Symptoms of diffuse toxic goiter

The pathogenesis of clinical symptoms of diffuse toxic goiter is caused by the influence of excess thyroid hormones on various organs and systems of the body. The complexity and multiplicity of factors involved in the development of thyroid pathology determine the variety of clinical manifestations of the disease.

In addition to cardinal symptoms such as goitre, eyelashes, tremors and tachycardia, patients, on the one hand, have increased nervous excitability, tearfulness, fussiness, excessive sweating, a feeling of heat, small temperature fluctuations, unstable stools, swelling of the upper eyelids, increased reflexes. They become uncomfortable, suspicious, excessively active, suffer from sleep disturbances. On the other hand, adynamia is often observed, sudden attacks of muscle weakness.

The skin becomes elastic, hot to the touch, the hair is dry, brittle. There is a small tremor in the fingers of elongated arms, closed eyelids, sometimes the whole body (a symptom of the "telegraph pole"). Tremor can reach such intensity that the handwriting of the patient changes, becomes uneven and illegible. An important sign of the disease is the presence of goiter. Usually the thyroid gland is soft and enlarged diffusely and evenly. The size of the goiter can vary: it increases with excitement, after the beginning of treatment it gradually decreases, sometimes becomes denser. Over the gland in individual patients palpable and palpable systolic murmur is heard. But the magnitude of goiter does not determine the severity of the disease. Severe thyrotoxicosis can be observed even if its small size.

It is accepted to allocate 5 degrees of augmentation of a thyroid gland:

1. iron, invisible to the eye, the isthmus is probed;
2. lateral lobes are well felt, gland is noticeable when swallowing;
3. an enlargement of the thyroid gland is noticeable upon examination ("thick neck");
4. goitre is clearly visible, the configuration of the neck is changed;
5. a craw of huge sizes.

Since 1962, the world uses the classification of goiter sizes recommended by WHO. According to the 1994 WHO classification, the following degrees of thyroid enlargement are distinguished:

• 0 degree - no goiter,
• 1 - the struma is palpable, but not visible,
• 2 - the struma is palpable and is visible at a normal position of the neck.

The most common symptom for diffuse toxic goiter is progressive weight loss with a saved or even increased appetite. Increased secretion of thyroid hormones leads to an increase in the expenditure of energy resources in the body, which causes a decrease in body weight. In the absence of fatty tissue energy supply of the body is due to increased catabolism of exogenous and endogenous protein. Diffuse toxic goiter (stinging disease) is not always accompanied by weight loss. Sometimes there is an increase in body weight, the so-called "fat Basedov", which is associated with the features of the pathogenesis of the disease and requires the selection of a method of treatment.

For many years, it was believed that eye changes in patients with diffuse toxic goiter are one of the symptoms of the disease and are caused by an excess of thyroid hormones. However, it turned out that exophthalmos can occur both in hyperthyroidism and hypothyroidism, with thyroiditis in Hashimoto, and in some cases may precede the appearance of symptoms of the thyroid gland pathology or develop against the background of euthyroidism.

Ophthalmopathy is an autoimmune disease caused by the formation of specific immunoglobulins that cause changes in the retrobulbar fiber and the muscles of the orbit. More often, ophthalmopathy is combined with autoimmune diseases of the thyroid gland, namely diffuse toxic goiter. The pathogenesis of the disease was associated sequentially with an excess of thyroid hormones, TSH, LATS, LATS-protector, exophthalmine-producing hormones, microsomal antibodies, the presence of exophthalmic-producing antibodies. Apparently, the genetic defect in the immune control system is associated with the specificity of tissue damage. It is established that the surface membranes of some orbital muscles have receptors capable of fixing antigen-antibody complexes arising in autoimmune thyroid diseases.

The main changes occur in the extraocular muscles, depend on the duration of the disease. In the early stages, there is interstitial edema, diffuse cell infiltration, leading to degeneration and decay of muscle fibers. Muscles pale, swollen, sharply enlarged in volume. The next phase is the activation of endomysial fibroblasts, which, producing collagen and mucopolysaccharides, lead to proliferation of connective tissue and fibrosis, muscle fibers lose the ability to relax, which leads to limited mobility. The process of reduction is violated. Increased muscle volume leads to an increase in intraorbital pressure, disruption of fluid from the interstitial spaces. Venous stasis develops, causing edema of the eyelids and orbital fiber. In the later stages, fatty degeneration of muscles is observed. AF Brovkina identifies 2 forms of ophthalmopathy - edematous exophthalmos and endocrine myopathy. Foreign researchers speak about edematic and myopathic stages of ophthalmopathy as stages of a single process with predominant disturbances in retroorbital fiber or muscles of the orbit.

Patients are concerned about lacrimation, photophobia, a feeling of pressure, "sand" in the eyes, puffiness of the eyelids. In thyrotoxic exophthalmos, an important diagnostic feature is the absence of doubling. Exophthalmos are usually bilateral, less often unilateral. The degree of exophthalmos can be determined using the Gerthel exophthalmometer. With diffuse toxic goiter, the protrusion of the eye sometimes increases significantly. Exophthalmos is accompanied by increased shine of the eye, develops gradually, sometimes for several days or hours. Its severity usually does not correspond to the severity of thyrotoxicosis.

In addition to exophthalmos, other eye symptoms also occur in patients: a wide opening of the eye cracks (Delrymple's symptom), a rare flashing (Stelvag symptom), increased eye shine (Gref's symptom), a lagging of the upper eyelid from the iris when viewed down, so that a white band appears sclera (Kocher's symptom), weakness of convergence (Moebius symptom). Sometimes there is a symptom of Jellinek - darkening of the skin on the eyelids. These signs, especially the protrusion of the eyeballs and the wide opening of the eye slits, give the face a characteristic expression of fright. When fixing the eye - the so-called angry look.

When the eyes of the middle and severe degree are affected, there is a decrease in visual acuity, double vision as a constant symptom, and injection of vessels of the sclera. Develops lagophthalmus - the inability to completely close eyelids, possibly the ulceration of the cornea and sclera with the subsequent attachment of a secondary infection. The aforementioned eye symptoms are aggravated.

In the foreign literature, the NOSPECS classification, first proposed in 1969, is used. Werner:

• 0 - no pathological changes from the eyes;
• I - shortening of the upper eyelid - "surprised look", wide eyepiece and Gref's symptom;
• II - changes in soft tissues of the orbit;
• III - protrusion of eyeballs (the increase exceeds the norm by 3 mm or more);
• IV - defeat of orbital muscles, restriction of movement of eyeballs;
• V - changes in the conjunctiva;
• VI - defeat of the optic nerve.

V. G. Baranov considered it expedient to distinguish between 3 degrees of gravity of exophthalmos:

• I - small exophthalmos - (15,9 ± 0,2) mm, edema of the eyelids;
• II - moderate exophthalmos - (17,9 ± 0,2) mm, with significant edema of the eyelids and expressed symptoms of the defeat of the eye muscles;
• III - pronounced exophthalmos - (22,8 + 1,1) mm, corneal ulceration, diplopia, severe limitation of mobility of eyeballs.

In 3-4% of patients on the front surface of the leg develops a kind of lesion of the skin and subcutaneous fat, called pretybial myxedema. Clinically, the pretybial myxedema is characterized by a one- or two-sided, clearly defined compaction of purplish-cyanotic color on the anteromedial surfaces of the shins. Edema occurs as a result of impaired glucoprotein metabolism, carbohydrate components of which are found in edematous substance - mucin. For a long time, the cause of pre-bacterial myxedema was vascular sclerosis and circulatory stasis, leading to trophic disorders. The diencephalic lesions of the brain, the hypersecretion of thyrotropin by the anterior pituitary gland in patients after removal of the thyroid gland, the change in the function of the gland and pituitary gland against the background of disturbed mechanisms of neurotropic regulation were considered as etiological factors. To date, the most likely mechanism for the development of prebial and myxedema is autoimmune. McKenzie found in the blood of most patients pretybialnoi myxedema LATS-factor.

In men, there is sometimes a thickening of the phalanges of the fingers (thyroid acropathy), caused by edema of dense phalangeal tissues and periosteal neoplasm of bone tissue.

In the clinical picture of thyrotoxicosis, cardiovascular disorders are also characteristic. "Patients with the disease Basedova suffer heart and die from the heart" (Moebius). Cardiovascular disorders in diffuse toxic goiter are caused, on the one hand, by the pathological sensitivity of the cardiovascular system to catecholamines, on the other hand by the direct effect of excess thyroxin on the myocardium. It is noted the summation of the effect of excessive secretion of thyroid hormones and the effect of increased sympathetic activity on the heart and peripheral circulation. The resulting hemodynamic disorders, the discrepancy between the level of delivery, consumption and utilization of oxygen by the heart muscle lead to severe exchange-dystrophic damage and the development of thyrotoxic cardiomyopathy, manifestations of which in the clinic are rhythm disturbances (tachycardia, extrasystole, fibrillation and atrial flutter) and heart failure. The processes underlying the thyrotoxic cardiomyopathy are reversible. An almost constant symptom of thyrotoxicosis is tachycardia, against which there may be attacks of atrial fibrillation. For tachycardia is characteristic that it does not change when the patient changes position and does not disappear during sleep. Another of its peculiarities is a weak reaction to cardiac glycoside therapy. The pulse rate can reach 120-140 beats per minute, and with movement, physical stress and excitement, it is 160 or more. The patients feel the beating of the pulse in the neck, head, abdomen.

The dimensions of the heart are widened to the left, systolic murmurs are heard. Characteristic of the large pulse pressure due to excessive increase in systolic and low diastolic. The electrocardiogram does not show any characteristic features. Often there are high pointed tines P and T, there is a flickering of the atria, extrasystole. Sometimes on an electrocardiogram one can see depression of the ST segment and a negative T wave. Changes in the end part of the ventricular complex can be observed both in the absence of anginal pains and in the presence of angina pectoris; they are usually reversible. As compensation for thyrotoxicosis is achieved, there is a positive trend in ECG changes.

Often in patients with diffuse toxic goiter (Graves' disease), there are violations from the gastrointestinal tract. Patients complain of a change in appetite, a disorder of the stool, attacks of abdominal pain, vomiting. Sometimes spastic constipation is observed. In severe cases, the liver is affected. There is an increase in her size, soreness in the right hypochondrium, sometimes jaundice. With adequate therapy of thyrotoxicosis, liver function abnormalities are reversible. When diffuse toxic goiter also affects the function of the pancreas. Patients often observe an increase in the level of glycemia, a test for glucose tolerance is broken. When the symptoms of thyrotoxicosis are eliminated, the parameters of carbohydrate metabolism are normalized.

Women have menstrual irregularities right up to amenorrhea. In men suffering from thyrotoxicosis, libido decreases, potency, sometimes there is a violation of gynecomastia. Under the influence of thyroid hormones there is a rapid destruction of cortisol, resulting in pronounced thyrotoxicosis develops hypocorticism. With a long-term diffuse toxic goiter (Graves' disease), depletion of the adrenal cortex also occurs, which causes relative adrenal insufficiency.

The study of thyrotoxicosis clinic shows that patients do not always have clear signs of the disease. Often there is no large increase in the thyroid gland, constant tachycardia, characteristic facial expressions, eye symptoms. Patients are disturbed by periodically arising attacks of palpitation, accompanied by unpleasant sensations in the field of heart, a dyspnea or short wind. Outside attacks, the heart rate can be within normal limits, ECG without any peculiarities, the level of thyroid hormones in the blood is not changed. During the seizure, the content of triiodothyronine and thyroxine in the blood was sharply increased.

Triiodothyronine toxicosis, taking place against the background of a normal level of thyroxin in the blood, but an increased level of triiodothyronine, occurs in 5% of cases of diffuse toxic goiter, and in autonomous adenomas - up to 50%. One of the reasons for the violation of the ratio of thyroxin and triiodothyronine in the thyroid gland may be a deficiency of iodine leading to compensatory synthesis of the most active hormone.

Another reason for the isolated increase in the level of T3 can be the accelerated peripheral transition of T ₄ to T ₃. Symptoms of the flow of this form of thyrotoxicosis does not have any peculiarities.

In the literature, patients with a thyrotoxicosis course were complicated by attacks of partial or complete paralysis of the proximal parts of skeletal muscles in combination with vegetative disorders: sweating, thirst, tachycardia, increased blood pressure, increased excitability. Sometimes markedly expressed manifestations of periodic paralysis in the form of transient weakness in the legs.

Thyrotoxicosis in the elderly is a common phenomenon. According to Geffrys, its frequency among them is 2.3%. The disease develops gradually, against a background of somatic pathology. At the forefront are weight loss, loss of appetite, muscle weakness. Patients rather calm than excited. A characteristic difference of the clinical picture is the rapid development of heart failure, cardiac arrhythmias in the form of atrial fibrillation, refractory to the usual therapeutic doses of cardiac glycosides. With thyrotoxic ciliary arrhythmia, the risk of developing embolism is as high as in rheumatic mitral stenosis. Thyrotoxic ciliary arrhythmia develops with subclinical hyperthyroidism. Latent forms of ischemic or hypertensive cardiopathy, which are common in hyperthyroidism, in the elderly are converted into explicit forms (heart failure, atrial fibrillation, thoracic "toad"). Very rarely in elderly patients with thyrotoxicosis there is exophthalmos, they often have no goiter. Sometimes there is a so-called apathetic form of thyrotoxicosis. Clinical manifestations include apathy, depression, severe weight loss, heart failure, atrial fibrillation, proximal myopathy. Patients have an apathetic face, wrinkled skin, blepharoptosis, atrophy of the temporal muscles, which can be explained by the relative deficiency of catecholamines or a decrease in their response. The level of thyroid hormones in the elderly can be at the upper limit of the norm or slightly elevated. It is believed that hyperthyroidism in them develops by increasing the sensitivity of peripheral tissues to the action of hormones. Diagnosis can help test with thyreoliberin. A normal response to the administration of TRH excludes the diagnosis of thyrotoxicosis, with the exception of forms caused by selective pituitary thyroid hormone resistance.

[1], [2], [3], [4], [5], [6]

Degrees of severity of thyrotoxicosis

By the severity of thyrotoxicosis, a mild, moderate and severe disease is isolated.

With a mild degree, the pulse does not exceed 100 beats per minute, weight loss is 3 ~ 5 kg, eye symptoms are absent or slightly expressed, an increase in absorption of ¹³¹ I in 24 hours.

The average severity is characterized by an increase in tachycardia to 100-120 beats / minute, a marked tremor, a weight loss of up to 8-10 kg, an increase in systolic pressure and a decrease in diastolic pressure, an increase in the uptake of thyroid isotopes from the first hours.

A severe form (aurantic, visceropathic) develops with a relatively long history of the disease, without treatment. Weight loss reaches the degree of cachexia, the pulse rate exceeds 120-140 bpm. To the listed symptoms are added violations of the liver, cardiovascular system. Atrial fibrillation and myopathy, adrenal insufficiency are observed.

[7], [8], [9], [10]

Thyrotoxic crisis

Thyrotoxic crisis is the most difficult, life-threatening complication of diffuse toxic goiter. It develops when suddenly all the symptoms of hyperthyroidism become aggravated, more often several hours after a non-surgically performed operation against a background of insufficiently compensated thyrotoxicosis. The role of provoking factors can play stressful situations, physical overstrain, infections, surgical interventions, tooth extraction. In the pathogenesis of the thyrotoxic crisis, the main role is played by the sudden release into the blood of large quantities of thyroid hormones, the increase in adrenal insufficiency, the activity of the higher parts of the nervous system, the sympathetic-adrenal system. Developing in the thyrotoxic crisis, functional and morphological disturbances in various organs and tissues are caused, on the one hand, by a sharp increase in the level of thyroid hormones in the blood, excessive production of catecholamines or an increase in the sensitivity of peripheral tissues to them, on the other hand, by deficiency of the hormones of the adrenal cortex, the reserve capacity of the crisis can result in a fatal outcome. Patients become restless, blood pressure rises significantly. A considerable excitation, a tremor of extremities, expressed muscular weakness develops. There are violations of the gastrointestinal tract: diarrhea, nausea, vomiting, abdominal pain, jaundice. There is a violation of kidney function, a decrease in diuresis up to anuria. Heart failure may develop. Sometimes this is accompanied by acute liver atrophy. Further excitation is replaced by a stuporous state and loss of consciousness, the development of a clinical picture of coma.

The prognosis is determined by the timeliness of diagnosis and treatment.