Coma due to hypothyroidism causes emergency clinic. Development of hypothyroid coma: causes, symptoms, therapy. Hypothyroid coma - features of this condition

Hypothyroid coma is the most dangerous complication that occurs with hypothyroidism.

Coma can affect patients who have suffered from hypothyroidism for a long time and have not received the necessary treatment, most often these are elderly women.

Why does this condition occur? The main cause of coma is incorrect or untimely treatment.

If the patient consults a doctor too late, treatment may not always help, as numerous complications develop.

If a specialist makes an incorrect diagnosis and prescribes inadequate treatment, this can also lead to coma, even if the patient sought help at the initial stage of the disease.

Coma may occur if replacement hormones are withdrawn. This usually happens due to the patient's fault.
In addition, there may be an increased need for hormones in the body due to certain factors:

• severe hypothermia;
• hypoglycemia;
• injuries;
• bleeding;
• infectious diseases;
• after oxygen starvation;
• after certain medications;
• with a large dose of alcohol;
• after irradiation.

The functioning of most organs and systems in the body is disrupted. Water retention and tissue swelling occur.

A large amount of fluid leads to the following manifestations:

• dilation of veins;
• liver enlargement;
• cardiac dysfunction;
• bradycardia;
• hypothermia;
• breathing problems;
• decreased blood flow activity;
• cerebral edema.

If the level of thyroid hormones drops quickly, the activity of metabolic processes in the brain decreases. Because of this, hypoxia occurs.

60% of cases of hypothyroid coma end in the death of the patient.

Symptoms of hypothyroid coma

How does hypothyroid or myxedema coma manifest? This condition arises slowly and develops gradually.
The following symptoms may appear:

If at least a couple of signs appear, you need to urgently contact a specialist.
Your doctor may look for the following symptoms:

1. Low temperature – below 35 o C.
2. Digestive system disorder – intestinal obstruction, liver enlargement.
3. Anemia, as well as the symptoms that are associated with it.
4. Problems with the cardiovascular system – low heart rate, low blood pressure, thready pulse.

In addition, the following symptoms very often appear:

1. Disruption of the nervous system - stupor.
2. Pale and dry skin, waxy appearance.
3. – decrease in blood sugar levels.
4. Swelling in the limbs and face, low sodium levels in the blood.
5. Violation of normal breathing - temporary cessation of breathing, a small number of inhalations and exhalations.

The main precursors of this condition:

• drowsiness;
• weak breathing;
• a sharp drop in pressure.

Constipation and severe excitability (to the point of psychosis) may also occur. Convulsions are also possible. The comatose state develops gradually, so you can see a doctor in time; in this case, you should never waste time.

Stages of development

Three phases of coma development are observed:

1. The first phase is characterized. Consciousness becomes confused, however, not always.
2. In the second phase, patients often disoriented, convulsions may occur.
3. And the third phase - this is loss of consciousness. It is usually irreversible.

The duration of each phase can vary from several hours to a month, and even more. However, in rare cases, a very sudden development of hypothyroid coma is possible.

Signs of an oncoming coma are very characteristic:

1. The patient's face becomes yellowish.
2. Eyelids and lips swell.
3. Sometimes the feet and hands may swell.
4. The skin becomes dry and cold.
5. Usually the body temperature decreases, however, if an infectious disease is present, the temperature may even increase.
6. The patient breathes heavily and rarely.

If measures are not taken, hypothermia, muscle atonia and significant disruption of brain function occur. The patient's condition is similar to lethargic sleep.

Interesting!

Hypothyroid coma can lead to symptoms such as hallucinations and memory loss. This happens because the functioning of the brain is disrupted. Irreversible changes may occur.

Diagnosis of hypothyroid coma

What examination is needed to identify the disease? Since the signs of myxedema coma are very clear, making a diagnosis is not difficult.

However, a general examination of the patient and a number of tests still need to be performed. In addition, it sometimes happens that myxedematous coma manifests itself atypically. That is, there are no clear symptoms indicating this particular disease.

To make an accurate diagnosis, the following studies are prescribed:

1. Blood tests to determine the level of thyroxine in the blood serum, as well as other thyroid hormones.
2. Blood test for potassium and glucose levels.
3. X-ray of the thyroid gland - to obtain information about changes in the structure of the gland.
4. Ultrasound of the thyroid gland - helps determine the volume of the thyroid gland.
5. Analysis of the amount of cortisol in the blood - a low level indicates an approaching coma.
6. Ultrasound of the heart and kidneys is performed if necessary.

After all the necessary tests, the doctor prescribes treatment. However, if an ultrasound can be performed in a short time, the results of blood tests will have to wait a long time.

Therefore, these tests cannot be performed if the patient is very unwell and symptoms are increasing. In such cases, minimal research is carried out, focusing more on the symptoms.

Treatment of hypothyroid coma

What is used in the treatment of coma:

1. Hormone replacement treatment is an important part of treatment for this condition. Glucocorticoids are prescribed.
2. In addition, Prednisolone is prescribed. It is also important to increase your blood sugar levels to normal.
3. Therefore, if the glucose level has dropped, injections or drips of glucose solution are used.
4. If the pressure decreases, use Albumin or Reopoliglucin.
5. In addition, Angiotensinamide is administered using a dropper. It increases vascular resistance.
6. Sometimes, against the background of hypotension, heart failure occurs, then various cardiac drugs are used. It is important to normalize blood pressure and prevent disturbances in the cardiovascular system.

Since myxedematous coma is characterized by respiratory failure, therapy to restore it is necessary. Use oxygen inhalation through the nose.

If the patient is in serious condition, artificial ventilation is performed. If the patient’s condition sharply worsens, Cordiamine is administered intravenously; it stimulates respiratory function.

Sometimes injections are given three or four times.

Be sure to normalize the patient's temperature, but it is not advisable to use heating pads. As soon as they start, the temperature returns to normal.

To prevent complications such as pneumonia, antibiotics are prescribed. And if the level of sodium in the blood is low, it is administered intravenously.

If emergency care is needed, thyroid hormones are administered intravenously until the levels return to normal.

Their dose is gradually reduced. B and vitamin A are also administered intravenously. Be sure to warm the patient.

The patient is wrapped in blankets and the room temperature is maintained at a high temperature.

Further forecast

Myxedematous coma can lead to death if it is not recognized and treated in time. Therefore, you need to monitor your health very carefully if you are diagnosed with...

This disorder is difficult to treat. Even with intensive care, most patients die. And if the patient survives, he suffers complications in various internal organs.

In rare cases, with very rapid treatment and with a slowly developing coma, it is possible to save life and health, without serious long-term consequences.

It is necessary to strictly follow the doctor's instructions, do not change medications yourself or reduce the dose of medications. Hormone therapy must be used strictly according to the scheme.

Myxedematous coma is a critical form of hypothyroidism, so it is important to stop the disease before it progresses to such complications.

Hypothyroid coma is a consequence of hypothyroidism. It is characterized by an unconscious state due to the deterioration of metabolic processes - thyroid hormones. Also, the development of Hypothyroid coma can occur due to heart failure, infection, consequences of food intoxication and medications, the main reason being a lack of thyroid hormones. The main impetus may be brain hypoxia - a lack of oxygen due to impaired cerebral circulation, due to a decrease in metabolic processes.

Hypothyroid coma is divided into 3 forms:

1.Primary hypothyroidism. When there is a disturbance in the biosynthesis of thyroid hormones (the cause of a defect in embryonic development) due to autoimmune processes, or the use of thyreostatic drugs and radioactive iodine. This also includes incorrectly selected treatment for the patient and x-ray therapy of the thyroid gland, which could fail.

2.Secondary hypothyroidism. Its causes include the consequences of traumatic disorders. For example, a failure of the nervous system, inflammatory processes in the hypothalamic-pituitary region, which could lead to disruption of the thyroid-stimulating function of the pituitary gland. Other traumatic consequences are a tumor of the pituitary gland, hypophysectomy, and any other disorders of the pituitary gland.

3. Tertiary hypothyroidism. Consequences of thyrotropin-releasing hormone disorder.

The most common cause of coma is primary hypothyroidism.

Symptoms of Hypothyroid Coma

Since hypothyroid coma occurs as a result of hypothyroidism, the initial symptoms will be those of hypothyroidism [see hypothyroidism]. These include depression, sluggishness, cold intolerance, muscle weakness, in some cases there is weight gain, attention problems, lethargy, decreased libido, puffy eyes, confusion, apathy, constipation, etc.

As a result, the harbingers of coma are:

Severe depression of consciousness

Severe hypothermia

Shock

Hypoventilation of the lungs in combination with

accumulation of fluid in the pleural cavity

accumulation of fluid in the pericardial cavity

accumulation of fluid in the abdominal cavities

A sharp decrease in diuresis

Intestinal obstruction.

There are also several syndromes that are also symptoms of hypothyroid coma:

1. Acute hallucinatory-paranoid syndrome, with which there is cerebral crisis and cerebral ataxia

2. Signs of renal failure;

3. Secondary cerebral edema, manifested by pronounced neurological manifestations, while the cerebrospinal fluid remains normal.

4. Consequences of hyperthermia caused by infection;

5.Secondary adrenal insufficiency syndrome;

6. Myocardial failures and cardiovascular failure are observed;

7. Atony of intestinal smooth muscles with the formation of megacolon;

8. Atony of the gallbladder;

9.Secondary disorders of the neuromuscular system and the function of motor nerve centers;

10. hemorrhagic consequences of coma.

Hypothyroid coma occurs in two phases

1. Coma - complete loss of consciousness and cessation of motor activity, absence of all reflexes..

2.Precoma – depressive state, apathy, confusion, decreased breathing, decreased blood pressure, bradycardia, lethargy, and in some cases a stuporous state occurs.

Diagnosis of hypothyroid coma

There is a rare pulse, bradycardia with a heart rate of up to 35 heart rate/min, severe hypothermia (up to 24-25 ° C), and rare breathing up to 12 times per minute.

Biochemical analysis to determine the level of protein and iodine SBI - 20-25 mmol/l

An ECG shows:

P segment lengthening<3,

Voltage reduction

Depression of the 5-T segment,

Flattening, partial or complete inversion of the T wave,

Often signs of coronary circulatory insufficiency

Consequences of hypothyroid coma

All that needs to be done in this case is emergency help.hypothyroid coma.

There is no guarantee that the patient will come out of a coma; it depends on many factors, or more precisely on how severe the coma is. In cases where the symptoms of coma are too pronounced - severe bradycardia, heavy breathing, then the prognosis is greatly complicated and the mortality rate in this case is 50%

It is also necessary to receive timely and correct - adequate treatment to bring you out of a coma.

Hypothyroid coma is the most severe complication of hypothyroidism. It occurs due to profound deficiency of thyroid hormones, which develops in untreated or insufficiently treated patients. It is more common in older women (60 years and older) during the cold season. Provoking moments are cooling, massive bleeding, pneumonia, cardiovascular failure, hypoxia, hypoglycemia, and various injuries. In some cases, the development of coma is facilitated by the use of phenobarbital, phenothiazides, narcotic substances or anesthetics in normal therapeutic doses.

Clinical picture. A constant symptom of hypothyroid coma is a decrease in body temperature, sometimes up to 24°C, due to low basal metabolism and inadequate production of thermal energy. Coma is accompanied by increasing inhibition of the central nervous system (stupor and coma itself), prostration, and complete inhibition of deep tendon reflexes.

Severe cardiovascular failure is manifested by progressive bradycardia and arterial hypotension, and the smooth muscle atony characteristic of hypothyroidism is manifested by acute urinary retention syndrome or rapid dynamic and even mechanical (megacolon) intestinal obstruction. Gastrointestinal bleeding and persistent bleeding from the gums are often observed. Hypoglycemic conditions may develop. Without adequate treatment, a further decrease in body temperature occurs, breathing slows down, hypercapnia and respiratory acidosis increase. Cardiac weakness and arterial hypotension progress, which in turn leads to oliguria, anuria and metabolic acidosis. Brain hypoxia is accompanied by dysfunction of vital centers of the central nervous system. The immediate cause of death is usually increasing cardiovascular and respiratory failure.

Urgent Care. Hydrocortisone is administered intravenously (50-100 mg, daily dose up to 200 mg), thyroxine is prescribed (daily dose 400-500 mcg) as a slow infusion.

Along with this, oxygen therapy is carried out in combination with artificial ventilation. To combat anemia, blood or red blood cell transfusions are indicated (the latter is preferable). Infusion therapy is carried out with great caution, while glucocorticoids are administered.

To suppress a concomitant infection or prevent an outbreak of a dormant infection, vigorous antibiotic therapy must be prescribed. In patients in a coma, atony of the bladder is constantly observed, so a permanent urinary catheter is placed.

Emergency medical care, ed. B. D. Komarova, 1985

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

Hypothyroid coma (HC) is an urgent, extremely severe complication of long-term uncompensated hypothyroidism, in which mortality reaches 50-80%. Doctors of various specialties are often not prepared for timely diagnosis and adequate therapy of GC. Hypothyroid coma is a complication of any form of hypothyroidism, but is much more common in primary hypothyroidism. Data on the incidence and prevalence of GC are sparse. Thus, a survey of 800 medical centers in Germany over a two-year period revealed 24 cases of GC, with the average age of patients being 73 years. Myxedematous coma was first described in 1879. Only 60 years later, a report of its second case appeared in the literature. To date, approximately 300 cases of death from coma have been described in the literature; Thus, although this complication is currently quite rare, it is important to recognize it due to its 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 men, the majority of patients with HC are women in the last decade of life. Acute decompensation of long-term hypothyroidism usually develops under the influence of provoking factors that aggravate severe thyroid insufficiency. The most common provoking factors of GC are hypothermia, intoxication, trauma, anesthesia, surgery, anesthesia, bleeding, as well as infectious diseases, hypoxic conditions, alcohol consumption and stressful situations. Other causes of GC are inadequate treatment of hypothyroidism, a sharp reduction in the daily dose or discontinuation of thyroid hormones (TG). The development of GC is provoked by such severe concomitant diseases as myocardial infarction and cerebral stroke. In elderly people, pneumonia and sepsis are common causes of GC. 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 of drugs that depress the central nervous system (phenothiazines, tranquilizers, barbiturates, antihistamines), as well as amiodarone, lithium preparations, diuretics and b-blockers. Provoking factors are presented in more detail in Table 1.
Reasons for late diagnosis
In most cases, HC is difficult and late to diagnose, since long-term hypothyroidism often does not have clear clinical manifestations and occurs under the masks of other diseases. Late diagnosis of hypothyroidism is mainly associated with the gradual development of clinical symptoms, each of which in itself is not specific. Individual dominant symptoms of hypothyroidism with minimal severity or absence of characteristic manifestations are assessed by practitioners as signs of another independent disease. Since HA is more common in female and elderly patients, mainly in the cold season, the clinical symptoms of the disease are perceived as natural age-related changes in the body. In addition, the paucity of subjective data, unclear manifestations of hypothyroidism, and polymorbidity, characteristic of elderly patients, also do not allow a correct diagnosis to be made in a timely manner. The diagnosis of GC is extremely difficult even in the absence of anamnestic information about hypothyroidism. Diagnosis of cases of GC with atypical course is also problematic. One of the variants of the atypical clinical picture of decompensated hypothyroidism is myxedematous delirium, the so-called myxedema of the insane, manifested by acute psychosis against the background of severe disorders of memory and thinking. The literature describes a clinical case in which GC occurred under the guise of a brainstem stroke. A rare variant of the course of GC is a condition resembling neurogenic oropharyngeal dysphagia.
Clinical picture
The development of GC is preceded by a precomatous state, when all the symptoms of hypothyroidism sharply worsen. The severity of clinical manifestations, as a rule, occurs gradually over several weeks or months. The main manifestations of severe hypothyroidism are present: dry skin, sparse hair, hoarse voice, periorbital edema and dense swelling of the extremities, macroglossia and slowed deep tendon reflexes, hypothermia. In addition to hyponatremia and hypoglycemia, clinical and biochemical blood tests may demonstrate anemia, hypercholesterolemia, high serum LDH and creatine kinase concentrations.
If it is possible to obtain information about the patient’s previous treatment, we will find there indications of previous thyroid disease, radioiodine therapy, thyroidectomy, or thyroid hormone therapy that was unreasonably interrupted.
Thus, a physical examination will show us a postoperative scar on the neck from thyroidectomy, a non-palpable thyroid gland, or the presence of a goiter. Much less frequently (in about 5% of cases), the cause of GC is pituitary or hypothalamic in origin. In one of the observations, a combination of two causes of GC was noted - primary thyroid and pituitary insufficiency due to Sheehan syndrome. Of the 24 patients observed in Germany, 23 had primary hypothyroidism and one had central hypothyroidism. Patients observed: hypoxia in 80%, hypercapnia in 54% and hypothermia with t°<35°С у 88%. 6 пациентов (25%) умерли, несмотря на лечение тиреоидными гормонами.
GK is characterized by increasing depression of the central nervous system from lethargy and disorientation to coma. Specific clinical symptoms of GC are impaired tolerance to cold, hypothermia (rectal temperature less than 36°C), although with concomitant pathology, low-grade fever, severe mucinous edema of the face and extremities, and characteristic hypothyroid skin changes may occur. Hypothermia is present in almost all patients and can be truly profound (less than 26°C). In many of the presented case histories, hypothermia was the key (first clinical) symptom in the diagnosis of GC. 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 HC, like hypothyroidism, include nonspecific ECG changes, cardiomegaly, bradycardia, and decreased cardiac contractility. Decreases in stroke and cardiac output were associated with decreased cardiac contractility, but overt heart failure was rare. Cardiac enlargement may be 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 hormones are not prescribed.
Changes in the respiratory system are manifested by decreased breathing, alveolar hypoventilation with hypercapnia, which, together with deterioration of cerebral blood flow, aggravate brain hypoxia. Deterioration of respiratory muscle function and obesity may further exacerbate hypoventilation. Depression of respiratory function leads to alveolar hypoventilation and progression of hypoxemia, and, as an extreme manifestation, to hypercapnic anesthesia and coma. Although there is a multifactorial nature in the development of coma, the main factor seems to be depression of the respiratory center, supported by hypercapnia. Most patients require mechanical ventilation, regardless of the cause of hypoventilation. Respiratory function may also be impaired due to 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 initiation of thyroid hormone therapy, mechanical ventilation should continue.
A characteristic symptom of GC 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, and gastrointestinal bleeding is common. The course of GC 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, a decrease in myocardial contractility and oliguria progress. Patients may experience bladder atony with acute urinary retention. Brain hypoxia is accompanied by dysfunction of vital centers of the central nervous system, and 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 itself as mental disorders, including thinking disorders, personality changes, neuroses and psychoses. 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 deficiency of thyroid hormones. Subsequently, confusion develops against the background of severe drowsiness. Occasionally, acute psychoses are observed that do not have specific features that can imitate paranoid or affective psychosis. In these cases, patients with GC are often misdiagnosed as having a 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 dysfunction of the central nervous system, when their depression has not yet reached its maximum extent. HA causes profound changes in electrolyte metabolism, which is one of the specific diagnostic signs. In all cases of coma with hyponatremia, it is necessary to exclude GC. Laboratory diagnostic signs of GC include: hyponatremia, hypochloremia, hypoglycemia, increased creatinine, creatinine phosphokinase, transaminases and lipids, hypoxia, hypercapnia, anemia and leukopenia. An ECG study reveals sinus bradycardia, low wave voltage, reduction and inversion of the T wave, and ST segment depression. The presence of reasonable suspicion is the basis for immediate initiation of thyroid hormone therapy, without waiting for the results of serum TSH and free thyroxine (T4) analysis. Even in the presence of the previously mentioned disorders characteristic of GC, such as hypothermia, hypoventilation and hyponatremia in weakened, somnolent or comatose patients, the diagnosis must be substantiated, appropriate tests must be taken and sent to the laboratory, after which therapy began. Although in most patients the clinical manifestations may be so obvious that serum TSH and T4 tests are only necessary 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 nonthyroidal systemic diseases may exhibit a syndrome-like phenomenon of “euthyroidism,” which may mimic hypothyroidism. In these circumstances, TSH secretion is reduced and its blood level may not be as high as might be expected. As noted previously, approximately 5% of cases of GC developed from central hypothyroidism and may be associated with normal or decreased serum TSH levels. Regardless of whether primary or secondary thyroid deficiency is present, all patients with GC have low serum levels of total and free T4 and triiodothyronine (T3). In patients with euthyroid syndrome, serum T3 levels may be unusually low (25 ng/mL).
Treatment
Therapy with thyroid hormones alone without correction of all other metabolic disorders, previously prescribed, is inadequate for recovery. Due to the potentially high mortality rate in the absence of vigorous comprehensive therapy, all patients should be placed in an intensive care unit (resuscitation department), where pulmonary and cardiac status, central venous pressure and pulmonary artery pressure should be carefully monitored.
Significant difficulties in treating GC are primarily due to the critical severity of the patient's condition. Treatment with 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 administered, if necessary, tracheal intubation and artificial ventilation to help eliminate respiratory acidosis.
Emergency treatment measures for GC include the administration of TG 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 TG administration are possible. The intravenous route of administration is accompanied by a rapid increase in TG levels (on average after 3-4 hours) to subnormal levels with a further slow increase over 5-7 days. In domestic practice, there are no thyroid hormone preparations for intravenous administration. Oral use of levothyroxine, despite a slow increase in TG levels with prolonged retention of them at the hypothyroid level, causes a clinical response after 24-72 hours. The absorption of L-T4 after oral administration is variable, but the clinical response develops quickly, even with myxedematous ileus. Intensive intravenous L-T4 therapy in the early hours (100-500 mcg over 1 hour) dramatically reduces mortality. During the first day, L-T4 is administered intravenously, at a dose of 300-1000 mcg/day, then maintenance doses are used - 75-100 mcg/day. When the patient’s well-being improves and the drug can be taken independently, the patient switches to oral administration. Eutirox is a levothyroxine preparation that has a wide range of dosages: 25, 50, 75, 100, 125 and 150 mcg. Therapy with Eutirox allows you to improve the quality of treatment: ensure accurate dose selection and, accordingly, better compensation for hypothyroidism.
The convenience of taking the drug and the absence of the need to divide tablets increases patient adherence 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 elevated TSH levels, restores physical and mental activity, and prevents the adverse effects 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 levothyroxine dosage 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 makes emergency therapy difficult, 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 mcg) intravenously or through a gastric tube (100 mcg initially, then 25-50 mcg every 12 hours), given the faster metabolic and central nervous system effects. In addition, there is an opinion that GC is accompanied by a pronounced impairment of the peripheral conversion of thyroxine to 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 preparations for intravenous administration. It must 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 mcg/day) are prescribed.
200-400 mg/day is administered intravenously. 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 and a 5% glucose solution are introduced. Fluid administration is carried out in a volume of no more than 1 liter per day to avoid myocardial overload and an increase in hyponatremia. Hyponatremia is eliminated as the TG concentration increases. For hypoglycemia, 20-30 ml of a 40% glucose solution is administered.
Rapid warming of the patient is contraindicated due to deterioration of hemodynamics due to rapid peripheral vasodilation with the development of collapse and arrhythmias. Passive warming is recommended (increasing room temperature by 1 degree per hour, wrapping in blankets). Prescription of sedatives should be avoided even when the patient is agitated, which is controlled by TG replacement therapy. In the future, infectious and other concomitant diseases that cause decompensation of hypothyroidism are treated. In case of concomitant infection, antibiotic therapy is carried out. 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 provoked by various drugs, systemic diseases and other reasons. It usually develops in older women in the winter and is combined with manifestations of hypothyroidism, such as hypothermia, hyponatremia, hypercapnia and hypoxia. Treatment should begin immediately in the intensive care unit or intensive care unit. Although thyroid hormone therapy is life-threatening, it is undoubtedly necessary and is carried out using T4, T3 or a combination of both. Additional measures such as mechanical ventilation, rewarming, fluid resuscitation, antibiotics, vasopressors, and corticosteroids may be important to the success of treatment.

Literature
1. Benfar G, de Vincentiis M. Postoperative airway obstruction: a complication of a previously undiagnosed hypothyroidism. Otolaryngol Head Neck Surg 2005;132:343-4.
2. Chernow B, Burman KD, Johnson DL, et al. T3 may be a better agent than T4 in the critically ill hypothyroid patient: evaluation of transport across the blood-brain barrier in a primate model. Crit Care Med 1983;11:99-104.
3. Cullen MJ, Mayne PD, Sliney I. Myxoedema coma. Ir J Med Sci 1979;148:201-6.
4. Fliers E, Wiersinga WM. Myxedema coma. Rev Endocr Metabol Disord 2003;4:137-41.
5. Hylander B, Rosenqvist U. Treatment of myxoedema coma: factors associated with fatal outcome. Acta Endocrinol (Copenh) 1985;108:65-71.
6. MacKerrowSD, Osborn LA, Levy H, et al. Myxedema-associated cardiogenic shock treated with intravenous triiodothyronine. Ann Intern Med 1992;117:1014-5.
7. Mathes DD. Treatment of myxedema coma for emergency surgery. Anesth Analg 1997;85:30-6.
8. Nicoloff JT, LoPresti JS. Myxedema coma: a form of decompensated hypothyroidism. Endocrinol Metab Clin North Am 1993;22:279-90.
9. Reinhardt W, Mann K. Incidence, clinical picture, and treatment of hypothyroid coma: results of a survey. Med Klin 1997;92:521-4.
10. Ringel MD.Management of hypothyroidism and hyperthyroidism in the intensive care unit. Crit Care Clin 2001;17:59-74.
11. Rodriguez I, Fluiters E, Perez-Mendez LF, et al. Factors associated with mortality of patients with myxoedema coma: prospective study in 11 cases treated in a single institution. J Endocrinol 2004;180:347-50.
12. Turhan NO, Kockar MC, Inegol I. Myxedematous coma in a laboring woman suggested a pre-eclamptic coma: a case report. Acta Obstet Gynecol Scand 2004;83:1089-91.
13. Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Phys 2000;62:2485-90.
14. Wartofsky L. Myxedema Coma. A Department of Medicine, Washington Hospital Center, Washington, DC 20010-2975, USA, 2005
15. Yamamoto T, Fukuyama J, Fujiyoshi A. Factors associated with mortality of myxedema coma: report of eight cases and literature survey. Thyroid 1999;9:1167-74.
16. Yamamoto T. Delayed respiratory failure during the treatment of myxedema coma. Endocrinol Jpn 1984;31:769-75.
17. Zwillich CW, Pierson DJ, Hofeldt FD, et al. Ventilatory control in myxedema and hypothyroidism. N Engl J Med 1975;292:662-5.

Hypothyroid coma is the most severe complication of hypothyroidism, occurring
repentant due to profound deficiency of thyroid hormones,
which occurs in untreated or insufficiently treated patients. More often
occurs in older people during the cold season. provoking
These moments are cooling, bleeding, pneumonia, cardiac failure.
sufficiency, hypoxia, hypoglycemia, various injuries. In some
In cases of coma, the development of coma is facilitated by the use of phenobarbital, phenothiazines
derivatives, the use of narcotic substances or anesthetics in ordinary
therapeutic doses.
Symptoms A constant symptom of hypothyroid coma is a sharp
decrease in body temperature due to low basal metabolic rate and
inadequate generation of thermal energy. Coma is accompanied by increasing
significant inhibition of the central nervous system (lethargy, depression, stupor
pores and coma itself), prostration develops, complete depression of deep
ky tendon reflexes. Due to alveolar hypoventilation,
carbon dioxide retention occurs, leading to an increase in PC02 and a decrease
Po2, which, together with a decrease in cerebral blood flow, promotes cerebral
ral hypoxia.
Severe cardiovascular failure manifests itself progressively
bradycardia and arterial hypotension. Characteristic of hypothyroidism
Smooth muscle atony is manifested by acute urinary retention syndrome
or fast dynamic and even mechanical (megacolon) intestinal leakage
mileage. Gastrointestinal bleeding is often observed, persistent
bleeding from the gums. Hypoglycemic conditions are possible.
Without adequate treatment, a further decrease in temperature occurs
body, breathing begins, hypercapnia and respiratory acidosis increase.
Cardiac weakness and arterial hypotension progress, which in turn
turn leads to oliguria, anuria and metabolic acidosis. Hypoxia
brain is accompanied by dysfunction of vital centers of the central nervous system. Not-
the mediocre cause of death is usually increasing cardiovascular
vascular and respiratory failure.
Diagnosis. Hypothyroid coma is characterized by depression of the central nervous system due to lethargy
and disorientation to the point of true coma, sometimes convulsions in the form of small seizures
epilepsy, hypothermia, hypoventilation, hypotension, bradycardia, edema
face, especially periorbital edema, dry, pale with a jaundiced tint
skin, enlarged tongue, decreased tendon reflexes. Laboratory
studies reveal hypercapnia, respiratory or mixed acidosis, hy-
ponatremia, hypoglycemia, hypercholesterolemia, increased activity
creatine phosphokinase in blood serum and protein in cerebrospinal fluid
tee. ECG shows bradycardia, low voltage in all leads, inversion
T wave, myocardial conduction disturbances.
Urgent Care. At the prehospital stage, measures are taken to
combat hypoxia - oxygen therapy, intubation if necessary
and artificial ventilation. To correct hypoglycemia it is necessary
introduce 20-30 ml of 40% glucose solution.
In the hospital (intensive care unit) after taking blood for
content of triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone
pituitary gland (TSH), electrolytes, blood gases, liver and kidney tests
carry out further measures aimed at treating hypothyroidism
coma, including the elimination of hypothermia, the fight against hypoventilation, hy-
percapnia and hypoxia, use of glucocorticoids; application of adequate
no dose of thyroid hormones; treatment of concomitant infectious and other
many diseases that led to the development of coma.
To eliminate hypothermia, the patient must be warmed, for which
the air temperature in the room should not be lower than 25 C. Warming the patient
by using local heat applications is contraindicated, since
due to cutaneous vasodilation, collapse and arrhythmia may occur. Pro-
administer oxygen therapy in combination with artificial ventilation.
Infusion therapy is prescribed with great caution with simultaneous
administration of glucocorticoids and under constant cardiac monitoring
eat. In hypothyroid coma, hyponatremia is usually observed, so
administration of hypotonic solutions is contraindicated.
Therapy for hypothyroid coma in a hospital begins with intravenous
administration of hydrocortisone hemisuccinate - 200-400 mg/day, and this is the amount
The quality of the drug is administered in divided doses every 6 hours. Introduction
glucocorticoids should precede the administration of thyroid hormones,
due to the fact that hypothyroidism is often combined with chronic adrenal
insufficiency (Schmidt's syndrome) or panhypopituitarism, with
which there is a decrease in the function of the adrenal cortex. Ignoring
this condition when administered thyroid hormones can create acute
adrenal insufficiency.
Hormone replacement therapy is carried out with levothyroxine, daily
a dose of 400-500 mcg is administered by slow infusion. In the following days, the dose
Roxine is reduced to 50-100 mcg/day.
Patients in hypothyroid coma are contraindicated
drugs that have a depressant effect on the central nervous system. Moreover, due to
with decreased metabolism in patients with hypothyroidism there is an increase
sensitivity to all drugs, especially drugs
digitalis and morphine preparations.
To suppress co-infection or prevent an outbreak
dormant infections must be actively treated with antibiotics.
Due to the fact that patients in a coma have atony of the muscles,
bladder, a permanent urinary catheter is required.