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A 28-year-old man presented to the casualty department with a one-day history of abdominal pain and bloating following a heavy intake of alcohol. The patient had no urinary, respiratory or cardiovascular symptoms and had recently opened his bowels normally. A previous episode of ureteric colic 3 years earlier was the only medical history of note. On examination the patient was apyrexial with a pulse rate of 97 beats/min and a blood pressure of 190/100 mmHg. He was noted to have tense abdominal swelling and there was evidence of free intraperitoneal fluid. On palpation there was generalised abdominal tenderness; bowel sounds were present and there were no external signs of trauma. The abdominal X-ray was considered to be normal as were the full blood count and serum amylase but the renal function was mildly impaired with a high potassium. The patient was admitted for observation and given intravenous fluids overnight. The next morning the renal function had further deteriorated (urea 12.9 mmol/l, creatinine 337 μmol/l) and the patient had become oliguric. A tentative diagnosis of acute renal failure secondary to an acute abdomen was made and a renal physician was asked to see the patient. No obvious cause of renal impairment such as hypovolaemia or sepsis was identified. An abdominal ultrasound was requested and this showed substantial volumes of free intraperitoneal fluid but the kidneys and other abdominal organs appeared normal as did the portal vein, hepatic veins and inferior vena cava. An abdominal paracentesis was performed and revealed a straw-coloured fluid with a very low protein level (less than 10 g/l).
- What radiological investigation is indicated and what abnormality do you expect it to show?
- How can the features of acute renal failure be explained in this case?
A cystogram is the next radiological investigation indicated, as this history is suggestive of an intraperitoneal rupture of the bladder causing urinary ascites and peritonitis. In this case the cystogram showed a massive intraperitoneal leak (figure) and a 4-cm tear in the dome of the bladder was identified at surgery and repaired.
The diffusion of urea and electrolytes across the peritoneal membrane secondary to urinary ascites causes an elevation in serum urea and creatinine levels. In addition, the constant flow of urine from the ruptured bladder into the peritoneal cavity can give the false impression of oliguria if urine volumes are measured from a bladder catheter.
Bladder ruptures can be extraperitoneal or intraperitoneal, depending on the site of injury although a mixed picture occurs in a small percentages of cases. Intraperitoneal bladder ruptures are usually associated with blunt abdominal trauma (excluding iatrogenic causes) and unlike extraperitoneal leaks, they are not usually associated with pelvic fractures. Intraperitoneal bladder ruptures usually occur in the dome of the bladder in contrast to extraperitoneal leaks which are most often located in the lateral walls. The diagnosis can be confirmed by a cystogram and if performed carefully then almost 100% of ruptures can be detected, although if a post-drainage film is omitted, then up to 20% of cases may be missed.1 In the case of an intraperitoneal bladder rupture, a cystogram will show contrast collecting within the peritoneal cavity and outlining bowel loops which appear as cylindrical filling defects. When the patient is in the supine position, free intraperitoneal contrast settles in the most dependent part of the pelvis and in this situation the cystogram has the configuration of an hourglass. The well-defined lower portion represents the urinary bladder and the upper part is formed by free contrast in the pelvic cavity. The waist of the hourglass is the point from which contrast escapes from the bladder. If there are other significant traumatic injuries, the diagnosis can also be made by performing computed tomographic cystography, although some authors do not feel that this is as sensitive as conventional cystography.2
In the majority of cases of intraperitoneal bladder rupture there is a history of significant abdominal trauma but it is important to realise that, following a period of heavy alcohol intake, the distended urinary bladder is very susceptible to injury and can be ruptured by surprisingly minor incidents. Furthermore, the intoxicated patient may fail to recall any relevant episode of trauma. In this case, the patient only gave a history of falling onto his abdomen when specifically questioned about trauma. Although these cases are rare they are important because the correct diagnosis is usually not made at presentation causing an increase in mortality and morbidity. In a recent paper, 20 isolated intraperitoneal bladder ruptures were reviewed and the mean time between presentation and diagnosis was found to be 5.4 days.3 In many of these cases heavy alcohol intake was considered to be one of the most important factors associated with a delay in diagnosis and management.
In urinary ascites there are relatively high concentrations of urea and electrolytes in the peritoneal cavity compared with blood levels, and therefore diffusion of these substances takes place, back across the peritoneal membrane. This results in an elevation of serum urea, creatinine and potassium levels with an associated metabolic acidosis and hyponatraemia which can simulate the biochemical changes of acute renal failure.4
In conclusion, it is important to suspect an intraperitoneal bladder rupture in any patient with a history of non-specific abdominal pain following an alcoholic bout, even in the absence of any urinary symptoms. If the correct diagnosis is not made initially, the patient may develop biochemical changes which are very similar to those of acute renal failure causing a further delay in appropriate management, with an associated increase in morbidity and mortality.
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