Table of contents
- 1. Acute Pancreatitis
- 1.1. Introduction
- 1.2. Causes
- 1.3. Symptoms
- 1.4. Diagnostic Criteria
- 1.5. Prognosis
- 1.6. Management
- 1.7. Complications
- 1.8. Treatment
- 1.9. References / Further Reading
- 2. Chronic Pancreatitis
- 3. Pancreatic Adenocarcinoma
- 4. Insulinoma
- 5. IgG4 Disease
.
See "References / Further Reading"
Acute Pancreatitis
Introduction
- Acute onset of pancreatic and peripancreatic inflammation
- Rate is rising (10-45 cases / 100,000), 5% mortality rate.
- Classification:
-
Severity Criteria Mild Pancreatitis
(Most Cases)
Acute pancreatitis that does not meet
"severe" criteria".
Severe Pancreatitis
- 20% of acute pancreatitis
- up to 20% mortality
Organ failure
- hypoxemia
- hypotension
- renal failure
OR
Complications:
- Pancreatic Necrosis
- Fluid collections
-
- Premature activation of intracellular pancreatic trypsinogen to trypsin conversion (activation).
- Triggers inflammatory cascade, causing capillary leak --> Can cause SIRS
Causes
- 80% of all acute pancreatitis are from Gall Stones or EtOH
-
Causes of Pancreatitis G - Gall Stones (45%) (MOST COMMON)
- Microlithiasis
E - Ethanol (35%) (MOST COMMON)
T - Tumors (choledochocele)
S - Steroids
M - Mumps
A - Autoimmune (IgG4, Polyarteritis Nodosa?, SLE?)
- (Other infections: viral [CMV, MUMPS], parasitic [toxoplasma, Ascaris lumbricoides])
S - Scorpion bite
H - Hypertriglyceridemia (TG > 5.6) Hypercalcemia
E - ERCP (post-ERCP), Emboli, Ischemia
D - Drugs
- SAND Mnemonic
- S - Simvastatin
- A - Azathioprine, 6-MP
- N - NSAIDS?
- D - Diuretics (Furosemide, hydrochlorthiazide)
- Mesalamine, asparaginase, didanosine
Others:
- Pancreas divisum (two congenital pancreatic ducts)
- Genetic, Ischemia
Symptoms
- Sudden onset pain in epigastric region with radiation to the back.
- (more comfortable seated position than supine).
- Nausea, vomiting, fever.
- Pleural Effusions --> dyspnea. (from capillary leak).
Diagnostic Criteria
-
Diagnostic Criteria for Acute Pancreatitis Need at least two of:
1. Typical clinical symptoms
2. Elevated serum amylase and/or lipase level> 3x ULN
3. Typical findings on cross-sectional imaging.
- Lipase has a longer half-life, MUCH more specific.
- Amylase is less specific (can see in salivary glands, fallopian tubes rises sooner.
- Non-specific, also seen in:
- Perforated peptic ulcer
- Intestinal ischemia
- Acute hepatitis or cholecystitis
- Rupture ectopic pregnancy
- Parotidis
- CKD
- Macroamylasemia
- Bening condition - multimers of amylase that are poorly filtered (need to do SPEP to find out).
- Gullo Syndrome
- Rare cause of benign amylase and sometimes even lipase elevations.
- Non-specific, also seen in:
- Contrast CT - only if clinical picture is not clear.
- Pancreatic or peripancreatic edema (+inflammatory stranding), fluid collections
- Pancreatic necrosis (but rare on initial imaging).
- Splenic vein thrombosis?
Prognosis
- Ranson Criteria (need parameters on admission + 48hrs later).
- Problem: Complexity, and cannot make initial analysis.
- Apache Score (MORE COMMON)
- The Acute Physiology and Chronic Health Evaluation (APACHE) II
- More accurate than Ranson, but cumbersome. (i.e. need ABG, etc...)
- Hemoconcentration
- Potential predictor of morbidity and mortality (marker of capillary leak).
- **Elevated BUN (serum)** Most important, most reliable, can trend.
- Elevated Creat
- Elevated Hematocrit
- Others:
- Medical comorbidities
- >75,
- BMI > 30
Management
- ADMIT ALL
- ICU if hemodynamically unstable or breathing challenges
- Require:
- Narcotic analgesia
- Bowel rest (NPO)
- Aggressive early fluids (Pancreas can sequester a lot of fluid) --> decrease ECV --> AKI + other organs.
- High risk of necrotizing pancreatitis (contrast CT often demonstrates inflammation and hypoperfusion).
- Monitor hypovolemia signs (tachycardia, hypotension, dry MM, hematocrit).
- Rehydration helps prevent organ failure.
- Other therapies:
- NG Tube --> NOT INDICATED
- Usually not needed, unless have ileus as a result from pancreatitis
- ERCP --> USUALLY NOT
- ERCP: AVOID, can worsen: in gall stones or worsening sympsoms + rising liver chemistry
- ONLY in two scenarios:
- 1. Concominant ascending cholangitis (fever, RUQ pain, and jaundice)
- 2. Gallstone pancreatitis who is not improving clinically and has worsening liver chemistry tests.
- Starting: Naso-Jejunal feeding
- Criteria: Start as soon as feasible NJ feeding, especially if no signs of improvement in first 72-92hrs.
- Avoid IV nutrition (high risk fungemia, bacteremia).
- Surgery
- Cholecystectomy indicated prior to discharge if pt has gall stone pancreatitis, and no other complications. (previously done as O/P once pancreas "cools off")
- Also done if pancreas is necrotic, due to high risk of mortality. But usually need repeat OR to keep removing necrotic tissue. Various drains are currently investigated.
- Antibiotics --> NOT INDICATED
- In the past used carbapenems, but now not indicated, even if necrosis is present.
- Studies: NO BENEFIT on mortality (predisposis to intra-abdominal fungal infections)
- If significant pancreatic necrosis --> can consider percutaneous fine-needle aspiration (culture + Gram stain).
- Abx only for culture-proven infected necrosis of the pancreas.
- If documented necrotizing pancreatitis and develop clinical instability (Fever, Hypotension)
- Must sample pancreatic bed (endoscopically, percutaneously, or surgical).
- May need drainage, if infected.
- Probiotics --> worsen outcomes
Complications
- Pseudocysts (Most Common)
- Fluid collection without solid degree (no epithelial layer) - Most common complication
- Often walled off pancreatic necrosis
- Pancreatic fluid collections due to destruction of main pancreatic duct or branches.
- Often have continued abdominal pain, failure to thrive, hospitalization etc..
- Can have mass effect on stomach
- Pseudocysts typically resolve spontaneously, and do not need treatment.
- If persist or have mass effect: surgical decompression, percutaneously, endoscopically.
- Fluid collection without solid degree (no epithelial layer) - Most common complication
- Leaking Pancreatic Ducts (30%)
- If untreated, can develop fistulas.
- Treated with:
- Endoscopic stenting.
- Can use octreotide to decrease secretions.
- Pancreatic enzymes to replace what is lost.
- Bowel rest.
- Splenic Vein Thrombosis
- Anticoagulation not recommended.
- Secondary to inflammation around that vein in pancreas.
- Can cause gastric varices.
- Diabetes
- If lost a lot of pancreas.
Treatment
- IV HYDRATION -> Aggressive!!!
- High risk of necrotizing pancreatitis (contrast CT often demonstrates inflammation and hypoperfusion).
- Monitor hypovolemia signs (tachycardia, hypotension, dry MM, hematocrit).
- Rehydration helps prevent organ failure.
- Notes On Other Therapies
- Antibiotics? --> NOT INDICATED in acute pancreatitis, even if necrosis is present. In the past used carbapenems.
- Studies show no benefit of prophylactic abx in severe necrotic pancreatitis. (abx raise risk of abdominal fungal infections)
- If significant pancreatic necrosis --> can consider percutaneous fine-needle aspiration (culture + Gram stain).
- Treat only if culture-proven infected necrosis of the pancreas.
- ERCP ?
- -> Can worsen pancreatitis. Only indicated if gallstone pancreatitis and worsening liver chemistry + instability (or if concerning for ascending cholangitis).
- NG suction? --> NOT INDICATED
- Early feeding decreases hospital stay, mortality. No need to NG suction.
- Probiotics contraindicated: increases mortality.
- Surgery:
- If necrotic, high mortality.
- However have to repeat OR many times, keep taking out necrotic tissue.
- Investigated various drains.
- Antibiotics? --> NOT INDICATED in acute pancreatitis, even if necrosis is present. In the past used carbapenems.
References / Further Reading
- Banks PA, Freeman ML; Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 2006;101(10):2379-2400. PMID: 17032204
- MKSAP 16
Chronic Pancreatitis
- Defined as:
- Irreversible descrution of pancreatic parenchyma causing variable degrees of endocrine and exocrine dysfunction.
- Heterogenous disorder, huge variation.
- Most patients:
- Constant severe abdominal pain radiating to the back.
- Signs of exocrine dysfunction: weight loss, diarrhea
- Signs of endocrine dysfunction: IDDM (lose function)
- Vitamin D/A/E/K deficient.
- Causes:
- Toxic:
- **Habitual alcohol** (>10y of 50g/day of EtOH, any drink glass of wine, can of beer, or shot is 10g)
- 5 drinks/day raises risk significantly.
- Tobacco use (also raises risk).
- **Habitual alcohol** (>10y of 50g/day of EtOH, any drink glass of wine, can of beer, or shot is 10g)
- Genetic (Cystic Fibrosis, Serine protease inhibitor, Kazal type I, Pancreatic secretory trypsin inhibitor)
- Obstructive (Pancreatic solid tumor, Intraductal papillary mucinous neoplasm, Pancreas divisum, Trauma)
- Other (Recurrent acute pancreatitis, Autoimmune)
- Toxic:
- Classified:
- Large Duct -
- Small Duct - hard to diagnose, often hard to see changes on imaging.
- Diagnosis:
- No gold standard, typically based on clinical symptoms.
- Cross section imaging helpful (pancreatic calcifications, ductal dilatation, parenchymal atrophy and/or focal inflammatory masses)
- Often times amylase/lipase are normal (no parenchyma to produce).
- Endoscopic Ultrasound
- MRCP (ECRP can make it worse)
- Direct stimulation of function: (hard to perform, often not available)
- cholecystokinin or secretin stimulation --> looking for minimal change disease.
- Early exocrine changes.
- Management:
- Prevent further damage, treat symptoms.
- Counsel to avoid exposures (alcohol, tobacco)
- Treat reversible causes (strictures, stones, etc..), endoscopically stent or remove stone.
- Enteric-coated pancreatic enzymes
- For exocrine insufficiency (take with meals, at least 30,000u of lipase daily - 10,000/meal + snacks).
- Ensure replacing fat-soluble vitamins. (ADEK)
- Non-Enteric-coated pancreatic enzymes
- Used for pain control
- Theoretical: limits stimulation of pancreas by inhibiting cholecystekinin feedback loop.
- Must be on PPI (enzymes denatured by low pH)
- Endocrine insufficiency
- Hard to manage, patients lose glucagon production.
- Very labile plasma glucose.
- Treat with INSULIN.
- Pain management:
- Avoid opioids as long as possible.
- Often opioid dependence.
- Can use Vitamin A/E, selenium (antioxidant)
- Other:
- Transcranial Magnetic Stimulation (Preliminary studies improved pain, but not yet available).
- Celiac plexus blockade (corticosteroids or neurolysis [ethanol], either percutaneously or endoscopic U/S). Usually short-lived benefit.
- Surgery
- Last resort, if all medical mgmt exhausted.
- Operative resection or lateral pancreaticojejunostomy (if obstruction).
- Total resection rare, makes pts insulin dependent and may not improve pain.
Pancreatic Adenocarcinoma
Insulinoma
- Presenting with neuroglycopenic symptoms and recurrent hypoglycemic episodes.
- First test: 8h fasting glucose (will be low!), and can directly measure insulin (will be inappropriately high)
- Imaging:
- Start with CT (r/o large tumors and metastasis)
- if CT negative, (can miss small <2cm lesions) do endoscopic ultrasound (90% detection).
IgG4 Disease
- IgG4 Disease is a spectrum of conditions causing autoimmune pancreatitis.
- Systemic fibroinflammatory disease that can affect pancreas, bile duct, salivary glands, retroperitoneum, lymph nodes.
- See lymphoplasmacytic infiltrate that is rich in IgG Subclass 4 (IgG4 positive cells).
- Most cases described in Japan (0.82/100,000 ppl).
- Assessment:
- Screen with serum IgG4
- Diagnostic when see on tissue pathology
- Rapidly responds to corticosteroid therapy.