What Is a Myxedema Coma?

Myxedema coma often has infections, stress and the use of sedatives before the onset of hypothyroidism, such as fatigue, cold, abdominal distension, constipation, lethargy and slow movements, memory loss and so on. If not treated in time, a myxedema coma occurs, also known as a hypothyroidism crisis. ^[1]

Myxedema coma

Myxedema coma (myxedema coma) is a severe state of hypothyroidism, which is mostly induced by infection and the use of sedatives. Myxedema coma is an advanced stage of hypothyroidism that cannot be diagnosed and treated in time. Its characteristics are in addition to severe hypothyroidism, hypothermia, coma, and sometimes shock. This disease often occurs in elderly female patients. Although the incidence is not high, it has a higher mortality rate, and its risk is no less than that of diabetic coma.

Pathogenesis of myxedema coma

Incidence of myxedema coma

This disease is a rare complication of severe myxedema. This kind of case was first reported in the United Kingdom in 1879, but its understanding was not enough. After the second case was reported by Summers in 1953, as the level of awareness of the disease improved, many authors successively introduced the same cases. By 1964 A total of 131 cases were reported in the literature. Urbanic et al. Introduced that in patients with hypothyroidism hospitalized within 10 years, the incidence of coma was only 0.1%.

Myxedema coma pathophysiology

In most cases, the pituitary gland and adrenal glands are normal. In a few cases, the pituitary gland can be enlarged and the adrenal gland atrophy or bleeding. The liver may have fatty changes and fibrosis. The basement membrane of the glomeruli and tubules thickened and the cytoplasm was abnormal. In a group of 48 autopsies, no special brain changes were seen.

The disease is mainly manifested as loss of mind and hypothermia. Others include decreased ventilation, hypotension, imbalance of body fluids and electrolytes, and peripheral circulation failure. Many of the pathophysiology of these manifestations remain uncertain. The cause of coma may be a combination of multiple factors: brain cells can not work properly at low body temperature, resulting in a high degree of inhibition; cardiac output and cerebral blood flow are reduced, causing cerebral hypoxia; subarachnoid space or choroidal edema degeneration, causing cerebrospinal fluid pressure Increased; decreased use of sugar by brain cells during hypoglycemia; reduced vital capacity and alveolar ventilation, significantly increased carbon dioxide tension, and anesthesia of carbon dioxide; severe infection and hyponatremia can also cause coma; thyroid hormone deficiency, many important in the brain Enzyme activity is inhibited and so on.

Hypothermia may be the result of reduced basal metabolism and insufficient thermal energy. When cold, the thyroid hormone in the patient's circulation does not increase correspondingly with physiological needs. Therefore, winter is the peak season of the disease.

Reduced ventilation causes carbon dioxide retention, which causes carbon dioxide anesthesia and respiratory acidosis. Inhibition of the respiratory center affects nerve conduction in the respiratory muscles, weakens the contraction of respiratory muscles, and obstructs alveolar capillaries. In addition, mucopolysaccharides are deposited, and the upper airway is blocked when the tongue falls backwards in a coma; the effects of edema on the respiratory muscles, obesity, emphysema, and upper respiratory infections can reduce ventilation; and sedation and anesthetics can reduce breathing Central sensitivity.

Patients with hypothyroidism have an overall increase in sodium, while myxedema presents with hyponatremia in a coma, an increase in overall water and sodium in the urine, and a decrease in glomerular filtration rate and renal blood flow. The diuretic decrease may be caused by the deposition of renal mucopolysaccharides, increased urine osmotic concentration, and decreased blood osmotic concentration, resulting in imbalance of intracellular and external interstitial balance. Impaired renal dilution may be the cause of hyponatremia. Plasma volume is reduced while extracellular volume is increased, capillary permeability is enhanced, serum exudates, the protein content in the exudate is high, and the edema is non-depressive.

Patients with primary myxedema have elevated TSH, but no change is caused by hypopituitarism. TSH's response to TRH is significantly higher in patients with primary disease than in patients with pituitary. Patients may have reduced adrenal function. With prolonged hypothermia or reduced adrenal function, hypoglycemia may occur, which is related to decreased intestinal glucose absorption and insufficient glycogen mobilization.

Reduced respiratory function, carbon dioxide anesthesia, hyponatremia, cerebral edema, lack of thyroid hormones and hypoglycemia, etc., can produce various comorbidities in the nervous system, such as mental retardation, forgetfulness, mood swings, lethargy, depression and delusions of persecution, etc. Some patients may have a major seizure.

Muscle volume increases, muscle contraction and relaxation slows, and eventually causes reflexes to slow. Paralyzed intestinal obstruction can occur due to loss of intestinal elasticity and lack of peristalsis.

Patients may also have urinary retention. When the condition is severe, food intake is further reduced and cachexia is present. Due to the increased fragility of capillaries, there may be gastrointestinal or skin bleeding.

Clinical classification of myxedema coma

Myxedema can be clinically divided into three types: primary (thyroid), secondary (pituitary) and tertiary (hypothalamus). The former accounts for the vast majority of cases, and the latter two account for about 4%. Primary cases occur mostly after autoimmune thyroiditis, and can also be removed by most or all of the thyroid gland after surgery, radioactive iodine, or local radiation therapy. A few are found for no reason and are idiopathic; secondary cases are caused by pituitary tumors. Or it may be caused by hypofunction of the anterior pituitary gland caused by other reasons; those caused by hypothalamic disorders are tertiary myxedema. Regardless of the cause, coma can occur in anyone with hypothyroidism that progresses to the terminal stage.

Clinical manifestations of myxedema coma

(1) Drowsiness, unconsciousness and even coma.

(2) Respiratory failure, manifested as shallow breathing, hypoventilation, CO2 retention, etc.

(3) hypothermia.

(4) Slow heart rate and low voltage.

(5) Water poisoning.

(6) Acute urinary retention and paralytic intestinal obstruction. ^[1]

Myxedema coma auxiliary examination

Myxedema coma laboratory test

1. In patients with primary hypothyroidism, TT3, FT3, TT4, and FT4 decrease, and TSH increases.

2. Determination of thyroid iodine uptake rate: significantly lower than normal.

3 Anemia, blood lipids and muscle enzymes were significantly increased.

4 Blood gas analysis: showed respiratory failure, CO2 retention, respiratory acidosis.

Myxedema coma other examination

ECG: low voltage, sinus bradycardia, low voltage, atrioventricular block, ST-T changes. ^[1]

Differential diagnosis of myxedema and coma

Primary and secondary hypothyroidism are often difficult to distinguish clinically. Most of them are primary in terms of etiology. Determination of TSH is helpful in distinguishing primary, secondary, or tertiary hypothyroidism. Glucocorticoids are used at the beginning of emergency treatment, so this identification is not necessarily required. However, for further etiology treatment after the condition improves, this test is meaningful.

The diagnosis of typical cases is not difficult, and for less typical cases, it is often difficult to confirm under emergency conditions. Clinically, this disease is easy to be confused with other systemic diseases, especially some cardiovascular, gastrointestinal, and nervous system diseases, and other common causes of coma, which should be ruled out as soon as possible for easy treatment. ^[2]

Myxedema coma treatment

1. Replacement therapy: L-thyroxine (L-T4) is 2 g per kilogram of body weight, and the intravenous injection is completed within 5 to 10 minutes, followed by 100 g daily. After the patient is awake, the patient will take the oral dose instead. Generally within 24 hours of medication, blood pressure, pulse, body temperature and mental state can be significantly improved. Starting with T3, the effect is better. Intravenous injection of 10 g, once every 4 to 6 hours. Use L-T4 when the condition improves. You can also use thyroid tablets, nasal feeding 80mg, then every 8h, after the condition improves, change to a maintenance amount.

2. Keep your body temperature, but not heat.

3 If necessary, endotracheal intubation and mechanical ventilation.

4 Appropriate fluid replacement after measuring blood glucose and electrolytes, pay attention to observation of water retention.

5. Hydrocortisone intravenous drip is 100 ~ 200mg / d.

6. Remove incentives, such as infection. ^[1]

Prevention of myxedema and coma

If the disease is not treated in time, the prognosis is poor, and respiratory failure is the main cause of death. In the past, the mortality rate of this disease was as high as 80%. With the improvement of diagnosis and treatment, it has been reduced, but it is still about 50%. Many factors, such as a significant decrease in body temperature, prolonged coma, hypotension, cachexia, and failure to identify and promptly affect the prognosis. Laboratory test results are of little value in judging prognosis.