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Pediatric Critical Care Medicine

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Title: Pediatric Critical Care Medicine


1

CNS Other Infections
Pediatric Critical Care Medicine Emory
University Childrens Healthcare of Atlanta
2
Aseptic Meningitis
  • Viral, atypical bacteria, fungal, TB

3
Etiologies Viruses and Bacteria
  • - Adenovirus
  • - Arbovirus
  • - Enteroviruses
  • - Herpesviruses
  • - HIV
  • - Influenza A/B
  • - Japanese encephalitis
  • - Measles
  • - Mumps
  • - Rubella
  • - Rabies
  • - Lymphocytic choriomeningitic virus
  • - Bartonella henslae
  • - Bordetella pertussis
  • - Borrelia burgdorferi
  • - Brucella spp.
  • - Chlamydia spp.
  • - Ehrlichia, Leptospria spp.
  • - Mycobacteria spp.
  • - Mycoplasma spp.
  • - Rickettsia spp.
  • - Treponema pallidum

4
Etiologies Fungal and Others
  • Aspergillus fumigatus
  • Blastomyces dermatitidis
  • Candida spp.
  • Crytococcus neoformans
  • Coccidioides immitis
  • Histoplasma capsulatum
  • Toxoplasma gondii
  • Entamoeba histolytica
  • Acanthamoeba
  • Trichinella
  • Naegleria

5
TB Meningitis
  • Most serious complication of TB infection
  • Fatal without effective treatment, significant
    morbidity even with treatment
  • In children CNS involvement occurs during primary
    infection (rather than reactivation)
  • Usually results from hematogenous spread from a
    primary focus (lungs)
  • Variable presentation, but usually onset is
    insidious
  • More rapid in infants and young children

6
TB Meningitis
7
Clinical Staging
Stage Signs and Symptoms
Stage 1 (Early) Days to weeks Fever, HA, malaise Lethargy, behavior changes No neuro deficits No alteration of consciousness
Stage 2 (intermediate) Weeks to months Meningeal irritation Minor neuro deficits (CN)
Stage 3 (late) Months to years Abnormal movements Convulsions Stupor or coma Severe neuro deficits
8
Diagnosis
  • Isolation or identification of mycobacterium is
    the gold standard for diagnosis
  • Possible in about 80 of cases
  • PCR, ADA, ELISA have varying degrees of accuracy
  • Typically 10-500 WBCs, with predominance of
    lymphs
  • CSF glucose lt40, protein moderately elevated
    (150-200)
  • CSF can be normal in children with unruptured
    tuberculomas
  • Neuroimaging will be very helpful
  • Look for the primary TB site

9
Treatment
  • Typically requires at least 3 or 4 drug therapy
  • Isoniazid, rifampin, pyrazinamide /- ethambutol
    or streptomycin
  • WHO recommends at least a 4 month course for TB
    meningitis
  • Steroids have been shown to significantly reduce
    the neurologic sequelae of TBM
  • They often require a shunt for hydrocephalus
  • Prognosis varies but depends on clinical stage
    at the time treatment is started

10
Encephalitis and Myelitis
11
Encephalitis
  • Refers to inflammation of the brain parenchyma
  • Pathology shows
  • Inflammation and destruction of neurons
  • Pathogen detection by direct visualization,
    staining, etc
  • Referred to as postinfectious encephalitis when
    in temporal association with viral infection or
    immunization
  • ADEM when it includes spinal cord
  • Can cause significant alterations in sensorium
    and seizures
  • Many patients require ICU

12
Etiology
  • In neonates, the most common etiology is HSV
    (usually type 2), but also entero- and adenovirus
  • In older children arthropod-borne viruses
    (arboviruses) and enteroviruses are the most
    common
  • Arbo EEE, WEE, St. Louis, West Nile, JE
  • Entero polio, echo, coxsackie, etc
  • Subacute sclerosing panencephalitis is a now
    rare complication of measles infection
  • Tick borne bacteria can also be implicated
  • Borrelia, Rickettsia, ehrlichiosis

13
Pathogenesis
  • Once a virus crosses the epithelium (usually at
    a mucosal surface) viral replication occurs,
    followed by viremia
  • Viruses can penetrate the CSF from the blood,
    or by spread from peripheral neurons (rabies and
    HSV)
  • Once in the CNS the virus attaches to host
    cells
  • Viral genome replication takes over, affecting
    the other functions of the cell
  • Interferon in particular inhibits viral
    penetration, replication, translation, and
    assembly
  • The inflammatory process may turn on the host

14
Clinical Manifestations
  • Varies depending on affected site, severity,
    and host factors
  • May or may not involve meninges (rabies)
  • Nonspecific symptoms in neonates
  • May not have maternal h/o HSV
  • Older children have acute onset of fever, HA,
    seizures, behavior changes, AMS, or coma, /-
    prodrome
  • Depends on site of involvement
  • May have paralysis or paraplegia if spinal cord
    involved
  • Look for rashes (erythema migrans)

15
Diagnosis
  • CSF findings are non-specific
  • Cells and protein may be normal or slightly
    elevated
  • May see predominance of lymphs
  • May get a diagnosis from culture, antigen
    detection, PCR, or antibody titers
  • PCR stays positive for months, highly sensitive
    and specific
  • EEG can help distinguish focal from
    generalized encephalitis
  • HSV has characteristic periodic lateralized
    epileptiform discharges (PLEDs)

16
Neuroimaging
Etiology Site of involvement on MRI
HSV Inferomedial temporal and frontal lobes
Japanese encephalitis Bilateral thalami and basal ganglia
Rabies Hippocampal, cerebellar, mesencephalic areas
Eastern equine encephalitis Disseminated brain stem and basal ganglia
17
Management
  • Children with suspected encephalitis warrant
    ICU monitoring
  • Antimicrobial therapy is appropriate until
    bacterial meningitis has been ruled out
  • Antiviral therapy should be started when
    appropriate
  • HSV acyclovir
  • CMV ganciclovir or foscarnet
  • Flu A/B amantadine/rimantadine (A only),
    oseltamivir (A and B)
  • No specific therapy for entero- and arboviruses
  • Consider IVIG in immune compromised patients

18
HSV Encephalitis
  • HSV is the most common cause of fatal
    encephalitis in childhood
  • Mostly HSV-1 after neonatal period
  • Encephalitis can result from both primary and
    recurrent HSV infection
  • Primary CNS if via olfactory and trigeminal
    nerves
  • Disseminated HSV in the neonate affects the CNS
    by hematogenous spread

19
HSV Clinical Presentation
  • Neonatal
  • Older children
  • Skin vesicles, scarring
  • Eye involvement (chorioretinitis, optic atrophy)
  • Brain (microcephaly, encephalomalacia)
  • Disseminated disease (sepsis, ARDS, MODS)
  • Older children have typical symptoms of
    encephalitis
  • Behavior, personality, and speech changes are
    particular to HSV
  • Progression may still be rapid and fatal in
    non-neonates

20
Diagnosis
  • Swabs from conjunctiva, nasopharynx, rectum,
    skin lesions
  • MRI may show temporal or frontal involvement
  • PLEDs on EEG
  • HSV PCR is 95 sensitive and 100 specific
    (gold standard)
  • Please dont do a brain biopsy

21
HSV Treatment and Prognosis
  • ACYCLOVIR 20 mg/kg q8h for 14-21 days in
    neonates
  • 10 mg/kg q8h in older children
  • Need a negative CSF PCR before stopping therapy
  • Steroids have not been proven in children
  • Early treatment reduces morbidity and mortality
  • Relapse occurs in 12 of adult patients
  • Disseminated neonatal disease has 50 mortality
    and 50 of survivors have significant sequelae

22
ADEM
  • Acute Disseminated Encephalomyelitis

23
ADEM Introduction
  • ADEM is an inflammatory demyelinating disorder of
    the CNS
  • Mostly seen in children and young adults
  • Can be multiphasic (must distinguish from MS)
  • Often preceeded by respiratory or GI viral
    illness
  • Has also been reported after immunizations
  • MMR and rabies vaccines

24
ADEM Clinical Presentation
  • Mean age of presentation is 7 years, slightly gt
    males
  • Fever, HA rapidly progresses to AMS and
    multifocal neuro deficits
  • Evolution may occur over a few days
  • Deficits depend on affected areas
  • White matter, spinal cord, optic nerves
  • Ataxia and extrapyramidal symptoms are common
  • UMN signs in affected limbs
  • Fulminant presentation with rapid deterioration
    is rare, but usually occurs in children lt 3 yrs

25
ADEM Diagnosis
  • The Brighton collaboration has published a very
    complicated clinical definition of ADEM
  • Based on varying levels of diagnostic certainty
    histopathology, imaging, presentation, etc
  • CSF is not helpful in making a diagnosis of ADEM
  • May show pleocytosis or be normal
  • 10 of cases have oligoclonal bands
  • Myelin basic protein may be increased
  • EEG may show focal or generalized slowing

26
Neuroimaging
27
ADEM Treatment
  • Mainstay of treatment is methylprednisolone 20-30
    mg/kg/day for 3-5 days
  • Taper over 3-6 weeks
  • Plasmapheresis and IVIG have also been used
  • Considered when meningoencephalitis cannot be
    excluded
  • Concern that steroids would worsen possible
    infection
  • Combing either of these with steroids show no
    added benefit

28
ADEM Prognosis
  • Most children with mild to moderate illness and
    appropriate treatment achieve good recovery
  • Acute mortality is rare
  • Fulminant cases are at higher risk of mortality
  • 1/3 of cases have residual deficits
  • Motor, visual, autonomic, developmental, epilepsy
  • Relapses may occur during the steroid taper
  • Recurrent attacks can occur after full recovery

29
Brain and Spinal Cord Abscess
30
Brain and Spinal Cord Abscess
  • May occur as a primary infection or as a
    complication of bacterial meningitis (more rare)
  • Rogers says that intensivists like them because
    they are a serious, potentially fatal infection
    that requires immediate intervention

31
Abscesses Etiologies
  • Most common pathogens include anaerobes, GNs,
    streptococci, and staph
  • Neonates most commonly get GNs Citrobacter,
    Enterobacter, Proteus
  • In other populations the organism depends on
    predisposing factors
  • CHD a-hemolytic strep
  • Endocarditis strep, S. aureus
  • Post-trauma staph
  • Otitis/sinusitis strep, Bacteroides fragilis,
    Proteus spp., pseudomonas, H.flu

32
Abscesses Pathogenesis
  • May occur via hematogenous or direct spread
  • Cyanotic heart disease is the most common
    underlying condition (esp. TOF)
  • Polycythemia ? higher viscosity ? microinfarcts
  • Bacteria love it!
  • Chronic pulm infection, bacterial endocarditis,
    and immune compromise also increase risk
  • Direct spread may occur from chronic otitis,
    mastoiditis, sinusitis, trauma, NS procedures
  • Meningitis is a rare cause if treated
    appropriately
  • Except in neonates with GN meningitis

33
Abscesses Pathogenesis
  • Bugs localize at the gray-white junction ?
    cerebritis
  • Stage 1 Early cerebritis (Day 1-3)
  • Leukocyte infiltration, focal edema, no clear
    demarcation
  • Stage 2 Late cerebritis (Day 4-9)
  • Central liquefaction necrosis (yum!), fibroblast
    infiltration, capsule formation
  • Stage 3 Continued capsule formation
  • Stage 4 Late capsule formation (2 weeks out)
  • Dense fibrous capsule, marked edema

34
Abscesses Pathogenesis
  • Entire process may take 4-6 weeks
  • May progress faster or rupture into ventricular
    system
  • Sites of infection vary but cerebral are most
    common
  • Kids with CHD get them in MCA distribution
  • Otitis can spread to unilateral temporal lobe or
    cerebellum

35
Abscesses Diagnosis
  • LP would be contraindicated in a patient with
    brain or spinal cord abscess
  • ButCSF may show pleocytosis, ? protein, normal
    glc
  • Blood cultures and cultures from other potential
    foci would help
  • Get imaging

36
Abscesses Imaging
37
Abscesses Imaging
38
Abscesses Treatment
  • Surgical drainage or excision is required in many
    cases
  • Usually under CT guidance
  • Smaller abscesses may be manageable with
    antibiotics alone
  • Empiric therapy is usually a 3rd/4th gen
    cephalosporin metronidazole
  • Add vanc if staph is suspected
  • Tailor therapy once an organism is defined
  • IV therapy for at least 6 weeks

39
Abscesses Prognosis
  • Mortality is high in several groups
  • Newborns, young infants
  • Children with multiple large abscesses and CHD
  • Intramedullary abscess of spinal cord (vs.
    subdural or epidural spinal abscesses)
  • Rupture of an abscess can be life-threatening
  • Residual defects are common
  • Hemiparesis, CN palsies, cognitive defects,
    epilepsy
  • Early decompression improves outcome

40
Cerebritis ? Vasculitis
41
Shunt Infections
  • 2/3 of all shunt infections are caused by staph
    spp
  • Staph epi, aureus, and other coag-negative types
    have been frequently isolated in several series
  • GN enterics (E.coli, Klebsiella, Proteus,
    Pseudomonas) make up 6-20
  • Strep causes 8-10
  • Multiple organisms are found in 10-15
  • Incidence has declined over the past few years
  • 70-85 of infections are within 6 months of
    surgery

42
Pathogenesis
  • Shunts are foreign bodies and interfere with
    natural host defense mechanisms
  • Chemotaxis and phagocytosis
  • Staph can also form biofilm which increases
    bacterial adherence and decreases effect of
    antibiotics
  • Infection may occur through different
    mechanisms
  • Wound or skin breakdown over shunt
  • Colonization at the time of surgery
  • Retrograde from the distal end of shunt
  • Hematogenous seeding (infrequent)

43
Clinical Presentation
  • Fever, headache, vomiting, lethargy, altered
    mental status
  • Check for wounds and look for cellulitis along
    the shunt
  • Infection may spread to the distal end of the
    shunt and cause peritonitis

44
Diagnosis
  • Isolation of organisms from CSF or equipment
  • Other CSF studies are variable
  • If there is associated shunt malfunction there
    may be an increase in ventricular size on CT
  • Distal shunt infections can also cause abdominal
    pseudocysts

45
Treatment
  • Antibiotics are a mainstay of treatment
  • Some propose shunt removal or externalization
    only if there is no response to antibiotics
  • Associated ventriculitis may clear more quickly
    with externalization
  • Cover staph with cloxacillin or vanc an
    aminoglycoside
  • Rifampin is often added
  • Intraventricular therapy is sometimes indicated

46
CNS Fungal Infections
  • Aspergillus, Cryptococcus

47
CNS Fungal Infections
Predisposing Condition Fungal Pathogen
Prematurity Candida albicans
Primary immunodeficiency (CGD, SCID) Candida, Cryptococcus, Aspergillus
Corticosteroids Cryptococcus, Candida
Cytotoxic agents Aspergillus, Candida
Secondary immunodeficiency (AIDS) Cryptococcus, Histoplasma
Iron chelator therapy Zygomycetes
IV drug abuse Candida, Zygomycetes
Ketoacidosis, renal acidosis Zygomycetes (Mucor)
Trauma, foreign body Candida
48
CNS Fungal Infections
  • Dont forget about the fungi that can cause
    disease in a healthy host
  • Cryptococcus, Histoplasma, Blastomyces,
    Coccidioides, Sporothrix
  • Fungal infections are on the rise worldwide due
    to increasing prevalence of HIV

49
Fungal Meningitis
  • Most common causes are Cryptococcus neoformans,
    C. immitis, Candida, and Aspergillus
  • Fungal meningitis in general has a more insidious
    onset than bacterial
  • Symptoms may develop over days
  • Always consider it with subacute/chronic
    presentation
  • C.neoformans may develop more quickly in patients
    on high-dose steroids or with HIV

50
Fungal Meningitis
  • Rhinocerebral syndrome is a major presentation of
    zygomycosis
  • Rhizopus and Mucor spp
  • Associated with poorly controlled DM
  • Orbital pain, nasal discharge, facial edema,
    proptosis
  • May invade carotids, trigeminal nerve and
    adjacent brain structures
  • May also present with sudden neuro deficit due to
    vasculitis
  • Can rarely cause mycotic aneurysmal bleed

51
Diagnosis
  • Have a low index of suspicion in immune
    compromised patients with fever and CNS signs
  • CSF usually has high protein, low glucose, and
    20-500 WBCs
  • Cell count may be LOW (lt20) with AIDS or high
    dose steroids
  • India ink prep can identify gt50 of
    C.neoformans cases (up to 80 in AIDS)

52
Diagnosis
  • - Cultures are frequently negative
  • Candida takes days to grow, histo/coccidio take
    weeks
  • - Methenamine stain of an aspirate or biopsy can
    help identify Aspergillus and Zygomycetes, which
    can cause tissue invasion and necrosis

53
Treatment
Fungus Initial Regimen Second Regimen Other Considerations
Candida Amphotericin B flucytosine x 2 wks Fluconazole x 8-10 weeks Remove shunt if appicable.
Cryptococcus Ampho B flucytosine x 2 wks Fluconazole x 8-10 weeks Repeat LP after 2wks of ampho. Stop steroids.
Coccidio Ampho x 4wks Fluconazole or ampho 4eva Serial monitoring of CSF
Aspergillus High dose ampho excision PO vori or ampho x 1 yr Excision is key.
54
Prognosis
  • Depends on underlying disease process
  • Why are they immune suppressed?
  • Candida meningitis has a mortality of 10-20
  • Only 50 of patients with coccidioidal meningitis
    survive initial treatment
  • Survivors have a high risk of relapse
  • A cryptococcal vaccine has been developed, not
    sure if it is available yet

55
Parasitic CNS Infections
  • Neurocysticercosis and Cerebral Malaria

56
Neurocysticercosis
  • - Most common parasitic CNS infection.
  • Important cause of epilepsy in the tropics.
  • - Most cases present with seizures.
  • 1/3 present with raised ICP.
  • - Endemic in Latin America, Mexico, India,
    sub-Saharan Africa, and China.
  • Including developed countries.
  • gt1000 new cases are diagnosed in the US each year.

57
Taenia solium Life Cycle
58
Neurocysticercosis
  • Parenchymal
  • Extraparenchymal
  • Seizures in 70-90 of patients
  • 1/3 will have raised ICP
  • 4 have focal neuro deficits
  • May have encephalitis
  • Numerous cysts
  • Diffuse cerebral edema
  • Poor prognosis
  • Rare in children
  • Obstructive hyrdocephalous or chronic meningitis
  • Spinal involvement
  • Radicular pain
  • Cord compression
  • Transverse myelitis
  • Ophthalmic involvement
  • Vision deficits

59
Neurocysticercosis
60
Treatment
  • - Praziquantel and albendazole are both effective
  • - But albendazole is better tolerated and
    penetrates CSF better.
  • 15 mg/kg/day x 28 days
  • - There are some times to NOT use cysticidal
    therapy
  • Markedly raised ICP inflammatory response will
    be bad, give only steroids
  • Ophthalmic NCC
  • Calcified lesions parasite is already dead
  • - Use steroids to reduce cerebral edema or if
    there is encephalitis
  • - Repeat CT in 3-6 months to assess lesions

61
Cerebral Malaria
  • Last one!

62
Cerebral Malaria
  • Clinical syndrome characterized by CNS
    dysfunction associated with Plasmodium falciparum
    infection
  • Becoming more common in developed countries due
    to increases in international travel and
    migration
  • Pathophysiology is different in children who grew
    up in endemic areas vs. those who are non-immune

63
Etiology
  • P. falciparum causes almost all life-threatening
    malaria.
  • Transmitted by anopheline mosquitos
  • Sporozoites enter the bloodstream and visit the
    liver before invading erythrocytes
  • Trophozoites and schizonts are sequestered in
    the microcirculation of vital organs
  • Obstructs blood flow and impairs function of
    parenchymal cells
  • Thats bad

64
Epidemiology
  • Endemic in tropical areas
  • Southeast Asia, Central/South America, Africa
  • 300-500 million cases and 1.5-3 million deaths
    annually
  • One of the top 3 infectious disease killers
    worldwide

65
Pathogenesis
  • - Plasmodial infections stimulate monocyte
    release of cytokines (TNF, IL-1, IL-6)
  • - Pathogenesis of cerebral malaria is not well
    understood
  • Likely multi-factorial mechanisms of neuro
    dysfunction
  • May be due to obstruction of microvasculature
  • Increased CSF lactate production
  • - Global ischemia doesnt seem occur
  • - Pathologic hallmark is engorgement of cerebral
    capillaries with infected erythrocytes

66
Clinical Presentation
  • - Suspect it in any child who has visited (or
    even landed in an airport!) an endemic area and
    develops CNS symptoms.
  • - Fever, HA, irritability, altered mental status.
  • - Seizures are common.
  • - Retinopathy (including hemorrhages)
  • - Metabolic acidosis
  • - Hypoglycemia (associated with poor prognosis)
  • In non-immune adults it is from hyperinsulinemia
  • In African children it is impaired
    gluconeogenesis.
  • -Hemolytic anemia, may be severe.

67
Diagnosis
  • CSF is usually acellular consider other
    diagnosis if there is pleocytosis
  • Protein and glucose are normal, CSF lactate is up
  • Associated with GN sepsis
  • Parasite count ranges from barely detectable to
    gt20
  • May not be detectable at first
  • Need blood smears q6h x 48hrs to rule out

68
Treatment
  • - Children with severe malaria need parenteral
    therapy
  • Cinchona alkaloids (quinine, quinidine)
  • Artermisinin compounds (not available in N.
    America)
  • - Side effects include cinchonism, but serious CV
    effects may occur if drugs are given undiluted or
    too fast
  • Hypotension, arrythmias
  • Watch QT during infusion
  • - Supportive care is important, many children die
    in the first 24 hours.
  • - Watch glucose, fluid balance, renal function,
    HCT.
  • - Exchange transfusion may be indicated for
    parasitemia gt10 or if not responding to therapy.
  • - Steroids appear to increase bleeding and offer
    no benefit.

69
Prognosis
  • Mortality in non-immune patients is 15-26
  • Many patients die in the first 4 days from renal
    failure or pulmonary edema
  • African children have similar mortality but they
    die in the first 24 hours
  • Often from herniation, severe hypoglycemia,
    anemia
  • Survivors have significant neurologic sequelae

70
Prevention
  • No vaccine is available for malaria.
  • Prophylaxis is recommended for travelers.
  • Mefloquine or atovaqone-proguanil.
  • Protection from mosquito bites is also important.
  • Repellant, netting, protective clothing.
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