6 T ropical infections and infestations

ACKNOWLEDGEMENT
ACKNOWLEDGEMENT
The authors acknowledge the contribution of  Professor Ahmed Hassan Fahal MBBS, FRCS, FRCSI, FRCSG, MD, MS, FRCP (London), Professor of  Surgery , University of  Khartoum, Khartoum, Sudan, in the section relating to Mycetoma. ACKNOWLEDGEMENT
The authors acknowledge the contribution of  Professor Ahmed Hassan Fahal MBBS, FRCS, FRCSI, FRCSG, MD, MS, FRCP (London), Professor of  Surgery , University of  Khartoum, Khartoum, Sudan, in the section relating to Mycetoma. ACKNOWLEDGEMENT
The authors acknowledge the contribution of  Professor Ahmed Hassan Fahal MBBS, FRCS, FRCSI, FRCSG, MD, MS, FRCP (London), Professor of  Surgery , University of  Khartoum, Khartoum, Sudan, in the section relating to Mycetoma.

AMOEBIASIS Introduction
AMOEBIASIS Introduction
Amoebiasis is caused by Entamoeba histolytica. The disease is common in the Indian subcontinent, Africa and parts of Central and South America, where almost half  the population is infected. The majority remain asymptomatic carriers. The mode of  infection is via the faecal–oral route and the disease occurs as a result of  substandard hygiene and sanitation; therefore, the population from the poorer socioeconomic strata are more vulnerable. The prevalence of E. histolytica stool samples in high-endemic zones such as South East Asia averages 10%; the incidence of amoebic liver abscesses in such populations, however, can be as high as 21 per 100 /uni00A0 000 population. -
To be able to:
Diagnose and treat these conditions, particularly as
•
emergencies. The ease of global travel has connected
areas where tropical infections are common to areas
where they are not. Patients with such an infection who
are recently returned from the tropics will mostly present
as emergencies
To realise:
That the ideal management involves a multidisciplinary
•
approach between the surgeon, physician, radiologist,
pathologist and microbiologist. In case of doubt, in a
dif
/f_i
cult situation, there should be no hesitation in seeking
help from a specialist centre
AMOEBIASIS Introduction
Amoebiasis is caused by Entamoeba histolytica. The disease is common in the Indian subcontinent, Africa and parts of Central and South America, where almost half  the population is infected. The majority remain asymptomatic carriers. The mode of  infection is via the faecal–oral route and the disease occurs as a result of  substandard hygiene and sanitation; therefore, the population from the poorer socioeconomic strata are more vulnerable. The prevalence of E. histolytica stool samples in high-endemic zones such as South East Asia averages 10%; the incidence of amoebic liver abscesses in such populations, however, can be as high as 21 per 100 /uni00A0 000 population. -
To be able to:
Diagnose and treat these conditions, particularly as
•
emergencies. The ease of global travel has connected
areas where tropical infections are common to areas
where they are not. Patients with such an infection who
are recently returned from the tropics will mostly present
as emergencies
To realise:
That the ideal management involves a multidisciplinary
•
approach between the surgeon, physician, radiologist,
pathologist and microbiologist. In case of doubt, in a
dif
/f_i
cult situation, there should be no hesitation in seeking
help from a specialist centre
AMOEBIASIS Introduction
Amoebiasis is caused by Entamoeba histolytica. The disease is common in the Indian subcontinent, Africa and parts of Central and South America, where almost half  the population is infected. The majority remain asymptomatic carriers. The mode of  infection is via the faecal–oral route and the disease occurs as a result of  substandard hygiene and sanitation; therefore, the population from the poorer socioeconomic strata are more vulnerable. The prevalence of E. histolytica stool samples in high-endemic zones such as South East Asia averages 10%; the incidence of amoebic liver abscesses in such populations, however, can be as high as 21 per 100 /uni00A0 000 population. -
To be able to:
Diagnose and treat these conditions, particularly as
•
emergencies. The ease of global travel has connected
areas where tropical infections are common to areas
where they are not. Patients with such an infection who
are recently returned from the tropics will mostly present
as emergencies
To realise:
That the ideal management involves a multidisciplinary
•
approach between the surgeon, physician, radiologist,
pathologist and microbiologist. In case of doubt, in a
dif
/f_i
cult situation, there should be no hesitation in seeking
help from a specialist centre

ASIATIC CHOLANGIOHEPATITIS Introduction
ASIATIC CHOLANGIOHEPATITIS Introduction
This disease, also called oriental cholangiohepatitis, is caused by infestation of  the hepatobiliary system by a trematode, Clonorchis sinensis. It has a high incidence in the tropical regions of  South East Asia, particularly among those living in the major sea ports and near river estuaries. The organism, - which is a type of liver fluke, develops in snails that act as an intermediate host. Free swimming from snails, the cercariae penetrate the flesh of freshwater fish, crabs and crayfish, which also act as an intermediate host. Ingestion of  infected fish, crabs and crayfish, when eaten raw or improperly cooked, causes the infection in humans and other fish-eating mammals, es - which are the definitive hosts. Two other parasites, Opisthorchis , which has the same life cycle as Clonorchis , and Fasciola , the metacercariae of  which colonise vegetation, can cause similar damage to the biliary channels. - ASIATIC CHOLANGIOHEPATITIS Introduction
This disease, also called oriental cholangiohepatitis, is caused by infestation of  the hepatobiliary system by a trematode, Clonorchis sinensis. It has a high incidence in the tropical regions of  South East Asia, particularly among those living in the major sea ports and near river estuaries. The organism, - which is a type of liver fluke, develops in snails that act as an intermediate host. Free swimming from snails, the cercariae penetrate the flesh of freshwater fish, crabs and crayfish, which also act as an intermediate host. Ingestion of  infected fish, crabs and crayfish, when eaten raw or improperly cooked, causes the infection in humans and other fish-eating mammals, es - which are the definitive hosts. Two other parasites, Opisthorchis , which has the same life cycle as Clonorchis , and Fasciola , the metacercariae of  which colonise vegetation, can cause similar damage to the biliary channels. - ASIATIC CHOLANGIOHEPATITIS Introduction
This disease, also called oriental cholangiohepatitis, is caused by infestation of  the hepatobiliary system by a trematode, Clonorchis sinensis. It has a high incidence in the tropical regions of  South East Asia, particularly among those living in the major sea ports and near river estuaries. The organism, - which is a type of liver fluke, develops in snails that act as an intermediate host. Free swimming from snails, the cercariae penetrate the flesh of freshwater fish, crabs and crayfish, which also act as an intermediate host. Ingestion of  infected fish, crabs and crayfish, when eaten raw or improperly cooked, causes the infection in humans and other fish-eating mammals, es - which are the definitive hosts. Two other parasites, Opisthorchis , which has the same life cycle as Clonorchis , and Fasciola , the metacercariae of  which colonise vegetation, can cause similar damage to the biliary channels. -

Aetiology and pathology
Aetiology and pathology
Cassava (tapioca) is a root vegetable that is readily available and inexpensive and is therefore consumed as a staple diet by people from a poor background. It contains derivatives of cyanide that are detoxified in the liver by sulphur-containing amino acids. The less well o ff among the population lack such amino acids in the diet. This results in cyanogen toxicity , causing the disease. Several members of  the same family have been known to su ff er from this condition; this strengthens the theory that cassava toxicity is an important cause because family members eat the same food. Macroscopically , the pancreas is firm and nodular with extensive periductal fibrosis, with intraductal calcium carbon - ate stones of  di ff erent sizes and shapes that may show branches and resemble a staghorn. T he ducts are dilated. Microscop - ically , intralobular, interlobular and periductal fibrosis is the predominant featur e, with plasma cell and lymphocyte infiltra - tion. There is a high incidence of  pancreatic cancer in these patients. Pathology of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Almost exclusively occurs in resource-poor countries and is
due to malnutrition; alcohol is not a cause
Cassava ingestion is regarded as an aetiological factor because
of its high content of cyanide compounds
Dilatation of pancreatic ducts with large intraductal stones
Fibrosis of the pancreas as a whole
A high incidence of pancreatic cancer in those affected by the
disease
Aetiology and pathology
Cassava (tapioca) is a root vegetable that is readily available and inexpensive and is therefore consumed as a staple diet by people from a poor background. It contains derivatives of cyanide that are detoxified in the liver by sulphur-containing amino acids. The less well o ff among the population lack such amino acids in the diet. This results in cyanogen toxicity , causing the disease. Several members of  the same family have been known to su ff er from this condition; this strengthens the theory that cassava toxicity is an important cause because family members eat the same food. Macroscopically , the pancreas is firm and nodular with extensive periductal fibrosis, with intraductal calcium carbon - ate stones of  di ff erent sizes and shapes that may show branches and resemble a staghorn. T he ducts are dilated. Microscop - ically , intralobular, interlobular and periductal fibrosis is the predominant featur e, with plasma cell and lymphocyte infiltra - tion. There is a high incidence of  pancreatic cancer in these patients. Pathology of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Almost exclusively occurs in resource-poor countries and is
due to malnutrition; alcohol is not a cause
Cassava ingestion is regarded as an aetiological factor because
of its high content of cyanide compounds
Dilatation of pancreatic ducts with large intraductal stones
Fibrosis of the pancreas as a whole
A high incidence of pancreatic cancer in those affected by the
disease
Aetiology and pathology
Cassava (tapioca) is a root vegetable that is readily available and inexpensive and is therefore consumed as a staple diet by people from a poor background. It contains derivatives of cyanide that are detoxified in the liver by sulphur-containing amino acids. The less well o ff among the population lack such amino acids in the diet. This results in cyanogen toxicity , causing the disease. Several members of  the same family have been known to su ff er from this condition; this strengthens the theory that cassava toxicity is an important cause because family members eat the same food. Macroscopically , the pancreas is firm and nodular with extensive periductal fibrosis, with intraductal calcium carbon - ate stones of  di ff erent sizes and shapes that may show branches and resemble a staghorn. T he ducts are dilated. Microscop - ically , intralobular, interlobular and periductal fibrosis is the predominant featur e, with plasma cell and lymphocyte infiltra - tion. There is a high incidence of  pancreatic cancer in these patients. Pathology of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Almost exclusively occurs in resource-poor countries and is
due to malnutrition; alcohol is not a cause
Cassava ingestion is regarded as an aetiological factor because
of its high content of cyanide compounds
Dilatation of pancreatic ducts with large intraductal stones
Fibrosis of the pancreas as a whole
A high incidence of pancreatic cancer in those affected by the
disease

Amoeboma
Amoeboma
This is a chronic granuloma arising in the large bowel, most commonly seen in the caecum. It is prone to occur in long standing amoebic infection that has been treated intermittently with drugs without completion of  a full course, a situation that arises from indiscriminate self-medication, particularly in resource-poor countries. Hence this is more often seen in such countries. should be suspected when a patient from an endemic area with generalised ill health and pyrexia has a mass in the right iliac fossa with a history of  blood-stained mucoid diarrhoea. Such a patient is highly unlikely to hav e a carcinoma because altered bowel habit is not a feature of  right-sided colonic carcinoma. While iron deficiency anaemia is a classical elective presenta - - tion of  a caecal carcinoma, the same is present in an amoe - boma because of  chronic malnutrition. Amoeboma
This is a chronic granuloma arising in the large bowel, most commonly seen in the caecum. It is prone to occur in long standing amoebic infection that has been treated intermittently with drugs without completion of  a full course, a situation that arises from indiscriminate self-medication, particularly in resource-poor countries. Hence this is more often seen in such countries. should be suspected when a patient from an endemic area with generalised ill health and pyrexia has a mass in the right iliac fossa with a history of  blood-stained mucoid diarrhoea. Such a patient is highly unlikely to hav e a carcinoma because altered bowel habit is not a feature of  right-sided colonic carcinoma. While iron deficiency anaemia is a classical elective presenta - - tion of  a caecal carcinoma, the same is present in an amoe - boma because of  chronic malnutrition. Amoeboma
This is a chronic granuloma arising in the large bowel, most commonly seen in the caecum. It is prone to occur in long standing amoebic infection that has been treated intermittently with drugs without completion of  a full course, a situation that arises from indiscriminate self-medication, particularly in resource-poor countries. Hence this is more often seen in such countries. should be suspected when a patient from an endemic area with generalised ill health and pyrexia has a mass in the right iliac fossa with a history of  blood-stained mucoid diarrhoea. Such a patient is highly unlikely to hav e a carcinoma because altered bowel habit is not a feature of  right-sided colonic carcinoma. While iron deficiency anaemia is a classical elective presenta - - tion of  a caecal carcinoma, the same is present in an amoe - boma because of  chronic malnutrition.

Classification
Classification
In 2003, the WHO Informal Working Group on Echinoco - ccosis (WHO-IWGE) proposed a standardised ultrasound ( Table 6.1 ). This is universally accepted, particularly because it helps to decide on the appropriate management. Three groups have been recognised: /uni25CF Group 1: Active group – cysts larger than 2 cm and often fertile. /uni25CF Group 2: Transition group – cysts starting to degenerate and entering a transitional stage because of  host resistance or treatment but may contain viable protoscolices. /uni25CF Group 3: Inactive group – degenerated, partially or totally calcified cysts; unlikely to contain viable protoscolices. Classification
In 2003, the WHO Informal Working Group on Echinoco - ccosis (WHO-IWGE) proposed a standardised ultrasound ( Table 6.1 ). This is universally accepted, particularly because it helps to decide on the appropriate management. Three groups have been recognised: /uni25CF Group 1: Active group – cysts larger than 2 cm and often fertile. /uni25CF Group 2: Transition group – cysts starting to degenerate and entering a transitional stage because of  host resistance or treatment but may contain viable protoscolices. /uni25CF Group 3: Inactive group – degenerated, partially or totally calcified cysts; unlikely to contain viable protoscolices. Classification
In 2003, the WHO Informal Working Group on Echinoco - ccosis (WHO-IWGE) proposed a standardised ultrasound ( Table 6.1 ). This is universally accepted, particularly because it helps to decide on the appropriate management. Three groups have been recognised: /uni25CF Group 1: Active group – cysts larger than 2 cm and often fertile. /uni25CF Group 2: Transition group – cysts starting to degenerate and entering a transitional stage because of  host resistance or treatment but may contain viable protoscolices. /uni25CF Group 3: Inactive group – degenerated, partially or totally calcified cysts; unlikely to contain viable protoscolices.

Clinical features and diagnosis
Clinical features and diagnosis
The disease is slowly progressive and a ff ects the skin, upper respiratory tract and peripheral nerves. In tuberculoid leprosy , the damage to tissues occurs early and is localised to one part of  the body , with limited deformity of  that organ. Neural involvement is characterised by thickening of  the nerves, which are tender. There may be asymmetrical well-defined anaesthetic hypopigmented or erythematous macules with elevated edges and a dry and rough surface – lesions called leprids. In lepromatous leprosy , the disease is symmetrical and extensive. Cutaneous involvement occurs in the form of  several pale macules that form plaques and nodules called lepromas. The deformities produced are divided into primary , which are caused by leprosy or its reactions, and secondary , resulting from e ff ects such as anaesthesia of  the hands and feet. Nodu lar lesions on the face in the acute phase of  the lepromatous variety are known as ‘leonine facies’ (looking like a lion). Later, there is wrinkling of  the skin, giving an aged appearance to a Gerhard Domagk , 1895–1964, German physician, Lecturer in Pathologic Anatomy , University of  Munster, Germany , discovered prontosil in 1935, for which he was awarded the Nobel Prize in Physiology or Medicine in 1939. of  the lateral cartilages and septum of  the nose with collapse of the nasal bridge and lifting of  the tip of  the nose ( Figure 6.17 ). There may be paralysis of  the branches of  the facial nerve in the bony canal or of the zygomatic branch. Blindness may be - attrib uted to exposure keratitis or iridocyclitis. Paralysis of  the orbicularis oculi causes incomplete closure of the eye, epiphora and conjunctivitis ( Figure 6.18 ). The hands are typically clawed - ( Figure 6.19 ) because of involvement of  the ulnar nerve at the - elbow and the median nerve at the wrist. Anaesthesia of  the hands makes these patients vulnerable to frequent burns and injuries. Similarly , clawing of  the toes ( Figure 6.20 ) occurs as a result of  involvement of  the posterior tibial nerve. When the lateral popliteal nerve is a ff ected, it leads to foot drop, and the nerve can be felt to be thickened behind the upper end of the fibula. Anaesthesia of  the feet predisposes to trophic ulceration ( Figure 6.21 ), chronic infection, contraction and autoamputa - tion. Involvement of  the testes causes atrophy , which in turn results in gynaecomastia ( Figure 6.22 ). Confirmation of  the diagnosis is obtained by a skin smear or skin biopsy , which shows the classical histological and microbiological features . Summary box 6.13 Leprosy: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF
Typical clinical features and awareness of the disease should
help to make a diagnosis
The face has an aged look, with collapse of the nasal bridge
and ocular changes
Thickened peripheral nerves, patches of anaesthetic skin, claw
hands, foot drop and trophic ulcers are characteristic
Microbiological examination of the acid-fast bacillus and typical
histology on skin biopsy are con
/f_i
rmatory
Clinical features and diagnosis
The disease is slowly progressive and a ff ects the skin, upper respiratory tract and peripheral nerves. In tuberculoid leprosy , the damage to tissues occurs early and is localised to one part of  the body , with limited deformity of  that organ. Neural involvement is characterised by thickening of  the nerves, which are tender. There may be asymmetrical well-defined anaesthetic hypopigmented or erythematous macules with elevated edges and a dry and rough surface – lesions called leprids. In lepromatous leprosy , the disease is symmetrical and extensive. Cutaneous involvement occurs in the form of  several pale macules that form plaques and nodules called lepromas. The deformities produced are divided into primary , which are caused by leprosy or its reactions, and secondary , resulting from e ff ects such as anaesthesia of  the hands and feet. Nodu lar lesions on the face in the acute phase of  the lepromatous variety are known as ‘leonine facies’ (looking like a lion). Later, there is wrinkling of  the skin, giving an aged appearance to a Gerhard Domagk , 1895–1964, German physician, Lecturer in Pathologic Anatomy , University of  Munster, Germany , discovered prontosil in 1935, for which he was awarded the Nobel Prize in Physiology or Medicine in 1939. of  the lateral cartilages and septum of  the nose with collapse of the nasal bridge and lifting of  the tip of  the nose ( Figure 6.17 ). There may be paralysis of  the branches of  the facial nerve in the bony canal or of the zygomatic branch. Blindness may be - attrib uted to exposure keratitis or iridocyclitis. Paralysis of  the orbicularis oculi causes incomplete closure of the eye, epiphora and conjunctivitis ( Figure 6.18 ). The hands are typically clawed - ( Figure 6.19 ) because of involvement of  the ulnar nerve at the - elbow and the median nerve at the wrist. Anaesthesia of  the hands makes these patients vulnerable to frequent burns and injuries. Similarly , clawing of  the toes ( Figure 6.20 ) occurs as a result of  involvement of  the posterior tibial nerve. When the lateral popliteal nerve is a ff ected, it leads to foot drop, and the nerve can be felt to be thickened behind the upper end of the fibula. Anaesthesia of  the feet predisposes to trophic ulceration ( Figure 6.21 ), chronic infection, contraction and autoamputa - tion. Involvement of  the testes causes atrophy , which in turn results in gynaecomastia ( Figure 6.22 ). Confirmation of  the diagnosis is obtained by a skin smear or skin biopsy , which shows the classical histological and microbiological features . Summary box 6.13 Leprosy: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF
Typical clinical features and awareness of the disease should
help to make a diagnosis
The face has an aged look, with collapse of the nasal bridge
and ocular changes
Thickened peripheral nerves, patches of anaesthetic skin, claw
hands, foot drop and trophic ulcers are characteristic
Microbiological examination of the acid-fast bacillus and typical
histology on skin biopsy are con
/f_i
rmatory
Clinical features and diagnosis
The disease is slowly progressive and a ff ects the skin, upper respiratory tract and peripheral nerves. In tuberculoid leprosy , the damage to tissues occurs early and is localised to one part of  the body , with limited deformity of  that organ. Neural involvement is characterised by thickening of  the nerves, which are tender. There may be asymmetrical well-defined anaesthetic hypopigmented or erythematous macules with elevated edges and a dry and rough surface – lesions called leprids. In lepromatous leprosy , the disease is symmetrical and extensive. Cutaneous involvement occurs in the form of  several pale macules that form plaques and nodules called lepromas. The deformities produced are divided into primary , which are caused by leprosy or its reactions, and secondary , resulting from e ff ects such as anaesthesia of  the hands and feet. Nodu lar lesions on the face in the acute phase of  the lepromatous variety are known as ‘leonine facies’ (looking like a lion). Later, there is wrinkling of  the skin, giving an aged appearance to a Gerhard Domagk , 1895–1964, German physician, Lecturer in Pathologic Anatomy , University of  Munster, Germany , discovered prontosil in 1935, for which he was awarded the Nobel Prize in Physiology or Medicine in 1939. of  the lateral cartilages and septum of  the nose with collapse of the nasal bridge and lifting of  the tip of  the nose ( Figure 6.17 ). There may be paralysis of  the branches of  the facial nerve in the bony canal or of the zygomatic branch. Blindness may be - attrib uted to exposure keratitis or iridocyclitis. Paralysis of  the orbicularis oculi causes incomplete closure of the eye, epiphora and conjunctivitis ( Figure 6.18 ). The hands are typically clawed - ( Figure 6.19 ) because of involvement of  the ulnar nerve at the - elbow and the median nerve at the wrist. Anaesthesia of  the hands makes these patients vulnerable to frequent burns and injuries. Similarly , clawing of  the toes ( Figure 6.20 ) occurs as a result of  involvement of  the posterior tibial nerve. When the lateral popliteal nerve is a ff ected, it leads to foot drop, and the nerve can be felt to be thickened behind the upper end of the fibula. Anaesthesia of  the feet predisposes to trophic ulceration ( Figure 6.21 ), chronic infection, contraction and autoamputa - tion. Involvement of  the testes causes atrophy , which in turn results in gynaecomastia ( Figure 6.22 ). Confirmation of  the diagnosis is obtained by a skin smear or skin biopsy , which shows the classical histological and microbiological features . Summary box 6.13 Leprosy: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF
Typical clinical features and awareness of the disease should
help to make a diagnosis
The face has an aged look, with collapse of the nasal bridge
and ocular changes
Thickened peripheral nerves, patches of anaesthetic skin, claw
hands, foot drop and trophic ulcers are characteristic
Microbiological examination of the acid-fast bacillus and typical
histology on skin biopsy are con
/f_i
rmatory

Clinical features
Clinical features
The typical patient with an amoebic liver abscess is a young adult male with a history of  insidious onset of  non-specific symptoms, such as abdominal pain, anorexia, fever, night sweats, malaise, cough and weight loss. These symptoms gradually progress to more specific symptoms of  pain in the right upper abdomen and right shoulder tip, hiccoughs and a non-productive cough. A past history of  bloody diarrhoea or travel to an endemic area raises the index of  suspicion. Examination reveals a patient who is toxic and anaemic. The patient will have upper abdominal rigidity , tender hepato megaly , often with tender and bulging intercostal spaces and overlying skin oedema, a pleural e ff usion and basal pneumo nitis – the last fea ture is usually a late manifestation. Occasion ally , a tinge of  jaundice or ascites may be present. Rarely , the patient ma y present as an emergency owing to the e ff ects of rupture of  an abscess into the peritoneal, pleural or pericardial cavity . Clinical features
The larval stage in the lungs causes pulmonary symptoms – dry cough, chest pain, dyspnoea and fever – referred to as Loef fler’s syndrome. The adult worm can grow up to 45 cm long. Wilhelm Loe ffl er , 1887–1972, Professor of  Medicine, Zurich, Switzerland. Jean Martin Charcot , 1825–1893, French neurologist and Professor of  Pathology at Hôpital Universitaire la Pitié-Salpêtrière, Paris, France. Ernst von Leyden , 1832–1910, Professor of  Medicine, Berlin, Germany . to thrive, particularly in children, and abdominal pain. Worms that migrate into the common bile duct can produce ascending cholangitis and obstructive jaundice, while features of acute pancreatitis may be caused by a worm in the pancreatic duct. Small intestinal obstruction can occur, particularly in chil - dren, owing to a bolus of  adult worms incarcerated in the ter - minal ileum. This is a surgical emergency . Rarely , perforation of  the small bowel may occur from ischaemic pressure necrosis from the bolus of  worms. A high index of  suspicion is necessar y so as not to miss the diagnosis. If  a person from a tropical country , or one who has recently returned after spending some time in an endemic area, presents with pulmonary , gastr ointestinal, hepatobiliary and pancreatic symptoms, ascariasis should be high on the list of  possible diagnoses. Clinical features
As the parasite can colonise virtually every organ in the body , the condition can be protean in its presentation. When a sheep farmer who is otherwise healthy complains of  a gradually enlarging painful mass in the right upper quadrant with the physical findings of  a liver swelling, a hydatid liver cyst should be considered. The liver is the organ most often a ff ected. The lung is the next most common. The parasite can a ff ect any organ ( Figures 6.10 and 6.11 ) or several organs in the same patient ( Figure 6.12 ). The disease may be asymptomatic and discovered coin cidentally at postmortem or w hen an ultrasonography or CT scan is done for some other condition. Symptomatic dis ease presents with a swelling causing pressure e ff ects. Thus, a hepatic lesion causes dull pain from str etching of the liver capsule, and a pulmonar y lesion, if  large enough, causes dys pnoea. Daughter cysts may communicate with the biliary tree, causing obstructive jaundice and all the usual clinical features associated with it in addition to symptoms attributable to a parasitic infestation ( Figure 6.13 ) . Features of  raised intracra nial pr essure or unexplained headaches in a patient from a sheep-rearing community should raise the suspicion of  a cere bral hydatid cyst. The patient may present as an emergency with severe abdominal pain f ollowing minor trauma, when the CT scan may be diagnostic ( Figure 6.14 ). Rarely , a patient may present as an emergency with features of anaphylactic shock without any obvious cause. Such a patient may subsequently cough up white material that contains scolices that have travelled into the - - tracheobronchial tree from rupture of  a hepatic hydatid on the diaphragmatic surface of  the liver. -
TABLE 6.1
Classi
/f_i
cation of hepatic hydatid cyst
Stage
Description
CL (cystic lesion)
Unilocular anechoic cystic lesion without internal echoes or septations
CE (cystic echinococcosis) 1
Uniformly anechoic cyst with
/f_i
ne internal echoes that represent protoscolices after rupture of a
vesicle, called ‘hydatid sand’
CE 2
Cyst with internal septation representing the walls of the daughter cyst described as multivesicular,
honeycomb, cartwheel or rosette formation
3A: daughter cysts with detached laminated membrane
CE 3
(transitional stage) description of
3B- daughter cysts inside a solid matrix
daughter cyst
CE 4
Daughter cysts can no longer be seen
(inactive/degenerative)
Mixture of hypoechoic and hyperechoic features – like a bag of wool
CE 5
Calci
/f_i
cation of the wall; either partial or complete
(inactive/degenerative)
Figure 6.10
Computed tomographic scan showing a hydatid cyst of
the pancreas. A differential diagnosis of hydatid cyst or a tumour was
considered. At exploration, the patient was found to have a hydatid
cyst, which was excised. This was followed by 30 months of treatment
with albendazole. The patient remains free of disease.
Clinical features
Patients present electively with weight loss, chronic cough, malaise, evening rise in temperature with sweating, vague abdominal pain with distension and alternating constipation and diarrhoea. As an emergency , they present with features of distal small bowel obstruction from strictures of  the small bowel, particularly the terminal ileum. Rarely , a patient may present with features of  peritonitis from perforation of  a tuber - culous ulcer in the small bowel ( Figure 6.37 ) . Examination shows a chronically ill patient with a ‘doughy’ feel to the abdomen from areas of localised ascites. In the a mass may be felt in the right iliac fossa. In hyperplastic type, in - ano , which addition, some patients may present with fistula- is typically multiple with undermined edges and watery dis - charge. As this is a disease mainly seen in certain resource-poor countries, patients may present late as an emergency from intestinal obstruction. Abdominal pain and distension, consti pation and bilious and faeculent vomiting are typical of  such a patient, who is usually in extremis. There may be involvement of  other systems, such as the genitourinary tract, when the patient complains of  frequency of  micturition. Clinical examination does not show any abnor mality . The genitourinary tract should then be investigated. Summary box 6.24 Tuberculosis: clinical features /uni25CF /uni25CF /uni25CF /uni25CF
Stricture in the
terminal ileum
Perforation in the
terminal ileum
Figure 6.37
Emergency limited ileocolic resection: specimen showing
a tuberculous stricture in the terminal ileum and perforation of a trans
verse ulcer just proximal to the stricture.
Intestinal tuberculosis should be suspected in any patient
from an endemic area who presents with weight loss, malaise,
evening fever, cough, alternating constipation and diarrhoea
and intermittent abdominal pain with distension
The abdomen has a doughy feel; a mass may be found in the
right iliac fossa
The emergency patient presents with features of distal small
bowel obstruction – abdominal pain, distension, bilious and
faeculent vomiting
Peritonitis from a perforated tuberculous ulcer in the small
bowel can be another emergency presentation, though rare
Clinical features
The typical patient with an amoebic liver abscess is a young adult male with a history of  insidious onset of  non-specific symptoms, such as abdominal pain, anorexia, fever, night sweats, malaise, cough and weight loss. These symptoms gradually progress to more specific symptoms of  pain in the right upper abdomen and right shoulder tip, hiccoughs and a non-productive cough. A past history of  bloody diarrhoea or travel to an endemic area raises the index of  suspicion. Examination reveals a patient who is toxic and anaemic. The patient will have upper abdominal rigidity , tender hepato megaly , often with tender and bulging intercostal spaces and overlying skin oedema, a pleural e ff usion and basal pneumo nitis – the last fea ture is usually a late manifestation. Occasion ally , a tinge of  jaundice or ascites may be present. Rarely , the patient ma y present as an emergency owing to the e ff ects of rupture of  an abscess into the peritoneal, pleural or pericardial cavity . Clinical features
The larval stage in the lungs causes pulmonary symptoms – dry cough, chest pain, dyspnoea and fever – referred to as Loef fler’s syndrome. The adult worm can grow up to 45 cm long. Wilhelm Loe ffl er , 1887–1972, Professor of  Medicine, Zurich, Switzerland. Jean Martin Charcot , 1825–1893, French neurologist and Professor of  Pathology at Hôpital Universitaire la Pitié-Salpêtrière, Paris, France. Ernst von Leyden , 1832–1910, Professor of  Medicine, Berlin, Germany . to thrive, particularly in children, and abdominal pain. Worms that migrate into the common bile duct can produce ascending cholangitis and obstructive jaundice, while features of acute pancreatitis may be caused by a worm in the pancreatic duct. Small intestinal obstruction can occur, particularly in chil - dren, owing to a bolus of  adult worms incarcerated in the ter - minal ileum. This is a surgical emergency . Rarely , perforation of  the small bowel may occur from ischaemic pressure necrosis from the bolus of  worms. A high index of  suspicion is necessar y so as not to miss the diagnosis. If  a person from a tropical country , or one who has recently returned after spending some time in an endemic area, presents with pulmonary , gastr ointestinal, hepatobiliary and pancreatic symptoms, ascariasis should be high on the list of  possible diagnoses. Clinical features
As the parasite can colonise virtually every organ in the body , the condition can be protean in its presentation. When a sheep farmer who is otherwise healthy complains of  a gradually enlarging painful mass in the right upper quadrant with the physical findings of  a liver swelling, a hydatid liver cyst should be considered. The liver is the organ most often a ff ected. The lung is the next most common. The parasite can a ff ect any organ ( Figures 6.10 and 6.11 ) or several organs in the same patient ( Figure 6.12 ). The disease may be asymptomatic and discovered coin cidentally at postmortem or w hen an ultrasonography or CT scan is done for some other condition. Symptomatic dis ease presents with a swelling causing pressure e ff ects. Thus, a hepatic lesion causes dull pain from str etching of the liver capsule, and a pulmonar y lesion, if  large enough, causes dys pnoea. Daughter cysts may communicate with the biliary tree, causing obstructive jaundice and all the usual clinical features associated with it in addition to symptoms attributable to a parasitic infestation ( Figure 6.13 ) . Features of  raised intracra nial pr essure or unexplained headaches in a patient from a sheep-rearing community should raise the suspicion of  a cere bral hydatid cyst. The patient may present as an emergency with severe abdominal pain f ollowing minor trauma, when the CT scan may be diagnostic ( Figure 6.14 ). Rarely , a patient may present as an emergency with features of anaphylactic shock without any obvious cause. Such a patient may subsequently cough up white material that contains scolices that have travelled into the - - tracheobronchial tree from rupture of  a hepatic hydatid on the diaphragmatic surface of  the liver. -
TABLE 6.1
Classi
/f_i
cation of hepatic hydatid cyst
Stage
Description
CL (cystic lesion)
Unilocular anechoic cystic lesion without internal echoes or septations
CE (cystic echinococcosis) 1
Uniformly anechoic cyst with
/f_i
ne internal echoes that represent protoscolices after rupture of a
vesicle, called ‘hydatid sand’
CE 2
Cyst with internal septation representing the walls of the daughter cyst described as multivesicular,
honeycomb, cartwheel or rosette formation
3A: daughter cysts with detached laminated membrane
CE 3
(transitional stage) description of
3B- daughter cysts inside a solid matrix
daughter cyst
CE 4
Daughter cysts can no longer be seen
(inactive/degenerative)
Mixture of hypoechoic and hyperechoic features – like a bag of wool
CE 5
Calci
/f_i
cation of the wall; either partial or complete
(inactive/degenerative)
Figure 6.10
Computed tomographic scan showing a hydatid cyst of
the pancreas. A differential diagnosis of hydatid cyst or a tumour was
considered. At exploration, the patient was found to have a hydatid
cyst, which was excised. This was followed by 30 months of treatment
with albendazole. The patient remains free of disease.
Clinical features
Patients present electively with weight loss, chronic cough, malaise, evening rise in temperature with sweating, vague abdominal pain with distension and alternating constipation and diarrhoea. As an emergency , they present with features of distal small bowel obstruction from strictures of  the small bowel, particularly the terminal ileum. Rarely , a patient may present with features of  peritonitis from perforation of  a tuber - culous ulcer in the small bowel ( Figure 6.37 ) . Examination shows a chronically ill patient with a ‘doughy’ feel to the abdomen from areas of localised ascites. In the a mass may be felt in the right iliac fossa. In hyperplastic type, in - ano , which addition, some patients may present with fistula- is typically multiple with undermined edges and watery dis - charge. As this is a disease mainly seen in certain resource-poor countries, patients may present late as an emergency from intestinal obstruction. Abdominal pain and distension, consti pation and bilious and faeculent vomiting are typical of  such a patient, who is usually in extremis. There may be involvement of  other systems, such as the genitourinary tract, when the patient complains of  frequency of  micturition. Clinical examination does not show any abnor mality . The genitourinary tract should then be investigated. Summary box 6.24 Tuberculosis: clinical features /uni25CF /uni25CF /uni25CF /uni25CF
Stricture in the
terminal ileum
Perforation in the
terminal ileum
Figure 6.37
Emergency limited ileocolic resection: specimen showing
a tuberculous stricture in the terminal ileum and perforation of a trans
verse ulcer just proximal to the stricture.
Intestinal tuberculosis should be suspected in any patient
from an endemic area who presents with weight loss, malaise,
evening fever, cough, alternating constipation and diarrhoea
and intermittent abdominal pain with distension
The abdomen has a doughy feel; a mass may be found in the
right iliac fossa
The emergency patient presents with features of distal small
bowel obstruction – abdominal pain, distension, bilious and
faeculent vomiting
Peritonitis from a perforated tuberculous ulcer in the small
bowel can be another emergency presentation, though rare
Clinical features
The typical patient with an amoebic liver abscess is a young adult male with a history of  insidious onset of  non-specific symptoms, such as abdominal pain, anorexia, fever, night sweats, malaise, cough and weight loss. These symptoms gradually progress to more specific symptoms of  pain in the right upper abdomen and right shoulder tip, hiccoughs and a non-productive cough. A past history of  bloody diarrhoea or travel to an endemic area raises the index of  suspicion. Examination reveals a patient who is toxic and anaemic. The patient will have upper abdominal rigidity , tender hepato megaly , often with tender and bulging intercostal spaces and overlying skin oedema, a pleural e ff usion and basal pneumo nitis – the last fea ture is usually a late manifestation. Occasion ally , a tinge of  jaundice or ascites may be present. Rarely , the patient ma y present as an emergency owing to the e ff ects of rupture of  an abscess into the peritoneal, pleural or pericardial cavity . Clinical features
The larval stage in the lungs causes pulmonary symptoms – dry cough, chest pain, dyspnoea and fever – referred to as Loef fler’s syndrome. The adult worm can grow up to 45 cm long. Wilhelm Loe ffl er , 1887–1972, Professor of  Medicine, Zurich, Switzerland. Jean Martin Charcot , 1825–1893, French neurologist and Professor of  Pathology at Hôpital Universitaire la Pitié-Salpêtrière, Paris, France. Ernst von Leyden , 1832–1910, Professor of  Medicine, Berlin, Germany . to thrive, particularly in children, and abdominal pain. Worms that migrate into the common bile duct can produce ascending cholangitis and obstructive jaundice, while features of acute pancreatitis may be caused by a worm in the pancreatic duct. Small intestinal obstruction can occur, particularly in chil - dren, owing to a bolus of  adult worms incarcerated in the ter - minal ileum. This is a surgical emergency . Rarely , perforation of  the small bowel may occur from ischaemic pressure necrosis from the bolus of  worms. A high index of  suspicion is necessar y so as not to miss the diagnosis. If  a person from a tropical country , or one who has recently returned after spending some time in an endemic area, presents with pulmonary , gastr ointestinal, hepatobiliary and pancreatic symptoms, ascariasis should be high on the list of  possible diagnoses. Clinical features
As the parasite can colonise virtually every organ in the body , the condition can be protean in its presentation. When a sheep farmer who is otherwise healthy complains of  a gradually enlarging painful mass in the right upper quadrant with the physical findings of  a liver swelling, a hydatid liver cyst should be considered. The liver is the organ most often a ff ected. The lung is the next most common. The parasite can a ff ect any organ ( Figures 6.10 and 6.11 ) or several organs in the same patient ( Figure 6.12 ). The disease may be asymptomatic and discovered coin cidentally at postmortem or w hen an ultrasonography or CT scan is done for some other condition. Symptomatic dis ease presents with a swelling causing pressure e ff ects. Thus, a hepatic lesion causes dull pain from str etching of the liver capsule, and a pulmonar y lesion, if  large enough, causes dys pnoea. Daughter cysts may communicate with the biliary tree, causing obstructive jaundice and all the usual clinical features associated with it in addition to symptoms attributable to a parasitic infestation ( Figure 6.13 ) . Features of  raised intracra nial pr essure or unexplained headaches in a patient from a sheep-rearing community should raise the suspicion of  a cere bral hydatid cyst. The patient may present as an emergency with severe abdominal pain f ollowing minor trauma, when the CT scan may be diagnostic ( Figure 6.14 ). Rarely , a patient may present as an emergency with features of anaphylactic shock without any obvious cause. Such a patient may subsequently cough up white material that contains scolices that have travelled into the - - tracheobronchial tree from rupture of  a hepatic hydatid on the diaphragmatic surface of  the liver. -
TABLE 6.1
Classi
/f_i
cation of hepatic hydatid cyst
Stage
Description
CL (cystic lesion)
Unilocular anechoic cystic lesion without internal echoes or septations
CE (cystic echinococcosis) 1
Uniformly anechoic cyst with
/f_i
ne internal echoes that represent protoscolices after rupture of a
vesicle, called ‘hydatid sand’
CE 2
Cyst with internal septation representing the walls of the daughter cyst described as multivesicular,
honeycomb, cartwheel or rosette formation
3A: daughter cysts with detached laminated membrane
CE 3
(transitional stage) description of
3B- daughter cysts inside a solid matrix
daughter cyst
CE 4
Daughter cysts can no longer be seen
(inactive/degenerative)
Mixture of hypoechoic and hyperechoic features – like a bag of wool
CE 5
Calci
/f_i
cation of the wall; either partial or complete
(inactive/degenerative)
Figure 6.10
Computed tomographic scan showing a hydatid cyst of
the pancreas. A differential diagnosis of hydatid cyst or a tumour was
considered. At exploration, the patient was found to have a hydatid
cyst, which was excised. This was followed by 30 months of treatment
with albendazole. The patient remains free of disease.
Clinical features
Patients present electively with weight loss, chronic cough, malaise, evening rise in temperature with sweating, vague abdominal pain with distension and alternating constipation and diarrhoea. As an emergency , they present with features of distal small bowel obstruction from strictures of  the small bowel, particularly the terminal ileum. Rarely , a patient may present with features of  peritonitis from perforation of  a tuber - culous ulcer in the small bowel ( Figure 6.37 ) . Examination shows a chronically ill patient with a ‘doughy’ feel to the abdomen from areas of localised ascites. In the a mass may be felt in the right iliac fossa. In hyperplastic type, in - ano , which addition, some patients may present with fistula- is typically multiple with undermined edges and watery dis - charge. As this is a disease mainly seen in certain resource-poor countries, patients may present late as an emergency from intestinal obstruction. Abdominal pain and distension, consti pation and bilious and faeculent vomiting are typical of  such a patient, who is usually in extremis. There may be involvement of  other systems, such as the genitourinary tract, when the patient complains of  frequency of  micturition. Clinical examination does not show any abnor mality . The genitourinary tract should then be investigated. Summary box 6.24 Tuberculosis: clinical features /uni25CF /uni25CF /uni25CF /uni25CF
Stricture in the
terminal ileum
Perforation in the
terminal ileum
Figure 6.37
Emergency limited ileocolic resection: specimen showing
a tuberculous stricture in the terminal ileum and perforation of a trans
verse ulcer just proximal to the stricture.
Intestinal tuberculosis should be suspected in any patient
from an endemic area who presents with weight loss, malaise,
evening fever, cough, alternating constipation and diarrhoea
and intermittent abdominal pain with distension
The abdomen has a doughy feel; a mass may be found in the
right iliac fossa
The emergency patient presents with features of distal small
bowel obstruction – abdominal pain, distension, bilious and
faeculent vomiting
Peritonitis from a perforated tuberculous ulcer in the small
bowel can be another emergency presentation, though rare

Clinical presentation
Clinical presentation
As mycetoma is painless, presentation is late in the majority . It presents as a slowly progressive, painless, subcutaneous swell ing commonly at the site of  presumed trauma. The swelling is variable in its physical characteristics: firm and rounded, soft and lobulated, rarely cystic and often mobile . Multiple secondary nodules may evolve; they may suppurate and drain through multiple sinus tracts. The sinuses may close transiently after discharge during the active phase of  the disease. Fresh adjacent sinuses may open while some of  the old ones may heal completely . They coalesce and form abscesses, the discharge being serous, serosanguineous or purulent. During the active phase of the disease the sinuses discharge grains, the colour of which can be black, yellow , white or red depending upon the organism. Pain supervenes when there is secondary bacterial infection. The common sites a ff ected are those that come into contact with soil during daily activities: the foot in 70% ( Figure 6.23 and the hand in 12% ( Figure 6.24 ). In endemic areas the knee ( Figure 6.25 ), arm, leg, head and neck ( Figure 6.26 and perineum ( Figure 6.27 ) can be involved. Rare sites are the chest, abdominal wall, facial bones, mandible, testes, paranasal sinuses and eye. In some patients there may be areas of  local hyperhidrosis over the lesion. This may be due to sympathetic o veractivity or increased local temperature due to raised arterial blood flow caused by the chronic inflammation. In the majority of  patients, the regional lymph nodes are small and shotty . Lymphadenopathy is common. This may be due to secondary bacterial infection, lymphatic spread of  mycetoma or a local immune response to the disease. The condition remains localised; constitutional distur bances are a sign of  secondary bacterial infection. Cachexia and anaemia from malnutrition and sepsis may be seen in late cases. It can be fatal, especially in cases of  cranial mycetoma. - - - - ) ), thigh -
Figure 6.24
Mycetoma of the hand.
Figure 6.25
Mycetoma of the knee.
Figure 6.26
Actinomycetoma of the head and neck.
Figure 6.27
Extensive satellite inguinal actinomycetoma from a pri
mary foot lesion involving the anterior abdominal wall and perineum.
Clinical presentation
As mycetoma is painless, presentation is late in the majority . It presents as a slowly progressive, painless, subcutaneous swell ing commonly at the site of  presumed trauma. The swelling is variable in its physical characteristics: firm and rounded, soft and lobulated, rarely cystic and often mobile . Multiple secondary nodules may evolve; they may suppurate and drain through multiple sinus tracts. The sinuses may close transiently after discharge during the active phase of  the disease. Fresh adjacent sinuses may open while some of  the old ones may heal completely . They coalesce and form abscesses, the discharge being serous, serosanguineous or purulent. During the active phase of the disease the sinuses discharge grains, the colour of which can be black, yellow , white or red depending upon the organism. Pain supervenes when there is secondary bacterial infection. The common sites a ff ected are those that come into contact with soil during daily activities: the foot in 70% ( Figure 6.23 and the hand in 12% ( Figure 6.24 ). In endemic areas the knee ( Figure 6.25 ), arm, leg, head and neck ( Figure 6.26 and perineum ( Figure 6.27 ) can be involved. Rare sites are the chest, abdominal wall, facial bones, mandible, testes, paranasal sinuses and eye. In some patients there may be areas of  local hyperhidrosis over the lesion. This may be due to sympathetic o veractivity or increased local temperature due to raised arterial blood flow caused by the chronic inflammation. In the majority of  patients, the regional lymph nodes are small and shotty . Lymphadenopathy is common. This may be due to secondary bacterial infection, lymphatic spread of  mycetoma or a local immune response to the disease. The condition remains localised; constitutional distur bances are a sign of  secondary bacterial infection. Cachexia and anaemia from malnutrition and sepsis may be seen in late cases. It can be fatal, especially in cases of  cranial mycetoma. - - - - ) ), thigh -
Figure 6.24
Mycetoma of the hand.
Figure 6.25
Mycetoma of the knee.
Figure 6.26
Actinomycetoma of the head and neck.
Figure 6.27
Extensive satellite inguinal actinomycetoma from a pri
mary foot lesion involving the anterior abdominal wall and perineum.
Clinical presentation
As mycetoma is painless, presentation is late in the majority . It presents as a slowly progressive, painless, subcutaneous swell ing commonly at the site of  presumed trauma. The swelling is variable in its physical characteristics: firm and rounded, soft and lobulated, rarely cystic and often mobile . Multiple secondary nodules may evolve; they may suppurate and drain through multiple sinus tracts. The sinuses may close transiently after discharge during the active phase of  the disease. Fresh adjacent sinuses may open while some of  the old ones may heal completely . They coalesce and form abscesses, the discharge being serous, serosanguineous or purulent. During the active phase of the disease the sinuses discharge grains, the colour of which can be black, yellow , white or red depending upon the organism. Pain supervenes when there is secondary bacterial infection. The common sites a ff ected are those that come into contact with soil during daily activities: the foot in 70% ( Figure 6.23 and the hand in 12% ( Figure 6.24 ). In endemic areas the knee ( Figure 6.25 ), arm, leg, head and neck ( Figure 6.26 and perineum ( Figure 6.27 ) can be involved. Rare sites are the chest, abdominal wall, facial bones, mandible, testes, paranasal sinuses and eye. In some patients there may be areas of  local hyperhidrosis over the lesion. This may be due to sympathetic o veractivity or increased local temperature due to raised arterial blood flow caused by the chronic inflammation. In the majority of  patients, the regional lymph nodes are small and shotty . Lymphadenopathy is common. This may be due to secondary bacterial infection, lymphatic spread of  mycetoma or a local immune response to the disease. The condition remains localised; constitutional distur bances are a sign of  secondary bacterial infection. Cachexia and anaemia from malnutrition and sepsis may be seen in late cases. It can be fatal, especially in cases of  cranial mycetoma. - - - - ) ), thigh -
Figure 6.24
Mycetoma of the hand.
Figure 6.25
Mycetoma of the knee.
Figure 6.26
Actinomycetoma of the head and neck.
Figure 6.27
Extensive satellite inguinal actinomycetoma from a pri
mary foot lesion involving the anterior abdominal wall and perineum.

Culture
Culture
A variety of microorganisms are capable of producing myce - tomata that can be identified by their textural description, morphology and biological activities in pure culture. Deep surgical biopsy is always needed to obtain the grains that are the source of  culture. T he grains extracted through the sinuses are usually contaminated and not viable and hence should be avoided. Several media may be used to isolate and grow these organisms. In the absence of  the classical triad of  mycetoma, the demonstration of  significant antibody titres against the caus - ative organism may be of  diagnostic value and aid follow up. T he common serodiagnostic tests are immunoelectrophoresis and ELISA. Summary box 6.16 Mycetoma: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Usually presents late as it is painless
Triad of painless subcutaneous mass, multiple sinuses and
seropurulent discharge
Clinical picture may be deceptive as there may be deep-seated
extension
May spread to lymph nodes
Can be confused with Kaposi’s sarcoma
Radiologically can be mistaken for osteosarcoma
MRI shows typical ‘dot-in-circle’ sign
Open biopsy and FNAC are con
/f_i
rmatory
Ideally this should be a combined e ff ort between the physician and the surgeon. In actinomycetoma, combined drug therapy with amikacin sulphate and co-trimoxazole in the form of cycles is the treatment of  choice. Amoxicillin–clavulanic acid, rifampicin, sulphonamides, gentamicin and kanamycin are used as a second line of  treatment. Long-term drug treatment can have serious side e ff ects. In eumycetoma, ketoconazole, itraconazole and voriconazole are the drugs of  choice. They may need to be used for up to a year. Use of  these drugs should be closely monitored for side e ff ects. While not cura tive, these drugs help to localise the disease by forming thickly encapsulated lesions that are then amenable to surgical excision. Medical treatment for both types of  mycetoma must continue until the patient is cured and also in the postoperative period. Culture
A variety of microorganisms are capable of producing myce - tomata that can be identified by their textural description, morphology and biological activities in pure culture. Deep surgical biopsy is always needed to obtain the grains that are the source of  culture. T he grains extracted through the sinuses are usually contaminated and not viable and hence should be avoided. Several media may be used to isolate and grow these organisms. In the absence of  the classical triad of  mycetoma, the demonstration of  significant antibody titres against the caus - ative organism may be of  diagnostic value and aid follow up. T he common serodiagnostic tests are immunoelectrophoresis and ELISA. Summary box 6.16 Mycetoma: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Usually presents late as it is painless
Triad of painless subcutaneous mass, multiple sinuses and
seropurulent discharge
Clinical picture may be deceptive as there may be deep-seated
extension
May spread to lymph nodes
Can be confused with Kaposi’s sarcoma
Radiologically can be mistaken for osteosarcoma
MRI shows typical ‘dot-in-circle’ sign
Open biopsy and FNAC are con
/f_i
rmatory
Ideally this should be a combined e ff ort between the physician and the surgeon. In actinomycetoma, combined drug therapy with amikacin sulphate and co-trimoxazole in the form of cycles is the treatment of  choice. Amoxicillin–clavulanic acid, rifampicin, sulphonamides, gentamicin and kanamycin are used as a second line of  treatment. Long-term drug treatment can have serious side e ff ects. In eumycetoma, ketoconazole, itraconazole and voriconazole are the drugs of  choice. They may need to be used for up to a year. Use of  these drugs should be closely monitored for side e ff ects. While not cura tive, these drugs help to localise the disease by forming thickly encapsulated lesions that are then amenable to surgical excision. Medical treatment for both types of  mycetoma must continue until the patient is cured and also in the postoperative period. Culture
A variety of microorganisms are capable of producing myce - tomata that can be identified by their textural description, morphology and biological activities in pure culture. Deep surgical biopsy is always needed to obtain the grains that are the source of  culture. T he grains extracted through the sinuses are usually contaminated and not viable and hence should be avoided. Several media may be used to isolate and grow these organisms. In the absence of  the classical triad of  mycetoma, the demonstration of  significant antibody titres against the caus - ative organism may be of  diagnostic value and aid follow up. T he common serodiagnostic tests are immunoelectrophoresis and ELISA. Summary box 6.16 Mycetoma: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Usually presents late as it is painless
Triad of painless subcutaneous mass, multiple sinuses and
seropurulent discharge
Clinical picture may be deceptive as there may be deep-seated
extension
May spread to lymph nodes
Can be confused with Kaposi’s sarcoma
Radiologically can be mistaken for osteosarcoma
MRI shows typical ‘dot-in-circle’ sign
Open biopsy and FNAC are con
/f_i
rmatory
Ideally this should be a combined e ff ort between the physician and the surgeon. In actinomycetoma, combined drug therapy with amikacin sulphate and co-trimoxazole in the form of cycles is the treatment of  choice. Amoxicillin–clavulanic acid, rifampicin, sulphonamides, gentamicin and kanamycin are used as a second line of  treatment. Long-term drug treatment can have serious side e ff ects. In eumycetoma, ketoconazole, itraconazole and voriconazole are the drugs of  choice. They may need to be used for up to a year. Use of  these drugs should be closely monitored for side e ff ects. While not cura tive, these drugs help to localise the disease by forming thickly encapsulated lesions that are then amenable to surgical excision. Medical treatment for both types of  mycetoma must continue until the patient is cured and also in the postoperative period.

Diagnosis
Diagnosis
The disease may remain dormant for many years. Clinical features are non-specific and include fever, malaise, anorexia and upper abdominal discomfort. The complete clinical picture can consist of  fever with rigors due to ascending cholangitis, the common bile duct. Acute pancreatitis may occur because of  obstruction of  the pancreatic duct by an adult worm. Particularly when presenting in non-endemic areas, it should be noted that if  a person from an endemic area complains of symptoms of  biliary tract disease, Clonorchis infestation should be high in the di ff erential diagnosis. In advanced cases, liver function tests are abnormal. Confirmation of  the condition is by examination of  stool or duodenal aspirate, which may sho w the eggs or adult worms. Ultrasonography findings may be characteristic, showing uni form dilatation of  small peripheral intrahepatic bile ducts with only minimal dilatation of  the common hepatic and common bile ducts, although the latter are much more dilated when the obstruction is caused by stones. The thickened duct walls sho increased echogenicity and non-shadowing echogenic foci in the bile ducts, representing the worms or eggs. ERCP will con firm these findings. Summary box 6.6 Asiatic cholangiohepatitis: pathogenesis and diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Occurs in Far Eastern tropical zones
The causative parasite is
Clonorchis sinensis
,
Opisthorchis
Fasciola
Produces bile duct hyperplasia, intrahepatic duct dilatation and
stones
Increases the risk of cholangiocarcinoma
May remain dormant for many years
When active, there are biliary tract symptoms in a generally
unwell patient
Stool examination for eggs or worms is diagnostic
Ultrasonography of the hepatobiliary system and ERCP is also
diagnostic
Diagnosis
It is mainly males who are a ff ected because females generally cover a greater part of  their bodies with clothing, thus making them less prone to mosquito bites. In the acute presentation, there are episodic attacks of  fever with lymphadenitis and lymphangitis. - Occasionally , adult worms may be felt subcutaneously . Chronic manifestations appear after repeated acute attacks - over several years. The adult worms cause lympha tic obstruc - tion, resulting in massive lower limb oedema. Obstruction to the cutaneous lymphatics causes skin thickening, not unlike the peau d’orange appearance in breast cancer, thus exacerbating the limb swelling. Secondary streptococcal infection is common. Recurrent attacks of  lymphangitis cause fibrosis of  the lymph channels, resulting in a grossly swollen limb with thickened skin, producing the condition of elephantiasis ( Figure 6.8 ). Bilateral lower limb filariasis is often associated with scrotal and penile elephantiasis. Early on, there may be a hydrocele underlying scrotal filariasis ( Figure 6.9 ). Chyluria and chylous ascites may occur. A mild form of the disease can a ff ect the respiratory tract, causing dry cough, and is referred to as tropical pulmonary eosinophilia. The con dition of  filariasis is clinically very obvious, and thus investi gations in the full-blown case are superfluous. Eosinophilia is common and a nocturnal peripheral blood smear may show the immature forms, or microfilariae. The parasite may also be seen in chylous urine, ascites and h ydrocele fluid.
Figure 6.8
Left lower limb
/f_i
lariasis – elephantiasis (courtesy of Profes
sor Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).
Diagnosis
There should be a high index of  suspicion. Investigations show a raised eosinophil count; serological tests, such as ELISA and immunoelectrophoresis, point towards the diagnosis. Ultra - - sonography and CT scan are the investigations of  choice. The CT scan shows a smooth space-occupying lesion with - several septa. Ultrasonography of  the biliary tract may show abnormality in the gallbladder and bile ducts, when h ydatid infestation of  the biliary system should be suspected. An MRCP may even show multiple cysts communicating with the biliary tree ( Figure 6.13 ). Ultimately , the diagnosis is made by a combination of  good history and clinical examination supplemented by serology and imaging. Summary box 6.9 Hydatid disease: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.11
Anteroposterior
(a)
and lateral
(b)
views of computed tomographic scans showing a large hydatid cyst of the right adrenal gland. The
patient presented with a mass in the right loin and underwent an adrenalectomy (courtesy of Dr PP Bhattacharyya, Kolkata, India).
In the UK, the usual sufferer is a sheep farmer
While any organ may be involved, the liver is by far the most
commonly affected
Elective clinical presentation is usually in the form of a painful
lump arising from the liver
Anaphylactic shock due to rupture of the hydatid cyst is the
emergency presentation
CT scan is the best imaging technique – the diagnostic feature
is a space-occupying lesion with a smooth outline with septa
Figure 6.12
Computed tomographic scan showing disseminated
hydatid cysts of the abdomen. The patient was started on albendazole
but was lost to follow-up (courtesy of Dr PP Bhattacharyya, Kolkata,
India).
Diagnosis
The disease targets the anterior horn cells, causing lower motor neurone paralysis. Muscles of  the lower limb are a ff ected twice as frequently as those of  the upper limb ( Figures 6.30 and 6.31 ). Fortunately , only 1–2% of su ff erers develop paralytic symptoms but, when they do occur, the disability causes much misery ( Figure 6.32 ). When a patient develops fe ver with muscle weakness, Guillain–Barré syndrome needs to be excluded. The latter has sensory symptoms and signs. Cerebrospinal fluid analysis should help to di ff erentiate the two conditions. Diagnosis
The patient, usually male, is almost always below the age of 40 years and from a poor socioeconomic background. The clinical presentation is abdominal pain, thirst, polyuria and features of  gross pancreatic insu ffi ciency causing steatorrhoea and malnutrition. The patient looks ill and emaciated. Initial routine blood and urine tests confirm that the patient has type 1 diabetes mellitus. This is known as fibro calculous pancreatic diabetes, a label that is aptly descriptive of  the typical pathological changes. Serum amylase is usually nor mal; in an acute exacerbation, it may be elevated. A plain abdominal radiograph shows typical pancreatic calcifica in the form of  discrete stones in the duct ( Figure 6.33 ). Ultra sonography and CT scanning of  the pancreas confirm the diagnosis. An ERCP , as an investigation, should only be done when the procedure is also being considered as a therapeutic manoeuvre for removal of ductal stones in the pancreatic head by papillotomy . Diagnosis of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.33
Plain radiograph of the abdomen showing large stones
along the main pancreatic duct typical of tropical chronic pancreatitis
(courtesy of Dr V Mohan, Chennai, India).
The usual sufferer is a type 1 diabetic under 40 years of age
Serum amylase may be elevated in an acute exacerbation
Plain radiograph shows stones along the pancreatic duct
Ultrasonography and CT scan of the pancreas con
/f_i
rm the
diagnosis
ERCP should be used as an investigation only when combined
with a therapeutic procedure
Diagnosis
Any of  the cervical group of  lymph nodes (jugulodigastric, submandibular, supraclavicular, posterior triangle) can be involved. The patient has the usual general manifestations of tuberculosis: evening pyrexia, cough (maybe from pulmonary tuberculosis) and malaise; if  the su ff erer is a child, failure to thrive is a significant finding. Locally there will be regional lymphadenopathy where the lymph nodes may be matted; in late stages a cold abscess may form – a painless, fluctuant, mass which is not warm; significantly there are no signs of inflammation ( Figure 6.34 ), hence it is called a ‘cold abscess’. This is a clinical manifestation of  underlying caseation. Left untreated, the cold abscess, initially deep to the deep fascia, bursts through into the space just beneath the superficial fascia. This produces a bilocular mass with cr oss-fluctuation. This is called a ‘collar-stud’ abscess. Eventually this may burst thr ough the skin, discharging pus and forming a tuberculous sinus and eventually might ulcerate ( Figure 6.35 ) . The latter typically has watery discharge with undermined edges as the tubercle bacilli destroy the subcutaneous tissue faster than the rest and thrive in the relatively anoxic environment. Diagnosis
The disease may remain dormant for many years. Clinical features are non-specific and include fever, malaise, anorexia and upper abdominal discomfort. The complete clinical picture can consist of  fever with rigors due to ascending cholangitis, the common bile duct. Acute pancreatitis may occur because of  obstruction of  the pancreatic duct by an adult worm. Particularly when presenting in non-endemic areas, it should be noted that if  a person from an endemic area complains of symptoms of  biliary tract disease, Clonorchis infestation should be high in the di ff erential diagnosis. In advanced cases, liver function tests are abnormal. Confirmation of  the condition is by examination of  stool or duodenal aspirate, which may sho w the eggs or adult worms. Ultrasonography findings may be characteristic, showing uni form dilatation of  small peripheral intrahepatic bile ducts with only minimal dilatation of  the common hepatic and common bile ducts, although the latter are much more dilated when the obstruction is caused by stones. The thickened duct walls sho increased echogenicity and non-shadowing echogenic foci in the bile ducts, representing the worms or eggs. ERCP will con firm these findings. Summary box 6.6 Asiatic cholangiohepatitis: pathogenesis and diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Occurs in Far Eastern tropical zones
The causative parasite is
Clonorchis sinensis
,
Opisthorchis
Fasciola
Produces bile duct hyperplasia, intrahepatic duct dilatation and
stones
Increases the risk of cholangiocarcinoma
May remain dormant for many years
When active, there are biliary tract symptoms in a generally
unwell patient
Stool examination for eggs or worms is diagnostic
Ultrasonography of the hepatobiliary system and ERCP is also
diagnostic
Diagnosis
It is mainly males who are a ff ected because females generally cover a greater part of  their bodies with clothing, thus making them less prone to mosquito bites. In the acute presentation, there are episodic attacks of  fever with lymphadenitis and lymphangitis. - Occasionally , adult worms may be felt subcutaneously . Chronic manifestations appear after repeated acute attacks - over several years. The adult worms cause lympha tic obstruc - tion, resulting in massive lower limb oedema. Obstruction to the cutaneous lymphatics causes skin thickening, not unlike the peau d’orange appearance in breast cancer, thus exacerbating the limb swelling. Secondary streptococcal infection is common. Recurrent attacks of  lymphangitis cause fibrosis of  the lymph channels, resulting in a grossly swollen limb with thickened skin, producing the condition of elephantiasis ( Figure 6.8 ). Bilateral lower limb filariasis is often associated with scrotal and penile elephantiasis. Early on, there may be a hydrocele underlying scrotal filariasis ( Figure 6.9 ). Chyluria and chylous ascites may occur. A mild form of the disease can a ff ect the respiratory tract, causing dry cough, and is referred to as tropical pulmonary eosinophilia. The con dition of  filariasis is clinically very obvious, and thus investi gations in the full-blown case are superfluous. Eosinophilia is common and a nocturnal peripheral blood smear may show the immature forms, or microfilariae. The parasite may also be seen in chylous urine, ascites and h ydrocele fluid.
Figure 6.8
Left lower limb
/f_i
lariasis – elephantiasis (courtesy of Profes
sor Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).
Diagnosis
There should be a high index of  suspicion. Investigations show a raised eosinophil count; serological tests, such as ELISA and immunoelectrophoresis, point towards the diagnosis. Ultra - - sonography and CT scan are the investigations of  choice. The CT scan shows a smooth space-occupying lesion with - several septa. Ultrasonography of  the biliary tract may show abnormality in the gallbladder and bile ducts, when h ydatid infestation of  the biliary system should be suspected. An MRCP may even show multiple cysts communicating with the biliary tree ( Figure 6.13 ). Ultimately , the diagnosis is made by a combination of  good history and clinical examination supplemented by serology and imaging. Summary box 6.9 Hydatid disease: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.11
Anteroposterior
(a)
and lateral
(b)
views of computed tomographic scans showing a large hydatid cyst of the right adrenal gland. The
patient presented with a mass in the right loin and underwent an adrenalectomy (courtesy of Dr PP Bhattacharyya, Kolkata, India).
In the UK, the usual sufferer is a sheep farmer
While any organ may be involved, the liver is by far the most
commonly affected
Elective clinical presentation is usually in the form of a painful
lump arising from the liver
Anaphylactic shock due to rupture of the hydatid cyst is the
emergency presentation
CT scan is the best imaging technique – the diagnostic feature
is a space-occupying lesion with a smooth outline with septa
Figure 6.12
Computed tomographic scan showing disseminated
hydatid cysts of the abdomen. The patient was started on albendazole
but was lost to follow-up (courtesy of Dr PP Bhattacharyya, Kolkata,
India).
Diagnosis
The disease targets the anterior horn cells, causing lower motor neurone paralysis. Muscles of  the lower limb are a ff ected twice as frequently as those of  the upper limb ( Figures 6.30 and 6.31 ). Fortunately , only 1–2% of su ff erers develop paralytic symptoms but, when they do occur, the disability causes much misery ( Figure 6.32 ). When a patient develops fe ver with muscle weakness, Guillain–Barré syndrome needs to be excluded. The latter has sensory symptoms and signs. Cerebrospinal fluid analysis should help to di ff erentiate the two conditions. Diagnosis
The patient, usually male, is almost always below the age of 40 years and from a poor socioeconomic background. The clinical presentation is abdominal pain, thirst, polyuria and features of  gross pancreatic insu ffi ciency causing steatorrhoea and malnutrition. The patient looks ill and emaciated. Initial routine blood and urine tests confirm that the patient has type 1 diabetes mellitus. This is known as fibro calculous pancreatic diabetes, a label that is aptly descriptive of  the typical pathological changes. Serum amylase is usually nor mal; in an acute exacerbation, it may be elevated. A plain abdominal radiograph shows typical pancreatic calcifica in the form of  discrete stones in the duct ( Figure 6.33 ). Ultra sonography and CT scanning of  the pancreas confirm the diagnosis. An ERCP , as an investigation, should only be done when the procedure is also being considered as a therapeutic manoeuvre for removal of ductal stones in the pancreatic head by papillotomy . Diagnosis of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.33
Plain radiograph of the abdomen showing large stones
along the main pancreatic duct typical of tropical chronic pancreatitis
(courtesy of Dr V Mohan, Chennai, India).
The usual sufferer is a type 1 diabetic under 40 years of age
Serum amylase may be elevated in an acute exacerbation
Plain radiograph shows stones along the pancreatic duct
Ultrasonography and CT scan of the pancreas con
/f_i
rm the
diagnosis
ERCP should be used as an investigation only when combined
with a therapeutic procedure
Diagnosis
Any of  the cervical group of  lymph nodes (jugulodigastric, submandibular, supraclavicular, posterior triangle) can be involved. The patient has the usual general manifestations of tuberculosis: evening pyrexia, cough (maybe from pulmonary tuberculosis) and malaise; if  the su ff erer is a child, failure to thrive is a significant finding. Locally there will be regional lymphadenopathy where the lymph nodes may be matted; in late stages a cold abscess may form – a painless, fluctuant, mass which is not warm; significantly there are no signs of inflammation ( Figure 6.34 ), hence it is called a ‘cold abscess’. This is a clinical manifestation of  underlying caseation. Left untreated, the cold abscess, initially deep to the deep fascia, bursts through into the space just beneath the superficial fascia. This produces a bilocular mass with cr oss-fluctuation. This is called a ‘collar-stud’ abscess. Eventually this may burst thr ough the skin, discharging pus and forming a tuberculous sinus and eventually might ulcerate ( Figure 6.35 ) . The latter typically has watery discharge with undermined edges as the tubercle bacilli destroy the subcutaneous tissue faster than the rest and thrive in the relatively anoxic environment. Diagnosis
The disease may remain dormant for many years. Clinical features are non-specific and include fever, malaise, anorexia and upper abdominal discomfort. The complete clinical picture can consist of  fever with rigors due to ascending cholangitis, the common bile duct. Acute pancreatitis may occur because of  obstruction of  the pancreatic duct by an adult worm. Particularly when presenting in non-endemic areas, it should be noted that if  a person from an endemic area complains of symptoms of  biliary tract disease, Clonorchis infestation should be high in the di ff erential diagnosis. In advanced cases, liver function tests are abnormal. Confirmation of  the condition is by examination of  stool or duodenal aspirate, which may sho w the eggs or adult worms. Ultrasonography findings may be characteristic, showing uni form dilatation of  small peripheral intrahepatic bile ducts with only minimal dilatation of  the common hepatic and common bile ducts, although the latter are much more dilated when the obstruction is caused by stones. The thickened duct walls sho increased echogenicity and non-shadowing echogenic foci in the bile ducts, representing the worms or eggs. ERCP will con firm these findings. Summary box 6.6 Asiatic cholangiohepatitis: pathogenesis and diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Occurs in Far Eastern tropical zones
The causative parasite is
Clonorchis sinensis
,
Opisthorchis
Fasciola
Produces bile duct hyperplasia, intrahepatic duct dilatation and
stones
Increases the risk of cholangiocarcinoma
May remain dormant for many years
When active, there are biliary tract symptoms in a generally
unwell patient
Stool examination for eggs or worms is diagnostic
Ultrasonography of the hepatobiliary system and ERCP is also
diagnostic
Diagnosis
It is mainly males who are a ff ected because females generally cover a greater part of  their bodies with clothing, thus making them less prone to mosquito bites. In the acute presentation, there are episodic attacks of  fever with lymphadenitis and lymphangitis. - Occasionally , adult worms may be felt subcutaneously . Chronic manifestations appear after repeated acute attacks - over several years. The adult worms cause lympha tic obstruc - tion, resulting in massive lower limb oedema. Obstruction to the cutaneous lymphatics causes skin thickening, not unlike the peau d’orange appearance in breast cancer, thus exacerbating the limb swelling. Secondary streptococcal infection is common. Recurrent attacks of  lymphangitis cause fibrosis of  the lymph channels, resulting in a grossly swollen limb with thickened skin, producing the condition of elephantiasis ( Figure 6.8 ). Bilateral lower limb filariasis is often associated with scrotal and penile elephantiasis. Early on, there may be a hydrocele underlying scrotal filariasis ( Figure 6.9 ). Chyluria and chylous ascites may occur. A mild form of the disease can a ff ect the respiratory tract, causing dry cough, and is referred to as tropical pulmonary eosinophilia. The con dition of  filariasis is clinically very obvious, and thus investi gations in the full-blown case are superfluous. Eosinophilia is common and a nocturnal peripheral blood smear may show the immature forms, or microfilariae. The parasite may also be seen in chylous urine, ascites and h ydrocele fluid.
Figure 6.8
Left lower limb
/f_i
lariasis – elephantiasis (courtesy of Profes
sor Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).
Diagnosis
There should be a high index of  suspicion. Investigations show a raised eosinophil count; serological tests, such as ELISA and immunoelectrophoresis, point towards the diagnosis. Ultra - - sonography and CT scan are the investigations of  choice. The CT scan shows a smooth space-occupying lesion with - several septa. Ultrasonography of  the biliary tract may show abnormality in the gallbladder and bile ducts, when h ydatid infestation of  the biliary system should be suspected. An MRCP may even show multiple cysts communicating with the biliary tree ( Figure 6.13 ). Ultimately , the diagnosis is made by a combination of  good history and clinical examination supplemented by serology and imaging. Summary box 6.9 Hydatid disease: diagnosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.11
Anteroposterior
(a)
and lateral
(b)
views of computed tomographic scans showing a large hydatid cyst of the right adrenal gland. The
patient presented with a mass in the right loin and underwent an adrenalectomy (courtesy of Dr PP Bhattacharyya, Kolkata, India).
In the UK, the usual sufferer is a sheep farmer
While any organ may be involved, the liver is by far the most
commonly affected
Elective clinical presentation is usually in the form of a painful
lump arising from the liver
Anaphylactic shock due to rupture of the hydatid cyst is the
emergency presentation
CT scan is the best imaging technique – the diagnostic feature
is a space-occupying lesion with a smooth outline with septa
Figure 6.12
Computed tomographic scan showing disseminated
hydatid cysts of the abdomen. The patient was started on albendazole
but was lost to follow-up (courtesy of Dr PP Bhattacharyya, Kolkata,
India).
Diagnosis
The disease targets the anterior horn cells, causing lower motor neurone paralysis. Muscles of  the lower limb are a ff ected twice as frequently as those of  the upper limb ( Figures 6.30 and 6.31 ). Fortunately , only 1–2% of su ff erers develop paralytic symptoms but, when they do occur, the disability causes much misery ( Figure 6.32 ). When a patient develops fe ver with muscle weakness, Guillain–Barré syndrome needs to be excluded. The latter has sensory symptoms and signs. Cerebrospinal fluid analysis should help to di ff erentiate the two conditions. Diagnosis
The patient, usually male, is almost always below the age of 40 years and from a poor socioeconomic background. The clinical presentation is abdominal pain, thirst, polyuria and features of  gross pancreatic insu ffi ciency causing steatorrhoea and malnutrition. The patient looks ill and emaciated. Initial routine blood and urine tests confirm that the patient has type 1 diabetes mellitus. This is known as fibro calculous pancreatic diabetes, a label that is aptly descriptive of  the typical pathological changes. Serum amylase is usually nor mal; in an acute exacerbation, it may be elevated. A plain abdominal radiograph shows typical pancreatic calcifica in the form of  discrete stones in the duct ( Figure 6.33 ). Ultra sonography and CT scanning of  the pancreas confirm the diagnosis. An ERCP , as an investigation, should only be done when the procedure is also being considered as a therapeutic manoeuvre for removal of ductal stones in the pancreatic head by papillotomy . Diagnosis of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.33
Plain radiograph of the abdomen showing large stones
along the main pancreatic duct typical of tropical chronic pancreatitis
(courtesy of Dr V Mohan, Chennai, India).
The usual sufferer is a type 1 diabetic under 40 years of age
Serum amylase may be elevated in an acute exacerbation
Plain radiograph shows stones along the pancreatic duct
Ultrasonography and CT scan of the pancreas con
/f_i
rm the
diagnosis
ERCP should be used as an investigation only when combined
with a therapeutic procedure
Diagnosis
Any of  the cervical group of  lymph nodes (jugulodigastric, submandibular, supraclavicular, posterior triangle) can be involved. The patient has the usual general manifestations of tuberculosis: evening pyrexia, cough (maybe from pulmonary tuberculosis) and malaise; if  the su ff erer is a child, failure to thrive is a significant finding. Locally there will be regional lymphadenopathy where the lymph nodes may be matted; in late stages a cold abscess may form – a painless, fluctuant, mass which is not warm; significantly there are no signs of inflammation ( Figure 6.34 ), hence it is called a ‘cold abscess’. This is a clinical manifestation of  underlying caseation. Left untreated, the cold abscess, initially deep to the deep fascia, bursts through into the space just beneath the superficial fascia. This produces a bilocular mass with cr oss-fluctuation. This is called a ‘collar-stud’ abscess. Eventually this may burst thr ough the skin, discharging pus and forming a tuberculous sinus and eventually might ulcerate ( Figure 6.35 ) . The latter typically has watery discharge with undermined edges as the tubercle bacilli destroy the subcutaneous tissue faster than the rest and thrive in the relatively anoxic environment.

Differential diagnosis
Differential diagnosis
Mycetoma should be distinguished from Kaposi’s sarcoma, malignant melanoma, fibroma and foreign body (thorn) gran uloma. A radiograph that demonstrates the presence of  bone destruction in the absence of  sinuses is suggestive of  tuberculo sis. The radiological features of  advanced my cetoma are simi lar to those of  primary osteogenic sarcoma. Primary osseous mycetoma is to be di ff erentiated from chronic osteomyelitis, osteoclastoma, bone cysts and syphilitic osteitis. In endemic areas the dictum should be ‘any subcutaneous swelling must be considered a m ycetoma until proven otherwise’. Moritz Kaposi , 1837–1902, Hungarian-born Professor of Dermatology viral cause was discovered in 1994. Ernest Codman , 1869–1940, American surgeon. Codman’s triangle can be seen in osteosarcoma, Ewing’s sarcoma, subperiosteal abscess and haematoma. Several imaging techniques are available to confirm the diag - nosis: plain radiography , ultrasonography , CT and magnetic resonance imaging (MRI). Plain radiograph In the early stages, soft-tissue shadows (often multiple) with calcification and obliteration of  the fascial planes may be seen. As the disease progresses, the cortex may be compressed from the outside by the granuloma, leading to bone scalloping. Peri - osteal reaction with new bone spicules may create a sun-ray appearance and Codman’s triangle, not unlike an osteogenic sarcoma ( Figure 6.28 ). Late in the disease, ther e may be multi - ple punched-out cavities throughout the bone. Ultrasonography This can di ff erentiate between eumycetoma and actinomy - cetoma as well as between mycetoma and other conditions. In eumycetoma, the grains produce numerous sharp bright hyper-reflective echoes. There are m ultiple thick-walled cavi - ties with absent acoustic enhancement. In actinomycetoma, the findings are similar but the grains are less distinct. The size and e xtent of  the lesion can be accurately determined ultrasonically , a finding useful in planning surgical treatment. - - - - - , University of Vienna, Austria, described pigmented sarcoma of the skin in 1872. The
Figure 6.28
Plain radiograph of the knee showing multiple large cavi
ties involving the lower femur, upper tibia and
/f_i
bula, with well-de
/f_i
ned
margins and periosteal reaction typical of eumycetoma.
(b) Magnetic resonance imaging This helps to assess bone destruction, periosteal reaction and particularly soft-tissue involvement ( Figure 6.29 ) . MRI usually shows multiple 2- to 5-mm lesions of  high signal intensity , which indicates the granuloma, interspersed within a low-intensity matrix denoting the fibrous tissue. The ‘dot-in-circle’ sign, which indicates the presence of  grains, is highly characteristic. Computed tomography CT findings in mycetoma are not specific but are helpful to detect early bone involvement.
Granuloma
Dot-in-circle sign
Figure 6.29
(a)
Magnetic resonance imaging (MRI) of the foot showing
multiple lesions of high signal intensity, which indicates granuloma,
interspersed within a low-intensity matrix, which is the
/f_i
brous
tissue and the ‘dot-in-circle’ sign, which indicates the presence of
grains.
(b)
MRI showing massive upper thigh and lower abdominal
actinomycetoma.
Differential diagnosis
Mycetoma should be distinguished from Kaposi’s sarcoma, malignant melanoma, fibroma and foreign body (thorn) gran uloma. A radiograph that demonstrates the presence of  bone destruction in the absence of  sinuses is suggestive of  tuberculo sis. The radiological features of  advanced my cetoma are simi lar to those of  primary osteogenic sarcoma. Primary osseous mycetoma is to be di ff erentiated from chronic osteomyelitis, osteoclastoma, bone cysts and syphilitic osteitis. In endemic areas the dictum should be ‘any subcutaneous swelling must be considered a m ycetoma until proven otherwise’. Moritz Kaposi , 1837–1902, Hungarian-born Professor of Dermatology viral cause was discovered in 1994. Ernest Codman , 1869–1940, American surgeon. Codman’s triangle can be seen in osteosarcoma, Ewing’s sarcoma, subperiosteal abscess and haematoma. Several imaging techniques are available to confirm the diag - nosis: plain radiography , ultrasonography , CT and magnetic resonance imaging (MRI). Plain radiograph In the early stages, soft-tissue shadows (often multiple) with calcification and obliteration of  the fascial planes may be seen. As the disease progresses, the cortex may be compressed from the outside by the granuloma, leading to bone scalloping. Peri - osteal reaction with new bone spicules may create a sun-ray appearance and Codman’s triangle, not unlike an osteogenic sarcoma ( Figure 6.28 ). Late in the disease, ther e may be multi - ple punched-out cavities throughout the bone. Ultrasonography This can di ff erentiate between eumycetoma and actinomy - cetoma as well as between mycetoma and other conditions. In eumycetoma, the grains produce numerous sharp bright hyper-reflective echoes. There are m ultiple thick-walled cavi - ties with absent acoustic enhancement. In actinomycetoma, the findings are similar but the grains are less distinct. The size and e xtent of  the lesion can be accurately determined ultrasonically , a finding useful in planning surgical treatment. - - - - - , University of Vienna, Austria, described pigmented sarcoma of the skin in 1872. The
Figure 6.28
Plain radiograph of the knee showing multiple large cavi
ties involving the lower femur, upper tibia and
/f_i
bula, with well-de
/f_i
ned
margins and periosteal reaction typical of eumycetoma.
(b) Magnetic resonance imaging This helps to assess bone destruction, periosteal reaction and particularly soft-tissue involvement ( Figure 6.29 ) . MRI usually shows multiple 2- to 5-mm lesions of  high signal intensity , which indicates the granuloma, interspersed within a low-intensity matrix denoting the fibrous tissue. The ‘dot-in-circle’ sign, which indicates the presence of  grains, is highly characteristic. Computed tomography CT findings in mycetoma are not specific but are helpful to detect early bone involvement.
Granuloma
Dot-in-circle sign
Figure 6.29
(a)
Magnetic resonance imaging (MRI) of the foot showing
multiple lesions of high signal intensity, which indicates granuloma,
interspersed within a low-intensity matrix, which is the
/f_i
brous
tissue and the ‘dot-in-circle’ sign, which indicates the presence of
grains.
(b)
MRI showing massive upper thigh and lower abdominal
actinomycetoma.
Differential diagnosis
Mycetoma should be distinguished from Kaposi’s sarcoma, malignant melanoma, fibroma and foreign body (thorn) gran uloma. A radiograph that demonstrates the presence of  bone destruction in the absence of  sinuses is suggestive of  tuberculo sis. The radiological features of  advanced my cetoma are simi lar to those of  primary osteogenic sarcoma. Primary osseous mycetoma is to be di ff erentiated from chronic osteomyelitis, osteoclastoma, bone cysts and syphilitic osteitis. In endemic areas the dictum should be ‘any subcutaneous swelling must be considered a m ycetoma until proven otherwise’. Moritz Kaposi , 1837–1902, Hungarian-born Professor of Dermatology viral cause was discovered in 1994. Ernest Codman , 1869–1940, American surgeon. Codman’s triangle can be seen in osteosarcoma, Ewing’s sarcoma, subperiosteal abscess and haematoma. Several imaging techniques are available to confirm the diag - nosis: plain radiography , ultrasonography , CT and magnetic resonance imaging (MRI). Plain radiograph In the early stages, soft-tissue shadows (often multiple) with calcification and obliteration of  the fascial planes may be seen. As the disease progresses, the cortex may be compressed from the outside by the granuloma, leading to bone scalloping. Peri - osteal reaction with new bone spicules may create a sun-ray appearance and Codman’s triangle, not unlike an osteogenic sarcoma ( Figure 6.28 ). Late in the disease, ther e may be multi - ple punched-out cavities throughout the bone. Ultrasonography This can di ff erentiate between eumycetoma and actinomy - cetoma as well as between mycetoma and other conditions. In eumycetoma, the grains produce numerous sharp bright hyper-reflective echoes. There are m ultiple thick-walled cavi - ties with absent acoustic enhancement. In actinomycetoma, the findings are similar but the grains are less distinct. The size and e xtent of  the lesion can be accurately determined ultrasonically , a finding useful in planning surgical treatment. - - - - - , University of Vienna, Austria, described pigmented sarcoma of the skin in 1872. The
Figure 6.28
Plain radiograph of the knee showing multiple large cavi
ties involving the lower femur, upper tibia and
/f_i
bula, with well-de
/f_i
ned
margins and periosteal reaction typical of eumycetoma.
(b) Magnetic resonance imaging This helps to assess bone destruction, periosteal reaction and particularly soft-tissue involvement ( Figure 6.29 ) . MRI usually shows multiple 2- to 5-mm lesions of  high signal intensity , which indicates the granuloma, interspersed within a low-intensity matrix denoting the fibrous tissue. The ‘dot-in-circle’ sign, which indicates the presence of  grains, is highly characteristic. Computed tomography CT findings in mycetoma are not specific but are helpful to detect early bone involvement.
Granuloma
Dot-in-circle sign
Figure 6.29
(a)
Magnetic resonance imaging (MRI) of the foot showing
multiple lesions of high signal intensity, which indicates granuloma,
interspersed within a low-intensity matrix, which is the
/f_i
brous
tissue and the ‘dot-in-circle’ sign, which indicates the presence of
grains.
(b)
MRI showing massive upper thigh and lower abdominal
actinomycetoma.

Epidemiology and pathogenesis
Epidemiology and pathogenesis
The condition predominantly occurs in the ‘mycetoma belt’ that lies between latitudes 15° south and 30° north, compris - ing the countries of  Sudan, Somalia, Senegal, India, Y emen, Mexico, V enezuela, Columbia, Argentina and a few others. The route of  infection is inoculation of the organism that is resident in the soil through a traumatised area. Although in the vast majority there is no history of  trauma, the portal of  entry is always an area of  minor unrecognised trauma in a bare-footed individual walking in a terrain full of  thorns. Hence the foot is the commonest site a ff ected. Mycetoma is not contagious. Once the granuloma forms it increases in size, and the overlying skin becomes stretched, smooth, shiny and attached - -
Figure 6.23
Mycetoma of the foot.
develop. Eventually it invades the deeper structures. This is usually gradual and delayed in eumycetoma. In actinomyce toma, invasion to deeper tissues occurs earlier and is more extensive. The tendons and nerves are spared until late in the disease. This may explain the rarity of  neurological and tro phic c hanges even in patients with longstanding disease. Tro phic changes are rare because the blood supply is adequate. Summary box 6.15 Mycetoma: pathogenesis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Mostly occurs in the ‘mycetoma belt’
There are two types – eumycetoma and actinomycetoma
Caused by fungi or bacteria entering through a site of trauma,
which may not be apparent; hence the foot is most commonly
affected
Produces a chronic, speci
/f_i
c, granulomatous, progressive,
destructive in
/f_l
ammatory lesion
Results in tissue destruction, deformity, disability and
sometimes death
Epidemiology and pathogenesis
The condition predominantly occurs in the ‘mycetoma belt’ that lies between latitudes 15° south and 30° north, compris - ing the countries of  Sudan, Somalia, Senegal, India, Y emen, Mexico, V enezuela, Columbia, Argentina and a few others. The route of  infection is inoculation of the organism that is resident in the soil through a traumatised area. Although in the vast majority there is no history of  trauma, the portal of  entry is always an area of  minor unrecognised trauma in a bare-footed individual walking in a terrain full of  thorns. Hence the foot is the commonest site a ff ected. Mycetoma is not contagious. Once the granuloma forms it increases in size, and the overlying skin becomes stretched, smooth, shiny and attached - -
Figure 6.23
Mycetoma of the foot.
develop. Eventually it invades the deeper structures. This is usually gradual and delayed in eumycetoma. In actinomyce toma, invasion to deeper tissues occurs earlier and is more extensive. The tendons and nerves are spared until late in the disease. This may explain the rarity of  neurological and tro phic c hanges even in patients with longstanding disease. Tro phic changes are rare because the blood supply is adequate. Summary box 6.15 Mycetoma: pathogenesis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Mostly occurs in the ‘mycetoma belt’
There are two types – eumycetoma and actinomycetoma
Caused by fungi or bacteria entering through a site of trauma,
which may not be apparent; hence the foot is most commonly
affected
Produces a chronic, speci
/f_i
c, granulomatous, progressive,
destructive in
/f_l
ammatory lesion
Results in tissue destruction, deformity, disability and
sometimes death
Epidemiology and pathogenesis
The condition predominantly occurs in the ‘mycetoma belt’ that lies between latitudes 15° south and 30° north, compris - ing the countries of  Sudan, Somalia, Senegal, India, Y emen, Mexico, V enezuela, Columbia, Argentina and a few others. The route of  infection is inoculation of the organism that is resident in the soil through a traumatised area. Although in the vast majority there is no history of  trauma, the portal of  entry is always an area of  minor unrecognised trauma in a bare-footed individual walking in a terrain full of  thorns. Hence the foot is the commonest site a ff ected. Mycetoma is not contagious. Once the granuloma forms it increases in size, and the overlying skin becomes stretched, smooth, shiny and attached - -
Figure 6.23
Mycetoma of the foot.
develop. Eventually it invades the deeper structures. This is usually gradual and delayed in eumycetoma. In actinomyce toma, invasion to deeper tissues occurs earlier and is more extensive. The tendons and nerves are spared until late in the disease. This may explain the rarity of  neurological and tro phic c hanges even in patients with longstanding disease. Tro phic changes are rare because the blood supply is adequate. Summary box 6.15 Mycetoma: pathogenesis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Mostly occurs in the ‘mycetoma belt’
There are two types – eumycetoma and actinomycetoma
Caused by fungi or bacteria entering through a site of trauma,
which may not be apparent; hence the foot is most commonly
affected
Produces a chronic, speci
/f_i
c, granulomatous, progressive,
destructive in
/f_l
ammatory lesion
Results in tissue destruction, deformity, disability and
sometimes death

FILARIASIS Introduction
FILARIASIS Introduction
Filariasis is mainly caused by the parasite Wuchereria bancrofti , which is transmitted by the mosquito. Variants of  the parasite called Brugia malayi and Brugia timori are responsible for caus - ing the disease in about 10% of  those infected. The condition a ff ects more than 120 million people worldwide, two-thirds of whom live in India, China and Indonesia. According to the World Health Organization (WHO), after lepr osy , filariasis is the most common cause of  long-term disability . Once the host has been bitten by the mosquito, the matured eggs enter the human circulation to hatch and grow into adult worms; the process of matura tion takes almost a year. The adult worms mainly colonise the lymphatic system.
or
FILARIASIS Introduction
Filariasis is mainly caused by the parasite Wuchereria bancrofti , which is transmitted by the mosquito. Variants of  the parasite called Brugia malayi and Brugia timori are responsible for caus - ing the disease in about 10% of  those infected. The condition a ff ects more than 120 million people worldwide, two-thirds of whom live in India, China and Indonesia. According to the World Health Organization (WHO), after lepr osy , filariasis is the most common cause of  long-term disability . Once the host has been bitten by the mosquito, the matured eggs enter the human circulation to hatch and grow into adult worms; the process of matura tion takes almost a year. The adult worms mainly colonise the lymphatic system.
or
FILARIASIS Introduction
Filariasis is mainly caused by the parasite Wuchereria bancrofti , which is transmitted by the mosquito. Variants of  the parasite called Brugia malayi and Brugia timori are responsible for caus - ing the disease in about 10% of  those infected. The condition a ff ects more than 120 million people worldwide, two-thirds of whom live in India, China and Indonesia. According to the World Health Organization (WHO), after lepr osy , filariasis is the most common cause of  long-term disability . Once the host has been bitten by the mosquito, the matured eggs enter the human circulation to hatch and grow into adult worms; the process of matura tion takes almost a year. The adult worms mainly colonise the lymphatic system.
or

FURTHER READING
FURTHER READING
AMOEBIASIS Barnes SA, Lillemore KD. Liver abscess and hydatid disease In: Zinner NJ, Schwartz I, Ellis H (eds). Maingot’s abdominal operations, 10th edn, vol. 2. New Y ork: Appleton and Lange, McGraw-Hill, 1997: 1527–45. Blessmann J, Van Linh P , Nu PA et al . Epidemiology of  amebiasis in a region of  high incidence of  amebic liver abscess in central Viet - nam. Am J Trop Med Hyg 2002; 66 (5): 578–83. Bruns BR, Scalea TM. Complex liver abscess. In: Diaz JJ, Efron DT (eds). Complications in acute care surgery. Cham: Springer Internation - al Publishing, 2017: 189–97. Shirley D-AT , Watanabe K, Moonah S. Significance of  amebiasis: 10 reasons why neglecting amebiasis might come back to bite us in the gut. PLoS Negl Trop Dis 2019; 13 (11): e0007744. Tanyuksel M, Petri Jr WA. Laboratory diagnosis of  amebiasis. Clin Mi - crobiol Rev 2003; 16 (4): 713–29.
(a)
).
Carrero JC, Reyes-Lopez M, Serrano-Luna J, Shibayama M, Unzueta J, Leon-Sicairos N, de la Garza M. Intestinal amoebiasis: 160 years of  its first detection and still remains as a health problem in developing countries. Int J Med Microbiol 2020; 310 (1): 151358. Das AK. Hepatic and biliary ascariasis. J Global Infect Dis 2014; 65. Steinberg R, Davies J, Millar AJ et al. Unusual intestinal sequelae after operations for Ascaris lumbricoides infestation. Paediatr Surg Int 19 (1–2): 85–7. Wani RA, Parray FQ, Bhat NA et al. Non-traumatic terminal ileal perforation. World J Emerg Surg 2006; 10 : 1–7. ASIATIC CHOLANGIOHEPATITIS Choi BI, Han JK, Hong ST , Lee KH. Clonorchiasis and cholangiocarcinoma: etiologic relationship and imaging diagnosis. Clin Microbiol Rev 2004; 17 (3): 540–52. V erweij KE, van Buuren H. Oriental cholangiohepatitis (recurrent pyogenic cholangitis): a case series from the Netherlands and brief review of  the literature. Neth J Med 2016; 74 (9): 401-5. FILARIASIS Lim KH, Speare R, Thomas G, Graves P . Surgical treatment of  genital manifestations of  lymphatic filariasis: a systematic review . Surg 2015; 39 (12): 2885–99. Manjula Y , Kate V , Ananthakrishnan N. Evaluation of sequential intermittent pneumatic compression for filarial lymphoedema. Med J India 2002; 15 (4): 192–4. Barnes SA, Lillemore KD. Liver abscess and hydatid disease. In: Zinner NJ, Schwartz I, Ellis H (eds). Maingot’s abdominal operations, 10th edn, vol. 2. New Y ork: Appleton and Lange, McGraw Hill, 1997: 1527–45. Botezatu C, Mastalier B, Patrascu T . Hepatic hydatid cyst–diagnose 6 (2): and treatment algorithm. J Med Life 2018; 11 (3): 203. Chiodini P . Parasitic infections. In: Russell RCG, Williams NS, Bulstrode CJK (eds). 2003; 24th edn. London: Arnold, 2004: 146–74. WHO Informal Working Group. International classification of ultrasound images in cystic echinococcosis for application in clinical and field epidemiological settings. Acta Trop 2003; 85 (2): 253–61. LEPROSY Anderson GA. The surgical management of  deformities of  the hand in leprosy . Bone Joint J 2006; 88 (3): 290–4. MYCETOMA Fahal AH. Management of mycetoma. Expert Rev Dermatol 2010; 5 (1): 87–93. Hassan MA, Fahal AH. Mycetoma. In: Kamil R, Lumby J (eds). World J Tropical surgery. London: Westminster Publications Ltd, 2004: 786– 90. Natl TROPICAL CHRONIC PANCREATITIS Barman KK, Premlatha G, Mohan V . Tropical chronic pancreatitis. Postgrad Med J 2003; 79 : 606–15. TYPHOID Aziz M, Qadir A, Aziz M, Faizullah. Prognostic factors in typhoid perforation. J Coll Physicians Surg Pak 2005; 15 (11): 704–7. Olsen SJ, Pruckler J, Bibb W et al. Evaluation of  rapid diagnostic tests for typhoid fever. J Clin Microbiol 2004; 42 (5): 1885–9. FURTHER READING
AMOEBIASIS Barnes SA, Lillemore KD. Liver abscess and hydatid disease In: Zinner NJ, Schwartz I, Ellis H (eds). Maingot’s abdominal operations, 10th edn, vol. 2. New Y ork: Appleton and Lange, McGraw-Hill, 1997: 1527–45. Blessmann J, Van Linh P , Nu PA et al . Epidemiology of  amebiasis in a region of  high incidence of  amebic liver abscess in central Viet - nam. Am J Trop Med Hyg 2002; 66 (5): 578–83. Bruns BR, Scalea TM. Complex liver abscess. In: Diaz JJ, Efron DT (eds). Complications in acute care surgery. Cham: Springer Internation - al Publishing, 2017: 189–97. Shirley D-AT , Watanabe K, Moonah S. Significance of  amebiasis: 10 reasons why neglecting amebiasis might come back to bite us in the gut. PLoS Negl Trop Dis 2019; 13 (11): e0007744. Tanyuksel M, Petri Jr WA. Laboratory diagnosis of  amebiasis. Clin Mi - crobiol Rev 2003; 16 (4): 713–29.
(a)
).
Carrero JC, Reyes-Lopez M, Serrano-Luna J, Shibayama M, Unzueta J, Leon-Sicairos N, de la Garza M. Intestinal amoebiasis: 160 years of  its first detection and still remains as a health problem in developing countries. Int J Med Microbiol 2020; 310 (1): 151358. Das AK. Hepatic and biliary ascariasis. J Global Infect Dis 2014; 65. Steinberg R, Davies J, Millar AJ et al. Unusual intestinal sequelae after operations for Ascaris lumbricoides infestation. Paediatr Surg Int 19 (1–2): 85–7. Wani RA, Parray FQ, Bhat NA et al. Non-traumatic terminal ileal perforation. World J Emerg Surg 2006; 10 : 1–7. ASIATIC CHOLANGIOHEPATITIS Choi BI, Han JK, Hong ST , Lee KH. Clonorchiasis and cholangiocarcinoma: etiologic relationship and imaging diagnosis. Clin Microbiol Rev 2004; 17 (3): 540–52. V erweij KE, van Buuren H. Oriental cholangiohepatitis (recurrent pyogenic cholangitis): a case series from the Netherlands and brief review of  the literature. Neth J Med 2016; 74 (9): 401-5. FILARIASIS Lim KH, Speare R, Thomas G, Graves P . Surgical treatment of  genital manifestations of  lymphatic filariasis: a systematic review . Surg 2015; 39 (12): 2885–99. Manjula Y , Kate V , Ananthakrishnan N. Evaluation of sequential intermittent pneumatic compression for filarial lymphoedema. Med J India 2002; 15 (4): 192–4. Barnes SA, Lillemore KD. Liver abscess and hydatid disease. In: Zinner NJ, Schwartz I, Ellis H (eds). Maingot’s abdominal operations, 10th edn, vol. 2. New Y ork: Appleton and Lange, McGraw Hill, 1997: 1527–45. Botezatu C, Mastalier B, Patrascu T . Hepatic hydatid cyst–diagnose 6 (2): and treatment algorithm. J Med Life 2018; 11 (3): 203. Chiodini P . Parasitic infections. In: Russell RCG, Williams NS, Bulstrode CJK (eds). 2003; 24th edn. London: Arnold, 2004: 146–74. WHO Informal Working Group. International classification of ultrasound images in cystic echinococcosis for application in clinical and field epidemiological settings. Acta Trop 2003; 85 (2): 253–61. LEPROSY Anderson GA. The surgical management of  deformities of  the hand in leprosy . Bone Joint J 2006; 88 (3): 290–4. MYCETOMA Fahal AH. Management of mycetoma. Expert Rev Dermatol 2010; 5 (1): 87–93. Hassan MA, Fahal AH. Mycetoma. In: Kamil R, Lumby J (eds). World J Tropical surgery. London: Westminster Publications Ltd, 2004: 786– 90. Natl TROPICAL CHRONIC PANCREATITIS Barman KK, Premlatha G, Mohan V . Tropical chronic pancreatitis. Postgrad Med J 2003; 79 : 606–15. TYPHOID Aziz M, Qadir A, Aziz M, Faizullah. Prognostic factors in typhoid perforation. J Coll Physicians Surg Pak 2005; 15 (11): 704–7. Olsen SJ, Pruckler J, Bibb W et al. Evaluation of  rapid diagnostic tests for typhoid fever. J Clin Microbiol 2004; 42 (5): 1885–9. FURTHER READING
AMOEBIASIS Barnes SA, Lillemore KD. Liver abscess and hydatid disease In: Zinner NJ, Schwartz I, Ellis H (eds). Maingot’s abdominal operations, 10th edn, vol. 2. New Y ork: Appleton and Lange, McGraw-Hill, 1997: 1527–45. Blessmann J, Van Linh P , Nu PA et al . Epidemiology of  amebiasis in a region of  high incidence of  amebic liver abscess in central Viet - nam. Am J Trop Med Hyg 2002; 66 (5): 578–83. Bruns BR, Scalea TM. Complex liver abscess. In: Diaz JJ, Efron DT (eds). Complications in acute care surgery. Cham: Springer Internation - al Publishing, 2017: 189–97. Shirley D-AT , Watanabe K, Moonah S. Significance of  amebiasis: 10 reasons why neglecting amebiasis might come back to bite us in the gut. PLoS Negl Trop Dis 2019; 13 (11): e0007744. Tanyuksel M, Petri Jr WA. Laboratory diagnosis of  amebiasis. Clin Mi - crobiol Rev 2003; 16 (4): 713–29.
(a)
).
Carrero JC, Reyes-Lopez M, Serrano-Luna J, Shibayama M, Unzueta J, Leon-Sicairos N, de la Garza M. Intestinal amoebiasis: 160 years of  its first detection and still remains as a health problem in developing countries. Int J Med Microbiol 2020; 310 (1): 151358. Das AK. Hepatic and biliary ascariasis. J Global Infect Dis 2014; 65. Steinberg R, Davies J, Millar AJ et al. Unusual intestinal sequelae after operations for Ascaris lumbricoides infestation. Paediatr Surg Int 19 (1–2): 85–7. Wani RA, Parray FQ, Bhat NA et al. Non-traumatic terminal ileal perforation. World J Emerg Surg 2006; 10 : 1–7. ASIATIC CHOLANGIOHEPATITIS Choi BI, Han JK, Hong ST , Lee KH. Clonorchiasis and cholangiocarcinoma: etiologic relationship and imaging diagnosis. Clin Microbiol Rev 2004; 17 (3): 540–52. V erweij KE, van Buuren H. Oriental cholangiohepatitis (recurrent pyogenic cholangitis): a case series from the Netherlands and brief review of  the literature. Neth J Med 2016; 74 (9): 401-5. FILARIASIS Lim KH, Speare R, Thomas G, Graves P . Surgical treatment of  genital manifestations of  lymphatic filariasis: a systematic review . Surg 2015; 39 (12): 2885–99. Manjula Y , Kate V , Ananthakrishnan N. Evaluation of sequential intermittent pneumatic compression for filarial lymphoedema. Med J India 2002; 15 (4): 192–4. Barnes SA, Lillemore KD. Liver abscess and hydatid disease. In: Zinner NJ, Schwartz I, Ellis H (eds). Maingot’s abdominal operations, 10th edn, vol. 2. New Y ork: Appleton and Lange, McGraw Hill, 1997: 1527–45. Botezatu C, Mastalier B, Patrascu T . Hepatic hydatid cyst–diagnose 6 (2): and treatment algorithm. J Med Life 2018; 11 (3): 203. Chiodini P . Parasitic infections. In: Russell RCG, Williams NS, Bulstrode CJK (eds). 2003; 24th edn. London: Arnold, 2004: 146–74. WHO Informal Working Group. International classification of ultrasound images in cystic echinococcosis for application in clinical and field epidemiological settings. Acta Trop 2003; 85 (2): 253–61. LEPROSY Anderson GA. The surgical management of  deformities of  the hand in leprosy . Bone Joint J 2006; 88 (3): 290–4. MYCETOMA Fahal AH. Management of mycetoma. Expert Rev Dermatol 2010; 5 (1): 87–93. Hassan MA, Fahal AH. Mycetoma. In: Kamil R, Lumby J (eds). World J Tropical surgery. London: Westminster Publications Ltd, 2004: 786– 90. Natl TROPICAL CHRONIC PANCREATITIS Barman KK, Premlatha G, Mohan V . Tropical chronic pancreatitis. Postgrad Med J 2003; 79 : 606–15. TYPHOID Aziz M, Qadir A, Aziz M, Faizullah. Prognostic factors in typhoid perforation. J Coll Physicians Surg Pak 2005; 15 (11): 704–7. Olsen SJ, Pruckler J, Bibb W et al. Evaluation of  rapid diagnostic tests for typhoid fever. J Clin Microbiol 2004; 42 (5): 1885–9.

Fine-needle aspiration cytology
Fine-needle aspiration cytology
Fine-needle aspiration cytology (FNAC) can yield an accurate diagnosis and helps in distinguishing between eumycetoma and actinomycetoma. The technique is simple, rapid and sensitive. Fine-needle aspiration cytology
Fine-needle aspiration cytology (FNAC) can yield an accurate diagnosis and helps in distinguishing between eumycetoma and actinomycetoma. The technique is simple, rapid and sensitive. Fine-needle aspiration cytology
Fine-needle aspiration cytology (FNAC) can yield an accurate diagnosis and helps in distinguishing between eumycetoma and actinomycetoma. The technique is simple, rapid and sensitive.

HYDATID DISEASE
HYDATID DISEASE
HYDATID DISEASE
HYDATID DISEASE

Histopathological diagnosis
Histopathological diagnosis
Deep biopsy is obtained under general or regional anaesthesia, although the chance of  local spread is high. The biopsy should be adequate, contain grains and should be fixed immediately in 10% formal saline. Three types of  host tissue reaction occur against the organism. Theodor Langhans , 1839–1915, Professor of  Pathological Anatomy , University of  Berne, Switzerland. polymorphonuclear leukocytes. The innermost neutro - phils are closely attached to the surface of  the grain, some - times invading the grain and causing its fragmentation. The hyphae and cement substance disappear and only remnants of  brown pigmented cement are left behind. Outside the zone of  neutrophils there is granulation tissue containing macrophages , lymphocytes, plasma cells and few neutrophils. The mononuclear cells increase in num - ber towards the periphery of  the lesion. The outermost zone of  the lesion consists of  fibrous tissue. /uni25CF Type II: the neutrophils largely disappear and are re - placed by macrophages and multinucleated giant cells that engulf  the grain material. This consists largely of  pigment - ed cement substance although hyphae are sometimes iden - tified. /uni25CF Type III: this is characterised by the formation of  a well-organised epithelioid granuloma with Langhans-type giant cells. The centre of  the granuloma will sometimes contain remnants of  fungal material. Histopathological diagnosis
Deep biopsy is obtained under general or regional anaesthesia, although the chance of  local spread is high. The biopsy should be adequate, contain grains and should be fixed immediately in 10% formal saline. Three types of  host tissue reaction occur against the organism. Theodor Langhans , 1839–1915, Professor of  Pathological Anatomy , University of  Berne, Switzerland. polymorphonuclear leukocytes. The innermost neutro - phils are closely attached to the surface of  the grain, some - times invading the grain and causing its fragmentation. The hyphae and cement substance disappear and only remnants of  brown pigmented cement are left behind. Outside the zone of  neutrophils there is granulation tissue containing macrophages , lymphocytes, plasma cells and few neutrophils. The mononuclear cells increase in num - ber towards the periphery of  the lesion. The outermost zone of  the lesion consists of  fibrous tissue. /uni25CF Type II: the neutrophils largely disappear and are re - placed by macrophages and multinucleated giant cells that engulf  the grain material. This consists largely of  pigment - ed cement substance although hyphae are sometimes iden - tified. /uni25CF Type III: this is characterised by the formation of  a well-organised epithelioid granuloma with Langhans-type giant cells. The centre of  the granuloma will sometimes contain remnants of  fungal material. Histopathological diagnosis
Deep biopsy is obtained under general or regional anaesthesia, although the chance of  local spread is high. The biopsy should be adequate, contain grains and should be fixed immediately in 10% formal saline. Three types of  host tissue reaction occur against the organism. Theodor Langhans , 1839–1915, Professor of  Pathological Anatomy , University of  Berne, Switzerland. polymorphonuclear leukocytes. The innermost neutro - phils are closely attached to the surface of  the grain, some - times invading the grain and causing its fragmentation. The hyphae and cement substance disappear and only remnants of  brown pigmented cement are left behind. Outside the zone of  neutrophils there is granulation tissue containing macrophages , lymphocytes, plasma cells and few neutrophils. The mononuclear cells increase in num - ber towards the periphery of  the lesion. The outermost zone of  the lesion consists of  fibrous tissue. /uni25CF Type II: the neutrophils largely disappear and are re - placed by macrophages and multinucleated giant cells that engulf  the grain material. This consists largely of  pigment - ed cement substance although hyphae are sometimes iden - tified. /uni25CF Type III: this is characterised by the formation of  a well-organised epithelioid granuloma with Langhans-type giant cells. The centre of  the granuloma will sometimes contain remnants of  fungal material.

Imaging techniques
Imaging techniques
On ultrasonography , an abscess cavity in the liver is seen as a - hypoechoic or anechoic lesion with ill-defined borders; internal echoes suggest necrotic material or debris ( Figure 6.1 ). The - investigation is very accurate and is used for aspiration, both - diagnostic and therapeutic. When there is doubt about the diagnosis, a computed tomography (CT) scan may be helpful ( Figure 6.2 ). Diagnostic aspiration is of  limited value exce pt for estab - lishing the typical colour of  the aspirate, which is sterile and odourless unless it is secondarily infected. A CT scan may show a raised right hemidiaphragm, a pleural e ff usion and evidence of pneumonitis ( Figure 6.3 ) . - An ‘apple-core’ deformity on barium enema would arouse suspicion of  a carcinoma. A colonoscopy with biopsy is man - datory because the radiological and macr oscopic appearance may be indistinguishable from a carcinoma. In doubtful cases, vigorous medical treatment is given and the pa tient undergoes colonoscopy again in 3–4 weeks, as these masses are known to regress completely on a full course of  drug therapy . If  symp toms persist even partially following full medical treatment in a patient who has recently returned from an endemic area, a colonic carcinoma must be excluded forthwith. This is because a dormant colonic carcinoma may become apparent as a result of  infestation with amoebic dysentery causing ‘traveller’s diar rhoea’. However, it must be borne in mind that an amoeboma and a carcinoma can coexist. Summary box 6.2 Diagnostic pointers for infection with Entamoeba histolytica /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.1
Ultrasound of the liver showing a large amoebic liver
abscess with necrotic tissue in the right lobe.
Bloody mucoid diarrhoea in a patient from an endemic area or
following a recent visit to such a country
Upper abdominal pain, fever, cough, malaise
In chronic cases, a mass in the right iliac fossa may be
an amoeboma but caecal cancer must be excluded by
colonoscopy and biopsy
Sigmoidoscopy shows typical ulcers – biopsy and scrapes may
be diagnostic
Serological tests are highly sensitive and speci
/f_i
c outside
endemic areas
Ultrasonography and CT scans are the imaging methods of
choice
Imaging techniques
On ultrasonography , an abscess cavity in the liver is seen as a - hypoechoic or anechoic lesion with ill-defined borders; internal echoes suggest necrotic material or debris ( Figure 6.1 ). The - investigation is very accurate and is used for aspiration, both - diagnostic and therapeutic. When there is doubt about the diagnosis, a computed tomography (CT) scan may be helpful ( Figure 6.2 ). Diagnostic aspiration is of  limited value exce pt for estab - lishing the typical colour of  the aspirate, which is sterile and odourless unless it is secondarily infected. A CT scan may show a raised right hemidiaphragm, a pleural e ff usion and evidence of pneumonitis ( Figure 6.3 ) . - An ‘apple-core’ deformity on barium enema would arouse suspicion of  a carcinoma. A colonoscopy with biopsy is man - datory because the radiological and macr oscopic appearance may be indistinguishable from a carcinoma. In doubtful cases, vigorous medical treatment is given and the pa tient undergoes colonoscopy again in 3–4 weeks, as these masses are known to regress completely on a full course of  drug therapy . If  symp toms persist even partially following full medical treatment in a patient who has recently returned from an endemic area, a colonic carcinoma must be excluded forthwith. This is because a dormant colonic carcinoma may become apparent as a result of  infestation with amoebic dysentery causing ‘traveller’s diar rhoea’. However, it must be borne in mind that an amoeboma and a carcinoma can coexist. Summary box 6.2 Diagnostic pointers for infection with Entamoeba histolytica /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.1
Ultrasound of the liver showing a large amoebic liver
abscess with necrotic tissue in the right lobe.
Bloody mucoid diarrhoea in a patient from an endemic area or
following a recent visit to such a country
Upper abdominal pain, fever, cough, malaise
In chronic cases, a mass in the right iliac fossa may be
an amoeboma but caecal cancer must be excluded by
colonoscopy and biopsy
Sigmoidoscopy shows typical ulcers – biopsy and scrapes may
be diagnostic
Serological tests are highly sensitive and speci
/f_i
c outside
endemic areas
Ultrasonography and CT scans are the imaging methods of
choice
Imaging techniques
On ultrasonography , an abscess cavity in the liver is seen as a - hypoechoic or anechoic lesion with ill-defined borders; internal echoes suggest necrotic material or debris ( Figure 6.1 ). The - investigation is very accurate and is used for aspiration, both - diagnostic and therapeutic. When there is doubt about the diagnosis, a computed tomography (CT) scan may be helpful ( Figure 6.2 ). Diagnostic aspiration is of  limited value exce pt for estab - lishing the typical colour of  the aspirate, which is sterile and odourless unless it is secondarily infected. A CT scan may show a raised right hemidiaphragm, a pleural e ff usion and evidence of pneumonitis ( Figure 6.3 ) . - An ‘apple-core’ deformity on barium enema would arouse suspicion of  a carcinoma. A colonoscopy with biopsy is man - datory because the radiological and macr oscopic appearance may be indistinguishable from a carcinoma. In doubtful cases, vigorous medical treatment is given and the pa tient undergoes colonoscopy again in 3–4 weeks, as these masses are known to regress completely on a full course of  drug therapy . If  symp toms persist even partially following full medical treatment in a patient who has recently returned from an endemic area, a colonic carcinoma must be excluded forthwith. This is because a dormant colonic carcinoma may become apparent as a result of  infestation with amoebic dysentery causing ‘traveller’s diar rhoea’. However, it must be borne in mind that an amoeboma and a carcinoma can coexist. Summary box 6.2 Diagnostic pointers for infection with Entamoeba histolytica /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.1
Ultrasound of the liver showing a large amoebic liver
abscess with necrotic tissue in the right lobe.
Bloody mucoid diarrhoea in a patient from an endemic area or
following a recent visit to such a country
Upper abdominal pain, fever, cough, malaise
In chronic cases, a mass in the right iliac fossa may be
an amoeboma but caecal cancer must be excluded by
colonoscopy and biopsy
Sigmoidoscopy shows typical ulcers – biopsy and scrapes may
be diagnostic
Serological tests are highly sensitive and speci
/f_i
c outside
endemic areas
Ultrasonography and CT scans are the imaging methods of
choice

Introduction and pathology
Introduction and pathology
Hydatid disease is caused by Echinococcus granulosus, commonly called the dog tapeworm. The disease is globally distributed and, while it is common in the tropics, it is much less common in other countries; for example, in the UK the occasional patient may come from a rural sheep-farming community . The dog is the definitive host and is the commonest source of  infection transmitted to the intermediate hosts – humans, sheep and cattle. In the dog, the adult worm reaches the small intestine and the eggs are passed in the faeces. These eg gs are - highly resistant to extremes of  temperature and may survive for long periods. In the dog’s intestine, the cyst wall is digested, allowing the protoscolices to develop into adult worms. Close contact with an infected dog causes contamination by the oral route, with the ovum thus gaining entry into the human gas - trointestinal tract. The cyst is characterised by three layers: an outer peri - cyst , which is derived from compressed host organ tissues; an intermediate hyaline ectocyst , which is non-infective; and an inner endocyst , which is the germinal membrane and contains viable parasites that can separate, forming daughter cysts. A variant of  the disease occurs in colder climates caused by Echinococcus multilocularis, in which the cyst spreads from the outset by actual invasion rather than expansion. Introduction and pathology
Hydatid disease is caused by Echinococcus granulosus, commonly called the dog tapeworm. The disease is globally distributed and, while it is common in the tropics, it is much less common in other countries; for example, in the UK the occasional patient may come from a rural sheep-farming community . The dog is the definitive host and is the commonest source of  infection transmitted to the intermediate hosts – humans, sheep and cattle. In the dog, the adult worm reaches the small intestine and the eggs are passed in the faeces. These eg gs are - highly resistant to extremes of  temperature and may survive for long periods. In the dog’s intestine, the cyst wall is digested, allowing the protoscolices to develop into adult worms. Close contact with an infected dog causes contamination by the oral route, with the ovum thus gaining entry into the human gas - trointestinal tract. The cyst is characterised by three layers: an outer peri - cyst , which is derived from compressed host organ tissues; an intermediate hyaline ectocyst , which is non-infective; and an inner endocyst , which is the germinal membrane and contains viable parasites that can separate, forming daughter cysts. A variant of  the disease occurs in colder climates caused by Echinococcus multilocularis, in which the cyst spreads from the outset by actual invasion rather than expansion. Introduction and pathology
Hydatid disease is caused by Echinococcus granulosus, commonly called the dog tapeworm. The disease is globally distributed and, while it is common in the tropics, it is much less common in other countries; for example, in the UK the occasional patient may come from a rural sheep-farming community . The dog is the definitive host and is the commonest source of  infection transmitted to the intermediate hosts – humans, sheep and cattle. In the dog, the adult worm reaches the small intestine and the eggs are passed in the faeces. These eg gs are - highly resistant to extremes of  temperature and may survive for long periods. In the dog’s intestine, the cyst wall is digested, allowing the protoscolices to develop into adult worms. Close contact with an infected dog causes contamination by the oral route, with the ovum thus gaining entry into the human gas - trointestinal tract. The cyst is characterised by three layers: an outer peri - cyst , which is derived from compressed host organ tissues; an intermediate hyaline ectocyst , which is non-infective; and an inner endocyst , which is the germinal membrane and contains viable parasites that can separate, forming daughter cysts. A variant of  the disease occurs in colder climates caused by Echinococcus multilocularis, in which the cyst spreads from the outset by actual invasion rather than expansion.

Introduction
INTRODUCTION
Most surgical conditions in the tropics (regions of  the Earth surrounding the equator) are associated with parasitic infesta tions and infections related to poor hygienic conditions. With the ease of  international travel, diseases that are common in the tropics may present in areas of  the world where the not commonly seen, especially as emergencies. This chapter deals with the conditions that a surgeon might occasionally see when working in an area where such diseases are uncommon. Typically the patient would be a visitor a tropical climate or a local resident who has visited the tropics either on holiday or to work. The life cycles of  the parasites will not be described. The principles of  surgical treatment are dealt with in the appropriate sections although, for operative details, referral to a relevant textbook is advised.

Investigations
Investigations
The haematological and biochemical investigations reflect the presence of  a chronic infective process: anaemia, leukocytosis, raised inflammatory markers – erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) – hypoalbuminaemia and deranged liver function tests, particularly elevated alkaline phosphatase. Serological tests are more specific, with the majority of patients showing antibodies in serum. These can be detected by tests for complement fixation, indirect haemagglutination (IHA), indirect immunofluorescence , counter-immunoelectro - phoresis and enzyme-linked immunosorbent assay (ELISA). These tests are extremely useful in detecting acute infection in non-endemic areas. IHA has a very high sensitivity in acute amoebic liver abscess in non-endemic regions and remains ele - vated for some time. The persistence of  antibodies in a large majority of the population in endemic areas precludes its use as a diagnostic investigation in those loca tions. A combination of  serological tests detecting antibodies in combination with detection of the parasite by antigen detection or DNA poly - merase chain reaction is likely to be more beneficial in such cases, though with the limitation of  cost and accessibility in developing nations. While amoebiasis may a ff ect the entire colon, it has a pre - dilection for the caecum and ascending colon. A colonoscopy may rev eal discrete exudate-covered areas of  ulceration with normal areas in between. Investigations
As with most parasitic infestations, an increase in the eosinophil count is common. Stool examination may show ova. Sputum or bronchoscopic washings may show Charcot–Leyden crystals or the larvae. Chest radiograph may show flu ff y exudates in Loe ffl er’s syndrome. A barium meal and follow-through may show a bolus of  worms in the ileum or lying freely within the small bowel ( Figur e 6.4 ). Ultrasonography may show a worm in the gallbladder, the common bile duct ( Figure 6.5 ) or pan - creatic duct. On magnetic resonance cholangiopancreatog - raphy (MRCP), an adult worm may be seen in the common bile duct in a patient presenting with features of  obstructive jaundice ( Figure 6.6 ) . In patients with intestinal obstruction, plain abdominal radiograph may show tubular structures within dilated small bowel, denoting the presence of  worms, - which would also show up on a contrast CT scan as curvilinear structures. - - Summary box 6.4 Ascariasis: pathogenesis - /uni25CF /uni25CF com - /uni25CF /uni25CF /uni25CF /uni25CF -
It is the commonest intestinal nematode affecting humans
Typically found in a humid atmosphere and poor sanitary
conditions, hence is seen in the tropics and resource-poor
countries
Larvae cause pulmonary symptoms; adult worms cause
gastrointestinal, biliary and pancreatic symptoms
Distal ileal obstruction is due to a bolus of worms; ascending
cholangitis and obstructive jaundice are due to infestation of
the common bile duct
Acute pancreatitis occurs when a worm is lodged in the
pancreatic duct
Perforation of the small bowel is rare
BARIUM SEEN INSIDE
THE ROUNDWORM
Figure 6.4
Barium meal and follow-through showing roundworms in
the course of the small bowel with barium seen inside the worms in
an 18-year-old patient who presented with bouts of colicky abdominal
pain and bilious vomiting, which settled with conservative manage
ment (courtesy of Dr PP Bhattacharyya, Kolkata, India).
Investigations
Raised ESR and CRP , low haemoglobin and a positive Mantoux test are usual, although the last is not significant in a patient from an endemic area. The Mantoux test (tuberculin skin test), although in use for over a hundred years, has now been superseded by interferon-gamma (IFN- γ ) release assays. This is an in vitro blood test of  cellular immune response. Antigens unique to M. tuberculosis are used to stimulate and measure T-cell release of  IFN- γ . This helps to earmark patients A collar-stud abscess is so-called because it resembles a collar stud (which has two parts) used in shirts with detachable collars, now largely out of  fashion. Charles Mantoux , 1877–1947, physician, Le Cannet, Alpes Maritimes, France, described the intradermal tuberculin skin test in 1908. Franz Heinrich Paul Ziehl , 1857–1926, German bacteriologist and professor in Lübeck, Germany . With pathologist Ziehl–Neelsen stain, also known as the acid-fast stain, which is used to identify acid-fast bacteria. Friedrich Carl Adolf  Neelsen , 1854–1898, pathologist and professor at the Institute of  Pathology , University of  Rostock, Germany . Summary box 6.22 Tuberculous cervical lymphadenitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF who have latent or subclinical tuberculosis and thus will benefit from treatment. Sputum for culture and sensitivity (the result may take several weeks) and staining by the Ziehl–Neelsen method for acid-fast bacilli (the result is obtained much earlier) should be carried out. Specific investigations would include aspiration of the pus from a cold abscess for culture and sensitivity . If  the mass is still in the early stages of  adenitis, excision biopsy should be done. Here, part of  the lymph nodes should be sent fresh and unfixed to the laboratory , which should be warned of the arrival of the specimen so that the tissue can be appropriately processed immediately .
Figure 6.35
Cervical tuberculous ulcer with typical overhanging
edges (courtesy of Professor Ahmed Hassan Fahal, FRCS MD MS,
Khartoum, Sudan).
This is a common condition at any age
A matted lymph nodal mass is the typical clinical feature
In later stages the mass may be cystic, denoting an abscess
The abscess denotes underlying caseation and does not show
any features of in
/f_l
ammation – hence called a cold abscess
Ultimately the abscess may burst, forming a sinus
Diagnosis is clinched by culture of pus and biopsy of the lymph
node
Involvement of other systems must be excluded
Treatment is mainly medical
Investigations
General investigations are the same as those for suspected tuberculosis anywhere in the body . They have been detailed in the previous section under investigations for tuberculous cervical adenitis. A barium meal and follow-through (or small bowel enema) shows strictures of  the small bowel, particularly the ileum, typ ically with a high subhepatic caecum with the narrow ileum entering the caecum directly from below upwar ds in a straight line rather than at an angle ( Figures 6.38 and 6.39a aroscopy r eveals the typical picture of  tubercles on the bowel serosa, multiple strictures, a high caecum, enlarged lymph fluid may be helpful. A chest radiograph is essential ( Figur e 6.39b ) as there may be features of  pulmonary tuberculosis. If  the pa tient complains of  urinary symptoms, urine is sent for microscopy and culture; the finding of  sterile pyuria should alert the clinician to the possibility of  tuberculosis of  the uri - nary tract, when the appropriate investig ations should be done. A flexible cystoscopy would be very useful in the presence of sterile pyuria. A contracted bladder (‘thimble’ bladder) with ureteric orifices that are in-dra wn (‘golf-hole’ ureter) may be seen; these changes are due to fibrosis. In the patient presenting as an abdominal emergency , urea and electrolytes may show evidence of  gross dehydration. A plain abdominal radiograph shows typical small bowel obstruc - tion – valvulae conniventes (concertina e ff ect) of  dilated jeju - num and featureless ileum with evidence of  fluid between the loops. Summary box 6.25 Intestinal tuberculosis: investigations /uni25CF - /uni25CF γ /uni25CF /uni25CF /uni25CF - /uni25CF
Raised in
/f_l
ammatory markers, anaemia and positive sputum
culture
IFN-
release assays for subclinical infection
Ultrasonography of the abdomen may show localised areas of
ascites
Chest radiograph shows pulmonary in
/f_i
ltration
Barium meal and follow-through shows multiple small bowel
strictures particularly in the ileum, with a subhepatic caecum
If symptoms warrant, the genitourinary tract is also investigated
Investigations
The haematological and biochemical investigations reflect the presence of  a chronic infective process: anaemia, leukocytosis, raised inflammatory markers – erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) – hypoalbuminaemia and deranged liver function tests, particularly elevated alkaline phosphatase. Serological tests are more specific, with the majority of patients showing antibodies in serum. These can be detected by tests for complement fixation, indirect haemagglutination (IHA), indirect immunofluorescence , counter-immunoelectro - phoresis and enzyme-linked immunosorbent assay (ELISA). These tests are extremely useful in detecting acute infection in non-endemic areas. IHA has a very high sensitivity in acute amoebic liver abscess in non-endemic regions and remains ele - vated for some time. The persistence of  antibodies in a large majority of the population in endemic areas precludes its use as a diagnostic investigation in those loca tions. A combination of  serological tests detecting antibodies in combination with detection of the parasite by antigen detection or DNA poly - merase chain reaction is likely to be more beneficial in such cases, though with the limitation of  cost and accessibility in developing nations. While amoebiasis may a ff ect the entire colon, it has a pre - dilection for the caecum and ascending colon. A colonoscopy may rev eal discrete exudate-covered areas of  ulceration with normal areas in between. Investigations
As with most parasitic infestations, an increase in the eosinophil count is common. Stool examination may show ova. Sputum or bronchoscopic washings may show Charcot–Leyden crystals or the larvae. Chest radiograph may show flu ff y exudates in Loe ffl er’s syndrome. A barium meal and follow-through may show a bolus of  worms in the ileum or lying freely within the small bowel ( Figur e 6.4 ). Ultrasonography may show a worm in the gallbladder, the common bile duct ( Figure 6.5 ) or pan - creatic duct. On magnetic resonance cholangiopancreatog - raphy (MRCP), an adult worm may be seen in the common bile duct in a patient presenting with features of  obstructive jaundice ( Figure 6.6 ) . In patients with intestinal obstruction, plain abdominal radiograph may show tubular structures within dilated small bowel, denoting the presence of  worms, - which would also show up on a contrast CT scan as curvilinear structures. - - Summary box 6.4 Ascariasis: pathogenesis - /uni25CF /uni25CF com - /uni25CF /uni25CF /uni25CF /uni25CF -
It is the commonest intestinal nematode affecting humans
Typically found in a humid atmosphere and poor sanitary
conditions, hence is seen in the tropics and resource-poor
countries
Larvae cause pulmonary symptoms; adult worms cause
gastrointestinal, biliary and pancreatic symptoms
Distal ileal obstruction is due to a bolus of worms; ascending
cholangitis and obstructive jaundice are due to infestation of
the common bile duct
Acute pancreatitis occurs when a worm is lodged in the
pancreatic duct
Perforation of the small bowel is rare
BARIUM SEEN INSIDE
THE ROUNDWORM
Figure 6.4
Barium meal and follow-through showing roundworms in
the course of the small bowel with barium seen inside the worms in
an 18-year-old patient who presented with bouts of colicky abdominal
pain and bilious vomiting, which settled with conservative manage
ment (courtesy of Dr PP Bhattacharyya, Kolkata, India).
Investigations
Raised ESR and CRP , low haemoglobin and a positive Mantoux test are usual, although the last is not significant in a patient from an endemic area. The Mantoux test (tuberculin skin test), although in use for over a hundred years, has now been superseded by interferon-gamma (IFN- γ ) release assays. This is an in vitro blood test of  cellular immune response. Antigens unique to M. tuberculosis are used to stimulate and measure T-cell release of  IFN- γ . This helps to earmark patients A collar-stud abscess is so-called because it resembles a collar stud (which has two parts) used in shirts with detachable collars, now largely out of  fashion. Charles Mantoux , 1877–1947, physician, Le Cannet, Alpes Maritimes, France, described the intradermal tuberculin skin test in 1908. Franz Heinrich Paul Ziehl , 1857–1926, German bacteriologist and professor in Lübeck, Germany . With pathologist Ziehl–Neelsen stain, also known as the acid-fast stain, which is used to identify acid-fast bacteria. Friedrich Carl Adolf  Neelsen , 1854–1898, pathologist and professor at the Institute of  Pathology , University of  Rostock, Germany . Summary box 6.22 Tuberculous cervical lymphadenitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF who have latent or subclinical tuberculosis and thus will benefit from treatment. Sputum for culture and sensitivity (the result may take several weeks) and staining by the Ziehl–Neelsen method for acid-fast bacilli (the result is obtained much earlier) should be carried out. Specific investigations would include aspiration of the pus from a cold abscess for culture and sensitivity . If  the mass is still in the early stages of  adenitis, excision biopsy should be done. Here, part of  the lymph nodes should be sent fresh and unfixed to the laboratory , which should be warned of the arrival of the specimen so that the tissue can be appropriately processed immediately .
Figure 6.35
Cervical tuberculous ulcer with typical overhanging
edges (courtesy of Professor Ahmed Hassan Fahal, FRCS MD MS,
Khartoum, Sudan).
This is a common condition at any age
A matted lymph nodal mass is the typical clinical feature
In later stages the mass may be cystic, denoting an abscess
The abscess denotes underlying caseation and does not show
any features of in
/f_l
ammation – hence called a cold abscess
Ultimately the abscess may burst, forming a sinus
Diagnosis is clinched by culture of pus and biopsy of the lymph
node
Involvement of other systems must be excluded
Treatment is mainly medical
Investigations
General investigations are the same as those for suspected tuberculosis anywhere in the body . They have been detailed in the previous section under investigations for tuberculous cervical adenitis. A barium meal and follow-through (or small bowel enema) shows strictures of  the small bowel, particularly the ileum, typ ically with a high subhepatic caecum with the narrow ileum entering the caecum directly from below upwar ds in a straight line rather than at an angle ( Figures 6.38 and 6.39a aroscopy r eveals the typical picture of  tubercles on the bowel serosa, multiple strictures, a high caecum, enlarged lymph fluid may be helpful. A chest radiograph is essential ( Figur e 6.39b ) as there may be features of  pulmonary tuberculosis. If  the pa tient complains of  urinary symptoms, urine is sent for microscopy and culture; the finding of  sterile pyuria should alert the clinician to the possibility of  tuberculosis of  the uri - nary tract, when the appropriate investig ations should be done. A flexible cystoscopy would be very useful in the presence of sterile pyuria. A contracted bladder (‘thimble’ bladder) with ureteric orifices that are in-dra wn (‘golf-hole’ ureter) may be seen; these changes are due to fibrosis. In the patient presenting as an abdominal emergency , urea and electrolytes may show evidence of  gross dehydration. A plain abdominal radiograph shows typical small bowel obstruc - tion – valvulae conniventes (concertina e ff ect) of  dilated jeju - num and featureless ileum with evidence of  fluid between the loops. Summary box 6.25 Intestinal tuberculosis: investigations /uni25CF - /uni25CF γ /uni25CF /uni25CF /uni25CF - /uni25CF
Raised in
/f_l
ammatory markers, anaemia and positive sputum
culture
IFN-
release assays for subclinical infection
Ultrasonography of the abdomen may show localised areas of
ascites
Chest radiograph shows pulmonary in
/f_i
ltration
Barium meal and follow-through shows multiple small bowel
strictures particularly in the ileum, with a subhepatic caecum
If symptoms warrant, the genitourinary tract is also investigated
Investigations
The haematological and biochemical investigations reflect the presence of  a chronic infective process: anaemia, leukocytosis, raised inflammatory markers – erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) – hypoalbuminaemia and deranged liver function tests, particularly elevated alkaline phosphatase. Serological tests are more specific, with the majority of patients showing antibodies in serum. These can be detected by tests for complement fixation, indirect haemagglutination (IHA), indirect immunofluorescence , counter-immunoelectro - phoresis and enzyme-linked immunosorbent assay (ELISA). These tests are extremely useful in detecting acute infection in non-endemic areas. IHA has a very high sensitivity in acute amoebic liver abscess in non-endemic regions and remains ele - vated for some time. The persistence of  antibodies in a large majority of the population in endemic areas precludes its use as a diagnostic investigation in those loca tions. A combination of  serological tests detecting antibodies in combination with detection of the parasite by antigen detection or DNA poly - merase chain reaction is likely to be more beneficial in such cases, though with the limitation of  cost and accessibility in developing nations. While amoebiasis may a ff ect the entire colon, it has a pre - dilection for the caecum and ascending colon. A colonoscopy may rev eal discrete exudate-covered areas of  ulceration with normal areas in between. Investigations
As with most parasitic infestations, an increase in the eosinophil count is common. Stool examination may show ova. Sputum or bronchoscopic washings may show Charcot–Leyden crystals or the larvae. Chest radiograph may show flu ff y exudates in Loe ffl er’s syndrome. A barium meal and follow-through may show a bolus of  worms in the ileum or lying freely within the small bowel ( Figur e 6.4 ). Ultrasonography may show a worm in the gallbladder, the common bile duct ( Figure 6.5 ) or pan - creatic duct. On magnetic resonance cholangiopancreatog - raphy (MRCP), an adult worm may be seen in the common bile duct in a patient presenting with features of  obstructive jaundice ( Figure 6.6 ) . In patients with intestinal obstruction, plain abdominal radiograph may show tubular structures within dilated small bowel, denoting the presence of  worms, - which would also show up on a contrast CT scan as curvilinear structures. - - Summary box 6.4 Ascariasis: pathogenesis - /uni25CF /uni25CF com - /uni25CF /uni25CF /uni25CF /uni25CF -
It is the commonest intestinal nematode affecting humans
Typically found in a humid atmosphere and poor sanitary
conditions, hence is seen in the tropics and resource-poor
countries
Larvae cause pulmonary symptoms; adult worms cause
gastrointestinal, biliary and pancreatic symptoms
Distal ileal obstruction is due to a bolus of worms; ascending
cholangitis and obstructive jaundice are due to infestation of
the common bile duct
Acute pancreatitis occurs when a worm is lodged in the
pancreatic duct
Perforation of the small bowel is rare
BARIUM SEEN INSIDE
THE ROUNDWORM
Figure 6.4
Barium meal and follow-through showing roundworms in
the course of the small bowel with barium seen inside the worms in
an 18-year-old patient who presented with bouts of colicky abdominal
pain and bilious vomiting, which settled with conservative manage
ment (courtesy of Dr PP Bhattacharyya, Kolkata, India).
Investigations
Raised ESR and CRP , low haemoglobin and a positive Mantoux test are usual, although the last is not significant in a patient from an endemic area. The Mantoux test (tuberculin skin test), although in use for over a hundred years, has now been superseded by interferon-gamma (IFN- γ ) release assays. This is an in vitro blood test of  cellular immune response. Antigens unique to M. tuberculosis are used to stimulate and measure T-cell release of  IFN- γ . This helps to earmark patients A collar-stud abscess is so-called because it resembles a collar stud (which has two parts) used in shirts with detachable collars, now largely out of  fashion. Charles Mantoux , 1877–1947, physician, Le Cannet, Alpes Maritimes, France, described the intradermal tuberculin skin test in 1908. Franz Heinrich Paul Ziehl , 1857–1926, German bacteriologist and professor in Lübeck, Germany . With pathologist Ziehl–Neelsen stain, also known as the acid-fast stain, which is used to identify acid-fast bacteria. Friedrich Carl Adolf  Neelsen , 1854–1898, pathologist and professor at the Institute of  Pathology , University of  Rostock, Germany . Summary box 6.22 Tuberculous cervical lymphadenitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF who have latent or subclinical tuberculosis and thus will benefit from treatment. Sputum for culture and sensitivity (the result may take several weeks) and staining by the Ziehl–Neelsen method for acid-fast bacilli (the result is obtained much earlier) should be carried out. Specific investigations would include aspiration of the pus from a cold abscess for culture and sensitivity . If  the mass is still in the early stages of  adenitis, excision biopsy should be done. Here, part of  the lymph nodes should be sent fresh and unfixed to the laboratory , which should be warned of the arrival of the specimen so that the tissue can be appropriately processed immediately .
Figure 6.35
Cervical tuberculous ulcer with typical overhanging
edges (courtesy of Professor Ahmed Hassan Fahal, FRCS MD MS,
Khartoum, Sudan).
This is a common condition at any age
A matted lymph nodal mass is the typical clinical feature
In later stages the mass may be cystic, denoting an abscess
The abscess denotes underlying caseation and does not show
any features of in
/f_l
ammation – hence called a cold abscess
Ultimately the abscess may burst, forming a sinus
Diagnosis is clinched by culture of pus and biopsy of the lymph
node
Involvement of other systems must be excluded
Treatment is mainly medical
Investigations
General investigations are the same as those for suspected tuberculosis anywhere in the body . They have been detailed in the previous section under investigations for tuberculous cervical adenitis. A barium meal and follow-through (or small bowel enema) shows strictures of  the small bowel, particularly the ileum, typ ically with a high subhepatic caecum with the narrow ileum entering the caecum directly from below upwar ds in a straight line rather than at an angle ( Figures 6.38 and 6.39a aroscopy r eveals the typical picture of  tubercles on the bowel serosa, multiple strictures, a high caecum, enlarged lymph fluid may be helpful. A chest radiograph is essential ( Figur e 6.39b ) as there may be features of  pulmonary tuberculosis. If  the pa tient complains of  urinary symptoms, urine is sent for microscopy and culture; the finding of  sterile pyuria should alert the clinician to the possibility of  tuberculosis of  the uri - nary tract, when the appropriate investig ations should be done. A flexible cystoscopy would be very useful in the presence of sterile pyuria. A contracted bladder (‘thimble’ bladder) with ureteric orifices that are in-dra wn (‘golf-hole’ ureter) may be seen; these changes are due to fibrosis. In the patient presenting as an abdominal emergency , urea and electrolytes may show evidence of  gross dehydration. A plain abdominal radiograph shows typical small bowel obstruc - tion – valvulae conniventes (concertina e ff ect) of  dilated jeju - num and featureless ileum with evidence of  fluid between the loops. Summary box 6.25 Intestinal tuberculosis: investigations /uni25CF - /uni25CF γ /uni25CF /uni25CF /uni25CF - /uni25CF
Raised in
/f_l
ammatory markers, anaemia and positive sputum
culture
IFN-
release assays for subclinical infection
Ultrasonography of the abdomen may show localised areas of
ascites
Chest radiograph shows pulmonary in
/f_i
ltration
Barium meal and follow-through shows multiple small bowel
strictures particularly in the ileum, with a subhepatic caecum
If symptoms warrant, the genitourinary tract is also investigated

LEPROSY Introduction
LEPROSY Introduction
Leprosy , also called Hansen’s disease, is a chronic infectious disease caused by an acid-fast bacillus, Mycobacterium leprae, that is widely prevalent in the tropics. Globally , India, Brazil, Nepal, Mozambique, Angola and Myanmar account for 91% of  all cases; India alone accounts for 78% of  the world’s disease. Patients su ff er not only from the primary e ff ects of  the disease but also from social discrimination, sadly compounded by use of  the word ‘leper’ for one a ffl icted with this disease. Close contact over a long duration (several years) is required for disease transmission. Ignorance of  this fact on the part of the general public results in ostracism and social stigma. His - tory records that in the distant past su ff erers were made to wear cow bells so that other people could avoid them. The use of the term ‘leper’, still used metaphorically to denote an outcast, does not help to break down the social barriers that continue to exist against the su ff erer. LEPROSY Introduction
Leprosy , also called Hansen’s disease, is a chronic infectious disease caused by an acid-fast bacillus, Mycobacterium leprae, that is widely prevalent in the tropics. Globally , India, Brazil, Nepal, Mozambique, Angola and Myanmar account for 91% of  all cases; India alone accounts for 78% of  the world’s disease. Patients su ff er not only from the primary e ff ects of  the disease but also from social discrimination, sadly compounded by use of  the word ‘leper’ for one a ffl icted with this disease. Close contact over a long duration (several years) is required for disease transmission. Ignorance of  this fact on the part of the general public results in ostracism and social stigma. His - tory records that in the distant past su ff erers were made to wear cow bells so that other people could avoid them. The use of the term ‘leper’, still used metaphorically to denote an outcast, does not help to break down the social barriers that continue to exist against the su ff erer. LEPROSY Introduction
Leprosy , also called Hansen’s disease, is a chronic infectious disease caused by an acid-fast bacillus, Mycobacterium leprae, that is widely prevalent in the tropics. Globally , India, Brazil, Nepal, Mozambique, Angola and Myanmar account for 91% of  all cases; India alone accounts for 78% of  the world’s disease. Patients su ff er not only from the primary e ff ects of  the disease but also from social discrimination, sadly compounded by use of  the word ‘leper’ for one a ffl icted with this disease. Close contact over a long duration (several years) is required for disease transmission. Ignorance of  this fact on the part of the general public results in ostracism and social stigma. His - tory records that in the distant past su ff erers were made to wear cow bells so that other people could avoid them. The use of the term ‘leper’, still used metaphorically to denote an outcast, does not help to break down the social barriers that continue to exist against the su ff erer.

Learning objectives
Learning objectives
To be able to list: The common surgical infections and infestations that • occur in the tropics To appreciate: That many patients do not seek medical help until late • in the course of the disease because of socioeconomic reasons To be able to describe: The emergency presentations of the various conditions, as • patients may not seek treatment until they are very ill Learning objectives
To be able to list: The common surgical infections and infestations that • occur in the tropics To appreciate: That many patients do not seek medical help until late • in the course of the disease because of socioeconomic reasons To be able to describe: The emergency presentations of the various conditions, as • patients may not seek treatment until they are very ill Learning objectives
To be able to list: The common surgical infections and infestations that • occur in the tropics To appreciate: That many patients do not seek medical help until late • in the course of the disease because of socioeconomic reasons To be able to describe: The emergency presentations of the various conditions, as • patients may not seek treatment until they are very ill

MYCETOMA Introduction
MYCETOMA Introduction
Mycetoma is a chronic, specific, granulomatous, progressive, destructive inflammatory disease that involves the skin, subcu taneous tissues and deeper structures. The causative organism may be true fungi, when the condition is called eumyce toma; when caused by bacteria it is called actinomycetoma. The /uni00A0 pathognomonic feature is the triad of  painless subcuta - neous mass, multiple sinuses and seropurulent discharge. It causes tissue destruction, deformity and disability , and death in extreme cases.
Figure 6.22
Typical leonine facies and gynaecomastia in leprosy.
MYCETOMA Introduction
Mycetoma is a chronic, specific, granulomatous, progressive, destructive inflammatory disease that involves the skin, subcu taneous tissues and deeper structures. The causative organism may be true fungi, when the condition is called eumyce toma; when caused by bacteria it is called actinomycetoma. The /uni00A0 pathognomonic feature is the triad of  painless subcuta - neous mass, multiple sinuses and seropurulent discharge. It causes tissue destruction, deformity and disability , and death in extreme cases.
Figure 6.22
Typical leonine facies and gynaecomastia in leprosy.
MYCETOMA Introduction
Mycetoma is a chronic, specific, granulomatous, progressive, destructive inflammatory disease that involves the skin, subcu taneous tissues and deeper structures. The causative organism may be true fungi, when the condition is called eumyce toma; when caused by bacteria it is called actinomycetoma. The /uni00A0 pathognomonic feature is the triad of  painless subcuta - neous mass, multiple sinuses and seropurulent discharge. It causes tissue destruction, deformity and disability , and death in extreme cases.
Figure 6.22
Typical leonine facies and gynaecomastia in leprosy.

Management
Management
Surgical management is directed mainly towards the rehabili - tation of the patient who has residual paralysis, the operations being tailored to the particular individual’s disability . Children especially may show improvement in their muscle function for up to 2 years after the onset of  the illness. Ther eafter, many patients learn to manage their disability by incorporating various manoeuvres (‘trick movements’) into their daily life. The surgeon must be cautious in considering such a patient for any form of  surgery . Surgical treatment in the chronic form of  the disease is the domain of  a highly specialised orthopaedic surgeon who needs (b) to work closely with the physiotherapist both in assessing and in rehabilitating the patient. Operations are only considered after a very careful and detailed assessment of  the patient’s needs. A multidisciplinary team, consisting of  the orthopaedic surgeon, neurologist, physiotherapist, orthotist and the family , should decide upon the need for and advisability of  any sur gical procedure. A description of  the operations for the various disabilities is beyond the scope of  this book. The reader should therefore seek surgical details in a specialist textbook. In 2012, WHO declared India a polio-free country . Summary box 6.18 Poliomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.31 (a, b)
A 12-year-old patient with polio showing marked
wasting of the left upper arm muscles with
/f_l
exion contractures of the
left knee and hip; there is equinus deformity of the foot (courtesy of Dr
SM Lakhotia, MS and Dr PK Jain, MD, DA, Kolkata, India).
A viral illness that is preventable
Presents with protean manifestations of fever, headache and
muscular paralysis without sensory loss, more frequently
affecting the lower limbs
Treatment is mainly medical and supportive in the early stages
Surgery should only be undertaken after very careful
assessment as most patients learn to live with their disabilities
Surgery is considered for the various types of paralysis in the
form of tendon transfers and arthrodesis, which is the domain
of a specialist orthopaedic surgeon
Figure 6.32
A young patient with polio showing paralysis of the
lower limb and paraspinal muscles causing marked scoliosis and a
deformed pelvis.
Management
Surgical management is directed mainly towards the rehabili - tation of the patient who has residual paralysis, the operations being tailored to the particular individual’s disability . Children especially may show improvement in their muscle function for up to 2 years after the onset of  the illness. Ther eafter, many patients learn to manage their disability by incorporating various manoeuvres (‘trick movements’) into their daily life. The surgeon must be cautious in considering such a patient for any form of  surgery . Surgical treatment in the chronic form of  the disease is the domain of  a highly specialised orthopaedic surgeon who needs (b) to work closely with the physiotherapist both in assessing and in rehabilitating the patient. Operations are only considered after a very careful and detailed assessment of  the patient’s needs. A multidisciplinary team, consisting of  the orthopaedic surgeon, neurologist, physiotherapist, orthotist and the family , should decide upon the need for and advisability of  any sur gical procedure. A description of  the operations for the various disabilities is beyond the scope of  this book. The reader should therefore seek surgical details in a specialist textbook. In 2012, WHO declared India a polio-free country . Summary box 6.18 Poliomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.31 (a, b)
A 12-year-old patient with polio showing marked
wasting of the left upper arm muscles with
/f_l
exion contractures of the
left knee and hip; there is equinus deformity of the foot (courtesy of Dr
SM Lakhotia, MS and Dr PK Jain, MD, DA, Kolkata, India).
A viral illness that is preventable
Presents with protean manifestations of fever, headache and
muscular paralysis without sensory loss, more frequently
affecting the lower limbs
Treatment is mainly medical and supportive in the early stages
Surgery should only be undertaken after very careful
assessment as most patients learn to live with their disabilities
Surgery is considered for the various types of paralysis in the
form of tendon transfers and arthrodesis, which is the domain
of a specialist orthopaedic surgeon
Figure 6.32
A young patient with polio showing paralysis of the
lower limb and paraspinal muscles causing marked scoliosis and a
deformed pelvis.
Management
Surgical management is directed mainly towards the rehabili - tation of the patient who has residual paralysis, the operations being tailored to the particular individual’s disability . Children especially may show improvement in their muscle function for up to 2 years after the onset of  the illness. Ther eafter, many patients learn to manage their disability by incorporating various manoeuvres (‘trick movements’) into their daily life. The surgeon must be cautious in considering such a patient for any form of  surgery . Surgical treatment in the chronic form of  the disease is the domain of  a highly specialised orthopaedic surgeon who needs (b) to work closely with the physiotherapist both in assessing and in rehabilitating the patient. Operations are only considered after a very careful and detailed assessment of  the patient’s needs. A multidisciplinary team, consisting of  the orthopaedic surgeon, neurologist, physiotherapist, orthotist and the family , should decide upon the need for and advisability of  any sur gical procedure. A description of  the operations for the various disabilities is beyond the scope of  this book. The reader should therefore seek surgical details in a specialist textbook. In 2012, WHO declared India a polio-free country . Summary box 6.18 Poliomyelitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.31 (a, b)
A 12-year-old patient with polio showing marked
wasting of the left upper arm muscles with
/f_l
exion contractures of the
left knee and hip; there is equinus deformity of the foot (courtesy of Dr
SM Lakhotia, MS and Dr PK Jain, MD, DA, Kolkata, India).
A viral illness that is preventable
Presents with protean manifestations of fever, headache and
muscular paralysis without sensory loss, more frequently
affecting the lower limbs
Treatment is mainly medical and supportive in the early stages
Surgery should only be undertaken after very careful
assessment as most patients learn to live with their disabilities
Surgery is considered for the various types of paralysis in the
form of tendon transfers and arthrodesis, which is the domain
of a specialist orthopaedic surgeon
Figure 6.32
A young patient with polio showing paralysis of the
lower limb and paraspinal muscles causing marked scoliosis and a
deformed pelvis.

POLIOMYELITIS Introduction
POLIOMYELITIS Introduction
Poliomyelitis is an enteroviral infection that sadly still a ff ects children in certain parts of  the world – this is in spite of  e ff ec - tive vaccination having been universally available for several decades. The virus enters the body by inhalation or ingestion. Clinically , the disease manifests itself  in a wide spectrum of symptoms – fr om a few days of  mild fever and headache to the extreme variety consisting of  extensive paralysis of  the bulbar form that may not be compatible with life because of involvement of  the respiratory and pharyngeal muscles. - POLIOMYELITIS Introduction
Poliomyelitis is an enteroviral infection that sadly still a ff ects children in certain parts of  the world – this is in spite of  e ff ec - tive vaccination having been universally available for several decades. The virus enters the body by inhalation or ingestion. Clinically , the disease manifests itself  in a wide spectrum of symptoms – fr om a few days of  mild fever and headache to the extreme variety consisting of  extensive paralysis of  the bulbar form that may not be compatible with life because of involvement of  the respiratory and pharyngeal muscles. - POLIOMYELITIS Introduction
Poliomyelitis is an enteroviral infection that sadly still a ff ects children in certain parts of  the world – this is in spite of  e ff ec - tive vaccination having been universally available for several decades. The virus enters the body by inhalation or ingestion. Clinically , the disease manifests itself  in a wide spectrum of symptoms – fr om a few days of  mild fever and headache to the extreme variety consisting of  extensive paralysis of  the bulbar form that may not be compatible with life because of involvement of  the respiratory and pharyngeal muscles. -

Pathogenesis
Pathogenesis
y are The organism enters the gut through food or water contam - inated with the cyst. In the small bowel, the cysts hatch and a large number of  trophozoites are released and carried to the colon, where flask-shaped ulcers form in the submucosa. from The tr ophozoites multiply , ultimately forming cysts, which either enter the portal circulation or are passed in the faeces as an infective form that infects other humans as a result of insanitary conditions. Having entered the portal circulation, the trophozoites are filtered and trapped in the interlobular veins of  the liver. They multiply in the portal triads, causing f ocal infarction of hepatocytes and liquefactive necrosis as a result of  proteolytic enzymes produced by the trophozoites. The areas of necro - sis eventually coalesce to form the abscess cavity . The term ‘amoebic hepatitis’ is used to describe the microscopic picture in the absence of  macroscopic abscess, a di ff erentiation only in theory because the medical treatment is the same. The right lobe is inv olved in 80% of  cases, the left in 10% and the remainder are multiple. One possible explanation for the more common involvement of  the right lobe of  the liver is that b lood from the superior mesenteric vein runs on a straighter course through the portal vein into the larger lobe. in The abscesses are most common high in the diaphragmatic surface of  the right lobe. This may cause pulmonary symptoms coloured, odourless, ‘anchovy sauce’-like fluid that is a mixture of  necrotic liver tissue and blood. There may be secondary infection of  the abscess, which causes the pus to smell. While pus in the abscess is sterile unless secondarily infected, trophozoites may be f ound in the abscess wall in a minority of cases. Untreated abscesses are likely to rupture. Chronic infection of  the large bowel may result in a gran ulomatous lesion along the large bowel, most commonly seen in the caecum, called an amoeboma. Summary box 6.1 Amoebiasis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
E. histolytica
is the most common pathogenic amoeba in
humans
The vast majority of carriers are asymptomatic
Insanitary conditions and poor personal hygiene encourage
transmission of the infection
In the small intestine, the parasite hatches into trophozoites,
which invade the submucosa to produce
/f_l
ask-shaped ulcers in
the colon
In the portal circulation, the parasite causes liquefactive
necrosis in the liver, producing an abscess, the commonest
extraintestinal manifestation
The majority of abscesses occur in the right lobe of the liver
A mass in the course of the large bowel may indicate an
amoeboma
Pathogenesis
y are The organism enters the gut through food or water contam - inated with the cyst. In the small bowel, the cysts hatch and a large number of  trophozoites are released and carried to the colon, where flask-shaped ulcers form in the submucosa. from The tr ophozoites multiply , ultimately forming cysts, which either enter the portal circulation or are passed in the faeces as an infective form that infects other humans as a result of insanitary conditions. Having entered the portal circulation, the trophozoites are filtered and trapped in the interlobular veins of  the liver. They multiply in the portal triads, causing f ocal infarction of hepatocytes and liquefactive necrosis as a result of  proteolytic enzymes produced by the trophozoites. The areas of necro - sis eventually coalesce to form the abscess cavity . The term ‘amoebic hepatitis’ is used to describe the microscopic picture in the absence of  macroscopic abscess, a di ff erentiation only in theory because the medical treatment is the same. The right lobe is inv olved in 80% of  cases, the left in 10% and the remainder are multiple. One possible explanation for the more common involvement of  the right lobe of  the liver is that b lood from the superior mesenteric vein runs on a straighter course through the portal vein into the larger lobe. in The abscesses are most common high in the diaphragmatic surface of  the right lobe. This may cause pulmonary symptoms coloured, odourless, ‘anchovy sauce’-like fluid that is a mixture of  necrotic liver tissue and blood. There may be secondary infection of  the abscess, which causes the pus to smell. While pus in the abscess is sterile unless secondarily infected, trophozoites may be f ound in the abscess wall in a minority of cases. Untreated abscesses are likely to rupture. Chronic infection of  the large bowel may result in a gran ulomatous lesion along the large bowel, most commonly seen in the caecum, called an amoeboma. Summary box 6.1 Amoebiasis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
E. histolytica
is the most common pathogenic amoeba in
humans
The vast majority of carriers are asymptomatic
Insanitary conditions and poor personal hygiene encourage
transmission of the infection
In the small intestine, the parasite hatches into trophozoites,
which invade the submucosa to produce
/f_l
ask-shaped ulcers in
the colon
In the portal circulation, the parasite causes liquefactive
necrosis in the liver, producing an abscess, the commonest
extraintestinal manifestation
The majority of abscesses occur in the right lobe of the liver
A mass in the course of the large bowel may indicate an
amoeboma
Pathogenesis
y are The organism enters the gut through food or water contam - inated with the cyst. In the small bowel, the cysts hatch and a large number of  trophozoites are released and carried to the colon, where flask-shaped ulcers form in the submucosa. from The tr ophozoites multiply , ultimately forming cysts, which either enter the portal circulation or are passed in the faeces as an infective form that infects other humans as a result of insanitary conditions. Having entered the portal circulation, the trophozoites are filtered and trapped in the interlobular veins of  the liver. They multiply in the portal triads, causing f ocal infarction of hepatocytes and liquefactive necrosis as a result of  proteolytic enzymes produced by the trophozoites. The areas of necro - sis eventually coalesce to form the abscess cavity . The term ‘amoebic hepatitis’ is used to describe the microscopic picture in the absence of  macroscopic abscess, a di ff erentiation only in theory because the medical treatment is the same. The right lobe is inv olved in 80% of  cases, the left in 10% and the remainder are multiple. One possible explanation for the more common involvement of  the right lobe of  the liver is that b lood from the superior mesenteric vein runs on a straighter course through the portal vein into the larger lobe. in The abscesses are most common high in the diaphragmatic surface of  the right lobe. This may cause pulmonary symptoms coloured, odourless, ‘anchovy sauce’-like fluid that is a mixture of  necrotic liver tissue and blood. There may be secondary infection of  the abscess, which causes the pus to smell. While pus in the abscess is sterile unless secondarily infected, trophozoites may be f ound in the abscess wall in a minority of cases. Untreated abscesses are likely to rupture. Chronic infection of  the large bowel may result in a gran ulomatous lesion along the large bowel, most commonly seen in the caecum, called an amoeboma. Summary box 6.1 Amoebiasis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
E. histolytica
is the most common pathogenic amoeba in
humans
The vast majority of carriers are asymptomatic
Insanitary conditions and poor personal hygiene encourage
transmission of the infection
In the small intestine, the parasite hatches into trophozoites,
which invade the submucosa to produce
/f_l
ask-shaped ulcers in
the colon
In the portal circulation, the parasite causes liquefactive
necrosis in the liver, producing an abscess, the commonest
extraintestinal manifestation
The majority of abscesses occur in the right lobe of the liver
A mass in the course of the large bowel may indicate an
amoeboma

Pathology and life cycle
Pathology and life cycle
The fertilised eggs can survive in a hostile environment for a long time. The hot and humid conditions in the tropics are ideally suited for the eggs to turn into embryos. The fertilised eggs are present in soil contaminated with infected faeces, becoming infective in about 3 weeks. Faecal–oral contamina tion causes human infection. The eggs are ingested and the larvae are released in the jejunum, from where they travel to the liver via the portal sys tem and the lymphatics. The larvae reach the lungs via the sys temic circulation, where they undergo maturation for 2 weeks. The developed larvae reach the alveoli, are coughed up, swallowed and continue their maturation in the small intestine. Sometimes, the young worms migrate from the tracheobron c hial tree into the oesophagus, thus finding their way into the gastrointestinal tract, from where they can migrate to the mon bile duct or pancreatic duct. The mature female, once in the small bowel, produces innumerable eggs that are fertilised and thereafter excreted in the stool to perpetuate the life cycle. Eg gs in the biliary tract can form a nidus for a stone. Pathology and life cycle
The fertilised eggs can survive in a hostile environment for a long time. The hot and humid conditions in the tropics are ideally suited for the eggs to turn into embryos. The fertilised eggs are present in soil contaminated with infected faeces, becoming infective in about 3 weeks. Faecal–oral contamina tion causes human infection. The eggs are ingested and the larvae are released in the jejunum, from where they travel to the liver via the portal sys tem and the lymphatics. The larvae reach the lungs via the sys temic circulation, where they undergo maturation for 2 weeks. The developed larvae reach the alveoli, are coughed up, swallowed and continue their maturation in the small intestine. Sometimes, the young worms migrate from the tracheobron c hial tree into the oesophagus, thus finding their way into the gastrointestinal tract, from where they can migrate to the mon bile duct or pancreatic duct. The mature female, once in the small bowel, produces innumerable eggs that are fertilised and thereafter excreted in the stool to perpetuate the life cycle. Eg gs in the biliary tract can form a nidus for a stone. Pathology and life cycle
The fertilised eggs can survive in a hostile environment for a long time. The hot and humid conditions in the tropics are ideally suited for the eggs to turn into embryos. The fertilised eggs are present in soil contaminated with infected faeces, becoming infective in about 3 weeks. Faecal–oral contamina tion causes human infection. The eggs are ingested and the larvae are released in the jejunum, from where they travel to the liver via the portal sys tem and the lymphatics. The larvae reach the lungs via the sys temic circulation, where they undergo maturation for 2 weeks. The developed larvae reach the alveoli, are coughed up, swallowed and continue their maturation in the small intestine. Sometimes, the young worms migrate from the tracheobron c hial tree into the oesophagus, thus finding their way into the gastrointestinal tract, from where they can migrate to the mon bile duct or pancreatic duct. The mature female, once in the small bowel, produces innumerable eggs that are fertilised and thereafter excreted in the stool to perpetuate the life cycle. Eg gs in the biliary tract can form a nidus for a stone.

Pathology
Pathology
In humans, the parasite matures into the adult worm in the intrahepatic biliary radicles, where it may reside for many years. The intrahepatic bile ducts are dilated, with epithelial hyperplasia and periductal fibrosis. These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and dreaded complication of  this parasitic infestation. The eggs or dead worms may form a nidus for stone forma - tion in the gallbladder or common bile duct, which becomes thickened and much dilated in the late stages. Intrahepatic bile duct stones ar e also caused by the parasite producing mucin - rich bile. The dilated intrahepatic bile ducts may lead to chol - angitis, liver abscess and hepatitis. Pathology
The bacillus inhabits the colder parts of  the body; hence, it is found in the nasal mucosa and skin in the region of the ears, foramen. The disease is transmitted from the nasal secretions of  a patient, the infection being contracted in childhood or early adolescence. After an incubation period of  several years, the disease presents with skin, upper respiratory or neurologi cal manifestations. The bacillus is acid fast but weakly so when compared with Mycobacterium tuberculosis. The disease is broadly classified into two groups: leproma tous and tuberculoid. In lepromatous leprosy , there is wide spread dissemination of  abundant bacilli in the tissues, with macrophages and few lymphocytes. This is a reflection of  the poor immune response, resulting in depleted host resistance from the patient. In tuberculoid leprosy , on the other hand, the patient shows a strong immune response with scant bacilli in the tissues, epithelioid granulomas, numerous lymphocytes and giant cells. The tissue damage is inversely proportional to the host’s immune response. There are various grades of  the disease between the two main spectra called dimorphous or borderline variant. Summary box 6.12 Mycobacterium leprae : pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Leprosy is a chronic curable infection caused by
M. leprae
It occurs mainly in tropical regions and resource-poor countries
The majority of cases are located in the Indian subcontinent
Transmission is through nasal secretions, the bacillus inhabiting
the colder parts of the body
It is attributed to poor hygiene and insanitary conditions
The incubation period is several years
The initial infection occurs in childhood
Lepromatous leprosy denotes a poor host immune reaction
Tuberculoid leprosy occurs when host resistance is stronger
than the virulence of the organism
Pathology
There are two types: ulcerative and hyperplastic. In both types, there may be marked mesenteric lymphadenopathy . /uni25CF Ulcerative type: The organism colonises the lymphat ics of  the terminal ileum, causing transverse ulcers with typical undermined edges. The serosa is usually studded with tubercles. Histology shows caseating granuloma with giant cells ( Figure 6.36 ). This pathological entity , referred to as the ulcerative type, denotes a severe form of  the dis ease in which the virulence of  the organism overwhelms ★
Burrill Bernard Crohn , 1884–1983, gastroenterologist, Mount Sinai Hospital, New Y ork, NY , USA, described regional ileitis in 1932 along with Leon Ginzburg and Gordon Oppenheimer. ulcers lead to multiple strictures that may present later with luminal narrowing and intestinal obstruction. /uni25CF Hyperplastic type: This occurs when host resistance has the upper hand over the virulence of  the organism. There is a marked inflammatory reaction causing hyper - plasia and thickening of  the terminal ileum because of its abundance of  lymphoid follicles, thus resulting in nar - rowing of  the lumen and obstruction. Macroscopically , this type ma y be confused with Crohn’s disease. Ileocaecal right iliac tuberculosis ( Figure 6.37 ) may present with a - fossa mass and features of  intestinal obstruction. As a result of  fibrosis, there is shortening of  the bowel with the cae - cum being pulled up into a subhepatic position with resul - tant widening of  the ileocaecal angle beyond 90°. Summary box 6.23 - Tuberculosis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF
Figure 6.36
Histology of ileocaecal tuberculosis showing epithelioid
cell granuloma (black arrows) with caseation (star) (courtesy of Dr AK
Mandal, New Delhi, India).
Increasingly being seen in non-endemic areas, mostly among
immigrants from endemic areas
Two types are recognised – ulcerative and hyperplastic
The ulcerative type occurs when the virulence of the organism
is greater than the host defence and forms strictures
The opposite occurs in the hyperplastic type and presents with
a mass
Small bowel strictures are common in the ulcerative type,
presenting with obstructive symptoms, while the hyperplastic
type mainly affects the ileocaecal area and presents with a right
iliac fossa mass and obstructive symptoms
In peritoneal tuberculosis, the parietal and visceral peritoneum
is studded with tubercles
Localised areas of ascites (loculated) depicts peritoneal
involvement
Encasement of bowel in a
/f_i
brotic sac (cocoon) may be seen in
the plastic type of peritoneal tuberculosis, which presents with
obstruction
The lungs and other organs, particularly of the genitourinary
system, may also be involved simultaneously
Pathology
Following ingestion of contaminated food or water, the organ ism colonises the Peyer’s patches in the terminal ileum, causing hyperplasia of  the lymphoid follicles followed by necrosis and ulceration. The microscopic picture shows erythrophagocyto sis with histiocytic proliferation ( Figure 6.40 ). If  the patient is left untreated or inadequately treated, the ulcers may lead to perforation and bleeding. The bowel may perforate at several sites, including the large bow el. Daniel Elmer Salmon , 1850–1914, veterinary pathologist, Chief  of  the Bureau of  Animal Industry , Washington, DC, USA. Johann Conrad P eyer , 1653–1712, Professor of  Logic, Rhetoric and Medicine, Scha ff hausen, Switzerland, described the lymph follicles in the intestine in 1677. e Widal , 1862–1929, Professor of  Internal Pathology , and later of  Clinical Medicine, The Faculty of  Medicine, Paris, France. Georges Fernand Isidor A typical patient is from an endemic area or has recently visited such a country and su ff ers from a high temperature for 2–3 weeks. The patient may be toxic with abdominal distension from paralytic ileus and may have melaena due to haemor - rhage from a typhoid ulcer; this can lead to hypovolaemia. Blood and stool cultures confirm the nature of  the infection and exclude malaria. Although obsolete in some parts of the world, the Widal test is still done on the Indian subcontinent. The test looks for the pr esence of  agglutinins to O and H antigens of Salmonella Typhi and Paratyphi in the patient’s serum. In endemic areas, laboratory facilities may sometimes be limited. Certain other tests have been developed that identify sensitive and specific markers for typhoid fever. Practical and cheap kits are available for their rapid detection that need no special expertise and equipment. These are MultiTest Dip-S-Ticks to detect immunoglobulin G (IgG), Tubex to detect immunoglobulin M (IgM) and TyphiDot to detect IgG and IgM. These tests are particularly valuable when blood cultures are negative (as a result of prehospital treatment or self-medication with antibiotics) or facilities for such an investigation are not available. In the second or third week of  the illness, if  there is severe generalised abdominal pain, this indicates a perforated typhoid ulcer unless otherwise proven. The patient, who is already very ill, deteriorates further with classical features of peritonitis. An erect chest radiograph or a lateral decubitus film (in the very ill, as they usually are) will show free gas in the peritoneal cav - ity . In fact, any patient being treated for typhoid fever who shows a sudden deterioration accompanied by abdominal signs should be considered to have a typhoid perforation until proven otherwise. - - -
Figure 6.40
Histology of enteric perforation of the small intestine
showing erythrophagocytosis (arrows) with predominantly histiocytic
proliferation (courtesy of Dr AK Mandal, New Delhi, India).
Diagnosis of bowel perforation secondary to typhoid /uni25CF /uni25CF /uni25CF /uni25CF
The patient presents in, or has recently visited, an endemic
area
The patient has persistent high temperature and is very toxic
Positive blood or stool cultures for
Salmonella
Typhi and the
patient is already on treatment for typhoid
After the second week, signs of peritonitis usually denote
perforation, which is con
/f_i
rmed by the presence of free gas
seen on a radiograph
Pathology
In humans, the parasite matures into the adult worm in the intrahepatic biliary radicles, where it may reside for many years. The intrahepatic bile ducts are dilated, with epithelial hyperplasia and periductal fibrosis. These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and dreaded complication of  this parasitic infestation. The eggs or dead worms may form a nidus for stone forma - tion in the gallbladder or common bile duct, which becomes thickened and much dilated in the late stages. Intrahepatic bile duct stones ar e also caused by the parasite producing mucin - rich bile. The dilated intrahepatic bile ducts may lead to chol - angitis, liver abscess and hepatitis. Pathology
The bacillus inhabits the colder parts of  the body; hence, it is found in the nasal mucosa and skin in the region of the ears, foramen. The disease is transmitted from the nasal secretions of  a patient, the infection being contracted in childhood or early adolescence. After an incubation period of  several years, the disease presents with skin, upper respiratory or neurologi cal manifestations. The bacillus is acid fast but weakly so when compared with Mycobacterium tuberculosis. The disease is broadly classified into two groups: leproma tous and tuberculoid. In lepromatous leprosy , there is wide spread dissemination of  abundant bacilli in the tissues, with macrophages and few lymphocytes. This is a reflection of  the poor immune response, resulting in depleted host resistance from the patient. In tuberculoid leprosy , on the other hand, the patient shows a strong immune response with scant bacilli in the tissues, epithelioid granulomas, numerous lymphocytes and giant cells. The tissue damage is inversely proportional to the host’s immune response. There are various grades of  the disease between the two main spectra called dimorphous or borderline variant. Summary box 6.12 Mycobacterium leprae : pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Leprosy is a chronic curable infection caused by
M. leprae
It occurs mainly in tropical regions and resource-poor countries
The majority of cases are located in the Indian subcontinent
Transmission is through nasal secretions, the bacillus inhabiting
the colder parts of the body
It is attributed to poor hygiene and insanitary conditions
The incubation period is several years
The initial infection occurs in childhood
Lepromatous leprosy denotes a poor host immune reaction
Tuberculoid leprosy occurs when host resistance is stronger
than the virulence of the organism
Pathology
There are two types: ulcerative and hyperplastic. In both types, there may be marked mesenteric lymphadenopathy . /uni25CF Ulcerative type: The organism colonises the lymphat ics of  the terminal ileum, causing transverse ulcers with typical undermined edges. The serosa is usually studded with tubercles. Histology shows caseating granuloma with giant cells ( Figure 6.36 ). This pathological entity , referred to as the ulcerative type, denotes a severe form of  the dis ease in which the virulence of  the organism overwhelms ★
Burrill Bernard Crohn , 1884–1983, gastroenterologist, Mount Sinai Hospital, New Y ork, NY , USA, described regional ileitis in 1932 along with Leon Ginzburg and Gordon Oppenheimer. ulcers lead to multiple strictures that may present later with luminal narrowing and intestinal obstruction. /uni25CF Hyperplastic type: This occurs when host resistance has the upper hand over the virulence of  the organism. There is a marked inflammatory reaction causing hyper - plasia and thickening of  the terminal ileum because of its abundance of  lymphoid follicles, thus resulting in nar - rowing of  the lumen and obstruction. Macroscopically , this type ma y be confused with Crohn’s disease. Ileocaecal right iliac tuberculosis ( Figure 6.37 ) may present with a - fossa mass and features of  intestinal obstruction. As a result of  fibrosis, there is shortening of  the bowel with the cae - cum being pulled up into a subhepatic position with resul - tant widening of  the ileocaecal angle beyond 90°. Summary box 6.23 - Tuberculosis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF
Figure 6.36
Histology of ileocaecal tuberculosis showing epithelioid
cell granuloma (black arrows) with caseation (star) (courtesy of Dr AK
Mandal, New Delhi, India).
Increasingly being seen in non-endemic areas, mostly among
immigrants from endemic areas
Two types are recognised – ulcerative and hyperplastic
The ulcerative type occurs when the virulence of the organism
is greater than the host defence and forms strictures
The opposite occurs in the hyperplastic type and presents with
a mass
Small bowel strictures are common in the ulcerative type,
presenting with obstructive symptoms, while the hyperplastic
type mainly affects the ileocaecal area and presents with a right
iliac fossa mass and obstructive symptoms
In peritoneal tuberculosis, the parietal and visceral peritoneum
is studded with tubercles
Localised areas of ascites (loculated) depicts peritoneal
involvement
Encasement of bowel in a
/f_i
brotic sac (cocoon) may be seen in
the plastic type of peritoneal tuberculosis, which presents with
obstruction
The lungs and other organs, particularly of the genitourinary
system, may also be involved simultaneously
Pathology
Following ingestion of contaminated food or water, the organ ism colonises the Peyer’s patches in the terminal ileum, causing hyperplasia of  the lymphoid follicles followed by necrosis and ulceration. The microscopic picture shows erythrophagocyto sis with histiocytic proliferation ( Figure 6.40 ). If  the patient is left untreated or inadequately treated, the ulcers may lead to perforation and bleeding. The bowel may perforate at several sites, including the large bow el. Daniel Elmer Salmon , 1850–1914, veterinary pathologist, Chief  of  the Bureau of  Animal Industry , Washington, DC, USA. Johann Conrad P eyer , 1653–1712, Professor of  Logic, Rhetoric and Medicine, Scha ff hausen, Switzerland, described the lymph follicles in the intestine in 1677. e Widal , 1862–1929, Professor of  Internal Pathology , and later of  Clinical Medicine, The Faculty of  Medicine, Paris, France. Georges Fernand Isidor A typical patient is from an endemic area or has recently visited such a country and su ff ers from a high temperature for 2–3 weeks. The patient may be toxic with abdominal distension from paralytic ileus and may have melaena due to haemor - rhage from a typhoid ulcer; this can lead to hypovolaemia. Blood and stool cultures confirm the nature of  the infection and exclude malaria. Although obsolete in some parts of the world, the Widal test is still done on the Indian subcontinent. The test looks for the pr esence of  agglutinins to O and H antigens of Salmonella Typhi and Paratyphi in the patient’s serum. In endemic areas, laboratory facilities may sometimes be limited. Certain other tests have been developed that identify sensitive and specific markers for typhoid fever. Practical and cheap kits are available for their rapid detection that need no special expertise and equipment. These are MultiTest Dip-S-Ticks to detect immunoglobulin G (IgG), Tubex to detect immunoglobulin M (IgM) and TyphiDot to detect IgG and IgM. These tests are particularly valuable when blood cultures are negative (as a result of prehospital treatment or self-medication with antibiotics) or facilities for such an investigation are not available. In the second or third week of  the illness, if  there is severe generalised abdominal pain, this indicates a perforated typhoid ulcer unless otherwise proven. The patient, who is already very ill, deteriorates further with classical features of peritonitis. An erect chest radiograph or a lateral decubitus film (in the very ill, as they usually are) will show free gas in the peritoneal cav - ity . In fact, any patient being treated for typhoid fever who shows a sudden deterioration accompanied by abdominal signs should be considered to have a typhoid perforation until proven otherwise. - - -
Figure 6.40
Histology of enteric perforation of the small intestine
showing erythrophagocytosis (arrows) with predominantly histiocytic
proliferation (courtesy of Dr AK Mandal, New Delhi, India).
Diagnosis of bowel perforation secondary to typhoid /uni25CF /uni25CF /uni25CF /uni25CF
The patient presents in, or has recently visited, an endemic
area
The patient has persistent high temperature and is very toxic
Positive blood or stool cultures for
Salmonella
Typhi and the
patient is already on treatment for typhoid
After the second week, signs of peritonitis usually denote
perforation, which is con
/f_i
rmed by the presence of free gas
seen on a radiograph
Pathology
In humans, the parasite matures into the adult worm in the intrahepatic biliary radicles, where it may reside for many years. The intrahepatic bile ducts are dilated, with epithelial hyperplasia and periductal fibrosis. These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and dreaded complication of  this parasitic infestation. The eggs or dead worms may form a nidus for stone forma - tion in the gallbladder or common bile duct, which becomes thickened and much dilated in the late stages. Intrahepatic bile duct stones ar e also caused by the parasite producing mucin - rich bile. The dilated intrahepatic bile ducts may lead to chol - angitis, liver abscess and hepatitis. Pathology
The bacillus inhabits the colder parts of  the body; hence, it is found in the nasal mucosa and skin in the region of the ears, foramen. The disease is transmitted from the nasal secretions of  a patient, the infection being contracted in childhood or early adolescence. After an incubation period of  several years, the disease presents with skin, upper respiratory or neurologi cal manifestations. The bacillus is acid fast but weakly so when compared with Mycobacterium tuberculosis. The disease is broadly classified into two groups: leproma tous and tuberculoid. In lepromatous leprosy , there is wide spread dissemination of  abundant bacilli in the tissues, with macrophages and few lymphocytes. This is a reflection of  the poor immune response, resulting in depleted host resistance from the patient. In tuberculoid leprosy , on the other hand, the patient shows a strong immune response with scant bacilli in the tissues, epithelioid granulomas, numerous lymphocytes and giant cells. The tissue damage is inversely proportional to the host’s immune response. There are various grades of  the disease between the two main spectra called dimorphous or borderline variant. Summary box 6.12 Mycobacterium leprae : pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Leprosy is a chronic curable infection caused by
M. leprae
It occurs mainly in tropical regions and resource-poor countries
The majority of cases are located in the Indian subcontinent
Transmission is through nasal secretions, the bacillus inhabiting
the colder parts of the body
It is attributed to poor hygiene and insanitary conditions
The incubation period is several years
The initial infection occurs in childhood
Lepromatous leprosy denotes a poor host immune reaction
Tuberculoid leprosy occurs when host resistance is stronger
than the virulence of the organism
Pathology
There are two types: ulcerative and hyperplastic. In both types, there may be marked mesenteric lymphadenopathy . /uni25CF Ulcerative type: The organism colonises the lymphat ics of  the terminal ileum, causing transverse ulcers with typical undermined edges. The serosa is usually studded with tubercles. Histology shows caseating granuloma with giant cells ( Figure 6.36 ). This pathological entity , referred to as the ulcerative type, denotes a severe form of  the dis ease in which the virulence of  the organism overwhelms ★
Burrill Bernard Crohn , 1884–1983, gastroenterologist, Mount Sinai Hospital, New Y ork, NY , USA, described regional ileitis in 1932 along with Leon Ginzburg and Gordon Oppenheimer. ulcers lead to multiple strictures that may present later with luminal narrowing and intestinal obstruction. /uni25CF Hyperplastic type: This occurs when host resistance has the upper hand over the virulence of  the organism. There is a marked inflammatory reaction causing hyper - plasia and thickening of  the terminal ileum because of its abundance of  lymphoid follicles, thus resulting in nar - rowing of  the lumen and obstruction. Macroscopically , this type ma y be confused with Crohn’s disease. Ileocaecal right iliac tuberculosis ( Figure 6.37 ) may present with a - fossa mass and features of  intestinal obstruction. As a result of  fibrosis, there is shortening of  the bowel with the cae - cum being pulled up into a subhepatic position with resul - tant widening of  the ileocaecal angle beyond 90°. Summary box 6.23 - Tuberculosis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF
Figure 6.36
Histology of ileocaecal tuberculosis showing epithelioid
cell granuloma (black arrows) with caseation (star) (courtesy of Dr AK
Mandal, New Delhi, India).
Increasingly being seen in non-endemic areas, mostly among
immigrants from endemic areas
Two types are recognised – ulcerative and hyperplastic
The ulcerative type occurs when the virulence of the organism
is greater than the host defence and forms strictures
The opposite occurs in the hyperplastic type and presents with
a mass
Small bowel strictures are common in the ulcerative type,
presenting with obstructive symptoms, while the hyperplastic
type mainly affects the ileocaecal area and presents with a right
iliac fossa mass and obstructive symptoms
In peritoneal tuberculosis, the parietal and visceral peritoneum
is studded with tubercles
Localised areas of ascites (loculated) depicts peritoneal
involvement
Encasement of bowel in a
/f_i
brotic sac (cocoon) may be seen in
the plastic type of peritoneal tuberculosis, which presents with
obstruction
The lungs and other organs, particularly of the genitourinary
system, may also be involved simultaneously
Pathology
Following ingestion of contaminated food or water, the organ ism colonises the Peyer’s patches in the terminal ileum, causing hyperplasia of  the lymphoid follicles followed by necrosis and ulceration. The microscopic picture shows erythrophagocyto sis with histiocytic proliferation ( Figure 6.40 ). If  the patient is left untreated or inadequately treated, the ulcers may lead to perforation and bleeding. The bowel may perforate at several sites, including the large bow el. Daniel Elmer Salmon , 1850–1914, veterinary pathologist, Chief  of  the Bureau of  Animal Industry , Washington, DC, USA. Johann Conrad P eyer , 1653–1712, Professor of  Logic, Rhetoric and Medicine, Scha ff hausen, Switzerland, described the lymph follicles in the intestine in 1677. e Widal , 1862–1929, Professor of  Internal Pathology , and later of  Clinical Medicine, The Faculty of  Medicine, Paris, France. Georges Fernand Isidor A typical patient is from an endemic area or has recently visited such a country and su ff ers from a high temperature for 2–3 weeks. The patient may be toxic with abdominal distension from paralytic ileus and may have melaena due to haemor - rhage from a typhoid ulcer; this can lead to hypovolaemia. Blood and stool cultures confirm the nature of  the infection and exclude malaria. Although obsolete in some parts of the world, the Widal test is still done on the Indian subcontinent. The test looks for the pr esence of  agglutinins to O and H antigens of Salmonella Typhi and Paratyphi in the patient’s serum. In endemic areas, laboratory facilities may sometimes be limited. Certain other tests have been developed that identify sensitive and specific markers for typhoid fever. Practical and cheap kits are available for their rapid detection that need no special expertise and equipment. These are MultiTest Dip-S-Ticks to detect immunoglobulin G (IgG), Tubex to detect immunoglobulin M (IgM) and TyphiDot to detect IgG and IgM. These tests are particularly valuable when blood cultures are negative (as a result of prehospital treatment or self-medication with antibiotics) or facilities for such an investigation are not available. In the second or third week of  the illness, if  there is severe generalised abdominal pain, this indicates a perforated typhoid ulcer unless otherwise proven. The patient, who is already very ill, deteriorates further with classical features of peritonitis. An erect chest radiograph or a lateral decubitus film (in the very ill, as they usually are) will show free gas in the peritoneal cav - ity . In fact, any patient being treated for typhoid fever who shows a sudden deterioration accompanied by abdominal signs should be considered to have a typhoid perforation until proven otherwise. - - -
Figure 6.40
Histology of enteric perforation of the small intestine
showing erythrophagocytosis (arrows) with predominantly histiocytic
proliferation (courtesy of Dr AK Mandal, New Delhi, India).
Diagnosis of bowel perforation secondary to typhoid /uni25CF /uni25CF /uni25CF /uni25CF
The patient presents in, or has recently visited, an endemic
area
The patient has persistent high temperature and is very toxic
Positive blood or stool cultures for
Salmonella
Typhi and the
patient is already on treatment for typhoid
After the second week, signs of peritonitis usually denote
perforation, which is con
/f_i
rmed by the presence of free gas
seen on a radiograph

Pulmonary hydatid disease
Pulmonary hydatid disease
The lung is the second commonest organ a ff ected after the liver. The size of  the cyst can vary from very small to a considerable size. The right lung and lower lobes are slightly more often involved. The cyst is usually single, although multiple cysts do occur and concomitant hydatid cysts in other organs, such as the liver, are not unknown. The condition may be silent and found incidentally . Symptomatic patients present with cough, expectoration, fever, chest pain and sometimes haemoptysis. Silent cysts may present as an emergency because of  rupture or an allergic reaction. - Uncomplicated cysts present as rounded or oval lesions on chest radiography . Erosion of  the bronchioles results in air being introduced between the pericyst and the laminated membrane and gives a fine radiolucent crescent, the ‘meniscus’ or ‘crescent’ sign ( Figur e 6.15 ). This is often regarded as a sign of impending rupture. When the cyst ruptures, the crumpled collapsed endocyst floats like a lily on the residual fluid, giving rise to the ‘water-lily’ sign on CT scan ( Figure 6.16 ) . Rup - ture into the pleural cavity r esults in pleural e ff usion. CT scan - defines the pathology in greater detail. The mainstay of  treatment of  pulmonary hydatid is sur - gery . Medical treatment is less successful and considered when surgery is not possible because of  poor general condition or dif - - fuse disease a ff ecting both lungs, or recurrent or ruptured cysts. The principle of surgery is to preserve as much viable lung tissue as possible. T he exact procedure can vary: cystotomy , capitonnage, pericystectomy , segmentectomy or occasionally pneumonectomy . Summary box 6.11 Pulmonary hydatid disease /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
The second most common organ involved
Size of the cyst has a wide variation
May present as an incidental
/f_i
nding
Clinical presentation may be elective or as an emergency
because of rupture
Plain radiograph shows ‘meniscus’ or ‘crescent’ sign; CT
shows ‘water-lily’ sign
Ideal treatment is surgical – various choices are available
(b) Owing to the stigma attached to the word ‘leper’, RG Cochrane suggested that the best name for leprosy is ‘Hansen’s disease’. Robert Greenhill Cochrane , 1899–1985, medical missionary who became an international authority on leprosy; he devoted his time to leprosy patients in South East Asia, particularly India. Gerhard Henrik Armauer Hansen , 1841–1912, physician in charge of  a leper hospital near Bergen, Norway .
Figure 6.15
Hydatid cysts of the lung, one intact (solid arrow), one
ruptured (hollow arrow) showing the lamellar membrane
/f_l
oating like
a water lily (solid arrowhead) (courtesy of Professor Saibal Gupta,
MS, FRCS, Professor of Cardiovascular Surgery, Kolkata, India and
Dr
/uni00A0
Rupak Bhattacharya, Kolkata, India).
Figure 6.16
Computed tomographic scan showing the ‘water-lily’ sign
(arrow). While on a high-altitude trip a young mountaineer complained
of sudden shortness of breath, cough and copious expectoration
consisting of clear
/f_l
uid and
/f_l
aky material. At
/f_i
rst thought to be due
to pulmonary oedema, it turned out to be ruptured hydatid cyst,
successfully treated by surgery (courtesy of Professor Saibal Gupta,
MS, FRCS, Pr
ofessor of Cardiovascular Surgery, Kolkata, India and Dr
Rupak Bhattacharya, Kolkata, India).
Pulmonary hydatid disease
The lung is the second commonest organ a ff ected after the liver. The size of  the cyst can vary from very small to a considerable size. The right lung and lower lobes are slightly more often involved. The cyst is usually single, although multiple cysts do occur and concomitant hydatid cysts in other organs, such as the liver, are not unknown. The condition may be silent and found incidentally . Symptomatic patients present with cough, expectoration, fever, chest pain and sometimes haemoptysis. Silent cysts may present as an emergency because of  rupture or an allergic reaction. - Uncomplicated cysts present as rounded or oval lesions on chest radiography . Erosion of  the bronchioles results in air being introduced between the pericyst and the laminated membrane and gives a fine radiolucent crescent, the ‘meniscus’ or ‘crescent’ sign ( Figur e 6.15 ). This is often regarded as a sign of impending rupture. When the cyst ruptures, the crumpled collapsed endocyst floats like a lily on the residual fluid, giving rise to the ‘water-lily’ sign on CT scan ( Figure 6.16 ) . Rup - ture into the pleural cavity r esults in pleural e ff usion. CT scan - defines the pathology in greater detail. The mainstay of  treatment of  pulmonary hydatid is sur - gery . Medical treatment is less successful and considered when surgery is not possible because of  poor general condition or dif - - fuse disease a ff ecting both lungs, or recurrent or ruptured cysts. The principle of surgery is to preserve as much viable lung tissue as possible. T he exact procedure can vary: cystotomy , capitonnage, pericystectomy , segmentectomy or occasionally pneumonectomy . Summary box 6.11 Pulmonary hydatid disease /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
The second most common organ involved
Size of the cyst has a wide variation
May present as an incidental
/f_i
nding
Clinical presentation may be elective or as an emergency
because of rupture
Plain radiograph shows ‘meniscus’ or ‘crescent’ sign; CT
shows ‘water-lily’ sign
Ideal treatment is surgical – various choices are available
(b) Owing to the stigma attached to the word ‘leper’, RG Cochrane suggested that the best name for leprosy is ‘Hansen’s disease’. Robert Greenhill Cochrane , 1899–1985, medical missionary who became an international authority on leprosy; he devoted his time to leprosy patients in South East Asia, particularly India. Gerhard Henrik Armauer Hansen , 1841–1912, physician in charge of  a leper hospital near Bergen, Norway .
Figure 6.15
Hydatid cysts of the lung, one intact (solid arrow), one
ruptured (hollow arrow) showing the lamellar membrane
/f_l
oating like
a water lily (solid arrowhead) (courtesy of Professor Saibal Gupta,
MS, FRCS, Professor of Cardiovascular Surgery, Kolkata, India and
Dr
/uni00A0
Rupak Bhattacharya, Kolkata, India).
Figure 6.16
Computed tomographic scan showing the ‘water-lily’ sign
(arrow). While on a high-altitude trip a young mountaineer complained
of sudden shortness of breath, cough and copious expectoration
consisting of clear
/f_l
uid and
/f_l
aky material. At
/f_i
rst thought to be due
to pulmonary oedema, it turned out to be ruptured hydatid cyst,
successfully treated by surgery (courtesy of Professor Saibal Gupta,
MS, FRCS, Pr
ofessor of Cardiovascular Surgery, Kolkata, India and Dr
Rupak Bhattacharya, Kolkata, India).
Pulmonary hydatid disease
The lung is the second commonest organ a ff ected after the liver. The size of  the cyst can vary from very small to a considerable size. The right lung and lower lobes are slightly more often involved. The cyst is usually single, although multiple cysts do occur and concomitant hydatid cysts in other organs, such as the liver, are not unknown. The condition may be silent and found incidentally . Symptomatic patients present with cough, expectoration, fever, chest pain and sometimes haemoptysis. Silent cysts may present as an emergency because of  rupture or an allergic reaction. - Uncomplicated cysts present as rounded or oval lesions on chest radiography . Erosion of  the bronchioles results in air being introduced between the pericyst and the laminated membrane and gives a fine radiolucent crescent, the ‘meniscus’ or ‘crescent’ sign ( Figur e 6.15 ). This is often regarded as a sign of impending rupture. When the cyst ruptures, the crumpled collapsed endocyst floats like a lily on the residual fluid, giving rise to the ‘water-lily’ sign on CT scan ( Figure 6.16 ) . Rup - ture into the pleural cavity r esults in pleural e ff usion. CT scan - defines the pathology in greater detail. The mainstay of  treatment of  pulmonary hydatid is sur - gery . Medical treatment is less successful and considered when surgery is not possible because of  poor general condition or dif - - fuse disease a ff ecting both lungs, or recurrent or ruptured cysts. The principle of surgery is to preserve as much viable lung tissue as possible. T he exact procedure can vary: cystotomy , capitonnage, pericystectomy , segmentectomy or occasionally pneumonectomy . Summary box 6.11 Pulmonary hydatid disease /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
The second most common organ involved
Size of the cyst has a wide variation
May present as an incidental
/f_i
nding
Clinical presentation may be elective or as an emergency
because of rupture
Plain radiograph shows ‘meniscus’ or ‘crescent’ sign; CT
shows ‘water-lily’ sign
Ideal treatment is surgical – various choices are available
(b) Owing to the stigma attached to the word ‘leper’, RG Cochrane suggested that the best name for leprosy is ‘Hansen’s disease’. Robert Greenhill Cochrane , 1899–1985, medical missionary who became an international authority on leprosy; he devoted his time to leprosy patients in South East Asia, particularly India. Gerhard Henrik Armauer Hansen , 1841–1912, physician in charge of  a leper hospital near Bergen, Norway .
Figure 6.15
Hydatid cysts of the lung, one intact (solid arrow), one
ruptured (hollow arrow) showing the lamellar membrane
/f_l
oating like
a water lily (solid arrowhead) (courtesy of Professor Saibal Gupta,
MS, FRCS, Professor of Cardiovascular Surgery, Kolkata, India and
Dr
/uni00A0
Rupak Bhattacharya, Kolkata, India).
Figure 6.16
Computed tomographic scan showing the ‘water-lily’ sign
(arrow). While on a high-altitude trip a young mountaineer complained
of sudden shortness of breath, cough and copious expectoration
consisting of clear
/f_l
uid and
/f_l
aky material. At
/f_i
rst thought to be due
to pulmonary oedema, it turned out to be ruptured hydatid cyst,
successfully treated by surgery (courtesy of Professor Saibal Gupta,
MS, FRCS, Pr
ofessor of Cardiovascular Surgery, Kolkata, India and Dr
Rupak Bhattacharya, Kolkata, India).

ROUNDWORM ( ASCARIS LUMBRICOIDES ) Introduction
ROUNDWORM ( ASCARIS LUMBRICOIDES ) Introduction
Ascaris lumbricoides, commonly called the roundworm, is the commonest intestinal nematode to infect humans and a ff ects a quarter of  the world’s population. The parasite causes pulmonary symptoms as a larva and intestinal symptoms as an adult worm. ROUNDWORM ( ASCARIS LUMBRICOIDES ) Introduction
Ascaris lumbricoides, commonly called the roundworm, is the commonest intestinal nematode to infect humans and a ff ects a quarter of  the world’s population. The parasite causes pulmonary symptoms as a larva and intestinal symptoms as an adult worm. ROUNDWORM ( ASCARIS LUMBRICOIDES ) Introduction
Ascaris lumbricoides, commonly called the roundworm, is the commonest intestinal nematode to infect humans and a ff ects a quarter of  the world’s population. The parasite causes pulmonary symptoms as a larva and intestinal symptoms as an adult worm.

Spread
Spread
Local spread occurs predominantly along tissue planes. The organism multiplies to form colonies that spread along the fascial planes to skin and underlying structures. Lymphatic spread, more common in actinomycetoma, occurs to the regional lymph nodes, and increases with repeated inade quate surgical excision procedures. During the active phase of  the disease, these lymphatic satellites may suppurate and discharge; lymphadenopathy may also be due to secondary bacterial infection. Spread via the bloodstream can occur. T he apparent clinical features of  mycetoma are not always a reliable indicator of  the extent and spread of  the disease. Some small lesions with few sinuses may have many deep connecting tracts, through w hich the disease can spread quite extensively . Therefore, surgery in mycetoma under local anaes thesia is contraindicated. Spread
Local spread occurs predominantly along tissue planes. The organism multiplies to form colonies that spread along the fascial planes to skin and underlying structures. Lymphatic spread, more common in actinomycetoma, occurs to the regional lymph nodes, and increases with repeated inade quate surgical excision procedures. During the active phase of  the disease, these lymphatic satellites may suppurate and discharge; lymphadenopathy may also be due to secondary bacterial infection. Spread via the bloodstream can occur. T he apparent clinical features of  mycetoma are not always a reliable indicator of  the extent and spread of  the disease. Some small lesions with few sinuses may have many deep connecting tracts, through w hich the disease can spread quite extensively . Therefore, surgery in mycetoma under local anaes thesia is contraindicated. Spread
Local spread occurs predominantly along tissue planes. The organism multiplies to form colonies that spread along the fascial planes to skin and underlying structures. Lymphatic spread, more common in actinomycetoma, occurs to the regional lymph nodes, and increases with repeated inade quate surgical excision procedures. During the active phase of  the disease, these lymphatic satellites may suppurate and discharge; lymphadenopathy may also be due to secondary bacterial infection. Spread via the bloodstream can occur. T he apparent clinical features of  mycetoma are not always a reliable indicator of  the extent and spread of  the disease. Some small lesions with few sinuses may have many deep connecting tracts, through w hich the disease can spread quite extensively . Therefore, surgery in mycetoma under local anaes thesia is contraindicated.

Surgical treatment
Surgical treatment
Surgery is indicated for small, localised lesions, resistance to medical treatment or for a better response after medical treatment in patients with massive disease. Excision may need to be much more extensive than suggested at first on clinical appearance because the disease may extend to deeper planes that are not clinically apparent. The surgical options are wide local and debulking excisions and amputations. Amputation, used as a life-saving procedure, is indicated in advanced myce toma refractory to medical treatment with severe secondary bacterial infection. The amputation rate is 10–25%. Postoperative medical treatment should continue for an adequate period to prevent recurr ence. The recurrence rate varies from 25% to 50%. This can be local or distant, to r egional lymph nodes. Recurrence is usually due to inadequate surgical excision, use of  local anaesthesia, lack of  surgical experience, non-compliance with drugs for financial reasons and lack of health education. Georges Guillain , 1876–1961, Professor of  Neurology , The Faculty of  Medicine, Paris, France. Jean Alexandre Barré , 1880–1967, Professor of  Neurology , Strasbourg, France. Guillain and Barré described the condition in a joint paper in 1916 while serving as Medical O ffi cers in the French Army during the First World War. Mycetoma: management /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.30
Polio affecting
predominantly the upper limb
muscles with wasting of the
intercostal muscles.
Ideally combined management by physician and surgeon
Medical treatment with appropriate long-term antibiotics
In large lesions medical treatment to reduce the size followed
by excision
Beware of serious drug side effects
Surgery in the form of wide excision and amputation as a life-
saving procedure
High recurrence rate
Surgical treatment
Surgery is indicated for small, localised lesions, resistance to medical treatment or for a better response after medical treatment in patients with massive disease. Excision may need to be much more extensive than suggested at first on clinical appearance because the disease may extend to deeper planes that are not clinically apparent. The surgical options are wide local and debulking excisions and amputations. Amputation, used as a life-saving procedure, is indicated in advanced myce toma refractory to medical treatment with severe secondary bacterial infection. The amputation rate is 10–25%. Postoperative medical treatment should continue for an adequate period to prevent recurr ence. The recurrence rate varies from 25% to 50%. This can be local or distant, to r egional lymph nodes. Recurrence is usually due to inadequate surgical excision, use of  local anaesthesia, lack of  surgical experience, non-compliance with drugs for financial reasons and lack of health education. Georges Guillain , 1876–1961, Professor of  Neurology , The Faculty of  Medicine, Paris, France. Jean Alexandre Barré , 1880–1967, Professor of  Neurology , Strasbourg, France. Guillain and Barré described the condition in a joint paper in 1916 while serving as Medical O ffi cers in the French Army during the First World War. Mycetoma: management /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.30
Polio affecting
predominantly the upper limb
muscles with wasting of the
intercostal muscles.
Ideally combined management by physician and surgeon
Medical treatment with appropriate long-term antibiotics
In large lesions medical treatment to reduce the size followed
by excision
Beware of serious drug side effects
Surgery in the form of wide excision and amputation as a life-
saving procedure
High recurrence rate
Surgical treatment
Surgery is indicated for small, localised lesions, resistance to medical treatment or for a better response after medical treatment in patients with massive disease. Excision may need to be much more extensive than suggested at first on clinical appearance because the disease may extend to deeper planes that are not clinically apparent. The surgical options are wide local and debulking excisions and amputations. Amputation, used as a life-saving procedure, is indicated in advanced myce toma refractory to medical treatment with severe secondary bacterial infection. The amputation rate is 10–25%. Postoperative medical treatment should continue for an adequate period to prevent recurr ence. The recurrence rate varies from 25% to 50%. This can be local or distant, to r egional lymph nodes. Recurrence is usually due to inadequate surgical excision, use of  local anaesthesia, lack of  surgical experience, non-compliance with drugs for financial reasons and lack of health education. Georges Guillain , 1876–1961, Professor of  Neurology , The Faculty of  Medicine, Paris, France. Jean Alexandre Barré , 1880–1967, Professor of  Neurology , Strasbourg, France. Guillain and Barré described the condition in a joint paper in 1916 while serving as Medical O ffi cers in the French Army during the First World War. Mycetoma: management /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.30
Polio affecting
predominantly the upper limb
muscles with wasting of the
intercostal muscles.
Ideally combined management by physician and surgeon
Medical treatment with appropriate long-term antibiotics
In large lesions medical treatment to reduce the size followed
by excision
Beware of serious drug side effects
Surgery in the form of wide excision and amputation as a life-
saving procedure
High recurrence rate

TROPICAL CHRONIC PANCREATITIS Introduction
TROPICAL CHRONIC PANCREATITIS Introduction
Tropical chronic pancreatitis is a disease a ff ecting the younger generation from poor socioeconomic strata in resource-poor countries, seen mostly in southern India. The aetiology remains obscure, with malnutrition, dietary , familial and genetic factors being possible causes. Alcohol ingestion does not play a part in the aetiology . - TROPICAL CHRONIC PANCREATITIS Introduction
Tropical chronic pancreatitis is a disease a ff ecting the younger generation from poor socioeconomic strata in resource-poor countries, seen mostly in southern India. The aetiology remains obscure, with malnutrition, dietary , familial and genetic factors being possible causes. Alcohol ingestion does not play a part in the aetiology . - TROPICAL CHRONIC PANCREATITIS Introduction
Tropical chronic pancreatitis is a disease a ff ecting the younger generation from poor socioeconomic strata in resource-poor countries, seen mostly in southern India. The aetiology remains obscure, with malnutrition, dietary , familial and genetic factors being possible causes. Alcohol ingestion does not play a part in the aetiology . -

TUBERCULOSIS OF SMALL INTESTINE Introduction
TUBERCULOSIS OF SMALL INTESTINE Introduction
Infection by M. tuberculosis is common in the tropics. In these days of  international travel and increased migration, tuber culosis in general and intestinal tuberculosis in particular are no longer clinical curiosities in non-endemic countries. Any patient, particularly one who has recently arrived from an endemic area and who has fea tures of  generalised ill health and altered bowel habit, should arouse suspicion for intestinal tuberculosis. The increased prevalence of  human immuno deficiency virus (HIV) infection worldwide has also made tuberculosis more common. The infection is transmitted by swallowing of  infected sputum in a patient with pulmonary tuberculosis, by drinking infected unpasteurised milk or by a haematogenous route . TUBERCULOSIS OF SMALL INTESTINE Introduction
Infection by M. tuberculosis is common in the tropics. In these days of  international travel and increased migration, tuber culosis in general and intestinal tuberculosis in particular are no longer clinical curiosities in non-endemic countries. Any patient, particularly one who has recently arrived from an endemic area and who has fea tures of  generalised ill health and altered bowel habit, should arouse suspicion for intestinal tuberculosis. The increased prevalence of  human immuno deficiency virus (HIV) infection worldwide has also made tuberculosis more common. The infection is transmitted by swallowing of  infected sputum in a patient with pulmonary tuberculosis, by drinking infected unpasteurised milk or by a haematogenous route . TUBERCULOSIS OF SMALL INTESTINE Introduction
Infection by M. tuberculosis is common in the tropics. In these days of  international travel and increased migration, tuber culosis in general and intestinal tuberculosis in particular are no longer clinical curiosities in non-endemic countries. Any patient, particularly one who has recently arrived from an endemic area and who has fea tures of  generalised ill health and altered bowel habit, should arouse suspicion for intestinal tuberculosis. The increased prevalence of  human immuno deficiency virus (HIV) infection worldwide has also made tuberculosis more common. The infection is transmitted by swallowing of  infected sputum in a patient with pulmonary tuberculosis, by drinking infected unpasteurised milk or by a haematogenous route .

TUBERCULOSIS
TUBERCULOSIS
Although tuberculosis can a ff ect all systems in the body , in the tropical world the surgeon is most often faced with tuberculosis a ff ecting the cervical lymph nodes and the small intestine. Therefore, in this chapter tuberculous cervical lymphadenitis and tuberculosis of  the small bowel will be described. TUBERCULOSIS
Although tuberculosis can a ff ect all systems in the body , in the tropical world the surgeon is most often faced with tuberculosis a ff ecting the cervical lymph nodes and the small intestine. Therefore, in this chapter tuberculous cervical lymphadenitis and tuberculosis of  the small bowel will be described. TUBERCULOSIS
Although tuberculosis can a ff ect all systems in the body , in the tropical world the surgeon is most often faced with tuberculosis a ff ecting the cervical lymph nodes and the small intestine. Therefore, in this chapter tuberculous cervical lymphadenitis and tuberculosis of  the small bowel will be described.

TUBERCULOUS CERVICAL LY M P H A D E N I T I S Intr
TUBERCULOUS CERVICAL LY M P H A D E N I T I S Introduction
This is common in the Indian subcontinent. A young person who has recently arrived from an endemic area, presenting with cervical lymphadenopathy , should be diagnosed as having tuberculous lymphadenitis unless otherwise proven. With acquired immune deficiency syndrome (AIDS) being globally prevalent, this is not as rare in the West in the indigenous population as it used to be.
Figure 6.34
Cervical tuberculous: cold abscess about to burst.
TUBERCULOUS CERVICAL LY M P H A D E N I T I S Introduction
This is common in the Indian subcontinent. A young person who has recently arrived from an endemic area, presenting with cervical lymphadenopathy , should be diagnosed as having tuberculous lymphadenitis unless otherwise proven. With acquired immune deficiency syndrome (AIDS) being globally prevalent, this is not as rare in the West in the indigenous population as it used to be.
Figure 6.34
Cervical tuberculous: cold abscess about to burst.

TUBERCULOUS CERVICAL LY M P H A D E N I T I S Introduction
TUBERCULOUS CERVICAL LY M P H A D E N I T I S Introduction
This is common in the Indian subcontinent. A young person who has recently arrived from an endemic area, presenting with cervical lymphadenopathy , should be diagnosed as having tuberculous lymphadenitis unless otherwise proven. With acquired immune deficiency syndrome (AIDS) being globally prevalent, this is not as rare in the West in the indigenous population as it used to be.
Figure 6.34
Cervical tuberculous: cold abscess about to burst.

TYPHOID Introduction
TYPHOID Introduction
Typhoid fever is caused by Salmonella Typhi , also called the typhoid bacillus, a Gram-negative organism. Like most infec tions occurring in the tropics, the organism gains entry into the human gastrointestinal tract as a result of  poor hygiene and inadequate sanitation. It is a disease normally managed by physicians, but the surgeon may be called upon to treat the patient with typhoid fever because of  perforation of  a typhoid ulcer. TYPHOID Introduction
Typhoid fever is caused by Salmonella Typhi , also called the typhoid bacillus, a Gram-negative organism. Like most infec tions occurring in the tropics, the organism gains entry into the human gastrointestinal tract as a result of  poor hygiene and inadequate sanitation. It is a disease normally managed by physicians, but the surgeon may be called upon to treat the patient with typhoid fever because of  perforation of  a typhoid ulcer. TYPHOID Introduction
Typhoid fever is caused by Salmonella Typhi , also called the typhoid bacillus, a Gram-negative organism. Like most infec tions occurring in the tropics, the organism gains entry into the human gastrointestinal tract as a result of  poor hygiene and inadequate sanitation. It is a disease normally managed by physicians, but the surgeon may be called upon to treat the patient with typhoid fever because of  perforation of  a typhoid ulcer.

Treatment
Treatment
Medical treatment is very e ff ective and should be the first choice in the elective situation, with surgery being reserved for complications. Metronidazole and tinidazole are the e ff ective drugs. After treatment with metronidazole and tinidazole, diloxanide furoate, a luminal amoebicide that is not e ff ective against hepatic infestation, is used for 10 days to destroy any intestinal amoebae. Aspiration is carried out when imminent rupture of  an abscess is expected, especially when involving the left lobe. Pigtail catheter drainage may be considered in those pa who are not responding to intravenous metronidazole in the first 48–72 hours to improve antibiotic penetration. If  there is evidence of secondary infection, appropriate drug treatment is added. The threshold for draining a left liver lobe abscess - - should be low , given its propensity for rupture into either the peritoneal, pleural or pericardial cavity . tions Surgical treatment should be reserved for the complica of rupture into the pleural (usually the right side), peritoneal or pericardial cavities. Resuscitation, drainage and appropriate la vage with vigorous medical treatment are the key principles. In the large bowel, severe haemorrhage and toxic megacolon are rare complications. In these patients, the general principles of a surgical emergency apply , the principles of management being the same as for any toxic megacolon. Resuscitation is followed by resection of  bowel with exteriorisation. Then the patient is given vigorous supportive therapy . All such cases are tients managed in the intensive care unit, as would any patient with toxic megacolon whatever the cause. An amoeboma that has not regressed after full medical treatment should be managed with colonic resection, particu - larly if  cancer cannot be excluded.
Figure 6.2
Computed tomographic scan showing an amoebic liver
abscess in the right lobe.
Figure 6.3
Computed tomographic scans showing multiple amoebic
liver abscesses with extension into the chest.
Amoebiasis: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Medical treatment is very effective
For large abscesses, repeated aspiration or pigtail catheter
drainage is combined with drug treatment
Surgical treatment is reserved for complications, such as
rupture into the pleural, peritoneal or pericardial cavities
Acute toxic megacolon and severe haemorrhage are intestinal
complications that are treated with intensive supportive therapy
followed by resection and exteriorisation: subtotal colectomy
with terminal ileostomy and closure of the rectal stump
When an amoeboma is suspected in a colonic mass, cancer
should be excluded by appropriate imaging and biopsy
Treatment
The pulmonary phase of  the disease is usually self-limiting and requires symptomatic treatment only . For intestinal disease, patients should ideally be under the care of  a physician for treatment with anthelminthic drugs. Certain drugs may cause rapid death of  the adult worms and, if  there are many worms in the terminal ileum, the treatment may actually precipitate acute intestinal obstruction from a bolus of  dead worms. Children who present with features of  intermittent or subacute obstruction should be given a trial of conservative management in the form of  intravenous fluids, nasogastric suction and hypertonic saline enemas. The last of  these helps to disentangle the bolus of  worms and also increases intestinal motility . Surgery is reserved for complications, such as intestinal obstruction that has not resolved on a conservative regime, or when perforation is suspected. At laparotomy , the bolus ms in the terminal ileum is milked through the of wor ileocaecal valve into the colon for natural passage in the
(a)
(b)
Figure 6.5
Ultrasound scan showing a live worm (arrow) in the gallbladder
ryya, Kolkata, India).
Figure 6.6
Magnetic resonance cholangiopancreatography showing
a roundworm in the common bile duct (CBD). The worm could not
be removed endoscopically. The patient underwent an open chole
cystectomy and exploration of the CBD (this can also be addressed
laparoscopically in some centres).
(a)
and the common bile duct (CBD)
(b)
(courtesy of Dr A Bhattacha
stool. Postoperatively , hypertonic saline enemas may help in the extrusion of  the worms. Strictures, gangrenous areas or perforations need resection and anastomosis. If  the bowel wall is healthy , enterotomy and removal of  the worms may be performed ( Figure 6.7 ). Rarely , when perforation occurs as a result of  roundworm, the parasites may be found lying free in the peritoneal cavity . It is safer to bring out the site of  perforation as an ileostomy because, in the presence of  a large number of  w orms, the clo sure of  an anastomosis may be at risk of  breakdown from the activity of  the residual worms in the bowel. When a patient is operated upon as an emergency for a suspected complication of  roundworm infesta tion, the actual diagnosis at operation may turn out to be acute appendicitis, typhoid perforation or a tuberculous stricture and the pr ence of  roundworms is an incidental finding. Such a patient requires the appropriate surgery depending upon the primary pathology . Common bile duct or pancreatic duct obstruction from a roundw orm can be treated by endoscopic removal at endo scopic retrograde c holangiopancreatography (ERCP), failing which laparoscopic or open exploration of  the common bile duct is necessary . Cholecystectomy is also carried out. A full w any surgical course of  antiparasitic treatment must follo intervention. Summary box 6.5 Ascariasis: diagnosis and management /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.7
(a)
Roundworms seen through the bowel wall (arrowed).
worms.
Barium meal and follow-through will show worms scattered in
the small bowel
Ultrasonography may show worms in the common bile duct
and pancreatic duct
Plain abdominal radiograph and contrast CT scan will show the
worms as tubular or curvilinear structures
Conservative management with anthelminthics is the
/f_i
rst line
of treatment even in obstruction
Surgery is a last resort for acute abdomen – various options are
available
(b)
Roundworm being removed through enterotomy.
(c)
Removed round
Treatment
Praziquantel and albendazole are the drugs of  choice. However, the surgeon faces a challenge when there are stones not only in the gallbladder but also in the common bile duct. Cholecystec tomy with exploration of  the common bile duct is performed when indicated; currently , both procedures are performed lapa roscopically as a single-stage procedure. R epeated washouts are necessary during the exploration of  the common bile duct as there are stones, biliary debris, sludge and mud in the dilated duct. This should be followed b y choledochoduodenostomy . As this is a disease with a prolonged and relapsing course, some surgeons prefer to do a choledochojejunostomy to a Roux loop. The Roux loop is brought up to the abdominal wall, referred to as ‘an access loop’, which allows the interventional radiologist to deal with any future stones. As a public health measure, people who have emigrated from an endemic area should be o ff ered screening for César Roux , 1857–1934, Professor of  Surgery and Gynaecology , Lausanne, Switzerland, described this method of  forming a jejunal conduit in 1908. Otto Eduard Heinrich Wucherer , 1820–1873, German physician who practised in Brazil. Joseph Bancroft , 1836–1894, English physician who worked in Australia. Peau d’orange is French for ‘orange peel skin’. hepatobiliary system. This condition can be diagnosed and treated, and even cured, when it is in its subclinical form. Most importantly , the risk of  developing the dreadful disease of  cholangiocarcinoma is eliminated. Summary box 6.7 Asiatic cholangiohepatitis: treatment /uni25CF - /uni25CF /uni25CF w -
Medical treatment can be curative in the early stages
Surgical treatment is cholecystectomy, exploration of the
common bile duct and some form of biliary–enteric bypass
Prevention: consider offering hepatobiliary ultrasonography
as a screening procedure to recently arrived migrants from
endemic areas
Treatment
Medical treatment with diethylcarbamazine is very e ff ective in the early stages before the gross deformities of elephantiasis have developed. In the early stages of  limb swelling, intermit tent pneumatic compression helps, but the treatment has to be repeated over a prolonged period. Summary box 6.8 Filariasis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF A hydrocele is treated by the usual operation of excision and eversion of  the sac with, if  necessary , excision of  redun - dant scrotal skin. Operations for reducing the size of  the limb are hardly ever done these days because the procedures are so rarely successful.
Caused by
Wuchereria bancrofti
, which is carried by the
mosquito
Lymphatics are mainly affected, resulting in gross limb swelling
Eosinophilia occurs; immature worms may be seen in a
nocturnal peripheral blood smear
Gross forms of the disease cause a great deal of disability and
misery
Early cases are very amenable to medical treatment
Intermittent pneumatic compression gives some relief
The value of various surgical procedures is largely unproven
and hence they are rarely performed
Figure 6.9
Filariasis of the scrotum and penis (courtesy of Professor
Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).
Treatment
Here, the treatment of  hepatic hydatid is outlined because the liver is most commonly a ff ected, but the same general princi - ples apply whichever organ is involved. These patients should be treated in a tertiary unit where good teamwork between an expert hepatobiliary surgeon, an experienced physician and an interv entional radiologist is available. Surgical treatment by minimal access therapy is best summarised by the mnemonic PAIR (puncture, aspira - tion, injection and reaspiration). This is done after adequate drug treatment with albendazole, although praziquantel has
Figure 6.13
Magnetic resonance cholangiopancreatography showing
a large hepatic hydatid cyst with daughter cysts communicating with
the common bile duct, causing obstruction and dilatation of the entire
biliary tree (courtesy of Dr B Agarwal, New Delhi, India).
also been used, both of  these drugs being available only on a ‘named patient’ basis. Whether the patient is treated only medically or in combi nation with surgery will depend upon the clinical group (which gives an idea as to the activity of  the disease), the number of cysts and their anatomical position. Radical total or partial pericystectomy with omentoplasty or hepatic segmentectomy (especially if  the lesion is in a peripheral part of  the liver) are some of  the surgical options. During the operation, scolicidal agents ar e used, such as hypertonic saline (15–20%), ethanol (75–95%) or 5% povidone–iodine (although some use a 10% solution). This may cause sclerosing cholangitis if  biliary rad icles are in communication with the cyst wall. A laparoscopic approach to these procedures is being tried (see next section, Laparoscopic management ). Obviously , cysts in other organs need to be treated in accor dance with the actual anatomical site, along with the general principles described. An asymptomatic cyst tha t is inactive (group 3) may be left alone. Summary box 6.10 Hydatid cyst of the liver: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Currently , surgeons trained in minimal access surgery perform hydatid surgery using minimal access. Laparoscopic marsupial - isation of the cyst (deroofing), consisting of removal of the cyst containing the endocyst along with daughter cysts, is the most common procedure. In the initial steps, the cyst is aspirated, taking care not to spill any contents, using povidone–iodine or hypertonic saline as a scolicidal agent. Any communication with the biliary tr ee is oversewn and pedicled omentum is sutured to the margins of  the cyst. If  the cyst is small and superficial, a cystopericystectomy is performed at centres experienced enough to do more advanced surger y , removing the entire cyst intact.
Figure 6.14
Computed tomographic (CT) scan of the upper abdomen
showing a hypodense lesion of the left lobe of the liver; the periphery
of the lesion shows a double edge. This is the lamellar membrane of
the hydatid cyst that separated after trivial injury. The patient was a
14-year-old girl who developed a rash and pain in the upper abdomen
after dancing. The rash settled down after a course of antihistamines.
The CT scan was performed 2 weeks later for persisting upper
abdominal pain.
Ideally managed in a tertiary unit by a multidisciplinary team of
hepatobiliary surgeon, physician and interventional radiologist
Leave asymptomatic and inactive cysts alone – monitor size by
ultrasonography
Active cysts should
/f_i
rst be treated by a full course of
albendazole
Several procedures are available – PAIR, pericystectomy
with omentoplasty and hepatic segmentectomy; appropriate
management is customised according to the particular patient
and organ involved
Increasingly, a laparoscopic approach is being tried
Treatment
A herbal derivative from the seeds of Hydnocarpus wightianus (Chaulmoogra) was the mainstay of  treatment, with some success, until the advent of  dapsone (diamino-diphenyl sulphone). Dapsone, one of  the principal drugs, was a deriv - ative of  prontosil red and was discovered by Domagk. This is used according to the WHO guidelines along with rifampicin and clofazimine. During treatment, the patient may develop acute manifesta tions. These are controlled with steroids. Multiple drug therapy for 12 months is the key to treatment. A team approach between an infectious diseases specialist, plastic surgeon, ophthalmologist, and hand or orthopaedic surgeon is important. Surgical treatment is indicated in advanced stages of  the - disease for functional disability of  limbs, cosmetic disfigure - ment of  the face and visual problems. These entail major reconstructive surgery , whic h is the domain of  the plastic surgeon. Surgery for deformities in the hand is aimed at returning the ability to achieve a grasp and a pinch grip. Tendon trans fers (pioneered by Brand and Tovey) are used to recreate the (a) (b) Paul Wilson Brand CBE, FRCS, 1914–2003, was born to missionary parents in Southern India, and qualified in London in 1943. He himself  was a dedicated missionary who was ‘ An extraordinary gifted orthopaedic surgeon who straightened crooked hands and unravelled the riddle of  leprosy .’ As a pioneer in tendon transfer techniques , he established and practised initially in New Life Center, V ellore, South India and Schie ff elin Leprosy Research Centre, Karigiri, South India. Initially he trained as a carpenter and builder and maintained that his training as a carpenter helped him in his expertise in tendon transplantation. When he was awarded the CBE, his wife, Margaret, came to know about it when she found a letter from Her Majesty’s Government informing him of  the award while emptying the pockets of  his trousers before they were put into the wash. He later moved to Louisiana State University , Baton Rouge, LA, where he continued his work, and finally to Seattle as Emeritus Professor of  Orthopaedics at the University of  Washington, Seattle, USA. Margaret Brand , alongside her husband, Paul Brand, also contributed immensely to the health of  leprosy patients by concentrating on research to prevent blind ness in leprosy . She became known as ‘the woman who first helped lepers to see’. Frank Tovey OBE , 1921–2019, another English surgeon at about the same time (1951–1967), also performed extensive tendon transfers and facial and other reconstructive sur gery on patients with leprosy in southern India in the State of  Mysore. In this he was helped by his wife, Winifred, who organised the physiotherapy and rehabilitation of  the patients and established village diagnostic and treatment centres. function of  the lumbricals that have been lost due to dam - - age to the ulnar nerve. In the foot, damage to the common peroneal nerve leads to a foot drop due to paralysis of  tibialis -
Figure 6.17
Lateral view of the face showing collapse of the nasal
bridge due to destruction of nasal cartilage by leprosy.
Figure 6.18
Frontal view of the face showing eye changes in leprosy:
paralysis of orbicularis oculi and loss of eyebrows.
Figure 6.19
(a, b)
Typical bilateral claw hand
from leprosy due to involvement of the ulnar and
median nerves.
Figure 6.20
Claw toes from involvement of
the posterior tibial nerve by leprosy; also note
autoamputation of toes of the right foot.
anterior. If  a foot-drop splint is not adequate, then once again a tendon transfer (tibialis posterior into the dorsum of  the foot) will improve function. Ulcers resulting from an insensate foot should be completely debrided followed by protection with a plaster cast. The general surgeon may be called upon to treat a patient when the deformity is so advanced that amputation is required or an abscess needs drainage as an emergency . All surgical procedures obviously need to be done under antileprosy drug tr eatment. This is best achieved by a team approach. Educating patients about the dreadful sequelae of the disease so that they seek medical help ear ly is important. It is also necessary to educate the general public that patients su ff ering from the disease should not be made social outcasts. Summary box 6.14 Leprosy: treatment /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.21
Bilateral trophic ulceration of the feet due to anaesthesia
of the soles resulting from leprosy; also note claw toes on the left foot.
Multiple drug therapy for a year
Team approach
Surgical reconstruction requires the expertise of a hand
surgeon, orthopaedic surgeon and plastic surgeon
Education of the patient and general public should be the
keystone in prevention
Treatment
The treatment is mainly medical, with exocrine support using pancreatic enzymes, treatment of diabetes with insulin and the management of  malnutrition. Treatment of  pain should be along the lines of  the usual analgesic ladder: non-opioids, followed by weak and then strong opioids and, finally , referral to a pain clinic. Surgical treatment is necessary for intractable pain, partic - ularly when there are stones in a dilated duct. Removal of  the - stones, with a side-to-side pancreaticojejunostomy to a Roux loop, is the procedure of  choice . As most patients are young, pancreatic resection is only very rarely considered, and only as a last resort, when all available methods of  pain relief  have tion been exhausted. - Summary box 6.21 Treatment of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF
Mainly medical – pain relief, insulin for diabetes and pancreatic
supplements for malnutrition
Surgery is reserved for intractable pain when all other methods
have been exhausted
Operations are side-to-side pancreaticojejunostomy; resection
in extreme cases
Treatment
This must be combined management between the physician and the surgeon. Tuberculous infection at other sites must Friedrich Neelsen , he developed the mainstay . The reader is asked to look up details of medical treatment in an appropriate source. Treatment
On completion of  medical treatment, the patient’s small bowel is reimaged to look for significant strictures. If  the patient has features of  subacute intermittent obstruction, bowel resection, in the form of  limited ileocolic resection with anastomosis between the terminal ileum and ascending colon for ileocolic hyperplastic disease, strictureplasty for single ileal stricture, bowel resection for multiple closely placed strictures or right hemicolectomy for extensive ileocolic disease precluding limited resection, is performed as deemed appropriate. The surgical principles and options in the elective patient are very similar to those for Crohn’s disease, where resections should be kept as conservative as possible. The emergency patient presents a great challenge. Such a patient is usually from a poor socioeconomic background, hence the late presentation of acute, distal, small bow el obstruction. The patient is extremely ill from dehydration, malnutrition, anaemia and probably active pulmonary tuberculosis. Vigor - ous resuscitation should precede the operation. At laparotomy , the minimum life-saving procedure is carried out, such as a resection of  diseased segment with proximal ileostomy and dis - - tal ileal or colonic mucus fistula to avoid anastomosis, w hich has a high chance of  leaking in the presence of  active infection and poor general condition. If, however, the general condition ) . Lap - of  the patient permits, a one-stage resection and anastomosis ma y rarely be performed. Thereafter, the patient should ideally be under the com bined care of  the physician and surgeon for a full course of standard multidrug antitubercular chemotherapy (intensive and maintenance phases) and improvement in nutritional sta tus, which may take up to 6–12 months. T he patient who had a simple bypass procedure is reassessed and, when the disease is no longer active (as evidenced by return to normal inflamma (a) - tory markers, weight gain, negative sputum culture), an elec - tive right hemicolectomy is done to remove the blind loop. This may be supplemented with strictureplasty for short strictures - at intervals or resection of  a segment with several strictures. Perforation is tr eated by thorough resuscitation followed by resection of  the a ff ected segment. Anastomosis is performed, - provided it is regarded as safe to do so, when peritoneal (b)
SUBHEPATIC
CAECUM
Figure 6.38
(a, b)
Series of a barium meal and follow-through showing strictures in the ileum, with the caecum pulled up into a subhepatic
position.
SUBHEPATIC
CAECUM
SUBHEPATIC
CAECUM
PULMONARY
INFILTRATION
Figure 6.39
Barium meal and follow-through
(a)
and chest radiograph
(b)
in a patient with extensive intestinal and pulmonary tuberculosis,
showing ileal strictures with high caecum and pulmonary in
/f_i
ltration.
encountered; otherwise, as a first stage, resection and ileostomy are performed followed by restoration of  bowel continuity as a second stage later on after a full course of  antitubercular chemotherapy and improvement in nutritional status. Summary box 6.26 Tuberculosis: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Patients should ideally be under the combined care of a
physician and surgeon
Vigorous supportive and full drug treatment are mandatory in
all cases
Symptomatic strictures are treated by the appropriate
resection, e.g. local ileocolic resection or strictureplasty
or resection as an elective procedure once the disease is
completely under control
Acute intestinal obstruction from distal ileal stricture is treated
by thorough resuscitation followed by resection with ileostomy
or primary anastomosis
One-stage resection and anastomosis can rarely be considered
if the patient’s general condition permits
Perforation is treated by appropriate local resection and
anastomosis or ileostomy if the condition of the patient is very
poor; this is later followed by restoration of bowel continuity
after the patient has fully recovered with antitubercular
chemotherapy
Treatment
Vigorous resuscitation with intravenous fluids and antibiotics in an intensive care unit gives the best chance of  stabilising the patient’s condition. Metronidazole, cephalosporins and gentamicin are used in combination. Chloramphenicol, despite its potential side e ff ect of  aplastic anaemia, is still used occasionally in resource-poor countries. Laparotomy is then carried out. Several surgical options are available, and the most appro priate operative procedure should be chosen judiciously depending upon the general condition of  the patient, the site of  perforation, the number of  perforations and the degree of (a) (b) ration ( Figure 6.41 ) after freshening the edges, wedge resec - tion of the ulcer area and closure, resection of bowel with or without anastomosis (exteriorisation), closure of the perfo - ration and side-to-side ileotransverse anastomosis, ileostomy or colostom y where the perforated bowel is exteriorised after refashioning the edges. After closing an ileal perforation, the surgeon should look of perforation or necrotic patches in the small for other sites or lar ge bowel that might imminently perforate, and deal with them appropriately . Thorough peritoneal lavage is essential. The linea alba is closed, leaving the rest of  the abdominal wound open for delayed closure, as wound infection is almost inevitable and dehiscence not uncommon. In the presence of rampant infection, laparostomy may be a good alternative. When a typhoid perforation occurs within the first week of illness, the prognosis is better than if  it occurs after the second or third week because, in the early stages, the patient is less nutritionally compromised and the body’s defences are more r obust. Furthermore, the shorter the interval between diagno - sis and operation, the better the prognosis. - Summary box 6.28 Treatment of bowel perforation from typhoid /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.41
(a, b)
Typhoid perforation of the terminal ileum (arrow in
Manage in intensive care
Resuscitate and give intravenous antibiotics
Laparotomy – choice of various procedures
Commonest site of perforation is the terminal ileum
Having found a perforation, always look for others
In the very ill patient, consider some form of exteriorisation
Close the peritoneum and leave the wound open for secondary
closure
Treatment
Medical treatment is very e ff ective and should be the first choice in the elective situation, with surgery being reserved for complications. Metronidazole and tinidazole are the e ff ective drugs. After treatment with metronidazole and tinidazole, diloxanide furoate, a luminal amoebicide that is not e ff ective against hepatic infestation, is used for 10 days to destroy any intestinal amoebae. Aspiration is carried out when imminent rupture of  an abscess is expected, especially when involving the left lobe. Pigtail catheter drainage may be considered in those pa who are not responding to intravenous metronidazole in the first 48–72 hours to improve antibiotic penetration. If  there is evidence of secondary infection, appropriate drug treatment is added. The threshold for draining a left liver lobe abscess - - should be low , given its propensity for rupture into either the peritoneal, pleural or pericardial cavity . tions Surgical treatment should be reserved for the complica of rupture into the pleural (usually the right side), peritoneal or pericardial cavities. Resuscitation, drainage and appropriate la vage with vigorous medical treatment are the key principles. In the large bowel, severe haemorrhage and toxic megacolon are rare complications. In these patients, the general principles of a surgical emergency apply , the principles of management being the same as for any toxic megacolon. Resuscitation is followed by resection of  bowel with exteriorisation. Then the patient is given vigorous supportive therapy . All such cases are tients managed in the intensive care unit, as would any patient with toxic megacolon whatever the cause. An amoeboma that has not regressed after full medical treatment should be managed with colonic resection, particu - larly if  cancer cannot be excluded.
Figure 6.2
Computed tomographic scan showing an amoebic liver
abscess in the right lobe.
Figure 6.3
Computed tomographic scans showing multiple amoebic
liver abscesses with extension into the chest.
Amoebiasis: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Medical treatment is very effective
For large abscesses, repeated aspiration or pigtail catheter
drainage is combined with drug treatment
Surgical treatment is reserved for complications, such as
rupture into the pleural, peritoneal or pericardial cavities
Acute toxic megacolon and severe haemorrhage are intestinal
complications that are treated with intensive supportive therapy
followed by resection and exteriorisation: subtotal colectomy
with terminal ileostomy and closure of the rectal stump
When an amoeboma is suspected in a colonic mass, cancer
should be excluded by appropriate imaging and biopsy
Treatment
The pulmonary phase of  the disease is usually self-limiting and requires symptomatic treatment only . For intestinal disease, patients should ideally be under the care of  a physician for treatment with anthelminthic drugs. Certain drugs may cause rapid death of  the adult worms and, if  there are many worms in the terminal ileum, the treatment may actually precipitate acute intestinal obstruction from a bolus of  dead worms. Children who present with features of  intermittent or subacute obstruction should be given a trial of conservative management in the form of  intravenous fluids, nasogastric suction and hypertonic saline enemas. The last of  these helps to disentangle the bolus of  worms and also increases intestinal motility . Surgery is reserved for complications, such as intestinal obstruction that has not resolved on a conservative regime, or when perforation is suspected. At laparotomy , the bolus ms in the terminal ileum is milked through the of wor ileocaecal valve into the colon for natural passage in the
(a)
(b)
Figure 6.5
Ultrasound scan showing a live worm (arrow) in the gallbladder
ryya, Kolkata, India).
Figure 6.6
Magnetic resonance cholangiopancreatography showing
a roundworm in the common bile duct (CBD). The worm could not
be removed endoscopically. The patient underwent an open chole
cystectomy and exploration of the CBD (this can also be addressed
laparoscopically in some centres).
(a)
and the common bile duct (CBD)
(b)
(courtesy of Dr A Bhattacha
stool. Postoperatively , hypertonic saline enemas may help in the extrusion of  the worms. Strictures, gangrenous areas or perforations need resection and anastomosis. If  the bowel wall is healthy , enterotomy and removal of  the worms may be performed ( Figure 6.7 ). Rarely , when perforation occurs as a result of  roundworm, the parasites may be found lying free in the peritoneal cavity . It is safer to bring out the site of  perforation as an ileostomy because, in the presence of  a large number of  w orms, the clo sure of  an anastomosis may be at risk of  breakdown from the activity of  the residual worms in the bowel. When a patient is operated upon as an emergency for a suspected complication of  roundworm infesta tion, the actual diagnosis at operation may turn out to be acute appendicitis, typhoid perforation or a tuberculous stricture and the pr ence of  roundworms is an incidental finding. Such a patient requires the appropriate surgery depending upon the primary pathology . Common bile duct or pancreatic duct obstruction from a roundw orm can be treated by endoscopic removal at endo scopic retrograde c holangiopancreatography (ERCP), failing which laparoscopic or open exploration of  the common bile duct is necessary . Cholecystectomy is also carried out. A full w any surgical course of  antiparasitic treatment must follo intervention. Summary box 6.5 Ascariasis: diagnosis and management /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.7
(a)
Roundworms seen through the bowel wall (arrowed).
worms.
Barium meal and follow-through will show worms scattered in
the small bowel
Ultrasonography may show worms in the common bile duct
and pancreatic duct
Plain abdominal radiograph and contrast CT scan will show the
worms as tubular or curvilinear structures
Conservative management with anthelminthics is the
/f_i
rst line
of treatment even in obstruction
Surgery is a last resort for acute abdomen – various options are
available
(b)
Roundworm being removed through enterotomy.
(c)
Removed round
Treatment
Praziquantel and albendazole are the drugs of  choice. However, the surgeon faces a challenge when there are stones not only in the gallbladder but also in the common bile duct. Cholecystec tomy with exploration of  the common bile duct is performed when indicated; currently , both procedures are performed lapa roscopically as a single-stage procedure. R epeated washouts are necessary during the exploration of  the common bile duct as there are stones, biliary debris, sludge and mud in the dilated duct. This should be followed b y choledochoduodenostomy . As this is a disease with a prolonged and relapsing course, some surgeons prefer to do a choledochojejunostomy to a Roux loop. The Roux loop is brought up to the abdominal wall, referred to as ‘an access loop’, which allows the interventional radiologist to deal with any future stones. As a public health measure, people who have emigrated from an endemic area should be o ff ered screening for César Roux , 1857–1934, Professor of  Surgery and Gynaecology , Lausanne, Switzerland, described this method of  forming a jejunal conduit in 1908. Otto Eduard Heinrich Wucherer , 1820–1873, German physician who practised in Brazil. Joseph Bancroft , 1836–1894, English physician who worked in Australia. Peau d’orange is French for ‘orange peel skin’. hepatobiliary system. This condition can be diagnosed and treated, and even cured, when it is in its subclinical form. Most importantly , the risk of  developing the dreadful disease of  cholangiocarcinoma is eliminated. Summary box 6.7 Asiatic cholangiohepatitis: treatment /uni25CF - /uni25CF /uni25CF w -
Medical treatment can be curative in the early stages
Surgical treatment is cholecystectomy, exploration of the
common bile duct and some form of biliary–enteric bypass
Prevention: consider offering hepatobiliary ultrasonography
as a screening procedure to recently arrived migrants from
endemic areas
Treatment
Medical treatment with diethylcarbamazine is very e ff ective in the early stages before the gross deformities of elephantiasis have developed. In the early stages of  limb swelling, intermit tent pneumatic compression helps, but the treatment has to be repeated over a prolonged period. Summary box 6.8 Filariasis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF A hydrocele is treated by the usual operation of excision and eversion of  the sac with, if  necessary , excision of  redun - dant scrotal skin. Operations for reducing the size of  the limb are hardly ever done these days because the procedures are so rarely successful.
Caused by
Wuchereria bancrofti
, which is carried by the
mosquito
Lymphatics are mainly affected, resulting in gross limb swelling
Eosinophilia occurs; immature worms may be seen in a
nocturnal peripheral blood smear
Gross forms of the disease cause a great deal of disability and
misery
Early cases are very amenable to medical treatment
Intermittent pneumatic compression gives some relief
The value of various surgical procedures is largely unproven
and hence they are rarely performed
Figure 6.9
Filariasis of the scrotum and penis (courtesy of Professor
Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).
Treatment
Here, the treatment of  hepatic hydatid is outlined because the liver is most commonly a ff ected, but the same general princi - ples apply whichever organ is involved. These patients should be treated in a tertiary unit where good teamwork between an expert hepatobiliary surgeon, an experienced physician and an interv entional radiologist is available. Surgical treatment by minimal access therapy is best summarised by the mnemonic PAIR (puncture, aspira - tion, injection and reaspiration). This is done after adequate drug treatment with albendazole, although praziquantel has
Figure 6.13
Magnetic resonance cholangiopancreatography showing
a large hepatic hydatid cyst with daughter cysts communicating with
the common bile duct, causing obstruction and dilatation of the entire
biliary tree (courtesy of Dr B Agarwal, New Delhi, India).
also been used, both of  these drugs being available only on a ‘named patient’ basis. Whether the patient is treated only medically or in combi nation with surgery will depend upon the clinical group (which gives an idea as to the activity of  the disease), the number of cysts and their anatomical position. Radical total or partial pericystectomy with omentoplasty or hepatic segmentectomy (especially if  the lesion is in a peripheral part of  the liver) are some of  the surgical options. During the operation, scolicidal agents ar e used, such as hypertonic saline (15–20%), ethanol (75–95%) or 5% povidone–iodine (although some use a 10% solution). This may cause sclerosing cholangitis if  biliary rad icles are in communication with the cyst wall. A laparoscopic approach to these procedures is being tried (see next section, Laparoscopic management ). Obviously , cysts in other organs need to be treated in accor dance with the actual anatomical site, along with the general principles described. An asymptomatic cyst tha t is inactive (group 3) may be left alone. Summary box 6.10 Hydatid cyst of the liver: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Currently , surgeons trained in minimal access surgery perform hydatid surgery using minimal access. Laparoscopic marsupial - isation of the cyst (deroofing), consisting of removal of the cyst containing the endocyst along with daughter cysts, is the most common procedure. In the initial steps, the cyst is aspirated, taking care not to spill any contents, using povidone–iodine or hypertonic saline as a scolicidal agent. Any communication with the biliary tr ee is oversewn and pedicled omentum is sutured to the margins of  the cyst. If  the cyst is small and superficial, a cystopericystectomy is performed at centres experienced enough to do more advanced surger y , removing the entire cyst intact.
Figure 6.14
Computed tomographic (CT) scan of the upper abdomen
showing a hypodense lesion of the left lobe of the liver; the periphery
of the lesion shows a double edge. This is the lamellar membrane of
the hydatid cyst that separated after trivial injury. The patient was a
14-year-old girl who developed a rash and pain in the upper abdomen
after dancing. The rash settled down after a course of antihistamines.
The CT scan was performed 2 weeks later for persisting upper
abdominal pain.
Ideally managed in a tertiary unit by a multidisciplinary team of
hepatobiliary surgeon, physician and interventional radiologist
Leave asymptomatic and inactive cysts alone – monitor size by
ultrasonography
Active cysts should
/f_i
rst be treated by a full course of
albendazole
Several procedures are available – PAIR, pericystectomy
with omentoplasty and hepatic segmentectomy; appropriate
management is customised according to the particular patient
and organ involved
Increasingly, a laparoscopic approach is being tried
Treatment
A herbal derivative from the seeds of Hydnocarpus wightianus (Chaulmoogra) was the mainstay of  treatment, with some success, until the advent of  dapsone (diamino-diphenyl sulphone). Dapsone, one of  the principal drugs, was a deriv - ative of  prontosil red and was discovered by Domagk. This is used according to the WHO guidelines along with rifampicin and clofazimine. During treatment, the patient may develop acute manifesta tions. These are controlled with steroids. Multiple drug therapy for 12 months is the key to treatment. A team approach between an infectious diseases specialist, plastic surgeon, ophthalmologist, and hand or orthopaedic surgeon is important. Surgical treatment is indicated in advanced stages of  the - disease for functional disability of  limbs, cosmetic disfigure - ment of  the face and visual problems. These entail major reconstructive surgery , whic h is the domain of  the plastic surgeon. Surgery for deformities in the hand is aimed at returning the ability to achieve a grasp and a pinch grip. Tendon trans fers (pioneered by Brand and Tovey) are used to recreate the (a) (b) Paul Wilson Brand CBE, FRCS, 1914–2003, was born to missionary parents in Southern India, and qualified in London in 1943. He himself  was a dedicated missionary who was ‘ An extraordinary gifted orthopaedic surgeon who straightened crooked hands and unravelled the riddle of  leprosy .’ As a pioneer in tendon transfer techniques , he established and practised initially in New Life Center, V ellore, South India and Schie ff elin Leprosy Research Centre, Karigiri, South India. Initially he trained as a carpenter and builder and maintained that his training as a carpenter helped him in his expertise in tendon transplantation. When he was awarded the CBE, his wife, Margaret, came to know about it when she found a letter from Her Majesty’s Government informing him of  the award while emptying the pockets of  his trousers before they were put into the wash. He later moved to Louisiana State University , Baton Rouge, LA, where he continued his work, and finally to Seattle as Emeritus Professor of  Orthopaedics at the University of  Washington, Seattle, USA. Margaret Brand , alongside her husband, Paul Brand, also contributed immensely to the health of  leprosy patients by concentrating on research to prevent blind ness in leprosy . She became known as ‘the woman who first helped lepers to see’. Frank Tovey OBE , 1921–2019, another English surgeon at about the same time (1951–1967), also performed extensive tendon transfers and facial and other reconstructive sur gery on patients with leprosy in southern India in the State of  Mysore. In this he was helped by his wife, Winifred, who organised the physiotherapy and rehabilitation of  the patients and established village diagnostic and treatment centres. function of  the lumbricals that have been lost due to dam - - age to the ulnar nerve. In the foot, damage to the common peroneal nerve leads to a foot drop due to paralysis of  tibialis -
Figure 6.17
Lateral view of the face showing collapse of the nasal
bridge due to destruction of nasal cartilage by leprosy.
Figure 6.18
Frontal view of the face showing eye changes in leprosy:
paralysis of orbicularis oculi and loss of eyebrows.
Figure 6.19
(a, b)
Typical bilateral claw hand
from leprosy due to involvement of the ulnar and
median nerves.
Figure 6.20
Claw toes from involvement of
the posterior tibial nerve by leprosy; also note
autoamputation of toes of the right foot.
anterior. If  a foot-drop splint is not adequate, then once again a tendon transfer (tibialis posterior into the dorsum of  the foot) will improve function. Ulcers resulting from an insensate foot should be completely debrided followed by protection with a plaster cast. The general surgeon may be called upon to treat a patient when the deformity is so advanced that amputation is required or an abscess needs drainage as an emergency . All surgical procedures obviously need to be done under antileprosy drug tr eatment. This is best achieved by a team approach. Educating patients about the dreadful sequelae of the disease so that they seek medical help ear ly is important. It is also necessary to educate the general public that patients su ff ering from the disease should not be made social outcasts. Summary box 6.14 Leprosy: treatment /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.21
Bilateral trophic ulceration of the feet due to anaesthesia
of the soles resulting from leprosy; also note claw toes on the left foot.
Multiple drug therapy for a year
Team approach
Surgical reconstruction requires the expertise of a hand
surgeon, orthopaedic surgeon and plastic surgeon
Education of the patient and general public should be the
keystone in prevention
Treatment
The treatment is mainly medical, with exocrine support using pancreatic enzymes, treatment of diabetes with insulin and the management of  malnutrition. Treatment of  pain should be along the lines of  the usual analgesic ladder: non-opioids, followed by weak and then strong opioids and, finally , referral to a pain clinic. Surgical treatment is necessary for intractable pain, partic - ularly when there are stones in a dilated duct. Removal of  the - stones, with a side-to-side pancreaticojejunostomy to a Roux loop, is the procedure of  choice . As most patients are young, pancreatic resection is only very rarely considered, and only as a last resort, when all available methods of  pain relief  have tion been exhausted. - Summary box 6.21 Treatment of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF
Mainly medical – pain relief, insulin for diabetes and pancreatic
supplements for malnutrition
Surgery is reserved for intractable pain when all other methods
have been exhausted
Operations are side-to-side pancreaticojejunostomy; resection
in extreme cases
Treatment
This must be combined management between the physician and the surgeon. Tuberculous infection at other sites must Friedrich Neelsen , he developed the mainstay . The reader is asked to look up details of medical treatment in an appropriate source. Treatment
On completion of  medical treatment, the patient’s small bowel is reimaged to look for significant strictures. If  the patient has features of  subacute intermittent obstruction, bowel resection, in the form of  limited ileocolic resection with anastomosis between the terminal ileum and ascending colon for ileocolic hyperplastic disease, strictureplasty for single ileal stricture, bowel resection for multiple closely placed strictures or right hemicolectomy for extensive ileocolic disease precluding limited resection, is performed as deemed appropriate. The surgical principles and options in the elective patient are very similar to those for Crohn’s disease, where resections should be kept as conservative as possible. The emergency patient presents a great challenge. Such a patient is usually from a poor socioeconomic background, hence the late presentation of acute, distal, small bow el obstruction. The patient is extremely ill from dehydration, malnutrition, anaemia and probably active pulmonary tuberculosis. Vigor - ous resuscitation should precede the operation. At laparotomy , the minimum life-saving procedure is carried out, such as a resection of  diseased segment with proximal ileostomy and dis - - tal ileal or colonic mucus fistula to avoid anastomosis, w hich has a high chance of  leaking in the presence of  active infection and poor general condition. If, however, the general condition ) . Lap - of  the patient permits, a one-stage resection and anastomosis ma y rarely be performed. Thereafter, the patient should ideally be under the com bined care of  the physician and surgeon for a full course of standard multidrug antitubercular chemotherapy (intensive and maintenance phases) and improvement in nutritional sta tus, which may take up to 6–12 months. T he patient who had a simple bypass procedure is reassessed and, when the disease is no longer active (as evidenced by return to normal inflamma (a) - tory markers, weight gain, negative sputum culture), an elec - tive right hemicolectomy is done to remove the blind loop. This may be supplemented with strictureplasty for short strictures - at intervals or resection of  a segment with several strictures. Perforation is tr eated by thorough resuscitation followed by resection of  the a ff ected segment. Anastomosis is performed, - provided it is regarded as safe to do so, when peritoneal (b)
SUBHEPATIC
CAECUM
Figure 6.38
(a, b)
Series of a barium meal and follow-through showing strictures in the ileum, with the caecum pulled up into a subhepatic
position.
SUBHEPATIC
CAECUM
SUBHEPATIC
CAECUM
PULMONARY
INFILTRATION
Figure 6.39
Barium meal and follow-through
(a)
and chest radiograph
(b)
in a patient with extensive intestinal and pulmonary tuberculosis,
showing ileal strictures with high caecum and pulmonary in
/f_i
ltration.
encountered; otherwise, as a first stage, resection and ileostomy are performed followed by restoration of  bowel continuity as a second stage later on after a full course of  antitubercular chemotherapy and improvement in nutritional status. Summary box 6.26 Tuberculosis: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Patients should ideally be under the combined care of a
physician and surgeon
Vigorous supportive and full drug treatment are mandatory in
all cases
Symptomatic strictures are treated by the appropriate
resection, e.g. local ileocolic resection or strictureplasty
or resection as an elective procedure once the disease is
completely under control
Acute intestinal obstruction from distal ileal stricture is treated
by thorough resuscitation followed by resection with ileostomy
or primary anastomosis
One-stage resection and anastomosis can rarely be considered
if the patient’s general condition permits
Perforation is treated by appropriate local resection and
anastomosis or ileostomy if the condition of the patient is very
poor; this is later followed by restoration of bowel continuity
after the patient has fully recovered with antitubercular
chemotherapy
Treatment
Vigorous resuscitation with intravenous fluids and antibiotics in an intensive care unit gives the best chance of  stabilising the patient’s condition. Metronidazole, cephalosporins and gentamicin are used in combination. Chloramphenicol, despite its potential side e ff ect of  aplastic anaemia, is still used occasionally in resource-poor countries. Laparotomy is then carried out. Several surgical options are available, and the most appro priate operative procedure should be chosen judiciously depending upon the general condition of  the patient, the site of  perforation, the number of  perforations and the degree of (a) (b) ration ( Figure 6.41 ) after freshening the edges, wedge resec - tion of the ulcer area and closure, resection of bowel with or without anastomosis (exteriorisation), closure of the perfo - ration and side-to-side ileotransverse anastomosis, ileostomy or colostom y where the perforated bowel is exteriorised after refashioning the edges. After closing an ileal perforation, the surgeon should look of perforation or necrotic patches in the small for other sites or lar ge bowel that might imminently perforate, and deal with them appropriately . Thorough peritoneal lavage is essential. The linea alba is closed, leaving the rest of  the abdominal wound open for delayed closure, as wound infection is almost inevitable and dehiscence not uncommon. In the presence of rampant infection, laparostomy may be a good alternative. When a typhoid perforation occurs within the first week of illness, the prognosis is better than if  it occurs after the second or third week because, in the early stages, the patient is less nutritionally compromised and the body’s defences are more r obust. Furthermore, the shorter the interval between diagno - sis and operation, the better the prognosis. - Summary box 6.28 Treatment of bowel perforation from typhoid /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.41
(a, b)
Typhoid perforation of the terminal ileum (arrow in
Manage in intensive care
Resuscitate and give intravenous antibiotics
Laparotomy – choice of various procedures
Commonest site of perforation is the terminal ileum
Having found a perforation, always look for others
In the very ill patient, consider some form of exteriorisation
Close the peritoneum and leave the wound open for secondary
closure
Treatment
Medical treatment is very e ff ective and should be the first choice in the elective situation, with surgery being reserved for complications. Metronidazole and tinidazole are the e ff ective drugs. After treatment with metronidazole and tinidazole, diloxanide furoate, a luminal amoebicide that is not e ff ective against hepatic infestation, is used for 10 days to destroy any intestinal amoebae. Aspiration is carried out when imminent rupture of  an abscess is expected, especially when involving the left lobe. Pigtail catheter drainage may be considered in those pa who are not responding to intravenous metronidazole in the first 48–72 hours to improve antibiotic penetration. If  there is evidence of secondary infection, appropriate drug treatment is added. The threshold for draining a left liver lobe abscess - - should be low , given its propensity for rupture into either the peritoneal, pleural or pericardial cavity . tions Surgical treatment should be reserved for the complica of rupture into the pleural (usually the right side), peritoneal or pericardial cavities. Resuscitation, drainage and appropriate la vage with vigorous medical treatment are the key principles. In the large bowel, severe haemorrhage and toxic megacolon are rare complications. In these patients, the general principles of a surgical emergency apply , the principles of management being the same as for any toxic megacolon. Resuscitation is followed by resection of  bowel with exteriorisation. Then the patient is given vigorous supportive therapy . All such cases are tients managed in the intensive care unit, as would any patient with toxic megacolon whatever the cause. An amoeboma that has not regressed after full medical treatment should be managed with colonic resection, particu - larly if  cancer cannot be excluded.
Figure 6.2
Computed tomographic scan showing an amoebic liver
abscess in the right lobe.
Figure 6.3
Computed tomographic scans showing multiple amoebic
liver abscesses with extension into the chest.
Amoebiasis: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Medical treatment is very effective
For large abscesses, repeated aspiration or pigtail catheter
drainage is combined with drug treatment
Surgical treatment is reserved for complications, such as
rupture into the pleural, peritoneal or pericardial cavities
Acute toxic megacolon and severe haemorrhage are intestinal
complications that are treated with intensive supportive therapy
followed by resection and exteriorisation: subtotal colectomy
with terminal ileostomy and closure of the rectal stump
When an amoeboma is suspected in a colonic mass, cancer
should be excluded by appropriate imaging and biopsy
Treatment
The pulmonary phase of  the disease is usually self-limiting and requires symptomatic treatment only . For intestinal disease, patients should ideally be under the care of  a physician for treatment with anthelminthic drugs. Certain drugs may cause rapid death of  the adult worms and, if  there are many worms in the terminal ileum, the treatment may actually precipitate acute intestinal obstruction from a bolus of  dead worms. Children who present with features of  intermittent or subacute obstruction should be given a trial of conservative management in the form of  intravenous fluids, nasogastric suction and hypertonic saline enemas. The last of  these helps to disentangle the bolus of  worms and also increases intestinal motility . Surgery is reserved for complications, such as intestinal obstruction that has not resolved on a conservative regime, or when perforation is suspected. At laparotomy , the bolus ms in the terminal ileum is milked through the of wor ileocaecal valve into the colon for natural passage in the
(a)
(b)
Figure 6.5
Ultrasound scan showing a live worm (arrow) in the gallbladder
ryya, Kolkata, India).
Figure 6.6
Magnetic resonance cholangiopancreatography showing
a roundworm in the common bile duct (CBD). The worm could not
be removed endoscopically. The patient underwent an open chole
cystectomy and exploration of the CBD (this can also be addressed
laparoscopically in some centres).
(a)
and the common bile duct (CBD)
(b)
(courtesy of Dr A Bhattacha
stool. Postoperatively , hypertonic saline enemas may help in the extrusion of  the worms. Strictures, gangrenous areas or perforations need resection and anastomosis. If  the bowel wall is healthy , enterotomy and removal of  the worms may be performed ( Figure 6.7 ). Rarely , when perforation occurs as a result of  roundworm, the parasites may be found lying free in the peritoneal cavity . It is safer to bring out the site of  perforation as an ileostomy because, in the presence of  a large number of  w orms, the clo sure of  an anastomosis may be at risk of  breakdown from the activity of  the residual worms in the bowel. When a patient is operated upon as an emergency for a suspected complication of  roundworm infesta tion, the actual diagnosis at operation may turn out to be acute appendicitis, typhoid perforation or a tuberculous stricture and the pr ence of  roundworms is an incidental finding. Such a patient requires the appropriate surgery depending upon the primary pathology . Common bile duct or pancreatic duct obstruction from a roundw orm can be treated by endoscopic removal at endo scopic retrograde c holangiopancreatography (ERCP), failing which laparoscopic or open exploration of  the common bile duct is necessary . Cholecystectomy is also carried out. A full w any surgical course of  antiparasitic treatment must follo intervention. Summary box 6.5 Ascariasis: diagnosis and management /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.7
(a)
Roundworms seen through the bowel wall (arrowed).
worms.
Barium meal and follow-through will show worms scattered in
the small bowel
Ultrasonography may show worms in the common bile duct
and pancreatic duct
Plain abdominal radiograph and contrast CT scan will show the
worms as tubular or curvilinear structures
Conservative management with anthelminthics is the
/f_i
rst line
of treatment even in obstruction
Surgery is a last resort for acute abdomen – various options are
available
(b)
Roundworm being removed through enterotomy.
(c)
Removed round
Treatment
Praziquantel and albendazole are the drugs of  choice. However, the surgeon faces a challenge when there are stones not only in the gallbladder but also in the common bile duct. Cholecystec tomy with exploration of  the common bile duct is performed when indicated; currently , both procedures are performed lapa roscopically as a single-stage procedure. R epeated washouts are necessary during the exploration of  the common bile duct as there are stones, biliary debris, sludge and mud in the dilated duct. This should be followed b y choledochoduodenostomy . As this is a disease with a prolonged and relapsing course, some surgeons prefer to do a choledochojejunostomy to a Roux loop. The Roux loop is brought up to the abdominal wall, referred to as ‘an access loop’, which allows the interventional radiologist to deal with any future stones. As a public health measure, people who have emigrated from an endemic area should be o ff ered screening for César Roux , 1857–1934, Professor of  Surgery and Gynaecology , Lausanne, Switzerland, described this method of  forming a jejunal conduit in 1908. Otto Eduard Heinrich Wucherer , 1820–1873, German physician who practised in Brazil. Joseph Bancroft , 1836–1894, English physician who worked in Australia. Peau d’orange is French for ‘orange peel skin’. hepatobiliary system. This condition can be diagnosed and treated, and even cured, when it is in its subclinical form. Most importantly , the risk of  developing the dreadful disease of  cholangiocarcinoma is eliminated. Summary box 6.7 Asiatic cholangiohepatitis: treatment /uni25CF - /uni25CF /uni25CF w -
Medical treatment can be curative in the early stages
Surgical treatment is cholecystectomy, exploration of the
common bile duct and some form of biliary–enteric bypass
Prevention: consider offering hepatobiliary ultrasonography
as a screening procedure to recently arrived migrants from
endemic areas
Treatment
Medical treatment with diethylcarbamazine is very e ff ective in the early stages before the gross deformities of elephantiasis have developed. In the early stages of  limb swelling, intermit tent pneumatic compression helps, but the treatment has to be repeated over a prolonged period. Summary box 6.8 Filariasis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF A hydrocele is treated by the usual operation of excision and eversion of  the sac with, if  necessary , excision of  redun - dant scrotal skin. Operations for reducing the size of  the limb are hardly ever done these days because the procedures are so rarely successful.
Caused by
Wuchereria bancrofti
, which is carried by the
mosquito
Lymphatics are mainly affected, resulting in gross limb swelling
Eosinophilia occurs; immature worms may be seen in a
nocturnal peripheral blood smear
Gross forms of the disease cause a great deal of disability and
misery
Early cases are very amenable to medical treatment
Intermittent pneumatic compression gives some relief
The value of various surgical procedures is largely unproven
and hence they are rarely performed
Figure 6.9
Filariasis of the scrotum and penis (courtesy of Professor
Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).
Treatment
Here, the treatment of  hepatic hydatid is outlined because the liver is most commonly a ff ected, but the same general princi - ples apply whichever organ is involved. These patients should be treated in a tertiary unit where good teamwork between an expert hepatobiliary surgeon, an experienced physician and an interv entional radiologist is available. Surgical treatment by minimal access therapy is best summarised by the mnemonic PAIR (puncture, aspira - tion, injection and reaspiration). This is done after adequate drug treatment with albendazole, although praziquantel has
Figure 6.13
Magnetic resonance cholangiopancreatography showing
a large hepatic hydatid cyst with daughter cysts communicating with
the common bile duct, causing obstruction and dilatation of the entire
biliary tree (courtesy of Dr B Agarwal, New Delhi, India).
also been used, both of  these drugs being available only on a ‘named patient’ basis. Whether the patient is treated only medically or in combi nation with surgery will depend upon the clinical group (which gives an idea as to the activity of  the disease), the number of cysts and their anatomical position. Radical total or partial pericystectomy with omentoplasty or hepatic segmentectomy (especially if  the lesion is in a peripheral part of  the liver) are some of  the surgical options. During the operation, scolicidal agents ar e used, such as hypertonic saline (15–20%), ethanol (75–95%) or 5% povidone–iodine (although some use a 10% solution). This may cause sclerosing cholangitis if  biliary rad icles are in communication with the cyst wall. A laparoscopic approach to these procedures is being tried (see next section, Laparoscopic management ). Obviously , cysts in other organs need to be treated in accor dance with the actual anatomical site, along with the general principles described. An asymptomatic cyst tha t is inactive (group 3) may be left alone. Summary box 6.10 Hydatid cyst of the liver: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Currently , surgeons trained in minimal access surgery perform hydatid surgery using minimal access. Laparoscopic marsupial - isation of the cyst (deroofing), consisting of removal of the cyst containing the endocyst along with daughter cysts, is the most common procedure. In the initial steps, the cyst is aspirated, taking care not to spill any contents, using povidone–iodine or hypertonic saline as a scolicidal agent. Any communication with the biliary tr ee is oversewn and pedicled omentum is sutured to the margins of  the cyst. If  the cyst is small and superficial, a cystopericystectomy is performed at centres experienced enough to do more advanced surger y , removing the entire cyst intact.
Figure 6.14
Computed tomographic (CT) scan of the upper abdomen
showing a hypodense lesion of the left lobe of the liver; the periphery
of the lesion shows a double edge. This is the lamellar membrane of
the hydatid cyst that separated after trivial injury. The patient was a
14-year-old girl who developed a rash and pain in the upper abdomen
after dancing. The rash settled down after a course of antihistamines.
The CT scan was performed 2 weeks later for persisting upper
abdominal pain.
Ideally managed in a tertiary unit by a multidisciplinary team of
hepatobiliary surgeon, physician and interventional radiologist
Leave asymptomatic and inactive cysts alone – monitor size by
ultrasonography
Active cysts should
/f_i
rst be treated by a full course of
albendazole
Several procedures are available – PAIR, pericystectomy
with omentoplasty and hepatic segmentectomy; appropriate
management is customised according to the particular patient
and organ involved
Increasingly, a laparoscopic approach is being tried
Treatment
A herbal derivative from the seeds of Hydnocarpus wightianus (Chaulmoogra) was the mainstay of  treatment, with some success, until the advent of  dapsone (diamino-diphenyl sulphone). Dapsone, one of  the principal drugs, was a deriv - ative of  prontosil red and was discovered by Domagk. This is used according to the WHO guidelines along with rifampicin and clofazimine. During treatment, the patient may develop acute manifesta tions. These are controlled with steroids. Multiple drug therapy for 12 months is the key to treatment. A team approach between an infectious diseases specialist, plastic surgeon, ophthalmologist, and hand or orthopaedic surgeon is important. Surgical treatment is indicated in advanced stages of  the - disease for functional disability of  limbs, cosmetic disfigure - ment of  the face and visual problems. These entail major reconstructive surgery , whic h is the domain of  the plastic surgeon. Surgery for deformities in the hand is aimed at returning the ability to achieve a grasp and a pinch grip. Tendon trans fers (pioneered by Brand and Tovey) are used to recreate the (a) (b) Paul Wilson Brand CBE, FRCS, 1914–2003, was born to missionary parents in Southern India, and qualified in London in 1943. He himself  was a dedicated missionary who was ‘ An extraordinary gifted orthopaedic surgeon who straightened crooked hands and unravelled the riddle of  leprosy .’ As a pioneer in tendon transfer techniques , he established and practised initially in New Life Center, V ellore, South India and Schie ff elin Leprosy Research Centre, Karigiri, South India. Initially he trained as a carpenter and builder and maintained that his training as a carpenter helped him in his expertise in tendon transplantation. When he was awarded the CBE, his wife, Margaret, came to know about it when she found a letter from Her Majesty’s Government informing him of  the award while emptying the pockets of  his trousers before they were put into the wash. He later moved to Louisiana State University , Baton Rouge, LA, where he continued his work, and finally to Seattle as Emeritus Professor of  Orthopaedics at the University of  Washington, Seattle, USA. Margaret Brand , alongside her husband, Paul Brand, also contributed immensely to the health of  leprosy patients by concentrating on research to prevent blind ness in leprosy . She became known as ‘the woman who first helped lepers to see’. Frank Tovey OBE , 1921–2019, another English surgeon at about the same time (1951–1967), also performed extensive tendon transfers and facial and other reconstructive sur gery on patients with leprosy in southern India in the State of  Mysore. In this he was helped by his wife, Winifred, who organised the physiotherapy and rehabilitation of  the patients and established village diagnostic and treatment centres. function of  the lumbricals that have been lost due to dam - - age to the ulnar nerve. In the foot, damage to the common peroneal nerve leads to a foot drop due to paralysis of  tibialis -
Figure 6.17
Lateral view of the face showing collapse of the nasal
bridge due to destruction of nasal cartilage by leprosy.
Figure 6.18
Frontal view of the face showing eye changes in leprosy:
paralysis of orbicularis oculi and loss of eyebrows.
Figure 6.19
(a, b)
Typical bilateral claw hand
from leprosy due to involvement of the ulnar and
median nerves.
Figure 6.20
Claw toes from involvement of
the posterior tibial nerve by leprosy; also note
autoamputation of toes of the right foot.
anterior. If  a foot-drop splint is not adequate, then once again a tendon transfer (tibialis posterior into the dorsum of  the foot) will improve function. Ulcers resulting from an insensate foot should be completely debrided followed by protection with a plaster cast. The general surgeon may be called upon to treat a patient when the deformity is so advanced that amputation is required or an abscess needs drainage as an emergency . All surgical procedures obviously need to be done under antileprosy drug tr eatment. This is best achieved by a team approach. Educating patients about the dreadful sequelae of the disease so that they seek medical help ear ly is important. It is also necessary to educate the general public that patients su ff ering from the disease should not be made social outcasts. Summary box 6.14 Leprosy: treatment /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.21
Bilateral trophic ulceration of the feet due to anaesthesia
of the soles resulting from leprosy; also note claw toes on the left foot.
Multiple drug therapy for a year
Team approach
Surgical reconstruction requires the expertise of a hand
surgeon, orthopaedic surgeon and plastic surgeon
Education of the patient and general public should be the
keystone in prevention
Treatment
The treatment is mainly medical, with exocrine support using pancreatic enzymes, treatment of diabetes with insulin and the management of  malnutrition. Treatment of  pain should be along the lines of  the usual analgesic ladder: non-opioids, followed by weak and then strong opioids and, finally , referral to a pain clinic. Surgical treatment is necessary for intractable pain, partic - ularly when there are stones in a dilated duct. Removal of  the - stones, with a side-to-side pancreaticojejunostomy to a Roux loop, is the procedure of  choice . As most patients are young, pancreatic resection is only very rarely considered, and only as a last resort, when all available methods of  pain relief  have tion been exhausted. - Summary box 6.21 Treatment of tropical chronic pancreatitis /uni25CF /uni25CF /uni25CF
Mainly medical – pain relief, insulin for diabetes and pancreatic
supplements for malnutrition
Surgery is reserved for intractable pain when all other methods
have been exhausted
Operations are side-to-side pancreaticojejunostomy; resection
in extreme cases
Treatment
This must be combined management between the physician and the surgeon. Tuberculous infection at other sites must Friedrich Neelsen , he developed the mainstay . The reader is asked to look up details of medical treatment in an appropriate source. Treatment
On completion of  medical treatment, the patient’s small bowel is reimaged to look for significant strictures. If  the patient has features of  subacute intermittent obstruction, bowel resection, in the form of  limited ileocolic resection with anastomosis between the terminal ileum and ascending colon for ileocolic hyperplastic disease, strictureplasty for single ileal stricture, bowel resection for multiple closely placed strictures or right hemicolectomy for extensive ileocolic disease precluding limited resection, is performed as deemed appropriate. The surgical principles and options in the elective patient are very similar to those for Crohn’s disease, where resections should be kept as conservative as possible. The emergency patient presents a great challenge. Such a patient is usually from a poor socioeconomic background, hence the late presentation of acute, distal, small bow el obstruction. The patient is extremely ill from dehydration, malnutrition, anaemia and probably active pulmonary tuberculosis. Vigor - ous resuscitation should precede the operation. At laparotomy , the minimum life-saving procedure is carried out, such as a resection of  diseased segment with proximal ileostomy and dis - - tal ileal or colonic mucus fistula to avoid anastomosis, w hich has a high chance of  leaking in the presence of  active infection and poor general condition. If, however, the general condition ) . Lap - of  the patient permits, a one-stage resection and anastomosis ma y rarely be performed. Thereafter, the patient should ideally be under the com bined care of  the physician and surgeon for a full course of standard multidrug antitubercular chemotherapy (intensive and maintenance phases) and improvement in nutritional sta tus, which may take up to 6–12 months. T he patient who had a simple bypass procedure is reassessed and, when the disease is no longer active (as evidenced by return to normal inflamma (a) - tory markers, weight gain, negative sputum culture), an elec - tive right hemicolectomy is done to remove the blind loop. This may be supplemented with strictureplasty for short strictures - at intervals or resection of  a segment with several strictures. Perforation is tr eated by thorough resuscitation followed by resection of  the a ff ected segment. Anastomosis is performed, - provided it is regarded as safe to do so, when peritoneal (b)
SUBHEPATIC
CAECUM
Figure 6.38
(a, b)
Series of a barium meal and follow-through showing strictures in the ileum, with the caecum pulled up into a subhepatic
position.
SUBHEPATIC
CAECUM
SUBHEPATIC
CAECUM
PULMONARY
INFILTRATION
Figure 6.39
Barium meal and follow-through
(a)
and chest radiograph
(b)
in a patient with extensive intestinal and pulmonary tuberculosis,
showing ileal strictures with high caecum and pulmonary in
/f_i
ltration.
encountered; otherwise, as a first stage, resection and ileostomy are performed followed by restoration of  bowel continuity as a second stage later on after a full course of  antitubercular chemotherapy and improvement in nutritional status. Summary box 6.26 Tuberculosis: treatment /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Patients should ideally be under the combined care of a
physician and surgeon
Vigorous supportive and full drug treatment are mandatory in
all cases
Symptomatic strictures are treated by the appropriate
resection, e.g. local ileocolic resection or strictureplasty
or resection as an elective procedure once the disease is
completely under control
Acute intestinal obstruction from distal ileal stricture is treated
by thorough resuscitation followed by resection with ileostomy
or primary anastomosis
One-stage resection and anastomosis can rarely be considered
if the patient’s general condition permits
Perforation is treated by appropriate local resection and
anastomosis or ileostomy if the condition of the patient is very
poor; this is later followed by restoration of bowel continuity
after the patient has fully recovered with antitubercular
chemotherapy
Treatment
Vigorous resuscitation with intravenous fluids and antibiotics in an intensive care unit gives the best chance of  stabilising the patient’s condition. Metronidazole, cephalosporins and gentamicin are used in combination. Chloramphenicol, despite its potential side e ff ect of  aplastic anaemia, is still used occasionally in resource-poor countries. Laparotomy is then carried out. Several surgical options are available, and the most appro priate operative procedure should be chosen judiciously depending upon the general condition of  the patient, the site of  perforation, the number of  perforations and the degree of (a) (b) ration ( Figure 6.41 ) after freshening the edges, wedge resec - tion of the ulcer area and closure, resection of bowel with or without anastomosis (exteriorisation), closure of the perfo - ration and side-to-side ileotransverse anastomosis, ileostomy or colostom y where the perforated bowel is exteriorised after refashioning the edges. After closing an ileal perforation, the surgeon should look of perforation or necrotic patches in the small for other sites or lar ge bowel that might imminently perforate, and deal with them appropriately . Thorough peritoneal lavage is essential. The linea alba is closed, leaving the rest of  the abdominal wound open for delayed closure, as wound infection is almost inevitable and dehiscence not uncommon. In the presence of rampant infection, laparostomy may be a good alternative. When a typhoid perforation occurs within the first week of illness, the prognosis is better than if  it occurs after the second or third week because, in the early stages, the patient is less nutritionally compromised and the body’s defences are more r obust. Furthermore, the shorter the interval between diagno - sis and operation, the better the prognosis. - Summary box 6.28 Treatment of bowel perforation from typhoid /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 6.41
(a, b)
Typhoid perforation of the terminal ileum (arrow in
Manage in intensive care
Resuscitate and give intravenous antibiotics
Laparotomy – choice of various procedures
Commonest site of perforation is the terminal ileum
Having found a perforation, always look for others
In the very ill patient, consider some form of exteriorisation
Close the peritoneum and leave the wound open for secondary
closure