A Case of J.D.

3 yrs old female admitted due to Dengue Fever

In Partial Fulfillment of the

Course NCM 101 RLE
August 18, 2007

Submitted to:
Mrs. Rosalie Uriarte, R.N.

Submitted by:
Balio, Maria Aiza
Barriga, Rodwick Rodan
Diao, May
Gamboa, Antonio
Gavas, Kate Margaret
Lim, Melissa Katrina
Pacheco, Christy Joy
Penera, Love Joy Marie
Salubre, Donna
Tingabngab, Ryan
Tuvilla, Ana Chloe
Villalba, Carleen

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 TABLE OF CONTENTS

I. INTRODUCTION……………………………………………………………………….. 3
A. General Objectives…………………………………………………………………... 3
B. Specific Objectives…………………………………………………………………... 3
C. Scope and Limitation………………………………………………………………... 4
II. ASSESSMENT
A. Assessment tool……………………………………………………………………... 4
B. Laboratory Results…………………………………………………………………... 10
III. ANATOMY AND PHYSIOLOGY………………….………………………………... 11
IV. PATHOPHYSIOLOGY
A. Narrative Forms…………………………………….………………………………... 13
B. Schematic Diagram………………………………………………………………... 19
V. MEDICAL MANAGEMENT
A. Doctor’s Order
Ideal Management……………..………………………………………………………... 20
Actual Management……………………………………………………………………... 22
B. Drug Study……………………………..……………………………………………... 23
VI. NURSING MANAGEMENT………………………………………………………... 28
VII. DISCHARGE PLAN…………………………………………………………………. 31
VIII. PROGNOSIS………………………………………………………………….......... 33
IX. CONCLUSION……………………………………………………….…………......... 33
X. RECOMMENDATION…………..…………………………………...………………... 34
XI. APPENDIX
Doctor’s Orders…………………………………………….……..……………………... 34
Nurse’s Notes……………………………………………….………………………........ 36
Special Endorsement………………………………………………………………….. 39
List Of tables…………………...……………………………………………………… 39
XII. BIBLIOGRAPHY……………………………………………………………………... 40

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I. INTRODUCTION
This is a case of patient J.D., a 3-year-old female brought to Maria Reyna hospital last
Thursday, July 30, 2007 with complaints of fever. Tests were done and the doctor then came up
with the primary diagnosis of Dengue Fever Grade 3.
Dengue hemorrhagic fever (DHF) is an acute febrile diseases caused by one of four
closely related virus serotypes of the genus Flavivirus, family Flaviviridae. Dengue is transmitted
to humans by the Aedes aegypti (rarely Aedes albopictus) mosquito, that feeds during the day.
This infectious disease is manifested by a sudden onset of fever, with severe headache, muscle
and joint pains and rashes; the dengue rash is characteristically bright red petechia and usually
appears first on the lower limbs and the chest - in some patients, it spreads to cover most of the
body. There may also be gastritis with some combination of associated abdominal pain, nausea,
vomiting or diarrhea.
Cases of DHF also show higher fever, haemorrhagic phenomena, thrombocytopenia and
haemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which
has a high mortality rate.

A. General Objectives
At the end of 1 hour case presentation, the group will be able to discuss briefly the
diagnosed illness which is Dengue Fever Grade 3 as experienced by the patient. We will also
be able to concisely provide the information of the disease, the plan of care and post-disease
interventions. Finally, we shall be able to accentuate the value on both pharmacological and
non-pharmacological management of the condition.

B. Specific Objectives
At the end of 1 hour case presentation, the group will be able to:
1. give the appurtenant data as to the demographic data and general
information and/or background of the patient;
2. discuss the development of the disease as manifested by the patient;
3. discuss a simple pathophysiology of the disease process as assessed and
manifested by the patient;
4. present the formulated nursing diagnoses and each equivalent interventions;
5. discuss drug studies;
6. confer prognosis, discharge planning, conclusions and recommendations as
the post-disease projections; and

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C. Scope and Limitation
This case presentation will attempt to cover and discuss the disease process and
present condition of the patient as assessed in the two days of duty, at Ext 3, Maria Reyna
Hospital. It will also present the nursing and medical care as provided during the 16 hours of
duty (July 30-31, 2007).
This case presentation will be limited only to the laboratory reports, signs and symptoms
as evidenced by and observed from the patient within the engaged days and how the medical
team (doctors, nurses, SN, etc.) has managed each of them. We will also be focusing only to
the verbalization of the patient’s mother for the subjective cues since patient cannot express
properly.

II. ASSESSMENT
COLLEGE OF NURSING
Xavier University
Ateneo de Cagayan

NURSING HISTORY AND ASSESSMENT RECORD

NAME OF PATIENT: J.D. CHIEF COMPLAINT: Fever

AGE: 3 years old DIAGNOSIS: Dengue Fever Grade 3
DATE TIME () AM NAME OF ATTENDING PHYSICIAN:
July 30, 2007 ( ) PM Dr. Anne Agnes

ADMITTED BY: ADMITTED FROM

( ) Ambulatory ( ) Wheelchair ( ) Home
( ) Stretcher () Other, Cuddled by mother ( ) ER

Vital Signs upon Admission

Temperature Pulse Respirations Blood Pressure Height Weight
36.4 °C 76 bpm 25 cpm 90/60 mmHg 3’8 11 kg.
Vital Signs upon Assessment (July 31, 2007)
Temperature Pulse Respirations Blood Pressure Height Weight
38.2 °C 79 bpm 28 cpm 100/60 mmHg 3’8 11 kg.

Comments: As verbalized by the mother, “init man jd kayo siya ma’am, ge-hilanat npd siguro”

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Language/Dialects spoken: Bisaya
( ) Oriented to Unit () Not Oriented
Reason: ( ) Confused ( ) Comatose
( ) Critical () Language Barrier
Comments: The patient is only 3 years old, and she is still not able to talk yet.

RELIGION: Roman Catholic Status: Child

INFORMANT ( ) Patient () others (specify)

Jenny Dejos (mother)
CHIEF COMPLAINT/ REASON FOR HOSPITALIZATION
Fever

Duration / Onset of Problem: July 27, 2007. (3 days prior to admission)

Treated for Symptoms Before? ( ) No () Yes (explain)
Patient JD was admitted to Sambitan Hospital for chief complaints of fever, after an hour
of medical treatment, the physician then referred them to be transferred to Maria Reyna Hospital
for further management.
ALLERGIES
() None Known ( ) Yes (specify allergen and reaction)

MAJOR ILLNESS, OPERATIONS, AND HOSPITALIZATIONS

Medical History () Heart Disease Family History () Heart Disease
() Hypertension () Hypertension
() Stroke () Stroke
() Substance Abuse () Substance Abuse

() Lung Disease () Lung Disease

() Renal Disease () Renal Disease

() Cancer () Cancer

() Others () Others

Comments: The mother verbalized, “ Ai, sakit sa dughan? Oo, akong papa ug mama in-ana
man siya. Baga? Kanang asthma, naa pud mi ana. Highblood pud to sa akong bana nga side.
Wala naman lain. ”

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SURGICAL HISTORY / HOSPITALIZATIONS (Include Dates):
 At three months old, April 2007, she was hospitalized due to an asthma attack.
 And on August 2007, he was hospitalized again and was diagnosed to have
amoeba.
 And consecutively every 6 months patient JD returns to the hospital due to an
asthma attack.
Comments: The mother verbalized, “ Adtong ika-tulo niya nga bulan, na-ospital ni siya kay
giasthma siya. Tapos tulo ka bulan human ato, na-ospital napud siya kay nagka amoeba siya.
Nagsige na dayon siya ug balik-balik sa ospital hangtud pag 2 years old niya kay tungod sa
asthma ra japun.”
PHYSICAL ASSESSMENT
I. NEUROLOGICAL ASSESSMENT
Level of Consciousness: Conscious, alert, doesn’t talk
Mental Status: The patient was not well groomed; she wore a baby shirt and loose shorts. Her
hair was tangled. The mother verbalized, “Gubot man gud kaayu iyang mga dextrose, lisud
kaayu siya atimanon kay saputon pud siya ug dali.”
Speech: inappropriate, talks and uses incoherent words.
Pupils: Illuminated Pupil constricts, black in color, equal in size.
Pupil Size 3 mm
Comments: Pupil size was 4mm.When the penlight was directed to the client’s eyes, her pupils
constricted to 3mm,her pupils exhibited PERRLA (pupils, equally round, responsive to light and
accommodation).

II. RESPIRATORY ASSESSMENT

Respiratory Rate: 28 cpm, tachypnea (Normal Range: 15-25 cpm)
Pattern: regular but rapid, shallow breathing
Characteristics: costal type of breathing, involving the external intercostal muscles, can be
observed by the movement of chest upward and outward.
Adventitious sounds: inspiratory crackles
Cough: dry unproductive cough
Comments: The mother verbalized, “Asthmatic man gud ni siya, nisabay rapud ni iyang hubak
sa pagkaadmit niya tungod sa Dengue. Pero ginagmay raman pud,dili man pud grabe.”

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III. CARDIOVASCULAR ASSESSMENT
Skin Color: presence of erythema, pale, ecchymosis on the right cubital area, right dorsal area
of the arm and the right pedal part of the foot.
Pulse Rate and Characteristics:
Apical: 78 bpm, regular pace Radial: left -79 bpm, right- 79 bpm
(Normal symmetrical and equal)
Edema none upon assessment
Chest Pain (describe): The mother verbalized.” Wala man siguro sakit, ambot. Dili man sad
siya makasturya.” During assessment, the patient showed grimace and she was crying when
she was coughing.

IV. PERIPHERAL – VASCULAR ASSESSMENT

Peripheral Pulses: left-79 bpm, right- 79 bpm

Homan’s Sign: ()

Comments: When the client’s foot was forcefully dorsiflexed, she showed no signs of grimace
that displays feeling of pain. This then indicates absence of deep vein thrombosis of the calf
muscles.

V. MUSCULO-SKELETAL ASSESSMENT
Range of Motion The patient is unable to walk or feed for herself. In doing her ADL, she is
dependent with her mother and her support persons.
Muscles:
Contractures of muscle: (+) there was a visible contracture of her muscle in the left
pedal part of her foot.
Fasciculation of muscle: no fasciculation
() Weakness () Contractures () Pain
() Paralysis () Joint Swelling
Comments: During the assessment of the musculo-skeletal system, the patient was
uncooperative and voluntarily moves her extremities.
VI. SKIN ASSESSMENT
Skin Color: pale; (+) erythema on both sides of the arms and legs, (+) ecchymosis on the right
cubital area, right dorsal area of the arm and the right pedal part of the foot.

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Comment: “Nanaghan lagi ni iyang pula-pula sa lawas tungod sa Dengue, unya dali ra kayo
gakabun-ugan.”
Uniformity: Generally uniform except in areas of lighter pigmentation like palms, lips, nail beds.
Temperature: 38.2 °C ; febrile
Commments: During the duty hours the temperature of the patient increases and decreases for
some time.
Burns/ Decubiti Present: () No
Comments: (+) ecchymosis, coolness of skin, and discomfort on the frontal parietal bone,
cubital part of the right arm and the pedal part of the left foot. The mother verbalized,”
Nanglagum iyang kamot ug tiil tungod kay giturok man siya sa nurse gud adtong pagkaadmit
niya, kapila siya giturok ma-o nang in-ana ang labas. Nawa ang resulta, sa ulo giturok.Lihok
man sad gud ni siya oi,”

VII. NUTRITION / METABOLIC PATTERN

General Appearance: () Well-nourished
Meal Pattern: Bottle Fed per demand
Changes in Eating Habits? () No Amount: 1/2 glass, 125 cc
Appetite: () Good
Appetite Changes? () No
Weight Loss/ Gain: none Special diet: none
Comments: “Gainom man siya ug gatas, ginagmay lang sad, kay magsige man sad ug
katulog.Dili man sad siya mamili sa iyang gatas, Ganado man sad siya mukaon.”

TEETH: () Own

Comments: Smooth, light yellowish tooth enamel, pink gums, (+) carries visible on the upper
and lower first molars.

VIII. ELIMINTATION PATTERN

Bladder: No Difficulty
Amount and color of urine: 700cc/day, pale yellow urine

Intake (oral): 250 cc (water and food intake)

Bowel: No Difficulty; Diarrhea

Amount of bowel: 500 cc/day; 2 full diapers a day
Frequency of bowel movement: two (2) times per day

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Characteristics of stool: Watery yellowish liquid
Comments: The mother verbalized, “Wala man siya galisod ug kalibang or ihi.”

IX. SLEEP / REST PATTERN

Sleeps: 6 -7 hours/day; interrupted with no difficulty going to sleep; without snoring
Comments: The mother verbalized, “Magsige man siya ug mata2x, paimnon ug tambal dayon
maglisud ug ginhawa.putol-putol jud iyang katulog ai.”
Using of sleeping aids: () No
Comments: The mother verbalized, “ makatulog man siya, pero magsige lagi siya ug mata2x
kay tungod sa iyang oxygen sa ilong ug paimnon ug tambal. Murag mga 7 ka oras man siya
gakatulog, putol2x lang lagi.”

X. ACTIVITY / EXERCISE
Activity of Daily Living (I = Independent, A = with assistance, D = Dependent)
Eating: Dependent Bathing: Dependent Dressing: Dependent
Grooming: Dependent Toileting: Dependent Ambulating: Dependent
ACTIVITY LEVEL: () Sedentary
Comments: At three years old, patient JD still isn’t able to walk because of a foot deformity on
her right foot, due to a genetic birth defect. The patient is usually lying down in a dorsal
recumbent position. “Gapasagdan raman namo na siya sa sulod sa balay unya naa ra gyud na
siya sa iyang duyan kay di man siya maka lakaw. Naigo gyud siguro siya ug lamok na naai
dengue kay daghan man gyud lamok sa amua kay duol man mi sa kana bitaw mga kahoy na
ginahimo ug rubber, mao na nga daghan gyud lamok” “ Kanang mga lamok, gapa aso man mi
kada gabie ana para mawala kay dibah mawala man nah sila pag magpa aso”, as verbalized by
the mother.

XI. BEHAVIOR PATTERN (COPING/VALUES)

Behavior: () Moderately anxious
Comments: the patient shows irritability with the attendants that will approach her, her mother
verbalized, “Na trauma man gud ni akong anak, kay daghan kaayu gipangturok sa iyang kamot,
ug sa tiil para sa dextrose. Dili pud siya ganahan nga duolan siya. Sapoton man gud ni siya. “
Psychiatric History: The mother verbalized,” Special child man daw akong anak, ambot kung
unsa na. Pero makita baya nako sa iyaha nga naa siya deperensya, ulahi iyang pangutok. Ug

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 maklaro pud baya sa hitsura niya, ug nilihokan, nawa ra gani. Dili pa pud siya kalakaw o
makasturya man lang nga tulo naman tana ni siya ka tuig. ”

XII. PAIN: () No

XIII. ROLE/ RELATIONSHIP PATTERN
Occupation: Child, 3rd child of the 3 siblings
With whom does the patient live? Parents
Anticipating returning home? () Yes
Persons available to assist at home: Mother and Aunt

B. Laboratory Results
Hematology
7/31/07 5:24 am
Test Result Unit Reference
WBC 10.5 10^3/ul 5.0-100
Hemoglobin 13.5 g/dl 11.0-16.5
Hematocrit 41.0 % 35.0-50.0
Platelet 45 10^3/ul 150-350

Differential count
Segmenters 62.0 % 55-65
Lymphocytes 37.0 % 25-35
Monocytes 1.0 % 2-4
Eosinophils % 1-3
Basophil % 0-1
Bands % 1-2
Reticulocytes 10^5/l 0.5-1.5
Bloodtyping

Urinalysis 8/1/07
Color: yellow Microscopic findings Crystals Cast
Transparency: clear RBC: 1-3/hpf Amorphous urates/ Coarse granular
Specific gravity: 1.010 PUS cells: 0-1/hpf PO4: Fine granular
PH: 7.5 Epithelial cells: rare Calcium oxalates: Pus case
Sugar: negative Mucus Threads: Uric acid: Waxy cast
Protein: negative Renal cell: Triple PO4: RBC cast
Yeast cell: Others
Bacteria: rare Pregnancy test:
Urine ketone:
Laboratory Interpretation: Hemolysis shows a low platelet count; Urinalysis shows that child
has presence of blood in urine.

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III. ANATOMY AND PHYSIOLOGY
Blood is a liquid with suspended cells 30-50% by volume. These cells are of three basic
types, erythrocytes or RBCs, leucocytes or WBCs and thrombocytes or platelets.
Blood components
Normally, 7-8% of human body weight is from blood.  This essential fluid carries out the
critical functions of transporting oxygen and nutrients to our cells and getting rid of carbon
dioxide and other waste products.  In addition, it plays a vital role in our immune system and in
maintaining a relatively constant body temperature.  Blood is a highly specialized tissue
composed of many different kinds of components.  Four of the most important ones are red
cells, white cells, platelets, and plasma.  All humans produce these blood components--there
are no populational or regional differences.
Red Blood Cells
Red blood cells, or erythrocytes , are relatively large microscopic cells without nuclei.  In
this latter trait, they are similar to the primitive prokaryotic cells of bacteria.  Red cells normally
make up 40-50% of the total blood volume.  They transport oxygen from the lungs to all of the
living tissues of the body and carry away carbon dioxide.  The red cells are produced
continuously in our bone marrow from stem cells.   Hemoglobin is the gas transporting protein
molecule that makes up 95% of a red cell.  Each red cell has about 270,000,000 iron-rich
hemoglobin molecules.  People who are anemic generally have a deficiency in red cells.  The
red color of blood is primarily due to oxygenated red cells.
White Blood Cells
White blood cells, or leukocytes, exist in variable numbers and types but make up a very
small part of blood's volume--normally only about 1%.  Most are produced in our bone marrow
from the same kind of stem cells that produce red cells.  Some white cells (called lymphocytes)
are a major part of the immune system.  Other white cells (called granulocytes and
macrophages) protect our bodies from infection by surrounding and destroying bacteria, viruses,
fungi, or other parasites.  They also have the function of getting rid of old, unneeded blood cells
as well as foreign matter such as dust and asbestos.  The red cells remain viable for only about
120 days before they are removed from the blood and their components recycled in the spleen. 
Individual white cells before they are removed from the blood usually only last 18-36 hours.
Platelets
Platelets, or thrombocytes, are cells that clot blood at the site of wounds.  They do this
by adhering to the walls of blood vessels, thereby plugging the rupture in the vascular wall. 
They also can release coagulating chemicals which cause clots to form in the blood that can

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plug up narrowed blood vessels.  There are more than a dozen types of blood clotting factors
and platelets that need to interact in the blood clotting process.  Recent research has shown
that platelets help fight infections by releasing proteins that kill invading bacteria and some other
microorganisms.  In addition, platelets stimulate the immune system.  Individual platelets are
about 1/3 the size of red cells.  They have a lifespan of 9-10 days.  Like the red and white blood
cells, platelets are produced in bone marrow from stem cells.
Plasma
Plasma is the relatively clear liquid protein and salt solution which carries the red cells,
white cells, and platelets.  Normally, 55% of our blood's volume is made up of plasma.  About
95% of it consists of water.  As the heart pumps blood to cells throughout the body, plasma
brings nourishment to them and removes the waste products of metabolism.  Plasma also
contains blood clotting factors, sugars, lipids, vitamins, minerals, hormones, enzymes,
antibodies, and other proteins.  It is likely that plasma contains some of every protein produced
by the body--approximately 500 have been identified in human plasma so far.
Normal blood values
The values for blood may vary in relationship to the altitude of your geographic location.
Check with your Hematology Department if the normal values do not appear on your
hematology report forms. The following values are for sea level.
Hematocrit - Men:   45% (38-51%)
                   Women:   40% (36-47%)
Hemoglobin - Men:         14-17 gm.%
                   Women:    12-16 gm. %
                   Children:   12-14 gm. %
Blood Counts Per cu. Mm Percent
Erythrocytes (RBC)
Men 5.0 (4.5-6.0) million
Women 4.5 (4.3-5.5) million
Reticulocytes 1.0%
Differential White Count
Leukocytes, total (WBC) 5,000-10,000 100%
Lymphocytes 1,000-4,000 20-40%
Segmented neutrophils 2,500-6,000 40-60%
Band neutrophils 0-500 0-5%
Juvenile neutrophils 0-100 0-1%
Myelocytes 0 0%
Eosinophils 50-300 1-3%
Basophils 0-100 0-1%
Monocytes 200-800 4-8%
Platelets 200,000-500,000

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Certain types of disease associated with the abnormality of blood cells are:

 Anemia- deficiency in erythrocytes or hemoglobin

 Aplastic anemia- a form of anemia where there is lack of formation of blood cell
elements in the bone marrow.
 Leukemia- a progressive, malignant disease of the blood and blood-forming organs
characterized by uncontrolled proliferation and development of leukocytes. It is
diagnosed by microscopic detection of abnormal in the blood and bone
marrow.
 Leukocytosis- an increase in the number of leukocytes in the blood.
 Leucopenia- reduction in the number of leukocytes in the blood.
 Polycythemia- excessive number of erythrocytes.
 Thrombocytopenia- decrease in the number of blood platelets.

IV. PATHOPHYSIOLOGY
A. Narrative Forms
Dengue hemorrhagic fever (DHF) is an acute febrile disease, found in the tropics, with a
geographical spread similar to malaria. Caused by one of four closely related virus serotypes of
the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no
cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur.
Dengue is transmitted to humans by the Aedes aegypti (rarely Aedes albopictus) mosquito, who
feeds during the day.
Dengue viruses are transmitted to humans through the bites of infective female Aedes
mosquitoes. Mosquitoes generally acquire the virus while feeding on the blood of an infected
person. After virus incubation for 8-10 days, an infected mosquito is capable, during probing and
blood feeding, of transmitting the virus, to susceptible individuals for the rest of its life. Infected
female mosquitoes may also transmit the virus to their offspring by transovarial (via the eggs)
transmission, but the role of this in sustaining transmission of virus to humans has not yet been
delineated.
Humans are the main amplifying host of the virus, although studies have shown that in
some parts of the world monkeys may become infected and perhaps serve as a source of virus
for uninfected mosquitoes. The virus circulates in the blood of infected humans for two to seven

13
days, at approximately the same time as they have fever; Aedes mosquitoes may acquire the
virus when they feed on an individual during this period.
The pathogenesis of DHF and DSS (Dengue Shock Syndrome) is still controversial. Two
theories, which are not mutually exclusive, are frequently cited to explain the pathogenetic
changes that occur in DHF and DSS. The most commonly accepted is known as the secondary
infection or immune enhancement hypothesis. This hypothesis implies that patients
experiencing a second infection with a heterologous dengue virus serotype have a significantly
higher risk for developing DHF. Preexisting heterologous dengue antibody recognizes the
infecting virus and forms an antigen-antibody complex, which is then bound to and internalized
by immunoglobulin Fc receptors on the cell membrane of leukocytes, especially macrophages.
Because the antibody is heterologous, however, the virus is not neutralized and is free to
replicate once inside the macrophage. Thus, it is hypothesized that prior infection, through a
process known as antibody-dependent enhancement (ADE), enhances the infection and
replication of dengue virus in cells of the mononuclear cell lineage. It is thought that these cells
produce and secrete vasoactive mediators in response to dengue infection, which causes
increased vascular permeability leading to hypovolemia and shock. The other hypothesis
assumes that dengue viruses, like all animal viruses, vary and change genetically as a result of
selection pressures as they replicate in humans and/or mosquitoes and that there are some
virus strains that have greater epidemic potential. Phenotypic expression of genetic changes in
the virus genome may include increased virus replication and viremia, severity of disease
(virulence), and epidemic potential. They are not mutually exclusive, and both are most probably
valid. Excellent reviews have recently been published on both viral pathogenesis and
immunopathogenesis, which have summarized the evidence concluding that both viral and host
immunologic factors are involved in the pathogenesis of severe dengue disease.
Virologic Factors
Detectable for various periods ranging from 2 to 12 days, depending on the strain of
virus and the immune status of the individual. It has been suggested that the severity of the
disease associated with dengue infection is determined by the number of cells infected with the
virus and that the number of cells infected is related to ADE infection of peripheral blood
leukocytes in secondary infections. It follows that viremias should be higher in secondary
infections, but this is not borne out by experimental infection of lower primates or by clinical
studies on humans. In fact, the opposite has usually been observed; that is, viremias are usually
higher in primary infections. In secondary infections, the virus may be complexed with antibody,
making it undetectable by most current virus isolation techniques.

14
Host Immune Factors
There is a large body of evidence, mostly obtained in vitro, suggesting that heterotypic,
nonneutralizing antibody binds with dengue virus, facilitating the entry of the virus into cells of
the monocytic line and hence facilitating infection. These data, along with epidemiologic
observations that the majority of patients with reported DHF cases are experiencing a
secondary infection, form the basis for the hypothesis that preexisting heterotypic dengue
antibody is a risk factor for DHF. The lack of a good animal model for human disease and
limitations of human clinical studies have made it difficult to confirm this hypothesis. In recent
years, however, detailed, well-designed studies that support the concept of
immunopathogenesis of dengue infection in humans have been conducted. The results of these
studies have been comprehensively reviewed in a recent article. Briefly, the data show that
dengue virus-specific memory CD41 CD82 and CD42 CD81 lymphocytes are detectable in
humans after natural dengue infections. Infection with a single dengue serotype induces both
serotype-specific and serotypecross- reactive CD41 memory T cells, while CD81 T lymphocytes
have virus-specific cytotoxic activity. The pathogenetic mechanism responsible for the increased
vascular permeability observed in DHF and DSS is not known, but it has been suggested that
cytokines and chemical mediators such as tumor necrosis factor (TNF), interleukin-1 (IL-1), IL-2,
IL-6, platelet-activating factor (PAF), complement activation products C3a and C5a, and
histamine may play a role. CD41 T lymphocytes produce a number of cytokines, including
gamma interferon (IFN-g), IL-2, IL-4, IL-5, IL-6, IL-10, and lymphotoxin. Moreover,
monocytes/macrophages which are infected by dengue viruses produce TNF, IL-1, IL- 1B, IL-6,
and PAF. Finally, cytokine and chemical mediator production is induced by other cytokines.
Thus, once cytokines are produced, a complex network of induction may further increase the
levels of cytokines and chemical mediators, resulting in even higher levels with synergistic
effects on vascular permeability. Kurane and Ennis have proposed a model of
immunopathogenesis based on these observations (92). Briefly, it is hypothesized that dengue
virus infections of monocytes/macrophages is enhanced by ADE. This enhancement is
facilitated by the fact that the dengue virus-specific CD41 T lymphocytes produce IFN-g, which
in turn up-regulates the expression of FC-g receptors. The increased number of dengue virus-
infected monocytes/macrophages results in increased T-cell activation, which results in the
release of increased levels of cytokines and chemical mediators. Kurane and Ennis)
hypothesized that the rapid increase in the levels and the synergistic effects of mediators such
as TNF, IL-2, IL-6, IFN-g, PAF, C3a, C5a, and histamine induce increased vascular
permeability, plasma leakage, shock, and malfunction of the coagulation system, which may

15
lead to hemorrhage. In summary, available evidence suggests that both viral and host immune
factors are involved in the pathogenesis of severe dengue disease. Unfortunately, the role of
each is not fully understood and the lack of an animal model makes this a difficult area to study.
It would appear that different clinical pathologic manifestations of the disease may be caused by
different pathogenetic mechanisms. For example, it has been suggested that hepatic injury may
relate more to viral factors whereas vascular permeability may be mediated predominantly by
the immune response. Clearly, the strain of virus is important since ADE apparently occurs only
with selected virus strains when tested in vitro. Also, the rate of virus replication and infectivity in
various tissues varies with the strain of virus. Collectively, the data suggest that only certain
strains of dengue virus are associated with major epidemics and severe disease, and it is most
likely that these are the viruses that infect cells of the monocytic line via ADE.
Precipitating and Predisposing Factors
Ethnicity is nonspecific, but the disease's distribution is geographically determined
especially in tropical countries. People infected with DHF are more susceptible because they
are near places where vectors nest specially in areas where there are stagnant water. Fewer
cases have been reported in the black population than in other races. No gender predilection is
known; however, fewer cases of DHF/DSS have been reported in men than in women.
In endemic areas, a high prevalence of immunity in adults may limit outbreaks to
children specially those under 15 years old.
Clinical Manifestations
Signs and Symptoms
The three stages of clinical presentation are named febrile, toxic and convalescent. The
patients initially develop an abrupt onset of high fever (39–40°C) with malaise, headache,
nausea, vomiting, myalgia and, sometimes, abdominal pain. During the acute febrile stage,
which lasts 2–7 days, hemorrhagic manifestation is invariably present but usually mild. Petechial
hemorrhage on the skin is commonly found. Also, a positive tourniquet test is frequently
observed. Bleeding at the nose, gastrointestinal tract and gums is relatively less common
compared with petechiae, but may be severe. Recently, menorrhagia has been more prevalent
because of the increasing number of affected adolescents. However, hematuria is extremely
rare. Hepatomegaly is commonly found, and the liver is usually soft and tender.
Thrombocytopenia and rising hematocrit due to plasma leakage are usually detectable before
the onset of the subsequent toxic stage. An abrupt fall to normal or subnormal levels of
temperature, varying degrees of circulatory disturbance will develop, known as the toxic stage,

16
lasts 24–48 hours. Ultimately, the majority of patients have rapid uneventful recovery without
sequelae in the convalescent stage.
Diagnosis
The clinical diagnosis of DHF is based on four major characteristic manifestations: (i)
sustained high fever lasting 2–7 days; (ii) hemorrhagic tendency such as a positive tourniquet
test, petechiae or epistaxis; (iii) thrombocytopenia (platelet count  100 x 109/L); and (iv)
evidence of plasma leakage manifested by hemoconcentration (an increase in hematocrit 
20% above average for age, sex and population), pleural effusion and ascites. Close
observation, serial hematocrit and daily platelet count monitoring are suggested in order to
accomplish the clinical diagnostic criteria. Pleural effusion can be demonstrated by a chest X-
ray in right lateral decubitus view at 12–24 hours after defervescence. These applications may
be problematic in a busy pediatric practice in a dengue-endemic area. A study in Vietnam
suggested using fever and hemoconcentration together with either bleeding or
thrombocytopenia as clinical criteria of DHF. However, some patients with bleeding or anemia
will not have a rising hematocrit. Therefore, the minimal criteria should include fever and
evidence of plasma leakage together with either bleeding or thrombocytopenia. Further
evaluation in a large prospective series from other dengue-endemic regions is warranted. The
severity of DHF is categorized into four grades: grade I, without overt bleeding but positive for
tourniquet test; grade II, with clinical bleeding diathesis such as petechiae, epistaxis and
hematemesis; grade III, circulatory failure manifested by a rapid and weak pulse with narrowing
pulse pressure ( 20 mmHg) or hypotension, with the presence of cold clammy skin and
restlessness; and grade IV, profound shock in which pulse and blood pressure are not
detectable. It is note-worthy that patients who are in threatened shock or shock stage, also
known as dengue shock syndrome, usually remain conscious.
Daily platelet count monitoring are suggested in order to accomplish the clinical
diagnostic criteria. Pleural effusion can be demonstrated by a chest X-ray in right lateral
decubitus view at 12–24 hours after defervescence. These applications may be problematic in a
busy pediatric practice in a dengue-endemic area. A study in Vietnam suggested to use fever
and hemoconcentration together with either bleeding or thrombocytopenia as clinical criteria of
DHF. However, some patients with bleeding or anemia will not have a rising hematocrit.
Therefore, the minimal criteria should include fever and evidence of plasma leakage together
with either bleeding or thrombocytopenia.
The diagnosis of dengue infection is confirmed by testing positive for either virus
isolation using cultureor polymerase chain reaction from the clinical specimens such as serum

17
in the early febrile stage, or serological studies. The positive serological studies define as a
fourfold or more increase in the hemagglutination inhibition test between acute and
convalescent sera or positive test for dengue-specific IgM/IgG performed by enzyme-linked
immunosorbent assay (ELISA). The secondary dengue infection is defined when the
hemagglutination inhibition titer was 1:2560 or more, or the ratio of IgG and IgM was > 1.8.
Treatment
The mainstay of treatment is supportive therapy. Increased oral fluid intake is
recommended to prevent dehydration. If the patient is unable to maintain oral intake,
supplementation with intravenous fluids may be necessary to prevent dehydration and
significant hemoconcentration. A platelet transfusion is rarely indicated if the platelet level drops
significantly (below 20,000) or if there is significant bleeding.
The presence of melena may indicate internal gastrointestinal bleeding requiring platelet
and/or red blood cell transfusion.
It is very important to avoid Aspirin and non-steroidal anti-inflammatory medications.
These drugs are often used to treat pain and fever, but in this case, they may actually aggravate
the bleeding tendency associated with some of these infections. If dengue is suspected,
patients should receive instead acetaminophen preparations to deal with these symptoms.

18
PREDISPOSING FACTORS PRECIPITATING FACTORS:

Sex: Female predominance, 3:1 ratio to men (Pan Health Lifestyle: J.D. is usually just left alone in the “duyan” since
Organization 2003) she cannot walk leaving her more exposed to mosquitoes
Age: Children; specially under the age 15 – patient is 3 years old wandering in the area
Cognitive Limitations: the child still does not talk at the age 3; all Lack of knowledge regarding precautionary measures
activities are dependent Lack of guidance from the mother
Environmental Constrains/ Factors: more prevalence of cases in
tropical countries – Philippines is a tropical country
Exposure to Environmental Hazards: they live in an open area with
so many trees which increases the likelihood to be in contact with
carriers of the virus
Race: less prevalent in blacks
Time of day: infected mosquitoes usually feed during daytime
(morning)

Contact to female Aedes aegypti mosquitoes infected with the dengue virus of
the serotype Flavivirus

Secondary infection or immune enhancement Bite from mosquito carrying the virus
hypothesis:

Virus travel to various glands

Second infection with a heterologous dengue virus
serotype
Incubation Multiply
period (5-8
Preexisting heterologous dengue antibody recognizes the days)
infecting virus

19
V. MEDICAL MANAGEMENT
A. Doctor’s Order
Ideal Management
The management of DF is symptomatic and supportive.
 Bed rest is advisable during the acute febrile phase.
 Antipyretics or sponging are required to keep the body temperature below 40C. Aspirin
should be avoided since it may cause gastritis, bleeding and acidosis; paracetamol is
preferable.
 Analgesics or mild sedatives may be required for patients with severe pain.
 Oral fluids and electrolyte therapy are recommended for patients with excessive sweating
or vomiting.
In DHF-endemic areas, patients should be monitored until after they become afebrile
and after platelet counts and haematocrit determinations are normal. In mild to moderate cases
of DHF (Grades I and II), intravenous fluid therapy may be given for a period of 12-24 hours at
an outpatient clinic. Patients who continue to have elevated haematocrit, platelet counts below
50,000/mm3, or present with any type of spontaneous haemorrhage other than petechiae
should be hospitalized. In general, there is no need to hospitalize all patients with suspected
DHF, since only about one-third will develop shock.
Febrile phase
The management of DHF during the febrile phase is similar to that of DF. Antipyretics
may be indicated but salicylates should be avoided. It should be noted that antipyretics do not
shorten the duration of fever in DHF. Paracetamol is recommended and should be used only to
keep the temperature below 39oC. Patients with hyperpyrexia are at risk of convulsions. High
fever, anorexia and vomiting lead to thirst and dehydration. Therefore, copious amounts of fluids
should be given orally, to the extent tolerated. Oral rehydration solutions, such as those used for
the treatment of diarrhea diseases* and/or fruit juices are preferable to plain water. Patients
should be closely monitored for the initial signs of shock. The critical period is during the
transition from the febrile to the afebrile phase, and usually occurs after the third day. Serial
hematocrit determinations are an essential guide for treatment, since they reflect the degree of
plasma leakage and the need for intravenous administration of fluids. Hemoconcentration
usually precedes the blood pressure and pulse changes. Hematocrit should be determined daily
from the third day, until the temperature has remained normal for one or two days. If hematocrit
determination is not possible, hemoglobin determination may be carried out as an alternative,
but this is less sensitive.

20
Volume replacement in DHF
Although there is massive plasma leakage, particularly in shock cases, judicious volume
replacement is mandatory. The required volume should be charted on a two or three hourly
basis or even more frequently in shock cases. The rate of intravenous fluid replacement should
be adjusted throughout the 24-48 hour period of leakage by serial hematocrit determinations,
with frequent assessments of vital signs and urine output, in order to ensure adequate volume
replacement and to avoid over-volume infusion. The volume of fluid replacement should be the
minimum that is sufficient to maintain effective circulation during the period of leakage.
Excessive volume replacement and continuation after leakage stops will cause massive pleural
effusion, ascites, and pulmonary congestion/edema with respiratory distress when reabsorption
of the extravasated plasma occurs in the convalescent stage. In general, the volume required is
maintenance plus 5-8% deficit. The fluid administered to correct dehydration from high fever,
anorexia and vomiting is calculated according to the degree of dehydration and electrolyte loss
and should have the following composition: 5% glucose in one-half or one-third physiological
saline solution (PSS). In the case of acidosis, onefourth of the total fluids should consist of
0.167 mol/liter of sodium bicarbonate (i.e. three-quarters PSS plus glucose plus one quarter
sodium bicarbonate). When there is significant hemoconcentration, the fluids used for
replacement therapy should have a composition similar to plasma. The volume and composition
are similar to those used in the treatment of diarrhea with mild to moderate isotonic dehydration
(5-8% deficit). The necessary volume of replacement fluid is equivalent to the amount of fluids
and electrolytes lost: thus, 10ml/kg should be administered for each 1% of normal body weight
lost. Since the rate of plasma leakage is not constant (it is more rapid when body temperature
drops), the volume and rate of intravenous fluid therapy should be adjusted according to the
volume and rate of plasma loss. Plasma loss can be monitored by changes in the hematocrit,
vital signs or volume of urine output. However, even where there is massive plasma loss,
judicious fluid replacement is necessary to avoid over hydration. In older children and adults
who weigh more than 40 kgs, the volume needed for 24 hours should be calculated as twice
that required for maintenance.
The fluid replacement should be the minimum volume that is sufficient to maintain
effective circulation during the period of leakage (24-48 hours). Excessive replacement will
cause respiratory distress (from massive pleural effusion and ascites), pulmonary congestion
and edema.
Sedatives

21
 In some cases, treatment with sedatives is necessary to calm an agitated child.
Hepatotoxic drugs should be avoided. Chloral hydrate, administered orally or rectally, is highly
recommended at a dosage of 12.5-50 mg per kilogram of body weight (but no more than 1 g) as
a single hypnotic dose. Agitation/ restlessness that results from poor tissue perfusion often
subsides when adequate fluid volume replacement is given.
Oxygen therapy
Oxygen therapy should be provided for all patients in shock, but it must be remembered
that an oxygen mask or tent may lead to increased patient anxiety.
Blood transfusion
Blood grouping and cross-matching should be carried out as a systematic precaution on
every patient in shock, particularly in cases with prolonged shock. Blood transfusion is indicated
in cases with significant hemorrhagic manifestations. It may be difficult to recognize internal
hemorrhage if there is hemoconcentration. A decrease in the hematocrit, example: from 0.5
(50%) to 0.4 (40%), without clinical improvement, despite the administration of sufficient fluids,
indicates significant internal hemorrhage. Fresh whole blood is preferable and the volume of
blood administered should be only enough to raise the red blood cell concentration to normal.
Fresh frozen plasma and/or concentrated platelets may be indicated in some cases when
disseminated intravascular coagulation causes massive bleeding. Disseminated intravascular
coagulation is common in severe shock, and may play an important role in the development of
massive bleeding and lethal shock. The results of hematological tests (e.g. prothrombin time,
partial thromboplastin time, and fibrinogen degradation products) should be studied in all
patients with shock to monitor the onset and severity of disseminated intravascular coagulation.
Results of these tests will determine the prognosis.

Actual Management
Dengue is spread by the bite of an Aedes mosquito. The mosquito transmits the disease
by biting an infected person and then biting someone else and blood test and Tourniquet Test
(Rumpel Lead Test) and is a diagnostic test used to detect dengue virus. A test is (+) when 20
or more petechiae per 2.5 cm square or 1 inch square are observed.
Paracetamol is used for fever to lower the temperature of the patient and to provide and
analgesia which is the cessation of pain brought by headaches.
Dopamine adjunct to standard measures to improve blood pressure, cardiac output, urine
output in treatment of shock unresponsive to fluid replacement.
Dobutamine increases cardiac output without significantly increased heart rate.

22
 Famotidine is a histamine H2 antagonist. It relieves signs and symptoms of allergic
reactions. Prevention and treatment of stress-induced upper GI bleeding in critically ill patients.
It can be administered orally.
Salbutamol is used as a bronchodilator to control and prevent reversible airway
obstruction caused by asthma or COPD. It can be administered through inhalation or orally.
Hydroxyzine decreases nausea and vomiting, decreases allergic symptoms associated
with release of histamine and relief anxiety. It is well absorbed following PO/IM administration. It
maybe combined with opioid analgesics.

B. Drug Study

NAPREX

Generic name: Paracetamol

Classification: Non-narcotic Analgesic
Actual dosage: 100/ml 1.2 ml qº 4 for T>38º C
Action: Thought to produce analgesia by blocking generation of pain impulses, probably by
inhibiting prostaglandin synthesis in the CNS or the synthesis or action of other substances
that sensitize pain receptors to mechanical or chemical stimulation. It is thought to relieve
fever by central action in the hypothalamic heat regulating center.
Therapeutic Effects: Analgesia. Antipyresis.
Contraindication: Previous hypersensitivity. Products containing alcohol, aspartame,
saccharin, sugar, or tartrazine should be avoided in patients who have hypersensitivity or
intolerance to these compounds.
Indication: Mild pain or fever.
Adverse Effects: Hemat: hemolytic anemia, neutropenia, leukopenia, pancytopenia. Hepatic:
liver damage, jaundice. Metabolic: hypoglycemia. Derm: rash, urticaria.
Nursing Considerations:
 Use cautiously in patients with history of chronic alcohol use because hepatotoxicity has
occurred after therapeutic doses.
 PO: Administer with a full glass of water.
 May be taken with food or on an empty stomach
 Use liquid form for children and patients who have difficulty swallowing.

23
 Acetaminophen may produce false-positive decreases in glucose levels in home monitoring
systems; drug may cause a false-positive test result for the urinary 5-hydroxyindoleacetatic
acid.
 Toxicity and Overdose: If overdose occurs, acetylcysteine (Acetadote) is the antidote.

ITERAX

Generic Name: hydroxyzine

Classification: antianxiety agents, antihistamines, sedative/hypnotics
Actual Dose: 2 mg/ml 2.5 ml BID PO

Action: Acts as a CNS depressant at the subcortical level of the CNS. Has anticholinergic,
antihistaminic, and antiemetic properties.
Therapeutic Effects: Sedation. Relief of anxiety. Decreased nausea and vomiting. Decreased
allergic symptoms associated with release of histamine, including pruritis.
Indications: Treatment of anxiety. Preoperative sedation. Antiemetics. Antipruritic. May be
combined with opiod analgesics.
Contraindication: Hypersensitivity. Pregnancy.
Adverse Effects: CNS: drowsiness, agitation, ataxia, dizziness, headache, weakness.
Resp: wheezing. GI: dry mouth, bitter taste, constipation, nausea. GU: urinary retention. Derm:
flushing. Local: pain at IM site, abscesses at IM sites. Misc: chest tightness.
Nursing Considerations:
 Do not confuse hydroxyzine with hydralazine.
 PO: Tablets may be crushed and capsules opened and administered with food or fluids for
patients having difficulty swallowing.
 Shake suspension well before administration.

DOPAMINE
Classification: Inotropics. Vasopressors.
Dosage: 1ml/hour
Action: small doses (0.5-3 mcg/kg/min) stimulate dopaminergic receptors, producing renal
vasodilation. Larger doses (2-10 mcg/kg/min) stimulate dopaminergic and beta1-adrenergic
receptors, producing cardiac stimulation and renal vasodilation. Doses greater that
10mcg/kg/min stimulate alpha-adrenergic receptors and may cause renal vasoconstriction.

24
 Therapeutic Effects: Increased cardiac output, increased blood pressure, and improved
renal blood flow.
Indication: Adjunct to standard measures to improve: Blood pressure, Cardiac output, urine
output in treatment of shock unresponsive to fluid replacement.
Contraindication: Tachyarrhythmias, Pheochromocytoma. Hypersensitivity to bisulfites.
Adverse Effects: CNS: headache. EENT: mydriasis (high dose). Resp: dyspnea. CV:
arrhythmias, hypotension, angina, ECG changes, palpitations, vasoconstriction. GI: nausea,
vomiting. Derm: piloerection. Local: irritation at IV site.
Nursing Considerations:
 Monitor urine output frequently throughout administration. Report decrease in urine output
promptly.
 Palpate peripheral pulses and assess appearance of extremities routinely throughout
dopamine administration. Notify physician if quality of pulse deteriorates or if extremities
become cold or mottled
 If hypotension occurs, administration rate should be increased. If hypotension continues,
more potent vasonconstrictors (norepinephrine) may be administered.
 High Alert: IV vasoactive medications are potentially dangerous. Have second practitioner
independently check original order, dosage calculations and infusion pump setting. Do not
confuse dopamine with dobutamine
 Correct hypovolemia with volume expanders before initiating dopamine therapy.
 Extravasion may cause severe irritation, necrosis, and sloughing of tissue. Administer into a
large vein and assess administration site frequently. If extravasion occurs, affected area
should be infiltrated liberally with 10-15 ml ml of 0.9% NaCl containing 5-10 mg of
phentolamine. Reduce proportionally for pediatric patients. Infiltration within 12 hr of
extravasion produces immediate hyperemic changes.
 Continuous Infusion: Dilute immediately before administration. Yellow or brown
discoloration indicates decomposition. Discard solution that is cloudy, discolored, or contains
a precipitate. Solution is stable for 24 hr. infusion must be administered via infusion pump to
ensure precise amount delivered. Rate of administration is titrated according to patient
response (heart rate, presence of ectopic activity, blood pressure, urine flow, peripheral
perfusion, cardiac output). Decrease rate gradually when discontinuing to prevent marked
decreases in blood pressure.
 Toxicity and Overdose: If excessive hypertension occurs, rate of infusion shoul be
decreased or temporarily discontinued until blood pressure is decreased. Although

25
 additional measures are usually not necessary because of the short duration of dopamine,
phentolamine may be administered if hypertension continues.

DOBUTAMINE HYDROCHLORIDE
Classification: Inotropics
Actual dosage: .8 ml/hour
Action: Stimulates beta1 (myocardial)-adrenergic receptors with relatively minor effect on heart
rate or peripheral blood vessels.
Therapeutic Effects: Increased cardiac output without significantly increased heart rate.
Indication: short term (<48 hr) management of heart failure caused by depressed contractility
from organic heart disease or surgical procedures.
Contraindication: Hypersensitivity to dobutamine or bisulfites. Idiopathic hypertrophic subaortic
stenosis.
Adverse Effects: CNS: headache. Resp: shortness of breath. CV: hypertension, increased
heart rate, premature ventricular contractions, angina pectoris, arrhythmias, hypotension,
palpitations. GI: nausea, vomiting. Local: phlebitis. Misc: hypersensitivity reactions
including skin rash, fever, bronchospasm or eosonophilia, nonanginal chest pain.
Nursing Considerations:
 High Alert: IV vasoactive medications are potentially dangerous. Have second practitioner
independently check original order, dosage calculations and infusion pump setting. Do not
confuse dobutamine with dopamine.
 Correct hypovolemia with volume expanders before initiating dobutamine therapy.
 Administer into a large vein and assess administration site frequently. Extravasion may
cause pain and inflammation.
 Palpate peripheral pulses and assess appearance of extremities routinely throughout
dobutamine administration. Notify physician if quality of pulse deteriorates or if extremities
become cold or mottled.
 Concentration should not exceed 5 mg of dobutamine per ml. slight pink color of solution
does not alter potency. Solution is stable for 24 hr at room temperature.
 Continuous Infusion: Administer via infusion pump. Rate of administration is titrated
according to patient’s response (heart rate, presence of ectopic activity, blood pressure,
urine output, CVP, PCWP, cardiac output). Dose should be titrated so heart rate does not
increase by > 10% of baseline.

26
 Toxicity and Overdose: If overdose occurs, reduction or discontinuation of therapy is the
only treatment necessary because of the short duration of dobutamine.

COMBIVENT

Generic name: salbutamol

Classification: bronchodilators
Actual dosage: 1 nebule q 6º
Action: Binds to beta2- adrenergic receptors in airway smooth muscle, leading to activation of
adenyl cyclase and increased levels of cyclic-3’.5’-adenosine monophosphate (cAMP).
Increases in cAMP activate kinases, which inhibit the phosphorylation of myosin and
decrease intracellular calcium. Decreased intracellular calcium relaxes smooth muscle
airways. Relaxation of airway smooth muscle with subsequent bronchodilation. Relatively
selective for beta2 (pulmonary) receptors. Therapeutic Effects: Bronchodilation.
Indications: Used as a bronchodilator to control and prevent reversible airway obstruction
caused by asthma. Or COPD. Inhaln: Used as a quick-relief agent for acute bronchospasm
and for prevention of exercise-induced bronchospasm.
Contraindication: Hypersensitivity to adrenergic amines. Hypersensitivity to fluorocarbons
(some inhalers).
Adverse Effects: CNS: nervousness, restlessness, tremor, headache, insomnia, hyperactivity
in children. CV: chest pain, palpitations, angina, arrhythmias, hypertension. GI: nausea and
vomiting. Endo: hyperglycemia. F and E: hypokalemia. Neuro: tremor.
Nursing Considerations:
 Monitor pulmonary function tests before initiating therapy and periodically during therapy to
determine effectiveness of medication.
 Observe for paradoxical bronchospasm (wheezing). If condition occurs, withhold medication
and notify physician or other health care professional immediately.
 Do not confuse salbutamol with salmeterol.
 For nebulization or IPPB, the .5-.83-, 1- and 2-mg/ml solutions do not require dilution before
administration. The 5 mg/ml (.5%) solution must be diluted with 1-2.5 ml of 0.9& NaCl for
inhalation. Diluted solutions are stable for 24 hr at room temperature or 48 hr if refrigerated.
For nebulizer, compressed air or oxygen flow should be 6-10 L/min; a single treatment of 3 ml
lasts about 10 min.

27
 VI. NURSING MANAGEMENT
Name of Patient: __J.D. __ Age: _3__ Room no.: _Ext3_ Hospital No.:______________
Diagnosis/Impression: __ DHF3 _____ Attending Physician/s: ______Dr. Agnes____________________________

NURSING CARE PLAN

CUES NURSING OBJECTIVES INTERVENTION RATIONALE EVALUATION

DIAGNOSIS

Subjective: Ineffective  At the end of  Assess/monitor  Tachypnea is usually present  At the end of
airway 5 mins nursing respiratory rate. Note in some degrees, and may be 5 mins of
The mother clearance r/t intervention, the the inspiratory / pronounced on admission or nursing
verbalized, bronchospasm patient will be expiratory ratio. during stress, concurrent acute intervention,
“Asthmatic man able to breathe process. Respirations may be the client was
gud ni siya, properly. shallow and rapid. able to breathe
nisabay rapud ni  Assist the patient to  Elevation of the head of the properly
iyang hubak sa  At the end of assume position of bed facilitates respiratory
pagkaadmit niya 8 hrs, the comfort, e.g, elevate function by use of gravity. Side  At the end of
tungod sa significant head of bed, side lying lying position facilitates 8 hrs nursing
Dengue.” others of the position. breathing. intervention the
patient will be  Encourage/assist with  Provides the patient with significant
Objective: able to know abdominal or pursed-lip some means to cope with and others of the
what actions breathing exercises. reduce air-trapping. patient knew
 RR= 28 cpm, must be done Health teachings to the and
tachypnea (normal when the significant others of the understood the
15-25 cpm) patient has patient: actions to be
 Pattern= regular asthma attack.  Keep environmental  Precipitators of allergic type of done in case of
but rapid, shallow pollution to a minimum, respiratory reactions that can asthma attack.
breathing e.g., dust, smoke, trigger onset of respiratory
 Adventitious feather pillows episodes.
sounds: inspiratory according to individual
crackles situation.
 dry unproductive  Increase fluid intake  Hydration helps decrease the
cough noted to 4-6 glasses/day and viscosity of secretions. Using
provide warm/tepid warm liquids may decrease

28
 liquids instead of cold. bronchospasm.
 Administer nebulizers  Promotes relaxation of
or bronchodilators as smooth muscle reducing air-
ordered spasm and wheezing.
Bronchodilators decreases
mucosal edema and smooth
muscle spasm.

Name of Patient: __J.D. __ Age: _3__ Room no.: _Ext3_ Hospital No.:______________
Diagnosis/Impression: __ DHF3 _____ Attending Physician/s: ______Dr. Agnes____________________________

NURSING CARE PLAN

CUES NURSING OBJECTIVES INTERVENTION RATIONALE EVALUATION

DIAGNOSIS

Subjective: Hyperthermia r/t  At the end of  Monitor patient’s  Fever pattern may aid in After 8 hrs of
Infectious 30 mins. Client temperature diagnosis. nursing
As verbalized disease. will manifest a  Limit or add bed  number of blankets should interventions, the
by the mother: reduce in the linens as indicated be altered to maintain near patient will manifest
“init man jd temperature normal temperature a decrease in
kayo siya from 38.2C to  Do Tepid Sponge  Tepid Sponge bath will temperature from
ma’am, ge- 37.0C bath. Avoid use of facilitate in the decrease of 38.2C to 37.0C
hilanat npd  At the end of alcohol temperature. Alcohol may
siguro” 16 hrs. Client cause chills actually elevating At the end of 16
will temperature and dryness of hrs of nursing
Objective: demonstrate skin. interventions, the
temperature  administer  Use to reduce fever by its patient will maintain
within normal antipyretics central action on the a temperature
 Temp: 38.2 range of 36.5 hypothalamus. ranging from 36.5C
 Skin is warm, to 37.5C.  regulate IVF to  Increase metabolic rate to 37.5C
rough and dry accomplish fluid associated with fever cause
to touch replacement as loss of body fluids.
ordered

29
Name of Patient: __J.D. __ Age: _3__ Room no.: _Ext3_ Hospital No.:______________
Diagnosis/Impression: __ DHF3 _____ Attending Physician/s: ______Dr. Agnes____________________________

NURSING CARE PLAN

CUES NURSING OBJECTIVES INTERVENTION RATIONALE EVALUATION

DIAGNOSIS

Subjective: Ineffective  At the end of  Have the client use  To prevent trauma to  At the end of 1 hr
protection r/t 1 hr the client’s moistened toothette or a the oral mucosa that nursing
“Nanaghan lagi decrease platelet family will very soft child’s could result in bleeding. interventions, the
ni iyang pula- count explain toothbrush instead of a client’s family was
pula sa lawas precautions to toothbrush. Have the able to explain the
tungod sa take to prevent client use alcohol free precautions to take
Dengue, unya new bleeding dental products to prevent new
dali ra kayo  Teach the client and  To provide information bleeding
gakabun-ugan”  At the end of family the signs of and promote
As verbalized 16 hrs. Client bleeding, precautions to independence in the part
by the mother will be free of take to prevent bleeding of the family.  At the end of 16
any evidence and action to take if hrs nursing
Objective: of new bleeding begins interventions,
bleeding  Caution the client to Client was free of
 Hemolysis: avoid OTC medications, any evidence of
Platelet 45 especially Aspirin, without  Medications, like new bleeding
10^3/ul permission of the Aspirin, that contain
 Urinalysis: physician salicylates can increase
RBC:1-3/hpf  Give medications orally bleeding
 ecchymosis or intravenously only as
on the right ordered. Apply pressure
cubital area, for longer time than used
right dorsal to invasive sites such as  Additional pressure is
area of the arm venipuncture sites. needed to stop bleeding
and the right of invasive sites.
pedal part of
the foot.

30
VII. DISCHARGE PLAN
Objectives: This discharge plan aims to continue treatment and care of the client by involving
significant others to participate in the plan of care.

Medications Encourage strict compliance of regimens to attain therapeutic effects.

Instruct parents to continue to give the prescribed medications as
directed by attending physician.
 Iterax Hydroxyzine-2 mg/mL 2.5 mL BID PO
 Naprex Paracetamol-100 mg/mL 1.2 mL qº 4 for T>38º C
 Salbutamol-1 nebule q 6º
 Hydroxyzine- Antianxiety agents, antihistamines and sedatives/
hypnotics. Acts as a CNS depressant at the subcortical level of the
CNS. Has an anticholinergic, antihistaminic, and antiemetic property.
Its Therapeutic effects are sedation, relief of anxiety, decrease nausea
and vomiting and decrease allergic symptoms associated with release
of histamine, including pruritus.
 Paracetamol- an antipyretic and analgesic agent which inhibits the
synthesis of prostaglandins that may serve as mediators of pain and
fever, primarily in the CNS. Have no significant anti-inflammatory
properties or GI toxicity.
 Salbutamol- A bronchodilator used to control and prevent reversible
airway obstruction caused by asthma or COPD. Binds beta2-adrenergic
receptors in airway smooth muscles, leading to activation of adenyl
cyclase and increased levels of cyclic-3’,5’-adenosine monophosphate
(cAMP). Results in the decreased of intracellular calcium which relaxes
smooth muscle airways.
Exercise Daily active exercises are advised to facilitate fast recovery and
restoration of muscle functions.
Passive Range of Motion exercises to prevent contraction of the
muscles and maintain joint flexibility.
Make sure that the patient receives a lot of rest. Rest is important in
order for the body to rejuvenate and repair body tissues.

31
Treatment Instruct parents to continue giving all the medications prescribed by the
physician and to return to the hospital for scheduled follow-up.
Assess parents’ understanding of treatment regimen as well as
concerns and fears.
Health Teachings Give family and significant others verbal and written information on the
following:
 Medications and their generic and drug names, dosages, indications,
precautions and adverse effects and strict adherence to them.
 Proper hygiene especially proper hand washing.
 Proper diet and nutrition like taking in fruits and vegetables.
 Increase fluid intake up to 1 to 2 liters/day (fruit juices and water).
 Necessity of follow-up appointments; confirm date and time with the
physician.
 Regular exercise and adequate rest and sleep.
Out Patient Follow Instruct parents to return to their attending physician for scheduled
Up follow-up visit.
Advice parents to report to the physician any recurrence or severity of
symptoms, adverse effects of the medication and any development of
complications.
Encourage family to ask and inquire to the physician if there are things
they are unclear of.
Diet Encourage family to increase fluid intake (milk, fruit juices, and water)
to compensate for the losses from sweating and to permit adequate
volume of urine for excreting the wastes.
Maintain a high calorie diet (carbohydrates, glucose, sucrose and
starch).
Advice a high protein diet (eggs, milk and high protein beverages) to
compensate loss of tissue proteins. Proteins have high nutritive factors
and are readily digestible.
Increase intake of foods containing vitamin A, ascorbic acid, calcium,
phosphorus, sodium and B complex vitamins.
Fats should be avoided (butter and fried foods).
Diet must be free of spices and fibers.
Spirituality Encourage family to attend any religious activities or to go to Mass
regularly.

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 Encourage family to read the bible and to pray to God always. To ask
for guidance and to pray for healing and restoration of health.
Ask family to reflect on this verse: "For I will restore health to you and
heal you of your wounds," says the Lord. (Jeremiah 30:17)

VIII. PROGNOSIS

Most people who develop dengue fever recover completely within two weeks. Some,
however, may go through several weeks of feeling tired and/or depressed.
The duration of dengue fever is 2 weeks typically but sometimes months before weakness or
joint pains disappear. The acute phase of up to 1 week is followed by a 1- to 2-week period of
convalescence which is characterized by weakness, malaise, and anorexia.
The prognosis for uncomplicated dengue fever is very good, and almost 100% of
patients fully recover. It is because medications and therapies are already available. There is
also preventive measures that are out in the market which can lower the incidence of this
disease; However, as many as 6-30% of all patients die when DHF occurs. The death rate is
especially high among the youngest patients (under one year old) because of their low immune
system to fight this illness. In places where excellent medical care is available, very close
monitoring and immediate treatment of complications lowers the death rate among DHF patients
to about 1%. Nevertheless, death rate continues to increase because of the poor facilities the
country has; especially in far flung areas where Dengue is prevalent. There is the uneven
distribution of resources and lack of information dissemination which leave the innocent victims
defenseless.
Overall, prognosis of Dengue Hemorrhagic fever is high provided with the facilities and
resources.

IX. CONCLUSION

Dengue hemorrhagic fever (DHF) is a viral infection caused by one of four closely
related virus serotypes of the genus Flavivirus, family Flaviviridae and transmitted to humans by
the Aedes aegypti mosquito that feeds during the day. Patient with dengue fever will, as WHO
defines dengue, experience sudden onset of Fever, Haemorrhagic tendency,
Thrombocytopaenia and evidence of plasma leakage. The mainstay of treatment is supportive
therapy through rehydration. A platelet transfusion is rarely indicated if the platelet level drops
significantly (below 20,000) or if there is significant bleeding. Avoidance of Aspirin and non-

33
steroidal anti-inflammatory medications must be emphasized. Prevention of dengue includes
mosquito control and use of mosquito nets, repellents containing NNDB or DEET, cover
exposed skin, use DEET-impregnated bednets, and avoiding endemic areas.
This information enables the proponents to derive this case analysis and present these
findings to fellow student nurses. The proponents were able to enhance their learning about
Typhoid Fever with their appropriate nursing management and consideration.

X. RECOMMENDATION

Primary prevention of dengue mainly resides in eliminating or reducing the mosquito

vector for dengue. Spraying the surroundings with chemicals that could kill mosquitoes is one
way to prevent this disease. At our climate today, the eradication of stagnant water is also
useful in controlling mosquito-borne diseases. Defogging every afternoon is another way to
avoid Dengue with the use of dried leaves of scratch paper.
Personal prevention would include the use of mosquito nets and repellants. Although
repellants would be costly, defogging and use of mosquito nets is more recommended at the
same time it is also effective.

XI. APPENDIX

Doctor’s Orders
DATE TIME
7/30 12:30am >Please admit to Ext. 3 under the service of Dr. Agnes
>secure consent to care
>TPR with BP q hour (infant cuff)
>diet for age, no choco-colored food
>lab: CBC wit blood typing with APTT, PTPA
UA- wash genitalia before attaching urine bag
>change IVF/site to voluven 500cc, run 300cc as fast drip then
regulate at 200gtt
>side drip with dopamine drip prepared as follows

Dopamine 4cc
D5LR 46cc
50 cc @ 4cc/hr via IP
>side drip with dobutamine drip prepared as follows:

Dobutamine 13cc
D5LR 37cc
50cc @ 1.5cc/hr via SP

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 >medication 1. Paracetamol 100/ml 1.2 ml q 4° for T ≥ 38°C
2. Famotidine 9g IVT q 12°
>I and O q shift
> refer for SBP <80, for narrow pulse pressure ≤ 20 for active
bleeding or any unusualities
>attending by AP
>refer accordingly or inhalation of 1Lpm via nasal canula

7/30 1:15 am >Fastdrip 10cc voluven

>decrease dapamine to 3cc/hr
>voluven at 10gtts/min IVFTF plain LR @ 10gtts/min
>D5LR @10gtts/min
>combivent 1 nebule now then q 6°
>cerftriaxone 19 O.D IV drip ANST. 1st dose

7/30 1:40 am >decsrease dobutamine 1cc/r

>decrease dapamine 2cc/hr
>regulate D5LR
>furosemide 10g IVT now

7/30 2:30 am >furosemide 100g IVT now

7/30 3:00am >off dopamine drip now

7/30 11:15am >run 100 cc PLR hour

>increase dobutamine to 1.5cc/hr
>resume dopamine at 1cc/hr
>recheck and refer BP 30 min after fast drip

7/30 11:50am >increase PLR to 10gtts/min

7/30 12:00 pm >decrease PLR to 5 gtt/min

>remove dobutamine deep
>decrease D5LR to 10 gtts/min
Repeat CBC, platelet in AM (7/31/07)

7/30 5:00pm > decrease dobutamine drip to 1cc/hr

7/30 7:00pm >retain PLR line- regulated @ 10 gtts/min

>SD increase Dopamine @ 2cc/hr
>dobutamine drip to 1cc/hr

7/31 6:00am >decrease dopamine drip to 1cc/hr

7/31 9:00am >furosemide 10mg IVTT now

>iterax 2mg/ml 2.5 ml BID PO
>maulain: IVF rate of PLR @ 10gtts/hr
>IVFTF: D5IMB500cc @10gtts/gr
>maintain Dopamine drip @1cc/hr and dobutamine drip @ 1cc/hr
>CBC, platelet in AM (Aug 1, 07)

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 7/31 11:20am >decrease dobutamine drip to 0.8cc/hr

7/31 5:00pm >d/c dobutamine drip; recheck 30 mins after; refer

7/31 6:00pm >d/c PLR; change to D5IMB 500cc @ 10gtts/min

Nurse’s Notes
07/30/07 1:30AM  received from ER per stretcher
 with IVF of Voluven 500cc fast drip 300cc then regulated @
10 gtts/min and D5LR 500 cc @ 10 gtts/min
 started with side drip of D5W 46cc and Dopamine 4cc @
2cc/hr via infusion pump
 started with another side drip of D5W 37cc and Dobutamine
13cc @ 1 L/min via nasal cannula
 visited by Dr. Agnes with orders – carried out
 labs taken
 vital signs monitored and recorded
 due meds and nebulization – given
 Dopamine and Dobutamine drip off temporarily
 I & O measured and recorded
 needs attended
6 AM  endorsed
(signed)
6 AM  Received lying on bed sleeping with D5LR @ 400cc level
regulated @10 gtts/min infusing well @ R temporo parietal
area.
 with side drip of Voluven @ 75cc level regulated @
20gtts/min
 with O2 inhilation via nasal cannula @ 2 LPM
 with ecchymoses @ upper extremities
(signed)
07/30/07 2 PM  Received on bed with IVF infusing well
 Vital signs taken & recorded
 With O2 @ 1 l/min via nasal cannula
 Due meds given
 I & O measured & recorded
 Kept watch for unusualities
 Needs attended
10 PM  Endorsed
(signed)
07/30/07 10 PM  Received on bed with INF @ left fontanel of DLR, L @ 10
gtts/min
 IVF @ right fontanel D5LR 500cc @ 10 gtts/min – removed
 Side drip of dopamine @ 2 cc/hr & Dobutamine drip @ 1cc/hr
attached to DLR mainline
 With O2 inhalation @ 1 L/min via nasal cannula
 Vital signs monitored & recorded
 Due meds & nebulization – given
 For repeat CBC & platelet in AM – done

36
  I & O measured & recorded
 Needs attended
 Endorsed
(signed)
07/31/07 6 AM  Received lying on bed with DLR @ 600cc level regulated @
10 gtts/min infusing well @ left tempoparietal area
 With generalized petechiae
 With narrow pulse – noted
 Initial v/s taken: BP=130/60 mmHg, T= 37.7 C, P= 120 bpm,
R=18 bpm
 Bedside care done
8:30AM  Seen & examined by Dr. Dumato with new orders carried out
Diet for AGE  Served & consumed half of share with fair appetite
 Health teachings imparted with emphasis on:
 Proper nutrition
 Proper hygiene
 Medical regimen compliance
 I & O measured & recorded
 Kept observed for any unusualities
 Endorsed with latest v/s: BP= 110/70 mmHg’ PR= 117 bpm,
1 PM RR= 35 bpm, T= 37.2 C
addendeum  No urine output noted
 Hot & cold compress applied to hypogastric area
 Endorsed
(signed)
07/31/07  With side drip of Dobutamine regulated @ 1 mgtts/min via
syringe pump
 With side drip of Dopamine regulated @ 1 gtts/min via
infusion pump
 With generalized petechiae noted
 With productive cough with whitish asputum
 Initial v/s taken: BP= 130/70 mmHg, PR= 152 bpm, RR= 36
bpm, T= 37.9 C
 Bedside care done
9 AM  Seen & examined by Dr. Agnes with new orders carried out
DFA  Served & consumed small amount of share with poor
appetite
 Health teachings imparted with emphasis on:
 Proper nutrition
 Safety precaution
 Observed for any unusualities
 I & O measured & recorded
 Endorsed with latest v/s: BP= 120/80 mmHg, PR= 125 bpm,
RR= 33 bpm, T= 37.5 C
(signed)
07/31/07 2 PM  Received asleep on be with ongoing IVF of DLR 1 L @ 450
level regulated @ 10 gtts/min infused in the left side of
forehead
 With side drip of Dopamine @ 10 ml level @ soluset
attached to IP regulated @ 1 cc/hr

37
  With side drip of Dobutamine @ 5 ml level regulated @ 0.8
cc/hr attached to syringe pump
 Presence of rashes in the upper lower extremiries
 Positive ecchymoses in the upper & lower extremities
 Appered weak & irritable when touched
 Febrile – T= 37.9 C
 Vital signs taken & minitored
 Bedside care done
5 PM  Seen & examined by Dr. Dumato
 Diet – consumed share with fair appetite - - no choco colored
food emphasized
5:30 PM  Dobutamine discontinued
6:00 PM  Seen & examined by Dra. Agnes with orders carried out by
NOD
 Above IVF DLR 1 L changed to D5IMB 500cc @ 10 gtts/min
 Health teachings imparted with emphasis on:
 Proper fluid intake
 Small frequent feeding
 Proper sanitation
10 PM  Endorsed asleep on bed
(signed)
08/01/07 6-2pm  Received lying on bed with ongoing IVF of #3 D5IMB 500cc
@ 250 ml level regulated @ 10 gtts/min hooked @ the
forehead infusing well
 With side drip of D5W 46 cc + dopamine 1cc regulated 1
cc/hr in soluset via infusion pump
 With occasional productive cough noted
 Afebrile
 v/s taken & recorded as follows: T=37.2 C, PR= 120 bpm,
RR= 30 bpm, BP= 120/80 mmHg
 bedside care done
 due meds given
12:00nn  nebulization done
 adequate rest rendered
 needs attended
 I & O monitored & recorded
 Health Teachings imparted to the mother:
 Proper hygiene
 Proper nutrition and diet
 Keeping back dry
 Endorsed with latest v/s T= 37.2 C, PR= 142 bpm, RR=37
bpm, BP= 120/70 mmHg
(signed)
08/01/07 10PM-6AM  Received on bed with IVF going on
 With sd: of Dopamine @ 1 cc/hr
 v/s taken & recorded
 due meds given
 O2 maintained @ 1 L/min via nasal cannula
 I & O measured & recorded
 Kept rested

38
  Watched for unusualities
 Endorsed
(signed)

Special Endorsement
REFERRAL SLIP
  
Refer to : Dr. Ann Agnes
c/c: cold clammy skin, hypotension
history and physical endings on admission
 
july27-onset fever
july28-still with fever with cough
july29-morning-lysis of fever and later with clummy skin
 
Medication Given
ceftazidime 100 mg/kg/day q12xdose
hydrocortisone 4mg/kg/dose q4IVx2dose
salbutamol nebulization

List of Tables

Hematology Report……………..10
Urinalysis…………………………10
Nursing Diagnosis 1………….…28
Nursing Diagnosis 2…….………29
Nursing Diagnosis 3…….……...30
Discharge Plan………………….31
Doctor’s Orders…………….…...34
Nurse’s Notes………….……......36
Special Endorsement.................39

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XII. BIBLIOGRAPHY

Books

Kozier, B. Fundamentals of Nursing. Pearson Education South Asia PTE LTD, Philippines. pp.
1260-1261.

Ladwig, G. Nursing Diagnosis Handbook: A guide to Plan Care 7th Edition. Elsevier Inc.,
Singapore 2006. pp. 853-859, 533-539, 635-641,964-971.

Geissler, ALice C., et al.Nursing Care Plans 2nd edition. F.A Davis Company. Philadelphia:
1989. pp. 767-770.

Marieb, Elaine N. Essentials of Human Anatomy and Physiology 7th edition. San Francisco:
Pearson Education Inc.. 2003. pp. 433-436

Lippincott W. Nursing 2003 Drug Handbook 23rd edition. Schilling McCann Philadelphia: 2003.
pp. 101-102, 341-343, 355-356, 116.

Skidmore-Roth. Mosby’s Nursing Drug Reference. Philadelphia: Lippicott Williams and Wilkins.
2003. pp. 235-241, 25,222.

Internet:

DHF. Available: http://en.wikipedia.org/wiki/Dengue_fever [August 4, 2007]

Dengue Fever. Available: http://www.who.int/mediacentre/factsheets/fs117/en/ [August

6,2007]

Dengue. Available: http://training.seer.cancer.gov/module_abstracting/unit03_sec02_

part06_page04_blood_values.html [August 13, 2007]

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