Acute Pancreatitis
Acute inflammation of the pancreas that is subclassified by severity into:
The Glasgow Criteria are adverse prognostic factors:
- Admission
- Age >55
- WCC >15 1,000/mm3
- Glucose >10 mmol/L
- AST >250 U/L
- Within 48 hours
- ↓ In Hct >10%
- ↑ In urea >1.8 mmol/L
- Calcium <2 mmol/L
- PaO2 <60 mmHg
- Mild acute pancreatitis
No organ failure or complications. - Moderate acute pancreatitis
- Transient (<48 hours) organ failure
- Local complications
Peripancreatic fluid collections, which can be:- Necrosis
Non-viable pancreas that may be sterile or infected. Necrosis:- Usually develops early
- Is established by 96 hours
- Is a major prognostic factor
- Pseudocysts
- Cysts
- Necrosis
- Systemic complications
- Severe acute pancreatitis
As moderate, but with persistent single or multiorgan failure.
Epidemiology and Risk Factors
Pathophysiology
Aetiology
Precipitants include:
- Biliary obstruction
35-40%.- Gallstones
- Malignancy
- Drugs
- Alcohol
35%. - Antibiotics
- Metronidazole
- Nitrofurantoin
- Erythromycin
- Tetracyclines
- Sulphonamides
- Diuretics
- Furosemide
- Thiazides
- Toxins
- Methyl alcohol
- Scorpion venom
- Organophosphates
- Alcohol
- Metabolic
- Hyperlipidaemia
- Hypercalcaemia
- Hyperparathyroidism
- DKA
- ESRD
- Infections
- Viral
- HIV
- EBV
- Mumps
- Bacteria
- Mycoplasma
- Legionella
- Campylobacter
- Parasites
- Ascariasis
- Viral
- Immune
- Polyarteritis nodosa
- SLE
- TTP
- Pregnancy
- Trauma
- Iatrogenic
- Postoperative
An enjoyable mnemonic for some of these causes is:
- Idiopathic
- Gall stones
- Ethanol
- Trauma
- Steroids
- Mumps
And other viruses. - Autoimmune
- Scorpions
- Hyperlipidaemia
- ERCP
- Drugs
Clinical Manifestations
Diagnostic Approach and DDx
Investigations
Laboratory:
Amylase has been replaced by lipase, and has little current role in the diagnosis of pancreatitis.
- Blood
- Lipase
90% sensitive and specific for acute disease.- Elevations from non-pancreatic causes are typically <3× ULN
- LFTs
For biliary obstruction. - Triglycerides
>1000 mg/dL diagnostic of hypertriglyceridaemic pancreatitis, absent other causes. - Calcium
- Lipase
Imaging:
- Contrast CT
- Pancreatitis
Loss of normal contrast enhancement. - Necrosis
- Pancreatitis
- Ultrasound
- Usually limited by bowel gas
- Cannot quantify necrosis
- Provides assessment of biliary tree
CBD dilation most important finding. - May provide guidance for needle aspiration
Management
Surgical management of pancreatitis is associated with very high mortality; supportive treatment is first line and and surgical management should only be resorted to if it is otherwise unavoidable.
Resuscitation:
- C
- Volume resuscitation
- Aggressive volume resuscitation required for offsetting distributive shock and correcting hypovolaemia
- >10mL/kg associated with ↑ ARDS and ↑ abdominal compartment syndrome
- Haemodynamic support
- Volume resuscitation
Specific therapy:
Carbapenems have exceptional penetration into pancreatic tissue, and are effective against most culprit organisms.
- Pharmacological
- Antibiotics
- Low threshold for IV antibiotics if suspecting infected collection
- Prophylactic antimicrobials may have a role in severe disease
- NSAIDs
Appropriate post-ERCP in mild gallstone pancreatitis as analgesics and may ↓ severity. - Insulin/dextrose
If hypertriglyceridaemia.- Goal is to promote anabolism
- Effect achieved when enough insulin is provided such that the BSL does not rise in the face of dextrose infusion
- Antibiotics
- Procedural
- Open necrosectomy
- Infected collections should be managed non-operatively for >4 weeks to allow fibrous walls and liquefaction to occur
- Indications for surgery usually are other abdominal complication, e.g.:
- Perforation
- Bleeding
- Mesenteric ischaemia
- Needle aspiration
- For gallstone pancreatitis:
- Cholecystectomy
Indicated due to high (up to 90%) rate of recurrence.- Mild cases can proceed immediately
- More severe disease should be stabilised first
- ERCP
- ↓ Morbidity and mortality in mild gallstone pancreatitis
- Cholecystectomy
- Plasmapheresis
For hypertriglyceridaemia, with very little supportive evidence.
- Open necrosectomy
Supportive care:
Feeding:
- Maintains gut mucosal barrier
- Corrects nutritional deficiencies
Many patients malnourished on presentation. - ↓ Risk of secondary infection of necrotic pancreatic tissue
- G
- Feeding
- If non-intubated:
- Oral diet as clinically tolerated
- If intubated:
- EN should be started once resuscitation finished
- PN indicated only if EN fails or is contraindicated
EN ↓ infection, organ failure, and mortality compared with PN. - NJ feeding may be preferable to NG to avoid ↑ pancreatic secretion
- If hypertriglyceridaemic:
- Zero-fat diet initially
- Low-fat diet once triglycerides normal
- If non-intubated:
- Feeding
Disposition:
Marginal and Ineffective Therapies
Prophylactic antifungal therapy is not recommended.
Various therapies aimed at generally ↓ pancreatic exocrine function are without evidence, and include:
- Octreotide
- Somatostatin
- H2-antagonists
- Atropine
- Calcitonin
- Glucagon
- Fluorouracil
Interventions aimed to ↓ protease secretion are also without evidence, and include:
- Aprotinin
- Gabexate mesilate
Anaesthetic Considerations
Complications
- Death
5-10% mortality in severe disease. - B
- ARDS
- C
- Shock
- Distributive
- Hypovolaemic
- Shock
- G
- Abdominal compartment syndrome
- Pancreatic cysts
Do not merit surgical intervention unless:- Gastric outflow obstruction
- Biliary obstruction
- Infected necrosis
- Usually arise at 10-14 days
- Carbapenem or tazocin preferable for good solid organ penetration
- Pancreatic abscess
Infected collections are a major contributor to morbidity and mortality.- Usually arise at 4 weeks
- Amenable to percutaneous drainage
Prognosis
Poor prognostic signs:
- Pancreatic necrosis
- Pancreatic head necrosis is as severe as whole pancreatic necrosis
- Pancreatic tail necrosis usually has a good prognosis
Key Studies
- WATERFALL (2022)
- 249 of a planned 744 patients from Spain, France, Italy, and Mexico with acute pancreatitis
- Aggressive vs moderate fluid resuscitation
- Aggressive group:
- 20mL/kg bolus
- 3mL/kg/hr infusion for 48 hours
- Moderate group:
- 10mL/kg bolus
- 1.5mL/kg/hr for 20 hours
- Aggressive group:
- Stopped early for harm in the aggressive group
- ↑ Severity of pancreatitis
References
- de-Madaria E, Buxbaum JL, Maisonneuve P, et al. Aggressive or Moderate Fluid Resuscitation in Acute Pancreatitis. New England Journal of Medicine. 2022;387(11):989-1000.