Lapkas DHF Dep Anak Complete

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Case Report

DENGUE HEMORRHAGIC FEVER

Presenter : Lucyana Carolina S (100100213)

Indah Khairani Nst (100100237)

Supervisor : dr. Oke Rina, Sp.A (K)

__________________________________________________________________

INTRODUCTION

Dengue is a mosquito-borne disease caused by any one of four closely related

dengue viruses (DENV-1, -2, -3 and -4). Infection with one serotype of DENV provides

immunity to that serotype for life, but provides no long-term immunity to other

serotypes. Thus, a person can be infected as many as four times, once with each

serotype. Dengue viruses are transmitted from person to person by Aedes mosquitoes (

most often Aedes aegypti ) in the domestic environment.5

Dengue Haemorrhagic Fever (also known as Severe Dengue) was first

recognized in the 1950s during dengue epidemics in the Philippines and Thailand.

Today, severe dengue affects most Asian and Latin American countries and has become

a leading cause of hospitalization and death among children in these regions.Typical

cases of DHF are characterized by four major clinical manifestations : high fever,

haemorrhagic phenomena, and often, hepatomegaly and circulatory failure.1

In 2013, cases have occurred in Florida (United States of America) and Yunnan

province of China. Dengue also continues to affect several south American countries

notably Honduras, Costa Rica and Mexico. In Asia, Singapore has reported an increasein cases after a lapse of several years and outbreaks have also been reported in Laos. In

2014, trends indicate increases in the number of cases in the Cook Islands, Malaysia,

Fiji and Vanuatu, with Dengue Type 3 (DEN 3) affecting the Pacific Island countries

after a lapse of over 10 years.1


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An estimated 500 000 people with severe dengue require hospitalization each

year, a large proportion of whom are children. About 2.5% of those affected die.2

Transmission

WHO/TDR/Stammers

The Aedes aegypti mosquito is the primary vector of dengue. The virus is

transmitted to humans through the bites of infected female mosquitoes. After virus

incubation for 410 days, an infected mosquito is capable of transmitting the virus for

the rest of its life. Infected humans are the main carriers and multipliers of the virus,

serving as a source of the virus for uninfected mosquitoes. Patients who are already

infected with the dengue virus can transmit the infection (for 45 days; maximum 12)

viaAedesmosquitoes after their first symptoms appear.2

The Aedes aegyptimosquito lives in urban habitats and breeds mostly in man-

made containers. Unlike other mosquitoes Ae. aegypti is a daytime feeder; its peak

biting periods are early in the morning and in the evening before dusk. Female Ae.

aegyptibites multiple people during each feeding period. Aedes albopictus, a secondary

dengue vector in Asia, has spread to North America and Europe largely due to the

international trade in used tyres (a breeding habitat) and other goods (e.g. lucky

bamboo). Ae. albopictus is highly adaptive and therefore can survive in cooler

temperate regions of Europe. Its spread is due to its tolerance to temperatures below

freezing, hibernation, and ability to shelter in microhabitats.2


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Characteristics

Dengue fever is a severe, flu-like illness that affects infants, young children and

adults, but seldom causes death. Dengue should be suspected when a high fever (40C/

104F) is accompanied by two of the following symptoms: severe headache, pain

behind the eyes, muscle and joint pains, nausea, vomiting, swollen glands or rash.

Symptoms usually last for 27 days, after an incubation period of 410 days after the

bite from an infected mosquito.3

Severe dengue (DHF) is a potentially deadly complication due to plasma

leaking, fluid accumulation, respiratory distress, severe bleeding, or organ impairment.

Warning signs occur 37 days after the first symptoms in conjunction with a decrease in

temperature (below 38C/ 100F) and include: severe abdominal pain, persistent

vomiting, rapid breathing, bleeding gums, fatigue, restlessness, blood in vomit. The next

2448 hours of the critical stage can be lethal; proper medical care is needed to avoid

complications and risk of death.2,3

EPIDEMIOLOGY

Dengue fever (DF) is the fastest emerging arboviral infection spread by Aedes

aegypti mosquitoes with major public health consequences for millions of people

around the world, and in particular the South-East Asia and Asia-Pacific Regions of the

World Health Organization (WHO). Of the 2.5 billion people globally at risk of DF and

its severe forms dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS)

South-East Asia accounts for approximately 1.3 billion or 52%. As the disease spreads

to new geographical areas, the frequency of the outbreaks has increased along with a

rapidly changing disease epidemiology.

7

A dengue epidemic requires the presence of :

The vector mosquito (usually Aedes aegypti).

The dengue virus.

A large number of susceptible human hosts.


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CLASSIFICATION

The 1997 WHO classification of dengue virus infection

2

The 2009 revised dengue case classification3

Grading severity of dengue haemorrhagic fever

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

considered to be DSS. The presence of thrombocytopenia with concurrent

haemoconcentration differentiates grades I and II DHF from DF.4


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Grade I: Fever accompanied by non-specific constitutional symptoms; the only

haemorrhagic manifestation is a positive tourniquet test and/or easy bruising.

Grade II: Spontaneous bleeding in addition to the manifestations of Grade I patients,

usually in the forms of skin or other haemorrhages.

Grade III: Circulatory failure manifested by a rapid, weak pulse and narrowing of pulse

pressure or hypotension, with the presence of cold, clammy skin and restlessness.

Grade IV: Profound shock with undetectable blood pressure or pulse. Grading the

severity of the disease at the time of discharge has been found clinically and

epidemiologically useful in DHF epidemics in children in the WHO Regions of the

Americas, South-East Asia and the Western Pacific, and experience in Cuba, Puerto

Rico and Venezuela suggests that grading is also useful for adult cases.4

CLINICAL FEATURES & DIAGNOSIS

WHO 1997 case definitions for DF, DHF and DSS2

Dengue Fever

Probable

- An acute febrile illness with two or more of the following manifestations: headache,

retro-orbital pain, myalgia, arthralgia, rash, haemorrhagic manifestations and leucopenia

And

- Supportive serology (a reciprocal haemagglutination-inhibition antibody titre 1280, a

comparable IgG enzyme-linked immunosorbent assay (ELISA) titre or a positive IgMantibody test on a late acute or convalescent-phase serum specimen)

Or

- Occurrence at the same location and time as other DF cases


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Confirmed

A case confirmed by one of the following laboratory criteria :

- Isolation of the dengue virus from serum or autopsy samples

- An at least four-fold change in reciprocal IgG/IgM titres to one or more dengue virus

antigens in paired samples

- Demonstration of dengue virus antigen in autopsy tissue, serum or cerebrospinal fluid

samples by immunohistochemistry, immunofluorescence or ELISA

- Detection of dengue virus genomic sequences in autopsy tissue serum or cerebrospinal

fluid samples by polymerase chain reaction (PRC)

Reportable

- Any probable or confirmed case should be reported

Dengue Hemorrhagic Fever

For a diagnosis of DHF, a case must meet all four of the following criteria :

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

- A haemorrhagic tendency shown by at least one of the following :

A positive tourniquet test

Petechiae, ecchymoses or purpura

Bleeding from the mucosa, gastro-intestinal tract, injection sites or other

locations

Haematemesis or melaena

- Thrombocytopenia 100,000 cells/mm3 (100x109/L)

- Evidence of plasma leakage owing to increased vascular permeability shown by:

An increase in haematocrit 20% above average for age, sex and population


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A decrease in the haematocrit after intervention 20% of baseline

Signs of plasma leakage such as pleural effusion, ascites or hypoproteinaemia

Dengue Shock Syndrome

For a case of DSS, all four criteria for DHF must be met, in addition to evidence of

circulatory failure manifested by :

- Rapid and weak pulse

And

- Narrow pulse pressure (< 20 mmHg or 2-7 kPa)

Or manifested by

- Hypotension for age

And

- Cold, clammy skin and restlessness

The Course of Dengue Illness4

Febrile phase4

Patients typically develop high-grade fever suddenly. This acute febrile phase

usually lasts 27 days and is often accompanied by facial flushing, skin erythema,

generalized body ache, myalgia, arthralgia and headache. Some patients may have sore

throat, injected pharynx and conjunctival injection. Anorexia, nausea and vomiting are

common. It can be difficult to distinguish dengue clinically from non-dengue febrile

diseases in the early febrile phase. A positive tourniquet test in this phase increases the

probability of dengue. In addition, these clinical features are indistinguishable between

severe and non-severe dengue cases. Therefore monitoring for warning signs and other

clinical parameters is crucial to recognizing progression to the critical phase. Mild

haemorrhagic manifestations like petechiae and mucosal membrane bleeding (e.g. nose

and gums) may be seen. Massive vaginal bleeding (in women of childbearing age) and

gastrointestinal bleeding may occur during this phase but is not common. The liver is


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often enlarged and tender after a few days of fever. The earliest abnormality in the full

blood count is a progressive decrease in total white cell count, which should alert the

physician to a high probability of dengue.

Critical phase

Around the time of defervescence, when the temperature drops to 37.538oC or

less and remains below this level, usually on days 37 of illness, an increase in capillary

permeability in parallel with increasing haematocrit levels may occur. This marks the

beginning of the critical phase. The period of clinically significant plasma leakage

usually lasts 2448 hours. Progressive leukopenia followed by a rapid decrease in

platelet count usually precedes plasma leakage. At this point patients without an

increase in capillary permeability will improve, while those with increased capillary

permeability may become worse as a result of lost plasma volume. The degree of

plasma leakage varies. Pleural effusion and ascites may be clinically detectable

depending on the degree of plasma leakage and the volume of fluid therapy. Hence

chest x-ray and abdominal ultrasound can be useful tools for diagnosis. The degree of

increase above the baseline haematocrit often reflects the severity of plasma leakage.

Shock occurs when a critical volume of plasma is lost through leakage. It is often

preceded by warning signs. The body temperature may be subnormal when shock

occurs. With prolonged shock, the consequent organ hypoperfusion results in

progressive organ impairment, metabolic acidosis and disseminated intravascular

coagulation. This in turn leads to severe haemorrhage causing the haematocrit to

decrease in severe shock. Instead of the leukopenia usually seen during this phase of

dengue, the total white cell count may increase in patients with severe bleeding. In

addition, severe organ impairment such as severe hepatitis, encephalitis or myocarditisand/or severe bleeding may also develop without obvious plasma leakage or shock.

Those who improve after defervescence are said to have non-severe dengue. Some

patients progress to the critical phase of plasma leakage without defervescence and, in

these patients, changes in the full blood count should be used to guide the onset of the

critical phase and plasma leakage.


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Those who deteriorate will manifest with warning signs. This is called dengue

with warning signs. Cases of dengue with warning signs will probably recover with

early intravenous rehydration. Some cases will deteriorate to severe dengue.

Recovery phase 4

If the patient survives the 2448 hour critical phase, a gradual reabsorption of

extravascular compartment fluid takes place in the following 4872 hours. General

well-being improves, appetite returns, gastrointestinal symptoms abate, haemodynamic

status stabilizes and diuresis ensues. Some patients may have a rash of isles of white in

the sea of red. Some may experience generalized pruritus. Bradycardia and

electrocardiographic changes are common during this stage. The haematocrit stabilizes

or may be lower due to the dilutional effect of reabsorbed fluid. White blood cell count

usually starts to rise soon after defervescence but the recovery of platelet count is

typically later than that of white blood cell count.Respiratory distress from massive

pleural effusion and ascites will occur at any time if excessive intravenous fluids have

been administered. During the critical and/or recovery phases, excessive fluid therapy is

associated with pulmonary oedema or congestive heart failure.

The various clinical problems during the different phases of dengue can be summarized

as in Table 2.1

Table 2.1 Febrile, critical and recovery phases in dengue

1 Febrile phase

Dehydration; high fever may cause neurological disturbances and febrile seizures in

young children.

2 Critical phaseShock from plasma leakage; severe haemorrhage; organ impairment

3 Recovery phase

Hypervolaemia (only if intravenous fluid therapy has been excessive and/or has

extended into this period)


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Severe dengue 4

Severe dengue is defined by one or more of the following:

(i) plasma leakage that may lead to shock (dengue shock) and/or fluid accumulation,

with or without respiratory distress, and/or

(ii) severe bleeding, and/or

(iii) severe organ impairment.

As dengue vascular permeability progresses, hypovolaemia worsens and results

in shock. It usually takes place around defervescence, usually on day 4 or 5 (range days

37) of illness, preceded by the warning signs. During the initial stage of shock, the

compensatory mechanism which maintains a normal systolic blood pressure also

produces tachycardia and peripheral vasoconstriction with reduced skin perfusion,

resulting in cold extremities and delayed capillary refill time. Uniquely, the diastolic

pressure rises towards the systolic pressure and the pulse pressure narrows as the

peripheral vascular resistance increases. Patients in dengue shock often remain

conscious and lucid. The inexperienced physician may measure a normal systolic

pressure and misjudge the critical state of the patient. Finally, there is decompensation

and both pressures disappear abruptly. Prolonged hypotensive shock and hypoxia may

lead to multi-organ failure and an extremely difficult clinical course (Textbox D). The

patient is considered to have shock if the pulse pressure (i.e. the difference between the

systolic and diastolic pressures) is 20 mm Hg in children or he/she has signs of poor

capillary perfusion (cold extremities, delayed capillary refill, or rapid pulse rate). In

adults, the pulse pressure of 20 mm Hg may indicate a more severe shock.

Hypotension is usually associated with prolonged shock which is often complicated by

major bleeding. Patients with severe dengue may have coagulation abnormalities, butthese are usually not sufficient to cause major bleeding. When major bleeding does

occur, it is almost always associated with profound shock since this, in combination

with thrombocytopaenia, hypoxia and acidosis, can lead to multiple organ failure and

advanced disseminated intravascular coagulation. Massive bleeding may occur without

prolonged shock in instances when acetylsalicylic acid (aspirin), ibuprofen or

corticosteroids have been taken.


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Unusual manifestations, including acute liver failure and encephalopathy, may be

present, even in the absence of severe plasma leakage or shock. Cardiomyopathy and

encephalitis are also reported in a few dengue cases. However, most deaths from dengue

occur in patients with profound shock, particularly if the situation is complicated by

fluid overload.

Severe dengue should be considered if the patient is from an area of dengue risk

presenting with fever of 27 days plus any of the following features:

There is evidence of plasma leakage, such as:

high or progressively rising haematocrit;

pleural effusions or ascites;

circulatory compromise or shock (tachycardia, cold and clammy extremities, capillary

refill time greater than three seconds, weak or undetectable pulse, narrow pulse pressure

or, in late shock, unrecordable blood pressure).

Thereis significant bleeding.

Thereis an altered level of consciousness (lethargy or restlessness,coma, convulsions).

Thereis severe gastrointestinal involvement (persistent vomiting, increasing or intense

abdominal pain, jaundice).

There is severe organ impairment (acute liver failure, acute renal failure,

encephalopathy or encephalitis, or other unusual manifestations, cardiomyopathy) or

other unusual manifestations.

Laboratory Findings3

Thrombocytopenia and haemoconcentration are constant findings in DHF. A

drop in the platelet count to below 100 000 per mm

3

is usually found between the thirdand eighth day of illness, often before or simultaneous with changes in the haematocrit.3

A rise in the haematocrit level, indicating plasma leakage, is always present,

even in non-shock cases, but is more pronounced in shock cases. Haemoconcentration

with an increase in the haematocrit of 20% or more is considered to be definitive

evidence of increased vascular permeability and plasma leakage. It should be noted that


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the haematocrit level may be affected either by early volume replacement or by

bleeding.3

The time-course relation-ship between a drop in the platelet count and a rapid

rise in the haematocrit appears to be unique for DHF; both changes occur before

defervescence and before the onset of shock.3,6,7

In DHF, the white-blood-cell count may be variable at the onset of illness,

ranging from leukopenia to mild leukocytosis, but a drop in the total white- blood-cell

count due to a reduction in the number of neutrophils is virtually always observed near

the end of the febrile phase of illness. Relative lymphocytosis, with the presence of

atypical lymphocytes, is a common finding before defervescence or shock. A transient

mild albuminuria is sometimes observed, and occult blood is often found in the stool. 6,7

In most cases, assays of coagulation or fibrinolytic factors show a reduction in

fibrinogen, prothrombin, factor VIII, factor XII, and antithrombin III. A reduction in

antiplasmin (plasmin inhibitor) has been noted in some cases. In severe cases with

marked liver dysfunction, reductions are observed in the levels of the prothrombin

factors hat are vitamin-K dependent, such as factors V, VII, IX and X. Partial

thromboplastin time and prothrombin time are prolonged in about one-half and one-

third of DHF patients, respectively. Thrombin time is prolonged in severe cases. Platelet

function has also been found to be impaired. Serum complement levels, particularly that

of C3, are reduced.6

The other common findings are hypoproteinaemia (due to a loss of albumin),

hyponatraemia, and elevated levels of serum aspartate aminotransferase. Metabolic

acidosis may frequently be found in prolonged shock. Blood urea nitrogen is elevated at

the terminal stage of shock. X-ray examination of the chest reveals pleural effusion,

mostly on the right side, as a constant finding, and the extent of pleural effusion iscorrelated with the severity of disease. In shock, bilateral pleural effusion is a common

finding.6,7

Guidance for diagnosis of DHF/DSS2

The following manifestations have been selected as indicating a provisional

diagnosis of DHF/DSS. They are not intended to be substitutes for the above case


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definitions. The use of these criteria may help clinicians to establish an early diagnosis,

ideally before the onset of shock, as well as to avoid over diagnosis.

Clinical

The following clinical observations are important indicators of DHF/DSS:

High fever of acute onset

Haemorrhagic manifestations (at least a positive tourniquet test)

Hepatomegaly (observed in 9096% of Thai and 67% of Cuban children

with DHF)

Shock

Laboratory2

These laboratory findings support the above clinical observations:

Thrombocytopenia (100 000 cells per mm3or less)

Haemoconcentration (haematocrit elevated at least 20% above average for age, sex

and population).

The first two clinical observations, plus one of the laboratory findings (or at least

a rising haematocrit), are sufficient to establish a provisional diagnosis of DHF. 2

In monitoring haematocrit, one should bear in mind the possible effects of pre-

existing anaemia, severe haemorrhage or early volume replacement therapy. Moreover,

pleural effusion observed on a chest X-ray, or hypoalbuminaemia, can provide

supporting evidence of plasma leakage, the distinguishing feature of DHF. For a patient

with a provisional diagnosis of DHF, if shock is present, a diagnosis of DSS is

supported.

2

TREATMENT4

A stepwise approach to the management of dengue

Step I. Overall assessment

I.1 History, including information on symptoms, past medical and family history

I.2 Physical examination, including full physical and mental assessment


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I.3 Investigation, including routine laboratory and dengue-specific laboratory

Step II. Diagnosis, assessment of disease phase and severity

Step III. Management

III.1 Disease notification

III.2 Management decisions. Depending on the clinical manifestations and other

circumstances, patients may:

be sent home (Group A);

be referred for in-hospital management (Group B);

require emergency treatment and urgent referral (Group C).

Treatment according to groups A

C

Group Apatients who may be sent home

These are patients who are able to tolerate adequate volumes of oral fluids and

pass urine at least once every six hours, and do not have any of the warning signs,

particularly when fever subsides.

Ambulatory patients should be reviewed daily for disease progression

(decreasing white blood cell count, defervescence and warning signs) until they are out

of the critical period. Those with stable haematocrit can be sent home after being

advised to return to the hospital immediately if they develop any of the warning signs

and to adhere to the following action plan:

Encourageoral intake of oral rehydration solution (ORS), fruit juice and other fluids

containing electrolytes and sugar to replace losses from fever and vomiting. Adequate

oral fluid intake may be able to reduce the number of hospitalizations. [Caution: fluidscontaining sugar/glucose may exacerbate hyperglycaemia of physiological stress from

dengue and diabetes mellitus.]

Give paracetamol for high fever if the patient is uncomfortable. The interval of

paracetamol dosing should not be less than six hours. Tepid sponge if the patient still

has high fever. Do not give acetylsalicylic acid (aspirin), ibuprofen or other non-


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steroidal anti-inflammatory agents (NSAIDs) as these drugs may aggravate gastritis or

bleeding. Acetylsalicylic acid (aspirin) may be associated with Reyes Syndrome.

Instruct the care-givers that the patient should be brought to hospital immediately if

any of the following occur: no clinical improvement, deterioration around the time of

defervescence, severe abdominal pain, persistent vomiting, cold and clammy

extremities, lethargy or irritability/restlessness, bleeding (e.g. black stools or coffee-

ground vomiting), not passing urine for more than 46 hours.

Group Bpatients who should be referred for in-hospital management

Patients may need to be admitted to a secondary health care centre for close

observation, particularly as they approach the critical phase. These include patients with

warning signs, those with co-existing conditions that may make dengue or its

management more complicated (such as pregnancy, infancy, old age, obesity, diabetes

mellitus, renal failure, chronic haemolytic diseases), and those with certain social

circumstances (such as living alone, or living far from a health facility without reliable

means of transport).

If the patient has dengue with warning signs, the action plan should be as

follows:

Obtaina reference haematocrit before fluid therapy. Give only isotonic solutions such

as 0.9% saline, Ringers lactate, orHartmanns solution. Start with 57 ml/kg/hour for

12 hours, then reduce to 35 ml/kg/hr for 24 hours, and then reduce to 23 ml/kg/hr

or less according to the clinical response.

Reassessthe clinical status and repeat the haematocrit. If the haematocrit remains the

same or rises only minimally, continue with the same rate (23 ml/kg/hr) for another 2

4 hours. If the vital signs are worsening and haematocrit is rising rapidly, increase the

rate to 510 ml/kg/hour for 12 hours. Reassess the clinical status, repeat the

haematocrit and review fluid infusion rates accordingly.


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Givethe minimum intravenous fluid volume required to maintain good perfusion

and urine output of about 0.5 ml/kg/hr. Intravenous fluids are usually needed for only

2448 hours. Reduce intravenous fluids gradually when the rate of plasma leakage

decreases towards the end of the critical phase. This is indicated by urine output and/or

oral fluid intake that is/are adequate, or haematocrit decreasing below the baseline value

in a stable patient.

Patients with warning signs should be monitored by health care providers until the

period of risk is over. A detailed fluid balance should be maintained. Parameters that

should be monitored include vital signs and peripheral perfusion (14 hourly until the

patient is out of the critical phase), urine output (46 hourly), haematocrit (before and

after fluid replacement, then 612 hourly), blood glucose, and other organ functions

(such as renal profile, liver profile, coagulation profile, as indicated).

If the patient has dengue without warning signs, the action plan should be as

follows:

Encourageoral fluids. If not tolerated, start intravenous fluid therapy of 0.9% saline or

Ringers lactate with or without dextrose at maintenance rate. For obese and overweight

patients, use the ideal body weight for calculation of fluid infusion. Patients may be able

to take oral fluids after a few hours of intravenous fluid therapy. Thus, it is necessary to

revise the fluid infusion frequently. Give the minimum volume required to maintain

good perfusion and urine output. Intravenous fluids are usually needed only for 2448

hours.

Patientsshould be monitored by health care providers for temperature pattern,volumeof fluid intake and losses, urine output (volume and frequency), warning

signs,haematocrit, and white blood cell and platelet counts. Other laboratory tests (such

as liver and renal functions tests) can be done, depending on the clinical picture and the

facilities of the hospital or health centre.


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Group C patients who require emergency treatment and urgent referral when they

have severe dengue

Patients require emergency treatment and urgent referral when they are in the

critical phase of disease, i.e. when they have:

severe plasma leakage leading to dengue shock and/or fluid accumulation with

respiratory distress;

severe haemorrhages;

severe organ impairment (hepatic damage, renal impairment,cardiomyopathy,

encephalopathy or encephalitis).

All patients with severe dengue should be admitted to a hospital with access to

intensive care facilities and blood transfusion. Judicious intravenous fluid resuscitation

is the essential and usually sole intervention required. The crystalloid solution should be

isotonic and the volume just sufficient to maintain an effective circulation during the

period of plasma leakage. Plasma losses should be replaced immediately and rapidly

with isotonic crystalloid solution or, in the case of hypotensive shock, colloid solutions.

If possible, obtain haematocrit levels before and after fluid resuscitation.

There should be continued replacement of further plasma losses to maintain

effective circulation for 2448 hours. For overweight or obese patients, the ideal body

weight should be used for calculating fluid infusion rates. A group and cross-match

should be done for all shock patients. Blood transfusion should be given only in cases

with suspected/severe bleeding. Fluid resuscitation must be clearly separated from

simple fluid administration. This is a strategy in which larger volumes of fluids (e.g.

1020 ml boluses) are administered for a limited period of time under close monitoringto evaluate the patients response and to avoid thedevelopment of pulmonary oedema.

The degree of intravascular volume deficit in dengue shock varies. Input is typically

much greater than output, and the input/output ratio is of no utility for judging fluid

resuscitation needs during this period.

The goals of fluid resuscitation include improving central and peripheral

circulation (decreasing tachycardia, improving blood pressure, pulse volume, warm and


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pink extremities, and capillary refill time 50%), repeat a second bolus of

crystalloid solution at 1020 ml/kg/hr for one hour. After this second bolus, if there is

improvement, reduce the rate to 710 ml/kg/hr for 12 hours, and then continue to

reduce as above. If haematocrit decreases compared to the initial reference haematocrit

(


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If thepatientscondition improves, give a crystalloid/colloid infusion of 10 ml/kg/hr

for one hour. Then continue with crystalloid infusion and gradually reduce to 57

ml/kg/hr for 12 hours, then to 35 ml/kg/hr for 24 hours, and then to 23 ml/kg/hr or

less, which can be maintained for up to 2448 hours.

If vital signs are still unstable (i.e.shock persists), review the haematocrit obtained

before the first bolus. If the haematocrit was low (


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Parameters that should be monitored include vital signs and peripheral perfusion

(every 1530 minutes until the patient is out of shock, then 12 hourly). In general, the

higher the fluid infusion rate, the more frequently the patient should be monitored and

reviewed in order to avoid fluid overload while ensuring adequate volume replacement.

If resources are available, a patient with severe dengue should have an arterial line

placed as soon as practical. The reason for this is that in shock states, estimation of

blood pressure using a cuff is commonly inaccurate. The use of an indwelling arterial

catheter allows for continuous and reproducible blood pressure measurements and

frequent blood sampling on which decisions regarding therapy can be based. Monitoring

of ECG and pulse oximetry should be available in the intensive care unit.

Urine output should be checked regularly (hourly till the patient is out of shock,

then 12 hourly). A continuous bladder catheter enables close monitoring of urine

output. An acceptable urine output would be about 0.5 ml/kg/hour. Haematocrit should

be monitored (before and after fluid boluses until stable, then 46 hourly). In addition,

there should be monitoring of arterial or venous blood gases, lactate, total carbon

dioxide/bicarbonate (every 30 minutes to one hour until stable, then as indicated), blood

glucose (before fluid resuscitation and repeat as indicated), and other organ functions

(such as renal profile, liver profile, coagulation profile, before resuscitation and as

indicated).

Changes in the haematocrit are a useful guide to treatment. However, changes

must be interpreted in parallel with the haemodynamic status, the clinical response to

fluid therapy and the acid-base balance. For instance, a rising or persistently highhaematocrit together with unstable vital signs (particularly narrowing of the pulse

pressure) indicates active plasma leakage and the need for a further bolus of fluid

replacement. However, a rising or persistently high haematocrit together with stable

haemodynamic status and adequate urine output does not require extra intravenous

fluid. In the latter case, continue to monitor closely and it is likely that the haematocrit

will start to fall within the next 24 hours as the plasma leakage stops.


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A decrease in haematocrit together with unstable vital signs (particularly

narrowing of the pulse pressure, tachycardia, metabolic acidosis, poor urine output)

indicates major haemorrhage and the need for urgent blood transfusion. Yet a decrease

in haematocrit together with stable haemodynamic status and adequate urine output

indicates haemodilution and/or reabsorption of extravasated fluids, so in this case

intravenous fluids must be discontinued immediately to avoid pulmonary oedema.

PREVENTION

There is no vaccine to prevent dengue fever. Use personal protection such as

full-coverage clothing, mosquito nets, mosquito repellent containing DEET. If possible,

travel during times of the day when mosquitos are not so active. Mosquito abatement

(control) programs can also reduce the risk of infection.

At present, the only method to control or prevent the transmission of dengue virus is to

combat vector mosquitoes through:

preventing mosquitoes from accessing egg-laying habitats by environmental

management and modification;

disposing of solid waste properly and removing artificial man-made habitats;

covering, emptying and cleaning of domestic water storage containers on a

weekly basis;

applying appropriate insecticides to water storage outdoor containers;

using of personal household protection such as window screens, long-sleeved

clothes, insecticide treated materials, coils and vaporizers;

improving community participation and mobilization for sustained vector

control;

applying insecticides as space spraying during outbreaks as one of the

emergency vector control measures;


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active monitoring and surveillance of vectors should be carried out to determine

effectiveness of control interventions.


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CASE REPORT

Name : CVAge : 2 years and 6 month old

Sex : Female

Date of Admission : October, 3rd2014

Chief Complaint : Fever

History:

Patient has suffered a high fever 5 days ago before referred to HAM Hospital.

High fever onset sudden and does not recover with fever-reducing drugs. Night sweats

(-). Seizures (-).

Besides fever, patient also complained pain at the joints of her arms and legs,

pain around the eyes and suffering a headache during fever.

Red spots were seen on the second day of fever. Spots originally appeared on the

chest and abdomen, and gradually getting more on the hands and legs, and so the entire

body.She has no history of pale, nosebleeds, bleeding gums, vomiting of blood or tarry,

nor bloody urination.

She also having a discomfort feeling at the center of the abdomen. Previously,

he had vomited once on the second day of fever, with the smell of sour, colorless, an

amount of about 2-3 teaspoons. History of tarry faeces was found, within 2 days ago.

History of DHF or DF were not encountered. There was a finding that patients

neighbor also affected by dengue. However, no family members having the same

complaint.

History of previous illness : The patient was treated by midwive before the admission

to HAM Hospital.

History of drugs : Unidentified


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Pregnant History

There is no history of fever, hypertension, diabetic mellitus, and consumed herbal

medicine.

Birth History

Sectio caesarea; attended by midwives; BW 3100 gram; cyanotic (-).

Immunization History

Completed

Feeding History

From birth to 6 months : Breast milk

From 6 to 12 months : Breast milk + rice porridge

From 12 months until now : daily menu

History of Growth and Development

Sitting : 5 months

Crawling : 8 months

Standing : 14 months

Walking : 14 months

Physical Examination

Generalized status

Body weight: 10 kg, Body length: 87 cmBW/age: -2


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Presens status

Level of Consciousness: Compos Mentis, Blood pressure 100/70 mmHg, HR: 92 bpm,

RR: 24 bpm, body temperature: 37,3oC, body weight : 10 kg, body length : 87 cm

Anemic (-), Icteric (-), Cyanosis (-), Edema (-), Dyspnea (-).

Localized status

Head :

Eye: Isochoric pupil (3mm/3mm), light reflex (+/+), inferior palp. conjunctiva pale (-/-),

icteric sclera (-/-).

Nose, Ear and Mouth were normal

Neck:

TVJ: R+2 cmH2O, Lymph node enlargement (-).

Thorax:

Symmetrical fusiformis, Chest retraction (-), HR : 92 bpm, reguler, murmur (-), RR: 24

x/i, regular, rales (-).

Abdomen:

Soepel, Normoperistaltic. Liver was enlargement 1cm BAC(D), spleen and renal were

unpalpable.

Extremities:

Pulse 92 bpm, regular, adequate pressure and volume, warm acral, CRT < 3, Blood

Pressure 100/70 mmHg, Petechie (+)

Urogenital:

Female, within normal limit.


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Laboratory Findings on HAM Hospital (October 3rd

2014)IGD:

Parameters Value Normal Value

Complete Bl ood Count

Hemoglobin 14,7 g/dL 1318

Leucocyte 5.600 /mm3 4.00011.000

Trombocyte 34.000 /uL 150.000450.000

ESR 8 mm/hour 010

Hematocrite 42 % 39 - 54

Eritrocyte 5.6 mil/mm 4.506.50

MCV 87 fl 8l -99

MCH 29 pg 2731

MCHC 33 g/dl 3137

RDW 13 % 10 - 15

PDW 7 fl 1018

MPV 6 fl 8.112.4

Leucocytes Count :

Neutrophil % 56.30 3780

Lymphocyte % 33.20 2040

Monocyte % 9.50 2 - 8

Eosinophil % 0.60 16

Basophil % 0.400 01

Neutrophil absolute 10 /L 4.43 2.76.5

Lymphocyte absolute 103/L 2.62 1.53.7

Monocyte absolute 10 /L 0.75 0.20.4

Eosinophil absolute 10 /L 0.05 00.10Basophil absolute 10 /L 0.03 00.1

Differential Diagnosis:

Dengue Hemorrhagic fever

Dengue Fever

Typhoid fever


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Malaria

Rheumatoid Fever

Chikungunya

Working Diagnosis:

Dengue Hemorrhagic Fever Grade II

Management:

Bed Rest

IVFD RL 10cc/ kgBB 100gtt/min micro

Paracetamol 3x1 cth

Diet daily menu

Diagnostic Planning:

Check Complete Blood Count, Electrolyte and Blood Glucose Level


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FOLLOW UP

October 3rd 2014

S Fever (-), Petechie (+), pain at joints of knee, arms, legs and around eyes (+), headache (+)

O Sens: Alert, Anemic (-). Icteric (-). Edema (-). Cyanosis (-) Dyspnoe (-). Body Temperature :

36,8 0C . Body weight: 10 kg, Body length: 87 cm.

Head Eye: Isochoric pupil (3mm/3mm), light reflex (+/+), inferior palpebra

conjunctiva pale (-/-), icteric sclera (-/-).

Nose, Ear and Mouth were within normal limit.

Neck VJP: R+2 cmH2O, Lymph node enlargement (-).

Thorax Symmetrical fusiformis, Chest retraction (-), HR :88bpm, reguler, murmur (-),

RR: 26 x/i, regular, rales (-).

Abdomen Soepel. Normoperistaltic. Liver was enlargement 1 cm BAC(D), spleen and

renal unpalpable.

Extremities Blod pressure: 100/70mmHg, Pulse 88 bpm, regular, adequate pressure and

volume, warm acral, CRT < 3, petekie (+)

Genital Female, within normal limit

A DHF grade 2

P - Bed Rest

- IVFD RL 10cc/kgBB 100 gtt/min micro

- Paracetamol 3xcth1

-

Diet daily menu 1000 kkal + 20 gram protein

Planning:

CBC/6hoursUrinalisis

IgG IgM Anti Dengue

October 4t

2014

S Fever (-), Petechie (+), pain at joints of knee, arms, legs and around eyes (+), headache (+)



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October 5t

2014

S Fever (-), Petechie (+),pain at joints of knee, arms, legs and around eyes (+), headache (+)


36,50C . Body weight: 10 kg, Body length: 87 cm.


36,7 C . Body weight: 10 kg, Body length: 87 cm.




Neck TVJ R+2 cmH2O, Lymph node enlargement (-).

Thorax Symmetrical fusiformis, Chest retraction (-), HR : 80 bpm, reguler, murmur (-),


Abdomen Soepel Normoperistaltic. Liver was enlargement 1 cm BAC, spleen and renal

unpalpable.

Extremities Blood pressure: 110/80 mmHg, Pulse 80 bpm, regular, adequate pressure and

volume, warm acral, CRT < 3


A Dengue Hemorrhagic Fever grade II

P - Bed Rest

-

IVFD RL 10cc/kgBB 100 gtt/min macro


- Diet daily menu 1000 kkal + 20 gram protein

Hasil Lab:

Hb: 12,5/Ht: 36.00/Leu:5890/Trombocyte:26000

Anti DHF Ig.M : -

Ani DHF Ig.G : +

CRP : +

Procalcitonin : 1,66


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Abdomen Soepel Normoperistaltic. Liver was enlargement 1 cm BAC, spleen and renal

unpalpable.





P - Bed Rest

- IVFD RL 10cc/kgBB 100 gtt/min macro


-

Diet daily menu 1000 kkal + 20 gram protein

Hasil Lab:

Hb: 12,5/Ht:36,5/Leu: 5660/Trombocyte: 61000

October 6t

2014

S Fever (-), Petechie (+),pain around eyes (+), headache (+)









Abdomen Soepel Normoperistaltic. Liver, spleen and renal unpalpable.



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P -

Bed Rest

- IVFD D5% NaCl 0,45% 30cc/jam



- Hasil Lab:

- Hb: 11,9/Ht: 36,5/Leu: 6100/Trombocyte: 76.000

October 7t

2014

S Fever (-), Petechie (+),pain around eyes (+), headache (+)









Abdomen Soepel Normoperistaltic. Liver, spleen and renal unpalpable.

Extremities Blood pressure: 110/80mmHg, Pulse 84 bpm, regular, adequate pressure and




P -

Bed Rest

- IVFD D5% NaCl 0,45% 30cc/jam

-

Paracetamol 3xcth1

Hasil Lab:

Hb:11,9/ Ht: 36,5/Leu: 6220/Trombocyte: 81.000


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Discussion

CV, female, 2 years and 6 month old, was arrived at HAM Hospital on October

3rd and was diagnosed as having DHF Grade 2 at Emergency Unit at HAM Hospital.

This diagnosis was made based on clinical findings, found in the patient such as

sudden high fever that last for 5 days and does not fully recovered after having fever

reducing drugs. The others symptoms on this patient were pain on joints, around the

eyes and headache. These happened during the fever and still going on when he

admitted to HAM Hospital. Besides that, he also felt uncomfortable on his abdomen and

vomited once on day-2 of fever.

From the physical examination of inspection the patient, we can see he looks

restlessness and having reddish or red spots all over his body, which indicating there is a

spontaneous bleeding of skin. From palpation, we found hepatomegaly, one of thesymptoms of DHF.

Thrombocytopenia and haemoconcentration are constant findings in DHF. A

drop in the platelet count to below 100 000 per mm3 is usually found between the third

and eighth day of illness, often before or simultaneous with changes in the haematocrit.

A rise in the haematocrit level, indicating plasma leakage, is always present, even in

non-shock cases, but is more pronounced in shock cases. Haemoconcentration with an

increase in the haematocrit of 20% or more is considered to be definitive evidence of

increased vascular permeability and plasma leakage. It should be noted that the

haematocrit level may be affected either by early volume replacement or by bleeding. In

patient, about 7,4 - 48,7% of hematocrit elevation was not found, with the normal

ranging of 39-54% hematocrit count. There is a decreased in hematocrit from 52% to

36% after intervention 20% of baselineas the evidence of plasma leakage owing to

increased vascular permeability. Besides that, supportive serology (a reciprocal


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haemagglutination-inhibition antibody titre 1280, a comparable IgG enzyme-linked

immunosorbent assay (ELISA) titre or a positive IgM antibody test on a late acute or

convalescent-phase serum specimen) support a probable case of dengue fever. Our

patient has Anti DHF IgG positive makes an early diagnose of probable a dengue fever

case.

Therefore, according to WHO classification, our patient falls under Dengue

Hemorrhagic Fever with the grading of 2 by the physical and laboratory examinations.


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Conclusions

The conclusion of this paper is a girl, 2 years and 6 month old, diagnosed with Dengue

Hemorrhagic Fever Grade 2. The patient received :

-

Bed Rest

- IVFD RL 100 gtt/min micro

-

Paracetamol 3xcth1



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REFERENCES

1. Barniol J, Gaczkowski R, Barbato EV, da Cunha RV, Salgado D, Martnez E, et al.

Usefulness and applicability of the revised dengue case classification by disease:

multi-centre study in 18 countries. BMC Infect Dis. 2011;11:106.

2. Dengue haemorrhagic fever: diagnosis, treatment, prevention and control. 2nd

edition. Geneva : World Health Organization. 1997

3. Deen JL, Harris E, Wills B, Balmaseda A, Hammond SN, Rocha C, et al. The WHO

dengue classification and case definitions: time for a reassessment. Lancet.

2006;368:1703.

4.

World Health Organization. Geneva, Switzerland: WHO; 2009. Dengue: Guidelines

for Diagnosis, Treatment, Prevention and Control.

5. U.S. Department of Health and Human Services. Dengue and Dengue Hemorrhagic

Fever. Centers for Disease Control and Prevention.

6. WebMD. Dengue Fever. http://www.webmd.com/a-to-z-guides/dengue-fever-

reference

7. Handbook For Clinical Management of Dengue. WHO 2012. ISBN 9789241504713

Documents

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