Coagulopathy Puns

"HILLSBOROUGH COUNTY, Fla. — The Department of Health is investigating multiple reports of people becoming "severely ill" after smoking synthetic blends"

"These individuals displayed symptoms associated with coagulopathy, a condition where the blood's ability to clot is impaired," DOH-Hillsborough said in a press release. "While the symptoms reported have varied, most cases have had bruising, nosebleeds, bleeding gums, vomiting blood, blood in urine or stool, and heavy menstrual bleeding."

DOH-Hillsborough said if you or anyone you know exhibits symptoms after smoking spice you should call 911 immediately.

"The department is working to identify and investigate possible cases, and is coordinating with hospitals, emergency medical services, and other healthcare providers to keep an eye out for other potential patients."

There was a very similar incident also in Hillsborough Country Florida back in 2018 and brodifacoum was confirmed in samples then, however there is no information in regards to this specific incident as of yet. This new incident just occurred this week.

I have no idea why someone would use brodifacoum unless it was a mis-synth of a structurally related coumarin cannabinoid being identified/assumed as brodifacoum because it's also a coumarin.

Regardless please be aware and use extra caution and be aware of the symptoms of coagulopathy.

UPDATE: 2 people have died directly linked to this new incident with 41+ hospitalized. Reportedly spreading throughout Florida but mainly Hillsborough.

https://www.tampabay.com/news/health/2021/12/15/2-dead-41-hospitalized-in-hillsborough-from-poisonous-batch-of-spice/

I'll try this again for y'all. Little bit of background, I post this stuff on my Instagram: @fisherad1. Y'all know there is character limits, which may be why there is a bit of disconnect. I do this because I publish a lot of articles and read a lot, many in EMS or military medicine do not have the same access as I, so I try to share a little bit, given character limits. I enjoy spreading knowledge about trauma care. This is not something I have to do or an assignment. Some of your comments were useful, thank you.

Three types of coagulopathy in hemorrhagic shock.

1. Trauma Induced Coagulopathy
2. Acute Traumatic Coagulopathy
3. Iatrogenic Coagulopathy

The iatrogenic coagulopathy (lethal triad) is a combination of coagulopathy, acidosis, and hypothermia, where each is the result of and cause of the others. The lethal triad is also referred to as iatrogenic due to crystalloid administration and poor hypothermia prevention. For many years, the best defense against the lethal triad in prehospital medicine was hypothermia prevention. More recently, there has been a resurgence of using whole blood to address the coagulopathy and acidosis. The lethal triad is preventable if we treat our patients with an evidenced based approach. However, the lethal triad is only a partial cause of shock. Trauma induced coagulopathy (TIC) is the overarching theme and can happen anytime after injury.[1] Where acute traumatic coagulopathy (ATC) happens within 30 min after the injury. While the lethal triad is part of the exogenous pathway, (ATC) is an endogenous arm and far more complicated. The drivers of ATC are poorly understood by many physicians and scientists, but there are basic mechanisms that are universal.

ATC was first described in 2003 by Brohi et al. [2] They found that approximately 25% of severely injured patients presented with ATC and it could exacerbate the hemorrhage. ATC was associated with functional reductions in clot generation and clot strength, consumption of coagulation factors, systemic anticoagulation, and hyperfibrinolysis.[2,3]

Using laboratory data, ATC is defined and characterized by reduction in clot generation and strength, as well as minor prolonged clotting times—prothrombin time (PT) >18 seconds, partial activated thromboplastin time (aPTT) >60 seconds, and thrombin time (TT) >15 seconds.[2,4]

Hyperfibrino

In pathoma it mentions a similar picture to dic with some changes and something to do with decreased anti plasmin.. Can someone please explain it? I can't go back to the lectures and can't make sense of what I've noted

Thank you 😭

Publicação no link. O que acham dessa publicação?

https://onlinelibrary.wiley.com/doi/abs/10.1111/jth.14817

I'm posting on here since I couldn't find any explanation on the net or in my books, hoping maybe someone here has a logical explanation!

Why do defects in platelets predominantly manifest as superficial bleeding (petechiae, purpura, or ecchymoses), while coagulation factor defects e.g. hemophilia mainly manifest as deep bleeding in the joints / internal organs?

Is there any scientific explanation to this preponderance or is it just a take it or leave it phenomenon?

TIA !

A couple weeks ago when I was working I had a decompensated cirrhotic (EtoH) present with LLQ pain and a spontaneous (per her history) intramuscular hematoma. Stable vital signs (although on BB), Hct down 10 pts from about a month ago (37 -> 27). plts ~100, INR about 2.7 if I recall correctly, BUN wasn't crazy but she had an AKI as well (Cr of 1.6-7 I think). In my experience IR usually isn't interested taking these patients for emergently for embolization until after the coagulopathy has had a chance to get better as sometimes these spontaneously resolve.

That night I gave her 10 mg IV vit K , FFP, typed and crossed her with the expectation that her hct would drop (which it did, to 24 by 6 AM and then 19 later that day), INR had corrected (but was probably transient at that time point). I was a little surprised the day team didn't consult IR at that point, but they did take her the day after when she continued to need blood and didn't find anything to embolize.

I was wondering in your institutions how often or quickly does IR try to embolize these patients and what has been your experience. From my N of 3-4 now (across several different hospitals), I find that IR is hesitant to take them unless they fail reversal of the coagulant and when they do they often don't find any active bleeding (presumably the hematoma snowballs and starts shearing slow venous bleeders that can't be embolized is how I have had it described to me). Most of my patients who present with this end up dying (including her, unfortunately) so I wonder what I could be doing better (perhaps putting more pressure on IR to immediately take the patient that night)? Any thoughts?