SEIZURE
HISTORY OF PRESENT ILLNESS
4 days PTA
Persistence of fever
Intermittent abdominal pain specifically located at the epigastric area
Post prandial projectile vomiting with mucoid appearance,
Cough and colds.
HISTORY OF PRESENT ILLNESS
1 DAY PTA
persistently afebrile
Persistence of intermittent epigastric pain
Episode of postprandial vomiting
Non-projectile and watery.
HISTORY OF PRESENT ILLNESS
DOC
Perinatal
Uncomplicated delivery
Postnatal
Term, VSD, no complications
PAST MEDICAL HISTORY
Patient had history of Typhoid fever when he was younger.
No history of previous illnesses such as measles, mumps, chickenpox,
tuberculosis, pneumonia, asthma, allergies, eye or ear problems, or seizures
No history of operations or injuries.
FAMILY HISTORY
conscious, well nourished, coherent, well developed, weak looking and irritable, not in
cardiorespiratory distress. and appears his chronological age of 5 years old and 3 months
VITAL SIGNS
Blood Pressure 90-50mmHg N:95-110/60-75mmHg
Pulse Rate 114 bpm N:65-110bpm
Respiratory Rate 22cpm N:20-25cpm
Temperature 36.8C N: 36.5-37.5C
O2 Saturation 99% N: 100-95%
ANTHROPOMETRIC MEASUREMENTS
SKIN
Inspection
moist, mild pallor, acyanotic
Palpation
good skin turgor, good capillary refill
Nail unit
pink, no nail clubbing or koilonychia, no cyanosis.
REGIONAL EXAMINATION
HEAD
Inspection
hair color is black, thin and well distributed, smooth with no patterns of hair
loss.
No lumps and scales and flakes in scalp
Skull is normocephalic with no lump.
Palpation
No cervical lymphadenopathy
Trachea is in midline and thyroid cartilage moves with deglutition
REGIONAL EXAMINATION
EYES
Inspection MOUTH
Symmetrical Inspection
Eyebrows are well distributed Dry lips, chappy with dried blood
Pink palpebral conjunctiva Pink oral mucosa
gum bleeding and hyperemic
tonsils and posterior palate
EARS
No erythema, lesions, tenderness
REGIONAL EXAMINATION
RESPIRATORY
Inspection
Symmetrical chest expansion, no use of accessory muscles A:P diameter 1:2
Percussion
Resonant on all lung fields
Auscultation
Equal vesicular and bronchovesicular sounds on anterior lung fields
No adventitious sounds were noted; (-) crackles, wheezes, stridor
REGIONAL EXAMINATION
CARDIOVASCULAR
Inspection
No precordial bulge
Palpation
(-) heaves (-) thrills
Auscultation
Normal rate, regular rhythm
No murmurs
REGIONAL EXAMINATION
ABDOMEN
Inspection
Not distended, no scars
Auscultation
Normoactive bowel sounds
Palpation
Soft (+)abdominal guarding (-) abdominal tenderness (-) hepatosplenomegaly
(-) Rovsings and Murphys sign
Abdominal circumference: 67 cm
REGIONAL EXAMINATION
EXTREMITIES
Inspection
no swelling noted on both extremities
Palpation
No tenderness, good equal pulses
No loss of motion
REGIONAL EXAMINATION
NEUROLOGIC EXAM
GCS 14-15/15
Normal general behavior
Scarce stream of talk
Appropriate mood
No hallucinations
Oriented to 3 spheres
No sensory and motor deficits
(-) Kernigs (-) Brudzinski (-) Nuchal rigidity
REGIONAL EXAMINATION
Cranial nerves
II (+) direct and consensual light reflex
Pupils EBRTL 2-3mm
III. IV, V Intact EOM
V Good masseter tone
Intact facial sensation
VII No facial symmetry
IX (-) drooling of saliva
(+) swallow
(+) cough
(+) lingual and guttural sounds
(-) nasal twang
(-) dysphonia
Phosphorus 0.74-1.52
laboratory
CHEST, AP/L VIEWS
laboratory
laboratory
laboratory
KUB ULTRASOUND
COURSE IN THE WARDS
S O A P
ER
Primary Impression
DENGUE WITH WARNING SIGNS
SALIENT FEATURES
1. Malaria
Patient had history of fever, cough, abdominal pain,
anorexia, nausea, and vomiting. PE finding of abdominal
tenderness.
2. Influenza
Considered due to history of fever, poor activity,
cough, and colds.
Differential diagnosis
3. Typhoid fever
Considered due to history of fever,
abdominal pain, cough, and poor
activity. PE finding of abdominal
tenderness.
Differential diagnosis
4. Japanese encephalitis
Considered due to history of fever. JE virus is a
flavivirus related to dengue.
5. Yellow fever
A possibility due to symptoms of fever,
anorexia, nausea, and vomiting.
Differential diagnosis
6. Bleeding dyscrasia:
Hemophilia A & B
Von Willebrand disease
Disseminated Intravascular Coagulation
Idiopathic Thrombocytopenic Purpura
DHF: Pathogenesis
Secondary infection with another serotype leads to
antibody mediated enhancement
Heterotypic antibodies are non protective and fail to
neutralise the virus
Virus-antibody complexes taken up by monocytes
Virion multiplication in human monocytes is promoted
Activation of CD4+ and CD8+ lymphocytes release of
cytokines
Complement system activated with depression of C3 & C5
Homologous Antibodies Form
Non-infectious Complexes
Dengue 1 virus
Neutralizing antibody to Dengue 1 virus
Non-neutralizing
antibody
Complex formed by neutralizing antibody
and virus
Hypothesis on Pathogenesis
of DHF (Part 2)
Dengue 2 virus
Non-neutralizing antibody to Dengue 1
2
virus
Complex formed by non-neutralizing
antibody and virus
Hypothesis on Pathogenesis
of DHF (Part 3)
Antibody-dependent enhancement
is the process in which certain strains
of dengue virus, complexed with
antibodies, can enter a greater
proportion of cells of the
mononuclear lineage, thus increasing
virus production
Plasma leaks - Pathophysiology
Host response
Subsequent infection
Previous IgG
Neutralizing (protective)
non neutralizing (replication enhancing)
Loss of volume
Reduces pulse pressure
during the critical phase when the fluid is oozing out - would result in
Pathophysiology of DHF
People do not die of hemorrhage in DHF
They die
Either due to shock and 20 organ failure
Or due to Pulmonary edema & fluid over load during the recovery
phase
EPIDEMIOLOGY
Genus Flavivirus
Family Flaviviridae
Single-stranded RNA
4 serotypes (DEN-1 to 4)
50 nm diameter with
multiple copies of 3
structural proteins (( membrane
membrane
bilayer
bilayer and
and single-stranded
single-stranded RNA)
RNA)
Vector Profile
Aedes mosquitoes
A.
A. aegypti
aegypti
A.
A. albopictus
albopictus
A.
A. polynesiensis
polynesiensis
Tropical and
subtropical species
Urban places
Immature stages are
found in water-filled
habitats
The Host
Viral
Replication WBC and
Lymphatics
Replication and Transmission
Replication in
the salivary
gland
Female
mosquito ingests
infected blood
Dengue Fever
Three phases
Febrile phase
Critical phase
Recovery phase
Febrile Phase
Critical Phase
Recovery Phase
Febrile Phase
facial flushing
skin erythema
Sudden onset of generalized body ache
myalgia and arthralgia
high-grade fever headache
Lasts for 2-7 days sorethroat, injected pharynx,
and conjunctival injection
anorexia, nausea and
vomiting
Febrile Phase
(+) hemorrhagic
manifestations
RT-PCR
NS1
IgM
IgG
CBC
TREATMENT
GROUP B
Obtain a reference
hematocrit before Reassess the
Give the minimum
fluid therapy clinical status,
intravenous fluid volume
repeat HCT and
required to maintain good
review fluid
perfusion and urine output
infusion rates
of about 0.5 mL/kg/hr
accordingly
Isotonic solutions
5-7 mL/kg/hour for
1-2h If there are
worsening of vital Reduce intravenous fluids
3-5 mL/kg/hr for 2- signs and rapidly gradually when the rate of
4h rising HCT, increase plasma leakage decreases
2-3 mL/kg/hr or less the rate to 5-10 towards the end of the
according to mL/kg/hour for 1-2 critical phase
clinical response hours
NOT RECOMMENDED
Children < 9 y/o and Adults > 45 y/o
Allergic to dengue vaccine
Immunocompromised individuals
Pregnant or Breastfeeding individuals
Chloroquine use
Improves Dengue-
related Symptoms
M.C. Borges, L.A. Castro, et al.
Objective
Antiviral effect
Raising the intracellular pH -> interfere with endosome-mediated entry
Interfere with the post-translational processing of viral glycoproteins
Anti-inflammatory activity
TNF-a inhibitor
Limitations of the Study
But did not alter the duration of the disease or the intensity and days of fever