Hypertransaminasemia in non-cirrhotic critically-ill patients

Table 1 Major etiologies of hypertransaminasemia in non-cirrhotic critically ill patients is summarized

Etiology	Clinical context	Biochemical pattern	Key diagnostic clues	Management focus	Ref.
HLI	Shock, cardiac arrest, severe hypoxaemia	Massive ALT/AST > 1000 U/L; bilirubin initially normal	Acute haemodynamic collapse; ≥ 50 % ALT/AST decline ≤ 72 h	Fluid resuscitation, vasopressors, optimise oxygen delivery	[2,6,7]
DILI	Polypharmacy, known hepatotoxins	Hepatocellular, cholestatic or mixed	Temporal drug link; RUCAM limited in ICU	Drug withdrawal; NAC (acetaminophen); selective corticosteroids	[13,17]
SALI	Septic shock, bacteraemia/fungaemia	Mild-moderate ALT/AST; cholestatic bilirubin rise	Imaging rules-out obstruction; conjugated hyperbilirubinaemia	Source control, guideline antibiotics, perfusion optimisation	[22]
PNALD	> 2 weeks PN, minimal enteral feed	Cholestasis ± mild ALT/AST	GGT/ALP rise; exclude other cholestasis	Early enteral nutrition, fish-oil lipids, avoid overfeeding	[30]
Multifactorial/unclear	Combined shock, sepsis, drugs, PN	Variable	No single dominant trigger	Multimodal supportive care; hepatology consult	[3]

HLI: Hypoxic liver injury; DILI: Drug-induced liver injury; SALI: Sepsis-associated liver injury; PNALD: Parenteral-nutrition-associated liver disease; RUCAM: Roussel Uclaf causality assessment method; ICU: Intensive care unit; NAC: N-acetylcysteine; ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; PN: Parenteral nutrition; GGT: Gamma-glutamyl transferase; ALP: Alkaline phosphatase.