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DOI:
https://doi.org/10.37051/mir-34-002213Keywords:
ammonia, hyperammonia, cirrhosis, acute liver injury, cardiac arrest, encephalopathyAbstract
If hyperammonemia, defined by an increase in plasma ammonium concentration, is a situation that any intensivist may encounter, its etiological and therapeutic management remains relatively unfamiliar to clinicians. However, the consequences of hyperammonemia can be severe, particularly when levels exceed 150 µmol/L, where neurological complications (such as cerebral edema and brain herniation) become life-threatening.
From an etiological perspective, it is essential to distinguish hepatic causes, which account for 80-90% of cases, from non-hepatic causes, which pose an additional diagnostic challenge, including portosystemic shunts, drug-induced origins, inherited metabolic disorders, etc.
Various symptomatic treatments—both pharmacological and non-pharmacological—can be implemented alongside the treatment of the underlying cause, if identified, to rapidly reduce ammonia levels and, consequently, morbidity and mortality.
This review aims to help intensivists better understand the underlying pathophysiological mechanisms and clinical situations that should prompt consideration of hyperammonemia, identify the main etiologies in this context, and propose a therapeutic approach based on current scientific knowledge to improve patient outcomes.