2024 Author: Josephine Shorter | [email protected]. Last modified: 2023-12-16 21:43
Uremic coma
What is uremic coma?
Uremic coma (uremia) or uremic blood develops due to endogenous (internal) intoxication of the body caused by severe acute or chronic renal failure.
Causes of uremic coma
In most cases, uremic coma is a consequence of chronic forms of glomerulonephritis or pyelonephritis. In the body, toxic metabolic products are formed in excess, due to which the amount of excreted daily urine sharply decreases and coma develops.
The extrarenal causes of the development of uremic coma include: drug poisoning (sulfonamide series, salicylates, antibiotics), industrial poisoning (methyl alcohol, dichloroethane, ethylene glycol), shock conditions, indomitable 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 a violation of the acid-base balance, metabolic acidosis develops (a condition in which the body contains too many acidic foods).
Uremic coma symptoms
The clinical picture of uremic coma develops gradually, slowly. It is characterized by a pronounced asthenic syndrome: apathy, increasing general weakness, increased fatigue, headache, daytime sleepiness and sleep disturbance at night.
Dyspeptic syndrome is a loss of appetite, often before anorexia (refusal to eat). The patient has a dry and bitter taste in the mouth, there is a smell of ammonia from the mouth, thirst increases. Stomatitis, gastritis, enterocolitis often join.
Patients with an increasing 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 on the skin you can observe the deposition of crystals of uric acid, similar to powder. Hematomas and hemorrhages are visible, pastiness (pallor and decreased elasticity of the facial skin against a background of slight edema), edema in the lumbar region and the region of the lower extremities.
Hemorrhagic syndrome is manifested by uterine, nasal, gastrointestinal bleeding. On the part of the respiratory system, its 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 from the central nervous system. The patient's reaction decreases, he falls into a state of stupor, which ends in a coma. In this case, periods of sudden psychomotor agitation, accompanied by delusions and hallucinations, can be observed. With an increase in the coma, involuntary twitching of certain muscle groups is permissible, the pupils narrow, tendon reflexes increase.
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 clinical manifestations such as disorders of the digestive system, encephalopathy, pericarditis, anemia, and skin symptoms.
The second most important pathogenetic sign is a shift in the water-electrolyte balance. In the early stages, the kidney's ability to concentrate urine is impaired, which is manifested by polyuria. At the terminal stage of renal failure, oliguria develops, then anuria.
The progression of the disease leads to the fact that the kidneys lose their ability to retain sodium and this leads to salt depletion of the body - hyponatremia. Clinically, this is manifested by weakness, decreased blood pressure, skin turgor, increased heart rate, and 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 mouth and abdomen. Hypocalcemia and hyperphosphatemia are the causes of paresthesias, seizures, vomiting, bone pain, and the development of osteoporosis.
The third most important link in the development of uremia is a violation of the acid state of the blood and tissue fluid. In this case, metabolic acidosis develops, accompanied by shortness of breath and hyperventilation.
Article author: Mochalov Pavel Alexandrovich | d. m. n. therapist
Education: Moscow Medical Institute. IM Sechenov, specialty - "General Medicine" in 1991, in 1993 "Occupational Diseases", in 1996 "Therapy".
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