Early intravenous unfractionated heparin and outcome in acute lung injury and acute respiratory distress syndrome – a retrospective propensity matched cohort study

Patients admitted to the Intensive Care Unit (ICU) of a tertiary referral center in the Netherlands between November 2004 and October 2007 were screened. Patients who developed ALI (consensus definition) were included. In this cohort, the impact of heparin use on mortality was assessed by logistic regression analysis in a propensity matched case–control design.Of 5,561 admitted patients, 2,138 patients had a length of stay？>？48？hours, of whom 723 were diagnosed with ALI (34%), of whom 164 received intravenous heparin. In a propensity score adjusted logistic regression analysis, heparin use did not influence 28-day mortality (odds ratio 1.23 [confidence interval 95% 0.80–1.89], nor did it affect ICU length of stay.Administration of therapeutic doses of intravenous unfractionated heparin was not associated with reduced mortality in critically ill patients diagnosed with ALI. Heparin treatment did not increase transfusion requirements. These results may help in the design of prospective trials evaluating the use of heparin as adjunctive treatment for ALI.Acute lung injury (ALI), and its more severe form Acute Respiratory Distress Syndrome (ARDS), are characterized by an exaggerated pulmonary pro-inflammatory and pro-coagulant response of the host against some form of insult. In sepsis, activation of coagulation as well as defective anticoagulant pathways and inhibition of fibrinolysis all contribute to systemic coagulopathy [1]. Similar disturbances in coagulation and fibrinolysis have been found locally in models of ALI [2-4] and in lungs of patients with ALI/ARDS [5,6]. There is evidence that this coagulopathy contributes to pulmonary inflammation [7,8], as the extent of coagulopathy is independently associated with adverse clinical outcomes in patients with ALI/ARDS [8,9]. As such, the pathogenesis of ALI/ARDS shares many similarities to sepsis [5,6] independent of the occurrence of sepsis [8]. Mechanical ventilation also induces fibrin deposition in the lung, there