Dr. Salazar presented a fascinating case of a male who presented with the sudden onset of severe epigastric abdominal pain and was found to have pancreatitis.
Etiology
There are several causes of acute pancreatitis, with gallstones (40%) and alcohol (30%) being the most common. Other common causes include:
Drugs (Furosemide, Thiazides, Sulfas, Estrogen, ACE inhibitors, Valproic Acid, Mesalamine, 6MP/AZA, Dapsone, DPP-4 inhibitor)
Pancreatic Obstruction (From a tumor or annular pancreas)
Hypertriglyceridemia(Needs to be a triglyceride level more than 1000 although it is generally more than 4500)
Hypercalcemia
Post ERCP (5% of cases, most patients present with an asymptomatic rise in amylase)
Ischemic causes, including vasculitis, cholesterol emboli, hypovolemic shock
Post-traumatic (Blunt abdominal trauma, pancreatic/biliary surgery)
Autoimmune (inc. IgG4, +ANA)
Infectious causes, such as Coxsackie, mumps, EBV, CMV, HAV, HBV, mycoplasma, Tb
Scorpion sting
Classifications of Pancreatitis
Acute pancreatitis is classified as mild acute, moderately severe acute, or severe acute.
Mild Acute= Absence of organ failure, local, or systemic complications
Moderately Severe Acute= No organ failure (or transient <48 hours organ failure) and/or local complications
Severe Acute= Persistent organ failure >48hr
Presentation of Pancreatitis
Classically, this presents with epigastric abdominal pain
Radiates to back (50% of patients).
Constant
Often relief when leaning forward.
You can also have RUQ if this is gallstone pancreatits. Other symptoms include Nausea/Vomiting (90% of patients) and dyspnea (thought to be secondary to diaphragmatic inflammation or pleural effusion).
Be aware that about 5-10% have painless disease and unexplained hypotension!
Diagnosis of Pancreatitis
Diagnosis of acute pancreatitis requires two of three criteria:
1. Acute onset of upper abdominal pain
2. Serum amylase or lipase level increased by at least three times the upper limit of normal
The amylase level does not correspond with severity!
You can get a false positive amylase elevation with acidemia, renal failure, macroamylasemia, or other abdominal/salivary gland process
Lipase is more specific, but you can still get a false positive with renal failure, DKA, HIV, macrolipasemia, or other abdominal process.
3. Characteristic findings on cross-sectional imaging
How do you prognosticate in pancreatitis?
There are several classification systems that have been developed to prognosticate and classify pancreatitis.
The American College of Gastroenterology (ACG) generally recommends just taking the following into account.
Patient characteristics: Age >55 years, obesity (body mass index >30 kg/m2), altered mental status, and presence of comorbid disease
SIRS Criteria, especially if >48 hours
Laboratory findings: BUN >20 mg/dl or rising BUN, hematocrit >44% or rising hematocrit, elevated creatinine
Radiology findings, including pleural effusions, pulmonary infiltrates, and multiple or extensive extrapancreatic collections
How do I know if my patient needs the ICU?
The following guidelines are suggested for determining ICU admission.
Pulse <40 or >150
SBP <80, DBP>120, or MAP <60
RR >35
Serum Na+ <110 or >170
Serum K+ <2.0 or >7.0
PaO2 <50
Serum Glucose >800mg/dL
pH <7.1 or >7.7
Anuria
Coma
Consider admitting the following patients to the ICU to minimize sequelae in the following populations:
SIRS >48 hours
Age >60
Cardiac, pulmonary disease or obesity
Hematocrit >44, BUN >20, or creatinine >1.8
Management of Pancreatitis
Management focuses on appropriate hydration, pain/nausea control, and nutrition as well as close monitoring.
1. Hydration- Most beneficial in the first 12 to 24 hours!!!
Your goal is to treat with 5-10 mL/kg/hr of isotonic crystalloid.
LR is preferred over Normal Saline as this was found to reduce SIRS. It is contraindicated if hypercalcemic.
BUN during first 24 hours of hospitalizations predict mortality!
Hydration is key because inadequate hydration was associated with development of necrotizing pancreatitis and lactic acidosis. However over-vigorous fluid resuscitation associated with increased need for intubation and increased risk of abdominal compartment syndrome.
2. Nutrition- Earlier enteral nutrition is key. It has been associated with reduced infectious complications, organ failure, and mortality compared with total parenteral nutrition. Enteral feeding prevents infections by promoting gut mucosal health and barrier function necessary for preventing leakage or translocation of bacteria that can infect other tissues.
In mild acute pancreatitis, initiate oral nutrition when pain and nausea allow.
If severe pancreatitis and planned NPO >7d, give enteral nutrition at 48-72 hours. (NJ is preferred over NG).
3. Analgesia
You can use meperidine, morphine, or hydromorphone. There is a risk of Sphincter of Oddi spasm with morphine HOWEVER this has not been shown to adversely affect outcome (i.e. there is no aggravation of pancreatitis & no increased cholecystitis )
Fentanyl use for analgesia has been increasing due to safety profile in renal impairment though short lived.
References
Sabatine, M. S. (2014). Pocket medicine (Fifth edition.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins.
Smellie WS. Hypertriglyceridaemia in diabetes. BMJ. 2006;333(7581):1257–1260. doi:10.1136/bmj.39043.398738.DE
Vege, SS. Management of acute pancreatitis. In: UpToDate, Witecomb, DC (Ed), UpToDate, Waltham, MA, 2014.
Wu BU, Hwang JQ, Gardner TH, Repas K, Delee R, Yu S, Smith B, Banks PA, Conwell DL. Lactated Ringer's solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clin Gastroenterol Hepatol. 2011 Aug;9(8):710-717.e1. doi: 10.1016/j.cgh.2011.04.026. Epub 2011 May 12. PubMed PMID: 21645639.
Wu BU, Johannes RS, Sun X, Conwell DL, Banks PA. Early changes in blood urea nitrogen predict mortality in acute pancreatitis.Gastroenterology. 2009 Jul;137(1):129-35. doi: 10.1053/j.gastro.2009.03.056. Epub 2009 Apr 1. PubMed PMID: 19344722
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