Pediatric nueroinfections . TBM, Viral meningoencephalitis ,nueroinfections pediatric nuerology pediatric nueroinfections tbm tubercular meningitis bacterial meningiti meningitis , pediatric meningitis , viral viral encephalitis

1. NEUROINFECTIONS
Moderator : Dr. Suvarna P Reddy
Presenter : Dr. Vinaykumar S Appannavar

2. CONTENTS
• Introduction
• Bacterial meningitis
• Viral meningoencephalitis
• Tubercular meningitis

3. INTRODUCTION
• Infection of the central nervous system (CNS) is a significant cause of morbidity and
mortality in children.
• Nonetheless, viral infections remain a significant cause of CNS disease
• Regardless of the etiology, many patients with CNS infection have similar clinical
manifestations.
• Common symptoms include headache, nausea, vomiting, anorexia, photophobia,
restlessness, altered state of consciousness, and irritability.
• Common signs include fever ,Neck pain and rigidity, focal neurologic deficits, seizures,
obtundation, and coma.

4. BACTERIAL MENINGITIS

5. INTRODUCTION
• It is an inflammation of the leptomeninges triggered by bacteria present in the
subarachnoid space.
• The outcome of bacterial meningitis is not primarily dependent on the organism,
but the inflammation reaction that it produces.
• It occurs in all age groups with manifestation depending on the age,
immunological status and other co-existing morbidities
• Most of the cases occur between 1 month and 5 years of age.

6. ETIOLOGY
• The most common organisms responsible are
1. Streptococcus pneumonia
2. Neisseria meningitidis
3. Hemophilus influenzae type b (Hib)
• This traid is responsible for more than 80% of all
cases

7. ETIOLOGY
• Prospective surveillance shows most common serotypes of S. pneumonia were 6, 1,19,
14,4,5,45,12 and 7
• The risk of pneumococcal meningitis is increased in children with congenital or acquired CSF
leak across a mucocutaneous barrier, such as a lumbar dural sinus, cranial or midline facial
defects (cribriform plate), fistulas of the middle ear (stapedial foot plate) or inner ear
(oval window, internal auditory canal, cochlear aqueduct), or CSF leakage as a result of
basilar or other skull fracture.
• The risk of pneumococcal bacterial meningitis was historically increased by more than 30-
fold in children with cochlear implants.

8. ETIOLOGY
• Neisseria meningitidis - Serogroups A, B, C, X, Y and W135 are responsible for
almost all meningococcal disease. The risk of cases occurring in contacts at centers is
approximately in 1,000.
• Children younger than 5yr of age have the highest rates of meningococcal infection,
and a second peak in incidence occurs in persons between 15 and 25 yrs of age.
• Haemophilus influenzae Type b - Invasive infections occurred primarily in infants 2
month to 2yr of age, the peak incidence was at 6-9 month of age, and 50% of cases
occurred in the 1st yr of life.
• In India, the burden of invasive H. Influence is substantial, with incidence of Hib
meningitis to be 50-60 cases per 1,00,000 children less than 5 years of age
• The risk to children was markedly increased among family or daycare center contacts
of patients with H. influenzae type b disease.

9. PATHOGENESIS
• Most cases of BM result from
bacteraemia and mostly after
colonization of
nasopharyngeal mucosa by
pathogens
• Transmission of respiratory
pathogen is from person to
person and in neonates by
vertical transmission, during
delivery, after delivery or
following IV cannulation and
ventilation.

11. CLINICAL FEATURES
• A high index of suspicion is essential to reduce morbidity and mortality in bacterial
meningitis.
• Presentation – Fever, seizures, vomiting and abnormal behaviour.
• In neonates , subtule presentation of symptoms – irregular fever, incessant cry,
lethargy, refusal of feeds, persistant vomiting with no clinical focus of sepsis on clinical
examination.
• Altered sensorium with a bulging frontanelle in a non crying child is suggestive of
raised ICP.
• The signs and symptoms of meningitis are related to the nonspecific findings associated
with a systemic infection and the manifestations of meningeal irritation.

12. CLINICAL FEATURES
• Nonspecific findings include fever, anorexia and poor feeding, headache,upper
respiratory symptoms, myalgias, arthralgias,photophobia tachycardia, hypotension,
and various cutaneous signs, such as petechiae, purpura, or an erythematous
macular rash. The rash of meningococcemia istypifiedby an initial petechial rash
that evolves into ecchymotic and purpuric lesions.
• Meningeal irritation is manifested as nuchal rigidity, back pain, Kernig sign and
Brudzinski sign
• Increased ICPis suggested by headache, emesis, bulging fontanel or diastasis,
oculomotor (anisocoria,ptosis)or abducens nerve paralysis, hypertension with
bradycardia,apnea or hyperventilation, decorticate ordecerebrate posturing,
stupor, coma, or signs of herniation.
• Approximately 10–20% of children with bacterial meningitis have focalneurologic
signs.

13. • Seizures (focal or generalized)related to cerebritis, infarction, or electrolyte
disturbances occur in 20–30% of patients withmeningitis. Poor prognosis is
suggested when seizures persist after the fourth day of illness, which can be
refractory to treatment.
• Alteration in mental status is common among patients with meningitis and may
be the consequence of increased ICP, cerebritis, or hypotension; manifestations
include irritability, lethargy, stupor, andcoma.

14. DIAGNOSIS
• Lumbar puncture is the most important step in the diagnosis of meningitis.
Contraindications
(1) Evidence of increased ICP
(2) Severe cardiopulmonary compromise requiring prompt resuscitative measures for shock or in
patients in whom positioning for the LP would further compromise cardiopulmonary function
(3) Local infection
Thrombocytopenia – count <20,000 cells/cum is a relative contraindication for LP.

15. DIAGNOSIS
• Some clinicians obtain a head CT scan prior to LP to evaluate for evidence of increased
ICP. Neurosonogram in case of neonates.
• Lumbar puncture –
• Blood culture

16. Repeat lumbar puncture : Needed ?
• Patients who were adequately responded to antibiotics does not require repeat LP.
• Indications
I. No clinical improvement after 48hours of appropriate antibiotic therapy
II. Highly resistant pneumococcal meningitis, particularly who have also received
adjunctive dexamethasone therapy
III. Neonatal meningitis
IV. Meningitis caused by gram-negative organisms
V. Meningitis complicating CSF shunt

17. MANAGEMENT
• SS

18. • Vancomycin – trough of 15-20 µg/mL. An alternative dosing regimen outside the
neonatal period includes:
• <3 mo 15 mg/kg/dose q8h, - 45mg/kg/day
• 3-11 mo 15 mg/kg/dose q6h, - 60mg/kg/day
• 1-8 yr 20 mg/kg/dose q6h, - 80mg/kg/day
• 9-13 yr 20 mg/kg/dose q8h, - 60mg/kg/day
• ≥14 yr 15 mg/kg/dose q8h. – 45mg/kg/day

19. Corticosteroids
• It has found to ameliorate the
inflammation.
• Beneficial effects in H. influenzae and
S. Pneumoniae
• Dexamethasone therapy to be started
early
• Dose : 0.15mg/kg/dose every 6th
hourly for 2-4 days
• Side effects : Gastrointestinal
haemorrhage

20. COMPLICATIONS
• Acute complications acute CNS complications can include
seizures, increased ICP, cranial nerve palsies, stroke, cerebral
or cerebellar herniation, and thrombosis of the dural venous
sinuses
• Subdural effusions may result in a bulging fontanel, diastasis of
sutures, enlarging head circumference, emesis, seizures,fever.
• SIADH occurs in some patients leads to hyponatremia and
reduced serum osmolality.
• In meningitis caused by N. meningitidis, pericarditis or arthritis
may occur
• Thrombocytosis, eosinophilia, and anemia may develop during
therapy for meningitis

21. • The combination of endotoxemia
and severe hypotension initiates the
coagulation cascade; the
coexistence of ongoing thrombosis
may produce symmetric peripheral
gangrene.
• Sequelae include regression and
delay in milestones, mental
retardation, motor deficit
hemiplegia, spasticity, cranial nerve
palsies, seizures, hearing loss,
behavioural problems.

23. PREVENTION
• Prophylaxis for prevention of development of Hib meningitis in household contacts –
Rifampin 20/mg/kg/day, Vaccine - H.influenzae type b conjugate vaccine – 2mo of age
• For N. Meningitidis – Rifampin 20/mg/kg/day,
- Alternative options include
1. Ceftriaxone 125mg IM once for children under age 15yr, or
2. Ceftriaxone 250mg IM once for persons older than 15yr, or
3. Ciprofloxacin 500mg orally once.
vaccine - a quadrivalent conjugate meningococcal vaccine (types A,C, Y ,and W-
135; Menactra and Menveo) a two-dose vaccine series for children,with
• first dose -11-12yr age and a
• Second dose 16-18yr.

24. • Vaccines against S. pneumonia
- PCV13 conjugate vaccine is recommended for children younger
than 5yr of age

25. VIRAL MENINGOENCEPHALITIS

26. INTRODUCTION
• Viral meningoencephalitis is an acute inflammatory process involving the
meninges and/or brain parenchymal tissue.
• Theseinfections are caused by a number of different pathogens, and quite
often, no pathogen can be identified from the CSF and brain tissue specimens.
• The CSF is characterized by pleocytosis and the absence of microorganisms on
Gram stain and routine bacterial culture.
• Outcomes arequite variable because cases of meningoencephalitis caused by
some pathogens are self-limited whereas others cause significant long-term
neurologic sequelae.

27. ETIOLOGY
• In more than 70% of cases of VE the etiological agent remains unidentified in spite of
extensive lab workup.
• Herpesviridae Family – HSV is the most common cause of non- epidemic VE (90% - HSV-1)
• Arboviridae Family – these are important cause of VE worldwide.
Alphaviruses – Eastern equine virus, Western equine virus , Venenzulan equine virus,
Flaviviruses – St. Louis encephalitis virus, JEV, West nile viruses
Bunyaviruses – La Crosse virus
• Enterovirus Family – Coxsakie A2,4-7,9,10,16 and B1-5,echoviruses 1-9, 11-25, 27,30,33
and enterovirus 71.

28. ETIOLOGY
• JE is the most widespread of the arboviral encephalitidis. Affecting China, India, Japan,
Pakistan and Philipines.
• Culex species mosquitos
• Pigs and wild birds are reservoir of infection , Human and pigs – dead end hosts.
• Mumps virus can cause acute VE, or a delayed immune-mediated encephalitis.
• It is well-known that dengue infections can also result in encephalopathy and neurological
complications.
• Immunocomprimised area at risk of encephalitis from CMV, EBV and Human herpes virus-6

29. PATHOGENESIS
• Neurologic damage is caused by direct invasion and destruction of neural tissues by
actively multiplying viruses or by a host reaction to viral antigens.
• Tissue sections of the brain generally are characterized by meningeal congestion
and mononuclear infiltration, perivascular cuffs of lymphocytes and plasma cells,
some perivascular tissue necrosis with myelin breakdown, and neuronal disruption
in various stages ultimately, neuronophagia and endothelial proliferation
• A marked degree of demyelination with preservation of neurons and their axons is
considered to represent predominantly “postinfectious” or an autoimmune
encephalitis.

30. • In HSV encephalitis,
The cerebralcortex (classically the temporal lobes involvement)is often
severely affected.
• Arboviruses tend to affect the entire brain, while rabies has a predilection for
the basal structures.

31. CLINICAL FEATURES
• The onset of meningoencephalitis is generally acute, although CNS signs and symptoms are
often preceded by a nonspecific febrile illness of a few days’ duration.
• The presenting manifestations in older children include headache and hyperesthesia, and in
infants, irritability and lethargy.
• Headache is most often frontal or generalized; adolescents frequently complain of retrobulbar
pain. Fever, nausea and vomiting, photophobia, and pain in the neck, back, and Legs are
common.
• Uncontrolled body movements and seizures.
• Focal neurologic signsmay be persistent, fluctuating, or migratory.
• WNV and nonpolio enteroviruses may cause anterior horn cellinjury and acute flaccid paralysis.

32. CLINICAL FEATURES
• Loss of bowel and bladder control and unprovoked emotional outbursts may also
occur.
• Focal seizures and focal neurological deficits are more common in HSE.
• The presence of multifocal lower motor neuron signs in a patient – poliomyelitis
• In JE most of the people are asymptomatic and less than1% develop clinical
disease.

33. DIAGNOSIS
• It relies on a combination of analyzing the CSF by PCR, serology, and brain biopsy.
• It is supported by associated symptoms and LP, which usually shows a mild mononuclear
predominance

34. • Electroencephalogram(EEG) and MRI – Investigation of choice
• EEG typically shows diffuse slow-wave activity, although focal changes in
temporal regions can be observed in HSV meningoencephalitis.
• MRI of the brain may demonstrate focal brain lesions that correlate with clinical
disease, including temporal lobe involvement. Hyperdense lesions may also be
identified on T2 and FLAIR imaging.

35. MANAGEMENT
• Stabilization of patient
• Supportive care
• Specific treatment
• Treatment of immediate complications
• Treatment of secondary complications
• Rehabilitation

36. General management
• Assessment by GCS
• Monitoring of fluids, cardiorespiratory status and electrolytes
• Effective use of sedatives and anticonvulsants
• ICP management
• Nutrition
• Care of bowel and bladder

37. Treatment of immediate complications
• Control of ICP
- Head end elevation to 30%
- IV Dexona, Mannitol or oral glycerol maybe used to reduce CE
• Control of convulsions
- Lorazepam – preferred
- IV phenytoin or phosphenytoin is next drug of choice
- Midazolam infusion/propofol – in refractory seizures

38. Specific treatment
• Antibiotics – Preferably a cephalosporin
• Antiviral therapy – For most forms of VE there is no specific
treatment. Acyclovir should be started early.
• Acyclovir – used in HSE, it reduces both mortality and morbidity
and has advantage over vidarabine.
• Use of corticosteroids is controversial.

39. Treatment of secondary complications
• Following may arise in course of the disease
- Cerebral infarction, CVT, Aspiration pneumonia, upper GI
bleeding, urinary tract infections, DIC
• Bedsores
• Deep venous thrombosis – Compression stockings
• Physiotherapy

40. Rehabilitation
• Multidisciplinary approach
• Assessment of cognition, memory, speech, vision, hearing and
motor impairment should be made at discharge
• Speech therapist
• Counselling

41. TUBERCULAR MENINGITIS

42. INTRODUCTION
• CNS tuberculosis accounts for 1% of all cases of a TB
• Most Common form is TB meningitis in Indian children
• Incidence 1-4%
• Almost always associated with primary tuberculosis
• Most Common route is lymphohematogenous spread
• It is Highly clinical suspicious with diagnostic difficulty and lack of
standardized criteria. morbidity and mortality is high for TBM

43. PATHOGENESIS
• DC

45. CLINICAL FEATURES
• 75 to 85% below age 5 yrs, uncommon <6M, rare < 3M
• Peak incidence is 3-5 yrs.
• Onset is subacute or chronic, taking more than 3 wks.
• Clinical manifestation grouped in to 3 stages
STAGE 1: ( early )
• prodromal stage lasts 2 to 3 wks.
• symptoms nonspecific i.e low-grade fever, anorexia sleep disturbance, apathy,
irritability, fatigue, headache, vomiting, but child is conscious.

46. • STAGE 2 ( intermediate )
1 ] Convulsions
2 ] Signs of meningeal irritation
3 ] Neurological deficits
a) cranial nerves palsy
b) motor deficits
4 ] Signs of raised intracranial
pressure
5 ] Impaired consciousness
• STAGE 3 ( advanced )
1) Progressive neurological deficits with
dilated pupils
2) Signs of brain stem compression (
opisthotonos posture, neck retractions,
decorticate, and decerebrate posture,
Hyperpyrexia, monoplegia, hemiplegia,
paraplegia )
3) Movement disorders
4) Deep coma and death

48. DIAGNOSIS
• MODIFIED AHUJA CRITERIA
A) MANDATORY FEATURES
1) Fever lasting more than 14 days
2) Abnormal CSF findings pleocytosis with more than 20 cells and more
than 60 % are lymphocytes proteins > 100 mg / dl, sugar < 60 % of blood sugar
B) PLUS ANY TWO OF FOLLOWING CRITERIA
1) Evidence of extra neural TB
2) Positive family history of exposure to case
3) Positive mantoux reaction
4) Abnormal CT scan findings - exudate in basal cistern, hydrocephalus, infarcts, gyral
enhancements.

49. • AIIMS PROTOCOL FOR DIAGNOSIS OF TB MENINGITIS
Demonstration of acid fast bacilli in the CSF or fulfilment of following criteria
CSF showing
Predominant lymphocyte pleocytosis > 50/mm3
protein > 60 mg/dl sugar
< 2/3 of blood sugar

50. Algorithm
by RNTCP

51. Algorithm
by RNTCP

52. INVESTIGATIONS
• Chest X-ray
• USG abdomen
• Montoux test
• CBNAAT
• CSF Analysis
• Nueroimaging

53. MANAGEMENT

54. ATT –PEDIATRIC RNTCP GUIDELINES -2019

55. • Corticosteroids(usually prednisolone) 2mg/kg/day daily for 4
weeks and then gradually tapered over 1-2 weeks before stopping.
• Alternately dexamethasone 0.4mg/kg/day followed by oral
prednisolone can be used. Total duration of steroids 6 – 8 wks.
• Seizures which occurs after first week, or associated with
tuberculoma or infract require initiation of antiepileptic drugs.
• Seizures are acute symptomatic, they do not require the longterm
treatment.

56. • Phenobarbitone should not be used for treatment as it is a cerebral
depressant and induces hepatic microenzymes, induces hepatotoxicity.
• Management of cerebral edema - Mannitol
• Glycerol, acetazolamide can be used for chronic raised intracranial
pressure.

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