Green urine, but no infection.

In September, 2007, an unconscious 88-year-old woman was brought to the emergency room. She had undergone a hysterectomy and radiotherapy because of carcinoma of the cervix 30 years previously; 10 years later she had developed neurogenic bladder dysfunction, requiring intermittent self-catheterisation. She had had mild renal insuffi ciency (creatinine 100 μmol/L) and mild hydronephrosis unilaterally, because of ureteric obstruction following the irradiation. Her medical history also included bilateral femoral artery angioplasty, a transient ischaemic attack, and group B streptococcal endocarditis with remaining mild mitral valve insuffi ciency. Medications included an ACE-inhibitor, aspirin, and dipyridamole for the past 4 years. On presentation she was unresponsive and hyperventilating (20 breaths per min) with a body temperature of 33·0°C, an irregular pulse (110 beats per min), and a blood pressure of 110/60 mm Hg. Auscultation showed no new cardiac abnormalities, and neurological evaluation was unremarkable. The electrocardiogram showed atrial fi brillation (110 beats per min). Blood gas analysis on supplemental oxygen, corrected for hypothermia, showed a pH of 7·08, pCO2 1·85 kPa, bicarbonate 3·6 mmol/L, and pO2 18·5 kPa, indicative of metabolic acidosis with incomplete respiratory compensation. 1300 mL of green purulent urine was emptied from the bladder on catheterisation. Urosepsis was suspected, blood samples were taken, and she was rehydrated with saline and treated with ceftriaxone and 8·4% NaHCO3. 1 h later laboratory test results showed a normal anion gap hyperchloraemic acidosis (anion gap 16, sodium 147 mmol/L, and chloride 127 mmol/L). Lactate (1 mmol/L), potassium (4·3 mmol/L), albumin (34 g/L), and glucose (7·9 mmol/L) were normal. Until this point she had received 1250 mL 0·9% NaCl (saline) and 200 mL of 8·4% NaHCO3. Repeat analysis showed sodium 159 mmol/L, chloride 131 mmol/L, potassium 3·4 mmol/L, and bicarbonate 7·0 mmol/L. Although the saline was replaced by 5% glucose solution, 1·5 L/day, with 4 mmol potassium added, plasma sodium and chloride concentrations inceased to 170 mmol/L and 143 mmol/L, respectively, over the next 2 days. Urine cultures were negative. Hyperchloraemia and hypernatraemia because of endogenous reuptake of urinary chloride in the bowel was suspected. Cystoscopy showed a large bladder wall defect with a vesicojejunal fi stula on CT (fi gure). Our patient refused additional procedures and was discharged to a nursing home with oral bicarbonate supplementation. She passed away 2 months later. Our patient had a hyperchloraemic metabolic acidosis because of a fi stula between bladder and jejunum caused by previous radiotherapy; it is possible that the fi stula caused the group B streptococcal endocarditis 3 years before presentation. The ileal and colonic mucous membrane harbours a Cl/HCO3 transporter that exchanges intraluminal chloride (in our patient, a large amount via the communication to the bladder) for bicarbonate; sodium is actively reabsorbed, leading to potassium excretion. This explains the hyperchloraemic acidosis that can be seen in patients following ureter implantation into the sigmoid commonly presenting with hypokalaemia. However, in our patient, renal insuffi ciency and ACE-inhibitor use induced normokalaemia, and correction of the acid-base status provoked hypokalaemia. Saline infusion and bicarbonate supplementation during initial resuscitation resulted in additional sodium re-uptake and worsening of hyperchloraemia and hypernatraemia. Several other factors may have contributed to the observed acidosis, for example elevated bladder pressure between the selfcatheterisations promoting fl uid movement through the fi stula. In addition, the proximal localisation of the fi stula could have extended ileal and colonic transit time, augmenting intestinal chloride uptake. Enterovesical fi stula can occur years after pelvic radiotherapy; the importance of taking into account the patient’s history cannot be emphasised enough.