Multinodular goiter ICD 10. Autoimmune diseases of the thyroid gland

Diffuse toxic goiter, in most cases, is characterized by a relatively short history: the first symptoms usually appear 4-6 months before visiting a doctor and making a diagnosis. As a rule, the key complaints are associated with changes in the cardiovascular system, the so-called catabolic syndrome and endocrine ophthalmopathy.
  The main symptom of the cardiovascular system is tachycardia and quite pronounced palpitations. Patients can feel heartbeats not only in the chest, but also in the head, arms, and stomach. Heart rate at rest with sinus tachycardia caused by thyrotoxicosis can reach 120-130 beats per minute.
  With long-term thyrotoxicosis, especially in elderly patients, pronounced dystrophic changes in the myocardium develop, a frequent manifestation of which is supraventricular rhythm disturbances, namely atrial fibrillation (flicker). This complication of thyrotoxicosis rarely develops in patients under 50 years of age. Further progression of myocardial dystrophy leads to the development of changes in the ventricular myocardium and congestive heart failure.
  As a rule, catabolic syndrome is expressed, manifested by progressive weight loss (sometimes by 10-15 kg or more, especially in persons with initial excess weight) against the background of increasing weakness and increased appetite. The skin of patients is hot, sometimes there is severe hyperhidrosis. A feeling of heat is typical; patients do not freeze at a sufficiently low temperature in the room. Some patients (especially the elderly) may experience evening low-grade fever.
  Changes in the nervous system are characterized by mental lability: episodes of aggressiveness, agitation, chaotic unproductive activity are replaced by tearfulness, asthenia (irritable weakness). Many patients are not critical of their condition and try to maintain an active lifestyle against the background of a rather severe somatic condition. Long-term thyrotoxicosis is accompanied by persistent changes in the patient’s psyche and personality. A frequent but nonspecific symptom of thyrotoxicosis is fine tremor: fine trembling of the fingers of outstretched arms is detected in most patients. In severe thyretoxicosis, tremors can be detected throughout the body and even make it difficult for the patient to speak.
  Thyrotoxicosis is characterized by muscle weakness and a decrease in muscle volume, especially the proximal muscles of the arms and legs. Sometimes quite pronounced myopathy develops. A very rare complication is thyrotoxic hypokalemic periodic paralysis, which is manifested by periodically occurring sharp attacks of muscle weakness. Laboratory tests reveal hypokalemia and increased CPK levels. It is more common among representatives of the Asian race.
  Intensification of bone resorption leads to the development of osteopenia syndrome, and thyrotoxicosis itself is considered one of the most important risk factors for osteoporosis. Frequent complaints of patients are hair loss and brittle nails.
  Changes in the gastrointestinal tract develop quite rarely. Elderly patients may have diarrhea in some cases. With long-term severe thyrotoxicosis, dystrophic changes in the liver (thyrotoxic hepatosis) can develop.
  Menstrual irregularities are quite rare. Unlike hypothyroidism, moderate thyrotoxicosis may not be accompanied by a decrease in fertility and does not exclude the possibility of pregnancy. Antibodies to the TSH receptor cross the placenta, and therefore children born (1%) to women with diffuse toxic goiter (sometimes years after radical treatment) may develop transient neonatal thyrotoxicosis. In men, thyrotoxicosis is often accompanied by erectile dysfunction.
  In severe thyrotoxicosis, a number of patients exhibit symptoms of thyroidogenic (relative) adrenal insufficiency, which must be differentiated from true. To the already listed symptoms are added hyperpigmentation of the skin, exposed parts of the body (Jellinek’s symptom), and arterial hypotension.
  In most cases, with diffuse toxic goiter, there is an increase in the size of the thyroid gland, which, as a rule, is diffuse in nature. Often the gland is significantly enlarged. In some cases, a systolic murmur can be heard over the thyroid gland. However, goiter is not an obligate symptom of diffuse toxic goiter, since it is absent in at least 25-30% of patients.
  Of key importance in the diagnosis of diffuse toxic goiter are changes in the eyes (“bulging”), which are a kind of “calling card” of diffuse toxic goiter, i.e. Their detection in a patient with thyrotoxicosis almost unambiguously indicates diffuse toxic goiter, and not about another disease. Very often, due to the presence of severe ophthalmopathy in combination with symptoms of thyrotoxicosis, the diagnosis of diffuse toxic goiter is obvious already upon examination of the patient.
  The clinical picture of thyrotoxicosis may differ from the classic version. So, if in young people diffuse toxic goiter is characterized by a detailed clinical picture, in elderly patients its course is often oligo- or even monosymptomatic (heart rhythm disturbance, low-grade fever). In the “apathetic” version of the course of diffuse toxic goiter, which occurs in elderly patients, clinical manifestations include loss of appetite, depression, and physical inactivity.
  A very rare complication of diffuse toxic goiter is a thyrotoxic crisis, the pathogenesis of which is not entirely clear, since a crisis can develop without an extreme increase in the level of thyroid hormones in the blood. The cause of a thyrotoxic crisis may be acute infectious diseases accompanying diffuse toxic goiter, surgical intervention or radioactive iodine therapy against the background of severe thyrotoxicosis, withdrawal of thyrostatic therapy, or administration of a contrast iodine-containing drug to the patient.
  Clinical manifestations of a thyrotoxic crisis include a sharp worsening of the symptoms of thyrotoxicosis, hyperthermia, confusion, nausea, vomiting, and sometimes diarrhea. Sinus tachycardia over 120 beats/min is recorded. Atrial fibrillation, high pulse pressure followed by severe hypotension are often observed. The clinical picture may be dominated by heart failure and respiratory distress syndrome. Manifestations of relative adrenal insufficiency are often expressed in the form of skin hyperpigmentation. The skin may be jaundiced due to the development of toxic hepatosis. Laboratory tests may reveal leukocytosis (even in the absence of concomitant infection), moderate hypercalcemia, and increased alkaline phosphatase levels. Mortality during thyrotoxic crisis reaches 30-50%.

Included: endemic conditions associated with iodine deficiency in the natural environment, both directly and as a result of iodine deficiency in the mother’s body. Some of these conditions cannot be considered true hypothyroidism, but are a consequence of inadequate secretion of thyroid hormones in the developing fetus; there may be a connection with natural goitrogenic factors. If necessary, identify concomitant mental retardation, use an additional code (F70-F79). Deleted: subclinical hypothyroidism due to iodine deficiency (E02)

• • E00.0 Congenital iodine deficiency syndrome, neurological form. Endemic cretinism, neurological form
  • E00.1 Congenital iodine deficiency syndrome, myxedema form Endemic cretinism: hypothyroid, myxedema form
  • E00.2 Congenital iodine deficiency syndrome, mixed form. Endemic cretinism, mixed form
  • E00.9 Congenital iodine deficiency syndrome, unspecified. Congenital hypothyroidism due to iodine deficiency NOS. Endemic cretinism NOS
• E01 Thyroid diseases associated with iodine deficiency and similar conditions. Excluded: congenital iodine deficiency syndrome (E.00-), subclinical hypothyroidism due to iodine deficiency (E02)
  • E01.0 Diffuse (endemic) goiter associated with iodine deficiency
  • E01.1 Multinodular (endemic) goiter associated with iodine deficiency. Nodular goiter associated with iodine deficiency
  • E01.2 Goiter (endemic), associated with iodine deficiency, unspecified Endemic goiter NOS
  • E01.8 Other thyroid diseases associated with iodine deficiency and similar conditions. Acquired hypothyroidism due to iodine deficiency NOS
• E02 Subclinical hypothyroidism due to iodine deficiency
• E03 Other forms of hypothyroidism.

Excluded: hypothyroidism associated with iodine deficiency (E00 - E02), hypothyroidism following medical procedures (E89.0)

• • E03.0 Congenital hypothyroidism with diffuse goiter. Goiter (non-toxic) congenital: NOS, parenchymal, Deleted: transient congenital goiter with normal function (P72.0)
  • E03.1 Congenital hypothyroidism without goiter. Aplasia of the thyroid gland (with myxedema). Congenital: thyroid atrophy, hypothyroidism NOS
  • E03.2 Hypothyroidism caused by drugs and other exogenous substances
  • E03.3 Post-infectious hypothyroidism
  • E03.4 Thyroid atrophy (acquired) Excluded: congenital atrophy of the thyroid gland (E03.1)
  • E03.5 Myxedema coma
  • E03.8 Other specified hypothyroidisms
  • E03.9 Hypothyroidism, unspecified. Myxedema NOS
• E04 Other forms of non-toxic goiter.

Excluded: congenital goiter: NOS, diffuse, parenchymal goiter associated with iodine deficiency (E00 - E02)

• • E04.0 Non-toxic diffuse goiter. Non-toxic goiter: diffuse (colloid), simple
  • E04.1 Non-toxic uninodular goiter. Colloid node (cystic), (thyroid). Non-toxic mononodous goiter. Thyroid (cystic) node NOS
  • E04.2 Non-toxic multinodular goiter. Cystic goiter NOS. Polynodous (cystic) goiter NOS
  • E04.8 Other specified forms of non-toxic goiter
  • E04.9 Non-toxic goiter, unspecified. Goiter NOS. Nodular goiter (non-toxic) NOS
• E05 Thyrotoxicosis [hyperthyroidism]
  • E05.0 Thyrotoxicosis with diffuse goiter. Exophthalmic or toxic goiter. NOS. Graves' disease. Diffuse toxic goiter
  • E05.1 Thyrotoxicosis with toxic uninodular goiter. Thyrotoxicosis with toxic mononodous goiter
  • E05.2 Thyrotoxicosis with toxic multinodular goiter. Toxic nodular goiter NOS
  • E05.3 Thyrotoxicosis with ectopia of thyroid tissue
  • E05.4 Artificial thyrotoxicosis
  • E05.5 Thyroid crisis or coma
  • E05.8 Other forms of thyrotoxicosis. Hypersecretion of thyroid stimulating hormone
  • E05.9 Thyrotoxicosis, unspecified. Hyperthyroidism NOS. Thyrotoxic heart disease (I43.8*)
• E06 Thyroiditis.

Deleted: postpartum thyroiditis (O90.5)

• • E06.0 Acute thyroiditis. Abscess of the thyroid gland. Thyroiditis: pyogenic, purulent
  • E06.1 Subacute thyroiditis. De Quervain's thyroiditis, giant cell, granulomatous, non-purulent. Deleted: autoimmune thyroiditis (E06.3)
  • E06.2 Chronic thyroiditis with transient thyrotoxicosis.

Deleted: autoimmune thyroiditis (E06.3)

• • E06.3 Autoimmune thyroiditis. Hashimoto's thyroiditis. Chasitoxicosis (transient). Lymphadenomatous goiter. Lymphocytic thyroiditis. Lymphomatous struma
  • E06.4 Drug-induced thyroiditis.
  • E06.5 Chronic thyroiditis: NOS, fibrous, woody, Riedel
  • E06.9 Thyroiditis, unspecified
• E07 Other thyroid diseases
  • E07.0 Hypersecretion of calcitonin. C-cell hyperplasia of the thyroid gland. Hypersecretion of thyrocalcitonin
  • E07.1 Dyshormonal goiter. Familial dyshormonal goiter. Pendred's syndrome.

Deleted: transient congenital goiter with normal function (P72.0)

• • E07.8 Other specified diseases of the thyroid gland. Tyrosine-binding globulin defect. Hemorrhage, infarction in the thyroid gland.
  • E07.9 Thyroid disease, unspecified

Such a nosological unit as nodular goiter, the ICD 10 code of which is from E00 to E07, respectively, is not one disease, but a clinical syndrome. It combines formations quite diverse in shape and structure that form in the area of ​​the thyroid gland. Most often, pathological changes in the structure of the organ are caused by a lack of iodine in the patient’s body.

The disease is usually endemic. It has been noted that in certain areas among the population the incidence rate may exceed 40%. Most often women in the age group of 40 years and over are affected. If we talk about characteristic symptomatic manifestations, they may be absent if the pathological process is mild. In more severe cases, nodular goiter can manifest itself in the form of various dysfunctions of this organ, as well as symptoms of compression of surrounding organs and tissues.

If we talk about the structure of such a human endocrine organ as the thyroid gland, then first of all we will determine that it consists of follicular cells. Each such cell is a microscopic ball that is filled with a specific liquid - keloid. As the pathological process develops, the follicle increases in size, forming a so-called node. The neoplasm can be represented by only one node or be formed from a large number of modified follicles. This is already the so-called diffuse nodular goiter.

QjZIYKBrYHs

If we talk about the reason for the development of such pathological changes in the thyroid gland, it has not yet been precisely established. As mentioned above, most experts associate the formation of pathological changes in follicles with a lack of iodine in the human body. This theory is based on the fact that, according to statistical data, in areas with low levels of this chemical element in water and food, the incidence of nodular goiter among the population is quite high. However, how can we explain the fact that such a pathology is often detected in areas that are fairly free in iodine content?

According to another theory, diseases (classification code corresponds to column E0-07) develop as a result of increased load on the thyroid gland. As a rule, this is associated with a violation of the functioning of the entire human body. What factors can provoke an increase in the size of the follicles and form cystic formations on their basis?

1. Hereditary predisposition to disruption of the endocrine system.
2. Environmental factors. This includes increased radiation, water and air pollution with waste products from industrial enterprises.
3. Various human immune disorders or diseases.
4. Prolonged stressful situations.
5. Age-related changes in the tissues that form the thyroid gland can also contribute to the development of this pathology.

The difficulty of determining the cause of such a goiter (ICD 10 defines it as E01-07) may be due to the fact that the patient’s body is affected by not one, but several unfavorable factors. However, regardless of the determining factors, the symptomatic manifestations of the pathology are always the same.

Clinical picture

In the early and uncomplicated stages of the pathological process, it is almost impossible to determine the presence of nodular goiter without special studies. The patient has no specific complaints. The diagnosis in this case can be made by chance, for example, as a result of examining the thyroid gland using ultrasound. On the screen, the doctor identifies the presence of nodes or cysts in the organ tissue.

Only at a later stage will the patient notice a change in the contours of the neck due to the growth of the cystic formation. This disease is called euthyroidism. The absence of clinical symptoms is due to the fact that hormone production in this case is not impaired. The patient will mainly be concerned about the resulting cosmetic defect. Only in some cases can unpleasant squeezing sensations appear in the throat area.

Diffuse goiter is considered the most severe in terms of symptomatic manifestations. Its clinical course is very similar to thyrotoxicosis. When interviewing a doctor, the patient makes the following complaints:

1. Unpleasant sensations appear in the throat area. Sometimes it's just a feeling of pressure, but pain can also appear.
2. The patient complains of difficulty swallowing food.
3. When the cystic formation puts pressure on the trachea, complaints of impaired respiratory function appear.
4. Changes in the functioning of the cardiovascular system may be detected, for example, in the form of increased heart rate and arrhythmia. This symptomatic manifestation will have an additional code in the patient's medical history.
5. The patient notices that he has lost weight for no specific reason.
6. The work of the sweat glands increases.
7. The skin may be very dry.
8. The patient notes increased nervousness or, conversely, is prone to depression.
9. The process of memorizing a large amount of information may be disrupted.
10. Sometimes there are complaints of intestinal dysfunction or constipation.

Classification of the disease

If we talk about the classifications most often used in medical practice for this pathology, then those are used that are based on the characteristics of the degree of enlargement of the organ. An example would be the classification proposed by Dr. O.V. Nikolaev. Unlike ICD 10, it does not use coding, but simply indicates the degree of enlargement of the thyroid gland in the medical history:

1. Zero degree of pathology is characterized by the absence of obvious violations of the shape and size of the organ. Even palpation examination will not help make a diagnosis. The patient has no characteristic complaints.
2. In the first degree, there are no cosmetic defects in the neck area, but upon palpation, the doctor may note a slight enlargement of the thyroid gland. It is during this period that the first functional disturbances in the functioning of the organ may appear.
3. If the thyroid gland is clearly visible during the act of swallowing, then the patient is diagnosed with the second stage of the disease. During this period, the organ is easily palpable. The patient begins to complain of periodic difficulties when swallowing or breathing.
4. The third degree code for this pathology is set in the case when the patient’s gland is so enlarged that it changes the usual contour of the neck. During this period, all the main symptomatic manifestations of the disease can be identified in the patient.
5. If symptomatic manifestations increase and there is a significant cosmetic defect in the neck area, the person is given the fourth degree of the disease.
6. The fifth degree is the most severe. In this case, the gland grows to large sizes, which leads to compression of regional organs and tissues. The functioning of most organs and systems is disrupted.

There is a classification according to ICD 10. It is based not only on symptomatic manifestations, but also takes into account the causes of the development of the disease. There are 3 types of disease:

1. Endemic goiter, which is formed due to iodine deficiency.
2. A non-toxic form of goiter, in which the presence of one or several nodes is distinguished.
3. Thyrotoxicosis form of pathology.

Therapeutic measures

Experts believe that for mild forms of nodular goiter, therapy is usually not needed. The patient's health condition is monitored. And only in the presence of intensive cyst growth can treatment tactics be chosen. In this case, the question of which technique to use, conservative or operative, is decided.

JIjKxkEB-F4

If a conservative, or, in other words, medicinal method is chosen, the patient is prescribed medications that can suppress the increased production of hormones by this gland. In addition to this, iodine preparations may be prescribed.

Surgical treatment is indicated for significant enlargement of cysts, for example, if the patient has a diffuse toxic goiter of severe severity. The surgical technique in this case is designed to remove the formed cysts. In this case, part of the affected gland (a lobe or half of the gland) is also removed. If a malignant neoplasm is detected, depending on the area of ​​the lesion, the entire thyroid gland may be removed.

In order to understand what the ICD 10 code for diffuse nodular goiter is and what it means, you need to understand what the designation “ICD 10” represents. It stands for “international classification of diseases” and is a normative document whose task is to unite methodological approaches and compare materials among doctors around the world. That is, in simple terms, this is an international classification of all known diseases. And the number 10 indicates the version of the revision of this classification, at the moment it is the 10th. And diffuse nodular goiter as a pathology belongs to class IV, which includes diseases of the endocrine system, metabolic and digestive disorders, which have alphanumeric codes from E00 to E90. Diseases of the thyroid gland occupy positions from E00 to E07.

If we talk about diffuse nodular goiter, it should be remembered that the classification according to ICD 10 combines into a group various pathologies of the thyroid gland, which differ both in the reasons for their appearance and in morphology. These are nodular neoplasms in the tissues of the thyroid gland (uninodular and multinodular), and pathological proliferation of its tissues due to dysfunction, as well as mixed forms and clinical syndromes associated with diseases of the endocrine organ.

They can also be diagnosed in different ways, some pathologies visually “disfigure” the neck, some can only be felt during palpation, others, in general, are determined only using ultrasound.

The morphology of the diseases allows us to distinguish the following types: diffuse, nodular and diffuse nodular goiter.

One of the changes made by the 10th revision to the ICD was the classification of thyroid pathologies not only by morphological characteristics, but also by the reasons for their appearance.

Thus, the following types of goiter are distinguished:

• endemic origin due to iodine deficiency;
• euthyroid or non-toxic;
• thyrotoxic conditions.

For example, if we consider the endemic goiter ICD 10 that has arisen as a result of iodine deficiency, it is assigned the code E01. The official wording is as follows: “Diseases of the thyroid gland associated with iodine deficiency and similar conditions.” Since this group combines diffuse and nodular forms of endemic goiter, as well as their mixed forms, diffuse nodular goiter can be classified under this international classification code, but only as a type that has developed as a result of iodine deficiency.

ICD 10 E04 code implies sporadic non-toxic forms of goiter. This includes both diffuse and nodal types - one node or many. That is, diffuse nodular goiter, which is not caused by iodine deficiency, but, for example, by a genetic predisposition to thyroid dysfunction, can be “marked” with the alphanumeric code E04.

If you pay attention to the group of diseases under the ICD code E05, the main concept of these pathologies will be thyrotoxicosis. Thyrotoxicosis is a condition in which toxic poisoning of the body occurs due to an excess of thyroid hormones in the blood, for example, thyroid adenoma. The main causes of such processes are toxic types of goiter: diffuse toxic goiter, nodular toxic goiter (single and multinodular) and their mixed form. So the toxic type of diffuse nodular goiter belongs specifically to group E05.

However, it is not always possible to see one doctor. There are times when there is a need to move to another city or country. Or there is an opportunity to continue treatment in a foreign clinic with more experienced specialists. And doctors need to exchange research and laboratory test data. It is in such cases that the importance and usefulness of such a document as ICD 10 is felt. Thanks to it, the boundaries between doctors from different countries are erased, which naturally saves both time and resources. And time, as we know, is very valuable.

ICD-10: types of goiter

ICD 10 - International Classification of Diseases, 10th revision, was created to systematize data on diseases according to their type and development.

To designate diseases, a special encoding has been developed, which uses capital Latin letters and numbers.

Thyroid diseases are classified as class IV.

Goiter, as a type of thyroid disease, is also included in ICD 10 and has several types.

Types of goiter according to ICD 10

Goiter is a clearly defined enlargement of the thyroid gland tissue, resulting from dysfunction (toxic form) or due to changes in the structure of the organ (euthyroid form).

The ICD 10 classification provides for territorial foci of iodine deficiency (endemic), due to which the development of pathologies is possible.

This disease most often affects residents of regions with iodine-poor soils - these are mountainous areas, areas far from the sea.

The endemic type of goiter can seriously affect thyroid function.

The classification of goiter according to ICD 10 is as follows:

1. Diffuse endemic;
2. Multinodular endemic;
3. Non-toxic diffuse;
4. Non-toxic single-node;
5. Non-toxic multi-node;
6. Other specified species;
7. Endemic, unspecified;
8. Non-toxic, unspecified.

A non-toxic form is one that, unlike the toxic one, does not affect the normal production of hormones; the reasons for the enlargement of the thyroid gland lie in the morphological changes of the organ.

An increase in volume most often indicates the development of a goiter.

Even with visual defects, it is impossible to immediately determine the cause and type of disease without additional tests and studies.

For an accurate diagnosis, all patients must undergo ultrasound examinations and donate blood for hormones.

Diffuse endemic process

Diffuse endemic goiter has an ICD 10 code - E01.0, and is the most common form of the disease.

In this case, the entire parenchyma of the organ is enlarged due to acute or chronic iodine deficiency.

Patients experience:

• weakness;
• apathy;
• headaches, dizziness;
• suffocation;
• difficulty swallowing;
• Digestive problems.

Later, pain in the heart area may develop due to a reduced concentration of thyroid hormones in the blood.

In severe cases, surgery and goiter removal are indicated.

Residents of iodine-deficient areas are advised to regularly take iodine-containing foods, vitamins, and undergo regular examinations.

Multinodular endemic process

This species has code E01.1.

With pathology, several well-defined neoplasms appear on the tissues of the organ.

Goiter grows due to iodine deficiency, characteristic of a particular area. The symptoms are as follows:

• hoarse, hoarse voice;
• sore throat;
• breathing is difficult;
• dizziness.

It should be noted that only as the disease progresses do the symptoms become pronounced.

At the initial stage, fatigue and drowsiness are possible; such signs can be attributed to overwork or a number of other diseases.

Non-toxic diffusion process

The code in ICD 10 is E04.0.

Enlargement of the entire thyroid gland area with no changes in functionality.

This happens due to autoimmune disorders in the structure of the organ. Signs of the disease:

• headaches;
• suffocation;
• characteristic neck deformity.

Complications in the form of hemorrhages are possible.

A number of doctors believe that euthyroid goiter can not be treated until it narrows the esophagus and trachea and does not cause pain and spasmodic cough.

Non-toxic single-node process

Has code E04.1.

This type of goiter is characterized by the appearance of one clear neoplasm on the thyroid gland.

The knot causes discomfort if it is treated incorrectly or untimely.

As the disease progresses, a pronounced bulge appears on the neck.

As the node grows, nearby organs are compressed, which leads to serious problems:

• voice and breathing disorders;
• difficulty swallowing, digestive problems;
• dizziness, headaches;
• improper functioning of the cardiovascular system.

The area of ​​the node can be very painful, this is due to the inflammatory process and swelling.

Endemic goiter, unspecified

It has a code according to ICD 10 - E01.2.

This type is caused by territorial iodine deficiency.

It does not have certain pronounced symptoms; the doctor cannot determine the type of disease even after the required tests.

The disease is assigned based on endemic characteristics.

Non-toxic multi-node process

The non-toxic multi-node type has code E04.2. in ICD 10.

Pathology of the structure of the thyroid gland. in which there are several clearly defined nodular neoplasms.

The lesions are usually located asymmetrically.

Other types of non-toxic goiter (specified)

Other specified forms of non-toxic goiter of the disease, which are assigned code E04.8, include:

1. A pathology in which both diffuse tissue proliferation and the formation of nodes are detected - diffuse-nodular form.
2. The growth and adhesion of several nodes is a conglomerate form.

Such formations occur in 25% of cases of the disease.

Unspecified nontoxic goiter

For this type of goiter, code E04.9 is provided in ICD 10.

It is used in cases where the doctor, as a result of an examination, rejects the toxic form of the disease, but cannot determine what kind of pathology of the thyroid gland structure is present.

The symptoms in this case are varied; tests do not provide the full picture.

How will ICD 10 help?

This classification was developed primarily for recording and comparing the clinical picture of diseases and for statistical analysis of mortality in individual territories.

The classifier benefits the doctor and the patient, helps to quickly make an accurate diagnosis and choose the most advantageous treatment strategy.

Nodular and diffuse goiter of the thyroid gland

Characteristics

The features of the disease can be read from its name:

• Diffuse - means that there is no clear macroscopic (observable with the naked eye) boundary between the affected and healthy areas of the gland. In the early stages, it is difficult to see during microscopic examination. Sick cells and their groups are almost evenly distributed among healthy ones.
• Goiter refers to the tendency of pathological areas to gather together into so-called nodes. They become visible during ultrasound examination immediately before the onset of the disease.

The mechanism of development of the disease is associated with an increased influence of thyroid-stimulating hormone (TSH) on gland tissue. It is produced in the pituitary gland. This hormone stimulates the growth and development of gland cells. With pathology, an increase in its cells is observed, and then in the tissue itself (hypertrophy). This leads to an increase in the amount of hormones (thyronines) produced by the thyroid gland. In the first stages, their release is controlled by the hypothalamic-pituitary system of the brain. After a few years (the time depends on external factors), immune cells, due to a failure of the protective system, begin to attack the hypertrophied cells of the gland. This is called an autoimmune process. The cell wall is destroyed, hormones enter the blood en masse.

Causes of pathology

The development of diffuse goiter is associated only with autoimmune processes, the predisposition to which is inherited. This is proven by the fact that in children whose families have endocrine pathology, nodular goiter is more common. The disease itself occurs under the influence of external factors. Therefore, its start dates vary. Average age is considered to be between 30 and 50 years. Women suffer from this pathology 8 times more often.

External factors provoking the development of the disease:

• stress;
• injuries;
• chronic pathologies of the upper respiratory tract.

Clinic of the disease

Diffuse goiter occurs hidden for several years. Often it is detected already in the presence of certain complications. All of them are associated with increased production of thyroid hormones. As a result, not a positive, but a toxic effect on the body is manifested.

Early signs

The disease can be suspected by its early symptoms. They are considered obvious only if there are shifts in the levels of thyroid hormones and TSH. In the early stages, all signs may suddenly appear and disappear (unstable).

The first symptoms include:

• tachycardia (increased heart rate);
• underweight with good nutrition;
• causeless headaches;
• sweating

Late symptoms and complications

At the height of the disease, the patient experiences persistence of these symptoms. A number of new symptoms appear. They are all grouped as follows:

• Endocrine. High metabolism causes weight loss along with increased appetite. Women under 40-45 years old experience irregularities in the menstrual cycle. They are also characterized by an early onset of menopause.
• Neurological. Patients are irritable and mentally unstable. Tremors of the limbs, insomnia and weakness when moving (especially when trying to get up from a chair or bed) are often noted.
• Cardiological. Various heart rhythm disturbances (tachycardia, extrasystole, atrial fibrillation), arterial hypertension and heart failure. The latter joins in the later stages of the disease. It is characterized by shortness of breath, swelling in the legs, and an enlarged abdomen due to ascites (fluid accumulation in the abdominal cavity).
• Dermatological. Excessive sweating over time leads to dermatitis (inflammation of the skin) in the natural folds of the body. With long-term diffuse goiter, changes affect the nails. They become brittle and deformed.
• Ophthalmological. Patients' eyes protrude from their sockets. This makes them visually larger. Due to constant tension, the upper and lower eyelids acquire a striated appearance.

Diagnosis and degree of gland enlargement

To make a diagnosis, a combination of several symptoms with an increase in the amount of thyroid hormones is necessary. The TSH level can be either elevated or decreased.

The difference in the degrees of enlargement of the gland is of great clinical significance. Before the widespread dissemination of laboratory and instrumental research methods, they were considered the main criterion for the stage of the disease and the effectiveness of treatment. These include:

• Grade 0 is assigned when there are no changes in the thyroid gland. At the same time, there is clinical and/or laboratory evidence of an increase in the production of its hormones.
• Grade 1 is assigned to a slight enlargement of the gland. Outwardly it is not defined in any way. This can only be noticed by palpation (palpation with fingers).
• Grade 2 means that the enlargement of the gland can be detected during swallowing. A number of patients feel a lump in their throat.
• Grade 3 is a permanent visual enlargement of the gland. The patient constantly feels a lump in the throat.
• The 4th degree is set when the gland is enlarged, leading to neck deformation. A number of authors identify another 5th degree, when changes affect not only the anterior, but also the lateral surfaces of the neck.

Treatment

Therapy for diffuse goiter involves three options:

• conservative drug treatment;
• radioiodine therapy;
• surgical treatment.

The choice of method depends on the stage of the disease, condition and individual characteristics of the patient. Sometimes a combination of these is used.

Drug treatment involves taking medications that reduce the production of thyroid hormones and/or block their action. The main remedy is Mercazolil. It interferes with the synthesis of hormones. Its intake is carried out under the control of thyronine levels. Beta blockers (Concor, Egilok, Anaprilin, Bidop, etc.), potassium preparations (Asparkam, Panangin) and sedatives of plant origin (valerian, motherwort) are prescribed as adjuvant therapy.

Radioiodine therapy is used when the disease progresses (clinical and laboratory-instrumental deterioration) throughout the year, despite drug treatment. The procedure involves administering the isotope iodine-131. It selectively accumulates in the thyroid gland. When its nuclei decay, radioactive radiation is emitted. It destroys gland cells. This is especially true for those who have a high metabolic rate. The result of therapy is the removal of all hypertrophied tissue.

Surgical treatment is performed only if there is no effect from drug therapy and rapid (within 1-2 months) enlargement of the gland. The purpose of the method is to excise hypertrophied tissue. Sometimes they resort to complete resection (removal) of the gland.

All these methods must be carried out while observing a special diet. It involves the exclusion of fatty, fried and smoked foods. Salt is limited to 6-8 g per day (in the presence of arterial hypertension - up to 3). The only meat allowed is chicken and lean beef. Fish (preference is given to freshwater) can be eaten stewed with vegetables. All gray porridges are allowed (buckwheat, pearl barley, barley).

12171 0

Diffuse toxic goiter (DTZ)- Graves' disease, Parry's disease, Graves' disease - a genetically determined autoimmune disease manifested by persistent hyperproduction of thyroid hormones by a diffusely enlarged thyroid gland under the influence of specific thyroid-stimulating autoantibodies.

ICD-10 CODE
E05.0. Thyrotoxicosis with diffuse goiter.

Epidemiology

The incidence is approximately 5-6 cases per 100 thousand population. The disease most often manifests itself between the ages of 16 and 40 years, predominantly in females.

Etiology and pathogenesis

The main role in the development of the disease belongs to hereditary predisposition with the inclusion of autoimmune mechanisms. 15% of patients with DTD have relatives with the same disease. Approximately 50% of patients' relatives have circulating thyroid autoantibodies. Provoking factors can be mental trauma, infectious diseases, pregnancy, taking large doses of iodine and prolonged exposure to the sun. B lymphocytes and plasma cells mistakenly recognize thyrocyte TSH receptors as antigens and produce thyroid-stimulating autoantibodies. By binding to the TSH receptors of thyrocytes like TSH, they trigger the adenylate cyclase reaction and stimulate thyroid function. As a result, its mass and vascularization increase, and the production of thyroid hormones increases.

Clinical picture

Thyrotoxicosis with thyrotoxicosis is usually severe. An excess of thyroid hormones has a toxic effect on all organs and systems, activates catabolic processes, as a result of which patients lose weight, muscle weakness, low-grade fever, tachycardia, and atrial fibrillation appear. Myocardial dystrophy, adrenal and insulin insufficiency and cachexia subsequently develop.

The thyroid gland, as a rule, is evenly enlarged, soft-elastic in consistency, painless, and displaces when swallowing.

The clinical picture is due to the influence of excess thyroid hormones on the organs and systems of the body. The complexity and multiplicity of factors involved in pathogenesis determine the variety of clinical manifestations of the disease.

When analyzing complaints and the results of an objective examination, various symptoms are identified that can be combined into several syndromes.

Damage to the central and peripheral nervous system. Under the influence of excess thyroid hormones, patients experience increased excitability, psycho-emotional lability, decreased concentration, tearfulness, fatigue, sleep disturbances, tremor of the fingers and the whole body (telegraph pole syndrome), increased sweating, persistent red dermographism and increased tendon reflexes.

Eye syndrome caused by hypertonicity of the muscles of the eyeball and upper eyelid due to disruption of autonomic innervation under the influence of excess thyroid hormones.

• Dalrymple's sign(exophthalmos, thyroid exophthalmos) - widening of the palpebral fissure with the appearance of a white strip of sclera between the iris and the upper eyelid.
• Graefe's symptom- lag of the upper eyelid from the iris when fixing the gaze on an object slowly moving downwards. In this case, a white strip of sclera remains between the upper eyelid and the iris.
• Kocher's sign- when you fix your gaze on an object slowly moving upward, a white strip of sclera remains between the lower eyelid and the iris.
• Stellwag's sign- rare blinking of the eyelids.
• Möbius sign- loss of ability to fix gaze at close range. Due to the weakness of the adductor eye muscles, the eyeballs fixed on a nearby object diverge and take their original position.
• Repnev-Melekhov symptom- “angry look.”

Eye symptoms (thyroid exophthalmos) in DTG should be distinguished from endocrine ophthalmopathy, an autoimmune disease that is not a manifestation of DTG, but is often (40-50%) combined with it. With endocrine ophthalmopathy, an autoimmune process affects the periorbital tissues. Due to the infiltration of orbital tissues by lymphocytes and the deposition of acidic glycosaminoglycans produced by fibroblasts, edema and an increase in the volume of retrobulbar tissue, myositis and proliferation of connective tissue in the extraocular muscles develop. Gradually, infiltration and edema turn into fibrosis and changes in the eye muscles become irreversible.

Endocrine ophthalmopathy Clinically manifested by disorders of the extraocular muscles, trophic disorders and exophthalmos. Patients are bothered by pain, double vision, a feeling of “sand” in the eyes, and lacrimation. Conjunctivitis and keratitis often develop with ulceration of the cornea due to its drying out when the eyelids do not close completely. Sometimes the disease takes on a malignant course, asymmetry and protrusion of the eyeballs develop until one of them completely falls out of the orbit.
There are 3 stages of endocrine ophthalmopathy:
I - swelling of the eyelids, feeling of “sand” in the eyes, lacrimation;
II - diplopia, limited abduction of the eyeballs, upward gaze paresis;
III - incomplete closure of the palpebral fissure, corneal ulceration, persistent diplopia, optic nerve atrophy.

Damage to the cardiovascular system is manifested by tachycardia, atrial fibrillation, the development of dyshormonal myocardial dystrophy (“thyrotoxic heart”), and high pulse pressure. Cardiac disorders are associated both with the direct toxic effect of hormones on the myocardium and with increased work of the heart due to the increased needs of peripheral tissues for oxygen under conditions of increased metabolism. As a result of an increase in stroke and cardiac output and acceleration of blood flow, systolic blood pressure (BP) increases. A systolic murmur appears at the apex of the heart and over the carotid arteries. A decrease in diastolic blood pressure in thyrotoxicosis is associated with the development of adrenal insufficiency and a decrease in the production of glucocorticoids, the main regulators of vascular wall tone.

Damage to the digestive system manifested by unstable stools with a tendency to diarrhea, attacks of abdominal pain, and sometimes jaundice, which is associated with impaired liver function.

Damage to other glands:
Dysfunction of the adrenal cortex, in addition to reducing diastolic blood pressure, also causes hyperpigmentation of the skin. Pigmentation often appears around the eyes - Jellinek's sign.
Increased breakdown of glycogen and the entry of large amounts of glucose into the blood forces the pancreas to work in maximum tension mode, which ultimately leads to its insufficiency - thyroidogenic diabetes mellitus develops. The course of existing diabetes mellitus in patients with DTG significantly worsens.
Other hormonal disorders in women include ovarian dysfunction with menstrual irregularities and fibrocystic mastopathy (thyrotoxic mastopathy, Velyaminov's disease), and in men - gynecomastia.

Catabolic disorder syndrome manifested by weight loss with increased appetite, low-grade fever and muscle weakness.

Pretibial myxedema- another manifestation of DTZ - develops in 1-4% of cases. In this case, the skin of the anterior surface of the leg becomes swollen and thickened. Itching and erythema often occur.

Diagnostics

Diagnosis of DTZ, as a rule, does not cause difficulties. A characteristic clinical picture, an increase in the level of T 3, T 4 and specific antibodies, as well as a significant decrease in the level of TSH in the blood allow a diagnosis to be made. Ultrasound and scintigraphy make it possible to distinguish thyrotoxicosis from other diseases manifested by thyrotoxicosis. Ultrasound reveals a diffuse enlargement of the thyroid gland, the tissue is hypoechoic, “hydrophilic”; Doppler mapping reveals increased vascularization - a picture of a “thyroid fire”. During radionuclide scanning, increased uptake of radioactive iodine by the entire thyroid gland is observed.

Treatment

Treatment Goals

Elimination of thyrotoxicosis and related disorders. Currently, three methods of treating DTG are used - medication, surgery and treatment with radioactive iodine.

Drug treatment

Drug treatment is indicated for newly diagnosed DTG. To block the synthesis of thyroid hormones, thyreostatics are used: thiamazole, propylthiouracil. Thiamazole is prescribed in a dose of up to 30-60 mg/day, propylthiouracil - up to 100-400 mg/day. After achieving a euthyroid state, the dose of the drug is reduced to a maintenance dose (5-10 mg/day), and to prevent the goitrogenic effect of the thyreostatic, sodium levothyroxine (25-50 mcg/day) is additionally prescribed. The combination of a thyrostatic agent with levothyroxine sodium works on the “block and replace” principle. Symptomatic treatment includes the prescription of sedatives and β-blockers (propranolol, atenolol). In case of adrenal insufficiency or endocrine ophthalmopathy, glucocorticoids (prednisolone 5-30 mg/day) must be prescribed. The course of treatment is continued for 1-1.5 years under the control of TSH levels. Persistent remission for several years after discontinuation of thyreostatics indicates recovery. With a small volume of the thyroid gland, the probability of a positive effect from conservative therapy is 50-70%.

Surgical treatment

Surgical treatment is indicated in the absence of a lasting effect from conservative therapy; large volume of the thyroid gland (more than 35-40 ml), when it is difficult to expect an effect from conservative therapy; complicated thyrotoxicosis and compression syndrome.

Preparation for surgery is based on the same principles as in the treatment of patients with thyrotoxicosis. In case of intolerance to thyreostatics, large doses of iodine are used, which have a thyreostatic effect. To do this, a short course of preparation is carried out with Lugol's solution. Over the course of 5 days, the dose of the drug is increased from 1.5 to 3.5 teaspoons per day with the obligatory intake of 100 mcg/day of sodium levothyroxine. In case of severe thyrotoxicosis, the course of preoperative preparation includes glucocorticoids and plasmapheresis.

Subtotal subfascial resection of the thyroid gland is performed according to O.V. Nikolaev, leaving a total of 4-7 g of thyroid parenchyma on both sides of the trachea. It is believed that maintaining this amount of tissue adequately supplies the body with thyroid hormones. In recent years, there has been a tendency to perform thyroidectomy for DTG, which eliminates the risk of relapse of thyrotoxicosis, but leads to severe hypothyroidism, as in treatment with radioactive iodine.

The prognosis after surgery is usually good. Postoperative hypothyroidism should hardly be considered a complication. Rather, this is a natural outcome of the operation, associated with excessive radicalism, justified by the prevention of relapse of thyrotoxicosis. In these cases, hormone replacement therapy is necessary. Relapse of thyrotoxicosis occurs in 0.5-3% of cases. If there is no effect from thyreostatic therapy, treatment with radioactive iodine or reoperation is prescribed.

Postoperative complications

The most serious complication after surgery performed for toxic goiter is thyrotoxic crisis. Mortality during a crisis is very high, reaching 50% or more. Currently, this complication is observed extremely rarely.

The main role in the mechanism of development of the crisis is assigned to acute adrenal insufficiency and the rapid increase in the level of free fractions of T 3 and T 4 in the blood. At the same time, patients are restless, body temperature reaches 40 ° C, the skin becomes moist, hot and hyperemic, severe tachycardia and atrial fibrillation occur. Subsequently, cardiovascular and multiple organ failure quickly develops, which becomes the cause of death.

Treatment is carried out in a specialized intensive care unit. It includes the administration of large doses of glucocorticoids, thyreostatics, Lugol's solution, β-blockers, detoxification and sedation therapy, correction of water and electrolyte disorders and cardiovascular failure.

To prevent thyrotoxic crisis, surgery is performed only after compensation of thyrotoxicosis.

Treatment with radioactive iodine

Treatment with radioactive iodine (131 I) is based on the ability of β-rays to cause the death of the follicular epithelium of the thyroid gland, followed by its replacement with connective tissue. This process is accompanied by suppression of the functional activity of the organ and relief of thyrotoxicosis. Currently, radioactive iodine therapy is recognized as the most rational way to treat diffuse toxic goiter in the absence of direct indications for surgery (presence of compression syndrome). Such treatment is especially indicated in case of high surgical risk (severe concomitant diseases, old age), when the patient categorically refuses surgery, and when the disease relapses after surgical treatment.

A.M. Shulutko, V.I. Semikov