Purulent Meningitis in Children

1. Purulent Meningitis in Children Jiang Li Department of Neurology Children’s Hospital Chongqing University of Medical Sciences

2. Purulent Meningitis • Acute infection of central nervous system(CNS). 90% of cases occur in the age of 1mo-5yr. • The inflammation of meninges caused by various bacteria.Common features in clinical practices include: fever, increased intracranial pressure, meningeal irritation.  One of the most potentially serious infections, associated with high mortality (about 10%) and morbidity.

3. Etiology • 1.1 Pathogens: • Main pathogens: Neissria meningitidis, streptoccus pneumoniae, Haemophilus influenzae. (2/3 of purulent meningitis are caused by these pathogens) • Pathogens in special populations (neonate & <3mo infants , malnutrition, immunodeficiency): gramnegative enteric bacilli, group B streptococci, staphlococcus aureus

4. 1.2 Major risk factors for meningitis • Immature immunologic function and attenuated immunologic response to pathogens  Low level of immunoglobulin, defects of complement and properdin system  Immature or impaired blood-brain-barrier (BBB)  Immature BBB function: maturation at about 1yr  Impaired BBB: Congenial or acquired defects across mucocutaneous barrier

5. 1.3 Access of bacteria invasion  Typical access---hematogenous dissemination  Bacteria colonizing the mucous membranes of the nasopharynx invasion into local tissue  bacteremia  hematogenous seeding to the subarachnoid space  Mode of transmission: Person to person contact through respiratory tract secretions or droplets

6. Access of bacteria invasion • Bacteria spread to the meninges directly: through anatomic defects in the skull or head trauma • Invasion from parameningeal organs: such as paranasal sinuses or middle ear

7. 2. Pathology • Structure of meninges

8. Pathology • Characterized by leptomeningeal and perivascular infiltration with polymorphonuclear leukocytes and an inflammatory exudate. • Exudate which may be distributed from convexity of brain to basal region of cranium. • Exudate is more thickness due to streptococcus pneumoniae than other pathogens.

9. 3. Clinical manifestations • The younger the child is, the higher incidence of meningitis will be. ½-2/3 of cases occur less than 1yr of age. • Mode of presentation:  Acute or fulminant onset: symptoms and signs of sepsis; meningitis evolve rapidly over a few hours and death within 24 hours; usually infected with Neissria meningitides (N. meningitides).

10. Mode of presentation • Subacute onset: Precede by several days of upper respiratory tract or gastrointestinal symptoms; difficult to pinpoint the exact onset of meningitis; usually with meningitis due to Haemophilus influenzae (H influenzae) and streptoccus pneumococcus (S pneumococcus).

11. Clinical manifestations • Common features of meningitis:  signs of systemic infection : fever(90-95%), anorexia,shock, alteration of mental status and consciousness  neurological signs:  increased intracranial pressure: headache, vomiting(82%), herniation  meningeal irritation: nuchal rigidity(77%), kernig sign, brudzinski sign

12. brudzinski sign

13. Clinical manifestations • Seizure (20-30%)  Focal or generalized  Due to cerebritis, infarction, electrolyte disturbances  Frequently noted with H influenzae & S pneumococcal meningitis  Persist after 4th day and difficult to treat with poor prognosis

14. Clinical manifestations • Alteration of mental status and consciousness  Including: irritability, lethargy, stupor obtundation, coma  Due to increased intracranial pressure, cerebritis, hypotension  Often with pneumococcal or meningococcal meningitis  Comatose patients with a poor prognosis

15. Clinical manifestations • The symptoms and signs are not evident in neonates and infants younger than 3mo of age; and patients already received irregular antibiotic therapy.

16. Clinical manifestations Comparison of the manifestations of meningitis between different age groups

17. 4. Diagnosis • Earlier diagnosis and prompt initiation of effective antibiotic treatment is critical for minimizing sequelae of purulent meningitis.  Suspected cases: febrile infants with seizure, meningeal irritability, increased intracranial pressure, altered mental status  Pay attention to the atypical symptoms and signs in neonate, infant and patient already received irregular antibiotic therapy

18. Diagnosis • Diagnosis is confirmed by analysis of cerebrospinal fluid ( CSF)  Suggestion bacterial meningitis  Increased pressure (90%)  Appearance: slightly cloudy to purulent  Raised white blood cells,consisting chiefly of polymorphonuclear leukocytes  Raised protein concentration, decreased glucose concentration (80%)

19. Diagnosis • Confirmation of the diagnosis: isolation from the CSF of a specific bacterial pathogen by microscopy or a positive culture or rapid antigen- detection test of CSF  Gram-stained smear of CSF: identify the causative organism in 70-90% of cases  CSF culture: positive in about 80% of cases. definitive diagnosis, determination of antibiotic sensitivity.  PCR: amplifies bacterial DNA (H influenzae, N. meningitidis)

20. 5. Differential diagnosis • Purulent meningitis caused by different pathogens  Neissria meningitidis:  Occur in epidemics (type A,C), which is more common in spring, or sporadic all the year (type B,C,Y)  Sudden onset with various cutaneous signs ( petechiae, purpura, or an erythematous macular rash)

21. Differential diagnosis  Streptococcus pneumoniae:  Young infants ( <1yr) are most susceptible population  Peak season: spring and winter  Easier to have subdural effusion and hydrocephalus  Easily have a protracted course and relapse

22. Differential diagnosis • Haemophilus influenzae  Occurs predominantly in infants 2mo to 2yr of age  Many cases are in winter  Higher incidence of subdural effusion • Others pathogens: staphylococcus aureus, gramnegative enteric bacilli  Special susceptible population: neonate, <3mo infants, malnutrition, immunodeficiency  Severe infection, difficult to treat

23. Differential diagnosis • Meningitis caused by other microorganisms  Viral meningitis/encephalitis:  Less severe systemic infectious symptoms  Usually not develop after 2-3weeks  CSF: normal glucose

24. Differential diagnosis  Tuberculous meningitis  Subacute onset and progress  A history of close contact with known cases of tuberculosis  Evidence of acute or healed tubercular infection on chest x-ray  Tuberculin skin test : OT, PPD  CSF

25. Cerebrospinal fluid in neurologic infection

26. 6. Complications and sequelae • 6.1 Subdural effusion • Definitive diagnosis: volume of fluid in subdural space >2ml, protein>0.4g/L, • Incidence: develop in 10-30% of patients, asymptomatic in 85-90% of patients; especially common in infants 4-6 month of age ( rare in children over 1yr);

27. subdural effusion • Causative organisms: 45% of cases of meningitis caused by H influenzae, 30% by S pneumoniae, 9% by N meningitidis

28. subdural effusion  Indications:  No response to a sensitive antibiotic therapy  Prolonged fever or fever reoccurring after an afebrile interval with effective treatment  Bulging fontanel, widening of sutures, enlarging head circumference, emesis,seizure, altered consciousness.  Improved CSF profile with more serious clinical manifestations

29. subdural effusion • Diagnosis methods:  Cranial translucent test  B ultrasonic examination and CT  Subdural space puncture normal subdural effusion

30. Complications 6.2 Ventriculitis 6.3 hydrocephalus

31. Circulation of cerebrospinal fluid(CSF)

32. Complications • 6.2 Ventriculitis • Usually occurs in neonates and infants (<1yr), with severe prognosis • The main cause is delayed diagnosis and treatment of meningitis.

33. Ventriculitis • Diagnosis:  B ultrasonic examination or neuroimaging studies( CT, MRI): enlarged lateral ventricle  Lateral ventricle puncture: bacteria and inflammatory cells in ventricular fluid, WBC>50x106/L, Glucose<1.6mmol/L, or protein>400mg/L.

34. Circulation of cerebrospinal fluid(CSF)

35. Complications 6.3 hydrocephalus :  Communicating hydrocephalus: adhered or destroyed arachnoid granulation around the cistern at the base of the brain  Obstructive hydrocephalus: following obstructed of the cerebral aqueduct, or the foramina of Magendie and Luschka 6.4 others: Deafness, blindness, paralysis, epilepsy, mental retardation

36. Treatment • 7.1 Antibacterial therapy • Therapy principles: early treatment, antibiotics susceptible to pathogens and with high permeability through BBB, given intraveninously, enough dose, enough course of antibiotic therapy

37. Antibacterial therapy  Susceptible to pathogens  First choice: Cefotaxime, Ceftriaxone (3dr generation of cephalosporins, high permeability through BBB, products of metabolism also has effect, CSF sterilization within 24h)  Other choice: Penicillin, Chloromycin, Cefuroxime, Ceftazidime ( delayed effect to make CSF sterile, high incidence of relapse and deafness)

38. Antibiotic therapy of bacterial meningitis

39. Treatment 7.2 Supportive care • Maintenance fluid and thermal energy supplement:  Fluid administration: 60-80ml/kg/day  Fluid infusion with dehydration therapy

40. Treatment •  increased intracranial pressure •  Osmotic therapy: intravenous mannitol 0.5- • 1g/kg/every time, q4-6h •  Combination with intravenous dexamethasone: • 0.3-0.5mg/kg/day •  Endotracheal intubation and hyperventilation

41. Treatment • Subdural effusion  Few volume could be absorbed with treatment spontaneously  Subdural puncture: take out 15ml/each time (unilateral puncture), less than 30ml/each time ( bilateral puncture), everyday or every other day  Stripping operation: for the cases not cure after 3-4weeks

42. Treatment • Others:  Ventriculitis : lateral ventricle puncture and injection of antibiotics locally  Epilepsy: AEDs