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Biomedical subjects

David R King

Publications and source records attributed to David R King.

10 recordsLinked to original sources
PubMed2006

Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury.

OBJECTIVE: Two series of experiments were designed to evaluate whether early arginine vasopressin improves acute outcome following resuscitation from traumatic brain injury and severe hemorrhagic hypotension. DESIGN: Prospective randomized, blinded animal study. SETTING: University laboratory. SUBJECTS: Thirty-three swine. INTERVENTIONS: In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure approximately 20 mm Hg), survivors (n = 16) were initially resuscitated with 10 mL/kg crystalloid. After 30 mins, crystalloid and blood with either 0.1 unit x kg(-1) x hr(-1) arginine vasopressin or placebo was titrated to a mean arterial pressure target >or=60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure >or=60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO2 was administered periodically. In series 2 (n = 14), the identical protocol was followed except the shock period was 20 mins and survivors (n = 10) received a bolus of either arginine vasopressin (0.2 units/kg) or placebo during the initial fluid resuscitation. MEASUREMENTS AND MAIN RESULTS: In series 1, by 300 mins after traumatic brain injury with arginine vasopressin (n = 8) vs. placebo (n = 8), the fluid and transfusion requirements were reduced (both p < .01), intracranial pressure was improved (11 +/- 1 vs. 23 +/- 2 mmHg; p < .0001), and the CO2-evoked intracranial pressure elevation was reduced (7 +/- 2 vs. 26 +/- 3 mm Hg, p < .001), suggesting improved compliance. In series 2, with arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (p < .05). With arginine vasopressin, five of five animals survived 300 mins, whereas three of five placebo animals died. The survival time with placebo was 54 +/- 4 mins (p < .05 vs. arginine vasopressin). CONCLUSIONS: Early supplemental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury.

Animals↗
PubMed2006

Simulation training for a mass casualty incident: two-year experience at the Army Trauma Training Center.

BACKGROUND: Civilian and military mass casualty incidents (MCI) are an unfortunate reality in the 21st century, but there are few situational training exercises (STX) to prepare for them. To fill this gap, we developed a MCI STX for U.S. Army Forward Surgical Teams (FST) in conjunction with the U.S. Army Trauma Training Center. METHODS: After a standardized briefing, each FST has 60 minutes to unpack, setup, and organize a standard equipment cache into an emergency room, operating room, and intensive care unit. In an adjacent room, five anesthetized swine are prepared with standardized, combat-relevant injuries. The number and acuity of the total casualties are unknown to the FST and arrive in waves and without warning. A realistic combat environment is simulated by creating resource limitations, power outages, security breaches, and other stressors. The STX concludes when all casualties have died or are successfully treated. FSTs complete a teamwork self-assessment card, while staff and FST surgeons evaluate organization, resource allocation, communication, treatment, and overall performance. Feedback from each FST can be incorporated into an updated design for the next STX. RESULTS: From 2003-2005, 16 FSTs have completed the STX. All FSTs have had collapses in situational triage, primary/ secondary surveys, and/or ATLS principles (basic ABCs), resulting in approximately 20% preventable deaths. CONCLUSIONS: We concluded (1) a MCI can overwhelm even combat- experienced FSTs; (2) adherence to basic principles of emergency trauma care by all FST members is essential to effectively and efficiently respond to this MCI; (3) by prospectively identifying deficiencies, future military or civilian performance during an actual MCI may be improved; and (4) this MCI STX could provide a template for similar programs to develop, train, and evaluate civilian surgical disaster response teams.

Animals↗
PubMed2005

Ubiquitin immunoreactivity in cerebrospinal fluid after traumatic brain injury: clinical and experimental findings.

OBJECTIVE: Recent data indicate that ubiquitin is increased in serum after trauma and might regulate immune functions. Its cellular source is unknown. Because there have been no previous studies after traumatic brain injury (TBI), we determined whether ubiquitin immunoreactivity is increased in cerebrospinal fluid (CSF) after TBI. DESIGN AND SETTING: Prospective observational study of patients, with a subsequent interventional study of animals. SUBJECTS: The subjects were 14 patients with TBI, five patients with nontraumatic subarachnoid hemorrhage, ten nonneurologic controls, and seven cross-bred swine. INTERVENTIONS: Standardized TBI. MEASUREMENTS AND MAIN RESULTS: Ubiquitin immunoreactivity was analyzed by enzyme-linked immunosorbent assay and immunoblotting. Hemolysis was assessed spectrophotometrically. CSF ubiquitin levels (mean +/- sd) were 19 +/- 3 ng/mL in nonneurologic control patients, 81 +/- 48 ng/mL at 7 +/- 2 hrs after TBI (p = .002), and at the end of operation in patients with nontraumatic subarachnoid hemorrhage they were 104 +/- 68 ng/mL (p = .001). CSF and serum ubiquitin were measured for 7 days in six patients with TBI. In survivors (n = 3), CSF ubiquitin levels progressively recovered, whereas in nonsurvivors (n = 3), the levels increased until death. There was no difference in serum ubiquitin levels between survivors/nonsurvivors and there was no correlation between serum and CSF ubiquitin levels. In swine, CSF ubiquitin levels peaked at 8- to 30-fold higher than baseline at 60 min post-TBI and then declined with a half-life of 1.3 hrs. In CSF with hemolysis, peak ubiquitin levels were five-fold higher than without hemolysis (p < .05). Ubiquitin and hemoglobin correlations in CSF and after in vitro lysis of erythrocytes suggested that erythrolysis could account for no more than 23 +/- 16% of the CSF ubiquitin. CONCLUSIONS: CSF ubiquitin levels are increased more than four-fold in patients after TBI and nontraumatic subarachnoid hemorrhage. Peak CSF ubiquitin measurements in patients with TBI probably underestimated the actual peak, on the basis of data from the animal model. The progressive rise in CSF ubiquitin in patients with TBI who died suggests that lack of clearance could reflect lethal progression to irreversible brain damage. Erythrolysis is one potential source of CSF ubiquitin.

Adult↗
PubMed2005

Early vasopressin improves short-term survival after pulmonary contusion.

UNLABELLED: Arginine vasopressin (AVP) is a promising treatment for several types of irreversible shock, but its therapeutic potential has not been examined after severe chest trauma. Two series of experiments were performed to fill this gap. METHODS: Series 1: anesthetized, mechanically-ventilated pigs (n = 20, 29 +/- 1 kg) received a blast to the chest, followed by a "controlled" arterial hemorrhage to a mean arterial pressure (MAP) <30 mm Hg. At 20 minutes, a 10 mL/kg normal saline (NS) bolus was followed by either 0.1 U/kg AVP bolus or NS, in randomized, blinded fashion. From 30-300 minutes, either AVP (0.4 U/kg/hr plus NS) or NS alone was infused as needed to MAP>70 mm Hg. Series 2: Swine (n = 15) received the chest injury followed by partial left hepatectomy to produce "uncontrolled" hemorrhage. Resuscitation was the same as in series 1. RESULTS: The blast created bilateral parenchymal contusions (R > L), hemo/pneumothorax and progressive cardiopulmonary distress. In Series 1, there were 3/20 deaths before randomization, 0/8 deaths after resuscitation with AVP versus 4/9 deaths with NS (p = 0.029). In surviving animals, with AVP versus NS, fluid requirements and peak airway pressures were lower while P/F was higher (all p < 0.05). In Series 2, with uncontrolled hemorrhage, there were 5/15 deaths before randomization. Upon resuscitation with AVP versus NS, survival time and blood loss were both improved, but the differences did not reach statistical significance. CONCLUSIONS: After severe chest trauma with controlled hemorrhage, early AVP decreased mortality, reduced fluid requirements and improved pulmonary function. With uncontrolled hemorrhage, early AVP did not increase the risk for bleeding.

Animals↗
PubMed2005

Systemic coagulation changes caused by pulmonary artery catheters: laboratory findings and clinical correlation.

BACKGROUND: A higher rate of pulmonary embolism has been associated with pulmonary artery (PA) catheters; however, no mechanism has been described. Conventional tests of coagulation reveal no changes related to PA catheterization. The purpose of this study was to determine whether PA catheterization resulted in a hypercoagulable state detectable by thrombelastography (TEG). METHODS ANIMAL: Healthy, anesthetized, swine (n = 19) underwent PA catheterization. Samples were drawn from 7F femoral arterial catheters before and two hours after PA catheterization, at 5 mL/min, and analyzed (native whole blood, n = 15, kaolin activated blood, n = 4) by TEG (Hemoscope, Niles, IL) at precisely two minutes. Human: An IRB-approved prospective, observational trial was conducted in critically ill patients (n = 19). Samples were drawn from 22-gauge radial artery catheters, before and three hours after PA catheterization. Kaolin-activated TEG samples were analyzed at precisely five minutes. Data are mean +/- SE; Groups were compared with analysis of variance and significance was assessed at the 95% confidence interval. RESULTS: In both animals and patients, PA catheterization truncated R times (time to initial fibrin formation). In swine, the R times were 17.6 +/- 1.3 minutes (native) and 3.8 +/- 0.4 (kaolin) before PA catheterization, and decreased to 6.3 +/- 1.0 minutes (p = 0.002) and 1.9 +/- 0.5 minutes (p = 0.010) afterward. There were no changes in pH or temperature during the experiment. In patients, 4 of 19 were excluded for protocol violations. The R time was 6.3 +/- 1.0 minutes (kaolin) before and 3.0 +/- 0.3 minutes after catheterization (p = 0.003). No changes were observed in conventional coagulation parameters, temperature or pH. CONCLUSION: In healthy swine, and critically ill patients, PA catheters may enhance thrombin formation and fibrin polymerization, indicating a systemic hypercoagulable state. This may explain why PA catheters are associated with an increased risk of pulmonary emboli.

Adult↗
PubMed2005

Resuscitation with a hemoglobin-based oxygen carrier after traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) remains an exclusionary criterion in nearly every clinical trial involving hemoglobin-based oxygen carriers (HBOCs) for traumatic hemorrhage. Furthermore, most HBOCs are vasoactive, and use of pressors in the setting of hemorrhagic shock is generally contraindicated. The purpose of this investigation was to test the hypothesis that low-volume resuscitation with a vasoactive HBOC (hemoglobin glutamer-200 [bovine], HBOC-301; Oxyglobin, BioPure, Inc., Cambridge, MA) would improve outcomes after severe TBI and hemorrhagic shock. METHODS: In Part 1, anesthetized swine received TBI and hemorrhage (30 +/- 2 mL/kg, n = 15). After 30 minutes, lactated Ringer's (LR) solution (n = 5), HBOC (n = 5), or 10 mL/kg of LR + HBOC (n = 5) was titrated to restore systolic blood pressure to > or = 100 mm Hg and heart rate (HR) to < or = 100 beats/min. After 60 minutes, fluid was given to maintain mean arterial pressure (MAP) at > or = 70 mm Hg and heterologous whole blood (red blood cells [RBCs], 10 mL/kg) was transfused for hemoglobin at < or = 5 g/dL. After 90 minutes, mannitol (MAN, 1 g/kg) was given for intracranial pressure > or = 20 mm Hg, LR solution was given to maintain cerebral perfusion pressure at > or = 70 mm Hg, and RBCs were given for hemoglobin of < or = 5 g/dL. In Part 2, after similar TBI and resuscitation with either LR + MAN + RBCs (n = 3) or HBOC alone (n = 3), animals underwent attempted weaning, extubation, and monitoring for 72 hours. RESULTS: In Part 1, relative to resuscitation with LR + MAN + RBCs, LR + HBOC attenuated intracranial pressure (12 +/- 1 mm Hg vs. 33 +/- 6 mm Hg), improved cerebral perfusion pressure in the initial 4 hours (89 +/- 6 mm Hg vs. 60 +/- 3 mm Hg), and improved brain tissue PO2 (34.2 +/- 3.6 mm Hg vs. 16.1 +/- 1.6 mm Hg; all p < 0.05). Cerebrovascular reactivity and intracranial compliance were improved with LR + HBOC (p < 0.05) and fluid requirements were reduced (30 +/- 12 vs. 280 +/- 40 mL/kg; p < 0.05). Lactate and base excess corrected faster with LR + HBOC despite a 40% reduction in cardiac index. With HBOC alone and LR + HBOC, MAP and HR rapidly corrected and remained normal during observation; however, with HBOC alone, lactate clearance was slower and systemic oxygen extraction was transiently increased. In Part 2, resuscitation with HBOC alone allowed all animals to wean and extubate, whereas none in the LR + MAN + RBCs group was able to wean and extubate. At 72 hours, no HBOC animal had detectable neurologic deficits and all had normal hemodynamics. CONCLUSION: The use of HBOC-301 supplemented by a crystalloid bolus was clearly superior to the standard of care (LR + MAN + RBCs) after TBI. This may represent a new indication for HBOCs. Use of HBOC eliminated the need for RBC transfusions and mannitol. The inherent vasopressor effect of HBOCs, especially when used alone, may misguide initial resuscitation, leading to transient poor global tissue perfusion despite restoration of MAP and HR. This suggests that MAP and HR are inadequate endpoints with HBOC resuscitation. HBOC use alone after TBI permitted early extubation and excellent 72-hour outcomes.

Analysis of Variance↗
PubMed2004

Changes in intracranial pressure, coagulation, and neurologic outcome after resuscitation from experimental traumatic brain injury with hetastarch.

BACKGROUND: In a model of traumatic brain injury (TBI), 2 protocols compared changes in intracranial pressure (ICP), coagulation, and neurologic outcome after intravenous fluid (IVF) resuscitation with either Hextend (HEX, 6% hetastarch in lactated electrolyte injection) or standard of care, crystalloid plus mannitol (MAN). METHODS: In the nonsurvivor protocol, swine (n = 28) received a fluid percussion TBI and hemorrhage (27 +/- 3 mL/kg). At 30 minutes, resuscitation began with lactated Ringer's (LR) or HEX. After 60 minutes, MAN (1 g/kg) or placebo was given plus supplemental IVF to maintain cerebral perfusion pressure (CPP) > or = 70 mm Hg for 240 minutes. Swine in the survivor group (n = 15) also underwent TBI and hemorrhage, and resuscitation with HEX was compared to that of normal saline (NS)+MAN. Neurologic outcome and coagulation were evaluated for 72 hours. RESULTS: In the nonsurvivor protocol, HEX, LR+MAN, and HEX+MAN attenuated the time-related rise of ICP and prevented ICP >20 mm Hg versus LR alone (P < .05). HEX alone maintained CPP (relative to baseline) and decreased total IVF by 50% versus LR +/- MAN (P < .05). MAN had no additive effect with HEX. Coagulation, measured by thromboelastograph reaction time (R), was 11 +/- 1 and 9 +/- 1 minutes at baseline and after TBI (before randomization). At 240 minutes after HEX or LR+MAN, R was 6 +/- 1 or 7 +/- 2 minutes, which indicates a hypercoagulable state, but there was no difference between treatments. In the survivor protocol, ICP and CPP were similar with NS+MAN versus HEX, but IVF requirement was 161 +/- 20 versus 28 +/- 3 mL/kg (P < .05). Motor scores were higher on days 2 and 3 with HEX (P < .05). At 72 hours, R was 28 +/- 14 versus 26 +/- 6 minutes with NS+MAN versus HEX, which indicates a hypocoagulable state, but there was no difference between treatments. CONCLUSIONS: Hextend as the sole resuscitation fluid after severe TBI reduces fluid requirement, obviates the need for mannitol, improves neurologic outcome, and has no adverse effect on the coagulation profile relative to the crystalloid plus mannitol standard of care.

Animals↗
PubMed2004

Modified rapid deployment hemostat bandage terminates bleeding in coagulopathic patients with severe visceral injuries.

BACKGROUND: We recently reported that a new dressing, the Modified Rapid Deployment Hemostat (MRDH) controlled bleeding in hypothermic coagulopathic swine after traumatic liver avulsion. The purpose of this study was to evaluate the MRDH in coagulopathic trauma patients undergoing abbreviated laparotomy. METHODS: A prospective, observational clinical trial of the MRDH dressing was performed at our Level One Trauma Center in patients with high-grade visceral injuries with coagulopathy who failed conventional therapy and required packing. Attending surgeons graded the injury and the adequacy of hemostasis following application of the dressing. Patients were followed until discharge or death. RESULTS: Ten patients were enrolled: nine severe hepatic injuries, and one major abdominal vascular injury. All patients were hypothermic, acidotic, and clinically coagulopathic. Intraoperative hemostasis was immediately obtained after MRDH placement in all cases except one. There was one death. CONCLUSION: The Modified Rapid Deployment Hemostat terminates bleeding from severe visceral injuries in coagulopathic patients undergoing abbreviated laparotomy.

Abdominal Injuries↗
PubMedDate not supplied

An unusual cause of septicemia and death in a burn patient: discussion and review.

Sepsis remains a common source of morbidity and mortality for seriously burned patients. Sources of sepsis are varied, although some are dramatically more common than others. Rarely, the burn surgeon may be confronted with an infectious source that remains unelucidated until postmortem examination. This case report describes the hospital course and subsequent death of a severely burned patient with sepsis, the source of which was only discovered on postmortem examination by our county medical examiner.

Acinetobacter Infections↗