a 66-year - old male patient with a history of hypertension and heavy alcoholism was referred to asan medical center for further evaluation of an abdominal distension that had developed 15 days prior . on admission ,
the patient had experienced 6 kg of weight loss during the previous 2 months . a physical examination revealed fever ( 38.2c ) and abdominal tenderness .
laboratory investigations revealed an elevated white cell count of 10.610/l and a c - reactive protein level of 6.69 mg / dl ( the reference value is < 0.6 mg / dl ) .
other findings were unremarkable , including serum amylase / lipase levels and the results of liver function tests .
esophagogastroduo - denoscopy ( egd ) , colonoscopy , and enhanced abdominopelvic computed tomography ( ct ) were performed under suspicion of a cancer of gastrointestinal origin .
abdominopelvic ct revealed chronic calculous cholecystitis , pancreatic duct stone , and associated peripancreatic fat necrosis accompanied by periesophageal fluid collection and a moderate amount of ascites ( fig .
subsequent laboratory tests showed elevated pancreatic enzymes ( serum levels of amylase and lipase of 773 u / l and 589 u / l , respectively ) .
additional enhanced chest ct showed an incidental tubular low attenuated lesion within the lumen of the ascending aorta ( fig .
ascitic fluid examinations showed exudative fluid that was negative for malignant cells . under the impression of acute necrotizing pancreatitis complicated by exudative ascites resulting in periesophageal fluid collection , the patient remained in a fasting state , and received intravenous ( iv ) fluids and broad - spectrum antibacterial therapy .
due to persistent fever and elevating c - reactive proteins despite these treatments , the patient underwent follow - up abdominal ct 2 weeks later , which revealed a newly developed left kidney infarction , pleural effusion , and pericardial effusion .
in addition , marked thickening of the distal esophageal wall and an increased extent of loculated paraesophageal fluid were also found on the ct imaging ( fig .
2 ) . a subsequent chest ct revealed multiple floating masses in the ascending aorta and mediastinal fat necrosis ( fig .
the aortic mass was confirmed to be highly mobile on transesophageal echocardiography ( tee ) .
therefore , we proceeded with urgent surgery , which included mediastinal debridement and removal of aortic thrombi under cardiopulmonary bypass . in the operating room , we found severe necrotizing mediastinitis with multifocal abscess formation and 2 of the highly mobile thrombi attached loosely to the aortic intima in the ascending aorta .
the total pump and aortic clamping times were 52 minutes and 23 minutes , respectively .
after mediastinal debridement and removal of the mobile thrombi , the inflammatory anterior pericardium was further resected , which was followed by massive irrigation ( > 10 l ) of the whole surgical field .
additionally , we found the inflamed distal esophagus to be suggestive of an infected pseudocyst and planned to perform distal esophageal resection ; however , the patient s family declined further esophageal procedures in consideration of the additional surgical risks .
postoperatively , vital signs were stable and the patient fasted for 2 weeks until the absence of an esophageal fistula or perforation on egd was confirmed .
in addition , the patient underwent anticoagulation with iv heparin , which was switched to oral warfarin to prevent potential thromboembolism .
the patient was able to ingest full meals , and a follow - up ct confirmed significant improvement of the lesions in the distal esophagus , which had been thickened diffusely with fat necrosis ( fig .
two years after surgery , the patient was doing well clinically , without any complications .
this was an extremely rare case of a patient with multiple aortic mural thrombi and necrotizing mediastinitis caused by acute pancreatitis .
although most cases of acute pancreatitis are self - limited , one - fourth of patients have been reported to develop vascular complications , such as hemorrhage into a pseudocyst , erosion of the peripancreatic arteries , splanchnic venous thrombosis , and formation of pseudoaneurysms .
arterial thrombus formation , however , is very uncommon , and aortic involvement is extremely rare . in a review of the literature , we were only able to find 3 cases of aortic mural thrombi formation secondary to acute pancreatitis , all of which involved the retropancreatic aorta . to our knowledge
, this is the first report in the literature describing thrombi in the ascending aorta .
we initially thought that the intramural aortic mass on the chest ct was a pseudolesion due to motion artifacts that turned out to be multiple floating thrombi in the ascending aorta according to subsequent ct evaluations and tee .
primary aortic thrombosis is defined as the development of thrombosis without underlying atheromatous lesions in the aorta .
the etiologies of primary aortic thrombosis are diverse , ranging from chemotherapy to treat cancer to heparin - induced thrombocytopenia and inflammatory bowel disease .
in addition , primary aortic thrombosis has been reported to occur in extremely rare cases of acute pancreatitis . although the pathophysiology of acute pancreatitis leading to aortic thrombosis is not clear , several hypotheses have been suggested .
first , acute severe pancreatitis emits proteolytic enzymes that injure the vascular wall directly , which may result in its acting as a nidus for intraluminal thrombus formation .
second , the activation of thrombogenic factors from pancreatitis , such as fibrinogens and platelets , can also be triggered by the release of trypsin into the blood stream .
lastly , acute pancreatitis possibly can lead to hypovolemia , which can increase the risk of vascular stasis and vasospasm .
after the second set of imaging evaluations in the present case , we assumed that the acute pancreatitis had progressed and was complicated by a paraesophageal pseudocyst , which subsequently developed into phlegmonous esophagitis and resultant acute mediastinitis .
these inflammatory processes in the mediastinum might have been facilitated by the thrombogenic environment in the proximal aorta . in conclusion , we experienced a rare case of acute pancreatitis resulting in necrotizing mediastinitis , paraesophageal pseudocyst , and multiple aortic thrombi .
it was successfully treated by medical therapies combined with an urgent operation in which mediastinal debridement and complete removal of the aortic thrombi were performed .
 the formation of aortic thrombi is an extremely rare complication of acute pancreatitis . 
 here we report a case of acute pancreatitis complicated by a paraesophageal pseudocyst , necrotizing mediastinitis , and the formation of multiple thrombi in the ascending aorta . 
 the patient was successfully treated by surgical therapy , which included extensive debridement of the mediastinum and removal of the aortic thrombi under cardiopulmonary bypass . 
 although esophageal resection was not carried out concomitantly , the lesions were resolved and the patient remained free of complications over 2 years of follow - up care . 
Case report
Discussion