ESPEN Congress Brussels 2005 Therapeutic endoscopy of pancreatic diseases. How endoscopy may improve nutrition? Myriam Delhaye
Therapeutic endoscopy of pancreatic diseases. How endoscopy may improve nutrition? Myriam Delhaye Medico-surgical Department of Gastroenterology Erasme Hospital Brussels - Belgium 27th ESPEN Congress, Brussels, Belgium 27-30 August 2005
Acute pancreatitis Definition Acute inflammatory process of the pancreas may involve Peripancreatic tissues Remote organ systems Symposium of Atlanta 1992 Bradley, Arch Surg 1993; 128: 586
Acute pancreatitis Mortality Mild in 80% of cases < 1% Severe in 20% of cases Sterile necrosis 10% Infected necrosis 25% Atlanta criteria Organ failure Local complications Ranson's score 3 Apache II score 8 CRP 15 mg/dl CTSI 7
Severe Acute pancreatitis Prophylactic antibiotics Nutritional support Endoscopic therapy
Severe Acute pancreatitis Nutritional support: TEN vs TPN Infection p = 0.004 0,45 RR Complications other than infection 0.61 NS Surgical interventions p = 0.05 0,48 Mortality NS 0,66 1 Length of stay 2.9 d (1.6 4.3) p < 0.01 Meta analysis of 6 RCT (n = 263 patients) Marik, BMJ 2004; 328: 1407
Severe Acute pancreatitis Nutritional support TEN Nasogastric tube No radiological assistance endoscopic No change in - mortality - total hospital stay - days in ICU Nasojejunal tube Endoscopic placement Risk of dislocation No adverse effect - on acute phase response - on pain, analgesics Eatock, Am J GE 2005; 100: 432
Acute pancreatitis Indications for endoscopic treatment Biliary AP: EBS + extraction of CBD stones Fluid collections: drainage procedures
Predicted mild Biliary AP Predicted severe Cholangitis Jaundice Improving No cholangitis No jaundice No CBD stone Cholecystectomy + IOC Unfit for cholecystectomy Biliary symptoms or already suggesting CBD stones cholecystectomised No improvement after 48 h Elective EBS Early EBS morbidity mortality If CBD stones present at IOC EBS
Acute pancreatitis Fluid collections: drainage procedures Necrosis (> 30%) Clinical deterioration organ failure persistent symptoms > 7d clinical suspicion sepsis CT-guided percutaneous FNA of pancreatic necrosis Sterile Infected Supportive care Adapt antibiotherapy MRI/S-MRCP
Acute pancreatitis Fluid collections: drainage procedures MRI/S-MRCP Partial MPD rupture Organized liquefied necrosis Transpapillary stent bridging the rupture NO YES Surgical necrosectomy Endoscopic transmural > 2 4 W after onset drainage Technical/Clinical success 72% Telford, GE 2002; 56: 18 Baron, GE 1996; 111: 755 Baron, GE 2002; 56: 7
67 y.o. man with biliary AP ERCP + ES + removal of a CBD stone within 24h of symptom onset T 2 MRI at admission T 2 MRI 6 w after onset CE-CT 6 w after onset C D E F Transmural drainage of the infected pancreatic collection
Chronic pancreatitis Definition Relapsing or continuing inflammatory disease of the pancreas irreversible morphologic changes pain ± loss of exocrine/ endocrine function International Workshop on Pancreatitis, Cambridge 1983
Causes of malnutrition in patients with CP calorie intake due to pain after meals Pancreatic exocrine insufficiency fat malabsorption late in the course of CP < large functional reserve synthesis/secretion of lipase [H CO3] secretion low intraduodenal ph lipase activity extrapancreatic lipolysis marginal Pancreatic endocrine insufficiency Coexistent alcoholism, liver disease
Nutritional management in CP Appropriate management of pain analgesics 30 min before meals endoscopic therapy
Severe chronic pancreatitis Parenchyma decreased compliance Ducts obstruction stones 18% strictures 47% both 32% Tissue hypertension Ischemia pain oxydative stress mediators of inflammation fibrosis Pancreatic fibrogenesis NO CURATIVE TREATMENT AVAILABLE
Selection of patients with severe CP for endoscopic therapy Obstruction of the MPD by stones/strictures/both Fluid collections < downstream ductal obstruction < disruption of the MPD Obstruction of the CBD < fibrotic changes in the pancreas < compression by a pancreatic pseudocyst
Pain and MPD obstruction Endotherapy = 1st choice of treatment
ESWL (40% of cases) 3000-5000 Shock waves mj/mm 2 0.28 = 3 0.33 = 4 0.37 = 5 0.42 = 6 0.47 = 7 0.54 = 8 4-8 < 5 if ERCP follows Chronic pancreatitis Pain and MPD obstruction 1st step of endotherapy = fragmentation of obstructive pancreatic ductal stones Bidimensional X ray focusing system
ESWL 3000-5000 Shock waves mj/mm 2 0.28 = 3 0.33 = 4 0.37 = 5 0.42 = 6 0.47 = 7 0.54 = 8 4-8 < 5 if ERCP follows Chronic pancreatitis Pain and MPD obstruction 1st step of endotherapy = fragmentation of obstructive pancreatic ductal stones
After ESWL Chronic pancreatitis Pain and MPD obstruction 2nd step of endotherapy: EPS, stone extraction, NPC EPS Stone extraction NPC
Cannulatome Torque device Position 1 Position 2
10F Teflon Bougie Maxforce Balloon 6mm x 4cm Soehendra stent retriever
Pancreatic stenting for severe CP
Chronic pancreatitis Pain and MPD obstruction 3rd step of endotherapy: pancreatic stenting (50-60% of patients with CP)
Technical results of MPD drainage Initial technical success (86%): decrease in MPD ± complete clearance ESWL = the only independent predictive factor for technical success Dumonceau, GIE 1996; 43: 547
Pain and MPD obstruction in CP Clinical results of endoscopic therapy Short-term FU < 2 y Clinical success 82-94% Predictive factors Technical success of ductal drainage ( MPD ) Medium-term FU 2-5 y 48-84% Short duration of disease Low frequency of pain Absence of MPD stricture Long-term FU 14 y 66% Short duration of disease No current smoking ESWL + endotherapy as early as possible in the course of CP
Which test for malabsorption screening in CP? Correlation between the acid steatocrit and the TBT 60 patients with CP (10 mild, 50 severe) Acid steatocrit (AS) = fatty layer / (fatty layer + solid layer) x 100 fatty layer water layer Acid Triolein Mean values steatocrit Breath for AS Test compared to TBT results ingestion 24h stools, of (n=60 a normal standard CP) diet lipid-rich (80-100 test g fat/d) meal 80 homogenization (30 g) containing 5 µci of 14 p<0.0001 C glycerol 70 sample trioleatecentrifugation in acid environment 60 % lipid 14 CO phase 2 exhaled on dry compared feces in volumetric to the total % 50 Normal TBT (n=17) N: CO< 2 10% of the sample 40 N: > 3% Acid Steatocrit value (%) 30 20 10 0 Pathological TBT (n=43) solid layer AS = 60% AS = 12% AS = 7% Dumasy et al, Am J GE 2004; 99: 1350
Evolution of exocrine dysfunction 100 Proportion of patients (%) 90 80 70 60 50 40 30 20 10 0 1 to 5 (n=27) 6 to 10 (n=15) >10 (n=18) Abnormal steatocrit Clinical steatorrhea Present when AS 30% Sens 38% Spec 100% Duration of CP (years) Pancreatic exocrine insufficiency underestimated in patients with CP when its assessment is based on the presence of clinical steatorrhea Dumasy et al, Am J GE 2004: 99: 1350
2,5 Impact of malabsorption on BMI Loss of BMI per year (kg/m2/y) 2 1,5 1 0,5 0 NS p<0.03 No malabsorption (n=13) Treated malabsorption (n=19) Untreated malabsorption (n=28) (24 without clinical steatorrhea) Ammann, GE, 1999; 116: 1132 p<0.03 Undetected Untreated malabsorption harmful effect on weight loss Dumasy et al, Am J GE 2004; 99: 1350
Impact of endotherapy on the pancreatic Test exocrine function in patients with CP Patients Literature data Improved (%) Worsened (%) No change (%) TBT 22 55 32 14 11 Steatorrhea 12 50 42 8 11 FU (m) Delhaye, GE 1992 PABA test 18 61 - - 32 Ohara, AJGE 1996 Steatorrhea 19 47 11 42 40 Adamek, Gut 1999 Steatorrhea 13 77 - - 7 Brand, AJGE 2000 Diarrhea 377 51 17-59 Rösch, Endoscopy 2002
Exocrine pancreatic function after endotherapy endotherapy in CP postponed the functional exocrine impairment for about 10 years
Predictive factors for exocrine insufficiency Developing steatorrhea Yes n = 18 No n = 22 Alcoholic etiology 89% 55% p=0.018 Recurrent symptomatic ductal obstruction further ESWL 72% 36% p=0.025 N hospit. for pain/y 0.24 0.11 p=0.024 Duration of endotherapy (m) 47 13 p=0.021 exocrine pancreatic function dependent on early relief of ductal obstruction
Impact of endotherapy on the pancreatic endocrine function in patients with CP Literature data Patients Improved (%) Worsened (%) No change (%) FU (m) 41 10 13 77 14 Delhaye, GE 1992 12 17-83 31 Ohara, AJGE 1996 234 8 21 71 59 Rösch, Endoscopy 2002
Risk factors for diabetes mellitus in CP n: 453 patients; surgery: n=231; FU: 7 ± 6.8 y RR 3,2 2,4 1,7 1 Alcoholic cause of CP Pancreatic calcifications Distal pancreatectomy 0,8 Pancreatic drainage p=0.04 p<0.001 p<0.0001 NS Malka, GE 2000; 119: 1324
Endocrine pancreatic function after endotherapy endotherapy in CP did not prevent the appearance of DM
Predictive factors for endocrine insufficiency Developing diabetes Yes n = 25 No n = 15 Alcoholic etiology* 84% 40% p=0.007 Age at onset (y) 42 32 p=0.016 Age at study entry (y) 47 35 p=0.002 Amount of tobacco (pack-years) 47 20 p<0.001 *Significant by multivariate analysis endocrine pancreatic function dependent on alcohol consumption habits role in development of fibrosis
Conclusions Severe acute pancreatitis Nutritional support TEN > TPN Nasogastric feeding Ξ Nasojejunal feeding Early ERCP + EBS in severe biliary AP Endoscopic transmural drainage for organized liquefied necrosis 4 W after onset symptomatic infected Transpapillary bridging stent for partial MPD rupture
Conclusions Severe chronic pancreatitis Pain & ductal obstruction ENDOTHERAPY = first choice long-term benefit for about 2/3 of patients hospit. rate overtime delaying functional exocrine impairment good clinical outcome associated with cessation or absence of smoking alcohol abuse risks of diabetes mellitus steatorrhea
Acknowledgements Department of Gastroenterology M. Arvanitakis M. Baize Pr. M. Cremer Pr. J. Devière O. Le Moine A. Vandermeeren Department of Radiology C. Matos D. Van Gansbeke M. Zalcman A. Van Gossum G. Verset Scientific Secretary Department of Digestive Surgery J. Closset Pr. M. Gelin C. Piesen