How to relieve eye symptoms in thyrotoxicosis. Treatment of eye symptoms of thyrotoxicosis

The eye symptoms of thyrotoxicosis do not fundamentally differ from those with an independent disease of endocrine ophthalmopathy.

Ectodermal disorders are manifested by brittle nails, hair loss. Relatively rare are abdominal pain, unstable stool with a tendency to diarrhea, thyrotoxic hepatosis. Ovarian dysfunction up to amenorrhea, fibrocystic mastopathy, gynecomastia, impaired carbohydrate tolerance, tyrogenic relative (with normal cortisol levels) adrenal insufficiency (moderate melasma, hypotension) are possible. Diseases associated with Graves' disease: endocrine ophthalmopathy, pretibial myxedema. The latter occurs in 1-4% of cases, manifested by swelling, thickening and hypertrophy of the skin of the anterior surface of the lower leg. Acropathy is extremely rare: periosteal osteopathy of the feet and hands radiographically resembles “soap foam”.

Laboratory signs of confirmation of thyrotoxicosis in DTG are an imbalance in the levels of thyroid hormones [thyroxine (T 4) and triiodothyronine (T 3)] and thyroid stimulating hormone (TSH) of the pituitary gland. To diagnose the disease and evaluate the effectiveness of the treatment, it is most appropriate to determine the levels of free (sv.) fractions of T 4 , T 3 and TSH. With a persistent and significant increase in the levels of St. T 4, St. T 3 and low TSH in combination with the corresponding clinical symptoms state thyrotoxicosis. The detection of elevated titers of thyroid autoantibodies [antibodies to microsomal antigen (AT-MS), thyrocyte peroxidase (AT-TPO), the second colloid antigen, thyroglobulin (AT-TG)] confirms the autoimmune genesis of the disease.

Ultrasound examination (ultrasound) in DTG is of secondary importance and can only confirm the diffuse nature of the increase in the thyroid gland. A puncture biopsy, performed under ultrasound guidance, followed by a cytological examination of the obtained biopsy specimen, is performed in cases of detection of nodular formations against the background of diffuse enlargement of the thyroid gland or doubts about the goodness of the disease. Scintigraphy is not used for the differential diagnosis of the nature of thyroid diseases. It can only be used for a comparative assessment of the functional activity of the diffusely enlarged parenchyma of the gland and the nodular formations identified in it, determining the volume and functional activity of the thyroid residue after surgical treatment, as well as identifying ectopic foci of the thyroid tissue.

Thyrotoxic crisis is an urgent clinical syndrome, which is a combination of severe thyrotoxicosis with thyroid adrenal insufficiency. The main reason is inadequate thyreostatic therapy. Provoking factors are: surgery, infectious and other diseases. It is clinically manifested by a developed syndrome of thyrotoxicosis, pronounced anxiety up to psychosis, motor hyperactivity, alternating apathy and disorientation, hyperthermia (up to 40 ° C), suffocation, pain in the heart, abdomen, nausea, vomiting, signs of acute heart failure, hepatomegaly. Perhaps the development of thyrotoxic coma.

Currently, there are three ways to treat DTG - complex drug thyrostatic therapy, surgery and radioactive iodine. It is not possible to establish any general pattern in the choice of one or another method of treating DTG on a global and even European scale. A number of the largest clinics with many years of experience in surgical thyroidology remain adherents of their own practice that has developed over decades. In many countries, especially in the USA, and in recent years in Western Europe, the number of operations for DTG has been significantly reduced and the main method of treatment is radioactive iodine therapy. In Russia, most of the CIS countries, Japan, preference is still given to surgical treatment.

Drug therapy provides a stable cure only in 20–25% of patients with DTG. It can be used as a stand-alone treatment or as a preparation for surgery or radioiodine therapy. The disadvantages of thyrostatic therapy include a high risk of thyrotoxicosis recurrence after its withdrawal, a low probability of stable remission, and the occurrence of side effects.

In our country, indications for surgical treatment of DTG are quite clearly formulated: ineffectiveness of conservative therapy for 1-2 years; severe degree of thyrotoxicosis with a complicated course; large size of the thyroid gland; recurrence of thyrotoxicosis with the abolition of thyreostatics; intolerance to medications (thyreostatics); combination of DTG with neoplastic processes in the thyroid gland.

The operation for DTG in specialized surgical departments, careful preoperative preparation, qualified performance of the operation technique with a high level of anesthetic support, provision of adequate postoperative intensive care made it possible to minimize possible complications and mortality, to achieve quite satisfactory immediate results of treatment. Surgical treatment, which in our country is performed in approximately 40% of patients with DTG, impresses with its efficiency and speed of elimination of the pathological process. Of course, one should not underestimate the importance of specific complications that undoubtedly overshadow the results of treatment (damage to the laryngeal nerves, parathyroid glands), the genesis of which is complex and multicomponent (although traditionally they are primarily attributed to insufficient special qualifications of the surgeon). In recent years, the percentage of these complications has decreased significantly, however, even in specialized departments, they cannot be completely avoided.

In DTG surgery, two main problems remain relevant and unresolved: postoperative recurrence of thyrotoxicosis and hypothyroidism. According to the literature, at present, persistent euthyroidism after surgical treatment of DTG is achieved only in 25-30% of patients. The frequency of recurrence of thyrotoxicosis ranges from 0.5 to 34% without a tendency to decrease, and postoperative hypothyroidism from 0.2 to 70% and depends on the time of repeated examinations of patients. Therefore, the problem of preserving the function of the remaining thyroid tissue, as well as the search for markers for predicting the outcomes of surgical intervention in DTG, is very relevant.

In Russia, since the middle of the last century, the methods of operation for DTG according to O. V. Nikolaev or E. S. Drachinskaya have been recognized and become generally accepted. The majority of domestic surgeons and at present, with DTG, perform subtotal subfascial resection of the thyroid gland, leaving a minimum amount of tissue (4-8 g) in the tracheoesophageal grooves (according to O. V. Nikolaev).

Existing methods for determining the volume of tissue left, as well as methods for preventing complications in the surgical treatment of DTG, do not have wide practical application. At the same time, in modern conditions, the general trend is to recognize postoperative hypothyroidism as a predictable outcome of the operation, not attributing it to negative consequences and complications, but considering it as the goal of radical surgical intervention.

An effective treatment for DTG is radioactive iodine therapy. In the USA, some countries of Western Europe, preference is given to radioiodine therapy, which is an alternative to surgical treatment in its radical nature. The drug of choice is the isotope I 131 . Contraindications are significant size of the thyroid gland, ophthalmopathy, impaired hematopoiesis, young age, pregnancy and lactation. In 70-90% of patients after radioiodine therapy, hypothyroidism develops, requiring lifelong replacement therapy. In Russia, this method is still inaccessible.

Toxic adenoma of the thyroid gland(nodular toxic goiter, functional autonomy, Plummer's disease) - thyroid adenoma, in which there is an increased level of thyroid hormones in the blood. It is more common in women at any age, mainly at the age of 40-50 years. It grows slowly - within 5-10 years. The adenoma is usually small (2–2.5 cm in diameter). Signs of thyrotoxicosis often occur only after the adenoma reaches a certain size, sometimes after 3–8 years from the onset of its development.

Plummer's disease is a form of functionally active thyroid adenoma characterized by TSH-independent excess iodine uptake and increased production of thyroxine by thyrocytes. Functional autonomy (FA) of the thyroid gland can be unifocal (toxic nodular goiter), multifocal (multinodular toxic goiter) and disseminated (diffuse distribution of autonomously functioning thyrocytes in the form of small-nodular areas). FA is the second most common (after DTG) cause of thyrotoxicosis.

As a result of prolonged iodine deficiency, thyrocytes malfunction, which manifests itself in their acquisition of the ability to autonomously absorb iodine and produce thyroxine. Normally, no more than 10% of thyrocytes function autonomously in the thyroid gland. In the initial stages of FA, thyroid scintigraphy reveals areas that excessively absorb the radiopharmaceutical (RP), against the background of its normal uptake by the surrounding thyroid tissue. At the same time, thyrotoxicosis is absent and a normal level of TSH (compensated FA) is determined. As the degree of autonomy and the volume of autonomously functioning tissue increase, the uptake of iodine by the surrounding tissue decreases, the secretion of TSH (decompensated FA) is gradually suppressed, and clinically pronounced thyrotoxicosis develops. FA is the most common cause of thyrotoxicosis in the elderly and senile age. In areas of iodine endemia, FA, as a rule, does not progress to the stage of decompensation. The latter in 80% of observations is associated with exogenous intake of excess iodine. With compensated FA, thyrotoxicosis develops in about 5% of patients per year.

The clinical picture of the disease is determined by the degree of FA compensation. With euthyroidism and subclinical thyrotoxicosis (T 3 and T 4 are normal, TSH is lowered), FA may not be clinically manifested in any way. Compensated FA in the absence of nodules in the thyroid gland is a scintigraphic finding. Scintigraphy is usually undertaken when examining a nodular or multinodular goiter. Decompensated FA is manifested by thyrotoxicosis syndrome. Clinical symptoms are similar to those in DTG: palpitations, poor heat tolerance, increased sweating and, as a result, thirst, weight loss, despite increased appetite, shortness of breath. Excitability, irritability, anxiety, hyperkinesia and emotional lability, insomnia, muscle weakness in the proximal sections, tremor of the outstretched and spread fingers, increased deep tendon reflexes are also possible signs. The skin is usually warm, moist, flushed on the face, thin hair falling out, and menstruation is scanty or absent. Autoimmune ophthalmopathy is not typical; only "separate" eye symptoms may occur. In some elderly patients, only weakness, palpitations, atrial fibrillation, shortness of breath are noted, and there is almost no effect from the use of cardiac glycosides. By the way, DTG in the elderly is sometimes not recognized for a long time due to the lack of symptoms, as a result of which various disorders are attributed to age-related changes.

FA is characterized by the presence of a nodular formation in the thyroid gland (according to palpation and ultrasound data), uneven absorption of radiopharmaceuticals during scintigraphy, and a high titer of antibodies to TSH receptors in 70–80% of cases. In addition, high titers of AT-TPO and AT-TG can be detected.

In case of nodular formation of the thyroid gland, the main tasks are the exclusion of a malignant tumor and the identification or determination of a risk factor for the development of decompensated FA of the thyroid gland. In nodular and multinodular toxic goiter, the incidence of thyroid cancer is 3-10%.

Nodular toxic goiter is more often detected at a young age, and multinodular - at the age of 50-70 years. More than half of elderly patients have nodular forms of toxic goiter.

To determine the tactics of treatment and choose the volume of surgical intervention, it is necessary to carry out differential diagnostics between DTG with nodes and toxic thyroid adenoma, as well as preoperative and intraoperative verification of the morphological structure of thyroid FA.

There are different opinions regarding the choice of treatment method, scope and nature of surgical intervention in thyroid FA. Most authors recommend surgical treatment for nodular and multinodular toxic goiter. With solitary toxic adenoma - subtotal resection of the lobe, with multinodular - subtotal, marginally subtotal and total thyroidectomy. If malignancy of the node is suspected, hemithyroidectomy with isthmusectomy. It should be noted that multinodular toxic goiter is one of the main risk factors for the development of recurrent toxic goiter after its surgical treatment.

With euthyroidism or slight suppression of TSH at normal levels of sv. T 3 and St. T 4 , as well as in the absence of goiter, data for thyrotoxicosis in the past, the capture of 99m Tc-pertechnetate with suppressive scintigraphy is less than 2%, observation is indicated (annual scintigraphy and examination of TSH levels, f. T 3 , f. T 4) without active treatment with a ban on the introduction of iodine preparations. Thyreostatics (thyrozol, propicil) are indicated only as a preparation for surgery and radioactive iodine therapy. The operation is indicated for FA with an autonomous tissue volume of more than 3 cm in diameter, nodular, multinodular toxic goiter. In other cases, as well as with contraindications to surgery, radioactive iodine therapy is indicated.

In recent years, ethanol sclerotherapy has been used in clinical practice for toxic adenomas. This method is used when the size of the formation is up to 3 cm in diameter, the exclusion of its malignant nature and the presence of a closed non-infiltrated capsule.

Disorders of the thyroid gland, expressed in hyperfunctions, which lead to an increased content of hormones, are considered to be. Pathology develops against the background of diseases of the endocrine system, in particular, diffuse toxic goiter. The syndrome has a number of characteristic features and eye symptoms of thyrotoxicosis are distinguished into a separate category. They are noticeable not only visually, but also cause significant discomfort to the patient.

Causes of the development of eye symptoms of thyrotoxicosis

There are conflicting opinions regarding the relationship between increased concentrations of hormones and the onset of ophthalmic disorders.

It is assumed that the hyperfunction of the thyroid gland affects the nervous, autonomic systems and some others. As a result, metabolic, metabolic processes go wrong, changes are observed, which can be considered the causes of eye symptoms.

In particular, the following phenomena are observed:

Increased muscle tone in the eye area.
The growth of fatty, connective tissues, which disrupts the functionality of normal tissues.
Inflammation of the optic nerve.
Increased eye pressure.
Circulatory disorders.
Formation of puffiness, stagnant areas.

It is believed that these phenomena lead to the characteristic symptoms of thyrotoxicosis on the part of the visual system. In addition, there is an assumption that hormonal disruptions lead to impaired lymph flow, the quality of which can also provoke violations of a similar nature.

How do voice symptoms manifest?

Disorders of the ophthalmic type in thyrotoxicosis are combined into a separate symptomatology, which consists of a combination of different syndromes and manifestations. The group of signs characteristic of thyrotoxicosis, in particular, with diffuse toxic goiter, includes the following phenomena:

Rare blinking. If on average a healthy person blinks 15-20 times per minute, then with thyrotoxicosis this number is reduced to 5-7 times. (Stelwag symptom).
Expanded eyes. From the outside, it seems that a person has a strong surprise, although this sign is not associated with an emotional state (Dalrymple's symptom).
Puffiness, swelling of the eyelid. (symptom of Ekrot).
Slow movement of the upper eyelid or its delay (Gref's symptom).
Difficulties in examining an object, eyeballs do not move synchronously, there is no way to fix the gaze (Mobius symptom).
Displacement of the eyelid relative to its normal position. It can be any direction. Depending on the development of the disease, there may be a slight displacement or leading to exposure of the sclera (Kocher's symptom).
When trying to track an object, the eyelid begins to noticeably twitch, sometimes stop involuntarily (Wilder's symptom).
When laughing, the eyes remain indifferent, the person does not squint them, their shape practically does not change (Brahm's symptom).
Insufficient discharge of tears, which additionally provokes infectious and other inflammatory diseases.

The above symptoms are quite common. To it is added a significant deterioration in vision, pain, a feeling of sand in the eyes, bifurcation.

In total, there are more than 30 names of symptoms that characterize one or another ophthalmic disorder, pathological process.

Stages of manifestation of eye symptoms

GS DTZ is mainly expressed in exophthalmos or in a specific protrusion of the eyeballs. There is a certain scheme for assessing the condition of the eyes, according to which experts draw conclusions about the severity of changes that have already occurred. It is for exophthalmos that the following classification is characteristic:

1 degree. It is considered the initial stage, the motor activity of the eyes is not yet impaired, forward displacement or protrusion is within 16 mm.
2 degree. In addition to moderate dysfunction of the oculomotor muscles, conjunctival disorders begin to develop, and slight swelling is formed. Exophthalmos up to 18 mm.
3 degree. The condition is characterized by the inability to completely close the eyelids, inflammatory processes develop, ulcers on the cornea. The mobility of the eyeball is significantly deteriorating. Protrusion up to 23 mm.
4 degree. At this stage, not only is it almost impossible to preserve vision, but also the eye itself. The displacement of the apple exceeds 24 mm, inflammatory processes, erosion are aggravated, the optic nerves atrophy, and others.

Other symptoms of thyrotoxicosis

Simultaneously with the eye symptoms of diffuse toxic goiter, signs of the disease develop, which are reflected in other body functions.

Of the main distinguish:

Rapid weight loss.
Digestive problems, frequent stools.
Trembling in the hands.
Emotional unreasonable swings, nervousness.
Excessive sweating.
Memory impairment, restlessness.

Diseases of the endocrine system are well diagnosed, the main thing is to do it in a timely manner, until the symptoms lead to irreversible consequences, including from the side of vision.

In the early stages of the disease, until the goiter has reached an impressive size, serious changes have not yet occurred regarding the visual system, for example, only 1 degree of exophthalmos has been diagnosed, other symptoms have not yet been expressed, then treatment can only be medication.

Blockers of intensive hormone production, antithyroid drugs and other drugs are prescribed at the discretion of the doctor.

If there is no positive dynamics, it is not possible to control the work of the endocrine system, or the patient initially applied at an advanced stage of the disease, a decision is made on surgical intervention. The operation may be preceded by special preparatory therapy.

Treatment and maintenance of the eyes

Simultaneously with the treatment of the underlying pathology, supportive therapy is carried out to reduce ophthalmic symptoms. What it will be depends on the totality of the expressed syndromes. Therapy may include the following:

Elimination of acute inflammation.
Antibacterial therapy aimed at limiting the development of infectious foci.
Treatment of ulcerative formations on the cornea.
Prescribing physiotherapy, such as x-ray therapy.

Depending on the degree of tissue damage, the types of development of pathological processes, a decision is made on the method of treating the eye symptoms of thyrotoxicosis. In the initial stages, it is likely that the state of the visual system will normalize or go into a stage of long-term remission. To do this, it is important to control the functions of the endocrine system and, in general, prevent a serious hormonal imbalance. It will also be useful to carry out the prevention of eye diseases.

If thyroid disease has developed for a long time, eye complications can become irreversible. Foci of adipose or connective tissue may form, nerves may atrophy, and the structure of muscle fibers may change.

In such cases, surgical intervention is prescribed, since the tissues will not be able to recover on their own. If the situation is not yet critical, then the operation is reconstructive.

With complicated ophthalmopathy treatment is orbital decompression, involving the removal of part of the walls of the orbits, which allows you to return the position of the eyeball. According to indications, surgical manipulations and other directions can be carried out.

In order to prevent irreversible consequences both on the part of the visual system and on the whole health of the whole organism, it is necessary to undergo a diagnosis of the endocrine system in a timely manner. In the initial stages of many hormonal diseases, it is possible to cope with the problem in a conservative way, to detect the pathological process at the initial stage.

In cases where the disease proceeds for a long time, and the patient either does not go to the doctor for any reason, or is treated incorrectly, the thyroid gland continues to grow, and the goiter can reach large sizes (Fig. 6). At the same time, the configuration of the neck changes significantly, and there may even be problems with the passage of food through the esophagus.

Rice. 5. Characteristic view of a patient with thyrotoxicosis. . Rice. 6. Large goiter

Indeed, these symptoms may be enough to make a diagnosis, but the clinical picture of the disease is so many-sided and varied, there are so many large and small symptoms that just listing them can take several pages.

A sick person complains of muscle weakness, fatigue, decreased performance, irritability, tearfulness, poor sleep, a feeling of heat, excessive sweating, weight loss, a feeling of pressure in the neck, palpitations that increase with physical and emotional stress, trembling of the limbs, and sometimes whole body, loose stools, with a tendency to diarrhoea. Sometimes patients themselves note an increase in the thyroid gland and bulging eyes. Women complain about menstrual irregularities. With all the variety of complaints, the most characteristic of them are palpitations, weight loss and muscle weakness.

Of the other complaints that should alert and force you to see a doctor, the following should be highlighted:

Irritability;

Mental imbalance;

excessive sweating;

Poor tolerance to high temperatures;

Hand trembling (small tremor);

Weakness;

fatigue;

stool disorder (diarrhea);

Frequent and excessive urination (polyuria);

Menstrual disorders.

Decreased sex drive.

Changes in the thyroid gland in Graves' disease are manifested mostly in the form of a diffuse, uniform increase in it. In most cases, iron is increased by 2-3 times compared to the norm (60-80 g compared to the normal weight of 25 g).

Currently, the size of the thyroid gland is measured using an ultrasound method (the normal volume in men is 25 ml, in women - 18 ml).

The degree of enlargement of the thyroid gland often does not correspond to the severity of thyrotoxicosis. As a rule, in men with a pronounced clinical form of thyrotoxicosis, the gland is slightly enlarged, it is difficult to palpate, since the increase occurs mainly due to the lateral lobes of the gland, which tightly cover the trachea. A small, non-palpable gland is noted in 3-5% of patients. In some cases, with diffuse enlargement of the gland, one lobe (usually the right one) may be larger.

With diffuse toxic goiter, the thyroid gland is usually soft or moderately dense in consistency, not soldered to the underlying tissues, easily displaced when swallowed. The thyroid gland may take a retrosternal position. Sometimes a goiter develops from an extra lobe or ectopic (unusually located) gland tissue, making examination difficult.

Pressure on the gland is often painful. One of the characteristic signs of goiter in Graves' disease is that its volume in different periods of the disease is subject to large fluctuations, which is explained by the varying degree of blood filling of the gland.

During auscultation, the doctor can hear vascular noises over the thyroid gland, the occurrence of which is associated with increased blood filling of the gland and accelerated blood flow in its vessels.

Often the disease is accompanied by a change in the eyes. Sometimes it is bulging eyes that make you turn to the doctor. The appearance of eye symptoms is associated with a violation of the tone of the eye muscles. Due to the variability, as well as non-specificity, the significance of eye symptoms is small.

Eye symptoms vary and may be completely absent. Exophthalmos (bulging eyes, protrusion of the eyeballs) is the most characteristic symptom of thyrotoxicosis. Exophthalmos usually develops gradually, although it can appear suddenly. In some cases, bulging is present only on one side, more often on the right. Exophthalmos gives the patient an angry, surprised or frightened look. Sometimes the look expresses horror.

On examination, the doctor may detect other eye symptoms. They are named after the authors who observed them. Graefe's symptom is the lag of the upper eyelid from the iris when fixing the sight of a slowly moving downward object, and therefore a white stripe of sclera remains between the upper eyelid and the iris. Graefe's symptom can also be observed in healthy people with myopia. When looking up, an area of the sclera is also found between the lower eyelid and the iris (Kocher's symptom).

Widely opened palpebral fissures give the face an expression of fright, concentration (Delrymple's symptom). Convergence disorder, that is, the loss of the ability to fix an object at close range, is called the Mobius symptom. Rare blinking is characteristic - 2-3 times per minute compared to 3-5 in the norm (Stelvag's symptom).

Jellinek's symptom is characterized by brown pigmentation of the eyelids and skin around the eyes. In some cases, there is a trembling of the closed eyelids (Rosenbach's symptom), the absence of wrinkling of the forehead when looking up (Geoffroy's symptom). Krauss's symptom is expressed in a strong glare of the eyes. In addition to diffuse toxic goiter, this symptom can be observed in tuberculosis, rheumatism, functional disorders of the nervous system, as well as in healthy people. In some patients, there is an inability to squint the eyes (Kocher). Zenger pointed to a soft, cushion-like swelling of the eyelids (Senger's symptom), which in the later stages of the disease can turn into a bag-like drooping of the eyelids.

The appearance of eye symptoms is associated with a violation of the tone of the eye muscles. Due to the variability, as well as non-specificity, the significance of eye symptoms is small.

Ocular symptoms of diffuse toxic goiter should be distinguished from ophthalmopathy(edematous exophthalmos, malignant exophthalmos, neurodystrophic exophthalmos, endocrine ophthalmoplegia and other names). Ophthalmopathy is caused by the influence of the so-called exophthalmic factor, which is a precursor in the biosynthesis of thyroid-stimulating hormone from the pituitary gland. An important role is given to autoimmune processes.

Rice. 7. Ophthalmopathy

The protrusion of the eyeball and its exit from the orbit occurs as a result of an increase in the volume of tissue located behind the eyeball (retrobulbar). The increase in the volume of the retrobulbar tissue is due to edema, lymphocytic and fatty infiltration, venous congestion and an increase in the volume of the eye muscles due to their edema.

With endocrine exophthalmos, patients complain of pain and pressure in the eyeballs, photophobia, a feeling of "sand" in the eyes, doubling and lacrimation. As a result of paralysis of the eye muscles, the movement of the eyes up and to the sides is limited.

There are three degrees of ophthalmopathy, in which the protrusion (constancy) of the eyeball is 16, 18 and 22-23 mm, respectively. With significant ophthalmopathy (III degree), the eyeballs protrude from the orbits, the eyelids and conjunctiva are edematous, inflamed, keratitis develops due to the constant drying of the cornea and its ulceration, which can lead to blindness. Edema of the retroorbital (retrobulbar) tissue not only leads to the expulsion of the eyeball from the orbit - exophthalmos, but also causes compression of the optic nerve with loss of vision, and can also cause thrombosis of the retinal vessels.

Endocrine ophthalmopathy is more often observed after 40 years, but can occur at any age. Men are more often affected. Usually, ophthalmopathy is bilateral, less often (at the beginning of the disease) unilateral.

Ophthalmopathy develops against the background of diffuse toxic goiter, however, the correlation between the severity of thyrotoxicosis and the severity of ophthalmopathy is not always observed. Endocrine ophthalmopathy occurs against the background of normal and even reduced thyroid function, with inflammatory diseases of the gland, autoimmune thyroiditis. Sometimes ophthalmopathy occurs after surgical treatment of diffuse toxic goiter or treatment with radioactive iodine. Occasionally, ophthalmopathy precedes thyroid disease.

In addition to diffuse toxic goiter, exophthalmos can occur with a high degree of myopia, glaucoma. It can be familial or congenital. Unilateral and bilateral exophthalmos requires a special examination by an ophthalmologist, a neuropathologist, since the causes of its occurrence may be inflammatory processes and brain tumors, congenital anomalies of the skull, etc.

It is wrong to think that the disease is limited only to the defeat of one thyroid gland. With thyrotoxicosis, damage to many body systems is observed.

Neuromuscular system. In the clinical picture of diffuse toxic goiter, disorders of the central and peripheral nervous system occupy one of the first places. The outstanding domestic therapist S. P. Botkin (1885) considered mental changes to be the most significant symptom of Graves' disease, "more permanent and characteristic than goiter and bulging eyes."

Persons suffering from diffuse toxic goiter are usually animated, excited, restless, emotionally labile. They are verbose, quick in their movements, fussy, hurried, irritable, whiny, touchy, often experiencing a state of fear. The most insignificant reasons can cause tears. Characterized by a quick change of mood, lack of concentration, loss of the ability to concentrate. Some patients cannot sit still for a single minute. They easily come into conflict with others, become quarrelsome, self-centered. Feelings of anxiety and gloomy forebodings are replaced by feelings of deep anxiety. There may be outbursts of rage.

Many patients complain of persistent insomnia. Their sleep is intermittent, shallow, with nightmares. Graves' disease is a fertile ground for the development of mental disorders. Sometimes there is a manic state, followed by a depressive mood.

A characteristic symptom of the disease is a small tremor (trembling) of the fingers of outstretched hands (Marie's symptom). Sometimes the tremor of the hands is so pronounced that patients can hardly fasten buttons, hold a cup of tea in their hands, or perform any other precise movements. Handwriting may change. In severe thyrotoxicosis, trembling of the head, tongue, drooping eyelids, feet, and the whole body is observed (a symptom of the "telegraph pole"). Thyrotoxic trembling is characterized by a small scope and a fast rhythm. It is the subtle form of tremor in the form of rapid fine trembling that is characteristic of Graves' disease, in contrast to neurological pathology, in which the tremor is more sweeping.

An early and frequent symptom of diffuse toxic goiter is muscle weakness, which may be accompanied by paresis and muscle atrophy. Especially characteristic is the weakness of the muscles of the arms, shoulder girdle, pelvis. Muscle weakness (myopathy) usually develops slowly, over several months or years. Patients have difficulty walking, climbing stairs. In severe cases, the patient cannot stand up without assistance. The occurrence of myopathy is associated with disorders of protein and energy metabolism in muscle tissue. After successful treatment of diffuse toxic goiter, myopathy disappears.

Periodic paralysis (thyrotoxic myoplegia) is manifested by a sudden short-term paroxysmal muscle weakness that occurs when walking or standing for a long time. In severe cases, there may be complete paralysis of all skeletal muscles. The duration of the attack is from several hours to several days. Thyrotoxic myoplegia disappears under the influence of antithyroid treatment. The occurrence of an attack of periodic paralysis is associated with a decrease in the level of potassium in the blood serum.

Patients have a youthful, youthful appearance. If the disease began in childhood or adolescence (before the end of bone growth), body growth often exceeds the norm. Young patients usually have thin hands, thin fingers with a pointed terminal phalanx ("Madonna's hands").

In severe forms of toxic goiter, especially in the elderly, osteoporosis and increased bone fragility may occur. This is due to a violation of protein and phosphorus-calcium metabolism.

Leather in patients with diffuse toxic goiter, it is elastic, tender, with a slight feeling of velvety, thin, transparent. Its elasticity is maintained despite the weight loss that accompanies thyrotoxicosis. There are no wrinkles or dull skin. There is slight redness of the face and neck.

As a result of increased metabolism and heat production, the skin may be moist, warm or hot to the touch. Wet, pink skin is a characteristic sign of thyrotoxicosis. The hands and feet are usually warm, in contrast to neurocirculatory asthenia. With a slight increase in ambient temperature or with light work, the moisture of the skin easily turns into perceptible perspiration.

In severe thyrotoxicosis, the skin of the eyelids, armpits, genitals, anus, as well as in places where clothing is rubbed, can be pigmented. Sometimes there is an almost diffuse brown coloration of large areas of the skin or even the entire body. Pigmentation of the mucous membranes, on the contrary, is rarely detected.

In a small proportion of patients with diffuse toxic goiter (3-4%), a peculiar skin lesion occurs, called pretibial myxedema. The skin of the anterior surface of the legs is affected, it becomes edematous, thickened, rough, rough, with protruding hair follicles, reminiscent of orange peel or pigskin. Skin changes are often accompanied by significant redness and itching. These swollen spots are sensitive to pressure, but finger pressure does not pit. The legs look swollen and have a shapeless appearance.

A biopsy (microscopic examination) of these areas of the skin reveals changes characteristic of hypothyroidism. The cause of pretibial myxedema is not clear. Sometimes it appears (as well as ophthalmopathy) a few months after surgical treatment of diffuse toxic goiter or treatment with radioactive iodine.

Subcutaneous adipose tissue in most patients with diffuse toxic goiter is poorly developed. Despite a good or even increased appetite, patients lose weight. Within a few months, they can lose 10-15 kg or more in weight. In severe forms of thyrotoxicosis, in neglected, undiagnosed or poorly treated cases, a sharp exhaustion develops - cachexia. This is explained by a significant increase in metabolic processes, enhanced combustion of fat reserves and loss of water. In rare cases, patients with diffuse toxic goiter may be overweight (the so-called "fat Basedow").

With thyrotoxicosis, skin appendages suffer. The hair is thin, brittle and falls out easily. Hair growth on the body, in the armpits and other places is sparse. The fragility of nails is increased, their longitudinal striation is observed.

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Diffuse toxic goiterTreatment of diffuse toxic goiter

6. Ectodermal disorders: fragility of nails, hair loss.

7. Digestive system: abdominal pain, unstable stool with a tendency to diarrhea, thyrotoxic hepatosis.

8. Endocrine glands: ovarian dysfunction up to amenorrhea, fibrocystic mastopathy, gynecomastia, impaired carbohydrate tolerance, tyrogenic relative, that is, with a normal or increased level of cortisol secretion, adrenal insufficiency (moderate melasma, hypotension).

Conservative pharmacological treatment

The main means of conservative treatment are the drugs Mercazolil and methylthiouracil (or propylthiouracil). The daily dose of Mercazolil is 30-40 mg, sometimes with very large goiter and severe thyrotoxicosis, it can reach 60-80 mg. The maintenance daily dose of Mercazolil is usually 10-15 mg. The drug is taken continuously for 1/2-2 years. Reducing the dose of Mercazolil is strictly individual, it is carried out, focusing on the signs of elimination of thyrotoxicosis: pulse stabilization (70-80 beats per minute), weight gain, disappearance of tremor and sweating, normalization of pulse pressure.

Radioiodine therapy (RIT) is one of the modern methods of treating diffuse toxic goiter and other thyroid diseases. During treatment, radioactive iodine (isotope I-131) is administered into the body in the form of gelatin capsules orally (in rare cases, a liquid solution of I-131 is used). Radioactive iodine, which accumulates in the cells of the thyroid gland, exposes the entire gland to beta and gamma radiation. In this case, the cells of the gland and tumor cells that have spread beyond its limits are destroyed. Conducting radioiodine therapy implies mandatory hospitalization in a specialized department.

Absolute indications for surgical treatment are allergic reactions or a persistent decrease in leukocytes observed during conservative treatment, large goiter (enlargement of the thyroid gland above grade III), heart rhythm disturbances like atrial fibrillation with symptoms of cardiovascular insufficiency, pronounced goiter effect of Mercazolil.

The operation is performed only when the state of drug compensation is reached, since otherwise a thyrotoxic crisis may develop in the early postoperative period.

Nodular toxic goiter - hyperthyroidism due to an autonomously functioning thyroid adenoma (TG) in the form of one or more nodules. The function of the remaining parts of the gland is suppressed by low TSH levels due to high levels of thyroid hormones. These sites are identified by their ability to accumulate radioactive iodine after TSH injection. Nodules and cysts in the thyroid gland are often incidental findings detected by ultrasound. In patients with a solitary thyroid nodule identified clinically or by ultrasound, the possibility of cancer should be considered.

SURGERY. All malignant and some benign tumors of the thyroid gland are subject to surgical treatment.

Indications for surgical treatment

The presence in the anamnesis of irradiation of the neck (suspicion of a malignant process)

The large size of the node (more than 4 cm) or the compression symptoms caused by it

Progressive node growth

Dense knot consistency

The young age of the patient.

The volume of the operation for a solid benign nodular formation is the removal of a lobe with / without the isthmus of the gland; with highly differentiated cancer (papillary or follicular) - extremely subtotal thyroidectomy.

Indications for surgical intervention: diffuse toxic goiter of moderate and severe form, nodular toxic goiter (thyrotoxic adenoma), large goiter that compresses the organs of the neck, regardless of the severity of thyrotoxicosis. Before surgery, it is necessary to bring the functions of the thyroid gland to a euthyroid state.

Contraindications to surgical intervention: mild forms of thyrotoxicosis, in old malnourished patients due to high operational risk, in patients with irreversible changes in the liver, kidneys, cardiovascular and mental diseases.

2.Indications and contraindications for hernia repair. The main stages of the hernia operation. Principles of reliable plasty of hernial orifices.

In general, all hernias should be repaired if the patient's local or systemic status portends a reliable outcome. A possible exception to this rule is a hernia that has a wide neck and a small bag, i.e., signs indicating the possibility of a slow increase in the hernia. Hernia bandages and surgical straps have been successfully used in the treatment of small hernias in situations where surgery is contraindicated, but the use of hernia bandages is not recommended for patients with femoral hernias.

Contraindications to surgery: absolute - acute infection, severe diseases - tuberculosis, malignant tumors, severe respiratory and heart failure, etc. Relative - early age (up to six months), decrepitude, the last 2-3 months of pregnancy, urethral stricture, prostate adenoma (hernia repair is performed after their elimination).

The operation in all cases consists of two stages: I / the actual hernia repair - the selection of the hernial sac, opening it, repositioning the viscera, stitching and bandaging the sac in the cervical region and cutting it off - is performed the same for all forms of hernias; 2/plasty (suturing) of the hernia orifice - it is performed differently even with the same form of hernia, depending on this, different methods of hernia repair are distinguished.

Anesthesia - traditionally local (novocaine or lidocaine) - for small hernias in adults, anesthesia is used for all other hernias in adults, including complicated large incisional hernias and in neuropaths, as well as in children.

Preoperative preparation - hygienic bath and shaving of the surgical field, cleansing enema on the eve of the operation. In the postoperative period - the prevention of pulmonary complications, the fight against flatulence. The timing of getting up varies depending on the characteristics of the patient and the operation.

The last most important stage of the operation - hernial orifice plasty is performed in various ways: 1) by stitching together local homogeneous tissues (autoplastic methods); 2) using additional biological or synthetic materials (alloplastic methods).

3.Mallory-Weiss syndrome. Definition. The reasons. Clinic. Diagnostics. differential diagnosis. Conservative treatment. indications for surgery.

Mallory-Weiss syndrome is a longitudinal rupture of the esophageal mucosa that occurs with a strong urge to vomit or during vomiting itself. Clinically, Malory-Weiss syndrome will be manifested by the presence of blood in the vomit. Moreover, blood may be absent during the first bouts of vomiting, when only a rupture of the mucosa occurs. In addition to vomiting with an admixture of blood, patients with this syndrome may have abdominal pain, black stools (melena). Diagnosis of the Mallory-Weiss syndrome. Of the instrumental methods for diagnosing Malory-Weiss syndrome, endoscopic examination (fibroesophagogastroduodenoscopy) is of the greatest value. This study allows you to see the longitudinal rupture of the mucosa of the esophagus. In addition, if bleeding is detected, then it can be tried to stop it endoscopically (see Treatment of Mallory-Weiss Syndrome). In the anamnesis of patients with Malory-Weiss syndrome, one can often find mention of the use of alcoholic beverages in large quantities, as a result of which vomiting occurred. When examining a patient with Malory-Weiss syndrome, one can find common signs of all bleeding: pallor of the skin, cold sticky sweat, lethargy, tachycardia, hypotension, and possibly even the development of shock.

In a clinical blood test, there will be a decrease in the number of red blood cells, hemoglobin levels, an increase in the number of platelets, which indicates the presence of bleeding. Conservative therapy for Malory-Weiss syndrome is used to restore the volume of circulating blood. For this, various crystalloid (NaCl 0.9%, glucose 5%, Ringer's solution, etc.), colloidal solutions (albumin, aminoplasmal, etc.) are used, in case of severe blood loss, hemotransfusion can be used (erythrocyte mass, fresh frozen plasma) (or urge to vomit) use metoclopramide (cerucal). In order to stop bleeding, a Blackmore probe is used. This probe has 2 balloons. With the help of the lower balloon, the probe is fixed in the stomach in the correct position, after which the second balloon is inflated, located in the lumen of the esophagus. The hemostatic effect is achieved by mechanical compression of the bleeding vessels of the esophagus. In order to stop bleeding, it is possible to use sodium etamsylate, calcium chloride, aminocaproic acid, octreatide. When performing fibroesophagogastroduodenoscopy and detecting a longitudinal rupture of the esophageal mucosa with bleeding, you can try to stop this bleeding endoscopically. It uses:

1. Pricking the bleeding site with adrenaline

A solution of epinephrine hydrochloride is injected into the area of bleeding, as well as around the source of bleeding. The hemostatic effect is achieved due to the vasoconstrictive action of adrenaline.

2. Argon-plasma coagulation

This method is one of the most effective and at the same time one of the most technically difficult. The use of the method of argon-plasma coagulation allows to achieve stable hemostasis.

3. Electrocoagulation

It is also a fairly efficient method. Often the use of electrocoagulation is combined with the introduction of adrenaline.

4. Introduction of sclerosants

This method lies in the fact that the hemostatic effect is achieved by the introduction of sclerosing drugs (polidocanol).

5. Vessel ligation

In Malory-Weiss syndrome, endoscopic ligation of bleeding vessels is often used. The use of endoscopic vessel ligation is especially justified in the combination of Malory-Weiss syndrome and portal hypertension with esophageal varicose veins.

6. Clipping of vessels

In essence, this method is similar to the previous one. The only difference is that not a ligature is applied to the bleeding vessel, but a metal clip. Clips can be applied using the applicator. Unfortunately, endoscopic clipping of vessels is not always possible due to the technical difficulties of applying clips to vessels.

in. In Malory-Weiss syndrome, surgical treatment is resorted to in case of failure of conservative therapy and endoscopic methods of treatment. With Malory-Weiss syndrome, the Baye operation will be performed:

Access: median laparotomy.

Operation: gastrotomy, stitching of bleeding vessels.

TICKET #3

1. Goiter and thyrotoxicosis. Complications during and after surgery. Clinic of complications, their treatment and prevention.

Intraoperative complications: bleeding, air embolism, damage to the recurrent nerve, removal or damage to the parathyroid glands with subsequent development of hypoparathyroidism. If both recurrent nerves are damaged, the patient develops acute asphyxia and only immediate tracheal intubation or tracheostomy can save the patient. In patients with thyrotoxicosis in the postoperative period, the most dangerous complication is the development of a thyrotoxic crisis. The first sign of a thyrotoxic crisis is a rapid increase in body temperature up to 40°C, accompanied by increasing tachycardia. Blood pressure first rises and then decreases, neuropsychiatric disorders are observed.

In the development of the crisis, the main role is played by the insufficiency of the function of the adrenal cortex, due to operational stress. Treatment of the crisis should be aimed at combating adrenal insufficiency, cardiovascular disorders, hyperthermia and oxygen deficiency.

Tracheomalacia. With a long-term goiter, especially with retrosternal, retrotracheal and retroesophageal, due to its constant pressure on the trachea, degenerative changes occur in the tracheal rings and their thinning - Tracheomalacia. After removal of the goiter immediately after the extubation of the trachea or in the immediate postoperative period, it may kink in the area of softening or convergence of the walls and narrowing of the lumen. Acute asphyxia occurs, which can lead to the death of the patient if an urgent tracheostomy is not performed (see "Inflammatory diseases of the trachea").

Postoperative hypothyroidism - insufficiency of the thyroid gland, due to its complete or almost complete removal during surgery, develops in 9--10% of operated patients. Hypothyroidism is characterized by general weakness, constant feeling of fatigue, apathy, drowsiness, and general lethargy of patients. The skin becomes dry, wrinkled, swollen. Hair begins to fall out, pain in the limbs appears, sexual function weakens.

Treatment: prescribe thyroidin and other thyroid drugs. With the development of microsurgical techniques and advances in immunology, allotransplantation of the thyroid gland using a transplant on a vascular pedicle began to be performed. Free replanting of pieces of gland tissue under the skin, into the muscle is also used, however, these operations usually give a temporary effect, therefore, in practice, substitution therapy is mainly used.

2.Oblique inguinal hernia. clinical picture. Diagnostics. differential diagnosis. Operation methods. Congenital inguinal hernia.

Oblique inguinal hernias are formed as a result of protrusion of the hernial sac through the internal inguinal ring corresponding to the lateral inguinal fossa. The hernial sac is covered with a common vaginal membrane of the spermatic cord and repeats its course.

Depending on the stage of development, it is customary to distinguish the following forms of oblique inguinal hernias (according to A.P. Krymov): 1) initial hernia, in which the sac is determined only in the inguinal canal; 2) channel form - the bottom of the bag reaches the outer opening of the inguinal canal; 3) cord form - a hernia exits through the external opening of the inguinal canal and is located at different heights of the spermatic cord; 4) inguinal-scrotal hernia - the hernial sac with the contents descends into the scrotum (in women - into the fiber of the labia majora).

Congenital inguinal hernias are always oblique. They develop in case of non-closure of the vaginal process of the peritoneum. The latter, communicating with the peritoneal cavity, forms a hernial sac. At the bottom of the hernial sac lies the testicle, since its own shell is at the same time the inner wall of the hernial sac. Congenital inguinal hernias are often combined with dropsy of the testicle or spermatic cord.

The diagnosis of an inguinal hernia is usually not difficult. A characteristic objective sign is a protrusion of the anterior abdominal wall in the inguinal region, which increases with straining and coughing. With an oblique inguinal hernia, it has an oblong shape, is located along the inguinal canal, often descends into the scrotum.

Finger examination of the hernial canal allows you to determine its direction and differentiate the type of hernia. With an oblique inguinal hernia, the finger does not determine the presence of bone when moving it along the inguinal canal, since this is prevented by the muscular aponeurotic elements of the inguinal triangle. Without removing the finger from the hernial canal, the patient is asked to strain or cough - a symptom of a cough impulse is determined. Differential diagnosis. Inguinal hernia should be differentiated from femoral hernia, dropsy of the testicular membranes, cysts of the spermatic cord and Nukov's canal, cryptorchidism, varicocele, inguinal lymphadenitis, tumors in the area of the inguinal canal. When differentiating a hernia, dropsy, testicular tumor, it is advisable to use the transillumination method. A light source (flashlight) is installed on one side of the scrotum, and on the other side, using a tube, the glow is determined. With a hernia and a tumor of the testicle, there is no glow, but with dropsy it is determined. Cryptorchidism is characterized by a high location of the "tumor" at the root of the scrotum, its non-displacement and the impossibility of repositioning into the abdominal cavity.

The presence of an inguinal hernia is an indication for surgical treatment. More than 200 methods have been proposed for the restoration and reconstruction of the abdominal wall with inguinal hernias. They can be conditionally divided into three groups:

Methods of strengthening the anterior wall of the inguinal canal without dissection of the aponeurosis of the external oblique muscle of the abdomen. This group includes the methods of Ru, Ru-Oppel, Krasnobaev. They are used for uncomplicated inguinal hernias in childhood.

Methods aimed at strengthening the anterior wall of the inguinal canal after dissection of the aponeurosis of the external oblique muscle of the abdomen (methods of the operation of Martynov, Girard, Spasokukotsky, Kimbarovsky, etc.).

3. Methods of hernioplasty associated with the strengthening of the posterior wall of the inguinal canal and the movement of the spermatic cord. This group includes the methods of Bassini, Kukudzhanov, McVey, Shuldice, Postempsky, etc.

When choosing a hernioplasty method, it must be remembered that in the genesis of the formation of inguinal hernias, the leading role is played not by the weakness of the aponeurosis of the external oblique muscle of the abdomen and the expansion of the external inguinal ring, but by the weakening of the posterior wall of the inguinal canal and an increase in the diameter of its deep opening. Based on this premise, for all direct, most oblique hernias and recurrent hernias, methods of plasty of the posterior wall of the inguinal canal should be used. Strengthening of its anterior wall can be used in children and young men with small oblique inguinal hernias. The expediency of such surgical tactics is confirmed by the statistics of long-term results of hernia repair.

The peculiarity of the operation for congenital inguinal hernia lies in the method of processing the hernial sac. The latter is isolated at the neck, bandaged and crossed. The distal part of the sac is not removed, but cut along its entire length, then turned out and sewn behind the spermatic cord and testicle (similar to the Winckelmann operation for dropsy of the testicle). Plastic surgery of the inguinal canal is performed according to one of the methods listed above.

The sequence of surgery for inguinal hernia is the same for various methods and consists of the following steps:

The first stage is the formation of access to the inguinal canal. Exposure of the inguinal canal is achieved by a skin incision made parallel to the inguinal ligament and above it by 2 cm, about 10-12 cm long. Accordingly, the aponeurosis of the external oblique muscle of the abdomen is dissected and the pupart ligament is exposed.

The second stage is the isolation from the surrounding tissues and the removal of the hernial sac. Sewing the neck of the bag before cutting it off is done either from the outside or from the inside with a purse-string suture, but always under the control of the eye.

The third stage is the suturing of the deep inguinal opening to normal sizes (0.6-0.8 cm) with its expansion or destruction.

The fourth stage of the operation is plastic surgery of the inguinal canal.

A large number of operations proposed for the treatment of inguinal hernias differ from each other only in the final stage - the method of inguinal canal plasty.

3.Symptomatic acute ulcers: stress, hormonal, medicinal. Clinic. Diagnostics. differential diagnosis. Complications. Surgical tactics. Indications and features of surgical treatment. Zollinger-Ellison syndrome.

The disease occurs in stressful situations associated with a serious pathology of internal organs, severe surgical interventions, burns, polytrauma, taking certain drugs, etc.

Depending on the cause of the occurrence, the following types of acute ulcers are distinguished:

1) stress ulcers - in patients with multiple trauma (polytrauma), shock, sepsis, severe major operations on the organs of the chest cavity, abdomen, on large vessels and operations on the brain;

2) Cushing's ulcer - after brain surgery, with traumatic brain injury and brain tumors due to central stimulation of gastric secretion and an increase in its aggressive properties in relation to the gastric mucosa;

3) drug ulcers that occur when taking acetylsalicylic acid, indomethacin, voltaren, steroid hormones, cytostatic drugs.

Typical signs of all acute ulcers are sudden massive life-threatening bleeding or perforation of the ulcer. The best way to diagnose acute ulcers is endoscopic examination. It should be borne in mind that before the onset of bleeding, acute ulcers are usually asymptomatic.

Acute erosive gastritis. This disease is characterized by superficial flat rounded or elongated defects in the gastric mucosa (erosion). Unlike ulcers, they do not destroy the muscularis mucosa (lamina muscularis mucosae). The causes of their occurrence are severe stress, multiple injuries, extensive burns (Curling's ulcer), extensive traumatic operations, taking certain medications; the main clinical symptoms are bleeding (hematemesis, melena), shock. The diagnosis is established by endoscopic examination.

Drugs (steroid hormones, acetylsalicylic acid, butadione, indomethacin, atophane) reduce the formation of mucus, destroy the protective barrier of the mucous membrane, and cause hemorrhages. With the abolition of drugs, ulcers and erosions heal quickly.

Mucosal ischemia plays a key role in the development of hemorrhagic gastritis, as it contributes to the weakening of its protective barrier.

Treatment. In acute ulcers and erosive gastritis, conservative treatment is first performed.

Surgical treatment is rarely used. Preference is given to selective proximal vagotomy, chipping and ligation of bleeding vessels, less often gastric resection or even gastrectomy (in exceptional cases).

A simple ulcer of Dieulafoy is amenable only to surgical treatment: the bleeding artery is cut off and tied up through the gastrotomy opening or the ulcerated area is excised and a suture is placed on the edges of the wound in the wall of the stomach. Bleeding often recurs.

Zollinger-Ellison syndrome (pancreatic adenoma ulcerogenic, gastrinoma) is a tumor of the islet apparatus of the pancreas, characterized by the occurrence of peptic ulcers of the duodenum and stomach, not amenable to treatment and accompanied by persistent diarrhea. Clinical manifestations of the disease are pains in the upper abdomen, which have the same patterns in relation to food intake as in the case of a normal duodenal ulcer and stomach, but unlike them, they are very stubborn, very intense and do not respond to antiulcer therapy.

Characterized by persistent heartburn and belching sour. An important symptom is diarrhea caused by the ingestion of a large amount of hydrochloric acid into the small intestine and, as a result, increased motility of the small intestine and slow absorption. Stools are profuse, watery, with a lot of fat. Perhaps a significant decrease in body weight, which is typical for malignant gastrinemia.

Ulcers of the stomach and duodenum in Zollinger-Ellison syndrome do not heal even with prolonged appropriate therapy. Many patients experience esophagitis, sometimes even with the formation of narrowing of the esophagus. Palpation is determined by severe pain in the upper abdomen, and the area of the projection of the lower part of the stomach, there may be a positive Mendel's symptom (local pain in the projection of the ulcer). In the case of a malignant course of the disease, tumor formations in the liver and its significant increase are possible.

The main method of treatment (in 80%) is gastrectomy. In order to decide on the complete removal of the stomach, one must be sure of the presence of Zollinger-Ellison syndrome. If there is no such confidence, then some authors (V. M. Sitenko, V. I. Samokhvalov, 1972) recommend resorting to diagnostic vagotomy or resection of the unoperated stomach and, if a month after them, gastric secretion remains extremely high, perform extirpation of the stomach in a planned order, without waiting for the development of ulcer complications. The indication for gastrectomy is the presence of multiple gastrinoma, single gastrinoma with metastases, as well as recurrence of the ulcer after removal of the tumor.

As already mentioned, gastrinomas are often multiple, located in different parts of the pancreas and in different organs, which makes it extremely difficult to find them during surgery. Therefore, attempts to treat patients with Zollinger-Ellison syndrome by removing the tumor alone are usually unrealistic. True, cases of successful treatment of such patients with such an intervention under the control of operational pH-metry of the gastric mucosa are described (A. A. Kurygin, 1987). In these individual observations, after the removal of single gastrinomas, achlohydria occurred already on the operating table. However, such observations are extremely rare and not always reliable.

Removal of pancreatic adenoma is justified and reliable in Werner-Morrison syndrome, in which the patient is not threatened by the development of ulcers in the stomach and duodenum.

TICKET #4

1.Thyroiditis and strumitis. Definition. Concepts. Clinic. Diagnostics. differential diagnosis. Conservative and surgical treatment. Hashimoto's and Fidel's thyroiditis.

The inflammatory process that develops in the previously unchanged thyroid gland is called thyroiditis, and that develops against the background of goiter is called strumitis. The cause of thyroiditis and strumitis is an acute or chronic infection.

Acute thyroiditis or strumitis begins with fever, headache, and severe pain in the thyroid gland. The pain radiates to the occipital region and ear. A swelling appears on the front surface of the neck, which is displaced when swallowing. A severe complication of thyroiditis is the development of purulent mediastinitis. Sometimes sepsis develops. That is why hospitalization for the purpose of active treatment is shown to all patients.

Treatment: prescribe antibiotics; when an abscess is formed, its opening is shown in order to avoid the spread of the purulent process to the neck and mediastinum.

Chronic lymphomatous thyroiditis Hashimoto. The disease is classified as an autoimmune organ-specific pathological process, in which antibodies formed in the body are specific to the components of one organ. With Hashimoto's thyroiditis, under the influence of unknown causes, the thyroid gland begins to produce altered hormonally inactive iodine proteins that differ from thyroglobulin. Penetrating into the blood, they become antigens and form antibodies against thyroid acinar cells and thyroglobulin. The latter inactivate thyroglobulin. This leads to a disruption in the synthesis of normal thyroid hormones, which causes an increase in the secretion of TSH by the pituitary gland and hyperplasia of the thyroid gland. In the late stages of the disease, the thyroid function of the gland is reduced, the accumulation of iodine in it decreases.

Clinic and diagnosis: Hashimoto's thyroiditis occurs more often in women over the age of 50 years. The disease develops slowly (1-4 years). The only symptom for a long time is an enlarged thyroid gland. It is dense to the touch, but not soldered to the surrounding tissues and is mobile on palpation. Later, discomfort and signs of hypothyroidism appear. Regional lymph nodes are not enlarged.

Of great importance in the diagnosis is the detection of antithyroid autoantibodies in the patient's serum. The final answer is obtained by puncture biopsy.

Treatment: conservative, includes the appointment of thyroid and glucocorticoid hormones The dose of thyroid hormones is chosen individually, the average daily dose of thyroidin is 0.1-0.3 g The daily dose of prednisolone is 20-40 mg for 1 1/2 - 2 months with a gradual decrease in dose .

If a malignant degeneration is suspected, with compression of the neck organs by a large goiter, an operation is indicated. Produce subtotal resection of the thyroid gland. After the operation, treatment with thyroidin is necessary due to the inevitably developing hypothyroidism.

Chronic fibrous thyroiditis of Riedel. The disease is characterized by the proliferation of connective tissue in the thyroid gland, which replaces its parenchyma, and the involvement of surrounding tissues in the process. The etiology of the disease has not been established.

Clinic and diagnostics. The thyroid gland is diffusely enlarged, of stony density, soldered to the surrounding tissues. There are moderate signs of hypothyroidism. Pressure on the esophagus, trachea, vessels and nerves cause the corresponding symptoms.

Treatment: before surgery, it is almost impossible to exclude a malignant tumor of the thyroid gland, therefore, with Riedel's thyroiditis, surgical intervention is indicated. The maximum possible excision of fibrosing thyroid tissue is performed, followed by replacement therapy.

2. 2. Direct and oblique inguinal hernias (anatomical and clinical differences). Causes of hernia recurrence. Operation methods.

Causes of recurrence of inguinal hernias are diverse. They can be systematized as follows:
1) causes existing before the operation; 2) reasons depending on the type of operation performed and its technical execution; 3) causes that arose in the postoperative period.

To the first group of causes of relapses relate:
1) late surgery in the presence of significant changes in the tissues of the inguinal region (it has long been noted [A.I. Baryshnikov, 1965] that the longer a hernia exists, the deeper morphological changes it causes in the inguinal canal, the more often relapses occur in the postoperative period);
2) the elderly age of the patient (in this group of patients, recurrent hernias are observed most often, which is associated primarily with progressive degenerative changes in the tissues of the inguinal region: the results of studies by Yu.N. Nesterenko and Yu.B. Salov are especially demonstrative in this regard ( 1980), which are presented in Table 13);
3) the presence of concomitant chronic diseases that cause sharp fluctuations in intra-abdominal pressure (prostatic hypertrophy, urethral stricture, chronic constipation, chronic bronchitis, pulmonary emphysema, etc.);
4) insufficient examination and sanitation of the patient before surgery, leaving foci of infection in the body, which can lead to complications in the postoperative period (chronic tonsillitis, pustular and infectious diseases).

Co. the second group of causes of relapses relate:
1) the wrong choice of the method of operation, without taking into account the pathogenetic conditions for the formation of a hernia and those changes in the inguinal canal that occur in patients with inguinal hernias (for example, strengthening with direct and recurrent hernias only the anterior wall of the inguinal canal, leaving an enlarged deep opening of the inguinal canal and a high inguinal interval);
2) gross defects in surgical technique (insufficient hemostasis, insufficiently high allocation of the hernial sac, viewing the second hernial sac, slipping of the ligature from the stump of the hernial sac, leaving the transverse fascia unsutured or destroying it during the operation, stitching tissues with high tension, suturing to the inguinal ligament superficial fascia instead of the aponeurosis of the external oblique muscle, suturing to the inguinal ligament not the entire thickness of the muscles, but only the surface layer, insufficient separation of the stitched tissues from fatty tissue, damage to blood vessels and nerves). With alloplastic methods of operations, the most common cause of complications is the use of plastic materials that cause a high tissue reaction.

To The third group of causes of relapses include:
1) inflammatory complications from the surgical wound (suppuration, infiltrates, ligature fistulas);
2) an early load on a scar that has not yet formed;
3) hard physical work in the late postoperative period.

Girard method. Inguinal canal plasty is performed by suturing the internal oblique and transverse abdominal muscles to the pupart ligament over the spermatic cord. Then, the inner leaf of the dissected aponeurosis of the external oblique muscle of the abdomen is sutured to the pupart ligament. On top of it, the outer leaf of the aponeurosis is sewn, thus creating an aponeurotic duplication. The external opening of the inguinal canal is formed so that it passes the tip of the finger (spermicular cord). Sutures are applied to the skin.

Spasokukotsky's method. It differs from the Girard method in that the internal oblique and transverse muscles are sutured to the inguinal ligament simultaneously (with one suture), along with the internal leaf of the aponeurosis of the external oblique muscle of the abdomen. Then, an arc chamber is also created from the sheets of the aponeurosis.

The Kimbarovsky method (Kimbarovsky sutures) is the most commonly used modification of the Girard-Spasokukotsky operation in clinical practice. The essence of the modification is the use of original sutures in plastic surgery, which provide a comparison of homogeneous tissues. To do this, the first injection of the needle is done, retreating 1 cm from the edge of the upper leaf of the aponeurosis. The needle passes through the entire thickness of the underlying muscles and returns to the anterior surface of the aponeurosis at its very edge. Then the inguinal ligament is captured with the same needle. The remaining sutures are applied in the same way. When the threads are tightened, the upper leaf of the aponeurosis turns up and covers the muscles. As a result, the edges of the muscles wrapped in aponeurosis are sutured in front of the spermatic cord to the inguinal ligament.

Martynov's method. The steps of the operation are the same as for the Girard method. Plastic surgery is performed by suturing the inner leaf of the aponeurosis of the oblique abdominal muscle to the pupart ligament, followed by the formation of a duplication from the aponeurosis.

3. Pyloric stenosis of ulcerative etiology. Clinic. stages of stenosis. Diagnostics. differential diagnosis. Preoperative preparation of patients with decompensated pyloroduodenal stenosis. Indications (absolute and relative) for operations. Types of operations.

Cicatricial stenosis of the duodenum and the outlet of the stomach develops in 10-15% of patients with peptic ulcer. It was previously stated that stenosis always forms at the level of the ulcer. However, the narrowing of the outlet section of the stomach and duodenum is not always due to the cicatricial process. Swelling and inflammation of the tissues in the area of the ulcer during an exacerbation of the disease can sometimes be accompanied by a violation of the evacuation of gastric contents, which is eliminated with effective antiulcer treatment. Depending on the degree of violation of the evacuation of the contents of the stomach, it is customary to distinguish three degrees of stenosis of the outlet section of the stomach or duodenum: compensated, subcompensated and decompensated.

At the compensated stage of stenosis, patients are in a satisfactory condition, they do not have vomiting with stagnant stomach contents, with X-ray

Anatomical and physiological data and symptoms of lesions of the first pair of craniocerebral insufficiency

The patient states that objects sometimes seem distorted, beveled, twisted around their axis, and sometimes too distant from the patient. Name the symptom(s).

Will the patient reject any notion that the symptoms are stress related?

Eye symptoms of thyrotoxicosis are fundamentally different from an independent disease of endocrine ophthalmopathy.

6. Endocrine ophthalmopathy (EOP)- defeat of periorbital tissues of autoimmune origin, in 95% of cases combined with autoimmune diseases of the thyroid gland (TG), clinically manifested by dystrophic changes in the oculomotor muscles (OOM) and other structures of the eye. There are 3 degrees of severity of the image intensifier:

I. Swelling of the eyelids, a feeling of "sand in the eyes", lacrimation, in the absence of diplopia.

II. Diplopia, limitation of abduction of the eyeballs, paresis of the gaze upward.

III. Vision-threatening symptoms: incomplete closure of the palpebral fissure, corneal ulceration, persistent diplopia, optic nerve atrophy.

EOP is an independent autoimmune disease, however, in 90% of cases it is combined with diffuse toxic goiter (DTG), in 5% with autoimmune thyroiditis, in 5-10% of cases there is no clinically detectable pathology of the thyroid gland. In some cases, DTZ manifests later than the EOP. The ratio of men to women is 5:1, in 10% of cases the image intensifier tube is unilateral. Anti-TSH receptor antibodies (AT-TSH) have several functionally and immunologically distinct subpopulations. Mutant variants of AT-TSH can cause immune inflammation of the retrobulbar tissue. Immune inflammation of the retrobulbar tissue leads to excessive deposition of glycosaminoglycans and a decrease in the volume of the orbital cavity with the development of exophthalmos and HDM dystrophy. The severity of EOP does not correlate with the severity of concomitant thyroiditis.

EOP begins gradually, often on one side. Chemosis, feeling of pressure behind the eyeballs, increased photosensitivity, sensation of a foreign body, "sand in the eyes". Further, the symptoms increase according to the described degrees of severity. Instrumental research methods (ultrasound, MRI of the orbits) make it possible to determine the protrusion of the eyeball, the thickness of the HDM, including in the framework of monitoring and evaluation, the effectiveness of treatment.

7. Ectodermal disorders: fragility of nails, hair loss.

8. Digestive system: abdominal pain, unstable stool with a tendency to diarrhea, thyrotoxic hepatosis.

9. Endocrine glands: ovarian dysfunction up to amenorrhea, fibrocystic mastopathy, gynecomastia, impaired carbohydrate tolerance, tyrogenic relative, that is, with a normal or increased level of cortisol secretion, adrenal insufficiency (moderate melasma, hypotension).

10. Diseases associated with DTG: endocrine ophthalmopathy, pretibial myxedema (1-4%; swelling and thickening and hypertrophy of the skin of the anterior surface of the lower leg), acropathy (extremely rare; periosteal osteopathy of the feet and hands radiographically resembles "soap foam").

11. Thyrotoxic crisis- an urgent clinical syndrome, which is a combination of severe T. with tyrogenic adrenal insufficiency. The main reason is inadequate thyreostatic therapy. Provoking factors are: surgery, infectious and other diseases. Clinically: advanced T. syndrome, severe mental anxiety up to psychosis, motor hyperactivity, followed by apathy and disorientation, hyperthermia (up to 40 0 C), suffocation, pain in the heart, abdominal pain, nausea, vomiting, acute heart failure, hepatomegaly , thyrotoxic coma.

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