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Severe Acute Type B Aortic Dissection Complicated by Acute Pancreatitis: A Case Report Jin Jie,1 Wu Yongfa,1 Wang Yuxin,2 Liao Mingfang,1 and Qu Lefeng,1 Shanghai, China
A 52-year-old man presented with sudden abdominal pain and intermittent vomiting. The patient underwent contrast-enhanced computed tomography scan and was diagnosed with an acute type B aortic dissection involving the celiac trunk superior mesenteric artery and extending to the renal artery. The patient was treated with thoracic endovascular aortic repair. After the procedure, the patient still complained of left upper abdomen abdominal pain, and an abdominal mass was detected on physical examination. Imaging revealed a 15-cm cystic lesion involving the pancreatic tail and serum amylase measured at 556 U/L. A definitive diagnosis of severe acute pancreatitis was made. The patient was treated with injection of somatostatin, ultrasound-guided puncture drainage, and jejunal nutrition tube placement. The patient was discharged with symptom free after 30 days and well recovered in subsequent follow-up 12 months later.
Acute aortic dissection (AAD) is a relatively rare but very fatal disease, and aortic dissections are divided into 2 groups based on their location: type A (ascending aorta) and type B (descending aorta). The overall in-hospital mortality of AAD in China is relatively high and estimated to be 17.7%.1 Acute type B aortic dissection (ABAD) often presents with several clinical symptoms which can easily be mistaken and prolong diagnosis. The classic symptom of an aortic dissection is described as sudden-onset tearing chest/back pain2; some patients present with complaints of abdominal pain, chest congestion, limb weakness, and other vague symptoms. Compared with uncomplicated ABAD, almost 25% of patients
with complicated ABAD present with malperfusion syndrome or hemodynamic instability, resulting in a high risk of morbidity and mortality.3 According to the International Registry of Acute Aortic Dissection (IRAD) database, malperfusion syndrome is reported in about 10e21% of patients with type B aortic dissection and typically leads to paraparesis, paraplegia, lower limb ischemia, abdominal pain, nausea, and/or diarrhea.4e6 Herein, we report the successful management of a special case of ABAD, which was complicated by acute pancreatitis. The diagnostic workup and the treatment strategy are described in the following.
CASE REPORT The authors declare no conflicts of interest to disclose. This study was supported by the grants from Shanghai Government Grant (12JC1411202) and National Natural Science Foundation of China (81470576). 1 Department of Vascular and Endovascular Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, China. 2 Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, China.
Correspondence to: Qu Lefeng, PhD, No. 415 Fengyang Road, Huangpu District, Shanghai, China; E-mail: [email protected] Ann Vasc Surg 2018; 47: 279.e19–279.e24 http://dx.doi.org/10.1016/j.avsg.2017.07.044 Ó 2017 Elsevier Inc. All rights reserved. Manuscript received: March 23, 2017; manuscript accepted: July 31, 2017; published online: 6 September 2017
A 52-year-old man was admitted to our department with acute onset epigastric pain, associated with mild vomiting and hematochezia. His past medical history included long-standing hypertension (diagnosed 10 years prior), which was poorly controlled. After arrival, the patient complained of left upper abdominal pain. His initial vital signs showed a blood pressure of 213/108 mm Hg, a pulse of 92 bpm, and a respiration rate of 14 inspirations/min. On physical examination, there was slight abdominal tenderness in the left upper quadrant without rebound, and bowel sounds were positive (2/min). Electrocardiography demonstrated scarce atrial premature beats and bilateral bundle branch block. Clinically significant laboratory values were as 279.e19
279.e20 Case reports
Annals of Vascular Surgery
Fig. 1. Contrast-enhanced computed tomography scan of the aortic vasculature. (A) The extent of the dissection, from left subclavian artery to renal artery, showing the right renal artery arising from the true lumen and the left renal artery supplied by the false lumen. The white
arrows indicate the true and false lumen. (B) The first intimal tear was located close to the root of left subclavian artery (white arrow head). (C) Thrombosis of the celiac trunk (white arrow head). (D and E) the SMA was partially occluded (white arrow head).
follows: WBC count 11.8 109/L, 88.1% neutrophils (NEUT), serum potassium of 1.78 mmol/L, a serum amylase of 58 U/L, blood glucose of 10.9 mmol/L, ALT of 159 IU/L, and AST of 205 IU/L. Contrast-enhanced computed tomography scan (CTA) of the whole aorta demonstrated an ABAD, extending to the renal artery and involving celiac trunk and superior mesenteric artery (SMA). An intimal tear was located in the left subclavian artery (LSA), and the celiac trunk was occluded with thrombus. The true lumen of SMA was patent but thin because of pressure from the false lumen and local thrombosis. The right renal artery arose from the true lumen, and the left renal artery was supplied by the false lumen (Fig. 1). The liver and spleen demonstrated signs of ischemia, related to vascular occlusion, and the left adrenal gland appeared a small mass, possibly related to the patient’s hypokalemia (Fig. 2). Initially, the patient was treated conservatively with maximum fluid replacement, bowel rest, antihypertensive medication, as well as liver-protecting treatment and potassium supplementation. The patient’s clinical course was complicated by blood pressure instability, elevating transaminase levels, reduced albumin, and only gradual improvement of serum potassium (2.5 mmol/L). Four days after admission, the patient underwent placement of a temporary pacemaker, and thoracic endovascular aortic repair (TEVAR) (include traditional covered stent and a restricted bare stent in the distal descending aorta and a chimney graft in the left subclavian) was performed. During
the operation, a moderate pleural effusion was found in the left thorax which drained 400 mL of hemorrhagic fluid. Unfortunately, the patient suffered from postoperative cognitive dysfunction, which was attributed to anesthesia. A brain computed tomography (CT) was carried in time and showed nothing unusual. In the early postoperative period, laboratory results showed improvement, but the patient still reported vague abdominal pain. Four days status after TEVAR, the patient demonstrated marked abdominal pain, abdominal distension, vomiting, and fever. On physical examination, a large left upper abdominal mass was palpated. CTA demonstrated that the aortic dissection, celiac trunk, and SMA were in good condition (Fig. 3), while a massive encapsulated effusion in the pancreatic tail forming a pancreatic pseudocyst (Fig. 4A). Laboratory tests revealed a high serum/urine amylase (556/1,011 IU/L) (Fig. 5). A diagnosis of severe acute pancreatitis (SAP) was made, and appropriate treatment strategies were initiated, including administration of a protease inhibitor, antibiotics, fluid infusion, and fasting. Gastroenterology was consulted, recommending close observation and percutaneous tube drainage of the pancreatic pseudocyst as a safe, efficient method of therapy. Almost 800-mL jelly-like liquid was drained from the pancreatic tail, and the patient reported immediate symptomatic relief. The level of amylase in the drained liquid measured more than 24,000 U/L. In addition, a nasojejunal nutrition tube was placed for gastric rest and nutritional support.
Volume 47, February 2018
Case reports 279.e21
Fig. 2. CT images related to the aortic dissection (white arrow head ). (A) Ischemia signs of liver and spleen; gastric retention (lack of gastrointestinal peristalsis). (B)
A left adrenal mass (15.9 mm). (C) An inconspicuous ischemic area in the pancreas tail.
Fig. 3. Radiologic examination by spiral CTA after TEVAR. The aorta and main vessels after repair. (A) The segment of thoracic aortic was well remolded, and
the chimney graft in left subclavian artery was patency. (BeD) The celiac trunk and SMA demonstrate repatency (white arrow head ).
The aforementioned treatment strategies resulted in normalization of serum amylase at 10 days status after drainage of the pseudocyst. The patient’s condition gradually stabilized, but the pancreas continued to drain at a rate of 100e150 mL/day. CT and ultrasound imaging failed to reveal effusion in the pancreatic tail (Fig. 4B). The patient was subsequently discharged 30 days after admission. At 1 year outpatient follow-up and in telephone interviews, the patient reported a full recovery with no symptomatic recurrence.
DISCUSSION Complications of aortic dissection are not uncommon and can include rupture, hemorrhage, and malperfusion, but SAP is a rare complication of an aortic dissection. Reports of aortic dissection associated with pancreatitis are reported in the literature, mostly in the form of case reports (Table I). A total of 8 patients suffering from this
279.e22 Case reports
Annals of Vascular Surgery
Fig. 4. CT scanning contrast before and after the treatment of SAP. (A) Pancreatic pseudocyst in the pancreas tail. (B) The cyst disappeared after percutaneous tube drainage, the arrow was the shadow of tube.
Fig. 5. Trend of laboratory results in the process of treatment, which toward to a positive direction.
situation have been described, and all of the dissection involved the visceral artery, which show that the onset of SAP was closely related to the visceral arterial ischemia after aortic dissection. Acute pancreatitis is a deadly disease that can be caused by a variety of factors. About 85% of cases are related to bile stones or excessive alcohol consumption, but pancreatic ischemia should be considered when no other reasons can be defined.13 The pancreas is an organ that is highly susceptible to ischemia14,15; its blood supply mainly comes from branches of celiac trunk and SMA. AP may be
caused by ischemia-reperfusion injury, which may be caused by the exposure to oxygen-free radicals, the activation of polymorphonuclear leukocytes, failure of adequate microvascular perfusion, increased cellular acidosis, or a disturbance of intracellular homeostasis.15 Ischemia-reperfusion injury to the pancreas is known to occur in various clinical settings, including CPR, shock, and complex great vessels operations.13,15,16 Hideaki et al. have also described a case of ischemia-reperfusioneinduced pancreatitis, which was caused by the sudden and transient deterioration of the pancreatic circulation, as a result of the ABAD.6
Volume 47, February 2018
Case reports 279.e23
Table I. Summary of all reported cases of aortic dissection relate to pancreatitis Author
Year 7
Age/sex
Dissection
Pombo et al. Goff et al.8 Baydina et al.9
1991 42/M Type B 1992 Middle/M Type B 2008 52/M Type A
Umeda et al.10 Hamamoto6 Hideaki11 Pham and Nable2 Zheng et al.12
2011 2012 2012 2013 2014
49/M 47/M 60/M 69/F 47/M
Type Type Type Type Type
A B B B A
Clinical feature
Developed epigastric pain Unknown Severe epigastric pain
Treatment
Surgical reconstruction Conservative therapy Whether surgery was unknown Sudden chest pain Conservative therapy Sudden back pain Conservative therapy Asymptomatic Conservative therapy Epigastric pain Conservative therapy Sudden upper abdominal pain Conservative therapy
Outcome
Discharge Discharge Discharge Recovery Discharge Discharge Discharge Dead
Table II. Schematic representation of the patient’s in-hospital treatment
All aortic dissections are characterized by separation of the tunica media in a course parallel to that of the flow of blood.17 The intimal flap divides aorta into a true and a false lumen, which affects branches along the wall and results in malperfusion syndrome.18 In the present case, treatment focused on addressing intestinal ischemia, hypokalemia, and ABAD. Careful reading of the CTA scans identified 2 branch vessels of the pancreas that were damaged seriously and an inconspicuous ischemic area present in the pancreas tail, which was ignored by us (Fig. 2C). We speculated that the SAP was induced by reperfusion, related to the aortic dissection and subsequent repair operation. Four days before the operation, serum amylase was normal, and the abdominal discomfort was relieved. After TEVAR, the patient’s situation get worse, which reflected in the sudden increased abdominal symptoms and pancreatic pseudocyst. When the ABAD was repaired, the SMA widened, and the celiac trunk was partial recanalized, causing a generous amount of blood flow to return to the pancreas, possibly resulting in a delayed SAP.
Severe ABAD complicated by acute pancreatitis is not straightforward to diagnose or manage. Similar to the 8 cases in the literature, CT and level of amylase are important tests. The treatment strategies should be planned according to the individual patient. For example, conservative treatment is effective but requires stable conditions. Our experience illustrates a difficult condition and successful treatment method (Table II). In conclusion, aortic dissection complicated by SAP is an uncommon occurrence but a very real possibility in the emergency setting. AP should be considered when encountering a complex aortic dissection as timely and correct diagnosis and treatment of the disease are essential to proper clinical management. REFERENCES 1. Li Y, Yang N, Duan W, et al. Acute aortic dissection in China. Am J Cardiolds 2012;110:1056e61. 2. Pham TV, Nable JV. Aortic dissection presenting with pancreatitis. Am J Emerg Med 2013;31:e1e2. 3. Fattori R, Cao P, De Rango P, et al. Interdisciplinary expert consensus document on management of type B aortic dissection. J Am Coll Cardiol 2013;61:1661e78.
279.e24 Case reports
4. Suzuki T, Mehta RH, Ince H, et al. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003;108(10 suppl 1):II312e7. 5. Fattori R, Tsai TT, Myrmel T, et al. Complicated acute type B dissection: is surgery still the best option a report from the International Registry of Acute Aortic Dissection. JACC Cardiovasc Interv 2008;1:395e402. 6. Hamamoto M. Acute ischemic pancreatitis associated with acute type B aortic dissection: a case report. Ann Vasc Dis 2012;5:385. 7. Pombo F, Marini M, Beraza A, et al. Aortic dissection presenting as acute pancreatitis: CT diagnosis. Comput Med Imaging Graph 1991;15:407e9. 8. Goff WB 2nd, Lawrence DP, Burkhard TK. Aortic dissection in acute pancreatitis. J Am Osteopath Assoc 1992;92: 921e3. 9. Baydin A, Genc S, Aygun D, et al. Acute pancreatitis after acute Aortic dissection: report of a case and review of the literature. Fırat Tıp Dergisi 2008;13:271e3. 10. Umeda I, Hayashi T, Ishiwatari H, et al. A case of severe acute pancreatitis and ischemic gastropathy caused by acute aortic dissection. Nihon Shokakibyo Gakkai Zasshi 2011;108: 103e10.
Annals of Vascular Surgery
11. Eiaki O, Ohno H. A case of acute aortic dissection with hyperplastic asymptomatic acute pancreatitis and pancreatic cyst: report of 1 cases of virtual. Respir Circ 2012;60:337e40. 12. Zheng Z, Liu J, Huang Y, et al. Acute pancreatitis induced by acute type A aortic dissection: a Case report. J Cardiovasc Dis Res Vol 2014;5:65. 13. Hackert T, Hartwig W, Fritz S, et al. Ischemic acute pancreatitis: clinical features of 11 patients and review of the literature. Am J Surg 2009;197:450e4. 14. Tsai K, Wang SS, Chen TS, et al. Oxidative stress: an important phenomenon with pathogenetic significance in the progression of acute pancreatitis. Gut 1998;42:850e5. 15. Sakorafas GH, Tsiotos GG, Sarr MG. Ischemia/reperfusioninduced pancreatitis. Dig Surg 1999;17:3e14. 16. Burkey SH, Valentine RJ, Jackson MR, et al. Acute pancreatitis after abdominal vascular surgery. J Am Coll Surg 2000;191:373e80. 17. Roberts WC. Aortic dissection: anatomy, consequences, and causes. Am Heart J 1981;101:195e214. 18. Gaxotte V, Cocheteux B, Haulon S, et al. Relationship of intimal flap position to endovascular treatment of malperfusion syndromes in aortic dissection. J Endovasc Ther 2003;10:719e27.
A 52-year-old man presented with sudden abdominal pain and intermittent vomiting. The patient underwent contrast-enhanced computed tomography scan and was diagnosed with an acute type B aortic dissection involving the celiac trunk superior mesenteric artery and extending to the renal artery. The patient was treated with thoracic endovascular aortic repair. After the procedure, the patient still complained of left upper abdomen abdominal pain, and an abdominal mass was detected on physical examination. Imaging revealed a 15-cm cystic lesion involving the pancreatic tail and serum amylase measured at 556 U/L. A definitive diagnosis of severe acute pancreatitis was made. The patient was treated with injection of somatostatin, ultrasound-guided puncture drainage, and jejunal nutrition tube placement. The patient was discharged with symptom free after 30 days and well recovered in subsequent follow-up 12 months later.
Acute aortic dissection (AAD) is a relatively rare but very fatal disease, and aortic dissections are divided into 2 groups based on their location: type A (ascending aorta) and type B (descending aorta). The overall in-hospital mortality of AAD in China is relatively high and estimated to be 17.7%.1 Acute type B aortic dissection (ABAD) often presents with several clinical symptoms which can easily be mistaken and prolong diagnosis. The classic symptom of an aortic dissection is described as sudden-onset tearing chest/back pain2; some patients present with complaints of abdominal pain, chest congestion, limb weakness, and other vague symptoms. Compared with uncomplicated ABAD, almost 25% of patients
with complicated ABAD present with malperfusion syndrome or hemodynamic instability, resulting in a high risk of morbidity and mortality.3 According to the International Registry of Acute Aortic Dissection (IRAD) database, malperfusion syndrome is reported in about 10e21% of patients with type B aortic dissection and typically leads to paraparesis, paraplegia, lower limb ischemia, abdominal pain, nausea, and/or diarrhea.4e6 Herein, we report the successful management of a special case of ABAD, which was complicated by acute pancreatitis. The diagnostic workup and the treatment strategy are described in the following.
CASE REPORT The authors declare no conflicts of interest to disclose. This study was supported by the grants from Shanghai Government Grant (12JC1411202) and National Natural Science Foundation of China (81470576). 1 Department of Vascular and Endovascular Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, China. 2 Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, China.
Correspondence to: Qu Lefeng, PhD, No. 415 Fengyang Road, Huangpu District, Shanghai, China; E-mail: [email protected] Ann Vasc Surg 2018; 47: 279.e19–279.e24 http://dx.doi.org/10.1016/j.avsg.2017.07.044 Ó 2017 Elsevier Inc. All rights reserved. Manuscript received: March 23, 2017; manuscript accepted: July 31, 2017; published online: 6 September 2017
A 52-year-old man was admitted to our department with acute onset epigastric pain, associated with mild vomiting and hematochezia. His past medical history included long-standing hypertension (diagnosed 10 years prior), which was poorly controlled. After arrival, the patient complained of left upper abdominal pain. His initial vital signs showed a blood pressure of 213/108 mm Hg, a pulse of 92 bpm, and a respiration rate of 14 inspirations/min. On physical examination, there was slight abdominal tenderness in the left upper quadrant without rebound, and bowel sounds were positive (2/min). Electrocardiography demonstrated scarce atrial premature beats and bilateral bundle branch block. Clinically significant laboratory values were as 279.e19
279.e20 Case reports
Annals of Vascular Surgery
Fig. 1. Contrast-enhanced computed tomography scan of the aortic vasculature. (A) The extent of the dissection, from left subclavian artery to renal artery, showing the right renal artery arising from the true lumen and the left renal artery supplied by the false lumen. The white
arrows indicate the true and false lumen. (B) The first intimal tear was located close to the root of left subclavian artery (white arrow head). (C) Thrombosis of the celiac trunk (white arrow head). (D and E) the SMA was partially occluded (white arrow head).
follows: WBC count 11.8 109/L, 88.1% neutrophils (NEUT), serum potassium of 1.78 mmol/L, a serum amylase of 58 U/L, blood glucose of 10.9 mmol/L, ALT of 159 IU/L, and AST of 205 IU/L. Contrast-enhanced computed tomography scan (CTA) of the whole aorta demonstrated an ABAD, extending to the renal artery and involving celiac trunk and superior mesenteric artery (SMA). An intimal tear was located in the left subclavian artery (LSA), and the celiac trunk was occluded with thrombus. The true lumen of SMA was patent but thin because of pressure from the false lumen and local thrombosis. The right renal artery arose from the true lumen, and the left renal artery was supplied by the false lumen (Fig. 1). The liver and spleen demonstrated signs of ischemia, related to vascular occlusion, and the left adrenal gland appeared a small mass, possibly related to the patient’s hypokalemia (Fig. 2). Initially, the patient was treated conservatively with maximum fluid replacement, bowel rest, antihypertensive medication, as well as liver-protecting treatment and potassium supplementation. The patient’s clinical course was complicated by blood pressure instability, elevating transaminase levels, reduced albumin, and only gradual improvement of serum potassium (2.5 mmol/L). Four days after admission, the patient underwent placement of a temporary pacemaker, and thoracic endovascular aortic repair (TEVAR) (include traditional covered stent and a restricted bare stent in the distal descending aorta and a chimney graft in the left subclavian) was performed. During
the operation, a moderate pleural effusion was found in the left thorax which drained 400 mL of hemorrhagic fluid. Unfortunately, the patient suffered from postoperative cognitive dysfunction, which was attributed to anesthesia. A brain computed tomography (CT) was carried in time and showed nothing unusual. In the early postoperative period, laboratory results showed improvement, but the patient still reported vague abdominal pain. Four days status after TEVAR, the patient demonstrated marked abdominal pain, abdominal distension, vomiting, and fever. On physical examination, a large left upper abdominal mass was palpated. CTA demonstrated that the aortic dissection, celiac trunk, and SMA were in good condition (Fig. 3), while a massive encapsulated effusion in the pancreatic tail forming a pancreatic pseudocyst (Fig. 4A). Laboratory tests revealed a high serum/urine amylase (556/1,011 IU/L) (Fig. 5). A diagnosis of severe acute pancreatitis (SAP) was made, and appropriate treatment strategies were initiated, including administration of a protease inhibitor, antibiotics, fluid infusion, and fasting. Gastroenterology was consulted, recommending close observation and percutaneous tube drainage of the pancreatic pseudocyst as a safe, efficient method of therapy. Almost 800-mL jelly-like liquid was drained from the pancreatic tail, and the patient reported immediate symptomatic relief. The level of amylase in the drained liquid measured more than 24,000 U/L. In addition, a nasojejunal nutrition tube was placed for gastric rest and nutritional support.
Volume 47, February 2018
Case reports 279.e21
Fig. 2. CT images related to the aortic dissection (white arrow head ). (A) Ischemia signs of liver and spleen; gastric retention (lack of gastrointestinal peristalsis). (B)
A left adrenal mass (15.9 mm). (C) An inconspicuous ischemic area in the pancreas tail.
Fig. 3. Radiologic examination by spiral CTA after TEVAR. The aorta and main vessels after repair. (A) The segment of thoracic aortic was well remolded, and
the chimney graft in left subclavian artery was patency. (BeD) The celiac trunk and SMA demonstrate repatency (white arrow head ).
The aforementioned treatment strategies resulted in normalization of serum amylase at 10 days status after drainage of the pseudocyst. The patient’s condition gradually stabilized, but the pancreas continued to drain at a rate of 100e150 mL/day. CT and ultrasound imaging failed to reveal effusion in the pancreatic tail (Fig. 4B). The patient was subsequently discharged 30 days after admission. At 1 year outpatient follow-up and in telephone interviews, the patient reported a full recovery with no symptomatic recurrence.
DISCUSSION Complications of aortic dissection are not uncommon and can include rupture, hemorrhage, and malperfusion, but SAP is a rare complication of an aortic dissection. Reports of aortic dissection associated with pancreatitis are reported in the literature, mostly in the form of case reports (Table I). A total of 8 patients suffering from this
279.e22 Case reports
Annals of Vascular Surgery
Fig. 4. CT scanning contrast before and after the treatment of SAP. (A) Pancreatic pseudocyst in the pancreas tail. (B) The cyst disappeared after percutaneous tube drainage, the arrow was the shadow of tube.
Fig. 5. Trend of laboratory results in the process of treatment, which toward to a positive direction.
situation have been described, and all of the dissection involved the visceral artery, which show that the onset of SAP was closely related to the visceral arterial ischemia after aortic dissection. Acute pancreatitis is a deadly disease that can be caused by a variety of factors. About 85% of cases are related to bile stones or excessive alcohol consumption, but pancreatic ischemia should be considered when no other reasons can be defined.13 The pancreas is an organ that is highly susceptible to ischemia14,15; its blood supply mainly comes from branches of celiac trunk and SMA. AP may be
caused by ischemia-reperfusion injury, which may be caused by the exposure to oxygen-free radicals, the activation of polymorphonuclear leukocytes, failure of adequate microvascular perfusion, increased cellular acidosis, or a disturbance of intracellular homeostasis.15 Ischemia-reperfusion injury to the pancreas is known to occur in various clinical settings, including CPR, shock, and complex great vessels operations.13,15,16 Hideaki et al. have also described a case of ischemia-reperfusioneinduced pancreatitis, which was caused by the sudden and transient deterioration of the pancreatic circulation, as a result of the ABAD.6
Volume 47, February 2018
Case reports 279.e23
Table I. Summary of all reported cases of aortic dissection relate to pancreatitis Author
Year 7
Age/sex
Dissection
Pombo et al. Goff et al.8 Baydina et al.9
1991 42/M Type B 1992 Middle/M Type B 2008 52/M Type A
Umeda et al.10 Hamamoto6 Hideaki11 Pham and Nable2 Zheng et al.12
2011 2012 2012 2013 2014
49/M 47/M 60/M 69/F 47/M
Type Type Type Type Type
A B B B A
Clinical feature
Developed epigastric pain Unknown Severe epigastric pain
Treatment
Surgical reconstruction Conservative therapy Whether surgery was unknown Sudden chest pain Conservative therapy Sudden back pain Conservative therapy Asymptomatic Conservative therapy Epigastric pain Conservative therapy Sudden upper abdominal pain Conservative therapy
Outcome
Discharge Discharge Discharge Recovery Discharge Discharge Discharge Dead
Table II. Schematic representation of the patient’s in-hospital treatment
All aortic dissections are characterized by separation of the tunica media in a course parallel to that of the flow of blood.17 The intimal flap divides aorta into a true and a false lumen, which affects branches along the wall and results in malperfusion syndrome.18 In the present case, treatment focused on addressing intestinal ischemia, hypokalemia, and ABAD. Careful reading of the CTA scans identified 2 branch vessels of the pancreas that were damaged seriously and an inconspicuous ischemic area present in the pancreas tail, which was ignored by us (Fig. 2C). We speculated that the SAP was induced by reperfusion, related to the aortic dissection and subsequent repair operation. Four days before the operation, serum amylase was normal, and the abdominal discomfort was relieved. After TEVAR, the patient’s situation get worse, which reflected in the sudden increased abdominal symptoms and pancreatic pseudocyst. When the ABAD was repaired, the SMA widened, and the celiac trunk was partial recanalized, causing a generous amount of blood flow to return to the pancreas, possibly resulting in a delayed SAP.
Severe ABAD complicated by acute pancreatitis is not straightforward to diagnose or manage. Similar to the 8 cases in the literature, CT and level of amylase are important tests. The treatment strategies should be planned according to the individual patient. For example, conservative treatment is effective but requires stable conditions. Our experience illustrates a difficult condition and successful treatment method (Table II). In conclusion, aortic dissection complicated by SAP is an uncommon occurrence but a very real possibility in the emergency setting. AP should be considered when encountering a complex aortic dissection as timely and correct diagnosis and treatment of the disease are essential to proper clinical management. REFERENCES 1. Li Y, Yang N, Duan W, et al. Acute aortic dissection in China. Am J Cardiolds 2012;110:1056e61. 2. Pham TV, Nable JV. Aortic dissection presenting with pancreatitis. Am J Emerg Med 2013;31:e1e2. 3. Fattori R, Cao P, De Rango P, et al. Interdisciplinary expert consensus document on management of type B aortic dissection. J Am Coll Cardiol 2013;61:1661e78.
279.e24 Case reports
4. Suzuki T, Mehta RH, Ince H, et al. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003;108(10 suppl 1):II312e7. 5. Fattori R, Tsai TT, Myrmel T, et al. Complicated acute type B dissection: is surgery still the best option a report from the International Registry of Acute Aortic Dissection. JACC Cardiovasc Interv 2008;1:395e402. 6. Hamamoto M. Acute ischemic pancreatitis associated with acute type B aortic dissection: a case report. Ann Vasc Dis 2012;5:385. 7. Pombo F, Marini M, Beraza A, et al. Aortic dissection presenting as acute pancreatitis: CT diagnosis. Comput Med Imaging Graph 1991;15:407e9. 8. Goff WB 2nd, Lawrence DP, Burkhard TK. Aortic dissection in acute pancreatitis. J Am Osteopath Assoc 1992;92: 921e3. 9. Baydin A, Genc S, Aygun D, et al. Acute pancreatitis after acute Aortic dissection: report of a case and review of the literature. Fırat Tıp Dergisi 2008;13:271e3. 10. Umeda I, Hayashi T, Ishiwatari H, et al. A case of severe acute pancreatitis and ischemic gastropathy caused by acute aortic dissection. Nihon Shokakibyo Gakkai Zasshi 2011;108: 103e10.
Annals of Vascular Surgery
11. Eiaki O, Ohno H. A case of acute aortic dissection with hyperplastic asymptomatic acute pancreatitis and pancreatic cyst: report of 1 cases of virtual. Respir Circ 2012;60:337e40. 12. Zheng Z, Liu J, Huang Y, et al. Acute pancreatitis induced by acute type A aortic dissection: a Case report. J Cardiovasc Dis Res Vol 2014;5:65. 13. Hackert T, Hartwig W, Fritz S, et al. Ischemic acute pancreatitis: clinical features of 11 patients and review of the literature. Am J Surg 2009;197:450e4. 14. Tsai K, Wang SS, Chen TS, et al. Oxidative stress: an important phenomenon with pathogenetic significance in the progression of acute pancreatitis. Gut 1998;42:850e5. 15. Sakorafas GH, Tsiotos GG, Sarr MG. Ischemia/reperfusioninduced pancreatitis. Dig Surg 1999;17:3e14. 16. Burkey SH, Valentine RJ, Jackson MR, et al. Acute pancreatitis after abdominal vascular surgery. J Am Coll Surg 2000;191:373e80. 17. Roberts WC. Aortic dissection: anatomy, consequences, and causes. Am Heart J 1981;101:195e214. 18. Gaxotte V, Cocheteux B, Haulon S, et al. Relationship of intimal flap position to endovascular treatment of malperfusion syndromes in aortic dissection. J Endovasc Ther 2003;10:719e27.