Introduction

The urinary bladder is usually protected by pelvic structures owing to its deep location in the pelvis with a low injury rate of 0.87 to 1.6% among the blunt abdominal trauma cases [1,2]. Mechanisms of bladder injuries includes direct force towards a distended bladder, shearing force secondary to pelvic fracture, penetrating trauma and iatrogenic causes [2-4]. Traumatic urinary bladder injuries can be further classified into bladder contusion, extra peritoneal rupture (60%), intraperitoneal rupture (25%), and combined intraperitoneal and extra peritoneal ruptures (6%) [1,5,6]. Extra peritoneal bladder rupture (EBR) is two-fold more common than intraperitoneal rupture, and intraperitoneal bladder rupture (IBR) often results from blunt force compressing on a distended bladder. In rare circumstances, IBR can occur spontaneously. Reported causes and risk factors of spontaneous bladder rupture (SBR) include chronic bladder disease, prolonged urinary retention, alcohol binge drinking, postpartum period and radiotherapy for pelvic malignancies [7]. We report a case of a middle-aged male without any history of trauma presenting to a rural facility with signs and symptoms consistent with acute peritonitis. CT scan findings were initially thought suggestive of perforated bowel with pneumoperitoneum and large volume free fluid, with blood analysis indicating significant acute kidney injury. On exploratory laparotomy the patient was found to have a 4cm posterior bladder wall injury. Our case highlights that in patients with acute abdomen, with imaging consistent with ascites and no history of liver disease urinary ascites and bladder perforation should be considered as prompt surgical repair reduces complications including intra-abdominal sepsis.

Case Presentation

A middle-aged Australian male presented to the emergency department with a 12-hour history of acute severe generalised abdominal pain on waking. The patient gave a history of excessive alcohol consumption the night prior to presentation however denied abdominal trauma. Patient had no significant past medical history (no known history of liver or renal disease), no medications, and surgical history was only significant for a colonoscopy one month prior to investigate per rectal bleeding which demonstrated internal haemorrhoids and a 3mm hyperplastic polyp in sigmoid colon. He had no history of intravenous drug use, no history of blood transfusions or recent tattoos. The patient was normotensive with a blood pressure of 138/81mm Hg, heart rate of 90 beats per minute, had a temperature of 37.0 degrees Celsius and a respiratory rate of 20 breaths per minute. On abdominal examination, he was generally peritonitic with board like rigidity with generalised guarding in all four quadrants. An in-dwelling urinary catheter (IDC) was inserted prior to surgical review and the urine drained clear. Biochemical analysis of blood for electrolytes, renal and liver function on presentation were indicative of an acute kidney injury with a potassium of 5.2mmol/L (135-145mmol/L), creatinine of 271 umol/L (40-100 umol/L), eGFR 24 mL/min/1.73m^2, urea 8.6mmol/L (2.7-7.1 mmol/L) and normal liver function with a total bilirubin 13 umol/L (<20 umol/L), conjugated bilirubin <4 umol/L (<4umol/L), alkaline phosphatase 80 U/L (30-110U/L), gamma-glutamyl transferase 20 U/L (<38U/L), alanine aminotransferase 32 U/L (<34 U/L), aspartate aminotransferase 35 U/L (<31U/L) and lipase of 24 U/L (<60 U/L). Baseline eGFR was >90 mL/min/1.73m^2 and creatinine level was 82 umol/L. Full blood count demonstrated a white cell count (WCC) of 17.7 x 10^9/L (4.0 – 11.0x10^9/L), Haemoglobin of 146g/L and a C-reactive protein of 32 mg/L (<2 mg/L). A venous blood gas was performed which demonstrated an elevated lactate at 2.6 mmol/L, which normalised to 2.3 on repeat venous blood gas after fluid resuscitation. Urine analysis for microscopy demonstrated >500 leukocytes, 350 red blood cells and 30 epithelial cells, with urine myoglobin of 19. Computed tomography (CT) abdomen (after bladder catheterisation) with intravenous contrast and images in portal venous phase demonstrated pneumoperitoneum, with free air in left upper and lower abdomen, large volume free fluid with concern for perforation of bowel (Figure 1 and Figure 2).

Figure 1: Coronal views of a CT abdomen pre-operatively showing a catheterised bladder with tip of catheter appear to be external to bladder dome.

Figure 2: Axial and coronal views of a computed tomography (CT) scan Preoperative showing moderate volume ascites (arrow) without haemoperitoneum.

Figure 3: Coronal views of a postoperative CT Cystogram particularly showing 10mm thickening along superior bladder surface without contrast extravasation.

After aggressive fluid resuscitation in emergency, a decision was made for urgent exploratory laparotomy. A midline laparotomy was performed with initial findings of 850mls of blood tinged free fluid in the peritoneal cavity, which had macroscopic appearance of blood stained urine. All large and small bowel looked macroscopically normal. A 4cm posterior aspect bladder perforation without ureteric involvement was found with a three-layer bladder wall closure performed and a post repair leak test demonstrating no evidence of leak. A thorough abdominal washout was performed with 1L of normal saline prior to closure of the laparotomy wound. Free fluid was sent for microscopic analysis, which demonstrated 1+ leucocytes. No epithelial cells or organisms were noted. The patient was admitted to the surgical ward post operatively with patient controlled anaesthetic infusion and rectus sheath blocks for analgesia. Post operatively, the IDC was draining clear fluid. The creatinine normalised on post-operative day one (97 umol/L) and eGFR returned to baseline of >90 mL/min/1.73m^2 on day 2 post operation. The patient was discharged home on day 7 post operation with an IDC in situ. He was reviewed in the urology outpatient clinic 2-weeks post discharge with a CT cystogram prior to review (Figure 3). CT cystogram demonstrated no extravasation of contrast, with bladder wall superiourly appearing thickened at 10mm and no free fluid in pelvis (Figure 3). The patient recovered well and a trial of void and Catheter removal was performed successfully at initial post operative review. Patient was discharged back into care of his general practitioner without further urology follow up. Imaging preoperative showed free air under the diaphragm, resulting in initial suspicious for bowel perforation. Free air seen on imaging is presumed secondary to introduction of air into the bladder during catheterisation and movement of this air into the peritoneal cavity through the bladder wall defect. Despite significant urine leakage into the peritoneal cavity demonstrated on CT imaging, the patient was never anuric, the bladder defect did not involve the ureters and thus some urine draining into the bladder was drained via the indwelling catheter.