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.

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.

The role of donor chronic alcohol abuse in the development of primary graft dysfunction in lung transplant recipients.

Primary graft dysfunction (PGD) following lung transplantation is clinically similar to the acute respiratory distress syndrome. Because alcohol abuse independently increases the incidence of acute respiratory distress syndrome in at-risk individuals, we hypothesized that donor alcohol use is correlated with an increased risk of PGD. As a pilot study, we collected alcohol use histories using a validated instrument, the Alcohol Use Disorder Identification Test questionnaire, from 74 donors and correlated these with the development of PGD in corresponding recipients. Nineteen percent (14/74) of donors were classified as heavy alcohol users, as defined by the Alcohol Use Disorder Identification Test scores≥8. In the 1st 4 days post-transplantation, similar percentages of recipients developed grade 3 PGD on at least 1 day (heavy alcohol user=29% [4/14] versus lighter alcohol user=27% [16/60]); however, recipients receiving a lung from a heavy alcohol user were more likely to have multiple and consecutive days of grade 3 PGD, especially in the 1st 48 hours post-transplant. Both median length of stay in the intensive care unit and hospital were somewhat longer in the heavy alcohol user group (9 versus 7 days and 19.5 versus 17.5 days, respectively). If these preliminary findings are validated in a multi-center study, they would have important implications not only for our understanding of the pathophysiology of PGD but also for the development of novel treatments based on the evolving evidence from experimental and clinical studies on how alcohol abuse renders the lung susceptible to acute edematous injury.

Left ventricular assist device management in the ICU.

OBJECTIVES: To review left ventricular assist device physiology, initial postoperative management, common complications, trouble shooting and management of hypotension, and other common ICU problems. DATA SOURCE: Narrative review of relevant medical literature. DATA SYNTHESIS: Left ventricular assist devices prolong the lives of patients with end-stage heart failure, and their use is increasing. Continuous-flow left ventricular assist devices have replaced first-generation pulsatile devices. These patients present unique management concerns. In the immediate postimplant period, care must be taken to support the unassisted right ventricle. Invasive monitors for blood pressure, pulmonary artery catheterization, and echocardiography are essential to optimize left ventricular assist device settings and cardiac performance. Anticoagulation is necessary to prevent devastating thrombotic and embolic complications, but bleeding is a major source of morbidity due to inherent bleeding diatheses and prescribed anticoagulants. Infection of the device can be life threatening, and all infections must be aggressively treated to avoid seeding the device. Patients are at risk of ventricular arrhythmias because of their underlying disease, as well as the placement and position of the inflow cannula. Aortic valve stenosis and insufficiency develop over time and can lead to thrombosis or heart failure. Cardiopulmonary resuscitation with chest compressions must be performed with care or not at all due to risk of dislodging the device. CONCLUSION: Intensivists are increasingly likely to encounter patients requiring mechanical circulatory support with left ventricular assist devices at various points in the trajectory of their disease, from the immediate postimplant period to subsequent admissions for complications, and at end of life. A basic understanding of left ventricular assist device physiology is essential to the safe and effective care of these patients.