Pediatric emergency medicine trisk 564

TABLE 93.13
SYSTEMIC HEPARIN ADMINISTRATION AND ADJUSTMENT


TABLE 93.14
TRANSFUSION REACTIONS

TRANSFUSION REACTIONS
Clinical Recognition


Reactions to transfused blood products may be acute (during or within 24 hours of
transfusion) or delayed (days to weeks posttransfusion). The most feared, but fortunately
now uncommon transfusion reaction, is an acute hemolytic transfusion reaction. This
type of reaction occurs due to the presence of a complement-fixing RBC antibody that
causes rapid and often severe intravascular hemolysis. The patient will have a newly
positive DAT (Coombs). The uncommon occurrence of this problem is, in large part, a
tribute to careful blood banking practices and close attention to the administration of the
properly identified RBC product to the correct recipient thereby avoiding infusion of
ABO-incompatible red cells. The release of proinflammatory cytokines as a result of
complement activation gives rise to the characteristic symptoms of apprehension, fever,
chills, abdominal or flank pain, chest tightness, and hypotension as well as activation of
the coagulation cascade potentially manifesting as DIC. Other potentially lifethreatening transfusion reactions include transfusion-related acute lung injury (TRALI),
transfusion-associated circulatory overload (TACO), anaphylactic transfusion reaction,
and septic transfusion reaction ( Table 93.14 ). TRALI is defined as acute lung injury
with hypoxemia (PaO2 /FiO2 ≤300 or room air O2 saturation <90%) that occurs within 6
hours of a transfusion in a patient without prior risk factors for acute lung injury.
Respiratory symptoms can be severe and may progress to respiratory failure in some
cases. While symptoms typically resolve within 48 to 72 hours, the associated mortality
is about 10%. TACO should be considered prior to transfusion in patients at risk for
circulatory volume overload such as patients with chronic anemia or those with

compromised cardiac function. Delayed hemolytic transfusion reactions can occur days
to weeks after an RBC transfusion. These reactions may be due to formation of an
antibody in response to a newly encountered RBC antigen or an amnestic response of an
antibody that originally developed in response to a previous transfusion but was
undetectable at the time of the most recent cross-match. The rate of RBC destruction is
usually slower with a delayed hemolytic transfusion reaction than with an acute
hemolytic reaction, so patients may have symptoms of anemia and hyperbilirubinemia,
but not shock and renal insult.
While nonhemolytic and febrile transfusion reactions are more common, they may be
difficult to distinguish from the more dangerous hemolytic reaction prior to laboratory
evaluation. Consultation with the blood bank and/or hematology can provide guidance
regarding assessment for possible transfusion reaction.

Management
In the event of a suspected transfusion reaction, the transfusion should be stopped
immediately. The blood bank should be alerted to the concern for a possible transfusion
reaction. Supportive care to ensure adequate respiratory support and end-organ
perfusion is essential. Evaluation and management considerations by reaction type are
highlighted in Table 93.14 . The name, identification number, and blood type of the
patient should be compared with those on the unit of blood to ensure that the blood was


given to the patient for whom it was intended. Laboratory testing to evaluate for
hemolysis, coagulopathy, and renal function should be sent to exclude the possibility of
a hemolytic reaction (see Table 93.14 ). Additionally, an aliquot of the unit should be
returned to the blood bank for confirmation of the original compatibility testing and
labeling. For patients with severe acute hemolysis, aggressive fluid resuscitation,
sometimes including diuretic therapy is needed to maintain urine output and minimize
the toxic effects of free hemoglobin on the renal tubules.
Suggested Readings and Key References

Anemia
Bansal D, Oberoi S, Marwaha RK, et al. Approach to a child with bleeding in the
emergency room. Indian J Pediatr 2013;80:411–420.
Drucker NA, Wang SK, Newton C. Pediatric trauma-related coagulopathy: balanced
resuscitation, goal-directed therapy and viscoelastic assays. Semin Pediatr Surg 2019;
28:61–66.
Hayward CP, Moffat KA. Laboratory testing for bleeding disorders: strategic uses of
high and low-yield tests. Int J Lab Hematol 2013;35:322–333.
Jackson J, Carpenter S, Anderst J. Challenges in the evaluation for possible abuse:
presentations of congenital bleeding disorders in childhood. Child Abuse Negl
2012;36:127–134.
Blood Loss
Janz TG, Johnson RL, Rubenstein SD. Anemia in the emergency department: evaluation
and treatment. Emerg Med Pract 2013;15:1–15; quiz 15–16.
Tobian AA, Heddle NM, Wiegmann TL, et al. Red blood cell transfusion: 2016 clinical
practice guidelines from AABB. Transfusion 2016;56(10):2627–2630.
Tyrrell CT, Bateman ST. Critically ill children: to transfuse or not to transfuse packed
red blood cells, that is the question. Pediatr Crit Care Med 2012;13:204–209.
Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper
gastrointestinal bleeding. N Engl J Med 2013;368:11–21.
Hemolytic Anemia
Dhaliwal G, Cornett PA, Tierney LM Jr. Hemolytic anemia. Am Fam Physician
2004;69:2599–2606.
Ladogana S, Maruzzi M, Samperi P, et al; AIHA Committee of the Italian Association
of Paediatric Onco-haematology (AIEOP). Diagnosis and management of newly
diagnosed childhood autoimmune haemolytic anaemia. Recommendations from the
Red Cell Study Group of the Paediatric Haemato-Oncology Italian Association. Blood
Transfus 2017;15(3):259–267.
Petz LD. A physician’s guide to transfusion in autoimmune haemolytic anaemia. Br J
Haematol 2004;124:712–716.