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 is a severe, life-threatening complication that occurs in patients with diffuse toxic goiter. It is rare in children. Etiology. Most often, thyrotoxic crisis develops as a complication after strumectomy in the postoperative period, if the operation is performed without achieving compensation for the disease. A crisis can occur with undiagnosed toxic goiter (or insufficiency of its treatment) under the influence of provoking factors (infections, purulent inflammatory diseases, intoxication, mental and physical trauma, extrathyroidal operations, insufficient pain relief, abrupt cancellation of thyreostatic therapy, reaction to certain drugs, etc.) . It develops more often in the summer. Pathogenesis. The main pathogenetic factors of thyrotoxic crisis, according to most researchers, are a significant increase in the level of thyroid hormones, an increase in adrenal insufficiency, a sharp increase in the activity of the higher parts of the central nervous system, the hypothalamic-pituitary and sympathetic-adrenal systems. A sharp increase in the secretion of thyroid hormones leads to an increase in oxidative processes in the body, activation of the catabolism of proteins, fats, glycogen; glucose production increases, water-salt metabolism is disturbed, which is accompanied by a loss of water, sodium chloride, calcium, phosphorus, and potassium. Along with this, the accumulation of energy (adenosine triphosphate) in the cell decreases. To make up for the missing energy, the metabolic processes in the body, the functions of organs and systems increase even more. The influence of any stressful effect on the background of hyperactivity of the higher parts of the nervous, hypothalamic-pituitary and sympathetic-adrenal systems, severe metabolic disorders, relative insufficiency of the adrenal glands in diffuse toxic goiter, dysfunctions of organs and systems, especially cardiovascular, for a long time in a state of functional stress, can lead to the development of a thyrotoxic crisis. Clinic. Thyrotoxic crisis is characterized by a sharp exacerbation of all symptoms of diffuse toxic goiter, an acute onset. After strumectomy, the crisis develops in the first 1-2 days, sometimes within the first hours. Appear nausea, indomitable vomiting, leading to dehydration, profuse sweating, mental and motor agitation, insomnia, fear of death, headache, pain in the wound, ears, teeth. The skin is hyperemic (cyanotic), hot, moist, then becomes dry. Tissue turgor is reduced. Visible mucous membranes are dry, red. Frequent and deep breathing, up to 40-60 in 1 min. Body temperature rises to 39-40 ° C and above. Tachycardia up to 160-180 in 1 min, arrhythmia (extrasystole, atrial fibrillation). The pulse is weak, labile, pulse pressure is increased, then decreases. Muscular adynamia, violation of the act of swallowing, choking, dysarthria. With the predominance of the phenomena of adynamia, the patient's face is mask-like, with an expression of horror, sharply hyperemic. Widely opened palpebral fissures, rare blinking, corners of the mouth are lowered. With the further development of the crisis, there is a sharp excitement (up to psychosis), hallucinations, delirium, followed by lethargy and complete loss of consciousness. Hyperthermia above 41 ° C, tachycardia up to 200 beats per minute, severe hypotension, respiratory failure, weakness. Reflexes fade. Diuresis is reduced to anuria. The cause of death is mainly acute cardiac, adrenal or liver failure. Children are characterized by a milder form of thyrotoxic crisis: symptoms of damage to the nervous system, a marked increase in body temperature, and dyspeptic disorders predominate, while cardiovascular disorders are less pronounced. Clinical manifestations are of primary diagnostic value, since thyrotoxic crisis requires immediate therapy. Of the laboratory studies carried out in parallel with the therapy of a crisis, the most informative are the level of thyroid hormones and the concentration of protein-bound iodine, which increase significantly during a thyrotoxic crisis. Of auxiliary importance are hypocholesterolemia, leukocytosis, hyperglobulinemia with hypoproteinemia, transient glucosuria, creatinuria, hypokalemia, and an increase in urobilinogen release. Thyrotoxic crisis is differentiated with cardiovascular insufficiency in patients with thyrotoxicosis, and also, due to a number of similar symptoms, with diabetic, uremic, hepatic coma. A characteristic clinical picture and specific laboratory parameters play a decisive role in the diagnosis of a thyrotoxic crisis. Treatment of a thyrotoxic crisis should be carried out immediately and should be aimed at lowering the level of thyroid hormones in the blood, stopping adrenal insufficiency, eliminating cardiovascular and neurovegetative disorders, dehydration, hypoxia, and hyperthermia. In order to reduce the flow of thyroid hormones into the blood, 1% Lugol's solution is injected intravenously, in which potassium is replaced by sodium, - 100-250 drops in 300-800 ml of 5% glucose solution or 5-10 ml of 10% sodium iodide solution every 8 hours (B . G. Baranov, V. V. Potin, 1977). Lugol's solution is also administered through a probe into the stomach, in a microclyster or, in the absence of vomiting, orally in milk, 20-25 drops 3 times a day. Along with Lugol's solution, Mercazolil is prescribed in a loading dose - up to 60 mg / day, one hour before the administration of iodine preparations, in order to avoid the accumulation of iodine in the thyroid gland. The drugs can be dissolved in 100-150 ml of 5% glucose and administered through a tube. From the 2-3rd day, Mercazolil is given at a dose of 10-20 mg 3 times a day in combination with Lugol's solution (20 drops each). To stop adrenal insufficiency, intravenous glucocorticoids (2-5 mg / kg of body weight according to prednisolone) and DOK.SA (0.5 mg / kg / day) are prescribed intramuscularly. When the condition improves, glucocorticoids are administered intramuscularly, reducing the dose. In order to reduce the toxic effect of thyroid hormones, to eliminate neurovegetative disorders, P-blockers are used (Inderal - 0.5 mg / kg of body weight), sympatholytic agents (rausedil - 0.1 ml / year of life, 0.1% solution; reserpine - 0.1 mg 4 times a day). The introduction of sedative and neuroplegic agents is recommended. With severe psychomotor agitation, chlorpromazine is used (1-2 mg / kg of weight of a 2.5% solution intramuscularly or intravenously), droperidol (0.5 mg / kg of weight intramuscularly). One of the urgent tasks is to combat disorders of cardiovascular activity (cardiac glycosides, isoptin, papaverine, cocarboxylase, panangin, diuretics, etc.). To eliminate dehydration, infusion therapy is carried out by intravenous drip injection of 5% glucose solution, isotonic sodium chloride solution. Correction of pronounced microcirculatory disorders is carried out by introducing solutions of albumin, gelatinol, rheopolyglucin, plasma. At the same time, measures are being taken to replenish the loss of electrolytes and normalize the acid-base state. With repeated vomiting, a 10% solution of sodium chloride (10-20 ml) is injected intravenously. To reduce hyperthermia, lytic mixtures are used, wrapping the body with ice bubbles (head, heart area, inguinal region, lower limbs), cooling with fans (at low air temperature in the room). Constantly provide humidified oxygen. With cerebral edema, intravenous administration of a 40% glucose solution, intramuscular administration of a 25% solution of magnesium sulfate (0.2 ml / kg of weight) are indicated. Apply B vitamins (thiamine, pyridoxine, cyanocobalamin), ascorbic acid, antihistamines, antibiotics. It is necessary to replenish the body's energy costs (except for intravenous administration of plasma, plasma substitutes) by the intake of nutrient solutions through a nasal probe. While swallowing, they give easily digestible food (kissels, juices, sweet drinks, etc.). The patient should be provided with physical and mental rest, everything necessary for intubation, artificial lung ventilation, defibrillation, chest compressions should be prepared. It is necessary to monitor the condition of vital organs and systems. Treatment of thyrotoxic crisis is carried out until the complete elimination of clinical and metabolic manifestations (at least 7=10 days). If the condition does not improve within 2 days, exchange hemotransfusion, plasmapheresis, or peritoneal dialysis are recommended. After leaving the coma, continue treatment with Mercazolil, Reserpine. The prognosis for thyrotoxic crisis is determined by the timeliness of diagnosis and treatment. Despite complex intensive therapy, the mortality rate is high (at least 25%).

Thyrotoxic crisis is an acute condition that develops against the background of thyrotoxicosis with. A crisis occurs quite rarely, mainly in patients with a severe form of the disease or with improper treatment of goiter.

Causes

Thyrotoxic crisis occurs with a sharp increase in: thyroxine and triiodothyronine. However, a similar high level of hormones is observed in normal thyrotoxicosis. It turns out that this is not the only condition for the development of a crisis.

According to modern medical concepts, adrenal insufficiency and an increase in the activity of the sympathetic nervous system also play a significant role in the development of a crisis.

As a rule, the crisis develops after surgery to remove the gland or radioiodine therapy. Surgical intervention, as well as treatment with radioactive iodine, should be carried out only after the patient has achieved a medical condition, that is, a normal level of thyroid hormones in the blood. Failure to comply with these conditions can lead to a crisis. Much less often, a thyrotoxic crisis develops simply against the background of severe diffuse toxic goiter.

There are certain factors that contribute to the development of a crisis:

infectious diseases;
Psycho-emotional;
Any surgical intervention;
Injuries;
Existing somatic diseases;
Pregnancy and childbirth.

Symptoms of a thyrotoxic crisis

Thyrotoxic crisis develops rapidly within a day, and sometimes within a few hours. The earliest signs of a crisis are disorders of the nervous system. A person becomes restless, anxious, tearful, mood swings are noted,. There may be more severe mental disorders up to psychosis or impaired consciousness.

Damage to the heart manifests itself in the form, blockades,. The patient's heart rate can reach two hundred beats per minute. An increase in body temperature and sweating are also characteristic.

Often patients with a crisis complain of muscle weakness, which makes it difficult for them to make any movements. At the same time, there is a pronounced tremor of the limbs. In addition, there are symptoms of damage to the digestive tract. Often there are, with, abdominal pain.

Important! Thyrotoxic crisis may be complicated or. These conditions are life threatening.

Diagnostics

The diagnosis is determined on the basis of the clinical picture of the pathological condition, as well as the anamnesis (the presence of diffuse toxic goiter, surgery on the gland).

The following studies can help in the diagnosis of a thyrotoxic crisis:

Treatment of thyrotoxic goiter

Thyrotoxic crisis is a real threat to the life of the patient. Therefore, if symptoms of this pathological condition occur, it is necessary to take the patient to the hospital.

When treating a crisis, the doctor pursues the following goals:

Maintaining the basic functions of the body;
Inhibition of the synthesis and release of thyroid hormones;
Reducing the effect of thyroid hormones on target organs;
Identification and subsequent elimination of the provoking factor.

Maintenance of basic bodily functions

As a result of excessive sweating, vomiting, diarrhea, the patient has a significant, which is fraught with dangerous consequences. To correct this condition, the patient is injected intravenously with a large volume of fluids and electrolytes.

Treat with antiarrhythmic drugs, and congestive heart failure with diuretics and cardiac glycosides. To combat progressive adrenal insufficiency, glucocorticosteroids are prescribed.

Inhibition of synthesis and release of thyroid hormones

To suppress the synthesis of thyroid hormones, antithyroid drugs are prescribed (Mercazolil, Tyrozol). Initially, a large dose of the drug is prescribed, in the following days the dose is gradually reduced. The drug begins to act after an hour. However, the desired therapeutic effect can be achieved only after a few days.

Slowing down the release of hormones can be achieved by the introduction of iodine preparations. These medications may be given by your doctor as oral drops or as an intravenous infusion.

Reducing the effect of thyroid hormones on target organs

To eliminate heart palpitations, arrhythmias, anxiety, psycho-emotional arousal, beta-blockers (Propranolol) are used. The positive effect of the drug is observed already ten minutes after administration. To stop psycho-emotional arousal, the patient is prescribed tranquilizers.

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 if emergency care is not provided.

Causes of thyrotoxic crisis

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 period. Pathology is generated by violations in the implementation of appropriate treatment - the lack of proper training to normalize hormonal levels through replacement therapy.

Factors that can trigger the development of a thyrotoxic crisis:

nervous tension;
physical fatigue;
intercurrent infections and intoxications;
surgical interventions;
tooth extraction;
the introduction of radioactive iodine, resulting in the breakdown of thyroid follicles;
exposure to the thyroid gland of x-rays.

Thyrotoxic crisis: symptoms and signs

The development of a thyrotoxic crisis occurs quickly - within a few hours (in rare cases, the duration of development can be 2-3 days). There are 2 main stages in the growth process:

period of excitation: associated with the activation of the sympathetic-adrenal system
phase of progression of cardiac pathologies: associated with the attenuation of compensatory mechanisms.

Against the background of the classical clinical picture of toxic goiter (bulging eyes, goiter, tremor, tachycardia), patients experience:

increase in excitement;
rise in body temperature to 39-41 degrees;
there is a sharp headache;
anxiety, ;
tachycardia 140-200 beats per minute;
possible atrial fibrillation;
rise in blood pressure;
shortness of breath, shortness of breath with the possible development of pulmonary edema;
nausea, vomiting, profuse diarrhea;
severe muscle weakness;
it is possible to develop dehydration with the patient falling into stupor and coma.

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.

Forecast

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

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.

Crisis diagnostics

The diagnosis is determined on the basis of the clinical picture of the pathological condition, as well as the anamnesis (the presence of diffuse toxic goiter, surgery on the gland).

Laboratory diagnosis of the disease:

Increase in thyroid hormones: increase in T3 and T4
Decreased thyroid stimulating hormone (TSH)
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)
There may be an increase in blood glucose levels
Thyrotoxicosis is characterized by a decrease in the level of cholesterol in the blood.

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.

Treatment

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.

When treating a crisis, the doctor pursues the following goals:

Maintaining the basic functions of the body;
Inhibition of the synthesis and release of thyroid hormones;
Reducing the effect of thyroid hormones on target organs;
Identification and subsequent elimination of the provoking factor.

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.

First aid before the doctor arrives

A thyrotoxic crisis requires emergency care even before the patient is admitted to the hospital. It should begin before the arrival of the doctor:

the victim should be laid down;
create conditions for access to fresh air;
measure pressure;
determine the frequency of pulse and respiration;
to measure the temperature;
note the condition of the skin (humidity, color);
if possible ask about the time of urination (kidney condition).

Since the symptoms of fever are pronounced during a thyrotoxic crisis, cooling will be an important task of first aid:

do not use salicylates (aspirin) to combat fever;
the patient must be freed from warm clothing;
if possible put in a cool bath;
pack with ice packs: head, neck, chest, stomach;
rub the skin with ethyl alcohol, alcohol or acetic solution;
in the cold season, open the window, cover the patient with snow (packed in bags);
you can cover the patient with a wet sheet, spray with cold water;
continue cooling until the ambulance arrives.

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.

The crisis is dangerous to human life, if you do not take emergency measures to stop the attack.

Algorithm of actions (emergency care) for thyrotoxic crisis:

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

After providing first aid for a thyrotoxic crisis and stabilizing the patient's condition, the tactics of therapy are selected depending on the specifics of the clinical picture.

To reduce the risk of developing a thyrotoxic crisis, a person suffering from thyrotoxicosis should:

receive adequate therapy for the underlying disease; avoid any kind of stress;
avoid intense physical activity;
be attentive to your health, receive adequate therapy for all concomitant diseases.

Thyrotoxic crisis is an extremely life-threatening complication of thyrotoxicosis, which, fortunately, is quite rare these days.

Thyrotoxic crisis: clinic, differential diagnosis, prognosis. Causes, symptoms and principles of treatment of thyrotoxic crisis Thyrotoxic crisis is accompanied by

Thyrotoxic crisis (thyroid crisis) is a rare urgent complication of hyperthyroidism, in which the manifestations of thyrotoxicosis increase to a life-threatening degree. Thyrotoxic crisis is most commonly seen in patients with moderate to severe preexisting Graves' disease and is usually triggered by some form of stress. Thyrotoxic crisis is suspected and treated based on clinical impression due to the absence of pathognomonic features or any confirmatory tests.

What provokes a Thyrotoxic crisis (thyroid crisis):

Thyrotoxic crisis is usually preceded by surgery for hyperthyroidism. The frequency of surgically caused crisis has decreased significantly in recent years due to the use of antithyroid drugs and iodine preparations in the treatment and preoperative preparation of patients with hyperthyroidism. Currently, thyrotoxic crisis most often occurs for iatrogenic reasons. According to the available data, thyrotoxic crisis occurs in 1-2% of patients hospitalized for hyperthyroidism.

A risk factor for thyroid storm is unrecognized or untreated hyperthyroidism. Dobyns states that true thyroid storm occurs only in Graves' disease (diffuse toxic goiter), the most common cause of hyperthyroidism. Other authors report intoxication of multinodular goiter as a precursor (provocative) factor of thyrotoxic crisis. The distribution of the frequency of thyrotoxic crisis among both sexes is the same as in Graves' disease: in women, thyrotoxic crisis is observed 9 times more often than in men.

The duration of uncomplicated thyrotoxicosis preceding the onset of a crisis varies from 2 months to 4 years. Patients with a thyroid crisis have symptoms of hyperthyroidism for less than 2 years. An accurate prediction of the development of thyrotoxicosis in a particular patient is impossible due to the absence of predisposing factors associated with age, sex or race.

Provoking factors of thyrotoxic crisis
Many different factors have been described as triggers. The most common cause of a crisis is a surgical operation on the thyroid gland in the treatment of hyperthyroidism. Modern preoperative preparation of the patient significantly reduces this complication, but does not exclude its occurrence. Other surgical factors that have been shown to precipitate a thyroid crisis include non-thyroid surgery and ether anesthesia.

Medical causes of thyrotoxic crisis are numerous and currently prevail over surgical ones. The most common provoking factor of thyrotoxic crisis is infection, especially bronchopulmonary. In diabetic patients, the thyrotoxic crisis is provoked by ketoacidosis, hyperosmolar coma, and insulin-induced hypoglycemia. Factors that increase the level of circulating thyroid hormones contribute to the occurrence of a thyrotoxic crisis in sensitive patients; they include the following: premature withdrawal of antithyroid drugs; the introduction of radioactive iodine; the use of iodine-containing contrasts in x-ray examination; thyroid hormone poisoning; the use of a saturated solution of potassium iodide in patients with non-toxic goiter; rough palpation of the thyroid gland in patients with thyrotoxicosis. Additional factors associated with the development of a crisis include cerebrovascular accident, embolism in the pulmonary artery system, toxicosis of pregnant women and emotional stress. Finally, hospitalization associated with rough diagnostic procedures can lead to a crisis.

Pathogenesis (what happens?) during Thyrotoxic crisis (thyroid crisis):

The exact pathogenetic mechanisms of thyrotoxic crisis have not been determined. The explanation of its occurrence by excess production or secretion of thyroid hormones seems very attractive. The results of the study of thyroid function show its increase during a crisis in the vast majority of patients, however, the degree of this increase does not differ significantly from that observed in uncomplicated thyrotoxicosis. It has been suggested that the cause of the thyrotoxic crisis is an increase in the level of free triiodothyronine (T3) or free thyroxine (T4). However, a crisis is also observed in the absence of an increase in T3 or T4. Apparently, the occurrence of a crisis, in addition to an excess of the amount or form of thyroid hormones, must be influenced by something else.

It has been suggested that adrenergic hyperactivity is due either to sensitization of the patient to thyroid hormones or to a violation of the interaction between thyroid hormones and catecholamines. In a thyroid crisis, the plasma levels of adrenaline and norepinephrine do not increase. One of the authors proposes an explanation for the thyrotoxic crisis by the existence in the heart of two different adenylcyclase systems, one of which is sensitive to adrenaline, and the other to thyroid hormones. Further studies are needed to elucidate the role of catecholamines in the pathogenesis of thyroid storm.

According to another theory, the pathogenesis of thyroid storm is based on a change in the peripheral response to the action of thyroid hormone, which leads to increased lipolysis and excessive heat production. According to this theory, excessive lipolysis, due to the interaction of catecholamines and thyroid hormones, leads to excessive production of thermal energy and an increase in temperature. Ultimately, the body's tolerance to the effects of thyroid hormones is depleted, which leads to "decompensated thyrotoxicosis." This theory is the most stable; more importance here is given to a change in the response to thyroid hormones, and not to a sudden increase in their concentration in the blood.

Symptoms of Thyrotoxic crisis (thyroid crisis):

Symptoms and signs of a thyrotoxic crisis usually occur suddenly, but a prodromal period is also possible here with a barely noticeable increase in the manifestations of thyrotoxicosis.

The earliest signs of a thyrotoxic crisis are fever, tachycardia, sweating, CNS hyperexcitability, and emotional lability. In the absence of treatment, a hyperkinetic toxic state develops with an intensification of symptoms. Progression to congestive heart failure, refractory pulmonary edema, circulatory collapse, coma, and death may occur within 72 hours.

The increase in body temperature ranges from 38 ° to 41 ° C. The pulse rate is usually 120-200 beats / min, but in some cases it reaches 300 beats / min. Sweating may be profuse, leading to dehydration due to insensible fluid loss.

In 90% of patients with a thyrotoxic crisis, a CNS disorder is observed. Symptoms are highly variable - from lethargy, anxiety and emotional lability, manic behavior, excessive arousal and psychosis to confusion, stupefaction and coma. There may be extreme muscle weakness. Sometimes there is thyrotoxic myopathy, usually affecting the proximal muscles. In severe forms, the distal muscles of the extremities, as well as the muscles of the trunk and face, may be involved. Approximately 1% of patients with Graves' disease develop "myasthenia gravis", creating serious diagnostic difficulties. The response of thyrotoxic myopathy to edrophonium (tensilon test) is incomplete, in contrast to the complete response observed in myasthenia gravis. Patients with thyrotoxicosis may also have hypokalemic periodic (paroxysmal) paralysis.

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

Most patients with thyroid storm develop gastrointestinal symptoms. Before the onset of a thyrotoxic crisis, there is usually a weight loss of more than 44 kg. Diarrhea and hyperdefecation seem to herald the onset of a thyroid storm and may be severe, contributing to dehydration. In a thyrotoxic crisis, there is often anorexia, nausea, vomiting, and cramping abdominal pain. Jaundice and painful hepatomegaly due to passive hepatic congestion or even hepatic necrosis have been reported. The occurrence of jaundice is a poor prognostic sign.

Apathetic thyrotoxicosis- this is a rare, but clinically well-defined form of thyrotoxicosis; it is usually seen in the elderly and often goes undiagnosed. Thyrotoxic crisis in such patients may develop without the usual hyperkinetic manifestations, while they may quietly fall into a coma and die. There are a number of clinical features of apathetic thyrotoxicosis that may help in the diagnosis. As a rule, this is a patient over 60 years old, with lethargy, slow reaction and a calm, even apathetic face. A goiter is usually present, but may be small and multinodular. The usual ocular symptoms of thyrotoxicosis (exophthalmos, dilated palpebral fissure, and lagophthalmos) are absent, but blepharoptosis (drooping of the upper eyelid) often occurs. There is extreme emaciation and weakness of the proximal muscles. Symptoms in such patients, as a rule, have a longer prescription than in patients with the usual form of thyrotoxicosis.

"Masked" thyrotoxicosis is observed when the symptoms associated with the dysfunction of any one organ system dominate, masking the previous thyrotoxicosis. In patients with apathetic thyrotoxicosis, thyrotoxicosis is often masked by signs and symptoms associated with the cardiovascular system. Such patients often present to the ED with atrial fibrillation or congestive heart failure. According to one observation, thyrotoxicosis was not suspected in any of the 9 patients due to the dominance of cardiovascular symptoms. Congestive heart failure in such cases may be refractory to conventional therapy until treatment for thyrotoxicosis is initiated.

The pathogenesis of an apathetic response to thyrotoxicosis is unclear. Age is not a determining factor here, since apathetic thyrotoxicosis has also been described in children. The physician must maintain a high degree of suspicion for apathetic thyrotoxicosis. Every elderly patient with a small goiter and any of the above symptoms and signs may have this form of thyrotoxicosis.

Diagnosis of Thyrotoxic crisis (thyroid crisis):

Thyrotoxic crisis is diagnosed purely clinically due to the lack of laboratory methods to distinguish it from thyrotoxicosis. Although the clinical presentation of thyroid storm is highly variable, there are a number of guidelines to help make this diagnosis. Most patients with thyroid storm have a history of hyperthyroidism, ophthalmologic signs of Graves' disease, elevated pulse pressure, and palpable enlargement of the thyroid gland (goiter). However, in some cases, the history is not available and the usual signs of Graves' disease are absent, including overt goiter, which is absent in almost 9% of patients with Graves' disease.

Common diagnostic criteria for thyroid storm are as follows: body temperature above 37.8 ° C; significant tachycardia, inappropriate to the degree of temperature rise; dysfunction of the central nervous system, cardiovascular or digestive system; excessive peripheral manifestations of thyrotoxicosis. Some authors consider fever, accompanied by disproportionate tachycardia, almost the only sign of a thyrotoxic crisis. It should be noted, however, that the diagnosis of thyroid storm requires more than just fever in a patient with hyperthyroidism.

There are no laboratory tests to confirm the diagnosis of thyroid storm. Serum levels of T3 and T4 are usually elevated, but not to such an extent that this indicator can be used to make a differential diagnosis between thyrotoxic crisis and uncomplicated thyrotoxicosis. Absorption of radioactive iodine by the thyroid gland during a thyrotoxic crisis is often very significant, but in some cases it may be below the average values recorded in patients with uncomplicated thyrotoxicosis. A rapid (1-2 hour) radioactive iodine study is recommended after initiation of beta-blockers but before treatment with antithyroid drugs and iodine preparations. This study is not performed in acute cases as it delays the initiation of therapy. Other authors recommend a 15-minute study of dynamic blood flow in the thyroid gland using Tc. Although this test can demonstrate an overactive thyroid gland, it cannot determine the presence (or absence) of a thyroid storm.

Data from routine laboratory studies in thyrotoxic crisis show wide variability. Nonspecific abnormalities may be noted on complete blood count, electrolyte levels, and liver function tests. The presence of a bacterial infection can only be reflected by a shift of the leukocyte formula to the left without changing the total number of leukocytes in the peripheral blood. Hyperglycemia (greater than 120 mg/dL) is common; sometimes there is hypercalcemia. According to one series of observations, all patients with thyrotoxic crisis have a low level of cholesterol in the blood; its mean value is 117 mg/dl. A stress-inappropriate low plasma cortisol level was also noted, suggesting a lack of adrenal reserve.

Treatment of Thyrotoxic crisis (thyroid crisis):

The importance of early thyroid crisis treatment, whose diagnosis is based on clinical impression, is difficult to overestimate. Before starting treatment, blood should be taken for thyroid function testing and cortisol levels, as well as for a complete clinical blood count and routine biochemical studies. Shown cultural studies to detect infection. It is desirable to draw up a clear treatment plan in order to avoid unnecessary delay in the implementation of specific therapy.

The goals of specific treatment are as follows: maintaining the basic functions of the body at the physiological level; inhibition of the synthesis of thyroid hormones; slowing down the release of thyroid hormones; blockade of the effects of thyroid hormones in the periphery; identification and correction of provoking factors. One should strive to simultaneously achieve all of these goals.

Maintenance of basic bodily functions
Adequate hydration with intravenous fluids and electrolytes has been shown to compensate for the so-called insensible losses, as well as losses through the gastrointestinal tract. Additional oxygen is needed due to its increased consumption. In a crisis, hyperglycemia and hypercalcemia may occur; they are usually corrected with fluids, but in some cases specific therapy is required to reduce unacceptably high levels of calcium and glucose. Fever is controlled with antipyretics and a cooling blanket. Acetylsalicylic acid should be used with caution or not used at all, since salicylates increase the level of free T) and T4 due to a decrease in protein binding. This consideration is rather theoretical, since no adverse effects have been noted with the use of acetylsalicylic acid. In thyrotoxic crisis, sedatives should also be used with caution. Sedation depresses consciousness, which reduces the value of this parameter as an indicator of clinical improvement in the patient's condition. In addition, it can cause hypoventilation.

Congestive heart failure is treated with digitalis and diuretics, although failure due to hyperthyroidism may be refractory to digitalis. Cardiac arrhythmias are treated with conventional antiarrhythmic drugs. The use of atropine should be avoided as its parasympatholytic effect may increase heart rate. In addition, atropine can neutralize the action of propranolol.

Intravenous glucocorticoids are given at a dose equivalent to 300 mg hydrocortisone per day. The role of the adrenal glands in the pathogenesis of thyroid storm is unclear, but the use of hydrocortisone has been shown to improve patient survival. Dexamethasone has some advantages over other glucocorticoids, as it reduces the conversion of T4 to T3 in the periphery.

Inhibition of thyroid hormone synthesis
The antithyroid drugs propylthiouracil (PTU) and methylmazol block the synthesis of thyroid hormones by inhibiting the organization of tyrosine residues. This action begins within an hour after administration, but the full therapeutic effect is not achieved even after a few weeks. Initially, a loading dose of PTK is prescribed (900-1200 mg, and then 300-600 mg per day for 3-6 weeks or until a therapeutic effect is obtained (control of thyrotoxicosis). An acceptable alternative is the appointment of methylmazole at an initial dose of 90-120 mg, followed by the introduction 30-60 mg per day Both drugs are administered orally or via a nasogastric tube, as their parenteral forms are not available.PTU has an advantage over methyl mazol: it inhibits the peripheral conversion of T4 to T3 and causes a faster therapeutic effect.Although these drugs inhibit the synthesis of again formed thyroid hormones, they do not affect the release of already accumulated hormones.

Decreased release of thyroid hormones
The introduction of iodine preparations immediately slows down the release of thyroid hormones from their places of accumulation. Iodides can be given as strong iodine solutions (30 drops orally every day) or as sodium iodide (1 g every 8 to 12 hours by slow intravenous infusion). Iodide should be administered one hour after the loading dose of the antithyroid drug to prevent the utilization of iodine by the thyroid gland during the synthesis of a new hormone.

Blockade of peripheral effects of thyroid hormones
Adrenergic blockade is the basis of the treatment of thyrotoxic crisis. In an extensive series of observations by Waldstein et al. (1960) noted an increase in the survival of patients when using reserpine. Subsequently, guanethidine was shown to be effective in alleviating the symptoms and signs of thyrotoxicosis due to sympathetic hyperactivity. Currently, the beta-blocker propranolol is the drug of choice. In addition to reducing sympathetic hyperactivity, propranolol partially blocks the conversion of T4 to T3 in the periphery.

Propranolol can be given intravenously at a rate of 1 mg/min, with a cautious dose increase of 1 mg every 10 to 15 minutes until a total dose of 10 mg is reached. The positive effects of the drug (control of cardiac and psychomotor manifestations of thyrotoxic crisis) are observed after 10 minutes. The lowest dose sufficient to control thyrotoxic symptoms should be used; if necessary, this dose can be repeated every 3-4 hours. The oral dose of propranolol is 20-120 mg every 4-6 hours. When administered orally, propranolol is effective for approximately 1 hour. Propranolol has been successfully used in the treatment of thyroid storm in children. Young children may require high doses of the drug (240-320 mg/day orally).

The usual precautions should be observed when prescribing propranolol to patients with bronchospastic syndrome and heart block. In the case of its use, a preliminary ECG study is carried out in order to assess conduction disturbances. In patients with congestive heart failure, the beneficial effects of the drug (decrease in heart rate and some arrhythmias) and the risk of its use (inhibition of myocardial contractility with beta-adrenergic blockade) should be compared. Urbanic believes that in this situation the benefits of treatment with propranolol outweigh its risks, but the author recommends prior administration of digitalis preparations.

Propranolol alone should not be relied upon in the treatment of thyrotoxicosis or thyroid storm. Two cases of thyrotoxicosis in patients who received seemingly quite adequate therapy with propranolol for thyrotoxicosis are described. It is known that with a single or repeated oral dose of propranolol, its plasma level is very variable in controls and in patients with thyrotoxicosis. Treatment of thyrotoxic crisis should be sufficiently flexible and individualized.

One of the authors recommends a gradual decrease in the dose of propranolol as the thyrotoxic crisis is relieved. He believes that an objective assessment of the patient's condition may be difficult, since propranolol masks the symptoms of hypermetabolism. In patients already treated with beta-blockers, the symptoms of a thyroid crisis may be masked, which is associated with a risk of late diagnosis of a thyrotoxic crisis.

Alternatives to propranolol are guanethidine and reserpine, which also provide effective autonomic blockade. Guanethidine reduces the stores of catecholamines and blocks their release. When administered orally at 1-2 mg/kg per day (50-150 mg), it is effective after 24 hours, but its maximum effect may be observed after a few days. Toxic reactions are cumulative and include postural hypotension, myocardial decompensation, and diarrhea. The advantage of guanethidine over reserpine is the absence of a pronounced sedative effect characteristic of reserpine.

The action of reserpine is aimed at reducing the reserves of catecholamines. After the initial dose (1-5 mg intramuscularly), the drug is administered every 4-6 hours at 1-2.5 mg. Improvement of the patient's condition can be observed after 4-8 hours. Side effects of reserpine include drowsiness, mental depression (which can be severe), cramping abdominal pain, and diarrhea.

Identification and elimination of provoking factors
A thorough assessment of the provoking factors of thyrotoxic crisis is carried out. Treatment of thyroid storm should not be delayed until these factors are identified; appropriate examination can be carried out as the patient's condition stabilizes. A provocative factor is identified in 50-75% of cases.

Recovery
After the start of treatment, symptomatic improvement is observed after a few hours, primarily due to adrenergic blockade. The elimination of the thyrotoxic crisis requires the destruction of circulating thyroid hormones, the biological half-life of which is 6 days for T4 and 22 hours for T3. Thyrotoxic crisis can last from 1 to 8 days (average duration - 3 days). If standard crisis control methods fail, alternative therapeutic options can be resorted to, including peritoneal dialysis, plasmapheresis, and charcoal hemoperfusion to remove circulating thyroid hormones. After recovery from a thyroid crisis, radioactive iodine therapy is the treatment of choice for hyperthyroidism.

Mortality
In the absence of treatment of a thyrotoxic crisis, mortality approaches 100%. With the use of antithyroid drugs, there is a decrease in mortality. According to available data, the lowest mortality in thyroid storm over a 10-year period is 7%; its usual rate is 10-20%. In many cases, the cause of death is a previous disease. The main means of reducing mortality, of course, is to prevent the development of a thyrotoxic crisis. Early recognition and timely treatment of this complication of hyperthyroidism gives the patient a better chance of survival.

Prevention of Thyrotoxic crisis (thyroid crisis):

Prevention of thyrotoxic crisis is, first of all, in the timely diagnosis and proper treatment of thyrotoxicosis. Patients with thyrotoxicosis should always refrain from any surgical interventions (unless, of course, they are associated with a threat to life). Before surgery on the thyroid gland, the patient must undergo a thorough examination and good treatment.