KOREKSI (2)final dhf(sumi)

CASE REPORT

Dengue Haemorrhagic Fever

Presenter: Thaneswaran .M

Sumita .M

Day/Date: Tuesday/30th November 2010

Supervisor : dr.Hj.Tiangsa br.Sembiring,SpA(K)

INTRODUCTION

Dengue fever (DF) or Dengue haemorrhagic fever (DHF) is a growing public

health problem in the subtropics. In South-East Asia, with a total population of 1.5

billion, approximately 1.3 billion people live at risk of acquiring DF or DHF.

Currently, DHF is the leading cause of hospital admissions and death among

children in this region.1

Dengue, the most common arboviral illness transmitted worldwide, is caused

by infection with 1 of the 4 serotypes of dengue virus, family Flaviviridae, genus

Flavivirus ,single-stranded nonsegmented RNA viruses. 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).9 Most patients with dengue infection have

only mild disease or classic dengue fever, with influenza-like symptoms, severe

headache, and aching joints and muscles. However, in a small percentage of

patients maybe half a million people every year potentially lethal forms of

dengue called dengue hemorrhagic fever and dengue shock syndrome develop.2

Dengue virus transmission follows two general patterns which is 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

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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. Transmission appears to begin in urban centers

and then spreads to the rest of a country. 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.2

At present, the only method of controlling or preventing dengue and DHF

is to combat the vector mosquitoes. Aedes aegypti breeds primarily in man-made

containers like earthenware jars, metal drums and concrete cisterns used for

domestic water storage, as well as discarded plastic food containers, used

automobile tyres and other items that collect rainwater. It can also breed

extensively in natural habitats such as tree holes and leaf axils. In recent years,

Aedes albopictus, a secondary dengue vector in Asia, has become established in

the United States, several Latin American and Caribbean countries, in parts of

Europe and in one African country. The rapid geographic spread of this species

has been largely attributed to the international trade in used tyres. Dengue

continues to be a global challenge because the pathogenesis of DHF is not fully

understood, there is no immediate prospect of a vaccine and the mosquito control

measures are inadequate. The wide spread DHF epidemics during 2003 reinforces

the belief that DHF has come to stay in this country and will continue to spread to

newer areas unless vector control measures are taken up on war footing.3

EPIDEMIOLOGY

Dengue haemorrhagic fever is now endemic in more than 100 countries in

Africa, the Americas, the Eastern Mediterranean, Southeast Asia and the Western

Pacific, Southeast Asia and the Western Pacific are most seriously affected. Some

2500 million people two fifths of the world.’s population are now at risk from

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dengue. WHO currently estimated 50 million cases of dengue infection worldwide

every year and during epidemics of dengue, attack rates among susceptibles are 40

to 90%. An estimated 500,000 cases of DHF require hospitalization each year, of

whom a very large proportion are children.3

Figure 1: Dengue, countries or areas at risk, 2008

Indonesia is the largest country in the region with a population of 245

million. Almost sixty per cent of the people live on the island of Java, which is

most severely afflicted by periodic outbreaks of dengue disease. However, the

disease is endemic in many large cities and small towns throughout the country

and has also spread to certain smaller villages, where population movement and

density are high.Epidemic DF has been reported in all 27 Indonesian provinces,

whereas in 1968 only two provinces had reported dengue cases.1

Figure 2: The incidence rate and case-fatality rate of DHF in Indonesia in

2005.

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An increase in commercial air travel has subsequently aided the

transmission of the virus between populations so that dengue is now endemic in

over 100 countries throughout tropical and sub-tropical areas of the world. The

main vector Aedes aegypti is found worldwide between latitudes 35ºN and

35ºS .The principle areas affected include the Caribbean, South and Central

America, Mexico, Africa, the Pacific Islands, South East (SE) Asia, Indian sub-

continent, Hawaii, and Australia (see Figure 1). By 2002, more than 2.5 billion

people were at risk of infection (roughly 40% of the world’s population). An

estimated 50-100 million illnesses occur annually, 250,000-500,000 of which are

dengue haemorrhagic fever, many of these in children. The estimated global

mortality rate is 25,000 per annually.4

VIROLOGY

The genome of Dengue virus consists of a single stranded, non

segmented, positive sense ribonucleic acid (RNA) of about 11 kb in length . The

genome is translated into a single polypeptide which is co- and post-

translationally processed by host signalases as well as the virus encoded serine

protease into the three structural and seven non structural proteins (NS) in the

order C-prM-E-NS1-NS2A-NS2B-NS3-NS4A-NS4B-NS5 that traverse the

Endoplasmic Reticulum (ER) membrane .Dengue and other flaviviruses are

thought to replicate in the cytoplasm, mature on intracellular membranes and

egress by exocytosis and in some cases by budding at the plasma membrane . The

host ER is the primary site of envelope glycoprotein biogenesis, genomic

replication, and particle assembly of flaviviruses. In the course of productive

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infection, flaviviruses induce proliferation and hypertrophy of the ER membranes

Moreover, a large amount of flaviviral proteins are synthesized in infected cells,

thus overwhelming the ER folding capacity. As a natural consequence, we

hypothesize that these events will lead to the activation of the ER stress response

which in turn will modulate various signaling pathways resulting in cell survival

or death decisions.5

TRANSMISSION

Transmission occurs following a bite from an infected Aedes mosquito. It

is most widely transmitted by Ae. aegypti and Ae. albopictus (Asia, Philippines

and Japan), other Aedes species also transmit disease in specific areas; Ae.

polynesiensis, Ae. scutellaris and Ae. pseudoscutallaris (Pacific Islands and New

Guinea), Ae. polynesiensis (Society Islands) and Ae. niveus (Philippines).4

The cycle of transmission typically involves humans and mosquitoes. The

virus is spread from an infected human to a mosquito and then to another human,

often in areas where there are dense human populations. The mosquito can

transmit dengue if it immediately bites another host. Humans are the main

reservoir for the dengue virus, although nonhuman primates in Asia and Africa

may also be infected.2,4

Figure 3: Mechanism of transmission

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Humans serve as the primary reservoir for dengue; however, certain non human

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. The mosquito can transmit dengue if it immediately bites another host.2

VECTORS

A. aegypti, found worldwide in the tropics and subtropics, is the principal

vector. The Aedes mosquito prefers to breed in water-filled receptacles, usually

close to human habitation. They often rest in dark rooms (e.g. in bathrooms and

under beds) and breed in clean, stagnant water in containers that collect rainwater,

such as tires, tin cans, pots, and buckets.4

Figure 4: Vector

Female Aedes are highly susceptible to dengue virus, feeds preferentially

on human blood, is a daytime feeder, has an almost imperceptible bite, and is

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capable of biting several people in a short period for one blood meal.6 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.3

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.2

PATHOGENESIS

After an infected mosquito has bitten a person, the virus replicates in

regional lymph nodes and is disseminated through the lymphatic system and

blood to other tissues. Replication in the reticuloendothelial system and skin

results in viremia. The incubation period ranges from 3 to 14 days, but it is

usually 4 to 7 days. Infection with dengue virus of any of the four serotypes

causes a spectrum of illness, ranging from no symptoms or mild fever to severe

and fatal hemorrhage, depending largely on the patient’s age and immunologic

condition.6

Viral virulence and immune responses have been considered as two major

factors responsible for the pathogenesis of DHF. Virological studies areattempting

to define the molecular basis of viral virulence. The immunopathological

mechanisms appear to include a complex series of immune responses. A rapid

increase in the levels of cytokines and chemical mediators apparently plays a key

role in inducing plasma leakage, shock and haemorrhagic manifestations. It is

likely that the entire process is initiated by infection with a socalled virulent

dengue virus, often with the help of enhancing antibodies in secondary infection,

and then triggered by rapidly elevated cytokines and chemical mediators produced

by intense immune activation.3

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The pathogenesis of DHF is poorly understood. DHF caused by primary or secondary

dengue infection is due to the occurrence of abnormal immune response involv ing

production of cytokines or chemokines, activation of T-lymphocytes and disturbance

of the hemostatic system. The elevated mediators include C3a, C5a, tumor necrosis

factor-α, interleukin (IL)-2, IL-6, IL-10, interferon-α and histamine.9–14 Halstead

described the antibody-dependent enhancement whereby, upon the second infection

with a heterotypic dengue virus,15 the subneutralizing concentration of the cross-

reacting antibody from the previous infection may opsonize the virus and enhance its

uptake and replication in the macrophage or mononuclear cells. Secondary infection

with a heterotypic dengue virus is associated with increased risk of developing DHF in

individuals who have recovered from a primary dengue virus with a first serotype. The

level of T-cell activation in a secondary dengue infection is also enhanced, occurring

as a phenomenon known as original antigenic sin,16,17 and is undergoing

programmed cell death. Many dengue- specific T-cells are of low affinity for the

infected virus and show higher affinity for other, probably previously encountered

serotypes. Profound T-cell activation and death during acute dengue infection may

suppress or delay viral elimination, leading to the higher viral loads and increased

immunopathology found in patients with DHF. 7

Most patients who develop dengue hemorrhagic fever or dengue shock

syndrome have had prior infection with one or more dengue serotypes. In

individuals with low levels of neutralizing antibodies, nonneutralizing antibodies

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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.2

PATHOPHYSIOLOGY

Two main pathophysiological changes occur in DHF/DSS are increase in

vascular permeability that gives rise to loss of plasma from vascular compartment

and disorder in haemostasis.6

a. Evidence of plasma leakage

The plasma leakage is due to the increased vascular permeability induced

by several mediators such as C3a, C5a during the acute febrile stage and

prominent during the toxic stage. Capillary damage allows fluid, electrolytes,

small proteins, and, in some instances, red cells to leak into extravascular spaces.3

The evidence of plasma leakage includes hemoconcentration, hypoproteinemia/

hypoalbuminemia, pleural effusion, ascites, threatened shock and profound shock.

The rising hematocrit may not be evidenced because of either severe bleeding or

early intravenous fluid replacement.7

b. Bleeding tendency

The bleeding diathesis is caused by vasculopathy, thrombocytopenia,

platelet dysfunction and coagulopathy.2

Vasculopathy

A positive tourniquet test indicating the increased capillary fragility is

found in the early febrile stage. It may be a direct effect of dengue virus as it

appears in the first few days of illness during the viremic phase.7

Thrombocytopenia and platelet dysfunction

Patients with DHF usually have platelet counts less than 100 × 109/L.

Thrombocytopenia is most prominent during the toxic stage. The mechanisms of

thrombocytopenia include decreased platelet production and increased peripheral

destruction. 3

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Additionally, the increased peripheral destruction is markedly prominent

during 2 days before defervescence. The bone marrow then revealed

hypercellularity with an increase in the megakaryocyte, erythroblast and myeloid

precursors. Hemophagocytosis of young and mature erythroid and myeloid cells,

lymphocytes and platelets was observed.Survival of patients and transfused

platelets was markedly decreased because of immune-mediated injury of platelets.

Platelet dysfunction as evidenced by the absence of adenosine diphosphate (ADP)

release was initially demonstrated in patients with DHF during the convalescent

stage by Mitrakul et al. in 1977. The subsequent study during the febrile and early

convalescent stages by Srichaikul et al. in 1989 also demonstrated the impaired

platelet aggregation response to ADP that returned to a normal response 2–3

weeks later. An increase in plasma β-thromboglobulin and platelet factor 4,

indicating increased platelet secretory activity, was observed. The platelet

dysfunction might be the result of exhaustion from platelet activation triggered by

immune complexes containing dengue antigen.7

Coagulopathy

During the acute febrile stage, mild prolongation of the prothrombin time

and partial thromboplastin time, as well as reduced fibrinogen levels, have been

demonstrated in several studies. Variable reductions in the activities of several

coagulation factors, including prothrombin, factors V, VII, VIII, IX and X,

antithrombin and α-antiplasmin, have been demonstrated. Fibrin degradation

product or D-dimer is slightly elevated.9

Low levels of anticoagulant proteins C and S and antithrombin III were

found to be associated with increasing severity of shock, presumably due to

plasma leakage. Elevated levels of tissue factor, thrombomodulin and

plasminogen activator inhibitor-1 reflect endothelial, platelet and/or monocyte

activation and may be a secondary response to direct activation of fibrinolysis by

the dengue virus. The coagulation abnormality is well compensated for in the

majority of patients without circulatory collapse. Most of the patients have serum

aspartate transaminase (AST) and alanine transaminase (ALT) levels threeand

twofold higher than normal, respectively. There is focal necrosis of hepatic cells,

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swelling appearance of Councilman bodies and hyaline necrosis of Kupffer cells.

Proliferation of mononuclear leucocytes and less frequently polymorphonuclear

leucocytes occurs in the sinusoids and occasionally in the portal areas.2,9

CLINICAL FEATURES

Classic dengue or “breakbone fever” is characterized by a sudden onset of

high-grade fever, accompanied by a severe headache, pain behind the eyes (retro-

orbital pain), and fatigue, and it is often associated with severe myalgias,

particularly of the lower back, arms, and legs, and arthralgias, especially of the

knees and shoulders.The fever usually lasts five to seven days. A rash, typically

macular or maculopapular and often confluent with the sparing of small islands of

normal skin has been reported in about half of infected persons. It usually appears

near the time of defervescence, often lasts for two to four days, and may be

accompanied by scaling and pruritus. Other signs and symptoms include flushed

facies (usually during the first 24 to 48 hours), lymphadenopathy, injected

conjunctivae, an inflamed pharynx, and mild respiratory and gastrointestinal

symptoms. 6

Fever in persons with symptomatic dengue fever may be as high as 39,4 –

41,1°C (103 - 106°F).3 The fever typically begins on the third day and lasts 5-7

days, abating with the cessation of viremia. Fever is often preceded by chills,

erythematous mottling of the skin, and facial flushing (a sensitive and specific

indicator of dengue fever). Occasionally, and more commonly in children, the

fever abates for a day and then returns, a pattern that has been called saddleback

fever. Patients are at risk for development of dengue hemorrhagic fever or dengue

shock syndrome at approximately the time of defervescence.2

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Gum bleeding, epistaxis,cmenorrhagia, and gastrointestinal hemorrhage are

only occasionally seen. Very rare complications of dengue fever include

myocarditis, hepatitis, and neurologic abnormalities, such as encephalopathy and

neuropathies. Laboratory findings commonly associated with dengue fever

include thrombocytopenia, leukopenia with lymphopenia, mild-to-moderate

elevations of hepatic aminotransferases and lactate dehydrogenase, and

hyponatremia.6

DIAGNOSIS

The WHO guidelines propose the following classification for

symptomatic dengue infection :

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Figure 1 Manifestation of dengue virus infection

To fulfil the WHO case definition for DHF, the following must all be

present.9,10

1. Fever or history of acute fever, lasting 2-7 days, occasionally biphasic.

2. Bleeding (haemorrhagic tendencies), evidenced by at least one of the

following:

a. a positive tourniquet test (TT)

b. petechiae, ecchymosis, or purpura

c. bleeding from the mucosa, gastrointestinal tract, injection sites or

other locations

d. haematemesis or melena

3. Thrombocytopaenia (100,000 cells per mm3 or less)

4. Evidence of plasma leakage due to increased vascular permeability,

manifested by at least one of the following:

a. a rise in the haematocrit equal or greater than 20% above average

for age, sex and population

b. a drop in the haematocrit following volume-replacement treatment

equal to or greater than 20% of baseline

c. signs of plasma leakage such as pleural effusion, ascites, and

hypoproteinaemia.

The onset of shock may be subtle, indicated by raised diastolic pressure

and increased PVR in an alert patient.2 To fulfil the case definition for Dengue

Shock Syndrome (DSS), the four criteria above for DHF (fever, haemorrhagic

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tendencies, thrombocytopaenia, and plasma leakage) must all be present plus

evidence of circulatory failure manifested as: 10

a. Rapid and weak pulse

b. Narrow pulse pressure (<20 mmHg)

c. Hypotension for age (this is defined as systolic pressure < 80 mmHg for

those less than five years of age, or <90 mmHg for those five years of age

and older.)

d. Cold clammy skin and restlessness.

The diagnosis of dengue infection is confirmed by testing positive for

either virus isolation using culture, polymerase chain reaction (PCR) from the

clinical specimens such as serum in the early febrile stage, or serological studies.6

In both primary and secondary dengue infections, there is a relatively transient

appearance of antidengue immunoglobulin M (IgM) antibodies. These disappear

after 6-12 wk, which can be used to time a dengue infection.10

In 2nd primary dengue infections, most antibody is of the IgG class. The

positive serological studies define as a fourfold or more increase in the

hemagglutination inhibition test, complement fixation, enzyme immunoassay, or

neutralization test, between acute and convalescent sera or positive test for

dengue-specific IgM/IgG performed by enzyme-linked immunosorbent assay

(ELISA).6 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.

Crossreactions with other flaviviruses interfere with serologic testing,

particularly the ELISA for IgG, and this affects the interpretation of test results in

travelers exposed to other flavivirus infections, including those previously

vaccinated against flavivirus infections, such as yellow fever and Japanese

encephalitis.6

The most commonly used test for the diagnosis of dengue is the IgM

capture ELISA, but this test is negative early in the course of the disease, should

be performed only four to five days after the onset of symptoms, and gives only a

probable diagnosis. Usually such samples should be collected not earlier than 5

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days nor later than 6 wk after onset. Rheumatoid factor may lead to an IgM

capture assay that is false positive for dengue.6,10

Primary infections are characterized by an increase in dengue-specific IgM

antibodies 4 to 5 days after the onset of fever and by an increase in IgG antibodies

only after 7 to 10 days. IgM antibodies are detectable for three to six months,

whereas IgG antibodies remain detectable for life. In secondary infections, the

level of IgM antibodies is lower than in primary infections and the antibodies are

sometimes even absent, whereas levels of IgG antibodies rise rapidly in secondary

infections, even during the acute phase. Thus, the presence of high titers of IgG

early in the course of the disease is a criterion for secondary infection.6

CLASSIFICATION

DHF is lassified into four grade of severity, where grades III and IV are

considered to de DSS. The presence of thrombocytopenia with concurrent

haemoconcentration differentiates grades I and II DHF from DF: 9

1. Grade I is defined as fever and non-specific constitutional signs and

symptoms; the only haemorrhagic manifestation is a positive TT and/or

easy bruising.

2. Grade II is the same as grade I but includes spontaneous bleeding, usually

in the form of skin or other haemorrhages.

3. Grade III is circulatory failure manifested by a rapid, weak pulse and

narrowing of the pulse pressure or hypotension, with the presence of cold,

clammy skin and restlessness.

4. Grade IV is profound shock with undetectable blood pressure or pulse.

Grades III and IV are define are as DSS.

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Figure 2 The spectrum of dengue illness

In addition, the guidelines list indicators that may be used to guide the

diagnosis of DHF/DSS. These indicators may help clinicians to establish an early

diagnosis, ideally before the onset of shock but are not intended to be substitutes

for the case definitions. The listed indicators of DHF/DSS are: high fever of acute

onset, hemorrhagic manifestations (at least a positive TT), hepatomegaly, shock,

thrombocytopaenia, and hemoconcentration. The first two clinical observations,

plus one of the laboratory findings establishes a provisional diagnosis of DHF.

The of shock in a patient with a provisional diagnosis of DHF supports the

diagnosis of DSS.8

DIFFERENTIAL DIAGNOSIS

Early in the febrile phase, the differential diagnose for DHF/DSS includes

a wide spectrum of viral, bacterial and parasitic infections. Chikungunya fever

may be difficult to differentiate clinically from DF and mild or early cases of

DHF.8 In addition, DHF can also mimic Kawasaki disease, yellow fever,

hantavirus infections, meningococcemia and other viral hemorrhagic fevers.8

By the third or fourth day, laboratory findings may establish a diagnosis

before shock occurs. Shock virtually rules out a diagnosis of chikungunya fever.

Marked thrombocytopenia with concurrent haemoconcentration differentiates

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DHF/DSS from diseases such as endotoxin shock from bacterial infection or

meningococcaemia.9

The differential diagnosis of dengue fever includes viral respiratory and

influenza-like diseases, the early stages of malaria, mild yellow fever, scrub

typhus, viral hepatitis, and leptospirosis. Four arboviral diseases have dengue-like

courses but without rash: Colorado tick fever, sandfly fever, Rift Valley fever, and

Ross River fever.10

In dengue fever, pancytopenia may occur after the 3-4 days of illness. A

recent systematic review found that patients with dengue had significantly lower

total WBC, neutrophil, and platelet counts than patients with other febrile

illnesses in dengue-endemic populations. Leukopenia, often with lymphopenia, is

observed near the end of the febrile phase of illness.2 Neutropenia may persist or

reappear during the latter stage of the disease and may continue into

convalescence with white blood cell counts of <2,000/mm3.10

Other abnormalities include moderate elevations of the serum

transaminase levels, consumption of complement, mild metabolic acidosis with

hyponatremia, occasionally hypochloremia, slight elevation of serum urea

nitrogen, and hypoalbuminemia.10

The most common hematologic abnormalities during dengue hemorrhagic

fever and dengue shock syndrome are hemoconcentration with an increase of

>20% in hematocrit, thrombocytopenia, prolonged bleeding time, and moderately

decreased prothrombin level that is seldom <40% of control. Fibrinogen levels

may be subnormal and fibrin split products elevated.3

Thrombocytopenia has been demonstrated in up to 50% of dengue fever

cases. Platelet counts of less than 100,000 cells/μL are seen before defervescence

and the onset of shock. The platelet count and hematocrit level should be

monitored at least every 24 hours to facilitate early recognition of dengue

hemorrhagic fever and every 3-4 hours in severe cases of dengue hemorrhagic

fever or dengue shock syndrome.2

Cultures of blood, urine, CSF, and other body fluids should be performed

as necessary to exclude or confirm other potential causes of the patient's

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condition. Arterial blood gas should be assessed in patients with severe cases to

assess pH, oxygenation, and ventilation. Typing and crossmatching of blood

should be performed in cases of severe dengue hemorrhagic fever or dengue

shock syndrome because blood products may be required.2

Serum specimens should be sent to the laboratory for serodiagnosis, PCR,

and viral isolation. Serodiagnosis is made based on a rise in antibody titer in

paired IgG or IgM specimens. Results vary depending on whether the infection is

primary or secondary. The IgM capture enzyme-linked immunosorbent assay

(MAC-ELISA) has become the most widely used assay, although other tests,

including complement fixation (CF), neutralization test (NT), hemagglutination

inhibition (HI), and IgG ELISA are also used.10

Imaging Studies

Chest radiography of the chest reveal pleural effusions (left > right) in

nearly all patients with dengue shock syndrome. Bilateral pleural effusions are

common in patients with dengue shock syndrome.2

Positive and reliable ultrasonographic findings include fluid in the chest

and abdominal cavities, pericardial effusion, and a thickened gallbladder wall.

Thickening of the gallbladder wall may presage clinically significant vascular

permeability. The electrocardiogram may show sinus bradycardia, ectopic

ventricular foci, flattened T waves, and prolongation of the P-R interval.2,10

MANAGEMENT

There is no specific treatment for DHF. Dengue fever is usually a self-

limited illness, as there are no specific antiviral medications for dengue infections,

and only supportive care is required. Therapy for DHF is wholly symptomatic and

aims at controlling the clinical manifestations of shock and hemorrhage.7

No specific diet is necessary for patients with dengue fever. Patients may

become dehydrated from fever, lack of oral intake, or vomiting. Patients who are

able to tolerate oral fluids should be encouraged to drink oral rehydration solution,

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http://emedicine.medscape.com/article/157325-overview

fruit juice, or water to prevent dehydration. Return of appetite after dengue

hemorrhagic fever or dengue shock syndrome is a sign of recovery. Bedrest is

recommended for patients with symptomatic dengue fever, dengue hemorrhagic

fever, or dengue shock syndrome. Table 1 shows high risk patients and some

indication for admission to hospital.9

Table 1 - High-risk dengue patients and indication for admission to hospital/ICU

High-risk dengue patients that need special attention

Infants under 1 year of age

Overweight/obese patients

Massive bleeding

Change of consciousness, especially restlessness and irritability or coma

Presence of underlying diseases e.g. thalassemia, G-6-PD deficiency, heart

disease

Indication for admission

Excessive family concern or cannot be followed up

Very weak, cannot eat or drink, not drinking/feeding poorly

Spontaneous bleeding

Platelet counts ≤ 100,000 cells/mm3 and/or rising Hct 10-20%

Clinical deterioration in defervescence

Severe abdominal pain/vomiting

Significant dehydration requiring intravenous fluids

Admit immediately if there are signs of shock. These signs are as follows:

Rapid pulse with no fever

Prolonged capillary refill time

Cold clammy skin, mottling

Narrowing of pulse pressure ≤ 20 mmHg, e.g. 100/80

Hypotension

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Oliguria, no urine for 4-6 hours

Change of consciousness: drowsiness to stupor, restlessness, irritability

(encephalopathy)

World Health Orgnization, Dengue Haemorrhagic Fever: 1997

The treatment of dengue fever in the febrile phase is symptomatic (Table

2). Fever is treated with paracetamol. Salicylates and other nonsteroidal anti-

inflammatory drugs should be avoided as these may predispose a child to mucosal

bleeding.6 Patients who do not receive a proper treatment usually die within 12–24

hours after shock ensues. The most important aspect in managing patients with

DHF is close observation by the attending physicians and nurses with frequent

clinical and laboratory monitoring.8

Table 2 - Steps to the management of the febrile phase

Resting, oral fluids

Reduction of fever: Tepid sponge after a dose of paracetamol 10-15 mg/kg/day for

high fever ≥ 39oC, every 4 to 6 hours

Nutritional support: Soft, balanced, nutritious diet, juice and electrolyte solution -

plainwater is not adequate.Avoid black- or red-colored food or drinks (may be

mistaken for bleeding)

Other supportive and symptomatic treatment

Domperidone -1 mg/kg/day in three divided doses in case of severe

vomiting for 1-2 days. One single dose may be adequate

H2-blockers (ranitidine) - recommended in case of gastrointestinal

bleeding

Antibiotic - not necessary; it may lead to complications

Steroid is ineffective in preventing shock DHF. It may cause harm

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Intravenous fluids: In case of doubt, provide intravenous fluids, guided by serial

hematocrit, blood pressure, and urine output levels. The volume of fluid should be

targeted at treating mild to moderate isotonic dehydration (5-8% deficit); just

correct dehydration, and discontinue it as soon as possible

If sent home- Advise about warning signs and symptoms of shock and ask to

report immediately if any of the following symptoms occur

Clinical deterioration in defervescence (no fever or low-grade fever)

Any type of bleeding

Severe vomiting/abdominal pain

Intense thirst

Drowsiness, desire for sleeping all the time

Refusal to eat or drink

Cold, clammy skin and extremities, restlessness, irritability, decreased

urine output or no urine for 4-6 hours

Behavioral changes e.g. confusion, use of foul language

Follow up preferably everyday - from the 3rd day until afebrile for 24-48 hours.

Important points to evaluate are :

History of bleeding, abdominal pain, vomiting, appetite, fluid intake,

and urine output

Physical examination: vital signs, liver size and tenderness

Blood counts: WBC ≤ 5,000 cells/mm3 with lymphocytosis and

increase in atypical lymphocytes – and platelet counts ≤ 100,000

cells/cumm – indicates progression to critical phase. Rising Hct of 10-

20% - indicates that the patient has progressed to the critical phase

Liver function tests in every patient who shows a change in

consciousness, restlessness, confusion and irritability


Patients who develop signs of dehydration, such as tachycardia, prolonged

capillary refill time, cool or mottled skin, restlessness, acute abdominal pain,

diminished pulse amplitude, altered mental status, decreased urine output, rise in

hematocrit levels, narrowed pulse pressure, or hypotension, should be hospitalized

as require admission for intravenous fluid administration.9

21 | P a g e

Ringer’s lactate is infused at a rate of 7 mL/kg over 1 hour. After 1 hour, if

hematocrit level decreases and vital parameters improve, the fluid infusion rate

should be decreased to 5 mL/kg over the next hour and to 3 mL/kg/hour for 24-48

hours. When the patient is stable, as indicated by normal blood pressure,

satisfactory oral intake and urine output, the child can be discharged.8

If at 1 hour the hematocrit level rises and vital parameters do not show

improvement, the fluid infusion rate should be increased to 10 mL/kg over the

next hour. In case of no improvement, the fluid infusion rate should be further

increased to 15 mL/kg over the third hour. If no improvement is observed in vital

parameters and hematocrit level at the end of 3 hours, colloids or plasma infusion

(10 mL/kg) should be administered (Figure 3). Once the hematocrit level and vital

parameters are stable the infusion rate should be gradually reduced and

discontinued over 24-48 hours.8,9

22 | P a g e

Figure 3 Management for DHF grade I and II

Intravenous fluids should be stopped when the hematocrit level falls below

40% and adequate intravascular volume is present. At this time, patients reabsorb

extravasated fluid and are at risk for volume overload if intravenous fluids are

continued. Do not interpret a falling hematocrit value in a clinically improving

patient as a sign of internal bleeding.2

The most important element of treatment in a critically ill patient or in a

patient with DSS is providing intensive care with close monitoring of blood

pressure, hematocrit levels, platelet count, urinary output, hemorrhagic

manifestations, and level of consciousness (Table 3). With adequate and

appropriate fluid replacement, DSS is rapidly reversible.8,9

23 | P a g e

Table 3

Steps to the management of the critical phase/DHF and dengue shock

syndrome

General measures

Give oxygen via face mask/nasal cannula in case of shock/impending

shock. NCPAP should be preferred if there is acute respiratory failure

associated with DSS

Frequent monitoring

Stop bleeding with proper techniques e.g. anterior nasal packing for

massive epistaxis

Avoid blind invasive procedures e.g. no nasogastric tube insertion, no

gastric lavage

Essential nursing care

Sedation is needed in some cases to restrain an agitated child. Chloral

hydrate(12.5-50 mg/kg), orally or rectally, is recommended.

Long-acting sedatives should be avoided

Monitoring of children with DHF/DSS

Vital signs should be checked every 15-30 minutes until the patient is

stable, and every 1-2 hours thereafter

Hematocrit levels must be checked every 2 hours for 6 hours, then

every 4 hours until the patient is stable. Monitoring at every 12 hours

during recovery

Fluid balance sheet: type of fluid, amount, rate etc

Accurate measurement of urine output

Serum electrolytes and blood gases should be checked every 12 hours

DIC profile and liver function tests as and when indicated

Weight should be measured every 12 hours

Obtain laboratory tests

In uncomplicated DHF cases, Hematocrit and platelet counts are the

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only necessary tests

In those at high risk of complicated DHF

Blood grouping/cross matching

Blood glucose

Blood electrolyte (Na, Ca, K, CO2)

Liver function test

Renal function test (BUN, creatinine, uric acid)

Blood gas

Coagulogram (PTT, PT, TT)

IV fluid

IV fluids should be given only when the patient enters the critical phase:

thrombocytopenia ≤ 100,000, rising Hct of 10-20%. IV fluid before critical phase

cannot prevent shock, but may cause fluid overload

Type of IV fluid used: isotonic salt solution (normal saline or Ringer 's lactate)

In young infants without shock-N/2 saline in 5% dextrose; colloid solutions in

patients who already have volume overload, i.e., massive pleural effusion

Fluid replacement rate – minimum necessary to maintain effective circulatory

volume, excess amount will leak into the pleural and peritoneal spaces

Initial rate of administration

DSS grade III – 10 mL/kg/hour for 1-2 hours

Grade IV – Free flow or 20 mL/kg/dose IV bolus until BP can be

measured (usually within 5-15 minutes), then reduce the rate to 10

mL/kg/hour for 1-2 hours

Non-shock patients: normal maintenance or + 5%deficit and then

reduce the rate to minimum after 2-4 hours, if possible. Body weight <

15 kg: 4-7 mL/kg/hour. Body weight 15-40 kg: 3-5 mL/kg/hour

Colloids: The initial rate is 10 mL/kg/hour; this will reduce Hct by

about 10 percentage points e.g. from 53 to 43%. After that, reduce to 5,

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then to 3 mL/kg/hour

Increase or decrease the rate of IV fluid depending on: clinical signs of shock,

hematocrit level, urine output

In case of no response to IV fluids: consider and correct

Massive plasma leakage

Concealed internal bleeding – decrease in Hct

Hypoglycemia – Blood sugar < 60 mg%

Hyponatremia, hypocalcemia – electrolytes

Acidosis – indicates metabolic acidosis in blood gas analysis

Duration of IV fluid infusion: between 24-48 hours as plasma loss may continue

for 24-48 hours. It should be discontinued when the hematocrit level falls to

approximately 40%, with stable vital signs. A good urine flow indicates sufficient

circulating volume. Reabsorption of extravasated plasma occurs 48 hours after the

termination of shock (manifested by a further drop in hematocrit levels after

intravenous fluid administration has been stopped), and hypervolemia, pulmonary

edema or heart failure may occur if more fluid is given. It is extremely important

that a drop in hematocrit levels at this later stage is not interpreted as a sign of

internal bleeding.Strong pulse and blood pressure and adequate dieresis are good

signs at this stage. The return of the patient’s appetite is also a sign of recovery.

Blood and platelet transfusion

The indications for fresh whole blood or packed red cell transfusion are

significant blood loss > 10% (6-8 mL/kg), hemolysis, concealed

internal bleeding

Dose: Fresh whole blood 10 mL/kg/dose, packed red cells 5

mL/kg/dose

Indication for platelet transfusion: significant bleeding with

thrombocytopenia or if platelet count is less than 10,000/mm3 (10-20

mL/kg of platelets). Mild reductions in platelet counts are usually not

associated with significant bleeding. Platelets return to normal within 7-

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9 days. Only 0.4% of DHF patients need platelet transfusion


In children with hypotension (DSS grade III), Ringer’s lactate solution,

10-20 mL/kg, should be infused over 1 hour or given as bolus 20 mL/kg if blood

pressure is unrecordable (DSS grade IV). The bolus may be repeated twice if there

is no improvement. If there is no improvement in vital parameters and hematocrit

level rises, colloids 10 mL/kg should be rapidly infused. If the hematocrit level is

falling without improvement in vital parameters, blood transfusion is necessary,

presuming that lack of improvement is due to occult blood loss (Figure 4). Once

improvement starts, the fluid infusion rate should be gradually decreased.9

Patients who are unresponsive to fluids may have myocardial dysfunction

and decreased left ventricular performance, which may be easily detected by

echocardiography. Low platelet count may not be predictive of bleeding. Platelets

or blood should not be transfused based upon platelet count alone. In children

with severe thrombocytopenia in absence of significant bleeding, platelet infusion

does not alter the outcome. Infusion of fresh frozen plasma and platelet

concentrates may be beneficial in patients with disseminated intravascular

coagulation.8,9

27 | P a g e

Figure 4 Management for DSS

COMPLICATIONS

The complications can occur from DHF include 2,9

1. Electrolyte imbalance : Hyponatremia, Hypocalcemia

2. Fluid overload (overhydration) : avoid the common causes of fluid

overload, which are:

a. Early IV fluid therapy- in the febrile phase

b. Excessive use of hypotonic solutions

c. Non-reduction in the rate of IV fluid after initial resuscitation

d. Blood loss replaced with fluids in cases with occult bleeding

e. Judicious fluid removal using colloids with controlled diuresis

(furosemide 1 mg/kg infusion over 4 hours) or dialysis

28 | P a g e

3. Large pleural effusions, ascites

4. Disseminated intravascular coagulation

CRITERIA FOR DISCHARGING IN PATIENTS

Patients who are resuscitated from shock rapidly recover. Patients with

dengue hemorrhagic fever or dengue shock syndrome may be discharged from the

hospital when they meet the following criteria:2,9

1. Afebrile for at lease 24 hours without antipyretics

2. Good appetite, clinically improved condition

3. Adequate urine output

4. Stable hematocrit level

5. At least 48 hours since recovery from shock: stable pulse, blood

pressure and breathing rate

6. Absence of respiratory distress from pleural effusion and no ascites

7. Platelet count greater than 50,000 cells/μL

8. No evidence of external or internal bleeding

9. Convalescent confluent petechial rash

PROGNOSIS

Significant morbidity and mortality can result if early recognition and

monitoring of severe forms are not done. If left untreated, the mortality of DHF or

DSS patients may be as high as 40-50%. Early recognition of illness, careful

monitoring and appropriate fluid therapy alone have decreased mortality to 1%. If

shock is identified when pulse pressure starts to drop and intravenous fluids are

administered, the outcome will be excellent. Infrequently, there is residual brain

damage caused by prolonged shock or occasionally by intracranial hemorrhage.10

Recovery is fast and most patients recover in 24-48 hours without any

sequelae. The outcome may not be so good if the patient develops cold

extremities. Most deaths from DHF/DSS are caused by prolonged shock, massive

bleeding, fluid overload and acute liver failure with encephalopathy. Severe

refractory shock, DIC, ARDS, liver failure and neurological manifestations singly

29 | P a g e

or in combination were the commonest causes of death in a recent series. The case

fatality rate is high with shortage of experienced medical teams.9

PREVENTION AND CONTROL

At present, no specific drug or vaccine is available against the dengue

virus. The control is primarily dependent on vector control.1,8,9

1) Environmental changes: improved water supply, mosquito proofing of

overhead tanks, cisterns and underground reservoirs.

2) Personal protection: protective clothing, mats, aerosol coils (pyrethrum),

repellents e.g., DEET, permethrin impregnated in cloth, insecticide-treated

mosquito nets and curtains.

3) Biological control: by larvivorous fish: Gambria affinis and Peorilia

reticulate. Bacteria – Bacillus thuringiensis H-14, Bacillus sphaericus – in

polluted water.

4) Chemical control: 1% temephos sand granules. Space sprays – malathion,

fenitrothion, pirimiphos (only in major DHF epidemics). Insect growth

regulators – interfere with development of the immature stages of the

mosquito in larvae or disruption of pupal stage.

The aim of doing this paper is to report a case of grade II dengue

hemorrhagic fever of an 6 year-old girl that was admitted at the Infection Unit of

Pediatric Ward Haji Adam Malik General Hospital.

30 | P a g e

CASE

EN, a 6 year-old girl, 19 kg, 116 cm, was admitted to the Infection Unit of

Pediatric Ward Haji Adam Malik General Hospital on October 29th, 2010 at 02.00

am with chief complaint was fever. The fever occured suddenly since 3 days ago

with a characteristic of high fever which relieved with fever relieving medication.

Shivers and seizures were not found. .

Pain behind the eyes was not found. Patient experienced epistaxis 1 day

ago. Small red patches were found on hands and legs since a day ago. Neither

gingival bleeding and black stool.Patient complained of fatigue since 3 days ago.

Nausea and vomiting were found since 3 days ago with a frequency of 3x/day.

Volume: ¼ Aqua cup. Micturition and defecation were normal.

History of previous illness: This patient was referred from RSU Dr.Hadrianus

Sinaga for the diagnosis of the Dengue Haemorrhagic

Fever.

History of drugs usage : Ringer Lactat,Cefadroxil,Parasetamol,Ranitidine

PHYSICAL EXAMINATION

Generalized Status:

Body weight (BW) : 19 kg Body length (BL) : 120 cm

BW/ BL : 90,4% (normoweight)

Consciousness: Was Clear Body Temperature : 38,6 ۫CAnemic (-), icteric (-), cyanosis (-), oedema (-), dyspnea (-)

Localized Status:

Head : Eye: light reflexes (+/+), isochoric pupil (right=left), pale inferior

conjunctival palpebral (-/-), palpebra edema (-/-)

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Mouth/Ears /Nose: Within normal limit

Neck : Lymph node enlargement (-), JVP: R-2cmH₂O

Chest : Symmetrical fusiformic, retraction of epigastric (-)

HR: 123 bpm, regular, no murmur

RR: 20 rpm, regular, no rales

Abdominal : Soepel, peristaltic was normal,

Liver : Not palpable

Spleen: Not palpable

Extremities : Pulse: 123 bpm, regular, pressure/volume: adequate

BP: 90/50 mmHg, CRT < 3’’ cold acral, ptechiae (+) o/t superior-

inferior dextra-sinistra extremities

Rumple leed : (+)

Urogenital : Female, within normal limit

Laboratorium Findings (October 29th 2010) from

Emergency Unit of Adam Malik

Test Result Normal Value

Complete Blood CountHemoglobin (Hb)Erytrocyes (RBC)Leucocytes (WBC)Hematocrit Thrombocyte MCVMCHMCHCRDW

12.20 g%5.2 x 106/mm3

2,5 x 103/ mm3

45,90 %55x 103/ mm3

80.70 fL26.80pg33.20g%13.30 %

11-15g%3.0-5.3x106mm3

5.000-10.000x103/mm3

36-46%150-400x103mm3

83-103fL28-34pg32-36g%39-46%

Cell CountNeutrophilLymphocyteMonocyteEosinophilBasophil

52% 35,20%11,60%0,00%1,200%

37- 80% 20-40%

2-8% 1-6% 0-1%

Differential diagnosis :- DHF grade II

- Chikugunya

Working diagnosis : DHF grade II

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Management :

IVFD RL 5 cc/BW 95gtt/i micro

Paracetamol 3x250 mg

Diet porridge 1450kkal with 38 grams of protein.

Investigation Plan : Routine Blood Count/6 hour

Follow Up

Follow Up October 29th 2010 06.00 am

S Fever (+) 4th day, epistaxis (+), red spots in body (+)

O Consciousness: Was Clear T: 38,0 ۫C BW: 19,0 kg BL: 116cm

BW/BL: 90,4 % (normoweight)

Head : Eyes: Light reflexes (+/+), isochoric pupil, pale inferior

palpebral conjunctiva (-), Ears/Nose/Mouth: Within normal

limits,

Neck : Lymph nodes enlargement (-), JVP: R-2cmH₂O

Chest : Symmetrical fusiformic, retraction of epigastrial (-),

HR : 100 bpm, regular, no murmur

RR : 30 rpm, regular, no rales

Abdomen : Soepel, normal peristaltic, epigastrial pain (-),

Liver / Spleen: Not palpable

Extremities: Pols 100 bpm, regular, Pressure/Volume:adequate,

CRT < 3” warm acral, BP :90/60mmHg, ptechiae (+) o/t superior-inferior

dextra-sinistra extremities

A DHF Grade II

P IVFD RL 5 cc/BW/hour 95 gtt/i micro

Paracetamol 3x250 mg

Diet porridge 1450 kkal with 38 grams of protein

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Investigation plan :

- Routine Blood Count / 6 hours

- consult to Infection Division

- Lab examination IgG and IgM anti dengue

Laboratory findings at 12.00 pm:

Hb : 12,7 g%

Ht : 44,80 %

L : 3,17 x 103/ mm3

Plt : 51 x 103/ mm3


Hb : 13,00 g%

Ht : 45,40 %

L : 3,84 x 103/ mm3

Plt : 47 x 103/ mm3

Follow Up October 30th 2010 06.00 am

S Fever (-) 5th day, epistaxis (-), red spots in body (+)

O Consciousness : Was Clear T: 37,1 ۫C BW: 19 kg BL: 116cm

BW/BL: 90,4 %


palpebral conjunctiva (-), Ears/Nose/Mouth: Within

normal limits,






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Extremities : Pols 98 bpm, regular, Pressure/Volume:adequate,



Investigation plan : Waiting for IgG and IgM anti dengue lab result

A DHF Grade II

P IVFD RL 3cc/BW 57 gtt/i micro


Laboratory findings at 06.00 am :

Hb : 12,10 g%

Ht : 44.80%

L : 7,35 x 103/ mm3

Plt : 41 x 103/ mm3


Hb : 12,40 g%

Ht : 45,10 %

L : 9,19 x 103/ mm3

Plt : 57 x 103/ mm3

Laboratory findings at 06.00 pm :

Hb : 13,30 g%

Ht : 42.80 %

L : 5,11 x 103/ mm3

Plt : 66 x 103/ mm3


Hb : 12,60 g%

Ht : 42.50%

L : 6,54 x 103/ mm3

Plt : 72 x 103/ mm3

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Imunoserologi : Virus

Anti DHF IgM : Positif

Anti DHF IgG : Positif

Follow Up October 31st 2010 06.00 am

S Fever (-) 6th day, red spots in body (+)

O Consciousness : Was Clear T: 36,7C BW: 19 kg BL: 116cm

BW/BL: 90,4%,



limits,










A DHF Grade II

P IVFD RL 3 cc/BW/hour 57 gtt/i micro


- Investigation : - Routine Blood Count at 06.00pm

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Hb : 11,50 g%

Ht : 39.60 %

L : 7,22 x 103/ mm3

Plt : 64 x 103/ mm3


Hb : 11,4 g%

Ht : 38.50 %

L : 7,39 x 103/ mm3

Plt : 65 x 103/ mm3

Follow Up October 1st 2010 06.00 am

S Fever (-)

O Consciousness : Was Clear T: 36,8C BW: 19 kg BL: 116cm

BW/BL: 90,4%



limits,







37 | P a g e


CRT < 3” warm acral, BP :90/60mmHg

A DHF Grade II

P IVFD RL 3 cc/BW/ hour 57 gtt/i micro



Hb : 11,40 g%

Ht : 37.40 %

L : 6,96 x 103/ mm3

Plt : 93 x 103/ mm3

Patient is discharged from the hospital.

DISCUSSION

According to WHO, all 4 criteria must be fulfilled to make the diagnosis

of DHF, which are: 1) fever or history of acute fever lasting 2-7 days; 2) bleeding

(haemorrhagic tendencies); 3) thrombocytopaenia (100.000 cells per mm3 or

less); and 4) evidence of plasma leakage due to increased vascular permeability.

In this patient all of the criteria were found, which were 1) sudden of high-grade

38 | P a g e

fever since 3 days ago; 2) small red patches (petechies) on hands and legs and

history of bleeding nose as haemorrhagic tendencies; and from the laboratory

results were 3) thrombocytopaenia (platelet 55.000/mm3) and 4) raised of

hematocrit (44,9%) as the evidence of plasma leakage.

Laboratory examinations of IgM and IgG are important to find out

whether its primary or secondary infections. Primary infections are characterized

by an increase in dengue-specific IgM antibodies 4 to 5 days after the onset of

fever and by an increase in IgG antibodies only after 7 to 10 days. IgM antibodies

are detectable for three to six months, whereas IgG antibodies remain detectable

for life.In this patient,IgM and IgG were checked on day 5th .Both IgM and Ig G

were positive and this concludes that this patient has been exposed with one of the

dengue serotypes earlier and currently suffering the secondary infection. Isolation

of most strains of dengue virus from clinical specimens can be accomplished in

which the sample is taken in the first few days of illness and processed without

delay to know the serotype of the dengue virus .Specimens that may be suitable

for virus isolation include acute phase serum, plasma or washed buffy coat from

the patient, autopsy tissues from fatal cases, especially liver, spleen, lymph nodes

and thymus, and mosquitoes collected in nature. In this patient,serotype of the

denque virus could not been found as isolation of virus were not done.

The severity of DHF are classified into 4 gradings according to WHO

guidelines which are:

1. Grade I is defined as fever and non-specific constitutional signs and

symptoms; the only haemorrhagic manifestation is a positive TT and/or

easy bruising.

2. Grade II is the same as grade I but includes spontaneous bleeding,

usually in the form of skin or other haemorrhages.

39 | P a g e

3. Grade III is circulatory failure manifested by a rapid, weak pulse and

narrowing of the pulse pressure or hypotension, with the presence of

cold, clammy skin and restlessness.

4. Grade IV is profound shock with undetectable blood pressure or pulse.

Grades III and IV are define are as DSS.

Spontaneous bleeding (petechiaes and history of epistaxis) was found

because the girl had petechiaes on her extremities. Thus, the patient was

diagnosed as DHF grade II.

There is no specific treatment for DHF, only supportive care is required.

Therapy for DHF is wholly symptomatic and aims at controlling the clinical

manifestations of shock and hemorrhage. This patient was given intravenous fluid

(RL) and paracetamol. This patient was discharged from hospital after the routine

blood count showed that platelet and hematocrit level were in normal value

(93000/mm3 and 37.40%).

SUMMARY

It has been reported a case of a 6-year-old girl with dengue haemorrhagic

fever grade II. The diagnosis was established based on history taking, clinical

manifestation, and laboratory findings. Treatment for this patient was only

supportive and symptomatic. This patient was discharged from hospital after the

condition the routine blood count of platelet and hematocrit level were in normal

value.

REFERENCES

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Gorp, E., C., M., Soemantri. 2006. Changing Epidemiology of Dengue

Haemorrhagic Fever in Indonesia. Available from :

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2010]

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