Biomedical subjects

A B Peitzman

Publications and source records attributed to A B Peitzman.

At least 37 records · Page 2Linked to original sources

PubMed1997

Management of blunt splenic trauma: significant differences between adults and children.

BACKGROUND: Although highly successful in children, nonoperative management of blunt splenic injury in adults is less defined. The purpose of this study was to determine whether mechanism of injury, grade of splenic injury, associated injuries, and pattern of injury differ between adults and children (younger than 15 years of age). METHODS: Four hundred eleven patients (293 adults and 118 pediatric patients) with blunt splenic injury were admitted to an affiliated adult/pediatric trauma program from 1989 to 1994. Computed tomography (CT) scans were interpreted in a blinded fashion. Mechanism of injury was significantly different for adults versus children (p < 0.05): motor vehicle crash (66.9% versus 23.7%), motorcycle (8.8% versus 0.8%), sports (2.4% versus 16.9%), falls (8.8% versus 25.4%), pedestrian/automobile (4.4% versus 11.0%), bicycle (1.4% versus 9.3%), and other (7.3% versus 12.7%). RESULTS: Higher injury severity scores, lower Glasgow Coma Scales, and higher mortality indicated that the adults were more severely injured than the children. Fifty-nine percent of the adults and 7% of the children required immediate laparotomy for splenic injury. Both CT grade and quantity of blood on CT predicted the need for exploration in adults but not in children. An injury severity score above 15 and high-energy mechanisms correlated with the need for operative intervention. CONCLUSIONS: Rather than children simply being physically different, they are injured differently than adults, hence the high rate of nonoperative management.

Accidents, Traffic↗

PubMed1997

Efficacy of inhaled nitric oxide in oleic acid-induced acute lung injury.

OBJECTIVE: To assess the efficacy of inhaled nitric oxide in improving pulmonary hypertension and gas exchange following oleic acid-induced acute lung injury. DESIGN: Prospective, pharmacologic study. SETTING: Surgical research laboratory at the University of Pittsburgh, Pittsburgh, PA. SUBJECTS: Instrumented, intubated pigs weighing 16 to 27 kg. INTERVENTIONS: Intravenous oleic acid and inhaled nitric oxide. MEASUREMENTS AND MAIN RESULTS: All pigs treated with intravenous oleic acid (0.11 mL/kg) developed a severe lung injury with pulmonary hypertension, accompanied by impaired oxygenation, intrapulmonary shunting, and increased extravascular lung water (p < .05 compared with baseline). Following nitric oxide inhalation, although pulmonary hypertension decreased in a dose-dependent fashion, no amelioration in pulmonary gas exchange was observed, as reflected by PaO2 and intrapulmonary shunt. Plasma nitrite and nitrate concentrations, the stable end products of nitric oxide metabolism, did not increase following nitric oxide exposure in this model of severe lung injury. CONCLUSIONS: The effect of inhaled nitric oxide, restricted to relieving pulmonary vasoconstriction in this model of lung injury, may have limited benefit in improving pulmonary gas exchange when diffusion is impaired by severe lung injury and inflammatory thickening of the alveolar-capillary barrier. Nitric oxide inhalation may have better results when used at an earlier, less severe stage of acute lung injury.

Administration, Inhalation↗

PubMed1997

Prospective study of blunt aortic injury: Multicenter Trial of the American Association for the Surgery of Trauma.

BACKGROUND: Blunt aortic injury is a major cause of death from blunt trauma. Evolution of diagnostic techniques and methods of operative repair have altered the management and posed new questions in recent years. METHODS: This study was a prospectively conducted multi-center trial involving 50 trauma centers in North America under the direction of the Multi-institutional Trial Committee of the American Association for the Surgery of Trauma. RESULTS: There were 274 blunt aortic injury cases studied over 2.5 years, of which 81% were caused by automobile crashes. Chest computed tomography and transesophageal echocardiography were applied in 88 and 30 cases, respectively, and were 75 and 80% diagnostic, respectively. Two hundred seven stable patients underwent planned thoracotomy and repair. Clamp and sew technique was used in 73 (35%) and bypass techniques in 134 (65%). Overall mortality was 31%, with 63% of deaths being attributable to aortic rupture; mortality was not affected by method of repair. Paraplegia occurred postoperatively in 8.7%. Logistic regression analysis demonstrated clamp and sew (p = 0.002) and aortic cross clamp time of > or = 30 minutes (p = 0.01) to be associated with development of postoperative paraplegia. CONCLUSIONS: Rupture after hospital admission remains a major problem. Although newer diagnostic techniques are being applied, at this time aortography remains the diagnostic standard. Aortic cross clamp time beyond 30 minutes was associated with paraplegia; bypass techniques, which provide distal aortic perfusion, produced significantly lower paraplegia rates than the clamp and sew approach.

Adolescent↗

PubMed1997

Effects of hemodilution on long-term survival in an uncontrolled hemorrhagic shock model in rats.

Prehospital guidelines for the treatment of penetrating trauma recommend rapid volume resuscitation to normal blood pressure. There is evidence, however, that fluid resuscitation to normal blood pressure in the setting of uncontrolled hemorrhagic shock (UHS) causes increased bleeding, hemodilution, and mortality. To test this hypothesis, we evaluated the effects of blood pressure and hemodilution on survival in a rat model of UHS. UHS was produced in rats by preliminary bleed of 3 mL/100 g followed by a 75% tail amputation. Experimental design consisted of three phases: a prehospital phase, with uncontrolled bleeding and resuscitation to either 40 or 80 mm Hg with lactated Ringer's solution (LR) or lactated Ringer's solution and whole blood (WB); followed by a hospital phase, with control of the bleeding and continued resuscitation to mean arterial pressure (MAP) > 80 mm Hg and hematocrit near 30%; followed by a 3-day observation phase. There were four treatment groups, n = 8 in each group: group I, MAP = 80 mm Hg with LR only; group II, MAP = 80 mm Hg with WB and LR; group III, MAP = 40 mm Hg with LR only; and group IV, MAP = 40 mm Hg with WB and LR. All group I rats died within 2.5 hours. There were no significant differences in survival among groups II, III, and IV. Base deficit, arterial pH, and lactate levels were significantly worse in the rats resuscitated to a MAP of 80 mm Hg with LR (group I). The effects of blood pressure alone, hemodilution alone, and their interaction were significantly related to base deficit and arterial pH. Hemodilution, but not blood pressure as an end point in resuscitation, was significantly related to lactate levels. The high mortality in this model of uncontrolled hemorrhage was attributable to the effects of blood pressure, hemodilution, and the interaction between the two variables, rather than simply continued blood loss from increased hydrostatic pressure.

Animals↗

PubMed1997

Asymptomatic aortic stenosis and unexpected death in the trauma patient.

We report the cases of two young trauma patients with asymptomatic aortic stenosis who died after nonlethal blunt traumatic injuries. In both cases, their deaths were attributed to their underlying valvular disease. Awareness of the incidence of asymptomatic aortic stenosis and its potential physiologic hazard to the trauma victim may facilitate management of these difficult patients.

Accidents, Traffic↗

PubMed1997

Physiologic and molecular characterization of the role of nitric oxide in hemorrhagic shock: evidence that type II nitric oxide synthase does not regulate vascular decompensation.

To determine the role of nitric oxide (NO) in decompensated and irreversible hemorrhagic shock, rats were subjected to hemorrhagic shock (HS) for 3 or 5 h. Lung, liver, and plasma samples were studied for evidence of NO formation using Northern analysis and immunohistochemistry for Type II NOS, as well as measurement of plasma nitrite/nitrate, cyclic GMP, and nitrosylated hemoglobin levels. Comparisons were made with similarly instrumented time-matched sham rats. Type II NOS mRNA and protein were detectable in lung and liver only in the irreversible phase of HS (5 h). A large accumulation of nitrosylated hemoglobin and nitrite/nitrate appeared in the irreversible phase. Significant accumulation of cyclic GMP or nitrite/nitrate was not detectable in the decompensation phase. Despite the hemodynamic decompensation at 3 h of HS, Type II NOS mRNA and protein expression, as well as NO metabolites were not elevated. To assess whether NO plays a physiologically significant role in decompensation, rats in the decompensation phase and sham animals were subjected to nonspecific NOS inhibition. Both groups displayed a similar magnitude and duration of blood pressure elevation. Hemodynamic decompensation in HS is not mediated by Type II NOS induction. NO production increases only after prolonged HS; significant NO production is observed only in severe, irreversible HS.

Animals↗

PubMed1997

Abdominal trauma: use of oral contrast material for CT is safe.

PURPOSE: To determine the potential risk of aspiration pneumonitis associated with use of oral contrast material in computed tomography (CT) performed for evaluation of abdominal trauma. MATERIALS AND METHODS: In 510 consecutive adult patients, a dilute 2.5% solution of diatrizoate meglumine and sodium was administered orally or by means of a nasogastric tube as part of a routine protocol for CT evaluation of acute abdominal trauma. A retrospective review of medical records was performed to determine evidence of aspiration pneumonitis occurring before or after CT. RESULTS: None of the patients had aspiration of contrast material or gastric contents attributable to the CT examination. CONCLUSION: Use of contrast material for stomach and bowel opacification during CT for evaluation of abdominal trauma appears to be safe. Proper preparation and administration of contrast material and control of the patient's airway are essential to ensure the safety of this procedure.

Abdominal Injuries↗

PubMed1997

Inhibition of nitric oxide synthesis during severe shock but not after resuscitation increases hepatic injury and neutrophil accumulation in hemorrhaged rats.

Hemorrhagic shock results in hepatocellular dysfunction and hepatic injury that may contribute to the development of liver failure and multiple organ dysfunction in trauma patients. The specific mediators involved in this process remain incompletely defined. We have previously demonstrated that inhibition of nitric oxide (NO) synthesis in a rat model of moderately severe hemorrhagic shock increases hepatic injury, suggesting that NO synthesis is beneficial after hemorrhage. To further define the role of NO in hepatic function during hemorrhagic shock, rats were subjected to a severe hemorrhagic shock insult in which they were bled to a mean arterial pressure of 40 mmHg until 40% of their shed blood had been returned and then were resuscitated. Rats were treated with the NO synthase inhibitor L-nitroarginine methyl ester (L-NAME) or the NO donor S-nitroso-N-acetylpenicillamine beginning either during the hypotensive period or after resuscitation. When instituted during the hypotensive period, low dose L-NAME infusion significantly increased hepatic injury. When L-NAME was infused after resuscitation, no increase in hepatic injury was detected even when the L-NAME dose was increased by a factor of four. The increased hepatic injury produced by L-NAME was associated with increased myeloperoxidase content in the lung, suggesting that L-NAME led to a greater accumulation of neutrophils during shock. Administration of the NO donor S-nitroso-N-acetylpenicillamine reduced hepatocellular enzyme release. Our results suggest that ongoing NO synthesis during the hypotensive phase of hemorrhagic shock is essential in preventing shock-induced hepatic injury and this may be due, in part, to the interaction between NO and circulating neutrophils.

Alanine Transaminase↗

PubMed1996

Metallothionein and HSP-72 are induced in the liver by hemorrhagic shock and resuscitation but not by shock alone.

BACKGROUND: Previous reports have indicated that HSP-72 and metallothionein mRNA undergo induction in the liver after resuscitated hemorrhagic shock. In this study we investigated whether unresuscitated shock triggers induction and whether protein induction also occurs. METHODS: Rats were subjected to resuscitated and unresuscitated shock protocols of varying severity; livers were isolated and processed for Northern, Western, and immunohistochemical analysis. Cadmium binding assay was used to measure metallothionein protein. RESULTS: Unresuscitated shock led to no induction of HSP-72 or metallothionein. Severe resuscitated shock led to prompt induction of HSP-72 mRNA and protein in hepatocytes, up to 20-fold over sham group; metallothionein mRNA induction appeared later than HSP-72 and did not lead to elevated protein levels. Mild resuscitated shock had little effect. CONCLUSIONS: These findings indicate resuscitated severe shock, not shock alone, leads to induction of HSP-72 and metallothionein in the liver. Metallothionein expression lags behind HSP-72 expression.

Animals↗

PubMed1996

Acute aortic dissection after blunt chest trauma.

Medial dissection of the aorta after blunt trauma is a rare occurrence. We report the case of a 79-year-old woman injured in a motor vehicle crash who suffered an acute DeBakey type I aortic dissection.

Accidents, Traffic↗

PubMed1996

Resuscitation from severe hemorrhage.

The potential to be successfully resuscitation from severe traumatic hemorrhagic shock is not only limited by the "golden 1 hr", but also by the "brass (or platinum) 10 mins" for combat casualties and civilian trauma victims with traumatic exsanguination. One research challenge is to determine how best to prevent cardiac arrest during severe hemorrhage, before control of bleeding is possible. Another research challenge is to determine the critical limits of, and optimal treatments for, protracted hemorrhagic hypotension, in order to prevent "delayed" multiple organ failure after hemostasis and all-out resuscitation. Animal research is shifting from the use of unrealistic, pressure-controlled, hemorrhagic shock models and partially realistic, volume-controlled hemorrhagic shock models to more realistic, uncontrolled hemorrhagic shock outcome models. Animal outcome models of combined trauma and shock are needed; a challenge is to find a humane and clinically realistic long-term method for analgesia that does not interfere with cardiovascular responses. Clinical potentials in need of research are shifting from normotensive to hypotensive (limited) fluid resuscitation with plasma substitutes. Topics include optimal temperature, fluid composition, analgesia, and pharmacotherapy. Hypotensive fluid resuscitation in uncontrolled hemorrhagic shock with the addition of moderate resuscitative (28 degrees to 32 degrees C) hypothermia looks promising in the laboratory. Regarding the composition of the resuscitation fluid, despite encouraging results with new preparations of stroma-free hemoglobin and hypertonic salt solutions with colloid, searches for the optimal combination of oxygen-carrying blood substitute, colloid, and electrolyte solution for limited fluid resuscitation with the smallest volume should continue. For titrating treatment of shock, blood lactate concentrations are of questionable value although metabolic acidemia seems helpful for prognostication. Development of devices for early noninvasive monitoring of multiple parameters in the field is indicated. Molecular research applies more to protracted hypovolemic shock followed by the systemic inflammatory response syndrome or septic shock, which were not the major topics of this discussion.

Animals↗

PubMed1995

Hemorrhagic shock.

A great deal has been learned about the pathophysiologic condition of hemorrhagic shock. The response of the hormonal and inflammatory mediator systems in patients in hemorrhagic shock appears to represent a distinct set of responses different from those of other forms of shock. The classic neuroendocrine response to hemorrhage attempts to maintain perfusion to the heart and brain, often at the expense of other organ systems. This intense vasoconstriction occurs via central mechanisms. The response of the peripheral microcirculation is driven by local tissue hypoperfusion that results in vasodilation in the ischemic tissue bed. Activation of the systemic inflammatory response by hemorrhage and tissue injury is an important component of the pathophysiologic condition of hemorrhagic shock. Activators of this systemic inflammatory response include ischemia/reperfusion injury and neutrophil activation. Capillary "no-flow" with prolonged ischemia and "no-reflow" with reperfusion may initiate neutrophil activation in patients in hemorrhagic shock. The mechanisms that lead to decompensated and irreversible hemorrhagic shock include (1) "arteriolar hyposensitivity" as manifested by progressive arteriolar vasodilation and decreased responsiveness of the microcirculation to alpha-agonists, and (2) cellular injury and activation of both proinflammatory and counterinflammatory mechanisms. These changes represent a failure of the microcirculation. Redistribution of cardiac output and persistent gut ischemia after adequate resuscitation may also contribute to the development of irreversible hemorrhagic shock. Treatment of hemorrhagic shock includes rapid operative resuscitation to limit activation of the mediator systems and abort the microcirculatory changes that result from hemorrhagic shock. Volume resuscitation and control of hemorrhage, should occur simultaneously. The end point in volume resuscitation of hemorrhagic shock must be maintenance of organ system and cellular function. Whether we use adequate urine output, correction of lactic acidemia, optimization of oxygen delivery, or oxygen consumption as our specific goal, the general objective is to provide adequate crystalloid solution and packed red blood cells to achieve and maintain normal organ and cellular perfusion and function.

Adrenal Glands↗

PubMed1995

Percutaneous iliosacral screw fixation: early treatment for unstable posterior pelvic ring disruptions.

OBJECTIVE: Open reduction and internal fixation of unstable posterior pelvic ring injury provides better bony stability and less long term morbidity than nonoperative treatment. However, open reduction and internal fixation of the posterior pelvis may involve substantial intraoperative blood loss, reported infection rates of 6 to 25%, and wound complications in 25%. Our hypothesis was that percutaneous cannulated iliosacral screws placed by fluoroscopic control would provide early, rapid, definitive stabilization with minimal blood loss, infection, and wound complications. DESIGN: A retrospective medical record and radiographic study. MATERIALS, METHODS, MEASUREMENTS AND MAIN RESULTS: Twenty consecutive patients with an unstable posterior pelvic ring injury treated by percutaneous fixation (41 screws) under fluoroscopic guidance were reviewed. Average patient age was 34 years, trauma score was 14.4 +/- 3.3, and Injury Severity Score was 22.9 +/- 10.6. Mechanisms were motor vehicle collisions (11), falls (3), crush injury (3), and pedestrian/auto (3). Pelvic injuries were classified as Tile B (5) or Tile C (15). Associated injuries were present in 80%. Seventy-five percent of patients underwent pelvic fixation less than 72 hours after injury with closed percutaneous screw placement achieved in 60%, assisted by open reduction in 25% or aided by anterior external fixation in 15%. Mean operative time was 52 minutes for patients requiring percutaneous screws only (7 of 20 patients, 35%), whereas average blood loss was 233 mL for all cases (including open anterior and posterior procedures). No loss of fixation or wound complications occurred during 9.6 months follow-up. CONCLUSIONS: Percutaneous iliosacral screw fixation for unstable posterior pelvic disruption provided early fixation with minimal operative time, minimal blood loss, and wound-related morbidity.

Adolescent↗

PubMed1995

Benign cervical prevertebral soft tissue swelling in traumatic asphyxia.

Two cases of benign cervical prevertebral soft tissue swelling following traumatic asphyxia are presented. Neither were associated with neck pain, neck tenderness, or mechanism of injury associated with cervical injury, and each resolved spontaneously. Traumatic asphyxia, which results in significant craniofacial swelling, may also result in swelling of the retropharyngeal soft tissues, which may be detected on cervical radiography. Cervical prevertebral soft tissue swelling in the setting of traumatic asphyxia should not be misinterpreted as suggestive of spinal injury in the absence of other findings.

Adult↗

PubMed1995

Evolution of management of major hepatic trauma: identification of patterns of injury.

Nonoperative management of hemodynamically stable patients following blunt hepatic trauma identified by computed tomography (CT) has been reported in up to 20% of patients presenting with hepatic injury, predominantly low grade. We reviewed 128 consecutive adult patients sustaining blunt hepatic trauma with the hypothesis that severe hepatic injuries (grades III to V) could be safely managed nonoperatively and to determine anatomic pattern and severity of hepatic injuries. Sixty-two of the 128 patients (47%) went directly for laparotomy, based on physical findings or positive peritoneal lavage. Sixty-six patients were hemodynamically stable and underwent abdominal CT scanning; 70% (46 of 66) were successfully managed nonoperatively. Fifty-one percent of grade III and IV injuries were treated nonoperatively. However, the majority of patients with grade V injuries were unstable, and 92% required laparotomy. Twenty-six of 46 patients treated nonoperatively (56%) had injury to the posterior segment of the right lobe of the liver or a "split liver." In retrospect, only 33% of patients with hepatic injury required laparotomy for therapy of the liver injury. Hemodynamic stability and anatomic pattern of injury on presentation were important factors in successful nonoperative management of hepatic injury.

Adolescent↗

PubMed1995

Functional outcome of patients with unstable pelvic ring fractures stabilized with open reduction and internal fixation.

An unstable pelvic ring fracture represents a severe injury and is associated with high morbidity and mortality. Little data are available assessing the long-term functional limitations, including disability, in a patient with an unstable pelvic ring fracture. The purpose of this study was to describe the impairment and functional outcome (disability) for patients with unstable pelvic ring fractures managed with open reduction and internal fixation (ORIF). Disability was measured at a minimum of 1 year postinjury using the Sickness Impact Profile (SIP), a measure of the health-related quality of life as perceived by the patient. Of the 230 consecutive patients with a pelvic ring fracture, 54 had unstable fractures requiring ORIF; 48 patients were available at a 1 year follow-up. The follow-up roentgenograms confirmed an osseous union and an anatomic alignment of the pelvis. Thirty-seven (77%) of the patients had mild disability (total SIP < 10); 11 (23%) of the patients had moderate disability (SIP > 10) at 1 year. Of the patients who were employed preinjury, 76% were employed 1 year postinjury; 62% had returned to full time work and 14% had returned with job modification. Of the 7 patients who had been in school, 6 had returned full time and 1 student returned part time. Mean SIP scores for subcategories were: physical health = 6.8 +/- 9.4, psychosocial health = 7.4 +/- 12.7, work = 17.6 +/- 25.5, home management = 8.3 +/- 13.0, ambulation = 10.7 +/- 13.7, and mobility = 5.3 +/- 13.0. Despite the magnitude of the bony injuries, the majority of patients with unstable pelvic ring fractures managed with ORIF had mild disability 1 year postinjury; the majority of the patients had returned to work.

Activities of Daily Living↗

PubMed1995

Inhibition of nitric oxide synthase during hemorrhagic shock increases hepatic injury.

The function of nitric oxide (NO) in hemorrhagic shock is controversial. Increased NO synthesis has been temporally correlated with severe shock and has been associated with vascular hyporeactivity to vasoconstrictor agents in isolated vascular rings. Its role in local tissue perfusion, however, is unknown. We studied the role of NO in shock-induced hepatic injury in a rodent model of decompensated hemorrhagic shock by inhibiting its synthesis with Nw-nitro-L-arginine methyl ester (L-NAME). L-NAME infusion (5 micrograms/kg/min) increased the shock-induced hepatic injury and this effect was reversible with L-arginine. L-NAME had only transient effects on systemic mean arterial blood pressure, which quickly returned to pre-L-NAME levels. We conclude that NO synthesis serves a protective function in preventing shock-induced hepatic injury and we postulate that this effect may be due to modulation of the local hepatic circulation.

Analysis of Variance↗

PubMed1995

Improved outcome with fluid restriction in treatment of uncontrolled hemorrhagic shock.

BACKGROUND: Recent studies have challenged current guidelines for prehospital fluid resuscitation. However, long-term studies evaluating the consequences of fluid restriction in uncontrolled hemorrhagic shock are lacking. This study was done to examine the long-term effects of deliberate hypotension in the treatment of uncontrolled hemorrhage. STUDY DESIGN: Uncontrolled hemorrhagic shock was produced in 40 rats by a preliminary bleed (3 mL per 100 g) followed by 75 percent tail amputation. Experimental design consisted of three phases: a "prehospital phase" (90 minutes of uncontrolled bleeding with or without treatment with lactated Ringer's [LR] solution), followed by a "hospital phase" (60 minutes, including control of hemorrhage and fluid resuscitation including blood), and a three day observation phase. Forty rats were studied in four treatment groups (ten rats per group). Group 1 consisted of untreated controls (no resuscitation). Group 2 had no fluid during the prehospital phase. Group 3 had prehospital resuscitation to a mean arterial pressure (MAP) of 40 mm Hg with LR, and group 4 had prehospital resuscitation to MAP of 80 mm Hg with LR. Groups 2, 3, and 4 received fluid and blood to MAP of 80 mm Hg and hematocrit of 30 percent in the hospital phase. RESULTS: All rats in group 1 (untreated) died within 2.5 hours. Five rats in group 2 (no prehospital FR) survived 90 minutes; however, only one survived three days. In group 3, all ten rats survived 2.5 hours and six survived three days. In group 4, eight rats died within 90 minutes, but none survived long-term. Blood loss (mL per 100 g) for each group was 3.75 0.6 for group 1, 3.35 0.1 for group 2, 4.15 0.8 for group 3, and 8.45 0.6 for group 4, (p < 0.05, group 4 compared with groups 1, 2, and 3). CONCLUSIONS: Attempts to achieve normal MAP during uncontrolled bleeding increased blood loss, hemodilution and mortality. Hypotensive resuscitation resulted in less acidemia and improved long-term survival.

Animals↗