NEPHROLOGY

RENAL COLIC

Renal colic is a painful attack that develops when there is a sudden obstruction to the outflow of urine from the kidney. An attack most often occurs during urolithiasis - during the passage of urinary stones from the kidney through the ureter into the bladder. Less commonly, renal colic develops in other diseases (tuberculosis and tumors of the urinary system, injuries of the kidney, ureter, etc.).

Etiology: The most common cause of the development of renal colic is urolithiasis, hydronephrosis, nephroptosis, dyskinesia of the upper urinary tract. Less commonly, the cause of renal colic may be a tumor of the kidney or renal pelvis, a tumor of the ureter, tuberculosis of the upper urinary tract, obstruction of the ureter or pelvis by blood clots, or polycystic disease.

Pathogenesis: It is based on acute occlusion of the upper urinary tract with the development of intrapelvic hypertension and disorder of the hemodynamics of the kidney and urodynamics of the upper urinary tract. Subsequently, as hypoxia intensifies, urodynamic disorders develop in the form of hypokinesia and hypotension.

Clinical manifestations:

1. The presence of a provoking factor: running, jumping, riding a bicycle, motorcycle, walking, but sometimes an attack occurs at rest.

1. The attack usually begins suddenly. The intensity of the pain syndrome may vary. The pain is initially felt in the lumbar region from the side of the diseased kidney and spreads along the ureter towards the bladder and genitals. The patient is excited, rushes about, takes a forced position. An increased urge to urinate and cutting pain in the urethra may occur. Nausea, vomiting. Marked weakness.
2. Possible increased body temperature, chills, hyperhidrosis.
3. Blood tests: leukocytosis, accelerated ESR.
4. The duration of renal colic ranges from several minutes to several hours. Less commonly, an attack with short breaks can last for several days.

Differential diagnosis: acute surgical pathology of the abdominal organs (attack of cholelithiasis, acute cholecystopancreatitis, appendicitis, intestinal obstruction); inflammatory diseases of the pelvic organs; dissecting aortic aneurysm; intervertebral disc herniation; Exacerbation of chronic intestinal diseases, diverticulitis.

Help with renal colic:

1. Place the patient in a warm bath at a temperature of 37-39C 0 or a warm heating pad on the lumbar region.
2. Antispasmodics and painkillers: atropine 0.1% - 1.0 ml s.c. + analgin 50% - 2.0 ml i.m.; platifilin 0.2% - 1.0 ml subcutaneously + analgin 50% - 2.0 ml intramuscularly; no-spa 2.0 ml + analgin 50% - 2.0 ml IM; baralgin 5.0 ml IM. If there is no effect, Promedol 2% - 1.0 ml or Morphine 1% - 1.0 ml.
3. According to indications: vascular (cordiamin, caffeine, mezaton), anticonvulsants (Relanium 2-4 ml intravenously; aminazine 2.5% 1-4 i/m).
4. If renal colic persists for 4-6 hours, there is severe pain, or the temperature rises to febrile levels, consult a urologist.
5. Indications for emergency treatment and early consultation with a urologist: herniation of a stone, stone in a single kidney, urinary infection with fever, severe obstruction of the ureter, proximal location of a large stone in the ureter, severe symptoms with progressive deterioration of the patient's condition.

ACUTE RENAL FAILURE

Acute renal failure (ARF) – rapid, potentially reversible impairment of kidney function, developing over a period of one day to a week, leading to disruption of the excretion of nitrogen metabolism products from the body and disorders of water, electrolyte and acid-base balance. Half of hospital cases of acute renal failure are iatrogenic; most often they are caused by extensive surgical interventions.

Surge arrester classification:

1. Prerenal acute renal failure: associated with impaired cortical circulation, causing a drop in blood flow in the kidneys, a sharp decrease in glomerular filtration and oligo-anuria, renal function is preserved, but changes in blood flow in the renal arteries and a decrease in blood volume lead to a decrease in the volume of blood coming through the kidneys, and, consequently, to insufficient purification.

2. Renal acute renal failure: in 85% of cases it is caused by ischemic and toxic damage to the kidneys, which occurs with severe damage to the renal parenchyma and in 15% of cases by other causes (inflammation in the renal parenchyma and interstitium, vasculitis and thrombosis of the renal vessels).

3. Postrenal acute renal failure: occurs when there is a sudden cessation of urine flow from

renal pelvis for various reasons (stones, tumors, ligation

ureters during gynecological operations, retroperitoneal fibrosis).

4. Arenal: Develops in patients who have had their

one or both functioning kidneys.

Etiology:

Prerenal : decreased cardiac output (cardiogenic shock, cardiac tamponade, arrhythmias); systemic vasodilation; sequestration of fluid in tissues; dehydration of the body; liver diseases.

Renal: ischemia; exogenous intoxication (poisoning with salts of heavy metals, poisonous mushrooms, alcohol surrogates); hemolysis (transfusion complications, malaria); inflammatory kidney diseases; infectious diseases (septicemia, leptospirosis, meningococcal infection); positional compression syndrome (crash – syndrom); damage to the renal vessels; injury or removal of a single kidney.

Postrenal: extrarenal obstruction; intrarenal obstruction; urinary retention.

Classification of acute renal failure according to E.M. Tareev (1983).

1. Initial stage with a predominance of general phenomena characteristic of the underlying disease (burns, injuries, poisoning, infections). During this phase, which lasts several hours or days, urine output decreases markedly.

2. Oligo-anuric: clinical signs of kidney damage come first. Diuresis decreases to 500-600 ml. The level of urea, creatine, potassium, magnesium, sulfates, phosphates in the blood increases, and acidosis increases.

3. The stage of diuresis is divided into two periods:

A) Early period of diuresis: there is an increase in diuresis over 300 ml per

day, but the urea level continues to increase and the condition does not improve.

B) Late period of diuresis: the amount of urine increases to 1500 ml and

The level of azotemia gradually decreases. The end of this period

is the normalization of blood urea. Polyuria may develop because

destroyed tubules lose their ability to reabsorb. With inadequate

management of the patient, dehydration, hypokalemia, and often infections develop

4. Stage of restored diuresis (recovery). This stage may last

from 3-6 months to 2-3 years. Complete recovery is impossible with irreversible

damage to most nephrons. In this case, a decrease in glomerular

filtration and concentrating ability of the kidneys is preserved, which actually

indicates a transition to chronic renal failure.

Treatment:

Etiotropic treatment:

Prerenal acute renal failure: restoration of adequate blood supply to the kidney tissue - correction of dehydration, hypovolemia and acute vascular insufficiency. In case of blood loss, blood transfusions are performed, mainly plasma.

Renal acute renal failure: Treatment largely depends on the underlying disease. Glomerulonephritis or diffuse connective tissue diseases as a cause of acute renal failure often require the administration of glucocorticoids or cytostatics. Correction of hypertension, scleroderma crisis, and late gestosis is very important. Nephrotoxic medications should be stopped immediately. To treat uric acid tubular obstruction, intensive alkalizing infusion therapy and allopurinol are used.

Postrenal acute renal failure: In this condition, it is necessary to eliminate the obstruction as soon as possible.

Treatment of acute renal failure by stages:

Stages of initial oliguria (up to a day):

1. IM and IV pain relief: analgesics, baralgin, neuroleptanalgesia (droperidol, fentanyl, tramal, ketonol)

2. Restoration of bcc depending on the genesis of shock: crystalloids + glucose 5%; reopolyglucin, polyglucin, hemodez; plasma, albumin, blood transfusions.

3. For hemolysis, prednisolone 60 – 120 mg IV

4. For high blood pressure: clonidine IM, sublingually or sodium nitroprusside 3 mcg/kg/min for no more than 3 days or pentamin 5% 0.5 - 1.0 ml IM, s.c.

5. Normalization of cardiac output:

a) with normal blood pressure, dobutamine (Dobutrex) 10-20 mcg/kg/min;

b) with low blood pressure, dopamine 5-15 mcg/kg/min;

6. For septic shock - antibiotics, except aminoglycosides;

Stage of persistent oliguria (up to 3 days) - diuresis less than 500 ml/day:

1. Limit protein from food to 40 g/day.
2. Control of blood pressure and diuresis. Amount of fluid administered: diuresis + 400 ml. For diarrhea and vomiting – correction according to fluid loss.
3. Stimulation of diuresis: mannitol IV 50-100 ml of 2.5% solution or furosemide 60-100 mg IV (minimum single dose 0.5 mg/kg body weight, optimal single dose 1.0 mg/kg, maximum single dose dose 3.0 mg/kg body weight) 4-6 injections per day, maximum daily dose not more than 1000 mg, or dopamine IV 1-2 mcg/kg/min (if the effect is obtained, another 24-72 hours from dose reduction ).
4. Correction of acidosis: sodium bicarbonate intravenously. Calculation of sodium bicarbonate infusion is carried out according to the formula: number of ml of 4% sodium bicarbonate = 0.2 · BE · patient's body weight in kg (BE - base deficiency according to acid-base balance analysis).
5. Prevention of hyperkalemia: glucose - insulin mixture (glucose solution 40% - 100 ml + insulin 10 units + calcium gluconate solution 10% - 10-20 ml IV drip.
6. Prevention of infectious complications: III generation cephalosporins, macrolides + metronidazole. It is prohibited to prescribe nephrotoxic antibacterial drugs (aminoglycosides).
7. Daily monitoring of serum urea, creatinine, potassium levels, if necessary, 2 times a day.

If ineffective, the use of extrarenal cleansing methods is indicated

Extrarenal cleansing methods:

Hemodialysis is a method of correcting water-electrolyte and acid-base balance and removing various toxic substances from the body, based on dialysis and blood ultrafiltration.

Indications for emergency hemodialysis: hyperkalemia 6.5 mmol/l or more; urea level more than 35 mmol/l; severe acidosis (decrease in the level of standard bicarbonate to 8-10 mmol/l of plasma or base deficiency according to acid-base balance analysis of more than 14-16 mmol/l); deterioration of the clinical condition (threat of pulmonary edema, cerebral edema, nausea, vomiting, diarrhea, etc.).

Contraindications to hemodialysis: coronary thrombosis, severe vascular lesions of the central nervous system, acute stage of thromboembolic disease, inability to use heparin.

Peritoneal dialysis: intracorporeal dialysis, which involves injecting a dialysate solution into the abdominal cavity for several hours.

Course and prognosis:

Death in acute renal failure most often occurs from uremic coma, hemodynamic disorders and sepsis. Mortality in patients with oliguria is 50%, without oliguria - 26%. The prognosis is determined both by the severity of the underlying disease and the clinical situation. In uncomplicated acute renal failure, the probability of complete recovery of renal function over the next 6 weeks in patients who have survived one episode of acute renal failure is 90%.

LUPUS CRISES

Autoimmune lupus crises (LC) - these are acute or subacute conditions that develop over a short period of time (from several days to 1-2 weeks) against the background of the maximum degree of SLE activity, characterized by rapid progression of the lupus process with the development of multiple organ failure with the threat of death, requiring emergency intensive care.

General clinical and laboratory manifestations :

Fever (above 38˚C) with chills, asthenic syndrome, weight loss to 10-12 kg within 2-3 weeks, severe reaction of the reticuloendothelial system (lymphadenopathy, enlarged liver and spleen), damage to the skin and mucous membranes, polyserositis, increased ESR up to 60-70 mm/hour, hypergammaglobulinemia (more than 25%), LE cells (5:1000 or more), high titers of antibodies to n-DNA, ANF, Sm nuclear antigen.

Clinical options for VC:

Hematological crisis - a rapid (within 2-3 days) decrease in the level of blood cells, often with the development of hemorrhagic syndrome of varying severity. There are several types of hematological crises: hemolytic, thrombocytopenic, pancytopenic.

Classic lupus crisis - The development of a crisis in the acute and subacute course of the disease occurs at the onset of SLE in case of untimely administration of adequate therapy or during the first 2-3 years against the background of progression of lupus nephritis. In a chronic course, this version of the crisis develops at 5-7 years of illness and later. As a rule, the leading clinical diagnosis is rapidly progressive lupus nephritis with nephrotic syndrome.

Cerebral crisis – V The clinical picture of cerebral crisis is dominated by neurological symptoms with signs of severe damage to the central and peripheral nervous system.

Abdominal crisis - abdominal pain syndrome of a permanent nature, which increases over 1-2 days and does not differ in any specificity. Symptomatic therapy has no effect.

Treatment of the main variants of VK:

Therapy for hematological crisis

1. Suppressive therapy:

¨ classical pulse therapy with methylprednisolone 1000 mg/day for 3 consecutive days (until the crisis stops), if necessary, additional pulses;

¨ prednisolone orally at a dose of 60-80 mg/day for 6-10 weeks;

¨ intravenous immunoglobulin (sandoglobulin, normal human immunoglobulin), especially during thrombocytopenic crisis, according to the scheme: 500 mg/kg per day for 5 days, then 400 mg/kg once a month for 6-12 months;

¨ transfusion of blood cells (washed red blood cells, platelet concentrate), blood products (fresh frozen plasma);

¨ anticoagulants according to indications.

2. Maintenance therapy: after 6-10 weeks of taking the suppressive dose of prednisolone, begin a slow reduction over 6-8 months to a maintenance dose of 10-15 mg/day.

Therapy for classical lupus crisis

1. Suppressive therapy:

¨ synchronous intensive therapy (plasmapheresis 3-6 procedures with the introduction of 1000 mg of methylprednisolone after each procedure and 1000 mg of cyclophosphamide once). If ineffective, continue administration of methylprednisolone 250 mg/day for another 2-3 weeks;

¨ prednisolone orally at a dose of 60-80 mg/day for 6-12 weeks;

¨ blood products (albumin, fresh frozen plasma), plasma replacement agents;

¨ correction of cardiovascular disorders according to indications (diuretics, calcium antagonists, beta blockers, ACE inhibitors, cardiac glycosides).

2. Maintenance therapy:

¨ after 6-12 weeks of taking a suppressive dose of prednisolone, begin a slow reduction over 10-12 months to a maintenance dose of 10-15 mg/day;

¨ cyclophosphamide 1000 mg IV once a month for the first 6 months, then 1000 mg IV once every 3 months for 18-24 months or monthly synchronous intensive therapy (plasmapheresis + IV drip of 1000 mg methylprednisolone + 1000 mg cyclophosphamide 12 months);

¨ if there is no effect, intravenous immunoglobulin (sandoglobulin, normal human immunoglobulin) according to the scheme: 500 mg/kg per day for 5 days, then 400 mg/kg once a month for 6-12 months;

¨ long-term use of anticoagulants (phenyline, syncumar, warfarin) and antiplatelet agents (aspirin, trental, ticlopidine, chimes).

Therapy for cerebral crisis

1. Suppressive therapy:

¨ combination pulse therapy: classic 3-day pulse with methylprednisolone with the addition of 1000 mg of cyclophosphamide on the 2nd day or synchronous intensive therapy (plasmapheresis 3-6 procedures with the introduction of 1000 mg of methylprednisolone after each procedure and 1000 mg of cyclophosphamide once); in cases of development of convulsive syndrome and coma, intravenous administration of methylprednisolone up to a total dose of 10 g and up to 2 g of cyclophosphamide is allowed for 5-10 days;

¨ prednisolone orally at a dose of 50-60 mg/day for 6-12 weeks;

¨ heparin 20,000 units/day or fraxiparin 0.3-1.0 ml/day for 3-4 weeks;

¨ according to indications, lumbar puncture and diuretics;

¨ if there is no effect, intralumbar administration of GCS or methotrexate at a dose of 10 mg in combination with dexamethasone (20 mg) once a week for 2-7 weeks;

¨ according to indications, sedatives, anticonvulsants, metabolic drugs, antipsychotics.

2. Maintenance therapy:

¨ reducing the suppressive dose of prednisolone over 10-12 months to a maintenance dose of 5-10 mg/day;

¨ cyclophosphamide IV or IM 200 mg per week or monthly 1000 mg IV for 12 months, then 200 mg IV once a month or 1000 mg IV once every 3 months for 2- 5 years until lasting effect is obtained;

¨ long-term use of anticoagulants and antiplatelet agents;

¨ according to indications, metabolic agents, antihypoxants, antidepressants, sedatives, anticonvulsants.

Treatment of abdominal crisis

1. Suppressive therapy:

¨ combination pulse therapy: classic 3-day pulse with methylprednisolone with the addition of 1000 mg of cyclophosphamide on the 2nd day;

¨ prednisolone orally at a dose of 50-60 mg/day for 6-8 weeks;

¨ heparin 10,000-20,000 units/day or fraxiparin 0.3-1.0 ml/day for 3-4 weeks.

2. Maintenance therapy: reducing the suppressive dose of prednisolone over 8-10 months to a maintenance dose of 5-10 mg/day; cyclophosphamide IV 800 mg once a month – 6 months, then 400 mg IV once a month for 12-18 months; long-term use of anticoagulants (phenyline, syncumar, warfarin).

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Hematological data	Initial phase	Final phase
Peripheral blood
Reticulocytosis
Spherocytosis
Decreased erythrocyte resistance
Bone marrow
Normoblastosis
Erythroblastosis

Observations show that anemia reaches a particularly severe degree in the case when the hemolytic crisis is not accompanied by a response reticulocyte wave, and in the sternal punctate, instead of erythroblastosis, a picture of acute erythroblastopenia is found - the so-called aplastic (Gasser), or rather, aregenerative (A. G. Alekseev) crisis The difference between the aregenerative state and true bone marrow aplasia (erythroblastophthisis) is its fundamentally reversible nature.

“Decompensation” of the hemolytic process, expressed in the development of anemia, occurs due to increased breakdown of blood and the inhibitory effect of the spleen on the bone marrow (secondary hypersplenism). This assumption is supported by the fact that, in parallel with the development of anemia, the number of leukocytes and blood platelets decreases.

Histological examination of the spleen shows a sharp blood filling of the pulp, while the venous sinuses are poor in blood. The base of the pulp, the so-called Billroth cords, is literally stuffed with red blood cells, which are captured by splenic macrophages. As a result of increased hemolysis, a large amount of iron-containing pigment, hemosiderin, is released, which is deposited in the tissues (mainly in the same splenic pulp). At the same time, iron-free breakdown products of hemoglobin are formed; through the venous sinuses and splenic vein they enter the liver in the form of dynamic (i.e., associated with globulins) bilirubin, which gives an indirect van den Berg reaction.

Similar, although less pronounced manifestations of erythrophagocytosis and erythrolysis with the formation of hemosiderin and bilirubin are also found in Kupffer cells of the liver, bone marrow, and lymph nodes.

Table 26 a. Blood picture in the microspherocytic form of hemolytic disease. Microspherocytes predominate. Peripheral blood reticulocytes in huge numbers.

Pathogenesis. The main pathogenetic factor of congenital microspherocytic hemolytic disease is the increased breakdown of abnormal red blood cells, as a result of which the physiological balance between erythropoiesis and erythrolysis is disrupted. At present, there is no doubt that hemolysis in these cases is not intravascular, but intracellular - it occurs in the organs of the reticulo-histiocytic system, mainly in the spleen and to a lesser extent in the Kupffer cells of the liver, bone marrow and lymph nodes.

According to our observations (1949-1952), erythrocytes in the blood of the splenic vein (obtained during splenectomy) in patients with spherocytic hemolytic anemia have a higher osmotic resistance compared to erythrocytes of peripheral blood. This fact confirms the “screening” role of the splenic filter, which consists in the fact that in the spleen, osmotically unstable spherocytes prepared for hemolysis disintegrate.

Increased destruction of spherocytes in the spleen is due to the physical characteristics of the latter - their reduced osmotic and mechanical resistance. Thick, swollen red blood cells agglutinate and pass through the narrow mouths of the venous sinusoids with great difficulty. They are retained in the splenic pulp, where they are exposed to splenic hemolysin - lysolecithin and are captured by splenic macrophages. The latter is proven by experiments with blood perfusion through the extirpated spleen immediately after surgery - there were much more spherocytes in the splenic pulp than in the peripheral blood.

The inferiority of erythrocytes in congenital hemolytic disease is proven by data according to which the content of hydrophilic colloids, potassium salts and lipoid phosphorus (lecithin) is reduced in spherocytes. According to Young et al., the main genetic defect of erythrocytes in hereditary spherocytosis is a violation of the resynthesis of adenosine triphosphoric acid (ATP) and (or) other phosphorus compounds necessary to maintain the normal biconcave shape of erythrocytes. According to Dacie, the basis of congenital inferiority of erythrocytes is a poorly studied enzyme deficiency, leading to a disorder in the intracellular metabolism of carbohydrates and lipoids. It is possible that the reduced osmotic stability of erythrocytes, causing their premature spherulation with subsequent lysis, is associated with a greater degree of lipid loss by maturing erythrocytes.

As Japanese researchers (Nakao et al.) have shown, there is a close connection between the energy metabolism of erythrocytes and their shape, which is effected by ATP.

In the presence of 50% of the initial amount of ATP, red blood cells retain their disk shape; When ATP levels fall below 10% of normal, red blood cells lose potassium ions and become spherical.

There is an assumption that a decrease in the level of ATP occurs due to its accelerated breakdown due to increased activity of adenosine triphosphatase (ATPase), an enzyme that ensures the permeability of the erythrocyte membrane to potassium ions.

According to modern authors, the membrane of erythrocytes contains actomyosin-like proteins that have contractile function and ATPase activity. Based on this, it is suggested that impaired cation transport in hereditary spherocytosis is associated with a mutant protein, and the spherical shape of erythrocytes is the result of altered contractile properties of this protein.

Spherocytosis and reduced osmotic stability of red blood cells in hemolytic disease persist even after surgical removal of the spleen. This fact, noted by us (1949) and repeatedly confirmed by other authors, refutes the doctrine of hypersplenism as the primary cause of hemolysis.

The duration of stay of red blood cells in the circulating blood during hemolytic disease is sharply reduced. The average residence time of red blood cells in the bloodstream can be only 12-14 days (instead of the normal 120-125 days). Consequently, in order to maintain normal blood composition with such intensive breakdown, the bone marrow must renew the entire cellular composition of the blood in an extremely short time - within 2 weeks. In rare cases of hemolytic disease, increased erythropoietic function of the bone marrow so overcomes the breakdown of red blood cells that even polyglobulia develops. When the increased regeneration of blood elements in the bone marrow is not able to compensate for the massive destruction of red blood cells in the spleen, anemia develops.

So, the main role in the pathogenesis of familial hemolytic disease belongs to congenital inferiority, resp. reduced osmotic resistance of red blood cells, leading through the stage of spherocytosis to their accelerated destruction in the spleen. This position, in particular, is proven by the crossover experiments of Dacie and Mollison, which showed that red blood cells from a healthy donor transfused to a patient with spherocytosis retain a normal life expectancy (120 days). On the contrary, erythrocytes-spherocytes from patients with congenital hemolytic disease, including patients in clinical remission after splenectomy, transfused into a healthy recipient, quickly, within 14-20 days, undergo complete destruction. The same erythrocytes-spherocytes, transfused to a healthy person whose spleen was removed due to injury, are found in large quantities in the recipient’s blood 32 days later (Schrumpf). Thus, due to the new environmental conditions created in the body after splenectomy, the period of residence of low-resistant spherocytes in the bloodstream increases significantly, approaching their normal period of residence in the peripheral blood. Therefore, despite even some vicarious increase in the blood-destructive function of other organs of the reticulo-histiocytic system after splenectomy, the phenomena of hemolytic jaundice and anemia sharply decrease and practical recovery occurs.

Diagnosis. The diagnosis of congenital hemolytic disease sometimes presents certain difficulties. The most typical manifestations of hemolysis - yellowness of the sclera and integument - are not always clearly expressed and may not be noticed by the doctor, especially if the patient is examined under artificial light. To recognize jaundice in the evening, it is recommended to examine the patient under the light of a blue lamp. It is even better to use a fluorescent lamp when visiting patients.

The course of the disease is cyclical; it is characterized by alternating exacerbations (crises) and remissions.

Forecast. The prognosis for life is usually favorable. Cases of death from exacerbation of the hemolytic process during the period of regeneration crisis are relatively rare. Death in hemolytic disease can occur from cholangitis (due to calculous cholecystitis) or from intercurrent infections. Timely splenectomy sharply reduced mortality.

Treatment. The only effective therapeutic measure for the congenital form of hemolytic disease is splenectomy. In principle, one should agree with the position expressed by Cazal that every case of congenital hemolytic disease is indicated for surgical intervention (from the point of view of preventing possible complications). In practice, however, the benign course of the disease, as well as, although rare, deaths from operations limit the indications for surgery. Splenectomy is certainly indicated for severe anemia and frequent crises, for splenic infarctions and attacks of hepatic colic.

Splenectomy is urgently indicated in acute hemolytic crisis caused by intracellular (splenic) hemolysis; The more anemic the patient, the more urgent the operation. The latter must be carried out under the protection of a blood transfusion.

The effect of splenectomy is immediate, a few hours after removal of the spleen; already on the operating table, the number of red blood cells in the circulating blood increases by 1,000,000 or more, which is explained by the entry of blood deposited in the spleen into the general bloodstream. The resulting “autotransfusion” does not eliminate the need for additional blood transfusions after surgery.

Splenectomy leads to rapid disappearance of the symptoms of the disease - jaundice and anemia.

According to P. A. Herzen, “the results obtained with hemolytic jaundice can be called a triumph of splenectomy.”

After splenectomy, siderocytes appear in the blood, and this symptom becomes lifelong; other blood changes that occur after splenectomy: - hyperleukocytosis and especially hyperthrombocytosis - are temporary.

In patients with microspherocytic hemolytic anemia who have undergone splenectomy, as a rule, complete clinical recovery occurs (disappearance of jaundice and anemia), although red blood cells retain pathological qualities for life. In some patients, for a number of years after splenectomy, red blood cells turn out to be even less stable and more spherical than before the operation (our observations, Fig. 52, Table 27).

The fact that increased hemolysis in the body ceases after splenectomy is explained by the removal of an organ that plays a major role in the processes of blood breakdown.

Turning off the splenic filter (as a result of splenectomy) helps to preserve in the bloodstream the least stable forms of erythrocytes, spherocytes, which before the operation were retained in the spleen and, undergoing decay, “went into circulation.”

Sometimes relapses of the disease are observed, but to a lesser extent than before splenectomy, because the reticulo-histiocytic elements preserved in other organs are not able to compensate for the lost hemolytic function of the spleen. The pathogenesis of relapses is usually explained by vicarious hyperplasia of the surviving accessory spleens.

Blood (erythrocyte mass) transfusion for congenital hemolytic anemia should be considered indicated in the case of severe hemolytic crisis, when preparing the patient for surgery (when the patient is severely anemic) and in the postoperative period. Blood transfusions must be carried out taking into account Rh compatibility.

For persistently recurrent hepatic colic, splenectomy (not cholecystectomy!) is indicated, since due to the normalization of increased hemolysis, the formation of pigment stones stops and the symptoms of pseudocholelithiasis disappear. In case of indications for cholecystectomy, dictated by the complication of true cholelithiasis or cholecystitis, the operation of removing the gallbladder is combined with splenectomy.

After the operation, sanatorium-resort treatment with mineral waters (Zheleznovodsk) is indicated.

Hemolytic crisis is a disease that occurs from the destruction of a large number of red blood cells (hemolysis) in the blood. Their destruction occurs faster than the human body can produce the same new blood cells.

How does a hemolytic crisis occur?

An acute hemolytic crisis can be caused by a hereditary predisposition of red blood cells, as well as the occurrence of immune hemolytic anemia, when antibodies destroy red blood cell cells.

Also, a crisis can occur when transfusion of blood that is incompatible with the donor, or if the material is bacterially contaminated. Red blood cells can also be destroyed when a number of blood diseases occur.

Taking certain medications (quinidine, sulfonamides, etc.) can also cause a hemolytic crisis if the patient had hereditary hemolytic anemia. Also, people susceptible to the disease include those who are exposed to intense physical activity, go in for parachuting, paragliding and mountaineering. That is, those sports in which the human body experiences a sharp change in atmospheric pressure.

Hemolytic crisis: symptoms

Hemolytic crisis can be diagnosed by a combination of several characteristic symptoms:

• the person turns pale;
• he is shivering;
• body temperature rises sharply;
• cramping pain occurs in the abdomen and lower back;
• mucous membranes turn yellow.

Brain phenomena such as a sharp decrease in vision, dizziness, and even loss of consciousness also occur. The concentration of reticulocytes in the blood increases, bilirubin and free hemoglobin increase in the plasma.

Blood plasma may appear yellow or pink. The content of urea and free hemoglobin increases. Acute renal failure may develop, which can progress to complete anuria, and in some cases even to uremia.

Hemolytic crisis: emergency care

To provide first aid, it is necessary to warm the human body; for this you can use a heating pad. The use of drugs such as heparin, metipred or prednisone is very effective. They are administered intravenously.

It is necessary to carry out therapy using hormonal and antihistamine drugs. These include:

• gluconate;

The basis for a favorable outcome after a hemolytic crisis is how quickly the patient is transported to the nearest hematology hospital, where he can receive emergency care.

During the initial examination of the patient in the hospital, the diagnosis is clarified. In severe cases, a blood transfusion is performed, for which donor blood is selected, the red blood cells of which must be completely compatible with the patient’s blood.

To do this, use a washed erythrocyte suspension, which must be prepared 5-6 days before the procedure. If the patient is found to be poisoned by hemolytic poisons, then the most effective procedure is therapeutic plasmapheresis. It allows you to very quickly cleanse the blood of the agent that caused hemolysis, as well as immune complexes and antibodies. Transfusion therapy can be carried out only after a complete examination of the patient, so as not to cause increased hemolysis.

CRISES(French) crisis fracture, attack) is a term used to designate sudden changes in the body, which are characterized by a paroxysmal appearance or intensification of symptoms of the disease and are transient in nature. Systematization of Crises is extremely complex, because this term refers to phenomena that often differ in pathogenesis and wedge, manifestations. Thus, the terms “blast crisis”, “reticulocyte crisis” are used in hematology to designate acute changes in blood composition in leukemia, pernicious anemia; in ophthalmology the terms “glaucomatous crisis” and “glaucomocyclic crisis” are often used for glaucoma; in surgery - “rejection crisis” during organ or tissue transplantation; in neurology - “myasthenic. crisis" with myasthenia gravis, "tabetic crisis" with tabes dorsalis, "solar crisis" with solaritis; in gastroenterology - “stomach, intestinal crisis.” The listed K. refer to the natural manifestations of certain pathols, conditions or diseases. Along with them, there is another group of K., which act as a leading wedge, a sign of the disease. This group includes cerebral K., hypertensive K., thyrotoxic, addisonic, catecholamine, hypercalcemic, hemolytic, erythremic and some others.

Cerebral crises

Cerebral crises can be divided into primary and secondary. Primary cerebral K. develop with functional or organic damage to the brain, Ch. arr. due to a disorder of the centers regulating autonomic functions, including vascular tone, and the functions of a number of internal organs. Thus, in their essence they are more often cerebral vegetative K. However, the wedge, manifestations of primary cerebral K. can be a consequence of dysfunction of other parts of the brain. Depending on the location of the lesion or dysfunction of the brain, blood cells can be temporal, hypothalamic (diencephalic) or brain stem. Secondary cerebral K. (visceral-cerebral K.) are characterized by neurol, disorders caused by somatic diseases.

A special place is occupied by vascular cerebral K., which manifest themselves as unstable disorders of brain function as a result of transient cerebrovascular accident and can be either primary or secondary.

Depending on the volume and localization of vascular changes in the brain, generalized cerebral K. and regional (covering a separate vascular basin) are distinguished.

The pathogenesis of primary cerebral K. is complex. In their origin, disruption of the functions and state of the limbic-reticular system, as well as the endocrine glands, is of great importance. These disorders are manifested by cerebral autonomic crisis, mono- or polysymptomatic. In this case, the reflex mutual regulation between individual functions, which underlies the provision of all homeostatic and adaptive functions of a person, is lost (see Adaptation, Homeostasis).

When the process is localized in the upper parts of the brain stem, in the area of ​​the vestibular nuclei and nuclei of the vagus nerve, which are closely interconnected, there is a predominance of the parasympathetic direction of cerebral K. Similar K. can also occur with damage to the anterior parts of the hypothalamus. Damage to the posterior parts of the hypothalamic region, in which adrenergic structures are most represented, having a special connection with the adaptation apparatus, leads to the development of sympathetic-adrenal K.

Cerebral vascular K. is based on either the mechanism of cerebral vascular insufficiency, or microembolism, or angiodystonic phenomena with a change in the permeability of the vascular wall. Vascular cerebral K., which occurs by the mechanism of cerebrovascular insufficiency, is often caused by the influence of extracerebral factors (changes in blood pressure, a drop in cardiac activity, blood loss, etc.), which, in the presence of stenosis of one of the vessels supplying the brain, cause the development of cerebral ischemia due to a decrease in blood flow into the basin of this vessel. This mechanism occurs especially often in atherosclerosis.

The development of vascular blood vessels can also be facilitated by disturbances in the nervous regulation of cerebral circulation. In cerebral K., cerebral ischemia is usually shallow and short-lived, and therefore focal cerebral symptoms disappear after restoration of cerebral blood flow. Microembolisms that underlie some vascular cerebral K. in atherosclerosis, rheumatism, and vasculitis of various etiologies are cardiogenic (from cardiosclerosis, heart defects, myocardial infarction) and arteriogenic (from the aortic arch and main arteries of the head). The source of emboli are small pieces of parietal thrombi, cholesterol crystals and atheromatous masses from disintegrating atherosclerotic plaques, as well as platelet aggregates. Blockage of a small vessel by an embolus, accompanied by perifocal edema, leads to the appearance of focal symptoms that disappear after the disintegration or lysis of the embolus and reduction of edema or after the establishment of full collateral circulation. In some cases, transient cerebral symptoms that develop without pronounced fluctuations in blood pressure are caused by changes in physical-chemical. properties of blood: an increase in its viscosity, an increase in the number of formed elements, a decrease in oxygen content, hypoglycemia, etc. These factors, in conditions of a decrease in blood supply to the brain, can lead to a drop below the critical level in the amounts of oxygen and glucose delivered to the brain tissue, to a delay in the removal of metabolic end products , especially in the area of ​​the affected vessel, which leads to the appearance of focal symptoms. According to E. V. Schmidt (1963), cerebral vascular K. are often observed against the background of an atherosclerotic stenotic process in the extracranial parts of the vertebral and carotid arteries; sometimes K. arise in patients with patol, tortuosity and kinks of these vessels, as a result of which, in certain positions of the head, disruption of cerebral blood flow may occur. Osteochondrosis of the cervical spine in combination with atherosclerosis of the main arteries of the head often causes the occurrence of regional vascular K., caused by the fact that osteophytes in the area of ​​the uncovertebral joints, during forced turns of the head, compress the vertebral artery passing nearby.

The basis of the pathogenesis of cerebral K. in congenital heart defects are disorders of general hemodynamics, hron, hypoxemia caused by circulatory failure in the systemic circle, anomalies in the development of cerebral vessels. K. in patients with acquired heart defects are caused by a transient insufficiency of blood supply to the brain due to weakening of cardiac activity and fluctuations in blood pressure leading to brain hypoxia. In case of coronary heart disease, cerebral K. arise as a result of patol, afferent impulses, promoting the involvement of peripheral and central parts of the blood in the process. n. With. Various cerebral K., arising from cardiac arrhythmias, are caused by acute cerebral circulatory failure, causing cerebral hypoxia.

Cerebral vascular K. in diseases of the gastrointestinal tract. tract are caused by patol, impulses from the reflexogenic zones of the affected organ to the segmental spinal autonomic centers with the subsequent spread of irritation to the central autonomic formations (limbic-reticular system), which causes secondary cerebral angiodystonic disorders. In the pathogenesis of cerebral K. in liver failure, disturbances of various types of metabolism are important, with intoxication playing a leading role. The basis of the pathogenesis of cerebral K. in acute and chronic renal failure is metabolic disorders, the development of azotemia, acidosis.

Pathomorphol, changes are described only in cerebral vascular K. These data were obtained based on a study of the brain of patients who died during K., complicated by cerebral edema, acute left ventricular or renal failure, or (much less often) acute development of perforated ulcers of the stomach and intestines. Morfol, changes in the brain with vascular cerebral K. may consist in the impregnation of vascular walls with protein masses and blood, accompanied by their focal necrobiosis, sometimes with parietal thrombosis (see), in the development of miliary aneurysms (see), in small perivascular hemorrhages ( see) and plasmorrhagia (see), the appearance of foci of perivascular) melting (encephalolysis), sometimes in focal or diffuse edema (see), focal loss of nerve cells, proliferation of astrocytes (diffuse or focal). Each vascular K., no matter how mild it is, usually leaves behind changes.

Wedge, the picture of cerebral K. is polymorphic. Cerebral K., caused by neuroses (see), occur with a predominance of cardiovascular disorders. With organic damage to the temporal structures (mainly the right hemisphere), cerebral K. are characterized by complex psychopathols, phenomena that include olfactory and auditory hallucinations (see), states of depersonalization (see) and derealization (see). In this case, vegetative-visceral disorders are usually pronounced with a tendency towards a parasympathetic direction.

Hypothalamic K. are very diverse in wedge, manifestations (see Hypothalamic syndrome). Sometimes Hypothalamic K. occurs in the form of Gowers syndrome: attacks of pain in the epigastric region, lasting approx. 30 minutes, accompanied by pallor of the skin, irregular breathing rhythm, cold sweat, fear of death and sometimes ending in vomiting and polyuria. With lesions of the brain stem wedge, the picture of K. is varied, but more often, especially with caudal localization of the process, vagoinsular K. occurs.

Cerebral vascular K. in the domestic literature are usually called transient cerebrovascular accidents (TCI), in foreign literature - transient ischemic attacks. Transient include those cases of cerebral circulatory disorders in which the wedge, symptoms persist no longer than 24 hours.

Cerebral vascular K. in atherosclerosis (see) often occurs without cerebral symptoms or the latter are mildly expressed, as well as vegetative ones, but paleness of the face and increased sweating are often observed; Blood pressure in most cases is normal, less often low or moderately high. The most characteristic is the sudden development of transient focal brain symptoms. K.'s development is often provoked by physical and mental overstrain, emotional overload, painful attacks, overheating, neuroendocrine changes that occur during menopause, and sudden meteorolemia. changes.

If cerebral vascular K. is caused by discirculatory disorders in the internal carotid artery, which supplies most of the cerebral hemisphere, then focal symptoms often manifest themselves as paresthesia in the form of numbness, sometimes with a tingling sensation in the skin of the face or limbs on the opposite side; often paresthesias appear simultaneously in half of the upper lip, tongue, on the inner surface of the forearm, and hand. Paralysis or paresis of the muscles of the face and tongue on the opposite side may occur, as well as speech disorders in the form of motor or sensory aphasia (see), apractical disorders, loss of the opposite field of vision (see Hemianopsia), disturbance of the body diagram, etc. Transient crossed optics -pyramidal syndrome (reduced vision or complete blindness in one eye and paresis of the opposite limbs) is considered pathognomonic for stenosis or occlusion of the internal carotid artery in the neck (see Alternating syndromes). Transient visual impairment on the side of the insufficiently functioning carotid artery and paresthesia on the opposite half of the body in hypertension are described as Petzl crises.

Cerebral vascular K., caused by discirculation in the basin of the vertebral and basilar arteries, is characterized by stem symptoms: dizziness of a systemic nature, impaired coordination, swallowing, double vision, nystagmus, dysarthria, bilateral patol, reflexes. Various visual and optic-vestibular disorders, short-term memory loss, and orientation disturbances associated with discirculation in the posterior cerebral artery basin also often appear (see Cerebral circulation).

Wedge, manifestations of vascular cerebral K. in vasculitis, diabetes mellitus and blood diseases are similar to atherosclerotic cerebral K., therefore, one should take into account the features of the somatic disease in which K. occurs.

Wedge, the picture of cerebral vascular K. in hypertension or symptomatic arterial hypertension is characterized by a rapid and significant increase in blood pressure, pronounced cerebral and autonomic symptoms.

Cerebral vascular K. in hypotension develop against the background of low blood pressure and are characterized by pallor of the skin, weakening of the pulse, increased sweating, general weakness, dizziness, and a feeling of blurred vision (see Arterial hypotension).

Viscerocerebral K. often occur with various heart diseases, according to the wedge, their manifestations are polymorphic (see Cardiocerebral syndromes). Thus, with congenital heart defects, cephalgic K., syncope (see Fainting), epileptiform, cyanotic-dyspneic K. are possible. The appearance of attacks of loss of consciousness in patients with “blue” heart defects is a formidable symptom. Cephalgic and syncopal K. also occur in patients with acquired heart defects. In coronary heart disease, cardiocerebral K. are expressed in the appearance of transient focal cerebral symptoms, as well as a variety of vegetative symptoms. Wedge, manifestations of cerebral K. that occur with cardiac arrhythmias include loss of consciousness, cephalalgia, and dizziness. Thus, with Morgagni-Adams-Stokes syndrome, simple or convulsive types of fainting are noted; with paroxysmal tachycardia (see) and atrial fibrillation, fainting, pale face, dizziness and other transient symptoms may occur. A variety of cerebral K. (migraine- and meniere-like, fainting) occur with peptic ulcers of the stomach and duodenum, as well as with diseases of the liver and biliary tract. In patients with hron, pancreatic insufficiency, K. manifests itself in the form of cerebral vascular disorders, hypoglycemic conditions. Various cerebral K. can also be observed in acute and chronic renal failure.

The duration of cerebral vascular K. ranges from several minutes to days. The outcome in most cases is favorable, however, hypertensive cerebral K. can sometimes be followed by cerebral edema or severe left ventricular failure, pulmonary edema and result in death. The course and outcomes of cerebral K. with focal lesions of the brain are usually determined by the nature of the organic process against which K. arises. The course of viscerocerebral K. also depends mainly on the nature and severity of the disease of the internal organs that caused K. Viscerocerebral K. more often arise in period of exacerbation of somatic disease; regression of cerebral disorders also occurs as the function of internal organs improves.

Treatment

Therapy of primary cerebral K. is carried out taking into account the underlying disease, the topic of damage to the nervous system and the initial tone of the autonomic nervous system in the interictal period. If in primary cerebral K. sympathetic tone predominates, adrenolytic substances are used (aminazine, propazine, pyrroxan, ergo- and dihydroergotamine), antispasmodics, vasodilators and hypotensive drugs - reserpine, papaverine, dibazol, nicotinic acid, xanthinol nicotinate (complamin, xavin ), cinnarizine (stugeron). It is also recommended to administer lytic mixtures and, occasionally, ganglion-blocking agents. Increased tone of the parasympathetic department c. n. With. in case of primary cerebral K., it is necessary to prescribe centrally acting anticholinergic drugs internally: cyclodol a (Artane, Parkinsan), amizil a, etc. Calcium preparations are administered intravenously. If these K. are accompanied by allergic symptoms, antihistamines are used (diphenhydramine, pipolfen, suprastin, tavegil). With dysfunction of both departments c. n. With. agents that have adrenergic and anticholinergic effects are used: belloid, bellataminal, bellaspon. In case of severe K., it is necessary to administer cardiovascular drugs (cordiamin, camphor, adrenaline, mesaton).

When treating cerebral vascular K. of atherosclerotic origin, attention should be paid to maintaining blood pressure at a normal level, improving cardiac activity, and using vasodilators. For heart failure, 0.25-1 ml of 0.06% corglycone solution or 0.05% strophanthin solution in 10-20 ml of 20% glucose solution is administered intravenously, as well as cordiamin, camphor oil subcutaneously. In case of a sharp drop in blood pressure, 1% mezaton solution is prescribed subcutaneously (0.3-1 ml) or intravenously (0.1-0.3-0.5 ml 1% solution in 40 ml 5-20-40% solution -ra glucose), caffeine and ephedrine subcutaneously. To improve cerebral blood flow, intravenous or intramuscular administration of aminophylline is prescribed. In some cases, it is possible to use anticoagulants under the control of the blood coagulation system. There is data indicating the prospects of using antiplatelet agents for repeated cerebral vascular K. of atherosclerotic origin - drugs that prevent the formation of platelet aggregates, in particular acetylsalicylic acid, prodectin.

For hypotonic K., caffeine 0.1 g orally, ephedrine 0.025 g orally, mesaton 1 ml of 1% solution or cortin - 1 ml subcutaneously, and sedatives are prescribed.

Viscerocerebral K. require complex treatment, which is carried out depending on the nozol, the form of somatic disease, and also on the nature of the K.

Hypertensive crises

Hypertensive crises are observed in patients suffering from hypertension (see) or arterial hypertension (see Arterial hypertension).

The occurrence of hypertensive blood pressure is characterized by a cyclical nature. Factors contributing to their occurrence may be psycho-emotional stress, hormonal changes in women (menstrual cycle, menopause), meteorol. influences, etc.

The pathogenetic mechanisms of hypertensive K. are not fully disclosed; More often, arterial hypertension occurs in response to emotional stress, accompanied by the formation of foci of excitation in the structures of the c. n. With.

Hypothalamoreticular formations are most closely related to the occurrence of vascular hypertensive reactions. Under normal conditions, the pressor effect is opposed by powerful depressor baroreceptor and humoral influences (prostaglandins, kinins, etc.), acting on the principle of self-regulation.

Hypertensive K. is accompanied by changes in the pituitary-adrenal system, which is manifested by increased secretion of ACTH, vasopressin, glucocorticoids and aldosterone. During K., the content of catecholamines in the blood and their excretion in the urine increases. The effect of these pressor agents on the reactivity and tonic contraction of arterioles is realized to a large extent through their influence on the active transport of ions (an increase in the intracellular content of sodium and calcium).

Excitation of the hypothalamoreticular structures of the brain can lead to disturbances in intrarenal hemodynamics: a persistent decrease in blood flow in the renal cortex and a transient increase in blood flow in the medulla. As a result of ischemia of the renal cortex, the production of renin increases, and the increase in blood flow in the renal medulla promotes increased formation of renal prostaglandins and kinins, which counteract the hypertensive response. The ability of the kidneys to produce humoral substances with pressor and depressor effects depends on the degree and duration of disturbances in intrarenal hemodynamics. Increased production of renin leads to increased formation of angiotensin, which in turn stimulates the production of aldosterone.

The occurrence of hypertensive blood pressure, its severity and consequences are largely determined by the state of the mechanisms of autoregulation of cerebral blood flow. Experimental studies on rabbits have shown that when the reactivity of the subcortical centers changes, the usual adaptive depressor reflex from the baroreceptors of the carotid sinus weakens, changes to a pressor reflex and can cause the occurrence of hypertensive K.

Hypertensive blood pressure is accompanied by a rise in blood pressure. Usually there is a severe headache, often of a bursting nature, pain in the eyeballs - spontaneous and aggravated by eye movement, nausea, sometimes vomiting, noise and ringing in the ears, non-systemic dizziness. Patients experience feelings of anxiety and tension; sometimes there is psychomotor agitation or, on the contrary, drowsiness and stupor. Of the vegetative symptoms, the most common are a feeling of heat in the face, hyperemia or pallor, tachycardia, chills, paresthesia in the limbs and back, polyuria. In severe cases, meningeal symptoms may be observed. Lumbar puncture reveals increased cerebrospinal fluid pressure. Focal neurol symptoms also occur, often mildly expressed; sometimes focal or general epileptic seizures are observed; in the fundus - swelling of the discs (nipples) of the optic nerves, pinpoint hemorrhages.

According to the wedge, course and hemodynamic parameters, two types of hypertensive crises are distinguished. K. of the first type (hyperkinetic) develop rapidly, proceed relatively easily, and are accompanied by severe vegetative-vascular disorders (headache, agitation, tremors, tachycardia). At the moment of K., predominantly systolic and pulse pressure increases; minute blood volume, venous pressure and blood flow velocity increase significantly, but the total peripheral resistance to blood flow does not increase and may even decrease. K. usually ends after 1-3 hours, and sometimes there is profuse urination. Such K. occur Ch. arr. in patients with early stages of hypertension (I or II A).

Hypertensive K. of the second type are much more severe. In the clinic, the leading symptoms are brain symptoms: severe headache, dizziness, drowsiness, nausea and vomiting. Often these K. are accompanied by transient visual disturbances, other focal neurol, symptoms. With such K., not only systolic, but especially diastolic pressure increases. Minute blood volume and venous pressure often do not change, but the total peripheral resistance to blood flow increases significantly. This is the so-called eukinetic variant of hypertensive K. In the presence of coronary heart disease, K. of the second type can occur with reduced cardiac output, but a significantly increased general peripheral resistance to blood flow (hypokinetic variant). Crises of the second type usually occur in patients with stage II B and III hypertension, last 3-5 days, and can be complicated by acute coronary insufficiency, left ventricular failure, and focal cerebrovascular accidents. In some cases, during K. an increased amount of patol and elements in the urine sediment is detected.

There are also cardiac hypertensive K., in which in the wedge, the picture is dominated by a disturbance of cardiac activity. According to the wedge, the manifestations distinguish three variants of hypertensive cardiac K. 1) asthmatic, 2) anginal with myocardial infarction, 3) arrhythmic.

In the first option, a sharp increase in blood pressure is accompanied by acute left ventricular failure with attacks of cardiac asthma (see), and in severe cases with pulmonary edema (see). In the second option, against the background of a sharp increase in blood pressure, in addition to cardiac asthma, attacks of angina pectoris and the development of myocardial infarction are observed. The third variant of hypertensive cardiac K. is accompanied by a sudden sharp tachycardia, which may be caused by paroxysmal tachycardia or paroxysm of atrial fibrillation.

Treatment

To relieve hypertensive blood pressure, antihypertensive drugs are used.

In case of hypertensive blood pressure of the first type, the patient's condition allows the use of medications that lower blood pressure 1.5-2 hours after their administration. The drug of choice may be reserpine (rausedil). The drug is administered intramuscularly at a dose of 1.0-2.5 mg. If necessary, the drug is re-administered after 4-6 hours. The total dose per day should not exceed 5 mg. A combination of reserpine with furosemide at a dose of 80 mg orally or ethacrine at a dose of 100 mg orally is more effective. Intramuscular or intravenous administration of 0.5% dibazole solution in a dose of 6-12 ml is also indicated. Magnesium sulfate for the relief of hypertensive K. type 1 is administered intramuscularly or intravenously (slowly) in a dose of 10-20 ml of 25% solution.

Hypertensive K. of the second type require a rapid, within 10-15 minutes, reduction in blood pressure and elimination of hypervolemia and cerebral edema. For this purpose, clonidine (hemiton, catapressan, clonidine) is administered intravenously or intramuscularly at a dose of 0.15-0.30 mg. The effect occurs within 10-15 minutes. If necessary, a second injection is prescribed after 1-4 hours. Clonidine inhibits the release of norepinephrine in the medulla oblongata; its effect is in many ways similar to the effect of ganglion blockers. A rapid and strong decrease in vascular tone in the systemic and pulmonary circulation is achieved by administering ganglion blockers - benzohexonium and pentamine (under blood pressure control). Non thymine is slowly injected into a vein in a dose of 0.2-0.5-0.75 ml of 5% solution, diluted in 20 ml of isotonic sodium chloride solution. For intramuscular injection, use 0.3-0.5-1 ml of 5% pentamine solution. The hypotensive effect of pentamine administered intramuscularly can be enhanced by droperidol (1-3 ml of 0.25% solution intramuscularly). Ganglion blockers are especially indicated during the development of left ventricular heart failure during K. Arfonad (trimetaphan, camsilate) is a ganglion blocker that is used to urgently lower blood pressure in case of intractable arterial hypertension and cerebral edema. The drug is administered intravenously (500 mg of arfonade per 500 ml of 5% glucose solution), starting from 30-50 drops per minute and gradually increasing to 120 drops per minute until the desired effect is obtained.

Diuretics (furosemide, dichlothiazide, hypothiazide) can be of great help in eliminating hypervolemia and cerebral edema. They are prescribed parenterally in combination with the above drugs.

Catecholamine crises

Catecholamine crises are typical for pheochromocytoma (see). They are characterized by a sudden significant rise in blood pressure and a variety of autonomic and metabolic disorders. They are based on hyperproduction of catecholamines (see), in particular adrenaline and norepinephrine. Arterial hypertension is caused not only by the vasoconstrictor effect of catecholamines, but is also associated with activation of the renin-angiotensin-aldosterone system.

Catecholamine K. in pheochromocytoma can be provoked by physical. overstrain, neuro-emotional impact, pressure on the tumor, but often the immediate cause remains unclear. The crisis is developing rapidly. The patient is pale, covered in sweat, very excited, trembling, and experiencing a feeling of fear. He complains of severe headache and dizziness, chest pain. Systolic pressure increases sharply (up to 250-300 mm Hg), diastolic pressure can remain at the same level or also increase (up to 150-170 mm Hg). There is tachycardia and cardiac arrhythmia in the form of extrasystole or atrial fibrillation. Leukocytosis with eosinophilia in the peripheral blood, low glycemia and glycosuria are characteristic. A huge amount of catecholamines is determined in the urine, much greater than with hypertensive K. Catecholamine K. lasts from several minutes to several hours and ends suddenly. Sometimes during the period of exit from K. there is a sharp drop in blood pressure, up to collapse.

Treatment

Treatment of catecholamine K. involves the use of adrepolit and ches to their agents, which block the action of catecholamines at the effector level and thereby reduce blood pressure. The most commonly used drugs are phentolamine (Regitine) and tropafene. Phentolamine is administered intramuscularly in 1 ml of 0.5% solution. Tropafen is prescribed intravenously 1 ml of 2% solution.

Thyrotoxic crises

Thyrotoxic crises are a severe complication of thyrotoxicosis (see). A crisis can be triggered by any significant external irritant (stressor), infection, physical. or mental trauma, overheating, strumectomy with insufficient preoperative preparation (so-called postoperative K.). In some cases, the immediate cause of K. remains unclear. The pathogenesis of thyrotoxic K. is caused by the entry into the blood of large quantities of thyroid hormones, leading to sudden changes in the function of the liver, adrenal glands, and heart.

Thyrotoxic K. is characterized by an acute onset and lightning-fast course. Clinically, thyrotoxic K. is manifested by severe mental agitation, often with delirium and hallucinations, sharp tremor of the limbs, sharp tachycardia (up to 150-200 pulses per minute), sometimes with paroxysms of atrial fibrillation, severe sweating, uncontrollable vomiting, diarrhea; fever develops. A large amount of acetone is detected in the urine. Characterized by a decrease in the function of the adrenal cortex, up to acute adrenal insufficiency. Sometimes jaundice appears, which can be combined with acute fatty degeneration of the liver. K.'s duration varies from 2 to 4 days. In severe cases, a coma develops (see Coma) with a fatal outcome. The cause of death may be heart failure, acute fatty liver, or insufficiency of the adrenal cortex.

Treatment

Treatment of thyrotoxic K. consists of eliminating dehydration and intoxication and combating the phenomena of acute insufficiency of the adrenal cortex. 2-3 liters of isotonic sodium chloride solution with 5% glucose solution, 150-300 mg of hydrocortisone or equivalent doses of prednisolone are administered intravenously per day. Sedatives, reserpine, and cardiac glycosides are prescribed. In order to suppress the secretion of thyroid hormones, it is recommended to prescribe thyreostatics (Mercazolil); Sometimes intravenous administration of 1% Lugol's solution, prepared with sodium iodide instead of potassium, is carried out in the amount of 100-250 drops in 1 liter of 5% glucose solution. In K.'s therapy, anaprilin (Inderal) can be used at a dose of 0.04-0.06 g per day. In extremely severe forms, local hypothermia is used.

Hypercalcemic crises

Hypercalcemic crises are most often a complication of primary hyperparathyroidism (see), caused by adenoma or hyperplasia of the parathyroid glands. The main pathogenetic factor is hypercalcemia (see). The development of calcium is associated with calcium intoxication when its concentration in the blood exceeds a critical level (14-17 mg%).

Hypercalcemic K. develops suddenly as a result of the action of some provoking factor: rough palpation of the parathyroid gland area, the prescription of a calcium-rich dairy diet or antacid drugs to a patient with hyperparathyroidism. The initial symptom of K. is often abdominal pain localized in the epigastrium. Nausea appears or intensifies, eventually turning into uncontrollable vomiting, accompanied by thirst, and the temperature rises. Severe joint pain, myalgia, muscle weakness, and cramps are noted. The ECG shows sinus tachycardia and shortening of the Q-T interval. Lethargy, confusion, and then coma (against the background of vascular collapse and azotemia) quickly develop. Coma usually occurs with hypercalcemia reaching 20 mg%. K. may result in the death of the patient.

Sometimes hypercalcemic K. is accompanied by acute metastatic pulmonary calcification, acute renal failure, and acute pancreatitis.

Treatment

In case of hypercalcemic K., it is important to create forced diuresis using furosemide, prescribed at a dose of 100 mg/hour with isotonic sodium chloride solution intravenously, and the use of hemodialysis with calcium-free dialysate. Urgent surgery to remove parathyroid adenoma or hyperplastic parathyroid glands is the treatment of choice in cases of primary hyperparathyroidism causing hypercalcemic K.

Hypocalcemic crises

Hypocalcemic crises are a condition opposite to hypercalcemic K., i.e., acute tetany develops (see).

Most often, hypocalcemic K. occurs as a complication of operations on the thyroid gland. Other causes may include idiopathic hypoparathyroidism with insensitivity to parathyroid hormone; damage to the parathyroid glands by a metastatic or infiltrative tumor process: a sharp deficiency in the body of vitamin D or magnesium ions; hypocalcemia with the administration of large doses of calcitonin, glucagon, mithromycin, phosphorus salts, and long-term use of phenobarbital. The main pathogenetic mechanism of hypocalcemic K. is a severe calcium deficiency in the body. K. develops when total calcium decreases to 7.5 mg% and below, and ionized calcium to 4.3 mg% and below.

K. is characterized by muscle spasms, convulsions, difficulty breathing, and on the ECG the Q-T interval is lengthened. During severe K., asphyxia may occur due to spasm of the muscles of the larynx.

Treatment

For hypocalcemic K., intravenous administration of 10-20 ml of 10% gluconate or calcium chloride is indicated.

Addisonian crises

Addisonian crises develop in patients with chronic, adrenal insufficiency (see Addison's disease) with inadequate treatment, the addition of intercurrent infections and intoxications, as well as as a result of surgery for concomitant diseases. The mechanism of occurrence of K. in Addison's disease is due to a rapid and sharp increase in the deficiency of mineralo- and glucocorticoids.

K. develops, as a rule, acutely within several hours. The onset of K. is manifested by a rapid increase in the symptoms of Addison's disease. The general condition sharply worsens, general weakness increases, appetite sharply decreases, nausea appears, then uncontrollable vomiting and diarrhea. Adynamia intensifies, dehydration increases. In the blood, the concentration of sodium and chlorides sharply decreases and the level of potassium increases, the content of residual nitrogen increases, severe hypoglycemia is often observed, leukocytosis increases and ROE accelerates. The daily release of 17-corticosteroids, 17-hydroxycorticosteroids, and aldosterone is reduced. If untimely and irrational treatment is used, coma may develop with a fatal outcome.

Treatment

Treatment of Addisonian K. consists of hormone replacement therapy, combating dehydration and electrolyte imbalance. 2-3 liters of 5% glucose solution prepared in isotonic sodium chloride solution are administered intravenously per day along with hydrocortisone in a dose of 200-500 mg or prednisolone in an amount of 50-150 mg. In combination with the above treatment, an oil solution of deoxycorticosterone is administered at a dose of 20-40 mg per day intramuscularly at intervals of 6 hours. In case of indomitable vomiting, 10% sodium chloride solution is administered intravenously in an amount of 10-20 ml. If necessary, mezaton and norepinephrine hydrotartrate are prescribed.

Hemolytic crises

Hemolytic crises are characterized by the sudden and rapid development of hemolytic anemia (see). K. may be a consequence of autoimmune processes in the patient’s body; may occur as a result of poisoning with hemolytic poisons or transfusion of incompatible blood (by Rh factor or group); can be triggered by various indifferent factors in individuals with enzymopathy (deficiency of glucose-6-phosphate dehydrogenase in erythrocytes). Hemolytic K. is characterized by acute chills and fever, severe headache, olive-yellow coloration of the skin, and severe shortness of breath. Sometimes abdominal pain occurs, reminiscent of an acute abdomen. Uncontrollable vomiting develops with huge masses of bile, often liquid feces. Urine is the color of black beer or a strong solution of potassium permanganate. In severe cases, K. may be complicated by acute renal failure.

Hemolysis develops rapidly, jaundice begins 2-3 hours after the onset of the disease and reaches a maximum after 15-20 hours. During the first 24 hours, severe normochromic anemia appears. If the course is favorable, hemolysis ends within 2-4 weeks. significant improvement or complete recovery occurs. In severe cases, death from anemic coma or uremia is possible (see).

Treatment

For autoimmune hemolytic K., the treatment of choice is glucocorticoid hormones, prescribed in large doses (prednisolone 50-100 mg per day orally). In case of acute toxic hemolytic K., with enzymopathies and paroxysmal hemoglobinuria, repeated blood transfusions of 250-500 ml are indicated, for a total of up to 1 - 2 liters per day (in the absence of signs of renal failure); intravenous administration of fluids (40% glucose solution; polyglucin) up to 400-500 ml per day; prescribing medium doses of glucocorticoids (25-40 mg prednisolone per day). An effective method of combating acute uremia is hemodialysis (see). In acute hemolytic K. caused by intracellular hemolysis (in patients with Minkowski-Choffard disease), splenectomy is indicated under the protection of a blood transfusion.

Erythremic crises

Erythremic crises occur with polycythemia (see) against the background of a sharp increase in the number of red blood cells. They are characterized by severe weakness, drowsiness, headache, vomiting, dizziness, tinnitus (wedge, the picture may resemble Meniere's syndrome). Patients feel a rush to the head, a feeling of heat. Erythremic K. essentially belong to cerebral K. They are based on a violation of cerebral hemodynamics due to erythremia, a sharp thickening of the blood.

Treatment

With erythremic K., repeated bloodletting, the use of leeches, the administration of anticoagulants, as well as symptomatic drugs are indicated.

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D.K. Lunev, E. A. Nemchinov, M. L. Fedorova.

Acute hemolysis is a severe pathological condition characterized by massive destruction of red blood cells, the rapid occurrence of normochromic hyperregenerative anemia, jaundice syndromes, hypercoagulation, resulting in severe hypoxic, intoxication syndromes, thrombosis, acute renal failure, which pose a threat to the patient’s life.

Treatment of hemolytic crisis in enzymatic erythropathy
(symptomatic taking into account etiopathogenesis):

Prednisolone - 2-3 mg/kg/day - first intravenously, then orally until the reticulocyte count normalizes

Transfusion of washed red blood cells with a hemoglobin content below 4.0 mmol/l (6.5 g/%), (transfusion of red blood cells without selecting an individual donor is dangerous)

Prevention of hypothermia in the presence of cold autoAT

Splenectomy in chronic cases (if corticosteroid therapy is ineffective for 6 months)

Principles of emergency treatment

1. Elimination of the action of the etiological factor

2. Detoxification, disaggregation, anti-shock measures, fight against acute renal failure

3. Suppression of antibody formation (during immune genesis).

4. Replacement blood transfusion therapy.

5. Gravity surgery methods

First aid

Rest, warming the patient, hot sweet drink

For cardiovascular failure - dopamine, adrenaline, oxygen inhalation

For severe pain, IV analgesics.

In case of autoimmune HA, transfusions of blood incompatible with blood group and Rh factor, it is advisable to administer drugs

In case of immune genesis of hemolysis (including post-transfusion) - prednisolone 90-200 mg IV bolus

Qualified
and specialized medical care

Detoxification therapy: rheopolyglucin, 5% glucose, saline solution including solutions of acesol, disol, trisol up to 1 l/day intravenously in a heated drip (up to 35°); sodium bicarbonate 4% 150 - 200.0 ml intravenous drip; enterodesis orally 5 g in 100 ml boiled water 3 times a day

Maintain diuresis of at least 100 ml/h with intravenous fluid administration and diuretics

Excretion of free hemoglobin can be increased by alkalinizing the urine. To do this, sodium bicarbonate is added to IV fluids, which increases urine pH to > 7.5

Correction of microcirculation and hemorheology disorders: heparin 10-20 thousand units/day, rheopolyglucin 200-400.0 ml IV drip, Trental 5 ml IV drip in 5% glucose, chimes 2 ml IM

Antihypoxants - sodium hydroxybutyrate 20% 10 -20 ml intravenous drip

Antioxidants (especially during a crisis of paroxysmal nocturnal hemoglobinuria, hemolytic disease of newborns) - tocopherol acetate 5, 10, 30% solution in oil, 1 ml IM (warm to body temperature), aevit 1.0 ml IM or orally 0 .2 ml 2-3 times a day

Prevention and treatment of hemosiderosis - desferal IM or IV drip 500-1000 mg/day

Administration of heparin for the prevention of hemolytic-uremic syndrome in hemolytic anemia caused by neuraminidase, as well as transfusion of washed red blood cells (free from anti-T-Ag)

In severe condition, a decrease in hemoglobin less than 80 g/l and Er less than 3X1012 g/l - transfusions of washed (1, 3, 5, 7 times) red blood cells or red blood mass with selection using the Coombs test

For acute immune hemolysis - prednisolone 120-60-30 mg/day - according to a decreasing regimen

Cytostatics - azathioprine (125 mg/day) or cyclophosphamide (100 mg/day) in combination with prednisone when other therapy does not help. Sometimes - vincristine or the androgenic drug danazol

Immunoglobulin G 0.5-1.0 g/kg/day IV for 5 days

Plasmapheresis, hemosorption (removal of immune complexes, microclots, toxins, pathological metabolites)

Splenectomy for microspherocytosis, chronic autoimmune GA, a number of enzymopathies

Treatment of DIC syndrome, acute renal failure in full