One of the most controversial aspects of the management of myxoedema coma is which thyroid hormone medication to give and how to give it (dose, frequency, and route of administration). Because of the relative rarity of this condition, the paucity of reported treatment results, and the difficulties inherent in performing a controlled investigation, the optimum treatment remains uncertain, and several approaches will be discussed. Some of the differences of opinion relate to whether to administer T4 and rely on the patient to con vert it to the more active T3, or to give T3 itself. One must balance the need for quickly attaining physiologically effective thyroid hormone levels against the risk of precipitating a fatal tachyarrhythmia or myocardial infarction. T4 provides a steady smooth onset of action with a lower risk of adverse effects.

Parenteral preparations of either T4 or T3 are available for intravenous administration. Although oral forms of either T3 or T4 can be given by nasogastric tube in the comatose patient, this route is fraught with risks of aspiration and uncertain absorption, particularly in the presence of gastric atony or ileus.

Parenteral preparations of T4 may be available in ampoules of 100 and 500 μg. A loading dose of 200– 400 μg of levothyroxine may be given intravenously. After this initial ‘loading’ dose, a maintenance dose of 1.6 μg/ kg body weight, reduced to 75% if being intravenously administered, can be given thereafter. This method may be at tended by increases in serum T4 to within the normal range within 24 h and by significant decrements in serum TSH. After clinical improvement the patient may be switched to oral therapy. Larger doses of T4 probably have no advantage and may, in fact, be more dangerous. Due to its conversion from T4, a progressive increase in serum T3 is seen after 300– 600 μg doses of T4, as has been described by Ridgway et al. .

The approach to therapy employing an initial large intravenous bolus dose of T4 followed by maintenance therapy has been considered optimal, but other evidence suggests improved outcomes with lower doses of thyroid hormone. This was also indicated in a prospective trial in which patients were randomized to receive either a 500- μg loading dose of intravenous T4 followed by a 100- μg daily maintenance dose, or only the maintenance dose. The overall mortality rate was 36.4% with a lower mortality rate in the high- dose group (17%) versus the low dose group (60%). Although suggestive, the difference was not statistically significant. Factors associated with a worse outcome included a decreased level of consciousness, lower Glasgow coma score, and increased severity of illness on entry as determined by an APACHE II score of more than 20.

T4 treatment has been generally considered effective, but there is one important drawback to total reliance on T3 generation from T4. The rate of conversion of T4 to T3 is reduced in many systemic illnesses (the euthyroid sick or low T3 syndrome) and hence T3 generation may be reduced in myxoedema coma as a consequence of any associated illness. Theoretically then, one might administer T4, see increases in serum T4 levels confirming adequate absorption, but fail to witness any significant fall in TSH or dramatic clinical improvement. As a consequence, small supplements of T3 should be given along with T4 during the initial few days of treatment, especially if obvious associated illness is present. Irrespective of the type of treatment selected, all patients should have continuous ECG monitoring with reduction in thyroid hormone dosage should arrhythmias or ischaemic changes be detected.

T3 is available for intravenous use (Triostat) in 1 ml vials containing 10 μg/ ml. When therapy is approached with T3 alone, it may be given as a 10– 20 μg bolus followed by 5– 10 μg every 4 h for the first 24 h, dropping to 5– 10 μg every 6 h for days 2– 3, by which time oral administration should be feasible. T3 has a much quicker onset of action than T4 and increases in body temperature and oxygen consumption may occur 2– 3 h after intravenous T3, compared to 8– 14 h after intravenous T4. A patient with pro found secondary myxoedema believed due to postpartum pituitary necrosis has been reported who presented with cardiogenic shock which responded to T3 but not T4 therapy. Because of the high mortality rate in myxoedema coma, advocates for T3 therapy argue that the more rapid onset of action could make the difference between life and death. But the benefits of the more rapid onset of action need to be weighed against the greater risk of complications. As a consequence, it is difficult to justify the high risk/ benefit ratio of a regimen that uses rapid replacement with relatively large doses of intravenous T3 alone. Such treatment would be marked by large and unpredictable fluctuations in serum T3 levels, and high serum T3 levels during treatment with thyroid hormone have been associated with fatal outcomes.

 A more conservative but seemingly rational course of management is to provide combined therapy with both T4 and T3. Rather than administer 300– 500 μg T4 intravenously initially, a dose of 4 μg/ kg lean body weight (or about 200– 300 μg) is given, and an additional 100 μg is given 24 hours later. By the third day, the dose is reduced to a daily maintenance dose of 50 μg, which can be given by mouth as soon as the patient is conscious. Simultaneously with the initial dose of T4, a bolus of 5– 20 μg T3 is given and intravenous T3 is continued at a dosage of 2.5– 10 μg every 8– 12 hours until the patient is conscious and taking maintenance T4 [46]. Sensitivity to thyroid hormone in terms of cardiac risk varies, depending on age, cardiac medications, and the presence of underlying hypoxaemia, coronary artery disease, congestive failure, and electrolyte imbalance. Clinical improvement has been seen with even a single dose of only 2.5 μg T3 . It is wise to monitor the patient for any un toward effects of therapy before administering each dose of thyroid hormone.

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ضمن محفلها الأسبوعي في كربلاء.. دار علوم نهج البلاغة تقدم محاضرة عن أساليب التزييف السياسي التاريخي

أكاديمية التطوير الإداري تشكل فريقًا بحثيًّا من خريجيها لرفع كفاءة الأداء المؤسسي

شعبة الخطابة تقيم ورشة تخصصية عن سلوك الخطيب الحسيني في بغداد

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ألمانيا.. رئيس الأطباء يدعو للإسراع بتطبيق "ضريبة السكر"

بين الفائدة والضرر.. جدل حول تأثير الشاي والقهوة على العظام

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حرارة المحيطات عند مستويات مقلقة.. وعودة "إل نينيو" تقترب

باحثون يحددون تأثير القهوة على الميكروبيوم والمزاج

المزيد

مواضيع ذات صلة

Myxoedema Coma: Hyponatraemia

Diagnosis of Myxoedema Coma

Pathophysiology of Unstable Hemoglobin Disorders

Central Hypothyroidism

Severe Iodine Deficiency and natural Goitrogens

Iatrogenic Hypothyroidism

Pathobiology of Sickle Cell Disease: The Basis of Phenotypic Diversity

The Unique Systems Biology of Sickle Cell Anemia

Abnormalities of Sickle Red Blood Cells

Abnormal Molecular Behaviors of Sickle Hemoglobin

Clinical Assessment and Systemic Manifestations of Hypothyroidism: Diagnostic Accuracy

Clinical Aspects of Hypothyroidism due to Different Aetiologies