2. Definition
• Transfusion of large volume of blood products over a short period of
time to a patient who has severe or uncontrolled hemorrhage
Adults
Replacement of one entire blood volume (70mls/kg) within 24h
Transfusion of >10 units of packed red blood cells in 24h
Transfusion of >4 units of PRBCs in 1h when ongoing need is
foreseeable
Replacement of 50% of total blood volume within 3hrs
3. Paediatric population
Transfusion of 100% TBV within 24hrs
Transfusion to replace ongoing hemorrhage of 10% TBV per minute
Replacement of 50% TBV by blood products within 3 hrs
6. Electrolyte imbalance
• Metabolic complications are usually seen after massive transfusion.
Hyperkalemia: Stored blood has high potassium levels because of hemolysis and
irradiation
Hypocalcemia: Citrate chelates calcium
• Risk is substantially greater in a patient with preexisting liver disease or ischemia
induced hepatic dysfunction
o The indications for calcium replacement during transfusion are:
• Blood given at a very fast rate (Liver does not get sufficient time to metabolize
citrate)
• Liver diseases.
• Massive blood transfusion (citrate load is too high)
• Severe hypothermia (decreases citrate metabolism).
7. Hypomagnesemia because of large volume of poor magnesium fluid
and citrate overload
Hypokalemia because of reentry into transfused red blood cells,
release of stress hormones, or metabolic alkalosis
8. Management of electrolyte imbalances
• Laboratory monitoring
potassium, free calcium, sodium and chloride abnormalities
• Hypocalcemia replaced with either calcium chloride (2 to 5 Ml per
500mL of blood given) or calcium gluconate (10 to 20 ml per 500 ml
of blood transfused)
• Hyperkalemia – insulin, glucose
9. Acid base abnormalities
• Blood gases show variable results.
• Acidic pH of stored blood causes acidosis while citrate metabolism
causes alkalosis.
• pH falls 0.1 pH unit/week due to the production of lactic acid and
pyruvic acids by the red cells
• In massive transfusion alkalosis is more common due to citrate
intoxication (one molecule of citrate generates 3 molecules of
bicarbonate).
10. Management of acid base abnormalities
• Blood gas analysis – base deficits and lactate levels are monitored to
assess adequacy of resuscitation in restoring oxygen delivery and
tissue perfusion
11. Coagulation abnormalities
• Massive blood transfusion causes dilutional coagulopathies especially
dilutional thrombocytopenia (stored blood has no platelets and
concentration of other clotting factors is also less).
• Dilutional coagulopathies leading to disseminated intravascular
coagulation (DIC) is the usual cause of death after massive blood
transfusion
• Tissue trauma causes activation and consumption of coagulation
factors( consumptive coagulopathy)
12. • Prolonged shock, hypoxia and hypothermia result in reduced activity
of coagulation factors
• Renal dysfunction: failure to clear activation peptides that act as
competitive inhibitors
oLaboratory monitoring
CBC( platelet count)
PT, Aptt, INR, fibrinogen levels
13. management
• Treatment should be initiated only if (not prophylactically after 3-4 units as practiced in past)
• There is bleeding from surgical site which is not getting controlled by surgical hemostasis or there
is bleeding from intravenous site, mucous membranes or petechial hemorrhages.
• PT, APTT > 1.5 times of normal
• Fibrinogen < 75 mg/dL
• Platelet count < 50,000
Treatment includes
• Fresh blood (collected and used within 6 hours without refrigeration)- best modality of treatment.
(Provides all coagulation factors and platelets)
• Fresh frozen plasma.
• Specific blood component therapy.
• Platelets.
14. Hypothermia
• Significant hypothermia is only seen with massive transfusion.
• Blood should be warmed to 37°C before infusion
• Reduce rate of infusion
15. Volume overload
• Overzealous resuscitation
• Transfusion associated circulatory overload is characterized by acute
respiratory distress, tachycardia, increased blood pressure, acute
pulmonary edema etc
• Common in the elderly, children, patients with compromised left
ventricular function
• The intravenous infusion of blood product significantly raises the
central venous pressure, resulting in increased trans-vascular fluid
extravasation and pulmonary edema
16. Tissue hypoxia
• Decrease in 2,3 DPG in stored blood can shift oxygen dissociation
curve to left and at least theoretically can produce tissue hypoxia
• 2,3 DPG decreases hemoglobin’s affinity for oxygen, thereby shifting
the entire oxygen-binding curve to right
17. Volume overload/tissue hypoxia intervention
• Fluid (colloids/crystalloids resuscitation) only until blood available
• Typed/cross-matched RBCs is ideal
• Administering PRBCs, FFP and platelet concentrate in a 1:1:1 ratio
for example: 6PRBCs : 6 units of FFP and 6 units of pooled platelets.
18. Transfusion related acute lung injury
• Manifest as hypoxia within 6hrs of transfusion
• Probably due to damage alveolar capillary membrane by to anti-HLA
antibodies or anti-leukocytic antibodies
• Managed like ARDS : oxygen therapy, clearing of the airway, ensuring
adequate breathing and circulation