

Pancreatitis
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17 Slides • 7 Questions
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Poll
How frequent you encounter cases of acute pancreatitis in ED
Once a week
Once a month
Once in three months
Once in 6 months
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One of the most common GI condition that require admission
Mostly may only have one episode of AP, 15- 30% will have at least recurrence once, 5-25% will ultimately have chronic pancreatitis
A complex that has variable courses, difficult to predict its development
Mild to moderate pancreatitis!
20% were severe acute pancreatitis (AP), with 20% mortality
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Word Cloud
What do you think the causes of acute pancreatitis
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Acute pancreatitis begins with injury to the acinar cells, leading to inappropriate intracellular activation of trypsinogen to trypsin. This initiates a cascade activating other digestive enzymes, the kinin system, and the complement system, resulting in autodigestion of pancreatic tissue.
Pathophysiology
Mechanism of Acinar Cell Injury and Enzyme Activation
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Ductal obstruction (e.g., gallstones) causing pressure buildup, interstitial edema, and enzyme-rich fluid accumulation.
Calcium dysregulation, which increases cytosolic calcium and triggers premature trypsin activation.
Ethanol, a common but complex cause, likely interferes with multiple intracellular pathways, though its exact mechanism remains unclear.
Triggers of Acinar Injury
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Word Cloud
What in the history and physical examination that can suggest “Acute Pancreatitis”
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Upper quadrant pain, usually epigastric,
Constant pain
Radiating to the back
Exacerbated by eating, or lying supine
Abdominal Pain
Pain described as lower abdominal pain or dull or colicky pain is highly unlikely to be pancreatitis.
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Mild Pancreatitis | Moderate Pancreatitis | Severe pancreatitis |
|---|---|---|
without local complications/ organ failure | With transient organ failure (recovery within 48 hours), and/or local complications | persistent organ failure (recovery >48 hours) with or without local complications |
Self limiting, discharged within 1 week | Have protracted courses over weeks/ month | |
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more specific to pancreatic injury;
remain elevated longer after symptoms
also elevated in DM, renal disease, appendicitis. and cholecystitis
more sensitive in delayed presentation, or related to alcohol use/ hyperTG
Lipase
Rises within a few hours after onset of symptoms
Peaks within 48 hours,
Normalizes in 3 -5 days
20% with pancreatitis whom may caused by alcohol and hyperTG will have normal amylase
Amylase
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Investigation
to identify the cause of pancreatitis, severity and complication.
Transabdominal US if gallstone is not yet ruled out.
CXR: especially with respi complaints, to evaluate effusion/ infiltrates
In patients who meet the clinical presentation and laboratory criteria, routine early CT, with or without IV or PO contrast, is not recommended for multiple reasons.
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Poll
Role of CT scan in Acute Pancreatitis?
To confirm diagnosis of AP
To identify complication of AP
To assess severity in all AP patients at arrival
No treatment for pancreatic necrosis from CT detected in first few days
Magnitude of morphology change in CT does not correlate with severity
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Poll
Which scoring would you use for Acute Pancreatitis in ED?
IMRIE Score
Ranson Scores
Bedside Index Scoring in Acute Pancreatitis (BISAP) score
APACHE II score
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When diagnosis is unclear
To identify complication
Best after >72 hours if symptoms persists or worsen
When CT is USEful
Not for early diagnosis/ assess severity
No evidence that early CT have improves outcome
Finding often lags behind symptoms
May underestimate it's severity if done too early (<72hours)
When CT is NOT useful
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None is superior to another
Most data not collected until 48h of admission
CRP >190mg/L within 48h (PPV 31.7%) or absolute increase >90,g/L (PPV 27.4%) for predicting severe disease
SIRS at admission and persist until 48h predicts severity
age >55 years
obesity
altered mental status
comorbidities
BUN >20mg/dL
Hct >44%
increasing creatinine
large extrapancretic fluid collection, pleural effusion, pulmonary infiltrates
Additional findings predicts severe cases
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Multiple Choice
A 50-year-old woman complains of epigastric pain that radiates to the back associated with nausea and vomiting. Her vitals are: BP 100/50 mm Hg, HR 110/min, T 37.8oC and SpO2 95% under room air. Her pain score is 9/10. Her serum amylase level is 200 U/L.
What is the best initial management for this patient?
a) IV gelofusine, tramadol and arrange for hepatobiliary ultrasound
b) IV morphine, erect chest radiograph and arrange for ERCP
c) Keep nil by mouth, IV tramadol and abdominal CT
d) Administer Hartmann’s solution, erect chect radiograph and IV cefuroxime
e) IV fentanyl, normal saline and bedside ultrasound
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#1 Catabolic state, increasing caloric and nutritional requirements.
#2 Gut mucosal damage—> translocating of bacteria from the bowel lumen to the portal circulation and mesenteric lymphatics >> organ failure, sepsis, and secondary infection of pancreatic and peripancreatic necrosis
In ED, if nausea and vomiting resolves, may serve oral painkillers and start low fat solid diet (calories)
Nutritional therapy
As soon as diagnosis is made (ED)
Intravascular depletion due to fluid sequestration from pancreatic, peripancreatic and systemic edema
Recommend to titrate IV fluid to measurable target of perfusion (Generally 2.5 to 4L in the first 12- 24 hours)
Watchout for risk of overload in high risk patients
Crystalloids!
Fluid resuscitation
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Fluid resuscitation
Control nausea and vomiting
Early nutrition
No role for antibiotic (acute pancreatitis is not source of infection)
Management in ED
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Multiple Select
Regarding acute pancreatitis
a. Obstructive biliary pancreatitis requires urgent decompression
b. Parenteral opioid is the analgesia of choice.
c. Nasogastric tube suction relieves pain.
d. Hyperglycaemia is a feature of poor prognosis.
e. Peritonitis is an early finding.
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