Transfusion Therapy - PowerPoint Presentation

Slide1
Slide2

 Transfusion TherapySlide3

According to a survey conducted by the Committee on Blood and Blood Products of the American Society of

Anesthesiologists,much

of all blood given to patients is during the

perioperative

period. The anesthesiologist should be an expert on the implications and the complications associated with blood transfusions and should be a leader of acute transfusion medicine in the hospital setting.Slide4

Blood transfusions are given to increase oxygen-carrying capacity and intravascular volume. Slide5

Factors

Class I

Class II

Class III

Class IV

Blood loss (mL)

750

750-15001500-20002000 or moreBlood loss (% blood volume)1515-3030-4040 or morePulse (beats/min)100100120140 or higherBlood pressureNormalNormalDecreasedDecreasedPulse pressure (mm Hg)Normal or increasedDecreasedDecreasedDecreasedCapillary refill testNormalPositivePositivePositiveRespirations per minute14-2020-3030-4035Urine output (mL/hr)3020-305-10NegligibleCentral nervous system: mental statusSlightly anxiousMildly anxiousAnxious, confusedConfused, lethargicFluid replacement (3-1 rule)CrystalloidCrystalloidCrystalloid + bloodCrystalloid + blood

American College of Surgeons' Classes of Acute HemorrhageSlide6

In 2006, the American Society of Anesthesiologists Practice Guidelines offered these recommendations:   

1

.    Transfusion is rarely indicated when the hemoglobin concentration is greater than 10 g/

dL

and is almost always indicated when it is less than 6 g/

dL

, especially when the anemia is acute.   

2.    The determination of whether intermediate hemoglobin concentrations (6 to 10 g/dL) justify or require RBC transfusion should be based on the patient's risk for complications of inadequate oxygenation.    3.    The use of a single hemoglobin “trigger” for all patients and other approaches that fail to consider all important physiologic and surgical factors affecting oxygenation is not recommended.    4.    When appropriate, preoperative autologous blood donation, intraoperative and postoperative blood recovery, acute normovolemic hemodilution, and measures to decrease blood loss (i.e., deliberate hypotension and pharmacologic agents) may be beneficial.    5.    The indications for transfusion of autologous RBCs may be more liberal than those for allogeneic RBCs because of less frequent (but still significant) risks associated with the former.Slide7

The following indications were recommended in the 6th edition of

Anesthesia

with the rule of thumb that administration of 1 unit of packed RBCs will increase

hematocrit

value by 3% to 5%:

   1.    Blood loss greater than 20% of blood volume  

2.    Hemoglobin level less than 8 g/dL    3.    Hemoglobin level less than 10 g/dL with major disease (e.g., emphysema, ischemic heart disease)    4.    Hemoglobin level of less than 10 g/dL with autologous blood    5.    Hemoglobin level less than 12 g/dL and ventilator dependentSlide8

In view of the aforementioned considerations, the following steps are recommended for patients who are

hypovolemic

and require blood transfusion:   

1

.    Infuse crystalloids or colloids.  

  2.    Draw a blood sample for typing and

crossmatching

.    3.    If crossmatched blood is not ready to give, use type-specific or type O Rh-negative cells or type O Rh-positive cells for males or postmenopausal females without a history of transfusions; type-specific, partially crossmatched blood; or type-specific, crossmatched blood.Slide9

During emergency transfusion of more than two units of type O Rh-negative,

uncrossmatched

whole blood, the patient probably cannot be switched to his or her blood type (A, B, or AB) as soon as the blood bank determines the correct blood type. Slide10

Switching could cause major intravascular

hemolysis

of donor RBCs by increasing titers of transfused anti-A and anti-B. Continued use of O Rh-negative whole blood results only in minor

hemolysis

of recipient RBCs, with

hyperbilirubinemia

as the only complication. The patient must not be transfused with his or her correct blood type until the blood bank determines that the transfused anti-A and anti-B has decreased to levels that permit safe transfusion of type-specific blood.Slide11

Complications

Changes in Oxygen Transport

Coagulopathy

Dilutional Thrombocytopenia

Low Levels of Factors V and VIII

Disseminated Intravascular Coagulation-like Syndrome (DIC)

Hemolytic Transfusion ReactionSlide12

coagulopathy

This

coagulopathy

is caused by a combination of factors, of which the most important are the volume of blood given and the duration of hypotension or

hypoperfusion

. Slide13

Patients who are well

perfused

and are not

hypotensive

for a long period (e.g., 1 hour) can tolerate multiple units of blood without developing a

coagulopathy

. Slide14

The patient who is

hypotensive

and has received many units of blood probably has a

coagulopathy

from a condition that resembles disseminated intravascular coagulation (DIC) and dilution of coagulation factors from stored bank bloodSlide15

When such bleeding occurs, the differential diagnosis for a patient who did not have a

pretransfusion

coagulopathy

(e.g., hemophilia) is

dilutional

thrombocytopenia, low factors V and VIII, a DIC-like syndrome, or hemolytic transfusion reaction.

Clinical manifestations include oozing into the surgical field, hematuria, gingival bleeding, petechial bleeding from venipuncture sites, and ecchymoses.Slide16

Dilutional Thrombocytopenia

When the platelet count is less than 50,000 to

75,000/mm,

a bleeding problem is likely and is probably a combination of

dilutional

thrombocytopenia and DIC. Platelet therapy would be appropriate in this situation.

For unexplained reasons, patients with an acutely induced thrombocytopenia (e.g., from blood transfusions) develop a hemorrhagic diathesis at a much higher platelet count than do patients with a chronically induced thrombocytopenia (e.g., idiopathic

thrombocytopeniac purpura). A higher platelet count is required to maintain adequate hemostasis with a surgical incision or trauma because damaged capillaries require platelets to plug the holes. Slide17

Low Levels of Factors V and VIII

Most of the factors are stable in stored blood, with two exceptions: factors V and

VIII.These

factors gradually decrease to 15% and 50% of normal, respectively, in whole blood after 21 days of storage. Packed RBCs even have fewer coagulation factors. Consequently, administration of fresh frozen plasma (FFP), which contains all the factors except platelets, has been recommended on a therapeutic or a prophylactic basis.

However, this practice is of questionable benefit because only 5% to 20% of factor V and 30% of factor VIII are needed for adequate

hemostasis

during surgery.

Although low factors V and VIII appear to be an unlikely primary cause of bleeding during massive blood transfusion, such deficiencies may intensify bleeding from other causes, usually dilutional thrombocytopenia in the case of blood transfusion.Slide18

Disseminated Intravascular Coagulation-like Syndrome (DIC)

DIC is likely with

thrombocytopenia,

hypofibrinogenemia

,

and

lysis of a clot within 2 hours.Slide19

Drugs Used to Improve

Hemostasis

desmopressin

(1-deamino-8-

d

-arginine vasopressin [DDAVP]), a synthetic analog of the

antidiuretic

hormone vasopressin. It increases the levels of factor VIII and von Willebrand factor and is a well-established therapy for hemophilia and von Willebrand disease. It also reduces blood loss and transfusion requirement in patients with normal preoperative coagulation status who are undergoing spinal or cardiac surgery. However, the ultimate role of desmopressin remains to be determined.It can cause hypotension, hyponatremia, and increased platelet adhesion.Slide20

aprotinin

, a serine protease inhibitor that inhibits

fibrinolysis

and improves platelet function. It has been used to decrease blood loss in multiple surgical procedures, including cardiopulmonary bypass. However, its ultimate place in the treatment of

coagulopathies

has not been established.Slide21

tranexamic

acid, is also an

antifibrinolytic

drug. Two studies found a decreased blood loss from total-knee

arthroplasty

. Presumably, release of the pneumatic tourniquet releases

fibrinolytic

material, which is inhibited by tranexamic acid.Slide22

Citrate Intoxication

Citrate intoxication is not caused by the citrate ion per se; it occurs because citrate binds calcium. The signs of citrate intoxication are those of

hypocalcemia

: hypotension, narrow pulse pressure, and increased

intraventricular

end-diastolic pressure and central venous pressure. However, citrate intoxication is very rare. Having hypothermia, liver disease, liver transplantation, or hyperventilation or being a pediatric patient increases the possibility of citrate intoxication.

infusion of more than 1 unit of blood every 10 minutes is necessary for ionized calcium levels to begin to decrease.Slide23

Hyperkalemia

For significant

hyperkalemia

to occur clinically, bank blood must be given at a rate of 120 

mL

/min or more.

As with citrate intoxication, hyperkalemia is rare and this also rules against the routine administration of calcium. Calcium may cause cardiac arrhythmias, particularly in patients anesthetized with halothane. Calcium administration should be based on diagnostic signs of hyperkalemia (i.e., peak T wave). Slide24

Temperature

Perhaps the safest and most common method of warming blood is to pass it through plastic coils or plastic cassettes in a warm water (37° to 38°C) bath or warming plates. These heat exchangers should have upper (e.g., 43°C) and lower (e.g., 33°C) temperature limits .Slide25

Acid-Base Abnormalities

As a result of accumulation of lactic and

pyruvic

acids by RBC metabolism and

glycolysis

, the pH of bank blood continues to decrease to about 6.9 after 21 days of storage. A large portion of the acidosis can be accounted for by the P

co

2 of 150 to 220 mm Hg. the metabolic acid-base response to blood transfusion was variable. Blood transfusions provide a substrate, namely, citrate, in large quantities for the endogenous generation of bicarbonate, and this accounts for the significant incidence of metabolic alkalosis after blood transfusions.Slide26

Transfusion Reactions Slide27

Hemolytic Transfusion Reaction

From 2004 to 2006, three of the four most common causes of transfusion-related deaths were hemolytic transfusion reactions, septic transfusions (e.g., bacterial contamination), and transfusion-related acute lung injury (TRALI).

Intravascular

hemolysis

occurs when there is a direct attack on transfused donor cells by recipient antibody and complement. Such a reaction can occur from infusion of as little as 10 

mL

of blood. If properly treated, death is

rare.Slide28

The classic signs and symptoms of a hemolytic transfusion reaction

chills, fever, chest and flank pain, and nausea—are masked by anesthesia.

Under general anesthesia, the only signs may be

hemoglobinuria

, bleeding diathesis, or hypotension. The presenting sign is usually

hemoglobinuria

.Slide29

Laboratory tests that should be performed if hemolytic transfusion reaction is suspected include serum

haptoglobin

, plasma and urine hemoglobin,

bilirubin

, and direct

antiglobulin

determinations. The direct

antiglobulin test can confirm the presence of hemolytic transfusion reaction because it shows that there is antibody attached to transfused donor RBCs.Slide30

Treatment

If a hemolytic reaction is suspected, blood and urine samples should be sent to the laboratory for examination.

The blood bank should check all paperwork to ensure that the correct blood component was transfused to the patient.

Laboratory tests should be performed to determine the presence of

hemoglobinemia

: a direct

antiglobulin test, repeat compatibility testing, repeat other serologic tests (i.e., ABO and Rh), and analysis of urine for hemoglobinuria.Slide31

Although there are several consequences of intravascular

hemolysis

, mainly the renal and coagulation systems are affected. The exact cause of acute renal failure from intravascular

hemolysis

is controversial, but the most common hypothesis is that hemoglobin in the form of acid

hematin

precipitates in the distal tubule and causes mechanical tubular blockage.Slide32

The magnitude of the precipitation probably is inversely related to the volume of urine flow and its

pH.

The primary emphasis of therapy should be directed toward maintaining urinary output in excess of 75 

mL

/hr by generous administration of intravenous fluids and diuretics.

One approach is the administration of lactated Ringer's solution to maintain the central venous pressure between 10 and 15 cm H

2O while initially administering 12.5 to 50 g of mannitol. If this is ineffective, the dose of mannitol may be increased or the use of more potent diuretics, such as furosemide, which increases blood flow to the renal cortex, may be required to maintain adequate urinary output. Alkalinization of the urine to prevent precipitation of acid hematin in the distal tubules is of questionable value but is easy and therefore recommendedSlide33

DIC commonly occurs with hemolytic transfusion reactions, probably because RBC

stroma

is severed, releasing

erythrocytin

, which activates the intrinsic system of coagulation. This activated coagulation leads to fibrin formation. Subsequently, platelets and factors I, II, V, and VII are consumed. As soon as a hemolytic transfusion reaction is recognized, platelet count,

prothrombin

time, and partial

thromboplastin time should be determined to provide baseline values with which subsequent laboratory values can be compared.Slide34

Hypotension during a hemolytic transfusion reaction may result from activation of the kallikrein system.After a series of reactions, plasma kininogen is converted to bradykinin, a potent vasodilator that can cause hypotension. Slide35

Steps in the Treatment of a Hemolytic Transfusion Reaction

1.    STOP THE TRANSFUSION.   

2.    Maintain the urine output at a minimum of 75 to 100 

mL

/hr by the following methods:    a.    Generously administer fluids intravenously and possibly

mannitol

(12.5 to 50 g, given over 5 to 15 minutes).    b.    If intravenously administered fluids and

mannitol are ineffective, administer furosemide (20 to 40 mg) intravenously.    3.    Alkalinize the urine; because bicarbonate is preferentially excreted in the urine, only 40 to 70 mEq of sodium bicarbonate per 70 kg of body weight is usually required to raise the urine pH to 8, whereupon repeat urine pH determinations indicate the need for additional bicarbonate.    4.    Assay urine and plasma hemoglobin concentrations.    5.    Determine platelet count, partial thromboplastin time, and serum fibrinogen level.    6.    Return unused blood to blood bank for repeat crossmatch.    7.    Send patient's blood and urine sample to blood bank for examination.    8.    Prevent hypotension to ensure adequate renal blood flow.Slide36

Delayed Hemolytic Transfusion Reaction (Immune

Extravascular

Reaction)

the level of antibody at the time of transfusion is too low to be detected or too low to cause RBC destruction. RBC destruction occurs only when the level of antibody is increased after a secondary stimulus (i.e.,

anamnestic

response). Slide37

These delayed reactions are often manifested only by a decrease in the post-transfusion

hematocrit

value. However, jaundice and

hemoglobinuria

can occur in these patients and can cause some impairment in renal function but only rarely do they lead to death. Unlike immediate reactions, antibodies most commonly involved in delayed hemolytic reactions are those in the

Rh

and Kidd systems rather than the ABO system.Slide38

Although improved blood-banking procedures have decreased the incidence of immediate hemolytic transfusion reactions, the delayed hemolytic reaction may not be preventable, because

pretransfusion

testing is unable to detect very low levels of antibody present in potential blood recipients.Slide39

Nonhemolytic Transfusion Reactions

Nonhemolytic

reactions to blood transfusions usually are not serious and are febrile or allergic in nature.

The most common adverse reactions to blood transfusions are the less serious febrile reactions.

The symptoms consist of chills, fever, headache,

myalgia

, nausea, and nonproductive cough occurring shortly after blood transfusion caused by

pyrogenic cytokines and intracellular contents released by donor leukocytes.Slide40

A direct

antiglobulin

test readily differentiates a hemolytic reaction from a febrile reaction because this test rules out the attachment of an RBC antibody to transfused donor RBCs.

There is no clear consensus on whether the transfusion should be terminated when a febrile reaction occurs.Slide41

Allergic reactions can be minor,

anaphylactoid

, or anaphylactic.

Anaphylactoid

is similar to anaphylaxis clinically but are not mediated by

IgE

. Most allergic transfusion reactions are minor and are thought to be caused by the presence of foreign protein in the transfused blood.

The most common symptom is urticaria associated with itching. Occasionally, the patient has facial swelling. When these reactions are clearly not a serious hemolytic reaction, the transfusion does not need to be discontinued. Antihistamines are used to relieve the symptoms of the allergic reaction.Slide42

These are anaphylactic reactions caused by the transfusion of

IgA

to patients who are

IgA

deficient and have formed anti-

IgA

. This type of reaction does not involve red cell destruction and it occurs very rapidly, usually after the transfusion of only a few milliliters of blood or plasma.Slide43

Infectivity of Blood

Ninety percent of post-transfusion hepatitis is caused by the hepatitis C virus.

Many blood components, such as FFP and platelet concentrates, also transmit hepatitis at an incidence equal to that of whole blood and packed RBCs. Certainly the HCV nucleic acid technology testing represents a dramatic increase in blood safety, although HCV RNA can be below detection by this process, which probably represents the occasional ongoing transmission risk.

It is a major health care advance or even a miracle that HIV is only rarely transmitted by blood transfusions except in some developing countriesSlide44

Transfusion-Related Acute Lung Injury

Transfusion-related acute lung injury (TRALI) is now the leading cause of transfusion-related mortality , although it probably is

underdiagnosed

and

underreported.This

injury manifests as

noncardiogenic

pulmonary edema. Clinically, symptoms and signs appear 1 to 2 hours after transfusion and are in force within 6 hours. Fever, dyspnea, fluid in the endotracheal tube, and severe hypoxia are typical. During anesthesia, a persistent decrease in blood oxygen saturation can be the presenting sign. Although the chest radiograph is characteristic of pulmonary edema, circulatory overload (i.e., left atrial hypertension) is not present. Slide45

All blood components, especially FFP, are implicated as caustic factors. There is no specific therapy other than stopping the transfusion and instituting critical care supportive measures. However, the transfusion should be immediately stopped and the blood bank notified for a different donor and quarantining all units from that donor. Most patients recover in 96 hours, although TRALI remains the leading cause of transfusion-related death.Slide46