Acute pancreatitis is an inflammatory condition of the pancreas characterized by abdominal pain and elevated pancreatic enzymes. The most common causes are gallstones and alcohol. In severe cases, pancreatic enzymes activate prematurely and digest the pancreas. This can lead to systemic inflammatory response and organ failure. Diagnosis is based on abdominal symptoms and blood tests showing elevated pancreatic enzymes. Severity is assessed using criteria like Marshall score and need for ICU care. Treatment involves hydration, pain control, treating the underlying cause, preventing infection, and nutrition support. Surgery is usually not needed for sterile pancreatic necrosis but may be for infected necrosis after 4 weeks.

1. ACUTE PANCREATITIS
Abbas Qaddomi ( intern)
1

2. INTRODUCTION
 Acute pancreatitis(AP) is an inflammatory condition
of the pancreas characterized clinically by
abdominal pain and elevated levels of pancreatic
enzymes in the blood.
 AP was the most common gastroenterology
discharge diagnosis with a cost of 2.6 billion dollars.
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3.  Worldwide the incidence of acute pancreatitis
ranges from 5 to 80/100,000 population
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4. ETIOLOGY
 Gallstones : reflux of bile into the pancreatic duct
due to transient obstruction of the ampulla during
passage of gallstones
 gallstone obstructing the pancreatic duct, leading to
ductal hypertension.
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5.  Alcohol : amount for many years
 Generation of toxic metabolites such as
acetaldehyde and fatty acid ethyl esters
 Sensitization of acinar cells to cholecystokinin
(CCK)-induced premature activation of zymogens
 Ethanol also increases the protein content of
pancreatic juice, decreases bicarbonate levels, and
trypsin inhibitor concentration
ETIOLOGY
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6.  Hereditary Pancreatitis

 Tumors
 Hyperlipidemia
 Iatrogenic
ETIOLOGY
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8. PATHOPHYSIOLOGY
 Acinar cell injury: auto-digestion of pancreatic
substance by inappropriately activated enzymes (
trypsinogen )
 Intrapancreatic Events : Leukocyte
chemoattraction, release of cytokines, and
oxidative stress
 Systemic Events systemic inflammatory response
syndrome (SIRS) Organ failure
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9. ABDOMEN PAIN-CARDINAL SYMPTOM
 SITE: usually experienced first in the epigastrium
 but may be localized to either upper quadrant or felt diffusely throughout the abdomen or lower chest
 ONSET: characteristically develops quickly, generally following substantial meal and precedes NV
 SEVERITY: frequently severe, reaching max. intensity within minutes rather than hours
 NATURE: “boring through”, “knifing” (illimitable agony)
 DURATION: hours-days
 COURSE: constant (refractory to usual doses of analgesics, not relieved by vomiting)
 RADIATION: directly to back(50%), chest or flanks
 RELEIVING FACTOR: sitting or leaning/stooping forward due to shifting forward of abdominal
contents and taking pressure off from inflamed pancreas
 AGGRAVATING FACTOR: food/alcohol intake, walking, lying supine
Pain described as dull, colicky, or located in the lower abdominal region is not
consistent with AP and suggests an alternative etiology
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10. OTHER MANIFESTATIONS
 Nausea, frequent and effortless vomiting, anorexia,diarrhea
 Due to reflex pylorospasm
 More intense in necrotizing than in edematous pancreatitis
 Persistent retching
 despite empty stomach
 Hiccups
 Due to gastric distension/diaphragmatic irritation
 Fever
 Low grade, seen in infective pancreatitis
 Weakness, Anxiety, Sweating
 Indicates severe attack
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11. ABDOMEN EXAMINATION
 Physical findings vary depending upon the severity of acute
pancreatitis
 Tenderness + Rebound tenderness:
 epigastrium/upper abdomen
 Distension:
 Ileus(BS decreased or absent)
 ascites with shifting dullness
 Guarding -upper abdomen
 tensing of the abdominal wall muscles to guard inflamed organs
within the abdomen from the pain of pressure upon them
 Rigidity(involuntary stiffness)-unusual
 Tensing of the abdominal wall muscles to guard inflamed organs
even if patient not touched
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12. DIAGNOSTIC CRITERIA
 Most often established by the presence of 2 of the 3 following
criteria
(1) abdominal pain consistent with the disease,
(2) serum amylase and/or lipase greater than three times the upper limit
of normal, and/or
(3) characteristic findings from abdominal imaging.
_____________________________________________________
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Transabdominal ultrasound should be performed in all patients with
acute pancreatitis
CT and/or MRI of the pancreas should be reserved for patients
 in whom the diagnosis is unclear(typical pain with normal enzymes)
 who fail to improve clinically within the first 48–72 h after hospital
admission (e.g., persistent pain, fever, nausea, unable to begin oral
feeding)
 to evaluate complications
 Genetic testing may be considered in young patients ( < 30 years
old) if no cause is evident and a family history of pancreatic
disease is present
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13. CLASSIFICATION OF ACUTE PANCREATITIS
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14. ASSESSMENT OF DISEASE SEVERITY
 systemic inflammatory response syndrome (SIRS)
 modified Marshall scoring system
 SOFA
 APACHE II
 Ranson's criteria
 BISAP 14

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18. INDICATIONS FOR ICU ADMISSION
 Patients with severe acute pancreatitis
 Patients with acute pancreatitis and one or more of the following
parameters:
 •Pulse <40 or >150 beats/minute
 •Systolic arterial pressure <80 mmHg or mean arterial pressure
<60 mmHg or diastolic arterial pressure >120 mmHg
 •Respiratory rate >35 breaths/minute
 •Serum sodium <110 mmol/L or >170 mmol/L
 •Serum potassium <2.0 mmol/L or >7.0 mmol/L
 •PaO2 <50 mmHg
 •pH <7.1 or >7.7
 •Serum glucose >800 mg/dL
 •Serum calcium >15 mg/dL
 •Anuria
 •Coma 18

19. INITIAL MANAGEMENT
 Aggressive hydration during 12-24
 Decrease morbidity and mortality
 Hematocrit and BUN has been widely recommended as
surrogate markers for successful hydration
 No absolute numbers recommended
 Goal to decrease Hct and BUN and maintain normal cr
 In elderly and cardiac/renal comorbidities hydration is
monitored by
 Central venous pressure via CV line or
 Intrathoracic blood volume index
 Better/more accurate correlate with cardiac index than CVP
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20. PAIN CONTROL
 should be treated with analgesics. uncontrolled pain
can contribute to the hemodynamic instability
 Attention to adequate fluid resuscitation should be
the first priority in addressing abdominal pain, as
hypovolemia from vascular leak and
hemoconcentration can cause ischemic pain and
resultant lactic acidosis.
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21.  should be administered intravenously
 mild pain , NSAID (metamizole 2g/8h IV)
 severe pain opioid analgesia
 Morphine is to be avoided, due to its potential to
cause sphincter of Oddi spasm
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PAIN CONTROL

22. ROLE OF ERCP
 most gallstones that cause AP readily pass to the
duodenum and are lost in the stool
 should be performed early in the course (within 24
hours of admission) for patients with:
 gallstone pancreatitis
 Cholangitis
 common bile duct obstruction (visible stone on
imaging)
 dilated common bile duct
 increasing liver tests without cholangitis
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23. PREVENTING POST-ERCP
PANCREATITIS
 Over the past 15 years, the risk of post-ERCP
pancreatitis has decreased to 2 – 4 % and the risk
of severe AP to < 1 / 500
 guidewire cannulation
 pancreatic duct stents
 rectal NSAIDs
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24. THE ROLE OF ANTIBIOTICS IN AP
 Prophylactic antibiotics are not recommended in
patients with acute pancreatitis, regardless of the
type or disease severity
 Infected necrosis should be considered in patients
with pancreatic or extrapancreatic necrosis who
deteriorate or fail to improve after 7 – 10 days of
hospitalization
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25.  As SIRS may be indistinguishable from sepsis
syndrome, so if infection is suspected, antibiotics
should be given while source of infection is being
investigated
 Once blood and other cultures are found negative,
antibiotics should be discontinued
 The antibiotics shown to penetrate and used in
clinical trials include carbapenems, quinolones,
metronidazole, and high-dose cephalosporins
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26.  Routine administration of antifungal agents along
with prophylactic or therapeutic antibiotics is not
recommended
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27. NUTRITION
 Clinical and experimental studies showed that
bowel rest is associated with intestinal mucosal
atrophy and increased infectious complications
because of bacterial translocation from the gut
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28.  In mild AP oral feedings can be started immediately if
there is no nausea/vomiting, and the abdominal
pain/tenderness/Ileus has resolved(amylase return to
normal, patient feel hunger
 low-fat soft diet has been shown to be safe compared
with clear liquids,
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NUTRITION

29. NUTRITION
IN SEVERE AP
 In severe AP, enteral nutrition is recommended to
prevent infectious complications.
 Parenteral nutrition should be avoided, unless the
enteral route is not available, not tolerated, or not
meeting caloric requirements
 Nasogastric delivery and nasojejunal delivery of
enteral feeding appear comparable in efficacy and
safety
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30.  high protein, low fat, semi-elemental feeding
formulas
 Signs that the formula is not tolerated include
increased abdominal pain, vomiting (with
nasogastric feeding), bloating, or diarrhea
 Parenteral
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NUTRITION
IN SEVERE AP

31. ROLE OF SURGERY IN AP
 Cholecystectomy should be performed after recovery in
all patients with gallstone pancreatitis including those
who have undergone an endoscopic sphincterotomy
 In case of mild gallstone AP, cholecystectomy should be
performed before discharge to prevent a recurrence of
AP
 clinical suspicion of CBD stones is high ------- ERCP
 clinical suspicion of CBD stones is moderate -------MRCP or
EUS
 clinical suspicion of CBD stones is low ---------- intraoperative
cholangiogram 31

32.  In case of necrotizing biliary AP, in order to prevent
infection, cholecystectomy is to be deferred until active
inflammation subsides and fluid collections resolve or
stabilize
 Failure to perform a cholecystectomy is associated with
a 25 to 30 percent risk of recurrent acute pancreatitis,
cholecystitis, or cholangitis within 6 to 18 weeks
 population-based study found that cholecystectomy
performed for recurrent attacks of AP with no stones /
sludge on ultrasound and no significant elevation of liver
tests during the attack of AP was associated with a > 50
% recurrence of AP
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33.  If patient unfit for surgery(comorbid/elderly), biliary
sphincherotomy alone may be effective to reduce
further attacks of AP
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34. Sterile necrosis infected necrosis
Asymptomatic Does not mandate
intervention regardless of
size, location and
extension
surgical, radiologic, and/or
endoscopic drainage should
be delayed preferably for
more than 4 weeks
• to allow liquefaction of
the contents and the
development of a
fibrous wall around the
necrosis
• Initially treated with
antibiotics
Stable
Symptomatic
(associated
with GOO or
bile
obstruction)
minimally invasive
methods of
necrosectomy are
preferred to open
necrosectomy
Urgent debridement unstable
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36.  Thank you
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