A.

Personal Data
Name: Irvin Magno
Address: Brgy. 17, Batac City
Hospital Number:
Gender: Male
Age: 29
Date of Birth: 09/24/1991
Place of Birth: Batac City
Civil Status: Married
Religion: Baptist
Educational Attainment: Vocational Graduate
Occupation: Farming
Chief Complaint: Sharp epigastric pain (9/10) radiating from left upper quadrant to
back accompanied by nausea and vomiting.
Admitting Diagnosis: Acute Pancreatitis
Date and Time of Admission: 10/05/2020 @ 6:05PM
Admitting Physician: Dr. G
Attending Physician: Dr. S
Final Diagnosis: Acute Pancreatitis, Resolved
Date and Time of Discharge: 10/11/2020
B. Pathophysiology
A. Anatomy and Physiology
The illustration in Figure 1 demonstrates the anatomical relationships between the
pancreas and organs surrounding it in the abdomen. The pancreas is a long,
slender organ most of which is located posterior to the bottom half of the
stomach. The regions of the pancreas are the head, body, tail and uncinate process
(Figure 2). The distal end of the common bile duct passes through the head of the
pancreas and joins the pancreatic duct as it enters the intestine (Figure 2). Because
the bile duct passes through the pancreas before entering the intestine, diseases of
the pancreas such as a cancer at the head of the pancreas or swelling and/or
scarring of the head of the pancreas from pancreatitis can block the bile duct
system resulting in jaundice in a patient. As seen in Figure 1, the pancreas is
situated deep in the abdomen and thus is usually protected from trauma. However,
occasionally severe trauma as might occur from a steering wheel in an auto
accident can crush the pancreas against the vertebral column that sites just behind
the pancreas. Such an injury can result in pancreatitis.

Figure 1. Cross sectional anatomy of the abdomen. This cartoon represents the
anatomical features of a slice of the abdomen at the level depicted in the upper
right hand corner of the figure. Anterior to the pancreas are the stomach, colon,
omentum and loops of small intestine. Posterior to the pancreas are the portal
vein, inferior vena cava, aorta, superior mesenteric artery and vein, kidneys and
vertebrae. The distal common bile duct passes through the head of the pancreas.

Figure 2. Anatomic regions and blood vessels of the pancreas. The anatomic
regions are the head, neck, body and tail. Behind the pancreas lie the portal vein,
inferior vena cava, aorta and the superior mesenteric artery and vein. The distal
common bile duct passes through the head of the pancreas.

The pancreas receives blood from two major arterial supplies (Figure 2). Because
of the dual blood supply, ischemia to the pancreas from vascular obstruction is
uncommon. Venous blood leaving the pancreas is via the splenic vein as the
spleen is continuous to the tail of the pancreas; this vein empties into the portal
vein which carries blood from the GI tract to the liver. Diseases such as
pancreatitis and pancreatic cancer can cause thrombosis and/or blockage of the
draining of the spleen and pancreas. In this case the spleen becomes engorged
with blood causing its enlargement which results in several undesirable
consequences.

The pancreas is connected by the nervous system containing both sensory neurons
and effector neurons. The sensory neurons function for pain perception so that
diseases of the pancreas cause significant pain while the effector neurons are
involved in regulating the secretions of both the exocrine and endocrine pancreas.
It is important to point out that there are important inter-relationships between the
endocrine (Islets of Langerhans) and exocrine pancreas. As shown in figure, the
blood flow from the endocrine pancreas enters the capillaries of the exocrine
tissue surrounding each of the islets before entering the general circulation (4).
Thus, the exocrine pancreatic tissue surrounding the islets is exposed to very high
concentrations of hormones such as insulin coming from the islets. Normally, the
islet hormones promote the function of the exocrine gland including the
regulation of digestive enzyme synthesis (13, 14, 32).
The pancreas is divided into an exocrine portion (acinar and duct tissue) and an
endocrine portion (islets of Langerhans). The exocrine portion, comprising 85%
of the mass of the pancreas is composed of acinar tissue which synthesizes, stores
and secretes digestive enzymes; and ductal tissue which secretes water and
NaHCO3. The endocrine portion secretes its hormones into the blood stream. The
blood flow from the endocrine pancreas passes to the exocrine pancreas before
entering the general circulation.

Functions
The pancreas has both exocrine and endocrine function. The exocrine function is
devoted to secretion of digestive enzymes, ions and water into the intestine of the
gastrointestinal (GI) tract. The digestive enzymes are necessary to break down
carbohydrates, proteins and lipids into molecules that can be absorbed across the
surface lining of the GI tract into the body. Proteases, the enzymes involved in
digestion of proteins include trypsinogen and chymotrypsinogen. The enzyme
involved in the digestion of fats is lipase. Amylase, also secreted by the pancreas
breaks down starch and other carbohydrates. Secretion of this proenzyme is via
the hormones gastrin, cholecystokinin and secretin which are secreted by cells in
the stomach and duodenum in response to distension and or food.
Of note, there are digestive enzymes secreted by our salivary glands, stomach
and surface epithelium of the GI tract that also contribute to digestion of a meal.
However, the exocrine pancreas is necessary for most of the digestion of a meal
and without it there is a substantial loss of digestion that results in malnutrition.
The cells are filled with granules containing the digestive enzyme. These are
secreted in an inactive form called zymogens or proenzymes. Zymogens are
released through exocytosis in which calcium plays an important role.
These exocrine cells release their enzymes into a series of progressively larger
tubes called ducts that eventually join together to form the main pancreatic duct.
The main pancreatic duct runs the length of the pancreas and drains the fluid
produced by the exocrine cells into the duodenum.
The ions and water secreted are also critical for pancreas function as the resultant
fluid is necessary to carry the digestive enzymes through the pancreatic ductal
system into the intestine. In addition, the pH of the pancreatic secretions is
alkaline due to a very high concentration of NaHCO3 in the fluid. A major
function of the NaHCO3 is to neutralize the acidic pH of the gastric contents
delivered to the intestine from the stomach. A neutral pH in the intestinal lumen is
necessary for normal digestion and absorption.
The second functional component of the pancreas is the endocrine pancreas. The
endocrine pancreas is composed of small islands of cells called islets of
Langerhans. These endocrine cells don’t release their secretions into the
pancreatic ducts, instead they release hormones such as insulin and glucagon into
the bloodstream and these hormones in turn help control blood sugar.
 Approximately 3 million cell clusters called pancreatic islets are present in the
pancreas. Within these islets are 4 types of cells which are involved in the regulation of
blood glucose levels. Each type of cell secretes a different type of hormone: α cells
secrete glucagon which increases glucose in the blood, β cells secrete insulin which
decreases sugar in the blood, δ cells secrete somatostatin which regulates and stops α
and β cells and γ cells secrete pancreatic polypeptide. These act to control blood
glucose through secreting glucagon to increase levels of glucose and insulin too
decrease it.
B. Readings
Definition
Pancreatitis (inflammation of the pancreas) is a serious disorder that can range in
severity from a relatively mild, self-limiting disorder to a rapidly fatal disease that
does not respond to any treatment. Acute pancreatitis is commonly described as
an auto digestion of the pancreas by the exocrine enzymes it produces, principally
trypsin. Eighty percent of patients with acute pancreatitis have biliary tract disease
or a history of long-term alcohol abuse. Other less common causes of pancreatitis
include bacterial or viral infection, with pancreatitis occasionally developing as a
complication of mumps virus. Many disease processes and conditions have been
associated with an increased incidence of pancreatitis, including surgery on or
near the pancreas, medications, hypercalcemia, and hyperlipidemia. Up to 10% of
cases are idiopathic, and there is a small incidence of hereditary pancreatitis.
Despite the great advances in critical care medicine over the past 20 years, the
mortality rate of acute pancreatitis has remained at about 10%. Diagnosis of
pancreatic problems is often difficult and treatments are therefore delayed because
the organ is relatively inaccessible. There are no easy ways to see the pancreas
directly without surgery, and available imaging studies are often inadequate. In
addition to the acute form, there are hereditary and chronic forms of pancreatitis
which can devastate a person over many years. Sufferers often endure pain and
malnutrition, and are most likely left with a higher risk of pancreatic cancer.
 Mortality is high because of shock, anoxia, hypotension, or fluid and electrolyte
imbalances. Attacks of acute pancreatitis may result in complete recovery, may
recur without permanent damage, or may progress to chronic pancreatitis.

Causes and Risk Factors

1. History of Gallstones
The most common cause of acute pancreatitis is stones in the gallbladder.
Gallstones pass through the common bile duct to enter the small intestine. At the
entry of the small intestine, the main pancreatic duct joins or lies immediately next
to the common bile duct. It is believed that stones that get stuck in the common
bile duct impinge on the main pancreatic duct, causing an obstruction of the
normal flow of pancreatic fluid and leading to pancreatic injury. Another way that
a stone can cause pancreatitis is by causing a backflow of bile into the pancreatic
duct, resulting in pancreatic injury.
2. History of binge alcoholic drinking and chronic alcoholism
Excessive ethanol consumption is a common risk factor for acute
pancreatitis. Ethanol could lead to the onset of pancreatitis because of its effect on
intrapancreatic digestive enzyme activation through sensitizing acinar cells to
pathologic stimuli or stimulating the release of cholecystokinin from duodenal
cells.
3. High triglyceride level
The exact mechanism is unclear but it is thought to involve increased
concentrations of chylomicrons in the blood. Chylomicrons are usually formed 1-3
hours post-prandially and cleared within 8 hours. However, when triglycerides
levels exceed 1,000mg/dL, chylomicrons are almost always present. These low
density particles are very large and may obstruct capillaries leading to local
ischemia and acidemia. This local damage can expose triglycerides to pancreatic
lipases. The degradation of triglycerides to free fatty acids can lead to cytotoxic
injury resulting in further local injury that increases inflammatory mediators and
free radicals, eventually manifesting as pancreatitis.
4. Hypercalcemia
 In acute pancreatitis, hypercalcemia can be a causative factors. It is
believed that this will accelerates intrapancreatic conversion of trypsinogen to
trypsin which can lead to pancreatic damage due to auto digestion. Calcium plays
an important role in the activation of pancreatic enzymes.
5. Recent abdominal surgery and abdominal trauma
Acute pancreatitis occurs after a number of surgical procedures most
commonly operations performed on or near the pancreas. It is generally believed
that post-operative pancreatitis results from iatrogenic injury to the gland.
In view of central and relatively unprotected location of the pancreas in
the abdomen, it is surprising that pancreatic injury and traumatic pancreatitis are
relatively uncommon. They be associated with either penetrating or blunt trauma,
in the latter case resulting from compression of pancreas against the spine.
6. Tumors
Tumors that originate in the periampullary area like in the duodenum,
distal bile duct and pancreatic head will cause obstruction. Hence, obstruction and
backflow of bile and pancreatic enzymes.
7. Drugs
Certain drugs like use of steroids and H2 blocker antagonist receptor can
cause acute pancreatitis by direct damage to acinar cells.
8. Infections
Rising antibody titers to mumps virus and coxsackie virus and to
Mycoplasma pneumonia have been noted up to 30% of patients with acute
pancreatitis in whom no other factor has been identified as possibly causing the
episode of pancreatitis. It is assumed that these agents may induce pancreatitis by
infecting pancreatic acinar cells which may cause local injury.

Pathogenesis

Regardless of etiology, the initial step in pathogenesis of acute pancreatitis is

triggered by activation of intrapancreatic digestive enzyme and acinar cell injury. This
activation will lead in the so called auto digestion and cell destruction. This will
initiate inflammatory response leading to the release of chemical mediators which in
turn occurrence of inflammatory manifestations. After sometime, it will progress and
will develop into systemic inflammatory response syndrome. SIRS together with
hypoperfusion, sepsis and shock will lead to multi organ failure and eventually death.

Normally, pancreatic enzymes are released via the pancreatic duct however in
pancreatitis, pancreatic enzymes are released in the bloodstream causing damage to the
blood vessel walls leading to interstitial leakage and wrecking of extravascular havoc.
This will now be evident as interstitial edema in the radiographic exam. Among others,
this phenomenon will damaged fat cells, releases free fatty acids in which circulating
calcium will bind to it. As such, hypocalcemia occurs and this can be a measure or
determines the extent of enzymatic damage.

If necrosis occurs it is termed necrotizing pancreatitis which is a severe form.

Continuous hypoperfusion and hypoxia due to hypercoagulability secondary to
inflammatory response,this will lead ro necrosis. In turn, there will be accumulation of
large vacuoles acinar cells which is composed of enzymes and necrotic collections.
This will develop fibrosis around its periphery and will be seen as pseudocyst and
formation of walled-off pancreatic necrosis. This will be a good ground for bacterial
invasion and multiplication. If this persist, it can lead to perforation and pancreatic
contents will leak to the peritoneum leading to peritonitis, Cullen sign and Grey
Turner sign.

Signs and symptoms

Symptoms of acute pancreatitis include the following:

 Abdominal pain (cardinal symptom): Characteristically dull, boring, and

steady; usually sudden in onset and gradually becoming more severe until
reaching a constant ache; most often located in the upper abdomen and may
radiate directly through to the back. Pain is frequently acute in onset (24 to 48
hours after a heavy meal or alcohol ingestion); may be more severe after meals
and unrelieved by antacids.

 Nausea and vomiting, sometimes with anorexia

 Patients may have a history of the following:

 Recent operative or other invasive procedures

 Family history of hypertriglyceridemia

 Previous biliary colic and binge alcohol consumption (major causes of acute
pancreatitis)

The following physical findings may be noted, varying with the severity of the
disease:

 Fever (76%) and tachycardia (65%); hypotension

 Abdominal tenderness, muscular guarding (68%), and distention (65%);

diminished or absent bowel sounds

The following uncommon physical findings are associated with severe necrotizing
pancreatitis:

 Cullen sign (bluish discoloration around the umbilicus resulting from

hemoperitoneum)
 Grey-Turner sign (reddish-brown discoloration along the flanks resulting from
retroperitoneal blood dissecting along tissue planes); more commonly, patients
may have a ruddy erythema in the flanks secondary to extravasated pancreatic
exudate.

Diagnosis

Acute pancreatitis is confirmed by medical history, physical examination, and

typically a blood test (amylase or lipase) for digestive enzymes of the pancreas. Blood
amylase or lipase levels are typically elevated 3 times the normal level during acute
pancreatitis. In some cases when the blood tests are not elevated and the diagnosis is
still in question, abdominal imaging, such as a computed tomography (CT) scan, might
be performed.

After diagnosis is confirmed, certain imaging tests might be performed during

hospitalization or after to help identify the cause. Such tests include:
 Transabdominal ultrasound

This is commonly performed during hospitalization to specifically evaluate the

gallbladder for stones because gallstones are the most common cause of acute
pancreatitis. Ultrasound uses sound waves that bounce off the pancreas, gallbladder,
liver, and other organs, and their echoes generate electrical impulses that create an
image called a sonogram on a video monitor. If gallstones are causing inflammation,
the sound waves will also bounce off of them, showing their location.

 Endoscopic ultrasound (EUS)

This test is not commonly required during acute pancreatitis. Compared to

transabdominal ultrasound, it is relatively more invasive, in that a physician passes a
flexible thin tube down into the stomach. A camera and ultrasound probe are attached
to the end of the tube, which enable the physician to look at images of the gallbladder,
pancreas, and liver. The images are more sensitive than those of transabdominal
ultrasound in detecting small stones in the gallbladder and bile ducts that may have
been missed. It can also visualize the pancreas for abnormalities.

 Magnetic resonance cholangiopancreatography (MRCP)

MRCP uses magnetic resonance imaging (MRI), a noninvasive procedure that

produces cross-section images of parts of the body. After being lightly sedated, the
patient lies in a cylinder-like tube. The technician injects dye into the patient’s veins,
which helps show the pancreas, gallbladder, and pancreatic and bile ducts. This is
another sensitive test for evaluating the gallbladder, bile ducts, and pancreas for causes
of acute pancreatitis.

 Computerized tomography (CT)

A CT scan is a noninvasive radiograph (x-ray) that produces 3-dimensional

images of parts of the body. The patient lies on a table that slides into a donut-shaped
machine. Typically not performed initially for an episode of acute pancreatitis, it may
be performed when a diagnosis is uncertain or several days into hospitalization to
evaluate the extent of pancreatic damage when a patient is not recovering as quickly as
expected.

Risk Stratification of Acute Pancreatitis

In most cases, acute pancreatitis resolves with therapy, but approximately 15% of
patients develop severe disease.3 Severe acute pancreatitis can lead to life-threatening
failure of multiple organs and to infection. Therefore, it is extremely important to seek
medical attention if experiencing signs or symptoms of acute pancreatitis. Several
clinical risk-scoring systems are available to help physicians predict who is most likely
to develop severe acute pancreatitis. These scores rely on several pieces of clinical
data collected at admission and during the first 48 hours of hospitalization. Commonly
used scoring systems include:

 The Ranson criteria

 The APACHE II score

Treatment

Fluids
One of the primary therapies for acute pancreatitis is adequate early fluid
resuscitation, especially within the first 24 hours of onset. Pancreatitis is
associated with a lot of swelling and inflammation. Giving fluids intravenously
prevents dehydration and ensures that the rest of the organs of the body get
adequate blood flow to support the healing process.
Nutritional Support
Initially, no nutrition is given to rest the pancreas and bowels during the
first 24 to 48 hours. After 48 hours, a plan to provide nutrition should be
implemented because acute pancreatitis is a highly active state of inflammation
and injury that requires a lot of calories to support the healing process. In most
cases, patients can start to take in food on their own by 48 hours. If this is not
possible, then a feeding tube that is passed through the nose into the intestines can
be used to provide nutrition. This method is safer than providing nutrition
intravenously. There is no benefit to using probiotics for acute pancreatitis.
 Pain Control
Intravenous medications, typically potent narcotic pain medications, are
effective in controlling pain associated with acute pancreatitis. Nausea is a
common symptom and can be due to pancreatic inflammation as well as slowing
of the bowels. Effective intravenous medications are available for nausea. Pain
and nausea will decrease as the inflammation resolves.
Treatment of Underlying Issues

In addition to providing supportive care, underlying causes need to be

promptly evaluated. If the acute pancreatitis is thought to be due to gallstones,
medication, high triglycerides, or high calcium levels within the patient’s body (or
other external causes), directed therapy can be implemented.

Endoscopic Retrograde Cholangiopancreatography (ERCP)

ERCP is a procedure in which a physician with specialized training passes

a flexible, thin tube with a camera attached to the end through the patient’s mouth
and into the first part of the small intestine, where the bile duct and pancreatic
duct exit. With this device, a small catheter can be passed into the bile duct to
remove gallstones that might have gotten stuck and are the cause of pancreatitis.
In certain situations, a special catheter can also be passed into the pancreatic duct
to help the pancreas heal.

The Following Procedures can be performed with ERCP:

 Sphincterotomy
Using a small wire on the endoscope, a physician finds the muscle that
surrounds the pancreatic duct or bile duct and makes a tiny cut to enlarge the
duct opening. When a pseudocyst is present, the duct is drained.
 Gallstone Removal
 The endoscope is used to remove pancreatic or bile duct stones with a tiny
basket. Gallstone removal is sometimes performed along with a
sphincterotomy.
 Stent Placement
Using the endoscope, a physician places a tiny piece of plastic or metal
that looks like a straw into a narrowed pancreatic or bile duct to keep it open.
 Balloon Dilatation
Some endoscopes have a small balloon that a physician uses to dilate, or
stretch, a narrowed pancreatic or bile duct. A temporary stent can be placed
for a few months to keep the duct open.
It is well documented that one of the main side effects of ERCP is
pancreatitis; however, there are several clearly defined situations when urgent
ERCP is indicated for acute pancreatitis.
Antioxidant therapies
Basic and clinical evidence suggests that the development of both acute
pancreatitis (AP) and chronic pancreatitis (CP) can be associated with oxidative stress.
Findings show that free radical activity and oxidative stress indices are higher in the
blood and duodenal juice of patients with pancreatitis.
Based on these findings, the idea of using antioxidant regimens in the
management of both AP and CP as a supplement and complementary in combination
with its traditional therapy is reasonable. In practice, however, the overall
effectiveness of antioxidants is not known, and the best mixture of agents and dosages
is not clear. Currently, a trial of a mixture of antioxidants containing vitamin C,
vitamin E, selenium, and methionine is reasonable as one component of overall
medical management.

In summation, there is no definite consensus on the dosage, length of therapy, and

ultimately, the benefits of antioxidant therapy in the management of AP or CP. Further
well-designed clinical studies are needed to determine the appropriate combination of
agents, time of initiation, and duration of therapy.

Treatment Considerations for Severe Acute Pancreatitis

Necrotizing Pancreatitis:
The definition of severe acute pancreatitis includes cases in which a
portion of pancreatic tissue is no longer viable because of injury, this is called
necrosis. Over time, the body will resorb this dead tissue. In some cases, this dead
tissue can become a source of infection. When infection is suspected, diagnosis
can be made by needle biopsy, and if confirmed, medical treatment with
antibiotics is required along with consideration of drainage.

Prognosis
The overall mortality in patients with acute pancreatitis is 10-15%. Patients with
biliary pancreatitis tend to have a higher mortality than patients with alcoholic
pancreatitis. This rate has been falling over the last 2 decades as improvements in
supportive care have been initiated. In patients with severe disease (organ failure),
who account for about 20% of presentations, mortality is approximately 30%.
This figure has not decreased in the past 10 years. In patients with pancreatic
necrosis without organ failure, the mortality approaches zero.