May 23, 2020

Disclaimer: This post explores some of the pathophysiologic findings in severe SARS-CoV-2 infection. It explores possible mechanisms-based and posits theories BUT, this is not a clinical post. The hypothesis and findings here are not confirmed and extrapolation to management is unclear. Understanding of the mechanisms of COVID-19 is badly needed if we are to find treatments that may be beneficial. The leading cause of mortality in patients with COVID-19 is hypoxemic respiratory failure most frequently resulting in ARDS.  However, the mechanisms that bring patients from infection to ARDS are unknown:  is it diffuse alveolar damage (DAD), endothelial damage, or some combination of both? Although it may seem ridiculous to consider these two entities as separate, as the alveolar-capillary interface is submicrons in size, we want to know if one of these two entities is driving the injury more than the other? There have been some interesting pathological reports that have been published looking at the histopathology of COVID-19, and many more discussions about the similarities to other viral pneumonias (i.e. H1N1). A recent publication in NEJM compares the pathology of COVID-19 vs H1N1.

May 21, 2020

Background: Upper endoscopy allows for the identification of the source of bleeding as well as hemostatic treatment for actively bleeding lesions In patients with upper gastrointestinal bleeding (UGIB).  Definitive treatment with endoscopic hemostatic treatment can potentially stop bleeding in high-risk lesions and reduce further bleeding and the need for surgery. The optimal time for endoscopy to be performed is unknown.  The definition of urgent varies depending on which study you read, ranging from 2 hours up to 12 hours. Additionally, most previous studies only enrolled patients who were not hemodynamically unstable or high-risk, which is frequently what we are dealing with in the emergency department. The Glasgow-Blatchford score is a validated risk-assessment score for the prediction of clinical outcomes, including the need for intervention and risk of death.  The score ranges from 0 to 23, with higher scores indicting a higher risk of further bleeding or death. A threshold score of ≥7 has been shown to be the most accurate predictor of whether a patient will need endoscopic treatment.2 There are conflicting results regarding urgent endoscopy (within 6 hours after admission) and mortality.

May 19, 2020

While the rate of prepublications on COVID19 continue to be cranked out, we at REBEL EM have reduced our blog post production. It’s not because we’re reading less, but  we’ve reported enough on small, retrospective, observational studies that don’t tell us anything more than we already know.  At this point in time we know enough about what does and doesn’t work, so we wanted to focus on important literature that may affect practice. Going forward that will be our focus with updates in a less rapid-fire rate and more useful way to digest the information. For this COVID-19 update we have picked four papers that are we thought are worthy of mention.

May 18, 2020

Background: Getting the basics right in all illness is vital. In sepsis, this means appropriate use of antibiotics, judicious fluid resuscitation, and early identification.  Vasopressor support is also essential in the sickest sepsis patients (i.e. septic shock). Should the metabolic cocktail (thiamine, vitamin C and hydrocrotisone) be part of that initial package? We’ve previously reviewed the key articles in this area: CITRIS-ALI, VITAMINS, and the original before and after Marik trial. Now we have our next RCT, the HYVCTTSSS trial. From a pathophysiologic standpoint, Vitamin C levels are thought to be low in critically ill patients with sepsis. Vitamin C is an antioxidant that prevents vascular endothelial damage and helps maintain microvascular integrity. Additionally, it is a cofactor for catecholamine synthesis which helps maintain vascular tone and cardiac output.  Glucocorticoids have been shown to reduce time to shock relief and length of ICU stay, but not mortality. The addition of thiamine can help promote oxalate decomposition, which reduces vitamin C metabolites from depositing and crystalizing in kidneys.  While these medications are cheap, the more important question is do they improve patient-oriented outcomes? The previous literature on whether this translates to patient oriented benefits has been mostly negative thus far.

May 17, 2020

There is a lot we still do not know when it comes to COVID-19 pathophysiology. We are learning every day, and as we navigate the waters of the unknown, there are a few that boldly dare to try and understand what is happening in this disease process that may go against mainstream thinking. COVID-19 is new and therefore will require new thinking and new questions but should also be balanced with not grasping for straws and randomly doing things that could be deleterious. Below is a proposed lung injury model that may be right or could be wrong. However, the only way we can further understanding is by feedback and edits until we can get to the right answer. The purpose of this post is not to tell you what you are doing is wrong, but instead putting a model out there so that we can work on this together to find an answer. This is not a recommendation on how to treat patients, but a proposal that needs feedback and work. We felt it was a good starting place for all of us to work together to figure this thing out. Thank you to Dr. Farid Jalali, MD for putting his thoughts down on COVID-19 acute lung injury to help as a starting point.