Objectives:Limited literature exists examining the use of enteral clonidine to transition patients from dexmedetomidine for management of agitation. The aim of this study was to evaluate dexmedetomidine discontinuation within 8 h of enteral clonidine administration in addition to the rates of dexmedetomidine re-initiation in patients who failed clonidine transition.Methods:A single-center, retrospective analysis evaluated critically ill adult patients from 1 February 2013 to 28 February 2014, who used dexmedetomidine and clonidine for sedation management. Patients were excluded if they received enteral clonidine for reasons other than sedation management. Secondary aims of the study observed time to dexmedetomidine discontinuation, agitation (Richmond Agitation Sedation Scale) and delirium ratings (Confusion Assessment Method for the intensive care unit), clonidine dose, and enteral clonidine discontinuation.Results:In all, 26 patients were evaluated. Demographics included a mean age of 54.4 (±16.7) years, Acute Physiology and Chronic Health Evaluation II score of 18 (interquartile range = 14–22), and 80.7% of admissions to the cardiac surgery intensive care unit. Dexmedetomidine discontinuation occurred in 17 (65.4%) patients within 8 h of receiving clonidine. The total median clonidine exposure per intensive care unit day was 0.35 mg/ICU day (interquartile range = 0.2–0.5) in patients who discontinued dexmedetomidine within 8 h and 0.5 mg/ICU day (interquartile range = 0.4–1.0) (p = 0.036) in patients who did not. We observed similar Richmond Agitation Sedation Scale and Confusion Assessment Method for the intensive care unit scores and rates of hypotension. Unintentional use of clonidine beyond ICU and hospital stay was observed in 54% and 23% of patients, respectively.Conclusion:Enteral clonidine may be an effective and safe alternative to transition patients off of dexmedetomidine for ongoing sedation management. Clinicians should critically evaluate the need for clonidine at ICU and hospital discharge. More studies comparing the use of clonidine to transition from dexmedetomidine infusions are needed.

A dexmedetomidine stewardship program, including an institution-specific prescribing guideline and a pharmacist-driven quality assurance program may ensure guideline compliance and decreased use of dexmedetomidine at an academic medical center.

No abstract

Ranolazine, an antianginal agent, has activity at muscle and neuronal sodium channels. Congenital genetic mutations to sodium channels in humans and supratherapeutic ranolazine concentrations in animal models have produced similar neurologic adverse reactions. We describe a case of neurologic adverse effects in an 81-year-old woman with coronary artery disease, renal impairment, and mild neurologic disease who received ranolazine for symptomatic control of a non-ST-segment elevation myocardial infarction. Just over 48 hours after a dose increase, she experienced new-onset dysarthia, dysmetria, hallucinations, worse tremors, and difficulty with word finding. Her workup for acute stroke and infectious causes was negative. Her symptoms abated 2 days after ranolazine was discontinued. The patient was at risk for ranolazine adverse effects due to the high dose administered and her advanced age, renal impairment, and baseline mild neurologic disease. Use of the Naranjo adverse drug reaction probability scale indicated a probable relationship (score of 5) between the patient's neurologic adverse events and the ranolazine therapy. To our knowledge, this is the first case report illustrating rare but debilitating neurologic adverse effects of ranolazine. Health care practitioners should be aware of the adverse effects of ranolazine and avoid doses greater than 500 mg twice/day in patients older than 80 years or those with a creatinine clearance of less than 30 ml/minute.

Introduction:The rate of severe bleeding and thrombotic complications on ECLS remains high (20-40%) and leads to poor outcomes. Platelet dysfunction on ECLS has been described, but it is seldom considered in goal directed hemostasis management. TEG® with platelet mapping (TEG-PM) measures functional aspects of clot formation and the percent of Platelet Inhibition (PI) on specific platelet surface receptors. Data provided by TEG-PM might enhance our ability to titrate goal-directed hemostasis management, thereby minimizing bleeding complications. Our primary objectives were 1) to determine the frequency and magnitude of PI in children on ECLS, and 2) to determine if PI is independently associated with severe bleeding or mortality in children requiring ECLS. Methods: An IRB approved retrospective chart review was performed of children from birth to 18 years, who required ECLS from 9/30/2011-12/31/2012. Data collected included demographics, coagulation tests, TEG®-PM, the number and type of blood products transfused, the number and type of medications given within 24 hours prior to each TEG sample, the number and severity of bleeding and thrombotic complications. Severe bleeding was defined as intracranial, pulmonary or gastrointestinal bleeding. The magnitude of PI was defined as the median (IQR) of all values measured per patient. To assess the frequency of PI, a threshold of > 50 % PI was considered significant. We separately evaluated adenosine diphosphate (ADP) and arachidonic acid (AA) receptor inhibition. Data are presented as median (IQR). results: In 24 patients, we reviewed 54 TEG®-PM samples. The median number of TEG samples analyzed per patient was 2 (1-3), age was 9 months (0.9-73), heparin dose was 40 U/kg/hr (30-50) and duration on ECLS was 8 days (6-10). Severe bleeding occurred in 42 % (10/24) patients and thrombotic complications in 16 % (4/24). ICU mortality was 54 %( 13/24). We found > 50 % ADP-PI in 92 % (22/24) patients and 80 % (46/54) TEG®-PM samples. We found > 50 % AA-PI in 75 % (18/24) patients and 47 % (25/53) TEG®-PM samples. In the 54 samples analyzed, the magnitude of ADP-PI was 84 % (50-97) and AA-PI was 51% (11-72). The magnitude of AA-PI was higher in the severe bleeding group 59 % (34-77) compared to the non-bleeding group 36.6 % (4-61), (p=0.045). Upon logistic regression no variables were independently associated with severe bleeding. None of patients had received direct platelet inhibitors such as aspirin and dipyridamole. The patients had received known platelet inhibitors including: H2 Blockers 66% (16/24), inhaled Nitric Oxide (iNO) 50 % (12/24) and milrinone 42 %( 10/24) within 24 hours prior to the TEG sample reviewed. Use of these medications was not associated with increased ADP-PI, as the magnitude of ADP-PI was similar for patients received H2 blockers 84 %( 36-97) and those did not on H2 Blockers 85 % (52-97), (p =0.93); those on iNO 97 % (60-96) and not on iNO 73 % (46-97), (p=0.54); those on milrinone 74 % (44-96) and not on milrinone 86 % (53-98), (p =0.23). These a...