Acute Pancreatitis is higher in women due

 Acute inflammatory process of the pancreas to a higher prevalence of

 Should be suspected in patients with severe gallstones
acute upper abdominal pain Alcohol - 25-35%
 Requires biochemical or radiologic evidence to - Alcohol may act by
establish diagnosis increasing the synthesis
of enzymes by
Atlanta classification pancreatic acinar cells to
Acute pancreatitis can be divided into two broad synthesize the digestive
categories: and lysosomal enzymes
1) Interstitial edematous acute pancreatitis, that are thought to be
which is characterized by acute inflammation of responsible for acure
the pancreatic parenchyma and peripancreatic pancreatitis or over-
tissues, but without recognizable tissue sensitization of acini to
necrosis. cholecystokinin
2) Necrotizing acute pancreatitis, which is HyperTriglycedidemia - Serum triglyceride
characterized by inflammation associated with >1000mg/dL can
pancreatic parenchymal necrosis and/or precipitate attacks of
peripancreatic necrosis acute pancreatitis
- 1-14%
Classification - Both primary (genetic) and
 Mild acute pancreatitis: absence of organ secondary (acquired)
failure and local or systemic complications; disorders of lipoprotein
intersitial pancreatitis – self-limited metabolism are
 Moderately severe acute pancreatitis: transient associated with
organ failure (resolves within 48 hours) and/or hypertriglyceridemia-
local or systemic complications without induced pancreatitis
persistent organ failure (>48 hours) - Acquired causes: obesity,
 Severe acute pancreatitis: persistent organ DM, hypothyroidism,
failure that may involve one or multiple organs; pregnancy and
necrotizing pancreatitis medications (estrogen,
tamoxifen, beta blockers)
Etiologies (G-A-T-E-D) ERCP (endoscopic - 3% - diagnostic ERCP
Etiology Notes retrograde cholangio - 5% - therapeutic ERCP
Gallstones - Most common (40-70%) pancreatography) - 25% sphincter of Oddi
- 2 factors have been manometric studies
suggested: 1) reflux of - Multiple operator, patient,
bile into the pancreatic and procedure related
duct due to transient factors increase the risk of
obstruction of the postERCP pancreatitis
ampulla during passage - Risk factors: lack of ERCP
of gallstones experience, sphincter of
2) obstruction at the Oddi dysnfunction,
ampulla secondary to difficult cannulation,
stone or edema resulting therapeutic>diagnostic
from the passage of the ERCP
stone Drugs - <5%
- Risk of developing acute - Prognosis of drug-induced
pancreatitis in patients pancreatitis is generally
with gallstones is excellent and mortality is
greater in men low
- However, the incidence - Mechanisms: immunologic
of gallstone pancreatitis reactions (6-
 marcaptopurine, more intense when supine;
aminosalicylates, relieved upon sitting with
sulfonamides); direct toxic the trunk flexed and knees
effect (diuretics, drawn up
sulfonamides)
accumulation of a toxic Gallstones pancreatitis: pain
metabolite (valproic acid, well-localized; onset of pain is
didanosine, pentamidine, rapid; reaching maximum
tetracycline), ischemia intensity 10-20 minutes
(diuretics, azathipine), Other - Severe acute pancreatitis:
intravascular thrombosis dyspnea due to
(estrogen) increased diaphragmatic inflammation,
viscosity of pancreatic pleural effusions, or ARDs
juice (diuretics and - Nausea and vomiting
steroids) Signs
Others - Genetic risk: may present as General PE - Distressed and anxious
recurrent acute patient
pancreatitis, childhood - Low-grade fever, tachycardia,
pancreatitis without a hypotension
known cause; mutations Shock - Hypovolemia secondary to
in the CFTR gene exudation of blood and
(autosomal recessive plasma proteins into the
pancreatitis), SPINK1, retroperitoneum
CTRC - Systemic effects of
- Pancreatic duct injury – proteolytic and lipolytic
blunt or penetrating enzymes released into the
trauma can damage the circulation
pancreas – however Disorientation, - Alcohol withdrawal,
uncommon due to the hallucination, hypotension/shock,
retroperitoneal location of agitation, coma electrolye imabalnce
the pancreas (hyponatremia), hypoxemia,
- Infections: viral (mumps, fever, toxic effects of
coxsackie virus, hepatitis pancreatic enzymes o CNS
B, CMV, varicella-zoster, Abdominal - Guarding more prominent in
herpes simplex, HIV), tenderness the upper abdomen
Bacteria (mycoplasma, Bowel sounds - Decreased or absent
legionella, leptospira, Jaundice - due to the edema of the
salmonella) (infrequent) pancreatic head with
- Fungi (aspergillus) compression of the
- Parasites (Toxoplasma, intrahepatic position of the
cryptosporidium, ascaris) CBD
- possible choledocholithiasis
Clinical manifestations (gallstone pancreatitis)
Symptoms - co-existent liver disease
Abdominal pain - Major symptom Pulmonary - basilar rales
- Quality: steady and boring in findings - atelectasis
character - pleural effusion (most
- Location: epigastrium and frequently left sided)
periumbilical region; may - ARDs
also be in RUQ Cullen’s sign - Blue discoloration around the
- Radiation: back, chest, umbilicus (results from
flanks, lower abdomen hemiperitoneum)
- Effects of position changes: Turner’s sign - Blue-red-purple or green-
 brown discoloration of the acute cholecystitis
flanks (reflects tissue commonly experience
catabolism of hemoglobin) increased discomfort while
Panniculitis with - 0.5 cm tender red nodules the area around the
subcutaneous fat that commonly appear over gallbladder fossa is
nerosis the distal extremities but palpated and may have an
may also occur over the associated inspiratory
scalp, trunk, buttocks arrest (Murphy’s sign)
- May be accompanied by - Mild elevations in serum
polyarthritis and aminotransferases and
thrombophlebitis in the legs amylase, along with
Differential diagnosis hyperbilirubinemia may be
- Includes other causes of epigastric abdominal seen
pain - But amylase or lipase
elevations of greater than
DDx Notes three times the upper limit
Peptic ulcer - Longstanding epigastric of normal are not usually
disease pain associated with
- Usually intermittent cholecystitis
- Does not radiate to the - Abd CT: gallbladder wall
back edema and pericholecystic
- May have a history of stranding
NSAID use or prior infection Perforated viscus - Sudden onset abdominal
with Helicobacter pylori pain and have peritoneal
- Normal amylase and lipase signs with guarding,
Choledocholithiasi - History of gallstones or rigidity and rebound
s biliary manipulation such as tenderness that are not
Or cholangitis ERCP associated with acute
- Serum ALT and AST pancreatitis
concentrations are - May have elevated
typically elevated early in amylase but elevations are
the course of biliary unlikely to be three times
obstruction the upper limit of normal
- Later, patients have - Upright chest films and abd
elevations in serum CT  free air can be seen
bilirubin, alkaline - Abd CT: free fluid,
phosphatase, exceeding phlegmon, bowel wall
the elevations in serum ALT pathology with adjacent
and AST inflammation
- Serum amylase and lipase Intestinal - Abdominal pain with
are normal obstruction anorexia, emesis,
Cholecystitis - It may be difficult to obstipation or constipation
differentiate acute - Elevation in serum amylase
cholecystits from acute and lipase
pancreatitis because an - History of prior abdominal
elevated serum amylase be surgeries or Crohn’s
found in both disease; on PE, may have
- Right upper quadrant or prior surgical scars or
epigastrium hernias
- Radiate to the right - Abd CT: dilated loops of
shoulder or back bowel with air fluid levels,
- Unlike patients with acute the etiology and site of
pancreatitis, patients with obstruction
 Mesenteric - Pain is often periumbilical define organ failure:
ischemia and out of proportion to 1) Respiratory
findings on physical 2) Cardiovascular
examination 3) Renal
- Risk factors: advanced age, - Persistent organ failure (>48
atherosclerosis, cardiac hours): most important clinical
arrythmias, severe cardiac finding with regard to severity
valvular disease, recent MI, Late (>2 - Protracted course of illness and
intraabdominal malignancy weeks) may require imaging to evaluate fo
- Patients may have local complications
elevations in amylase or - Persistent organ failure (>48
lipase but are usually less hours): most important clinical
marked than elevations finding with regard to severity
seen in acute pancreatitis - May require supportive measures
- Abd CT: focal or segmental (dialysis, ventilator support, TPN)
bowel wall thickening or
intestinal pneumatosis with Severity of Acute Pancreatitis
portal vein gas Severity Remarks
- Arterial or venous Mild - without local complications or
thrombosis or hepatic or organ failure
splenic infarcts may be - self-limited and subsides within 3-
seen 7 days after treatment
Hepatitis - Acute right upper quadrant - oral intake may be resumed if
pain, anorexia, general patient is hungry, has ormal bowel
malaise function and has no
- Dark urine, acholic stools, nausea/vomiting
jaundice and pruritus Moderatel - transient organ failure (resolves in
- PE: scleral icterus and y severe <48 hours) or local or systemic
tender hepatomegaly. complications in the absence of
Others - Inferior myocardial persistent organ failure
infarction Severe - persistent organ failure (>48 hours)
- Dissecting aortic aneurysm - CT scan or MRI should be obtained
- Connective tissue disorders to assess for necrosis and/or
with vasculitis complications
- Pneumonia
- DKA – often accompanied Diagnostics
by abdominal pain and Diagnostics Remarks and Expected Findings
elevated total serum Amylase - Acute pancreatitis: increased level
amylase; closely mimicking (>3x) N:23-85 U/L
pancreatitis; BUT serum - Returns to normal after 3-7 days
lipase is not elevated in - DDx for elevated amylase:
DKA macroamylasemia, papillary
cystadenocarcinoma of the ovary,
Revised Atlanta Classification: Clinical Course, benign ovarian cyst, carcinoma of
Definitions and Classifications the lung, intestinal infarction,
perforated viscus
Phases of Acute Pancreatitis Lipase - Acute pancreatitis: increased level
Phase Remarks (>3x); N: 0-160 U/L
Early (<2 - Severity is defined by clinical - Preferred test (more specific than
weeks) parameters amylase)
- Most exhibit SIRs and are - Elevated for 7-14 days
predisposed to organ failure Complete - Leukocytosis (15,000-20,000uL)
- Three organs should be assessed to blood - Hemoconcentration with
count hematocrit values >44% and a
failure to decrease levels in 24 Management
hours from admission   Usually, the disease is self-limited and subsides
necrotizing pancreatitis spontaneously
Renal - Azotemia (BUN >22mg/dL)  Resolution occurs within 3-7 days after
function associated with increased mortality treatment is instituted
due to loss of plasma into the
retroperitoneal space and Managemen Remarks
peritoneal cavity t
Serum - Hyperglycemia: due to decreased Conventional - Analgesics for pain
chemistry insulin release, increased glucagon measures - No oral alimentation (NPO)
release, increased output of - Oxygen via nasal cannula
adrenal glucocorticoids and Fluid - Most important intervention:
catecholamines; resuscitation safe, aggressive fluid resuscitation
- Hypocalcemia: due to decreased - Initial IVF: aggressive hydration
albumin (Normal calcium 2.2-2.7 at a rate of 5 to 10 mL/kg per
mmol/L or 8.5-10.5 mg/dL) hour of isotonic crystalloid
- Hyperbilirubinemia, serum ALP solution (eg, normal saline or
and AST: transiently elevated; lactated Ringer's solution) to all
particularly in acute biliary patients with acute pancreatitis,
obstruction from unless cardiovascular, renal, or
choledocholithiasis (gallstone other related comorbid factors
pancreatitis) preclude aggressive fluid
- ALT concentration 150 IU/L (~3 replacement
fold elevation) may distinguish - Severe volume depletion
gallstone pancreatitis from other (hypotension and tachycardia):
causes LR or PNSS at 15-20cc/hr in 30
- Markedly elevated serum LDH mins followed by 3 mg/kg/hr
levels: poor prognosis infusion to maintain urine output
- Hypertriglycerdemia >1000mg/dL >0.5cc/kg/hr
may precipitated attacks of acute - Fluid requirements are
pancreatitis reassessed at frequent intervals
ABG - Hypoxemia (arterial PO2 in the first six hours of admission
<60mmHg): may herald the onset and for the next 24 to 48 hours.
of ARDs - Targeted resuscitation strategy:
Abdominal - Helpful in indicating the severity of measure hematocrit and BUN
CT scan acute pancreatitis and the risk of every 8-12 hours and serum
morbidity and mortality electrolytes daily
- Aids in evaluating for - Adequate fluid replacement can
complications of acute pancreatitis be assessed by an improvement
- CT Imaging in Acute Pancreatitis in vital signs (goal heart rate
 2 types of pancreatitis are <120 beats/minute, mean
recognized on imaging: 1) arterial pressure between 65 to
interstitial 2) necrotizing 85 mmHg), urine output (>0.5 to
 Best evaluated 3-5 days into 1 cc/kg/hour) and reduction in
hospitalization when patients hematocrit (goal 35 to 44
are not responding to percent) and BUN over 24 hours,
supportive care t look for local particularly if they were high at
complicatons such as necrosis the onset
 Perfusion defects after IV - Monitoring the BUN may be
contrast may not appear until particularly important, as both
48 to 72 hours after onset of the BUN at the time of admission
acute pancreatitis and the change in BUN during the
 first 24 hours of hospitalization opiates, fentanyl can depress
predict mortality respiratory function. It can be
- low urine output may reflect the given both as a bolus as well as
development of acute tubular constant infusion. The typical
necrosis rather than persistent dose for the bolus regimen ranges
volume depletion. from 20 to 50 micrograms with a
- In the initial stages (within the 10-minute lock-out period (time
first 12 to 24 hours) of acute from the end of one dose infusion
pancreatitis, fluid replacement to the time the machine starts
has been associated with a responding to another demand).
reduction in morbidity and - Meperidine has been favored
mortality over morphine for analgesia in
- Inadequate hydration can lead to pancreatitis because studies
hypotension and acute tubular showed that morphine caused an
necrosis. increase in sphincter of Oddi
- Persistent hemoconcentration at pressure.
24 hours has been associated Abdominal - Helpful in indicating the severity
with development of necrotizing CT scan of acute pancreatitis and the risk
pancreatitis of morbidity and mortality
- Aids in evaluating for
Interpretation of hematocrit complications of acute
 Rising or persistently high pancreatitis
HCT: - CT Imaging in Acute Pancreatitis
(+) unstable VS (particularly  2 types of pancreatitis are
narrowing pulse pressure)  recognized on imaging: 1)
active plasma leakage and interstitial 2) necrotizing
need for bolus fluid  Best evaluated 3-5 days into
replacement hospitalization when patients
(+) stable and adeq UO, don’t are not responding to
require extra IVF supportive care t look for
 Decrease in HCT local complicatons such as
(+) unstable VS (narrowing necrosis
pulse pressure, tachycardia, - Perfusion defects after IV contrast
met acid, poor UO)  major may not appear until 48 to 72
hemorrhage and need for hours after onset of acute
urgent blood transfusion pancreatitis
(+) stable VS and adeq UO  ERCP - For severe acute biliary
hemodilution and/or pancreatitis with organ failure
reabsorption of extravasated and/or cholangitis within 24-72
fluid  IVF must be hours
discontinued Resumption - Early refeeding umproved
Pain control - Uncontrolled pain can contribute of diet outcome and allowed early
to the hemodynamic instability discharge
- Opioids are safe and effective at - Mild Acute Pancreatitis: oral
providing pain control in patients feedings (low fat solid diet, clear
with acute pancreatitis liquids) can be started
- Hydromorphone or fentanyl immediately if there is no nausea
(intravenous) may be used for and vomiting and abdominal pain
pain relief in acute pancreatitis. has resolved
Fentanyl is being increasingly - Severe Acute Pancreatitis:
used due to its better safety enteral nutrition is recommended
profile, especially in renal to prevent infectious
impairment. As with other complications
 - Parenteral nutrition should be Dx:
generally avoided unless the  Serum lipase, amylase
enteral route is not tolerated, not  CBC
available or not meeting caloric  BUN, crea
requirements  RBS, FBS, Lipid Profiles
Fine needle - Consider if no improvement in 7- o Serum glucose levels should be
aspiration of 28 days despite above measures monitored hourly in patients with
pancrease severe pancreatitis and hyperglycemia
Role of - In patients with gallstone (blood glucose greater than 180 to 200
surgery pancreatitis, cholecystectomy mg/dL) should be treated as it can
should be performed prior to increase the risk of secondary pancreatic
discharge to prevent recurrence infections. Hyperglycemia may result
of acute pancreatitis from parenteral nutritional therapy,
decreased insulin release, increased
Sample Order gluconeogenesis, and decreased glucose
Admit patient to _____ utilization. The management of
Secure consent for admission and procedures hyperglycemia is discussed in detail,
NPO strictly, resume diet slowly after 3rd to 6th day if separately.
without pain or vomiting  Serum Ca, Na, K, Mg, Phos, Alb, Uric Acid
IVF o Electrolytes should be monitored
- Initial IVF: aggressive hydration at a rate of 5 to 10 frequently in the first 48 to 72 hours
mL/kg per hour of isotonic crystalloid solution (eg, and especially with aggressive fluid
normal saline or lactated Ringer's solution) to all resuscitation.
patients with acute pancreatitis, unless o Hypocalcemia should be corrected if
cardiovascular, renal, or other related comorbid ionized calcium is low or if there are
factors preclude aggressive fluid replacement signs of neuromuscular irritability
- Severe volume depletion (hypotension and (Chvostek's or Trousseau's sign). For low
tachycardia): LR or PNSS at 15-20cc/hr in 30 mins Ca: Calcium gluconate slow IV or
followed by 3 mg/kg/hr infusion to maintain urine incorporate in IVF
output >0.5cc/kg/hr o Low magnesium levels can also cause
Monitor VS q2h including progress of abdominal pain hypocalcemia and should be corrected.
Monitor VS q1/q2 including progression of abdominal  LDH, Alk Phos
pain - Patients with acute pancreatitis should be  AST, ALT
monitored closely in the first 24 to 48 hours. Patients  TB, DB, IB
with organ failure will need ongoing monitoring for  ABG
other complications that might arise  ECG (rule out MI)
 Vital signs including oxygen saturation should  Plain Abd Xray supine and upright – to evaluate
be monitored and supplemental oxygen perforated viscus
administered to maintain arterial oxygen  Abdominal CT scan with pancreatic protocol
saturation of greater than 95 percent.  UTZ of liver, HBT, and Pancreas
 Blood gas analysis should be performed if
oxygen saturation is less than 90 percent or if Tx:
the clinical situation demands. Hypoxia may be Medical Therapy
due to splinting, atelectasis, pleural effusions, 1) H2 blockers: Ranitidine 50mg IV q8h OR
opening of intrapulmonary shunts, or acute 2) Omeprazole 40mg cap OD pre BF
respiratory distress syndrome (ARDS). Patients Pain relief: Meperidine HCl 25-50mg IVq6-8h
with persistent or progressive hypoxia should be Insert NGT if with ileus and hook to bedside bottle
transferred to an intensive care unit (ICU) for CBG monitoring
ventilatory support. Refer accordingly
Monitor I and O qshift
 Urine output should be measured hourly and Surgical option
fluids should be titrated to maintain urine 1) If with severe hemorrhage, necrotizing
output (>0.5 to 1 cc/kg/hour) pancreatitis, pancreatic abscess or large
 pseudocyst (5-6cm), do surgical drainage
(necrocystectomy)
2) If with associated gallstone/ileus, insert NGT to
decompress bowl
3) Cholecystectomy prior to discharge for
gallstone pancreatitis since recurrence rate is
high