Myxedema Coma Secondary to Central Hypothyroidism: A Rare but Real Cause of Altered Mental Status in Pediatrics

2016 ◽  
Vol 87 (5) ◽  
pp. 350-353 ◽  
Author(s):  
Michael D. Thompson ◽  
Rohan K. Henry
2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A971-A972
Author(s):  
Yumna Hamid ◽  
Steven Douedi ◽  
Johnathan Nold ◽  
Raquel Kristin Ong ◽  
Jennifer Cheng ◽  
...  

Abstract Background: Myxedema coma is a severe manifestation of hypothyroidism that typicallypresents with altered mental status and requires close monitoring in the intensive care unit dueto 30-60% mortality rate. Clinical Case: A 56 year old white male with type 1 diabetes with recurrent DKA, polysubstanceabuse, Bipolar disorder on lithium and post surgical hypothyroidism presented due to change inmental status after being brought in by sister. Patient was found to be lethargic with confusionthat worsened over the last week. The patient was admitted several times in the past monthsecondary to pneumonia, sepsis, and recurrent DKA. On physical examination, he found to have lethargy, macroglossia, hyporeflexia, and periorbitaledema. Patient had acute respiratory failure with metabolic encephalopathy, bradycardia,tachypnea, severe hyperglycemia, hypotension of 77/51, tachypnea of 31 breaths per minuteand hyponatremia. Laboratory findings showed T4 levels 2.87(n=5.28-9.87ug/dL) withundetectable FT4 and elevated TSH (>50, n=0.300-4.500uIU/mL). Electrolyte panel showedhyponatremia (133, n=136-145mmol/L), hyperglycemia up to 532mg/dL and lithium levels werewithin normal limits (n=0.5-1.5 mmol/L). Urine drug screen was positive for cocaine. A CT scanof the head was negative. His myxedema score was diagnostic (>60). The patient wasdiagnosed with myxedema coma and admitted to the ICU. Patient was treated with IV LT4 400mcg, LT3 10mcg and hydrocortisone 100mg and started onIV LT4 100mcg daily, LT3 2.5mcg daily and hydrocortisone 100mg Q8 hours. There was wideglycemic variation from 46-532 mg/dL on POCT. The patient improved clinically, with resolutionof lethargy, confusion, fatigue, improved appetite, and improved lab work of FT3 2.30 (n=2.28-3.96pg/mL), FT4 at 0.76 (n=0.50-1.26ng/dL) and was downgraded from the ICU. On hospitalday four, he was transitioned to oral levothyroxine and discharged home. Conclusion: It is important to diagnose early and promptly manage decompensatedhypothyroidism in the setting of other comorbidities such as hyperglycemia in diabetes andpolysubstance abuse. The cocaine in the system may cause tachypnea and tachycardia. Manyconditions may have altered mental status, but with a history of hypothyroidism, Myxedemacoma should be on the differential due to its high mortality rate.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A943-A943
Author(s):  
Aisha Parihar

Abstract Background: Myxedema coma, a misnomer for severe hypothyroidism, is a rare endocrine emergency with an incidence of 1.08 cases per million people per year and a high mortality rate ranging from 30-50%. A delay in diagnosis and treatment worsens the prognosis and increases morbidity and mortality. Delayed management often leads to decompensation, presenting as uncontrolled persistent hypothermia, severe electrolyte derangements, and a potential for ventilator requirement needing ICU care. We present a patient in hypothyroid crisis who was promptly managed in a non-ICU setting who demonstrated a relatively early improvement in vital signs, thyroid lab values, and return to baseline mental status. Clinical Case: A 75 year old female with past medical history of hypothyroidism, atrial fibrillation, hypertension, coronary artery disease, depression, tardive dyskinesia, and dementia presented to the hospital in the month of December due to confusion after a mechanical fall that resulted in a head laceration requiring multiple stitches. Trauma work up included a CT scan of the head that was negative. On presentation, patient was also hypothermic, bradycardic, hypotensive, and lethargic with an altered mental status. Sepsis work up was negative. TSH was checked on day of admission and found to be significantly elevated to > 100 mcIU/mL, consistent with severe hypothyroidism. Free T4 and total T3 levels were low. Patient was immediately given intravenous levothyroxine 300 mcg followed by oral levothyroxine 125 mcg daily. In addition, intravenous hydrocortisone 100 mg every 8 hours was started until adrenal insufficiency was ruled out with a normal cortisol level. Upon discussion with family, it was learned that patient had not been taking her home medications indicating non-compliance to thyroid replacement therapy as the etiology for her hypothyroid crisis. Within a day of initiating therapy, TSH levels drastically improved with a reduction by 50%. Bradycardia, hypotension, and hypothermia resolved as well. In three days, patient’s mentation improved back to baseline and TSH, free T4, and total T3 continued to normalize. Conclusion: This case demonstrates how prompt recognition of hypothyroid crisis and immediate therapy can lead to early improvement in outcomes such as reversibility of mental status, normalization of vital signs and lab values, prevention of escalation of care to an ICU setting, and overall morbidity and mortality.


2016 ◽  
Vol 2016 ◽  
pp. 1-4
Author(s):  
Pratik Patel ◽  
Mikhael Bekkerman ◽  
Cristina Varallo-Rodriguez ◽  
Rajendra Rampersaud

Hypothyroidism is a prevalent condition in the general population that is treatable with appropriately dosed thyroid hormone replacement medication. Infrequently, patients will present with myxedema coma, characterized by hypothermia, hypotension, bradycardia, and altered mental status in the setting of severe hypothyroidism. Myxedema coma has also been known to manifest in a number of unusual and dangerous forms. Here, we present the case of a woman we diagnosed with an uncharacteristic expression of myxedema coma and nonconvulsive seizure complicated by a right middle cerebral artery infarct.


Author(s):  
Keng Lam ◽  
Sameer K. Kulkarni ◽  
Manya Khrlobyan ◽  
Pamela K. Cheng ◽  
Caroline L. Fong

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
T. M. Skipina ◽  
S. Macbeth ◽  
E. L. Cummer ◽  
O. L. Wells ◽  
S. Kalathoor

Abstract Introduction Acute encephalopathy, while a common presentation in the emergency department, is typically caused by a variety of metabolic, vascular, infectious, structural, or psychiatric etiologies. Among metabolic causes, hyperammonemia is relatively common and typically occurs in the setting of cirrhosis or liver dysfunction. However, noncirrhotic hyperammonemia is a rare occurrence and poses unique challenges for clinicians. Case presentation Here we report a rare case of a 50-year-old Caucasian female with history of bladder cancer status post chemotherapy, radical cystectomy, and ileocecal diversion who presented to the emergency department with severe altered mental status, combativeness, and a 3-day history of decreased urine output. Her laboratory tests were notable for hyperammonemia up to 289 μmol/L, hypokalemia, and hyperchloremic nonanion gap metabolic acidosis; her liver function tests were normal. Urine cultures were positive for Enterococcus faecium. Computed tomography imaging showed an intact ileoceal urinary diversion with chronic ileolithiasis. Upon administration of appropriate antibiotics, lactulose, and potassium citrate, she experienced rapid resolution of her encephalopathy and a significant reduction in hyperammonemia. Her hyperchloremic metabolic acidosis persisted, but her hypokalemia had resolved. Conclusion This case is an example of one of the unique consequences of urinary diversions. Urothelial tissue is typically impermeable to urinary solutes. However, when bowel segments are used, abnormal absorption of solutes occurs, including exchange of urinary chloride for serum bicarbonate, leading to a persistent hyperchloremic nonanion gap metabolic acidosis. In addition, overproduction of ammonia from urea-producing organisms can lead to abnormal absorption into the blood and subsequent oversaturation of hepatic metabolic capacity with consequent hyperammonemic encephalopathy. Although this is a rare case, prompt identification and treatment of these metabolic abnormalities is critical to prevent severe central nervous system complications such as altered mental status, coma, and even death in patients with urinary diversions.


Author(s):  
Marjorie J. Kenerly ◽  
Priyank Shah ◽  
Hiten Patel ◽  
Rilee Racine ◽  
Yash Jani ◽  
...  

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