Thromboembolic Events During Continuous Vasopressin Infusions: A Retrospective Evaluation

Abstract

Published guidelines suggest that vasopressin has a role in shock treatment, although its safety has not been adequately evaluated in a clinical setting. Vasopressin causes platelet aggregation and has been associated with the release of factor VIII coagulant and von Willebrand factor. To compare the incidence of venous thromboembolism (VTE) in patients with a diagnosis of shock who received vasopressin with those who did not receive vasopressin for hemodynamic support. A retrospective, single-center, cohort study was conducted at an academic, tertiary care center with 350 patients with a diagnosis of shock. Patients from the intensive care unit were randomly selected and separated into 2 groups for comparison of those receiving only catecholamines with those receiving vasopressin with or without catecholamines for hypotension. Patients with diabetes insipidus or variceal hemorrhage and those with any documented history of VTE were excluded. The primary outcome, VTE occurrence, was defined as a positive Doppler ultrasound, spiral computed tomography, or documented diagnosis in the discharge records. Frequency and type of risk factors for VTE were compared between the 2 study arms. A risk factor modeling approach was performed, using logistic regression to identify potential confounders and effect modifiers in the relationship between vasopressin and VTE. There were 175 patients in each arm of the study. The crude incidence of VTE was 7.4% and 8% in the vasopressin and catecholamine groups, respectively (p = 0.84). No significant difference in the incidence of deep venous thrombosis (vasopressin 5.1%, control 7.4%; p = 0.51) or pulmonary embolism (vasopressin 2.3%, control 0.6%; p = 0.37) was found between groups. After adjusting for covariates, there was no statistically significant difference in the incidence of VTE between the 2 arms (p = 0.72). This investigation provides initial evidence that vasopressin infusions do not increase the risk of VTE in patients with shock.