Ascariasis-Hepatobiliary and pancreatic...
2
SELECTED SUMMARIES Karyadi D. Vitamin A fortified monosodium glutamate and health. growth, and survival of children: A controlled field trial. Am 1 c/in Nutr 1988;48:1271-6. 13 McDowell EM, Keenan KP, Huang M. Effects of vitamin A depriva- tion on hamster tracheal epithelium. A quantitative morphologic study. Virchows Arch lBJ 1984;45:197-219. 14 Puengtomwatanakul S, Sirisinha S. Impaired biliary secretion of immunoglobulin A in vitamin A-deficient rats. Proc Soc Exp BioI Med 1986;182:437-42. 15 Nauss KM, Phua C-C, Ambrogi L, Newberne PM. Immunological changes during progressive stages of vitamin A deficiency in the rat. 1 Nutr 1985;115:909-18. Ascariasis-Hepatobiliary and pancreatic involvement Khuroo MS, Zargar SA, Mahajan R. (Department of Gastroenterology, Sher-i- Kashmir Institute of Medical Sciences, Srinagar, Kashmir, India.) Hepatobiliary and pancreatic ascariasis in India. Lancet 1990;335:1503-6. SUMMARY Over a 6-year period, the authors studied S()()patients with hepatobiliary and pancreatic disease due to Ascaris lumbricoides. Two hundred and seventy four patients had duodenal ascariasis, in 171 the worms had entered the biliary system, in 40 the liver, in 8 the gall bladder, and 7 patients had pancreatic ascariasis. The most common clinical manifestation was biliary colic with the others being, in descending order of frequency, acute cholangitis, acute cholecystitis, acute pancreatitis and liver abscess. Roundworms in the duodenum manifest as biliary colic or acute pancreatitis. The procedure of choice for acute cholangitis was endoscopic biliary decompression; removal of worms from the ampullary orifice led to prompt relief of biliary colic and acute pancreatitis. Only 4 patients died, the mortality being related to acute pancreatitis, pyogenic cholangitis and liver abscess. Worms were seen to move in and out of the ductal systems. In 12 patients the worms persisted in the biliary tree at 3 weeks and had to be removed either through surgery or by endoscopy using a basket. During a mean follow up period of 48 months, 76 patients had re-invasion of the biliary tree by the round- worms. Intrahepatic and bile duct calculi developed in 7 patients in whom dead worms formed a nidus for stone formation. COMMENT Over 1 billion of the world's population is estimated to be infected with Ascaris lumbricoides (roundworms) and of these about 20 000 die annually. 1 The adult fertilized female lays 200000 eggs a day in the human small intestine and the eggs are generally excreted in the faeces. If the climate is warm and humid the ova embryonate. On re- ingestion by humans larvae develop in the duodenum. The larvae penetrate the intestinal wall and are carried to 189 16 Ongsakul M. Sirisinha S, Lamb AJ. Impaired blood clearance of bacteria and phagocytic activity in vitamin A-deficient rats. Proc Soc Exp BioI Med 1985;178:204-8. 17 Subcommittee on vitamin A deficiency Prevention and Control, Food and Nutritional Board, National Research Council. Vitamin A supplementation: Methodologies for field trials. Washington D.C.:National Academy Press, 1987. S. K.ACHARYA Birmingham England the lung via the portal venous circulation. They cross the alveolar capillary walls of the lung and migrate up the respiratory tree to the epiglottis where they are swallowed. The larvae mature into adult worms in the small intestine and the females produce eggs in about two months. By bridging the gut lumen the adult worms maintain their position in the small bowel. Though ascariasis is a benign condition, migration of worms to extraintestinal sites is potentially fatal. Migration occurs in response to anthelminthic drugs, purgatives, intercurrent illness and often without any cause. The propensity for worms to invade the biliary tree is a result of their preference to migrate through small orifices. They may produce no symptoms within the hepatobiliary system.? but this is rare. Worms usually cause cholecystitis, suppurative cholangitis, liver abscess, haemobilia and acute pancreatitis. Late complications such as biliary calculi and hepatic granulomas also occur. 2 In 1946, the clinical patterns of biliary ascariasis were clearly recognized-right upper quadrant pain and tender- ness accompanied by vomiting worms or passing them in the stool.' However, the dangers of roundworms migrat- ing to. the biliary tree were recognized much earlier, ~ as was surgical removal from the bile ducts.' The earliest reports from India were of acute haemorrhagic pancreatitis due to roundworms." Antemortem demonstration of ascariasis in the biliary tree on intravenous cholangio- graphy was described in 1964 7 and on endoscopic retrograde cholangiopancreatography (ERCP) in 1984. 8 The largest series on biliary ascariasis is from China." All these factors notwithstanding the finest descriptions of hepatobiliary and pancreatic ascariasis have come from the authors of the present study. 10,11 In this report from Kashmir, the common presentation of the patients has been recurrent biliary colic and cholan- gitis which is identical to the symptoms described earlier from South Africa.? Biliary ascariasis must be considered a possible diagnosis in all patients with fever and right upper quadrant pain. Rigidity on physical examination indicates complications such as an abscess or suppurative cholangitis. As only half the patients vomited worms following a colic, the absence of vomiting or passing worms in the stool should not negate the diagnosis. Other
Transcript of Ascariasis-Hepatobiliary and pancreatic...
SELECTED SUMMARIES
Karyadi D. Vitamin A fortified monosodium glutamate and health.growth, and survival of children: A controlled field trial. Am 1 c/inNutr 1988;48:1271-6.
13 McDowell EM, Keenan KP, Huang M. Effects of vitamin A depriva-tion on hamster tracheal epithelium. A quantitative morphologicstudy. Virchows Arch lBJ 1984;45:197-219.
14 Puengtomwatanakul S, Sirisinha S. Impaired biliary secretion ofimmunoglobulin A in vitamin A-deficient rats. Proc Soc Exp BioIMed 1986;182:437-42.
15 Nauss KM, Phua C-C, Ambrogi L, Newberne PM. Immunologicalchanges during progressive stages of vitamin A deficiency in the rat.1 Nutr 1985;115:909-18.
Ascariasis-Hepatobiliary and pancreaticinvolvement
Khuroo MS, Zargar SA, Mahajan R. (Department ofGastroenterology, Sher-i- Kashmir Institute of MedicalSciences, Srinagar, Kashmir, India.) Hepatobiliary andpancreatic ascariasis in India. Lancet 1990;335:1503-6.
SUMMARYOver a 6-year period, the authors studied S()()patients withhepatobiliary and pancreatic disease due to Ascaris lumbricoides.Two hundred and seventy four patients had duodenal ascariasis,in 171 the worms had entered the biliary system, in 40 the liver,in 8 the gall bladder, and 7 patients had pancreatic ascariasis.
The most common clinical manifestation was biliary colic withthe others being, in descending order of frequency, acutecholangitis, acute cholecystitis, acute pancreatitis and liverabscess. Roundworms in the duodenum manifest as biliary colicor acute pancreatitis. The procedure of choice for acute cholangitiswas endoscopic biliary decompression; removal of worms fromthe ampullary orifice led to prompt relief of biliary colic andacute pancreatitis. Only 4 patients died, the mortality beingrelated to acute pancreatitis, pyogenic cholangitis and liverabscess.
Worms were seen to move in and out of the ductal systems. In12 patients the worms persisted in the biliary tree at 3 weeksand had to be removed either through surgery or by endoscopyusing a basket. During a mean follow up period of 48 months,76 patients had re-invasion of the biliary tree by the round-worms. Intrahepatic and bile duct calculi developed in 7 patientsin whom dead worms formed a nidus for stone formation.
COMMENTOver 1 billion of the world's population is estimated to beinfected with Ascaris lumbricoides (roundworms) and ofthese about 20 000 die annually. 1 The adult fertilizedfemale lays 200000 eggs a day in the human small intestineand the eggs are generally excreted in the faeces. If theclimate is warm and humid the ova embryonate. On re-ingestion by humans larvae develop in the duodenum.The larvae penetrate the intestinal wall and are carried to
189
16 Ongsakul M. Sirisinha S, Lamb AJ. Impaired blood clearance ofbacteria and phagocytic activity in vitamin A-deficient rats. ProcSoc Exp BioI Med 1985;178:204-8.
17 Subcommittee on vitamin A deficiency Prevention and Control,Food and Nutritional Board, National Research Council. VitaminA supplementation: Methodologies for field trials. WashingtonD.C.:National Academy Press, 1987.
S. K.ACHARYABirmingham
England
the lung via the portal venous circulation. They cross thealveolar capillary walls of the lung and migrate up therespiratory tree to the epiglottis where they are swallowed.The larvae mature into adult worms in the small intestineand the females produce eggs in about two months. Bybridging the gut lumen the adult worms maintain theirposition in the small bowel.
Though ascariasis is a benign condition, migration ofworms to extraintestinal sites is potentially fatal. Migrationoccurs in response to anthelminthic drugs, purgatives,intercurrent illness and often without any cause. Thepropensity for worms to invade the biliary tree is a resultof their preference to migrate through small orifices. Theymay produce no symptoms within the hepatobiliarysystem.? but this is rare. Worms usually cause cholecystitis,suppurative cholangitis, liver abscess, haemobilia andacute pancreatitis. Late complications such as biliarycalculi and hepatic granulomas also occur. 2
In 1946, the clinical patterns of biliary ascariasis wereclearly recognized-right upper quadrant pain and tender-ness accompanied by vomiting worms or passing them inthe stool.' However, the dangers of roundworms migrat-ing to. the biliary tree were recognized much earlier, ~as was surgical removal from the bile ducts.' The earliestreports from India were of acute haemorrhagic pancreatitisdue to roundworms." Antemortem demonstration ofascariasis in the biliary tree on intravenous cholangio-graphy was described in 19647 and on endoscopicretrograde cholangiopancreatography (ERCP) in 1984.8The largest series on biliary ascariasis is from China."All these factors notwithstanding the finest descriptionsof hepatobiliary and pancreatic ascariasis have come fromthe authors of the present study. 10,11
In this report from Kashmir, the common presentationof the patients has been recurrent biliary colic and cholan-gitis which is identical to the symptoms described earlierfrom South Africa.? Biliary ascariasis must be considereda possible diagnosis in all patients with fever and rightupper quadrant pain. Rigidity on physical examinationindicates complications such as an abscess or suppurativecholangitis. As only half the patients vomited wormsfollowing a colic, the absence of vomiting or passingworms in the stool should not negate the diagnosis. Other
190
clinical presentations are 'acalculous cholecystitis', acutepancreatitis and liver abscess. The presentation of thepatients with cholecystitis was right hypochondrial painand fever; ultrasonography demonstrated a thickenedand distended gall bladder. The number of patients withpancreatic ascariasis is likely to be underestimatedbecause an ERCP, the 'gold standard' for demonstrating'worms in the pancreatic duct,is rarely performed duringan attack of acute pancreatitis.
Several imaging modalities have been used to demon-strate hepatobiliary and pancreatic ascariasis. The easiestand most economical investigation, however, is a plainX-ray of the abdomen which in the South African seriesconfirmed the presence of worms in the right hypochon-drium in most patients.? Ultrasonography is useful inidentifying worms and diagnosing complications.'! Themorphology of the worm can be demonstrated simply andsafely." The authors have clearly shown that ERCP isuseful in documenting ascariasis in the duodenum, biliarytree and pancreatic duct. After injection of contrast, theworms are visualized as characteristic filling defects. Anadditional advantage is that patients with suppurativecholangitis can have the worms extracted or endoscopicdrainage carried out. 12
While much of the data in this paper has already beenpublished.P'!' the major new contribution of the presentarticle is the long term follow up of patients with hepato-biliary and pancreatic ascariasis. Patients were seen everymonth or earlier if symptoms recurred. Ultrasonographyand ERCP were carried out. Seventy-six patients hadre-invasion of the biliary tree by roundworms and all weresymptomatic. Multiple episodes of re-invasion occurredin those who had had a sphincterotomy. Eight patientshad acute pancreatitis of whom. one died, while sevenpatients had biliary stones which were removed atsurgery. Histological examination revealed worm segmentsto be the nidus of the stones.
Ascariasis is a major epidemiological problem in Kashmirwith .a more than 60% prevalence in children.P Thefactors contributing to this are believed to be the wet soil,poor sanitation and water supply, the use of humanexcreta as a fertilizer and the consumption of raw vege-tables. Host factors are not clear. 14
Active measures must now be taken to prevent hepato-
THE NATIONAL MEDICAL JOURNAL OF INDIA VOL. 4, NO.4
biliary and pancreatic ascariasis in particular, andascariasis in general. Roundworms should be eradicatedfrom those already infected. Prevention involves personal,family and community hygiene, construction of latrinesand efficient disposal systems, and sterilizing humanfaeces meant/destined for use as fertilizer. 1 The WHOsuggests mass therapy for helminths in populations whereover 50% are infected, as in Kashmir. The drugs re-commended are pyrantel palmoate, mebendazole andalbendazole. To produce a demonstrable reduction in therate of reinfection, therapy should be repeated every4 to 6 months. 1
REFERENCESWorld Health Organization. WHO model prescribing information:Drugs used in parasitic disease. Geneva:Worid Health Organiza-tion,1990:82-3.
2 Lloyd DA. Hepatobiliary Ascariasis in Children. Surg Ann 1982;14:277-97.
3 Yang SCH, Laube PJ. Biliary Ascariasis. Ann Surg 1946;123:299-303.
4 Cromwell BC. The dangers of ascariasis. Am J Med Sci 1920;159:380--98.
5 Muir JB. Removal of Ascaris from the common bile duct. Br Med J1932;1:1077-8.
6 Ghosh KK. Acute haemorrhagic pancreatitis due to roundworm.J Indian Med Assoc 1951;21:437-8.
7 Aggarwal SK, Aggarwal SP, Aggarwal DC. Demonstration of around worm in the common bile duct AJR 1964;91:869-70.
8 Kalro RH, Esmail JH, Contractor QQ, Desai HG. Biliaryascariasis. Indian J GastroenteroI1984;3:163-4.
9 Chang CC, Han CT. Biliary ascariasis in childhood. A clinicalanalysis of 788 cases. Chin MedJ 1966;85:167-71.
10 Khuroo MS, Zargar SA. Biliary Ascariasis: A common cause ofbiliary and pancreatic disease in an endemic area. Gastroenterology1985;88:418-23.
11 Khuroo MS, Zargar SA, Mahajan R, Bhat RL, Javid G. Sonographicappearances in biliary ascariasis. Gastroenterology 1987;93:267-72.
12 Kamath PS, Joseph DC, Channdran R, Rao SR, Sri Prakash ML,D'Cruz AJ. Biliary ascarisis: Ultrasonography, endoscopic retrogradecholangiopancreatography, and biliary drainage. Gastroenterology1986;91:730--2.
13 Khuroo MS, Mahajan R, Zargar SA, Javid G, Sapru S. Prevalenceof biliary tract disease in India: A sonographic study in adult popula-tion in Kashmir. Gut 1989;30:201-5.
14 Mahmoud AAF. Parasitic protozoa and helminths: Biological andimmunological challenges. Science 1989;246:1015-22.
P. S. KAMATHBangalore
