Blood transfusion complications. Transfusion shock: when someone else's blood becomes poison Citrate and potassium intoxication

Complications arising from blood transfusion can be divided into three groups.

1. Hemolytic.

2. Non-hemolytic.

3. Certain syndromes that occur during blood transfusion.

The most severe and still occurring complications of blood transfusion should be considered hemolytic complications (primarily blood transfusion shock). This complication develops when transfusion of blood of a different group. At the same time, massive hemolysis of red blood cells develops in the vascular bed; the released hemoglobin enters the renal tubules and clogs them, as it settles in acidic urine. Acute renal failure develops.

Subjective signs of transfusion shock are severe lower back pain, dizziness, chills, and loss of consciousness. The clinical picture is dominated by manifestations of cardiovascular failure; systolic blood pressure can drop to 50 mmHg. Art. and below. Along with this, tachycardia is observed, the pulse is so weak in filling and tension that it is determined only in the central arteries. The patient's skin is pale, cold, covered with sticky cold sweat. In the lungs, dry rales are detected by auscultation (signs of interstitial pulmonary edema). The leading symptom is renal failure, which is manifested by a decrease in urine output per hour, less than 10 ml. Urine is cloudy and pink. Laboratory indicators include azotemia (increased creatinine, blood urea), hyperkalemia, acidosis. Depending on the level of blood pressure, there are three degrees of transfusion shock: I- Blood pressure - 90 mm Hg. Art.; II- 70 mm Hg. Art.; III- below 70 mm Hg. Art.

Treatment of transfusion shock should be two-stage.

1. At the first stage, it is necessary to stop the blood transfusion at the first signs of shock, leave the needle in the vein: massive infusion therapy will be carried out through it:

1) for infusion, both crystalloid solutions (5-10% glucose solution, Ringer-Locke solution, saline solution) and drugs that affect the rheological properties of blood (reopolyglucin, solutions of hydroxylated starch) are used. The goal of infusion therapy is to stabilize systolic blood pressure at least at 90–100 mmHg. Art.;

2) it is also necessary to administer prednisolone intravenously in an amount of 60–90 mg, which will increase vascular tone, maintain blood pressure, and correct immune disorders;

3) a bilateral perinephric blockade is performed with a 0.25% solution of novocaine in order to maintain intrarenal blood flow, as well as pain relief;

4) when blood pressure stabilizes, it is necessary to resort to diuretics - Lasix in high doses (240-360 mg) intravenously - in order to reduce the severity of acute renal failure and prevent its progression.

2. At the second stage of care for a patient with transfusion shock, measures from the group of symptomatic therapy are carried out, i.e. they are required only when individual symptoms occur. This group includes:

1) prescription of antihistamines;

2) the use of cardiovascular drugs and analeptics;

3) administration of euffilin intravenously (10 ml of 2.4% solution, slowly);

4) correction of acid-base imbalances;

5) hemodialysis if indicated;

Complications of a blood transfusion nature, such as the most severe - blood transfusion shock, are rightfully considered more dangerous for the patient. Doctors call the most common cause of complications and reactions of a blood transfusion nature a disrupted blood transfusion process that is incompatible with the Rh factor or inappropriate with the ABO system (about 60% of all cases).

Causes, features and changes in organs

The main factors causing complications, in more cases, are violations of the provisions of the rules of blood transfusion, inconsistency with the methods by which blood type is determined, and incorrect sampling when checking for compatibility. During the process of blood transfusion, which turns out to be incompatible according to the group's indications, massive hemolysis occurs inside the vessels, which is caused by the destruction of the donor's red blood cells, which occurs under the influence of agglutinins in the patient.

The pathogenesis of the shock state is characterized by such damaging agents as the main components of hemolysis (amines of biogenic origin, free hemoglobin, thromboplastin). Large concentrations of the listed substances provoke the occurrence of pronounced vasospasm, which is replaced by paretic dilation. This difference is the main reason for the resulting oxygen starvation of tissues and impaired microcirculation.

At the same time, the permeability of the vessel walls increases, the viscosity of the blood increases, which significantly worsens its rheological qualities, and further reduces the level of microcirculation. Due to hypoxia for a long time, and the simultaneous concentration of acidic metabolites, dysfunctions of organs and systems, as well as their morphological changes, appear. The stage of shock begins, at which immediate, emergency help is required.

The difference that characterizes blood transfusion shock is disseminated intravascular coagulation syndrome, which is accompanied by significant changes in hemostasis and microcirculatory process. All hemodynamic parameters change sharply. The syndrome is considered the main factor in the pathogenetic picture of disorders in the lungs, endocrine glands and liver. The main provocation of its development - the highest point of the clinical picture - is the full penetration of thromboplastin into the bloodstream from destroyed red blood cells - erythrocytes.

The kidneys at this time undergo characteristic changes associated with the concentration in the renal tubules of hematin hydrochloride (a metabolite of free hemoglobin) and the remnants of destroyed red blood cells. In combination with simultaneous spasm of the renal vessels, these changes cause a decrease in renal blood flow and a decrease in glomerular filtration. This combined clinical picture of disorders reveals the main reason why acute renal failure develops.

During the clinical picture of complications encountered during blood transfusion, there are 3 main periods:

  • the actual onset of shock;
  • the occurrence of acute renal failure;
  • the process of disappearance of clinical signs of shock - convalescence.

Shock of a blood transfusion nature occurs specifically during the transfusion process, and/or immediately after it. It can last for a few minutes or for several hours. In some cases, shock does not manifest itself in a clear clinical picture, and is sometimes accompanied by pronounced manifestations that can be fatal.

Symptom Clinic

Signs of the onset of shock are:

  • general anxiety;
  • sudden excitement for a short period;
  • feeling of cold, chills;
  • painful sensations in the abdomen, chest, lower back;
  • heavy breathing and shortness of breath;
  • the appearance of a bluish tint of the skin and mucous membranes, signs of cyanosis.

Doctors call the appearance of pain in the lumbar region a “marker” symptom, or a pathognostic (pathognomonic) manifestation that characterizes this pathological condition.

It is accompanied by a gradual (or sharp) increase in disturbances of circulatory origin, signs of a state of shock (the appearance of tachycardia, a decrease in blood pressure, a failure of the heart rhythm with manifestations of acute cardiovascular failure).

Such manifestations as:

  • change in facial skin color - redness, pallor;
  • vomit;
  • the appearance of temperature;
  • “marbling” of the skin;
  • convulsions;
  • involuntary defecation and urination.

Doctors consider persistent hemolysis of blood vessels to be one of the symptoms of the early manifestation of a state of shock, with indicators of the breakdown of red blood cells - signs of hemoglobinemia or hemoglobinuria, hyperbilirubinemia, jaundice (enlarged liver). The urine turns brown, tests show a high protein content and destruction of red blood cells. The development of disturbances in the hemocoagulation process also begins sharply, the clinical picture of which is manifested by profuse bleeding. The severity and level of hemorrhagic diathesis depend on the same factors of the hemolytic process.

Doctors should be sure to monitor the blood transfusion process during operations performed under anesthesia, as symptoms may be mild or not appear at all.

Course of the pathology

The extent of the condition largely depends on the volume of incompatible red blood cells transfused, the type of primary disease and the condition of the patient before the blood transfusion procedure.

The level of pressure determines to what degree experts classify transfusion shock:

  • 1st degree shock occurs when systolic blood pressure exceeds 90 mmHg. Art.
  • Stage 2 is characterized by pressure in the range of 71 mm Hg. Art. up to 90 mm Hg Art.
  • Stage 3 is diagnosed when systolic blood pressure is less than 70 mmHg. Art.

In most cases, timely assistance and properly performed medical procedures make it possible to stop the circulatory disorder, bring the patient out of shock, and eliminate its consequences.

Although characteristic is considered to be an increase in temperature some time after the transfusion, the appearance of yellowness of the sclera and skin, with a gradual increase, and increased headache. After a certain period of time, functional disorders in the kidney area may begin, and acute renal failure may develop. This pathology continues through alternating stages: anuria-polyuria-recovery period.

When hemodynamic factors are stable, the following occurs:

  • a sharp decrease in daily diuresis;
  • state of overhydration of the body;
  • increased levels of creatinine, plasma potassium and urea.

Principles and methods of treatment procedures

At the first manifestation of symptoms of transfusion shock, the blood transfusion process is immediately stopped, the drip for transfusion is disconnected, and saline solution is started to be infused. In this case, it is strictly forbidden to remove the needle from the vein, since you may lose ready-made access to the vein.

The main focus of recovery from shock is to restore all functions of the body, maintain them, relieve the syndrome, and eliminate the consequences in order to prevent further development of disorders.

Types of treatment procedures

  • Infusion therapeutic methods. To stabilize hemodynamics and restore microcirculation, blood replacement solutions are transfused - rheopolyglucin is considered the best option (polyglucin and gelatin preparations are also used).

In addition, a 4% solution of sodium bicarbonate (soda solution) or lactasol is started to be administered as early as possible in order to initiate an alkaline reaction in the urine, which is an obstacle to the formation of hematin hydrochloride. In the future, it is advisable to transfuse solutions of polyions, which promote the excretion of free hemoglobin and also prevent the degradation of fibrinogens. The volume of the infusion procedure is controlled by the value of central venous pressure.


Forecasts

The patient’s future condition, and often life, depends on how timely and competently the rehabilitation therapy is carried out and all the appropriate measures are taken. If all procedures are carried out correctly in the first period (4-6 hours), doctors’ forecasts are positive, as is the patient’s complete return to a full-fledged lifestyle. Moreover, timely assistance in 75% of cases prevents severe organ dysfunction.

Post-transfusion reactions:

Allergic;

Pyrogenic;

Antigenic (non-hemolytic);

Blood transfusion complications

All complications after blood transfusion can be divided into 3 groups.

1. Mechanical errors

Air embolism

Thromboembolism

Thrombophlebitis

Circulatory overload

2. Reactive complications

2.1Blood transfusion shock as a result of:

Incompatibility of components according to the AB0 system

Incompatibilities of components according to the Rh system

Incompatibility of components with respect to antigens of other serological systems

2.2. Post-transfusion shock due to transfusion of poor-quality medium

Bacterial contamination

Overheating, hypothermia, hemolysis

Expiration of shelf life

Violation of storage temperature conditions

2.3. Anaphylactic shock

2.4. Citrate shock (with the simultaneous transfusion of a large amount of canned blood).

2.5. Massive transfusion syndrome

2.6. Acute pulmonary failure syndrome

3. Transmission of infectious diseases

3.1. Syphilis infection

3.2. Malaria infection

3.3. Viral hepatitis infection

3.4. HIV infection

3.5. Infection with herpes viral infections

Blood transfusion reactions

In addition to complications after blood transfusion, a person may experience hemotransfusion reactions , which, unlike complications, do not pose a threat to life. These include:

A) pyrogenic reactions

B) allergic reactions.

Pyrogenic reactions arise due to the ingress of pyrogens along with blood components. Pyrogens are produced by many bacteria, as well as as a result of poor asepsis when collecting blood. The reaction is manifested by increased body temperature, chills, and headache.

Allergic reactions appear a few minutes after the start of transfusion, due to sensitization to plasma proteins and various immunoglobulins. Manifested by shortness of breath, suffocation, skin rashes, swelling of the face, and urticaria. Occur more often during plasma and albumin transfusions.

Antigenic (non-hemolytic reactions) as a result of sensitization of the recipient with antigens during repeated transfusion, during pregnancy.

Manifested by chills, vomiting, lower back pain, shortness of breath, urticaria, temperature 39-40, in severe cases there may be bronchospasm, acute respiratory failure, loss of consciousness.

Prevention: compliance with the rules of asepsis and antisepsis when collecting and storing blood.

Careful collection of transfusion history.

The use of blood components with less pronounced reactive properties.

Individual selection of blood transfusion media.

Treatment.

Stop the transfusion without leaving the vein, add antihistamines, glucocorticosteroids, adrenaline, anti-shock solutions, blood substitutes, cardiac glycosides, fight against hyperthermia.

Mechanical errors

1. Air embolism

An air embolism occurs when the system is not filled correctly, due to air entering the patient’s vein along with blood during transfusion.

1.as a result of improper filling of the system

2. as a result of untimely stop of transfusion during blood transfusion under pressure.

Clinic: difficulty breathing, shortness of breath, pain and a feeling of pressure behind the sternum, cyanosis of the face, tachycardia.

Treatment: massive air embolism with the development of clinical death requires immediate resuscitation measures - chest compressions, mouth-to-mouth artificial respiration, calling a resuscitation team.

Prevention consists in strict compliance with all technical 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.

2. Thromboembolism- embolism with blood clots in the pulmonary arteries.

Causes: separation of a blood clot from varicose veins of the lower extremities, separation of blood clots forming in the vein near the tip of the needle, entry of blood clots formed in the transfused blood.

Pulmonary embolism clinic: 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 patients develop collapse - cold sweat, drop in blood pressure, rapid pulse.

Treatment activators of fibrinolysis - streptases (streptodecases, urokinases),

Continuous intravenous administration of heparin (25,000-40,000 units per day), immediate jet administration of at least 600 ml of fresh frozen plasma under the control of a coagulogram, euphyllin, cardiac glycosides and other therapeutic measures are indicated.

Prevention correct preparation, stabilization of blood, use of disposable systems for transfusion using filters. In case of needle thrombosis, repeated puncture of the vein with another needle is necessary; in no case should you try to restore the patency of the thrombosed needle in various ways.

3. Thrombophlebitis the formation of blood clots in the inflamed vein.

Cause: violation of aseptic rules, multiple infusion punctures.

Clinic: pain along the vein, redness, swelling, upon palpation - painful compaction along the vein.

Treatment: dressings with heparin ointment, alcohol compresses.

4. Circulatory overload SHF manifests itself and develops more often in patients with myocardial damage.

Cause: the introduction of a large amount of fluid in a short period of time and, as a result, expansion and cardiac arrest.

Clinic: difficulty breathing, chest tightness, facial cyanosis, decreased blood pressure, tachycardia, arrhythmias, increased central venous pressure.

Help: stop infusion, intravenous cardiac glycosides, diuretics, vasopressor amines (mesaton).

Reactive complications:

Blood transfusion shock

Causes:

Develops as a result of blood transfusion:

  1. incompatible according to the ABO system (during a biological test or during a blood transfusion);
  2. Rh incompatibility – (spasm after blood transfusion or after 6-12 hours the course is less violent).

    Clinically, transfusion shock manifests itself:

  • Short-term excitement;
  • Pain in the chest, abdomen, lower back;
  • Tachycardia occurs;
  • Blood pressure decreases;
  • The skin is first hyperemic, then suddenly becomes pale. If a person is under anesthesia, then signs of developing shock are severe bleeding from the surgical wound, persistent low blood pressure, and in the presence of a urinary catheter, the appearance of cherry or black urine.
  • After 1-2 days, urine the color of “meat slop” appears;
  • The amount of urine “oliguria” decreases;
  • Urine production stops (anuria).

    Algorithm of the nurse's action

    Actions Target
    1. stop intravenous infusion of donor blood - prevention of worsening transfusion shock
    2. maintain contact with the vein — for infusion antishock therapy (as prescribed by a doctor)
    3. call a doctor — assessing the recipient’s condition, giving prescriptions
    4. measure A/D and count pulse — monitoring the recipient’s condition
    5. provide a flow of fresh air — prevention of hypoxia
    6. Perform bladder catheterization (as prescribed by a doctor) - monitoring kidney function and collecting urine for clinical analysis (detecting hemolysis of red blood cells)
    7. fulfillment of doctor’s medication prescriptions

    solution of promedol 1% 1 ml

    mezaton 2 ml or ephedrine 5% 2 ml or norepinephrine 0.2% 1 ml, solution of prednisolone 30-60 mg or hydrokartisone 125 mg;

    diphenhydramine 1% 2 ml or pipolfen 2.5% 2 ml or tavegil 2.5%, calcium chloride 10% 10ml, aminophylline 2.4% 10ml

    diuretics: 20% mannitol (15-50 g) lasix 100 mg once, up to 1000 per day

    antishock solution (polyglucin, gelatinol,

    4% sodium bicarbonate solution.

    According to indications, the patient is connected to hemodialysis.

    for pain relief

    to increase blood pressure

    to relieve spasm from the renal arteries

    to reduce the deposition of hemolysis products in the distal tubules of the nephron

    to maintain blood volume and stabilize blood pressure

    Correction of acid-base balance

    Removal from the body of substances that led to the development of shock

    8. repeated A/D measurement and pulse counting — monitoring the effectiveness of measures to eliminate blood transfusion shock

    Citrate shock

    Occurs as a result of transfusion of large quantities of blood prepared with sodium citrate, which binds calcium, causing hypocalcemia.

    Clinic: a metallic taste in the mouth, pain behind the sternum, interfering with inhalation, a drop in blood pressure, bradycardia and convulsions (twitching of the muscles of the lips, tongue, lower leg, in severe cases - respiratory failure up to stoppage and asystole.

    For prevention development of citrate shock during transfusion of large doses of blood and plasma, after each transfusion 500 ml of blood must be injected into a vein with 10%-10 ml of calcium chloride or calcium gluconate. Introduce the medium at a rate of 40-60 drops/min.

    Treatment: stop administration, 10 ml of calcium chloride or 10-20 ml of calcium gluconate must be injected into the vein and monitor the ECG.

    Hypocalcemia may occur during rapid transfusion of long-term stored blood (more than 14 days);

    Clinic: bradycardia.

    Prevention: Slow, drip administration (50-70 ml/min.)

    The use of washed red blood cells,

    Massive transfusion syndrome

    It occurs when up to 3 liters of whole blood from many donors are introduced into the recipient’s bloodstream in a short period of time.

    Clinic: bradycardia, ventricular fibrillation, asystole, wound bleeding, acidosis, anemia, development of hepatic renal failure.

    Help: The use of fresh frozen plasma, rheopolyglucin, heparin, cardiac glycosides, aminophylline, protease inhibitors, plasmapheresis.

    Prevention: Avoid transfusion of whole blood in large quantities.

    Transfusions only for strict indications

    Use of blood components and products.

    The use of the patient's autologous blood (prepared before a planned operation) or taken from the patient's body cavities.

    Acute pulmonary failure syndrome

    After 3-7 days of storage, microclots form in the blood and aggregation of formed elements occurs. The lungs are the first filter on the path of transfused blood. The capillaries of the lungs retain microclots, which leads to thromboembolism of the pulmonary capillaries, and subsequently to the development of acute pulmonary failure.

    Clinic: shortness of breath, cyanosis, tachycardia, moist rales, increased breathing of auxiliary muscles.

    Prevention: use for transfusion of disposable systems using filters, blood transfusion with a shelf life of less than 7-10 days.

    Septic shock

    Occurs when transfusion of poor quality blood occurs,

    Clinic: characterized by a sharp increase in temperature to 39-41ºС, chills, drop in blood pressure, abdominal pain, cramps, vomiting

    Symptoms of multiple organ failure: anuria, enlarged liver, yellowness of the skin, dullness of heart sounds.

    Prevention: visual macroscopic assessment of transfused blood. Blood transfusion with a valid expiration date.

    Treatment: cessation of transfusion, administration of large doses of antibiotics, detoxification therapy, antishock therapy, corticosteroids, cardiac glycosides, plasmapheresis.

Blood transfusion shock is a collective concept that unites a number of similar clinical conditions that arise in response to extremely strong effects on the body of various factors, with hypotension, a critical decrease in blood flow in tissues, the development of tissue hypoxia and hypothermia.

When transfusing blood, the possible development of this severe condition should be taken into account.

Etiology

This transfusion complication occurs due to violation of the rules for manipulating blood or its components, errors in determining the blood group and the compatibility of the recipient’s and donor’s blood components.

The main factors leading to the development of a shock state are: the ABO antigenic system and the Rh factor system. There are also a huge number of other antigenic systems, but they rarely give such a complication.

Pathogenesis

Shock is an allergic reaction of type II - cytotoxic. It develops immediately during the transfusion or after a certain time after the procedure.

The development of hemolysis inside the vessels during blood infusion is possible if red blood cells begin to be destroyed due to incompatibility with the antigenic profile of the recipient's plasma.

The basis for the development of a shock state is the breakdown of red blood cells. This process leads to the release of specific substances that provoke spasm of blood vessels, and then their pathological dilation. The permeability of the vessel wall increases, which leads to the release of plasma into the tissue and thickening of the blood.

The release of a large number of substances into the blood that promote the formation of blood clots leads to the development of disseminated intravascular coagulation syndrome. Its pathogenesis is characterized by an initial increase in blood clotting with the formation of many small blood clots.

After consumption, when the blood can no longer clot, massive bleeding occurs. There is a disruption of blood flow in small vessels, which leads to insufficient oxygen supply to the internal organs, and, consequently, to their damage.

All organs suffer, including the kidneys. The breakdown products of hemoglobin accumulate in their glomeruli, which leads to a drop in the rate of blood filling and the development of kidney failure.

Shock clinic

There are 3 stages that appear in case of incompatibility:

  1. Actually a shock.
  2. Pathology of the kidneys, which is expressed by acute failure.
  3. Recovery period.

The state of shock can last from several minutes to a couple of hours. It is possible to trace a clear relationship between the appearance of symptoms of transfusion shock and the transfusion

The patient's condition is initially characterized by a feeling of anxiety, causeless agitation, pain in the chest, abdominal and lumbar pain, chills, difficulty breathing, and bluish skin.

Low back pain is one of the most characteristic features of the development of this complication. Subsequently, vascular disorders begin to appear.

Characteristic symptoms:

  1. Tachycardia.
  2. A sharp decrease in blood pressure.
  3. The appearance of signs of acute heart failure.

A common manifestation is changes in the patient’s facial skin (redness followed by pallor), skin spotting, dyspeptic disorders, increased body temperature, and inability to control urination.

Symptoms of blood transfusion shock - which develops inside the vessels, and. Its manifestations:

  • Free hemoglobin to the blood.
  • Hemoglobin in urine.
  • Hyperbilirubinemia.
  • Jaundice.
  • Hepatomegaly.
  • The color of urine changes: a brownish tint appears (in urine analysis - proteinuria and altered red blood cells).

As a result of hemolysis and the development of disseminated intravascular coagulation syndrome, a disruption of the blood coagulation system occurs, which is expressed by increased bleeding and the occurrence of hemorrhagic diathesis.

When blood is infused during surgeries performed using general anesthesia, symptoms may be erased. Surgeons may notice abnormal bleeding from the wound and urine the color of meat slop.

Anesthesiologists focus on a sharp drop in pressure. The duration and severity of pathological processes depend on the number of incompatible red blood cells injected, the characteristics of the pathological process in the patient and his state of health before the transfusion.

Degrees

There are 3 degrees of shock, the definition of which is based on systolic pressure:

  • I Art. — SBP above 90 mm Hg. Art.
  • II Art. — SBP ranges from 71 to 90 mm Hg. Art.
  • III Art. — SBP below 70 mmHg. Art.

The possible outcome of shock is directly proportional to the course and duration of the reduced pressure. Most often, anti-shock measures help reverse changes in blood vessels and prevent complications of this condition.

Associated symptoms

After a while, there may be an increase in temperature, yellow coloration of the eyeballs, and constant headaches. This indicates the development of acute renal failure (ARF). It manifests itself in the form of three subsequent phases: oligo- or anuria, polyuria and the recovery phase.

Against the background of unchanged hemodynamic conditions, a sharp decrease in the amount of urine excreted is observed, initial signs of hydration of the body are observed, and the level of creatinine, urea and potassium in the plasma increases (oliguria phase).

After some time, diuresis is restored. Despite this, high levels of trace elements in the blood may persist (polyuria phase). In the future, with a favorable outcome, the filtration capacity of the kidneys is restored.

This pathological condition ends with the restoration of all pathological processes in the body (the period of convalescence).

Transfusion shock is a condition that requires emergency care. The algorithm of actions in this situation can be presented as follows:

  • Removing the patient from a state of shock.
  • Measures to prevent pathological changes in important organs and correct them.
  • Relief of developing DIC syndrome.
  • Prevention of development of acute renal failure.

If adverse symptoms appear, the first action of the nurse or doctor is to stop the transfusion procedure and replace the system with saline solutions.

The most important factor is time: the faster medical interventions are performed, the better the prognosis for the patient.

Infusion therapy

All shock treatment regimens begin with infusions.

First of all, it is necessary to replenish the circulating blood volume (CBV) and restore hemostatic function (dextrans with a molecular weight of 40-70 thousand units are used - rheopolyglucin, gelatinol).

Early infusion of a 4% solution of sodium bicarbonate or lactosol is also indicated. In this way, compensation for metabolic acidification of the blood is ensured, and the synthesis of hematin hydrochloride does not occur.

Subsequently, a crystalloid infusion is performed (with a solution of 0.9% sodium chloride or Ringer's solution) to reduce the amount of free Hb and prevent the destruction of fibrinogen. The amount of infused drugs must be controlled by the volume of diuresis and pressure values.

Drug therapy

It is necessary to raise the patient's blood pressure, as well as ensure normal renal blood flow. A triad of standard antishock drugs: prednisolone (a glucocorticosteroid to increase blood pressure), furosemide (a diuretic) and aminophylline (a phosphodiesterase inhibitor). Antihistamines and opioid painkillers (fentanyl) are also used.

Efferent methods

An effective method of anti-shock therapy is plasmapheresis - removal of about 2 liters of plasma followed by infusion of fresh frozen plasma and colloid solutions. Symptomatic correction of disorders of the internal organs.

If necessary, medications are prescribed that stimulate the activity of important body systems. If symptoms characteristic of a decrease in the respiratory function of the lungs appear, the patient may be transferred to a ventilator. In case of severe anemia (hemoglobin concentration less than 70 g/l), it is possible to transfuse washed red blood cells compatible in blood group with the patient's red blood cells.

Correction of the hemostatic system

Anticoagulants are used, transfusions of fresh frozen plasma and antienzyme drugs (Gordox) are performed to inhibit fibrinolysis.

Since the development of acute renal failure is possible in the future, treatment of transfusion shock is also aimed at correcting the functional state of the kidneys. Furosemide and mannitol are used and correction is performed with crystalloid solutions.

If there is no effect, hemodialysis may be used. During the recovery period, specific symptoms are treated.

Prevention

To avoid the development of shock during transfusion, you need to follow some rules (this is a kind of prevention):

  • Before a blood infusion, you need to collect a detailed history, in which it is important to focus on previous transfusions or infusions.
  • Comply with all rules for conducting compatibility tests (if there are errors or inaccuracies, repeat the procedure).

Indications for blood transfusion

In addition to the development of a state of shock, other complications associated with the infusion of blood components are also possible. These may be pyrogenic or allergic reactions, thrombosis or acute aneurysm. Therefore, it is important to treat it carefully and use it only for certain indications.

Absolute readings:

  1. Massive blood loss (more than 15% of blood volume).
  2. Shock states.
  3. Severe traumatic operations with heavy bleeding.

Relative readings:

  1. Anemia.
  2. Severe intoxication.
  3. Disturbance of the hemostasis system.

Contraindications

There are also a number of prohibitions. Absolute contraindications:

  • Acute heart failure.
  • Myocardial infarction.

Relative contraindications:

  • Heart defects.
  • The presence of blood clots or emboli in the vascular bloodstream.
  • Cerebral circulation disorders.
  • Tuberculosis.
  • Kidney or liver failure.

It is important to know that if there are absolute indications, then blood or its components are transfused in any case. Even if there are contraindications.

Conclusion

Transfusion shock is a serious and not the only complication that occurs during transfusions, therefore, even in an emergency, all necessary tests should be carefully carried out and the rules of blood transfusions should be followed.

If signs of transfusion shock are observed, it is important to begin treatment as quickly as possible, which will improve the prognosis for the patient.

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.