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I.

INTRODUCTION

Gastroenteritis is a catchall term for infection or irritation of the digestive tract,

particularly the stomach and intestine. It is frequently referred to as the stomach or

intestinal flu, although the influenza virus is not associated with this illness. Major

symptoms include nausea and vomiting, diarrhea, and abdominal cramps. These

symptoms are sometimes also accompanied by fever and overall weakness.

Gastroenteritis typically lasts about three days. Adults usually recover without problem,

but children, the elderly, and anyone with an underlying disease are more vulnerable to

complications such as dehydration.

Bacterial gastroenteritis is frequently a result of poor sanitation, the lack of safe

drinking water, or contaminated food—conditions common in developing nations.

Natural or man-made disasters can make underlying problems in sanitation and food

safety worse. In developed nations, the modern food production system potentially

exposes millions of people to disease-causing bacteria through its intensive production

and distribution methods. Common types of bacterial gastroenteritis can be linked to

Salmonella and Campylobacter bacteria; however, Escherichia coli 0157 and Listeria

monocytogenes are creating increased concern in developed nations. Cholera and

Shigella remain two diseases of great concern in developing countries, and research to

develop long-term vaccines against them is underway.

Gastroenteritis is an uncomfortable and inconvenient ailment, but it is rarely life-

threatening in the United States and other developed nations. However, an estimated

220,000 children younger than age five are hospitalized with gastroenteritis symptoms

in the United States annually. Of these children, 300 die as a result of severe diarrhea

and dehydration. In developing nations, diarrheal illnesses are a major source of

mortality. In 1990, approximately three million deaths occurred worldwide as a result of

diarrheal illness.

Gastroenteritis is a general term referring to inflammation or infection of the

gastrointestinal tract, primarily the stomach and intestines.[1] It can be caused by

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infection with bacteria, viruses, or other parasites, or less commonly reactions to new

foods or medications. It often involves stomach pain (sometimes to the point of

crippling), diarrhea and/or vomiting, with non-inflammatory infection of the upper small

bowel, or inflammatory infections of the colon. It usually is of acute onset, normally

lasting fewer than 10 days and self-limiting. Sometimes it is referred to simply as

'gastro'. It is often called the stomach flu or gastric flu even though it is not related to

influenza. If inflammation is limited to the stomach, the term gastritis is used, and if the

small bowel alone is affected it is enteritis. As such, this has a relationship on the

concept fluids and electrolyte. Because dehydration the most common complication of

gastroenteritis if not treated or no immediate intervention done it could lead to shock

and eventually can lead to death.

A case of patient KA, 3-year old, Filipino child, from Macasandig, Cagayan de

Oro City, was admitted for the second time in Oro Doctor’s Hospital due to Loose Bowel

Movement and vomiting.

In the morning prior to the patient’s admission, the patient had an onset of loose

watery, foul-smelling, mucoid, with blood-streaked stool. This is in an amount

approximately equivalent to a ¼ of a cup, similarly occurring for 8 episodes,

accompanied by abdominal discomfort and vomiting for two consecutive episodes. The

patient was negative for fever, and was given Flagyl for relief; however, due to

persistent diarrhea, the patient opts for admission.

From the patient’s presenting signs and symptoms, along with the aid of some

laboratory studies, the physician arrived with a diagnosis of Acute Gastroenteritis with

some Dehydrations, especially Amebiasis; and, Urinary Tract Infection.

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b. General Objectives:

After 2 weeks of case study on Patient AR, the group will be able to acquire

knowledge about Gastroenteritis with some dehydration especially Amoebiasis and their

complications; gain proficiency on nursing interventions which are essential and suitable

for the patient and significant others with the above mentioned disease condition.

Furthermore, provide support and encouragement on the patient and the family in

dealing with the client’s condition.

c. Specific Objectives:

This case study specifically aims to do the following after 2 hours of case

presentation:

1. Discuss the Anatomy and Physiology of the organs interconnected to the client’s

disease condition.

2. Provide information about the description and progress of Gastroenteritis with

some dehydration especially Amoebiasis that are specific to the client.

3. Itemize the predisposing and precipitating factors that lead to Gastroenteritis with

some dehydration especially Amoebiasis

4. List the ideal medical and nursing intervention appropriate to the disease condition

5. Present the formulated and prioritized nursing care plan for the client

6. Provide a study of the medications ordered for the client and the rationale for its

prerequisite

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7. Convey additional information that is necessary for the improvement of care given

to the client maybe utilized as health teaching to the client.

d. Scope and Limitation of the Study

This study includes the collection of information specifically to the patient’s health

condition. The study also includes the assessment of the physiological and

psychological status, adequacy of support systems and care given by the family as well

as other health care providers.

The scope of this study would include:

a. Data collected via assessment, interviews with the patient, family members

and clinical records.

b. Actual and ideal problems for 3 days including the initial assessment and its

appropriate nursing intervention that would be applied within his stay in the hospital at

PGH hospital.

c. Developing a plan of care that will reduce identified predicaments and

complications.

d. Coordinating and delegating interventions within the plan of care to assist the

client to reach maximum functional health.

e. Further evaluating the effectiveness of nursing interventions that have been

rendered to the client.

An array of factors influencing the limitations of this study includes:

a. Data collected is limited only to assessment and interview to the patient,

patient’s chart and nurse on duty.

b. The interaction, assessment and care were only limited to a total of 16 hours

(2 days clinical duty, 1 day assessment) with actual nursing intervention done.

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c. The lack of complete family history obtained was due to lack of laboratory

examinations or diagnostic examinations results like x-ray which data or results

obtained is in the chart of the client during the time of care.

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II. ASSESSMENT

Pediatric Assessment Tool

A. Client Profile:

Name: KA

Age: 3

Birthday: May 15,2006

Birthplace: Polymedic Hospital CDO

Address: Calacala Macasandig, CDO

Religion: Roman Catholic Current Educational Level: N/A

Name of School: N/A

Name of Parents/Guardian: EA & CA

Name of Informant: CA Relation to client: Mother

Attending Physician: Dr. C. Red

Date of Admission: 2/15/10 Room/Ward#: 304

No. of Days Admitted: 2

Chief Complaint/s upon admission: LBM & Vomiting

Medical Diagnosis, if any: Acute Gastroenteritis w/ some dehydration

Current Medications:

Name of Drug/s Dosage Indications Remarks


PCM 250/5 9.5 ml PO Fever
Gentamicin 25g IVTT Bacterial Infection
Diloxamide 5ml PO Tx for entamoeba

Furoate hystolitica
Domperidone 3ml TID Vomiting
Zinc Sulfate 5ml OD PO Zinc deficiency

Past hospitalization, if any: twice, because of Amoeba. First at Sabal clinic then 2 nd at

Oro Doctor’s hospital

Past treatments, if any: informant cannot remember

I. HEALTH PERCEPTION- HEALTH MANAGEMENT PATTERN

Apperance: weak & pale, poor skin turgor, appears restless; thin & small for age; poor

muscle tone, sunken eyes, appears restless

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Grooming: well groomed, appropriately dressed, neat & clean without any foul/bad

body odor.

Posture: erect

Height: 37 in (0.94m) Weight: 15 kgs.

PR: 90 bpm RR: 24cpm Temperature: 37.2

Immunizations received including date:

Child is fully immunized when he was 9 mos. Old according to his mother

(February 2007).

II. NUTRITIONAL METABOLIC PATTERN

Skin-Color: brownish

Lesions: none, but there are scars on both knees

Texture: slightly dry but smooth to touch

Hair-Color: black

Lesions: none

Texture: smooth and shiny

Nail-color: pale pink with a delayed capillary refill of 1-3 seconds.

Condition: clean

Oral Mucosa-Teeth: whitish

Condition: no visible dental carries

Daily Food Intake:

Breakfast/Lunch/Dinner: his meal varies; he only eats rice & viand once in a day

either during breakfast, lunch or dinner. Other meals consist of biscuit or milk and/or

juice.

Snacks: biscuit and juice/coke

Food supplements: none

Vitamins taken: Ener 4 plus & Pro-zinc but for only 2 months

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III. ELIMINATION

Bowel-Habits:

Frequency : 1-3 times a day

Color: varies, yellow or brown, there is a change in stool color

Consistency: formed & cylindrical, but now watery

Amount: approxiamately ½ cup

Bladder Habits:

Frequency: anytime of the day

Color: orange or yellow

Amount: scanty amount ranging from ½-3/4 cup per micturation

IV. ACTIVITY-EXERCISE PATTERN

Daily activities: upon waking up, he eat his meal, watch tv or play; he sleeps at noon

then play till night

Leisure activities: watch tv, ride a bike, play

Exercise routine: none specifically but considered biking as one

V. SLEEP-REST PATTERN

Time of sleep: sleeps 8-11pm wakes up at 6 am

Quality: good & well rested

Sleep aid/s: none: sometimes he watches television until he falls asleep

VI. SENSORY-PERCEPTUAL PATTERN

Vision: good, recognizes objects from a far

Aid/s for vision: none

Hearing: good but do not pay attention most of the time when called by his name

Aid/s for hearing: none

Smell: N/A

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VII. COGNITIVE PATTERN

Ability to express:

When he wants to eat he grabs a plate , when he wants to pee he takes off his

shorts. If he wants to sleep he lies on bed. If he wants something but cant express it

verbally he cries out loud. He cannot speak properly and mother admitted that her child

(the Patient) has special needs and has a developmental delay in speech.

VIII. ROLE-RELATIONSHIP PATTERN

Ordinal position of client in the family: youngest/ 3rd child of 3

Primary caregiver of client: mother, but he was taken care by a nanny when he was

few months old until he reached 2 years old.

Other support system of client: older sister, father.

B. Laboratory Results

Hematology

Date: 2/15/2010

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CBC

Hgb 187 g/L M (40-175)

 elevated Hgb suggests hemoconcentration from polycythemia or dehydration

Hct 0.56 M (0.41)

 high Hct indicates polycythemia or hemoconcentration resulting from blood

loss and dehydration

RBC 6.7 (4.0-6.0 012/L)

 Increases in the RBC count are most commonly seen in polycythemia vera,

chronic pulmonary disease with hypoxia and secondary polycythemia, and

dehydration with hemoconcentration

WBC 17.4 (4.5-10 x 012/L)

 elevated WBC (leukocytosis) count commonly signals infection, such as an

abscess, meningitis, appendicitis, or tonsillitis

Differential Count

Neutrophils 0.87 (0.50-0.70)

 increased level suggests an inflammatory disorders

Lymphocytes 0.13 (0.20-0.40)

 decreased lymphocytes indicates severe debilitating illnesses, such as heart

failure, renal failure, advanced tuberculosis, defective lymphatic circulation, high

levels of adrenal corticoids, immunodeficiency

Platelet Count 240 (150-400 : 109/L)

 within normal range

Fecalysis

Date: 2/16/2010

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Color: Yellow usually found in milk-fed children

Consistency: Watery possibly caused by inflammatory bowel syndrome,

carcinoma, typhoid, Shigella, amebae

Pus Cells: 8-12 / hpf 

Entamoeba histolitica: Cyst  positive

Others: Bacteria  few

Urinalysis

Date: 2/16/2010

Physical Characteristics

Color: Yellow  normal

Transparency: Hazy  may be caused by precipitation of urates, uric acid,

or calcium oxalate

Specific gravity: 1.030  Urine with a high specific gravity is associated with

dehydration, uncontrolled diabetes mellitus, and

nephrosis

Albumin: +1  may be present during dehydration

Chemical Tests

pH: 6.0  acidic

Sugar: (-)  normal

Cells

Pus cells: 4-6/ hpf 

RBC: 4-5/ hpf  damage to the glomerular membrane or to the

genitourinary tract is indicated

Others

Bacteria: Moderate  may present in UTI

Crystals

Amorphous Urates: Plenty  not of a major clinical significance

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Amorphous Phosphate: Few  may be found in urine that has stool at room

temperature for several hours

C. Developmental Stages

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a. Developmental Task Theory of Robert Havighurst

A developmental task is a task which arises at or about a certain period in the life

of an individual. Havighurst has identified six major age periods: infancy and early

childhood (0-5 years), middle childhood (6-12 years), adolescence (13-18 years), early

adulthood (19-29 years), middle adulthood (30-60 years), and later maturity (61+).

Basing on Havighurst’s Theory, the patient belongs in the infancy and early

childhood stage. According to the patient’s mother the patient learned to walk when he

was already almost 2 years old and started to talk just recently. The patient has control

on his elimination but is not able to relate emotionally to his parents and cannot

distinguish right from wrong when in fact according to Havighurst these things should

already be mastered in this stage.

b. Psychosexual Theory of Sigmund Freud

The psychosexual stages of Sigmund Freud are five different developmental

periods during which the individual seeks pleasure from different areas of the body

associated with sexual feelings. These stages are as follows:

Oral Birth to to 1year

Anal 2 to 3years

Phallic 4 to 5years

Latency 6 to 12years

Genital 13 and Up

Basing on this theory, the patient belongs to the anal stage the time wherein the

child’s feeling of self-control is enhanced through making a positive toilet training

experience. According to the mother when a child wants to void or defecate he takes off

his shorts and goes to the comfort room.

c. Psychosocial Theory of Erik Erickson

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Erik Erickson envisioned life as a sequence of levels of achievement. Each

stage signals a task that must be achieved. He believed that the greater the task

achievement, the healthier the personality of the person. Failure to achieve a task

influences the person’s ability to progress to the next level. Stages of Erikson’s

Psychosocial Theory are as follows:

 Infancy Birth – 18 months Trust vs. Mistrust

 Early Childhood 18 months – 3 years Autonomy vs. Shame

 Late Childhood 3 – 5 years Initiative vs. Guilt

 School Age 6 – 12 years Industry vs. Inferiority

 Adolescence 12 – 20 years Identity vs. Role Confusion

 Young Adulthood 18 – 25 years Intimacy vs. Isolation

 Adulthood 25 – 65 years Generativity vs. Stagnation

 Maturity 65 years to death Integrity vs. Despair

Basing on this theory, the patient belongs to late childhood stage with the central

task of “initiative vs. guilt.” The mother verbalized that her son has a developmental

delay and depends on her in most of his activities of daily living. According to Erikson a

child in this stage must develop initiative in doing things without the help of other

people; failure to do so may indicate a negative resolution for this stage such as having

a poor self-esteem, lack of self-confidence and pessimism which are apparent to the

patient and thus reflect a negative aspect of guilt.

d. Cognitive Theory of Jean Piaget

Cognitive development refers to how a person perceives, thinks, and gains

understanding of his or her world through the interaction and influence of genetic and

learning factors. This is divided into five major phases:

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Sensorimotor Phase Birth to 2 years

Pre-conceptual Phase 2 – 3 years

Intuitive Thought Phase 4 – 6 years

Concrete Operations Phase 7 – 11 years

Formal Operational Phase 12 – adulthood

Basing on this theory, patient belongs to the pre-conceptual stage in which a

child uses an egocentric approach to accommodate the demands of an environment.

The child in this stage according to Piaget has rapid language development and

associates words with objects but in the case of the patient he has a developmental

delayed in speech and started to talk just recently.

D. Body Map

1) D5LR 500 cc,


2

regulated @ 55 ml/hr

2)Vomiting, developmental

delay in speech

3) Mid abdominal pain,

3 Loss of appetite

4) Frequent loose, watery,

bowel movement

4
1

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III. ANATOMY AND PHYSIOLOGY

Anatomy of the Digestive System

If a human adult’s digestive tract were stretched out, it would be 6 to 9 m (20 to

30 ft) long. In humans, digestion begins in the mouth, where both mechanical and

chemical digestion occur. The mouth quickly converts food into a soft, moist mass. The

muscular tongue pushes the food against the teeth, which cut, chop, and grind the food.

Glands in the cheek linings secrete mucus, which lubricates the food, making it easier to

chew and swallow. Three pairs of glands empty saliva into the mouth through ducts to

moisten the food. Saliva contains the enzyme ptyalin, which begins to hydrolyze (break

down) starch—a carbohydrate manufactured by green plants.

Once food has been reduced to a soft mass, it is ready to be swallowed. The

tongue pushes this mass—called a bolus—to the back of the mouth and into the

pharynx. This cavity between the mouth and windpipe serves as a passageway both for

food on its way down the alimentary canal and for air passing into the windpipe. The

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epiglottis, a flap of cartilage, covers the trachea (windpipe) when a person swallows.

This action of the epiglottis prevents choking by directing food from the windpipe and

toward the stomach.

Mouth

The mouth plays a role in digestion, speech, and breathing. Digestion begins

when food enters the mouth. Teeth break down food and the muscular tongue pushes

food back toward the pharynx, or throat. Three salivary glands—the sublingual gland,

the submandibular gland, and the parotid gland—secrete enzymes that partially digest

food into a soft, moist, round lump. Muscles in the pharynx swallow the food, pushing it

into the esophagus, a muscular tube that passes food into the stomach. The epiglottis

prevents food from entering the trachea, or windpipe, during swallowing.

Esophagus

The presence of food in the pharynx stimulates swallowing, which squeezes the

food into the esophagus. The esophagus, a muscular tube about 25 cm (10 in) long,

passes behind the trachea and heart and penetrates the diaphragm (muscular wall

between the chest and abdomen) before reaching the stomach. Food advances through

the alimentary canal by means of rhythmic muscle contractions (tightenings) known as

peristalsis. The process begins when circular muscles in the esophagus wall contract

and relax (widen) one after the other, squeezing food downward toward the stomach.

Food travels the length of the esophagus in two to three seconds.

A circular muscle called the esophageal sphincter separates the esophagus and

the stomach. As food is swallowed, this muscle relaxes, forming an opening through

which the food can pass into the stomach. Then the muscle contracts, closing the

opening to prevent food from moving back into the esophagus. The esophageal

sphincter is the first of several such muscles along the alimentary canal. These muscles

act as valves to regulate the passage of food and keep it from moving backward.

Stomach

The stomach, located in the upper abdomen just below the diaphragm, is a

saclike structure with strong, muscular walls. The stomach can expand significantly to

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store all the food from a meal for both mechanical and chemical processing. The

stomach contracts about three times per minute, churning the food and mixing it with

gastric juice. This fluid, secreted by thousands of gastric glands in the lining of the

stomach, consists of water, hydrochloric acid, an enzyme called pepsin, and mucin (the

main component of mucus). Hydrochloric acid creates the acidic environment that

pepsin needs to begin breaking down proteins. It also kills microorganisms that may

have been ingested in the food. Mucin coats the stomach, protecting it from the effects

of the acid and pepsin. About four hours or less after a meal, food processed by the

stomach, called chyme, begins passing a little at a time through the pyloric sphincter

into the duodenum, the first portion of the small intestine.

Liver

The liver is the largest internal organ in the human body, located at the top of the

abdomen on the right side of the body. A dark red organ with a spongy texture, the liver

is divided into right and left lobes by the falciform ligament. The liver performs more

than 500 functions, including the production of digestive liquid called bile that plays a

role in the breakdown of fats in food. Bile from the liver passes through the hepatic duct

into the gallbladder, where it is stored. During digestion bile passes from the gallbladder

through bile ducts to the small intestine, where it breaks down fatty food so that it can

be absorbed into the body. Nutrientrich blood passes from the small intestine to the

liver, where nutrients are further processed and stored. Deoxygenated blood leaves the

liver via the hepatic vein to return to the heart.

Small Intestine

Most digestion, as well as absorption of digested food, occurs in the small

intestine. This narrow, twisting tube, about 2.5 cm (1 in) in diameter, fills most of the

lower abdomen, extending about 6 m (20 ft) in length. Over a period of three to six

hours, peristalsis moves chyme through the duodenum into the next portion of the small

intestine, the jejunum, and finally into the ileum, the last section of the small intestine.

During this time, the liver secretes bile into the small intestine through the bile duct. Bile

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breaks large fat globules into small droplets, which enzymes in the small intestine can

act upon. Pancreatic juice, secreted by the pancreas, enters the small intestine through

the pancreatic duct. Pancreatic juice contains enzymes that break down sugars and

starches into simple sugars, fats into fatty acids and glycerol, and proteins into amino

acids. Glands in the intestinal walls secrete additional enzymes that break down

starches and complex sugars into nutrients that the intestine absorbs. Structures called

Brunner’s glands secrete mucus to protect the intestinal walls from the acid effects of

digestive juices. The small intestine’s capacity for absorption is increased by millions of

fingerlike projections called villi, which line the inner walls of the small intestine. Each

villus is about 0.5 to 1.5 mm (0.02 to 0.06 in) long and covered with a single layer of

cells. Even tinier fingerlike projections called microvilli cover the cell surfaces. This

combination of villi and microvilli increases the surface area of the small intestine’s

lining by about 150 times, multiplying its capacity for absorption. Beneath the villi’s

single layer of cells are capillaries (tiny vessels) of the bloodstream and the lymphatic

system. These capillaries allow nutrients produced by digestion to travel to the cells of

the body. Simple sugars and amino acids pass through the capillaries to enter the

bloodstream. Fatty acids and glycerol pass through to the lymphatic system.

Large Intestine

A watery residue of indigestible food and digestive juices remains unabsorbed.

This residue leaves the ileum of the small intestine and moves by peristalsis into the

large intestine, where it spends 12 to 24 hours. The large intestine forms an inverted U

over the coils of the small intestine. It starts on the lower right-hand side of the body and

ends on the lower left-hand side. The large intestine is 1.5 to 1.8 m (5 to 6 ft) long and

about 6 cm (2.5 in) in diameter. The large intestine serves several important functions. It

absorbs water— about 6 liters (1.6 gallons) daily—as well as dissolved salts from the

residue passed on by the small intestine. In addition, bacteria in the large intestine

promote the breakdown of undigested materials and make several vitamins, notably

vitamin K, which the body needs for blood clotting. The large intestine moves its

remaining contents toward the rectum, which makes up the final 15 to 20 cm (6 to 8 in)

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of the alimentary canal. The rectum stores the feces—waste material that consists

largely of undigested food, digestive juices, bacteria, and mucus—until elimination.

Then, muscle contractions in the walls of the rectum push the feces toward the anus.

The Urinary System:

The Urinary System performs the functions of producing and excreting urine from

the body. The constancy of body fluid volumes and the level of many important

chemicals depend on normal urinary system function. It performs vital excretory

functions and eliminates the dissolved organic waste products generated by the body’s

cells. It is also responsible for regulating blood volume and blood pressure by adjusting

the volume of water lost in the urine and releasing the hormones erythropoietin and

rennin. Urinary system also regulates blood concentrations of sodium, potassium,

chloride and other ions by controlling the quantities lost in the urine; stabilizes blood pH

by controlling the loss of ions in the urine; and conserves valuable nutrients by

selectively preventing losses while eliminating waste products.

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The body takes nutrients from food and converts them to energy. After the body

has taken the food that it needs, waste products are left behind in the bowel and in the

blood. Thus, the urinary system keeps the chemicals and water in balance by removing

a type of waste called urea from the blood. Urea is produced when proteins, found in

meat products, are broken down in the body.

• Kidneys: bean shaped, purplish-brown organs located retroperitoneally. Their

function is to:

o Remove liquid waste from the blood in the form of urine.

o Keep a stable balance of salts and other substances in the blood.

o Produce erythropoietin, a hormone that aids the formation of red blood

cells.

• The kidneys remove urea from the blood through tiny filtering units called

nephrons. Each nephron consists of a ball formed of small blood capillaries,

called a glomerulus and a small tube called a renal tubule. Urea, together with

water and other waste substances, forms the urine as it passes through the

nephrons and down the renal tubules of the kidney.

• Ureters: narrow tubes that carry urine from the kidneys to the bladder. Muscles

in the ureter walls continually tighten and relax forcing urine downward, away

from the kidneys. If urine backs up, or is allowed to stand still, a kidney infection

can develop. About every 10 to 15 seconds, small amounts of urine are emptied

into the bladder from the ureters.

• Bladder: it serves as a reservoir for urine. This triangle-shaped, hollow organ

located in the lower abdomen is held in place by ligaments that are attached to

other organs and the pelvic bones. The bladder's walls relax and expand to store

urine and contract and flatten to empty urine through the urethra.

• Sphincter muscles: circular muscles that help keep urine from leaking by

closing tightly like a rubber band around the opening of the bladder.

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• Nerves in the bladder: alert a person when it is time to urinate, or empty the

bladder.

• Urethra: it is the passageway of urine to the external environment. The brain

signals the bladder muscles to tighten, which squeezes urine out of the bladder.

At the same time, the brain signals the sphincter muscles to relax to let urine exit

the bladder through the urethra. When all the signals occur in the correct order,

normal urination occurs.

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IV. PATHOPHYSIOLOGY

A. Narrative

Infectious agents usually cause acute gastroenteritis. These agents cause

diarrhea by adherence, mucosal invasion, enterotoxin production, and/or cytotoxin

production.

These mechanisms result in increased fluid secretion and/or decreased

absorption. This produces an increased luminal fluid content that cannot be adequately

reabsorbed, leading to dehydration and the loss of electrolytes and nutrients.

Diarrheal illnesses may be classified as follows:

• Osmotic, due to an increase in the osmotic load presented to the intestinal

lumen, either through excessive intake or diminished absorption

• Inflammatory (or mucosal), when the mucosal lining of the intestine is inflamed

• Secretory, when increased secretory activity occurs

• Motile, caused by intestinal motility disorders

The small intestine is the prime absorptive surface. The colon then absorbs

additional fluid, transforming a relatively liquid fecal stream in the cecum to well-formed

solid stool in the rectosigmoid.

Disorders of the small intestine result in increased amounts of diarrheal fluid with a

concomitantly greater loss of electrolytes and nutrients.

Microorganisms may produce toxins that facilitate infection. Enterotoxins are

generated by bacteria (ie, enterotoxigenic Escherichia coli, Vibrio cholera) that act

directly on secretory mechanisms and produce typical, copious watery (rice water)

diarrhea. No mucosal invasion occurs. The small intestines are primarily affected, and

elevation of the adenosine monophosphate (AMP) levels is the common mechanism.

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Cytotoxin production by bacteria (ie, Shigella dysenteriae, Vibrio

parahaemolyticus, Clostridium difficile, enterohemorrhagic E coli) results in mucosal cell

destruction that leads to bloody stools with inflammatory cells. A resulting decreased

absorptive ability occurs.

Enterocyte invasion is the preferred method by which microbes such as Shigella

and Campylobacter organisms and enteroinvasive E coli cause destruction and

inflammatory diarrhea. Similarly, Salmonella and Yersinia species also invade cells but

do not cause cell death. Hence, dysentery does not usually occur. However, these

bacteria invade the bloodstream across the lamina propria and cause enteric fever such

as typhoid.

Diarrheal illness occurs when microbial virulence overwhelms normal host

defenses. A large inoculum may overwhelm the host capacity to mount an effective

defense. Normally, more than 100,000 E coli are required to cause disease, while only

10 Entamoeba or Giardia cysts may suffice to do the same. Some organisms (eg, V

cholera, enterotoxigenic E coli) produce proteins that aid their adherence to the

intestinal wall, thereby displacing the normal flora and colonizing the intestinal lumen.

In addition to the ingestion of pathogenic organisms or toxins, other intrinsic

factors can lead to infection. An alteration of normal bowel flora can create a biologic

void that is filled by pathogens. This occurs most commonly after antibiotic

administration, but infants are also at risk prior to colonization with normal bowel flora.

The normally acidic pH of the stomach and colon is an effective antimicrobial

defense. In achlorhydric states (ie, caused by antacids, histamine-2 [H2] blockers,

gastric surgery, decreased colonic anaerobic flora), this defense is weakened.

Hypomotility states may result in colonization by pathogens, especially in the

proximal small bowel, where motility is the major mechanism in the removal of

organisms. Hypomotility may be induced by antiperistaltic agents (eg, opiates,

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diphenoxylate and atropine [Lomotil], loperamide) or anomalous anatomy (eg, fistulae,

diverticula, antiperistaltic afferent loops) or is inherent in disorders such as diabetes

mellitus or scleroderma.

The immunocompromised host is more susceptible to infection, as evidenced by

the wide spectrum of diarrheal pathogens in patients with AIDS.

The exact mechanism of vomiting in acute diarrheal illness is not known,

although serotonin release has been postulated as a cause, stimulating visceral afferent

input to the chemoreceptor trigger zone in the lower brainstem. Preformed neurotoxins

produced by Staphylococcus aureus and Bacillus cereus, when ingested, can cause

severe vomiting.

Entamoeba sp exist in 2 forms:

• Trophozoite

• Cyst

The motile trophozoites feed on bacteria and tissue, reproduce, colonize the lumen

and the mucosa of the large intestine, and sometimes invade tissues and organs.

Trophozoites predominate in liquid stools but rapidly die outside the body. Some

trophozoites in the colonic lumen become cysts that are excreted with stool.

Cysts predominate in formed stools and resist destruction in the external

environment. They may spread directly from person to person or indirectly via food or

water. Amebiasis can also be sexually transmitted by oral-anal contact.

E. histolytica trophozoites can adhere to and kill colonic epithelial cells and PMNs

and can cause dysentery with blood and mucus but with few PMNs in stool.

Trophozoites also secrete proteases that degrade the extracellular matrix and permit

invasion into the intestinal wall and beyond. Trophozoites can spread via the portal

circulation and cause necrotic liver abscesses. Infection may spread by direct extension

25
from the liver to the right lung and pleural space or, rarely, through the bloodstream to

the brain and other organs.

When cyst is swallowed, it passes through the stomach unharmed and shows no

activity while in an acidic environment. When it reaches the alkaline medium of the

intestine, the metacyst begins to move within the cyst wall, which rapidly weakens and

tears. The quadrinucleate amoeba emerges and divides into amebulas that are swept

down into the cecum. This is the first opportunity of the organism to colonize, and its

success depends on one or more metacystic trophozoites making contact with the

mucosa.

Mature cyst in the large intestines leaves the host in great numbers (the host

remains asymptomatic). The cyst can remain viable and infective in moist and cool

environment for at least 12 days, and in water for 30 days. The cysts are resistant to

levels of chlorine normally used for water purification. They are rapidly killed by

purification, desiccation and temperatures below 5 and above 40 degrees.

The metacystic trophozoites of their progenies reach the cecum and those that

come in contact with the oral mucosa penetrate or invade the epithelium by lytic

digestion.

The trophozoites burrow deeper with tendency to spread laterally or continue the

lysis of cells until they reach the sub-mucosa forming flash-shape ulcers. There may be

several points of penetration.

From the primary site of invasion, secondary lesions maybe produced at the

lower level of the large intestine.

Progenies of the initial colonies are squeezed out to the lower portion of the

bowel and thus, have the opportunity to invade and produce additional ulcers.

Eventually, the whole colon may be involved.

26
E. histolytica has been demonstrated in practically every soft organ of the body.

Trophozoites which reach the muscularis mucosa frequently erode the

lymphatics or walls of the mesenteric venules in the floor of the ulcers, and are carried

to the intrahepatic portal vein.

If thrombi occur in the small branches of the portal veins, the trophozoites in

thrombi cause lytic necrosis on the wall of the vessels and digest a pathway into the

lobules.

The colonies increase in size and develop into abscess.

A typical liver abscess develops and consists of:

• Central zone necrosis

• Median zone of stoma only

• An outer zone of normal tissue newly invaded by amoeba. Most amoebic

abscess of the liver are in the right lobe.

Next to the liver, the organ which is the frequent site of extra-intestinal amoebiasis is

the lungs. This commonly develops as an extension of the hepatic abscess.

27
28
29
30
V. MEDICAL MANAGEMENT

A. Ideal and Actual Management

IDEAL MANAGEMENT RATIONALE ACTUAL


MANAGMENT
I. Acute Gastroenteritis
especially Amebiasis
A. Medical Therapy
1. Metronidazole Kills trophozoites of E histolytica in
(Flagyl, Protostat) intestine and tissue. Does not PERFORMED
eradicate cysts from intestines.
2. Tinidazole (Fasigyn, 5-nitroimidazole derivative with
Tindamax) selective antimicrobial activity
against anaerobic bacteria and
protozoa. The mechanism by which
tinidazole exhibits activity against
Giardia and Entamoeba species is
not known.
3. Paromomycin Amebicidal aminoglycoside antibiotic
(Humatin) that is poorly absorbed. Active only
against intraluminal form of
amebiasis. Used to eradicate cysts
of E histolytica following treatment
with metronidazole or tinidazole for
an invasive disease.
4. Anthelmintics Parasite biochemical pathways are
different from the human host; thus,
toxicity is directed to the parasite,
egg, or larvae.
5. Iodoquinol (Yodoxin) Halogenated hydroxyquinoline.
Luminal amebicide; acts primarily in
bowel lumen because it is poorly
absorbed. Best tolerated when given
with meals. Because it is active only
against intraluminal form of
amebiasis, it is used to eradicate
cysts of E histolytica after treatment
of invasive disease.
6. Chloroquine Inhibits growth by concentrating
phosphate (Aralen) within acid vesicles of parasite,
which increases internal pH of
organism. Also inhibits hemoglobin
utilization and metabolism of
parasite. Highly effective in
treatment of amebic liver abscess
when administered with emetine or
dehydroemetine. Like emetine and
dehydroemetine, it is not effective
against luminal forms.
7. Dehydroemetine Preferred over emetine because it is
(Mebadin) less toxic. Eradicates amebic tissue
infections, including liver abscess,
but does not act on luminal forms.
Luminal amebicide also must be
used to eradicate the bowel luminal

31
infection. Only effective against the
trophozoite forms and not the cyst
form.
8. Diloxanide furoate Luminal amebicide; acts primarily in
(Furamid, bowel lumen because it is poorly
Entamizole, absorbed. Used to eradicate cysts of
PERFORMED
Furamide) E histolytica after treatment of
invasive disease. Not available in
the United States.
B. Supplemental /
Dietary
1. Supplemental Zinc More recent advances in the science
Therapy of diarrhea treatment include
recognition for the role of zinc
supplementation in reducing disease
severity and occurrence, and
development of an oral rehydration
PERFORMED
solution of lower osmolarity for
global use. The combination of oral
rehydration and early nutritional
support promises to safely and
effectively assist a patient through
an episode of diarrhea.
2. Moderate Oral rehydration therapy is as
Dehydration effective as intravenous therapy in
rehydrating and replacing
• Oral electrolytes in children with mild to
rehydration moderate dehydration and therefore
solutions contain should be the therapy of first choice.
glucose plus
electrolytes.
PERFORMED
• Rehydration
protocols
(Moderate):
100cc/kg of ORS
plus replacement
over 4 hours

3. Diet Appropriate for All children should be returned to


Age age-appropriate age appropriate diets upon initial
unrestricted diets. rehydration. “Resting the gut” is an
inappropriate approach; early
refeeding has been shown to reduce
PERFORMED
illness duration, improve nutritional
outcomes and decrease changes to
intestinal permeability. Foods high in
simple sugars should be avoided
due to osmotic load.
4. Highly specific diets This had been commonly
(e.g., the BRAT recommended. Certain benefits exist
[bananas, rice, from green bananas and pectin in PERFORMED
applesauce, and persistent diarrhea
toast diet)
5. Functional foods: Reviews have evaluated studies of
Probiotics their use in preventing or reducing

32
the severity or duration of diarrheal
illnesses among children, including
diarrhea caused by rotavirus or
associated with antibiotic use. These
products have included various
species of lactobacilli or
bifidobacteria or the nonpathogenic
yeast Saccharomyces boulardii. The
mechanism of action might include
competition with pathogenic bacteria
for receptor sites or intraluminal
nutrients, production of antibiotic
substances, and enhancement of
host immune defenses
C. Diagnostic
Procedures
1. Imaging Studies
a. Chest May reveal an elevated right
radiography hemidiaphragm and a right-sided
pleural effusion in patients with
amebic liver abscess.
b. Ultrasonography Preferred for the evaluation of
amebic liver abscess because of its
low cost, rapidity, and lack of
adverse effects. A single lesion is
usually seen in the posterosuperior
aspect of the right lobe of the liver.
Multiple abscesses may occur in
some patients.
c. CT May be slightly more sensitive than
ultrasonography. In cerebral
amebiasis, CT shows irregular
lesions without a surrounding
capsule or enhancement.
d. MRI Reveals high signal intensity on T2-
weighted images. Perilesional
edema and enhancement of rim are
noted after injection of gadolinium
(86%).
2. Invasive Studies
a. Rectosigmoidosc Provides valuable materials for
opy and diagnostic information in intestinal
colonoscopy with amebiasis. Small mucosal ulcers
biopsy covered with yellowish exudates are
observed. The mucosal lining
between ulcers appears
normal. Rectosigmoidoscopy and
colonoscopy should be considered
before using steroids in patients in
whom inflammatory bowel disease is
suspected. Biopsy results and a
scraping of ulcer edge may reveal
trophozoites.
b. Aspiration of the Occasionally required to rule out a
liver abscess pyogenic abscess. Aspiration
amebic liver abscess yields an

33
anchovy-pastelike material that lacks
WBCs due to lysis by the parasite.
Amebae are visualized in the
abscess fluid in a minority of patients
with amebic liver abscess. Aspiration
of liver is indicated only for large
abscesses (>12 cm), imminent
abscess rupture, failure of medical
therapy, or presence of left lobe
abscesses.
3. Stool cultures Indicated in cases of dysentery or
where the diagnosis of AGE is PERFORMED
unclear.
a. Light Examination of a fresh stool smear
microscopy: for trophozoites that contain
ingested RBCs is rather insensitive.
Routine microscopy cannot
distinguish the E dispar and E
moshkovskii (nonpathogenic
amebae) from E histolytica.
b. An enzyme Specifically detect E histolytica in
immunoassay fresh stool specimens is
kit commercially available.
c. PCR-based Have been developed but are not
diagnostic tests widely available. Field studies that
directly compared PCR with stool
culture or antigen-detection tests for
the diagnosis of E histolytica
infection suggest that these methods
are equally comparable.
4. Serum Should be considered in cases of
electrolytes moderate to severe dehydration,
PERFORMED
when the case is not straightforward,
or when IV fluids are required
a. Antibody tests Serum antibodies against amebae
are present in 70-90% of individuals
with symptomatic intestinal E
histolytica infection. Antiamebic
antibodies are present in as many as
99% of individuals with liver abscess
who have been symptomatic
for longer than a week. Serologic
examination should be repeated a
week later in those with negative test
on presentation.
i. Indirect Detects antibody specific for E
hemagglutinati histolytica. The antigen used in IHA
on antibody consists of a crude extract of
(IHA) test axenically cultured organisms.
Antibody titers of more than 1:256 to
the 170-kd subunit of the galactose-
inhibitable adherence lectin are
noted in approximately 95% of
patients with extraintestinal
amebiasis, 70% of patients with
active intestinal infection, and 10%
of asymptomatic individuals.

34
i. EIA As sensitive and specific as the IHA
test and has replaced IHA in most
laboratories.
ii. Immunodiffusi Simple to perform, making it ideal for
on (ID) the laboratory that has only an
occasional request for amebic
serology. However, it requires a
minimum of 24 hours to complete,
compared with 2 hours for the IHA or
EIA test. ID is slightly less sensitive
than IHA and EIA, but is equally
specific.

b. The galactose Present in the serum of 75% of


lectin antigen subjects with amebic liver abscess
and may be particularly useful in
patients presenting acutely, before
an IgG serum anti-amebic antibody
response occurs.
5. Histologic Histopathologic findings include
Findings nonspecific mucosal thickening and
focal ulcerations with or without
amebae in a diffusely inflamed
mucosal layer. Classic flask-shaped PERFORMED
ulcers may be seen with ulceration
extending through the mucosa and
muscularis mucosa into the
submucosa
II. Urinary Tract Infection
A. Medical
Therapy
1. Broad To promote comfort and decrease
Spectrum complications by targeting the
Antibiotics specific bacteria and acts in a
a. Cephalosporin specific way to inhibit bacterial
b. growth. Typically begins before the
Ampicillin/amin culture and sensitivity results are
oglycoside known. Then, later, on the basis of
combination sensitivity report, a more specific PERFORMED
c. Sulfonamides antibiotic may be prescribed.
(Bactrim)
d.
Fluoroquinolon
es (Cipro)S
e. Nitrofurantoin
(Macrobid)
2. Analgesic: A urinary analgesic containing azo
Phenazopyridine dyes, may be prescribed to relieve
(Pyridium) the discomfort associated with the
infection or the burning sensation
often felt with cystitis.

B. Dietary
Modifications

35
1. Diet as tolerated Certain foods are known to irritate
with restrictions on the bladder, such as caffeine,
bowel irritants alcohol, tomatoes, spicy foods,
chocolate, and some berries. Clients PERFORMED
should be encouraged to avoid
bladder irritants during the acute
phase of the UTI
2. Cranberry juice Have been used to acidify the urine.
and Ascorbic Acid The use of these dietary measures
(Vitamin C) is under investigation. The tannin
proanthocyanidins is thought to
block bacteria from attaching to the
bladder wall, thus flushing it from the
urinary system.
3. Increase Fluid To treat and prevent UTI, encourage
Intake increased fluid intake, especially
water, if the client is not required to
restrict fluids. The desired amount is
PERFORMED
3 to 4 L/day. Increased fluids flush
the urinary system and are important
in preventing urolithiasis in clients
treated with sulfa drugs.
C. Diagnostic Findings
1. Urine Cultures Useful for documenting a UTI and
can identify the specific organism
present. UTI is diagnosed by a
bacteria in the urine culture. A
colony count of at least 105 colony PERFORMED
forming units (CFU) per millilitre of
urine on a clean-catch midstream or
catheterized specimen is a major
criterion for infection.
2. Cellular Studies Microscopic hematuria is preset in
about half of patients with an acute
UTI. Pyuria (greater than 4 white
blood cells per high-power field) PERFORMED
occurs in all patients with UTI;
however, it is not specific for
bacterial infection.
3. Other Studies
a. Multiple Test Includes testing for WBCs, known as
dipstick the leukocyte esterase test, and
nitrite testing (Griess nitrate
reduction test). If the leukocyte
esterase test is positive, it is
assumed that the patient has pyuria
and should be treated. The Griess
nitrate reduction test is considered
positive if bacteria that reduce
normal urinary nitrates to nitrites are
present.
b. Test for STD May be performed because acute
urethritis caused by sexually
transmitted organisms or acute
vaginitis infections may be
responsible for symptoms similar to
those of UTIs.

36
c. CT scan May detect pyelonephritis and
abscesses
d. Ultrasonography Is extremely sensitive for detecting
obstruction, abscess, tumors and
cysts.
e. Transrectal To assess the prostate and bladder.
ultrasonography It is the procedure of choice for men
with recurrent and complicated UTIs.
f. Intravenous Indicated to visualize the ureters or
Urogram to detect strictures or stones, and it
is necessary for an accurate
diagnosis of reflux nephropathy.

37
C. Drug Study

Name of Patient: Kenneth Amolato Age: 4 years old Room No.: 304 Hospital No.
Diagnosis/Impression: Acute Gastroenteritis with some dehydration Attending Physician: Dr. Red

38
Name of Drug Date Drug Dose, Frequency, Mechanism of Action Specific Contraindication Adverse Effects Nursing Precaution
(Generic &Brand Ordered Classification Route Indication
Name)
paracetamol 2/15/10 Analgesic, Dose: Acts directly on Treatment of • >Hyperse Anemia, >administer with
anti- 250/5 4.5 ml the mild to nsitivity jaundice, food and provide
inflammatory Frequency: hypothalamus to moderate • >Pregnan hypoglycaemic small, frequent
, Antipyretic q4h cause pain,fever cy coma, rash, meals if GI upset
Route: vasodilation and • >Lactation uticaria, occurs
PO sweating which • >Chronic hypersensitivity >ensure that client
will reduce fever alcoholism reaction,headach is well hydrated
• >Hepatic e,liver toxicity, >monitor for
dysfunction chest pain,renal severe reactions
dysfunction, >do not exceed
bone marrow recommended
suppression doses
>do not take drug
for more than 10
days
gentamicin 2/15/10 Anti-infective Dose: Inhibits protein Serious >hypersensitivity >dizziness, >Avoid long-term
25 mg synthesis in infections deafness, therapies because
Frequency: susceptible caused by lethargy, of increased risk
q8h gram (-); appears susceptible hypotension, of toxicity
Route: to disrupt strains of stomatitis, >Ensure adequate
IVTT functional Escherichia hypertension, hydration of
integrity of coli, hepatic toxicity, patient before and
bacterial cell enterobacter, palpitations, during therapy
membrane proteus and increased >Monitor hearing
causing cell staphylococcu salivation, with long term
death s species polyuria, dysuria therapy
>monitor client’s
weight regularly
>watch for signs
and symptoms of
hypersensitivity
reactions

Diloxanide 2/16/10 Anti- Dose: Destroys the Treatment of >children below >flatulence >Follow-up stool
fuorate protozoal 5ml trophozite Entamoeba 2 years of age >nausea exam should be
Frequency: Entamoebe hystolitica and >vomiting done no earlier
TID hystolytica that other >abdominal than 2 weeks after
Route: eventually form protozoal cramps the end of the
PO into cysts. The infections, >pruritis treatment to 39
cysts are intestinal >uticaria determine efficacy
secreted with amoebiasis
asymptomatic
VI. NURSING MANAGEMENT

ASSESSMENT DIAGNOSIS OBJECTIVE IMPLEMENTATION RATIONALE EVALUATION

40
Subjective Cues: Diarrhea related to Short term goals: Independent: To be
As verbalized by the inflammation and At the end of 45- • Discuss with the SO the • Helps identify implemented;
SO: presence of toxins as minutes of effective patient’s recent exposure causative however,
“Sige ra nah siya ug evidenced by: nursing to different/ foreign and environmental interventions are
kalibanga, usahay interventions, the change in drinking water/ factors. directed towards
muabot ug walo (8) sa Increased bowel significant others food intake. the improvement of
isa ka adlaw” sounds/ peristalsis will be able to: the patient’s
“Sige basa iyang tae” • Observe and record frequency during
Frequent watery stools a. Verbalize changes in stool • Helps differentiate elimination and the
understanding of frequency , individual disease promotion of
Changes in stool color causative factors characteristics, amount and assesses comfort.
Objective Cues: of the illness. and precipitating factors. severity of episodes.

Increased bowel b. Demonstrate • Rest decreases


sounds/ peristalsis appropriate • Promote bedrest, intestinal
behavior to assist provide bedside motility and
Frequent watery stools with resolution of commode. reduces the
causative factors. metabolic rate
Changes in stool color when infection
c. Verbalize or hemorrhage
rationale for is a
treatment complication.
regimen. Urge to
defecate may
Long term goals: occur without
Within the time warning and be
frame of 8-hours uncontrollable,
after effective increasing risk
nursing interventions, • Remove stool promptly. of
the patient will be Provide room incontinence/
able to: deodorizers. falls if facilities
are not closed

41
a. Re-establish as hand.
a more normal • Restrict solid food
stool consistency. intake as indicated.
• Reduces noxious
b. Reduce odors to avoid undue
frequency of client embarrassment.
stools. • Provide for changes in
dietary intake such as low • To allow for
c. Re-establish fiber and low fat diet. bowel rest/
normal pattern of reduced
bowel functioning. • Restart oral fluid, intestinal
gradually offer clear workload.
liquids hourly, and avoid
cold fluids. • To avoid
foods/
substances
that precipitate
diarrhea.

• Provides colon
rest by omitting
Dependent: or decreasing
• Administer anti- stimulus of
diarrheal medications as foods/ fluids.
ordered. Gradual
resumption of
liquids may
• Administer intravenous prevent
fluids as ordered. cramping and
recurrence of
Collaborative: diarrhea,
however, cold
• Consult dietitian for fluids can

42
further assessment and increase
recommendations intestinal
regarding food preferences motility.
and nutritional support.

• To decrease
gastrointestinal
• Monitor laboratory motility and
values for fluid and minimize fluid
electrolyte imbalance. loss.

• To correct fluid and


electrolyte
imbalance.

• Dietitians have
a greater
understanding
of the
nutritional
value of foods
that may be
helpful in
assessing
specific foods.

• Indicates the
need for fluid
and electrolyte
supplements.

43
ASSESSMENT DIAGNOSIS OBJECTIVES INTERVENTION RATIONALE EVALUATION

44
Deficient fluid Volume At the end of 65 Independent:
Subjective Cue: related to active fluid minutes after • Discuss with the • Helps identify To be
As verbalized by volume loss as effective nursing S.O.the factors related causative implemented;
the SO: evidenced by : interventions are to occurrence of deficit environmental however, the
“Usahay ginasuka ra carried out, the S.O as individually factors interventions are
gihapon niya ang iya pallor will be able to: appropriate directed towards
ginainom nga tubig.” diaphoresis the improvement of
frequent vomiting a.) Verbalize • weigh daily and • although the patient’s
restlessness understandin compare with 24-hour weight gain and hydration status
decreased urine g of fluid balance. Mark fluid intake greater and prevent any
output causative /measure edematous than output may complications that
75cc upon factors anal; abdomen, limbs not accurately may arise from
Objective Cues: assessment b.) Verbalize reflect intravascular deficiency of the
pallor delayed capillary understandin volume, these patient’s fluid
diaphoresis refill-3 seconds g of purpose measurement status.
frequent vomiting weight loss of individual provide useful data
restlessness decreased therapeutic for comparison
decreased urine skin/tongue interventions
output turgor and • Ascertain client’s • Relieve thirst
75cc upon dry skin/mucous medications beverage preference. and discomfort of
assessment membranes c.) Demonstrate And set up a 24-hour dry mucous
delayed capillary elevated Hgb and behaviors to schedule for fluid membranes and
refill-3 seconds Hct monitor and intake- encourage augments
weight loss Hgb:187g/dl NV:40- correct foods with high fluid parenteral
decreased 75 deficits as content replacement
skin/tongue Hct: 0.5 g/dl indicted
turgor NV: 0.2 Long term: • Turn frequently,
dry skin/mucous elevated SG- 1.030 Gently massage skin, • Tissues are
membranes NV: 1.010-1.025 Within the time and protect bony susceptible to
elevated Hgb and frame of 8 hours prominences breakdown
Hct after effective because of
Hgb:187g/dl NV:40- nursing vasoconstriction
75 interventions are and increased

45
Hct: 0.5 g/dl carried out, the cellular fragility
NV: 0.2 patient will be able
elevated SG- 1.030 to: • Provide skin and • Skin and
NV: 1.010-1.025 mouth care. Bathe mucous
a.) Demonstrate every other day using membranes are dry
improved fluid mild soap. Apply lotion with decreased
balance as indicated elasticity because
evidenced by of vasoconstriction
individually and reduced
adequate urinary intracellular H2O.
output with normal Daily bathing may
specific gravity. increase dryness
Moist mucous
membranes, good
skin turgor and • Provide safety • Decreased
prompt capillary precautions as cerebral perfusion
refill inidicated: e.g. use of frequently result in
side rails where changes in
appropriate bed in low mentation/ altered
postion thought process
requriung protective
measure to prevent
client injury
Collaborative:

• Monitor Laboratoty
studies as indicated;
e.g. electrolyte,
glucose. Ph/PCO2 and
coagulation studies

46
Dependent:

 Administer
IV solutions as • crystalloid
indicated; provide prompt
• Isotonic solutions; circulatory
• e.g. 0.9 NaCl (NS). improvement,
5% Dextrose/ water; Although the
• .45% NaCl ( half benefit may be
NS), Lactated Ringer transit
Solution
• Colloid; e.g. • used to
Dextran; albumin promote both
electrolyte and -----
• administer Sodium H2O of renal
if indicated excretion of
metabolic ---
• corrects
plasma protein
concentration
deficits, thereby
increasing
intravascular
osmotic pressure
and facilitating
return of fluid into
vascular
compartment
• Maybe given to
correct severe

47
acidosis while
correcting fluid
imbalance.

ASSESSMENT DIAGNOSIS OBJECTIVES INTERVENTION RATIONALE EVALUATION

48
Subjective cues: Ineffective Tissue Short term goals: Independent: To be
As verbalized by the Perfusion related to implemented;
SO: mal-absorption of food At the end of 45- • Maintain bedrest. • Decreased however,
“ Ginasuka ra niya nutrients as evidenced minutes of effective myocardial interventions are
iyang mga kinaon mao by: nursing interventions workload and directed towards
wala kayo siya gana the significant others O2 early
mukaon” Changes in stool – will be able to: consumption, manifestations of
“Sige siya ug libang frequent watery stools. maximizing adequate nutrient
dayon basa iyang tae” a. Identify causative effectiveness absorption and
Presence of blood in factors. of tissue improvement in the
the stool. • Elevate head of bed perfusion. condition.
b. Verbalize and maintain head/neck
Objective cues: Abdominal tenderness understanding of on midline or neutral • To promote
condition, therapy position. circulation/ venous
Changes in stool – Altered skin regimen, side effects drainage.
frequent watery stools. characteristics of medications and • Provide for diet
when to contact restrictions, as
Presence of blood in Imbalanced intake/ healthcare provider. indicated, while
the stool. output- decreased providing adequate • Restriction of
output c. Demonstrate calories to meet the protein helps
Abdominal tenderness behaviors to body’s needs such as limit BUN.
improve/ maintain protein restriction.
Altered skin circulation.
characteristics • Encourage quiet,
Long term goals: restful atmosphere.
Imbalanced intake/
output- decreased Within the time
output frame of 8-hours of • Conserves energy/
effective nursing • Provide small/ easily lower tissue O2
interventions, the digested foods as demands.
patient will be able to tolerated.
demonstrate increased • To promote

49
perfusion as • Encourage rest after digestion.
individually appropriate meals.
( skin warm, vital signs
within client’s normal • To maximize blood
range, alert/ oriented, flow to stomach
balanced intake/ Dependent: enhancing digestion.
output)
• Administer vitamin
supplements and vitamin
b12 injections, folate and
calcium as indicated. • Supplements may
be needed for life to
Collaborative: prevent anemia
because absorption is
• Refer to impaired.
multidisciplinary team.

• Provides assistance
in planning
individualized
• Monitor laboratory treatment and
studies such as hgb and support.
hct.
• Provides
information about
circulatory volumes.

50
ASSESSMENT DIAGNOSIS OBJECTIVE IMPLEMENTATION RATIONALE EVALUATION

51
Subjective Cue: Imbalanced nutrition less Short term Goals: Independent: To be
than body requirement At the end of 1 hour implemented;
As verbalized by the related to insufficient with Purposeful and • Encourage Caloric • Diet however,
SO: intake of nutrients effective nursing intake appropriate for change is a interventions are
“ Nagiwang na siya secondary to poor interventions, the body type and lifestyle. complicate directed towards
karon kumpara adtong appetite as evidenced Significant others will d process the improvement
wala pa siya na-admit.” by: be able to: that of the patient’s
“ Lahi na iyang timbang involves metabolic status
karon ug atong sauna” Appears thin and small a. Verbalize at changing and ensure that
for age the same time, patterns adequate nutrition
demonstrates that have is met for the
Unwillingness to eat selection of foods or been firmly patient’s daily
Objective cues: meals that will • Encourage patient to established needs.
Loss of weight with achieve a cessation of be aware of nutritional by family
Appears thin and small inadequate food intake weight loss. habits that may prevent to and
for age under eating: personal
Poor muscle tone b. Verbalize a. To realize the factors.
Unwillingness to eat • BMI -16.98% understanding of time needed for
* Underweight causative factors eating. • Hurried
Loss of weight with * Weight:15kgs when known and eating may
inadequate food intake * Height: 37 in. necessary b. To focus on eating result in
independent and to avoid other under
Poor muscle tone interventions for diversional activities eating
• BMI -16.98% further complications because
* Underweight of the condition. c. To observe for cues satiety is
* Weight: 15Kgs that will lead for the not
* Height: 37 in. c. Suggest client to eat realized
behaviors in relation until 15-20
to the lifestyle d. To eat in a minutes
changes of the patient designated place after
and to regain or ingestion of
maintain appropriate e. To recognize actual foods.

52
weight according to Its hunger versus • This
Age. desire to eat. controls
environme
Long term Goals: • Establish appropriate nt stimuli
short and long range for eating
At the end of 1 goals to the patient and and other
Week with purposeful the significant others by impulse
and effective nursing suggesting ways to obtain eating.
interventions, the proper nutrition and
client will be able to: hydration.

a. Regain its weight • Attention to


within 10% of ideal the social
body weight. aspects of
eating is
b. Display important
normalization of in both the
Laboratory values and • Discourage beverages hospital
be free of signs of that are caffeinated or and home
malnutrition as carbonated. settings.
reflected in defining
characteristics. • Depending
Dependent: on the
c. Start an etiological
appropriate program • Administer factors of
of exercise intended pharmaceuticals agents the
for cessation of weight as indicated: problem,
reduction. a. Vitamins/ minerals improveme
(iron) supplement, nt in
including chewable nutritional
multivitamins. status may
b. Medication (e.g, take a long
antacids, time.

53
anticholinergics, Without
antiemetics and anti- realistic
diarrheals) short term
goals to
provide
tangible
rewards,
c. High-calorie patient
nutrient-rich dietary may lose
supplements, such as interest in
meal replacement addressing
shake. this
problem.

• These may
decrease
appetite
and lead to
Collaborative: early
satiety.
• Consult dietitian for
further assessment and
recommendations • To correct
regarding food preferences deficiencie
and nutritional support. s as well
as to
enhance
food
satisfaction
• Monitor laboratory and
values that indicate stimulate
nutritional well appetite.
being/deterioration:

54
a. Serum albumin • Multivitami
b. Transferrin n pills are
c. RBC and WBC not a
counts replaceme
d. Serum electolyte nt for a
healthy
diet,
however.
Instead,
they are a
supplemen
t to healthy
eating.

• High
calorie
nutrient
rich diet is
indicated
for the
patient to
promote
adequate
nutrition to
the patient.

• Dietitians
have a
greater

55
understand
ing of the
nutritional
value of
foods that
may be
helpful in
assessing
specific
foods.

• This
indicates
degree of
protein
depletion
(2.5g/dl
indicates
severe
depletion;
3.8-4.5g/dl
is normal)

• Decreased
in
malnutritio
n indicates
anemia
and
resistance
to infection.

56
ASSESSMENT DIAGNOSIS OBJECTIVES INTERVENTION RATIONALE EVALUATION

57
Subjective Cue: Impaired verbal Short term Goals: Independent: To be
As verbalized by the Communication related At the end of 30 implemented;
SO: to a decreased minutes with • Listen for errors in • Provides however, the
“Dugay ra nah siya transmission of purposeful and conversation or provide opportunity to clarify interventions are
nga dili kayo makalitok messages with an effective nursing feedback. content and meaning. directed towards
ug sturya. ‘Mama’ ra absent of ability to interventions, the the assistance of
gyud nah iya receive information Significant others • A test for the client in the
gakahibal-an” secondary to delayed will be able to: • Ask client to follow Receptive aphasia. promotion of
growth and simple commands. verbal/speech
development as a. Verbalize or • This will prevent developments that
evidenced by: indicate increasing the are appropriate for
Objective cues: understanding of • Never talk in front of patient’s sense of the patient’s age.
Age = 4 years old communication patient as though he or frustration and
Age = 4 years old difficulty and she comprehends feelings of
Speak or verbalizes with plans for ways of nothing. And Keep helplessness. And
Speak or verbalizes difficulty handling this distractions such as will keep patient
with difficulty condition. television and radio at a focused, decrease
Difficulty expressing minimum when talking to stimuli going to the
Difficulty expressing thoughts verbally b. Establish patient. brain for
thoughts verbally method of interpretation, and
Problems in receiving communication in enhance the nurse’s
Problems in receiving the type of sensory which needs can ability to listen.
the type of sensory input being sent or be expressed.
input being sent or sending the type of • Talk directly to the • Stimulates harmony
sending the type of input necessary for Long term Goals: patient, speak slowly & and further enhances
input necessary for understanding At the end of 1 distinctly begin with yes word/idea
understanding week with or no questions. Do not association. Loud
Absence of eye contact. purposeful and speak loudly unless talking does not
Absence of eye effective nursing patient is hearing- improve the patient’s
contact. interventions, the impaired. ability to understand
client will be able to: if the barriers are
primary language,

58
a. Participate in aphasia, or a sensory
therapeutic deficit.
communication
properly. • Maintain eye contact • Patients may have
with patient when defect in field of
b. Demonstrate speaking. Stand close, vision or may need to
congruent within patient’s line of see the nurse’s face
verbal and vision (generally midline). or lips to enhance
nonverbal understanding of
communication. what is being
Dependent: communicated.
c. To use a form
of • Check for Doctor’s • Help alleviate
communication order regarding the condition or minimize
to get needs client’s condition. dysfunction
met and to
relate effectively Collaborative: • Fatigue may have
with persons • Consult a speech an adverse effect on
and his or her therapist for additional learning ability.
environment. help. See that patient is
well-rested before each
session with the speech
therapist.

59
VII. DISCHARGE PLANNING

Medication >encourage strict medication compliance

such as antibiotic therapy.

>teach patient and SO to take his

medications at the right time, dose, and

route to promote fast recovery.

>provide proper instructions to patient

and SO about the significance of each

medication to provide correct knowledge

about the medication.

>avoid skipping of medication.

>continue medication as ordered by the

physician.
Exercise >provide safe environment on which the

patient can exercise.

>encourage regular exercise without

over exercising or restraining the body.

>teach patient to do active range of

motion.

>instruct the patient and his SO in taking

adequate rest periods.


Treatment >rapid replacement of body fluids is the

most important treatment.

>give buko juice to provide rehydration if

not available; give ORESOL to replace

fluid as in moderate dehydration at

75ml/kg in 4-6hours. Continue intake

until condition improves.

>control measures to eliminate vector by

promoting cleanliness.

>seek immediate medical assistance for

any unusualities of the patient that still

60
persist after the treatment.

>instruct patient and SO to do follow-up

exam or check-ups after discharge.


Health Teachings >teach the patient and SO to thoroughly

wash hands with soap and running water

before touching any food. Use paper

towel or hand towel to dry hands.

>clean bathrooms and toilets often. Pay

particular attention to toilet seats.

>instruct patient and SO to provide good

sanitation to their surroundings.

>avoid eating uncooked foods,

particularly meats, vegetables and fruits

which cannot be peeled before eating.

>avoid drinks containing ice.

>avoid being under the sun and try to

keep cool in order to prevent further loss

of body fluids in sweat.

>instruct patient and SO to follow

intended duration of antibiotic therapy

while providing safety precautions for

complications and allergic reactions.


Out-Patient >Instruct patient and SO to:

• Follow schedule for check-ups.

• Comply with further examinations.

• Maintain medications as ordered by

the physician.

>if complications or signs and symptoms

will occur, immediately consult health

care provider.
Diet >encourage fluid intake such as water,

buko juice or ORS to promote hydration.

>foods high in simple sugars like milk,

61
yogurt, orange juice, or soda should be

avoided to decrease osmotic load that

might worsen diarrhea.

>avoid greasy and citrus foods, ice

cream, coffee and alcohol, they can

aggravate the condition.

>consume a low-fiber diet.

>traditional BRAT diet-bananas, rice,

applesauce and toast- is tolerated by the

tender gastrointestinal system, but not

nutritious.
Spirituality >establish an environment that promotes

free expression of feelings and concerns.

Provide calm, peaceful setting when

possible.

>encourage patient to have optimistic

perspective with regards to the disease

condition.

>establish a strong foundation of faith to

promote the feeling of wellness.

VIII. PROGNOSIS

Criteria Good Poor Justification


Onset of Illness  >The illness started when the patient

manifested a signs and symptoms of

62
having a loose watery foul-smelling,

mucoid, with blood streaked stool,

approximately ¼ cup per episode of 8

episodes.

>There are also complains of vomiting

for 2 episodes along with abdominal

discomfort.

>Negative for fever, and diarrhea

prompted admission.
>The illness is a self limiting process of

healing.

>This can be easily prevented through

safety precautions from the primary


Duration of Illness 
care giver.

>Palliative care is to be given for the

patient to relieve its signs and

symptoms related to the illness.


>Since the illness is a self limiting

process, this can be easily modified

through proper sanitation, hygiene and

constant supervision of the patient.

>Moreover, modifications can be done


Precipitating
 through non-pharmacologic,
Factors
independent interventions such as

increasing fluid intake and pain

management, to relieve the patient’s

condition and reduce the severity of the

symptoms.
Predisposing  >The patient’s condition is not a familial

Factors risk and also not a genetic condition.

>Also, this can be managed through

environmental awareness and

preservation of clean surroundings.

63
>The patient’s age is a possible factor

that makes him vulnerable to such

causative agents.
>The patient does not comply with

medication given because there times

Attitude and when the patient refuses to take the

Willingness to Take  medication and cry.

Treatment >There is presence of vomiting when

the medication is given; making PO

medications ineffective for the patient.


>Patient’s age is 4 years old and has a

developmental delay in speech, so it

Level of also affects the cognitive process of the



Consciousness patient which leads him into having a

difficulty in focusing a certain

phenomenon.
The family supports him in every

difficulty he is having. They support him

in any way they could and provide him

Family Support  with full support.

>The family is also financially stable

without any complaints of money as a

source of family stressors.

Calculation:

Poor: 3/7 X 100% = 42.86%

Good: 4/7 X 100% = 57.14%

100%

Overall Prognosis:

Acute Gastroenteritis is usually resolved within two to three days and there

are no long term effects. When dehydration occurs, recovery is extended by a few

64
days. So, overall, patient has a good prognosis since he has no longer manifested

any signs and symptom. Also, this illness is a self limiting process which can be

prevented through proper supervision of the patient and provide a clean

environment.

IX. RECOMMENDATIONS

The researcher of this study would like to recommend the following:

• For the patient significant others, she should provide good hygiene to the

patient to prevent further infections from occurring. She should have strict

compliance of medications to the patient to promote continuous healing and

good prognosis. She would be able to identify foods that can precipitate

discomfort and thus it should be avoided.

65
• For the following student nurses, they should continually provide interventions

to help alleviate patient’s condition. They should impart health teachings to

the mother regarding promotion of proper hydration and nutrition for the

patient. They should also give emphasis on promoting hand washing before

feeding the child. They should also review all their insights regarding the

patient’s condition so that application would be manifested in the next nursing

duty if ever given with a patient who has the same condition.

• For the health care team they should continue to monitor the patient’s

condition so that if signs and symptoms of the patient will aggravate,

immediate medical and nursing intervention would be given.

X. CONCLUSION

The patient in this study has under taken both pharmacologic and and non

pharmacologic treatment regimens. Appropriate nursing interventions were made to

maintain core vital signs within normal range. Nursing care and administration of

prescribed medications were done to promote patients wellness and prevent further

complications. Teachings were also done for it is very important to understand

66
treatments and interventions. All of these were made for the welfare of the patient

and promote timely recovery.

XI. Bibliography:

• Johnson, D.R. “Introductory Anatomy: Digestive System.” Centre for

Human Biology, UK

http://www.leeds.ac.uk/chb/lectures/anatomy8.html

Accessed May 2005.

• “Anatomy of the Digestive System.” Emedicine Consumer Health

http://www.emedicinehealth.com/resources/40933-6.asp

67
• MIMS. Philippines. 08 Feb 2010. http://www.mims.com/Page.aspx?

menuid=mng&name=racecadotril&h=racecadotril&CTRY=PH&searchstring=r

acecadotril

• Association for Medical School Pharmacology.America, Ltd., Ambler, Pa.2005

http://www.amspc.org/Knowledge_Objectives/DrugList/GI.asp

• Doenges, Marilynn, et al. (2008). Nurse’s Pocket Guide: Diagnoses,

Prioritized Intervention, and Rationales. 11th ed. Philadelphia: F.A Davis

Company

• Udan, Josie. (2009). Medical-Surgical Nursing: concepts and clinical

application. 2nd edition. Philippines: Guani print house.

• Black, J. & Hawks, J. (2009). Medical-Surgical Nursing Clinical Management

for Positive Outcomes. 8th ed. Singapore: Elsevier Pte Ltd.

• American Academy of Pediatrics Provisional Committee on Quality

Improvement Subcommittee on Acute Gastroenteritis. Practice parameter: the

management of acute gastroenteritis in young children. Pediatrics. 1996;

97:424-35.

• Burkhart, David. (1999). Management of Acute Gastroenteritis in Children.

American Family Physician. http://www.aafp.org/afp/991201ap/2555.html

• UCCH: Pediatric Chiefs. (2010). Acute Gastroenteritis.

http://pediatrics.uchicago.edu/chiefs/inpatient/AcuteGE.htm

• Hughes, James. (2003). Managing Acute Gastroenteritis in Children. National

Center of Infectious Diseases.

http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5216a1.htm

• Dhawan, Vinod. (2010). Amebiasis – Treatment and Medication. CDC: E-

Medicine. http://emedicine.medscape.com/article/996092-treatment

• Nick J. Diet for Gastroenteritis. Buzzle.com Intelligent Life on the Web. 15

Feb 2009.

• http://www.buzzle.com/articles/diet-for-gastroenteritis.html

• Gastroenteritis Diet. Student health Service, Nutrition Clinic. 2007.

www.sfsu.edu/~shs

68
• Gastroenteritis. The Free Dictionary by Farlex. Farlex, Inc. 2010.

http://medical-dictionary.thefreedictionary.com/Acute+gastroenteritis

• Michael Vincent F Tablang et al. Gastroenteritis, Viral. Emedicine:WebMB. 21

Dec 2009. http://emedicine.medscape.com/article/176515-overview

• Caleb K. King et al. Managing Acute Gastroenteritis Among Children: Oral

Rehydration, Maintenance and Nutritional Therapy. MMWR

Recommendations and Reports. Center for Disease Control and Prevention,

U.S.A. 10 Nov. 2005.

http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5216a1.htm

XII. APPENDIX

A. DOCTOR’S ORDER

DATE TIME ORDER


02/15/10 > Please admit under the service of
Dr. Red
> Secure consent to care
> TPR q 4
> Allergies, none
> Problem: LBM, vomiting
> Venocylis w/ D5lr 500cc @ 55-60cc/hr
in 8hours then reassess hydration status
> Labs: CBC @8pm, Stool exam, U/A

69
 Meds: Paracetamol 5ml PRN for
fever
 ORS as vol/vol replacement, give
dropper by dropper
> Monitor v/s q 4h
> I and O q shift
> Chart amount, frequency and character

of stool
> will inform AP- informed
> refer accordingly
4:00pm > Hydration status q 2h
> Domperidone, 3ml 3x a day, PRN for

vomiting
> Zinc sulfate syrup, 5ml OD PC
> Gentamycin 25mg, q 8h IVTT, ANST
6:10pm > Diet for age
11:00pm > IVTFTF: D5IMB 500cc@ 50cc/hr
2/16/10 12:40pm > IVTFTF 1 D5IMB 500cc @ 52Mgtts
Afebrile > Continue meds
(+) appetite > 1 banana per meal
BNI with soft stool > Diloxamide ferorate ( Dilfur) 5.0ml TID
2/17/10 4am > IVTFT:D51MB 500cc @ 50cc/hr
> Nacecodotril( Hidrasev) 10mg 2 sachet

in 15ml of water q 8hr


(+) poor appetite > change present IVF with D5LR 1L

LBM 2x @ 56-58cc/hr
(+) weak looking > continue meds
> Full diet
> Reassess after 8hrs
> Refer accordingly
11:44pm > IVF: D5LR 1L @ 56-58cc/hr
2/18/10 11:55am > MGH
> IVFTWC and IV meds to consume
Home Meds:

 Dicixamide Fuonate 5ml TID x

8days

 Erceuryl 1ysp TID x 7days

 Hidusec 10mg 2 sachets TID x

3days

 Prozine syrup 1tsp

 Hydrite for volume per volume

replacement
> Follow-up after 7days

70
B. NURSES NOTES

DATE TIME NURSES NOTES


2/15/10 3:30pm > a case of 4 yr old male child is admitted due to LBM

under the service of Dr. Red


> vital signs taken and recorded
>weight taken-15kg
>afebrile
>seen and examined by Dr. Red
>consent to care signed by the patients father
>AD informed
>still for U/E and S/E
D5LR 500cc 4:00pm >started with venoclysis regulated at 55-60cc/hr
>CBC not yet done - patient vomited @2pm
>transferred to ward per wheelchair
>endorsed to NOD
Gentamicin >skin testing done and will due at 4:45pm
4:15pm >received awake from ER per wheelchair with an

ongoing IVF of D5LR 500ml @ 450cc level regulated

@ 55cc/hr infusing well on left arm.


>assisted and placed on bed comfortably
>appears restless
>poor skin turgor noted
>initial v/s taken with T = 32.3 degrees Celsius;

P = 82 bpm; R = 19 cpm
>bedside care done
>adequate rest periods provided
>back kept dry
6:30pm >above IVF on KSS status
>consumed share with poor appetite
>health teachings reinforced to patients mother with

emphasis on:

a. proper hygiene

b. proper food preparation

c. medication compliance

d. increase in fluid intake


8:30pm > above IVF#1 D5LR 520cc @30cc level reinserted

71
and regulated @ 55cc/hr infusing well on R arm
10:00pm >endorsed with latest signs of T = 37.1 degrees

Celsius; P = 92 bpm; R = 25 cpm


2/15/10 6:00pm >received on bed with ongoing D5NM 500cc @ 100cc

level regulated 55-60cc/hr


>(-) vomiting, (-) LBM
>still for stool exam
>due meds given
>ff up @ 500cc/hr
>kept watched
6:00pm >endorsed
2/16/10 6:00am >with ongoing IVF of #3D5MB 500cc @ 200cc level

regulated @ 50cc/hr infusing well on R arm with no

signs of infiltration noted


>initial vital signs taken T = 36.9 degrees Celsius; P =

88 bpm; R = 18 cpm; afebrile


>not in respiratory distress
>weak and pale
9:20am >specimen collected and sent to laboratory for stool

exam
9:35am >above IVF consumed and followed up with 500cc

D5IMB regulated @ 50cc/hr


2:00pm >endorsed with latest vital signs of T = 36.2 degrees

Celsius; PR = 112 bpm; RR = 19 cpm


2-10pm
2:30pm >appears calm
>good skin turgor noted
>v/s taken and recorded as follows: T = 38.2 degrees

Celsius; P = 132 bpm; RR = 22cpm


>consumed one pack of biscuits and one glass of

Gatorade with fair appetite


2/17/10 6:00am >no abnormalities noted
2-10pm
6:00pm >DFA consumed half share with poor appetite
10-6am >afebrile
>on CTAU and CFAS monitoring
>(+) BM, (-) vomit

C. FLUID INTAKE AND OUTPUT 24 hour RECORD

DATE INTAKE OUTPUT


2/17/10 PO IV TOTAL URINE OTHERS TOTAL
6-2PM 90 450 540 75 60 135
2-10PM 45 400 430 20 520 540
10-6AM 150 350 450 BMI1X

D. STOOL MONITORING RECORD

DATE/SHIFT STOOL APPROXIMATELY CONSISTENCY COLOR

72
FREQUENCY AMOUNT
Feb. 15, 10
2-10 0 - - -
10-6 0 0 - -
Feb. 16, 10
6-2 1 130 cc Loose, watery Yellowish

foul smelling
2-10 1 20 cc Watery foul Yellowish

smelling
10-6 2x 250 cc Smelling watery Yellowish
Feb. 17,10
6-2 0 - - -
2-10 5 520 cc Watery Yellowish

E. VOMIT MONITORING RECORD

DATE FREQUENCY QUANTITY CHARACTERISTIC COLOR


Feb. 15, 10
2-10 1 50 Watery Orange
Feb. 16, 10
6-2 1 60 Watery Whitish

73

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