Erratum to: The management of intra-abdominal infections from a global perspective: 2017 WSES guidelines for management of intra-abdominal infections.

[This corrects the article DOI: 10.1186/s13017-017-0141-6.].

Erratum to: Antimicrobials: a global alliance for optimizing their rational use in intra-abdominal infections (AGORA).

[This corrects the article DOI: 10.1186/s13017-016-0089-y.].

Erratum to: 2016 WSES guidelines on acute calculous cholecystitis.

[This corrects the article DOI: 10.1186/s13017-016-0082-5.].

2016 WSES guidelines on acute calculous cholecystitis.

Acute calculus cholecystitis is a very common disease with several area of uncertainty. The World Society of Emergency Surgery developed extensive guidelines in order to cover grey areas. The diagnostic criteria, the antimicrobial therapy, the evaluation of associated common bile duct stones, the identification of "high risk" patients, the surgical timing, the type of surgery, and the alternatives to surgery are discussed. Moreover the algorithm is proposed: as soon as diagnosis is made and after the evaluation of choledocholitiasis risk, laparoscopic cholecystectomy should be offered to all patients exception of those with high risk of morbidity or mortality. These Guidelines must be considered as an adjunctive tool for decision but they are not substitute of the clinical judgement for the individual patient.

The epidemic of pre-injury oral antiplatelet and anticoagulant use.

BACKGROUND: As the population ages, an increasing number of trauma patients are taking antiplatelet and anticoagulant medications (ACAP) prior to their injuries. These medications increase their risk of hemorrhagic complications, particularly intracerebral hemorrhage. Clopidogrel and warfarin are common and their mechanisms well understood, but optimal reversal methods continue to evolve. The novel direct thrombin and factor Xa inhibitors are less well described and do not have existing antidotes. METHODS: This article reviews the relevant literature on traumatic outcomes with use of ACAP medications, as well as data on ideal reversal strategies. Suggested algorithms are introduced, and future research directions discussed. RESULTS: Although they are beneficial in preventing clot formation, once bleeding occurs ACAP medications contribute to increased morbidity and mortality, particularly in geriatric patient populations. The efficacy of clopidogrel reversal with platelet transfusions and DDAVP remains unclear. Warfarin use is best treated with the algorithm-driven use of plasma, vitamin K, prothrombin complex concentrates (PCCs) and possibly recombinant factor VIIa depending upon specific patient and injury factors. Optimal treatment for direct thrombin and factor Xa inhibitors has yet to be developed, but PCCs are promising for rivaroxaban and apixaban while dabigatran is best treated with medication cessation and the possible addition of activated PCCs or hemodialysis. CONCLUSION: New developments in reversal of the ACAP medications are promising, particularly PCCs for warfarin and the factor Xa inhibitors. Function assays and clear antidotes are needed for the thrombin and Xa inhibitors. Research on outcomes and appropriate treatments is actively ongoing.

Planned re-laparotomy and the need for optimization of physiology and immunology.

Planned re-laparotomy or damage control laparotomy (DCL), first described by Dr. Harlan Stone in 1983, has become a widely utilized technique in a broad range of patients and operative situations. Studies have validated the use of DCL by demonstrating decreased mortality and morbidity in trauma, general surgery and abdominal vascular catastrophes. Indications for planned re-laparotomy include severe physiologic derangements, coagulopathy, concern for bowel ischemia, and abdominal compartment syndrome. The immunology of DCL patients is not well described in humans, but promising animal studies suggest a benefit from the open abdomen (OA) and several human trials on this subject are currently underway. Optimal critical care of patients with OA's, including sedation, paralysis, nutrition, antimicrobial and fluid management strategies have been associated with improved closure rates and recovery.

Nutritional support in patients following damage control laparotomy with an open abdomen.

INTRODUCTION: Damage control laparotomy (DCL) and the open abdomen have been well accepted following either severe abdominal trauma or emergency surgical disease. As DCL is increasingly utilized as a therapeutic option, appropriate management of the post-DCL patient is important. Early caloric support by enteral nutrition (EN) in the critically ill patient improves wound healing and decreases septic complications, lung injury, and multi-system organ failure. However, following DCL, nutritional strategies can be challenging and, at times, even daunting. CONCLUSIONS: Even though limited data exist, the use of early EN following DCL seems safe, provided that the patient is not undergoing active resuscitation or the bowel is not in discontinuity. It is unknown as to whether EN in the open abdomen reduces septic complications, prevents enterocutaneous fistula (ECF), or alters the timing of definitive abdominal wall closure. Future investigation in a prospective manner may help elucidate these important questions.

Acute lower GI bleeding for the acute care surgeon: current diagnosis and management.

Lower gastrointestinal bleeding is a common cause for hospital admission that results in significant morbidity and mortality. After initial resuscitation of the patient, the diagnosis and treatment of lower gastrointestinal bleeding remains a challenge for acute care surgeons. Identifying the source of bleeding can be difficult since many patients bleed intermittently or stop bleeding spontaneously. It is therefore important for the acute care surgeon to be familiar with the different diagnostic and therapeutic modalities and their advantages and disadvantages in order to guide the management of the acutely bleeding patient. This review summarizes the current methods available for the diagnosis and treatment of acute lower gastrointestinal bleeding and proposes an algorithm for the management of these patients.

A 20-year experience with portal and superior mesenteric venous injuries: has anything changed?

OBJECTIVES: To identify predictive factors causing mortality in patients with injuries to the portal (PV) and superior mesenteric veins (SMV). DESIGN: Retrospective analysis of prospectively collected data. MATERIALS AND METHODS: Adults admitted with blunt or penetrating PV and SMV injuries at an academic level I trauma center during a 20-year period. RESULTS: Of 26,387 major trauma victims admitted from 1987 through 2006, 26 sustained PV or SMV injuries (PV=15, SMV=11). Mechanism of injury was penetrating in 19 (73%) and 20 were in shock. Active hemorrhage occurred in 21. Most patients had associated injuries (2.9+/-1.8/patient). Mean Injury Severity Score (ISS) was 27.8+/-16.8. All PV injuries underwent suture repair and 27% of SMV injuries were ligated. Overall mortality was 46% (PV=47%, SMV=45%). Stab wounds had a lower mortality (31%) compared to gunshot wounds (67%) and blunt injuries (57%). Nonsurvivors had a higher ISS (35.8 vs. 20.9; p=0.02), more associated injuries (3.7 vs. 2.2; p=0.02), were older, and had active hemorrhage. Active hemorrhage (p=0.04) was independently related to death while shock on admission (odds ratio=6.1, p=0.61) trended toward higher mortality. CONCLUSION: Despite improvements in trauma care, mortality of PV and SMV injuries remains high. Shock, active hemorrhage, and associated injuries were predictive of increased mortality.

Hyperthermia induced after recirculation triggers chronic neurodegeneration in the penumbra zone of focal ischemia in the rat brain.

Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed the effects of HT induced after recirculation of focal brain ischemia on infarct size during long survival times. Adult male Wistar rats underwent intra-luminal occlusion of the left middle cerebral artery for 60 min followed by HT (39.0-39.5 degrees C) or normothermia. Control procedures included none and sham surgery with and without HT, and middle cerebral artery occlusion alone. Part I: 6-h HT induced at recirculation. Part II: 2-h HT induced at 2-, 6-, or 24-h recirculation. Part III: 2-h HT initiated at recirculation or 6-h HT initiated at 2-, 6- or 24-h recirculation. Survival periods were 7 days, 2 or 6 months. The effects of post-ischemic HT on cortex and striatum were evaluated histopathologically by measuring the area of remaining tissue in the infarcted hemisphere at -0.30 mm from bregma. Six-hour HT initiated from 6-h recirculation caused a significant decrease in the remaining cortical tissue between 7-day (N = 8) and 2-month (N = 8) survivals (98.46 +/- 1.14 to 73.62 +/- 8.99%, respectively). When induced from 24-h recirculation, 6-h HT caused a significant reduction of the remaining cortical tissue between 2- (N = 8) and 6-month (N = 9) survivals (94.97 +/- 5.02 vs 63.26 +/- 11.97%, respectively). These data indicate that post-ischemic HT triggers chronic neurodegenerative processes in ischemic penumbra, suggesting that similar fever-triggered effects may annul the benefit of early recirculation in stroke patients over the long-term.

Hyperthermia induced after recirculation triggers chronic neurodegeneration in the penumbra zone of focal ischemia in the rat brain

Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed the effects of HT induced after recirculation of focal brain ischemia on infarct size during long survival times. Adult male Wistar rats underwent intra-luminal occlusion of the left middle cerebral artery for 60 min followed by HT (39.0-39.5°C) or normothermia. Control procedures included none and sham surgery with and without HT, and middle cerebral artery occlusion alone. Part I: 6-h HT induced at recirculation. Part II: 2-h HT induced at 2-, 6-, or 24-h recirculation. Part III: 2-h HT initiated at recirculation or 6-h HT initiated at 2-, 6- or 24-h recirculation. Survival periods were 7 days, 2 or 6 months. The effects of post-ischemic HT on cortex and striatum were evaluated histopathologically by measuring the area of remaining tissue in the infarcted hemisphere at -0.30 mm from bregma. Six-hour HT initiated from 6-h recirculation caused a significant decrease in the remaining cortical tissue between 7-day (N = 8) and 2-month (N = 8) survivals (98.46 ± 1.14 to 73.62 ± 8.99 percent, respectively). When induced from 24-h recirculation, 6-h HT caused a significant reduction of the remaining cortical tissue between 2- (N = 8) and 6-month (N = 9) survivals (94.97 ± 5.02 vs 63.26 ± 11.97 percent, respectively). These data indicate that post-ischemic HT triggers chronic neurodegenerative processes in ischemic penumbra, suggesting that similar fever-triggered effects may annul the benefit of early recirculation in stroke patients over the long-term.

Postischemic hyperthermia induces Alzheimer-like pathology in the rat brain.

This study addresses the effects of induced hyperthermia on post-ischemic rat brain evaluated histologically and/or immunohistochemically after 7-day, 2-month or 6-month survival. Hyperthermia (38.5 degrees - 40 degrees C) maintained (by heating the cage environment to 34-35 degrees C) for two consecutive periods of 5 and 9 h timed, respectively, from 4- and 21-h recirculation following 10-min global ischemia (two-vessel occlusion + hypotension) induced chronic neuronal death that became apparent in the rat forebrain from 7-day to 2-month survival. Associated immunohistochemical findings after 2 or 6 months of recovery included: (1) complement activation (membrane attack complex formation); (2) generalized overexpression of ubiquitin in surviving forebrain neurons; (3) persistent activation of macrophages; (4) presence of gemistocytic astrocytes in the hippocampus; (5) maturation of amyloid plaques (identified by immunohistochemistry using anti-human beta-A4 primary antibody) in cerebral cortex; and (6) intracellular deposits identified by anti-human hyperphosphorylated tau protein antibodies. This novel non-transgenic, self-sustained model of neurodegeneration triggered by the association of two prevalent insults to the aging human brain (ischemia and hyperthermia) presents morphological features similar to those of Alzheimer's disease. This finding raises the possibility that febrile complications of acute brain injuries may similarly impair human cognitive function in the long run.

The 15-year evolution of an urban trauma center: what does the future hold for the trauma surgeon?

BACKGROUND: Safer cars, decreased violence, and nonoperative management have changed the trauma patient's nature. We evaluated changes in a Level I trauma center over 15 years and considered their effect on trauma surgeons. METHODS: From January 1985 through August 1999, 16,799 trauma registry patients were analyzed for mechanism of injury, Injury Severity Score, and procedures. RESULTS: Mean Injury Severity Score decreased from 15.9 to 10.7 and length of stay fell from 8.0 days to 5.9 days. There were significant decreases in penetrating trauma admissions and percentage of patients with Abbreviated Injury Scale score > 3 for head, chest, and abdomen. Frequency of craniotomy, thoracotomy, and laparotomy dropped dramatically. CONCLUSION: Significant decreases in injury severity, penetrating violence, and operations have occurred over 15 years. These changes will have profound effects on the practice of trauma surgeons and on surgical education.

Management of penetrating pancreatic trauma: an 11-year experience of a level-1 trauma center.

INTRODUCTION: We present our experience in the management of penetrating pancreatic injuries, focusing on factors related to complications and death. METHODS: Retrospective trauma registry-based analysis of 62 consecutive patients with penetrating pancreatic injuries during an 11-year period. Overall injury severity was assessed by the injury severity score (ISS) and the penetrating abdominal trauma index (PATI). Pancreatic injuries were graded according to the American Association for the Surgery of Trauma (AAST) Organ Injury Scaling (OIS). Complications were characterised using standardised definitions. Mortality was recorded as early (within 48 h after admission) and late (after 48 h). RESULTS: Thirty patients suffered gunshot wounds and 24 had grade I pancreatic injuries. Shotgun and gunshot wounds were more destructive than stab wounds (higher PATI, number of intraabdominal injuries and mortality). Seventeen patients died. Most deaths occurred within 1 h after admission due to massive bleeding and severe associated injuries. Only one death was potentially related to the pancreatic injury. Mortality rate also correlated with pancreatic injury grading. Sixty-one patients had associated intraabdominal injuries. Combined pancreaticoduodenal injuries were present in 13 patients, and five died. Simple drainage was the most common procedure performed. Pancreas-related complications were found in 12 out of 47 patients who survived more than 48 h; intraabdominal abscess (n=7) that was associated with colon injuries, and pancreatic fistula (n=5). CONCLUSION: An approach based on injury grade and location is advised. Routine drainage is recommended; distal resection is indicated in the presence of main duct injury, and the management of severe injuries will be tailored according to the overall physiologic status, presence of associated injuries, and duodenal viability. Morbidity and mortality is mainly due to associated injuries.

Hypertonic saline and pentoxifylline prevent lung injury and bacterial translocation after hemorrhagic shock.

Previous reports have shown beneficial effects of pentoxifylline (PTX) and hypertonic saline (HS) in the treatment of hemorrhagic shock. We compared the effects of these solutions to those of conventional lactated Ringer's (LR) treatment on bacterial translocation (BT), lung injury and total and differential cell count in the bronchoalveolar lavage fluid (BAL) after hemorrhagic shock. Rats (280-330 g) were bled to a MAP of 35 mmHg for 1 h and then randomized into 4 groups: LR (3x shed blood); HS (7,5% NaCl, 4 mL/kg); LR+PTX (25 mg/kg) and SHAM (no shock, no treatment). Additionally, total shed blood was reinfused. At 24 h lung injury was analyzed by a pathologist blinded to the groups, and a score was calculated. BT was determined by microbiological cultures of mesenteric lymph node complex. BAL was performed on a separate set of animals that received the same treatments. Lung score was significantly higher in LR group (11.5+/-1.4) as compared to HS (6.8+/-0.9), and PTX treated animals (7.2+/-0.9). The percentage of neutrophils in the BAL of LR animals (15.8%) was also significantly higher as compared with HS (5.25%) and PTX groups (9.72%). BT was noted in 50% of rats for LR group, 30% for PTX, 10% for HS and 0% for sham group. HS and PTX reduced BT and lung injury after hemorrhage. Attenuation of lung injury could be the result of less neutrophil infiltration into the lungs of HS and PTX treated animals. LR resuscitation caused pronounced lung injury and BT.

Traumatic brain injury: patterns of failure of nonoperative management.

OBJECTIVE: The circumstances of failure for nonoperative management of blunt traumatic brain injury have been poorly defined. In this study, all trauma patients identified over a 12-year period with progression of neurologic injury requiring craniotomy were retrospectively reviewed. METHODS: Data collected included demographic information, mechanism of injury, field and admission vital signs, and Glasgow Coma Scale score, medications, associated injuries, and coagulopathy. Head computed tomographic scans were reviewed, and anatomic findings were correlated with clinical changes (change in mental status or elevation of intracranial pressure) that led to subsequent CT scan and craniotomy. RESULTS: Of 20,100 patients, there were 852 who had computed tomographic scans with acute intracranial injuries on admission; 462 patients were managed nonoperatively. Fifty-seven patients had progression of neurologic injury (34 < 24 hours = early; 23 > 24 hours = late) that required surgery. CONCLUSION: Of the variables investigated, only anatomic location of injury was found to be predictive of early failure of nonoperative management. Frontal intraparenchymal hematomas are particularly prone to early failure. Clinical examination and intracranial pressure monitoring are equally important in detecting failure and should be an integral part of nonoperative management.

Hypertonic saline resuscitation diminishes lung injury by suppressing neutrophil activation after hemorrhagic shock.

UNLABELLED: Hypertonic saline (HS) resuscitation after hemorrhage and sepsis has been shown to markedly reduce the development of lung injury in animals, compared with traditional resuscitation with lactated Ringer's (LR). These experiments examined the effect of HS on lung injury after hemorrhage without sepsis. The effects of HS and LR resuscitation on neutrophil trafficking, neutrophil adhesion, and neutrophil oxidative burst were studied. METHODS: BALB/c mice were hemorrhaged to a mean arterial pressure of 40 torr for 1 h. Animals were resuscitated with shed blood and either 4 mL/kg of 7.5% HS or LR in twice the volume of the shed blood. Lung histology was examined 24 h after hemorrhage. Lung myeloperoxidase content and bronchoalveolar lavage fluid neutrophil counts were obtained. Peripheral blood smears were obtained to determine the neutrophil percentage. Peripheral blood neutrophil CD11b expression and neutrophil H2O2 production were assayed by flow cytometry. RESULTS: HS animals had less lung injury than LR animals. The mean myeloperoxidase activity in HS versus LR animals was 1.79+/-1.33 U/100 mg versus 3.0+/-1.33 U/100 mg, respectively. The percentage of neutrophils in the bronchoalveolar lavage fluid of HS animals (3.8%+/-.8) was significantly less than that of LR animals (10.8%+/-2.1). This corresponded to a significantly higher peripheral blood neutrophil count in HS animals compared with LR animals, 41% vs. 20%, respectively. There was no difference in neutrophil expression of the CD11b integrin between the HS and LR groups. The neutrophils of LR animals had basal H2O2 production that was 107% greater than that of controls; HS suppressed this hemorrhage-induced activation by > 60%. HS resuscitation after hemorrhagic shock protects against the development of lung injury. This protection is due, in part, to suppression of the hemorrhage-induced neutrophil oxidative burst. HS resuscitation offers immunomodulatory potential after hemorrhagic shock.