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Acute ischemic stroke is the third leading cause of death in the United States and the leading cause of adult disability. The direct and indirect costs of stroke care exceed $51 billion annually. In 1996, the US Food and Drug Administration approved the first treatment for acute ischemic stroke, intravenous tissue plasminogen activator. Later that year, the National Institute of Neurologic Disorders and Stroke (a branch of the National Institutes of Health) convened a consensus conference on the Rapid Identification and Treatment of Acute Ischemic Stroke, setting goals for stroke care in the United States. Since then, it has become imperative that emergency physicians understand the pathophysiology of stroke, the basis and rationale for treatment, and the therapeutic approaches. This article reviews the state of the art of acute stroke treatment, its foundation, as well as its future.

The long-term goals of developing research within the specialty of emergency medicine include the following: (1) to continue to improve the quality and quantity of emergency patient care; (2) to maximize the research potential of emergency health care professionals to develop new emergency research talent and enthusiasm; and (3) to establish the academic research credentials of the specialty of emergency medicine to become competitive for federal research funding, and further improve emergency patient care. This article addresses the process by which the infrastructure for emergency medicine research can be developed at academic medical centers and provides recommendations. The roles of the academic chair, research director, senior researcher, and departmental faculty are discussed.

Cervical epidural hematoma is an uncommon cause of neck pain. It may occur spontaneously or after trauma and has also become associated with many underlying conditions. Most patients present with paraparesis or tetraparesis. We describe the case of a healthy 60-year-old woman in whom a spontaneous cervical epidural hematoma developed while she was swimming. She presented with transient hemiparesis and recovered without surgery. This case is unusual with respect to the patient's neurologic presentation and her spontaneous recovery without neurologic sequelae.

Study Objective: To characterize the role of emergency medicine residency programs in determining emergency medicine career choice among medical students., Design: Observational, cross-sectional, descriptive study. Information on student career choice was obtained through a targeted query of the National Resident Matching Program data base, simultaneously stratified by specialty and school, and adjusted for class size., Participants: All accredited emergency medicine residency programs and four-year allopathic medical schools., Results: Fifty-two schools (42%) had a closely affiliated emergency medicine residency program, ie, one based primarily at the institution's main teaching hospital(s). This configuration was associated with a 70% increase in the median proportion of students choosing emergency medicine as a career when compared to the 73 schools with no closely affiliated emergency medicine residency (5.1% vs 3.0%, P < .0001). When institutions were stratified by overall commitment to emergency medicine, the median proportion of students choosing emergency medicine as a career was 2.9% for institutions with a minimal commitment to emergency medicine (neither an academic department of emergency medicine nor a closely affiliated emergency medicine residency), 4.1% for institutions with a moderate commitment to emergency medicine (either a department of emergency medicine or an emergency medicine residency, but not both), and 5.7% for institutions with a substantial commitment to emergency medicine (a department of emergency medicine and an emergency medicine residency) (P < .0001). When institutional commitment to emergency medicine was examined in a simple multivariate model, only the presence of an emergency medicine residency was associated independently with student career choice (P < .001)., Conclusion: An emergency medicine residency program that is closely affiliated with a medical school is strongly and independently associated with a quantitatively and statistically significant increase in the proportion of students from that school who choose a career in emergency medicine. These data support the proposition that, if emergency medicine is to meet national manpower shortage needs by attracting students to the specialty, it must establish residency programs within the primary teaching hospital(s) of medical schools. Such a configuration does not currently exist in the majority of schools.

Study Objective: To evaluate the safety of high-dose IV narcotics in patients requiring analgesia for painful emergency department procedures., Design: Prospective multicenter clinical trial., Setting: Five adult urban EDs., Methods and Measurements: All patients received IV meperidine (1.5 to 3.0 mg/kg) titrated to analgesia followed by a painful procedure. Vital signs and alertness scale were recorded at regular intervals, and patients were observed for four hours. Adverse events were monitored and documented. Comparisons between baseline and postanalgesia intervals were made with a repeated measures ANOVA (Dunnett's test)., Results: Although statistically significant changes in vital signs and alertness scale occurred, they were not clinically significant. Opiate reversal with naloxone was not needed in any patient, and no significant respiratory or circulatory compromise occurred., Conclusion: This study of 72 patients demonstrates that high-dose narcotic analgesia is appropriate, well tolerated, and safe when used in selected patients before painful procedures in the ED. Narcotic antagonists and resuscitation equipment nonetheless should be available to maximize safety.

Study Objective: To determine whether blood pressure declines spontaneously during the first minutes and hours of focal cerebral ischemia., Design: Multiple blood pressure measurements as part of an urgent stroke therapy trial (treatment within 90 minutes of stroke onset)., Setting: Thirteen hospitals in three metropolitan communities., Participants: Sixty-nine patients (mean age, 65 +/- 9 years) with acute ischemic stroke who were participants in a phase I urgent stroke therapy trial of recombinant tissue plasminogen activator., Main Outcome Measure: Blood pressures recorded at the scene of stroke by life-squad personnel, in the emergency department, and in the ICU., Results: The mean time from stroke onset to the time of first blood pressure measurement was 19 +/- 13 minutes. Twenty-four of the 69 patients in the urgent stroke therapy trial had an initial systolic blood pressure of at least 160 mm Hg. Of these, 23 had a significant decline in systolic and diastolic blood pressure during the first 90 minutes after the onset of stroke (mean change in systolic pressure, -29 +/- 22 mm Hg, P < .001; mean change in diastolic pressure, -10 +/- 14 mm Hg, P < .01). No patients received antihypertensive therapy during the time in which the decline in blood pressure was noted., Conclusion: Mildly or moderately elevated blood pressure frequently declines spontaneously during the first minutes and hours of focal cerebral ischemia and generally does not require urgent pharmacologic treatment.

Ancrod has been used in Europe for over 15 years for peripheral vascular disease, deep vein thrombosis, and central retinal venous thrombosis, and in patients at risk for thromboembolism. In a double-blind, randomized, placebo-controlled study at University Hospitals in Cincinnati, 20 acute cerebral infarction patients received a series of IV infusions of ancrod (ten) or placebo (ten) for seven days. Early fibrinolysis with a small decrease in fibrinogen was observed, and d-dimers were elevated at four hours, indicating early clot lysis. At three months, patients with moderate to severe strokes (less than 40 on the Scandinavian Stroke Scale) in the ancrod group showed average improvement by a factor of 3 over the placebo group. No bleeding, abnormal laboratory results, or deaths occurred, but ancrod was discontinued in one patient who had seizures. As a result of this study, a double-blind multicenter international clinical trial to further assess the safety and effectiveness of ancrod is being planned.

Transcutaneous cardiac pacing holds promise as the initial cardiac pacing technique for emergency patients. Determination of the extent of myocardial injury associated with the use of commercial transcutaneous pacemaker devices has been limited. This study was undertaken to document electrocardiographic, enzymatic, and histologic changes following transcutaneous pacing. Ten mongrel dogs were paced with a transcutaneous cardiac pacemaker for 30 minutes. Electrical pulses of 100 mA lasting 20 ms each were delivered at a rate of 80/min via cutaneous electrodes on the anterior and posterior thorax. Myocardial damage was assessed by serial electrocardiograms (ECGs), serial creatine kinase (CK) determinations with myocardial band (MB) fractionation, and gross and microscopic pathologic examination. Double blind reading of the ECGs showed no significant changes after pacing. CK levels peaked an average of 78 units over baseline levels at 4 hours; however, there was no rise in the CK MB fraction. Pathologic examination revealed micro-infarcts adjacent to intramural vessels in 5 animals, but no clinically significant myocardial injury in the 10 dogs. The absence of enzymatic, cardiographic, and clinically significant pathologic findings was statistically significant (P less than .05). Transcutaneous pacing at low currents and for short periods appears to be a safe technique. This pacing technique deserves further evaluation, and may hold promise as a clinical tool during resuscitation.

The treatment of cardiovascular collapse and anaphylactic shock is largely empiric. A simple animal model was developed to evaluate the hemodynamic alterations in anaphylaxis. Eight adult New Zealand white rabbits of both sexes were studied. All animals weighed 3.8 kg to 5.3 kg. Sensitization was accomplished with a 2-mL subcutaneous dose of horse serum followed in two days with a 2-mL intravenous (IV) dose. At least 14 days elapsed after the IV dose before a 1-mL challenge dose of horse serum was given. On the day of the challenge dose, a femoral arterial catheter, arterial temperature probe, and right atrial catheter were placed under methoxyflurane anesthesia. The temperature probe was positioned in the aortic arch. The methoxyflurane was discontinued and the only sedation given during the shock phase was IV diazepam (0.1 mg/kg to 0.5 mg/kg). At least 30 minutes after methoxyflurane was discontinued, the challenge dose of horse serum was given through the right atrial catheter. Before and during the shock phase cardiac rhythm, arterial pressure, and intravascular temperature were monitored continuously. Cardiac outputs (CO) were performed by a thermodilution technique using 0.8 mL room temperature saline injectate through the right atrial catheter. Temperature deflection of the aortic probe was recorded and cardiac output was calculated. After giving the challenge dose, CO was measured at three, five, ten, 15, 25, 35, 45, and 60 minutes. All eight animals showed a significant (P less than .0005) fall in CO, cardiac index, and blood pressure within three minutes. The fall in cardiac index was 50% or more in all animals. Two animals died as a result of shock.(ABSTRACT TRUNCATED AT 250 WORDS)

A pilot study was performed to evaluate the endotracheal administration of diazepam. Five mongrel dogs were anesthetized and orotracheally intubated. Diazepam in a dose of 0.5 mg/kg was delivered through a red rubber catheter placed through the endotracheal tube. Diazepam levels were then measured at 0, 30, and 60 seconds, and at 2, 5, 15, 30, and 60 minutes. Arterial blood gas determinations were performed at 0, 10, 30, 60, and 90 minutes. In all dogs peak serum levels averaged 1,500 ng/ml +/- 541 ng/ml, which is well above therapeutic anticonvulsant levels (150 ng/ml to 600 ng/ml). Arterial pH an PCO2 did not change dramatically from control values during the period of study. Arterial PO2 showed a transient drop of approximately 10 to 30 mm Hg within the first 60 minutes, but returned nearer the control values by the end of 90 minutes. the endotracheal administration of diazepam has been shown to be effective in achieving rapid therapeutic serum levels of the drug. Further study is needed to determine any deleterious effects on the lungs before this method of administration can be recommended for use in humans.

Cerebral ischemic insult is one of the most clinically significant conditions leading to irreversible brain cell damage and death. Animal studies have suggested that lowered intracellular pH due to the severe brain lactic acidosis following ischemia interferes with normal cell structure and function and leads to brain cell necrosis. Therefore, efforts directed to decreasing brain lactate may be beneficial in preventing brain cell damage and death. The goal of our study was to evaluate the effectiveness of postinsult treatment with dichloroacetate (DCA) in controlling increases in brain lactate following partial global ischemia (PGI) in rats. PGI was induced by bilateral carotid artery occlusion and induced hypotension. Animals that received DCA immediately after a 30-minute ischemic insult (n = 5) or 15 minutes after the end of an ischemic insult (n = 5) had cortical lactate levels that were significantly lower (P less than .005) than lactate levels in untreated insulted animals and that were not significantly different than those previously obtained with preinsult DCA treatment in rats subjected to 30 minutes of PGI. Treatment of rats with DCA following PGI may be effective in reducing cortical lactate levels and hence may limit irreversible damage to brain cells following cerebral ischemia.

During hemorrhagic shock, decreased perfusion and poor tissue oxygenation lead to increased lactate production. Previous animal studies have suggested that sodium dichloroacetate (DCA), an agent that decreases lactate production, can improve hemodynamics and survival when administered after severe hemorrhage. We used an unanesthetized porcine hemorrhagic shock model to assess the effect of DCA on survival time when administered during fatal hemorrhage. Immature female swine weighing 14 to 20 kg were splenectomized and instrumented with chronic indwelling aortic and right atrial catheters one week prior to hemorrhage. On the day of the experiment, the unanesthetized animals' aortic catheter was connected to a roller pump and blood was removed at a rate of 1.0 mL/kg/min until death occurred. Experimental animals (n = 8) received sodium dichloroacetate (25 mg/mL distilled water) 100 mg/kg IV bolus beginning 15 minutes after the start of hemorrhage followed by a 3 mg/kg/min constant IV infusion. Control animals (n = 8) received an equal volume of normal saline. Arterial pressure, heart rate, blood gases, serum lactate, and serum glucose were measured at baseline and every 15 minutes during hemorrhage. There were no significant differences in survival time (controls, 63 +/- 2.8 min; DCA-treated, 60 +/- 3.7 min), lactate levels, or blood pressures between the two groups. These results suggest that DCA does not decrease serum lactate or improve survival time when administered during ongoing severe hemorrhagic shock. Further study should be directed at the effects of DCA as an adjunctive treatment after hemorrhage has been controlled and tissue perfusion restored.

Recent studies of thoracic pressure changes during external cardiopulmonary resuscitation (CPR) suggest that there may be a significant difference in the rate of delivery of intravenous drugs when they are administered through the extrathoracic inferior vena cava (IVC) rather than the intrathoracic superior vena cava (SVC). Comparison of delivery of a radionuclide given using superior and inferior vena caval access sites was made during normal blood flow and during CPR. Mean times from injection to peak emission count in each ventricle were determined. There were no significant differences between mean peak times for SVC or IVC routes during normal flow or CPR. When peak times were corrected for variations in cardiac output, there were no significant differences between IVC and SVC peak times during normal flow. During CPR, however, mean left ventricular peak time, when corrected for cardiac output, was significantly shorter (P less than .05) when the SVC route was used. The mean time for the counts to reach half the ventricular peak was statistically shorter (P less than .05) in both ventricles with the SVC route during the low flow of CPR. This suggests that during CPR, increased drug dispersion may occur when drugs are infused by the IVC route and thus may modify the anticipated effect of the drug bolus. These results suggest that during CPR, both the cardiac output and the choice of venous access are important variables for drug delivery.

Sodium dichloroacetate (DCA) has been shown to lower elevated serum lactate levels produced by hypoxia, exercise, and phenformin. We conducted a study to investigate the effect of DCA treatment on lactic acidosis following resuscitation from asphyxial cardiac arrest. Conditioned dogs were anesthetized with pentobarbital (30 mg/kg), endotracheally intubated, and mechanically ventilated to maintain an arterial pCO2 of 30 to 40 mm Hg. Asphyxial cardiac arrest was produced by endotracheal tube occlusion for six to eight minutes. After five minutes of cardiac arrest, the endotracheal tube was unclamped and closed-chest CPR was begun. Six animals received DCA 100 mg/kg IV push after one minute of CPR. Control animals (n = 6) received an equal volume of saline. CPR was continued until the return of a spontaneous pulse, when mechanical ventilation was resumed. Arterial and venous blood gases, glucose, and lactate levels were obtained at baseline and 15, 30, 45, 60, 90, and 120 minutes after resuscitation. Mean arterial blood pressure, pulse, and glucose, and venous and arterial blood gases were similar in both groups throughout the study. By 45 minutes after resuscitation, the DCA-treated group showed a significantly faster rate of decline in lactate levels that continued to the final sampling period. By 90 minutes, arterial lactate in DCA animals was not significantly different from baseline (pre-arrest) values. DCA given during cardiac arrest will cause a more rapid normalization of arterial lactate after successful resuscitation. Further studies are needed to evaluate the effects of lowered lactic acid on survival and neurological outcome following cardiac arrest.

The ECG and the determination of serum enzymes creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) may be falsely normal early in acute myocardial infarction. Myoglobin, an oxygen-carrying protein found in cardiac muscle and striated skeletal muscle, presents an attractive alternative to CPK and LDH in the emergency department setting for identification of acute myocardial infarction. Myoglobin levels may be elevated in the serum within one hour after myocardial cell death with peak levels reached within four to six hours. We report a study of 59 patients presenting to a community hospital with chest pain and subsequent hospitalization. Twenty-one had an acute myocardial infarction. Presenting (0 hour) myoglobin determination was positive in 13 of 21 individuals, while CPK-MB was positive in only three. Serum myoglobin elevation at three hours identified all 21 patients with myocardial infarction with the CPK-MB determination positive in 19. Serum myoglobin elevation may permit early identification of myocardial infarction, with subsequent verification using CPK-MB determination, allowing appropriate intensive care admission for careful monitoring of these patients.

Drug administration via peripheral vein, central vein, and intracardiac routes is generally assumed to be equally effective during cardiopulmonary resuscitation (CPR). Experiments were performed in an animal model to evaluate this assumption. Twelve mongrel dogs weighing greater than 20 kg were studied. Arterial blood pressure and electrocardiogram were monitored continuously. Cardiac outputs were evaluated before CPR to determine control. After thoracotomy and fibrillation of the heart, cardiac massage was started and the rate of compression adjusted to give 30% of control cardiac output. A lidocaine bolus of 1.5 mg/kg was given via peripheral vein in four dogs, central vein in four dogs, and intracardiac (left ventricle) in four dogs. Drug levels were sampled through an aortic catheter at the level of the coronary artery ostia every 20 sec for five min, every 30 sec for 10 min, and every 60 sec for 15 min. There was no significant difference in the appearance of effective levels or time of peak levels in the three groups. The peak levels were highest in the central venous group, while peripheral venous and intracardiac peak levels were 63% and 31%, respectively, of the central venous peak. Duration of effective levels was 20 min in the intracardiac group, 14.5 min in the central venous group, and 9.6 min in the peripheral venous group. Further studies are needed to determine whether changes are needed in drug administration during CPR in man.

Although time has been recognized as a critical factor in the treatment of other arterial occlusive disorders, it has been an underemphasized variable in the treatment of acute stroke. Animal models of cerebral arterial occlusion have demonstrated that neurologic recovery is more likely the shorter the duration of occlusion. Complete recovery does not occur if the occlusion persists more than six hours. Prior trials have only rarely begun treatment within six hours of stroke onset. Over the past five years, we have participated in three stroke trials and have tried to identify factors that lead to delays in treatment. Factors that affect the time from stroke onset to arrival at the hospital include recognition of acute stroke by the patient, prehospital care personnel, and physicians. After arrival at the hospital, factors that can significantly delay treatment include the time to obtain computed tomography and the site of treatment (emergency department vs ICU). With proper attention, the time from patient arrival until treatment should be less than one hour. Future efforts should be directed toward reducing the time from stroke onset until arrival at the hospital. Education of the public, high-risk patients, prehospital care providers, and physicians may aid in these efforts.

Many different designs for studies of various aspects of cardiopulmonary resuscitation (CPR) in dogs are described in the literature. No single technique is generally accepted. We present a systematized approach to the study of CPR in the canine model. Cardiac output, arterial blood pressure, and electrocardiogram were recorded for three different methods. The methods studied were closed chest compression, closed chest compression with an automatic gas-powered chest compressor, and open chest manual cardiac massage. Cardiac output for both types of external chest compression were less than 17% of control in all cases. With open chest cardiac massage, systemic arterial blood pressures were in the 50 mm Hg to 100 mm Hg range and cardiac output of up to 70% of control was achieved. Using a metronome to obtain compression rate and the arterial blood pressure to guide the efficacy of compression, consistent levels of cardiac output could be achieved for up to 30 minutes using open chest cardiac massage. Closed chest massage in man results in a cardiac output of 25% to 30% of normal when performed under optimal conditions. A cardiac output of 25% to 30% of control cannot be achieved in large dogs with external chest compression, and hence is not a good model to stimulate CPR in man.

Controversy exists as to whether ethanol intoxication causes exaggerated hypotension or increased mortality during hemorrhagic shock. Previous studies have used anesthetized animals. This limits data interpretation as anesthetic agents, particularly pentobarbital, have well-documented effects on hemodynamics and the response to hemorrhage. We studied the effects of moderate ethanol intoxication on blood pressure and survival time during fatal hemorrhagic shock in unanesthetized swine. Immature female swine weighing 15 to 20 kg were splenectomized and instrumented with chronic indwelling aortic catheters, right atrial catheters, and gastrostomy tubes. Four to seven days later the unanesthetized animals underwent hemorrhagic shock. Thirty minutes prior to the start of hemorrhage, the experimental group (n = 8) received 3 mL/kg of 100% ethanol mixed as a 1:3 solution with water through a gastrostomy tube. The control group (n = 8) received an equal amount of water. The distal aortic catheter was connected to a roller pump and blood was removed at a rate of 1 mL/kg/min until the animal died. Arterial pressure, heart rate, lactate ethanol and glucose levels, hematocrit, and arterial blood gases were measured in both groups at baseline and every 15 minutes thereafter. A mean ethanol level of 1,500 to 1,700 micrograms/mL was produced in the experimental group from baseline through 60 minutes. Data were analyzed using Student's two-tailed t test, and analysis of variance for repeated measures. There was no significant difference in survival time between the control (63.1 +/- 2.8 min) and ethanol (59.9 +/- 5.9 min) groups. Systolic blood pressure was significantly lower in the ethanol group after 15 minutes of hemorrhage (81 +/- 22 to 59 +/- 14 mm Hg, P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

We examined the effect of an inflated pneumatic antishock garment (PASG) on simulated drug delivery through a distally placed venous catheter, during both normal flow and cardiopulmonary resuscitation (CPR). A PASG device was applied to anesthetized mongrel dogs and was inflated to 60 mm Hg. A small bolus of radionuclide was injected through an intravenous catheter placed distal to the PASG. Emission counts were made over both ventricles during conditions of normal flow and then during CPR following cardiac arrest. Mean times from injection to peak counts were determined. A control group of animals with central venous catheters but no PASG was studied similarly. There were no clinically appreciable differences between groups during normal flow. During CPR the PASG animals showed a mean delay of 90 seconds to the left ventricle peak. This difference was not statistically significant. We conclude that, in this canine model, acceptable delivery of drugs can be obtained by venous infusion into a limb with a PASG inflated.

Stroke therapy trials have historically allowed for late patient entry (ie, within 24 to 48 hours from stroke onset) despite evidence suggesting the importance of early intervention. Experimental studies of cerebral infarction suggest treatment may be most effective when begun within three hours and may be only marginally effective when begun after 12 hours. Lysis of an acute intra-arterial thrombus in the setting of thrombolytic therapy is also time dependent. We describe an ongoing dose-escalation study of tissue plasminogen activator (tPA) as ultra-early therapy for cerebral infarction. The protocol requires that hemorrhage be ruled out by computed tomography scan of the brain prior to tPA infusion, and the infusion must begin within 90 minutes of symptom onset. The two primary goals of the study are to assess safety and potential efficacy. Preliminary results from the study and the future of ultra-early stroke intervention are discussed.