Acute mesenteric ischemia (AMI) is often caused by superior mesenteric artery (SMA) embolization. We report a rare case of synchronous celiac axis and SMA embolization in an elderly woman with initially mild abdominal pain. Ultimately, a second contrast-enhanced computed tomography revealed extensive necrosis from the stomach to the transverse colon together with liver ischemia due to hours of occlusion. Multiorgan failure made palliation the only option, and she died the following evening. Autopsy revealed a fragile atherosclerosis-asso-ciated thrombus. Careful examination and repeat diagnostic tests should be performed in patients with mild abdominal symptoms at risk for AMI

Hamada, Takashi

Hirayama, Takanori

Kuroki, Tamotsu

Maeda, Shigeto

Matsuoka, Yuki

Miura, Shiro

Takeshita, Hiroaki

Tokunaga, Takayuki

Yamanouchi, Kosho

Yamashita, Mampei

Yoneda, Akira

English

Okayama University Scientific Achievement Repository

A lthough acute mesenteric ischemia (AMI) only accounts for 2% of cases of gastrointestinal dis-ease,  it is a life-threatening surgical emergency associ-ated with mortality rates as high as 40% to 70% [1].  Usually,  most cases of AMI are caused by embolization of the superior mesenteric artery (SMA).  In general,  embolism occurs when a piece of a blood clot,  foreign object,  or other bodily substance occludes a blood ves-sel and obstructs the flow of blood.  By contrast,  thrombosis is when a thrombus,  or blood clot,  devel-ops in a blood vessel and reduces the flow of blood through that vessel.  Herein,  we report a rare case of synchronous embolization of both the celiac axis (CA) and SMA caused by an atherosclerosis-associated thrombus.Case ReportAn 83-year-old Japanese woman who had been pre-viously treated for atrial fibrillation (AF) and hyperten-sion presented to a general practitioner with slight abdominal pain and vomiting.  She was admitted to the facility,  and intravenous treatment of rehydration ther-apy was performed.  No remarkable findings were observed on laboratory tests or computed tomography (CT) except for atherosclerosis.  Vital signs were as fol-lows: body temperature,  35.8°C; blood pressure,  112/98 mmHg; pulse,  58 beats/min.  Abdominal pain continued intermittently,  always resolving with analge-sics such as non-steroidal anti-inflammatory drugs.  However,  on the following day (18 h from onset),  abdominal pain recurred with an increase in intensity.  After a bout of hematemesis 2 h later,  laboratory tests (Table 1) and CT scan findings revealed intestinal Acta Med.  Okayama,  2021Vol.  75,  No.  4,  pp.  523-527CopyrightⒸ 2021 by Okayama University Medical School.http ://escholarship.lib.okayama-u.ac.jp/amo/Case ReportSynchronous Total Occlusion of the Celiac Axis and  Superior Mesenteric Artery: An Autopsy CaseMampei Yamashitaa＊,  Tamotsu Kurokia,  Yuki Matsuokab,  Shiro Miurab,  Takashi Hamadaa,   Takanori Hirayamaa,  Akira Yonedaa,  Takayuki Tokunagaa,  Kosho Yamanouchia,   Hiroaki Takeshitaa,  and Shigeto MaedaaDepartments of  aSurgery,  bPathology,  National Hospital Organization Nagasaki Medical Center,   Omura,  Nagasaki 856-8562,  JapanAcute mesenteric ischemia (AMI) is often caused by superior mesenteric artery (SMA) embolization.  We report a rare case of synchronous celiac axis and SMA embolization in an elderly woman with initially mild abdominal pain.  Ultimately,  a second contrast-enhanced computed tomography revealed extensive necrosis from the stomach to the transverse colon together with liver ischemia due to hours of occlusion.  Multiorgan failure made palliation the only option,  and she died the following evening.  Autopsy revealed a fragile atherosclerosis-asso-ciated thrombus.  Careful examination and repeat diagnostic tests should be performed in patients with mild abdominal symptoms at risk for AMI.Key words:  atherosclerosis,  celiac axis,  mesenteric ischemia,  superior mesenteric artery,  thromboembolismReceived September 4, 2020 ; accepted January 22, 2021.＊Corresponding author. Phone : +81-957-52-3121; Fax : +81-957-54-0292E-mail : kakugali_zenz@yahoo.co.jp (M. Yamashita)Conflict of Interest Disclosures: No potential conflict of interest relevant to this article was reported.necrosis.  The patient became hemodynamically unsta-ble and was immediately intubated and administered catecholamines prior to transfer to our hospital.On admission to hospital,  22 h later from the onset,  the vital signs were as follows: body temperature,  33.3°C; blood pressure,  70/33 mmHg; and pulse rate,  90 beats/min and irregular.  Laboratory studies revealed an elevated white blood cell count (17,000/μL) and thrombocytopenia (41,000/μL).  Aspartate transami-nase,  alanine aminotransferase,  and lactate dehydro-genase levels were drastically elevated at 15,318 IU/L,  7,106 IU/L,  and 18,045 IU/L,  respectively.  A decrease in prothrombin activity (9.8%) was observed.  Arterial blood gas analysis revealed a pH of 7.027 and a lactic acid concentration of 135 mg/dL.  Contrast-enhanced CT (CE-CT) showed poor contrast and pneumatosis of the digestive tract,  extending from the stomach to the transverse colon and liver,  and portal venous gas resulting from the total obstruction of the CA and SMA.  The evidence of both sepsis and multiorgan failure due to extensive intestinal necrosis with hypothermia,  aci-dosis,  and coagulopathy halted all efforts for curative treatment,  and palliative treatment was begun.  The patient died the following evening.  Figure 1 shows the passage of symptoms and CT imaging from the onset to admission in our hospital.An autopsy was performed 2 h following her death with the consent of the bereaved family.  Macroscopic-ally,  the GI tract from the stomach to the transverse colon,  liver,  and gallbladder were a dark red color (Fig. 2A).  Histologically,  the necrotic digestive tract showed severe submucosal edema,  emphysematous change,  and hemorrhage.  The liver showed necrosis with lipid droplet deposition around the central vein.  In the abdominal aorta,  ulcers and an atherosclerosis-as-sociated thrombus were confirmed upstream of the CA,  and the CA and SMA were found to be totally occluded (~2 cm) by the thrombus (Fig. 2B, C).  At the entrance 524 Yamashita et al. Acta Med.  Okayama　Vol.  75,  No.  4Table 1　 Changes of laboratory date over timePractitioner Practitioner Our hospitalTime (hours) 0 20 22Hematology　WBC (/μL) 5,500 22,000 17,000　RBC (×106/μL) 4.46 4.25 3.04　Hb (g/dL) 14.6 13.9 9.9　PLT (×103/μL) 172 57 41Coagulation　PT (%) - - 9.8　PT-INR - - 5.0　APTT (sec) - - 92.0　D-dimer (μg/mL) - - 405.1　FDP (μg/mL) - - 870.8Biochemistry　T-Bil (mg/dL) 1.0 2.2 1.7　AST (U/L) 28 15,158 15,318　ALT (U/L) 17 6,468 7,106　LDH (U/L) 316 24,459 18,045　BUN (mg/dL) 19.1 21.8 23.0　Cre (mg/dL) 0.87 1.97 2.66　CPK (U/L) 56 91 336　CRP (mg/dL) 0.55 0.66 0.43　K (mEq/L) 4.6 7.2 8.4Blood gas analysis　pH - - 7.027　Lactate (mg/dL) - - 135.0The Time shows the progress from presenting the practitioner.of the CA,  thromboembolism was detected in addition to local thrombosis (Fig. 2D, E),  and there was a trace of a broken thrombus upstream of the atherosclerosed portion (Fig. 2F).  There was no thrombus formation in the atria despite the history of AF.DiscussionAMI is a life-threatening surgical emergency and accounts for 2% of patients with gastrointestinal dis-eases and up to 10% of that in patients aged > 70 years and causes acute abdominal pain [2].  Risk factors for AMI include heart failure,  AF,  coronary heart disease,  arterial hypertension,  and peripheral arterial occlusion [3].  Among patients with thrombosis of the SMA,  33% were found to have thrombosis or severe atherosclerotic changes of the CA.  Furthermore,  synchronous embo-lism of the CA was present in 10 out of 83 SMA-embolized patients [4].  There are a few reports of syn-chronous occlusion of the CA and SMA [5 , 6].  In our case,  results of the autopsy confirmed atherosclerotic changes upstream of the CA,  along with minor throm-bosis of the CA and SMA.  A huge fragile thrombus,  formed on the atherosclerotic plaque,  was peeled off and trapped synchronously into the CA and SMA,  causing extensive and fatal abdominal organ necrosis within just a few hours.Clinically,  the initial stage of AMI,  which is charac-terized by a sudden onset of cramp-like abdominal pain,  is followed by a deceptive pain-free interval after approximately 3 to 6 h,  caused by a decline in intramu-ral pain receptors as a result of sustained underperfu-sion of the intestinal wall.  Subsequently,  the mucosal barriers collapse with bacterial translocation and gan-grene of the intestinal wall,  with peritonitis resulting from bacterial infiltration,  ileus,  sepsis,  and multior-gan failure [2].  In cases of CA occlusion alone,  most patients remain asymptomatic owing to the gradual progression,  as well as the vast collateral circulation from the SMA [6].  In our case,  the patient’s initial abdominal pain,  which resolved with analgesics on her first admission,  was possibly the initial sign that sug-gested AMI.  Based on her initial symptoms,  laboratory tests,  and CT scan results,  the necrotic change of the digestive tract had not started yet,  although the throm-bus might have been at the entrance of the CA and SMA.  The CA and SMA were synchronously emboli-zed,  and extensive necrosis,  including that of the stom-ach,  occurred before collateral circulation could develop.The prognosis of AMI is poor unless diagnosis and treatment are performed promptly.  The mortality rate August 2021 Synchronous Occlusion of the CA and SMA 525CT, laboratory test CT, laboratory test CE-CT, laboratory testslight abdominal painvomitingTime passage fromonset (hours)CT(axial)intermittent pain strong pain Instability of hemodynamichematemesis0 18 20 22 25CT(sagittal)CASMASymptoms†Fig. 1　 The timeline of the patientʼs symptoms and corresponding computed tomography (CT) images.  On the initial CT scan,  athero-sclerosis was observed at the entrance of the celiac axis and the superior mesenteric artery; however,  no signs of intestinal necrosis were found.  On subsequent CT scans,  intestinal necrosis was observed,  and blood flow could not be visualized at the CA and the SMA.rises from 0% to 10% in those with swift treatment to 50% to 60% in those with treatment delays of 6 to 12 h and 80% to 100% in those with treatment delays of more than 24 h after symptom onset [7].  AMI results from arterial embolism in 50% of patients,  arterial thrombosis in 20%,  nonocclusive mesenteric ischemia in 20%,  and venous thrombosis in 10% [8].  If AMI is suspected,  biphasic CE-CT is the diagnostic tool of choice.  The sensitivity and specificity of CE-CT are 93% and 100%,  respectively [9].  Pneumatosis intestinalis,  portal venous gas,  bowel dilation,  and massive ascites are the findings noted with respect to intestinal necro-sis.  Diagnosis and treatment within 6 to 12 h from the onset are life-saving; in our case,  repeat laboratory tests within 6 h and early stage CE-CT should have been performed before hematemesis prompted such mea-sures.  Calcification and stenosis in the CA and SMA could have been revealed in more detail if CE-CT had been performed,  and minor changes could have been detected earlier with more frequent laboratory tests.  Furthermore,  our patient had previously been treated for AF,  and atherosclerosis had already been observed in the CA and SMA by CT.  Thus,  the possibility of AMI could have been suspected based on the symptoms of 526 Yamashita et al. Acta Med.  Okayama　Vol.  75,  No.  4AD EFB CCASMACASMAFig. 2　 Autopsy findings.  (A) Extensive necrosis from the stomach to the transverse colon.  (B) An ulcer and a thrombus (white arrow-head) caused by atherosclerosis,  upstream of the celiac axis (CA).  The CA and the superior mesenteric artery (SMA) were totally occluded by the thrombus; however,  the renal arteries (black arrow heads) were intact.  (C) In the sagittal section,  approximately 2 cm of the CA and SMA were occluded by the thrombus.  (D ,E) Macroscopic and histological section of the CA.  There was a covering thrombus (white and black dotted line,  respectively) that was peeled off upstream.  (F) There was a trace of a broken thrombus (white arrow) on the atheroma (black dotted line).mild,  intermittent abdominal pain and vomiting.Endovascular intervention can be performed for synchronous occlusion of the CA and SMA,  with low rates of complication and mortality as long as the via-bility of the digestive tract is maintained [5].  More specifically,  endovascular intervention includes the possibility of angiographically directed catheter-aspira-tion embolectomy and/or catheter lysis with recombi-nant tissue plasminogen activator,  urokinase,  or pros-taglandin E1 [10].  Surgery is the only option for patients with intestinal infarction,  acute peritonitis,  or failure of endovascular intervention.  It is difficult to recognize transmural bowel necrosis; therefore,  even if the necrotic intestine could be resected at initial surgery,  a second-look surgery should be considered to ensure resection of any nonviable intestine.As mentioned above,  severe atherosclerotic changes or embolism in the CA may coexist with occlusion in the SMA.  Even in cases with mild abdominal symp-toms,  conducting repeat laboratory tests within 6 h and a CE-CT should be considered to exclude AMI in any patient with a high risk of AMI.In conclusion,  we investigated a rare case of syn-chronous total occlusion of the CA and SMA confirmed on autopsy.  Such AMI cases have high mortality,  thus,  a high suspicion for the possibility should be present and repeat diagnostic tests ordered to allow for timely intervention.References 1.  van den Heijkant TC,  Aerts BAC,  Teijink JA,  Buurman WA and Luyer MDP: Challenges in diagnosing mesenteric ischemia.  World J Gastroenterol (2013) 19: 1338-1341. 2.  Klar E,  Rahmanian PB,  Bücker A,  Hauenstein K,  Jauch KW and Luther B: Acute mesenteric ischemia: a vascular emergency.  Dtsch Arztebl Int (2012) 109: 249-256. 3.  Dahlke MH,  Asshoff L,  Popp FC,  Feuerbach S,  Lang SA,  Renner P,  Slowik P,  Stoeltzing O,  Schlitt HJ and Piso P: Mesenteric ischemia -outcome after surgical therapy in 83 patients.  Dig Surg (2008) 25: 213-219. 4.  Acosta S,  Ogren M,  Stemby NH,  Bergqvist D and Björck M: Clinical implications for the management of acute thromboembolic occlu-sion of the superior mesenteric artery autopsy findings in 213 patients.  Ann Surg (2005) 241: 516-522. 5.  San Norberto EM,  Gutierrez VM,  Gonzalez-Fajardo JA,  Chehayeb J,  Ibanez MA and Vaquero C: Percutaneous treatment of liver fail-ure and acute mesenteric ischaemia.  Eur J Vasc Endovasc Surg (2012) 43: 35-37. 6.  Farma JM and Hoffman JP: Nonneoplastic celiac axis occlusion in patients undergoing pancreaticoduodenectomy.  Am J Surg (2007) 193: 341-344; discussion 344. 7.  Paes E,  Vollmar JF,  Hutschenreiter S,  Schoenberg MH and Schölzel E: Diagnostik und therapie des akuten mesenterialinfark-tes.  Chir Gastroenterol (1990) 6: 473-480. 8.  Sise MJ: Acute mesenteric ischemia.  Surg Clin North Am (2014) 94: 165-181. 9.  Aschoff AJ,  Stuber G,  Becker BW,  Hoffmann MHK,  Schmitz BL,  Schelzig H and Jaeckle: Evaluation of acute mesenteric isch-emia: accuracy of biphasic mesenteric multi-detector CT angiogra-phy.  Abdom Imaging (2009) 34: 345-357.10.  Schoots IG,  Levi MM,  Reekers JA,  Lameris JS and van Gulik TM:  Thrombolytic therapy for acute superior mesenteric artery occlu-sion.  J Vasc Interv Radiol (2005) 16: 317-329.August 2021 Synchronous Occlusion of the CA and SMA 527

Synchronous Total Occlusion of the Celiac Axis and Superior Mesenteric Artery: An Autopsy Case

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Synchronous Total Occlusion of the Celiac Axis and Superior Mesenteric Artery: An Autopsy Case

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