Early diagnosis of persons infected with human immunodeficiency virus (HIV) through diagnostic testing and screening is a critical priority for individual and public health. Emergency departments (EDs) have an important role in this effort. As EDs gain experience in HIV testing, it is increasingly apparent that implementing testing is conceptually and operationally complex. A wide variety of HIV testing practice and research models have emerged, each reflecting adaptations to site-specific factors and the needs of local populations. The diversity and complexity inherent in nascent ED HIV testing practice and research are associated with the risk that findings will not be described according to a common lexicon. This article presents a comprehensive set of terms and definitions that can be used to describe ED-based HIV testing programs, developed by consensus opinion from the inaugural meeting of the National ED HIV Testing Consortium. These definitions are designed to facilitate discussion, increase comparability of future reports, and potentially accelerate wider implementation of ED HIV testing.
Abstract. Calcium chloride (CaCl 2 ) is ineffective in severe calcium channel antagonist overdoses. Digoxin increases intracellular calcium by inhibiting the sodium-potassium adenosine triphosphatase enzymes. Objective: To examine the effect of calcium and digoxin on the treatment of verapamil toxicity. Methods: Sixteen dogs were instrumented to monitor hemodynamics. Verapamil toxicity (50% decrease in mean arterial pressure) was induced with verapamil (VER) at 6 mg/kg/hr and maintained for 30 minutes by titrating the VER rate. Following toxicity, the dogs received either digoxin (0.018 mg/kg) (DIG) (n = 8) or saline (No-DIG) (n = 8). Both groups received VER at three sequential rates (1 mg/kg/hr from 0 to 90 min, 6 mg/kg/hr from 90 to 130 min, and 18 mg/kg/hr from 130 to 170 min). Calcium boluses were given (500 mg at 0 and 15 min; 1 g at 140, 150, and 160 min). Data were analyzed using a repeated-measures analysis of covariance comparing DIG vs No-DIG across the infusion rates and time. Animal weight, dose of VER administered during the toxicity phase, and baseline values were included as covariates. Mortality rates were compared at 230 minutes following a total dose of 500 mg of VER. Results: The DIG group had a higher systolic blood pressure (SBP) than the No-DIG group during the 1-mg/kg/hr (early p = 0.028, late p = 0.01), 6-mg/kg/hr (p = 0.051), and 18-mg/kg/hr (p = 0.038) VER 1 This is because the overdoses of the sustained-release preparation, which contains large doses of the drug, result in profound toxicity over an extended period of time. Toxicity develops when intracellular calcium is decreased in cardiac and vascular smooth muscle, which is why intravenous (IV) calcium chloride (CaCl 2 ) is used as one of the initial therapies. In large-dose calcium channel antagonist overdoses, calcium is usually ineffective, and other therapies such as atropine, glucagon, cardiac pacing, vasopressors, 2 Even with these therapies, fatalities occur.In the presence of calcium channel antagonist toxicity, IV calcium increases intracellular calcium by creating a large extracellular-to-intracellular concentration gradient and forcing calcium through unblocked calcium channels.2 In large overdoses, calcium is ineffective because few if any channels are unblocked and calcium is unable to enter the cell.Digoxin increases intracellular calcium by initially inhibiting the sodium-potassium adenosine triphosphatase (Na-K ATPase) pump. This inhibition results in an increased intracellular sodium, which is then exchanged for calcium by an exchange mechanism that is not blocked by the calcium channel antagonist. Since calcium has limited effect in large calcium channel antagonist overdoses, the addition of digoxin may facilitate the movement of calcium intracellularly by passing the blocked calcium channels. Our hypothesis was that calcium plus a high therapeutic dose of digoxin would be more effective than calcium alone in reversing the hemodynamic effects of verapamil in an animal model of severe verapamil toxicity.
Although transient, cocaine blunted the hypotensive response to acute controlled hemorrhage and resulted in tachycardia.
Calcium chloride (CaCl 2 ) alone is an ineffective antidote in severe calcium channel antagonist overdoses. Digoxin has been evaluated as a therapy to increase the effectiveness of calcium in severe calcium channel antagonist overdoses. Objective: To determine if there is a dose-dependent hemodynamic effect of digoxin in the setting of severe verapamil toxicity treated with high-dose CaCl 2 . Methods: Eight dogs were instrumented to measure systolic and diastolic blood pressure, cardiac output, pulmonary artery pressures, and left ventricular pressures. Verapamil toxicity (50% decrease in mean arterial pressure) was induced with verapamil 6 mg/kg/hr and maintained for 30 minutes by titrating the verapamil rate. Following verapamil toxicity, each dog received one dose of digoxin equivalent to 0, 1, 1.5, 2, 3, 4, 6, or 8 times the loading dose of digoxin (0.009 mg/ kg). The verapamil rate was changed to 4 mg/kg/hr and continued for the next five hours. CaCl 2 boluses were given (0.5 g immediately following verapamil toxicity and 1 g at one, two, and three hours). Measurements were compared with the loading dose of digoxin using linear regression analysis.
Abstract. Objective: Cocaine toxicity frequently manifests as seizures and status epilepticus. Frequently, dextrose is administered to patients with cocaine-induced seizures. The objective of this study was to examine the effect of pre-existing hyperglycemia on cocaine neurotoxicity and death in mice. Methods: Swiss albino mice received intraperitoneal dextrose at a dose of 1 g/kg (12.5%) (hyperglycemic group, n = 98). The euglycemic group (n = 98) received an equal volume of 0.9% saline. After 60 minutes, all the animals received intraperitoneal cocaine at a dose of 90 mg/kg. The times to onset of ataxia, seizure, and death were recorded in seconds. Times to events were compared using a Kaplan-Meier method and results were compared using the logrank test. The overall percentage outcomes were compared using chi-square. Results: The ataxia rates (hyperglycemic 97%, euglycemic 97%, 2 = 0, p = 1), seizure rates (hyperglycemic 85%, euglycemic 82%, 2 = 0.292, p = 0.589), and survival rates (hyperglycemic 62%, euglycemic 51%, 2 = 0.2514, p = 0.113) were similar between the groups. The survival following a seizure was significantly higher in the hyperglycemic group (hyperglycemic 57%, euglycemic 41%, 2 = 4.439, p = 0.035). The median ataxia time was earlier in the hyperglycemic group (190 sec) than in the euglycemic group (166 sec) (p = 0.031). Seizures occurred no earlier in the hyperglycemic group (331 sec) than in the euglycemic group (342 sec) (p = 0.207). Survival times were not different for the hyperglycemic group (9,133 sec) and the euglycemic group (7,593 sec) (p = 0.394). Survival times following seizures were not different for the hyperglycemic group (8,095 sec) and the euglycemic group (5,816 sec) (p = 0.0752). Conclusions: In mice with pre-existing hyperglycemia, ataxia occurred earlier and survival following cocaine-induced seizures was longer than for euglycemic mice. No significant difference in the overall percentage of seizures and death was detected. Pre-existing hyperglycemia had minimal effect on worsening cocaine toxicity in mice. Key words: cocaine; neurotoxicity; hyperglycemia. ACADEMIC EMERGENCY MEDICINE 2000; 7:974-979 C OCAINE is a frequent cause of seizures and status epilepticus treated by emergency physicians and out-of-hospital care providers. The initial management of all seizures includes stabilization of the airway and cervical spine, ensuring adequate oxygenation, and evaluation and treatment of hypoglycemia. Glucose determination is important because hypoglycemia is a common cause of seizures and status epilepticus, and can easily be corrected by the administration of dextrose. 1Many out-of-hospital care protocols administer dextrose without an evaluation of the glucose level. In addition, some physicians recommend the administration of dextrose if the bedside determination is less than 120 mg/dL because these tests may not detect hypoglycemia if a lower level is used. 2Hyperglycemia worsens neurologic outcome and increases mortality in experimental models of cerebral ischemia.3-5 Co...
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