Laparoscopic resection of choledochal cyst with Roux-en-Y hepaticojejunostomy: a case report and review of the literature.

BACKGROUND: Choledochal cysts are associated with ductal strictures, stone formation, cholangitis, rupture, secondary biliary cirrhosis and increased incidence of cholangiocarcinoma. The surgical approach to choledochal cysts has evolved from the cyst-enterostomy to a complete excision with more recent use of minimally invasive approaches. We report a complete minimally invasive approach to a Type 1 choledochal cyst and summarize the literature containing large case series of similar approaches. METHODS AND OPERATIVE TECHNIQUE: A 38-year-old female with a history of vague epigastric pain for multiple years was diagnosed with a Type 1 choledochal cyst on MRCP. The operative approach was an elective laparoscopic resection of choledochal cyst and Roux-en-Y hepaticojejunostomy. There were no intraoperative complications and discharge occurred on postoperative day three. Approximately 1 month after resection, she was diagnosed with a small retrohepatic fluid collection which was treated percutaneously and was diagnosed as a hematoma. A PubMed literature review focusing on surgical approaches to Type 1 choledochal cysts methods of repair and postoperative complications was performed and summarized. RESULTS AND DISCUSSION: The literature search performed on the subject of choledochal cyst management in adults and laparoscopic approaches resulted in a review of twenty-one articles. Ten of the articles were review articles regarding surgical approach and management of the disease. An additional two were case reviews, and eight reported on laparoscopic approaches to management of choledochal cysts. In this paper, we summarize the eight articles that provide information on the laparoscopic management and outcomes for choledochal cysts. While operative times were longer on the laparoscopic procedures, hospital stay was shorter and there was no increase in complication rates. The most common complications reported were postoperative bile leak followed by anastomotic stricture. CONCLUSION: This case highlights the management of laparoscopic resection of choledochal cyst as a viable, safe and feasible approach based on this case and a literature review.

Formal quality improvement curriculum and DMAIC method results in interdisciplinary collaboration and process improvement in renal transplant patients.

BACKGROUND: Broad-based formal quality improvement curriculum emphasizing Six Sigma and the DMAIC approach developed by our institution is required for physicians in training. DMAIC methods evaluated the common outcome of postoperative hyponatremia, thus resulting in collaboration to prevent hyponatremia in the renal transplant population. METHODS: To define postoperative hyponatremia in renal transplant recipients, a project charter outlined project aims. To measure postoperative hyponatremia, serum sodium at admission and immediately postoperative were recorded by retrospective review of renal transplant recipient charts from June 29, 2010 to December 31, 2011. An Ishikawa diagram was generated to analyze potential causative factors. Interdisciplinary collaboration and hospital policy assessment determined necessary improvements to prevent hyponatremia. Continuous monitoring in control phase was performed by establishing the goal of <10% of transplant recipients with abnormal serum sodium annually through quarterly reduction of hyponatremia by 30% to reach this goal. RESULTS: Of 54 transplant recipients, postoperative hyponatremia occurred in 92.6% of patients. These potential causes were evaluated: 1) Hemodialysis was more common than peritoneal dialysis. 2) Alemtuzumab induction was more common than antithymocyte globulin. 3) A primary diagnosis of diabetes existed in 16 patients (30%). 4) Strikingly, 51 patients received 0.45% sodium chloride intraoperatively, suggesting this as the most likely cause of postoperative hyponatremia. A hospital policy change to administer 0.9% sodium chloride during renal transplantation resulted in normal serum sodium levels postoperatively in 59 of 64 patients (92.2%). CONCLUSION: The DMAIC approach and formal quality curriculum for trainees addresses core competencies by providing a framework for problem solving, interdisciplinary collaboration, and process improvement.

Trajectory of metabolic derangement in infants with necrotizing enterocolitis should drive timing and technique of surgical intervention.

BACKGROUND: Seven clinical metrics of metabolic derangement (MD7) have improved the timing of surgical intervention in infants with necrotizing enterocolitis (NEC). We compared surgical NEC outcomes based on MD7 at our center (unit S) with a similar center (unit B) that based its intervention on abdominal radiograph. STUDY DESIGN: Premature infants undergoing surgical care for NEC were evaluated. MD7 included positive blood culture, acidosis, bandemia, hyponatremia, thrombocytopenia, hypotension, and neutropenia. Surgical recommendations were stratified as observation or intervention. Good outcomes included full enteric feeding by discharge and poor outcomes were death or dependence on parenteral nutrition. For unit S and unit B, the frequency, median, and mode of MD7 component per case were determined for observation and intervention. Mann-Whitney U test and Wilcoxon matched pairs were used to compare positive MD7 frequency for observation with intervention. Institutional mortality was compared and metabolic severity of unit cohorts was evaluated by incidence of MD7 in each. RESULTS: From March 2005 to July 2008, forty-one infants at unit S underwent 62 surgical evaluations. Observation was elected in 38 (median 1 MD7 per case, mode 0). Operative intervention occurred in 24 (median 4 MD7 per case, mode 4). Proportional MD7 difference between observation and intervention was significant (p = 0.018, U = 6). From February 2007 to December 2008, sixty-five unit B infants received 81 evaluations, recommending 37 observations (median 2 MD7 per case, mode 2), and 44 interventions (median 3 MD7 per case, mode 3). MD7 proportions between observation and intervention were not significant (p = 0.318, U = 16). Poor outcomes rates for unit S and unit B infants were 24% and 66%, respectively (p = 0.0001). Severity of MD7 did not differ between institutions (p = 0.53, U = 19). CONCLUSIONS: These data demonstrate variability in surgical approach to NEC. The MD7 panel describes the trajectory of metabolic derangement, defines more timely surgical intervention, and demonstrates that waiting for free air is too late.

Timing of surgical intervention in necrotizing enterocolitis can be determined by trajectory of metabolic derangement.

PURPOSE: Seven metrics of metabolic derangement were evaluated as contributors to clinical decision support for operative intervention in infants with suspected necrotizing enterocolitis (NEC). METHODS: Records of infants with suspected NEC without radiologic evidence of free air were queried for presence of 7 components of metabolic derangement (CMD), consisting of positive blood culture, acidosis, bandemia, thrombocytopenia, hyponatremia, hypotension, or neutropenia. Cases were stratified by clinical decision after each surgical evaluation as observation (OBS) or intervention (INT). Good outcome was defined as full enteric feeding by discharge and bad outcome as death or ongoing parenteral alimentation. Eleven infants undergoing operative intervention after an initial decision to observe were evaluated as matched pairs. Components of metabolic derangement/case and frequency of each CMD were determined for OBS and INT. Mann-Whitney U test was used to compare proportions of CMD in each group. Outcome was compared using chi(2). Observation was then stratified by outcome to determine whether 3 or more metabolic derangements warranting operative intervention would have changed initial clinical decision. The 11 matched cases were similarly analyzed using Wilcoxon-matched pairs. RESULTS: Between March 2005 and July 2008, 35 infants with NEC received 53 surgical evaluations. A median of 1 CMD/case was defined in 32 instances of OBS. Surgical intervention was carried out in 19 infants with a median of 3 CMD/case. Mann-Whitney U test indicated significant difference in the frequencies of each CMD component in OBS vs INT (P = .04). Good outcome was achieved in 75% of OBS and 63% of INT (non-significant, NS). Analysis of OBS by outcome demonstrated a median 1 CMD/case of 25 with good outcome and 3 CMD/case in infants with bad outcome. Frequency of CMD was significantly higher in infants with bad outcome (P = .02). Wilcoxon-matched pair analysis of the 11 infants with paired evaluations demonstrated a similar distribution and frequency of CMD. CONCLUSION: Progressive metabolic derangement of infants with NEC can be clinically tracked. The appearance of any 3 of these 7 metrics indicates timely operative intervention. Application of CMD trajectory to timing of surgical intervention may improve outcome and define the relationship between specific CMD and operative risk.

Application of International Classification Injury Severity Score to National Surgical Quality Improvement Program defines pediatric trauma performance standards and drives performance improvement.

BACKGROUND: The American College of Surgeons National Surgical Quality Improvement Program is becoming a core methodology to define performance as a ratio of observed to expected events. We hypothesized that application of this using International Classification of Injury Severity Score (ICISS) for individual patient risk stratification to a group of hospitals contributing data to the National Pediatric Trauma Registry (NPTR) would apply objective evidence of actual injuries to define an expected standard and identify performance outliers. METHODS: Using a blinded code, children entered into phase III of the NPTR were aggregated by treating hospital. Individual patient ICISS survival probability (Ps) were calculated using survival risk ratios (SRR) derived from the phase II NPTR dataset (n = 53,253). For each center, sample size, observed mortality, and ICISS Ps were calculated. Probability of mortality (Pm) was computed as 1 - Ps. Logistic regression was used to develop a predictive model for mortality. Logit transformation of Pm was performed to adjust for the skew of minor injury in children and reduce overestimation of low Pm fatalities. Mean Pm was computed for each center and multiplied by its volume to determine expected frequency. Observed to expected ratio (O/E) and 95% confidence interval were calculated to define expected performance and outliers above or below 1 SD of the mean O/E. RESULTS: Patients treated at 30 pediatric trauma centers (mean volume = 451 +/- 258/patients per center) were evaluated. Mean O/E was 1.001 with SD = 0.404. Twenty-two centers fell within the reference range; O/E of 12 centers exceeded 1, suggesting performance below expectation. Trauma center volume, as reflected by sample, did not correlate to O/E performance. CONCLUSIONS: Application of ICISS Ps from a national pediatric benchmark population simplifies determination of expected mortality necessary to compute the expected component of National Surgical Quality Improvement Program. Analysis of these ratios of expected to observed mortality demonstrates variance among centers, defines performance against peers using the same benchmarks, and can drive performance improvement based on the objective evidence of injury diagnoses actually encountered.

The effect of delay in rehabilitation on outcome of severe traumatic brain injury.

BACKGROUND: Expeditious care within minutes of severe injury improves outcome and is the driving force for development of trauma care systems. Transition from hospital care to rehabilitation is an important step in recovery after trauma-related injury. We hypothesize that delay in the transition from acute care to rehabilitation adversely affects outcome and diminishes recovery after traumatic brain injury (TBI). METHODS: After institutional review board approval, the trauma registry of our regional level I pediatric trauma center was queried for all children with severe blunt TBI (initial Glasgow Coma Scale score

Surgical quality improvement: a simplified method to apply national standards to pediatric trauma care.

BACKGROUND: The emerging "pay for performance" national initiative mandates the development of valid metrics for risk stratification and performance assessment. The International Classification Injury Severity Score (ICISS) predicts survival from injury and is calculated as the product of survival risk ratios (SRRs) for a patient's 3 worst injuries. Survival risk ratios are derived as the proportion of fatalities for every International Classification of Diseases, Ninth Edition, Clinical Modification, diagnosis in a "benchmark" population. We hypothesized that the ICISS prediction model derived from the National Pediatric Trauma Registry (NPTR) would accurately predict mortality in an independent sample from a single pediatric trauma center (PTC) and could be applied to the NSQIP methodology to analyze performance. METHODS: The ICISS survival probabilities (Ps) were calculated for PTC patients using SRRs computed from 102,608 NPTR records. Records with a single diagnosis and Ps of 1 were excluded from the analysis. Receiver operator characteristics analysis (ROC) was used to evaluate the accuracy of Ps to predict mortality. The Hosmer-Lemeshow statistic was used to determine the degree that the NPTR-derived expected probabilities matched the observed mortality profile at the PTC. Program performance from 2000 to 2004 was then evaluated using Ps adjusted by logit transformation to predict expected mortality (E) for each year cohort. Observed mortality divided by expected mortality (O/E) was calculated for each year group to compare PTC performance to the NSQIP standard of one. The influence of injury severity on these results was determined by evaluating the correlation between O/E and mean Ps of each year cohort. RESULTS: A total of 1523 records were analyzed. The ROC area under the curve (AUC ) for Ps was .947 (confidence interval, .934-.957). The Hosmer-Lemeshow statistic (chi(2) = 5.102; df = 8; P = .747, not significant) indicated the model fit the data well. Adjusted O/E ratio after logit transformation of Ps for the PTC demonstrated initial performance slightly below standard (1.000778) followed by performance better than expected for the subsequent 4 years (range, .6466-.9784). The ratio of observed (O) to expected (E) demonstrated no correlation to mean Ps (r(2) = .378; P = .208). CONCLUSION: These data validate the application of injury diagnosis derived survival probabilities as objective metrics for determining performance using the NSQIP methodology. Incorporation of these objective predictors of expected outcome to calculation of the risk adjusted O/E ratio enables trend analysis of program performance over time. The lack of significant correlation between O/E and mean Ps demonstrates that NSQIP does indeed reflect process of care while adjusting for severity of patient pathologic condition.

Risk stratification simplified: the worst injury predicts mortality for the injured children.

BACKGROUND: The International Classification Injury Severity Score (ICISS) uses anatomic injury diagnoses to predict probability of survival (Ps) computed as the product of the survival risk ratios (SRR) of the three most severe injuries. SRRs are derived as the proportion of fatalities for every International Classification of Diseases-9th Revision-Clinical Modification diagnosis in a "benchmark" population. Pediatric-specific SRRs were computed from 103,434 entries in the National Pediatric Trauma Registry. We hypothesized that ICISS was a valid pediatric outcome predictor, and that the child's most severe injury; i.e., the lowest SRR, is the major driver of outcome, which can be used alone to predict survival. METHODS: Receiver operator characteristic analysis was used to assess the predictive validity of ICISS. SRRs derived from 53,235 phase II patients were used as the training set to calculate the Ps for 50,199 phase III children comprising the test set. The survival probability (Ps) computed from the standard three diagnoses was compared with that computed from only the worst injury (lowest SRR). Records with a single diagnosis or Ps of 1, indicating no mortality potential, were excluded from the analysis. Nagelkerke pseudo R2 defined what proportion of the predicted Ps was the effect of the worst injury alone versus the traditional Ps. RESULTS: A total of 25,239 records with at least two diagnoses with SRRs indicating risk of mortality were analyzed. The area under the receiver operator characteristic curve for traditional Ps was 0.935, compared with 0.932 for that calculated using only the lowest SRR. The difference of 0.003 was not significant (z = 1.061, p = 0.2888, NS). Nagelkerke pseudo R2 for the lowest SRR was 0.455 compared with 0.462 for the traditional three diagnosis Ps, which shows that the majority of Ps predictive power is related to the single injury with the lowest SRR. Further analysis demonstrated that this effect was related to frequency of coexistent injuries with no mortality risk rather than definable difference in severity. CONCLUSION: These data validate ICISS as predictive of pediatric injury survival. The dominant effect of the worst injury reflects an epidemiologic characteristic of pediatric trauma that will identify specific injuries for best practice analysis and focused injury prevention.

Interferon-gamma inhibits enterocyte migration by reversibly displacing connexin43 from lipid rafts.

Necrotizing enterocolitis (NEC) is associated with the release of interferon-gamma (IFN) by enterocytes and delayed intestinal restitution. Our laboratory has recently demonstrated that IFN inhibits enterocyte migration by impairing enterocyte gap junctions, intercellular channels that are composed of connexin43 (Cx43) monomers and that are required for enterocyte migration to occur. The mechanisms by which IFN inhibits gap junctions are incompletely understood. Lipid rafts are cholesterol-sphingolipid-rich microdomains of the plasma membrane that play a central role in the trafficking and signaling of various proteins. We now hypothesize that Cx43 is present on enterocyte lipid rafts and that IFN inhibits enterocyte migration by displacing Cx43 from lipid rafts in enterocytes. We now confirm our previous observations that intestinal restitution is impaired in NEC and demonstrate that Cx43 is present on lipid rafts in IEC-6 enterocytes. We show that lipid rafts are required for enterocyte migration, that IFN displaces Cx43 from lipid rafts, and that the phorbol ester phorbol 12-myristate 13-acetate (PMA) restores Cx43 to lipid rafts after treatment with IFN in a protein kinase C-dependent manner. IFN also reversibly decreased the phosphorylation of Cx43 on lipid rafts, which was restored by PMA. Strikingly, restoration of Cx43 to lipid rafts by PMA or by transfection of enterocytes with adenoviruses expressing wild-type Cx43 but not mutant Cx43 is associated with the restoration of enterocyte migration after IFN treatment. Taken together, these findings suggest an important role for lipid raft-Cx43 interactions in the regulation of enterocyte migration during exposure to IFN, such as NEC.

Hypertrophic pyloric stenosis in newborns younger than 21 days: remodeling the path of surgical intervention.

BACKGROUND: According to currently accepted diagnostic criteria, ultrasonography confirms hypertrophic pyloric stenosis (HPS) when the pyloric muscle thickness (MT) is greater than 4 mm and the pyloric channel length (CL) is greater than 15 mm. Hypertrophic pyloric stenosis frequently presents in newborns younger than 21 days; yet, the diagnostic criteria in this younger population remain poorly defined. We, therefore, sought to define the diagnostic criteria for HPS in newborns younger than 21 days. METHODS: Ultrasonographic measures of pyloric MT and CL were obtained by retrospective chart review (2000-2006) at a single institution for all newborns (aged 10 days to 6 weeks) with an intraoperatively proven diagnosis of HPS. Demographic characteristics and ultrasonographic measurements were collected, and features differentiating younger (21 days or younger) from older newborns were assessed. Measures of pyloric MT and CL were analyzed in 7-day increments, and comparisons were made between newborns aged 21 days or less and newborns 22 to 42 days of age. Based upon these features, a set of ultrasonographic parameters to establish the diagnosis of HPS in younger patients was defined. RESULTS: Three hundred fourteen newborns (83% male) underwent pyloromyotomy of whom 64% (n = 200) had a preoperative pyloric ultrasound. Sixty newborns (19%) were younger than 21 days, of whom 51 (85%) had preoperative ultrasonography. The ultrasound measurement of HPS was significantly decreased in younger vs older newborns: (MT, 3.7 +/- 0.65 vs 4.6 +/- 0.82 mm, P < .05; CL, 16.9 +/- 2.8 vs 18.2 +/- 3.4 mm, P < .05). Importantly, the mean ultrasound measurement for young newborns with HPS typically fell within the currently defined "normal" or "borderline" range. A linear relationship was determined to exist between pyloric MT and CL and patient age, suggesting the use of 3.5 mm as a "cutoff" in younger patients. CONCLUSIONS: These findings suggest that current guidelines to diagnose HPS do not accurately diagnose HPS in children younger than 3 weeks, and these findings raise the need to evaluate the decision analysis algorithm using prospective studies.

A critical role for TLR4 in the pathogenesis of necrotizing enterocolitis by modulating intestinal injury and repair.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in preterm infants and is characterized by translocation of LPS across the inflamed intestine. We hypothesized that the LPS receptor (TLR4) plays a critical role in NEC development, and we sought to determine the mechanisms involved. We now demonstrate that NEC in mice and humans is associated with increased expression of TLR4 in the intestinal mucosa and that physiological stressors associated with NEC development, namely, exposure to LPS and hypoxia, sensitize the murine intestinal epithelium to LPS through up-regulation of TLR4. In support of a critical role for TLR4 in NEC development, TLR4-mutant C3H/HeJ mice were protected from the development of NEC compared with wild-type C3H/HeOUJ littermates. TLR4 activation in vitro led to increased enterocyte apoptosis and reduced enterocyte migration and proliferation, suggesting a role for TLR4 in intestinal repair. In support of this possibility, increased NEC severity in C3H/HeOUJ mice resulted from increased enterocyte apoptosis and reduced enterocyte restitution and proliferation after mucosal injury compared with mutant mice. TLR4 signaling also led to increased serine phosphorylation of intestinal focal adhesion kinase (FAK). Remarkably, TLR4 coimmunoprecipitated with FAK, and small interfering RNA-mediated FAK inhibition restored enterocyte migration after TLR4 activation, demonstrating that the FAK-TLR4 association regulates intestinal healing. These findings demonstrate a critical role for TLR4 in the development of NEC through effects on enterocyte injury and repair, identify a novel TLR4-FAK association in regulating enterocyte migration, and suggest TLR4/FAK as a therapeutic target in this disease.

Interferon-gamma inhibits intestinal restitution by preventing gap junction communication between enterocytes.

BACKGROUND & AIMS: Necrotizing enterocolitis (NEC) is characterized by interferon-gamma (IFN-gamma) release and inadequate intestinal restitution. Because enterocytes migrate together, mucosal healing may require interenterocyte communication via connexin 43-mediated gap junctions. We hypothesize that enterocyte migration requires interenterocyte communication, that IFN impairs migration by impairing connexin 43, and that impaired healing during NEC is associated with reduced gap junctions. METHODS: NEC was induced in Swiss-Webster or IFN(-/-) mice, and restitution was determined in the presence of the gap junction inhibitor oleamide, or via time-lapse microscopy of IEC-6 cells. Connexin 43 expression, trafficking, and localization were detected in cultured or primary enterocytes or mouse or human intestine by confocal microscopy and (35)S-labeling, and gap junction communication was assessed using live microscopy with oleamide or connexin 43 siRNA. RESULTS: Enterocytes expressed connexin 43 in vitro and in vivo, and exchanged fluorescent dye via gap junctions. Gap junction inhibition significantly reduced enterocyte migration in vitro and in vivo. NEC was associated with IFN release and loss of enterocyte connexin 43 expression. IFN inhibited enterocyte migration by reducing gap junction communication through the dephosphorylation and internalization of connexin 43. Gap junction inhibition significantly increased NEC severity, whereas reversal of the inhibitory effects of IFN on gap junction communication restored enterocyte migration after IFN exposure. Strikingly, IFN(-/-) mice were protected from the development of NEC, and showed restored connexin 43 expression and intestinal restitution. CONCLUSIONS: IFN inhibits enterocyte migration by preventing interenterocyte gap junction communication. Connexin 43 loss may provide insights into the development of NEC, in which restitution is impaired.

Nitric oxide inhibits enterocyte migration through activation of RhoA-GTPase in a SHP-2-dependent manner.

Diseases of intestinal inflammation like necrotizing enterocolitis (NEC) are associated with impaired epithelial barrier integrity and the sustained release of intestinal nitric oxide (NO). NO modifies the cytoskeletal regulator RhoA-GTPase, suggesting that NO could affect barrier healing by inhibiting intestinal restitution. We now hypothesize that NO inhibits enterocyte migration through RhoA-GTPase and sought to determine the pathways involved. The induction of NEC was associated with increased enterocyte NO release and impaired migration of bromodeoxyuridine-labeled enterocytes from terminal ileal crypts to villus tips. In IEC-6 enterocytes, NO significantly inhibited enterocyte migration and activated RhoA-GTPase while increasing the formation of stress fibers. In parallel, exposure of IEC-6 cells to NO increased the phosphorylation of focal adhesion kinase (pFAK) and caused a striking increase in cell-matrix adhesiveness, suggesting a mechanism by which NO could impair enterocyte migration. NEC was associated with increased expression of pFAK in the terminal ileal mucosa of wild-type mice and a corresponding increase in disease severity compared with inducible NO synthase knockout mice, confirming the dependence of NO for FAK phosphorylation in vivo and its role in the pathogenesis of NEC. Strikingly, inhibition of the protein tyrosine phosphatase SHP-2 in IEC-6 cells prevented the activation of RhoA by NO, restored focal adhesions, and reversed the inhibitory effects of NO on enterocyte migration. These data indicate that NO impairs mucosal healing by inhibiting enterocyte migration through activation of RhoA in a SHP-2-dependent manner and support a possible role for SHP-2 as a therapeutic target in diseases of intestinal inflammation like NEC.

The role of the intestinal barrier in the pathogenesis of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the leading cause of death from gastrointestinal disease in neonates and is increasing in frequency because of recent advances in neonatal care. NEC develops in a stressed preterm infant in the setting of intestinal barrier disruption, systemic inflammation, and leads to, multisystem organ failure. The intestinal barrier lies at the interface between microbes within the intestinal lumen and the immune system of the host, and has both immunological and mechanical components. These components serve to protect the host from invading pathogens and, at the same time, provide a surface area for nutrient absorption. Factors that lead to impairments in the function of the intestinal barrier may predispose the host to the invasion of gut-derived microbes and to the development of systemic inflammatory disease. This process, termed "bacterial translocation," may be compounded during instances in which the mechanisms that regulate the repair of the intestinal barrier are disrupted. Bacterial translocation is of particular concern to the newborn patient, in which immaturity of the mechanical barrier and incomplete development of the host immune system combine to render the host at particular risk for the development of intestinal inflammation. This review will serve to provide an overview of recent evidence regarding the components of the intestinal barrier, and the mechanisms by which disruptions in barrier function may contribute to the pathogenesis of NEC.

An analysis of proctoscopy vs computed tomography scanning in the diagnosis of rectal injuries in children: which is better?

BACKGROUND: Current dogma suggests that the diagnosis of rectal injury can be made after physical examination and proctoscopy (PR). However, anecdotal evidence suggests that these modalities lack specificity when applied to children and that computed tomography (CT) scanning may be superior. A direct comparison between CT scanning and PR has not been performed. We therefore sought to compare CT with PR in the diagnosis of rectal injury by analyzing our large institutional experience. METHODS: To assess institutional outcome, the charts of all children younger than 18 years admitted to our level I trauma center (1999-2004) were prospectively collected and retrospectively assessed. Demographics, diagnostic accuracy (PR vs CT), and outcome (length of stay, days in the intensive care unit [ICU], Injury Severity Score, and missed injury) were assessed. RESULTS: There were 24 injuries (63% boys, 71% blunt, 100% survival), and diagnostic modality included the following: PR, 37.5%; CT, 37.5%; laparotomy alone, 8%. Length of stay (PR 5.7 +/- 6.2 vs CT 13.7 +/- 22.2, NS) were similar between groups. Of the missed rectal injuries, 66% of patients undergoing PR had missed injuries that were ultimately detected by CT whereas 33% of the patients undergoing CT scan had a missed injury. CONCLUSION: CT is at least as accurate as PR in diagnosing pediatric rectal injury. Consideration of early scanning as opposed to PR may improve diagnosis and outcome in these patients.