Oct 12, 1990 - Infection in a urachal cyst presenting in a 42-year-old man with no premorbid symptoms is an extremely rare event. We describe such a case ...
Journal of the Royal Society of Medicine Volume 84 June 1991
367
Case reports
Urachal cyst presenting with abscess formation
Case presented to Clinical Section, 12 October 1990
V C Lees FRCS Department of Plastic Surgery, Frenchay Hospital, Frenchay, Bristol BS16 ILE P T Doyle FRCS Department of Urology, Addenbrookes Hospital, Cambridge CB2 2QQ Keywords: urachus; urachal cyst; abscess
Infection in a urachal cyst presenting in a 42-year-old man with no premorbid symptoms is an extremely rare event. We describe such a case and outline the pp ate investigation and management.
Case report The case is reported of a 42-year-old man who presented with a one week history of lower abdominal pain, reddening around the umbilicus (see Figure. 1), and a 3-day history of dysuria. He was treated for thes symptoms by his general practitioner with amoxycilnin and co-trimoxazole.- There no other history of note. Positive findings on examination were a temperature of 38°C, periumbilical erythema and hypogastric tendernes. Investigations showed a white cell count of 13.7x 1O9A/ in the presence of normal urine microsoopy and renal function. An ultrasound of the lower abdomen revealed an 11 x5 x 3 cm mass arising from the superior surface of the bladder and extending to the umbilicus. Appearances were consistent with an abscess occurring in a urachal remnant. The abscess was formally drained and packed. Culture of the pus obtained grew Staphylococcus aureus. The appropriate antibiotics were given systemically. One week later the wound was clean and was closed over a corrugated drain. Cystoscopy was simultaneousl performed and showed
F
ng. .
Figure 1. Admilssion photograph showing periumbilical erythema
Figure . Micturating cystogram. The arrows point to the lobulated
filling defec in the dome of the bladder. The Raytec marker of the pack in th abscess cavity is seen at the apex of the bladder
a lesion in the dome of the bladder; possibly neoplastic. A micturating cystogram showed a lobulated filling defect in the superior aspect of the bladder (see Figure 2). Two weeks later -he was readmitted and underwent elective partial cystectomy with removal of the urachal remnant. Histology of the resection specimen showed granulomatous changes only with no evidence of neoplasia. Postoperatively he has made an uneventful recovery.
Discussion Urachal remnants may present as patent urachus, vesicourachal diverticulum, urachal sinus or urachal cyst. Infection occurring within a cyst is a rare manifestation of urachal disease"6. From these reports it appears that the peak incidence of infected urachal cysts is in infancy and again in early adulthood. This fact may be interpreted as evidence for the existence of congenital and acquired forms of urachal disease, with acquired disease representing the partial reopening of the channel which is believed to have closed at birth7. Presentation of an infected cyst in the 5th decade and beyond is extremely rare. Blichert-Toft and Nielson3 reported 17 cases from the world literature in this age group and Berman et aW6 have reported one further case. The former authors stress the point that 85% ofthe cases of urachal tract sepeis which they reviewed were treated by incision and drainage alone. Thus there are only a few cases in this age group where histological confirmation of the cyst has been obtained and the diagnosis established beyond doubt. The diagnosis in this case was confirmed by ultrasound. The role of high resolution ultrasound in defining urachal anomalies is established8'. The mucosal lesion shown on micturating cystogram proved to be a granulomatous reaction in response to the adjacent infected cyst. Recommended treatment of infected cysts comprises a two stag procedure of initial incision and drinage followed later by excision ofthe urachal remnant. Exision ofthe cyst mass at the first operation has been advocated where the patient's general condition permits and where the cyst mass is not too large3.56. Antibiotics are administered according to bacterial sensitivity. It should be stressed that simple incision and drainage of the abscess with fulguration of the tract is associated with a 30% cyst recurrence. Further, removal of the whole urachal tract precludes the possibility of late neoplastic change.
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References 1 Goldman IL, Caldamene AA, Gauderer M, Hampel N, Wesselhoeft CW, Elder JS. Infected urachal cysts: a review of 10 cases. J Urol 1988;140:375-8 2 Blichert-Toft M, Nielson OV. Disease of the urachus simulating intra-abdominal disorders. Am J Surg 1971;122:123 3 Blichert-Toft M, Nielson OV. Congenital patent urachus and acquired variants. Diagnosis and treatment. Review of the literature and report of 5 cases. Acta Chir Scand 1971;137:807-14 4 Sterling JA, Goldsmith R. Lesions of the urachus appear in the adult. Ann Surg 1953;137:120 5 Newman BM, Karp MP, Jewett TC, Coonery DR. Advances in the management of infected urachal cysts. J Paediatr Surg, 1986;21:1051-2
6 Berman SM, Tolia BM, Laor E, Reid RE, Schweizer SP, Freed SZ. Urachal remnants in adults. Urology 1988;31:17-21 7 Blichert-Toft M, Kock F, Nielson OV. Anatomic variations of the urachus related to clinical appearance and surgical treatment of urachal disorders. Surg Gynecol Obstet 1973;137:51 8 Avni EF, Matos C, Regemarter G, Goolaerts JP, Diard F. Symptomatic patent urachus in children: the contribution of ultrasound. European Society of Paediatric Radiology, Toronto 1987;30:482-5 9 Morin ME, Tan A, Baker DA, Sue HK. Urachal cyst in the adultultrasound diagnosis. J Urol 1979;132:831
(Accepted 29 January 1991. Correspondence to Mr P T Doyle, Department of Urology, Addenbrookes Hospital, Cambridge CB2 2QQ)
Sarcoidosis and acute myeloid leukaemia
Case presented to Section of Rheumatology & Rehabilitation, 30 June 1990
E A Murphy MB ChB MRCP' J A Murphy MB ChB MRCP2 R Jackson MB MRCPI3 R D Sturrock MD FRCP' 'Centre for Rheumatic Diseases, Departments of 2Haematology and 3Pathology, Glasgow Royal Infirmary, Glasgow G4 OSF Keywords: sarcoid; acute myeloid leukaemia; glomerulonephritis; aspergillosis
A 52-year-old man with a long history of uveitis had a diagnosis of sarcoid made when he developed a seronegative polyarthropathy and was shown to have non-caseating granulomata in biopsies of bone-marrow and liver. He died 10 years later of acute myeloid leukaemia and widespread invasive aspergillosis, having developed porphyria cutanea tarda, alcoholic liver disease, cardiac failure and mesangioproliferative glomerulonephritis in the interim. Case report A 52-year-old man was referred to the rheumatology clinic in 1980 because of a history ofjoint pains over the preceding few months. He had a long history of uveitis and secondary glaucoma. X-rays showed no erosions and testing for rheumatoid factor was negative. He was noted to be anaemic with a haemoglobin of about 8 g/dl and he underwent bone marrow biopsy when initial investigations failed to reveal a cause for the anaemia. This showed a hypercellular marrow with increased reticulin staining, raising the possibility of an underlying myeloproliferative disorder. In view of this, a repeat bone-marrow biopsy was carried out 6 months later which was again hypercellular, and in addition showed the presence of a non-caseating epithelioid granuloma. Liver biopsy at this time showed similar granulomata and moderate fatty change compatible with a history of excessive alcohol intake. The result of a Kveim test was equivocal, chest X-ray was normal and pulmonary function tests showed a reduction in the transfer factor. Review of the initial hand X-rays showed coarse trabeculation, typical of sarcoid bone disease (Figure 1). On the basis ofthese findings, and the history of uveitis, a diagnosis of sarcoid was made. Because of persistent anaemia and recurrent uveitis, the patient was commenced on low dose prednisolone, on which he remained, in varying doses, until his death. Some months later, he developed a blistering skin rash which was confirmed as porphyria cutanea tarda. Over the next few years, he remained anaemic and had recurrent uveitis but was otherwise well.
Figure 1. Hand radiographs at the time of presentation
In 1984, he was admitted as an emergency because of increasing breathlessness. A diagnosis of biventricular cardiac failure was made. There was no evidence of recent myocardial infarction and echocardiography showed a small pericardial effusion but no evidence of any primary myocardial or valvular problem. He was again anaemic with a leucoerythroblastic blood film on this occasion, and bonemarrow examination was once more hypercellular with no distinguishing morphological features. With appropriate therapy, he improved over the course of 2 weeks and remained well for the next 4 years despite persistent anaemia and an abnormal blood film. In 1988 he was noted to have renal impairment with a urea of over 20 mmol/l and creatinine over 300 umolfl. Bone-marrow appearances were unchanged. Renal biopsy showed mesangioproliferative glomerulonephritis with mesangial IgA deposition. In 1989, when he again complained of tiredness and malaise, his haemoglobin was found to be 5 g/dl. The peripheral blood film was again leucoerythroblastic with many abnormal monocytoid cells. The bone-marrow was hypercellular showmng erythroid hyperplasia with a left shift of the myeloid series. One week after admission his condition deteriorated over several hours with increasing breathlessness, widespread bronchospasm and severe hypoxia. He was transferred to the intensive therapy unit (ITU) for assisted ventilation. His peripheral blood film had deteriorated and showed numerous blast cells and bone marrow aspirate confirmed the diagnosis of acute myeloid leukaemia (FAB classification M4). Cytogenetic examination of the bone marrow demonstrated no abnormality. Before speific therapy could be commenced, he deteriorated fturther and died 36 h after arrival in the ITU. Postmortem examination confirmed the pre-mortem diagnoses. In addition, there was evidence of established hepatic cirrhosis and widespread invasive aspergillus infection with colonies in several tissues, including lung, trachea, myocardium and pancreas (Figure 2).
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