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Transcript
ENCEPHALITIS,CEREBRAL EDEMA
5/14/2017
Dr. Alka Stoelinga
1
• Encephalitis means inflammation of brain parenchyma
• Cause: usually viral
• Brain inflammation also develops in bacterial and fungal
meningitis
• Not an isolated entity
• Usually associated with meningeal inflammation
together
• Also term as “Meningoencephalitis”
• Commonest virus is Herpes simplex which reaches
brain via the Olfactory nerve
• Meningism is the triad of
• Nuchal rigidity (neck stiffness)
• Photophobia (intolerance of bright light)
• Headache.
5/14/2017
Dr. Alka Stoelinga
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Etiology:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
5/14/2017
Arbo virus
Japanese B encephalitis
Herpes simplex
Coxsackie
Epstein-Barr viruses
Adenovirus
Varicella zoster
Influenza
Measles
Entero virus
Mumps (Aseptic meningitis)
HIV
Rabies
Dr. Alka Stoelinga
3
Clinical features:
• Acute onset of Fever, Headache, Meningism and
Drowsiness in mild cases.
• In severe illness: focal signs(e.g Aphasia,
hemiplegia or cranial nerve palsies), siezures and
coma may develop
• Coma: Rapid deterioration in sensorium
• Altered consciousness, focal signs and seizure are
more common in encephalitis as compared to
meningitis
• Patient may agitate(while in meningitis patients is
usually calm, conscious, drowsy and nonagitated)
5/14/2017
Dr. Alka Stoelinga
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Examination:
1.
2.
3.
4.
5.
Coma/Altered level of consciousness
Meningeal signs may be present
Focal neurological deficits
Hypertonia/Brisk reflexes/Extensor plantar
Opthalmoscopic examination: Look for
papilloedema
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Dr. Alka Stoelinga
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Investigation:
1. CT scan head :Shows area of edema
1. In Herpes simplex encephalitis CT scan show low
density lesions in the temporal lobes
2. MRI head
3. EEG : Shows slow wave changes
4. CSF analysis
•
•
•
•
Cell: 10-2000
Mainly Lymphocytes
Glucose usually normal
Protein normal or Slightly raised
5. Viral serology of blood and CSF
6. PCR: Herpes simplex virus DNA can be detected
by PCR
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Dr. Alka Stoelinga
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Management:
•
•
•
•
Supportive
Fluid balance
Control of seizure
Treatment of raised ICP:Dexamethasone 4mg
QID for raised intracranial pressure
• Herpes simplex encephalitis: Acyclovir
 Dose: 10mg/kg/dose IV 10 hourly
 Acyclovir should be given to all suspected
cases of viral encephalitis
• Anticonvulsants if presence of Epilepsy
5/14/2017
Dr. Alka Stoelinga
7
Prognosis:
• Mortality is 10-30% when antiviral drugs are
used, without antiviral mortality is 70%
• Survivors may have cognitive impairment or
developed epilepsy
Complications:
1. Focal Neurological deficit
2. Loss of cognitive function
3. Seizure
5/14/2017
Dr. Alka Stoelinga
8
CEREBRAL MALARIA
• Severe form of falciparum malaria
• Common in tropical area
• Treatable condition
Pathogenesis :
• Sequestration of parasitized RBC into blood
vessels of internal organs: Brain
• Rouleax formation
• Cerebral anoxia
• Hemolysis
5/14/2017
Dr. Alka Stoelinga
9
Clinical features:
• Chills, Persistent high fever, headache, orthostatic hypotension, myalgia
• Red blood cell (RBC) sludging that leads to capillary blockage at several
sites
• The three initial stages of Cerebral Malaria are:
1. Cold Stage: It ranges from chills to extreme shaking for 1-2 hours
2. Hot Stage: It is characterized by a high fever up to 107°F (41.7°C)
for 3-4 hours
3. Wet Stage: It is characterized by profuse sweating for 2-4 hours
• There are three primary symptoms of cerebral malaria which are
common in both adults and children:
1. Impaired consciousness with non-specific fever,
2. Generalized convulsions and neurological abnormalities, and
3. Coma that lasts for 24-72 hours, initially rousable and then
unrousable
5/14/2017
Dr. Alka Stoelinga
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• It also manifests with
– signs of increased intracranial pressure
– Hemiplegia
– Encephalopathy
– Delirium
– seizures and
– Coma
• If not treated on time, it can lead to complications like
– Jaundice
– Hemoglobinuria
– a tender and enlarged spleen
– acute renal failure
– Uremia
5/14/2017
Dr. Alka Stoelinga
11
Examination:
•
•
•
•
•
•
Altered consciousness
Pallor
Icterus
Bleeding manifestation
No focal neurological deficit
Splenomegaly
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Dr. Alka Stoelinga
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Investigation:
 Peripheral blood smear:
 Thick and Thin smear
 CSF analysis
 Blood Sugar, electrolytes, ABG, urea, creatinine
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Dr. Alka Stoelinga
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Treatment of Severe P. falciparum Malaria/ Cerebral Malaria
Regimen
Regimen 1
First Drug
Second Drug
Artesunate 2.4 mg/kg bw iv or im on
Doxycycline100mgs BID (2.2mg/kg BID for <45kgs[4])
admission; then at 12 h and 24 h, then once a for 7 days OR
day for 7 days
Mefloquine 15 mg/kg (750 mg) base, then 10 mg/kg
(500 mg) base at 6–8 hours and (if >60 kg) followed by
5 mg/kg (250 mg) at 16 hours (Total 1500 mg) OR
Clindamycin 20mg base/kg/day divided in three doses
for 7 days in pregnancy
Regimen 2
Artemether 3.2 mg/kg bw i.m. given on
admission then 1.6 mg/kg bw per day for 7
days
Same as above
Regimen 3
Quinine 20 mg salt/kg bw on admission (iv
Doxycycline OR Clindamycin as above
infusion or divided im injection), then 10
mg/kg bw every 8 h; infusion rate should not
exceed 5 mg salt/kg bw per hour; course for 3
days for malaria acquired in Africa and South
America, 7 days for malaria acquired in SE Asia
Regimen 4
Quinidine gluconate 10 mg salt/kg (equivalent Doxycycline OR Clindamycin as above
to 6.2 mg base/kg) iv infused over 1–2 hours,
followed immediately by 0.02 mg/kg/min salt
(equivalent to 0.0125 mg/kg/min base)
continuous iv infusion; course for 3 days for
malaria acquired in Africa and South America,
7 days for malaria acquired in SE Asia
5/14/2017
Dr. Alka Stoelinga
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INTRACRANIAL SPACE OCCUPYING
LESION(ICSOL)
5/14/2017
Dr. Alka Stoelinga
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TUBERCULOMA (TBM)
• Non-neoplastic mass
• Tumor like growth of Tuberculous tissue in the
central nervous system, characterized by
symptoms of an expanding cerebral, Cerebellar,
or spinal mass
• Presents as ring enhancing lesion
• Seizure: Partial seizure
• Focal neurological deficit
• Headache
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Dr. Alka Stoelinga
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Investigation:
1. CT scan head: Ring enhancing lesion
2. AFB smear
3. Mantoux
4. CXR
Treatment:
• Similar to that of tubercular meningitis
5/14/2017
Dr. Alka Stoelinga
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5/14/2017
Dr. Alka Stoelinga
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NEUROCYSTICERCOSIS (NCC)
• Cysticercosis, is an infection which results from
the ingestion of the eggs of the pork tapeworm
(uncooked/undercooked pork meat), Taenia
solium
• Neurocysticercosis, is when the brain or spinal
cord (CNS) is affected by the larval stage of T.
solium
• Neurocysticercosis is the most common
helminthic (tapeworm) infestation to affect the
CNS worldwide
• Is the prime cause of acquired epilepsy.
5/14/2017
Dr. Alka Stoelinga
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Clinical features:
•
•
•
•
•
Seizures: Partial/ Generalised
Hydrocephalus
Features of raised ICP
Stroke, focal neurological deficits
Meningitis
5/14/2017
Dr. Alka Stoelinga
20
Investigations:
1. Neuroimaging:
– MRI(early stage)/CT head(late phase)
•
•
•
•
Ring enhancing lesion
Scolex
Calcification
Perilesional edema
2. Fundoscopy
3. Soft tissue X-ray
4. Serologic test: ELISA
5/14/2017
Dr. Alka Stoelinga
21
Treatment:
• Treatment of seizure Antiepileptics
• Treatment of Hydrocephalus if present
• Cysticidal therapy
Indicated for active lesions
Albendazole 15mg/kg/d for 8-28 days
Praziquantel
• In immature cyst stage  High dosage of
corticosteroids
• In the colloid cyst stage Surgical removal of the
cyst, along with albendazole is indicated
• In calcified dead cysts No treatment
5/14/2017
Dr. Alka Stoelinga
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•
•
•
•
•
•
TBM
Secondary to primary or
post primary TB
Bigger size than NCC
Situated in the midline and
margins are thick and
irregular
More perilesional edema
seen
Calcification
Midline shift and
hydrocephalus
5/14/2017
NCC
• Due to ingestion of T.solium egg
• Small size <10mm and are
multiple in number
• Usually situated in the periphery
with well defined margins
• Less perilesional edema
• Calcification
• Hydrocephalus is uncommon
Dr. Alka Stoelinga
23
BRAIN ABSCESS
Predisposing factors:
• Hematogenous spread: Can occur from any site of primary
infection but is commonly associated with:
1. Infection of chest, including lung abscess, bronchiectasis and
empyema
2. Infection of heart such as infective endocarditis
3. Infection of bone or dental abscess can be primary site of
infection
• Direct/Local spread: Penetrating injury of skull, PNS, Middle
ear
• Mostly involve Frontal and temporal lobes
5/14/2017
Dr. Alka Stoelinga
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• Causative organisms:
– Mixed aerobic and anaerobic organisms are
involved
Staph aureus
Streptococcus milleri
Enterobacteriae
5/14/2017
Dr. Alka Stoelinga
25
Clinical feature:
• Illness develops more gradually than acute
bacterial meningitis.
• Fever, headache, drowsiness, altered
sensorium
• Partial seizure
• Focal neurological deficit
• Features of meningitis
• Septicemia
5/14/2017
Dr. Alka Stoelinga
26
Investigations:
• Neuroimaging: CT
scan head
 Single or multiple
ring enhancing
lesion with
perilesional
edema(central low
density and
surrounding
edema)
• CSF analysis usually
not helpful and C/I
if there is evidence
of raised ICP
• Blood :
TC,DC,ESR,C/S
5/14/2017
Dr. Alka Stoelinga
27
5/14/2017
Dr. Alka Stoelinga
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Treatment:
• Emperic antibiotic therapy must be started
 Inj Benzyl penicillin 2 million units IV hourly +Inj
Chloramphenicol 1-2 gm IV 6 hourly + Inj Metronidazole
500mg IV 6 hourly
• Steroid: Inj Dexamethasone 4-25 mg 6 hourly followed by
tappering of dose to reduce cerebral edema
• Along with drainage of Pus
• 3rd generation
Cephalosporin+Metronidazole+Cloxacillin/Vancomycin
• Antibiotics should be continued for 6-8 weeks.
5/14/2017
Dr. Alka Stoelinga
29