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We shopped both locations, nice ladies! One of my favorite places ever. I come to Estes Park at least once every 3 months. Always something amazing to see and do! Love It. Great place to visit. Rocky Mountain national park. Beautiful lakes. Friendly people. Enjoyed shorter hikes around Sprague And Lily Lakes.

Very peaceful and enjoyable walk on a nice flatter trail. Location was awesome as we got up early and headed to Rocky Mt NP. This hotel is nearby few restaurants and shops and 5 min from Estes Park downtown charm. The room was cozy and pretty good size. I would recommend this hotel to anyone. The hotel was a short way out of town but we could park easily.

The pool was very good with a couple of changing facilities. Pool towels were plentiful but very small. Not in the middle of Estes Park, but not far, so it was fairly quiet despite being there in the midst of Elkfest unexpected. Great value and not far from Rocky Mountain National Park. Best of all, we walked out the second morning, and 3 young bull elk were grazing alongside the parking lot.

Near downtown Estes Park. Beautiful property with a pond on the edge of a golf course. Stunning views of the Continental Divide and Stanley Hotel. Minutes away from Rocky Mountain National Park. Rooms were clean and comfortable one of our rooms even had a fireplace and they provided us with wood for it. The decor of the lodge was so cute. The bed was very comfortable and the bathroom great for its size. The decking was really handy for cooking out. The property was very convenient to everything we wanted to do in Estes Park. The villa we stayed at was well taken care of.

Very clean and tidy. The staff was very friendly as well. Quiet location, we drove through the Rocky Mountain National Park and ended here, a nice place to end your day! All points of interest are close by, Estes Park is a drive though and not walkable! Great views from the hot tub! Great location, friendly and very helpful staff, very clean and spacious rooms, good choice of food for breakfast, fantastic hotel you won't be disappointed will definitely be staying there again.

Loved absolutely everything about my stay. Everything from the staff to the facilities were just excellent. Cannot day one negative thing about the hotel. Highly recommend The balcony on the river was awesome and the room felt more homey than a usual hotel room in a good way. It was close to everything and the location was just beautiful. The best part of the stay really is the town of Estes Park. The hotel had a great location within walking distance to main drag.

The room was a great size and very clean. The staff was very nice and the breakfast was one of the best we have had at a hotel!! The pool area was amazing, probably the best indoor Hotel pool I've been to. The game room was a hit with my son. Nice team, great breakfast and the first hotel I have ever seen that offers popcorn and movies. The location and the aesthetic of the hotel is great. The manager and staff were very pleasant and helpful. We had a problem with our AC and it was fixed immediately. The continental breakfast was more than enough to satisfy anyone's wants and it was nice to not have to take the time to go out to eat.

The rooms were cleaned thoroughly every day and the ladies were very friendly. Room was clean and big and had enough facilities. View in the room is awesome, if you have mountain view. Invite Hosts List Your Property. We have more than 70 million property reviews, and they're all from real, verified guests. The only way to leave a review is to first make a booking. That's how we know our reviews come from real guests who have stayed at the property. When guests stay at the property, they check out how quiet the room is, how friendly the staff is, and more.

After their trip, guests tell us about their stay. We check for naughty words and verify the authenticity of all guest reviews before adding them to our site. Register — opens a dialog box. Sign in — opens a dialog box. Hotels in Estes Park Be a Booker. Search hotels and more in Estes Park Type your destination. Error: Enter a destination to start searching. I'm traveling for work.

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Tartaruga gigante continua a recusar alimento RTP. Famosos ao Minuto. Que desafios enfrenta? Os melhores carros para comprar em StarsInsider. A vida da Princesa Diana em imagens StarsInsider. Sabia que pode congelar estes alimentos? Eu vou ao nascimento do meu filho' MaisFutebol. Meghan ou Kate? There are no randomized controlled trials to guide treatment and the published literature contains a high ratio of reviews to original data. For the purpose of these guidelines, acute mesenteric ischaemia AMI is defined as sudden acute arterial or venous occlusion or drop in circulating pressure resulting in insufficient blood flow within the mesenteric circulation to meet the metabolic demands placed upon it.

Isolated colonic ischaemia and focal segmental ischaemia secondary to adhesions, hernias or other forms of extrinsic compression are excluded. Chronic mesenteric ischaemia and ischaemic colitis are separate entities and are not considered in these guidelines. Searches were limited to human studies. Abstracts from original publications were screened for relevance and full publications evaluated where appropriate. Lists of quoted literature within these articles were also screened for additional relevant publications.

Evidence from non-experimental descriptive studies such as comparative studies, correlation studies and case controlled-studies. Evidence from expert committee reports or opinions or clinical experience of respected authorities or both. Answer: Most patients present with abdominal pain of sudden onset.

The early phase of AMI can be characterized by an initial discrepancy between the severity of the abdominal pain and minimal findings on physical examination. Patients can also present with symptoms of nausea, vomiting and initial forced evacuation, early in the course of the disease. The location of pain varies, but as ischemia progresses to infarction, it becomes diffuse.

The development of transmural infarction may also be signalled by fever, bloody diarrhoea and shock. Background: The available evidence comes from level II and III studies, with mostly small and retrospective observational case-series. However, they all consider pain as the main symptom in most cases [ 14 , 35 ]. However, these symptoms are not specific for AMI.

A retrospective series of AMI patients identified significant comorbidities that predispose to AMI such as ischaemic heart disease, atrial fibrillation, hypertension, diabetes mellitus or renal insufficiency in most patients [ 47 ]. As the disease progresses and ischemia leads to intestinal necrosis, pain becomes more diffuse and signs of peritoneal irritation [ 14 ] and bloating appear [ 39 ]. The patient may develop bloody diarrhoea, fever, signs of shock, multiple organ failure and a reduction in consciousness [ 37 , 39 ]. Recommendation: Acute mesenteric ischaemia AMI should be suspected in patients with acute abdominal pain in whom there is no clear diagnosis, particularly when the pain is disproportionate to the physical examination findings and in the elderly with a history of cardiovascular comorbidities LOE: III.

Arteriosclerosis, hypertension, diabetes, hyperlipidemia, dehydration, antiphospholipid syndrome, estrogens. Hypercoagulable disorders, sickle cell disease, right sided heart failure, DVT, malignancies, hepatitis, pancreatitis, sepsis hepato-splenomegaly, cirrhosis. Shock, hypovolemia, hypotension, digitalis, diuretics, beta-blockers, alpha-adrenergics, enteral nutrition, critical care support. Cardiac ischemia, tachyarrhythmia, rheumatic fever, and other conditions that predispose to the formation of atrial thrombi are risk factors of the disease [ 35 , 36 , 38 , 42 , 49 ].

The sudden onset of severe pain with spontaneous emptying of the bowel vomiting and diarrhoea but no significant physical findings is a classic sign of an EAMI. These patients usually report prodromal symptoms of mesenteric angina [ 36 ] postprandial abdominal pain, nausea and weight loss before the acute episode resulting from pre-existent vascular insufficiency [ 10 , 39 ]. The main risk factors for TAMI are atherosclerotic disease and dyslipidaemia [ 49 , 50 ].

There may be a history of other vascular events and previous vascular surgery. Although occasionally idiopathic, most patients have an identifiable risk factor [ 10 , 51 , 53 ]. Other risk factors include hypercoagulability states protein C and S deficiency, polycythaemia or Leiden factor V mutation , portal hypertension, abdominal trauma, abdominal infection, acute pancreatitis, malignancy, nephrotic syndrome, cirrhosis or splenomegaly [ 10 , 40 , 49 , 51 , 52 , 53 , 55 , 56 , 57 ]. Oral contraceptives, pregnancy and the puerperium are risk factors in young women [ 35 , 58 ].

Venous vascular occlusion is usually peripheral, involving short segments of bowel [ 53 ]. Half of the patients complain of nausea and vomiting. Untreated cases may result in portal hypertension with the development of oesophageal varices [ 39 ]. VAMI is not usually associated with postprandial syndrome, although bloating, abdominal distension, fever and occult blood in stools may be present [ 59 ]. It usually occurs in patients that are critically ill, sedated and artificially ventilated and is difficult to recognize.

It is poorly understood, but can be explained by a combination of low cardiac output and vasoconstriction. Risk factors for NOMI include age over 50, history of acute myocardial infarction, congestive heart failure, aortic insufficiency, cardiopulmonary bypass, kidney or liver disease or major abdominal surgery. Notably, many patients with NOMI may have none of these factors [ 10 ]. The diagnosis should be suspected in patients with mesenteric hypoperfusion secondary to circulatory shock or vasoactive drugs including amines, cocaine and digitalis when there is a significant unexpected deterioration in their clinical course [ 40 , 41 , 43 , 60 ].

Acute or insidious pain without defecation , bloating, abdominal distension and the presence of occult blood in the stools are all consistent with NOMI in a critically ill patient [ 10 , 21 , 36 , 45 , 54 ]. Most patients display signs of sepsis and abdominal distension as a late clinical sign [ 10 ].

Mitsuyoshi et al. Although they were able to demonstrate early detection and improved survival, the numbers involved were small. Large doses of vasopressors alone can cause bowel ischaemia by non-occlusive, low perfusion mechanisms NOMI. AMI has been associated with drug toxicity. Several case reports link cardiotoxins, such as digitalis, in combination with furosemide-induced fluid depletion, calcium-channel blockers [ 36 ], cocaine linked to arterial thrombosis , organophosphates, ergotamine, phenobarbital, ethylene glycol or tricyclic antidepressants to NOMI in ICU patients.

Snake bites have also been associated with NOMI [ 62 , 63 ]. NOMI has also been described in patients who have undergone the stress of a surgical procedure or trauma and are receiving enteral nutrition in intensive care units. The reported incidence of AMI in these patients is 0. The proposed mechanism is an imbalance between demand created by the enteral feeding and supply decreased by systemic hypo-perfusion and mesenteric vasoconstriction. Recommendations: AMI secondary to an arterial embolism EAMI should be suspected in patients with atrial fibrillation who have a sudden onset of abdominal pain.

AMI resulting from arterial thrombosis TAMI should be suspected in patients with evidence of atherosclerotic disease particularly with a recent history of postprandial syndrome. Answer: Any procedure which involves vascular manipulation even unintentional can precipitate AMI. Background: Acute mesenteric ischaemia has been associated with several procedures and may complicate any abdominal surgery [ 21 ].

VAMI is a recognised complication of laparoscopic colorectal surgery. The latter two were independent predictors of thrombosis in multivariate analysis. Manipulation of mesenteric vessels and raised intra-abdominal pressure may play a role in the pathophysiology [ 65 ]. EAMI may occur when atheromatous plaques are dislodged by angiography of the coronary or cerebral circulation [ 10 ]. Aortic catheterization can induce cholesterol embolization [ 59 ]. AMI may be seen after colonoscopy.

The decreased intravascular volume resulting from fasting and colon preparation, reduction of vascular tone through medications used for conscious sedation and the mechanical effects of colonoscopy may work together to create a low flow state precipitating acute mesenteric ischemia [ 66 ]. Possible predisposing conditions include connective tissue disease, advanced age, cardiovascular disease and immunosuppression. Several factors low cardiac output, use of vasopressors and underlying atherosclerotic disease contribute to severe hypoperfusion and NOMI is the most frequent pathophysiological event [ 41 ].

Intra-aortic balloon pumps cause embolic showers particularly if placement involves excessive manipulation of a diseased aorta [ 50 ]. Answer: It is difficult to predict prognosis at presentation based exclusively on clinical findings. However, older patients with delayed presentation and abdominal signs of peritonitis or organ failure generally have a worse prognosis. A number of scoring systems have been proposed for AMI, but these have not been validated in large-scale studies.

Background: The moribund patient with significant co-morbidities and poor performance status is unlikely to benefit from intervention. Most of the literature considers old age and late diagnosis as bad prognostic factors for arterio-occlusive disease. However, in VAMI longer duration of symptoms before hospital admission may be related to better outcome. In a series of patients with AMI mortality was In arterial occlusion, all symptoms but abdominal pain indicate disease progression. The presence of peritoneal irritation is associated with bowel necrosis and worse prognosis [ 14 , 42 ].

Renal failure and acidosis resulting from shock and sepsis are independent risk factors for mortality [ 7 , 35 ]. In a retrospective study of 58 patients resection at first or second look procedure and no recent major cardiovascular intervention were associated with better survival rates [ 21 ]. A larger retrospective series of patients identified older age, bandemia, elevated serum aspartate aminotransferase, increased blood urea nitrogen and metabolic acidosis as independent predictors of death in AMI [ 7 ].

However, they may provide a useful indicator of morbidity and mortality. Other scoring systems for predicting outcome from AMI have shown early promise, but require validation in further studies [ 2 , 30 , 68 ].


Recommendation: Management decisions should not be based exclusively on clinical findings. However, patients with advanced age, late presentation, peritonitis and signs of organ failure are unlikely to benefit from invasive procedures and should be considered for palliative care only LOE: III.

Answer: There is no specific laboratory test that can be routinely used for early detection of AMI. Background: The ideal plasma biomarker for AMI should be specific for bowel ischemia and highly sensitive. As ischemia starts from the mucosa and progresses to the serosa, a mucosa-derived marker would be most useful for early diagnosis [ 70 ].

Serum L-lactate is a specific marker of tissue hypo-perfusion [ 73 ]. The liver can clear large quantities of L-lactate from the porto-mesenteric circulation and as a result serum lactate level does not correlate with intestinal infarction [ 74 ]. Lactic acidosis develops late in the course of AMI with extensive transmural infarction and tissue hypoperfusion due to sepsis.

The fibrinolytic marker D-dimer does not differentiate patients with AMI from those with non-acute mesenteric ischemia and that there is no difference in D-dimer levels between patients with resectable and irresectable bowel necrosis [ 76 ]. The most common laboratory abnormalities found in AMI are hemoconcentration, leukocytosis, metabolic acidosis with high anion gap and lactate concentration, and high levels of serum amylase, aspartate aminotransferase, lactate dehydrogenase and creatine phosphokinase.

None of these is sufficiently sensitive or specific to diagnose AMI [ 10 , 77 ]. Answer: The most sensitive and specific diagnostic tool is biphasic multidetector computed tomography MDCT with intravenous contrast. Background: The diagnostic work-up of AMI requires a non-invasive test that confirms the diagnosis and differentiates it from other abdominal pathology. A plain abdominal radiograph has no role in the early detection of AMI, since a normal radiograph does not exclude the diagnosis.

Radiographic signs in patients with AMI are nonspecific and appear when bowel infarction has already occurred [ 78 ]. No relevant trials supporting the use of angiography for diagnosis can be found in the recent literature [ 79 , 80 ]. MDCT should be the first line imaging method in suspected AMI due to its high diagnostic accuracy [ 81 , 82 , 83 , 84 , 85 ]. This imaging modality also allows other causes of acute abdominal pain to be excluded.

In this context biphasic CT involves the acquisition of scans in the arterial and venous phases. Scans are also acquired before intravenous contrast is given. Pre-contrast scans detect vascular calcification, hyper-attenuating intravascular thrombus and intramural haemorrhage, while contrast-enhanced CT allows the identification of thrombus in the mesenteric arteries and veins, abnormal enhancement of the bowel wall and the presence of embolism or infarction of other organs.

Sagittal reconstructions are used to assess the origin of the mesenteric arteries [ 83 ]. The use of oral contrast is generally not feasible in patients with AMI. The transit time for oral contrast through the bowel will delay definitive treatment in AMI and the associated vomiting and an adynamic ileus limit the useful passage of oral contrast material [ 83 , 86 ]. MDCT has a high specificity and sensitivity [ 82 ]. The high diagnostic accuracy of MDCT is based on specific features of AMI such as occlusion of mesenteric vessels and the non-specific appearance of bowel wall thickening and intestinal pneumatosis [ 88 ].

Pneumatosis Intestinalis presence of air within the bowel wall usually indicates transmural infarction in AMI, particularly if it is associated with portomesenteric venous gas, but this sign is not specific for either infarction or ischemia. NOMI represents the most difficult diagnostic challenge in AMI; usually these critically ill patients are sedated and intubated and diagnosis may rely only on clinical suspicion and imaging studies. The administration of intravenous contrast may be contraindicated, hence a lesser sensitivity and utility of MDCT [ 89 ].

The diagnosis of NOMI should be confirmed by selective catheter angiography [ 90 , 91 ]. Modified from Furukawa et al. Recommendations: In cases of suspected AMI, multidetector computerised tomography scanning MDCT with intravenous contrast should be performed immediately. Answer: Laparoscopy can be used for diagnosis and second-look.

Background : Several articles with small series of patients address the use of laparoscopy in AMI [ 94 , 95 , 96 ]. In cases of uncertainty regarding the diagnosis or the extent of bowel necrosis, laparoscopy can offer a minimally invasive way to asses it, even in the ICU bedside laparoscopy. Laparoscopic second-look procedures can be offered in a planned or on-demand fashion. However, there is no strong evidence to support the routine use of laparoscopy in AMI. Supplementary oxygen should be given and crystalloids are the fluid of choice. Supplementary oxygen should be given [ ] and the evaluation of organ delivery of oxygen assessed using accepted clinical markers such as peripheral perfusion, mental status, and urine output [ 97 , ].

A recent Cochrane Review [ ] has shown no advantage of colloids over crystalloids in reducing mortality when used for intravenous fluid resuscitation. The choice of fluid will have a cost implication, and colloids are more expensive than crystalloids. As there is no evidence that colloids improve survival rates or reduce morbidity, crystalloids should be preferred on economic grounds.

Evidence suggests that the use of hydroxyethyl starch might increase mortality and should be avoided until further proof of safety can be provided [ , , , , ]. Fluid volume status should be quickly assessed and fluid replacement should start promptly but should not delay diagnosis and intervention LOE: IV.

Crystalloids should be used for fluid replacement, hydroxyethyl starch should be avoided LOE: Ia. Answer: Vasopressors reduce splanchnic perfusion and should be avoided in AMI whenever possible. Pressors also reduce the effectiveness of angiography. However, when required consideration should be given to using a pressor which has less effect on mesenteric blood flow. Background: AMI results from insufficient blood flow within the mesenteric circulation to meet the metabolic demands placed upon it. This may be confounded by hypovolaemia and circulatory failure. The use of vasopressors to improve cardiac function should be balanced against the adverse effect of further splanchnic vasoconstriction [ 3 , ].

Consideration should be given to the use of drugs such as dobutamine, low dose dopamine and milrinone, which have been shown to have less impact on mesenteric blood flow [ 39 ]. Vasopressors should not be used until the patient has been adequately volume resuscitated. Cardiac output can also be improved by rate control in atrial fibrillation. Recommendations: Vasopressor drugs should be avoided in AMI. If vasopressor drugs are required after adequate volume replacement, preference should be given to those with minimal effect on the splanchnic circulation LOE: IV.

Broad-spectrum antibiotic cover should be given. Background: Loss of the integrity of the mucosal barrier facilitates bacterial translocation and occurs in the early stages of AMI. Although no specific studies have examined the role of prophylactic antibiotics in AMI, broad spectrum antibiotics such as a penicillin or a third generation cephalosporin in combination with metronidazole would be expected to reduce the consequences of bacterial translocation and should be given early [ ].

Answer: Open embolectomy is widely used in this scenario. However, if expertise and appropriate resources are available, and there is no evidence of bowel necrosis, endovascular techniques should be attempted.

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Background: The established treatment is open surgical embolectomy. However, an increasing number of cases of successful percutaneous treatment have been reported with overall results comparable to the open approach [ 91 , ]. Open embolectomy is usually performed via a midline incision approaching the SMA just below the pancreas at the mesenteric root [ 98 ]. A transverse arteriotomy is then made after proximal and distal clamping and embolectomy catheters are used to clear the artery proximally and distally.

High pressure proximal flushing should be avoided so as not to dislodge the thrombus in the aorta and produce further emboli. After completing the thrombectomy the artery should be flushed gently with heparinized saline. The arteriotomy is then closed in a standard fashion.

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Endovascular embolectomy is achieved by percutaneous mechanical aspiration [ ] or thrombolysis [ , ] and permits percutaneous transluminal angioplasty PTA , if necessary, with or without stenting [ , ]. Recommendation: In cases where immediate surgical intervention is not required the decision to perform endovascular or open vascular surgery for EAMI should be determined by the personal experience and technical capabilities of the surgeon and the available resources LOE: IV.

Background: Endovascular treatment should be considered as soon as possible for acute thrombosis of a diseased superior mesenteric artery SMA [ 91 , 98 , , , ]. This should be performed before intestinal infarction occurs and when the ischaemia is potentially reversible. The commonest interventions are PTA and stenting. Other endovascular techniques include percutaneous aspiration thrombectomy, local fibrinolysis or intra-arterial drug perfusion such as heparin or papaverine.

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If surgery is needed to resect ischaemic bowel before vascular intervention, or when percutaneous treatment has failed, retrograde open mesenteric stenting ROMS has been suggested [ ]. Conventional bypass surgery is another option [ 98 ]. There are a variety of bypass procedures, providing either antegrade or retrograde flow, with vein or synthetic grafts. An antegrade bypass from supraceliac aorta to superior mesenteric trunk using an endogenous vein graft will give the best result.

An alternative approach would be a renal-mesenteric bypass. However, the most practical option for proximal mesenteric atherosclerotic occlusive disease is a retrograde bypass from common iliac with a synthetic graft. Where vascular expertise is not available it may be reasonable to resect the necrotic bowel first and transfer the patient for urgent interventional angiography or vascular surgery [ 91 ]. When vascular expertise is not available it may be reasonable to resect the necrotic bowel first and transfer the patient for urgent interventional angiography or vascular surgery LOE: III.

Answer: The first line treatment for mesenteric venous thrombosis is anticoagulation. Background: VAMI is usually managed without surgery. Anticoagulation with a continuous infusion of unfractionated or low molecular weight heparin is the first line treatment for VAMI and should also be started in patients diagnosed at operation [ 80 , 91 , 98 , , , , ]. Isolated thrombosis of the superior mesenteric vein is usually compensated by sufficient collateral circulation.

However, additional complete thrombosis of the portal vein leads to venous infarction of segments of small intestine of varying severity and may require laparotomy. Patients who deteriorate during medical treatment can be considered for endovascular treatment. Many techniques have been described such as transjugular intrahepatic portosystemic shunting TIPS with mechanical aspiration thrombectomy and direct thrombolysis, percutaneous transhepatic thrombolysis, indirect thrombolysis via the SMA and thrombolysis via a surgically placed superior mesenteric vein SMV catheter.

A number of case-series advocate prompt direct thrombolysis on the basis of reported reduction in both early complications infarction and late sequelae portal hypertension [ ]. Contraindications to thrombolytic treatment are well established and can be divided into absolute central nervous system tumours, recent haemorrhagic stroke, gastrointestinal GI bleed and uncontrolled hypertension and relative pregnancy, remote history of GI bleeding, and recent major surgery. Background: The treatment of NOMI is based on correcting the clinical or pharmacological conditions that generate splanchnic vasoconstriction, improving mesenteric perfusion and early recognition and resection of infarcted bowel [ 99 ].

The main factor in improving mesenteric perfusion is the restoration of circulatory volume and hemodynamic stability coupled with the use of vasodilators administered directly into the SMA in order to reverse the intestinal vasospasm that causes ischemia. The diagnosis of NOMI should be confirmed by selective mesenteric angiography and, if there are no contraindications, the infusion of vasodilators directly into the SMA [ 90 ].

Other prostacyclin analogues have also been used [ 61 ]. Recommendation: NOMI should be managed by correcting the underlying cause wherever possible and improving mesenteric perfusion by direct infusion of vasodilators. Answer: The common feature in the management of AMI is the need for surgical exploration in the presence of peritonitis.

Patients with AMI and signs of peritonitis should undergo immediate surgery if comorbidities and clinical condition make curative treatment possible. With severe pre-existing medical conditions, pre-terminal state or extreme old age, the decision to proceed to laparotomy may not be appropriate. Background: Across the literature there is agreement that peritonitis secondary to bowel necrosis mandates surgery without delay if curative treatment is to be achieved [ 98 , ]. All other priorities type of AMI, level of occlusion, etc. Background: Patients with AMI who have severe sepsis or septic shock and undergo life-saving surgery should have a damage control approach.

This includes immediate laparotomy with resection of ischaemic bowel and no anastomosis or stoma , open thrombectomy if indicated , transfer to the intensive care unit to continue resuscitation prior to planned definitive procedures [ ]. A temporary abdominal closure via a negative pressure wound therapy NPWT device should be considered since they have been shown to promote wound healing and facilitate subsequent abdominal closure [ , ].

Answer: Assessment is based on the macroscopic appearance of the bowel: its colour, motility and bleeding of cut ends. Background: Necrotic bowel will be clearly identifiable at laparotomy [ , ]. In the acute setting, hypotension, vascular impairment and the concurrent use of vasopressors may confound this assessment and could result in excessive resection [ ].

It is often better to adopt a damage limitation approach and schedule a second-look procedure under these circumstances. Intra-operative assessment with Doppler ultrasound of the vascular arcade, [ , ], fluorescein angiography [ , ] and indocyanine green angiography [ ] have shown promise, but not been used extensively. Ischemic bowel should be reassessed after adequate fluid resuscitation and revascularization. If any doubt remains about the viability of the bowel, a second-look procedure should be performed LOE: IV.

Answer: The removal of large amounts of small bowel can result in short bowel syndrome SBS and intestinal failure. Thus extensive resections should be carefully considered. Background: Vascular occlusion in TAMI usually occurs in the proximal SMA and the consequent ischemia may extend from the terminal portion of the duodenum to the transverse colon [ 36 ].

In contrast, in EAMI most emboli lodge in the superior mesenteric artery distal to the origin of the middle colic artery. This maintains perfusion of the inferior pancreaticoduodenal arteries and spares the proximal jejunum from ischaemia [ 10 , 36 , ].

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Restoring bowel continuity will improve the functional results of extensive small bowel resection and may avoid long term TPN. In younger patients the option of long term parenteral nutrition or the option of subsequent intestinal transplantation could make a more extensive resection reasonable. Recommendation: The benefits of extensive small bowel resection should be balanced against the resultant quality of life, morbidity and mortality especially in elderly patients.

Answer: An anastomosis should be performed only in adequately resuscitated and stable patients when there is no question about the viability of the bowel. Background: Bowel anastomosis should be avoided in the presence of severe sepsis or septic shock or when the patient is inadequately resuscitated. Where limited necrosis is found, there is no doubt about the viability of the remaining bowel, the patient has been adequately resuscitated and there is no evidence of shock, some authors advocate anastomosis with a planned second-look [ 94 ].