lecture

1. CNS infection
Presented by Nancy Mohammed Alaa
Assistant lecturer of Pediatrics
Assiut university

2. 1-epidemiology
• In general, viral infections of the CNS are much
more common than bacterial infections, which, in
turn, are more common than fungal and parasitic
infections.
• Infections caused by rickettsiae (Rocky Mountain
• spotted fever, Ehrlichia) are relatively uncommon
but assume important roles under certain
epidemiologic circumstances.
• Mycoplasma spp. can also cause infections of the
CNS, although their precise contribution is often
difficult to determine

3. 2-types
• 1-meningitis
• 2-encephalitis
• 3-meningioencephalitis

4. 1-meningitis
• Etiology
• a-bacterial organisms are age-dependent
• b-viral can be seasonal
• c-fungal most common in immunocompromised
• d-tuberculosis
• e-parasite (rare

5. • A-Pyogenic meningitis
• Neonatal meningitis
• mostly reflect maternal GI and genitourinary flora E coli, Strep
pneumoniae, Salmonella species, Pseudomonas aeruginosa, Strep
fecalis, Staph aureus
• Beyond Neonatal period
• 2 month ‐2 years —
• • H. influenzae( 60‐70%)
• • S. pneumoniae
• • Neisseria meningitidis
• • Group B streptococcus (18 percent).
• 2 ‐18 years —
• N. meningitidis ‐ 59 percent of cases,
• S. pneumoniae (approximately 25 percent)
• Hib (approximately 8 percent).

10. Route of spread
• Hematogenous spread
• • Direct spread :
• ‐ Contiguous focus (eg, sinusitis, mastoiditis,
otitis media)
• ‐Through an injury, such as a skull fractures
and foreign body (ventricular shunt).

11. presentation
• A-Neonate
Bulging fontanelle
• Fever/ hypothermia
• Persistent vomiting
• Alternating irritability and drowsiness
• Refusal to feed
• Poor tone and cry
• Shock
• Seizure

12. :• B-child and adult
• 2 presentations:
•
1) Dramatically acute presentation:
Rapid progressive manifestations of shock, purpura,
DIC, altered sensorium, usually death within 24
hours

14. • 2) Acute presentation :
progress over several days
Nonspecific findings:
• Fever, Anorexia, lethargy, URI or GIT sx,
• Petechie/ purpura/ macular rash
• f/o shock
S/o meningeal irritation
f/o raised ICP: headache, vomiting, bulging AF,
hypertension, posturing, papillaedema
Focal neurological signs ( 10‐ 20%)
Altered mental status

16. 2-encephalitis
• encephalitis has been defined as encephalopathy
plus two or more of fever, seizure, focal neurological
findings, compatible electroencephalogram (EEG),
abnormal diagnostic imaging or CSF pleocytosis

17. • Etiology
•
Viral:
• Mumps, measles, rubella, enterovirus
• HSV, CMV, EBV, Varicella
• Japanese encephalitis, West Nile, Russian spring
summer, Equine virus
• Rabies
• Lymphocytic choriomeningitis
• Dengue
• Influenz

18. • Nonviral:
• Rickettsia
• Mycoplasma pneumoniae
• Bacterial: TB, Enteric fever, Shigella etc.
• Spirochetal
• Fungal
• Protozoal

19. Route of spread
• The majority of cases of herpes encephalitis are
caused by herpes simplex virus-1 (HSV-1), the
same virus that causes cold sores which is spread
through droplets, casual contact, and sometimes
sexual contact, though most infected people
never have cold sores.
• About 10% of cases of herpes encephalitis are due
to HSV-2, which is typically spread through sexual
contact.

20. • Clinical picture
• Acute onset
• High fever
• Rash±
• Headache
• Vomiting
• Altered sensorium
• Seizures
• Neurological deficits( HSV: focality +)
• H/o similar illness in the community

21. 3-meningioencephalitis
Organisms located in the subarachnoid space may spread
to the adjacent cortical mantle. When there are signs of
both meningeal and cerebrocortical involvement, the
term meningoencephalitis is appropriate

22. -prognosis
• 1-Bacterial infection: early recognition, diagnosis and
start of treatment are associated generally with better
outcomes. HIB, pneumococcal and meningococcal
vaccines decreases the incidence of meningitis
• 2-causes of Recurrent meningitis:
• • # of cribriform plate or sinuses, pilonidal sinus,
• congenital fistulae, immune deficiency dis

23. monitoring
• With appropriate treatment: CSF culture and
gram stain will become negative in 24-48
hours, glucose will normalize in 72 hrs. Cell
counts and proteins will take days to
normalize.
• Clinical symptoms: Fever and headaches may
persist for 7-10 days

24. diagnosis
Diagnostic criteria and tests
A-A complete and detailed history and physical examination
with details of length of illness and details of presenting
symptoms, preceding illness, past medical history. Also history
of exposure: travel, sick contact, insect bites, sexual activities,
animal contacts
.
B-Initial labs: CBC, CMP, CPR, UA, blood cultures; CSF: with
opening pressure, cultures, cytology, serology
C-Initial imaging: CT head without contrast to rule out space-
occupying lesions, hemorrhage or trauma.
MRI of brain and spine if concern for myelitis/encephalitis

27. complications
•
1-meningitis
• Inflammation of spinal roots/ Nerves
• Neuropathy of 2, 3, 7, 8 N:
•
Inflammation of cranial Nerves
• Hydrocephalus
• Communicating type:
Adhesive thickening of arachnoid villi around cisterns
of brain l/t interference with CSF absorption
• Obstructive type:
Fibrosis & gliosis of aqueduct / foramina of Magendie
& Luschka
Subdural effusion
• Increased permeability of BBB causing exudation of
albumin rich fluid in subdural space

28. • Immediate Complications
• Subdural effusion/ empyema
• Ventriculitis
• Arachnoiditis
• Brain abscess
• Hydrocephalus
• Shock
• ARDS
• Myocarditis
• SIADH
Late complications/ Sequelae
• Hemiplegia/ monoplegia
• SN deafness
• Blindness
• Aphasia
• Ocular palsies ( squint)
• Mental retardation
• Seizure disorder

31. 9-management
• Key emergency management steps
• ABC
• Management of fluid & electrolytes
• Management of raised ICP
• Management of seizures
• Care of back, bladder & bowel
• Nutrition
• Neuro assessment: airway protection for severe altered mental status (GCS
below 8). Take precautions for increased intracranial pressure during
intubation. Consider ICP monitoring for evidence of elevated ICP. Treat
seizure activity: 50% of patients who presented with seizures progress to
status epilepticus, which is hard to control and correlates with poor neuro
outcomes.
• Cardiovascular support as needed; cerebral perfusion pressure is directly
affected by mean blood pressure.
• Antibiotics early; do not withhold antibiotics awaiting lumbar puncture.
Start antiviral if high suspicion of herpes infection.

32. • Management points not to be missed
• Electrolyte and fluid derangements are common:
• Diabetes insipidus: monitor urine output and check
sodium level for spike in UOP (Na in the 150s-160s).
• SIADH: late onset of electrolyte derangements with
oliguria and relative hyponatremia (Na can be below
125), increased risk of seizure activity. Correct
hyponatremia acutely to bring Na level above 125 with
3% saline if necessary (seizure threshold), then slow
correction to normal level (Na 140-145) over the next
36-48 hrs.
• At risk of hypokalemia secondary to GI losses,
hemodilution, osmotherapy, diuretics, sepsis.
• At risk for cerebral edema

33. Specific therapy
• Meningitis
• Antibiotics:
• Hib, Meningococcal, Pneumococcal, Gm negative: IV
Ceftriaxone/ Cefotaxime
• Hib: Ampicillin + Chloremphenicol
• Listeria: Ampicillin + Aminoglycoside
• Staph: Methicillin /Vancomycin
• Pseudomonas: Ceftazidime + Amonoglycoside
Duration of Tt:
10 ‐14 days in uncomplicated cases
Staph: 3‐4 weeks
Steroids:
• IV dexamethasone 15 mg/kg/dose 6 hourly X 5 days
• 1st dose : 15 min. before antibiotics
• Useful in reducing incidence of sensorineural
deafness