THE TOXIC EFFECTS OF CARBON DIOXIDE AND ACETAZOLAMIDE IN HEPATIC ENCEPHALOPATHY *

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Abstract
Cerebral blood flow (CBF) and metabolism (CMRO2) was determined in controls, in alert patients with hepatic cirrhosis and in patients with hepatic encephalopathy. Clinical and CMRO2 responses were compared following 5% CO2 inhalation and acetazolamide infusion. CMRO2 was normal in alert cirrnotics, but declined progressively as encephalopathy appeared and worsened. CO2 (5%) caused both clinical deterioration and decreased CMROo in patients having hepatic encephalopathy. Cerebral ammonia uptake (CMRNH3) decreased during CO2 inhalation. Acetazolamide infusions (2.0 g) caused no significant change in controls. However, when subjects with hepatic encephalopathy received 2.0 g acetazolamide, prompt clinical deterioration and CMRO2 reduction was observed. These changes following acetazolamide preceded any rise in arterial ammonia. Reversing blood alkalosis by CO2 inhalation worsens rather than improves subjects with hepatic encephalopathy. The results suggest that the major toxicity of acetazolamide in hepatic cirrhosis directly results from increased cerebral tissue CO2 tensions.