manifestations of thyrotoxic crisis. Thyrotoxic crisis: symptoms and treatment

Severe health problems begin with diseases of a small organ in the neck. Goiter chronic ailments lead to an increase in the thyroid gland. The extreme stage of complications is referred to as a thyrotoxic crisis. With such a complication, the result of clinical symptoms is a fatal outcome in 20% of cases. At the time of acute manifestations of dangerous conditions, the patient needs urgent help and constant monitoring by medical personnel.

Difficulties in the treatment of chronic diseases of the organ

A person has severe suffocation from unrest, allergic reactions, it becomes difficult to swallow - this may be a thyrotoxic crisis. The urgency of the problem remains to this day: the surgical method of treating the thyroid gland is not suitable. After the removal of the organ, complications occur that require constant drug therapy for the rest of your life.

Not all doctors recommend resorting to surgical removal of the thyroid gland, and few specialists are able to perform such an operation. A small organ is part of the body's lymphatic system. If you remove the link from the chain of complex processes, the infection will be able to penetrate freely into the region of the lungs, bronchi, and stomach.

A typical manifestation of a complication in a person with a removed thyroid gland is a stomach ulcer. The appointment of pills and other medicines is not able to make up for the lost function of the organ. Patients with chronic diseases are at risk of acquiring a thyrotoxic crisis. With the existing predisposition of the body to swelling of the tissues of the goiter, sick and close people are advised to familiarize themselves with the principles of first aid during clinical conditions.

Ways of acquiring complications

Thyrotoxic crisis is the result of various complications in the body:

The main cause of the crisis is the lack of iodine in the body. An increase in the organ can occur with the active process of the formation of connective tissue. Pathology occurs after a violation of protein metabolism in the human body.

External manifestations in clinical cases

If a deterioration in well-being began to appear with minor loads, this may be a thyrotoxic crisis. Symptoms of the disease begin to manifest themselves clearly after taking iodine preparations or thyroid hormones. Let's highlight the main signs, after which you need to urgently be examined by an endocrinologist. If more than three symptoms are detected, then we can assume the presence of a complication - a thyrotoxic crisis.

External manifestations by which you can independently assess the development of the disease:

The decline in well-being occurs earlier than in the past state of the body.
Often the pulse rises, exceeding 100 beats per minute.
Increased excitability is observed, irritation occurs due to every little thing.
The picture is supplemented by an increase in pressure.
An unreasonable increase in body temperature of more than 3 degrees.
There is dizziness, nausea, vomiting.
Disorder of the digestive system.
Broken breathing rate.

Procedure before the ambulance arrives

If a thyrotoxic crisis occurs, help should follow immediately. A lethal outcome is possible without the provision of initial actions that facilitate the supply of oxygen to the lungs and exclude blocking of vital metabolic processes. It is advisable to notice the previous points that are sources of deterioration in well-being.

Let's single out the main measures in case of complications:

Call for emergency help.
Place the patient on his back, put a roller under the neck.
In a stuffy room, it is required to open the windows, which will facilitate the flow of fresh air into the lungs of the patient.
Before the arrival of doctors, you can independently assess the condition: measure the pulse, pressure, temperature. External conditions are fixed: skin moisture, blanching of the face.
Interrogation of the patient helps to establish the moment of deterioration of health. But a person remains conscious during a thyrotoxic crisis.

How to make the patient feel better on his own?

The acute phase of the disease is accompanied by a breakdown in the functioning of the kidneys. Therefore, it is pointless to give medicines in the form of tablets. The drugs are administered intravenously or intramuscularly as prescribed by a doctor or an experienced specialist. At home, there is rarely such an opportunity, they use their own skills of elementary assistance to victims.

We single out the main measures to normalize the state:

If the body temperature is too high, which is often observed during a crisis, then they resort to cooling the body. This slows down metabolic processes, curbing the harmful effects of hormones. The patient is placed in a cool bath. If not, remove all clothing. An alternative option is the following: apply several compresses to different parts of the body. Reduces the temperature of wiping with alcohol solutions.
The person is being monitored until the ambulance arrives. The tongue can sink into the larynx, causing suffocation.
They help to drink as much clean liquid as possible so that dehydration does not occur.

What actions are taken by doctors?

If a thyroid crisis occurs, emergency care includes the appointment of drugs that reduce the action of thyroid hormones. These substances are actively produced by the thyroid gland when the organ malfunctions. The result of treatment is a decrease in their content in the blood serum.

The external manifestation of the disease becomes. Additional information about the state of the body is given by the results of the examination by the ECG method. Deviations are set:

atrial fibrillation;
sinus tachycardia;
violation of intraventricular conduction;
an increase in the amplitude of the teeth of the QRS complex and T.

Preparations

Treatment of a thyrotoxic crisis is necessary for any cause of a critical condition. The following types of medicines are used:

"Mercazolil" is administered intravenously at a dosage of 100 ml.
Enter sodium iodide solution.
Orally give at the rate of 30 drops per day.
Good results are noted after the injection of "Kontrykal".
A dropper is installed from solutions: 5% glucose, sodium chloride, albumin. Add vitamins B1, B2, nicotinamide.

The recovery period with medications is carried out for at least two weeks after critical conditions. Initially, they are used only after more than two days, iodine-containing substances are prescribed.

How to prevent the disease?

Carry out preventive measures to exclude the body - thyrotoxic crisis. Emergency care, the algorithm of which is clearly spelled out in the instructions for ambulance personnel, will be less painful, and there will be no irreversible consequences. So, treatment is carried out before operations in people with Antithyroid drugs are selected, iodine-containing substances are prescribed.

The fight against hyperthyroidism is a measure for the prevention of critical conditions. Doctors noted the prevalence of the disease among women. A crisis in the weaker sex appears 9 times more often than in men. A long-term complication can form at almost any age under the influence of certain factors.

Thyrotoxic crisis- life-threatening increase in symptoms of toxic goiter. It develops in patients with a severe form of the disease. Thyrotoxic crisis is observed in 0.5-19% of cases, which, apparently, is due to a different assessment of the condition of patients.

Etiology and pathogenesis of thyrotoxic crisis

A thyrotoxic crisis develops after operations for diffuse toxic goiter or its treatment with radioactive iodine, when these measures are carried out without first achieving the patient's euthyroid state. With undiagnosed or poorly treated diffuse toxic goiter, a thyrotoxic crisis is provoked by mental trauma, intercurrent infections, acute surgical diseases, insufficient pain relief during surgery, surgical trauma, intoxication, toxic infections, hyperthermia, diabetic ketoacidosis, physical activity, surgical intervention outside the thyroid gland ( tonsillectomy, cholecystectomy, tooth extraction, etc.), abrupt withdrawal of antithyroid drugs, pregnancy toxicosis, even normal delivery, reaction to adrenomimetics, glycosides, insulin and other drugs, etc. Most of these etiological factors of thyrotoxic crisis are intense cortical irritants adrenal glands, whose function was largely depleted prior to the crisis. In some cases, the cause of the thyrotoxic crisis remains unknown ("spontaneous" crisis).

The pathogenesis of thyroid storm is not well understood. Currently, most researchers believe that the main factors in the pathogenesis of a thyrotoxic crisis are a sharp increase in the release of thyroid hormones into the blood, an increase in relative adrenal insufficiency, hyperactivity of the higher parts of the nervous system, the hypothalamic-pituitary and sympathetic-adrenal systems.

P. E. Ogiy and A. N. Lyulka (1973) believe that the postoperative thyrotoxic crisis is the result of complex and deep disturbances in the relationship between the central nervous system, the function of the pituitary gland and the adrenal cortex during removal of the thyroid gland.

It is believed that the trigger mechanism of the thyrotoxic crisis is a sharp increase in the content of thyroid hormones in the blood. The role of thyroid hormones in the development of a thyrotoxic crisis was first pointed out in 1901 by A. Kocher. He associated the development of a postoperative crisis with the intoxication of the body with thyroxine and wound secretions absorbed during the operation during resection of the thyroid gland. C. Cravetto et al. (1958), J. Nauman (1961) found that during a thyrotoxic crisis in the blood, the most significant level of SBY is observed, which increases in parallel with the increase in clinical symptoms. Exacerbation of toxic goiter during treatment with radioactive iodine is associated with irritation of the thyroid gland [Klyachko V. R., 1957-1961] or with rupture of the walls of the follicles [Milk Sht., 1962], as a result of which thyroid hormones enter the blood intensively. Cases of thyrotoxic crisis have been described with the use of large doses of iodine in the treatment of diffuse toxic goiter [Mazovetsky A. G., 1960, etc.]. At the same time, a number of authors have shown that a sharp increase in thyroid hormones in the blood does not always lead to the development of a thyrotoxic crisis [Gurevich GM, 1955; Krivitsky D.I., 1963; Milku St., 1962]. Conversely, with a thyrotoxic crisis, there may be only a slight increase or a normal level of thyroid hormones, which is explained by an increase in the concentration of thyroid-binding proteins in diffuse toxic goiter.

It is believed that one of the main factors in the pathogenesis of a thyrotoxic crisis is an increase in relative adrenal insufficiency [Molodaya E.K., 1943; 1950; Lyulka A. N., 1954, 1964; Ogiy P. E., Lyulka A. N., 1973, etc.].

Changes in the functional state of the adrenal cortex in decompensated toxic goiter are reduced to increased incretion of cortisol [Povolotskaya GM, PavlyukP. M., 1971; Bezverkhaya T. P., 1975; Markov VV, Bezverkhaya TP, 1976, etc.] and acceleration of its metabolism under the influence of thyroid hormones. As a result of the change in cortisol metabolism, more cortisone and tetrahydrocortisone are produced, which are biologically less active than cortisol. Due to the increased metabolism of corticosteroids, the deficiency of these hormones in the body is felt even when their synthesis is enhanced. Stressful situations (mental and physical stress, intoxication, etc.), contributing to the increased consumption of corticosteroids, lead with toxic goiter to the depletion of the reserve capacity of the adrenal cortex, which can result in a crisis and death.

The main factors in the development of thyrotoxic crisis S. Zografsky (1977) considers the insufficiency of the function of the adrenal cortex and increased production of adrenaline by the medulla. M. Goodkind et al. (1961), W. Ftirthaler (1965) pay special attention to the effect of catecholamines on metabolic processes in the myocardium. Yu. M. Mikhailov (1968) believes that not only a decrease in the potential reserve of the adrenal cortex, but also pronounced disturbances in the metabolism of corticosteroids in the periphery, probably as a result of an increased release of adrenaline under the influence of a stressful situation, play a role in the pathogenesis of a thyrotoxic crisis. Adrenaline, contributing to an increase in the consumption of corticosteroids by tissues, increases the relative insufficiency of the adrenal cortex.

In recent years, the state of the kallikrein-kinin system has been given a certain importance in the pathogenesis of the thyrotoxic crisis. It has been established that during a thyrotoxic crisis, the activity of proteolytic enzymes increases, the processes of fibrinolysis and the release of plasmin increase. It has been shown that plasmin activates the kallikrein-kinin system [Pavlovsky D.P., 1977]. As a result of a sharp increase in the activity of kallikrein, the tone of the sympathetic division of the autonomic nervous system increases, which causes an increase in the incretion of thyroid and other hormones. This, in turn, leads to further activation of the kallikrein-kinin system and increases the yield of free kinins [Fesenko V.P., Babalich A.K., 1978]. A sharp increase in the content of thyroid hormones in the blood, excessive production of catecholamines or an increase in the sensitivity of peripheral tissues and (or) beta-adrenergic receptors to their normal content, as well as a sharp deficiency of adrenal hormones lead to the development of functional and morphological disorders in various organs and systems.

Clinical manifestations of thyrotoxic crisis are due to the action of thyroid hormones, catecholamines and a sharp deficiency of adrenal hormones.

Excessive production of thyroid hormones leads to the activation of protein breakdown, resulting in a negative nitrogen balance. Excretion of nitrogen with urine, excretion of ammonia and uric acid increase. The content of residual nitrogen and nitrogen of amino acids increases in the blood. There is creatinuria. Due to prolonged excess intake of thyroid hormones into the blood, carbohydrate metabolism is disturbed. Thyroid hormones act on the beta cells of the islets of Langerhans, either directly or indirectly, causing their depletion. In the latter case, an increase in blood sugar occurs as a result of increased neoglucogenesis processes, increased absorption of glucose in the intestine, inhibition of its fixation in the liver in the form of glycogen, and increased glycogenolysis due to a sharp increase in the effect of catecholamines by thyroid hormones.

An excess of thyroid hormones and a deficiency of mineral corticoids lead to a violation of water-salt metabolism: the excretion of water, sodium, chlorides, and magnesium from the body increases. Along with this, the content of potassium, calcium and other electrolytes in the blood plasma increases, which leads to dehydration and hypotension. Under the influence of thyroid hormones in the body, the consumption of ascorbic acid increases, as a result of which its content in the blood plasma, liver and adrenal glands decreases. An excess of thyroid hormones, as well as their metabolic products (triiodothyroacetic acid), causes a violation of oxidative phosphorylation, which is one of the causes of muscle weakness and an increase in body temperature (due to large heat release). The central mechanisms (excitation of the hypothalamic centers) also contribute to a large extent to an increase in body temperature. As a result of the suppression of myocardial monoamine oxidase activity by an excess of thyroid hormones, its sensitivity to catecholamines increases, which leads to tachycardia, degenerative lesions of the heart muscle, the development of heart failure, and collapse.

Due to a deficiency of glucocorticoids in a thyrotoxic crisis, adynamia, phenomena of acute cardiovascular insufficiency, gastrointestinal disorders (diarrhea, abdominal pain, sometimes simulating acute diseases of the abdominal organs, etc.), a sharp decrease in the body's resistance to adverse factors ( trauma, intoxication, infections, etc.), increases the permeability of the vascular wall, etc.

Mineralocorticoid deficiency causes a violation of water-salt metabolism (hyponatremia, hypochloremia, hyperkalemia), which leads to dehydration and hypotension.

Due to a drop in the tone of arterial vessels, cardiac activity and blood supply to the brain are disturbed, which causes an increase in cardiovascular insufficiency and mental disorders (psychosis, twilight states, etc.). The pathogenesis of heart failure in toxic goiter is mainly due to overload of the heart as a result of changes in hemodynamics and a decrease in myocardial contractility. During a crisis, the functional reserves of the myocardium decrease even more, and blood flow to the heart increases due to an increase in the volume of circulating blood, which is the reason for the frequent development of acute heart failure. V. P. Ostrovsky (1964, 1970), A. A. Savchenko (1970), oxygen starvation of the body, mainly of the tissue type, is of great importance in the development of a thyrotoxic crisis.

Intoxication of the body with thyroid hormones and adrenaline, along with an increase in relative adrenal insufficiency, in the absence of timely and targeted treatment, ultimately leads to death.

Classification thyrotoxic crisis

There is no generally accepted classification of thyrotoxic crisis. Some authors [Pirogov A.I., 1963; Ryabov Yu. V., 1963; Sukhanov V.I., 1964; Narychev L. A., 1965, etc.], depending on the severity, there are

easy,
middle and
severe thyrotoxic crisis.

Mild thyrotoxic crisis body temperature rises to 38 ° C, tachycardia up to 100 beats per minute, sleep disturbance are noted. During a moderate crisis, body temperature reaches 38-39°C, tachycardia 120-140 beats per minute, patients are excited, complain of headache, insomnia. In a severe crisis, body temperature is above 38 ° C, tachycardia is 150-160 beats per minute, arrhythmia often occurs.

However, P. E. Ogiy and A. N. Lyulka (1973) consider the above signs of a thyrotoxic crisis mainly as a pre-crisis state (crisis background). When assessing the condition of patients during a crisis, they take as a basis the suddenness, intensity, duration and degree of reduction in blood pressure, as well as the psychomotor reaction. For the convenience of assessing the condition of patients in the postoperative period, these authors propose to divide the pre-crisis condition into mild, moderate and severe.

With a mild degree of pre-crisis state, body temperature up to 38 ° C, tachycardia up to 120 beats per minute, disturbing sleep. In a state of moderate severity, the body temperature reaches 39 ° C, tachycardia - 120-140 beats per minute, the patient is excited, complains of headache, sweating. In a severe pre-crisis state, body temperature is above 39 ° C, tachycardia is 140 or more beats per minute, pronounced psychomotor agitation, headache, excessive sweating are noted, the patient assumes a characteristic posture (divorced and half-bent lower limbs and upper limbs scattered to the sides).

P. E. Ogiy and A. N. Lyulka distinguish between moderate and severe thyrotoxic crisis, believing that there is no mild thyrotoxic crisis.

With a thyrotoxic crisis of moderate severity systolic pressure does not change or increases, diastolic pressure decreases to 6.6 kPa (50 mm Hg) (increase in pulse pressure), tachycardia is observed up to 120-140 beats per minute, body temperature reaches 38-40 ° C, the patient excited, insomnia and excessive sweating are noted, consciousness is preserved.

In severe thyroid storm systolic pressure drops to 9.3-8 kPa (70-60 mm Hg), and diastolic - up to 2.6 kPa (20 mm Hg) and even to zero, tachycardia 140 beats per minute or more, often arrhythmia, body temperature 40 ° C and above, weakness, severe headache, insomnia, twilight consciousness, periodic loss of consciousness, profuse sweating are noted.

It should be noted that despite the undoubted conventionality of the proposed classification, it is quite acceptable. The allocation by the authors of the pre-crisis state and the thyrotoxic crisis itself is justified, because it allows one to correctly and timely assess changes in the patient's condition in the postoperative period and apply reasonable and effective methods of treatment.

A. S. Efimov et al. (1982) distinguish between the actual thyrotoxic crisis and thyrotoxic coma.

Potemkin V.V. Emergency conditions in the clinic of endocrine diseases, 1984

Thyrotoxic crisis is a very dangerous manifestation of endocrine pathology that can lead to serious consequences. Such a phenomenon can occur in the absence of due attention to the chronic course of thyrotoxicosis, attempts to treat it on their own, or improper surgical treatment of goiter. A thyrotoxic crisis is dangerous to a person's life, if emergency measures are not taken to stop the attack. Only urgent professional medical care can save a person.

Thyrotoxic crisis is a critical condition of a person in the form of an acute manifestation of thyrotoxicosis in toxic goiter of a diffuse type with an avalanche-like increase in dangerous symptoms. A sharp exacerbation of the disease is caused by an unexpected significant increase in the production of thyroid hormones with the release of an excessive amount of them into the blood. Diffusion toxic goiter (Graves' disease) implies an increased production of hormones, but during a crisis, this one increases several times.

Critical conditions are characterized by the fact that a sudden increase in the level of thyroid hormones is accompanied by signs of adrenal pathology (adrenal insufficiency), increased activity of the sympathetic-adrenal system and parts of the central nervous system, and excessive production of catecholamines. The lack of hormones of the adrenal cortex is especially acute.

Most often, a thyrotoxic crisis occurs after a surgical operation aimed at eliminating diffuse goiter, as well as when using an excessive dose of radioactive iodine during the treatment of thyrotoxicosis. Pathology is generated by violations in the implementation of appropriate treatment - non-transfer of a person to a euthyroid state, i.e. lack of proper training to normalize hormonal levels through replacement therapy.

The critical development of the disease can also occur in the absence of treatment or the use of improper therapy. Launched chronic thyrotoxicosis can be brought to a crisis by the following reasons: stress, physical overload, traumatic effects, surgical operations on other organs with improper anesthesia, infectious diseases, childbirth and complicated pregnancy in women, certain diseases (gastroenteritis, pneumonia), taking certain medications. agents (insulin, glycosides, adrenomimetics), withdrawal of drugs after prolonged use. In some cases, a so-called spontaneous crisis is recorded, which manifests itself without visible provoking factors.

Crisis symptoms

The development of a thyrotoxic crisis occurs quickly - within a few hours (in rare cases, the duration of development can be 2-3 days). In the growth of the process, 2 main stages can be distinguished: the period of excitation and the phase of progression of cardiac pathologies. The first stage is associated with the activation of the sympathetic-adrenal system, and the second stage is associated with the attenuation of compensatory mechanisms.

Signs of a crisis are intensively manifested symptoms of a toxic goiter of a diffuse type with an avalanche-like increase. The following symptoms are characteristic: nausea, unstoppable vomiting, increased sweating, severe diarrhea leading to dehydration, muscle adynamia. Against this background, there is an indomitable fear of mortal danger.

The appearance of a person changes dramatically: a hyperemic face of a mask-like appearance with a pronounced state of horror, eyes wide open with rare blinking. The injured person occupies a specific posture: spreading the arms and legs to the side, with the legs half-bent at the knees. The skin is moist and hot to the touch. Rapid breathing is heard (this is a sign of suffocation).

Symptoms of disorders of the cardiovascular system are manifested in the form of severe tachycardia (above 190 beats per minute), atrial fibrillation, tachypnea. Acute heart failure often develops. An increase in blood pressure is determined by the severity of the attack. An increase in diastolic pressure indicates the development of heart failure.

Renal pathologies are clearly expressed in the form of a significant decrease in the frequency of urination, up to anuria (complete blocking of urine output). The critical condition is aggravated by acute hepatic atrophy.

The progression of the crisis leads to neurogenic and motor disorders. The following manifestations are possible: an acute form of psychosis, hallucinations and delirium, clouding of consciousness, followed by prostration and the onset of a coma. Mental lesions cause developing lethargy, loss of orientation in space, confusion.

Treatment and emergency care

When a thyrotoxic crisis occurs, it is important to take emergency measures to stop the process of releasing an excessive amount of hormones into the blood and to prevent the involvement of other organs in the process.
Further treatment is aimed at restoring the functions of the thyroid gland and adrenal glands, eliminating disorders in various body systems, and normalizing metabolic processes.

Emergency medical care for the manifestation of an attack includes the following activities:

The introduction of a water-soluble composition of Hydrocortisone (Solu-Cortef) by intravenous drip. You can prescribe other corticosteroids: Prednisolone, Dexamethasone. Mineralocorticoids are sometimes used: deoxycorticosterone acetate, Desoxycorton.

Infusion therapy is carried out to exclude dehydration of the body. Sodium-containing solutions are used. For uncontrollable vomiting, an injection of sodium chloride or metoclopramide is given.

Cardiovascular therapy is carried out using beta2-blockers (Inderal, Propranolol, Obzidan, Anaprilin. If there are contraindications to the use of these drugs, Reserpine is prescribed. Sedatives, oxygen therapy, inhibitors of proteolytic enzymes (Aprotinin) are also recommended.

In a coma and the risk of cerebral edema, Mannitol, Furosemide, a solution of magnesium sulfate are urgently introduced.

The introduction of antithyroid drugs based on thiouracil (Tiamazol, Mercazolil) or on the basis of methimazole (Favistan, Tapazol). With a severe development of the crisis, 1% Lugol's solution is administered intravenously (50-150 drops of sodium iodide per 1 liter of 5% glucose solution). In the future, the introduction of Lugol's solution is shown.

If the measures taken do not give a positive result, then hemosorption is carried out.

After the provision of urgent medical care, it is the turn of the treatment scheme to eliminate the consequences of the crisis. The program includes the following activities:

Reducing the level of thyroid hormones: thyreostatics (Merkazolil), iodine preparations, Lugol's solution are used.

Relief of adrenal pathologies. Corticosteroids are prescribed: Hydrocortisone, Prednisolone, Dexamethasone, DOXA oil solution (in severe cases).

Symptomatic and anticonvulsant therapy (eg beta-blocker Propranolol).

To block psychomotor agitation: Seduxena, Haloperidol.

To exclude dehydration, intoxication and electrolyte imbalance: drip injection of Hemodez, glucose solution, saline solution, Ringer's solution.

Elimination of the risk of developing heart failure (sympathomimetics - Dobutamine or Dopamine, Cocarboxylase.

Thyrotoxic crisis is a severe and very dangerous manifestation of endocrine pathology. At the first signs of this critical condition, urgent hospitalization and the adoption of urgent effective measures of drug exposure are necessary.

Thyrotoxic crisis is a severe, life-threatening condition of the patient, which is a complication of thyrotoxicosis that develops with diffuse toxic goiter (Graves' disease). The development of a thyrotoxic crisis can be fatal. Fortunately, thyroid storm is not common. On average, according to different authors, in a few percent of cases. May develop in severe Graves' disease. Graves' disease, or diffuse toxic goiter, is a disease of the thyroid gland, which is accompanied by the release of an excess amount of thyroid hormones into the blood: T 3 and T 4. In a thyrotoxic crisis, there is a sharp increase in the production of thyroid hormones, many times higher than normal, that is, there is severe thyrotoxicosis, which determines the severity and danger of this condition.

Causes of thyrotoxic crisis

As mentioned above, thyrotoxic crisis is a complication of diffuse toxic goiter. The cause of a thyrotoxic crisis is the lack of treatment or improper treatment of severe thyrotoxicosis.

The main cause of thyrotoxic crisis is the performance of operations related to the thyroid gland (complete or partial removal of the thyroid gland), as well as the treatment with radioactive iodine in patients with thyrotoxicosis without first achieving a normal hormonal status.

Before surgical treatment, as well as before treatment with radioactive iodine in patients with thyrotoxicosis, preparation is necessary: you must first achieve the so-called euthyroid state - a state in which thyroid hormones (T3 and T4) are within normal limits. This is achieved by prescribing special drugs - thyreostatics, which block the synthesis of an excess amount of hormones.

There are also factors that can contribute to the occurrence of a thyrotoxic crisis, such as: stressful situations, intense physical activity, any surgical treatment, various infectious diseases, exacerbation of severe chronic diseases, pregnancy, childbirth. All these factors, if a patient has severe thyrotoxicosis without adequate treatment, can provoke the development of a thyrotoxic crisis.

The patient is conscious. At the beginning of the development of the crisis, the patient is very excited, fussy, aggressive, psychosis may develop, then, on the contrary, the state of pronounced excitement may be replaced by apathy, inactivity, and severe weakness. There may be an intense headache.

A sign of thyrotoxic coma is a feeling of pronounced palpitations (heart rate increases to 200 beats per minute), the pulse is frequent, irregular. The development of arrhythmias is characteristic. The level of blood pressure rises. Breathing is rapid, shallow. Severe (profuse) sweating is noted. The skin is hot, red. Body temperature can rise to 40-41 degrees Celsius.

Nausea is characteristic, there may be vomiting, abdominal pain, loosening of the stool (diarrhea), jaundice may appear. In severe cases, there may be loss of consciousness, the development of coma.

Manifestations are associated with the fact that an excess of thyroid hormones has a damaging effect on the cardiovascular system, nervous system, and adrenal glands.

Diagnosis of thyrotoxic crisis.

The diagnosis is established on the basis of data on the presence of thyrotoxicosis in the patient, exacerbation of the symptoms of the disease after stressful situations, and surgical treatment. The characteristic clinic of thyrotoxic crisis, its acute onset is taken into account.

Laboratory diagnosis of the disease:

1. Increase in thyroid hormones: increase in T3 and T4
2. Decreased thyroid-stimulating hormone (TSH)
3. Decrease in cortisol - the hormone of the adrenal glands (as a result of a thyrotoxic crisis, damage to the adrenal glands occurs with the development of adrenal insufficiency)
4. There may be an increase in blood glucose levels
5. Thyrotoxicosis is characterized by a decrease in the level of cholesterol in the blood.

It is necessary to perform an ECG: tachycardia (increased heart rate), various types of arrhythmias are recorded. The development of atrial fibrillation (atrial fibrillation) is characteristic. These changes are associated with the cardiotoxic effect of excess thyroid hormones, that is, an increase in T3 and T4 in the blood has a damaging effect on the cardiovascular system.

On ultrasound of the thyroid gland: an increase in the size of the thyroid gland, an increase in the speed of blood flow in the tissue of the gland is determined.

Treatment of thyrotoxic crisis

Thyrotoxic crisis is a very dangerous, severe, life-threatening condition. Treatment is carried out only in a hospital in an intensive care unit. It is necessary to start treatment as early as possible. If a thyrotoxic crisis is suspected, emergency hospitalization is necessary. Lack of timely treatment threatens the life of the patient.

Treatment consists in prescribing thyreostatic drugs (for example, Tyrozol, Mercazolil), which block the synthesis of thyroid hormones, drugs of the beta-blocker group, which reduce the heart rate, palpitations, and are used to treat arrhythmias.

Glucocorticosteroid hormones are also used to treat advanced adrenal insufficiency. To reduce the symptoms of intoxication, infusions of a large amount of liquid, electrolytes are used.

With an increase in blood pressure numbers, antihypertensive drugs (drugs that lower blood pressure) are used.

If the patient is excited, in case of development of psychosis, tranquilizers are applied.

In case of high fever, antipyretics are used, cooling procedures are applied (wipe with alcohol solutions, ice packs can be used for cooling).

Thyrotoxic crisis is a severe, life-threatening condition. Immediate hospitalization required. Self-treatment, which can lead to the death of the patient, is extremely dangerous and unacceptable. From the auxiliary treatment in a hospital, it is possible to recommend the use of neurotropic vitamin preparations (preparations of B vitamins: Milgamma, Neuromultivit and others).

Complications of thyrotoxic crisis

The development of adrenal insufficiency, severe arrhythmias, progression of heart failure, which, if not treated in time, leads to the death of the patient.

Prevention of thyrotoxic crisis

Timely detection of signs of thyrotoxicosis is necessary. If surgical treatment of the thyroid gland is planned (resection or extirpation of the thyroid gland) or treatment with radioactive iodine is planned, preliminary treatment of thyrotoxicosis is necessary with the achievement of a normal level of thyroid hormones. Treatment of thyrotoxicosis is carried out with thyreostatics (Tyrozol, Mercazolil), which reduce the synthesis of thyroid hormones. Only after reaching euthyroidism is surgical treatment or treatment with radioactive iodine carried out.

Forecast of thyrotoxic crisis

Depends on how timely treatment is started. With timely adequate therapy, the prognosis is favorable. In the absence of treatment, the prognosis is poor.

Cancer consultation

Question: Why am I prescribed medication before surgery on the thyroid gland?
Answer: If a patient who is scheduled for thyroid surgery is in a state of thyrotoxicosis, preliminary drug treatment with thyreostatics is necessary until euthyroidism is achieved. Only after this is it possible to perform surgery to avoid a thyrotoxic crisis.

Question: If there is a suspicion of the development of a thyrotoxic crisis, is outpatient treatment possible?
Answer: No, treatment is possible only in the intensive care unit of a hospital, as this is a serious, life-threatening condition.

Doctor endocrinologist Artemyeva Marina Sergeevna

Thyrotoxic crisis is a complication of diffuse toxic goiter, which occurs as a result of a sudden sharp increase in the level of thyroid hormones in the blood. This condition is life-threatening for the patient, but fortunately, it is quite rare.

You will learn about why and how this pathology occurs, about its symptoms, the principles of diagnosis and treatment from our article.

Causes and mechanism of the development of the disease

The likelihood of developing a thyrotoxic crisis does not depend on how severe thyrotoxicosis is. It is almost impossible to predict this state.

The vast majority of crises occur after thyroid surgery or radioactive iodine treatment. It is believed that the stress that the body experiences during the operation provokes the release of a large amount of thyroxine and triiodothyronine into the blood, which is manifested by the corresponding symptoms. Radioactive iodine leads to a crisis in cases where the patient begins to receive therapy against the background of an increased level of thyroid hormones in the blood.

This pathology can be provoked by:

, mental trauma;
traumatic injury or surgery on any part of the body in a person suffering from thyrotoxicosis;
severe infectious diseases;
complications - or hypoglycemia;
unauthorized refusal to take thyreostatic drugs;
body load (including x-ray examinations of internal organs with contrast or taking iodine-containing drugs);
radiation therapy;
acute violation of cerebral circulation ();
thromboembolism, in particular pulmonary embolism;
rough palpation (palpation) of the thyroid gland;

The mechanism for the development of a thyrotoxic crisis includes 3 consecutive links:

1. Hyperthyroidism (in this case, an increased level of thyroxine and free triiodothyronine is determined in the blood).
2. Relative insufficiency of adrenal function (it is believed that there is an inverse relationship between the functioning of the thyroid gland and adrenal glands, therefore, a sharp increase in the level of thyroid hormones is accompanied by development; in addition, it is considered an autoimmune process).
3. Increased activity of the sympathoadrenal system (this is one of the mechanisms for mobilizing the defenses of any organism when exposed to psycho-emotional or other types of stress (including after surgery or in severe somatic pathology, including thyrotoxicosis); thyroid hormones increase tissue sensitivity to catecholamines).

All these processes determine the development of the clinical symptoms, which will be discussed in the next section.

Symptoms of pathology

In patients with thyrotoxicosis, excitation can be replaced by lethargy and impaired consciousness up to coma.

Clinical manifestations of thyrotoxic crisis are diverse. The main ones are:

labile psycho-emotional state of the patient (excitation, anxiety, which, when the condition worsens, are replaced by lethargy);
weakness, trembling in the muscles;
(patients complain of interruptions in the work of the heart, a feeling of fading, palpitations, and so on);
tachycardia (rapid heartbeat up to 120-200, and in severe cases up to 300 beats per minute);
(increased blood pressure), in the late stage - hypotension (as a result of dehydration);
headache and dizziness;
loss of appetite up to its complete absence;
nausea and vomiting;
expressed;
diffuse cramping pains in the abdomen;
yellowing of the skin and visible mucous membranes (this indicates stagnation in the liver of blood and significantly worsens the patient's prognosis for life and recovery);
stool disorders (diarrhea), contributing to the development of dehydration (dehydration) of the patient's body;
increase in body temperature to febrile values (39-40-41 ° C);
decrease in the frequency of urination up to a complete cessation (this condition is called "anuria");
disturbances of consciousness up to a coma.

There are symptoms of this pathology, as a rule, suddenly, however, some patients pay attention to the manifestations of the prodromal period - some aggravation of the signs of thyrotoxicosis.

At the initial stage of the crisis, patients notice an increase in body temperature, chills, palpitations, sweating. They become irritable and emotionally labile (their mood changes dramatically). If medical care is not provided at this stage, the symptoms of the pathology increase, and the patient's condition progressively worsens.

During a thyrotoxic crisis, 2 phases are distinguished:

subacute (lasts from the moment the first symptoms of pathology appear until the development of impaired consciousness);
acute (develops after 1-2 days, and in severe cases even faster - after 12-24 hours of illness; the patient falls into a coma, he develops insufficiency of the functions of many internal organs - the heart, adrenal glands, liver (this increases the likelihood of death)) .

Thyrotoxic crisis in the elderly

In this age group of patients, a thyrotoxic crisis may develop without pronounced clinical symptoms. Thyrotoxicosis is often not diagnosed in them. At the same time, against the background of a seemingly satisfactory condition, a person quietly goes into a coma and then dies.

To prevent the irreversible, it is still important to diagnose hyperthyroidism in the elderly and senile. There are clinical characteristics that will help to suspect thyrotoxicosis in such patients and refer them to the appropriate investigations:

age over 60;
calm facial expression, often apathetic;
slow reaction of a person to what is happening around him;
small goiter;
lean physique up to extreme emaciation;
muscle weakness;
drooping of the upper eyelid (blepharoptosis);
cardiovascular pathology (atrial flutter,); the dominance of these symptoms very often masks thyrotoxicosis; in this case, heart failure is usually resistant to standard therapy, its symptoms regress only when the patient begins to take drugs against thyrotoxicosis.

Diagnostic principles

The process of making a diagnosis includes:

collection by the doctor of the patient's complaints, anamnesis of his life and disease;
objective examination;
laboratory diagnostic methods;
instrumental research.

Let's consider each of the points in more detail.

Complaints and anamnesis

The rate of development of the disease matters - with a thyrotoxic crisis, the patient's condition worsens, one might say, before our eyes. It is also characterized by a connection with any surgical intervention (especially on the thyroid gland), trauma, severe somatic or infectious disease, treatment with iodine preparations.

Objective examination

By examining the patient, palpation (palpation), percussion (tapping) and auscultation (listening) of various organs, the doctor can detect the following changes characteristic of this pathology:

high body temperature in combination with severe sweating of the patient in the absence of data indicating infectious processes are the most characteristic symptoms of a thyrotoxic crisis that require the start of intensive treatment;
signs of damage to the central nervous system (changes in the psycho-emotional status of the patient, symptoms of dysmetabolic encephalopathy, impaired consciousness up to coma);
symptoms of damage to the digestive system (diffuse pain on palpation of the abdomen, yellowness of the skin and visible mucous membranes, an increase in the liver due to stagnation of blood in it and necrosis of hepatocytes);
signs of damage to the heart and blood vessels (cardiac arrhythmias, in particular, sinus tachycardia, atrial flutter, chronic heart failure, increased systolic ("upper") arterial
pressure; in the presence of symptoms such as vomiting, diarrhea, severe sweating, dehydration (dehydration) of the body occurs, resulting in a decrease in blood pressure, collapse; often this condition becomes the leading cause of death of the patient);
external signs (visually noticeable and palpable enlargement of the thyroid gland, bulging eyes (exophthalmos)).

Laboratory diagnostics

Studies are carried out in parallel with intensive therapy, since the patient does not have time to wait for test results - if he has symptoms of a thyrotoxic crisis, treatment should be started immediately.

As a rule, they carry out:

a clinical blood test (mostly, it is within the normal range; moderate leukocytosis (an increase in the level of leukocytes) can be detected with some shift of the leukocyte formula to the left, and with dehydration, signs of blood clotting);
determination of the level of thyroid hormones in the blood (free thyroxine and triiodothyronine are elevated; in some cases (in persons suffering from systemic connective tissue diseases or diabetes mellitus), the thyroxine level may not change - this condition is called low thyroxine syndrome);
biochemical analysis of blood (increased blood sugar level (despite the fact that the patient does not suffer from diabetes mellitus), protein globulin, calcium, AlAT, AsAT, bilirubin, alkaline phosphatase; prothrombin index, fibrinogen, total blood protein levels are reduced).

Methods of instrumental diagnostics

Of these, in the diagnosis of thyrotoxic crisis, only a 24-hour test for the absorption of radioactive iodine matters, the results of which in this pathology will be above the norm.

Auxiliary research methods that allow to establish the nature of damage to other organs are:

electrocardiography (ECG);
Ultrasound of the abdominal organs;
computed tomography and others.

The need for their implementation is determined individually, based on a specific clinical situation.

Differential Diagnosis

Since this disease is not characterized by any symptoms peculiar to it, but proceeds with many completely versatile clinical manifestations, it should be distinguished from a number of pathologies that may be accompanied by them. These are:

vascular crises;
heart failure of a different origin;
pneumonia;
spicy ;
psychoses of other etiology;
hepatic, diabetic, uremic coma;
periodic thyrotoxic paralysis;
malignant hyperthermia;
sepsis;
acute intoxication with certain drugs, including neuroleptics;
alcoholic delirium.

Principles of treatment

If a thyrotoxic crisis is suspected, the patient should be immediately hospitalized in the intensive care unit and intensive care unit. Treatment begins immediately, without waiting for laboratory confirmation of a preliminary diagnosis.

The patient may be prescribed:

Timely initiated adequate therapy of thyrotoxic crisis leads to stabilization of the patient's condition within a day after its onset. Continue treatment until the symptoms of the pathology finally regress. As a rule, this happens within 1-1.5 weeks.

Prevention measures

To reduce the risk of developing a thyrotoxic crisis, it is necessary for a person suffering from thyrotoxicosis.