Welcome to the emDOCs.net podcast with Brit Long, MD (@long_brit) and Manpreet Singh, MD (@MprizzleER)! Join us as we review our high-yield posts from our website emDOCs.net.
Today on the emDocs cast with Brit Long, MD (@long_brit) we cover two topics: Decompensated Hypothyroidism and Euglycemic Diabetic Ketoacidosis
To continue to make this a worthwhile podcast for you to listen to, we appreciate any feedback and comments you may have for us. Please let us know!
Subscribe to the podcast on one of the many platforms below:
Welcome to the emDOCs.net podcast with Brit Long, MD (@long_brit) and Manpreet Singh, MD (@MprizzleER)! Join us as we review our high-yield posts from our website emDOCs.net.
Today on the emDocs cast with Brit Long, MD (@long_brit) we cover two topics: Decompensated Hypothyroidism and Euglycemic Diabetic Ketoacidosis
To continue to make this a worthwhile podcast for you to listen to, we appreciate any feedback and comments you may have for us. Please let us know!
Subscribe to the podcast on one of the many platforms below:
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.[1,2,3] Unfortunately, it is incredibly easy to miss as it commonly presents with a constellation of nonspecific symptoms similar to many common ED chief complaints. Due to the thyroid’s varied affects, hypothyroidism can affect a vast array of organ systems.[4]
Typically, a patient maintains homeostasis until a precipitating event induces decompensated hypothyroidism like infection, ischemia, ingestion, PE, burns, hyponatremia, or cold exposure. It is most often seen in female elderly patients and tends to occur during the winter months.[6]
While decompensated hypothyroidism presenting symptoms vary significantly, some main features typically remain consistent.
1. Altered Mental Status: Though often called ‘Myxedema Coma’, decompensated hypothyroid patients rarely present in a true coma. Instead they typically present altered, lethargic, or delirious.[5,7]
2. Low and Slow: Patients are typically hypothermic, bradycardic, hypotensive, hypoxemic, hypercapnic, and hypoglycemic. Hypothermia is extremely common in decompensated hypothyroidism. Be aware that a normal temperature in a decompensated hypothyroid patient is actually concerning for an underlying infection.[4] The loss of thyroid hormone typically results in decreased HR and loss of motor tone. Hypotension is often refractory to both volume resuscitation and vasopressors. The hypotension does not resolve until thyroid hormone administration.[4] Respirations are slow with low tidal volumes, which may lead to both hypoxia and hypercapnia and pending respiratory failure.[10] Hypoglycemia can also occur.
3. Precipitating event: Precipitating events often require treatment. Focusing solely on the decompensated hypothyroidism may miss a treatable and reversable underlying pathology.[8]
4. History of hypothyroidism: While some decompensated hypothyroidism patients may have no previous history of hypothyroidism others may already have been diagnosed previously. [8,9] An anterior midline neck scar, history of radioactive iodine ablation, or levothyroxine on the medication list all indicate of a history of hypothyroidism. [4]
The initial work-up consists of TSH and free T4 to evaluate thyroid function. Hypothyroidism typically presents with an elevated TSH and a decreased T4. More rarely, the hypothyroidism is due to a central etiology, which would result in a low TSH and a low T4.[4] Concurrently the physician should evaluate the patient for both a precipitating factor and derangements resulting from the hypothyroidism. Additional tests include CBC, metabolic panel, cultures, VBG, CXR, and ECG. Due to altered mental status, we recommend head CT as well.
Although the TSH and T4 may aid in the diagnosis of hypothyroidism the levels of these tests do not determine whether the patient is in compensated vs. decompensated hypothyroidism.[4,14] Decompensated hypothyroidism is a clinical diagnosis, and once suspected the provider should immediately begin treatment.
The initial treatment consists of the typical ED evaluation of large bore IVs, supplemental oxygen as needed, and cardiac monitoring as well as evaluation and stabilization of the airway, breathing, and circulation. These patients can be a difficult airway due to lingual edema and the physiologic derangements. After a primary and secondary survey reveals a clinical suspicion for decompensated hypothyroidism, the next step is to identify and treat the precipitating factors as listed above. One should strongly consider empiric antibiotics administration, as infection is often the common underlying precipitant. Vasopressors may also be used if indicated, however it is important to note that they may be ineffective without thyroid hormone replacement. Begin resuscitation with IV fluids and glucose.
Though thyroid hormone replacement should be administered immediately once the diagnosis is suspected, with 100 mg of stress dose IV hydrocortisone recommended as well. Since the hypothyroidism may be associated with adrenal insufficiency, thyroid replacement without steroids could lead to an adrenal crisis. [4,15] Laboratory results are not needed prior to treatment.
IV thyroxine (T4) with the dose of 4mcg/kg, typically between 100-500 mcg is the first line treatment. The levothyroxine IV doses are then tapered over the following days until patient can tolerate oral medications. Elderly patients or those at risk for cardiac side effects should be given doses on the lower end, while otherwise healthy patients can receive doses on the higher end of the dose range.[4,15] T4 is the preferred first line agent as T3 may precipitate cardiac arrythmias in patients with underlying cardiac disease. [1,4,15]
Limited studies have evaluated the prevalence of missed decompensated hypothyroidism diagnosis in the ED. However, one study demonstrated only 21% of primary overt hypothyroidism was 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.[6]
The ambiguity and non-specific symptoms seen in both compensated and decompensated hypothyroidism likely contribute to the difficulty in obtaining the diagnosis. Another complicating factor is that the precipitating cause may reasonably explain the patient’s presentation. By recognizing and treating the precipitating cause, the physician may miss the additional overt and decompensating hypothyroidism. Although it is imperative to treat the precipitating event, the mortality of missing decompensated hypothyroidism can reach 100% if left untreated.[1] These mistakes may be amplified in the ED due to increased anchoring bias due to its fast-pace.
As this rare disease can mimic many others, the diagnosis is extremely difficult. Remember that hypothyroidism is a laboratory diagnosis, but decompensated hypothyroidism is a clinical diagnosis. It must be considered even in patients with multiple non-specific complaints if they fit the disease profile. One should also consider the demographics and time of year, as the classic decompensated hypothyroidism case is that of a confused, hypothermic, and hypotensive elderly woman presenting during the winter months. Lastly, a history of hypothyroidism or midline anterior neck scar should also raise clinical suspicion for this disease. Once suspected, immediately treat with stress dose steroids and IV T4. Provide IV antibiotics, as patients typically have an underlying infection. Be careful rushing to intubate these patients, as they have physiologically and anatomically difficult airways.
EDKA
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.
EDKA has a 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.
There is a 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 value. Symptoms include nausea, vomiting, malaise, and fatigue. Vomiting may be one of the most common findings.
Consider obtaining electrolytes, glucose, renal function, serum ketones, and a venous blood gas. Beta-hydroxybutyrate and pH recommended by the American College of Endocrinology for diagnosis.
Management is similar to DKA, plus glucose. Fluids, electrolytes, insulin. 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.