Hypothyroid coma

Hypothyroid coma is an extremely severe manifestation of hypothyroidism, characterized by the most acute exacerbation of all symptoms of the disease and loss of consciousness.

The main reasons leading to the development of hypothyroid coma:

  • hypothermia;
  • infectious and inflammatory processes, in particular, pneumonia (it proceeds without fever, tachycardia, leukocytosis);
  • surgical interventions;
  • injuries;
  • treatment with sedatives, tranquilizers, neuroleptics, sleeping pills, especially when using these funds often and in large doses;
  • long-undiagnosed hypothyroidism and, therefore, prolonged absence of treatment;
  • unsystematic treatment, taking replacement agents in insufficient doses, especially in the cold season;
  • alcohol abuse, alcohol intoxication;
  • gastrointestinal and other bleeding;
  • hypoglycemia of any origin;
  • hypoxia of any origin.

The pathogenesis of hypothyroid coma is based on a severe, progressive violation of all types of metabolism, caused by prolonged thyroid insufficiency, which is manifested by a sharp inhibition of oxidative enzymatic processes in the brain tissue. Of great importance is also the toxic effect of carbon dioxide that accumulates in the body due to alveolar hypoventilation, as well as hypothermia, marked adrenal insufficiency, cardiovascular insufficiency. The following symptoms are characteristic of hypothyroid coma:

  • the gradual development of coma: progressive lethargy, drowsiness, gradually replaced by complete loss of consciousness;
  • the patient’s skin is dry, scaly, pale jaundice, cold, body temperature is significantly reduced (“hypothermic coma”);
  • face pasty, puffy, pale yellowish color, characteristic dense swelling of hands, legs, feet;
  • severe bradycardia, deafness of heart tones;
  • hypotension, the development of left ventricular failure;
  • rare breathing;
  • accumulation in serous cavities (abdominal, pleural, pericardial cavity) mucin-like substance, which is manifested by shortening percussion sound in the lateral abdomen, expanding the boundaries of the heart, the appearance of dull percussion sound above the lungs with the disappearance of vesicular respiration in this area; recognition of this syndrome contributes to ultrasound;
  • reduced muscle tone;
  • a sharp decline and even disappearance of tendon reflexes;
  • oligoanuria;
  • atony of smooth muscles, which is manifested by syndromes of acute urinary retention or rapidly developing dynamic and even mechanical (megacolon) intestinal obstruction.

Laboratory data:

  • anemia, increased ESR;
  • dramatically reduced blood levels of T3, T4;
  • a study of indicators of acid-base balance and blood gas composition reveals hypercapnia and pronounced acidosis, hypoxia;
  • hypoglycemia is possible;
  • reduced levels of cortisol in the blood;
  • significantly increased cholesterol and beta-lipoproteins in the blood.
local_offerevent_note November 18, 2019

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