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Biomedical subjects

B J Zink

Publications and source records attributed to B J Zink.

At least 19 recordsLinked to original sources
PubMed2001

Traumatic brain injury outcome: concepts for emergency care.

Injury to the brain is the leading factor in mortality and morbidity from traumatic injury. The devastating personal, social, and financial consequences of traumatic brain injury (TBI) are compounded by the fact that most people with TBI are young and previously healthy. From the emergency physician's standpoint, patients with severe TBI are those with a presenting Glasgow Coma Scale score of less than 9. Over the past 30 years, mortality from severe traumatic brain injury for those patients who survive to the hospital has been reduced by half from nearly 50% to approximately 25%. Because most of the pathologic processes that determine outcome are fully active during the first hours after TBI, the decisions of emergency care providers may be crucial. This review addresses new concepts and information in the pathophysiology of TBI and secondary brain injury and demonstrates how emergency management may be linked to neurologic outcome.

Brain↗
PubMed2001

Effects of ethanol and naltrexone in a model of traumatic brain injury with hemorrhagic shock.

BACKGROUND: Ethanol predisposes to traumatic injury and causes respiratory depression and cardiovascular compromise in models of traumatic brain injury (TBI) and hemorrhagic shock (HS). Endogenous opioids may play a role in ethanol intoxication and TBI. We studied the effects of ethanol and the opiate antagonist agent naltrexone (NTX) in a TBI/HS model. METHODS: Fifty-six pigs (20 kg) were anesthetized with isoflurane, intubated, instrumented, and subjected to fluid percussion TBI with concurrent 30 ml/kg hemorrhage over 30 min. Seven groups were studied: Control, EtOH, NTX, INJ, INJ/EtOH, INJ/NTX, and INJ/EtOH/NTX. Ethanol (2 g/kg IV) was given preinjury, followed by infusion of 0.4 g/kg/hr. NTX 0.3 mg/kg intravenous was given 5 min postinjury. Parameters monitored for 120 min postinjury included minute ventilation (VE), blood pressure (MAP), cerebral perfusion pressure (CPP), cerebral venous lactate (Lac), arterial and cerebral venous blood gases, and brain tissue PtiO2. RESULTS: Ethanol levels at injury were 220 mg/dL. Ethanol-treated animals had depression of hypercapnic ventilatory response, which was reversed by administration of naltrexone. MAP and CPP were significantly lower in injured animals, but were not significantly improved by NTX. Cerebral venous pH was lower and lactate was higher in ethanol-treated animals. CONCLUSION: In this TBI/HS model, NTX reverses ethanol-induced depression of hypercapnic ventilatory response but does not improve MAP, CPP, or metabolic acidosis. This suggests that the respiratory effects of ethanol in TBI, but not the hemodynamic effects, may be mediated by opiate receptor activation.

Animals↗
PubMed2000

Effect of initially limited resuscitation in a combined model of fluid-percussion brain injury and severe uncontrolled hemorrhagic shock.

OBJECT: Studies of isolated uncontrolled hemorrhage have indicated that initial limited resuscitation improves survival. Limited resuscitation has not been studied in combined traumatic brain injury and uncontrolled hemorrhage. In this study the authors evaluated the effects of limited resuscitation on outcome in combined fluid-percussion injury (FPI) and uncontrolled hemorrhage. METHODS: Twenty-four swine weighing 17 to 24 kg each underwent FPI (3 atm) and hemorrhage to a mean arterial pressure (MAP) of 30 mm Hg in the presence of a 4-mm aortic tear. Group I (nine animals) was initially resuscitated to a goal MAP of 60 mm Hg; Group II (nine animals) was resuscitated to a goal MAP of 80 mm Hg; and Group III (control; six animals) was not resuscitated. After 60 minutes, the aortic hemorrhage was controlled and the animals were resuscitated to baseline physiological parameters and observed for 150 minutes. Mortality rates were 11%, 50%, and 100% for Groups I, II, and III, respectively (Fisher's exact test; p = 0.002). The total hemorrhage volume was greater in Group II (69+/-32 ml/kg), as compared with Group I (41+/-18 ml/kg) and Group III (37+/-3 ml/kg) according to analysis of variance (p < 0.05). In surviving animals, cerebral perfusion pressure, cerebral blood flow (CBF), cerebral venous O2 saturation (ScvO2), and cerebral metabolic rate of O2 did not differ among groups. Although CBF was approximately 50% of baseline during the period of limited resuscitation in Group I, ScvO2 remained greater than 60%, and arteriovenous O2 differences remained within normal limits. CONCLUSIONS: In this model of FPI and uncontrolled hemorrhage, early aggressive resuscitation, which is currently recommended, resulted in increased hemorrhage and failure to optimize cerebrovascular parameters. In addition, a 60-minute period of moderate hypotension (MAP = 60 mm Hg) was well tolerated and did not compromise cerebrovascular hemodynamics, as evidenced by physiological parameters that remained within the limits of cerebral autoregulation.

Animals↗
PubMed1999

Effects of ethanol on brain lactate in experimental traumatic brain injury with hemorrhagic shock.

OBJECTIVE: Previous studies of traumatic brain injury (TBI) and hemorrhagic shock (HS) models, have shown cardiorespiratory depression in ethanol-treated animals. This study investigated the effects of ethanol (ET) on brain lactate concentrations and acidosis in a TBI/HS model. METHODS: Anesthetized swine were instrumented and subjected to injury (INJ) consisting of fluid percussion TBI of 3 atm with concurrent 30 ml/kg graded hemorrhage over 30 min. Three groups were studied: Sham, INJ and INJ/ET. ET was given preinjury as a 2-g/kg i.v. bolus over 30 min, and an infusion of 0.4 g kg(-1) h(-1). Cardiorespiratory and cerebral physiologic data were monitored continuously for 150 min postinjury. Cerebral and renal blood flow was measured with colored microspheres. Brains were frozen in situ with liquid nitrogen. Lactate was measured with an enzymatic method. RESULTS: ET levels at injury were 219+/-24 mg/dl. The INJ/ET group had increased mortality, impaired ventilation, and reduced renal blood flow. Brain (cortical) lactate levels were significantly higher and cerebral venous lactate concentrations were increased in the INJ/ET group during the postinjury period. Cerebral venous glucose was significantly higher in the INJ/ET group, and cerebral venous pH was significantly lower. CONCLUSION: In this TBI/HS model, ethanol-induced increases in lactate concentrations in brain tissue and cerebral venous blood are associated with respiratory depression and reduced organ blood flow.

Analysis of Variance↗
PubMed1998

Effects of ethanol in an experimental model of combined traumatic brain injury and hemorrhagic shock.

OBJECTIVES: Given that clinical and laboratory studies suggest that ethanol and hemorrhagic shock (HS) potentiate traumatic brain injury (TBI), the authors studied the effects of ethanol in a model of combined TBI and HS. METHODS: A controlled porcine model of combined TBI and HS was evaluated for the effect of ethanol on survival time, hemodynamic function, and cerebral tissue perfusion. Anesthetized swine (17-24 kg) were instrumented, splenectomized, and subjected to fluid percussion TBI with concurrent 25-mL/kg graded hemorrhage over 30 minutes. Two groups were studied: control (n = 11) and ethanol (n = 11). Ethanol, 3.5 g/kg intragastric, was given 100 minutes prior to TBI/HS. Systemic and cerebral physiologic and metabolic parameters were monitored for 2 hours without resuscitation. Regional cerebral blood flow (rCBF) and renal blood flow were measured with dye-labeled microspheres. Data were analyzed with 2-sample t-test and repeated-measures ANOVA. RESULTS: Ethanol levels at the time of injury were 162 +/- 68 mg/dL. Average TBI was 2.65 +/- 0.35 atm. Survival time was significantly shorter in the ethanol group (60 +/- 27 min vs 94 +/- 28 min, p = 0.011). The ethanol group had significantly lower mean arterial pressure, cerebral perfusion pressure, and cerebral venous O2 saturation in the postinjury period. Cerebral O2 extraction ratios and cerebral venous lactate levels were significantly higher in the ethanol group. A trend toward lower postinjury rCBF in all brain regions was observed in the ethanol group. CONCLUSION: In this TBI/HS model, ethanol administration decreased survival time, impaired the hemodynamic response, and worsened measures of cerebral tissue perfusion.

Analysis of Variance↗
PubMed1998

Patients with alcohol problems in the emergency department, part 1: improving detection. SAEM Substance Abuse Task Force. Society for Academic Emergency Medicine.

Medical and social problems related to alcohol use are frequently seen in the ED. Often, the tempo of emergency medicine practice seems to preclude assessment beyond that required by the acute complaint. However, detection of ED patients with alcohol problems can occur using brief screening tools. This article was developed by members of the SAEM Substance Abuse Task Force, and describes screening tools that have been used successfully to identify at-risk and dependent drinkers. Their brevity, reproducibility, and accuracy vary somewhat, but screening can be realistically performed in the busy ED setting. The early detection of patients with alcohol problems would provide the opportunity for early intervention, and may reduce subsequent morbidity and mortality in this patient population.

Adult↗
PubMed1998

Patients with alcohol problems in the emergency department, part 2: intervention and referral. SAEM Substance Abuse Task Force. Society for Academic Emergency Medicine.

Early intervention and appropriate referral of patients with alcohol problems have the potential to reduce alcohol-related morbidity and mortality. Part 1 of this series introduced screening tools that can be applied in the ED to allow early detection of at-risk drinkers. This article was developed by members of the SAEM Substance Abuse Task Force and describes assessment and intervention techniques once the at-risk or dependent drinkers has been identified. Appropriate aftercare and referral of patients found to have alcohol problems are also discussed.

Alcoholism↗
PubMed1998

Acute ethanol intoxication in a model of traumatic brain injury with hemorrhagic shock: effects on early physiological response.

OBJECT: Traumatic brain injury (TBI) is exacerbated by hypotension and hypoventilation. Because previous studies have shown a potentiating effect of ethanol (EtOH) on TBI and hemorrhagic shock (HS), the authors investigated the effects of EtOH on the early physiological response to TBI with and without HS. METHODS: Anesthetized swine, weighing approximately 20 kg each, underwent fluid-percussion TBI of 3 atm with or without 30 ml/kg hemorrhage for a period of 30 minutes. The mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure (CPP), cardiac output, cerebral venous oxygen saturation, and metabolic parameters were monitored for 3 hours postinjury. Ventilation and the response to hypercapnia were also measured. Regional cerebral blood flow and renal blood flow were measured using dye-labeled microspheres. Five groups were studied: control, TBI, TBI/EtOH, TBI/HS, and TBI/HS/EtOH. The EtOH (3.5 g) was given intragastrically 100 minutes preinjury. The TBI/HS/EtOH group demonstrated a 3-hour mortality rate of 56% and postinjury apnea requiring ventilation in 44% of animals compared with 0% in all other groups. Minute ventilation and the hypercapnic ventilatory response were significantly reduced in the postinjury period in the TBI/HS/EtOH group. The animals in this group had significantly lower CPP and cardiac output in the first 60 minutes postinjury, as well as lower renal and cerebral blood flow. Postinjury cerebral venous lactate levels were higher, and cerebral venous pH was lower in the TBI/HS/EtOH group. CONCLUSIONS: In this model of TBI, acute EtOH intoxication in the presence of HS potentiates the physiological and metabolic alterations that may contribute to secondary brain injury.

Acute Disease↗
PubMed1996

Traumatic brain injury.

Traumatic brain injury (TBI) contributes significantly to the mortality and morbidity rates of traumatized patients. This article presents current concepts in the pathophysiology of TBI, including mechanisms of injury, biomolecular mediators of injury, and the occurrence of secondary injury. Emergency management, monitoring, and imaging of TBI also are reviewed.

Algorithms↗
PubMed1996

Alcohol, central nervous system injury, and time to death in fatal motor vehicle crashes.

OBJECTIVES: Motor vehicle crash (MVC) studies have found that alcohol (ALC) is associated with increased mortality and decreased time to death (TTD). Clinical and experimental data suggest that ALC potentiates central nervous system injury (CNSI). We hypothesize that ALC-intoxicated, MVC fatalities with CNSI are more likely to die in the immediate postinjury period than are sober victims with CNSI. Methods; DESIGN: A retrospective cohort of 401 MVC fatalities from four Michigan counties for the time period 1985 to 1991 was studied. MEASUREMENTS: Medical examiner records were reviewed to determine age, blood alcohol concentration (BAC), and TTD. Injury severity was calculated with the Abbreviated injury Scale (1985 version). Anatomical profile scores and G scores were also calculated and used to identify CNSI subjects. ANALYSIS: chi 2 and Student's t test were used, and odds ratios with 0.95 confidence intervals (CIs) were calculated. RESULTS: ALC(+) cases (BAC > or = 100 mg/dl) (n = 99) were significantly younger and more frequently had TTD < 1 hr than ALC(-) cases (n = 233): odds ratio 1.62[0.95 CI (1.02 to 2.58)]. Overall, CNSI cases (n = 297) were significantly younger and had fewer thoracic injuries, but did not have significantly shorter TTD, compared with non-CNSI cases. However, ALC(+) CNSI cases (n = 77) were over twice as likely to have TTD < 1 hr ¿odds ratio 2.04 [0.95 CI (1.13 to 3.70)]¿. For ALC(+) isolated CNSI cases, the odds ratio for TTD < 1 hr, compared with nonisolated CNSI cases was 8.25 (0.95; CI 0.66 to 102.5). Injury Severity Score, anatomical profile, and G scores were not significantly different for ALC(+) CNSI cases, compared with ALC(-) CNSI cases, whether isolated or nonisolated. CONCLUSIONS: These data suggest that alcohol intoxication is associated with increased frequency of early death in MVC victims with CNSI, despite there being no detectable difference in anatomical injury scoring.

Accidents, Traffic↗
PubMed1995

Lack of a hyperkalemic response in emergency department patients receiving succinylcholine.

OBJECTIVE: To determine whether serum potassium (K) levels increase significantly following succinylcholine (SCh)-assisted intubation in ED patients. METHODS: A prospective, noncontrolled, consecutive case series design was used to evaluate the change in serum K levels in ED patients who received SCh for emergency intubation. The study was performed at an academic medical center staffed by board-certified emergency physicians. The subjects were 100 consecutive prescreened ED patients with various diagnoses who received SCh for intubation. The eligible subjects had serum K levels determined prior to and 5 minutes after administration of a 1.0-1.5-mg/kg i.v. dose of SCh. Serum K levels were measured by the ion-selective electrode assay method. RESULTS: The mean change in serum K levels was -0.04 mmol/L (95% CI -0.14 to 0.06). The maximum increase was 1.10 mmol/L. The serum K level rose in 46 cases, decreased in 46 cases, and was unchanged in eight cases. No instance of SCh-induced cardiac arrest was identified. CONCLUSION: Changes in serum K levels following SCh administration in prescreened ED patients were minimal. A hyperkalemic response is uncommon in ED patients who undergo SCh-assisted intubation.

Adolescent↗
PubMed1995

Effects of ethanol on respiratory function in traumatic brain injury.

It has been observed that traumatic brain injury (TBI) increases the susceptibility of the brain to subsequent hypoxia, and prolonged apnea occurs in ethanol (EtOH)-treated animals following brain injury. This investigation tests the hypothesis that EtOH suppresses ventilation and hypercapnic respiratory drive following TBI. Immature pigs were anesthetized with halothane and received a 2 to 3 atm fluid-percussion brain injury. Respiratory parameters, including tidal volume, frequency, ventilation (VE), and arterial blood gases were measured on 100% O2 and on 5% to 6% inspired CO2 in O2 prior to and at 10, 60, 120, and 180 minutes after TBI. Hypercapnic response sensitivity (S) was measured as the change in VE per mm Hg increase in PaCO2. Intracranial pressure, mean arterial blood pressure, heart rate, brain temperature, glucose, and EtOH levels were also monitored. Three groups were studied: the first group of six received EtOH (3.5 gm/kg, intragastrically) without brain injury; the second group of six received TBI without EtOH; the third group of eight received EtOH and TBI. Ethanol levels were 121 +/- 13 (standard error of the mean) mg/dl in the EtOH/TBI group (136 +/- 25 in the EtOH group) at the time of injury, and 175 +/- 12 mg/dl in the EtOH/TBI group (200 +/- 20 mg/dl in the EtOH group) at 120 minutes after injury. The EtOH/TBI animals had significantly lower VE and S, and higher PaCO2 following brain injury (p < 0.05, repeated-measures analysis of variance). No significant differences were identified between groups for pH, PaCO2, intracranial pressure, heart rate, brain temperature, or glucose levels. Ethanol intoxication leads to significant impairment of respiratory control following traumatic brain injury and may contribute to brain injury in intoxicated trauma victims.

Alcoholic Intoxication↗
PubMed1994

4-Methylpyrazole blocks acetaminophen hepatotoxicity in the rat.

STUDY OBJECTIVE: To determine whether 4-methylpyrazole inhibits the hepatotoxic effects of acetaminophen in a rat model. DESIGN AND TYPE OF PARTICIPANTS: A nonblinded experiment using male Sprague-Dawley rats. INTERVENTIONS: Animals were divided into four groups. Groups 1 through 3 received 2,000 mg/kg acetaminophen by gavage; group 4 acted as a control. At four or eight hours, group 2 received 400 mg/kg 4-methylpyrazole; group 3 received 50 mg/kg 4-methylpyrazole. Blood samples were taken for measurements of serum AST and ALT levels. Livers were removed for microscopic examination and grading of necrosis. RESULTS: Lower AST and ALT levels were obtained for both the 400-mg/kg (P < .01) and 50-mg/kg (P < .05) doses of 4-methylpyrazole administered four hours after acetaminophen. Although mean AST and ALT levels also were lower when 400 and 50 mg/kg 4-methylpyrazole were administered eight hours after acetaminophen, these results were not statistically significant. Median necrosis scores were 3 for rats receiving acetaminophen alone, 0.5 for those receiving acetaminophen and 400 mg/kg 4-methylpyrazole (P < .05), 1 for those receiving acetaminophen and 50 mg/kg 4-methylpyrazole (P < .05), and 0 for control rats (P < .05). CONCLUSION: When administered four hours after a toxic dose of acetaminophen, 4-methylpyrazole significantly inhibits hepatotoxicity in the rat, as reflected by lower levels of serum transaminases and lesser degrees of hepatic necrosis.

Acetaminophen↗
PubMed1993

Effects of ethanol in traumatic brain injury.

The effects of ethanol intoxication on brain injury and cerebral blood flow (CBF) were investigated in a porcine fluid-percussion model of traumatic brain injury (TBI). Immature swine, under halothane anesthesia (1%), had a TBI delivered with a fluid-percussion device. The experimental group (n = 10) received ethanol (3.5 gm/kg) via gastric tube followed in 1 h by TBI. Two groups of control animals received normal saline and TBI (n = 10) or ethanol and no TBI (n = 5). Mean arterial blood pressure (MAP), intracranial pressure (ICP), arterial blood gases, and serum lactate were monitored for 3 h after the injury. CBF was measured with radiolabelled 15-micron diameter microspheres. Neuropathologic changes were evaluated and graded after formalin perfusion and brain removal at 3 h postinjury. The ethanol level 60 min post-head injury was 198 +/- 70 (SD) mg/dL in the ethanol+TBI group. At 90 min postinjury and thereafter, ethanol+TBI animals compared with TBI only animals had significantly lower MAP (63 +/- 26 mmHg vs 91 +/- 15 mmHg) and lower cerebral perfusion pressure (50 +/- 25 mmHg vs 78 +/- 15), and at 180 min postinjury, lower CBF (87 +/- 37% vs 62 +/- 79% of preinjury levels). Ethanol+TBI animals had higher blood lactates (28 +/- 11 mg/dL vs 13 +/- 6 mg/dL) than TBI only animals. Ethanol+TBI animals also had significantly longer postinjury apneas (11 +/- 8 min vs 0.6 +/- 0.4 min), with three of ten ethanol-treated animals never recovering spontaneous respiration. Ethanol intoxication produced hemodynamic and respiratory changes, which may have a deleterious effect on outcome and mortality after brain injury.

Alcoholic Intoxication↗
PubMed1993

Methohexital for orthopaedic procedures in the emergency department.

The past two decades have seen more and more orthopaedic procedures performed in the emergency department. Methohexital would seem to be a useful adjunct drug for the performance of these procedures because of its well-known attributes (eg, rapid induction and recovery, brief duration, and minimal hemodynamic changes). A search of the literature revealed no previous studies on the use of methohexital in the emergency department. Therefore, the authors undertook a 1-year prospective study of all patients in their emergency department who received methohexital for orthopaedic procedures. The study's hypothesis was that methohexital is a safe drug for use in orthopaedic procedures in the emergency department. Additionally, the authors sought to determine the drug's indications for use, patterns of usage, and effects on the respiratory and cardiovascular systems. The data presented here are a subset of data previously presented and published.

Adolescent↗