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Raul Coimbra

Publications and source records attributed to Raul Coimbra.

At least 37 records · Page 2Linked to original sources

The use of recombinant factor VIIa for severe intractable bleeding during spine surgery.

STUDY DESIGN: A report on the use of recombinant activated factor VII in 4 patients who developed severe intractable bleeding and coagulopathy during spine surgery. OBJECTIVE: To describe the role of recombinant activated factor VII for hemostasis during spine surgery. SUMMARY OF BACKGROUND DATA: Recombinant activated factor VII is indicated for the treatment of bleeding episodes and the prevention of bleeding during surgery in patients with hemophilia with inhibitors. However, its use in adults undergoing spine surgery has not yet been reported. METHODS: Four patients who underwent multilevel spine surgery through an anterior approach incurred massive bleeding and subsequently became coagulopathic. Standard hemostatic techniques were performed and blood products were transfused. Persistence of the bleeding prompted the use of recombinant activated factor VII. RESULTS: Treatment with recombinant activated factor VII led to an improvement in prothrombin time and partial thromboplastin time and brought about cessation in gross, nonsurgical bleeding intraoperatively. No clinically relevant thrombotic complications related to the drug were noted. CONCLUSIONS: Recombinant activated factor VII is promising as an adjunctive hemostatic agent for patients with perioperative bleeding problems during spine surgery. Efficacy is seen even at low doses.

Adult↗

Acute cholecystitis with a hemocholecyst as an unusual presentation of gallbladder cancer: report of a case.

Several atypical presentations of gallbladder carcinoma have been reported, but one of the rarest is intraluminal hemorrhage. We report a case of carcinoma of the gallbladder disclosed by an emergency cholecystectomy, performed for acute cholecystitis caused by a hemocholecyst. The diagnostic approaches and characteristics of a hemocholecyst associated with carcinoma of the gallbladder are discussed.

Adenocarcinoma↗

Osmotic regulation of cell function and possible clinical applications.

Inflammation and immunosuppression can cause acute respiratory distress syndrome, multiple organ failure, and sepsis, all of which are lethal posttraumatic complications in trauma patients. Prevention of the inflammation and immunosuppression has been a main focus of trauma researcher for many years. Recently, hypertonic resuscitation has attracted attention as a possible therapeutic approach to counteract such deleterious immune responses in trauma patients. We have begun to understand how hypertonic fluids affect immune cell signaling, and a number of experimental and clinical studies have started to reveal valuable information on the clinical efficacy and the limitations of hypertonic resuscitation fluids. Knowledge of how osmotic cues regulate immune cell function will enable us to fully exploit the clinical potential of hypertonic resuscitation to reduce inflammatory and anergic complications in trauma patients.

Animals↗

The epidemiology of serious and fatal injury in San Diego County over an 11-year period.

BACKGROUND: Analysis of the mechanism and severity of injury over time may permit a more focused planning of acute care and trauma prevention programs. METHODS: A retrospective, population-based study examining severe traumatic injury in a single county was undertaken. Three overlapping data sets were used to form a composite injury data set. RESULTS: There were 55,664 patients included in the study. A total of 40,897 (73.5%) patients survived and 14,767 (26.5%) died. Of those patients who died, 8,910 (60.3%) died in the field and were not transported to a trauma center. There was an increase in the mean age of all trauma victims (3 years) and an increase of 5 years in fatally injured patients. The mean Injury Severity Score decreased from 14.7 to 11.6 (p < 0.01); however, Injury Severity Score for fatal patients remained constant (39.7). The overall injury rate remained unchanged (195 per 10(5)), whereas the fatal injury rate decreased by 22% (45.9 per 10(5)) over the 11-year study period. The leading cause of injury was motor vehicle crash, followed by assault. The leading cause of fatal injury was suicide, followed by homicide. CONCLUSION: A combination of three independent injury data sources generated a composite data set of serious and fatal injury. This regional injury analysis was the most comprehensive overview of injury in our region. Important observations included the following: there has been no change in the overall incidence of severe injury within our county; the incidence of fatal traumatic injury has significantly decreased; the leading causes of nonfatal injury do not correlate with the rank order of fatal injury; intentional injury was the leading cause of injury deaths; and scene fatalities represent a poorly studied group of patients who may benefit from primary prevention and injury control research.

Accidents, Traffic↗

Inhibition of enteral enzymes by enteroclysis with nafamostat mesilate reduces neutrophil activation and transfusion requirements after hemorrhagic shock.

BACKGROUND: The gut origin of the inflammatory response in trauma patients has been difficult to define. "In vivo" generation of neutrophil-activating factors by gut proteases may be a cause of multiorgan failure after hemorrhagic shock, and can be prevented with the serine protease inhibitor nafamostat mesilate (Futhan). The objective of this study was to determine the effect of nafamostat mesilate given by enteroclysis on enteric serine protease activity, neutrophil activation, and transfusion requirements during hemorrhagic shock. METHODS: Sixteen pigs weighing 21 to 26 kg were divided into control and treatment groups. A laparotomy was performed under anesthesia, and catheters were placed in the duodenum, midjejunum, and terminal ileum. Pigs were bled 30 mL/kg over 30 minutes and maintained at a mean arterial pressure of 30 mm Hg for 60 minutes. Shed blood was then used to maintain a mean arterial pressure of 45 mm Hg for another 3 hours. Treated animals received 100 mL/kg of 0.37 mmol/L nafamostat mesilate in GoLYTELY through the duodenal catheter at 1 L/h. Control animals received GoLYTELY only. Samples of enteral content and blood were taken at baseline, after shock, and at 30-minute intervals during resuscitation. Animals were killed after 3 hours of resuscitation. Enteral trypsin-like activity at the three gut sites was measured by spectrophotometry. Activation of naive human neutrophils by pig plasma was measured by the percentage of cells having pseudopods larger than 1 microm on microscopy. Lung, liver, and small bowel were analyzed by histology and myeloperoxidase assay. RESULTS: Both control and nafamostat mesilate-treated groups had significant reductions in protein and protease levels in the duodenum during enteroclysis; however, only nafamostat mesilate-treated animals had persistent suppression of protease activity throughout the experiment. Nafamostat mesilate-treated animals had a lower transfusion requirement of shed blood, 18.1 +/- 4.5 mL/kg versus 30 +/- 0.43 mL/kg (p = 0.002). Nafamostat mesilate-treated animals had significantly less neutrophil activation than controls at 150 minutes after resuscitation (33.7 +/- 6.48% vs. 42.4 +/- 4.57%,p = 0.01) and 180 minutes after resuscitation (31.1 +/- 3.31% vs. 46.9 +/- 4.53%, p = 0.0002). Lung myeloperoxidase activity was lower in nafamostat mesilate-treated animals (0.31 +/- 0.14) than in control animals (0.16 +/- 0.04, p = 0.04). Histology of liver and small intestine showed less injury in nafamostat mesilate-treated animals. CONCLUSION: Nafamostat mesilate given by means of enteroclysis with GoLYTELY significantly reduces enteral protease levels, leukocyte activation, and transfusion requirements during resuscitation from hemorrhagic shock. This strategy may have clinical promise.

Animals↗

The effect of age on functional outcome in mild traumatic brain injury: 6-month report of a prospective multicenter trial.

OBJECTIVE: Elderly patients (aged 60 years and older) have been demonstrated to have an increased mortality after isolated traumatic brain injury (TBI); however, the prognosis of those patients surviving their hospitalization is unknown. We hypothesized that surviving elderly patients would also have decreased functional outcome, and this study examined the functional outcome of patients with isolated TBI at discharge and at 6 months posthospitalization. METHODS: This was a multicenter prospective study of all patients with isolated moderate to severe TBI defined as Head Abbreviated Injury Scale score of 3 with an Abbreviated Injury Scale score in any other body area of 1. Patients surviving to discharge gave their consent and were enrolled. Data collected included demographics, Glasgow Coma Scale (GCS) score at admission, and neurosurgical interventions. Outcome data included discharge disposition and Glasgow Outcome Scale score and modified Functional Independence Measure (FIM) score at discharge and at 6 months. RESULTS: Two hundred thirty-five patients were enrolled, with 44 (19%) aged greater than or equal to 65 years. Mechanisms of injury were falls (34%), assaults (28%), motor vehicle collisions (14%), pedestrian (11%), and other (12%). Falls were more common in the older patients and assaults in the younger group. The mean admitting GCS score was 12.8 (95% confidence interval [CI], 12.4-13.3), with older patients having a higher mean GCS score, 14.1 (95% CI, 13.6-14.6) versus 12.5 (95% CI, 12.0-13.1; p = 0.03). There were no differences in the percentage of patients admitted to the intensive care unit or requiring neurosurgical intervention between younger and older patients. Because there were few elderly patients with low GCS scores who survived to discharge, outcome measures focused on those patients with GCS scores of 13 to 15. A greater percentage of elderly were discharged to rehabilitation (28% vs. 16%, p =0.08). The mean discharge FIM score was 10.4 (95% CI, 9.8-11.0) for the elderly versus 11.4 (95% CI, 11.1-11.7) for the young (p =0.001), with 68% elderly and 89% young discharged with total independent scores of 11 to 12. At 6 months, the difference narrowed, but the mean FIM score was still greater for the young group, 11.7 (95% CI, 11.6-11.9) versus 11.0 (95% CI, 10.6-11.4; p < 0.001). CONCLUSION: Functional outcome after isolated mild TBI as measured by the Glasgow Outcome Scale and modified FIM is generally good to excellent for both elderly and younger patients. Older patients required more inpatient rehabilitation and lagged behind their younger counterparts but continued to recover and improve after discharge. Although there were statistically significant differences in the FIM score at both discharge and 6 months, the clinical importance of these small differences in the mean FIM score to the patient's quality of life is less clear. Measurable improvement in functional status during the first 6 months after injury is observed in both groups. Aggressive management and care of older patients with TBI is warranted, and efforts should be made to decrease inpatient mortality. Continued follow-up is ongoing to determine whether these outcomes persist at 12 months.

Abbreviated Injury Scale↗

LPS-stimulated PMN activation and proinflammatory mediator synthesis is downregulated by phosphodiesterase inhibition: role of pentoxifylline.

BACKGROUND: Excessive production of reactive oxygen species by PMN is associated with tissue damage during inflammation. LPS interacts with the cell surface receptor CD14, which generates transmembrane signals through Toll-like protein 4 leading to mitogen activated protein kinase (MAPK) p38 activation, cytokine synthesis, PMN beta2-integrin expression and oxidative burst. Phosphodiesterase inhibition decreases proinflammatory cytokine production and tissue injury after LPS challenge. Its effects on PMN function after LPS stimulation, however, have not been fully investigated. We hypothesized that LPS-induced TNF-alpha synthesis and subsequent PMN beta2-integrin expression and oxidative burst are downregulated by concomitant treatment with the non-specific phosphodiesterase inhibitor pentoxifylline (PTX). METHODS: Whole blood was incubated with HBSS (control), LPS (100 microg/mL), fMLP (1 micromol/L), LPS+PTX (2 mmol/L) and fMLP+PTX for different time intervals at 37C. Oxidative burst, CD14, and CD-11b expression were measured by flow cytometry. Serum TNF-alpha levels were measured by ELISA. In an attempt to localize the site of action of PTX (proximal or distal to PKC) cell surface receptors were bypassed by PMA stimulation (1 microg/mL) and oxidative burst was measured with and without PTX. RESULTS: Up-regulation of CD14 expression was similar in LPS and LPS+PTX groups. LPS stimulation caused a significant increase in PMN oxidative burst, CD11b expression, and TNF-alpha serum levels. In addition, PMA and fMLP stimulation also caused significant increase in oxidative burst compared with controls. Concomitant addition of PTX to LPS led to a significant decrease in PMN oxidative burst (65%; p < 0.0001), PMN CD11b expression (20%; p = 0.012), and TNF-alpha levels (93%; p < 0.0001). Also, PMA- and fMLP-induced PMN oxidative burst were significantly decreased by PTX [77.5% (p < 0.0001) and 50% (p < 0.01), respectively]. CONCLUSIONS: These results suggest that PTX-inhibition of oxidative burst occurs distal to PKC and may be either due to direct inhibition of NADPH oxidase or inhibition of MAPK phosphorylation, leading to decreased adhesion molecule expression and TNF-alpha synthesis. Its use in clinical scenarios in which PMN are primed may be of clinical relevance.

Analysis of Variance↗

Resuscitation affects microcirculatory polymorphonuclear leukocyte behavior after hemorrhagic shock: role of hypertonic saline and pentoxifylline.

We have previously shown that lung injury following fluid resuscitation either with hypertonic saline (HS) or lactated Ringer's (LR) plus pentoxifylline (PTX) attenuated acute lung injury when compared with LR resuscitation. The objective of the present study is to determine whether our previous observations are accompanied by changes in polymorphonu-clear leukocyte (PMN) behavior. To study this, PMN-endothelial cell interactions, microcirculatory blood flow, lung histology, lung PMN infiltration (MPO, Myeloperoxidase), and lung intra-cellular adhesion molecule-1 (ICAM-1) expression were assessed in a controlled hemorrhagic shock model followed by LR, HS, and LR+PTX resuscitation in rodents. Rats (240-300 g) were bled to a mean arterial pressure (MAP) of 35 mm Hg for 1 hr and then randomized into three groups: HS (7.5% NaCl, 4 ml/kg); LR (3x shed blood); and LR+PTX (25 mg/kg). Additionally, total shed blood was reinfused. A sham group underwent no shock and no treatment. The internal spermatic fascia was exteriorized and the microcirculation was observed by closed-circuit TV coupled to a microscope, 2 and 6 hrs after treatment. The number of leukocytes sticking to the venular endothelium was determined 2 hrs after fluid resuscitation. Microcirculatory blood flow was measured by an optical Doppler velocimeter. Lung histology and lung MPO immunostaining were assessed at 6 hrs, and lung ICAM-1 expression was determined by immunostaining at 2 hrs following fluid resuscitation. Two hours after treatment, HS (1.4 +/- 0.4), LR+PTX (1.7 +/- 0.3), and sham (0.4 +/- 0.2) groups presented significant reductions in leukocyte adherence (cells/100 microm venule length), compared with the LR group (4.0 +/- 0.9, P < 0.05). No differences were observed 6 hrs after treatment on leukocyte adherence and microcirculatory blood flow. ICAM-1 expression was significantly higher in LR-treated animals compared with the HS, LR+PTX, and sham groups (P < 0.01). PMN infiltration and overall lung injury were significantly attenuated by HS and LR+PTX. These results support earlier studies that indicated the potential application of HS and PTX in shock therapy and the increase in PMN-endothelial cell interaction and lung injury after LR resuscitation.

Animals↗

Intraarterial pulmonary pentoxifylline improves cardiac performance and oxygen utilization after hemorrhagic shock: a novel resuscitation strategy.

UNLABELLED: The role of pentoxifylline (PTX) as a resuscitation adjunct in hemorrhagic shock is unclear. PTX infusion into the pulmonary artery and its effects on cardiac performance and oxygen utilization have not been defined. We hypothesized that pulmonary PTX is superior to systemic PTX or lactated Ringer's (LR) solution alone. The effects of LR solution, systemic PTX, and pulmonary PTX on cardiac performance and oxygen utilization in a hemorrhagic shock model in dogs were compared. Animals were bled to a mean arterial blood pressure (MAP) of 40 mm Hg maintained for 30 min and randomized into 3 resuscitation groups: LR solution (2x shed blood), systemic PTX (10 mg/kg bolus i.v.) in addition to LR solution (2x shed blood) + PTX (5 mg/kg for 45 min i.v.), and pulmonary PTX (10 mg/kg bolus + 5 mg/kg for 45 min via a pulmonary artery catheter) plus LR solution (2x shed blood, i.v.). Arterial blood gases, hemoglobin levels, MAP, cardiac index, systemic vascular resistance index, pulmonary vascular resistance index, oxygen delivery, oxygen consumption, and oxygen extraction ratio (O(2)ER) were measured serially. No differences in blood loss, hemoglobin, and MAP were observed. Pulmonary PTX increased cardiac index to levels more than baseline (P = 0.012) and decreased systemic vascular resistance index and pulmonary vascular resistance index to levels less than baseline (P < 0.0001). Pulmonary PTX increased oxygen delivery and oxygen consumption to baseline levels. Postresuscitation O(2)ER levels in LR-treated animals remained more than baseline (P < 0.0001). Systemic and pulmonary PTX significantly decreased O(2)ER compared with shock levels. PTX resuscitation is superior compared with LR solution alone. Intraarterial pulmonary PTX administration is safe, and improves cardiac performance as well as O(2) utilization. IMPLICATIONS: This study shows that a novel route (via the pulmonary circulation) used to administer pentoxifylline after hemorrhagic shock leads to superior cardiac performance in comparison with administration via lactated Ringer's solution or i.v. systemic pentoxifylline.

Animals↗

Pentoxifylline reduces acute lung injury in chronic endotoxemia.

BACKGROUND: Pentoxifylline (PTX) attenuates end-organ injury in models of sepsis and hemorrhage. PTX is thought to act by inhibiting phosphodiesterase, thus increasing cAMP and decreasing tumor necrosis factor-alpha (TNF-alpha) synthesis. The effects of PTX on neutrophil and endothelial cell adhesion molecules and, ultimately, organ injury in a chronic endotoxemia model have not been studied. We hypothesized that continuous infusion of PTX reduces acute lung injury (ALI) caused by chronic lipopolysaccharide (LPS) exposure. MATERIALS AND METHODS: Male Sprague-Dawley rats were given continuous infusion of LPS, PTX + LPS combined, or saline (sham) by implantable pumps. Neutrophil CD11b expression, lung histopathology, lung intercellular adhesion molecule-1 (ICAM-1) expression assessed by immune staining, serum TNF-alpha, serum interleukin-6 (IL-6), and bronchoalveolar lavage (BAL) IL-8 were evaluated at different time points. Lung injury was graded in a blinded fashion from 0 (normal) to 4 (severe) for interstitial inflammation, neutrophil infiltration, congestion, and edema. Total lung injury score (TLIS) was calculated by adding listed categories. White cell count in the peripheral blood and in the BAL was also performed. RESULTS: Animals treated with PTX + LPS showed a significant reduction in lung injury score, a marked decrease in ICAM-1 expression, and a significant decrease in IL-8 levels in the BAL and serum IL-6 levels when compared with LPS-treated animals. CONCLUSIONS: Continuous infusion of PTX reduces ALI caused by chronic endotoxemia. The effect seems to be a result of decreased expression of endothelial and epithelial ICAM-1 and modulation of proinflammatory cytokine synthesis.

Animals↗

Diagnosis and monitoring of hemorrhagic shock during the initial resuscitation of multiple trauma patients: a review.

The initial management of the multiple trauma victim requires evaluation for potential hemorrhage and ongoing monitoring to assess the efficacy of resuscitation and avoid complications related to hemorrhagic shock. A variety of strategies exist to assess circulatory status, including hemodynamic monitoring, tissue perfusion measurement, and use of serum markers of metabolism. We review available technologies used to assess fluid status and tissue perfusion in patients with blood loss or hemorrhagic shock, discuss how these methods can be used effectively and efficiently during initial trauma resuscitation to guide therapy and disposition, and suggest directions for future research to improve outcomes by providing more appropriate and timely care and avoiding unnecessary complications.

Biomarkers↗

A twelve-year analysis of disease and provider complications on an organized level I trauma service: as good as it gets?

BACKGROUND: The development of trauma systems reduces preventable mortality and the measurement of standardized complications creates further opportunity for improvement in morbidity. The annual incidence of complications in a trauma population has been previously reported but the frequency change over time in a single institution is not well studied. METHODS: All patients who were hospitalized for more than 24 hours, who died, were admitted to the Intensive Care Unit (ICU) or Intermediate Care Unit (IMU), or were inter-facility transfers prospectively evaluated for 12 consecutive years. A total of 13,382 patients were studied (range, 862-1234 patients per year). Complication events were collected using 135 standardized definitions including disease and provider outcomes. RESULTS: The overall incidence of complications has remained stable over time. Provider events, disease events, and patients developing three or more complications have remained unchanged as well. Specific disease complications including pneumonia, deep vein thrombosis (DVT), and small bowel obstruction have fallen over time. Improvements in provider errors have also occurred. CONCLUSION: This data suggests that most complications have a finite threshold despite the use of a stable trauma staff, implementation of standardized protocols, and emphasis on consistency of practice. Further reductions will require new research for disease-related treatment and new strategies for consistency and error reduction rather than our current models of continuous quality improvement.

Academic Medical Centers↗

Characterization of two classes of pancreatic shock factors: functional differences exhibited by hydrophilic and hydrophobic shock factors.

Pancreatic tissue homogenate induces a powerful pathophysiologic response sufficient to produce lethal shock in a rat. However, limited progress has been made in the biochemical characterization of these pancreas-derived active factors or their mechanisms of action. It has been shown that the pancreas is a major source of these shock-inducing factors and that they are generated by pancreatic proteinases. Porcine pancreas was homogenized and the filtered homogenate was subjected to organic extraction both before and after incubation for 2.5 h at 37 degrees C. The aqueous and lipid extracts of pancreatic homogenates were collected and analyzed for their ability to activate human neutrophils and to induce lethal shock in the rat. Neutrophil activation, a presumed hallmark of shock, was determined by chemiluminescence and myeloperoxidase (MPO) release. Only the intact homogenate and lipid extracts stimulated the neutrophils, and the aqueous extracts proved to be inactive. Neutrophils exhibited enhanced cellular activation when exposed to substimulatory levels of either formyl-methionyl-leucyl-phenylalanine (FMLP) or platelet-activating factor (PAF) followed by substimulatory levels of the lipid extracts, but not by the aqueous extracts. Both the lipid and aqueous extracts induced dramatic decreases in heart rate and blood pressure when injected in the rat, often resulting in lethal shock. In all cases, incubation of the homogenates at 37 degrees C enhanced the potency of the extracts. Our results demonstrated that the pancreas-derived homogenate and lipid factors were capable of inducing both neutrophil activation and shock. These results support the hypothesis that shock is produced via neutrophils that have been activated by inflammatory components. However, the shock-inducing factors in the aqueous extracts (i.e., hydrophilic fraction of the homogenate) apparently function via a pathway independent of neutrophil activation. This is the first evidence that there are both hydrophobic and hydrophilic factors generated in tissue homogenates capable of inducing shock, and that these different chemical classes of factors appear to function via separate mechanisms.

Animals↗

Does sexual dimorphism influence outcome of traumatic brain injury patients? The answer is no!

BACKGROUND: The protective effect of female gender on posttraumatic mortality or acute complications after traumatic brain injury (TBI) has been postulated. This effect might be seen if TBIs were analyzed by severity. To assess potential gender effects, we performed a retrospective case-controlled study matching female patients to male counterparts for overall injury severity; hemodynamic status at admission; and head, chest, and abdomen Abbreviated Injury Scale score. METHODS: All female patients sustaining TBI admitted over 6.5 years were reviewed. An overall comparison between women (n = 914) and their male matched counterparts (n = 916) was performed. Patients were then stratified according to the severity of head injury on the basis of admission Glasgow Coma Scale (GCS) score into three groups: group 1, GCS score of 13 to 15 (788 female patients, 769 male patients); group 2, GCS score of 9 to 12 (40 female patients, 42 male patients); and group 3, GCS score < 9 (63 female patients, 87 male patients). Cohorts were compared for mortality or the development of acute respiratory distress syndrome, pneumonia, and systemic sepsis using standard definitions. A subset analysis was performed excluding patients with age above 50 years (789 women, 811 men) to exclude the effects of menopause on the results. RESULTS: There was no statistically significant difference in outcome overall or in subset analysis of mild (group 1), moderate (group 2), or severe (group 3) TBI. The exclusion of patients older than 50 years showed no protective effect of female gender on outcome. CONCLUSION: Gender does not play a role in posttraumatic mortality or in the incidence of acute complications after any degree of TBI.

Adolescent↗

Female gender does not protect blunt trauma patients from complications and mortality.

BACKGROUND: The protective effect of gender on posttraumatic mortality or acute complications (acute respiratory distress syndrome [ARDS], pneumonia, and sepsis) is unclear. To assess potential effects, we performed a retrospective case-controlled study, matching patients for injury factors including overall severity (Injury Severity Sscore), the presence of shock (systolic blood pressure [SBP] < 90 mm Hg) at admission, and the presence of closed head injury (CHI). METHODS: All female patients admitted over a 61/2-year period were reviewed and divided into four groups: group 1, SBP > 90, no CHI; group 2, SBP < 90, no CHI; group 3, SBP > 90, with CHI; and group 4, SBP < 90, with CHI. Each cohort was matched one to one with an equivalent male counterpart. Cohorts were compared for mortality or the development of ARDS, pneumonia, and systemic sepsis using standard definitions. RESULTS: Overall, 1,229 female patients were identified for study. The average Injury Severity Score was 16.3 and overall mortality was 2.7%. Analysis of the groups described previously demonstrated no statistically significant difference in the development of ARDS, pneumonia, systemic sepsis, or overall mortality between male and female patients including patients presenting with shock, CHI, or both. CONCLUSION: We conclude that female gender offers no protection from the development of ARDS, pneumonia, sepsis, or decreased mortality after blunt trauma.

Adolescent↗

Intestinal lymphoma causing intussusception in HIV(+) patient: a rare presentation.

Ten-percent of all malignancies affecting the HIV(+) patient population are lymphomas. Lymphoma involving the gastrointestinal tract may be more common than anticipated in this select group of patients. Because this patient population is frequently seen by the surgeon for abdominal complaints, the diagnosis of enteric lymphoma should be entertained and the general surgeons should be aware of its frequency. We report a case of intussusception caused by enteric lymphoma in an HIV(+) patient.

Adult↗