RASingh MD FRCPC AGAF Clinical Assistant Professor of Medicine Division of Gastroenterology UBC Disclosures Speaker honorarium from Takeda ID: 915425
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Slide1
Management of Acute and Chronic Pancreatitis
R.A.Singh
MD FRCPC AGAFClinical Assistant Professor of MedicineDivision of Gastroenterology, UBC
Slide2Disclosures
Speaker honorarium from: Takeda
Abbvie Janssen Pentax Clinical Research Funds Celgene
Gilead
Takeda
Janssen
No financial disclosures for this specific talk
Slide3Learning Objectives
Distinguish the pathophysiology, complications and management between acute and chronic pancreatitisDistinguish between the in- patient management between acute and chronic pancreatitis
Slide4Introduction
Acute Pancreatitis (AP) and Chronic Pancreatitis(CP) are two distinct disease statesMost common cause of AP is gallstones and alcohol
Less common cause include hyperlipidemia, hypercalcemia, celiac disease, autoimmune, drugsChronic Pancreatitis is rarely dealt with in hospitalCP is usually caused by alcoholSmoking is an independent risk factor for CP progression
Slide5Pathophysiology
Acute pancreatitis is caused by acute inflammation of the pancreatic parenchymaAcute inflammation can lead to systemic inflammatory response syndrome ( SIRS)
SIRS can lead to respiratory depression, renal failure and hypovolemic shock Sepsis is typically caused by transmural lumenal bacterial migration
Slide6Pathophysiology
Chronic pancreatitis is caused by chronic inflammation and fibrosis This damage can lead to exocrine dysfunction ( diarrhea) or endocrine dysfunction ( diabetes) and cancerPain is common
Acute on chronic pancreatitis is caused by acute parenchymal inflammation on the background of CPThis leads to self limited abdominal pain and short stays in hospitalSerious acute complications are rare
Slide7Case 1
35 year old woman presents with 24 h of epigastric pain, emesisHistory of alcohol abuse ( 1 bottle vodka/d)No meds
T 36.8, P 92, BP 147/92, RR 15 SaO2 95% on Rm airTender in EpigastriumJVP difficult to seeChest clearWBC,19.4,HGB 175,urea 4.9,Cr 80,GLU 8,Ca 2.20,LFTs N, Lipase 620Diagnosis : Acute Alcoholic Pancreatitis
Slide8CT: Normal Pancreas
Slide9Case 1
Slide10Case 1
Initial resuscitation should be aggressive 250-300 cc/hMonitor urine output
CIWA protocolAvoid excessive analgesics/sedationDVT ProphylaxisPractical Nursing Issues: Wide range narcotics dangerous
Monitor urine output (poorly done)
Monitor
Resp
/ O2 saturations
Check for DVT prophylaxis
Slide11Case 1 ( 12 h post admission)
Patient has been on the ward for 2 hUrine output 50cc/hrPain under control. BP/P stable . RR 22/min SaO2 92%
No evidence of withdrawalConcerns?RR is increased , SaO2 decreasedNext stepsNotify MRP, ABG, CXR, increase O2CXR shows bilateral pleural effusions and evidence of pulmonary edemaABG( Room Air) pH 7.32 PO2 60, PCO2 55 BE 6
Slide12Case 1
ICU asked to assessPatient brought to ICU for observation Patient continues to deteriorate in ICU and is intubated within 2 hr of admission to ICU ( 16 h post admission)
Practical Nursing Issues: AP patients can deteriorate quickly, changes in respiratory status can be subtle
Slide13Case 1
Severity of Pancreatitis difficult to assess on admission Number of Scoring Models to assess Severity
Ranson’s Criteria is the most commonly used :Admission Age >55 48h Fall in HCT >10% WBC >16,000 Increase BUN>1.98 GLU > 11 Ca < 2mmol
LDH >350 pO2 <60mmHg
AST >250 BE>4
Fluid
Seq
>6L
Severe Pancreatitis greater or equal to 3
Slide14Case 1
Radiographic Evidence of Necrosis, Significant Peripancreatitic edema/fluid indicate severe pancreatitisAdmission CT may not show necrosis or significant
peripancreatic edema
Slide15Case 1 (72 h Post Admission)
Slide16Case 1
Severe Pancreatitis based on Ranson’s Criteria and CT Enteral feeds should be considered for all patients with severe pancreatitis
Feeding should start by 72h NG feeds likely acceptableSemi elemental feeds
Slide17Case 1: Role for ERCP?
ERCP indicated for biliary pancreatitis with jaundice, dilated biliary tree, ascending cholangitisIf risk for stone is low or moderate, less invasive imaging with MRCP or EUS indicated first
Slide18ERCP (CBD Stones)
Slide19EUS (for CBD stones)
Slide20MRCP
Slide21Case 1
Patient recovers and is dischargedShe represents to hospital 2 months later with LUQ pain, early satiety and intermittent emesis. VSS; afebrileLab work shows a mild increase in lipase, normal WBC
CT shows a large 9 x 6 cm loculated cyst in the lesser sac compressing the stomachDiagnosis : Pseudocyst
Slide22Pancreatic Pseudocyst
Slide23Pancreatic Pseudocyst Drainage
Percutaneous DrainageEndoscopic Drainage ( ERCP v EUS approach)
Surgical
Slide24Percutaneous Drainage
Largely historical interestUsed primarily for acutely infected fluid collections Drainage results poor
Fistula formation
Slide25Surgical Drainage
More morbid than endoscopic drainageIndicated for Complex loculated
pseudocystsIndicated for Cysts not causing bulge in the stomachIndicated for failed drainage procedures
Slide26Pseudocyst Drainage (Surgical)
Slide27Pseudocyst Drainage ( Endoscopic)
ERCP approach. Needle knife cut followed by placement of double pigtail stentsEUS guided
EUS guided and placement of fully covered metal stentEchoendoscope is not the ideal scope for pseudocyst draineage
Slide28Pseudocyst Drainage (Endoscopic)
Slide29Pseudocyst (Endoscopic Drainage)
Slide30Acute Pancreatitis Key Points
First 48 h crucialAggressive fluid resuscitation requiredUrine output should be monitored
Remember DVT prophylaxisBeware of respiratory compromise and sepsisEnteral feeding should be started early in SAPPseudocyst drainage can often be managed endoscopically
Slide31Case 2
43 yo man presents with epigastric pain for weeks. Some nausea. No vomiting.Vitals stable; afebrile
CBC, lytes, BUN/Cr normal. GLU 10.5Lipase 250CT Atrophic Pancreas, Numerous Calcifications in Pancreatic parenchyma. No peripancreatic edema or fluidDx Acute exacerbation of CP
Slide32Chronic Pancreatitis: Imaging
Slide33Chronic Pancreatitis: Management
IV fluids and analgesicsLittle risk of infection, SIRS or respiratory failureSymptoms usually settle in a few days
Push for Alcohol and smoking cessationComplications are typically long term such as pancreatic insufficiency, biliary obstruction and cancerMay be a role for pancreatic enzymes for pain controlMinimal role for EUS guided celiac plexus blockade
Slide34Chronic Pancreatitis: Risk of Cancer
Well documented increased riskNo surveillance guidelinesTumour is often difficult to distinguish from focal chronic pancreatitis
Slide35Chronic Pancreatitis: Key Points
Hospitalized patients follow a benign courseManagement is largely supportivePriority is to eliminate triggers ( e.g. alcohol and smoking)
Pancreatic enzymes can be used to treat pain or steatorrhea