Patrick J. O'Neill

Diagnosis and Management of Complicated Intra-abdominal Infection in Adults and Children: Guidelines by the Surgical Infection Society and the Infectious Diseases Society of America

Evidence-based guidelines for managing patients with intra-abdominal infection were prepared by an Expert Panel of the Surgical Infection Society and the Infectious Diseases Society of America. These updated guidelines replace those previously published in 2002 and 2003. The guidelines are intended for treating patients who either have these infections or may be at risk for them. New information, based on publications from the period 2003-2008, is incorporated into this guideline document. The panel has also added recommendations for managing intra-abdominal infection in children, particularly where such management differs from that of adults; for appendicitis in patients of all ages; and for necrotizing enterocolitis in neonates.

Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America.

Evidence-based guidelines for managing patients with intra-abdominal infection were prepared by an Expert Panel of the Surgical Infection Society and the Infectious Diseases Society of America. These updated guidelines replace those previously published in 2002 and 2003. The guidelines are intended for treating patients who either have these infections or may be at risk for them. New information, based on publications from the period 2003-2008, is incorporated into this guideline document. The panel has also added recommendations for managing intra-abdominal infection in children, particularly where such management differs from that of adults; for appendicitis in patients of all ages; and for necrotizing enterocolitis in neonates.

Trial of Short-Course Antimicrobial Therapy for Intraabdominal Infection

BACKGROUND The successful treatment of intraabdominal infection requires a combination of anatomical source control and antibiotics. The appropriate duration of antimicrobial therapy remains unclear. METHODS We randomly assigned 518 patients with complicated intraabdominal infection and adequate source control to receive antibiotics until 2 days after the resolution of fever, leukocytosis, and ileus, with a maximum of 10 days of therapy (control group), or to receive a fixed course of antibiotics (experimental group) for 4±1 calendar days. The primary outcome was a composite of surgical-site infection, recurrent intraabdominal infection, or death within 30 days after the index source-control procedure, according to treatment group. Secondary outcomes included the duration of therapy and rates of subsequent infections. RESULTS Surgical-site infection, recurrent intraabdominal infection, or death occurred in 56 of 257 patients in the experimental group (21.8%), as compared with 58 of 260 patients in the control group (22.3%) (absolute difference, -0.5 percentage point; 95% confidence interval [CI], -7.0 to 8.0; P=0.92). The median duration of antibiotic therapy was 4.0 days (interquartile range, 4.0 to 5.0) in the experimental group, as compared with 8.0 days (interquartile range, 5.0 to 10.0) in the control group (absolute difference, -4.0 days; 95% CI, -4.7 to -3.3; P<0.001). No significant between-group differences were found in the individual rates of the components of the primary outcome or in other secondary outcomes. CONCLUSIONS In patients with intraabdominal infections who had undergone an adequate source-control procedure, the outcomes after fixed-duration antibiotic therapy (approximately 4 days) were similar to those after a longer course of antibiotics (approximately 8 days) that extended until after the resolution of physiological abnormalities. (Funded by the National Institutes of Health; STOP-IT ClinicalTrials.gov number, NCT00657566.).

Role of Kupffer cells in interleukin-6 release following trauma-hemorrhage and resuscitation.

Although Interleukin-6 (IL-6) plays an important role in the pathophysiology of traumahemorrhage and resuscitation, the cellular origin of this inflammatory cytokine remains unknown. This study was undertaken to determine whether Kupffer cells (KC) are a major source of IL-6 release following traumahemorrhage and resuscitation. KC numbers were significantly (p > .05) reduced in vivo with gadolinium chloride (GdCI3; 10 mg/kg IV). KC-reduced (KC(−)) and KC-normal (saline-treated; KC(+)) rats underwent laparotomy (i.e., trauma-induced), followed by either sham operation or hemorrhage. Hemorrhaged rats were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of the shed blood volume was returned as Ringers lactate, and then resuscitated with Ringers lactate (four times shed blood volume over 1 h). Results indicate that KC reduction per se had no effect on any measured parameter at any time. At 0.5 and 2.0 h postresuscitation, mean arterial pressure, heart rate, cardiac output, stroke volumen, and hematocrit were reduced to a similar extent in both the KC(+) and KC(−) hemorrhage groups. KC reduction did, however, significantly reduce plasma IL-6 concentration (means ± S.E.; U/ml) at both 0.5 h (KC(+) = 709 ± 391 vs. KC(−) = 159 ± 5) and at 2.0 h (KC(+) = 527 ± 394 vs. KC(−) = 83 ± 20) postresuscitation. In conclusion, this study demonstrates that KC are a major source of in vivo IL-6 release following trauma-hemorrhage and resuscitation.

An evaluation of multidetector computed tomography in detecting pancreatic injury: results of a multicenter AAST study.

BACKGROUND Efforts to determine the suitability of low-grade pancreatic injuries for nonoperative management have been hindered by the inaccuracy of older computed tomography (CT) technology for detecting pancreatic injury (PI). This retrospective, multicenter American Association for the Surgery of Trauma-sponsored trial examined the sensitivity of newer 16- and 64-multidetector CT (MDCT) for detecting PI, and sensitivity/specificity for the identification of pancreatic ductal injury (PDI). METHODS Patients who received a preoperative 16- or 64-MDCT followed by laparotomy with a documented PI were enrolled. Preoperative MDCT scans were classified as indicating the presence (+) or absence (-) of PI and PDI. Operative notes were reviewed and all patients were confirmed as PI (+), and then classified as PDI (+) or (-). As all patients had PI, an analysis of PI specificity was not possible. PI patients formed the pool for further PDI analysis. As sensitivity and specificity data were available for PDI, multivariate logistic regression was performed for PDI patients using the presence or absence of agreement between CT and operative note findings as an independent variable. Covariates were age, gender, Injury Severity Score, mechanism of injury, presence of oral contrast, presence of other abdominal injuries, performance of the scan as part of a dedicated pancreas protocol, and image thickness < or =3 mm or > or =5 mm. RESULTS Twenty centers enrolled 206 PI patients, including 71 PDI (+) patients. Intravenous contrast was used in 203 studies; 69 studies used presence of oral contrast. Eight-nine percent were blunt mechanisms, and 96% were able to have their duct status operatively classified as PDI (+) or (-). The sensitivity of 16-MDCT for all PI was 60.1%, whereas 64-MDCT was 47.2%. For PDI, the sensitivities of 16- and 64-MDCT were 54.0% and 52.4%, respectively, with specificities of 94.8% for 16-MDCT scanners and 90.3% for 64-MDCT scanners. Logistic regression showed that no covariates were associated with an increased likelihood of detecting PDI for either 16- or 64-MDCT scanners. The area under the curve was 0.66 for the 16-MDCT PDI analysis and 0.77 for the 64-MDCT PDI analysis. CONCLUSION Sixteen and 64-MDCT have low sensitivity for detecting PI and PDI, while exhibiting a high specificity for PDI. Their use as decision-making tools for the nonoperative management of PI are, therefore, limited.

Mechanism of splenic immunosuppression during sepsis: key role of Kupffer cell mediators.

Studies indicate that the liver, in particular the Kupffer cells, appear to be key contributors in the systemic inflammatory mediator response associated with shock and sepsis. Although several of these agents have been implicated as mediators of depressed immunoresponsiveness observed during sepsis, it remains unknown whether or not mediators released specifically by Kupffer cells play any significant role in producing the cellular dysfunction in distant organs. The aim of this study, therefore, was to determine whether or not acute Kupffer cell reduction before the onset of sepsis would protect splenic lymphocyte function. Kupffer cell number was reduced by prior (48 hours) treatment of mice with gadolinium chloride (GdCl2, 10 mg/kg of body weight, intravenously) or saline vehicle. Animals were then subjected to either sham-CLP (sham) or polymicrobial sepsis in the form of cecal ligation and puncture (CLP). Plasma and splenocytes were harvested at 2 or 24 hours after CLP. Splenocyte cultures were exposed to 2.5 micrograms concanavalin A/mL to assess their ability to release lymphokines. Cytokine (interleukin (IL)-2, IL-6, interferon-gamma, tumor necrosis factor-alpha) concentration in plasma or cell supernatants was assessed by bioassay. The results indicated that GdCl2 treated mice exhibited a marked reduction in circulating IL-6 levels at both 2 and 24 hours after CLP. Furthermore, the reduction of Kupffer cell number before the onset of sepsis completely prevented the depression of splenocyte IL-2 and interferon-gamma release, capacity. Thus mediators released by Kupffer cells during the systemic inflammatory response to polymicrobial sepsis play a significant role in producing immune dysfunction in resident splenic lymphocytes. In view of this, it appears that modulation of Kupffer cell hyperactivity during sepsis may be a novel approach for maintaining distant organ host defense mechanisms.

Trauma center variation in splenic artery embolization and spleen salvage: A multicenter analysis

BACKGROUND This study aimed to evaluate if variation in management of blunt splenic injury (BSI) among Level I trauma centers is associated with different outcomes related to the use of splenic artery embolization (SAE). METHODS All adult patients admitted for BSI from 2008 to 2010 at 4 Level I trauma centers were reviewed. Use of SAE was determined, and outcomes of spleen salvage and nonoperative management (NOM) failure were evaluated. A priori, a 10% SAE rate was used to group centers into high- or low-use groups. RESULTS There were 1,275 BSI patients. There were intercenter differences in age, injury severity, and grade of spleen injury (Spleen Injury Scale [SIS]). Mortality was similar by center; however, BSI treatment varied significantly by center. Overall, SAE use was highest at center A compared with B, C, and D (19%, 11%, 1%, and 4%, respectively; p < 0.01). High SAE use centers had significantly higher spleen salvage rates and fewer NOM failures. Differences in the use of SAE (25% vs. 2%, p < 0.01) and salvage rate (67% vs. 56%, p = 0.03) were most dramatic between high- and low-use SAE centers for Grade 3 and 4 injured spleens. In patients who received initial NOM, multivariate logistic regression analysis showed that SAE was an independent predictor of spleen salvage (odds ratio, 5; 95% confidence interval, 1.8–13.5; p < 0.01) as were lower age, lower SIS, and Injury Severity Score (ISS). Patients treated at high SAE use centers were more likely to leave the hospital with their spleen in situ (odds ratio, 3; 95% confidence interval, 1.7–6.3; p < 0.01). CONCLUSION Significant practice variation exists in the use of SAE in treating BSI at Level I trauma centers. Centers with higher rates of SAE use have higher spleen salvage and less NOM failure. SAE was shown to be an independent predictor of spleen salvage. LEVEL OF EVIDENCE Therapeutic study, level IV.

Pentobarbital coma for refractory intra-cranial hypertension after severe traumatic brain injury: mortality predictions and one-year outcomes in 55 patients

OBJECTIVE To identify predictors of mortality and long-term outcomes in survivors after pentobarbital coma (PBC) in patients failing current treatment standards for severe traumatic brain injuries (TBI). This is a retrospective cohort study of severe TBI patients receiving PBC at Level I Trauma Center and tertiary university hospital. METHODS Four thousand nine hundred thirty-four patients were admitted to the trauma intensive care unit with severe TBI (head Abbreviated Injury Scale >or= 3) between April 1998 and December 2004. Six hundred eleven received intracranial pressure (ICP) monitoring and 58 received PBC. Three patients underwent craniotomy for intracranial mass lesion and were excluded. The study group received standardized medical management for severe TBI including opiates, benzodiazepines, elevation of the head of bed, avoidance of hypotension and hypercapnia and hyperosmolar therapy (HOsmRx). In addition, 31 of 55 patients (56%) underwent placement of intraventricular catheters for cerebrospinal fluid drainage. If routine medical management and cerebrospinal fluid diversion failed to control ICP, then the patient was determined to have refractory intracranial hypertension (RICH) and PBC treatment was initiated. PBC was performed with pentobarbital infusion with continuous electroencephalogram monitoring to ensure adequate burst suppression. The measurements include serum sodium (Na) and osmolality (Osm) were assessed as indicators for initiation of PBC and to estimate the 50% mortality cut-points when controlling for ICP. Follow-up functional outcomes were assessed using the Glasgow Outcome Scale and stratified according to admission Glasgow Coma Scale score and Marshall computed tomography classification. Of the 55 PBC patients, 22 (40%) survived at discharge. 19 of 22 had long-term follow-up (1 year or more) available. Of these, 13 (68%) were normal or functionally independent (Glasgow Outcome Scale score 4 or 5). Serum Na and Osm were associated with death (p < 0.05) when controlling for ICP. The 50% mortality cut-points were Na of 160 mEq/L and Osm of 330 mOsm/kg H2O. Median minimum cerebral perfusion pressure after PBC was 42 mm Hg in survivors and 34 mm Hg in nonsurvivors (p = 0.013). CONCLUSIONS In patients with severe TBI and RICH, survival at discharge of 40% with good functional outcomes in 68% of survivors at 1 year or more can be achieved with PBC after failure of HOsmRx. Based on 50% mortality cut-points, analysis suggests the limits of HOsmRx to be Na of 160 mEq/L and Osm of 330 mOsm/Kg H2O. Maintenance of higher cerebral perfusion pressure after PBC is associated with survival. PBC treatment of RIH may be even more important when other treatments of RIH, such as decompressive craniectomy, are not available.

Risk factors for blunt cerebrovascular injury in children: do they mimic those seen in adults?

BACKGROUND Eastern Association for the Surgery of Trauma guideline for the evaluation of blunt cerebrovascular injury (BCVI) states that pediatric trauma patients should be evaluated using the same criteria as the adult population. The purpose of our study was to determine whether adult criteria translate to the pediatric population. METHODS Retrospective evaluation was performed at a Level I trauma center of blunt pediatric trauma patients (age <15 years) presenting over a 5-year period. Data obtained included patient demographics, presence of adult risk factors for BCVI (Glasgow coma scale ≤8, skull base fracture, cervical spine fracture, complex facial fractures, and soft tissue injury to the neck), presence of signs/symptoms of BCVI, method of evaluation, treatment, and outcome. RESULTS A total of 1,209 pediatric trauma patients were admitted during the study period. While 128 patients met criteria on retrospective review for evaluation based on Eastern Association for the Surgery of Trauma criteria, only 52 patients (42%) received subsequent radiographic evaluation. In all, 14 carotid artery or vertebral artery injuries were identified in 11 patients (all admissions, 0.9% incidence; all screened, 21% incidence). Adult risk factors were present in 91% of patients diagnosed with an injury. Major thoracic injury was found in 67% of patients with carotid artery injuries. Cervical spine fracture was found in 100% of patients with vertebral artery injuries. Stroke occurred in four patients (36%). Stroke rate after admission for untreated patients was 38% (3/8) versus 0.0% in those treated (0/2). Mortality was 27% because of concomitant severe traumatic brain injury. CONCLUSION Risk factors for BCVI in the pediatric trauma patient appear to mimic those of the adult patient.

Decompressive craniectomy or medical management for refractory intracranial hypertension: An AAST-MIT propensity score analysis

BACKGROUND Moderate/severe traumatic brain injury (TBI) management involves minimizing cerebral edema to maintain brain oxygen delivery. While medical therapy (MT) consisting of diuresis, hyperosmolar therapy, ventriculostomy, and barbiturate coma is the standard of care, decompressive craniectomy (DC) for refractory intracranial hypertension (ICH) has gained renewed interest. Since TBI treatment guidelines consider DC a second-tier intervention after MT failure, we sought to determine if early DC (<48 hours) was associated with improved survival in patients with refractory ICH. METHODS Eleven Level 1 trauma centers provided clinical data and head computed tomographic scans for patients with a Glasgow Coma Scale (GCS) score of 13 or less and radiographic evidence of TBI excluding deaths within 48 hours. Computed tomographic scans were graded according to the Marshall classification. A propensity score to receive DC (regardless of whether DC was performed) was calculated for each patient based on patient characteristics, physiology, injury severity, GCS, severity of intracranial injury, and treatment center. Patients who actually received a DC were matched to patients with similar propensity scores who received MT for analysis. Outcomes were compared between early (<48 hours of injury) primary or secondary DC and matched controls and then between early primary DC only and matched controls. RESULTS There were 2,602 patients who met the inclusion criteria ,of whom 264 (10.1%) received DC (either primary or secondary to another cranial procedure) and 109 (5%) had a DC that was primary. Variables associated with performing a DC included sex, race, intracranial pressure monitor placement, in-house trauma attending, traumatic subarachnoid hemorrhage, midline shift, and basal cistern compression. There was no survival benefit with early primary DC compared with the controls (relative risk, 1.07; 95% confidence interval, 0.67–1.73; p = 0.77), and resource use was higher. CONCLUSION Early DC does not seem to significantly improve mortality in patients with refractory ICH compared with MT. Neurosurgeons should pause before entertaining this resource-demanding form of therapy. LEVEL OF EVIDENCE Therapeutic care/management, level III.