Complications of donor and patient apheresis

 

Complication rates of donors:
Overall rate ranges between 0.81 to 2%
complication rate requiring hospitalization 1/200,000
this is in comparison to between 10 to 20% in whole blood donors.

Common reactions: hematoma, pain, citrate toxicity, vasovagal, vasovagal with syncope

 

Complication rate of therapeutic apheresis (for patients)
reported to be approximately 4.75%
reactions include: allergic febrile transfusion reactions, citrate toxicity, hypotension, vasovagal
mortality rate in therapeutic apheresis estimated to be 3 per 10,000 procedures

Citrate toxicity: a calcium chelator that inhibits coagulation. Normally citrate is distributed throughout the entire extracellular fluid it is rapidly metabolized and any calcium deficit is mobilized from albumin. Secondarily parathyroid mobilizes bone stores and renal handling of calcium increases urinary calcium resorption. Despite these companies employ mechanisms it is still possible to to see clinically significant hypocalcemia. Factors that have been associated with citrate toxicity are hypoventilation, hypoalbuminemia, total amount of citrate and the rate of infusion (high rate intermittent).

**Citrate toxicity cannot cause bleeding from inhibiting coagulation factors. This is because in order to prevent coagulation calcium levels must be reduced to 0.2 mmol per liter. This level of hypocalcemia is incompatible with life and occurs only in the machine and not in the patient.

Remember that between 40 to 55% of total calcium is albumin bound. Transfusing albumin is normally stripped of calcium and can cause a significant decrease in calcium store. It is recommended to add calcium gluconate to albumin prior to administration. You can also give intravenous calcium gluconate or slow the rate of infusion.

Keep in mind citrate also chelates magnesium. Clinical signs of hypomagnesiumemia include muscle spasm weakness decreased vascular tone and cardiac contractility abnormality. Important to remember that hypomagnesemia inhibits parathyroid hormone action and can be a secondary cause of hypocalcemia in addition to citrate toxicity.

Citrate is metabolized into bicarbonate. In settings where the patient cannot excrete bicarbonate significant metabolic alkalosis with resultant hypokalemia has been observed. Therefore remember to check your potassium before initiating therapy and replete as necessary.

 

ALLERGIC and ANAPHYLACTOID
urticaria and other allergic reactions that are seen in blood donors typically are an allergy to ethylene oxide. Ethylene oxide is used to sterilize the disposables. The combined plasma proteins and initiate an immune response. This is seen in donors of multiple donations.

Anaphylactic reactions may be triggered by ethylene oxide, hydroxyethyl starch, immunoglobulin A, albumin.

Immunoglobulin A deficiency is seen in one in 700 Caucasian. Must use IgA deficient blood products.

Anaphylaxis isnormally triggered by complement fragments C3a C5a as well as anti-bodies to immunoglobulin G & E.

ACE inhibitors:
electrostatic materials in the apheresis columns as well as enzymatic activity in donor albumin convert bradykininogen to bradykinin. Furthermore ace inhibitors in addition to blocking angiotensin-converting enzyme also block kninases (degradation enzymes of bradykinin). This leads to unopposed bradykinin activity which clinically presents flushing hypotension bradycardia dyspnea. That's why you want to stop all ace inhibitor therapy between one and two days prior to the procedure. If that didn't happen and you are suspecting this, immediately discontinue the procedure.

THROMBOCYTOPENIA OF PLASMA EXCHANGE
therapeutic plasma exchange expect to see a reduction in platelets anywhere between 0 to 71%. In the hematopoetic stem cell collections anywhere between 24 and 54% has been reported.
Plasma exchange also reduces coagulation factors, so monitor go as as well as fibrinogen. This is especially important in hemostatic challenged patients.

Reversing heparin induced bleeding - protamine sulfate dose of 1 mg for every 100 units of heparin.