MYXEDEMA LÀ GÌ
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StatPearls
Continuing Education Activity
Myxedema coma is a rare fatal condition resulting from long-standing hypothyroidism with loss of the adaptive mechanism khổng lồ maintain homeostasis. Hypothyroidism due to lớn any cause, including autoimmune disease, iodine deficiency, congenital abnormalities, or medications lượt thích lithium and amiodarone, can precipitate myxedema coma if left untreated. Even with early diagnosis and treatment of myxedema coma, the mortality rate is variable, with some reports as high as 60% and others as low as đôi mươi to 25% in the presence of advanced intensive tư vấn care. Early recognition, a thorough history, physical exam, and early treatment are paramount in managing myxedema coma. This activity nhận xét the cause, pathophysiology, và presentation of myxedema & highlights the role of the interprofessional team in management.
Objectives:
Describe the history và physical exam of a patient with myxedema coma.
Identify the etiology of myxedema coma.
Outline the management options available for myxedema coma.
Review the importance of an interprofessional team for improving outcomes of myxedema coma.
Access không lấy phí multiple choice questions on this topic.
Introduction
Myxedema coma is a rare & extreme complication of hypothyroidism with multiple organ abnormalities associated with altered sensorium, it can be fatal. Hypothyroid patients exhibit multiple physiologic alterations to lớn compensate for the deficiency of thyroid hormone. Factors like infection can overwhelm these homeostatic mechanisms and can lead to myxedema coma. Myxedema coma can be an initial presentation of any size of hypothyroidism, irrespective of the cause.<1> Even with early diagnosis & treatment of myxedema coma, the mortality rate is variable, with some reports as high as 60% and others as low as đôi mươi to 25% even with intensive care.
Myxedema is commonly used often in the context of hypothyroidism and myxedema coma, it also means edema of the skin and soft tissue in hypothyroidism.<2> Myxedema coma is a misnomer. Neither the patients have classic nonpitting edema, nor are they in a coma. The most salient feature of myxedema coma is deteriorating mentation.
A high index of suspicion, early recognition, admission to intensive care units, and treatment with intravenous levothyroxine và hydrocortisone are paramount in the management of myxedema coma.<3> History of any thyroid dysfunction, thyroid medication, adherence with thyroid medication, thyroid surgery, & history of any drugs that may affect thyroid function require assessment in any patient suspected myxedema coma.<4>
Etiology
Disrupted homeostatic mechanisms in hypothyroid patients lead to myxedema coma. There are many Precipitating factors. The most important are:
Infections: urinary tract infection, pneumonia, viral infections, influenza, etc.
Burns, carbon dioxide retention, & trauma
Congestive heart failure
Epidemiology
The exact incidence and prevalence of myxedema coma are not known, but some authors estimate an incidence of approximately 0.22 per 1000000 per year in the western world; however, there is no sufficient epidemiological data from other countries.<4> Myxedema coma is more common in females (80% of cases), as hypothyroidism is more common in women (four-fold more than men).<12> The population aged more than 60 years are more liable lớn have myxedema coma.<13> Since the patients are usually hypothermic, myxedema coma is more common in the winter (90% of cases).<14> This fact is explained by decreased heat production with age & hypothyroidism and decreased thermoregulation with age.<15>
Pathophysiology
The thyroid gland begins development during the fourth gestational week as an endodermal thickening of the floor of the primitive pharynx. Its final resting place is located in the anterior inferior visceral compartment of the neck và lies deep khổng lồ the omohyoid, sternohyoid, và sternothyroid muscles. It is encased in the pretracheal fascia and accompanied by the pharynx, trachea, esophagus, and recurrent laryngeal nerve.<16> The thyroid has two lobes linked by an isthmus. It sometimes has a pyramidal lobe (40% of the population) that extends upward from the isthmus và is responsible for the production of two major hormones: thyroxine (T4), triiodothyronine (T3).<17> These hormones are responsible for regulating whole-body metabolism, which can decrease by as much as 40 to lớn 50 percent in the complete absence of these hormones & increase by as much as 60 lớn 100 percent with full secretion.
The metabolically active hormones the thyroid secretes are T4 & T3 (around 93% T4 và 7% T3). T3 is four times more potent than T4, và the vast majority of T4 converts to lớn T3 in the tissues. The half-life of T4 is seven days, while T3 has a much shorter half-life. Multiple proteins bind to T3 and T4. These proteins include thyroxine-binding globulin, transthyretin (TTR), & albumin. Production of the thyroid hormones by follicles lined by cuboidal epithelial cells occurs inside the thyroid gland. These follicles secrete colloid, which is composed of thyroglobulin and contains the thyroid hormones T3 & T4. At least 50 milligrams of iodine per year or 1 milligram per week are necessary for adequate hormone production.<18>
Iodine is concentrated within the thyroid cell by a sodium-iodide symporter that pumps one iodide molecule và two sodium ions. The serum TSH màn chơi highly influences the activity of this symporter. A peroxidase enzyme then oxidizes iodide ions to lớn iodine.<19> Then organification occurs by binding iodine to lớn the amino acid tyrosine located within the thyroglobulin molecule. Thyroglobulin is stored in the thyroid gland & contains approximately 30 molecules of T4 and a few molecules of T3. In the complete absence of the production of thyroid hormone, the thyroid contains enough reserve lớn last about 2 to lớn 3 months.
Thyroid hormone influences virtually all cells in the toàn thân by activating or repressing a variety of genes after binding to lớn thyroid hooc môn receptors. Ninety percent of the intracellular thyroid hooc môn that binds to và influences cellular function is T3, which has been converted from T4 by the removal of an iodide ion. The thyroid hooc môn receptors associated with the DNA within the target genes are bound to lớn retinoid X receptors at specific thyroid hooc môn response elements. Once bound, the transcription process begins, & hundreds of new intracellular proteins, mostly enzymes, are formed. One particular gene of importance is the gen that regulates the expression of calcium ATPase, which is especially important in maintaining efficient cardiac output.<20> Thyroid hormones bởi have some non-genomic effects on cells, which include the regulation of ion channels và oxidative phosphorylation. These effects are possibly under the mediation of the thyroid hormone-binding of the plasma membrane, cytoplasm, and cellular organelles. Other effects of thyroid hormone include increased Na-K-ATPase activity, increased carbohydrate metabolism, increased miễn phí fatty acids (decreased cholesterol, phospholipids, và triglycerides), increased vitamin requirements as a consequence of increased enzymes that use vitamins as cofactors, & overall increased metabolism. In light of thyroid hormone being responsible for a vast majority of bodily functions at the genetic and cellular level, it is easy to see how the extreme absence of this hormone, as seen in myxedema coma, is associated with a high mortality rate and has a broad spectrum of presenting symptoms.<21>
Myxedema coma is a potentially fatal complication, & prompt diagnosis is an important factor in reducing mortality.
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<5> Identifying a precipitating cause is imperative. It is worth noting that a patient usually presents with hypothermia & is not febrile.<22> However, an investigation for an infectious cause is warranted, particularly if the patient is minimally hypothermic as it may be masking the underlying infection.<15> Particular drugs such as lithium và amiodarone have multiple case reports associating their use and precipitation of myxedema coma given their mechanism of kích hoạt on the inhibition of thyroid hooc môn release.<23> Lithium also inhibits cAMP production in response to lớn TSH. Patients on lithium also have been shown to have an exaggerated TSH response khổng lồ TRH.<24> Amiodarone inhibits thyroid hooc môn entry into peripheral tissues, inhibits 5’-deiodinase, converts T4 khổng lồ T3, và releases excess iodine.<25> Other precipitating factors such as hypoglycemia, hypoxemia, and hypercapnia may also be secondary to myxedema coma itself.
A brief mô tả tìm kiếm of organ system-specific pathologic manifestations is described below.
Cardiac Manifestations
Diastolic hypertension is one of the cardiovascular compensatory mechanisms in hypothyroidism. Hypothermia & decreased respiratory drive cause peripheral vasoconstriction, resulting in loss of protective mechanism và development of hypotension. Common cardiovascular symptoms include hypotension, shock, arrhythmia, and heart block. Myxedema causes decreased myocardial contractility & reduced cardiac output, which leads to hypotension.<26> Bradycardia, flattened T waves, low voltage, bundle branch blocks, & complete heart blocks are common EKG findings.<27> Low voltage on EKG can be representative of pericardial effusion due to the accumulation of fluid rich in mucopolysaccharides và merits investigation.<28> Fatal arrhythmias are important to recognize in Myxedema và chronic hypothyroidism<5>. There have been cases showing QT interval prolongations leading khổng lồ “torsades de pointes,” which resolves with treatment of myxedema. Myocardial infarction is important to lớn rule out as aggressive T4 replacement may increase the risk of myocardial infarction.<29>
Neurological Manifestations
Myxedema coma course is commonly a slow progression to lớn coma. Typically patients vày not present with coma, especially in the early phase, but they present with lethargy. Hence the name of myxedema coma itself can be misleading. Other findings may include depression, disorientation, decrease deep tendon reflexes, psychosis, slow mentation, paranoia, và poor recall.<30> One case describes a rare presentation of a patient with status epilepticus.<31> Lumbar punctures, which are usually done during the investigation of underlying causes to rule out infections, can show increased pressure & high protein count in these situations, attributable to increased meningeal permeability và cerebral blood flow and a decrease in metabolism.<32>
Respiratory Manifestations
Hypoventilation in myxedema coma is due to impaired hypoxic và hypercapnic ventilatory response và the associated diaphragmatic muscle weakness.<33> The primary cause of coma in myxedema appears khổng lồ be due to lớn respiratory depression due to lớn decreased response khổng lồ hypercapnia.<27> Also, swelling of the tongue & vocal cords leads to obstructive sleep apnea contributing khổng lồ respiratory failure. Another issue that can contribute is a reduction in tidal volume due to pleural effusion or ascites.<34>
Gastrointestinal Manifestations
Myxedema coma commonly causes abdominal pain, nausea, vomiting, ileus, anorexia, constipation, and ascites.<35> Ileus is of particular importance as it can lead lớn megacolon. Ascites have also been seen in cases of myxedema but are not common. There are reports of only a few cases in the literature. These gastric complications may also cause issues with the absorption of oral medications. Gastrointestinal bleeding can occur as myxedema has a higher risk of bleeds due khổng lồ coagulopathy-related complications.<36><37>
Renal và Electrolyte Manifestations
Typical findings in myxedema coma are hyponatremia and decreased glomerular filtration rate.<38> Hyponatremia occurs mainly due khổng lồ decreased water transport khổng lồ the distal nephron.<39> Other causes can be an increase in antidiuretic hormone (ADH).<40> Hyponatremia is also a key factor in the patient’s altered mental status và development of a coma.<41> Urinary sodium excretion is increased or normal. Urinary osmolality elevates relative lớn plasma osmolality.<42> Patients may also have bladder atony causing urinary retention.
Hematologic Manifestations
Patients with myxedema coma have an increased risk of bleeding due to lớn an acquired von Willebrand syndrome type 1 và a decrease in factors V, VII, VIII, IX, và X.
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<43> This is unlike those with only mild hypothyroidism, which causes a hypercoagulable state. Cases have shown that acquired von Willebrand syndrome is reversible with T4 therapy.<44>
