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Biomedical subjects

J N Love

Publications and source records attributed to J N Love.

At least 19 recordsLinked to original sources
PubMed2006

Lack of toxicity from pediatric beta-blocker exposures.

The risk of toxicity in a child who is unintentionally exposed to a beta-blocking drug remains uncertain. The current study further defines this risk, particularly in the common scenario of ingestion of one or two tablets. A prospective cohort of 208 pediatric patients, 6 months to 6 years of age, reported to two regional poison centers serves as the study population. Data were collected with a standardized instrument during the care of each patient and for a minimum of 24 hours after exposure. No instances of serious toxicity typical of beta-blocker intoxication, such as 'shock-like' states, arrhythmias or seizures were observed in this series. Furthermore, there were no reported episodes of hypoglycemia, symptomatic bradycardia or bronchospasm. Nine instances of altered mental status or behavioral changes were reported. All appeared to be minor in nature. The most serious outcome was charcoal aspiration during gastrointestinal decontamination. This study adds to a growing body of evidence suggesting that exposure to one or two beta-blocker tablets places children at very little, if any, risk of toxicity.

Adrenergic beta-Antagonists↗
PubMed2002

Cardiovascular depression resulting from atenolol intoxication.

A case of massive atenolol ingestion leading to hypotension in association with PR and QRS interval prolongation on the electrocardiogram is presented. These clinical findings are identical to those attributed to the membrane-stabilizing activity of propranolol and other lipophilic beta-blockers. It is commonly believed that hydrophilic agents such as atenolol lack this activity. A review of the literature reveals that hydrophilic beta-blockers may have membrane-stabilizing activity, though much higher concentrations are required to produce this action in comparison with lipophilic agents. This case and a review of the literature provides a potential pathophysiological basis for atenolol-induced haemodynamic depression.

Adrenergic beta-Antagonists↗
PubMed2000

Urinary retention resulting from incarceration of a retroverted, gravid uterus.

Urinary retention resulting from urethral obstruction by a retroverted, gravid uterus is an uncommon disorder that is reported only once in the Emergency Medicine literature. Yet these patients may present in extreme distress and precipitate considerable confusion regarding the cause of and solution to this problem. No study evaluating outcome, risk of complications, or therapy exists. We present two cases that clarify diagnostic and therapeutic controversies and provide a better understanding of what is known about the pathophysiology and treatment alternatives.

Adult↗
PubMed2000

Acebutolol overdose resulting in fatalities.

Two fatal cases of Acebutolol intoxication are presented that demonstrate its clinical characteristics and potential lethality. A review of the literature suggests that acebutolol is one of the most toxic beta blockers when taken as an overdose. In addition to demonstrating characteristics of membrane-stabilizing activity, both fatal cases demonstrate significant QTc prolongation and ventricular tachycardia. The latter findings suggest an impact on ventricular repolarization not seen with Propranolol intoxication. Clarification of these findings has important implications regarding identification and treatment of this potentially fatal intoxication.

Acebutolol↗
PubMed2000

Acute beta blocker overdose: factors associated with the development of cardiovascular morbidity.

OBJECTIVE: To identify factors in exposures to beta blockers (beta-adrenergic receptor antagonists) that are associated with the development of cardiovascular morbidity and contribute to disposition decisions from the emergency department. METHODS: Prospective cohort of 280 beta blocker exposures reported to 2 regional poison centers. Multiple logistic regression was used to determine association of various clinical factors and outcome. RESULTS: In this series of beta blocker exposures, 41 (15%) developed cardiovascular morbidity and 4 (1.4%) died. A history of cardioactive coingestant was the only factor significantly associated with the development of cardiovascular morbidity (p < .05). When cases reporting cardioactive coingestants were excluded, a history of ingesting a beta blocker with membrane stabilizing activity was significantly associated with the development of cardiovascular morbidity (p < .05). All those in whom the timing of symptoms could be determined, developed symptoms within 6 hours of ingestion. CONCLUSIONS: The single most important factor associated with the development of cardiovascular morbidity in beta blocker ingestion is a history of a cardioactive coingestant, primarily calcium channel blockers, cyclic antidepressants, and neuroleptics. In the absence of such coingestion, exposure to a beta blocker with membrane stabilizing activity is associated with an increased risk of cardiovascular morbidity. Beta blocker ingestion is unlikely to result in symptoms if the patient remains asymptomatic for 6 hours after the time of ingestion.

Adrenergic beta-Antagonists↗
PubMed2000

The effect of sodium bicarbonate on propranolol-induced cardiovascular toxicity in a canine model.

STUDY OBJECTIVE: To evaluate the potential utility of sodium bicarbonate in an established model of acute propranolol toxicity. METHODS: Two minutes after the completion of a propranolol infusion (10 mg/kg), a bolus of 1.5 mEq/kg of sodium bicarbonate solution (1 mEq/mL) followed by an infusion of 1.5 mEq/kg over the next 26 minutes (n = 6) or an equivalent timing and volume of 5% dextrose solution (n = 6) was administered in each dog. Targeted cardiovascular parameters included heart rate, mean arterial pressure, left ventricular dP/dtmax, and QRS interval. RESULTS: Propranolol infusion significantly depressed heart rate (p < 0.0001), mean arterial pressure (p < 0.0001), dP/dtmax (p < 0.0001) and prolonged the QRS interval (p < 0.0001). Sodium bicarbonate failed to significantly improve these targeted parameters when compared to control animals. CONCLUSION: In this canine model of propranolol toxicity, intravenous sodium bicarbonate appears to be an ineffective single therapy. Furthermore, these results may suggest a different mechanism of sodium channel blockade for propanolol than that of type IA antiarrhythmic agents.

Animals↗
PubMed1998

A potential role for glucagon in the treatment of drug-induced symptomatic bradycardia.

Nine cases of symptomatic bradycardia are presented in which treatment with intravenous glucagon was administered when atropine failed to improve the patient's condition significantly. Although the cause often was not obvious at presentation, all nine subjects took oral medications that could have contributed to the development of symptomatic bradycardia. Eight of nine patients demonstrated clinical improvement 5 to 10 min after glucagon administration, which was consistent with its peak clinical action. Beta-blockers, calcium channel blockers, and digoxin were ultimately thought to have contributed to the majority of these presentations. This report suggests that glucagon may have a role in the treatment of symptomatic bradycardia, particularly in the presence of beta-adrenergic blockade and perhaps calcium channel blockade. Furthermore, the results in these cases suggest that future clinical trials should not be limited to drug-induced symptomatic bradycardia.

Adrenergic beta-Antagonists↗
PubMed1997

Glucagon therapy in the treatment of symptomatic bradycardia.

Symptomatic bradycardia is commonly seen in the emergency department. Effective drug therapy for this clinical scenario is limited. Although glucagon has been used in no clinical trial in this setting, its cardiac activity may prove useful, particularly in the setting of beta-adrenergic blockade. We report a case series comprising three patients taking maintenance beta-blocker therapy who presented to the ED with symptomatic bradycardia and hypotension and in whom glucagon therapy obviated the need for further treatment. Further study is warranted to evaluate and define the role of glucagon in the treatment of symptomatic bradycardia.

Adrenergic beta-Antagonists↗
PubMed1997

Characterization of fatal beta blocker ingestion: a review of the American Association of Poison Control Centers data from 1985 to 1995.

OBJECTIVE: To characterize beta blocker-related deaths. METHODS: This is a retrospective review of beta blocker-related exposure data and fatality case abstracts reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System during the 11 year period, 1985 to 1995. Historical and laboratory data were used to determine those fatalities which resulted primarily from beta blocker intoxication. RESULTS: Of 52,156 reported beta blocker exposures, 164 were fatal. In 38 cases, beta blockers were implicated as the primary cause of death. Propranolol was responsible for the greatest number of exposures (44%) and implicated as the cause of death in a disproportionately high percentage of fatalities (71%). Patients were generally young women; 63% were female and 92% were less than 50 years old. The dysrhythmias most often noted in fatal cases were bradycardia and asystole. Cardiopulmonary arrest did not develop until patients were in the care of health care personnel in 59% of cases. Though glucagon was initiated more often than any other intervention in fatal intoxications (83%), optimal dosing and maintenance infusions appear to have been underutilized. CONCLUSIONS: The predominance of fatalities associated with propranolol compared to other beta blockers reflects both its greater frequency of use over the time period studied and its greater toxicity. Since 59% developed. cardiac arrest after reaching health care personnel, further study should focus on identifying medical intervention that can reduce mortality in this group.

Administration, Oral↗
PubMed1996

Hemodynamic effects of calcium chloride in a canine model of acute propranolol intoxication.

STUDY OBJECTIVE: To evaluate the hemodynamic effects of calcium chloride in a canine model of acute propranolol toxicity. METHODS: Two minutes after the completion of a propranolol infusion (10 mg/kg), a bolus of .125 mL/kg 10% CaCl solution followed by an infusion of .375 mL/kg over the next 30 minutes or a bolus and subsequent infusion of an equivalent volume of normal saline solution was administered to each dog. RESULTS: CaCl yielded significant improvements in propranolol-induced decreases in cardiac index and stroke volume compared with saline solution-treated control animals (overall alpha = .05). Furthermore, CaCl administration resulted in earlier improvement in propranolol-induced alterations in mean arterial pressure, maximal left ventricular pressure change over time, and peripheral vascular resistance compared with saline solution (overall alpha = .05). We observed no difference between treatment groups in response to propranolol-induced bradycardia or QRS-interval prolongation. CONCLUSION: In this model of acute propranolol toxicity, CaCl therapy improved depressed hemodynamic status, mainly by a positive inotropic action.

Acute Disease↗
PubMed1995

Toxic psychosis: an unusual presentation of propranolol intoxication.

Timely diagnosis of acute propranolol intoxication requires a high index of suspicion and a knowledge of the multiple ways in which these patients may present to the emergency department. We report a case of severe propranolol intoxication that presented as an acute psychotic episode preceding cardiovascular decompensation and seizures by several hours. Though acute reversible psychosis has been appreciated after initiating or increasing propranolol dosage therapeutically, this association has not been reported in the literature regarding beta blocker overdose or intoxication. Propranolol psychosis and several other pertinent aspects of this case are discussed.

Acute Disease↗
PubMed1994

Beta-blocker toxicity: a clinical diagnosis.

An overdose of the beta-blocking agent metoprolol is presented in which the patient remained asymptomatic despite blood levels that were more than 25 times that reported to be the upper limit of therapeutic. This case emphasizes the need to diagnose beta-blocker toxicity on clinical grounds, not on blood levels that correlate poorly with the severity of symptoms. Furthermore, the question is raised as to whether patients are at any subsequent risk for morbidity, if they have not demonstrated signs or symptoms within 4 hours of ingestion.

Adult↗
PubMed1993

Luxation of the globe.

Emergency physicians encounter globe luxation, anterior dislocation of the eyeball beyond retracted lids, in a limited number of clinical circumstances. The authors present a case of spontaneous luxation followed by a general discussion of luxation. An understanding of the pathophysiology of various causes of luxation and the appropriate method and timing of reduction allows appropriate evaluation, treatment, and follow-up, thereby limiting patient discomfort, recurrence, and perhaps long-term visual impairment.

Adult↗
PubMed1993

A comparison of combined amrinone and glucagon therapy to glucagon alone for cardiovascular depression associated with propranolol toxicity in a canine model.

Multiple inotropic agents may be required to improve hypotension associated with beta-blocker toxicity. This study compared combined amrinone and glucagon therapy to glucagon alone and saline control for the treatment of propranolol-induced cardiovascular depression in a canine model. Six animals were pretreated with 10 mg/kg of propranolol intravenously (i.v.), which resulted in significant depression in heart rate (HR), cardiac output (CO), mean arterial pressure (MAP), and maximal left ventricular change in pressure over time (dP/dt max) (P < .0001). Each canine received i.v. amrinone (4 mg/kg) plus glucagon (20 micrograms/kg) therapy during a 2-minute period after propranolol infusion was completed. Cardiovascular parameters were monitored at 1, 6, 11, 21, and 31 minutes after treatment was rendered. Results were compared with those of a previous study, consisting of six animals that received glucagon therapy alone (20 mg/kg) and six controls (normal saline only) in an identical protocol. The addition of i.v. amrinone to glucagon therapy did not increase significantly, HR, CO, stroke volume, or dP/dt max compared with glucagon alone. Total systemic peripheral resistance was reduced significantly during 31 minutes of observation after the administration of combined therapy compared with the control; glucagon alone also reduced systemic peripheral resistance at 1 and 6 minutes. At all time periods except 1 minute of observation there was a significant reduction in MAP when comparing combined therapy with that of glucagon therapy alone. In this model, the addition of amrinone to glucagon therapy seems to have a detrimental effect on the ability of glucagon to increase MAP resulting from propranolol toxicity.

Amrinone↗
PubMed1992

Isolated anterolateral proximal fibular head dislocation.

A 28-year-old woman fell and sustained an isolated anterolateral dislocation of the proximal fibula. This injury generally presents with a characteristic history and associated physical examination and radiographic findings, but the subtle nature of the salient findings contributes to a high degree of misdiagnosis. Emergency physicians should be familiar with this injury because early reduction reduces long-term morbidity.

Adult↗
PubMed1992

A comparison of amrinone and glucagon therapy for cardiovascular depression associated with propranolol toxicity in a canine model.

This study's objective is to evaluate the ability of glucagon and amrinone to reverse propranolol induced cardiovascular depression in a canine model, compared to a control of normal saline. The study design included 18 animals which received intravenous propranolol (10 mg/kg) resulting in significant depression in heart rate, cardiac output, mean arterial pressure, maximal ventricular dP/dt and stroke volume. Each canine was randomly assigned to one of three treatment groups; controls (normal saline only), glucagon (20 micrograms/kg bolus) and amrinone (4 mg/kg bolus). Cardiovascular parameters were monitored at 1, 6, 11, 21 and 31 min after treatment was rendered. Multiple comparison procedures at each time period controlled the overall alpha-level at .05. Compared to control animals, both amrinone and glucagon were effective in reversing propranolol-induced depression of dP/dtmax at 6 and 11 min for glucagon and 11 min for amrinone and cardiac output at 1, 6 and 11 min for glucagon and 1 min for amrinone. Amrinone and glucagon significantly increased stroke volume over control values at 1 min and tended to do so at the remaining time periods. The two days caused a similar degree of arteriolar vasodilation which was significantly greater than that seen in control animals at 1 and 6 min. Beta blocker induced bradycardia did not respond significantly to amrinone while glucagon induced a tachycardia which is unique to canines. It is concluded that in this canine model, amrinone appears to be an effective therapeutic alternative to glucagon for reversing depressed dP/dtmax, cardiac output and stoke volume induced by propranolol toxicity. Unlike glucagon, amrinone appears to lack positive chronotropic activity which may limit its clinical utility in the treatment of beta blocker overdose.

Amrinone↗
PubMed1982

Mechanical transmission of anaplasmosis by tabanids (Diptera: Tabanidae).

The role of tabanids in the mechanical transmission of anaplasmosis was further clarified by determining the number of horse fly bites needed to transmit the disease and the length of time that horse flies remain mechanically infective. Transmission of anaplasmosis from acutely infected calves to susceptible splenectomized calves was accomplished with as few as 10 horse fly bites. These flies were shown to remain mechanically infective for at least 2 hours after they had obtained a partial blood meal from an acutely infected calf. These data emphasize the efficiency of horse flies in the mechanical transmission of anaplasmosis and indicate that relatively short-distance barriers may not be adequate to prevent transmission between infected and noninfected herds.

Anaplasmosis↗