SURGICAL PROBLEMS IN

E. Q. ARCHAMPONG F.R.C.S., F.R.C.S.Ed.

C. G. CLARK M.D., Ch.M., F.R.C.S., F.R.C.S.Ed.

Department of Surgery, University College Hospital Medical School

INFESTATION WITH PATHOGENIC amoebae is geographically the most widely distributed of the protozoal diseases. The general surgeon is liable to be faced with complications arising from amoebiasis wherever he works. With increased intercontinental travel the condition is now more frequently encountered in countries with a high standard of living, where it may be confused with other diseases of the colon. In endemic areas the disease is often diagnosed too readily, and the manifestations of the disease are liable to differ, depending perhaps on the nutritional state of the patient. Differences occur in clinical presentation, and the course of the disease varies in different communities. It is not surprising therefore that there is controversy regarding management. An attempt has been made in this paper to provide some guidance for the surgeon faced with the complications of amoebiasis.

Pathogenesis Amoebiasis is an infection due to histolytica, which is ingested with contaminated . The lesions produced by E. histolytica in the colonic mucosa involve principally the caecum, ascending colon, and rectosigmoid, the latter fortunately allowing access to biopsy material for diagnosis. Craig and Faust' found that in symptomatic patients the lesions were generalized throughout the colon in 60% of cases and localized in the remainder. The initial lesion seen on sigmoidoscopy is a characteristic punched-out ulcer, or undermined ulcers with yellowish-grey exudate in the base. Un- fortunately, in the there is often associated oedema and attendant inflammation which may obscure the typical ulcers, thus making it impossible to differentiate amoebic from other forms of dysentry on proctoscopy. At first there is only a mild cellular reaction to the amoebae, and in the early stages the serosa and muscular wall of the colon show little change. Later, because of secondary invasion, the intes- tinal wall becomes a little thickened by oedema, though invasion of lymphatics by amoebae is seldom demonstrated and regional lymph- From a Postgraduate Lecture (Ann. Roy. Coll. Surg. Engl. 1973, vol. 52) 36 SURGICAL PROBLEMS IN AMOEBIASIS adenopathy is rare. This results in a tendency to underestimate the severity of the lesion if for any reason laparotomy is performed. Amoebic lesions generally heal without extensive cicatrization, though the regenerated mucous membranes may be thin and atrophic, with deficient glands and mucus production. Occasionally pseudopolypi occur, and more rarely an amoebic (amoeboma) is found in the region of the caecum or rectosigmoid. These are uncommon lesions in actively treated patients, but when they occur early revision of the diag- nosis is imperative. The mild cellular reaction to amoebae may permit ready access of the parasite to the vascular tree; however, the low incidence of extra- intestinal foci (2-5% ) suggests that most amoebae perish before estab- lishing metastatic foci. Amoebic abscess may occur in the lung, pleura, or pericardium, and occasionally in the brain, but the commonest ectopic site is the . Many amoebae undoubtedly invade the portal vein and are transported to the liver, but Craig and Faust' have emphasized that it is the liver whose resistance is decreased by other factors such as alcoholism which becomes affected. Most amoebic liver abscesses are solitary, sterile, and situated in the right lobe of the liver. They result from misdiagnosis and delayed or ineffective treatment. Symptoms If the definition of amoebiasis as an infection with the pathogenic E. histolytica be accepted, then the disease may be regarded as occurring in invasive and non-invasive forms. The latter is symptomless, the organism living commensally in the colon and being discovered only on routine stool examination. Although amoebiasis is regarded primarily as a tropical infection, 5-10% of subjects in temperate climates harbour either amoebae or amoebic cysts3. If the stools are examined because of irregular bowel action the amoebic trophozoite may be found, but unless it contains engulfed red cells it may be entirely blameless. The unfortunate tendency to attribute an aetiological role to E. histolytica in all situations has contributed to a state of amoebophobia which is increasingly encountered in visitors to tropical and subtropical countries. The symptomatology of invasive amoebiasis is not well understood, particularly in the temperate regions of the world, where perhaps from a higher standard of living the manifestations are often mild. An aver- age attack may manifest itself as no more than a windy looseness of stools with 2-3 postprandial defaecations daily, preceded by colic and aching in the rectum4. Passage of macroscopic may or may not be evident. The finding of E. histolytica in the stools and permanent relief of symptoms with specific treatment are confirmatory evidence of the disease. Untreated, symptoms may wax and wane or progress to the more serious disease. 37 E. Q. ARCHAMPONG AND C. G. CLARK Because of the poorer standard of living and health the disease takes a more severe form in developing countries, and occasionally this variety may be seen in temperate latitudes. The presentation may simu- late the clinical picture of shigellosis, with high fever and acute fulminating characterized by diarrhoea with blood, pus, and mucus. This later deteriorates into passage of copious exudate replacing the liquid stools, leading to profound fluid and electrolyte disturbance. Abdominal tenderness is frequent and later distension supervenes.

Diagnosis The diagnosis is confirmed by the identification of the parasite in fresh stool specimens, ulcer scrapings, and rectal biopsy specimens. In nearly all symptomatic patients haemotophagous trophozoites of E. histolytica are seen; occur only in mild cases and then identification is aided by flotation methods5. Characteristic punched-out or undermined ulcers, the floor covered with yellowish-grey exudate, may be seen at sigmoidoscopy in half the patients with active colitis6, but the appearances are seldom diagnostic since it is not always possible to differentiate amoebiasis from other causes of dysentery on the basis of mucosal changes. The procedure, however, affords the means for biopsy and obtaining fresh stool speci- mens; it is safe and requires no preparation besides bowel evacuation shortly before examination. The characteristic sigmoidoscopic appear- ance is one of inflamed, oedematous mucosa, ulcers being often but not always identifiable. Although recent advances have made possible the culture of E. his- tolytica7, 8 this technique is of limited value in the laboratory investiga- tion of the disease, yielding a lower incidence of positive results than microscopical examination7. Amoebiasis confined to the colon produces little change in the peri- pheral blood, and even in the presence of secondary infection a white cell count of 10,000/mm3 is seldom exceeded9' 10. Anaemia is not a feature of the uncomplicated disease and patients with a raised erythro- cyte sedimentation rate are often found to harbour hepatic abscesses. Barium enema examination is of little value except perhaps for the location of ulcers high in the sigmoid colon, and in severe cases may be dangerous. Ulceration is demonstrable in about 25-35% of dysenteric patients, usually associated with irritability of the colon'1. Serological tests may prove useful in specific circumstances. In par- ticular the gel diffusion precipitin test of Maddison12 has given reliable results. Its limitation is its inability to differentiate recent from past in- fection with E. histolytica It is in the investigation of complications of invasive amoebiasis that the gel diffusion test is most useful. In non- 38 SURGICAL PROBLEMS IN AMOEBIASIS endemic areas a negative reaction to the test may virtually exclude amoebiasis; in the endemic areas, however, where the problem of diag- nosis of complicated lesions is most difficult, positive reactions have limited value. Efforts to develop a more discriminative technique have so far been unavailing. The of amoebic lies mainly between the other infective causes of colitis-bacillary dysentery, salmonellosis, and balantidiasis. Granulomatous conditions such as , Crohn's disease, schistosomiasis, and neoplasms of the large bowel need careful consideration. The diagnosis is conditional on the finding of amoebae in all cases, but due regard needs to be given to the fact that amoebiasis may coexist with other bowel lesions.

Treatment of amoebic colitis The large number of drugs currently available for the treatment of amoebiasis makes caution necessary in the choice of the most appro- priate regimen. The ideal drug would be one capable of destroying E. histolytica in both tissues and bowel lumen. From the studies of Powell13 and Haddock14 it is evident that , given in doses of 800 mg 3 times daily for 5 days, closely approaches this ideal. The drug has a high margin of safety, only occasionally producing nausea and vomiting. Its clinical use is limited by the lack of a parenteral preparation. In the event of persistent or recurrent symptoms a second course of the drug may be administered or one of the combinations of older drugs described by Wilmot5: 1. (a) 250 mg 4 times daily for 10 days (erythromycin has been used in tetracycline-sensitive individuals); (b) furo- ate 0.5 g 3 times daily for 10 days; and (c) 600 mg of base immediately, followed by 300 mg 6-hourly, then 150 mg twice daily for 14 days. 2. (a) 90 mg intramuscularly daily for 10 days; (b) tetracycline 250 mg 4 times daily for 10 days; and (c) diloxanide furoate 0.5 g 3 times daily for 10 days. There is little to choose between these regimens; the second, how- ever, has the disadvantage of requiring bed rest and strict supervision. In patients with severe disease, particularly when complications such as are suspected, supplementing metronidazole with tetracycline improves the prognosis. This antibiotic probably exerts no antiamoebic effects but acts on the bacterial associates in the synergistic amoeba- bacterial relationship. Where patients suffer repeated recurrences of intestinal amoebiasis a source of reinfection is highly probable. This is frequently found to be 39 E. Q. ARCHAMPONG AND C. G. CLARK a carrier; his detection and treatment are of vital importance in the control of the disease. The surgical problem in amoebiasis In the management of amoebiasis and its complications certain prin- ciples have emerged which must first be discussed. Patients with amoebic dysentery are best regarded as potential candidates for surgery. This outlook serves the purpose of focusing attention on the possible com- plications and, by intensifying treatment, possibly reduces the incidence of these events; this would also make for enhancement of the survival rate in patients who eventually undergo operation. For similar reasons it is preferable for semi-emergency operations for complications of amoebiasis (e.g., a recurrent hepatic abscess) to be deferred until 3-4 days of antiamoebic and antibiotic therapy has been given. Further, when patients presenting for elective surgery are found on examination to harbour amoebic infection operation should be withheld until the full course of treatment has been given. Finally, owing to the poor state of health of most patients with amoebiasis, especially in the endemic areas, incisions into tissues con- taining amoebae often become secondarily infected and considerable tissue damage from sloughing is the result. In particular, resections of bowel carry a high risk of suture-line dehiscence with generalized peri- tonitis. It is therefore essential that a proximal defunctioning colostomy or, if necessary, ileostomy be considered in all prospective candidates for colonic surgery in amoebiasis. Where the colon is clearly devitalized, exteriorization may prove a safer procedure.

Acute complications of amoebiasis Perforation. Perforation with peritonitis is a relatively uncommon event in amoebic colitis; it remains, however, a serious and has been reported in 3-5% of autopsies on patients dying of amoebiasis1'0 1-5. The rupture may occur in an amoebic ulcer or in an amoeboma, and the rupture may be extra- or intraperitoneal. The sites liable to perforation are the caecum, ascending colon, and rectosigmoid. Perforations are more frequently retroperitoneal than intraperitoneal, and the clinical course and prognosis are largely determined by the success of the walling-off process. With a background of considerable experience of amoebic disease Wilmot'0 discerned two main clinical categories in the peritonitis which occurs in amoebic colitis. In the first the patient often has severe amoebic dysentery and the clinical picture of generalized peritonitis develops gradually. There is usually no dramatic point in the patient's illness to indicate perforation, nor are the signs of peritoneal con- tamination-guarding, rigidity, and absent bowel sounds-prominent. 40 SURGICAL PROBLEMS IN AMOEBIASIS Erect or lateral abdominal X-rays may show free peritoneal air, yet perforations can seldom be demonstrated in the colon. Indeed, for this reason laparotomy is generally contraindicated owing to the friability and gross oedema of the inflamed intestinal walls. Treatment is therefore usually conservative and consists in intensive antiamoebic and anti- bacterial chemotherapy, replacement of fluids and electrolytes, and intestinal decompression by nasogastric suction. Mortality is high and may exceed 75o/o16, but is even higher when these cases are managed operatively. The reasons for the high mortality are multifactorial, and judgement whether or not to intervene demands experience. If lapa- rotomy is performed, then consideration should be given to a temporary diverting ileotomy. Clearly a more aggressive approach to the treatment of these patients is required and it is likely that in the majority the diagnosis of perforation is made too late. In those with severe symptoms daily abdominal X-rays should be taken, as is the practice in acute ful- minating colitis. In a situation with such a high mortality the previous bad results of surgery should not be taken as an absolute indication for continued conservative measures. In the second group the attack of dysentery is less severe and the patient may not be actively experiencing symptoms at the time of per- foration. The episode is usually marked by with muscle spasm, guarding, and rebound tenderness. The full picture of paralytic ileus with increasing toxicity then follows. The perforation is usually confirmed by erect X-rays of the abdomen. Treatment is primarily that of the acute peritonitis, with antibiotics (tetracycline, ampicillin, or a combination of penicillin and streptomycin) and fluid and electrolyte replacement as well as decompression by means of gastroduodenal in- tubation. Laparotomy is performed as soon as the patient's condition admits of this. Simple suture of the perforation is usually not success- ful because of the friable oedematous bowel; faecal diversion is carried out by means of a proximal colostomy, supplemented where possible by exteriorization of the affected colon. Occasionally perforations are mul- tiple and extensive, involving the caecum and the entire colon. Haemorrhage. Patients in tropical climates with amoebic colitis are frequently anaemic because of nutritional deficiency, and mild blood loss from ulcerating lesions may aggravate this. Massive haemorrhage is rare, but persistent passage of blood may occur when a rapidly ad- vancing ulcer erodes a large artery before obliterating endarteritis has occurred2 or when extensive mucosal ulceration is associated with bac- terial infection. These cases are best managed conservatively because location of the source of haemorrhage in an oedematous bowel is difficult. In life-threatening circumstances colectomy may have to be performed, but severe haemorrhage carries a high mortality even in spite of re- peated blood transfusion and intensive antiamoebic treatment. 41 E. Q. ARCHAMPONG AND C G. CLARK The availability of blood is often a limiting factor in the treatment of patients and can lead to undue conservatism in blood replacement for haemorrhage. In the United Kingdom and elsewhere haemorrhage from the alimentary tract may in certain circumstances be treated by repeated transfusion of 2-3 1. over a period of many days. There is no doubt that blood transfusion of this magnitude is less readily available in other countries. In the occasional case of severe haemorrhage the possibility of surgical intervention must be considered, although the procedure at operation will be determined by the circumstances, partial or total colectomy with a temporary ileostomy being the most logical procedures. Amoebic appendicitis and typhlitis. Amoebic typhilitis is the re- sult of localized caecal amoebiasis which presents with symptoms similar to those of appendicitis. True amoebic appendicitis is rare but has been reported in 7-40% of patients dying from amoebiasis'5 17. In both circumstances constipation rather than diarrhoea is not uncommon. Ten- derness and guarding may be present in the right iliac fossa, so that the differential diagnosis from bacterial appendicitis may be extremely difficult. A palpable mass is sometimes present in amoebiasis but may be obscured by local muscle spasm. Appendicectomy in the presence of amoebiasis may be disastrous, for the bowel is friable and may easily tear"8' 19 or the suture line may slough, with attendant high mortal- ity20' 21. However, the risks of leaving an obstructive appendicitis without operation are also considerable. In areas where amoebiasis is endemic it has become common prac- tice to treat this type of syndrome, whether due to bacterial or amoebic appendicitis or typhlitis, with a conservative regimen unless peritonitis occurs. Intensive acute amoebicidal therapy is begun and a policy of 'wait and see' is adopted. Even where diagnostic facilities are good the problem still exists, for bacterial appendicitis may complicate invasive amoebiasis or alternatively caecal amoebiasis may exist without the diagnosis being readily apparent. In some circumstances therefore lapa- rotomy is likely to be performed; if the diagnosis is amoebiasis it seems quite clear that the appendix should not be removed, the tissues should be handled with great care, and the abdomen closed with drainage of the caecal area. The majority of patients with amoebic infection of the caecum or appendix recover with conservative measures. Interval appendicectomy must be considered several weeks after the cessation of antiamoebic treatment. A mistake in diagnosis and laparotomy may affect the prog- nosis but need not be disastrous if the condition is recognized and left alone. Occasionally stenosis of the right colon may develop, requiring subsequent treatment. Rarely amoebic form the apex of an intussusception22' 23, introducing a further problem in the diagnosis of right iliac fossa pain. 42 SURGICAL PROBLEMS IN AMOEBIASIS Postdysenteric colitis. This term was applied by Stewart24 in 1950 to the syndrome of diarrhoea with mucus and blood which sometimes follows severe amoebic dysentery despite elimination of the parasites by specific treatment. Since then the condition has also been recognized by Powell and Wilmot25' 26. Symptoms often persist for weeks or months, but the patient is seldom toxic and the condition is usually self-limiting. At sigmoidoscopy a red oedematous mucosa with ulceration is seen, and contrast radiography demonstrates loss of haustrations with ulcera- tion and impressions from the oedematous mucosa. The importance of this condition lies in its differentiation from other diseases of the large bowel such as carcinoma and non-specific ulcera- tive colitis or Crohn's disease of the colon. When sigmoidoscopic and radiological examination are inconclusive laparotomy may be justified, but the emergence of diseases such as non-specific colitis in races hitherto unaffected by this disease is increasing, and revision of the diagnosis is mandatory. There is no reason why amoebiasis and non- specific colitis should not coexist, particularly in areas of endemic amoebiasis. If postdysenteric colitis is diagnosed, then since most of these patients are not acutely ill a therapeutic trial of treatment for non- specific colitis is justifiable. The logical approach is to give sulphasalazine first in a dose of Ig 4 times daily; if this is not tolerated steroid enemata given cautiously is the next line of treatment. Ideally, treatment should be guided by biopsy through the fibreoptic colonoscope, though this is unlikely to be available for routine use for some years. Delayed complications Amoeboma. The commonest long-term complication of amoebic colitis is the amoeboma, which is pathologically a firm granulomatous mass containing multiple abscesses. The lesion contains vegetative forms of E. histolytica; it is not encapsulated and has a tendency to spread, with further granulation and abscess formation. This may result in the formation of enterocolic amoebic fistulae. A series of 230 cases of amoeboma was reviewed by Spicknall and Peirce27; in 40°/O of these the disease was located in the caecum, in 26% in the rectum and anal canal, in 10% in the transverse colon, and in 5o/1 in the sigmoid. Multiple lesions were reported in up to 10%/" of cases. The diagnosis of an amoeboma is rendered difficult by the variable symptoms and signs. A history of diarrhoea may be absent. The symptoms of anorexia, malaise, fever, , and anaemia are non-specific, and presentation with intermittent diarrhoea, intestinal obstruction, or a palpable mass may also occur in colonic or rectal carcinoma. The differential diagnosis further includes diverticulitis, benign tumours, Crohn's disease, schistosome granulomas, and tuber- 43 E. Q. ARCHAMPONG AND C. G. CLARK culous and mycotic lesions of the colon. The diagnostic difficulty is not completely resolved by barium enema or sigmoidoscopy and biopsy. Eveni when amoebae are demonstrated a carcinoma is not excluded. Repeated biopsy is needed and the lesion must be seen to regress with treatment. Often diagnosis is only established by laparotomy and histo- logical examinationi of the excised specimen. Amoebomas in most patients resolve with antiamoebic and anti- biotic treatment. The process is slow and may take several months; it requires careful follow-up with rectal examinations and repeated sigmoidoscopy and barium enema. Failure to regress may be the result of extensive infectioni or pronouniced cicatrization and constitutes an im- portant indicationi for operative intervention. Intestinal obstruction, ileocaecal intussusception, and fistula formation are less commonly en- counitered as the indicationis for operative treatment. Provided surgery is undertaken after adequate antiamoebic treatment, resection of amoeboma carries the sanme operative risks as with other coloniic tumours.

Fistulae. Fistulae connlectinig coloniic lesionis are rare; however, en- terocolic fistulae are occasionally found. They arise from in deep ulcers or amoebomas lying adjacent to other viscera or through perforation with a localized abscess which secondarily erodes another viscus. Shaff28 and Grigsby2 described two clinical groups of patients. The first group has the better prognosis; symptoms are mild and often suggestive of partial intestinal obstruction with occasional diarrhoea. The obstructed segments may be demonstrated by contrast radiography, but only the large fistulous tracks are outlined. The diagnosis in this group is liable to be confused with similar complications in diverti culitis, regional enteritis, and fungal granulomas. The treatmenit is essentially conservative with amoebicides and anti- biotics, and on this some fistulae heal completely. When subsequent examination shows evidence of persisting disease the fistula may be managed as for other intestinal fistulae-a proximal colostomy to divert the faecal stream and an en bloc resection of the affected intestinal segments with the fistulous track, followed by an end-to-end anastomosis. The seconid group is attended by high mortality (80%/,), for these patients present with localized or generalized peritonitis consequent on leakage at the site of the fistula. The patients are toxic and show evidence of peripheral circulatory failure. Management is primarily conservative and includes intenisive resuscitation with parenteral fluids, antibiotics, amoebicides, and hydrocortisone. A proximal defunctioning colostomy may be attempted under local anaesthesia. Patients surviving the initial episode are managed as in the first group. 44 SURGICAL PROBLEMS IN AMOEBIASIS Amoebiasis cutis. This is a rare condition occurring in the skin surrounidinig all amoebic fistula. It is frequently encountered in the ab- dominal wall from intestinal and hepatic lesions, the chest wall from liver abscesses, and the perineum and genitalia from lesions of the lower intestinal tract. Occasionally the lesion follows operation for ulnsus- pected amoebiasis. There is progressive necrosis of the skin and subcutanieous fat, which is replaced by granulations; this presumably represents a synergistic amoeba-bacterial invasion29 3 The skin lesion will not heal unless the underlying amoebic abscess and fistula has been controlled by amoebicides and antibiotics. It may be necessary to divert the faecal stream by a proximal colostomy as a preliminary to the treatment of the fistula. In extensive lesions scar excision with grafting of the residual ulcer may be attempted if the amoebic and bacterial infection has been eradicated as well as the fistula.

Liver involvement in amoebiasis Hepatic involvemenit is perhaps the most common complication of amoebiasis. At least one-third of patients dying of amoebiasis are found to have hepatic lesions at autopsy:1, and 50%/0 of 320 patients seen at Kerle Ba Hospital with amoebiasis had signs of liver involvement. Despite its high incidence it was not until recently that its true patho- logical nature became evident2' ". The amoebae on arrival in the liver from the colonic lesions largely perish, and such areas of focal necrosis as occasionally arise heal with little fibrosis. The only proven lesion in the liver is the amoebic abscess; most authorities agree that the so- called amoebic hepatitis represents collections of small focal abscesses rather than a diffuse lesion of the parenchyma. The clinical features often reflect the site, size, and number of ab- scesses as well as the degree of involvement of adjacent tissues<'. When pain and tenderness are not localized it frequently transpires that the abscess is deeply placed. A painful, tender, enlarged liver is the hall- mark of the more superficially placed abscess, often with capsular involvement. The pain is dull, but pressure on the related intercostal spaces reveals exquisite tenderness. When the pleura is involved by the inflammatory process cough is a troublesome symptom. Superiorly and posteriorly placed abscesses are clinically latent until extension oc- curs through the central tendon of the diaphragm. Abscesses located in the left lobe are difficult to diagnose because of atypical manifesta- tions. Tenderness in the epigastrium or along the left costal margin associated with low-grade pyrexia, weight loss, and anaemia are the common signs. Occasionally amoebic involvement of the spleen occurs and this further confuses the clinical findings. The diagnosis is most frequently made at exploratory laparotomy or autopsy. 45 E. Q. ARCHAMPONG AND C. G. CLARK The diagnosis of is essentially dependent on signs in the abdomen. The history of previous diarrhoea and the finding of E. histolytica in the stool are confirmatory. Among the ancillary investi- gations the indirect haemagglutination and complement fixation tests are useful, particularly when both tests are positive2. The complement fixation test of Craig is frequently positive in , but false positives and false negatives limit its usefulness. Radiologically, elevation or localized upward bulging of the right leaf of the diaphragm is a common feature; basal consolidation, pleural thickening, and effusion may also occur. The introduction of 20% so- dium diatrizoate (Hypaque) into the abscess cavity at the time of aspiration may reveal the extent and location of the abscess cavity. Hepatic angiography, portal venography, and percutaneous splenography are additional radiographic measures which may be invoked in difficult cases. In recent years liver scanning has provided additional information on the location and extent of amoebic liver abscesses. Access to isotopes and high cost, however, limit its use to- the larger centres in non- endemic areas. The diagnosis of amoebic liver involvement eventually rests on the response to a therapeutic trial of metronidazole or hydro- chloride. The aspiration of the characteristic brownish pus further clinches the diagnosis. If no pus is obtained liver biopsy with a Vim- Silverman needle may be helpful. If the diagnosis remains in doubt open drainage is imperative, for the mortality from undiagnosed ab- scesses is inordinately high. Treatment. The advent of metronidazole has transformed manage- ment of amoebic liver abscess. Three regimens have been tried and proved equally effective: (a) a single dose of 2.4 g; (b) 800 mg 3 times daily for 5 days; and (c) 400 mg 3 times daily for 10 days20. In re- sistant cases emetine hydrochloride 65 mg intramuscularly for 10 days and chloroquine sulphate or diphosphate 600 mg of base initially and 300 mg 3 times daily for 3 days by mouth may be given. Addition of 2 g of tetracycline daily by mouth for 14 days improves the results. When emetine hydrochloride is used care should be taken to confine the patient to bed, and repeated electrocardiography should give due warning of toxic effects in the form of increased heart rate, flattening and inversion of the T waves, and prolongation of the Q-T and P-R intervals. Aspiration of a liver abscess is indicated when a large hepatic swelling becomes evident, oedema or marked tenderness become noticeable in the intercostal spaces, or persistent symptoms raise suspicion of failure of response to amoebicides. Initially closed drainage is preferable, but 46 SURGICAL PROBLEMS IN AMOEBIASIS in the presence of secondary infection open drainage is essential. In these cases tube drainage is contraindicated in view of reports of in- creased morbidity and mortality from this procedure35. When closed aspiration has been successful renewed fever, pain and leucocytosis should be regarded as specific indications for repeat aspiration. Because of the deeper position of amoebic abscesses of the left lobe there is a danger of spillage into the peritoneal cavity. These cases are thus best managed by needle aspiration at an open operation. Repeat aspiration under vision may be necessary. Complications. The most commonly encountered complications of amoebic liver abscess are rupture and pleuropulmonary extension. Rup- ture into the peritoneal cavity occurs in 2-100/% of cases of liver abscess31' 3. With intraperitoneal spillage of pus the clinical picture is indistinguishable from that of perforation of a peptic ulcer. A history of amoebic dysentery and the finding of hepatomegaly and intercostal tenderness usually point to ruptured liver abscess. Generalized peritonitis from a ruptured amoebic abscess has been reported as carrying a high mortality-50-75/0/ . The traditional management of these cases has been by simple aspiration of the ruptured liver, exploratory laparotomy being advocated only when this fails. Archampong37 reported survival in 4 consecutive cases of free intraperitoneal rupture managed by aggressive fluid and antibiotic atnd antiamoebic therapy; this calls for a reappraisal of the conservative attitude to management of this complication. Rupture may occur into parts of the bowel such as the duodenum, stomach, and colon. The patient usually shows only mild systemic disturbance and the lesions heal rapidly with antiamoebic therapy38. Amoebic abscesses occasionally rupture through the pleura and lungs or into the pericardium. Treatment of these complications is essentially conservative, supplemented by aspiration. The prognosis with pulmonary rupture is good; patients with intrapericardial rupture, however, fre- quently succumb within a few hours.

REFERENCES I. CRAIG, C. F., and FAUST, E. C. (1964) Clinical , 7th edn. Philadelphia, Lea and Febiger 2. GRIGSBY, W. P. (1969) Surg. Gynec. Obstet., 128 609. 3. OCHSNER, A. (1969) In Abdominal Operations, ed. R. Maingot. London, Butterworths. 4. WALTERS, J. (1970) Trans. roy. Soc. trop. Med. Hyg., 64, 220. 5. WILMOT, A. J. (1969) Practitioner, 203, 643. 6. RAIL, G. A. (1946) J. trop. Med., 49, 68. 7. ANTIA, F. P.,PDESAI, H. G., JEEJEEBHoY, K. N., and BORKAR, A. V. (1965) J. trop. Med. Hyg., 68, 53. 8. SHAFFER, J. G., SHLAES, W. H., and RADKE, R. A. (1965) Amoebiasis: a Biomedical Problem. Springfield, IlI.,Thomas. 9. POWELL, S. J. (1959) Amer. J. trop. Med., 8, 331. 10. WILMOT, A. J. (1962) Clinical Amoebiasis. Oxford, Blackwell. 11. MIDDLEMISS. H. (1961) Tropical Radiology. London, Heinemann. 12. MADDISON, S. E. (1965) Exp. Parasit., 16, 224. 13. POWELL, S. J. (1967) Trans. roy. Soc., trop. Med. Hyg. 61, 765. 14. HADDOCK, D. R. W., and AWADZI, J. K. (1970) Ghana nmed. J., 9, 31. 15. CLARK, H. C. (1925) Amer. J. trop. Med., 5, 157. 16. BAKER, E. M. (1958) S. Afr. med. J., 32, 643 47 E. Q. ARCHAMPONG AND C. G. CLARK 17. ANDERSON, H. H., BOSTOCK, W. L., and JOHNSTONE, H. G. (1953) Anmoebiasis: Pathology, Diagnosis. and Chemotherapy. Springfield, Ill., Thomas. 18. JAMES, K. L. (1946) Proc. roy. Soc. Med., 39, 766. 19. NEVIN, R. (1947) Ann. roy. Coll. Surg. Engl., 1, 169. 20. KLEITSCH, W. P., and KISNER, P. (1951) Ann. Surg., 133. 139. 21. McCoy, G. W., HARDY, A. V., GORMAN, A. E., BUNDESEN, H.. CONNOLLY, J. 1., and RAWLINGS, I. D. (1936) Nat. Inst. Health Bull., No. 166. 22. BOWESMAN, C. (1960) Surgery and Clinical Pathology in the Tropics. London, Livingstone. 23. ODUNJO, E. 0. (1969) W. Afr. med. J., 18, 117. 24. STEWART, G. T. (1950) Brit. med. J. 1, 405. 25. POWELL, S. J., and WILMOT, A. J. (1966) Gut, 7, 438. 26. POWELL, S. J. (1969) Ghana nied. J., 8, 100. 27. SPICKNALL, G. G., and PEIRCE, E. G. (1954) New EngI. J. miied., 250, 1055. 28. SHAFF, B. L., and WOLFOWITZ, J. (1962) Brit. J. Surg., 49, 535. 29. ENGMAN. M. F., and MELENEY, H. E. (1931) Arch. Dernm. Syph. (Chic.) 24, 1. 30. CAPETANAKIS, J., and DoXIADES, T. (1966) Amer. J. Proctol. 17, 58. 31. WRAY, C. H., STARK, C. E., BRACKNEY, E. L., and MORETZ, W. H1. (1964) Anmer. Surg., 30, 780. 32. KEAN, B. H. (1955) Arch. intern. Med., 96, 667. 33. KEAN, B. H. (1957) Anmer. J. dig. Dis., 2, 342. 34. KINNEY, T. D., and FERREBEE, J. N. (1948) Arch. Path., 45, 41. 35. JORDAN, P. H. JR., (1955) Ann. Surg., 141, 70. 36. DEBAKEY, M. E., and OCHSNER, A. (1951) Int. Abstr. Surg._ 92, 209. 37. ARCHAMPONG, E. Q. (1972) Brit. J. Surg., 59, 179. 38. ACEVEDO, A. (I96 1) Dis. Colon Rect., 4, 235.

COURSES AND SYMPOSIA COUNTY OF HAMPSHIRE MEDICAL FEDERATION PROGRAMME OF LECTURES of surgical interest to be given at the Postgraduate Medical Centre, Royal Hampshire Coun:y Hospital, Winchester (0962-63535 Ext. 356). Lunchtime meetings Lunch 12.30 p.m. Lecture 1.15 p.m. January 16 Lumbar disc problems - Mr. R. K. Jackson, F.R.C.S. February 6 The control of insulin and glucagon in relation to diabetes mellitus - Professor V. Marks, D.M., F.R.C.P.Ed. February 27 Hirschsprung's disease - Mr. N. V. Freeman, F.R.C.S. Evening meetings 8.15 p.m. January 16 E.C.1 Club - Breast - Professor Sir James Fraser, F.R.C.S. February 21 E.C.1 Club (combined meeting with B.M.A.) - Terminal care - Dr. Cicely Saunders, O.B.E., M.R.C.S.

ST. GEORGE'S HOSPITAL AND S.W. METROPOLITAN ORTHOPAEDIC TRAINING SCHEME PROGRAMME Thurs. 25th Jan., 8.00 p.m. "A discussion on the talus' - Mr. J. Morris. Chairman: Mr. W. Murphy. Thurs. 1st Feb., 8.00 p.m. Short Papers: Joint meeting with South-West Metropolitan Orthopaedic Club. Chairman: Mr. G. F. Walker. Thurs. 8th Feb., 8.00 p.m. Journal club. Chairman: Mr. W. Murphy. Thurs. 15th Feb., 8.00 p.m. "The problem knee'' - Mr. P. R. French. Tues. 20th Feb., 2.00 p.m. Clinical conference: Rowley Bristow Orthopaedic Hospital, Pyr- ford, Surrey. Chairman: Mr. A. G. Apley. Thurs. 22nd Feb., 8.00 p.m. "Ewing's tumour'' - Mr. I. S. Duff. Chairman: Mr. T. L. Bowen, Thurs. 1st Mar., 8.00 p.m. "Hazards of diagnostic irradiation'' - Dr. B. C. H. Ward. Chairman: Mr. T. L. Bowen. Thurs. 8th Mar., 8.00 p.m. Journal club. Chairman: Mr. W. Murphy. Thurs. 15th Mar., 8.00 p.m. Bone tumour registry: St. Luke's Hospital, Guildford. Tues. 20th Mar., 2.00 p.m. Clinical conference: Queen Mary's Hospital for Children, Car- shalton, Surrey. Chairman: Mr. T. L. Bowen. Thurs. 22nd Mar., 8.00 p.m. Registrars' meeting - Mr. S. Richardson. Chairman: Mr. R. Bendall. All evening meetings at The Medical Centre, St. James' Hospital, Sarsteld Road, Balham, S.W.12. 01-672 1222. 48