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Big Manuscript submitted for publication data conclusions are useful guides buy cheap cialis black 800 mg online erectile dysfunction doctors san francisco, but do not 12 discount 800 mg cialis black with mastercard impotence 17 year old male. Instead order 800 mg cialis black visa impotence yahoo, they describe a Steiman J, Anderson A, Jeevanandam V (2013) Transapical approach for mitral valve repair during median value, which in the current feld of bio- insertion of a left ventricular assist device. N Engl J Med prosthesis in patients undergoing left ventricular assist 345(20):1435–1443 device implantation. J Heart Lung Transplant 34(12):1617–1623 of continuous fow ventricular assist device in a patient 4. Circ regurgitation after implantation of a left-ventricular Heart Fail 7(1):215–222 assist device. Ann outcomes after continuous-flow left ventricular Thorac Surg 100(4):67–69 348 W. May-Newman K, Chillcott S, Stahovich M, McCalmont V, J Card Surg 27(6):760–766 Ortiz K, Hoagland P, Jaski B (2011) Aortic valve closure 34. Ann Thorac Surg 92(4):1414–1418 ical prosthetic valve supported with left ventricular 35. J Cardiovasc Comput Tomogr 5(1):66–67 (2012) Liberal use of tricuspid-valve annuloplasty dur- 25. Eur of left ventricular outfow tract after left ventricular assist J Cardiothorac Surg 41(1):213–217 device implantation in patients with aortic valve pathol- 36. Fujita T, Kobayashi J, Hata H, Seguchi O, Murata Y, cuspid regurgitation on long-term survival. J Am Coll Yanase M, Nakatani T (2014) Right heart failure and Card 43(3):405–409 benefts of adjuvant tricuspid valve repair in patients 28. Curr Opin Cardiol with left-ventricular assist device implants and tricus- 27(3):288–295 pid valve regurgitation: propensity score-adjusted 30. Interact Cardiovasc mechanism of tricuspid regurgitation following Thorac Surg 21(6):741–747 implantation of endocardial leads for pacemaker or 39. Krabatsch References – 352 © Springer International Publishing Switzerland 2017 A. Predictors of signifcant valve pathology, and normal function recovery are younger age and short duration of and geometry of both the lef and right side of the the disease. Unfortunately, only few cases of myocardial recovery is likely to be sustained for a myocardial recovery in patients sufering from toxic longer time, in the next step, the strategy for with- cardiomyopathy (mostly afer chemotherapy) have drawal of ventricular support should be discussed. Our limited experience shows recur- Tere are several options: rence of heart failure and dilatation of the lef ventri- 1. First, oversewing of the apex of the lef ventricle echocardiography on pump should be performed. If and of the prosthetic anastomosis to the echocardiography shows normal size of the lef ven- ascending or descending aorta. In the case of tricle with satisfactory contractility, echocardiogra- anastomosis to the ascending aorta median phy at reduced pump speed and then an of-pump sternotomy and in the case of anastomosis to study should be scheduled during outpatient visits. Afer an anticoagulation bolus, the bal- and through a subcostal incision with partial loon is infated for 3–4 min and the pump stopped. Te balloon should be and the driveline can be removed, with the defated afer 3–4 min and the pump started for infow and outfow grafs ligated and the 10–20 s, and then the procedure may be repeated 3–5 infow cannula lef in situ. Ligation of the outfow graf is also possible inserted individually designed titanium plug through a small subcostal incision to stop (Fittkau GmbH, Berlin, Germany) is sintered backfow, with transection of the driveline with titanium spheres and becomes overgrown below the skin, while the outfow graf, pump, with tissue , therefore requiring anticoagula- and driveline remain in situ. It is unclear whether In all cases except ligation or interventional reevaluation of the myocardial recovery some closure of the outfow graf, we recommend com- months later would be helpful. Interventional clo- plete removal of the driveline because of the sure of the outfow graf or ligation of the outfow potential risk of infection. Ligation of the outfow Minimally invasive Driveline remains in the Patients with high risk for graft approach, no need for body. Percutaneous No risk of damage or Driveline remains in the Patients with high risk for 34 interventional closure bleeding body. J Heart Lung Transplant 29(11):1316–1317 Krabatsch T, Potapov E et al (2011) Heart failure rever- 5. Morales Chapter 38 Ventricular Assist Device Support for Hypoplastic Left Heart Syndrome, Fontan Failure, and End-Stage Systemic Right Ventricular Dysfunction – 381 Fabrizio De Rita, Antonio Amodeo, and Asif Hasan Chapter 39 Continuous-Flow Pumps in Infants, Jarvik Infant System, and Destination Therapy in Pediatrics – 391 Antonio Amodeo, Sergio Filippelli, Arianna Di Molfetta, Gianluigi Perri, and R. Jarvik 355 35 Mechanical Circulatory Support in Pediatric Population: Clinical Considerations, Indications, Strategies, and Postoperative Management O. Te main etiologies leading to end-stage heart of mechanical ventilation, escalation of inotropic failure requiring mechanical support in children support, inability to tolerate enteral feeds, rise of are dilated cardiomyopathy, myocarditis, and liver function tests, increase in creatinine levels, congenital heart disease. Since end-stage heart altered mental status, low central venous satura- failure is rather uncommon in the pediatric popu- tion (<60%), or elevated lactate. Defnition of the underlying pathology and of the medical therapy, the question arises if exclusion of any residual defect or coronary mechanical support can/should be applied to injury in children with congenital heart save the patient’s life. Since heart transplantation may 35 However, during the child’s treatment, the clini- become necessary, contraindications for cian may be confronted with the question if the transplantation must be considered. Obtaining consent is time consuming but extremely important in establishing a trustful 35. Generally accepted indications are whether the intra-atrial septum is intact or critical cardiogenic shock and progressive decline the aortic and pulmonary valves are despite inotropic support. An intracardial thrombus must clinical presentation is a child who is hemody- be ruled out. Although the vast majority of patients cannulation may become necessary if the needing a long-term device are candidates for cardiac chamber is small, e. Children with a body surface transplantation), recovery of myocardial area larger than 1–1. Depending on body 8 size and patient’s needs, pump chambers of difer­ 7 ent sizes can be chosen 6 5 4 60 ml 50 ml 3 2 30 ml 25 ml 1 15 ml 10 ml 10 20 30 40 50 60 Body Weight [kg] 358 O. Considerations in children with congenital medical support of right ventricular function in heart disease. For children with congenital the intensive care unit is crucial to avoid second- heart diseases, an individualized approach is ary heart failure. Support for children with a A standard protocol for antithrombotic ther- univentricular heart is possible at every stage apy has been proposed [10]. Anticoagulation is of palliation (aortopulmonary shunt, withheld during the frst 24 h until bleeding has superior caval vein anastomosis, and Fontan completely stopped. However, the prognosis is initiated with unfractionated heparin and switched worse in patients with a univentricular to low molecular heparin in infants or warfarin in physiology as compared to patients with children older than 1 year of age. Examples 35 of strategies to lower the adverse event rate include Postoperative management starts in the operat- earlier initiation of unfractionated heparin, higher ing room. To support the right ventricle during target ranges for low molecular heparin and war- weaning from cardiopulmonary bypass, inhaled farin, higher dosages of antiplatelet drugs, and nitric oxide, milrinone, and epinephrine are rec- introduction of a third agent. Transesophageal echocardiog- adverse events such as infections or thromboem- raphy is used to rule out infow obstruction of bolic events. Tereby, the unloading of the lef right ventricular function is severely impaired ventricle is mandatory and must be verifed not despite maximal medical therapy and optimal only directly afer cardiopulmonary bypass but lef ventricular pump settings, the implantation also during follow-up examinations. Directly afer bypass dence of incomplete unloading such as mitral the heparin efect should be completely antago- valve insufciency or increased lef ventricular nized. Initial accurate hemostasis is necessary to dimensions must prompt a careful reassessment minimize the need for blood products and avoid to rule out incorrect position of the cannula, sub- volume overload of the right ventricle.

Tis chapter focuses on the masticatory muscles buy cialis black 800 mg line erectile dysfunction and diabetes type 1, mimetic Considerations muscles (muscles of facial expression) purchase cialis black 800mg fast delivery erectile dysfunction protocol jason, and tongue muscles buy cialis black 800mg overnight delivery erectile dysfunction causes and remedies. In the upper face, when elevating a coronal or forehead fap, Masticatory Muscles dissection in the avascular plane between the periosteum and temporoparietal fascia protects the temporal branch of the Te muscles of mastication are derived from the frst bran- facial nerve. Nasal subunits: 2A, Tip; 2B, Columellar; 2C, Dorsal; 2D, Right and left dorsal side wall; 2E, Right and left alar base; 2F, Right and left alar side wall. Periorbital subunits: 3A, Lower eyelid; 3B, Upper eyelid; 3C, Lateral canthal; 3D, Medial canthal. Auricular subunits: 8A, Helical; 8B, Antihelical; 8C, Triangular fossa; 8D, Conchal; 8E, Lobe. Table 5-2 Layers of Facial Musculature Some have suggested that there are four layers of facial muscles; layer four is unique because these muscles are inner- Layer 1 Depressor anguli oris, zygomaticus minor, orbicularis vated from their superfcial surface, whereas the muscles in oculi layers one through three receive innervation from their deep Layer 2 Depressor labii inferioris, risorius, platysma, zygomaticus surfaces (Table 5-2). Te regional position of the facial nerve is shown in relation to surgically important anatomic layers. Tese muscles function formation and bolus control by pressing the cheek against the to close the oropharyngeal opening via contraction of the teeth during mastication. Defcit of the hypoglossal nerve results in a protruded tongue pointing toward the injury or lesion. Tis is due to Musculature of the Tongue the fan-shaped insertion of the bilateral genioglossus muscles Te musculature of the tongue is composed of four intrinsic that cross the midline anteriorly. Te intrinsic muscles of the tongue are the superior and inferior longitudinal muscles, the transverse muscles, and the The Facial Nerve vertical muscles. Te extrinsic muscles are the genioglossus, hyoglos- face varies markedly from person to person. All are inner- understanding of the anatomic literature and recognition of Temporalis muscle Insertion on both sides of coronoid process of mandible: Anterior Posterior Superior lateral pterygoid muscle Figure 5-4 Muscles of mastication. Te pterygomandibular ligament A space between the mandible and the medial pterygoid is where local anes- Pterygomandibular thetic is injected for a block of the space inferior alveolar nerve. Tere are commonly anastomoses between the buccal foramen between 6 and 8 mm medial to the tympanomastoid and zygomatic branches, but the temporal and mandibular suture and just lateral to the styloid process. Because bution and branching pattern of the facial nerve become of the degree of morbidity associated with damage to these quite variable. Te a description of the most commonly accepted pattern, repre- temporal branch leaves the parotid and runs within the senting around 24% of individuals. Te fve arch between 8 and 35 cm anterior to the external auditory 15 branches, or rami, of the facial nerve are the temporal (or canal. Te marginal mandibular nerve exits the 16 21 posterior to the superfcial temporal vessels. Dingman and Grabb, in their rior branch is 2 cm posterior to the anterior extent of the classic dissection study, identifed the majority of marginal 17 zygomatic arch. Anterior to the facial vessels, temporalis fascia, or within the temporal fat pad between the the nerve is above the mandibular border 100% of the time. Te number of branches varies from one to four, but two Several landmarks are available in the temporal region. Estimation of the temporal branch distribution can be made Te marginal mandibular nerve is protected throughout by drawing a triangle from the earlobe to the lateral brow the majority of its course by the platysma muscle. About 2 cm 18 and lateral extent of the highest forehead crease or from a lateral to the corner of the mouth, the nerve becomes more point 0. Te distribution of the marginal mandibular nerve Another approach, although somewhat more technique- must be discussed with regard to surgical approaches to the sensitive, is to refect the platysma superiorly and visually lower face, because injury to this nerve results in paralysis of identify and protect the marginal branch of the facial nerve the lip and chin, producing a notable deformity; in addition, (Figure 5-7). The Ligaments and Adhesions of the Face The Trigeminal Nerve: Cranial Nerve V Te retaining ligaments of the face are responsible for anchor- Sensation of the face is supplied by the trigeminal nerve, ing the overlying dermis to the facial skeleton and for main- otherwise known as cranial nerve V. Te ligaments have been described as local anesthesia are a fundamental prerequisite to facial fasciocutaneous or osteocutaneous. Osteocutaneous ligaments are much forehead, nasal dorsum, anterior scalp to the vertex stronger attachments that extend directly from the perios- superiorly, and dura mater of the anterior cranial fossa. Tese are present as the zygomatic osteo- Te ophthalmic and ciliary nerves provide sensation to cutaneous ligaments, also referred to as McGregor’s patch, the skin and conjunctiva of the upper eyelid and cornea, and the mandibular cutaneous ligaments extending from the respectively. Sensation to the maxillary dentition and mucosal to the bridge of the nose; this area contains the angular sensation of the maxillary sinus are via the anterior, vein that connects with the superior ophthalmic vein and middle, and posterior superior alveolar nerves. Historically this process was thought to be due to an dural innervation in both the middle and posterior anatomic defciency of valves in the these veins; however, it cranial fossa. Maxilla and Mandible Other nerves that provide sensory innervation of the face Te vascular supply to the maxilla and mandible are of par- include the great auricular nerve (C2-C3) and the lesser ticular importance to the facial surgeon in orthognathic and occipital nerve, which provide sensation to the skin of the ear trauma surgery. In an intact mandible, the blood supply is The Vascular Supply of the Face almost exclusively from the inferior alveolar artery; however, after traumatic or surgical insult, centripetal fow from the 30,31 Te arterial supply of the face arises primarily from the exter- periosteum provides a sustaining arterial supply. Te central face, including the periorbital In the maxilla the vascular supply is somewhat more region, upper two thirds of the nose, and central forehead, complex. Arterial anastomosis of the nasopalatine, descend- receive some anastomotic arterial supply via the ophthalmic ing palatine, and palatal vascular supply from the ascending division of the internal carotid artery. After down-fracture neous perforating arteries, such as the facial and infraorbital of the maxilla for orthognathic surgery, the blood supply of arteries. Laterally, the face is supplied by larger, more ana- the ascending pharyngeal artery and the ascending palatine 32 tomically consistent fasciocutaneous perforators, including branch of the facial artery provide sustaining arterial supply. Venous drainage Te cutaneous angiosome concept provides some oppor- is via a plexus around the capsule and venous channels in the tunity for surgical treatment planning, particularly when retrodiscal tissue. Generally, the concept is that regional segments of bone, muscle, nerve, and overlying skin 27 Blood Supply to the Nose are supplied by a common vessel. Venous drainage of the face is primarily through the inter- Te proximal vascular supply to the nose is from the oph- nal jugular vein. Te facial vein and anterior division of the thalmic artery via the anterior ethmoidal artery and the retromandibular vein join to become the facial vein that dorsal nasal and external nasal arteries. Te internal jugular plies the nasal tip via the superior labial and angular arteries. Te external jugular vein the angular artery may result in loss of vascular supply to the receives blood from the posterior division of the retroman- nasal tip; this has implications in revision rhinoplasty. Kesselbach’s plexus is the rich vascular network of the Of clinical importance is the complex and extensive com- nasal septum and is responsible for 90% of nosebleeds. Four munication between extracranial veins and intracerebral arteries anastomose at this site: the nasopalatine branch of veins. Many of these venous anastomoses may allow retro- the descending palatine artery anastomoses with the septal grade bacterial contamination and result in thrombosis of the branches of the sphenopalatine artery, the anterior ethmoidal cavernous sinus or devastating infections. Te dangerous area artery, and the superior lateral branches of the superior labial of the face is a triangle formed by the corners of the mouth branch of the facial artery (see Figure 5-10). Te approximate position of the duct can be Te oral cavity extends from the oral aperture to the palato- estimated by drawing an imaginary line from the tragus to a glossal fold. It contains the tongue and 20 deciduous (then midpoint between the upper lip and columella.

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Ronco G buy 800 mg cialis black fast delivery impotence tumblr, Giorgi-Rossi F cheap 800mg cialis black otc erectile dysfunction protocol scam or real, Carozzi F et al (2008) Results at recruitment from a randomized controlled trial comparing human papillomavirus testing alone with conventional cytology as the primary cervical cancer screening test buy cialis black 800 mg on line erectile dysfunction stress. Eurogin 2011, Lisbon, Portugal Chapter 44 Molecular Niches for the Laboratory Diagnosis of Sepsis Donna M. In this review, the human and financial impact of sepsis, are summarized as well as the predisposing factors, symptoms, and com- mon modes of bacterial pathogenesis. Important clinical and laboratory criteria for the diagnosis of sepsis and key aspects of the Surviving Sepsis Campaign Guidelines are detailed as they relate to diagnosis, therapy, and resuscitation from the septic event. Clinical laboratories must expand their understanding of the complexities related to diagnosing and treating sepsis in order to expand their role as productive members of interdisciplinary health care teams focused on improving survival from sepsis and limiting the financial impact that sepsis imparts on our health care systems. Unfortunately, current microbiology laboratory methods are too slow to support rapid interventions, typically requiring >24 h to detect the presence of bloodstream pathogens (hematopathogens) and at least 3–5 days to confirm selection of appro- priate antimicrobial therapy. Moreover, cultures from septic patients are often falsely negative due to preemptive therapy, the presence of fastidious organisms, or microbes that are present in low density. As a result, empiric, broad-spectrum treat- ment is common, and is a costly approach that may fail to effectively target the D. Wolk (*) Department of Pathology , University of Arizona College of Medicine , 1501 N. Wolk correct microbe, may inadvertently harm patients via antimicrobial toxicity, and may contribute to the evolution of drug-resistant microbes. Clearly new rapid labo- ratory methods, which enhance the laboratory capabilities to diagnose bloodstream infections, will be a useful and welcome addition to clinical microbiology laboratories. The Impact of Sepsis Morbidity and Mortality Bloodstream infections can lead to sepsis, a multi-symptom manifestation of blood- stream infection that causes rapid fatalities across all demographic populations. Cases of sepsis, primarily caused by bloodstream infections, are increasing dramatically, recently doubling in incidence [1–3 ] , which is expected to increase by as much as 1. Sepsis is a growing problem to health care systems worldwide, affecting 18 million people and equaling the number of fatalities from acute myocardial infarction [9 ]. Economic Burden of Sepsis Sepsis occurs in approximately 2 % of all hospitalizations and 75 % of intensive care patients , with enormous concomitant social and economic burden. Sepsis can be a fatal outcome for post-surgical patients in a variety of settings including, transplantation, wound surgery, splenectomy, intra- abdominal surgery, and cancer surgery [14–19]. Patients with hematologic cancers are 15 times more likely than the average person to suffer from severe sepsis [20 ]. The use of cytotoxic agents is largely responsible for immune suppression in these patients, which pre- disposes them to sepsis. In addition, malignant neoplasms can provide entry for bacteria into the bloodstream. The poorest outcomes are observed in patients over age 85, with a mortality rate over 38. At the other end of the age spectrum, children share elevated mortality rates [11 ]. Indeed, due to hospital-associated drug-resistant infections, the simple act of hospitalization increases risk for blood- stream infections and sepsis. For gram negative hematopathogens, the bacterial cell wall endotoxin, a lipopolysaccharide from the cell wall, initiates the human inflammatory response. For gram positive hematopathogens, it is the lipotechoic acid, peptidoglycan, and extracellular products (toxins) that trigger the response. An inflammatory response follows, functioning to mount protective host responses, such as vascular, cellular, and chemical. The pathogenesis of sepsis involves pro-in fl ammatory mediators, anti-in fl ammatory mediators, and vaso-in fl ammatory mediators. Other physiological changes include reduced protein C activity, micro-plugging of vessels, cellular necrosis (ischemic injury), fibrinolysis inhibition, apoptosis, leukocyte-mediated tissue injury, endothelial dysfunction, and cytopathic hypoxia. While some patients may die of infection due to their lack of ability to mount an effective immune response, sepsis also results from a human immune response to bacteria (or other pathogens), which goes awry and out of control (Fig. Patient survival is dependent on whether or not physicians can balance the patient immune response to microbial pathogens and bring patients’ systems back to homeostasis. Pathophysiology of Sepsis, a Disease Gradient Due to the widespread inflammatory response [23], disease symptoms are widely variable and include fever, chills, hypotension, neutrophilic leukocytosis or neutro- penia, hypothermia (especially in the elderly), diaphoresis, apprehension, change in 44 Molecular Niches for the Laboratory Diagnosis of Sepsis 849 Fig. There are also noninfectious causes of inflammation, which must be eliminated before treatment for microbial sepsis (not drawn to scale). Reprinted with permission from Elsevier mental status, tachypnea, tachycardia, hyperventilation and respiratory alkalosis, reduced vascular tone, and ultimately organ dysfunction. There are consensus definitions that define the serial stages of sepsis [21 ] , a pro- gression of disease detailed below. Severe sepsis, which is sepsis plus signs of hypoperfusion, hypotension, or organ dysfunction. Septic shock, which is refractory arterial hypotension or hypoperfusion despite adequate intravascular fluid resuscitation. Hypoperfusion may be manifested as lactic acidosis, oliguria, or mental status changes. Wolk Rapid Antibiotic Therapy Saves More Lives than Any Other Intervention In cases of sepsis, rapid intervention with appropriate antimicrobial therapy can be critical to patient survival [24, 25]. For aerobes, anaerobes, and fungi, appropriate antibiotic therapy increases survival by approximately 25–45 %. Eliminating delays in appropriate antibiotic administration increases survival by ~7–10 %/h [26]. Diagnostic Approach to the Septic Patient Unfortunately, despite the enormous human and financial impact of sepsis, this diagnosis remains largely a clinical one [28], due to the lack of rapid, sensitive, and specific laboratory tests to detect the causative pathogens. In order to provide a more accurate diagnosis, there is a significant need to improve the speed and diag- nostic breadth of laboratory detection methods for hematopathogens, bloodstream infections, and sepsis. Requirements for an Interdisciplinary Sepsis Team As with all complex diseases, the diagnostic approach to sepsis is multifaceted. Laboratory collaboration with Emergency Medicine Departments and Critical Care Services is essential. Laboratories can participate by partnering with the entire health care team, setting goals to provide rapid laboratory testing to maximize effec- tiveness of early goal-directed therapy, improve targeted antibiotic therapy, shorten antibiotic treatment duration, avoid development of antibiotic resistance and side effects, decrease mortality and morbidity, decrease length of stay, and decrease overall hospital costs. The clinical microbiology laboratory must help drive antibi- otic intervention in partnership with pharmacists and physicians. Upon presentation of a patient with symptoms of infection, physicians will seek the primary site of infection and attempt to direct therapy to that primary site. For instance, important factors include the source of infection, community- or hospital-acquired; prior or current medications; recent manipulations or surgery; underlying or chronic diseases; and travel history. Combining a variety of clinical assessments with various laboratory tests from clinical microbiology, hematology, chemistry, point-of-care testing, and blood gas laboratories is an important aspect of the optimum care and treatment of septic patients. Other Evidence-Based Sepsis Guidelines The Surviving Sepsis Campaign is a worldwide consortium of health care providers committed to improving the outcomes for patients with sepsis [21, 30 ].

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Current use of damage-control laparotomy buy cialis black without prescription injections for erectile dysfunction side effects, closure rates buy cialis black uk erectile dysfunction main causes, and predictors of early fascial closure at the frst take-back cheap cialis black 800mg otc erectile dysfunction drugs forum. Temporary abdominal closure for trauma and intra-abdominal sepsis: different patients, different outcomes. A protocol for a scoping and qualitative study to identify and evaluate indications for damage control surgery and damage control interventions in civilian trauma patients. Weuster M, Bruck A, Lippross S, Menzdorf L, Fitschen-Oestern S, Behrendt P, Iden T, Hocker J, Lefering R, Seekamp A, Kluter T. Impact of hemorrhage on trauma outcome: an over- view of epidemiology, clinical presentations, and therapeutic considerations. Hypothermic coagulopathy in trauma: effect of varying levels of hypothermia on enzyme speed, platelet function, and fbri- nolytic activity. Late fascial closure in lieu of ventral hernia: the next step in open abdomen management. Damage control resuscitation is associated with a reduction in resuscitation volumes and improvement in survival in 390 damage control laparotomy patients. The conjoint effect of reduced crystalloid administration and decreased damage-control laparotomy use in the development of abdominal compartment syn- drome. It’s all in the gut: introducing the concept of acute bowel injury and acute intestinal distress syndrome. Strategies for modulating the infammatory response after decompression from abdominal compartment syndrome. Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome. Neutrophils are primed for cytotoxicity and resist apoptosis in injured patients at risk for multiple organ failure. A novel mechanism for neutrophil priming in trauma: potential role of peritoneal fuid. Peritoneal negative pressure therapy prevents multiple organ injury in a chronic porcine sepsis and ischemia/reperfusion model. Peritoneal fuid: a potential mechanism of systemic neutrophil priming in experimental intra-abdominal sepsis. Effect of acute, slightly increased intra-abdominal pressure on intestinal permeability and oxidative stress in a rat model. Intestinal crosstalk: a new paradigm for understanding the gut as the “motor” of critical illness. The role of abdominal compliance, the neglected parameter in critically ill patients - a consensus review of 16. The role of abdominal compliance, the neglected parameter in critically ill patients - a consensus review of 16. The role of intesti- nal mucosa injury induced by intra-abdominal hypertension in the development of abdominal compartment syndrome and multiple organ dysfunction syndrome. Infammation, coagulopathy, and the pathogenesis of multiple organ dysfunction, syndrome. Epithelial barrier dysfunction: a unifying theme to explain the pathogen- esis of multiple organ dysfunction at the cellular level. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical rele- vance to gastric mucosal pH and abdominal compartment syndrome. Decompressive laparotomy for abdominal compart- ment syndrome--a critical analysis. Prospective study examining clinical outcomes associated with a negative pressure wound therapy system and Barker’s vacuum packing tech- nique. Time to frst take-back operation predicts successful primary fascial closure in patients undergoing damage control laparotomy. Bao J, Tan S, Yu W, Lin Z, Dong Y, Chen Q, Shi J, Duan K, Bai X, Xu L, Li J, Li N. Post-pyloric enteral nutrition in septic patients: effects on hepato-splanchnic hemodynamics and energy status. Indications for Open Abdomen 5 in the Non-trauma Setting Hany Bahouth and Yoram Kluger 5. Although the indications for this technique vary among care providers, it is agreed that that this approach revolutionized the management of critically injured patients [1, 2]. Overall, about 10–15% of all laparotomies for trauma are managed with damage control techniques. In non-trauma setting, the causes for the physiologic derange- ments observed are diverse and different from that of the injured. Despite this deference, the basic pathophysiology that results in acidosis, coagulopathy, and hypothermia remains the same. With better understanding of damage control principles, the open abdomen strat- egy, frst described almost 120 years ago by McCosh , became a common and appreciated philosophy practiced enthusiastically by surgeons in non-trauma emer- gency general surgery. In spite of the adoption of the open abdomen technique in non-trauma emer- gency surgery, the indications that defne its appropriate application are poorly agreed among surgeons [6–11]. This is due to the lack of well-constructed random- ized studies exploring the concept in the non-trauma settings as well as defciency of common language and classifcation system of surgical emergencies that may favor from open abdomen strategies. Kluger described in various published studies and the inclusions of heterogeneous patient population contribute to the paucity of evidence-based data [6–8, 11]. In their review, looking at the indications for open abdomen in non-trauma surgery, Atema et al. The most frequent single indication for the open abdomen management was a planned relaparotomy strategy. There are no defnitive physiological or anatomical criteria to aid surgeons to properly consider and select damage control strategy in non-trauma surgical patients. Nevertheless some of the indications and physiological-based criteria were extrapolated from the trauma arena; temperature lower than 35°C, pH less than 7. Several studies identifed peritonitis as an independent predictor of failure of fascial closure [14–16]. Higher fascial closure rates were achieved at the frst re-exploration and less likely during the second or third take back [17]. Shorter period of open abdomen was also associated with higher fascial closure rates [18–20]. The mortality rates of patients submitted for the open abdomen exceed 30% and are dependent on the causative event leading to the selection of the open abdomen strategy [22]. In this chapter, we will review the most common indications for the open abdo- men technique in the non-trauma setting and their utility and effcacy. Based on small retrospective studies in the 1980s and 1990s, enthusi- astic adoption of the strategy for patients diagnosed with severe peritonitis was recorded [23, 24]. Most abdominal sepsis results from pathologies in the hepatobili- ary tree, pancreatic necrosis/infection, or hollow viscus perforation/necrosis. The main surgical focus in the septic abdomen should be therefore to obtain source control by means of peritoneal lavage, debridement of infected/necrotic tissue, and defnitive or temporary measures to control anatomic integrity and to restore opti- mal function [25]. In severe secondary peritonitis, a staged approach may be compulsory for three different reasons or any of their combination [26].

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