1. CNS INFECTIONS
DR. TA OGUNLESI (FWACP)

2. SPECTRUM OF CNS INFECTIONS
Pyogenic Meningitis
Aseptic Meningitis
Tuberculous Meningitis
Encephalitis
Cerebral abscess
Cerebral thrombophlebitis
DR. TA OGUNLESI (FWACP)

3. MENINGITIS
Meningitis is an infection that is located predominantly in the leptomeninges and CSF. It consists of both meningeal irritation & inflammatory changes in the CSF.
Meningism refers to the presence of meningeal irritation without inflammatory changes in the CSF.
DR. TA OGUNLESI (FWACP)

4. MENINGITIS
A potentially serious infection in infants and older children.
It is associated with a high rate of acute complications and risk of chronic morbidity.
Meningitis may be caused by:
Bacteria
Viruses
Mycobacterium
Fungus
DR. TA OGUNLESI (FWACP)

5. BACTERIAL (PYOGENIC) MENINGITIS
Bacterial meningitis:
-is a life-threatening illness resulting from bacterial infection of the meninges.
-is the most common form of childhood meningitis in the developing world.
DR. TA OGUNLESI (FWACP)

6. HOW DO ORGANISMS REACH THE BRAIN?
Usually haematogenous route i.e through the bloodstream from other parts of the body especially the lungs, joints, pericardium, ear, nose and throat.
Local extension from contiguous extra-cerebral infection (eg, otitis media, mastoiditis, or sinusitis).
Direct implantation of bacteria into the meninges usually complicates head and neck surgery, penetrating head injury, comminuted skull fracture, and osteomyelitic erosion.
DR. TA OGUNLESI (FWACP)

7. PATHOGENESIS
Bacteria gain entry to the CSF through the choroid plexus of the lateral ventricles and the meninges and then circulate to the extracerebral CSF and subarachnoid space.
They rapidly multiply because the CSF concentrations of complement and antibody are inadequate to contain bacterial proliferation.
The presence of bacterial cell wall components stimulates the local production of tumor necrosis factor, interleukin-1, prostaglandin E, Nitric Oxide and other cytokine inflammatory mediators.
DR. TA OGUNLESI (FWACP)

8. PATHOGENESIS
This inflammatory response is characterized by neutrophilic infiltration, increased vascular permeability, alterations of the blood-brain barrier and vascular thrombosis.
This results in marked inflammatory reaction causing cerebral oedema and cerebritis. Cerebral perfusion declines and infarction may occur in the cerebral tissue.
DR. TA OGUNLESI (FWACP)

9. PATHOLOGY Features include:
Meningeal exudate distributed around the cerebral vessels, sulci and brain surface.
Ventriculitis.
Subdural effusions and empyema.
Perivascular inflammatory infiltrates resulting in vasculitis, thrombosis and cortical necrosis.
DR. TA OGUNLESI (FWACP)

10. PATHOLOGY
Inflammation of spinal nerves and roots produces meningeal signs.
Inflammation of the cranial nerves produces cranial neuropathies of oculomotor, facial, abducens and vestibulo-cochlear nerves.
DR. TA OGUNLESI (FWACP)

11. PATHOLOGY
Increased ICP is due to cerebral oedema from cell death (cytotoxic), cytokine-induced increased capillary vascular permeability (vasogenic) and possibly, increased hydrostatic pressure from obstructed CSF flow (interstitial).
Raised CSF protein levels are due in part to increased vascular permeability of the blood-brain barrier and the loss of albumin-rich fluid from the capillaries and veins traversing the subdural space.
Hypoglycorrhachia (reduced CSF glucose levels) is due to decreased glucose transport by the cerebral tissue.
DR. TA OGUNLESI (FWACP)

12. EPIDEMIOLOGY Meningitis occur worldwide
Since the introduction of the Haemophilus influenzae type b vaccine, the prominence of that organism in the aetiology of childhood meningitis has declined.
Meningococcal meningitis occurs in epidemics along the meningitis belt of Africa which stretches through Mali, Burkina Faso, Chad, Niger and Nigeria.
DR. TA OGUNLESI (FWACP)

13. EPIDEMIOLOGY
Most cases are Under-5 and 70% are aged less than 2 years.
Males are more affected than females except in cases of L. monocytogenes infection where the females predominate.
L. monocytogenes is an unusual cause of neonatal meningits in the developing world.
DR. TA OGUNLESI (FWACP)

14. RISK FACTORS Overcrowding
Parameningeal infections (sinusitis, otitis media, mastoiditis, orbital cellulitis)
Splenectomy
Head injuries with open wound
Sickle cell anaemia
Congenital or acquired CSF leakage
Chemotherapy
Congenital immune deficiency syndromes
HIV
DR. TA OGUNLESI (FWACP)

15. AETIOLOGIES OF BACTERIAL MENINGITIS
Neonates
Group B Streptococcus species
Escherichia coli
Streptococcus pneumoniae
Listeria monocytogenes
Infants and Children
Haemophilus influenzae
Neisseria meningitidis
Staphylococcus aureus
DR. TA OGUNLESI (FWACP)

16. CLINICAL FEATURES
The onset of acute meningitis has two predominant patterns:
The more dramatic but less common presentation is sudden onset with rapidly progressive manifestations and reduced levels of consciousness frequently resulting in death within 24 hr.
More often, meningitis is preceded by several days of upper respiratory tract or gastrointestinal symptoms, followed by nonspecific signs such as increasing lethargy and irritability.
DR. TA OGUNLESI (FWACP)

17. CLINICAL FEATURES
Neonatal: Features are usually NON-SPECIFIC. These include:
Fever
Poor feeding
Irritability
Lethargy
Apnea
Seizures (cerebral oedema, SIADH, subdural collections, cerebral abscess, sinus thrombosis)
Bulging fontanelle
Jaundice
Shrill cry
Opisthotonus
DR. TA OGUNLESI (FWACP)

18. CLINICAL FEATURES
Infants & Older children: Features are more-specific.
Nuchal rigidity
Opisthotonus
Bulging fontanelle
Convulsions
Photophobia
Headache
Alterations of the sensorium
Irritability
Lethargy
Cushing’s triad (hypertension, bradycardia, irregular respiration)
Vomiting
Coma
DR. TA OGUNLESI (FWACP)

19. CLINICAL FEATURES
Kernig and Brudzinski signs are rarely present in neonates and young infants but are helpful indicators in older children.
Skin findings include maculopapular rash, petechial or purpuric rash.
About 15% of patients have focal neurologic signs at diagnosis.
Seizures are observed in about 33% of patients.
Papilloedema
Maculopapular rash (meningococcal)
Oculomotor palsy
Abducens palsy
Decorticate and decerebrate posturing
DR. TA OGUNLESI (FWACP)

20. MENINGISM Neck stiffness without CSF changes. Causes include:
Tonsillitis
Retropharyngeal abscess
Severe otitis media
Severe pneumonia
Tetanus
Dystonic reaction to drugs in the phenothiazine group
DR. TA OGUNLESI (FWACP)

21. DIAGNOSIS Meningitis is a medical emergency.
LP should be performed when bacterial meningitis is suspected.
LP is contraindicated in the presence of (1) evidence of increased ICP (cushing’s triad, papilloedema) (2) severe cardiopulmonary compromise (3) infection of the skin overlying the site of the LP.
If an LP is delayed, immediate empirical therapy should be initiated while awaiting CT scanning for evidence of a brain abscess or increased ICP.
DR. TA OGUNLESI (FWACP)

22. DIAGNOSIS
The presence of CSF pleocytosis (>30/mm3 in neonates and >5/mm3 in older children), raised protein (>150mg/dL in neonates & > 45mg/dL in older children), reduced glucose (less than 50% of simultaneously determined RBS) elevated lactate (>4.2mmol/L) and raised lactate dehydrogenase (>17U/L) are suggestive of meningitis.
The diagnosis is confirmed when bacteria are isolated from the CSF.
DR. TA OGUNLESI (FWACP)

23. DIAGNOSIS
Serologic studies (Latex agglutination or Counterimmuno electrophoresis) to detect bacterial antigens in urine, CSF or blood in the presence of CSF inflammation also is highly suggestive of meningitis.
Blood cultures may reveal the responsible bacteria in 80–90% of cases of childhood meningitis.
DR. TA OGUNLESI (FWACP)

24. DIAGNOSIS
With partial antibiotic therapy, CSF becomes rapidly sterilised if the pathogen was pneumococcus or meningococcus but cellular changes, an increase in protein, and low glucose levels persist.
Imaging studies: Transfontanelle USS, CT scan, MRI
DR. TA OGUNLESI (FWACP)

25. MANAGEMENT Highlights include: (1) antibiotic therapy
(2) fluid & electrolytes therapy
(3) steroid therapy
(4) serial monitoring of serum electrolytes & urea
DR. TA OGUNLESI (FWACP)

26. DRUG TREATMENT (1) Choice of antibiotic agent:
Must be based on local pattern of bacterial aetiologies.
Must be bactericidal.
Must be able to penetrate the BBB sufficiently.
(2) Peculiarities of antibiotic treatment of meningitis:
High dose required
Longer duration of treatment
DR. TA OGUNLESI (FWACP)

27. DRUG TREATMENT OF NEONATAL MENINGITIS
Traditionally, initial empirical antimicrobial treatment consists of the combination of ampicillin and an aminoglycoside.
Ampicillin covers for group B streptococci, enterococci, L monocytogenes, some strains of E coli, and H influenzae type b. Ampicillin also achieves adequate levels in CSF.
Cefotaxime and Ceftriaxone are two third-generation cephalosporins which have good CSF penetration and are effective against gram-negative microbes.
DR. TA OGUNLESI (FWACP)

28. DRUG TREATMENT OF NEONATAL MENINGITIS
Aminoglycosides (eg, gentamicin, tobramycin, amikacin), have good activity against most gram-negative bacilli, including P aeruginosa.
However, aminoglycosides achieve only marginal levels in both CSF and ventricular fluid.
DR. TA OGUNLESI (FWACP)

29. DRUG TREATMENT OF NEONATAL MENINGITIS
Etiologic agent and clinical course dictate duration of treatment; however, a 14- to 21-day treatment is usually adequate for group B streptococcal infection. It may take longer to sterilize the CSF with gram-negative bacillary meningitis, and 3-4 weeks of treatment is usually necessary.
Re-examination of CSF for chemistries and culture may be necessary hours following initiation of treatment to assess response to treatment, especially in neonates with gram-negative bacillary meningitis.
DR. TA OGUNLESI (FWACP)

30. DRUG TREATMENT OF MENINGITIS IN CHILDREN
Initial empirical antibiotic treatment should have good coverage for H. influenzae, S. pneumoniae and N. meningitidis.
Traditionally, a combination of IV chloramphenicol and IV ampicillin or IV penicillin G may be used.
DR. TA OGUNLESI (FWACP)

31. DRUG TREATMENT OF MENINGITIS IN CHILDREN
Due to the problem of high resistance of H. influenzae and S. pneumoniae to the traditional regime, initial antimicrobial therapy is currently done with IV ceftriaxone or IV cefotaxime combined with IV vancomycin.
Subsequent treatment should be tailored to the sensitivity pattern of the CSF isolate.
DR. TA OGUNLESI (FWACP)

32. GUIDE TO ANTIBIOTIC THERAPY
DOSE (mg/kg/d)
DOSE INTERVAL
Ampicillin
400
Q6hourly
Vancomycin 60
Penicillin G
300,000U
Cefotaxime
Ceftriaxone
100
Q12hourly
Chloramphenicol
Ceftazidime
150
Q8hourly
DR. TA OGUNLESI (FWACP)

33. DRUG TREATMENT OF MENINGITIS IN CHILDREN
Appropriate antibiotics should be continued for at least 10 days but it is often guided by the patient's hospital course.
In cases of N. meningitidis infection, a 7-day course of penicillin may be adequate.
LP may be repeated either before discontinuing treatment or 24 hours after cessation of antibiotics. Invariably, the CSF should be sterile within hours following initiation of the proper antibiotic therapy.
A repeat LP is often indicated when there is no remarkable improvement in the clinical state of the patient.
DR. TA OGUNLESI (FWACP)

34. DRUG TREATMENT OF MENINGITIS IN CHILDREN
Corticosteroids (IV Dexamethasone 0.2mg/kg stat, then 0.15mg/kg 6hourly) are recommended. It should be commenced at least 1 hour before the commencement of antibiotics and should be given for up to 4 days.
Corticosteroids decrease inflammation and reduce the risk of nerve palsies and cerebritis with decrease in the incidence of neurologic and audiologic sequelae.
DR. TA OGUNLESI (FWACP)

35. ANTICONVULSANT THERAPY
Adequate airway and oxygenation must be maintained during seizure activity.
Phenobarbitone (20 mg/kg IV dose at a rate of 1 mg/kg/min) often is effective in controlling seizures.
Phenytoin (15-20 mg/kg IV at a rate of 1 mg/kg/min) also may be used to treat seizure activity.
DR. TA OGUNLESI (FWACP)

36. ANTI-CONVULSANT THERAPY
If these drugs are not effective, a bolus of IV diazepam may be administered ( mg/kg/dose). Because the anticonvulsant effect of this drug is brief, it may be better to administer phenytoin (5 mg/kg/d IV q12h) along with it to provide continued seizure control.
Lorazepam (Ativan) is a long-acting benzodiazepine and can be administered safely (0.05 mg/kg/dose q4-6h).
DR. TA OGUNLESI (FWACP)

37. OTHER ASPECTS OF MANAGEMENT
Fluid restriction to 75-80% of the total maintenance volume is recommended.
Adequate caloric intake.
Mannitol ( g/kg/dose IV) usually is administered over minutes. It draws water from brain tissues into the vascular space by osmosis. This reduces the ICP and cerebral oedema.
Audiometry to detect hearing deficit at the point of discharge and 6 weeks later.
DR. TA OGUNLESI (FWACP)

38. COMPLICATIONS OF MENINGITIS
Short term
Cerebral oedema
Dural venous sinus thrombosis
Subdural effusion & empyema
Syndrome of Inappropriate ADH secretion
Cranial nerve palsies (VI & VIII commonly)
DR. TA OGUNLESI (FWACP)

39. COMPLICATIONS OF MENINGITIS
Short Term
Hydrocephalus (post-neonatal)
Cerebral abscess
Hemiplegia, quadriplegia
Ataxia
Ventriculitis
Cerebral or cerebellar herniation
DR. TA OGUNLESI (FWACP)

40. COMPLICATIONS OF MENINGITIS
Long term
Sensorineural deafness
Cerebral palsy
Mental retardation
Seizure disorders
DR. TA OGUNLESI (FWACP)

41. COMPLICATIONS OF MENINGITIS
Long Term
Microcephaly
Cortical blindness
Learning disability
Behavioural disorders
DR. TA OGUNLESI (FWACP)

42. PROGNOSIS Determinants of poor prognosis include:
Age younger than 6 mo
Aetiology – Streptococcus pneumoniae
Presence of focal neurologic deficits on admission
Presence of altered sensorium on admission
Hyponatraemia
Prolonged or difficult-to-control seizures, especially after the fourth hospital day.
DIC
Endotoxic shock
DR. TA OGUNLESI (FWACP)

43. PREVENTION Chemoprophylaxis:
Rifampicin (10mg/kg q12hrly for 2 days) for close contacts of N. meningitidis and H. influenzae cases.
Ceftriaxone ( mg stat) for close contacts of N. meningitidis cases.
Immunization:
Meningococcal polysaccharide vaccine (A, C, Y, W-135 type)
H. Influenzae type b vaccine
Conjugate pneumococcal vaccine
DR. TA OGUNLESI (FWACP)

44. ASEPTIC MENINGITIS
An illness characterized by serous inflammation of the linings of the brain (ie, meninges), usually with an accompanying mononuclear pleocytosis. Clinical symptomatology varies from very mild to severe and life threatening.
DR. TA OGUNLESI (FWACP)

45. ASEPTIC MENINGITIS
Aseptic meningitis syndrome is not caused by pyogenic bacteria, but can be caused by multiple conditions including infectious viral and non-viral causes and many noninfectious etiologies.
Hence, this term is NO longer synonymous with viral meningitis, although the two often are used interchangeably.
DR. TA OGUNLESI (FWACP)

46. INFECTIOUS AETIOLOGY Viruses
Enteroviruses – (Polio, coxsackievirus, echovirus)
HSV types 1 and 2
Varicella-zoster virus
Adenovirus
Epstein-Barr virus
LCMV (Lymphocytic choriomeningitis virus)
HIV
Influenza virus types A and B
DR. TA OGUNLESI (FWACP)

47. INFECTIOUS AETIOLOGY Bacteria Partially treated pyogenic meningitis
Parameningeal infections
Mycoplasma pneumoniae
M tuberculosis
Borrelia burgdorferi
Treponema pallidum
Brucella species
DR. TA OGUNLESI (FWACP)

48. INFECTIOUS AETIOLOGY Fungi Parasites Histoplasma capsulatum
Coccidioides immitis
Blastomyces dermatitides
Parasites
Toxoplasma gondii
Taenia solium (cysticercosis)
DR. TA OGUNLESI (FWACP)

49. NON-INFECTIOUS AETIOLOGY
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Trimethoprim-sulfamethoxazole, amoxicillin
Isoniazid
Intrathecal methotrexate
Intrathecal cystine arabinoside
Vaccination (DPT)
SLE
Migranes
DR. TA OGUNLESI (FWACP)

50. CLINICAL FEATURES
The time course of acute viral meningitis varies. The onset may occur within a matter of hours or evolve more slowly over a few days. Usually, maximum deficit appears within 3-6 days after exposure.
The diagnosis may be suggested by associated skin manifestations such as the rash of varicella zoster or mild maculopapular rash of enteroviruses. Occasionally, patients may exhibit altered levels of consciousness including confusion and visual hallucinations.
DR. TA OGUNLESI (FWACP)

51. CLINICAL FEATURES Headache Fever Stiff neck Photophobia Drowsiness
Myalgias & malaise
Sore throat
Abdominal pain, nausea, and vomiting
Focal signs, seizures, and profound lethargy are rare.
DR. TA OGUNLESI (FWACP)

52. DIAGNOSIS
Suspicion of viral meningitis is based on the clinical presentation of meningitis and presence of certain CSF findings.
Presence of LESS than 500 mononuclear cells/mm3 of CSF (pleocytosis) is characteristic. Occasionally, early examination may reveal acellular fluid or predominance of polymorphonuclear leukocytes, but the typical mononuclear pleocytosis develops in about 48 hours.
DR. TA OGUNLESI (FWACP)

53. DIAGNOSIS
CSF pressure may be elevated, whereas the glucose level is characteristically NORMAL.
CSF protein level usually is elevated ( mg/dL).
DR. TA OGUNLESI (FWACP)

54. DIAGNOSIS
The WBC count usually is not elevated, but an increase or decrease can occur, usually with a lymphocytic predominance.
A high serum amylase level is observed in patients with mumps because of involvement of the salivary glands or pancreas.
Other test results include LOW levels of tumor necrosis factor (TNF) and lactate.
DR. TA OGUNLESI (FWACP)

55. DIAGNOSIS
Serology: 4-fold or higher increase in antibody titer between acute and convalescent sera. Virus-specific immunoglobulin M (IgM) antibodies provide a quick and more accurate early diagnosis.
CX-Ray and tuberculin test in suspected Tuberculous meningitis.
DR. TA OGUNLESI (FWACP)

56. MANAGEMENT
Rapid institution of antibiotic therapy until pyogenic cause is excluded.
No specific treatment exists for most of the viruses; therefore, treatment, for the most part, is supportive (analgesics, anti-emetics, intravenous fluids).
Headache and fever usually can be treated with judicious doses of acetaminophen.
DR. TA OGUNLESI (FWACP)

57. MANAGEMENT
Severe hyperthermia (>40°C) may require vigorous therapy, but mild temperature elevation may serve as a natural defense mechanism, and some people believe it should be left untreated.
Strict isolation is not necessary. When enteroviral infection is suspected, take precautions in handling stools and wash hands carefully.
DR. TA OGUNLESI (FWACP)

58. DRUG THERAPY Anti-viral like acyclovir, valacyclovir and foscarnet
Isoniazid, rifampicin, and pyrazinamide are combined for tuberculosis.
Penicillin and ceftriaxone are used for actinomycetes and spirochetes.
Doxycycline or rifampin can be used for Brucella infection.
DR. TA OGUNLESI (FWACP)

59. DRUG THERAPY
Antifungal agents of choice include amphotericin B, fluconazole, and flucytosine.
Occasionally, dexamethasone is useful when meningitis is associated with signs of intracranial hypertension but the general trend is to avoid corticosteroids because of their inhibitory effects on host immune responses.
DR. TA OGUNLESI (FWACP)

60. PROGNOSIS
Aseptic meningitis is usually a benign disease; most people usually experience full recovery in 5-14 days after onset of symptoms. However, fatigue and lightheadedness may persist longer in some people.
Seizures, encephalitis & deafness are common complications of mumps & varicella zoster meningitis.
DR. TA OGUNLESI (FWACP)

61. ENCEPHALITIS
Acute viral encephalitis is the inflammation of the brain tissue.
It is often an unusual manifestation of common viral infections and most commonly affects children and young adults.
DR. TA OGUNLESI (FWACP)

62. ENCEPHALITIS
In general, viral encephalitis can be divided into 4 separate categories based on the cause and pathogenesis of the following complications:
Acute viral encephalitis
Post-infectious encephalomyelitis
Slow viral infections of the CNS
Chronic degenerative diseases of the CNS presumed to be of viral origin.
DR. TA OGUNLESI (FWACP)

63. AETIOLOGY Measles virus Poliovirus Herpes simplex virus (HSV)
Rabies virus
Human immunodeficiency virus-1 (HIV-1)
Mumps virus
Arboviruses (Eastern Equine, Western Equine, West Nile, St. Louis, Japanese B, Venezuelan)
DR. TA OGUNLESI (FWACP)

64. PATHOGENESIS The viruses enter the CNS through 2 distinct routes:
hematogenous dissemination (MOST COMMON)
neuronal retrograde dissemination.
DR. TA OGUNLESI (FWACP)

65. PATHOGENESIS
Arbovirus encephalitides are zoonoses transmitted by an insect bite and then undergoes local replication in the skin.
Transient viremia leads to seeding of the reticuloendothelial system and muscles. After continuous replication, secondary viremia leads to seeding of other sites, including the CNS.
Leptomeningitis, demyelination, extensive neuronal damage occur.
Various degrees of repair, which may include calcification occur in survivors.
DR. TA OGUNLESI (FWACP)

66. CLINICAL FEATURES
Viral encephalitis is marked by acute onset of a febrile illness associated with conjunctivitis, rhinorrhea, diarrhoea and skin rashes.
Features of leptomeningeal irritation (eg, headache, fever, neck stiffness).
Focal neurological signs; seizures; and alteration of consciousness, starting with lethargy and progressing to confusion, stupor and prolonged coma.
DR. TA OGUNLESI (FWACP)

67. CLINICAL FEATURES Behavioural and speech disturbances are common.
Abnormal movements may occur.
Involvement of the hypothalamic/pituitary axis can lead to hyperthermia or poikilothermia.
DR. TA OGUNLESI (FWACP)

68. CLINICAL FEATURES
Findings from physical examination are not usually diagnostic.
Abnormal movements including tremor may be seen.
Increased intracranial pressure can also lead to papilledema and cranial nerve VI palsy.
DR. TA OGUNLESI (FWACP)

69. CLINICAL FEATURES Focal neurological deficits: Opisthotonus Pareses
Tremors
Ataxia
Hypotonia
Diplopia
Accentuated reflexes and extensor plantar responses may be observed.
DR. TA OGUNLESI (FWACP)

70. DIFFERENTIAL DIAGNOSES
Aseptic meningitis
Subdural haematoma
Cavernous sinus syndromes
Intracranial haemorrhage
Acute confusional states
Seizure disorders
DR. TA OGUNLESI (FWACP)

71. DIAGNOSIS FBC typically shows lymphocytosis
LP: CSF examination reveals:
mildly elevated protein (60-80 mg/dL)
normal glucose
moderate pleocytosis, up to 1000 leukocytes/mm3.
Mononuclear cells usually predominate.
DR. TA OGUNLESI (FWACP)

72. DIAGNOSIS
Viral CSF cultures for enteroviruses, mumps, and certain arboviruses may be positive.
Serology: ELISA for specific IgM and IgG; PCR
CT scan/MRI (focal oedema, haemorrhages)
EEG (abnormal patterns occur in encephalopathies)
DR. TA OGUNLESI (FWACP)

73. MANAGEMENT Appropriate management of the airway Bladder function
Fluid and electrolyte balance
Nutrition
Prevention of bedsores
Secondary pulmonary infection
Hyperpyrexia.
DR. TA OGUNLESI (FWACP)

74. MANAGEMENT
Increased intracranial pressure should be managed in the ICU setting with:
Head elevation
Gentle diuresis
Mannitol
Hyperventilation.
DR. TA OGUNLESI (FWACP)

75. MANAGEMENT
Seizures control with phenytoin, carbamazepine, benzodiazepines and valproic acid.
Drugs (none for arboviruses; ribavirin 400mg/dose for Lassa, acyclovir 10mg/kg/dose for HSV)
Physiotherapy
DR. TA OGUNLESI (FWACP)

76. COMPLICATIONS Secondary bacterial respiratory infections
Seizure disorders
SIADH with hyponatraemia
Ataxia
Speech, visual and auditory deficits
Mental retardation
Behavioural disorders
DR. TA OGUNLESI (FWACP)