Supportive and Preventive Medicine

Rivaroxaban 10 mg orally once daily was compared with enoxaparin 40 mg subcutaneously daily

for 10 days, followed by placebo in acutely ill hospitalized patients. The rates of asymptomatic or

symptomatic VTE, pulmonary embolism, or death were comparable; however, the bleeding rates were

increased in the rivaroxaban group (N Engl J Med 2013;368:513-23). A subsequent study evaluating

rivaroxaban 10 mg/day orally with placebo in patients at high risk of VTE demonstrated a decrease in

rates of symptomatic VTE (0.18 vs 0.42%; HR 0.44, 95% CI, 0.22-0.89); however, low overall VTE and

bleeding event rates limit widespread use. Further studies must identify the populations most likely to

benefit from extended prophylaxis (N Engl J Med. 2018;379:1118-27).

LMWH is preferred to vitamin K antagonists and DOACs for prophylaxis in critically ill patients

HIT is a severe, immune-mediated reaction that potentially leads to life-threatening complications

such as myocardial infarction, skin necrosis, stroke, and VTE (around 50%–75% of patients with HIT

develop symptomatic thrombosis).

(prior 2 weeks) who present with a new thrombosis and low Plt.

Frequency of HIT

Higher in patients receiving unfractionated heparin than in patients receiving LMWH, occurring

in 1%–5% of patients versus less than 1%, respectively

Occurs in less than 1% of ICU patients

Higher risk in cardiac or orthopedic surgical patients receiving unfractionated heparin (15%) than

in medical patients (0.1%–1%)

Alternative causes of thrombocytopenia in critically ill patients include extracorporeal devices, intra-

aortic balloon pumps, sepsis, disseminated intravascular coagulation, bleeding, and medications (eg,

linezolid, carbamazepine, phenytoin, valproic acid). Plts may decrease after surgery on cardiopulmonary

bypass and subsequently recover; however, a secondary decrease in Plt may signal potential HIT.

Clinical diagnosis of HIT

Suspected when a patient has a decrease in absolute Plt to less than 150,000/mm3 or a relative

decrease of at least 50% from baseline, skin lesions at injection sites, or systemic reactions after

intravenous boluses

Typical onset is 5–10 days after heparin exposure, though onset can be delayed and can occur up

to 3 weeks after therapy cessation.

Recent heparin exposure, within the last 90 days, may result in rapid-onset HIT, occurring within

hours after rechallenge.

their Plt checked before anticoagulant therapy is initiated.

Probability of HIT

4T score

Segregates patients into low, intermediate, and high clinical probability on the basis of four

criteria

ii.

Four clinical features incorporated: (1) thrombocytopenia, (2) timing of thrombocytopenia, (3)

presence of thrombosis or other clinical sequelae, and (4) other causes of thrombocytopenia

iii.

A low probability 4T score (3 or less) has a high negative predictive value (0.998), whereas an

intermediate or high probability score (4 or greater) has a low positive predictive value (0.64

and 0.14, respectively) (Blood 2012;120:4160-7).