Caring for the Patient with Acute Pancreatitis. Disclosure. Objectives
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1 Caring for the Patient with Acute Pancreatitis Bruce D. Askey, MS, ANP-BC Associate Lecturer Fitzgerald Health Education North Andover, MA Adult Nurse Practitioner Dept. of Hepatology/Gastroenterology Guthrie Clinic Sayre, PA/Ithaca, NY Disclosure No real or potential conflict of interest to disclose No off-label, experimental or investigational use of drugs or devices will be presented. 2 Objectives Upon completion of the learning activity the participant will be able to: Describe the pathophysiology of acute pancreatitis. Discuss the potential complications of acute pancreatitis. Discuss the management of acute pancreatitis. 3 1
2 American College of Gastroenterology The information for this presentation was taken from the guidelines set forth by the American College of Gastroenterology. 1 Source: 1. Tenner, et al. American college of gastroenterology guideline: Management of acute pancreatitis. The American Journal of Gastroenterology advance online publication, 30 July 2013; doi: /ajg Acute Pancreatitis by the Numbers >200,000 annual hospitalizations >$2.5 billion annual cost 75 85% will have a mild clinical course which resolves in 5 7 days Mild attack Only 1% mortality Severe attack Results in mortality rate approaching 20% 5 Definition Autodigestion of pancreatic and peripancreatic tissues by naturally occurring pancreatic digestive enzymes Trypsin: Digests proteins Amylase: Digests carbohydrates Lipase: Digests fats 6 2
3 Pathophysiology Enzymes Generally stored in an inactive form within the pancreas Activated in the small intestine Pancreatitis occurs when the enzymes are activated within the pancreas itself. 7 Local Effect of Enzymes 8 Risk factors have been identified, but exact pathophysiologic mechanism not fully understood Pathophysiology 9 3
4 Symptoms Epigastric pain Bandlike pattern that often bores straight through to the back Chemical burn Nausea, vomiting, anorexia Fever, diaphoresis, dehydration 10 Physical Exam Looks mildly uncomfortable to toxic Epigastric pain with palpation Abdominal distension, possibly hypoactive bowel sounds Dehydration, orthostatic Tachycardia Hypotension 11 Grey-Turner s sign: Flank ecchymosis=high mortality Physical Exam 12 4
5 Physical Exam Cullen s sign: Periumbilical ecchymosis=high mortality 13 Diagnostics Increased pancreatic enzymes Degree of elevation parallels degree of inflammation Lipase: More specific than amylase Amylase WBC often elevated 14 Causes of Increased Serum Amylase Pancreatic Pancreatitis, CA Intra-abdominal Acute cholecystitis CBD obstruction Perforated hollow viscus Ischemia, infarction Acute appendicitis Salpingitis Ruptured ectopic pregnancy Tumors Ovarian cysts Papillary cystadenoma of ovary Lung carcinoma Miscellaneous Morphine Endoscopy Sphincter of Oddi spasm 15 5
6 Causes of Increased Serum Amylase Salivary glands Mumps Effects of ETOH Scorpion sting Renal insufficiency Macroamylasemia Miscellaneous Anorexia nervosa Head trauma w/intracranial bleed DM ketoacidosis HIV 16 Diagnostics Elevated BUN/creatinine suggests dehydration Decreased calcium often an ominous sign Elevated liver enzymes often indicates gallstone pancreatitis 17 Diagnostics: Imaging Ultrasound Noninvasive/inexpensive No dye allergy or renal concerns No radiation Can often be done at the bedside Excellent for seeing gallstones The pancreas is often poorly seen. 18 6
7 Diagnostics: Imaging CT scan Excellent modality to view the pancreas Can see pancreatic tumors that may not be seen with ultrasound Can use specific pancreatic protocol Dye allergy and renal failure limits its use 19 Diagnostics: Imaging MRI Excellent modality to view the pancreas Can see pancreatic tumors that may not be seen with ultrasound Can use specific pancreatic protocol The presence of a pacemaker limits its use 20 Differential Diagnosis Choledocholithiasis Perforated ulcer Mesenteric ischemia Intestinal obstruction Salpingitis Ectopic pregnancy 21 7
8 Predisposing Conditions Gallstones Alcohol Hyperlipidemia Hereditary Hyperparathyroidism/ hypercalcemia ERCP Postoperative Pancreatic trauma Cystic fibrosis Pregnancy Vascular diseases Infectious agents 22 Predisposing Conditions Structural abnormalities Ampullary Biliary Sphincter of Oddi Main PD Accessory PD Medications 23 Gallstones Responsible for 35 70% of all cases Treatment with cholecystectomy, sphincterotomy Shown to decrease recurrence of pancreatitis 24 8
9 Impacted Gallstones Endoscopic Retrograde Cholangiopancreaography (ERCP) Useful in gallstone pancreatitis when CBD stone impaction is suspected With +US, should be performed prior to discharge 26 Alcohol Responsible for 30% of pancreatitis Pathogenesis remains unclear. Toxic metabolite hypothesis Direct toxicity to acinar cells Reflux of duodenal contents by sphincter of Oddi relaxation Eventual necrosis, fibrosis and chronic pancreatitis 27 9
10 Hypertriglyceridemia Most with hx of DM or hypertriglyceridemia Some cases are induced by drugs (e.g., estrogens). Most cases are in excess of 1000 mg/dl (11.3 mmol/l). Possible for mg/dl ( mmol/l) to cause 28 Medications Azathioprine Sulfonamides Bactrim Oral 5-ASA Antibiotics Metronidazole Tetracycline Nitrofurantoin Valproic acid Corticosteroids Furosemide Estrogens Methyldopa Aldomet Pentamidine Didanosine Octreotide DPP-4 inhibitor GLP-agonist Others 29 ERCP-induced Risk is ~5%. Octreotide, nifedipine, steroids, non-ionic dyes do not decrease incidence. Increased with multiple attempts at cannulation Sphincterotomy does not increase risk further
11 Penetrating or blunt injury Compression by the spine Can require ERCP to rule out transection Pancreatic Trauma 31 Danger Signs 1 st 24 Hours Encephalopathy Hypoxemia Tachycardia >130/min Hypotension <90 mm Hg Hct>50% 0.5 proportion Oliguria Azotemia 32 On admission Age >55 years WBC>16,000/mm 3 Glucose>200 mg/dl (11.1 mmol/l) LDH>350 international unit/l AST>250 unit/l Ranson s Criteria 33 11
12 During 1 st 48 hours Ranson s Criteria Hct decrease>10% (0.1 proportion) BUN increase>5 mg/dl (1.8 mmol/l) Calcium<8 mg/dl (2 mmol/l) PaO 2 <60 mm Hg Base deficit>4 meq/l Fluid sequestration>6l 34 Ranson s Criteria <3 signs=excellent prognosis 3 5 signs=10 20% mortality 6 signs 50% mortality General rule 3 signs=severe pancreatitis 35 Atlanta Criteria 2013 Mild acute pancreatitis Absence of organ failure Absence of local complications Moderately severe acute pancreatitis Local complications and/or Transient organ failure (<48 hours) Severe acute pancreatitis Persistent organ failure (>48 hours) 36 12
13 Complications Hypovolemia Adult Respiratory Distress Syndrome (ARDS) Disseminated Intravascular Coagulation (DIC) Infection/pancreatic necrosis 37 Complications Hypovolemia ml/hour of crystalloid Can require more fluid based on clinical status Lactated Ringer s solution can be more effective than normal saline Goal: Decrease the BUN Reassess within 6 hours of admission 38 Complications Hypovolemia (cont.) Assess breath sounds for rales Monitor electrolytes Monitor heart rate and blood pressure Monitor central venous pressure, cardiac output and pulmonary artery pressures if central line is in place Assess for heart failure 39 13
14 Complications Adult respiratory distress syndrome (ARDS) Occurs between days 2 7 of acute pancreatitis Monitor respiratory rate and status Monitor oxygen saturations 40 Complications Disseminated intravascular coagulation (DIC) Trypsin activates prothrombin resulting in coagulation and depletion of clotting factors Assess for signs of bleeding Monitor complete blood count (CBC) Monitor PT/INR/PTT 41 Complications Infection/pancreatic necrosis Monitor temperature CT Aspiration with C/S and appropriate antibiotics 42 14
15 Supportive Care Essential Close clinical surveillance NPO IV fluid replacement Nutritional support Relief of pain 43 Supportive Care No proven benefit Antibiotics (unless infection is identified) Reduction of pancreatic secretion H-2 blocker, NG suction, glucagon, anticholinergic, somatostatin 44 Case Study GK is a 47-year-old male with no past medical history who presents to the emergency room complaining of a 10-h history of severe continuous epigastric pain, which bores through to his back. He reports associated nausea and vomiting
16 Case Study He routinely drinks 20 cans of beer daily and has done so for the past 25 years. 1 drink=12 oz (0.35 L) of beer, 5 oz (0.15 L) of wine, 1.5 oz (0.04 L) of 80-proof liquor He is on no medications and has no allergies but admits that he has never had a physical and goes to the ER when he needs something from the doctors. 46 Case Study His blood pressure is 94/52 mm Hg and his heart rate is regular at 128 beats per minute. In light of the fact that this presentation is about acute pancreatitis, you suspect that he has the condition. What tests will confirm acute pancreatitis? What is the likely etiology in this case? 47 Case Study: Additional Information White blood cell count=14,500 mm 3 N: ,000 mm 3 Blood glucose=350 mg/dl (19.4 mmol/l) N: mg/dl ( mmol/l) LDH=290 international units/l N: international units/l AST=410 units/l N: 8 48 units/l Associates, Inc
17 What is his Ranson s score? Based on his Ranson s score, what is his prognosis? 49 On admission Age>55 years WBC>16,000/mm 3 Glucose>200 mg/dl (11.1 mmol/l) LDH>350 international units/l AST>250 units/l Ranson s Criteria 50 Ranson s Criteria During 1 st 48 hours Hct decrease>10% (0.1 proportion) BUN increase>5 mg/dl (1.8 mmol/l) Calcium<8 mg/dl (2 mmol/l) PaO 2 <60 mm Hg Base deficit>4 meq/l Fluid sequestration>6 L 51 17
18 Ranson s Criteria <3 signs=excellent prognosis 3 5 signs=10 20% mortality 6 signs 50% mortality General rule 3 signs=severe pancreatitis 52 Case Study How should this patient be managed? What lab parameters should be monitored? What clinical parameters should be assessed? What do you get when you cross an elephant with a rhino? 53 Questions? 54 18
19 End of Presentation Thank you for your time and attention. Bruce D. Askey, MS, ANP-BC 55 Images/Illustrations: Unless otherwise noted, all images/ illustrations are from open sources, such as the CDC or Wikipedia or property of FHEA or author. All websites listed active at the time of publication. 56 Copyright Notice Copyright by Fitzgerald Health Education All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording or any information storage and retrieval system, without permission from Fitzgerald Health Education Requests for permission to make copies of any part of the work should be mailed to: Fitzgerald Health Education 85 Flagship Drive North Andover, MA
20 Statement of Liability The information in this program has been thoroughly researched and checked for accuracy. However, clinical practice and techniques are a dynamic process and new information becomes available daily. Prudent practice dictates that the clinician consult further sources prior to applying information obtained from this program, whether in printed, visual or verbal form. Fitzgerald Health Education disclaims any liability, loss, injury or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents of this presentation. 58 Fitzgerald Health Education 85 Flagship Drive North Andover, MA Fax Website: fhea.com Learning & Testing Center: fhea.com/npexpert 59 20
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