Cannula associated deep vein thromboses in COVID-19 patients supported with VV ECMO.

BACKGROUND: VV ECMO is increasingly used as a rescue strategy for hypercarbic and hypoxic respiratory failure refractory to conventional management, and more than 14,000 patients with COVID-19 related respiratory failure have been supported with VV ECMO to date. One of the known complications of VV ECMO support is the development of cannula-associated deep vein thromboses (CaDVT). The purpose of this study was to identify the incidence of CaDVT in COVID-19 patients supported with VV ECMO as compared to non-COVID-19 patients. We hypothesized that due to the hypercoagulable state and longer duration of VV ECMO support required for patients with COVID-19, a higher incidence of CaDVT would be observed in these patients. METHODS: This is a single center, retrospective observational study. About 291 non-trauma adult patients who were cannulated for VV ECMO and managed at our institution from January 1, 2014 to January 10, 2022 were included. The primary outcome was the presence of CaDVT 24 h after decannulation in COVID-19 versus non-COVID-19 patients. Our secondary outcome was continued presence of DVT on follow up imaging. CaDVT were defined as venous thrombi detected at prior cannulation sites. RESULTS: Both groups had a high incidence of CaDVT. There was no significant difference in the incidence of CaDVT in COVID-19 patients compared to non-COVID-19 patients (95% vs 88%, p = 0.13). Patients with COVID-19 had an increased incidence of persistent CaDVT on repeat imaging (78% vs 56%, p = 0.03). CONCLUSION: Given the high number of post-decannulation CaDVT in both groups, routine screening should be a part of post ECMO care in both populations. Repeat venous duplex ultrasound should be performed to assess for the need for ongoing treatment given the high incidence of CaDVT that persisted on repeat duplex scans.

The emerging role for neutrophil mitochondrial metabolism in lung inflammation.

Recent advances shed light on the importance of mitochondrial metabolism in supporting essential neutrophil functions such as trafficking, NETosis, bacterial killing, and modulating inflammatory responses. Mitochondrial metabolism is now recognized to contribute to a number of lung diseases marked by neutrophilic inflammation, including bacterial pneumonia, acute lung injury, and chronic obstructive pulmonary disease. In this mini review, we provide an overview of neutrophil metabolism focusing on the role of mitochondrial programs, discuss select neutrophil effector functions that are directly influenced by mitochondrial metabolism, and present what is known about the role for mitochondrial metabolism in lung diseases marked by neutrophilic inflammation.

Effects of a single bolus of hydroxocobalamin on hemodynamics in vasodilatory shock.

PURPOSE: Hydroxocobalamin has been observed to cause transient hypertension in healthy subjects, but rigorous studies examining its efficacy are lacking. MATERIALS AND METHODS: Adults in shock who received hydroxocobalamin from 2017 to 2021 were analyzed retrospectively. Hourly hemodynamics from 24 h before and after treatment were collected, and the difference and hourly change of mean arterial pressure (MAP), systolic blood pressure (SBP), diastolic blood pressure (DBP), and norepinephrine-equivalent dose (NED) were examined in mixed-effects models. RESULTS: This study included 3992 hemodynamic data points from 35 patients and is the largest case series to date. In the mixed effects model, there was no difference in MAP 24-h after hydroxocobalamin administration (estimated fixed effect [EFE] -0.2 mmHg, p = 0.89). A two-piecewise mixed model found that the hourly change in MAP was not different from zero in either the pre-administration (EFE 0.0 mmHg/h, p = 0.80) or post-administration segments (EFE 0.0 mmHg/h, p = 0.55). Analysis of the SBP, DBP, and NED also found similar insignificant results. CONCLUSIONS: Although hydroxocobalamin has been observed to cause hypertension in healthy subjects, our results suggest that in patients with shock, hydroxocobalamin may not be effective in improving hemodynamics at 24 h after administration.

Acute Limb Ischemia Caused by Inadvertent Arterial Drug Self-Injection: A Case Report.

BACKGROUND A predictable consequence of long-term injection drug use is the destruction of the native venous system; as a consequence, people who inject drugs may eventually move to injection into skin and subcutaneous tissue, wounds, muscles, and arteries. These practices put people who inject drugs at risk for injection-related soft-tissue infection, vascular damage, ischemia, and compartment syndrome, all of which have overlapping presenting symptoms. CASE REPORT A 35-year-old man who injects drugs presented with foot swelling and discoloration initially concerning for necrotizing fasciitis or compartment syndrome. After progression despite appropriate antimicrobial and surgical treatment for soft-tissue infection, he was diagnosed with arterial insufficiency and resultant distal ischemia. This diagnosis was discovered only after obtaining additional history of the patient's drug use practices. Just prior to his symptoms, he had unintentionally injected a formed thrombus into his dorsalis pedis artery. CONCLUSIONS Intra-arterial injection of drugs can cause ischemia through a variety of mechanisms, including direct vessel trauma, arterial spasm, toxicity from the drug of abuse or an adulterant, embolism of particulate matter, and as proposed here, direct injection of preformed thrombus. Medical providers should be aware of the steps of injection drug use and their associated risks so that they can ask appropriate questions to focus their differential diagnosis, increase their understanding of common or current local injection practices, and develop rapport with the patient. Patient education on safe injection techniques may also reduce the risk of serious complications.