Myxedema là gì

Myxedema là một sử dụng để mô tả dữ dội hypothrdoism. Myxedema cũng được sử dụng để mô tả những thay đổi ngoài da xảy ra trong hypothrdoisim và đôi khi cường giáp. Trong hoàn cảnh này, hỗn hợp dùng để chỉ sự lắng đọng của mucopolysaccharide trong lớp hạ bì, mà kết quả trong sưng của khu vực ảnh hưởng. Khi thay đổi da xảy ra trong cường giáp, chủ yếu Graves disease, nó được gọi là myxedema pretibial.

Myxedema hôn mê đôi khi được gọi là cuộc khủng hoảng myxedema, là một phổ biến, life-threatening clinical ailment that signifies severe hypothyroidism with physiological decompensation. The condition normally happens in patients who undiagnosed hypothyroidism for many years and is usually hastened by heart failure, nhiễm trùng, vết thương, cerebrovascular disease, or drug therapy. Patients with myxedema coma are commonly seriously -ill with notable hypothermia have a depressed mental status.
A medical emergency, myxedema coma demands immediate attention. If the diagnosis is presumed, direct supervision is needed before establishing the diagnosis due to the high mortality rate associated with this condition. Patients with myxedema coma should be attended to in an intensive care unit with non-stop cardiac monitoring. The first steps in therapy include airway control, glucocorticoid therapy, thyroid hormone replacement, and supportive measures.
Sinh lý bệnh
Myxedema coma transpires as a consequence of long-standing, undiagnosed, or undertreated hypothyroidism and is normally hastened by a systemic illness. Myxedema coma can be due to any of the causes of hypothyroidism, ordinarily chronic autoimmune thyroiditis. This can also befall patients who had thyroidectomy or experienced radioactive iodine therapy for hyperthyroidism. Rare causes may comprise subsequent hypothyroidism and medicines such as amiodarone and lithium
Given the significance of thyroid hormones in cell metabolism, long-standing hypothyroidism is connected with reduced metabolic rate and reduced oxygen consumption, which affects all body systems. This ends in hypothermia, which is a powerful predictor of mortality. Another outcome is reduced drug metabolism leading to overdosing of medications especially sedatives, hypnotics, and analgesic agents; this can accelerate myxedema coma.
Cardiac contractility is an impartment, low cardiac output volume, commencing low cardiac output, bradycardia and at times hypotension. Reduced stroke volume in critical cases may also be due to pericardial effusions triggered by the accumulation of fluid heavy in mucopolysaccharides within the pericardial sac. Congestive heart failure is rarely observed in the vacancy of preexisting cardiac disease.
Electrocardiographic conclusions can include bradycardia,low voltage, varying degrees of the block, nonspecific ST-segment changes, flattened or inverted T waves, extended Q-T interval, and ventricular or atrial arrhythmias.
The reduction of the effect of beta-adrenergic receptors leads to the pervasiveness of the effect of alpha-adrenergic receptors, increased catecholamines, and enhanced systemic vascular resistance, causing some sufferers to have diastolic hypertension and a restricted pulse pressure.
Plasma capacity is limited, and capillary permeability rises, causing fluid buildup in tissue and expanses and pericardial effusions.
Notwithstanding the term myxedema coma, many patients do not present in a coma, but manifest variable degrees of altered consciousness. Brain function is impacted by reduction in oxygen delivery and subsequent damage, lowered glucose usage and reduced cerebral blood flow. Hyponatremia can also lead to altered mental function.
The main pulmonary outcome of myxedema coma is hypoventilation, which results from central depression of ventilatory drive with reduced responsiveness to hypoxia and hypercapnia. Other participating factors to hypoventilation involve respiratory muscle instability, reflex obstruction by a large tongue, and obesity-hypoventilation syndrome. Fluid buildup may cause pleural flows and lowered diffusing capacity.
Kidney function may be compromised with reduced glomerular filtration rate because of low cardiac output and peripheral vasoconstriction or because of rhabdomyolysis. Hyponatremia is prevalent in patients with myxedema coma and is generated by increased serum antidiuretic hormone and impaired water excretion.
The gastrointestinal tract in myxedema coma can be remarked by mucopolysaccharide infiltration and edema. Cũng thế, neuropathic changes can cause malabsorption, gastric-atony, , megacolon, impaired peristalsis, and paralyticileus, Ascites may happen due to enlarged capillary permeability, suy tim, or other adjustments. Gastrointestinal bleeding secondary to an associated coagulopathy may occur.
Myxedema coma is associated with a greater risk of bleeding created by coagulopathy related to an acquired von Willebrand syndrome (kiểu 1) and lowers factors V, VII, VIII, IX, and X. . Patients may also have microcytic anemia secondary to hemorrhage, or macrocytic anemia produced by normocytic normochromic anemia, or vitamin B12 deficiency, which can be subordinate to reduced oxygen requirement and decreased erythropoietin

United States
Myxedema coma is a rare outcome of untreated hypothyroidism, and the exact predominance in the United States is not known.
A study from Spain showed that the incidence rate of myxedema coma is 0.22 per million per year. A study by Ono et al estimated the annual frequency of myxedema coma in Japan to be 1.08 per million people.

Myxedema coma is a medical emergency. If the ailment is not promptly diagnosed and treated, the mortality rate can be more than 50%. Even with prompt recognition and timely medical intervention, mortality rates are as high as 25%.
The most common circumstances of death are a respiratory failure, nhiễm trùng huyết, and gastrointestinal bleeding.
Myxedema coma bears a high mortality and morbidity rate. vì thế, timely identification and proper management are critical. Factors leading to a poor prognosis are older age, steadfast hypothermia, or bradycardia, lower degree of awareness by Glasgow Coma Scale, multiorgan impairment indicated by high APACHE (Acute Physiology and Chronic Health Evaluation) II score. The study above by Ono et al. reported that, as revealed through multivariable logistic regression, a higher in-hospital mortality rate was associated with older age and catecholamine use (with or without steroids).

Suy giáp là gì ( Theo chủ động tuyến giáp)?

Patient Education
Các bệnh nhân được xác định có suy giáp cần được tư vấn liên quan đến yêu cầu của việc thay thế hormone tuyến giáp hàng ngày và quan sát kiểm tra tuyến giáp trên cơ sở thường xuyên.
Bệnh nhân có tiền sử viêm tuyến giáp hoặc những người đã trải qua chiếu xạ tuyến giáp hoặc phẫu thuật tuyến giáp nên được khuyến cáo rằng suy giáp có thể xảy ra trong tương lai. Họ cần được giáo dục về các triệu chứng của suy giáp và nên hiểu tầm quan trọng của tìm tư vấn y tế kịp thời để kiểm tra và thử nghiệm.

Chăm sóc y tế
Myxedema hôn mê là một cấp cứu y tế đòi hỏi phải có sự quan tâm kịp thời. Nếu chẩn đoán nghi ngờ, immediate management is needed before confirming the diagnosis due to the high linked mortality rate. Patients with myxedema coma should be administered in an intensive care unit with consistent cardiac monitoring. Initial steps in control include the elements below.
Airway management
Preservation of adequate airway is crucial, since most patients have discouraged mental status along with respiratory failure. Mechanical ventilation is commonly needed during the first 36-48 giờ, nhưng một số bệnh nhân yêu cầu hỗ trợ hô hấp kéo dài càng lâu càng 2-3 tuần.
thay thế hormone tuyến giáp
The ideal form of therapy and doses of thyroid hormone therapy in myxedema coma continue to be controversial due to the rarity of the condition and lack of clinical trials. Some clinicians advocate the administration of levothyroxine (T4), while others prefer a combination of T4 and liothyronine (T3) The American Thyroid Association recommends combination therapy with T4 and T3.
Because of declining gastrointestinal absorption, intravenous thyroid hormone therapy is advised.
Một liều tải tĩnh mạch 300-600 microgram levothyroxin (T4) được thay thế bởi một liều tiêm tĩnh mạch mỗi ngày 50-100 microgram. liều lớn hơn của T4 lẽ không có lợi thế và có thể nguy hiểm. Sự kết thúc dưới của dải liều được hỗ trợ ở những bệnh nhân cao cấp, những nguy cơ bị các biến chứng tim mạch như loạn nhịp, nhồi máu cơ tim và loạn nhịp, và ở những bệnh nhân bị bệnh động mạch vành, vì liệu pháp T4 đầy đủ liều có thể làm trầm trọng thêm thiếu máu cơ tim bằng cách nâng cao mức tiêu thụ oxy của cơ tim.
Since the rate of conversion of T4 to the active hormone T3 can be reduced in these patients, the addition of T3 along with T4 has been advised. T3 has a quicker onset of action than T4, as rises in body temperature and oxygen consumption has been stated to be faster with T3 therapy compared to T4. T3 therapy is given as a bolus of 5-20 micrograms intravenously and to be maintained at a dosage of 2.5-10 micrograms every 8 hours depending on the patient’s age and coexistent cardiac risk factors.

treatmen levothyroxin tĩnh mạcht ở những bệnh nhân suy giáp nặng thường dẫn đến sự cải thiện trong tim mạch, thận, phổi, and metabolic framework within a week. Serum T4 and T3 concentrations may advance or normalize with a similar time frame, with more progressive improvement in serum TSH. như vậy, the therapeutic endpoints in myxedema coma should be enhanced mental status, improved cardiac function, and improved pulmonary function.
Analysis of thyroid hormones every 1-2 days is suggested. Failure of TSH to decrease or of thyroid hormone levels to increase suggests the need to increase doses of T4 and add T3.
The treatment is adapted to the oral form once the patient can take medications by mouth.
Glucocorticoid therapy
Patients with primary hypothyroidism may have lined primary adrenal insufficiency while patients with secondary hypothyroidism may have linked hypopituitarism and secondary adrenal insufficiency. The other reason for the treatment with corticosteroids is the possible risk of precipitating acute adrenal insufficiency caused by faster metabolism of cortisol that follows T4 therapy.
Stress doses of intravenous glucocorticoids should be given the chance of adrenal insufficiency is barred by a random serum cortisol, which is beneficial only if very low, hoặc là, tốt hơn, by an ACTH stimulation test.
Hydrocortisone at a dose of 50-100 mg every 8 hours is administered. An option is a dexamethasone at a dose of 2-4 mg every 12 giờ. Dexamethasone has the benefit of not impacting the serum cortisol concentration and can be used immediately without altering the results of the ACTH stimulation test, which can be implemented at any time. If the test is negative, corticosteroids can be stopped without tapering.
Supportive measures
Treat hypothermia by passive rewarming using ordinary blankets and a warm room. Active rewarming using external tools carries a risk of vasodilatation and deteriorating hypotension and should be avoided. The use of a rectal probe helps to discover the true core temperature and to monitor rewarming.
Treat related infection. Given the severity of the condition, contamination infection should always be acknowledged, and empiric broad-spectrum of antibiotics be considered until suitable cultures are proven negative.
hạ natri máu nặng đúng với hạn chế mặn nước miễn phí.
hạ đường huyết đúng với dextrose tiêm tĩnh mạch.
Hạ huyết áp được thường khắc phục bằng liệu pháp hormone tuyến giáp. Nếu huyết áp vẫn tiếp tục là thấp, sử dụng thận trọng của dịch truyền tĩnh mạch với dung dịch muối sinh được khuyến khích. hạ huyết áp chịu lửa có thể được điều trị bằng thuốc co mạch như dopamin. Tuy nhiên, patients should be weaned off the vasopressor as soon as possible because of the risk of the pressor-induced ischemic event.
Patients who are awake, no longer reliant on a ventilator, and medically stable may be transported from the intensive care unit to a medical ward.