ACUTE PANCREATITIS
Alex Mutua
Bsc clinical medicine
Pancreatitis is an inflammatory process in
which pancreatic enzymes auto digest the
gland.
Pancreatitis can also recur intermittently,
contributing to the functional and morphologic
loss of the gland; recurrent attacks are
referred to as chronic pancreatitis.
Both forms of pancreatitis may present in the
emergency department (ED) with acute
clinical findings.
Diagnostic imaging is unnecessary in most
cases but may be obtained when the diagnosis
is in doubt, when severe pancreatitis is
present, or when an imaging study might
provide specific information needed to answer
a clinical question.
GOALS OF MEDICAL MANAGEMENT
provide aggressive supportive care,
to decrease inflammation,
to limit infection or superinfection, and
to identify and treat complications as
appropriate.
ANATOMY
The pancreas is an elongated, tapered organ behind
the stomach.
The right side of the organ—called the head—is the
widest part of the organ and lies in the curve of the
duodenum
The tapered left side extends slightly upward—called
the body of the pancreas—and ends near the spleen—
called the tail.
pancreas is made up of 2 types of glands:
Exocrine. The exocrine gland secretes digestive
enzymes.
Endocrine. The endocrine gland, which consists of
the islets of Langerhans, secretes hormones into the
bloodstream.
CAUSES
Most common causes
Long-standing alcohol consumption
Alcoholics are usually admitted with an acute
exacerbation of chronic pancreatitis.
Occasionally, however, pancreatitis can develop in
a patient with a weekend binging habit
biliary stone disease: gallstones passing into the bile
duct and temporarily lodging at the sphincter of Oddi.
Mnemonic: GET SMASHED
Gallstones
Ethanol (Alcohol)
Trauma
Steroids
Mumps
Autoimmune disease, such as SLE
Scorpion venom (a rare and unlikely cause in most countries)
Hypercalcaemia
Endoscopic retrograde cholangio-pancreatography (ERCP)
Drugs, such as Azathioprine, NSAIDs, or Diuretics
pathophysiology
PATHOPHYSIOLOGY
There is a premature and exaggerated
activation of the digestive enzymes within
the pancreas.
The resulting pancreatic inflammatory
response causes an increase in vascular
permeability and subsequent fluid loss into the
third space (transcellular space, e.g.
peritoneal cavity)
Enzymes are released from the pancreas into the
systemic circulation, causing autodigestion of
fats (resulting in a ‘fat necrosis’) and blood vessels
(sometimes leading to hemorrhage in
the retroperitoneal space).
Fat necrosis can cause the release of free fatty acids,
reacting with serum calcium to form chalky deposits in
fatty tissue, resulting in hypocalcemia.
In acute pancreatitis, parenchymal edema and
peripancreatic fat necrosis occur first; this is known as
acute edematous pancreatitis.
When necrosis involves the parenchyma,
accompanied by hemorrhage and dysfunction of the
gland, the inflammation evolves into hemorrhagic or
necrotizing pancreatitis.
CLASSIFICATION- according to
severity
Mild acute pancreatitis which is characterized by
the absence of organ failure and local or systemic
complications
Moderately severe acute pancreatitis which is
characterized by transient organ failure (resolves
within 48 hours) and/or local or systemic
complications without persistent organ failure (>48
hours)
Severe acute pancreatitis which is characterized
by persistent organ failure that may involve one or
multiple organs
RANSONS CRITERIA
The original Ranson's criteria is a scoring system that
uses 11 parameters to assess the severity of acute
pancreatitis.
The 11 parameters are age, white blood cell count
(WBC), blood glucose, serum aspartate transaminase
(AST), serum lactate dehydrogenase (LDH), serum
calcium, fall in hematocrit, arterial oxygen (PaO2),
blood urea nitrogen (BUN), base deficit, and
sequestration of fluids
AT ADMISSION:
Age in years > 55 years
WBC count > 16000 cells/mm3
Blood glucose > 11.11 mmol/L (> 200 mg/dL)
Serum AST > 250 IU/L
Serum LDH > 350 IU/L
AFTER 48 HOURS:
Serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
Hematocrit fall > 10%
Oxygen (hypoxemia PaO2 < 60 mmHg)
BUN increased by 1.8 or more mmol/L (5 or more
mg/dL) after IV fluid hydration
Base deficit (negative base excess) > 4 mEq/L
Sequestration of fluids > 6 L
PRESENTATION
The cardinal symptom of acute pancreatitis is
abdominal pain
characteristically dull, boring, and steady.
Usually, the pain is sudden in onset and gradually
intensifies in severity until reaching a constant
ache.
Most often, it is located in the upper abdomen,
usually in the epigastric region, but it may be
perceived in the flanks,
The pain radiates to the back in approximately one
half of cases.
Nausea and vomiting are often present,
accompanying anorexia.
Diarrhea can also occur.
Positioning can be important, because the discomfort
frequently improves with the patient sitting up and
bending forward.
Physical examination
Fever (76%) and tachycardia (65%) are common
abnormal vital signs; hypotension may be noted
Abdominal tenderness with guarding (68%), and
distention (65%)
bowel sounds are often diminished or absent because
of gastric and transverse colonic ileus;
guarding tends to be more pronounced in the upper
abdomen
A minority of patients exhibit jaundice (28%)
Some patients experience dyspnea (10%), which may
be caused by irritation of the diaphragm (resulting
from inflammation
In severe cases, hemodynamic instability is evident
(10%) and hematemesis or melena sometimes
develops (5%)
patients with severe acute pancreatitis are often pale,
diaphoretic, and listless
RARER SIGNS
Rarer signs that are often described are
Grey Turner’s Sign (bruising in the flanks)
and
Cullen’s Sign (bruising around the
umbilicus), representing retroperitoneal
haemorrhage
Tetany may occur from hypocalcaemia
secondary to fat necrosis
Differential diagnosis
Peritonitis
Perforated viscus
Peptic ulcer disease
Bowel obstruction
Mesenteric ischemia
Investigations
Serum amylase and lipase amylase or lipase levels at
least 3 times above the reference range are generally
considered diagnostic of acute pancreatitis
LFTs: Elevated ALT (alanine aminotransferase)suggests
gallstone pancreatitis
Complete blood count: leukocytosis with left shift
C- reactive protein: high levels indicate severity of
disease
Serum electolytes and renal functions
Radiographs
Limited use
Perform to rule out perforated viscus
A CXR should be undertaken to look for pleural
effusion or signs of ARDS.
ultrasonography
May detect gallstones (demonstrating dilation of the
bile ducts)
Can not determine severity
COMPUTED TOMOGRAPHY
generally not indicated for patients with mild
pancreatitis unless a pancreatic tumor is suspected
(usually in elderly patients).
It is always indicated in patients with severe acute
pancreatitis and is the imaging study of choice for
assessing complications.
Scans are seldom needed within the first 72 hours
after symptom onset unless the diagnosis is
uncertain, because inflammatory changes are often
not radiographically present until this time
OTHER STUDIES
Magnetic resonance
cholangiopancreatography (MRCP). not as
sensitive as endoscopic retrograde
cholangiopancreatography (ERCP)but it is
safer, noninvasive, and fast,
Endoscopic retrograde
cholangiopancreatography (ERCP)
MANAGEMENT - MILD
The patient is kept NPO
Intravenous (IV) fluid hydration is provided.
Analgesics are administered for pain relief.
Antibiotics are generally not indicated.
Feeding should be introduced enterally as the
patient’s anorexia and pain resolves. Patients
can be initiated on a low-fat diet initially
MANAGEMENT - SEVERE
require intensive care.
The goals of medical management are
to provide aggressive supportive care,
to decrease inflammation,
to limit infection or superinfection, and
to identify and treat complications as
appropriate.
In moderately severe to severe pancreatitis, oral
feeding may not be tolerated due to postprandial
pain, nausea or vomiting related to gastroduodenal
inflammation and/or extrinsic compression from fluid
collections leading to gastric outlet obstruction.
Patients may require parenteral feeding if caloric and
protein needs are not met.
when the local complications start improving, oral
feeds can be initiated and advanced as tolerated.
ANTIBIOTICS
Up to 20 percent of patients with acute pancreatitis
develop an extrapancreatic infection (eg, bloodstream
infections, pneumonia, and urinary tract infections)
Extrapancreatic infections are associated with an
increase in mortality.
When an infection is suspected, antibiotics should be
started while the source of the infection is being
determined.
COMPLICATIONS OF ACUTE
PANCREATITIS
SYSTEMIC
LOCAL
SYSTEMIC COMPLCATIONS
Disseminated Intravascular Coagulation (DIC)
Acute Respiratory Distress Syndrome (ARDS)
Hypocalcaemia
Hyperglycaemia
Secondary to destruction of islets of
Langerhans and subsequent disturbances to
insulin metabolism
Hypovolemic shock and multiorgan failure
LOCAL COMPLICATIONS
Pancreatic Necrosis
Ongoing inflammation eventually leads to
ischaemic infarction of the pancreatic tissue,
such progression should be suspected in
patients with evidence of persistent systemic
inflammation for more than 7-10 days after
the onset of pancreatitis.
Pancreatic necrosis is prone to infection
LOCAL COMPLICATIONS
Pancreatic Pseudocyst
A pancreatic pseudocyst is a collection of
fluid containing pancreatic enzymes, blood, and necrotic tissue;
they can occur anywhere within or adjacent to the pancreas,
however are usually seen in the lesser sac obstructing the
gastro-epiploic foramen by inflammatory adhesions..
They are typically formed weeks after the initial acute
pancreatitis episode. They lack an epithelial lining,
Pseudocysts may be found incidentally on imaging or can
present with symptoms of mass effect, such as biliary
obstruction or gastric outlet obstruction.
They are prone to haemorrhage or rupture, and can become
infected.
