This document provides an overview of acute bacterial meningitis in children. It begins with an introduction discussing central nervous system infections in children in the tropics. It then covers the epidemiology, classification, pathogenesis, clinical presentation, diagnosis, treatment, complications and prevention of acute bacterial meningitis. The main causative bacteria are Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis. Clinical features include fever, headache, vomiting, seizures and altered mental status. Diagnosis involves lumbar puncture and analysis of cerebrospinal fluid. Treatment requires prompt administration of antibiotics along with management of increased intracranial pressure and other complications. Prevention strategies include vaccination programs.

1. State Specialist Hospital Gombe(SSHG)
Department of Paediatrics
Dr. Ibrahim Adamu
22 September, 2022
Moderator: Dr Rukaiyya

2. OUTLINE
• Introduction
• Epidemiology
• Classification
• Pathogenesis
• Clinical manifestation
• Principles of Management
• Conclusion
• References

3. OVERVIEW
• Infections of the central nervous system (CNS) are among the most
common neurologic disorders in children in the tropics
• These infection are divided into 2: those affecting meninges primarily
and those confined to the parenchyma
is inflammation of the leptomeninges including
subarachnoid space leading to constellation of signs and symptoms
• It is a life-threatening medical emergency that requires prompt
recognition and treatment.
Superficial cortical structures and blood vessels are not spared

4. OVERVIEW
is a form of
purulent meningitis and one of the
most challenging of pediatric
emergencies anywhere in the
world
• Its importance world-wide derives
principally from its neurologic
sequelae

5. CLASSIFICATION
• Leptomeningitis
- Acute bacterial meningitis (pyogenic)
- Aseptic meningitis (lymphocytic)
• Fungal meningitis
• Protozoal meningitis
• Chemical meningitis
• Tuberculous meningitis
• Others: Spirochaetal meningitis, Lyme meningitis

6. ACUTE BACTERIAL MENINGITIS

7. INTRODUCTION
• Bacterial meningitis is of the cranial and spinal
leptomeninges with evidence of a bacterial pathogen in the CSF
• There are basically 2 clinical entities of ABM
- Neonatal meningitis
- Meningitis in older children
• Effective immunization with H. influenza type b conjugated vaccine
has dramatically reduced the incidence of Hib meningitis in developing
countries.

8. EPIDEMIOLOGY
• Globally >1.2 million cases occur each year
• 80% to 95% of cases involve infants and children <5 yr old
with the greatest risk in 3-8 months olds
• About 135,000 treated cases die (11%)
• Case-fatality rate up to 70% (without treatment)
• One in five survivors may be left with permanent
sequelae
• In Africa, it constitutes 1-6% of paediatrics admission and
8-40% die from the disease

9. EPIDEMIOLOGY
- Infants
- Male sex
- Poor socioeconomic conditions and overcrowding
- Congenital and acquired deficiencies in host defense mechanisms
- Blacks race
- Lack of immunization
- Genetically susceptibility
- Household contacts and group day care centre contacts
- Contiguous infection e.g. Otitis media

10. EPIDEMICS
• Due to Neisseria meningitides
• Highest in “meningitis belt” in sub-Saharan Africa
• Extends from Senegal (west) to Ethiopia (east)
• Characterised by seasonal epidemics in dry season
• Punctuated by explosive epidemics in 8-12 yrs cycle (1000 cases
per 100,000 population)
• During epidemics: 350 million people at risk
• Epidemics generally caused by Serotype A, sometimes C
Latest epidemic in Nigeria

11. EPIDEMIOLOGY

12. AETIOLOGY
• Causative pathogens of
meningitis are largely age
dependent
• Generally, S. pneumoniae is
the commonest organism in
the southern parts of Nigeria
and N. meningitidis in the
northern parts while the
prevalence of H. influenzae is
variable
Age Agents
Neonate or < 2months Generally, organisms causing
neonatal sepsis
 Klebsiella sp
 Staphylococcus aureus
 Escherichia coli
 Group B & D Streptococci
2 months – 5 year  Haemophilus influenza
 Streptococcus pneumoniae
 Neisseria meningitides
 M. Tuberculosis
6 - 12 years  Streptococcus pneumoniae
 Neisseria meningitidis

13. PATHOPHYSIOLOGY
• Bacterial meningitis commonly follows a haematogenous spread,
bacteraemia precedes the condition or occurs at the same time
• May arise from a contiguous focus or direct invasion of the CSF by
bacteria e.g instrumentation
• After gaining entry into the CSF there is rapid bacterial proliferation
• Release of immunogenic fragments by bateria triggers cytokine release
• The pathophysiological consequence of the cytokine-induced damage
include cerebral edema, vascular thrombosis and intense focal
inflammatory response
The mechanism of oedema is multifactorial

14. causes raised intracranial pressure, manifesting
with headache, vomiting and altered consciousness
• May be absent in infant
• The increased vascular permeability allows leakage of albumin into
the CSF causing increase in CSF proteins
• The CSF glucose level is reduced due to increased metabolic
demand, reduced glucose transport and shift to anaerobic
metabolism
PATHOPHYSIOLOGY

15. occurs as a result of local damage to
vessels.
• The thrombotic process and inflammatory infiltration of blood vessels
cause luminal narrowing leading to ischaemia and infarction
• Infarctions may cause focal or generalized seizures, with further
deterioration of consciousness
can cause cerebritis or ventriculitis
• Inflammatory reaction around spinal nerves causes meningeal signs
PATHOPHYSIOLOGY

16. • Acute or sudden onset which is most frequently associated with NM
• Subacute with an insidious onset preceding non-specific febrile illness
(with URI or GIT symptoms) usual with Hib and SP
• Typically, young infants initially have minimal and subtle manifestations
which lead to difficulty with early clinical diagnosis
• Nonspecific findings include
• Fever, anorexia and poor feeding
• Symptoms of upper respiratory tract infection
• Myalgias, arthralgias, tachycardia, hypotension
• Cutaneous signs, such as petechiae, purpura, or an erythematous
macular rash
CLINICAL PRESENTATION

17. • Increased ICP
-
• Seizures (focal or generalized) due to cerebritis, infarction, or
electrolyte disturbances occur
The fontanel may not be raised or tense in the dehydrated infant even if the CSF pressure is raised
CLINICAL PRESENTATION

18. • Alterations of mental status - include irritability, lethargy, stupor,
obtundation, and coma
• Meningeal irritation is manifested as nuchal rigidity, back pain, Kernigs
sign, and Brudzinski sign
• In some children, particularly in those younger than 12-18 mo, Kernigs
and Brudzinski signs are not consistently present
• In neonates, they may presents with fever, high pitched cry, seizures,
change in alertness, vomiting, poor feeding, paradoxic irritability,
hypertonia/hypotonia, bulging fontanels & opisthotonos
Meningismus refers to meningeaI irritation especially nuchal rigidity, not due to CNS infection
CLINICAL PRESENTATION

20. • Subdural effusion manifest in infants <18mo with
-
• Anaemia due to sudden hemolysis is not uncommon in children
with H.i.b. meningitis
• In N.M meningococcaemia, petechiae and purpura, shock and DIC
may be observed
CLINICAL PRESENTATION

21. DIAGNOSIS
• The first essential in diagnosis is a high index of suspicion
• Investigations
- Lumbar Puncture
- E/U/Cr
- FBC with differentials
- Blood/Urine cultures
- LFT
- Coagulation profile – if DIC is suspected.
- CT/MRI

22. Lumbar Puncture
Clear Cloudy/turbid/
Purulent
Clear/turbid/xantho-
chromic
Clear Clear/cloudy
< 180 Raised >200 Usually raised normal/raised Usually raised
< 5, predominantly
lymphocytes upto
30 in neonates
↑↑↑ 1000s mainly
polymorphs or
pleocytosis
↑↑ 100s
Mainly lymphocytes
↑ mainly
lymphocytes
Usually ↑ (PMN
predominates)
No organism seen Positive No organism seen No organism seen Negative
Negative Positive Negative, but +ve in LJ
medium
Negative Negative
10 – 40 upto 30 in
neonates
↑↑ ↑↑↑: early 100-300
Late: >1000
Normal or slightly
↑: 50-150
Usually ↑
1/2 - 2/3rd of
concurrent RBS
< ½ -concurret 2/3rd
of nt RBS
< ½ -concurret 2/3rd of
nt RBS
Normal Normal or
decreased

23. Differential diagnoses
• Febrile Seizures
• Encephalitis
• SAH
• ICSOL
• Cerebral Malaria
• Tuberculoma
• Cerebral Abscess
• Tetanus
• Malignant infiltrations of the meninges

24. TREATMENT
• Treatment of acute bacterial meningitis is aimed at sterilization of the
CSF by the use of appropriate antibiotics and management of
associated life-threatening complications.
• Antibiotics of choice should be bactericidal, excellent CSF
pharmacokinetics and broad spectrum
• Empirical treatment while awaiting cultures is recommended then
modified based on the sensitivity pattern
• A balance is sought between what is ideal and what is available and
affordable and still reasonably effective

25. • In the neonatal period, and up to the age of 2 mo, a 3rd generation cephalosporin
- or 100mg/kg/day -is combined with 100-
200mg/kg/day If not responding, consider 5mg/kg/day
• A less frequently recommended treatment is high dose 300-400
mg/kg/day and 100 mg/kg/day
• Use of the 3rd generation cephalosporins e.g 100mg/kg/day avoids
the problem of increasing resistance to AMP/CHL
• 300,000IU/kg + 100mg/kg
• In epidemics, a single dose of long-acting oily chloramphenicol given l.M is
effective
Ceftrixone is not recommended in the neonatal period
TREATMENT

26. • IVF restriction to 1/2-1/3 of requirement = 50-60 ml/kg/d for the first
48-72. However, fluid restriction can only be instituted in absence of
hypovolaemia and shock
Treat Septic shock
Raised intracranial pressure
• Hyperventilation
• IV mannitol 0.5-1g/kg; may be repeated after 6 hours
• Nurse head up at 300
TREATMENT

27. • Vital signs: PR, BP, RR, T
• Intensive nursing
• Management of unconscious patient
• Complete neurologic evaluation on admission and daily thereafter
• Serum electrolytes, serum and urine osmolality
• Monitor head circumference
TREATMENT

28. Seizures
• Diazepam IV or rectally
• Phenobarbitone 10-15 mg/kg stat then 5 mg/kg
• Phenytoin IV 15-20 mg/kg over 30-45 min; then 5 mg/kg
• Phenytoin is advantageous because it inhibits ADH and does not
depress level of consciousness
Dexamethasome therapy
• Modulation of the inflammatory response
• IV dexamethasone 0.15mg/kg
Phenytoin is more advantageous
TREATMENT

29. COMPLICATIONS
SIADH & Shock Seizure disorder
Cerebral oedema Intellectual impairment
Cranial nerve palsies Deafness
Hydrocephalus Cortical blindness
DIC Behavioural abnormalities
Patients with raised intracranial pressure may also have poor peripheral circulation because of altered brain stem
function. Shock may then be confused with raised intracranial pressure

30. PREVENTION
• Hib conjugate vaccine
• Pneumococcal conjugate Vaccine
• Meningococcal polysaccharide vaccine (ACWY135)
• Bivalent A & C vaccine
• A single IM dose is effective but short-lived
• Meningococcal: Rifampicin 10mg/kg/dose B.D for 2 days
• H.influenza: Rifampicin 20mg/kg for 4days
e.g SCA, Splenectomy
• PCV & Meningococcal Vaccine( ACWY135)

31. PROGNOSIS
• Prognosis depends on age, duration of illness and immunologic status
of the individual
• On the whole, it is estimated that about 40% of children may develop
neurologicaI abnormalities
• Deafness is common sequalae of bacteria meningitis. Overall, 10% of
children have persistent bilateral or unilateral hearing loss
• Deep coma, meningococcaemia, shock are poor prognostic signs

32. ACUTE ASEPTIC MENINGITIS

33. • Aseptic meningitis refers to a syndrome consistent with sign and
symptoms of meningeal inflammation but with negative routine CSF
culture
• It is an acute inflammation of the meninges due mainly to a variety of
viruses
• Most of cases are benign and self-limiting and complete recovery
without sequelae occurs in 95% of the children.
INTRODUCTION

34. AETIOLOGY
- Enterovirus, Arbovirus, HSV and Mumps virus
- Cryptococcus, Histoplasmosis
- Amoebiasis, Toxoplasmosis, Strongyloides, Cysticercosis
- Kawasaki disease
- Acute Leukemia
- NSAIDS, Chemotherpeutic agents
• Other bacteria: Leptospira, Mycoplasma, Tuberculosis, Rickettsia

35. CLINICAL MANIFESTATION
• Child is usually febrile, irritable, nauseated and may vomit feeds
• Headache or back pain may be present
• There may be an associated exanthematous rash suggesting
enterovirus infection
• Nuchal rigidity
• Convulsions are rare
• Progressive loss of consciousness as in bacterial meningitis is
uncommon.

36. INVESTIGATIONS
: The CSF is usually clear with moderate
lymphocytosis. The glucose level is within normal limits with the
exception of aseptic meningitis following mumps, where the CSF sugar
is somewhat raised. The CSF protein is usually normal or slightly raised
• Specific viral studies may be necessary with throat swabs, urine and
stool specimens. Antigenic or genomic PCR methods also help to
determine the aetiology if facilities are available.

37. TREATMENT
• There is no specific treatment for viral meningitis
• May be admitted to observe or for symptomatic management
• It is wise to start proper antibiotic treatment bearing in mind that
partially treated bacterial meningitis has CSF changes suggestive of
aseptic meningitis
• In addition, some centres treat all cases of aseptic meningitis with
acyclovir, fungal with amphotericin B

38. CONCLUSION
• Meningitis is a medical emergency once suspected
• It is a reportable disease under IDSR
• Despite better antimicrobial agents and advances in medical intensive
care technology, the mortality and long-term morbidity rates for
children is still significantly high
• In poor countries, the problem is compounded by increasing level of
poverty, overcrowding, poor immunization coverage etc.

39. REFERENCES
•Jonathan C. Azubuilke, Kanu E. Nkanginieme, Paediatrics and Child
Health in a Tropical Region 3rd edition
• Nelson Textbook of Paediatrics 19th Edition
• Robert M. Kliegman, Bonita F. Stanton, Joseph W. St. Geme III, Nina F.
Schor, & Richard E. Behrman Pediatric Textbook 4th Edition
• Website: http://www.emedicine/medscape.com/shock578763.
Accessed on Saturday, 2-10-2022, 3:36pm

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