Page 2210 - Hematology_ Basic Principles and Practice ( PDFDrive )

Chapter 132 Thrombocytopenia Caused by Platelet Destruction, Hypersplenism, or Hemodilution 1957

the possibility of postoperative thrombotic thrombocytopenic uremic syndrome (HUS); thrombocytopenia and microangiopathic
purpura (TTP) should be considered. 6 hemolysis that begin approximately 1 week after a prodromal diar-
Mild to moderate platelet count decreases that occur soon after rheal illness; and fungemia-associated thrombocytopenia (onset, 1–3
transfusion of blood products are common and can be explained by weeks after complex illness involving indwelling catheters and broad-
hemodilution; however, a marked platelet count fall after transfusion spectrum antibiotic usage). In contrast, thrombocytopenia of insidi-
may be the result of passive alloimmune thrombocytopenia (PAT) or ous onset that progresses over several years suggests chronic liver
sepsis because of contaminated blood products (see Fig. 132.2). disease, with evolution to portal hypertension and associated spleno-
Other characteristic temporal features of thrombocytopenia megaly (e.g., cirrhosis secondary to alcohol or hepatitis C) or a slowly
include postenterohemorrhagic Escherichia coli–associated hemolytic progressive BM disorder (e.g., myelodysplasia).

TABLE Differential Diagnosis of Thrombocytopenia in Laboratory Evaluation
132.2 Pregnancy
Laboratory evaluation of patients with thrombocytopenia is sum-
Incidental thrombocytopenia of pregnancy (gestational marized in Table 132.3 (also see Chapter 129). The blood film is
thrombocytopenia)
Preeclampsia or eclampsia a examined to exclude pseudothrombocytopenia, which is character-
ized by in vitro platelet clumping. This phenomenon, which is
DIC secondary to: evident in approximately one in 1000 blood samples, is most often
Abruptio placentae caused by naturally occurring GPIIb/IIIa (α IIbβ 3)-reactive autoanti-
Endometritis bodies that induce aggregation of platelets in the presence of the
Amniotic fluid embolism calcium-chelating anticoagulant ethylenediamine tetraacetic acid
Retained fetus (EDTA). Because the platelet aggregates are not counted by the
Preeclampsia or eclampsia a
Peripartum or postpartum thrombotic microangiopathy electronic particle counter, the automated platelet count appears
falsely low. The correct platelet count usually can be determined by
TTP collecting the blood into sodium citrate or heparin or by performing
HUS
the count on nonanticoagulated finger prick samples; maintaining
a Preeclampsia or eclampsia usually is not associated with overt DIC. the blood sample at 37°C often attenuates platelet clumping. EDTA-
DIC, Disseminated intravascular coagulation; HUS, hemolytic uremic syndrome;
TTP, thrombotic thrombocytopenic purpura. dependent pseudothrombocytopenia has no pathologic significance
other than potentially placing a patient in jeopardy for inappropriate
Transfusion of
blood product
500
Heparin bolus
Normal platelet count
400 nadir after major surgery
Platelet count (× 10 9 /L) 300 Rapid- Bacterial

200
contamination
onset HIT
100 Typical-onset
HIT
Sepsis, multiorgan failure
PAT
Postsurgery TTP D-ITP, PTP
0
0 1 2 3 4 5 6 7 8 9 10
Postoperative day (day 0 = day of surgery)
Fig. 132.2 TIMING OF ONSET AND SEVERITY OF THROMBOCYTOPENIA: IMPLICATIONS
FOR DIFFERENTIAL DIAGNOSIS. The usual postoperative platelet count nadir is seen between postopera-
tive days 1 to 3 (inclusive). Early and progressive platelet count declines often reflect severe postoperative
complications such as sepsis and multiorgan failure; severe thrombocytopenia can (rarely) indicate postsurgery
thrombotic thrombocytopenic purpura. Thrombocytopenic disorders that begin approximately 1 week after
surgery are often immune mediated: moderate thrombocytopenia can indicate heparin-induced thrombocy-
topenia (HIT), both “typical onset” or (if heparin is not being given) “delayed onset”; very severe thrombo-
cytopenia can indicate drug-induced immune thrombocytopenia (D-ITP) or (rarely) posttransfusion purpura.
An abrupt decline in platelet count after receiving a heparin bolus in a patient who has received heparin within
the past 7–100 days can indicate “rapid-onset” HIT; thrombocytopenia that begins abruptly after transfusion
of a blood product can indicate sepsis from bacterial contamination or (rarely) passive alloimmune thrombo-
cytopenia caused by transfusion of platelet-reactive alloantibodies. D-ITP, Drug-induced immune thrombo-
cytopenia; HIT, heparin-induced thrombocytopenia; PAT, passive alloimmune thrombocytopenia; PTP,
posttransfusion purpura; TTP, thrombotic thrombocytopenic purpura. (Reprinted, with permission, from Grein-
acher A, Warkentin TE: Acquired non-immune thrombocytopenia. In: Marder VJ, Aird WC, Bennett JS, et al, editors:
Hemostasis and thrombosis: Basic principles and clinical practice, ed 6, Philadelphia, 2013, Lippincott Williams &
Wilkins, p 796.)