Two Cases of Myxedema Coma Successfully Treated with Low-Dose Thyroid Hormone Replacement.

2000 ◽  
Vol 11 (1) ◽  
pp. 22-26
Author(s):  
Akira Fujiyoshi ◽  
Toshihide Yamamoto
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.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A946-A947
Author(s):  
Aysegul Bulut ◽  
Khaled AlSibai ◽  
Catalina Norman

Abstract Introduction: Hypothyroidism usually affects red blood cell line most commonly seen as normochromic normocytic anemia. We present a unique case of a patient with pancytopenia in the setting of severe hypothyroidism, which improved following IV thyroid hormone replacement. Case: An 85-year-old female with history of type II diabetes mellitus and hypothyroidism who was admitted for open reduction and internal fixation (ORIF) of a displaced left femur fracture following a mechanical fall. Patient has a long-standing history of hypothyroidism on replacement with levothyroxine 75 mcg, which was inadvertently discontinued at the nursing home 2 weeks prior to presentation. CBC on admission was notable for pancytopenia with macrocytic anemia with hemoglobin of 6.2 g/dl (baseline of 11), leukopenia with WBC of 4.2 x103/ul and thrombocytopenia with platelet of 77 X 103 /ul. TSH was 83 uIU/mL (reference range: 0.34 - 5.6) and Free T4 was < 0.11 ng/dl (reference range: 0.93 - 1.7). Patient was on the verge of developing myxedema coma as she presented with hypotension with blood pressure of 103/55 mmHg, hyponatremia 133 mmol/L and mild change in mental status. There was no evidence for hypothermia or bradycardia. Presence of a small thigh hematoma on examination partially explained the acute drop in hemoglobin. Iron panel, folic acid and vitamin B12 levels were found to be within normal range. Patient had no active of infection to suggest sepsis and she did not receive any myelosuppressive medication. Rapid replacement with IV levothyroxine was started before proceeding with surgery to prevent development of myxedema coma. Free T4 normalized at 1.05 ng/dl after receiving a total of 700 mcg of IV levothyroxine on day 5 of hospitalization. ORIF was done with no complications. Pancytopenia resolved upon thyroid replacement therapy and she was discharged on her regular dose of levothyroxine 75 mcg daily. Discussion: Most common hematologic abnormality associated with hypothyroidism is normochromic normocytic anemia. Currently, there are less than 10 reported cases of pancytopenia associated with hypothyroidism. The exact mechanism is unclear but proposed hypothesis is transient bone marrow hypoplasia. The most common clinical presentation, as seen in our patient, is profound hypothyroidism with ultimate outcome of myxedema coma. Most of these patients had resolution of pancytopenia following adequate thyroid hormone replacement. Interestingly, all cases have been reported in female patient population. Further research is needed to understand pathophysiology, risk factors, prognosis and the risk of pancytopenia recurrence in patients with severe hypothyroidism. More importantly, hypothyroidism must certainly be entertained as a differential diagnosis of pancytopenia.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nikita Limara Rabelo Pagan ◽  
Melanie Quintana Serrano ◽  
Mary J Rodriguez Malave ◽  
Meilyn Reyes

Abstract Myxedema coma is a severe form of hypothyroidism representing a endocrinologic emergency. It requires prompt identification and management, as mortality rates exceed 50%. Its rarity stems from early recognition and thyroid medication availability. Its presentation can be non-specific, making it a challenging diagnosis. This is a 67-year-old male inmate who was brought to the ED due to hypoactivity. He had a long-standing history of bipolar disorder, and hypothyroidism receiving oral levothyroxine. On evaluation, patient had slowed mentation, GCS 14/15, sluggish reactive pupils, macroglossia, diffuse non-pitting edema, and delayed relaxation of the deep tendon reflexes in the extremities. Vital signs were abnormal; T: 35.2 °C, RR: 10 rpm, SpO2: 84 %, BP: 137/89 mmHg and HR: 42 bpm without chronotropism. 12-lead ECG revealed a complete atrioventricular block (AV block), with non-conductive P waves and idioventricular rhythm. Patient became hemodynamically unstable, transcutaneous pacemaker was placed. Dopamine infusion was initiated for adequate mean arterial pressure. Subsequently, a femoral transvenous pacemaker was performed. However, neurological deterioration prompted mechanical ventilation. Exploring reversible AV block etiologies, laboratory results were markedly elevated for TSH at 184.775 ng/mL and decreased T4 at 1.5 ng/mL. Lithium levels were therapeutic. Myxedema coma was identified and timely treatment was provided with intravenous thyroid hormone replacement, intravenous hydrocortisone, and supportive care. Patient was transferred to an ICU where TSH was monitored. After 5 days of receiving IV thyroid hormone replacement therapy, TSH improved. However, patient remained dependent on transvenous pacemaker, for which permanent pacemaker had to be placed. With further therapy, patient’s neurological status improved leading to extubation, and subsequent discharge. Thyroid hormones play a vital role in the electrical current of the heart; hence, disturbances may potentiate cardiac arrhythmias. Sinus bradycardia and QT interval prolongation are commonly seen. As the severity of hypothyroidism progresses, high-grade AV block may be encountered, being third degree AV block the most challenging and severe. Patients with high-degree AV block in the setting of reversible etiologies, commonly, do not need a permanent pacemaker. On the contrary, our patient developed complete dependence of the pacemaker for adequate cardiac synchrony, despite adequate replacement therapy. With this case, we illustrate the importance of a thorough evaluation in patients with AV block of unknown origin, with special attention to reversible etiologies. Thyroid function abnormalities should be promptly identified and managed for better outcomes. Furthermore, it may decrease cardiac death risk and the need for invasive procedures, such as permanent pacemaker placement.


1980 ◽  
Vol 95 (4) ◽  
pp. 472-478 ◽  
Author(s):  
A. Eugene Pekary ◽  
Jerome M. Hershman ◽  
Clark T. Sawin

Abstract. Basal serum TSH and the peak TSH response to a 500 μg TRH bolus were measured in 57 euthyroid and in 29 hypothyroid subjects either receiving graded thyroid hormone replacement or acutely removed from full replacement therapy. Serum TSH, total T4 and T3 were determined by sensitive radioimmunoassay methods. The peak versus basal TSH data for hypothyroid patients were linear within individuals. The regression slope of the peak versus basal TSH data for all hypothyroid subjects did not differ significantly from the corresponding slope for all euthyroid subjects. Basal and peak TSH versus T3 and T4 data for hypothyroid patients were also linear within each individual. Moreover, the regression of the basal TSH values averaged over the non-replacement to full replacement state against the TSH versus T3 slope had a significant negative correlation. This trend leads to an array of regression lines which average to the familiar hyperbolic relationship between thyrotrophin and thyroid hormone levels in man.


Prescriber ◽  
2018 ◽  
Vol 29 (12) ◽  
pp. 30-33
Author(s):  
Anh Tran ◽  
Steve Hyer ◽  
Gabriella Bathgate ◽  
Onyebuchi Okosieme

2018 ◽  
Vol 8 (1) ◽  
pp. 24-28
Author(s):  
Sukriti Kumar ◽  
Sumit Rungta ◽  
Manish Gutch ◽  
Annesh Bhattacharya ◽  
Syed Mohd Razi ◽  
...  

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