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PAPER OF
ENGLISH NURSING
“DENGUE HAEMORRHAGIC FEVER”
Created by:
Group 10
AndriFibriyanto (11.11011037)
BagusAdiSaputera (11.11011039)
FirjonSepartagusWalHabby (11.11011047)
KhoirulHidayat (11.11011050)
S1 NURSING STUDY PROGRAM
FACULTY OF HEALTH SCIENCE
UNIVERSITY OF MUHAMMADIYAH JEMBER
2012
PREFACE
Thanks to God that we have completed this paper entitled “DENGUE
HAEMORRHAGIC FEVER”, to fulfill the project of English Nursing subject. We
would like to express our gratitude to all those who have given us the possibility to
complete this paper. We want to thank to Mr. Sigit, M.Kep the lecturer of S1 Nursing
Study Faculty of Health Science University of MuhammadiyahJember. We also
would like to thank to all of our friends in S1 Nursing Study Faculty of Health
Science University of MuhammadiyahJember for giving us supports and encourage
us to finish this paper.
We realized that this paper far from perfectness, so we apologize and we
really appreciate and welcome any constructive criticisms and suggestions to improve
this paper.
Jember, June 2012
CONTENT
The development of aexample of assessment steps developed from the nursing
process which includes:
1. Assessment - collection of patient data
2. Determining the Nursing Diagnosis with identification of nursing diagnoses,
goals and outcomes
3. Planning – Actually putting together and writing the care plan (include
interventions)
4. Implementation - putting the Care plan into action
5. Evaluation – How will you evaluate it and ensure it is periodically updated
DENGUE HAEMORRHAGIC FEVER (DHF)
Dengue fever and dengue hemorrhagic fever (DHF) are acute febrile diseases,
that occurs in the tropics. 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 Aedesaegypti (rarely
Aedesalbopictus) mosquito, which feeds during the day.
The first epidemics occurred almost simultaneously in Asia, Africa, and North
America in the 1780s. The disease was identified and named in 1779. A global
pandemic began in Southeast Asia in the 1950s and by 1975 DHF had become a
leading cause of death among children in many countries in that region. Epidemic
dengue has become more common since the 1980s – by the late 1990s, dengue was
the most important mosquito-borne disease affecting humans after malaria, there
being around 40 million cases of dengue fever and several hundred thousand cases of
dengue hemorrhagic fever each year. There was a serious outbreak in Rio de Janeiro
in February, 2002 affecting around one million people and killing sixteen.
Significant outbreaks of dengue fever tend to occur every five or six years.
There tend to remain large numbers of susceptible people in the population despite
previous outbreaks because there are four different strains of the dengue virus and
because of new susceptible individuals entering the target population, either through
childbirth or immigration.
There is significant evidence, originally suggested by S.B. Halstead in the
1970s, that dengue hemorrhagic fever is more likely to occur in patients who have
secondary infections by serotypes different from the primary infection. One model to
explain this process is known as antibody-dependent enhancement (ADE), which
allows for increased uptake and virion replication during a secondary infection with a
different strain. Through an immunological phenomena, known as original antigenic
sin, the immune system is not able to adequately respond to the stronger infection,
and the secondary infection becomes far more serious. This process is also known as
superinfection.
1. Signs and Symptoms
This infectious disease is manifested by a sudden onset of fever, with severe
headache, muscle and joint pains (myalgias and arthralgias – severe pain gives it the
name break-bone fever or bonecrusher disease) 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.
Some cases develop much milder symptoms which can, when no rash is
present, be misdiagnosed as influenza or other viral infection. Thus travelers from
tropical areas may inadvertently pass on dengue in their home countries, having not
been properly diagnosed at the height of their illness. Patients with dengue can only
pass on the infection through mosquitoes or blood products while they are still
febrile.
The classic dengue fever lasts about six to seven days, with a smaller peak of
fever at the trailing end of the fever (the so-called “biphasic pattern”). Clinically, the
platelet count will drop until the patient’s temperature is normal.
Cases of DHF also show higher fever, hemorrhagic phenomena,
thrombocytopenia, and hemoconcentration. A small proportion of cases lead to
dengue shock syndrome (DSS) which has a high mortality rate.
Conclusion symptomsof dengue haemorrhagic fever:
Fever within 5 to 6 days after you have been bitten by an infected mosquito
High fever, up to 105 degrees Fahrenheit
Severe headache
Retro-orbital (behind the eye) pain
Severe joint and muscle pain
Nausea and vomiting
Rash
2. Causative Agent
Arthropod-borne virus belonging to the family Flaviviridae. There are four
known serotypes: DEN-1, DEN-2, DEN-3, and DEN-4.
Mode of Transmission is Aedesaegypti
The viruses are transmitted via the bite of various day-feeding mosquitoes of
the subgenus Stegomyia. The principal vector is Aedesaegypti. Once infected, a
mosquito remains infective for life. Infected humans circulate the virus in their blood,
mosquitoes ingest viruses when feeding on the infective individual. Humans serve as
an amplifying host, though some monkeys may also serve as a source of the virus.
Female mosquitoes can also transmit the virus transovarially, passing it down to the
next generation.
3. Diagnosis
The diagnosis of dengue is usually made clinically. The classic picture is high
fever with no localizing source of infection, a petechial rash with thrombocytopenia
and relativeleukopenia.
There exists a WHO definition of dengue hemorrhagic fever that has been in
use since 1975; all four criteria must be fulfilled:
a. Fever
Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from
mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea).
Thrombocytopenia (<100,000 platelets per mm³ or estimated as less than 3 platelets
per high power field).
Evidence of plasma leakage (hematocrit more than 20% higher than expected, or drop
in hematocrit of 20% or more from baseline following IV fluid, pleural effusion,
ascites, hypoproteinemia).
b. Encephalitic occurrences
Dengue shock syndrome is defined as dengue hemorrhagic fever plus:
Weak rapid pulse
Narrow pulse pressure (less than 20 mm Hg)
Cold, clammy skin and restlessness
Dependable, immediate diagnosis of dengue can be performed in rural areas by the
use of Rapid Diagnostic Test kits, which also differentiate between primary and
secondary dengue infections. Serology and polymerase chain reaction (PCR) studies
are available to confirm the diagnosis of dengue if clinically indicated.
4. Incubation Period
The incubation period of dengue fever is approximately four days.
5. Pathogenesis/Pathophysiology
Dengue infection is caused by 1 of 4 related, but antigenically distinct, viral
serotypes: dengue virus 1 (DENV-1), dengue virus 2 (DENV-2), dengue virus 3
(DENV-3), and dengue virus 4 (DENV-4). Albert Sabin speciated these in 1944.
Each serotype is known to have several different genotypes. Dengue viruses are
small, spherical, single-stranded enveloped RNA viruses of the family Flaviviridae,
genus Flavivirus.
Infection with one dengue serotype confers lifelong homotypic immunity and
a very brief period of partial heterotypic immunity, but each individual can eventually
be infected by all 4 serotypes. Several serotypes can be in circulation during an
epidemic.
Dengue viruses are transmitted by the bite of an infected Aedes mosquito.
Globally, aaegypti is the predominant highly efficient mosquito vector for dengue
infection, but Aalbopictus and other Aedes species can also transmit dengue with
varying degrees of efficiency.
Aedes mosquito species have adapted well to human habitation, often
breeding around dwellings in small amounts of stagnant water found in old tires or
other small containers discarded by humans. Female Aedes mosquitoes are daytime
feeders. They inflict an innocuous bite and are easily disturbed during a blood meal,
causing them to move on to finish a meal on another individual, making them
efficient vectors. Entire families who develop infection within a 24- to 36-hour
period, presumably from the bites of a single infected vector, is not unusual.
Humans serve as the primary reservoir for dengue; however, certain
nonhuman primates in Africa and Asia also serve as hosts. Mosquitoes acquire the
virus when they feed on a carrier of the virus. The mosquito can transmit dengue if it
immediately bites another host. In addition, transmission occurs after 8-12 days of
viral replication in the mosquito’s salivary glands (extrinsic incubation period). The
mosquito remains infected for the remainder of its 15- to 65-day lifespan. Vertical
transmission of dengue virus in mosquitoes has been documented. The eggs of Aedes
mosquitoes withstand long periods of desiccation, reportedly as long as 1 year, but
are killed by temperatures of less than 10°C.
Once inoculated into a human host, dengue has an incubation period of 3-14
days (average 4-7 d). Following incubation, a 5- to 7-day acute febrile illness ensues.
Recovery is usually complete by 7-10 days. DHF or DSS usually develops around the
third to seventh day of illness, approximately at the time of defervescence. The major
pathophysiological abnormalities that occur in DHF and DSS are plasma leakage and
bleeding. Plasma leakage is caused by increased capillary permeability and may be
manifested by hemoconcentration, as well as pleural effusion and ascites. Bleeding is
caused by capillary fragility and thrombocytopenia and may present various ways,
ranging from petechial skin hemorrhages to life-threatening gastrointestinal bleeding.
Most patients who develop DHF or DSS have had prior infection with one or
more dengue serotypes. In individuals with low levels of neutralizing antibodies,
nonneutralizing antibodies to one dengue serotype, when bound by macrophage and
monocyte Fc receptors, have been proposed to result in increased viral entry and
replication, and increased cytokine production and complement activation. This
phenomenon is called antibody-dependent enhancement. In addition, certain dengue
strains, particularly those of DEN-2, have been proposed to be more virulent, in part
because more epidemics of DHF have been associated with DEN-2 than with the
other serotypes.
6. Prevention
a. Vaccine development
There is no commercially available vaccine for the dengue flavivirus.
However, one of the many ongoing vaccine development programs is the Pediatric
Dengue Vaccine Initiative which was set up in 2003 with the aim of accelerating the
development and introduction of dengue vaccine(s) that are affordable and accessible
to poor children in endemic countries. Thai researchers are testing a dengue fever
vaccine on 3,000-5,000 human volunteers within the next three years after having
successfully conducted tests on animals and a small group of human volunteers. And,
a number of other vaccine candidates are entering phase I or II testing.
b. Mosquito control
Primary prevention of dengue mainly resides in eliminating or reducing the
mosquito vector for dengue. Public spraying for mosquitoes is the most important
aspect of this vector. Application of larvicides such as Abate® to standing water is
more effective in the long term control of mosquitoes. Initiatives to eradicate pools of
standing water (such as in flowerpots) have proven useful in controlling mosquito-
borne diseases. Promising new techniques have been recently reported from Oxford
University on rendering the Aedes mosquito pest sterile. US and British researchers
have also genetically engineered a strain of flightless mosquito that may help curb the
spread of Dengue fever.
Recently, researchers at the Federal University of Minas Gerais, in Brazil,
have developed a world-awarded new technology to monitor and control the
mosquito, using traps, chemical attractants, handheld computers and GPS
georeferenced maps. The MI Dengue system can show precisely where the
mosquitoes are inside the urban area, in a very short period of time.
c. Personal protection
Personal prevention consists of the use of mosquito nets, repellents containing
NNDB or DEET ((N,N-Diethyl-meta-toluamide; also known as N,N’-Diethyl-3-
methylbenzamide), covering exposed skin, use of DEET-impregnated bednets, and
avoiding endemic areas.
7. Treatment
The mainstay of treatment is supportive therapy. Increased oral fluid intake is
recommended to prevent dehydration. Supplementation with intravenous fluids may
be necessary to prevent dehydration and significant hemoconcentration if the patient
is unable to maintain oral intake. A platelet transfusion is indicated in rare cases 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 though in this case
they may actually aggravate the bleeding tendency associated with some of these
infections. Patients should instead receive acetaminophen preparations to deal with
these symptoms if dengue is suspected.Having a strong immune system also benefits
recovery from dengue.
8. Complications
Neurologic manifestations such as seizures and encephalitis/encephalopathy
have been reported in rare cases of dengue infection. Some of these cases did not
manifest other typical features of dengue infection. Other neurological complications
associated with dengue infection include neuropathies, Guillain-Barré syndrome, and
transverse myelitis.
Liver failure has been associated with DHF/DSS epidemics. Whether this is a
viral effect or a product of prolonged liver hypoperfusion remains
unclear.Overhydration is a well-recognized complication of DF and DHF/DSS.
NURSING MANAGEMENT FOR DENGUE HEMORRHAGIC FEVER (DHF)
1. Definition
Dengue is a tropical virus disease transmitted by mosquitoes and
characterized by fever, headache, pain in the limbs, and rash (Brooker,
2001).Dengue fever is a disease primarily in children, adolescents, or adults, with
clinical signs of fever, sore muscles, or joints accompanied by leukopenia, with /
without rash (rash) and lymphadenopathy, biphasic fever, severe headache, pain on
the movement of the eyeball, taste menyecap impaired, mild thrombocytopenia, and
bleeding spots (ptekie) spontaneous (Noer, et al, 1999).Dengue hemorrhagic fever is
a disease caused by dengue viruses (arboviruses) that enters the body through the
bite of the mosquito Aedesaegypti (Suriadi&Yuliani, 2001).
2. Pathophysiology
Dengue virus enters the body through the bite of aedesaegypti mosquito and
then reacted with the antibody and virus-antibody complexes formed in circulation
will activate the complement system (Suriadi&Yuliani, 2001).Dengue virus enters
the body through mosquito bites and infection first causes dengue fever. Body
reaction is a reaction commonly seen in infections by viruses. A very different
reaction would seem, when someone gets repeated infections with different dengue
virus types. And DHF can occur when a person is infected after the first time, got the
other dengue virus infection recurs. Re-infection will cause an anamnestic antibody
reaction, giving rise to the concentration of antigen-antibody complex (virus-
antibody complexes) is high (Noer, et al, 1999).
A. Nursing Assessment of Dengue Hemorrhagic Fever (DHF)
1. Identity
Dengue Hemorrhagic Fever (DHF) is a tropical disease that often causes the
death of children, adolescents and adults (Effendy, 1995).
2. Main complaint
Patients complain of fever, headache, weakness, heartburn, nausea and
decreased appetite.
3. History of present illness
Medical history showed headache, muscle pain, soreness throughout the body,
pain on swallowing, weakness, fever, nausea, and decreased appetite.
4. History of previous illness
No illness in specific.
5. Family history of disease
A history of DHF disease on other family members is crucial, since DHF
disease is a disease that can be transmitted through mosquito bites aigepty
aides.
6. Environmental Health History
Normally less clean environment, lots of clean water puddles like tin cans, old
tires, where the drinking water of birds that are rarely changed the water, the
tub is rarely cleaned.
7. Historical Growth
Physical Examination for Dengue Hemorrhagic Fever (DHF)
B. Nursing Diagnosis of Dengue Hemorrhagic Fever (DHF)
1. Hyperthermia related to dengue virus infection process.
2. Risk for fluid deficit related to movement of the intravascular to the
extravascular fluid.
3. Risk for fluid volume deficit related to excessive bleeding, intravascular to the
extravascular fluid displacement.
4. Risk for impaired nutritional needs less than body requirements related to
inadequate nutritional intake due to nausea and decreased appetite.
5. Risk for hemorrhage related to a decrease of blood clotting factors
(thrombocytopenia).
6. Anxiety: parents related to the child's condition.
7. Knowledge deficit: about disease, prognosis, the effect of the procedure, and
the care of sick family members associated with less exposure / recall
information.
C. Nursing Care Plans
DP 1: Hipertermie associated with the dengue virus infection
Purpose: Normal body temperature
Criteria: body temperature between 36-37, lost muscle pain
Intervention:
1. Assess the patient's body temperature
Rational: find an increase in body temperature, facilitate intervention
2. Give a warm water compress
Rational: reduce heat by conduction heat transfer. Warm water slowly to
control heat transfer without causing hypothermia or shivering.
3. Provide / instruct the patient to drink plenty of 1500-2000 cc / day (as
tolerated)
Rational: To replace fluids lost due to evaporation.
4. Instruct patient to wear clothing that is thin and easy to absorb sweat
Rational: To provide a sense of comfort and clothes that easily absorb
sweat and thin does not stimulate an increase in body temperature.
5. Observation of intake and output, vital signs (temperature, pulse, blood
pressure) every 3 hours or as indicated
Rationale: Early detection and knowing the lack of fluid and electrolyte
balance in body fluids. Vital Signs is a reference to determine the
patient's general condition.
6. Collaboration: intravenous fluid and drug administration according to the
program.
Rational: Fluid is very important for patients with high body temperature.
Drugs, especially to reduce the patient's body heat.
DP 2: The risk of fluid volume deficit related to intravascular fluid into the
extravascular emigration.
Objectives: There was no fluid deficit volume
Criteria: Input and output balanced, Vital signs within normal limits, no sign pre
shock, Capilarry refill
Intervention:
1. Keep an eye on vital signs every 3 hours / as indicated
Rational: Vital signs help identify fluctuations in intravascular fluid
2. Observation of capillary refill.
Rational: Indications adequacy of peripheral circulation
3. Observation of intake and output. Record the color of urine /
concentration, BJ
Rational: The decline of concentrated urine output with an increase in BJ
suspected dehydration.
4. Advise to drink 1500-2000 ml / day (as tolerated)
Rationale: To meet the needs of body fluids/oral
5. Collaboration: intravenous fluid administration
6. Rational: May increase the amount of body fluids, to prevent hipovolemic
shock.
DP 3: The risk of hypovolemic shock associated with excessive bleeding,
intravascular fluid into the extravascular emigration.
Objectives: There was no hypovolemic shock
Criteria: Vital signs within normal limits
Intervention:
1. Monitor the patient's general condition
Rational: To monitor the condition of the patient during treatment,
especially when paused bleeding. Nurses immediately know the signs pre
shock / shock.
2. Observation of vital signs every 3 hours or more.
Rationale: Nurses need to continue observation vital sign to ensure it does
not happen pre shock / shock.
3. Explain to the patient and family sign of bleeding, and report immediately
if there is bleeding
Rational: By involving the patient’s family and signs of bleeding can be
identified and appropriate action is fast and can be given.
4. Collaboration: intravenous fluid administration
Rationale: Intravenous fluids needed to overcome the great loss of body
fluids.
5. Collaboration: checks: HB, PCV, platelet
Rational: To determine the rate of leakage of blood vessels that
experienced by patients and for reference to further action.
DP 4: Risk of impaired nutritional needs less than body requirements related to
inadequate nutritional intake due to nausea and decreased appetite.
Objectives: There was no need for nutritional disorders
Criteria: There are no signs of malnutrition, weight-balanced show.
1. Intervention:
Review the history of nutrition, including food preferences
Rationale: Identify deficiencies, assuming the possibility of intervention
2. Observation and record the patient's food intake
Rational: Keep an eye on calorie input / lack of quality of food
consumption
3. BB Weigh each day (if possible)
Rational: Keep an eye on weight loss / monitor the effectiveness of
interventions.
4. Give a little but often and the food or eat between meals
Rationale: Food may slightly decrease and increase input weaknesses also
prevent gastric distention.
5. Give and Bantu oral hygiene.
Rationale: Increased appetite and input/oral
6. Avoid foods that stimulate and contain gas.
Rational: Reduce distension and gastric irritation.
DP 5: The risk of bleeding associated with a reduction factor of blood clotting
factors (thrombocytopenia)
Objectives: There was no bleeding
Criteria: BP 100/60 mmHg, N: 80-100x/s regular, strong pulse, No sign of
further bleeding, platelets increase.
Intervention:
1. Monitor signs of decreased platelets are accompanied by clinical signs.
Rational: Decreased platelet count is a sign of leakage of blood vessels at
some stage can cause clinical signs such as epistaxis, ptike.
2. Instruct patient to take plenty of rest (bed rest)
Rational: the patient activity can lead to uncontrolled bleeding.
3. Provide information to clients and families to report any signs of bleeding
such as hematemesis, melena, epistaxis.
Rational: The involvement of patients and families can help to handling
early if there is bleeding.
4. The anticipation of bleeding: use a soft toothbrush, pet oral hygiene,
given the pressure took 5-10 minutes after each blood.
Rational: To prevent further bleeding.
5. Collaboration, monitor platelets every day
Rational: The platelets are monitored every day, it can be seen the rate of
leakage of blood vessels and the possibility of the patients experienced
bleeding.
DP 6: parental anxiety associated with the child's condition.
Purpose: anxiety is reduced / controlled.
Criteria: the client reported no physical manifestations of anxiety, there is no
manifestation of behavior due to anxiety.
Intervention:
1. Assess and document the patient's anxiety level.
Rational: to facilitate intervention.
2. Assess patient's coping mechanisms used to cope with anxiety in the past.
Rational: maintaining adaftif coping mechanisms, increasing the ability to
control anxiety.
3. Do the approach and provide motivation to patients to express their
thoughts and feelings.
Rational: the approach and motivation to help the patient to externalizing
perceived anxiety.
4. Patient's motivation to focus on the reality that exists today, positive
expectations for therapy that in lead.
Rational: a tool to identify the coping mechanisms needed to reduce
anxiety.
5. Give positive reinforcement to continue their daily activities while in a
state of anxiety.
Rational: create trust in the patient that he was able to overcome the
problem and give confidence in myself as evidenced by the self
recognition others in his abilities.
6. Instruct the patient to use relaxation techniques.
Rational: creating a sense of calm and comfortable.
7. Provide factual information (real and true) to patients and families
regarding diagnosis, treatment and prognosis.
Rational: increase knowledge, reduce anxiety.
8. Collaboration of anti anxiety drugs.
Rational: reduce anxiety as needed.
D. Implementation
1. Prevent the lack of fluid volume
a. Observe signs - vital signs at least every 4 hours
b. Monitor sign - a sign of the increasing shortage of liquid: turgor is not
elastic, crown - sunken fontanel, decreased urine production
c. Observe and record intake and output
d. Provide adequate hydration according to the needs of the body
e. Monitoring laboratory values: electrolyte / blood, BJ urine, serum body
f. Maintain an adequate intake and output
g. Monitor and record the weight
h. Monitor the provision of intravenous fluids per hour through
i. Reducing fluid loss does not appear (insesible water loss / IWL)
2. Adequate tissue perfusion
a. Assess and record the signs - Vital signs (quality and frequency of pulse,
blood pressure, capillary refill)
b. Assess and record the circulation in the extremities (temperature,
humidity and color)
c. Assess the possibility of the death of tissue in the extremities such as
cold, pain, swelling of the feet)
3. The need for adequate nutrition
a. Allow the child to eat foods that can be tolerated child. Plan to improve
the nutritional quality at the child's appetite increases.
b. Give the food is accompanied by a nutritional supplement to improve
the quality of nutritional intake
c. Advised the parents to provide food with a small portion technique but
often
d. Weigh every day at the same time and with the same scale
e. Maintaining a patient's oral hygiene
f. Explain the importance of adequate intake nutrition to cure
4. Maintain normal body temperature
a. Measure signs - body temperature of vital signs
b. Teach the family in the temperature measurement
c. Perform "tapid sponge" (wipe) with plain water
d. Increase fluid intake
e. Provide therapy to lower the temperature
5. Adaptive support family coping
a. Assess feeling and parent or family to full stress situation.
b. Allow parent and family for give the response be completely and
identification factor about most parent’s worried
c. Identification coping that usually be used and how to manage situation
E. Evaluation
1. Normal body temperature
2. Fluid does not occur deficit volume
3. Hypovolemic shock does not occur
4. Nutritional needs are not an interruption occurs
5. No bleeding
6. Anxiety is reduced / controlled
7. parents understand about the conditions, procedures and effects of the
treatment process.
CONCLUSION
Dengue fever and dengue hemorrhagic fever (DHF) are acute febrile diseases,
that occurs in the tropics. 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 Aedesaegypti (rarely
Aedesalbopictus) mosquito, which feeds during the day.
Arthropod-borne virus belonging to the family Flaviviridae. There are four
known serotypes: DEN-1, DEN-2, DEN-3, and DEN-4.
Symptomsof dengue haemorrhagic fever:Fever within 5 to 6 days after you
have been bitten by an infected mosquito, high fever, up to 105 degrees Fahrenheit,
severe headache, retro-orbital (behind the eye) pain, severe joint and muscle pain,
sausea and vomiting and rash.
BIBLIOGRAPHY
http://en.wikipedia.org/wiki/Dengue_Haemorrhagic_Fever.html
http://corex-c.blogspot.com/2011/01/DHF.html
http://nursingbegin.com/DHF/html
http://id.wikipedia.org/wiki/dengue-hemorrhagic-fever
http://www.edtech.vt.edu/edtech/id/assess/assess.html
http://www.state.mn.us/mn/externalDocs/dengue_hemorrhagic_fever.pdf
http://www.york.ac.uk/res/dec/resources/papers/cog%20comp%20DHFt.pdf