History and exam
Key diagnostic factors
common
presence of risk factors
Key risk factors include recent heparin exposure (within past 100 days) and recent orthopaedic or cardiovascular surgery.
history of recent heparin exposure
Received unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux for the past 5-10 days (range 4-5 days) or within the past 100 days.
The risk of HIT, according to heparin type, in order from highest to lowest is as follows: unfractionated heparin >LMWH >fondaparinux.[16][32]
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history of HIT
Patients with a remote history of HIT who are re-exposed to unfractionated heparin or low molecular weight heparin for at least 4 days are at risk of recurrence.
absence of conditions and medications that cause thrombocytopenia
Increases the likelihood of HIT (e.g., sepsis; absence of drugs such as vancomycin, carbamazepine, sulfa drugs, antineoplastic agents, glycoprotein IIb/IIIa antagonists, quinine/quinidine).[53]
history of recent surgery or trauma
Postoperative and trauma patients who receive heparin have the highest incidence of HIT (1% to 5%), whereas HIT is very uncommon in medical patients who receive prophylactic doses of heparin (<1%), and is extremely rare in obstetric patients (<0.1%).[10][11][12][13][14]
Surgery/trauma releases platelet factor 4 (PF4), which increases the likelihood of HIT in patients exposed to heparin. The higher levels of PF4 produced by surgical and non-surgical trauma favour the stoichometric concentrations of PF4 and heparin required to form the antigen recognised by HIT antibodies.[35]
The timing of the platelet fall in relationship to surgery/trauma is important because these events are also alternative causes of thrombocytopenia/thrombosis.
features consistent with recent venous or arterial thromboembolic event (e.g., PE, DVT, stroke, MI)
New unilateral leg oedema and/or tenderness and/or discoloration is suggestive of deep vein thrombosis (DVT).
Chest pain, tachypnoea, hypotension, and tachycardia are features of pulmonary embolism (PE) and myocardial infarction (MI).
New focal neurological deficits are suggestive of stroke.
Thrombosis precedes thrombocytopenia in approximately 25% of patients with HIT.[52]
Ratio of venous to arterial thrombotic events in HIT is 2.4 to 4.1.[52]
Patients with cerebral venous thrombosis may present with headache, nausea, vomiting, and/or neurological deficits.
uncommon
necrosis at heparin injection site(s)
May occur without thrombocytopenia.
Other diagnostic factors
common
absence of bleeding
No or minimal petechiae/ecchymosis or other signs of bleeding.
Despite sometimes profound thrombocytopenia, bleeding in patients with HIT is rare.
uncommon
signs of adrenal haemorrhagic necrosis
Occurs in 3% to 5% of HIT patients.[54]
May present with abdominal pain, refractory hypotension, and Addisonian crisis.
acute systemic reaction
Fever, chills, tachycardia, hypertension, dyspnoea, or cardiopulmonary arrest within 30 minutes of a dose of heparin or low molecular weight heparin.
Usually accompanied by an abrupt drop in platelet count.
signs of venous limb gangrene
Rarely, patients with HIT-provoked deep vein thrombosis (DVT) will present with venous limb gangrene (as a consequence of inappropriate treatment with a vitamin K antagonist).[7][Figure caption and citation for the preceding image starts]: Venous limb gangrene of left foot in HIT: (A) dorsal aspect; (B) medial aspect; and (C) plantar aspectRozati H, Shah SP, Peng YY. Lower limb gangrene postcardiac surgery. BMJ Case Reports. 2013; doi:10.1136/bcr-2012-008362 [Citation ends].
Risk factors
strong
recent heparin exposure (within past 100 days)
The risk of HIT, according to heparin type, in order from highest to lowest is as follows: unfractionated heparin >low molecular weight heparin (LMWH) >fondaparinux.[16][32]
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There is a consensus that differences in the polysaccharide chain length and degree of sulfation of the drugs explains this ranking.[33][34] Fondaparinux, at one third the length of heparin, still stimulates the formation of antiheparin/platelet factor 4 (PF4) HIT antibodies, but only rarely triggers the platelet activation required to elicit the clinical manifestations of HIT.[2]
HIT typically develops 5 to 10 days after exposure to heparin (range of 4-15 days). It is important to be aware that, even if HIT antibody formation occurs during the typical day 5 to 10 window period, thrombocytopenia can occur later (even after heparin exposure has been discontinued).
recent orthopaedic or cardiovascular surgery
Postoperative and trauma patients who receive heparin have the highest incidence of HIT (1% to 5%), whereas HIT is very uncommon in medical patients who receive prophylactic doses of heparin (<1%), and is extremely rare in obstetric patients (<0.1%).[10][11][12][13][14]
A key link between patient population and risk for HIT is the circulating level of platelet factor 4 (PF4). The higher levels of PF4 produced by surgical and non-surgical trauma favour the stoichometric concentrations of PF4 and heparin required to form the antigen recognised by HIT antibodies.[35]
weak
female sex
Women appear to have a 1.5- to 2-fold increased risk of HIT compared with men.[17] For reasons that are unclear, the difference according to sex is less apparent when low molecular weight heparin is the cause of HIT.
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