five minute incubation at room temperature, and
then examined for hemolysis or agglutination. This
crossmatch serves only as a check on the ABO
matching of the donor and recipient. Modern blood
bank practices now allow for the use of an electronic
crossmatch in which ABO compatibility between
donor and recipient is assured by verification by a
computerized data system (Judd 1998).
As mentioned, a full red cell crossmatch is
called for if there is a history of antibody formation
in the recipient. The crossmatch is performed in a
manner similar to an antibody screen, including an
antiglobulin testing step, only donor red cells rather
than panel red cells are used.
Transfusion recipients are monitored closely
during and immediately following the transfusion. If
ABO incompatibility is the cause of the reaction,
intravascular hemolysis will occur during or within
an hour following the transfusion. Laboratory
findings consistent with a significant release of
hemoglobin into the circulation include substantially
reduced plasma concentrations of haptogloblin (a
hemoglobin binding protein) and hemopexin (a
heme binding protein), the appearance of unbound
hemoglobin in the plasma and hemoglobin and
hemosiderin in the urine, and an increased plasma
concentration of bilirubin. Red cell lysis is marked
by increased plasma concentrations of red cell injury
markers (e.g., lactate dehydrogenase). Hemolysis
occurs quickly and the clearance of plasma hemoglo-
bin and its breakdown products is rapid, so the
plasma markers of hemolysis peak within hours after
the transfusion and dissipate promptly. Therefore,
blood should be collected for these laboratory studies
soon after the recognition that a transfusion reaction
may have occurred. A direct antiglobulin test should
also be performed to provide evidence that the
hemolysis, if present, is due to antibodies.
Extravascular hemolysis can occur when there is
incompatibility of non-ABO blood group systems
including the Rh system. If alloantibodies are pre-
sent at the time of the transfusion, acute extravascu-
lar hemolysis will result. The findings of hemo-
globin release into the plasma are not present but
there is evidence of increased hemoglobin recycling
in the form of an elevated plasma concentration of
bilirubin. Red cell injury markers also show an
increase in their plasma concentration and the direct
antiglobulin test is positive. Delayed extravascular
hemolysis can be caused by an anamnestic immune
response even when there is no detectable antibody
present at the time of pretransfusion testing. Typical
laboratory findings will only be present if the
response is brisk.
Note that it is exceedingly unlikely for ABO or
Rh incompatibility to occur if the donor and recipi-
ent are typed as being compatible. Transfusions that
are ABO or Rh incompatible are almost always due
to clerical errors when releasing the red cell units or
identification errors when hanging the red cell units.
That is why the first step in the investigation of a
transfusion reaction, after immediate discontinuation
of the transfusion and institution of resuscitative
measures, is a check for discrepancies among the
compatibility tag, the product bag label, and the
patient’s hospital identification band.
INFECTION
The laboratory evaluation of infection has two
parts, the tentative classification of an illness as
infectious and the definitive demonstration, identifi-
cation, and characterization of the pathogen respon-
sible. Tentative classification rests primarily on the
clinical presentation but there are laboratory findings
that may contribute. They include characteristic
changes in the plasma concentrations of markers of
the injury and function of the involved tissues and
changes in the plasma concentrations of markers of
the acute phase response.
The presence of a pathogen can be demonstrated
by microscopic visualization of the organism in
material sampled from the patient or by culture of
the organism from the material. Some pathogens
are, however, extremely difficult or impossible to
visualize or culture; infection by these pathogens is
demonstrated by the presence of microbial sub-
stances or by an active immune response (Figure
9.3).
The identification of a pathogen entails, at a
minimum, the elucidation of the genus of the patho-
gen, as antimicrobial susceptibilities are largely de-
fined at the genus level. Pathogens may be further
identified as to species and, sometimes, as to strain
if classification at that level is important in making
therapeutic decisions and if the technical difficulty of
performing the classification is not unreasonable.
For most pathogens, identification includes deter-
mining the species of the organism. Characteriza-
tion of a pathogen consists of the determination of
the antimicrobial susceptibilities of the organism.
Characterization of the organism by high resolution
Tissue Injury
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