Is there an effective treatment for edematous exophthalmos and other forms of the disease? How do vowel symptoms manifest? Features of symptoms of increased thyroid function
In cases where the disease lasts a long time, and the patient either does not see a doctor for some reason or is not treated correctly, the thyroid gland continues to enlarge, and the goiter can reach large sizes (Fig. 6). In this case, the configuration of the neck changes significantly, and problems may even arise with the passage of food through the esophagus.
Rice. 5. The characteristic look of a patient with thyrotoxicosis.
. Rice. 6. Large goiter
Indeed, these symptoms may be sufficient 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, increased fatigue, decreased performance, irritability, tearfulness, poor sleep, feeling hot, increased sweating, weight loss, a feeling of pressure in the neck, palpitations that increase with physical and emotional stress, trembling of the limbs, and sometimes of the whole body, unstable chair with a tendency to diarrhea. Sometimes patients themselves note an increase thyroid gland and bulging eyes. Women complain of menstrual irregularities. With all the variety of complaints, the most characteristic of them are palpitations, loss of body weight and muscle weakness.
Among other complaints that should alert you and force you to see a doctor, the following should be highlighted:
Irritability;
Mental imbalance;
Excessive sweating;
Poor tolerance to high temperatures;
Hand trembling (fine tremor);
Weakness;
Fatigue;
Stool disorder (diarrhea);
Frequent and excessive urination (polyuria);
Menstrual irregularities.
Decreased sexual desire.
Changes in the thyroid gland in Graves' disease manifest themselves mostly in the form of a diffuse, uniform increase. In most cases, the iron is increased 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 assessed using the 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 severe clinical form of thyrotoxicosis, the gland is slightly enlarged and 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 observed in 3-5% of patients. In some cases, with diffuse enlargement of the gland, one lobe (usually the right) may be larger.
In diffuse toxic goiter, the thyroid gland is usually of a soft or moderately dense consistency, not fused to the underlying tissues, and is easily displaced when swallowing. Thyroid may occupy a retrosternal position. Sometimes a goiter develops from an additional lobe or ectopic (unusually located) gland tissue, which makes examination difficult.
Pressing on the gland is often painful. One of the characteristic signs of goiter in Graves' disease is that its volume during different periods of the disease is subject to large fluctuations, which is explained varying degrees blood supply to the gland.
During auscultation, the doctor can listen to vascular noises above the thyroid gland, the occurrence of which is associated with increased blood supply to the gland and accelerated blood flow in its vessels.
The disease is often accompanied by changes in the eyes. Sometimes it is bulging eyes that make you see a doctor. The appearance of eye symptoms is associated with impaired tone eye muscles. Due to inconsistency and 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 sign of thyrotoxicosis. Exophthalmos usually develops gradually, although it can appear suddenly. In some cases, bulging eyes are present only on one side, usually the right. Exophthalmos gives the patient an angry, surprised or frightened appearance. Sometimes the look expresses horror.
During the examination, the doctor may detect other eye symptoms. They are named after the authors who observed them. Graefe's symptom is a lag upper eyelid from the iris when the vision fixes an object slowly moving downward, due to which a white strip 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, there is also a section of sclera between the lower eyelid and the iris (Kocher's sign).
Widely opened palpebral fissures give the face an expression of fear and concentration (Delrymple's symptom). Convergence disorder, that is, the loss of the ability to fixate an object at close range, is called Moebius' symptom. Rare blinking is characteristic - 2-3 times per minute compared to 3-5 normally (Stellwag's symptom).
Jellinek's sign is characterized by brown pigmentation of the eyelids and skin around the eyes. In some cases, trembling of closed eyelids (Rosenbach's symptom) and absence of wrinkling of the forehead when looking up (Geoffroy's symptom) are observed. 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. Some patients experience the inability to squint their eyes (Kocher). Zenger indicated a soft, cushion-like swelling of the eyelids (Zenger's sign), which in the later stages of the disease can develop into a bag-like drooping of the eyelids.
The appearance of eye symptoms is associated with impaired tone of the eye muscles. Due to inconsistency and non-specificity, the significance of eye symptoms is small.
The 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 thyroid-stimulating hormone pituitary gland An important role is played by autoimmune processes.
Bulging 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 retrobulbar tissue is caused by edema, lymphocytic and fatty infiltration, venous stagnation 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, double vision 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 (stability) 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 swollen, inflamed, and keratitis develops due to constant drying of the cornea and its ulceration, which can lead to blindness. Swelling of the retroorbital (retrobulbar) tissue not only leads to the ejection of the eyeball from the orbit - exophthalmos, but also causes compression optic nerve with vision loss, and can also cause retinal vascular thrombosis.
Endocrine ophthalmopathy It is more common after 40 years of age, but can occur at any age. Men are more often affected. Usually the ophthalmopathy is bilateral, less often (at the beginning of the disease) unilateral.
Ophthalmopathy develops against the background of diffuse toxic goiter, but a 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 decreased function of the thyroid gland, 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 diseases.
In addition to diffuse toxic goiter, exophthalmos can occur with a high degree of myopia and glaucoma. It may be familial or congenital. Unilateral and bilateral exophthalmos requires special examination see an ophthalmologist or neurologist, since its causes may be inflammatory processes and tumors brain, congenital anomalies of the skull, etc.
It is wrong to think that the disease is limited only to damage to 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 Russian therapist S.P. Botkin (1885) considered changes in the psyche 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, and emotionally labile. They are verbose, quick in their movements, fussy, hasty, irritable, whiny, touchy, and often experience a state of fear. The smallest things can cause tears. Characterized by rapid mood swings, lack of concentration, and loss of the ability to concentrate. Some patients cannot sit still for a single minute. They easily come into conflict with others, become quarrelsome and self-centered. The feeling of anxiety and gloomy forebodings are replaced by a feeling of deep anxiety. Outbursts of rage may occur.
Many patients complain of persistent insomnia. Their sleep is intermittent, shallow, with nightmares. Graves' disease represents fertile ground for the development of mental disorders. Sometimes it occurs manic state, giving way to a depressive mood.
A characteristic symptom of the disease is a slight tremor (shaking) of the fingers of outstretched hands (Marie's symptom). Sometimes hand tremors are so pronounced that patients have difficulty fastening buttons, holding a cup of tea in their hands, or performing any other precise movements. Handwriting may change. In severe thyrotoxicosis, trembling of the head, tongue, drooping eyelids, feet, and the whole body is observed (the “telegraph pole” symptom). Thyrotoxic tremors are characterized by a small amplitude and a fast rhythm. It is the subtle form of tremor in the form of rapid small trembling that is characteristic of Graves' disease, in contrast to neurological pathology, in which the tremor is more widespread.
An early and frequent symptom of diffuse toxic goiter is muscle weakness, which may be accompanied by paresis and muscle atrophy. Weakness of the muscles of the arms, shoulder girdle, and pelvis is especially characteristic. Muscle weakness (myopathy) usually develops slowly over several months or years. Patients have difficulty walking and climbing stairs. In severe cases, the patient cannot get up without outside help. The occurrence of myopathy is associated with disorders of protein and energy metabolism in muscle tissue. After successful treatment diffuse toxic goiter myopathy disappears.
Periodic paralysis (thyrotoxic myoplegia) is manifested by sudden short-term paroxysmal muscle weakness that occurs when walking or standing for long periods of 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 normal. Young patients usually have thin hands, thin fingers with a pointed terminal phalanx (“Madonna hands”).
In severe forms of toxic goiter, especially in older people, 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, elastic, tender, with a slight velvety feeling, thin, transparent. Its elasticity is maintained despite the weight loss that accompanies thyrotoxicosis. There are no wrinkles or dullness of the skin. There is slight redness of the face and neck.
As a result increased metabolism and heat production, the skin may be moist, warm, or hot to the touch. damp, Pink colour skin is a characteristic sign of thyrotoxicosis. The hands and feet are usually warm, in contrast to neurocirculatory asthenia. At slight increase ambient temperature or when easy work skin moisture easily turns into noticeable sweating.
In severe cases of thyrotoxicosis, the skin of the eyelids, armpits, genitals, anus, and also in places where clothing rubs may become pigmented. Sometimes there is an almost diffuse brown discoloration 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 on the front surface of the legs is affected, it becomes swollen, thickened, rough, rough, with protruding hair follicles, reminiscent of an orange peel or pork skin. Skin changes are often accompanied by significant redness and itching. These swollen areas are sensitive to pressure, but finger pressure does not cause a pit. The legs look swollen and have a shapeless appearance.
A biopsy (microscopic examination) of these areas of skin reveals changes characteristic of hypothyroidism. The cause of pretibial myxedema is not clear. Sometimes it appears (just like ophthalmopathy) several months after surgical treatment of diffuse toxic goiter or treatment with radioactive iodine.
Subcutaneous fatty tissue in most patients with diffuse toxic goiter it is poorly developed. Despite the good or even increased appetite, patients lose weight. Over the course of several months, they can lose 10-15 kg or more in weight. In severe forms of thyrotoxicosis, in advanced, undiagnosed or poorly treated cases, severe exhaustion develops - cachexia. This is explained by a significant increase in metabolic processes, increased combustion of fat reserves and loss of water. In rare cases, patients with diffuse toxic goiter may have overweight(the so-called “fat Basedov”).
With thyrotoxicosis, skin appendages are affected. Hair is thin, brittle, and falls out easily. Body hair growth armpits and other places are scarce. The fragility of the nails is increased, and their longitudinal striations are observed.
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Diffuse toxic goiterTreatment of diffuse toxic goiter
6. Ectodermal disorders: brittle 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, relative thyrogenic, that is, with normal or increased levels 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). Daily dose Mercazolil is 30-40 mg, sometimes with very large goiters 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 based on the signs of elimination of thyrotoxicosis: stabilization of the pulse (70-80 beats per minute), increase in body weight, disappearance of tremor and sweating, normalization of pulse pressure.
Radioiodine therapy (RIT) is one of the modern methods treatment of diffuse toxic goiter and other diseases of the thyroid gland. During treatment, radioactive iodine (isotope I-131) is introduced into the body in the form gelatin capsules orally (in rare cases, a liquid solution of I-131 is used). Radioactive iodine that accumulates in the cells of the thyroid gland exposes the entire gland to beta and gamma radiation. In this case, gland cells and tumor cells that have spread beyond its boundaries are destroyed. Radioiodine therapy requires mandatory hospitalization in a specialized department.
The absolute indications for surgical treatment are allergic reactions or a persistent decrease in leukocytes observed during conservative treatment, big sizes goiter (enlargement of the thyroid gland above grade III), heart rhythm disturbances such as atrial fibrillation with symptoms cardiovascular failure, pronounced goitrogenic effect of Mercazolil.
The operation is performed only when a state of drug compensation has been achieved, since otherwise a thyrotoxic crisis may develop in the early postoperative period.
Nodular toxic goiter is hyperthyroidism due to an autonomously functioning adenoma of the thyroid gland (thyroid gland) in the form of one or more nodules. The function of other parts of the gland is suppressed low level TSH due to high levels of thyroid hormones. These areas 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 single nodular formation in the thyroid tissue, identified clinically or using ultrasound, the possibility of cancer should be considered.
SURGERY. All malignant and some benign formations thyroid gland
Indications for surgical treatment
· History of irradiation of the neck area (suspicion of a malignant process)
Large size of the node (more than 4 cm) or compression symptoms caused by it
Progressive growth of the node
Dense consistency of the knot
· Young age of the patient.
The scope of the operation for a solid benign nodular formation is removal of a lobe with or without the isthmus of the gland; for 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 compressing the organs of the neck, regardless of the severity of thyrotoxicosis. Before surgery, it is imperative 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 the high operational risk, in patients with irreversible changes liver, kidneys, cardiovascular and mental diseases.
2.Indications and contraindications for hernia repair. The main stages of herniotomy surgery. Principles of reliable hernial orifice repair.
In general, all hernias should be repaired if the local or systemic status of the patient predicts a reliable outcome. A possible exception to this rule is a hernia that has a wide neck and a small sac, i.e., signs indicating the possibility of a slow enlargement of the hernia. Hernia bandages and surgical belts are 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 illnesses – tuberculosis, malignant tumors, severe respiratory and heart failure, etc. Relative – early age (up to six months), state of decrepitude, last 2-3 months of pregnancy, urethral strictures, adenoma prostate gland(hernia repair is performed after they are eliminated).
The operation in all cases consists of two stages: I/ the herniotomy itself - isolating the hernial sac, opening it, realigning the insides, stitching and ligating the sac in the neck area and cutting it off - is performed in the same way for all forms of hernias; 2/ plastic (suturing) of the hernial 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 postoperative hernias and in neuropaths, as well as in children.
Preoperative preparation - hygienic bath and shaving surgical field, cleansing enema on the eve of surgery. In the postoperative period - prevention of pulmonary complications, 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 - plastic surgery of the hernial orifice is performed different ways: 1) by suturing local homogeneous tissues (autoplastic methods); 2) using additional biological or synthetic materials (alloplastic methods).
3.Mallory-Weiss syndrome. Definition. Causes. 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, Mallory-Weiss syndrome will be manifested by the presence of blood in the vomit. Moreover, blood may be absent during the first attacks of vomiting, when the mucous membrane just ruptures. In addition to vomiting mixed with blood, patients with this syndrome may have abdominal pain and black stools (melena). Diagnosis of Malory-Weiss syndrome. Of the instrumental methods for diagnosing Mallory-Weiss syndrome, endoscopic examination (fibroesophagogastroduodenoscopy) is of greatest value. This study allows you to see a longitudinal tear in the mucous membrane of the esophagus. In addition, if bleeding is detected, an attempt can be made to stop it endoscopically (see Treatment of Malory-Weiss syndrome). In the anamnesis of patients with Mallory-Weiss syndrome, one can often find mention of drinking alcoholic beverages in large quantities, which resulted in vomiting. When examining a patient with Mallory-Weiss syndrome, one can detect common signs of all bleeding: pale skin, cold sticky sweat, lethargy, tachycardia, hypotension, and possibly even the development of shock.
IN clinical analysis blood there will be a decrease in the number of red blood cells, hemoglobin levels, and an increase in the number of platelets, which indicates the presence of bleeding. Conservative therapy for Malory-Weiss syndrome is used to restore circulating blood volume. For this, various crystalloid (NaCl 0.9%, glucose 5%, Ringer's solution, etc.), colloid solutions (albumin, aminoplasmal, etc.) are used; in case of severe blood loss, blood transfusion (packed red blood cells, fresh frozen plasma) can be used. For vomiting (or the urge to vomit) use metoclopramide (Cerucal). To stop bleeding, a Blackmore probe is used. This probe has 2 balloons. Using the lower balloon, the probe is fixed in the stomach in correct position, after which the second balloon located in the lumen of the esophagus is inflated. The hemostatic effect is achieved through mechanical compression of the bleeding vessels of the esophagus. To stop bleeding, it is possible to use sodium ethamsylate, calcium chloride, aminocaproic acid, and octreatide. When performing fibroesophagogastroduodenoscopy and detecting a longitudinal rupture of the mucous membrane of the esophagus with bleeding, you can try to stop this bleeding endoscopically. This uses:
1. Injection of 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 vasoconstrictor effect 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 argon plasma coagulation method allows achieving stable hemostasis.
3. Electrocoagulation
Also quite an effective method. The use of electrocoagulation is often combined with the administration of adrenaline.
4. Administration of sclerosants
This method consists in the fact that the hemostatic effect is achieved through the introduction of slerating drugs (polidocanol).
5. Vessel ligation
For Mallory-Weiss syndrome, endoscopic ligation of bleeding vessels is often used. The use of endoscopic vascular ligation is especially justified in cases of combination of Malory-Weiss syndrome and portal hypertension with varicose veins of the esophagus.
6. Vessel clipping
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. Clip application is possible using an applicator. Unfortunately, endosopic clipping of vessels is not always possible due to the technical difficulties of applying clips to vessels.
V. With Mallory-Weiss syndrome surgical treatment resort in case of ineffectiveness conservative therapy and endoscopic treatment methods. For Mallory-Weiss syndrome, a Bayeux operation will be performed:
Access: median laparotomy.
Operation: gastrotomy, suturing of bleeding vessels.
TICKET No. 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 experiences 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- development of thyrotoxic crisis. The first sign of thyrotoxic crisis is rapid rise body temperature up to 40°C, accompanied by increasing tachycardia. Blood pressure first increases and then decreases, and neuropsychic disorders are observed.
In the development of the crisis, the main role is played by insufficiency of the adrenal cortex function, caused by operational stress. Treatment of a crisis should be aimed at combating adrenal insufficiency, cardiovascular disorders, hyperthermia and oxygen deficiency.
Tracheomalacia. With long-standing goiter, especially with retrosternal, retrotracheal and retroesophageal goiter, 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 extubation of the trachea or in the immediate postoperative period, it may bend in the area of softening or bring the walls closer together and narrow the lumen. Acute asphyxia occurs, which can lead to the death of the patient if urgent tracheostomy is not performed (see " Inflammatory diseases trachea").
Postoperative hypothyroidism - insufficiency of thyroid function, caused by its complete or almost complete removal during surgery, develops in 9-10% of operated patients. Hypothyroidism is characterized general weakness, constant feeling fatigue, apathy, drowsiness, general lethargy of patients. The skin becomes dry, wrinkled, and swollen. Hair begins to fall out, pain in the limbs appears, sexual function weakens.
Treatment: thyroidin and other thyroid medications are prescribed. With the development of microsurgical technology and advances in immunology, allotransplantation of the thyroid gland began to be performed using a graft on a vascular pedicle. Free implantation of pieces of gland tissue under the skin, into the muscle is also used, however, these operations usually give a temporary effect, so in practice they mainly use replacement therapy.
2.Indirect inguinal hernia. Clinical picture. Diagnostics. Differential diagnosis. Methods of operations. Congenital inguinal hernia.
Indirect 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 follows its course.
Depending on the stage of development, it is customary to distinguish following forms oblique inguinal hernias (according to A.P. Krymov): 1) initial hernia, in which the sac is identified only in the inguinal canal; 2) canal form - the bottom of the bag reaches the external opening of the inguinal canal; 3) cord form - the 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 its contents descends into the scrotum (in women - into the tissue of the labia majora).
Congenital inguinal hernias are always oblique. They develop in case of non-fusion 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 membrane is at the same time inner wall hernial sac. Congenital inguinal hernias are often combined with hydrocele of the testicle or spermatic cord.
The diagnosis of an inguinal hernia is usually not difficult. A characteristic objective sign is protrusion of the anterior abdominal wall in the groin area, increasing with straining and coughing. With an oblique inguinal hernia, it has an oblong shape, is located along the inguinal canal, and 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 indirect inguinal hernia, the finger does not detect the presence of bone when moving it along the inguinal canal, since the muscular aponeurotic elements of the inguinal triangle interfere with this. Without removing the finger from the hernial canal, the patient is asked to push or cough - the symptom of a cough impulse is determined. Differential diagnosis. An inguinal hernia should be differentiated from a femoral hernia, hydrocele of the testicular membranes, spermatic cord and canal cysts, cryptorchidism, varicocele, inguinal lymphadenitis, tumors in the inguinal canal area. When differentiating a hernia, hydrocele, or 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, the glow is determined using a tube. With a hernia and tumor of the testicle there is no glow, but with dropsy it is detected. Cryptorchidism is characterized by high location“tumors” at the root of the scrotum, its immobility and the impossibility of reduction into the abdominal cavity.
The presence of an inguinal hernia is an indication for surgical treatment. More than 200 methods have been proposed for restoration and reconstruction of the abdominal wall for inguinal hernias. Conventionally, they can be divided into three groups:
Methods for strengthening the anterior wall of the inguinal canal without dissecting the aponeurosis of the external oblique abdominal muscle. 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 abdominal muscle (operation methods of Martynov, Girard, Spasokukotsky, Kimbarovsky, etc.).
3. Hernioplasty methods associated with strengthening the posterior wall of the inguinal canal and moving the spermatic cord. This group includes the methods of Bassini, Kukudzhanov, McVey, Shouldice, Postempsky, etc.
When choosing a hernioplasty method, it is necessary to remember 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 indirect hernias and recurrent hernias methods of plastic surgery of the posterior wall of the inguinal canal should be used. Strengthening the anterior wall can be used in children and young men with small indirect inguinal hernias. The feasibility of such surgical tactics is confirmed by statistics on long-term results of hernia repair.
The peculiarity of the operation for congenital inguinal hernia lies in the method of treating the hernial sac. The latter is isolated at the neck, bandaged and cut. The distal part of the sac is not removed, but is cut along its entire length, then turned out and sutured behind the spermatic cord and testicle (similar to the Winkelmann operation for testicular hydrocele). Plastic surgery of the inguinal canal is performed using one of the methods listed above.
The sequence of surgery for an inguinal hernia is the same for different 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 2 cm above it, about 10-12 cm long. Accordingly, the aponeurosis of the external oblique abdominal muscle is cut through the wound and the Poupartian ligament is exposed.
The second stage is isolation from the surrounding tissues and removal of the hernial sac. Stitching of the neck of the pouch before cutting it off is done either from the outside or from the inside using a purse-string suture, but always under the control of the eye.
The third stage is suturing the deep inguinal opening to normal size (0.6-0.8 cm) if it is expanded or destroyed.
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 plastic surgery of the inguinal canal.
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 when stressful situations associated with serious pathology internal organs, severe surgical interventions, burns, polytrauma, taking certain medications, etc.
Depending on the cause of 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, large vessels and brain operations;
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) medicinal ulcers problems that occur when taking acetylsalicylic acid, indomethacin, voltaren, steroid hormones, cytostatic drugs.
Typical signs all acute ulcers are sudden massive life-threatening bleeding or perforation of the ulcer. The optimal way to diagnose acute ulcers is endoscopic examination. It should be borne in mind that until bleeding occurs, acute ulcers are usually asymptomatic.
Acute erosive gastritis. This disease is characterized by superficial flat, round or elongated defects in the gastric mucosa (erosions). Unlike ulcers, they do not destroy the muscular plate of the mucous membrane (lamina muscularis mucosae). The causes of their occurrence are severe stress, multiple injuries, extensive burns (Curling ulcer), extensive traumatic operations, taking certain medications; basic clinical symptoms- bleeding (hematemesis, melena), shock. The diagnosis is made by endoscopic examination.
Medicines (steroid hormones, acetylsalicylic acid, butadione, indomethacin, atophan) reduce the formation of mucus, destroy the protective barrier of the mucous membrane, and cause hemorrhages. When drugs are discontinued, ulcers and erosions heal quickly.
Ischemia of the mucous membrane plays a key role in the development of hemorrhagic gastritis, as it helps to weaken its protective barrier.
Treatment. For acute ulcers and erosive gastritis conservative treatment is performed initially
Surgical treatment is rarely used. Preference is given to selective proximal vagotomy, puncture and ligation of bleeding vessels, less often gastrectomy or even gastrectomy (in exceptional cases) is performed.
A simple Dieulafoy's ulcer can only be treated surgically: the bleeding artery is punctured and tied 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 (ulcerogenic pancreatic adenoma, gastrinoma) is a tumor of the islet apparatus of the pancreas, characterized by the occurrence of peptic ulcers of the duodenum and stomach, which cannot be treated and is accompanied by persistent diarrhea. Clinical manifestations of the disease are pain in the upper abdomen, which have the same patterns in relation to food intake as with a regular ulcer of the duodenum and stomach, but unlike them, they are very persistent, have great intensity and do not respond to antiulcer therapy.
Characterized by persistent heartburn and sour belching. An important sign are diarrhea caused by contact with small intestine large quantity hydrochloric acid and, as a result, increased motility of the small intestine and slower absorption. The stool is copious, watery, with a lot of fat. A significant decrease in body weight is possible, 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 a narrowing of the esophagus. Palpation reveals severe pain in the upper abdomen and the projection area of the lower stomach; there may be a positive Mendelian sign (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 complete removal stomach, you need to 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 this, gastric secretion remains extremely high, performing gastric extirpation as planned order, without waiting for the development of complications of the ulcer. Indications for gastrectomy are the presence of multiple gastrinomas, a single gastrinoma with metastases, as well as recurrence of the ulcer after tumor removal.
As already indicated, gastrinomas are often multiple, located in different parts of the pancreas and in various organs, which makes it extremely difficult to find them during surgery. Therefore, attempts to treat patients with Zollinger-Ellison syndrome by tumor removal alone are usually unrealistic. True, cases of successful treatment of such patients with a similar intervention under the control of operational pH-metry of the gastric mucosa have been described (A. A. Kurygin, 1987). In these individual observations, after removal of single gastrinomas, already operating table achlohydria set in. 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 at risk of developing ulcers in the stomach and duodenum.
TICKET No. 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 developing against the background of goiter is called strumitis. The cause of the development of thyroiditis and strumitis is 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 indicated for all patients.
Treatment: antibiotics are prescribed; When an abscess forms, its opening is indicated to avoid the spread of the purulent process to the neck and mediastinum.
Hashimoto's chronic lymphomatous thyroiditis. 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 acinar cells of the thyroid gland and thyroglobulin. The latter inactivate thyroglobulin. This leads to disruption of the synthesis of normal thyroid hormones, which causes increased secretion of TSH from the pituitary gland and hyperplasia of the thyroid gland. In the later stages of the disease, the thyroid function of the gland is reduced, and the accumulation of iodine in it decreases.
Clinical presentation and diagnosis: Hashimoto's thyroiditis most often occurs in women over 50 years of age. 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 is not fused with the surrounding tissues and is mobile during palpation. Subsequently, discomfort and signs of hypothyroidism appear. Regional lymph nodes are not enlarged.
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 administration of thyroid and glucocorticoid hormones. The dose of thyroid hormones is selected individually, the average daily dose of thyroidine is 0.1--0.3 g. The daily dose of prednisolone is 20--40 mg for 1 1/2 - 2 months with a gradual dose reduction. .
If malignant degeneration is suspected, or if the organs of the neck are compressed by a large goiter, surgery is indicated. Subtotal resection of the thyroid gland is performed. After surgery, treatment with thyroidin is necessary due to the inevitably developing hypothyroidism.
Chronic fibrous thyroiditis of Riedel. The disease is characterized by the growth of connective tissue in the thyroid gland, replacing 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, stony in density, fused with the surrounding tissues. There are moderate signs of hypothyroidism. Pressure on the esophagus, trachea, blood vessels and nerves causes the corresponding symptoms.
Treatment: before surgery it is almost impossible to exclude a malignant tumor of the thyroid gland, therefore, for Riedel's thyroiditis it is indicated surgical intervention. 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 recurrent hernias. Methods of operations.
Causes of recurrence of inguinal hernias diverse. They can be systematized as follows:
1) reasons existing before the operation; 2) reasons depending on the type of operation performed and its technical execution; 3) reasons that arose in the postoperative period.
TO the first group of causes of relapse relate:
1) late surgery in the presence of significant changes in the tissues of the groin area (it has long been noted [A.I. Baryshnikov, 1965] that the longer the 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 groin area: 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) presence of accompanying chronic diseases causing sharp fluctuations in intra-abdominal pressure (prostatic hypertrophy, urethral stricture, chronic constipation, Chronical bronchitis, emphysema, etc.);
4) insufficient examination and sanitation of the patient before surgery, leaving foci of infection in the body that can lead to complications postoperative period(chronic tonsillitis, pustular and infectious diseases).
Co. second group of causes of relapse relate:
1) incorrect choice method of operation, without taking into account the pathogenetic conditions of hernia formation and those changes in the inguinal canal that occur in patients with inguinal hernias (for example, strengthening in direct and recurrent hernias only the anterior wall of the inguinal canal, leaving an expanded deep opening of the inguinal canal and a high inguinal space);
2) gross defects in surgical technique (insufficient hemostasis, insufficiently high isolation 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 surgery, suturing tissue with high tension, suturing the superficial inguinal ligament 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 superficial layer, insufficient separation of the sutured tissues from the fatty tissue, damage to blood vessels and nerves). With alloplastic methods of surgery, 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 relapse includes:
1) inflammatory complications from the surgical wound (suppuration, infiltrates, ligature fistulas);
2) early load on a scar that has not yet formed;
3) heavy physical work in the late postoperative period.
Girard's method. Inguinal canal plastic surgery 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 abdominal muscle is sutured to the Pupart ligament. The outer layer of the aponeurosis is sewn on top of it, thus creating an aponeurotic duplication. The external opening of the inguinal canal is formed so that it allows the tip of the finger (spermatic cord) to pass through. Sutures are placed on the skin.
Spasokukotsky's method. It differs from the Girard method in that the internal oblique and transverse muscles along with the internal leaf of the aponeurosis of the external oblique abdominal muscle are sutured to the inguinal ligament simultaneously (with one suture). Then an arch structure is also created from the leaves of the aponeurosis.
The Kimbarovsky method (Kimbarovsky sutures) is the most commonly used in clinical practice modification of the Girard-Spasokukotsky operation. The essence of the modification is the use of original sutures during plastic surgery, ensuring comparison of homogeneous tissues. To do this, the first injection of the needle is made at a distance of 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 placed in the same way. When the threads are tightened, the upper layer of the aponeurosis is tucked in and covers the muscles. As a result, the edges of the muscles wrapped in the aponeurosis are sutured in front of the spermatic cord to the inguinal ligament.
Martynov's method. The stages of the operation are the same as with the Girard method. Plastic surgery is performed by suturing the inner layer of the aponeurosis of the oblique abdominal muscle to the Poupart ligament, followed by the formation of a duplicate 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 gastric outlet develops in 10-15% of patients with peptic ulcer disease. It was previously stated that stenosis always forms at the level of the ulcer. However, the narrowing of the outlet 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 the period of exacerbation of the disease can sometimes be accompanied by impaired evacuation of gastric contents, which is eliminated with effective antiulcer treatment. Depending on the degree of disturbance in the evacuation of gastric contents, it is customary to distinguish three degrees of stenosis of the outlet of the stomach or duodenum: compensated, subcompensated and decompensated.
At the compensated stage of stenosis, patients are in a satisfactory condition, they do not vomit with stagnant stomach contents;
The ocular symptoms of thyrotoxicosis are not fundamentally different from those with an independent disease of endocrine ophthalmopathy.
Ectodermal disorders are manifested by brittle nails and hair loss. Abdominal pain, unstable stools with a tendency to diarrhea, and thyrotoxic hepatosis are relatively rare. Possible ovarian dysfunction up to amenorrhea, fibrocystic mastopathy, gynecomastia, impaired carbohydrate tolerance, relative thyrogenic (with normal cortisol levels) adrenal insufficiency (moderate melasma, hypotension). Diseases associated with Graves' disease: endocrine ophthalmopathy, pretibial myxedema. The latter occurs in 1-4% of cases, manifesting itself as swelling, thickening and hypertrophy of the skin on the anterior surface of the 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 assess the effectiveness of the treatment, it is most advisable to determine the levels of free (free) fractions T 4, T 3 and TSH. With persistent and significant increase levels of St. T 4, St. T 3 and low TSH in combination with the corresponding clinical symptoms indicate thyrotoxicosis. The detection of elevated titers of thyroid autoantibodies [antibodies to microsomal antigen (AT-MS), thyrocyte peroxidase (AT-TPO), second colloidal antigen, thyroglobulin (AT-TG)] confirms the autoimmune genesis of the disease.
Ultrasound examination (ultrasound) for DTG is of auxiliary value and can only confirm the diffuse nature of the thyroid enlargement. A puncture biopsy, carried out targeted under ultrasound control, followed by a cytological examination of the resulting biopsy is performed in cases of detection of nodular formations against the background diffuse increase thyroid gland or doubts about the benignity of the disease. Scintigraphy is not used for differential diagnosis of the nature of thyroid diseases. It can only be used for comparative assessment functional activity diffusely enlarged gland parenchyma and nodular formations identified in it, determining the volume and functional activity of the thyroid remnant after surgical treatment, as well as identifying ectopic foci of thyroid tissue.
Thyrotoxic crisis is an urgent clinical syndrome, which is a combination of severe thyrotoxicosis with thyrogenic adrenal insufficiency. The main reason is inadequate thyreostatic therapy. Provoking factors are: surgery, infectious and other diseases. Clinically manifested by a full-blown syndrome of thyrotoxicosis, severe anxiety up to psychosis, motor hyperactivity, alternating apathy and disorientation, hyperthermia (up to 40°C), suffocation, pain in the heart, abdominal area, nausea, vomiting, signs of acute heart failure, hepatomegaly. Possible development of thyrotoxic coma.
Currently, there are three methods of treating DTG - complex drug thyreostatic therapy, surgery and radioactive iodine. It is not possible to establish any general pattern in the choice of one or another treatment method for DTG on a global or even European scale. A number of the largest clinics with many years of experience in surgical thyroidology remain committed to their own practice that has developed over decades. In many countries, especially in the USA, and in last years Western Europe, the number of operations for DTG is significantly reduced and the main method of treatment is radioactive iodine therapy. In Russia, most CIS countries, and Japan, preference is still given to surgical treatment.
Drug therapy provides a lasting cure in only 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 thyreostatic therapy include high risk the development of relapse of thyrotoxicosis after its discontinuation, low probability of stable remission, and the occurrence of side effects.
In our country, the 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 thyroid gland size; relapses of thyrotoxicosis upon discontinuation of thyreostatics; intolerance to medications (thyreostatics); combination of DTG with neoplastic processes in the thyroid gland.
Performing surgery for DTG in specialized surgical departments, carefully preoperative preparation, qualified performance of surgical technique during high level Anesthesia care and provision of adequate postoperative intensive care allowed us to minimize possible complications and mortality and achieve quite satisfactory immediate treatment results. Surgical treatment, which in our country is performed in approximately 40% of patients with DTG, is captivating with its effectiveness and speed of elimination of the pathological process. Of course, one should not downplay the importance of specific complications that undoubtedly overshadow the results of treatment (damage laryngeal nerves, parathyroid glands), the genesis of which is complex and multicomponent (although traditionally they are primarily attributed to the 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 relapse thyrotoxicosis and hypothyroidism. According to the literature, persistent euthyroidism after surgical treatment of DTG is currently achieved only in 25-30% of patients. The frequency of relapse of thyrotoxicosis ranges from 0.5 to 34% without a tendency to decrease, and of 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 finding markers for predicting the outcome of surgical intervention in DTG, is very relevant.
In Russia, since the middle of the last century, surgical techniques for DTZ according to O. V. Nikolaev or E. S. Drachinskaya have gained recognition and become generally accepted. Most domestic surgeons even currently perform subtotal subfascial resection of the thyroid gland in cases of DTG, leaving minimum quantity 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 during the surgical treatment of DTG, do not have wide practical application. At the same time, in modern conditions the general tendency is to recognize postoperative hypothyroidism as a predictable outcome of surgery, without attributing it to negative consequences and complications, but is considered as the goal of radical surgical intervention.
An effective method of treating DTG is radioactive iodine therapy. In the USA and some Western European countries, preference is given to radioiodine therapy, which is a radical alternative to surgical treatment. The drug of choice is the isotope I 131. Contraindications include significant size of the thyroid gland, ophthalmopathy, hematopoietic disorders, young age, pregnancy and lactation. In 70-90% of patients after radioiodine therapy, hypothyroidism develops, requiring lifelong replacement therapy. In Russia this method is not yet widely available.
Toxic thyroid adenoma(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 of any age, mainly at the age of 40–50 years. It grows slowly - over 5–10 years. The adenoma is usually small in size (2–2.5 cm in diameter). Signs of thyrotoxicosis often appear only after the adenoma reaches a certain size, sometimes after 3–8 years from the beginning of its development.
Plummer's disease is one of the forms of functionally active thyroid adenoma, characterized by excessive iodine uptake independent of TSH and increased production of thyroxine by thyrocytes. Functional autonomy (FA) of the thyroid gland can be unifocal (nodular toxic 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 cause (after DTG) of the development of thyrotoxicosis.
As a result of prolonged iodine deficiency, the functioning of thyrocytes is impaired, manifested 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. In this case, thyrotoxicosis is absent and a normal TSH level is determined (compensated PA). As the degree of autonomy and the volume of autonomously functioning tissue increases, iodine uptake by the surrounding tissue decreases, TSH secretion gradually suppresses (decompensated FA) and clinically significant thyrotoxicosis develops. FA is the most common cause of thyrotoxicosis in the elderly and senile. In areas of iodine endemia, FA usually does not progress to the stage of decompensation. The latter in 80% of observations is associated with the exogenous intake of excess iodine. With compensated FA, thyrotoxicosis develops in approximately 5% of patients per year.
The clinical picture of the disease is determined by the degree of PA compensation. With euthyroidism and subclinical thyrotoxicosis (T 3 and T 4 are normal, TSH is low), FA may not manifest itself clinically. Compensated FA in the absence of nodules in the thyroid gland is a scintigraphic finding. Scintigraphy is usually performed when examining a nodular or multinodular goiter. Decompensated FA is manifested by thyrotoxicosis syndrome. Clinical symptoms similar to that of DTD: palpitations, poor heat tolerance, increased sweating and, as a result, thirst, loss of body weight, despite increased appetite, shortness of breath. Excitability, irritability, anxiety, hyperkinesis and emotional lability, insomnia, muscle weakness in the proximal parts, tremor of fingers extended forward and outstretched, increased deep tendon reflexes - also possible signs. The skin is usually warm, moist, the face is flushed, thin hair is falling out, and menstruation is scanty or absent. Autoimmune ophthalmopathy is not typical; only “isolated” eye symptoms may occur. Some elderly patients experience only weakness, palpitations, atrial fibrillation, shortness of breath and almost no effect from the use of cardiac glycosides. By the way, DTD in the elderly is sometimes not recognized for a long time due to the lack of expression 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), 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 to exclude malignant tumor and identification or determination of a risk factor for the development of decompensated thyroid FA. In nodular and multinodular toxic goiter, the detection rate of thyroid cancer is 3–10%.
Nodular toxic goiter is more often detected at a young age, and multinodular goiter - at the age of 50–70 years. More than half of elderly patients have nodal forms toxic goiter.
To determine treatment tactics and select the extent of surgical intervention, it is necessary to carry out differential diagnosis between DTG with nodes and toxic thyroid adenoma, as well as preoperative and intraoperative verification of the morphological structure of the thyroid FA.
There are different opinions regarding the choice of treatment method, volume and nature of surgical intervention for thyroid FA. Most authors recommend surgical treatment for nodular and multinodular toxic goiter. For solitary toxic adenoma - subtotal resection of the lobe, for multinodular adenoma - subtotal, extremely subtotal and total thyroidectomy. If malignancy of the node is suspected, hemithyroidectomy with isthmusectomy is performed. It should be noted that multinodular toxic goiter is one of the main risk factors for the development of recurrent toxic goiter after surgical treatment.
With euthyroidism or slight suppression of TSH with normal levels of St. T 3 and St. T4, as well as in the absence of goiter, data for thyrotoxicosis in the past, the uptake of 99m Tc-pertechnetate with suppression scintigraphy is less than 2%, observation (annual scintigraphy and study of TSH levels, free T3, free T4) without active treatment is indicated with a ban on the administration of iodine preparations. Thyrostatic agents (tyrosol, propicil) are indicated only as preparation for surgery and radioactive iodine therapy. The operation is indicated for FA with a volume of autonomous tissue more than 3 cm in diameter, nodular, multinodular toxic goiter. In other cases, as well as in cases of contraindications to surgery, radioactive iodine therapy is indicated.
In recent years, sclerotherapy with ethanol 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, its malignant nature is excluded and the presence of a closed, non-infiltrated capsule.
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Graefe's symptom |
Retraction of the upper eyelid - when looking down, a piece of sclera appears between the upper eyelid and the iris. |
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Kocher's sign |
When looking up, a section of sclera is revealed between the lower eyelid and the iris - a lag of the lower eyelid. |
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Moebius sign |
Violation of convergence of the eyeballs (loss of the ability to fix gaze at close distances). |
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Stellwag's symptom |
Rare flashing. |
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Delrymple's sign |
When looking directly, a strip of sclera is revealed between the upper eyelid and the iris (wide opening of the palpebral fissures). |
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Jellinek's sign |
Eyelid hyperpigmentation |
Endocrine (edematous) ophthalmopathy
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Domestic classification |
Classification (WernerS.C.) |
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I. Swelling of the eyelids, feeling of “sand in the eyes”, lacrimation, absence of diplopia |
I. Non-infiltrative (retraction of the upper eyelid, convergence disorder) |
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II. Infiltrative (edema of the eyelids, chemosis, dry conjunctivitis) |
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II. Diplopia, limited eye abduction |
III. Exophthalmos, lagophthalmos |
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IV. Changes oculomotor muscles(diplopia) |
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III. Incomplete closure of the palpebral fissure, corneal ulceration, persistent diplopia, optic nerve atrophy |
V. Corneal erosion, incomplete closure of the palpebral fissure |
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VI. Optic nerve compression |
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active inactive |
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CASE HISTORY OUTLINE
I. GENERAL INFORMATION ABOUT THE PATIENT.
II. ANAMNESIS
Complaints and active questioning of the patient. Identify the complaints inherent in thyrotoxicosis: weight loss, constant palpitations, pain in the heart, increased blood pressure; trembling of the hands (handwriting may change), the whole body, tearfulness, fussiness, irritability, feeling hot, sweating, rapid exhaustion, mood changes; frequent loose stool up to 6 or more times a day without mucus and blood, polyuria. Slight fluctuations in body temperature are possible. Identify signs of decompensation from the cardiovascular system: shortness of breath, swelling.
A goiter of significant size exerts mechanical pressure on neighboring organs, which may be accompanied by unpleasant sensations in the neck when the collar is buttoned, a feeling of pressure, a lump in the throat, difficulty swallowing, frequent coughing, and hoarseness.
It must be remembered that toxic goiter can be accompanied by damage not only to the cardiovascular, nervous, digestive systems, but also by damage to the neuromuscular (muscle weakness), skeletal system (pain in the back and bones), manifestation of ophthalmopathy (swelling of the eyelids , feeling of “sand in the eyes”, lacrimation, diplopia) and changes in the function of other glands internal secretion(oligomenorrhea, amenorrhea, decreased libido, decreased fertility, sexual weakness and gynecomastia in men, symptoms of hyperglycemia, skin hyperpigmentation).
2. History of the present illness. Find out at what time he considers himself sick. What were the first signs of the disease? To trace the connection of the disease with previous acute respiratory infections, sore throat, mental trauma, change of place of residence, surgical intervention. For women, take into account childbirth, pregnancy, abortion and their connection with health status.
Establish the dynamics of the development of the disease. Determine the time of occurrence of complications: atrial fibrillation, heart failure, jaundice and signs of ophthalmopathy, etc. Find out whether the patient has previously consulted a doctor. What treatment was prescribed and what was the effect. Have you previously undergone surgical treatment of thyroid tumors or nodules in the thyroid gland? Are you currently taking thyreostatics? Draw a diagram of the medical history according to E.M. Tareev.
3. Life history of the patient. What kind of child was born, what infections did he suffer in childhood? Education. Predisposing factors in the development of the disease are heredity and residence in iodine-deficient areas. There is or has been an occupational hazard in the past. Describe in detail the nature of the work performed by the patient; whether it is associated with mental or physical stress, with moving mechanisms, frequent business trips, or night shifts. The presence of concomitant diseases that could contribute to dysfunction of the thyroid gland, for example, chronic adnexitis, chronic cholecystitis, chronic hepatitis, chronic tonsillitis, chronic sinusitis, etc. Does the patient have bad habits(alcohol abuse, smoking). Gynecological history. The onset of menstruation, its frequency, the number of pregnancies, abortions, miscarriages, and trace their connection with the disease. How long have you been on sick leave and for what disease? Material and living conditions.
III. OBJECTIVE EXAMINATIONS
External examination. General condition of the patient. Position, movement activity. Consciousness, adequacy of behavior. Height, body weight, BMI (weight kg/height m2). youthful appearance, characteristic angry facial expression (Reprev-Melikhov symptom).
Skin and mucous membranes. The skin is thin, warm, translucent, moist, velvety, tender. Some patients have vitiligo, skin hyperpigmentation, especially in areas of friction, urticaria, scratch marks, alopecia on the scalp, and thinning nails. In rare cases, pretibial myxedema occurs, which is manifested by swelling, thickening and hypertrophy of the skin of the anterior surface of the leg. The skin turns purplish-red and resembles the peel of an orange. Even less common is acropathy - swelling of the soft and underlying bone tissues in the area of the hands (phalanxes of the fingers, wrist bones) and feet. Along with this, there is damage to the nail plates, which look like watch glasses. The affected areas of the skin are hyperpigmented with pronounced hyperkeratosis, painless on palpation.
Changes in the organ of vision. Identify the presence of ocular symptoms (exophthalmos, Moebius, Stellwag, Delrymple, Hellinik, eye gloss, Graefe, Kocher, Rosenbach, Geoffroy). Determine the degree of ophthalmopathy (I, II, III, tearing, scleral vascular injection, corneal ulceration).
The cardiovascular system. Ripple carotid arteries, elevating apical impulse. The pulse is frequent (90 beats or more), does not change when the patient changes position. Blood pressure level in both arms: there is an increase in systolic pressure with a decrease in diastolic pressure (increase in pulse pressure). Boundaries of the heart. Width vascular bundle. Auscultation. Loud heart sounds, systolic murmur. Heart rhythm disturbances: tachycardia, extrasystole, paroxysmal or constant atrial fibrillation. Presence of signs of heart failure (formation of a “thyrotoxic heart”).
Respiratory system. Breathing through the nose. Breathing rate. Percussion, auscultation of the lungs. Predisposition to pneumonia with atypical course.
Digestive system. Presence of manifestations of hepatitis (hepatomegaly), jaundice. Measure the Kurlov ordinates of the liver.
Genitourinary system.
Specifics of changes endocrine system . In women, note the presence of fibrocystic mastopathy. In men, gynecomastia may be detected.
Neuromuscular system and mental state. Characteristic is a combination of damage to the peripheral and central nervous systems, thyrotoxic myopathy and myoatrophy, which makes it difficult for patients to get up from a chair; in rare cases, periodic paralysis, paresis, and fascicular twitching are observed. Tendon reflexes are increased, Marie's symptom (tremor of the fingers of outstretched arms), tremor of the whole body ("telegraph pole symptom") are detected.
Dysfunction of the central nervous system is manifested by tearfulness, fussiness, irritability, increased excitability, mood lability, loss of the ability to concentrate, sleep disorders, sometimes depression, psychoses and hallucinations are extremely rare.
IV. PRELIMINARY DIAGNOSIS.
It is necessary to analyze complaints, medical history, and objective status. Identify the main syndromes:
Indicate the most likely main (preliminary) diagnosis:
Diffuse toxic goiter, degree of enlargement of the thyroid gland or
Nodular/multinodular toxic goiter.
V. PLAN FOR EXAMINATION OF THE PATIENT.
Data from laboratory and instrumental studies should confirm the preliminary diagnosis. In each proposed study, indicate probable deviations. For example: General urine analysis - proteinuria, bacteriuria.
General blood analysis. general urine analysis. Determination of blood cholesterol, glucose, urea content, creatinine, total protein, protein fractions; liver function tests. X-ray of the chest, and, if necessary, X-ray of the esophagus with barium to diagnose compression of surrounding organs by the large thyroid gland. ECG. Laboratory confirmation of thyrotoxicosis (suppressed TSH, elevated T4 and/or T3). Ultrasound of the thyroid gland. Ultrasound of the thyroid gland allows you to evaluate: the anatomical location of the gland, the contours of the lobes, structure, echogenicity, parenchyma, volume of the thyroid gland (Volume of the thyroid lobe (ml) = Length (cm) x Width (cm) x Thickness (cm) x 0.5); visualize palpable and detect non-palpable lesions and evaluate their structures. Scintigraphy of the thyroid gland (for nodes). Determination of antibodies to TPO (thyroid peroxidase), antibodies to TG (thyroglobulin), antibodies to the TSH receptor.
Other examinations as indicated in the presence of complications or concomitant diseases.
Consultations with specialized specialists: ophthalmologist (for endocrine ophthalmopathy - a complete ophthalmological examination), neurologist and others.
UI. DATA OF LABORATORY AND INSTRUMENTAL EXAMINATION OF THE PATIENT.
Emphasize deviations from normal values.
VII. DIFFERENTIAL DIAGNOSIS Differential diagnosis is carried out according to the leading syndrome:
Thyrotoxicosis syndrome. In iodine-deficient regions in the etiological structure of thyrotoxicosis, the first place in prevalence is shared by Graves' disease and various clinical forms functional autonomy of the thyroid gland (most often multinodular toxic goiter). In clinical practice, it is most often necessary to differentiate these diseases.
Heart rhythm disturbances: tachycardia, atrial fibrillation, arterial hypertension ( cardiopsychoneurosis tachyarrhythmias, climacteric neurosis, rheumatism,
Catabolic syndrome: fever of unknown origin, psychosis and psychopathy, artificial thyrotoxicosis (taking thyroid hormone drugs), drug addiction: cocaine, amphetamines; pheochromocytoma, adrenal insufficiency.
Endocrine ophthalmopathy (EOP): exophthalmos with hydrocephalus, fibrocystic osteodystrophy, bilateral orbital tumor, brain tumor, xanthomatosis, craniostenosis.
VIII. FINAL DIAGNOSIS AND ITS RATIONALE
A final detailed clinical diagnosis is formulated, indicating toxic goiter, the degree of enlargement of the thyroid gland, the severity of thyrotoxicosis, the presence of complications and concomitant diseases. Justify the presence of thyrotoxicosis, severity and compensation. Examples of diagnoses:
Basic: Diffuse toxic goiter of grade I (WHO), moderate severity, uncompensated.
Related: Chronic pyelonephritis, active, latent course.
Complications: Myocardial dystrophy. HIst.
Basic: Diffuse toxic goiter of degree II (WHO), severe, uncompensated.
Complications: Thyrotoxic heart: permanent form of atrial fibrillation, tachysystolic variant, myocardial dystrophy. HIIAst. Endocrine ophthalmopathy stage II, active phase.
Basic: Nodular toxic goiter of the II degree (WHO), severe course.
Complications: thyrotoxic heart, atrial fibrillation, myocardial dystrophy. N II A Art.
IX. ETIOLOGY AND PATHOGENESIS
Indicate the modern understanding of etiology and pathogenesis of this disease. Possibilities of prevention.
X. MEDICAL PURPOSE. Indicate the general principles of treatment of this disease. Rationale for the choice of treatment methods: conservative, surgical, treatment J 131. When carrying out conservative therapy, it is necessary to take into account the following: individual selection of the dose of thyreostatic drugs, the possibility of their toxic effect, justification of the indications for prescribing beta-blockers (persistent tachycardia, extrasystole), cardiac glycosides (permanent form of atrial fibrillation, heart failure). In the presence of ophthalmopathy, along with treatment with thyreostatics, glucocorticoids (prednisolone) are prescribed. For severe progressive ophthalmopathy, pulse therapy with glucocorticoids, irradiation of the orbital field of the orbit, orbital decompression, and surgery on the extraocular muscles and eyelids are indicated. Local therapy includes treatment of conjunctivitis and keratitis. Prescribe medications to treat concomitant pathologies and complications. Write out prescriptions.
XI. FORECAST. The prognosis should include three main aspects regarding life, regarding recovery (full or partial) and the degree of disability.
With a mild form of thyrotoxicosis, patients are able to work. Work in conditions of high temperature, associated with high physical activity, mental stress, and exposure to the sun is contraindicated. In patients with moderate severity of the disease, the ability to work is temporarily lost until a state of clinical euthyroidism is achieved. In patients with severe thyrotoxicosis, ability to work depends on the severity of complications remaining after treatment (ophthalmopathy, heart failure, cardiac arrhythmia) and is determined individually in each case.
PATIENT'S ILLNESS HISTORY CHART
OBESITY (METABOLIC SYNDROME)
Basic theoretical principles
Obesity– a chronic relapsing disease characterized by excessive accumulation of adipose tissue in the body.
Pattern of distribution of adipose tissue determined using the waist circumference/hip circumference (W/H) ratio. Magnitude WC/VR for men > 1.0 and women > 0.85 indicates the abdominal type of obesity. An indicator of the clinical risk of developing metabolic complications of obesity is also the size of the waist circumference.
There are a large number of obesity criteria, the most widely used is the body mass index (BMI), which is the ratio of body weight (bm) expressed in kilograms to the square of height in meters. BMI = weight (kg) / height (m2).
CLASSIFICATION OF OBESITY BY BMI (WHO, 1997) AND THE RISK OF METABOLIC COMPLICATIONS
|
Underweight |
Increased risk of other diseases |
|
|
Normal b.t. | ||
|
Obesity |
Elevated |
|
|
Obesity 1 tbsp | ||
|
Obesity level 11 |
Very tall |
|
|
Obesity 111st degree |
Extremely high |
|
|
FROM husband (cm) |
>94 and >102 |
Promoted and Tall |
|
FROM women (cm) |
Promoted and Tall |
Obesity classifications
According to etiological principle:
Nutritional-constitutional;
Hypothalamic;
Endocrine;
Iatrogenic.
By type of adipose tissue deposition:
Abdominal (android, central);
Gynoid (gluteo-femoral);
Mixed.
Obesity increases the risk of many diseases that often determine the patient's ability to work:
Diabetes mellitus type 2, impaired glucose tolerance
Arterial hypertension, stroke, myocardial infarction
Coronary heart disease, heart failure
Cancer (hormone dependent and independent)
Gallstone disease, steatohepatitis
Deforming arthritis, osteochondrosis
Varicose veins
Respiratory disorders (night apnea)
PARAMETERS OF METABOLIC SYNDROME
|
options |
meaning |
|
>27 kg/m2 |
|
|
>Female 0.85 |
|
|
FROM to 40 years | |
|
>140/90 mmHg |
|
|
Fasting glycemia |
>6.1 mmol/l |
|
After 2 hours GTT | |
|
Uric acid |
>480 mmol/l |
|
testosterone |
Female >+1№ |
|
triglycerides |
>2.3 mmol/l |
|
cholesterol |
>5.2 mmol/l |
|
<0,9 ммоль/л |
|
|
Albuminuria |
>20 mg/day |
|
Fibrinogen |
>300 mg/dl |
Scheme of primary examination of patients
The ocular symptoms of thyrotoxicosis are fundamentally distinguished from the independent disease of endocrine ophthalmopathy.
6. Endocrine ophthalmopathy (EOP)- damage to periorbital tissues of autoimmune origin, in 95% of cases combined with autoimmune diseases thyroid gland (TG), clinically manifested dystrophic changes oculomotor muscles (OMM) and other structures of the eye. There are 3 degrees of severity of EOP:
I. Swelling of the eyelids, feeling of “sand in the eyes”, lacrimation, in the absence of diplopia.
II. Diplopia, limited abduction of the eyeballs, upward gaze paresis.
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 (DTZ), in 5% with autoimmune thyroiditis, in 5-10% of cases there is no clinically detectable thyroid pathology. In some cases, DTZ manifests itself later than the image intensifier. The male to female ratio is 5:1, in 10% of cases the image intensifier is unilateral. Antibodies to TSH receptors (AT-TSH) have several functionally and immunologically distinct subpopulations. Mutant variants of AT-TSH can cause immune inflammation of 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 dystrophy of the orbital cavity. The severity of EOP does not correlate with the severity of concomitant thyroidopathy.
The image intensifier begins gradually, often on one side. Chemosis, feeling of pressure behind the eyeballs, increased sensitivity to light, sensation 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 eyeball, including as part of monitoring and evaluation, and the effectiveness of treatment.
7. Ectodermal disorders: brittle 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, relative thyrogenic, that is, with normal or increased levels of cortisol secretion, adrenal insufficiency (moderate melasma, hypotension).
10. Diseases associated with thyrotoxicosis: endocrine ophthalmopathy, pretibial myxedema (1-4%; swelling and thickening and hypertrophy of the skin of the anterior surface of the leg), acropathy (extremely rare; periosteal osteopathy of the feet and hands radiographically resembles “soap foam”).
11. Thyrotoxic crisis– urgent clinical syndrome, which is a combination of severe T. with thyrogenic adrenal insufficiency. The main reason is inadequate thyreostatic therapy. Provoking factors are: surgery, infectious and other diseases. Clinically: full-blown T. syndrome, severe mental anxiety up to psychosis, motor hyperactivity, alternating with 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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