There has been a plethora of literature regarding nonoperative management of blunt splenic injuries published since the original EAST practice management guideline was written. Nonoperative management of blunt splenic injuries is now the treatment modality of choice in hemodynamically stable patients, irrespective of the grade of injury, patient age, or the presence of associated injuries. Its use is associated with a low overall morbidity and mortality when applied to an appropriate patient population. Nonoperative management of blunt splenic injuries should only be considered in an environment that provides capabilities for monitoring, serial clinical evaluations, and has an operating room available for urgent laparotomy. Patients presenting with hemodynamic instability and peritonitis still warrant emergent operative intervention. Intravenous contrast enhanced computed tomographic scan is the diagnostic modality of choice for evaluating blunt splenic injuries. Repeat imaging should be guided by a patient's clinical status. Adjunctive therapies like angiography with embolization are increasingly important adjuncts to nonoperative management of splenic injuries. Despite the explosion of literature on this topic, many questions regarding nonoperative management of blunt splenic injuries remain without conclusive answers in the literature.
Most original hepatic guidelines remained valid and were incorporated into the greatly expanded current guidelines as appropriate. Nonoperative management of blunt hepatic injuries currently is the treatment modality of choice in hemodynamically stable patients, irrespective of the grade of injury or patient age. Nonoperative management of blunt hepatic injuries should only be considered in an environment that provides capabilities for monitoring, serial clinical evaluations, and an operating room available for urgent laparotomy. Patients presenting with hemodynamic instability and peritonitis still warrant emergent operative intervention. Intravenous contrast enhanced computed tomographic scan is the diagnostic modality of choice for evaluating blunt hepatic injuries. Repeated imaging should be guided by a patient's clinical status. Adjunctive therapies like angiography, percutaneous drainage, endoscopy/endoscopic retrograde cholangiopancreatography and laparoscopy remain important adjuncts to nonoperative management of hepatic injuries. Despite the explosion of literature on this topic, many questions regarding nonoperative management of blunt hepatic injuries remain without conclusive answers in the literature.
Level I evidence now exists to recommend the use of computed tomographic scan, especially multidetector computed tomography with multiplanar reconstructions, in the evaluation of patients with SBO because it can provide incremental clinically relevant information over plains films that may lead to changes in management. Patients with evidence of generalized peritonitis, other evidence of clinical deterioration, such as fever, leukocytosis, tachycardia, metabolic acidosis, and continuous pain, or patients with evidence of ischemia on imaging should undergo timely exploration. The remainder of patients can safely undergo initial nonoperative management for both partial and complete SBO. Water-soluble contrast studies should be considered in patients who do not clinically resolve after 48 to 72 hours for both diagnostic and potential therapeutic purposes. Laparoscopic treatment of SBO has been demonstrated to be a viable alternative to laparotomy in selected cases.
We demonstrate for the first time that human Tregs are increased in potency after severe injury. Most significantly, Tregs are important mediators of the suppression of T cell activation and the reduction in TH1 cytokine production found after injury.
Severe injury primes the innate-immune system for increased Toll-like receptor 4 (TLR4)-induced proinflammatory cytokine production by macrophages. In this study, we examined changes in TLR4 signaling pathways in splenic macrophages from burn-injured or sham mice to determine the molecular mechanism(s) responsible for the increased TLR4 responsiveness. Using flow cytometry and specific antibodies, we first looked for injury-induced changes in the expression levels of several TLR-associated signaling molecules. We found similar levels of myeloid differentiation primary-response protein 88 (MyD88) and interleukin-1 receptor-associated kinase-M (IRAK-M) and somewhat lower levels of total p38, extracellular signal-regulated kinase (ERK), and stress-activated protein kinase (SAPK)/c-jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPKs) in burn compared with sham macrophages. However, with the use of antibodies specific for the phosphorylated (activated) forms of the three MAPKs, we found that macrophages from burn mice showed a twofold increase in purified lipopolysaccharide (LPS)-stimulated p38 activation as compared with cells from sham mice on days 1 and 7 post-injury, whereas ERK and SAPK/JNK activation was increased by burn injury only on day 1. Using the specific p38 inhibitor (SB203580), we confirmed that the increase in tumor necrosis factor alpha production by LPS-stimulated burn macrophages requires p38 activation. Although we demonstrated that injury increases macrophage TLR4 mRNA expression and intracellular expression of TLR4-myeloid differentiation protein-2 (MD-2) protein, macrophage cell-surface expression of TLR4-MD-2 was not changed by burn injury. Our results suggest that the injury-induced increase in TLR4 reactivity is mediated, at least in part, by enhanced activation of the p38 signaling pathway.
IV contrast media in elderly trauma patients is not associated with an increased risk of AKI. Development of AKI within 72 hours of admission is associated with mortality and increased length of stay.
In a large regional trauma cooperative, increasing age and Injury Severity Score were independent predictors of survival among older patients incurring traumatic RFs. Admission to high-volume trauma centers, preexisting congestive heart failure, and intubation added to mortality. Therapies associated with improved survival were patient-controlled analgesia and tracheostomy. Further regional cooperation should allow development of standard care practices for these challenging patients.
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