preclinicalnotes

how well do you expect them to do after admission?

fortunately some guy named JH Ranson developed some criteria in 1974. (a quick google search turns up almost nothing about him, making this a rare occasion where the namesake didn’t get nearly enough fanfare. I don’t even know if it’s a him, but the 70s weren’t great on gender equality and clinical research was no exception.)

medicine is full of mnemonics and this is no exception. you’ll want to use “GA LAW and CHOBBS” here.

At admission / 0-hour:

Glucose (blood) >200 mg/dL

Age > 55 y/o

Lactate dehydrogenase (LDH) > 350 IU/L

Aspartate transaminase (AST) > 250 IU/L

WBC > 16000

At 48 hours:

Calcium (serum) < 8mg/dL

Hematocrit falls in excess of 10%

Oxygen (PaO2) < 60mmHg

BUN increase greater than 5 mg/dL (despite adequate hydration)

Base deficit > 4 mEq/L

Sequestration of fluid > 6L

Some societies alter the parameters above if the patient has gallstone pancreatitis--for our purposes (studying/entry-level clinical practice aka medical student) just stick with the criteria as written as I’m not sure the gallstone differentiation is universally accepted.

Anyway, now you have the criteria, how will they fare? What’s their prognosis?

Each criteria is worth one point.

< 2 points: 2% mortality

3-4 points: 16% mortality

5-6 points: 40% mortality

Background: In von Willebrand disease, your patient has an inherited deficiency of von Willebrand factor (vWF), an important part of clot formation. This is the most common inherited (autosomal dominant) bleeding disorder. vWF tethers platelets to damaged endothelium, and binds factor VIII to inhibit degradation by protein C (if you know the clotting cascade, you know this helps lyse clots).

Clinical vignette: Often features a post-menarche, pre-menopausal female (take stock of this general age range) with history of frequent nosebleeds and/or heavy menstruation (mucosal bleeds). Lab work will show anemia (low Hgb, Hct) and depleted factor VIII. Restoring factor VIII will fail to improve their symptoms.

Back to vasopressin: Vasopressin (and its analogues) stimulates release of vWF and factor VIII from endothelial stores, and can be given IV (obv since you can use it in a code) or intranasal. Being mindful of the primary effect of vasopressin, you must keep an eye out for hyponatremia as water retention dilutes serum ion concentrations.

At 9:20, Dr. Williams draws “chemo man.”

unless it’s in the eye…

Lipid A is the endotoxin that causes sepsis and septic shock. It does this by recruiting macrophages and granulocytes, which then increase production of pyrogens like IL-1, PGEs, and inflammatory mediators like TNF-alpha and interferon. These proteins work to induce fever (pyrogen!), hypotension, and increased vascular permeability as well as DIC and death.

This is not a toxin the bacteria actively secretes, but is released when the immune system begins destroying them.

Other relevant components of Gram negative bacteria:

The O antigen is used to classify Gram negative bacteria (as in E. coli O157:H7 outbreaks).

Heat stable exotoxin is specific to ETEC (toxogenic/Traveler’s diarrhea).

K1 capsular antigens cause neonatal meningitis.

something to look out for in boards questions and real patients.

hypoglycemia normally presents with tachycardia/palpitations, tremors, and sweating. block the beta receptors and the only overt warning sign you’re left with is sweating [still a sympathetic mechanism, but uses acetylcholine post-ganglionic instead of norepi].