Resident Version

Thyroid Storm Module

Created by Dr. Kathleen Colleran

Objectives:

1)  Recognize three signs and symptoms of thyroid storm and why they occur

2)  Be able to appropriately evaluate a patient with suspected thyroid storm

3)  List three treatments for thyroid storm

References:

1.  McKeown, N, et al. Hyperthyroidism. Emergency Medicine Clinics of North America
23:669-85, 2005.

2.  Migneco A, et al. Management of Thyrotoxic Crisis. Eur Rev Med Pharmacol Sci. 9:69-74, 2005.

3.  Douglas S Ross, MD, Treatment of Thyroid storm @ 2006 UpToDate .


Discussion Outline:

I. Overview

Thyroid storm is a medical emergency that includes hyperthyroidism, cardiovascular instability, thermogenic instability, and neurogenic instability. The diagnosis of thyroid storm is based on signs and symptoms and is a clinical diagnosis. Being able to recognize the manifestations of thyroid storm is essential to expedite treatment and prevent morbidity and mortality. Even with appropriate treatment mortality rates for thyroid storm remain high at 25%.

All forms of hyperthyroidism can culminate in thyroid storm. Table 1 list causes of hyperthyroidism. Grave’s disease accounts for most cases of thyroid storm because it is common and severe hyperthyroidism can occur.

Thyroid storm typically occurs in a patient with underlying hyperthyroidism, either previously known or unknown, who develops a second illness or stressor. The second stressor results in an acute catecholamine surge. The catecholamine surge in the presence of hyperthyroidism leads to tachyarthymias, high output cardiac failure and cardiovascular instability. Elevated catecholamine in the setting of hyperthyroidism causes hyperthermia leading to thermodynamic instability. The combination also causes tremors, hyperreflexia, mania, concentration and memory disturbances and culminates in neuropsychiatric instability.

II. Common precipitants of thyroid storm

Thyroid storm can mimic several conditions including sepsis, pheochromocytoma, psychosis, adrenal insufficiency, intoxication, and autonomic insufficiency. Common precipitants of thyroid storm are listed in table 2.

Table 1. Causes of hyperthyroidism / Table 2. Precipitants of Thyroid Storm
Graves’ Disease
Toxic Multinodular Goiter
Toxic Adenoma
Thyroiditis
Exogenous Thyroid Hormone
Thyroiditis
Jod Basedow
TSH Secreting Pituitary Adenoma
Molar Pregnancy
Struma Ovarii / Pregnancy
Trauma
Infection
Myocardial Infarction
Surgery
Intoxication
ETOH
Cocaine
Amphetamines
Iodine ( in MNG, Toxic adenoma)
Radioactive Iodine
IV Contrast
Amiodarone

III. Clinical Assessment

The diagnosis of thyroid storm is made by clinical suspicion based on patient history, signs and symptoms and physical exam findings. Waiting for thyroid function tests to return leads to unnecessary treatment delays and can be catastrophic.

Most patients will report a history of symptoms consistent with hyperthyroidism including unexplained weight loss, insomnia, heat intolerance, tremors, and palpitations.

They will present with an acute worsening of those symptoms in addition to severe agitation.

Significant physical exam findings include agitation and inability to sit still. Temperature is usually elevated, significant tachycardia is present and blood pressure is labile. Skin is moist and warm to touch. Eye examination may demonstrate stare, lid lag, or exopthalmos if Graves’ disease is present. Thyroid exam findings depend on the etiology of hyperthyroidism (Table 3). Muscle weakness and hyperreflexia may be present. Additionally, patients perform poorly on the mini mental status exam. Standard laboratory analysis including a full metabolic profile and CBC is nonspecific.

Table 3.

Graves’ Disease / Diffusely enlarged gland ± bruit
Toxic Multinodular Goiter / Nodular goiter
Toxic Adenoma / Solitary nodule
Thyroiditis / ± tenderness
Exogenous thyroid intake / Nonpalpable gland
TSH secreting pituitary tumor / Diffusely enlarged gland
Molar pregnancy / Diffusely enlarged gland
Strumii ovarie / Nonpalpable gland

IV. Treatment

Treatment of thyroid storm is empiric based on clinical suspicion. Patients should be admitted to an intensive care unit. Treatment is multifactorial and includes supportive care and pharmacologic intervention. Pharmacologic treatment is aimed at blocking thyroid hormone synthesis, release, conversion to T3, and action on cells. Figure 1 demonstrates where pharmacologic therapies are acting.

·  Fluid as patients are volume deplete

·  Cooling blankets if hyperthermia is present

·  Beta blockade to minimize catecholamine excess

o  Propranolol 20-40 mg q 6 hours to decrease heart rate to < 100 bpm

o  Esmolol if concern regarding cardiac output (fast acting/short t ½ life.)

·  Thionamides:

o  Propothyouricil (PTU) 150 mg po q 6 hours if patient is able to take p.o.

Or

o  Methimazole 10-20 mg pr q 6 hours

·  SSKI or Lugol's solution: administer 1-2 hours following thionamide administration.

·  Steroids: Dexamethasone 1 mg q 6-8 hours

·  Treat underlying precipitating stressor if present

·  If no response consider emergent thyroidectomy or plasmaphoresis.

·  Aviod aspirin; it increases free thyroid hormone levels by competing with binding sites on Thyroid binding globulin

Figure 1.

Thionamides Iodine PTU β-blockers

Propranolol Steroids

Steroids

V. Pharmacology:

·  PTU has a shorter t ½ and faster onset of action than methimazole.

·  PTU preferentially blocks conversion of T4 to T3 (active hormone)

·  PTU is preferred during pregnancy as methimazole may cause congenital defects

·  Both agents can cause agranulocytosis and hepatitis (<0.1%). These adverse events are idiosyncratic can occur randomly; therefore monitoring WBC or LFTs are not useful. Patients should be educated to get a blood test done if they develop symptoms of neutropenia including: unexplained fever, sore throat, or mouth sores; or if they develop symptoms of hepatitis including: right upper quadrant pain, jaundice, or nausea or vomiting.


CASE

D.Y. is a 19 yr old male who was involved in a low speed motor vehicle accident. At the scene, he complained of neck pain. A C-collar was placed and he was transferred by ambulance to the local Emergency room. On initial presentation he was warm to touch, anxious with a mild tremor, and tachycardic with a HR of 125. He was tender over the c-spine but demonstrated no focal neurological deficits. The remainder of his physical exam was nonspecific. An XRAY of the C-spine was ordered. Over the course of his ER stay he became progressively agitated, confused and combative. His HR increased to 160 and temperature rose to 40◦ C. He was visibly shaking and unable to sit still. He required sedation and restraints. He was intubated for airway protection and respiratory support and was transferred to a tertiary care center and admitted to an ICU bed. A full metabolic panel, CBC, blood and urine cultures, and a toxicology screen were ordered. EKG showed sinus tachycardia, CXR was negative, C-spine was difficult to interpret and a CT was ordered.

1. What should be initial management step and what further tests should be ordered?

2. What would be reasonable treatment for his diagnosis, and what precipitated it?


Review Questions

1. A 64 yr. old male presents to the ED with angina and hyperthyroidism. He is scheduled to undergo cardiac catheterization.

This procedure will result in a worsening of his hyperthyroidism if he has which of the following:

a. Viral Thyroiditis

b. Toxic Multinodular Goiter

c. Graves’ Disease

d. Hashimotos Thyroiditis

e. Thyroid Hormone Resistance

2. A 40-yr-old female with Grave’s disease was recently started on methimazole. One month later she comes to the clinic for a routine follow-up. She reports low grade fevers, myalgias, arthralgias, and general malaise.

The most important test to order now is which of the following?

a. TSH

b. ALT

c. TSI

d. WBC

e. Radio iodine uptake

Post Module Evaluation

Please place completed evaluation in an interdepartmental mail envelope and address to Dr. Wendy Gerstein, Department of Medicine, VAMC (111).

1) Topic of module:______

2) On a scale of 1-5, how effective was this module for learning this topic? ______

(1= not effective at all, 5 = extremely effective)

3) Were there any obvious errors, confusing data, or omissions? Please list/comment below:

______

4) Was the attending involved in the teaching of this module? Yes/no (please circle).

5) Please provide any further comments/feedback about this module, or the inpatient curriculum in general:

6) Please circle one:

Attending Resident (R2/R3) Intern Medical student