Biomedical subjects

E R Geller

Publications and source records attributed to E R Geller.

At least 19 recordsLinked to original sources

PubMed1999

Critical analysis of injuries sustained in the TWA flight 800 midair disaster.

BACKGROUND: Previous reports of commercial airline disasters have reviewed incidents occurring at takeoff and landing. The purpose of the present study, which represents the first analysis of aviation injuries incurred during a midflight incident, was to examine the injuries sustained by the victims of the TWA Flight 800 disaster and to determine any correlation of injuries with structural damage and seat location. METHODS: Complete autopsy records, toxicology screening, and forensic analysis were reviewed. Injuries were assessed by anatomic region and severity by using the Abbreviated Injury Scale. The National Transportation Safety Board report of the investigation was applied to correlate individual injuries with seat location and structural damage. A comparison was performed against injury data from takeoff and landing incidents. RESULTS: All 230 passengers of TWA Flight 800 were recovered as fatalities. Head, thoracic, and abdominal injuries were multiple and severe, contributing to the mortality of the occupants. Analysis revealed that the severity of injury and anatomic injury pattern did not generally correlate with seating position or structural damage. A comparison of these injuries with those of takeoff and landing crashes showed differences in injury pattern and severity. CONCLUSION: Passengers of Flight 800 sustained instantaneous fatal blunt force injury. Analysis of the data revealed no global correlation between seat position and pattern of injury. In contrast to injuries incurred during crashes at takeoff and landing, these midflight injuries were too extreme to warrant a reappraisal of current passenger protective safety measures or standards.

Abbreviated Injury Scale↗

PubMed1996

Shotgun slug injuries: case report and literature review.

Shotguns are usually used to fire multiple pellets; however, they are capable of firing a single projectile in the form of a slug. Although rare, shotgun slug injuries are severe, producing wounds comparable to those inflicted by high-velocity weapons with the potential for even more tissue destruction because of the slug's size and mass. We report the first survivor of a close range shotgun slug injury, with a review of this weapon's unique projectile ballistics and the relevant literature.

Abdominal Injuries↗

PubMed1996

Renal gluconeogenesis and blood flow during endotoxic shock.

OBJECTIVES: To determine whether endotoxic shock decreases the renal gluconeogenic capacity and the renal artery blood flow. METHODS: An in-vivo, murine, nonrecirculating kidney perfusion model was studied in a trauma research laboratory. Each of 12 fasted, male Holtzman rats (shock n = 6, control n = 6) was injected with 1 mL of normal saline or endotoxin (20 mg/kg). Five hours after the injection, all the rats were anesthetized and blood samples were obtained for the determination of the plasma glucose. Right renal artery blood flow was measured by an ultrasonic small-animal flow meter. The kidney was then perfused via the renal artery with 37 degrees C, oxygenated, glucose-free Krebs-Henseleit solution in the presence of 100 mumol of phloridzin to inhibit the cellular uptake of glucose. Renal glucose production was determined by measuring glucose in both renal vein effluent and urine. After 30 minutes of equilibration, 5 mmol of lactate and 0.5 mmol of pyruvate were added to the perfusate as a gluconeogenic substrate. Renal vein and ureteral effluent samples were collected after 5, 10, and 15 minutes. RESULTS: The endotoxic shock group showed hypoglycemia (p < 0.05) as well as a decrease in renal artery blood flow (p < 0.05). Gluconeogenic stimulation was demonstrable in both the control and the endotoxic shock groups after 15 minutes of perfusion with substrate (p < 0.05). However, renal gluconeogenesis was significantly attenuated in the endotoxic shock group compared with the control. CONCLUSIONS: Renal glucose production in response to a gluconeogenic substrate is significantly attenuated during the hypoglycemic phase of endotoxic shock. Endotoxic shock also causes a significant decrease of renal artery blood flow.

Animals↗

PubMed1995

Laparoscopic-assisted percutaneous endoscopic gastrostomy.

The authors report the successful use of laparoscopic-assisted percutaneous endoscopic gastrostomy (LAPEG) in two children. Attempts at simple percutaneous endoscopic gastrostomy in both patients had failed. Subsequently, LA-PEG was easily accomplished. This technique consisted of a combination of upper gastrointestinal endoscopy and laparoscopy. The gastrostomy was placed under direct vision in the lesser gastric curvature, hence minimizing the risk of developing gastroesophageal reflux.

Adolescent↗

PubMed1993

Effect of diltiazem on altered glucose regulation during endotoxic shock.

Endotoxic shock is associated with profound metabolic alterations including hypoglycemia and hyperlactiacidemia. We studied hepatic glucose production and the role of diltiazem in affecting these metabolic alterations in a rat model of endotoxic shock. Fasted rats were intravenously injected with saline, endotoxin (20 mg/kg), endotoxin (20 mg/kg) plus diltiazem (1.2 mg/kg), or saline plus diltiazem. Five hours after the injections, the rats were anesthetized and blood samples were obtained for plasma glucose and lactate. The livers of all rats were then perfused in situ with an oxygenated 37 degrees C glucose-free Hanks' balanced salt solution at a rate of 30 ml/min via the portal vein and effluent was collected from the inferior vena cava. After 30 min equilibration, 5 mM lactate was added to the perfusate as a gluconeogenic substrate. Endotoxic groups exhibited hypoglycemia (64.5 +/- 12.7 mg/dl) and hyperlacticacidemia (4.3 +/- 0.63 mM). Diltiazem administration improved the hypoglycemia (96.9 +/- 9.1 mg/dl) and attenuated the hyperlacticacidemia (2.2 +/- 0.7 mM) in the endotoxic group. Gluconeogenic stimulation with lactate was demonstrated in both the control (18.1 +/- 2.3 vs 12.8 +/- 1.86 microns/g/hr, P < .05) and endotoxic (16.6 +/- 2.3 vs 9.8 +/- 1.1, P < .05) groups. However, stimulation in the endotoxic groups was significantly less compared with control. Gluconeogenic stimulation in the endotoxic group was unaffected after diltiazem administration. These data suggest that diltiazem treatment in endotoxic shock improves hypoglycemia and attenuates hyperlacticacidemia. These metabolic alterations are not associated with an improvement in substrate-specific stimulation of gluconeogenesis.

Animals↗

PubMed1993

Effective treatment of acute alkali injury of the rat esophagus with early saline dilution therapy.

BACKGROUND: Controversy persists regarding the appropriate treatment of acute alkali injury to the esophagus. The current study establishes a controlled model of alkali esophageal injury and examines the efficacy of saline dilution therapy. STUDY HYPOTHESIS: Early saline dilution therapy effectively reduces esophageal injury resulting from acute alkali exposure. METHODS: The esophagi were harvested from 60 Sprague-Dawley rats. Each end was cannulated with a 20-gauge catheter. Specimens were maintained in an oxygen-perfused saline bath (37 C) during a 60-minute experimental period and then fixed immediately in 10% formalin solution for histologic examination. Three experimental groups (A, B, and C) were perfused with 50% NaOH solution at time zero. Treatment with saline perfusion was performed immediately in group A, five minutes after injury in group B, and 30 minutes after injury in group C. The positive control group D was perfused with saline at time zero. A negative control, group E, was perfused with 50% NaOH at time zero. This group did not receive subsequent treatment with saline. Pathologic examination was performed in a blinded fashion using a score of 0 to 3 (0, no injury; 1, minimal; 2, moderate; 3, severe) for seven histologic criteria: epithelial viability, extent of injury, cornified epithelial cell differentiation, granular cell differentiation, epithelial cell nuclei, muscle cells, and muscle cell nuclei. RESULTS: The positive control group demonstrated scores of zero. Nonparametric analysis showed a significant difference among treatment groups for each injury category. Trend analysis revealed a significant progression of injury for each category associated with time to treatment. Discriminant analysis indicated that the muscle cells category was the most useful category with which to distinguish injury among groups. CONCLUSION: In our model, saline lavage decreased objective evidence of esophageal injury after a severe alkaline exposure, and early therapy enhanced this beneficial effect.

Acute Disease↗

PubMed1993

Analysis of injuries following the crash of Avianca Flight 52.

Analyses of injuries sustained in airline disasters have been hampered by the frequent association of burn injury and by poor documentation. This report analyzes autopsy data from the crash of Avianca Flight 52 on Long Island, New York. There were 158 passengers of whom 73 died. The majority of persons had multiple organ injuries (average, 3.8/victim). Severe neurologic trauma included subarachnoid hemorrhage (65%), skull fracture (32%), and brain laceration (22%). Chest injuries included rib fractures (80%: average, 8.3/victim), hemothorax (58%), sternal fracture (22%), and lung contusion (33%). Orthopedic injuries (average, 4.4/victim) included pelvic (22%), tibial (37%), femur (22%), thoracic spine (33%), cervical spine (22%), and lumbar fractures (5%). Cardiovascular injuries included aortic transection (25%), heart laceration (14%), and major vascular injury (10%). Intra-abdominal injuries included liver (10%), spleen (8%), and kidney (10%). Unrestrained infants suffered severe injuries. Deaths in this airline disaster were from severe head and upper body injuries. This report may allow reappraisal of current restraint and safety measures.

Abdominal Injuries↗

PubMed1993

Diltiazem preserves hepatic gluconeogenesis following hemorrhagic shock.

Prolonged hemorrhagic shock is characterized by the progression from hyperglycemia to hypoglycemia and failure to respond to standard methods of resuscitation. Previous studies have shown that the transition to irreversible shock is accompanied by attenuation of hepatic gluconeogenic capacity and a rising level of intracellular calcium. Additionally, it has been observed that diltiazem improves survival following prolonged hemorrhagic shock in rats. We examined the effect of resuscitation containing diltiazem upon hepatic gluconeogenesis during early and late phases of hemorrhagic shock in a rat model. Fasted male Sprague-Dawley rats (250-350 g) were rapidly bled to a mean arterial pressure of 40 mm Hg for a period of 30 minutes (group A) or 120 minutes (group B). At the end of the hemorrhagic shock period, rats were randomized to resuscitation utilizing lactated Ringer's (LR) solution, or LR+diltiazem (DZ, 1.2 mg/kg). Following resuscitation, rats underwent laparotomy and in situ liver perfusion with an oxygenated 37 degrees C glucose-free Krebs solution via the portal vein. After equilibration, 5 mmol/L lactate and 0.5 mmol/L pyruvate were added to the perfusate as substrate and effluent samples collected. Serum glucose concentration and portal venous flow did not differ significantly between DZ and LR groups throughout the study periods. In group A, hepatic glucose production was significantly elevated in DZ animals when compared with controls (p < 0.05). A similar significant improvement in gluconeogenesis was observed following 120 minutes of hemorrhagic shock in group B (p < 0.05). Additionally, treated rats (DZ, both groups A and B) demonstrated improved gluconeogenic response to substrate when compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Alterations in renal gluconeogenesis and blood flow during hemorrhagic shock.

The role of renal gluconeogenesis following hemorrhagic shock was studied. Hemorrhagic shock was induced in fasted, anesthesized rats by reduction of blood pressure to 40 mm Hg for either 30 or 150 min. Plasma samples were obtained for plasma glucose determination, and right renal arterial blood flow was determined with the help of an ultrasonic transit time blood flowmeter in hemorrhagic shock and control rats. The kidney was perfused via the renal artery with 37 degrees C oxygenated, glucose-free Krebs-Henseleit solution in the presence of 100 microM phloridzin to inhibit the cellular reuptake of glucose. Renal glucose production was determined by measuring glucose in both renal vein effluent and urine. After 30 min of equilibration, 5 mM lactate and 0.5 mM pyruvate were added to the perfusate as a gluconeogenic substrate, and effluent samples were collected after 5, 10, and 15 min. Moderate hyperglycemia was observed in vivo following 30 min of hemorrhagic shock, and significant hypoglycemia (P < .05) was observed following 150 min of hemorrhagic shock. Renal arterial flow was significantly decreased at 30 min (P < .05) and 150 min (P < .05) of hemorrhagic shock. Renal glucose production with and without substrate after 30 min of hemorrhagic shock was similar compared to control. Renal glucose production after 150 min of hemorrhagic shock was significantly decreased (P < .05) compared to control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Altered cellular calcium regulation and hepatic glucose production during hemorrhagic shock.

The relationship between intracellular Ca2+ and glucose production in the liver during early and late states of hemorrhagic shock was studied. Rats were anesthetized with intraperitoneal sodium pentobarbital and both femoral arteries and one femoral vein were cannulated. Rats were divided into two groups. One group was subjected to hemorrhagic shock by rapid withdrawal of blood to a mean arterial pressure of 40 mm Hg and maintained in shock for either 30 or 150 min. Rats in the control group were observed for the same time period. Hepatic glucose production was evaluated in both groups by a nonrecirculating liver perfusion model with and without lactate as a substrate. Intracellular free Ca2+ in hepatocytes was measured using the Ca2+ selective indicator Fura-2, under basal and epinephrine-stimulated conditions. Hyperglycemia and hyperlacticacidemia were observed in vivo at 30 min of hemorrhagic shock, whereas hypoglycemia and hyperlacticacidemia were observed at 150 min of shock. Hepatic glucose production in isolated perfused livers was significantly depressed at 30 min in animals subjected to shock (P less than 0.05). Lactate-induced glucose production was significantly attenuated at 30 and 150 min (P less than 0.05). Basal Ca2+, in isolated hepatocytes, at 30 and 150 min of hemorrhagic shock was significantly (P less than 0.05) higher than in controls. The hemorrhagic shock rat hepatocytes failed to evaluate intracellular free Ca2+ upon stimulation with 10(-5) M epinephrine. These results demonstrate that hemorrhagic shock is associated with an increase in hepatocyte intracellular Ca2+ concentration along with attenuation of hormone-mediated mobilization of calcium and substrate specific stimulation of hepatic glucose production.

Animals↗

PubMed1991

T3 preserves respiratory function in sepsis.

Sepsis produces profound hypothyroidism. This hypothyroid state is associated with altered lung metabolism and structural integrity. We studied the respiratory function of rats during sepsis-induced hypothyroidism with or without T3 treatment. Forty-four male Holtzman rats underwent cecal ligation and puncture (CLP). Treatment was administered at six hours after surgery consisting of intraperitoneal injection of T3 (15 micrograms/kg, n = 19) or saline (n = 25). At 20 hours (Group A) or 30 hours (Group B) following CLP, respiratory drive was assessed by serial occlusion pressure technique (P0.1). The rats were killed and static elastance determined by serial air inflation to 10 cc. The lungs were excised for weight determination. The P0.1 values were significantly greater in T3-treated animals over controls in Group A (9.3 +/- 0.7 vs. 6.6 +/- 2.2, p less than 0.05 by t test); elastance was significantly improved by T3 treatment in Group B (p less than 0.05 by two-way ANOVA). Lung weight, pH, pO2, pCO2, respiratory rate (RR), and mortality were not significantly different between groups. Control animals were hypothyroid by 20 hours after CLP (T3 less than 12.5 ng/dL) whereas T3-treated animals were euthyroid (T3 = 145 +/- 43 ng/dL). Pulmonary dysfunction frequently accompanies sepsis; the euthyroid state appears protective. We found a significantly improved respiratory drive in septic animals with T3 treatment. Lung elastance was similarly improved in late sepsis with T3 treatment. The data suggest that T3 treatment preserves respiratory function in septic rats as evidenced by respiratory drive and compliance.

Airway Resistance↗

PubMed1991

Beneficial effects of diltiazem in hemorrhagic shock.

The role of calcium channel blockade on metabolic alterations in a hemorrhagic shock model was studied. Experiments were performed on anesthetized Sprague-Dawley rats to evaluate the effect of diltiazem on hyperglycemia and hyperlacticacidemia following hemorrhagic shock. Rats were bled rapidly to a blood pressure of 40 mm Hg and maintained at that level for 2 hr. At 30 min into hemorrhagic shock, rats received either saline or diltiazem (1.2 mg/kg, i.v.) as treatment. Blood samples were obtained preshock and at 30-min intervals. Plasma glucose and lactate increased significantly in both groups at 30 min. Diltiazem treatment significantly reduced the plasma glucose and heart rate during hemorrhagic shock (P less than 0.05). Plasma lactate increased similarly in both groups. Survival analysis indicates significant (P less than 0.05) improvement in the diltiazem-treated group. These data suggest that diltiazem has a beneficial effect in hemorrhagic shock in rats.

Animals↗

PubMed1991

Inflammatory complications following penetrating cardiac trauma.

Two cases with pericardial and myocardial inflammatory complications following penetrating cardiac trauma are presented. A high index of suspicion with liberal usage of echocardiography, serial electrocardiograms, and careful patient follow-up will preclude this diagnostic oversight.

Adult↗

PubMed1991

Autologous fibrin gel: bactericidal properties in contaminated hepatic injury.

Fibrin glue is an effective hemostatic agent in a variety of clinical situations; its utility is limited by potential transmission of viral infection. We studied the bactericidal properties of fibrin gel (FG) in a murine contaminated hepatic injury model and in vitro by agar plate culture method. Intra-abdominal abscess formation and adhesion rate were assessed following controlled liver injury in association with abdominal contamination with 10(7) Bacteroides fragilis and hepatorrhaphy (H, n = 15) or FG (n = 12). Animals treated by hepatorrhaphy had a significantly greater intra-abdominal abscess rate (15/15 vs. 4/12, p less than 0.05) and adhesion rate (14/15 vs. 6/12, p less than 0.05) than animals treated with FG. Fibrin gel is bactericidal to Bacteroides fragilis, Enterobacter faecium, Escherichia coli, and Staphylococcus aureus but has no effect against Klebsiella pneumoniae or Pseudomonas aeruginosa; the plasma component appears active. Fibrin gel demonstrates significant improvement in adhesion formation and intra-abdominal abscess rate when compared with suture hepatorrhaphy. Fibrin gel appears protective in contaminated hepatic injury.

Abscess↗

PubMed1989

Intra-abdominal sepsis following liver trauma.

Of 330 consecutive patients with liver trauma having a celiotomy over a 5-year period, 295 (89%) survived more than 72 hours. Of these 295, 35 (12%) developed sepsis, and 11 (31%) of these septic patients died. The sources of the sepsis in 30 of these patients included: abdominal abscesses--23, pneumonia or empyema--seven, acalculous cholecystitis--two, gangrene of right colon--two, and thigh abscess--one. In five other patients, the source of the sepsis was not found, even at autopsy. The mortality rate in the 30 patients with one or more identifiable foci of infection was 23%. In contrast, when the source of the sepsis could not be found, the mortality rate was 80% (4/5) (p less than 0.05). Factors associated with an increased incidence of abdominal abscess included: splenectomy, 75% (3/4); liver packs, 63% (5/8); 20+ units of blood, 57% (8/14); Class IV-V liver injury, 35% (8/23); 10-19 units of blood, 25% (7/28); colon injury, 19% (7/36); and open (Penrose) drainage of the abdomen, 11% (23/213). None of 82 patients without drains developed an intra-abdominal abscess. Thus early control of an identifiable source of infection provides the best results with sepsis following liver trauma. The most effective method for preventing intra-abdominal abscesses appears to be avoidance of drains in mild (Class I-II) liver injuries. The use of a closed system in the most severe injuries is still controversial and needs to be addressed in a prospective trial.

Abdomen↗

PubMed1988

Enhancement of mitochondrial function in sepsis.

Recent reports from our laboratory have challenged the concept that sepsis selectively damages or interferes with mitochondrial function. To address the lingering skepticism that mitochondrial assays in surviving animals might not detect this "injury," we injected rats with a lethal dose of Escherichia coli endotoxin and compared hepatic, cardiac, and skeletal muscle mitochondrial function in these animals with that of control rats. Mitochondrial function was serially determined during a four-hour postmortem period by measuring the respiratory control ratio, the adenosine diphosphate-oxygen ratio, and protein levels. Hepatic mitochondria ceased to function within 30 minutes of the time of death. Cardiac and skeletal muscle mitochondria functioned normally up to four hours after death in both septic and control animals. Mitochondria from septic animals had a significantly higher respiratory control ratio than those from control rats. Thus, sepsis appears to enhance rather than damage mitochondrial function up to four hours after death.

Animals↗

PubMed1988

Comparison of 1% sodium tetradecyl sulfate to a thrombogenic sclerosant cocktail for endoscopic sclerotherapy.

This preliminary report suggests superior efficacy of a mixture of Sodium Tetradecyl Sulfate, thrombin and cefazolin (ST-Thr-Cef) over 1% Sodium Tetradecyl Sulfate (ST) in the early control of variceal bleeding. The overall management of patients treated with ST-Thr-Cef was superior as indicated by fewer hospital days and lesser transfusion requirements. Though trends were suggestive, we were unable to demonstrate a survival advantage for patients treated with ST-Thr-Cef. There was a low number of complication in both treatment groups and they were easily managed.

Adult↗

PubMed1986

Mitochondrial death in sepsis: a failed concept.

The concept of early selective mitochondrial injury has been proposed to explain the global metabolic dysfunction observed in the septic state. A two phase study was undertaken to test the validity of this hypothesis. In the initial phase, an endotoxin shock model was employed in the rat to delineate the function of skeletal muscle mitochondria. Mitochondrial function was determined polarimetrically, comparing state three and state four rates, respiratory control index (RCI) and ADP:O ratios. No significant alteration in these parameters was observed in the endotoxic state. Phase II of the study was designed to investigate mitochondrial function in a bacterial peritonitis rat model. Both liver and skeletal muscle mitochondrial function were determined to control for possible alterations in liver metabolism. Neither muscle nor liver mitochondria exhibited functional impairment during sepsis. We conclude from this study that neither endotoxemia nor peritonitis selectively "kills" mitochondria as previously suggested.

Animals↗