• 40 years old Pakistani man
• Referred from Quriat hospital with 7 days h/o
lt sided body weakness and slurred speech
and 1 day h/o fever , confusion and
• 5 days prior to presentation he was seen in
private clinic and he was prescribed aspirin
• He had GTC convulsion the night before
• Past history:
• Drug history:
• Family history:
• Occupational history
• Travel history:
• Social history
Head & Neck:
RESP: clear, no added sounds
CVS: 140/mit, irregular pulse, s1s2, no murmur
ABD: soft, no mass palpable, no tenderness, BS+
CNS: uncooperative for detailed examination.
He Looks drowsy.
No neck stiffness
Power: lt side 4/5, rt side : normal
Pupils: equal and reactive.
MSKS; nad, no dvt or pedal edema
Skin: warm to touch,
• Chest x-ray: looks normal
• Ct head: normal
• Echo: Mildly dilated LV with global hypokinesia
with severe LV dysfunction ( EF=30%) , small
soft thrombus in LA extending from LAA, Mild
MR, no Pericardial effusion.
Impression: cardiomyopathy with LA clot.
Treatment in ED
• In Quriat:
Phenrgan 25 mg , Diazepam 10 mg,
Adenosine , inderal.
• In ED:
IVF: NS 500 ml
Paracetamol 1 gm
Diltiazem 12.5 mg iv slowly
Ceftrixone 2 gm IV
Rare live- threatening exacerbation of hyperthyroidism
life-threatening decompensation of poorly controlled, untreated,
or unrecognized thyrotoxicosis
• Common in female, 2 % of thyrotoxic patients , occurs
predominately in Graves’ disease.
• Mortality : 20 % ( if aggressively treated)
• Clinical diagnosis.
• Patients typically appear markedly hypermetabolic with high fevers,
tachycardia, nausea and vomiting, tremulousness, agitation, and
• Late in the progression of disease patients may become stuporous
or comatose with hypotension
• Increase in catecholamine-binding sites+ acute stress
• In conjunction with high levels of free T4 and T3.
• Hormone levels in thyroid storm are not generally
distinguishable from poorly controlled thyrotoxicosis.
• Generally the case except in hyperthyroid patient with
sudden cessation of antithyroid drugs and blunt or
penetrating trauma to the thyroid gland in which
hormone leaks from injured acini, rapid rises in T4 and T3
• Often Dramatic
• Many findings of thyrotoxicosis are evident on exam
but certain features distinguish thyroid storm.
• Distinguished from thyrotoxicosis by the presence :
1- fever up to 40- 41 degree
2-marked tachycardia ( up to 150/min)
3-central nervous system dysfunction
4- gastrointestinal symptoms(Severe nausea,
vomiting, or diarrhea, and hepatic failure with
5-Decompensation of one or more organ systems,
such as shock or heart failure
• Altered mental status is a hallmark of thyroid
storm, ranging from restlessness and agitation to
delirium, psychosis, seizures, and coma.
• Gastrointestinal symptoms are often pronounced
and can lead to dehydration and hypotention
• Abdominal pain can mimic bowel obstruction.
• An unusual complication of severe thyrotoxicosis
is cholestatic jaundice, which carries a bad
prognosis if hepatic failure ensues
Diagnostic criteria of thyroid storm
A score of 45 or more is highly suggestive of
thyroid storm; a score of 25 to 44 supports the
diagnosis; and a score below 25 makes thyroid
PRECIPITANTS OF THYROID STORM
• Infection/sepsis • Iodine-131 therapy
• Cerebral vascular accident • Premature withdrawal of antithyroid
• Myocardial infarction therapy
• Congestive heart failure • Ingestion of thyroid hormone
• Pulmonary embolism • Iodinated contrast agents
• Visceral infarction • Amiodarone therapy
• Emotional stress • Iodine ingestion
• Acute manic crisis • Anesthesia induction
Trauma • Miscellaneous drugs (chemotherapy,
• Thyroid surgery pseudoephedrine, organophosphates,
• Nonthyroid surgery Pregnancy-Related
• Blunt and penetrating trauma to the • Toxemia of pregnancy
• Vigorous palpation of the thyroid gland • Hyperemesis gravidarum
• Burns • Parturition and the immediate
• Diabetic ketoacidosis
• Hyperosmolar nonketotic coma
Aspirin can increase serum free T4 and T3 concentrations by
interfering with protein binding
Can occur without any obvious precipitating factors in pt
with long-standing untreated hyperthyroidism
• In elders, the hyperadrenergic features of
thyrotoxicosis may be masked, facial muscles may lack
expression, and mental status may be depressed
leading to the syndrome of apathetic hyperthyroidism.
Patients with multinodular goiters and those older than
70 are most likely to present in this manner. New-onset
atrial fibrillation and congestive heart failure
exacerbations are often the presenting symptoms of
apathetic hyperthyroidism. In addition, elders with
thyrotoxicosis may have significant weight loss without
increased appetite, suggestive of occult cancer
• Free T4 and free T3 elevation with TSH suppression .
• Hyperglycemia : common, 50 % of patients,
( related to glycogenolysis and catecholamine-mediated
antagonism of insulin)
• Bone: Mild hypercalcemia is seen in 10% of patients
(hormone-mediated bone resorption, osteoporosis )
• LFT: mild increases in serum AST, ALT, bilirubin, and,
most commonly ALP .
• CBC: leukocytosis with a left shift, a mild normocytic
3-Treatment of underlying precipitating factors
• The same principles of treatment are more often
applied to patients with severe hyperthyroidism
who do not fully meet the criteria for thyroid
General Supportive Measures
• critical to final outcome
• Aggressive Volume resuscitation and replacement of
glycogen stores(D5/0.9NS 125–1000 mL/hr depending
on volume status and CHF)
• Some pts may require diuresis because of congestive
• Tylenol with caution( hepatic dysfunction) , avoid
aspirin and NSAID.
• Cooling blanket, fans, ice packs, ice lavage
• Benzodiazepines for agitation and hypomania
• Avoid interventions that may increase thyroid
hormone levels or accentuate adrenergic stimuli .
iodinated contrast media or amiodarone, both of
which present an iodine load that may enhance
thyroid hormone production.
aspirin and NSAIDS( interfere with protein
binding of thyroid hormone, leading to increases
in free T4 and T3.)
Drugs such as pseudoephedrine, ketamine, and
albuterol that increase sympathomimetic.
• Consists of multiple medications each of which has a
different mechanism of action:
1-A beta-blocker to control the symptoms induced by
increased adrenergic tone.
2-A thionamide, such as methimazole , to block new hormone
3-An iodinated radiocontrast agent (if available) to inhibit the
peripheral conversion of T4 to T3.
4-An iodine solution to block the release of thyroid hormone.
5- Glucocorticoids: to reduce T4-to-T3 conversion and possibly
treat the autoimmune process in Graves' disease.
• Important aspect in treatment
• Block the peripheral hyperadrenergic activity
• Propranolol : drug of choice [ it also blocks
conversion of T4 to T3]
• Used with caution if the patient has
congestive heart failure or other
contraindications to beta-blockade.
• However , that control of tachycardia may
lead to improvement in cardiac function.
PO: 60−80 mg PO every 6 hr or
IV: 1.0 mg IV slow push test dose, then repeat
q15 min to desired effect ( up to 5 mg) then 2–
3 mg every 3 hr
• Metoprolol 50 mg PO every 6 to 12 hr
• Esmolol :250–500 µg/kg bolus, then 50–
100 µg/kg/min infusion
• Strict contraindication to beta-blocker: reserpine
0.5 mg PO every 6 hr
• Propylthiouracil, methimazole, carbimazole.
• Block de novo thyroid hormone synthesis within 1-2 hours.
• No effect on the release of preformed hormone.
• Some consider PTU the drug of choice in thyroid storm,
because PTU blocks T4-to-T3 conversion in the periphery.
• However, we prefer methimazole as long as other drugs
(such as iopanoic acid) are coadministered to block T4-to-
• Methimazole has a longer duration of action( 4h) than
PTU(75 min) and is therefore more effective unless PTU is
given at regular frequent intervals.
• Since thionamide therapy may be interrupted, even in an
ICU, we prefer to use the longer-acting drug
• High dose.
• Can be given PO , PR, IV
• IV route should be considered only IF oral or rectal
administration is not feasible or ineffective
• Propylthiouracil: 600–1000 mg loading dose, then 200–
250 mg every 4 hr
• Methimazole 20–25 mg initially, then 20–25 mg every 4 hr
• No READY MADE IV preparation .
• PTU can be prepared for IV administration by dissolving the
tablets in isotonic saline made alkaline (pH 9.25) with
• Methimazole can be dissolved in pH-neutral isotonic saline
and prepared for intravenous administration by filtering
through a Millipore filter and and given 30 mg every 6 hr
Iodinated radiocontrast agents
• Iopanoic acid and other iodinated radiocontrast agents
used for oral cholecystography have been used to treat
• Little published data on their efficacy in thyroid storm.
• Potent inhibitors of T4-to-T3 conversion.
• extremely useful in treating severe hyperthyroidism or
in preparing hyperthyroid patients for urgent surgery
• In severe hyperthyroidism : 0.5 to 1 g given OD.
• Given 1-2 h after thionamide
• Blocks the release of T4 and T3 from the
• higher than usual dose.
• Given 1-2 after thionamide
• It has been suggested that 10 drops of Lugol's
solution can be directly added to intravenous
fluids since it is sterile .
• Doses and routes:
Saturated solution of potassium iodide (SSKI)
5 gtt by mouth, NG, or PR every 6 hr
Lugol's solution 8 gtt by mouth, NG, or PR
every 6 hr
Sodium Iodide 500 mg in solution prepared by
pharmacy IV every 12 hr
1. Reduce T4-to-T3 conversion ( main action)
2. It also block the hormone release.
3. Relative adrenal insufficiency that can occur in thyroid storm
4. May have a direct effect on the underlying autoimmune process if
the thyroid storm is due to Graves' disease.
• It improves outcome .
• Hydrocortisone 300 mg IV, followed by 100 mg every 6 hr
• Dexamethasone 2–4 mg IV every 6 hr
• Not routinely use in patients with severe, but not life-threatening,
• Lithium has also been given to acutely block the release of
• its renal and neurologic toxicity limit its utility.
• Used if the patient is allergic to iodine,
• lithium carbonate 300 mg by mouth or NG every 6 hr
• Cholestyramine, an anion exchange resin, binds thyroid
hormone in the bowel lumen, thus interrupting
• L-Carnitine has been described in thyroid storm, its
suggested mechanism being the inhibition of thyroid
hormone entry into cell nuclei
• Plasmapheresis, plasma exchange, or dialysis has been
tried when traditional therapy has not been successful
Congestive Heart failure.
If rate-related, high-output failure
• Beta-blockade is first-line therapy
• ACEI, digoxin, diuretics as needed
If depressed EF
• Avoid beta-blocker or 1/4 dose
• ACEI if BP adequate
• Digoxin and furosemide as needed
• Beta-blocker preferred for rate control.
• Calcium channel blockers: can cause
hypotension; diltiazem 10-mg test dose. Avoid
• Digoxin less effective but may be tried
• Amiodarone should be avoided due to iodine
• Refractory to conversion to sinus unless euthyroid
Identifying and Treating the
• CXR, urinalysis, and blood cultures
• ECG and troponin