LE

LEСTURES 2.

 

Bleeding. Blood loss. Transfusion of blood.
Extreme conditions.
Cardiopulmonary resuscitation

               

Bleeding and blood loss.

 

Bleeding (haemorrhagia) – withdrawal of blood from the blood vessels if they are damaged or breach permeability of the wall. Loss of blood causes the body changes and creates a great threat to the life of the patient. Sometimes even minor bleeding in the brain, bleeding in the pericardial cavity can cause death of the patient. From timely and qualified medical professional action largely depends the fate of man. Causes of bleeding may be injured tissues, vessel walls, the violation of their permeability, homeostasis, and various blood diseases (hemophilia, thrombocytopenia, leukemia, etc.). Some adverse environmental factors may increase blood – high temperature, low pressure, or lower – cold water, etc.

 

Bleeding is physiological (menstruation), and abnormal. Depending on the principle underpinning the classification distinguishes between different types of bleeding.

 

 

I. For anatomical localization

 

1. Arterial bleeding (Fig. 1.) – Occurs when damage to the arterial blood vessels are the most dangerous kind: death may occur within a few minutes. The sign of bleeding from the arteries is bright red blood that flows pulsating jet. When pressing the central end of the vessel bleeding stops.

 

Fig. 1. Arterial bleeding

 

 

2. Venous bleeding (Fig. 2.) – Unlike the arterial, venous blood flows evenly and slowly and has a maroon color. When pressing the central end of the veins bleeding stops. If the damage is large veins, especially in the neck, death can occur as a result of air embolism (air intake in the vessel). Air plug (embolus) may override the right half of the heart and pulmonary artery. Death occurs from reflex cardiac arrest and paralysis of the respiratory center.

 

Fig. 2. Venous bleeding

 

 

3. Capillary bleeding (Fig. 3.) – With this kind of bleeding blood all surface wounds. By staining the blood occupies a middle position between the arterial and venous. This is particularly dangerous bleeding in hemophilia, liver disease or sepsis, when a decrease in coagulation properties of blood. Under normal conditions, capillary bleeding stops itself.

Fig. 3. Capillary bleeding

 

 

4. Parenchymal hemorrhage (Fig. 4.) – It occurs when trauma and rupture of internal organs (liver, spleen, lungs, kidneys, etc.) when damaged all vessels (arteries, veins, capillaries). This type of bleeding is extremely dangerous, as damaged blood vessels of these organs caot contraction due to connective tissue stroma of parenchymal organs, and also due to the formation of anticoagulant substances in organ damage.

Fig. 4. Parenchymal hemorrhage

 

 

II. By reason of distinguish.

 

1. Traumatic hemorrhage (haemorrhagia per rhexin), resulting in mechanical damage of the vessel wall. They are usually in open and closed injuries, burns, frostbite, actions surgeon during surgery. This group includes bleeding developing in traumatic injuries have abnormal blood vessels (aneurysms, hemorrhoids, varicose veins).

 

2. Erosive bleeding (haemorrhagia per diabrosin), resulting in violation of the integrity of the vascular wall abscess or necrotic process, germination and decay tumors, etc. (Fig. 5).

Fig.5. Erosive bleeding

 

 

3. Haemorrhagia per diapedesin, arising from abnormal vascular wall permeability and observed in a number of diseases (hemorrhagic diathesis, beri-beri, uremia, sepsis, holemiya, toxins). This condition is associated with vascular functional and morphological changes in their wall.

 

III. By the time of occurrence.

 

1. Primary, which occur immediately after injury vessels.

 

2. Secondary arising shortly after the bleeding stops (eg, slipping ligature or festering wounds and melting pots in it).

 

 

IV. According to clinical manifestations.

 

 

1. External bleeding when blood poured from the wound in the environment.

 

2. Internal, when there is bleeding in the intestine (intestinal bleeding) or cavity – haemoperitoneum (accumulation of blood in the abdominal cavity), hemothorax (in the pleural cavity) haemopericardium (in the pericardium), hemarthrosis (in the joint cavity) and others.

 

3. Hidden (occult) bleeding occurring without obvious clinical signs. For example, the progression of gastric ulcer and duodenal ulcer detect clinically occult bleeding is difficult, but the presence of blood can be easily detected in a laboratory study of fecal occult blood reaction (Gregersen). Untimely discovered hidden bleeding can lead to severe anemia.

 

 

V. Depending on the rate of bleeding and amount of blood loss.

 

1. Acute bleeding is most dangerous. Rapid loss of 30% of blood volume (CBV) leads to severe anemia, hypoxia of the brain and can result in death of the patient.

 

2. Chronic bleeding – blood loss occurs slowly and gradually, in connection with which the body has time to adapt to the gradual reduction of BCC.

 

Clinic. Examining the patient, who emerged bleeding must address three questions: what blood, how much blood is lost, or bleeding continues. Common signs of bleeding include: pale skin and mucous membranes, giddiness, fatigue, thirst, blackout, flickering “flies”, nausea, decreased arterial and venous pressure, pulse rapid, low-volume and tension, breath frequently. Late assisting death can occur from the loss of functional capacity of blood (carrying oxygen, carbon dioxide, nutrients, metabolic products, etc.) and circulatory disorders (acute heart failure, hemorrhagic shock). Consequences of bleeding depends on several factors. Crucial in predicting the effects of bleeding has volume and rate of blood loss. Accepted distinguish three degrees of acute blood loss: mild – up to 20% of the original BCC (up to 1 liter of blood), moderate – 30% of BCC (up to 1.5 liters of blood) and severe loss of blood – more than 30% of BCC (over 1.5 liter of blood). Rapid blood loss – about one third of the bcc (1.5 l) – life-threatening, blood loss more than 50% of circulating blood volume is fatal. Under some circumstances, death can occur from blood loss less than 1.5 liters. The speed and volume of blood loss depends on the nature and type of the damaged vessel. Fastest blood loss occurs when damage to large arteries. More dangerous side damage their walls than a full cross a gap, because the latter type of vascular injury is reduced, and the inner shell wraps it inside the vessel, which reduces or completely stops bleeding. Sometimes even bleeding from large arteries can stay alone. This affects a number of factors: the reduction in blood pressure due to bleeding that lasts, total vasospasm as compensation factor, reducing the damaged vessel, especially after its complete cutting; tucking the middle of the inner and middle walls in place of rupture.

 

Adaptive-compensatory mechanisms in acute blood loss are: venospazm; influx of tissue fluid; tachycardia oligouriya, hyperventilation, peripheral arteriolospazm; activation of the sympathoadrenal system, activation of blood coagulation and stimulation of hematopoiesis.

 

         Generally, in the body there is a so-called spontaneous hemostasis system that independently, without any help cope with bleeding. This includes: 1) reaction vessels (vasospasm), 2) activation of platelets (cells mechanism – adhesion, platelet aggregation and thrombus formation), and 3) blood coagulation system (13 factors).

 

According to the classical theory of enzyme A. Schmidt (1861) clotting process consists of three phases: the first phase – formation of blood and tissue thromboplastin (lasts 3-5 minutes, the other two – 2-5 seconds), the second phase – the conversion of prothrombin to thrombin; 3rd phase – formation of fibrin that stops bleeding and blood loss. Extremely dangerous bleeding may occur in disorders of blood coagulation and blood diseases (hemophilia syndrome, disseminated intravascular coagulation, thrombocytopenic purpura disease).

 

The reaction of the body to blood loss depends on his general condition, age and gender of the victims. It should be noted that women and donors easier to tolerate blood loss. This is due to the fact that during menstruation in women and periodic blood donations from donors produced compensatory mechanisms. It is difficult to tolerate blood loss, children and the elderly. In the elderly due to age-related changes in the heart, blood vessels (atherosclerosis) adaptation of the cardiovascular system to hemorrhage is much lower than in the young. However, remember that sometimes minor bleeding, especially in the matter of the brain, can be extremely dangerous due to destruction of vital centers, and bleeding in the subdural, epidural, subarachnoid space of the skull can lead to compression of the brain, a violation of its functions and death.

 

Important for establishing the amount of blood loss is the determination of red blood cells, hemoglobin, and hematocrit. Approximate volume of blood loss can be calculated using Alhovera index (the ratio of heart rate to systolic blood pressure (BP), which normally is 0.5.

 

Treatment. Depending on the conditions of medical care and training of medical workers, stop bleeding may be temporary and final. Temporary stop bleeding conducted at the scene and during transport the victim to a hospital. The final stop bleeding is in the hospital, and in some cases by surgery.

 

 

There are several ways to temporarily stop bleeding:

 

1. Compressive bandage. It is imposed on victims bleeding from veins and small arteries: the wound is covered with several layers of sterile gauze, and the top layer of sterile cotton wool, which are tightly fixed to the circular limb bandaging.

 

2. Maximum flexion the limbs at the joint (Fig. 6.). Active bleeding from the femoral artery in the inguinal bending popliteal artery at the knee, the brachial artery at the elbow. This kind of stop the bleeding at the expense of flexion or abduction limb by bandages.

 

а                                                            б                                                  в

 

Fig. 6. Maximum bending the limb: a – bleeding from the femoral artery, b – bleeding from the popliteal artery in – bleeding from the brachial artery;

 

3. Pressing the blood vessels in the wound. Dressed sterile glove or hand quickly processed alcohol, chlorhexidine and index finger inserted into the wound, pressed vessels in a place where there is a stream of blood

 

4. Tight tamponade wound. To do this, take a strip of gauze or sterile gauze and a large napkin with tweezers consistently and tightly fill the entire wound. Typically, such a stop is performed with deep wounds.

 

5. Overlay clamp bleeding vessels. It is used in cases of inability to stop bleeding from a deep-seated vessels of the limbs, pelvis, abdominal or thoracic cavities.

 

6. Pressing a vessels. Active bleeding from large vessels (Fig. 7.8): a) the subclavian artery is pressed against the first rib at a point located above the collarbone outside the place of attachment sternocleidomastoideus muscle to handle chest, armpit – in the armpit to the head of the humerus; aorta – to the spinal column, and b) the carotid artery can squeeze, pressing her finger to the transverse process of the cervical vertebra VI, which corresponds to a point in the middle sternocleidomastoideus muscle, with its inner side, c) femoral artery pressed to the horizontal branch pubic bone below the middle ligamentum inguinale. Pressing a popliteal artery performed by compressing tissue in the popliteal fossa with a bent knee (Fig. 9).

                 

Fig. 7. Pressing the brachial artery.

 

 

 

 

а                                                              б

 

Fig. 8. Pressing: a – subclavial artery b – carotid artery.

 

 

 

 

 

а                                                                                          б

 

Fig. 9. Pressing: a – femoral artery, b – popliteal artery.

 

 

The most typical place temporary stop the bleeding by pressing vessels listed in Fig. 10.

 

 

Fig.10. The most common places finger pressing arteries.

 

 

Overlay hemostatic tourniquet. The most commonly used Esmarch tourniquet (Fig. 11).

 

 

Fig. 11. Types of tourniquet: 1 – Esmarch tourniquet 2 – tow-twist, 3 –

 

improvised tourniquet using a belt.

 

This method is essential, especially when you stop arterial bleeding. With such bleeding proximal tourniquet is placed upon the (central) end of the vessel in relation to the wound. Before laying tourniquet limb covered clothes or wrapped in a towel, bandage. Plait and stretch wrapped limb. Need to ensure that tours tow not crossed, and housed together. The ends of the bundle fix. During one of the tours harness to leave a note with a timestamp overlay harness. With proper imposition of “blood” tourniquet limb fades below the tourniquet is not felt ripple artery bleeding stops. With insufficient tightening the tourniquet limb becomes cyanotic, stored pulse below tourniquet, bleeding increases. In these cases, you must remove the tourniquet, after pressing artery finger and apply it tighter. Note also that in too tight tightening tourniquet limb paralysis may occur due to trauma nerves. Victim of imposed twist as soon as possible to deliver the hospital for the final stop bleeding. “Blood” tourniquet can be left on the limb no longer 1.5-2 hours. In the longer term there may come a limb necrosis. If during this time could not perform the operation, the tourniquet is removed, the artery is pressed with your finger and 3-5 min tourniquet again impose slightly above or below the previous location (Fig. 12).

 

 

Fig. 12. Methods applying a tourniquet: a – prepare to imposing bundle b – stopping blending, the first round, d – the final appearance of the overlay tourniquet and bandages to the wound, e, f – applying a tourniquet to the thigh.

 

 

In the absence of a special bundle you can use a belt, rope, handkerchief and so on. To gain compression improvised tourniquet insert stick and twist-twisting by conducting stop bleeding (Fig. 13.).

Fig. 13. Stop bleeding by using sticks, twist.

 

 

When bleeding from the neck vessels can be used splint Cramer. At the same time on the opposite side from bleeding impose curved splint Kramer (Fig. 14).

 

Fig. 14. Temporary stop bleeding from the neck vessels.

 

 

 

When venous bleeding apply a so-called “venous” tourniquet. His impose below the damage blood vessels and tighten slightly. This ending is blue, the pulse of the artery is preserved, and the bleeding stops.

 

The final stop bleeding in surgical hospital conducted in accordance with all the requirements imposed for surgery.

 

 

I. Mechanical methods.

 

 

1. Fitting the clamp and ligature (Fig. 15).

 

Fig. 15 Clamp and ligature on vessel.

 

 

 

2. Suturing blood vessels in the wound. Stitch suture sterile material (silk, polyester, catgut). This is the most common method of stopping bleeding from vessels (Fig. 16).

 

 

 

Fig. 16. Suturing blood vessels in the wound

 

 

3. Ligaturing at distance. Suitable for infected wounds or if technical difficulties of detecting vessels in the wound (Fig. 17).

 

 

 

Fig. 17 Ligaturing at distance.

 

 

4. Overlay vascular suture. It can be a side and circular perimeter around the vessel. It is possible to use special suture with atraumatic needles or apparatus for mechanical stitching vessels using tantalum brackets (Fig. 18).

 

 

Fig. 18. Overlay vascular suture.

 

II. Physical methods.

 

1. Often used cold. Basically, this method is used in small capillary bleeding. To do this, use rubber or plastic bags filled with ice (Fig. 19).

 

 

Fig. 19. Ice pack.

 

 

1. Electrocautery (Fig. 20). Coagulation is usually performed under

 

Fig. 20. Electrocautery vessels.

 

 

operation for bleeding from small vessels using a special device – diathermy. Besides using diathermocoagulation (Fig. 21), kriocoagulation, laser photocoagulation (Fig. 22), arhonoplazmocoagulation (Fig. 23), the radio wave coagulation, termocoagulation (Fig. 24).

 

Fig. (21)  diathermocoagulation

 

 

 

 

Fig. 22. laser photocoagulation

 

 

 

 

Fig. 23. arhonoplazmocoagulation

 

 

Fig. 24. termocoagulation

 

Radiowave coagulation

 

3. Use hot (60-800S) isotonic sodium chloride solution. Damp cloth with this solution, is applied for several minutes before the bleeding site. The method is mainly used in operations on the chest, abdomen and neurosurgery.

 

III. Chemical methods.

 

1. Vasoconstrictor drugs. They are based on a spasm of blood vessels and improve blood clotting. These drugs include epinephrine, norepinephrine, drugs sporyni others. Depending on the type of bleeding these medications are used topically, parenterally or orally.

 

2. Drugs that increase blood clotting. This group includes fibrinogen, 4% solution epsylonaminocapron acid, tranexamic acid, Aprotinin, desmopressin, vasopressin, calcium chloride (10%), vikasol, 3% solution of hydrogen peroxide others. Locally most commonly used 3% hydrogen peroxide solution. Napkins, tampons moistened with water and put on the wound.

 

IV. Biological methods are based on the properties of body tissues to promote thrombosis. Biological assets are divided into two groups. For drugs first group includes drugs topical application: dry plasma, fibrin, gelatin sponge fibrynna film thrombin trombostat etc., which fills bleeding wound.

 

In the second group of drugs biological hemostatic products include: fresh frozen plasma, fibrinogen, cryoprecipitate, antihemophilic globulin, antihemophilic plasma, recombinant clotting factors (VII A, VIII, IX) and others. These drugs are mainly administered parenterally (intravenously).

 

 

Complications Bleeding

 

 

In clinical practice, during and after the bleeding may have conditions that require immediate assistance.

 

Collapse – acute cardiovascular failure, which develops due to decreased vascular tone and acute weakness of the heart muscle.

 

Clinic. Occurs in patients with sudden pallor of cyanotic tinge, skin covered with cold sweat, pulse is threadlike, reduced blood pressure, breathing becomes frequent, shallow. Unlike syncope in patients with collapse of consciousness is usually retained.

Treatment. The first step is to stop the bleeding, warm the patient, introduce 0.5 ml of 0.1% solution of adrenaline or 1 ml of 5% solution of ephedrine, 0.5 ml of lobeline, apply oxygen cushion. In severe cases, the transfusion of blood components, administered cardiac drugs.

 

Hemorrhagic shock caused by severe bleeding. Development of shock and its severity depends on the amount and rate of blood loss. Every hemorrhage accompanied by centralization of circulation: a protective biological reaction that is aimed at providing vital organs: heart, lungs, liver, brain, etc.. However, continued centralization of circulation accompanied by the release of the liquid part of the blood into the interstitial space. Blood in the peripheral vessels thickens, slowing its movement speed, red blood cells clumped together, leading to intravascular coagulation and blood clots. These intravascular clots block the capillaries, causing disturbance of microcirculation in organs and tissues. Consequently, the syndrome of small emission heart deteriorating supply of oxygen (developing circulatory, hemic and hypoxic hypoxia).

 

Depending on the severity distinguish three stages of hemorrhagic shock:

 

I stage – compensated hemorrhagic shock (when blood loss more than 1000 ml). Patients in the mind, somewhat excited. Skin pale, marked tachycardia (90-100 bpm. / Min). Blood pressure in the normal range, although reduced cardiac output, urine output decreases to 20-35 ml per hour.

 

Second stage – decompensated hemorrhagic shock (when blood loss 1500 ml). The patient’s condition worsens, increases pale skin, there is tachycardia (heart rate to 120 bpm. / Min), systolic blood pressure decreased to 100 mm Hg, pulse pressure increases. Appears respiratory failure. Under hypoxic tissues in the body are formed toxic products (lactic, pyruvic acid, etc.), resulting in metabolic acidosis. Changing the acid-base balance negatively reflected on the many functions of the body: the contractile ability of the myocardium, renal excretory function, the function of the central nervous system.

 

Third stage – irreversible hemorrhagic shock (blood loss more than 1500 ml). The patient’s condition worsens and manifested deep functional disorders of the central nervous system, respiratory, circulatory, etc.. Thus, the sharp decrease in blood flow through the kidneys completed the development of necrosis and renal tubules. About irreversible shock may indicate prolonged hypotension (over 12 hours), confusion, anuria, acrocyanosis.

 

Treatment. All measures in the treatment of hemorrhagic shock should be directed to stop the bleeding. After the bleeding stops, or simultaneously with it (during surgery) spend infusion-transfusion therapy. Infusion engaged in 2-3 veins. Originally spend puncture of peripheral veins, and perform catheterization main veins (subclavian, jugular or great saphenous vein of the lower extremities, etc.). Massive infusion therapy performed under the control of central venous pressure (CVP). All solutions should be warm. Update bleeding donor blood on a “drop by drop” is not practiced. Remember that even the immediate removal of blood loss transfusion does not always reach the goal.

Today, restoration BCV is mainly due to substitutes. Yes, blood loss, even up to 30% of BCV with success can compensate for infusion of various crystalloid and colloid solutions. Only blood loss of more than 30% of BCV may require transfusion of some blood components (red cell, platelet, etc.).

Importance in the treatment of patients with hemorrhagic shock with transfusion means hemodynamic effects (colloidal plasma substitutes) – reopolyglukine, reohlyuman, polifer, perftoran, zhelatynol, and crystalloid preparations – salt and electrolyte solution (Ringer-Locke solution, 7.5% sodium chloride solution , loktosole).

In severe cases, blood transfusions and blood substitutes solutions combined with the appointment of vasoconstrictor (norepinephrine, epinephrine, ephedrine, mezaton), heart (strophanthin, korglikon, digoxin) and hormones (hydrocortisone, prednisone). They are introduced only intravenously. Subcutaneous or intramuscular injection of drugs due to hemodynamic disorders is ineffective. Along with these patients demonstrated oxygen therapy. In severe cases, the controlled breathing with breathing apparatus. The patient should be warm, warm cover. For such patients should maintain strict oversight, particularly in terms of hemodynamics (heart rate, blood pressure) and hemogram (number of erythrocytes, hemoglobin, hematocrit).

 

The doctrine of blood. Samples of blood transfusion.

 

Infusion-transfusion therapy (infusio – pour, transfusio – pour) – a method of influencing physiological properties of organ systems (cardiovascular, respiratory, metabolic, etc.) on morphological, biochemical, and functional status of the blood and extracellular fluid and providing mechanisms of homeostasis by infusion or transfusion of blood, blood components, products or different liquids. The first attempts at transfusion (transfusion) rooted in antiquity and related blood transfusion from person to person, from animal to animal. The first blood transfusion was performed in a 1492 court physician of Pope Innocent VIII, who took the blood of three boys in order to rejuvenate the old pope. However, blood transfusion ended in complete failure – Pope died after boys. This case is long delayed development transfusion. And only in 1666 the first successful blood transfusion from dog to dog made an English anatomist and physiologist Richard Louyer.

 The first successful human blood transfusion was held June 15, 1667 the court physician of French King Louis XIV, philosopher and mathematician Jean Baptiste Denis for assistance surgeon Emmereza patient, who had a fever and was very exhausted after multiple bloodletting. They had a small amount of transfused blood (about 270 ml) of the carotid artery lamb in hand vein of the patient, after which he recovered. However, frequent failures and adverse effects of blood transfusion on long delayed development of this problem. Only in 1820, British obstetrician and physiologist James Blandel made transfusion of human blood 10 women dying from postnatal uterine bleeding, 5 of them were saved. In 1832 Russian obstetrician in St. Petersburg K. Wolf also done successful blood transfusion (from a man) to save women from the presence of bleeding in the postpartum period. It should be noted that for the period from 1832 to the end of the 1 century in the Russian Empire conducted a total of 60 blood transfusions, 22 of them made Kyiv surgeon, Professor SP Kolomnin.

The importance of the development was the discovery hemotransfusiology Austrian scientist Karl Landsteiner, who discovered in the blood of different people specific protein (agglutinogen A and B agglutinins α and β), and a pattern agglutination test (agglutination of red blood cells), based on which in 1901 he described the three blood groups. In 1907, the Czech psychiatrist J. Jansky, studying hemagglutination searching for the causes of mental disorders, has opened a fourth group of blood. After a year on the basis of classification yang Ottenberh doctor from New York developed a method of accurately determining blood groups before transfusion. Opening Jansky and test Otenberha possible to start a blood transfusion in vain, and on scientific grounds, without putting the patient’s life danger. In 1921, J. Jansky proposed international classification of blood groups. Discovery of blood groups became a scientific rationale for the widespread introduction of blood transfusion in medical practice. The first successful blood transfusion taking into account group membership made in 1919 Russian scientist VV Shamov anemic woman, after repeated uterine bleeding. Name the first young girl donor, unfortunately, remains unknown.

An important discovery in the field of blood transfusion was done also in 1914 A. Hustenom (Hustin A.), which is to prevent blood clotting suggested sodium citrate, which is commonly used until recently.

In 1940, Karl Landsteiner and Winner found in erythrocytes of a new antigen-Rh (Rh) and Levin co-authors have shown its association with hemolytic jaundice iewborns. Since then initiated a new approach to Transfusion therapy in view of not only blood, but also the Rh factor.

Today infusion-transfusion therapy in Ukraine dealing Institute of Hematology and Blood Transfusion, provincial and city stations and department Transfusion therapy in large hospitals (regional, city, district). The achievements of modern science allow wide use of infusion-transfusion therapy in clinical practice as an effective means of treating patients.

All questions of infusion-transfusion therapy settle doctors. They are legally responsible for the accuracy of blood transfusions.

 

Fundamentals isoserology system and blood groups.

Success transfusion is closely associated with the development of the doctrine of blood. Today we know that in the blood are erythrocytes agglutinogen A and B, and H oligosaccharide, the latter is group 0 erythrocytes and has antigenic determinants. Serum agglutinins are a (anti-A) and b (anti-B). The interaction of similar agglutinogen of agglutinins is agglutination. Blood is incompatible when mixing it has the same name agglutinogen (AB) and agglutinins (ab). Depending on the availability of blood and agglutinogen agglutinins are four blood types.

 

No agglutination test                          positive agglutination

The first (I) 0 group (ab) – red blood cells do not contain agglutinogen. Serum available only both agglutinins (a and b), can agglutinate erythrocytes three other groups.

 

The second (II) Group A (b) – erythrocytes containing agglutinogen A that agglutinated sera of groups that have agglutinins a. Serum agglutinins is b, which agglutinated red blood cells that contain agglutinogen B.

 

The third (III) Group B (a) – erythrocytes containing agglutinogen in which agglutinated agglutinin b. A serum agglutinins agglutinated erythrocytes of blood groups with agglutinogen A.

 

The fourth (IV) group AB (0) – erythrocytes containing agglutinogen AB and agglutinated sera previous three blood groups. In this group serum no agglutinins because it agglutinated erythrocytes of other blood groups.

 

Note that agglutinogen A has its variations, and so, consequently, blood group A (II) has a subgroup A1 (II), A2 (II), and group AB (IV) – A1B (IV) and A2V (IV).

Blood genetically caused an appropriate set of antigens contained in red blood cells is constant and does not change with age, influenced by illness or other reasons. Note that only agglutinins serum adsorbed on the surface of red blood cells (agglutinogen), and the last stick together and precipitate. Severity depends on the agglutination titer (number agglutinogen, agglutinins, giving an agglutination test), ambient temperature and other factors. The reaction between serum and erythrocytes of one species of organisms that causes agglutination of red blood cells, called isoagglutination. Bonding erythrocytes of one type of animal serum, the second is called heteroagglutination.

Method for determining blood groups. Determination of blood groups AB0 carry the system through the identification of specific antigens and antibodies and is based on the phenomenon of agglutination using two methodological approaches:

 

1. To determine the presence of erythrocyte antigens A, using: a) standard sera with specific isoagglutinins b) monoclonal antibodies (MAbs).

2. In determining the presence of serum isoagglutinins a and b using the standard red blood cells known blood group.

 

Determination of blood in humans conducted by doctors, technicians specialized and certified laboratories in accordance with the following account of the results in a special journal or make them as a stamp in the passport. When taking a patient to hospital treatment initial determination of blood performed by specially trained doctors centralized laboratory (clinical) laboratories. The results of blood grouping recorded in a special journal and form with the date and signature of the person who conducted it. This form fixated at patient medical card. In addition, the result of which is specified in this form, the attending physician records on the title page and countersign, specifying the date.

In urgent cases where the patient requires urgent transfusion of blood components, and blood grouping laboratory doctor caot organize blood grouping holds doctor with the obligatory provision of the tube with the blood of the patient to the laboratory for final determination of group membership.

Determination of blood in all cases necessarily carried out using standard sera two series each group or monoclonal antibodies. In doubtful cases, additional check presence isoagglutinins using standard erythrocytes.

Determination of blood using standard sera. Standard serum produced in ampoules special laboratories institutions of the blood. Sera stored in a refrigerator at +6-20 C. Shelf serum indicated on the label (6 months from date of manufacture). Each ampoule serum must have a passport-label indication of blood, number series, titer, expiry date, place of manufacture. Use vials without labels is strictly prohibited! All the standard whey depending on the blood group with its color-coded: 0 (I) – a colorless, A (II) – dove, In (III) – red and AB (IV) – yellow. Appropriate labeling sera are on the labels in the form of colored stripes. The label vials of serum 0 (I) of strips no label serum A (II) group has two strips of blue color, serum B (III) of three strips of red and serum AB (IV) group – four strips of yellow. Serum should be fair and transparent, ampoule – intact. The presence of flakes, sediment, turbidity is featured unsuitability sera. Each must have its serum titer. Titer of serum – that it most dilution at which agglutination still possible. The higher the titer, the more reliable serum. For the determination of blood is desirable to use serum titer, not below 1:32. Note that when a significant dilution of serum agglutination may not occur. Serum levels of the group should have its own series and high activity, the first signs of agglutination should appear within 30 seconds. The series describes the serum made from the blood of a certain person.

For the determination of blood using whole blood, washed red blood cells, red blood cells in plasma, serum or in 0.9% sodium chloride. In patients with anemia stabilize blood heparin.

Determination of blood carried indoors with a satisfactory illumination at temperatures from +15 to +25 ^oC (optimum 18-24 ^oC). His conduct on special (with grooves) or conventional porcelain plates or skeet. Recent divided crayons into four squares in a clockwise direction represent sectors blood groups: 0 (I) A (II), B (III), AB (IV). According to each sector plates with a pipette put one drop of serum two series. Then the patient rubbed cotton swab dipped in alcohol pad 96 ˚ ultimate phalanx third or fourth fingers of his left hand and hold a special puncture needle (Scarifiers). The first drop of blood removed gauze ball, and the next drop collected in sterile capillary Panchenkova or using different angles slides and consistently bring in the sera, stirring them. Value of blood and serum should be 1:10 (0.01 mL studied blood or red blood cells and 0.1 ml of each serum two batches). Mixed separate glass rods or angles objective lenses every drop of blood (red blood cells) with the appropriate serum, gently take a porcelain plate (plate) and shake. Then leave for 1-2 min at rest and shake again. Monitoring the progress of the reaction is carried out at least 5 min. Because possible agglutination, such as erythrocytes A2 (II) and A2B (IV) blood groups. After 3-4 minutes until the mixture drops of serum to erythrocytes, where there was agglutination, add 1 drop of 0.9% sodium chloride solution and continue to watch 5 minutes shaking periodically plate.

Reaction isoagglunation in each drop may be positive or negative. In case of a positive reaction in the mixture appear visible to the naked eye small red grains (agglutinins), which consist of bonded red blood cells. Small grains gradually stick together into larger grains, sometimes in flakes of irregular shape, resulting in serum completely or partially discolored. In case of a negative reaction liquid at all times (5 minutes) is uniformly colored and it is not observed granularity (agglutinins). Results of reactions in drops of sera of the same group (two batches) should coincide.

Interpretation of the results of agglutination test in determining the blood groups are presented in Table 1.

Table 1

Variants of blood group

 

 

0(І)                                                     А(ІІ)                                              В(ІІІ)                                           АВ(IV)

   

 

Determination of blood using monoclonal antibodies «tsoliklon». «Tsoliklon» (monoclonal antibodies) are used instead of standard sera. Tsoliklon against antigens A and B produced by two different tumor hybridomas are formed by the interaction of B lymphocytes mouse with myeloma cells of mouse. Ascitic fluid produced by hybridoma containing immunoglobulin M (IgM), which are directed against specific antigens of groups A and B of AB0 blood. Determination of blood carried in the blood without preservant and stabilized using preservant (Glugitsir, tsytroglukofosfat, heparin, sodium citrate). Tsoliklony give quick and expressive agglutination reaction compared with standard sera. They come in vials or ampoules of 20, 50, 100 and 200 doses (1 dose = 0.1 ml). Tsoliklon painted in red – anti-A and blue – anti-B. They were stored in a refrigerator at + (2 ± 6) ˚ C. Storage time – 2 years. Determination of blood is carried out at temperatures from 15 to 25 ˚ C. On a plate put two drops tsoliklon anti-A and two drops tsoliklon anti-B on the opposite side. Along with these drops cause a drop studied blood (0.01 ml), 10 times less than the tsoliklon (1:10) and mixed some sticks or different angles of the objective glass. Agglutination reaction occurs in the first 3-5 s and shows small red grains, and later flakes. Monitoring should be conducted for 2.5 min. The following options agglutination test: 1) no agglutination with tsoliklon anti-A and anti-B blood contains no agglutinogen A and B, this blood belongs to 0 (I) group, 2) tsoliklon agglutination observed with anti-A, erythrocytes containing agglutinogen A – blood A (II) group, 3) agglutination occurs with tsoliklon anti-B – Blood B (III) group, 4) tsoliklon agglutination observed with anti-A and anti-B, erythrocytes containing agglutinogen A and B – AB blood (IV) group. Given the high activity tsoliklon, if the reagent anti-AB blood group determination can be made with only one series of monoclonal antibodies anti-A and anti-B.

monoclonal antibodies for determining blood groups

 

Table 2

Variants of blood group by monoclonal antibodies.

 

Determination of blood groups by monoclonal antibodies

 

In the case of positive agglutination test with both monoclonal antibodies anti-A and anti-B blood group is identifying AB (IV) should be additional control analysis of the blood sample with 0.9% sodium chloride. This mix one large drop (0.1 ml) of 0.9% sodium chloride solution with a small (0.01 ml) studied blood drop. Lack of agglutination in the studied blood indicates that the blood belongs to AB (IV).

Determination of blood according to standard erythrocytes. From the patient’s veins take 4 ml of blood in a test tube and centrifuged. At the plate, divided into sectors, applied in accordance with signatures drop of serum. They’ll add 10-20% suspension of erythrocytes standard 0 (I) and (II) and In (III) in a ratio of 1:5, plate shaking for 3 min, then’ll add a drop of isotonic sodium chloride solution, the result is evaluated after 5 min . Possible 4 options agglutination reactions: 1) no agglutination with erythrocytes 0 (I) and determined with erythrocytes A (II) and B (III) – blood group 0 (I), 2) negative agglutination with erythrocytes 0 (I) and A ( II) and positive groups of erythrocytes B(III) – blood group A (II) 3) no agglutination with erythrocytes 0 (I) and B (III) groups and positive erythrocytes with A (II) groups – blood group B (III ), 4) negative agglutination with erythrocytes 0 (I) A (II), B (III) group – investigated blood AB (IV) groups (Table 3).

Table 3.

Variants of blood according to standard erythrocytes.

 

 

In case of discrepancies in the results in the determination of blood donors by monoclonal antibodies erythrocytes and standard use of such blood for transfusion to patients is not permitted, and blood sent for detailed research to a specialized laboratory. If the results of the two tests do not meet the blood recipient, which needed urgent blood transfusion, in which case he can pour Rh compatible red cell mass group 0 (I) or Rh-negative red cell mass group 0 (I).

It should be noted that the blood of man, like all the other features inherited from classical laws of genetics and defined a set of genes that she received a maternal or paternal chromosome. If we know the blood of both parents, it is easy to predict what blood group can have children.

 

Errors in determining the blood group membership

Technical errors: a) a false location standard serum, erythrocytes or monoclonal antibodies b) mismatch volume ratio serum or erythrocyte monoclonal antibodies and studied blood c) premature conclusions (5 min) of the sample result (at slow agglutination), d) incorrect entry studied blood e) nonspecific reaction – agglutination that occurs with fresh blood at temperatures above +25 ° C, f) nonspecific reaction cold antibody for its specification plate or plate placed in a thermostat at a temperature of +37 ° C in 5 min, followed by false agglutination disappears and remains true e) Failure to control reactions with serum group AB (IV) or isotonic sodium chloride solution when dealing with monoclonal antibodies g) pollution or use wet pipettes, plates, rods.

Errors associated with inferiority standard serum, erythrocytes, or monoclonal antibodies studied blood: a) weak standard serum titer below 1:32 or expired storage or weak forms antigen A (mostly) or B (rarely), b) not preserved or harvested in violation of aseptic serum, erythrocytes, monoclonal antibodies c) non-specific agglutination of erythrocytes studied blood (“coin columns,” Thomsen phenomenon, which is associated with bacterial contamination of blood or prolonged its location at room temperature). To prevent errors associated with psevdoagglutination should use test with saline. For this study to drops of blood which came agglutination, but not earlier than 3 minutes, add a drop of saline, mixed and shaking plate, observed for 5 min. Adding saline increases true agglutination and eliminates false.

Errors associated with the biological properties of blood: a) low titer agglutinogen studied blood to determine blood by standard sera or agglutinins for erythrocytes standard, b) the presence of groups A (II) and AB (IV) weak agglutinogen A2 A2V with that there is a weak and late agglutination. Thus errors may occur, in which blood group A2B (IV) is defined as blood group B(III), and blood A2 (II) – as a group 0 (I).

In all cases, unclear or questionable results should be repeated determination of blood through other series sera tsoliklon or “cross method” using standard erythrocytes.

 

The clinical significance of blood group compatibility.

 Modern transfusiology numbering several thousand and several hundred agglutinogen serum agglutinins (system MNSs; P; Kell; Duffy; Kidd et al.). And so today should be considered that the ideal blood group compatibility is not. In the case of blood transfusion must remember Otenberha rule whereby agglutination erythrocytes blood flows (donor) and not the patient, as agglutinins blood flows, bred in the patient’s blood and it caot agglutinate erythrocytes. This allows you to pour in some cases not only one groupe blood, but blood, red blood cells which caot be agglutinated serum of the patient. Thus, red is not the first group agglutinated sera of all groups, and therefore blood 0 (I) group can be transfused to any patient (universal donor).

 

The concept of the Rh factor

Rh factor – a special D-antigen, which was first detected in erythrocytes of monkeys breed macaques (Macacus rhesus). It is found in 85% of their blood called the Rh-positive. In the other 15%, this factor is absent, their blood is called Rh negative. Rhesus factor is strong enough antigen. Transfusion of Rh-positive blood people with Rh-negative blood they made specific Rh antibodies that cause Rh disease; posttransfusion reaction, anaphylactic shock may occur. Rhesus antibodies occur in people with Rh-negative blood for life in their immunization Rh factor people with Rh-positive blood. When blood transfusion should be aware that in addition to Rh (D), there are several types of Rh factor. For their designations used nomenclature Winner or Fischer-Reis (Rh (D), Rh ‘(C), Rh” (E), d, c, e). Various combinations of Rh antigens on the surface of red blood cells create 18 theoretically possible phenotypes, ie the system of blood groups Rh. Note that, unlike the AB0 system in human blood serum practically no natural antibodies of Rh. They are only immune iature and result from Rh-incompatible transfusion or pregnancy.

 

Methods for determining Rh membership

Determination of Rh membership can be carried out in blood taken directly to the spot study of finger-preserved blood and red blood cells, which precipitated from blood taken without stabilizer. You may store blood samples for 3 days at + (2-6) oC.

Defining the Rh blood belong carried out in two stages: first, blood donors tested standard serum anti-D (Rh) or monoclonal reagents anti-D-super, and then blood, which gave a negative reaction with serum anti-D (Rh), explore additional with standard sera Antirhesus containing, in addition to anti-D (Rh), antibody anti-C (rh ‘) and anti-E (rh”). Antibodies anti-C (rh ‘) and anti-E-(rh”) can be found in serum both in pure form and in mixtures with antibodies anti-D (Rh).

Determination of Rh-factor, like blood, perform laboratory doctor specialized and certified laboratories. In determining Rh blood belonging to use force instructions available to the antirhesus serum, erythrocytes and monoclonal bodies. In all cases, prior to the definition of group membership levels. Rhesus factor is hereditary and is not dependent on blood, sex and other characteristics of the person.

1. Method for determining Rh membership by standard sera.

Antirhesus serum produced normally in the form of universal, ie deprived group antibodies. Such serum suitable for the determination of Rh-blood people belonging any groups AB0 system. However, under certain circumstances antirhesus serum made from the blood of different groups AB0 system. In these cases, when determining the Rh factor to consider group specificity of serum. Antirhesus serum group 0 (I) determine the Rh factor only in erythrocytes of group 0 (I); antirhesus serum group A (II) – Rh factor only in erythrocytes 0 (I) and A (II), serum Antirhesus group B(III ) – Rh factor only in erythrocytes of group 0 (I) and B (III) antirhesus serum group AB (IV), and specially made universal determine Rh factor in erythrocytes of group AB (IV) and any other blood group.

 During each study to verify the specificity and activity of serum antirhesus to put control. To control use standard Rh-positive erythrocytes group 0 (I) or the same group that studied the blood, and standard Rh-negative erythrocytes necessarily the same group that studied the blood.

Determination of Rh factor must be done in two batches antirhesus standard sera. If the standard serum active in different conditions (for example, one of them contains a complete antibody and therefore active in a saline environment, and the second contains incomplete antibodies and active in the colloidal environment – in gelatin or polyglucin) then determine Rh membership should be made by various methods, as shown in the accompanying instructions for each series of serum

2. Determination of Rh factor – D (Rh) using a standard universal reagent (in test tubes without heating).

To do this, use a standard universal reagent Antirhesus – anti-Rh (D) and standard erythrocytes to control. In tripod put 2 rows of test tubes by the number of samples in each row of red blood cells and 2 tubes for control research – standard Rh-positive and Rh-negative erythrocytes. In vitro inscription surname and initials of the person whose blood tested. According designate and control tubes. In all tubes 1st row make 2 drops (0.1 ml) of the standard universal reagent Antirhesus. In all tubes 2nd row make 2 drops (0.1 ml) of 0.9% sodium chloride and one drop (0.05 ml) 33% solution polyglucin. In each pair of tubes made in accordance with the designation 1 drop (0.05 ml) studied blood, standard Rh-positive and Rh-negative erythrocytes. Content tubes mixed by shaking and then slowly turn around its axis, tilting almost to a horizontal position so that the contents poured on the walls. Typically, agglutination occurs already for 1 minute. However, the formation of stable antigen-antibody complex and distinct reactions, contact with reagent red blood cells should last at least 3 minutes. After 3 min in a test tube add 2-3 mL of 0.9% sodium chloride and stirred the contents of 2-3-fold rotation tubes without shaking it.

The result was assessed by the presence or absence of agglutination test. If agglutination as large lumps or flakes bonded with erythrocytes studied blood believe Rh positive (Rh +). In the absence of agglutination (homogeneous color) studied blood Rh-negative (Rh-). However, these results should be considered credible only after checking the control samples, ie, in the case of a positive reaction with standard Rh-positive erythrocytes and negative – with Rh-negative, and after viewing the results in the 2nd control number. All tubes 2nd reference number agglutination should not be. The presence of agglutination in any of the control tube row indicates a nonspecific agglutination of red blood cells and caot take into account the outcome of the study as probable. In these cases, to determine Rh belonging to apply another antirhesus sera, including serum antibodies with complete or washed erythrocytes warm 0.9% sodium chloride leaching of these autoantibodies.

 

3. Determination of Rh affiliation rapid method using serum Antirhesus AB (IV) blood, diluted 20-30% albumin solution or 30-33% solution polyglucin without heating.

At the bottom of the Petri cup put a drop of this standard serum AB (IV) blood that contains antibodies antirhesus and next drop of Rh-negative serum AB (IV) group, which does not contain antibodies. These drops’ll add investigated blood 2-3 times smaller in volume, stirred with a glass rod or turn corners objective glass, shake the cup 3-4 minutes, then’ll add 1 drop of isotonic sodium chloride solution. Results read after 5 min. If agglutination of red blood cells studied with antirhesus serum and no reaction with Rh-negative control serum – Rh-positive blood. In the absence of agglutination test in both serum – blood Rh-negative.

The main causes of errors in determining the Rh factor by standard sera can be: reduced activity antirhesus sera violation proportions studied blood and serum discrepancy temperature regime, reducing exposure (less than 1 hour), lack of control and specific tests.

 

4. Determination of Rh factor using monoclonal antibodies.

Monoclonal reagents (antibodies) are designed to detect specific antigens of Rh on human erythrocytes. They are used instead isoimmune serum or in parallel with them. Monoclonal test reagents – a monoclonal antibody produced by heterohibrydoma. Monoclonal anti-D-antibodies produced in the form of full (IgM) and incomplete (IgG) antibodies. Anti-D-IgM-antibodies cause direct agglutination of red blood cells with D-antigen and can be used in any modification of the direct agglutination

Defining the Rh blood belonging using monoclonal antibodies should be performed in two stages: first, the blood of the patient examined using reagent monoclonal antibodies anti-D, if you get a negative reaction with this reagent, the additional conducting studies such blood with monoclonal reagent standard anti-C. Monoclonal antibodies used in direct agglutination reactions on the plane, in vitro and in mikroplati. Determination of antigens D and C can be conducted in the native blood, taken from the preservative, in blood taken without preservative.

Agglutination test on the plane. On a plate or glass slide causing a large drop (0.1 ml) reagent Antirhesus along put a small drop (0.05 ml) studied blood and mixed them. Agglutination test begins 10-15. Clear agglutination occurs within 30-60 s. Reaction assessed after 3 min after mixing the reagent with blood.

Agglutination test in test tubes. This washed red blood cells from blood study and prepare with them 5% suspension in saline. In test tube 1 drop of reagent (about 0.1 ml) and’ll add 1 drop of 5% suspension of erythrocytes. Contents of the tube thoroughly mixed by shaking and incubated (aged) 30 min at room temperature. Then the tube is centrifuged at a speed of 1500-2000 rpm. / Min for 1 min. Gently shaking the test tube, evaluate its contents. A negative reaction precipitate erythrocytes can be easily broken and forms a homogeneous opaque suspension. If a positive result, sediment is not broken, but remains in the form of one or several large bunches (agglutinates) against the backdrop of clear fluid.

Agglutination test for mikroplate. In hole mikroplate make 1 drop (0.05 ml) of test reagent and mixed with a drop of 5% suspension of erythrocytes, washed in saline. Leave on for 45-60 min incubation at room temperature. The result of the reaction is measured by drawing sediment that formed at the bottom of the hole. A negative result of sediment uniform, homogeneous. If a positive result, sediment settles unevenly, its edges jagged.

It should be noted that some people with Rh-negative blood are carriers of certain specific Rh-antigens. In this connection, in all cases, blood transfusions should be tried on Rh compatibility. Is not allowed to transfer to the card-patient information from a passport or other documents on the blood group and Rh affiliation, they can be made inaccurate data.

 

Preparing the patient for transfusion

In all cases, before each transfusion of blood or blood components to determine group membership and Rh blood of the patient and donor. In addition, to be held mandatory tests for compatibility, are distinguished: 1) individual test for compatibility by AB0 system, 2) test for the Rh factor (in preparation for transfusion), 3) the biological sample (early transfusion).

To perform the first two tests should have serum of the patient. It should be fresh, received daily blood transfusions or before (but not more than one day prior to transfusion), provided it has been stored at +4, +6 ˚ C.

For serum in patients taking 4.5 ml of blood in a test tube without stabilizer, which immediately inscription surname and initials of the patient, his blood group and date. Then put in a test tube rack and place in the refrigerator to defend. If you want to speed up the separation of serum from blood tube centrifuged 5-7 min at a speed of 2000-3000 rpm. / Min. After coagulation and clot retraction of it separates whey, which it used for tests for compatibility. Subject to store serum in the refrigerator shelf life – up to 2 days.

Blood donor for samples taken from the bottle after it prepared for transfusion.

Sample of individual compatibility of blood groups engaged by the system AB0 serum from the recipient. It is performed in a well-lit room at room temperature within +15-25 ˚ C. On a white surface (porcelain plate, plate) pipette applied drop of serum of the patient, and near it is 5-10 times smaller drop of blood donor (10:1), and then mixed with a dry glass rod or angles objective glass. Then gently shaking the plate for 5 min while monitoring the outcome of the reaction. No agglutination test (test negative) indicates the blood compatibility of donor and recipient for blood group AB0 system. The appearance of agglutination (test positive) sign of incompatibility and transfusion of blood inadmissibility. It should be remembered that the low titer group antibodies in serum of patients with mild or activity agglutinogen A the donor (subgroup A2), it may come much later. Therefore, the observation must be conducted at least 5 min. In doubtful cases, perform thermal breakdown of individual compatibility.

Thermal analysis of individual compatibility: the bottom of the Petri cup put 2-3 drops of serum of the patient and donor blood drop in the ratio of 10:1, they are mixed with a glass rod (drop must be sufficiently large and massive). For better assessment tests recommended to put a drop on a glass slide. Between him and the cup is placed a circle of white filter paper. Cup immersed float on a water bath at a temperature of 44-48 ˚ C for 10 min (for water bath using apparatus “Rh-1”, in his absence – a pan of not less than 2 liters). To reduce evaporation serum (drying drops) Petri recommend cover paper circle. After 10 minutes, take out the cup and evaluate the results. The sample should be evaluated in the first minute, shaking a glass slide with a drop of over a white background or on the lighted lamp (in the absence of filter paper). When these conditions are not met, the vystyhanni drops can occur nonspecific agglutination. Sometimes desiccation drop and roll fibrin on its surface can be formed film to be carefully removed by touching its edge needle. The presence of agglutination (test positive) indicates the incompatibility of individual blood donor and recipient, and pour this blood test for categorically forbidden. After individual compatibility test conducted on blood compatibility of Rh factor.

The test of the compatibility of the Rh factor (from 33% solution polyglucin): this test is carried out in vitro without heating for 5 min. In test tube 2 drops serum of the patient, 1 drop of blood and 1 drop of specially prepared 33% solution polyglucin. Then the contents of the tube mixed by shaking and render such provision, that he poured on the walls of the tube. This procedure is continued for 5 minutes. Then pour into the tube 3-4 ml isotonic sodium chloride solution, mix it and see the light. If the contents of the tube is uniformly painted, with no signs of agglutination, blood donor is compatible with the blood of the patient relative to the Rh factor Rho (D) and can transfused. In due to the fact that, in determining the Rh affiliation identified different types of Rh factor, lately instead of the above test for Rh compatibility proposed test using 10% gelatin solution.

Test for compatibility with 10% gelatin solution and more accurate in assessing visual. She performed in vitro at +46-48 ˚ C for 10 min. In test tube one drop of blood donor, then’ll add two drops of warmed up to dilution 10% gelatin solution and 2-3 drops of blood serum of the patient. Contents of the tube mixed (by shaking) and placed for 10 minutes in a water bath at a temperature of +46-48 ˚ C. Then the tube is removed, added to 5.8 ml of it isotonic sodium chloride solution, mix the contents by 1-2-fold reversal tube and see the light with the naked eye or through a magnifying glass. The presence of agglutination of a suspension of small, sometimes large lumps against lit or completely discolored fluid means that the blood donor is not compatible with the blood of the patient and it can be transfused to him. If the contents of the tube is evenly colored, with a slight opalescence and it is not observed agglutination of red blood cells, blood donor is compatible with the blood of the patient. In doubtful cases, the test should be repeated or to a new one.

The test of the Rh compatibility is important, especially if the patient burdened transfusion history, and women – and obstetric history.

Test for Rh compatibility spend as transfusion of Rh-positive blood Rh-positive patients, and Rh-negative blood Rh-negative patient. Sample spend with each vial of blood, packed red blood cells, washed red blood cells. Remember that tests on a group and Rh compatibility in any case not replace one another. With these tests it appears compatibility between agglutinogen agglutinins and blood that manifest themselves in different situations. Only two of the samples may prevent timely transfusion of incompatible blood or blood components.

 Biological samples is carried out immediately after venopuncture by jet 3 single injection of 15 ml of blood every 3 min (packed red blood cells, washed red blood cells, plasma). It should be remembered that the biological test for compatibility in children in the same way as in adults, three times, but smaller portions: children under 2 years – 2 ml to 5 years – 5 ml, 10 years – 10 ml, children , over 10 years – 10-15 ml. To prevent blood clotting in the needle during a three-minute interval transfusions goes liquid drops (20 drops per minute). Blunders infusion is indicated dose levels not bolus and infusion: the drip infusion can pour much larger number of incompatible blood without severe reactions, but the subsequent development posttransfusion shock. When biological samples carefully observe the patient (complaints, appearance, breathing, pulse). And only in the absence of clinical manifestations of reactions at triple infusion patient Transfusion fluids (biological test is negative) to continue the rest of transfusion transfusion liquid – infusion or bolus – depending on the evidence. In the case of incompatible blood infusions behavior of the patient becomes restless, feeling it worse: fever appears, sensation in the chest. The patient complains of pain in the lower back, abdomen, head. Pulse usually becomes small and frequent, reduced blood pressure. Breathing becomes shallow and faster. The facial skin becomes cyanotic red color, which varies pallor. If you have any of the signs described transfusion of blood or blood components or other liquids should be discontinued. The patient is subject to medical supervision, with the interpreter cause reactions or complications and spend the necessary treatment. Biological test compatibility practically prevents the possibility transfusion of incompatible blood system AB0, transfusion of tainted blood (hemolyzed, infected, superheated), and detects individual sensitivity of each recipient to the donor’s blood. Transfusion patient components and blood products can be made only with the consent of the patient. He must know what he faces the rejection of the application Transfusion means, at the same time should be informed that they may be adverse effects of such treatment. This requires modern international conventions on human rights and laws of Ukraine (Decree of the Supreme Council of Ukraine of 11.09.1992, the “Basic Law of Ukraine on Health Care”).

 

Blood transfusions, blood products, blood substitutes.

Complications of blood transfusions.

Indications and contraindications for transfusion of blood components, products and substitutes

 

Today, blood is regarded as average transaction transplantation of tissue that is fraught with serious complications. We must remember that, despite the strict requirements of the definition of group membership and Rh blood donor and recipient, the body begins still immune conflict because, in addition to erythrocyte and plasma factors, there are many others that do not count – leukocyte , platelet others. Expressed immune conflict can arise even at minimum volume of blood transfusion. So recently the practice of introducing new principles transfusion tactics – component infusion-transfusion therapy, which is based on a differentiated approach to the use of blood components (packed red blood cells, washed red blood cells, platelet and leukocyte plasma mass) and its protein products (albumin, fibrinogen, polibiolinu etc.) as well as substitutes.

Components and blood products give a more pronounced treatment effect is less dangerous in immunological terms, because they contain a smaller set of antigens in their composition. When using blood components frequency of complications and reactions decreases by several times compared with the transfusion of whole blood. So today believe that absolute indications for transfusion of whole blood can occur only in extreme situations – for large blood loss, wheo blood components. Under existing regulations, currently allowed only one groupe transfusion and one Rh blood, erythrocytes and plasma. Only in rare cases – with absolute indication for transfusion, lack one groupe donated blood components – acceptable transfusion “universal” 0 (I) blood group one Rh no more than 500 ml. Children need to transfuse only one groupe and one Rh blood. In similar situations in the absence of plasma one groupe can use plasma group AB (IV) transfusion recipients of any blood, plasma group A(II) orB (III) – recipients of 0 (I). Rules group compatibility cryoprecipitate transfusions are the same as for plasma. Components and blood products administered only to compensate for the deficiency of specific cellular and plasma components of blood. Their transfusion may only be exercised in the absolute indications and only in cases where the possibility of alternative treatments have been exhausted.

In absolute indications include: 1) acute blood loss (more than 30% of BCV), 2) traumatic shock II-III level.

All other indications for hemotransfusion belong to a relative anemia; continuing bleeding, coagulation of blood disorders, decreased immunity, regeneration, reactivity, etc. ..

Note that the approach to the transfusion of blood components and each patient should be individualized, taking into account the indications and contraindications. There are absolute and relative contraindications to transfusion.

Absolute contraindications to transfusion are: acute cardiopulmonary failure, accompanied by pulmonary edema.

Relative contraindications: acute thrombosis and embolism, heart disease with circulatory failure, hypertension III stage, kidney disease, liver disorders of cerebral circulation allergic disease (polyvalent allergy, bronchial asthma) tuberculosis, rheumatism and others. In these states use hemotransfusion should be used with extreme caution

Choosing transfusion environment. The proper decision on the choice transfusion medium dose, method and route of administration will depend on the success of Transfusion therapy and its safety. Blood transfusions to treat anemia, leukopenia, thrombocytopenia, disorders of blood clotting when observed deficiency of certain blood components, is not justified, because to replenish spent some factors other in the introduction which is not necessary. Therapeutic effect of blood in such cases lower likelihood of complications increases and blood flow is much greater than the introduction of concentrated components or blood products. Yes, hemophilia patient must enter only factor VIII. To cover the costs of the body in it through the blood to enter several liters of fresh blood, whereas this need will only several milliliters antihemophilic globulin (cryoprecipitate). Therefore, patients should be given only to those components or blood products they need.

 

Transfusion product.

With Transfusion of, instead of whole blood, the most common are erythrocyte mass, washed red blood cells, fresh frozen plasma (Table 3.1).

Table (3.1) Transfusion product

 

 

Components of blood.

Red cell mass obtained from preserved blood by removing the plasma. It contains the same amount of hemoglobin and erythrocytes and blood, but to a much lesser extent. It is less citrate dissolved antigens and antibodies, plasma protein factors that determines its lower reactogenicity. Erythrocyte mass stored at +4-8 ^oC Storage time erythrocyte mass depends on the preservative. Red cell mass harvested on a solution gluhytsyr or cytroglukofosfat, stored 21 days at a solution cyglufad – up to 35 days.

The main indications for the use of packed red blood cells is a significant reduction in the number of red blood cells resulting in acute or chronic blood loss.

However, the use of packed red blood cells to replenish BCV currently considered impractical because 30% of transfused red blood cells because of their immune incompatibility immediately deposited in the microvasculature that enhances the growth of hemic hypoxia, and the remaining 70% are beginning to bind oxygen only after 24 hours. Therefore, indications for transfusion of packed red blood cells believed hemoglobin level below 75 g / dL, hematocrit – 0.25 g / l, and in some cases even hemoglobin level below 50 g / l. Thus the volume of transfused packed red blood cells should not exceed 50% of the blood volume. If the same fill BCV only components of the blood, the patient developed rapidly effect “swamping lungs.” Erythrocyte mass may be used in conjunction with blood products and fresh frozen plasma and give greater effect than the use of whole blood.

Washed red blood cells – is laundered 1-3-fold in saline (after removal of plasma) donor erythrocytes. Storage time washed red blood cells up to 24 hours from the moment of harvesting (in a refrigerator at +4-8 ^oC), it is better to pour the first 3 hours. Transfusion of washed erythrocytes shown in case of severe anemia and sensitization of the patient to the factors plasma donor.

Leucocyte mass – a component of blood that contains mostly white blood cells. Leukocyte mass obtained by settling of blood or by cytoforez. Leucocyte mass produced in bottles of 50 ml. This number contains one dose leukocyte mass, which corresponds to the number of leucocytes in 500 ml of blood. During the transfusion of leukocyte mass necessary to consider group affiliation blood donor and recipient. Keep leukocyte mass can be no longer than one day. Leucocyte mass used in radiation leukopenia and infectious origin, sepsis, drug agranulocytosis, to accelerate healing. Poured leukocyte mass at intervals of 2-3 days at a rate of 30-40 drops per minute.

Platelet mass consists of 60-70% suspension of platelets in 40 ml of plasma. Used immediately after harvesting (extempore), store it caot. Platelet mass is widely used in thrombocytopenic bleeding (ulcer thrombocytopenic purpura, platelet deficiency, etc..). Infusion of platelet accelerates clotting time and blood clot retraction. Transfusion conducted taking into account group and Rh compatibility with speeds of 30-40 drops per minute intravenously.

Fresh frozen plasma – the most effective type of plasma that almost fully retains its biological functions, including most of the clotting factors (II, V, VII, VIII, X, XI, XII i XIII). After preparation of the plasma its frozen and stored at – 20 ° C throughout the year. It stores all labile factors of hemostasis. Immediately before transfusion of fresh frozen plasma propagated in water at a temperature of +37-38 ^oC. Thawed plasma can be stored for no more than 1 hour. Fresh frozen plasma should be one group with the blood of the patient in the system AB0. In the absence odnohrupnoyi plasma in emergency situations allowed plasma transfusion group A(II) of the patients with blood group 0 (I), plasma B (III) – patients with blood group 0 (I) and plasma group AB (IV) – a patient with any -what blood type.

Dry plasma is produced by drying in vacuum at +37-38 ˚ C. Dry plasma stored up to three years. Before transfusion it is dissolved twice with distilled water or isotonic sodium chloride at a temperature of +37 ˚ C.

Transfusion of plasma shown in patients with traumatic shock, bleeding, hypoproteinemia with others.

Besides the usual native, fresh frozen or dry plasma produced plasma Special: antistaphylococcus, antihaemophilic, antipseudomonas et al. However, it should be noted that recently, native to transfusion, fresh frozen plasma and other are restrained. This is due to the fact that the period of seroconversion in HIV infection lasts about six months (PM Perehrestenko, 2002.). Accordingly, the proposed transition to quarantinesation plasma, which is based in unused harvested tested plasma for 6 months, followed by re-examination of the donor, and only after obtaining negative test results for HIV plasma stored six months, can be used.

Preparations of blood.

Albumin is a major fraction of plasma. With 400 ml of plasma produced 6 grams of protein, including 55-60% albumin. Albumin is produced in the form of 5, 10 and 20% solutions. 5% solution used for the rapid increase in CBV and 10-20% – for correction of hypoproteinemia. Term storage at +4-8 ˚ C – up to 5 years.

Uses albumin to treat malnourished patients with severely reduced protein levels (with hypoproteinemia), and dehydration (hypovolemia) during burn shock, anemia.

Protein – protein solution plasma produced at doses of 100-200 ml. Contains 75-80% albumin, 20-25% alpha and beta globulins. Indications for transfusion of protein are the same as for albumin.

Cryoprecipitate. It is a plasma protein fraction of blood. One dose contains 100 units of antihemophilic globulin (VIII clotting factor), fibrinogen, and fibrynostabilizing factor (Factor XIII). The drug is used in bleeding, especially in reducing the number VIII and XIII of clotting factors and hemophilia. The drug was diluted with distilled water in an amount specified on the label, injected intravenously or jet-jet method based on group affiliation blood recipient. After entering the first 5 ml of cryoprecipitate to detect hypersensitivity in the patient perform a biological sample. The optimum storage temperature – +30 ° C. (24 months).

 Fibrinogen is made from fresh blood by drying. It contains the active antihemophilic globulin. Available in 250-500 ml vials containing 1.2 g of fibrinogen. Shelf life – 2 years. Before infusion of fibrinogen diluted twice distilled water or isotonic sodium chloride solution.

Apply with various bleeding, fibrinolysis, DIC syndrome, traumatic shock.

Immunobiological preparations made from donated plasma and placental through active immunization of donors corresponding antigen. They contain a large set of antibodies against various bacteria and viruses. The resulting antibody drug has a high specific activity compared to the causative agent.

Among these drugs are widely used antistaphylococcal g-globulin poliglobulin, Antirhesus (D), anti-influenza, antihepatic immunoglobulin others. All immunological drugs produced in ampoules of 1, 1.5, 5 ml and stored in a refrigerator at 2-10 ˚ C. Storage time- up to three years. Enter the scheme intramuscularly.

Blood substitutes (tabl.3.2.) – A drug that when injected into the patient’s body carry the therapeutic effect, similar to blood. Blood substitutes are mainly used to correct changes in the body: high blood pressure, detoxification, rehabilitation BCV, synthesis of the protein fractions of blood, etc.. Typically, this means Plasma.

Depending on the actions of all substitutes are divided into six groups:

1. Blood substitutes hemodynamic actions, they are called anti-shock. Mechanism of action aimed at normalization of hemodynamics, increased CBV. In addition, they reduce stasis and aggregation of red blood cells, improves blood rheology. This group of substitutes include: Refortan; stabizol; infezol; polifer; perftoran; reopolyglukine; reohlyuman; zhelatynol others.

2. Solutions desintoxication steps: a) Neogemodez b) polidez c) enterodez etc. Therapeutic effect of the action of these solutions is due to the fact that they bind toxins and remove them through the kidney barrier. In addition, these drugs improve blood rheology, microcirculation and create conditions for the transition of intracellular fluid into the vascular bed, which in turn leads to an increase in CBV and improve hemodynamics. Recently, for detoxification use multiple drugs or one complex. For their production technology and applying homeopathic ingredients vegetable, mineral, animal, catalysts, vitamins, neurotransmitters, embryonic tissues.

3. Tools for parenteral nutrition. The infusion of these solutions is shown in cases where the patient from one reason or another caot eat it or not absorbed in the gastrointestinal tract. Preparations for parenteral nutrition can be divided into three groups: protein, fat and preparations for carbohydrate metabolism. The basic principle underlying the parenteral nutrition is to provide the body with energy, proteins, fats and carbohydrates, which makes it possible to resist such aggressive factors like infection, burns, trauma and surgery. Today distinguish full and partial parenteral nutrition. Complete nutrition involves the introduction into the body intravenously all components that provide livelihoods.

By protein drugs include: a) hidrolizyn b) aminopeptyd c) infuzamin d) polyamine and others. It basically hydrolysates, which are made from whey protein blood of animals and humans by hydrolysis enzymes bases, acids. They are a mixture of amino acids and simple peptides. Produced these drugs in vials 200-400 ml. Introduction to protein drugs creates a positive nitrogen balance – a “golden rule” parenteral nutrition. It is known that the average amount of nitrogen in the protein is 16% (at 6.25 g protein contained 1 g of nitrogen). If you know the amount of nitrogen that is released, you deduct the right amount of protein.

To correct fat metabolism fat emulsion used – a white milk similar fluid. To produce fat emulsions used primarily fats of vegetable origin. Issued fat emulsion in bottles of 400 ml. These include: infuzolipol, lipofundyn, lipomayz, intralipid, lipofizan etc.. With body fat emulsions provided essential fatty acids and fat-soluble vitamins.

To ensure carbohydrate metabolism are widely used in various concentrations of glucose, glucose is better than fructose and sugar inversion (a mixture of glucose to fructose). Useful than carbohydrates, the energy source is alcohols (ethanol, sorbitol, xylitol).

4. Regulators fluid and electrolyte and acid-base status. For this purpose, use saline crystalloid solutions: 0.85% sodium chloride solution, Ringer-Locke (9 g sodium chloride, potassium chloride, 0.25 g calcium chloride 0.23 g, sodium 0.2 g, glucose 1 g, 1000 ml of water) and others. Saline solutions are used primarily to correct fluid and electrolyte metabolism during dehydration, intoxication, large hemorrhages. They are rapidly absorbed and excreted from the bloodstream and the body in general.

5. Blood substitutes-hemocorrectors. They have one of the main functions of blood – oxygen transfer. These include hemoglobin solution, emulsion fluorocarbon compounds. Most use perftoran, which is a submicron emulsion based perfluoroorganic compounds and has a strong gas transport function. It can be transfused without blood, it captures from the respiratory tract in 3 times more oxygen than red blood cells can be stored in the refrigerator for up to 3 years.

6. Blood substitutes complex action. This multifunctional solutions combined hemodynamic and desintoxication action; desintoxication actions in complex with amino acids and more. The combination of infusion of blood components and plasma substitutes became the leading principle transfusion medicine known as controlled hemodilution.

tabl. 3.2. Blood substitutes

 

 

Methods and techniques blood transfusion

In all cases, before each transfusion of blood or blood components to determine group membership and Rh blood of the patient and donor. In addition, to be held mandatory tests for compatibility, are distinguished: 1) individual test for compatibility by AB0 system, 2) test for the Rh factor (in preparation for transfusion), 3) the biological sample (early transfusion). Dosage, the method and means of transfusion of any fluid transfusion physician determined in each case.

Direct transfusion provides blood directly from donors (previously examined) patients without phase stabilization or preservation of blood. Only in this way can transfuse whole blood. Direct transfusion carry only intravenously (Fig. 4.).

 

donor                                                           recipients

         

Fig.4. Direct blood transfusion

 

At present the method of direct transfusion of blood is considered as a necessary medical event in the extreme situation in the development of sudden massive blood loss and absence in the doctor’s arsenal required number of blood components (packed red blood cells, fresh frozen plasma, cryoprecipitate, etc.). In some cases, instead of direct transfusion of blood before transfusion resort freshly made “warm” blood (from previously examined donor). However, according to AI Vorobiev (2001), no “warm” blood does not exist – transfused blood clots, extremely dangerous for the patient (the composition is completely different environment than in the bloodstream). Blood transfusions, scouted for AIDS and other vector-borne infection is allowed only when health reasons and lack of fresh blood or its respective components must be documented in by hospital doctors to address consultation and consent of the patient or his relatives. Transfusion of blood scouted in such cases does not remove the responsibility from the doctor for her complete study after transfusion!

Indirect transfusion carried out by means of disposable filter, which directly joins bottle, this is the main method of transfusion. Intravenous (venopunction, venosection, catheterization vein) is the most effective way to transfusion. Much less in medical practice using such routes of administration as intraarterial, intraosseous and others.

 

Indirect blood transfusion

 

Venosection, catheter.

Exchange transfusion partial or complete removal of blood from the bloodstream recipient with simultaneous substitution of adequate or more blood. The main objective of this operation – removal together with the blood of various poisons (for poisoning, endogenous intoxication), decomposition products of hemolysis and antibodies (in transfusion shock, severe toxicosis, poisoning, acute renal failure, etc.). Exchange transfusion can be successfully replaced by therapeutic plasmapheresis, which removes up to 2 liters of plasma substitute plasma substitute its rheological and fresh frozen plasma.

Autotransfusion – transfusion to the patient’s own blood. His conduct after the preparation of the preservation of his own blood and in patients before major surgery. Planned autotransfusion has several advantages over blood transfusion: risk eliminated complications associated with incompatibility, transfer of infectious diseases (hepatitis, AIDS, etc.)., Risk alo immunization et al. Autotransfusion exercise in patients with major surgery, accompanied by significant blood loss, when an abnormal liver function and kidney, which significantly increases the risk of possible posttransfusion complications of donor blood or red blood cells. Method autotransfusion contraindicated in the presence of inflammation, sepsis, liver and kidneys, as well as pancytopenia. Absolutely contraindicated application method autotransfusion in pediatric practice.

Reinfusion of blood is a kind autotransfusion and the patient is transfusion of blood that flowed in the wound or serous body cavities (abdominal, thoracic) and was in them no more than 12 hours (longer, increasing the risk of infection).

This method is widely used in ectopic pregnancy, rupture of the spleen, wounds of the chest, abdomen, in traumatic operations. For its implementation requires proper equipment, which consists of a sterile vessel, scoop, set of tubes, electric pumps, disposable systems and others., Or “sel-seyver” which independently collects, cleans, filters the blood spilled and then sends it to the bloodstream.

Stabilizers for spilled blood is standard hemopreservatives (sodium citrate, cyglufad, Glugitsir, cytroglukofosfat etc..) Or heparin (10 mg in 50 ml of isotonic sodium chloride to 450 ml of blood). In most cases, the collected blood during surgery diluted isotonic sodium chloride solution in a 1:1 ratio and add 1000 OD of heparin in 1000 mL of blood.

Transfusion made via infusion filter. It is better to transfusion through a special micro.

Fig 5. System for infusion

 

The speed of Transfusion fluids. In shock, especially when combined with massive blood loss when there threatening volemic and anemic violation when you need to quickly increase blood volume, should be performed transfusion jet way in one or more veins. In all other cases, transfusion Transfusion fluids typically spend slow-drip method. This method allows you to enter a large number of transfusion fluids without much risk associated with congestion of the cardiovascular system. An infusion rate of 20 ml per minute is considered jet, and a rate of 15 ml per minute, which corresponds to approximately 40-60 drops per minute – droplets.

Preparation of transfusion fluids. After visual quality assessment Transfusion liquid that was kept in the refrigerator in a bottle, it should be warm (regardless of routes of administration). Transfusion refrigerated liquids poorly tolerated, these fluids can cause severe reactions, especially in critically ill and children. To reheat a bottle of fluid transfusion should be placed in a thermostat or heated in a water bath to a temperature not higher than +37 ˚ C. This bottle is immersed in clean dishes with warm water whose temperature is gradually increased from +25 ˚ to +36-37 ˚ C (no higher!) By pouring more hot water. Each time this bottle is removed, pour water, stirred it and measure the temperature. The water level in the vessel must be adequate and meet the level of the liquid in the bottle. Label the bottle before diving record eraser. You must refrain from the use of improper methods warming: bottle wraps a towel dipped in boiling water, heating over a gas burner, electric stove, use hot objects such as hot lid sterilizer, et al. Improper heating of blood or blood components leads to denaturation of plasma proteins, hemolysis of red blood cells and other changes, resulting in transfusion arise serious complications that can result in death of patients. Repeated heating of the blood is not allowed.

Saline, non-pyrogenic distilled water to dissolve dried blood products must also have the appropriate temperature (+20-30 ˚ C). When the solvent is an urgent need to warm up in warm water at a temperature of about +30 ˚ C for 10-15 minutes.

During the installation of the system for transfusion blood erythrocyte mass, plasma vial gently stirred. This bottle several times transferred from a vertical to a horizontal position and slowly rotated around the axis.

Installation of the system. After macroscopic evaluation, heating of blood or other fluid conducting mounting system. For this release the tube from bottle wrappers, gauze, paraffin and grease with a solution of iodoform or alcohol. If cork bottle closed aluminum plate, her unbend and open areas cork smeared antiseptic. Transfusion Transfusion environments, substitutes and others. carried out only using disposable systems for intravenous infusion. Installation of the system is carried out in accordance with the instructions printed on the package. The system is not suitable for use if the package is swollen, compromised his integrity or expired shelf life. After careful filling system (prevention of air embolism) check a blood donor, conduct tests on individual Rh compatibility, perform biological sample.

Transfusion liquids must comply with all requirements of asepsis and antisepsis. Installation of the system must be carried out cleanly washed hands, touching hands and other objects needles treated with antiseptic and peel the skin at the site of puncture.

 

In a transfusion should observe the following rules:

 

1. Once punctured bottle with any liquid transfusion should be used immediately, it can not postpone and reuse later.

2. Transfuse should be using a single system with the bottle, which stocked Transfusion liquid.

3. Do not use for transfusion fluid from the bottle with impaired tightness and without visual assessment of its contents.

4. At the end of transfusion leave 20 ml liquid and store it in the refrigerator for two days.

5. In the absence of complications of transfusion liquid medical professional should remove the label from the bottle, glue it in by hospital, a bottle with lukewarm water and send it to the station of blood transfusion.

 

Complications of blood transfusion and blood products

 

All complications of transfusion are divided into three main groups: 1) complications of mechanical nature, 2) the complications associated with the change of reactivity, and 3) Transmission complications associated with infection of the patient donor blood and its components.

 

Complications of mechanical nature arise mainly due to violations of guidelines and techniques transfusion of transfusion fluids.

Life-threatening complication is air embolism. The air that enters the system during its filling and goes into a vein, moves to the right half of the heart, and then – in the pulmonary artery and its branches, blocking them. Thus there is a sudden loss of consciousness, stop breathing (apnea) and heart (syncope). Skin becomes pale, cyanotic. Pulse is not detected, blood pressure is measured.

First aid is a rapid lowering of the head end of the bed, holding Ventilator closed cardiac massage. Doctors II the IV intercostal space to the right of the sternum puncturing right half of the heart and suck frothy blood of 200-250 ml.

Sometimes a blood transfusion may be complicated by embolism blood clots (thromboembolism). These problems may be caused by: improper preservation (stabilization) blood transfusion incorrect technique and distance thrombus, which was formed to transfusion (chronic thrombophlebitis) in the veins due to increased venous pressure. Often occurs embolism pulmonary artery and its branches. Closing the main branches of the pulmonary artery or its branches followed by the small retrosternal pain, acute respiratory failure (dyspnea), cardiac abnormalities (collapse), tensioeck veins. Quickly stops breathing and circulation. Such a course of complications resulting from a massive embolism of the main pulmonary artery trunk. Death usually occurs within a few minutes. When embolism small branches over time develop pulmonary infarction.

At the first signs of this complication should immediately stop the transfusion of blood type analgesic, antispasmodic, cardiac drugs. For the prevention of pulmonary infarction, pneumonia prescribed fibrinolytic drugs (fibrinolysin, streptaza, urokinase), anticoagulants (heparin, fraxyparyn, calcyparyn, FRAGMIN et al.). Absolutely contraindicated “washing” trombotic needles during blood transfusions, since there is a danger of embolism. It is strictly forbidden as transfusion of blood in the vein pressure (air injection using pears in a bottle with blood). Prevention of embolic clots or thromb is to use droppers with filters, check the quality of blood.

Along with these complications may arise phlebitis, thrombophlebitis in the area of ​​the vein into which carry infusion. In patients there pain along the vein, and palpation determine cord similar. Treatment consists in assigning a hot compress, anticoagulants (heparin, fraxyparyn, pelentan, fenilin etc.). Electrophoresis with heparin, holding limb immobilization; imposing bandage with ointment (indovazyn, troksovazyn).

Thrombophlebitis in the area of v/v infusion

During the transfusion of large quantities of blood components or blood products may develop acute enlargement of the heart. The patient feeling chest compression, pain in the heart, tachycardia, decreased blood pressure.

At the first signs of circulatory overload should immediately stop the transfusion, to phlebotomy (200-250 ml), appoint heart medications (consists of digoxin, strophanthin, korglukon etc.).

 

Complications associated with the change of reactivity.

Posttransfusion fever caused by endotoxin in getting Transfusion environment or the interaction of antibodies with recipient transfused leukocytes, platelets or immunoglobulins donor. Fever usually occurs within 1.5-2 h after injection Transfusion fluid. The patient feeling the heat, the body temperature rises to 38-39 ˚ C, appears headache, nausea, vomiting, and sometimes shortness of breath, pain in the bones back. In these cases, the patient must be warm (cover with blankets, put a heating pad feet, drink hot tea). If severe the reaction must enter painkillers (promedol, omnopon, tramadol, etc.), cardiovascular drugs (caffeine, cordiamin, strophanthin, corglukon), antihistamines (suprastin, diphenhydramine, diazolin), corticosteroids (hydrocortisone, prednisolone), antipyretics agents (acetylsalicylic acid askofen, Amidopyrine), intravenous 10% solution of calcium chloride (10 mL), 5% glucose (500 mg) with a 5% solution of ascorbic acid (5.10 ml).

Allergic reactions occur in recipients who have sensitization to various plasma proteins blood. They arise in the case of repeated transfusions of blood, plasma protein preparations. Signs of an allergic reaction occur already during the transfusion or within 15-20 minutes after its completion. It is manifested by fever up to 39-40 ˚ C, fever, sweating, headache, allergic swelling of various parts of the body, urticaria, wheezing, tachycardia, decreased blood pressure. Therapeutic activities are reduced to stopping blood transfusions. The patient should immediately introduce 10 ml of 10% solution of calcium chloride, 10 ml of 5% solution of ascorbic acid, antihistamines (diphenhydramine, suprastin, diazolin), in severe cases – corticosteroids (hydrocortisone, prednisolone). According to indications introduced strophanthin, corglukon, caffeine, etc. kordiamin.

Transfusion shock occurs after transfusion of incompatible blood (errors in determining blood group, Rh factor, conducting tests for compatibility). It may be caused as a result of transfusion of infected blood or blood that was accidentally frozen and thawed or heated to temperatures above +40 ˚ C. The main cause of this complication is massive intravascular destruction of red blood cells transfused incompatible donor, their hemolysis and formation of toxic degradation products (histamine, serotonin, callikrein, bradykinin, etc.) that cause a decrease in vascular tone and cardiac activity. Sometimes erythrocyte hemolysis occurs in the recipient under the influence of agglutinins blood donor, especially for non-compliance rules – only onegroups blood transfusion.

Clinic. On motion of Transfusion shock distinguish three periods: I – actually shock, II – kidney failure, III – recovery. The first period Transfusion shock (first few hours) appears immediately after the introduction of 20-40 mL of incompatible blood. In the patient has a sudden reddening of the skin, irritability, anxiety, fear of death, in the chest, pain, tachycardia, decreased. blood pressure. Following this, the patient’s shortness of breath, weakness, pale skin, acrocyanosis, nausea, vomiting, loss of consciousness with spontaneous discharge of feces and urine. One of the earliest and permanent signs Transfusion shock is intravascular hemolysis, which manifests hemoglobinemiya (increase in hemoglobin in the blood) and hemoglobinuria (presence of hemoglobin in the urine – red urine). To determine intravascular hemolysis in a clean dry test tube with anticoagulant (2-3 drops of heparin, 1-2 ml of preservation solutions for collecting blood or sodium citrate) make 3-5 ml of the patient’s blood and centrifuged. The appearance of a pink or red color of blood plasma indicates elevated levels of free hemoglobin and the presence of intravascular hemolysis. If the patient was not provided timely and adequate medical care, he has developed the second period – the clinical picture of renal failure. Kidney damage is due to occlusion of the renal tubules and capillaries damaged red blood cells, hemoglobin and its derivatives. The main feature of this period is oliguria (low urine). In severe cases developed anuria (absence of urine). The blood accumulates urea, creatinine, nitrogenous wastes, potassium, magnesium, phosphorus, causing water retention in the tissues. There generalized swelling of the body, the lungs, the brain. In some cases develop uremia – nitrogen poisoning slag, which is manifested by headache, weakness, dry skin, increased blood pressure. Along with this, there is parenchymal toxic hepatitis. During this period, whose duration is 1-2 weeks, death can occur due to uremia and heart failure.

If the patient is undergoing oligoanuria, then comes the third period – the period of recovery, which is characterized by a gradual recovery of renal function. There is a state of increased urination (polyuria). For a day patient identifies to 3-5 liters of urine, which creates conditions for dehydration (dehydration), electrolyte metabolism disorders – blood sharply reduced amounts of potassium (hypokalemia), severe cardiac activity. With favorable motion of Transfusion shock from blood gradually released toxic products (nitrogenous waste products), normalized rates of water-electrolyte metabolism, reduced kidney function, liver. Recovery of the patient, usually lasts 3-6 months.

Mortality from Transfusion shock observed in 20-30% of cases.

Treatment. It should begin immediately after the first signs of shock. It is urgent to stop the transfusion of blood or packed red blood cells, to give drink hot tea cornering patient heaters, cover with warm blankets, blanket. Intravenous 1% solution promedol or omnopon, glucose with insulin, vitamins. To increase blood pressure intravenously to enter corticosteroids (hydrocortisone, prednisolone), 400-450 ml dextran. In order to remove products of hemolysis of red blood cells carry out forced diuresis, which should be at least 75-100 mL / h, with 20% solution of mannitol (15-20 g) and furasemid (100 mg single dose, up to 1000 per day). To correct acid-alkaline balance injected 400-500 ml of 4% sodium bicarbonate. To combat hyperkalemia injected calcium supplements (calcium gluconate, calcium chloride). Volume of transfusion-infusion therapy should be adequate diuresis.

From the first days after the development of shock should be heparin or its analogs.

In cases where comprehensive treatment is preventing renal failure (in the second period Transfusion shock) to eliminate uremia treatment is carried out in specialized departments, where, if necessary, have the opportunity to hemodialysis machine using “artificial kidney”. During this period it is necessary to limit the introduction of liquids. The amount of liquid that is injected into the body must be equal to that which the patient loses the urine, feces, vomit, exhaled air. With the development of anuria should stop pouring osmotically active plasma substitutes, as a result of hydration may develop pulmonary edema, brain. Patients should be on the protein diet with fluid restriction to 600-700 ml per day.

At the stage of polyuria is necessary to prevent dehydration and electrolyte disturbances. Along with these measures serve to restore the function of the kidneys and liver. The patient is injected intravenously 20-40% glucose (200-400 ml) of ascorbic acid and insulin (40-50 units per 100 grams of dry glucose). For the purpose of detoxification and improved rheological properties of blood injected gemodez reopolyglukine, reohlyuman, albumin, plasma protein, etc..

In order to accelerate the excretion of toxic products to patients prescribed enterosorbent (enterosgel) treatment, siphon enema.

If transfusion of infected blood simultaneously with the above treatment administered intravenously large doses of antibiotics, including sensitivity to these microorganisms.

Equally important is the careful nursing of Transfusion shock. We conduct breathing exercises as preventing pneumonia, infectious complications in the mouth, in time to change clothes, stretch folds sheets, return the patient to hold back massage and so on.

 

Citrate shock develops in a large number of blood transfusions with a high content of sodium citrate. Toxic dose of sodium citrate is 10 mg / kg / min, which corresponds to the introduction of canned 2-3 ml of blood per 1 kg of body weight recipient for 1 min.

Clinically citrate shock manifested anxiety, accelerated heart rate, arrhythmia, lower blood pressure, breathing difficulties, convulsions. Signs citrate shock appear during blood transfusion or end it. To prevent shock citrate recommended for every 500 ml of blood donor introduce 10 ml of 10% solution of calcium chloride or calcium gluconate, since the introduction of citrate blood sodium citrate combines with calcium serum, causing the above disorders in the body.

Gear complications associated with infection of the patient with blood donor. Infect a patient at blood transfusion can hepatitis, syphilis, AIDS, malaria, toxoplasmosis, brucellosis and others. Among these diseases are the most common viral hepatitis. It occurs in 2-3% of recipients and often complicated by cirrhosis. In 10-15% of patients with hepatitis implantation leads to death. The incubation period of hepatitis B (serum hepatitis) – 9-26 weeks.

It should be noted that in recent years, cases of syphilis implantation fresh made transfusion of blood. In blood stored for more than 4 days at 4 ˚ C, syphilitic spirochete dying. For prevention HIV infection all donated blood undergoes testing for the detection of antibodies to the virus. Parallel conduct activities aimed at extracting donors who are at risk for AIDS.

Along with the penetration of the blood recipient specific infection through blood transfusion can occur bacterial contamination of blood his usual microbes (staphylococcus, streptococcus, Pseudomonas aeruginosa, Proteus, etc.). This occurs in violation of the rules of asepsis during preparation of the blood and blood transfusion. Medical worker who carries blood must strictly follow the rules of asepsis.

 

Monitor patients during and after transfusion Transfusion fluids.

During and after transfusion Transfusion fluids of patients establish closer care. Changing the status of the patient, his behavior or appearance of any complaints should be regarded as the first manifestation of complications. After transfusion Transfusion liquids patient prescribed bed rest for 2 hours. Two hours to measure body temperature, while its increase – repeat measurements every hour for 4 h. The day after the transfusion patient prescribed a general analysis of blood and urine. In posttransfusion period is important to monitor the excretion of urine, the number of urine and its color. The appearance of a pink or brown color indicates the development Transfusion complications. Only careful monitoring of the general condition of the patient, the level of blood pressure, body temperature, the number and nature of urine makes it possible to discover the beginning of complications.

Most reactions and complications occur usually within the first day. In case of complications posttransfusion should stop the transfusion, immediately inform your doctor and he has informed the hospital administration and blood transfusion station.

Documentation associated with transfusion Transfusion fluids. Blood Service hospital must have a well-established and promptly executed documentation. In each hospital chief physician orders assigned material compliance officer for registration (receiving, storing and issuing) Transfusion fluids, disposable systems for transfusion, the standard serum, erythrocytes for blood group and Rh affiliation etc.. In small hospitals accounting Transfusion fluids can be delivered to the home nurse hospital.

All Transfusion fluids that come into the hospital, according to invoices, log in magazines and issuing receipts. In these magazines hold registration issued environments transfusion requirements for hospital departments. Liquids that postponed (tightness, clots, etc.) blamed for the act.

Health care workers who are assigned accounting Transfusion fluids responsible for enforcing the correct mode of storage and recording of temperature refrigerator in a special journal temperature control storage of blood and other fluids.

Each transfusion of blood, blood components, medications and blood products in the record by hospital, according to the form in “Leaves registration transfusion fluids.” Leaf glued to the map inpatients. In his absence, recording is carried out in a protocol in the diary by hospital or by stamp, presenting the following data: 1) the date and time of transfusion, and 2) the indications for transfusion, and 3) the method of transfusion (routes of administration, rate of transfusion), the number of transfused fluid, 4) passport data of each vial of blood, packed red blood cells (surname, initials donor blood group, Rh membership number, or a series of drug vial, blood substitutes, date of preparation of the blood, packed red blood cells), 5) Results of control check of the patient’s blood the system AB0, 6) Results of control check blood donor, taken from the vial for AB0 system, 7) the results of tests on the compatibility of blood groups of donor and recipient for the AB0 system, 8) method and the results of tests on compatibility for the Rh factor, 9) result of biological samples, 10) signature physician.

Registration of each transfusion of Transfusion fluid doable as in “ Journal of registration transfusion of transfusion fluids.” Journal of plants in each department of a hospital, where they spent transfusion of Transfusion fluids.

Careful record blood and other fluids enables to control the work of medical staff promptly identify and prevent errors and violations during infusion therapy.

 

Methods of sampling blood from a finger.

 

1. Warn patient to blood sampling for he came in the morning and on an empty stomach.

2. Treat pulp fourth finger left hand a cotton ball soaked with alcohol, then with ether.

3. Take a left hand finger of the patient, gently pressing the flesh.

4. Take the right puku needle-scarifier and place it strictly perpendicular to the spot.

5. Vkola rapid movement of the entire length of needles (2-3 mm) skin cross across the fingerprint lines.

6. Remove the swab first drop of blood.

7. Collect blood in sterile capillary Panchenkov, lightly pressing the pulp of the finger.

8. Attach to the puncture watt ball soaked with alcohol.

9. Take a cotton ball blood traces.

10.Poprosit patient pressed a finger to his hand to stop the bleeding.

 

Determination of blood using standard sera.

 

1. Put on a clean plate, top left and right labels blood groups: I (0), II (A), III (B).

2. Apply under each separately labeled standard serum drops two series.

3. Treat pulp ultimate phalanx fourth finger left hand swab with alcohol.

4. Puncture Scarifiers skin.

5. Take away the first drop of blood a cotton ball.

6. Apply using a single glass rod blood on the plate along with serum (in the ratio 1:10).

7. Mix every drop of blood and serum together a glass rod.

8. Watch agglutination test for 3 min.

9. Add 1 drop of 0.9% solution of NaCl.

10. Assessment results in 2-3 minutes.

 

 

 

Determination of blood group according to standard erythrocytes.

You must have:

– Standard erythrocytes O (I) A (II), B (III) group;

– Prepared from blood donors with known blood group, retention period for 2-3 days at 4-8⁰C;

– Accessories that are necessary in determining the blood by standard serum.

Technique of reactions: 1) the subject of the veins taking blood for plasma and 2) the marked plate put 6 drops examinee plasma (0.1 ml) is added to each drop of 0.01 ml standard erythrocytes O(I) A (II ), B (III) blood (2 series), 3) and subsequent reading of agglutination reactions are similar, as in the study using standard sera. Evaluation of results:

 

 

Determination of blood group through monoclonal antibodies anti-A and anti-B.

 

SUPPLIES: scarifier, alcohol, cotton, plate, glass rods, monoclonal antibodies anti-A and anti-B, two vials of diluent substantive lenses.

1. Uncover vial monoclonal antibodies anti-A and anti-B and dilute monoclonal antibodies solvent NaCl

2. Put on a plate monoclonal antibodies two drops of anti-A and two drops monoclonal antibodies anti-B on the opposite side.

3. Mix different edges slides studied blood from monoclonal antibodies ratio of 1:10.

4. After 2-3 min. evaluate the results.

 

Evaluation of results:

 

 

Determination of Rh-factor

According antigenic system in human blood is a 6 core antigen D, d, C, c, E, e Rh factor. Depending on the presence or absence of erythrocyte most active antigen RhD blood dilyat Rh positive (Rh +), or Rh negative (Rh-). Rh antigen is launched from 8-9 weeks, the most active in the 3-4 a month’s embrion i remains unchanged for life. Antibodies in the plasma to the Rh-antigen produced only with admission in foreign organism it isoantygen. Determination of Rh-factor exercise by antirhesus sera and anti-D-monoclonal antibodies.

1. Determination of Rh-factor using standard sera Antirhesus.

 Express Method: In a cup or Petri a test tube put 1 drop of serum Antirhesus, it adds a little drop of blood under study (in proportsii 10:1). Complex “antigen- antibodies ” (agglutination) read no more than 3 minutes. In the presence agglutination blood Rh + (positive), in the absence Rh-( negative).

Laboratory method: Scanning in test tube, but the above components is added 10% solution of gelatin. Reaction to read after incubation test tube at t + 42-48⁰ C. In the presence agglutination blood Rh + (positive), in the absence Rh-( negative).

2. Determination of Rh-factor with anti-D-monoclonal antibodies: mixed on a plate 0.1 ml of anti-D-monoclonal reagent and a small drop (0.01ml) studied blood. REACTIONS read through 3 minutes. In the presence agglutination blood Rh + (positive), in the absence Rh-( negative).

Possible errors in the determination of blood ABO system i Rh-factor: a) low quality reagents and b) technical errors (bad lighting, temperature – below 15⁰ C or higher + 25⁰, carelessness of the reaction, not adding physiological solution- psevdoagglutination, inappropriate relations reagent and blood, c) features studied blood – associated with disease or bacterial contamination, hemolyzed blood.

 

Definition of individual compatibility of blood before transfusion.

 

SUPPLIES: plates, pipette, syringe, needle, tourniquet, roller, blood donor, centrifuge, test tubes.

 

1. Take 5 ml of blood from a vein of the patient.

2. From centrifuged blood (or refrigerate for 12 hours) for obtaining serum.

3. Apply 1-2 drops of serum pipette patient plate.

4. Watch the reaction of 5 min., Shaking plate.

5. Evaluate results.

 

Determination of Rh compatible blood before transfusion.

 

SUPPLIES: Petri cup, pipettes, syringes, alcohol, needle, tourniquet, roller, wool, blood donor, centrifuge, test tubes.

 

1. Take 5 ml of blood from a vein of the patient.

2. From centrifuged blood (or refrigerate for 12 hours) for obtaining serum.

3. In Petri apply pipette 1-2 drops of serum.

4. Mix blood donor with patient serum at a ratio of 1:10.

5. Petri cup, put in a water bath at a temperature of 44-48 ˚ C for 10 min.

  6. Evaluate result, placing a petri cup on white background.

 

Preparing the patient for transfusion:

 

In all cases, before each transfusion of blood or blood components should:

1. Identify group and Rh blood affiliation of the patient and donor;

2. Conduct individual test for compatibility in the system AB0 (in preparation for transfusion);

3. Make a test for compatibility for Rh factor (in preparation for transfusion);

4. Conduct biological sample (early transfusion).

5. If the patient had a history of Surgery reactions or hypersensitivity to enter even compatible for ABO blood group and Rh factor of red blood cells, then selecting compatible erythrocytic means necessary to indirect Coombs test.

 

Choosing indications and contraindications for blood transfusions.

 Today allogene blood transfusion is regarded as a secondary operation transplantation of tissue that is fraught with serious complications and consequences associated with exposure to the organism recipients of different antigens and immune function components. Therefore, in recent years the practice of Transfusion therapy is increasingly being implemented by introducing components and blood products (not whole blood) which is more pronounced therapeutic effect and less dangerous. When using blood components frequency of complications and reactions decreases by several times compared with the transfusion of whole blood. So today believe that absolute indications for transfusion of whole blood can occur only in extreme situations – for large blood loss, wheo blood components. Under existing regulations, currently allowed only one groupe transfusion and one Rh blood, erythrocytes and plasma. Only in rare cases – with absolute indication for transfusion, lack one groupe donated blood components – acceptable transfusion “universal” 0 (I) blood group one Rh no more than 500 ml. Childreeed to transfuse only one groupe and one Rh blood. In similar situations in the absence of plasma one groupe can use plasma group AB (IV) transfusion recipients of any blood, plasma group A(II) or B(III) – recipients of 0 (I). Rules group compatibility cryoprecipitate transfusions are the same as for plasma. Components and blood products administered only to compensate for the deficiency of specific cellular and plasma components of blood. Their transfusion may only be exercised in the absolute indications and only in cases where the possibility of alternative treatments have been exhausted.

 

The method of determining the quality and transfusion systems for infusion-transfusion therapy.

Dosage, routes, methods of transfusion of any fluid transfusion doctor determines in each case.

Direct transfusion provides blood directly from donors (previously examined) patients without phase stabilization or preservation of blood. Direct blood transfusions carry only intravenously via a special system. Remember that blood transfusion scouted AIDS and other vector-borne infection is allowed only when health reasons and lack of blood or its respective components must be documented in by hospital doctors to address consultation and consent of the patient or his relatives. Transfusion of blood scouted in such cases does not remove the responsibility from the doctor for her complete study after transfusion!

Indirect transfusion carried out by means of disposable filter, which directly joins bottle, this is the main method of transfusion.

Exchange transfusion. Partial or complete removal of blood from the bloodstream recipient with simultaneous substitution of adequate or more blood. The main objective of this operation – removal together with the blood of various poisons (for poisoning, endogenous intoxication), decomposition products of hemolysis and antibodies (in Transfusion shock, severe toxicosis, poisoning, acute renal failure, etc.)..

Autotransfusion – transfusion to the patient’s own blood. His conduct after harvesting and conservation autologous blood of patients before major surgery (maximum term determined by the nature of its storage preservative – to 42 days, usually 4-5 days before surgery).

Ways transfusion of Transfusion vehicles. The most effective way to transfusion is intravenous fluids (venopunction, venosection – catheterisation of veins). Much less in medical practice using intraarterial, intraosseous and others.

Systems for infusion-transfusion therapy. To make infusion-transfusion therapy (transfusion of Transfusion products) now use special (sterile, non-pyrogenic, non-toxic, disposable) of prefabricated, so-called “devices”: 1. “The device for blood transfusion, blood substitutes and infusion solutions” in diameter injectioeedle – 1.2 mm (red label). 2. “Device for infusion of blood substitutes and infusion solutions” with a diameter injectioeedle – 0.8 mm (blue label). Such systems (devices) should be used strictly in accordance with the instructions. Do not use in case of violation of the integrity of the package and the expiration date. Each package drawn with technique and tagged filling system (№ 1, № 2) Transfusion means substitutes or other infusion solutions.

Intravenous fluids. (Financial support: package of sterile disposable system, 70^o ethanol, tourniquet, sterile cotton balls, wipes, plasters, scissors, clamps (kortsanh), soap, towel, rubber gloves, Transfusion agent.

Wash your hands twice with running water and soap and dry them with a towel.

Compare the label on the bottle, check its integrity, shelf-life, transparent liquid and remove the central part of the metal cover.

Treat the hands of alcohol, open the package and take scissors system.

Treat a cotton ball cork bottle, take the system in the left hand and right – put the needle closer to the drip through a rubber cork in a bottle and close the clamp.

 The speed of Transfusion fluids. In shock, especially when combined with massive blood loss should be performed transfusion Transfusion Liquid jet way in one or more veins. In all other cases, transfusion fluids typically spend slow-drip method. Infusion at a speed of 20 ml or more per minute is considered jet, and a rate of 15 ml per minute, which corresponds to approximately 40-60 drops per minute – droplets.

 

Transfusion complications.

Examined patients department undergoing blood transfusion or transfusion of other transfusion facilities, simultaneously addresses the issue of hemolytic transfusion complications character. Hemolytic transfusion complications character, usually relating to the incompatibility of the blood donor and recipient for erythrocyte antigens ABO system, rhesus Rh0 (D) and for the second antigen serological systems. From this group of complications most often Transfusion shock, allergic reactions, citrate shock posttransfusion fever and others.

 

Resuscitation measures in surgical patients.

 

Terminology terminal states

                                               

 

1. Terminal called immediately preceding the death of a pathological condition in which the patient is unable unassisted developed to eliminate critical violations vital functions.

 

2. Types of terminal states (in order of development):

 

A) Preagony

B) Terminal pause.

B) Agony.

D) Clinical death.

 

Preagony

 

1. Preagony – terminal condition characterized by gross violations of functions of vital organs and homeostasis of retained control of the centers of the cerebral cortex.

2. Conditions of formation and time limits:

 

A) Preagony may be absent (electric shock). B) may last from several minutes to several hours ( bleeding).

 

Clinical signs:

 

A) Status of the nervous system:

 

a) consciousness:

– Confused, inhibited,

– The possible impairment of consciousness to sopor;

b) reflexes traumatic facial nerve:

– Pupillary, corneal, ciliated and others are not changed;

c) tendon reflexes:

– Weakened;

d) muscle tone:

– not disturbed;

e) spontaneous movements:

– Possible.

 

B) Skin and visible mucous membranes: a) color:

 

– Pale skin,

– Cyanosis or acrocyanosis,

– The possible presence of spots on the skin surface hypostasis limbs.

 

B) respiratory system:

 

a) shallow breathing;

b) tachypnea, rolling in bradypnoe;

c) the presence of pathological types of breathing:

 

– Cheyne-Stokes Kussmaul et al.

 

D) circulatory system:

 

a) critical hypotension;

b) tachycardia, bradycardia rolling in;

c) possible cardiac arrhythmia by type of arrhythmia, atrioventricular block, sinus arrhythmia.

 

D) Diuresis:

 

a) decrease in minute diuresis as a manifestation of disorder of tissue perfusion.

 

4. Intensive care.

 

A) Provide adequate ventilation:

 

a) support the airway:

– Reorganization of the tracheobronchial tree by suction;

– Lavage tracheobronchial tree (in the presence of viscous mucus that is difficult separated);

– sanation fiberbronchoscopy (to remove small foreign bodies from the trachea and bronch, for visually controlled aspiration);

– Protection airway using artificial tubular air leading vehicles (air duct, laryngeal mask, endotracheal tube, etc..)

b) Assisted mechanical ventilation (with adequate frequency of breathing);

c) controlled ventilation (with inadequate frequency of breathing).

 

B) Providing adequate blood oxygen saturation:

 

a) feeding the patient breathing mixtures with high oxygen content:

– Through nasal catheters (with adequate depth and frequency independent breath);

– Using the ventilator (during assisted or controlled ventilation).

 

C) Ensuring effective systemic hemodynamics:

 

a) restore the BCV;

b) restore vascular tone;

c) restoring force of heart contractions;

d) restore normal heart rhythm.

 

D) Ensuring effective microcirculation:

 

a) improve the rheological properties of blood;

b) removal of vascular spasm;

c) effective control of microcirculation – minute diuresis.

 

Terminal pause

 

1.Terminal pause called supraliminal inhibition of vital functions of the body, especially – breathing.

 

2. Conditions of formation and time limits:

 

A) may be absent.

 

B) arises as a result of inhibition of the cerebral cortex with complete exclusion of the regulation of vital body functions against temporary increased vagal tone.

 

B) Duration:

 

a) 20-90 seconds;

b) determined the threshold sensitivity of the respiratory center to CO2 is by reducing reflex activity significantly higher than under normal conditions;

c) stops when a carbon dioxide concentration above the threshold of the respiratory center, causing the appearance of pulses that stimulate contraction of respiratory muscles.

 

3. Clinical manifestations:

 

A) Status of the nervous system:

a) there is no consciousness;

b) reflexes traumatic facial nerve (pupillary, corneal, ciliated and others) are available;

c) tendon reflexes – no;

d) muscle tone weak or absent;

e) no spontaneous movements.

 

B) Skin and visible mucous membranes: a) color:

 

– Pale skin;

– Cyanosis or acrocyanosis;

– The possible presence of spots on the skin surface hypostasis limbs.

 

B) The system of breathing – breathing is absent.

 

D) circulatory system:

 

a) pulse in the peripheral arteries is absent;

b) the carotid pulse weak tension.

 

4. Intensive care:

 

A) Provide adequate ventilation:

 

a) Support airway – putting duct or laryngeal mask if it has not been done before;

b) controlled ventilation.

 

B) Providing adequate blood oxygen saturation:

 

a) feeding the patient breathing mixtures with high oxygen content. C) Ensuring effective systemic hemodynamics:

a) restore the BCV;

b) restore vascular tone;

c) restoring force of heart contractions;

d) restore normal heart rhythm.

 

D) Ensuring effective microcirculation:

 

a) improve the rheological properties of blood;

b) removal of vascular spasm;

c) effective control of microcirculation (by volume diuresis minute).

 

Agony

 

 

1. Agony – terminal condition characterized by short-term increase in activity of the vital functions, followed by progressive inhibition them until termination.

 

2. Conditions of formation and time limits:

 

A) The agony can be absent (eg, electric shock). B) may last from several seconds to several minutes.

 

3. Clinical signs:

 

A) Status of the nervous system:

a) consciousness – a possible partial clarification of consciousness to sopor;

b) reflexes traumatic facial nerve (pupillary, corneal, ciliated and others) can partially recover;

c) tendon reflexes variable;

d) the muscle tone of varying severity;

e) spontaneous movements possible.

 

B) Skin and visible mucous membranes: a) color:

 

– Pale skin;

– Cyanosis or acrocyanosis less pronounced than in previous stages;

– Possible restoration of the natural color of the skin.

 

B) respiratory system:

 

a) Stage agony begins with superficial breaths;

b) gradually become deeper breaths, often with the inclusion of auxiliary muscles;

c) when there is insufficient oxygen supply to the respiratory muscle strength reductions gradually weakens, leading to a decrease in the depth of breathing and its complete stop.

 

D) circulatory system:

 

a) blood pressure is restored to a level of moderate hypotension;

b) tachycardia, bradycardia rolling in;

c) pulse at the periphery defined.

 

4. Intensive care:

 

A) Provide adequate ventilation:

 

a) support the airway:

– Reorganization of the tracheobronchial tree by suction;

– Sanation fiber bronchoscopy;

b) Assisted mechanical ventilation (with adequate frequency, but lack the depth of breathing);

c) controlled ventilation (with inadequate frequency of breathing).

 

B) Providing adequate blood oxygen saturation:

 

a) feeding the patient breathing mixtures with high oxygen content. C) Ensuring effective systemic hemodynamics:

a) restore the BCV;

b) restore vascular tone;

c) restoring force of heart contractions;

d) restore normal heart rhythm.

 

D) Ensuring effective microcirculation:

 

a) improve the rheological properties of blood;

b) removal of vascular spasm;

c) effective control of microcirculation (by volume diuresis minute).

 

Clinical death

 

1. Clinical death – terminal condition characterized by complete cessation of functioning of vital systems with the possibility of renewal for a short period before the onset of irreversible changes in the cerebral cortex.

 

2. Time limits:

A) There comes a point in circulatory arrest and continues to develop in the cerebral cortex of irreversible damage to neurons.

 

B) The duration of clinical death:

a) iormal conditions – up to 5 minutes;

b) depends on the supply of glycogen ieurons and speeds metabolic processes:

– Duration of clinical death decreases with decreasing supply of glycogen, which is caused by prolonged state of hypoxia and ischemia of the brain in accelerated gas in the period immediately preceding death;

– The rate of metabolic processes depend on body temperature (hypothermia prolongs and hyperthermia – cuts) and the presence of endocrine disorders ( hyperthyroidism reduces and hypothyroidism – lengthens).

 

3. Signs of clinical death:

 

A) The main features, if that can reliably diagnose clinical death:

a) absence of spontaneous breathing;

b) lack of pulse in the carotid or femoral arteries;

c) pupil dilation.

 

B) Support (features that allow suspect the presence of a critical state at a distance from the patient and encourage greater action by checking the main characters):

a) lack of awareness;

b) pallor and / or cyanosis of the skin;

c) lack of independent movements;

d) twitching (may occur in the first few seconds when a sudden stop circulation);

e) possible unnatural posture.

 

Notes

– Diagnosis of clinical death must be set for 10-15 seconds;

– Lack of reflexes is not a sign of clinical death, although there is, because when you stop the circulation do not have time to check all reflexes, and for the assessment of CNS rather explore the state of the pupils.

 

 

4. Immediate treatment measures:

 

a) an early challenge to health care;

b) early onset complex cardiopulmonary and cerebral resuscitation by P. Safar;

c) Early defibrillation;

d) Early specialized assistance.

 

Brain Death

 

At some intracerebral pathology, and also after resuscitation activities sometimes have a situation where central nervous system functions, especially the cerebral cortex are completely and irreversibly lost, when heart function is preserved, maintained or supported by AT vasopressors, and mechanical ventilation is provided breathing. This state is called brain death. The diagnosis of brain death put extremely difficult. There are following her criteria:

– Full and steady lack of consciousness;

– Persistent lack of spontaneous breathing;

– The disappearance of responses to external stimuli and beloved types of reflexes;

– Atony of muscles;

– The disappearance of thermoregulation;

– Full and stable absence of spontaneous or induced brain electrical activity (according to EEG).

 

The diagnosis of brain death is important for organ transplantation. After her statement possible taking their organs for transplant recipients. In such cases, the diagnosis additionally required:

– Angiography of cerebral vessels;

– Conclusion specialists (neurologist, resuscitator, forensic medical expert, as well as officially representative of the hospital), confirming brain death.

 

In most countries, according the law “brain death” is equivalent to the biological.

 

 

Social death

 

1. Social death – a pathological condition characterized by complete irreversible brain damage, which caot restore brain functions and the body without external assistance continued to maintain their livelihoods caot.

 

2. Reasons for Development:

 

A) Untimely taken or improperly performed resuscitation:

a) After 4-5 minutes of circulatory arrest;

b) for events of basic life support is controlled by the signs of their effectiveness.

 

3. Signs of social death:

 

A) Self breath absent.

B) Hemodynamics supported cardio and vasotonic drugs.

B) Consciousness and reflexes were absent – prohibitive coma.

D) EEG – contours in all leads.

 

4. Emergency measures:

 

A) Support of vital functions:

a) controlled mechanical ventilation to ensure adequate gas exchange;

b) vasotonic therapy aimed at ensuring adequate microcirculation in all regions of the vasculature;

c) ensuring the effective operation of the kidneys.

 

B) Diagnosis of brain death by the relevant protocol.

 

Cardiopulmonary and cerebral resuscitation (by P. Safar)

 

I the stage – elementary (basic) support life.

 

Purpose – immediate oxygenation:

 

A) Ensure the effective ventilation.

 

B) mechanical ventilation.

 

B) providing artificial circulation.

 

Stage II – Further (Extended) support life.

 

The goal – the restoration of effective cardiac independent:

 

A) Drug therapy.

 

B) ECG diagnosis.

 

B) Electro therapy.

 

Stage III – continued support life (Treatment of post resuscitation disease).

 

Purpose – to restore all functions of the body, primarily – CNS (“cerebral resuscitation”):

 

A) Assessment of damage to the central nervous system (brain death diagnosis) and the prevention of repeated stops circulation.

B) Recovery of higher brain functions (anoxic encephalopathy therapy).

B) Intensive care violations arising in other organ systems during clinical death and complications of intensive therapy.

 

I stage resuscitation (BLS – basic life support)

 

1. Title: elementary (basic) support life.

 

A) Objective: immediate oxygenation.

B) Steps:

a) ensure the possibility of effective ventilation;

b) mechanical ventilation;

c) providing artificial circulation.

 

2. Contents stages:

A) Ensure the effective ventilation:

a) causes impaired patency of the upper airway during clinical death:

– Tongue;

– Swelling of the vocal cords;

– Swelling of the tongue;

– Foreign object in the airway;

– Pathological airway liquid contents;

b) the reasons for breach tours chest with clinical death:

– Compression of the chest from the outside (for example, the victim pressure of a heavy object or dusted the ground);

– Limiting chest excursion through tight bandaging ( mothers who breast cancer tight bandage to stop lactation);

c) the possibility of efficient breach causes swelling of the lungs:

– Valve pneumothorax;

– Hydro or hemothorax;

– Empyema;

– Atelectasis;

d) methods of patency of the upper airway:

– When the tongue:

 

• perform “triple reception Peter Safar”:

 

 

-mouth opening injured finger wrapped handkerchief (gauze cloth on clamps) exemption it from existing foreign bodies and fluids (vomit, sputum, algae, plug jaws, blood clots, etc.);

 

 

head-rejecting most backward, resting under the neck improvised roller (eg own forearm). In the majority of victims tongue stops to close the entrance to the upper respiratory tract;

 

–         output mandible to the front;

 

• enter the duct bend to the tongue, followed by rotation by 180 ° as you type.

 

• Enter esophageal stoppers

Introduction esophageal stoppers

 

• Set the laryngeal mask.

 

• Endotracheal intubation

 

Introduction laryngoscope                                                                                            Intubation using laryngoscope through the mouth

 

 

– When the vocal cords and edema swelling of the tongue with complete obturation:

 

-perform crycoconicotomy or puncture the crycothyreoid membrane  perform tracheostomy.

 

– If swelling of the tongue with incomplete obturation:

 

Introduction esophageal obturator

Perform nasothracheal intubation using the bronchoscope.

 

In the presence of a foreign object in the mouth:

– Remove the foreign object by using the index and middle fingers, using them as tweezers;

– Remove the foreign object by using medical instruments (tweezers, forceps, surgical clamp, etc.).

 

With the localization of foreign body from vocal cords:

 

– Clutching the back of the patient so that the animators were clasped his hands in the epigastric area of the victim, rhythmically compress the chest, creating increased pressure in the airways that chasing foreign body in the oropharynx;

 

– Perform reception Heymlih (underdiaphragm push): rhythmic clicking the epigastric area in the diaphragm.

Perform reception Heymlih

 

With the localization of foreign body deep in the trachea or bronch, or in the presence of viscous liquid pathological content:

– Create drainage of body affected (head below waist), standing on one knee and putting the victim on his stomach on the second knee, tapping on the back to achieve the shift to a foreign object out of the trachea;

 

 

 

 

 

 

 

 

 

 

 

 

 

 

– sanation bronchoscopy.

 

 In the presence of airway liquid or foam pathological content:

 

– Aspiration by suction.

 

B) Measures to ensure the possibility of effective ventilation:

 

• release the chest of the patient objects, compressing it;

• release the chest from tight bandages imposed.

 

In valvular pneumothorax:

 

transfer valve in open pneumothorax by needle puncture with a thick gleam in midclavicular line in II intercostal space.

 

In the presence of large amounts of fluid in the pleural cavity:

 

Emergency puncture of pleural cavity in VII-IX intercostal space on the posterior axillary line.

 

B) ALV:

 

a) the types ventilation performed during clinical death

 

– without apparatus (“mouth to mouth”, “mouth to nose”);

– Hand-held devices (Ambu bag and the like);

– Forced ventilation apparatus;

b) the mode of ventilation:

– respiratory volume – the volume corresponding physiological inspiration – 500-800 ml;

– Respiratory rate – 12-14 breaths per minute;

c) effective control of ventilation:

– The effectiveness of ventilation is judged by the presence of chest excursion. With effective ventilation chest on inspiration rises and falls on expiration;

– Chest on expiration does not drop:

 

Artificial lung ventilation. Frequent and shallow breathing until the absence of respiratory movements of the chest, along with the general features of respiratory arrest (bluish skin and mucous membranes, speeding up, and later infrequent, irregular filling pulse, convulsions, loss of consciousness), is indicated for the auxiliary or artificial ventilation lung before stopping breathing and cardiac activity and the onset of collapse (sudden drop in blood pressure).

 

Before artificial respiration victim should be put back, unbutton clothing that compresses the chest (collar, belt, bra) and provide a free airway.

 

Anyone who assists, kneels at the head of the victim, with one hand holding it in the most abandoned back position, thumb second hand pulls the lower jaw. Then it makes a deep breath, either directly or through cheesecloth tightly covering the patient’s mouth his lips and makes a complete exhalation (part from 1 children up to 8 years, easy for children under 1 year), while watching the expansion of the chest. To prevent release of air through the nose clamp affected his fingers, which is located near the forehead to hold the head in a ghost position. Output air is passively by spontaneous decay and reduce the volume of the chest of the patient.

Fig. Methods of artificial ventilation by “mouth-to-mouth”

(A – injection with simultaneous control of lifting the chest, B – passive exhalation).

 

Little baby breathe air at once, his mouth and nose, holding them with his lips.

 

Important in carrying out artificial respiration rhythm is implementation breaths: adults – 4 second cycles – rescuer breathes air into itself, for 5 – blown into the victim (for 1.5 s), children under 8 years – 2s bars – rescuer breathes air a, 3 – blown into the victim (for 1.5 s).

 

          When the victim appear open or closed injuries of the lower and upper jaws used method of mechanical ventilation “from mouth to nose.” Head injured alleged victim as possible and held with one hand, which lies at its crown, the second hand to slightly raise the lower jaw and close the mouth. Anyone who assists, makes a deep breath and his lips tightly covering nose victim – is blowing air. If chest collapses enough mouth affected during exhalation air slightly open.

Fig. Methods of artificial ventilation by “mouth-to-nose.”

 

 

 

The most common mistake during artificial respiration by these methods is the lack of throwing heads, thus not restored airway and air is blown, into the stomach of the victim. This protrusion going to appear under the costal area. To prevent the air from the gastric contents, which can get into the airways necessary after several insufflation pressed his hand on the middle of the upper abdomen.

 

On admission to the oral cavity of gastric contents head and shoulders of the victim to return to the side and back to clear his mouth.

 

Artificial respiration preferably carried out in a dry warm place, as the cooling of the body affected increases anoxia.

 

From frequent respiratory movements whoever assists may experience dizziness and weakness, then it is advisable to replace. Injection of air should be long and hard. Performance indicators ventilation is seen expanding the chest with air injection, redness of the skin and restoring independent breathing (chest victim rises in time with the breath).

 

♦ with valvular pneumothorax (converted to open);

 

♦ when ingested by inhaling air into the stomach (Selika execute method that is pressed to the spine of the thyroid cartilage that covers the lumen of the esophagus and prevents further flow of air into the stomach and accusations of gastric contents into the oropharynx).

 

D) providing artificial blood circulation:

a) The main types of lung:

– Hand indirect heart massage;

– Indirect heart massage with hand apparatus (Kardiopamp, Kardiovent);

– Hardware indirect heart massage (chest massager);

b) the method of indirect cardiac massage without aids

– Determine the point of compression:

 

♦ 1-way – divided into three parts chest on the edge of the lower and middle thirds of the sternum in the midline mid put on one of the hands, on the second hand is placed strictly on the same point;

 

♦ 2nd way – from the xiphoid process up retreating to a distance corresponding to the thickness of two fingers of the victim, was found just above the point of the fly on one hand, on the second hand is placed strictly on the same point;

– The shift sternum towards chest spine:

♦ in adults – 4-5 sm;

♦ in primary school children – 3–4 sm;

♦ in neonates and infants – 2-3 sm;

 

– Specification of indirect cardiac massage:

♦ patient should lie on a solid basis;

♦ pressing the chest performed transfer weight on hands animators, and not through the power of his muscles. This reanimator should not bend your elbows. To help comply with this rule is intended method of crossed fingers, in which the fingers of one hand at the top, held between the fingers second hand and cover tightly brush;

♦ pressing chest rhythmically performed with a frequency of 90-100 compressions per minute (adults);

♦ ratio of compressions and vduvan air into the lungs of the victim – 15:2 at any number of animators;

The victim put her back on a firm footing. Anyone who assists, becoming the side and palms of hands without bending them (Fig. A) (bases of palms, not fingers!), Superimposed on each other (Fig. Б), click in the area on 2 fingers above the lower edge of the sternum (Fig. B) whole body body with a frequency of no less than 60 times per minute. This hand is not detached from the surface of the chest (Fig. Г). The amplitude of the chest in an adult is about 4-5 sm (Fig. Д).

 

 

 

 

 

 

 

 

 

 

 

 

Children 1-8 years closed cardiac massage should be done with one hand with frequency of 80 times per minute, and infants – the tips of the thumb, with a frequency of 120 clicks per minute. Point fingers applying for children under 1 year – on one finger width below the nipple line between. Caution should be carried out heart massage in the elderly, because the rough performed massage can be rib fractures.

 

 

c) the method of indirect heart massage by Kardiopamp (the “compression-decompression”):

 

 

– The method is based on the idea of ​​using decompression of the chest to increase blood flow to the heart in an artificial diastole;

– For indirect heart massage by Kardiopamp need:

♦ make the front surface of the chest of clothes;

♦ for better contact wet spot compression water;

– A point on which set Kardiopamp, corresponds to the point at hand indirect compression massage;

– Technique:

♦ to create artificial systole reanimator, holding both hands Kardiopamp per disc, click on it with a force controlled by the indicator;

♦ to create improved diastolic reanimator chest tightens up, holding two hands per disc Kardiopamp;

 

d) monitor the effectiveness of cardiopulmonary bypass:

– Effective massage is indirect, in which pulse wave caused by compression, felt at the radial artery. Pulse wave, which is determined only by the carotid arteries is insufficient to overcome the intracranial pressure and, therefore, does not provide perfusion of the brain.

 

If measures of cardiopulmonary resuscitation carries one person, then every fifteen compressions chest stop heart massage for two or three seconds, and this time made two strong injection by the method of “from mouth to mouth” or “mouth-to-nose” .

 

 

When helping two people required after every five taps on the chest give the command “Inspiration” and, at this time, the second rescuer should hold one blowing air into the lungs.

 

 

 

D) Monitoring the effectiveness of the full range of resuscitation:

 

a) restoring the normal color of skin:

– Disappears cyanosis of the skin and visible mucous;

– Pale skin becomes pink;

 

b) Recovery of reflex activity of the brain:

– Constriction of the pupils.

 

Stage II resuscitation (ACLS – advanced cardiac life support)

 

 

3. Title: Further (Extended) support life.

 

A) Purpose: restoring self-circulation.

B) Steps:

a) drug therapy circulatory arrest;

b) electrocardiographic evaluation form circulatory arrest;

c) electric pulse therapy (defibrillation / cardioversion).

 

4. Contents stages:

 

A) Drug therapy circulatory arrest: a) objectives:

 

– Increased electrical activity and force reductions myocardiocytes;

– Restoration of vascular tone;

– Artificial circulatory centralization;

– Increased sympathetic influence on the heart by blocking the parasympathetic nervous system;

– Increasing the efficiency of electric pulse therapy;

 

b) drugs:

 

– Adrenaline hydrochloride – a-and b-agonists, promotes blood circulation centralization at the expense of its redistribution from peripheral organs in favor of the brain and myocardium (a-adrenomimetic effect), increases myocardial contractility, which helps restore and strengthen their heart rate (b- adrenomimetic effect), increases cardiac output and blood pressure in early spontaneous reperfusion;

 

– Atropine Sulfate – M cholineblocker, removes inhibitory effect of acetylcholine on the activity of the sinus and atrioventricular nodes;

 

– Amiodarone – antiarrhythmic drug of first choice, improves the efficiency of electric pulse therapy for ventricular fibrillation or ventricular tachycardia without pulse refractory to electrical discharge;

 

– Lidocaine – local anesthetic with antiarrhythmic action, suppresses ventricular extrasystoles and increases ventricular fibrillation threshold applies in the absence of amiodarone (joint application of lidocaine and amiodarone unacceptable!)

 

– Novokainamid – antiarrhythmic drug that prolongs the effective refractory period, blocking vagal reactions;

 

– Sodium bicarbonate – a component of the extracellular buffer system is introduced in order to restore the sensitivity of the myocardium to adrenaline in baseline hyperkalemia, severe metabolic acidosis, overdose of tricyclic antidepressants or phenobarbital;

 

c) route of administration:

– Better to introduce drugs into the central vein, but it is effective is put into a peripheral vein;

– Inability to obtain intravenous access can use alternative means of input – endotracheal, it is necessary to take into account that not all drugs can be administered into the trachea (sodium bicarbonate). In the lumen of the trachea or drugs administered through an endotracheal tube (endotracheal intubation if done) or through a catheter introduced through microcricoconycotomy;

– Intramuscular or subcutaneous injection, and prescriptions in tablet form under the tongue is not used because under cardiopulmonary bypass significantly reduced absorption of drugs from the tissues;

– Intracardiac administration of drugs at this time, according to the recommendations of the European Council on Resuscitation, not recommended;

d) doses of medication depending on the route of administration:

 

 

 

Notes: 1) the introduction of drugs into the trachea dose should be doubled and diluted with saline to 10 ml, 2) 1 mM NaHCO3 contained in 1 ml of 8.4% solution.

 

B) Electrocardiographic diagnosis of the type of circulatory arrest:

Cardiomonitor

 

 

a) the types of circulatory arrest during clinical death:

– Asystole;

– Ventricular fibrillation;

– Ventricular tachycardia without a pulse;

– Electromechanical dissociation (“inefficient heart”);

b) Characteristics of circulatory arrest:

 

– Asystole – the complete absence of electrical activity of the myocardium, the worst kind of circulatory arrest, as often occurs in the later period of clinical death, ie after 3-4 min. from the time of development;

 

♦ ECG wonder contours in all assignments:

 

The complete absence of electrical activity in the myocardium (asystole)

 

– Ventricular fibrillation – the presence of disordered electrical activity of the myocardium in which the reduction of individual myocardiocytes not interoperable and do not obey a single pacemaker, originally developed as a form of cardiac arrhythmia in acute myocardial ischemia (heart attack), electric shock, secondary develops in “inefficient heart “as a result of myocardial ischemia, as the development of clinical death goes into asystole;

♦ ECG feature: the line of waves of different amplitudes without clearly defined teeth;

 

Ventricular fibrillation

 

-Ventricular tachycardia without pulse – synchronous contraction of the ventricles myocardiocytes own high frequency at which in diastole they do not have time to be filled with blood;

♦ ECG feature: the same kind of waves with high frequency and precise rhythm, electromechanical dissociation – ordered electrical activity myocardiocytes compliance with cyclic reduction sequence in which systolic ejection insufficient for efficient blood circulation is often a primary form of circulatory arrest, later replaced by ventricular fibrillation and asystole:

 

 Syncope

 

In milder cases, often a state of fainting or swoon (brief loss of consciousness, anemia caused by cerebral arteries), which remains painful reaction kornealny reflex (closing eyelids in mild irritation of the cornea of ​​the eye), pupillary response to light. Causes of syncope are quite varied (injury status after surgery, illness, lack of oxygen in the air, great physical and mental strain of little people trained, etc.). Unconscious lay flat on his back, without raising his head, fired from clothes that hinder breathing, raise the legs to improve blood supply to the brain, rubbed his limbs, give a sniff to cause breathing ammonia or conduct painful stimulation (pressing the trapezoid muscle) and quickly cause a health worker.

 

Acute vascular FAILURE

 

Collapse occurs due to decreased sympathetic tone of the autonomic nervous system or increase – parasympathetic (vagal). This reduces resistance arterioles, accompanied by their extension and a violation of correspondence between content vascular and BCV. As a consequence, decreases venous flow: CO, circulation of the brain.

 

Reasons:

 

1) vasovagal reaction in pain;

2) sudden change in body position (orthostatic collapse);

3) barbiturate poisoning;

4) side effects ganglion blocking, narcotics, sedatives, antiarrhythmic, local anesthetic means;

5) spinal and epidural anesthesia.

 

Clinic: general weakness, dizziness, tinnitus, cold clammy sweat, pallor, sometimes yawning, nausea, vomiting, decreased AT, slowing heart rate, decrease in urine output, and sometimes loss of consciousness (fainting). Most of collapse is transient iature, but by its duration may develop shock.

 

Emergency. Often enough to give the patient the horizontal position, slightly lift the lower limbs, give a sniff of 10% ammonia solution, free from neck compression garments sprinkle face with cold water, rub the body, stop giving the drugs that caused the collapse, warm the patient, eliminate all adverse factors may be the cause of the collapse. In severe cases, the vasoconstrictor: mezaton (0.2 – 0.3 ml of 1% solution) or noradrepalin gidrotartrat (0.5-1 ml of 0.1% solution) in 10-20 ml of isotonic sodium chloride intravenous. In cases of prolonged collapse intravenous plasma substitutes – reopoliglukin, drugs hydroxyetil starch (200 – 400 ml) hormones – hydrocortisone (3 – 5 mg / kg) or prednisolone (0.5 – 1 mg / kg). In case of significant bradycardia intravenous atropine sulfate (0.5 – 1 ml of 1% solution).

 

Coma

 

Coma – a condition which is characterized by loss of consciousness, disturbances of reflex activity, the functions of vital organs and systems, lack of conscious reactions to external and internal stimulation. With deep coma patient caot withdraw from a state property even strong stimulationes. Often coma is a complication, and sometimes end-stage disease, endogenous or exogenous intoxications (failure of kidney, liver). Often coma develops in the primary lesion of the brain (brain injury, metabolic disorders). Particularly severe and deep coma is in terminal patients (preagony, agony, clinical death).

 

In the pathogenesis of coma is important anoxia whole brain or its activating structures. In many cases, coma, the brain receives sufficient and even “excessive” amount of blood saturated with oxygen and glucose, but the destruction of cells or subcellular structures, synapses or activating structures gives all exchanges brain: energy, exchange of neurotransmitters like.

 

Clinic. Despite pas different nature and mechanisms of different types of places, in their clinical picture much in common. The most characteristic symptoms: lack of awareness, change reflex responses (decrease, increase, negative), decrease or increase muscle tone of tongue, violation breathing (Cheyne rhythms – Stokes Biota, Kussmaul, hypo-or hyperventilation, apnea), swallowing. Often have less AT, change rate, oligo-, anuria, water metabolism disorder (dehydration, hyperhydration), electrolyte balance (hypo-, hyperkaliemia, hipernatriemia etc.), CBS, thermoregulation.

 

Classifications of com – the etiology, pathogenesis, depth and severity of CNS lesions. The most common is the classification of coma depth and degree of severity:

 

1. Light coma. Consciousness and spontaneous movements do not, patients do not respond to the question, protective response adequate corneal and tendon reflexes and pupillary response to light saved, but can be reduced, respiration and blood circulation of the brain is affected.

 

2. Severe coma. Consciousness is lost, caused by uncoordinated movements may stem symptoms (impaired swallowing), respiratory disorders (abnormal rhythms), hemodynamics and function of the pelvic organs.

 

3. Deep coma. Consciousness lost defensive reactions are negative, the disappearance of the corneal reflex, atony of muscles, areflection, often hypothermia, severe respiratory failure, circulatory functions of internal organs.

 

4. Terminal (prohibitive) coma. Consciousness lost defensive reactions are negative, areflection, dilated pupils, critical disorder of the vital functions (AT is not defined or minimum level, sleep apnea), which requires special measures to support life.

 

To determine the depth of coma often use scale deep coma Glasgow. In Glasgow clinical signs are differentiated by their degree of the severity, as reflected in scores. For information about the degree of change in consciousness points summarize. The greater the total score, the lower the degree of inhibition of brain and vice versa. If the total score 15 – no commas.

 

 Determining the severity of coma for Glasgow

 

Clinical signs

 

A) Open Eyes

Arbitrary

In the language of address

On painful stimulation

There is not

 

B) The motor response

Executes commands

Focused on pain stimulation

No focused to pain stimulation

Tonic flexion to pain stimulation

Tonic extension to pain stimulation

There is not

 

B) Language

Oriented full-tangled-Unknown words – inaudible sounds-No

 

Balls

1) No 2) 13-14 – stunning, 3) 10-12, sopor; 4) 4 – 9 – coma; 5) 3 – brain death.

 

During the inspection clarify information history (trauma, brain disease – meningitis, encephalitis, cerebral hemorrhage, etc.). They exhibit a disease that can lead to coma (diabetes, liver, kidney, adrenal, thyroid glands, etc.). Specify whether the patient took drugs in large doses, does not suffer from drug addiction, substance abuse, or was he attacks the court (before or immediately prior to deterioration). It is important to test it carefully as targeted treatment after such examination is much more effective than emergency polytherapy.

One of the main goals of treatment of patients who are in a coma, the maximum blood oxygenation prevention (treatment) cerebral hypoxia.

If pulmonary ventilation is ineffective or deep coma <8 points, begin ventilation. If necessary, carry out intubation tracheal tube with inflate cuff. Inflate cuff prevents aspiration of sputum, gastric contents into the lungs. If after intubation continues to stand out a large number of sputum, conduct periodic cautious aspiration of her lungs through the endotracheal tube. To facilitate output secret, the patient should be put in drainage position. In the stomach to release it from the injected fat content probe (in violation of swallowing and breathing – just after intubation). Gastric emptying is especially important in cases of poisoning. Induce vomiting in patients who are in a coma, is unacceptable! After gastric lavage patient is injected through a tube activated carbon or other sorbent that binds toxic products.

 

To ensure adequate oxygen to the brain circulatory support is required. This constantly monitor AT, frequency and rhythm of the heart, spend correcting arrhythmias, AT. Provide intravenous route of administration of drugs, mainly catheterization main veins (brachial, subclavian or internal jugular).

 

    In case of significant hypotension injected sympathomimetic, plasma substitutes. Systolic AT maintained in the range 110 -120 mm Hg. col. for patients with normal levels (if it is able to find out), in elderly patients with hypertension disease – within their usual level. To avoid hypotension in patients who are in a coma, enter dopamine (1 – 2mkg / (kg-min)), which also has less negative influence on the renal blood flow than most agonists. If the patient is in a state of shock, it should eliminate the other (extracerebral) factors in its development. In cases where a known substance which caused the poisoning, an early start to enter antidotes and antagonists. An important component of treatment is to eliminate generalized seizures, as repeated attacks by the court, regardless of the reasons that caused exacerbate the brain damage. Reduce the depth of coma may contribute to normalization of body temperature, so it should start as soon as possible. Especially harmful hyperthermia for brain – increasing its metabolic needs, deepens breathing disorder water– electrolyte balance. Lowering body temperature under these conditions can be achieved outside cooling body, the introduction of non-narcotic analgesics. In cases of hypothermia spend a gradual warming of the body to a temperature not lower than 36 ° C.

 

 

Asphyxia

 

 Asphyxia – a critical body condition associated with a deficiency of oxygen and accumulation of carbon dioxide in the body. Distinguish acute asphyxia Having arisen from rapid dysfunction of the respiratory, circulatory, central nervous system and subacute with gradual impairment of respiratory and hemodynamics. Symptoms of acute respiratory disorders are signs of hypoxia: there are dyspnea, cyanosis, ortopnoz, tachycardia. However, there are also signs of hypercapnia – the accumulation of excess carbon dioxide, which is accompanied by a decrease in blood pH.

 

 On the mechanism of acute respiratory disorders isolated extrapulmonary and pulmonary causes.

 By extrapulmonary causes include:

 1) violation of the central regulation of respiration:

 a) acute cardiovascular disorders (thromboembolism, stroke, swelling of the brain);

 b) brain injury;

 c) intoxication by drugs that act on the respiratory center (narcotic drugs, barbiturates, etc.);

 d) infectious, inflammatory and neoplastic processes that lead to lesions of the brain;

 d) coma, leading to cerebral hypoxia;

 2) disruption of the respiratory muscles associated with lesions of the medulla oblongata and the motor neurons of the cervical and thoracic spinal cord:

 a) The neurotropic action of bacterial toxins and viruses (poliomyelitis, botulism, tetanus, encephalitis, etc.);

 b) spinal cord injury;

 c) poisoning curariform agents, organophosphorus compounds;

 d) myasthenia;

 3) the integrity and mobility of the chest – the so-called traumatic asphyxia caused by compression of the chest, abdomen with increasing intrathoracic pressure;

 4) Violation of oxygen transport in large blood loss, acute circulatory failure and poisoning “bleeding” poisons (carbon monoxide, methemoglobin forming).

 

 In pulmonary causes asphyxia include:

 1) obstructive disorders – impaired airway:

 a) obstruction airway foreign bodies, sputum, blood (with pulmonary hemorrhage), vomitus, amniotic fluid;

 b) mechanical noise during compression of air access from outside (increase, suffocation);

 c) the development of acute stenosis of the upper airway during allergic swelling of larynx, vocal cords;

 d) neoplastic processes of the respiratory tract;

 e) violation of the act of swallowing, paralysis of the tongue with its retraction;

 e) obstruction of the respiratory tract that may accompany acute farynhotracheobronchitis, acute tracheobronchitis, severe attacks of asthma;

 g) farynheal and laryngeal paralysis with symptoms of hypersecretion and edema of vocal cords;

 c) Custody of laryngeal edema development;

 2) restrictive disorders – disorders ductility (elongation) of lung tissue, leading to a decrease in respiratory surface of the lungs:

 a) acute pneumonia;

 b) pulmonary atelectasis;

 c) spontaneous pneumothorax;

 d) pleural effusion;

 e) pulmonary edema;

 e) massive pulmonary embolism.

 Causes of asphyxia varied, but the main feature is its violation of the act of breathing.

 

 Accepted distinguish several phases of asphyxia.

The first phase is characterized by enhanced activity of the respiratory center. There is increased blood pressure, increased heart rate and increased. Prolonged and enhanced breath (inspiratory dyspnea). Patients experience dizziness, blackout, excited. There is a pronounced cyanosis.

The second phase is characterized by decrease in breathing, often accompanied by increased exhalation (expiratory dyspnea) and a significant slowing of heart rate (vagus pulse), blood pressure gradually decreases, marked acrocyanosis.

The third phase is characterized by a temporary (from several seconds to several minutes) cessation of activity of the respiratory center, at which time blood pressure is greatly reduced spinal fade, eye reflexes, loss of consciousness occurs, develops hypoxic coma.

The fourth phase is manifested rare deep convulsive “sighs” – so-called terminal (agonal) breathing lasts a few minutes.

 

 Severe complications that arise when asphyxia is ventricular fibrillation of the heart, brain and lung edema, anuria. With the development of asphyxia pupil constricted, then they expand, when you stop breathing pupillary and corneal reflexes were absent.

 Duration of asphyxia (from its beginning until death) can vary widely, the sudden cessation of pulmonary ventilation duration asphyxia is not more than 5-7 minutes.

 In patients with asthma asphyxia develops in asthmatic condition. Asphyxia may occur suddenly and progress rapidly after exposure to allergens, especially with the introduction of drugs. Asphyxia may develop gradually. With increasing respiratory failure show signs of hypoxic-hiperkapnic coma.

 

Emergency. Causes of pulmonary ventilation define complex emergency medical measures. In the presence of obstructive syndrome to restore airway, freeing them of mucus, blood, vomit. Helping begins with drainage sloping posture. To restore the airway should perform the following steps: straighten your head in the vertebral-occipital junction, lift and push forward and chin up. To remove a foreign body from the area glottis using two methods – jerk epigastric towards diaphragm or compression of the lower parts of the thorax. Later make bronchoaspiration by introduced through the nose into the trachea rubber suction catheter with liquid contents. After removal of content spend no hardware artificial respiration, and if necessary transferred to hardware breathing. The patient was hospitalized with the continuation of artificial respiration hardware.

 With the rise of asphyxia shown urgent intubation using the laryngoscope, and sometimes tracheostomy. In the presence of foreign bodies in the larynx, trachea intubation may increase asphyxia, in connection with what makes tracheostomy followed Term hospitalization.

 Acute respiratory disorders due to acute hemodynamic disorders, damage the respiratory center, as well as lesions of the respiratory muscles, immediately transmitting auxiliary ventilation with subsequent transfer of patient-controlled hardware artificial respiration.

 In acute respiratory failure, which developed as a result of severe hemodynamic disturbances with the development of acute heart failure, cardiac glycosides injected (0.5-1 ml 0.06% solution korglikon or 0.5-0.75 ml of 0.05% solution of strophanthin intravenously in 20 ml of 40% glucose solution).

 

DROWNING

 

Drowning – is a form of mechanical asphyxia, which develops due to ingress of liquid into the upper respiratory tract and bronchoalveolar space.

 

Pathophysiological changes that occur in the body due drowning due to the following reasons:

 

1) aspiration of liquid into the respiratory tract preserved spontaneous breathing;

 

2) cessation of gas exchange due laryngospasm;

 

3) heart stopped due to mental (fear) or reflex (shock, cold shock) effects.

 

The first mechanism of the terminal state of the water is called real (true wet) drowning, second – asphyxia drowning, third – syncope. It should be borne water temperature: in cold water during clinical death can significantly lengthen (20 – 30 minutes or more). Intoxicated prolonged period of dying by 1.5 – 2 min. The nature of the pathophysiological changes in osmolarity pours water that gets into the lungs (sea or freshwater).

 

 

 

 

Real (true wet) drowning (70 -80% of cases) is accompanied by breath. The long delay leads to hypoxia and the accumulation of CO2 in the blood. This induced respiratory center and there shee involuntary respiratory excursions under water, the depth and frequency is increasing. Water enters the lungs, washes surfactant and cessation of gas exchange occurs.

 

A lethal dose of aspirated water – 20 ml / kg, but death may occur after aspiration and 10 ml / kg of water. Even a relatively small amount of aspirated water (1 – 3 ml / kg) caused loss of consciousness, profound hypoxemia due to shunting of blood flow, which in severe cases up to 50% of MVH.

 

When filling the lungs with fresh water (hypotonic fluid) alveoli are stretched, the water enters the bloodstream by direct diffusion through the destroyed alveolar-capillary membrane. For a few minutes there is a sharp increase in BCV (1.5 times more), developing state hypotonic hydration: water penetrates into erythrocytes, causing hemolysis and hyperkalemia. In severe hypoxia join stagnation in the large and small circles circulation.

 

Real drowning in seawater – revenues hyperosmolar fluid in the alveoli – leads to a rapid movement of the liquid part of blood, together with proteins in the lumen of the alveoli, and electrolytes – in the vascular bed. Developing hypertension dehydration: increased hematocrit numbers of sodium, potassium, magnesium, calcium, chlorine plasma. Movement of gases in the respiratory tract during breathing (spontaneous or mechanical ventilation) promotes liquid contents of the alveoli and the formation of these stable protein foam.

 

Clinic. The course of true drowning has three periods:

 

1) initial – consciousness is preserved, arousal, inadequate response pas environment underestimation of what happened, the refusal of medical care, sometimes general movanist, severe depression, cyanosis, chills, “goose” skin, rapid breathing, hear a noise in the upper airways, coughing attacks, tachycardia, hypertension, vomiting water;

 

2) increasing the overall agonal ~ Cyanosis (skin turns purple-blue), tachycardia and hypertension vary bradycardia (or bradiarrhythmia) and hypotension, loss of consciousness, breathing becomes rarer, whooping, accompanied by pink foam from the nasal passages and mouth;

 

3) clinical death – lost consciousness, acute cyanosis of the skin and mucous membranes, puffiness of the face, neck swelling veins, sleep apnea, asystole, areflexia, pupil dilation.

 

Asphyxia drowning (10-15% of cases), usually the result of a sharp slowdown CNS under the influence of alcohol, sudden acute illness (acute myocardial infarction, acute cerebrovascular accident, an attack of epilepsy, etc.) or injury (fracture in the cervical spine as a result of diving, mechanical damage to water immersion). There is no uncoordinated movements and attempts to get out of the water, and hyperventilation, and water without interference enters the upper respiratory tract, but there are muscle spasms larynx that prevents water filling the lungs. There psevdorespiratory breaths in of closed vocal cords, the lungs rises sharply negative pressure, which leads to the formation of alveoli resistant foam. Simultaneously, a large amount of water enters the stomach.

 

In the future, if the victim is rescued, spasm of the glottis after terminal pause varies atony, and water fills the lungs. Because the flow of water into the lungs prior to pathophysiological disorders caused by hypoxia, stagnation less pronounced. Cyanosis of the skin and mucous membranes in such cases is less pronounced compared with real drowning.

 

Clinic. At the initial period of rapidly changing agonal, which is characterized by trismus and laryngospasm that not hinder mechanical ventilation. Prolonged asphyxia, after which comes atony and breaking the vocal cords, accompanied by pale pink foam formed during psevdorespiratory breaths and pumping blood plasma to alveoli. The course of clinical death is similar to that in real drowning, making it difficult to differentiate in this period.

 

In cases syncopal drowning, which is a consequence of reflex heart and breathing stop, immediately, a period of clinical death. Breathing and heartbeat No, there is also the selection of foam and fluid from the respiratory tract, characterized by sudden pallor of skin (“white drowning“). This type of predictive drowning most favorable to provide intensive care.

 

Notably, asystole and apnea during syncopal drowning occur simultaneously, while in cases of genuine drowning first heart stops, and when asphyxiation- breathing. However, all kinds drowning primarily fade functions of the cerebral cortex.

 

Emergency. Regardless of the type drowning the absence of signs of life assistance should be directed to restore breathing and circulation. Well-trained rescuer starts conducting ventilation by mouth to mouth or mouth to nose even when transporting the victim to the boat or shore. The boat should not spend time on the release of the respiratory tract from aspirated fluid – enough to release the upper respiratory tract of sand, silt and proceed to the immediate phase of cardio-pulmonary reanimation. At the rescue station, if appropriate equipment and trained personnel, immediately fully conduct specialized stage cardio-pulmonary reanimation. For preservation of consciousness, breathing and heart activity conducted sedation, warm, oxygen inhalation, immediate hospitalization.

 

If a large amount of fluid from the respiratory tract during mechanical ventilation of its output using aspirator. If not, and the water makes mechanical ventilation, it can partially withdraw, raising the victim’s waist so that your upper body and head hanging down, or “bend” it through his thigh bent at the knee, simultaneously pressing the  back. These measures should be carried out in exceptional cases as quickly as possible and only in the “blue” drowning. In victims of syncopal type drowning (“white” drowning) to spend time removing water from the airway should not be (another mechanism dying).

 

The most effective method of removing fluid from the respiratory tract and stomach is its aspiration using aspirator through intubation tube and gavage. No way to remove fluid from the respiratory tract should not try to remove all of the liquid or a substantial part of it: it is almost impossible. It is better to repeat aspiration after intubation the background reliably tuned mechanical ventilation with oxygen inhalation.

 

In cases of severe bronchospasm, atelectasis, increasing pulmonary edema, even preserved spontaneous breathing showed mechanical ventilation with inhalation of 100% oxygen through a mask with positive pressure on inspiration (not less than 40 – 60 sm of water. col.) And positive end-expiratory pressure in (3 – 5 sm of water. col.) followed intubation tracheal tube cuff (with preserved consciousness before intubation should enter intravenous 50 – 80 mg / kg sodium oxybutyrate or 0.2 -0.3 mg / kg diazepam). In the case of upper airway obstruction or massive pulmonary edema if endotracheal intubation is not possible, immediately conduct tracheostomy. Probe into the stomach should be introduced only after intubation and leave it for the duration of assistance, including during transport to the hospital, because 60% of victims with recovery of vital organs occurs vomiting.

 

After recovery of the heart of the victim transported to the hospital on a stretcher with lowered head end of compulsory inhalation of oxygen on the background ventilation or preserved spontaneous breathing. During transport in the presence of appropriate indications cardio-pulmonary reanimation conduct activities taking into account the threat of rapidly progressive pulmonary edema. In cases drowning in freshwater pulmonary edema may develop immediately after drowning due hypervolemia. However, even if there are no signs of pulmonary edema after restoration of breathing and heartbeat, he can develop after a latent period – from 15 minutes to 3 days. Therefore, in addition to conventional measures, held in stages cardio-pulmonary reanimation when existing signs right ventricular heart failure (sudden general cyanosis, swelling of the neck veins), should be immediately removed from the ulnar, femoral, subclavian or jugular vein at least 400 – 500 ml of blood. Parallel conduct activities correction of pulmonary edema.

 

In the melting of fresh water to the development of hemolysis requires bloodletting, even if there is no threat of pulmonary edema. This withdrawn blood substitute solutions of glucose, Ringer-lactate, and if drowning in seawater – colloidal solutions (reopolyglukine, Refortan). In cases of massive hemolysis, which requires replacement of a large part of the blood of the victim, conduct transfusion (in the hospital).

 

One of the important conditions for the successful elimination of the consequences of hemolysis is support alkaline blood infusion of 200 – 300 ml of 4% sodium hydrocarbonate with subsequent control of blood pH and further correction acid-base status in hospital.

 

Victims, derived from clinical death, to moderately and gradually warm. For him remove wet clothes dried body towels and sheets, rubbing the skin irritable liquids (ethyl alcohol or camphor) envelops in a blanket and rubbing the skin under her, putting a warm heating pad (through the fabric). In the hospital after restore breathing and heart activity and preserved consciousness exercise constant surveillance, prevention of late pulmonary edema, pneumonia, hepatic, renal, adrenocortical insufficiency, etc..

 

Symptomatic therapy is performed under the control of homeostasis, where necessary carry out its correction.

 

According saved respiration and heart activity in cases of lost consciousness conducting combat cerebral edema in the absence of spontaneous or inadequate spontaneous breathing exercise ventilation. Spend a permanent toilet trachea and bronchi, washed them through an endotracheal tube or bronchoscope isotonic sodium chloride solution.

 

In all cases shown prolonged continuous oxygen therapy (especially if drowning in seawater).

 

To correct metabolic acidosis shown rekeying 4% sodium hydrocarbonate controlled parameters acid-base status.

 

To normalize the permeability of the vascular wall intravenously administered rutin (30 – 40 ml), sodium thiosulfate (10ml 5% solution), corticosteroids (hydrocortisone – 4 – 5 mg / kg, prednisolone – 1 – 2 mg / kg or more per day).

 

Measures BCV normalization in drowning in seawater: transfusion dry blood plasma, serum albumin, dextran, Refortan. When drowning in fresh water to reduce hypervolemia used bloodletting with exchange blood transfusion, plasmapheresis, ultrafiltration.

 

Sometimes patients after latency is developing rapidly progressive pulmonary edema. Therefore, all escaped to conduct chest radiography for detecting early signs of pulmonary edema that is not clinically detected. The mechanism of repeated pulmonary edema is not quite clear, possibly pathogenic role water, chemicals or of infection, destruction of surfactant.

 

Immediate treatment in cases of pulmonary edema after drowning is oxygen inhalation and intravenous administration of 1 liter of blood plasma or other oncotic fluid. You can try to stop the introduction of pulmonary edema diuretic. For inhibition of alveolar tissue reaction indicated the introduction of large doses of corticosteroids. Required prophylactic administration of antibiotics.

Auther- doc.L.Yu.Ivashchuk