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DHF

Dengue Hemmorhagic Fever

Dr. DWI LINGGA UTAMA, SpA (K)


Homologous Antibodies Form
Non-infectious Complexes

1
1

1
1 Dengue 1 virus
Neutralizing antibody to Dengue 1 virus

Non-neutralizing antibody
1 Complex formed by neutralizing antibody and virus
Heterologous Antibodies
Form Infectious Complexes
2

2 2
2

2
Dengue 2 virus

Non-neutralizing antibody to Dengue 1 virus


2
Complex formed by non-neutralizing
antibody and virus
Heterologous Complexes Enter More
Monocytes, Where Virus Replicates

2
2
2
2
2
2 2
2
2

2 Dengue 2 virus

Non-neutralizing antibody

2 Complex formed by non-neutralizing


antibody and Dengue 2 virus
Secondary heterologous dengue infection

Virus Previously
replication antibody
Virus-antibody complex respons

Endothelial Complement
Platelet agregation
disturbances activation

Hageman factor Anafilatoxin


Platelet activation Coagulation
destruction by activation
Releasing factor III
RES platelet
Kinin
Thrombocytopeni
system Capillary
a
Consumptive Kinin permeability
coagulopathy increase
FDP
Platelet Decreasing coagulation increasing
function function
disturbances
Massive SHOC
bleeding K
Suvatte, 1978
Pathogenesis of bleeding on
Secondary heterologous dengue infection

Virus replication Anamnestic antibody respons

Complex virus-antibody

Complemen activation
Complemen

Anafilatoxin (C3a, C5a)


Urine Histamin
Capillary permeability increase
Ht increase
30% shock Plasma leakage Natrium
decrease
Hipovolemia Intra serous
fluid
Anoxia Acidosis
Shock
Death
Criteria from WHO (1999)
Clinical :
Fever 2 7 days
Bleeding : RL test (+)/spontaneous bleeding
Hepatomegaly
Shock 2 clinical + lab
Laboratories :
Low platelet count (<100.000 /ul)
Hemoconcentrate (>20%)
DHF
Grading of Illness
Grade I
Unspecified febrile, Tourniquet test
positive
Grade II
Grade I + spontaneous bleeding
Grade III
Circulatory failure (restless, fast &
small pulse, pulse pressure < 20mmHg,
hypotension, cyanosis, cold & moist
extremities)
Grade IV
Shock, undetected pulse and blood
INTERPRETASI HASIL
PEMERIKSAAN IgM dan IgG
IgM IgG Interpretasi
(+) (-) Infeksi primer
(+) (+) Infeksi sekunder
(-) (+) Tersangka infeksi
sekunder
(-) (-) Tidak ada infeksi
MUNCULNYA IgM DAN IgG PADA PASIEN
YANG TERINFEKSI VIRUS DENGUE
Warning Signs for
Dengue Shock Alarm Signals
Severe abdominal pain
Prolonged vomiting
Four Criteria for DHF Abrupt change from fever
Fever
Hemorrhagic manifestations
Excessive capillary
permeability
100,000/mm3 platelets
to hypothermia
Initial Warning Signals Change in level of
Disappearance of When Patients Develop
consciousness (irritability
DSS:
fever
3 to 6 days after onset of
Drop in platelets
Increase in hematocrite
Ref: CDC Atlanta, 2003

or somnolence)
Dengue virus infections
10,000
Asymptomatic Symptomatic
9,000 1,000

Undifferentiated Fever Dengue Fever Dengue Hemorrhagic Fever


(Viral syndrome) (DF) (DHF)
400 100
500

Plasma leakage
50DF, 50 DHF
Non-shock Shock
DHF DSS
(Dengue shock syndrome)
48 1-2
Systolic + Diastolic
2
= 5

Natural course of DHF


Day 1 2 3 4 5 6 7 8 9

Fever Shock

Pleural effusion,
Ascites

Plasma leakage Stop leakage Reabsorption

IV fluid: NSS, DAR, DLR


W Colloid: 10%Dextran,
B 10%Haes-steril
C M+5% Deficit
(= 4,600 ml in adult)
WBC 8,000 5,000
Platelet count 200,000+ 100,000
Hct rising 20%
Albumin 3.5 gm
%
Cholesterol Professor Siripen Kalayanarooj
100 mg%
Warning signs of shock
Clinical deterioration when no fever
Severe abdominal pain
Excessive vomiting
Irritable/ restless, Persistent crying
in infants
Sweating, cold clammy skin, ottling
Drowsy, behavior change
No urine for 4 6 hours
Detection of shock :
Difficult because of good consciousness
Rapid pulse without fever
Narrowing of pulse pressure eg.100/80, 110/90
mmHg
Rapid and weak pulse
Poor peripheral circulation (capillary refill > 2
sec)
Irritable/ restless
Confusion, speak fowl language, behavior change
Delayed capillary refill time
Convalescent rash
Pentingnya pemantauan demam pada
Demam Dengue
Tips
Pada Demam Dengue:
setelah suhu reda,
klinis & nafsu makan membaik

Time of fever defervescence


(Saat suhu reda)
emp

Hari sakit/demam
Time of fever defervescence
Demam Berdarah Dengue
Tips
Pada DBD setelah suhu turun:
Klinis memburuk, lemah, gelisah,
tangan kaki dingin, nafas cepat,
diuresis berkurang,
tidak ada nafsu makan

emp Time of fever defervescence

Fase demam Fase syok Fase konv

Hari sakit
Monitor H-1 H-2 H-3 H-4 H-5 H-6 H-7 H-8 H-9 H-10
Tek darah

Nadi

Frek nafas

Suhu

Kesadaran
Pemantauan berkala selama
Jantung perawatan
Paru

Hati

Lingkaran perut Pemeriksaan Fisik


Pem penunjang
Refleks

Diuresis
Balans cairan
Hb

Leukosit & HJ Obat-obatan


Hematokrit Transfusi darah
Trombosit

AGD & elektrolit

Cairan

Foto toraks

Diuresis

Transfusi darah
Returning Home Criteria for the Patient

No fever for 24 hours without


antipiretic
Good appetite
Clinically better
Stable Hematocrit
Three days after shock recovery
Platelet count increased (>50.000/ul)
No respiratory distress found
(because of pleural efusion or acidosis)
Hematom
pada bekas tusukan
Perdarahan pada DIC
darah merembes dari tusukan jarum

Kasa basah, darah segar merembes


Perdarahan saluran cerna
pada DSS
Pembesaran hati korelasi
positif dengan perdarahan
sal cerna
Perdarahan hebat akibat DIC
pada DSS
dipther
ia
Diphtheria
Is an acute infectious disease of the childhood
characterized by local inflammation of the
epithelial surface , formation of a membrane ,
and severe toxemia

Epidemiology : -
Age groups : Pre school age children

Caused by ---- Gram positive bacilli,


Corynebacterium diphtheria
Cont ..
Source : -
- secretions and discharge from an infected
person or carrier
Human are chief reservoirs
Mode of transmission : -
Contact or through droplets of secretion
Portal of entry :
Respiratory tract
May enter through the conjuntiva or skin
wound
Risk factors
1. Poor nutrition.
2. Outbreak in the community.
3. Crowded or unsanitary living conditions.
4. Low vaccine coverage among infants and
children.
5. Lack of mass immunization programmes amongst
children and adults at high risk.
Pathogenesis
Entry ------ the bacilli multiply locally in the throat and
elaborate a powerful exotoxin ----- produce local and
systemic symptoms.
Local lesions :
Exotoxin causes necrosis of the epithelial cells and
liberates serous and fibrinous material which forms a
grayish white pseudomembrane

The membrane bleeds on being dislodged

Surrounding tissue is inflamed and edematous


Cont
Systemic lesions :
Exotoxin affects the heart , kidney and CNS

Heart :
Myocardial fibers are degenerated and the heart
is dilated
Conduction disturbance

CNS : polyneuritis

Kidney : renal tubular necrosis


Clinical features
Incubation period : 2 5 days

Onset : acute with fever ( 39 C ) , malaise ,


headache and loss of appetite

Child looks very sick and toxic

Delirium

Circulatory collapse ( myocarditis )


Local manifestation
Depend on the site of Faucial diphtheria :
lesion: Redness and swelling over
Nasal diphtheria : fauces
Unilateral or bilateral Exudates on the tonsils
serosanguineous ( blood and coalesces to form grayish
serous fluid ) discharge from white pseudo membrane
the nose Regional lymph nodes are
Excoriation of upper lip inflamed
Toxemia is minimal Sore throat and
dysphagia
Cont
Laryngotracheal diphtheria :
Membrane over the larynx results in
brassy ( hardness ) cough and
hoarse voice
Respiration ------- noisy Unusual sites :
Suprasternal and subcostal
Conjunctiva and
recession
Restlessness
skin
Increasing respiratory effort In the skin :
Use of accessory muscles Ulcers ( tender )
Diagnosis

clinical history , examination and identification of


diphtheria bacilli from the site of lesion.

Culture

Fluorescent antibody technique


Schick Test
Schick test: It is an intradermal test,
the test is carried out by injecting
intradermally into the skin of
forearm 0.2 ml of diphtheria toxin,
while into the opposite arm is
injected as a control, the same
amount of toxin which has been
inactivated by heat.
Interpretation
Negative reaction: If a person had immunity to diphtheria,
no reaction will be observed on either arm.

Positive reaction: An area of in duration 10-15 mm in


diameter generally appears within 24-36 hours reaching
its maximum development by 4-7 days, the control arm
shows no change. The person is susceptible to diphtheria.

False positive reaction: A red flush develops in both arms,


the reaction fades very quickly, and disappears by 4th day.
This is an allergic type of reaction found in certain
individuals
Combined reaction: the control arm shows pseudo
positive reaction and the test arm is true +ve reaction,
susceptible and need vaccination
Differential diagnosis
Nasal diphtheria :
Foreign body in nose ,
Rhinorrhea

Laryngeal diphtheria :
Croup
Acute epiglottitis
Laryngotracheobronchitis
Peritonsillar abscess
Retropharyngeal abscess
Cont .
Faucial diphtheria :
Acute streptococcal membranous tonsillitis
( high grade fever , child less toxic )

Viral membranous tonsillitis :


high grade fever ,
WBC : normal or low ,
Antibiotic : no effects
Treatment
Principles :
Neutralization of free circulating toxin by
administration of antitoxin

Antibiotic to eradicate bacteria

Supportive and symptomatic therapy

Management of complication
Antitoxin
Diphtheria antitoxin :
Pharyngeal or laryngeal diphtheria of 48 hours
duration : 20,000 to 40,000 units.
Nasopharyngeal lesions : 40,000 60,000 units
Extensive disease of 3 or more days duration or
patient with swelling of neck : 80,000 120,000
units
Antitoxin may be repeated if the clinical
improvementis slower
Antibiotics
Penicillin :
Procaine penicilline ( 3 6 lac units IM at 12
hourly intervals till the patient is able to swallow )
Oral penicillin ( 125 250 mg qid )

Erythromycin ( 25 30 mg / kg / day ) for 14 days

Three negative cultures at 24 hours intervals


should be obtained before the patient is
declared free of the organism
Supportive and symptomatic therapy

Bed rest for 2 3 weeks ( to reduce cardiac


complications )

Antipyretics and sedative ( if required )

Monitor rate and rhythm of the heart


Management of complication
Respiratory obstruction :
Humidified oxygen
Tracheostomy

Myocarditis :
Fluids and salt restriction
Sedation and oxygen supply
Diuretics and digoxin

Neurological complications :
Palatal paralysis ( NG feeding )
Generalised weakness ( as polio )
Prognosis
Death may occur due to : -

Respiratory obstruction

Myocarditis

Respiratory paralysis
MEASL
ES
Measles
Highly contagious viral illness
First described in 7th century
Near universal infection of childhood in
prevaccination era
Common and often fatal in developing
areas
Paramyxovirus (RNA)
Rapidly inactivated by heat and light
Measles Pathogenesis
Respiratory transmission of virus
Replication in nasopharynx and regional
lymph nodes
Primary viremia 2-3 days after exposure
Secondary viremia 5-7 days after
exposure with spread to tissues
Measles Clinical Features
Incubation period 10-12 days

Prodrome
Stepwise increase in fever to
103F or higher
Cough, coryza, conjunctivitis
Koplik spots
Measles Clinical Features
Rash
2-4 days after prodrome, 14 days after
exposure
Maculopapular, becomes confluent
Begins on face and head
Persists 5-6 days
Fades in order of appearance
Measles Complications

Diarrhea
Otitis media
Pneumonia
Encephalitis
Hospitalization
Death

Based on 1985-1992 surveillance data


TREATMENT

NO SPECIFIC THERAPY IS AVAILABLE


Ensure adequate nutrition and fluid intake
Antibiotics for eye/ear infection, or
pneumonia
Measles Vaccine
Composition Live virus
Efficacy 95% (range, 90%-98%)
Duration of
Immunity Lifelong
Schedule 2 doses