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with spontaneous healing. Where surgical control is
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required, ideally reattempted until sepsis is eradicated and nutrition
optimized, which may take several months.
operation should not be
Localized intraperitoneal
collections
Following peritonitis, pus may collect in localized
pockets within the peritoneum. These may be
dependent anatomical spaces in the abdomen when
the patient lies supine, such subphrenic spaces and
pelvis or non- anatomical, where pus exists walled off
by loops of bowel and omentum.
Risk factors
• Preoperative: perforated viscus or peritonitis at
presentation, obesity, immunocompromised by
drugs or disease, for example, corticosteroid use,
diabetes, malnutrition
• Operative: peritonitis, soiling with luminal contents during surgery, inadequate intra- operative
lavage, retained infected material (such as faecolith from perforated appendix and gallstones following cholecystectomy)
• Postoperative: presence of an organism resistant
to the antibiotics used
Clinical features
The patient may present with a swinging pyrexia or a
pyrexia that has persisted since surgery. There is malaise,
weight loss, anaemia and leucocytosis. If antibiotics
have been given without a diagnosis, the presentation of
an abscess may be disguised and may only manifest
weeks or even months after the original episode
Postoperative complications 45
Subphrenic abscess
Anatomy
The subphrenic region lies between the diaphragm
above and the transverse colon with mesocolon
below and is divided further by the liver and its ligaments (Figure 5.2). The right and left subphrenic
Right
subphrenic
space
Liver
Right
subhepatic
space
(Morison’s
pouch)
Kidney
Duodenum
Hepatic
flexure of colon
(a)
Left
subphrenic
space
Liver
Left
subhepatic
space
(lesser sac)
Stomach
Pancreas
Duodenum
Special investigations
• Full blood count: A polymorph leucocytosis is
common, with a white cell count typically 15–20 ×
9
10
/L.
• CRP is raised.
• CT scan will confirm the diagnosis and anatomical
site of the collection and determine whether it is
drainable by a radiologically guided percutaneous
approach.
Transverse
colon
Omentum
(b)
Figure5.2 The anatomy of the subphrenic spaces
(sagittal views): (a) right and (b) left.
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spaces lie between the diaphragm and the liver and
are separated from each other by the falciform ligament. The right and left subhepatic spaces are below
the liver, the right forming Morison’s pouch
left being the lesser sac, which communicates with
the former through the foramen of Winslow.
right extraperitoneal space lies between the bare area
of the liver and the diaphragm. About twosubphrenic abscesses occur on the right side. Rarely
they may be bilateral.
7
and the
8
The
thirds of
Aetiology
The underlying cause is a peritonitis involving the
upper abdomen– leakage following biliary or gastric
surgery or a perforated peptic ulcer. Rarely, infection
occurs from haematogenous spread or from direct
spread from a primary chest lesion, for example,
empyema.
Clinical features
In addition to the features of a localized collection of
pus (see previous sections), there may be right upper
quadrant pain and pain referred to the shoulder tip
with localized upper abdominal or chest wall tenderness. There may be signs of fluid or collapse at the
lung base. In late cases, a swelling may be detected
over the lower chest wall or upper abdomen. In many
cases, there are no localizing features.
Special investigations
• Chest X- ray may show the following:
– elevation of the diaphragm on the affected
side;
– pleural effusion and/or collapse of the lung
base;
– gas and a fluid level below the diaphragm.
• CT scan will demonstrate an abscess.
Treatment
In early cases, where there is absence of gas and free
fluid on X-
ray, the patient is placed on broad-
spectrum antibiotic therapy. If there is clinical or
radiological evidence of a localized abscess, or if
resolution fails to occur on antimicrobial chemotherapy, percutaneous drainage may be carried out
under ultrasound or CT guidance. If this fails, or the
abscess is loculated, surgical drainage is
performed.
Pelvic abscess
A pelvic abscess may follow any general peritonitis,
but it is particularly common after acute appendicitis
(75%) or after gynaecological infections. In men, the
abscess lies between the bladder and the rectum; in
women, it lies between the uterus and posterior fornix of the vagina anteriorly and the rectum posteriorly
(pouch of Douglas
Left untreated, the abscess may burst into the rectum or vagina or may discharge onto the abdominal
wall, particularly if there has been a previous laparotomy incision at the time of the original episode of
peritonitis. Occasionally, the abscess may rupture
into the peritoneal cavity.
Clinical features
• General features of intraperitoneal pus (see
above).
Local: diarrhoea, mucus discharge per rectum and
•
the presence of a tender extrinsic mass felt on rectal or vaginal examination. Rarely, this may be
large enough to be palpated abdominally.
Treatment
• Broad- spectrum antibiotic therapy adjusted
according to microbiological sensitivities when
available. Anti- fungal agents may be added in certain cases (e.g. immunosuppressed and chronic
infection).
•
Percutaneous radiologically guided drainage using
ultrasound or CT. This carries a risk of vascular
and hollow viscus injury.
• Internal drainage is possible when the abscess
points into the vagina or rectum.
9
).
7
James Rutherford Morison (1853–1939), Professor of
Surgery, University of Durham, Durham, UK.
8
Jacob Winslow (1669–1760), Danish; became the Professor
of Anatomy and Surgery in Paris, France.
9
James Douglas (1675–1742), Obstetrician and Anatomist,
London, UK.
Delirium
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Delirium is an ‘acute confusional state’, which presents
as an altered state of consciousness, cognitive function
and behaviour. Typically, it develops over 1 to 2days
and is common in, but not confined to, elderly patients
undergoing major surgery. Patients may develop visual
or auditory hallucinations; become restless, agitated
and aggressive, or lethargic; have disturbed sleep; and
lack cooperation with simple requests. It is associated
with poorer surgical outcomes, in part as a consequence of the delirium and in part the underlying condition that prompted the state of delirium.
Risk factors
• Preoperative: the elderly, past or current cognitive
impairment or dementia, other comorbidity, metabolic derangement, alcohol and other substance
abuse, and sleep deprivation.
• Operative: type of surgery (more common in
major surgery); opiate and benzodiazepine use,
especially benzodiazepine premedication; surgical blood loss and requirement for transfusion.
The use of spinal anaesthesia for hip surgery, for
example, is associated with less delirium than a
general anaesthetic. Ketamine and dexmedetomidine as part of the anaesthetic regimen are associated with less delirium.
• Postoperative: inadequate pain relief, opiates,
electrolyte imbalance, anaemia, infection, sensory
deprivation (such as loss of glasses or hearing
aids), and malnutrition.
Management
Management usually involves assistance from Care of
the Elderly or psychiatric teams. Initial management
requires careful review of history and repeat examination for any new signs, such as pyrexia, new murmurs
and neurological deficits (suggesting a new cerebral
event). Investigations should aim to exclude other
possible causes:
•
Pain: A common cause of confusion, but its treat-
ment may also cause confusion. Use of blocks in
preference to drugs to reduce immediate postoperative pain helps.
• Hypoxia: Haemoglobin saturations should be
checked, and oxygen administered if necessary; a
Postoperative complications 47
CT pulmonary angiogram may be necessary to
exclude a PE.
Sepsis: Common (urinary tract and/or chest)
•
and uncommon sources should be considered,
and urine, sputum and any drain fluids cultured.
CT imaging may be required to exclude a complication of the surgery such as an anastomotic
leak.
•
Electrolyte disturbance, especially hyponatremia.
Myocardial infarction: Troponin and serial ECGs.
•
•
Arrhythmia: An ECG is necessary to exclude a
change in rhythm, for example, new atrial
fibrillation.
•
D- dimers will exclude a thrombo- embolic event if
negative.
Medication review to check:
•
– critical preoperative drugs have not been omit-
ted inadvertently;
– currently prescribed drugs for any that may be
responsible, such as pain killers, sedatives and
GABAergic drugs (benzodiazepines).
Drips, drains and catheters can prompt confusion:
•
These should be avoided or removed as soon as
possible.
Complications ofminimally
invasive surgery
Minimally invasive operative techniques have
become commonplace for many surgical procedures.
The use of such techniques is associated with their
own complications, some of which are listed later.
Management follows standard surgical principles,
but early diagnosis, achieved by an awareness of what
might go wrong, is important.
Radiological intervention
The interventional radiologist has taken on many
procedures that used to be the preserve of the surgeon, but it is often the surgeon who is left to diagnose and manage the complications. Typical
complications of radiological intervention include
the following.
1
Imaging ‘guided’ needle core biopsy of mass or
lesion
General: bleeding; perforation of viscus; inadvertent puncture of other organs or vessels; and arte-
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riovenous malformation (especially in liver and
kidney).
Cancer: seeding of tumour along the biopsy track,
thereby disseminating it
Transarterial procedure
2
General: arterial dissection; distal embolization;
thrombosis; loss of guidewire; false aneurysm
Angioplasty: vessel rupture
Embolization of a bleeding bowel: infarction and/
or perforation
3
Transvenous procedure (e.g. caval filter
placement)
General: bleeding, thrombosis, thromboembolism
and loss of guidewire
Transcoelomic procedure (e.g. abscess
4
drainage)
General: bleeding, bowel injury and bladder injury
Endoluminal surgery
Upper and lower GI endoscopy, together with any
procedures performed, carry their own risks, the most
common of which is perforation.
Upper GI endoscopy: oesophageal perforation;
1
haemorrhage from varices or from peptic ulcer if
clot displaced
Endoscopic retrograde cholangiopancreatogra-
2
phy (ERCP): perforation, cholangitis and
pancreatitis
3 Lower GI endoscopy: perforation, especially if
snaring polyp or stenting stricture
Laparoscopic surgery
1 Port insertion: perforation of viscus; perforation of
bladder; puncture of the aorta (especially if aneurysmal), vena cava or iliac vessels; and puncture of
the uterus
Insufflation: vagal stimulation causing profound
2
bradycardia, CO
3 Collateral damage: unseen collateral visceral or
vascular damage by surgical instruments; trauma
due to excess force applied by instruments
(which act as levers magnifying the exerted
force), for example, causing avulsion of vessels;
mis- identification of structures (e.g. aorta
divided instead of renal artery during
nephrectomy).
4
Port closure: visceral perforation; inadequate
closure, leading to hernia
retention and embolism.
2
Additional resources
Case 1: Postoperative dyspnoea
Case 2: Inside out
Case 3: A wound leak
Case 4: Postoperative infection
Acute infections
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Christopher Watson
Learning objectives
✓ To know the common surgical infections and their management.
✓ To be particularly cognisant of tetanus and gas gangrene, including
prophylaxis and treatment.
6
There is an important general principle in treating
acute infection anywhere in the body; antibiotics are
invaluable when the infection is spreading through
the tissues (e.g. cellulitis, peritonitis, pneumonia), but
drainage is essential when abscess formation occurs.
Diabetic patients are very prone to infection; anyone presenting with an infection should have their
blood tested for glucose, and an HbA1c checked if
doubt exists.
Cellulitis
Cellulitis is a spreading inflammation of connective
tissues. It usually affects the skin and subcutaneous
tissue, but the term may also be applied to pelvic, perinephric, pharyngeal and other connective tissue
infections. There is usually a prior breach of the skin,
usually of a limb, which admits the infecting organism. The common causative agent is the β- haemolytic
Group A streptococcus (Strep. pyogenes) in around
two- thirds of cases, with staph. aureus involved in
most of the other cases. The invasiveness of streptococcus is due to the production of hyaluronidase and
streptokinase, which dissolve the intercellular matrix
and the fibrin inflammatory barrier, respectively.
Predisposing factors include diabetes, venous insufficiency, eczema and obesity. It is also more common
in those immunosuppressed by drugs or disease.
Characteristically, the skin is dark red with local
oedema (peau d’orange) and hot; it blanches on pressure. There may be blistering and, in severe cases,
cutaneous gangrene. Cellulitis is often accompanied
by lymphangitis and lymphadenitis, and there may be
an associated septicaemia.
Treatment
Any pustules, ulcers or areas of skin breakdown are
swabbed, and the margin of the inflammation is
marked so that progression or regression of infection
can be readily assessed. The limb is immobilized, elevated, and antibiotics begun. Typically, the first- line
antibiotics will be flucloxacillin, with co- amoxiclav if
the infection is near the eyes. Second choice, in case of
allergy, would be clarithromycin, erythromycin or doxycycline. If methicillininfection is possible, then vancomycin is added.
Careful observation is necessary to ensure necrotizing
fasciitis does not ensue (see later in this chapter).
resistant staph. aureus (MRSA)
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
Erysipelas
Erysipelas is a superficial form of cellulitis affecting
the upper dermis and superficial cutaneous lymphatics.
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The culprit is nearly always a Group A beta- haemolytic
streptococcus.
Abscess
An abscess is a localized collection of pus, usually, but
not invariably, produced by pyogenic organisms.
They typically occur under the arms, complicating
pilonidal disease, and around the anus and genitals.
Occasionally, a sterile abscess results from the injection of irritants into soft tissues (e.g. a corticosteroid
injection).
An abscess commences as a hard, red, painful
swelling, which then softens and becomes fluctuant.
If not drained, it may discharge spontaneously onto
the surface or into an adjacent viscus or body cavity.
There are the associated features of bacterial infection, namely a swinging fever, malaise, anorexia and
sweating with a polymorph leucocytosis.
Treatment
An established abscess, in any situation, requires
drainage. Antimicrobial agents cannot diffuse in sufficient quantity to sterilize an abscess completely. Pus
left undrained continues to act as a source of toxaemia and becomes surrounded by dense, fibrous
1
tissue.
The technique of abscess drainage depends on
the site. The classic method, which is applicable to
a superficial abscess, is to wait until there is fluctuation and to insert the tip of a scalpel blade at this
point. The track is widened by means of sinus forceps, which can be inserted without fear of damaging adjacent structures. If there is room, the
surgeon’s finger can be used to explore the abscess
cavity and break down undrained loculi. Drainage
is then maintained until the abscess cavity heals–
from below outwards, since otherwise the superficial layers can close over, with recurrence of the
abscess. Occasionally, the abscess may be kept
open with use of a drain, and the drain is gradually
withdrawn until complete healing is achieved.
Packing of most abscesses after drainage can generally be avoided.
Deep abscesses can be localized and drained
percutaneously using ultrasound or computed
tomography (CT) guidance.
Boil
A boil (furuncle) is an abscess that involves a hair follicle and its associated glands. It is, therefore, not found
on the hairless palm or sole but is usually encountered
where the skin is hairy, injured by
and macerated by sweat; thus, it occurs particularly on
the neck, axilla and the perianal region. It is usually
due to the staphylococcus aureus, and like cellulitis,
occurs more commonly in patients with diabetes or
other immune compromise.
Occasionally, a furuncle may be the primary source
of a staphylococcal septicaemia and may be responsible for osteomyelitis, perinephric abscess or empyema, particularly in debilitated patients. A boil on the
face may be complicated by a septic phlebitis spreading along the facial veins, resulting in thrombosis of
the cavernous sinus.
friction or is dirty
Differential diagnosis
Hidradenitis suppurativa: Multiple infected foci in the
axillae or groins due to infection of the apocrine sweat
glands of these regions are usually misdiagnosed as boils.
They generally do not respond to antimicrobial therapy,
but some will respond to treatment with a monoclonal
antibody against tumour necrosis factor (TNF) (e.g. adalimumab). Excision of the affected skin is often necessary;
if this is extensive, the defect may require skin grafting.
Treatment
When pus is visible, the boil should be incised.
Recurrent crops of boils should be treated by improving the general hygiene of the patient and by the use
of ultraviolet light and hexachlorophene baths, but
systemic antibiotic therapy is seldom indicated.
Carbuncle
1
An old surgical aphorism states that the sun should never
set on undrained pus, something that is still relevant today.
A carbuncle is an area of subcutaneous necrosis
that discharges onto the surface through multiple
sinuses. It is usually staphylococcal in origin. The
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subcutaneous tissues become honeycombed by small
abscesses separated by fibrous strands. The condition
is often associated with general debility, and diabetes,
in
particular, must be considered.
Treatment
Surgery is rarely indicated initially. Antibiotic therapy
is given, and the carbuncle merely protected with
sterile dressings. Occasionally, a large sloughing area
eventually requires excision and a skin graft. Diabetes,
if present, must be controlled.
Specific infections
Tetanus
Tetanus is now a rare disease in the Western world,
thanks to a comprehensive immunization policy. In
the developing world, it remains prevalent with a high
mortality.
Pathology
Tetanus is caused by Clostridium tetani, an anaerobic, exotoxin- secreting, Gram- positive bacillus. It
is characterized by formation of a terminal spore
(‘drumstick’) and is a normal inhabitant of soil and
faeces. The bacillus remains at the site of inoculation and produces a powerful exotoxin, tetanospasmin. Tetanospasmin principally affects
inhibitory neurones that secrete γacid (GABA) and glycine. By blocking the inhibitory effects of these neurones, there is unopposed
excitatory activity from motor and autonomic neurones. Motor effects include increase in muscle
tone, with rigidity and reflex spasms; autonomic
effects include sympathetic overactivity with tachycardia, increased cardiac output and reduced
vascular tone.
Tetanus follows the implantation of spores into a
deep, devitalized wound where anaerobic conditions
occur. Infection is related less to the severity of the
wound than to its nature; thus, an extensive injury
that has received early and adequate wound toilet is
far less risky than a contaminated puncture wound
that has been neglected.
aminobutyric
Clinical features
The incubation time is 24 hours to 24days, the initial
injury often being trivial and forgotten. Muscle spasm
first develops at the site of inoculation and then
involves the facial muscles and the muscles of the
neck and spine. As a rule, it is the trismus of the facial
spasm (producing the typical ‘risus sardonicus’) that
is the first reliable indication of developing tetanus.
This may be so severe that it becomes impossible for
the patient to open his or her mouth (‘lockjaw’). The
period of spasm is followed, except in mild cases, by
violent and extremely painful convulsions, which
occur within 24–72 hours of the onset of symptoms
and may be precipitated by some trivial stimulus,
such as a sudden noise. The convulsions, like the
muscle spasm, affect the muscles of the neck, face
and trunk. Characteristically, the muscles remain in
spasm between the convulsions. The temperature is a
little elevated, but the pulse is rapid and weak.
In favourable cases, the convulsions, if present at all,
become less frequent and then cease and the tonic
spasm gradually lessens. It may, however, be some
weeks before muscle tone returns to normal and the
risus sardonicus disappears. In fatal cases, paroxysms
become more severe and frequent; death occurs from
asphyxia due to involvement of the respiratory muscles
or from exhaustion, inhalation of vomit or pneumonia.
Poor prognostic features are a short incubation
period from the time of injury to the onset of spasm
(under 5 days) and the occurrence of convulsions
within 48 hours of the onset of muscle spasm.
Differential diagnosis
• Hypocalcaemic tetany: characteristically affects the
limbs, producing carpopedal spasm (Chapter40).
• Strychnine poisoning: flaccidity occurs between
convulsions, whereas in tetanus, the spasm
persists.
• Meningitis: neck stiffness.
•
Epilepsy.
• Conversion disorder (previously known as hysteria).
Treatment
Prophylaxis
Active immunization
This comprises two initial injections of tetanus toxoid
(formalin- treated exotoxin) at an interval of 6weeks.
Booster doses are given at intervals of 10 years or at
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the time of any injury. Toxoid should be given to any
population at risk of injury, particularly the elderly in
whom cover may have lapsed.
Wound toilet
The risk of tetanus can be reduced almost to zero if
penetrating and contaminated wounds are adequately
excised to remove all dead tissue and a course of prophylactic penicillin (or erythromycin for penicillinsensitive patients) is given. Antibiotic therapy is no
substitute for thorough wound debridement.
Passive immunization
This is done to neutralize the toxin. Patients who have
previously received toxoid should be given a booster
dose. If toxoid has not been given in the past, human tetanus immunoglobulin (HTIG), prepared from fully immunized subjects, should be given if the wound is heavily
contaminated or is a puncture wound, and more than 6
hours have elapsed before treatment is received. HTIG is
not sufficient to confer longcourse of toxoid immunization should also be given.
term immunity; therefore, a
Curative treatment
Control ofconvulsions
The patient is nursed in isolation, quiet and darkness,
and is heavily sedated. In severe cases, pharmacological
paralysis with tracheostomy and mechanical ventilation
is required, and this may have to be continued for several
weeks. It is terminated when the spasms and rigidity are
absent during a trial period without muscle relaxants.
Control ofthe local infection
Excision and drainage of any wound is carried out
under a general anaesthetic. Higherythromycin if the patient is penicillin sensitive) is
administered.
dose penicillin (or
Nutrition
Feeding via a fine- bore nasogastric tube may be needed
to maintain the general condition and electrolyte balance.
Necrotizing soft tissue
infections
These are bacterial infections characterized by rapidly
progressive tissue destruction, systemic toxicity and
high mortality. The three main types of necrotizing
soft tissue infections are:
•
Polymicrobial infection, with multiple organisms
present
Single organism infection, usually a haemolytic
•
Group A streptococcal infection but may also be
staph. aureus (including MRSA)
•
Gas gangrene, typically due to Clostridium
perfringens
Clinical features
Although there are three main sorts of necrotizing
infection, in reality, presentation and treatment are
similar. An oftenwhether accidental or surgical, is followed by infection with a bacterium producing powerful exotoxins,
which result in tissue destruction.
Around the wound, an area of rapidly spreading cellulitis appears. At the same time, the patient develops
intense pain at the site of infection out of proportion to
the initial external appearance of the skin. This is followed by rapid features of systemic sepsis and confusion. The local manifestations progress, with swelling
of the tissues, skin discolouration, blistering and the
appearance of black (necrotic) spots; these features
may be delayed if the infection is more deeply seated.
overlooked initial breach in the skin,
Risk factors
As with the other infections described in this chapter,
patients at risk of necrotizing infections include those
who are immunosuppressed by drugs or disease,
such as diabetes mellitus or malignancy, as well as
the elderly and the obese. In addition, surgery or
infections around the perineum are prone to develop
into necrotizing infections.
Investigation
• Skin swabs are often negative, but blistered or
ulcerated areas may be more revealing.
• Blood cultures.
• CT and magnetic resonance imaging (MRI) scans
will identify gas within soft tissues.
• Creatine kinase may be risen due to myonecrosis.
Treatment
Treatment involves a high index of suspicion, with
cellulitis often being the initial differential diagnosis.
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Skin and blood cultures are obtained and high- dose,
spectrum antibiotics are commenced immedi-
broadately, but the mainstay of treatment is a radical
debridement of all the affected area.
The infection spreads extensively along fascial
planes, so the true extent of spread may not be apparent until surgery. Wounds are widely debrided and
left open, which allows them to be reassessed twice a
day with further debridement performed until all the
affected area is cleared. The resulting defect may
require covering with skin or a composite tissue graft,
which can only be performed after the infection has
settled.
Mortality from necrotizing infections is high.
Polymicrobial infection:
‘Synergistic gangrene’
Polymicrobial infection, also known as synergistic
gangrene, progressive bacterial gangrene and
Meleney’s gangrene,
action of two or more organisms, commonly aerobic
haemolytic staphylococcus and microaerophilic nonhaemolytic streptococcus. Where it affects the scrotum and perineum, it has been termed Fournier’s
gangrene.
3
2
is caused by the synergistic
Group Astreptococcal infection
Necrotizing fasciitis was the term used historically to
describe the necrotizing soft tissue infection caused
by Group A streptococcus (strep. pyogenes), the ‘flesheating bug’ of media fame. Streptococcus is a common
skin commensal, and infection follows entry of the
bacteria through an oftensuch as a cut, graze, insect bite or puncture wound.
trivial break in the skin,
Gas gangrene
Pathology
Gas gangrene results from infection by Clostridium
perfringens (welchii) and other Clostridium species.
The organism, a Gram- positive, anaerobic sporeforming bacillus like Clostridium tetani, also pro-
duces powerful exotoxins. The toxins have various
activities, including phospholipase, collagenase,
proteinase and hyaluronidase, which facilitate
aggressive local spread of infection along tissue
planes, with liberation of CO
tein destruction. The organisms are found in soil
and faeces.
Gas gangrene is a typical infection of deep
penetrating wounds, particularly of war, but sometimes involvement of the abdominal wall or cavity
may follow operations upon the alimentary system.
Occasionally, gas gangrene complicates amputation
of an ischaemic lower limb or follows abortion or
puerperal infection. It may also arise in drug addicts
giving themselves subcutaneous injections of contaminated heroin.
, H2S and NH3 by pro-
2
Clinical features
The incubation period is about 24 hours. Severe
sudden onset of pain is characteristic, together
with severe toxaemia with tachycardia, shock and
vomiting. The temperature is first elevated and
then becomes subnormal. The affected tissues are
swollen, and crepitus is palpable due to gas in the
tissues. The skin becomes gangrenous, and the
infection spreads along the muscle planes, producing at first dark red swollen muscle and then
frank gangrene. The gas imparts a typical foul
smell.
Treatment
Prophylaxis
Debridement
Adequate excision of wounds removes both the organisms and the dead tissues that are essential for their
anaerobic growth. Seriously contused wounds (such as
those produced by a gunshot) or contaminated wounds
are left open and lightly packed with gauze; primary closure should be avoided. Delayed primary suture can
then safely be performed after 5–6 days, by which time
the wound is usually healthy and granulating.
2
Frank L Meleney (1889–1963), Professor of Clinical
Surgery, Columbia University, OH, USA.
3
Jean Alfred Fournier (1832–1914), ‘Professeur des maladies
cutanées et syphilitiques’, Hôpital St Louis, Paris, France.
Antimicrobial therapy
Penicillin is given in all heavily contaminated
wounds and to patients undergoing amputation of
an ischaemic leg.
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Curative treatment
In the established case, all involved tissue must be excised.
Involvement of all muscle groups in a limb is an indication for amputation, which in the lower limb may mean a
disarticulation at the hip. Highand other supportive measures as required. Hyperbaric
oxygen therapy, to eliminate the anaerobic environment,
has been used with varying degrees of success.
dose penicillin is given,
Anthrax
Anthrax is caused by Bacillus anthracis, a Grampositive, aerobic spore- forming bacillus that lives in
the soil. It may manifest in one of three ways:
Cutaneous anthrax– infection through a break in
1
the skin.
Gastrointestinal anthrax– spore entry through the
2
gut mucosa.
3
Inhalational anthrax – inhalation of spores caus-
ing pulmonary disease.
It is an occupational disease of people working with
wool (‘wool sorter’s disease’) and the hides from
infected animals.
Cutaneous anthrax is the most common manifestation and presents as a painless, pruritic papule that
develops into a vesicle 1–2cm in diameter. The vesicle
ruptures, undergoes necrosis and enlarges to form a
black eschar with surrounding oedema. Associated
features include lymphangitis and regional lymphadenopathy as well as general manifestations of sepsis.
Gastrointestinal anthrax manifests as nausea, vomiting, fever and abdominal pain, with bloody diarrhoea
and features suggestive of an acute abdomen. Symptoms
first appear 2–5days after the ingestion of contaminated
food. Haemorrhagic mesenteric adenitis and ascites are
late features, and mortality is around 50%.
Prophylaxis and treatment of anthrax are with
ciprofloxacin.
contaminated food, originally described with contaminated sausages (botulus is Latin for sausage).
The botulinum toxin is a heatdestroyed by cooking) that penetrates cholinergic
neurones and prevents neurotransmitter (acetylcholine) release at the neuromuscular junction,
thus inhibiting muscular contraction. While botulism is itself a condition more familiar to infectious
disease units, the toxin is widely used in surgery
for conditions as diverse as fissure in ano, achalasia
and hyperhidrosis (excess sweating, especially of
thepalms).
labile toxin (hence
Actinomycosis
Actinomyces are Gram- positive anaerobic bacteria
that commonly colonize the mouths of cattle in
whom they cause a condition called lumpy jaw, a
manifestation of abscesses in the jaw; if an abscess
discharges through the skin as a sinus, the resultant
pus is said to have a characteristic appearance of
sulphur granules.
Actinomyces species, most commonly Actinomyces
israelii, can cause human disease (actinomycosis).
They are commensals in human mouths and may
cause infection particularly in the presence of poor
dental hygiene or previous irradiation (Chapter 20).
In addition to the mouth, A. israelii is a commensal of
the female genital tract and the gastrointestinal tract.
Actinomycosis may follow perforated appendicitis or
colonic surgery, or may present as chronic pelvic pain
in women, associated with weight loss and vaginal
discharge, especially in the presence of an intrauterine
device. It is characterized by an indolent infection,
often with a palpable mass and presence of discharging sinuses. While the diagnosis may be difficult to
make, the treatment is less challenging since the
organism responds to penicillin.
Botulism
Botulism is caused by an exotoxin of Clostridium
botulinum and is associated with ingestion of
Additional resources
Case 5: An inamed neck
Case 6: A sore neck
Case 7: A hidden infection
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