TNF receptor I mediates chemokine production and neutrophil accumulation in the lung following systemic lipopolysaccharide.

BACKGROUND: Tumor necrosis factor (TNF)-alpha is a critical effector of lipopolysaccharide (LPS)-induced acute lung injury, and its effects are mediated by two structurally related receptors, RI and RII. Cellular adhesion molecules and C-X-C chemokines (Keratinocyte chemoattractant (KC) and macrophage inflammatory protein [MIP]-2) regulate tissue neutrophil polymorphonuclear neutrophil (PMN) accumulation in a multitude of inflammatory states. We hypothesized that TNFRI signaling dictates PMN accumulation in the lung via regulation of chemokine molecule production. Therefore, the purposes of this study were to (1) delineate LPS-induced lung TNF-alpha production and (2) characterize the contribution of both TNF receptors to lung chemokine production and neutrophil influx following systemic LPS. METHODS: Wild-type or TNFRI and TNFRII knockout (KO) mice were injected with vehicle (saline) or LPS (Escherichia coli 0.5 mg/kg intraperitoneally). After 2, 4, 6, or 24 h, lungs were analyzed for TNF-alpha and chemokine (KC and MIP-2) protein expression (enzyme-linked immunosorbent assay) and PMN accumulation (myeloperoxidase assay). RESULTS: There was an increase in total lung TNF-alpha (vehicle, 5.0 +/- 1.2 pg/mg total protein vs LPS, 950 +/- 318; P < 0.05) after LPS. Lung chemokine production and PMN accumulation were also increased compared to vehicle-injected mice. Lung chemokine production and PMN accumulation were significantly lower in TNFRI KO, but not TNFRII KO, mice, despite no difference in TNF-alpha production (TNFRI KO, 925 +/- 301 vs TNFRII KO, 837 +/- 267, P = 0.82). CONCLUSIONS: Acute lung injury following systemic LPS administration is characterized by increased lung (1) TNF-alpha production, (2) C-X-C chemokine production, and (3) neutrophil accumulation. The maximal effect of LPS-induced lung neutrophil accumulation appears to be dependent upon the TNFRI receptor but not the TNFRII receptor. .

Life-threatening dog attacks: a devastating combination of penetrating and blunt injuries.

BACKGROUND/PURPOSE: Children often are the victims of dog attacks. Although bite injuries sustained in an attack characteristically are attributed to the penetrating component of the bite, the blunt nature of a bite may represent the most serious and devastating component of injury. The purpose of this study was to characterize a group of children suffering life-threatening dog bites and examine the predominant aspect of injury. METHODS: Thirty-nine children were admitted to the trauma service at a regional pediatric trauma center with the diagnosis of dog bite injury over a 6-year period (1994 through 1999). Patient demographics, site and description of injury, and surgical procedures performed were recorded from a chart review. RESULTS: Mean age of the 35 children included for analysis was 5.4 years (range, 0.8 to 17 years). Twenty-five (71%) injuries occurred in the head and neck region. Eight (23%) children sustained life-threatening injuries. Of these, blunt force was the predominant injury in 6. This resulted in 1 (20%) arterial occlusion requiring vascular reconstruction, 2 (40%) permanent neurologic injuries (stroke, spinal cord transection), and 1 (20%) death (exsanguination). CONCLUSIONS: On evaluation of a dog attack, the focus generally is on the obvious penetrating aspect of the bite. Yet, we found the blunt component of injury can have devastating consequences reflected in acute arterial, brain, and spinal cord injury. Even in the absence of significant penetrating trauma, further evaluation should be considered to exclude occult blunt arterial or neurologic injury.

Suppression of tumor necrosis factor alpha production by cAMP in human monocytes: dissociation with mRNA level and independent of interleukin-10.

BACKGROUND: Elevation of cellular cAMP inhibits lipopolysaccharide(LPS)-stimulated tumor necrosis factor alpha (TNF-alpha) production and increases the expression of interleukin (IL)-10 in mononuclear cells. TNF-alpha gene expression obligates activation of the transcription factor nuclear factor kappaB (NF-kappaB). Exogenous IL-10 inhibits NF-kappaB in monocytes and thus attenuates TNF-alpha production. We examined the role of endogenous IL-10 in the regulation of NF-kappaB activation and TNF-alpha production in human monocytes by cAMP. METHODS: Human monocytes were stimulated with Escherichia coli LPS (100 ng/ml) with and without forskolin (FSK, 50 microM) or dibutyryl cyclic AMP (dbcAMP, 100 microM). Cytokine (TNF-alpha and IL-10) release was measured by immunoassay. TNF-alpha mRNA was measured by reverse transcription polymerase chain reaction, and NF-kappaB DNA binding activity was assessed by gel mobility shift assay. RESULTS: cAMP-elevating agents inhibited LPS-stimulated TNF-alpha release (0.77 +/- 0.13 ng/10(6) cells in LPS + dbcAMP and 0.68 +/- 0.19 ng/10(6) cells in LPS + FSK, both P < 0.05 vs 1.61 +/- 0.34 ng/10(6) cells in LPS alone). Conversely, cAMP enhanced LPS-stimulated IL-10 release (100 +/- 21.5 pg/10(6) cells in LPS + dbcAMP and 110 +/- 25.2 pg/10(6) cells in LPS + FSK, both P < 0.05 vs 53.3 +/- 12.8 pg/10(6) cells in LPS alone). Neither TNF-alpha mRNA expression nor NF-kappaB activation stimulated by LPS was inhibited by the cAMP-elevating agents. Neutralization of IL-10 with a specific antibody did not attenuate the effect of cAMP-elevating agents on TNF-alpha production. CONCLUSION: The results indicate that cAMP inhibits LPS-stimulated TNF-alpha production through a posttranscriptional mechanism that is independent of endogenous IL-10.

The synergistic relationship between a level I trauma center and a regional pediatric trauma center.

A regional pediatric trauma center and a level I trauma center with pediatric commitment in the same city developed a synergistic relationship addressing all aspects of care for pediatric trauma patients. Although it is unlikely that this model could be used in its entirety by all similar institutions, the principles may prove helpful in creating guidelines and relationships. Categorization, optimal use of resources, timely transportation of seriously injured children to the appropriate facility, and maintaining urgent care capabilities of each institution to care for seriously injured children are imperative. The combined effort resulted in our level I trauma center being verified by the American College of Surgeons and designated by our state Health Department as meeting all the criteria for pediatric trauma care. This experience should encourage every pediatric trauma center located in a children's hospital to become a regional pediatric trauma center. The real benefit from the relationship is that injured children receive optimal care at both institutions.

L-arginine attenuates lipopolysaccharide-induced lung chemokine production.

Chemokines stimulate the influx of leukocytes into tissues. Their production is regulated by nuclear factor-kappaB (NF-kappaB), an inducible transcription factor under the control of inhibitory factor kappaB-alpha (IkappaB-alpha). We have previously demonstrated that L-arginine (L-Arg) attenuates neutrophil accumulation and pulmonary vascular injury after administration of lipopolysaccharide (LPS). We hypothesized that L-Arg would attenuate the production of lung chemokines by stabilizing IkappaB-alpha and preventing NF-kappaB DNA binding. We examined the effect of L-Arg on chemokine production, IkappaB-alpha degradation, and NF-kappaB DNA binding in the lung after systemic LPS. To block nitric oxide (NO) production, a NO synthase inhibitor was given before L-Arg. LPS induced the production of chemokine protein and mRNA. L-Arg attenuated the production of chemokine protein and mRNA, prevented the decrease in IkappaB-alpha levels, and inhibited NF-kappaB DNA binding. NO synthase inhibition abolished the effects of L-Arg on all measured parameters. Our results suggest that L-Arg abrogates chemokine protein and mRNA production in rat lung after LPS. This effect is dependent on NO and is mediated by stabilization of IkappaB-alpha levels and inhibition of NF-kappaB DNA binding.

Neonatal cholestasis.

In simplest terms, cholestasis is defined as a decrease in bile flow. The clinical manifestations of cholestasis occur because of accumulation of substances normally excreted in the bile; namely bilirubin, bile acids, and cholesterol. Accumulation of bilirubin leads to jaundice and dark urine. Accumulation of bile acids is associated with pruritus, and accumulation of cholesterol causes hypercholesterolemia and xanthomas. There are many causes of cholestasis in early infancy ranging from normal physiologic jaundice to complete biliary obstruction associated with biliary atresia.

Cervical spine trauma in the injured child: a tragic injury with potential for salvageable functional outcome,.

BACKGROUND/PURPOSE: Cervical spine injuries are uncommon in children, and, therefore, presumptive immobilization and diagnosis remain controversial. The purpose of this study was to review the author's experience with cervical spine injuries in children to determine the incidence, injury mechanism, pattern of injury, and subsequent functional outcome. METHODS: Fifty-two children over a 6-year period (1994 to 1999) with a cervical spine injury secondary to blunt trauma were identified (1.3% incidence). The functional independent measure (FIM) was assessed at the time of discharge in each of 3 categories: communication, feeding, and locomotion. RESULTS: Mean age of the study children was 10.7 +/- 0.7 years. Eight children (15%) were less than 5 years old, and 4 (8%) were less than 2 years old. The mechanism of injury included motor vehicle crash (52%), falls (15%), bicycle accidents (11%), sports-related injuries (10%), pedestrian accidents (8%), and motorcycle crashes (4%). Seven patients died yielding an overall mortality rate of 13%. Injuries were distributed along the cervical spinal cord as follows: 5 atlanto-occipital dislocations, 28 C1 to C3 injuries, 17 C4 to C7 injuries, and 2 ligamentous injuries. FIM scores were recorded for 18 patients. Seventeen communicated independently, 14 fed themselves independently, and 12 had independent locomotive function. CONCLUSIONS: Cervical spine injuries occur in children across a spectrum of ages. Although atlanto-occipital dislocation is a highly lethal event, children with C1 to C7 injuries have a high likelihood of reasonable independent functioning.

Thirty years of clinical trials in acute respiratory distress syndrome.

OBJECTIVE: To systematically review clinical trials in acute respiratory distress syndrome (ARDS). DATA SOURCES: Computerized bibliographic search of published research and citation review of relevant articles. STUDY SELECTION: All clinical trials of therapies for ARDS were reviewed. Therapies that have been compared in prospective, randomized trials were the focus of this analysis. DATA EXTRACTION: Data on population, interventions, and outcomes were obtained by review. Studies were graded for quality of scientific evidence. MAIN RESULTS: Lung protective ventilator strategy is supported by improved outcome in a single large, prospective trial and a second smaller trial. Other therapies for ARDS, including noninvasive positive pressure ventilation, inverse ratio ventilation, fluid restriction, inhaled nitric oxide, almitrine, prostacyclin, liquid ventilation, surfactant, and immune-modulating therapies, cannot be recommended at this time. Results of small trials using corticosteroids in late ARDS support the need for confirmatory large clinical trials. CONCLUSIONS: Lung protective ventilator strategy is the first therapy found to improve outcome in ARDS. Trials of prone ventilation and fluid restriction in ARDS and corticosteroids in late ARDS support the need for large, prospective, randomized trials.

Chemokines as mediators of diseases related to surgical conditions.

Chemokines are important mediators of inflammation. Animal studies suggest that inhibition of chemokine action results in a decrease in inflammation. Novel anti-inflammatory agents directed against chemokines are now available. Surgeons are uniquely positioned to treat multiple chemokine-mediated diseases. In this article, we review the biology and nomenclature of chemokines as well as their role in neutrophil migration. Further, the potential role of chemokines in various diseases related to surgical conditions, including adult respiratory distress syndrome, atherosclerosis, inflammatory bowel disease, and solid organ rejection, is reviewed. Finally, the idea that chemokines could be targets for novel therapeutic agents is discussed.

Operative management of injured children at an adult level I trauma center.

BACKGROUND: The geographic distribution of trauma centers results in a significant number of children being treated in adult centers. The emphasis on nonoperative management of pediatric blunt trauma has heightened concern that in adult trauma centers, an aggressive operative approach will continue to be used. We hypothesized that pediatric commitment at a Level I trauma center results in appropriate nonoperative care of injured children as established by regional pediatric trauma centers. METHODS: The records of 1,792 consecutively treated children admitted to the trauma service during a 6-year period (January of 1990 to December of 1995) were reviewed. Patients were stratified into one of three age groups: 0 to 5, 6 to 11, and 12 to 17 years of age. RESULTS: Mean age of the study patients was 10.0 +/- 0.1 years, 1,147 were boys (64%), and their mean Injury Severity Score was 7.3 +/- 0.3. The injury mechanism was blunt in 1,550 (87%) and 132 (7%) required laparotomy. In the 0- to 5-year-old blunt mechanism group, 6% underwent laparotomy or thoracotomy from 1990 to 1992. In comparison, only 1% of this age group had a laparotomy from 1993 to 1995 (p < 0.05, Fisher's exact test). A similar trend was found in the 6- to 11-year-old children after blunt injury (4% laparotomy rate from 1990 to 1992; 2% from 1993-1995). CONCLUSION: There has been a declining trend in the operative management of blunt pediatric trauma, especially in children less than 6 years old, whereas the operative management of penetrating injuries has remained stable. These data confirm that pediatric commitment in a Level I trauma center results in nonoperative treatment of injured children commensurate with that established in regional pediatric trauma centers.

Differential inducible nitric oxide synthase expression in systemic and pulmonary vessels after endotoxin.

Inducible nitric oxide synthase (iNOS) is associated with vascular hypocontractility in systemic vessels after endotoxin lipopolysaccharide (LPS) administration. Although lung iNOS is increased after LPS, its role in the pulmonary circulation is unclear. We hypothesized that whereas iNOS upregulation is responsible for LPS-induced vascular dysfunction in systemic vessels, iNOS does not play a significant role in the pulmonary artery (PA). Using isolated aorta (AO) and PA rings, we examined the effect of nonselective NOS inhibition [N(G)-monomethyl-L-arginine (L-NMMA); 100 micromol/l] and selective iNOS inhibition (aminoguanidine, AG; 100 micromol/l) on alpha(1)-adrenergic-mediated vasoconstriction (phenylephrine; 10(-9) to 10(-3) M) after LPS (Salmonella typhimurium, 20 mg/kg ip). We also determined the presence of iNOS using Western blot and immunohistochemistry. LPS markedly impaired AO contractility (maximal control tension 1,076 +/- 33 mg vs. LPS 412 +/- 39 mg, P < 0.05), but PA contractility was unchanged (control 466 +/- 29 mg vs. LPS 455 +/- 27 mg, P > 0.05). Selective iNOS inhibition restored the AO's response to vasoconstriction (LPS + AG 1,135 +/- 54 mg, P > 0.05 vs. control and P < 0.05 vs. LPS), but had no effect on the PA (LPS + AG 422 +/- 38 mg, P > 0.05 vs. control and LPS). Western blot and immunohistochemistry revealed increased iNOS expression in the AO after LPS, but iNOS was not detected in the PA. Our results suggest that differential iNOS expression after LPS in systemic and pulmonary vessels contributes to the phenomenon of sepsis/endotoxemia-induced systemic hypotension and pulmonary hypertension.

Nonoperative management of solid organ injuries in children results in decreased blood utilization.

BACKGROUND: The administration of blood products to injured children has been recognized as a potential risk of nonoperative management. The purpose of this study was to evaluate blood utilization in the management of solid organ injuries in pediatric blunt abdominal trauma victims. METHODS: One hundred sixty-one children (< or =16 years old) with solid organ injuries over an 8-year study period (1990 through 1997) were identified from the trauma registries at 2 urban regional trauma centers. RESULTS: Mean age of the study patients was 7.9+/-0.4 years, 95 (59%) were boys, and their mean injury severity score (ISS) was 17.8+/-1.2. Patients were divided into 4-year study cohorts (1990 through 1993 and 1994 through 1997) to examine changes in operative management and blood utilization. For each time period examined, those treated nonoperatively received fewer blood transfusions (46% v 9% and 44% v 13%, P<.05 by Fisher's Exact test), and the hospital length of stay was shorter (12.3+/-2.1 v 5.0+/-0.7 and 7.8+/-1.9 v 4.2+/-0.4 days, P<.0001 by analysis of variance/Scheffe's) compared with the laparotomy cohort. CONCLUSIONS: The appropriate nonoperative management of injured children actually reduces the risks of receiving blood transfusion and decreases the length of hospital stay compared with aggressive operative intervention. Blood transfusion should be reserved only for those injured children with solid organ injuries who are hemodynamically unstable.

Inhibition of PARS attenuates endotoxin-induced dysfunction of pulmonary vasorelaxation.

Endotoxin (Etx) causes excessive activation of the nuclear repair enzyme poly(ADP-ribose) synthase (PARS), which depletes cellular energy stores and leads to vascular dysfunction. We hypothesized that PARS inhibition would attenuate injury to mechanisms of pulmonary vasorelaxation in acute lung injury. The purpose of this study was to determine the effect of in vivo PARS inhibition on Etx-induced dysfunction of pulmonary vasorelaxation. Rats received intraperitoneal saline or Etx (Salmonella typhimurium; 20 mg/kg) and one of the PARS inhibitors, 3-aminobenzamide (3-AB; 10 mg/kg) or nicotinamide (Nic; 200 mg/kg), 90 min later. After 6 h, concentration-response curves were determined in isolated pulmonary arterial rings. Etx impaired endothelium-dependent (response to ACh and calcium ionophore) and -independent (sodium nitroprusside) cGMP-mediated vasorelaxation. 3-AB and Nic attenuated Etx-induced impairment of endothelium-dependent and -independent pulmonary vasorelaxation. 3-AB and Nic had no effect on Etx-induced increases in lung myeloperoxidase activity and edema. Lung ATP decreased after Etx but was maintained by 3-AB and Nic. Pulmonary arterial PARS activity increased fivefold after Etx, which 3-AB and Nic prevented. The beneficial effects were not observed with benzoic acid, a structural analog of 3-AB that does not inhibit PARS. Our results suggest that PARS inhibition with 3-AB or Nic improves pulmonary vasorelaxation and preserves lung ATP levels in acute lung injury.

Cardiotrophin-1 attenuates endotoxin-induced acute lung injury.

Cardiotrophin-1 (CT-1) is a recently discovered member of the gp130 cytokine family, which includes IL-6, IL-11, leukemia inhibitory factor, ciliary neurotrophic factor, and oncostatin M. Recent evidence suggests that, like other members of this family, CT-1 may possess anti-inflammatory properties. We hypothesized that in vivo CT-1 administration would attenuate endotoxin (ETX)-induced acute lung injury. We studied the effects of CT-1 (100 microgram/kg ip, 10 min prior to ETX) in a rat model of ETX-induced acute lung injury (Salmonella typhimurium lipopolysaccharide, 20 mg/kg ip). Six hours after ETX, lungs were harvested for determination of neutrophil accumulation (myeloperoxidase, MPO, assay) and lung edema (wet-to-dry weight ratio). Mechanisms of pulmonary vasorelaxation were examined in isolated pulmonary artery rings at 6 h by interrogating endothelium-dependent (response to acetylcholine) and endothelium-independent (response to sodium nitroprusside) relaxation following alpha-adrenergic (phenylephrine)-stimulated preconstriction. CT-1 abrogated the endotoxin-induced lung neutrophil accumulation: 2.3 +/- 0.2 units MPO/g wet lung (gwl) vs 6. 3 +/- 0.3 units MPO/gwl in the ETX group (P < 0.05 vs ETX, P > 0.05 vs control). Similarly, CT-1 prevented ETX-induced lung edema: wet-to-dry-weight ratio, 4.473 +/- 0.039 vs 4.747 +/- 0.039 in the ETX group (P < 0.05 vs ETX, P > 0.05 vs control). Endotoxin caused significant impairment of both endothelium-dependent and -independent pulmonary vasorelaxation, and CT-1 attenuated this injury. Thus, cardiotrophin-1 possesses significant anti-inflammatory properties in a model of endotoxin-induced acute lung injury.

Driveway crush injuries in young children: a highly lethal, devastating, and potentially preventable event.

BACKGROUND/PURPOSE: The aim of this study was to investigate driveway-related injuries in children, identify associated risk factors, and evaluate outcome compared with other mechanisms of blunt trauma. METHODS: A 6-year review (1991 to 1996) of pediatric (age less than 18 years) pedestrian injuries treated at two urban trauma centers was conducted: one regional pediatric trauma center and one level I trauma center with pediatric commitment. Five hundred twenty-seven children injured in pedestrian accidents were identified from the trauma registry; 51 children (10%) sustained traumatic injuries as a result of being struck in their driveway. Data are reported as mean +/- SEM. RESULTS: Children less than 5 years of age (n = 41) had an injury severity score (ISS) of 12.3+/-2.3, 15 (37%) sustained closed head injury, 13 (37%) had torso trauma, 19 (46%) skeletal trauma, and eight (20%) died. Children > or = 5 years old (n = 10) had an ISS of 10.7+/-2.4, three (30%) sustained closed head injury, four (40%) torso trauma, six (60%) skeletal trauma, and none died. In contrast, all other pediatric pedestrian accidents analyzed over the same time period had a mortality rate of only 2% (11 of 476). CONCLUSIONS: Pediatric driveway trauma carries a significant risk of head injury and a 10-fold increase in mortality in children under 5 years of age when compared with all other pediatric pedestrian accidents. More emphasis must be placed on injury prevention and public education to prevent this devastating mechanism of injury in these young, vulnerable children.

Endotoxin differentially impairs receptor-mediated relaxation in rat isolated pulmonary and thoracic aortic vessels.

PURPOSE: The purpose of this study was to determine the effect of endotoxin on vasorelaxation in the pulmonary and systemic circulations in response to the following agonists that require generation of cyclic adenosine monophosphate: (1) beta-adrenergic receptor stimulation with isoproterenol; (2) H2 receptor stimulation with dimaprit; and (3) adenylate cyclase stimulation with forskolin. METHODS: Male Sprague-Dawley rats weighing 250 to 350 g were injected with endotoxin (20 mg/kg intraperitoneal) or saline. Six hours later, the cumulative dose response to beta-adrenergic receptor stimulation (isoproterenol), H2 receptor stimulation (dimaprit), and adenylate cyclase stimulation (forskolin) was determined in isolated rat pulmonary artery and thoracic aortic rings preconstricted with phenylephrine. RESULTS: Endotoxin caused significant impairment of relaxation to isoproterenol in the pulmonary artery, but the response in the aorta was not different from the control response. In the pulmonary circulation, endotoxin converted the response to dimaprit from vasorelaxation to vasoconstriction. On the other hand, dimaprit resulted in vasorelaxation in the thoracic aorta after endotoxin; however, the response was impaired compared with the control response. Endotoxin did not affect the dose response to forskolin in either the pulmonary artery or the thoracic aorta. CONCLUSION: From these data, we conclude that endotoxin causes regional specific changes in vascular reactivity. These changes in vascular reactivity result in preserved vasorelaxation in the systemic circulation and impairment of vasorelaxation in the pulmonary circulation in response to endotoxin.

Is routine pathological evaluation of pediatric hernia sacs justified?

BACKGROUND/PURPOSE: Herniorrhaphy is the most common general surgical procedure performed on children, and hernia sac material is one of the most common tissue specimens microscopically examined in the authors' surgical pathology laboratory. The risk of accidental vas deferens ligation has prompted the recommendation that all hernia sacs be examined pathologically. The authors hypothesized that the incidence of unrecognized vas deferens or epididymis ligation is actually very low and may not warrant routine pathological examination of all pediatric hernia sacs. METHODS: Over a 3-year period (1994 to 1996), pathology reports from all hernia repairs at the authors' institution were reviewed. A total of 1,494 inguinal hernia sacs were pathologically evaluated from 1,077 pediatric patients (417 were bilateral). Pathological diagnoses not affecting clinical management (ie, chronic inflammation, irritated hernia sacs, embryonal remnants, adrenal cortical rests) were classified as incidental findings. Identification of true vas deferens was classified as a positive finding. RESULTS: The study population had a mean age of 3.9 +/- 0.1 years and 963 (89%) were boys. The incidence of vas deferens injury from herniorrhaphy was found to be 0.13% (2 of 1,494), and these were recognized by the pediatric surgeon in the operating room. CONCLUSIONS: When vas deferens injury is suspected, the sample should always be sent to the pathology department for confirmation. However, no occult carcinoma or other pathology was identified, and the remainder of the histological findings did not change the clinical treatment of any child. Given a fixed cost of pathological analysis, elimination of routine hernia sac examination may result in substantial annual savings. Therefore, in the current era of cost containment, recommendations for routine pathological examination of excised pediatric hernia sacs should be reevaluated.

Ultrasound is an effective triage tool to evaluate blunt abdominal trauma in the pediatric population.

BACKGROUND: Although computed tomography has been considered the diagnostic modality of choice for pediatric patients with blunt abdominal trauma (BAT), it is costly, time-consuming, requires sedation, and may be associated with complications in young children. Abdominal ultrasonography (US) is a promising modality in the evaluation of BAT that is quick, noninvasive, repeatable, and cost-effective. We hypothesized that emergency department US, performed by trauma surgeons, is a useful triage tool for pediatric BAT that reduces the need for computed tomography. METHODS: The 230 children (<18 years old) with suspected BAT were initially evaluated with US in the emergency department by surgeons. Subsequent computed tomographic scan or exploratory laparotomy was performed as indicated by the key clinical pathway. RESULTS: Twelve children (5.2%) had documented intra-abdominal injuries. All five injured children with significant intraperitoneal fluid were identified by US. Of the seven patients who had intra-abdominal injury not detected by US, six sustained solid organ injuries that were managed nonoperatively. Extrapolated reductions in hospital charges due to the decreased number of computed tomographic scans total $130,000. CONCLUSIONS: Using US as a triage tool may dramatically reduce the cost of pediatric BAT evaluation while being able to quickly identify significant intraperitoneal fluid that requires further evaluation and possible laparotomy.

Successful management with octreotide of a child with L-asparaginase induced hemorrhagic pancreatitis.

BACKGROUND: Octreotide is a synthetic somatostatin analogue which has been suggested for use in the management of acute pancreatitis. While studies have looked at octreotide use in the setting of pancreatitis due to chronic alcohol use or trauma, little is known of its role in management of drug induced acute pancreatitis; particularly in the pediatric setting. PATIENTS AND METHODS: We present a case of a 5 1/2-year-old white female who developed severe, necrotizing, hemorrhagic pancreatitis with pseudocyst formation secondary to L-asparaginase use as a part of her therapy for acute lymphoblastic leukemia (ALL). She was managed initially with intravenous fluids, bowel rest, nasogastric suctioning, parenteral narcotices, and broad spectrum antibiotics. In addition, within 12 hours of admission to The Children's Hospital (TCH) in Denver, Colorado, she began therapy with octreotide (5 micrograms/kg/day IV divided b.i.d.). With this management, her pseudocyst decompressed without need for surgical intervention, her pancreatitis fully resolved, and she recovered full pancreatic function without any long-term sequelae. CONCLUSION: Use of octreotide may have served a role in limiting the severity of the disease process in this case. Further studies need to be done to verify its usefulness in this setting.