Thyroid Emergencies

EXECUTIVE SUMMARY

• Myxedema coma and thyroid storm are thyroid emergencies that require urgent recognition because of associated complications and high mortality.
• Myxedema coma occurs primarily during the winter and typically affects female patients older than 60 years of age.
• Presenting symptoms of myxedema coma include hypothermia, bradycardia, metabolic abnormalities, and central nervous system dysfunction. Treatment typically includes
  300 mcg to 500 mcg intravenous T4, stress dose steroids, supportive care, and admission to the intensive care unit.
• Thyroid storm is seen commonly in female patients between the ages of 30 and 45 years and occurs more frequently in the summer.
• Hyperthermia, tachycardia, and central nervous system dysfunction are a few of the primary symptoms of thyroid storm and should be treated with a multifaceted regimen, including methimazole or propylthiouracil, propranolol, iodine administered one hour after the methimazole or propylthiouracil, glucocorticoids, and supportive therapy.

Thyroid Emergencies

Introduction

Thyroid emergencies, while rare, are life-threatening conditions that require prompt recognition, diagnosis, and treatment to optimize patient outcomes. There are two primary thyroid emergencies, myxedema coma, caused by lack of thyroid hormone, and thyroid storm, caused by increased action of thyroid hormone. A thorough understanding of the signs and symptoms for both emergencies is integral to timely management and prevention of further morbidity and mortality.

Case Introduction

A 50-year-old female presents for altered mental status. Her husband states that she has been very stressed lately. She has seen her primary care doctor and was supposed to start medication for her palpitations but has not done so yet. Her presenting vital signs are heart rate 160 bpm, blood pressure 175/85 mmHg, temperature 102.5°F, and oxygen saturation 94% on room air. She is agitated and sweaty. Her electrocardiogram (ECG) shows atrial fibrillation. What are your primary concerns with this patient? What steps are needed to stabilize her? What workup should you perform in the emergency department?

Normal Thyroid Physiology

The normal process of thyroid hormone production starts with the release of thyrotropin-releasing hormone (TRH) from the hypothalamus.¹ TRH then stimulates cells in the anterior pituitary gland to release thyroid-
stimulating hormone (TSH).¹ TSH subsequently binds to receptors in the thyroid gland, which initiates the production of thyroid hormone and results in the release of thyroxine (T4) and triiodothyronine (T3) into the bloodstream.^1,2 Thyroid hormone is responsible for the regulation of many bodily processes, including the activation or repression of gene transcription, regulation of ion channels, metabolism, and enzyme function.²

Myxedema Coma

Epidemiology

Myxedema coma is a relatively rare disease, with some reports estimating an incidence between 0.22 to 1.08 per million people per year.^2,3 Given that this disease is a result of a significant deficiency of thyroid hormone, the epidemiology of myxedema coma is very similar to hypothyroidism — a chronic disorder involving thyroid hormone deficiency.^4,5 Based on reports, between 60% and 80% of myxedema coma patients are female, with most cases occurring in individuals older than 60 years of age.^2-5 Most commonly, myxedema coma is seen in patients with previously diagnosed hypothyroidism.¹ Of note, more than 90% of myxedema coma cases occurred during the winter, and mortality rates approach 25% to 60% across various studies.^2,3,5 Even with treatment, mortality rates remain elevated, which may be affected by the age of the patients, a lack of prompt diagnosis, or the absence of effective therapy modalities.^2,5 Regardless, given the scarcity of studies analyzing myxedema coma, more reports are needed to evaluate epidemiologic data associated with this disease.⁴

Pathophysiology

Myxedema coma is a result of significant deficiency of thyroid hormone.⁶ Given the far-reaching role of thyroid hormone, the severe deficiency of thyroid hormone seen in myxedema coma is associated with a wide variety of symptomatology and significant morbidity and mortality.² Common presentations include a combination of hypothermia, cardiac depression, slowing of metabolic functions, and central nervous system depression.^2,7,8 It should be noted that while mental depression is common, true coma (unresponsiveness) is unusual. Often, another insult is a precipitating event for myxedema coma.⁸ Sudden discontinuation of thyroid hormone replacement therapy frequently is a precipitating factor.¹ Other known precipitants include infection, hypothermia, heart failure, gastrointestinal bleeding, trauma, surgery, cerebrovascular accidents, anterior pituitary dysfunction, and drugs, such as anesthetics, sedatives, tranquilizers, narcotics, barbiturates, amiodarone, phenytoin, rifampin, lithium, diuretics, and beta-blockers.^2,6,9 Metabolic insults, particularly acidosis, hypoglycemia, hyponatremia, hypoxemia, and hypercapnia, also may be precipitating factors for the development of myxedema coma.^6,9 This can greatly complicate the diagnosis of myxedema coma, since many of the aforementioned conditions can present with similar symptomatology and may delay the diagnosis of myxedema coma.

Presentation

Signs and Symptoms. Given the broad spectrum of roles that thyroid hormone plays within the body, it is not surprising that a significant deficiency of thyroid hormone, as seen in myxedema coma, will present with a variety of symptoms. A hallmark of myxedema coma is hypothermia (below 35.5°C or 95.9° F) and depressed central nervous system functioning, ranging from lethargy to coma.^6,8-10 However, manifestations within other organ systems are common. Neurologically, patients may have decreased deep tendon reflexes, ataxia, seizures, disorientation, and psychosis.^2,9,11,12 Hypoventilation often is present, due to impaired respiratory drive and diaphragmatic muscle weakness, which may contribute to an eventual coma.² Additional respiratory manifestations include macroglossia and swelling of the vocal cords, causing airway obstruction, and pleural effusions leading to reduced tidal volumes.^2,6 Cardiovascular presentations, such as hypotension, bradycardia, heart block, QT interval prolongation, pericardial effusion, and decreased cardiac contractility, are seen commonly in these patients.^2,9 Gastrointestinal dysfunction may present as abdominal pain, nausea, vomiting, decreased appetite, or constipation, or may manifest more severely and include gastrointestinal bleeding, paralytic ileus progressing to toxic megacolon, or ascites.^2,9,12

Endocrine signs and symptoms on presentation may include fatigue, dry skin, nonpitting edema, coarse and sparse hair, cold intolerance, hypoglycemia, and hyponatremia, which may further exacerbate imminent coma.^6,12 Additionally, bladder atony can cause significant urinary retention.^2,9,12 Moreover, myxedema coma can present with coagulopathies, such as acquired Von Willebrand disease, factor deficiencies, or disseminated intravascular coagulation due to underlying sepsis, with all of these pathologies associated with elevated bleeding risk and potential decompensation.^2,9

Ultimately, given the many possible findings associated with myxedema coma, it is important to take a thorough history. Clinicians should inquire about a history of thyroid dysfunction, thyroid medications, compliance with medication regimen, history of thyroid surgery, and exposure to any common triggers to myxedema coma.² Key findings from the physical examination, such as goiter, dry skin, edema, alopecia, macroglossia, impaired reflexes, hypothermia, bradycardia, and hypotension, should prompt further investigation and close monitoring.^2,8,12 Warning signs of impending decompensation include absence of mild diastolic hypertension, severe hypothermia, and significantly depressed mentation.^2,8

Diagnostic Tools

The diagnosis of myxedema coma may be made based on clinical presentation alone, particularly in the setting of altered mental status, hypothermia, and suspicious precipitating factors.^13,14 While there is no laboratory value that specifically designates this diagnosis, there are a variety of characteristic findings that should increase suspicion for this disease.⁶ In the setting of possible myxedema coma, it is important to consider a full laboratory workup, including thyroid labs, serum chemistry, calcium, complete blood count, liver function tests, creatinine phosphokinase, blood gases, electrocardiogram (ECG), and chest radiography. Based on physical exam findings, it may be appropriate to consider lumbar puncture, blood culture, urinalysis, and urine culture if there is any concern of underlying infection, given that signs of infection in these patients often are masked by hypothermia and bradycardia.^6,8,12

In the setting of myxedema coma, thyroid hormone levels typically are quite low, with T4 levels often undetectable and TSH levels low, normal, or high depending on the etiology of illness.^6,8 Patients often present with hyponatremia, due to decreased free water clearance, and hypoglycemia, which likely is a result of decreased metabolism.⁵ Additionally, mild elevations in creatinine and blood urea nitrogen (BUN) are common, especially in the setting of shock.^6,9

Elevations in creatinine phosphokinase, a consequence of altered membrane permeability and subsequent rhabdomyolysis, also will result in kidney injury and electrolyte abnormalities.^5,9 The laboratory workup may reveal renal dysfunction, with elevated antidiuretic hormone (ADH) causing impaired free water excretion and decreased glomerular filtration rate.^6,9 In the setting of end-organ dysfunction, liver function tests may be elevated.⁵ A mild normocytic anemia and leukopenia often are present, with occasional elevations in partial thromboplastin and bleeding times.^5,14

Blood gases may show hypercapnia in the setting of respiratory acidosis, particularly in patients with impaired respiratory drive.^2,5,12 Chest radiography may demonstrate pleural effusions and/or cardiomegaly, with echocardiogram indicated if there is suspicion for pericardial effusion.⁵ Characteristic electrocardiogram findings may include bradycardia, decreased voltages, nonspecific ST and T wave changes, complete heart block, bundle branch blocks, or torsades de pointes.^5,9

In the setting of coma, an electroencephalography may be obtained and often demonstrates low amplitude waveforms and decreased alpha-wave activity.⁹ Lastly, an infectious workup often is high yield, and there should be a low threshold to obtain blood and urine cultures given the significant mortality associated with underlying infection in this disease.^6,8 Lumbar puncture may show increased opening pressure and high protein count, likely associated with decreases in metabolism and increased membrane permeability.^2,5

Ultimately, evaluation of myxedema coma with various diagnostic tools is helpful to evaluate the severity of complications associated with this condition and assess potential triggers. Table 1 summarizes the exam and laboratory findings associated with myxedema coma.

Diagnostic scoring systems have been created based on clinical presentation and laboratory findings and may assist clinicians in evaluating the likelihood of myxedema coma diagnosis.^6,15 (See Table 2.)

Treatment and Disposition

Myxedema coma is a life-threatening illness that requires prompt recognition, rapid treatment, and early supportive care to optimize outcomes.^6,8 Administration of thyroid hormone is the mainstay of treatment, although controversy exists regarding the quantity of hormone and the use of T4 vs. T3, or a combination of both.^6,8 There is an absence of randomized controlled trial data. However, existing case studies provide guidance.^6,8,15 Based on a review of the literature, initial doses
of greater than 500 mcg of T4 or
75 mcg of T3 appear to be associated with higher mortality.^8,15 It is recommended that initial dosing be chosen carefully to avoid precipitating further decompensation. Early treatment should be intravenous, given the altered gastric absorption that accompanies this disease process.² Additionally, while more studies are necessary, initial data suggest that the use of T3 may carry a higher risk of cardiac effects, including fatal arrhythmia and ischemia.^8,15 A reasonable initial treatment regimen would be intravenous (IV) dose of 300 mcg to 500 mcg T4, with the addition of 10 mcg T3 if there is no response within 24 hours.^8,12,15 Repeat TSH and T4 values should be obtained and, if therapy is effective, should demonstrate improvement within this timeframe.¹⁵ Maintenance on 100 mcg T4 IV can be continued until oral doses of 50 mcg to 100 mcg T4 are well tolerated.⁸ Alternatively, initial therapy of 200 mcg to 300 mcg T4 and 10 mcg to 25 mcg T3, with subsequent dosing of 10 mcg IV every eight hours may be considered; however, patient risk factors and comorbidities should be weighed carefully, given the potential for elevated mortality.^8,15

Stress dose glucocorticoids, such as 100 mg IV hydrocortisone every eight hours, should be given in the emergency department (ED), especially given the high mortality associated with adrenal crisis.^5,8 Additionally, even in the absence of clinical signs of infection, empiric antibiotics should be administered because of the high rates of concomitant infection.^6,9

Beyond replacement of thyroid hormone, supportive care is essential to optimize outcomes.^8,11,15 Hypothermia should be approached with external warming through regular blankets, since peripheral warming may lead to cardiovascular decompensation.^5,8 Hypovolemia may be corrected cautiously with IV normal saline, although the patient should be monitored carefully for hyponatremia.^5,8 Endotracheal intubation and mechanical ventilation should be initiated in the setting of respiratory depression.^5,8,15 Glucose and electrolyte repletion may be indicated based on laboratory studies.²

Clinicians should investigate the underlying precipitant of myxedema coma and treat accordingly.^6,8,15 The patient ultimately should be admitted to the intensive care unit.¹¹

Factors associated with poor prognosis include increased age, cardiac dysfunction, and worsening hypothermia. Overall mortality is reported to be between 25% to 60% even in the setting of favorable prognostic factors.^2,5

Thyroid Storm

Epidemiology

Thyroid storm, decompensated thyrotoxicosis, is a life-threatening condition associated with elevated activity of thyroid hormone that overwhelms physiologic capabilities.⁹ Studies estimate that the incidence of thyroid storm is between 0.55 to 0.76 per 100,000 people per year, and 4.8 to 6.28 per 100,000 hospitalized patients per year.^16,17 Although rare, the mortality of thyroid storm without treatment is between 80% and 100%, which highlights the importance of recognizing this disease process.¹⁸ Across studies, it was noted that approximately two-thirds of patients presenting with thyroid storm were female, commonly between the ages of 30 and 45 years of age.^16,18,19 Compared to thyrotoxicosis, the mortality rate of thyroid storm is 12 times higher and is present in 1% to 2% of hospital admissions for hyperthyroidism.^9,17,19 Despite improvements in treatment, reports suggest that the mortality rate of thyroid storm is between 8% and 50% even with appropriate therapies.^18,19

Risk factors for poor prognosis include increased age, neurologic changes, delays in treatment, need for dialysis, and mechanical ventilation.¹⁹ The most common cause of death in patients with thyroid storm is multi-organ failure.¹⁸

Pathophysiology

Similar to myxedema coma, thyroid storm involves significant dysfunction but with the excess production and release of thyroid hormone.¹⁹ Thyroid storm develops as a result of rapid increases in thyroid hormone levels, often in the setting of underlying hyperthyroidism.¹⁸ Increased production of thyroid hormone or TSH may develop in the setting of a precipitating factor and may lead to the development of thyroid storm.¹⁸ Excess thyroid hormone interacts with circulating catecholamines and promotes hyperactivity of the sympathetic nervous system.^6,19 Graves’ disease is the most common cause of thyroid storm. However, toxic multinodular goiter, subacute thyroiditis, ectopic thyroid tissue, metastatic thyroid carcinoma, exogenous thyroid replacement therapy intake, and hydatidiform mole also are potential underlying illnesses.^6,18

In addition to underlying predisposing conditions, a precipitating event usually is required to trigger thyroid storm.¹⁹ Most commonly, this is due to discontinuation of antithyroid therapy or infection, but other common causes include surgery, diabetic ketoacidosis, myocardial infarction, trauma, hypoglycemia, pulmonary embolism, exposure to iodinated contrast, cerebrovascular accidents, eclampsia, stress, or medications, such as amiodarone.^6,18,19 Finally, the black market for thyroid supplementation is rising. Patients are seeking out unregulated medications from other countries or using prescriptions not prescribed to them. Clinicians should take a thorough history in any patients with unexplained and unresponsive tachycardia.

Presentation

Signs and Symptoms. The constellation of hyperthermia, altered mental status, and hemodynamic compromise is a common presentation of thyroid storm.²⁰ Extremely elevated temperature, between 104°F and 106°F, often with diaphoresis and heat intolerance, is a classic presenting feature.¹⁹ Cardiac dysfunction, including tachycardia, palpitations, systolic hypertension, postural hypotension, atrial fibrillation, and high output cardiac failure with pulmonary edema also are associated with thyroid storm.^{6,18,19,20,21} Central nervous system involvement also is common, ranging from agitation, anxiety, and delirium to psychosis, seizures, and coma.^19,21

Gastrointestinal manifestations, such as nausea, vomiting, diarrhea, and increased appetite, can be seen.^18,19 Tremors, hyperreflexia, weight loss, hair loss, jaundice, and vision changes also may be present in these patients to varying degrees.^18,19,21 Physical exam findings relate closely to presenting symptoms and may include high temperature, tachycardia, tremors, moist skin, hyperreflexia, exophthalmos, goiter, and/or thyroid gland tenderness.^6,18,19 Of note, atypical presentations of thyroid storm are common among elderly patients, typically involving stupor, coma, cardiac failure, and few of the classic signs of thyroid hormone excess.²¹

Diagnostic Tools

Diagnosis of thyroid storm primarily is clinical, but laboratory and imaging studies are helpful in assessing complications and necessary interventions.^18,19 Regardless, especially in the setting of known or suspected underlying hyperthyroidism, the workup should not delay treatment.¹⁹ Thyroid function tests in the setting of thyroid storm will show high total and free T4 and T3, although extremely high levels of thyroid hormone may not always be present.^6,18,19 TSH levels typically are severely suppressed but may be normal or elevated depending on the etiology of thyroid dysfunction.^5,18,19 Leukocytosis may be seen, particularly in the setting of underlying infection, which often is a precipitating factor.^6,19 Blood glucose may be slightly elevated because of inhibition of insulin and gluconeogenesis and may be accompanied by ketoacidosis or lactic acidosis.^6,18,19 Serum electrolytes typically are within normal range, except for calcium, which may be elevated due to thyroid hormone-mediated bone resorption.^6,19

Renal and liver function tests should be obtained to evaluate for the presence of end-organ dysfunction.¹⁸ Additionally, serum cortisol levels should be assessed to determine underlying adrenal insufficiency.¹⁸ Table 3 summarizes the physical exam and laboratory findings associated with thyroid storm.

Chest radiography and blood and urine cultures should be obtained to evaluate possible infection.¹⁸ An ECG should be obtained to evaluate tachyarrhythmias, such as atrial fibrillation, and ischemia.¹⁸ In women of childbearing age, pregnancy and gestational trophoblastic disease should be excluded via measurement of human chorionic gonadotropin (HCG) levels.²¹ Thyroid ultrasound can be obtained to assess for toxic nodular goiter and other structural abnormalities.¹⁸

Similar to myxedema coma, diagnostic scoring systems have been created to assist clinicians with the diagnosis of thyroid storm.^6,21,22 (See Table 4.) These criteria can be used for informed decision-making prior to receiving results from the laboratory workup to avoid treatment delays.^19,21,22

Treatment and Disposition

Prompt treatment of thyroid storm is imperative to optimize outcomes and prevent long-term complications.⁶ The treatment of this disease is multifaceted and focuses on five separate mechanisms: controlling adrenergic tone, blocking thyroid hormone synthesis, limiting thyroid hormone release, reducing peripheral T4 to T3 conversion, and decreasing enterohepatic circulation of thyroid hormone.^5,19,21

Beta-adrenergic blockade should be initiated quickly and can be given first if readily available to control the hyperadrenergic state resulting from excess thyroid hormone. Propranolol at 1 mg/min to 2 mg/min IV for 15 minutes can be initiated promptly, with follow-up doses at 20 mg to 120 mg orally every four to six hours.²¹ In the setting of bronchospasm or other beta-blocker contraindication, equivalent dosing of esmolol or diltiazem, respectively, can be administered.^19,21

Thionamide should be given, as soon as possible, to block thyroid hormone synthesis.^18,19 Either methimazole or propylthiouracil (PTU) may be administered, with initial doses of methimazole ranging between 40 mg and 120 mg orally and PTU at 600 mg to 1,000 mg orally or via nasogastric tube.¹⁸ After the loading dose, additional dosing of antithyroid medications should be administered every four hours, at 20 mg for methimazole and 200 mg to 250 mg for PTU.¹⁸ While there is some controversy over which thionamide to use, both therapies are found to be effective in the treatment of thyroid storm.²¹ PTU traditionally has been the treatment of choice in thyroid storm because of its additional benefit of inhibiting peripheral conversion for T4 to T3. However, its unfavorable side effect profile, including severe liver injury and acute liver failure, raises safety concerns, and official recommendations have shifted to methimazole.^6,16,21 In the setting of first-trimester pregnancy, PTU still is the treatment of choice.²¹

Next, thyroid hormone release must be blocked by administration of iodine at least one hour after thionamide therapy.^6,18,21 It is important that this is delayed for at least one hour from the initial treatment to avoid worsening the underlying condition. This can be given as five to 10 drops orally of Lugol’s solution every six hours or five drops of saturated solution of potassium iodide every six to eight hours.^18,21

Reduction of peripheral conversion of T4 to T3 is achieved primarily via glucocorticoids, such as hydrocortisone 100 mg IV every eight hours or dexamethasone 2 mg every six hours.^18,19,21 Additionally, some reports have suggested that glucocorticoid use in thyroid storm may optimize survival rates, likely secondary to prevention of underlying adrenal crises.¹⁸ Finally, reduction of enterohepatic thyroid hormone circulation can be achieved with cholestyramine, a bile acid resin, at a dose of 4 mg orally two to four times per day.²¹

Supportive therapy is a mainstay of treatment while the other treatments are taking effect.^6,19 Judicious administration of isotonic IV fluids, supplemental oxygen, cooling blankets, and acetaminophen is appropriate, with escalation of therapy based on hemodynamic stability of the patient.^6,18 When possible, treatment of the underlying cause of thyroid storm should be initiated.¹⁸ In the setting of potential infection, empiric treatment with broad-spectrum antibiotics is warranted.⁶ Patients presenting with thyroid storm should be admitted to the intensive care unit.¹⁹

Other Thyroid Emergencies and Presentations

Hashimoto’s Disease

Hashimoto’s disease is one of the most common autoimmune disorders.²³ It also is the most common cause of hypothyroidism.²³ This disease most commonly affects white females.²⁴ Hashimoto’s disease has a variety of presenting symptoms, including dysphonia, dysphagia, fatigue, bradycardia, hair thinning, dry skin, arthritis, cognitive decline, constipation, and myoclonus. Diagnosis of this disease can be made by laboratory values and histology. Laboratory studies will reveal antithyroid antibodies, specifically anti-TPO, elevated TSH, and low T4.^23,24 Histology reveals loss of architecture and lymphocytic invasion of thyroid tissue.

These patients may present to the emergency department for evaluation of their symptoms. Oral synthetic thyroid hormone is the mainstay of treatment. Glucocorticoids may have a role in acute thyroiditis.²⁵ Supplements, such as vitamin D and selenium, also have been shown to be beneficial.²⁵ Most patients with significant myxedema will require hospitalization. For those being discharged or where there will be a delay in inpatient care, the emergency physician should consider initiating daily thyroid replacement treatment. Although the full dose of oral levothyroxine replacement is 1.6 mcg/kg, lower doses are suggested in older patients, those with cardiac disease, and those with severe long-standing disease. Follow-up should be ensured for titration of the thyroid function.²⁶

Graves’ Disease

Like Hashimoto’s disease, Graves’ disease is an autoimmune etiology of hyperthyroidism and is the leading cause of hyperthyroid. Similarly, middle-age females are the population affected most commonly. A wide array of presenting symptoms is possible, including heat intolerance, palpitations, diarrhea, eye pain, and exophthalmos. The ocular findings in Graves’ disease frequently are obvious and may be the finding that tips the provider off to the presence of underlying thyroid disease. Proptosis or exophthalmos is the most taught and is specific to Graves’ disease. Lid lag, or von Graefe sign, and lid retraction, or Dalrymple sign, are two other ocular manifestations.

Active Graves’ disease presenting as severe hyperthyroidism is treated like thyroid storm. Beta-blocking medications have demonstrated effectiveness in treating the systemic and ocular symptoms. In addition, glucocorticoids often are added to minimize peripheral conversion of T4 to T3.²⁷ Newer medications specifically targeting thyroid eye disease have entered the market. Definitive treatments include radioactive iodine, thyroidectomy, and antithyroid drugs.²⁷

Postpartum Thyroiditis

Pregnancy is known to have a significant impact on thyroid function. This can occur in previously controlled patients as well as new manifestations of disease during the potential for and following pregnancy. Postpartum thyroid dysfunction has been found in approximately 8% of postpartum women, and it more than doubles in postpartum patients with diabetes.²⁸ The usual time course is three to six months after delivery, but it can occur up to 12 months postpartum. The pathophysiology behind this is thought to be restoration of the immune system after its suppression during the pregnancy. While the immune system reconstitutes, a surge of antibodies can be released.²⁹ Current recommendation do not call for routine screening of postpartum patients. Indications for screening for thyroiditis in the postpartum period include postpartum depression, difficulty with lactation, or other symptoms of thyroid disease.³⁰ This diagnosis can be challenging, since many of the symptoms of thyroid disease can mimic symptoms of the postpartum period and other hormone derangements and adjustments.

Apathetic Hyperthyroidism

Apathetic hyperthyroidism is a rare condition found primarily in the elderly. It is an abnormal presentation of thyrotoxicosis. Patients may present with atrial fibrillation, heart failure, generalized weakness, thyromegaly, and weight loss. Unlike standard thyrotoxicosis, the presentation is vague and often misdiagnosed.^31,32 In patients presenting with these vague complaints, and especially those presenting with atrial fibrillation, thyroid studies should be sent. In these patients, treatment of the underlying thyrotoxicosis often will resolve the atrial fibrillation, which may be refractory to other efforts until the thyrotoxicosis is addressed.

Thyroid Abscess

Thyroid abscesses are a rare complication of procedures or goiter but represent a life-threatening emergency.^33,34 Because of the proximity of the thyroid to the airway, any swelling of the tissue represents a significant compromise to airway patency. (See Figure 1.) These patients often present with goiters or thyroglossal fistula, or abscesses can occur after procedures.^33,34 Staphylococcus, Streptococcus, Pneumococcus, or anaerobes are the most common infective organisms.^33,34 Symptoms of thyroid abscess include neck pain, swelling, stridor, fever, difficulty swallowing, voice change, and difficulty breathing. The provider will need a high suspicion to make this diagnosis, since it is rare. Computed tomography, plain films, and ultrasound all are useful diagnostic modalities in confirming the diagnosis. Subspecialty consult, otolaryngology, intravenous antibiotics, early airway support, and close observation for rupture and progression to mediastinitis are necessary.

Summary

Thyroid emergencies can present across the spectrum from asymptomatic laboratory abnormalities to symptomatic hypothyroid or hyperthyroid to coma or storm. Emergency medicine clinicians should be comfortable evaluating and treating these patients. Table 5 summarizes thyroid function studies and how to interpret them. It is important to note that a TSH level, by itself, does not definitively diagnose either hyperthyroidism or hypothyroidism.

Thyroid emergencies like myxedema coma and thyroid storm, while rare, are associated with significant mortality and require swift recognition and treatment to optimize outcomes. Both diseases are primarily diagnosed clinically, and a thorough workup is essential to identify complications and underlying causes. Prompt administration of thyroid hormone and glucocorticoids for myxedema coma, or beta-blockers and antithyroid therapy for thyroid storm, is essential to prevent further decompensation. Supportive care is a mainstay of treatment for both conditions, and careful monitoring in the intensive care unit is required to improve the chance for recovery.

Case Conclusion

The 50-year-old female patient presents for altered mental status. Her presenting vital signs are heart rate
160 bpm, blood pressure 175/85 mmHg, temperature 102.5°F, and 94% oxygen saturation on room air. What are the primary concerns in this patient?

This patient appears to be in thyroid storm. Currently, she is relatively stable. She should be monitored closely. She should be given antipyretics and cooling measures. A toxicology screen and basic laboratory tests should be obtained, as well as cultures and an ECG. As long as there is no concern for concomitant substance use, particularly cocaine, beta-blockers can be initiated as well as methimazole. Steroids can be administered concomitantly. Iodine should be administered in a delayed fashion. This patient should be admitted to the intensive care unit.

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