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Thyrotoxic Storm Following Thyroidectomy Treatment & Management

  • Author: Peter F Czako, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA  more...
Updated: Jan 21, 2015

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.[5] 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.

Blocking thyroid hormone synthesis

Antithyroid compounds propylthiouracil (PTU) and methimazole (MMI) are used to block the synthesis of the thyroid hormone. PTU also blocks peripheral conversion of T4 to T3 and hence is preferred in thyroid storm over MMI. MMI is the common agent used in hyperthyroidism. PTU and MMI block the incorporation of iodine into thyroglobulin within 1 hour of ingestion. A history of hepatotoxicity or agranulocytosis from previous thioamide therapy precludes use of PTU and MMI.

The US Food and Drug Administration (FDA) had added a boxed warning, the strongest warning issued by the FDA, to the prescribing information for propylthiouracil. The boxed warning emphasizes the risk for severe liver injury and acute liver failure, some of which have been fatal. The boxed warning also states that propylthiouracil should be reserved for use in those who cannot tolerate other treatments such as methimazole, radioactive iodine, or surgery.

The decision to include a boxed warning was based on the FDA's review of postmarketing safety reports and meetings held with the American Thyroid Association, the National Institute of Child Health and Human Development, and the pediatric endocrine clinical community.

The FDA has identified 32 cases (22 adult and 10 pediatric) of serious liver injury associated with propylthiouracil (PTU). Of the adults, 12 deaths and 5 liver transplants occurred, and among the pediatric patients, 1 death and 6 liver transplants occurred. PTU is indicated for hyperthyroidism due to Graves disease. These reports suggest an increased risk for liver toxicity with PTU compared with methimazole. Serious liver injury has been identified with methimazole in 5 cases (3 resulting in death).

PTU is considered as a second-line drug therapy, except in patients who are allergic or intolerant to methimazole, or for women who are in the first trimester of pregnancy. Rare cases of embryopathy, including aplasia cutis, have been reported with methimazole during pregnancy. The FDA recommends the following criteria be considered for prescribing PTU. For more information, see the FDA Safety Alert.

  • Reserve PTU use during first trimester of pregnancy, or in patients who are allergic to or intolerant of methimazole.
  • Closely monitor PTU therapy for signs and symptoms of liver injury, especially during the first 6 months after initiation of therapy.
  • For suspected liver injury, promptly discontinue PTU therapy and evaluate for evidence of liver injury and provide supportive care.
  • PTU should not be used in pediatric patients unless the patient is allergic to or intolerant of methimazole, and no other treatment options are available.
  • Counsel patients to promptly contact their health care provider for the following signs or symptoms: fatigue, weakness, vague abdominal pain, loss of appetite, itching, easy bruising, or yellowing of the eyes or skin.

Blocking thyroid hormone secretion

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.[6]

The intravenous preparation of sodium iodide (given as 1 g slow infusion q8-12h) has been taken off of the market.

Blocking peripheral action of thyroid hormone

Propranolol is the drug of choice to counter peripheral action of thyroid hormone. Propranolol blocks beta-adrenergic receptors and prevents conversion of T4 to T3. It produces dramatic improvement in clinical status and greatly ameliorates symptoms. Propranolol produces the desired clinical response in thyroid storm only after large doses. Intravenous administration of propranolol requires continuous monitoring of cardiac rhythm.

Presently, esmolol is the ultra-short-acting beta-blocking agent used successfully in thyrotoxicosis and thyroid storm.

Noncardioselective beta-blockers (eg, propranolol, esmolol) cannot be used in patients with congestive cardiac failure, bronchospasm, or history of asthma. Guanethidine or reserpine can be used instead in these cases.[7]

Successful treatment with reserpine in cases of thyroid storm resistant to large doses of propranolol has been documented. However, guanethidine and reserpine cannot be used in the presence of cardiovascular collapse or shock.

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.[8] 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.

Contributor Information and Disclosures

Peter F Czako, MD, FACS Chief, Division of Endocrine Surgery, Medical Director, North Tower Operating Rooms, Surgical Administration, William Beaumont Hospital; Associate Professor, Department of Surgery, Oakland University William Beaumont School of Medicine; Royal Oak Surgical Associates, PC

Peter F Czako, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, Michigan State Medical Society, American Association of Endocrine Surgeons, Detroit Surgical Society

Disclosure: Nothing to disclose.


Nafisa K Kuwajerwala, MD Staff Surgeon, Breast Care Center, William Beaumont Hospital

Nafisa K Kuwajerwala, MD is a member of the following medical societies: American College of Surgeons, American Society of Breast Surgeons, American Society of Breast Disease

Disclosure: Nothing to disclose.

Gunateet Goswami, MD Consulting Staff, Internal Medicine Associates, Mount Clemens, Michigan; Consulting Staff, Department of Cardiology, Henry Ford Hospital

Gunateet Goswami, MD is a member of the following medical societies: American Medical Association, American Society of Echocardiography, Michigan State Medical Society

Disclosure: Nothing to disclose.

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.

Pankaj Chaturvedi, MBBS, MS, FACS Professor of Head and Neck Surgery, Department of Head and Neck Surgery, Tata Memorial Hospital, India

Pankaj Chaturvedi, MBBS, MS, FACS is a member of the following medical societies: American Association for the Advancement of Science, American Head and Neck Society, Association of Surgeons of India

Disclosure: Nothing to disclose.

Venkata Subramanian Kanthimathinathan, MD Fellow in Bariatric/Advanced Laparoscopic Surgery, University of Missouri Healthcare

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Dean Toriumi, MD Associate Professor, Department of Otolaryngology, University of Illinois Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, 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, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;SymbiaAllergySolutions<br/>Received income in an amount equal to or greater than $250 from: Symbia<br/>Received from Allergy Solutions, Inc for board membership; Received honoraria from RxRevu for chief medical editor; Received salary from Medvoy for founder and president; Received consulting fee from Corvectra for senior medical advisor; Received ownership interest from Cerescan for consulting; Received consulting fee from Essiahealth for advisor; Received consulting fee from Carespan for advisor; Received consulting fee from Covidien for consulting.

Additional Contributors

Mimi S Kokoska, MD Physician, Department of Otolaryngology-Head and Neck Surgery, Aurora Health Care

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 Association for Physician Leadership, American College of Surgeons, American Head and Neck Society

Disclosure: Nothing to disclose.

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Pathophysiologic mechanisms of Graves disease relating thyroid-stimulating immunoglobulins to hyperthyroidism and ophthalmopathy. T4 is levothyroxine. T3 is triiodothyronine.
Table. Symptoms and Signs of Thyroid Storm When Compared with Uncomplicated Thyrotoxicosis
Uncomplicated Thyrotoxicosis Thyroid Storm
1. Heat intolerance, diaphoresis 1. Hyperpyrexia, temperature in excess of 106o C, dehydration
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
4. Anxiety, restlessness 4. Confusion, agitation, delirium, frank psychosis, seizures, stupor or coma
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