uremic coma

What is uremic coma?

Uremic coma (uremia) or urination develops as a result of endogenous (internal) intoxication of the body caused by severe acute or chronic kidney failure.

Causes of uremic coma

In most cases, uremic coma is the result of chronic forms of glomerulonephritis or pyelonephritis. In the body, toxic metabolic products are formed in excess, which sharply reduces the amount of daily urine excreted and coma develops.

Extrarenal reasons for the development of uremic coma include: drug poisoning (sulfanilamide series, salicylates, antibiotics), industrial poisoning (methyl alcohol, dichloroethane, ethylene glycol), shock, intractable diarrhea and vomiting, transfusion of incompatible blood.

In pathological conditions of the body, a violation occurs in the circulatory system of the kidneys, as a result of which oliguria develops (the amount of urine excreted is about 500 ml per day), and then anuria (the amount of urine is up to 100 ml per day). The concentration of urea, creatinine and uric acid gradually increases, which leads to the appearance of symptoms of uremia. Due to an imbalance in the acid-base balance, metabolic acidosis develops (a condition in which the body contains too many acidic foods).

Symptoms of uremic coma

The clinical picture of uremic coma develops gradually, slowly. It is characterized by a pronounced asthenic syndrome: apathy, increasing general weakness, increased fatigue, headache, drowsiness during the day and sleep disturbance at night.

Dyspeptic syndrome is manifested by loss of appetite, often to anorexia (refusal to eat). The patient has dryness and a taste of bitterness in the mouth, smells of ammonia from the mouth, increased thirst. Stomatitis, gastritis, enterocolitis often join.

Patients with growing uremic coma have a characteristic appearance – the face looks puffy, the skin is pale, dry to the touch, traces of scratching are visible due to unbearable itching. Sometimes powder-like deposits of uric acid crystals can be observed on the skin. Hematomas and hemorrhages, pastosity (pallor and decreased elasticity of the skin of the face against the background of slight edema), edema in the lumbar region and the region of the lower extremities are visible.

Hemorrhagic syndrome is manifested by uterine, nasal, gastrointestinal bleeding. On the part of the respiratory system, his disorder is observed, the patient is worried about paroxysmal shortness of breath. Blood pressure drops, especially diastolic.

The increase in intoxication leads to severe pathology of the central nervous system. The patient’s reaction decreases, he falls into a state of stupor, which ends in a coma. In this case, there may be periods of sudden psychomotor agitation, accompanied by delusions and hallucinations. With an increase in a coma, involuntary twitches of individual muscle groups are acceptable, the pupils narrow, and tendon reflexes increase.

The pathogenesis of uremic coma

The first important pathogenetic and diagnostic sign of the onset of uremic coma is azotemia. In this condition, residual nitrogen, urea and creatinine are always elevated, their indicators determine the severity of renal failure.

Azotemia causes such clinical manifestations as disorders of the digestive system, encephalopathy, pericarditis, anemia, skin symptoms.

The second most important pathogenetic sign is a shift in water and electrolyte balance. In the early stages, there is a violation of the ability of the kidneys to concentrate urine, which is manifested by polyuria. In the terminal stage of renal failure, oliguria develops, then anuria.

The progression of the disease leads to the fact that the kidneys lose the ability to retain sodium and this leads to salt depletion of the body – hyponatremia. Clinically, this is manifested by weakness, a decrease in blood pressure, skin turgor, increased heart rate, thickening of the blood.

In the early polyuric stages of the development of uremia, hypokalemia is observed, which is expressed by a decrease in muscle tone, shortness of breath, and often convulsions.

At the terminal stage, hyperkalemia develops, characterized by a decrease in blood pressure, heart rate, nausea, vomiting, pain in the oral cavity and abdomen. Hypocalcemia and hyperphosphatemia are the causes of paresthesia, seizures, vomiting, bone pain, and osteoporosis.

The third most important link in the development of uremia is a violation of the acid state of the blood and tissue fluid. At the same time, metabolic acidosis develops, accompanied by shortness of breath and hyperventilation.

Leave a Reply