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Pancreatitis chap. 87 tintinalli

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Pancreatitis and Cholecystitis TINTINALLI S CHAP. 82 (7e) Clinical features Cullen sign bluish discoloration around umbilicus Grey Turner sign bluish ... – PowerPoint PPT presentation

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Title: Pancreatitis chap. 87 tintinalli


1
Pancreatitis and Cholecystitis TINTINALLIS
CHAP. 82 (7e)
2
acute pancreatitis
  • Most common causes
  • Alcohol
  • Biliary dz
  • Drugs
  • Infection
  • Inflammation
  • Trauma
  • Metabolic disorders
  • make up most of the cases

3
pathophysiology
  • Activation of digestive zymogens in pancreatic
    acinar cells gt autodigestion of pancreas
  • Edema
  • Interstitial hemorrhage
  • Vascular damage
  • Coagulation
  • Cellular necrosis

4
clinical features
  • Midepigastric pain or LUQ pain
  • Constant, boring pain that radiates to the back,
    flanks, chest, or lower abdomen
  • Pain can be exacerbated by supine position
    relieved by sitting with trunk knees flexed
  • Nausea/vomiting
  • Abdominal bloating (gut hypomobility) dec. BS
  • Low grade fevers
  • Tachycardia
  • Hypotension (from 3rd spacing shock MODS)
  • Pleural effusion (left sided) rarely ARDS

5
Clinical features
  • Cullen sign bluish discoloration around
    umbilicus
  • Grey Turner sign bluish discoloration of the
    flanks

6
diagnosis
  • Labs
  • Amylase pancreas/salivary glands. Most
    sensitive at 36 hrs
  • Lipase pancreas also found in gastric and
    intestinal mucosa. Longer half-life so will be
    elevated even when amylase at baseline
  • Preferred test
  • Absolute levels do NOT correlate w/ severity of
    dz

7
imaging
  • Plain Films
  • Used to r/o other causes
  • May see sentinel loop indicating regional ileus
  • May see left sided pleural or pericardial
    effusions
  • US
  • Used to see dilatation of biliary tree or
    gallstones
  • Pancreatic edema or pseudocysts

8
Imaging
  • CT -Better to visualize severity of dz and other
    anatomy

9
prognostic markers
  • Usually pancreatitis is a self-limiting dz
  • 5-10 of cases suffer significant
    morbidity/mortality
  • Ranson criteria at presentation
  • Age gt 55
  • BGL gt 200 mg/dL
  • WBC ct gt 16,000/L
  • AST gt 250 units/L
  • LDH gt 700 IU/L

10
treatment
  • rest the pancreas
  • NPO
  • FLUID RESUSCITATION!
  • Maintain Urine OP of 0.5ml/kg
  • Parenteral narcotics
  • Antiemetics
  • If biliary pancreatitis, then requires emergent
    decompression
  • Abx If abscess. No evidence for
    prophylactic/mild cases

11
disposition
  • Mild dz that can be managed with outpt therapy
    can go home pts tolerating PO and pain
    controlled
  • All others.admit
  • Pancreatic abscesses need a surgeon

12
chronic pancreatitis
  • Chronic inflammation of pancreas that causes
    irreversible damage to its structure and function
  • Most cases are alcohol related
  • Pathophysiology
  • Interstitial inflammation w/ duct obstruction
    dilatation leading to parenchymal loss fibrosis
  • Eventual impairment of both exocrine and
    endocrine pancreatic functions
  • Significant malabsorption syndrome does not occur
    until gt 90 of glandular function is lost

13
clinical features
  • Abdominal pain (midepigastric radiating to back)
  • Nausea/vomiting
  • Pain worse after alcohol or fatty meals
  • Pts will look chronically ill
  • Cachectic
  • Steatorrhea
  • Clubbing
  • Polyuria
  • Stigmata of liver dz

14
diagnosis
  • Amylase/lipase may be normal
  • Glucose tolerance impaired (elev. fasting BS)
  • Elevated bilirubin alk phos
  • CXR will see calcifications in pancreas
  • CT or US will show complications of chronic
    pancreatitis (pseudocysts or abscesses)

15
treatment
  • IV narcotics
  • Antiemetics
  • Correct fluid and electrolyte abnormalities
  • Relief of mechanical obstruction or complications
  • Correction of malabsorption
  • Alteration of dz course
  • 5 year mortality rate of chronic alcoholic
    pancreatitis in pts who continue to drink alcohol
    is 50

16
disposition
  • Most chronic pancreatitis pts can go home after
    any complications have been ruled out/addressed
  • Secure follow-up
  • Admit if pt has intractable pain

17
Cholecystitis
  • 4 major biliary tract emergencies
  • Biliary colic (symptomatic cholelithiasis)
  • Cholecystitis
  • Gallstone pancreatitis
  • Ascending cholangitis
  • 4 Fs (the classical presenting pt)
  • Female
  • Forty
  • Fat
  • Flatulence

18
pathophysiology
  • Bile is made and secreted by hepatocytes stored
    in GB
  • Wall of GB innervated
  • with sympathetic
  • parasympathetic
  • nerves from celiac
  • plexus

19
pathophysiology
  • Bile
  • Water (80)
  • Bile acids (10)
  • Lecithin other phospholipids (4-5)
  • Cholesterol (1)
  • Conjugated bilirubin
  • Electrolytes
  • Mucous
  • Various proteins
  • Cholecystokinin (CCK) is stimulus for release of
    bile into small intestine

20
types of gallstones
  • Cholesterol (70)
  • Radiolucent (calcium content lower here)
  • Pigment (20)
  • Black (pts w/ adv. liver dz hemolytic d/o)
  • Brown (pts of Asian descent, bacterial/parasitic
    infection)
  • Radiopaque (more calcium here)
  • Mixed (10)

21
Clinical features of acute cholecystitis
  • Pain persisting gt 6 hours
  • Nausea vomiting, anorexia
  • Fever /- chills
  • Hx of similar attacks/documented gallstones
  • Pain becomes more localized to RUQ
  • Murphys sign
  • Signs of systemic toxicity, dehydration
  • Localized peritoneal toxicity, distention
  • Hypoactive bowel sounds

22
specific presentations
  • Kids infrequent. Gallstones may be idiopathic or
    due to hemolytic disorders, cystic fibrosis,
    obesity, ileal resection or long-term TPN
  • Pregnancy increase of GB sludge/gallstones,
    predisposes cholelithiasis but rarely
    cholecystitis
  • Elderly more likely to present with biliary
    sepsis/GB gangrene increased perioperative
    mortality (19)

23
diagnosis
  • High clinical suspicion
  • US (modality of choice) CT not as sensitive
  • Labs will most likely be normal
  • CBC, CMP normal range
  • Lipase to r/o pancreatitis
  • Urine to r/o pyelo, uti, ectopic, kidney stones
  • Plain films (esp. CXR to r/o pneumonia)
  • EKG to r/o AMI ACS
  • HIDA (sens. of 97 and spec. of 90)

24
complications
  • Mallory-Weiss tears
  • Fluid electrolyte abnormalities
  • Gallstone pancreatitis
  • Ascending cholangitis (mortality can reach 100
    if no tx or improper tx)
  • Cholecystitis leading to GB empyema
  • Emphysematous (gangrenous) cholecystitis

25
Treatment disposition
  • If pt presents in shock, then IV fluids /-
    vasopressors, broad spectrum abx surgery to
    decompress biliary tree
  • GB empyema develop gm neg. sepsis
  • Broad spectrum axbx, fluids, stat surgery
  • Gangrene of GB (segmental ischemia of GB wall)
    risk of perforation -gt surgery
  • Emphysematous cholecystitis (gangrene of entire
    GB) pts are in septic shock

26
Contrast CT scan showing emphysematous
cholecystitis with gallbladder wall disruption
(arrow), gas formation (arrowhead), and a biloma
Contrast CT scan showing gallstones (arrow) with
gallbladder rupture and fluid localized at the
gallbladder fossa (arrowhead)
27
Abdominal radiograph of acalculous emphysematous
cholecystitis demonstrating curvilinear air
pattern conforming to the shape of the
gallbladder wall
CT images of emphysematous cholecystitis - same
patient
28
Ultrasound findings of acalculous cholecystitis
include marked gallbladder wall thickening and
pericholecystic fluid.
Transverse ultrasound demonstrates marked
gallbladder wall thickening and pericholecystic
fluid collection in a patient with AIDS who was
managed conservatively
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