Congenital AV fistula; Umbilical fistula (patent vitellointestinal
duct).
Acquired:
2.
¾
Traumatic:
–
Following surgery—intestinal fistulas (biliary,
pancreatic, faecal).
–
Following instrumental delivery or difficult labour
(vesicovaginal fistula, rectovaginal fistula, ureterovaginal
fistula).
¾
Inflammatory—intestinal actinomycosis, tubercu losis.
¾
Malignancy—when the growth of one organ penetrates
into the nearby organ (rectovesical fistulas as in carcinoma
rectum, vesicouterine fistulas as in uterine cancer).
External fistula
x Orocutaneous
x Branchial fistula
x Thyroglossal fistula
x Enterocutaneous fistula
x Appendicular fistula
Internal fistula
x Tracheo-oesophageal fistula
x Cholecystoduodenal fistula
x Colovesical fistula
x Rectovesical fistula
Clinical Features of Sinus/Fistula
Discharge from the opening of sinus.
No floor.
Raised indurated edge, indurated base, nonmobile.
Often sprouting granulation tissue over the sinus opening.
Bone thickening in osteomyelitis.
Surrounding skin may be erythematous in inflammatory;
bluish in tuberculosis; excoriated in faecal fistula; pigmented
in chronic sinuses/fistulas.
Discharge typical of the cause will be evident which will be
obvious after applying pressure over surrounding area.
Induration is a feature of all chronic fistulas except tuberculosis.
Thickening of the bone underneath on palpation if sinus is
adherent to bone or if there is osteomyelitis.
Enlargement of regional lymph nodes will be evident.
Sinus may be single or multiple.
Fig. 1.74: Typical sinus in the thigh due to osteomyelitis
of the greater trochanter.
FISTULA
It is an abnormal communication between the lumen of one
viscus to another or the body surface or between the vessels.
Fistula means “flute” or “a pipe or tube.”
Fig. 1.75: Multiple discharging sinus foot. It is commonly due to
mycetoma (Madura foot). It could also be due to tuberculosis, chronic
pyogenic osteomyelitis or malignancy.
CAUSES OF PERSISTENCE OF A SINUS OR FISTULA
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B
x A foreign body or necrotic tissue underneath, e.g. suture,
sequestrum
x Insufficient or nondependent drainage
x Persistent obstruction in the lumen, e.g. in faecal fistula, biliary
fistula (distal obstruction)
x Lack of rest, persistent infection
x Wall become lined with epithelium or endo thelium
x Dense fibrosis prevents contraction and healing
x Specific infections: Tuberculosis, actinomycosis
x Presence of malignant disease, post-irradiation
Note:
The most common cause of sinus in neck is tuberculosis. Commonly it is
tuberculous lymphadenitis. It shows yellowish cheesy discharge with bluish
margin. Usually tuberculous sinus/ulcer does not show any induration.
31
CHAPTER 1C General Surgery: Sinus and Fistula
Fig. 1.79: Pilonidal sinus showing primary and secondary sinus.
Fig. 1.80: Fistula in ano both sides.
A B
Figs. 1.76A and B: Secondaries in neck causing discharging sinus.
(A) and (B) in two different patients.
Fig. 1.77: Mandibular sinus. It is usually due to infected tooth causing
osteomyelitis of mandible. It also could be due to tumour, trauma,
actinomycosis and radiation. X-ray (orthopantomogram), study of
discharge and biopsy are relevant investigations. Such sinus should
be excised with extraction of the causative tooth.
Fig. 1.78: Discharging sinus in the neck due to tuberculosis
of lymph nodes with a cold abscess underneath.
Fig. 1.8 1: Postoperative gastrointestinal fistula. Note the skin excoriation.
It can be controlled by using zinc oxide cream local application.
DIFFERENT DISCHARGES IN A SINUS/FISTULA
B
x Purulent—bacterial infection
x Caseous—tuberculous
x Sulphur granules—actino-
mycosis
x Mucus—branchial fistula
Note:
x Saliva—parotid fistula
x Faeces—faecal fistula
x Bile—biliary, duodenal fistula
x Bone—osteomyelitis sinus
x Urine—urinary fistula
• Streptococcal pus is watery with blood stain.
• Staphylococcal pus is yellow and creamy.
• Green or greenish blue pus s due to Pseudomonas aeruginosa infection.
• Anchovy sauce pus is seen amoebic liver abscess.
• Gas gangrene produces sickly sweet odour—decayed apple like.
• E. coli pus is usually odourless.
• Anaerobic bacteria and proteus vulgaris cause typical odour due to prote-
olysis. Bacteroids cause typical over ripe Camembert cheese like odour.
• Faecal fistula causes foul smelling discharge with gas bubble in it.
• Tuberculous sinus discharges caseating cheesy material.
When a man looses his health he begins to take care of it.— John Billings
32
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Investigations
Fistulogram/sinusogram using ultrafluid lipiodol or water
soluble iodine dye (Lipiodol is poppy seed oil containing
40% iodine).
Discharge for C/S, AFB, cytology, staining.
Biopsy from the edge for tuberculosis and malignancy.
Chest X-ray; X-ray of the part; MRI (most reliable) of the part.
ESR.
CT sinusogram.
Probing gently with care.
Digital examination of the rectum and proctoscopy in fistula
SRB's Manual of Surgery
in ano.
Treatment
Treat the cause.
Excision of sinus or fistulas. Always specimen should be
sent for histology.
Antibiotics, antitubercular drugs, rest, adequate drainage.
MEDIAN MENTAL SINUS
It is a chronic infective acquired condition wherein there is
infection of roots of one or both lower incisor teeth forming
root abscess which eventually tracks down between two halves
of lower jaw in the midline presenting as discharging sinus on
the point of chin at midline.
Treatment:
started;
Antibiotics, after doing discharge study (C/S)
Lay opening and excision of the sinus track with
extraction of incisor tooth/teeth.
SEQUESTRUM (SEE TABLE)
Sequestrum is dead bone in situ.
It can be pyogenic, tubercular (feathery), Salmonella
(granular), syphilitic (ivory), tubular and ring (in amputation stump).
It can be unformed—means separation between sequestrum
and adjacent normal bone has not occurred or formed—
means there is proper adequate separation between normal
bone and sequestrum by forming granulation tissue. Radiologically formed sequestrum shows clear lucent area/zone of
demarcation.
Sequestrum is denser because of the absence of decalcifica-
tion in the dead bone as there is no blood supply (dead bone
is dense bone).
Sequestrum should be formed prior to surgical interven-
tion—sequestrectomy and saucerisation.
Features
Usually painless discharging sinus in the midline on the
point of chin.
Often incisor infection may be revealed (in many patients
clinically tooth looks normal even though root is infected
invariably).
It is often mistaken for infected sebaceous cyst.
Osteomyelitis of the mandible is the possible complication.
Differential diagnosis:
sinus; Osteomyelitis.
Investigations:
mandible may not reveal the disease); Discharge study for
C/S, cytology, AFB.
Fig. 1.82: Median mental sinus. Note the origin of the sinus from the
root/roots of the lower incisor/incisors.
Infected sebaceous cyst; Tuberculous
Dental X-ray is diagnostic (Plain X-ray
A
Figs. 1.83A and B: Diagram and X-ray showing osteomyelitis with
sequestrum and sinus. Sequestrum is dead bone in situ.
Types of sequestrum
T
Tubular/diaphyseal Pyogenic—common
Feathery Tuberculosis (vertebra, ribs)
Granular Salmonella
Ring/tubular Amputation stump and at Steinmann pin
area
Fine sandy Viral osteomyelitis—rare
Coarse sandy Tuberculosis
Button like Small separated sequestrum and in radiation
osteomyelitis
Black In actinomycosis (fungal) and due to H2S
Kiss sequestrum In peridiscal tuberculosis
B
A
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B
C
Figs. 1.84A to C: Osteomyelitis patient with scar. Also showing on
table photo of sequestrectomy and saucerisation.
PREAURICULAR SINUS
It is a congenital entity occurring due to imperfect fusion of
the six tubercles which form ear cartilage. Sinus opening
may be seen at the root of the helix or on the tragus. Track
is quiet deep running backwards, slightly upwards towards
the helix. It usually ends blindly. Outer opening of the sinus
often closed causing formation of a cystic swelling (preauricular cyst) which contains fluid which is often infected.
Preauricular sinus in no instance will communicate with the
external auditory meatus. Bursting of this swelling leads into
formation of ulcer like lesion. It can be unilateral or bilateral.
Occasionally multiple sinuses are seen. Opening of the sinus
occurs in a small triangular area in front of the ear at the level
of the tragus. Scarring is common around the opening due
to repeated infection.
Features
It is seen since childhood.
Often swelling appears and apparently disappears repeatedly.
Pain and discharge is common.
It causes a cosmetic problem in young individual.
Discharge study, ESR, sinusogram to assess the track is
needed. MR sinusogram is beneficial.
Differential diagnosis: Cold abscess, sebaceous cyst.
Investigation: Sinusogram, discharge study.
Treatment: Excision under general anaesthesia with removal
of entire track is essential. If track is not removed properly
recurrence will occur.
33
CHAPTER 1C General Surgery: Sinus and Fistula
A B C
Figs. 1.85A to C: X-ray pictures showing features of osteomyelitis
with sequestrum, sinus, cavity of tibia and metatasral bones in diabetic
patients.
The drops of rain make a hole in the stone not by violence, but by oft falling.
A B
Figs. 1.86A and B: Preauricular sinus. During excision, methylene blue
is injected into the track initially and later it is excised using elliptical
incision.
D. Infectious Diseases
T
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C hapter Outline
·
Surgical Infection
·
Cellulitis
·
Erysipelas
·
Lymphangitis
·
Abscess
·
Metastatic and Pyaemic
Abscess
·
Bacteraemia
·
Septicaemia
·
Pyaemia
·
Boil (Furuncle)
·
Hidradenitis Suppurativa
·
Carbuncle
·
Pott’s Puffy Tumour
·
Pyogenic
Granuloma (Granuloma
Pyogenicum)
·
Impetigo
SURGICAL INFECTION
Surgical infection is a major problem in surgical practice.
Asepsis (prevention of entry of organisms) and antisepsis
(killing of the bacteria in the skin or tissues) has made a
difference in surgical practice. Epithelial surfaces act as
mechanical barrier and phagocytes, antibodies; complements, macrophages, leukocytes, opsonins, etc. act as
protective mechanisms.
Malnutrition, diabetes mellitus, obesity, uraemia, jaundice,
malignancy, immunosuppression, radiotherapy, chemotherapy, HIV, ischaemia, foreign body, haematoma are the
risk factors for surgical infections. Virulence of organisms,
blood supply, body immunity and support of antibiotics are
the decisive factors in proper response to control infection.
Surgical infection can be superficial surgical site infection in
the wound or deep surgical site infection in deeper fasciomuscular layers or organ space infection like abdomen/
thoracic cavity, etc.
Health care associated infection occurs after hospital
admission in intensive unit/postoperative ward, etc.
·
Erythrasma
·
Scrum Pox
·
Tetanus
·
Gas Gangrene
·
Tuberculosis
·
Leprosy
·
Syphilis (Great Pox)
·
Actinomycosis
·
Madura Foot (Mycetoma
Pedis)
·
Rabies (Hydrophobia)
·
Anthrax
·
Nosocomial and
Opportunistic Infections
·
Necrotising Fasciitis
·
Acute Pyomyositis
·
Surgical Site Infection
·
HIV Infection and AIDS
SOUTHAMPTON WOUND GRADING SYSTEM FOR
B
EALING AND INFECTION
H
x Grade 0 is normal healing
x Grade 1 is with bruising/mild erythema
x Grade 2 is severe erythema with other features of inflammation
at or around wound
x Grade 3 is serous or bloody discharge
x Grade 4 is presence of pus or deep infection or tissue breakdown
or significant haematoma.
ASEPSIS wound score system is used to assess the wound
infection.
ASEPSIS wound scoring
Parameters Score
• Additional treatment
1. Antibiotics 10
2. Pus drainage 05
3. Wound debridement 10
• Serous discharge—for 5 days of first 7 days of
wound infection
• Erythema—for 5 days of first 7 days of wound
infection
•
Purulent fluid—for 5 days of first 7 days of
wound infection
• Separation of deep tissues—for 5 days of first 7
days of wound infection
• Isolation of bacteria 10
• Stay in the hospital (in-patient) more than 14
days due to infection
Fig. 1.87: Severe sepsis with necrosis in the limb after trauma.
0–5 daily
0–5 daily
0–10 daily
0–10 daily
05
CELLULITIS
It is spreading inflammation of subcutaneous tissue and
fascial planes.
Infection may follow a small scratch or wound or incision or
insect/snake/scorpion bite.
It can be superficial or deep. More common superficial type
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is easier to diagnose.
It is common in diabetics, immunosuppressed people and
old age.
It is common in face, lower limb, upper limb and scrotum
wherein subcutaneous tissue is lax.
Note:
Cellulitis occurring in children is never primary but secondary to an
underlying bone infection—Morison’s aphorism (James Morison, 1939—
Surgeon,
Durham, Newcastle).
CAUSATIVE AGENTS
B
x Commonly due to Streptococcus pyogenes and other Gram +ve
organisms. Release of streptokinase and hyaluronidase cause
spread of infection.
x Often Gram –ve organisms like Klebsiella, Pseudo monas, E. coli
are also involved (usually Gram –ve organisms cause secondary
infection).
SEQUELAE
B
x Infection can get localised to form pyogenic abscess
x Infection can spread to cause bacteraemia, septicaemia,
pyaemia
x Often infection can lead to local gangrene
x Extensive necrosis of skin and subcutaneous tissue—necrotizing
fasciitis.
Diabetes to be treated with insulin. Ketosis if present should
be confirmed by assessing urine ketone bodies and treated
subsequently with intravenous insulin.
Often patient may be in septicaemia; patient in such condition
should be treated with higher antibiotics, critical care with fluid
management, along with maintaining adequate urine output.
Catheterization is required; monitoring is done with—renal
function tests, haematocrit (platelet count), liver function tests,
prothrombin time and serum electrolyte estimation.
Fig. 1.88: Cellulitis face. Note the oedema of the face and eyelids.
35
CHAPTER 1D General Surgery: Infectious Diseases
Clinical Features
Fever, toxicity (tachycardia, hypotension).
Swelling is diffuse and spreading in nature.
Pain and tenderness, red, shiny area with stretched warm skin.
Cellulitis will progress rapidly in diabetic and immunosup-
pressed individuals.
Tender regional lymph nodes may be palpable which signify
severity of the infection.
No edge; no pus; no fluctuation; no limit.
Investigations
Total count raises, differential count, platelet count
(decreases) to be done.
Liver function tests, blood urea and serum creatinine in
severe cases.
Blood sugar estimation, urine test for ketone bodies, glyco-
sylated haemoglobin estimation.
Deep vein thrombosis (DVT) often may mimic cellulitis of
lower limb. Venous Doppler and ultrasound of soft tissues
of the limb may require in such situation.
Treatment
Elevation of limb or part to reduce oedema so as to increase
the circulation and bandaging.
Antibiotics—penicillins, cephalosporins.
Dressing (often glycerine dressing is used as it reduces the
oedema because of its hygroscopic action glycerine magnesium sulphate dressing).
A
B
C
D
Figs. 1.89A to D: Note the cellulitis in different patients. It is common in
lower limbs. There is no edge without any formed pus. It should never
be incised with certain exceptions like Ludwig’s angina. It is treated by
antibiotics. It can cause bacteraemia/septicaemia.
Oedema gives rise to soft pitting, while if pus present, induration can always be felt.—Allan B Kanavel
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