Platelet Count Trends and Prevalence of Heparin-Induced Thrombocytopenia in a Cohort of Extracorporeal Membrane Oxygenator Patients.

OBJECTIVES: To assess the prevalence of heparin-induced thrombocytopenia and to study platelet count trends potentially suggestive of heparin-induced thrombocytopenia in a population of extracorporeal membrane oxygenator patients. DESIGN: Retrospective cohort study. SETTING: A total of 926-bed teaching hospital. PATIENTS: Extracorporeal membrane oxygenator patients who survived longer than 48 hours from extracorporeal membrane oxygenator initiation between January 1, 2009, and December 31, 2013. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Demographic and clinical data were collected prospectively on all extracorporeal membrane oxygenator patients. Heparin-induced thrombocytopenia testing results and platelet count variables were obtained from the electronic medical record. We used our institutional algorithm to interpret the results of heparin-induced thrombocytopenia testing. Ninety-six extracorporeal membrane oxygenator patients met the inclusion criteria. Eight patients met the algorithm criteria for heparin-induced thrombocytopenia diagnosis and seven of those had documented thromboembolic event while on extracorporeal membrane oxygenator (prevalence of heparin-induced thrombocytopenia and heparin-induced thrombocytopenia related thrombosis, 8.3 and 7.3, respectively). Heparin-induced thrombocytopenia positive patients were younger; all underwent venoarterial extracorporeal membrane oxygenator; spent more hours on extracorporeal membrane oxygenator; had significantly higher heparin-induced thrombocytopenia enzyme-linked immunosorbent assays optical density; had a higher prevalence of thromboembolic events and reached platelet count nadir later. There was no difference in mortality between heparin-induced thrombocytopenia positive and negative patients. Comparison of platelet count trends revealed that there was no statistically significant difference between the predefined study groups. CONCLUSIONS: Prevalence of heparin-induced thrombocytopenia and heparin-induced thrombocytopenia-related thrombosis among extracorporeal membrane oxygenator patients at our institution is relatively high. Using platelet count trends to guide decision to test for heparin-induced thrombocytopenia is not an optimal strategy in extracorporeal membrane oxygenator patients. Without a validated pretest probability clinical score, serosurveillance in a defined high-risk group of extracorporeal membrane oxygenator patients may be needed.

Pulse Oximetry Is Unreliable in Patients on Veno-Venous Extracorporeal Membrane Oxygenation Caused by Unrecognized Carboxyhemoglobinemia.

Continuous bedside pulse oximetry (SpO2) is universally used to monitor oxygenation for patients supported on veno-venous extracorporeal membrane oxygenation (VV-ECMO). Yet, elevated carboxyhemoglobin (COHb), a known event in VV-ECMO, diminishes the reliability of SpO2. This retrospective cohort study aims to assess the accuracy of SpO2 compared with oxyhemoglobin (SaO2) and quantify COHb levels by co-oximetry in the VV-ECMO population. Forty patients on VV_ECMO from 2012 to 2017 underwent 1,119 simultaneous SaO2 and SpO2 measurements. Most patients were male (60%) with average age of 46 years. SpO2 overestimated SaO2 values by 2.35% at time of cannulation and 0.0061% for each additional hour on VV-ECMO (p < 0.0001). Twenty-nine (72.5%) patients developed elevated COHb (>3% of hemoglobin saturation) at least once during VV-ECMO support and 602 (40.2%) arterial blood gases yielded elevated COHb levels. Mean duration for ECMO with elevated COHb was 244 hours compared with 98 hours in patients without (p < 0.0048). Patients who developed COHb were younger (mean age 40 vs. 55 years, p < 0.024) and had single-site double-lumen cannulation (odds ratio = 4.5, p = 0.23). At time of cannulation, mean COHb was 2.18% and increased by 0.0054% for each additional hour (p < 0.0001). For every 1% increase in COHb, SaO2 decreased by 1.1% (p < 0.0001). During VV-ECMO, SpO2 often overestimates SaO2 by substantial margins. This is attributable to rising COHb levels proportional to duration on VV-ECMO. In this population where adequate oxygen delivery is often marginal, clinicians should be wary of the reliability of continuous pulse oximetry to assess oxygenation.

Contemporary Use of Veno-Arterial Extracorporeal Membrane Oxygenation for Refractory Cardiogenic Shock in Acute Coronary Syndrome.

BACKGROUND: Refractory cardiogenic shock (RCS) in acute myocardial infarction (AMI) is associated with high rates of mortality. Smaller ventricular assist devices, such as the intraaortic balloon pump, provide limited support. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) offers more robust mechanical ventricular support, but is not widely utilized by interventional cardiologists. This study aimed to evaluate the patient characteristics and outcomes of VA-ECMO with RCS in the setting of AMI. METHODS AND RESULTS: A retrospective chart review of all VA-ECMO cannulations between 2009 and 2014 was performed, and patients with an indication of RCS in AMI were identified. A total of 15 patients underwent VA-ECMO placement for AMI with RCS. One-third of these patients presented with out-of-hospital cardiac arrest, and 60% had ST-elevation myocardial infarction. The Intraaortic balloon pump was placed in addition to VA-ECMO in 60% of patients. Median duration of VA-ECMO support was 45 hours. Successful wean off VA-ECMO was obtained in 50% of the patients, and vascular complications occurred in 53% of patients. The survival rate at discharge was 47%, and all survivors were alive at 30 days post discharge. CONCLUSION: VA-ECMO is infrequently used in patients for cardiopulmonary resuscitation in the AMI setting. When used judiciously, it has good clinical outcomes in this group of patients. However, use of VA-ECMO should be individualized based on vascular anatomy for best results. Close cooperation among interventional cardiologists, cardiovascular surgeons, cardiologists, cardiac intensivists, and perfusionists is essential for success of this therapy for RCS in AMI.

Transfusion therapy and acute lung injury.

Transfusion-related acute lung injury (TRALI) remains the deadliest complication of transfusion. Consensus definitions of TRALI have been developed but remain controversial. Recent evidence supports a strong relationship between blood transfusion and the development of acute lung injury in the critically ill and trauma population. Plasma and platelet transfusions have been the most commonly implicated blood products. The 'two hit' model may best explain the immune and nonimmune pathogenesis of TRALI. Current treatment remains largely supportive; effective measures for decreasing the incidence of TRALI include the use of predominantly male plasma and apheresis platelets. Greater understanding of the blood component and patient risk factors for TRALI will hopefully lead to novel treatment and preventive strategies for reducing the risk of this life-threatening syndrome.