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DR. TA OGUNLESI (FWACP)1 CNS INFECTIONS. DR. TA OGUNLESI (FWACP)2 SPECTRUM OF CNS INFECTIONS Pyogenic Meningitis Aseptic Meningitis Tuberculous Meningitis.

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Presentation on theme: "DR. TA OGUNLESI (FWACP)1 CNS INFECTIONS. DR. TA OGUNLESI (FWACP)2 SPECTRUM OF CNS INFECTIONS Pyogenic Meningitis Aseptic Meningitis Tuberculous Meningitis."— Presentation transcript:

1 DR. TA OGUNLESI (FWACP)1 CNS INFECTIONS

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

3 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.

4 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

5 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.

6 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.

7 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.

8 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.

9 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.

10 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.

11 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.

12 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.

13 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.

14 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

15 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 Streptococcus pneumoniae Neisseria meningitidis Staphylococcus aureus

16 DR. TA OGUNLESI (FWACP)16 CLINICAL FEATURES The onset of acute meningitis has two predominant patterns: (1)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. (2)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.

17 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

18 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

19 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

20 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

21 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.

22 DR. TA OGUNLESI (FWACP)22 DIAGNOSIS The presence of CSF pleocytosis (>30/mm 3 in neonates and >5/mm 3 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.

23 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.

24 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

25 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

26 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

27 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.

28 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.

29 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.

30 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.

31 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.

32 DR. TA OGUNLESI (FWACP)32 GUIDE TO ANTIBIOTIC THERAPY ANTIBIOTICDOSE (mg/kg/d) DOSE INTERVAL Ampicillin 400Q6hourly Vancomycin60Q6hourly Penicillin G300,000UQ6hourly Cefotaxime Q6hourly Ceftriaxone100Q12hourly Chloramphenicol100Q6hourly Ceftazidime150Q8hourly

33 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.

34 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.

35 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.

36 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).

37 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.

38 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)

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

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

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

42 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

43 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

44 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.

45 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.

46 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

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

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

49 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

50 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.

51 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.

52 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.

53 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).

54 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.

55 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.

56 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.

57 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.

58 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.

59 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.

60 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.

61 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.

62 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.

63 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)

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

65 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.

66 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.

67 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.

68 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.

69 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.

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

71 DR. TA OGUNLESI (FWACP)71 DIAGNOSIS FBC typically shows lymphocytosis LP: CSF examination reveals: (1)mildly elevated protein (60-80 mg/dL) (2)normal glucose (3)moderate pleocytosis, up to 1000 leukocytes/mm 3. (4)Mononuclear cells usually predominate.

72 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)

73 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.

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

75 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

76 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


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