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Minimally Invasive Approach toIntestinal Bleeding
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Embolization has shown to lower mortality compared to emergent surgery and is successful 90–95%. The goal of embolization is to decrease the blood ow to the bleeding site enough to achieve hemostasis, while collaterals prevent ischemia to adjacent tissues. Failed endoscopic treatment is an indication for embolization by interventional radiology as well as massive GI bleeding that requires over fourunits of blood or hemorrhagic shock. Embolization can be done with a temporary agent or permanent device. Micro-coils are the preferred agent used for GI bleeds. An angiogram is rst done to identify the bleeding site, and then agent is then delivered via a vascular catheter into the selected artery. A completion angiogram is repeated to conrm hemostasis.
Variceal bleeding accounts for about 10% of UGI bleeds and can be treated with combination therapy including medical management (vasopressin and beta block­ade) and endoscopic variceal band ligation. Sclerotherapy is also an option, but it is less effective than banding. Variceal ligation is like hemorrhoidal banding, with placement of small elastic bands in the distal esophagus. Rebleeding may require additional therapies designed at decreasing portal hypertension.
Operative intervention for an UGI bleed is required in about 5% of patients and carries a mortality upward of 25–30%. Emergent operative intervention should only be considered in patients who have failed repeat attempts at endoscopic approaches and embolization. In hemodynamically stable and symptomatic patients, endo­scopic and radiologic options can be exhausted and repeated before surgical man­agement is considered.
By the time surgery is considered, these patients are usually unstable, and there­fore the use of the laparoscopic approach is not typically utilized. Unstable patients may not be able to tolerate the pneumoperitoneum. For the open approach, a mid­line laparotomy is performed. Bleeding gastric ulcers should be treated with resec­tion if technically feasible due to the risk of malignancy. Intraoperative endoscopy can be useful in identication and localization of the bleeding ulcer. If the location of the ulcer is not amenable for resection, a gastrotomy is most often performed fol­lowed by biopsy to rule out malignancy. Here, oversewing of the ulcer for hemosta­sis is performed. Biopsies should be taken from all four quadrants of the ulcer edge for maximum diagnostic yield. If the ulcer is present along the lesser curvature at the incisura and the ulcer requires resection, an antrectomy with a gastroduodenos­tomy (Bilroth I) or gastrojejunostomy (Bilroth II) reconstruction should be considered.
For duodenal ulcers, persistent bleeding is typically caused by an ulcer in the posterior wall which has eroded into the gastroduodenal artery. Ligation of the GDA is most effective for hemostasis. The duodenum is mobilized by performing a Kocher maneuver, and a duodenotomy made with a longitudinal incision along the anterior wall of the stomach, starting approximately 2cm proximal to the pylorus, extending through the pylorus and onto the anterior wall of the duodenum for approximately 3–4cm in length. The gastroduodenal artery is then ligated by plac­ing three sutures in a gure of eight fashions at the site of the bleeding vessel within the ulcer, in the superior, inferior, and medial positions. This three-point ligation (visualizing the face of a clock: 12, 3, and 6) with permanent suture is imperative
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Gastroduodenal artery
Transverse pancreatic artery
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Fig. 1 Three-point ligation of gastroduodenal artery. In Asensio, Ciof (Eds.) Atlas of Trauma/ Emergency Surgical Techniques. Philadelphia, PA: Elsevier/Saunders
A. M. Kapil and K. A. Davis
given the collateral blood supply from the transverse pancreatic arteries (see Fig.1). When performing the three-point ligation, it is important to be cognizant of the location of the ampulla of Vater. A probe or small catheter may be used in the ampulla to help identify its location and prevent injury to the common bile duct. After hemorrhage control is obtained, the longitudinal duodenotomy is then closed in a transverse fashion, thereby constructing a Heineke-Mikulicz pyloroplasty.
2 Lower GI Bleed
A patient with lower GI bleed presents with hematochezia, rarely with melena even if the bleed is originating in the right colon. Patients with a lower GI bleed usually have normocytic RBCs, while iron deciency anemia suggests a chronic bleed. Unlike an UGI bleed, patients usually have normal BUN-creatinine ratio. Any patient presenting with a lower GI bleed should have an upper GI bleed ruled out.
After initial assessment of a patient’s hemodynamic stability, a colonoscopy is the next step in diagnosis and treatment. The most common causes of acute severe LGIB include diverticulosis, angioectasia, post-polypectomy bleeding, and isch­emic colitis.
A colonoscopy allows for identication of the bleed about 50% of the time. However, an unprepped bowel can decrease the rate of cecal intubation preventing the identication of bleeding sites. It is imperative to carefully inspect the colonic mucosa both on insertion and withdrawal since culprit lesions often bleed intermit­tently and may be missed when not actively bleeding. The endoscopist should intu­bate the terminal ileum to rule out proximal blood suggestive of a small bowel
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lesion or rarely an upper source. An adult or pediatric colonoscope with a large working channel (at least 3.3mm) should be used because the larger working chan­nel facilitates suctioning of blood, clots, and residual stool and allows for the pas­sage of large diameter (e.g., 10Fr) endoscopic hemostasis tools. Endoscopic therapy options for acute LGIB include injection (most commonly dilute epinephrine), con­tact thermal therapies (bipolar/multipolar electrocoagulation, heat probe), noncon­tact thermal therapy (argon plasma coagulation), through-the-scope clipping devices, and band ligation. Endoscopic clips are an attractive treatment modality for diverticular bleeding. Compared to contact thermal therapies, clips avoid the theo­retical risk of transmural injury and perforation in the thin-walled colon. Control of diverticular bleeding using clips can be accomplished either by targeted clip place­ment directly on the bleeding stigma or by closure of the diverticular orice in a “zipper-like” fashion resulting in bleeding tamponade (see Fig.2).
If a colonoscopy is unsuccessful in identication of the source of the bleed, then imaging studies can be helpful inlocalizing the source (see Fig. 3). Classically, a nuclear scintigraphy (tagged RBC study) was the next line for investigation, as it is highly sensitive for bleeding and can identify bleeding rates of less than 0.5cc/min. More recently, CT angiography has been used to identify bleeding sources, either to guide future embolization or to guide surgical intervention in an actively bleeding patient who transiently responds to resuscitation. A mesenteric angiogram can allow
Fig. 2 Algorithm for the management of patients presenting with acute LGIB stratied by bleed­ing severity. From LL, Gralnek IM.ACG Clinical Guideline: Management of Patients With Acute Lower Gastrointestinal Bleeding [published correction appears in Am J Gastroenterol. 2016 May;111(5):755]. Am J Gastroenterol. 2016;111(4):459–474, with permission
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a b
A. M. Kapil and K. A. Davis
c
d
e
Fig. 3 Identication of LGI bleed. From Takeuchi N, Emori M, Yoshitani M, Soneda J, Takada M, Nomura Y. Gastrointestinal Bleeding Successfully Treated Using Interventional Radiology. Gastroenterology Res., with permission. (a) Endoscopy with massive clots over stomach. (b) Contrast enhanced CT with extravasation from the posterior walls of the lower stomach body. (c) Angiogram reveals extravasation from the posterior gastric artery. (d) A microcatheter in the pos­terior gastric artery. (e) The artery has been successfully occluded. (f) Endoscopy reveals Bormann 3 type cancer at the posterior walls of the lower gastric body
for treatment as well as diagnosis, although higher rates of bleeding are required for identication (1–2cc/min). All three of these radiographic modalities will be suc­cessful if the patient is actively bleeding at the time of the study. Embolization
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during angiography can be done as well if an active bleed is identied at that time. As described in UGI bleed, embolization can be done using a temporary or perma­nent agent. However, there is more concern for ischemia in the colon after emboli­zation because there are fewer collateral vessels in the colon. Patients who undergo embolization for colonic hemorrhage should be closely monitored for ischemia and/ or perforation in the post-procedural time frame.
Surgery for continuing massive hemorrhage is reserved for hemodynamic instabil­ity, massive transfusion requirements, and persistent hemorrhage despite other inter­ventions. If the bleeding is localized and other interventions continue to fail, a segmental colectomy can be done; however, this is associated with a rebleed rate of up to 15%. On the other hand, the subtotal colectomy has a high morbidity and mortality rate.
A subtotal colectomy is preferred for the hemodynamically unstable patient with an unknown source of bleeding. A large midline incision would be made allowing adequate exposure. The resection would be from terminal ileum to proximal rectum. After resection, if the patient continued to be hemodynamically unstable, a damage control approach should be taken. A temporary abdominal closure would be done, and the patient is left in discontinuity. This allows for further resuscitation in the ICU, and the patient would be brought back when she or he is stable. At the second look laparotomy, a decision can be made if for an ileorectal anastomosis versus an ileostomy.
If the patient is hemodynamically stable, a laparoscopic approach to a segmental colectomy can be attempted. In both, right and left laparoscopic colectomies, the patient will be positioned in a lithotomy position. For a right colectomy, the ports would be placed in similar fashion to a laparoscopic appendectomy. A 12mm peri­umbilical port and additional 5mm ports in the left lower quadrant and suprapubic region are placed, with an additional port in the left upper quadrant. The cecum and the hepatic exure would be mobilized, taking care not to injure the duodenum which lies below. The 12mm supraumbilical port can be upsized to allow for extrac­tion of the colon. A laparoscopic left colectomy can be done in a similar fashion with the working ports on the right side of the abdomen. If the patient is adequately resuscitated at the time of surgery, reanastomosis is feasible and should be favored over stoma formation.
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3 Small Bowel Bleeding
Massive small bowel bleeding is rare, accounting for 0.4% of all intestinal bleeds; thus, no effective method has been established for diagnosis. If upper and lower endoscopy are negative in the face of continued bleeding, the small bowel needs to be evaluated. A CT angiogram, arteriography, and nuclear scintigraphy can again help with localization of these bleeds. Wireless capsule endoscopy, double balloon enteroscopy, and a radionuclide Meckel’s scan can also be used to localize bleeding sites in the small intestine. In patients who are unstable and require exploration, on­table push enteroscopy can be helpful in identifying the bleeding site, as intestinal peristalsis may cause blood to accumulate distal to the site of hemorrhage
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A. M. Kapil and K. A. Davis
Case reports and small studies however have evaluated the usefulness of laparo­scopic approach to diagnosis and treatment in resuscitated patients with normal vital signs. A laparoscopic evaluation of the small bowel can help to identify the source of small bowel bleeding if the portion of bowel is lled with blood. The intestinal wall should be explored for local prominence, pitting, overlapping, and abnormal mesentery. The suspected bleeding segment should be palpated carefully with clamps to feel its hardness, exibility, and activity. If a Meckel’s diverticulum is identied while laparoscopically evaluating the bowel, a small bowel resection can be done. The resected bowel should include a few centimeters of small bowel distal to the Meckel’s diverticulum, because the bleeding site would likely be distal to the diverticulum.
In conclusion, nonsurgical management, including medical therapy, resuscita­tion, and correction of coagulopathy, remains the primary management for GI bleeding. The minimally invasive techniques in these diseases focus on endoscopy. Again the acute care surgeon should be familiar with doing therapeutic endoscopy. Endoscopy and interventional radiology treatments decrease mortality in these patients and have high rates of success. Surgery is a last line of treatment as it car­ries a high morbidity and mortality. The laparoscopic approach can be utilized in selective patients, but as the indication for surgery is most likely to be continued instability, the open approach is most often utilized.
References
1. Lee KKC, You JHS, Wong ICK, Kwong SKS, Lau JYW, Chan TYK, Lau JTF, Leung WYS, Sung JJY, Chung SSC. Cost-effectiveness analysis of high-dose omeprazole infusion as adjuvant therapy to endoscopic treatment of bleeding peptic ulcer. Gastrointest Endosc. 2003;57(2):160. https://doi.org/10.1067/mge.2003.74.
2. Kumar NL, Claggett BL, Cohen AJ, Nayor J, Saltzman JR.Association between an increase in blood urea nitrogen at 24 hours and worse outcomes in acute nonvariceal upper GI bleeding. Gastrointest Endosc. 2017;86(6):1022–1027.e1. https://doi.org/10.1016/j.gie.2017.03.1533. Epub 2017 Apr 2.
3. Colucci G, Stutz M, Rochat S, etal. The effect of desmopressin on platelet function: a selec­tive enhancement of procoagulant COAT platelets in patients with primary platelet function defects. Blood. 2014;123(12):1905–16.
4. Gralnek IM, Dumonceau JM, Kuipers EJ, et al. Diagnosis and management of nonvariceal upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) guideline. Endoscopy. 2015;47(10):a1–46.
Further Reading
Ahad S, Figueredo EJ.Laparoscopic colectomy. Med Gen Med. 2007;9(2):37. Ba MC, Qing SH, Huang XC, Wen Y, Li GX, Yu J.Application of laparoscopy in diagnosis and
treatment of massive small intestinal bleeding: report of 22 cases. World J Gastroenterol. 2006;12(43):7051–4. https://doi.org/10.3748/wjg.v12.i43.7051.
Blatchford O, Murray WR, Blatchford M.A risk score to predict need for treatment for upper-
gastrointestinal haemorrhage. Lancet. 2000;356(9238):1318–21.
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Casas A, Gadacz T. Laparoscopic management of peptic ulcer disease. Surg Clin N Am.
1996;76(3):512–22.
Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J.Portal hypertensive bleeding in cirrhosis: risk
stratication, diagnosis, and management: 2016 practice guidance by the American Association for the study of liver diseases. Hepatology. 2017;65(1):310–35. https://doi.org/10.1002/
hep.28906. Epub 2016 Dec 1. Erratum in: Hepatology. 2017 Jul;66(1):304.
Greco L, Koller S, Philp M, Ross H.Surgical management of lower gastrointestinal hemorrhage:
an analysis of the ACS NSQIP database. Journal Of Current Surgery. 2017;7(1–2):4–6. Jordan PH Jr. Surgery for peptic ulcer disease. Curr Probl Surg. 1991;28(4):265–330. Lau JY, Sung JJ, Lee KK, Yung MY, Wong SK, Wu JC, Chan FK, Ng EK, You JH, Lee CW, Chan
AC, Chung SC.Effect of intravenous omeprazole on recurrent bleeding after endoscopic treat-
ment of bleeding peptic ulcers. N Engl J Med. 2000;343(5):310–6. https://doi.org/10.1056/
NEJM200008033430501.
Lee CW, Sarosi GA Jr. Emergency ulcer surgery. Surg Clin North Am. 2011;91(5):1001–13.
https://doi.org/10.1016/j.suc.2011.06.008.
Leontiadis GI, Sharma VK, Howden CW.Systematic review and meta-analysis of proton pump
inhibitor therapy in peptic ulcer bleeding. BMJ. 2005;330(7491):568. https://www.proquest.
com/scholarly- journals/systematic- review- meta- analysis- proton- pump/docview/1777629388/
se- 2?accountid=15172.
Zang L, Wei-Guo H, Yan X-W, Zhang T, Ma J-J, Ye Q, Feng B, Wang M-L, Ai-Guo L, Li J-W.Jie
Zhong, and min-Hua Zheng. Journal of Laparoendoscopic & advanced surgical. Techniques.
2010:521–5. McDonald MP, Broughan TA, Hermann RE, Philip RS, Hoerr SO.Operations for gastric ulcer: a
long-term study. Am Surg. 1996;62(8):673–7. Raphaeli T, Menon R.Current treatment of lower gastrointestinal hemorrhage. Clin Colon Rectal
Surg. 2012;25(4):219–27. Shada AL, Dunst CM, Pescarus R, etal. Laparoscopic pyloroplasty is a safe and effective rst- line
surgical therapy for refractory gastroparesis. Surg Endosc. 2016;30:1326–32. Stanley AJ, Laine L.Management of acute upper gastrointestinal bleeding. BMJ. 2019;364:l536.
https://doi.org/10.1136/bmj.l536.
Strate LL, Gralnek IM.ACG clinical guideline: management of patients with acute lower gastroin-
testinal bleeding [published correction appears in Am J Gastroenterol. 2016 May;111(5):755].
Am J Gastroenterol. 2016;111(4):459–74. Takeuchi N, Emori M, Yoshitani M, Soneda J, Takada M, Nomura Y.Gastrointestinal bleeding
successfully treated using interventional radiology. Gastroenterology Res. 2017;10(4):259–67. Villanueva C, Colomo A, Bosch A, Concepción M, Hernandez-Gea V, Aracil C, Graupera I, Poca M,
Alvarez-Urturi C, Gordillo J, Guarner-Argente C, Santaló M, Muñiz E, Guarner C.Transfusion
strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013;368(1):11–21. Erratum
in: N Engl J Med 2013 Jun 13;368(24):2341. Lin HJ, Lo WC, Lee FY, Perng CL, Tseng GY.A prospective randomized comparative trial show-
ing that omeprazole prevents rebleeding in patients with bleeding peptic ulcer after successful
endoscopic therapy. Arch Intern Med. 1998;158(1):54–8. Samakar K, Tschen J, Astudillo A, Wallen J, Garberoglio C.Laparoscopic treatment of bleeding
duodenal ulcer. Loma Linda University Medical Center, SAGES; 2012. Sung JJY, Chan FLK, Chen M, etal. Asia-Pacic working group consensus on nonvariceal upper
gastrointestinal bleeding. Gut. 2011;60(9):1170–7.
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Bowel Ischemia
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FrancescoPata, AntonioPata, GianlucaPellino, GaetanoGallo, andGiancarloD’Ambrosio
The term “bowel ischemia” encompasses a wide range of diseases, ranging from self-limiting conditions, usually responding to conservative treatment, to surgical emergencies, associated with high mortality rates. In acute setting, according to anatomy, different pathogenesis, and clinical evolution, we can classify them in two main categories: acute mesenteric ischemia (AMI) and colon ischemia (CI), also named ischemic colitis (IC). Bowel ischemia may also be secondary to other pathol­ogies, such as strangulated hernia and intestinal occlusion, but, in these cases, it should be regarded as a complication of the related disease and falls outside the scope of the present chapter.
While AMI is a surgical emergency with high mortality, CI may be treated con- servatively in most cases, and surgery is indicated in case of gangrene, perforation, or unresponsive disease (Table1). In this chapter, we provide an overview of the
F. Pata (*) Department of Surgery, Nicola Giannettasio Hospital, Corigliano-Rossano, Italy
Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy
A. Pata Cardiology Unit, Azienda Ospedaliera Pugliese-Ciaccio, Catanzaro, Italy
G. Pellino Department of Advanced Medical and Surgical Science, Università degli Studi della Campania “Luigi Vanvitelli”, Naples, Italy
Colorectal Surgery, Vall d’Hebron University Hospital, Barcelona, Spain
G. Gallo Department of Surgery, Sapienza University of Rome, Rome, Italy
G. D’Ambrosio Department of General Surgery, Surgical Specialties and Organ Transplantation, Sapienza University, Rome, Italy
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 F. Coccolini et al. (eds.), Mini-invasive Approach in Acute Care Surgery, Hot Topics in Acute Care Surgery and Trauma,
https://doi.org/10.1007/978-3-031-39001-2_18
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Table 1 Differences between acute mesenteric ischemia (AMI) and colon ischemia (CI)
Acute mesenteric ischemia (AMI)
Incidence 1:1000 hospital admission 15–17 cases/100,000 person-years Site Small bowel Large Bowel Mechanism Usually occlusive (90%): embolism,
arterial trombosis, venous trombosis
Clinical features
Main Diagnostic tool
Treatment Usually surgical: resection of
Prognosis Poor Favorable Mortality 50–90% according to lenght of the
Special subtype
Acute onset abdominal pain out of proportionin comparison tondings of clinical examination CTA (Computed tomography angiography)
ischemic bowel +/ revascularization in occlusive pathology if early recognized
intestinal segmented affected and the delay of surgery
VenousAcute Mesenteric Ischaemia (VAMI): Mild symptoms,
younger patients, usually medical therapy (unfractioned o low-weight heparin) if no gangrene. Better prognosis. Usually associated with hypercoagulable conditions
Colon ischemia (CI)
Usually not occlusive: transient ipoperfusion +/ colonic wall more prone to ischemia (drugs, medical/surgical conditions) Abdominal pain, urgency for defecation, rectal bleeding (or bloody diarrhea)
Colonoscopy (aCT scan with intravenous contrast is often required before endoscopy to exclude perforation, gangrene or other disease) Medical (conservative). Surgery in case of gangrene/fuliminat IC or unresponsive disease for 2–3weeks
10% (85% spontaneous resolution in 2–3weeks)
Isolated Right Colon Ischemia (IRCI): more frequently occlusive mechanism. Less frequently associated with diarrhea/ rectal bleeding. Worse prognosis. Fivefold need for surgery and a higher mortality (twofold). Usually associated with atrial brillation, coronary artery disease and severechronic kidney disease
F. Pata et al.
epidemiology, pathogenesis, diagnosis, and clinical management of bowel isch­emia, highlighting the role of mini-invasive surgery in this setting.
1 Acute Mesenteric Ischemia
1.1 Introduction
Acute mesenteric ischemia (AMI) is a relatively rare condition, accounting 1 per 1000 acute admissions in Europe and in the USA [1, 2]. The median age is 70years [3], but any age can be affected. As the incidence increases with the age, many patients present several comorbidities and the clinical features are misleading, the diagnosis is often late, and the high mortality is ranging from 60 to 80% [4]. “The diagnosis is impossible, the prognosis hopeless, and the treatment useless”, a fre­quently cited quote by Cokkinis in 1930 [5], describes the challenge represented by AMI in the current practice.
The common pathogenetic mechanism is represented by an inadequate perfu-
sion or insufcient venous drainage of a territory tributary of the superior
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mesenteric artery (SMA) sufcient (for amount and time) to injure the small bowel wall, leading, if untreated, to ischemia, gangrene, and perforation. The exten­sion of bowel loop ischemia, the timing of surgery, and preexisting patient diseases are the main determinants of mortality.
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1.2 Etiopathogenesis
Four types of AMI can be identied according to the characteristic mechanisms of ow disruption [3, 68]:
1. Embolic acute mesenteric ischemia (EAMI) (45%)
2. Thrombotic acute mesenteric ischemia (TAMI) (25%)
3. Nonocclusive mesenteric ischemia (NOMI) (20%)
4. Venous acute mesenteric ischemia (VAMI) (10%)
The etiology may justify some differences in the past medical history, clinical picture, and prognosis. TAMI occurs as a complication of an atherosclerotic plaque usually at the origin of the superior mesenteric artery, so patients may have an his­tory of postprandial abdominal pain, weight loss, and “food fear” (angina abdomi- nis) and frequently present an history of other atherosclerotic disease and associated factors, as myocardial infarction, stroke, arterial hypertension, and diabetes [9]. As usually involves the origin of SMA, TAMI may result in a global ischemia of the small bowel and right colon, and the prognosis is poor. Emboli usually lodge 3–10cm distal to the origin of SMA, distally to the origin of pancreatic-duodenal artery and middle colic artery, so EAMI spares the rst jejunal loops and the trans­verse colon [10]. Atrial brillation and a recent episode of arterial embolism are, respectively, detected in one-half and one-third of patients, and the onset of symp­tom is dramatic [11]. NOMI usually occurs in critically ill, shocked patients for an episode of low cardiac output, with mesenteric hypoperfusion, often exacerbated by vasoactive drugs. As patients are often mechanically ventilated, unconscious ICU patients, the diagnosis is very challenging and clinical presentation misleading.
VAMI is usually a consequence of a slow process, symptoms tend to be milder, with a more insidious outset, and the patients presents lately, some days after the onset of symptoms with a gradually worsening abdominal pain evolving over 3–10days, but with further delayed presentations in some patients [12]. As the arte­rial perfusion is preserved and an irreversible ischemia happens lately, a prompt anticoagulant therapy resolves the disease in the majority of cases without surgery. Patients are younger than other groups and hypercoagulable states are the main causative factor.
1.3 Clinical Presentation andDiagnosis
AMI usually presents with acute abdominal pain disproportionated to ndings of clinical examination. Nausea, vomiting, and diarrhea may be present [13].