I.

VITAL INFORMATION

Name: I.E.S. Date of Interview: February 16, 2017; 09:00am

Age: 2 years old Informant:
Sex: Male Relationship to Patient: Mother
Address: Brgy. Cagamutan Norte, Leganes, Iloilo
Civil Status: Child
Date and Time Admitted: February 14, 2017; 02:00am
Chief Complaint: Epistaxis (According to Chart)
"Nagadugo iya ilong tapos sige-sige iya nga hilanat" (According to the Mother)
Ward: Sta. Teresita Ward
Bed No.: 102 C
Allergies: No known allergies to food, animal, drug, and other environmental stimuli.
Religious Affiliation: Roman Catholic
Physicians Initial: Dr. G/ Dr. C.
Impression/Diagnosis: Dengue Fever with Warning Signs

II. CLINICAL ASSESSMENT

1. History of Present Illness

a. Usual Health Status
I.E.S. was an energetic, playful and loving child as claimed by her mother. He usually
woke up at around 8am in the morning and sleeps at around 8pm in the evening. He was breastfed
until he was 1 year and 7 months and then changed into formula milk (Bonakid).......
b. Chronologic Story
February 2, 2017, 12 days PTC, IES started to experience nonproductive cough
accompanied by warm flushed skin. Temperature was not taken. Loss of appetite was observed.
"Pirmiro gainubo sya pero indi bala siling nga sigi-sigi. Ginalangaang sya tapos daw waay na sya
gana magkaon", as verbalized by his mother. No medications were taken nor consult made.
February 5, 2017, 9 days PTC, IES was still experiencing nonproductive cough and on
and off fever ranging from 37.5-37.8 degrees accompanied by episodes of vomiting with previous
meal taken but no phlegm was noted. TSB was done, Tempra 3ml q4h was administered. "Ang
ginakaon nya ginasuka nya man tungod sa iya ubo", as verbalized by his mother.
February 7, 2017, 7 days PTC, they sought consult with a private physician (Dr. G.) and
was prescribed with Salbutamol 3ml tid for 5 days, Ceterizine 3ml before bedtime for 5 days, and
unrecalled antibiotic bid to be taken for 1 week.
February 11, 2017, 3 days PTC, IES still had a nonproductive cough and his motgher
claimed that his fever increased ranging form 37.8-38.6 degrees inspite of the medications being
taken. TSB was done and Tempra 3ml q4h was administered by his mother but only offered minimal
relief with fever ranging 37.5-38.3. "sigi-sigi man painom ko sa iya sang bulong galing daw naglala pa
guid ya iya nga hilanat", as verbalized by his mother.
February 12 2017, 2 days PTC, IES still had nonproductive cough and intermittent fever
ranging from 37.8-38.6 degrees. This was accompanied with loose, watery, brownish stools, dryness
of lips and loss of appetite. "Indi na guid sya ya magkaon, uyon nya mainom na lang ka gatas" as
claimed by his mother.
February 13, 2017, 1 day PTC, small drips of blood was coming out into the nose of IES
while he wasa crying. No management was done. "Gintrapuhan ko lang ilong nya. Waay ko lang
ginbutangan ice", as verbalized by his mother.
February 14, 2017, IES experienced again minimal nosebleeding accompanied with
nonproductive cough and intermittent fever ranging still at 37.8-8.6 degrees. He was irritable,
reestless and crying a lot. He was immediately brought to WVSU-MC Emergency Department for
consultation. At the ER, IES experienced sudden drainage of large amount of blood from his nose.
History taking, physical examination, and laboratory eaxams were done. Thus, the admission.
c. Relevant Family History
 None as claimed by his mother.
2. Past Health Problems/Status
a. Chilhood Illness
Epistaxis
b. Immunization
Complete as claimed by the mother.
c. Allergies
No known allergies to food, animal, drug, and other environmental stimuli.
d. Accidents and Injuries
2016- LIp Trauma
e. Hospitalization for Serious Illness
2016- Lip Trauma
f. Medications
Bon-vita (Vitamin C) 3ml, once a day

3. Family History of Illness

(+) Allergic Cough- Grandmother (Praternal)
(+) Diabetes Mellitus- Grandmother (Maternal)

III. TEXTBOOK DISCUSSION

1. Definition:
Dengue Hemorrhagic Fever
Dengue is the most common arthropod-borne viral (arboviral) illness in humans. It is
transmitted by mosquitoes of the genus Aedes, which are widely distributed in subtropical
and tropical areas of the world.
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. Dengue fever is typically a
self-limiting disease with a mortality rate of less than 1%. When treated, dengue
hemorrhagic fever has a mortality rate of 2-5%, but when left untreated, the mortality rate
is as high as 50%.
The earliest known documentation of dengue feverlike illness was in the Chinese
Encyclopedia of Symptoms during the Chin Dynasty (CE 265-420). The illness was called
"the water poison" and was associated with flying insects near water.

Earliest recorded outbreak

Outbreaks of febrile illnesses compatible with dengue fever have been recorded
throughout history, with the first epidemic described in 1635 in the West Indies. In 1779-
1780, the first confirmed, reported outbreak of dengue fever occurred almost
simultaneously in Asia, North America, and Africa. In 1789, the American physician
Benjamin Rush 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. A denguelike epidemic in East Africa in
the early 1820s was called, in Swahili, ki denga pepo ("it is a sudden overtaking by a
spirit"). The English version of this term, Dandy fever, was applied to an 1827-28
Caribbean outbreak, and in the Spanish Caribbean colonies, that term was altered to
dengue.

Increased distribution after World War II

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 and capable vectors. The first epidemic of
dengue hemorrhagic fever in the modern era 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 are
Europe and Antarctica. In the 1950s, 9 countries reported dengue outbreaks; currently,
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 downthe island nations of Malaysia,
the Philippines, New Guinea, northeastern Australia, and several Pacific islands, including
Tahiti, Palau, Tonga, and the Cook Islands. Hyperendemic transmission is reported in
Vietnam, Thailand, Indonesia, Pakistan, India, Malaysia, and the Philippines. Dengue
continues to extend its range.

DENV-1 and DENV-2

Serotype 1 dengue (DENV-1) was introduced into a largely susceptible population in
Cuba in 1977. Serosurveys indicated that more than 44% of the population was infected,
with only mild disease reported. The first dengue hemorrhagic fever epidemic in the
Americas occurred in Cuba in 1981 and involved serotype 2 dengue (DENV-2), with
hundreds of thousands of cases of dengue in both children and adults, 24,000 cases of
dengue hemorrhagic fever, 10,000 cases of dengue shock syndrome, and 158 reported
deaths. In 1997, Asian genotype DENV-2 was reintroduced, and dengue shock syndrome
and dengue hemorrhagic fever were seen only in adults who had previously been
infected with DENV-1 in 1977.
Disease and case-fatality rates were higher in those who had been infected with
DENV-2 20 years after their initial DENV-1 infection than those who were infected 4 years
apart. Data from other countries supports the finding that the severity of secondary
dengue infections appears to intensify with longer intervals between infections. Since
then, dengue fever and dengue hemorrhagic fever cases have progressively increased.

Dengue fever
Dengue presents in a nonspecific manner similarly to that of many other viral and
bacterial illnesses. Fever typically begins on the third day of illness and persists 5-7 days,
abating with the cessation of viremia. Fever may reach 41C. Occasionally, and more
frequently in children, the fever abates for a day and recurs, a pattern that is termed a
saddleback fever; however, this pattern is more commonly seen in dengue hemorrhagic
fever.
Leukopenia, lymphopenia near the end of the febrile phase, and thrombocytopenia
are common findings in dengue fever and are believed to be caused by direct destructive
actions of the virus on bone marrow precursor cells. The resulting active viral replication
and cellular destruction in the bone marrow are believed to cause the bone pain.
Approximately one third of patients with dengue fever may have mild hemorrhagic
symptoms, including petechiae, gingival bleeding, and a positive tourniquet test (>20
petechiae in an area of 2.5 X 2.5 cm). Dengue fever is rarely fatal.

Dengue hemorrhagic fever

Dengue hemorrhagic fever occurs less frequently than dengue fever but has a more dramatic
clinical presentation. In most of Asia, where it first was described, dengue hemorrhagic fever is
primarily a disease of children. However, in the Americas, and more recently reported in Taiwan,
dengue hemorrhagic fever has an equal distribution in all ages.
 Dengue hemorrhagic fever typically begins with the initial manifestations of dengue fever. The
acute febrile illness (temperatures 40C), like that of dengue fever, lasts approximately 2-7 days.
However, in persons with dengue hemorrhagic fever, the fever reappears, giving a biphasic or
saddleback fever curve.
Along with biphasic fever, patients with dengue hemorrhagic fever have progressive
thrombocytopenia, increasing hematocrit (20% absolute rise from baseline) and low albumin (signs of
hemoconcentration preceding shock), more obvious hemorrhagic manifestations (>50% of patients
have a positive tourniquet test), and progressive effusions (pleural or peritoneal). Lymphocytosis,
often with atypical lymphocytes, commonly develops before defervescence or the onset of shock.
Transaminase levels may be mildly elevated or present in the several thousands associated with
hepatomegaly in those patients with acute hepatitis. Low fibrinogen and elevated fibrin split products
are signs of disseminated intravascular coagulation. Severe metabolic acidosis and circulatory failure
can occur. The critical feature of dengue hemorrhagic fever is plasma leakage. Plasma leakage is
caused by increased capillary permeability and may manifest as hemoconcentration, as well as
pleural effusion and ascites. Bleeding is caused by capillary fragility and thrombocytopenia and may
manifest in various forms, ranging from petechial skin hemorrhages to life-threatening gastrointestinal
bleeding.
Liver damage manifests as increases in levels of alanine aminotransferase and aspartate
aminotransferase, low albumin levels, and deranged coagulation parameters (prothrombin time,
partial thromboplastin time). [24, 25] In persons with fatal dengue hepatitis, infection was
demonstrated in more than 90% of hepatocytes and Kupffer cells with minimal cytokine response
(tumor necrosis factor [TNF]alpha, interleukin [IL]2). This is similar to that seen with fatal yellow
fever and Ebola infections. As the term implies, dengue shock syndrome is essentially dengue
hemorrhagic fever with progression into circulatory failure, with ensuing hypotension, narrow pulse
pressure (< 20 mm Hg), and, ultimately, shock and death if left untreated. Death may occur 8-24
hours after onset of signs of circulatory failure. The most common clinical findings in impending shock
include hypothermia, abdominal pain, vomiting, and restlessness.

Secondary infection
The immunopathology of dengue hemorrhagic fever/dengue shock syndrome remains
incompletely understood. Most patients who develop dengue hemorrhagic fever or dengue shock
syndrome have had prior infection with one or more dengue serotypes. In 20-30% of dengue
hemorrhagic fever cases, the patient develops shock, known as the dengue shock syndrome.
Worldwide, children younger than 15 years constitute 90% of dengue hemorrhagic fever patients.
When an individual is infected with another serotype (ie, secondary infection) and produces low levels
of nonneutralizing antibodies, these antibodies, directed against 1 of 2 surface proteins (precursor
membrane protein and envelope protein), when bound by macrophage and monocyte Fc receptors,
have been proposed to fail to neutralize virus and instead form an antigen-antibody complex
This results in increased viral entry into macrophages bearing IgG receptors, allowing unchecked
viral replication with higher viral titers and increased cytokine production and complement activation,
a phenomenon called antibody-dependent enhancement. The affected macrophages release
vasoactive mediators that increase vascular permeability, leading to vascular leakage, hypovolemia,
and shock. This mechanism, along with individual host and viral genome variations, plays an active
role in pathogenesis. Infants born to mothers who have had dengue, as maternally derived dengue
neutralizing IgGs wane, are also thought to be at risk for enhanced disease. Some researchers
suggest that T-cell immunopathology may play a role, with increased T-cell activation and apoptosis.
Increased concentrations of interferon have been recorded 1-2 days following fever onset during
symptomatic secondary dengue infections. The activation of cytokines, including TNF-alpha, TNF
receptors, soluble CD8, and soluble IL-2 receptors, has been correlated with disease severity. Certain
dengue strains, particularly those of DENV-2, have been proposed to be more virulent, in part
because more epidemics of dengue hemorrhagic fever have been associated with DENV-2 than with
the other serotypes. Current evidence suggests that those with a history of dengue fever are at
highest risk for dengue hemorrhagic fever or dengue shock syndrome if they are infected with a
different dengue strain.
 ` Causative Agent:
Dengue infection is caused by dengue virus (DENV) which is a single-stranded RNA virus
(approximately 11 kilobases long) with an icosahedral nucleocapsid and covered by a lipid envelope.
The virus is in the family Flaviviridae, genus Flavivirus, and the type-specific virus is yellow fever. The
dengue virus has 4 related but antigenically distinct serotypes: DENV-1, DENV-2, DENV-3, and
DENV-4. Genetic studies of sylvatic strains suggest that the 4 serotypes evolved from a common
ancestor in primate populations approximately 1000 years ago and that all 4 separately emerged into
a human urban transmission cycle 500 years ago in either Asia or Africa. Albert Sabin speciated these
viruses in 1944. Each serotype is known to have several different genotypes. Viral genotype and
serotype, and the sequence of infection with different serotypes, appear to affect disease severity.

Mode of transmission
A strain of Arbovirus caused Dengue Hemorrhagic Fever and transmitted by the Aedes
(subgenus Stegomyia) mosquito. Globally, Aedes aegypti is the predominant highly efficient mosquito
vector for dengue infection, but the Asian tiger mosquito, Aedes albopictus, 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. Humans are their preferred hosts. Female Aedes mosquitoes are daytime feeders. They
inflict an innocuous bite, usually on the back of the neck and the ankles, and are easily disturbed
during a blood meal, causing them to move on to finish a meal on another individual, making them
efficient vectors. Not uncommonly, entire families develop infection within a 24- to 36-hour period,
presumably from the bites of a single infected mosquito.

Characteristics of an Aedes aegypti mosquito:

` 1. Daybiting
2. Low-flying
3. In urban area
Hosts for transmission
Humans serve as the primary reservoir for dengue. Certain nonhuman primates in Africa
and Asia also serve as hosts but do not develop dengue hemorrhagic fever. Mosquitoes acquire the
virus when they feed on a carrier of the virus. Persons with dengue viruses in their blood can transmit
the viruses to the mosquito 1 day before the onset of the febrile period. The patient can remain
infectious for the next 6-7 days. 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 virus does not adversely affect the mosquito. The mosquito
remains infected for the remainder of its life. The life span of A aegypti is usually 21 days but ranges
from 15 to 65 days. Vertical transmission of dengue virus in mosquitoes has been documented. [12]
The eggs of Aedes mosquitoes withstand long periods of desiccation, reportedly as long as 1 year,
but are killed by temperatures of less than 10C. Rare cases of vertical dengue transmission have
been reported. In addition, rare reports of human-to-human transmission via needle-stick injuries
have been published

Incubation Period
Incubation period of 3-14 days (usually about 4-7).
Stages
First 4 days:
>febrile or invasive stage --- starts abruptly as high fever, abdominal pain and
headache; later flushing which may be accompanied by vomiting, conjunctival infection and epistaxis
4th to 7th day:
>toxic or hemorrhagic stage --- lowering of temperature, severe abdominal pain,
vomiting and frequent bleeding from GIT in the form of melena; unstable BP, narrow pulse pressure
and shock; death may occur; vasomotor collapse
7th to 10th day:
>convalescent or recovery stage --- generalized flushing with intervening areas of
blanching appetite regained and blood pressure already stable

Severity Grading

* Grade I: fever + Herman's sign (flushes and redness of skin with lighter color at the
center of the rash)
* Grade II: Grade I symptoms + bleeding (epistaxis or nosebleeding, gingival bleeding,
hematemesis or upper gastrointestinal bleeding; e.g: vomiting of blood), and melena or dark stool.
* Grade III: Grade II + Circulatory Collapse (hypotension, cold clammy skin and weak
pulse)
*Grade IV: Grade III + Shock.

Signs and Symptoms

1. Fever
2. Irritability
3. Restlessness
4. Low blood pressure
5. Weak and rapid pulse
6. Petechial rash
7. Chills
8. Erythematous mottling of the skin
9. Facial flushing, which may last for 2-3 days.
10. Headache
11. Retro-orbital pain
12.Severe myalgias: Especially of the lower back, arms, and legs 13.
Arthralgias: Usually of the knees and shoulders
14. Nausea and vomiting
15. Rash: A maculopapular or macular confluent rash over the face, thorax, and flexor
surfaces, with islands of skin sparing
16. Weakness
17. Altered taste sensation
18. Anorexia
19. Sore throat
20. Lymphadenopathy

Epidemiolgy
Southeast Asia
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. A 5-year
prospective study in Thai children examined the relative economic burden of dengue infection in
children on the local population. 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. 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.

Prognosis
Dengue fever is typically a self-limiting disease with a mortality rate of less than 1%. When
treated, dengue hemorrhagic fever has a mortality rate of 2-5%. When left untreated, dengue
hemorrhagic fever has a mortality rate as high as 50%. Survivors usually recover without sequelae
and develop immunity to the infecting serotype. The fatality rate associated with dengue shock
syndrome varies by country, from 12-44%.
A 2005 review from Singapore of 14,209 patients found that useful predictors of death included
the following: Atypical presentations; Significant comorbid illness; Abnormal serum markers (including
albumin and coagulation studies); Secondary bacterial infections.
Factors that affect disease severity include the following: Patient age; Pregnancy; Nutritional
status; Ethnicity; Sequence of infection with different dengue serotypes; Virus genotype; Quality and
extent of available medical care.
Complications and sequelae of dengue virus infections are rare but may include the following:
Cardiomyopathy; Seizures, encephalopathy, and viral encephalitis; Hepatic injury; Depression;
Pneumonia; Iritis; Orchitis; Oophoritis.

MANAGEMENT

1. Medical Management

Because dengue hemorrhagic fever is caused by a virus, there is no specific medicine or

antibiotic to treat it. For typical dengue, the treatment is purely concerned with relief of the symptoms
(symptomatic).
Rest and oral rehydration therapy is recommended for patients with moderate dehydration
caused by high fever and vomiting.
Aspirin and nonsteroidal anti-inflammatory drugs should only be taken under a doctor's
supervision because of the possibility of worsening hemorrhagic complications.
Acetaminophen (Tylenol) and codeine may be given for severe headache and for the joint and
muscle pain (myalgia).
Patients who develop signs of dengue hemorrhagic fever warrant closer observation.
Admission for intravenous fluid administration is indicated for patients who develop signs of
dehydration, such as the following: Tachycardia; Prolonged capillary refill time; Cool or mottled skin;
Diminished pulse amplitude; Altered mental status; Decreased urine output; Rising hematocrit;
Narrowed pulse pressure; Hypotension.
Do not give Aspirin because it contains at antiplatelet property which promotes bleeding.
Treatment is solely supportive and includes: Fluids; Analgesics (not aspirin) for fever and
muscles aches; Replacement of plasma or plasma expanders if patient has internal or gastrointestinal
beeding.

2. Nursing Management

Independent:
Close monitoring of vital signs in critical period (between days 2 to day 7 of fever) is
critical.
Increased oral fluid intake is recommended to prevent dehydration.
Tepid Sponge Bath to manage high fever.
Treatment is purely concerned with relief of the symptoms (symptomatic)
Educate patients, especially those who have experienced prior dengue fever, to avoid
mosquito bites, including the use of appropriate mosquito repellants and peridomestic vector control,
when traveling to dengue-endemic areas.
Dependent:
Because dengue is caused by a virus, there is no specific medicine or antibiotic to treat it.
Aspirin and nonsteroidal anti-inflammatory drugs should be avoided as these drugs may
worsen the bleeding tendency associated with some of these infections.
Acetaminophen (Tylenol) and codeine may be given for severe headache and for the joint
and muscle pain (myalgia). (DHF) Oxygen and sedatives may be administered.
Collaborative:
A platelet transfusion is indicated in rare cases if the platelet level drops significantly
(below 20,000) or if there are significant bleeding. The presence of melena or blood in the stool may
indicate internal gastrointestinal bleeding requiring platelet, FFP and/or red blood cell transfusion.

SCHEMDI
DRUGS
CARE PLAN
GOALS
LABS, ADDTNL LABS