Today on the emDocs cast with Brit Long, MD (@long_brit) we cover two topics: Decompensated Hypothyroidism and Euglycemic Diabetic Ketoacidosis.

Part 1: Decompensated Hypothyroidism

– Decompensated hypothyroidism, AKA Myxedema Coma, is a diagnosis we must recognize early in the ED as delayed or missed diagnosis carries significant mortality and morbidity. Unfortunately, it can be difficult to diagnose with its nonspecific symptoms.

– Classic picture is an elderly female patient in winter months who is altered and hypothermic.

– Variety of precipitating causes: Infection/sepsis (most common cause), environmental exposure (cold), hypoglycemia, PE, CHF, stroke, intoxication, MI, burn, trauma, anemia, medications (noncompliance, amiodarone, beta blockers, sedatives, opioids, lithium, phenytoin)

– Presentation:

  • Altered Mental Status: Myxedema coma is a misnomer. These patients typically don’t present in true coma, but rather with altered mental status or confusion.
  • Low and Slow: Hypothermic, bradycardic, hypotensive, hypoxemic, hypercapnic, and hypoglycemic. Hypothermia is extremely common in decompensated hypothyroidism. A normal temperature in a decompensated hypothyroid patient is concerning for underlying infection.
  • Precipitating event: Must treat underlying etiology/precipitating cause (ie, infection needs antibiotics).
  • History of hypothyroidism: Look for anterior midline neck scar, history of radioactive iodine ablation, or levothyroxine on the medication list.

– Obtain ECG, CXR, renal and liver function, electrolytes, CBC, CK, coagulation panel, VBG, UA. Due to AMS, head CT is likely recommended. May find hyponatremia, hyperkalemia, elevated liver enzymes, elevated CK, AKI, coagulopathy. ECG may show bradycardia, low voltage, QT prolongation.

– Treatment: Priorities include airway, hemodynamics, managing underlying etiology, steroids and thyroid hormone administration, supportive care.

  • Airway: difficult airway due to lingual edema and physiologic derangements.
  • Resuscitate with fluids and vasopressors, though patients often do not improve until they receive steroids and thyroid hormone.
  • Replete glucose.
  • Broad-spectrum antibiotics recommended.
  • Passive rewarming.
  • IV steroids to include hydrocortisone and IV thyroxine (T4) at 4 mcg/kg, or 100-500 mcg IV. T3 is controversial but can be considered in those who do not respond to T4 or those who are critically ill; however, it increases risk of arrhythmia.

– How often do we miss it? Studies suggest only 21% of primary overt hypothyroidism is diagnosed in the ED, with median time to diagnosis being 3 days. Of patients found to be in decompensated hypothyroidism only 50% were initially diagnosed in the ED. Mortality can reach 100% if not treated.

– Why do we miss it? Ambiguity and nonspecific symptoms. The precipitating cause may explain the patient’s presentation and signs/symptoms, and clinicians may anchor on this.

– How do we improve? Decompensated hypothyroidism is a clinical diagnosis, not based on labs (though they can assist us). Consider the condition in those with the ‘low and slow’ features,  those with multiple non-specific complaints, those who fail to respond to vasopressors and fluids, and repeat episodes of hypoglycemia.

Part 2: Euglycemic DKA


Diabetic ketoacidosis (DKA) is an endocrine emergency. A subset of diabetic patients may present with relative euglycemia with acidosis, known as euglycemic diabetic ketoacidosis (EDKA), which is often misdiagnosed due to a serum glucose < 250 mg/dL.

– EDKA was first described in 1973 by Munro et al., followed by the publication of a larger case series in 1993. The recognition and incidence of EDKA have increased in recent years, specifically with sodium-glucose cotransporter-2 (SGLT2) inhibitors in insulin-deficient patients with chronic type 2 diabetes, type 1 diabetes, or latent autoimmune diabetes.


Complex pathophysiology, which likely includes an absolute insulin deficiency or relative insulin deficiency with severe insulin resistance. This leads to increased glucagon and fatty acid release.

– Mechanism also includes reduced glucose availability and production during a fasting state and/or increased urinary glucose excretion.

– SGTL2 inhibitors work on the sodium-glucose cotransporter-2 protein, which is located in the proximal renal tubules and responsible for absorption of up to 90% of filtered glucose. This increases urinary excretion and blocks the reabsorption of glucose, resulting in glucosuria, reduced serum availability of carbohydrates, and volume depletion.

– Wide variety of conditions associated with EDKA, including fasting state, gastroparesis, renal disease, liver disease, intoxication, pregnancy, infection, SGLT2 inhibitor use, self-treatment with insulin for DKA prior to ED presentation.


– Close to 50% of patients experience a delay in diagnosis due to relatively normal glucose values.

– Symptoms include nausea, vomiting, malaise, and fatigue. Vomiting may be one of the most common findings.


– Beta-hydroxybutyrate and pH recommended by the American College of Endocrinology for diagnosis.

– Consider obtaining electrolytes, glucose, renal function, serum ketones, and a venous blood gas.


Similar to DKA = fluids and address underlying condition => potassium => insulin and glucose

– Balanced crystalloid fluid resuscitation with 1-2 L during the first 1-2 hours.

– Replete potassium based on level. For potassium < 3.5 mEq/L, replete potassium first. Potassium supplementation is recommended at 10mEq/L IV for those with serum potassium 3.5-5.5 mEq/L. If serum potassium is > 5.5 mEq/L, potassium supplementation can be held.

– For patients with serum potassium between 3.5-5.5 mEq/L, initiate insulin at a rate of 0.05-0.1 units/kilogram/hour alongside dextrose 5% to avoid hypoglycemia and improve resolution of ketosis.

– Insulin is utilized to resolve ketoacidosis, no matter the serum glucose level, and insulin infusion is recommended even if patients do not use insulin for home serum glucose control.

– Monitor glucose and serum electrolytes every hour. SGLT2 inhibitors should be discontinued, but they may be restarted after resolution of EDKA. Due to need for monitoring and insulin infusion, admission to the ICU is likely needed.


– Clinicians should consider EDKA in patients with nausea, vomiting, malaise, or fatigue in those with chronic liver disease, starvation, pregnancy, or on SGLT2 inhibitor.

– A glucose < 250 mg/dL should not be used to exclude DKA.

– If EDKA is possible, serum pH, bicarbonate, and ketones should be obtained.

– Treatment includes intravenous fluids, insulin, and glucose, as well as management of the underlying etiology (ie, antibiotics for infection).

The post emDOCs Podcast – Episode 19: Decompensated Hypothyroidism and Euglycemic Diabetic Ketoacidosis appeared first on – Emergency Medicine Education.

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