Urology 5th year, 4th lecture/part one (Dr. Ali Kamal)

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The lecture has been given on Apr. 13th, 2011 by Dr. Ali Kamal.

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Urology 5th year, 4th lecture/part one (Dr. Ali Kamal)

  1. 1. Schistosomiasis of the bladder<br />Geographical distribution<br />The disease is endemic in many parts of Africa, in Israel, Syria, Saudi Arabia, Iran, Iraq and along the shores of China’s great lakes. Dwellers of the Nile valley have suffered for centuries. Marshes or slow-running fresh water provide a favourable habitat for the particular freshwater snail (Bulinus truncatus) which is the intermediate host.<br />Mode of infestation  <br />The disease is acquired while bathing in infected water. The free-swimming, bifid-tailed embryos (cercaria) of the trematode Schistosoma haematobium penetrate the skin. Shedding their tails, they enter blood vessels and are swept to all parts of the body, but flourish in the liver where they live on erythrocytes. They develop into male and female worms. Schistosoma haematobium has an affinity for the vesical venous plexus which they reach through the portosystemic anastomotic channels.<br />Having reached the bladder, the female moves forward until she enters a submucous venule so small that she completely blocks it. She now proceeds to lay about 20 ova in a chain. Each ovum is provided with a terminal spine which penetrates the vessel wall. A heavily infected subject passes many hundreds of ova a day. If the ova reach fresh water, the low osmotic pressure causes their envelope to burst and the ciliated miracidium emerges. To survive, it must reach and penetrate the intermediate host within 36 hours. Within the snail’s liver the miracidium enlarges and gives rise to myriads of daughter cysts which are set free on the death of the snail. A single miracidium releases thousands of cercariae to complete the life cycle.<br />Infected watercercaria penetrate skinlivermale and female wormsvesical venous plexussubmucous venule blocked by the femaleshed 20 ovaeach ovum has terminal spine and penetrate vessel wallwhen in urine and contact with fresh water burst miracidium enter snail daughter cystswhen death of the snailthousands of cercaria.<br />Clinical features<br />After penetration of the skin, urticaria lasting for about 5 days can occur (swimmer’s itch). After an incubation period ranging from 4 to 12 weeks, high evening temperature, sweating and asthma, together with leucocytosis and eosinophilia, occur. Usually, an asymptomatic period of several months supervenes before the ova are released, causing the typical early sign and symptom of intermittent, painless, terminal haematunia. Men are three times more often affected than women. Patients often present at a very late stage.<br />Examination of the urine<br />The last few millilitres of an early morning urine specimen . Examination on several consecutive days may be required, but a negative result does not exclude bilharziasis, especially in patients no longer resident in bilharzial districts.<br />Cystoscopy<br />Dependent on the length of time for which the disease has remained untreated, cystoscopy will reveal one or more of the following.<br />1.     Bilharzial pseudotubercles are the earliest specific appearance. <br />2.     Bilharzial nodules are due to the fusion of tubercles in the presence of secondary infection. They are larger and greyer than those in 1.<br />3.     ‘Sandy patches’ are the result of calcified dead ova with degeneration of the overlying epithelium. They occur around one or both ureteric orifices . <br />4.     Ulceration is the result of sloughing of mucous membrane containing dead ova or, what is even more common, sloughing of a bilharzial papilloma. <br />5.    Fibrosis is mainly the result of secondary infection. The capacity of the bladder becomes much reduced and contracture of the bladder neck may be found.<br />6.     Granulomas. Bilharzial masses are due to an aggregation of nodules. They are sessile and soft, and bleed readily when touched.<br />7.    Papillomas are distinguished from those in 6, by being more pedunculated <br />8.     Carcinoma is a common end result in grossly infected bilharziasis of the bladder which has been neglected for years. It usually commences, not in a papilloma, but in an ulcer, and is therefore a squamous cell carcinoma (due to metaplasia). It is usually advanced and will require radical cystectomy <br />Treatment<br />Lesions 1—6, can be expected to heal in response to systemic treatment by antimony or other preparations (e.g. praziquantel and metriphonate). <br />In addition to general treatment, healing of bilharzial ulcers and granulomas is by light diathermy coagulation.<br /> Bilharzial papillomas and carcinomas do not respond and require the same surgical measures as nonbilharzial papillomas and carcinomas.<br />Other complications and their treatment<br />• Secondary bacterial cystitis is commonly present and requires treatment.<br />• Urinary calculi, especially vesical and ureteric, occur more frequently when bilharzial lesions of the bladder are present.<br />•  Stricture of the ureters affects the last inch of the ureters. These often respond to dilatation, but sometimes re-implantation of the affected ureter is necessary.<br />• Prostatoseminal vesiculitis.<br />• Fibrosis of the bladder and bladder neck should be treated in the same way as that of nonbilharzial origin.<br />• Bilharzial urethral strictures are often accompanied by fistulae, and can be cured only by excision of the fistulous tracts and urethroplasty.<br /> <br /> <br />Schistosomiasis. Plain films. Upper left: Extensive calcification in the wall of a contracted bladder.<br />Right: Extensive calcification of the bladder and both ureters up to the renal pelves. The ureters are dilated and<br />tortuous.<br /> Lower left: Extensive calcification of seminal vesicles and ampullae of vasa.<br />Schistosomiasis. Upper left: Excretory urogram showing markedly contracted bladder. Lower<br />right ureter dilated probably secondary to vesicoureteral reflux. Right: Excretory urogram at 2 hours showing<br />a fairly normal right kidney. The upper ureter is distorted. Arrows point to calcified wall. The lower ureter is<br />quite abnormal. The calyces and pelvis of the left kidney are dilated, but the kidney shows atrophy secondary<br />to nonspecific infection. The upper ureter is dilated and displaced by elongation due to obstruction. Arrows<br />show calcification. Linear calcification can be seen in the periphery of the lower half of the bladder wall (arrows).<br />Lower left: Nodular squamous cell carcinoma of the bladder. Dilated left lower ureter probably secondary<br />to obstruction by tumor. Nonvisualization of the right ureter caused by complete occlusion.<br />

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