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On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023
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Image from Hao J, Liu M, Mo Z. Case Rep Med. 2012;2012:271345. [Open access.] PMID: 23049563; PMCID: PMC3461311.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
The above image shows lateral eyebrow loss, a sign of Sheehan syndrome, a pituitary apoplexy.
Endocrine emergencies consist of several relatively uncommon but potentially life-threatening conditions, and their diagnostic and management challenges can lead to delays in timely recognition and treatment.
Adapted images from Patel P, Bekkerman M, Varallo-Rodriguez C, Rampersaud R. Case Rep Crit Care. 2016;2016:3438080. [Open access.] PMID: 27872766, PMCID: PMC5107213.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
An elderly woman presented with a nonconvulsive seizure and myxedema coma. Top row: Electroencephalogram (EEG) on admission (left) and 10 days later (right). Vertical arrows = paroxysmal discharges. Bottom row: Head computed tomography (CT) scan on admission (left) and 14 days later (right), with the latter showing a large right, nonhemorrhagic middle cerebral artery infarct. The infarct liked developed as a result of cerebral vasoconstriction caused by a combination of myxedema coma and epileptic activity.
Myxedema Coma
Myxedema coma is a rare but life-threatening endocrine emergency commonly seen in patients with a history of hypothyroidism.
Myxedema coma is typically triggered by an inciting event such as an infection, a gastrointestinal (GI) bleed, trauma, initiation of new medication, or hypoglycemia. Symptoms/signs include altered mental status, decreased respiratory rate, hypothermia, hypotension, bradycardia, hyponatremia, and hypoglycemia.[1]
Adapted images from Takamura A, Sangen R, Furumura Y, Usuda D, Kasamaki Y, Kanda T. Clin Case Rep. 2017;5(4):399-402. [Open access.] PMID: 28396755, PMCID: PMC5378864.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
These are admission images from an elderly woman with myxedema coma who presented with new-onset severe hypothyroidism and renal failure. Top left (thyroid sonogram): Normal-sized thyroid with small nodules. Bottom left (electrocardiogram [ECG]): Low-voltage waves throughout. Right (chest radiograph): Cardiomegaly and pleural effusion.
In patients with myxedema coma, the ECG may show low voltages (due to pericardial effusion), and chest radiography can reveal a large cardiac silhouette.
In patients with suspected myxedema coma, blood studies should include levels of thyroid-stimulating hormone (TSH), free thyroxine (T4), free triiodothyronine (T3), and cortisol.[2] After the tests are drawn, initiate intravenous (IV) thyroid hormone replacement with T4 and/or T3.[2] If concomitant adrenal insufficiency is suspected, glucocorticoids (hydrocortisone) should be given.[3]
Left: Photo showing exophthalmos from Wikimedia Commons / vasser a. Right: CT scan of enlarged thyroid gland courtesy of Nicole Cimino-Fiallos, MD, FACEP, FAAEM.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
Thyroid Storm
Thyroid storm develops when excessive thyroid hormone release occurs.[4,5,6] Hyperthermia, hypertension, tachycardia, diaphoresis, and altered mental status may be seen in a patient with a history or signs of hyperthyroidism (eg, thinning hair, exophthalmos, goiter). Symptoms/signs of high-output heart failure may be present.[4,5,6]
Laboratory workup should include measurements of TSH, free T4, and free T3.[4,5,6] Reducing the sympathetic surge in these patients is critical. IV beta blockers (ideally propranolol) should be initiated to lower the heart rate to below 100 beats/minute, followed by IV administration of the antithyroid agent propylthiouracil (PTU) or methimazole to block thyroid hormone synthesis. After 1 hour, give iodine orally or via nasogastric tube to block the release of thyroid hormones. Consider administering steroids to decrease T4 conversion to T3.[4,5,6] Finally, patients with thyroid storm are hyperthermic; although passive cooling is encouraged, active cooling can precipitate peripheral vasoconstriction and worsen hypertension.[5]
Sonograms of Hashimoto thyroiditis (top) from Cappelli C, Pirola I, Gandossi E, Formenti A, Agosti B, Castellano M. Int J Endocrinol. 2015;2015:367054. [Open access.] PMID: 26273296, PMCID: PMC4530237. Micrograph of subacute thyroiditis (bottom) from Wikimedia Commons / Nephron.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
Thyroiditis
In acute thyroiditis, thyroid cells are destroyed quickly, large boluses of thyroid hormone are released into the circulation, and patients develop thyrotoxicosis.[7] If thyroid cells are damaged gradually over time, however, symptoms/signs of a hypoactive thyroid will develop.
Several different types of thyroiditis exist, including Hashimoto, postpartum, postradiation, Riedel, and de Quervain.[7] Many of these types are related to autoimmune disease. Some drugs can also cause thyroiditis, including lithium and amiodarone.[8] The diagnosis of thyroiditis often hinges on findings from the physical examination and laboratory testing, including levels of thyroglobulin and TSH, and the erythrocyte sedimentation rate. Treatment is dependent on the type of thyroiditis.[7]
Image from Naka N, Takenaka S, Nanno K, et al. World J Surg Oncol. 2007;5:27. [Open access.] PMID: 17338824, PMCID: PMC1821329.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
A patient suffered acute adrenal crisis after orthopedic surgery for a pathologic fracture. This CT scan depicts bilateral adrenal enlargement consistent with lung cancer metastases (asterisks).
Adrenal Crisis
Adrenal crisis may develop from primary adrenal insufficiency (caused by autoimmunity, metastatic disease, or ischemic or hemorrhagic lesions) or secondary adrenal insufficiency (caused by panhypopituitarism or pituitary corticotropic insufficiency).[4] However, the most common at-risk patients are those taking chronic steroids who develop adrenal suppression over time and then undergo abrupt steroid withdrawal.[4] In patients with sepsis and coagulopathy, Waterhouse-Friderichsen syndrome and hemorrhagic adrenalitis can also cause adrenal crisis.[9]
Adrenal crisis can be characterized by (1) the presence of at least two of the following symptoms: hypotension, nausea/vomiting, fatigue, hyponatremia, hypoglycemia, and hyperkalemia; and (2) improvement after parenteral administration of glucocorticoids.[10] Treatment of adrenal crisis consists of 100 mg IV hydrocortisone and IV fluid resuscitation, as well as management of the precipitating factors.[4,10]
Adapted images from (left) Aziz Siddiqui S, Soomro N, Ganatra A. Pak J Med Sci. 2013;29(1):220-3. [Open access.] PMID: 24353545, PMCID: PMC3809185; and (right) Raul G Palacios III, MD, Brooke Army Medical Center, via MedPix [public domain].
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
The images are from two patients with delayed presentation of congenital adrenal hyperplasia (CAH). Left: Clitoromegaly with normal labia and introitus. Right: CT scan with contrast through the adrenals showing marked symmetrical enlargement of the adrenals and no other significant abnormality.
Congenital Adrenal Hyperplasia
CAH is the most common form of pediatric primary adrenal insufficiency.[11] Females become virilized in utero and typically present at birth with ambiguous genitalia, but males can be more difficult to diagnose. Although most affected male patients are detected on newborn screening, those who do not undergo such testing are at high risk for serious complications and may present to the emergency department (ED) with symptoms/signs of salt wasting (which include lethargy, poor tone, vomiting, poor feeding, and failure to thrive).[11] Clinical manifestations typically appear around age 2-3 weeks in these male infants.
Patients with CAH should be treated with oral hydrocortisone for glucocorticoid replacement.[11]
Adapted images from Dolan RT, Butler JS, Mentee GP, Byrne M. J Med Case Rep. 2011;5:6. [Open access.] PMID: 21226896, PMCID: PMC3025966.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
These images were obtained in a patient with a right-side pheochromocytoma that presented as recurrent urinary tract infections. Top left (sonogram): Note the large, mixed cystic/solid adrenal mass. Top right (CT scan): A solid heterogeneous right adrenal mass is seen, with focal cystic degeneration and slight displacement of the right kidney. Bottom center: Postsurgical gross adrenal pheochromocytoma specimen.
Pheochromocytoma
Pheochromocytomas are neuroendocrine tumors that develop from the chromaffin cells of the adrenal medulla and secrete norepinephrine and epinephrine.[12,13] Left undiagnosed and/or untreated, these lesions can precipitate life-threatening hypertension or cardiac arrhythmias.[13] Patients with pheochromocytomas classically present with paroxysmal hypertension, sweating, headache, and palpitations.[12,13]
The gold standard for diagnosing pheochromocytomas is to measure the 24-hour urinary metanephrines (metabolites of norepinephrine and epinephrine).[12,13] Measurement of serum levels of metanephrines is more sensitive but less specific than urine testing. Treatment of these tumors involves emergent surgical resection.[12]
Adapted images from Makdsi F, Kolade VO. Cases J. 2009;2:8095. [Open access.] PMID: 19918451, PMCID: PMC2769401.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
The chest radiograph (left) shows subcutaneous emphysema (top arrow) and pneumomediastinum at the cardiac border (bottom arrow), findings that were confirmed on CT scan (right), in a patient with diabetic ketoacidosis (DKA).
Diabetic Ketoacidosis
DKA, a dangerous complication of diabetes, is defined by a triad of hyperglycemia, acidosis, and ketonuria or ketonemia.[14,15] Triggers that can cause the cascade of DKA include infection, steroid therapy, trauma, and medication noncompliance.
Patients with DKA are extremely hypovolemic,[14,15] so a rapid IV bolus of crystalloid fluid should be started (20 mL/kg in the first hour). Calculation of the total body water deficit may be helpful.
After an initial fluid bolus, an insulin infusion may be started, with the goal of reducing ketone production and correcting the acidosis.[14,15]
Adapted image from John S, Samuel S, Lakhan SE. J Med Case Rep. 2013;7:51. [Open access.] PMID: 23432798, PMCID: PMC3599740.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
Axial brain CT scans (A) and magnetic resonance imaging (MRI) scans (B-D) of a patient with diabetic hyperglycemic hyperosmolar syndrome (HHS). The CT scans show diffuse leukoencephalopathy involving the frontal, parietal, and temporal lobes. The MRI scans reveal extensive bilateral hemispheric white-matter abnormality.
Hyperglycemic Hyperosmolar Syndrome
HHS, another feared complication of uncontrolled diabetes, occurs less frequently than DKA but has a higher mortality rate.[16] It can also be triggered by infections, medication noncompliance, and trauma. Patients with HHS suffer from insulin resistance, resulting in increased gluconeogenesis, increased levels of cortisol and catecholamines, hyperglycemia, and osmotic diuresis.[16]
Laboratory studies will reveal high osmolarity (>320 mOsmol/kg), hyperglycemia, and an elevated blood urea nitrogen (BUN)/creatinine ratio, but no ketoacidosis.[16] Targeted treatment should include fluid volume replacement with crystalloids, initiation of insulin infusion, and correction of electrolyte imbalances.[16]
The above patient, who suffered from acute-onset headache and mild partial bilateral abducens palsy, was found to have tumefactive perivascular spaces, possibly resulting from small vessel disease (as suggested by the presence of chronic hypertension and diabetes and by her former cocaine use). After correction of the HHS, her headache and palsy improved.
Image from Abu-Abed Abdin A, Hamza M, Khan MS, Ahmed A. Case Rep Crit Care. 2016;2016:4275651. [Open access.] PMID: 27579186, PMCID: PMC4992786.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
This admission chest radiograph is from a patient with diabetes who had euglycemic DKA, was noncompliant with insulin, and suffered from cocaine intoxication.
Euglycemic DKA
Sodium-glucose cotransporter type 2 (SGLT2) inhibitors (eg, canagliflozin, dapagliflozin, empagliflozin), used to treat type 2 diabetes, can cause euglycemic DKA.[17] These drugs work by increasing the excretion of sugar in the patient's urine; when the amount of glucose in the blood decreases, insulin secretion also decreases. Moreover, patients with diabetes may choose to administer less insulin if their blood sugar is lower after starting on these agents. Lower levels of serum insulin and glucose can trigger ketoacidosis despite the presence of a normal blood sugar level. Euglycemic DKA should be treated with the same protocol as DKA.[17]
Adapted image from Albani A, Ferrau F, Angileri FF, et al. Int J Endocrinol. 2016;2016:7951536. [Open access.] PMID: 28074095, PMCID: PMC5198093.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
These coronal T2-weighted (A,B) and sagittal T1-weighted (C) MRI scans in patients with pituitary apoplexy show (A) the low-signal hemorrhagic content of the pituitary mass, (B) the high-signal cystic area inside the lesion and the focal mucosal thickening of the sphenoid sinus (arrow), and (C) a fluid-fluid intralesional level (asterisk), which is pathognomonic of pituitary apoplexy.
Pituitary Apoplexy
Pituitary apoplexy occurs when there is an acute hemorrhage or infarction of the pituitary gland, usually due to an adenoma.[18]
The diagnostic test of choice for pituitary apoplexy is MRI, which can identify a hemorrhage or infarct inside the sella turcica.[18] Vision changes are due to compression on the optic chiasm, and ophthalmoplegia results from compression of cranial nerves III, IV, and VI; surgical decompression may be required. The remainder of treatment is focused on replacing lost hormones. Corticosteroid replacement is used to treat the secondary adrenal insufficiency that often results from pituitary apoplexy.
Image from Wikimedia Commons / Hellerhoff.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
The above image reveals an empty sella turcica (arrow).
Sheehan Syndrome
Sheehan syndrome is a pituitary apoplexy presumably resulting from postpartum spasm of arterioles supplying the anterior pituitary and its stalk. Magnetic resonance imaging (MRI) in the immediate postpartum period will show swelling of the pituitary gland, while atrophy and an empty sella turcica (shown) will develop months to years later.[19]
Laboratory tests for Sheehan syndrome include a complete blood count (CBC) with differential count, a basic metabolic profile, thyroid function tests (TSH, free T3, free T4), and levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, estrogen, cortisol, and growth hormone (GH).[20]
Treatment of Sheehan syndrome includes replacement of ovarian, thyroid, and adrenocorticotropic hormones. Diabetes insipidus, a rare manifestation of the syndrome, can be treated with desmopressin.[20,21]
ECG courtesy of Heather Murphy-Lavoie of Charity Hospital, New Orleans.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
Hypercalcemic Crisis
Severe hypercalcemia is defined as an albumin-corrected calcium level above 14 mg/dL.[22] This condition affects most organ systems and thus often involves multisystem dysfunction. Primary hyperparathyroidism is the leading cause of hypercalcemia in otherwise healthy patients.[22,23] Patients may complain of gastrointestinal (GI) symptoms such as vomiting, abdominal pain, and constipation.
Findings on clinical examination and from laboratory studies may include signs of dehydration, renal colic, and acute kidney injury.[23] Some patients with hypercalcemia may present with confusion, poor concentration, or other nonspecific neurologic features. The ECG will likely exhibit a shortened QT interval (shown).[22,23]
Adapted image from Mageau A, Rigolet A, Benali K, et al. Medicine (Baltimore). 2016;95(10):e3089. [Open access.] PMID: 26962842, PMCID: PMC4998923.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
These are maximum-intensity projection, coronal positron emission tomography (PET) scans of a patient with life-threatening hypercalcemia and isolated sarcoidlike myositis who presented with abdominal pain. Left: Multiple linear and nodular intense fluorodeoxyglucose (FDG) uptake in the intercostal, back, shoulder, and thigh muscles. Right: Complete regression of the pathologic FDG uptake after 2 months of steroid treatment.
The initial treatment of hypercalcemic crisis involves fluid volume correction with crystalloid solution and forced calciuresis.[22,24] Normal saline infusion will reduce calcium levels but will not return the patient to normocalcemia. Loop diuretics may also help in lowering calcium levels.[24] IV bisphosphonates should be started after volume resuscitation has begun; these agents reduce serum calcium levels by inhibiting osteoclast activity.[22,24] However, most patients will ultimately require surgical parathyroidectomy.[23]
Image from Koufakis T, Gabranis I. Pan Afr Med J. 2014;17:65. [Open access.] PMID: 25018815, PMCID: PMC4085941.
On Strike or Working Overtime: 13 Endocrine Emergencies
Nicole Cimino-Fiallos, MD, FACEP, FAAEM | August 29, 2023 | Contributor Information
A patient with hypocalcemia demonstrates prolonged QT interval on ECG (left) and another manifestation of the condition, Trousseau sign (right).
Acute Hypocalcemia
Acute hypocalcemia is most often caused by parathyroid gland dysfunction. A decrease in parathyroid hormone (PTH) results in increased excretion, and decreased absorption, of calcium. Acute hypocalcemia manifests with carpopedal spasms, perioral numbness, extremity paresthesias, Chvostek sign, and Trousseau sign.[25] In severe cases, hypocalcemia can lower a patient's seizure threshold or potentially cause a cardiomyopathy.[25]
Individuals with symptomatic hypocalcemia should be considered for inpatient admission and treatment with IV calcium infusion.[25] If hypomagnesemia is also present, it should be corrected before the hypocalcemia.[25] Finally, in patients with hypoparathyroidism-caused hypocalcemia that is refractory to first-line therapies, the US Food and Drug Administration (FDA) has approved recombinant human PTH (1-84) for treatment.[25]
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Contributor Information
Author
Nicole Cimino-Fiallos, MD, FACEP, FAAEM
Emergency Medicine Specialist
US Acute Care Solutions;
Assistant Medical Director
Emergency Department
Meritus Medical Center
Hagerstown, MD
Disclosure: Nicole Cimino-Fiallos, MD, FACEP, FAAEM, has disclosed no relevant financial relationships.
Editor
Olivia Wong, DO
Section Editor
Medscape Drugs & Diseases
New York, NY
Disclosure: Olivia Wong, DO, has disclosed no relevant financial relationships.
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