gemc- meningitis and other cns infections- resident training
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This is a lecture by Frank Madore, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.TRANSCRIPT
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Project: Ghana Emergency Medicine Collaborative
Document Title: Meningitis and Other CNS Infections
Author(s): Frank Madore, MD
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Meningitisand other CNS infections
Frank Madore, MDHennepin County Medical Center
Minneapolis, MN, USA3
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BACKGROUNDBACKGROUND
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history first described by Viesseux in 1805 Flexner developed antiserum in 1913 antibiotic use began in 1930s-40s high morbidity and mortality to this day
– 20-40% depending on organism
– 30% with residual deficits changing landscape of causative
organisms based on vaccination patterns
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definitions meningitis – inflammation of the
meninges encephalitis – inflammation of brain
parenchymaa myelitis – inflammation of spinal cord
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epidemiology meningitis endemic in parts of Africa occurs in epidemics in US
– incidence is 5-10/100,000 per year, winter
– 80% are Neisseria and Strep pneumo
– viral meningitis twice as common, summer encephalitis less common but incidence
rising due to West Nile Virus rare brain abscesses due to sinusitis, otitis
media, immunocompromised
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MENINGITISMENINGITIS
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etiology streptococcus pneumoniae neisseria meningitidis (<45 yo) listeria monocytogenes aseptic
viral – HSV, enteroviruses, etc.
– fungal – crypto, histo, blasto, coccidioides
– parasites – toxo, neurocyster. trichinosis
– rickettsiae – RMSF, typhus
– non-infectious – post inf, drugs, systemic dz
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pathophysiology nasopharyngeal colonization → mucosal
invasion → enter blood stream → evade immune destruction → cross blood brain barrier into CSF
meningeal inflammation → increased permeability of BBB, vasculitis, edema, increased ICP
decreased cerebral perfusion, decreased CSF glucose, increased CSF protein
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risk factors age <5 or >60 male african descent crowding sickle cell disease malignancy etoh, DM recent ENT surgery or head injury
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clinical presentation headache fever nausea/vomiting seizures altered mental status nuchal rigidity photophobia many present atypically (old, young,
immune compromised, aseptic) 12
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clinical presentation often have a primary source of infection
on exam (PNA, UTI, sinusitis, OM, etc.) purpuric rash with menincococcemia Kernig Sign – can't extend knee to 180
while laying supine with hip in flexion Brudzinski Sign – 5 described, 2 used now
– contralateral – flexion of one hip causes flexion of the other hip
– neck – flexion of neck causes hip flexion jolt acceleration of headache
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complications acute – coma, seizure, loss of airway
reflexes, respiratory arrest, cerebral edema, DIC, dehydration, death
delayed – seizures, paralysis, cognitive deficits, hydrocephalus, hearing loss, ataxia, blindness, death
complications from viral meningitis are rare
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ENCEPHALITISENCEPHALITIS
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etiology usually viral – HSV, HHV, west nile virus,
arbovirus, VZV, EBV occasionally idiopathic, post infectious, or
bacterial (mycoplasma pneumoniae)
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pathophysiology innoculation occurs via various
mechanisms depending on the virus viremia, proliferation within neurons, or
invasion via nasal mucosa CSF invasion similar to meningitis but less
of an immune response if viral → fewer neurologic sequelae in most patients
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clinical presentation symptoms similar to meningitis, except: almost all have AMS personality changes focal neurologic signs higher incidence of seizure hallucinations, bizarre behavior
– may precede other signs → psych dx
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complications dependent on etiologic agent Japanese, Eastern equine, and St. Louis
encephalitis have high M&M West Nile Virus infects few but has
significant mortality HSV mortality dropped from 70% to 30%
with acyclovir
– survivors: seizure, motor/cognitive deficits TB M&M vary based on duration fungal mortality high, morbidity low
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CNS ABSCESSCNS ABSCESS
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etiology usually invasion from more common ENT
infections (otitis media, sinusitis, dental infections, etc.)
streptococcus milleri most common also bacterioides, staph aureus,
propionbacterium, enterobacteriae
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clinical presentation similar to encephalitis, often difficult to
differentiate clinically usually subacute (>2 weeks onset) course
of illness often have papilledema acute worsening can occur with rupture of
abscess into ventricles or with uncal herniaton
can mimic intracranial hemorrhage22
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complications mortality >50% without aggressive care
– <20% with surgical aspiration + abx 80% develop seizure disorder cognitive deficits, focal neuro deficits
common epidural abscess → paralysis, motor &
sensory deficits, bowel/bladder dysfunction
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DIAGNOSISDIAGNOSIS
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CT before LP?
unnecessary in most patients with suspected meningitis, except:
– focal neuro deficits
– altered mental status/coma
– papilledema
– seizures
– trauma
CT and LP should not delay treatment
abx → CT if needed → LP 25
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lumbar puncture
collect at least 3 tubes of 1 mL each
opening pressure = 5-20 cm H2O
cell count <5 WBC/mm3
differential <1 PMN/mm3
protein = 15-45 mg/dL
glucose = 60% blood glucose
gram stain/AFB
culture, specific antigen tests26
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adjuncts to LP blood cultures
– often have higher yields for bacteria CBC w/diff
– don't let it talk you out of an LP chemistry panel
– compare glucose to CSF, renal function CXR
– 50% w/strep pnuemo meningitis have PNA
EEG – encephalitis (HSV)27
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MANAGEMENTMANAGEMENT
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resuscitation fulminant presentation
– septic shock
– seizures
– cerebral edema
– hypoxia
– loss of airway reflexes standard supportive measures
– mannitol for cerebral edema
– empiric antibiotics as soon as possible29
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antibiotic regimen vancomycin plus
– ceftriaxone or
– cefotaxime or
– meropenem or
– chloramphenicol add ampicillin if >50 yrs neonates: cefotaxime + ampicillin special cases: penetrating trauma, post
neurosurgery, VP shunt30
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other medications acyclovir for suspected HSV INH, rifampin, etc. for TB amphotericin B for fungal (not in ED) flagyl for CNS abscess
– also early neurosurgical consultation
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steroids in meningitis dexamethasone has been shown to
reduce cerebral edema, ICP, CSF lactate past studies with variable results randomized controlled study in sub-
Saharan Africa showed no benefit in children
randomized controlled study in Vietnam showed reduction of long-term neurologic sequelae with dexamethasone >14 yo
– dexamethasone for strep pneumoniae 32
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chemoprophylaxis rifampin 600 mg x4 doses in household
contacts ciprofloxacin 500 mg x1 dose in HCW with
direct contact (intubation, suctioning)
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disposition admit can consider d/c if symptoms are classic
for viral meningitis and follow up within 24 hours can be ensured
– often viral meningitis is admitted on abx until bacterial causes can be excluded
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SUMMARYSUMMARY
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in conclusion... suspicion of CNS infection mandates LP
unless contraindications to blind LP exist
– in which case, perform HCT first do not delay abx for HCT or LP evaluation for CNS infection in a patient
with the right symptoms should not stop if another infection is found
– many have hematogenous spread from PNA or UTI
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QUESTIONSQUESTIONS
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