Group Reports 6

Medical Surgical Nursing 1

" Cholelithiasis (Gallstones) and Cholecystitis (Gall Bladder Infection) "

Teaching Lectures :

Ns. Idramsyah, M.Kep., Sp.Kep.MB.

Group 6 :

1. Alda Bhumi Nauli Barubara P01720322001

2. Indo Putra Ali Dayanto P01720322021
3. Tari Diaslara Putri P01720322039

PIONNER OF INTERNATIONAL CLASS

PROFESSIONAL NURSING PROGRAM

HEALTH POLYTECHNIC OF BENGKULU

ACADEMIC YEAR 2023/2024

 FOREWORD

In the name of Allah SWT, the Most Gracious and Most Merciful. We give thanks to
His presence who has bestowed His grace, guidance, and Inayah upon us. So that we can
complete the task of this paper.
This paper has been prepared optimally and received information from various sources
so that it can facilitate the preparation of papers. Even though we have collected various
references to build this paper, we realize that in the paper we have compiled there are still
many mistakes and deficiencies, therefore constructive criticism and suggestions are
needed. We prepared this paper with the aim of fulfilling the assignment for the Medical
Surgical Nursing course. Hopefully this paper can provide useful information for all of us.

Bengkulu. August 01 2023

Group 6

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 TABLE OF CONTENTS

FOREWORD........................................................................................................................................i
TABLE OF CONTENTS....................................................................................................................ii
CHAPTER I.........................................................................................................................................1
INTRODUCTION...............................................................................................................................1
A BACKGROUND......................................................................................................................1
B. FORMULATION OF THE PROBLEM................................................................................1
C. OBJECTIVE............................................................................................................................2
CHAPTERII........................................................................................................................................3
CONTENTS.........................................................................................................................................3
A UNDERSTANDING................................................................................................................3
D. PHYSIOLOGICAL ANATOMY...........................................................................................5
F. PATHOPHYSIOLOGY..........................................................................................................8
G. CLINICAL MANIFESTATIONS......................................................................................9
H. DIAGNOSTIC EXAMINATION.......................................................................................9
I. COMPLICATIONS...............................................................................................................10
J. THE CONCEPT OF NURSING CARE...............................................................................10
CHAPTER III....................................................................................................................................19
CLOSING..........................................................................................................................................19
A CONCLUSION......................................................................................................................19
B. CRITICISM AND SUGGESTIONS....................................................................................19
BIBLIOGRAPHY..............................................................................................................................20

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iii
 CHAPTER I
INTRODUCTION

A. BACKGROUND
According to Arif Kurniawan (2017), Cholelithiasis is gallstones formed due to an
imbalance of chemical content in bile which causes the deposition of one or more bile
components. Cholelithiasis is a public health problem and often occurs throughout the
world, although the prevalence varies in each region.

One of the factors that can trigger or cause cholelithiasis is the lifestyle of people who
are increasing, especially people with a middle and upper economy prefer to consume fast
food with high cholesterol so that blood cholesterol is excessive and settles in the
gallbladder and becomes a gallbladder and with a lack of knowledge and awareness about
the consequences of wrong food consumption is very dangerous for their health
(Adreyne, et al, 2016).

Cholecystitis is inflammation that occurs in the ducts of the gallbladder and is

divided into acute and chronic. In America 10-20% of the population suffers from
cholelithiasis (gallstones) and a third suffers from acute cholecystitis, while in Indonesia
the incidence of cholecystitis is not known with certainty, but research at the Anatomical
Pathology Laboratory of Al-Islam Hospital, Bantul in 2003 - 2007 showed an incidence of
cholecystitis of 174 cases (Elber, 2013).
Acute cholecystitis usually occurs due to obstruction of the cystic duct by a stone,
and usually occurs after obstruction of the cystic duct by a stone, obstruction will increase
pressure in the gallbladder and cause ischemia of the gallbladder wall and mucosa.
Retention of the gallbladder causes irritation and is often followed by bacterial
inflammation (Lemone, 2016). Specific clinical symptoms for diagnosing cholecystitis are
biliary colic (Keshav, 2015).

B. FORMULATION OF THE PROBLEM

The formulation of the problem in this paper is as follows:

1. What is meant by cholelithiasis and cholecystitis?

2. What is the epidemiology of cholelithiasis and cholecystitis?
3. What is the etiology of cholelithiasis and cholecystitis?
4. What is the anatomy and physiology of cholelithiasis and cholecystitis?
5. What are the classifications of cholelithiasis and cholecystitis?
6. What is the pathophysiology of cholelithiasis and cholecystitis?
7. What are the clinical manifestations of cholelithiasis and cholecystitis?
8. How is the diagnostic examination of cholelithiasis and cholecystitis?

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9. What are the complications of cholelithiasis and cholecystitis?
10. What is the concept of nursing care for cholelithiasis and cholecystitis?

C. OBJECTIVE
The purpose of making this paper is as follows:

1. Know the definition of cholelithiasis and cholecystitis

2. Know the epidemiology of cholelithiasis and cholecystitis
3. Know the etiology of cholelithiasis and cholecystitis
4. Know the anatomy and physiology of cholelithiasis and cholecystitis
5. Know the classification of cholelithiasis and cholecystitis
6. Know the pathophysiology of cholelithiasis and cholecystitis
7. Knowing the clinical manifestations of cholelithiasis and cholecystitis
8. Knowing how to do a diagnostic examination of cholelithiasis and cholecystitis
9. Knowing the complications of cholelithiasis and cholecystitis
10. Knowing the concept of nursing care for cholelithiasis and cholecystitis

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 CHAPTER II
CONTENTS

A. UNDERSTANDING

(Cahyono, 2014) Cholelithiasis is the presence of stones in the gallbladder whose

exact cause is not yet known, but some of the most important predisposing factors seem
to be metabolic disorders caused by changes in the arrangement of bile and infections
that occur in the gallbladder and cholesterol. Excessive precipitating in the gallbladder
but the mechanism is not known with certainty, hormonal factors during pregnancy, can
be associated with the slow emptying of the gallbladder and is one of the causes of the
high incidence of cholelithiasis, as well as the occurrence of infection or inflammation of
the bile plays a role in the formation of gallstones. .(Rendi, 2012) Cholelithiasis is a
deposit of one or more components including bile cholesterol, billirubin, salt, bile,
calcium, protein,fatty acids, and phospholipids.Cholelithiasis is also called gallstones,
gallstones, biliary calculus. The term cholelithiasis refers to the formation of stones in
the gallbladder. Gallbladder stones are a combination of several elements that form a
stone-like material that forms in the gallbladder. Gallstones are crystal deposits in the
gallbladder or in the bile ducts. Stones found in the gallbladder are called cholelithiasis,
while stones in the bile ducts are called choledocholithiasis (Nucleus Precise Newsletter,
issue 72, 2011).

Cholecystitis is inflammation that occurs in the ducts of the gallbladder and is

divided into acute and chronic.Cholecystitis is an inflammation or inflammation of the
gallbladder which usually occurs due to a blockage in the bile duct, namely in the form of
gallstones. (Smeltzer, 2010). Cholecystitis is an inflammatory disease of the gallbladder
which is often caused by gallstones but can also be caused by ischemia, motility
disorders, direct trauma to chemicals, microorganism infections, protozoa, parasites, and
allergic reactions. (Journal of Hepatobiliary Pancreas Surgery, 2016).Acute cholecystitis
usually occurs due to obstruction of the cystic duct by a stone, and usually occurs after
obstruction of the cystic duct by a stone, obstruction will increase pressure in the
gallbladder and cause ischemia of the gallbladder wall and mucosa.

B. EPIDEMIOLOGY

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 Cholelithiasis is very common in the general population and reports show that out of
11,840 autopsies, 13.1% were men and 33.7% were women with gallstones. the most
common age is 40–50 years and increases at the age of 60 with age, from 20 million
people in western countries 20% of women and 8% of men suffer from cholelithiasis over
the age of 40 (Cahyono, 2014). Approximately 12% of the total adult population in
western countries suffers from cholelithiasis, so around 20 million people suffer from
cholelithiasis. Every year, around 1 million cholelithiasis patients are found and 500,000
people undergo gallstone removal surgery (cholecystectomy or chole laparoscopy).

Cholecystitis is inflammation that occurs in the ducts of the gallbladder and is divided
into acute and chronic. In America 10-20% of the population suffers from cholelithiasis
(gallstones) and a third suffers from acute cholecystitis, while in Indonesia the incidence
of cholecystitis is not known with certainty, but research at the Anatomical Pathology
Laboratory of Al-Islam Hospital, Bantul in 2003 - 2007 showed an incidence of
cholecystitis of 174 cases (Elber, 2013).

C. ETIOLOGY
According to Cahyono 2014, the etiology of cholelithiasis is:
a. Cholesterol supersaturation in general composition.
The composition of bile that affects the formation of stones depends on the balance
of bile salts, cholesterol and lecithin. The higher the cholesterol level or the lower the
bile salt content will make the condition in the gallbladder become saturated with
cholesterol (cholesterol supersaturation).
b. Formation of cholesterol nuclei.
Cholesterol is transported by micelles (clumps containing phospholipids, bile salts
and cholesterol). If the saturation, cholesterol is higher then it will be transported by
vesicles where the vesicles can be described as a two-layered circle. If there is a large
concentration of cholesterol and it can be transported, the vesicles multiply in layers of
circles, in the end in the gallbladder, cholesterol transporters, both micelles and vesicles
combine to become one and in the presence of mucin protein will form cholesterol
crystals, fragmented cholesterol crystals will eventually be glued or united.
c. Decreased gallbladder function
The reduced ability to spray and damage to the gallbladder wall makes it easier for
someone to suffer from gallstones, weakened contractions will cause bile stasis and will
make the mucin produced in the bile accumulate along with the length of time bile is
accommodated in the gallbladder. The mucin will be thicker and more concentrated,
making it more difficult for the process of emptying bile. Some conditions that can
interfere with the contractile power of the gallbladder, namely: bile hypomotility, total
parenteral (causing bile acid to slow down), pregnancy, spinal cord injury, diabetes.

The causes of cholecystitis according to Susan Smeltzer (Brunner and Suddarth,

2015), namely:
1. Bile stasis
2. Infection (E. coli, streptococcus)
3. Gallbladder wall ischemia
4. Bile concentration
5. Cholesterol
6. Prostaglandins (which damage the mucous lining of the gallbladder wall)
7. Lysolecithin

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D. PHYSIOLOGICAL ANATOMY

The gallbladder is a pouch-like, hollow organ about 10 cm long, located in a

fossa that defines the anatomical boundary between the right and left lobes of the liver.
The gallbladder is a hollow, oval-shaped pouch like an advocate just below the right lobe
of the liver. The gallbladder has a fundus, body and neck. The fundus is round, blind end
of the gallbladder which extends slightly above the rim of the liver. The corpus is the
largest part of the gallbladder. The neck is the narrow part of the gallbladder that lies
between the body and the cystic duct area. The bile secreted continuously by the liver
enters the small bile ducts in the liver. The smaller bile ducts unite to form two larger
ducts which emerge from the undersurface of the liver as the right and left hepatic ducts
which soon unite to form the common hepatic duct. The hepatic duct joins the cystic duct
to form the choledochal duct (Syaifuddin, 2011).

1. Gallbladder anatomy
1) Bile structure
The gallbladder is a bushy pear-shaped pouch that lies on the visceral surface.
The gallbladder is covered by peritoneum except for the part attached to the liver,
which is located on the undersurface of the liver between the right and quadratus
lobes of the liver.
2) Bile consists of:
a) Vesika fela fundus: round in shape, usually protruding below the inferior
border of the liver, connected to the anterior abdominal wall at the level of
the cartilage of the tip of the right IX rib.
b) Corpus vesica fela: in contact with the visceral surface of the liver pointing
upwards backwards and to the left.
c) Vesika felea column: continues with the cystic duct which runs with the
lesser omentum, unites with the right side of the common hepatic duct to
form the doctus colledukus.

3) Bile liquid

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 Bile is a viscous, golden yellow (greenish yellow) liquid which is
produced continuously by liver cells, approximately 500-1000 ml a day. Bile is an
essential substance needed in the digestion and absorption of fat.

4) Elements of bile:
a) Salts - bile salts: synthesized by the liver from cholesterol, a steroid alcohol
that is produced in large quantities by the liver. Bile salts function to help
digest fat, emulsify fat with lipase glands from the pancreas.
b) Enterohepatic circulation: bile salts (bile pigments) are absorbed from the
small intestine into the portal vein, flowed back to the liver to be reused.
c) Bile pigments: are the main result of the breakdown of hemoglobin. Hepatic
cells transport hemoglobin from the plasma and secrete it into the bile. Bile
pigment has no function in the digestive process.
d) Bacteria in the small intestine: converts bilirubin into urobilin, which is a
substance that is absorbed from the intestine, is converted into stercobilin
which is secreted into the feces, causing yellow stools.

5) Bile duct
The bile ducts gather into the hepaticus duct and then unite with the cystic
duct, because it will be stored in the gallbladder. Bile undergoes thickening 5-10
times, removed from the gallbladder by the action of cholecystectomy, a hormone
produced in the mucous membrane of the upper small intestine where fat enters.
Cholecystokinin causes contraction of the gallbladder muscles. At the same time
relaxation occurs so that bile flows into the cystic duct and common duct
(Syaifuddin, 2011).

2. Bile physiology
Bile is a product of the liver, is a liquid that contains mucus, has a greenish-
yellow color and has an alkaline reaction. The composition of bile is bile salts, bile
pigments, cholesterol, lecithin, fat and organic salts. Bile pigments consist of
bilirubin and bilverdin. At the time of damage, the red blood cells break down into
globin and bilirubin, which are pigments that no longer contain iron.

Bilirubin formation occurs in the reticulordothelial system in the bone

marrow, spleen and liver. Bilirubin that has been released into the blood circulation is
called hemobilirubin while the bilirubin contained in the bile is called cholebilirubin.
Bile salts are formed in the liver, consisting of sodium glycocolate and sodium
taurocholic. These bile salts will cause cholesterol in the bile in a state of solution.

These bile salts have hydrotropic properties. Bile salts increase the action of
enzymes originating from the pancreas, namely trypsin amylase and lipase. Bile salts
increase absorption increasing the absorption of both neutral fats and fatty acids. Bile
is produced by the liver and stored in the gallbladder before being excreted into the
intestine.

At the time of digestion, the gallbladder circumference muscle is in a state of

relaxation. Simultaneously, the pressure in the gallbladder will increase and there
will be contractions in the gallbladder so that bile flows and enters the duodenum.

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 Stimulation of the sympathetic nerves results in contractions of the gallbladder
(Suratun, 2010).

E. CLASSIFICATION

According to the macroscopic appearance and chemical composition, gallstones are

classified into 3 (three) groups. (Sylvia and Lorraine, 2006)
1. Cholesterol stones Oval, multifocal or mulberry shaped and contain more than 70%
cholesterol. More than 90% of gallstones are cholesterol (stones containing > 50%
cholesterol). Three main factors are needed for the formation of cholesterol stones:
a. Cholesterol supersaturation
b. Gallbladder hypomotility
c. Nucleation or nidus formation is rapid

2. Pigment stone
Pigment stones constitute 10% of the total new types of bile containing <20%
cholesterol. Types include:
a. Calcium bilirubinan pigment stones (brown pigment)
It is brown or dark brown in color, soft, easily crushed and contains calcium-
bilirubinate as the main component. Brown pigment stones are formed due to stasis
factors and bile duct infection. Stasis can be caused by sphincter of Oddi
dysfunction, strictures, biliary surgery, and parasitic infections. If there is an
infection of the bile duct, especially EColi, the levels of B-glucuronidase enzymes
originating from bacteria will be hydrolyzed to free bilirubin and glucuronic acid.
Calcium binds bilirubin to become insoluble calcium bilirubinate. From the research
conducted, it was found that there is a close relationship between bacterial infection
and the formation of brown pigment stones. Generally these brown pigment stones
form in the bile ducts in infected bile.
b. Black pigment stone.
Black or brownish-black in color, shapeless, powdery and rich in black residue
that was not extracted.' Black pigment stones are the most common type of stone
found in patients with chronic hemolysis or liver cirrhosis. These black pigment
stones consist mainly of polymerized bilirubin derivatives. The pathogenesis of stone
formation is unclear. Generally, black pigment stones form in the gallbladder with
sterile bile

3. Mixed stone

4. Mixed stone between cholesterol and pigment which contains 20-50% cholesterol

According to Dr. Suparyanto, 2009 Cholecystitis based on the time it occurs is

divided into 2, namely:
1. Acute cholecystitis
Namely inflammation of the gallbladder which is usually caused by gallstones
in the cystic duct which is characterized by sudden pain
2. Chronic choletitis

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 Namely chronic inflammation of the gallbladder and is characterized by
recurrent pain with a sharp and intense quality.
Cholecystitis based on the onset of the disease is divided into 2, namely:
1. Calculus choletitis
Namely cholecystitis caused by gallstones in the cystic duct so that it can cause
a chemical reaction, autolysis occurs and edema and blood vessels in the
gallbladder will be compressed so that the vascular supply is disturbed. The
result will be gangrene of the gallbladder accompanied by perforation
2. Acalculous cholecystitis
Namely cholecystitis in the absence of gallstones. Acalculous cholecystitis
occurs after major surgery, severe trauma or burns. Other factors associated
with this type include: cystic duct obstruction due to torsion, primary bacterial
infection of the gallbladder, and repeated blood transfusions. Acalculous
cholecystitis occurs due to fluid and electrolyte changes (Brunner & Suddarth,
2010).

F. PATHOPHYSIOLOGY
Gallstone formation is divided into three stages:
a) supersaturated bile formation
b) nucleation or formation of rock nuclei, and
c) developed due to increased deposition.
Cholesterol solubility is the most important problem in the formation of all stones,
except pigment stones. Supersaturation of bile with cholesterol occurs when the ratio of
bile acids and phospholipids (especially lecithin) to cholesterol falls below a certain
value. Normally cholesterol is insoluble in media containing water. Bile is maintained in
liquid form by the formation of colloid which has a central core of cholesterol,
surrounded by a hydrophilic mantle of bile salts and lecithin. So excessive cholesterol
secretion, or low bile acid levels, or lecithin secretion occurs, is a lithogenic state. Stone
formation begins only when there is a nidus or core of cholesterol deposition.
At the level of cholesterol supersaturation, cholesterol crystals come out of solution to
form a nidus, and form a precipitate. At lower saturation levels, perhaps bacteria, parasitic
fragments, loose epithelial cells, or other debris particles are required to serve as seed
crystallization. Pigment stones consist of calcium salts and one of these four anions:
bilirubinate, carbonate, phosphate and fatty acid. Pigment (bilirubin) under normal
conditions will be conjugated in bile. Bilirubin is conjugated due to the presence of the
enzyme glucuronyl transferase if unconjugated bilirubin is caused by a lack or absence of
the enzyme glucuronyl transferase which will result in precipitation of the bilirubin. This
is because unconjugated bilirubin is not soluble in water but soluble in fat.
Cholecystitis is often associated with gallstones (cholelithiasis). The stone will cause
obstruction of the cystic duct which prevents emptying of bile resulting in increased
intraluminal pressure and irritation of the bile wall. The gallbladder distends and becomes

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 edematous, followed by venous stasis and cystic artery thrombosis. In addition, gallstones
in the gallbladder also cause mechanical trauma which will stimulate the release of
prostaglandins and initiate the inflammatory process. In some cases, cholecystitis can be
followed by a secondary infection which can cause gangrene and perforation of the
gallbladder. The infection is most often caused by the invasion of gram-negative bacteria
such as Escherichia coli and Klebsiella spp.

G. CLINICAL MANIFESTATIONS
The clinical symptoms of cholelithiasis vary from no symptoms to the appearance of
symptoms. More than 80% of gallbladder stones are asymptomatic (patients are not
aware of any symptoms). Clinical symptoms that arise in adults are usually found
symptoms:
a.Pain in the upper right abdomen
b. Non-specific dyspepsia
c.Nauseous vomit
d. Fever

Signs and symptoms that appear in people with cholecystitis are: (Murarif. 2015)
1. Pain
2. Nausea and vomiting
3. Fever
4. Jaundice
5. Dark colored urine.

H. DIAGNOSTIC EXAMINATION
1. Radiology
Ultrasound has replaced oral cholecystography as the diagnostic procedure of
choice because it can be performed quickly and accurately, and can be used in patients
with liver dysfunction and jaundice. In addition, ultrasound examination does not expose
the patient to radiation initiation. This procedure will give the most accurate results if the
patient has fasted at night so that the gallbladder is distended. The use of ultrasound is
based on reflected sound waves. Ultrasound examination can detect calculi in the
gallbladder or dilated collecting ducts.
2. Radiography: Cholecystography
Cholecystography is used when ultrasound is not available or when ultrasound
results are questionable. Oral cholangiography can be performed to detect gallstones and
assess the gallbladder's ability to fill, concentrate, contract and empty. Oral
cholecystography is not used in jaundiced patients because the liver is unable to deliver
contrast media to the obstructed gallbladder.
3. Sonograms
A sonogram can detect stones and determine if the gallbladder wall has
thickened.
4. ERCP (Endoscopic Retrograde Cholangiopancreatography)
This examination allows direct visualization of structures that can only be seen at
the time of laparotomy. This examination involves inserting a flexible fiberoptic

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 endoscope into the esophagus until it reaches the descending duodenum. A cannula is
inserted into the collecting duct and pancreatic duct, then a contrast agent is injected into
the duct to determine the presence of stones in the duct and allow visualization and
evaluation of the biliary tree.
5. Laboratory Examination
a. Increase in serum cholesterol.
b. Increase in phospholipids.
c. Cholesterol ester reduction.
d. Increase in serum prothrombin time.
e. Increase in total bilirubin, transaminase (Normal < 0.4 mg/dl).
f. Decreased urobilirubin.
g. Increase in white blood cells: 12,000 - 15,000/iu (Normal: 5000 - 10,000/iu).
h. Increased serum amylase, if the pancreas is involved or if there are stones in the main
duct (Normal: 17 - 115 units/100ml).

I. COMPLICATIONS
Complications that can occur in patients with cholelithiasis:
a. Asymptomatic
b. Cystic duct obstruction
c. Biliary colic
d. Acute cholecystitis
e. Pericholecystitis
f. Inflammation of the pancreas (pancreatitis)
g. Perforation
h. Chronic cholecystitis
i. Gallbladder hydrops
j. Gallbladder empyema
k. Cholecystoenteric fistula
l. Secondary gallstones (In 2-6% of patients, the ducts shrink again and gallstones
reappear)
m. Gallstone ileus (gallstone ileus)

Complications of cholecystitis include (kawalak. 2016):

a. Peritonitis
b. Gallstone ileus
c. Empyema
d. Cholangitis
e. Pancreatitis

J. THE CONCEPT OF NURSING CARE

A. ASSESSMENT

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1. Patient identity Includes: name, age, gender, address, place of residence, date of
birth, occupation and education. Cholelithiasis is usually found at the age of 20 -50
years and is more common in girls than boys (Cahyono, 2015).
2. Chief complaint Is the most important complaint felt by the client during the
assessment. Usually the main complaint that the client feels is abdominal pain in the
right upper quadrant, and nausea and vomiting.
3. Medical history
1) Current health history Is self-development of the main complaint through the
PQRST method, palliative or provocative (P), namely the main focus of the
client's complaints, quality (Q) namely how the pain is felt by the client,
regional (R) namely where the pain radiates, Safety (S) ), namely what position
can reduce pain or the client feels comfortable and Time (T), namely since when
did the client feel the pain.
2) Medical history First, check whether the client has ever suffered from the same
disease or had a history of previous illness.
3) Family health history (genogram) Assess whether or not the client's family has
ever suffered from cholelithiasis. Cholelithiasis is not declining, because this
disease attacks a group of people who have an unhealthy diet and lifestyle. But
people with a family history of cholelithiasis have a greater risk than those
without a family history.
4. Physical examination
1) General Condition :
a) General Appearance Assess the client's weight and height.
b) Awareness Awareness includes the quality and quantity of the client's
condition.
c) Vital signs Assess blood pressure, temperature, pulse and respiration.
2) Endocrine system Assess the state of the abdomen and gallbladder. Usually, in
this disease, the gallbladder can be seen and felt by the hand due to swelling of
the gallbladder.
3) Elimination System
Symptoms: discolored urine & feces.
Signs: abdominal distention, palpable mass in the right upper quadrant, dark,
concentrated urine, clay-colored stools, steatorrhoea.

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 4) Nutrition
Symptoms: anorexia, nausea/vomiting, intolerance to fat & food gas formation,
regurgitation regurgitation, epigastric pain, unable to eat, flatus, dyspepsia.
Signs: obesity, weight loss.
5) Pain/Comfort
Symptoms: severe upper abdominal pain, may radiate to the back or right
shoulder, middle epigastric colic associated with eating, pain begins suddenly &
usually peaks within 30 minutes.
Signs: loose pain, tense or stiff muscles when the right upper quadrant is
pressed.
6) Respiratory system
Signs: increased respiratory rate, depressed breathing characterized by short,
shallow breaths.
7) Security
Signs: fever, chills, jaundice, and sweaty & itchy skin (pruritus), bleeding
tendencies (vit. K deficiency).
B. NURSING DIAGNOSES
1. Nutritional deficit related to inability to absorb nutrients
2. Hypovolaemia bdincrease in capillary permeability
3. Acute pain BD physiological agents of injury
4. Impaired skin integrity bd changes in pigmentation
5. Risk of bleeding dd impaired liver function

C. INTERVENTION

NO DIAGNOSIS OBJECTIVE AND INTERVENTION

RESULT CRITERIA

1 Nutrition Deficit After carrying out Nutrition Management

bdinability to absorb nursing interventions
Observation
nutrients for ... x ... hours, it is
hoped that nutritional 1. Identification of
status problems can nutritional status
improve with the 2. Identify favorite foods

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following criteria: 3. Identify caloric needs
and types of nutrients
1. The portion of food
4. Identify the need for
consumed increases
use of a nasogastric
on a scale of 5
tube
2. Feelings of fullness
5. Monitor food intake
quickly decreased
6. Weight monitoring
on a scale of 5
7. Monitor laboratory
3. Abdominal pain
test results
decreased scale 5
Therapeutic
4. Canker sores
decreased scale 5 1. Facilitation of
5. Hair loss decreased determining dietary
scale 5 guidelines (eg food
6. Body weight pyramid)
improved on a scale 2. Serve food
of 5 attractively and at the
7. Body mass index appropriate
(BMI) improved on temperature
a scale of 5 3. Give high-fiber foods
8. The frequency of to prevent
eating improves on constipation
a scale of 5 4. Provide high calorie
9. Appetite improved and high protein
on a scale of 5 foods
10. Bowel sounds 5. Give food
improved on a scale supplements, if
of 5 necessary
11. Mucous membranes Education
improve on a scale
1. Teach the
of 5
programmed diet
Collaboration

2. Collaborative

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 administration of
medication before
meals (eg pain
relievers, anthletics),
if necessary
3. Collaborate with
nutritionists to
determine the number
of calories and types
of nutrients needed, if
necessary
2 Hypervolemia related to After carrying out Management of
increased capillary nursing interventions Hypervolaemia
permeability for ... x ... hours, it is
Observation
hoped that balance
problems will increase 1. Check for signs and
with, Outcome criteria: symptoms of
hypervolemia (eg
1. Fluid intake
dyspnea, orthopnea,
increases on a scale
edema)
of 5.
2. Monitor fluid intake
2. Urine output
and output
increases on a scale
3. TTV monitors
of 5.
Therapeutic
3. Food intake
increases on a scale 1. Limit fluid and salt
of 5. intake
4. Edema decreased 2. Elevate head of bed
scale 5. 30"-40"
5. Dehydration down Education
on a scale of 5 1. Teach how to limit
6. Improved skin fluids
turgor 5 Collaboration

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 1. Collaborative
administration of
diuretic drugs
3 Acute pain r/d After carrying out Pain management
Physiological injurious nursing interventions
Observation:
agents for ... x ... hours, it is
hoped that the problem 4. Identify the location,
of pain levels will characteristics,
improve with the results duration, frequency,
criteria: quality, intensity of
pain.
1 The ability to
5. Identify a pain scale
complete activities
6. Identify factors that
increases on a scale
aggravate and relieve
of 5.
pain.
1. Complaints of pain
Therapeutic:
decreased scale 5.
2. Grimace down scale 3. Provide non-
5 pharmacological
3. Anxiety down to a techniques to reduce
scale of 5 pain (warm
compresses, music
therapy).
4. environmental
controls that
exacerbate pain (room
temperature, lighting).
Education :

1. Describe pain relief

strategies.
2. Teach non-
pharmacological
techniques to reduce

15
 pain.
Collaboration :

1. Collaborative
administration of
analgesics, if
necessary
4 Impaired skin integrity After carrying out Skin Integrity Care
related to changes in nursing interventions
Observation
pigmentation for ... x ... hours, it is
expected that skin and 1. Identification of
tissue integrity causes of impaired
problems will increase skin integrity (eg
rapidly. Result criteria: changes in
circulation, changes
1. Network damage
in nutritional status,
decreased scale 5.
humidity, extreme
2. Redness decreased
environmental
to 5 scale.
temperatures,
3. Scar tissue
decreased mobility)
decreased scale 5.
Therapeutic
4. Skin temperature
improves on a scale 1. Use products made
of 5 from petroleum or oil
on dry skin.
2. Use products made
from mild/natural and
hypoallergenic on
sensitive skin
3. Avoid alcohol-based
products on dry skin
Education

1. Suggest using a
moisturizer (eg lotion,

16
 serum)
2. Suggest drinking
enough water
3. Suggest increasing
nutritional intake
4. Encourage increased
fruit and vegetable
intake

D. NURSING IMPLEMENTATION

Date No Clock/time Implementation

Tuesday, 1 08.00 1. Identify the pain the client is experiencing
01 August 2. Identify factors aggravating and relieving pain
2023 3. monitor fluid intake and output

1. measure TTV
2 08.15 2. Monitor laboratory test results
3. identify causes of impaired skin integrity (eg
altered circulation, altered nutritional status,
humidity, extremes of ambient temperature,
decreased mobility)

1. Provide nonpharmacological therapy

3 08.20 2. Provide high-fiber foods to prevent constipation
3. Use products made from potassium or oil on dry
skin

1. Explain about cholelithiasis to the client

2. Suggest repeating relaxation therapy when
4. 08.30 feeling anxious or in pain

17
E. NURSING EVALUATION

No Date and time O'clock Evaluation

1. Wednesday, 12.00 S: the client says the pain is reduced and begins to
02 August feel the appetite
2023 O : the client looks calm
A : problem solved
Network damage scale 3
Pain scale 4
Anxiety scale 5
P : The intervention was stopped, the patient went
home.

18
 CHAPTER III
CLOSING

A. CONCLUSION
One of the factors that can trigger or cause cholelithiasis is the lifestyle of people who
are increasing, especially people with a middle and upper economy prefer to consume fast
food with high cholesterol so that blood cholesterol is excessive and settles in the gallbladder
and becomes a gallbladder and with a lack of knowledge and awareness about the
consequences of wrong food consumption is very dangerous for their health (Adreyne, et al,
2016).

Acute cholecystitis usually occurs due to obstruction of the cystic duct by a stone, and
usually occurs after obstruction of the cystic duct by a stone, obstruction will increase
pressure in the gallbladder and cause ischemia of the gallbladder wall and mucosa.

B. CRITICISM AND SUGGESTIONS

To achieve the expected nursing outcomes, good relationships and involvement

between patients, families, and the healthcare team are needed. Nurses as health care workers
should have adequate knowledge and skills and be able to work together with other health
teams by providing nursing care to cholecystitis and cholecystitis patients.

19
 BIBLIOGRAPHY

Journal Valima tunni mah. 2016. Factors Associated with Cholecystitis.

Kowalak, 2016. Textbook of Pathophysiology Jakarta: Book Publishers. EGC Medicine

Nurarif & Kusuma, 2016. (2013). Journal of Chemical Information and Modeling

SDKI DPP PPNI Working Group Team (2017), Indonesian Nursing Diagnostic Standards
Definition and Diagnostic Indicators, South Jakarta; Central Board of PPNI.

SIKI Working Group Team DPP PPNI (2018), Indonesian Nursing Intervention Standards
Nursing Definitions and Actions, South Jakarta; Central Board of PPNI.

PPNI DPP SLKI Working Group Team (2019), Indonesian Nursing Outcome Standards
Definition and Outcome Criteria, South Jakarta; Central Board of PPNI.

Wibowo. (2010). Journal Of Chemical Information and Modeling.

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