I am going to be completely honest here and mention that this particular article that I’m going to be looking at today looking at hypothermia in COVID is more for entertainment purposes at this juncture rather than actual data. The paper that I am using as a citation for this post was published on 30 January in the Journal of Critical Care. It is titled “cheap and simple, could it get even cooler? Mild hypothermia and COVID-19”. As always, I recommend that you read this article for yourself and do not trust me. The citation and link to the full free article is listed below. I would like to tip my hat to the authors at this time for this very interesting article.
I have discussed this ad nauseam before but the two main issues with COVID-19 seem to be the hypercoagulable state as well as the pro inflammatory state that we commonly called the “cytokine storm”. For the hypercoagulable state there are numerous studies currently ongoing which are looking at different anticoagulant and antiplatelet strategies to attempt to mitigate poor outcomes in our COVID-19 patients. With regards to the pro-inflammatory state, we have noticed the increase in interleukin 1, interleukin 6, tumor necrosis factor alpha, and other cytokines. We measure surrogates for this in our common routine labs that include ferritin as well as C-reactive protein.
Currently, in our armamentarium for fighting Covid we have corticosteroids including dexamethasone and methylprednisolone showing a decrease in mortality in COVID-19 patients. As recently as two days ago, data from the RECOVERY group has shown that tocilizumab in conjunction with corticosteroids could also decrease mortality in COVID-19 patients. I discussed this on the podcast yesterday and also on this blog. The truth is that there may be other anti-inflammatory mechanisms such as melatonin, colchicine, vitamin C, and other therapies that could potentially synergistically work with dexamethasone and tocilizumab to help reduce mortality.
The authors in this study agree that a multifaceted approach for managing patients with COVID would likely lead to better outcomes. The issue is, however, that organizing trials that are sufficiently powered to show these outcomes are quite challenging to create with the number of patients presenting to our hospitals currently declining. I would like to add that this is a good thing. The argument made by the authors, admittedly like in data, includes the fact that they believe that mild therapeutic hypothermia could be part of this multifaceted approach that also has limited risks. To quickly define what the authors meant by mild hypothermia, they mean that the patient should stay between 34°C to 35.9°C. They feel that a target of 34°C with small fluctuations sustained for 48 hours seems reasonable.
The authors offer a multifaceted approach as to how using mild therapeutic hypothermia could help out certain components such as inflammation, the respiratory system, the cardiovascular system, renal function, hemostasis, and infections. Then they explain how hypothermia could work in COVID.
With regards to inflammation, the authors state that therapeutic hypothermia will suppress the inflammatory phenomenon. They mention the different interleukins as well as tumor necrosis factor alpha that is decreased with hypothermia while interleukin 10 is increased. To me, these all sound like favorable affects of therapeutic hypothermia in our patients.
With regards to the respiratory effects, the authors admit that most of the gains are either theoretical or experimental and so therefore we do not really know if they will work or not in practice. Amongst the benefits that they describe is a decreased metabolic rate which will decrease the PaCO2 produced by the patients. They get far more into it than I am willing to get into at this time but they discuss how the hypothermia could increase the PaO2/FiO2 ratio.
Amongst the cardiovascular improvements potentially seen with therapeutic hypothermia, the author states that myocardial contractility, systolic function, as well as blood pressure typically improve. One could see a decrease in cardiac output due to a decrease in the heart rate as well as mild diastolic dysfunction with hypothermia so we have to keep an eye on this.
The renal benefits are also hypothetical where the author state that “Therapeutic hypothermia might be capable of attenuating kidney histopathological injury in systemic inflammation…”. As we all know, COVID is very significant systemic inflammation.
One of the more interesting components of this theory of using therapeutic hypothermia includes that of improving hemostasis in these patients. I guess hemostasis is not the right word but rather getting rid of the prothrombotic state that we see in COVID-19. Hematology is honestly not one of my strong suits but we all know when we cool patients down to 33°C that they tend to be far less coagulopathic than they are at baseline. This is why we obviously do not cool brain bleeds and patients that are actively bleeding after a cardiac arrest. I do not have access to TEG at my facility but we have all seen the wonky patterns that have been described at other institutions from Covid patients. The authors postulate that it is plausible that therapeutic hypothermia “reduces deviations from hemostasis throughout the whole spectrum of coagulopathy”. They state their sources for making this claim.
The part of infections really caught my eye where the others consider that therapeutic hypothermia. To simplify in my own words what the authors wrote, and again you should definitely read what they wrote, therapeutic hypothermia should bring down IL-6 and IL-6 helps viruses replicate. So if IL-6 is decreased, then Covid virus replication should be mitigated. The authors also discuss how therapeutic hypothermia could potentially help out with secondary infections. But my question honestly is how long we keep the patient cool to prevent secondary infections? In fact, when would we even started and how long will we continue it? And the truth is how well we actually be able to prove this in a study?
My personal take on hypothermia in COVID is that it is a very cool concept which I appreciate the authors digging into. Personally, I am not going to be implementing this strategy in my practice. To be honest, after the results of several trials looking at therapeutic hypothermia in cardiac arrest patients for neurological protection, I rarely use it in my practice. I use a strategy where I implement normothermia to a temperature of 36°C and avoid fever at all costs. I guess a hybrid way of sorts to use these types of therapies in Covid patients would include utilization of cooling blankets to avoid fever as well as scheduled acetaminophen which, at the end of the day, or a good way to do multimodal analgesia for our patients who are on mechanical ventilation. Obviously, that’s not a medical recommendation and if you do use scheduled acetaminophen on your critically ill patients, you already know that you need to be cognizant of the patient’s liver function.
What do you think about using hypothermia in COVID? Do you think that this is a possible strategy that could be used in the future?
Citation:
Raul dos Reis Ururahy, Marcelo Park, Cheap and simple, could it get even cooler? Mild hypothermia and COVID-19, Journal of Critical Care, 2021,ISSN 0883-9441, https://doi.org/10.1016/j.jcrc.2021.01.009.
Link to Article
Link to FULL FREE PDF
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