(Acta Paediatr Jpn 1992; 34: 350 - 357)

Dengue Encephalopathy

S.K. Hendarto, M.D. and Sri Rezeki Hadinegoro, M.D.

Departnient of Child Health, Medical Facult!,, Universitj, c?f’ Indonesia. Jakarta, Indonesia

Dengue encephalopathy or dengue hemorrhagic fever (DHF) with CNS involvement used
to be considered a relatively rare condition; but the number of cases reported in human
studies has been increasing every year. Diagnosis of dengue encephalopathy is based on
clinically diagnosed D H F according to the W.H.O. criteria (1980), with CNS
manifestations consisting of abrupt onset of hyperpyrexia, nontransient alteration of
- -
consciousness, headache, vomiting with or without seizures and normal CSF. Many
factors may be considered to be directly or indirectly associated with CNS signs and
symptoms in DHF, the main pathology being leakage of plasma into serous spaces and
abnormal hemostasis, leading to hypovolemic shock and hemorrhage in many organs of the
body. Acute liver failure is considered to be one of the main factors causing brain
pathology. One hundred fifty-two cases of dengue encephalopathy admitted during 3
periods at the Cipto Mangunkusumo Hospital in Jakarta were studied retrospectively. The
overall incidence was 152 out of 2,441 D H F cases, or 6.2%. The most pronounced
symptoms were hyperpyrexia, alteration of consciousness and convulsions. Laboratory
examination showed an unusually high increase of serum transaminases, hyponatremia,
and hypoxia. Neurologic abnormalities detected were hemiparesis and tetraparesis of the
extremities, and second nerve atrophy; such abnormalities were found in 10 out of the 152
cases, or 6.5%.

Key Words
Dengue hemorrhagic fever, Encephalopathy

Introduction

Dengue fever has been known for more than

Receired February 17. 1992
Correspondence address: S.K. Hendarto. M.D., Depart-
ment of Child Health. Medical Faculty. University of
Indonesia. Jakarta. Indonesia
Reproduced lrom the following with permission: Fuku-
yama Y . . Kamoshita S.. Ohtsuka C., Suzuki Y., eds.
Modern Perspectives of Child Neurology. Proceedings II
of the Joint Convention of the 5th International Child
Neurology Congress and the 3rd Asian & Oceanian
Congress of Child Neurology. Tokyo, November 4-9.
1990. Tokyo: The Japanese Society of Child Neurology.
1991; 345-51.
two decades as a tropical endemic infection
caused by dengue virus, a flavivirus from the
arbovirus or arthropod-borne virus group.
Formerly called “five days’ fever,” the classical
dengue infection had the well-known symp-
toms of acute febrile illness, headache, joint
and muscle pain, as found with any other viral
infection, and rash.
The main reservoir of dengue virus is man,
and it is mainly transmitted by Aedes aegypti
mosquitoes; in rural areas other species such
 Dengue encephalopathy (93) 35 I

as Aedes albopictus may play a role in the
spreading of this disease [ 13.
Aedes mosquitoes habitually multiply in
relatively clean water shaded from light;
female mosquitoes tend t o bite man at or
afternoon. Increased frequency of dengue
infection usually occurs during the rainy
season when the mosquitoes seek shelter from
the rain and invade the homes.
Dengue fever with hemorrhagic manifesta-
tions is called dengue hemorrhagic fever
(DHF), and is manifested as fever without
severe joint or muscle pain; deterioration with
bleeding tendency occurs after the first two
days of the illness and is after accompanied by
shock. If shock develops it is called dengue
shock syndrome (DSS). D H F has become a
major public health problem in tropical areas;
the number of cases has been increasing every
year, with an explosive outbreak approximately
every five years.
Serologic studies have identified 4 serotypes
of dengue virus in man, Den-I, 2, 3 and 4.
Serotype Den-3 is known to cause D H F with
severe clinical manifestations which are classi-
fied as grade 111 or 1V according to the
W.H.O. grading of D H F [2]. All the 4
serotypes of dengue virus have been identified
as causes of dengue infection in Indonesia [3].
The W.H.O. [Z] has proposed clinical
criteria for the diagnosis of D H F as follows:
Acute onset of fever, continuous for at least
2-7 days
Hemorrhagic manifestations proven by a
positive tourniquet test or by petechiae,
purpura, ecchymosis, epistaxis, gum bleed-
ing, hematemesis and/ or melaena
Liver enlargement
Shock, manifested by rapid and weak
pulse, narrowing of the pulse pressure to
20 mm or less, hypotension, clammy sweat
and restlessness
Laboratory evidence of thrombocytopenia
of less than 8O,OOO, with a steady rise of the
hematocrit to a hemoconcentration of
more than 20% in the acute phase of the
illness.

Table I . Age distribution of group I and I I D H F cases. 7-able 2. Classification of 98 cases of dengue encepha-
compared with cases of group 111 lopathy according to W H O classification

Age group Group I Group II Group I l l D H F grading Number of cases r:;

(years) N-358 N-754 N-98
D H F GR 1 - 0
<I 7 (1.9Q) 10 (1.3%) 10 (10.2%) D H F GR I1 22 22.6
14 148 (41 4%) 173 (22.8%) 37 (37.3%) D H F GR 111 13 13.3
5 9 105 (46.1'%,) 359 (47.6%) 40 (48.8%) D H F GR IV 63 64.3
> 10 38 (10.6%)) 212 (28.1%) I I (11.3%)
Total number 98 100.0

Table 3. Clinical manilestations in 3 groups of dengue encephalopathy

Clinical signs Group I Group I I Group I l l Total

and symptoms N-33 Y-2 I S-98 N-152
Abrupt onset of hyperpyrexia 33 (100.0'h) 21 (IOo.W%,) Y8 (IOo.ock)
Alteration of consciousness 33 (100.0(%) 21 (IOo.W&) 92 (93.8%) 146 (98.0%.)
Headache 10 (30.3%) 2 (9.5%) I3 ( 13.2%) 25 (16.4%)
Vomiting 23 (69.7%) 15 (71.4%) 23 (23.3%) 61 (40.4%)
Convulsions 28 (84.8%) I I (52.4%) 84 (84.9%) I23 (80.9%)
Neurologic abnormalities I0 (6.59;)
Hemiparesis 0 (0.0%) 2 (2.0%)
Tetraparesis 2 (9.57b) 2 (2.00?)
Optic atrophy I (9.5%) 0 (0.00?)
Normal CSF 21 (lOo.W+) 98 (lOo.O%)

Vol. 34 No. 3 June 1992

352 (94) Hendarro and Hadinegoro

The diagnosis of DHF is made if there are Mangunkusumo Hospital, Medical Faculty,
2 or more clinical manifestations with throm- University of Indonesia, Jakarta, at 3 different
bocytopenia and hemoconcentration. Confir- periods were evaluated.
mation of the diagnosis is made by virus The first group consisted of dengue
isolation or serologic hemagglutination inhibi- encephalopathy cases admitted from May Ist,
tory titer evaluation. 1975 to September 31st, 1976. The second
Outbreaks of DHF have occurred in many group were those admitted from January Ist,
tropical and subtropical areas including South- 1985, to December 31st, 1986. These 2 groups
East Asia, where Indonesia ranks second after had been studied previously by another author
Thailand in the number of cases detected; the [lo].
number in Indonesia reached its highest point The third group included cases of dengue
in 1983 with 11,875 cases, of which 491 died encephalopathy admitted from January lst,
~41. 1988, to December 31st, 1989.
Recently more cases have been reported in The method used was a retrospective
the literature of DHF with CNS manifestations evaluation of cases of dengue encephalopathy,
[5-91, which are now recognized as dengue
encephalopathies. In Indonesia, dengue en- Table 4. Other signs and symptoms of 98 cases of dengue
cephalopathy was first reported in 1981 [6]. encephalopathy during the pcriod 1988 1989 (Group 111)
The object of this study is to evaluate the
Signs and symptoms No. of cases %
clinical, laboratory findings and outcome of
D H F with CNS manifestations, or the so- Alteration of consciousness 92 9.3
called dengue encephalopathy, in patients Apathy 19 19.2
admitted to the Cipto Mangunkusumo Hospi- Somnolence 54 55.6
tal, Medical School, University of Indonesia, Stupor 14 14.1
in Jakarta at 3 different periods of time. Coma 5 5. I
Hepatoniegaly 62 62.6
Materials and Methods Hemorrhagic manifestations
Peleehiae 68 69.4
Three groups of cases with the diagnosis of Epistaxis 19 19.4
dengue encephalopathy admitted to the Cipto Hematcmcsis & melarna 54 55. I

I able 5 laboratory examinations in 98 c a m of dengue encephalopathy (Group 111)

Average Minimum Maximum

Hemoglobin (g d l . ) 11.4 4.4 18.2
tieniatocrit (vol 5 ) 36.0 20.0 52.9
I.eucoc)tes (pl) 6.300 3.ooo I5,XW
I’lateleta ( X 1.000) 82.7 4.0 368.0
Serum Sodium (niiiq 1.) 132.5 113.0 151.0
Serum Potassium ( m H q I.) 4.2 2.0 1.7
S.<;.O
‘1.(units) 357.x 25.0 1.x5o.o
S.G.P.1 (units) 299.0 10.0 I .785.0

No. of cases c/i

Primar!, infection 3 4.0
Secondary infection 31 43.0
f’resumptive secondary infeaton 25 34.6
Xot ewmined 39

Acta Paediair Jpn


based on the presence of CNS manifestations
in clinically proven D H F cases. CNS manifes-
tations were abrupt onset of high fever,
seizures, headache, vomiting, alteration of
consciousness and neurological abnormalities.
Seizures that had been diagnosed previously
as febrile convulsions were not included.
In all cases routine examinations of blood
were performed such as hemoglobin content,
white blood cells, hematocrit, blood platelets,
electrolytes, acid-base balance and serum
transaminases, and in most cases viral isolation
and hemagglutination inhibition tests. The
results of the first 2 groups were taken from
the investigation of Indra Roemaja Bahro-
emsyah, published in 1988 as a comparative
study.
Results
There were 358 cases of D H F in the first
group, 745 in the second [lo] and 1,329 in the
third, out of which dengue encephalopathy
was diagnosed in 33, 21 and 98 cases, or 9.2%,
2.5% and 7.3% respectively.
The age distribution of D H F cases in
group I showed a preponderance of the 1 4
Table 6. Outcomc of 98 cases of dengue encephalopathy
(Group 111)
No. of
cases
Death 51
Recovery 47
Neurologically normal 44
h'eurologically abnormal 3
Hemiparesis 2 Patho physiology
Tetraparesis I
Total 98
~~ ~
Table 7. Most pronounced symptoms in fatal cases
Symptoms No. of cases
Shock/ recurrent shock
Massive gastrointestinal bleeding
CNS manifestations
Total
Vol. 34 No. 3 June 1992
Dengue encephalopathy (95) 353
and 5-9 years age groups (87.5%), while a
high number of cases in group 11 were in the
5-9 years group (47.6%) (Table I). In all the
98 cases of dengue encephalopathy we studied,
more were found in the 14 and 5-9 years age
groups.
The WHO (1980) has classified D H F
according to the severity of clinical symptoms
into 4 grades as follows: grade 1, fever
accompanied by nonspecific constitutional
symptoms, the only hemorrhagic manifestation
being a positive tourniquet test; grade 11,
manifestations of grade I plus spontaneous
bleeding in skin or elsewhere; grade 111,
symptoms of circulatory failure such as rapid
and weak pulse, narrowing of pulse pressure
to 20 mmHg or less, or hypotension, with cold
any clammy skin or restlessness; and grade
IV, profound shock with undetectable blood
pressure and pulse.
In the 98 cases we studied, more than half
(77.6%) were classified as severe DHF (Table
2).
Evaluation of the clinical symptoms of the
3 groups is shown in Table 3. Besides the
* Clinical & Laboratory Evidence of DHF;DSS
* Abrupt Onset of Hyperpyrexia
* Alteration of Consciousness
% * Headache, Vomiting
* Neurological Abnormalities
52.0
* Normal CSF
47.9
Fig. I : Diagnosis of dengue encephalopathy
la, All organs
Plasma leakage
Hemorrhage
Prolonged shock
26 -. Edema - Metabolic acidosis
18 - Hemorrhage .- Hyponatremia
7 - Occlusion
51
Fig. 2: Pathophysiology of dcngue encephalopathy
354 (96) Hrndarro and Hudinegoro
classical manifestations of DHF such as
hepatomegaly and bleeding tendency, the
most prominent symptoms in dengue encepha-
lopathy are alteration of consciousness and
convulsions.
Out of the 98 cases of dengue encepha-
lopathy, 54 or 55.6(2) were in a state of
somnolence. while 14 or 14.1% were in a state
of stupor or coma. Other symptoms and signs
of D H F are shown in Table 4. Severe liver
enlargement was found in 62 or 62.6% of
cases; other symptoms were petechiae in 68 or
69.4gf : profuse nose bleeding in 19 or 19.4%:
and profuse gastrointestinal bleeding in 54 or
55.19; of cases.
Laboratory evaluation of the cases of
group 111 revealed mostly hemoconcentration
and thrombocytopenia. The maximum hemat-
ocrit value was 52.9 vol% and the lowest
platelet count was 4.000 (Table 5). Low
sodium and potassium levels were also noted
in most cases. Serum transaminases were
increased in 90 out of 98 cases (91.8%); they
were found to be normal in 8 cases only.
Serologic hemaglutination inhibition antibody
tests ( H I ) showed that out of 59 cases studied,
55 o r 77.6?+ had a secondary or presumptivc
secondary infection. In 39 cases, serologic HI
evaluation was not done due to technical
d iff cult ies.
The mortality of the 98 cases of dengue
encephalopathy in group 111 was 51. or 52%;
out of the 47 survivors, 3 were found to be
neurologically abnormal, with permanent
hemiparesis or tetraparesis of the extremities
(Table 6 ) .
Discussion
The incidence of dengue encephalopathy in
thc 3 groups evaluated was 9.2%. 2.4% and
7.3%. respectively.
The overall incidcnce in the 3 groups of
dengue encephalopathy was 152 out of 2,441
DHF cases admitted, or 6.2%.
A high frequency of DHF with CNS
manifestations was found during 1988 1989.
which may be correlated with the five-yearly
outbreak of dengue in 1988.
The age distribution of DHF cases indicated
a shift to the older age group [9, 101, which
can be explained by the hypothesis of
sccondary heterologous infection [ 121, which
states that infection with other strains of
dengue virus with clinical manifestations may
occur after a latent period of 6 months to 5
years. The shift to the older age group could
also be related to the increase in the number
of seropositive reactions against dengue with
increase of age. The finding of 4 serotypes of
dengue virus may also add to the risk of
secondary infection.
Cases of dengue encephalopathy have been
recorded since 1981, confirmed by viral
isolation and serological evidence [7- 91. Sero-
type Den-3 was usually found with the severe
type of dengue infection, DHF grades 111 and
IV. Such infections are usually complicated by
shock, profuse gastrointestinal bleeding and
CNS involvement. and end in death.
The diagnosis of dengue encephalopathy is
based on the clinical signs and symptoms of
DHF with cerebral manifestations such as are
found in other types of encephalitis/encepha-
lopathy: hyperpyrexia, alteration of conscious-
ness, headache, vomiting and neurological
abnormalities, with normal C S F (Fig. I).
Headache was usually found as a complaint in
the older age group.
Alteration of consciousness as one of the
most prominent symptoms of dengue en-
cephalopathy was found in 100% of groups I
and 11, and nearly 100% of group 111. That
alteration of consciousness was due to
encephalopathy and not simply to DHF could
be concluded by the fact that it does not occur
even in the most severe cases of D H F , except
terminally.
I n our study of 98 cases of group 111 of
confirmed DHF, the most pronounced symp-
toms in the 51 fatal cases were not the CNS
symptoms per se, but massive gastrointestinal
bleeding and shock, although all showed CNS
symptoms which were less pronounced than
the general symptoms. CNS symptoms seen
were alteration of consciousness, hyperpyrexia
and convulsions (Table 7).
The exact cause of death in the fatal cases
Acra Paediatr Jpn

could only be assumed clinically, since
autopsy is nearly impossible to obtain due to
local beliefs and religion in our country.
CSF examination in 152 cases in the 3
groups examined revealed normal values.
Pathophysiology of Dengue Encephalopathy
The basic pathophysiology of DHF/ DSS
is plasma leakage and abnormal hemostasis
leading to hypovolemic shock and hemor-
rhage. Hemorrhage may occur in any organ of
the body such as the heart, brain, liver or
gastrointestinal tract [9]. The pathophysiologic
changes in the brain due to plasma leakage
and hemorrhage are brain edema and intra-
cranial bleeding. Such bleeding may manifest
itself as intracerebral, intraventricular, sub-
dural or subarachnoid bleeding.
The causes of abnormal plasma leakage
and abnormal hemostasis are cellular damage,
direct or indirect, through an immunologic
process following secondary heterologous
infection or sequential dengue virus infection.
The pathophysiology of dengue infection is
set out in Fig. 2. An associated factor which
may directly or indirectly induce organ
involvement, including the brain, is dissemi-
nated intravascular coagulation (DIC) [9].
DIC causes occlusion of the brain vessels
and/or tissue hemorrhage in addition to the
already occurring brain hemorrhage and
edema which are common findings in autopsy
cases of dengue encephalopathy.
Prolonged shock may induce hypoxia and
metabolic acidosis with the consequence of
abnormal brain metabolism, leading to further
convulsions and alteration of consciousness.
Decreased serum sodium content, a common
finding in hypovolemic shock, may induce
convulsions, water intoxication and further
brain edema, especially if the serum sodium
falls below 120 meq/l.
Multiple organ involvement including the
brain occurred more frequency with prolonged
shock and DIC.
In the heart, bleeding in various parts of
the myocardium may lead to ischemia,
convulsions and coma. In the Nimmanitya
series [9], myocardial bleeding was found in
Vol. 34 No. 3 June 1992
Dengue encephalopathy (97) 355
all but one case.
In the gastrointestinal tract, focal petechiae
and submucosal bleeding were nearly always
found on autopsy, sometimes accompanied by
profuse hematemesis and melaena.
Recently, more investigators have pointed
out the important role of liver involvement in
DHF complicated by encephalopathy [9, 131.
Symptoms of acute liver failure which may
induce CNS involvement are an unusually
high increase of serum transaminases, pro-
longed plasma prothrombin time and jaundice.
In 98 cases studied in group 111, more than
90% showed an increase of serum trans-
aminases as a sign of liver failure.
Marked liver destruction was noted in all
nonfatal cases of dengue in the Nirnmannitya
study [9]. Liver failure was detected in cases of
Den-2 and Den-3 viral infection who died in
the first days of admission [Ill. Other
investigators suggested that liver failure may
be potentiated by the intake of drugs during
the early stages of the illness, such as
paracetamol, acetosal or antiemetics; however,
others found no correlation between serum
acetaminophen/paracetamol serum content
and the development of liver failure [14].
The possibility of associated Reye’s syn-
drome as a cause of acute liver failure was
also proposed [6, 81, but histopathological
liver biopsy examination in dengue encepha-
lopathy revealed different changes from those
seen in Reye’s syndrome [13]. Dengue anti-
bodies were found in nearly all virologically or
serologically confirmed cases of dengue en-
cephalopathy [13]; in one case flavivirus
antigen was detected. Dengue antigen was
detected in hepatocytes, Kupfer cells and
occasionally in acute inflammatory cells.
Dengue virus was not found in liver cell
cultures. Extensive necrosis of hepatocytes
was seen in massive or submassive distribution.
The degeneration underlying the necrosis was
coagulative. Innis et a1 [I31 found dengue
encephalopathy in about one third of cases of
primary dengue infection, mostly of serotypes
Den 1 and 3; contrary to the results of our
study, where it occurs with secondary or pre-
sumptive secondary infection with serotypes
356 (98) Hcndarro and Hadinegoro
Den-2 and 3, of which Den-3 infection caused
more severe clinical symptoms and a high
mortality rate.
A study reported by Wei-June Chen et a1
in 1990 on C S F and sera of clinically and
virologically diagnosed cases of dengue en-
cephalopathy stated that dengue IgM was
detected in 14 out of 20 sera; in one of the
positive specimens IgM could still be detected
up to 252 days after the onset of the illness
[14]. IgM was detected in all cases with CNS
symptoms (4 cases); the IgM titer in the CSF
was always lower than in the serum and faded
within 1 month of the illness.
All these studies of the possible pathophys-
iology of dengue encephalopathy suggest that
many factors may be associated with its
pathogenesis. That CNS manifestations were
due to encephalopathy and not encephalitis
was evident from autopsy findings, since
macroscopic and microscopic examination of
the brain revealed no evidence of encephalitis.
Treatment and Management of Dengue
Encephalopathy
Until now no satisfying standard treatment
or management has been proposed that will
ensure full recovery from the illness. Manage-
ment is directed to relief of symptoms and is
similar to the basic standard management of
D H F DSS.
The main aim of treatment is t o reduce
plasma leakage by volume replacement and to
minimir.e the bleeding.
In prolonged shock, plasma is added.
Blood or blood components such as packed
red cells are given to cases with profuse
gastrointestinal bleeding. Vinai Suvatte [ 151 in
his study used additional exchange blood
transfusion, which yielded a higher survival
rate than in previous studies; the survival rate
in his study was 72.2%. The use of corti-
costeroid to reduce brain edema is still
controversial, as brain edema is not the origin
of dengue encephalopathy; but in some
centres, corticosteroid is used for brain edema
if there is no sign of acute gastrointestinal
bleeding.
Conclusion
Many factors contribute t o the development
of CNS pathology with signs and symptoms
of brain involvement, or dengue encepha-
lopathy, as one of the most serious complica-
tions of DHF. Liver pathology or acute liver
failure is considered to be one of the main
factors involved, as well as pathologic abnor-
malities in other organs of the body.
Previously recognized as a relatively rare
complication of DHF, recent studies imply
that more cases of dengue encephalopathy will
be found in the future. More studies should be
done, especially in the field of prevention and
management; for the mortality rate is still very
high.
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