Anesthesiology and resuscitation. Acute renal failure (lecture notes)

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Anesthesiology and resuscitation. Acute renal failure (lecture notes)

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Lecture number 7. Acute renal failure

Acute renal failure (ARF) is a complication of a number of renal and extrarenal diseases characterized by a sharp deterioration or cessation of kidney function and manifested by the following symptom complex: oligoanuria, azotemia, hyperhydration, impaired CBS and water and electrolyte balance.

The forms of OOP include:

1) prerenal (hemodynamic);

2) renal (parenchymal);

3) postrenal (obstructive);

4) arenal.

Etiology

Reasons for the development of prerenal acute renal failure.

1. Decreased cardiac output (cardiogenic shock, paroxysmal arrhythmia, cardiac tamponade, pulmonary embolism, congestive heart failure).

2. Reduced vascular tone (sepsis, infectious-toxic shock, anaphylactic shock, overdose of antihypertensive drugs).

3. Decreased effective intravascular volume (blood loss, plasma loss, dehydration - loss of 7-10% of body weight, profuse vomiting, diarrhea, polyuria, hypovolemia with nephropathy in pregnancy, nephrotic syndrome, peritonitis, liver cirrhosis).

4. Violation of intrarenal hemodynamics (taking NSAIDs, ACE inhibitors, radiopaque drugs, sandimmune).

5. Water poisoning - hyperhydration (uncontrolled production of ADH in malignant tumors, inflammatory diseases of the central nervous system, drug overdose - drugs, barbiturates, antidiabetic sulfanilamide drugs, indomethacin, amitriptyline, cyclophosphamide).

Reasons for the development of renal acute renal failure.

1. Kidney ischemia (shock, dehydration).

2. Nephrotoxic damage due to exposure to:

1) drugs (aminoglycosides, NSAIDs, radiopaque agents, sulfonamides, phenacetin, barbiturates, cephalosporins, ampicillin, rimfapicin, sandimmune);

2) industrial nephrotoxins (salts of heavy metals: mercury, chromium, cadmium, lead, arsenic, platinum, bismuth, gold, uranium, barium);

3) household nephrotoxins (ethylene glycol, methyl alcohol, dichloroethane, carbon tetrachloride).

3. Intratubular obstruction by pigments:

1) hemoglobin (hemolysis - incompatible blood transfusion, mushroom poisoning, acetic acid, hemolytic anemia, hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura);

2) urates (gout, immunosuppressive therapy for multiple myeloma and leukemia in severe physical exertion, in people not adapted to the heat);

3) myoglobin (traumatic rhabdomyolysis, non-traumatic rhabdomyolysis in coma, electrical injury, frostbite, eclampsia, alcoholic and heroin myopathy, severe hypokalemia and hypophosphatemia, carbon monoxide poisoning, salts of mercury, zinc, copper, drugs, viral myositis, overdose of statins and fibrates);

4) inflammatory processes: OTIN of medicinal and infectious genesis (AIDS, HFRS, measles, mononucleosis, leptospirosis, mycoplasmosis, rickettsiosis) acute pyelonephritis, acute glomerulonephritis;

5) necrotic papillitis (diabetes mellitus, analgesic, alcoholic nephropathy);

6) vascular pathology (vasculitis - polyarteritis nodosa, Wegener's granulomatosis, systemic scleroderma; thrombosis of arteries or veins, bilateral embolism of the renal arteries, traumatic injury).

Reasons for the development of postrenal acute renal failure.

1. Pathology of the ureters:

1) obstruction (stone, blood clots, necrotic papillitis);

2) compression (tumor of the pelvic organs, retroperitoneal fibrosis).

2. Pathology of the bladder (stones, tumors, inflammatory obstruction of the bladder neck, prostate adenoma, impaired innervation in spinal cord lesions and diabetic neuropathy).

3. Urethral stricture.

Classification

OPN classification according to E. M. Tareev.

1. Shock kidney.

2. Toxic kidney.

3. Acute infectious kidney.

4. Vascular obstruction.

5. Urological kidney.

Options for the course of acute renal failure: cyclic, recurrent and irreversible.

Clinic

There are five stages in the clinical course of acute renal failure.

Stage I of acute renal failure is initial, it lasts from the moment the etiological factor occurs until the first signs appear. At this stage, therapeutic tactics are aimed at eliminating or mitigating the impact of the etiological factor: anti-shock therapy, replenishing the BCC, combating heart failure, alkalizing therapy for intravascular hemolysis, combating pain, treating septic conditions, etc. Along with etiological therapy, spasm of kidney vessels is eliminated under the control of hourly diuresis. The earlier diuresis stimulation is started, the better the prognosis.

Stage II of acute renal failure, or oligoanuric, is characterized by dysfunction of 70% of nephrons. Urination less than 500 ml per day indicates the development of oliguria, and its decrease to 50 ml per day. and below indicates anuria. Along with a violation of the water-excreting ability of the kidneys, the concentration and nitrogen-excreting functions also suffer. In the urine, the amount of electrolytes and nitrogen sharply decreases. At this stage, the most pronounced changes in hemostasis occur.

Treatment should be aimed at maintaining a constant internal environment in order to give time and opportunity for the renal epithelium to regenerate. A state of hyperhydration develops due to the loss of electrolytes during vomiting and diarrhea. Therefore, it is necessary to stimulate diuresis, but only under the control of central venous pressure. Improves renal blood flow. Since it is necessary to strictly control diuresis, catheterization of the bladder is performed. Impaired nitrogen excretion function of the kidneys leads to azotemia, therefore, to maximally prevent the breakdown of proteins in the body, it is necessary to introduce a sufficient amount of carbohydrates (at least 5 g/kg per day.). Fructose and glucose are introduced, adding xylitol (sorbitol) to them in proportions of 2: 1: 1, and if there is no fructose, then 3 parts of glucose and 1 part of sorbitol. If the course is severe and cannot be treated, then hemodialysis sessions are performed. If the etiological factor is removed, then after 5-7 days of treatment, diuresis begins to increase. The maximum duration of this stage is up to 2 weeks.

III stage of acute renal failure - early polyuric. It is characterized by a progressive increase in diuresis (by 200-300 ml per day) up to 3 liters. The nitrogen excretion and concentration functions of the kidneys have not yet fully recovered, but the concentration of potassium, magnesium, and phosphates is gradually normalizing. Intensive therapy in the early polyuric stage should include the same measures as in the previous one, except for the stimulation of diuresis. Often, hemodialysis is required. There is a high risk of dehydration.

IV stage of acute renal failure - late polyuria. The daily increase in urine reaches 500-1000 ml, and diuresis can reach 8-10 liters per day or more. In the kidneys, ion exchange processes begin to recover. Losses of potassium, magnesium, phosphorus and other electrolytes sharply increase, patients are at risk of dehydration and demineralization. Therefore, electrolytes and fluid are given intravenously at this stage.

Stage V OPN, or recovery stage. The concentration function of the kidneys is restored. Diuresis begins to gradually decrease to normal (2-3 liters per day) and urine density increases (1008-1028).

To determine the severity of the disease and the effectiveness of treatment, patients with acute renal failure are examined daily in the blood for indicators of CBS, the concentration of electrolytes, hemoglobin, sugar, total protein and protein fractions, urea, residual and urea nitrogen, creatinine, hematocrit, and in daily urine - density, the amount of electrolytes and nitrogen.

Treatment

The principles of treatment are as follows.

1. Treatment of shock: anti-shock measures, glucocorticosteroids.

2. Replenishment of BCC: polyglucin, reopoliglyukin, plasma, albumin, erythrocyte mass.

3. Treatment of infections: adequate antibiotic therapy.

4. Dehydration: isotonic, hypertonic, hypotonic solution of sodium chloride, glucose.

5. Poisoning with poisons: antidotes are introduced.

6. Urological kidney: elimination of obstruction.

7. Intratubular obstruction: continuous up to 60 hours intensive infusion alkalizing therapy (mannitol 10% solution 3-5 ml / kg / h with isotonic sodium chloride solution, sodium bicarbonate, glucose 400-600 ml / h, furosemide 30-50 mg /kg).

8. Elimination of spasm of renal vessels: eufillin 2,4% - 10 ml again after 4-6 hours, chimes 0,5% - 2-4-6 ml intravenously, trental 3-5 mg / kg per day, pentamine 0,5-1,0 mg/kg per day, benzohexonium 0,3-0,5 mg/kg per day, droperidol 0,12 mg/kg per day, dopamine 1,5-3 mg/kg.

9. Stimulation of diuresis (after stabilization of blood pressure and elimination of hypovolemia): aminofillin, mannitol, lasix.

10. Control of hourly diuresis, blood pressure, CVP.

Indications for acute hemodialysis: hypercatabolic acute renal failure, lack of effect from conservative therapy in non-catabolic acute renal failure for 2-3 days, hyperkalemia more than 6-6,5 mmol/l, decompensated metabolic acidosis with a base deficiency of more than 15 mmol/l, blood creatinine more than 600 µmol /l, blood urea more than 30 mmol/l, hyperhydration with the development of pulmonary or cerebral edema.

Author: Kolesnikova M.A.

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