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Successful Treatment of Myxedema Coma: A Case Report Donnie Lumban Gaol, Achnes Pangaribuan, Kurniyanto, Budi Setiawan, Hildebrand Hanoch Victor, Yunus Tanggo Departement of Internal Medicine, Faculty of Medicine, Universitas Kristen Indonesia, Jakarta

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Successful Treatment of Myxedema Coma: A Case Report

Donnie Lumban Gaol, Achnes Pangaribuan, Kurniyanto, Budi Setiawan, Hildebrand Hanoch Victor, Yunus Tanggo

Departement of Internal Medicine, Faculty of Medicine, Universitas Kristen Indonesia, Jakarta

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Background

Myxedema coma is a severe life threatening form of decompensatedhypothyroidism. Infections and discontinuation of thyroid supplements arethe major precipitating factors. The mortality rates may be as high as 25–60%even with best possible treatment.

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Case Report

Patient 48-year-old man, had history of thyroidectomy , 9

years ago with unknown of thyroid hormone therapy.

He was admitted with feeling fatigue, muscle weakness, headache, nausea, and decrease

mobility since one week ago.

Three days after admission patient was

found with confusion & lethargy without seizures.

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Case report

Complete blood test shows acute infection, uncontrolled glycemic. Chest x-ray figured pneumonia. Abdominal Ultrasonography revealed right pleura effusion, massive ascites and a normal-sized liver and spleen. Three days after admission patient was found with confusion & lethargy without seizures. Brain CT revealed normal.

We assessed patient with myxedema coma and treated with levothyroxine (thyrax) 100 mcg twice daily orally without laboratory result. From investigation revealed severe hypothyroidism with TSHs 11.1117 uIU/ml and free T4 < 0.4 ng/dl. After following the administration of thyroid replacement hormones for hypothyroid, her clinical condition improved gradually. Patient was given levothyroxine (thyrax) 100 mcg once daily as a maintenance therapy.

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Imaging Examination

USG : Right pleura effusion, massive ascites

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Chest x-ray : consolidation and thickening of right pleura CT Brain revealed Normal Scan

Imaging Examination

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Result Normal RangeErythrocyte sedimentation

rate 75 (H) <10 mm/hrHaemoglobin 12.2 (L) 14-16 g/dLLeukocytes 12.5 (H) 5-10 103/µL

Erythrocytes 3.95 (L) 4.5-5.5 106/mLHematocrites 34.5 (L) 40-48 %Trombocytes 659 (H) 150-400 x 103/ µL

MCV 87.4 82-92 /fLMCH 30.9 27-31 pg

MCHC 35.4 32-36 %Albumin 3.51 3.7-5.2 g/dLGlobulin 3.73 2.9-3.1 g/dL

AST 16 10-34 U/LALT 8 9-43 U/L

Fasting plasma glucose 270 (H) 70-110 mg/dLHbA1 14 (H) 4.5-6.3 %

Total cholesterol 156.5 150-250 mg/dLTriglycerides 83 40-160 mg/dL

HDL 30 35-55 mg/dLLDL 99 <155 mg/dL

Ureum 20 15-45 mg/dLCreatinin 0.91 0.7-1.1 mg/dLSodium 144 136-145 mmol/LPotasium 4.7 3.5-5.1 mmol/LChloride 91 99-111 mmol/L

TSHs 11.1117 0.35-4.94 µIU/mlFT4 < 0.40 0.7-1.48 ng/dL

LABORATORIUM RESULT

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Discussion

• Infections and history of thyroidectomy are the precipitating factors.

• Once clinicaly suspected to myxedema coma, treatment can be lifesaving and should be start promptly in anticipation of confirmation of the diagnosis by laboratory test.

PATIENT PleuropnemoniaHistory of Thyroidectomy

Clinical Presentations

clinically myxedema coma

treat as myxedema coma without laboratory confirmation

(do not delay treatment)

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Discussion

Our Patient

TSHs 11.1117 µIU/ml

FT4 < 0.40 ng/dL

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• Thyroid hormone therapy is the backbone of treatment of patients with myxedema coma and most authorities therefore recommend use of Thyroxine (T4) alone. Oral administration of T4 has proved to be equally effective compare with intravenous T4.

• The mechanism of ascites fluid formation in patients with myxedema is unclear. There are two main hypotheses.

• The first is that low levels of circulating thyroid hormones cause increased extravasation of plasma proteins because of abnormal capillary permeability and the lack of a compensatory increase in lymph flow and protein return rate.

• The second hypothesis is that hyaluronic acid accumulates in the skin and produces edema by a direct hygroscopic effect. However, hyaluronic acid has only been found in minute quantities in patients with myxedema ascites: not large enough to exert a direct hygroscopic effect. However, it could interact with albumin to form complexes that prevent the lymphatic drainage of extravasated albumin.

Discussion

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Conclussion

Early recognition and prompt treatment with thyroid hormone replacement is crucial in the management of myxedema coma due to potentially fatal condition

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