Transfusion medicine – clinical notes

Patient has an anaphylactic reaction to albumin? It is likely sodium caprylate which is an additive in the mixture.

Sequence of clinical presentation of symptomatic hypocalcemia:

#1 paresthesias

#2 shivering lightheadedness 

#3 twitching and tremors

#4 nausea and vomiting

#5 hypotension carpalpedal spasm tetany and seizure

hold Ace inhibitors 24 to 48 hours prior to apheresis especially with LDL apheresis

Human immunoglobulin M - half life 10 days in the serum is highly efficient at fixing complement and agglutination.

Human immunoglobulin A- serum half-life is 5-8 interesting is a monomer in the serum but it is a dimer in secretions

there are two subclasses of immunoglobulin A IgA1 and IgA2, if you're suspecting an anaphylactic reaction to a blood transfusion in somebody who is IgA deficient is best to check in anti-IGA level and not the absolute IGA level because you can be deficient in one particular subclass and therefore the anaphylactic reaction is directed against a particular subclass which is deficient. Bottom line is draw the anti-IgA.

anti human globulin -this is a probably specific anti-immunoglobulin G and an anti-complement used for ABO blood typing

P antigen is the receptor for parvovirus can give you a paroxysmal cold hemoglobinuria that fixes complement upon rewarming than causing hemolysis

But blood cell antigen Kidd fixes complement and can cause intravascular hemolysis, exposure to this antigen in previous transfusions creates anti-bodies that are known to fade from circulation over time.

Clinically significant red blood cell antigens are of course the ABO groups, but also include Rh Kell Duffy Kidd and Ss.

Buffy is the receptor for plasmodium vivax

Donated platelets come in two particular flavors those that are acquired by apheresis and those that are whole blood derived.

This is important clinically because when you are transfusing platelets that are derived from apheresis you must match crossmatch the plasma because they are red blood cell depleted. However if you are transfusing platelets that are whole blood derived you must match ABO blood group because you have red blood cells present in the mixture. Even having small amounts of red blood cells present in the mixture is a risk because that creates allo sensitization to other clinically significant red blood cell antigens and thus increasing the risk of harmful reactions in future transfusions.

On the coagulopathy of trauma

massive injury rapidly consumes platelets. Fun facts: the surface area of capillaries in your lungs can cover a football field, you have enough platelets to cover 82 ft.² large amounts of tissue injury creates endothelial micro tears which expose collagen tissue factor and other platelet aggregating substances. This is seen clinically because in trauma 5% present with with platelet counts less than 100,000.

In the setting of major trauma coagulopathy is exacerbated by the presence of hypothermia and metabolic acidosis. These clinical factors create a feedforward cycle that worsens coagulopathy and thus inevitably results with high mortality. This is the coagulopathy of trauma

ACIDOSIS

For example the activity of Xa is reduced by 55% when the pH goes from 7.4 to 7.0 furthermore the activity of the prothrombinase complex has been found to be reduced by 70% at a pH of 7.0 compared to normal physiological pH. 

Mechanisms of action of platelet dysfunction in the setting of acidosis

the presence of H+ adversely affects Na/H exchange transport across the platelet membrane. The increased proton gradient inhibits the alkalinaztion of the platelet cytosol. An alkaline cytosol is necessary for platelet degranulation. If the platelet cytosol pH remains less than 7.0 then it cannot degranulate.

Thus one platelets and turn acidotic microcirculation they are very much impaired

An interesting pathophysiological idea is that acidosis inferred from systemic pH is falsely high in comparison to the microenvironment of low flow regions in trauma patients. The point being that you can correct serum pH but low flow tissue beds have a systemic acidosis that process as a result of low flow.

HYPOTHERMIA

Every 10°C decrease reduces enzymatic activities broadly by 50%. This includes coagulation reactions. An interesting idea is that prothrombin and activated partial thromboplastin time assays should be performed at the core temperature of the patient to get a true indicator of the degree of coagulopathy. Core temperature is below 33°C are significantly impaired.

DILUTIONAL COAGULOPATHY FROM LARGE VOLUME RESUSCITATION IN SEPSIS

current guidelines for volume resuscitation in sepsis do not adequately address clotting factor replacement during significant hemorrhage. 

Current protocol from Gonzales et al Journal of trauma in 2007 - if continued bleeding following six units of RBC transfusion than two units of FFP for every additional five units of RBC. No formal criteria on platelets or cryoprecipitate.

Borgman et al in Journal trauma 2007- found improved survival with a higher FFP to RBC ratio.