ACHALASIA

GROUP 1
NAME :
1. Ranti Agustini (21117098)
2. Ridia Lokarina (21117100)
3. Rizky Amrin Sidiq (21117102)
4. Selvi Suci Hayati (21117104)
5. Sheli Sulistia Ningsih (21117106)
6. Shindy Prima Utami (21117108)
7. Sici Safitri (21117111)

Supervisor : Sukron, MNS

PROGRAM STUDI ILMU KEPERAWATAN

SEKOLAH TINGGI ILMU KESEHATAN
MUHAMMADIYAH PALEMBANG
TAHUN AJARAN 2018/2019

i
 FOREWORD

By chanting the name of Allah Almighty, the Most Merciful, the Most
Merciful, we pour out praise and praise for His presence, who has bestowed His
grace, guidance, and blessings on us, so that we can complete the paper on
Achalasia.
We have prepared this paper to the maximum and get help from various
parties so that it can facilitate the making of this paper. For this reason, we express
our gratitude to all those who have contributed to the making of this paper.
Apart from all that, we are fully aware that there are still deficiencies both
in terms of sentence formation and grammar. Therefore, with open arms we accept
all suggestions and criticisms from readers so that we can improve this paper.

Palembang, 19th March 2019

Penulis

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 TABLE OF CONTENTS

TITLE PAGE ..................................................................................................................... i

FOREWORD..................................................................................................................... ii

TABLE OF CONTENTS ................................................................................................ iii

BAB I PRELIMINARY .................................................................................................... 1

A. Background .................................................................................................................... 1

B. Problem Formulation...................................................................................................... 2

C. Purpose .......................................................................................................................... 2

BAB II DISCUSSION ....................................................................................................... 4

A. Understanding ................................................................................................................ 4

B. Physiological Anatomy .................................................................................................. 4

C. Epidemiology ............................................................................................................... 11

D. Etiology ........................................................................................................................ 11

E. Pathophysiology ........................................................................................................... 12

F. Clasification .................................................................................................................. 16

G. Clinical Manifestations ................................................................................................ 17

H. Diagnostic Check ......................................................................................................... 18

I. Complications ................................................................................................................ 20

J. Nursing Care.................................................................................................................. 21

BAB III Closing ............................................................................................................... 25

A. Conclusion ................................................................................................................... 25
B. Suggestion.................................................................................................................... 25

Biblioggraphy .................................................................................................................. 26

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 CHAPTER I
PRELIMINARY
A. Background
Acalacia is a primary disorder in esophageal motility. Acalacia is a motor
disorder characterized by a complete progressive relaxation of the lower
esophageal (LES), and progressively complete, loss of peristalsis in the
esophagus. Foods that have been swallowed have difficulty getting into the
upper abdomen and esophagus, LES becomes enlarged. One of several foods
can enter the esophagus and slowly into the stomach from time to time. There
is a danger of aspiration of isiesophagus into the lungs when someone is lying
down. Clients usually present progressively with (months and even years)
dysphagia, usually expressing the feeling that "something is stuck in the
throat".
Etiology of achalasia is not clearly known but there are several factoryang
role are neuromuscular dysfunction, emotional disorders and traumapsychic,
autoimmune, and infectious diseases. Acalacia is characterized by impaired
motility that is lower than two thirds of the esophagus. LES fails to relax
usually by swallowing. Inadequate function occurs because nerve impulses
cannot pass through the esophagus or sympathetic receptors absent from LES.
There may be degeneration of ganglion cells or impulse disorders from
Auerbach's plexus. Propulsion of the disorder and LES results constrict in the
accumulation of food and fluid in the lower esophagus. When the hydrostatic
pressure exceeds the resistance strength of the LES, the contents enter the
stomach. Reflux esophagitis with ulceration is produced. Aspiration of
vomiting of the esophageal contents can result in atelectasis and other lung
problems.
Acalacia often occurs in individuals in their 20s and 30s and appears
frequently in men and women. About 2 people per 200,000 per year will be
diagnosed with achalasia. Clients are often treated for gastroesophageal reflux
(GERD) disease before the diagnosis of achalasia is made.

1
 The initial manifestation of achalasia is dysphagia. It's hard for food and
fluids to pass LES. In the early stages of achalasia, the client may experience
external irritation because the esophageal spasm or may not be able to belch.
Clients can vomit undigested food, eat many hours beforehand and large
amounts of mucus that has been stimulated by irritation of the esophagus.
Upper respiratory tract infections, emotional disorders, overeating, obesity, and
pregnancy can make matters worse. Diagnostic test used to determine the
presence of achalasia including radiologic examination, esophagoscopy,
manometry.
B. Problem Formulation
In this paper, the author will discuss " Achalasia ", for which the main
issues discussed are:
1. What the meaning of the Achalasia?
2. What are the anatomy of the digestive system physiology?
3. How is the epidemiology of Achalasia?
4. How is the etiology of Achalasia?
5. How is the pathophysiology of Achalasia?
6. What are the classification of Achalasia?
7. What are the Clinical Manifestations of Achalasia?
8. What are the diagnostic check of Achalasia?
9. What are the compications of Achalasia?
10. How is nursing care in Achalasia?
C. Purpose
1. To knowing the meaning of the Achalasia?
2. To knowing the anatomy of the digestive system physiology?
3. To knowing the epidemiology of Achalasia?
4. To knowing the etiology of Achalasia?
5. To knowing the pathophysiology of Achalasia?
6. To knowing the classification of Achalasia?
7. To knowing the Clinical Manifestations of Achalasia?
8. To knowing the diagnostic check of Decompensation Cordis?

2
9. To knowing the compications of Achalasia?
10. To knowing nursing care in Achalasia?

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 BAB II
DISCUSSION
A. Understanding
Achalasia is a rare motility disorder where the relative obstruction of the
gastroesophageal junction becomes worse due to the absence of peristaltic
waves in the esophagus. Acalacia is the loss of esophageal peristalsis and
failure of relaxation of the lower esophageal sphincter. The failure to relax the
smooth muscle fibers of the gastrointestinal tract at the intersection of one part
with another in particular the failure of the esofagogaster sphincter to relax at
swallowing due to degeneration of ganglion cells in the organ (Dorland pocket
medical dictionary, 2007).
Achalasia is a motor disorder of the esophageal smooth muscle, where a
complete esophageal peristaltic muscle disorder is accompanied by a
disturbance of the lower esophageal girth muscle, failing to relax completely,
resulting in an esophageal emptying disorder. According to Behrman (1999),
achalasia is a rare motility disorder where the relative obstruction of the
gastroesophageal junction becomes worse due to the absence of peristaltic
waves in the esophagus. Whereas according to Yasmin Asih, et al (1998)
achalasia is the cessation or absence of peristaltic work in the lower 2/3 of the
esophagus and the failure of the cardiac sphincter to relax when swallowing.
Akalasia is a typical condition characterized by the absence of peristalsis of the
lower esophageal body and hypertonic lower esophageal sphincter (SEB) so
that it cannot relax completely when swallowing food. Histopathologically, this
disorder is characterized by degeneration of the myenteric plexus ganglua. As
a result of this condition there will be static food and will further cause
esophageal dilation (Fuad, 2006: 322)
B. Anatomical Physiology
1. Mouth
The mouth or oral cavity is the entrance to the digestive system and contains an
accessory organ that functions in the initial process of digestion. The vestibule
(buccal) cavity is located between the teeth and lips and cheeks as the outer

4
border. The main oral organ is restricted to the teeth and gums at the front, soft
and hard palate at the top, tongue at the bottom, and oropharynx at the back.

a) Lips
Lips are composed of skeletal muscle (orbicularis mouth) and connective
tissue. This organ serves to receive food and speech production.
 The outer surface of the lips is covered with skin containing hair
follicles, sweat glands, and sebaceous glands.
 Transitional areas have transparent epidermis. This part looks red
because it is skipped by many visible capillaries.
 The inner surface of the lips is the mucous membrane. The labia
frenulum section attaches the mucous membrane to the gum in the
midline.
b) Cheeks
The cheeks contain the bucinator maximization muscles. The cheek
epithelial layer is the subject of abrasion and the cell is constantly released to be
replaced with new cells that divide rapidly.

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c) Tongue
The tongue is attached to the floor of the mouth by the lingua frenulum.
The tongue functions to move food when chewed or swallowed, for taste, and in
speech production.
 The extrinsic muscles of the tongue begin in the bone and the tissues outside
the tongue and function in the movement of the tongue as a whole.
 The intrinsic muscles of the tongue have fibers facing various directions to
form angles to each other, this gives great mobility to the tongue.
 Papillae is the elevation of mucous tissue and connective tissue on the dorsal
surface of the tongue. These papillae cause the texture of the tongue to
become rough.
21 Papilla fungiform and circumvallate papilla have taste buds.
22 Watery secretions from the gland of Von Ebner, located in the tongue
muscle, mixed with food on the surface of the tongue and helps taste
taste.
 Lingua tonsils are aggregation of lymphoid tissue in the third third of the
tongue.
d) Salivary glands
The salivary gland secretes saliva into the oral cavity. Saliva consists of
dilute liquid containing enzymes and thick liquid containing mucus.
 There are three pairs of salivary glands, namely:
1. The parotid gland is the largest salivary gland, located slightly down and
in front of the ear and opening through the parotid duct (Stensen) to a
small elevation (papilla) located adjacent to the second molar on both
sides.
2. The submaxillary (submandibular) gland is approximately the size of a
walnut and is located on the inner surface of the mandible and opens
through the Wharton duct to the floor of the mouth on both sides of the
lingua frenulum.
3. The sublingual gland is located at the floor of the mouth and opens
through a small sublingual duct to the floor of the mouth.

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 Saliva consists mainly of serous secretion, which is 98% water and
contains amylase enzymes and various types of ions (sodium, chloride,
bicarbonate, and potassium), also more thick and less mucous secretions
containing glycoprotein (mucin), ions, and water.
 Saliva has the following functions.
1) Saliva chemically dissolves food for taste.
2) Saliva moisturizes and lubricates food so that it can be swallowed.
Saliva also provides moisture to the lips and tongue.
3) Amylase in saliva breaks down starch into polysaccharides and
maltose.
4) Waste substances such as uric acid and urea and various other
substances such as drugs, viruses, and metals are excreted into saliva.
5) Antibacterial and antibody substances in saliva function to cleanse the
oral cavity and help maintain oral health and prevent tooth loss.
 Nerve control in salivary secretions.
1) The flow of saliva can be triggered through psychic stimuli (thoughts
of food), mechanical (presence of food), or chemical (type of food).
2) Stimulus is carried through afferent fibers in cranial nerves V, VII,
IX, and X towards inferior and superior salivatory nuclei in the
medulla. All salivary glands are innervated by sympathetic and
parasympathetic fibers.
3) The volume and composition of saliva varies according to the type
of stimulus and the type of immunization (sympathetic or
parasympathetic system).
a. Parasympathetic stimuli result in vascular vasodilation and a lot
of serous secretions.
b. Sympathetic stimulation results in vasoconstriction of blood
vessels and thick and sticky mucous secretions.
c. In normal humans, the saliva secreted by minute is as much as
1ml. The secreted saliva can reach 1 L to 1.5 L in 24 hours.

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e) Teeth
Teeth are arranged in pockets (alveoli) in the mandible and maxilla.
 Dental anatomy
A. Each arch of the tooth line in the jaw forms a dental arch. The upper arch
is bigger than the bottom so that the upper teeth normally close the lower
teeth.
B. Humans have 2 arrangement of teeth; primary teeth (desiduous, milk
teeth) and secondary (permanent) teeth.
a. The primary tooth in half the dental arch (starting from the space
between the two front teeth) consists of 2 series teeth, one fang and
two graham, for a total of 20 teeth.
b. Secondary teeth start out at the age of 5 to 6 years. Half of the dental
arch consists of 2 series teeth, one fang, two remolar and three molars,
for a total of 32 pieces. The third molars are called wisdom teeth.
3) Dental components
a. The crown is the visible part of the tooth. One to three roots are
embedded from the part of the tooth that is embedded in the alveolar
jaw bone.
b. Crowns and roots meet on the neck that is covered by the gingival
(gums).
c. The periodontal membrane is the connective tissue that lines the
alveolar pouch and attaches to the cementum at the root. This
membrane holds teeth in the jaw.
d. The pulp cavity in the crown extends into the root canal, containing
a dental pulp containing blood vessels and nerves. The root canal
opens to the bone through the apical foramen.
e. Dentin covers the pulp cavity and forms the largest part of the tooth.
Dentine in the crown of the tooth is covered by e-mail and at the root
by the cementum. Email consists of 97% inorganic materials
(especially calcium phosphate) and is the hardest substance in the
body. This substance functions to protect, but can be eroded by

8
 enzymes and acids produced by oral bacteria and result in dental
caries. Fluoride in drinking water or intentionally applied to teeth
can strengthen email.
 Function of teeth. Teeth function in the process of mastication (mastication).
Food that enters the mouth is cut into small parts and mixed with saliva to
form a bolus of food that can be swallowed.
2. Pharynx

Pharynx Is a link between the oral cavity and esophagus. Derived

from Greek, namely Pharynk. There are three divisions of pharynx, namely:
1. Epipharynx (nasopharynx)
2. Mesopharynx (oropharynx)
3. Hypopharynx (pharyngopharynx)
Inside the pharyngeal arch are tonsils (tonsils), which are lymph
nodes which contain lymphocyte glands and are a defense against infection,
here lies a cross between the airway and the food path, located behind the
oral cavity and nasal cavity, in front of the vertebrae. To the top of the front
is associated with the nasal cavity, by means of a hole called koana, the state
of contact is related to the oral cavity through a hole called ismus fausium.
The consistency consists of; The superior part = the very high part of the
nose, the medium = the same height as the mouth and the inferior part = the
same height as the larynx. The superior part is called the nasopharynx, in
the nasopharynx empties into the tube which connects the pharynx to the
eardrum space, the media section is called the oropharynx, this section is

9
 bounded to the root of the tongue called the larynx, which connects the
oropharynx to the larynx.
3. Esophagus
The esophagus is innervated by sympathetic and parasympathetic
innervation (vagus nerve) of the esophageal plexus or commonly called
the Auerbach myenteric plexus which is located between the longitudinal
muscle and the circular muscle along the esophagus The esophagus has 3
functional parts. The upper part is the upper esophageal sphincter (upper
esophageal sphincter), a muscle ring that forms the upper part of the
esophagus and separates the esophagus from the throat. This sphincter
always closes to prevent food from the main part of the esophagus from
entering the throat.
The main part of the esophagus is referred to as the body of the
esophagus, a muscular duct which is approximately 20 cm long. The third
functional part of the esophagus is the lower esophageal sphincter, a
muscle ring located at the confluence of the esophagus and stomach. Like
the upper sphincter, the lower sphincter always closes to prevent food and
stomach acid from returning up / regurgitation into the esophageal body.
The upper sphincter will relax in the process of swallowing so that food
and saliva can enter the upper part of the esophageal body. Then, the
muscles of the upper esophagus located below the sphincter contract,
pressing food and saliva further into the esophagus.
Contractions called peristalsis will bring food and saliva to descend
into the stomach. When this peristaltic wave reaches the lower sphincter,
it opens and food enters the stomach. The esophagus functions to carry
food, fluid, secretions from the pharynx to the stomach through a process
of swallowing, where there will be a formation of bolus food with soft size
and consistency, the process of swallowing consists of three phases,
namely:

10
 1. Oral phase
Food in the form of a bolus due to the mechanical process moves on the
dorsum of the tongue towards the oropharynx, the mole palate and the
upper part of the posterior pharyngeal wall is raised.
2. Pharingeal phase
There is involuntary swallowing, the pharynx and fangs move up due
to contraction m. Stylofaringeus, m. Salipingopharynx, m. Thyroid and
m. Palatopharynx, laryngeal aditus enclosed by epiglottis and laryngeal
sphincter.
3. Oesophageal phase
Phase of swallowing (involuntary) displacement of bolus in food
caused by relaxation m. Cricopharynx, at the end of the lower
esophageal sphincter phase opens and closes again when the food has
passed.
C. Epidemiology
Achalasia is rare compared to other diseases. Most cases occur in middle
age with almost the same sex ratio, more common in adults even though it can
occur in childhood or baby. This disease is also not inherited and usually takes
years to cause symptoms. In the United States there are around 2000 cases of
achalasia every year, most of them at the age of 25-60 years and few in children.
D. Etiology
The cause of this disease is not yet known. However, histologically the
cause of achalasia is found in the form of degeneration of auerbach ganglion
plexus cells along the parachoracic esophagus which causes neurological control
and as a result primary peristaltic waves do not reach the lower esophageal
sphincter.
Based on the theory, the causes of achalasia include:
1. Genetic theory
Achalasia can be reduced in the range of 1% -2% of the population with
achalasia.

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 2. Infection theory
Akalasia is caused by:
a. Bacteria (diphtheria pertussis, dostridia, tuberculosis, syphilis)
b. Virus (herpes, varicella zooster)
c. Toxic substance (gas kombat)
3. Autoimmune theory
Akalasia is caused by an inflammatory response in the esophageal myenteric
plexus dominated by T lymphocytes which play a role in autoimmune diseases.
4. Degenerative theory
Achalasia is associated with the aging process with neurological status or
psychological illnesses such as Parkinson's or depression.
E. Pathophysiology

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 Contraction and relaxation of the lower esophageal sphincter is regulated
by stimulating neurotransmitters such as acetylcholine and P substance, as well
as inhibitory neurotransmitters such as nitric oxyde and vasoactve intestinal
peptide.
According to Castell there are two important defects in achalasia patients:
a. Obstruction of the esophageal and gastric junction due to an increase in
the lower esophageal sphincter (SEB) breaks well above normal and the
failure of SEB for perfect relaxation. Some authors cite an association
between increased SEB and sensitivity to the hormone gastrin. The human
SEB length is 3-5 cm while the normal basal SEB pressure is 20 mmHg.
The achalasia of SEB pressure increases by about twice or approximately
50 mmHg.

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b. The failure of SEB relaxation is due to a decrease in pressure of 30-40%
which normally falls to 100% which will result in food boluses not being
able to enter the stomach. This failure results in retention of food and
drinks in the esophagus. The inability of perfect relaxation will cause
residual pressure. If hydrostatic pressure accompanied by gravity can
exceed residual pressure, food can enter the stomach.
c. Abnormal esophageal peristalsis is caused by aperistaltic and dilated ⅔
lower part of the esophageal corpus. As a result of weak and uncoordinated
peristalsis, it is not effective in pushing food boluses through SEB. With
the development of research in the direction of motility, objectively it can
be determined that esophageal motility is manometric in normal and
achalasia conditions.
In other literature also states that the pathophysiology of achalasia,
namely:
1. Neuropathology
Several types of pathological abnormalities of achalasia have been
suggested. Some of these changes may be primary (eg loss of ganglion
cells and myenteric inflammation), where others (eg degenerative changes
of the vagus and the dorsal motor nucleus of the vagus, or the weakness of
the muscles and mucosa) are usually secondary causes from stasis and long
esophageal obstruction.
 Abnormalities in Extrinsic Conservation
Efferent nerve of n. vagus, with its cell bodies in the dorsal motor
nucleus, stimulates relaxation of LES and peristalsis which is the response
to the process of swallowing. With a light microscope, the vagus nerve
fibers look normal in achalasia patients. However, using an electron
microscope found a Wallerian degeneration of n. vagus with disintegration
of axoplasmic changes in Schwann cells and degeneration of the myehnn,
which are changes similar to nerve transection experiments.
 Abnormalities in Intrinsic Innervation.

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 Nitrergic neurons in the myenteric plexus stimulate inhibition along
the esophageal body and LES that arise during the process of swallowing.
This inhibition is important to produce a stable increase in contraction
along the esophagus, which results in peristaltic movements and relaxation
of LES. In achalasia, the intrinsic nervous system inhibitor of the
esophagus becomes damaged accompanied by inflammation and loss of
ganglion cells along Auerbach's myenteric plexus.
 Plain esophageal muscle abnormalities.
In the muscularis propria, especially in the circular smooth muscle it
is usually thickened in achalasia patients. Goldblum put forward in detail
several muscle disorders in achalasia patients after the esophagectomy
process. Muscle hypertrophy appears in all cases, and 79% of specimens
provide evidence of muscle degeneration which usually involves fibrosis
but includes likuefactive necrosis, changes in vacuolar, and dystrophic
calcification. It is also stated that degenerative changes are caused by
muscles that enlarge their blood supply due to prolonged obstruction and
esophageal dilation. Another possibility is that muscle hypertrophy is a
reaction to loss of innervation.
 Abnormalities in the esophageal mucosa.
Mucosal abnormalities, estimated secondary to chronic luminal
static that has been described in achalasia. In all cases, the squamous
mucosa of a person with achalasia indicates hyperplasia with
papillamatosis and basal cell hyperplasia. The series of p53 in the
squamous mucosa and CD3 + cells always exceeds CD20 + cells, this
situation is significant with chronic inflammation, which may be
associated with a high risk of squamous cell carcinoma in achalasia
patients.
 Skeletal Muscle Abnormalities.
Skeletal muscle function in the esophageal proximal and upper
esophageal spingter is impaired in achalasia patients. Although peristalsis
in skeletal muscles is normal but the amplitude of peristaltic contractions

15
 decreases. Massey et al. also reported that belching reflexes were also
disrupted. This causes the esophagus to massively dilate and acute airway
obstruction.
2. Neurophysiological abnormalities.
In a healthy esophagus, extracellular cholinergic neurons release
acetylcholine causing muscle contractions and increasing LES tone, where
inhibition of NO / VIP neurons mediates inhibition thereby inhibiting the
response of swallowing along the esophagus, which results in LES
peristalsis and relaxation. The key to the abnormality of achalasia is
damage from the postganglionic neuron inhibitor of the LES cyclic
muscle.
F. Classification
Based on etiology, achalasia can be divided into 2, namely:
1. Primary
It is the most common case of achalasia found in the United States. In
this type, the cause of achalasia is unknown, but it is thought to be caused by
a neurotropic virus which results in lesions of the dorsal vagus nucleus in the
brain stem and misenteric ganglia of the esophagus. However, some sources
also state that the auerbach plexus degeneration causes loss of neurological
control resulting in primary peristaltic waves not reaching the lower
esophageal sphincter (SEB) to stimulate relaxation. As for hereditary factors
that are quite influential in this achalasia disease.
2. Secondary
Akalasia is caused by other diseases, including:
 Infection (Chagas disease)
 Gastric carcinoma that invades the esophagus through radiation, toxins
or certain drugs.
 Intraluminer tumors, such as cardia tumors or extra luminous pushing
like pancreatic pseudocysts.
 Anti-cholinergic drugs or post vagotomy.
Clinical picture:

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 No. Symptoms Primary Secondary

Light to severe (> 1 Medium to severe (<6

1. Dysphagia
year) months)

2. Regurgitation Medium to severe Light

3. Weight loss Light (5 kg) Weight (15 kg)

4. Chest pain Mild to moderate Rarely

Pulmonary
5. Is being Rarely
complications

G. Clinical Manifestations
There are main signs of achalasia disease, namely:
1. Dysphagia (difficult to swallow)
The client has dysphagia or is difficult to swallow for solid or liquid food.
The nature of the onset of loss can occur for years before the diagnosis is
clearly known. The location of the obstruction is usually felt at the lower
retrosternal.
2. Regurgitation
Kilen has regurgitation or re-flow. This is related to the client's position (such
as when lying down) and often occurs at night because of the accumulation
of food in the esophagus that widens. However, the distinctive feature is that
the client does not feel sour or bitter.
3. Weight loss
This is because the client is afraid of eating due to odinophagia (pain
swallowing). However, if the disease has lasted a long time there will be
weight gain due to esophageal dilation due to food retention and will increase
hydrostatic pressure which will exceed the pressure of the lower esophageal
sphincter (SEB).
4. Symptoms that accompany the main symptoms, such as pain in the chest.
This symptom is experienced by about 30% of cases but not so felt by the
client. The nature of pain with a substernal location and is usually felt when

17
 drinking cold water. This is a result of complications in food retention in the
form of cough and aspiration pneumonia.
H. Diagnostic Check
1. Radiological examination
Radiological examination is very helpful in establishing a diagnosis
of an illness, this must be correlated with clinical findings and history of the
disease.12 In plain chest X-ray achalasia patients do not reveal air bubbles at
the top of the gaster, can also show an air fluid level image on the side posterior
mediastinum. Barium esophagogram examination with fluoroscopy
examination appears to be dilated in the distal two-thirds region of the
esophagus with abnormal peristalsis and a narrowing of the distal esophagus
or esophagogastric junction that resembles a bird-beak like appearance.
A chest x-ray can show widening of the mediastinum because the
dilated esophagus contains an air-fluid limit. Signs of chronic pulmonary
aspiration can be seen. Evaluation of 'cinefluoroscopic' esophagus will show
three stages:
• Stage 1 or mild achalasia, showing no or little dilatation with minimum
retention of contraceptive material proximal to the lower esophageal sphincter.
Contraction of the esophageal vessels can be seen in this stage and may be
difficult to distinguish from diffuse esophageal spasm.
• Stage 2, shows more dilatation with weak nonperistaltic contractions and
tapered esophagogaster joints, which describe the distal sphincter not being
relaxed or tightly closed.
• Stage 3, shows a very large esophagus with food retention and often looks
like sigmoide
2. Esophagoscopic examination
Esophagoscopy is a recommended examination for all achalasia
patients for several reasons, namely to determine the presence of retention
esophagitis and its severity, to see the cause of the obstruction, and to ensure
the presence or absence of signs of malignancy. On this examination, there is
a widening of the esophageal lumen with a distal narrowing, food debris and

18
 fluid in the proximal part of the narrowing area, pale esophageal mucosa,
edema and sometimes signs of esophagitis due to food retention. The lower
esophageal sphincter will open with a little pressure on the esophagoscope and
the esophagoscope can enter the stomach easily.
3. Manometric Examination
The point is to start the esophageal motor function by checking the
pressure inside the lumen of the esophageal sphincter. This examination shows
quantitative and qualitative motility abnormalities. Examination is done by
inserting a pipe for manometry through the mouth or nose. In the achalasia
assessed is the motor function of the esophageal body and lower esophageal
sphincter. The esophageal body is assessed for resting pressure and peristaltic
activity. The lower esophageal sphincter assessed is resting pressure and its
relaxation mechanism. The typical manometric feature is the increased
pressure of the esophageal body, there is no peristaltic movement along the
esophagus as a reaction to the swallowing process. The lower esophageal
sphincter pressure is normal or elevated and no sphincter relaxation occurs
during swallowing.
4. Barium swallowing or esophago gastro duodenoscopy (EGD); ± monitoring of
esophageal pH or manometer.
Radiological barium examination is usually combined with a gastric
and duodenal diagnostic examination (a series of upper gasyrointestinal
radiological examinations using barium sulfate) using barium sulfate in
swallowed liquid or suspended fluids. The mechanism of swallowing can be
seen directly by fluoroscopic examination or recording of radiographic images.
If an esophageal abnormality is suspected the radiologist can place the patient
in various positions.
5. Motility checks
It functions to check the esophageal motor parts by using a pressure
sensitive catheter or mini mg balloon placed in the stomach and then raising it
again. Pressure is then transmitted to transducers placed outside the patient's
body, measurement of changes in esophageal and gastric pressure greatly

19
 increases the understanding of esophageal activity in a healthy state or during
rest and during swallowing.
I. Complications
Some complications and achalasia as a result of food retention in the
esophagus are as follows:
1. Obstruction of the respiratory tract
Airway obstruction is a respiratory system failure to meet the body's
metabolic needs due to obstruction of the upper airway (from the nose to the
tracheal branching). This airway obstruction often causes respiratory failure.
2. Bronchitis
Bronchitis is an inflammation of the bronchial tubes or bronchi. Inflammation
is caused by viruses, bacteria, smoking, or air pollution (Samer Qarah, 2007).
The definition of acute bronchitis is coughing and sometimes sputum
production is no more than three weeks (Samer Qarah, 2007). The definition
of chronic bronchitis is coughing with sputum every day for at least 3 months
a year for at least 2 consecutive years.
3. Aspiration pneumonia
Aspiration pneumonia is a lung infection caused by inhalation of substances
into the respiratory tract.
4. Lung abscess
Lung abscess is defined as the death of lung tissue and the formation of
cavities that contain dead cells or fluids due to bacterial infection.
5. Meckel diverticulum
Meckel's diverticulum is a congenital disorder, which is a sac (diverticula)
that protrudes from the wall of the small intestine; diverticula can contain
gastric tissue or pancreatic tissue.
6. Esophageal perforation
Esophageal perforation is the rupture of the esophageal wall due to vomiting.
90% of causes of esophageal rupture are iatrogenic, which is usually caused
by medical instrumentation such as paraesophageal endoscopy or surgery.
And 10% is caused by vomiting

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 7. Small cell carcinoma
8. Sudden death
J. Nursing care
A. Assessment
1. Client Identity
Name, age, gender, occupation, entry date, address, MR number, etc.
2. Health History
a. Previous Medical History
Usually clients have experienced upper gastrointestinal disease.
b. Current Health History
Usually the client experiences dysphagia, regurgitation, pain behind the
sternum, anorexia and decreased body weight.
c. Family Health History
The presence or absence of family members who suffer from the same disease
as the client.
3. Physical Examination
a. Head and Neck
Usually the hygiene of the head is maintained and the neck usually does not
have enlarged lymph nodes
b. Eye
Usually the conjunctiva is not anemic, the sclera is not jaundiced and the
palpebra is not edema
c. Nose
Usually no abnormalities are found
d. Mouth
Usually oral and dental hygiene is maintained and the lips mucosa is dry
e. Ear
Usually abnormalities are not found
f. Chest / Thorax
 Lungs
I: usually symmetrical left and right

21
 P: usually fremitus left and right
P: usually sonor
A: usually vesicular, no ronchi, no wheezing
 Heart
I: Ictus is usually not visible
P: Usually Ictus is felt by 1 finger LMCS RIC V
P: usually the heart is within normal limits
A: usually regular rhythms
g. Abdomen
I: usually not ascites, concave
Q: Usually liver and spleen are not palpable
P: usually Tympani
A: usually a normal BU
h. Genitourinary
There are usually no abnormalities and complaints
i. Extremity
Usually there is no edema
4. Daily activities
a. Nutrition
Anorexia, nausea, vomiting, bad stomach, weight loss.
b. Rest / sleep
Weakness, fatigue, heavy activity arises shortness of breath, difficulty
sleeping
c. Elimination
Usually clients do not experience interference
d. Personal hygiene
Usually the client's cleanliness is maintained
B. Focus of Intervention
a. Disorders of nutrition fulfillment are less than the body's needs b / d
inadequate intakes are characterized by nausea vomiting.

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Objective: Nutritional needs are met with the results criteria: BB within
normal limits
Intervention:
• Assess client's nutritional needs
• Give clients a small but frequent meal
• Give food warm
• Give clients motivation to want to spend food
Rational :
• By knowing the nutritional needs of the client can be assessed the extent of
the client's nutritional deficiencies and determine the next step
• To reduce gastric fulfillment and facilitate absorption
• Warm food is expected to reduce nausea / vomiting
• Clients feel cared for and try to spend their food
b. Activity intolerance b / d physical weakness
Objective: Clients can carry out activities according to the level of tolerance
with the results criteria: Clients can carry out daily activities according to their
level of ability.
Intervention:
• Assess the cause of fatigue
• Help clients meet basic needs
• Provide a calm environment and uninterrupted resting period
• Provide a safe environment
Rational :
• To find out the factors that decrease activity tolerance
• Maximizing the fulfillment of the client's basic needs
• Save energy for activities
• Avoid injuries from accidents
C. Implementation
It is the application of an action plan that has been prepared with priority
problems and this activity is carried out by nurses to help meet client needs
and achieve expected goals.

23
 D. Evaluation
It is the final stage of the nursing process to determine the expected outcome
of the actions taken and the extent to which the client's problem is resolved.
The nurse carries out a review to determine the next action if the goal is not
achieved.

CHAPTER III
CLOSING
A. Conclusion

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 Achalasia is a primary esophageal motor disorder characterized by failure
of the hypertonic lower esophageal sphincter to relax during ingestion and loss
of peristalsisesophagus. Acalacia often occurs in individuals in their 20s and 30s
and appears as often in men and women. The factors that influence the
occurrence of achalasia disorders are neuromuscular dysfunction, emotional
disorders and psychological trauma, autoimmune and infectious diseases.
Achalasia sufferers can be helped by several therapies so that the disease
does not worsen, such as: calorie intake, medical treatment, dilatation measures,
psychotherapy, and surgery for cardiocotomyotomy (Heller's surgery).
However, the therapeutic nature of the installation is only palliative, because the
esophageal peristaltic function cannot be restored.
Treatment of a client with achalasia disorder can be done by performing
several diagnostic tests. Examination with barium contrast, you will see a picture
of narrowing and stenosis in the cardiaesophagus with a proximal part of the
esophageal dilation. In achalasia, the esophageal dilatation is seen, the dilated
part of the esophagus appears hypertrophy with thinning walls and at an
advanced stage shows elongation. Esophagoscopic examination to determine the
presence of retention esophagitis and its severity, see the cause of obstruction,
and to ensure the presence or absence of malignancy. At this examination, there
appears widening of the esophageal lumen with a narrowing of the internal,
leftover food and fluid in the proximal part of the narrowing area, esophageal
mucosa pale, edema and sometimes there are signs of aldebate retention
esophagitis. Manometric examination to determine motorikesophageal function
by checking the pressure inside the sphincter lumen esophagus. This
examination is to show motor abnormalities quantitatively and qualitatively.
B. Suggestion
By studdying this material, students are expected to be able to know about
Achalasia. So that it can deepen science.

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