CNS Infections EMERGENCY NEUROLOGY LECTURE SERIES August 24, 2011 Dr . Abdullah Al - Salti R4
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CNS Infections EMERGENCY NEUROLOGY LECTURE SERIES
August 24, 2011
Dr. Abdullah Al-Salti R4
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CNS Infections Case scenario
Bacterial meningitis . C.T before L.P Dexamethasone used Prophylaxes.
Viral encephalitis
L.P procedure.
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CASE 1
A 21-year-old college student was found poorly responsive in her room. She had complained of a headache for about 4 days that was refractory to NSAIDs.
In the ER, temperature was 39.5°C, with BP 145/100 mmHg, HR of 112 per minute and RR of 18 per minute.
She partly responded to verbal commands, localized symmetrically to noxious stimuli, and moaned incoherently.
Neurological examination showed nuchal rigidity, and normal brainstem reflexes, with symmetric hyperreflexia and flexor plantar responses.
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CASE 1
H.P.IONSET,
COURSE ,DURATION
CONSTITIUSIONAL SYMPTOMES.
SCREEN NUEROLOGICAL
SYSTEMS.
SYSTEMIC REVIEW.
WHAT IS SO FARE BEEN DONE ?
First thing to do
PMH.
SURGICAL HISTORY
MEDICATIONS.
FAMILY HISTORY.
HABITES.
SOCIAL .
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Examination :1. Focal neurological deficitst .
2. Signs of meninegeal irritation.
3. Signs of raised ICP.
4. General systemic exam.
Ddx:?
Investigasion ?
Treatments?
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CNS INFECTIONS
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CNS INFECTIONSOverview
Life-threatening problems with high associated mortality and morbidity.
Presentation may be acute, subacute, or chronic.
Clinical findings determined by anatomic site(s) of involvement, infecting pathogen, and host response.
Vulnerability of CNS to the effects of inflammation & edema mandates prompt diagnosis with appropriate therapy if consequences to be minimized.
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CNS InfectionsMeningitis
Bacterial, viral, fungal, chemical, carcinomatous
EncephalitisBacterial, viral
Meningoencephalitis
AbscessParenchymal, subdural, epidural
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INFECTIONS 4 routes which infectious agents can enter the CNS
a) hematogenous spreadi) most common
- usually via arterial route- can enter retrogradely (veins)
b) direct implantationi) most often is traumaticii) iatrogenic (rare) via lumbar punctureiii) congenital (meningomyelocele)
c) local extension (secondary to established infections) i) most often from mastoid, frontal sinuses, infected
tooth, etc.d) PNS into CNS
i) viruses- rabies- herpes zoster
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BACTERIAL MENINGITIS
Meningitis
refers to an inflammatory process of leptomeninges and CSF.
Meningoencephalitis
refers to inflammation to meninges and brain parenchyma.
Meningitis classified:
a) acute pyogenic i) usually bacterial meningitis
b) aseptici) usually acute viral meningitis
c) chronici) usually TB, spirochetes, cryptococcus.
Incidence of 3 cases/100,000 population/yr (~25,000 total cases).
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COMMON BACTERIAL PATHOGENS BASED ON PREDISPOSING FACTOR IN PATIENTS WITH MENINGITIS
Predisposing Factor
Age
0-4 wK
4-12 wk
3 mo to 18 yr
18-50 yr
>50 yr
Common Bacterial Pathogens
Streptococcus agalactiae, Escherichia coli, Listeria monocytogenes, Klebsiella pneumoniae, Enterococcus spp., Salmonella spp.
S. agalactiae, E. coli, L. monocytogenes, Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitidis
H. influenzae, N. meningitidis, S. pneumoniae
S. pneumoniae, N. meningitidis
S. pneumoniae, N. meningitidis, L..monocytogenes, aerobic gram-negative bacilli
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Clinical Features
Signs and symptoms:
rapid onset of fever
headache
photophobia
nuchal rigidity
lethargy, malaise
altered mentation
seizure
vomiting.
van de Beek D, de Gans J, Tunkel AR, et al. Community-acquired bacterial meningitisin adults. N Engl J Med 2006;354(1):44–53.
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Clinical Features Study of 493 adult patients with bacterial meningitis,
the presence of the ‘‘classic triad’’ of
fever, neck stiffness, and altered mental status was present in two-thirds of patients.
fever WAS the most common element, in 95%.
(N Engl J Med 1993;328(1):21–8. )
Older patients with S. pneumoniae meningitis are more likely to have the classic triad.
Weisfelt M, van de Beek D, Spanjaard L, et al. Community-acquired bacterial meningitis in older people. J Am Geriatr Soc 2006;54(10):1500–7.
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Physical examinationA careful neurological examination is important
to evaluate for :
focal deficits increased intracranial pressure (ICP).
Examination should include assessment for meningeal irritation Brudzinski’s sign Kernig’s sign
findings include purpura or petechia of the skin, which may occur with meningococcemia.
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(straightening of the knee with a flexed hip resulting in back and neck pain)
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(passive flexion of the neck resulting in flexion of the hips and knees)
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Bacterial meningitis
Investigations
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LPSingle most impt diagnostic test.
Mandatory, esp if bacterial meningitis suspected.
Tube #1 – glucose and protein
Tube #2 – cell count and differential
Tube #3 – gram stain and rountine culture, cyrptococcal antigen, AFB stain and culture
Tube #4 – VDRL, or viral studies (PCR)
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CSF CharacteristicsBacterialBacterial ViralViral FungalFungal TBTB
Opening Opening PressurePressure
ElevatedElevated Slight Slight elevatedelevated
Normal Normal or Highor High
Usually Usually highhigh
GlcGlc LowLow NormalNormal LowLow LowLow
ProPro Very Very highhigh
NormalNormal HighHigh HighHigh
RbcsRbcs FewFew NoneNone NoneNone NoneNone
Wbcs Wbcs (c/mm3)(c/mm3)
>>200200 <<200200 <<5050 20-3020-30
DiffDiff PMNsPMNs MonoMono MonoMono MonoMono
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CT Before LP in Patients with Suspected Meningitis
301 pts with suspected meningitis; 235 (78%) had CT prior to LP
CT abnormal in 56/235 (24%); 11 pts (5%) had evidence of mass effect
Features associated with abnl. CT were:
age >60, immunocompromise, H/O CNS dz, H/O seizure w/in 7d, & selected neuro abnls
Hasbun, NEJM 2001;345:1727
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CT head Before LP(Cont.)
96/235 pts (41%) who underwent CT had none of features present at baseline
CT normal in 93 of these 96 pts (NPV 97%).
Of the 3 remaining patients, only 1 had mild mass effect on CT, and all 3 underwent lumbar puncture with no evidence of brain herniation
Hasbun, NEJM 2001;345:1727
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Consideration for lumbar puncture without
neuroimagingDavid Somand, MDa,WilliamMeurer, MD
Department of Emergency Medicine, University of Michigan, Taubman Center B1354
SPC #5303, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5303, USA
Age less than 60.
Immunocompetent.
No history of CNS disease.
No recent seizure (less than 1 week).
Normal sensorium and cognition.
No papilledema.
No focal neurologic defecits.
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BACTERIAL MENINGITIS
Managements
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APPROACH TO THE PATIENT WITH SUSPECTED MENINGITIS
Decision-Making Within the First 30 Minutes
Clinical AssessmentClinical Assessment
Mode of presentationMode of presentation Acute (< 24 hrs)Acute (< 24 hrs) Subacute (< 7 days)Subacute (< 7 days) Chronic (> 4 wks)Chronic (> 4 wks)
Historical/physical exam cluesHistorical/physical exam clues Clinical status of the patient (ABCD)Clinical status of the patient (ABCD)
Integrity of host defensesIntegrity of host defenses
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Management algorithm for adults with suspected bacterial meningitis.
Practice Guidelines for the Management of Bacterial Meningitis
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BACTERIAL MENINGITISAntimicrobial Rx
Therapy is generally IV, high dose, & bolus.
Dosing intervals should be appropriate for drug being administered.
Utilize “cidal” therapy whenever possible.
Initiate therapy promptly (ie, within 30 mins)
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THE THERAPY OF MENINGITISCNS Penetration
Good Diffusion Penicillins 3rd & 4th Gen Cephs Chloramphenicol Rifampin TSX
Poor Diffusion Early Gen Cephs Clindamycin AMGs Tetracyclines Macrolides
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EMPIRIC THERAPY OF MENINGITIS IN THE ADULT
Clinical Setting Likely Pathogens Therapy
Community-acquired S. Pneumoniae
N. meningitidis
[Listeria]
[H. influenzae]
Ceftriaxone
2 gm
q12h
+
Vancomycin 1-2 gm
12h
+/_
Ampicillin 2 gm q4h
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EMPIRIC THERAPY OF MENINGITIS IN THE ADULT
Closed head trauma S. pneumoniae Pen G 3-4 mu q4h
Streptococci +
Vancomycin 1-2 gm q12h
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EMPIRIC THERAPY OF MENINGITIS IN THE ADULT
Clinical Setting Likely Pathogens Therapy
High risk patients S. aureus Vancomycin 2-3 gm/d
Compromised hosts Gram negative +
Neurosurgical bacilli Ceftazidime 2 gm q8h or
Open head injury Listeria Cefepime 2 gm q8h
Nosocomial [Ceftriaxone 2 gm q12h]
Elderly [Cefotaxime 2 gm q4h]
+/-
Ampicillin 2 gm q4h
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BACTERIAL MENINGITISDuration of ATB Rx
Pathogen Duration of Rx (d)
H. influenzae 7
N. meningitidis 7
S. pneumoniae 10-14
L. monocytogenes 14-21
Group B strep 14-21
GNRs 21
NEJ1997;336:708
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CORTICOSTEROIDS AND MENINGITIS
Recent European study in adults suggested that Rx with dexa associated with ↓ in risk of unfavorable outcome (25%→15%, RR 0.59) & in mortality (15%→7%, RR for death 0.48).
Benefit primarily pts w/S. pneumo.
Dose of dex was 10mg IV q6h X 4d; per protocol, dex given concurrent with or 15-20 mins before 1st dose of ATBs.
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Acute bacterial meningitis Antibiotic prophylaxis
Is recommended for high-risk exposures to patients with Neisseria or Hib meningitis.(potentially share secretions).
Regimens include :Single-dose ciprofloxacin or ceftriaxone.Rifampin 600 mg every 12 hours for five doses.
There is no indication for prophylaxis for exposure to pneumococcal meningitis.
Quinolone resistance has been reported to Neisseria, and this class of antibiotics is no longer recommended for prophylaxis in parts of the United States.
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PREDICTORS OF ADVERSE CLINICAL OUTCOMES IN PTS WITH COMMUNITY-
ACQUIRED BACTERIAL MENINGITIS Aronin et al, AIM1998;129:862
Retrospecitve study; 269 pts (84% culture +).
Adverse clinical outcome in 36% of pts(Death 27%, neuro deficit 9%).
↓BP, altered MS, and seizures on presentation all independently associated with adverse clinical outcome.
Adverse outcomes in 5% of low risk pts (0 features), 37% of intermediate risk pts (1 feature), and 63% of high risk pts (2-3 features).
Delay in administration of appropriate ATB Rx also associated with adverse clinical outcome.
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Viral MeningitisVery common• clinical course is less fulminant compared to
bacterial
Often caused by enteroviruses
Polioviruses Coxsackieviruses Echoviruses
Treatment is supportive
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VIRAL ENCEPHALITIS
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IntroductionEncephalitis is an acute inflammatory process
affecting the brain
Viral infection is the most common and important cause, with over 100 viruses implicated worldwide
Symptoms Fever Headache Behavioral changes Altered level of consciousness Focal neurologic deficits Seizures
Incidence of 3.5-7.4 per 100,000 persons per year
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VIRAL ENCEPHALITISEnteroviruses
Polioviruses
Coxsackieviruses
Echoviruses
Togaviruses
Eastern equine
Western equine
Venezuelan equine
St. Louis
Powasson
California
West Nile
Herpesviruses
Herpes simplex
Varicella-zoster
Epstein Barr
Cytomegalovirus
Myxo/paramyxoviruses
Influenza/parainfluenzae
Mumps
Measles
Miscellaneous
Adenoviruses
LCM
Rabies
HIV
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Patient HistoryDetailed history critical to determine the likely cause of
encephalitis.
Prodromal illness, recent vaccination, development of few days → Acute Disseminated Encephalomyelitis (ADEM) .
Biphasic onset: systemic illness then CNS disease → Enterovirus encephalitis.
Abrupt onset, rapid progression over few days → HSE.
Recent travel and the geographical context: Africa → Cerebral malaria Asia → Japanese encephalitis High risk regions of Europe and USA → Lyme disease
Recent animal bites → Tick borne encephalitis or Rabies.
Occupation Forest worker, exposed to tick bites Medical personnel, possible exposure to infectious diseases.
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History cont.Season
Japanese encephalitis is more common during the rainy season.
Arbovirus infections are more frequent during summer and fall.
Predisposing factors: Immunosuppression caused by disease and/or drug
treatment. Organ transplant → Opportunistic infections HIV → CNS infections HSV-2 encephalitis and Cytomegalovirus infection (CMV)
Drug ingestion and/or abuse
Trauma
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Initial SignsHeadache
Malaise
Anorexia
Nausea and Vomiting
Abdominal pain
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Developing SignsAltered LOC – mild lethargy to deep coma.
AMS – confused, delirious, disoriented.
Mental aberrations: hallucinationsagitationpersonality change behavioral disorders occasionally frank psychosis
Focal or general seizures in >50% severe cases.
Severe focused neurologic deficits.
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Neurologic SignsVirtually every possible focal neurological
disturbance has been reported.
Most CommonAphasiaAtaxia Hemiparesis.Involuntary movementsCranial nerve deficits (ocular palsies, facial
weakness)
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Other Causes of Encephalopathy
Anoxic/Ischemic conditions
Metabolic disorders
Nutritional deficiency
Toxic (Accidental & Intentional)
Systemic infections
Critical illness
Malignant hypertension
Mitochondrial cytopathy (Reye’s and MELAS syndromes)
Hashimoto’s encephalopathy
Traumatic brain injury
Epileptic (non-convulsive status)
CJD (Mad Cow)
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Differential Diagnosis
Distinguish Etiology
(1) Bacterial infection and other infectious conditions (2) Parameningeal infections or partially treated
bacterial meningitis (3) Nonviral infectious meningitides where cultures may
be negative (e.g., fungal, tuberculous, parasitic, or syphilitic disease)
(4) Meningitis secondary to noninfectious inflammatory diseases
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VIRAL ENCEPHALITIS
DIAGNOSIS.
LP:
CSF usually colorless
- slightly pressure
- initially a neutrophilic pleocytosis, which rapidly converts to lymphocytes
- proteins are
- glucose is normal
PCR for HSE and other viral infection is diagnostic .
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VIRAL ENCEPHALITISDIAGNOSIS.
MRI:
May show temporal or orbitofrontal cortex enhancement or edema in HSE.
In most other acute viral encephalities , neuroimaging finding are nonspecific.
Can exclude subdural bleeds, tumor, and sinus thrombosis.
EEG: Non specific Diffuse slowing . Focal abnormalities in the temporal region . HSV
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Treatment. Only HSV disease has specific therapy available. Acyclovir
is capable of improving patient outcome.
dose : 10 mg/kg intravenously every 8 hours. Duration 14-21 days.
ganciclovir can be used in CMV infections. pleconaril has shown promise in enteroviral.
Outcomes
Outcomes are variable depending on etiology.
EEE and St. Louis encephalitis generally have high mortality rates and Severe neurologic sequelae among survivors.
WNV is associated with significant morbidity and morality.
Mortality of HSV encephalitis before acyclovir was 60% to 70%, and with treatment approximately 30%.
Cognitive disability,seizures, and motor deficits are common sequelae seen among survivors