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57. Thyroid Storm: Glands Gone Wild!
Keywords
Thyroid stormHyperthyroidismEndocrinologyEndocrinological emergenciesT4, TSHThyroid Storm—It’s Raining ThyroxineCase
Palpitations and Diaphoresis
Pertinent History
Patient is a 53-year-old female who presents to the Emergency Department accompanied by her husband. She states she has felt like her heart was racing all day today, and she feels hot and sweaty. She denies any upper respiratory symptoms, chest pain, shortness of breath, abdominal pain, vomiting, or diarrhea. She feels slightly nauseated. Her husband also adds that she has been mildly confused over the past few days and seems to get lost in familiar areas or intermittently forgets what she is doing, but she seems more agitated today. They deny any hallucinations or substance abuse. She does not have a history of dysrhythmias or coronary artery disease. She has never had a stress test or undergone cardiac catheterization. Her husband brought the patient’s medication bottles with him. He denies that she has started any new medications, vitamins, or supplements recently.
Past Medical History
Gastroesophageal reflux disease (GERD), hyperthyroidism, arthritis.
Family History
Mother – hypertension, diabetes; Father – hypertension, Coronary Artery Disease, hyperlipidemia.
Surgical History
Cesarean section.
Social History
Nonsmoker, Consumes Alcohol Socially, Denies Intravenous Drug Use (IVDU)
Pertinent Physical Exam
Vitals: Heart Rate 160, Blood Pressure 130/74, Oxygen saturation (O2 sat) 98% on room air, Respiratory rate 24, Temperature 102.2 °F/39 °C.
Head, Ears, Eyes, Nose, and Throat: Normocephalic, atraumatic. Exophthalmos present bilaterally. Ears and nose unremarkable. Neck supple. Enlarged thyroid palpated with nodules.
Exophthalmos. (Image courtesy of Colin Kaide, MD)
Cardiovascular: Tachycardic, irregular rhythm. No murmurs . Intact symmetric distal pulses.
Pulmonary: Lungs clear to auscultation bilaterally (CTAB), appropriate chest wall excursion. Speaking in slightly shortened sentences secondary to tachypnea at rest.
Abdomen: Soft, Nontender/Nondistended, Positive bowel sounds.
Extremities: No clubbing, cyanosis, or edema.
Neuro: Hyperreflexia noted throughout all extremities. Generally tremulous at rest. No clonus or rigidity. No focal weakness or deficits. Appears anxious and delirious, occasionally staring off during questioning.
Skin: Diaphoretic. Thin hair.
Pertinent Diagnostic testing
Lab results | |||
|---|---|---|---|
Test | Results | Units | Normal range |
WBC | 13.3 | K/uL | 3.8–11.0 103 / mm3 |
Hgb | 11 | g/dL | (male) 14–18 g/dL (female) 11–16 g/dL |
Platelets | 212 | K/uL | 140–450 K /uL |
Creatinine | 0.8 | Mg/dL | 0.6–1.5 mg/dL |
Potassium | 4.3 | mEq/L | 3.5–5.5 mEq/L |
Glucose | 146 | Mg/dL | 65–99 mg/dL |
Lactate | 1.0 | Mmol/L | < 2.0 |
Uric acid | 11.6 | Mg/dL | (3.5–7.7 mg/dL) |
Troponin | <0.01 | Ng/ml | < 0.04 |
BNP | 170 | Pg/ml | <100 |
TSH | 0.0003 | μU/mL | Less than 9 μU/mL |
Free T4 | 6 | μU/mL | 5–13 μg/dL |
Chest X-Ray
No acute cardiopulmonary findings.
Computed Tomography Angiogram Chest
No pulmonary embolism identified. No focal consolidation or effusion bilaterally.
Urinalysis and Urine Drug Screen
Negative.
Electrocardiogram
Irregularly irregular rhythm rate of 160 bpm, narrow QRS, unable to identify P waves, nonspecific ST or T wave changes. Consistent with atrial fibrillation with rapid ventricular response.
Emergency Department (ED) Course
Patient’s home medications were brought to the ED by husband and include chondroitin, aspirin, omeprazole, and methimazole. On further discussion with the patient’s husband, he states they were recently traveling out of the country and she forgot to pack her medications, so she had not taken her methimazole for the past 5 days. Due to recent travel and new onset atrial fibrillation (a-fib), computer tomography angiography (CTA) of the chest was obtained to evaluate for pulmonary embolism, which was negative. Vitals were significant for tachycardia and hyperthermia. Labs were relatively unremarkable other than a mild leukocytosis, but she did not have overt signs of infection evident on her physical exam, chest X-ray, or urinalysis. Urine drug screen negative for tested substances. Electrocardiogram (EKG) showed atrial fibrillation with rapid ventricular response (RVR), which was new-onset atrial fibrillation as patient had no history of previous dysrhythmia. Given her history of hyperthyroidism and recent medication noncompliance, a clinical diagnosis of thyroid storm was suspected.
Update 1
Patient was given 1 mg IV propranolol every 15 minutes for heart rate control and 600 mg of oral propylthiouracil (PTU). 1 hour after PTU, 8 drops of Lugol’s solution iodine was administered. She was also given hydrocortisone 300 mg IV and acetaminophen for hyperpyrexia. Blood and urine cultures were drawn. As her medication noncompliance was a reasonable cause of thyroid storm without identified infectious etiologies, broad-spectrum antibiotics were held. On reassessment, patient’s heart rate improved to 138 from 160, her temperature was 98.6 °F/37 °C, she was more alert, oriented times 3, and answering questions appropriately. An admission to ICU was requested.
Learning Points: Thyroid Storm
Priming Questions
- 1.
How do you differentiate between hyperthyroidism and thyroid storm? What is used to make the diagnosis of thyroid storm?
- 2.
If so many people have thyroid dysfunction and hyperthyroidism, which subset of these people develop thyroid storm and who is predisposed?
3. When treating thyroid storm, does the order in which you give the medications make a difference?
Introduction/Background
- 1.
Hyperthyroidism progresses to thyroid storm in approximately 12% of patients [1].
- 2.
Thyroid storm is a life-threatening condition that can lead to end-organ damage and cardiovascular collapse if not treated emergently [2].
- 3.
The cause of progression from hyperthyroidism to thyroid storm is not well defined but is thought to be due to altered peripheral response to thyroid hormone and resulting adrenergic hyperactivity [3].
- 4.
The most common precipitating event of thyroid storm is infection, however, there are other physiologic triggers including burns, diabetic ketoacidosis (DKA), pulmonary embolism (PE), stroke, surgery, trauma, and parturition [4].
- 5.
Thyroid storm has a nonspecific presentation that mimics many other more common ED presentations, thus the physician must maintain a high index of suspicion for the diagnosis.
- 6.
The most common clinical features of thyroid storm are hyperpyrexia, tachycardia, central nervous system (CNS) dysfunction, and gastrointestinal (GI) manifestations [4–6].
- 7.
Mortality of thyroid storm is currently reported at 10% [7].
Physiology/Pathophysiology
- 1.
Hyperthyroidism is classically defined as low TSH and elevated free T3 and T4 hormone.
The hypothalamus secretes thyroid releasing hormone (TRH), which stimulates release of thyroid stimulating hormone (TSH) from the pituitary. TSH binds receptors on the thyroid cells to stimulate release of thyroid hormone [7].
The T4 form of the hormone, thyroxine, is the most prevalent type in circulation; however, triiodothyronine (T3) is the active form that binds nuclear receptors [8].
The ratio of T4 to T3 circulating in the blood stream is 20:1 [3].
The majority of circulating thyroid hormone is bound to proteins including thyroid binding globulin (TBG), albumin, and transthyretin [7]. The percentage of free hormone determines thyroid activity.
T4 undergoes conversion to T3 by 5′ deiodinase. T3 then enters the cells and binds to receptors, which affect gene regulation and transcription [7].
- 2.
Excess thyroid hormone has effects including elevated metabolic rate, increased temperature and heart rate, increased cardiac contractility, as well as muscle and CNS excitability.
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