Edited By: David Wald, MD
Temple University School of Medicine
The objectives of this module will be to:
- Review the presenting signs and symptoms of thyroid storm.
- Review the neuroendocrine axis of the thyroid gland.
- Review the principles of managing a patient with thyroid storm.
Thyroid storm is a rarely encountered clinical condition. Complicating the diagnosis is the broad range of symptoms that can be associated with this disease state. Typically, it manifests itself as a state of exaggerated hyperthyroidism accompanied by systemic organ decompensation. The etiology of thyroid storm can range from poorly controlled disease (grave's disease) to precipitant such as infection, surgery, diabetic ketoacidosis, etc. Prompt recognition and early treatment is paramount to limit the associated morbidity and mortality associated with the condition.
Initial Actions and Primary Survey
Because thyroid storm is rare, patient care will be initiated long before a definitive diagnosis is made and often before the diagnosis is suspected. These patients will be critically ill and will require a prompt and systematic primary and secondary survey to be performed.
The following measures should be instituted in all patients suspected of having thyroid storm;
- Close attention should be paid to the ABC's. Cardiopulmonary dysfunction can occur prompting aggressive airway management.
- Intravenous access should be obtained. Central venous access along with transducing the central venous pressure along with the placement of a pulmonary artery catheter may be necessary to assist in determining the patient's fluid status.
- Place the patient on a cardiac monitor and obtain an electrocardiogram
- Intravenous fluid administration may be necessary, be wary of the patient with pulmonary edema.
- Administer supplemental oxygen as needed.
Thyroid storm has a vast differential, keep in mind, conditions such as;
- Acute pulmonary edema
- Heat stroke
- Malignant hyperthermia
- Neuroleptic malignant syndrome
- Sepsis / septic shock
- Serotonin syndrome
- Sympathomimetic toxicity
- Tachyarrhythmias (atrial fibrillation, supraventricular tachycardia)
The classic triad of thyroid storm is high fever (sometimes as high as 106OF), exaggerated tachycardia, and central nervous system dysfunction.
- Patients may present with neurologic symptoms that range from restlessness and anxiety to agitation progressing to coma and eventually hypotension and death.
- Additional nonspecific complaints may be seen, that range ranging from weight loss, fatigue, proximal muscle weakness, psychosis, edema , heat intolerance or tremor to name a few.
- Cardiovascular complaints are also commonly encountered including; palpitations, tachyarrhythmias, hypertension, pulmonary edema, chest pain and dyspnea.
- The acute presentation is a hypermetabolic state of high fever, tachycardia, tremulousness, agitation, psychosis, nausea and vomiting. On the far end of the disease spectrum, late in presentation is a patient who may present comatose and hypotensive.
- Women are more commonly affected than men.
To understand the etiology of thyroid storm, let's first look at the neuroendocrine pathway.
The hypothalamus releases thyroid releasing hormone (TRH) which acts on the anterior pituitary gland. The anterior pituitary gland then releases thyroid stimulating hormone (TSH) which acts on the thyroid gland. The thyroid gland then releases prohormone thyroxine (T4) and a small amount of triiodothyronine (T3). T4 is the inactive form and will convert to its active form via the liver and kidney. Most of the converted T3 will bind to thyroid binding globule (TBG). T4 can also bind to TBG. Only a fraction of T4 and T3 remain unbound or 'free'. The free T4 and T3 are the most accurately correlate to clinical status.
The most common risk factor for thyroid storm is preexisting hyperthyroidism. The most common form of this is Graves' disease. Graves' disease results from over activity of the thyroid gland. This is due to an autoimmune attack on thyroid receptors which stimulate the thyroid to produce thyroid hormone. These patients commonly have the triad of exophthalmos, goiter and pretibial myxedema. Other etiologies include infectious (bacterial or viral), idiopathic (toxic multinodular goiter), iatrogenic (surgery or ingesting thyroid medication), drug-induced (iodine or amiodarone) and malignancy (thyroid toxic adenoma, pituitary tumors or struma ovarii).
Thyroid storm results when an incompletely treated hyperthyroid state is exacerbated usually by infection, surgery or trauma. Often times, the diagnosis must be made clinically given the need for immediate treatment and the longer lab times required processing thyroid panels.
The diagnosis of thyroid storm is usually made based on clinical findings alone. There are no laboratory criteria that definitively diagnose thyroid storm. However, patients will typically demonstrate laboratory findings consistent with a hyperthyroid state. These findings include;
- Elevated T3 and T4 levels
- Elevated T3 uptake
- Low TSH
These laboratory values should be viewed in context of the presenting signs and symptoms. In isolation, the laboratory studies can not distinguish between uncontrolled hyperthyroidism and thyroid storm.
Additional diagnostic studies may be indicated to further identify systemic or target organ dysfunction along with identifying a precipitating cause.
- Basic metabolic profile
- Complete blood count
- Hepatic function tests
- Chest radiograph
- Urinalysis / urine culture
- Blood cultures
At times treatment may need to be initiated based on clinical suspicion. The medical management of thyroid storm can be divided into four components.
1. Treatment directed against the thyroid gland
Blocking synthesis of thyroid hormone (Thionamide agents) is accomplished by Propylthiouracil (PTU) (PO or NG). Preferred over methimazole because PTU also reduces peripheral conversion of T4 to T3 in the peripheral tissues.
Blocking release of preformed thyroid hormone (administer inorganic iodine at least 1 hour after antithyroid medications): Lugol's solution or SSKI, can use lithium carbonate if allergic to iodine.
2. Treatment directed against the peripheral effects of thyroid hormone
Antagonize the hyperadrenergic effects of thyroid hormone with Beta adrenergic blocking agents: Propranolol, esmolol as an alternative
Inhibition of peripheral conversion of T4 to T3. PTU, propranolol, glucocorticoids
3. Treatment directed against systemic decompensation
Treat hyperthermia with Acetaminophen, avoid aspirin.
Treatment of dehydration, electrolyte imbalance and depleted glycogen stores with Dextrose containing i.v. fluids and electrolyte replacement as needed
4. Identification and treatment of the precipitating cause
Check a Chest radiograph, urinalysis, etc... and give antibiotics as needed
All patients with thyroid storm will require admission to the intensive care unit, close monitoring and aggressive care. For those patients with moderately exaggerated hyperthyroid symptoms who have stable vital signs and a normal mental status can often be admitted to a monitored setting. Patients with mild hyperthyroid symptoms may even be managed as an outpatient with close follow up after initiating therapy in the emergency department.
Pearls and Pitfalls
- Clinical recognition is the key to making this diagnosis.
- Do not be fooled by other conditions that may mimic thyroid storm i.e., sympathomimetic toxicity (methamphetamine abuse), neuroleptic malignant syndrome, septic shock.
- Careful with administration long acting beta blockers in attempt to slow tachycardia as this may precipitate cardiogenic shock.
- Shraga, Erik D et al. "Hyperthyroidism, Thyroid Storm, and Graves Disease: Differential Diagnoses & Workup" eMedicine.
- Basaria S, Cooper DS. Amiodarone and the thyroid. Am J Med. Jul 2005;118(7):706-14.
- Cooper DS. Antithyroid drugs. N Engl J Med. Mar 2005;352(9):905-17.
- Sherman, SC. Thyroid emergencies. In: Harwood-Nuss, Wolfson, AB, eds. Clinical Practice of Emergency Medicine. 4th ed. Lippincott Williams & Wilkins; 2005:854-859.