Pretreatment With the Tumor Nerosis Factor-α Blocker Etanercept Attenuated Ischemia-Reperfusion Renal Injury

Introduction

Tumor necrosis factor (TNF)-α mediates inflammation and apoptosis in ischemia-reperfusion (IR) injury of the kidneys. Etanercept, a soluble TNF-α receptor, has shown anti-inflammatory and anti-apoptotic effects in several animal models of renal injury, including chronic insufficiency and unilateral ureteral obstruction. We evaluated the protective effect of etanercept against experimental renal IR injury.

Methods

Male Sprague-Dawley (SD) rats were divided into 4 groups: saline-treated sham rats, etanercept-treated sham rats, saline-treated IR rats, and etanercept-treated IR rats. Renal messenger RNA (mRNA) levels of TNF-α and monocyte chemotactic protein-1 (MCP-1) were measured by real-time polymerase chain reaction (PCR) at 24 hours after IR injury. The protein levels of renal Bcl-2 associated X (Bax), B-cell lymphoma 2 (Bcl), extracellular signal-regulated kinase (ERK), and caspase-3 activation were evaluated using Western blot analysis. The degree of apoptosis of renal tubular cells was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays.

Results

At 24 hours after IR injury, the serum levels of blood urea nitrogen (BUN) and creatinine were significantly lower among etanercept-treated than saline-treated IR rats. Renal mRNA levels of TNF-α and MCP-1 in saline-treated IR rats were significantly higher than the levels in saline-treated sham rats, and TNF-α and MCP-1 mRNA levels in etanercept-treated IR rats were significantly lower than those in saline-treated IR rats. Etanercept pretreatment of IR-injured rats significantly increased EKR phosphorylation and reduced the renal Bcl-2/Bax ratio, the renal caspase-3 activation, and the number of TUNEL-positive apoptotic cells.

Conclusion

Etanercept improved resistance to renal injury during IR by enhancing the activation of ERK and increasing the Bcl-2/Bax ratio.     

Nitrovasodilator responses in pulmonary arterioles from rats with nitrofen-induced congenital diaphragmatic hernia

Background/Purpose

Many infants with congenital diaphragmatic hernias (CDHs) experience persistent pulmonary hypertension that is refractory to treatment with inhaled nitric oxide (NO). We have examined the responses of isolated pulmonary arterioles from prenatal and postnatal rats with and without nitrofen (2,4-dichlorophenyl-p-nitrophenyl ether)-induced CDH to a variety of activators of the NO-cyclic guanosine monophosphate (cGMP) pathway.

Methods

Right-sided CDH was induced in fetal rats by feeding nitrofen to pregnant rats on day 12 of gestation. Control rats were fed olive oil (vehicle). Third-generation pulmonary arterioles were isolated from the right lung of prenatal rats at term and from newborn rats within 8 hours after birth. Responses to increasing concentrations of sodium nitroprusside (SNP), atrial natriuretic peptide, or 8-bromo-cGMP were measured in pulmonary arterioles from control rats and from rats with nitrofen-induced CDH. Postnatal responses to 8-bromo-cGMP were also recorded in the presence of zaprinast, a type V phosphodiesterase inhibitor.

Results

Pulmonary arterioles from prenatal rats did not dilate in response to SNP, atrial natriuretic peptide, or 8-bromo-cGMP. Vasodilatory responses of postnatal pulmonary arterioles from control rats to SNP and 8-bromo-cGMP were significantly greater than for arterioles from rats with CDH. Zaprinast pretreatment resulted in similar responses for postnatal CDH and control arterioles to 8-bromo-cGMP.

Conclusions

Postnatal pulmonary arterioles from CDH rats exhibit altered nitrovasodilator responsiveness, which may be due to rapid degradation of cGMP.     

Effects of Thalidomide and Pentoxyphylline Over Local and Remote Organ Injury After Intestinal Ischemia/Reperfusion

Objective

We investigated the effects of thalidomide alone or in combination with pentoxyphylline upon intestinal ischemia/reperfusion (I/R) injury in the rat.

Materials and Methods

Twenty male Wistar rats were randomized into 5 groups: sham-operated (SHAM), control (CTL), thalidomide (400 mg/kg) treatment (THAL), pentoxyphylline (50 mg/kg) treatment and a combination group (THAL + POX). I/R was induced by clamping the superior mesenteric artery for 45 minutes, followed by 120 minutes of reperfusion. We measured serum concentrations of aspartate-aminotransferase (AST), lactate dehydrogenase (LDH), tumor necrosis factor (TNF)-α as well as lipid peroxidation and antioxidant status. Intestinal samples were morphologically analyzed, and dry to wet (W/D) ratios calculated in intestinal, lung and liver samples, as a measurement of tissue edema.

Results

Serum concentrations of AST, LDH, and TNF-α were increased after I/R in the CTL compared with the SHAM group (P < .05). Lipid peroxidation was also increased, and antioxidant capacity in serum, decreased (P < .05). The W/D ratio was elevated in all tissue samples as well (P < .05). Both thalidomide and pentoxyphylline effectively reduced AST, LDH, TNF-α, and lipid peroxidation levels, as well as attenuated tissue edema and intestinal injury induced by I/R (P < .05). Combination treatment showed only modest additive effects on lung W/D ratio and TNF-α levels.

Conclusion

Both drugs protected the intestine, lungs, and liver against intestinal I/R injury, probably by inhibition of TNF-α and lipid peroxidation. However, combination treatment showed small, additive effects.     

Enterogenesis by mechanical lengthening: morphology and function of the lengthened small intestine

Background/Purpose

The purpose of this study is to evaluate the function of the mechanically lengthened small intestine.

Methods

A jejunal segment was separated from intestinal continuity in rats. A screw was inserted into its proximal end, and the distal end was oversewn. The screw was advanced into the jejunal segment by 5 mm every other day. The jejunal segments were retrieved after 2 weeks. The length, weight, muscular thickness, alkaline phosphatase, and lactase activities of the jejunal segments were determined. Comparisons were made among normal jejunum, isolated jejunal segments without lengthening, and lengthened jejunal segments.

Results

Jejunal segments doubled in length after gradual mechanical stretching compared with the normal and isolated controls. The thickness of the muscular layer increased in both the isolated and lengthened groups. The total activity of alkaline phosphatase increased in jejunal segments that were lengthened, whereas the total lactase activity remained the same.

Conclusions

Mechanical force is a viable method for increasing intestinal length while preserving the intestinal function. This phenomenon may provide a new method for the treatment of patients with short bowel syndrome.     

Erythropoietin protects severe haemorrhagic shock-induced organ damage in conscious rats

Objective

Erythropoietin (EPO) has pleiotropic cytoprotective actions. We investigated the effects of EPO on the physiopathology and cytokine levels after haemorrhagic shock (HS) in conscious rats.

Methods

Rats received an intravenous injection of 300 U/kg EPO over 10 min followed by HS via withdrawal of 60% of total blood volume from a femoral arterial catheter (6 ml/100 g body weight) over 30 min. Mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 18 h after the start of blood withdrawal. Levels of biochemical parameters, including haemoglobin, GOT, GPT, BUN, creatinine (Cr), LDH, CPK, and lactate were measured at 30 min before the induction of HS and 0, 1, 3, 6, 9, 12, and 18 h after HS. Cytokine levels, including TNF-α and IL-6, in serum were measured at 1, 9, and 18 h after HS. The kidneys, liver, lungs, and small intestine were removed for pathology assessment at 48 h after HS.

Results

HS significantly increased HR, blood GOT, GPT, BUN, Cr, LDH, CPK, lactate, TNF-α, and IL-6 levels and decreased haemoglobin and MAP in rats. Pre-treatment with EPO improved survival rate, preserved the MAP, decreased the tachycardia and markers of organ injury, suppressed the release of TNF-α and IL-6 after HS in rats.

Conclusion

Pre-treatment with EPO suppresses the release of serum TNF-α and IL-6, along with decreasing the levels of markers of organ injury associated with HS, with such actions ameliorating HS-induced organ damage in rats.     

Glucagonlike peptide-2 analogue: a possible new approach in the management of inflammatory bowel disease

Background/purpose

Glucagonlike peptide-2α (GLP-2α) has been shown to be a growth factor for the small intestine. This study investigated the benefits of intravenous and intraluminal administration of GLP-2α using a rat model of inflammatory bowel disease (IBD).

Methods

Normal Fisher rats and HLA-B27 (IBD) rats were treated for 14 days as follows: Fisher, intravenous saline (n = 6); HLA-B27, intravenous saline (n = 6); HLA-B27, intravenous GLP-2α (50 μg/kg/d; n = 5); Fisher, intraluminal saline (n = 5); HLA-B27, intraluminal saline (n = 5); or intraluminal GLP-2α (50 μg/kg/d; n = 5). Rats were evaluated for frequency of diarrhea, and the bowel was analyzed for gross and microscopic lesions. Statistical evaluations were determined using analysis of variance (ANOVA). A P value of .05 was significant.

Results

Intravenous GLP-2α decreased diarrhea and the number of bowel lesions (P < .05). Microscopic inflammation was reduced by 24% but was not statistically significant. Intraluminal GLP-2α decreased the number of small intestine lesions (P < .05) and the microscopic inflammation (P < .05) but did not significantly reduce diarrhea or the overall number of bowel lesions.

Conclusions

GLP-2α ameliorates the signs of IBD in HLA-B27 rats. Intravenous GLP-2α reduces diarrhea more effectively than intraluminal administration, and both routes are equally effective in ameliorating inflammation. GLP-2α potentially provides a new modality for the treatment of IBD.     

The protective effect of curcumin on ischemia-reperfusion-induced liver injury

Objective

Reperfusion of the ischemic liver results in the generation of oxidative and nitrosative stresses and reaction product of peroxynitrite, which induce rapid cytotoxicity and liver injury. In this study we demonstrated that curcumin, an antioxidant, attenuated ischemia/reperfusion (I/R)-induced liver injury.

Materials and Methods

Ischemia was induced by clamping the common hepatic artery and portal vein of rats for 30 minutes. Thereafter, flow was restored and the liver was reperfused for 80 minutes. Blood samples collected prior to ischemia and after reperfusion were analyzed for methyl guanidine (MG), nitric oxide (NO), tumor necrosis factor-alpha (TNF-α), and adenosphate triphosphate (ATP). Blood levels of serum glutamic oxaloacetic transaminase (sGOT), serum glutamate pyruvate transaminase (sGPT), and lactic dehydrogenase (LDH), which served as indexes of liver injury, were measured.

Results

The protocol resulted in elevation of blood NO (P < .001), TNF-α (P < .001), and MG (P < .001). sGOT, sGPT, and LDH were elevated significantly (P < .001), whereas ATP was significantly diminished (P < .001). Pretreatment with curcumin (25 mg/kg) significantly attenuated the reperfusion liver injury, while the ATP content reversed. In addition, MG, TNF-α, and NO release were attenuated.

Conclusions

These results indicated that curcumin exerted potent anti-inflammatory effects in I/R-induced liver injury due to its antioxidant effects.     

Recombinant Human Erythropoietin Pretreatment Attenuates Heart Ischemia-Reperfusion Injury in Rats by Suppressing the Systemic Inflammatory Response

Background

Ischemia-reperfusion (I/R) injury may influence graft function after transplantation. Erythropoietin (EPO) attenuates I/R injury in various animal organs such as intestine, brain, and kidney.

Objective

To evaluate the effects of pretreatment with recombinant human EPO (rhEPO) on I/R-induced heart injury.

Materials and Methods

A rat model of I/R injury was established by ligating the left descending coronary artery for 30 minutes, followed by reperfusion for 4 hours. Fifty Sprague-Dawley rats were divided into 5 groups: sham operation; I/R; I/R+rhEPO, 100 U/kg; I/R+rhEPO, 1000 U/kg; and I/R+rhEPO, 5000 U/kg. Electrocardiograms were assessed continuously to note arrhythmia caused by reperfusion. Serum concentrations of interleukin (IL)-6 and IL-8, and tumor necrosis factor-α were measured at 2 and 4 hours after reperfusion.

Results

The rhEPO-treated animals exhibited dosage-dependent significant reduction in the incidence of ventricular arrhythmia caused by reperfusion, and markedly decreased serum concentrations of IL-6, IL-8, and tumor necrosis factor-α (P < .05) compared with the I/R group (P < .05).

Conclusion

The rhEPO attenuates myocardial I/R injury in rats, at least in part related to inhibition of the system inflammatory response.     

Augmentor of liver regeneration ameliorates renal tubular epithelial cell injury after rat liver transplantation

Background

Acute renal insufficiency and dysfunction are common complications after clinical liver transplantation. This study examined whether augmentor of liver regeneration (ALR) played a significant role to ameliorate renal tubular epithelial cell injury after liver transplantation.

Methods

Orthotopic liver transplantation was performed from Sprague-Dawley (SD) to SD rats. Twelve recipients were randomly divided into two groups: ALR group (with recombinated human ALR 100 μg/kg  ·  d intramuscular injection postoperation) versus normal saline-treated group (with the same volume of normal saline injected intramuscularly postoperation). Rats were sacrificed at day 3 posttransplantation. Renal morphological changes in recipients were assessed with light microscopy. The expressions of tumor necrosis factor-α (TNF-α), proliferating cell nuclear antigen (PCNA) and caspase-3 protein and mRNA in the kidney were evaluated by real-time polymerase chain reaction and immunohistochemical staining.

Results

Morphological changes in renal tubular epithelial cells were not significant in either group at day 3 posttransplantation. The intragraft expression of TNF-α and caspase-3 was strikingly promoted in the normal saline-treated group and PCNA attenuated compared to the ALR group.

Conclusion

These data suggested that ALR may play a role to reduce renal damage in liver transplant recipients.     

Intestine as Source of Cytokines and Growth Factors

Background

The activation status of intestinal immune system cells is much higher than that of analogous peripheral cells. Increased serum concentrations of proinflammatory cytokines have been reported in various pathologic conditions; however, the source of these mediators has not been elucidated.

Objective

To assess the role of the human intestine and its lymphatic system in production of growth factors and proinflammatory cytokines.

Material and Methods

Twenty liver transplant recipients and 20 donors were included in the study. Blood samples were obtained from the artery supplying the intestine, the portal vein, and a peripheral vein during liver harvesting in donors and after transplantation in recipients. An enzyme-linked immunosorbent assay was used to assess serum concentrations of IL-6, tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), and hepatocyte growth factor (HGF).

Results

In transplant recipients, IL-6 concentration in arterial blood was lower than that in portal blood (P < .049), whereas in donors, there was no significant difference in these concentrations. Neither recipients nor donors demonstrated significant differences in arterial or portal blood concentrations of TNF-α, TGF-β, or HGF.

Conclusions

In healthy human beings, the intestine is not a substantial source of IL-6, TNF-α, TGF-β, or HGF. However, in patients with liver cirrhosis, the intestine is an important source of IL-6 but not of the other studied growth factors and cytokines.     

Hypothermic Liver Machine Perfusion With EKPS-1 Solution vs Aqix RS-I Solution: In Vivo Feasibility Study in a Pig Transplantation Model

Objective

Hypothermic machine perfusion (HMP) is superior to simple cold storage for kidney preservation. We previous observed in a porcine liver transplantation model increased tumor necrosis factor-α (TNF-α) production eventually leading to poor recipient survival after HMP using standard kidney perfusion solution (KPS-1) compared with simple cold storage. We compared two solutions for HMP preservation of the liver: enriched KPS-1 (EKPS-1) and Aqix RS-I.

Methods

Pig livers were obtained after cold flushing with histidine-tryptophan-ketoglutarate solution. Subsequently, the livers were subjected to dual-vessel perfusion with two preservation solutions: EKPS-1 (n = 6) and Aqix RS-I (n = 3). After HMP preservation and transplantation, graft and recipient survival, hepatocellular damage (aspartate aminotransferase concentration), TNF-α production, and endothelial cell damage (hyaluronic acid clearance) were recorded.

Results

No primary graft nonfunction was observed. Recipient survival at postoperative day 3 was similar in both groups (33%). Aspartate aminotransferase concentration measured in serum samples after reperfusion was similar in both groups. After reperfusion, TNF-α concentration was higher and hyaluronic acid clearance was lower in the EKPS-1 group vs the Aqix RS-I group at 60, 120, and 180 minutes (all P < .05).

Conclusion

Hypothermic machine perfusion provided adequate longer term graft survival. After reperfusion, TNF-α production seems to be reduced, and endothelial cell dysfunction remains pronounced with Aqix RS-1 solution compared with EKPS-1 solution.     

Interferon-gamma induces caspase-8 in neuroblastomas without affecting methylation of caspase-8 promoter

Background

The expression of caspase-8, a cysteine protease that is crucial for the apoptotic cascade, is absent in a high percentage of neuroblastomas, the most frequent extracranial solid tumor of infants and children. Resistance of neuroblastomas to death-receptor (eg, tumor necrosis factor alpha (TNF-α) receptor)—mediated apoptosis is thought to be caused by loss of caspase-8 expression. Gene silencing by hypermethylation of caspase-8 promoter has been proposed for the loss of caspase-8 expression in neuroblastoma cells.

Methods

To further evaluate the role of caspase-8 in neuroblastoma, we assessed the induction of caspase-8 expression in neuroblastoma cells by treating the cells with a physiologic agent such as interferon-γ.

Results

The authors found that interferon-γ induces caspase-8 expression in neuroblastoma cells irrespective of the gene silenced by hypermethylation of caspase-8 promoter. The authors show that interferon-γ also regulates other apoptosis related gene expression. Moreover, they show that interferon-γ treatment in combination with TNF-α decreases neuroblastoma cell proliferation.

Conclusions

Interferon-γ induces procaspase-8 expression in neuroblastoma cells, and this induction is not dependent on demethylation of the caspase-8 promoter. Therapies aimed at inducing caspase-8 expression by adjunctive treatment, such as interferon-γ, may increase the effectiveness of current chemotherapeutic regimens.     

Laparoscopic partial versus total adrenalectomy for aldosterone producing adenoma

Purpose:

Laparoscopic surgery has become a standard method for adrenal treatment. Primary hyperaldosteronism is known to be frequently characterized by multiple adrenal lesions. The indication of laparoscopic partial or total adrenalectomy in patients with aldosterone producing adenoma (APA) remains controversial. We performed the 2 procedures and compared the outcomes of these 2 operations retrospectively.

Materials and Methods:

A total of 92 patients with primary hyperaldosteronism were laparoscopically treated at our institution from 1995 to 2004. A total of 29 patients underwent partial adrenalectomy or enucleation, while unilateral total adrenalectomy was performed in 63. A single pathologist examined the number and histopathological characteristics of APAs. Postoperative median followup was 60.3 and 29.3 months, respectively.

Results:

Laparoscopic adrenalectomies were successfully performed in each group, although the partial type had fewer ports and shorter operative time. All 63 patients with total adrenalectomy showed recovery from hypertension, suppressed plasma renin activity and high plasma aldosterone. Two of 29 patients with partial adrenalectomy or enucleation still experienced hypertension with high plasma aldosterone. Of the 63 extirpated specimens 17 adrenals (27.0%) demonstrated multiple space occupying lesions along with the main APA.

Conclusions:

Primary hyperaldosteronism is highly associated with multiple adrenal space occupying lesions. The risk-to-benefit ratio must be carefully weighed against the potential advantage of partial adrenalectomy. We chose total laparoscopic adrenalectomy in patients with unilateral APA and primary hyperaldosteronism.     

Adrenocortical cell transplantation reverses a murine model of adrenal failure

Purpose

Although adrenal insufficiency can be managed with steroid replacement, transplantation of adrenocortical cells may represent a more definitive therapy.

Methods

An adrenal failure model was created by adding stress to mice that underwent staged bilateral adrenalectomy. Murine adrenocortical cells were seeded onto collagen sponges. The grafts were implanted under the renal capsule during the first adrenalectomy. Some mice had an additional graft placed next to the kidney. A contralateral adrenalectomy and a laparotomy were performed 1 week after the first adrenalectomy. Two weeks later, blood was collected for corticosterone measurement; and implants were retrieved for adrenal-specific messenger RNA analysis and histology. Mice that underwent the same procedures but received a graft without cells served as controls.

Results

Control group mortality was 100%. Mice that had only one cell-seeded implant had 42% survival, whereas mice that had 2 cell-seeded implants had 100% survival. Retrieved implants demonstrated viable cells and expression of adrenocortical genes. The plasma corticosterone concentration in animals that survived was similar to that in normal mice.

Conclusion

Cells transplantation restored the adrenocortical function in these mice. Further optimization of this technique could bring a curative therapy to patients with adrenal insufficiency.     

Resource utilization and its management in splenic trauma

Background

This study compared resource utilization and its management for splenic injury at 2 level-I trauma centers and a pediatric referral center with other facilities in a state currently developing a trauma system.

Methods

Management strategy, length of stay, and total charges for children were compared among the pediatric referral center, trauma centers, and other facilities. Adult management, length of stay, and total charges were compared between trauma centers and other facilities.

Results

Nonoperative management was more frequent in children at the pediatric referral center than trauma centers or other facilities and was more common in adults at trauma centers than at other facilities. Mean length of stay and total charges for children were significantly greater at the pediatric referral center and trauma centers than at other facilities and for adults at trauma centers than at other facilities. Facility type was associated with length of stay and total charges when injury type and severity were controlled.

Conclusions

Nonoperative management of splenic injury is more common at trauma centers, and splenic trauma management may be more costly at trauma centers.     

Endoscopic Management of Urologic Complications Following Renal Transplantation: Impact of Ureteral Anastomosis

Objective

To evaluate the success of ureteral stent placement to treat or prepare for surgical treatment of urologic complications after renal transplantation, according to a type of ureteral anastomosis.

Patient and methods

From May 1989 to December 2006, we performed 703 kidney transplantations including 412 extravesical ureteroneocystostomy (according to Lich-Gregoire technique) and 265 transvesical ureteroneocystostomy (according to Politano-Leadbetter technique). We retrospectively analyzed our endoscopic management of urinary leaks and ureteral strictures. The criteria of success were the feasibility to place a ureteral stent, permitting good drainage of the upper renal graft tract before further endoscopic or surgical treatment.

Results

Forty-three urinary leaks or ureteral strictures occurred after extravesical ureteroneocystostomy (n = 21) or after Politano-Leadbetter anastomosis (n = 22). The success rate of endoscopic management was 75% (n = 16) for Politano-Leadbetter anastomosis versus 53% (n = 11) for the Lich-Gregoire anastomosis. There was no statistical difference (P = .1).

Conclusion

Ureteroneocystostomy according to Lich-Gregoire procedure were twice less complicated than those according to the Politano-Leadbetter technique, but were associated with a rate of failure of ureteral stent placement in urgency higher to 25%.     

The association of promoter gene polymorphisms of the tumor necrosis factor-α and interleukin-10 with severity of lactic acidosis during liver transplantation surgery

Background

Orthotopic liver transplantation (OLT) is a major operation, causing cytokine release and other inflammatory responses that can contribute to postreperfusion syndrome occurrence. During the systemic inflammatory response syndrome, increased lactate levels result from excessive cytokine production despite normal oxygen delivery and carbohydrate metabolism. The goal of the study was to determine the relationship between genetic polymorphisms in interleukin (IL)-10 (−1082G/A) or tumor necrosis factor (TNF)-α (−376 G/A) and lactate levels in patients during OLT surgery.

Patients and Methods

This prospective observational study in 40 consecutive adult patients who underwent OLT documented lactic acid levels at 5 times: Immediately after induction of anesthesia, at the end of the pre-anhepatic phase, at the end of the anhepatic phase, 1 hour after reperfusion, and at the end of surgery. Polymerase chain reaction (PCR; RFLP methodology) was used to examine IL-10 (−1082G/A) and TNF-α (−376 G/A) gene polymorphisms.

Results

Carriers of the IL-10/TNF-α genotype combination GG/GG showed significantly different changes in lactate levels at 1 hour after reperfusion and at the end of surgery. Lactate levels were significantly higher among patients heterozygous for TNF-α (AG genotype) compared with patients homozygous for TNF-α (GG genotype) at same times. In contrast, there was no significant difference among IL-10 polymorphic genotypes (−1082G/A).

Conclusion

Genetic factors play a role in the development of lactic acidosis after OLT. IL-10 (−1082G/A) and TNF-α (−376 G/A) gene polymorphisms could influence the variability of lactate levels after liver transplantation surgery.     

Posttraumatic small bowel obstruction in children

Background

The diagnosis of intestinal injuries in children after blunt abdominal trauma can be difficult and delayed. Most children who suffer blunt abdominal trauma are managed nonoperatively, making the diagnosis of intestinal injuries more difficult. We sought to gain information about children who develop intestinal obstruction after blunt abdominal trauma by reviewing our experience.

Methods

Review of records from a pediatric tertiary care center over an 11.5-year period revealed 5 patients who developed small bowel obstruction after blunt trauma to the abdomen. The details of these patients were studied.

Results

All patients were previously managed nonoperatively for blunt abdominal trauma. Intestinal obstruction developed 2 weeks to 1 year (median, 21 days) after the trauma. Abdominal x-ray, computerized tomography scan, or barium meal studies were used to establish the diagnosis. The pathology was either a stricture, an old perforation, or adhesions causing the intestinal obstruction. Laparotomy with resection and anastomosis was curative.

Conclusions

Posttraumatic small bowel obstruction is a clinical entity that needs to be watched for in all patients managed nonoperatively for blunt abdominal trauma.