Complications from transfusion of incompatible blood group. Transfusion shock: when someone else's blood becomes poison

– a concept that unites a set of severe pathological reactions that develop as a result of transfusion of blood or its components and are accompanied by dysfunction of vital organs. Post-transfusion complications may include air embolism and thromboembolism; blood transfusion, citrate, bacterial shock; circulatory overload, infection with blood-contact infections, etc. They are recognized on the basis of symptoms that arose during the blood transfusion or shortly after its completion. The development of post-transfusion complications requires immediate cessation of blood transfusion and emergency care.

General information

Post-transfusion complications are severe, often life-threatening, caused by blood transfusion therapy. Every year in Russia about 10 million blood transfusions are performed, and the incidence of complications is 1 case per 190 blood transfusions. To a greater extent, post-transfusion complications are characteristic of urgent medicine (surgery, resuscitation, traumatology, obstetrics and gynecology), occurring in situations requiring emergency blood transfusion and in conditions of time shortage.

In hematology, it is customary to distinguish between post-transfusion reactions and complications. Various types of reactive manifestations caused by blood transfusions occur in 1-3% of patients. Post-transfusion reactions, as a rule, do not cause serious and long-term organ dysfunction, while complications can lead to irreversible changes in vital organs and death of patients.

Causes of post-transfusion complications

A blood transfusion is a serious procedure that involves the transplantation of living donor tissue. Therefore, it should be carried out only after a balanced consideration of indications and contraindications, in conditions of strict adherence to the requirements of the technology and methodology for conducting blood transfusion. Such a serious approach will avoid the development of post-transfusion complications.

Absolute vital indications for blood transfusion are acute blood loss, hypovolemic shock, ongoing bleeding, severe posthemorrhagic anmia, disseminated intravascular coagulation syndrome, etc. The main contraindications include decompensated heart failure, grade 3 hypertension, infective endocarditis, pulmonary embolism, pulmonary edema, stroke, liver failure, acute glomerulonephritis, systemic amyloidosis, allergic diseases, etc. However, if there are serious reasons, blood transfusions can be carried out, despite contraindications, under the guise of preventive measures. However, in this case, the risk of post-transfusion complications increases significantly.

Most often, complications develop with repeated and significant transfusion of transfusion medium. The immediate causes of post-transfusion complications in most cases are iatrogenic in nature and may be associated with blood transfusion that is ABO and Rh antigen incompatible; use of blood of inadequate quality (hemolyzed, overheated, infected); violation of the timing and regime of storage and transportation of blood; transfusion of excessive doses of blood, technical errors during transfusion; underestimation of contraindications.

Classification of post-transfusion complications

The most complete and comprehensive classification of post-transfusion complications was proposed by A.N. Filatov, who divided them into three groups:

I. Post-transfusion complications caused by errors in blood transfusion:

circulatory overload (acute cardiac enlargement)
embolic syndrome (thrombosis, thromboembolism, air embolism)
peripheral circulatory disorders due to intra-arterial blood transfusions

II. Reactive post-transfusion complications:

bacterial shock
pyrogenic reactions

III. Infection with blood-contact infections (serum hepatitis, herpes, syphilis, malaria, HIV infection, etc.).

Post-transfusion reactions in modern taxonomy, depending on their severity, are divided into mild, moderate and severe. Taking into account the etiological factor and clinical manifestations, they can be pyrogenic, allergic, anaphylactic.

Post-transfusion reactions

They can develop within the first 20-30 minutes after the start of blood transfusion or shortly after its completion and last for several hours. Pyrogenic reactions are characterized by sudden chills and fever up to 39-40°C. An increase in body temperature is accompanied by muscle pain, cephalalgia, chest tightness, cyanosis of the lips, and pain in the lumbar region. Usually all these manifestations subside after warming the patient, taking antipyretic, hyposensitizing drugs or administering a lytic mixture.

At the first signs of thromboembolic post-transfusion complications, you should immediately stop the blood infusion, begin oxygen inhalation, thrombolytic therapy (administration of heparin, fibrinolysin, streptokinase), and, if necessary, resuscitation measures. If drug thrombolysis is ineffective, pulmonary embolectomy is indicated.

Citrate and potassium intoxication

Citrate intoxication is caused by both the direct toxic effect of the preservative - sodium citrate (sodium citrate), and a change in the ratio of potassium and calcium ions in the blood. Sodium citrate binds calcium ions, causing hypocalcemia. Usually occurs at high rates of administration of preserved blood. Manifestations of this post-transfusion complication include arterial hypotension, increased central venous pressure, convulsive muscle twitching, and ECG changes (prolongation of the Q-T interval). With a high level of hypocalcemia, the development of clonic seizures, bradycardia, asystole, and apnea is possible. The infusion of 10% calcium gluconate solution can weaken or eliminate citrate intoxication.

Potassium intoxication can occur with the rapid administration of red blood cells or canned blood stored for more than 14 days. In these transfusion media, potassium levels increase significantly. Typical signs of hyperkalemia are lethargy, drowsiness, bradycardia, and arrhythmia. In severe cases, ventricular fibrillation and cardiac arrest may occur. Treatment of potassium intoxication involves intravenous administration of a solution of gluconate or calcium chloride, the abolition of all potassium-containing and potassium-sparing drugs, intravenous infusions of saline, glucose and insulin.

Blood transfusion shock

The cause of this post-transfusion complication is most often the infusion of blood incompatible with AB0 or Rh factor, leading to the development of acute intravascular hemolysis. There are three degrees of transfusion shock: at stage I. systolic blood pressure decreases to 90 mm Hg. Art.; at stage II - up to 80-70 mm Hg. Art.; III Art. - below 70 mm Hg. Art. In the development of post-transfusion complications, periods are distinguished: transfusion shock itself, acute renal failure and convalescence.

The first period begins either during the transfusion or immediately after it and lasts up to several hours. There is short-term excitement, general anxiety, chest and lower back pain, shortness of breath. Circulatory disorders develop (arterial hypotension, tachycardia, cardiac arrhythmia), facial redness, and marbling of the skin. Signs of acute intravascular hemolysis are hepatomegaly, jaundice, hyperbilirubinemia, hemoglobinuria. Coagulation disorders include increased bleeding and disseminated intravascular coagulation syndrome.

The period of acute renal failure lasts up to 8-15 days and includes the stages of oliguria (anuria), polyuria and restoration of renal function. At the beginning of the second period, there is a decrease in diuresis, a decrease in the relative density of urine, after which urination may stop completely. Biochemical changes in the blood include an increase in the level of urea, residual nitrogen, bilirubin, and plasma potassium. In severe cases, uremia develops, leading to the death of the patient. In a favorable scenario, diuresis and renal function are restored. During the period of convalescence, the functions of other internal organs, water and electrolyte balance and homeostasis are normalized.

At the first signs of transfusion shock, the transfusion should be stopped while maintaining venous access. Infusion therapy with blood replacement, polyion, alkaline solutions (reopolyglucin, food gelatin, sodium bicarbonate) begins immediately. Antishock therapy itself includes the administration of prednisolone, aminophylline, and furosemide. The use of narcotic analgesics and antihistamines is indicated.

At the same time, drug correction of hemostasis, organ dysfunction (heart, respiratory failure), and symptomatic therapy are carried out. It is used to remove products of acute intravascular hemolysis. If there is a tendency to develop uremia, hemodialysis is required.

Prevention of post-transfusion complications

The development of post-transfusion reactions and complications can be prevented. To do this, it is necessary to carefully weigh the indications and risks of blood transfusion, and strictly follow the rules for collecting and storing blood. Blood transfusions should be carried out under the supervision of a transfusiologist and an experienced nurse authorized to perform the procedure. Preliminary control samples are required (determination of the blood group of the patient and the donor, compatibility test, biological test). Blood transfusion is preferably carried out using the drip method.

During the day after blood transfusion, the patient is subject to observation with monitoring of body temperature, blood pressure, and diuresis. The next day, the patient needs to undergo a general analysis of urine and blood.

Transfusion shock is a fairly rare but serious complication that develops during transfusion of blood and its components.

Occurs during the procedure or immediately after it.

Requires immediate emergency anti-shock therapy.

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. The release of a large amount of free hemoglobin into the blood 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, 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 is a characteristic symptom of shock and 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 mmHg;
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 is a rapid and dangerous reaction of the 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 serious 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) - to dilate the renal arteries and restore 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 (stage of oligoanuria) – strict limitation of the 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 and necessary procedure that heals and saves many people, but in order for donor blood to bring benefit and not harm to the patient, 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.

Video on the topic

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, decreased 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 are administered (50-150 mg of prednisolone or 250 mg of hydrocortisone) 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).

The most effective is the early addition of complex therapy with 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 pulmonary artery air embolism are sharp chest pain, shortness of breath, severe cough, cyanosis of the upper half of the body, weak rapid pulse, and a 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, use cardiovascular drugs, inhalation of oxygen, infusions 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), donor blood is introduced into the bloodstream 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. For therapeutic purposes, infusions of 10% calcium chloride, isotonic sodium chloride solution, 40% dextrose solution with insulin, and cardiac medications are used.

During a massive blood transfusion, in which blood that is group and Rh compatible from many donors is transfused, due to individual incompatibility of plasma proteins, a serious complication may develop - homologous blood syndrome. Clinical signs of this syndrome are pale skin with a bluish tint and a 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.

Hemotransfusion shock (hemolytic) is a complication that occurs when transfusion of blood that is completely or in any way incompatible. It usually occurs during or at the end of a blood transfusion.

What changes occur in the body?

This condition is characterized by the destruction of donor red blood cells in blood vessels under the influence of antibodies, the release of hemoglobin, biogenic amines, potassium, and tissue thromboplastin. Due to the influence of high concentrations of these substances, the following occurs:

severe vasospasm, there is a rapid transition from contraction to expansion. As a consequence of this, hypoxia occurs, blood microcirculation is impaired, its viscosity increases, and the permeability of the vascular walls increases.
Reduced oxygen content and the presence of acidic metabolites leads to disruption of the body systems and their morphological changes. Blood pH decreases.
The process of hemoglobin breakdown has a devastating effect on renal function. As a result of deposition of hematin hydrochloride in the kidney tubules, as well as spasm and the occurrence of vascular obstruction, acute renal failure develops. This leads to a gradual cessation of the filtering function of the organ, an increase in the level of creatinine and nitrogenous substances in the blood.

Hemotransfusion shock is characterized by the presence of thrombohemorrhagic syndrome. This disorder is provoked by thromboplastins, which penetrate into the blood due to the destruction of red blood cells and activate its coagulation.

With thrombohemorrhagic syndrome, blood clots form in small vessels, causing damage to all organs and systems, especially the lungs, liver, and endocrine glands.

For what reasons does shock occur?

Reasons why hemolytic shock can occur:

mistakes made by doctors when conducting serological tests (determination of blood groups, its Rhesus status) - their incompatibility;
non-compliance with blood transfusion techniques, impaired storage of donor blood, its poor quality (presence of bacteria, hemolysis, inappropriate temperature).

The first reason is the most common - if there is a discrepancy with the ABO (blood group) system or the Rh factor, transfusion shock occurs in 60% of cases.

Clinical picture and symptoms of hemolytic shock

The clinical picture of transfusion shock covers the following signs that appear at the onset of this condition:

increasing anxiety;
the occurrence of short-term excitement;
pain syndrome localized in the thoracic and lumbar region, as well as in the abdomen;
the patient feels chills and cold;
rapid and difficult breathing;
blue discoloration of the skin and mucous membranes.

Pain in the lower back is called a “marker” symptom or pathognostic manifestation characteristic of hemolytic shock. In this condition, circulatory disorders occur, characterized by:

arterial hypotension;
the appearance of sticky cold sweat;
cardiac arrhythmia with signs of acute heart failure;
rapid heartbeat accompanied by pain.

The state of transfusion shock is characterized by sustained hemolysis due to the breakdown of red blood cells. The acquisition of a brown color in urine and a high protein content (according to tests) is also a characteristic symptom. There is also a violation of the blood clotting process, the clinical manifestation of this symptom is manifested in profuse bleeding.

Rare symptoms are:

increased body temperature;
redness or, conversely, paleness of the skin on the face;
nausea and vomiting;
marbling of the skin;
the appearance of seizures;
fecal and urinary incontinence.

Symptoms during a procedure performed under anesthesia may not appear at all or may be mild. Careful observation by doctors of the blood transfusion procedure and emergency care when such a complication occurs is the key to its successful elimination.

Course of transfusion shock

The severity of this condition primarily depends on the patient’s well-being before the blood transfusion and on the volume of blood transfused. When it occurs, the doctor measures the blood pressure level and determines the degree of shock:

first degree – pressure level exceeds 90 mm Hg. Art.;
second degree – pressure from 70 to 90 mm Hg. Art.;
third – the pressure level drops below 70 mm Hg. Art.

The clinical picture of hemolytic shock also includes its periods. If the course of the complication is classic, these phases replace each other. With severe shock, there is a rapid change of symptoms; not all stages can be clearly tracked. The manifestations of transfusion shock itself are:

DIC syndrome (or thrombohemorrhagic syndrome);
hypotension.

The period of oliguria (decreased urine production) and anuria (cessation of urine flow into the bladder) includes:

development of renal block - a condition in which the outflow of urine is difficult;
the appearance of signs of renal failure, cessation of kidney function.

If emergency assistance was provided on time, a phase begins when diuresis is restored and the ability of the renal tubules to filter urine is restored. Then comes the rehabilitation period, during which the parameters of the coagulation system, the level of hemoglobin, bilirubin, and red blood cells are normalized.

Emergency procedures

Algorithm of manipulations in the event of hemolytic shock:

if the patient complains or has symptoms of such a condition, the doctor must stop the transfusion procedure;
the transfusion system needs to be replaced;
installation of a new catheter is required;
providing mask supply of humidified oxygen;
control of the volume of urine excreted;
calling a laboratory assistant, urgently taking a blood test to determine the number of red blood cells, hemoglobin levels, hematocrit, fibrinogen.

Take the following measures whenever possible:

measure central venous pressure;
analyze the content of free hemoglobin in urine and plasma;
determine electrolytes (potassium, sodium) in plasma, as well as acid-base balance;
do an ECG.

In the absence of reagents, a Baxter test can be performed to determine the incompatibility of the blood of the donor and recipient. It consists of injecting up to 75 ml of blood into the patient, followed by taking 10 ml of it (after 10 minutes) from another vein. After this, the tube is closed and centrifuged. Incompatibility can be determined if the plasma becomes pink in color when it is normally a colorless liquid.

Treatment options

Treatment of hemolytic shock and emergency care involve several types of procedures:

Methods of infusion therapy (infusion of rheopolyglucin, polyglucin, gelatin preparations to stabilize blood circulation and restore microcirculation). Treatment includes the administration of a 4% soda solution to create an alkaline reaction in the urine, which prevents the formation of hemin.
Depending on the level of central venous pressure, an appropriate volume of polyion solutions is transfused, removing free hemoglobin and preventing fibrin degradation.
Medication methods are used as first aid. They involve the use of classical drugs to recover from a state of shock - prednisolone, aminophylline, Lasix. Antiallergic medications, for example, tavegil, and narcotic analgesics (promedol) are also used.
Extracorporeal method. This treatment involves removing free hemoglobin, toxins and other products that disrupt the functions of body systems from the patient’s body. Plasmapheresis is used.
Correcting the functions of systems and individual organs - the use of medications depending on the pathology.
Correction of the blood coagulation system in renal failure - treatment to restore kidney function.

Prevention of hemolytic shock consists of:

strict adherence to the rules of blood transfusion;
storing it correctly;
thorough examination of donors;
correct conduct of serological tests.

Prevention is a very important condition when carrying out blood transfusions!

Forecasts

A successful outcome of a shock state is determined by the following points:

timely provision of emergency care;
competent implementation of rehabilitation therapy.

If these conditions were carried out during the first 4-5 hours of the complication, doctors predict in most cases the prevention of severe disturbances in the functioning of the body systems.

It must be stated that proper prevention is the key to successful blood transfusions. If a complication of blood transfusion such as transfusion shock does occur, proper treatment and emergency measures will help the patient recover and then return to a full life.

Details

BLOOD TRANSFUSION COMPLICATIONS

Blood transfusion complications are the most life-threatening for the patient. The most common cause of transfusion complications is blood transfusion that is ABO and Rh-incompatible (approximately 60%). The main and most severe transfusion complication is transfusion shock.

a) Complications from transfusion of blood incompatible with the ABO system. Blood transfusion shock

The reason for the development of complications in most cases is a violation of the rules provided for in the instructions for blood transfusion techniques, methods for determining ABO blood groups and conducting compatibility tests. When transfusion of blood or EVs that are incompatible with the group factors of the ABO system, massive intravascular hemolysis occurs due to the destruction of the donor's red blood cells under the influence of the recipient's agglutinins.

In the pathogenesis of hemotransfusion shock, the main damaging factors are free hemoglobin, biogenic amines, thromboplastin and other hemolysis products. Under the influence of high concentrations of these biologically active substances, a pronounced spasm of peripheral vessels occurs, quickly giving way to their paretic expansion, which leads to impaired microcirculation and oxygen starvation of tissues. An increase in the permeability of the vascular wall and blood viscosity worsens the rheological properties of the blood, which further disrupts microcirculation. The consequence of prolonged hypoxia and the accumulation of acidic metabolites are functional and morphological changes in various organs and systems, that is, a complete clinical picture of shock develops.

A distinctive feature of blood transfusion shock is the occurrence of disseminated intravascular coagulation syndrome with significant changes in the hemostasis and microcirculation system, and gross disturbances in central hemodynamics. It is DIC that plays the leading role in the pathogenesis of damage to the lungs, liver, endocrine glands and other internal organs. The starting point in its development is the massive entry of thromboplastin into the bloodstream from destroyed red blood cells.
Characteristic changes occur in the kidneys: hematin hydrochloride (a metabolite of free hemoglobin) and the remains of destroyed red blood cells accumulate in the renal tubules, which, along with spasm of the renal vessels, leads to a decrease in renal blood flow and glomerular filtration. The described changes are the cause of the development of acute renal failure.

Clinical picture. During complications during blood transfusion that is incompatible according to the ABO system, three periods are distinguished:
■ blood transfusion shock,
■ acute renal failure,
■ convalescence.

Transfusion shock occurs immediately during or after transfusion and lasts from several minutes to several hours. In some cases it is not clinically manifested, in others it occurs with severe symptoms leading to the death of the patient.

Clinical manifestations are initially characterized by general anxiety, short-term agitation, chills, pain in the chest, abdomen, lower back, difficulty breathing, shortness of breath, cyanosis. Pain in the lumbar region is considered a pathognomonic sign for this type of complication. Subsequently, circulatory disorders characteristic of a state of shock gradually increase (tachycardia, decreased blood pressure, sometimes cardiac arrhythmia with symptoms of acute cardiovascular failure). Quite often there are changes in facial color (redness followed by pallor), nausea, vomiting, increased body temperature, marbling of the skin, convulsions, involuntary urination and defecation.

Along with symptoms of shock, one of the early and persistent signs of transfusion shock is acute intravascular hemolysis. The main indicators of increased breakdown of red blood cells are hemoglobinemia, hemoglobinuria, hyperbilirubinemia, jaundice, and liver enlargement. Characteristic is the appearance of brown urine (in the general analysis - leached red blood cells, increased protein content).

A hemocoagulation disorder develops, which is clinically manifested by increased bleeding. Hemorrhagic diathesis occurs as a result of DIC syndrome, the severity of which depends on the degree and duration of the hemolytic process.

When incompatible blood is transfused during surgery under anesthesia, as well as during hormonal or radiation therapy, reactive manifestations may be erased and symptoms of shock are most often absent or mildly expressed.

The severity of the clinical course of shock is largely determined by the volume of incompatible red blood cells transfused, the nature of the underlying disease and the general condition of the patient before blood transfusion. Depending on the level of blood pressure, there are three degrees of transfusion shock:
I degree - systolic blood pressure above 90 mm Hg. Art.
II degree - systolic blood pressure 71-90 mm Hg. Art.
III degree - systolic blood pressure below 70 mm Hg. Art.

The severity of the clinical course of shock and its duration determine the outcome of the pathological process. In most cases, therapeutic measures can eliminate circulatory disorders and bring the patient out of shock. However, some time after the transfusion, the body temperature may rise, gradually increasing yellowness of the sclera and skin appears, and the headache intensifies. Subsequently, renal dysfunction comes to the fore, and acute renal failure develops.
Acute renal failure occurs in three alternating phases: anuria (oliguria), polyuria and restoration of renal function. Against the background of stable hemodynamic parameters, daily diuresis sharply decreases, hyperhydration of the body is noted, and the level of creatinine, urea and plasma potassium increases. Subsequently, diuresis is restored and sometimes increases to 5-6 liters per day, while high creatininemia and hyperkalemia may persist (polyuric phase of renal failure).

Treatment. When the first signs of transfusion shock appear, the blood transfusion is stopped, the transfusion system is disconnected and a system with saline solution is connected. Under no circumstances should the needle be removed from the vein so as not to lose ready venous access.
The main treatment is aimed at removing the patient from a state of shock, restoring and maintaining the function of vital organs, relieving hemorrhagic syndrome, and preventing the development of acute renal failure.

Principles of treatment of blood transfusion shock. Infusion therapy. To maintain blood volume and stabilize hemodynamics and microcirculation, transfusions of blood-substituting solutions are performed (the drug of choice is rheopolyglucin, it is possible to use polyglucin and gelatin preparations). It is also necessary to start administering a soda solution (4% sodium bicarbonate solution) or lactasol as early as possible to obtain an alkaline urine reaction, which prevents the formation of hematin hydrochloride. Subsequently, polyionic solutions are transfused to remove free hemoglobin and to prevent fibrinogen degradation. The volume of infusion therapy should correspond to diuresis and be controlled by the value of central venous pressure.

First-line medications. Classic drugs for the treatment of transfusion shock are prednisolone (90-120 mg), aminophylline (10.0 ml of 2.4% solution) and lasix (100 mg) - the so-called classic anti-shock triad. In addition, antihistamines (diphenhydramine, tavegil) and narcotic analgesics (promedol) are used.

Extracorporeal methods. A highly effective method is massive plasmapheresis (exfusion of about 2 liters of plasma with replacement of PSZ and colloidal solutions) to remove free hemoglobin and fibrinogen degradation products.

Correction of the function of organs and systems. According to indications, cardiac glycosides, cardiotonic drugs, etc. are used. In case of severe anemia (HB below 60 g/l), washed red blood cells of the same blood group as the recipient are transfused. With the development of hypoventilation, transfer to artificial ventilation is possible.
Correction of the hemostatic system. Heparin is used (50-70 IU/kg body weight), PSZ is transfused, and anti-enzyme drugs (contrical) are used.
When recovering from shock and the onset of acute renal failure, treatment should be aimed at improving renal function (aminophylline, Lasix and osmodiuretics), correcting the water and electrolyte balance. In cases where therapy does not prevent the development of uremia, progression of creatininemia and hyperkalemia, hemodialysis is required. In this regard, it is advisable to treat patients with acute renal failure in a specialized department equipped with an “artificial kidney” apparatus.

During the period of convalescence, symptomatic therapy is carried out.
Prevention consists of strict adherence to the rules for performing blood transfusion (careful implementation of all sequential procedures, especially reactions to the compatibility of transfused blood).

b) Complications during blood transfusion that is incompatible with the Rh factor and other erythrocyte antigen systems

Complications caused by incompatibility of transfused blood with respect to the Rh factor occur in patients who are sensitized to the Rh factor. This can occur when Rh-positive blood is administered to Rh-negative recipients who have been sensitized by a previous blood transfusion of Rh-positive blood (or, in women, by pregnancy with an Rh-positive fetus).

The cause of complications in most cases is an insufficiently complete study of the obstetric and transfusion history, as well as failure to comply with or violation of other rules preventing incompatibility for the Rh factor (primarily tests for individual compatibility for the Rh factor).
In addition to the Rh factor Rh0(D), complications during blood transfusion can be caused by other antigens of the Rh system: rh" (C), rh" (E), hr"(c), hr" (e), as well as antigens of the Lewis systems , Duffy, Kell, Kidd, Cellano. The degree of their immunogenicity and significance for the practice of blood transfusion is much lower.

The developing immunological conflict leads to massive intravascular hemolysis of transfused donor red blood cells by immune antibodies (anti-D, anti-C, anti-E) formed during the previous sensitization of the recipient. Next, the mechanism for the development of blood transfusion shock is triggered, similar to ABO incompatibility.

It should be noted that similar changes in the body (except for immune conflict) are observed when a large amount of hemolyzed blood is transfused.
Clinical picture. Clinical manifestations differ from complications of ABO incompatibility in that they have a later onset, a less violent course, slow and delayed hemolysis, which depends on the type of immune antibodies and their titer; When transfusion of blood incompatible with the Rh factor, symptoms appear 30-40 minutes, sometimes 1-2 hours and even 12 hours after the blood transfusion. In this case, the shock phase itself is less pronounced, and its picture is often blurred. Subsequently, a phase of acute renal failure also begins, but its course is usually more favorable.
Treatment is carried out according to the same principles as for ABO incompatibility.
Prevention consists of carefully collecting a transfusiological history and following the rules of blood transfusion.