Ammonia and nutritional therapy in the critically ill: when to worry, when to test and how to treat?

PURPOSE OF REVIEW: Hyperammonaemia is almost always develops in patients with severe liver failure and this remains the commonest cause of elevated ammonia concentrations in the ICU. Nonhepatic hyperammonaemia in ICU presents diagnostic and management challenges for treating clinicians. Nutritional and metabolic factors play an important role in the cause and management of these complex disorders. RECENT FINDINGS: Nonhepatic hyperammonaemia causes such as drugs, infection and inborn errors of metabolism may be unfamiliar to clinicians and risk being overlooked. Although cirrhotic patients may tolerate marked elevations in ammonia, other causes of acute severe hyperammonaemia may result in fatal cerebral oedema. Any coma of unclear cause should prompt urgent measurement of ammonia and severe elevations warrant immediate protective measures as well as treatments such as renal replacement therapy to avoid life-threatening neurological injury. SUMMARY: The current review explores important clinical considerations, the approach to testing and key treatment principles that may prevent progressive neurological damage and improve outcomes for patients with hyperammonaemia, especially from nonhepatic causes.

Liquorice Intoxication Can Lead to Cardiac Arrest!

A 45-year-old man was admitted to the Emergency Department with fatigue and muscular weakness. Soon after hospital admission, he developed "torsades de pointe" and was successfully resuscitated. The admission laboratory investigations had revealed a profound hypokalemia (1.65 mmol/L). The patient had a long-term use of alcohol-free "pastis" in an attempt to reduce his chronic ethanol consumption. As the beverage likely contained a significant amount of liquorice, the diagnosis of glycyrrhizin chronic intoxication was suspected. The diagnosis of liquorice-related pseudohyperaldosteronism was assessed by normal plasma aldosterone levels and low plasma renin activity. Intravenous and oral supplementation of potassium was required for 5 days, and the patient had an uneventful follow-up.