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Liver dysfunction associated with artificial nutrition in critically ill patients

Teodoro Grau1*, Alfonso Bonet2, Mercedes Rubio3, Dolores Mateo4, Mercé Farré5, José A Acosta6, Antonio Blesa7, Juan C Montejo8, Abelardo G de Lorenzo9, Alfonso Mesejo10 and the Working Group on Nutrition and Metabolism of the Spanish Society of Critical Care

Author Affiliations

1 Intensive Care Unit, Hospital Severo Ochoa. Av. Orellana s/n, 28911 Leganés, Madrid, Spain

2 Intensive Care Unit, Hospital Josep Trueta. Av. de Francia s/n, 17007 Girona, Spain

3 Cardiovascular Intensive Care Unit, Hospital Universitario 12 de Octubre. Av. de Córdoba s/n, 28041 Madrid, Spain

4 Intensive Care Unit, Newham University Hospital NHS Trust. Glen Road, Plaistow London E13 8SL, UK

5 Intensive Care Unit, Hospital Universitari Vall d'Hebró. Paseo Vall d'Hebró 119-129, 08035 Barcelona, Spain

6 Intensive Care Unit, General de Alicante. Maestro Alonso 109, 03010 Alicante, Spain

7 Intensive Care Unit, Hospital Clínico San Carlos. Profesor Martin Lagos s/n, 28040 Madrid, Spain

8 Intensive Care Unit, Hospital Universitario Doce de Octubre.Av. de Córdoba s/n, 28041 Madrid, Spain

9 Intensive Care Unit, Hospital Universitario La Paz. Paseo de la Castellana 261, 28046 Madrid, Spain

10 Intensive Care Unit, Hospital Universitario La Fe. Av. Campanar 21, 46009 Valencia, Spain

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Critical Care 2007, 11:R10 doi:10.1186/cc5670

Published: 25 January 2007

Abstract

Introduction

Liver dysfunction associated with artificial nutrition in critically ill patients is a complication that seems to be frequent, but it has not been assessed previously in a large cohort of critically ill patients.

Methods

We conducted a prospective cohort study of incidence in 40 intensive care units. Different liver dysfunction patterns were defined: (a) cholestasis: alkaline phosphatase of more than 280 IU/l, gamma-glutamyl-transferase of more than 50 IU/l, or bilirubin of more than 1.2 mg/dl; (b) liver necrosis: aspartate aminotransferase of more than 40 IU/l or alanine aminotransferase of more than 42 IU/l, plus bilirubin of more than 1.2 mg/dl or international normalized ratio of more than 1.4; and (c) mixed pattern: alkaline phosphatase of more than 280 IU/l or gamma-glutamyl-transferase of more than 50 IU/l, plus aspartate aminotransferase of more than 40 IU/l or alanine aminotransferase of more than 42 IU/l.

Results

Seven hundred and twenty-five of 3,409 patients received artificial nutrition: 303 received total parenteral nutrition (TPN) and 422 received enteral nutrition (EN). Twenty-three percent of patients developed liver dysfunction: 30% in the TPN group and 18% in the EN group. The univariate analysis showed an association between liver dysfunction and TPN (p < 0.001), Multiple Organ Dysfunction Score on admission (p < 0.001), sepsis (p < 0.001), early use of artificial nutrition (p < 0.03), and malnutrition (p < 0.01). In the multivariate analysis, liver dysfunction was associated with TPN (p < 0.001), sepsis (p < 0.02), early use of artificial nutrition (p < 0.03), and calculated energy requirements of more than 25 kcal/kg per day (p < 0.05).

Conclusion

TPN, sepsis, and excessive calculated energy requirements appear as risk factors for developing liver dysfunction. Septic critically ill patients should not be fed with excessive caloric amounts, particularly when TPN is employed. Administering artificial nutrition in the first 24 hours after admission seems to have a protective effect.