Overtreatment of Heparin-Induced Thrombocytopenia in the Surgical ICU. (Betters)

Harada MY, et al. Overtreatment of Heparin-Induced Thrombocytopenia in the Surgical ICU. Crit Care Med. 2017 Jan;45(1):28-34.

OBJECTIVE: Recent studies reveal a high occurrence of overdiagnosis of heparin-induced thrombocytopenia in surgical patients with critical illness. The optimal criteria for diagnosis of heparin-induced thrombocytopenia remain unclear, contributing to unnecessary treatment. We reviewed patients who were admitted to surgical ICUs and were suspected of heparin-induced thrombocytopenia to identify how often patients were correctly treated.

DESIGN: In this clinical prospective study, data were collected including age, sex, antiplatelet factor 4/heparin enzyme-linked immunosorbent assay, serotonin release assay, and Warkentin 4Ts scores. Heparin-induced thrombocytopenia-positive patients were defined as those with both positive antiplatelet factor 4/heparin enzyme-linked immunosorbent assay (optical density, ≥ 0.40) and positive serotonin release assay results.

SETTING: Urban tertiary medical center.

PATIENTS: Patients admitted to the surgical and cardiac ICU who were presumed to have heparin-induced thrombocytopenia and underwent antiplatelet factor 4/heparin enzyme-linked immunosorbent assay and serotonin release assay testing between January 1, 2011, and August 1, 2014.

INTERVENTIONS: None.

MEASUREMENTS AND MAIN RESULTS: A total of 135 patients had 4Ts, antiplatelet factor 4/heparin enzyme-linked immunosorbent assay, and serotonin release assay scores. A total of 11 patients (8.1%) had positive serotonin release assay and 80 patients had positive antiplatelet factor 4/heparin enzyme-linked immunosorbent assay; 10 patients were identified as heparin-induced thrombocytopenia positive. Positive serotonin release assay was noted in nine of 11 patients (81.8%) with antiplatelet factor 4/heparin enzyme-linked immunosorbent assay optical density greater than or equal to 2.0, compared with one of 22 patients (4.5%) with optical density values of 0.85-1.99, and one of 102 patients (1.0%) with optical density values of 0-0.84. Out of 135 patients, 29 patients (21.5%) received treatment with argatroban, lepirudin, or fondaparinux: 10 of 10 heparin-induced thrombocytopenia-positive patients (100%) compared with 19 of 125 heparin-induced thrombocytopenia-negative patients (15%).

CONCLUSIONS: Overtreatment of heparin-induced thrombocytopenia in the surgical ICU continues even with recent increased caution encouraging a higher antiplatelet factor 4/heparin enzyme-linked immunosorbent assay optical density threshold before initiating treatment. More stringent criteria should be used to determine when to order serologic testing and when the results of such testing should prompt a change in anticoagulant treatment. If antiplatelet factor 4/heparin enzyme-linked immunosorbent assay is used to consider immediate treatment, an optical density greater than or equal to 2.0 may be a more appropriate threshold.

Circuit Lifetime With Citrate Versus Heparin in Pediatric Continuous Venovenous Hemodialysis. (Duke)

Zaoral T, et al. Circuit Lifetime With Citrate Versus Heparin in Pediatric Continuous Venovenous Hemodialysis. Pediatr Crit Care Med. 2016 Sep;17(9):e399-405.

OBJECTIVES: To determine if there is a difference between regional citrate and global heparinized anticoagulation on circuit lifetimes during continuous venovenous hemodialysis in children.

DESIGN: Prospective “cross-over” trial.

SETTING: PICU, Department of Pediatrics, University Hospital Ostrava.

PATIENTS: Children 0-18 years old.

INTERVENTIONS: From 2009 to 2014, 63 eligible children (age, 89.24 ± 62.9 mo; weight, 30.37 ± 20.62 kg) received at least 24 hours of continuous venovenous hemodialysis. Each child received four continuous venovenous hemodialysis circuits with anticoagulants in the following order: heparin, citrate, heparin, citrate. Circuit life ended when transmembrane pressure was greater than or equal to 250 mm Hg for more than 60 minutes.

MEASUREMENTS AND MAIN RESULTS: The total mean circuit lifetime was 39.75 ± 10.73 hours. Citrate had a significantly longer median circuit lifetime (41.0 hr; CI, 37.6-44.4) than heparin (36.0 hr; CI, 35.4-36.6; p = 0.0001). Mortality was 33.33%. Circuit lifetime was significantly correlated to patient age (r = 0.606), weight (r = 0.763), and blood flow rate (r = 0.697). Transfusion rates (units of red cells per circuit of continuous venovenous hemodialysis) were 0.17 (0.0-1.0) with citrate and 0.36 (0.0-2.0) with heparin (p = 0.002).

CONCLUSIONS: We showed in our study that citrate provided significantly longer circuit lifetimes than heparin for continuous venovenous hemodialysis in children. Citrate was superior to heparin for the transfusion requirements. Citrate was feasible and safe in children and infants.

Failure of anticoagulant thromboprophylaxis: risk factors in medical-surgical critically ill patients. (Teppa)

Lim W, Meade M, Lauzier F, et al. Failure of anticoagulant thromboprophylaxis: risk factors in medical-surgical critically ill patients*. Crit Care Med. 2015 Feb;43(2):401-10.

Full-text for Children’s and Emory users.

OBJECTIVES: To identify risk factors for failure of anticoagulant thromboprophylaxis in critically ill patients in the ICU.

DESIGN: Multivariable regression analysis of thrombosis predictors from a randomized thromboprophylaxis trial.

SETTING: Sixty-seven medical-surgical ICUs in six countries.

PATIENTS: Three thousand seven hundred forty-six medical-surgical critically ill patients.

INTERVENTIONS: All patients received anticoagulant thromboprophylaxis with low-molecular-weight heparin or unfractionated heparin at standard doses.

MEASUREMENTS AND MAIN RESULTS: Independent predictors for venous thromboembolism, proximal leg deep vein thrombosis, and pulmonary embolism developing during critical illness were assessed. A total of 289 patients (7.7%) developed venous thromboembolism. Predictors of thromboprophylaxis failure as measured by development of venous thromboembolism included a personal or family history of venous thromboembolism (hazard ratio, 1.64; 95% CI, 1.03-2.59; p = 0.04) and body mass index (hazard ratio, 1.18 per 10-point increase; 95% CI, 1.04-1.35; p = 0.01). Increasing body mass index was also a predictor for developing proximal leg deep vein thrombosis (hazard ratio, 1.25; 95% CI, 1.06-1.46; p = 0.007), which occurred in 182 patients (4.9%). Pulmonary embolism occurred in 47 patients (1.3%) and was associated with body mass index (hazard ratio, 1.37; 95% CI, 1.02-1.83; p = 0.035) and vasopressor use (hazard ratio, 1.84; 95% CI, 1.01-3.35; p = 0.046). Low-molecular-weight heparin (in comparison to unfractionated heparin) thromboprophylaxis lowered pulmonary embolism risk (hazard ratio, 0.51; 95% CI, 0.27-0.95; p = 0.034) while statin use in the preceding week lowered the risk of proximal leg deep vein thrombosis (hazard ratio, 0.46; 95% CI, 0.27-0.77; p = 0.004).

CONCLUSIONS: Failure of standard thromboprophylaxis using low-molecular-weight heparin or unfractionated heparin is more likely in ICU patients with elevated body mass index, those with a personal or family history of venous thromboembolism, and those receiving vasopressors. Alternate management or incremental risk reduction strategies may be needed in such patients.