Based on the published literature, intranasal administration of fentanyl, sufentanil, ketamine, hydromorphone, midazolam, haloperidol, naloxone, glucagon, and, in limited cases, flumazenil may be a safe, effective, and well-tolerated alternative to intramuscular or intravenous administration in the prehospital and ED settings.
Acute heart failure (AHF) is defined by a constellation of signs and symptoms that manifest when new or decompensated ventricular dysfunction is triggered by an acute precipitant such as excessive preload, afterload, or myocardial ischemia. Despite being one of the most frequent causes of hospitalization and cardiovascular mortality, little to no progress has been made over the last few decades to advance the treatment of AHF. Current mainstays of pharmacotherapy for AHF including diuretics, vasodilators, and inotropes can improve symptoms; however, no currently approved agent has been shown to provide lasting outcome benefit for patients with AHF. First discovered in pregnant women where it is known to help with growth of the cervix and assist with the maternal cardiovascular and renovascular responses to pregnancy, relaxin is an endogenous neurohormone that has novel vasoactive properties. In particular, relaxin is a potent vasodilator with a number of pleiotropic effects that may affect cardiac remodeling, making relaxin an attractive compound for use in the management of AHF. Indeed, in two randomized controlled trials, a single 48-hour infusion of relaxin relieved symptoms of AHF with no evidence of major adverse effects. A signal of mortality benefit at 180 days was noted in both trials, prompting a third trial of relaxin powered for 180-day mortality that is currently under way. The pharmacology that underscores the potential benefit of relaxin is discussed and insight is provided into future clinical application of this novel drug should it prove to be the first therapy capable of reducing mortality in AHF.
IntroductionWhile moderate to severely elevated blood pressure (BP) is present in nearly half of all emergency department (ED) patients, the incidence of true hypertensive emergencies in ED patients is low. Administration of bolus intravenous (IV) antihypertensive treatment to lower BP in patients without a true hypertensive emergency is a wasteful practice that is discouraged by hypertension experts; however, anecdotal evidence suggests this occurs with relatively high frequency. Accordingly, we sought to assess the frequency of inappropriate IV antihypertensive treatment in ED patients with elevated BP absent a hypertensive emergency.MethodsWe performed a retrospective cohort study from a single, urban, teaching hospital. Using pharmacy records, we identified patients age 18–89 who received IV antihypertensive treatment in the ED. We defined treatment as inappropriate if documented suspicion for an indicated cardiovascular condition or acute end-organ injury was lacking. Data abstraction included adverse events and 30-day readmission rates, and analysis was primarily descriptive.ResultsWe included a total of 357 patients over an 18-month period. The mean age was 55; 51% were male and 93% black, and 127 (36.4%) were considered inappropriately treated. Overall, labetalol (61%) was the most commonly used medication, followed by enalaprilat (18%), hydralazine (18%), and metoprolol (3%). There were no significant differences between appropriate and inappropriate BP treatment groups in terms of clinical characteristics or adverse events. Hypotension or bradycardia occurred in three (2%) patients in the inappropriate treatment cohort and in two (1%) patients in the appropriately treated cohort. Survival to discharge and 30-day ED revisit rates were equivalent.ConclusionMore than one in three patients who were given IV bolus antihypertensive treatment in the ED received such therapy inappropriately by our definition, suggesting that significant resources could perhaps be saved through education of providers and development of clearly defined BP treatment protocols.
ABSTRACT. The aim of this study was to determine the frequency of subdural haematomas (SDHs) occurring in infants presenting following atraumatic cardiorespiratory collapse. This study was a review of retrospective case notes, brain imaging and post-mortem examinations carried out in the paediatric intensive care unit (PICU) and emergency department (ED) in a tertiary paediatric centre in the UK. The study included infants and children less than 4 years old dying in the ED or admitted to the PICU after atraumatic cardiorespiratory arrest. We identified macroscopic SDHs on brain imaging or post-mortem examination. Of those children who experienced a cardiorespiratory arrest from a non-traumatic cause and met inclusion criteria, 33 presented and died in the ED and 17 were admitted to the PICU. These children had a post-mortem examination, brain imaging or both. None of these infants had a significant SDH. One child had a small clot adherent to the dura found on post-mortem and two had microscopic intradural haemorrhage, but it is unclear in each case whether this was artefact, as each had otherwise normal brains. Subdural haematoma arising in infants or young children in the context of catastrophic cardiorespiratory compromise from a non-traumatic cause was not observed.
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