This may result from impaired production or increased destruction of platelets. Platelet transfusion is often indicated in neonates and young infants with
All components used for intrauterine transfusion or in neonates of 1.2 Kg or less must be irradiated and should have a reduced risk of CMV transmission such as seronegative donors, deglycerolized, leukocyte reduced by filtration. They must be cross match compatible with maternal serum.
1. Hemolyte Disease of the Newborn (HDN)
2. Hyperbibrulinemia: (unrelated to HDN)
Exchange transfusion is mandated at a bilirubin level of 18-20 mg% by 24-48 hours of age in a metabolically unstable, full term infant, and at a bilirubin level of 25 mg% in a metabolically stable infant.
- Liver conjugation system immaturity
- Hereditary red cell disorders (e.g. spherocytosis, elliptocytosis)
The most effective modality of treatment is whole blood exchange transfusion to detoxify endotoxins with or without antibiotics.
4. Disseminated Intravascular Coagulation (DIC)
Treatment is ideally with fresh whole blood exchange transfusion to provide clotting factors and remove fibrin degradation products.
Hyperviscosity in this disease is directly related to neurologic impairment in the neonate. It is important to note that the peripheral hematocrit is disproportionate to the central nervous system hematocrit and should not be used as a guideline to estimate the degree of viscosity. Decision is based on both clinical and metabolic status, lethargy, hypoglycemia, and hypocalcemia.
Table 25.3. Causes of neonatal anemia
1. Soft tissue rupture
2. Loss of vascular integrity leading to blood loss in body cavities
3. Twin-twin transfusion
4. Fetal-maternal transplacental bleeding
6. Blood sampling platelet counts below 50 x 109/L (50,000 mm3) and who are bleeding. Neonatal alloimmune thrombocytopenia at term is managed as for fetal transfusion (Table 25.1). However, in the neonate, this transfusion may occur with the first pregnancy and technically, the platelet transfusion is much simpler. The dose is 1 unit.
Granulocytic transfusions are used rarely in septic infants. Ideally exchange transfusion with fresh whole blood is effective in treating the septic neonate. However, granulocyte support may be useful in the treatment of gram-negative and Staphylococcal infections. The dose is 1 x 109 neutrophils in a volume of 15-20 ml. This dose and volume is approximately present in the fresh (less than 8 hours) buffy coat from a unit of whole blood, but a fresh granulocyte apheresis product is preferred, if available. The donors are usually selected to be CMV seronegative and the granulocytes are irradiated to prevent transfusion associated graft versus host disease (Chapter 37). Granulocyte products are never leukoreduced by filtration.
Fresh frozen plasma (FFP) is the treatment of choice to replace coagulation factors in a dose of 10-15 ml/Kg unless a specific concentrate is available. FFP increases clotting factor activity by 10-20%. This is used to treat bleeding in (1) hereditary coagulation factor deficiency or (2) maternal causes such as antenatal disseminated intravascular coagulation (DIC) or vitamin K deficiency. Rarely, cryo-precipitate is transfused in cases of DIC, often in conjunction with platelet transfusion. The dose is 1-2 units.
Clinical Decisions and Response Monitoring: Triggers, Targets, Functional Reserve and Threshold of Effect
The decision to transfuse any blood component should never be made exclusively on the basis of a laboratory test. In many instances, however, laboratory tests are important in guiding the appropriate use of blood components. The clinical practice of routinely transfusing patients merely on the basis of laboratory results such as a hemoglobin or hematocrit without regard for clinical symptoms has fallen into disrepute. A combination of clinical and laboratory features is the basis of good clinical judgment regarding the need for blood transfusion.
The reason is illustrated in Figure 26.1. This shows a general relationship between clinical symptomatology and laboratory test results. The abscissa, (y-axis) shows clinical symptoms. The ordinate (x-axis) shows a laboratory test which has a normal range and then increasing in the degree of abnormality. In more concrete terms, the clinical symptom could be fatigue or malaise and the laboratory test the hematocrit. Within the normal range of the hematocrit (arbitrarily 38-52), clinical symptoms such as fatigue cannot be attributed to the hematocrit. As the hematocrit becomes abnormal, (arbitrarily between 27-38), clinical symptoms due to anemia are unlikely in most patients. This is largely because of the ability of the heart to compensate by increasing cardiac output, which will likely occur as the hematocrit drops below 30. As the hematocrit drops further (21-27), some clinical symptoms may occur. This will, of course, depend on the specific clinical situation, the degree of the anemia, the rate of blood loss, and patient features such as age, physiological status, and cardiac function. The point at which clinical symptoms become evident is called the threshold of effect. The threshold of effect is not to be mistaken with the transfusion trigger. Patients with minimal symptoms of anemia who may respond to other forms of treatment, such as iron or vitamin B12 deficiency, etc. are not transfused at the threshold of effect. In addition, bedridden patients without any expectation of an immediate increase in exercise need, not be transfused at this threshold. As the degree of abnormality worsens, however, a point is reached where the clinical symptoms justify a blood transfusion. This point for any individual patient is known as the transfusion trigger. When a decision is made to transfuse the patient, consideration must be made as to the expected outcome. An adequate dose of the blood product should be given (in this case, the volume of red cells to be prescribed) in order to achieve a target
posttransfusion result. This should be below the threshold of effect in order to allow a safety margin in any individual patient and to ensure that there will be a satisfactory outcome (improvement in symptoms) from the blood transfusion. The transfusion target, however, need not be within the normal range. The degree of abnormality which an individual patient can sustain once laboratory results begin to shift from the normal range until it reaches the threshold of effect is called the functional reserve for that particular patient. Functional reserve is due to a compensatory mechanism, such as increased cardiac output, increased red cell 2, 3 diphosphoglyceric acid, etc.
These concepts are of importance in making appropriate clinical decisions with regard to the transfusion of individual patients. Applying these concepts to platelet transfusions is as follows: As the platelet count drops slightly below the normal range of 140 x 109/L, clinical bleeding will not occur, and the count may decrease to 30 x 109/L or lower before an increased risk of minor spontaneous clinical hemorrhage becomes evident (threshold). However, the transfusion trigger i.e., the decision to transfuse platelets, will be much lower than the 30 x 109/L, e.g., for example, 10 x 109/L. Once a decision is made to transfuse, the dose of platelets should result in a 20-40 x 109/L increase in the platelet count, i.e., the transfusion target will be beyond threshold of effect. It can be seen, therefore, from this example that the functional reserve in platelets is very large and extends well into the abnormal range. A further change in immune thrombocytopenic purpura (ITP)
is that the platelets are larger (Chapter 22). Therefore, in this condition, even very low platelet counts are tolerated for long intervals without apparent significant bleeding. These concepts can also be applied to the transfusion of fresh frozen plasma in a patient with liver disease. As the prothrombin time (PT) prolongs slightly, all available data indicates that there is little or no increase in clinical bleeding. At some arbitrary prolongation of the prothrombin time, a slight increase in bleeding risk of no clinical significance could become manifest (threshold of effect) if an invasive procedure were performed. The transfusion trigger should be beyond the threshold. Plasma at a dose of 10-15 ml/kg will likely result in a shortening of the PT below this threshold. Note that the transfusion target is not within the normal range. There is a common misconception in attempting to achieve a prothrombin time within the normal range prior to an invasive diagnostic or therapeutic procedure. In more concrete terms, using a thromboplastin with an ISI of 2.0, the upper normal PT could be 13 seconds, then the functional reserve is probably 14-16 seconds, the threshold of effect at 16 seconds, the transfusion trigger 18 at seconds and the transfusion target, 15 seconds.
If compensatory mechanisms are compromised, the above principles do not change, but the critical values may shift. This is illustrated in Figure 26.2. In this figure, the theoretical relationships between fatigue, a symptom of anemia, and hematocrit in two hemodynamically stable-iron deficient subjects aged 20 and 80 years is shown. The symptomatic threshold for the 20-year-old may be a hematocrit of 20; for the 80-year-old, at a hematocrit of 30. The transfusion trigger, however, for the 20-year-old could be a hematocrit of 10-14; for the 80-year-old, 24-27. The above assumes that there is no imminent threatening acute blood loss.
In monitoring the laboratory response to transfusion, for red blood cells, the hematocrit can be measured at 1-24 hours posttransfusion in the absence of ongoing blood loss. For platelets, the increment is measured at 10-60 minutes posttransfusion to measure 'recovery'; and at 18-24 hours to estimate survival. For plasma, the prothrombin time or activated partial thromboplastin time can be measured after plasma have undergone blood volume equilibration, usually after 3 minutes. However, 10-15 minute postplasma transfusion would be reasonable. Some clotting factors such as factor VII have short a half life (3 hours) and a low molecule weight (factors II, VII, IX, X), such that they will equilibrate with the extravascular space. Therefore, the beneficial effect of plasma transfusion as measured by a shortening of the prothrombin time tends to be short lived.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...