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46
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Complications
¾
Osteomyelitis of frontal bone.
¾
Spread of infection into intracranial cavity leads to
intracranial abscess (Extradural or subdural abscess)
(dumb-bell abscess). So may present with features of
raised intracranial tension like headache, coning and
convulsions.
¾
Pott’s Puffy tumor can be associated with cortical vein
thrombosis, epidural brain abscess/subdural empyema.
The cause of vein thrombosis is explained by diplopic
veins in frontal bone, which communicates with the dural
SRB's Manual of Surgery
venous plexus; septic thrombi can potentially evolve from
foci within the frontal sinus and propagate through this
venous system.
Treatment: Antibiotics and drainage under general anaes-
thesia before it spreads into cranial cavity.
Note:
Once it extends into cranial cavity, it is treated accor
neurosurgical decom
Osteomyelitis of skull bones requires radical removal with reconstruction
of skull defect.
pression (often using Dandy’s brain cannula);
PYOGENIC GRANULOMA (GRANULOMA
PYOGENICUM)
It is a common condition which occurs on the face, scalp,
fingers and toes.
It may be due to minor trauma or minor infection.
Infection leads to formation of unhealthy granu lation tissue
which protrudes through the wound.
It is also called as acquired lobular capillary haeman gioma.
Features: Usually single, well localised, red, firm, nodule,
which bleeds on touch. May or may not be tender.
Sites: Face, scalp, fingers, toes.
Differential diagnosis: Haemangioma; papilloma; skin
adnexal tumours; in recurrent cases, haemangioendothelioma
and melanoma.
Treatment: Excision, laser surgery; Later tissue has to be
sent for histopathological study.
dingly by formal
Fig. 1.113: Pyogenic granuloma lower lip.
IMPETIGO
It is highly infectious superficial skin infection caused
commonly by Staphylococcus but sometimes by streptococcal organisms.
It usually occurs in infants and children with formation of
multiple blisters in the face, neck and hands that rupture and
coalesce to cover with honey-coloured crust.
Red sores, itchy rashes, tender regional lymph nodes are
typical.
Impetigo may be non-bullous (impetigo contagiosa, most
common, common in nose and mouth); bullous (common
in <2 years, common in body/arms/legs); ecthyma (most
serious form involving deeper layer of the skin).
Staphylococcus aureus causes most nonbullous impetigo
and all bullous impetigo.
For persistent impetigo, culture of the wound (to identify
MRSA) and the nose (to identify a causative nasal reservoir)
is needed.
Treatment is oral antibiotics and topical antiseptics (Mupi-
rocin, fusidic acid).
Note:
Ecythma is an ulcerative form of impetigo. Ecthyma is characterized by
small, purulent, shallow, punched-out ulcers with thick, brown-black
crusts and surrounding erythema.
ERYTHRASMA
It is the infection caused by Corynebacterium minutissimum
involving foot, groin, axilla, subumbilical area and perineum
mimicking the tinea or intertrigo.
It is common in diabetics, obesity; common in females.
Superficial scaling, fissuring and maceration are common.
In groin, pink brown marginated patch with fine scaling is
common.
Erythrasma fluorescences a typical coral red colour under a
wood light. Absence of hyphae in skin scrapings differentiates it from tinea.
Treatment is topical and oral erythromycin or clindamycin.
A B
Figs. 1.112A and B: Pyogenic granuloma finger.
SCRUM POX
Scrum pox is a disease seen in rugby players (athletes with
close contact sports) wherein infection occurs during scrum-
ming. It is usually caused by Herpes rugbiorum or Herpes
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rugbiaforum (Herpes simplex virus type 1).
Scrum pox like condition can also be caused by Strepto-
coccus pyogenes where it is called as ‘scrum strep’. Similar
infection seen in wrestlers caused by Herpes gladiatorum and
is called as ‘mat pox’.
Rugby players within the scrum (forwards position) are more
prone for infection.
Vesicular lesions with pain, fever are the usual features.
Infection may complicate as keratitis, corneal scarring, sacral
ganglionitis and meningitis.
Antiviral drug like acyclovir (200 mg 5 times a day for 10
days) is the treatment. Valacyclovir is also used.
by acting on cholinesterase
↓enzyme
↓
Causing hyperexcitability and
reflex spasm of muscles
often with tonic, clonic convulsions
↓
Once toxin is fixed in nerve tissue,
it can no longer be neutralised by antitoxin
Aggravates the muscle
spasm
Cranial nerves involved in tetanus—trigeminal (trismus);
facial (risus sardonicus); vestibulocochlear nerve (hyperacusis);
vagus and hypoglossal (dysphagia).
Toxins
47
CHAPTER 1D General Surgery: Infectious Diseases
TETANUS
It is an infective condition caused by Clostridium tetani organisms leading to reflex muscle spasm, often associated with tonic
clonic convulsions.
Predisposing Factors for Tetanus
Absence of prior tetanus toxoid immunisation.
Trauma with lacerations, deep wounds, crush devitalised
wounds, presence of foreign body, wounds with anaerobic
environment in the tissues.
Chronic suppurative otitis media with perforation, caries teeth.
Improper sterilisation in the ward, labour (septic abortion)
and operation theatre.
Tattooing, rusted nails (there is a myth that only rusted
instrument will cause tetanus; this is not true), ear lobe prick,
colloquial perianal therapies,
Organism
Clostridium tetani is a Gram-positive, anaerobic, motile,
noncapsulated, organism with peritrichous flagella, and
terminal spores (Drum stick/tennis racket appearance).
Spore is the infective agent. They are found in soil, manure, dust.
Spore can gain entry through any wound, pricks, injuries
resulting from road traffic accidents, pene
trating injuries.
Pathog enesis
Spore
↓
Enters the wound
↓
It germinates in anaerobic media releasing bacteria,
which multiply
↓
Release of Exotoxins
Tetanospasmin Tetanolysin
Exotoxins released by Clostridium tetani are tetanospasmin
and tetanolysin (Exotoxin is the one which is released from
bacteria without their destruction/death. Endotoxin is the one
which is released with death of the bacteria). Tetanus bacteria
release only exotoxins.
Tetanospasmin, the common exotoxin released by the
multiplying bacteria once spore germinates travels along the
perineural sheath, lymphatics along the nerve, and through
blood to cause various effects.
Note:
• Tetanospasmin is oxygen stable, heat labile exotoxin (zinc dependent
metalloproteinase) and is a single polypeptide chain of 150 KDa which
gets cleaved into light (fragment A, 50 KDa) and heavy (fragment B,
100 KDa) parts; fragment B part binds to nerve receptors; fragment
A blocks neurotransmitter. It blocks the release of inhibitory neuro-
transmitters glycine and gamma amino butyric acid (GABA). Loss of
inhibition alters (increases) the firing rate of α motor neuron causing
rigidity, spasm, sympathetic overactivity. Tetanospasmin rapidly binds
to gangliosides at the presynaptic membrane of inhibitory motor
nerve endings.
• Tetanus is not communicable from person to person.
Clinical Features
SYMPTOMS
B
x Trismus is the most common symptom
x Jaw stiffness, pain and stiffness in the neck and back muscles
x Anxiousness, sweating, headache, delirium, sleeplessness
x Dysphagia, dyspnoea
INCUBATION PERIOD
B
x Time between the entry of spore and appearance of first
symptom
x Usually 7–10 days
x Shorter the incubation period worser the prognosis and more severe
the course of disease. If it is less than 3 days it is commonly fatal
Through lymphatics
Through the perineural sheath Circulation Haemolysis
↓↓
Enters the central nervous system
Blocks cholinesterase enzymes at Blocks the NMJ (neuroanterior horn cells muscular junction)
Even if you’re on the right track, you’ll get runover if you just sit there.—Arthur Godfrey
Toxaemia (through blood)
PERIOD OF ONSET
B
x Time between appearance of first symptom and appearance of
first sign
x Shorter the incubation period of onset the prognosis and vice versa.
If it is less than 2 days it is commonly fatal
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Signs
Trismus, due to spasm of masseter and pterygoids.
Risus sardonicus (smiling facies), a rigid smile due to spasm
of the facial muscle—zygomaticus major. Looks as if patient
is smiling.
Neck rigidity; spasm and rigidity of all muscles; hyperreflexia.
Respiratory changes—due to laryngeal muscle spasm, infec-
tion, aspiration.
Tonic clonic convulsions.
Abdominal wall rigidity often with haematoma formation.
Severe convulsion may often lead to fractures, joint disloca-
SRB's Manual of Surgery
tions and tendon ruptures.
Fever and tachycardia.
Retention of urine (due to spasm of urinary sphincter),
constipation (due to rectal spasm).
Rarely features of carditis are seen due to involve ment of
the cardiac muscle, which is dangerous, as it often leads to
cardiac arrest and death. Here steroids are very useful. It
presents with refractory bradycardia.
Symptoms will be aggravated by stimuli like light, noise.
Diaphragm and other muscles of respiration undergo spasm
causing tachypnoea, respiratory distress, respiratory infections, aspiration, cyanosis, respiratory failure with altered
PO
and PCO2 levels.
2
Urban tetanus. Due to repeated injections in IV drug abusers.
Postoperative tetanus due to improper sterilisation.
Even though it is classified as acute tetanus (tetanus develops
within 10 days) or chronic tetanus (tetanus develops from 10
days to 3 months) it is only of outcome value as therapy will
be same in both.
Post-abortion or puerperal tetanus develops due to practice
of improper sterilisation during abortion or delivery.
If patient is not given tetanus toxoid during the first attack, he
can develop second attack of tetanus at a later period called
as recurrent tetanus as patient who had once tetanus is not
immune for development of second attack of tetanus.
In children and adolescents chronic suppurative otitis media
(CSOM) with perforation of tympanic membrane can cause
tetanus—otitis tetanus.
DIFFERENT POSTURES IN TETANUS
B
x Opisthotonus: Posterior muscles are acting more, so backward
bending.
x Orthotonus: Straight posture. Both front and back muscles are
acting equally.
x Emprosthotonus: Forward bending as front muscles are acting
more.
x Pleurothotonus: Lateral bending as lateral muscles act more.
Types of Tetanus
x Generalized—commonest; Localized—less severe
x Cephalic—facial nerve muscles; Neonatal tetanus
Early tetanus: It is a severe form with a short incubation
period and poor prognosis.
Latent tetanus: Wound is healed and forgotten. After a long
incubation period, may be years later, under favourable
environment, spores release bacteria and cause tetanus. It
carries better prognosis. Latent tetanus is often called as
delayed tetanus.
Late tetanus: Disease develops many months after injury.
Ascending tetanus: Symptoms and signs progress from
below upwards.
Descending tetanus: Symptoms and signs progress from
above downwards.
Cephalic tetanus: Facial muscles are involved first (3rd, 4th,
6th and 7th cranial nerves can get involved). Facial nerve is
commonly involved in this type. Oculomotor nerve—3rd
nerve (ophthalmoplegia), hypoglossal nerve—12th nerve
(spasm of tongue) are other cranial nerves involved.
Localised tetanus: Here muscles adjacent to the wound or
muscles of one segment or one area develop spasm. It is due
to less virulent toxin or released toxins are of less concentration or only one or few segments of anterior horn cells of the
spinal cord are affected.
Bulbar tetanus: When muscles of deglutition and respiration
are involved. Highly fatal.
Tetanus neonatorum (7th day tetanus): Tetanus occurring
in neonates. Spread is through umbilical cord. It carries very
high, nearly 100% mortality.
Fig. 1.114: Different types of postures seen in tetanus.
COMPLICATIONS OF TETANUS
B
x Fracture bones; haematoma
x Aspiration pneumonia, respiratory failure, ARDS
x Carditis, arrhythmias—life-threatening
x DVT, pulmonary embolism
x Toxaemia; secondary infection—septicaemia
x Bedsore, malnutrition, stress gastric ulcers
x Mortality used to be very high in earlier days up to or more than
50%. It is reduced to 15–20% at present; but it is still higher in
children and elderly
x Repeated uncontrollable convulsions can lead into coma and death.
STAGING OF TETANUS
B
x Mildly ill: Rigidity, spasm, trismus and different postures.
x Seriously ill: Spasm, rigidity, severe respiratory infections,
dysphagia.
x Dangerously ill: Cyanosis with respiratory failure and tonic-clonic
convulsions, cyanosis.
ABLETT CLASSIFICATION OF SEVERITY GRADING OF
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B
TETANUS
x I Mild: Mild to moderate trismus; general spasticity; no respiratory
embarrassment; no spasms; little or no dysphagia.
x II Moderate: Moderate trismus; well-marked rigidity; mild to
moderate but short spasms; moderate respiratory embarrassment
with an increased respiratory rate greater than 30; mild dysphagia.
x III Severe: Severe trismus; generalised spasticity; reflex prolonged
spasms; increased respiratory rate greater than 40; apnoeic spells;
severe dysphagia; tachycardia greater than 120.
x IV Very severe: Grade III and violent autonomic disturbances
involving the cardiovascular system. Severe hypertension and
tachycardia alternating.
Note: Several other severity grading systems are adapted like of
Philips, Dakar, Udwadia, Black, Patel and Jong method.
DIFFERENTIAL DIAGNOSIS
B
x Strychnine poisoning (here patient is normal in between): Strych-
nine blocks neural synapse
x Trismus due to other causes like—dental, oral, tonsillar sepsis,
oral malignancy, temporomandibular joint dysfunction
x Meningitis
x Hydrophobia
x Convulsive disorders
x Metabolic cause like hypocalcaemia and hypomagnesaemia and
hypoglycaemia
x Drug induced extrapyramidal reaction by metoclopramide,
phenothiazines
Management of the Tetanus
Isolation
blood-brain barrier. Intrathecal injection of antitoxin is of less
value (circulating free toxin in the CSF can be neutralised in
first 48 hours during initial development of the spasm). It
should not be given intravenously. It is 100 times more potent
than anti-tetanus serum (ATS, equinus tetanus antitoxin).
Control of Muscle Spasms
Benzodiazepines are used mainly; they are GABA agonists
but do not restore glycinergic inhibition. Higher doses
of diazepam; lorazepam with a longer duration of action;
midazolam with shorter duration of action as infusion
(15 mg/hour). Diazepam and lorazepam contains propylene
glycol which may cause lactic acidosis; but midazolam does
not contain propylene glycol. Diazepam has got cumulative
effect by it metabolites oxazepam and desmethyldiazepam.
Phenobarbitones (anticonvulsants) and chlorpromazines are
also used.
Therapeutic paralysis with a nondepolarising neuromuscular
blocking agent with mechanical ventilation is often required.
Vecuronium and atracurium are used; pancuronium is also
used but may cause tachycardia and hypertension. Propofol
infusion, dantrolene, baclofen are other agents used. Intrathecal baclofen is also often used (500–200 mg infusion) which
is a GABA agonist but is invasive.
Centrally acting drugs like methocarbamol, mephenesin or
meprobamate is useful. Methocarbamol which is long acting
with high potency does not suppress respiration. It may
cause severe gastritis and haemorrhagic cystitis. Mephenesin
causes hypotension and haemoglobinuria. Meprobamate
causes thrombosis, haemolysis and uraemia but is most
potent muscle relaxant.
49
CHAPTER 1D General Surgery: Infectious Diseases
Isolation is advised in a dark quiet room to have a faster recovery;
ventilator and all supportive critical care facilities should be available. Tetanus per se being not a communicable disease does not
essentially require isolation.
Eliminating the Source of the Toxin
Clostridium tetani are sensitive to penicillins, metronidazole,
clindamycin, and erythromycin. Injection crystalline penicillin
20 lac 6th hourly; injection gentamicin and metronidazole are
given in secondary infection. Only problem with penicillin is that
it is GABA antagonist and may increase the convulsions, but
still it is the most commonly used drug. Metronidazole is more
effective and choice of drug at present—500 mg intravenously
8th hourly for 10 days.
Neutralizing the Unbound and Circulating Toxins
It is done ideally by Human Tetanus Immunoglobulin (HTIG/
ATG)—3000–6000 units. HTIG is given intramuscularly
usually to deltoid as a single dose or often in 2 or 3 divided
doses. HTIG (ATG) has got long half life (40 days). There is
no risk of hypersensitivity; it does not interfere with antibody
production; there is no preservative. It does not penetrate
Control of Autonomic Dysfunction
Autonomic dysfunction in tetanus causes haemodynamic
instability. Fluid therapy (8 liters/day), morphine (20–180
mg), phenothiazines [Chlorpromazine, phenoxybenzamine,
phentolamine (α-receptor blocker)], anticholinergics (atropine 100 mg hourly), α2 adrenergic agonists (clonidine,
dexmedetomidine) contribute to cardiovascular stability.
Beta blockers like propranolol should not be used. Sodium
valproate, angiotensin converting enzyme inhibitor, adenosine
are other drugs used for this purpose.
Magnesium sulphate as presynaptic neuromuscular blocker
reduces receptor responsiveness to the catecholamines and
also is an anticonvulsant and a vasodilator. Magnesium
sulphate infusion is rapidly emerging as a useful therapeutic
technique. It controls the autonomic dysfunction; intravenous loading dose of 5 gram given in 20 minutes followed
by infusion for maintenance should be given; one should
observe for hypermagnesaemia by observing ventilation
changes.
Managing Respiratory System Complications
Aspiration, pneumonia, ARDS (adult respiratory distress
syndrome), respiratory failure are common life-threatening
Ancients discovered much, and yet left much more to be discovered.
50
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complications. Ventilator support (IPPR) with endotracheal
intubation; paralyzing the patient; tracheostomy; regular
suctioning, respiratory physiotherapy for prevention of
bronchopneumonia and ARDS; regular monitoring by doing
arterial blood gas analysis (ABG), total count, chest X-ray.
Steroids may be beneficial in ARDS and in patients with
carditis.
Active Immunization
Tetanus toxoid should be given as disease will not give immunity
against further infection. To start—1st dose, 2nd dose after one
month, 3rd dose after 6 months.
SRB's Manual of Surgery
Wound Management
Wound debridement, drainage of pus when present and injec-
tion of HTIG 500 units into wound area to reduce the effects of
toxins locally.
Management of Complications
Respiratory (laryngospasm, aspiration, pneumonia, ARDS,
pulmonary oedema), renal (infection, failure), cardiac (arrhythmias, failure), gastrointestinal (stasis, ileus, diarrhoea, haemorrhage), fracture bones and vertebrae, muscle and tendon
injuries, DVT, thromboembolism, sepsis should be managed
accordingly.
Other Management
Good nursing care, prevention of bedsore and DVT (deep
vein thrombosis), nutrition (enteral through nasogastric tube
or parenteral using a central line)—are important. Care of
urinary catheter, prevention of urosepsis is important.
Steroids may be useful in ARDS and carditis.
Pyrexia or hyperpyrexia should be treated by tepid sponging,
intravenous paracetamol or steroids. It is a poor prognostic
indicator.
Hyperbaric oxygen even though routinely not used has got
beneficial effects in reversing the symptoms.
Cardiac pacemaker may be useful in refractory bradycardia
and arrhythmias.
Following treatment patient may develop muscle spasms or
tics which can be prevented by giving oral methocarbamol
for one year.
Monitoring during therapy: PCO
, PO2, haemotocrit, blood
2
urea, serum electro lytes, chest X-ray, ECG are done at regular
intervals.
Note:
• Culture media for Clostridium tetani is RCM (Robertson’s Cooked Meat)
media and nutrient agar.
• Serum antitoxin (antitetanus antibody) level more than 0.01 units/L is
protective against tetanus.
• When HTIG is not available or financial constraint is the matter then as
an alternative, equine tetanus antitoxin serum (ATS, antitetanus serum)
can be given. Full dose is 1, 00,000 units; half is given intramuscular
and another half given intravenously after initial testing for anaphylaxis
by injecting a test dose of 1000 units intravenously.
GENERAL MEASURES
B
x Isolation
x Avoid noise and light
x ATG 3,000 units IM
x ATS-50,000 IM and 50,000 IV—after test dose—not used now
x Antibiotics like injection penicillin 20 lacs 6th hourly
x injection tetanus toxoid 0.5 ml IM—to deltoid muscle
x IV fluids with TPN
x Urinary catheterisation
x Nasogastric tube is passed to prevent aspiration initially, later
for feeding
x Regular suction of throat
x Nasal oxygen when required
x Prevention of bedsore formation
x Prevention of DVT by low molecular weight heparin
x Good nursing care
SPECIFIC MEASURES
B
x IV diazepam 20 mg 6th hourly
x IV phenobarbitone 30 mg 6th hourly
x IV chorpromazine 25 mg 6th hourly
x Endotracheal intubation and ventilator support
x Tracheostomy if there is severe respiratory secretions
x Steroids
x Bronchodilators like deriphylline
x Wound care—debridement, drainage, and local injection of ATG
PROPHYLAXIS AGAINST TETANUS
B
x In adults, fresh immunisation to start—second in one month,
next in 6 months period. Tetanus toxoid 0.5 m
should be given once in every 4 years or after any significant
trauma
x In infants—triple antigen (DPT)—6 weeks, 10 weeks, 14 weeks,
18 months, and 5 years
x To pregnant mother tetanus toxoid injections are given in 4th and
6th months of pregnancy
x Additional booster dose given in major injuries or high-risk injuries
x ATG 500–1000 units IM given as a prophylaxis in road accidents,
severe burns, crush injuries, war wounds, penetrating wounds
and wounds of head and face. Here tetanus toxoid also should
be given separately at separate site IM
CAUSE OF DEATH IN TETANUS
B
x Respiratory failure with aspiration pneumonia and ARDS
x Severe carditis—an ominous sign
x Mortality is 45–50%—becoming less now in will equipped
centers (15%)
L IM. Booster dose
GAS GANGRENE
It is an infective gangrene caused by clostridial organisms
involving mainly skeletal muscle as oedematous myone-
crosis. Earlier it was called as malignant oedema.
Source and predisposing factors
¾
Contaminated, manured or cultivated soil, intestines are
the sources. Faecal flora commonly contains clostridial
organisms enters the wound; in presence of calcium
from blood clot or silica (silicic acid) of soil, it causes
infection.
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It is common in crush wounds, following road traffic
accidents, after amputations, ischaemic limb, gunshot
wounds, war wounds. Injury or ischaemia or necrosis of
the muscle due to trauma predisposes infection.
¾
Anaerobic environments in the wound—initial infection
with aerobic organism utilises existing oxygen in tissues
creating anaerobic environment to cause clostridial
sepsis.
Organisms: Clostridium Welchii (perfringens): Gram-posi-
tive, anaerobic central spore bearing, nonmotile, capsulated
organisms, most common—60%. Others are—Clostridium
oedematiens; Clostridium septicum; Clostridium histolyticum.
Note:
• Various strains include—A, B, C, D, E. ‘A’ strain is most common.
• Non-clostridial gas producing organisms like coliforms can also cause
gas gangrene.
CLOSTRIDIUM WELCHII PRODUCE TOXINS
B
x Alpha (most common); Beta; Epsilon; Iota
x Phi toxin—myocardial depressant
x Kappa toxin—destruction of connective tissue and blood vessels
x Bursting factor and circulating factor
Exotoxins
Limbs are commonly involved; but organs like liver can also
be affected.
Muscle glycogen is broken down into lactic acid, CO
and
2
hydrogen. Proteinase released by organism forms amino
acids which further releases ammonia and hydrogen
sulphide. Acid released earlier is neutralised by ammonia
and calcium to progress further multiplication of organisms.
Clinical Features
Incubation period is 1–2 days.
Features of toxaemia, fever, tachycardia (out of proportion
to fever) pallor.
Wound is under tension with foul smelling discharge (sickly
sweety/decaying apple odour).
Khaki brown coloured skin due to haemolysis.
Crepitus can be felt.
Jaundice may be ominous sign and also oliguria signifies
renal failure.
Frequent sites are adductor region of the lower limb and
buttocks and subscapular region in upper limb.
Clostridium Welchii can infect limbs, abdominal wall,
appendix, gallbladder, common bile duct, intestine, uterus
(during septic abortion).
51
CHAPTER 1D General Surgery: Infectious Diseases
Lecithinase is important toxin which is haemolytic,
membranolytic and necrotic causing extensive myositis. It
splits lecithin into phosphocholine.
Haemolysin causes extensive haemolysis.
Hyaluronidase helps in rapid spread of gas gangrene.
Proteinase causes breaking down of proteins in an infected
tissue.
Spores enter through the devitalised tissues commonly
in road traffic accidents, crush injury
↓
Spores germinate
↓
Released bacteria will multiply
↓
Exotoxins are released
cause their effects
Effects
Extensive necrosis of muscle with production of gas
(hydrogen sulphide; nitrogen; carbon dioxide) which
stains the muscle brown or black anaerobic myositis/
myonecrosis.
Usually muscle is involved from origin to insertion.
Often may extend into thoracic and abdominal muscles.
When it affects the liver it causes necrosis with frothy blood—
foaming liver, is characteristic.
Rapidly spreading infection which is also often fatal.
Clinical Types
Fulminant type causes rapid progress and often death due
to toxaemia, renal failure or liver failure or MODS or ARDS.
Massive type involving whole of one limb containing fully
dark-coloured gas filled areas.
Group type: Infection of one group of muscles, extensors of
thigh, flexors of leg.
Single muscle type affecting one single muscle.
Subcutaneous type of gas gangrene involves only subcu-
taneous tissue (i.e. superficial involvement). It is mainly of
anaerobic cellulitis type without muscle involvement usually
caused by less virulent clostridial organisms other than
clostridial welchii. It is usually superficial but may spread and
involve fascial planes. It causes necrosis with foul smelling
seropurulent discharge.
Fig. 1.115: Gas gangrene in upper limb. It is after effect of an
assault using an axe by a drunken husband.
Peace is so hard to nd because it is under your nose.
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SRB's Manual of Surgery
Fig. 1.116: Gas gangrene involving entire leg extensively. Note
the black/khaki coloured area. Patient died of toxaemia.
COMPLICATIONS OF GAS GANGRENE
B
x Septicaemia, toxaemia. Renal failure, liver failure
x Circulatory failure, DIC, secondary infection
x Death occurs in critically ill patients
Investigations
X-ray shows gas in muscle plane or under the skin.
Liver function tests, blood urea, serum creatinine, total count,
PO2, PCO2.
CT scan of the part may be useful especially in chest or
abdominal wounds.
Gram’s stain shows Gram-positive bacilli.
Robertson’s cooked meat media is used which causes meat
to turn pink with sour smell and acid reaction.
Clostridium Welchii is grown in culture media containing
20% human serum in a plate. Antitoxin is placed in one-half
of the bacteria grown plate sparing the other half. Zone of
opacity will be seen in that half of the plate where there is
no antitoxin. In the other half part of the plate where there is
antitoxin there is no opacity—Nagler reaction.
Liberal incisions are given. All dead tissues are excised and
debridement is done until healthy tissue bleeds.
Rehydration and maintaining optimum urine output (30 mL/
hour) (0.5 m
Electrolyte management.
In severe cases amputation has to be done as a life-saving
L/kg/hour).
procedure—stump should never be closed (Guillotine
amputation).
Often ventilator support is required.
Once a ward or operation theatre is used for a patient with gas
gangrene, it should be fumigated for 24–48 hours properly
to prevent the risk of spread of infection to other patients
especially with open wounds.
Hypotension in gas gangrene is treated with whole blood
transfusion.
Therapy should be concentrated in managing dehydration,
hypotension, infection, toxaemia by hydration, fresh whole
blood transfusion, passive immunisation, antibiotics, and
hyperbaric oxygen, doing radical wound excision with
removal of all dead tissues with foreign body or amputation
with critical care.
TUBERCULOSIS
Whilst meagre Phthisis gives a silent bow, her strokes are sure, but
her advances slow. No loud alarms, nor fierce assaults are shown:
She starves the fortress first, then takes the town.
—Samuel Garth, 1699
PREVENTION OF GAS GANGRENE
B
x Proper debridement of devitalised crushed wounds
x Devitalised wounds should not be sutured
x Adequate cleaning of the wounds with H
x Penicillin as prophylactic antibiotic.
Treatment
Injection benzyl penicillin 20 lacs 4th hourly + Injection
metronidazole 500 mg 8th hourly + Injection amino glycosides
(if blood urea is normal) or third generation cephalosporins
or metronidazole.
Fresh blood transfusion.
Polyvalent antiserum 25,000 units given intra venously after
a test dose and repeated after 6 hours (Welchii 10,000 IU,
oedematiens 10,000 IU, and septicum 5,000 IU).
Hyperbaric oxygen is very useful.
and normal saline
2O2
Fig. 1.117: Tuberculous lymphadenitis and tuberculous ulcer.
It is commonly caused by Mycobacterium tuber culosis;
occasionally by Mycobacterium bovis, M. kansasii,
M. fortuitum, M. marinum, M. ulcerans.
M. tuberculosis is gram neutral, acid fast, alcohol fast
straight or slightly curved rods.
It is prevalent in most of the developing countries and has
made its resurgence in the developed countries with the
advent of AIDS.
The characteristic lesion here is ‘tubercle’, which is an
avascular granuloma composed of a central zone containing
giant cells, with or without caseation necrosis, surrounded
by a rim of epithelioid cells, lymphocytes and fibroblasts.
It can occur in almost all organs in the body. Pre sen tation
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may vary depending on the individual sites.
General features are—low-grade fever with evening rise of
temperature; loss of appetite; decreased weight.
Investigations
ESR is often raised; peripheral smear—lympho cytosis.
AFB (acid-fast bacillus) staining using Ziehl-Neelsen stain.
Chest X-ray is done to rule out pulmonary tuber culosis.
Culture of the organism in Lowenstein Jenson media.
Mantoux skin test—read after 48 hours of inoculation.
Guinea-pig inoculation.
Relevant investigations depending on the site of the tuber-
culosis.
Interferon gamma release assay (IFN-g).
Treatment
Antituberculous drugs are given for 6 months to one year.
Specific treatment is given depending on the site of the
tuberculosis.
(Please refer individual chapters for details about tuberculosis at
different locations and also chapter drugs for Anti-tuberculous
Therapy.)
53
CHAPTER 1D General Surgery: Infectious Diseases
A
C
B
LEPROSY
It is caused by Mycobacterium leprae. It is a Gram-positive,
acid fast bacillus.
It mainly involves skin, nasal mucosa and peripheral neural
tissues.
It involves only the cooler parts of the body (So axilla, gluteal
region are not involved). Testicular involve ment is seen but
not the ovary. It does not involve the vital organs. Though not
acutely fatal, the disease leaves the victim severely deformed
and crippled for life.
TYPES
B
1. Multibacillary Types
x Lepromatous leprosy: It denotes little or no host resistance.
Bacilli are seen in large numbers in the superficial nodular lesions
and the patient is highly infective.
x Borderline lepromatous.
x Borderline.
2. Paucibacillary Types
x Borderline tuberculoid.
x Tuberculoid leprosy: Here strong host resistance is observed. The
disease is more localised, but it causes more deformities due to
early involvement of nerves. Bacilli are scanty in the lesion and
so infectivity is minimal.
D
Figs. 1.118A to D: A leprosy patient with the typical face
(leonine); skin patches; hand deformities and trophic changes;
trophic ulcer in heel.
Investigations: Regular checking of sensation of the
suspected area is done. Split skin smear, nerve biopsy
taken.
Treatment: Dapsone 100 mg daily; Rifampicin 600 mg once
a month; Clofazimine 50 mg daily + 300 mg once a month.
Note:
• For paucibacillary types, treatment is for 6 months.
• For multibacillary types, treatment is for 2 years or more.
SURGICAL COMPLICATIONS IN LEPROSY
B
a. Primary Deformities
x Leonine facies.
x Collapsed nasal bridge.
x Upper branch facial nerve palsy (causes lag ophthalmos).
x Keratitis and blindness.
x Claw hand either ulnar or combined ulnar and median nerves.
x Radial nerve palsy—wrist drop (1%).
x Clawing of toes due to involvement of posterior tibial nerve.
x Foot drop due to involvement of lateral popliteal nerve. (Medial
popliteal nerve which supplies the tibialis posterior is never
involved.)
Contd...
Right is right even if everyone is against it, and wrong is wrong even if everyone is for it.
54
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Contd...
b. Secondary Deformities
x Anaesthesia of the part makes it prone to trauma, infection,
infective gangrene, destruction, autoampu
less parts.
x Trophic ulcers in the foot are common.
Treatment of complications: Reconstructive surgeries; Release of
contractures; Tendon transfers; Arthrodesis; Ulcer management;
Physiotherapy and rehabilitation.
tation and function-
SYPHILIS (GREAT POX) (FRENCH DISEASE)
SRB's Manual of Surgery
It is concluded…that this disease which amongst the Italians is
called Gallicus, that is to say, the French disease, should now
be named Patursa, …a disease filthie and Saturnall. It is a filthie
disease, because it maketh women to be estee
irreligious…. There is a twofold kinde of causes…. The first is
the only influence or corruption of the aire, from whence we must
charitably thinke, that it infected those which were religious. The
second is conversation, as by kissing and sucking, as appeareth in
children, or by carnall copulation.
med unchast and
—Juan Almenor, 1502
It is a venereal infection caused by Treponema pallidum (Refer
Chapter 1B—Ulcer).
Congenital Syphilis
Here the infection is transmitted from the mother to foetus
through placenta.
Early congenital syphilis: It is seen in newborn.
x Features are:
– Rash, syphilitic snuffles
– Nasal discharge, weight loss
– Periostitis, meningitis, hepatosplenomegaly
– Pneumonia alba
Late congenital syphilis:
x Hutchinson’s triad:
– Interstitial keratitis
– 8th nerve deafness
– Hutchinson’s teeth: Peg shaped upper incisors
x Moon’s molar, molars with cusps
x Congenital neurosyphilis
x Cutaneous, skeletal or visceral gummas
x Saddle nose
x Sabre tibia, Clutton’s joint
x Perforated palate
Congenital syphilis is treated with penicillins.
ACTINOMYCOSIS
It is caused by Actinomyces israelii.
It is an anaerobic Gram-positive fungal like bacterium, which
is a branching filamentous organism. It is called as “Ray
fungus” because of sun-ray appearance.
Fig. 1.119: Saddle nose.
CLINICAL TYPES
B
x Facio-cervical: It is the most common type. Infection spreads
either from tonsil or from adjacent infected tooth. Initially an
induration develops. Nodules form with involvement of skin of
face and neck. It softens and bursts through the skin as sinuses
which discharge pus which contains sulphur granules (60%).
x Thorax: Lungs and pleura get infected by direct spread from
pharynx or by aspiration. Empyema develops. Later chest wall
nodules appear leading to sinuses with discharge (20%).
x In right iliac fossa: It presents as a mass abdomen with
discharging sinus.
x Liver is infected through portal vein (Honey comb liver).
x Pelvic: Pelvic actinomycosis can occur due to intra-uterine
devices.
Organism enters through deeper plane of the tissue, causes
subacute inflammation with induration and nodule formation. Eventually discharging sinus forms at the surface. Pus
collected in a swab or sterile tube will show sulphur granules.
Features:
¾
Discharging sinus with induration and nodules; No lymph
nodal involvement; Through blood spread it may cause
pyaemia and endanger life.
¾
Pus under microscopy shows branching filaments.
¾
Gram’s staining shows Gram-positive mycelia in centre
with Gram-negative radiating peripheral filaments.
These clubs are due to host reaction which are lipoid
material (antigen-antibody complex).
¾
Cultured in brain heart infusion agar and thiogly colate
media.
Differential diagnosis: Chronic pyogenic osteomyelitis;
Carcinomas at the site; Tuberculous disease
Treatment
¾
Penicillins for longer period (6–12 weeks).
¾
Tetracyclines, lincomycin, streptomycin.
¾
Dapsone and iodides may be useful.
¾
Antifungals are often given because it is fungal like bacterium.
¾
Surgical debridement is occasionally required.
¾
Welsh regimen—Injection amikacin 15 mg/kg IV daily
for 21 days; such cycle is repeated 3 times at a gap of
15 days—along with tablet trimothoprim (7 mg/kg)—
sulfamethoxazole (35 mg/kg) daily for 6 months.
MADURA FOOT (MYCETOMA PEDIS)
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It is a chronic granulomatous condition of the foot involving
subcutaneous and often deeper tissues causing multiple
discharging sinuses.
It was first identified in Madurai, Tamil Nadu (India) by Gill
(1842, Madura mycosis).
It is common in India and Africa.
It is common in Tamil Nadu.
It can be fungal (more common) or bacterial origin.
¾
Bacterial can be Actinomyces or Nocardia. Among bacte-
rial Nocardia madurae is most common.
¾
Bacterial mycetomas are by Actinomyces (A. israelii or
A. bovis) or by Nocardia or Actinomadura (red granules).
Occasionally it can be due to pyogenic bacteria like
Staphylococcus aureus (Botryomycosis). Bacterial mycetoma shows white/yellow/red granules which on smear
delineates thin filaments (1 µm). Nocardia asteroids can
primarily involve lungs later spreading to brain, kidney
and other organs as metastatic infection.
¾
Fungal eumycotic mycetoma is caused by Madurella
mycetomi or Madurella grisa. Fungal mycetoma causes
black granules, crushed smear of which shows thick stout
filaments (5 µm).
Organisms: Nocardia madurae (most common); Nocardia
brasiliensis; Nocardia asteroides; Actinomyces israelii.
Pathogenesis
Organism enters through a prick in the foot usually who walks bare-
foot
↓
Reaches deeper plane in the foot
↓
Evokes chronic granulomatous inflammation
↓
Causes pale, painless, firm nodule
↓
Formation of vesicles
↓
Burst to form a discharging sinuses.
Discharging granules may be Black, Red, Yellow.
In black type of Madura foot, infection is mainly subcutaneous.
In red and yellow types, it burrows into the deeper plane
including bone causing bone necrosis (osteomyelitis). Even-
tually gross swelling of the limb with multiple discharging
sinuses with disability will occur.
Muscles and bones are involved.
Tendons and nerves are spared until very late.
Regional lymph nodes are not involved.
Condition will deteriorate by secondary bacterial infection.
Note:
If infection occurs in hand, it is called as Madura hand.
MYCETOMA
B
x It is a chronic, granulomatous, progressive inflammatory condi-
tion involving subcutaneous tissue, skin and deeper tissues
x It may be bacterial (actinomycetoma) or fungal (eumycetoma)
x Painless subcutaneous tissue; multiple sinuses and seropurulent
discharges—triad of mycetoma
x Causes deformity, disability, destruction
x 70% occurs in foot; 12% in hands
x Local hyperhidrosis due to sympathetic over activity can occur
x Tiny, shotty regional lymph nodes can get enlarged due to
secondary infection or as localized immune response
x Osteomyelitis, Kaposi’s sarcoma, carcinoma are the differential
diagnoses
x ‘Dot in circle sign’ in MRI is characteristic
x FNAC and biopsy is very useful to confirm
x Immunoelectrophoresis and ELISA are having diagnostic value.
Features
Painless diffuse swelling in the foot of long duration.
Later multiple discharging sinuses develop on the skin.
Lymph node involvement will not occur unless secondary
bacterial infection is present.
Significant limb disability is common.
Common in males.
20% develop pain—due to secondary infection or bone
involvement.
Differential diagnosis:
Chronic osteomyeliti; Tuberculous
osteomyelitis; Carcinoma, Kaposi’s sarcoma.
Investigations
Discharge study will show branching filamentous appearance
of the organism.
Culture in Sabouroud’s dextrose agar medium.
Gram stain for actinomycosis will show sun-ray appearance
with Gram +ve centre and Gram –ve clubs.
X-ray of the foot is done to look for osteomyelitis.
FNAC and biopsy is confirmative as eumycetoma or actino-
mycetoma.
Ultrasound of area; MRI are useful. Dot in circle sign in MRI
is characteristic.
Immunoelectrophoresis and ELISA are having diagnostic
value showing antibody titre against causative organism.
Fig. 1.120: Madura foot. Note the multiple sinuses.
55
CHAPTER 1D General Surgery: Infectious Diseases
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