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eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Head & Neck Surgery
Nafisa K Kuwajerwala, MD, Staff Surgeon, Breast Oncology, William Beaumont Hospital
Gunateet Goswami, MD, Consulting Staff, Internal Medicine Associates, Mount Clemens, Michigan; Consulting Staff, Department of Cardiology, Henry
Ford Hospital; Thabet Abbarah, MD, FACS, Consulting Staff, Department of Otolaryngology, North Oakland Medical Centers; Venkata Subramanian
Kanthimathinathan, MD, Staff Physician, Department of General Surgery, Loma Linda University Medical Center; Pankaj Chaturvedi, MBBS, MS,
Associate Professor, Head and Neck Surgery, Department of Surgical Oncology, Tata Memorial Hospital, India
Updated: Sep 2, 2009
Introduction
Background
Thyroid storm is a clinical manifestation of an extreme hyperthyroid state that results in significant morbidity or disability or even death.
Previously, thyroid storm was a common complication of toxic goiter surgery during intraoperative and postoperative stages.
Preoperative control of the thyrotoxic state and use of radioiodine ablation has greatly reduced this phenomenon. Today, thyroid storm
more commonly is seen in a thyrotoxic patient with intercurrent illness or surgical emergency. Early recognition and prompt intervention
are necessary to prevail in management of this phenomenon.
Frequency
International
Presently, incidence is less than 10% among patients hospitalized for thyrotoxicosis.
Mortality/Morbidity
Although methods of diagnosis and management have improved considerably, reported mortality still is 20-30%.
Although it can develop in toxic adenoma or multinodular toxic goiter, thyroid storm is more commonly seen in toxicity secondary
to Graves disease.
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Sex
Age and sex predilection depends on the etiology of thyrotoxicity. Graves disease more frequently develops in females (ie, male-to-
female ratio ranges from 1:7 to 1:10); multinodular goiter more often manifests in the elderly population.
Clinical
History
Clinical features form the hallmark in diagnosing thyroid storm. Most patients have goiter, and many of those with Graves disease have
concurrent ophthalmopathy. Frequently, a past history of thyroid disease that has been partially treated exists.
Physical
An accentuation of signs and symptoms is seen in uncomplicated thyrotoxicosis. The point of transition from uncomplicated
thyrotoxicosis to thyroid storm is difficult to ascertain. Very few criteria define the change. However, certain clinical features (eg,
high-grade fever, mental obtundation, decompensation of one or more organ systems secondary to the severe state of
hypermetabolism) herald its onset.
The table below presents some changes in the symptoms and signs of thyroid storm when compared with uncomplicated
thyrotoxicosis. Importantly, some findings of thyroid storm (eg, atrial dysrhythmia) may also prevail in uncomplicated
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thyrotoxicosis. Therefore, the table represents only guidelines, not specific criteria to define thyroid storm.
2. Sinus tachycardia, heart rate 100-140 2. Heart rate faster than 140 beats/min, hypotension,
atrial dysrhythmias, congestive heart failure
3. Diarrhea, increased appetite with loss of weight 3. Nausea, vomiting, severe diarrhea, abdominal pain,
hepatocellular dysfunction-jaundice
Certain unusual presentations include chest pain, acute abdomen, status epilepticus, stroke, acute renal failure due to
rhabdomyolysis, and apathetic thyroidism. Lahey first described apathetic thyroidism (ie, masked hyperthyroidism) 60 years
ago.1 Apathetic thyroidism more frequently was seen in elderly patients but since has been described in all ages. Patients in this
variant group present without goiter, ophthalmopathy, or prominent symptoms of hyperthyroidism. These patients have a low
pulse rate and a propensity to develop thyroid storm due to delay in diagnosis.
Causes
A precipitating factor usually is found with thyroid storm. Presently, the most common cause of thyroid storm is intercurrent illness or
infection (ie, medical storm).
Some causes that rapidly increase the thyroid hormone levels include the following:
Surgery, thyroidal or nonthyroidal
Radioiodine therapy
Withdrawal of antithyroid drug therapy
Vigorous thyroid palpation
Iodinated contrast dye
Thyroid hormone ingestion
Differential Diagnoses
Workup
Laboratory Studies
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Presently, no specific diagnostic criteria to establish the diagnosis of thyroid storm exist.
Burch and Wartofsky have constructed an excellent clinical diagnostic point scale to facilitate a semiquantitative distinction
between uncomplicated thyrotoxicosis, impending storm, and established thyroid storm.2 Laboratory findings in thyroid storm
are consistent with those of thyrotoxicosis and include the following:
Elevated T3 and T4 levels
Elevated T3 uptake
Suppressed TSH levels
Elevated 24-hour radioiodine uptake
Elevated T4 and decreased TSH are the only abnormal findings needed for conformation of thyrotoxicosis. Treatment should
not be withheld for any laboratory confirmation of hyperthyroidism when thyroid storm is suspected clinically. A 2-hour
radioiodine uptake is advisable if thyroid storm is suspected and no past history of hyperthyroidism exists.
Other abnormal laboratory values that point toward decompensation of homeostasis include the following:
Increased BUN and creatinine kinase
Electrolyte imbalance from dehydration, anemia, thrombocytopenia, and leukocytosis
Hepatocellular dysfunction as shown by elevated levels of transaminases, lactate dehydrogenase, alkaline phosphatase,
and bilirubin
Elevated calcium levels
Hyperglycemia
Treatment
Medical Care
Management of thyroid storm is a multi-step process. Blocking the synthesis, secretion, and peripheral action of the thyroid hormone is
the ideal therapy. Aggressive supportive therapy then is used to stabilize homeostasis and reverse multiorgan decompensation.
Additional measures are taken to identify and treat the precipitating factor, followed by definitive treatment to avoid recurrence. Thyroid
storm is a fulminating crisis that demands an intensive level of care, continuous monitoring, and vigilance.
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After initiation of antithyroid therapy, hormone release can be inhibited by large doses of iodine, which reduce thyroidal
iodine uptake. Lugol solution or saturated solution of potassium iodide can be used.
Iodine therapy should be administered after approximately 1 hour following administration of PTU or MMI; iodine used
alone helps to increase thyroid hormone stores and may increase the thyrotoxic state.
The iodinated x-ray contrast agent, sodium ipodate, can be administered instead of iodine and also inhibits peripheral
conversion of T4 to T3. Potassium iodide (KI) decreases thyroidal blood flow and hence is used preoperatively in
thyrotoxicosis.
Patients intolerant to iodine can be treated with lithium, which also impairs thyroid hormone release. Patients unable to
take PTU or MMI also can be treated with lithium, as use of iodine alone is debatable. Unlike iodine, lithium is not subject
to the escape phenomenon; lithium blocks the release of thyroid hormone throughout its administration.
Plasmapheresis, plasma exchange, peritoneal dialysis exchange transfusion, and charcoal plasma perfusion are other
techniques used to remove excess circulating hormone. Presently, these techniques are reserved for patients who do
not respond to the initial line of management.
The intravenous preparation of sodium iodide (given as 1 g slow infusion q8-12h) has been taken off of the market.
Supportive measures
Aggressive fluid and electrolyte therapy is needed for dehydration and hypotension. This excessive hypermetabolic
state, with increased intestinal transit and tachypnea, leads to immense fluid loss. Fluid requirements may increase to
3-5 L/day. Therefore, invasive monitoring is advisable in elderly patients and in those with congestive cardiac failure.
Pressor agents can be used when hypotension persists following adequate fluid replacement.
Add glucose to IV fluids for nutritional support.
Multivitamins, especially vitamin B-1, are added to prevent Wernicke encephalopathy.
Hyperthermia is treated through central cooling and peripheral heat dissipation.
Acetaminophen is the drug of choice, as aspirin may displace thyroid hormone from binding sites and increase severity
of thyroid storm.
Cooling blankets, ice packs, and alcohol sponges encourage dissipation of heat. Use of a cooled humidified oxygen tent
is advised.
Use of glucocorticoids in thyroid storm is associated with improved survival rates. Initially, glucocorticoids were used to
treat potential relative insufficiency due to accelerated production and degradation owing to the hypermetabolic state.
However, the patient may have type 2 autoimmune deficiency, in which Graves disease coexists with absolute adrenal
insufficiency.
Glucocorticoids reduce iodine uptake and antibody titers of thyroid-stimulating antibodies with stabilization of the vascular
bed. In addition, dexamethasone and hydrocortisone have an inhibitory effect on conversion of T4 to T3. Therefore, a
stress dose of glucocorticoid (eg, hydrocortisone, dexamethasone) now is routine.
Cardiac decompensation, although seen more frequently in elderly patients, may appear in younger patients and in
patients without underlying cardiac disease.
Digitalization is required to control the ventricular rate in patients with atrial fibrillation.
Anticoagulation drugs may be needed for atrial fibrillation and can be administered in the absence of contraindications.3
Digoxin may be used in larger doses than those normally used in other conditions. Closely monitor digoxin levels to
prevent toxicity. As the patient improves, reduce digoxin dose.
Congestive cardiac failure is seen as a result of impaired myocardial contractility and may require Swan-Ganz catheter
monitoring.
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Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Antithyroid agents
These agents block thyroid hormone synthesis.
Propylthiouracil (PTU)
Thiourea agent that blocks production of thyroid hormones. In addition, inhibits peripheral deiodination of T4 to T3. Preferred over MMI
in thyroid storm.
Dosing
Adult
Pediatric
Not established
Interactions
Contraindications
Documented hypersensitivity; history of hepatotoxicity or agranulocytosis from previous thioamide therapy; pediatric patients (unless
allergic or intolerant to methimazole and no other treatment is an option)
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Monitor PT during therapy; may cause hypoprothrombinemia and bleeding; agranulocytosis may develop, monitor patients for
symptoms (eg, sore throat, fever, bleeding, bruising, malaise, stomatitis) and, if suspected, discontinue drug immediately; once
symptoms of hyperthyroidism have resolved, lower maintenance dose of PTU if serum TSH levels are elevated; risk of serious liver
injury, including liver failure and death, has been reported in adults and children by the FDA (carefully consider drug therapy, and if PTU
initiated, monitor for symptoms and signs of liver injury, especially during first 6 mo of therapy)
Methimazole (Tapazole)
Active moiety of parent compound carbimazole. Blocks incorporation of iodine into thyroglobulin within 1 h of ingestion.
Methimazole was initially thought to be associated with neonatal aplasia cutis (ie, defect in the neonatal scalp) and was thought to be
more likely to cross the placenta than PTU. However, recent studies by Wing et al concluded that PTU and MMI are equally effective
and safe in the treatment of hyperthyroidism in pregnancy.
Dosing
Adult
Pediatric
Not established
Interactions
Inhibits vitamin K activity and may potentiate activity of oral anticoagulants; toxicity increased with coadministration of lithium and
potassium iodide
Contraindications
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Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Monitor prothrombin time during therapy; agranulocytosis may develop (monitor patients for symptoms [eg, sore throat, fever, bleeding,
bruising, malaise, stomatitis] and, if suspected, discontinue drug immediately; may cause hypoprothrombinemia and bleeding; once
symptoms of hyperthyroidism have resolved, the presence of elevated serum TSH suggests that a lower maintenance dose of
methimazole should be used
Dosing
Adult
Pediatric
Not established
Interactions
Lithium increases toxicity of thiazide diuretics, haloperidol, phenothiazines, neuromuscular blockers carbamazepine, fluoxetine, and
ACE inhibitors
Contraindications
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Lithium toxicity is closely related to serum levels and can develop at therapeutic doses; serum lithium determinations are required to
monitor therapy
Inhibits thyroid hormone secretion. Contains 8 mg of iodide per drop. May be mixed with juice or water for intake.
Iodide treatment is reserved for the treatment of thyroid storm. It is also used for 10-14 d prior to surgical procedure, including
thyroidectomy. Can be used with Graves thyrotoxicosis but exacerbates thyrotoxicosis from toxic multinodular goiter and toxic
adenoma.
Dosing
Adult
Pediatric
Not established
Interactions
Contraindications
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Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
When used alone, iodine helps increase thyroid hormone stores and may increase the thyrotoxic state
Because iodine crosses the placenta, diagnosis or treatment with radioactive iodine (I131) is contraindicated in pregnancy
Nonradioactive iodide prevents release of T3/T4 from thyroglobulin and is used for treatment of hyperthyroidism in women who are not
pregnant
Infants born to mothers treated with prolonged courses of iodide appear to be at increased risk for goiter; therefore, iodide treatment
of women who are pregnant is indicated only in acute circumstances (eg, thyroid storm, immediately before surgical thyroidectomy)
Caution in renal failure and GI obstruction
One of the most effective inhibitors of deiodinase, which converts T4 to the more biologically active T3. Reduction in conversion of T4
to T3 can greatly reduce T3 levels and thyrotoxic symptoms.
Dosing
Adult
0.5-3 g/d PO
Pediatric
Not established
Interactions
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Risk of hypotension increases with increased dose; anuria may develop if agents are administered to patients with combined hepatic
and renal disease or severe renal impairment; prolonged iodine storage in tissues may lead to rebound thyrotoxicosis with potential to
cause ethionamide resistance
Glucocorticoids
These agents reduce iodine uptake and antibody titers of thyroid-stimulating antibodies with stabilization of the vascular bed.
Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant
synthesis, increases serum vitamin A concentration, and inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6,
IL-2, IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of
inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down
granulocyte aggregates and improves pulmonary microcirculation. Has inhibitory effect on conversion of T4 to T3.
Adverse effects include hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal
suppression, and death. Most of the adverse effects of corticosteroids are dose dependent or duration dependent.
Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining
property of hydrocortisone.
Patients can be switched from an IV to PO regimen in a 1:1 ratio.
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Dosing
Adult
2 mg IV q6h
Pediatric
Not established
Interactions
Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and
vaccines used for immunization
Contraindications
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt
discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease,
hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of
glucocorticoid use
Elicits anti-inflammatory properties and causes profound and varied metabolic effects. Modifies the body's immune response to
diverse stimuli.
Dosing
Adult
100 mg IV q8h
Pediatric
Not established
Interactions
Corticosteroid clearance may decrease with estrogens; may increase digitalis toxicity secondary to hypokalemia
Contraindications
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes, and myasthenia gravis
Analgesics
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating
properties.
Inhibits action of endogenous pyrogens on heat-regulating centers; reduces fever by a direct action on the hypothalamic
heat-regulating centers, which, in turn, increases the dissipation of body heat via sweating and vasodilation.
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Dosing
Adult
650 mg PO q4h
Pediatric
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 4 g/d
Interactions
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid
may increase hepatotoxicity
Contraindications
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hepatotoxicity possible in persons with long-standing alcoholism following various dose levels; severe or recurrent pain or high or
continued fever may indicate a serious illness; APAP is contained in many OTC products, and combined use with these products may
result in cumulative APAP doses that exceed recommended maximum dose
Beta-adrenergic blockers
These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.
DOC to counter peripheral action of thyroid hormone; blocks beta-adrenergic receptors; prevents conversion of T4 to T3.
Dosing
Adult
60-80 mg PO q4h
0.5-1 mg IV
Plasma level of 50 ng/mL
required for adequate effect
Pediatric
Not established
Interactions
Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease
propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of
hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol
Contraindications
Documented hypersensitivity; uncompensated congestive heart failure; bradycardia, cardiogenic shock; A-V conduction abnormalities
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate
symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely
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Esmolol (Brevibloc)
Ultra–short-acting agent that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. Particularly useful in
patients with elevated arterial pressure, especially if surgery is planned. Shown to reduce episodes of chest pain and clinical cardiac
events compared with placebo. Used successfully in thyrotoxicosis and thyroid storm. Can be discontinued abruptly if necessary.
Useful in patients at risk for experiencing complications from beta-blockade; particularly those with reactive airway disease,
mild-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick
discontinuation if needed.
Dosing
Adult
Pediatric
Not established
Interactions
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma
levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered
concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol
increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin,
haloperidol, phenothiazines, and catecholamine-depleting agents
Contraindications
Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; and A-V conduction
abnormalities
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of
hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient
closely
Antihypertensive agents
These agents reduce blood pressure.
Guanethidine (Ismelin)
For use in patients with congestive cardiac failure, bronchospasm, or history of asthma.
Dosing
Adult
1-2 mg/kg/d PO
Pediatric
Not established
Interactions
Tricyclic antidepressants, methylphenidate, thioxanthenes, phenothiazines, sympathomimetics, anorexiants, and haloperidol may
reduce effects of guanethidine; minoxidil, epinephrine, and norepinephrine may increase the toxicity of guanethidine
Contraindications
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Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in congestive heart failure, asthma, peptic ulcer disease, and regional vascular disease
Reserpine
For use in patients with congestive cardiac failure, bronchospasm, or history of asthma; successful treatment has been documented in
cases of thyroid storm resistant to large doses of propranolol.
Dosing
Adult
2.5-5 mg IM q4-6h
Pediatric
Not established
Interactions
Concurrent use of tricyclic antidepressants may decrease antihypertensive effects of reserpine; cardiac arrhythmias may develop when
either digitalis or quinidine are concurrently administered with reserpine
Contraindications
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients diagnosed with renal impairment and peptic ulcer disease
Follow-up
Combined use of propylthiouracil, iodine, and dexamethasone has an effect within 24-48 hours, and the serum levels of T3 and
T4 return to normal. Clinical signs of decreasing pulse, normal temperature, and improved mental status mark effective
management. Complete recovery takes 10-12 days. Dexamethasone can be tapered thereafter.
The three modalities of definitive management are radioiodine, antithyroid drugs, and surgery.
Prior to radioiodine therapy or surgery, a patient should be made euthyroid with antithyroid drugs and propranolol. Antithyroid
drugs are administered for 12-24 months, during which, a remission may occur. Antithyroid drugs are continued until a normal
metabolic state is reached. If in remission, the patient should be closely monitored for 6 months, as relapse is more common
during this period after discontinuation of therapy. Iodine is progressively withdrawn. Serially monitor patients until the thyroid
gland is sufficiently depleted of its hormone to allow radioiodine therapy. Delaying radioiodine ablation for several months may
be necessary because of the large doses of iodine used in management of thyroid storm. Some surgeons may reintroduce
iodine for 10 days prior to surgery if subtotal thyroidectomy is planned. Follow patients for up to 5 years.
Criteria established by Burch and Wartofsky help in early recognition of impending storm. In thyroid storm, management as
described improves the chance of survival.2
Deterrence/Prevention
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Precipitating factors are not found in all patients, but a meticulous search improves chances for a successful outcome.
Chest radiographs and blood, urine, and sputum cultures may be needed to identify intercurrent illness (eg, infection).
Judicious use of empiric antibiotics is needed if no obvious source is found.
Prevention of recurrence
Prevention of a recurrent crisis should be the main objective until completion of definitive therapy.
Vigilant monitoring of signs and symptoms of hyperthyroidism during preoperative or pre-anesthetic evaluation is
paramount.
Consider precipitating factors when deciding on treatment modalities.
Adequate control of the thyrotoxic state prior to initiation of definitive therapy is important. Carry out procedures only after
the patient is euthyroid.
Patient Education
For excellent patient education resources, visit eMedicine's Endocrine System Center. Also, see eMedicine's patient education articles
Thyroid Problems and Thyroid Storm.
Multimedia
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References
2. Burch HB, Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North
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3. Martin D. Disseminated intravascular coagulation precipitated by thyroid storm. South Med J. Feb 2009;102(2):193-5. [Medline].
4. Brooks MH, Waldstein SS, Bronsky D, Sterling K. Serum triiodothyronine concentration in thyroid storm. J Clin Endocrinol
Metab. Feb 1975;40(2):339-41. [Medline].
5. Ecker JL, Musci TJ. Treatment of thyroid disease in pregnancy. Obstet Gynecol Clin North
Am. Sep 1997;24(3):575-89. [Medline].
6. Gavin LA. Thyroid crises. Med Clin North Am. Jan 1991;75(1):179-93. [Medline].
7. Ingbar SH. Management of emergencies. IX. Thyrotoxic storm. N Engl J Med. Jun 2 1966;274(22):1252-4. [Medline].
8. Mackin JF, Canary JJ, Pittman CS. Thyroid storm and its management. N Engl J Med. Dec 26 1974;291(26):1396-8. [Medline].
9. Mazzaferri EL, Skillman TG. Thyroid storm. A review of 22 episodes with special emphasis on the use of guanethidine. Arch
Intern Med. Dec 1969;124(6):684-90. [Medline].
10. Migneco A, Ojetti V, Testa A. Management of thyrotoxic crisis. Eur Rev Med Pharmacol
Sci. Jan-Feb 2005;9(1):69-74. [Medline].
11. Milham S Jr. Scalp defects in infants of mothers treated for hyperthyroidism with methimazole or carbimazole during
pregnancy. Teratology. Oct 1985;32(2):321. [Medline].
12. Nakamura S, Nishmyama T, Hanaoka K. [Perioperative thyroid storm in a patient with undiscovered
hyperthyroidism]. Masui. Apr 2005;54(4):418-9. [Medline].
13. Prihoda JS, Davis LE. Metabolic emergencies in obstetrics. Obstet Gynecol Clin North Am. Jun 1991;18(2):301-18. [Medline].
14. Rosenberg IN. Thyroid storm. N Engl J Med. Nov 5 1970;283(19):1052-3. [Medline].
15. Scholz GH, Hagemann E, Arkenau C, Engelmann L, Lamesch P, Schreiter D. Is there a place for thyroidectomy in older patients
with thyrotoxic storm and cardiorespiratory failure?. Thyroid. Oct 2003;13(10):933-40. [Medline].
16. Tietgens ST, Leinung MC. Thyroid storm. Med Clin North Am. Jan 1995;79(1):169-84. [Medline].
17. Tintillani JE, Kelen GD, Stapazynski JS. Emergency Medicine A Comprehensive Study Guide. 5th ed. McGraw-
Hill;1999:1343-1345.
18. Utiger RD. The thyroid physiology; hyperthyroidism, hypothyroidism, and the painful thyroid. In: Endocrinology and
Metabolism. 2nd ed. New York, NY: McGraw-Hill;1987:438.
19. Wing DA, Millar LK, Koonings PP, et al. A comparison of propylthiouracil versus methimazole in the treatment of
hyperthyroidism in pregnancy. Am J Obstet Gynecol. Jan 1994;170(1 Pt 1):90-5. [Medline].
Keywords
thyrotoxic storm, thyroid storm, thyrotoxic crisis, thyroidectomy, thyroid disease, extreme hyperthyroid state, toxic goiter surgery,
thyrotoxicosis, Graves disease, toxic goiter
Author
Nafisa K Kuwajerwala, MD, Staff Surgeon, Breast Oncology, William Beaumont Hospital
Nafisa K Kuwajerwala, MD is a member of the following medical societies: American College of Surgeons
Disclosure: Nothing to disclose.
Coauthor(s)
Gunateet Goswami, MD, Consulting Staff, Internal Medicine Associates, Mount Clemens, Michigan; Consulting Staff, Department of
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Thabet Abbarah, MD, FACS, Consulting Staff, Department of Otolaryngology, North Oakland Medical Centers
Thabet Abbarah, MD, FACS is a member of the following medical societies: American College of Surgeons
Disclosure: Nothing to disclose.
Venkata Subramanian Kanthimathinathan, MD, Staff Physician, Department of General Surgery, Loma Linda University Medical
Center
Disclosure: Nothing to disclose.
Pankaj Chaturvedi, MBBS, MS, Associate Professor, Head and Neck Surgery, Department of Surgical Oncology, Tata Memorial
Hospital, India
Pankaj Chaturvedi, MBBS, MS is a member of the following medical societies: American Association for the Advancement of Science
and Association of Surgeons of India
Disclosure: Nothing to disclose.
Medical Editor
Mimi S Kokoska, MD, Associate Professor, Department of Otolaryngology-Head and Neck Surgery, University of Arkansas for
Medical Sciences; Chief, Department of Otolaryngology-Head and Neck Surgery, Central Arkansas Veterans Healthcare System
Mimi S Kokoska, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery,
American Academy of Otolaryngology-Head and Neck Surgery, American College of Physician Executives, American College of
Surgeons, American Head and Neck Society, and Arkansas Medical Society
Disclosure: Nothing to disclose.
Pharmacy Editor
Managing Editor
Dean Toriumi, MD, Department of Otolaryngology, Associate Professor, University of Illinois Medical Center
Disclosure: Nothing to disclose.
CME Editor
Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director,
Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and
Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of
Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive
Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown; Axis Three
Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board
membership; Syndicom Ownership interest Consulting; Oxlo Consulting; Medvoy Ownership interest Management position
Further Reading
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