Blood transfusion, when carefully followed, is a safe method of therapy. Violation of transfusion rules, underestimation of contraindications, and errors in transfusion technique can lead to post-transfusion complications.
The nature and severity of complications vary. They may not be accompanied by serious dysfunctions of organs and systems and may not pose a threat to life. These include pyrogenic and mild allergic reactions. They develop soon after transfusion and are expressed in increased body temperature, general malaise, and weakness. Chills, headache, itching of the skin, swelling of certain parts of the body (Quincke's edema) may appear.
Per share pyrogenic reactions accounts for half of all complications, they are mild, moderate and severe. With a mild degree, body temperature rises within 1 ° C, headache and muscle pain occur. Reactions of moderate severity are accompanied by chills, an increase in body temperature by 1.5-2 °C, increased heart rate and breathing. In severe reactions, stunning chills are observed, body temperature rises by more than 2 ° C (40 ° C and above), severe headache, muscle and bone pain, shortness of breath, cyanosis of the lips, and tachycardia are noted.
The cause of pyrogenic reactions are the breakdown products of plasma proteins and leukocytes of donor blood, and waste products of microbes.
If pyrogenic reactions occur, the patient should be warmed up, covered with blankets and heating pads applied to his legs, given hot tea, and given NSAIDs. For reactions of mild to moderate severity, this is sufficient. In case of severe reactions, the patient is additionally prescribed NSAIDs by injection, 5-10 ml of a 10% calcium chloride solution is injected intravenously, and a dextrose solution is infused drip-wise. To prevent pyrogenic reactions in severely anemic patients, washed and thawed red blood cells should be transfused.
Allergic reactions- a consequence of sensitization of the recipient’s body to Ig; more often they occur with repeated transfusions. Clinical manifestations of an allergic reaction: fever, chills, general malaise, urticaria, shortness of breath, suffocation, nausea, vomiting. For treatment, antihistamines and desensitizing agents are used (diphenhydramine, chloropyramine, calcium chloride, glucocorticoids), and for symptoms of vascular insufficiency - vascular tonics.
When transfusion of antigenically incompatible blood, mainly according to the ABO and Rh-factor system, develops blood transfusion shock. Its pathogenesis is based on rapidly occurring intravascular hemolysis of transfused blood. The main causes of blood incompatibility are errors in the actions of the doctor, violation of the rules of transfusion.
Depending on the level of decrease in SBP, three degrees of shock are distinguished: I degree - up to 90 mm Hg; II degree - up to 80-70 mm Hg; III degree - below 70 mm Hg.
During blood transfusion shock, periods are distinguished: 1) blood transfusion shock itself; 2) a period of oliguria and anuria, which is characterized by a decrease in diuresis and the development of uremia; the duration of this period is 1.5-2 weeks; 3) period of restoration of diuresis - characterized by polyuria and a decrease in azotemia; its duration is 2-3 weeks; 4) recovery period; lasts for 1-3 months (depending on the severity of renal failure).
Clinical symptoms of shock may occur at the beginning of the transfusion, after transfusion of 10-30 ml of blood, at the end of the transfusion, or shortly after it. The patient shows anxiety, complains of pain and a feeling of tightness behind the sternum, pain in the lower back, muscles, and sometimes chills. Shortness of breath and difficulty breathing are observed. The face is hyperemic, sometimes pale or cyanotic. Possible nausea, vomiting, involuntary urination and defecation. The pulse is frequent, weak filling, blood pressure decreases. If symptoms worsen rapidly, death may occur.
When incompatible blood is transfused during surgery under anesthesia, manifestations of shock are often absent or mild. In such cases, blood incompatibility is indicated by an increase or decrease in blood pressure, increased, sometimes significantly, tissue bleeding in the surgical wound. When the patient is recovered from anesthesia, tachycardia, a decrease in blood pressure are observed, and acute respiratory failure is possible.
Clinical manifestations of transfusion shock during blood transfusion that is incompatible with the Rh factor develop 30-40 minutes, and sometimes several hours after transfusion, when a large amount of blood has already been transfused. This complication is difficult.
When the patient recovers from shock, acute renal failure may develop. In the first days, a decrease in diuresis (oliguria), low relative density of urine, and an increase in uremia are noted. As acute renal failure progresses, complete cessation of urination (anuria) may occur. The content of residual nitrogen and urea and bilirubin increases in the blood. The duration of this period in severe cases lasts up to 8-15 and even up to 30 days. With a favorable course of renal failure, diuresis is gradually restored and a period of recovery begins. With the development of uremia, patients may die on the 13-15th day.
At the first signs of transfusion shock, the blood transfusion should be stopped immediately and, without waiting to determine the cause of the incompatibility, intensive therapy should be started.
1. Strophanthin-K, lily of the valley glycoside are used as cardiovascular drugs, norepinephrine is used for low blood pressure, diphenhydramine, chloropyramine or promethazine are used as antihistamines, glucocorticoids (50-150 mg prednisolone or 250 mg hydrocortisone) are administered to stimulate vascular activity and slowing down the antigen-antibody reaction.
2. To restore hemodynamics and microcirculation, blood replacement fluids are used: dextran [cf. they say weight 30,000-40,000], saline solutions.
3. In order to remove hemolysis products, Povidone + Sodium chloride + Potassium chloride + Calcium chloride + Magnesium chloride + Sodium bicarbonate, bicarbonate or sodium lactate are administered.
4. Furosemide and mannitol are used to maintain diuresis.
5. Urgently carry out a bilateral lumbar procaine blockade to relieve spasm of the renal vessels.
6. Patients are given humidified oxygen for breathing; in case of respiratory failure, mechanical ventilation is performed.
7. In the treatment of blood transfusion shock, early plasma exchange is indicated with the removal of 1500-2000 ml of plasma and its replacement with fresh frozen plasma.
8. The ineffectiveness of drug therapy for acute renal failure and the progression of uremia serve as indications for hemodialysis, hemosorption, and plasmapheresis.
If shock occurs, resuscitation measures are carried out in the institution where it occurred. Treatment of renal failure is carried out in special departments for extrarenal blood purification.
Bacterial toxic shock observed extremely rarely. It is caused by blood infection during preparation or storage. The complication occurs directly during transfusion or 30-60 minutes after it. Shaking chills, high body temperature, agitation, blackouts, rapid thready pulse, a sharp decrease in blood pressure, involuntary urination and defecation immediately appear.
To confirm the diagnosis, bacteriological examination of the blood remaining after the transfusion is of great importance.
Treatment involves the immediate use of anti-shock, detoxification and antibacterial therapy, including painkillers and vasoconstrictors (phenylephrine, norepinephrine), blood replacement fluids of rheological and detoxification action (dextran [average molecular weight 30,000-40,000], Povidone + Sodium chloride + Potassium chloride + Calcium chloride + Magnesium chloride + Sodium bicarbonate), electrolyte solutions, anticoagulants, broad-spectrum antibiotics (aminoglycosides, cephalosporins).
Early supplementation is most effective complex therapy exchange blood transfusions.
Air embolism can occur if the transfusion technique is violated - improper filling of the transfusion system (air remains in it), untimely termination of blood transfusion under pressure. In such cases, air can enter the vein, then into the right half of the heart and then into the pulmonary artery, clogging its trunk or branches. For the development of air embolism, a simultaneous entry of 2-3 cm 3 of air into the vein is sufficient. Clinical signs of air embolism pulmonary artery are sharp chest pain, shortness of breath, severe cough, cyanosis of the upper half of the body, weak rapid pulse, drop in blood pressure. Patients are restless, clutch their chests with their hands, and experience a feeling of fear. The outcome is often unfavorable. At the first signs of embolism, it is necessary to stop the blood transfusion and begin resuscitation measures: artificial respiration, administration of cardiovascular drugs.
Thromboembolism during blood transfusion occurs as a result of embolism by blood clots formed during its storage, or blood clots that break away from a thrombosed vein when blood is infused into it. The complication occurs as an air embolism. Small blood clots clog the small branches of the pulmonary artery, and a pulmonary infarction develops (chest pain; cough, initially dry, then with bloody sputum; increased body temperature). X-ray examination reveals the picture of focal pneumonia.
At the first signs of thromboembolism, immediately stop the blood infusion and use cardiovascular drugs, inhalation of oxygen, infusion of fibrinolysin [human], streptokinase, sodium heparin.
Massive blood transfusion is considered to be a transfusion in which, over a short period of time (up to 24 hours), blood is introduced into the bloodstream. donor blood in an amount exceeding 40-50% of the bcc (usually 2-3 liters of blood). When transfusing such a quantity of blood (especially long-term storage) obtained from different donors, the development of a complex symptom complex called massive blood transfusion syndrome. The main factors determining its development are the effect of cooled (refrigerated) blood, the intake of large doses of sodium citrate and blood breakdown products (potassium, ammonia, etc.) that accumulate in the plasma during its storage, as well as the massive entry of fluid into the bloodstream, which leads to overload of the cardiovascular system.
Acute cardiac enlargement develops when large doses of canned blood quickly enter the patient’s blood during jet transfusion or injection under pressure. There is shortness of breath, cyanosis, complaints of pain in the right hypochondrium, frequent small arrhythmic pulse, decreased blood pressure and increased central venous pressure. If there are signs of cardiac overload, the infusion should be stopped, bloodletting should be done (200-300 ml) and cardiac drugs (strophanthin-K, lily of the valley glycoside) and vasoconstrictors, 10% calcium chloride solution (10 ml) should be administered.
Citrate intoxication develops with massive blood transfusion. The toxic dose of sodium citrate is considered to be 0.3 g/kg. Sodium citrate binds calcium ions in the recipient’s blood, hypocalcemia develops, which, along with the accumulation of citrate in the blood, leads to severe intoxication, the symptoms of which are tremors, convulsions, increased heart rate, decreased blood pressure, and arrhythmia. In severe cases, dilation of the pupils, pulmonary and cerebral edema occur. To prevent citrate intoxication, it is necessary to administer 5 ml of a 10% calcium chloride solution or calcium gluconate solution for every 500 ml of preserved blood during blood transfusion.
Due to the transfusion of large doses of canned blood with long shelf life (more than 10 days), severe potassium intoxication, which leads to ventricular fibrillation and then cardiac arrest. Hyperkalemia is manifested by bradycardia, arrhythmia, myocardial atony, and a blood test reveals excess potassium content. Prevention of potassium intoxication is the transfusion of blood with short shelf life (3-5 days), the use of washed and thawed red blood cells. WITH therapeutic purpose use infusions of 10% calcium chloride, isotonic sodium chloride solution, 40% dextrose solution with insulin, and cardiac medications.
During massive blood transfusion, in which blood that is group and Rh compatible from many donors is transfused, due to individual incompatibility of plasma proteins, the development of serious complication - homologous blood syndrome. Clinical signs of this syndrome are pallor skin with a bluish tint, frequent weak pulse. Blood pressure is low, central venous pressure is high, and multiple fine moist rales are detected in the lungs. Pulmonary edema may increase, which is expressed in the appearance of large-bubble moist rales and bubbling breathing. There is a drop in hematocrit and a sharp decrease in blood volume, despite adequate or excessive compensation of blood loss; slowing down blood clotting time. The syndrome is based on impaired microcirculation, stasis of erythrocytes, microthrombosis, and blood deposition.
Prevention of homologous blood syndrome involves replenishing blood loss, taking into account the blood volume and its components. The combination of donor blood and blood-substituting fluids with hemodynamic (anti-shock) action (dextran [average molecular weight 50,000-70,000], dextran [average molecular weight 30,000-40,000]) that improve the rheological properties of blood (its fluidity) is very important ) due to the dilution of formed elements, reducing viscosity, improving microcirculation.
If massive transfusion is necessary, one should not strive to completely restore the hemoglobin concentration. To maintain the transport function of oxygen, a level of 75-80 g/l is sufficient. The missing blood volume should be replenished with blood substitute fluids. An important place in the prevention of homologous blood syndrome is occupied by autotransfusion of blood or plasma, i.e. transfusion of an absolutely compatible transfusion medium to the patient, as well as thawed and washed red blood cells.
Infectious complications. These include the transmission of acute infectious diseases with blood (influenza, measles, typhus, brucellosis, toxoplasmosis, etc.), as well as the transmission of diseases spread by serum (hepatitis B and C, AIDS, cytomegalovirus infection, malaria, etc.).
Prevention of such complications comes down to careful selection of donors, sanitary and educational work among donors, clear organization of the work of blood transfusion stations and donor points.
Lecture 4
Complications during transfusion of blood and its components
Blood transfusion complications are common in clinical practice and are mainly caused by violation of instructions for transfusion of blood and its components. According to statistics, complications during blood transfusion are observed in 0.01% of transfusions, and in 92% of cases they are associated with transfusion of incompatible blood according to the ABO system and Rh factor, in 6.5% - with transfusion of poor-quality blood, in 1% with underestimation of contraindications to blood transfusion, in 0.5% - with violation of transfusion technique.
Despite complex therapy and hemodialysis, mortality from blood transfusion complications remains high and reaches 25%.
The main causes of complications during blood transfusion are:
Incompatibility of the blood of the donor and recipient (according to the ABO system, Rh factor, other factors)
Poor quality of transfused blood (bacterial contamination, overheating, hemolysis, protein denaturation due to long storage periods, violation of storage temperature conditions, etc.).
Violations in transfusion technique (air and thromboembolism, acute cardiac enlargement).
Underestimation of the state of the recipient's body before transfusion (presence of contraindications to blood transfusion, increased reactivity, sensitization).
Transfer of pathogens of infectious diseases with transfused blood (syphilis, tuberculosis, AIDS, etc.).
As practice shows, the most common cause hemotransfusion complications is the transfusion of blood incompatible with the ABO group factors and the Rh factor. Most of of these complications is observed in obstetric-gynecological and surgical departments medical institutions for blood transfusion emergency indications(shock, acute blood loss, extensive injuries, surgical interventions etc.).
Complications caused by transfusion of blood, red blood cells, incompatible with the group and Rh factors of the ABO system.
The reason for such complications in the vast majority of cases is failure to follow the rules provided for in the instructions for blood transfusion techniques, the method for determining ABO blood groups and conducting compatibility tests.
Pathogenesis : massive intravascular destruction of transfused erythrocytes by natural agglutinins of the recipient with the release of destroyed erythrocytes and free hemoglobin, which have thromboplastin activity, into the plasma of the stroma, including the development of disseminated intravascular coagulation syndrome with pronounced violations in the hemostasis and microcirculation system with subsequent disturbances of central hemodynamics and the development of blood transfusion shock.
Blood transfusion shock. Transfusion shock may develop
1. in case of transfusion of incompatible blood (errors in determining the blood group, Rh factor, incorrect selection of a donor in relation to other isohemagglunic and isoserological characteristics).
2. When transfusion of compatible blood: a) due to insufficient consideration of the patient’s initial condition; b). Due to the introduction of low-quality blood; V). due to individual incompatibility of donor and recipient proteins.
Hemolysis of donor erythrocytes in the recipient’s bloodstream is the main cause of developing hemodynamic and metabolic disorders underlying blood transfusion shock.
Initial clinical signs of transfusion shock caused by transfusion of ABO-incompatible blood may appear immediately during the transfusion or shortly after it and are characterized by short-term agitation, pain in the chest, abdomen, and lower back. Subsequently, circular disorders characteristic of a state of shock (tachycardia, hypotension) gradually increase, a picture of massive intravascular hemolysis (hemoglobinemia, hemoglobinuria, bilirubinemia, jaundice) and acute dysfunction of the kidneys and liver develops. If shock develops during surgery under general anesthesia, its clinical signs may be severe bleeding from the surgical wound, persistent hypotension, and in the presence of a urinary tract, the appearance of dark cherry or black urine.
Heaviness clinical course shock largely depends on the volume of transfused incompatible red blood cells, with the nature of the underlying disease and the patient’s condition before blood transfusion playing a significant role.
Depending on the level blood pressure(maximum) there are three degrees of post-transfusion shock: 1st degree shock is characterized by a decrease in blood pressure to 90 mmHg, 11th degree shock - within 80-70 mmHg, 111th degree shock - below 70 mmHg. The severity of the clinical course of shock, its duration and prognosis are not related to the dose of blood transfused and the cause of the transfusion complication, as well as to the age of the patient, the state of anesthesia and the method of transfusion.
Treatment: stop transfusion of blood, red blood cells that caused hemolysis; in a complex of therapeutic measures, simultaneously with recovery from shock, massive (about 2-2.5 liters) plasmapheresis is indicated to remove free hemoglobin, fibrinogen degradation products, with replacement of the removed volumes with an appropriate amount of fresh frozen plasma or it in combination with colloidal plasma substitutes; to reduce the deposition of hemolysis products in the distal tubules of the nephron, it is necessary to maintain the patient’s diuresis at least 75-100 ml/hour using 20% mannitol (15-50 g) and furosemide 100 mg. One time, up to 1000 per day) correction Blood acid base 4% sodium bicarbonate solution; in order to maintain circulating blood volume and stabilize blood pressure, rheological solutions (reopolyglucin, albumin) are used; if it is necessary to correct deep (at least 60 g/l) anemia, transfusion of individually selected washed red blood cells; desensitizing therapy - antihistamines, corticosteroids, cardiovascular drugs. The volume of transfusion and infusion therapy should be adequate to diuresis. Control is normal level central venous pressure (CVP). The dose of administered corticosteroids is adjusted depending on hemodynamic stability, but should not be less than 30 mg. For 10 kg. Body weight per day.
It should be noted that osmotically active plasma expanders should be used before the onset of anuria. In case of anuria, their use is fraught with the appearance of pulmonary or cerebral edema.
On the first day of the development of post-transfusion acute intravascular hemolysis, intravenous heparin is indicated, up to 29 thousand units per day under the control of clotting time.
In cases where complex conservative therapy does not prevent the development of acute renal failure and uremia, progression of creatininemia and hyperkalemia, the use of hemodialysis in specialized institutions is required. The issue of transportation is decided by the doctor of this institution.
Reactions of the body that develop according to the type of hemotransfusion shock, the causes of which are transfusions of incompatible blood by Rh factors and other erythrocyte antigen systems develop somewhat less frequently than with transfusion of blood of different ABO groups.
Causes: these complications occur in patients who are sensitized to the Rh factor.
Isoimmunization with the Rh antigen can occur under the following conditions:
1. When repeated administration of Rh-positive blood to Rh-negative recipients;
2. When a Rh-negative woman is pregnant with a Rh-positive fetus, from which the Rh factor enters the mother’s blood, causing the formation of immune antibodies against the Rh factor in her blood.
The cause of such complications in the vast majority of cases is underestimation of obstetric and transfusion history, as well as failure to comply with other rules preventing Rh incompatibility.
Pathogenesis: massive intravascular hemolysis of transfused erythrocytes by immune antibodies (anti-D, anti-C, anti-E, etc.) formed during the previous sensitization of the recipient by repeated pregnancies or transfusions of erythrocytes incompatible with antigen systems (Rhesus, Call, Duffy, Kidd, Lewis, etc.).
Clinical manifestations This type of complications differs from the previous one by a later onset, a less violent course, and delayed hemolysis, which depends on the type of immune antibodies and their titer.
The principles of therapy are the same as in the treatment of post-transfusion type caused by blood (erythrocyte) transfusion incompatible with group factors of the ABO system.
In addition to the group factors of the ABO system and the Rh factor Rh 0 (D), complications during blood transfusion, although less frequently, can be caused by other antigens of the Rh system: ry 1 (C), rh 11 (E), hr 1 (c), hr (e), as well as antibodies from Duffy, Kell, Kidd and other systems. It should be noted that the degree of their antigenicity is less, therefore, the importance for the practice of blood transfusion of the Rh factor Rh 0 (D) is much lower. However, such complications still occur. They occur in both Rh-negative and Rh-positive individuals immunized through pregnancy or repeated blood transfusions.
The main measures to prevent transfusion complications associated with these antigens are taking into account the patient's obstetric and transfusion history, as well as fulfilling all other requirements. It should be emphasized that an indirect Coombs test is a particularly sensitive compatibility test, allowing the detection of antibodies and, therefore, incompatibility between the blood of the donor and the recipient. Therefore, an indirect Coombs test is recommended to be performed when selecting donor blood for patients with a history of post-transfusion reactions, as well as for sensitized individuals with different hypersensitivity to the introduction of red blood cells, even if they are compatible with ABO blood group and Rh factor. The test for isoantigen compatibility of transfused blood, as well as the test for compatibility for Rh factor-Rh 0 (D), is carried out separately from the test for compatibility for ABO blood groups and in no case replaces it.
The clinical manifestations of these complications are similar to those described above during transfusion of Rh-incompatible blood, although they are much less common. The principles of therapy are the same.
Post-transfusion reactions and complications associated with the preservation and storage of blood and red blood cells.
They arise as a result of the body’s reaction to the stabilizing solutions used in preserving blood and its components, to the metabolic products of blood cells formed as a result of its storage, to the temperature of the transfused transfusion medium.
Anaphylactic shock.
In clinical practice, reactions and complications of a non-hemolytic nature are quite common. They depend on the individual characteristics of the recipient, the functional state of the body, the characteristics of the donor, the nature of the transfusion environment, tactics and methods of blood transfusion. Freshly citrated blood is more reactogenic than canned blood. Plasma transfusion (especially native plasma) produces reactions more often than the use of red blood cells. An allergic reaction occurs as a result of the interaction of allergic antibodies (reaginins) with allergens from transfused donor blood or recipient plasma. This reaction occurs more often in patients suffering from allergic diseases. Sensitization of the recipient may be due to allergens of various origins: food (strawberries, Orange juice), medications, inhalation products, breakdown and denaturation products of protein. Allergic reactions are usually mild and go away within a few hours. They can occur at the time of blood transfusion, or 30 minutes, or several hours after the transfusion.
Clinical manifestations most often include the development of urticaria, edema, skin itching, headache, nausea and fever, chills, lower back pain. Anaphylactic shock rarely develops. Clinical manifestations of shock often occur 15-30 minutes after transfusion and are characterized by fever, headache, chills, and difficulty breathing due to bronchospasm. Then swelling of the face begins, hives all over the body, itching. Blood pressure decreases and heart rate increases. The reaction can proceed violently, and then there is an improvement. In most observations, the symptoms of anaphylactic shock last for the next 24 hours.
Treatment: stop blood transfusion, intravenous administration of antihistamines (diphenhydramine, suprastin, pipolfen, etc.), calcium chloride, adrenaline, corticosteroids, cardiovascular drugs, narcotic analgesics.
Massive transfusion syndrome. The syndrome is manifested by hemodynamic disturbances, the development of hepatic-renal and respiratory failure, increased bleeding, and metabolic changes. Most transfusiologists consider the introduction of more than 2500 ml of donor blood (40-50% of the circulating blood volume) into the patient’s bloodstream simultaneously within 24 hours to be a massive blood transfusion.
The reason for the development of massive transfusion syndrome lies in the specific conflict between the blood of the recipient and donors due to the presence of not only erythrocyte, but also leukocyte, platelet and protein antigens.
Complications that arise after massive blood transfusions are as follows:
1. Cardiovascular system disorders ( vascular collapse, asystole, bradycardia, cardiac arrest, ventricular fibrillation).
2. Blood changes (metabolic acidosis, hypocalcemia, hyperkalemia, increased blood viscosity, hypochromic anemia with leukopenia and thrombopenia: decreased levels of gamma globulin, albumin, citrate intoxication.
3. Hemostasis disorders (peripheral vascular spasm, wound bleeding, fibrinogenopenia, hypothrombinemia, thrombopenia, increased fibrinolytic activity.
4. Changes in internal organs (pinpoint hemorrhages, less often bleeding from the kidneys, intestines, hepatic-renal failure - oliguria, anuria, jaundice, pulmonary hypertension with the development of metabolic acidosis and respiratory failure).
5. Decreased immunobiological activity of the recipient, characterized by dehiscence of the sutures of the surgical wound, poor wound healing, and a protracted course of the postoperative period.
Bad influence massive transfusions of whole blood is expressed in the development of disseminated intravascular coagulation syndrome. An autopsy reveals minor hemorrhages in organs associated with microthrombi, which consist of aggregates of red blood cells and platelets. Hypodynamic disturbances occur in the systemic and pulmonary circulation, as well as at the level of capillary and organ blood flow.
The syndrome of massive transfusions, with the exception of traumatic blood loss, is usually the result of whole blood transfusions with already begun DIC syndrome, when, first of all, it is necessary to transfuse large quantities of fresh frozen plasma (1-2 liters or more) with a jet or frequent drops of its administration, but where transfusion of red blood cells (rather than whole blood) should be limited to vital indications.
In order to prevent and treat massive transfusion syndrome, it is necessary to:
Transfuse strictly single-group canned whole blood with the shortest possible shelf life. For patients with the presence of isoimmune antibodies, special blood selection should be performed. Patients with increased reactivity in postoperative period use washed erythrocyte suspension.
Along with blood transfusion, use low-molecular blood substitutes (polyglucin, reopoliglucin, hemodez, periston, reomacrodex, etc.) to replenish blood loss. For every 1500-2000 ml of blood transfused, inject 500 ml of plasma replacement solution.
During operations with extracorporeal circulation, the method of controlled hemodilution (dilution or dilution of blood) with low-molecular blood substitutes is used.
For hemostatic disorders in the immediate postoperative period, epsilonaminocaproic acid, fibrinogen, direct blood transfusion, platelet mass, concentrated solutions of dry plasma, albumin, gamma globulin, small doses of fresh red blood cells, and antihemophilic plasma are used.
In the postoperative period, osmotic diuretics are used to normalize diuresis.
Correction of acid-base balance disorders by introducing Tris buffer into the recipient’s bloodstream.
Treatment of DIC, a syndrome caused by massive blood transfusion, is based on a set of measures aimed at normalizing the hemostatic system and eliminating other leading manifestations of the syndrome, primarily shock, capillary stasis, disturbances in acid-base, electrolyte and water balance, damage to the lungs, kidneys, adrenal glands, anemia. It is advisable to use heparin (average dose 24,000 units per day with continuous administration). The most important method of therapy is plasmapheresis (removal of at least one liter of plasma) by replacing fresh frozen donor plasma in a volume of at least 600 ml. Blockade of microcirculation by blood cell aggregates and vascular spasm are eliminated with disaggregants and other drugs (reopolyglucin, intravenously, chimes 4-6 ml of 0.5% solution, euphyllin 10 ml of 2.4% solution, trental 5 ml). Protease inhibitors are also used - transilol, contrical in large doses - 80,000 - 100,000 units per intravenous administration. The need and volume of transfusion therapy is dictated by the severity of hemodynamic disorders. It should be remembered that whole blood cannot be used for DIC syndrome, and washed red blood cells cannot be transfused when the hemoglobin level decreases to 70 g/l.
Citrate intoxication . With a quick and massive transfusion of donor blood, a large amount of sodium citrate is introduced into the patient’s body with canned blood. The mechanism of action of citrate is a sudden decrease in the concentration of ionized calcium in the recipient’s plasma due to its combination with the citrate ion. This leads during blood transfusion or at the end of it to severe circulatory disorders due to disturbances in the rhythm of cardiac activity, including ventricular fibrillation, vasospasm of the pulmonary circulation, increased central venous pressure, hypotension, and convulsions.
Hypocalcemia develops during transfusions of large doses of whole blood or plasma, especially with high transfusion rates prepared using sodium citrate, which, by binding free calcium in the bloodstream, causes hypocalcemia. Transfusion of blood or plasma prepared using sodium citrate at a rate of 150 ml/min. reduces the level of free calcium to a maximum of 0.6 mmol/l, and at a rate of 50 ml/min. the content of free calcium in the recipient's plasma changes slightly. The level of ionized calcium returns to normal immediately after the transfusion is stopped, which is explained by the rapid mobilization of calcium from endogenous stores and metabolism of citrate in the liver.
In the absence of any clinical manifestations of temporary hypocalcemia, the standard prescription of calcium supplements (to “neutralize” citrate) is unjustified, since it can cause arrhythmia in patients with cardiac pathology. It is necessary to remember the category of patients who have initial hypocalcemia, or the possibility of its occurrence during various treatment procedures (therapeutic plasmapheresis with replacement of the exfused volume with plasma), as well as during surgical interventions. Particular attention should be paid to patients with the following concomitant pathology: hypoparothyroidism, D-vitaminosis, chronic renal failure, liver cirrhosis and active hepatitis, congenital hypocalcemia in children, pancreatitis, toxic-infectious shock, thrombophilic conditions, post-resuscitation conditions, long-term therapy with corticosteroid hormones and cytostatics.
Clinic, prevention and treatment of hypocalcemia: a decrease in the level of free calcium in the blood leads to arterial hypotension, increased pressure in the pulmonary artery and central venous pressure, lengthening QT interval on the ECG, the appearance of convulsive twitching of the muscles of the lower leg, face, disturbance of the breathing rhythm with transition to apnea with a high degree of hypocalcemia. Subjectively, patients initially perceive the increase in hypocalcemia as an unpleasant sensation behind the sternum, interfering with inhalation, an unpleasant taste of metal appears in the mouth, convulsive twitching of the muscles of the tongue and lips is noted, with a further increase in hypocalcemia - the appearance of clonic convulsions, impaired breathing until it stops, cardiac arrhythmias - bradycardia, up to asystole.
Prevention consists of identifying patients with potential hypocalcemia (tendency to seizures), administering plasma at a rate not higher than 40-60 ml/min, and prophylactically administering a 10% calcium gluconate solution - 10 ml for every 0.5 liter of plasma.
When clinical symptoms hypocalcemia, it is necessary to stop the plasma injection, administer 10-20 ml of calcium gluconate or 10 ml of calcium chloride intravenously, and monitor the ECG.
Hyperkalemia may occur in a recipient with rapid transfusion (about 120 ml/min) of long-stored canned blood or packed red blood cells (with a storage period of more than 14 days, the potassium level in these transfusion media can reach 32 mmol/l). The main clinical manifestation of hyperkalemia is the development of bradycardia.
Prevention: when using blood or red blood cells for more than 15 days of storage, transfusions should be done by drip (50-70 ml/min), it is better to use washed red blood cells.
To the group of complications associated with violation of transfusion technique blood complications include air and thromboembolism, acute expansion of the heart.
Air embolism occurs when the system is not filled correctly, resulting in air bubbles entering the patient’s vein. Therefore, the use of any pressure equipment during transfusion of blood and its components is strictly prohibited. When an air embolism occurs, patients experience difficulty breathing, shortness of breath, pain and a feeling of pressure behind the sternum, cyanosis of the face, and tychadriac. Massive air embolism with the development of clinical death requires immediate resuscitation measures- indirect cardiac massage, mouth-to-mouth artificial respiration, calling the resuscitation team.
Prevention of this complication lies in strict adherence to all rules of transfusion, installation of systems and equipment. It is necessary to carefully fill all tubes and parts of the equipment with the transfusion medium, ensuring that air bubbles are removed from the tubes. Monitoring of the patient during the transfusion should be constant until its completion.
Thromboembolism– embolism by blood clots, which occurs when clots of varying sizes enter a patient’s vein, formed in the transfused blood (erythrocyte mass) or, more rarely, carried with the blood flow from the patient’s thrombosed veins. The cause of embolism may be incorrect transfusion technique, when clots in the transfused blood enter the vein, or thrombi formed in the patient’s vein near the tip of the needle become emboli. The formation of microclots in canned blood begins from the first day of storage. The resulting microaggregates, entering the blood, are retained in the pulmonary capillaries and, as a rule, undergo lysis. When hit large number blood clots develop clinical picture thromboembolism of the branches of the pulmonary artery: sudden pain in the chest, a sharp increase or occurrence of shortness of breath, coughing, sometimes hemoptysis, pallor of the skin, cyanosis, in some cases collapse develops - cold sweat, drop in blood pressure, rapid pulse. In this case, the electrocardiogram shows signs of load on the right atrium and a possible shift of the electrical axis to the right.
Treatment of this complication requires the use of fibrinolysis activators - streptase (streptodecase, urokinase), which is administered through a catheter, preferably if there are conditions for its installation, in the pulmonary artery. With a local effect on a blood clot in a daily dose of 150,000 IU (50,000 IU 3 times). When administered intravenously daily dose streptase is 500,000 – 750,000 IU. Intravenous administration of heparin is indicated (24,000 - 40,000 units per day), immediate infusion of at least 600 ml. fresh frozen plasma under the control of a coagulogram.
Prevention of pulmonary embolism involves correct technique procurement and blood transfusion, which prevents blood clots from entering the patient’s vein, the use of filters and microfilters during blood transfusion, especially with massive and jet transfusions. In case of needle thrombosis, repeated puncture of the vein with another needle is necessary, without under any circumstances attempting to different ways restore patency of the thrombosed needle.
Acute cardiac enlargement occurs when the right heart is overloaded with an excessively large amount of blood quickly poured into the venous bed.
Infectious diseases, resulting from blood transfusion, clinically proceed in the same way as with the usual route of infection.
Serum hepatitis– one of the most severe complications that arise in a recipient during transfusion of blood or its components obtained from a donor who is either a virus carrier or was in the incubation period of the disease. Serum hepatitis is characterized severe course With possible outcome in liver dystrophy, in chronic hepatitis and cirrhosis of the liver.
The specific causative agent of post-transfusion hepatitis is the B-1 virus, discovered as the Australian antigen. The incubation period is from 50 to 180 days.
The main measure for the prevention of hepatitis is the careful selection of donors and identification of potential sources of infection among them.
Blood transfusion is often the only method of saving patients with massive blood loss, hematopoietic diseases, poisoning, and purulent-inflammatory pathologies. Hemotransfusion shock, which occurs when blood is incompatible, is an extremely serious condition that can be fatal. With a competent approach to the appropriateness of the procedure, taking into account contraindications for the patient, careful prevention, proper treatment and active monitoring of the patient, such a complication does not arise.
What is transfusion shock
Hemotransfusion shock refers to pathological conditions of extremely severe - life-threatening - disorder of all body functions that occur during blood transfusion.
The term blood transfusion comes from the Greek “haem” - blood and the Latin word “transfusion”, which means transfusion.
Blood transfusion shock is a dangerous and difficult to treat complication, manifesting itself in the form of a rapidly developing powerful inflammatory-anaphylactic reaction affecting all organs and systems.
Transfusion shock is a life-threatening complication of blood transfusion.According to medical statistics, this condition occurs in almost 2% of all blood transfusions.
Transfusion shock occurs either during the transfusion process or immediately after the procedure and lasts from 10–15 minutes to several hours. Thus, the first signs of infusion of blood of the wrong type occur when only 20–40 ml enters the patient’s body. It happens that a full-blown reaction is registered after 2–4 days.
In rare cases, the pathology does not give clear clinical signs, especially during general anesthesia, but more often it is accompanied by pronounced manifestations, which without intensive and emergency treatment lead to the death of the patient.
The danger of blood transfusion shock is a serious disruption of the heart, brain, insufficiency of liver and kidney function up to their failure, hemorrhagic syndrome (increased bleeding) with hemorrhages and bleeding that aggravate the condition of patients, intravascular thrombosis that threatens a drop in blood pressure.
Causes
Experts consider the most common cause of acute hemotransfusion complications to be the use of blood that is incompatible with the Rh factor Rh (a special protein present or absent on the surface of red blood cells - erythrocytes), which does not correspond to the group according to the ABO system (60% of all cases). Less commonly, a complication occurs when blood is incompatible with individual antigens.
Blood group compatibility - table
| Blood type | Can donate blood to groups | Can accept blood groups |
| I | I, II, III, IV | I |
| II | II, IV | I, II |
| III | III, IV | I, III |
| IV | IV | I, II, III, IV |
The blood transfusion procedure is a medical procedure, therefore leading causal factors are:
- violation of blood transfusion technique;
- inconsistency with the methodology and errors in determining the blood group and Rh factor;
- incorrect execution of samples when checking for compatibility.
Risk factors that aggravate the condition include:
- use of blood infected with bacteria or of poor quality due to violation of temperature conditions and shelf life;
- a large amount of incompatible blood transfused to the patient;
- appearance and severity primary disease, as a result of which blood transfusion was required;
- condition and age of the patient;
- allergic predisposition.
Clinical aspects of transfusion shock - video
Symptoms and signs
The clinical picture of shock is accompanied by characteristic manifestations, but experts always take into account that erased symptoms also occur. Moreover, the brief improvement that occurs in many patients is suddenly replaced by a state with obvious and acute manifestations severe renal-hepatic damage, which in 99% of cases is the main cause of death.
Therefore, both during and after blood transfusion, the patient must be under continuous monitoring.
Symptoms of transfusion shock - table
| By time of manifestation | Symptoms |
| Initial |
Lower back pain is a defining sign of the onset of shock during and after blood transfusion. It serves as a signal of catastrophic damage to the kidney tissue. |
| As the condition progresses |
|
| Late | With absence medical care:
|
Features of manifestations of the disease during general anesthesia
When incompatible blood is transfused into a patient who is under anesthesia during surgical operations, signs of shock are weak or absent.
The patient does not feel anything, does not complain, so early diagnosis of the development of pathology falls entirely on the doctors performing the operation.
Manifestations of jaundice during blood transfusion indicate the development pathological processes in the liver
An abnormal blood transfusion reaction is indicated by:
- an increase or, conversely, a drop in blood pressure below normal levels;
- increased heart rate;
- a sharp rise in temperature;
- paleness, cyanosis (blue discoloration) of the skin and mucous membranes;
- a noticeable increase in tissue bleeding in the area of the surgical wound;
- discharge of brown urine with inclusions resembling meat flakes in structure.
During surgical blood transfusion, it is necessary to insert a catheter into the bladder: in this case, you can visually track the color and type of urine released.
The degree of shock reaction is determined by the doctor based on blood pressure readings.
Degrees of transfusion shock - table
Diagnostics
Diagnosis is carried out on the basis of an analysis of the patient’s subjective sensations, special attention is paid to lower back pain - specific symptom. Of the objective signs, importance is attached to a sharp drop in pressure, redness of urine, decreased diuresis, rise in temperature and increased heart rate.
The analysis is difficult because in some cases the only sign of a complication is an increase in the patient’s temperature, so changes in this indicator are monitored for 2 hours after the transfusion.
Because the therapeutic measures in case of shock should be immediate, and it takes time to obtain test results, experienced specialists resort to the old method of determining the incompatibility of transfused blood, which was widely used in military hospitals in combat conditions - the Baxter test.
Baxter's test: after administering about 70–75 ml of donor blood to the patient, 10 minutes later a 10 ml sample is drawn from another vein into a test tube. Then centrifugation is carried out to separate the liquid part - plasma, which is normally colorless. Pink color indicates a high probability of developing transfusion shock as a result of incompatibility.
Laboratory tests reveal:
- Signs of hemolysis (destruction of red blood cells), which include:
- the appearance of free hemoglobin in the serum (hemoglobinemia reaches 2 grams per liter) already in the first hours;
- detection of free hemoglobin in the urine (hemoglobinuria) within 6–12 hours after the procedure;
- high content indirect bilirubin(hyperbilirubinemia), which persists for up to 5 days, along with the appearance of urobilin in the urine and an increase in the content of stool stercobilin.
- A positive reaction with a direct antiglobulin test (Coombs test), meaning the presence of antibodies to the Rh factor and specific globulin antibodies that are fixed on red blood cells.
- Detection of agglutination (sticking together) of red blood cells when examining blood under a microscope (a sign of the presence of an antigen or antibody).
- Decrease in hematocrit (the volume of the red blood cell fraction in the blood).
- Reduction or absence of haptoglobin (a protein that transports hemoglobin) in the blood serum.
- Oliguria (decreased amount of urine excreted) or anuria (urinary retention), indicating kidney dysfunction and the development of failure.
Difficulties differential diagnosis associated with the frequent absence or erasure of clinical symptoms of a reaction to blood transfusion. When studies determining the development of acute hemolysis are insufficient, additional serological tests are used.
Hemolysis - destruction of red blood cells and release of free hemoglobin - is the main laboratory indicator of incompatibility of blood transfused to a patient
Treatment
Treatment for blood transfusion shock is carried out in the department intensive care and includes a set of activities.
Emergency care algorithm
Emergency medical actions in case of blood transfusion complications are aimed at preventing coma, hemorrhagic syndrome and kidney failure.
Emergency care for shock during blood transfusion is aimed at stabilizing cardiac activity and vascular tone
At the first signs of shock:
- The transfusion procedure is immediately stopped and, without removing the needle from the vein, the dropper is closed with a clamp. Next, massive infusions will be administered through the left needle.
- Change the disposable transfusion system to a sterile one.
- Adrenaline is administered subcutaneously (or intravenously). If blood pressure does not stabilize after 10–15 minutes, the procedure is repeated.
- Heparin administration is started (intravenously, intramuscularly, subcutaneously) to prevent the development of disseminated intravascular coagulation syndrome, which is characterized by massive thrombus formation and bleeding.
- Infusion therapy is carried out to stabilize blood pressure to the minimum normal level of 90 mmHg. Art. (systolic).
- A solution of calcium chloride is injected intravenously (reduces the permeability of the vascular wall and relieves the allergic reaction).
- Perinephric (perinephric) blockade is carried out - introduction of Novocaine solution into the perinephric tissue according to A.V. Vishnevsky to relieve vasospasm, edema, maintain blood circulation in tissues and relieve pain.
- Infused into a vein:
- means for maintaining heart function - Cordiamine, Korglykon with glucose solution;
- antishock drugs (Kontrikal, Trasylol);
- Morphine, Atropine.
With the development of hemorrhagic syndrome:
- begin to transfuse the patient with freshly collected blood (same group), plasma, platelet and erythrocyte mass, cryoprecipitate, which have an effective anti-shock effect, preventing kidney damage;
- epsilon-aminocaproic acid is administered intravenously as a hemostatic agent for bleeding associated with increased fibrinolysis (thromt dissolution processes).
At the same time, instrumental measurements of blood pressure are taken and catheterization is performed. Bladder to monitor kidney function and collect urine for hemolysis.
Drug treatment
If blood pressure can be stabilized, active drug therapy is carried out.
Use:
- diuretics intravenously (then intramuscularly for 2–3 days) to remove free hemoglobin and reduce the risk of developing acute failure kidneys, liver or reducing its severity: Lasix, Mannitol. In this case, Furosemide (Lasix) is combined with Eufillin according to the scheme.
Important! If there is no therapeutic effect during the infusion of Mannitol, its administration is stopped due to the threat of developing pulmonary edema, brain edema and simultaneous tissue dehydration.
- antihistamines (antiallergic) agents to suppress the reaction of rejection of foreign blood components: Diphenhydramine, Suprastin, Diprazine;
- corticosteroids to stabilize the walls of blood vessels, relieve inflammatory edema, prevent acute pulmonary failure: Prednisolone, Dexamethasone, Hydrocortisone with a gradual dose reduction;
- as agents that improve microcirculation, prevent oxygen starvation of cells, and have a hemostatic (hemostatic) effect:
Troxevasin, Cyto-Mac, ascorbic acid, Etamzilat; - disaggregants that prevent the formation of blood clots: Pentoxifylline, Xanthinol nicotinate, Complamin;
- to relieve spasms of the bronchi and blood vessels: No-shpa, Eufillin, Baralgin (allowed only for stable blood pressure);
- analgesic and narcotic drugs for severe pain: Ketonal, Promedol, Omnopon.
- in case of bacterial contamination of the blood - antimicrobials wide spectrum.
Drugs for the treatment of blood transfusion shock - photo gallery
Suprastin is an antihistamine 
Prednisolone - hormonal drug 
Etamsylate is used for increased bleeding 
Eufillin dilates the lumen of blood vessels 
Ketonal is an effective pain reliever
Important! Do not prescribe antibiotics with nephrotoxicity side effect, including sulfonamides, cephalosporins, tetracyclines, streptomycin.
Infusion therapy
The treatment regimen, choice of medications and dosage are determined by the amount of diuresis (the volume of urine collected per unit of time).
Infusion therapy for the development of intravascular hemolysis - table
| Diuresis in ml per hour | |
| More than 30 | Less than 30 or anuria (lack of urination) |
| at least 5–6 liters of solutions are administered over 4–6 hours | the amount of fluid administered is reduced to a volume calculated using the formula 600 ml + volume of urine excreted |
|
|
| Stimulation of diuresis with infusion solutions begins only after the administration of drugs to alkalize urine in order to avoid damage to the renal tubules. | |
| Mannitol, Lasix to maintain diuresis rates of 100 ml/hour or more | Lasix. Mannitol is discontinued because its use against the background of anuria causes overhydration, which can lead to edema of the lungs and brain. |
| Diuresis is forced until the urine clears and free hemoglobin in the blood and urine is eliminated | If urine output does not increase within 20–40 minutes from the onset of hemolysis, disruption of renal blood flow may begin with the development of renal ischemia and nephronecrosis (death of organ cells). To remove toxins and free hemoglobin from the blood, plasmapheresis is performed and the question of the need for hemodialysis is raised, which can be performed only after the signs of hemolysis have been eliminated. |
| If a violation of the level of electrolytes is detected, solutions of potassium and sodium are added. | |
| Treatment of disseminated intravascular coagulation syndrome or acute coagulopathy (a dangerous condition of a sharp violation of blood clotting, leading to the development of massive bleeding), if necessary, blood transfusion is carried out in the amount of blood loss. | |
Blood purification
If possible, and especially with the development of anuria, indicating acute destructive processes in the kidneys, blood purification is carried out outside the patient's body - plasmapheresis.
The procedure involves taking a certain amount of blood and removing the liquid part from it - plasma containing free hemoglobin, toxins, and decay products. This purification of the blood occurs when its liquid part passes through special filters and is subsequently infused into another vein.
Plasmapheresis provides a rapid therapeutic effect due to the active removal of aggressive antibodies, hemolysis products, and toxins. It is performed using a device, completely eliminating the possibility of infection of the patient, and lasts about 1–1.5 hours.
Stabilization of organ function
To prevent the destruction of kidney, liver, and brain tissue during blood transfusion shock, measures are necessary to maintain their functioning.
The rapid progression of respiratory failure, hypoxia (decreased oxygen in the blood) and hypercapnia (increased amount of carbon dioxide) requires an emergency transfer of the patient to artificial respiration.
If symptoms of severe kidney failure appear (anuria, brown urine, lower back pain), the patient is transferred to hemodialysis - a method based on the extrarenal purification of the blood from toxins, allergens, and hemolysis products using an “artificial kidney” device. It is prescribed if renal failure does not respond to drug treatment and threatens the death of the patient.
Prevention
Prevention of transfusion shock consists of observing the principle: the medical approach to the blood transfusion procedure should be as responsible as for organ transplantation, including limiting the indications for transfusion, competently conducting tests and preliminary tests in accordance with the instructions.
Main indications for blood transfusion:
- Absolute indications for blood transfusion:
- acute blood loss (more than 21% of the circulating blood volume);
- traumatic shock grade 2–3;
- Relative indications for blood transfusion:
- anemia (hemoglobin level in the blood less than 80 g/l);
- inflammatory diseases with severe intoxication;
- continued bleeding;
- blood coagulation disorder;
- decline immune status body;
- long-term chronic inflammatory process(sepsis);
- some poisonings ( snake venom etc.).
To prevent the development of transfusion complications it is necessary:
- eliminate errors when determining a patient’s blood group and conducting compatibility tests;
- carry out a control re-determination of the patient’s blood group immediately before the blood transfusion procedure;
- eliminate the possibility of developing an Rh conflict, for which it is necessary to examine the patient’s Rh status and antibody titer, and perform compatibility tests;
- exclude the possibility of blood incompatibility due to rare serological factors using Coombs tests;
- use only disposable blood transfusion systems;
- visually assess the type and volume of urine excreted by the patient during and immediately after transfusion (volume, color);
- monitor and analyze symptoms of transfusion shock and hemolysis;
- carefully monitor the patient for 3 hours after blood transfusion (measure temperature, pressure, pulse rate every hour).
The prognosis for transfusion shock depends on the timeliness of emergency care and further therapy. If active, full treatment of pathology with manifestations of hemolysis, acute renal and respiratory failure, hemorrhagic syndrome is carried out in the first 6 hours after the onset of the disease, 75 out of 100 patients experience a complete recovery. In 25–30% of patients with severe complications, renal-hepatic dysfunction of the heart, brain, and pulmonary vessels develops.
Blood transfusion shock is the result of mistakes made medical personnel during transfusion of blood or its components. Transfusion from the Latin transfusio - transfusion. Hemo is blood. This means a blood transfusion is a blood transfusion.
The transfusion (blood transfusion) procedure is performed only in a hospital by trained doctors (in large centers there is a separate doctor - a transfusiologist). The preparation and conduct of the transfusion procedure requires a separate explanation.
In this material we will focus only on the consequences of mistakes made. It is believed that blood transfusion complications in the form of blood transfusion shock in 60 percent of cases occur precisely because of an error.
Blood transfusion shock is a consequence of immune and non-immune causes.
Immune causes include:
- Blood plasma incompatibility;
- Incompatibility of group and Rh factor.
Non-immune causes are as follows:
- Substances that increase body temperature enter the blood;
- Transfusion of infected blood;
- Disruptions in blood circulation;
- Failure to comply with transfusion rules.
For reference. The main and most common cause of this complication is non-compliance with blood transfusion technique. The most common medical errors are incorrect determination of blood type and violations during compatibility tests.
How does transfusion shock develop?
Transfusion shock is one of the most life-threatening conditions of the victim, which manifests itself during or after a blood transfusion.
After incompatible donor blood enters the recipient’s body, the irreversible process of hemolysis begins, which manifests itself in the form of destruction of red blood cells - erythrocytes.
Ultimately, this leads to the appearance of free hemoglobin, which results in impaired circulation, thrombohemorrhagic syndrome is observed, and blood pressure levels are significantly reduced. Multiple dysfunctions of internal organs and oxygen starvation develop.
For reference. At in a state of shock the number of hemolysis components increases, which causes a pronounced spasm of the vascular walls, and also causes an increase in the permeability of the vascular walls. Then the spasm turns into paretic expansion. This difference in the state of the circulatory system is the main reason for the development of hypoxia.
In the kidneys, the concentration of decomposition products of free hemoglobin and formed elements increases, which, together with the contraction of the walls of blood vessels, leads to the ontogenesis of renal failure.
The level of blood pressure is used as an indicator of the degree of shock, which begins to fall as shock develops. It is believed that during the development of shock there are three degrees:
- first. Mild degree, in which the pressure drops to the level of 81 - 90 mm. rt. Art.
- second. Average degree, at which the indicators reach 71 - 80 mm.
- third. Severe degree, in which the pressure drops below 70 mm.
The manifestation of blood transfusion complications can also be divided into the following stages:
- The onset of a shock post-transfusion state;
- The occurrence of acute renal failure;
- Stabilization of the patient's condition.
Symptoms
Signs of pathology development can appear both immediately after the blood transfusion procedure and in the subsequent hours after
her. Initial symptoms include: - Short-term emotional arousal;
- Difficulty breathing, shortness of breath;
- Manifestation of cyanosis in the skin and mucous membranes;
- Fever due to chills;
- Muscle, lumbar and chest pain.
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Spasms in the lower back primarily signal the beginning of transformations in the kidneys. Continued changes in blood circulation are manifested in the form of noticeable arrhythmias, pale skin, sweating and a steady decrease in blood pressure levels.
If at the first symptoms of transfusion shock the patient was not provided with medical assistance, then the following symptoms occur:
- Due to the uncontrolled growth of free hemoglobin, signs of hemolytic jaundice arise, characterized by yellowing of the skin and white membranes of the eyes;
- Actually, hemoglobinemia;
- The occurrence of acute renal failure.
Not so often, experts noticed the manifestation of such signs of transfusion shock as hyperthermia, vomiting syndrome, numbness, uncontrolled muscle contraction in the limbs and involuntary bowel movements.
If a blood transfusion is performed on a recipient who is under anesthesia, then blood transfusion shock is diagnosed based on the following criteria:
- Decreased blood pressure;
- Uncontrolled bleeding in the operated wound;
- Dark brown flakes are visible in the urinary drainage catheter.
Important! A patient who is under the influence of anesthesia cannot report how he is feeling, so the responsibility for the timely diagnosis of shock lies entirely with the medical staff.
First aid for shock
If during the transfusion procedure the patient experiences signs of shock similar to the symptoms of transfusion shock, then the procedure should be stopped immediately. Next, you should replace the transfusion system as soon as possible and pre-connect a convenient catheter into the vein running under the patient’s collarbone. It is recommended to carry out a perirenal bilateral blockade with novocaine solution (0.5%) in a volume of 70-100 ml in the near future.To avoid development oxygen starvation, you should establish a supply of humidified oxygen using a mask. The doctor should begin monitoring the volume of urine produced, and also urgently call laboratory technicians to collect blood and urine for an ambulance. full analysis, as a result of which the content values will become known red blood cells , free hemoglobin, fibrinogen.
For reference. If, when diagnosing post-transfusion shock, the laboratory does not have reagents to establish compatibility, then you can use the proven Baxter method, which was used in field hospitals. It is necessary to inject 75 ml of donor material into the victim, and after 10 minutes, take blood from any other vein.
The test tube must be placed in a centrifuge, which, using centrifugal force, will separate the material into plasma and formed elements. In case of incompatibility, the plasma acquires a pink tint, whereas in in good condition it is a colorless liquid.
It is also advisable to immediately measure central venous pressure, acid-base balance and electrolyte levels, as well as conduct electrocardiography.
Prompt implementation of anti-shock measures in most cases leads to an improvement in the patient's condition.
Treatment
After anti-shock treatment was carried out urgent action, there is a need for urgent restoration of basic blood indicators.
Blood transfusion shock is quite rare, but severe complication, which develops during transfusion of blood and its components.
Occurs during the procedure or immediately after it.
Requires immediate emergency anti-shock therapy.
Details about this state read below.
- blood group incompatibility according to the ABO system;
- incompatibility according to RH (Rhesus) factor;
- incompatibility with antigens of other serological systems.
Occurs due to violation of the rules of blood transfusion at any stage, incorrect determination of the blood group and Rh factor, errors during the compatibility test.
Features and changes in organs
The basis of all pathological changes is the destruction of red blood cells of incompatible donor blood in the recipient’s vascular bed, as a result of which the following enters the blood:
- Free hemoglobin - normally free hemoglobin is located inside red blood cells, its direct content in the bloodstream is insignificant (from 1 to 5%). Free hemoglobin is bound in the blood by haptaglobin, the resulting complex is destroyed in the liver and spleen and does not enter the kidneys. Release into the blood large quantity free hemoglobin leads to hemoglobinuria, i.e. all hemoglobin is not able to bind and begins to be filtered in the renal tubules.
- Active thromboplastin, an activator of blood coagulation and the formation of a thrombus (blood clot), is not normally present in the blood.
- Intraerythrocyte coagulation factors also promote clotting.
The release of these components leads to the following violations:
DIC syndrome, or disseminated intravascular coagulation syndrome - develops as a result of the release of coagulation activators into the blood.
Has several stages:
- hypercoagulation – multiple microthrombi are formed in the capillary bed, which clog small vessels, resulting in multiple organ failure;
- consumptive coagulopathy – at this stage, coagulation factors are consumed to form multiple blood clots. At the same time, the anticoagulation system of the blood is activated;
- hypocoagulation - at the third stage, the blood loses its ability to clot (since the main coagulation factor - fibrinogen - is no longer present), resulting in massive bleeding.
Oxygen deficiency – Free hemoglobin loses its connection with oxygen, and hypoxia occurs in tissues and organs.
Microcirculation disturbance- as a result of spasm of small vessels, which is then replaced by pathological expansion.
Hemoglobinuria and renal hemosiderosis– develops as a result of the release of a large amount of free hemoglobin into the blood, which, when filtered in the renal tubules, leads to the formation of hemosiderin (salt hematin - a breakdown product of hemoglobin).
Hemosiderosis in combination with vasospasm, it leads to disruption of the filtration process in the kidneys and accumulation of nitrogenous substances and creatinine in the blood, thus developing acute renal failure.
In addition, impaired microcirculation and hypoxia lead to disruption of the functioning of many organs and systems: liver, brain, lungs, endocrine system and etc.
Symptoms and signs
The first signs of transfusion shock may appear already during a blood transfusion or in the first few hours after the procedure.
- the patient is agitated and behaves restlessly;
- pain in the chest area, a feeling of tightness behind the sternum;
- breathing is difficult, shortness of breath appears;
- the complexion changes: more often it turns red, but it can be pale, cyanotic (blue) or with a marbled tint;
- lower back pain - characteristic symptom shock, indicates pathological changes in the kidneys;
- tachycardia - rapid heart rate;
- decreased blood pressure;
- Sometimes there may be nausea or vomiting.
After a few hours, the symptoms subside and the patient feels better. But this is a period of imaginary well-being, after which the following symptoms appear:
- Icterus (jaundice) of the eye sclera, mucous membranes and skin (hemolytic jaundice).
- Increased body temperature.
- Renewal and intensification of pain.
- Kidney and liver failure develops.
When receiving a blood transfusion under anesthesia, signs of shock may include:
- Fall in blood pressure.
- Increased bleeding from the surgical wound.
- The urinary catheter produces urine that is cherry-black or the color of “meat slop,” and there may be oligo- or anuria (decreased amount of urine or its absence).
- Changes in urinary excretion are a manifestation of increasing renal failure.
Course of the pathology
There are 3 degrees of transfusion shock depending on the level of decrease in systolic blood pressure:
- up to 90 mm Hg;
- up to 80-70 mm;
- below 70 mm. rt. Art.
There are also periods of shock characterized by a clinical picture:
- Shock itself is the first period in which hypotension (a drop in blood pressure) and DIC occur.
- The period of oliguria (anuria) – the impairment of kidney function progresses.
- The stage of diuresis restoration is the restoration of the filtering function of the kidneys. Occurs with timely provision of medical care.
- Convalescence (recovery) – restoration of the functioning of the blood coagulation system, normalization of hemoglobin, red blood cells, etc.
Anaphylactic shock - rapid and dangerous reaction body to an external irritant, which requires immediate medical attention. Following the link, we will consider the mechanism of development of this condition.
Types of treatment procedures
All therapeutic measures for blood transfusion shock are divided into 3 stages:
Emergency anti-shock therapy – to restore normal blood flow and prevent severe consequences. It includes:
- infusion therapy;
- intravenous administration of antishock drugs;
- extracorporeal methods of blood purification (plasmapheresis);
- correction of the function of systems and organs;
- correction of hemostasis (blood clotting);
- treatment of acute renal failure.
Symptomatic therapy – carried out after stabilization of the patient’s condition during the recovery period (recovery).
Preventive measures - identifying the cause of the development of shock and eliminating similar errors in the future, strict adherence to the sequence of transfusion procedures, conducting compatibility tests, etc.
First aid
If signs of transfusion shock or corresponding complaints from the recipient appear, it is necessary to urgently stop further blood transfusion without removing the needle from the vein, since anti-shock drugs will be administered intravenously and time cannot be wasted on new catheterization of the vein.
Emergency treatment includes:
Infusion therapy:
- blood replacement solutions (reopolyglucin) - to stabilize hemodynamics, normalize BCC (circulating blood volume);
- alkaline preparations (4% sodium bicarbonate solution) - to prevent the formation of hemosiderin in the kidneys;
- polyionic saline solutions (Trisol, Ringer-Locke solution) - to remove free hemoglobin from the blood and preserve fibrinogen (i.e., to prevent stage 3 of DIC, in which bleeding begins).
Drug antishock therapy:
- prednisolone – 90-120 mg;
- aminophylline – 2.4% solution in a dosage of 10 ml;
- lasix – 120 mg.
This is a classic triad for preventing shock, helping to increase blood pressure, relieve spasm of small vessels and stimulate kidney function. All drugs are administered intravenously. Also used:
- antihistamines (diphenhydramine and others) - for expansion renal arteries and restoration of blood flow through them;
- narcotic analgesics (for example, promedol) - to relieve severe pain.
An extracorporeal treatment method – plasmapheresis – involves taking blood, purifying it of free hemoglobin and fibrinogen breakdown products, then returning the blood to the patient’s bloodstream.
Correction of functions of systems and organs:
- transfer of the patient to mechanical ventilation (artificial ventilation) in case of a serious condition of the patient;
- transfusion of washed red blood cells - carried out when there is a sharp drop in hemoglobin levels (less than 60 g/l).
Correction of hemostasis:
- heparin therapy – 50-70 IU/kg;
- anti-enzyme drugs (contrical) - prevents pathological fibrinolysis, leading to bleeding in shock.
Treatment of acute renal failure:
- hemodialysis and hemosorption are procedures for purifying blood outside the kidneys, carried out when oligo- or anuria develops and previous measures are ineffective.
Principles and methods of treatment procedures
The basic principle of treating transfusion shock is emergency intensive care. It is important to start treatment as early as possible, only then can we hope for a favorable outcome.
Treatment methods differ fundamentally depending on diuresis indicators:
- Diuresis is preserved and is more than 30 ml/h - active infusion therapy is carried out with a large volume of infused liquid and forced diuresis, before which it is necessary to pre-administer sodium bicarbonate (to alkalinize urine and prevent the formation of hydrochloric acid hematin);
- Diuresis less than 30 ml/h (oligoanuria stage) – strict restriction administered fluid during infusion therapy. Forced diuresis is contraindicated. At this stage, hemosorption and hemodialysis are usually used, since renal failure is severe.
Forecasts
The patient's prognosis directly depends on the early provision of anti-shock measures and the completeness of treatment. Therapy in the first few hours (5-6 hours) ends with a favorable outcome in 2/3 of cases, i.e. patients recover completely.
In 1/3 of patients, irreversible complications remain, developing into chronic pathologies of systems and organs.
Most often this happens with the development of severe renal failure, thrombosis of vital vessels (brain, heart).
If emergency care is not provided in a timely or adequate manner, the outcome for the patient can be fatal.
Blood transfusion is a very important required procedure, which treats and saves many people, but in order for donor blood to bring benefit to the patient and not harm, it is necessary to carefully follow all the rules for its transfusion.
This is done by specially trained people who work in blood transfusion departments or stations. They carefully select donors; after blood collection, blood goes through all stages of preparation, safety testing, etc.
Blood transfusion, like preparation, is a carefully controlled process, carried out only by trained professionals. It is thanks to the work of these people that today this process is quite safe, the risk of complications is low, and the number of people saved is very large.
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