CNS infection
Presented by Nancy Mohammed Alaa
Assistant lecturer of Pediatrics
Assiut university
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
2-types
• 1-meningitis
• 2-encephalitis
• 3-meningioencephalitis
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
• 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).
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).
presentation
• A-Neonate
Bulging fontanelle
• Fever/ hypothermia
• Persistent vomiting
• Alternating irritability and drowsiness
• Refusal to feed
• Poor tone and cry
• Shock
• Seizure
:• B-child and adult
• 2 presentations:
•
1) Dramatically acute presentation:
Rapid progressive manifestations of shock, purpura,
DIC, altered sensorium, usually death within 24
hours
• 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
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
• Etiology
•
Viral:
• Mumps, measles, rubella, enterovirus
• HSV, CMV, EBV, Varicella
• Japanese encephalitis, West Nile, Russian spring
summer, Equine virus
• Rabies
• Lymphocytic choriomeningitis
• Dengue
• Influenz
• Nonviral:
• Rickettsia
• Mycoplasma pneumoniae
• Bacterial: TB, Enteric fever, Shigella etc.
• Spirochetal
• Fungal
• Protozoal
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.
• Clinical picture
• Acute onset
• High fever
• Rash±
• Headache
• Vomiting
• Altered sensorium
• Seizures
• Neurological deficits( HSV: focality +)
• H/o similar illness in the community
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
-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
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
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
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
• 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
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.
• 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
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
Cns infection    2019
Cns infection    2019
Cns infection    2019
Cns infection    2019
Cns infection    2019

Cns infection 2019

  • 1.
    CNS infection Presented byNancy 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.
  • 4.
    1-meningitis • Etiology • a-bacterialorganisms 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 andadult • 2 presentations: • 1) Dramatically acute presentation: Rapid progressive manifestations of shock, purpura, DIC, altered sensorium, usually death within 24 hours
  • 14.
    • 2) Acutepresentation : 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 hasbeen 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 inthe 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 appropriatetreatment: 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 andtests 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 ofspinal 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 emergencymanagement 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 pointsnot 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