Acute - PowerPoint PPT Presentation

Loading...

PPT – Acute PowerPoint presentation | free to download - id: 4026de-NzM2Y



Loading


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation
Title:

Acute

Description:

Acute & Chronic Pancreatitis 11/01/2005 Chp. 87 Tintinalli Bogdan Irimies D.O. Acute Pancreatitis: Epidemiology Clinical presentation can vary from mild abdominal ... – PowerPoint PPT presentation

Number of Views:52
Avg rating:3.0/5.0
Slides: 39
Provided by: BogdanI8
Learn more at: http://cchseast.org
Category:

less

Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: Acute


1
Acute Chronic Pancreatitis
  • 11/01/2005
  • Chp. 87 Tintinalli
  • Bogdan Irimies D.O.

2
Acute Pancreatitis Epidemiology
  • Clinical presentation can vary from mild
    abdominal pain to refractory shock
  • 90 of acute pancreatitis is secondary to acute
    cholelithiasis or ETOH abuse
  • List if causes is extensive Cholelithiasis,
    ETOH, drugs, infection, inflammation, trauma,
    metabolic disturbances

3
Drug Induced Pancreatitis
  • Drugs assoc. w/pancreatitis
  • Amiodarone, amlodipine
  • Antibiotics(macrolides,sulfa, FQs, rifampin)
  • Antiepileptics (carbamazepine, valproic acid,
    topiramate)
  • Hyperlipidemic drugs
  • Antineoplastic agents
  • Antipsychotics (risperdal)

4
Drug Induced Pancreatitis
  • Drugs contd
  • Antiretrovirals all types
  • Diuretics
  • GI agents H2 blockers, PPIs
  • Glucocorticoids
  • NSAIDS
  • ASA

5
Pathophysiology
  • Central cause appears to be activation of the
    digestive zymogens in the pancreatic acinar cells
    and subsequent autodigestion of the pancreas.
  • Number of factors(endotoxins, toxins, ischemia,
    infections, anoxia) trigger activation of
    proenzymes

6
Pathophysiology
  • Activated proteolytic enzymes such as trypsin
    digest cellular membranes within pancreas and
    cause edema, interstitial hemorrhage, vascular
    damage, coagulation and cellular necrosis.
  • This can lead to extension of localized process
    into generalized systemic inflammatory response
  • Can lead to shock, ARDS, Multi-organ system
    failure

7
Clinical Features
  • Major symptom is midepigastric or left upper
    quadrant pain described as constant, boring pain
    that radiates to back, flanks, chest or lower
    abdomen.
  • Nausea/vomiting or abdominal bloating
  • PE low grade fevers, tachycardia, /-
    hypotension

8
Clinical Features
  • Respiratory symptoms atelectasis, pleural
    effusion, ARDS
  • Abdominal exam epigastric tenderness,
    peritonitis, Cullen sign(bluish discoloration
    around umbilicus), Grey Turner sign (bluish
    discoloration of flanks)
  • Pts. May present in hypovolemic shock and MOSF
  • Hypotension secondary to 3rd spacing, hemorrhage,
    increased vascular permeability, vasodilation,
    cardiac depression, vomiting

9
Diagnosis
  • Amylase found in pancreas salivary glands
  • Low levels found in many tissues so this test is
    nonspecific
  • Amylase may be even normal in acute pancreatitis
  • Poor specificity

10
Diagnosis
  • Lipase found predominantly in pancreas but also
    in gastric, intestinal mucosa and liver
  • Cleared by the kidney so renal failure will
    elevate levels
  • Most appropriate cut-off is 2-3 x normal level
  • More accurate test than amylase, better
    specificity (90 vs. 75)

11
Diagnosis
  • Xrays of chest/abdomen useful for r/o other
    diagnosis.
  • Calcification of pancreas seen in chronic
    pancreatitis
  • May see sentinel loop, elevated hemi-diaphragm,
    pleural effusion
  • U/S may detect gallstones
  • CT best study for grading severity if disease,
    prognosis.

12
Diagnosis
  • Prognostic markers Ranson criteria predicts pt.
    outcome
  • Age gt55
  • BS gt200
  • WBC gt16,000
  • AST gt250
  • LDH gt700
  • Features portend a worse prognosis, but they have
    poor predictive value in acute setting and does
    not improve clinical judgment

13
Diagnosis
  • CT of abdomen
  • Estimates severity and prognosis
  • Complications include phlegmons, abscesses or
    pseudocysts.
  • Usually seen 2-3 weeks after acute pancreatitis

14
Complications of Acute Pancreatitis
  • Pulmonary pleural effusions, atelectasis,
    hypoxemia, ARDS
  • CV myocardial depression, hemorrhage,
    hypovolemia
  • Metabolic Hypocalcemia, hyperglycemia,
    Hyperlipidemia, coagulopathy/DIC
  • Others Colonic perforation, ARF. Arthritis,
    pseudocyst, abscess

15
Treatment
  • General principle rest the pancreas
  • Fluid resuscitation
  • NG tube only if needed
  • Pain control, anti-emetics
  • ATBX only in severe disease
  • Cover polymicrobial, GNB
  • IV imipenem or quinolone in combination w/Flagyl

16
Disposition
  • Pts. w/mild pancreatitis w/no evidence of
    systemic disease and low likelihood of biliary
    disease may be managed as outpts. if tolerating
    oral fluids and pain control is adequate
  • All others need to be admitted

17
Chronic Pancreatitis
  • Defined as chronic inflammatory condition that
    causes irreversible damage to pancreatic
    structure and function
  • Causes ETOH abuse, malnutrition, hyperPTH,
    pancreas divisum, ampullary stenosis, cystic
    fibrosis, hereditary, trauma, idiopathic

18
Chronic Pancreatitis
  • Chronic pancreatitis results in interstitial
    inflammation w/duct obstruction and dilation
    leading to parenchymal loss and fibrosis.
  • Loss of both exocrine and endocrine
  • Clinicically significant malabsorption occurs
    when 90 of pancreas is lost.

19
Chronic Pancreatitis
  • Presents as midepigastric abdominal pain, nausea,
    vomiting
  • Pts. May appear chronically ill, w/sign of
    pancreatic insufficiency such as weight loss,
    steatorrhea, clubbing, polyuria
  • Differentiating acute vs chronic pancreatitis is
    difficult b/c primary distinction is based on
    disease reversibility

20
Chronic Pancreatitis
  • Amylase and lipase may be normal if pancreas is
    fibrotic
  • CT scan may help ID pseudocyst or abscess
  • Tx IVFs anti-emetics, narcotics
  • Pancreatic extracts to improve absorption and
    pain
  • If pain is increasing or intractable, image
    pancreas to look for complications

21
Disposition
  • Pts. Maybe discharged home if all the
    complications have been ruled out
  • Hospitalize if intractable pain.

22
Questions
  • 1. Which of the following are common causes of
    pancreatitis
  • A. infection
  • B. Gallstones
  • C. ETOH
  • D. Drugs
  • E. all of above

23
Questions
  • 2. Which of the following are complications of
    pancreatitis
  • A. ARDS
  • B. Shock
  • C. pancreatic insufficiency
  • D. pleural effusions
  • E. all of above

24
Questions
  • 3. True or false many meds can cause
    pancreatitis?
  • 4. True or false Grey Turner and Cullens sign
    are signs of hemorrhagic pancreatitis?
  • 5. True or false There is no single lab test
    that can reliably diagnose pancreatitis?

25
Answers
  • 1. E
  • 2. E
  • 3. T
  • 4.T
  • 5. T

26
Case of the Day
  • HPI 54 y/o WF presented to ER after being found
    on the ground s/p fall by her son. Pt. was found
    to be lethargic, weak, dizzy. Pt. had been
    vomiting the preceding 2-3 days. C/O diffuse
    abdominal pain.
  • ROS weight loss 50 lbs. over past year, rest
    of ROS neg.

27
Case of the Day
  • PMHx 1. Anemia 2. GERD 3. HLD 4.
    Hypokalemia 5. Herniated disc
  • PSHX 1. TAH 2. Chole
  • NKDA
  • Meds Urocrit, Zyprexa, Prevacid, Vicodin
  • Soc Hx Denies ETOH, 1pk. Day smoker, no drugs
  • Fam Hx N/C

28
Physical Exam
  • VS 36.3, 96/60, 109, 14, 97 RA
  • Gen Ao x1 , cachetic, difficult to arouse
  • ENT mm dry, otherwise normal
  • CV Tachy, S1,S2 no m/c/r
  • Pulm LCTAx2
  • GI BS, soft, diffuse TTP, No R/R/G
  • Rectal heme stools (done by Dr. Holencik)
  • Neuro intact, no focal deficits
  • Ext good pulses, no edema

29
Labs
  • EKG ST 109 bpm
  • CBC WBC 8.5 10.7/32.4 Plt 440 MCV 102.2, Fe
    def. anemia
  • CMP Na 143, K 3.6, Cl 109 CO2 12, GLU 63 BUN 17
    Cr. 1.0 Alb. 3.3 AST/ALT nml, Amylase,lipase
    normal Mg 1.8
  • CPP neg. x 1, CXR NAD CT head neg.

30
Labs
  • UA 1 protein, 2 blood
  • ABG 7.24/26/95/10/96 RA
  • APAP/ASA neg.
  • UDS BZD TSH 0.23 (L) L.A. 1.6
  • ETOH 0.002
  • Serum acetones large amount
  • Serum Osm 294

31
D/Dx mental status change/metabolic acidosis
  • Methanol
  • Uremia
  • Dka
  • Inh/iron
  • Lactic acidosis
  • Ethylene glycol
  • ASA
  • CO
  • Cyanide
  • AKA/starvation
  • Tolulene

32
Alcoholic ketoacidosis(AKA)
  • AKA is a wide anion gap metabolic acidosis often
    assoc. w/acute cessation of ETOH consumption
    after chronic ETOH abuse.
  • Key features are ingestion of large amounts of
    ETOH, relative starvation, volume depletion

33
AKA
  • Relative starvation, lack of glucose/glycogen
    stores, insulin deficiency, production of
    counter-regulatory hormones
  • Lipolysis promoted w/conversion of acetyl Co A to
    ketones

34
Clinical Features
  • N/V abd. Pain
  • Tachycardia Tachypnea
  • SOB
  • Tremulousness
  • Dizziness
  • Hematemesis, melena
  • Hepatomegaly
  • Mental status change
  • Seizure/syncope
  • Muscle pain
  • Fever

35
Lab
  • ETOH low or none
  • Elevated anion gap caused by ketones
  • Serum ketones maybe neg. or high (assay detects
    AcAc/acetone, BHB predominant ketone in AKA)
  • Electrolytes hypophosphatemia, hypokalemia,
    hyponatremia, hypoglycemia
  • Acid Base maybe mixed met. Acidosis met.
    Alkalosis(vomiting, volume depletion)

36
Treatment
  • Glucose administration to promote insulin
    secretion
  • IVF D5NS , HCO3 if pHlt7.1
  • Thiamine
  • Admit for acidosis

37
Hyperkalemia EKG see III-19
  • Tall, tenting of T-waves
  • Prolongation of QRS P-R interval
  • Low amplitude p-waves
  • AV blocks
  • Sine wave, V. Fib, asystole

38
Hypokalemia see III-20
  • Flattening of T-waves, U waves present
  • ST-depression
  • T-wave inversion
  • Advanced PAT w/block
About PowerShow.com