Manifestations of thyrotoxic crisis. Thyrotoxic crisis: symptoms and treatment

Serious health problems begin with diseases of a small organ in the neck. Chronic goiter ailments lead to an enlargement of the thyroid gland. The extreme stage of complications is called thyrotoxic crisis. With this complication, the result of clinical symptoms is death in 20% of cases. At the time of acute manifestations of dangerous conditions, the patient requires urgent assistance and constant monitoring by medical personnel.

Difficulties in treating chronic organ diseases

A person experiences severe choking from excitement, allergic reactions, and it becomes difficult to swallow - this could be a thyrotoxic crisis. The relevance of the problem remains to this day: surgical treatment of the thyroid gland is not suitable. After organ removal, complications occur that require constant drug therapy for the rest of your life.

Not all doctors recommend surgical removal of the thyroid gland, and few specialists are able to perform such an operation. The small organ is part of the body's lymphatic system. If you remove a link from the chain of complex processes, the infection will be able to penetrate unhindered into the area 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 prescription of tablets and other medications is not able to compensate for the lost function of the organ. Patients with chronic diseases are at risk of developing a thyrotoxic crisis. If the body is predisposed to swelling of the tissues of the goiter area, patients and loved ones are advised to familiarize themselves with the principles of first aid during clinical conditions.

Ways to acquire complications

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

The main cause of the crisis is a lack of iodine in the body. Enlargement of the organ can occur during the active process of formation of connective tissue. Pathology occurs after a disruption of protein metabolism in the human body.

External manifestations in clinical cases

If your health begins to deteriorate with minor exertion, this may be a thyrotoxic crisis. Symptoms of the disease begin to manifest themselves clearly after taking iodine preparations or thyroid hormones. Let us highlight the main signs, after which you need to urgently be examined by an endocrinologist. If more than three symptoms are identified, 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:

A decrease in well-being occurs earlier compared to the previous state of the body.
The pulse often increases, exceeding 100 beats per minute.
There is increased excitability, irritation occurs due to every little thing.
The picture is complemented by an increase in pressure.
Unreasonable increase in body temperature of more than 3 degrees.
Dizziness, nausea, and vomiting appear.
Digestive system disorder.
Reduced breathing rate.

Procedure before the ambulance arrives

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

Let us highlight the main measures in case of complications:

Call emergency assistance.
Place the patient on his back and place a cushion under his neck.
In a stuffy room, you need to open the windows to facilitate the flow of fresh air into the patient’s lungs.
Before the doctors arrive, you can independently assess your condition: measure your pulse, blood pressure, and temperature. External conditions are recorded: skin moisture, facial pallor.
Questioning the patient helps to determine the moment of deterioration in health. But a person remains conscious during a thyrotoxic crisis.

How can you make your patient feel better on your own?

The acute phase of the disease is accompanied by kidney dysfunction. Therefore, giving medications in tablet form is pointless. 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 basic assistance to victims.

Let us highlight the main measures to normalize the condition:

If the body temperature is too high, which is often observed during a crisis, then resort to cooling the body. This slows down metabolic processes, inhibiting the harmful effects of hormones. The patient is placed in a cool bath. If there is none, remove all clothing. An alternative option is the following: apply several compresses to different parts of the body. Rubbing with alcohol solutions reduces the temperature.
The person is observed until the ambulance arrives. The tongue may become stuck in the larynx, causing suffocation.
Help drink as much clean liquid as possible to prevent dehydration.

What actions do doctors take?

If a thyrotoxic crisis occurs, emergency care includes the prescription of drugs that reduce the effect of thyroid hormones. These substances are actively produced by the thyroid gland when the organ’s functioning is disrupted. 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 provided by the results of an ECG examination. Deviations are set:

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

Drugs

Treatment of thyrotoxic crisis is necessary for any cause of critical illness. The following types of medications are used:

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

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

How to prevent the disease?

Preventive measures are taken to exclude the organism - thyrotoxic crisis. Emergency care, the algorithm of which is clearly stated in the instructions of the ambulance personnel, will be less painful, and irreversible consequences will not appear. Thus, 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 to prevent critical conditions. Doctors noted the predominance of the disease among women. Crisis in the weaker sex occurs 9 times more often than in men. A long-term complication can develop 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 severe forms of the disease. Thyrotoxic crisis is observed in 0.5-19% of cases, which is apparently due to different assessments of the patients’ condition.

Etiology and pathogenesis of thyrotoxic crisis

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 euthyroid state of the patient. In case of 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, traumatic surgery, intoxication, toxic infections, hyperthermia, diabetic ketoacidosis, physical activity, surgical intervention outside the thyroid gland ( tonsillectomy, cholecystectomy, tooth extraction, etc.), abrupt withdrawal of antithyroid drugs, toxicosis of pregnancy, even normal childbirth, reaction to adrenergic agonists, glycosides, insulin and other medications, etc. Most of these etiological factors of thyrotoxic crisis are intense irritants of the cortex adrenal glands, whose function was largely depleted before the crisis. In some cases, the cause of thyrotoxic crisis remains unknown (“spontaneous” crisis).

The pathogenesis of thyrotoxic crisis is not clear enough. Currently, most researchers believe that the main factors in the pathogenesis of thyrotoxic crisis are a sharp increase in the release of thyroid hormones into the blood, increased 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 postoperative thyrotoxic crisis is the result of complex and profound disturbances in the relationship between the central nervous system, the function of the pituitary gland and the adrenal cortex when the thyroid gland is removed.

It is believed that the trigger for a thyrotoxic crisis is a sharp increase in the level of thyroid hormones in the blood. The role of thyroid hormones in the development of thyrotoxic crisis was first pointed out in 1901 by A. Kocher. He associated the development of a postoperative crisis with intoxication of the body with thyroxine and wound secretions absorbed during surgery during resection of the thyroid gland. S. Cravetto et al. (1958), J. Nauman (1961) found that during a thyrotoxic crisis, the most significant level of SBI is observed in the blood, increasing 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 [Milku Sht., 1962], as a result of which thyroid hormones are intensively released into the blood. Cases of thyrotoxic crisis have been described when using 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 G. M., 1955; Krivitsky D.I., 1963; Milku Sht., 1962]. Conversely, during a thyrotoxic crisis there may be only a slight increase or 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 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 G.M., PavlyukP. M., 1971; Bezverkhaya T.P., 1975; Markov V.V., Bezverkhaya T.P., 1976, etc.] and acceleration of its metabolism under the influence of thyroid hormones. As a result of changes in cortisol metabolism, more cortisone and tetrahydrocortisone are produced, which are biologically less active than cortisol. Due to the increased metabolism of corticosteroids, a deficiency of these hormones in the body is felt even when their synthesis is increased. Stressful situations (mental and physical stress, intoxication, etc.), contributing to increased consumption of corticosteroids, lead to toxic goiter depleting the reserve capacity of the adrenal cortex, which can result in crisis and death.

S. Zografski (1977) considers the main factors in the development of thyrotoxic crisis to be insufficiency 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 influence of catecholamines on metabolic processes in the myocardium. Yu. M. Mikhailov (1968) believes that in the pathogenesis of thyrotoxic crisis, not only a decrease in the potential reserve of the adrenal cortex plays a role, but also pronounced disturbances in the metabolism of corticosteroids in the periphery, probably as a result of increased release of adrenaline under the influence of a stressful situation. Adrenaline, by increasing the tissue consumption of corticosteroids, increases the relative insufficiency of the adrenal cortex.

In recent years, the state of the kallikrein-kinin system has been given some importance in the pathogenesis of 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 intensify. It has been shown that plasmin activates the kallikrein-kinin system [Pavlovsky D. P., 1977]. As a result of a sharp increase in kallikrein activity, 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, excess production of catecholamines or increased 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 caused by the action of thyroid hormones, catecholamines and a sharp deficiency of adrenal hormones.

Excessive production of thyroid hormones leads to activation of protein breakdown, resulting in a negative nitrogen balance. The excretion of nitrogen in the urine and the excretion of ammonia and uric acid increase. The content of residual nitrogen and amino acid nitrogen increases in the blood. Creatinuria occurs. Due to prolonged excess intake of thyroid hormones into the blood, carbohydrate metabolism is disrupted. Thyroid hormones act on the beta cells of the islets of Langerhans, directly or indirectly causing their depletion. In the latter case, an increase in blood sugar occurs as a result of increased processes of neoglucogenesis, 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 mineralocorticoids lead to disruption 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, the consumption of ascorbic acid in the body increases, resulting in a decrease in its content in the blood plasma, liver and adrenal glands. An excess of thyroid hormones, as well as the products of their metabolism (triiodothyroacetic acid), causes a violation of oxidative phosphorylation, which is one of the causes of muscle weakness and increased body temperature (due to high heat generation). Central mechanisms (excitation of hypothalamic centers) also contribute to an increase in body temperature. As a result of the suppression of monoamine oxidase activity of the myocardium by excess 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 during a thyrotoxic crisis, adynamia, symptoms of acute cardiovascular failure, gastrointestinal disorders (diarrhea, abdominal pain, sometimes simulating acute diseases of the abdominal organs, etc.), and a sharp decrease in the body’s resistance to adverse factors occur. trauma, intoxication, infections, etc.), the permeability of the vascular wall increases, etc.

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

Due to a drop in arterial vascular tone, cardiac activity and blood supply to the brain are disrupted, which causes an increase in cardiovascular failure 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) attach great importance in the development of thyrotoxic crisis to oxygen starvation of the body, mainly of the tissue type.

Intoxication of the body with thyroid hormones and adrenaline, along with increased 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 degree of severity, they are distinguished

easy,
average and
severe thyrotoxic crisis.

For mild thyrotoxic crisis body temperature rises to 38°C, tachycardia up to 100 beats per minute, and sleep disturbances are noted. In a moderate crisis, the body temperature reaches 38-39°C, tachycardia 120-140 beats per minute, patients are excited, complaining of headaches and insomnia. In a severe crisis, the body temperature is above 38°C, tachycardia is 150-160 beats per minute, and arrhythmia often occurs.

However, P. E. Ogiy and A. N. Lyulka (1973) consider the above signs of 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 decrease 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 dividing the pre-crisis state into mild, moderate and severe.

With a mild degree of pre-crisis state, body temperature is up to 38°C, tachycardia is up to 120 beats per minute, and restless sleep. In a moderately severe condition, the body temperature reaches 39° C, tachycardia - 120-140 beats per minute, the patient is excited, complains of headache and sweating. In a severe pre-crisis state, the body temperature is above 39°C, tachycardia is 140 or more beats per minute, severe psychomotor agitation, headache, increased sweating are noted, the patient takes a characteristic pose (splayed and half-bent lower limbs and scattered upper limbs 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.

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

In severe thyrotoxic crisis systolic pressure decreases to 9.3-8 kPa (70-60 mm Hg), and diastolic pressure - 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, adynamia, severe headache, insomnia, twilight consciousness, periodic loss of consciousness, profuse sweating are noted.

It should be noted that despite the undoubted conventions of the proposed classification, it is quite acceptable. The authors’ identification of the pre-crisis state and the thyrotoxic crisis itself is justified, because it allows for a fairly correct and timely assessment of changes in the patient’s condition in the postoperative period and the use of reasonable and effective treatment methods.

A. S. Efimov et al. (1982) distinguish between thyrotoxic crisis itself 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. This phenomenon can occur in the absence of proper attention to the chronic course of thyrotoxicosis, attempts to treat it independently, or improper surgical treatment of goiter. Thyrotoxic crisis is dangerous for human life if emergency measures are not taken to stop the attack. Only urgent professional medical assistance can save a person.

Thyrotoxic crisis is a critical human condition in the form of an acute manifestation of thyrotoxicosis with diffuse-type toxic goiter 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 hormones by the thyroid gland with the release of excessive amounts of them into the blood. Diffusion toxic goiter (Graves' disease) implies increased production of hormones, but during a crisis this 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 shortage of adrenal hormones is especially acute.

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

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

The development of thyrotoxic crisis occurs quickly - within several hours (in rare cases, the duration of development can be 2-3 days). In the progression of the process, two 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 crisis are intensely manifested symptoms of toxic goiter of a diffuse type with an avalanche-like intensification. The following symptoms are typical: nausea, unstoppable vomiting, increased sweating, severe diarrhea leading to dehydration, muscle adynamia. Against this background, an indomitable fear of mortal danger arises.

The person’s appearance changes sharply: a hyperemic, mask-like face with a pronounced state of horror, eyes wide open with rare blinking. The injured person takes a specific position: spreading his arms and legs to the side, with his legs bent at the knees. The skin is moist and hot to the touch. You can hear rapid breathing (this is a sign of suffocation).

Symptoms of cardiovascular system disorders manifest themselves in the form of severe tachycardia (above 190 beats per minute), atrial fibrillation, and tachypnea. Acute heart failure often develops. The increase in blood pressure is determined by the severity of the attack. The development of heart failure is indicated by an increase in diastolic pressure.

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: acute form of psychosis, hallucinations and delusions, confusion of consciousness followed by prostration and the onset of a coma. Mental lesions cause developing lethargy, loss of spatial orientation, and confusion.

Treatment and emergency assistance

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

Emergency medical care in case of an attack includes the following measures:

Administration of the water-soluble composition of Hydrocortisone (Solu-Cortef) by intravenous drip. Other corticosteroids can be prescribed: Prednisolone, Dexamethasone. Mineralocorticoids are sometimes used: deoxycorticosterone acetate, deoxycortone.

Infusion therapy is carried out to prevent 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, and proteolytic enzyme inhibitors (Aprotinin) are also recommended.

In case of coma and risk of cerebral edema, Mannitol, Furosemide, and magnesium sulfate solution are urgently administered.

Administration of antithyroid drugs based on thiouracil (Thiamazol, Mercazolil) or based on methimazole (Favistan, Tapazol). In case of 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). Subsequently, the introduction of Lugol's solution is indicated.

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

After emergency medical care is provided, it is the turn of the treatment plan to eliminate the consequences of the crisis. The program includes the following activities:

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

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

Symptomatic and anticonvulsant therapy (for example, the beta blocker Propranolol).

To block psychomotor agitation: Seduxena, Haloperidol.

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

Eliminating 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 emergency effective medication measures 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 thyrotoxic crisis can be fatal. Fortunately, thyrotoxic crisis is not common. On average, according to various authors, in several 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 into the blood of an excess amount of thyroid hormones: T 3 and T 4. During a thyrotoxic crisis, there is a sharp increase in the production of thyroid hormones, many times higher than normal, that is, it occurs 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 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 treatment with radioactive iodine in patients with thyrotoxicosis without first achieving normal hormonal status.

Before surgical treatment, as well as before treatment with radioactive iodine in patients with thyrotoxicosis, preparation is necessary: one 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 excess amounts 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 the 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 a crisis, the patient is very excited, fussy, aggressive, psychosis may develop, then, on the contrary, a 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 and irregular. The development of arrhythmias is characteristic. Blood pressure levels increase. Breathing is rapid and shallow. Severe (profuse) sweating is noted. The skin is hot and red. Body temperature can rise to 40-41 degrees Celsius.

Nausea is typical, there may be vomiting, abdominal pain, loose stools (diarrhea), and jaundice may appear. In severe cases, loss of consciousness and coma may occur.

The manifestations are due to the fact that excess thyroid hormones have 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 symptoms of the disease after stressful situations, and surgical treatment. The characteristic clinical picture of thyrotoxic crisis and its acute onset are taken into account.

Laboratory diagnosis of the disease:

1. Increase in thyroid hormones: increase in T3 and T4
2. Decrease in thyroid-stimulating hormone (TSH)
3. Decrease in cortisol - a 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 blood cholesterol levels.

An ECG is necessary: 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.

Ultrasound of the thyroid gland: an increase in the size of the thyroid gland and an increase in the speed of blood flow in the gland tissue are 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 the development of a thyrotoxic crisis is suspected, emergency hospitalization in a hospital is necessary. Lack of timely treatment threatens the patient's life.

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

Glucocorticosteroid hormones are also used to treat developed adrenal insufficiency. To reduce the symptoms of intoxication, infusions of large amounts of fluid and electrolytes are used.

When blood pressure levels increase, antihypertensive drugs (drugs that lower blood pressure) are used.

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

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

Thyrotoxic crisis is a severe, life-threatening condition. Immediate hospitalization is required. Self-treatment is extremely dangerous and unacceptable, as it can lead to the death of the patient. As an auxiliary treatment in a hospital setting, 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 a timely manner, 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 (resection or extirpation of the thyroid gland) or treatment with radioactive iodine is planned, preliminary treatment of thyrotoxicosis is necessary to achieve normal levels of thyroid hormones. Treatment of thyrotoxicosis is carried out with thyreostatics (Tyrozol, Mercazolil), which reduce the synthesis of thyroid hormones. Only after achieving euthyroidism is surgical treatment or treatment with radioactive iodine performed.

Prognosis of thyrotoxic crisis

Depends on how timely treatment is started. With timely and adequate therapy, the prognosis is favorable. Without treatment, the prognosis is poor.

Consultation with a doctor

Question: Why am I prescribed medication before surgical treatment of 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, since this is a serious, life-threatening condition.

Endocrinologist Marina Sergeevna Artemyeva

Thyrotoxic crisis is a complication of diffuse toxic goiter, which occurs due to 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, its symptoms, principles of diagnosis and treatment from our article.

Causes and mechanism of disease development

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

The vast majority of cases of crisis occur after surgery on the thyroid gland or treatment with radioactive iodine. It is believed that the stress that the body experiences during surgery provokes the release of large amounts of thyroxine and triiodothyronine into the blood, which is manifested by corresponding symptoms. Radioactive iodine leads to a crisis in cases where the patient begins to receive therapy with it against the background of increased levels 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 medications);
radiation therapy;
acute cerebrovascular accident ();
thromboembolism, in particular pulmonary embolism;
rough palpation (palpation) of the thyroid gland;

The mechanism of development of thyrotoxic crisis includes 3 successively replacing each other 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 the adrenal glands, therefore, a sharp increase in the level of thyroid hormones is accompanied by the 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 thyrotosicosis); thyroid hormones increase the sensitivity of tissues to catecholamines).

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

Symptoms of pathology

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

The clinical manifestations of thyrotoxic crisis are varied. The main ones are:

labile psycho-emotional state of the patient (excitement, anxiety, which, when the condition worsens, is replaced by lethargy);
weakness, muscle tremors;
(patients complain of interruptions in the functioning of the heart, a feeling of it fading, palpitations, and so on);
tachycardia (rapid heart rate up to 120-200, and in severe cases up to 300 beats per minute);
(increased blood pressure), at a later stage - hypotension (as a result of dehydration);
headache and dizziness;
loss of appetite up to its complete absence;
nausea and vomiting;
expressed;
diffuse cramping pain in the abdominal area;
yellowing of the skin and visible mucous membranes (this indicates stagnation of blood in the liver 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);
reduction in the frequency of urination until complete cessation (this condition is called “anuria”);
disturbances of consciousness up to coma.

Symptoms of this pathology usually appear suddenly, but some patients also pay attention to the manifestations of the prodromal period - some worsening of the signs of thyrotoxicosis.

At the initial stage of the crisis, patients note an increase in body temperature, chills, palpitations, and 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, there are 2 phases:

subacute (lasts from the moment the first symptoms of the pathology appear until the development of disturbances of 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 category of patients, thyrotoxic crisis can develop without pronounced clinical symptoms. Thyrotoxicosis is often not diagnosed in them. At the same time, against the background of a seemingly satisfactory state, the person quietly goes into a coma and then dies.

To prevent the irreversible, it is still important to diagnose hyperfunction of the thyroid gland in elderly and senile people. There are clinical characteristics that will help to suspect thyrotoxicosis in such patients and refer them to appropriate studies:

age over 60 years;
calm facial expression, often apathetic;
slow human reaction to what is happening around him;
small goiter;
thin physique to the point of extreme emaciation;
muscle weakness;
drooping 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 diagnosis process includes:

collection by the doctor of the patient’s complaints, history of his life and illness;
objective examination;
laboratory diagnostic methods;
instrumental studies.

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

Complaints and anamnesis

The rate of development of the disease matters - during 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, requiring the initiation of intensive treatment;
signs of damage to the central nervous system (changes in the patient’s psycho-emotional status, symptoms of dysmetabolic encephalopathy, disturbances of consciousness up to coma);
symptoms of damage to the digestive organs (general pain on palpation of the abdomen, yellowness of the skin and visible mucous membranes, enlargement of 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 blood pressure
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 and collapse; often this condition becomes the leading cause of death of the patient);
external signs (visually noticeable and palpably detectable enlargement of the thyroid gland, bulging eyes (exophthalmos)).

Laboratory diagnostics

Research is 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:

clinical blood test (basically, it is within the normal range; moderate leukocytosis (increased level of leukocytes) with a slight shift in the leukocyte formula to the left can be detected, and in case of dehydration, signs of blood thickening);
determination of the level of thyroid hormones in the blood (free thyroxine and triiodothyronine are increased; 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 blood test (increased blood sugar level (even though the patient does not suffer from diabetes), globulin protein, calcium, ALT, AST, bilirubin, alkaline phosphatase; decreased prothrombin index, fibrinogen level, total blood protein).

Instrumental diagnostic methods

Of these, only a 24-hour radioiodine absorption test is important in the diagnosis of thyrotoxic crisis, the results of which in this pathology will be higher than normal.

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

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

The need for them is determined individually, based on the specific clinical situation.

Differential diagnosis

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

vascular crises;
heart failure of another origin;
pneumonia;
spicy ;
psychoses of other etiologies;
hepatic, diabetic, uremic coma;
periodic thyrotoxic paralysis;
malignant hyperthermia;
sepsis;
acute intoxication with certain medications, including antipsychotics;
alcoholic delirium.

Principles of treatment

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

The patient may be prescribed:

Timely initiation of adequate therapy for thyrotoxic crisis leads to stabilization of the patient’s condition within a day after its onset. Treatment is continued until the symptoms of the pathology completely regress. As a rule, this happens within 1-1.5 weeks.

Prevention measures

To reduce the risk of developing a thyrotoxic crisis, a person suffering from thyrotoxicosis needs.