Seelhammer, Troy G.

As the availability of extracorporeal membrane oxygenation (ECMO) expands, so has the need for interfacility transfer to ECMO centers. However, the impact of these transfers is unknown. We hypothesized that interfacility transfers would be associated with increased complications and mortality. This retrospective cohort study includes adult patients treated with venovenous (VV) ECMO at all four adult ECMO centers comprising our statewide registry. Complications, mortality, ECMO duration, length of stay, and disposition were compared based on cannulation at an ECMO center versus outside hospital and transferred by air versus ground after adjusting for baseline covariates/parameters. The study included 420 adult patients, 36% of whom were cannulated at an outside institution before transfer. Of these, 63% were transported by ground and the remainder by air. Risk adjusted logistic regression revealed similar odds of mortality between those cannulated at ECMO centers versus referring hospital and then transported (odds ratio [OR] = 0.77, confidence interval [CI] = 0.49–1.22). This study supports the practice of interfacility ECMO transfer.

This study described the outcomes of patients receiving topical, nebulized, endobronchial, or systemic tranexamic acid (TXA) for bleeding events while on extracorporeal membrane oxygenation (ECMO). We performed a single-center case series including adult patients >18 years old supported on either venovenous (VV) or venoarterial (VA) ECMO from January 1, 2014, to April 21, 2021. The primary outcome was hemostatic control defined as a composite of initial cessation of therapeutic interventions to mitigate bleeding or resumption of anticoagulation if previously held. Secondary outcomes included changes in transfusion requirements and lysis at 30-minute (LY30) values, venous thromboembolism (VTE) events, and seizures. In total, 47 patients were included for full analysis. There were 19 patients with surgical bleeds, 18 patients with medical bleeds, and 10 patients with multiple bleeds. Overall, initial hemostatic control was achieved in 79%, 67%, and 90% of patients, respectively. Pre- and post-TXA transfusion requirements were not significantly different (p = 0.2), although the intraindividual change in median LY30 was −5.1% compared with baseline (95% confidence interval [CI], −12.4% to −1.5%, p = 0.005). The occurrence of VTE and seizures was relatively low and similar among patient bleeding groups. Tranexamic acid provided initial hemostatic control in roughly three quarters of patients with bleeding events on ECMO and side effects were infrequent.

BACKGROUND: After hospital discharge, patients who had sepsis have increased mortality. We sought to estimate factors associated with postdischarge mortality and how they vary with time after discharge. METHODS: This was a retrospective study of hospital survivors of sepsis using time-varying Cox proportional hazard models, which produce a baseline hazard ratio (HR) and a second number (δHR) that reflects the amount by which the baseline HR changes with time. RESULTS: Of the 32,244 patients who survived sepsis at hospital discharge, 13,565 patients (42%) died (mean ± standard deviation: 1.41 ± 1.87 years) after discharge from the index hospitalization, while 18,679 patients were still alive at follow-up (4.98 ± 2.86 years). The mortality rate decreased with time after discharge: approximately 8.7% of patients died during the first month after discharge, 1.1% of patients died during the 12th month after discharge, and 0.3%% died during the 60th month; after Kaplan-Meier analysis, survival was 91% (95% confidence interval [CI], 91%–92%) at 1 month, 76% (95% CI, 76%–77%) at 1 year, 57% (95% CI, 56%–58%) at 5 years, and 48% (95% CI, 47%–48%) at 10 years after discharge. Organ dysfunction at discharge was associated with worse survival. In particular, elevated urea nitrogen at discharge (HR, 1.10 per 10 mg/dL, 95% CI, 1.08–1.12, P < .001) was associated with increased mortality, but the HR decreased with time from discharge (δHR, 0.98 per 10 mg/dL per year, 95% CI, 0.98–0.99, P < .001). Higher hemoglobin levels were associated with lower mortality (HR, 0.92 per g/dL, 95% CI, 0.91–0.93, P < .001), but this association increased with increasing time after discharge (δHR, 1.02 per g/dL per year, 95% CI, 1.01–1.02, P < .001). Older age was associated with an increased risk of mortality (HR, 1.29 per decade of age, 95% CI, 1.27–1.31, P < .001) that grew with increasing time after discharge (δHR, 1.01 per year of follow-up per decade of age, 95% CI, 1.00–1.02, P < .001). Compared to private insurances Medicaid as primary insurance was associated with an increased risk of mortality (HR, 1.17, 95% CI, 1.10–1.25, P < .001) that did not change with time after discharge. In contrast, Medicare status was initially associated with a similar risk of mortality as private insurance at discharge (HR, 1), but was associated with greater risk as time after discharge increased (δHR, 1.04 per year of follow-up, 95% CI, 1.03–1.05, P < .001). CONCLUSIONS: Acute physiologic derangements and organ dysfunction were associated with postdischarge mortality with the associations decreasing over time.

OBJECTIVES: To assess the wholistic costs of systemic anticoagulation delivery in heparin versus bivalirudin-based maintenance of adult patients supported on extracorporeal membrane oxygenation (ECMO). DESIGN: Single-center retrospective cohort study. SETTING: Large academic ECMO center. PATIENTS: Adults on ECMO receiving heparin or bivalirudin for primary maintenance systemic anticoagulation. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Electronic data were abstracted from a database maintained by our ECMO center, which transitioned to a preferred bivalirudin-based anticoagulation management in 2017. The pretransition group consisted of 126 patients (123 heparin and three bivalirudin), whereas the posttransition group included 275 patients (82 heparin and 193 bivalirudin). Drug costs were estimated using the wholesale acquisition cost, and laboratory assays costs were estimated using reimbursement fee schedules. Cost data were normalized to the duration of the ECMO run and reported in U.S. Dollar per ECMO day. Following the practice change, bivalirudin patients were less likely to receive AT supplementation (31.0 vs 12.4%; p < 0.0001) and had fewer coagulation assays ordered (6.1 vs 5.4 per ECMO day; p = 0.0004). After the transition, there was a dramatic decrease in costs related to AT assay assessments ($11.78 [interquartile range {IQR}, $9.48–$13.09] vs $1.03 [IQR, $0–$5.75]; p < 0.0001) and AT supplementation ($0 [IQR, $0–$312.82] vs $0 [IQR, $0–$0]; p < 0.0001) per ECMO day. Unadjusted survival at 28 days was higher posttransition (64.3 vs 74.9%; p = 0.0286). CONCLUSIONS: Antithrombin assays and supplementation compromise a significant proportion of heparin-based anticoagulation costs in ECMO patients and is substantially reduced when a bivalirudin-based anticoagulation strategy is deployed. A favorable association exists between the aggregate cost of administration of bivalirudin compared with heparin-based systemic anticoagulation in adults supported on ECMO driven by reductions in antithrombin activity assessments and the cost of antithrombin replacement.

Background: Patients supported on mechanical circulatory support devices experience vasodilatory hypotension due to high surface area exposure to nonbiological and non-endothelialized surfaces. Angiotensin II has been studied in general settings of vasodilatory shock, however concerns exist regarding the use of this vasopressor in patients with pre-existing cardiac failure. The objective of this study was to assess the systemic and central hemodynamic effects of angiotensin II in patients with primary cardiac or respiratory failure requiring treatment with mechanical circulatory support devices. Methods: Multicenter retrospective observational study of adults supported on a mechanical circulatory support device who received angiotensin II for vasodilatory shock. The primary outcome was the intraindividual change from baseline in mean arterial pressure (MAP) and vasopressor dosage after angiotensin II. Results: Fifty patients were included with mechanical circulatory devices that were primarily used for cardiac failure (n = 41) or respiratory failure (n = 9). At angiotensin II initiation, the norepinephrine equivalent vasopressor dosage was 0.44 (0.34, 0.64) and 0.47 (0.33, 0.73) mcg/kg/min in the cardiac and respiratory groups, respectively. In the cardiac group, MAP increased from 60 to 70 mmHg (intraindividual P < .001) in the 1 h after angiotensin II initiation and the vasopressor dosage declined by 0.04 mcg/kg/min (intraindividual P < .001). By 12 h, the vasopressor dosage declined by 0.16 mcg/kg/min ( P = .001). There were no significant changes in cardiac index or mean pulmonary artery pressure throughout the 12 h following angiotensin II. In the respiratory group, similar but nonsignificant effects at 1 h on MAP (61-81 mmHg, P = .26) and vasopressor dosage (decline by 0.13 mcg/kg/min, P = .06) were observed. Conclusions: In patients requiring mechanical circulatory support for cardiac failure, angiotensin II produced beneficial systemic hemodynamic effects without negatively impacting cardiac function or pulmonary pressures. The systemic hemodynamic effects in those with respiratory failure were nonsignificant due to limited sample size.