Computer-Based Substance Use Reporting and Acceptance of HIV Testing Among Emergency Department Patients.

More than 10 years after the Centers for Disease Control and Prevention recommended routine HIV testing for patients in emergency departments (ED) and other clinical settings, as many as three out of four patients may not be offered testing, and those who are offered testing frequently decline. The current study examines how participant characteristics, including demographics and reported substance use, influence the efficacy of a video-based intervention designed to increase HIV testing among ED patients who initially declined tests offered by hospital staff. Data from three separate trials in a high volume New York City ED were merged to determine whether patients (N = 560) were more likely to test post-intervention if: (1) they resembled people who appeared onscreen in terms of gender or race; or (2) they reported problem substance use. Chi Square and logistic regression analyses indicated demographic concordance did not significantly increase likelihood of accepting an HIV test. However, participants who reported problem substance use (n = 231) were significantly more likely to test for HIV in comparison to participants who reported either no problem substance use (n = 190) or no substance use at all (n = 125) (x2 = 6.830, p < 0.05). Specifically, 36.4% of patients who reported problem substance use tested for HIV post-intervention compared to 30.5% of patients who did not report problem substance use and 28.8% of participants who did not report substance use at all. This may be an important finding because substance use, including heavy alcohol or cannabis use, can lead to behaviors that increase HIV risk, such as sex with multiple partners or decreased condom use.

Methodology for AACT evidence-based recommendations on the use of intravenous lipid emulsion therapy in poisoning

Intravenous lipid emulsion (ILE) therapy is a novel treatment that was discovered in the last decade. Despite unclear understanding of its mechanisms of action, numerous and diverse publications attested to its clinical use. However, current evidence supporting its use is unclear and recommendations are inconsistent. To assist clinicians in decision-making, the American Academy of Clinical Toxicology created a workgroup composed of international experts from various clinical specialties, which includes representatives of major clinical toxicology associations. Rigorous methodology using the Appraisal of Guidelines for Research and Evaluation or AGREE II instrument was developed to provide a framework for the systematic reviews for this project and to formulate evidence-based recommendations on the use of ILE in poisoning. Systematic reviews on the efficacy of ILE in local anesthetic toxicity and non-local anesthetic poisonings as well as adverse effects of ILE are planned. A comprehensive review of lipid analytical interferences and a survey of ILE costs will be developed. The evidence will be appraised using the GRADE system. A thorough and transparent process for consensus statements will be performed to provide recommendations, using a modified Delphi method with two rounds of voting. This process will allow for the production of useful practice recommendations for this therapy.(AU)

Randomized trial of IV dexamethasone for acute migraine in the emergency department.

BACKGROUND: It is not yet clear if corticosteroids are useful for the treatment of migraine. We determined the efficacy of 10 mg of IV dexamethasone as adjuvant therapy for patients presenting to an emergency department (ED) with acute migraine. METHODS: This was a randomized, double-blind, placebo-controlled multicenter trial. Subjects were randomized to dexamethasone 10 mg IV or placebo. As primary treatment for their migraine, all subjects received IV metoclopramide. Our primary hypotheses were the following: a greater percentage of patients with migraine who received dexamethasone would 1) achieve a headache-free state in the ED and maintain it for 24 hours and 2) have no headache-related functional impairment after ED discharge when compared to placebo. RESULTS: A total of 656 patients were approached for participation and 205 were randomized. The persistent pain-free outcome was achieved in 25% of those randomized to dexamethasone and 19% of placebo (p = 0.34). No functional impairment after ED discharge occurred in 67% of those randomized to dexamethasone and 59% of placebo (p = 0.20). In the subgroup of subjects with migraine lasting longer than 72 hours, 38% of those randomized to dexamethasone were persistently pain-free vs 13% of placebo (p = 0.06). Side effect profiles were similar, with the exception of acute medication reactions, which occurred more commonly in the dexamethasone group. CONCLUSION: A moderate dose of IV dexamethasone should not be administered routinely for the emergency department-based treatment of acute migraine, although it might be useful for patients with migraine lasting longer than 72 hours.

Calcium and digoxin vs. calcium alone for severe verapamil toxicity.

UNLABELLED: 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, does 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 infusion rates. There were no deaths in the DIG group and four deaths in the No-DIG group (Fisher = 0.08). Neither ventricular tachycardia nor ventricular fibrillation developed in either group. Other hemodynamic parameters did not show significant changes. CONCLUSIONS: In a model of severe verapamil toxicity, digoxin plus calcium raised SBP and did not result in ventricular arrhythmias when compared with calcium alone.

The effect of hyperglycemia on cocaine neurotoxicity and death in mice.

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%, chi(2) = 0, p = 1), seizure rates (hyperglycemic 85%, euglycemic 82%, chi(2) = 0.292, p = 0.589), and survival rates (hyperglycemic 62%, euglycemic 51%, chi(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%, chi(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.

The hemodynamic effects of cocaine during acute controlled hemorrhage in conscious rats.

BACKGROUND: Cocaine is often associated with trauma; however, little is known about how its use alters the response to blood loss. The effect of cocaine on hemodynamics following acute hemorrhage was studied in a rat model. METHODS: Following baseline measurements, rats were administered either intravenous cocaine, or saline as a control. Both groups then underwent arterial catheter hemorrhage of 30% of total blood volume. Outcome variables include blood pressure, heart rate, hematocrit, pH, PCO2, PO2, and serum bicarbonate. RESULTS: Following hemorrhage, blood pressure decreased in both groups but the hypotension was significantly greater in the saline group than the intravenous cocaine group at 0 and 5 minutes posthemorrhage. Heart rate was increased significantly for the intravenous cocaine group compared to the saline group starting at 15 minutes postcocaine and lasting for the next 25 minutes. No difference was noted for hematocrit, pH, PO2, or serum bicarbonate. CONCLUSION: Although transient, cocaine blunted the hypotensive response to acute controlled hemorrhage and resulted in tachycardia.

Severe gamma-hydroxybutyrate withdrawal: a case report and literature review.

We report a case of gamma-hydroxybutyrate (GHB) withdrawal resulting in severe agitation, mental status changes, elevated blood pressure, and tachycardia hours after stopping chronic use of GHB. The patient admitted to substantial GHB abuse on a daily basis for 2.5 years. Previous attempts at cessation reportedly resulted in diaphoresis, tremors, and agitation. The patient's symptoms, negative polypharmacy history, and negative urine and blood toxicological analysis for alcohol, benzodiazepines, sedative-hypnotics, or other substances suggested the diagnosis of GHB withdrawal. Later analysis of a patient drug sample confirmed the presence of GHB. The patient required 507 mg of lorazepam and 120 mg of diazepam over 90 h to control agitation. This is one of the few reported cases of GHB withdrawal and one of the most severe. Given the increasing use of GHB, more cases of severe GHB withdrawal should be anticipated.

Intraarterial vs intravenous administration of antivenin for the treatment of Crotalidae atrox envenomation: a pilot study.

OBJECTIVE: Standard therapy for significant snake envenomation includes antivenin. i.v. administration is currently the only recommended route. Intraarterial (i.a.) administration has potential advantages over i.v. that could improve outcome. To study this, the authors compared i.v. and i.a. antivenin administrations for the treatment of experimental snake envenomations. METHODS: 14 adult female swine were anesthetized and prepared with femoral artery and ear vein catheters, and baseline hoof, forearm, and thigh circumference and volume displacement measurements were taken. Crotalidae atrox venom was injected into the subcutaneous tissue of the hoof. The doses of venom were 4.75, 9.50, 19.00, 37.90, 47.30, 56.90, and 66.40 mg. Immediately following injection of venom, polyvalent antivenin (Crotalidae) (0.285 mg/10 mL saline) was infused over 30 minutes into the femoral artery (i.a. group) or ear vein (i.v. group). As a control, 10 mL of saline was infused into the ear vein (i.a. group) or femoral artery (i.v. group). Measurements were recorded up to 48 hours. Linear mixed-effect regression models were used for each measurement and to compare the i.a. and i.v. groups. RESULTS: Venom dose and time after administrations were associated with increased circumferences and increased volumes (p < 0.05). i.v. administration was associated with larger hoof (1.26 cm) and forearm (0.42 cm) sizes and volume displacement (21.71 mL) when compared with i.a. administration ( p < 0.05). CONCLUSION: i.a. antivenin results in a modest but significant decrease in tissue edema when compared with i.v..

Sensitivity and specificity of salamandrid integumental transepithelial potential to prolactin.

The effects of ovine prolactin (oPRL), bovine growth hormone (bGH) and human placental lactogen (hPL) on in vivo integumental transepithelial potential (TEP) were examined in two salamandrid urodeles, adult terrestrial-phase Taricha granulosa and the juvenile red-eft stage of Notophthalmus viridescens. TEP in efts treated with 1.0 microgram oPRL/2 days fell from 73.3 +/- 6.1 to 15.2 +/- 5.5 mV by Day 7 (P less than 0.001), whereas the TEP of efts treated with either 1.0 or 10 micrograms bGH/2 days remained at control levels for as long as 24 days. TEP in efts treated with a single dose of 10 micrograms oPRL dropped from 65.74 +/- 4.1 to 23.0 +/- 3.4 mV (P less than 0.01) in 3 days. Efts treated with various doses of oPRL showed a linear log total dose response over the range of 0.05 to 10.0 micrograms oPRL/animal, with a minimum detectable total dose of 0.4 micrograms/g (0.01 IU/g). In the same experiments, tail height increased by Day 7 in efts treated every other day with 10.0 micrograms oPRL, but not 1.0 microgram oPRL or either 1.0 or 10.0 micrograms bGH/2 days. In Oregon newts injected every other day with 10 micrograms oPRL, TEP decreased by 33% in 8 days (P less than 0.05), whereas in animals treated with 10 micrograms bGH/2 days, TEP did not change from control values even after 23 days. TEP in Oregon newts receiving a single dose of 100 micrograms oPRL dropped to 68% of initial values within 2 days (P less than 0.05), but subsequently recovered to control values 3 weeks after the last injection.(ABSTRACT TRUNCATED AT 250 WORDS)