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Spontaneous bladder perforation: a rare complication of tuberculosis

Open ArchivePublished:February 01, 2010DOI:https://doi.org/10.1016/j.ijid.2009.10.006

      Summary

      Spontaneous bladder perforation secondary to tuberculosis (TB) is very rare. Only three cases have been reported so far in the literature. Due to its rarity, the diagnosis of spontaneous bladder perforation is often missed. Confirmation of TB via culture takes a long time and starting empirical treatment for TB is necessary. We relate our experience with a young woman who presented with clinical features of a perforated appendix and was only diagnosed with bladder perforation during laparotomy. She also had distal right ureteral stricture and left infundibular stenosis. The provisional diagnosis of TB was attained via typical histopathological features and a positive Mantoux test. She was started empirically on anti-TB treatment and recovered without any complications. Urine culture after 6 weeks confirmed the diagnosis of TB.

      Keywords

      1. Introduction

      Spontaneous intraperitoneal bladder rupture is rare;
      • Fugikawa K.
      • Yamamichi F.
      • Nonomura M.
      • Soeda A.
      • Takeuchi H.
      Spontaneous rupture of the urinary bladder is not a rare complication of radiotherapy for cervical cancer: report of six cases.
      the reported incidence is 1:126 000. The majority of cases are reported in men (79%), and the overall mortality is 47%.
      • Christiansen W.I.
      Genitourinary tuberculosis: review of 102 cases.
      In most cases, there is an underlying pathology that has weakened the bladder wall, precipitating the perforation. One of the rare causes is tuberculosis (TB). To date, there are only three cases reported in the English literature. Due to its rarity, the diagnosis of spontaneous bladder perforation is often missed. We present a case we encountered and discuss case management, stressing the need to start empirical treatment for TB while awaiting the confirmatory results of culture.

      2. Case report

      A 25-year-old unmarried woman was admitted for suprapubic pain, fever, dysuria and frequency of 5 days duration. There was no hematuria or per vaginal discharge. There was no previous history of similar complaints. She denied any sexual promiscuity. On examination, she was febrile and there was tenderness as well as guarding of the lower abdomen. Her white cell count was 11.4 × 109/l and platelet count 375 × 109/l. Serum urea was 84 mmol/l and creatinine 590 mmol/l. Her urine showed the presence of leukocytes. She was started on ciprofloxacin. An ultrasound of the abdomen carried out on the following day showed mild right hydronephrosis with moderate ascites. There were multiple cortical cysts of the left kidney and the bladder was partially distended. Clinically, there was also peritonitis and she was immediately posted for a laparotomy with the provisional diagnosis of perforated appendix.
      During surgery, it was found that she actually had a perforation of the bladder at the dome and anterior wall. The bladder was generally inflamed with an edematous mucosa. The ureteral orifices were inflamed and edematous. The edges of the perforated bladder were also necrotic. Part of the omentum was seen covering the perforated bladder wall. There was moderate ascites and multiple peritoneal deposits on the small and large bowel. The uterus, fallopian tubes, ovaries, and liver were otherwise normal. There was no enlarged lymph node.
      The necrotic edges of the bladder were resected and a watertight bladder repair in two layers was done using non-absorbable monofilament 3/0 sutures. The resected bladder edges and deposits on the omentum and bowel were sent for histopathological examination (HPE). A peritoneal washout was done. A Foley's catheter was inserted for bladder drainage; a drain was also placed in the pelvis.
      After surgery, she remained febrile and her antibiotic was changed to meropenem. Initial urine culture and sensitivity came back negative. However, the HPE specimens showed multiple granulomatous lesions. The granulomas consisted of central caseous necrosis surrounded by epithelioid cells, lymphocytes, multinucleated giant cells, foreign and Langhans type cells (Fig. 1, Fig. 2). Special stains (Ziehl–Neelsen, fungal stains) were, however, negative.
      Figure thumbnail gr1
      Fig. 1Histology of the bladder showing granuloma with caseating necrosis (×100).
      Figure thumbnail gr2
      Fig. 2Histology of the bladder showing granuloma with Langhans type giant cell (×200).
      On further questioning, she denied having been exposed to a TB patient. There was also no history of TB or prolonged chronic cough. Her chest X-ray was clear. Sputum and urine acid-fast bacilli (AFB) testing was also negative. However, a Mantoux test was positive, with a reading of 15 mm diameter. A repeat urine culture specifically for Mycobacterium tuberculosis was sent to the laboratory after obtaining the HPE results. HIV screening was negative. Anti-TB treatment was immediately commenced, consisting of isoniazid, rifampin, pyrazinamide, and ethambutol. Her fever then started to settle down.
      She was discharged after 10 days when there was no more abdominal pain or fever. A cystogram (Fig. 3) was done after 2 weeks and showed no contrast leak. The bladder was small and trabeculated with a capacity of only 120 ml. There was also a short segment of stricture and irregularity of the distal part of the right ureter with a grade 4 vesico-ureteral reflux. The Foley's catheter was removed. She recovered well and was asymptomatic when she was seen in the clinic one month later. An intravenous urogram (IVU) was done (Fig. 4) and it showed a distal right ureteral stricture with mild hydronephrosis, but no opacification of the left kidney or ureter. An ultrasound of the abdomen (Fig. 5) done concurrently showed dilatation of the calyces but not the renal pelvis of the left kidney. This is suggestive of infundibular stenosis, in keeping with the diagnosis of renal TB. The renal profile was normal. A review of the urine culture after 6 weeks of incubation showed that it was positive for M. tuberculosis.
      Figure thumbnail gr3
      Fig. 3Cystogram showing right distal ureteral stricture with vesico-ureteral reflux but no contrast leak.
      Figure thumbnail gr4
      Fig. 4Intravenous urogram showing non-opacification of the left kidney and ureter.
      Figure thumbnail gr5
      Fig. 5Ultrasound of the left kidney showing dilatation of the calyces but not the renal pelvis, in keeping with infundibular stenosis .
      At 3 months of follow-up, a repeat ultrasound of the abdomen showed that the left renal infundibular stenosis had resolved. She remained well and the anti-TB medication was completed at 6 months.

      3. Discussion

      TB is a dreaded disease in developing countries. Lately, its incidence has been on the increase in developed countries, in tandem with the increasing number of immigrants. Genitourinary TB (GUTB) has been inconsistently reported to account for 20–73% of all cases of extrapulmonary TB in the general population.
      • Chattopadhyay A.
      • Bhatnagar V.
      • Agarwala S.
      • Mitra D.K.
      Genitourinary tuberculosis in pediatric surgical practice.
      It is considered a severe form of extrapulmonary disease. GUTB occurs most frequently in the kidney (61%), ureter (19%), and urinary bladder (16%).
      • Hansen H.J.
      • Eldrup J.
      Spontaneous rupture of the urinary bladder: a late complication of Radiotherapy.
      Bladder TB occurs invariably secondary to TB of the kidney. The source is usually from small granulomas in the kidney, which shed bacteria intermittently. Large TB lesions in the kidney can also rupture and provide a period of prolonged bacteriuria. The mycobacteria are then washed along the ureter with the urine, to the bladder. The earliest form of bladder infection starts around one or both ureteral orifices, which then turn erythematous, inflamed, and edematous. With prolonged inflammation, there will be bladder exudates, ulcerations, fibrosis, and contracture of the bladder wall. This will lead to small, contracted, irreparably damaged bladders with intolerable frequency, pain, urgency, and hematuria.
      • McAleer S.J.
      • Johnson C.W.
      • Johnson Jr., W.D.
      Tuberculosis and parasitic and fungal infections of the genitourinary system.
      Bladder TB causing bladder perforation is extremely rare. To date, there are only three cases reported in the English literature.
      • Kumar R.V.
      • Banerjee G.K.
      • Bhadauria R.P.S.
      • Ahlawat R.
      Spontaneous bladder perforation: an unusual management problem of tuberculous cystitis.
      • Doig C.M.
      Perforation of a tuberculous bladder.
      • Heffernan S.J.
      Recurrent spontaneous rupture of the urinary bladder.
      Other causes of spontaneous bladder perforation include infections like schistosomiasis, inflammation of the bladder like eosinophilic cystitis, interstitial cystitis, enterocystoplasty, pelvic radiotherapy, malignant bladder tumors, erosion from indwelling catheter and giant vesical calculus, intra-arterial chemotherapy, atherosclerotic embolus, and following normal vaginal delivery.
      • Basavaraj D.R.
      • Zachariah K.K.
      • Feggetter J.G.
      Acute abdomen—remember spontaneous perforation of the urinary bladder.
      In most cases, the diagnosis was not obvious during initial evaluation. In a review by Schraut et al. of 100 cases of spontaneous bladder perforation, the diagnosis was only established intra-operatively.
      • Schraut W.H.
      • Huffman J.
      • Bagley D.H.
      Acute abdominal pain caused by spontaneous perforation of the urinary bladder.
      The presentation of spontaneous bladder perforation is usually lower abdominal pain, which later become diffuse with peritonitis and also oliguria or anuria. Biochemically, there will be evidence of renal dysfunction due to reabsorption of urea and creatinine via peritoneal self-dialysis. On ultrasound, there will be evidence of free intraperitoneal fluid. A cystogram is often diagnostic. Invariably, most patients will require laparotomy to confirm the diagnosis and repair the perforation.
      In our patient, her presentation pointed more to a diagnosis of perforated appendix. The diagnosis of bladder perforation was far from our mind since it is hardly seen and there was no predisposing factor. Therefore, we did not perform a cystogram. The presence of peritonitis was an indication for laparotomy, which we did perform. The intra-operative findings were very suggestive of chronic infection and TB was foremost in our minds since TB remains highly prevalent in our country.
      For a definite diagnosis, most patients would require a positive culture or histological analysis of biopsy specimens, possibly combined with PCR. Detection of AFB from urine samples by microscopy (Ziehl–Neelsen acid-fast stain) is not reliable, because of the possible presence of Mycobacterium smegmatis, which are also AFB. The biological activity of TB can only be assessed by cultivating mycobacteria. In our patient, despite the negative urine AFB stain, histopathological findings of chronic granulomatous inflammation with caseous necrosis and Langhans cells, combined with the positive Mantoux test, was highly suggestive of TB. Culture takes a few weeks. Therefore, we started empirical treatment with anti-TB drugs and this proved to be the right decision. Her condition improved clinically and the repair of the bladder healed well with no subsequent complications.
      The World Health Organization recommends an initial 2-month intensive phase of treatment with three or four drugs as anti-TB treatment, i.e., rifampin, isoniazid, pyrazinamide, and ethambutol (or streptomycin) to destroy almost all tubercle bacilli. This is followed by a 4-month continuation phase with only two drugs, most often rifampin and isoniazid.
      • Cek M.
      • Lenk S.
      • Naber K.G.
      • Bishop M.C.
      • Johansen T.E.
      • Botto H.
      • et al.
      EAU guidelines for the management of genitourinary tuberculosis.
      The Centers for Disease Control and Prevention (CDC) has recommended screening for HIV in patients with active TB.

      Centers for Disease Control and Prevention. Prevention and treatment of tuberculosis among patients infected with human immunodeficiency virus: principles of therapy and revised recommendations. MMWR 1998;47 (No. RR-20):23–25.

      HIV appears to be a potent facilitator of TB. Among the 9.27 million incident cases of TB in 2007, an estimated 1.37 million (14.8%) were HIV-positive.

      World Health Organization. Global tuberculosis control: surveillance, planning, financing. WHO Report 2009. WHO/HTM/TB/2009.411.Geneva: World Health Organization: 2009.

      For follow-up, patients should be re-evaluated at 3, 6, and 12 months after completion of their therapy. Relevant radiological investigations like ultrasound, intravenous urogram, cystogram, or a computerized tomography scan should be done at follow-up.
      • Dent R.E.
      • Batra A.K.
      Specific infections of the genitourinary tract.
      In conclusion, a diagnosis of bladder perforation, though remote, should be kept in mind in cases of acute abdomen and disproportionately elevated serum urea and creatinine levels. Based on typical HPE findings, anti-TB medication can be empirically started while awaiting the results of culture.

      Ethical approval

      The patient gave consent for the publication of this case report.

      Conflict of interest

      No conflict of interest to declare.

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