6: Transfusion Therapy

CHAPTER 6 Transfusion Therapy



James Duke, MD, MBA



1 How would knowledge of oxygen delivery impact the decision to transfuse?


A transfusion would be indicated when oxygen delivery falls to a critical level (DO2crit) and oxygen consumption (VO2) needs are not met. Recall that DO2 is a function of cardiac output (CO) and the arterial oxygen content (CaO2). Arterial oxygen content is a function of arterial oxygen saturation, the oxygen-carrying capacity of hemoglobin, the hemoglobin concentration, and, for the amount of oxygen dissolved in blood (unbound to hemoglobin), the partial pressure of oxygen.


Ordinarily DO2 exceeds VO2 by a factor of four (800 to 1200 ml/min vs. 200 to 300 ml/min). Thus the extraction ratio (O2ER = VO2/DO2) is 20% to 30%. As long as DO2 exceeds VO2, VO2 is “supply independent.” However, below DO2crit VO2 becomes “supply dependent,” and VO2 decreases as DO2 decreases, creating a situation in which end-organs are at risk for ischemia. It is at this point that a transfusion is clearly indicated.



2 At what point is DO2crit reached? What are our surrogate measures for DO2crit?


As long as the patient is euvolemic, DO2crit is not reached until hemoglobin decreases to about 3.5 g/dl. This also requires that pulmonary function is intact since it requires full hemoglobin oxygen saturation and oxygen dissolved in blood (not bound to hemoglobin). It should be noted that at this hemoglobin level the oxygen dissolved in blood becomes a major contributor (almost 75%) to the oxygen delivered. It should also be mentioned that the DO2crit is modified by the patient’s oxygen requirements above baseline (e.g., catabolic states such as sepsis, burns) and the presence of end-organ disease such as coronary artery disease.


Given that in the course of normal operating room conditions, DO2crit is unavailable, other variables are used to determine whether the patient is transfused. These include hypotension, tachycardia, urine output, the presence of lactic acidosis, signs of myocardial ischemia (new ST-segment depression >0.1 mV, new ST-segment elevation >0.2 mV, regional wall motion abnormalities by echocardiography), and low mixed venous oxygen saturation (<50%, requires pulmonary artery catheterization to determine).



3 What are the physiologic adaptations to acute normovolemic anemia?


During surgery acute blood loss is usually replaced with crystalloid solutions and, if in sufficient volume, results in acute normovolemic hemodilution. Compensatory changes include sympathetic stimulation, resulting in tachycardia and increased cardiac output. Decreased viscosity reduces afterload, increases preload, and improves flow at the capillary level. Since capillary flow is not maximal under resting conditions, capillary recruitment is an adaptive mechanism as well. In addition, there is redistribution of blood to the tissues that are oxygen supply dependent (e.g., heart and brain) and oxygen extraction is increased.


It is important to note that myocardial oxygen extraction is high under normal circumstances; thus the reserve is less. The brain has greater extraction reserve than the heart. Thus the heart is more dependent on increasing blood flow to increase oxygen delivery; the significance of this becomes clear in coronary artery disease. A failure for acute normovolemic anemia to deliver oxygen in excess of consumption is another argument in favor of blood transfusion.



4 Historically, a hemoglobin level of 10 g/dl (hematocrit of 30) was used as a transfusion trigger. Why is this is no longer an accepted practice?


In patients with coronary artery disease having signs of myocardial ischemia, this level of hemoglobin might be appropriate. Otherwise it has come to be viewed as a liberal transfusion trigger. Recall that in an otherwise normal situation, DO2crit has not been reached until hemoglobin decreases to 3.5 g/dl. Although no clinician probably pushes a patient to this extreme (unless the patient requests no transfusion based on religious reasons and the like), the less likely a transfusion is really indicated, the more the risks of transfusion negatively impact the risk/benefit ratio.


It is also interesting to note that men and women tend to be treated equally when the decision to transfuse is made, despite the fact that normal women are anemic relative to men. Using the same transfusion triggers hardly seems rational. Finally there is a concern that a transfusion might not substantially increase oxygen delivery (see discussion of blood storage lesions in question 8). These are strong arguments for closely scrutinizing the consideration to transfuse.



5 What are the risks of transfusion?


The risks include contracting an infectious disease through transfusion, transfusion reactions, and the immunomodulatory effects of transfusion.



6 What infectious diseases can be contracted from a transfusion and how significant is that risk?


At this point in time, the blood supply is as safe as it as ever been, with risks of contracting hepatitis or human immunodeficiency virus (HIV) in a developed nation estimated at 1 in 2.4 million units transfused. Donated blood is tested for hepatitis B (hepatitis B core antigen), hepatitis C (hepatitis C antibody), syphilis, HIV, human T cell lymphotropic virus, West Nile virus, and cytomegalovirus. Because of improvments in testing, the window between donation and seroconversion is becoming increasingly narrow.


However, there are new infectious risks, including contracting prion-mediated diseases (variant Creutzfeldt-Jakob disease (vCJD), parasitic disease (Chagas disease, malaria), and avian flu. There are concerns that severe acute respiratory syndrome will eventually be spread through the blood supply. The risks of these diseases vary with the geographic locality. For instance, malaria is a greater risk in undeveloped countries (as is HIV); the only known cases of contraction of vCJD through transfusion are in the United Kingdom.


Because platelets are stored at a higher temperature (20 to 22° C) than red blood cells (4° C) or other blood products, platelets are the blood component at greatest risk for bacterial infection. However, testing for sepsis in platelet units is improving, and the risk will likely decrease over time.



7 Review the major transfusion-related reactions



image Hemolytic transfusion reactions caused by ABO incompatibility are most commonly caused by clerical errors and transfusion of the wrong unit. Mistransfusion is thought to occur with a frequency between 1:14,000 and 1:18,000. Most reactions occur during or shortly after a transfusion. Clinical manifestations include fever; chills; chest, flank, and back pain; hypotension; nausea; flushing; diffuse bleeding; oliguria or anuria; and hemoglobinuria. General anesthesia may mask some of the clinical manifestations, and hypotension, hemoglobinuria, and diffuse bleeding may be the only signs. It should be noted that the signs of a severe hemolytic reaction might be missed while the patient is under general anesthesia or attributed to another cause.

image Anaphylactic reactions are caused by binding of IgE; present with bronchospasm, edema, redness, and hypotension; and require urgent treatment with epinephrine, fluid infusions, corticosteroids and antihistamines, and other therapies as indicated by severity and progression of symptoms.

image Febrile reactions may be an early sign of hemolytic transfusion reaction (but other symptoms should be present) or bacterial contamination of the blood product. Febrile nonhemolytic transfusion reactions usually occur in patients who have had prior transfusions; headache, nausea, and malaise are associated symptoms. The reaction is caused by leukocyte antibodies, and leukocyte-depleted red blood cells may be indicated for these patients. Antipyretics may decrease the symptoms if given before the transfusion; meperidine may decrease the severity of chills.

image Transfusion-related acute lung injury (TRALI) is in the top three of transfusion-related deaths, having a mortality of 50%. A form of noncardiogenic pulmonary edema, TRALI is also immune related and is usually noted within 6 to 12 hours after transfusion. Symptoms include hypoxia, dyspnea, fever, and pulmonary edema; treatment is supportive.

image Urticarial reactions secondary to mast cell degranulation do not require that the transfusion be stopped; antihistamines may be given.

image These transfusion reactions are compared in Table 6-1.


TABLE 6-1

Related posts:

76: Electroconvulsive Therapy 48: Alcohol and Substance Abuse 64: Pacemakers and Internal Cardioverter Defibrillators 41: Acute Respiratory Distress Syndrome (ARDS) 68: Heart Transplantation 46: Malignant Hyperthermia and Other Motor Diseases

Stay updated, free articles. Join our Telegram channel
Tags:
May 31, 2016 | Posted by in ANESTHESIA | Comments Off on 6: Transfusion Therapy

Full access? Get Clinical Tree
Get Clinical Tree app for offline access