Pancreatitis natural history, complications and prognosis

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Pancreatitis Main Page

Patient Information

Overview

Causes

Classification

Acute Pancreatitis
Chronic Pancreatitis
Hereditary Pancreatitis
Autoimmune Pancreatitis

Differential Diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Complications of pancreatitis should be suspected when there is persistence/recurrence of abdominal pain, secondary increases in pancreatic enzyme, increasing organ dysfunction, or the development of signs of sepsis.[1] There are several scoring systems used to help predict the severity of an attack of pancreatitis. The Apache II has the advantage being available at the time of admission as opposed to 48 hours later for the Glasgow criteria and Ranson criteria. However, the Glasgow criteria and Ranson criteria are easier to use.

Complications

Organ Failure

  • Modified Marshall Scoring System
Modified Marshall Scoring System
Organ System 0 1 2 3 4
Respiratory
PaO2/FiO2
>400 301-400 201-300 101-200 ≤101
Renal
Creatinine (μmol/l)
Creatinine (mg/dl)
≤134
<1.4
134-169
1.4-1.8
170-310
1.9-3.6
311-439
3.6-4.9
>439
>4.9
Cardiovascular
Systolic Blood Pressure (mmHg)
>90 <90, fluid responsive <90, not fluid responsive <90, pH <7.3 <90, pH <7.2

A score of 2 or more in any system defines the presence of organ failure.
A score for patients with pre-existing chronic renal failure depends on the extent of further deterioration of baseline renal function. No formal correction exists for a baseline creatinine ≥134 μmol/l or ≥1.4 mg/dl.

For non-ventilated patients, the FiO2 can be estimated from below:

Supplemental oxygen (l/min) FiO2 (%)
Room air 21
2 25
4 30
6–8 40
9–10 50
  • Transient organ failure = organ failure resolves within 48 h.
  • Persistent organ failure = organ failure persists for >48 h.[2][3][4]

Local Complications

▸ Should be suspected when there is persistence/recurrence of abdominal pain, secondary increases in pancreatic enzyme, increasing organ dysfunction, or the development of signs of sepsis.[1]

  • Acute Peripancreatic Fluid Collection (APFC)
▸ Peripancreatic fluid associated with interstitial edematous pancreatitis with no associated peripancreatic necrosis. This term applies only to areas of peripancreatic fluid seen within the first 4 weeks after onset of interstitial edematous pancreatitis and without the features of a pseudocyst.
CECT criteria
▸ Occurs in the setting of interstitial edematous pancreatitis.
▸ Homogeneous collection with fluid density.
▸ Confined by normal peripancreatic fascial planes.
▸ No definable wall encapsulating the collection.
▸ Adjacent to pancreas (no intrapancreatic extension).
  • Pancreatic Pseudocyst
▸ An encapsulated collection of fluid with a well defined inflammatory wall usually outside the pancreas with minimal or no necrosis. This entity usually occurs more than 4 weeks after onset of interstitial edematous pancreatitis to mature.
CECT criteria
▸ Well circumscribed, usually round or oval.
▸ Homogeneous fluid density.
▸ No non-liquid component.
▸ Well defined wall; that is, completely encapsulated.
▸ Maturation usually requires >4 weeks after onset of acute pancreatitis; occurs after interstitial edematous pancreatitis.
  • Acute necrotic collection (ANC)
▸ A collection containing variable amounts of both fluid and necrosis associated with necrotizing pancreatitis; the necrosis can involve the pancreatic parenchyma and/or the peripancreatic tissues.
CECT criteria
▸ Occurs only in the setting of acute necrotising pancreatitis.
▸ Heterogeneous and non-liquid density of varying degrees in different locations (some appear homogeneous early in their course).
▸ No definable wall encapsulating the collection.
▸ Location—intrapancreatic and/or extrapancreatic.
  • Walled-off necrosis (WON)
▸ A mature, encapsulated collection of pancreatic and/or peripancreatic necrosis that has developed a well defined inflammatory wall. WON usually occurs >4 weeks after onset of necrotising pancreatitis.
CECT criteria
▸ Heterogeneous with liquid and non-liquid density with varying degrees of loculations (some may appear homogeneous).
▸ Well defined wall, that is, completely encapsulated.
▸ Location—intrapancreatic and/or extrapancreatic.
▸ Maturation usually requires 4 weeks after onset of acute necrotizing pancreatitis

Systemic Complications

▸ Defined as exacerbation of pre-existing co-morbidity, such as coronary artery disease or chronic lung disease, precipitated by the acute pancreatitis.

Prognosis

There are several scoring systems used to help predict the severity of an attack of pancreatitis. The Apache II has the advantage being available at the time of admission as opposed to 48 hours later for the Glasgow criteria and Ranson criteria. However, the Glasgow criteria and Ranson criteria are easier to use.

APACHE II

Ranson Criteria

  • At admission:
  • Age in years >55years
  • White blood cell count > 16000/mcL
  • Blood glucose > 11 mmol/L (>200 mg/dL)
  • Serum AST > 250 IU/L
  • Serum LDH > 350 IU/L
  • After 48 hours:
  • Hematocrit fall > 10%
  • Increase in BUN by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
  • Hypocalcemia (serum calcium < 2.0 mmol/L (<8.0 mg/dL))
  • Hypoxemia (PO2 < 60 mmHg)
  • Base deficit > 4Meq/L
  • Estimated fluid sequestration > 6L

The criteria for point assignment is that a certain breakpoint be met at anytime during that 48 hour period, so that in some situations it can be calculated shortly after admission. It is applicable to both biliary and alcoholic pancreatitis.

Interpretation

  • If the score >=3, severe pancreatitis likely.
  • If the score < 3, severe pancreatitis is unlikely

Or

  • Score 0 to 2 : 2% mortality
  • Score 3 to 4 : 15% mortality
  • Score 5 to 6 : 40% mortality
  • Score 7 to 8 : 100% mortality

Glasgow Criteria

Glasgow's criteria[5]: The original system used 9 data elements. This was subsequently modified to 8 data elements, with removal of assessment for transaminase levels (either AST (SGOT) or ALT (SGPT) greater than 100 U/L).

  • On Admission
  • Age > 55 yr
  • WBC Count > 15 10 exp 9 /Lit
  • Blood Glucose > 10 mmol/L (No Diadetic History)
  • Serum Urea > 16 mmol/Lit ( No response to IV fluids)
  • Arterial oxygen saturation < 60
  • Within 48 hours

References

  1. 1.0 1.1 Banks, PA.; Bollen, TL.; Dervenis, C.; Gooszen, HG.; Johnson, CD.; Sarr, MG.; Tsiotos, GG.; Vege, SS.; Acosta, JM. (2013). "Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus". Gut. 62 (1): 102–11. doi:10.1136/gutjnl-2012-302779. PMID 23100216. Unknown parameter |month= ignored (help)
  2. Johnson, CD.; Abu-Hilal, M. (2004). "Persistent organ failure during the first week as a marker of fatal outcome in acute pancreatitis". Gut. 53 (9): 1340–4. doi:10.1136/gut.2004.039883. PMID 15306596. Unknown parameter |month= ignored (help)
  3. Mofidi, R.; Duff, MD.; Wigmore, SJ.; Madhavan, KK.; Garden, OJ.; Parks, RW. (2006). "Association between early systemic inflammatory response, severity of multiorgan dysfunction and death in acute pancreatitis". Br J Surg. 93 (6): 738–44. doi:10.1002/bjs.5290. PMID 16671062. Unknown parameter |month= ignored (help)
  4. Lytras, D.; Manes, K.; Triantopoulou, C.; Paraskeva, C.; Delis, S.; Avgerinos, C.; Dervenis, C. (2008). "Persistent early organ failure: defining the high-risk group of patients with severe acute pancreatitis?". Pancreas. 36 (3): 249–54. doi:10.1097/MPA.0b013e31815acb2c. PMID 18362837. Unknown parameter |month= ignored (help)
  5. Corfield AP, Cooper MJ, Williamson RC; et al. (1985). "Prediction of severity in acute pancreatitis: prospective comparison of three prognostic indices". Lancet. 2 (8452): 403–7. PMID 2863441.

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