Quiz 1

(Ref: Harrison 21st ed, p 893; Harrison 20th ed, p 812)  Citrate toxicity leads to excess generation of bicarbonate and resultant metabolic alkalosis. pH is inversely related to serum potassium. Since pH is rising, hypokalemia can occur. Hence, option a is seen.  If near expiry date blood is administered, then dextrose in the blood will be falling. This will cause sodium potassium pumps to fail. Hence, Potassium in blood can be elevated explaining option b.  Citrate toxicity will explain metabolic alkalosis. It leads to re-distribution of calcium and fall in ionized calcium. Hence option d is correct.

(Ref: Harrison 21st ed, p 894; Harrison 20th ed, p 812)  Option a is ruled out as history of trauma is given. Option b is ruled out as CVP will be reduced in patients with hemorrhagic shock.  Option c will require GURD Criteria with development of respiratory insufficiency and/or CNS features like coma.  Bleeding from orifices, NG tube and IV sites points to development of coagulopathy after MBT. Hence, answer is option d.  Bleeding following massive transfusion can occur due to hypothermia, dilutional coagulopathy, platelet dysfunction, fibrinolysis, or hypofibrinogenemia

(Ref: Harrison 21st ed, p 751; Harrison 20th ed, p 2995) Sideroblastic anemia occurs due to inability to form heme due to genetic reasons or drugs like INH. The first step that involves ALA Synthase activity has pyridoxal phosphate as a cofactor and pyridoxine supplementation has shown to resolve or reduce the severity of sideroblastic anemia.

(Ref: Harrison 21st ed, p 792; Harrison 20th ed, p 727) CML and Hairy cell leukemia lead to massive splenomegaly. CLL presents with cervical Lymphadenopathy and hepatosplenomegaly. But splenomegaly is not seen in aplastic anemia.

The combination of features of CRAB (Hypercalcemia, renal failure, anemia and bony lytic lesions) points to the etiology as multiple myeloma.

(Ref: Harrsion 20th edition, p 83-14; Harrison 19th edition, p 724 and morgan anesthesia: 5th edition, p 1173)
 The incidence of TRALI is more with plasma containing products. It is caused by donor anti – granulocyte antibodies in the plasma targeting the leucocyte antigens on the neutrophils sequestered in the lungs of the patient.
 The resultant acute lung injury does not respond to steroids, diuretics and needs supportive management in the form of non – invastive ventilation or CPAP.
 TRALI starts within 6 hours of transfusion and leads to fever with bilateral radiographic infiltrates.
The mortality rate is 5-10% and in most cases begings to resolve in 2-3 days and not weeks.

(Ref: Wintrobe’s hematology 11th edition 1704; Harrison 19th edition, p 138e-4/5)
Causes of FNHTR
1. HLA antibodies are most commonly found, followed by platelet – specific antibodies; and Granulocyte – specific antibodies
2. Another cause of FNHTRs is the transfusion of cytokines that have developed in vitro, especially in whole blood – derived platelet concentrates stored at room temperature.
3. Recent studies have shown that during storage, the leukocytes in platelet concentrates release cytokines that may be responsible for the febrile reaction. The incidence of FNHTRs to platelet concentrates increases with the age of the platelet concentrate and the leukocyte concentration in the product.
4. The possibility of bacterial contamination of the product must be considered as a possible cause of FNHTR. Symptoms caused by transfusion of bacteria or their toxins can be mild or may be fatal.
Platelet components are involved more often because they are stored at room temperature. However, certain organisms such as yersinia enterocolitica proliferate in red cells at storage temperatures of 1° to 6°C.

(Ref: Wintrobe’s hematology 11th edition 1657-58, Harrison 19th edition, p 685)
 CPDA – 1 is Citrate-Phosphate-Dextrose buffer supplemented with adenine. It was made available in the USA in 1978. CPDA-1 is now one of the standard anticoagulant preservative solutions in clinical use.
 The shelf life of RBC concentrates in CPDA-1 is 35 days.
 In CPD buffer life span is 28 days. The acid citrate dextrose buffer introduced at time of world war 2 also ensured a shelf life of 21 days.