Anti‐factor Xa (anti‐Xa) monitoring of unfractionated heparin (UFH) is associated with less time to achieve therapeutic anticoagulation compared to the activated partial thromboplastin time (aPTT). However, it is unknown whether clinical outcomes differ between these methods of monitoring. The aim of this research was to compare the rate of venous thrombosis and bleeding events in patients that received UFH monitored by anti‐Xa compared to the aPTT. A retrospective review of electronic health records identified adult patients that received UFH given intravenously (IV) for ≥2 days, with either anti‐Xa or aPTT monitoring at an academic tertiary care hospital. This was a pre/post study design conducted between January 1 to December 30, 2014 (aPTT), and January 1 to December 30, 2016 (anti‐Xa). All UFH adjustments were based on institutional nomograms. The primary outcome was venous thrombosis and the secondary outcome was bleeding, both of which occurred between UFH administration and discharge from the index hospitalization. A total of 2500 patients were in the anti‐Xa group and 2847 patients aPTT group. Venous thrombosis occurred in 10.2% vs 10.8% of patients in the anti‐Xa and aPTT groups, respectively (P = .49). Bleeding occurred in 33.7% vs 33.6% of patients in the anti‐Xa and aPTT groups, respectively (P = .94). Anti‐Xa monitoring was not an independent predictor of either outcome in multivariate logistic regression analyses. Our study found no difference in clinical outcomes between anti‐Xa and aPTT‐based monitoring of UFH IV.
Heparin-induced thrombocytopenia is a well-recognized complication of anticoagulation with heparin. We present the case of a patient with recent heparin-induced thrombocy1 Unfractionated heparin (UFH) currently remains the gold standard for anticoagulation in cardiopulmonary bypass (CPB) because of its low cost, safety profile, ease of dosing, and effective reversibility with protamine. Nevertheless, it is estimated that about 17% of patients on UFH will develop an immune response through the generation of immunoglobulin-G (IgG) antibodies against the complex of heparin with platelet factor 4, which results in type II HIT in 1% to 3% of those patients. 2 The consequent immune complex induces platelet activation and consumption, causing a drastic fall in platelet count, arterial or venous thrombosis (or both), and eventual bleeding. 2,3 Patients with an established diagnosis of HIT-for whom surgery that necessitates anticoagulation is planned-should therefore be administered an alternative drug.2 As a result of both blood stasis and alterations in enzymatic activity upon extreme temperature changes, deep hypothermic circulatory arrest (DHCA) further complicates the issues of anticoagulation, and increases the need for an alternative non-heparin-based anticoagulant. An alternative drug in such an instance is the bivalent, direct thrombin inhibitor bivalirudin, which achieves anticoagulation during CPB and DHCA. 4 We report a case of type II HIT in a patient undergoing emergency surgery for an acute type A aortic dissection, requiring CPB and DHCA, in whom we successfully used bivalirudin as an anticoagulant.
Case ReportAn 82-year-old man presented with chest pain and an inferior ST-elevation myocardial infarction. A computed tomographic (CT) angiogram also revealed a Stanford type A aortic dissection with a 6-cm ascending aortic aneurysm extending to the aortic arch and a large pericardial effusion with radiographic signs of tamponade. The patient also had severe aortic valve regurgitation, with a left ventricular ejection fraction of 0.62.Heparin had been initiated for atrial fibrillation at another hospital, before acute aortic dissection was diagnosed. The patient developed HIT, which was confirmed via enzyme-linked immunosorbent assay for the presence of antibodies against heparin and platelet factor 4 complex. Heparin was subsequently discontinued.The patient was taken to the operating room for repair of type A aortic dissection. Bivalirudin, a direct thrombin inhibitor, was used to achieve adequate anticoagulation
Background
Standard dose ganciclovir (SD-GCV) for treatment of CMV infection/disease is 5 mg/kg every 12 hours, although higher doses (7.5–10 mg/kg every 12 hours) may be considered for resistant CMV. Literature on safety/efficacy of high dose GCV (HD-GCV) is limited. We sought to evaluate safety and clinical outcomes of SD-GCV vs HD-GCV strategies.
Methods
Retrospective single center study of adult SOT recipients with CMV viremia from 1/1/2017-1/31/2019 who received IV GCV therapy. Primary objective was to compare incidence of cytopenias between SD-GCV and HD-GCV. Secondary outcomes compared CMV viremia clearance, incidence of CMV disease and recurrent viremia within 30 days, granulocyte colony stimulating factor (G-CSF) use, and antiviral resistance testing rates.
Results
We evaluated 121 patients: 74 received SD-GCV, 47 received HD-GCV. Baseline characteristics were similar between groups. Most patients received a liver transplant (46% SD vs 36% HD) and had D+/R- CMV serostatus (55.4% SD vs 68% HD). Induction immunosuppression occurred in 75%, mostly with anti-thymocyte globulin. Median baseline CMV viral loads were similar (4620 IU/mL SD vs 7770 IU/mL HD, p=0.25).
Incidence of cytopenias was similar between groups: leukopenia (43% SD vs 43% HD, p=0.96), neutropenia (15% SD vs 13% HD, p= 0.75), thrombocytopenia (24% SD vs 31% HD, p=0.62). HD-GCV did not significantly impact CMV clearance (HR: 0.79 [95% CI 0.52–1.21], p=0.27). There was no difference in incidence of CMV disease (35% SD vs 38% HD, p=0.72) or incidence of recurrent CMV viremia (15% SD vs 28% HD, p=0.098).
G-CSF requirement was not different (23.7% SD vs 14.3% HD, p=0.295), however, patients on HD-GCV received more doses of G-CSF (median 2 SD vs 5 HD, p=0.001). More patients in HD-GCV group were tested for antiviral resistance: 15 (21%) SD vs 20 (43%) HD, p=0.01. Of these, there was no difference in rate of resistance detection (7/15 (47%) SD vs 11/20 (55%) HD, p=0.95).
Conclusion
Therapy with HD-GCV did not demonstrate increased incidence of cytopenias compared to SD-GCV, nor did we observe improved time to CMV clearance or incidence of CMV disease between groups. Opportunities exist for improving stewardship of antiviral resistance testing and use of G-CSF when considering HD-GCV therapy.
Disclosures
All Authors: No reported disclosures
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