Immune heparin‐induced thrombocytopenia resulting from preceding exposure to heparin catheter flushes

Muslimani, Alaa; Ricaurte, Basma; Daw, Hamed

doi:10.1002/ajh.20849

Cited by 33 publications

(21 citation statements)

References 21 publications

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“…The standard dose of heparin used in flushing intravascular catheters has not been established. Most of those cases involved central vascular catheters with direct heparin flushing; infused quantities were approximately 1,000-2,000 units [10-12]. In a prospective argatroban study of 23 patients who developed HIT following exposure to heparin because of vascular catheter flushes, heparin doses were 10-13,000 units.…”

Section: Discussionmentioning

confidence: 99%

Thrombocytopenia caused by low-dose heparin supplementation of parenteral nutrition solution

Lee

Lim

et al. 2013

Blood Res

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Section: Discussionmentioning

confidence: 99%

Thrombocytopenia caused by low-dose heparin supplementation of parenteral nutrition solution

Lee

Lim

et al. 2013

Blood Res

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“…No dose of heparin is too low to cause HIT, as even small doses used for intravenous catheter flushes have been associated with HIT. 15,16 In a meta-analysis, the absolute risk for HIT with low molecular weight heparin was 0.2% (95% CI 0.1%-0.4%), and with unfractionated heparin was 2.6% (95% CI 1.5%-3.8%). 17 The lower risk of developing HIT with low molecular weight heparin is countered by its inferior lipolytic effects when compared to unfractionated heparin.…”

Section: See Related Article Pp 86-99mentioning

confidence: 99%

Challenges of cardiac inflammation imaging with F-18 FDG positron emission tomography

Bhambhvani

2017

Journal of Nuclear Cardiology

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Reliable hot spot inflammation imaging with fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) in suspected cardiac infection, cardiac sarcoidosis, or vulnerable coronary plaque is only possible when physiologic myocardial FDG uptake can be adequately suppressed. The gamut of perfusion-metabolism patterns possible in cardiac sarcoidosis 1 combined with the erratic and real possibility of inadequate suppression of normal myocardial FDG uptake is a sure recipe for head scratching and challenging image interpretation. A number of preparation methods aimed at suppressing physiologic myocardial glucose utilization have been described without clear consensus on the optimal method. In the present issue of the Journal of Nuclear Cardiology, Osborne and colleagues (doi:10.1007/s12350-016-0502-7) review various preparation protocols and success rates achieved in published studies for FDG cardiac PET and provide useful practical recommendations.A brief overview of cardiomyocyte metabolism is essential to appreciate the challenges and rationale of interventions. The heart uses various substrates as energy sources including free fatty acids (FFAs), glucose, and lactate. In the fasting condition, the normal myocardium utilizes FFAs as the major energy source (90%). Other sources include glucose and lactate.2 Postmeals or in the dysfunctional myocardium (example ischemic heart disease), myocardial metabolism shifts to glucose per the glucose-fatty acid cycle.2,3 Elevated blood insulin and glucose levels with decreased FFAs lead to a relative rise in myocardial glucose consumption. In contrast, during fasting, there is an increase in FFAs with decrease in insulin and glucose levels, shifting myocardial energy consumption away from glucose and toward FFAs. Hence interventions that facilitate myocardial FFAs metabolism while at the same time suppress physiologic glucose metabolism are imperative for successful FDG PET cardiac inflammation imaging. These include avoidance of strenuous exercise prior to imaging (to prevent skeletal muscle glucose utilization), high-fat with low (less than 5 g)-or no carbohydrate diet (to increase blood FFAs and minimize glucose and insulin levels), addition of a high-fat drink to this diet prior to FDG injection (to elevate blood FFAs), fasting for 4-18 hours (to decrease blood glucose and insulin levels and increase FFAs), and certain pharmacologic maneuvers. The latter include unfractionated heparin which induces lipolysis and up to fivefold increase in blood FFAs 4 and calcium channel blockers which reduce myocardial FDG uptake.5 Most studies combine two or more interventions with the goal of complete suppression of normal cardiac FDG uptake.Tang and colleagues in a meta-analysis involving 16 studies and 559 patients evaluated for cardiac sarcoidosis examined various patient preparations that impact the diagnostic performance of FDG PET. They conclude that duration of fasting and heparin administration significantly affected the diagnostic odds ratio (P = .01 and .04, respec...

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“…Two cases of HIT have been reported that were solely attributed to using heparin locking solutions in patients with indwelling infusion ports. 14,15…”

Section: Safetymentioning

confidence: 99%

“…9,[11][12][13] Use of UFH as a catheter locking solution also carries the risk of heparin-induced thrombocytopenia (HIT), although this has been reported in only a small number of patients. [14][15][16] Within the last decade, increasing evidence has shown an evolving role of citrates as alternatives to UFH as catheter locking solutions. 8,11,[17][18][19][20][21] The potential advantages of citrate catheter locking solutions include decreased hemodialysis catheter-related bloodstream infections (CRBSI), 8,18,20 decreased rates of catheter thrombosis, 8,18 reduced costs, 17,18,21 and lower risk of inadvertent systemic anticoagulation due to leakage of the locking solution into the bloodstream.…”

mentioning

confidence: 99%

Trisodium Citrate: An Alternative to Unfractionated Heparin for Hemodialysis Catheter Dwells

Pierce

Rocco

2010

Pharmacotherapy

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The use of tunneled hemodialysis catheters, or permcaths, either for temporary dialysis access before arteriovenous fistula or arteriovenous graft maturation or for long-term dialysis access, is associated with increased risk of catheter clotting and infection. Catheter locking solutions are routinely used to maintain patency in these catheters between dialysis sessions. Unfractionated heparin has traditionally been used for this purpose; however, trisodium citrate (also known as sodium citrate or citrate) has recently been shown to be an efficacious alternative to heparin as a locking solution. Citrate exerts both its anticoagulant and antimicrobial properties by chelating calcium to disrupt the normal coagulation pathway and by interfering with the formation of biofilm and the bacterial cell wall. Citrate is at least equivalent to heparin as an anticoagulant and antimicrobial agent for catheter locking, and in some clinical studies citrate was shown to be superior. Two different concentrations of sodium citrate were previously available; however, concerns of safety led to the removal of citrate 46.7% from the United States and Canadian markets in 2000, leaving only citrate 4% available for use as a catheter locking solution. The systemic hypocalcemic effects that were reported with citrate 46.7% have not been observed with citrate 4% in clinical trials, and the risk of systemic anticoagulation and bleeding was shown to be lower than that with unfractionated heparin. In addition, most comparative cost data indicate that citrate is a more cost-effective alternative than heparin; however, costs can vary by institution. Despite inconclusive evidence of clinical superiority, citrate 4% appears to provide a safe and at least equivocal alternative to heparin as a catheter locking agent.

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Immune heparin‐induced thrombocytopenia resulting from preceding exposure to heparin catheter flushes

Cited by 33 publications

References 21 publications

Thrombocytopenia caused by low-dose heparin supplementation of parenteral nutrition solution

Thrombocytopenia caused by low-dose heparin supplementation of parenteral nutrition solution

Challenges of cardiac inflammation imaging with F-18 FDG positron emission tomography

Trisodium Citrate: An Alternative to Unfractionated Heparin for Hemodialysis Catheter Dwells

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