Acute Pancreatitis

Most frequent GI cause for hospitalization + leading cause of in hospital deaths

CLASSIFICATIONS
Revised Atlanta Classification
– Interstitial edematous acute pancreatitis
– Necrotizing acute pancreatitis
According to Severity
– Mild acute pancreatitis – no organ failure/complications
– Mod pancreatitis – transient organ failure +/- local or systemic complications
– Severe acute pancreatitis – persistent organ failure (> 48hrs)

RISK FACTORS
Gallstones (most common), Alcohol, Hypertriglyceridemia, Post ERCP, Medications, Micro-organisms, Trauma, Genetic risk, Hypercalcemia

CLINICAL FEATURES
Severe epigastric pain, RUQ pain in some cases, nausea, vomiting Severe pancreatitis → Cullen sign, Grey Turner sign (suggest necrotizing / hemorrhagic pancreatitis)

LABORATORY
Hematocrit – elevated due to third spacing
Serum lipase – sensitivity and specificity of 82-100%, rises 4-8 hrs after attack, peaks at 24 hrs
CRP > 150, indicator for severe pancreatitis
BUN – most reliable to predict severity; every increase of BUN by 5 in 24 hrs = Odds ratio mortality 2.2
Calcium – check after initial treatment to make sure does not elevate
Triglycerides – usually caused if > 1000, risk if > 500
IgG4 – if autoimmune pancreatitis is suspected Genetic testing – if <35 and genetic factors suspected (PRSS1, SPINK1, CFTR, CTRC, CASR, Claudin-2)
CXR – pleural effusion / infiltrates within 24 hrs – necrosis + organ failure indication
CT – most frequently used to diagnose AP.
MRI / MRCP – increasingly used to diagnose AP + severity. MRI as effective as CT.

SCORING
Ranson’s Criteria or Apache II Score

TREATMENT

• Fluid Replacement – 5-10 ml/kg/hr. Also assess hydration status, if hypotension and tachycardia do 20 ml/kg  over 30 mins followed by 3 ml/kg/hr for 8-12 hrs. Monitor Cr and BUN.
• Hypertriglyceridemia – initial treatment with apheresis + insulin Apheresis → passing blood through machine to clean lipids, selected patients with severe HTGP – costly Insulin → @ 0.1-0.3 U/kg/hr + 5% dextrose (Glucose goal 150-200) [2].
• Pain Control – opioids are safe and effective. Hydromorphone or Fentanyl may be used for pain control.  Fentanyl is safer, in renal insufficiency as well. Be Careful of using morphine – may cause increased Sphincter of Oddi pressure.
• Feeding – NG tube in moderate to severe pancreatitis or those who can’t tolerate oral feeds. In the absence of ileus, nausea or vomiting, initiate oral feeds within 24 hrs as tolerated. Low residue, low fat, soft diet may be started or clear liquid diet.
• Antibiotics – 20% may develop infections – sepsis, URI, UTI – start antibiotics.  If cultures negative, stop antibiotics.

COMPLICATIONS
AKI is a frequent complication of severe pancreatitis, develops late in the course.  Carries poor prognosis, mortality rate > 75% – possibly due to volume depletion by complex vascular & humoral factors [1].
Pancreatic pseudocyst occurs more than 4 weeks after pancreatitis – usually drained by GI / IR
Thrombosis – splanchnic vein in about 1-24% with acute pancreatitis Pseudoaneurysm – rare, suspect when unexplained GI bleeding or sudden hematocrit drop

References:
1. Nassar et al. AKI associated with Acute Pancreatitis. CJASN. May 2019.
2. Gelrud et al. Hypertriglyceridemia-induced acute pancreatitis. Uptodate. (Accessed 24 May 2019)
3. Vege et al. Etiology & Predicting the severity of acute pancreatitis. Uptodate. (Accessed 24 May 2019)
4. Vege et al. Clinical manifestations & diagnosis of acute pancreatitis. Uptodate. (Accessed 24 May 2019)