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• W1575824741 abstract "Acute abdomen can often pose a diagnostic challenge. In the absence of conclusive clinical or radiological evidence, an exploratory laparatomy may be necessary to pinpoint the pathology. Sometimes, the aetiology may not be apparent even after laparatomy. We present a report of a patient where an insight into the nature of the surgical pathology was guided by the arterial blood gases and the acid-base picture. A 61-year-old female presented to the Emergency Department at our hospital with acute, severe abdominal pain. There had been no precipitating event. Examination demonstrated signs of generalised peritonitis. She remained afebrile, however, and her white cell count showed only a modest rise. Her past medical history included a hysterectomy and pelvic radiotherapy for cervical carcinoma, and no other significant comorbidities. She had also undergone two emergency laparotomies for peritonitis 18 months previously. The operative findings at the first laparatomy were pus in the peritoneal cavity, a thickened sigmoid colon but no apparent perforation. A second laparatomy a week later had revealed a small amount of clear peritoneal fluid only. One further admission with abdominal pain had been successfully treated conservatively. In view of the previous history of negative laparotomies, conservative management with intravenous fluids and antibiotics was commenced. An abdominal CT scan showed fluid in the peritoneal cavity. Twenty-four hours after admission she began to deteriorate, with increasing abdominal pain, tachycardia and tachypnoea; her urine output fell rapidly. Serial arterial blood gases (ABG) over this period showed a worsening metabolic acidosis. She was transferred to the ICU where invasive haemodynamic monitoring and mechanical ventilation of the lungs were instituted. Urine output remained poor despite optimisation of central venous and mean arterial pressures with fluids and inotropes. During the laparotomy, copious straw-coloured clear fluid was drained from the abdominal cavity. Despite a thorough search, no surgical reason could be found for the gross metabolic disturbance and severe peritonitis. This appeared to be another negative laparatomy in keeping with her past history. At this point the anaesthetist noted the presence of a normal anion gap and a hyperchloraemic metabolic acidosis on arterial blood gas analysis (pH 7.12, Pao2 20.9 kPa, Paco2 6.7 kPa, HCO3– 14.3 mmol.l−1 BE −12.6, Na+ 133 mmol.l−1, K+ 5.3 mmol.l−1, Cl– 112 mmol.l−1, and an anion gap of 10.2 mmol.l−1) and suggested the possibility of uro-peritoneum. Methylene blue was injected per urethra and dye was seen leaking from a small perforation located at the posterior aspect of the urinary bladder. A necrotic area surrounded the perforation; this was excised and the perforation repaired. Histology of the bladder biopsy showed inflammatory and necrotic tissue, reflecting previous local irradiation. Postoperatively, her biochemical profile normalised within 24 h, her condition improved over the following 48 h, and she was discharged on the 6th postoperative day. Spontaneous intraperitoneal rupture of the urinary bladder has been reported as a late complication of radiation therapy for cervical cancer [1]. Additional causes are distension resulting from outlet obstruction, alcohol intoxication, or a neurogenic bladder [2]. Bladder rupture can also occur due to malignant tumours, inflammatory lesions, diverticuli, calculi and following enterocystoplasty. Our patient had previously received pelvic radiotherapy for carcinoma of the cervix. It is important to note that presence of urine in the bladder on catheterisation does not exclude the possibility of a rupture [3]. Metabolic acidosis resulting from an abdominal sepsis is common. Hyperchloraemic, normal anion-gap acidosis in this setting is, however, unusual. This type of metabolic picture is generally due to gastro-intestinal loss of bicarbonate in conditions such as severe infective diarrhoea, villous adenoma, external pancreatic or biliary fistulas and chronic laxative abuse. Other causes include renal loss of base due to proximal and distal tubular acidosis, prolonged use of carbonic anhydrase inhibitors, hypoaldosteronism, and excessive saline administration in the presence of a chronic renal failure. Our patient developed peritonitis due to the intra-abdominal extravasation of urine. Accumulated urine acts like a dialysate, leading to a metabolic picture very similar to that following urinary diversion such as ileal conduit, uretero-sigmoidostomy or a vesico-colic fistula [4]. We have not found other reports of spontaneous rupture of bladder described with a hyperchloraemic acidosis. This case and its unusual method of diagnosis highlight the importance of the anaesthetist's understanding of acid-base physiology." @default.
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• W1575824741 date "2007-04-18" @default.
• W1575824741 modified "2023-10-13" @default.
• W1575824741 title "Diagnosis of bladder rupture by arterial blood gas analysis" @default.
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• W1575824741 doi "https://doi.org/10.1111/j.1365-2044.2007.05075_13.x" @default.
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