COMPLICATIONS OF BLOOD TRANSFUSION

Blood transfusion is considered to be a safe method of treatment if all the rules and regulations are carefully followed. Violation of the regulations, underestimation of contraindications, and technical errors can lead to serious post-transfusion reactions and complications.

Blood transfusion reactions. Unlike complications, these do not result in serious bodily dysfunctions and are therefore usually not life-threatening. They may be either pyrogenic or anaphylactic and occur promptly after transfusion. Their manifestations are as follows: fever, malaise and adynamia, rigors, headache, itching, Quincke's oedema.

Half of all the reactions and complications are due to pyrogenic reactions which may be mild, moderate or severe. In a mild reaction, the body temperature increases by 1 °C and the patient complains of headache and muscle pain. A moderate reaction involves rigors, a body temperature increase by 1, 5-2 °C, tachycardia and dyspnoea. Severe reactions are characterised by rigors, a body temperature rise by more than 2 °C to as high as 40 °C, severe headaches, pains in the muscles and bones, tachycardia, labial cyanosis and dyspnoea.

The pyrogenic reactions are mediated by the products of plasma protein decay, leucocytes of the donor's blood, products of microbial activity, breakdown of plasma and blood particles left over from previous transfusions.

In a pyrogenic reaction, the patient should be covered with warm clothing and hot water bottles applied to the feet, he/she should be given hot drinks as well as paracetamol. If it is a mild or moderate reaction, these measures may suffice. In severe reactions, apart from the above-mentioned measures, the patient is given promedol, analgin in injections, 5-10 ml of 10% calcium chloride and solutions of glucose are given intravenously. To prevent pyrogenic reactions in patients with severe anaemia, washed and frozen red blood cells should be transfused.

Allergic reactions because of the recipient's body being sensitive to immunoglobulins occur mostly in repeated transfusions. Clinical manifestations of anaphylaxis include rigors, fever, malaise, urticaria, dyspnoea, suffocation, nausea, vomiting. Antihistamines and desensitising agents (dimedrol, suprastin, calcium chloride, corticosteroids) are used, in case of vascular insufficiency vasopressors are administered.

Complications of blood transfusion. If blood incompatible mainly by the ABO group and Rh systems is transfused, the patient develops blood transfusion shock resulting from rapid intravascular haemolysis of the transfused blood. The main reasons of incompatibility of blood are technical errors.

The three degrees of shock are identified: degee 1 - a fall in systolic blood pressure to 90 mm Hg, degee 2 - a fall in systolic blood pressure to 80-70 mm Hg, degee 3 - a fall in systolic blood pressure below than 70 mm Hg.

The following periods are identified in the course of blood transfusion shock:

1) blood transfusion shock per se;

2) oliguria and anuria;

3) restoration of diuresis;

4) recovery.

Clinical symptoms and signs of shock can occur at the beginning of the procedure following transfusion of only 10-30 ml of blood, at the end of transfusion or immediately after transfusion. These usually involve restlessness, pain and a sensation of retrosternal uneasiness, lumbar or muscle pain, and sometimes rigors; the patient is dyspnoeic, tachycardic and hypotensive, his/her face being hyperaemic, sometimes pale or cyanotic. The may also experience nausea, vomiting, enuresis or even encopresis. Fulminant development of these manifestations may be fatal.

If incompatible, blood is transfused to a surgical patient under general anaesthesia during operation these signs of shock may manifest mildly, if at all. In such cases incompatibility is identified by the increase or decrease in blood pressure, cyanosis of the skin and visible mucus layer, an increase sometimes very pronounced bleeding tendencies of tissues in the operation wound. When the patient recovers consciousness, they may have tachycardia, hypotension, and acute respiratory arrest.

Clinical manifestations of blood transfusion shock after transfusing Rh incompatible blood occur after 30-40 minutes, and occasionally several hours after transfusion.

During recovery from blood transfusion shock, they can develop acute renal failure. Oliguria, hyposthenuria and progressing uraemia may be evident in the first few days. Progression of acute renal failure can lead to a cessation of urine production, or anuria. The levels of products of protein degradation, urea and bilirubin start to increase in the blood. In severe cases the period can last for 8-30 days. In favourable situations, the signs of renal failure subside, diuresis is gradually restored and the patient enters the recovery period. If uraemia sets in, death usually occurs within 3-15 days.

With the early signs of blood transfusion shock, transfusion must be stopped and intensive therapy started.

1. Cardiovascular agents like strophanthin, corglucon (in cardiovascular failure), norepinephrine (in hypotension), dimedrol, suprastin or diprazin are used as antihistamines, corticosteroids (50-150 mg of prednisolone or 250 mg of hydrocortisone) are given to stimulate vascular tone and inhibit the antigen - antibody reaction.

2. To accelerate the restoration of circulation rheopolyglukin and saline solutions are given.

3. To remove the products of haemolysis hydrocarbonate and sodium lactate are given.

4. To support diuresis haemodes, lasix and mannitol are given.

5. To reduce spasm of the renal vessels an emergency bilateral paranephric novocain (procaine) blockage is done.

6. Oxygen therapy is given and in respiratory failure artificial ventilation of the lung is provided.

7. Ineffective drug therapy of acute renal failure and progressing uraemia is an indication for haemodialysis or haemabsorption.

Bacterial - toxic shock only rarely occurs. It is caused by contamination of the blood during its preparation or storage. Complications occur either during transfusion or within 30-60 minutes. Rigors occur suddenly, fever, anxiety, semi-consciousness, fast and thready pulse, marked hypotension, enuresis and encopresis.

Bacteriological investigation of the blood left after transfusion plays a major role in confirmation of the diagnosis.

Treatment is by means of immediate antishock transfusion, detoxication and antibacterial substances, analgesic and vasoconstrictors (norepinephrine), solutions with rheologic and desintoxicating properties (rheopolyglukin, haemodes), electrolyte solutions, anticoagulants, broad-spectrum antibiotics (aminoglycosides, cephalosporins).

Most effective is the complex therapy with exchange blood transfusion.

Air embolism. This may be due to defective of transfusion techniques, namely incorrect filling of the blood giving system which results in air having been left in the tubes, when transfusion under pressure is not duly stopped. In such situations air can enter the patient's vein, reach the right cardiac chambers and obstruct the pulmonary artery and its branches. Air embolism may result from an instant entry of as much as 2-3 cm³ to the vein. Clinical signs of air embolism of the pulmonary artery are severe chest pain, dyspnoea, cough, cyanosis of the upper trunk, fast weak pulse and hypotension. The outcome is often unfavourable. With the early signs of embolism, transfusion must be stopped and resuscitation started: artificial ventilation, cardiovascular drug therapy.

Thromboembolism secondary to blood transfusion results from migration of a vein thrombus. The clinical features of this complication are similar to those of air embolism. Small thrombi obstruct smaller branches of the pulmonary artery causing lung infarction, whose clinical signs being as follows: chest pain, cough (progressing from being dry to that with bloody sputum), fever. Chest x-rays show signs of focal pneumonia.

With the early signs of thromboembolism transfusion must be stopped and cardiovascular drugs, oxygen, fibrinolysin, streptokinase and heparin given.

Transfusing an amount of donor's blood above 40-50% of the circulating blood volume (i.e. about 2-3 l) within a short period (up to 24 hours) is referred to as massive blood transfusion. In transfusing such an amount of blood (especially after long storage) from different donors there is a risk of massive blood transfusion syndrome. The factors that contribute to its development are as follows:

• exposure of blood to cold (refrigerator);

• administration of excessive amounts of sodium citrate and products of blood decay (e.g. potassium, ammonia), which accumulate in plasma during its storage;

• administration of excessive amounts of fluid that enters the blood stream and overloads the cardiovascular system.

Acute cardiac dilation of the heart results from large amounts of preserved blood being infused rapidly or under pressure. The clinical picture includes dyspnoea, cyanosis, right hypochondriac pain, fast weak arrhythmic pulse, arterial hypotension with venous hypertension. When there are signs of cardiac overload, transfusion should be stopped, cardiac drugs (strophanthin, corglucon) as well as vasoconstrictors and 10 ml of 10% calcium chloride is given.

Massive transfusion may cause citrate intoxication. The toxic dose of sodium citrate is considered to be as much as 0, 3 g/kg. Sodium citrate interacts with calcium ions in the recipient's blood and causes hypocalcaemia, which, combined with accumulation of citrate in the blood, leads to severe intoxication. The signs of the latter are as follows: tremor, twitching, fast pulse, hypotension, arrhythmia. In severe cases dilation of the pupils, cerebral and pulmonary oedema can be evident. To prevent citrate intoxication, it is required that following transfusion of each 500 ml of preserved blood 5 ml of 10% calcium chloride be given. To neutralise sodium, citrate solutions of calcium gluconate and calcium chloride are administered.

The transfusion of blood that has been stored for a long period (more than 10 days) can be followed by severe potassium intoxication that leads to ventricular fibrillations and further to cardiac arrest. Clinically, hyperkalaemia involves bradycardia, arrhythmia, myocardial atony. Prevention of potassium intoxication consists in transfusion of blood that has been stored for a short time (maximum 3-5 days) or the use of washed and frozen red blood cells. As a therapeutic measure, 10% calcium chloride, normal saline, 40% glucose with insulin as well as cardiac preparations are given.

In massive blood transfusions when compatible blood of the same group and Rh, obtained from different donors is transfused, individual incompatibility of plasma proteins can cause the development of a serious complication known as homological blood syndrome. Clinical signs of the syndrome include skin pallor with bluish discoloration, dyspnoea, anxiety, cool skin on touch, fast and weak pulse, arterial hypotension with venous hypertension. Multiple rhonchi are audible on auscultation of the lungs. Haematocrit falls and the circulating blood volume dramatically decreases, although sufficient blood has already been transfused; the blood clotting time slows down. A microcirculatory defect, red cell stasis, microthrombosis and deposition of blood all contribute to the pathogenesis of this syndrome.

Prevention of the syndrome of homological blood involves replacement of blood loss depending on the circulating blood volume and its components. It is important to combine donor's blood with anti-shock solutions (polyglukin, rheopolyglukin) that improve the rheologic properties of blood (fluidity) because of dilution of blood, reduction of its viscosity and acceleration of microcirculation.

In massive transfusion it is not necessary to fully replace the concentration of haemoglobin. To maintain the transport function of blood haemoglobin blood levels of at least 75-80 g/l will suffice. To replace the deficit in the circulating blood volume, solutions must be used. Of great importance in prevention of the syndrome of homological blood is autotransfusion of blood and plasma, i.e. the transfusion of absolutely compatible transfusion solutions as well as washed and frozen red blood cells.

Infectious complications. These include acute infections (e.g. influenza, measles, typhoid, brucellosis, toxoplasmosis) and diseases that are transmitted through serum (e.g. hepatitis B, C, HIV, cytomegalovirus infection, malaria). Prevention of such complications involves thorough choice of donors, education of donors, proper management of the blood banks' and blood stations' work.

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