Coma Hypothyroid

Hypothyroid coma: causes, symptoms and treatment

Hypothyroid coma, also known as coma myxedema, is a serious complication of hypothyroidism, characterized by a decrease in the level of metabolism and metabolic activity in the body. This condition can lead to decreased consciousness, loss of consciousness, and even death if not detected and treated promptly.

Causes

Hypothyroid coma usually occurs in patients with long-term and irreversible hypothyroidism, which occurs as a result of dysfunction of the thyroid gland. Other causes, including disturbances in thyroid hormone levels, can also lead to the development of this condition.

Symptoms

Hypothyroid coma can manifest itself with the following symptoms:

1. Decreased body temperature
2. Lower blood pressure
3. Increased sensitivity to cold
4. Slowing down of thought processes and movements
5. Drowsiness and decreased level of consciousness
6. Swelling and dry skin
7. Slowing heart rate and breathing

Treatment

Treatment of hypothyroid coma is associated with the immediate restoration of the level of thyroid hormones in the body. Patients may be given levothyroxine injections and other measures to maintain vital body functions, such as maintaining breathing, monitoring blood pressure and body temperature.

In conclusion, hypothyroid coma is a serious complication of hypothyroidism that can lead to death if not detected and treated promptly. Patients suffering from hypothyroidism should closely monitor their symptoms and seek immediate medical attention if they notice signs of a hypothyroid coma.

HYPOTHYROID COMA - (syn. thyrotoxic coma; s. hypothyroeideum, coma hypothyrioidea) is an acute pathological condition characterized by a massive, sometimes critical, decrease in body weight, body temperature and metabolic processes in the body in the presence of “classic” symptoms of hyperthyroidism (heart rate above 120 beats per minute, exophthalmos, weight loss, etc.) against the background of a pronounced compensatory increase in the level of thyroid hormones in the blood serum (thyrotoxicosis).

In the treatment of hypothyroid coma, hypothyroidism is used primarily rather than thyrostatics, since increased levels of triiodothyronine in the blood can lead to the release of large amounts of free fatty acids saturated with iron into the blood, which aggravates the depression of brain function.

Complaints, anamnesis and the results of an objective examination suggest hypothyroid coitis, and clinical and biochemical criteria further emphasize this assumption, especially with daily monitoring of the concentration of thyroid hormones in the serum and repeated determination of thyroid-stimulating hormone (TSH) in the first hours of the disease. The presence of thyroid disease should also be noted when the patient is discharged from the hospital. It is also necessary to identify the compliance of his hormonal profile with the main criteria for thyrotoxicosis and the diagnostic formulation of the diagnosis of this condition. To answer this question, it is necessary to compare the data obtained using various methods of laboratory and instrumental (for example, ultrasound of the thyroid gland and its cervical lymph nodes) studies, including with the results of treatment (determination of the dynamics of the level of thyroid hormones and brain function, biochemical composition of blood, etc.). Lack of response and assessment of the morphological variant of the disease as specific to it can lead to incorrect formulation of the final clinical diagnosis.

Thus, if clinical signs of the disease confirm the diagnosis of hypothyroidism, careful