Thyroid Emergencies

Hyper- and hypo-thyroidism are rarely emergencies because the hormones have a very long half-life, so clinical findings usually develop gradually. When thyroid emergencies do occur, they are usually due to an acute precipitant that derails the body’s compensation to thyroid disorders.

In the hyperthyroid state, the body’s metabolic rate and demand is increased. The body compensates by increasing cardiac output and dilating peripheral vasculature to promote heat loss and nutrient delivery.

Decompensated hyperthyroidism occurs when:

1. Metabolic demand is acutely increased beyond an already stretched supply
   • acute release of thryoid hormone (thyroid surgery, thyroiditis, radioactive iodine tx, iodinated contrast, withdrawal of thyroid tx, amiodarone)
   • trauma, surgeries
2. Supply is acutely decreased
   • hypoglycemia
   • hypovolemia (burn, sepsis, DKA)
   • MI
   • Increased SVR which decreases forward flow (adrenergic state, external cooling)
3. Cooling mechanisms are interrupted or exhausted
   • intense exercise
   • vasoconstriction (adrenergy)
   • anticholinergic medicines

Thyroid storm exists at the extreme end of the spectrum of decompensated hyperthyroidism and needs emergent aggressive treatment. Other decompensated hyperthyroidism also need treatment but rarely emergently. The diagnosis of thyroid storm is purely clinical. As you can see above, only a subset of precipitants for thyroid storm has anything to do with an acute change to the thyroid hormones themselves so cutoff levels for TSH and T4 are unreliable. I subscribe to Dr. LoPresti’s criteria for thyroid storm (need all five):

1. Hyperthyroid (by history or TSH/T4) or hypothyroidism on thyroid medications
2. Fever
3. AMS
4. Sympathomimetic
5. Precipitating event

The Burch score is, in my opinion, too cumbersome to use clinically:

The treatment for thyroid storm must be immediate, even before labs confirming or refuting hyperthyroidism have returned! Thankfully, the first doses of treatment will pose minimal harm whereas delays in treatment poses significant mortality. I was inspired to write this summary because the treatment is so counter-intuitive! So bear with me. The immediate treatment involves:

1. Supporting hemodynamics
   • Propanolol 1mg IV test dose. If tolerating, 1-2mg IV q15 min until HR <100 then start propanolol drip at load dose per hour
     • 60-80mg PO q4h
     • 3-5L LR despite the fact they have crackles or pulmonary edema on exam because this is from high output failure; don’t diurese; give fluids after heart rate improves
2. Block new thyroid hormone production
   • PTU; better for life-threatening cases because also blocks T4 to T3 conversion and shorter duration of action but is more hepatotoxic
     • AACE recommends 500mg PO load f/b 250mg q4h PO
     • Dr. Lopresti uses 150mg q8h without a load
     • uptodate recommends 200mg q4h without a load
   • Methimazole; teratogenic; better for severe but not lifethreatening because longer duration of action and less hepatotoxic
     • 20mg q6h PO
3. Block peripheral conversion; unnecessary in severe thyrotoxicosis unless life-threatening (thyroid storm)
   • Dexamethasone 4mg IV q6h
   • Hydrocortisone 300mg IV f/b 100mg q8h
   • HIDA scan oral contrast but US does not have this
4. Don’t actively cool the patient. Ice packs can cause vasoconstriction which can worsen heart failure depending on the initial insult. It can also induce shivering.
   • LA County-USC under Dr. Lopresti uses droperidol to treat hyperthermia in these patients

The subsequent treatment is to delay thyroid hormone release. Excessive iodine can produce iodolipid iodolactones in thyroid tissues which block TPO and inhibit new thyroglobulin synthesis and organification (Wolff-Chaikoff effect). It is important to wait 1 hour after giving PTU or methimazole before starting this treatment else the iodine will be incorporated into new thyroid hormone synthesis. However, before the era of PTU or methimazole, iodine-containing agents were used routinely on their own to treat thyroid storm. The providers simply need to be wary of the rebound effect (increased thyroglobulin production from downregulation of sodium iodide importer) 10 days later. I put this in a separate section because the treatments listed here should be delayed and you should therefore have time to obtain expert input.

1. Block enterohepatic circulation of thyroglobulins
   • cholestyramine 4g q6h
2. Further inhibit thyroglobulin synthesis and release
   • SSKI 5 drops PO q6h
   • Lugol’s 8 drops PO q6h
   • NaI 0.5mg IV q12h
3. Plasmapheresis

In the hypothyroid state, the body’s metabolic rate and demand is decreased. The body compensates by vasoconstricting peripheral vasculature to maintain perfusion and reduce heat loss.

Decompensated hypothyroidism occurs with vasodilation!

Myxedema coma is a giant misnomer. Few patients have myxedema in this era, which comes from long-standing untreated hypothyroidism, or comatose. I utilize the following criteria for decompensated hypothyroidism:

1. hypothyroid (lab tests, history, delayed recovery of deep tendon reflexes, dry skin)
2. low central temperature
3. signs of left forward heart failure (oliguria, depressed mental status, cool extr)
4. precipitating event (infection)

The treatment is thyroid hormone but T4 vs T3 and the dose is heavily debated. T3 definitely carries more risk of cardiac arrhythmia and high output heart failure though it is more effective in severe hypothyroidism in animal studies. T4, on the other hand, is safer but thought to be less effective. One article recommends using T4 in conscious patients and T3 in unconscious patients.

1. Thyroid supplementation
   • T4 500mcg IV load f/b 100mcg IV
   • T3 10mcg IV q8h until conscious; use only in young patients with no heart disease
2. Test and treat adrenal insufficiency (Schmidt’s syndrome) until test results return
   • 100mg hydrocortisone q8h
3. Passive, not active, rewarming. Expect to see 24h before successful rewarming.
4. Lean hard on fluids. Pressors might make things worse.