disseminated intravascular coagulation

So I think about... bleeding around the heart causing effusion and tamponade think about tension pneumothorax if you're bleeding into your chest wall or into your chest cavity and you can't expand your lungs then we think about hypoxemia could be from the bleeding into your chest and you can't expand your lungs could also just be from pulmonary injury or airway obstruction tracheal trauma that sort of thing Then we think about closed head injury, if you're having trouble breathing or moving air because the brain's having trouble making that communication, either through direct traumatic injury to the brain or through some nervous system issue that you've sustained.

And then one that we think about less often but is also I think equally as important is DIC, which is disseminated intravascular coagulation, which is where Um, you wind up losing clotting factors and becoming, um, hypocagable and then start bleeding and then you're back to square one.

So those are just the five trauma killers that we came up way back when we brainstormed.

There's obviously other things that can be deadly in trauma, but if we're thinking about hemorrhagic shock, obstructive shock, hypoxemia, high C-spine injury, closed head injury, and traumatic brain injury, and then sort of that subacute DIC, that gives us a pretty good mindset framework to start those patients in the field.

We have to think about tourniquet.

We have to think about our resuscitation, TXA, make sure that we've got oxygenation and ventilation, making sure that we're not hypoxic or hypotensive with traumatic brain injury.

We know that's going to increase our mortality.

So it gives us a good framework with which to base our exam, our history, our approach in the truck, even simple things like warming the back of the truck and keeping our patient warm when we, you know, you may say DIC, that doesn't hit us in the truck.

Platelets are the cells responsible for the initial plug when a blood vessel is damaged.

When they drop that fast in sepsis, we immediately fear DIC, disseminated intravascular coagulation.

DIC is a catastrophic complication.

The intense cytokine storm activates the coagulation cascade inappropriately, causing millions of microscopic blood clots to form in the tiny capillaries all over the body.

These microclots consume all of the body's platelets and clotting factors.

It's clotting to death and bleeding to death at the exact same time.

But his labs show his fibrinogen is incredibly high at 605.

How does that rule out DIC?

The first one is to look at bleeding or clotting disorders.

If a patient has unexplained bleeding, low fibrinogen could point to conditions like disseminated intravascular coagulation or congenital afibrinogenemia.

Secondarily, monitoring of DIC is important for laboratories to help clinicians.

Fibrinogen levels often drop in conceptive coagulopathies.

It's a part of DIC panels alongside PT, APTT, a platelet count, and D-dimer.

Liver assessment is also important.

Since fibrinogen is synthesized in the liver, low levels can reflect hepatic synthetic dysfunction.

Driven by analyzers that have lower maintenance and user-friendly interfaces, matching the U.S. market standards, trend towards the near-home model for healthcare needs.

concept of what's going on and thank goodness because that would have been so much more traumatic if I had been like oh I'm like really hemorrhaging you know it was it was like in that moment yeah I'm like

actively dying and meanwhile you're like I'm good just like developing DIC but like NPD

exactly so I don't know thank goodness for those those uh you know high ammonia levels keeping me feeling like that.

So my husband, and so really this is like, his trauma is really kicking in here because he's like, I just remember the hospitalist who is there now dealing with this hemorrhage because my OB had gone home because again, she wasn't working.

He's like, her white coat just had blood up to the elbow.

He's like, she was like, covered in your blood she had her arm up you know all the way inside of you and and he's like I just knew like this is not normal obviously um and so they did some labs and and they're giving me all the things and they're like you know she's in DIC um we need to take her to the ICU so Somehow throughout all this, the only thing I remember, other than just occasionally saying, I'm fine, was I remember when this doctor told me, she was like, Amber, we're going to take you to the ICU.

And I distinctly remember... like waking up to hear that and then just being like, fuck, and then going back to sleep.

Like I was like, that's not good.

Option C, pure red cell aplasia.

Option D, sepsis with DIC.

And option E, thrombotic thrombocytopenic purpura.

The question is asking about common complications of CLL.

Hypogammaglobulinemia is common and can be associated with significant risk for infections, primarily of mucocutaneous etiologies such as sinusitis and bronchitis.

In addition, women can have frequent urinary tract infections.

So these patients are at risk of sepsis and DIC, as mentioned in option D.

Yeah, but I don't think that's the answer here.

Because after the amniotic fluid embolism, I started to bleed uncontrollably.

And I went into what's called DIC, which is disseminated intravascular coagulation, which is where you bleed uncontrollably.

Your body forgets how to clot.

the blood.

Very frequent that I hear people using the term disseminated intravascular coagulopathy, and I'm not sure that we're using it correctly.

So number one, sorry, going on a tangent, but number one, can you talk about what's the real definition of that? And is acute obstetric coagulopathy a distinct form of DIC or is it its own entity? How can we sort of make sense of

all of this?

Yeah.

That's not what's happening in obstetric coagulopathy.

Not in the early days.

If you've lost control and you can't keep up with blood loss and the patient gets hypoxic, the hypoxia will stimulate a DIC.

But to start with, with somebody who's really, really bleeding out, you get massive activation of fibrinolysis and it will... break down all of the fibrinogen, fibrin, factor V, and the clots that have formed where you want them to locally in the uterus.

It's devastating.

This inflammation damages the lining of blood vessels throughout the entire body, which triggers the final, often lethal stage, DIC, or disseminated intravascular coagulation.

Disseminated intravascular coagulation.

Just the name sounds terrifying.

Yes.

And what does that lead to?

It often leads to DIC, or disseminated intravascular coagulation.

DIC.

Arrhythmia may occur due to hyperkalemia, hypercapnia, acidosis and sympathetic surge.

Disseminated intravascular coagulation, DIC, occurs in response to hypothermia and rhabdomyolysis.

The myoglobin released from damaged muscle effectively blocks the kidneys, so acute kidney injury and subsequent renal failure may occur.

Genetically, most MH is caused by mutations in the RYR1 gene encoding for the ryanidine receptor, but a small proportion, approximately 1%, are due to problems with the dihydropyridine receptor.

Interestingly, it's not always revealed during a patient's first anaesthetic.

What do we see? The cardinal features of MH are tachycardia, rise in ETCO2 and rise in temperature with rigidity following exposure to a triggering agent.

Progression to acidosis, hyperkalemia, hypoxia, arrhythmia and DIC ensues.

That being said, a rise in temperature can be a late sign.