Heparin-induced anaphylactic and anaphylactoid reactions: two distinct but overlapping syndromes

Warkentin, Theodore E.; Greinacher, Andreas

doi:10.1517/14740330902778180

Cited by 103 publications

(78 citation statements)

References 88 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The patient's recent heparin exposure resulted in formation of HIT antibodies such that repeat exposure to heparin via an IV bolus precipitated "rapid-onset" HIT. A repeat platelet count would have shown an abrupt platelet count fall [20,21]. HIT-associated anaphylactoid reactions occur 10 min (median) post-UFH bolus (the exact timing in our patient), and patients are typically described as hypertensive (not hypotensive as in PE), hypoxemic, dyspneic, and may have chest pain.…”

mentioning

confidence: 89%

Non–injection‐site necrotic skin lesions complicating postoperative heparin thromboprophylaxis

Tassava

Warkentin

2015

American J Hematol

View full text Add to dashboard Cite

A 75-year-old African-American man with Type II diabetes, hypertension, and hyperlipidemia was admitted with a painful right leg secondary to bilateral iliac artery obstruction. Admission hemoglobin level was 14.4 g/dL, white blood count was 11.9 3 10 9 /L (neutrophils, 10.4 3 10 9 /L), and the platelet count was 366 3 10 9 /L. Unfractionated heparin 5,000 IU thrice daily by subcutaneous injection was given for 5 days. Aortobifemoral bypass surgery was performed with full-dose intravenous heparin followed by daily subcutaneous unfractionated heparin thromboprophylaxis. After an initial decline, the platelet count rose to 480 3 10 9 /L on postoperative Day 4 (Day 10 after start of preoperative course of heparin), at which time the patient developed a swollen right leg. Vascular duplex revealed a gastrocnemius vein clot of indeterminate age, which was not treated.This patient was found to have a gastrocnemius vein thrombosis on Day 4 after surgery. Controversy exists over whether to anticoagulate deep muscular vein thromboses. No large randomized trials have been done, and some smaller studies show similar resolution with or without anticoagulation [1,2]. Thus, the decision to continue subcutaneous (SC) prophylactic-dose heparin was reasonable.On postoperative Day 5, a right leg patchy retiform purpuric skin rash developed (Fig. 1A). Arterial duplex showed improved but still poor arterial flow to the right leg. Skin biopsy (right medial thigh) showed intravascular thrombus in a mid-dermal vessel and partial epidermal necrosis, without vasculitis (Fig. 1B,C). Laboratory investigations, including complete blood count, measurement of antithrombin, protein C, protein S, ANCA, cryoglobulins, homocysteine, viral hepatitis serology, complement, and antiphospholipid antibodies, were normal/ negative. The necrotic skin rash was considered secondary to "transient ischemia" during the preceding vascular surgery. The patient was discharged to a rehabilitation facility off heparin.The patient's right lower limb rash included multiple discrete lesions extending from the thigh to the ankle with blisters, SC hemorrhage, and necrosis in an angulated branched configuration described as "retiform purpura." These lesions have a broad differential, including vasculitis, hypercoagulable state, purpura fulminans, cholesterol embolism, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, warfarin-induced skin necrosis, heparin-induced skin necrosis, cryoglobulinemia, and calciphylaxis [3][4][5]. The biopsy finding of epidermal necrosis and intravascular thrombus without vasculitis, calcification, or inflammatory cell infiltrate, plus the negative hypercoagulability testing, lack of infection, renal failure, hemolysis, and absence of warfarin therapy, rules out most of these entities. Additionally, skin necrosis from low blood flow alone can be seen in livedo racemosa, but this entity is accompanied by a perilesional violaceous reticulated skin discoloration, which was not seen [3,4].Our patient had received SC inj...

show abstract

mentioning

confidence: 89%

Non–injection‐site necrotic skin lesions complicating postoperative heparin thromboprophylaxis

Tassava

Warkentin

2015

American J Hematol

View full text Add to dashboard Cite

show abstract

“…Moreover, some literature reports have described cases of extensive cardiac thrombus, visceral angina, sudden spleen rupture and necrotic dermatitis [23−27]. HIT can also develop in the form of an anaphylactic reaction, whose first symptom is usually haemodynamic failure, including sudden cardiac arrest [18,28]. Cardiac surgery patients are at the highest risk for the most disastrous effects of HITT; those patients can be expected to develop acute closure of arterial and venous vessels (in patients after coronary vessel revascularisation) or valve dysfunction (predominantly when preceded by valve implantation into the mitral position) with dramatic haemodynamic consequences, usually leading to death [29−31].…”

Section: Hit Symptomsmentioning

confidence: 99%

Małopłytkowość poheparynowa

Krzych

Nowacka²,

Knapik³

2015

Anaesthesiol Intensive Ther

View full text Add to dashboard Cite

Heparin-induced thrombocytopenia (HIT) is a clinical immune-mediated syndrome; symptoms of HIT result from the development of arterial and venous thrombosis and are correlated with the severity of the thrombocytopenia. In all patients receiving heparin preparations in intensive care units, platelet counts should be monitored every 2−3 days throughout therapy, particularly during days 4−14 when HIT is most likely to develop. The major screening tests should always involve a clinical assessment of HIT probability (4Ts or HEP scoring systems) and enzymatic immunoassays (IgG antibodies) for patients with a moderate to high risk of HIT. The full possibilities of such advanced diagnostic procedures are limited in Poland because functional tests are still not widely available. If the diagnosis is questionable, all heparin preparations should be withdrawn and an alternative method of anticoagulation instituted until HIT has been conclusively excluded. The use of new-generation anticoagulants (direct thrombin or Xa factor inhibitors) is currently considered the treatment of choice. Old-generation anticoagulants should not be administered (vitamin K antagonists) as they can aggravate thrombosis. If administered, their action should be reversed by vitamin K once HIT is confirmed. Antithrombotic therapy with "new" anticoagulants should be carried out at least until platelet counts return to the baseline values; the recommended duration of therapy is 4 weeks in patients with isolated thrombocytopenia or 4 months in those with thrombotic complications. Vitamin K antagonists should not be applied until the normal platelet count is restored (usually > 150 G L -1 ). When the therapy with vitamin K antagonists is reintroduced, "old" antagonists should be administered simultaneously with a "new" anticoagulant for at least 5 days due to an initial decrease in protein C concentration concentration, provided that the therapeutic value of INR is maintained (> 2) for at least 2 days.

show abstract

“…Anaphylactoid reactions are a known feature of rapidonset HIT [11][12][13]. Table II lists the various signs and symptoms that have been reported [11][12][13].…”

Section: Commentarymentioning

confidence: 99%

“…Table II lists the various signs and symptoms that have been reported [11][12][13]. Most often, these reactions occur 5-30 min (median, 10 min) after intravenous bolus heparin administration.…”

Section: Commentarymentioning

confidence: 99%

See 1 more Smart Citation

Chills and limb pain following administration of low‐molecular‐weight heparin for treatment of acute venous thromboembolism

et al. 2011

View full text Add to dashboard Cite

Heparin-induced anaphylactic and anaphylactoid reactions: two distinct but overlapping syndromes

Cited by 103 publications

References 88 publications

Non–injection‐site necrotic skin lesions complicating postoperative heparin thromboprophylaxis

Non–injection‐site necrotic skin lesions complicating postoperative heparin thromboprophylaxis

Małopłytkowość poheparynowa

Chills and limb pain following administration of low‐molecular‐weight heparin for treatment of acute venous thromboembolism

Contact Info

Product

Resources

About