Case Presentation

(G.E.R.D)

INTRODUCTION
Gastroesophageal reflux disease (GERD), Gastric reflux disease, or Acid reflux disease
is defined as chronic symptoms or mucosal damage produced by the abnormal reflux in
the esophagus.

This is commonly due to transient or permanent changes in the barrier between the
esophagus

and the stomach. This can be due to incompetence of the lower esophageal sphincter,
transient

lower esophageal sphincter relaxation, impaired expulsion of gastric reflux from the
esophagus,

or a hiatal hernia

CASE ABSTRACT

This is a case of DC a 68 yr. old female residing at Kabihasnan., the patient was

received at PCH last July 22, 2009 at 05:39 pm with a chief complaint of D.O.B and

Abdominal pain. Initial vital signs were taken BP -90/60, T-36.3˚C, RR- 30 cpm, PR-

110 bpm. Initial diagnosis was(G.E.R.D) Gastroesopageal reflux disease. The patient

was subjected for ECG, Na, K+, CBC, and urinalysis and was given Ranitidine,

Domperidone, esomeprazole, hydryt and Kalium as prescribed.

LEARNING OBJECTIVES

General Objective
  To be able to know the comprehensive process of the disease condition

Specific Objectives

 To be able to perform or identify the patient in response to the disease condition

 To be able to discuss the normal anatomy and physiology

 To be able to trace the pathophysiology of the Disease

 To be able to know comprehensively the laboratory examinations, diagnostic

examinations and the treatment accompanied to the disease process of G.E.R.D

 To be able to assimilate all the learning experience garnered with this case study

 To be able to formulate an efficient and effective Nursing Care Plan

BIOGRAPHIC DATA

Name: DC

Age: 68

Gender: Female

Civil Status: Married

Date of Birth: December 8 1940

Address: kabihasnan

Place of Birth: Parañaque

Reiligion: Roman Catholic

Educational Attainment: Highschool

Language Spoken: Tagalog

Admitting Diagnosis/Impression: Community Acquired Pneumonia (Moderate to high

risk)

Admitting Physician: Dr. Karishma Sumilin

NURSING HISTORY

Chief Complaint: Difficulty of breathing

 History of present illness: 1 days prior to admission patient experience acute

pain, radiating upward(heartburn) with associated pericardial pain.

PAST MEDICAL HISTORY

Immunization status: not complete

Hospitalization: Fever

FAMILY HEALTH HISTORY

Health Stage and ages of (cause of death)

Siblings: none

Spouse: none

PHYSICAL EXAMINATION
Date Performed: July 22, 2009 No. Of Hospital Days: 1 days

1. Measurement:
1.1 Weight: 54 kgs Height: 5’4
1.2 Vital Signs:
 Temperature: 36.3 0C PR: 110 bpm RR: 30 cpm BP: 90/60 mmHg

2. General Appearance
The Client is conscious, coherent and oriented to place and person.
Looks according to his age.
3. Skin
Inspection: General color of the skin is brown, uniform in color except on part
not exposed to the sun.
Palpation: Skin is dry with poor skin turgor; with flush skin and warm to touch.

4. Head

Inspection: Normocepahalic, appears round, evenly distributed hair with no

dandruff, lesions and infestations.
Palpation: No mass noted.

5. Eyes

Inspection: Eyes are symmetrical, the conjunctiva is pink and with anicteric
sclera. Cornea and lens are smooth and clear. Pupil is equally round and reactive to
light.

6. Ears

Inspection: Symmetrical and proportional to the head. The external canal has
no purulent discharge.

Palpation: Upon palpation, both ears are non-tender with no presence of mass
or nodules.

7. Nose

Inspection: Nasal folds are symmetrical. Nasal septum is located at the

midline. Mucosa is pink and moist, and intact without presence of discharge.

Palpation: Airways are patent on both nasal nares. No tenderness on frontal

and maxillary sinuses.

8. Mouth

Inspection: Upon inspection of the mouth, the lips are pinkish and dry with
tongue located at the midline. Gums and mucosa are pinkish and with missing teeth.

9. Pharynx
 Inspection: Uvula is midline. Right tonsils and posterior pharyngeal wall are not
inflamed.

10. Neck

Inspection: Neck is symmetrical with full range of motion. No visible deformities

seen

Palpation: Trachea is midline. No swelling and tenderness of lymph nodes

noted. Thyroid gland is non-palpable, no mass noted.

11. Chest and Lungs

Inspection: Shape of the chest is symmetrical. No lesions noted. I&E ratio is 1:2
with dyspnea.

Palpation: Anterior-Posterior-Lateral ratio is 1:2 with symmetrical lung expansion

and symmetrical vocal/tactile fremitus.

Percussion: The sound of resonance was found at the 1st to 4th ICS and
dullness at left 5th ICS midclavicular line.

Auscultation: Bronchial sound is heard over trachea, bronchovesicular sound at

2nd and 3rd ICS and vesicular sound at the base of the lung. With crackles heard on the
lower posterior back.

12. Heart

Inspection: Precordium is normo-dynamic

Palpation: No presence of abnormal pulsations at precordium

 Auscultation: The point of maximum impulse is located at the 5th ICS MCL with
regular heart rhythm. Heart sounds S1 is louder at the apex; S2 is louder at the base.
No extra heart sound noted.

13. Breasts and Axillae Area: (NOT ASSESSED)

14. Abdomen

Inspection: The client’s abdomen is flat with symmetrical configuration. No scars,

lesions, striae noted. The color of the skin is slightly lighter than those areas exposed to
sun.

Auscultation: Bowel sound was normoactive.

Percussion: Tympanic sounds are heard over areas of RLQ and LLQ. Dullness
was heard over RUQ (liver), dullness over LUQ (spleen)

Palpation: There was no tenderness when palpated.

15. Genito-Urinary System: (NOT ASSESSED)

ANATOMY

The esophagus is a member of the digestive tract whose main responsibility is to

transfer food
from the pharynx to the stomach. It measures about 10 inches in length and is tubular
and

collapsible. The esophagus can be traced from the originating point of the larynx
running behind

the trachea. It traces down the mediastinum of the thorax until it runs into the
diaphragm, ending

just above the stomach’s opening. The esophageal hiatus refers to the opening in the
diaphragm.

Nonkeratinized stratified squamous epithelium lines the esophagus. The walls

themselves are

either created by skeletal muscles or by smooth muscle tissue. Skeletal muscle lines
the upper

1/3 of the esophagus, while the middle 1/3 is a combination of the two muscle tissues,
leaving

the remaining 1/3 as smooth muscle tissue. Where the stomach and the esophagus
meet, there is

a thickening of the circular muscle fibers, creating the gastroesophageal sphincter, or

the lower

esophageal sphincter. This sphincter is responsible for maintaining the food and fluids
inside the

stomach, preventing regurgitation up into the esophagus. Air in the lungs creates an
additional

pressure in the lower thoracic region, encouraging regurgitation of foods and fluids.
The Mechanisms of Swallowing

Deglutition is the term given to the process of swallowing, a highly mechanical and
functionally

complex process that allows the initiation of digestion to occur. Deglutition is typically
described

in three basic phases, allowing for clarity.

The initial stage of deglutition is preceded by mastication if there is a solid in the

process. This is

a voluntary stage, meaning that a human must begin this stage consciously. The oral
cavity

closes and the process of breathing is temporarily suspended. The bolus has been
formed through
the process of mastication, and the tongue then lifts the bolus firm against the
transverse palatine

folds of the hard palate. The mylohyoid muscle and the styloglossus muscle contract to
produce

this experience.

The secondary stage takes over from this point, passing the bolus through the pharynx.
The

second stage of deglutition is involuntary. Sensory receptors that are positioned at the
opening of

the oropharynx stimulate the secondary action. The tongue is pressing the bolus against
the

transverse palatine folds of the hard palate, which creates a seal against the
nasopharynx. This

not only prevents the bolus from entering the airway, but it also stimulates the pressure
senses of

the oropharynx and forces the bolus into the opening. The soft palate along with the
uvula close

off the rest of the nasopharynx while the bolus passes into the gullet, and the hyoid
bone and the

larynx elevate protectively. The constrictor muscles of the pharynx then contract in a
rhythmic

and intentional sequence in order to force the bolus through the pharynx, where it will
then enter

the esophagus. This entire stage can be completed in less then a second.

The final stage of deglutition is also involuntary, and it deals specifically with the bolus
entering

and passing through the esophagus. Peristalsis kicks in naturally and the bolus in
pressured down

the esophagus. Fluids are rushed through this entire process, all three stages, in under
a second,
while an average sized bolus takes approximately 5 to 8 seconds to complete the three
stages.

Pathophysiology

The development of GE reflux disease depends on a combination of the following four

factors: (1) defective anti-reflux mechanism, (2) the presence of caustic gastric
contents, (3) poor esophageal clearance, (4) diminished esophageal mucosal
resistance.

1) Anti-reflux mechanism

As intra-abdominal pressure is always greater than intrathoracic pressure, if it were not

for an anti-reflux barrier, GE reflux would be occurring almost constantly. The role of the
esophageal sphincter refers to a segment of specialized circular mucosa at the GE
junction approximately 3 cm in length which maintains a pressure 10 mmHg to 40
mmHg higher than the pressure of the stomach thereby preventing GE reflux.

Before the advent of widespread use of esophageal manometry, primary LES hypotonia
was felt to account for all cases of GE reflux disease. Using modern manometric
techniques, however, it has been demonstrated that only the minority (10-20%) of
patients with GE reflux disease do in fact have lower than normal LES pressures. It is
now believed by most investigators that the presence of transient LES relaxation
explains GE reflux in the majority of patients. Normally the LES relaxes briefly after a
peristaltic wave to allow passage of the bolus from the esophagus into the stomach.
Transient LES relaxation refers to inappropriate relaxation of the sphincter occurring
without a preceding peristaltic wave and lasting up to 30 seconds in duration. These
transient sphincter relaxations allow for reflux of caustic gastric contents into the
esophageal body.

The presence of a hiatus hernia, originally felt to be central in the pathogenesis of

GERD has continued to be the subject of much debate and controversy. Many patients
have GERD in the absence of hiatus hernias, and only the minority of patients with
hiatus hernias develop GE reflux. Recent studies on cats and human beings have
shown that the crural diaphragm does play a role in maintaining basal LES pressure. It
is unclear, however, how important a factor this is in most patients for maintaining LES
competence.

2) Gastric Contents

In order for gastroesophageal reflux to result in esophageal damage and symptomatic

heartburn there must be material in the stomach which is caustic to esophageal
mucosa. Clearly acid present in the stomach is the primary caustic agent, underscored
by the dramatic improvement almost all patients feel and endoscopic exam
demonstrates in patients with severe esophagitis. The role of other caustic agents such
as pepsin, bile salts, pancreatic enzymes and bicarbonate is less clear.

People with GE reflux disease have not been shown to be hypersecreters of gastric
acid, however, patients with delayed gastric emptying either on the basis of pyloric
stenosis or gastroparesis frequently develop resultant severe GE reflux.

3) Esophageal Clearance

In order for the caustic reflux to cause tissue damage it must be in contact with the
mucosa for a sufficient period of time. Normally refluxed material is cleared by a
combination of gravity and secondary peristalsis. In patients with disordered esophageal
peristalsis, particularly scleroderma, the material refluxed into the esophagus has the
opportunity to have prolonged contact with the esophageal mucosa thereby causing
severe erosive damage especially when the patient is supine. Additionally important
clearance is salivary and esophageal bicarbonate formation which helps neutralize the
refluxed acid.

4) Esophageal Mucosal Resistance

A more recently identified and poorly understood component of the defensive

mechanism in preventing GERD is esophageal mucosal resistance. The factors
involved in esophageal mucosal resistance to acid are much less well understood and
much more poorly developed than mucosal resistance factors of the stomach. What is
known, however, is that patients can develop erosive esophagitis in the setting of very
minimal GE reflux documented by a 24 hour pH probe, and on the other hand there are
patients with severe GE reflux as documented on pH probe which do not develop
significant esophageal damage.
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