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Gastric ischemia due to critical stenosis of the celiac trunk Isquemia gástrica secundaria a estenosis crítica del tronco celíaco doi.org/10.23938/ASSN.0248

C. Saldaña Dueñas, A. Elosua González, A. Guerra Lacunza

Contenido

Gastric ischemia due to critical stenosis of the celiac trunk 123

Abstract Resumen Abstract 123

Gastric ischemia (GI) results from diffuse or localized La isquemia gástrica resulta de la insuficiencia vascular Resumen 123 vascular insufficiency caused by different aetiologies difusa o localizada causada por diferentes etiologías such as systemic hypotension, vasculitis, disseminated como la hipotensión sistémica, la vasculitis, el trom- INTRODUCTION 124 thromboembolism and celiac or mesenteric stenosis. boembolismo diseminado y la estenosis mesentérica We present a case of gastric ischemia due to critical o celíaca. Presentamos un caso de isquemia gástrica CASE REPORT 124 stenosis of the celiac artery treated using endovascular secundaria a estenosis crítica del tronco celíaco trata- DISCUSSION 125 therapy. The celiac artery is the first major branch of da endovascularmente. El tronco celíaco es la primera the abdominal aorta and provides some of the blood rama de la aorta abdominal y aporta gran parte del flujo REFERENCES 127 supply to the stomach through the left gastric artery de sangre al estómago a través de la arteria gástrica iz- and other organs like the spleen (splenic artery branch) quierda y de otros órganos como el bazo (a través de la and the liver. Although the collateral blood supply to rama esplénica) y el hígado. Aunque las colaterales que the stomach is protective, systemic hypotension or irrigan el estómago son protectoras, la hipotensión sis- occlusion of the main arteries, as in the case of our pa- témica o la oclusión de las principales ramas como en tient, may result in gastric ischemia. The place- el caso que presentamos, pueden llevar a la isquemia ment is an alternative to surgery in patients with high gástrica. La colocación de endovasculares es una comorbidity and with good outcomes. The clinical alterativa terapéutica a la cirugía en pacientes con gran awareness of this syndrome will allow gastroenterol- comorbilidad y con buenos resultados. La sospecha clí- ogists and radiologists to appropriately diagnose and nica de este síndrome puede llevar tanto a gastroente- manage affected patients. rólogos como a radiólogos a un correcto diagnóstico y tratamiento de los pacientes afectos.

Keywords. Gastric ischemia. Gastric ulcer. Celiac trunk Palabras clave. Isquemia gástrica. Úlcera gástrica. Este- stenosis. Endovascular stent. nosis del tronco celíaco. Stent endovascular.

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Servicio de Digestivo. Complejo Hospitalario de Correspondencia: Navarra Cristina Saldaña Dueñas Servicio de Digestivo Complejo Hospitalario de Navarra Irunlarrea 3 Recepción: 09/10/2017 Aceptación provisional: 11/12/2017 31008 Pamplona Aceptación definitiva: 09/02/2018 e-mail: [email protected]

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INTRODUCTION chondrium tenderness to light palpation without rebound. Laboratory test revealed haemoglobin Gastric ischemia (GI) results from (Hb) of 8.9 g/dL, urea of 128 mg/dL, serum creati- diffuse or localized vascular insufficien- tine of 2.4 mg/dL and mild elevation of transam- inases with no other significant abnormalities. cy caused by different etiologies such as Two packed red blood cells were transfused. systemic hypotension, vasculitis, dissemi- Urgent esophagogastroduodenoscopy nated thromboembolism or celiac or mes- (EGD) was performed and a duodenal hemor- enteric stenosis1-4. We present a case of gas- rage was suspected due to the presence of fresh tric ischemia due to critical stenosis of the blood clots. Gastric alimentary content impaired celiac artery with an endovascular therapy proper visualization of gastric walls. A second approach. EGD revealed a large and deep ulcer, from the lesser curvature to the incisura angularis, with endoscopic signs of recent bleeding (Fig. 1a) CASE REPORT suggestive of ischemic origin that was confirmed by histological examination. A 66-year-old woman presented at the emer- Further evaluation by computed tomogra- gency department and postprandial acute dif- phy (CT) scan revealed splenic infarctions. fuse followed by three episodes The combination of suspected GI, impaired of . She had previous history of liver enzymes and splenic infarctions suggested type II diabetes, isquemic heart disease and pe- the implication of the celiac trunk. Furthermore, ripheral arteriopathy with chronic ischemia of calcified atheromatosis of the aorta and its main the lower limbs. abdominal branches were present in previous On admission, the patient was hemodynam- radiologic studies. ic stable and her physical examination was un- An endovascular approach was conducted: remarkable, except for epigastric and left hypo- a stent graft was placed in the celiac trunk after

Figure 1. a: Esophagogastroduodenoscopy (EGD) image identifying blood clots and a gastric ulcer with endoscopic signs of recent bleed- ing; b: EGD findings of an ulcer in healing period; c: Angiography study with a critical stenosis of celiac trunk; d: Angiography where a stent graft was placed in the celiac trunk after loading dose of clopidogrel.

124 An. Sist. Sanit. Navar. 2018, Vol. 41, Nº 1, enero-abril Gastric ischemia due to critical stenosis of the celiac trunk loading dose of clopidogrel (Fig. 1c, 1d). After the left gastric artery and also other or- the procedure, the patient had a new episode of gans as the spleen (by the splenic artery hematemesis with hemodynamic instability and branch) and the liver (by the common anemization (Hb of 8.7 g/dL, being 11 g/dL previ- hepatic artery)1. Although the collateral ously). She underwent a new EGD with an active blood supply to the stomach is protective, upper gastrointestinal bleeding coming from an ischemic ulcer in the fundus-proximal gastric systemic hypotension or occlusion of the body. An ulcer in healing period was present in main arteries, as the case of our patient, the lesser curvature (Fig. 1b). Another two con- may result in GI2. centrated red blood cells were transfused and The development of the ischemia leads antiplatelet therapy was discontinued. After 24 into main symptoms such as abdominal hours without symptoms and without bleeding, pain, ulcers, gastrointestinal bleeding, and a third episode of hematemesis was followed by even perforation2-5. The progression of the a haemorrhagic shock. No active bleeding was vascular occlusion can manifest as either detected in the urgent angiography and the EGD revealed an endoscopically non-treatable haem- acute or chronic abdominal . In acute orrhage. Urgent surgery was performed: large GI, patients can develop , vomiting, gastrostomy in the anterior wall visualizing an upper gastrointestinal bleeding, abdominal extensive lesion with detachment of the necrotic distention, and symptoms and signs relat- mucosa, affecting gastric fundus and body. After ed to underlying predisposing conditions haemosthasia and closure, the patient was ad- such as hypoperfusion or shock. In chronic mitted to the intensive care unit where she expe- GI, that may present as ischemic gastropa- rienced a new haemorrhagic shock non-treatable resis, patients usually develop abdominal endoscopically. A surgical total gastrectomy was completed followed by a deteriorating clinical pain, nausea, vomiting, overt or occult gas- course. The patient died three days after sur- trointestinal bleeding, anemia, diarrhoea, gery. and weight loss3,4. The diagnosis is based on endoscopic and radiological examination and may be DISCUSSION confirmed by anatomophatological study of biopsies. The CT scan findings comprise GI is mainly located at both the anterior gastric wall thickening as the result of fo- and posterior gastric walls near the anas- cal ulceration of the mucosa, intramural tomoses between the two arterial arches gas, gastric dilatation or even perforation1. over the lesser and greater curvatures1,3. Other radiological signs are thumbprinting, GI results from diffuse or localized vas- mucosal enhancement, intramural air, dila- cular insufficiency caused by different eti- tation and portal venous gas. CT scan helps ologies that may be classified by systemic in determining the etiology of ischemia in hypoperfusion (such as shock or sepsis) some cases. Findings such as thrombosis, or splanchnic vessel hypoperfusion sec- extensive vascular calcifications or tumour ondary to gastric , acute gastric progression may guide specific therapeutic dilatation, stenosis, thrombosis, embolism, modalities in certain clinical scenarios4. vasculitis or vasoconstriction3,4. Other rare Endoscopic findings vary on the etiol- causes of GI include endoscopic interven- ogy and chronicity. Early EGD could found tions (endoscopic submucosal dissection, the ischemia, as ulceration development injection sclerotherapy), postoperative may take one to two days. It is a safe pro- conditions (distal pancreatectomy with cedure as in ischemic , even though celiac axis resection, subtotal gastrectomy, the gastric wall is much thicker than the highly selective vagotomy, splenectomy, colonic wall. EGD also provides therapeu- gastric restrictive procedure using sta- tical options, for example in active bleed- plers, esophageal surgery) and even co- ing as in our patient. Some authors rec- caine abuse3,4. ommend avoiding cautery when necrosis The celiac artery is the first major is suspected because of the high risk of branch of the abdominal aorta and gives perforations, and prefer using hemoclips, some of the stomach blood supply through which are safer4.

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The systemic hypoperfusion appears this case, in order to ensure the blood sup- as gastric mucosal discoloration, loss of ply. The main techniques are angioplasty mucosal vascular pattern, diffuse erosions or vascular stenting6-9. Although stomach or ulcerations2-4. With reperfusion and pos- receives the main blood supply from the sible superinfection, both acute and chron- celiac artery, clinical improvement after re- ic inflammation become visible, and exu- vascularization of the superior mesenteric date or pseudomembrane may be evident artery, and even the inferior mesenteric ar- endoscopically4. tery, has been documented7,8. In patients with clinical or radiologi- The endovascular approach depends cal suspicious of GI, EGD should be per- on the setting (acute or chronic ischemia). formed in order to make a differential diag- Angiography can define the location of ar- nose, estimate its severity and extension, terial occlusion and provides the potential and evaluate the possibility of endoscopic for intervention, if mesenteric or GI is di- management. Some authors recommend agnosed prior to gastrointestinal infarction classifying and estimating the grade and 9. Although percutaneous transluminal severity of GI based on its endoscopic angioplasty and stenting is an alternative appearance3. They classify in mild (mot- treatment in chronic mesenteric ischemia, tled and pale gastric mucosa), moderate its role in the acute setting is controver- (mottled and pale gastric mucosa, numer- sial9. In acute thrombosis ischemia, even ous stellate gastric erosions or small ul- though other acknowledge management cerations) or severe (moderate plus large as selective catheterization and intra arte- and confluent gastric ulcerations) by the rial thrombolysis is safe as an alternative endoscopic findings. to surgery, it is contraindicated in patients Endoscopists usually make GI diagnosis who had recent surgery, trauma or severe according to endoscopic findings; unless gastrointestinal haemorrhage9. these are atypical, extensive or suspicious In our patient, the previous comorbid- of other diseases (malignancy, drug-in- ities and the loading dose of clopidogrel duced ulceration or viral infection), biop- prior to the stent may play a role in both sies are not obtained3,5. There is no agree- the reperfusion and the development of a ment if biopsies are mandatory in the early new haemorrhage. Despite aggressive man- EGD, because in the majority of cases the agement and optimal supportive care, GI histological examination do not suggest has a poor prognosis and, as in acute mes- the underlying cause. Early GI histologi- enteric ischemia, the mortality rate is high cal changes include capillary dilatation, (64-93%)8,9. An early diagnosis is critical to mucosal edema, vascular congestion, and guide potential interventions4,7. superficial necrosis, white mucosal coagu- In conclusion, GI should be suspected lative necrosis and full-thickness haemor- in individuals with underlying vascular, rhagic necrosis with deep ulceration of the predisposing condition for vascular com- gastric wall are seen at progresion3,4,6. promise, non-NSAIDs (non-steroid anti-in- Patients are usually treated conserva- flammatory drug), ulcer not related to tively unless signs of perforation, sepsis or Helicobacter pylori, atypical lesion, ulcer re- persistent bleeding (despite endoscopical fractoriness to standard peptic ulcer thera- intervention) are developed, in which case py, and severe recurrent hemorrhage4,5. gastrectomy is warranted5. The medical Although few cases have been report- management of GI includes fluid resuscita- ed, the clinical awareness of this syndrome tion, nasogastric tube as prevention of gas- will allow gastroenterologists, endosco- tric distension that worsen the ischemia, pists and radiologist to appropriately intravenous proton pump inhibitors, and diagnose and manage affected patients. broad-spectrum antibiotics if sepsis or gas- Even with poor prognosis, we have some tric pneumatosis are present.3 options of endoscopic and revasculization Angiographic interventions may be use- management that may lead to higher rates ful in vascular obstructive pathology, as in of success2-4,7.

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