In hypothyroid coma, the tone is vesicular breathing. Hypothyroid coma: causes and symptoms

Hypothyroid coma is a serious complication of diseases thyroid gland, contributing to a decrease in the production of thyroid hormones, is most often diagnosed in women of advanced and senile age. Development coma observed with a severe course of the pathological process against the background of the absence or untimely start of treatment.

Hypothyroid coma is a serious complication of thyroid disease. Most often it is diagnosed in women of advanced and senile age.

Symptoms

Distinctive feature hypothyroid coma - slow development with gradual onset of symptoms. Harbingers include:

• chronic fatigue;
• inhibition of reactions;
• apathy;
• decrease in body temperature;
• pallor skin;
• swelling of the face and limbs;
• slowing down of breathing;
• impaired renal function;
• decline blood pressure;
• the disappearance of tendon reflexes.

Examination of a patient with severe hypothyroidism allows the doctor to detect the following symptoms:

• violation metabolic processes: Availability excess weight, slowed circulation, body temperature below 35 ° C;
• dysfunction of the respiratory and cardiovascular systems. It manifests itself in the form of bradycardia, threadlike pulse, edema of the heart muscle, lowering blood pressure to critical levels. Heart sounds are muffled, the rhythm is beaten. Breathing becomes shallow, the number of inhalations and exhalations decreases sharply, the level of oxygen in the blood falls, and temporary stops in breathing are observed;
• dysfunction of the central nervous system: lack of reflexes, cerebral edema, progressive stupor;
• dermatological manifestations of hypothyroid coma: dryness, pallor and yellowish skin tone, brittle hair and nails, hyperkeratosis;
• severe swelling of the face and limbs;
• signs of anemia and hypoglycemia;
• dysfunction digestive system: hepatomegaly, dynamic intestinal obstruction.

Emergency care for hypothyroid coma

The development of hypothyroid coma in children and adults is an indication for placement in the intensive care unit. First aid includes:

• administration of a high dose of Triiodothyronine within the first hour. Supplemented with oxygen therapy and intravenous injections of Hydrocortisone, the use of cardiac drugs;
• the introduction of vitamins of group B and C, ATP one hour after the development of hypothyroid coma. If the value of the upper pressure exceeds 90 mm Hg. Art., use Lasix. In other cases, the introduction of Corazol, Cordiamin and Mezaton is indicated;
• the introduction of medium doses of Triiodothyronine. After normalization of body temperature and an increase in heart rate, the dosage of the drug is reduced. Oxygen therapy, passive warming of the patient, and the use of sodium oxybutyrate continue;
• intravenous administration Seduxena with the development of convulsive syndrome.

Causes of occurrence

In most cases, the development of a hypothyroid coma is facilitated by an untimely diagnosis of the disease. Hormone deficiency is aggravated by:

• abrupt withdrawal of therapy with Levothyroxine;
• hypothermia of the body;
• concomitant diseases: pneumonia, myocardial infarction, stroke, viral and bacterial infections;
• injuries, surgical interventions, massive blood loss, radiation exposure;
• reception drugs, suppressing the functions of the central nervous system;
• hypoglycemia;
• hypoxia.

A sharp drop in the level of thyroid hormones leads to a slowdown in metabolic processes in the tissues of the brain.

Lack of hormones provokes oxygen starvation of all internal organs.

Then a hypothyroid coma develops.

How is hypothyroid coma treated?

Myxedema coma is treated in stages, the therapeutic regimen includes:

• Substitute hormone therapy... For hypothyroid coma, L-thyroxine is used, which is administered together with glucocorticoids and triiodothyronine. After the return of consciousness and improvement of the state, glucocorticoids are canceled.
• Elimination of hypoglycemia is an important step in removing the patient from a hypothyroid coma. Normalizing blood glucose levels helps restore heart, kidney and brain function. Large volumes of 5% glucose solution are injected intravenously.
• Normalization of the functions of the respiratory system. Oxygen inhalation is carried out, in severe cases, mechanical ventilation. With a sharp deterioration in the condition, Cordiamine is administered, if necessary, the procedure is repeated 2-4 times.
• Function recovery of cardio-vascular system... To increase blood pressure, angiotensinamide is used, which increases peripheral vascular resistance. With the development of hypothyroid heart failure, Strofantin is administered.

Normalizing body temperature is an important part of treatment. Initially, the patient is warmed with blankets; the use of heating pads is not recommended. Some time after the administration of drugs, the temperature rises.

One of the most dangerous complications of hypothyroidism is hypothyroid coma. Most often it appears in patients with hypothyroidism, in the elderly and old age, while in most cases it affects women. Coma develops in patients with severe hypothyroidism who long time did not receive the necessary treatment, or received it out of time.

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ICD-10 code

E03 Other forms of hypothyroidism

Causes of hypothyroid coma

Untimely or inadequate treatment of hypothyroidism in most cases is explained by the delayed diagnosis of the disease. An aggravation of the deficiency of thyroid hormones is also observed due to the cancellation of the substitutional intake of levothyroxine (for example, in low-income patients), or as a result of a significant increase in the body's needs for hormones under the influence of some reasons, for example:

• due to hypothermia;
• due to concomitant diseases (pneumonia, heart attack, stroke, viral diseases, urogenital infection, etc.);
• due to injuries, massive bleeding, surgical interventions, radiation therapy;
• after X-ray examination;
• after taking medications that depress the functions of the central nervous system;
• as a result of taking a large dose of alcohol;
• due to hypoglycemia;
• after a state of hypoxia.

A sharp drop in the level of thyroid hormones leads to a decrease in the activity of metabolic processes in the brain. As a result, hypoxia increases with significant disruption of all types of metabolism and functions of most organs.

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Symptoms of a hypothyroid coma

Hypothyroid coma occurs slowly, gradually progressing and growing. First, there is a feeling of fatigue, lethargy, apathy, then you can observe the coldness of the extremities, pale skin, puffiness and dryness of the feet. Over time, breathing slows down, problems with urination begin (up to anuria), cardiac insufficiency develops, blood pressure decreases, tendon reflexes disappear.

During the examination of the patient, the doctor may pay attention to the following signs:

• deterioration of metabolic processes (an increase in body weight, a slowdown in blood circulation with a decrease in temperature indicators below 35 ° C);
• disorders of the function of the cardiovascular system (slowing heart rate, threadlike pulse, dropsy of the heart, lowering blood pressure);
• respiratory disorders (decrease in the number of breaths, decrease in blood oxygen saturation, temporary cessation of breathing during sleep);
• dysfunction of the nervous system (progressive stupor, loss of tendon reflexes);
• dermatological symptoms (skin dryness, pallor and waxy hue, deterioration of hair and nails, articular hyperkeratosis);
• severe swelling on the face and limbs, a drop in the level of sodium in the blood;
• an increase in anemia and associated symptoms;
• hypoglycemia;
• disorders of the digestive organs (enlargement of the liver, development dynamic obstruction intestines).

Diagnostics of the hypothyroid coma

The characteristic symptomatology of a hypothyroid coma usually leaves no doubt in the diagnosis, especially if the corresponding signs have developed against the background substitution treatment levothyroxine, radioiodine therapy, or after thyroid resection surgery.

Sometimes the difficulties encountered in diagnostics can be associated with general condition patients when it is not possible to conduct a full examination and some research. Often the doctor is forced to start providing emergency care even before receiving the survey results.

In rare cases, the clinical picture of the disease may be atypical, which undoubtedly complicates the diagnosis. For example, some of the key symptoms may be absent, for example, a decrease in temperature or pressure - this usually happens in the presence of a simultaneous infectious disease or persistent hypertension.

Hypothyroid coma treatment

Coma treatment is carried out in stages, with an impact in all directions.

• Substitute hormonal treatment glucocorticoids are the main therapy for patients. Usually, a combination of thyroid and glucocorticoid drugs is prescribed, starting with L-thyroxine, which is administered intravenously at a dose of 250 mg every 6 hours. On the second day, maintenance therapy is carried out at a dose of up to 100 mg / day. The effect of L-thyroxine becomes noticeable only after a few hours, therefore triiodothyronine is additionally prescribed in an amount of up to 50 μg. At the same time, prednisolone or hydrocortisone hemisuccinate is used. After the patient regains consciousness, and his condition improves, glucocorticoid drugs are canceled.
• Treatment of hypoglycemia is also an important step in improving the patient's condition, since bringing blood sugar levels back to normal helps restore the functioning of the brain, heart, and urinary system. For the treatment of hypoglycemia, an intravenous injection of 20-30 ml of glucose solution (40%) is used and drip injection 500-1000 ml of glucose solution (5%), under the obligatory control of blood pressure and urination.
• Treatment of respiratory disorders is an obligatory stage of therapy, because breathing of patients in a coma becomes weak and rare. Oxygen inhalation through the nose is used, and in severe situations - artificial lung ventilation. If the patient's condition has deteriorated sharply, then he is injected intravenously up to 4 ml of cordiamine - a stimulator of respiratory function. Cordiamine injections, if necessary, are repeated 3-4 times, while monitoring blood pressure.
• Treatment of disorders of the cardiovascular system, in particular, lowering blood pressure, is carried out with the use of rheopolyglucin, 10% albumin. The use of sympathotonics is highly discouraged, since in conjunction with treatment with thyroid drugs, this can cause myocardial infarction. To normalize blood pressure indicators, angiotensinamide is injected dropwise, which increases peripheral vascular resistance. If heart failure develops against the background of a decrease in blood pressure, then the introduction of cardiac drugs, for example, strophanthin, is used.
• Temperature normalization is very important for improving the condition of a patient who has experienced a thyrotoxic coma. To begin with, the patient should be warmed: for this it is better to use blankets. Active warming with heating pads is not recommended. Over time, when the action of thyroid hormones appears, the temperature readings will normalize.
• Normalization of the blood picture, elimination of anemia consists in blood or red blood cell transfusion, and such procedures can be performed more than once. Getting rid of anemia reduces the state of hypoxia of body tissues, including brain structures.

Emergency care for hypothyroid coma

With a hypothyroid coma, the patient is urgently hospitalized in the endocrinology department or in intensive care.

As an emergency aid, during the first hour, an urgent administration of triiodothyronine in an amount of 100 μg is carried out. Additionally, oxygen therapy is prescribed. Intravenous injections of hydrocortisone (100 mg), prednisolone (up to 50 mg), as well as the introduction of cardiovascular drugs are recommended.

After half an hour or an hour, ATP is introduced, vitamins gr. B, vitamin C solution (5% to 4 ml). If the systolic pressure readings exceed 90 mm Hg. Art., use the introduction of lasix. With a systolic pressure of less than 90 mm Hg. Art. use cordiamine, mezaton, corazole, cardiac drugs.

Then, every 4 hours, triiodothyronine is administered drip in an amount of 25 μg (with myocardial ischemia or cardiac insufficiency - no more than 10 μg twice a day). After normalization of temperature indicators and stabilization of heart contractions, the dosage of triiodothyronine is reduced. Oxygen therapy, the use of sodium oxybutyrate, and passive warming of the patient are continued.

For citation: Petunina N.A. Hypothyroid coma - modern approaches to diagnosis and treatment // BC. 2010. No. 14. S. 900

Hypothyroid coma (HA) is an urgent, extremely severe complication of long-term uncompensated hypothyroidism, in which the mortality rate reaches 50-80%. Doctors of various specialties are often not ready for timely diagnosis and adequate therapy of HA. Hypothyroid coma is a complication of any form of hypothyroidism, but it is much more common in primary hypothyroidism. Data on the frequency and prevalence of HA are scarce. So, poll 800 medical centers in Germany, 24 cases of HA were detected over a two-year period, with the average age of patients being 73 years. For the first time, myxedema coma was described in 1879. Only 60 years later in the literature there was a report about its second case. To date, there are approximately 300 deaths from coma in the literature; thus, although this complication is currently quite rare, it is important to be able to recognize it due to the high mortality rate. The vast majority of patients had undiagnosed primary hypothyroidism, and only one had secondary hypothyroidism.

Reasons for development
Since hypothyroidism is 8 times more common in women than in men, most HA patients are women in the last decade of their lives. Acute decompensation of long-term hypothyroidism usually develops under the influence of provoking factors that aggravate severe thyroid insufficiency. The most common triggers of HA are hypothermia, intoxication, trauma, anesthesia, surgical interventions, anesthesia, bleeding, and infectious diseases, hypoxic conditions, alcohol consumption and stressful situations... Other causes of HA are inadequate treatment of hypothyroidism, a sharp decrease in daily dose or stopping thyroid hormone (TG) intake. The development of HA is provoked by such severe concomitant diseases as myocardial infarction and cerebral stroke. In elderly people, pneumonia and sepsis are a common cause of HA. Pneumonia can be primary, or develop against the background of stroke or aspiration. In some cases, especially in elderly patients, its development is facilitated by long-term use. medicines oppressing the central nervous system(phenothiazines, tranquilizers, barbiturates, antihistamines), as well as amiodarone, lithium preparations, diuretics and b-blockers. In more detail provoking factors are presented in table 1.
Reasons for late diagnosis
In most cases, HA is difficult and late to diagnose, since long-term hypothyroidism often does not have clear clinical manifestations and proceeds under the mask of other diseases. Late diagnosis of hypothyroidism is mainly associated with the gradual development of clinical symptoms, each of which is not specific in itself. Certain dominant symptoms of hypothyroidism with minimal severity or absence of characteristic manifestations are assessed by practitioners as signs of another independent disease. Since GC is more common in female patients and the elderly, mainly in the cold season, clinical symptoms diseases are perceived as natural age changes organism. In addition, the paucity of subjective data, indistinct manifestations of hypothyroidism, polymorbidity, characteristic of elderly patients, also do not allow timely establishment of the correct diagnosis. It is extremely difficult to diagnose GC even in the absence of anamnestic information about hypothyroidism. It is also problematic to diagnose cases of HC of an atypical course. One of the atypical options clinical picture decompensated hypothyroidism is myxedema delirium, the so-called myxedema of insane, manifested acute psychosis against the background of severe memory and thinking disorders. A clinical case is described in the literature when GC proceeded under the guise of a stem stroke. A rare variant of the course of HA is a condition resembling neurogenic, rotopharyngeal dysphagia.
Clinical picture
The development of HA is preceded by a precomatose state, when all the symptoms of hypothyroidism are sharply aggravated. The aggravation of clinical manifestations, as a rule, occurs gradually over several weeks or months. The main manifestations of severe hypothyroidism are present: dry skin, thin hair, hoarse voice, periorbital edema and dense edema of the extremities, macroglossia and slowing of deep tendon reflexes, hypothermia. In addition to hyponatremia and hypoglycemia, clinical and biochemical analysis blood levels may exhibit anemia, hypercholesterolemia, high serum LDH and creatine kinase concentrations.
If it is possible to obtain information about the patient's previous treatment, then we will find there indications of a previous thyroid gland (thyroid) disease, radioiodine therapy, thyroidectomy, or thyroid hormone therapy that was unreasonably interrupted.
So, a physical examination will show us postoperative scar on the neck from thyroidectomy, non-palpable thyroid gland, or the presence of a goiter. Much less often (in about 5% of cases), the cause of HA is pituitary or hypothalamic genesis. In one of the observations, a combination of two causes of GC was noted - primary thyroid and pituitary insufficiency due to Sheehan's syndrome. Of the 24 patients observed in Germany, 23 had primary hypothyroidism and one had central hypothyroidism. The patients were observed: hypoxia in 80%, hypercapnia in 54% and hypothermia with t °<35°С у 88%. 6 пациентов (25%) умерли, несмотря на лечение тиреоидными гормонами.
HA is characterized by increasing depression of the central nervous system from lethargy and disorientation to coma. Specific clinical symptoms of HA are impaired cold tolerance, hypothermia (rectal temperature less than 36 ° C), although with concomitant pathology, subfebrile temperature, pronounced mucinous edema of the face and extremities, and characteristic hypothyroid skin changes may occur. Hypothermia is present in almost all patients and can be really deep (less than 26 ° C). In many of the presented case histories, hypothermia was the key (first clinical) symptom in the diagnosis of HA. The main criterion for the effectiveness of therapy and the prognosis of survival was body temperature. The worst prognosis was in patients with rectal temperature less than 33 ° C.
Other symptoms are increasing drowsiness, lack of verbal contact, and hyporeflexia. Severe cardiovascular failure is characterized by progressive bradycardia and arterial hypotension. Typical cardiovascular signs of HA, like hypothyroidism, include nonspecific ECG changes, cardiomegaly, bradycardia, and decreased cardiac contractility. Decreases in stroke and minute volume are associated with decreased cardiac contractility, but overt heart failure was rare. The expansion of the heart is possibly due to ventricular dilatation or pericardial effusion. Hypotension may be present due to decreased blood volume and may be refractory to treatment with vasopressors if thyroid hormone is not prescribed.
Changes in the respiratory system are manifested by decreased breathing, alveolar hypoventilation with hypercapnia, which, together with a deterioration in cerebral blood flow, aggravate cerebral hypoxia. Decreased respiratory function and obesity can further exacerbate hypoventilation. Inhibition of respiratory function leads to alveolar hypoventilation and progression of hypoxemia, and as an extreme manifestation - to hypercapnic anesthesia and coma. Although there is multifactoriality in the development of coma, depression of the respiratory center, supported by hypercapnia, seems to be the principal factor. Most patients need mechanical ventilation, regardless of the cause of hypoventilation. Respiratory function can also be impaired by pleural effusion or ascites, decreased lung volume, macroglossia, and edema (myxedema) of the nasopharynx and pharynx, which reduce the efficiency of airway conduction. Even after starting thyroid hormone therapy, mechanical ventilation should continue.
A characteristic sign of HA is hypothyroid polyserositis with accumulation of fluid in the pleural, pericardial and abdominal cavities. Acute urinary retention and rapid dynamic or mechanical intestinal obstruction are often observed, gastrointestinal bleeding is not uncommon. The course of HA can be complicated by severe hypoglycemia. Without adequate treatment, there is a further drop in body temperature and blood pressure, a decrease in respiration and heart rate, hypercapnia and hypoxia increase, and a decrease in myocardial contractility and oliguria progress. Patients may have bladder atony with acute urinary retention. Cerebral hypoxia is accompanied by a dysfunction of the vital centers of the central nervous system, the development of seizures is possible. The immediate cause of death is usually progressive cardiovascular and respiratory failure.
In rare cases, long-term undiagnosed severe hypothyroidism can manifest as mental disorders, including thought disorders, personality changes, neuroses and psychosis. Often such patients are first seen by psychiatrists. Among patients in psychiatric clinics, the incidence of hypothyroidism reaches 3%.
Decompensation of severe hypothyroidism is accompanied by various cognitive impairments, including attention, concentration, memory, orientation and perception, progressing against the background of increasing thyroid hormone deficiency. In the future, against the background of severe drowsiness, confusion develops. Occasionally, acute psychoses are observed that do not have specific features that can mimic paranoid or affective psychosis. In these cases, patients with HA are often mistakenly diagnosed with mental illness. At the same time, a combination of myxedema coma and mental illness is possible.
Diagnostics
Diagnosis and treatment of emergency conditions should be carried out at an earlier stage of CNS dysfunctions, when their depression has not yet reached the maximum degree. HA causes profound changes in electrolyte metabolism, which is one of the specific diagnostic signs. In all cases of coma with hyponatremia, GC should be excluded. Laboratory diagnostic signs of HA include: hyponatremia, hypochloremia, hypoglycemia, increased levels of creatinine, creatinine phosphokinase, transaminases and lipids, hypoxia, hypercapnia, anemia, and leukopenia. ECG examination reveals sinus bradycardia, low wave voltage, T wave depression and inversion, and ST segment depression. The presence of reasonable suspicion is the basis for the immediate initiation of thyroid hormone therapy, without waiting for the results of the analysis of serum TSH and free thyroxine (T4). Even in the presence of previously mentioned disorders characteristic of HA, such as hypothermia, hypoventilation and hyponatremia in debilitated, somnolent or comatose patients, the diagnosis must be justified, appropriate tests must be taken and sent to the laboratory, after which therapy is started. However, in most patients, the clinical manifestations can be so obvious that serum TSH and T4 tests are necessary only to confirm the diagnosis.
Today, in most clinics, both hormones can be determined within an hour or, if necessary, on an emergency basis. Although a significant increase in serum TSH may be expected, patients with severe non-thyroid systemic diseases may exhibit a phenomenon similar to the "euthyroid pathology" syndrome that can mimic hypothyroidism. Under these circumstances, the secretion of TSH is reduced and its level in the blood may not be as high as might be expected. As noted earlier, approximately 5% of HA cases developed on the basis of central hypothyroidism and may be associated with normal or decreased serum TSH levels. Regardless of whether there is primary or secondary thyroid insufficiency, all patients with HA have low serum total and free T4 and triiodothyronine (T3) levels. In patients with euthyroid disease, serum T3 levels may be unusually low (25 ng / ml).
Treatment
The previously prescribed therapy with thyroid hormones alone, without correcting all other metabolic disorders, is inadequate for recovery. Due to the potentially high mortality rate in the absence of vigorous complex therapy, all patients should be admitted to the intensive care unit (intensive care unit), where careful monitoring of pulmonary and cardiac status, CVP and pulmonary artery pressure should be carried out.
Significant difficulties in the treatment of HA are primarily due to the critical severity of the patient's condition. Treatment of GC is carried out taking into account the state of the cardiovascular system due to the high sensitivity of the myocardium to TG, and concomitant diseases. Oxygen therapy is carried out, if necessary, tracheal intubation and artificial ventilation of the lungs, which helps to eliminate respiratory acidosis.
Urgent therapeutic measures for GC include administration of triglycerides and glucocorticoids. Treatment is carried out under the control of body temperature (preferably rectal), respiratory rate, pulse, blood pressure, mental status. The administration of glucocorticoids precedes or is carried out simultaneously with TG. Intravenous and oral routes of administration of TG are possible. The intravenous route of administration is accompanied by a rapid increase in TG levels (on average after 3-4 hours) to subnormal values, followed by their slow growth within 5-7 days. In domestic practice, there are no preparations of thyroid hormones for intravenous administration. Oral use of levothyroxine, despite a slow increase in TG values ​​with long-term preservation of them at the hypothyroid level, causes a clinical response after 24-72 hours. The absorption of L-T4 when administered orally is variable, but the clinical response develops rapidly, even with myxedema ileus. Intensive intravenous therapy with L-T4 in the first hours (100-500 μg, for 1 hour) dramatically reduces mortality. During the first day, L-T4 is injected intravenously at a dose of 300-1000 mcg / day, then maintenance doses are used - 75-100 mcg / day. With the improvement of the patient's well-being with the possibility of self-administration of the drug, the transition to its oral administration is carried out. Eutirox is a levothyroxine preparation with a wide range of dosages: 25, 50, 75, 100, 125 and 150 mcg. Eutirox therapy allows to improve the quality of treatment: to ensure an accurate dose selection and, accordingly, better compensation for hypothyroidism.
Convenience of taking the drug, the absence of the need to divide the tablets increases the adherence of patients to treatment, which is especially important when taking the drug for life, improves the quality of life and creates convenience for patients.
Normalization of metabolic processes during replacement therapy with Eutirox replenishes the deficiency of thyroid hormones, normalizes the increased level of TSH, restores physical and mental activity, and prevents the adverse effect of a decrease in thyroid hormones on human health. The presence of a wide range of different dosages of the drug not only increases the accuracy of the dosage of levothyroxine and improves the degree of compensation for the disease, but also creates convenience for patients and improves their quality of life.
In the absence of L-T4 solutions for parenteral administration, which complicates emergency therapy, the drug is administered through a gastric tube. Due to the delayed clinical effects of L-T4, during the first day, it is possible to administer L-triiodothyronine (L-T3) in small doses (20-40 μg) intravenously or through a gastric tube (100 μg initially, then 25-50 μg each 12 hours), given the faster metabolic effect and the effect on the central nervous system. In addition, there is an opinion that HA is accompanied by a pronounced violation of the peripheral conversion of thyroxine into metabolically active triiodothyronine. However, intravenous administration of the drug is dangerous due to the significant risk of severe cardiovascular complications, which led to the discontinuation of T3 drugs for intravenous administration. It should be emphasized that the more severe the patient's condition, the lower the initial doses of TG should be used. The presence of coronary artery disease in a patient is a contraindication for the use of L-T3, and in this situation, small doses of L-T4 (50-100 μg / day) are prescribed.
Intravenous drip is administered 200-400 mg / day. water-soluble hydrocortisone (fractionally, every 6 hours). After 2-4 days, depending on the dynamics of clinical symptoms, the dose of glucocorticoids is gradually reduced. Particular attention is paid to anti-shock measures, plasma substitutes, 5% glucose solution are introduced. The introduction of fluid is carried out in a volume of no more than 1 liter per day in order to avoid myocardial overload and an increase in hyponatremia. Hyponatremia is eliminated as the concentration of TG increases. In case of hypoglycemia, 20-30 ml of a 40% glucose solution is injected.
Rapid warming of the patient is contraindicated due to the deterioration of hemodynamics due to rapid peripheral vasodilation with the development of collapse and arrhythmias. Passive warming is recommended (increasing the room temperature by 1 degree per hour, wrapping in blankets). Sedatives should be avoided even when the patient is agitated, which is stopped by TG replacement therapy. In the future, treatment of infectious and other concomitant diseases that caused hypothyroidism decompensation is carried out. With concomitant infection, antibiotic therapy is performed. The course of GC and its therapy can be complicated by the development of arrhythmias, myocardial infarction and severe heart failure.
conclusions
Hypothyroid coma is the most severe manifestation of decompensated hypothyroidism and is often fatal despite treatment. Decompensation of hypothyroidism to coma can be triggered by various drugs, systemic diseases and other reasons. It usually develops in older women during the winter season and is combined with manifestations of hypothyroidism, such as hypothermia, hyponatremia, hypercapnia, and hypoxia. Treatment should begin urgently in the ICU or intensive care unit. Although thyroid hormone therapy is life-threatening, it is undoubtedly necessary and is done with T4, T3, or a combination of both. Adjunctive measures such as mechanical ventilation, rewarming, fluid therapy, antibiotics, vasopressors, and corticosteroids can be critical to the success of treatment.

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Is an urgent, extremely severe complication of decompensated hypothyroidism. At the initial stages, it is manifested by increased fatigue, lethargy, apathy. Gradually there is a cold snap of the extremities, pale skin, edema of the lower extremities. In a serious condition, breathing slows down, loss of consciousness, urination is impaired, blood pressure decreases. Diagnostic methods: collection of clinical and anamnestic data, laboratory tests and study of the work of blood vessels and heart. Treatment includes therapy with thyroid drugs, restoration of vital functions of the body.

ICD-10

E03.5 Myxedema coma

General information

Myxedema, or hypothyroid, coma (HC) was first described in 1879, and an active search for treatment began in 1964. Despite the intensive development of endocrinology in recent decades, the success of the treatment of this condition is still determined by the timeliness of diagnosis. SCC develops as a complication of any form of hypothyroidism, but occurs mainly in patients with primary disease. Epidemiological data are scarce. According to studies conducted in Europe and the United States, hypothyroid coma is detected in 0.1% of patients, among whom elderly women predominate (average age - 73 years). In about half of them, the main diagnosis is established retrospectively - after stabilization of the condition.

Causes

The key factor in the development of coma is inadequate, untimely treatment of hypothyroidism - a sharp reduction in the daily dose or a complete cessation of the use of thyroid medications. The high-risk group consists of women over 50 years old, and the older the patient, the higher the likelihood of decompensation of the disease. The provoking causes of severe thyroid insufficiency include:

• Acute diseases. The onset of myxedema coma is promoted by stroke, myocardial infarction, infectious diseases, heart failure, and pneumonia. In addition, a coma can be triggered by hypothermia, internal bleeding, blood loss due to trauma, surgery.
• Metabolic disorders. The body's need for thyroid hormones increases with hypoglycemia, hyponatremia, acidosis, hyperkalemia, hypoxia, hypercapnia. In elderly people, metabolic disorders can occur with severe stress, alcohol consumption.
• Taking medications. The most dangerous is the use of drugs that inhibit the functions of the central nervous system. SCC is triggered by long-term treatment with phenothiazines, tranquilizers, barbiturates, antihistamines, lithium preparations, diuretics, and beta-blockers.

Pathogenesis

The key pathogenetic mechanism in the development of SCC is an acute deficiency of thyroid hormones, which provokes a decrease in metabolic processes in the brain and hypoxia. Cerebral circulation slows down, oxygen and glucose consumption by brain tissues decreases, carbohydrate, lipid, protein and water-salt metabolism is disturbed. There is tissue edema caused by lymphostasis, fluid accumulates in the serous cavities. The pathology of the cardiovascular system is formed - the borders of the heart increase, the volume of blood, the blood flow rate decreases, and bradycardia increases.

As a result of inhibition of the functions of the hypothalamic centers, inhibition of energy metabolism and changes in peripheral circulation, hypothermia develops. Failures in the autonomic nervous system cause shifts in the work of internal organs. Respiratory failure, hypercapnia, and cerebral edema are increasing, which is manifested by drowsiness, stupor and coma. Hypoventilation of the lungs and low resistance to infection lead to pneumonia. An additional toxic effect on the central nervous system is exerted by a high concentration of carbon dioxide in the blood.

Classification

There are two options for the onset and development of coma in hypothyroidism. First, the complication begins suddenly, accompanied by a sharp decrease in arterial and venous pressure, acute cardiovascular failure. Another, more common form of the course is a phased one: the coma develops gradually over several days or even months, the symptoms appear on the rise, from mild weakness to unconsciousness. There are four stages of SCC:

1. Harbinger. Drowsiness, bradycardia and vascular hypotension, poorly corrected by pressor drugs, increase. Breathing is reduced and weakened, hypothermia, excitability increase, convulsions occur.
2. Deceleration of central nervous system functions. The stage lasts from several hours to a month or longer. Reactions to light, sound and temperature change are inhibited, a state of stunnedness arises, a deep and prolonged sleep.
3. Predcoma. The condition lasts for hours or days. Periodically, unconsciousness occurs, the patient wakes up less and less often, often falls into a deep sleep. There is a narrowing of the pupils, spontaneous rare movements, involuntary emptying of the intestines and bladder.
4. Coma. Persistent loss of consciousness. There is no response to pain and bright light, body temperature drops, and brain functions are impaired. This stage is often irreversible and leads to death.

Symptoms of a hypothyroid coma

At the stage preceding the SCC, patients rarely pay attention to the deterioration of their condition. The main manifestations of hypothyroidism become heavier: the skin becomes drier, hair falls out more actively, the hoarseness of the voice increases, swelling around the eyes and swelling of the extremities increases, the temperature decreases slightly. With the development of hypothyroid coma, impaired tolerance to cold is determined, persistent hypothermia from 35-36 ° C in the early stages to 26 ° C and below in a state of deep coma. If the patient has a concomitant infection or other acute illness, the temperature can remain at the level of subfebrile values ​​for a long time. In most diagnostic cases, hypothermia is the first and key symptom of SCC, and the dynamics of body temperature is considered as a criterion for the effectiveness of treatment and is used to predict survival.

Other symptoms of myxedema coma are an increase in drowsiness, apathy, the patient's unwillingness to engage in conversation, emotional impoverishment, and suppression of reflexes. Determined by a decrease in the pulse, vascular hypotension, a slowdown in the breathing process, which is most pronounced in women with obesity, underdeveloped respiratory muscles. In the early stages of coma, acute urinary retention, chronic or acute intestinal obstruction, bleeding in various parts of the gastrointestinal tract are possible. Later, they are sometimes replaced by involuntary defecation and urination. Without adequate therapy, the phenomena of hypoglycemia, hypothermia, hypercapnia, hypoxia, vascular and muscle hypotension increase, respiration and heart rate are reduced. Oxygen starvation leads to a change in the work of the vital parts of the central nervous system. Respiratory and cardiovascular insufficiency becomes the cause of death.

Complications

Long-term undiagnosed hypothyroid coma can be complicated by mental disorders. Patients develop delusional disorders of thinking, hallucinations, personality changes, acute psychosis, neuroses. The state of decompensation of severe hypothyroidism is accompanied by a decrease in the cognitive sphere - attention, memory, intellectual abilities, and orientation in space and time deteriorate. In rare cases, acute psychotic conditions develop. They have no specific features, mimic paranoid or affective psychosis. This complicates the diagnosis and contributes to the misdiagnosis of a mental disorder.

Diagnostics

With a typical clinical picture, the diagnosis of a hypothyroid coma is not difficult. However, at a late stage, the general condition of patients is regarded as severe, and a full examination is extremely difficult to perform. The main activities for collecting data are carried out by an endocrinologist. During the initial survey of the patient or his relatives, an assumption is made about SCC, which must be differentiated from cerebral circulation disorder, mechanical intestinal obstruction, adrenal insufficiency, and intoxication. Comprehensive examination includes:

• Collecting anamnesis. Some patients have a confirmed diagnosis of hypothyroidism made 5 or more years ago. Often in the history of the disease or in the patient's responses there are indications of family history of endocrine diseases, radioiodine therapy, thyroidectomy, unreasonably interrupted treatment with thyroid hormones.
• Inspection. On physical examination, periorbital edema, dense edema of the feet, dryness and pallor (sometimes cyanosis) of the skin, hypothermia, slowness and lethargy of movements, and decreased tendon reflexes are determined. On the neck, a scar after thyroidectomy, non-palpable thyroid gland can be determined.
• Laboratory diagnostics. A general and biochemical analysis of blood and urine, a study of the level of electrolytes, hormones, specific markers of damage to the thyroid gland, myocardium, muscles. Laboratory diagnostic signs of SCC include: increased TSH concentration, low levels of free thyroxine and triiodothyronine, hypoxia, hypercapnia, anemia, leukopenia, hyponatremia, hypochloremia, hypoglycemia, increased levels of creatinine, creatine kinase, transaminases and lipids.
• Research of cardiovascular function. According to the results of the ECG, sinus bradycardia, low voltage of the teeth, depression of the ST segment are detected. Blood pressure measurement gives consistently low and low values ​​- from 90/60 mm. rt. Art. The pulse rate is less than 60 beats per minute.

Hypothyroid coma treatment

Vigorous complex therapy is necessary for all patients, as there is a potentially high probability of death. The efforts of doctors are aimed at compensating for respiratory, cardiac and vascular insufficiency, correcting metabolic disorders, and restoring hormone levels. The patient care scheme is as follows:

• Therapy with hormonal drugs. A combination of thyroid drugs and glucocorticoids is prescribed. The latter are canceled after the patient regains consciousness.
• Elimination of hypoglycemia. An increase in plasma sugar is necessary for the normal functioning of the heart muscle and brain structures. A glucose solution is injected intravenously with parallel monitoring of blood pressure and urination.
• Elimination of respiratory failure. Breathing of patients is reduced and weak. Oxygen inhalation therapy is carried out, artificial lung ventilation devices are connected. If the condition worsens, drugs are given to stimulate the respiratory center and airways.
• Elimination of heart failure. Shown are hypertensive drugs compatible with thyroid drugs. Cardiac glucosides are administered to correct heart failure.
• Elimination of hypothermia. Patients are warmed with blankets (no heating pads). When the action of thyroid drugs is manifested, the temperature rises to normal.
• Normalization of blood composition. Most patients need to prevent the development of anemia. A blood or erythrocyte mass transfusion is performed.

Forecast and prevention

Hypothyroid coma in advanced stages is difficult to treat. The prognosis is relatively favorable in middle-aged people, with early access to medical care, with the correct measures of emergency care and therapy. To prevent the development of SCC, the rules for the treatment of hypothyroidism should be strictly observed, immediately seek help from an endocrinologist if the state of health worsens, and concomitant serious diseases should be eliminated. It is unacceptable to independently cancel or change the scheme for taking thyroid hormonal drugs, developed by a doctor.

Hypothyroid coma is an extremely serious pathological condition that requires immediate medical attention. The essence of this pathology is a sharp decrease in the level of thyroid hormones in the blood. From a clinical point of view, such a disease is characterized by inhibition of the functional activity of the central nervous system with subsequent impairment of consciousness. With early seeking medical help, this pathological process has a relatively favorable prognosis. However, even with intensive therapy, some people with this diagnosis die.

Hypothyroid coma is also called myxedema coma. Its first descriptions were made in one thousand eight hundred and seventy-nine, but the most actively involved in this problem was from one thousand nine hundred and sixty-four. Despite the fact that medicine has made significant strides forward, the prognosis for this disease still depends on how timely it was diagnosed. In general, the frequency of occurrence of such a pathological process among the population is not high. At the same time, it was noticed that most often female representatives over fifty years old encounter him.

As we have already said, the main reason for the development of this disease is a sharp decrease in the level of thyroid hormones. As a rule, this occurs in those patients who have refused to take the necessary drugs for hypothyroidism. Self-decreasing dosage can also contribute to the onset of decompensation.

In addition, there are a number of factors that can contribute to the formation of a hypothyroid coma. First of all, these are various acute pathologies. Examples include myocardial infarction, pneumonia, and so on. At risk are also people who have lost a large volume of blood or have suffered severe hypothermia. An insufficient level of glucose in the blood, a decrease in sodium concentration, hypoxia, severe stress - all this refers to the predisposing moments.

Separately, it should be said that sometimes a hypothyroid coma can be triggered by taking certain medications. At the same time, the most dangerous are precisely those medicines that inhibit the activity of the central nervous system. An example is tranquilizers, barbiturates, and so on.

Numerous studies have established that there are two possible scenarios for the development of this disease. The first of them is characterized by a rapid deterioration in the condition of a sick person with a rapid depression of the functional activity of the central nervous and cardiovascular systems. In the second case, with such a pathological process, a clearly expressed staging can be traced. In other words, specific changes build up gradually over several days or even weeks.

Currently, there are four stages of hypothyroid coma. The first stage is characterized by initial changes, which include a decrease in blood pressure and a slowdown in heart rate, increasing drowsiness, seizures, and so on. At the second stage, signs are added that indicate a slowdown in the activity of the central nervous system. A person reacts poorly to external stimuli, falls into deep sleep. The third stage is established if the patient is increasingly unconscious, but sometimes he still comes to his senses. At the fourth stage, a persistent loss of consciousness occurs with a lack of response to external stimuli. The functional activity of the brain is increasingly impaired. This stage is often fatal.

Symptoms of a hypothyroid coma

At the initial stages, the increasing symptoms of hypothyroidism come to the fore in the clinical picture. A sick person pays attention to the fact that his skin became drier, hair began to actively fall out. Increasing edema is noted in the face and extremities. A characteristic point is a decrease in body temperature. At first, it drops to thirty-six or thirty-five degrees, and later it can even go up to twenty-six degrees.

Over time, symptoms such as drowsiness and lethargy, lack of interest in current events, suppression of reflexes join. The pulse becomes more rare, the blood pressure drops. In parallel, there is a slowdown in breathing. Often, the clinical picture is complemented by acute urinary retention and the absence of bowel movements. In the future, with the progression of the pathological process, involuntary urination may be observed.

In the absence of the necessary medical care, the severity of all the above symptoms increases. The body temperature continues to drop, the heart contracts even more slowly. Muscle hypotension develops, oxygen starvation sets in. The central nervous system is functioning worse and worse, due to which there is often a fatal outcome.

Diagnosis and treatment of the disease

This disease is diagnosed on the basis of a thorough physical examination and anamnesis. From laboratory tests, general and biochemical blood tests are used. It is imperative to determine the level of thyroid hormones. Additionally, it is recommended to evaluate the activity of the cardiovascular system using electrocardiography.

Medical treatment for hypothyroid coma should be provided as soon as possible. Initially, thyroid medications are prescribed in combination with glucocorticosteroids. At the same time, attention is directed to the elimination of respiratory and cardiovascular disorders. If necessary, the patient is injected with glucose, he is placed on artificial ventilation.

Prevention of the development of hypothyroid coma

To prevent the occurrence of such a condition, it is necessary to strictly follow all the doctor's recommendations in the presence of hypothyroidism, immediately seek medical help if the state of health has worsened.

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