Clinical Presentation

Thrombocytopenia is common in heparin-treated patients, yet only a minority have HIT. A clinical scoring system, the

"4 T's," helps predict which patients have HIT, based upon assessment of: Thrombocytopenia, Timing, Thrombosis, and the absence of oTher explanation(s) (see Table 44.1).7 Evaluation of this scoring system suggests that HIT antibod ies are unlikely (<5%) when a low score (<3) is obtained, but very likely (>80%) with a high score (>6).8 An intermediate score (4 or 5) usually indicates a clinical profile compatible with HIT but also with another plausible explanation, such as sepsis.

Most patients with HIT have moderate thrombocytope-nia, with platelet count nadirs usually between 20 to 150 x

109/L (median nadir, 55 x 109/L); only 5 to 10% develop a platelet count fall to less than 20 x I09/L.12 At least 90% of patients evince a 50% or greater platelet count fall; espe cially in postoperative patients (who usually exhibit throm-bocytosis after postoperative day 5), even a large platelet count fall may not necessarily cause the platelet count to fall below 150 x 109/L.3

Typically, the platelet count begins to fall five to 10 days after starting heparin, although a more rapid platelet count fall can occur if HIT antibodies are already present because of a recent exposure to heparin.9 This link between

Anti-PF4/heparin, platelet-activating IgG |

Decouper Des Flocons

Platelet (and microparticle) — leukocyte — endothelial aggregates

HIT-specific thrombosis (white clot)

1) tf Venous and/or arterial thrombosis

2) tÎ Risk for warfarin-associated microvascular thrombosis, e.g., venous limb gangrene

FIGURE 44.1 Pathogenesis of HIT: two explanations for thrombosis. Activation of platelets (Plt) by platelet-activating anti-platelet factor 4 (PF4)/heparin IgG antibodies (HIT antibodies), leading to formation of procoagulant, platelet-derived microparticles, and neutralization of heparin by PF4 released from activated platelets. This results in marked increase in thrombin (hypercoagulability state) characterized by an increased risk of venous and arterial thrombosis, as well as increased risk for coumarin-induced venous limb gangrene. However, it is also possible that unique pathogenetic mechanisms operative in HIT, including pancellular activation (platelets, endothelium, monocytes, neutrophils) explain unusual thromboses, such as arterial white clots. Reprinted, with permission.4

Platelet (and microparticle) — leukocyte — endothelial aggregates

HIT-specific thrombosis (white clot)

1) tf Venous and/or arterial thrombosis

2) tÎ Risk for warfarin-associated microvascular thrombosis, e.g., venous limb gangrene

FIGURE 44.1 Pathogenesis of HIT: two explanations for thrombosis. Activation of platelets (Plt) by platelet-activating anti-platelet factor 4 (PF4)/heparin IgG antibodies (HIT antibodies), leading to formation of procoagulant, platelet-derived microparticles, and neutralization of heparin by PF4 released from activated platelets. This results in marked increase in thrombin (hypercoagulability state) characterized by an increased risk of venous and arterial thrombosis, as well as increased risk for coumarin-induced venous limb gangrene. However, it is also possible that unique pathogenetic mechanisms operative in HIT, including pancellular activation (platelets, endothelium, monocytes, neutrophils) explain unusual thromboses, such as arterial white clots. Reprinted, with permission.4

"rapid-onset HIT" and recent heparin use is explained by the unusual transience of HIT antibodies, which become undetectable a median of 50 to 80 days (depending on the assay performed) after an episode of HIT.9 Indeed, the transience of HIT antibodies, together with the inability to regenerate HIT antibodies before day 5 following reexposure, provides a rationale for using heparin anticoagulation during cardiac or vascular surgery in a patient with previous HIT, provided that HIT antibodies are no longer detectable.10

Rarely, HIT begins several days after heparin already has been stopped (delayed-onset HIT); this syndrome is associated with strong positive tests for HIT antibodies.11 Some sera activate platelets in vitro without the need to add heparin.

Thrombosis is the most important complication of HIT, and occurs in most patients.1-3 Both venous and arterial thrombi (or both) can occur (see Table 44.2). The odds ratio for thrombosis ranges from 20 to 40.12

Venous Thrombosis and HIT

Venous thrombosis is the most common complication of HIT, usually manifesting as unilateral or bilateral lower-limb DVT.1,2 Indeed, DVT occurs in about 50% of patients with HIT, with about half of these also developing symptomatic pulmonary embolism. In one study, upper-limb DVT occurred in 10% of HIT patients with use of a central venous catheter (CVC); compared with controls, both HIT and CVC use were strongly associated with upper-limb DVT, illustrating that a localizing risk factor (vessel injury from the CVC) interacts with systemic hypercoagulability (HIT), thereby influencing the type and location of thrombosis.13

Phlegmasia Cerulea Dolens and Venous Limb Gangrene

Venous limb ischemia (phlegmasia cerulea dolens, venous limb gangrene) can result if coumarins such as warfarin are

TABLE 44.1 Clinical Scoring System for HIT: The "4 T's"

Points (0, 1, or 2 for each of 4 categories: maximum possible score = 8)

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