A CASE PRESENTATION ON LIVER ABCESS

Presented to the Faculty of the School of Nursing

Adventist Medical Center College
Brgy. San Miguel, Iligan City

In Partial Fulfillment
of the Requirements for the Degree
BACHELOR OF SCIENCE IN NURSING

Nur Mohammad Cornell

MARCH, 2019

TABLE OF CONTENTS
I. TITLE PAGE

II. TABLE OF CONTENTS

III. LIST OF TABLES

IV. LIST OF FIGURES

V. OBJECTIVES

General Objective

Specific Objectives

VI. DEFINITION OF TERMS

VII. INTRODUCTION

VIII. NURSING HEALTH HISTORY

Vital information

History of present health concern

Past history

Genogram

Physical assessment and review of systems

Gordons assessment

Diagnostic tests

IX. NORMAL ANATOMY AND PHYSIOLOGY

X. PATHOPHYSIOLOGY

XI. NURSING CARE PLANS

XII. DISCHARGE PLAN

XIII. REFERENCES \

XIV.
 LIST OF TABLES

1 PHYSICAL ASSESSMENT AND REVIEW OF SYSTEMS

2 GORDONS ASSESSMENT

3 NORMAL ANATOMY AND PHYSIOLOGY

4 NURSING CARE PLAN

 LIST OF FIGURES

1 GENOGRAM

2 PATHOPHYSIOLOGY
 OBJECTIVES

General Objectives:

At the end of one and a half hour of case presentation, the participants will be able to
learn about the disease process of Liver abcess

Specific Objectives:

At the end of one and a half hour of case presentation, the participants will be able to:

1. Relate the health history of the patient to Liver abcess.;

2. Categorize the physical assessment and review of system involved Liver abcess
3. Numerate at least 5 diagnostic tests related to Liver abcess.:
4. Discuss the anatomical structure and functions involved in Liver abcess.;
5. Summarize the pathophysiology, risk factors and manifestations of Liver abcess.;
6. Formulate appropriate nursing process for the client with Liver abcess.;. and
7. Organize a health education and discharge plan.

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 DEFINITION OF TERMS

Ascites. Is an accumulation of serous fluid in the abdominal cavity. The fluid

accumulates primarily because of low production of albumin by failing liver. An
insufficient amount of protein in the capillaries causes plasma to seep into the
abdominal cavity.

Hepatitis B. is an infection of your liver. It can cause scarring of the organ,

liver failure, and cancer. It can be fatal if it isn’t treated. It’s spread when people
come in contact with the blood, open sores, or body fluids of someone who has the
hepatitis B virus.

Hepatitis C. is the disease of the liver caused due to infection by hepatitis C

virus (HVC). It is one common causes of chronic liver disease and may to progressive
liver disease.

Hepatic encephalopathy. Is a decline in brain function that occurs as results

of severe liver disease. In this condition, your liver can’t adequately remove toxins
from your blood. This cause a buildup of toxins in your bloodstream, which can lead
to brain damage.

Uremia. Literally “urine in the blood”; the syndrome or group of symptoms

associated with end-stage renal failure. (LeMone, 2014)

2
 INTRODUCTION
The liver is subject to a variety of disorders and diseases. One is Abscesses which is

caused by acute appendicitis; those occurring in the bile ducts may result from gallstones or

may follow surgery. The parasite that causes amebic dysentery in the tropics can produce

liver abscesses as well. Various other parasites prevalent in different parts of the world also

infect the liver. Certain drugs may also damage the liver, producing jaundice.

Liver abscess is a pus-filled cyst in the liver. The liver abscess has a thin capsular

wall with a necroticcentre composed of a thick fluid. Typically,abscess fluid is odourless,

resembling ‘chocolate syrup’ oranchovy paste’ in half, and bacteriologically sterile,

althoughsecondary bacterial invasion may occur.

The liver is an organ in the digestive system that assists the digestive process and

carries out many other essential functions. These functions include producing bile to help

break down food into energy; creating essential substances, such as hormones; cleaning

toxins from the blood, including those from medication, alcohol and drugs; and controlling

fat storage and cholesterol production and release.

The condition can be caused by infections spread directly from nearby structures,

such as the bile-draining tubes, from the appendix or intestines, or carried in the bloodstream

from more distant parts of the body.It can also develop as a result of surgery or other trauma

to the liver.

Liver abscess is usually treatable and often can be cured with a course of antibiotics

or a combination of antibiotics and a surgical procedure to drain the abscessdepending on the

size, number, and complexity of the abscess(es) such the following cases:

A common sign of impaired liver function is jaundice, a yellowness of the eyes and skin

arising from excessive bilirubin in the blood. Jaundice can result from an abnormally high

3
level of red blood cell destruction (hemolytic jaundice), defective uptake or transport of

bilirubin by the hepatic cells (hepatocellular jaundice), or a blockage in the bile duct system

(obstructive jaundice). Failure of hepatic cells to function can result from hepatitis, cirrhosis,

tumors, vascular obstruction, or poisoning. Symptoms may include weakness, low blood

pressure, easy bruising and bleeding, tremor, and accumulation of fluid in the abdomen.

Blood tests can reveal abnormal levels of bilirubin, cholesterol, serum proteins, urea,

ammonia, and various enzymes. A specific diagnosis of a liver problem can be established by

performing a needle biopsy.

Bacterial abscess of the liver is relatively rare. It has been described since the time of

Hippocrates (400 BC), with the first published review by Bright appearing in 1936. In 1938,

Ochsner's classic review heralded surgical drainage as the definitive therapy; however,

despite the more aggressive approach to treatment, the mortality rate remained at 60-80%.

The development of new radiologic techniques, the improvement in microbiologic

identification, and the advancement of drainage techniques, as well as improved supportive

care, have decreased mortality rates to 5-30%; yet, the prevalence of liver abscess has

remained relatively unchanged. Untreated, this infection remains uniformly fatal.

Prior to the antibiotic era, liver abscess was most common in the fourth and fifth

decades of life, primarily due to complications of appendicitis. With the development of

better diagnostic techniques, early antibiotic administration, and the improved survival of the

general population, the demographic has shifted toward the sixth and seventh decades of life.

Frequency curves display a small peak in the neonatal period followed by a gradual rise

beginning at the sixth decade of life. Cases of liver abscesses in infants have been associated

with umbilical vein catheterization and sepsis. When abscesses are seen in children and

adolescents, underlying immune deficiency, severe malnutrition, or trauma frequently exists.

4
 VITAL INFORMATION
I. Biographical Data

Name: Boy A
Preferred to be called:

Age: 10 Years Old

Sex: Male
Time of Arrival to Unit: March 05,2019, 5:00pm
Mode of Admission: Wheel Chair
Mother’s Name: Mrs. S
Occupation: Elementary Teacher
Age: 41
Father’s Name: Mr. B
Occupation: Police Officer
Age: 42
Address: Diamla, Pualas , Lanao Del Sur
Religion: Islam
Primary Language: Maranao
Nationality: Filipino

II. Describe (Narrative Form)

1. Child’s Appearance & Behavior
2. Parent-child interaction
3. Siblings and other family members
4. Home environment

C. Chief Concern (Narrative of Present Illness)

D. Wt and Ht:

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Temp: ____ (oral, axilla, rectal)
Pulse _____ (regular/irregular)
Respiration _____ (regular/irregular)
BP:
E. Past History
1. Birth History
a. Mother’s health during pregnancy
b. Labor and delivery
c. Infant’s condition immediately after birth(APGAR)
2. Pregnancy, Labor and Delivery
a. Obstetric history (GP, TPAL)
b. Crisis during pregnancy
c. Prenatal attitude toward fetus
3. Perinatal History
a. Wt. and Ht. at birth
b. Loss of wt following birth and time of regaining birth wt
c. APGAR score, level of activity
d. Problem if any (birth injury, congenital anomalies)
4. Dietary History (Feeding History)
5. Immunization and boosters
6. Developmental milestones (growth pattern)
a. Approx. wt. at 6 mos, 1 yr, 2 yrs, 5 yrs
b. Approx.ht. at 1 yr, 2 yrs, 3 yrs, 4 yrs
c. Dentition (including age of onset, number of teeth and symptoms during teething)
d. Hold head steadily
e. Sitting alone without support
f. Walks without assistance
g. Says first words

F. Functional Health Pattern Assessment

1. Health Perception-Health Management Pattern
• Why has your child been admitted?
• How has your child’s general health been?
• What does your child know about this hospitalization?

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• Ask the child why he came to the hospital?
If answer is “For operation or for tests”,ask child to tell you about what had happened
before, during and after the operation or tests
• Has your child ever been in the hospital before?
• How was the hospital experience?
• What things were important to you and your child during that hospitalization? How
can we be most helpful now?
• What medications does your child take at home?
• Why are they given
• When are they given?
• How are they given (if a liquid, with a spoon, if a tablet, swallowed with water or
other)?
• Does he have any trouble taking medication? If so, what helps?
• Does he have any allergies to medications?
• What does your child know about this hospitalization?
• Ask the child why he came to the hospital
2. Nutritional and Metabolic Pattern
• What are the family’s usual meal times?
• Do family members eat together or at separate times?
• What are your child’s favorite foods, beverages and snacks?
• Average amounts consumed or usual size positions
• Special cultural practices, such as family eats only ethnic food
• What goods and beverages does your child dislike?
• What are his feeding habits (bottle, cup, spoon, eats by self, needs assistance, (any
special devices)?
• Does the child like the food served (warm, cold, one at a time)?
• How would you describe his usual appetite?(hearty eater, picky eater)
• Has his being sick affected your child’s appetite?
• Are there any feeding problems (excessive, fussiness, spitting up, colic), any dental
or gum problems that affect feeding?
• What do you do with these problems?
3. Elimination Pattern
• What are your child’s toilet habits? (diaper, toilet trained [day only or day and night],
use of words to communicate urination and defecation, potty chair, regular toilet, other
routines)?
• What is his usual pattern of elimination (bowel movements)
• Do you have any concerns about elimination(bed wetting, constipation, diarrhea)

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• What do you do for these problems?
• Have you ever noticed that your child sweats a lot?
4. Sleep-Rest Pattern
• What is your child’s usual hour of sleep and awakening?
• What is his schedule for naps/length of naps?
• Is there a special routine before sleeping (bottle, drink of water, bedtime story,
nightlight, favorite blanket, or toy or prayers)
• Is there a special routine during sleep time such as walking to go to the bathroom?
• What type of bed does he sleep on?
• Does he have his own room or share a room: if he shares a room, with whom?
• What are the home sleeping arrangements (along or with others, such as sibling
parent or other person)?

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9
 COMPLETE BLOOD COUNT AND PLATELET

TEST RESULT NORMAL NURSING

VALUE CONSIDERATION
RED BLOOD CELLS 3.87 4-6x10 12/L DECREASED
HEMATOCRIT 0.32 0.40-.54 DECREASED
HEMOGLOBIN 110.0 130-160 g/L DECREASED

WBC 17.44 5-10x10 9/L INCREASED

LYMPHOCYTES 0.2 0.25-0.35 DECREASED
SEGMENTERS 0.94 0.50-0.65 INCREASED
STABS 0 0.05-0.10 NORMAL
MONOCYTES 0.03 0.03-0.07 NORMAL
EOSINOPHILS 0 0.01-0.3 NORMAL
BASOPHILS 0 0-0.01 NORMAL
PLATELET COUNT 491 140-450x 10 INCREASED
9/L

POTASSIUM AND SODIUM

RESULT NORMAL
VALUE

POTASSSIUM 4.18 3.5-5.3 mmol/L

SODIUM 144.7 135-148mmol/L

CREATININE
NORMAL VALUE NURSING
CONSIDERATION

CREATININE 58.9 856 71-115mmol/L NORMAL

TPAG(TOT,PROTEIN,ALB/GLOB RATIO)

EXAMINATION RESULT NORMAL VALUE NURSING

CONSIDERATION
SGPT 35.92 (5-35U/L) INCREASED
ALKALINE PHOSPHATE 256.05 (53-141U/L) INCREASED

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EXAMINATION RESULT NORMAL NURSING
VALUE CONSIDERATION
TOTAL BILIRUBIN 20.1 (.7-20.u/L) NORMAL

B1 16.8 (1.7-17.1) NORMAL

B2 3.83 (0-3.34) INCREASED

Stool analysis:

Pus cells: 1-3/HPF Entaemoba hystolica

Urinalysis:
Protein: +2
WBC- /hpf: 1-3
RBC- 0-1
Bacterial : +1

ULTRASOUND-KUB
Impression
Hepatomegaly, Incidental finding
ofcomplex liver mass (segment 6) complex
mass in ipsilateral suprarenal area, likely
resolving abcess versus resolving
hematomas
Pre Nursing Responsibilities
 Obtain a history of the patient’s complains, including
sensitivity to the latex
 Ensure foods and liquids have been restricted
 Ensure patient has to remove external metallic objects
 Ensure patient to void prior to procedure , and to change
into gown, robe and foot coverings
 Instruct the patient to cooperate and follow the
instructions
 Place the patient into supine position on an examination
table

X-RAY OF THE CHEST

Impression Pre Nursing Responsibilities

Impression:  Obtain a history of patient’s complaints , including
 Within normal chest findings, in poor a list of known allergies
inspiratory phase  Ensure patient has to remove external metallic
 The small bowel loops in the objects
 Ensure patient to void prior to procedure , and to
change into gown, robe and foot coverings
 Instruct the patient to cooperate and follow the
instructions
 Place the patient in standing position

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CT SCAN ABDOMEN
Impression
1. Fluid collections in the intrahepatic
regions , which are indistinguishable
from the adjacent fluid –filled bowel
loops
2. Prominent sized liver
3. Bile sludge
 Ask the patient to inhale deeply and his breath
while the X-ray images are taken
Pre Nursing Responsibilities
 Ensure the patient has complied medication
restrictions and pretesting preparations
 Ensure that the patient has removed dentures and
all external metallic objects from the area to be
examined
 Obtain history of any allegies
 Have emergency equipment readily
 Instruct the patient to cooperate and follow the
instructions
 Establish an IV fluid line for the injection of
contrast medium
 Place the patient in supine position
 Instruct the patient to take slow, deep breaths of
nausea occurs
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 ANATOMY AND PHYSIOLOGY

Liver

The liver is the largest internal organ in the

body, and weighs about 3 pounds in an adult. The

liver is located in the right upper quadrant of the

abdomen, just below the diaphragm. A thick

capsule of connective tissue called Glisson's capsule

covers the entire surface of the liver. The liver is

divided into a large right lobe and a smaller left lobe. The falciform ligament divides

the two lobes of the liver. Each lobe is further divided into lobules that are

approximately 2 mm high and 1 mm in circumference.

These hepatic lobules are the functioning units of the liver. Each of the

approximately 1 million lobules consists of a hexagonal row of hepatic cells called

hepatocytes. The hepatocytes secrete bile into the bile channels and also perform a

variety of metabolic functions. Between each row of hepatocytes are small cavities

called sinusoids. Each sinusoid is lined with Kupffer cells, phagocytic cells that

remove amino acids, nutrients, sugar, old red blood cells, bacteria and debris from the

blood that flows through the sinusoids. The main functions of the sinusoids are to

destroy old or defective red blood cells, to remove bacteria and foreign particles from

the blood, and to detoxify toxins and other harmful substances. Approximately 1500

ml of blood enters the liver each minute, making it one of the most vascular organs in

the body. Seventy-five percent of the blood flowing to the liver comes through the

portal vein; the remaining 25% is oxygenated blood that is carried by the hepatic

artery.

13
 The hepatic portal system begins in the capillaries of the digestive organs and

ends in the portal vein. Consequently, portal blood contains substances absorbed by

the stomach and intestines. Portal blood is passed through the hepatic lobules where

nutrients and toxins are absorbed, excreted or converted.

Restriction of outflow through the hepatic portal system can lead to portal

hypertension. Portal hypertension is most often associated with cirrhosis. Patients

usually present with splenomegaly, ascites, GI bleeding and/or portal systemic

encephalopathy.

The consequences of portal hypertension are due to

portal systemic anastomosis formed by the body as an

attempt to bypass the obstructed liver circulation. These

collateral vessels form along the falciform ligament,

diaphragm, spleen, stomach and peritoneum. The

collaterals find their way to the renal vein where blood

drained from the digestive organs is let into the systemic

circulation.

The liver is responsible for important functions, including:

 Bile production and excretion

 Excretion of bilirubin, cholesterol, hormones, and drugs

 Metabolism of fats, proteins, and carbohydrates

 Enzyme activation

 Storage of glycogen, vitamins, and minerals

 Synthesis of plasma proteins, such as albumin and globulin, and clotting

factors

 Blood detoxification and purification

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 The liver synthesizes and transports bile pigments and bile salts that are needed

for fat digestion. Bile is a combination of water, bile acids, bile pigments, cholesterol,

bilirubin, phospholipids, potassium, sodium, and chloride. Primary bile acids are

produced from cholesterol. When bile acids are converted or "conjugated" in the

liver, they become bile salts.

Bilirubin is the main bile pigment that is formed from the breakdown of heme in

red blood cells. The broken-down heme travels to the liver, where is it secreted into

the bile by the liver. Bilirubin production and excretion follow a specific pathway.

When the reticuloendothelial system breaks down old red blood cells, bilirubin is one

of the waste products. This "free bilirubin" is a lipid soluble form that must be made

water-soluble to be excreted. The conjugation process in the liver converts the

bilirubin from a fat-soluble to a water-soluble form. The liver also plays a major role

in excreting cholesterol, hormones, and drugs from the body.

The liver plays an important role in metabolizing nutrients such as carbohydrates,

proteins, and fats. The liver helps metabolize carbohydrates in three ways:

 Through the process of glycogenesis, glucose, fructose, and galactose are

converted to glycogen and stored in the liver.

 Through the process of glycogenolysis, the liver breaks down stored glycogen

to maintain blood glucose levels when there is a decrease in carbohydrate

intake.

 Through the process of gluconeogenesis, the liver synthesizes glucose from

proteins or fats to maintain blood glucose levels.

The liver synthesizes about 50 grams of protein each day, primarily in the form of

albumin. Liver cells also chemically convert amino acids to produce ketoacids and

ammonia, from which urea is formed and excreted in the urine. Digested fat is

15
converted in the intestine to triglycerides, cholesterol, phospholipids, and

lipoproteins. These substances are converted in the liver into glycerol and fatty acids,

through a process known as ketogenesis.

Prothrombin and fibrinogen, substances needed to help blood coagulate, are both

produced by the liver. The liver also produces the anticoagulant heparin and releases

vasopressor substances after hemorrhage.

Liver cells protect the body from toxic injury by detoxifying potentially harmful

substances. By making toxic substances more water soluble, they can be excreted

from the body in the urine. The liver also has an important role in vitamin storage.

High concentrations of riboflavin or Vitamin B1 are found in the liver. 95% of the

body's vitamin A stores are concentrated in the liver. The liver also contains small

amounts of Vitamin C, most of the body's Vitamin D stores, and Vitamins E and K.

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Biliary tract

The biliary tract (or biliary tree) is the common anatomy

term for the path by which bile is secreted by the liver on its way

to the duodenum, or small intestine, of most members of the

mammal family. It is referred to as a tree because it begins with

many small branches which end in the common bile duct,

sometimes referred to as the trunk of the biliary tree. The duct is

present along with the branches of the hepatic artery and the

portal vein forming the central axis of the portal triad. Bile flows in opposite direction

to that of the blood present in the other two channels. The liver is usually excluded,

but sometimes included. Pressure inside in the

biliary tree can give rise to gall stone and lead to

cirrhosis of the liver. Blockage can cause

jaundice.

The biliary tract can also serve as a

reservoir for intestinal tract infections. Since

biliary tract is an internal organ, it has no

somatic nerve supply,and,therefore,colicky pain

due to infection and inflammation of the biliary tract is not a somatic pain but it may

be caused by luminal distension which causes stretching of the wall (the same

mechanism of pain in intestinal colic in intestinal obstruction in which intestine also

do not have somatic nerve supply)

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The path is as follows:

 Bile canaliculi >> Canals of Hering >> bile ductules (in portal tracts) >>

intrahepatic bile ducts >> left and right hepatic ducts >>

 merge to form >> common hepatic duct >>

 exits liver and joins >> cystic duct (from gall bladder) >>

 forming >> common bile duct >> joins with >> pancreatic duct >>

 forming >> ampulla of Vater >> enters duodenum

The anatomy of the biliary tree is a little complicated, but it is important to

understand. The liver's cells (hepatocytes) excrete bile into canaliculi, which are

intercellular spaces between the liver cells. These drain into the right and left hepatic

ducts, after which bile travels via the common hepatic and cystic ducts to the

gallbladder. The gallbladder, which has a capacity of 50 milliliters (about 5

tablespoons), concentrates the bile 10 fold by removing water and stores it until a

person eats. At this time, bile is discharged from the gallbladder via the cystic duct

into the common bile duct and then into the duodenum (the first part of the small

intestine), where it begins to dissolve the fat in ingested food.

The liver excretes approximately 500 to 1000 milliliters (50 to 100

tablespoons) of bile each day. Most (95%) of the bile that has entered the intestines is

resorbed in the last part of the small intestine (known as the terminal ileum), and

returned to the liver for reuse.

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The many functions of bile are best understood by knowing the composition of bile:

1. Bile Salts (cholates, chenodeoxycholate, deoxycholate): these are produced by

the liver's breakdown of cholesterol. They function in bile as detergents that

dissolve dietary fat and allow it to be absorbed. Hence, disruption of bile

excretion disrupts the normal absorption of fat, a process called

malabsorption. Patients develop diarrhea because the fat is not absorbed

(steatorrhea) , and develop deficiencies of the fat-soluble vitamins (A, D, E,

and K).

2. Cholesterol and phospholipids-while only

4% of bile is cholesterol, the secretion of

cholesterol and its metabolites (bile salts)

into bile is the body's major route of

elimination of cholesterol. Phospholipids,

which are components of cell membranes,

enhance the cholesterol solubilizing

properties of bile salts. Inefficient excretion

of cholesterol can cause an increased serum cholesterol. This predisposes to

vascular disease (heart attacks, strokes, etc.)

3. Bilirubin-while this comprises only 0.3% of bile, it is responsible for bile's

yellow color. Bilirubin is a product of the body's metabolism of hemoglobin,

the carrier of oxygen in red blood cells. Disruption of the excretion of this

component of bile leads to a yellow discoloration of the eyes and skin

(jaundice).

4. Protein and miscellaneous components

Bile production and recirculation is the main excretory function of the liver. Tumors

19
that obstruct the flow of bile from the liver can also impair other liver functions.

Therefore, it is necessary to understand these other functions to understand the

symptoms that these tumors can cause. These include:

Metabolic functions, such as the maintenance of glucose (blood sugar) levels

Synthetic functions, such as the synthesis of serum proteins such as albumin, blood

clotting (coagulation) factors, and complement (a mediator of inflammatory

responses)

Storage functions, such as the storage of sugar (glycogen), fat (triglycerides), iron,

copper, and fat soluble vitamins (A, D, E, and K)

Catabolic functions, such as the detoxification of drugs

Circulation of the blood in blood vessels

There are two circulatory routes of blood

as it flows through the blood vessels: the

systemic and the pulmonary circulation. In

systemic circulation, blood flows from the left

ventricle of the heart through blood vessels to

all parts of the body (except gas exchange

tissues of lungs) and back to the atrium. In

pulmonary circulation on the other hand, venous

blood moves from the right atrium to right

ventricle to pulmonary artery to lung arterioles

and capillaries where gases exchanged;

oxygenated blood returns to the left atrium via pulmonary veins; from left atrium,

blood enters the left ventricle.

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Hepatic Portal Circulation

The veins of the hepatic

portal circulation drain the

digestive organs, spleen, and

pancreas and deliver this blood to

the liver through the hepatic portal

vein. When you have just eaten,

the hepatic portal blood contains

large amounts of nutrients. Since

the liver is a key body organ

involve in maintaining the proper

glucose, fat and protein concentrations in the blood, this system “takes a detour “to

ensure that the liver processes these substances before they enter the systemic

circulation. As blood flows slowly through the liver, some of the nutrients are

removed to be stored or processed in various ways for later release to the blood. The

liver is drained by the hepatic veins that enter the inferior vena cava. Like the portal

circulation that links the hypothalamus of the brain and the anterior pituitary gland,

the hepatic portal circulation is a unique and unusual circulation. Normally, arteries

feed capillary beds, which in turn drain into veins. Here we see veins feeding the

liver circulation.

The inferior mesenteric vein, draining the terminal part of the large intestine,

drains into the splenic vein, which itself drains the spleen, pancreas and the left side

of the stomach. The splenic vein and superior mesenteric vein (which drains the

small intestine and the first part of the colon) join to form the hepatic portal vein. The

L. Gastric vein, which drains the right side of the stomach, drains directly into the

hepatic portal vein.

21
22
 ASSESSMENT NURSING DIAGNOSIS PLANNING INTERVENTIONS RATIONALE EVALUATION

Subjective: Acute Pain related to presence  After 5-6 hours of Independent: The patient was relieved
“Masakit” as verbalized by the of pus in the liver. nursing interventions, 1. Accept client’s  pain is subjective from any pain
patient the patient pain will description of pain. experience and cannot be
As verbalized by the wife decreased from 5 /10 to Acknowledge the
2/10
felt by others.
pain experience and
Objective: convey acceptance
T: 38.8-40.2 C Long term:
of client’s response
BP: 90/60 mmHg to pain
PR: 90-110 bpm After 2-3 days of nursing
2. Observe nonverbal  observations may/may
RR: 41-26 bpm intervention, the patient’s
pain will be relieved from cues/pain behaviors not be congruent with
O2sat: 95-97%
5/10 to 0. (e.g., how the verbal reports or may be
 Observed evidence of pain patient walks, holds only indicator present
 RUQ pain of 5/10, tenderness body, sits; facial when client is unable to
 Facial Grimace noted. expression; cool verbalize.
fingertips/toes,
which can mean
Lab result: constricted blood
vessels) and other
CT SCAN OF ABDOMEN: objective cues, as
4. Fluid collections in the noted
intrahepatic regions , which 3. Determine patient’s
are indistinguishable from  it may vary to individuals
acceptable level of
the adjacent fluid –filled coping capabilities.
bowel loops
pain/pain control
goals  to promote
5. Prominent sized liver
6. Bile sludge 4. Provide comfort nonpharmacological pain
measures (e.g., management.

23
ULTRASOUND:KUB touch,
Impression: Hepatomegaly, repositioning, use of
Incidental finding ofcomplex liver heat/cold packs,
mass (segment 6) complex mass in nurse’s presence)
ipsilateral suprarenal area, likely
quiet environment,
resolving abcess versus resolving  to distract attention and
and calm activitie
hematomas
5. Instruct patient to reduce tension.
X-ray of AP chest: encourage use of
Impression: Within normal chest relaxation
findings, in poor inspiratory phase techniques such as
The small bowel loops in the focused breathing,
imaging and
listening to calming
music. Encourage
also diversional
activities

Collaborative:
1. Administer
medication as
prescribed

 Metronidazole 250
mg q8h, IVTT
 Tazmed 2.25 grams
IV drip q8h
 Amikacin 250mg
slow IVTT

24
 Immunomax syrup 5
ml OD

 Ibuprofen (Dolan)
200/5 4 ml q6hr

25
 ASSESSMENT NURSING DIAGNOSIS PLANNING INTERVENTIONS RATIONALE EVALUATION
“Pila nan a siya kaadlaw Hyperthermia related to : Independent: The patient was able to
gilanat” as verbalized by SO increased metabolic rate maintain normal thermal
secondary to infection Short term goal: regulation as evidenced by by
Objective: Within 1 hr of nursing 1. Promote surface cooling by  To restore normal body temperature of 37.2 celcius
intervention patient will means of cool tepid sponge temperature by means of
Objective: decrease his body bath especially in groin and heat loss by evaporation and
T: 38.8-40.2 C temperature to 37.2 degree axilla conduction
BP: 90/60 mmHg Celsius 2. Maintain bed rest  To reduce metabolic
PR: 90-110 bpm demands
RR: 41-26 bpm Long term: 3. Increase fluid intake  Decrease in fluid intake may
O2sat: 95-97% cause dehydration
After 1 hour of nursing 4. Provide cool clothing  To enhance body
care, the SO will be able temperature
to identify contributing  To prevent further
 Skin is warm and dry to 5. Monitor vital signs
factors and importance of complication
touch noted
treatment.
 Flushed skin Dependent
 Firm skin turgor noted
 Body malaise
Administer medications as
prescribed

 Paracetamol 250/5 mg 7
RED BLOOD CELLS: 3.87(4-6x10 Antipyretic
ml po q4hr PRN
12/L)
HEMATOCRIT: 0.32(0.40-.54)  Metronidazole 250 mg
HEMOGLOBIN: 110(130-160 q8h, IVTT To treat underlying cause for
g/L)  Tazmed 2.25 grams IV infection
WBC: 17.44 (5-10x10 9/L) drip q8h
Lymphocytes: 0.10 (0.25-0.35)  Amikacin 250mg slow
Monocytes: 0.2(0.3-0.7) IVTT
Platelet: 491(140-450 x 9/L
ULTRASOUND:KUB
Impression: Hepatomegaly,

26
Incidental finding ofcomplex
liver mass (segment 6)
complex mass in ipsilateral
suprarenal area, likely resolving
abcess versus resolving
hematomas

27
 ASSESSMENT NURSING DIAGNOSIS PLANNING INTERVENTIONS RATIONALE EVALUATION

“Wala talaga siyang kumain” Imbalanced Nutrition: Less than Long term goal: Independent: Patient was able
as verbalized by SO body requirements related to  At the end of 2-3 display behaviors
Objective: increased metabolic demands. days patient will be 1. Provide small  To prevent nausea and and lifestyle
able to demonstrate frequent meals. vomiting changes to main
Objective: behaviors, lifestyle 2. Served high fiber  To prevent appropriate
changes to regain diet constipation weight
T: 38.8-40.2 C
and maintain 3. Increase fluid  To manage fluid
BP: 90/60 mmHg appropriate weight. intake to 2-3 liters/ imbalanced.
PR: 90-110 bpm
day.  To improve
RR: 41-26 bpm Short term 4. Encouraged metabolism
O2sat: 95-97% At the end of 5-6 hours exercise as
 Malnourished mother will be able to tolerated like
 Pale conjunctiva verbalized understanding passive ROM.
 Pale conjunctiva of causative factors when
 Body weakness known and necessary
 Vomiting interventions.

Dependent:
RED BLOOD CELLS: 3.87(4-6x10 Administer medication as
12/L) indicated
HEMATOCRIT: 0.32(0.40-.54) OMX cap , 1 cap mix
HEMOGLOBIN: 110(130-160 with h2o po OD
g/L)
WBC: 17.44 (5-10x10 9/L) Collaborative: Low salt
Lymphocytes: 0.10 (0.25-0.35)
Monocytes: 0.2(0.3-0.7)
Platelet: 491(140-450 x 9/L

28
 ASSESSMENT NURSING DIAGNOSIS PLANNING INTERVENTIONS RATIONALE EVALUATION

Short term: Independent The patient to maintain fluid

“Ilang araw na siyang Fluid Volume deficit related After 5-6 hours of nursing -To evaluate degree of fluid volume at functional level
nagtatae”: as verbalized by to loose watery stool interventions the patient 1. Assess vital signs; note deficit.
mother (Diarrhea) emonstrate behaviors to strength of peripheral pulses.
monitor and correct deficit -to correct/ replace losses to
Objective: as indicated. 2. Keep fluids within clients reverse pathophysiologic
T: 38.8-40.2 C . reach and encourage mechanisms.
BP: 90/60 mmHg frequent intake as
PR: 90-110 bpm appropriate.
RR: 41-26 bpm Long term:
O2sat: 95-97% After 2-3 days of nursing 3. Control humidity and -To reduce high fever and
interventions the patient will ambient air temperature as elevated metabolic rate.
 Decreased urine be able to maintain fluid appropriate. Reduce
output volume at a functional level beddings/clothes, provide
 Poor skin turgor as evidenced by individually tepid sponge bath.
 Pale conjunctiva adequate urinary output with -To promote comfort and
 Dry lips normal specific gravity, 4. Change position safety.
 Vomiting stable vital signs, moist frequently.
 Diarrhea mucous membranes, good
skin turgor and prompt
Urinalysis: capillary refill 5. Provide safety measures -To promote safety.
Protein: +2 when client is confused.
WBC- /hpf: 1-3 - to limit gastric/intestinal
RBC- 0-1 DEPENDENT: losses.
Bacterial : +1 1. Administer
medications as
indicated.(antidiarrhe
als)
 OMX cap , 1 cap

29
 mix with h2o po
OD
 Hidrasec 10 mg 1
sachet mix 5 ml h2o
TID To prevent peaks/valleys in
fluid level.

2. Establish 24-hour
fluid replacement
needs and routes to
be used.
o Erceflora po OD

o Flotera tab once a

day

30
 ASSESSMENT NURSING DIAGNOSIS PLANNING INTERVENTIONS RATIONALE EVALUATION
Subjective: Activity Intolerance related Short term: Independent: The patient was able to
“ to pain and fatigue Within 5-6 hrs or nursing Independent: • participate and perform
intervention the SO will his ADL’s
Objective: identify and participate 1. Evaluate current degree
T: 38.8-40.2 C alternative ways to of deficit in light of usual
BP: 90/60 mmHg maintain desired activity status To provide comparative baseline
PR: 90-110 bpm level
RR: 41-26 bpm 2. Adjust activities
O2sat: 95-97% (reduce intensity level or •To prevent over exertion
Long term: discontinue activities
After 2-3 days of nursing that cause undesired
 Decreased urine intervention the patient physiologic changes)
output will be able to perform •To reduce fatigue
his ADL’s 3. •Provide rest periods
 Poor skin turgor
between activities
 Pale conjunctiva
 Dry lips 4. •Promote comfort •To enhance ability to participate
 Vomiting measures and provide in activities
 Diarrhea for relief of pain
 Observed evidence of •Help to minimize frustration
pain 5. •Provide positive and rechannel energy
 RUQ pain of 5/10, atmosphere while
tenderness acknowledging difficulty
 Facial Grimace noted. of situation for the client

B1: 16.8 (1.7-17.1)

B2: 3.83 (0-3.34)
Total: 20.1 (.7-2.0u/L)

31
SGPT: 35.92 (5-35U/L)
Alkaline Phosphate: 256
.05(53-141U/L)

32
 Predisposing Factor:
 Age: 10 Years Old
Precipitating Factor:
 Gender: Male
 Infection: LBM (8 months)  Nutrition ( Junk foods, drinks
UTI (2015) soda every day, limit carbs
intake)
 Tropical areas

Entamoebahistolytica cyst might

ingested

Trophozite survives acidic stomach

Attachment to cecal mucosa and penetration of

epithelium by lytic digestion
Infection of liver

Invades to mesentery toward portahepatis

Activation of inflammatory
response

33
Release of kinins, histamine, and other
chemicals (chemical “alarms”)
 Capillaries become leaky
Blood vessel Neutrophils, monocytes
dilate and other WBCs enter the
Decreased albumin area

Decreased oncotic pressure,

Increased hydrostatic pressure

Redness Heat

Fluids and proteins leave the blood

 Paracetamol Fever vessel going to interstitial spaces of
250/5 mg 7 ml HYPERTHERMIA tissue
po q4hr PRN

Increased metabolic Edema

rate of tissue cells

Pain Swelling
Malaise  ACTIVITY
Nausea INTOLERANCE
LBM  FLUID DEFICIT
Abdominal pain Ibuprofen (Dolan)
(RUQ) 200/5 4 ml q6hr
 OMX cap , 1 cap mix with h2o po OD
ACUTE PAIN
 Erceflora po OD
 Flotera tab once a day
 Hidrasec 10 mg 1 sachet mix 5 ml h2o TID Failure of inflammatory
mechanism
 Metronidazole 250 mg RED BLOOD CELLS: 3.87(4-6x10 12/L)
Stool analysis: q8h, IVTT
Severe infection HEMATOCRIT: 0.32(0.40-.54)
 Tazmed 2.25 grams
Pus cells: 1-3/HPF HEMOGLOBIN: 110(130-160 g/L)
IV drip q8h
Entaemoba WBC: 17.44 (5-10x10 9/L)
 Amikacin 250mg slow
hystolica Lymphocytes: 0.10 (0.25-0.35)
IVTT
 Immunomax syrup 5 ml Monocytes: 0.2(0.3-0.7)
Platelet: 491(140-450 x 9/L
OD 34

 U ncleared area of
debris

Sac of pus (mixture of dead

neutrophils, broken-down tissue
cells, dead pathogens)
CT SCAN OF ABDOMEN:

1. Fluid collections in the intrahepatic regions , which

are indistinguishable from the adjacent fluid – Pus are walled off
filled bowel loops the liver
2. Prominent sized liver
3. Bile sludge
HEPATIC ABSCESS
ULTRASOUND:KUB
Blockage of bile duct
Impression: Hepatomegaly, Incidental finding ofcomplex liver
mass (segment 6) complex mass in ipsilateral suprarenal area,
likely resolving abcess versus resolving hematomas
Prevents bile from entering
small intestine
X-ray of AP chest:

Impression: Within normal chest Bile accumulates and

findings, in poor inspiratory Hepatomegaly backs-up into the liver
phase

The small bowel loops in the Pressure on liver cells

included abdomen, show
moderate amount of gas with
SGPT: 35.92
mucosal (5-35U/L), intestinal
thickening
Alkaline Phosphate: 256
ileus considered
.05(53-141U/L) 35
Proteins enter bloodstream Bile salts and bile pigments enter
bloodstream

Circulation of proteins
Circulation of bile pigments

Enters kidney circulation B1: 16.8 (1.7-17.1)

Jaundice B2: 3.83 (0-3.34)
Total: 20.1 (.7-
Protein in urine Urinalysis: 2.0u/L)
(Proteinuria) Protein: +2
WBC- /hpf: 1-3
DISTURBED BODY
RBC- 0-1
IMAGE
Bacterial : +1

36
 DRUG ORDER MECHANISM OF CONTRAINDICATIONS ADVERSE EFFECTS OF NURSING
ACTION INDICATIONS THE DRUG RESPONSIBILITIES/
PRECAUTIONS

Generic name: Paracetamol exhibits For treatment of mild to Hypersensitivity. Nausea, allergic The medication should
Paracetamol analgesic action by moderate pain and reaction, skin rashes, be given in orally
peripheral blockage of fever. acute renal tubular R> this is according to
Brand name: pain impulse generation. necrosis. the doctor’s order.
Boigesic It produces antipyresis
by inhibiting the Potentially Fatal: Very Assess patient for any
hypothalamic heat – rare, blood dyscrasias drug allergy to the
Classification: regulating center. Its (e.g., thrombocytopenia, medicine.
Analgesics and weak anti-inflammatory leukopenia, R> to determine if the
Antipyretics activity is related to neutropenia, patient is allergic to drug
inhibition of agranulocytosis); liver
prostaglandin synthesis damage. Intruct the patient/ give
Dosage: in the CNS. first health teaching
 250/5 mg 7 ml po before giving the
q4hr PRN patient.
R> to make the patient
prepare and know what
to expect

Give only the med for

presence of fever or
pain
R> overdose could lead
to drug-resistance

37
38
 Drug name Dosage Therapeutic Indication Contraindication Adverse effects Nursing responsibilities
action

Amikacin 250mg slow Inhibits protein Primarily for History of CNS: Neurotoxicity: 1. Before initial dose, C&S;
IVTT synthesis by short-term hypersensitivity drowsiness, unsteady renal function and
binding directly treatment of or toxic reaction gait, weakness, vestibulocochlear nerve function
to the30S serious infections with an clumsiness, paresthesias,
Drug class: ribosomal sub of respiratory aminoglycoside tremors, convulsions, 2. Monitor peak and trough
aminoglycosides unit ;bactericidal tract, bones, antibiotic. peripheral neuritis. amikacin blood levels: Draw
joints, skin, and blood 1 h after IM or
soft tissue, CNS immediately after completion of
Vestibular: dizziness,
(including IV infusion; draw trough levels
ataxia.
meningitis) and immediately before the next IM
peritonitis burns, GI: Nausea, vomiting,
or IV dose.
hepatotoxicity.
3. Monitor & report any changes
Metabolic: Hypokalemia, in I&O, oliguria, hematuria, or
hypomagnesemia. cloudy urine. Keeping patient
well hydrated reduces risk of
Skin: Skin rash, urticaria, nephrotoxicity; consult
pruritus, redness. physician regarding optimum
fluid intake.
Urogenital: Oliguria,
urinary frequency, 4. Monitor for and report
hematuria, tubular auditory symptoms (tinnitus,
necrosis, azotemia. roaring noises, sensation of
fullness in ears, hearing loss)
Other: Superinfections. and vestibular disturbances
(dizziness or vertigo,
nystagmus, ataxia).

39
40
 DRUG ORDER MECHANISM OF CONTRAINDICATIONS ADVERSE EFFECTS OF NURSING
INDICATIONS
ACTION THE DRUG RESPONSIBILITIES/
PRECAUTIONS

Generic name: A nitroimidazole For treatment of Hypersensitivity to Peripheral neuropathy, Check the prescribed
Metronidazole derivative that disrupts anaerobic infection other nitroimidazole manifested as medication for 3 time
bacterial and protozoal (skin and skin derivatives. numbness and tingling on the first encounter,
Brand name: DNA, inhibiting nucleic structures, lower in hands or feet, is before and after
Metronidazole acid synthesis. respiratory tract. usually reversible if withdrawing the med
Benzoate treatment is stopped R> so that the medicine
Therapeutic Effect: immediately after is properly checked
Classification: Produces bactericidal, neurologic symptoms according to the
Antibacterial, antiprotozoal, appear. Seizures occur doctor’s prescription.
antiprotozoal amebicidal, and ocassionally.
trichomonacidal effects. Give first health
Produces anti- teaching before giving
Dosage: inflammatory and the patient.
 250 mg q8h, immunosuppressive R> to make the patient
IVTT effects when applied prepare and know what
topically. to expect
ANST(-)
The med should be
given in IVT route
according to the doctor
R> Follow the doctor’s
order.

Question for
hypersensitivity on
41
metronidazole
R> to determine if the
med is applicable to
patient.

42
DRUG DOSAGE MECHANISM OF INDICATIONS C/I ADVERSE NURSING
CLASS ACTION REACTIONS CONSIDERATIONS

Analgesic 200/5 4 ml Anti-inflammatory, *Relief of mild to C/I with allergy CNS: headache, Administer in the
NSAID q6hr analgesic, and moderate pain to ibuprofen, dizziness, vertigo, nerve morning with a full
Propionic antipyretic activities *Fever reduction salicylates, or root lesion, asthenia, glass of water atleast
acide largely related to *Post surgery other insomnia 60 min before the first
derivative inhibition of *Headache & NSAIDS(more beverage, food, and
prostaglandin musculoskeletal common in CV: angina, medication of the day.
synthesis; pain patients with hypertension Patient must stay
*Soft tissue rhinitis, asthma, upright for 60min after
Inhibits both inflammation, chronic urticaria, GI: diarrhea, abdominal taking the tablet to
cyclooxygenase including nasal polyps) pain, dyspepsia, avoid potentially
(COX) 1 and 2. juvenile RA. gastric/esophageal serious esophageal
Slightly more Advanced kidney ulcers, nausea-vomiting erosion.
selective for COX1 and liver disease
RESPI: URTI, 1. Monitor serum
Asthma bronchitis, pneumonia calcium levels
before, during and
Active GI MUSCULOSKELETAl: after therapy
bleeding Back pain, myalgia, 2. Ensure adequate
joint pain intake of Vitamin
D and calcium.
3. Provide comfort
measures and
possible
analgesics for pain
and headache
4. Encourage
frequent small
meals if GI effects
are uncomfortable.

43
44
 DRUG DOSAGE MECHANISM OF INDICATIONS ADVERSE NURSING
CLASS ACTION REACTIONS CONSIDERATIONS
Generic Name :
Lactobacillus Supplements & 1 cap mix Lactobacillus * Preventing and . Hypersensitivity Nursing Responsibilities:
(Probiotics Adjuvant with h2o po acidophilus started treating diarrhea, Reactions  Can be taken with meals or
Therapy (lactic 2. Headache without meals
Brand Name: OMX OD the breakdown of including
acid producing 3. Disorientation  Assess if hypersensitive to
organisms, food and produce infectious
4. Nausea and Vomiting drug
combinations; lactic acid, hydrogen diarrhea.
 Assess for GI symptoms
Belongs to the peroxide, and other 5. Dizziness
class of Restoring the  Assess for skin rashes and
byproducts that make
antidiarrheal "friendly" other allergic reactions
the environment
microorganisms intestinal bacteria Teach to take medications
. Used in the hostile for undesired religiously to promote
organisms. During destroyed by
treatment of faster healing
diarrhea) fermentation it will antibiotics
produce lactate and treatment.
acetate. Lactobacillus Improving
acidophilus produces digestion and
the acids that make suppressing
food taste sour. disease-causing
Lactobacillus bacteria.
acidophilus enzyme
breaks down milk
sugar (lactose) into
simple sugars. People
who are lactose
intolerant do not
produce this enzyme.
For this reason,
Lactobacillus
acidophilus
supplements may be

45
beneficial for these
individuals

46
Name of Drugs Dosage Indications Containdications Mechanism of Action Side Effects N.
Responsibilities

47
Hidrasec 10 mg 1 sachet For the treatment of Known Hidrasec is an inhibitor A few cases of
mix 5 ml h2o TID acute diarrhea. hypersensitivity to of enkephalinase, drowsiness have
racecadotril. Renal theenzyme responsible been reported
Hidrasec should be or for breaking down during
given in conjunction hepaticimpairment. enkephalins. It is clinicaltrials.
with oral or aselective but Nausea and
parenteralrehydration reversible inhibitor and vomiting,
therapy in patients protects constipation,
wheredehydration endogenousenkephalins dizziness
has occurred or is which are andheadaches
suspected. physiologically active have also been
in the digestive tract. reported rarely.
The side effects
have been mild,
and equivalent in
nature,
frequency and
intensity tothose
reported with
placebo. Post-
marketing
surveillance
hasindicated side
effects to be
extremely rare in
general use.

No side effects
have been

48
 reported, up to
the present time,
po OD with the use of
Acute diarrhea with During antibiotic Erceflora is a the drug.
duration of ≤14 days therapy, Erceflora preparation consisting
due to infection, should be of suspension of
Erceflora drugs or poisons. administered in the Bacillus clausii spores,
Chronic or persistent interval between 1 normal inhabitants of
diarrhea with dose of antibiotic the intestine, with no
duration of >14 days. and the next. pathogenic powers.
Effects on the Administered orally,
Ability to Drive or Bacillus clausii spores,
Operate due to their high-
Machinery: resistance to both
Erceflora does not chemical and physical
interfere with the agents, cross the barrier
ability to drive or of the gastric juices
use machinery. reaching unharmed the
Use in pregnancy intestinal tract where
& lactation: There they are transformed
are no into metabolically
contraindications active vegetative cells.
regarding the use
of Erceflora during
pregnancy and
lactation.

49
DISCHA
RGE
PLAN
A.
OBJECT
IVE
1.
Summari
ze a
simple
and
producti
ve health
educatio
n plan;
2.
Adhere
prescribe
d
medicati
ons for
health

50
maintenance and resistance;
3. Promote a health lifestyle, maximize the level of health ;
4. Gains knowledge in managing the condition; and
5. Maintain and ensure adequate intake for nourishment

B. METHOD (N/A) REFER TO DRUG STUDY

2. EXERCISE/ACTIVITY and HOME ENIVRONMENT

1. Depending on the status, the patient is encouraged to return to usual activities gradually.

 Promoting proper skin and wound care.

 Maintaining good personal hygiene.
 Avoiding stress which can aggravate symptoms.
 Encouraging activity within prescribed limits but avoid fatigue.
 Protecting from injury when carrying out activities.
 Protecting patient from exposure to infectious agents.
 Maintaining good asepsis during treatments and procedures.
 Encouraging proper diet.

51
  Teach the family of how to promote comfort.
 Medicating patient as needed for pain.
 Providing comfort measures and relaxation techniques.
 Encouraging good oral hygiene.
 Encouraging rest for fatigue.
 Providing calm, supportive environment
RESTRICTIONS:
1. Strenuous activities
2. Heavy lifting greater than 5kg
3. Prolonged exposure to sunlighrt

HOME ENVIRONMENTAL HAZARDS:

a) Restrict smoker
b) Crowded area

3. TREATMENTS/THERAPIES
a) Attending the follow up check up :
 Educate client by adhering maintenance therapy, appropriate diet and having exercise will reduce likelihood

of occurrence and aggravation of disease.

52
 4. HEALTH TEACHING/EDUCATION
PREVENTION/PROMOTION
Health teaching about the disease, exercise and diet
 Instructs the patient about home-made interventions in reducing blood such as:
a.) Pineapple or calamansi juice to reduce blood pressure
b) chewing of raw or fried garlic after meals
c.) refrain from consumption of caffeinated beverages, such as coffee and chocolate

4. OPD Visit (N/A)

6. DIET
LOW FAT

53
References:

1. Taylor (2008) Nursing Diagnosis Pocket Guide (2th ed.).Philadelphia: Wolters

Kluwer Health/Lippincott Williams & Wilkins.

2. Lewis, Heitkemper ,Dirksen ,O'Brien,Bucher (2007): Assessment and

Management of Clinical Problems, liver, Pancreas and Biliary Tract problems,
Medical Surgical Nursing, MOSBY.1st Edition, 1101:15.

3. Ignatavicius & Workman (2006) Medical Surgical Nursing: Critical Thinking for
Collaborative Care. USA. Elsevier.

4. Smeltzer & Bare (2004). Medical- Surgical Nursing. Philadelphia. Lippincott

Williams & Wilkins.

5. Tortora (2011). Principles of Anatomy and Physiology , 14th Edition John Wiley
& Sons, 2008.

6. Weber & Kelley (2014). Health Assessment In Nursing. Philadelphia. Lippincott

Williams & Wilkins.

7. Goldman and Schafer (2016).Goldman-Cecil Medicine. 25th ed. Philadelphia,

PA: Elsevier Saunders.

8. Cecil, Goldman,Bennett (2000).Cecil Textbook of Medicine . 21st ed.

Philadelphia, PA: WB Saunders Comp

54
55