Dilated cardiomyopathy secondary to acute pancreatitis caused by hypertriglyceridemia

Dilated cardiomyopathy secondary to acute pancreatitis caused by hypertriglyceridemia A 30-year-old male presented to an outside facility with acute pancreatitis and triglycerides of 1594. He was transferred to our facility after becoming febrile, hypoxic and in acute renal failure with triglycerides of 4243. CT scan performed showed wall-off pancreatic necrosis. He underwent continuous renal replacement therapy and his acute renal failure resolved. He was treated with broad spectrum antibiotics and discharged. He developed a fever to 101 a week later and was found to have a large infected pancreatic pseudocyst. This was managed with an IR placed drain. This was continued for 6 weeks. He came to the emergency department several weeks later with shortness of breath and 3+ edema to bilateral lower extremities and lower abdomen. TTE performed showed an EF of 15%. He was diuresed 25 L during that stay. His heart failure was med- ically managed. We present this case of dilated cardiomyopathy secondary to acute pancreatitis. reports of dilated biventricular cardiomyopathy associated with INTRODUCTION pancreatitis. It has been reported that pancreatitis can cause Acute pancreatitis (AP) as defined by the revised Atlanta classi- Takotsubo Cardiomyopathy (TCM) [4–10]. TCM is a transient fication, has three levels of severity based largely on organ dys- disease with apical ballooning of the left ventricular wall during function [1]. Mild AP has no organ dysfunction. Moderately systole. The reported incidence is 2% of acute coronary syn- severe AP has organ dysfunction that remains <48 h or local or drome diagnoses [6]. There are a few case reports of pancrea- systemic complications without organ failure >48 h. Finally, titis induced TCM. Those cases resolved with treatment of the severe AP has persistent organ dysfunction >48 h. pancreatitis [4, 5, 7]. According to Carr’s review, hypertriglyceridemia is an uncom- mon cause of AP in 9% of cases. However, AP is seen in 14% of patients with hypertriglyceridemia. Triglyceride levels of <1000 mg/dL CASE REPORT should raise suspicion for other etiologies of AP [2]. Necrotizing pancreatitis occurs in 20% of patients with AP with a mortality A 30-year-old man with a past medical history of hypertrigly- rate of up to 30% [3]. ceridemia presented to an outside ER with nausea, vomiting Following a literature search of PubMed using keywords and abdominal pain. Lab studies were significant for pancrea- pancreatitis and cardiomyopathy, there were no published case titis (lipase 2730), hypertriglyceridemia (1594), blood glucose of Received: February 10, 2018. Accepted: May 1, 2018 Published by Oxford University Press and JSCR Publishing Ltd. All rights reserved. © The Author(s) 2018. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/ licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com Downloaded from https://academic.oup.com/jscr/article-abstract/2018/5/rjy104/4999375 by Ed 'DeepDyve' Gillespie user on 21 June 2018 2 J.W. Greer et al. Figure 1: Walled off pancreatic necrosis of admission CT. Figure 2: Worsening walled off pancreatic necrosis with extension to the para- colic gutters. 389 and BUN/Cr of 17/1.3. A CT of the abdomen showed AP. A found to have 3+ pitting edema up to his mid-abdomen. A chest subsequent lab draw showed BUN/Cr to 27/3.8, decrease in lip- x-ray showed bilateral pleural effusions and cardiomegaly. A TTE ase to 565, increase in triglycerides to 4243, and a BNP 15. He was performed which showed an EF of <15% and a moderate was transferred to our facility following worsening hypoxemia. pericardial effusion without tamponade. He had elevated tropo- A CT scan was performed: representative sections shown below nins, BNP of 2730, and elevated liver enzymes. CTA ruled out pul- demonstrated walled off pancreatic necrosis (Fig. 1). He was in monary embolism and showed a reduction in the left-sided acute renal failure on presentation and started on continuous abdominal abscess with some residual pockets of air. The patient renal replacement therapy. The renal failure resolved, he com- was sent to IR for a drain check and US-guided paracentesis. pleted a 7-day course of imipenem/cilistatin and was eventu- Approximately 2700 ml of ascitic fluid was removed and a persist- ally discharged 11 days after admission. ent moderate-sized abscess pocket with a fistulous tract of bowel A week later, he presented to his PCP for follow up and was was noted. He was diuresed almost 25 l during the hospital stay febrile with increasing abdominal pain. CT of the abdomen and and discharged with medical management of his heart failure. pelvis showed an 11 × 15 cm pancreatic fluid collection. His His drains were removed when drain check no longer demon- hemoglobin was 6.9 and he was transfused 3 units of PRBC. strated a cavity or fistula. After transfer to our facility, a repeat CT showed a small peri- He was followed in Cardiology clinic 2 months later with cardial and left pleural effusions, large volume ascites, a pan- stable NYHF class I–II symptoms. A cardiac MRI was performed creatic fluid collection within the lesser sac between the and showed enlargement of the heart with diffuse generalized anterior pancreas and posterior gastric body measuring 14 × hypokinesia consistent with dilated cardiomyopathy. With an 16.1 × 16.2 cm , and blood in both paracolic gutters and parare- ejection fraction of 22%. No evidence of myocardial infiltration. nal spaces (Fig. 2). He was referred to Interventional Radiology The patient remains in stable condition today. for drain placement. After drainage, he clinically improved and was discharged. His drains were followed in clinic and continued to drain DISCUSSION necrotic material 6 weeks following initial placement. He refused laparoscopic necrosectomy, preferring to continue with Our case is unique, in that, despite resolution of the AP and non-operative management via the IR drains. Follow up MRCP subsequent pancreatic necrosis, the patient’s heart failure per- revealed multiple intrabdominal fluid collections with the pre- sisted. ECGs throughout the acute period of illness were normal vious left-sided collection decompressing into the abdominal except for sinus tachycardia. Imaging revealed no evidence of wall prompting another drainage by IR. myocarditis or inflammation. There were no fistulous tracts At his next appointment, he was having lower extremity ede- visualized with MRCP to the pericardium as has been reported ma and acid reflux. He was treated with leg wraps and a PPI. in prior case reports [10]. Our patient’s echocardiogram is not Approximately 1 week later, the patient presented to the ED for consistent with the normal findings seen in TCM. The multiple shortness of breath and increased swelling. On exam, he was stressors over an extended period of time might contribute to Downloaded from https://academic.oup.com/jscr/article-abstract/2018/5/rjy104/4999375 by Ed 'DeepDyve' Gillespie user on 21 June 2018 Dilated cardiomyopathy secondary to acute pancreatitis 3 the non-transient nature of our patient’s heart failure and 2. Carr RA, Rejowski BJ, Cote GA, Pitt HA, Zyromski NJ. could represent a new subgroup of TCM patients. Systematic review of hypertriglyceridemia-induced acute There is not a role for routine screening given the rarity of pancreatitis: a more virulent etiology? Pancreatology 2016;16: pancreatitis induced heart failure. More studies will need to be 469–76. conducted to develop screening guidelines for patients with 3. On behalf of the Dutch Pancreatitis Study Group MJ. pancreatitis as there might be a subgroup that needs to be rou- Improving the outcome of acute pancreatitis. Digestive tinely screened. Further characterization of our patient’s heart Diseases (Basel, Switzerland) 2016;34:540–5. failure could aid in elucidating a cause, however, he refused 4. Hsu PC, Lin TH, Su HM, Lin ZY, Lai WT, Sheu SH. Acute nec- further studies. With so little published on pancreatitis induced rotizing pancreatitis complicated with ST elevation acute heart failure and ~90% of TCM cases being postmenopausal myocardial infarction: a case report and literature review. women, we would not advocate routine screening for heart fail- Kaohsiung J Med Sci 2010;26:200–5. ure with BNP or baseline echocardiogram [5, 8, 9]. 5. Bruenjes JD, Vallabhajosyula S, Vacek CJ, Fixley JE. Acute pancreatitis-induced Takotsubo cardiomyopathy in an African American Male. ACG Case Rep J 2015;3:53–6. CONCLUSION 6. Scantlebury DC, Prasad A. Diagnosis of Takotsubo cardio- To our knowledge, this represents the first case report of a myopathy. Circ J 2014;78:2129–39. patient with dilated biventricular cardiomyopathy induced by 7. Rajani R, Przedlacka A, Saha M, de Belder A. Pancreatitis pancreatitis. and the broken heart. Eur J Emerg Med 2010;17:27–9. 8. Pilgrim TM, Wyss TR. Takotsubo cardiomyopathy or transi- CONFLICT OF INTEREST STATEMENT ent left ventricular apical ballooning syndrome: a system- atic review. Int J Cardiol 2008;124:283–92. None declared. 9. Cheezum MK, Willis SL, Duffy SP, Moawad FJ, Horwhat JD, Huffer LL, et al. Broken pancreas, broken heart. Am J REFERENCES Gastroenterol 2010;105:237–8. 10. Khan MS, Shahbaz N, Zia HA, Hamza M, Iqbal H, Awab A. 1. Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Pancreaticopericardial fistula: a case report and literature Sarr MG, et al. Classification of acute pancreatitis—2012: review. Case Rep Crit Care 2016;2016:7169341. revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102–11. Downloaded from https://academic.oup.com/jscr/article-abstract/2018/5/rjy104/4999375 by Ed 'DeepDyve' Gillespie user on 21 June 2018 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Surgical Case Reports Oxford University Press

Dilated cardiomyopathy secondary to acute pancreatitis caused by hypertriglyceridemia

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Published by Oxford University Press and JSCR Publishing Ltd. All rights reserved. © The Author(s) 2018.
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Abstract

A 30-year-old male presented to an outside facility with acute pancreatitis and triglycerides of 1594. He was transferred to our facility after becoming febrile, hypoxic and in acute renal failure with triglycerides of 4243. CT scan performed showed wall-off pancreatic necrosis. He underwent continuous renal replacement therapy and his acute renal failure resolved. He was treated with broad spectrum antibiotics and discharged. He developed a fever to 101 a week later and was found to have a large infected pancreatic pseudocyst. This was managed with an IR placed drain. This was continued for 6 weeks. He came to the emergency department several weeks later with shortness of breath and 3+ edema to bilateral lower extremities and lower abdomen. TTE performed showed an EF of 15%. He was diuresed 25 L during that stay. His heart failure was med- ically managed. We present this case of dilated cardiomyopathy secondary to acute pancreatitis. reports of dilated biventricular cardiomyopathy associated with INTRODUCTION pancreatitis. It has been reported that pancreatitis can cause Acute pancreatitis (AP) as defined by the revised Atlanta classi- Takotsubo Cardiomyopathy (TCM) [4–10]. TCM is a transient fication, has three levels of severity based largely on organ dys- disease with apical ballooning of the left ventricular wall during function [1]. Mild AP has no organ dysfunction. Moderately systole. The reported incidence is 2% of acute coronary syn- severe AP has organ dysfunction that remains <48 h or local or drome diagnoses [6]. There are a few case reports of pancrea- systemic complications without organ failure >48 h. Finally, titis induced TCM. Those cases resolved with treatment of the severe AP has persistent organ dysfunction >48 h. pancreatitis [4, 5, 7]. According to Carr’s review, hypertriglyceridemia is an uncom- mon cause of AP in 9% of cases. However, AP is seen in 14% of patients with hypertriglyceridemia. Triglyceride levels of <1000 mg/dL CASE REPORT should raise suspicion for other etiologies of AP [2]. Necrotizing pancreatitis occurs in 20% of patients with AP with a mortality A 30-year-old man with a past medical history of hypertrigly- rate of up to 30% [3]. ceridemia presented to an outside ER with nausea, vomiting Following a literature search of PubMed using keywords and abdominal pain. Lab studies were significant for pancrea- pancreatitis and cardiomyopathy, there were no published case titis (lipase 2730), hypertriglyceridemia (1594), blood glucose of Received: February 10, 2018. Accepted: May 1, 2018 Published by Oxford University Press and JSCR Publishing Ltd. All rights reserved. © The Author(s) 2018. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/ licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com Downloaded from https://academic.oup.com/jscr/article-abstract/2018/5/rjy104/4999375 by Ed 'DeepDyve' Gillespie user on 21 June 2018 2 J.W. Greer et al. Figure 1: Walled off pancreatic necrosis of admission CT. Figure 2: Worsening walled off pancreatic necrosis with extension to the para- colic gutters. 389 and BUN/Cr of 17/1.3. A CT of the abdomen showed AP. A found to have 3+ pitting edema up to his mid-abdomen. A chest subsequent lab draw showed BUN/Cr to 27/3.8, decrease in lip- x-ray showed bilateral pleural effusions and cardiomegaly. A TTE ase to 565, increase in triglycerides to 4243, and a BNP 15. He was performed which showed an EF of <15% and a moderate was transferred to our facility following worsening hypoxemia. pericardial effusion without tamponade. He had elevated tropo- A CT scan was performed: representative sections shown below nins, BNP of 2730, and elevated liver enzymes. CTA ruled out pul- demonstrated walled off pancreatic necrosis (Fig. 1). He was in monary embolism and showed a reduction in the left-sided acute renal failure on presentation and started on continuous abdominal abscess with some residual pockets of air. The patient renal replacement therapy. The renal failure resolved, he com- was sent to IR for a drain check and US-guided paracentesis. pleted a 7-day course of imipenem/cilistatin and was eventu- Approximately 2700 ml of ascitic fluid was removed and a persist- ally discharged 11 days after admission. ent moderate-sized abscess pocket with a fistulous tract of bowel A week later, he presented to his PCP for follow up and was was noted. He was diuresed almost 25 l during the hospital stay febrile with increasing abdominal pain. CT of the abdomen and and discharged with medical management of his heart failure. pelvis showed an 11 × 15 cm pancreatic fluid collection. His His drains were removed when drain check no longer demon- hemoglobin was 6.9 and he was transfused 3 units of PRBC. strated a cavity or fistula. After transfer to our facility, a repeat CT showed a small peri- He was followed in Cardiology clinic 2 months later with cardial and left pleural effusions, large volume ascites, a pan- stable NYHF class I–II symptoms. A cardiac MRI was performed creatic fluid collection within the lesser sac between the and showed enlargement of the heart with diffuse generalized anterior pancreas and posterior gastric body measuring 14 × hypokinesia consistent with dilated cardiomyopathy. With an 16.1 × 16.2 cm , and blood in both paracolic gutters and parare- ejection fraction of 22%. No evidence of myocardial infiltration. nal spaces (Fig. 2). He was referred to Interventional Radiology The patient remains in stable condition today. for drain placement. After drainage, he clinically improved and was discharged. His drains were followed in clinic and continued to drain DISCUSSION necrotic material 6 weeks following initial placement. He refused laparoscopic necrosectomy, preferring to continue with Our case is unique, in that, despite resolution of the AP and non-operative management via the IR drains. Follow up MRCP subsequent pancreatic necrosis, the patient’s heart failure per- revealed multiple intrabdominal fluid collections with the pre- sisted. ECGs throughout the acute period of illness were normal vious left-sided collection decompressing into the abdominal except for sinus tachycardia. Imaging revealed no evidence of wall prompting another drainage by IR. myocarditis or inflammation. There were no fistulous tracts At his next appointment, he was having lower extremity ede- visualized with MRCP to the pericardium as has been reported ma and acid reflux. He was treated with leg wraps and a PPI. in prior case reports [10]. Our patient’s echocardiogram is not Approximately 1 week later, the patient presented to the ED for consistent with the normal findings seen in TCM. The multiple shortness of breath and increased swelling. On exam, he was stressors over an extended period of time might contribute to Downloaded from https://academic.oup.com/jscr/article-abstract/2018/5/rjy104/4999375 by Ed 'DeepDyve' Gillespie user on 21 June 2018 Dilated cardiomyopathy secondary to acute pancreatitis 3 the non-transient nature of our patient’s heart failure and 2. Carr RA, Rejowski BJ, Cote GA, Pitt HA, Zyromski NJ. could represent a new subgroup of TCM patients. Systematic review of hypertriglyceridemia-induced acute There is not a role for routine screening given the rarity of pancreatitis: a more virulent etiology? Pancreatology 2016;16: pancreatitis induced heart failure. More studies will need to be 469–76. conducted to develop screening guidelines for patients with 3. On behalf of the Dutch Pancreatitis Study Group MJ. pancreatitis as there might be a subgroup that needs to be rou- Improving the outcome of acute pancreatitis. Digestive tinely screened. Further characterization of our patient’s heart Diseases (Basel, Switzerland) 2016;34:540–5. failure could aid in elucidating a cause, however, he refused 4. Hsu PC, Lin TH, Su HM, Lin ZY, Lai WT, Sheu SH. Acute nec- further studies. With so little published on pancreatitis induced rotizing pancreatitis complicated with ST elevation acute heart failure and ~90% of TCM cases being postmenopausal myocardial infarction: a case report and literature review. women, we would not advocate routine screening for heart fail- Kaohsiung J Med Sci 2010;26:200–5. ure with BNP or baseline echocardiogram [5, 8, 9]. 5. Bruenjes JD, Vallabhajosyula S, Vacek CJ, Fixley JE. Acute pancreatitis-induced Takotsubo cardiomyopathy in an African American Male. ACG Case Rep J 2015;3:53–6. CONCLUSION 6. Scantlebury DC, Prasad A. Diagnosis of Takotsubo cardio- To our knowledge, this represents the first case report of a myopathy. Circ J 2014;78:2129–39. patient with dilated biventricular cardiomyopathy induced by 7. Rajani R, Przedlacka A, Saha M, de Belder A. Pancreatitis pancreatitis. and the broken heart. Eur J Emerg Med 2010;17:27–9. 8. Pilgrim TM, Wyss TR. Takotsubo cardiomyopathy or transi- CONFLICT OF INTEREST STATEMENT ent left ventricular apical ballooning syndrome: a system- atic review. Int J Cardiol 2008;124:283–92. None declared. 9. Cheezum MK, Willis SL, Duffy SP, Moawad FJ, Horwhat JD, Huffer LL, et al. Broken pancreas, broken heart. Am J REFERENCES Gastroenterol 2010;105:237–8. 10. Khan MS, Shahbaz N, Zia HA, Hamza M, Iqbal H, Awab A. 1. Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Pancreaticopericardial fistula: a case report and literature Sarr MG, et al. Classification of acute pancreatitis—2012: review. Case Rep Crit Care 2016;2016:7169341. revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102–11. Downloaded from https://academic.oup.com/jscr/article-abstract/2018/5/rjy104/4999375 by Ed 'DeepDyve' Gillespie user on 21 June 2018

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Journal of Surgical Case ReportsOxford University Press

Published: May 18, 2018

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