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Patient's Details:

Name : x
Age : 16y
Gender : Female
Race : Sarawak Iban
Address :Kapit
Reference Number :x
TPC Number
:x
Date of Admission :26-09-2016
Time of Admission :1700
___________________________________________________________________________________
Introduction.

x 16 year old female, newly married living with husband from Kapit who sought consult due to
recurrent abdominal pain associated with hematemesis. She is non-hypertensive, non-diabetic,
non-asthmatic, nulliparous with no known history of gastritis. She was able to do activities of
daily living independently without dyspnea or easy fatigability.
Chief Complaint
Three days prior to admission she had episodes of hematemesis associated with abdominal
pain.
History Presenting Illness
The history of present illness started three years ago 2013, prior to consult when patient
experienced recurrent abdominal pain. It was described as sudden onset, sharp and severe and
at times squeezing in character with a pain score of 4/10, initially localized over the left lower
quadrant of abdomen, specifically at umbilical and hypogastric region , occasionally radiating
to the left illiac region , lasting for a 15 minutes to 1 hour at times. The pain was relieved with
bedrest and with as needed intake of paracetamol tablet. The abdominal pain was occasionally
accompanied by undocumented fever furthermore she claim the fever usually with no chills and
rigor. During this time, she was working as a babysitter in Johor Bahru with her sister and once
rushed to nearest Medical Center due to an episodes of severe abdominal pain and associated
with hematemesis. It was the first episodes of her hematemesis. The blood was maroon red in
color. The quantitiy was two spoonful. It was also connected with nausea and vomiting after
the hematemesis. The vomiting was non bloody and and non bilious as well. The consult was
done at that time and treated as out patient and prescribed Paracetamol ,fever medicine and
cough syrup. The fever subsides but the abdominal pain was intermittent again.

A year later 2015, the persistence of the mentioned symptoms got worsen, she had recurrent
abdominal pain and also multiple episodes of hematemesis which the quantity of blood
gradually increased to 2 to 3 spoonful and it was marron in color. She did not care for any
treatment and. No records of any of the diagnostics done were mentioned. She took unrecalled
medications for the abdominal pain from and the pain reliever was continued as she needed.
Allegedly, she noticed she will have the pain before or after her meal. The pain severity will
also increases if she ate spicy food. However, symptoms recurred and became more frequent
during where she worked in Famous Bakery here at Kapit and she would take pain relievers
which afforded temporary relief.
Two months prior to consult, the symptoms worsened with additional findings of blood in
feces. She described it was bright red in color. At this time ,three days ago prior to her
admission ,patient experienced easy fatigability, generalized body malaise and traumatized by
recent episodes of hematemesis which massive around 4 spoonful in quantity and another
episodes of blood in feces. She consulted by a physician in Hospital Besar Kapit and she was
then advised that require hospitalization in district Hospital Sibu and endoscopy must be done.
Patient then decided to consult at the Hospital Sibu as referred.
Review of System
Respiratory system : no pharyngalgia, no chronic cough , no hemoptysis, and no
dyspnea

Circulatory system : no palpitation and breathlessness on exertion: no precordial pain,


no syncope.

Digestive system : no sour regurgitation and dysphagia,no diarrhea, no jaundice,loss of


appetite

Urinary system : no past history of edema and proteinuria; no polyuria, no urgency and
painful micturition,no visible hematuria.

Endocrine and metabolic system : no irritability, no impaired vision, exceeding thirsty


and polyuria

Nervous system : slight dizziness and headache occasionally, no memorial impairment


or speaking obstacle,

Mental status: no hallucination, delirium and orientation obstacle, no abnormal emotion

Glasgow Coma Scale : 15/15


Past Medical and Surgery History:
This is patient's first confirmed admission. As noticed before she had chronic abdominal pain
and with it associated symptoms in the past and treated as out patient. Otherwise there is no
significance of surgical history for her.

Drug and Food allergy:


No sensitivity reaction to any sustenance and drug noted.
Diet History:
Her daily intake of food mainly consist of vegetables which she like to eat. She will consume
meat twice or more in a week.
She likes fried food and also spicy food.
Menstrual History:
She achieve her menarche at age of 12.
Her menstrual cycle are constantly regular regardless of her stomach pain. She don't have any
premenstrual spasms during her period, she claimed her menses period are 5 days which the
pad will completely doused for the initial two days. Her keep going menstrual period began on
26-9-2016.
Family History:
Her parents and her kin are alive and healthy.
There was no hypertension, diabetes ,nor gastritis in the family. There was no family history of
pulmonary colorectal growth and appendicitis and there was no history of breast malignancy as
well.
Maritial History:
She just recently maried 3 months prior.
Her husband is 31 years of age working as a carpenter and month to month gets around RM
2000, which adequate for them.
They living in long house with a legitimate access of power and water supply.
She dont utilize any contraception before and now. There was no history of dyspareunia.
She is nulliparous.
Personal and Social History:
She doesn't smoke and denies history of any illict any drugs intake.
Occasionally she will drink liquor (Tuak) and alcohol beverage drinker, and not a heavy
drinker. She is not an alcoholic.

General Examination:
She was awake, coherent, ambulatory, not in cardiorespiratory distress lying comfortably in a supine
position. Anicteric sclerae, pink palpebral conjunctiva, no palpable cervical lymphadenopathy, no
anterior neck mass noted, and there is no jaundice , pallor, no clubbing , cyanosis or pedal edema seen
on her, There was no redness on tonsillar.
Vital signs are as below :
Temperature : 36.4 C
Blood pressure
: 120/70 mmHg
Pulse : 86 beat per minute, good volume, regular rhythm.
Respiratory rate
: 20 breaths per minute
Cardiovascular system examination
An adynamic precordium, not tachycardic, regular rhythm,
Normal 1st and 2nd heart sound was heard. Apex beat noted at the 5th Intescostalspace left midclavicular line, no murmurs/heaves/thrills.
Respiratory system examination
No gross deformity, chest expansion symmetry, equal vocal and tactile fremitus, resonance on
percussion and dullness on organ area.
Normal vesicular breath sound heard, no crackles/wheezes, clear breath sounds bilaterally.
.
Abdominal examination
On inspection, the abdomen shape was normal, flat abdomen and moves with respiration. There was no
surgical scar, no dilated vein, no visible pulsation and peristalsis noted .
On light palpitation, her abdomen was soft and tender at the left lower quadrant, specifically at left
hypogastric and left illiac regions. There is no guarding and rebound tenderness present. On deep
palpation, there was tenderness on the same pathological area with no hepatosplenomegaly . Both
kidneys were not ballotable.

Rovsing sign : negative


Psoas sign : negative
Obturator sign : negative

On percussion, there was no shifting dullness.


On auscultation, normal bowel sound present with no renal bruit.

Sumarry:
Shida Anak Dian newly wedded young lady, well built. Presented with hematemesis associated with
repetitive history of abdominal pain for a long time earlier , 3 years prior. Require hospitalization
promptly for further examination as referred from Hospital Kapit. With a positive discoveries on
physical examination , such as abdomen tenderness on palpation at the left lower quadrants.
She is a occasional drinker yet dont have any essentials past medical and surgical history. She loves to
eat spicy and fried food which usually trigger her abdominal pain. Despite the fact of her pain score
was just 4/10 the most extreme as she described but it might because of the pain killer she took as she
needed that may mimic the real pain score that varies.

Provisional Diagnosis:
My provisional diagnosis are upper gastrointestinal bleeding secondary to peptic ulcer disease
as my patient Shida was conspicuous by following symptoms , recurrent abdominal pain and
few episodes of hematemesis which with gradual increase of the quantity.
Besides Upper gastrointestinal bleeding may because of many reasons which would give a
couple of differential analysis as i state underneath. I might want to do further investigation to
which will lead to finish up my most likely diagnosis into a conclusion with a strong evidence
to support it .
Differential Diagnosis:
Condition

History

Peptic ulcer disease -NSAID use (often


(PUD)
with concomitant use
of corticosteroids)
-past ulcers is
common; ingestion of
food often transiently
improves abdominal
pain
- coffee-ground
emesis and
hematemesis are very
common

Examination
-mid-epigastric
tenderness to
palpation

Test
-upper GI endoscopy
(OGD):direct
visualisation of the ulcer
-Helicobacter pylori
serology or breath
test:positive for H
pylori

Oesophageal
varices

-intravenous drug use


that could lead to
chronic hepatitis,
chronic alcoholism, or
cirrhosis should
immediately arouse
suspicions of portal
hypertension and thus
varices.
-variceal bleeds often
lead to brisk
hematemesis

-stigmata of chronic
liver disease are often
present,
: jaundice,
hepatomegaly,
splenomegaly, ascites

-upper GI
endoscopy
(OGD):direct
visualisation of the
varices
-CT scan/portal
angiography:can
show collateral veins
and recanalised
umbilical vein
-transjugular
intrahepatic
portosystemic shunt
(TIPS) procedure: to
decompress
intractable
oesophageal variceal
bleeding

Mallory-Weiss tear

-classically, patients
note haematemesis
following retching or
vomiting, but any
increase in intraoesophageal pressure
(e.g., from seizures,
hiccups, or straining)
can cause a tear;
some tears develop
spontaneously;
alcohol use,
advanced age, and
presence of hiatal
hernias are common
underlying features

-bleeding is
sometimes
accompanied by midepigastric or
retrosternal pain

-upper GI
endoscopy
(OGD):direct
visualisation of
intramural dissections

Dieulafoy's lesions

-often present
painlessly; lesions are
submucosal vessels
that dive towards the
gastric lumen and,
through erosion,
rupture and produce
rapid blood loss;
regarded as
congenital arterial
dysplasias but are
most often
symptomatic in men
with alcohol histories,
cardiovascular
disease including
hypertension,
diabetes, or chronic
kidney disease

-often present with a


non-focal physical
examination; the
bleeding can be
intermittent

-upper GI endoscopy
(OGD):direct
visualization of lesion
-endoscopic
ultrasound:identificatio
n of lesion

Investigation :
1.Urine pregnancy test negative ( to rule out pregnancy )
2.Transabdominal Ultrasound
Impression : To rule out ectopic pregnancy and ureteric stone
3.Endoscopy Diagnosis: positive Helicobacter Pylori on histological examination of biopsies during
endoscopy procedure.
4.Chest X-ray
Normal
5. Full blood count - Normal
Result
WBC
6.9
RBC
4.05
Hemoglobin
12.6
Hematocrit
45.0
MCV
84.0
MCH
30.4
MCHC
34.2
Platlet
208
Lymphocyte
15.3 %
%
Neutrophil %
76.8 %
Monocyte %
6.5 %
Eosinophil %
1.3 %

Normal range
4.0 11.0 x10^9 g/L
2.5 5.5 x10^6 /ul
12.5 17.0 g/dL
35 47 %
76 96 fL
27 32 pg
30 35 g/dL
150 400 x 10^3 /uL
5 55 %

Remark
Normal
Normal
Normal
Normal
Normal
Normal
Normal
Normal
Normal

45 85 %

Normal
Normal
Normal

Basophil %
Lymphocyte
Neutrophil
Monocyte
Eosinophil
Basophil
RDW-SD
PDW
MPV
P-LCR

0.1 %
1.06 x 10^3 /ul
5.30 x 10^3 /ul
0.45 x10^3 /ul
0.09
0.01
39.5 fL
11.2 fL
10.2 Fl
26.0 %

Renal profile normal


Urea
Sodium
Potassium
Chloride
Creatinine

37 54 fL

Normal
Normal
Normal
Normal
Normal
Normal
Normal
Normal
Normal
Normal

Result
6
140
3.9
100
80

Normal range
1.7 6.4 mmol/L
135 150 mmol/L
3.5 5.0 mmol/L
98 107 mmol/L
44 88 mmol/L

Remarks
Normal
Normal
Normal
Normal
Normal

Coagulation Profile-normal
Prothrombin time
Activated Partial
Thromboplastin
Time

Blood glucose : 5.1mmol /L


-normal

ECG
-Normal sinus rhythm

Result
13.20
20.0

Normal range
10 14 seconds
20 35 seconds

Remarks
Normal
Normal

Final Diagnosis:
Upper Gastrointestinal bleeding secondary to peptic ulcer disease with confirmed Helicobacter
Pylori infection.
Management of the patient based on the Hospital Sibu :

Antibiotics therapy for two weeks


Proton Pump Inhibitors therapy for three weeks

Discussion:
Upper Gastrointestinal Bleeding
Upper gastrointestinal (UGI) bleeding is a common cause of morbidity and mortality among
urban dwellers in Malaysia. Despite advancements in endoscopy and pharmacology in the
treatment of peptic ulcer disease, the most frequent cause of such bleeding, the overall
mortality has remained constant. This is due to an increase in the proportion of elderly patients
developing complications of peptic ulcer disease. As such, early diagnosis, systematic
management and regular follow-up via endoscopy are vital.
A prospective records of UGI bleeding involving patients was documented in two surgical
wards of the government unit, Sibu Hospital between January 2016 to October 2016. All cases
aged 12 years and above admitted for hematemesis or malaena secondary to an upper
gastrointestinal cause, that is, proximal to the duodeno-jejunal flexure, were included in the
study. All patients underwent oesophagogastroduodenoscopy (OGDS) to conclude the causes.
The source of documentation are from admission records of Surgical Ward Sibu Hospital.
The result are summarized in Graph and Pie charts.

Bleeding was much more common in males than females (ratio 6:4). Among the factors
explaining this is the observation of the relative infrequency of smoking and alcohol abuse
among Malaysian women. Although the total number of patients diagnosed with peptic ulcer
disease over the period of this study was not recorded, the fact that primary presentations of
UGI bleeding from peptic ulcer disease made such a large contribution to the total number of
UGI bleeds stresses the importance of the early diagnosis and management of this condition.
Moreover the peak, the most elevated episodes were recorded on month January 32 patients
(16.5%) and the second were on June 27 patients (13.9%). At the same time high UGI were
noted in both male and female on that particular months. Based on this its highly suggestive
some ultimate variables that could be trigger more could be the festive periods of Christmas
and Gawai which the majority of Sarawakian celebrates here.

Genuine certainties the majority of them celebrate with high consumption of alcohol beverage,
furthermore with high intake of fried and barbecue grill sustenance together. This will more
prominent increment the risk of of UGI.
The other major predisposing factor to UGI bleeding apart from alcohol and smoking was drug
intake. NSAIDs, traditional drug therapy, anticoagulants and steroids were in use by patients in
this study. NSAIDs and aspirin are being increasingly employed in the management of arthritis,
cerebrovascular disease and coronary artery disease.

Peptic Ulcer Disease:


Peptic ulcer disease represents a serious medical problem. Interestingly, those at the highest
risk of contracting peptic ulcer disease are those generations born around the middle of the 20th
century. Ulcer disease has become a disease predominantly affecting the older population, with
the peak incidence occurring between 55 and 65 years of age. In men, duodenal ulcers were
more common than gastric ulcers; in women, the converse was found to be true. Thirty-five
percent of patients diagnosed with gastric ulcers will suffer serious complications. Although
mortality rates from peptic ulcer disease are low, the high prevalence and the resulting pain,
suffering, and expense are very costly. Ulcers can develop in the esophagus, stomach or
duodenum, at the margin of a gastroenterostomy, in the jejunum, in ZollingerEllison syndrome,
and in association with a Meckel's diverticulum containing ectopic gastric mucosa. Peptic ulcer
disease is one of several disorders of the upper gastrointestinal tract that is caused, at least
partially, by gastric acid. Patients with peptic ulcer disease may present with a range of
symptoms, from mild abdominal discomfort to catastrophic perforation and bleeding.
What is Peptic Ulcer Disease?
Gastric and duodenal ulcers are breaks in the gastric and duodenal mucosa. Both gastric and
duodenal ulcers relate to the corrosive action of pepsin and hydrochloric acid on the mucosa of
the upper gastrointestinal tract. Ulcers generally range between 3 mm and several centimeters
in diameter.
Symptoms
Most patients with peptic ulcer disease present with abdominal discomfort, pain or nausea. The
pain is located in the epigastrium and usually does not radiate. However, these symptoms are
neither sensitive nor specific. Pain radiating to the back may suggest that an ulcer has
penetrated posteriorly, or the pain may be pancreatic in origin. Pain radiating to the right upper
quadrant may suggest disease of the gallbladder or bile ducts. Patients may describe the pain of
peptic ulcer as burning or gnawing, or as hunger pains slowly building up for 12 hours, then
gradually decreasing. Use of antacids may provide temporary relief. Classically, gastric ulcer
pain is aggravated by meals, whereas the pain of duodenal ulcers is relieved by meals. Hence,
patients with gastric ulcers tend to avoid food and present with weight loss, while those with
duodenal ulcers do not lose weight. It is important to remember that although these patterns are
typical, they are not pathognomonic. The nature of the presenting symptoms alone does not permit a
clear differentiation between benign ulcers and gastric neoplasm.

Anatomy:
The stomach is located in the upper part of the abdomen just beneath the diaphragm (Figure 1). The
stomach is distensible and on a free mesentery, therefore, the size, shape, and position may vary with
posture and content. An empty stomach is roughly the size of an open hand and when distended with
food, can fill much of the upper abdomen and may descend into the lower abdomen or pelvis on
standing. The duodenum extends from the pylorus to the ligament of Treitz in a sharp curve that almost
completes a circle. It is so named because it is about equal in length to the breadth of 12 fingers, or
about 25 cm. It is largely retroperitoneal and its position is relatively fixed. The stomach and duodenum
are closely related in function, and in the pathogenesis and manifestation of disease.
The stomach may be divided into seven major sections. The cardia is a 12 cm segment distal to the
esophagogastric junction. The fundus refers to the superior portion of the stomach that lies above an
imaginary horizontal plane that passes through the esophagogastric junction. The antrum is the smaller
distal one-fourth to one-third of the stomach. The narrow 12 cm channel that connects the stomach
and duodenum is the pylorus. The lesser curve refers to the medial shorter border of the stomach,
whereas the opposite surface is the greater curve. The angularis is along the lesser curve of the stomach
where the body and antrum meet, and is accentuated during peristalsis.
The duodenum extends from the pylorus to the ligament of Treitz in a circle-like curve and is divided
into four portions. The superior portion is approximately 5 cm in length, beginning at the pylorus, and
passes beneath the liver to the neck of the gallbladder. The first part of the superior portion (23 cm) is
the duodenal bulb. The descending or second part of the duodenum takes a sharp curve and goes down
along the right margin of the head of the pancreas. The common bile duct and the pancreatic duct enter
the medial aspect of this portion of the duodenum at the major papilla either separately or together. The
duodenum turns medially, becoming the horizontal portion, and passes across the spinal column,
inclining upward for 58 cm. The ascending portion begins at the left of the spinal column, ascending
left of the aorta for 23 cm, and ends at the ligament of Treitz, where the intestine angles forward and
downward to become the jejunum.

Peptic Ulcer Disease: Causes


Protective vs. Hostile Factors
No gastric acid, no peptic ulcer is a misconception. Excessive gastric acid secretion is only one factor
in the pathogenesis of peptic ulcer disease. Decreased mucosal defense against gastric acid is another
cause. The integrity of the upper gastrointestinal tract is dependent upon the balance between hostile
factors such as gastric acid, H. pylori, NSAIDs and pepsin, and protective factors such as
prostaglandins, mucus,bicarbonate, and blood flow to mucosa affecting gastrointestinal mucosa

Injury to gastric and duodenal mucosa develops when deleterious effects of gastric acid overwhelm the
defensive properties of the mucosa. Inhibition of endogenous prostaglandin synthesis leads to a
decrease in epithelial mucus, bicarbonate secretion, mucosal blood flow, epithelial proliferation, and
mucosal resistance to injury. Lower mucosal resistance increases the incidence of injury by endogenous
factors such as acid, pepsin, and bile salts as well as exogenous factors such as NSAIDs, ethanol and
other noxious agents .

Helicobacter pylori
H. pylori is the etiologic factor in most patients with peptic ulcer disease and may predispose
individuals to the development of gastric carcinoma. H. pylori colonizes in the human stomach
(Figure 5). The method of H. pylori transmission is unclear, but seems to be person-to-person spread
via a fecal-oral route. The prevalence of H. pylori in adults appears to be inversely related to the
socioeconomic status. It is also thought that water is a reservoir for transmission of H. pylori.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDS)


A small but important percentage of patients have adverse gastrointestinal events associated with
NSAID use that results in substantial morbidity and mortality. Risk factors for the development of
NSAID-associated gastric and duodenal ulcers include advanced age, history of previous ulcer
disease, concomitant use of corticosteroids and anticoagulants, higher doses of NSAIDs, and serious
systemic disorders. The concept of gastroduodenal mucosal injury has evolved from the notion of
topical injury to concepts that involve multiple mechanisms.

NSAIDs initiate mucosal injury topically by their acidic properties. By diminishing the hydrophobicity
of gastric mucus, endogenous gastric acid and pepsin may injure surface epithelium. Systemic effects
of NSAIDs appear to play a predominant role through the decreased synthesis of mucosal
prostaglandins. The precursor of prostaglandins, arachidonic acid, is catalyzed by the two cyclooxygenase isoenzymes, cyclo-oxygenase-1 and cyclo-oxygenase-2. The gene for cyclo-oxygenase-1,
the housekeeping enzyme, maintains the homeostasis of organs. Cyclo-oxygenase-2, the inflammatory
enzyme, is inducible. Although NSAIDs can inhibit both pathways, only the gene for cyclooxygenase-2 contains a corticosteroid-responsive repressor element.
H. pylori is prevalent among 2263% of patients taking NSAIDs. Most studies do not show a
significant difference in H. pylori prevalence between NSAID users and nonusers. Gastritis in patients
on NSAID therapy appears to be related to underlying H. pylori rather than drug use. The lower
incidence of H. pylori among patients with gastric ulcers than those with duodenal ulcers is
presumably the result of NSAID use. NSAIDs are more likely to cause gastric than duodenal ulcers.
NSAIDs appear to cause ulcers by a mechanism independent of H. pylori based on the inhibition of
prostaglandin synthesis.
Gastrinoma (Zollinger-Ellison Syndrome)
The classic triad of Zollinger-Ellison syndrome involves peptic ulcers in unusual locations (i.e., the
jejunum), massive gastric acid hypersecretion, and a gastrin-producing islet cell tumor of the pancreas
(gastrinoma). Gastrinoma in the pancreas appears in approximately 50% of patients. Another 20% of
patients have it in the duodenum and others have it in the stomach, peripancreatic lymph nodes, liver,
ovary, or small-bowel mesentery.
Zollinger-Ellison syndrome accounts for only 0.1% of all duodenal ulcer disease. One fourth of patients
have this syndrome as part of the multiple neoplasia syndrome Type I (MEN I).
Patients with gastrinoma may have intractable ulcer disease. Because gastrin is trophic to the gastric
mucosa, endoscopy or x-ray may demonstrate hypertrophy of the gastric rugae. Patients may also
experience diarrhea (including steatorrhea from acid inactivation of lipase) and gastroesophageal
reflux. These symptoms are episodic in 75% of patients.
Hypercalcemia
Hypercalcemia has a direct bearing on the gastric acid hypersecretory state found in patients with
Zollinger-Ellison syndrome and MEN I. Intravenous calcium infusion in normal volunteers induces
gastric acid hypersecretion. Additionally, calcium has been demonstrated in vivo and in vitro to
stimulate gastrin release directly from gastrinomas. Resolution of hypercalcemia (by

parathyroidectomy) reduces the basal acid output and serum gastrin concentration in fasting gastrinoma
patients and those with MEN I, suggesting that resolution of hypercalcemia plays an important role in
the therapy of this subgroup of patients.

Genetic Factors
Genetic factors play a role in the pathogenesis of ulcer disease. The lifetime prevalence of developing
ulcer disease in first-degree relatives of ulcer patients is about three times greater than the general
population. Approximately 2050% of duodenal ulcer patients report a positive family history; gastric
ulcer patients also report clusters of family members who are likewise affected.
Smoking
The literature reveals a strong positive correlation between cigarette smoking and the incidence of ulcer
disease, mortality, complications, recurrences and delay in healing rates. Smokers are about two times
more likely to develop ulcer disease than nonsmokers. Cigarette smoking and H. pylori are co-factors
for the formation of peptic ulcer disease. There is a strong association between H. pylori infection and
cigarette smoking in patients with and without peptic ulcers. Cigarette smoking may increase
susceptibility, diminish the gastric mucosal defensive factors, or may provide a more favorable milieu
for H. pylori infection.
Stress
Numerous studies have revealed conflicting conclusions regarding the role of psychological factors in
the pathogenesis and natural history of peptic ulcer disease. The role of psychological factors is far
from established. Acute stress results in increases in pulse rate, blood pressure and anxiety, but only in
those patients with duodenal ulcers did acute stress actually result in significant increases in basal acid
secretion. There is no clearly established ulcer-type personality. Ulcer patients typically exhibit the
same psychological makeup as the general population, but they appear to perceive greater degrees of
stress. In addition, there is no evidence that distinct occupational factors influence the incidence of
ulcer disease.
Alcohol and Diet
Although alcohol has been shown to induce damage to the gastric mucosa in animals, it seems to be
related to the absolute ethanol administered (200 proof). Pure ethanol is lipid soluble and results in
frank, acute mucosal damage. Because most humans do not drink absolute ethanol, it is unlikely there
is mucosal injury at ethanol concentrations of less than 10% (20 proof). Ethanol at low concentrations
(5%) may modestly stimulate gastric acid secretions; higher concentrations diminish acid secretion.
Though physiologically interesting, this has no direct link to ulcerogenesis or therapy.
Some types of food and beverages are reported to cause dyspepsia. There is no convincing evidence
that indicates any specific diet causes ulcer disease. Epidemiologic studies have failed to reveal a

correlation between caffeinated, decaffeinated, or cola-type beverages, beer, or milk with an


increased risk of ulcer disease. Dietary alteration, other than avoidance of pain-causing foods, is
unnecessary in ulcer patients.

Peptic Ulcer Disease:

Diagnosis

Overview
Peptic ulcer disease is suspect in patients with epigastric distress and pain; however, these symptoms
are not specific. Lack of response to conventional treatment for peptic ulcer disease should suggest
conditions other than benign peptic ulcers, and should warrant endoscopy or abdominal imaging.
Radiological Diagnosis
Barium x-ray or upper GI series is a widely available and accepted method to establish a diagnosis
of peptic ulcer in the stomach (Figure 7) or duodenum (Figure 8).

Figure 7. A, X-ray of gastric ulcer in the antrum; B, corresponding illustration of


a gastric ulcer.

Figure 8. A, Duodenal ulcer; B, corresponding x-ray.


Though less invasive than endoscopy, the barium x-ray is limited by being less sensitive and accurate at
defining mucosal disease, or distinguishing benign from malignant ulcer disease (Figure 9). In patients
who have anatomic deformities from previous gastric surgery or scarring from chronic inflammation,
barium x-rays may be difficult to interpret. Generally, these x-rays have up to a 30% false negative and
a 10% false positive rate. Until 1970, peptic ulcers were diagnosed almost exclusively by radiological
methods. The most common inaccuracies of radiological diagnosis include the failure to recognize true
ulcers, or the misdiagnosis of a scar or a deformed duodenal bulb as a true ulcer. Since the 1970s,

increasing numbers of peptic ulcers are diagnosed by endoscopy.

Figure 9. Peptic ulcers; A. malignant; B. benign.

Laboratory Testing
Patients who respond to optimal therapy for peptic ulcer disease do not require specialized testing.
However, those with refractory (not healed after 8 weeks of therapy) or recurrent disease should have
serum gastrin and serum calcium measured to screen for gastrinoma and multiple endocrine neoplasia
(MEN). These patients should also undergo gastric acid analysis to determine whether the ulcer is
caused by gastric acid hypersecretion (basal acid output exceeding 10 mEq/hr) or decreased mucosal
protection.
Patients with refractory or recurrent peptic ulcer disease may have an underlying Helicobacter pylori
(H. pylori) infection. Histological examination of biopsies of the gastric antrum, obtained during
endoscopy, is the gold standard for diagnosis of H. pylori. Routinely, H. pylori is not cultured because
of the difficulty growing the organism. Serologic tests are available, but unfortunately, positive test
results indicate only past exposure and are not useful for determining if the infection has been cured.
Urea breath tests are simple and noninvasive, and have been used to diagnose H. pylori infection.
Because H. pylori produces large quantities of the enzyme urease, these breath tests have the potential
to be quite useful. 13C- and 14C-urea breath tests offer excellent diagnostic yield. Patients ingest a
solution containing 13C- or 14C-labeled urea and an exhaled breath is sampled for isotope-labeled
CO2 released by intragastric H. pylori urease activity. The test can be completed within 20 minutes
and is highly sensitive and specific.

Figure 10. Urea breath test determines the presence of H. pylori.


Serologic testing is an accepted method for detection of H. pylori. Mean levels of IgG and IgA
ELISA tests (enzyme-linked immunosorbent assay) are significantly higher in H. pylori-positive than

in H. pylori-negative patients. Sensitivity of this serum assay is generally in the range of 8095% and
specificity in the range of 7595%.
More recently, stool antigen testing has emerged as an alternative non-invasive means of detecting the
presence of H. pylori. These fecal assays have become a useful test, and recent studies have shown a
sensitivity value of 94% with specificity between 86-92%. Furthermore, it may be used to easily
document eradication of an H. pylori infection if performed at least four weeks after treatment.
Endoscopic Diagnosis
Gastrointestinal endoscopy allows the physician to visualize and biopsy the upper gastrointestinal tract
including the esophagus, stomach and duodenum. The enteroscope (a longer endoscope) allows
visualization of at least 50% of the small intestine, including most of the jejunum and different degrees
of the ileum. During these procedures, the patient is given a numbing agent to help prevent gagging.
Pain medication and a sedative may be administered prior to the procedure. The patient is placed in the
left lateral position (Figure 11).

Figure 11. Room set-up and patient positioning for endoscopy.


An endoscope (a thin, flexible, lighted tube) is passed through the mouth and pharynx and into the
esophagus. The forward-viewing scope transmits an image of the esophagus, stomach and duodenum
to a monitor visible to the physician . Air may be introduced into the stomach, expanding the folds of
tissue, and enhancing examination of the stomach.

Esophagogastroduodenoscopy (EGD) is the most direct and most accurate method of


establishing the diagnosis of peptic ulcer disease . In addition to identifying the ulcer, its
location and size, EGD also provides an opportunity to detect subtle mucosal lesions and to
biopsy lesions to establish histopathological basis. Endoscopic biopsies are indicated for all
gastric ulcers at the time of diagnosis, whereas duodenal ulcers are almost always benign, not
requiring biopsy in usual circumstances.

Endoscopic biopsy also appears the best and most accurate diagnostic method for H. pylori.

Histological examination with standard hematoxylin and eosin staining provides an excellent
means of diagnosis

In an effort to speed up the diagnosis of H. pylori following a biopsy of the gastric mucosa,
urease activity has been used. Biopsy specimens are placed in a urea and phenol red solution or
gel. If urease from H. pylori is present in the specimen, urea is hydrolyzed to release ammonia,
increasing pH in the solution and giving a pink color to the gel or solution. At 3 hours, this test
has a sensitivity of 90%. Using this technique, the diagnosis can be made sooner than standard
histopathological examination.

Peptic Ulcer Disease :Therapy


Overview
Most peptic ulcers heal if gastric acid production is adequately suppressed. The rationale behind
the treatment of peptic ulcer disease is twofold. The reduction of hostile factors is essential, as is
augmentation of protective factors. Antacids, histamine H2-receptor antagonists, proton pump
inhibitors (e.g., omeprazole, lansoprazole), and surgery succeed by neutralization or reduction of
gastric acid. Sucralfate and prostaglandin agents boost mucosal protection. The eradication of H.
pylori infection restores normal mucosal resistance, but unlike other treatment options, does not
require maintenance therapy to prevent ulcer recurrence. Patients should avoid factors known to
contribute to peptic ulcer disease, such as NSAIDs and smoking.
Medical Therapy
The goal of therapy for peptic ulcer disease is to relieve symptoms, heal craters, prevent
recurrences, and prevent complications. Medical therapy should include treatment with drugs,
and attempt to accomplish the following: 1) reduce gastric acidity by mechanisms that inhibit or
neutralize acid secretion, 2) coat ulcer craters to prevent acid and pepsin from penetrating to the
ulcer base, 3) provide a prostaglandin analog, 4) remove environmental factors such as NSAIDs
and smoking, and 5) reduce emotional stress (in a subset of patients).
Antacids neutralize gastric acid and are more effective than placebo in healing gastric and
duodenal ulcers. However, antacids have to be taken in relatively large doses 1 and 3 hours
after meals and at bedtime, and may cause side effects. The major side effect of magnesiumcontaining antacids is diarrhea caused by magnesium hydroxide.
Histamine H2-receptor antagonists reduce gastric acid production by blocking the H2 receptor on
the parietal cell (Figure 16). Examples of available H2 blockers used to treat gastric and duodenal
ulcers include cimetidine, ranitidine, famotidine and nizatidine. This group of compounds
effectively decreases acid secretion. H2-receptor antagonists are relatively safe. The choice of
drug should be dictated by cost, dosing schedule, convenience, and possible drug interactions.
The family of drugs known as as proton pump inhibitors, or PPIs, inactivates the parietal cell
hydrogen-potassium ATPase located on the lumenal surface. ATPase acts as a proton pump and
constitutes the final common pathway in the secretion of hydrogen ions. This class of medicines
is now considered the gold standard in medical therapy of peptic ulcer disease. Examples of
available PPIs include omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole.
Increasing the PPI dose can reduce acid secretion to the point of achlorhydria (unachievable by
H2 blockade). Thus, the proton pump inhibitors are the primary treatment when gastric
hypersecretion is resistant to other therapies. Proton pump inhibitors have been shown to prevent
NSAID-associated gastroduodenal ulcers, and to provide a safe and effective form of therapy.
Furthermore, studies have shown that PPIs are more effective than H2-receptor antagonists at
treating all types of peptic ulcer disease.

Sucralfate is the aluminum salt of a sulfated disaccharide. The drug forms a barrier or coating

over the ulcer crater, stimulates prostaglandin synthesis, and binds to noxious agents such as bile
salts. Although the exact mechanism of action is unclear, it appears sucralfates stimulate
prostaglandins, which promote improved mucosal integrity and enhance epithelial regeneration.
Because it requires multiple doses per day, patients are less likely to follow a sucralfate regimen
even though it has been shown to be as effective as an H2 blocker in healing both duodenal and
gastric ulcers. Sucralfate is not absorbed systemically, and its only remarkable side effect is
constipation.
Misoprostol is a prostaglandin E1 analog that increases mucosal resistance and inhibits acid
secretion to a minor degree. Misoprostol has been advocated for prophylaxis of NSAID-induced
mucosal injury. The drug has significant side effects, primarily mild to moderate diarrhea, and is
too costly to be used by most patients on long-term NSAIDs.
The suppression of gastric acid production promotes the healing of peptic ulcers. Unfortunately,
if acid suppression therapy is not maintained, peptic ulcers regularly recur. Since the long-term
cure of peptic ulcers accompanies the eradication of H. pylori, all ulcers associated with this
infection should be treated with the aim of infection eradication. Although H. pylori is sensitive
to a variety of antibiotics in vitro, its habitat beneath the gastric mucosa makes it difficult to
treat. The original treatment gold standard was 2 weeks of triple therapy, including bismuth,
tetracycline or amoxicillin, and metronidazole. Where compliance with this regimen can be
assured, H. pylori cure rate is 9095% or more; however, 20% of these cases develop side
effects.
Newer simpler regimens have been developed and H. pylori treatment recommendations are still
evolving. Today, the current gold standard of therapy is a triple combination of drugs that
includes a PPI (e.g. omeprazole or lansoprazole) plus amoxicillin and a newer antibiotic,
clarithromycin. All three medicines are to be taken twice per day for 7-14 days (preferably 14
days). Alternative drugs may be offered to those patients with certain allergies or medication
intolerances. Physicians should always offer patients with peptic ulcer disease and confirmed H.
pylori infection the option of curative therapy.
Gastric ulcers should be re-evaluated by multiple endoscopic biopsies and cytology to rule out
gastric carcinoma if they have not healed after 8 weeks of conventional medical therapy. If no
malignancy is seen on biopsy, aggressive treatment should be instituted for 6 weeks to eradicate
H. pylori and to suppress acid with full doses of a proton pump inhibitor. A gastric ulcer that does
not heal after this second aggressive course of medical therapy may suggest underlying
malignancy, even with negative repeat biopsies. Non-healing gastric ulcers should be resected
surgically.

Surgical Therapy
Over the past few decades in the United States, we have witnessed a declining need for surgery to
treat peptic ulcer disease. This decline may be explained primarily by the widespread use of H2
receptor antagonists, and now more recently, proton pump inhibitors. Complications such as

gastrointestinal hemorrhage, perforation, or gastric outlet obstruction remain the major


indications for surgical intervention.
The most common reason for surgical intervention for benign gastric ulcers is failure of the ulcer
to completely heal after an adequate trial of medical or endoscopic therapy. Patients are usually
given a 6-month trial of antisecretory agents prior to surgical consultation. The major concern
regarding non-healed ulcers is the high risk of underlying malignancies.
Due to the benign nature of duodenal ulcers, physicians can monitor the patients response to
medical regimens by following their symptoms. When patients with duodenal ulcers require
surgery, it is usually one of three procedures: vagotomy, vagotomy with antrectomy, or subtotal
gastrectomy. Vagotomy alone (without gastric resection) may involve truncal vagotomy with
drainage, selective vagotomy with drainage (Figure 18), or proximal gastric vagotomy alone
(without a drainage procedure).

Figure 18. Selective vagotomy.


Delayed gastric emptying may be caused by truncal vagotomy, and a concurrent drainage
procedure such as antrectomy (Figure 19), pyloroplasty (Figure 20), or gastroenterostomy may
be necessary as antral innervation (by Latarjet nerves) is nonfunctioning. Selective vagotomy
(proximal gastric vagotomy) does not necessitate a concomitant drainage procedure.

Figure 19. Antrectomy and truncal vagotomy for duodenal ulcer with Billroth I anastomosis.

Figure 20. Surgical technique of pyloroplasty and truncal vagotomy.


Morbidity resulting from the surgical procedure and the risk of recurrence of ulcers are two major
considerations. Proximal gastric vagotomy is probably the most preferred of surgical options
because the pylorus is preserved. Recurrence of ulcer disease is about the same with all three
types of surgical procedures, however, the incidence of dumping symptoms is higher with
vagotomy or vagotomy with antrectomy.
Endoscopic Therapy
The primary role of endoscopic therapy in peptic ulcer disease is to manage complications that
may arise.
Overview
Hemorrhage, perforation/penetration, and gastric outlet obstruction continue to be the major
complications associated with peptic ulcer disease, despite the availability of effective ulcer
medications. In the United States, the yearly complication rate ranges between 25%.
Hemorrhage
Rate of Incidence
Gastrointestinal hemorrhage affects 520% of patients (more often those with duodenal ulcers)
and is the most common complication of peptic ulcer disease. Bleeding occurs more often in men
than in women. Hemorrhage from ulcers stops spontaneously in approximately 7580% of cases.
Approximately one-fourth of all bleeding ulcers require surgery.

Endoscopic Therapy
Endoscopy is the preferred procedure for the diagnosis and treatment of an upper
gastrointestinal hemorrhage because of the low complication rate and accuracy. Stigmata on
ulcers may be seen during endoscopic procedures, and are important prognostic indicators
(Figure 21).

Figure 21. Classification of the stigmata of bleeding


ulcers, including prevalence and risks of further

bleeding; A, clean base; B, flat spot; C, adherent


clot; D, visible vessel; E, active bleeding.
After resuscitation and stabilization of the patient, gastric lavage is usually performed to remove
blood from the stomach prior to endoscopy. The goal of endoscopic therapy is to seal the
feeding vessel, and this may be accomplished in a variety of ways. The bleeding source is
identified in more than 95% of patients with significant upper GI hemorrhage (Figure 22).

Figure 22. A, Endoscopic view of an actively bleeding ulcer; B, crosssection of the stomach wall.
Thermally Active Methods
Thermal devices are the most widely tested modalities for endoscopic hemostasis. Heating leads
to edema, coagulation of tissue proteins, and contraction of arteries.Heat may be produced by
tissue absorption of laser light energy, passage of electrical current through tissue, or heat
diffusion from another source. Arterial coagulation is achieved with the laser by means of rapid
heating. The laser is effective for direct coagulation of 0.25-mm arteries and becomes less
effective with larger arteries. The BICAP, or bipolar circumactive probe, is a thermally active
contact or heater probe used to compress the target artery before heat delivery. After the initial
compression, the delivery of a small amount of heat welds the vessel walls together.
Photocoagulation can be achieved by use of the laser. The laser light can be focused on a
bleeding point to induce rapid tissue heating. This produces blood coagulation and tissue
necrosis. Endoscopic hemostasis may be achieved with two types of lasers: argon and Nd:YAG.
The Nd:YAG laser has longer wavelengths, greater coagulation capacity, and increased
perforation potential. Both lasers have been used in the endoscopic treatment of ulcer
hemorrhage (Figure 23).

Figure 23. Endoscopic laser coagulation of a bleeding ulcer.


Clinical trials of ulcer hemorrhage have confirmed that photocoagulation provides effective
hemostasis for active and non-bleeding visible vessels. The success rates with Nd:YAG are in the
range of 80100%. Important considerations that limit emergency laser hemostasis include
portability and cost. Additionally, the need for specific expertise by the endoscopist and
technician, special electrical outlets, eye protection, and technical considerations (difficulty in
aiming the laser beam) are further limiting factors in emergency situations.
Electrocoagulation
Heat generated from high-frequency electrical current is capable of coagulating or cutting
tissue. Thermal electrocoagulation is the classic treatment for bleeding during surgery and has
recently been used endoscopically to treat GI bleeding. Monopolar and multipolar endoscopic
electrodes are currently available, and both must contact the mucosal surface to be effective.
The multipolar electrocoagulation probe has two or more electrodes at the tip. Current is
concentrated much closer to the tip than in the monopolar probe, resulting in less depth of tissue
injury and lower perforation potential. The BICAP features six electrode plates in the tip, a
central irrigation channel, and two different diameter probes (Figure 24). It can achieve a
maximum temperature of 100oC and causes less tissue injury than the monopolar or Nd:YAG
electrocoagulation laser.

Figure 24. A, Endoscopic cauterization of a


bleeding ulcer using BICAP electrocoagulation;
B, corresponding endoscopic view.
Heater Probe
The heater probe is a hollow aluminum cylinder with an inner coil. The cylinder transfers heat
from its end or sides to tissue when positioned perpendicularly or tangentially. This probe may be
passed through the biopsy channels of larger endoscopes and positioned on bleeding lesions to

produce tamponade and heat (Figure 25). Studies have shown the heater probe to be safe and
effective for the treatment of ulcer bleeding or non-bleeding visible vessels, achieving hemostasis
and significantly improving clinical outcomes.

In a comparative study of the heater probe, BICAP, and medical therapy, the heater probe was
more than 95% effective in achieving initial hemostasis. Both the BICAP and heater probes
represent important endoscopic advances in endoscopic hemostasis, and have advantages over
laser therapy. These devices are less expensive, portable, easy to use, have target irrigation, and
allow tamponade and tangential coagulation.

Injection Therapy
Injection therapy for upper gastrointestinal bleeding is inexpensive, simple and widely used. A
sclerotherapy catheter with a small retractable needle is passed through the biopsy channel of the
endoscope. Non-bleeding visible vessels are treated by the injection of a solution at three or four
surrounding sites about 1-3 mm from the vessel. Subsequently, the visible vessel is injected. In
cases of bleeding vessels, injections are made around the bleeding point until hemostasis is
achieved. This is followed by injection into the vessel (Figure 26).

Several different sclerosant agents have been used alone or in combination to achieve endoscopic
hemostasis. Adrenaline; hypertonic saline and adrenaline combined; adrenaline and polidocanol;
pure ethanol; or combinations of dextrose, thrombin, and sodium morrhuate have shown
improvement in rebleeding, the need for urgent surgery, and mortality.
Combined injection and thermal treatment have theoretical advantages in the treatment of

bleeding ulcers. Injection with epinephrine produces vasoconstriction and activates platelet
coagulation, reducing blood flow and potentiating thermal therapy, which produces coaptive
coagulation. Recent studies have shown combination therapy (epinephrine injection and heater
probe) benefited patients with spurting bleeding, but not those with oozing bleeding.
Mechanical Therapy
Endoscopic hemoclips have recently been developed and made their way to the scene of
endoscopic therapy for peptic ulcer disease. These devices are small 3-4 mm titanium clips that
can be opened and closed while being operated through the working channel of the endoscope.
They may be used to pinch-off, or clip, a bleeding vessel. When fully deployed, they remain
fastened to the vessel after the endoscope has been removed from the patient. Emerging studies
have shown that hemoclips are an effective and safe method for treating certain forms of peptic
ulcer desease and should be used in the appropriate setting.

Radiological Therapy
Angiography is a useful diagnostic and therapeutic modality in treatment of bleeding gastric
and duodenal ulcers. Angiography can identify the site of bleeding in instances where
endoscopy has failed to be diagnostic. It should also be considered in patients at high risk for
surgical intervention.
Angiographic therapy includes two different embolization techniques for the treatment of GI
bleeding. Effective in 50% of cases, vasopressin intra-arterial infusion causes vasoconstriction
that results in the cessation of ulcer hemorrhage. Embolic material such as an absorbable gelatin
sponge, tissue adhesives, or other occlusion devices (such as microcoils) (Figure 27) can be
inserted through a catheter into the area of bleeding. Potential complications of embolization
therapy may include ischemia and perforation.

Surgical Therapy
When endoscopic hemostasis techniques are unavailable or fail to resolve bleeding or recurrent
hemorrhage, surgery provides another therapeutic option. Surgery is effective in the prevention of
recurrent ulceration and in excluding the presence of malignant disease. Emergent surgery
(Figures 2830) has a higher mortality rate than elective surgery, and resection procedures are
accompanied by higher mortality than oversewing the ulcer and selective vagotomy, or vagotomy
and pyloroplasty (Figure 29). The operative choice is related to the surgeons experience, ulcer
location, and overall condition of the patient. Truncal vagotomy and antrectomy (Figure 30)
provide high cure rates and low recurrence rates. Recurrence rates after vagotomy and
pyloroplasty are somewhat higher. Laparoscopic selective vagotomy provides an appealing
alternative for a subset of ulcer patients with lower morbidity, shorter recovery time, and a
shorter hospital stay.

Perforation
Approximately 510% of patients with peptic ulcers suffer a perforation into the abdominal
cavity (Figure 31). This rate is higher in men than in women. Approximately 15% of patients die
from ulcer perforation.

Two types of perforation of the stomach and duodenum have been observed. Free perforation
occurs when duodenal or gastric contents spill into the abdominal cavity with peritoneal
contamination by gastric, pancreatic and biliary juices. Clinically this produces an acute
abdomen, which is easily diagnosed. Contained perforation occurs when the ulcer produces a
full-thickness hole in the duodenum or stomach, but the omentum or other adjacent organs
prevent peritoneal contamination.
Perforations are most likely in elderly patients on chronic NSAID therapy, and are more
common in gastric than in duodenal ulcers. Initial symptoms of perforated duodenal or gastric
ulcers include severe abdominal pain, worse in the epigastrium, often accompanied by nausea
and vomiting. Typically the patient is acutely and severely ill. History and physical exam
suggest a diagnosis of perforation. The finding of free air on either an upright or decubitus
abdominal radiograph is noted in approximately 70% of cases (Figure 32).

An upper GI series with gastrografin will confirm the clinical impression of perforation if an xray is negative. Perforation is a contraindication for endoscopy because air insufflation may
exacerbate spillage of gastric contents or disrupt a sealed perforation.
Urgent surgical therapy is recommended in patients with uncontained, free perforated ulcers,
because spontaneous sealing is rare. In addition, gastric adenocarcinoma cannot be ruled out
and there is a greater potential for bacterial colonization. Aggressive surgical intervention helps
to decrease the high mortality associated with perforating gastric ulcers.

Penetration
Five to 10% of perforating ulcers may erode through the entire thickness of the gastric or
duodenal wall into adjacent abdominal organs. Such penetration can involve the pancreas, bile
ducts, liver, and the small or large intestine. The pancreas is the most common site of penetration
(Figure 33).

The acute onset of associated complications, such as pancreatitis, cholangitis, or diarrhea of


undigested food, may diagnose penetration. The diagnosis of penetration is more difficult than
perforation, and is based on a combination of severe ulcer symptoms, atypical pain distribution,
and diminished response to the usual therapy. Surgery is usually not recommended in the
management of penetration unless biliary complications are present or the underlying peptic
disease is severe.
Gastric Outlet Obstruction
Fewer than 5% of patients develop gastric outlet obstruction from pyloric stenosis. Duodenal
ulcers give rise to pyloric stenosis more often than gastric ulcers. Peptic ulcer disease may be
accompanied by varying degrees of obstruction caused by inflammatory swelling of the pyloric
channel or chronic scarring associated with fibrosis.
Patients with gastric outlet obstruction usually have a history of nausea, vomiting, and
epigastric pain or fullness. Laboratory findings may show anemia, low serum albumin, and
hyperkalemic alkalosis. Radiological exam is usually diagnostic, showing a large gastric
shadow with an air/fluid level (Figure 34). An upper GI series yields valuable information by
showing marked delay in gastric emptying and a large atonic stomach. Endoscopy is the best
test for evaluating gastric outlet obstruction after decompression of the stomach for 1224
hours.

Endoscopic Therapy
Endoscopic dilation of the gastric outlet obstruction is a reasonable course after the failure of
medical therapy. Balloon dilation can usually improve the acute problem by producing radial
forces on the strictured segment. Through-the-scope balloons are usually the first choice (over
guide wire balloons), using the largest balloon that can safely be passed into the segment. A welllubricated balloon is passed through the endoscopic biopsy channel and carefully positioned into
the stricture (Figure 35A). The balloon is inflated with contrast, water or air, and pressure is
maintained for the desired time (Figure 35B).
Dilation may also be performed over a guide wire that has been passed through the
stricture. Sequential balloon dilation is performed with fluoroscopy and endoscopic
evaluation. Figure 35C shows the strictured segment after balloon dilation.

Surgical Therapy
The goal of surgical therapy in gastric outlet obstruction is twofold: 1) improvement of the
obstruction and 2) treatment of the predisposing ulcer with an acid-reducing procedure.

Vagotomy and antrectomy (Figure 36) with gastroduodenal drainage, or truncal vagotomy with
drainage (Figure 37) are the recommended surgical procedures

Selective vagotomy with pyloroduodenal dilation is an alternative, but recurrent obstruction rates
are higher than with the other two surgeries.

(SURGERY CASE WRITE UP)


Submitted by RAHUL AUDENESEN

Date : 14th October 2016

Tittle : UPPER GASTROINTESTINAL BLEEDING SECONDARY TO PEPTIC ULCER


DISEASE .