POTD. Myxedema Coma.

A nice week of spring fling came and went. in honor of the return of the cold. lets have a discu-shin about an uncommon, but deadly cause of hypothyroidism - myxedema coma

  • Why do I care?

    • because mortality rates in treated MC approach 60%

      • if missed and untreated, mortality approaches 100%

  • How does it present?

    • Severe hypothyroidism --> everything slows down. hypothermia and decreased mental status are hallmarks, other common signs are hypotension, bradycardia, hyponatremia, hypoventilation, and hypoglycemia. 

      • interestingly, it is aka myxedema madness - as sometimes patients present with psychosis. 

      • due to its rarity it can be a confusing Ddx - think of a patient with multiple failing organs whose lethargic, hypotensive, and hypothermic

      • ddx include sepsis, CHF, tox, adrenal crisis

      • to make things more complicated, myxedema coma usually occurs in a patient with hypothyroidism as a result of a precipitant

      • any systemic insult can push a patient in to myxedema (overdose, CHF, CVA, sepsis, trauma, etc.)

  • so youre saying the differential diagnosis can actually be the cause?

    • YES I AM

  • So how will i recognize it????

    • You'll send a thyroid panel to the lab

    • and you'll realize that your standard treatments for whatever else may be present just are not working as well as you'd expect them to. 

      • BP will not respond to pressors as well you'd expect. 

  • How do I treat it?

    • controversial. most agree to adminster both T3 and T4 (levothyroxine)

      • T4: 4mcg/kg IV

        • followed by 75-100 mcg daily IV until patient tolerates PO

      • T3: 10mcg IV

        • followed by 2.5-10 mcg IV daily

    • concomitant adrenal insufficicnecy may be present

      • administer hydrocortisone 100 IV q8

  • where should i send this patient?

    • to the MICU. and get your endocrinologists involved. 

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Thyroid storm



Thyroid Storm

 

mask thyroid.gif

 

Background

 

Thyroid storm is a rare yet mortality rates reported between 10-30%

It is often presents in patients (pts) with established hyperthyroid disease (Graves' disease, toxic multinodular goiter, solitary toxic adenoma)

 

Precipitating Factors: Trauma, infection, DKA, CVA, PE, MI, etc.

 

Presentation and Diagnosis

 

Thyroid storm is a clinical diagnosis of a severe and exaggerated form of thyrotoxicosis.  

Look for a triad:

Extreme Fever (often >104F)

Tachycardia (can be accompanied with AFib, widened pulse pressure)

Altered Mental Status



Other findings:

Tremor

Lid Lag

Proptosis/Periorbital Edema

Pretibial plaques/nodules/non-pitting edema

Goiter/Thyroid Nodules

 

 

Labs:

low TSH and high free T4 and/or T3 concentrations

mild hyperglycemia, mild hypercalcemia, abnormal liver function tests, leukocytosis, or leukopenia

 

 

Management

 

Supportive Care

Fever: Cooling measures and antipyretics. 

Agitation: Benzodiazepines 

Vascular instability: IV fluids

 

Beta Blockers:

β blockade is critical in the management of the peripheral actions of increased thyroid hormone.

Propranolol 0.5-1mg IV over 10 mins followed by redosing 1-3mg every few hours OR 60-80mg PO q4h

Alternative metoprolol, esmolol or atenolol 



Thionamides - Inhibit New Synthesis by blocking T4-to-T3 conversion

PTU for the acute treatment of life-threatening thyroid storm -

Propylthiouracil (PTU) 600-1000mg PO loading dose with 200-400mg PO q6-8h, Hepatotoxic

Methimazole for severe, but not life-threatening for a longer duration of action 

Methimazole 20-25mg PO q4-6h - longer half-life compared to PTU.



Iodines - blocks the release of pre-stored hormone, and decreases follicular transport and oxidation.

SSKI 5 drops PO q6h or Lugol’s Solution 4-8 drops PO q6-8h

Works through “Wolff-Chaikoff effect,” in which high levels of iodide will inhibit T3/T4 synthesis and release

Give AFTER antithyroid drugs, no sooner than 30-60 mins following PTU/Methimazole.

Lithium 300mg PO q6-8h - for iodine allergy or contraindication to iodine usage 

 

Other therapies to consider: 

Steroids (Inhibit Peripheral Conversion) Hydrocortisone 300mg IVx1 and then 100mg IV q8h or Dexamethasone 2-4mg IV q6h

Cholestyramine (4 g orally four times daily) - bile acid sequestrants to reduce enterohepatic circulation of thyroid hormone

Plasmapheresis: Offers temporary stabilization for a patient that has been unresponsive to antithyroid medications



References: EMDocs, UpToDate




POTD: Alcoholic Ketoacidosis

Today’s topic will be for the people who used this 3-day weekend for a bender:

Alcohol Ketoacidosis (AKA)

Clinical Scenario:

Someone who has been on a bender and shows up to your ED after two days of vomiting, has a low bicarb, elevated anion gap, elevated lactate, urine ketones, and an elevated BHB level...probably has AKA. 

Background

  • Alcoholic ketoacidosis (AKA) is a starvation state in an alcoholic or binge drinker

  • Alcohol + No Food + Dehydration = AKA

  • Most often associated with acute cessation of alcohol consumption after chronic alcohol abuse

  • Can also be associated with first-time alcohol binge

  • one of the causes of anion-gap metabolic acidosis 

Clinical Features

  • episode of heavy drinking followed by vomiting and an acute decrease in alcohol consumption

  • N/V, nonspecific abdominal pain

  • can have associated gastritis or pancreatitis

  • normal mental status, but if patient is altered, look for toxic alcohol ingestion, postictal states from withdrawal seizures, or occult head injury

  • exam with acetone odor on breath

  • tachypnea (Kussmaul respiration), tachycardia, and signs of dehydration

Pathophysiology

ethanol metabolism.png

Nicotinamide adenine dinucleotide (NAD, or “Needs Additional Dextrose”) is depleted by ethanol metabolism, leading to inhibition of the Kreb’s cycle (or aerobic metabolism) in favor of ketone formation, depletion of glycogen stores, and suppression of insulin secretion  

Diagnosis

  • low, normal, or slightly elevated glucose

  • binge-drinking that ends in N/V and decreased intake

  • wide AG metabolic acidosis, especially one without an alternative diagnosis

  • (+) serum ketones

  • can have associated hypophosphatemia, hyponatremia, and hypokalemia

Treatment

  • Sugar and water!

  • Glucose stimulates insulin production, which stops lipolysis and halts further ketone formation. Glucose also increases oxidation of NADH to NAD, thereby further stopping ketone production. 

  • Start with 5% dextrose in NS. Once fluid and electrolyte losses are replaced, change fluids to 5% dextrose in 1/2 NS until oral intake is assured.

  • Give 100 mg thiamine (facilitates Krebs cycle)

  • Correct electrolytes

  • Repeat Chem7 to see if bicarb improving. If it’s not, consider ethylene glycol or methanol poisoning. This is the time for fomepizole and a call to your local toxicologist or poison center!

Disposition

Discharge if tolerating PO!

References

https://emcrit.org/toxhound/aka-aka/

https://lifeinthefastlane.com/ccc/alcoholic-ketoacidosis/

Tintanelli’s

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