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  • Poster presentation
  • Open Access

What is the role of carboxyhaemoglobin in patients with liver failure?

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Critical Care200711 (Suppl 2) :P397

  • Published:


  • Liver Failure
  • Physiological Parameter
  • Acute Liver Failure
  • Management System Database
  • Physiological Phenomenon


Patients with liver failure have haemodynamic and respiratory instability, the aetiology of which is unclear. Unregulated vasoactive mediators may have an important role in this physiological phenomenon. Carbon monoxide, a vasodilator, has been extensively studied and is easily measured using circulating carboxyhaemoglobin (COHb). The levels of circulating COHb have been reported as being elevated in patients with stable cirrhosis and hepatopulmonary syndrome. It is unknown whether the levels of COHb are elevated in patients with liver failure.


Patients admitted with acute liver dysfunction to the ITU between January 2003 and December 2005 were considered. Sixty-eight patients with acute liver failure (ALF) and 132 patients with decompensated chronic liver failure (DCLF) had a full dataset available on day 1 of admission. Patient demographics, physiological parameters, blood results and organ dysfunction were recorded prospectively and entered into a patient management system database (ICARE).


There was no statistical difference in patient demographics, organ failure scores or physiological parameters between the groups. The median COHb percentage for ALF was 0.9% (0.7–1.2) and for DCLF 1.5% (1.2–1.8). In patients with DCLF, COHb negatively correlated with PaO2 (r = -0.4, P = 0.05) and child Pugh (r = -0.4, P = 0.07). There was significant difference between grouped COHb and MAP in patients with ALF; there was a trend towards statistical significance with higher COHb. The arterial pH correlated with COHb in ALF (r = 0.4, P = 0.01).


These results suggest that COHb maybe an important mediator in haemodynamic and metabolic instability in ALF. In DCLF, COHb is an important factor in hypoxia and possible pulmonary shunting.

Authors’ Affiliations

King's College Hospital, London, UK


© BioMed Central Ltd. 2007