Background: Bleeding complications are common with extracorporeal membrane oxygenation (ECMO).We investigated whether a heparin monitoring protocol using activated partial thromboplastin time (aPTT) and thromboelastography (TEG) affected clinical outcomes. Methods: This retrospective chart review stratified cohorts by study interval: pre-protocol (January 2016-March 2017) or post-protocol (March 2017-December 2017. The protocol defined therapeutic anticoagulation as aPTT of 60-80 seconds and a TEG reaction (TEG-R) time of 2-4× baseline; pre-protocol management used aPTT alone. The primary endpoints were the rates of bleeding and thrombotic events (clinical/device thrombosis) as defined by Extracorporeal Life Support Organization (ELSO) guidelines.Secondary endpoints included time in therapeutic aPTT range, rate of physician compliance with the protocol, time to heparin initiation, intensive care unit length of stay, mortality, and antithrombin III (ATIII) supplementation.Results: The pre-protocol (n=72) and post-protocol (n=51) groups (age 60±12 years; 80% on venoarterial ECMO; average ECMO duration of 6 days) showed no difference in baseline characteristics. Major bleeding events occurred in 69% of pre-protocol patients, versus 67% of post-protocol patients (P=0.85). The post-protocol group had fewer retroperitoneal bleeds (P=0.01) and had a non-significantly lower rate of pulmonary or central nervous system (CNS) bleeding (P=0.07). Thrombotic events occurred in 21% of the pre-protocol group, versus 28% of the post-protocol group (P=0.39). Mortality during ECMO support was significantly lower in the post-protocol group (56.9% vs. 33.3%, P=0.01). The thrombosis rate was higher in patients who received ATIII than in those who did not (48.2% vs. 15.9%, P<0.01). Conclusions: Major bleeding did not differ between the treatment groups. However, we observed significantly less mortality and retroperitoneal bleeding in the post-protocol group, suggesting an important gain from the intervention. Further study of the value of ATIII supplementation in ECMO patients is needed since we observed that a lower baseline ATIII level may indicate higher risk for thrombosis.
We compared Brazilian, Indian, Siberian, Asian, and North American ginseng for potential interference with 3 digoxin immunoassays: fluorescence polarization (FPIA), microparticle enzyme (MEIA), and Tina-quant (Roche Diagnostics, Indianapolis, IN). We supplemented aliquots of a drug-free serum pool with ginseng extracts representing expected in vivo concentrations and overdose. We observed apparent digoxin-like immunoreactivity with FPIA, modest immunoreactivity with MEIA, and no apparent digoxin immunoreactivity with the Tina-quant with all ginsengs except Brazilian, which showed no immunoreactivity with any assay. When aliquots of serum pools prepared from patients receiving digoxin were supplemented with ginsengs, we observed falsely elevated digoxin values with FPIA, falsely lower digoxin values (negative interference) with MEIA, and no interference with the Tina-quant. Digoxin-like immunoreactive components of various ginsengs have moderate protein binding; monitoring free digoxin concentrations does not eliminate such interference. We also observed that Digibind (Burroughs Wellcome, Research Triangle Park, NC) can bind free digoxin-like immunoreactive components of ginsengs; such effects can be monitored by measuring apparent free digoxin concentrations. Indian, Asian, and North American ginsengs interfere with serum digoxin measurement by FPIA and MEIA; the Tina-quant is free of such interference. Digibind can bind free digoxin-like immunoreactive components of ginseng.
We report the case of an 82-year-old A pixaban is a novel oral anticoagulant (NOAC) that is used to prevent stroke in patients who have nonvalvular atrial fibrillation (AF). This drug has predictable therapeutic levels that do not require laboratory monitoring; however, there is no specific antidote to reverse its toxicity.1,2 We present a case of hemorrhagic pericarditis and cardiac tamponade after pacemaker implantation in a patient who was taking apixaban because of AF. Novel therapy and subsequent treatment are discussed. Case ReportAn 82-year-old man with sick sinus syndrome and paroxysmal AF presented at our catheterization laboratory from the clinic, with near-syncope and bradycardia (CHADS 2 score, 2 of 6). On 24-hour Holter monitoring, the predominant result was sinus rhythm. An echocardiogram revealed a normal left ventricular ejection fraction (>0.60), grade II (pseudonormal) diastolic dysfunction, no significant valvular regurgitation, and normal pulmonary artery pressures. A dual-chamber permanent pacemaker was implanted to treat the patient's brady-tachy syndrome and because ventricular pacing revealed pacemaker syndrome (hypotension that results from ventricular pacing due to the absence of the atrial kick that normally increases stroke volume during atrioventricular synchrony). During the procedure, the atrial lead was repositioned. One day postoperatively, the patient was discharged from the hospital after undergoing chest radiography (with normal findings), device interrogation, and incision evaluation. Because of his stroke risk, he was prescribed apixaban (5 mg twice/d) at discharge. He had normal renal function (Table I) and a body weight of 172 lb.During the week after pacemaker implantation, the patient developed fatigue, a low-grade fever (99.2 °F), nausea, moderate pleuritic chest pain, and a productive cough with clear sputum. He was readmitted to the hospital. His blood pressure had decreased from 130/77 mmHg after pacemaker implantation to 100/68 mmHg upon readmission, when he was taking no antihypertensive medications. Physical examination revealed an irregular, tachycardic rhythm (100-130 beats/min), and distended neck veins; auscultation yielded diminished bibasilar breath sounds but no quiet heart sounds. Laboratory data revealed acute kidney injury (Table I) and a substantially elevated erythrocyte sedimentation rate and fibrinogen level. The patient's platelet count and coagulation times were normal; his hemoglobin level had decreased from 15 g/dL after pacemaker implantation to 12 g/dL on readmission. He was taken to the cardiac intensive care unit, where he remained hemodynamically stable.Computed axial tomograms (CT) of the chest (Fig. 1) were not conclusive for right ventricular free-wall perforation, although a moderate-to-large circumferential pericardial effusion of 1.7 cm was detected; its Hounsfield density suggested the presence of Case Reports
Grapefruit juice increases bioavailability of a number of drugs because of inhibition of the P-glycoprotein pump and inhibition of intestinal cytochrome P450 3A4 enzyme. However, interaction between acetaminophen (also known as paracetamol in many parts of the world) and grapefruit juice has never been reported. The interaction of grapefruit juice with acetaminophen was examined in an in vivo mouse model. BALB/c mice were fed 200 microL of white grapefruit juice or pink grapefruit juice by oral gavage (three mice in each group) followed by oral delivery of 10, 50, or 100 mg/kg acetaminophen 1 hour later. Blood was withdrawn from the retro-orbital venous plexus at 1 hour and 2 hours after feeding with acetaminophen. The concentrations of acetaminophen in sera of mice were determined by fluorescence polarization immunoassay. White grapefruit juice increased concentrations of acetaminophen in mice both 1 hour and 2 hours after feeding compared to controls. In contrast, pink grapefruit juice increased acetaminophen concentrations 2 hours after feeding compared to controls. Because acetaminophen is almost completely absorbed these effects seems to be related to increased elimination half-life of acetaminophen because of interaction with grapefruit juice.
We studied the potential for detecting oleander with a new immunoassay (Digoxin III, Abbott Laboratories, Abbott Park, IL) by comparing results with those from the fluorescence polarization immunoassay (FPIA) and Digoxin II assay (Abbott). In aliquots of drug-free serum pools supplemented with pure oleandrin or oleander extract, we observed apparent digoxin values using all 3 immunoassays, but values obtained by the Digoxin III were higher than obtained by the other assays. We also observed significant apparent digoxin values in vivo in serum samples of mice 1 and 2 hours after feeding oleander extract. The average half-life of digoxin-like factors was 1.1 hours. In a serum pool (prepared from patients taking digoxin) supplemented with oleander extract, the observed digoxin values were falsely lowered when measured by the Digoxin II but falsely elevated when measured by the Digoxin III and FPIA. Monitoring free digoxin using the Digoxin III cannot eliminate this interference. Digibind neutralized digoxin-like factors of oleander extract; the effect can be monitored by observing a significant reduction in apparent free digoxin levels in the presence of Digibind as measured in protein-free ultrafiltrate using the Digoxin III. The Digoxin III is highly sensitive for measuring oleander.
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