ABSTRACT
Introduction: The current author encountered a patient with end-stage bladder cancer who developed hyperammonemia and impaired consciousness. Case: A 90-year-old man had repeated bleeding from a bladder tumor, so a urethral catheter was placed. During admission to the Palliative Care Unit, impaired consciousness and hyperammonemia were noted. Liver metastasis was not noted. Urinalysis revealed alkaluria and ammonium magnesium phosphate crystals, so production of ammonia by bacteria with the ability to hydrolyze urea was suspected. Levofloxacin was inefficacious. As a result of administration of metronidazole, however, consciousness improved, blood ammonia levels returned to normal, urine was acidic, and ammonium magnesium phosphate crystals disappeared. The bacterium with the ability to hydrolyze urea could not be identified. Discussion: In patients with advanced or end-stage bladder cancer like the current patient, ammonia produced by bacteria with the ability to hydrolyze urea can cause hyperammonemia and impaired consciousness even if the urinary tract is unobstructed.
ABSTRACT
Coma and other states of impaired consciousness represent a medical emergency. The potential causes are numerous, and the critical window for diagnosis and effective intervention is often short. The common causes of non-traumatic coma include central nervous system infections, metabolic encephalopathy (hepatic, uremic, diabetic ketoacidosis etc.), intracranial bleed, stroke and status epilepticus. The basic principles of management include 1) Rapid assessment and stabilization, 2) Focussed clinical evaluation to assess depth of coma, localization of lesion in the central nervous system and possible clues to etiology, and 3) Treatment including general and specific measures. Commonly associated problems such as raised intracranial pressure and seizures must be recognized and managed to prevent secondary neurologic injury.
ABSTRACT
We studied three patients with spontaneous mesencephalic hemorrhages. All presented with some degree of impaired consciousness and abnormal ocular movements. One patient had a convergence-retraction nystagmus with a unilateral hemorrhage confined to the dorsal midbrain. Another patient showed left third nerve palsy due to a unilateral hemorrhage that involved ventral midbrain. The third patient revealed left internuclear ophthalmoplegia with ataxia due to a pinpoint hemorrhage in the tegmentum of the left midbrain. The patients survived and major neurologic deficits recovered, but abnormal ocular movements persisted.