CASE PRESENTATION

APPENDICITIS ACUTA

Counsellor :

dr. H. Tisna Sukarna, Sp.A

Presented by :

Yenny Yan Saputra

0010011

DEPARTMENT OF PEDIATRIC
FACULTY OF MEDICINE MARANATHA CHRISTIAN UNIVERSITY
IMMANUEL HOSPITAL - MARANATHA TEACHING HOSPITAL
BANDUNG
2005
I. PATIENT IDENTITY

Name : Indri Irwanti Raharja Sex : Female

Place and date of birth : Bandung, 9th March 1998 RM : 00647472
Age : 10 year, 6 months old Reg : 5014852
Consignment from : Emergency Unit
Diagnose : Acute appendicitis + appendicular abcess

Date of hospitalized : 24th September 2005 Time : 13.51

Date of examination : 24th September 2005

Father :
Name : Mr. Iwan Raharja Age : 48 years old
Education : Senior High School
Occupation : Entrepreneur
Salary : Rp.-
Address : Jl Sadang no. 16 RT/RW : 1/3
Kelurahan Margahayu-Kecamatan Margahayu
Bandung

Mother :
Name : Mrs. Siti Fauziah Age : 44 years old
Education : Senior High School
Occupation : Entrepreneur
Salary : Rp. -
Address : Jl Sadang no. 16 RT/RW : 1/3
Kelurahan Margahayu-Kecamatan Margahayu
Bandung
II. ANAMNESIS

OAuto UHetero was given by patient’s mother on 24th September 2005

Chief complaint : Pain on the right lower quadrant

History of present illness :

Since 2 days before hospitalized [12nd September 2005], patient was
complained that she had an abdominal pain on the right lower abdomen. The
pain was like ????????. At first she felt the pain around her belly button but next
she felt it moved to her right lower abdomen. The patient’s mother added that she
thought her daugther was having a fever too, but the temperature wasn’t really
high and it was better when she gave her an antipiretic drug. She added that her
daugther was also vomiting, it was began with a nausea the followed by the
vomitting, consisted of water, food, and no blood. The nausea and vomitting
happened about 4 times, and each of it about ¼ mineral water in amount.
Since a day before hospitalized, the fever was self cured, and she wasn’t
vomiting anymore but the abdominal pain had became worst, and she felt it more
when she moved or even just lying on her bed.
The patient and her mother denied that she had had a trauma before, pain
when she was urinated, constipation or even diarrhea.
Sejak 1 hari SMRSI panas badan os turun dengan sendirinya dan os tidak muntah
lagi, tetapi os mengeluh perut kanannya menjadi semakin sakit sampai os menahan nyeri
dengan meringkuk.The fever was suddenly high and continuous, not up and down;
and it happened at night. In the morning, the fever still happened but the
temperature didn’t as high as the night. Shiver when the fever happened.
Convulsion when the fever happened was denied.
Patient also had had a cold, myalgia and headache at back area of the
head. Myalgia occurred most at the joint. Patient said that when the fever
happened, there was a red spot on skin at the extremities, both upper and lower
extremities and his lip feel to run dry . Patient had queasy and vomit 3 times in
oneday after eating counted a half a glasss containing food and without blood.
Since 1 days before hospitalized patient had bleeding from his nose 4
times, each about a half teaspoon, red colour, without had a trauma in the nose
before, also had bleeding from lip. Patient also denied that he felt ear pain,
hearing lost or there’s a discharge from the ear. Patient also denied that he felt
pain when swallowed. There’s no cough or breathless.
Patient denied had DHF (Dengue Hemorrhagic Fever).
Patient’s neighbour had being hospitalized at the hospital because of DHF
[Dengue Hemorrhagic Fever].
Urinate : color yellow, clear, frequency and volume normal, no abnormality or
changing,
no pain
Defecate : color brown – yellow with frequency 2 – 3 X daily, consistency flabby,
volume normal, no bleeding.
Medical effort :
The patient had seen the doctor on the second day of fever, and he had
given drugs for fever and cold [patient’s mother forgot branded name of the
drugs]. The preparations of the drugs were liquid and taken 3 times daily, ± ¾ - 1
tea spoon; patient’s mother forgot the color of the drugs. After taken the drugs,
the illness didn’t improved.

Obstetric and Birth History

Child : 7nd child from : 8 child, no stillbirth, no abortion

Birth: aterm, spontaneous, directly cry and helped by a midwife
Birth weight : 2500 gram, Birth length : 49 cm

Physical and Intelligence Development

Turn over : 4 month, appropriate with the developmental age

Sitting down without help : 8 month, appropriate with the developmental age
Walk alone without help : 15 month, appropriate with the developmental age
Talk 1 word : 12 month, appropriate with the developmental age
Talk 1 sentence : 18 month, appropriate with the developmental age
Read : 5 years , appropriate with the developmental
age
Write : 5 years , appropriate with the developmental
age
School : 5 years , appropriate with the
developmental age

Teeth
First eruption : 6 month. Now : complete permanent
teeth
Family Members

No. Name Age M/F Description

1. Mr. Iwan Raharja 48 M Father, healthy
years
2. Mrs. Siti Fauziah 44 F Mother, healthy
years
3. Santi Susanti 21 F Sister, healthy
years
4. Tanti Rianti 19 F Sister, healthy
years
5 Andi Pratama 17 M Brother, healthy
years
6. Dedi Rahmadi 15 M Brother, healthy
years
7. Tati Rahmawati 13 F Sister, healthy
years
8. Farah Fadilah 12 F Sister, healthy
years
9 Indri Irawati Raharja 10 F Patient, sick and being
years hospitalized because of acute
appendicitis
10 Nila 4 F Sister, healthy
years

Immunizations

Basic Booster Recommende

d
1. BCG √ X X X 6. HiB X
16/08/95
1 week Scar +
2. DPT √ √ √ X X X 7. MMR X
09/10/95 09/11/9 09/12/95
2 month 5 4 month
3
month
3. Polio √ √ √ √ X X 8. Hep.A X
16/08/95 09/09/9 09/10/95 09/12/95
1 week 5 2 month 4 month
1
month
4. Hep.B √ √ √ X X X 9. Varicella X
30/08/95 09/09/9 09/10/95
 3 weeks 5 2 month
1
month
5. √ X X X 10. X
Measles 09/05/96
9 month

Nutrition and Feeding

1. 0 – 4 months : breast feeding on demand

2. 4 – 6 months : breast feeding, cereal milk, fruits and extra milk,
average 3 X per day, quality good
3. 6 – 10 months : breast feeding, steamed rice, fruits and extra milk,
average 3 X per day, quality good
4. 10 – 12 months : breast feeding, cooked rice, fruits and extra milk,
average 3 X per day, quality good
5. 1 years – now : cooked rice, fruits, extra milk [regular family menu],
average 3 X per day, quality good, quantity less

Past Illness

Diarrhea :- Diphtheria : - Morbilli :-

Cold & cough :- Tetanus :- Renal
disease :-
Typhoid :- Hepatitis :- Asthma/allergic : -
Pneumonia : - TBC :- Pertusis :-
Varicella :- Convulsion :-
DHF :-

Family History

Asthma :- Blood disease :-

TBC :- Malignancy :-
Renal disease :- Diabetes mellitus :-
Etc. :-
III. PHYSICAL EXAMINATION

1. General appearance

Consciousness : compos mentis

Condition : moderate sickness
Activity and position : no force position, active movement
General condition : Mental : normal
Physic : weak

2. Vital signs

Pulse : 110 X per minutes / regular / strong /equal

Temperature : axiller, 37 oC
Respiration : type abdomino-thoracal / 28 X per minutes
Blood pressure : 110/80 mmHg.
Rumple leede test : positive

3. Anthropometric

Age : 10 year, 6 months old

Weight : 19 Kg
Height : 130 Cm
( 79,1 % standard Weight / Age )
( 104,5 % standard Height / Age )
( 70.1 % standard Weight / Height )
Nutrition status : PEM moderate
Head circumference : 51 Cm
Chest circumference : 49 Cm
Abdomen circumference : 46.5 Cm
Upper arms circumference : 20 Cm

4. Systematic examinations

4.1 Hair : black colored with well distribution, normal luxuriance,

not easy to yanked out
Skin : creamy yellow colored with no pale, no cyanosis,
petechiae positive on upper and lower extremities
Nail : capillary refill < 2 seconds
Lymph node : there’s no enlargement palpable on cervical nodes,
occipital nodes, retro auricular nodes, submandibular
nodes, axiller nodes even inguinal nodes
4.2 Head : no congenital abnormality
Eyes : normal palpebra, hyperemic conjunctiva +/+,
subconjungtival hemorrhage -/-, no icteric sclera, light
reflex positive both eyes, round and isochoric pupil
with 2 mm diameters

Ear, nose : crusta sanguinolenta +/+, no ear and nose

and throat secretion, no nasal flaring
Mouth : no foetor, wet mouth mucosa,dry lips mocosa and
bleeding no cyanosis lips, no gums bleeding, no
coated or tremor tongue, tonsil and pharynx normal

4.3 Neck : there’s no congenital abnormality, thyroid is palpable

normal, Jugular Venous Pressure 5 + 3 cmH2O

4.4 Thorax :
Lungs :
Inspection : shape and movement symmetric between right and left,
no retraction, no intercostals widening
Palpation : vocal fremitus normal - equal between right and left,
no intercostals widening
Percussion : sonor – equal between right and left and not found dullness
Auscultation : vocal resonance normal – equal between right and left,
vesicular breath sounds positive without ronchi and
wheezing

Heart :
Inspection : ictus cordis wasn’t seen
Palpation : ictus cordis was palpable at ICS 5 linea midclavicularis
sinistra, no thrill
Percussion : border on top : ICS 2 linea parasternalis sinistra
border on left : ICS 5 linea midclavicularis sinistra
border on right : ICS 4 linea sternalis dextra
Auscultation : regular heart sounds, no murmur

4.5 Abdomen :
Inspection : dome-shape, no darm contour or darm steifung
Palpation : soepel; liver 3 cm BAC 2 cm BPX spleen and ren
unpalpable; no abdominal tenderness
Percussion : tympani, traube’s space : tympani
Auscultation : bowl sound positive normal with frequency 2 – 4 x per
minutes

4.6 Genital : gender male, no congenital abnormality

 4.7 Anus & rectum : no congenital abnormality
no anal bleeding
4.8 Extremities : shape and movement normal – symmetrical between
right and left, there’s no congenital abnormality
petechie + at four extremties
4.9 Neurological : physiological reflex positive for both
examination legs, no pathological reflex, no atrophy, pareses,
paralysis, muscle tone normal [5]

IV. Laboratory finding

Blood :

Sysmex :??????????????

24/9/05 15/9/05 16/9/05 Normal

Hb 11.4 13 10,4 9,6 9,2 12 – 16 gr/dl

Ht ???? 39 29 26 26 37 – 47 gr/dl
Leko 20,000 - - 5500 - 5000 – 10000/mm3

Tc 341,000 10000 11000 8000 6000 150000 –

300000/mm

15/9/05 Normal
BT 1' 45" 1 – 3 minutes
CT 8' 30" 5 – 11 minutes

Serologic :

15/9/05 – Denque Blot Result

Anti dengue IgM Negative
Anti dengue IgG Positive
V. Resume

7 years and 6 months old boy, with 19 kg body weight, nutritional status
Protein and Energy Malnutrition Moderate, came to Immanuel Hospital on 14 th
September 2005 with febris as chief complain.

10th September 2005 11th September 2005 13th September 2005

th
14 September 2005
Febris [+] Went to the doctor Still febris Hospitalized
Petechiae [+] Petechiae [+]
Cephalgia [+] Cephalgia [+]
Myalgia [+] Myalgia [+]
Atralgia [+] Atralgia [+]
Dry lips mucosa Epistaxis [+]
Dry lips mucosa

The medicine was given à The disease didn’t improve

Febris suddenly high [39 oC] and continuous, happened at night. Rigoris
(+) Febris convulsion (-), myalgia (+), cephalgia (+), petechiae (+). His Lips had
dry and bleeding,Epistaksis (+), trauma on nose (-), vomit & nausea (+), history
of otitis media denied, history of URTI denied. Dyspnea (-), cough (-).

Past history : -

Family history : Patient’s neighbour had being hospitalized at the hospital

because of DHF [Dengue Hemorrhagic Fever].

Urinate : no hemorrhage

Defecate : no bleeding

Medical effort :
To the doctor on the second day of fever, gave drugs for fever and cold but
didn’t improved.
From physical examination:

General appearance : compos mentis, moderate sickness

Vital sign :
Pulse : 110 X per minutes / regular / strong /equal
Temperature : axiller, 37 oC
Respiration : type abdominothoracal / 28 X per minutes
Blood pressure : 110/80 mmHg.
Rumple leede test : positive

Systematic examination :

Head :
Eyes : hyperemic conjunctiva +/+
Ear, nose & throat : epistaksis positive, tonsil normal/no hyperemic
Mouth : wet mouth mucosa, dry lips mucosa and bleeding,
no
gums bleeding, coated tongue negative
Neck : no enlargement palpable of lymph node
Thorax : Shape & movement symmetric between left & right
Lung : VBS +/+, Rh -/-, Wh -/-
Heart : regular heart sounds, no murmur
Abdomen : flat-shape, soepel, no abdominal tenderness,
liver 3 cm under BAC 2 cm BPX,spleen no palpable, bowl sound
(+) normal
Extremities : petechiae positive both upper and lower extremities

Laboratory :

Blood :

Sysmex : ??????????????

24/9/05 15/9/05 16/9/05 Normal

Hb 11.4 13 10,4 9,6 9,2 12 – 16 gr/dl

Ht ???? 39 29 26 26 37 – 47 gr/dl
Leko 20,000 - - 5500 - 5000 – 10000/mm3

Tc 341,000 10000 11000 8000 6000 150000 –

300000/mm

15/9/05 Normal
 BT 1' 45" 1 – 3 minutes
CT 8' 30" 5 – 11 minutes
Serologic :
15/9/05 – Denque Blot Result
Anti dengue IgM Negative
Anti dengue IgG Positive

VI. Diagnose

Differential diagnose : Additional diagnose :

 Dengue Hemorrhagic Fever grade II PEM Moderate
 Typhoid Abdominalis

Working diagnose : Nutritional status :

Dengue Hemorrhagic Fever Grade II PEM Moderate

VII. Suggested Further Studies

1. Roentgen Thorax
2. Virus isolation
3. Widal/Gall Culture
4. Hb, Ht, Leukocyt, Tc, interval 4 hours
5. Diff count
6. Clotting time, Bleeding time, Clot retraction

VIII. Planning Therapy

- Non Medicamentose :
1. O2 1 – 2 L/min, up to 2 – 3 L/min
2. Fluid :
- Ringer Asetat for 20 gtt/min [14/9/05] change
- Ringer Laktat 500 cc + Adona [50 mg/bottle] 15 gtt/ Mnt

3. Transfusion :
1. FFP [Fresh Frozen Plasma]
 2. TC [Trombocyte Concentrate]
3. FWB [ Fresh Whole Blood]

4. Diet :
1. D II [15/9/05] 2000 kalori/day

- Medicamentose :
1. Kalmoxillin 3 x 1/3 vial
2. Vitacimin 3 x 1 tab
3. Dapyrin 3 x 2 Cth

IX. Prognosis

Quo ad vitam : dubia ad malam

Quo ad functionam : dubia ad malam

 X. DISCUSSION

DENGUE, DENGUE HAEMORRHAGIC FEVER, DENGUE SHOCK

SYNDROME

P Amin*, Sweety Bhandare**, Ajay Srivastava***

*Consultant BHIMS, **Resident, Cook Country Hosp. Chicago. ***Resident, Bombay Hospital,
Mumbai.

INTRODUCTION
Dengue is an acute mosquito-transmitted viral disease characterized by fever, headache, muscle
and joint pain, rash, nausea and vomiting. Some infections result in dengue haemorrhagic fever
(DHF), a syndrome that in its most severe form can threaten the patient’s life, primarily through
increased vascular permeability and shock. The case fatality in patients with dengue shock
syndrome can be as high as 44%.[1]

EPIDEMIOLOGY
Epidemics of an illness compatible with DF (dengue fever) were first reported in medical literature
in 1779 in Batavia (present-day Jakarta) and in 1780 in Philadelphia. Since then, epidemics have
been reported in Calcutta (1824, 1853, 1871 and 1905), the West Indies (1827), Hong Kong
(1901), Greece (1927-1928), Australia (1925-1926, 1942), the United States (1922), and Japan
(1942-1945).2

Dengue is predominant in tropical areas mostly in South-east Asia, Africa and Southern parts of
the US (Fig. 1). The first large epidemic of DHF (dengue haemorrhagic fever) occurred in Cuba in
1981 with 24,000 cases of DHF and 10,000 cases of DSS (dengue shock syndrome). In 1986
and 1987 massive outbreaks of dengue were reported in Brazil. In 1988, an epidemic of DF was
reported at 1700m above sea level in Guerrero State, Mexico3 and in 1990 almost one-fourth of
3,00,000 people living in lquitos, Peru contracted DF.4
TRANSMISSION
The known natural hosts for dengue viruses are man, lower primates, and mosquitoes. The
arthropod vectors are members of the genus Aedes that thrive both in urban and rural areas. The
predominant species implicated in disease transmission are A. aegypti and A. albopictus.

Aedes aegypti, considered the most effective vector, originated in the forests of Africa and is
found in Between 30 degrees north and 20 degrees south latitude.[11-14] The female mosquito
feeds during the daytime, with peak activity in the mornings and late afternoons. After feeding on
a viraemic individual, the mosquito may transmit the virus directly by change of host, or after 8 to
10 days during the time the virus multiplies in the salivary glands. The infected mosquito then
remains capable of transmission for its entire life. Transovarian transmission of dengue viruses
has been documented and A. aegypti eggs are highly resistant to desiccation and can survive for
extended periods.
Aedes albopictus is indigenous to Southeast Asia, feeds during the day, and has been shown to
have a higher biting frequency than A. aegypti. Recently, it has been introduced into Nigeria,
Europe, and the United States, apparently by shipments of used automobile tires. In the US
Aedes albopictus has spread as far north as Chicago. With the spread of adaptable cold-resistant
strains, the chances for a major outbreak in Europe have increased.
THE VIRUS
Dengue viruses are members of the family Flaviviridae, which include the Japanese encephalitis
virus and the yellow fever virus. Four dengue virus serotypes 1, 2, 3 and 4 and various biotypes
can be differentiated. The four serotypes are closely related antigenically.

Infection with one serotype provides life-long immunity to that virus but not to the others.

Mature Dengue virus consists of a single stranded ribonucleic acid genome (ssRNA), which has a
positive polarity. The genome is surrounded by an icosahedral nucleocapsid with a diameter of 30
nm. The nucleocapsid is covered by a lipid envelope of 10 nm thickness derived from host cell
membranes and contains the envelope and membrane proteins.

The viral genome is 11kb. The 5’end of the RNA has a type I cap structure but lacks a poly A tail
at the 3’ end. It contains a single open reading frame of about 10,000 nucleotides encoding three
structural and seven nonstructural proteins. The proteins are synthesized as a polyprotein of
about 3000 amino acids that is processed cotranslationally and posttranslationally by viral and
host proteases.

The structural proteins include a capsid protein rich in arginine and lysine residues and a
nonglycosylated prM protein. The major structural envelope protein is involved in the main
biologic functions of the virus particle such as cell tropism, acid catalyzed membrane fusion and
the induction of haemagglutination-inhibiting, neutralizing, and protective antibodies.

The non-structural proteins are addressed as NS1-7.

NS1, a glycoprotein is detected in high titers in patients with secondary dengue infections but its
function is unknown.

NS2 region, codes for two proteins (NS2A and NS2B), which are thought to be implicated in
polyprotein processing.

NS3 is the viral proteinase that functions that functions in the cytosol.
NS4 region codes for two small hydrophobic proteins that seem to be involved in the
establishment of the membrane bound RNA replication complex.

NS5 codes for a protein with a molecular weight of 105,000 and is the most conserved flavivirus
protein. This protein is believed to be the virus encoded RNA dependent RNA polymerase.

NS6 and NS7 function yet to be found.

CLINICAL FEATURES
The clinical features of dengue virus infection vary from an asymptomatic infection to a febrile flu
like infection (DF-dengue fever) to more severe form like DHF (dengue haemorrhagic fever),
which can lead to DSS (dengue shock syndrome). The clinical variability is poorly understood and
seems to be related to the age, sex and the immunologic and nutritional status of the patient.
DHF is most likely to develop in immune-competent, well-nourihed girls between the ages of 7
and 12 years. DHF is most common in children between ages 5 and 15 years.

DENGUE FEVER (DF)

The incubation period of dengue fever after the mosquito bite is usually 4 to 7 day (range is 3-14
days). DF may manifest with fever and a discrete macular or maculopapular rash. In this situation
the clinical differentiation from other viral ill nesses may not be possible, recovery is rapid and the
need for supportive treatment is minimal.

The fever in severe cases can rise up to 39 degrees Celsius or higher. It persists for 5 to 6 days.
Fever is characteristically biphasic and returns to almost normal in the middle of the febrile period
giving rise to the saddleback temperature chart. It reaches its highest level during the last 24
hours before abatement. Symptoms include headache, usually frontal, and retroorbital pain,
particularly when pressure is applied to the eyes. ("Fire is coming out of my eyes"). Arthralgias,
myalgias and a maculopapular rash may appear at the onset. Some patients report severe
backache (back-break fever), sore throat, or abdominal pain, which can be severe enough to be
confused with appendicitis. The febrile period usually lasts up to 6 days during which time the
rash may become diffusely erythematous with clear areas scattered in between, the so-called
"islands of white in sea of red". These patients are lethargic with accompanying anorexia and
nausea. Hepatomegaly can be present although splenomegaly is uncommon. Patients can have
nausea and vomiting. Thrombocytopenia is characteristic with and serum hepatic enzymes may
be elevated.

DENGUE HEMORRHAGIC FEVER (DHF)

The incubation period of DHF is unknown but is probably similar to that of DF. DHF commences
acutely with high fever and many of the symptoms of DF. However, drowsiness and lethargy are
more marked. There is increased vascular permeability, and abnormal haemostasis that can lead
to hypovolaemia and hypotension and in severe cases, result in hypovolaemic shock,
complicated by severe internal bleeding. The haemorrhagic manifestations appear usually by 3rd
day and consist of scattered petechiae over the trunk, limbs and axillae. The petechiae are
associated with a positive tourniquet test result. Bleeding at venepuncture sites is the rule and
there may be haemorrhage from GI tract, nose and gums. After 2-7 days as fever begins to
subside, signs of circulatory insufficiency can appear and pt is restless and sweaty, with cold
extremities.

Transudate leaking due to excessive capillary permeability causes pleural effusion

characteristically on the right side and abdominal ascites may be noted. In addition to the plasma
leakage, DIC is present. With appropriate treatment, this phase usually lasts 24-48 hours.
Neurologic manifestations indicate infectious encephalitis and the virus is isolated in the CSF and
brain tissue. Laboratory investigations in DHF reveal thrombocytopenia that may reach levels of
20,000 platelets/cubic mm. Haemoconcentration with haematocrit rise of 20% or more,
hypoalbuminaemia, hypovolaemia and moderately elevated serum aminotransferases and blood
urea nitrogen levels were documented. Partial thromboplastin time and thrombin time may be
prolonged. Hypofibrinogenaemia and complement depletion correlate with severity of the disease
(Fig. 3).

DENGUE SHOCK SYNDROME (DSS)

DSS is defined as DHF with signs of circulatory failure, including narrow pulse pressure (â 20 mm
Hg), or frank shock. The liver may be palpable and tender; and the liver enzymes are mildly
elevated but jaundice is rare. The four warning signs for impending shock are intense, sustained
abdominal pain, persistent vomiting, restlessness or lethargy, and a sudden change from fever to
hypothermia with sweating and prostration. The development of any of these signs or suggestion
of hypotension is indicative of hospital management to prevent shock. The patient may recover
rapidly after volume replacement but shock may recur during the period of excessive capillary
permeability. The case fatality rate in DHF can be as low as 0.2% if detected early and treated.
Once shock has set in, the fatality rate may be as high as 12% to 44%.

PATHOGENESIS
DHF is almost always found in individuals who had a previous experience with at least one of the
four serotypes of dengue virus. This leads to the hypothesis of heterotypic antibodies from a
previous dengue infection promoting the viral replication within the mononuclear leucocytes-the
phenomenon of antibody-dependent enhancement. Furthermore, the immunologic processes
aimed at eliminating dengue virus infected cells can result in release of histamine and substances
with vasoactive and procoagulant properties, the release of interferon-gamma, and the activation
of complement.
DHF results from an infection by a more virulent biotype of the virus or even from unfavourable
host factors such as concomitant bacterial infections. DHF is known to be more common in
Southeast Asia compared to Africa and America. Black individuals are relatively resistant to
DHF/DSS due to a speculated "resistant gene".

The cause of bleeding in DHF appears to be due to thrombocytopenia, platelet dysfunction,

disseminated intravascular coagulation and micro vascular injury.

DIAGNOSIS
The clinical criteria for diagnosis are as follows: (1) fever; (2) haemorrhagic manifestations,
including at least a positive tourniquet test result and a major or minor bleeding phenomenon; (3)
hepatic enlargement; (4) shock (high pulse rate and narrowing of the pulse pressure to 20 mmHg
or less, or hypotension). The laboratory criteria include (5) thrombocytopenia (â 100,000/mm3),
and (6) haemoconcentration (haematocrit increase ô 20%). Thrombocytopenia with concurrent
high haematocrit levels differentiates DHF from classic DF.

Currently routine laboratory diagnosis of dengue infections depends on virus isolation or the
detection of dengue virus-specific antibodies. The isolation of viruses from clinical specimens can
be carried out in cultured mosquito cells, such as AP-61 or C6/36 cells cultures. When dengue
virus serotype-specific monoclonal antibodies are used, virus identification by indirect
immunofluorescence can be achieved within 2 weeks. The development of mosquito inoculation
techniques has not only improved the sensitivity but also reduced the time required for virus
isolation and identification. Parenteral inoculation of adult. A. albopictus yields results in 7 days.
Virus isolation by intracerebral inoculation of Toxorhychitis splendens mosquito or its fourth instar
larvae can even be achieved within 2 to 5 days.

The serologic identification of the various types of dengue virus infection is complicated by the
occurrence of cross-reactive antibodies to antigenic determinants shared by all four dengue
viruses and other members of the flavivirus family. The commonly used serologic test is the
haemagglutination inhibition test. In a primary infection dengue haemagglutination inhibition
antibody titer is generally less than 1:20 in a sample collected within the first 4 days after the
onset of symptoms. In the convalescent phase sample (collected 1 to 4 weeks after the onset of
symptoms) a fourfold or greater rise in antibody titer is detected, with antibody titer â 1:1280.

A secondary dengue infection is characterized by the rapid appearance of broadly cross-reactive

antibodies. Haemagglutination inhibition titers of 1:20 in the acute-phase sample rise to ô to
1:2560 in the convalescent phase sample. An antibody titer of ô 1:1280 in the acute-phase
sample without a fourfold or greater increase in the second sample also is considered
presumptive of recent infection. An improved and less time-consuming method is a capture
enzyme-linked immunosorbent assay that can detect specific anti-dengue IgM in a single acute-
phase sample.

Recently commercial kits for the detection of specific IgG as well as IgM antibodies have become
available. They are based on a dot enzyme assay or a nitrocellulose membrane-based capture
format, respectively, and should be suitable for field research.

An alternative to virus isolation is the detection of viral RNA by reverse transcription polymerase
chain reaction. Reverse transcription polymerase chain reaction is a highly sensitive technique of
particular value in the early diagnosis of dengue infection, but at present is only available in
research settings.

TREATMENT
Patients with DF require rest, oral fluids to compensate for losses via diarrhoea or vomiting,
analgesics, and antipyretics for high fever (acetaminophen) but not aspirin, so that platelet
function will not be impaired. Steroids in DSS are not helpful. With the earliest suspicion of
threatened severe illness, an intravenous line should be placed so that fluids can be provided.
Monitoring of blood pressure, haematocrit, platelet count, haemorrhagic manifestations, urinary
output, and level of consciousness is important. Plasma leakage in DHF is very rapid and the
haematocrit may continue to rise even while intravenous fluids are being administered; however,
the "leaky capillary" period is short and intravenous fluids are usually required for only 1-2 days.
There is great variability from patient to patient, and the physician must adjust treatment using
serial haematocrit, blood pressure, and urinary output data. Insufficient volume replacement will
allow worsening shock, acidosis, and disseminated intravascular coagulation, while fluid overload
will produce massive effusions, respiratory compromise, and congestive heart failure. Because
patients have loss of plasma (through increased vascular permeability into the serous spaces)
they must be given isotonic solutions and plasma expanders, such as Ringer’s acetate or
Ringer’s lactate, plasma protein fraction, and Dextran. The recommended amount of total fluid
replacement in 24 h is approximately the volume required for maintenance, plus replacement of
5% of bodyweight deficit, but this volume is not administered uniformly throughout the 24 h. A
bolus of 10-20 ml of an isotonic solution per kg bodyweight is given in case of shock, and
repeated every 30 min until circulation improves and urinary output is adequate. Vital signs
should be measured every 30-60 min and haematocrit every 2-4 h, then less frequently as the
patient’s condition stabilizes.
Placement of a central-venous-pressure line is hazardous in patients with haemorrhagic
tendencies but may be necessary, especially when more than 60 ml/kg of fluids has been given
without improvement. An expert in a special care area should insert the line. It is used to estimate
filling pressures and to guide further intravenous fluid administration. An arterial line will help in
the assessment of arterial blood gases, acidbase status, coagulation profiles, and electrolytes in
the haemodynamically unstable patient, helping to identify early respiratory compromise.
Monitoring should be continued for at least a day after defervescence. Once the patient begins to
recover, extravasated fluid is rapidly reabsorbed, causing a drop in haematocrit. Before
discharge, the patient should meet the following criteria: absence of fever for 24 h (without
antipyretics) and a return of appetite; improvement in the clinical picture; hospital care for at least
3 days after recovery from shock; no respiratory distress from pleural effusion or ascites; stable
haematocrit; and platelet count greater than 50,000/ml76 Because convalescent-phase
diagnostic samples are often difficult to obtain, a second blood sample should always be taken on
the day of discharge.

PROSPECTS FOR CONTROL

Vaccine development
An effective vaccine will have to be tetravalent because pre-existing heterotypic dengue antibody
is a risk factor for DHF. Candidate attenuated vaccine viruses have been evaluated in phase I and
II trials in Thailand, and a tetravalent formulation is currently undergoing repeat phase I and II
trials. Advances have also been made with second generation recombinant dengue vaccines. A
cDNA infectious clone of the DEN-2 PDK-53 vaccine candidate virus has been constructed, and
work is in progress to construct chimeric viruses by inserting the capsid, premembrane, and
envelope genes of DEN 1, 3 and 4 into the DEN-2 PDK-53 backbone. These recombinants,
through genetic manipulation, may be made to replicate faster, be more immunogenic and safer.
However, an effective, safe and affordable vaccine is not an immediate prospect.

Vector control
At present dengue transmission can only be reduced by mosquito control. The task might seem a
simple matter of the treatment or elimination of infested containers. Source (container) reduction
campaigns have been very successful but they are hard to sustain, mainly because they are
labour intensive, require discipline and diligence, and are plagued by diminishing returns.
Emphasis has shifted first to organochloride insecticides and later to organophosphorus
larvicides, and aerosols targeted at adult mosquitoes and mostly applied outdoors as ultra-low
volume (ULV) concentrates. The aerosols are principally recommended for emergency control
during epidemic transmission as part of an integrated vector elimination effort, including
environmental management, source reduction and larvicides. Nevertheless, their routine use as
the principal response even before and after dengue epidemics has become widespread. This is
regrettable, because ULV aerosols have very limited surprisingly, therefore, there is no well-
documented example of interruption of a dengue epidemic by outdoor ULV treatments. Indoor
treatments are probably much more effective but are very labour-intensive and intrusive.
Dengue Haemorrhagic Fever Grade III & IV

Oxygenation [O2 2 – 4 L/min]

Change Plasma Volume As Soon As Possible [Crystalloid isotonic solution such
as RL/NaCl 0.9% 20 ml/kgBW quickly è bolus in 30 minutes]

Evaluation in 30 minutes, Is the shock handled ?

1. Check vital sign every 10 minutes
2. Observe fluid balance

Shock handled Shock isn’t handled

- Consciousness (+) -
Consciousness (-)
- Pulse >> - Pulse <<
- BP > 20 mmHg - BP < 20 mmHg
- Dyspnea/cyanosis (-) - Dyspnea/cyanosis
- Extremities è Warm - Extremities è Cold
- Diuresis : 1 ml/kgBW/hour - Skin è Cold
- Check blood
glucose

Fluid become Fluid

continue
10 ml/kgBW/hour 20 ml/kgBW/hour

Strict evaluation Add colloid/plasma

VS, bleeding, diuresis, Hb, Ht, Tc
Dextran/FPP
10 – 20
ml/kgBW/hour
[maks 30
ml/kgBW/hour]

Stabile in 24 hours Acidosis Correction

Fluid : 5 ml/kgBW/hour Evaluate in 1 hour

Fluid become 3 ml/kgBW/hour Shock handled Shock isn’t

handled
 Infusion STOP [≠ > 48 hour] Ht decrease Ht
increase

Transfusion FWB Colloid 20 ml/kgBW

10 ml/kgBW
Repeat if needed
XI. FOLLOW UP

Date Follow Up Doctor’s Order

14/9/05 Report New patient to dr Ferda New patient with D/ DHF
21.20 T = 110/80 mmHg advice :
N = 100 x/minute - Check Hb, Ht, L, Tc
Hb=14,6 (06.00)
Ht 42 - RA 250 cc loost change
Tc 12000 with RL 20 gtt/Minute
Leu = 5100 - Kalmoxillin 3 x 1/3 vial
- Dapyrin 2 cth if had
fever
- Prepare Tc 2 bags
15/3/05 Report patient to dr Ferda, Patient had - Check again Hb, Ht, Tc
01.30 fever temperature 380C - IgG, IgM anti dengue
- Prepare Tc 2 bags,
- Lab. result must be
report
15/9/05 Report patient had gum bleeding and - check BT, CT
05.30 lips - If there any TC, input
temperature 37,80C

15/9/05 Patient still get gum and lips bleeding - Therapy : continue
06.30 and somnolent - Infus RL 12 gtt/ mnt
- whoole blood (-)
- Tc (-)
- FFP transfusion 1 Bag
- Konsul to dr Tisna
- Dapyrin 3 x 2 tea
spoons
15/9/05 Patient still had fever - Transfusion :
12:30 Thrombosit 10.000 - FFP 3 bags and Tc 4
Bags
- Infus RL500cc + Adona
drip 50 mg for 15
gtt/mnt
Therapy
- Dapyrin 3 x 2 tea
spoons
- Vitacimin 3 x 1 tab
- Diet DI
-Observation BP, N,R, T
and manifestation
bleeding
15/9/05 Lab results reported to dr.Tisna, advice :
- Infus RL500cc + Adona
15.25 BP= 80/60 mmHg drip 50 mg release until
N= 100x/Mnt BP normal
R= 24x/mnt - Next infus RL + Adona
T= 380C 50
mg for 60 cc/hours
- 6 hours pos tranfusi
Check
Hb, Ht , Tc
Observation
15/9/05 Lab results reported to dr.Tisna post - Transfusion FFP 4 bags
23.30 transfusion, advice - Kalmethazone 3 x 2 mg
BP = 100/59 mmHg - RL release until BP
Tc = 8000 Stable
Consciousness = Somnolent - Check again after 4
Bleeding from lips still continuous hours
Hb, Ht, Tc
15/9/05 Patient had febris - Kalmetason 3 x 2 mg
23.35 Patient had bleeding continuous - RL release untul BP
stable
- Cool Compress
- more intake fluid
15/9/05 His familly are motivated, patient to enter ICU, but his familly
23.45 denied

16/9/05 Consciousness = Somnolent - transfusion whoole

01:30 Bleeding from lips still continuous blood
200 cc
- Observation Vital Sign
and bleeding

16/9/05 Report to dr Tisna, Advice: -Transfusion FFP 2 bags

02.57 Hb = 9,2 - Transfusion Whoole
Ht = 26 Blood 300 cc
Tc = 6000 - Observation vital sign
and
bleeding
16/9/05 Bp = 80/palpation - infus two line
7.50 N = 80 x/mnt - infus relese 400cc
Capilary Refill > 2 dtk - can repeat
- reported to dr Tisna
16/9/05 - - Transfusion Tc 4 bags
09.00-13.00 - FFP 2 bags
16/9/05 -Patient consciousness somnolent -
14.00 -Patient still bleeding continuous
 - General Condition poorly
16/9/05 Patient reproted to pass away ( death)
17.20