SALIENT FEATURES

A 60/M came in for consult due to epigastric pain which started 2 weeks prior to
consult. It was crampy to burning in character with VAS 5/10, aggravated by food and
slightly relieved by antacid. One day PTC, the patient had 2 episodes of vomiting and
the pain worsened to 8/10, with no relief upon intake of antacid. The patient is a known
smoker of 30-pack years, and a non-alcoholic drinker. He has controlled hypertension
and had no previous operations.
Upon physical examination, the patient is conscious and coherent. His vital signs
are normal and he has a normal BMI of 20.8. His abdomen is flat with normoactive
bowel sounds, tender epigastric area, no enlarged liver or spleen. His rectal exam is
normal. All the other PE findings are unremarkable.
DIFFERENTIAL DIAGNOSES
Cholelithiasis
Cholelithiasis involves the presence of gallstones which are concretions that form
in the biliary tract, usually in the gallbladder. It is considered as a differential because of
the patients presentation of epigastric pain not relieved by antacids, vomiting, localized
tenderness. The occurrence of gallstones is also prevalent in patients who are smokers,
which increases the risk of our patient.
Peptic Ulcer Disease
PUD is ruled in because the patient presents with burning epigastric pain which
occurs after meals and is slightly relieved by antacids. However, this is unlikely because
the patient has no dyspepsia including belching, bloating, distention, and fatty food
intolerance. He also did not experience heartburn or chest discomfort. Hematochezia,
presented by briskly bleeding ulcer, is a common manifestation of this disease.
However, the patient presented with none. He also did not have unexplained weight
loss, early satiety, anemia, and progressive dysphagia or odynophagia which are known
manifestations of this disease.
Gastritis
Gastritis, or the inflammation of the stomach lining, is ruled in because of the
presence of burning abdominal pain accompanied by vomiting. Smoking is also a risk
factor for having the disease. However, this diagnosis is unlikely because the use of
antacid did not relieve the pain. The patient also did not manifest indigestion, heartburn
and bloating.

CLINICAL ASSESSMENT & ANALYSIS OF THE CASE

The patients symptoms are most consistent of a gastrointestinal disorder. The
timing of epigastric pain followed by vomiting after meal highly suggests that the

abdominal pain is a manifestation of a gastrointestinal disorder. It is unlikely to be of

urinary tract in origin since findings in PE are unremarkable of any urinary tract disorder.
An abdominal mass that may cause the obstruction is unlikely for this patient because
of the absence of palpable mass during PE. In addition, normoactive bowel sounds
were heard upon physical exam. This indicates that there is no obstruction along the
gastrointestinal tract. A cardiovascular disorder is also less likely to cause the epigastric
pain since the patients blood pressure is controlled. Based on the history, the patient
experienced epigastric pain followed by food intake, which was not relieved by antacids.
This rules out the possibility that the cause of epigastric pain was solely due to
excessive acid in the stomach. This leads us to the possibility that there is something
more of an obstruction that produces the patients symptoms.
The patients symptomatology is most likely explained by the presence of
chlolelithiasis. After meal, the gallbladder secretes concentrated bile in the biliary tract
due to peptide hormone cholecystokinin (CCK), which is released from the duodenal
mucosa in response to ingestion of fats and amino acids. Gallstones usually produce
symptoms by causing inflammation or obstruction following their migration into the
cystic duct or common bile duct. They are formed when there is excess of essentially
water insoluble cholesterol in relation to phospholipids and bile acids. Unstable,
cholesterol-rich vesicles remain which aggregate into large vesicles from which
cholesterol crystals precipitate. When gallstones lodge and obstruct the ducts, it
produces increase intraluminal pressure and distention of the viscus that cannot be
relieved by repetitive biliary contractions. This results to visceral pain in the epigastrium
that is severe and steady in character. This explains why the patient manifested with
epigastric tenderness upon PE. The pain frequently radiates to the interscapular area,
right scapula, or shoulder. However, this was not experienced by our patient. Nausea
and vomiting usually accompany episodes of biliary pain. This explains why the patient
experienced 2 episodes of vomiting after meal. The patient also has an increased risk of
having gallstones because he is a smoker. The absence of fever or chills imply that
there is no complications such as cholecystitis, pancreatitis or cholangitis.
ANCILLARY TESTS
Hematologic Studies
A complete blood cell (CBC) count with differential, liver function panel, and
amylase and lipase should be done in patients with suspected gallstone complications.
Imaging
Ultrasonography is the preferred initial imaging test for the diagnosis of
suspected gallbladder or biliary disease, since it is 90-95% sensitive and 78-80%
specific. This is best performed following a fast of at least 8 hours. Findings such as
pericholecystic fluid, gallbladder wall thickening >4mm, and sonographic Murphys sign
are suggestive of acute cholecystitis. The presence of gallstones also helps to confirm
the diagnosis.
CT can also be done as a secondary imaging test to identify the extrabiliary
disorders and complications. It is often used in the workup of abdominal pain as it
provides excellent images of the abdominal viscera. It is superior to ultrasonography in

demonstrating gallstones in the common bile duct. Additional findings of subserosal

edema (in the absence of ascites), intramural gas and sloughed mucosa support the
diagnosis.
Endoscopic retrograde cholangiopancreatography (ERCP) may be useful for
visualizing the anatomy of the gallbladder in patients at high risk for gallstones if signs
of common bile duct obstruction are present.
Laboratory Tests
Although this criteria is not reliable in identifying all patients with the disease, it
can still be useful in arriving at the diagnosis. Laboratory criteria which may be observed
in cholelithiasis include:
o Leukocytosis with a left shift
o elevated alanine aminotransferase (ALT) and aspartate aminotransferase
(AST)
o bilirubin and alkaline phosphatase assays which indicates common bile duct
obstruction
o elevated amylase/lipase
o elevated alkaline phosphatase levels in 25% of patients; and
o urinalysis to rule out pyelonephritis and renal calculi.
MANAGEMENT
Initial Therapy and Antibiotic Treatment
The initial treatment includes bowel rest, intravenous hydration, correction of
electrolyte abnormalities, and analgesia. Since the patient has mild case of acute
cholelithiasis, antibiotic therapy with a single broad-spectrum antibiotic may already be
adequate instead of using intravenous antibiotic.
Cholecystectomy
Cholecystectomy or the removal of gallbladder can be done in complicated cases
as a definitive therapy. This can be done to our patient since he has no
contraindications such as high risk for general anesthesia because his blood pressure is
controlled, morbid obesity, end-stage liver disease with portal hypertension and severe
coagulopathy.
Endoscopy
Aside from diagnosis, endoscopy can also be used for therapeutic purposes.
ERCP can be done to visualize the anatomy and provide therapy by removing stones
from the common bile duct.
Prevention
Ursodeoxycholic acid treatment can prevent gallstone formation. It should be
administered at a dose of 600 mg daily for 16 weeks to reduce the incidence of
gallstones by 80%. Dietary change of decreased fat intake is prudent to decrease the
incidence of biliary colic attacks. However, it has not been shown to cause dissolution of
stones. Coffee consumption appears to be associated with a reduced risk of gallstone

disease. Regular exercise may also reduce the frequency of cholecystectomy.

REFERENCES
Kasper, D. et al. (2015). Harrisons Principles of Internal Medicine 19 th Edition. McGrawHill Education: USA.
Kumar, V. et al. (2015). Robbins and Cotran Pathologic Basis of Disease, 9 th Edition.
Elsevier Saunders, Philadelphia, PA.
Heuman, D. (2016). Cholelithiasis. Retrieved online on August 17, 2016 from
http://emedicine.medscape.com/article/175667-clinical
Anand, BS. (2015) Peptic Ulcer Disease. Retrieved online on August 17, 2016 from
http://emedicine.medscape.com/article/181753-overview
Wehbi, M. (2016). Acute Gastritis. Retrieved online on August 17, 2016 from
http://emedicine.medscape.com/article/175909-overview
University of Maryland Medical Center (n.d.) Gastritis. Retrieved online on August 17,
2016 from http://umm.edu/health/medical/altmed/condition/gastritis