scholarly journals Myxedema Coma Disguised as Alcohol Withdrawal

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A942-A943
Author(s):  
Dhivya Pahwa ◽  
Alexander Belkin ◽  
Neeraj Katriyar
Keyword(s):  
Mental Status ◽  
Alcohol Withdrawal ◽  
Clinical Symptoms ◽  
Female Gender ◽  
Laboratory Diagnosis ◽  
Medical Emergency ◽  
Thyroid Function Tests ◽  
Free T4 ◽  
Myxedema Coma ◽  
Multiple Organs

Abstract Introduction: Myxedema coma is a medical emergency whose symptoms may sometimes mimic other diseases such as alcohol withdrawal. Case: A 64-year-old male with a history of alcohol abuse and bipolar disorder (on no medications) presented to the emergency department after being found on the floor surrounded by multiple open alcohol bottles. He was a poor historian but reported a previous fall. Vitals on presentation were BP 109/70, HR 110, RR 22, SpO2 of 90% on room air, and rectal temperature of 97.6 F. The remainder of the exam revealed he was alert and oriented to self and place but not time; his neck was supple and no thyroid masses were palpated; he had tremors, head swelling and abdominal tenderness. Labs demonstrated CPK 1300 U/L, Creatinine 1.0 mg/dl, glucose 120 mg/dl, and sodium 142 mmol; urine toxicology was negative and alcohol level was not elevated. He was admitted and treated for suspected alcohol withdrawal and rhabdomyolysis with intravenous fluids and benzodiazepines. However, his mental status continued to decline; he became obtunded and was hypothermic and bradycardic. Thyroid function tests (TFT) revealed TSH 98.9 uIU/mL with free T4 0.27 ng/dl. He was subsequently managed for myxedema coma and given IV levothyroxine and hydrocortisone. He improved clinically after initiation of therapy and was transitioned to oral thyroid replacement. The patient was pending discharge to sub-acute rehab however his hospital course was later complicated by aspiration pneumonia. Discussion: Myxedema coma is a medical emergency as severe hypothyroidism leads to slowed functioning of multiple organs. Risk factors include female gender and age above 60 years; it is seen more commonly in colder months. Symptoms include decreased mental status, feelings of cold and tongue swelling while physical exam may reveal hypothermia, hypoventilation, bradycardia, an enlarged goiter, thinning hair and non-pitting edema. Lab studies usually reveal an elevated TSH with low T4; there may also be hyponatremia and hypoglycemia. Myxedema coma is a clinical and laboratory diagnosis; if there is clinical suspicion for myxedema coma, IV thyroid replacement should be administered promptly without waiting for lab results. Stress-dose steroids should also be administered and TFTs should be monitored every 48 hours. Clinical symptoms usually improve over one week of treatment. Mortality of myxedema coma is reported to be up to 40% in hospitalized patients. Our patient’s presentation of suspected alcohol withdrawal masked his diagnosis of myxedema coma. Conclusion: Physicians should keep myxedema coma in the differential for patients who present with suspected alcohol withdrawal and develop worsening mental status and hypothermia. Reference: DynaMed. (2020, October 22). Myxedema Coma. Retrieved October 23, 2020, from https://www-dynamed-com.arktos.nyit.edu/topics/dmp~AN~T1584563697784.

scholarly journals SAT-480 Myxedema Madness: A Rare Case of Severe Hypothyroidism Presenting as Psychosis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kevin Kohm ◽  
Shivani Vekaria ◽  
Jack Xu ◽  
Carol Nasr ◽  
Lauren Hogshire
Keyword(s):  
Mental Status ◽  
Suicide Attempts ◽  
Thyroid Stimulating Hormone ◽  
Medical Emergency ◽  
Thyroid Function Tests ◽  
Myxedema Coma ◽  
Rare Manifestation ◽  
Life Threatening ◽  
History Of ◽  
One Year

Abstract Introduction Myxedema coma is a rare, life-threatening medical emergency resulting from uncontrolled hypothyroidism. Myxedema coma refers to the neurological sequelae of severe hypothyroidism, which classically manifests as depressed mental status. Rarely, myxedema coma can present with a hyperactive mental state and psychosis. We present an unusual case of a drug overdose secondary to myxedema coma-induced psychosis. Clinical Case A 48 year old woman with a history of seizure disorder and hypothyroidism presented to the hospital after lamotrigine overdose. The patient’s spouse witnessed her ingest forty-five tablets of lamotrigine after an argument. The patient had no previous psychiatric diagnoses or suicide attempts. On examination, the patient was hemodynamically stable but was agitated, disoriented, and uncooperative. She had a normal neurologic exam and no peripheral edema. Her lamotrigine level was 25.4 ug/ml (2.5-15.0 ug/ml). The patient’s mental status did not improve with lamotrigine cessation. Psychiatry determined that the patient’s psychosis was not consistent with lamotrigine overdose. Given these recommendations, alternative causes of psychosis were considered. The patient’s husband stated she had not taken levothyroxine for over one year. Thyroid function tests revealed a thyroid stimulating hormone (TSH) of 299 mcIU/ml (0.35-5.50 mcIU/ml) with a free thyroxine (T4) level of 0.27 ng/dl (0.89-1.76 ng/gl). The patient was started on levothyroxine intravenously. After five doses of intravenous levothyroxine, her mental status improved to baseline and she was transitioned to oral levothyroxine. She denied that the lamotrigine ingestion was a suicide attempt. Based on the patient’s presentation and clinical course, we concluded that her overdose was due to severe hypothyroidism leading to myxedema madness. Conclusion Severe hypothyroidism with myxedema coma often presents with depressed mental status, which can manifest as progressive confusion, lethargy, and eventually coma. However, in the case of our patient, severe hypothyroidism presented as psychosis, a rare manifestation. Remarkably, the patient had no other obvious physical manifestations of severe hypothyroidism. Psychosis, though rare, has been seen in cases typically after thyroidectomy or in patients with previously undiagnosed Hashimoto’s thyroiditis. In this patient’s case, it is likely that her myxedema madness was precipitated by long-term nonadherence with her thyroid replacement therapy, as the patient had no prior psychiatric history. Additionally, her rapid reversal of symptoms after the administration of levothyroxine supports the diagnosis of hypothyroid-induced myxedema madness.

scholarly journals SAT-460 Myxedema Coma Mimicking Cardiogenic Shock Treated with Levothyroxine

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Bayan Chaker ◽  
Mahmoud Chaker ◽  
Hussam Alim ◽  
Louna S El-Zein
Keyword(s):  
Cardiogenic Shock ◽  
Early Recognition ◽  
Fluid Challenge ◽  
Cardiovascular Complications ◽  
Medical Emergency ◽  
High Dose ◽  
Thyroid Function Tests ◽  
Free T4 ◽  
Myxedema Coma ◽  
Patient Reported

Abstract Myxedema coma is a medical emergency with a mortality rate of 30–50%. It is a commonly missed diagnosis and can lead to multiple cardiovascular complications which are reversible with levothyroxine treatment. IV levothyroxine should be initiated based on clinical suspicion without waiting for laboratory results. We report a case of a 71-year-old female with a history of CABG 10 years ago, who presented to the emergency department with a syncopal episode. The patient denied aura, vomiting, jerky movements, rolling eye movements, bowel/bladder incontinence, and palpitations. She reported having exertional chest pain for a couple of months. Her home medications included metoprolol succinate 50 mg daily, hydralazine 50 mg twice daily, Imdur 30 mg daily, and levothyroxine 300 mcg daily which the patient reported taking rarely. On admission, the temperature was 36°C, HR 43, BP 75/49 which dropped to 60/40, RR 9, and SpO2 of 93% on 2LPM. Physical exam showed euvolemia with brisk reflexes and delayed relaxation. Blood work revealed Na of 133 mM/L (L), Cr 6.4 mg/dL (H) from a baseline of 2.4 mg/dL, and a troponin of 0.26 ng/mL (H). EKG showed first degree AV block with new T-wave flattening not seen on previous EKGs. A fluid challenge for hypotension elicited no response and the patient was started on a dopamine drip for cardiogenic shock, a heparin drip for ACS, and was transferred to the CCU. BP improved to 140s/70s with a HR remained in the 50s. On the 2nd day of admission, blood work revealed a TSH of >150 (H), free T4 of 0.6, total T3 of 34 (L) and a random cortisol of 15.5 microgram/dL. On the 3rd day of admission, the patient was given 200 mcg of IV levothyroxine. At that time, the patient was on a dopamine drip with a BP of 144/94 with a HR of 64. Twelve hours later, the patient’s BP went up to 197/105 with a heart rate of 65 prompting discontinuation of the dopamine drip and administration of hydralazine and amlodipine. On the morning of the fourth day of admission, BP went up to 236/116 with a HR of 75 and the patient was started on a nicardipine drip. Blood work 3 days after starting levothyroxine revealed a TSH of >150, free T4 of 0.9, and a total T3 of 70. The patient was discharged on levothyroxine 150 mcg daily, amlodipine 10 mg, hydralazine 50 mg q6hrs, and Imdur 30 mg daily. The patient’s myxedema score was 75 on admission. However, thyroid function tests were not checked with initial labs despite the presence of avert clinical features. As a result, the patient was started on a dopamine drip which could have been avoided. This underlines the importance of early recognition and management of myxedema coma. Having a low total T3 with a low normal FT4 could be explained by recent intake of high dose levothyroxine at home after a significant period of non-compliance. Fortunately, levothyroxine administration to this patient has reversed cardiovascular abnormalities including bradycardia and hypotension within hours when it was given promptly.

scholarly journals A comparative study on outcomes of preprandial versus postprandial thyroid function test

2019 ◽  
Vol 5 (6) ◽  
pp. 1662
Author(s):  
Vasim Ismail Patel ◽  
Akshay B. K.
Keyword(s):  
Thyroid Function ◽  
Subclinical Hypothyroidism ◽  
Clinical Symptoms ◽  
Thyroid Function Test ◽  
Thyroid Stimulating Hormone ◽  
Endocrine Gland ◽  
Thyroid Function Tests ◽  
Sample Collection ◽  
Free T4 ◽  
Group 2

<p class="abstract"><strong>Background:</strong> The thyroid is an<strong> </strong>endocrine gland. It secretes two hormones thyroxine (T<sub>4</sub>), triiodothyronine (T<sub>3</sub>). Hypothyroidism is a common condition encountered by a clinician. Subclinical hypothyroidism (SCH) defined as normal free thyroxine (T4) and elevated thyroid stimulating hormone (TSH), is primarily a biochemical diagnosis with or without clinical symptoms. Studies have observed that TSH levels vary at different times in a day. In practice not much importance is given to the timing of the sample collection (pre-prandial or post-prandial sate). SCH is diagnosed depending on TSH value. So the condition may be under or over diagnosed based on a single value. So we conducted this study to determine whether timing of sample collection had any significant relationship in the determination of levels of thyroid hormones.</p><p class="abstract"><strong>Methods:</strong> The study was carried on 114 patients who visited ENT department, NMCH between July 2018 and June 2019. Group-1 consisted of 38 normal patients. Group-2 consisted of 36 hypothyroidism patients GROUP-3 consisted of 40 subclinical hypothyroidism patients. Thyroid function tests (TSH and free T4) were done in fasting state and 2 hours postprandially.  </p><p class="abstract"><strong>Results:</strong> TSH values were found to be significantly lowered after food in all the three groups. Free T4 values did not show any statistically significant alteration after food.</p><p class="abstract"><strong>Conclusions:</strong> There was a significant decline in TSH values postprandially. This might lead to inappropriate diagnosis and management of patients as cases of hypothyroidism, especially in cases of sub clinical hypothyroidism.</p>

scholarly journals Hyponatremia as the Initial Presentation of Evolving Pituitary Apoplexy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A586-A586
Author(s):  
Jovan Milosavljevic ◽  
Asha Mary Thomas
Keyword(s):  
Mental Status ◽  
Pituitary Apoplexy ◽  
Pituitary Tumors ◽  
Altered Mental Status ◽  
Clinical Syndrome ◽  
Medical Emergency ◽  
Fluid Restriction ◽  
Free T4 ◽  
Acute Hemorrhage ◽  
Initial Testing

Abstract Pituitary apoplexy (PA) is a known, often under-recognized medical emergency and is characterized by ischemic or hemorrhagic necrosis of the pituitary gland. It is a rare clinical syndrome that occurs in 2-12% of pituitary tumors. Hyponatremia can occur secondary to hypocortisolism (12-40%) or, rarely, to the syndrome inappropriate antidiuretic hormone (ADH) secretion. We present the case of a 69-year-old man who presented with altered mental status on post-operative day 3 from total knee replacement surgery. Initial testing revealed hyponatremia of 124 mmol/L, low serum osmolality of 266 mOsm/kg, and high urine osmolality of 664 mOsm/kg with urine sodium of 179 mmol/L. Head computerized tomography revealed a sellar mass of 1.8 x 2.4 cm. Initial testing revealed low prolactin (0.7 ng/mL), normal TSH (0.458 mcIU/mL) with borderline low free T4 of 0.72 ng/dL. Morning cortisol was 12.7 mcg/dL with ACTH of 8.5 pg/mL. Cosyntropin stimulation test was done revealing baseline cortisol of 5.8 mcg/dL (at midnight), increasing to 25.8 mcg/dL after 30 minutes and to 30.9 mcg/dL 60 minutes after cosyntropin administration. His sodium and mental status initially improved with fluid restriction and salt tablets, for the assumed syndrome of inappropriate ADH secretion. The patient remained hemodynamically stable. On the fourth day, however, his mental status deteriorated. Magnetic resonance imaging revealed expansion of sella with hyperintense mass 2.2 x 2.0 x 2.8 cm with compression of the optic chiasm. He was given stress dose hydrocortisone and levothyroxine and underwent emergency transsphenoidal resection. Biopsy revealed acute hemorrhage within infarcted adenoma. Postoperatively, both the patient’s sodium and mental status improved significantly and he was discharged to home on hydrocortisone and levothyroxine. The main clinical concern in the management of PA remains under-diagnosis at presentation. Prognosis is dependent on management during the acute phase. PA can present as hyponatremia even in the absence of overt hypocortisolism, presumably due to inappropriate ADH secretion. Therefore, PA should be considered as one of the differential diagnoses in hemodynamically stable patients with altered mental status and hyponatremia.

scholarly journals Myxedema Coma: Improving Outcomes With Prompt Recognition and Therapy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A943-A943
Author(s):  
Aisha Parihar
Keyword(s):  
Mental Status ◽  
Vital Signs ◽  
Altered Mental Status ◽  
Morbidity And Mortality ◽  
Free T4 ◽  
Early Improvement ◽  
Delay In Diagnosis ◽  
Myxedema Coma ◽  
Artery Disease ◽  
Work Up

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 &gt; 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.

Could Thyroid Disorders Be Better Understood and Dealt as a Thyroid Syndrome

2020 ◽  
Vol 5 (08) ◽  
pp. 326-328
Author(s):  
Dr. Sushma Patil ◽  
Dr. Vikrant Patil
Keyword(s):  
Reference Range ◽  
Well Being ◽  
Thyroid Disorders ◽  
Thyroid Function Tests ◽  
Thyroid Disorder ◽  
Serum Concentrations ◽  
Comorbid Conditions ◽  
Free T4 ◽  
Research Perspective ◽  
Wide Range

Thyroid disorders are common worldwide. Thyroid dysfunction, both hypo- and hyperthyroidism may increase the risk of cardiovascular disorders. Current thyroid function tests may have limitations since they only measure the total or free T4 and/or T3 and TSH serum concentrations in peripheral blood and not the effect of T4 or T3 serum on different specific target tissues. Several comorbid conditions can interfere with the absorption or increase the clearance of levothyroxine. Among patients treated with thyroid replacement, under or overmedicated may-be at risk for adverse health consequences. A wide range of drugs may interfere with levothyroxine absorption, metabolism, and action. Patients report a lack of well-being, despite reaching euthyroid reference range of TSH, with psychological distress. If we will consider Thyroid related conditions as a syndrome then research perspective at the pathophysiology, interrelation between symptoms and comorbidities will be much broader that can lead researchers to get insights of different pathways in which thyroid gland functioning can be perceived and dealt therapeutically. The deliberation of thyroid disorder as a syndrome can affluence our knowledge of correlating cofounders, action of thyroid hormones on target tissues, underlying cause and thyroid health.

scholarly journals Determinants of Extraocular Muscle Volume in Patients with Graves' Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Samer El-Kaissi ◽  
Jack R. Wall
Keyword(s):  
Extraocular Muscle ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Thyroid Function Tests ◽  
Thyroid Scintigraphy ◽  
Free T4 ◽  
Receptor Antibody ◽  
Tsh Receptor Antibody ◽  
Antibody Positivity ◽  
Serum Tsh

Background. To examine factors contributing to extraocular muscle (EOM) volume enlargement in patients with Graves’ hyperthyroidism.Methods. EOM volumes were measured with orbital magnetic resonance imaging (MRI) in 39 patients with recently diagnosed Graves’ disease, and compared to EOM volumes of 13 normal volunteers. Thyroid function tests, uptake on thyroid scintigraphy, anti-TSH-receptor antibody positivity and other parameters were then evaluated in patients with EOM enlargement.Results. 31/39 patients had one or more enlarged EOM, of whom only 2 patients had clinical EOM dysfunction. Compared to Graves’ disease patients with normal EOM volumes, those with EOM enlargement had significantly higher mean serum TSH (0.020±0.005versus0.007±0.002mIU/L;Pvalue 0.012), free-T4 (52.9±3.3versus41.2±1.7 pmol/L;Pvalue 0.003) and technetium uptake on thyroid scintigraphy (13.51±1.7%versus8.55±1.6%;Pvalue 0.045). There were no differences between the 2 groups in anti-TSH-receptor antibody positivity, the proportion of males, tobacco smokers, or those with active ophthalmopathy.Conclusions. Patients with recently diagnosed Graves’ disease and EOM volume enlargement have higher serum TSH and more severe hyperthyroidism than patients with normal EOM volumes, with no difference in anti-TSH-receptor antibody positivity between the two groups.

scholarly journals A forgotten life-threatening medical emergency: myxedema coma

2016 ◽  
Vol 12 (2) ◽  
Author(s):  
Elisa Pizzolato ◽  
Alberto Peano ◽  
Letizia Barutta ◽  
Emanuele Bernardi ◽  
Elena Maggio ◽  
...  
Keyword(s):  
Life Support ◽  
Neurological Status ◽  
Medical Emergency ◽  
Myxedema Coma ◽  
Emergency Department Stay ◽  
Life Threatening ◽  
Appropriate Therapy ◽  
Alithiasic Cholecystitis ◽  
The Right ◽  
Tomography Scan

Nowadays myxedema coma is a rare medical emergency but, sometimes, it still remains a fatal condition even if appropriate therapy is soon administered. Although physical presentation is very non-specific and diversified, physicians should pay attention when patients present with low body temperature and alteration of neurological status; the presence of precipitating events in past medical history can help in making a diagnosis. Here we discuss one such case: an 83-year-old female presented with abdominal pain since few days. Laboratory tests and abdomen computed tomography scan demonstrated alithiasic cholecystitis; she was properly treated but, during the Emergency Department stay she experienced a cardiac arrest. Physicians immediately started advance cardiovascular life support algorithm and she survived. Later on, she was admitted to the Intensive Care Unit where doctors discovered she was affected by severe hypothyroidism. Straightway they started the right therapy but, unfortunately, the patient died in a few hours.

Delirium: Phenomenologic and Etiologic Subtypes

1991 ◽  
Vol 3 (2) ◽  
pp. 135-147 ◽  
Author(s):  
Christopher A. Ross ◽  
Carol E. Peyser ◽  
Ira Shapiro ◽  
Marshal F. Folstein
Keyword(s):  
Hepatic Encephalopathy ◽  
Cognitive Function ◽  
Cognitive Dysfunction ◽  
Mental Status ◽  
Alcohol Withdrawal ◽  
Analog Scale ◽  
Mini Mental Status Exam ◽  
Mental Status Exam ◽  
Exam Scores

While all delirious patients have clouding of consciousness (alteration of attention) and cognitive dysfunction, the level of alertness of different patients may range from stuporous to hyperalert. We, therefore, developed an analog scale to rate the alertness of delirious patients, and a separate scale to rate the severity of their clouding of consciousness. Based on these scales, patients were categorized overall as relatively “activated” (relatively alert despite clouding of consciousness), or “somnolent” (relatively stuporous along with clouding of consciousness). Cognitive function was estimated using the Mini-Mental Status Exam. Separate ratings were made of hallucinations, delusions, illusions, and agitated behavior. Activated and somnolent patients had similar ages, overall severity of delirium, and Mini-Mental Status Exam scores. Activated patients, however, were more likely to have hallucinations, delusions, and illusions than somnolent patients, and were more likely to have agitated behavior. Patients with hepatic encephalopathy were more likely to have somnolent delirium, while patients with alcohol withdrawal appeared more likely to have activated delirium. These data indicate that phenomenologic subtypes of delirium can be defined on the basis of level of alertness. These subtypes are validated in part by their differing associations with symptoms unrelated to alertness. These subtypes may have different pathophysiology, and thus, potentially different treatments.

scholarly journals Unusual Presentation of Myxedema Coma in Type 1 Diabetes Mellitus With Hyperglycemia and Polysubstance Abuse

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A971-A972
Author(s):  
Yumna Hamid ◽  
Steven Douedi ◽  
Johnathan Nold ◽  
Raquel Kristin Ong ◽  
Jennifer Cheng ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Mortality Rate ◽  
Mental Status ◽  
White Male ◽  
Altered Mental Status ◽  
Close Monitoring ◽  
Urine Drug Screen ◽  
Metabolic Encephalopathy ◽  
Myxedema Coma

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 (&gt;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 (&gt;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.

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