Myxedema


Article Author:
Ghada Elshimy


Article Editor:
Ricardo Correa


Editors In Chief:
Sisira Reddy
Joseph Nahas
CHOKKALINGAM SIVA


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
7/22/2019 11:02:26 AM

Introduction

Myxedema coma is a rare fatal condition as a result of long-standing hypothyroidism with loss of the adaptive mechanism to maintain homeostasis. Hypothyroidism due to any cause including autoimmune disease, iodine deficiency, congenital abnormalities or medications like lithium and amiodarone can precipitate myxedema coma if left untreated. Even with early diagnosis and treatment of myxedema coma, the mortality rate is variable with some reports as high as 60% and others as low as 20 to 25% in the presence of advanced intensive support care. Early recognition, with a thorough history and physical exam, and early treatment is paramount for myxedema coma. History of any thyroid dysfunction, thyroid medication, adherence with thyroid medication, thyroid surgery, and history of any drugs that may affect thyroid function require assessment in any patient suspected myxedema coma.[1][2][3]

Etiology

Precipitating factors are[4][5][6][7][8][9][10][11][12][13]:

  • Hypothermia
  • Hypoglycemia 
  • Hypoxemia 
  • Cerebrovascular accident
  • Drugs: amiodarone, lithium, sedatives, tranquilizers, anesthetics, narcotics, phenytoin, rifampin, diuretics, beta-blockers (given the slow drug metabolism in patients with hypothyroidism, these patients have a risk of an overdose of anesthetics and tranquilizers)
    • New case reports with anti-TNF therapy causing myxedema has documentation in the literature.
  • Infection
  • Winter months
  • Congestive heart failure 
  • Gastrointestinal bleeding
  • Surgery(given the effect on pituitary-thyroid axis with decrease thyroid hormones secretion after surgery in response to stress)
  • Burns
  • Carbon dioxide retention
  • Trauma
  • A new case report in 2019 showed that diabetic ketoacidosis precipitated myxedema coma in a patient after total thyroidectomy

Epidemiology

The exact incidence of myxedema coma is not known, but some authors estimate an incidence of approximately 0.22 per 1000000 per year in the western world; however, there is no sufficient epidemiological data from other countries.[3][8] Myxedema coma is more common in females as the hypothyroidism is more common in women (four-fold more than men).[14] Older population aged more than 60 years are more liable to get myxedema coma. Since the patients are usually hypothermic, myxedema coma is more common in winter months. This fact is explained by decrease heat production with age and hypothyroidism in addition to decreased thermoregulation with age.[15][16][13]

Pathophysiology

The thyroid gland begins development during the fourth gestational week as an endodermal thickening of the floor of the primitive pharynx. Its final resting place is located in the anterior inferior visceral compartment of the neck and lies deep to the omohyoid, sternohyoid, and sternothyroid muscles. It is encased in the pretracheal fascia and accompanied by the pharynx, trachea, esophagus, and recurrent laryngeal nerve. The thyroid has two lobes linked by an isthmus. It sometimes has a pyramidal lobe (40% of the population) that extends upward from the isthmus and is responsible for the production of two major hormones: thyroxine (T4), triiodothyronine (T3).[17][18] These hormones are responsible for regulating whole-body metabolism which can decrease by as much as 40 to 50 percent in the complete absence of these hormones and increase by as much as 60 to 100 percent with full secretion.[19][20][21]

The metabolically active hormones the thyroid secretes are T4 and T3 (around 93% T4 and 7% T3 ). Given the fact that T3 is four times more potent than T4, the vast majority of T4 converts to T3 in the tissues. The half-life of T4 is seven days while T3 has a much shorter half-life. Multiple proteins bind to T3 and T4. These proteins include thyroxine-binding globulin, transthyretin (TTR), and albumin. Production of the thyroid hormones by follicles lined by cuboidal epithelial cells occurs inside the thyroid gland. These follicles secrete colloid, which is composed of thyroglobulin and contains the thyroid hormones T3 and T4. At least 50 milligrams of iodine per year or 1 milligram per week are necessary for adequate hormone production.[19][20][21]

Iodine is concentrated within the thyroid cell by a sodium-iodide symporter that pumps one iodide molecule and two sodium ions into the cell. The serum TSH level highly influences the activity of this symporter. A peroxidase enzyme then oxidizes iodide ions to iodine. Then organification occurs by binding of iodine to the amino acid tyrosine located within the thyroglobulin molecule. Thyroglobulin is stored in the thyroid gland and contains approximately 30 molecules of T4 and a few molecules of T3. In the complete absence of production of thyroid hormone, the thyroid contains enough reserve to last about 2 to 3 months.[19][21]

Thyroid hormone influences virtually all cells in the body by activating or repressing a variety of genes after binding to thyroid hormone receptors.  Ninety percent of intracellular thyroid hormone that binds to and influences cellular function is T3, which has been converted from T4 by the removal of an iodide ion. The thyroid hormone receptors, which are associated with the DNA within the target genes, are bound to retinoid X receptors at specific thyroid hormone response elements. Once bound, the transcription process begins and hundreds of new intracellular proteins, mostly enzymes, are formed. One particular gene of importance is the gene that regulates the expression of calcium ATPase, which is especially important in maintaining efficient cardiac output. Thyroid hormones do have some non-genomic effects on cells, which include the regulation of ion channels and oxidative phosphorylation. These effects are possibly under the mediation of the thyroid hormone-binding of the plasma membrane, cytoplasm, and cellular organelles. Other effects of thyroid hormone include increased  Na-K-ATPase activity, increased carbohydrate metabolism, increased free fatty acids (decreased cholesterol, phospholipids, and triglycerides), increased vitamin requirements as a consequence of increased enzymes that use vitamins as cofactors, and overall increased metabolism. In light of thyroid hormone being responsible for a vast majority of bodily functions at the genetic and cellular level, it is easy to see how the extreme absence of this hormone, as seen in myxedema coma, is associated with a high mortality rate and has a broad spectrum of presenting symptoms.[21][22]

History and Physical

Myxedema coma is a potentially fatal complication, and prompt diagnosis is an important factor in reducing mortality.[9][23][16] Identifying a precipitating cause is imperative. It is worth noting that a patient usually presents with hypothermia and not febrile. However, an investigation for an infectious cause is warranted, particularly if the patient is minimally hypothermic as it may be masking the underlying infection. Particular drugs such as lithium and amiodarone have multiple case reports associating their use and precipitation of myxedema coma given their mechanism of action on the inhibition of thyroid hormone release. Lithium also inhibits cAMP production in response to TSH.  Patients on lithium also have been shown to have an exaggerated TSH response to TRH.[24][25] Amiodarone inhibits thyroid hormone entry into peripheral tissues, inhibits 5’-deiodinase, which converts T4 to T3 and releases excess iodine.[26][27][28] Other precipitating factors such as hypoglycemia, hypoxemia, and hypercapnia may also be secondary to myxedema coma itself. Patients are most commonly presenting for emergency services with altered mental status and hypothermia, below 35.5 degrees C (95.9 degrees F). The lower the body temperature, the worst is the prognosis. The absence of mild diastolic hypertension in severely hypothyroid patients is a warning sign of impending myxedema coma.[29][30][31] Due to the presence of altered mental status, a definitive history may be difficult to obtain. Important historical features include any thyroid dysfunction, the dosage of thyroid medication, adherence with thyroid medication, thyroid surgery, and history of any drugs that may affect thyroid function. A physical exam can help confirm the suspicion of thyroid history by findings of no palpable thyroid tissue, goiter, sparse hair, non-pitting edema, a surgical scar on the neck, or dry skin. Some elderly patients have atypical presentations, such as decreased mobility patients.[29][32][33][34]

Cardiac Findings

Common cardiovascular symptoms include hypotension, shock, arrhythmia, and heart block. Myxedema causes decreased myocardial contractility and reduced cardiac output, which leads to hypotension.[35][36] Bradycardia, flattened T waves, low voltage, bundle branch blocks, and complete heart blocks are common EKG findings.[35] Low voltage on EKG can be representative of pericardial effusion due to the accumulation of fluid rich in mucopolysaccharides and merits investigation.[37] Fatal arrhythmias are important to recognize in Myxedema and chronic hypothyroidism[9]. There have been cases showing QT interval prolongations leading to “torsades de pointes” which resolves with treatment of the myxedema. Myocardial infarction is important to rule out as aggressive T4 replacement may increase the risk of myocardial infarction.[38][39]

Neurological Findings

Myxedema coma course is commonly a slow progression to coma. Typically patients do not present with coma, especially in the early phase but they present with lethargy. Hence the name of myxedema coma itself can be misleading. Other findings may include depression, disorientation, decrease deep tendon reflexes, psychosis, slow mentation, paranoia, and poor recall.[40] One case describes a rare presentation of a patient with status epilepticus.[41] Lumbar punctures which are usually done during the investigation of underlying causes to rule out infections can show increased pressure and high protein count in these situations which is attributable to increased meningeal permeability and cerebral blood flow, and decrease in the metabolism.[42]

Respiratory Findings

Hypoventilation in myxedema coma is due to impaired hypoxic and hypercapnic ventilatory response and the associated diaphragmatic muscle weakness.[43][44] The primary cause of coma in myxedema appears to be due to respiratory depression due to decreased response to hypercapnia.[35] Also swelling of the tongue and vocal cords leads to obstructive sleep apnea contributing to the respiratory failure. Another issue that can contribute is a reduction in tidal volume due to pleural effusion or ascites.[45]

Gastrointestinal Findings

Myxedema coma commonly causes abdominal pain, nausea, vomiting, ileus, anorexia, and constipation. Ileus is of particular importance as it can lead to megacolon. Ascites has also been seen in cases of Myxedema but is not common. There are reports of only a few cases in the literature.[46][45] These gastric complications may also cause issues with the absorption of oral medications. Gastrointestinal bleeding can occur as myxedema has a higher risk of bleeds due to coagulopathy related complications.[47][48][49]

Renal and Electrolyte Findings

Typical findings in myxedema coma are hyponatremia and decreased glomerular filtration rate. Hyponatremia occurs mainly due to decreased water transport to the distal nephron. Other causes can be an increase in antidiuretic hormone (ADH). Hyponatremia is also a key factor in the patient’s altered mental status and development of coma. Urinary sodium excretion is increased or normal. Urinary osmolality elevates relative to plasma osmolality. Patients may also have bladder atony causing urinary retention.[50]([51][52][53]

Hematologic Findings

Patients with myxedema coma have an increased risk of bleeding due to an acquired Von Willebrand syndrome Type 1 and a decrease in factors V, VII, VIII, IX, and X.[48][47] This is unlike those with only mild hypothyroidism, which causes a hypercoagulable state. Cases have shown that acquired Von Willebrand syndrome is reversible with T4 therapy.[48][54]

Evaluation

A high index of clinician suspicion for myxedema coma is important. As discussed above, patients who present will most likely be women in the winter months with a history of thyroid disorders and a precipitating illness. The two most common findings will be altered mental status and hypothermia along with common findings of hypothyroidism. Other common signs include hyponatremia, hypotension, bradycardia, and hypoventilation. Laboratory results will show severely low or undetected low serum total T4, free T4, free T3, and elevated TSH. The underlying etiology for most patients is going to be a primary thyroid failure, but diagnosis can be difficult in some cases. In euthyroid sick syndrome, TSH will not be as elevated as expected. In a small percentage of patients, central hypothyroidism should be a consideration. In these patients, TSH may be inappropriately low. The method to distinguish central versus primary hypothyroidism is that the associated pituitary hormones will decrease as well.[55][23]

To summarize laboratory abnormalities in myxedema coma[56][57][58][57][56]:

  • Anemia ( either normocytic or macrocytic anemia)
  • Elevated creatinine phosphokinase( can lead to misdiagnosis of myocardial infarction)
  • Elevated transaminases
  • Hyperlipidemia (inhibition of lipoprotein lipase enzyme)
  • Hypoglycemia (due to downregulation of metabolism)[56]
  • Hyponatremia with low serum osmolarity and elevated creatinine (increase ADH with a decreased ability of kidneys to excrete water)
  • Leukopenia

Other investigations are required[57][13][59][13][57]:

  • Septic workup to rule out infection including cultures and chest X-ray, etc
  • EKG ( can show bradycardia with non-specific changes, decrease voltage, variable block or prolong QT interval)
  • Arterial blood gases can show hypoxia, hypercapnia, and respiratory acidosis
  • If cardiomegaly is present on imaging studies, further investigations to rule out pericardial effusion are necessary (echocardiogram is a necessary followup)
  • Neurological investigations like lumbar puncture usually show elevated protein with non-specific EEG changes

A retrospective study in 2014 proposed a diagnostic score on 14 patients with myxedema coma and seven patients without myxedema coma, where a score greater than or equal to 60 in the proposed scoring system is potentially diagnostic. Lower scores between 45 and 59 demonstrate a risk of developing myxedema coma. The scoring system was consisting of alterations of thermoregulatory, central nervous, cardiovascular, gastrointestinal, and metabolic systems, and the presence or absence of a precipitating event.[60]

Treatment / Management

Since myxedema coma has a high mortality rate up 60%, all patients require admission to the intensive care unit. There is documented higher mortality in elderly females, cardiac arrhythmias, persistent hypothermia, reduced consciousness, and sepsis.[61][62][63] Treating myxedema coma is a multisystem challenge. The identification of the precipitating factor is essential. Respiratory and airway management is a critical component in the management of the patient. Frequent monitoring of the arterial blood gas should be performed to monitor the hypercapnia and hypoxemia. Most will require mechanical ventilation as the altered mental status does leave patients more prone to aspiration and airway obstruction could occur due to the myxedema of the larynx. Patients should not stop receiving ventilator support until the resolution of both hypercapnia and hypoxemia as well as the patient regaining consciousness. Also, assessment for any pneumonia with imaging is needed to ensure the treatment of any precipitating factors. One should also initiate fluid resuscitation while monitoring sodium and slow re-warming to avoid further hypotension. Workup for infection etiology including lumbar puncture, blood, urine cultures, empiric antibiotics in addition to appropriate imaging and interventions as a working diagnosis necessitates.[64]

Hypothermia should be managed with warming blankets and increasing the temperature in the room. Care in warming the patient is advised as this will cause peripheral vasodilation and may lead to hypotension and shock. As the patient receives treatment with thyroid replacement, the hypothermia will slowly resolve. Hypotension requires careful management due to multiple issues that commonly present concurrently, such as hyponatremia, hypoglycemia, and hypothermia. As stated above, rapid rewarming of the patient will increase vasodilation worsening hypotension. This action necessitates the use of fluids to maintain hemodynamic stability. If hypotension is refractory to IV Fluid resuscitation, then vasopressors should be initiated until Levothyroxine has time to act. If hypoglycemia is present 5% to 10% dextrose with half normal saline should be administered carefully. The dilemma occurs if the patient presents with hyponatremia as well. Hypotonic fluids should be avoided. Low sodium can precipitate altered mental status, and correcting the deficiency is vital. There is a careful balance between fluid restriction and the need for fluids. A central venous line is also a recommendation.[65][49][53] If hyponatremia is severe (below 120 mmol/L) careful administration of 3% sodium chloride along with intravenous bolus furosemide to allow for proper diuresis. A 4 to 6 mmol/L increase in serum sodium concentration is shown to correct many neurological symptoms.[65][53]  Slow correction is vital as overcorrection increases the risk for osmotic demyelination syndrome. Current research suggests that the correct rate should not increase more than 6 to 8 mmol/L in 24 hours. Once serum sodium levels rise above mmol/L fluid restrictions should be sufficient in correcting serum sodium.[66][53]

Prompt initiation of thyroid hormone therapy is of paramount importance when myxedema coma is highly suspected, even before having thyroid hormone results back (even though results usually come back quickly in most clinical institutions). A delay could increase the mortality and morbidity of the patient.[67] Hydrocortisone is recommended to be administered prior to thyroid hormone therapy, especially if the patient is hypotensive to avoid adrenal crises; suggestions are that levothyroxine will increase cortisol metabolism and hypothyroidism may mask an underlying adrenal insufficiency.[68][69] A recommended course of therapy if possible is to draw blood for random cortisol, TSH, FT4, FT3 and administer  Hydrocortisone starting with a 100 mg IV initiating dose (total 200 to 400 mg daily) which can be stopped or weaned down based on cortisol when blood levels are back, and hypotension resolves. The administration of IV Levothyroxine should follow. Repeat TSH, FT4, and FT3 are the basis for dose adjustment.[67] 

According to the most recent ATA guidelines, the recommended initial dose is 200 to 400 mcg IV once (lower dose for elderly, or underlying cardiac disease or arrhythmia with some reports up to 500 mcg). Subsequently dosing is 1.6 mcg/kg/day, reduced to 75% when given IV as a preferred route, for patients may not be able to tolerate PO and the absorption could be impaired secondary to intestinal impaired motility and edema. TSH, FT4, FT3 should be measured at baseline and then every 24 to 48 hours until patient mental status starts to improve.[67][65] There is still a controversy on what is the optimal dose, for a higher dose may cause harm, particularly in elderly patients or in patients with underlying cardiac disease and arrhythmia.[61][2] Consider adding LT3 at a loading dose of 5 to 20 micrograms followed by 2.5 to 10 micrograms IV every 8 hours if no response within 24 hours (weak recommendation, low quality of evidence). Caution should be exercised again with patients who have underlying heart disease or a history of cardiac arrhythmia. Since the previous case series showed increased adverse outcomes with higher doses of LT3 therapy.[67][2] Another controversy is whether liothyronine (LT3) is appropriate for patients whose mental status does not improve in 24 to 48 hours after administration of levothyroxine or with undetectable FT3 levels. It is well known that the conversion of FT4 to FT3 at the cellular level will be impaired in severely ill patients and those who are on steroids.[67] However, this impaired conversion may sometimes be a protective mechanism to slow down metabolism in patients who are severely ill, to preserve organ function. Whether this phenomenon can be extrapolated to patients with myxedema coma is still controversial.[39] It remains very important, however, to properly dose LT3 for high levels correlate with increased mortality.[61]

One case report in 2017 split dose of levothyroxine to 200 mcg LT4 every 8 h in five consecutive doses (total dose of 1 mg) resulted in significant restoration of depleted thyroid status and clinical improvement within 48 h after treatment initiation. [70] Another case reports in 2019 treated the patient with a combination of levothyroxine 200 mcg with liothyronine 50 mcg for five days with a successful improvement of the patient's condition, so some reports recommended starting by 200 to 300 mcg levothyroxine with 10 to 25 mcg liothyronine as an alternative initial treatment.[71] While optimal levels for serum TSH and thyroid hormones are not well defined in these circumstances, failure of TSH to trend down or for thyroid hormone levels to improve could be considered indications to increase levothyroxine therapy and/or add LT3 therapy, whereas high serum triiodothyronine (FT3) is an indication to decrease therapy given safety concerns. An in vitro study on rats by Mooradian et al. concluded that aging is associated with reduced responsiveness to T3-stimulated up-regulation of beta-adrenergic receptor number in synaptosomal membranes and it did not improve with higher doses of LT3.[39]

The severity of myxedema coma should not rely solely on higher levels of TSH for it does not always correlate either secondary to suppression of the hypothalamic-pituitary axis in critically ill patients, a slower response in elderly or secondary hypothyroidism from pituitary causes. The expectation for serum FT4 to show normalization in 4 days after starting therapy.[72]

Differential Diagnosis

Differential diagnosis has its basis on signs and symptoms; for example, altered mental status or coma can point to an infection, stroke, drug overdose, systemic disease, etc.[73]

Prognosis

The prognosis for myxedema coma is difficult to establish due to the small number of cases reported. The mortality rate is variable with some reports as high as 60% and others as low as 20 to 25% in the presence of advanced intensive support care.[74] Poor prognosis is likely related to advanced age, bradycardia, and persistent hypothermia.[61]

Complications

If left untreated, myxedema coma is fatal. Complications of myxedema include coma, respiratory failure, myocardial ischemia, sepsis, and gastrointestinal hemorrhage.[9][23][16] 

Consultations

Endocrinology consult is warranted once the diagnosis of myxedema coma is suspected.

If the patient is experiencing arrhythmia or respiratory distress or multiorgan failure, an interprofessional team should be on board, including the cardiology team, pulmonary team, intensivists, and endocrinology team.

Deterrence and Patient Education

The patients should receive education about the importance of compliance with medications and the importance of monitoring thyroid function tests after starting certain medications like amiodarone, lithium, anti-TNF, etc.

Enhancing Healthcare Team Outcomes

Myxedema coma is often a fatal complication, and prompt diagnosis is an important factor in reducing mortality. Identifying a precipitating cause is imperative.[9][23][16]  Effective treatment calls for a team-based and patient-centered approach. Endocrinology consult is necessary on clinical suspicion.

These patients need care in an ICU setting. Besides the clinicians, ICU nurses play a critical role in management. Hypothermia requires management, and patients need IV hydration. The airways must remain patent, and any respiratory distress requires mechanical ventilation. Continuous cardiac monitoring is vital, as well as hemodynamics. Nurses should communicate any deviation from normal parameters to the team immediately. Also, patients required IV thyroid hormone replacement and corticosteroids. Other specialists involved in the care include pharmacists, endocrinologists, and pulmonologists. Since most patients are not able to eat, a dietary consult for TPN or enteral nutrition is needed. Pharmacists specializing in nutritional management must be involved and report to the team as challenges arise.

The medications used in the management of myxedema coma require the intervention of a pharmacist to ensure proper dosing, drug-drug interaction checking, and overall medication reconciliation; the pharmacist should communicate any concerns to the rest of the interprofessional team.

Prompt recognition of the condition by checking thyroid function tests and rapid intervention is essential for survival. 

After discharge, clinicians, nurses, and pharmacists should educate patients about the need to take thyroid hormone and undergo regular testing. Patients should be advised to report any new medication that may interfere with thyroid function or metabolism.

In summary, myxedema coma requires an interprofessional team approach, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to achieve optimal patient results. [Level V]

Outcomes

Myxedema is a serious disorder with high mortality. Most patients die from GI bleeding, sepsis, or respiratory failure despite optimal treatment. Poor prognostic factors include advanced age, persistent hypothermia, and altered mental status.


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Myxedema - Questions

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A 60-year-old female was found in a semi-comatose condition and brought to the emergency department. On physical exam, her height was 66 inches (167.6 cm), and weight was 123 lb (55.8 kg) (BMI=19.9 kg/m2). Her blood pressure was 80/40 mm; pulse rate was 50 beats/min with temperature 32C ( 89.6F). She was disoriented and lethargic. There was no palpable thyroid enlargement, but there was a scar in her neck. Laboratory test results demonstrate: hemoglobin 9 g/dl; hematocrit 25%; WBC count 9840 cells/mm3; platelet count 297,000 cells/mm3; creatinine 1.09 mg/dl sodium 126 meq/l; potassium 3.8 mEq/L; chloride 93 mEq/L; and bicarbonate 24.5 mEq/L. Chest radiography and CT brain didn’t reveal any abnormalities. Blood and urine cultures were sent. The patient was started on intravenous fluid resuscitation with broad-spectrum antibiotics. Which of the following is most likely to be seen in the ECG of this patient?



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A 65-year-old male with a history of bipolar disorder has experienced fatigue, muscle weakness, and dizziness for the past 3 weeks. His wife states that he has been experiencing memory problems recently. In the emergency department, he is bradycardiac, hypotensive, and hypothermic. He had a witnessed seizure episode inside the emergency department. On evaluation, he has hyponatremia with a serum sodium 118 mEq/L. The remaining laboratory workup is pending. What is the best next step in management?



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A 62-year-old female presented to the hospital with complaints of confusion and the inability to perform routine tasks. Her medical history includes a history of psoriasis for which she was started on anti-TNF therapy three months ago. She also has a history of celiac disease and hypertension. She doesn't smoke and doesn’t drink. She follows a gluten-free diet, and her medications are aspirin and hydrochlorothiazide. On physical exam, her height is 66 in (167.6 cm), and weight is 123 lb (55.8 kg). Her blood pressure is 80/40 mmHg, pulse rate is 50 beats/min with temperature 32 °C. She is disorientated and lethargic. There is no palpable thyroid enlargement. There is non-pitting edema in both legs with delayed deep tendon reflexes. Laboratory test results are: hemoglobin 9 g/dl, WBC 7740 cells/mm3, platelets 150,000 cells/mm3, creatinine 1.8 mg/dl, sodium 129 meq/l, potassium 3.8 mEq/L, chloride 93 mEq/L, bicarbonate 24.5 mEq/L with undetectable free T4. Chest radiography and brain CT don’t reveal any abnormalities. Blood and urine cultures were sent. The patient was started on intravenous fluid resuscitation. Which of the following are the two most important conditions that should be ruled out before starting therapy of this condition as they can precipitate crises?



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A 65-year-old female presents to the emergency department with confusion, lethargy, and lower extremity edema. Her vital signs are temperature 92.9F, HR: 49/min, BP: 110/90/min, RR: 8/min, and oxygen saturation: 90% on room air. Physical examination is remarkable for significant nonpitting lower extremity edema. Laboratory data demonstrates: TSH 150 mIU/L with free T4 less than 0.1 ng/dl and free T3 100 ng/dl (references: normal free T4: 0.7 to 1.8 ng/dl; normal free T3: 230-619 pg/dl, normal TSH: 0.5-5 mIU/L). Which of the following is the most likely pathologic response to this condition?



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A 60-year-old woman was found in a semi-comatose condition and brought to the emergency department. On physical examination, her height was 66 inches (167.6 cm), and weight was 123 lb (55.8 kg) (BMI=19.9 kg/m2). Her blood pressure was 80/40 mmHg; her pulse rate was 50 beats/min with temperature 32C ( 89.6F). She was disoriented and lethargic. There was no palpable thyroid enlargement, but a scar was seen in her neck. Laboratory test results demonstrate: hemoglobin 9 g/dl; hematocrit 25%; WBC count 9840 cells/mm3; platelet count 297,000 cells/mm3; creatinine 1.09 mg/dl sodium 126 meq/l; potassium 3.8 mEq/L; chloride 93 mEq/L; and bicarbonate 24.5 mEq/L. Chest radiography and CT brain didn’t reveal any abnormalities. Blood and urine cultures were sent. The patient was started on intravenous fluid resuscitation with broad-spectrum antibiotics. Which of the following is the next best step in the management of this patient?



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A 70-year-old male presents to the hospital with an altered mental status. Physical examination is remarkable for bradycardia, anasarca, and hypothermia. His family reveals that he had thyroid cancer and a thyroidectomy. He has not been seen by a healthcare provider in 5 years. Which of the following is the most accurate regarding this condition?



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A 63-year-old female presents to the emergency department with status epilepticus. As per her daughter, the patient doesn't have a prior history of seizures disorders. She has progressive paranoia and poor recall for the last 8 weeks. Her vital signs are temperature 92.9F, HR: 49/min, BP: 110/90 mmHg, RR: 8/min, and O2 Sat: 90%. Physical examination is remarkable for nonpitting lower extremity edema. Laboratory parameters demonstrate: TSH 150 mIU/L with free T4 less than 0.1 ng/dl and free T3 100 ng/dl (references: normal free T4: 0.7 to 1.8 ng/dl; normal free T3: 230-619 pg/dl, normal TSH 0.5-5 mIU/L). Which of the following is true regarding this disease?



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A 40-year-old male was found in a semi-comatose condition and brought to the emergency department. On physical examination, his blood pressure was 80/40 mmHg; his pulse rate was 50 beats/min with temperature 32°C. He was disoriented and lethargic. There was no palpable thyroid enlargement, but a scar was seen in his neck. Laboratory test results demonstrate: hemoglobin 10 g/dl; WBC count 5000 cells/mm3; platelet count 257,000 cells/mm3; creatinine 1.5 mg/dl sodium 129 meq/l; potassium 3.8 mEq/L; chloride 93 mEq/L; and bicarbonate 24.5 mEq/L. Chest radiography and CT brain didn’t reveal any abnormalities. Blood and urine cultures were sent.EKG showed sinus bradycardia with a prolonged QT interval. The patient was started on intravenous fluid resuscitation with broad-spectrum antibiotics. Which of the following is true regarding this patient clinical condition?



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A 67-year-old woman presents to the emergency department with an 8-week history of progressive confusion and cognitive decline. Her husband reports dramatic deterioration in her symptoms over the preceding 5 days with disorientation, falls and inability to perform routine tasks. Her appetite has been poor and she lost 11 lbs (5 kgs). Her medical history includes celiac disease and hypertension with bipolar disorder diagnosed 3 months ago. She smokes 20 cigarettes daily and does not drink. She follows a gluten-free diet and her medications are aspirin, sertraline and hydrochlorothiazide, and lithium. On physical exam, her height is 66 inches (167.6 cm) and weight is 123 lbs (55.8 kgs) (BMI=19.9 kg/m2). Her blood pressure is 80/40 mmHg, pulse rate is 120 beats/min with temperature 32 C (89.6 F). She is disorientated and lethargic. There is no palpable thyroid enlargement. Neurologic examination reveals delayed deep tendon reflex. Laboratory test results show hemoglobin 8.45 g/dl, hematocrit 23.2%, WBC count 8140 cells/mm3, platelets 297,000 cells/mm3, creatinine 1.09 mg/dl, sodium 126 mEq/L, potassium 3.8 mEq/L, chloride 93 mEq/L, and bicarbonate 24.5 mEq/L. Chest radiography and brain CT do not reveal any abnormalities. EKG shows sinus tachycardia with no other abnormalities. Blood and urine cultures are sent. The patient is started on intravenous fluid resuscitation with broad-spectrum antibiotics. What is the best next step in the management of this patient?



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A 40-year-old Asian woman with a history of cardiac arrhythmia and seizures is brought to the emergency department by her son as she was confused for the past three weeks. She was started on new medications six months ago, but she didn’t follow up with her doctor since then as she traveled to visit her son. She does not smoke or drink. She has delayed deep tendon reflexes. The patient is hypotensive with bradycardia, has hypothermia with hyponatremia, and anemia in her laboratory testing. Which of the following medications is the least likely reason for her symptoms?



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A 65-year-old male with a history of bipolar disorder has experienced fatigue, muscle weakness, and dizziness for the past three weeks. His wife states that he has been experiencing memory problems recently. In the emergency department, he is bradycardiac, hypotensive, and hypothermic. On evaluation, he has hyponatremia and hypoglycemia. He is started on dextrose 10% with half normal saline continuous infusion and broad-spectrum antibiotics. The patient remains hypotensive despite fluid resuscitation. The remaining laboratory workup is pending. What is the best next step in the management of this patient?



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A 28-year-old woman with a history of Prader-Willi syndrome and hypothyroidism presents to the emergency department with altered level of consciousness, lethargy, and lower extremity edema. She is taken care of exclusively by her caregiver. She ran out of levothyroxine three months ago. Vital signs reveal a temperature of 92.9 F, pulse 49/min, blood pressure 110/90 mmHg, respiratory rate 8/min, and SpO2 90%. The physical exam is significant for lethargy, bradycardia, and significant nonpitting lower extremity edema. Labs show sodium 129 mEq/L, blood glucose 54 mg/dL, TSH 110 IU/microL, and T4, T3 undetectable. Thyroid anti-peroxidase antibodies are also positive. Renal function, CBC, and serum cortisol are within normal limits. What is the most likely diagnosis?



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A 60-year-old female was found in a semi-comatose condition and brought to the emergency department. On physical exam, her height was 66 inches (167.6 cm), and weight was 123 lb (55.8 kg) (BMI=19.9 kg/m2). Her blood pressure was 80/40 mm; her pulse rate was 50 beats/min with temperature 32C ( 89.6F). She was disoriented and lethargic. There was no palpable thyroid enlargement, but there was a scar in her neck. Laboratory test results demonstrate: hemoglobin 9 g/dl; hematocrit 25%; WBC count 9840 cells/mm3; platelet count 297,000 cells/mm3; creatinine 1.09 mg/dl sodium 126 meq/l; potassium 3.8 mEq/L; chloride 93 mEq/L; and bicarbonate 24.5 mEq/L. Chest radiography and CT brain didn’t reveal any abnormalities. Blood and urine cultures were sent. What is the least accurate statement regarding hyponatremia in this patient?



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A 60-year-old female was found in a semi-comatose condition and brought to the emergency department. On physical exam, her height was 66 inches (167.6 cm), and weight was 123 lb (55.8 kg) (BMI=19.9 kg/m2). Her blood pressure was 80/40 mm; her pulse rate was 50 beats/min with temperature 32C ( 89.6F). She was disoriented and lethargic. There was no palpable thyroid enlargement, but there was a scar in her neck. Laboratory test results demonstrate: hemoglobin 9 g/dl; hematocrit 25%; WBC count 9840 cells/mm3; platelet count 297,000 cells/mm3; creatinine 1.09 mg/dl sodium 126 meq/l; potassium 3.8 mEq/L; chloride 93 mEq/L; and bicarbonate 24.5 mEq/L. Chest radiography and CT brain didn’t reveal any abnormalities. Blood and urine cultures were sent. Her family reveals she had rheumatoid arthritis and she was recently started on anti-TNF therapy. What is the least accurate statement for this condition?



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Myxedema - References

References

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