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Project: Ghana Emergency Medicine Collaborative Document Title: Meningitis and Other CNS Infections Author(s): Frank Madore, MD License: 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/ We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. These lectures have been modified in the process of making a publicly shareable version. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact [email protected] with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit http://open.umich.edu/privacy-and-terms-use. Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers. 1

GEMC: Meningitis and Other CNS Infections: Resident Training

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Page 1: GEMC: Meningitis and Other CNS Infections: Resident Training

Project: Ghana Emergency Medicine Collaborative Document Title: Meningitis and Other CNS Infections Author(s): Frank Madore, MD License: 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/

We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. These lectures have been modified in the process of making a publicly shareable version. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact [email protected] with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit http://open.umich.edu/privacy-and-terms-use. Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers.

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Page 2: GEMC: Meningitis and Other CNS Infections: Resident Training

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Meningitis and other CNS infections

Frank Madore, MD Hennepin County Medical Center

Minneapolis, MN, USA 3

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BACKGROUND

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history

n  first described by Viesseux in 1805 n  Flexner developed antiserum in 1913 n  antibiotic use began in 1930s-40s n  high morbidity and mortality to this day

–  20-40% depending on organism –  30% with residual deficits

n  changing landscape of causative organisms based on vaccination patterns

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definitions

n  meningitis – inflammation of the meninges n  encephalitis – inflammation of brain

parenchymaa n  myelitis – inflammation of spinal cord

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epidemiology n  meningitis endemic in parts of Africa n  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

n  encephalitis less common but incidence rising due to West Nile Virus

n  rare brain abscesses due to sinusitis, otitis media, immunocompromised

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MENINGITIS

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etiology n  streptococcus pneumoniae n  neisseria meningitidis (<45 yo) n  listeria monocytogenes n  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

n  nasopharyngeal colonization → mucosal invasion → enter blood stream → evade immune destruction → cross blood brain barrier into CSF

n  meningeal inflammation → increased permeability of BBB, vasculitis, edema, increased ICP

n  decreased cerebral perfusion, decreased CSF glucose, increased CSF protein

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risk factors

n  age <5 or >60 n  male n  african descent n  crowding n  sickle cell disease n  malignancy n  etoh, DM n  recent ENT surgery or head injury

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clinical presentation

n  headache n  fever n  nausea/vomiting n  seizures n  altered mental status n  nuchal rigidity n  photophobia n  many present atypically (old, young, immune

compromised, aseptic)

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clinical presentation n  often have a primary source of infection on

exam (PNA, UTI, sinusitis, OM, etc.) n  purpuric rash with menincococcemia n  Kernig Sign – can't extend knee to 180 while

laying supine with hip in flexion n  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

n  jolt acceleration of headache

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complications

n  acute – coma, seizure, loss of airway reflexes, respiratory arrest, cerebral edema, DIC, dehydration, death

n  delayed – seizures, paralysis, cognitive deficits, hydrocephalus, hearing loss, ataxia, blindness, death

n  complications from viral meningitis are rare

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ENCEPHALITIS

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etiology

n  usually viral – HSV, HHV, west nile virus, arbovirus, VZV, EBV

n  occasionally idiopathic, post infectious, or bacterial (mycoplasma pneumoniae)

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pathophysiology

n  innoculation occurs via various mechanisms depending on the virus

n  viremia, proliferation within neurons, or invasion via nasal mucosa

n  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

n  symptoms similar to meningitis, except: n  almost all have AMS n  personality changes n  focal neurologic signs n  higher incidence of seizure n  hallucinations, bizarre behavior

–  may precede other signs → psych dx

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complications

n  dependent on etiologic agent n  Japanese, Eastern equine, and St. Louis

encephalitis have high M&M n  West Nile Virus infects few but has significant

mortality n  HSV mortality dropped from 70% to 30% with

acyclovir –  survivors: seizure, motor/cognitive deficits

n  TB M&M vary based on duration n  fungal mortality high, morbidity low

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CNS ABSCESS

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etiology

n  usually invasion from more common ENT infections (otitis media, sinusitis, dental infections, etc.)

n  streptococcus milleri most common n  also bacterioides, staph aureus,

propionbacterium, enterobacteriae

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clinical presentation

n  similar to encephalitis, often difficult to differentiate clinically

n  usually subacute (>2 weeks onset) course of illness

n  often have papilledema n  acute worsening can occur with rupture of

abscess into ventricles or with uncal herniaton n  can mimic intracranial hemorrhage

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complications

n  mortality >50% without aggressive care –  <20% with surgical aspiration + abx

n  80% develop seizure disorder n  cognitive deficits, focal neuro deficits common n  epidural abscess → paralysis, motor & sensory

deficits, bowel/bladder dysfunction

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DIAGNOSIS

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CT before LP?

n  unnecessary in most patients with suspected meningitis, except: –  focal neuro deficits –  altered mental status/coma –  papilledema –  seizures –  trauma

n  CT and LP should not delay treatment n  abx → CT if needed → LP

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lumbar puncture

n  collect at least 3 tubes of 1 mL each n  opening pressure = 5-20 cm H2O n  cell count <5 WBC/mm3 n  differential <1 PMN/mm3 n  protein = 15-45 mg/dL n  glucose = 60% blood glucose n  gram stain/AFB n  culture, specific antigen tests

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adjuncts to LP

n  blood cultures –  often have higher yields for bacteria

n  CBC w/diff –  don't let it talk you out of an LP

n  chemistry panel –  compare glucose to CSF, renal function

n  CXR –  50% w/strep pnuemo meningitis have PNA

n  EEG – encephalitis (HSV) 27

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MANAGEMENT

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resuscitation

n  fulminant presentation –  septic shock –  seizures –  cerebral edema –  hypoxia –  loss of airway reflexes

n  standard supportive measures –  mannitol for cerebral edema –  empiric antibiotics as soon as possible

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antibiotic regimen

n  vancomycin plus –  ceftriaxone or –  cefotaxime or –  meropenem or –  chloramphenicol

n  add ampicillin if >50 yrs n  neonates: cefotaxime + ampicillin n  special cases: penetrating trauma, post

neurosurgery, VP shunt

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other medications

n  acyclovir for suspected HSV n  INH, rifampin, etc. for TB n  amphotericin B for fungal (not in ED) n  flagyl for CNS abscess

–  also early neurosurgical consultation

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steroids in meningitis

n  dexamethasone has been shown to reduce cerebral edema, ICP, CSF lactate

n  past studies with variable results n  randomized controlled study in sub-Saharan

Africa showed no benefit in children n  randomized controlled study in Vietnam showed

reduction of long-term neurologic sequelae with dexamethasone >14 yo –  dexamethasone for strep pneumoniae

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chemoprophylaxis

n  rifampin 600 mg x4 doses in household contacts

n  ciprofloxacin 500 mg x1 dose in HCW with direct contact (intubation, suctioning)

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disposition

n  admit n  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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SUMMARY

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in conclusion...

n  suspicion of CNS infection mandates LP unless contraindications to blind LP exist –  in which case, perform HCT first

n  do not delay abx for HCT or LP n  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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QUESTIONS

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