Thyrotoxic crisis after removal of the thyroid gland. Thyrotoxic crisis: causes, symptoms, treatment and emergency care

Thyrotoxic crisis is an acute and life-threatening metabolic disorder that manifests itself in an already existing condition. It is very dangerous for human life and can lead to death if help is not provided in a timely manner.

This is a pathological syndrome that occurs suddenly against the background of hyperthyroidism as a result of the release of a large amount of free thyroid hormones into the blood. At the same time, all signs of hyperthyroidism sharply worsen. That is, not just a lot of hormones triiodothyronine (T3) and thyroxine (T4) enter the blood, but a lot.

The prevalence is 0.5-19% in patients with severe hyperthyroidism. Those people who were not diagnosed with hyperthyroidism in a timely manner find themselves in a very difficult situation. As a result, they did not even suspect its possible exacerbation to the point of a life-threatening condition.

Why does thyrotoxic crisis develop?

Typically, only a small portion of the free hormones T3 and T4 is found in the blood. 99% of them are bound to plasma proteins, primarily thyroglobulin.

During a thyrotoxic crisis, too much T3 and T4 suddenly enters the blood while their connection with thyroglobulin decreases. In response to this, the adrenal glands begin to actively work, releasing adrenaline and norepinephrine, known as stress hormones. The combined actions of these active substances explain such a great danger of thyrotoxic crisis for humans. In addition, against the background of such a huge amount of hormones, the patient soon develops adrenal insufficiency - the function of the adrenal glands is depleted. The higher nervous system is activated - the subcortical centers of the hypothalamus and reticular formation. All this can lead to death if the patient is not provided with medical assistance in a timely manner.

At the same time, a thyrotoxic crisis can develop not only in a seriously ill person, but also in a completely normal course of the disease. But for this to happen, something extraordinary must happen.

What can start this process?

  • injection of radioactive iodine into the patient (causes the breakdown of thyroid follicles) or exposure to x-rays,
  • stress in patients with undiagnosed hyperthyroidism: myocardial infarction, surgery, trauma, sepsis, burns, nervous strain, physical activity, infectious diseases.
  • physical and emotional overload.
  • concomitant chronic diseases, if they suddenly worsen.
  • various medical procedures (including dental).
  • rise in body temperature (for example, against the background of the flu).
  • exacerbation of existing hyperthyroidism due to the severity of the underlying disease.
  • the appearance of thyroid hormones from outside, for example, through errors in dosage.
  • in women it can be triggered by pregnancy.

What's happening?

The maximum exacerbation of the symptoms of the disease begins. The severity of the condition depends on the concentration of free thyroid hormones in the blood. As a rule, only a few hours, or a day at most, pass from the onset of a strong provoking factor (for example, surgery) to the onset of symptoms of a crisis.

The patient becomes anxious, worried, his body temperature rises, his heartbeat increases, and his breathing quickens. The temperature rises quickly and can reach 40-41 °C or more in 3-4 hours. The pulse rate usually ranges from 120 to 200 beats per minute, but in some cases it reaches 300.

At first, the patient is usually excited and actively complains about his condition; then consciousness may be impaired. The person is anxious, emotionally unstable (cries, shows aggression, laughs), hyperactive and unfocused in behavior. Sometimes, against the background of a thyrotoxic crisis, hallucinations and psychosis develop - the patient becomes uncontrollable, does not respond to beliefs, and commits uncontrollable acts, including suicidal ones. Many patients begin to experience panic, fear of loss of consciousness, death.

As the crisis progresses, this state is replaced by lethargy, apathy, emotional dullness, and extreme muscle weakness. The thyrotoxic form of myopathy is manifested by a decrease in tone and rapid fatigue of the muscles of the neck, scapular region, arms and legs, and less often of the face and torso. Pain, involuntary twitching, convulsions, hypokalemic paroxysmal paralysis (paroxysmal severe muscle weakness) may be observed.

Sweating can be profuse, leading to dehydration due to insensible fluid loss.

Extreme muscle weakness may occur.

Among other symptoms of a crisis are trembling of the hands, which is noticeable from the outside and can gradually turn into convulsions; the appearance of disturbances in the heart rhythm (usually atrial fibrillation), a sharp increase in systolic blood pressure to 180-230 mm Hg. Art., nausea, vomiting, diarrhea. Due to the heavy load on the heart, heart failure may develop.

Cardiovascular disorders are present in 50% of patients, regardless of the presence of previous heart disease. Sinus tachycardia usually occurs. Arrhythmias may occur, especially atrial fibrillation, but with the addition of ventricular extrasystoles, as well as (rarely) complete heart block. In addition to an increase in heart rate, there is an increase in stroke volume, cardiac output and myocardial oxygen consumption. As a rule, pulse pressure increases sharply.

Most patients with thyrotoxic crisis develop gastrointestinal symptoms. Diarrhea and hyperdefecation contribute to dehydration (dehydration of the body).

Lack of appetite, nausea, vomiting and cramping abdominal pain often occur. Jaundice and painful hepatomegaly may occur.

Sometimes the patient complains of weakness, it is difficult for him to raise his arms and walk; Often, against the background of a thyrotoxic crisis, yellowness of the skin and sclera and diffuse abdominal pain appear. If the kidneys are involved in the pathological process, the person’s urine output stops or decreases.

Externally, the patient at the beginning of a thyrotoxic crisis looks frightened, his skin is red, moist, and hot when touched. Then, as the adrenal glands become exhausted and the body becomes dehydrated, the skin becomes dry, lips crack, and the patient becomes lethargic and lethargic.

There are 3 stages of crisis development:

Stage 1 - mortality is up to 10% and is characterized by the following symptoms:

Sinus tachycardia or tachyarrhythmia with existing atrial fibrillation, heart failure,

Hyperthermia (increase in body temperature to 38-41C) with profuse sweating,

General weakness

Gastrointestinal symptoms: nausea, vomiting, diarrhea (leads to dehydration).

Neurological symptoms: tremor, restlessness, agitation, muscle weakness primarily in the upper parts of the shoulder girdle, bulbar palsy (damage to the cranial nerves),

Dehydration (dehydration).

Stage 2 is characterized by the following:

Stupidity with delirium, stupor, stupor, hallucinations, with temporal and spatial disorientation.

Stage 3.

The mortality rate is up to 50% and the basis is an unconscious state, the patient enters a coma. It is further divided into: stage 3a - mortality less than 50% and stage 3b - mortality more than 50%.

What needs to be done as quickly as possible?

The average mortality rate in such a severe condition is 20%. Every fifth patient who experiences such a crisis dies. This means that the sooner a person receives medical care and the sooner he gets into the hands of specialists, the better his prognosis. In the absence of timely assistance, the probability of death is almost 100%.

Until the ambulance arrives, you need to lay the patient down, provide access to fresh air, assess his pulse, measure blood pressure, respiratory rate, and temperature. If the person is conscious, asking when they last urinated can give some idea of ​​whether their kidney function is intact.

Having quickly carried out measures to assess the patient’s condition, they move on to the most important stage of pre-medical care - cooling. Heat enhances the destructive effects of hormones, so combating it becomes a priority when providing first aid.

It must be remembered that body temperature rises rapidly during a crisis, so you cannot hesitate. A cool compress on the forehead will not help in this case.

The patient is freed from clothing and placed in a bath with cool water. Alternatively, you can apply ice packs to the head, neck, chest and abdomen (areas of greatest heat transfer) or rub the body with ethyl alcohol (or a weak solution of acetic acid).

During the cold season, you can open the windows in the room and cover the patient with bags of snow. If a cool bath, ice packs, and ethyl alcohol are not available, you must use any possible method of cooling the body: undress the patient, cover him with a wet sheet, or spray the skin with cold water and fan it so that when air moves, the water evaporates faster. Cooling should continue continuously until the arrival of doctors, and not as a one-time action.

During thyrotoxic crisis, renal and heart failure rapidly develop. Since these conditions are extremely life-threatening, you need to be prepared for the fact that you may have to carry out resuscitation measures. To do this, without losing sight of the patient for more than a few seconds, prepare everything necessary - look for a cushion to place under the neck, remove dentures from the patient’s mouth, if any, etc.

We must remember that during a thyrotoxic crisis, the absorption of drugs, if they are given in the form of tablets, practically does not occur. Therefore, tablets, including antipyretics, are ineffective - all drugs are administered intramuscularly or into a vein, if possible.

To combat dehydration, the patient is given plenty of fluids to drink in small sips. If a person is unconscious, then intravenous drip administration of drugs is necessary (400 ml of 0.9% sodium chloride solution or 5% glucose solution).

If a thyrotoxic crisis is provoked by an acute infectious disease, you can give the patient antibiotics (which depends on the disease).

Treatment of thyrotoxic crisis.

The goal of treatment is to stabilize the patient’s condition and immediately reduce high levels of thyroid hormones to the area of ​​euthyroidism and must be carried out in the intensive care unit of hospitals:

1. Drug treatment.

In order to suppress the secretion of thyroid hormones, immediately administer 10 mg of 10% sodium iodide or 1% Lugol's solution with sodium iodide, diluted in 1 liter of 0.9% sodium chloride or 5% glucose,

Thyrostatics in high dosage for the purpose of immediate blockade of the production of thyroid hormones: thiamazole 40-80 mg for 8 hours, Mercazolil 10 mg every 2 hours (daily dose up to 100-160 mg),

Hydrocortisone 400-600 mg per day or prednisolone 200-300 mg per day per 0.5-1.0 l 0.9% sodium chlorine or 5% glucose inhibit the conversion of T4 to T3, compensate for adrenal insufficiency,

Sedatives - diazepam, haloperidol,

Beta blockers (propranolol, esmolol) - reduce sensitivity to catecholamines, reduce heart rate, inhibit the conversion of T4 to T3,

Cardiac glycosides - strophanthin, corglycon,

Correction of dehydration by intravenous administration of saline solutions.,

Artificial nutrition, prevention of thromboembolic complications.

If necessary, provide respiratory support with mechanical ventilation and maintain blood pressure with cardiotonic medications.

2. Plasmapheresis.

Allows you to successfully remove excess T3 and T4 from the blood, carried out after correction of dehydration and stabilization of cardiovascular activity.

3. Surgical treatment.

In severe cases, total resection (complete removal) of the thyroid gland is performed.

Table of contents of the topic "Thyrotoxic crisis. Acute adrenal insufficiency (adrenal crisis). Ketoacidotic coma.":
1. Thyrotoxic crisis. Causes (etiology) of thyrotoxic crisis. Pathogenesis of thyrotoxic crisis. Clinic (signs) of thyrotoxic crisis.

3. Acute adrenal insufficiency (adrenal crisis). Causes (etiology) of adrenal insufficiency. Pathogenesis of adrenal crisis.
4. Clinic (signs) of adrenal insufficiency (adrenal crisis). Emergency care (first aid) for adrenal insufficiency (adrenal crisis).
5. Emergency conditions in diabetes mellitus. Ketoacidotic coma. Causes (etiology) of ketoacidotic coma. Pathogenesis of ketoacidotic coma.
6. Clinic (signs) of ketoacidotic diabetic coma.
7. Diagnosis of ketoacidotic diabetic coma. Emergency care (first aid) for ketoacidotic coma.
8. Principles of treatment of ketoacidotic diabetic coma. Treatment tactics for ketoacidotic coma. Insulin therapy. Method of continuous intravenous infusion of small doses of insulin.
9. Infusion therapy for ketoacidotic diabetic coma. Method of fractional administration of small doses of insulin for ketoacidotic coma. Method of fractional administration of large doses of insulin in ketoacidotic coma.

Treatment of thyrotoxic crisis aimed at combating intoxication of the body caused by an increase in the content of thyroid hormones in the blood; it is necessary to overcome acute adrenal insufficiency, eliminate dehydration, correct the activity of the cardiovascular system, etc.

Emergency care (first aid) for thyrotoxic crisis.

1. With a purpose suppression of thyroid hormone secretion immediate intravenous administration of 10 ml of 10% sodium iodite solution or intravenous administration of 1% Lugol's solution prepared with sodium iodide instead of potassium iodide, in the amount of 100-250 drops per liter of isotonic sodium chloride solution or 5% glucose solution.

2. For decreased thyroid function Mercazolil is prescribed at a dose of 10 mg every 2 hours (the total daily dosage can be increased to 100-160 mg). For vomiting, antithyroid drugs are administered rectally.

3. IV drip administration of 2-3 l of isotonic sodium chloride solution, 0.5-1.0 l of 5% glucose solution with hydrocortisone 400-600 mg/day, prednisolone 200-300 mg. The daily dose of hydrocortisone is determined by the severity of the patient's condition and, if necessary, can be increased.

4. With neuropsychic agitation IV administration of 2-4 ml of 0.5% seduxen solution or 2-4 ml of 0.25% droperidol solution is indicated.

5. For cardiovascular disorders according to indications, strophanthin 0.3-0.5 ml of 0.05% solution, korglykon 0.5-1 ml of 0.06% solution, cordiamin 1 ml of 25% solution, mezaton 0.5-1 are administered ml 1% solution. Rhythm and conduction disorders are treated according to the principles set out in the topic Cardiac Rhythm and Conduction Disturbances.

Effective method of treating thyrotoxic crisis is plasmapheresis, which allows you to quickly remove large amounts of thyroid hormones and immunoglobulins circulating in the blood.

Thyrotoxic crisis is a complication of diffuse toxic goiter, which occurs due to a sharp increase in the concentration of thyroid hormones in the blood plasma and is accompanied by an exacerbation of the symptoms of the underlying disease.

ICD-10 E05.5
MeSH D013958

Causes

Thyrotoxic crisis occurs as a result of inadequate treatment of toxic diffuse goiter (Graves' disease, Basedow's disease, hyperthyroidism). This autoimmune pathology is caused by increased secretion of hormones by overgrown thyroid tissue.

The incidence of thyrotoxic crisis in patients with moderate and severe forms of hyperthyroidism is 0.5-19%. The ratio of cases of crisis in women and men is 9:1.

Main provoking factors:

  • surgery on the thyroid gland to treat toxic diffuse goiter;
  • tooth extraction;
  • use of ether anesthesia during surgical procedures;
  • the use of radioactive iodine in the treatment of Graves' disease;
  • treatment of the thyroid gland with x-rays;
  • premature withdrawal or omission of medications used to correct hormonal status in hyperthyroidism;
  • taking products containing iodine, including contrast reagents during X-ray examinations;
  • rough palpation of the thyroid gland.

In addition, thyrotoxic crisis can be provoked by:

  • infectious diseases (especially those affecting the respiratory tract);
  • cerebrovascular accident;
  • pregnancy and childbirth;
  • stressful situations;
  • injuries;
  • excessive physical activity;
  • pulmonary embolism.

Pathogenesis

The pathogenesis of thyrotoxic crisis is based on a sharp increase in the level of free thyroid hormones - triiodothyronine (T3) and thyroxine (T4). In addition, this condition is characterized by the following processes:

  • increased adrenal insufficiency, which worsens the deficiency of their hormones;
  • activation of the sympathetic-adrenal system, as well as the subcortical centers of the hypothalamus and the reticular formation of the brain;
  • excess synthesis of catecholamines - substances that stimulate the activity of the endocrine glands.

The listed pathological changes lead to the fact that the body's reserve capabilities are depleted, and a life-threatening condition develops - a thyrotoxic crisis, requiring emergency care.

Symptoms

Manifestations of thyrotoxic crisis manifest suddenly. However, in some cases, a prodromal period is observed, during which a gradual, subtle increase in symptoms occurs.

Symptoms of thyrotoxic crisis:

  • fever – temperature rises to 38-40 °C;
  • sinus tachycardia - the pulse rate is at the level of 120-200 beats per minute, in some situations reaches 300 beats/min;
  • sweating - in severe cases, sweating is so profuse that there is a risk of dehydration;
  • headache;
  • trembling in the limbs;
  • anuria – decreased amount of urine excreted;
  • CNS disorders;
  • disturbances in the gastrointestinal tract.

Disorders in the functioning of the central nervous system are observed in 90% of patients in a state of crisis. Their specificity and severity vary significantly. Possible manifestations:

  • lethargy;
  • emotional lability (instability);
  • anxiety;
  • insomnia;
  • manic behavior;
  • excessive excitement;
  • confusion;
  • stunned.

In addition, most patients experience weakness involving the muscles of the face, trunk, and limbs.

In addition to sinus tachycardia, thyrotoxic crisis is accompanied by a number of disturbances in the functioning of the cardiovascular system. The main ones:

  • atrial fibrillation;
  • increased stroke volume and myocardial oxygen demand;
  • increased blood pressure;
  • shortness of breath, difficulty breathing.

The main gastrointestinal symptoms that occur during a crisis:

  • decreased appetite;
  • nausea, vomiting;
  • painful cramps in the abdomen;
  • diarrhea and hyperdefecation.

People over 60 years of age often develop an apathetic version of thyrotoxic crisis. Its signs:

  • apathy, slow reaction;
  • minor goiter;
  • absence of usual ophthalmic symptoms of hyperthyroidism;
  • blepharoptosis – drooping of the upper eyelids;
  • weight loss;
  • muscle weakness;
  • congestive heart failure.

Diagnostics

Thyrotoxic crisis is diagnosed based on the appearance of characteristic clinical symptoms (fever, tachycardia, central nervous system disorders and gastrointestinal disorders) against the background of toxic goiter. In addition, the previous action of the provoking factor is taken into account: surgery, treatment with radioactive iodine, infectious disease, and so on.

To confirm the diagnosis, laboratory and instrumental studies are carried out:

  • measurement of blood pressure (its increase is detected);
  • listening to heart sounds, measuring pulse;
  • ECG shows abnormal heart rhythm;
  • a blood test for hormones shows an increase in thyroxine and triiodothyronine, as well as a decrease in cortisol and thyroid-stimulating hormone;
  • a blood sugar test demonstrates hyperglycemia (glucose concentration exceeds 5.5 mmol/l).

Treatment

Treatment of thyrotoxic crisis includes several components:

  • neutralization of the provoking factor (for example, antibiotics are used to treat infectious diseases);
  • maintaining basic body functions (restoring electrolyte balance through infusions, oxygen inhalation, and so on);
  • elimination of thyrotoxicosis by normalizing the level of thyroid hormones.

Algorithm of action (emergency care) for thyrotoxic crisis:

  1. Administration of iodine-containing drugs - 10% iodide or Lugol solution diluted with sodium iodide and saline. The goal is to slow down the release of thyroid hormones.
  2. Oral administration or rectal administration (for vomiting) of Mercazolil to suppress thyroid function.
  • Intravenous infusions of sodium chloride solution with glucose and hydrocortisone, as well as the introduction of prednisolone. The goal is to rehydrate the body and normalize the functioning of the adrenal glands.
  1. Drip administration of a solution of seduxen or droperidol to relieve nervous excitement.

After providing first aid for a thyrotoxic crisis and stabilizing the patient’s condition, treatment tactics are selected depending on the specifics of the clinical picture. Typically, the following drugs are used:

  • to normalize cardiovascular activity - strophanthin, korglykon, cordiamine, metazone;
  • to eliminate fever - standard antipyretic drugs with the exception of acetylsalicylic acid;
  • to block the synthesis of thyroid hormones - propylthiouracil;
  • to reduce the intensity of peripheral effects from thyroid hormones - propranolol, reserpine, guanethidine.

Emergency care for thyrotoxic crisis in children is provided according to a similar scheme, but the doses of medications are adjusted. Plasmapheresis or hemosorption is also performed to accelerate the removal of thyroid hormones from the body.

Forecast

Thyrotoxic crisis has a favorable prognosis provided proper treatment. On average, 3 days after the start of therapy, the patient’s condition improves. Then constant correction of thyroid hormone levels is required.

Without emergency help, a thyrotoxic crisis is accompanied by a rapid worsening of symptoms:

  • dehydration develops;
  • refractory pulmonary edema occurs;
  • vascular collapse is observed;
  • in some cases, hepatomegaly occurs with subsequent liver necrosis.

The person loses consciousness, falls into a state, and then into a coma. Death may occur within 72 hours of the onset of signs of crisis.

Prevention

Thyrotoxic crisis and hypothyroid coma are severe complications of thyroid diseases. To prevent their development, it is necessary to correct the hormonal imbalance that occurs as a result of dysfunction of this endocrine organ.

Prevention of thyrotoxic crisis includes measures such as:

  • regularly taking antithyroid drugs according to the regimen prescribed by your doctor;
  • achieving a euthyroid state of the patient before performing surgical manipulations on the thyroid gland or before starting treatment with radioactive iodine.
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Thyrotoxic crisis is a complication of hyperthyroidism, in which the manifestations of thyrotoxicosis increase to a life-threatening degree.

Etiology and pathogenesis. Thyrotoxic crisis is most often observed in patients with moderate or severe previous Graves' disease (diffuse toxic goiter); it can develop after surgical treatment or radioiodine therapy for DTG against the background of uncompensated thyrotoxicosis. During a crisis, the binding of thyroid hormones decreases and the concentration of free forms of T3 and T4 increases; at the same time, the sensitivity of organs and tissues to catecholamines increases, and relative adrenal insufficiency develops. A provoking factor in the development of a thyrotoxic crisis can also be infection, psycho-emotional stress, surgical intervention, or exacerbation of a chronic disease.

Clinical picture. Under the influence of a trigger factor, the symptoms of thyrotoxicosis increase.

The earliest signs of a thyrotoxic crisis are fever, tachycardia, sweating, increased excitability of the central nervous system and emotional lability. The increase in body temperature ranges from 38 to 41 °C. The pulse rate is usually 120-200 beats/min, but in some cases it reaches 300 beats/min. Sweating can be profuse, leading to dehydration due to insensible fluid loss.

In 90% of patients with thyrotoxic crisis, a central nervous system disorder is observed. Symptoms are very variable - from lethargy, anxiety and emotional lability, manic behavior, excessive agitation and psychotic confusion, stupor and coma. Extreme muscle weakness may occur. Thyrotoxic myopathy sometimes occurs, usually affecting the proximal muscles. In severe forms, the distal muscles of the limbs, as well as the muscles of the trunk and face may be involved. Cardiovascular disorders are present in 50% of patients, regardless of the presence of previous heart disease. Sinus tachycardia usually occurs. Arrhythmias may occur, especially atrial fibrillation, but with the addition of ventricular extrasystoles, as well as (rarely) complete heart block. In addition to an increase in heart rate, there is an increase in stroke volume, cardiac output and myocardial oxygen consumption. As a rule, pulse pressure increases sharply. Terminal events may include congestive heart failure, pulmonary edema, and circulatory collapse. Most patients with thyrotoxic crisis develop gastrointestinal symptoms. Diarrhea and hyperdefecation contribute to dehydration. During a thyrotoxic crisis, there is often a lack of appetite, nausea, vomiting and cramping abdominal pain. Jaundice and painful hepatomegaly may occur.

Diagnostics. Clinical diagnostic criteria: body temperature above 38°C; significant tachycardia that does not correspond to the degree of temperature increase; dysfunction of the central nervous system, cardiovascular or digestive system; excessive peripheral manifestations of thyrotoxicosis. It should be noted, however, that the diagnosis of thyrotoxic crisis requires the presence of more than just fever in a patient with hyperthyroidism.

Laboratory tests reveal anemia, leukocytosis, hyperglycemia, hyperazotemia, hypercalcemia and increased activity of liver enzymes. Characterized by a significant increase in free T4 and T3.

Treatment. Emergency care begins with the administration of glucocorticoids 50-100 mg - hydrocortisone hemisuccinate every 4 hours. Antithyroid drugs are required - propylthiouracil(300-400 mg orally) or thiamazole(30-40 mg orally), and then repeat these doses after 6-8 hours to reduce the production of hormones by the thyroid gland. After 1 hour, iodine preparations are administered (sodium iodide 1-2 g intravenously over 24 hours or solution potassium iodide 5 drops orally every 6 hours) to prevent additional release of thyroid hormones. To prevent the development of symptoms of congestive heart failure, it is recommended propranolol(40-80 mg orally or 1-2 mg intravenously every 6-8 hours). Required oxygen therapy And infusion therapy: 0.9% sodium chloride solution and 5% solution glucose up to 3 liters per day. Can be used in complex therapy phenobarbital to enhance the synthesis of thyroxine-binding globulin and inactivate the conversion of T4 to T3, as well as for the purpose of sedation. If the temperature exceeds 40°C, antipyretics and cold applied to the extremities and blood vessels should be prescribed. It can be used as an additional treatment method plasmapheresis.

Forecast. If thyrotoxic crisis is left untreated, the mortality rate approaches 100%. With adequate therapy, mortality can reach 10-20%. The main means of reducing mortality, of course, is to prevent the development of thyrotoxic crisis.