I.

Introduction

Background & History

The origins of the word are not clear, but one theory is that it is derived from the Swahili
phrase "Ka-dinga pepo", which describes the disease as being caused by an evil spirit.The
Swahili word "dinga" may possibly have its origin in the Spanish word "dengue"
(fastidious or careful), describing the gait of a person suffering dengue fever, or,
alternatively, the Spanish word may derive from the Swahili.

Dengue, the most common arboviral illness transmitted worldwide, is caused by infection
with 1 of the 4 serotypes of dengue virus. Dengue is transmitted by mosquitoes of the
genus Aedes, which are widely distributed in subtropical and tropical areas of the world,
and is classified as a major global health threat by the World Health Organization
(WHO).

Initial dengue infection may be asymptomatic, may result in a nonspecific febrile illness,
or may produce the symptom complex of classic dengue fever (DF). A small percentage
of persons who have previously been infected by one dengue serotype develop bleeding
and endothelial leak upon infection with another dengue serotype. This syndrome is
termed dengue hemorrhagic fever (DHF). Some patients with dengue hemorrhagic fever
develop shock (dengue shock syndrome [DSS]), which may cause death.

Dengue virus transmission follows two general patterns—epidemic dengue and

hyperendemic dengue. Epidemic dengue transmission occurs when dengue virus is
introduced into a region as an isolated event that involves a single viral strain. If the
number of vectors and susceptible pediatric and adult hosts is sufficient, explosive
transmission can occur, with an infection incidence of 25-50%. Mosquito-control efforts,
changes in weather, and herd immunity contribute to the control of these epidemics. This
is the current pattern of transmission in parts of Africa and South America, areas of Asia
where the virus has reemerged, and small island nations. Travelers to these areas are at
increased risk of acquiring dengue during these periods of epidemic transmission.

Hyperendemic dengue transmission is characterized by the continuous circulation of

multiple viral serotypes in an area where a large pool of susceptible hosts and a
competent vector (with or without seasonal variation) are constantly present. This is the
predominant pattern of global transmission. In these populations, antibody prevalence
increases with age and most adults are immune. Hyperendemic transmission appears to
be a major risk for dengue hemorrhagic fever. Travelers to these areas are more likely to
be infected than are travelers to areas that experience only epidemic transmission.

Dengue fever–like illnesses were described in Chinese medical writings dating back to
265 AD. Outbreaks of febrile illnesses compatible with dengue fever have been recorded
throughout history. In 1789, Benjamin Rush, MD, published an account of a probable
dengue fever epidemic that had occurred in Philadelphia in 1780. Rush coined the term
breakbone fever to describe the intense symptoms reported by one of his patients.
Probable outbreaks of dengue fever occurred sporadically every 10-30 years until after
World War II. The socioeconomic disruptions caused by World War II resulted in
increased worldwide spread of dengue viruses.

The first epidemic of dengue hemorrhagic fever was described in Manila in 1953. After
that, outbreaks of dengue fever became more common. A pattern developed in which
dengue fever epidemics occurred with increasing frequency and were associated with
occasional dengue hemorrhagic fever cases. Subsequently, dengue hemorrhagic fever
epidemics occurred every few years. Eventually, dengue hemorrhagic fever epidemics
occurred yearly, with major outbreaks occurring approximately every 3 years. This
pattern has repeated itself as dengue fever has spread to new regions.

Although initial epidemics were located in urban areas, increased dengue spread has
involved suburban and rural locales in Asia and Latin America. The only continents that
do not experience dengue transmission include Europe and Antarctica. In the 1950s, 9
countries reported dengue outbreaks; today, the geographic distribution includes more
than 100 countries worldwide. Several of these countries had not previously reported
dengue, and many had not reported dengue in 20 years.

Dengue transmission spread from Southeast Asia into surrounding subtropical and
tropical Asian countries, southern China and southern Taiwan, the Indian subcontinent
and Sri Lanka, and down the island nations of Malaysia, the Philippines, New Guinea,
northeastern Australia, and several Pacific islands, including Tahiti, Palau, Tonga, and
the Cook Islands. Nepal has not reported dengue transmission. Hyperendemic
transmission is reported in Vietnam, Thailand, Indonesia, Pakistan, India, Malaysia, and
the Philippines.

Currently, dengue hemorrhagic fever is one of the leading causes of hospitalization and
death in children in many Southeast Asian countries, with Indonesia reporting the
majority of dengue hemorrhagic fever cases. Of interest and significance in prevention
and control, 3 surveillance studies in Asia report an increasing age among infected
patients and increasing mortality rate. Since 1982 in Singapore, more than 50% of deaths
have occurred in individuals older than 15 years. In Indonesia, young adults in Jakarta
and provincial areas make up a larger percentage of infected patients. During the 2000
epidemic in Bangladesh, up to 82% of hospitalized patients were adults, and all deaths
occurred in patients older than 5 years.

The epidemiology of dengue fever in Africa is more poorly characterized. Aedes aegypti
is present in a large portion of the Middle East and sub-Saharan Africa. Dengue fever is
present in 19 countries on the African continent. In a 1993 epidemic in the Comoros, an
estimated 60,000 persons were infected with dengue. Of note, no major dengue
hemorrhagic fever epidemics have occurred in Africa, despite the fact that all 4 dengue
serotypes circulate in the continent. This may be explained by a genetic factor in these
populations.
In the Americas, dengue epidemics were rare postwar because Aedes mosquitoes had
been eradicated from most of the region through coordinated vector-control efforts.
Systematic spraying was halted in the early 1970s because of environmental concerns. By
the 1990s, A aegypti mosquitoes repopulated most of the countries in which they had
been eliminated.

The first dengue hemorrhagic fever epidemic in the Americas occurred in Cuba in 1981,
with 24,000 cases of dengue hemorrhagic fever, 10,000 cases of dengue shock syndrome,
and 158 reported deaths. Since then, dengue fever and dengue hemorrhagic fever cases
have progressively increased. A aegypti is abundant year-round in most countries in the
Caribbean basin. Significant outbreaks of dengue have been reported in 2005 and 2006 in
Puerto Rico, the US Virgin Islands, the Dominican Republic, Barbados, Curacao, Cuba,
Guadeloupe, and Martinique.

Aedes albopictus, originally from Asia, is now found in limited areas of Brazil, Bolivia,
Colombia, the Dominican Republic, El Salvador, Guatemala, Honduras, Mexico, Cuba,
and the Cayman Islands. A aegypti is present in all countries in South America except
Chile. Hyperendemic circulation of all 4 dengue serotypes is present in the northern
countries of South America. Brazil (700,000 cases in 2002), Colombia, and Venezuela
report the most cases of dengue and dengue hemorrhagic fever, with low-level
transmission occurring year-round but with most occurring during periods of epidemic
transmission.

In 1986, the first clearly identified local transmission of dengue in the United States
occurred in Texas. Carriers of the virus were believed to have crossed the border from
Mexico; the local vector population was then infected. Since then, seasonal
autochthonous infection has been reported in both Texas and Hawaii.

Two competent vectors, A aegypti and A albopictus, are currently seasonally abundant in
some areas of the southwestern and southeastern United States, including Texas, Arizona,
New Mexico, Louisiana, Mississippi, Alabama, Georgia, and mid to south Florida. A
aegypti has also been reported sporadically in portions of North Carolina, South Carolina,
Tennessee, Arkansas, Maryland, and New Jersey. The range of A albopictus extends
almost as far north as the Great Lakes. Since many cases of dengue in US citizens occur
as a result of endemic transmission in some US territories, the Centers for Disease
Control and Prevention (CDC) currently conducts laboratory-based surveillance in Puerto
Rico.

Dengue fever does not naturally occur in the European Union and in continental
Europe because these areas do not have an appropriate vector population to allow further
spread of dengue from viremic patients returning from other countries. As such, the
disease is not statutorily notifiable in most member states. However, dengue does occur
in several overseas territories of European Union members. In recent decades, reports of
dengue infections in long-term expatriates, aid workers, military personnel, immigrants,
and travelers returning from the tropics and subtropics have been increasing.
Factors believed to be responsible for dengue's spread include explosive population
growth, unplanned urban overpopulation with inadequate public health systems, poor
standing water and vector control, climate change (increased virus transmission has been
associated with El Niño conditions), and increased international recreational, business,
and military travel to endemic areas. All of these factors must be addressed to control the
spread of dengue and other mosquito-borne infections.

II. Frequency

International

An estimated 2.5-3 billion people in approximately 110 countries worldwide are at risk
for dengue infection. Yearly, approximately 100 million people are infected with dengue,
and 250,000 individuals develop dengue hemorrhagic fever. Annually, approximately
24,000 deaths are attributed to dengue worldwide. The Pan American Health
Organization (PAHO) member states reported twice as many cases of dengue fever and
dengue hemorrhagic fever in 1998 as they did in 1997.

A recent 5-year prospective study in Thai children examined the relative economic
burden of dengue infection in children on the local population.4 Most disability-adjusted
life years (DALYs) lost to dengue resulted from long-duration illness in children who had
not been hospitalized. The infecting serotype appeared to be a determining factor of
DALYs lost, with DENV-2 and DENV-3 responsible for 30% and 29%, respectively.
The mean cost of illness from dengue was significantly higher than that from other febrile
illnesses.

Mortality/Morbidity

• Recovery from dengue infection is usually complete. Even patients who meet
strict criteria for dengue hemorrhagic fever or dengue shock syndrome usually
recover without sequelae.
• The fatality rate associated with dengue shock syndrome varies by country from
12-44%. In a 1997 Cuban epidemic, the fatality rate in patients who met criteria
for dengue hemorrhagic fever or dengue shock syndrome was approximately 6%.
The mortality rate associated with dengue fever is less than 1%.
• Data from the 1997 Cuban epidemic suggests that, for every clinically apparent
case of dengue fever, 13.9 cases of dengue infection went unrecognized because
of absent or minimal symptoms.
• Factors that affect disease severity include patient age, nutritional status,
ethnicity, the sequence of infection with different dengue serotypes, virus
genotype, and the quality and extent of available medical care.

Race

• Dengue affects all races. Some African and Haitian data demonstrate a relative
dearth of dengue hemorrhagic fever and dengue shock syndrome during dengue
 fever epidemics, suggesting that these populations may share a genetic advantage
to the virus. This merits further study.

Sex

• Dengue viruses affect both sexes.Age

• Dengue affects people of all ages. In Southeast Asia, where dengue is

hyperendemic, dengue hemorrhagic fever usually affects children younger than 15
years. However, in the Americas, where dengue is becoming progressively
hyperendemic, dengue hemorrhagic fever shows no age predilection.
 III.ANATOMY AND PHYSIOLOGY

Functions of Blood:

1 - Transportation:

o oxygen & carbon dioxide

o nutrients
o waste products (metabolic wastes, excessive water, & ions)

2 - Regulation - hormones & heat (to regulate body temperature)

3 - Protection - clotting mechanism protects against blood loss & leucocytes

provide immunity against many disease-causing agents

Components of Blood - average adult has about 5 liters:

1. Formed elements:

o Red blood cells (or erythrocytes)

o White blood cells (or leucocytes)
o Platelets (or thrombocytes)

2. Plasma = water + dissolved solutes

Red Blood Cells (or erythrocytes):

1 - biconcave discs

2 - lack a nucleus & cannot reproduce (average lifespan = about 120 days)

3 - transport hemoglobin (each RBC has about 280 million hemoglobin

molecules)

4 - Typical concentration is 4-6 million per cubic mm (or hematocrit [packed cell
volume] of about 42% for females & 45% for males)

5 - contain carbonic anhydrase (critical for transport of carbon dioxide)

 Determining the hematocrit

Erythropoiesis = formation of erythrocytes

• the body must produce about 2.5 million new RBCs every second
• in adults, erythropoiesis occurs mainly in the marrow of the sternum, ribs,
vertebral processes, and skull bones
• begins with a cell called a hemocytoblast or stem cell (below)
• rate is regulated by oxygen levels:

o hypoxia (lower than normal oxygen levels) is detected by cells in the

kidneys
o kidney cells release the hormone erythropoietin into the blood
o erythropoietin stimulates erythropoiesis by the bone marrow
Hemoglobin

• composed of globin (made up of 4 highly folded polypeptide chains) + 4 heme

groups (with iron)
• each molecule can carry 4 molecules of oxygen
• called oxyhemoglobin when carrying oxygen & called reduced hemoglobin when
not carrying oxygen
• can also combine with carbon dioxide & helps transport carbon dioxide from the
tissues to the lungs

White blood cells (or leucocytes or leukocytes):

• have nuclei & do not contain hemoglobin

• typical concentration is 5,000 - 9,000 per cubic millimeter
• types of WBCs:
o granular white blood cells include:
 neutrophils (50 - 70% of WBCs)
 eosinophils (1 - 4%)
 basophils (less than 1%)
o agranular (or non-granular) white blood cells include:
 lymphocytes (25 - 40%)
 monocytes (2 - 8%)

Granular white blood cells contains numerous granules in the cytoplasm, & their nuclei
are lobed. Agranular white blood cells have few or no granules in the cytoplasm & have a
large spherical nucleus. Granular white blood cells are produced in the bone marrow,
while agranular white blood cells are produced in lymph tissue, e.g., Lymph nodes
(specialized dilations of lymphatic tissue which are supported within by a meshwork of
connective tissue called reticulin fibers and are populated by dense aggregates of
lymphocytes and macrophages).

The primary functions of the various white blood cells are:

• Neutrophils - phagocytosis (bacteria & cellular debris); very important in

inflammation
• Eosinophils - help break down blood clots & kill parasites
• Basophils - synthesize & store histamine (a substance released during
inflammation) & heparin (an anticoagulant); functions(s) remain unclear
• Monocytes - phagocytosis (typically as macrophages in tissues of the liver,
spleen, lungs, & lymph nodes)
• Lymphocytes - immune response (including production of antibodies)
Some important characteristics of White Blood Cells (particularly neutrophils):

1 - phagocytic

2 - capable of diapedesis (also called extravasation)

3 - capable of ameboid movement

4 - exhibit chemotaxis (attracted to certain chemicals, such as those released by

damaged cells)

Platelets (or thrombocytes)

1 - formed in the bone marrow from cells called megakaryocytes

2 - have no nucleus, but can secrete a variety of substances & can also contract
(because they contain actin & myosin)

3 - normal concentration in the blood is about 250,000 per cubic millimeter

4 - remain functional for about 7 - 10 days (after which they are removed from the
blood by macrophages in the spleen & liver)

5- play an important role in hemostasis (preventing blood loss)

Plasma:

1 - Water - serves as transport medium; carries heat

2 - Proteins

• Albumins
o 60-80% of plasma proteins
o most important in maintenance of osmotic balance
o produced by liver
• Globulins
o alpha & beta
 some are important for transport of materials through the blood
(e.g., thyroid hormone & iron)
 some are clotting factors
 produced by liver
o gamma globulins are immunoglobulins (antibodies) produced by
lymphocytes
• Fibrinogen
o important in clotting
o produced by liver
3 - Inorganic constituents (1% of plasma) - e.g., sodium, chloride, potassium, & calcium

4 - Nutrients - glucose, amino acids, lipids & vitamins

5 - Waste products - e.g., nitrogenous wastes like urea

6 - Dissolved gases - oxygen & carbon dioxide

7 - Hormones

Hemostasis - prevention of blood loss from broken vessel:

1 - Vascular spasm - vasoconstriction of injured vessel due to contraction of smooth

muscle in the wall of the vessel. This 'spasm' may reduce blood flow & blood loss but
will not stop blood loss.

2 - Formation of a platelet plug - platelets aggregate at the point where a vessel ruptures.
This occurs because platelets are exposed to collagen (a protein found in the connective
tissure located just outside the blood vessel). Upon exposure to collagen, platelets release
ADP (adenosine diphosphate) & thromboxane. These substances cause the surfaces of
nearby platelets to become sticky and, as 'sticky' platelets accumulate, a 'plug' forms.

3 - Blood coagulation (clotting):

The result of all of this is a clot - formed primarily of fibrin threads (or polymers), but
also including blood cells & platelets.

Blood clots in the right places prevent the loss of blood from ruptured vessels, but in the
wrong place can cause problems such as a stroke (see below under inappropriate
clotting).

Clot retraction:

• "tightening" of clot
• contraction of platelets trapped within clot shrinks fibrin meshwork, pulling edges
of damaged vessel closer together. Over time (with the amount of time depending
on the amount of damage), the clot is dissolved and replaced with normal tissue.

Fibrinolysis:

• dissolution of clot
• mechanism = plasminogen (a plasma protein) is activated by many factors &
becomes PLASMIN. Plasmin then breaks down fibrin meshwork & phagocytic
WBCs remove products of clot dissolution
• Human Habitation
 IV. Pathophysiology

Environmental Factor Human Habitation

Bite of female
Aedes Aegypti

Replication of virus in the

dendrite cells

Immune mediators that serve

to share the quantity, type and
duration of cellular and
normal immune response to
both the initial and subsequent
virus infection

Thrombocytopenia Capillary fragility

Increase Capillary Permeability

Plasma
Hemoconcentrationn Petichial
Leakag
rash
e

Skin hemorrhage

Bleeding
 V. Patient’s Profile

Client’s Name or Initial: Mrs. A

Age: 21 years old
Sex: Female
Marital Status: Married
Religion: Catholic
Address: Phase1 blk.9 lot3 Francisco Homes San Jose Del Monte Bulacan
Birth Date and place of birth: April 27, 1987, Manila
Race/Nationality: Filipino
Usual Source of Medical Care: Health Center
Source and Reliability of Information: Patient

Reason for Seeking Care

1. Fever
2. Headache
3. Severe Vomiting
4. Body Rashes

Past Medical History

i. Pediatric/Childhood/Adult Illness:
Cough, Colds, Fever

ii. Injuries or accidents:

None

iii. Hospitalizations and operations:

None

iv. Obstetric History (for female clients only):

G1P1 Menarche at 13 years old

v. Immunization

BCG: /√/ at birth /√/ School Entrance

DPT: /x/ 1st dose /x/2nd dose /x/3rd dose
OPV: /x/ 1st dose /x/ 2nd dose /x/ 3rd dose
AMV: /x/
TT: /√/ 1st dose /√/ 2nd dose /√/ 3rd dose /√/ 4th dose /√/ 5th dose
Hepatitis B Vaccine: /x/ 1st dose /x/ 2nd dose /x/ 3rd dose /x/ 4th dose
 vi. Allergies

Food (specify): none

Drugs (specify): none
Chemicals (specify): none
Environmental Allergens (specify): none

Data Base
Two days prior to admission fever is on & off. A few hours prior to admission
patient develops vomiting 6x accompanied by poor appetite and body weakness.

Physical Assessment

V/S Gen.Survey : weak looking, ambulatory

BP: 90/60 HEENT: dry lips
Temp: 38.5 degree Celsius Lungs: clear breath sounds
RR: 23cpm Abdomen: soft, flat, slight epigastric
tenderness
PR: 100bpm Extremities: body rashes are present

Course in the Ward

The patient usually play with her cellphone & talks to her mother frequently. She
does not sleep often. She is ambulatory and can use the bathroom independently. She’s
usual elimination pattern is U=5x/day S=1x/day.

VI. Laboratory

Hematology

Hematology (American English) or haematology (British English) is the branch

of biology (physiology), pathology, clinical laboratory, internal medicine, and pediatrics
that is concerned with the study of blood, the blood-forming organs, and blood diseases.
Haematology includes the study of etiology, diagnosis, treatment, prognosis, and
prevention of blood diseases. The lab work that goes into the study of blood is performed
by a Medical Technologist.
Laboratory Result Prior to Admission (Oct. 4, 08)
VALUE UNITS NORMAL VALUE
WBC 6.20 10^g/l 5-10
RBC 4.09 10^12/uL 4.2-5.4
Hemoglobin 122 g/l 120-160
Hematocrit 0.37 0.37-0.47
Platelet 210x100 /mm3 140-340x100
Lymphocyte 0.47 0.20-0.40
Segmenters 0.53 0.50-0.70

Laboratory Result from Oct.4 to Oct.6

10/4 6pm 10/5 6am 10/5 6pm 10/6 6:20am
WBC
RBC
Hemoglobin 121 123 110 103
Hematocrit 0.36 0.37 0.33 0.31
Platelet 198x100 162x100 124x100 118x100
Lymphocyte
Segmenters

WBC- Normal

RBC-Normal

Hemoglobin- (10/5)
Decrease indicates hemorrhage

Hematocrit-(10/4 6pm), (10/5 6pm)

Decrease indicates hemorrhage

Platelet- (10/5 6pm)

Decrease indicates DIC, hemorrhage

Lymphocytes-(10/4 upon admission)

Increase indicates infection
 VII. Drug Study

Paracetamol (500mg/tab q 4 hours for fever)

Name of Action Indication Side effect Pharmacokinetics Nursing

Drug considertion

Paracetamol Inhibits Mild Pain. Hepatic Absorption: Well Assess overall

the Fever. failure, absorbed following oral health status and
synhesis hepatotoxic administration. Rectal alcohol usage
of Contraindic ity, renal absorption is variable. before
prostagl ation failure, Distribution: widely administration.
andin Previous neutropenia distributed. Crosses the
that may hypersensiti , placenta; enters breast Administer with
serve as vity. pancytopen milk in low food or an empty
mediator Products ia, concentrations. stomach.
s of pain containing leucopenia, Metabolism and
and alcohol, rash, excretion: 85%-95% Advise patient to
fever, aspartame, urticuria metabolized by the liver. avoid alcohol if
primaril saccharin Metabolites may be toxic taking this drug
y in the sugar, ot in overdose situation.
CNS. tartrazine Metabolites excreted by Avoid taking
Has no should be the kidneys. concurrently with
significa avoided. Half-Life: Neonates: 2- salicylates or
nt anti- 5hr; Adults: 1-3hr NSAIDs for more
inflamm than a few days,
atory Pharmacodynamics unless directed.
properti
es or GI rout ons pea dur Advise patient to
toxicity e et k atio consult physician
n if discomfort or
PO 0.5- 1- 3- fever is not
1hr 3hr 8hr relieved of routine
doses or if fever is
Rec 0.5- greater than 39.5C
t 1hr 1- 3- or lasts longer
3hr 4hr than 3 days.
Our Lady of Fatima University
Quezon City

A
Case Study
About
DENGUE

Prepared By:

Mariano, Efren (Leader)

Tano, John Leomar
Mostoles, Kleir Ann
Ravancho, Moonyeen

October 2008
 Table of Contents

I. Introduction

II. Frequency

III. Anatomy and Physiology

IV. Pathophysiology

V. Patients Profile

VI. Laboratory

VII. Drug Study

VIII. NCP

IX. Discharge Plan

 VIII. NCP

Subjective Nursing Dx Analysis Planning Implementation Rationale Evaluation

>”dalawang Increased Hypothalamus After 1 >Monitor core >For temperature After 1 hour of
araw na body temp. which controls hour of temp. assessment if change nursing intervention
akong r/t the bodys nursing >Monitor >To assess client the patient
nilalagnat inflammatory thermoregulation intervention BP,PR,RR stability temperature had been
at itoy process releases heat due the patient >Thermoregulation >To regulate body decreased.
pabalik- to the presence temp will temp. back into normal
balik” as of infection decrease. >Render TSB/ >To decrease temp
verbalize. warm bath
>Promote bedrest >To promote wellness
Objective: >Provide comfort >To reduce anxiety
>dry lips >Administer >To decrease temp
>pale color medication as
>weak prescribe
looking
>temp. of
38.5 degree
celcius
NCP

Subjective Nursing Analysis Planning Implementatio Rationale Evalution

Dx n
>”Anim na >Vomiting >G.I >After 1hr. >Encourage >To back flow >After 1hr.of
beses na r/t gastric irritation of nursing reverse the vomitous nursing
akong distention in intervention T-position intervention the
nagsusuka” response the filling of>Bed rest >To promote feeling of the
as verbalize. to the vomiting of comfort patient had been
presence the patient >Water therapy >To minimize decreased &
of blood will decrease the risk of patient had been
Objective: in the & the patient dehydration at comfort
>Weak G.I.T will be at >promote clean >for relaxation
looking comfort environment
>Dry lips
>Pale color
 IX. Discharge Planning

The discharge plan includes health teaching about Dengue Hemorrhagic Fever, its risk
factors, management and some complications of the condition if not managed or not
treated well, and methods of prevention and control.

As part of the plan, the patient the patient is advised to:

1. Report any signs and symptoms of DHF such as high fever, abdominal pain and
headache.
- early detection of signs and symptoms of the disease may decrease risk of
DHF’s complications

2. Clean environment:
- elimination of stagnant water
- cover water containers
- dispose old used tires
- clean water drainage
- proper disposal of garbage

3. Used insect propellant.

4. Avoid too many hanging clothes inside the house.

5. Drink adequate fluids at least eight glasses a day.

- may drink fruit juices such as calamansi juices for Vitamin C
supplementation

6. Eat foods rich in vitamins and minerals.

7. Use soft bristle toothbrush.

8. Report reoccurrence of fever and signs of bleeding to physician immediately.

.