Thyroiditis is an inflammatory lesion of the thyroid gland of acute, subacute, chronic, autoimmune nature. It is manifested by a feeling of pressure, painful sensations in the neck, difficulty swallowing, hoarseness of voice. With acute inflammation, the formation of an abscess is possible. The progression of the disease causes diffuse changes in the gland and a violation of its functions: at first the phenomenon of hyperthyroidism, and subsequently hypothyroidism, requiring appropriate treatment. Depending on the clinical features and course, acute, subacute and chronic thyroiditis are distinguished; according to etiology – autoimmune, syphilitic, tuberculosis, etc.
ICD 10
E06 Thyroiditis
Classification
In its practice, clinical endocrinology uses a classification based on the features of the mechanism of their development and clinical manifestation. There are the following forms of thyroiditis: acute, subacute and chronic. Acute form can spread to the whole lobe or the entire thyroid gland (diffuse) or occur with a partial lesion of the lobe of the gland (focal). In addition, inflammation in acute thyroiditis can be purulent or non-purulent.
Subacute thyroiditis occurs in three clinical forms: granulomatous, pneumocystic and lymphocytic form; the prevalence is focal and diffuse. The group of chronic thyroiditis is represented by Hashimoto’s autoimmune thyroiditis, Riedel’s fibroinvasive goiter and specific thyroiditis of tuberculous, syphilitic, and septic etiology. Purulent form of acute form and chronic fibroinvasive Ridel’s goiter are extremely rare.
Causes
The development of acute purulent thyroiditis occurs after acute or chronic infectious diseases – tonsillitis, pneumonia, sepsis, etc. as a result of hematogenic introduction of their pathogens into the thyroid tissue. Acute non-purulent form of thyroiditis can develop as a result of traumatic, radiation damage to the thyroid gland, as well as after hemorrhages in its tissues.
The basis of subacute (granulomatous) thyroiditis de Quervain is viral damage to thyroid cells by pathogens of various infections: adenoviruses, measles viruses, influenza, mumps. The disease develops 5-6 times more often in women, mainly between 20 and 50 years, clinically manifests itself a few weeks or months after the outcome of a viral infection. Outbreaks of de Quervain’s thyroiditis are associated with periods of the greatest viral activity. Subacute thyroiditis develops 10 times less often than autoimmune and is accompanied by reversible, transient thyroid dysfunction. Chronic nasopharyngeal infections and genetic hereditary factors predispose to the development of subacute thyroiditis.
With fibrous thyroiditis (Riedel’s goiter), there is a significant proliferation of connective tissue in the thyroid gland and compression of neck structures. The development of Riedel’s goiter is more common among women over 40-50 years old. The etiology of fibrous thyroiditis has not been definitively clarified: a certain role of infections in its development is assumed, some researchers tend to consider Riedel’s goiter as the outcome of autoimmune thyroid damage in Hashimoto’s thyroiditis. Patients who have undergone thyrotoxicosis, thyroid surgery, endemic goiter, genetic predisposition, as well as those suffering from autoimmune and allergic diseases, diabetes mellitus are prone to the development of fibrous thyroiditis.
Symptoms
Acute thyroiditis
In the purulent form of acute form, inflammatory infiltration of the thyroid gland is observed, followed by the formation of an abscess (abscess) in it. The purulent melting zone is turned off from secretory activity, but more often it captures a small part of the gland tissue and does not cause sharp disturbances of hormonal secretion.
Purulent thyroiditis develops acutely – with a high temperature (up to 40 ° C) and chills. There are sharp pains on the anterior surface of the neck with a shift to the back of the head, jaw, tongue, ears, which increase with coughing, swallowing and head movements. Intoxication is rapidly increasing: there is pronounced weakness, bruising, aching muscles and joints, headache, tachycardia is increasing. Often the patient’s condition is assessed as severe.
Local or diffuse enlargement of the thyroid gland, sharp soreness, dense (at the stage of infiltrative inflammation) or softened (at the stage of purulent melting and abscess formation) is determined by palpation consistency. There is hyperemia of the neck skin, local fever, enlargement and soreness of the cervical lymph nodes. The non-purulent form of acute thyroiditis is characterized by aseptic inflammation of the thyroid tissue and proceeds with less pronounced symptoms.
Subacute thyroiditis
The course of subacute form may have pronounced signs of inflammation: febrile body temperature (38 ° C and above), pain in the anterior surface of the neck with irradiation in the jaw, occiput, ear, weakness, increased intoxication. However, more often the development of the disease is gradual and begins with malaise, discomfort, moderate soreness and swelling in the thyroid gland, especially when swallowing, tilting and turning the head. The pain increases when chewing solid food. Palpation of the thyroid gland usually reveals an increase and soreness of one of its lobes. Neighboring lymph nodes are not enlarged.
Subacute thyroiditis in half of the patients is accompanied by the development of mild or moderate thyrotoxicosis. Patients’ complaints are associated with sweating, palpitations, tremor, weakness, insomnia, nervousness, intolerance to heat, joint pain.
An excessive amount of thyroid hormones secreted by the gland (thyroxine and triiodothyronine) has an inhibitory effect on the hypothalamus and reduces the production of the hormone regulator thyrotropin. In conditions of thyrotropin deficiency, there is a decrease in the function of the unchanged part of the thyroid gland and the development of hypothyroidism in the second phase of subacute thyroiditis. Hypothyroidism is usually not prolonged and pronounced, and with the attenuation of inflammation, the level of thyroid hormones returns to normal.
The duration of the stage of thyrotoxicosis (acute, initial) in subacute thyroiditis is from 4 to 8 weeks. During this period, there is pain in the thyroid gland and neck, a decrease in the accumulation of radioactive iodine by the gland, the phenomenon of thyrotoxicosis. In the acute stage, the reserves of thyroid hormones are depleted. As the intake of hormones into the blood decreases, the stage of euthyroidism develops, characterized by a normal level of thyroid hormones.
In cases of severe thyroiditis with a marked decrease in the number of functioning thyrocytes and depletion of the reserve of thyroid hormones, the stage of hypothyroidism with its clinical and biochemical manifestations may develop. The course of subacute thyroiditis is completed by the stage of recovery, during which the structure and secretory function of the thyroid gland are finally restored. The development of persistent hypothyroidism is rarely noted, in almost all patients who have undergone subacute thyroiditis, the function of the thyroid gland is normalized (euthyroidism).
Chronic fibrous thyroiditis
The course of chronic fibrous thyroiditis for a long time may not cause well-being disorders with a slow, gradual progression of structural changes in thyroid tissue. The earliest manifestation of fibrous thyroiditis is difficulty swallowing and a feeling of “lump in the throat”. In the advanced stage of the disease, respiratory disorders, swallowing, speech, hoarseness of voice, choking while eating develop.
Palpation determines a significant uneven increase in the thyroid gland (tuberosity), its compaction, inactivity when swallowing, dense “woody” consistency, painlessness. The lesion of the gland is usually diffuse in nature and is accompanied by a decrease in its functional activity with the development of hypothyroidism.
Compression of adjacent neck structures causes compression syndrome, manifested by headache, visual disturbances, tinnitus, difficulty in swallowing, pulsation of the cervical vessels, respiratory disorders.
Specific thyroiditis
Specific thyroiditis includes inflammatory and structural changes in thyroid tissue of the thyroid gland with its tuberculous, syphilitic, mycotic lesions. Specific thyroiditis has a chronic course; in cases of secondary infection, they become acute.
Complications
Purulent inflammation of the thyroid gland in acute thyroiditis, occurring with the formation of an abscess, is fraught with the opening of a purulent cavity into the surrounding tissues: mediastinum (with the development of mediastinitis), trachea (with the development of aspiration pneumonia, lung abscess). The spread of the purulent process on the neck tissue can cause the development of neck phlegmon, vascular damage, hematogenic spread of infection to the meningitis and brain tissue (encephalitis), the development of sepsis.
Neglect of subacute thyroiditis causes damage to a significant number of thyrocytes and the development of irreversible thyroid insufficiency.
Diagnostics
In all forms of thyroiditis, changes in the general blood test are characterized by signs of inflammation: neutrophilic leukocytosis, a shift of the leukocyte formula to the left, an increase in ESR. The acute form of thyroiditis is not accompanied by a change in the level of thyroid hormones in the blood. In the subacute course, at first there is an increase in the concentration of hormones (the stage of thyrotoxicosis), then their decrease occurs (euthyroidism, hypothyroidism). Ultrasound of the thyroid gland reveals its focal or diffuse enlargement, abscesses, nodes.
Scintigraphy of the thyroid gland clarifies the size and nature of the lesion. In the stage of hypothyroidism with subacute thyroiditis, there is a decrease in the absorption of iodine radioisotopes by the thyroid gland (less than 1%, at a rate of 15-20%); in the stage of euthyroidism with the restoration of thyrocyte function, the accumulation of radioactive iodine normalizes, and in the recovery stage due to an increase in the activity of regenerating follicles temporarily increases. Scintigraphy in fibrotic thyroiditis allows you to detect the size, fuzzy contours, altered shape of the thyroid gland.
Treatment
With mild forms of thyroiditis, you can limit yourself to the observation of an endocrinologist, the appointment of nonsteroidal anti-inflammatory drugs to relieve pain, symptomatic therapy. With pronounced diffuse inflammation, steroid hormones are used (prednisone with a gradual dose reduction).
In acute purulent thyroiditis, the patient is hospitalized in the surgery department. Active antibacterial therapy (penicillins, cephalosporins), vitamins B and C, antihistamines (mebhydroline, chloropyramine, clemastine, ciproheptadine), massive intravenous detoxification therapy (saline solutions, rheopolyglucine) are prescribed. When an abscess forms in the thyroid gland, it is surgically opened and drained.
Treatment of subacute and chronic thyroiditis is carried out by thyroid hormones. With the development of compression syndrome with signs of compression of neck structures, surgical intervention is resorted to. Specific thyroiditis is cured by the treatment of the underlying disease.
Prognosis and prevention
Early treatment of acute thyroiditis ends with a complete recovery of the patient in 1.5-2 months. Rarely, after suffering purulent thyroiditis, persistent hypothyroidism may develop. Active therapy of subacute thyroiditis makes it possible to achieve a cure in 2-3 months. Neglected subacute forms can last up to 2 years and take on a chronic character. Fibrous thyroiditis is characterized by long-term progression and development of hypothyroidism.
To prevent thyroiditis, the prevention of infectious and viral diseases plays a great role: hardening, vitamin therapy, healthy diet and lifestyle. It is necessary to carry out timely sanitation of chronic foci of infection: treatment of caries, otitis, tonsillitis, sinusitis, pneumonia, etc. The implementation of medical recommendations and prescriptions, prevention of self-reduction of the dose of hormones or their cancellation will avoid relapses of subacute thyroiditis.