Cheap and simple, could it get even cooler? Mild hypothermia and COVID-19

Autor: Marcelo Park, Raul dos Reis Ururahy
Rok vydání: 2020
Předmět:
medicine.medical_specialty
Central nervous system
PaCO2
CO2 partial pressure

Lung injury
Critical Care and Intensive Care Medicine
Cytokine storm
HF
heart failure

Article
03 medical and health sciences
0302 clinical medicine
Immune system
PaO2
O2 partial pressure

Hypothermia
Induced

Internal medicine
BALF
bronchoalveolar lavage fluid

Coagulopathy
Medicine
Humans
Respiratory system
ARDS
acute respiratory distress syndrome

PIP
peak inspiratory pressure

P/F
arterial O2 partial pressure/fractional inspired oxygen ratio

HR
heart rate

business.industry
SARS CoV2
Interleukin-6
SARS-CoV-2
Tumor Necrosis Factor-alpha
Mild therapeutic hypothermia
COVID-19
030208 emergency & critical care medicine
Hypothermia
A-aO2
alveolar-arterial O2 tension difference

medicine.disease
IL
interleukin

TNF-α
tumor necrosis factor- α

medicine.anatomical_structure
STEMI
ST-elevation myocardial infarction

030228 respiratory system
PMNs
polymorphonuclear leukocytes

Cardiology
IS
infarct size

Tumor necrosis factor alpha
medicine.symptom
business
Cooling
Cytokine Release Syndrome
Interleukin-1
Zdroj: Journal of Critical Care
ISSN: 1557-8615
Popis: Purpose The pathophysiology theories of COVID-19 attach the injury of target organs to faulty immune responses and occasionally hyper-inflammation. The damage frequently extends beyond the respiratory system, accompanying cardiovascular, renal, central nervous system, and/or coagulation derangements. Tumor necrosis factor-α (TNF-α) and interleukins (IL)-1 and − 6 suppression may improve outcomes, as experimentally shown. Targeted therapies have been proposed, but mild therapeutic hypothermia—a more multifaceted approach—could be suitable. Findings According to evidence derived from previous applications, therapeutic hypothermia diminishes the release of IL-1, IL-6, and TNF-α in serum and at the tissue level. PaCO2 is reduced and the PaO2/FiO2 ratio is increased, possibly lasting after rewarming. Cooling might mitigate both ventilator and infectious-induced lung injury, and suppress microthrombi development, enhancing V/Q mismatch. Improvements in microhemodynamics and tissue O2 diffusion, along with the ischemia-tolerance heightening of tissues, could be reached. Arrhythmia incidence diminishes. Moreover, hypothermia may address the coagulopathy, promoting normalization of both hypo- and hyper-coagulability patterns, which are apparently sustained after a return to normothermia. Conclusions As per prior therapeutic hypothermia literature, the benefits regarding inflammatory response and organic damage might be seen. Following the safety-cornerstones of the technique, the overall infection rate and infection-related mortality are not expected to rise, and increased viral replication does not seem to be a concern. Therefore, the possibility of a low cost and widely available therapy being capable of improving COVID-19 outcomes deserves further study.
Databáze: OpenAIRE