A.33 Acute Pancreatitis Flashcards

1
Q

A.33 Acute Pancreatitis

A

Acute pancreatitis is an inflammatory condition of the pancreas most commonly caused by gallstones or alcohol use. The typical manifestation includes sudden, severe epigastric pain that radiates to the back, nausea and vomiting, and epigastric tenderness on palpation.

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2
Q

A.33 Acute Pancreatitis
Etiology:

A

Most Common Causes
* Biliary Pancreatitis: ~40% of cases
* Alcohol-Induced: ~30% of cases
* Idiopathic: 15% - 25% of cases
Other Causes
* Severe Hypertriglyceridemia (>1,000 mg/dL), Hypercalcemia
* Post-ERCP
* Specific Medications: Steroids, Azathioprine, Sulfonamides, Loop and thiazide diuretics, Estrogen, Protease inhibitors, NRTIs, Anticonvulsants
* Scorpion Stings
* Viral Infections (e.g., Coxsackievirus B, Mumps)
* Trauma (e.g., surgical, accidental)

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3
Q

A.33 Acute Pancreatitis
Pathophysiology:

Mechanisms of Development

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  • Intrapancraetic activation of pancreatic enzymes: secondary to pancreatic duct outflow obstruction (e.g., gallstones, CF) or direct injury to pancreatic acinar cells (e.g., alcohol, drugs).
  • Increased proteolytic and lipolytic enzyme activity: contributes to pancreatic parenchyma damage.
  • Recruitment of inflammatory cells (neutrophils, macrophages): release of inflammatory cytokines.
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4
Q

A.33 Acute Pancreatitis
Sequelae of Pancreatitis (varying by severity):

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  • Capillary Leakage: Resulting in inflammatory cytokines and vascular injury, leading to vasodilation and increased vascular permeability—shifts fluid from the intravascular space into the interstitial space (third space loss)—potentially leading to hypotension and tachycardia.
  • Pancreatic Necrosis: Involves decreased pancreatic blood perfusion, multi-organ dysfunction, and further pancreatic tissue damage.
  • Hypocalcemia: Lipase breaks down pancreatic and mesenteric fat, leading to free fatty acids that bind calcium, resulting
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5
Q

A.33 Acute Pancreatitis
Clinical Features:

A

Pain:
* Constant, severe epigastric pain: typically radiates to the back, worsens after meals and when supine, may be accompanied by nausea and vomiting.
General Physical Examination:
* Signs of shock: tachycardia, hypotension, oliguria/anuria.
* Possible jaundice in patients with bile duct obstruction.
Abdominal Examination:
* Findings may include abdominal tenderness and distension.
* Ileus characterized by reduced bowel sounds and tympany on percussion.
* Ascites may be present.
Skin Changes (Rare):
* Cullen’s Sign: Periumbilical ecchymosis and discoloration (bluish-red).
* Grey Turner’s Sign: Flank ecchymosis with discoloration.
* Fox’s Sign: Ecchymosis over the inguinal ligament.

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6
Q

A.33 Acute Pancreatitis
Diagnosis:

A

Two of the three following criteria should be met for a diagnosis of acute pancreatitis to be made.
* Characteristic abdominal pain
* ↑ Serum pancreatic enzymes: lipase or amylase ≥ 3× ULN
* Characteristic findings of acute pancreatitis on cross-sectional imaging (e.g., abdominal ultrasound, contrast-enhanced CT abdomen)

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7
Q

A.33 Acute Pancreatitis
Laboratory Tests:

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Serum pancreatic enzymes:
- ↑ Lipase: ≥ 3× ULN is highly indicative of acute pancreatitis
- ↑ Amylase: ≥ 3× ULN (less sensitive and specific than lipase)
CBC:
↑ Hematocrit (Hct): marker of hemoconcentration
* Serial measurements: to guide IV fluid therapy with the aim of normalizing levels
* Persistently elevated Hct: third space fluid loss suggesting inadequate fluid resuscitation
* Sudden decrease in Hct: can indicate pancreatic hemorrhage (rare)
↑ WBC count
* Can be seen in early pancreatitis (a marker of severity)
* Worsening leukocytosis on serial evaluation is indicative of infected necrosis.
Inflammatory markers:
↑ CRP: Levels > 150 mg/L 3 days after onset can indicate severe or necrotizing pancreatitis.
↑ Procalcitonin: sensitive for infected necrosis
↑ Interleukin-6 (IL-6): can be seen in infected necrosis and used as a predictor for remote organ failure

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8
Q

A.33 Acute Pancreatitis
Imaging:

A

Ultrasound (US):

The most valuable initial test for all patients with acute pancreatitis.
Can identify gallstones and dilation of the biliary tract.
Signs indicative of pancreatitis include:
Indistinct pancreatic margins (edematous swelling).
Abnormalities in surrounding structures (e.g., fluid collections or ascites).
Evidence of necrosis, abscesses, and pancreatic pseudocysts.

CT Scan:

Recommended but less sensitive than MRI.

MRCP and ERCP:

MRCP: Noninvasive but less sensitive than ERCP.
ERCP: Can be combined with sphincterotomy and stone extraction, but may exacerbate pancreatitis.

X-Ray:

Sentinel Loop Sign: Dilation of a segment of the small intestine in the upper abdomen (duodenum/jejunum).

Additional Findings:

Colon cut-off sign: Gaseous distension of the descending and transverse colon, indicating obstruction at the splenic flexure.
Evidence of potential complications: pleural effusions, pancreatic calcifications, which may necessitate invasive procedures such as a drain placement.
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9
Q

A.33 Acute Pancreatitis
Treatment:

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General Measures:
- Admission: Patients should be hospitalized and monitored based on the severity of the condition (consider ICU as needed).
- Fluid Resuscitation: Initiate early hydration using crystalloids (e.g., lactated Ringer’s solution).
- Pain Management: Use IV opioids (e.g., fentanyl or hydromorphone), considering patient comfort.
- Bowel Rest: Maintain NPO (nothing by mouth) until the patient shows improvement in symptoms.
- Nutritional Support:
- Begin enteral feeding (oral or via nasogastric/nasointestinal tube) as soon as pain symptoms allow.
- Provide parenteral nutrition only for patients unable to tolerate enteral feeding.
Drug Therapy:
- Antibiotics: Not routinely recommended; should only be used in cases of infected necrosis.
- Fenofibrates: Considered in instances of hyperlipidemia-induced acute pancreatitis.
Biliary Pancreatitis:
- Urgent ERCP and Sphincterotomy: Perform within 24 hours for patients with evidence of choledocholithiasis and cholangitis.
- Cholecystectomy: Should be conducted in all patients with biliary pancreatitis, especially when pancreatitis is resolved or in the context of ongoing complications.

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10
Q

A.33 Acute Pancreatitis
Complications:

A

Localized:
- Bacterial Superinfection of necrotic tissue:
- Diagnosis: CT-guided percutaneous drainage and culture of the aspirate.
- Treatment: Surgical debridement and antibiotics.
- Prognosis: High mortality rate; multi-organ failure occurs in up to 50% of cases.
- Pancreatic Pseudocysts
- Pancreatic Abscess
- Pleural Effusion

Systemic:
- SIRS (Systemic Inflammatory Response Syndrome), Sepsis, DIC (Disseminated Intravascular Coagulation)
- Pneumonia and Respiratory Failure
- ARDS (Acute Respiratory Distress Syndrome)
- Shock
- Prerenal Failure due to volume depletion
- Hypocalcemia

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11
Q

A.33 Acute Pancreatitis
Prognosis:

A

Mortality:
* In patients without organ failure: < 1%
* In patients with organ failure: ~30%
* Higher mortality observed in patients with biliary pancreatitis compared to those with alcoholic pancreatitis.

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12
Q

A.33 Acute Pancreatitis
Key Predictors of Severity:

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  • Age: > 55 years
  • GI Bleeding
  • Abnormal Hematocrit within 48 hours:
  • Acute hemorrhagic pancreatitis: Low hematocrit
  • Third-space fluid loss: High hematocrit
  • Hypocalcemia and/or Hyperglycemia
  • Inflammatory Markers:
  • Elevated CRP (> 1 mg/dL), WBC count
  • Evidence of Shock and/or Organ Failure:
  • Elevated AST, ALT, BUN, creatinine
  • Arterial Blood Gas: Metabolic acidosis with a base deficit > 4 mmol/L
  • CT Findings:
  • Pancreatic edema, peripancreatic fluid collection, and/or necrosis of > 33% of the pancreas
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