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Biomedical subjects

R W Derlet

Publications and source records attributed to R W Derlet.

At least 37 records · Page 2Linked to original sources
PubMed1996

Fatal intracranial bleeding associated with prehospital use of epinephrine.

We present a case of paramedic misjudgment in the execution of a protocol for the treatment of allergic reaction in a case of pulmonary edema with wheezing. The sudden onset of respiratory distress, rash, and a history of a new medicine led the two paramedics on the scene to administer subcutaneous epinephrine. Subsequently, acute cardiac arrest and fatal subarachnoid hemorrhage occurred. Epinephrine has a proven role in cardiac arrest in prehospital care; however, use by paramedics in patients with suspected allergic reaction and severe hypertension should be viewed with caution.

Adult↗
PubMed1996

Minor head trauma: Is computed tomography always necessary?

STUDY OBJECTIVE: To determine the clinical value of routine computed tomography (CT) of the head in patients with normal mental status after minor head trauma. METHODS: We carried out a prospective study of a consecutive series of patients of all ages who presented to our urban university Level I trauma center emergency department with a Glasgow Coma Scale score of 15 and underwent CT of the head after loss of consciousness (LOC) or amnesia to event. A data form was filled out for each patient before CT. Patients with abnormal CT results were followed to discharge. We analyzed data with the chi 2 and student t tests. RESULTS: Of 1,382 patients, traumatic intracranial abnormality was identified on CT of the head in 84 (6.1%). Three patients in this group (.2%) required surgery. The subgroup of patients with history of LOC/amnesia but no symptoms or signs of a depressed skull fracture had a rate of abnormal CT findings of only 3% (24 of 789), and no patient in this group required medical or surgical intervention. Nausea and vomiting and signs of head trauma were significantly more common in the group with abnormal CT findings. CONCLUSION: Routine CT of the head in patients with history of LOC/amnesia but no symptoms or signs of depressed skull fracture has minimal clinical value and is not warranted. Patients with symptoms of head injury or apparent depressed skull fracture should undergo head CT because a small number will require surgery.

Adult↗
PubMed1996

The impact of health maintenance organization care authorization policy on an emergency department before California's new managed care law.

OBJECTIVE: To examine the effect on patient care of HMO-mandated calls for authorization prior to ED evaluation. The study examined this phenomenon prior to implementation of a California law that discourages such calls. METHODS: Concurrent data were collected for patients who presented to the ED and who had authorization calls made to their HMOs prior to their ED evaluations during the period September through December 1994. Data collected included: 1) the number of authorization calls made, 2) the frequency that ED care was deemed unnecessary by the HMO, 3) the outcomes of patients denied authorization, and 4) the time and personnel involved in completing calls. Follow-up phone calls were made to patients who left the ED after the HMO denied authorization for payment. RESULTS: The total ED census was 19,935 patient visits for the four-month period. Authorization calls were made for 4,642 (23%) of the ED visits. There were 545 patients (12%) in this group who had authorization denied and only 29 (5%) chose to remain in the ED for continued evaluation. The total time required to complete a call ranged from 20 minutes to 2.6 hours. Authorization calls and denials caused the following problems: 1) patients for whom calls were made were subject to delays in ED care; 2) at least seven patients referred to HMO clinics were referred back to the ED because the patient was too sick to receive clinic care; 3) patients were inconsistently asked to sign an against-medical-advice form when they chose to leave with unstable conditions; and 4) high-risk patients denied authorization included patients with final diagnoses of ectopic pregnancy, acute myocardial infarction, pulmonary embolus, respiratory failure, and sepsis. CONCLUSIONS: Calls for payment authorization prior to ED patient evaluation delay patient care and place some patients' health and safety in jeopardy.

California↗
PubMed1996

Conflicts between managed care organizations and emergency departments in California.

To control costs, managed care organizations have begun to restrict the use of hospital emergency departments by their enrollees. They are doing this by educating enrollees, providing better access to 24-hour urgent care, denying preauthorizations for care for some patients who do present to emergency departments, and retrospectively denying payment for certain patients who use emergency services. Changing traditional use of emergency departments has resulted in conflicts between managed care organizations and these departments. Because federal law mandates access to emergency care for all persons, disagreements occur over the precise definition of an emergency medical condition. In addition, conflicts occur over the scope and payment for the medical screening examination required by federal law of persons presenting to an emergency department. Finally, issues arise related to the safety of patients who present to emergency departments and request care but are denied care because the managed care organization does not authorize the visit. Recent legislation in California has attempted to reconcile differences between managed care practices and federal and state laws; however, areas of continued conflict need to be resolved to prevent possible adverse consequences for patients actually needing emergency care.

Emergency Service, Hospital↗
PubMed1995

Prospective identification and triage of nonemergency patients out of an emergency department: a 5-year study.

STUDY OBJECTIVE: To determine whether nonemergency patients can be prospectively identified by triage nurses and safely triaged out of the emergency department without treatment. METHODS: All adult patients (16 years or older) who presented to a university ED were provided an evaluation by a triage nurse. For a patient's case to be defined as nonemergency, four criteria were required: vital signs within a specific range, presence of 1 of 50 potentially nonemergent chief complaints, absence of key indicators found on screening examination, and absence of chest pain, abdominal pain, any severe pain, and inability to walk. Between July 1988 and July 1993, patients who satisfied these criteria were defined as nonemergency, refused care in the ED, and triaged out of the ED. Patients were referred to off-site clinics. The clinics had agreed to see patients in advance of the study, and the referral lists were frequently updated. Outcome data were obtained by telephone surveys to both triaged individuals and other health care providers. RESULTS: In this 5-year study, 176,074 adults presented to the ambulatory triage area in the ED, and 31,165 (18%) were defined as nonemergency, were not treated, and were referred elsewhere. Letters and telephone calls to all referral clinics, eight local EDs, and the coroner's office identified no instances of gross mistriage and only a small number of insignificant adverse outcomes. Telephone follow-up to individuals triaged away was successful in 34% of calls and showed that 39% of persons received care elsewhere on the same day, 35% received care within 3 days, and 26% decided not to seek medical care. A group of 1.0% sought care at other hospital EDs for minor complaints. CONCLUSION: A subset of patients with nonemergency problems can be prospectively identified and triaged out of the ED without significant adverse outcomes provided there is community support for follow-up care.

Adult↗
PubMed1995

Cardiotoxic drugs.

This article describes the cardiovascular effects and treatment of patients who have used cardiotoxic drugs. The discussion includes cocaine, methamphetamine, cyclic antidepressants, calcium channel blockers, beta-blockers, and digoxin. The authors review treatment controversies and emphasize the acute aspects of toxicity commonly seen in the emergency department.

Drug Overdose↗
PubMed1994

Flumazenil induces seizures and death in mixed cocaine-diazepam intoxications.

STUDY HYPOTHESIS: Administration of the benzodiazepine antagonist flumazenil may unmask seizures in mixed cocaine-benzodiazepine intoxication. DESIGN: Male Sprague-Dawley rats received 100 mg/kg cocaine IP alone, 5 mg/kg diazepam alone, or a combination of diazepam and cocaine. Three minutes later, groups were challenged with vehicle or flumazenil 5 or 10 mg/kg IP. Animal behavior, seizures (time to and incidence), death (time to and incidence), and cortical EEG tracings were recorded. INTERVENTIONS: Administration of flumazenil to animals after they had received a combination dose of cocaine and diazepam. RESULTS: In group 1, animals received cocaine followed by vehicle. This resulted in 100% developing seizures and death. Group 2 received diazepam alone followed by vehicle. Animals became somnolent and none died. Group 3 received diazepam followed by 5 mg/kg flumazenil. Animals became somnolent after diazepam and then active after flumazenil administration. In group 4, a combination of cocaine and diazepam was administered simultaneously. This resulted in no overt or EEG-detectable seizures and a 50% incidence of death. Group 5 received a similar combination of cocaine and diazepam, followed later by 5 mg/kg flumazenil. This resulted in an increased incidence of seizures, 90% (P < .01), and death, 100% (P < or = .01), compared with group 4. Group 6 received cocaine and diazepam followed by 10 mg/kg flumazenil. This also resulted in an increased incidence of seizures, 90% (P < or = .01), and death, 90% (P < or = .05), compared with group 4. CONCLUSION: Flumazenil can unmask seizures and increase the incidence of death in a model of combined cocaine-diazepam intoxications.

Animals↗
PubMed1993

Acute cocaine toxicity: the effect of agents in non-seizure-induced death.

Death from cocaine intoxication results from one or more of the multiple mechanisms including seizures, cardiovascular collapse, or apnea. In the free-moving rat model, continuous seizures are a major cause of death. To study other mechanisms of death unrelated to seizures in this model, we suppressed lethal seizures with diazepam (DZP) and investigated the effect of several pharmacological agents. Rats were pretreated with vehicle alone, diazepam 5 mg/kg alone, or a combination of DZP plus either nifedipine (NIFD) 2 mg/kg, propranolol (PROP) 10 mg/kg, or prazosin (PRAZ) 5 mg/kg. Five minutes after pretreatment, all animals received cocaine 100 mg/kg. Each test group consisted of 15 animals and all agents were given IP. Two animals in each group had cortical electrodes implanted. Animals that received vehicle followed by cocaine had 100% incidence of seizures and death. Those rats that received DZP alone followed by cocaine had no seizures and 53% death. Rats that received DZP plus NIFD or DZP plus PROP had suppression of seizures but no significant change in the incidence of death. The group that received DZP and PRAZ followed by cocaine had no seizures and 13% incidence of death (p < 0.001). Electroencephalogram recordings showed cortical electrical spike activity or spike-and-wave afterdischarges in all animals clinically observed to have seizures. In the absence of clinical seizure activity, no significant cortical spike activity was noted. It is concluded that animals protected from seizures with diazepam can still have nonseizure deaths after high-dose cocaine. The incidence of death in these animals is not reduced with nifedipine or propranolol pretreatment but is reduced with prazosin pretreatment.

Animals↗
PubMed1993

A clinical trial of escalating doses of flumazenil for reversal of suspected benzodiazepine overdose in the emergency department.

STUDY OBJECTIVE: To determine if flumazenil, when used in doses higher than those currently recommended, could reverse the effects of a benzodiazepine (BDZ) overdose in patients who might not otherwise respond and whether the higher dose was associated with increased adverse effects. DESIGN: Multicenter, randomized, double-blind, placebo-controlled, balanced, with parallel groups. Open-label flumazenil administration was available if a patient failed to respond or became resedated. SETTING: Sixteen emergency departments in the United States. POPULATION: Patients presenting to the ED with clinically significant signs and symptoms of a known or suspected BDZ overdose. INTERVENTIONS: Patients were randomized to receive 10 mL/min of placebo or flumazenil (1 mg/10 mL) each minute for ten minutes. If there was no response, up to 3 mg of open-label flumazenil could be administered. MEASUREMENTS AND MAIN RESULTS: Of 170 patients enrolled, 87 received flumazenil and 83 received placebo. The demographic characteristics of both groups were comparable. Ten minutes after the beginning of study drug infusion, patients were evaluated using the Clinical Global Impression Scale (CGIS), Glasgow Coma Scale (GSC), and Neurobehavioral Assessment Scale (NAS). The mean +/- SD CGIS score at ten minutes for BDZ-positive patients was 1.41 +/- 0.72 for patients who received flumazenil and 3.41 +/- 0.91 for the placebo group (P < .01). There was no difference in the mean CGIS score between the flumazenil (3.25 +/- 1.15) and placebo (3.75 +/- 0.69) groups in BDZ-negative patients. The GCS and NAS were also significantly better in patients who were BDZ-positive and received flumazenil. The mean +/- SD dose of flumazenil administered during the double-blind phase was 71.3 +/- 34.2 mL (7.13 mg) compared with 95.06 +/- 16.03 mL of placebo. Of the 39 patients who had BDZ-positive drug screens and received flumazenil, 29 (74%) responded to 3 mg or less. Six additional patients responded to 4 or 5 mg, and one patient responded to 8 mg. The most common adverse effects in patients who received flumazenil were injection site pain (10.3%), agitation (8%), vomiting (3.4%), dizziness (3.4%), headache (3.4%), tachycardia (3.4%), and crying (3.4%). Three patients developed seizures. Two were associated with significant tricyclic antidepressant overdoses and one with propoxyphene ingestion. Two patients had positive drug screens for BDZ. CONCLUSION: Flumazenil rapidly and effectively reverses the clinical signs and symptoms of a BDZ overdose. Most patients will respond to 3 mg or less, but a small number may require a higher dose for reversal of clinical symptoms. Patients with concomitant tricyclic antidepressant overdose may be at risk for developing seizures.

Adolescent↗
PubMed1992

Triage of patients out of the emergency department: three-year experience.

Because of severe emergency department (ED) overcrowding, the authors initiated a program of referring certain patients who were assessed as not needing emergency care away from the ED. A selected group of patients who presented to a busy university ED were refused treatment and triaged away following a medical screening examination performed by a nurse. In this 3-year study 136,794 patients presented to the triage area in the ED, of which 21,069 (15%) were refused care and referred elsewhere. Letters and calls to all referral clinics, eight local EDs, and the coroner's office identified no patients who had been grossly mistriaged, and only insignificant adverse outcomes could be identified. Additional follow-up on 3,740 individuals triaged away was performed by telephone. Responses from this survey indicated that 42% of persons received care elsewhere the same day, 37% within 2 days, and 22% decided not to seek medical care. A group of 1.6% sought care at other hospital EDs for minor complaints. The authors concluded that a group of patients can be selectively triaged out of the ED without significant adverse outcomes, which may offer one approach to the problem of ED overcrowding.

Adult↗
PubMed1992

Potentiation of cocaine and d-amphetamine toxicity with caffeine.

The effect of caffeine when combined with cocaine or amphetamine was studied in rats. Animals were pretreated with intraperitoneal vehicle (normal saline [NS]) or caffeine 100 mg/kg, then challenged with intraperitoneal cocaine (0, 35, 50, 70, or 90 mg/kg) or intraperitoneal d-amphetamine (0, 15, 25, 35, or 42 mg/kg). Animal behavior, time to, and incidences of seizures and death were recorded. This dose of caffeine alone did not cause seizures or death. Caffeine pretreatment significantly increased the incidence of overt seizures induced by either cocaine or amphetamine. Caffeine increased the incidence of cocaine-induced death from 10% to 90% at the 70 mg/kg cocaine dose (P less than .01). Caffeine increased amphetamine-induced death from 0% to 80% at 15 mg/kg (P less than or equal to .01), 10% to 70% at 25 mg/kg (P less than or equal to .01), and 30% to 80% at 35 mg/kg (P less than or equal to .01). To investigate mechanisms, additional animals were pretreated with the adenosine agonist, 2-chloroadenosine (2.5 and 10 mg/kg), before being challenged with NS, 90 mg/kg cocaine, or 42 mg/kg amphetamine. Pretreatment with 2-chloroadenosine had no affect in reducing cocaine or amphetamine toxicity. Combination pretreatment with caffeine and 2-chloroadenosine potentiated cocaine toxicity. The phosphodiesterase inhibitor, pentoxifylline, did not potentiate cocaine toxicity. The authors conclude that caffeine potentiates the acute toxicity of both cocaine and amphetamine, and that the failure of 2-chloroadenosine to alter this suggests that the toxicity of the stimulants cocaine and amphetamine may be modulated by nonspecific rather than specific adenosine- or phosphodiesterase-induced mechanisms.

2-Chloroadenosine↗
PubMed1992

Cocaine-induced respiratory depression and seizures are synergistic mechanisms of cocaine-induced death in rats.

STUDY OBJECTIVE: To determine if respiratory depression is an important mechanism of cocaine-induced death in conscious rats. DESIGN: Male Sprague-Dawley rats weighing between 200 and 300 g and fitted with cortical electrodes were pretreated intraperitoneally with either saline (vehicle), MK-801, or valproic acid for 30 minutes before challenge with 70 mg/kg IP cocaine followed by spontaneous breathing or mechanical ventilation after acute tracheostomy. Behavior, seizures, death, EEGs, and ECGs were observed and measured. MEASUREMENTS AND MAIN RESULTS: In group 1, animals received saline followed by cocaine. The incidence rates of seizures and death were 92% and 83%, respectively. Group 2 received saline followed by cocaine and then were ventilated mechanically through an acute tracheostomy after respiratory arrest (late mechanical ventilation). This group experienced seizures in 100% and death in 67% of animals. Group 3 also received saline followed by cocaine but were ventilated mechanically immediately after the first seizures (early mechanical ventilation). They had experienced seizures in 100% and death in 30%, the latter being significantly (P less than .025) reduced compared with group 1. In group 4, an anticonvulsant (1 mg/kg MK-801) was given before cocaine challenge, resulting in seizures in 10% (P less than .002 compared with group 1) and death in 90%. Group 5 received MK-801 followed by cocaine and then were ventilated mechanically after respiratory arrest (late mechanical ventilation). They experienced seizures in 20% (P less than .002 compared with group 1), and no animals in this group died (P less than .002 compared with group 1 or 4). Group 6 received an anticonvulsant (400 mg/kg valproic acid), followed by cocaine. This resulted in seizures in 20% (P less than .002 compared with group 1) and death in 90%. Group 7 received valproic acid followed by cocaine and then were ventilated mechanically (late mechanical ventilation). They experienced seizures in 30% (P less than .002 compared with group 1), and all animals survived (P less than .002 compared with group 1 or 6). CONCLUSION: Early mechanical ventilation reduces cocaine toxicity. Control of seizure activity with specific anticonvulsants allows delayed mechanical ventilation to protect against cocaine toxicity. This suggests that respiratory depression in conjunction with seizure activity plays a major role in the mechanisms of cocaine-induced death in this model.

Animals↗
PubMed1992

The effect of morphine and naloxone on cocaine toxicity.

The effect of morphine and naloxone on acute cocaine toxicity was studied. Male Sprague-Dawley rats were pretreated intraperitoneally (ip) with saline, morphine sulfate 25 mg/kg, or naloxone 1.0 mg/kg 15 minutes prior to challenge by cocaine. After pretreatment, each group was challenged with one of three doses of cocaine (35, 50, or 75 mg/kg ip). Each of the nine drug combinations was tested on at least 10 animals. Animals were observed for behavior, seizures, and death. The animals pretreated with saline and challenged with cocaine (35, 50, or 75 mg/kg) had seizure incidences of 0%, 40%, and 100%, respectively, after increasing doses. Pretreatment with morphine resulted in cocaine-induced seizures of 20%, 80% and 100%, respectively (p less than or equal to 0.05 with cocaine 35 and 50 mg/kg). Time to seizures in these groups did not differ significantly compared to the saline groups. Pretreatment with naloxone resulted in cocaine-induced seizures of 0%, 50%, and 60% (p less than or equal to 0.05 at the 75 mg/kg dose). The incidence of death was significantly increased by pretreatment with morphine in animals that received cocaine 50 or 75 mg/kg. The time to death was not significantly different compared to saline controls. The death rate in naloxone pretreated animals was not significantly different from the saline groups. In additional studies, high-dose naloxone pretreatment (10 mg/kg) also failed to provide protection from acute cocaine toxicity. In conclusion, cocaine toxicity is potentiated by morphine and does not appear to be altered by naloxone.

Animals↗
PubMed1991

Cocaine-induced respiratory depression in urethane-anesthetized rats: a possible mechanism of cocaine-induced death.

Urethane-anesthetized rats were used to study the mechanism of cocaine-induced death. Continuous recording of the changes in five physiological parameters, including respiratory rate (RR), electroencephalogram (EEG), blood pressure (BP), electrocardiogram (ECG), and body temperature (BT), were conducted after intraperitoneal (IP) administration of a single dose of cocaine HCl (70 mg/kg). In the control group (normothermic with core body temperature 37.7 +/- 0.1 degree C and spontaneously breathing), the death rate was 88% (15/17), and the average time to respiratory arrest was 12.99 +/- 1.40 min (mean +/- SEM). The first set of experiments investigated the contribution of hypothermia to cocaine-induced death. The hypothermic group (core body temperature 33.9 +/- 0.3 degrees C and spontaneously breathing) had a death rate of 81.5% (22/27), and an average time to respiratory arrest of 16.70 +/- 1.24 min, which was significantly (p les than 0.05) prolonged. A substantial decrease in respiratory rate was seen in normothermic group, while all the other measured parameters remained relatively stable until respiratory arrest. Sequential arterial blood gas data in this group showed a decrease in PaO2 from 116.0 +/- 5.7 mmHg to 57.7 +/- 4.6 mmHg, an increase in PaCO2 from 27.7 +/- 2.2 mmHg to 42.7 +/- 3.0 mmHg, and a decrease in pH from 7.467 +/- 0.039 to 7.357 +/- 0.003. To confirm that respiratory depression was an important mechanism of cocaine-induced death in this model, ten normothermic rats underwent mechanical ventilation, and all survived cocaine exposure. This study points to the important role of respiratory depression as a cause of cocaine-induced death.

Anesthesia↗