Urinary tract infection and coma

The high ammonia level, the triphasic wave pattern on EEG, and the absence of other causes of altered consciousness strongly suggested hyperammonaemic coma in our patient. Advanced age and normal liver function tests excluded an inherited metabolic disturbance and severe liver disease. She had no history of urinary diversion or evidence of vesico-colonic fistula, both of which are common causes of non-hepatic hyperammonaemia in adults.1,2 Urease production by urea splitting bacteria in repetitive UTIs resulted in hydrolysis of urinary urea to ammonium (NH^sub 4^^sup +^) and highly alkalinised urine. At a highly alkaline pH, ammonium is transformed into large amounts of ammonia (NH^sub 3^), a liposoluble free base that crosses cell membranes proportionally to the free base gradient, and inversely to the pH gradient.3 Urinary stagnation in a chronically distended bladder with increased surface area probably favoured ammonia diffusion through the bladder wall to the perivesical circulation. As most venous blood from the bladder drains directly into the hypogastric veins and inferior vena cava, bypassing the portal circulation and liver, the ammonia levels increased, causing encephalopathy.4,5 Other unidentified neurotoxic substances with biochemical properties similar to ammonia may also have contributed. Chronic urinary retention and hyperammonaemia should be considered in patients with altered consciousness or coma, particularly in elderly patients, in whom urinary outflow abnormalities and infections are common.