A woman with mild chronic renal insufficiency was being treated with glucocorticoids for a presumed chronic inflammatory disease. She developed peritonitis arising from a pelvic abscess, which was drained without complications. Unexpectedly, she became obtunded, and eventually, the neurologic dysfunction was linked to hyperammonemia in spite of normal liver function tests. Hyperammonemia was only transiently controlled in spite of protein restriction, repeated hemodialysis, and the use of biochemical means to reduce ammonia. A recurrent pelvic abscess was drained, and hyperammonemia disappeared. A review of ammonia and nitrogen metabolism indicates that bypassing the liver with shunting of ammonia into the systemic circulation should be added to the causes of symptomatic hyperammonemia. Treatment requires the elimination of the bacteria.