Identify precipitant (i.e. med noncompliance, DKA, infection).
When in doubt of diagnosis, the EP should treat given the high mortality rate, as a few doses of anti-thyroid medication are unlikely to harm euthyroid patient
Do not aggressively cool as this can lead to vasoconstriction
Careful cooling measures (ice packs & cooling blankets)
Acetaminophen (avoid aspirin or NSAIDS because they displace<unk>  hormone from TBG)
D5NS (most patients have depleted glycogen<unk> s)
Crackles in lungs are likely high output heart failure, NOT fluid overload
Rate control, inotropes, diuretics as needed (short acting always better)
Benzodiazepines are the preferred agent
Propranolol PO 60-80 mg q4hr (if can tolerate PO, no PR form)
Propranolol IV 1-2mg over 10 min; if tolerates then 1-2mg boluses q15 minutes until HR <100
Followed by drip at dose required for heart rate control (3-5mg/hr)
Relative contraindications are same as for other medical conditions (e.g. CHF, Reactive Airway Disease, see alternative therapies)
In addition to decreasing peripheral conversion, propranolol will improve tremor, hyperpyrexia, and agitation
Unlike other beta-blockers, propranolol also partially blocks conversion of T4 to T3
Followed by drip at dose required for heart rate control (3-5mg/hr)
Relative contraindications are same as for other medical conditions (e.g. CHF, Reactive Airway Disease, see alternative therapies)
In addition to decreasing peripheral conversion, propranolol will improve tremor, hyperpyrexia, and agitation
Unlike other beta-blockers, propranolol also partially blocks conversion of T4 to T3
Esmolol 250-500mcg/kg loading dose, then 50-100mcg/kg/min
B1 selective so can be used with active CHF, asthma, etc
Does not have T4 to T3 blocking properties of propranolol
B1 selective so can be used with active CHF, asthma, etc
Does not have T4 to T3 blocking properties of propranolol
Reserpine 2.5 - 5 mg IM q4h
Option for patients in whom beta-blockers are contraindicated 
Option for patients in whom beta-blockers are contraindicated 
Thionamides are the main class of medications which prevent new hormone synthesis by inhibiting the iodination of tyrosine residues by<unk>  peroxidase (TPO) enzymes. Propylthiouracil (PTU) is prefered over methimazole because it will also bock T4→T3 conversion
May provide PR, but PO or NG are preferred routes (IV formulations not available in US)
Note black box warning of hepatotoxicity so check LFTs prior
Avoid in patients with significant liver disease; use methimazole instead
Theoretically first line and offers advantage over methimazole
PTU has earlier onset of action and capacity to inhibit peripheral conversion of T4 to T3
However, no significant difference in mortality between PTU and methimazole
PTU has earlier onset of action and capacity to inhibit peripheral conversion of T4 to T3
However, no significant difference in mortality between PTU and methimazole
Longer acting than PTU
IV formulations may be available in Europe
Should be avoided in pregnancy by classic teaching (freely crosses placenta, birth defects)
Available in IV formulations outside America, but use supported by case reports only 
Give 1hr after PTU or methimazole to prevent increased hormone production (Jod-Basedow effect)
Block hormone release: (Wolff-Chaikoff effect) only after hormone synthesis is inhibited. Iodine concentration leads to transient decrease of T3/T4
5 drops (0.25 mL or 250mg) orally every 6 hours
Avoid potassium iodide if patient is on amiodarone
Can substitute radiocontrast dyes (Iopanoic acid, ipodate and iopanoate), PO Lugol solution, OR IV sodium iodide 
Consider if iodine allergic
Lithium carbonate 300mg PO q8hr
Lithium inhibits<unk>  hormone release from the gland and reduces iodination of tyrosine residues, but its use is complicated by the toxicity that can ensue
Treatment of choice for iodine-induced hyperthyroidism as the result of contrast load or amiodarone
Inhibits enterohepatic circulation of<unk>  hormone by binding to conjugated products and promote excretion
Often there may be associated adrenal insufficiency (also blocks T4>T3)
Hydrocortisone 300mg IV bolus, followed by 100mg TID for several days OR
Dexamethasone 4mg IV q6hr
Note that corticosteroids also inhibit conversion of T4 to T3 and block release of hormone from<unk>  gland
For recalcitrant<unk> , with remaining cardiac and neurologic symptoms
Especially in the case of fulminant liver failure, in which anti-thyroid drugs are contraindicated
Repeat sessions until TFTs normalize
Removes cytokines, auto-antibodies,<unk>  hormones,<unk>  hormone bound proteins
Second most common etiology of<unk>  (after medication noncompliance) is infection 
Low threshold to start broad spectrum antibiotics
Consider L-Carnitine (1 g PO q 12h) - blocks T3 & T4 entry into cell nuclei peripherally 
Consider Cholestyramine (4g PO q 6h) - decreases GI hormone recycling
Thyroid storm
Sympathomimetic ingestion
Adrenal crisis
Atherosclerosis
Cushing's syndrome
Aortic regurgitation
Diabetic ketoacidosis
Thyrotoxicosis