Teaching Clinic - Meningitis Flashcards
What is done to rule out normal ICP?
- Non contrast CT brain
- Fundoscopy (as normal CT brain does not rule out increased ICP): papilledema
LP:
*
TCC 307 (neutrophil 76%)
protein 1.87 g/L
glucose 1.1 mmol/L (blood 8.0)
Gram stain -ve
C/ST -ve
?? DDX
action?
Acute bacterial meningitis
Tuberculous meningitis
Other rare meningitis (parasitic infection, leptospirosis (transmitted by urine of animals near lakes))
Bacterial cerebritis (early small brain abscess not seen on CT scan)
Action: IV ceftriaxone (rocephin) + ampicillin (covers for leptospirosis) (total for 2 weeks)
how will CSF change after bacterial meningitis mx?
Lymphocyte predominant after treating bacterial meningitis is ok
BBB broken down: so elevated protein is ok
Glucose should improve the fastest (if below 50% not satisfied)
cause?
What to do next?
Persistent source of primary infection (e.g. pneumonia, bacterial endocarditis, mastoiditis or otitis media)
cerebritis or early small cerebral abscess
Inadequate immunity (prolonged antibiotics therapy required as for immunocompromised patient)
Consult micbio
MRI brain with gadolinium contrast
Consult cardiologist? echocardiogram
Explain condition to patient and relatives
What to do?
If impaired conciousness do Hstix and ECG
non contrast CT brain due to reduced GCS
What is seen and mx?
Hyperdensity in the pre-pontine cistern surrounding the pons
Hydrocephalus complicating subarachnoid hemorrhage
Consult neurosurgeon (due to intracerebral hemorrhage)
Do CT angiogram
Stenting, clipping
Cortical bone necrosis
Radiation induced arteritis: ischemia to the bone and cause necrotic bone and causing easier infection
Breakdown for result of patient 1
- SAH from ruptured pseudoaneurysm (dissection) of vertebrae
- RT induced arteritis and complicating osteomyelitis
- Infection spread from infected necrotic clivus complicating RT for NPC
- Infected necrotic bone –> non resolving meningitis
- Operation: infected necrotic bone: grew bacteroides (anaerobes)
Rx: vancomycin +metronidazole x 6 weeks and stents oinserted in sites of ruptured pseudoaneurysm
Common sx of ABM
sx triad: head, fever, photophobia
Most commonly reported Sx and signs: Fever, neck stiffness, altered mental state (GCS <14)
Timeline of ABM
B:
C: staph aureus rash
D: Ecchymosis (soles of foot)
E: meningococcal rash (neisseria meningitidis)
All start antibiotics before
Thrombocytopenia, DIC, sepsis
What meningitis?
Strept pneumoniae
Herpes labialis (mouth crust)
Strept suis meningitis presentation?
Deafness: occupational illness (can apply for compensation)
A: gram negative diplococci
B: gram negative bacilli (enterococci: e.coli, klebsiella)
C: streptococcus suis
D: drained skin lesion (gram positive diplococci)
ddx of ABM
Lab Ix in acute bacterial meningitis
C/I for lumbar puncture in ABM?
What antibiotics in ABM?
Duration of antibiotics in ABM?
3rd gen cephalosporins (cefotaxime, ceftriaxone)
If clinical condition not improve by 48 hours after commencing appropriate antibiotics what to consider?
Complications of ABM
Hydrocephalus, consult neurosurg for ventriculoperitoneal shunt and obtain CSF fluid
TB and fungal meningitis
Than had ischemic stroke (R hemiplegia and hemieglect) complication of meningitis
Bilateral CN6 palsy cause?
False localizing sign caused by increased ICP
basal meningies (gadolinium enhancement)
dilated ventricles
Rim enhancing tuberculous abscess (bottom left)
Thickened basal meninges (bottom right)
Circle of willis spread of infection (infective arteritis)
tuberculous meningitis
Spinal cord compression: paraplegia
anti-TNFa causes reactivation of TB (must know)
Can give isoniazid prophylaxis
Treatment for TBM
2 (isoniazid (peripheral neuropathy –> give vit B6), rifampicin, ethambutol, pyrazinamide) + 9 (isoniazid + rifampicin)
If HIV+ –> give dexamethasone
T1W gadolinium enhancement in brain and meninges
Abnormal gyral patterns
ddx: leptomeningeal carcinomatosis
PET CT done and found hypermetabolic lesions in lung
Bronchoscopy and LN and/or lesion biopsy: cryptococcus neoformans on indian ink stain
Liposomal amphoterin B and flucytosine given for 26 days
Thrombocytopenia due to flucytosine (myelosuppression)
Previous stroke from cardioembolic stroke from rheumatic heart disease
Abnormal gyral enhancement
What is most common fungal meningitis?
Mechanism of infection?
- Encapsulated yeast, worldwide distribution
- In soil, bird excreta, animals, can even colonize humans
- Via inhalation of small yeast forms from the environment (when immunocompromised –> can present with hilar lymphadenopathy)
- Once in host, develop large polysaccharide capsules that
- strongly resist phagocytosis
- Most pulmonary infections are asymptomatic
- Spread from lung and intrathoracic LN to circulate in
blood —> distant infection, most common to the CNS
Cryptococcus neoformans resistance?
- Primarily on cell-mediated immunity
- Natural killer cells (NK cells) - important in eliminating the initial infection in animal studies
- Complements - important to prevent dissemination from lung to the CNS
- Lymphocyte f(x) abnormal in most patients with disseminated cryptococcosis : CD4 T cells essential in
preventing dissemination & recurrence after Rx
What are predisposing factors for cryptococcus infection
- AIDS – HIV infection
- RE malignancies – lymphoma, and other cancers
- Sarcoidosis
- Organ transplantation
- Collagen vascular diseases
- Corticosteroid therapy
- DM
- Renal failure/dialysis
- Solid organ transplant recipients
- Idiopathic CD4 lymphocytopenia
- Other immunological disorders impaired CD4 T cell f(x)
Clinical features of cryptococcal CNS infection
Subacute/Chronic Meningitis OR Parenchymal syndromes
Most common presentation in normal host = meningitis
Others :
1. Cerebral abscesses
2. Isolated granulomatous lesion, cryptococcoma
3. Chronic — mimick progressive dementia
4. Visual loss with raised ICP poor Px
Cryptococcal parenchymal syndromes
- Diffuse granulomatous infiltrates
- Solitary abscesses
- Multiple microabscesses or macroabscesses
- Meningeal & subarachinoid inflammation –> vessel occlusion
- Vasculitis/arteritis (cryptococcus) —> small vessel thromboses formed by hyphae or pseudohyphae, or microinfarcts in areas of vasculitis
- Vessel wall invasion & SAH due to ruptured mycotic
aneurysm (emboli from cryptococcal endocarditis)
What to monitor with cryptococcal meningitis mx?
Reduce dose of amphotericin B and 5-flucytosine with renal
impairment
Toxicity of 5-flucytosine: Blood, Liver, Gastrointestinal
What to do before stopping rx for cryptococcal meningitis?
Before stopping Rx – repeating LP:
1. CSF glucose normal
2. CSF protein on declining trend
3. Indian Ink stain may be +ve when CSF culture turns -ve
(positive stain NOT = active disease)
If CSF still grows cryptococcus, acute Rx should be continued + consider dose adjustment or addition of other antifungal agents.
Mx for cryptococcal meningitis?
both amphotericin-B + flucytosine cross the blood placental barrier