Disclosure - eiseverywhere.com file3 Pathophysiology •Enzymes –Generally stored in an inactive...

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Caring for the Patient with Acute Pancreatitis Bruce D. Askey, MS, ANP-BC

Associate Lecturer

Fitzgerald Health Education Associates, Inc.

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.

© Fitzgerald Health Education Associates, Inc.

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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.


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American College of Gastroenterology

• The information for this presentation was taken from the guidelines set forth by the American College of Gastroenterology.1

– www.amjgastro.com – 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: 10.1038/ajg.2013.218


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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%


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Definition

• Autodigestion of pancreatic and peripancreatic tissues by naturally occurring pancreatic digestive enzymes

– Trypsin: Digests proteins

– Amylase: Digests carbohydrates

– Lipase: Digests fats


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http://www.amjgastro.com/

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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.


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Local Effect of Enzymes


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Pathophysiology

• Risk factors have been identified, but exact pathophysiologic mechanism not fully understood


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Symptoms

• Epigastric pain

– Bandlike pattern that often bores straight through to the back

– “Chemical burn”

• Nausea, vomiting, anorexia

• Fever, diaphoresis, dehydration


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Physical Exam

• Looks mildly uncomfortable to toxic

• Epigastric pain with palpation

• Abdominal distension, possibly hypoactive bowel sounds

• Dehydration, orthostatic

– Tachycardia

– Hypotension

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Associates, Inc. 11

Physical Exam (continued)

• Grey-Turner’s sign: Flank ecchymosis=High mortality


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Physical Exam

• Cullen’s sign: Periumbilical ecchymosis=High mortality


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Diagnostics

• Increased pancreatic enzymes

– Degree of elevation parallels degree of inflammation

– Lipase: More specific than amylase

– Amylase

• WBC often elevated


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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


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Causes of Increased Serum Amylase (continued)

• Salivary glands

– Mumps

– Effects of ETOH

– Scorpion sting

• Renal insufficiency

– Macroamylasemia

• Miscellaneous

– Anorexia nervosa

– Head trauma w/intracranial bleed

– DM ketoacidosis

– HIV


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Diagnostics

• Elevated BUN/creatinine suggests dehydration

• Decreased calcium often an ominous sign

• Elevated liver enzymes often indicates gallstone pancreatitis


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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.


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Diagnostics: Imaging (continued)

• 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


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Diagnostics: Imaging (continued)

• 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


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Differential Diagnosis

• Choledocholithiasis

• Perforated ulcer

• Mesenteric ischemia

• Intestinal obstruction

• Salpingitis

• Ectopic pregnancy


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Predisposing Conditions

• Gallstones

• Alcohol

• Hyperlipidemia

• Hereditary

• Hyperparathyroidism/ hypercalcemia

• ERCP

• Postoperative

• Pancreatic trauma

• Cystic fibrosis

• Pregnancy

• Vascular diseases

• Infectious agents


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Predisposing Conditions (continued)

• Structural abnormalities

–Ampullary

–Biliary

– Sphincter of Oddi

–Main PD

–Accessory PD

• Medications


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Gallstones

• Responsible for 35−70% of all cases

• Treatment with cholecystectomy, sphincterotomy

• Shown to decrease recurrence of pancreatitis


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Impacted Gallstones

Endoscopic Retrograde Cholangiopancreaography (ERCP)

• Useful in gallstone pancreatitis when CBD stone impaction is suspected

• With +US, should be performed prior to discharge


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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


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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 500−1000 mg/dL (5.65−11.3 mmol/L) to cause

28 © Fitzgerald Health Education

Associates, Inc.

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


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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.


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Pancreatic Trauma

• Penetrating or blunt injury

• Compression by the spine

• Can require ERCP to rule out transection


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Danger Signs‒ 1st 24 Hours

• Encephalopathy

• Hypoxemia

• Tachycardia >130/min

• Hypotension <90 mm Hg

• Hct>50% – 0.5 proportion

• Oliguria

• Azotemia

32 © Fitzgerald Health Education

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Ranson’s Criteria

• On admission

– Age >55 years

– WBC>16,000/mm3

– Glucose>200 mg/dL (11.1 mmol/L)

– LDH>350 international unit/L

– AST>250 unit/L


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Ranson’s Criteria (continued)

• During 1st 48 hours

–Hct decrease>10% (0.1 proportion)

–BUN increase>5 mg/dL (1.8 mmol/L)

–Calcium<8 mg/dL (2 mmol/L)

–PaO2<60 mm Hg

–Base deficit>4 mEq/L

– Fluid sequestration>6L


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• <3 signs=Excellent prognosis

• 3−5 signs=10−20% mortality

• ≥6 signs ≥50% mortality

• General rule – ≥3 signs=Severe pancreatitis


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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)


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Complications

• Hypovolemia

• Adult Respiratory Distress Syndrome (ARDS)

• Disseminated Intravascular Coagulation (DIC)

• Infection/pancreatic necrosis


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Complications (continued)

• Hypovolemia

– 250−500 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


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• 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


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• Adult respiratory distress syndrome (ARDS)

– Occurs between days 2−7 of acute pancreatitis

– Monitor respiratory rate and status

– Monitor oxygen saturations


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• 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


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• Infection/pancreatic necrosis

– Monitor temperature

– CT

– Aspiration with C/S and appropriate antibiotics


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Supportive Care

• Essential – Close clinical surveillance

– NPO

– IV fluid replacement

– Nutritional support

– Relief of pain


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Supportive Care (continued)

• No proven benefit – Antibiotics (unless infection is identified)

– Reduction of pancreatic secretion • H-2 blocker, NG suction, glucagon, anticholinergic,

somatostatin


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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.


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Case Study (continued)

• 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.”


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Case Study (continued)

• 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?


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Case Study: Additional Information • White blood cell count=14,500 mm3

– N: 4.5‒11.1,000 mm3

• Blood glucose=350 mg/dL (19.4 mmol/L)

– N: 80‒100 mg/dL (4.4‒5.6 mmol/L)

• LDH=290 international units/L

– N: 140‒280 international units/L

• AST=410 units/L

– N: 8‒48 units/L

© Fitzgerald Health Education Associates,

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What is his Ranson’s score? Based on his Ranson’s score, what is

his prognosis?


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Ranson’s Criteria

• On admission

– Age>55 years

– WBC>16,000/mm3

– Glucose>200 mg/dL (11.1 mmol/L)

– LDH>350 international units/L

– AST>250 units/L


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• During 1st 48 hours –Hct decrease>10% (0.1 proportion)

–BUN increase>5 mg/dL (1.8 mmol/L)

–Calcium<8 mg/dL (2 mmol/L)

–PaO2<60 mm Hg

–Base deficit>4 mEq/L

– Fluid sequestration>6 L


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• <3 signs=Excellent prognosis

• 3−5 signs=10−20% mortality

• ≥6 signs ≥50% mortality

• General rule

– ≥3 signs=Severe pancreatitis


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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?


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Questions?


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Thank you for your time and attention.

Bruce D. Askey, MS, ANP-BC

www.fhea.com [email protected]

End of Presentation

• 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.


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Copyright Notice

Copyright by Fitzgerald Health Education Associates, Inc. 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 Associates, Inc.

Requests for permission to make copies of any part of the work should be mailed to:


85 Flagship Drive

North Andover, MA 01845-6184


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http://www.fhea.com/

mailto:[email protected]

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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 Associates, Inc. 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.


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85 Flagship Drive

North Andover, MA 01845-6154 978.794.8366 Fax-978.794.2455

Website: fhea.com

Learning & Testing Center: fhea.com/npexpert

www.facebook.com/fitzgeraldhealth

@npcert


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