Meningitis Flashcards

(96 cards)

1
Q

What are the three layers of the meninges?

A

Dura mater (outermost), arachnoid mater (middle), and pia mater (innermost). The subarachnoid space lies between the arachnoid and pia mater.

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2
Q

What is the definition of meningitis?

A

Inflammation of the meninges (particularly the arachnoid and pia mater). Can be caused by bacteria, viruses, fungi, parasites, drugs, and other agents.

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3
Q

What is acute bacterial meningitis (ABM)?

A

An acute purulent infection within the subarachnoid space. It is the most common form of suppurative (pus-forming) central nervous system infection.

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4
Q

What is the annual incidence of acute bacterial meningitis worldwide?

A

Approximately 2-5 per 100,000 adults in developed countries, but 10-100 per 100,000 in developing countries. Highest incidence in children under 5 and adults over 60.

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5
Q

What is the mortality rate of acute bacterial meningitis?

A

10-30% despite appropriate antibiotics. Mortality is highest with Streptococcus pneumoniae (20-30%), lowest with Neisseria meningitidis (5-10%).

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6
Q

List the most common causes of acute bacterial meningitis by age group.

A

Neonates: Group B streptococci, E. coli, Listeria monocytogenes. Infants/children: S. pneumoniae, N. meningitidis, H. influenzae type b. Adults (18-50): S. pneumoniae, N. meningitidis. Adults >50: S. pneumoniae, Listeria monocytogenes, aerobic Gram-negative bacilli.

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7
Q

What is the most common cause of community-acquired bacterial meningitis in adults?

A

Streptococcus pneumoniae (pneumococcus) – responsible for 50-70% of cases. Mortality is 20-30%, highest among the common pathogens.

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8
Q

Which bacteria is the second most common cause of bacterial meningitis in adults?

A

Neisseria meningitidis (meningococcus) – responsible for 10-35% of cases. More common in adolescents and young adults, especially in crowded living conditions (college dorms, military barracks).

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9
Q

Which bacteria is an important cause of meningitis in the elderly, alcoholics, and immunocompromised patients?

A

Listeria monocytogenes – a Gram-positive rod that causes foodborne illness. Typically presents with subtle onset, may cause rhombencephalitis (brainstem involvement).

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10
Q

List the risk factors for acute bacterial meningitis.

A

Pneumonia, sinusitis, otitis media, alcoholism, diabetes mellitus, malignancy, splenectomy (aspheric/hyposplenism), hypogammaglobulinemia, complement deficiency (especially late complement components C5-C9 for meningococcus), basilar skull fracture with CSF leak, ventriculoperitoneal shunt, neurosurgery.

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11
Q

Why are patients with complement deficiency at increased risk for meningococcal meningitis?

A

Late complement components (C5-C9) form the membrane attack complex (MAC), which is required for direct lysis of Neisseria species. Deficiency leads to recurrent meningococcal infections.

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12
Q

Why are asplenic patients at increased risk for bacterial meningitis?

A

The spleen is critical for clearing encapsulated bacteria (S. pneumoniae, H. influenzae, N. meningitidis) via opsonization and phagocytosis. Asplenic patients should receive vaccination against these organisms.

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13
Q

What is the classic triad of acute bacterial meningitis?

A

1) Fever, 2) Headache, 3) Neck stiffness (nuchal rigidity). Present in only 40-60% of patients initially. The full triad is present in only 30-50% of cases.

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14
Q

List other clinical features of acute bacterial meningitis.

A

Altered mental status (lethargy, irritability, confusion, coma), nausea, vomiting, photophobia (sensitivity to light), and seizures (present in 20-30%).

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15
Q

What is the most common neurological sign in bacterial meningitis?

A

Altered mental status – present in 70-80% of patients. Ranges from lethargy and confusion to deep coma.

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16
Q

What percentage of patients with bacterial meningitis present with seizures?

A

20-30% – more common in children. Seizures may be focal or generalized. New-onset seizures are a poor prognostic sign.

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17
Q

What is nuchal rigidity?

A

Neck stiffness on passive flexion – a classic sign of meningeal irritation. Patient cannot touch chin to chest due to pain and muscle spasm.

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18
Q

What is Kernig’s sign and how is it elicited?

A

With the patient lying supine, the hip is flexed at 90° and the knee also flexed. If meningeal irritation is present, attempts to passively extend the knee elicits pain in the lower back or posterior thigh.

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19
Q

What is Brudzinski’s sign and how is it elicited?

A

With the patient lying supine, it is positive when passive flexion of the neck results in spontaneous flexion of the hips and knees. This occurs due to meningeal irritation.

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20
Q

What is the sensitivity of Kernig’s and Brudzinski’s signs?

A

Both signs have low sensitivity (approximately 30-50%) but high specificity (80-95%). Their absence does NOT rule out meningitis, but their presence strongly suggests it.

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21
Q

List the signs of raised intracranial pressure in meningitis.

A

Reduced level of consciousness, papilledema (optic disc swelling), dilated poorly reactive pupils, sixth nerve palsies (CN VI – causes impaired lateral gaze), decerebrate or decorticate posturing, and Cushing reflex (bradycardia, hypertension, irregular respirations).

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22
Q

What is Cushing’s reflex?

A

A physiological response to increased intracranial pressure: hypertension (widened pulse pressure), bradycardia, and irregular respirations. It is a late sign of brainstem compression and impending herniation.

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23
Q

What is the difference between decorticate and decerebrate posturing?

A

Decorticate posturing (flexion of arms, extension of legs) indicates damage above the midbrain. Decerebrate posturing (extension of both arms and legs) indicates damage to the brainstem (midbrain or pons). Decerebrate posturing carries a worse prognosis.

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24
Q

What is the normal opening pressure on lumbar puncture?

A

50-150 mm H₂O (approximately 5-15 cm H₂O). In bacterial meningitis, it is elevated to 200-300 mm H₂O.

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25
What are the typical CSF findings in acute bacterial meningitis?
Opening pressure: 200-300 mm H₂O (elevated). WBC: 10-10,000 cells/μL (mostly neutrophils, >80%). Glucose: <40 mg/dL (<2.2 mmol/L) – low (CSF:serum glucose ratio <0.4). Protein: >45 mg/dL (>0.45 g/L) – elevated. Gram stain: positive in 60-80% of untreated cases. Culture: positive in 80-90%.
26
What are the typical CSF findings in acute viral meningitis?
Opening pressure: 90-200 mm H₂O (normal or mildly elevated). WBC: 25-500 cells/μL (mostly lymphocytes). Glucose: normal (CSF:serum ratio >0.6). Protein: mildly elevated (usually <150 mg/dL). Gram stain: negative. Culture: rarely positive (PCR is more sensitive).
27
What are the typical CSF findings in tuberculous meningitis?
Opening pressure: elevated (often >300 mm H₂O). WBC: 100-500 cells/μL (lymphocytes). Glucose: markedly low (<40 mg/dL). Protein: markedly elevated (100-500 mg/dL or higher – may cause xanthochromia or clotting). Acid-fast bacilli stain: low yield (10-20%). Culture takes weeks. PCR (GeneXpert) is preferred.
28
What are the typical CSF findings in fungal meningitis (e.g., cryptococcal)?
Opening pressure: elevated (often >250 mm H₂O). WBC: 20-200 cells/μL (lymphocytes). Glucose: low to very low. Protein: elevated. India ink stain: positive in 50-80% of cryptococcal meningitis (encapsulated yeast). Cryptococcal antigen (CrAg) is highly sensitive and specific (>95%).
29
What is the most important diagnostic test for meningitis?
Lumbar puncture (LP) with CSF analysis – it is essential for diagnosis. However, CT scan should be performed before LP if there is concern for raised ICP or mass lesion (to prevent brain herniation).
30
When should CT scan be performed before lumbar puncture?
In patients with: 1) Immunocompromised state, 2) History of CNS disease (mass, stroke, abscess), 3) New-onset seizure within 1 week, 4) Papilledema, 5) Focal neurological deficit, 6) Altered level of consciousness, 7) Moderate-to-severe impairment of consciousness (GCS <12).
31
What is the empirical antibiotic regimen for community-acquired bacterial meningitis in adults (18-50 years)?
Ceftriaxone (2g IV every 12 hours) OR cefotaxime (2g IV every 4-6 hours) + vancomycin (15-20 mg/kg IV every 8-12 hours, with loading dose). Dexamethasone 0.15 mg/kg IV given 20 minutes before antibiotics.
32
What is the empirical antibiotic regimen for community-acquired bacterial meningitis in adults >50 years or with alcoholism/debilitating illness?
Ampicillin (2g IV every 4 hours) + ceftriaxone/cefotaxime + vancomycin – to cover Listeria monocytogenes (ampicillin is added). Plus dexamethasone as above.
33
What is the empirical antibiotic regimen for hospital-acquired, post-traumatic, or post-neurosurgical meningitis?
Ampicillin + ceftazidime (2g IV every 8 hours) OR meropenem (2g IV every 8 hours) + vancomycin. Cover for Pseudomonas aeruginosa (ceftazidime or meropenem) and Staphylococcus aureus (vancomycin).
34
What is the specific antibiotic for Streptococcus pneumoniae in meningitis?
Penicillin G (if susceptible) + ceftriaxone/cefotaxime/cefepime + vancomycin. However, due to increasing penicillin and cephalosporin resistance, vancomycin should be used empirically until susceptibilities are known.
35
What is the specific antibiotic for Neisseria meningitidis?
Penicillin G (24 million units/day IV in divided doses) OR ampicillin (12g/day IV) + ceftriaxone (2g IV every 12 hours) OR cefotaxime (2g IV every 4-6 hours).
36
What is the specific antibiotic for Listeria monocytogenes?
Ampicillin (2g IV every 4 hours) + gentamicin (1-2 mg/kg IV every 8 hours – synergistic). Duration: 21 days minimum. Listeria is NOT covered by cephalosporins (they are ineffective).
37
What is the specific antibiotic for Haemophilus influenzae type b?
Ceftriaxone (2g IV every 12 hours) OR cefotaxime (2g IV every 4-6 hours) OR cefepime (2g IV every 8 hours).
38
What is the specific antibiotic for Pseudomonas aeruginosa?
Ceftazidime (2g IV every 8 hours) OR cefepime (2g IV every 8 hours) OR meropenem (2g IV every 8 hours). Often combined with an aminoglycoside (gentamicin or tobramycin) for synergy.
39
What is the role of dexamethasone in bacterial meningitis?
IV dexamethasone 0.15 mg/kg every 6 hours for 2-4 days, with the first dose given 15-20 minutes BEFORE antibiotics. It inhibits TNF-α production, reduces subarachnoid inflammation, and reduces mortality and neurological sequelae (especially hearing loss). Strongest evidence for S. pneumoniae meningitis.
40
In which patients should dexamethasone be avoided in bacterial meningitis?
Dexamethasone may reduce CNS penetration of vancomycin and may be harmful in patients with septic shock. It should NOT be given if antibiotics have already been administered (no benefit if given after antibiotics).
41
What is the duration of antibiotic therapy for bacterial meningitis?
Neisseria meningitidis: 7 days. Haemophilus influenzae: 7 days. Streptococcus pneumoniae: 10-14 days. Listeria monocytogenes: 21 days. Gram-negative bacilli: 21 days.
42
What is chemoprophylaxis for meningococcal meningitis and who should receive it?
Rifampin (600 mg orally every 12 hours for 2 days) OR ceftriaxone (250 mg IM once) OR ciprofloxacin (500 mg orally once). Indicated for close contacts (household members, daycare, intimate contacts, healthcare workers with direct exposure to respiratory secretions).
43
What is the duration of chemoprophylaxis for H. influenzae type b meningitis?
Rifampin 20 mg/kg (max 600 mg) orally daily for 4 days. Indicated for all household contacts when there is at least one unvaccinated or incompletely vaccinated child under 4 years.
44
What is the most common cause of viral meningitis?
Enteroviruses (echoviruses, coxsackieviruses, polioviruses) – account for 80-90% of viral meningitis cases where a specific cause is identified. Most common in summer and early autumn.
45
List other causes of viral meningitis.
Varicella-zoster virus (VZV), Herpes simplex virus 2 (HSV-2) – more common than HSV-1 in meningitis, mumps virus, HIV, cytomegalovirus (CMV), Epstein-Barr virus (EBV), lymphocytic choriomeningitis virus (LCMV), and arboviruses (West Nile, St. Louis encephalitis, etc.).
46
What is the typical clinical presentation of viral meningitis?
Headache (almost always present – frontal or retro-orbital, with photophobia and pain on eye movement), fever (initially low-grade, becomes high-grade), neck stiffness, irritability, malaise, myalgia, anorexia, nausea, vomiting, diarrhea. Marked confusion, stupor, and coma are rare and suggest encephalitis.
47
What is the most important investigation for viral meningitis?
CSF analysis shows lymphocytic pleocytosis (25-500 WBC/μL, predominantly lymphocytes), normal or mildly elevated protein, normal glucose. CSF PCR is the gold standard for diagnosing enterovirus, HSV, VZV, CMV, EBV, and HHV-6 meningitis.
48
What is the treatment for viral meningitis?
Most cases are self-limited and require symptomatic treatment: analgesics, antipyretics, antiemetics, fluid and electrolyte management. HSV, EBV, VZV, or CMV meningitis requires antiviral therapy: acyclovir (10 mg/kg IV every 8 hours for 10-14 days) for HSV/VZV; ganciclovir/foscarnet for CMV.
49
What is the definition of encephalitis?
Inflammation of the brain parenchyma. Evidence of associated meningitis is present in many patients (giving meningoencephalitis).
50
What are the most common causes of viral encephalitis?
HSV-1 and 2 (most common cause of sporadic fatal encephalitis worldwide), arboviruses (West Nile, St. Louis encephalitis, Japanese encephalitis, Eastern/Western equine encephalitis), EBV, VZV, CMV, HIV, rabies (rare but almost uniformly fatal).
51
What is the most common cause of sporadic viral encephalitis worldwide?
Herpes simplex virus type 1 (HSV-1) – accounts for 10-20% of all viral encephalitis cases. Without treatment, mortality exceeds 70%; with acyclovir, mortality is 20-30%.
52
What is the classic presentation of HSV encephalitis?
Acute onset of fever, headache, altered mental status (lethargy, confusion, coma), seizures (focal or generalized), focal neurological deficits (aphasia, hemiparesis), behavioral changes (personality change, psychosis), hallucinations, and memory impairment.
53
What is the characteristic MRI finding in HSV encephalitis?
Focal bilateral temporal lobe involvement – T2-weighted and FLAIR images show hyperintensity in the medial temporal lobes, insular cortex, and orbital frontal cortex. Often asymmetric. Hemorrhage may occur in advanced cases.
54
What is the characteristic EEG finding in HSV encephalitis?
Periodic sharp-and-slow wave complexes originating in one or both temporal lobes (typically every 2-4 seconds). Highly suggestive of HSV encephalitis but not pathognomonic.
55
What is the treatment for HSV encephalitis?
IV acyclovir (10 mg/kg every 8 hours for 14-21 days, adjusted for renal function). Higher doses than for meningitis. Treatment should NOT be delayed for diagnostic confirmation – start empirically if HSV encephalitis is suspected.
56
What is the definition of a brain abscess?
A focal, suppurative (pus-forming) infection within the brain parenchyma, typically surrounded by a well-vascularized capsule. It is a neurosurgical emergency.
57
List the risk factors for brain abscess.
Otitis media (most common – leads to temporal lobe or cerebellar abscess), mastoiditis, sinusitis (frontal sinus – leads to frontal lobe abscess), dental infection (odontogenic – leads to frontal lobe abscess), head trauma (penetrating injury), neurosurgery, hematogenous spread from endocarditis, congenital heart disease (right-to-left shunt – paradoxical embolus), immunocompromised state.
58
What is the most common source of brain abscess?
Otitis media and mastoiditis – account for 30-50% of brain abscesses, typically causing temporal lobe or cerebellar abscess on the same side as the ear infection.
59
List the bacterial causes of brain abscess in immunocompetent patients.
Streptococcus species (especially S. intermedius, S. anginosus – most common), Proteus species, Escherichia coli, Bacteroides species (anaerobes), Staphylococcus aureus (especially post-traumatic or post-surgical).
60
List the causes of brain abscess in immunocompromised patients.
Nocardia species (Nocardia asteroides), Toxoplasma gondii (most common in HIV/AIDS – causes multiple ring-enhancing lesions), Aspergillus species, Candida species, Cryptococcus neoformans, Taenia solium (neurocysticercosis – parasitic, not truly an abscess).
61
What is the classic triad of brain abscess?
1) Headache (most common – 70-80%), 2) Fever (40-60%), 3) Focal neurological deficit (hemiparesis, aphasia, visual field defect – 40-60%). The full triad is present in less than 50% of patients initially.
62
What is the most common symptom of brain abscess?
Headache – present in 70-80% of patients. Usually progressive, may be localized to the side of the abscess, and worsens with Valsalva maneuver (coughing, sneezing, straining).
63
List other clinical features of brain abscess.
New-onset seizures (25-30% – may be focal or generalized), signs of raised intracranial pressure (papilledema, nausea/vomiting, altered mental status), nuchal rigidity (if abscess ruptures into the ventricle or if meningitis is present).
64
What is the best imaging modality for brain abscess?
Contrast-enhanced MRI (with gadolinium) is superior to CT. Shows a central hypointense (dark) area (necrotic pus) surrounded by a smooth, thin, ring-enhancing capsule with surrounding cerebral edema (vasogenic edema).
65
What does a brain abscess look like on contrast-enhanced CT?
A focal area of hypodensity (dark) surrounded by ring enhancement (bright rim) with surrounding hypodense edema. The ring is typically smooth and thin (<3 mm).
66
How do you differentiate a brain abscess from a necrotic brain tumor on imaging?
Abscess: smooth, thin, regular ring enhancement; central diffusion restriction on DWI (because pus is viscous); multiple lesions often satellite; surrounding edema. Necrotic tumor: thick, irregular, nodular ring enhancement; no central diffusion restriction; usually solitary.
67
What is the treatment for brain abscess?
1) High-dose parenteral antibiotics (empirical then targeted based on culture), 2) Neurosurgical drainage (aspiration or excision) – indicated for most abscesses >2.5 cm, those causing mass effect, or those in eloquent areas, 3) Treatment of underlying source (e.g., mastoidectomy, sinus drainage), 4) ICP management if needed (mannitol, steroids – controversial).
68
What is the empirical antibiotic regimen for brain abscess?
Ceftriaxone (2g IV every 12 hours) OR cefotaxime (2g IV every 6 hours) + metronidazole (500 mg IV every 8 hours – covers anaerobes) + vancomycin (if S. aureus or MRSA suspected). Duration: 4-8 weeks (typically 6 weeks).
69
Why is metronidazole important in brain abscess treatment?
Because anaerobes (Bacteroides, Fusobacterium, Peptostreptococcus) are common in brain abscesses originating from otitis media, sinusitis, or dental infections. Metronidazole has excellent CNS penetration and covers these organisms.
70
What is the duration of antibiotic therapy for brain abscess?
4-8 weeks (typically 6 weeks). Initial IV therapy for 2-4 weeks, followed by oral therapy if clinically stable and abscess is resolving on imaging. Serial imaging (CT/MRI) is needed to confirm resolution.
71
What is the mortality rate of brain abscess?
5-15% in the modern era with combined surgical and medical management. Higher mortality in: immunocompromised patients, multiple abscesses, rupture into ventricles (ventriculitis – mortality >50%), deep-seated abscesses, delayed diagnosis.
72
What is the complication of brain abscess rupture into the ventricle?
Ventriculitis (ependymitis) – a life-threatening complication with mortality >50%. Presents with sudden deterioration, high fever, meningismus, and purulent CSF. Requires IV and intraventricular antibiotics (e.g., intraventricular vancomycin + ceftazidime).
73
What is the most common long-term complication of bacterial meningitis?
Sensorineural hearing loss – occurs in 10-30% of survivors, most common with S. pneumoniae. Other complications: intellectual deficits, memory impairment, seizures (post-meningitis epilepsy), ataxia, hydrocephalus (communicating or obstructive), cortical blindness, and focal neurological deficits.
74
What is the vaccine available for Haemophilus influenzae type b (Hib) meningitis?
Hib conjugate vaccine (ActHIB, Hiberix, PedvaxHIB) – part of routine childhood immunization (given at 2, 4, 6, and 12-15 months). Has dramatically reduced Hib meningitis by >95% in vaccinated populations.
75
What is the vaccine available for Neisseria meningitidis?
Meningococcal conjugate vaccines: MenACWY (Menactra, Menveo) – covers serogroups A, C, W, Y; given at 11-12 years with booster at 16 years. MenB (Bexsero, Trumenba) – covers serogroup B; given at 16-18 years (shared clinical decision-making).
76
What is the vaccine available for Streptococcus pneumoniae?
Pneumococcal conjugate vaccine PCV13 (Prevnar 13) – covers 13 serotypes, given to children at 2, 4, 6, 12-15 months. Pneumococcal polysaccharide vaccine PPSV23 (Pneumovax 23) – for adults ≥65 and high-risk patients.
77
What is the WHO recommendation for meningococcal vaccination for Hajj pilgrims?
All Hajj and Umrah pilgrims must receive quadrivalent meningococcal vaccine (MenACWY) at least 10 days before arrival. The vaccine is valid for 3-5 years depending on the formulation.
78
What is the prophylaxis for close contacts of a patient with bacterial meningitis?
Meningococcus: rifampin (600 mg bid x 2 days), ceftriaxone (250 mg IM once), or ciprofloxacin (500 mg once). H. influenzae: rifampin (20 mg/kg/day x 4 days, max 600 mg/day). For pneumococcus: NO routine prophylaxis for close contacts.
79
What is the management of a patient with basilar skull fracture and CSF leak to prevent meningitis?
Prophylactic antibiotics are NOT routinely recommended (no proven benefit, may increase resistant organisms). Close observation for signs of meningitis. Surgical repair of persistent CSF leak (>7-14 days) is indicated to reduce meningitis risk.
80
What is the most common cause of recurrent meningitis?
Anatomical defects: basilar skull fracture with CSF leak (most common), Mondini dysplasia (inner ear malformation), dural ectasia, and neurocutaneous fistula. Also: complement deficiencies (meningococcus), hypogammaglobulinemia (encapsulated bacteria), and parameningeal foci (chronic otitis media, sinusitis).
81
What is Mollaret's meningitis?
Recurrent benign lymphocytic meningitis, most commonly caused by HSV-2. Presents with 2-10 episodes of fever, headache, meningismus, and CSF lymphocytic pleocytosis that resolves spontaneously within 2-7 days. Treatment: acyclovir.
82
What is the CSF finding in Mollaret's meningitis?
Lymphocytic pleocytosis (up to several thousand cells), elevated protein, normal glucose. Large 'Mollaret cells' (activated macrophages with irregular nuclei) may be seen. PCR for HSV-2 is positive in most cases.
83
What is the management of raised intracranial pressure in meningitis?
1) Head-up positioning (30-45°). 2) IV mannitol (1 g/kg bolus) or hypertonic saline (3% NaCl – 250 mL bolus). 3) Short-term hyperventilation (target PaCO₂ 25-30 mmHg) – temporizing measure only. 4) CSF drainage via external ventricular drain (EVD) if hydrocephalus is present. 5) Decompressive craniectomy for refractory herniation.
84
What is the role of hyperventilation in raised ICP?
Hyperventilation lowers PaCO₂, causing cerebral vasoconstriction and reducing cerebral blood volume, rapidly lowering ICP. However, it also reduces cerebral blood flow and may worsen ischemia. Use only as a temporizing measure for impending herniation, and not for prolonged periods.
85
What is the triad of Cushing's response to raised ICP?
Hypertension (with widened pulse pressure), bradycardia, and irregular respirations (Cheyne-Stokes or ataxic breathing). This is a late sign indicating brainstem compression and impending herniation.
86
What is the most common cause of meningitis in a patient with a ventriculoperitoneal (VP) shunt?
Coagulase-negative staphylococci (Staphylococcus epidermidis) – most common. Staphylococcus aureus (also common). Gram-negative bacilli (especially after abdominal surgery). Treatment: IV antibiotics (vancomycin + ceftazidime) plus shunt removal and replacement.
87
What is the most common cause of meningitis in a patient with HIV/AIDS?
Cryptococcal meningitis (Cryptococcus neoformans) – most common cause of subacute meningitis in advanced HIV (CD4 <100). Also: tuberculous meningitis, toxoplasmosis (encephalitis, not meningitis), neurosyphilis, and primary CNS lymphoma.
88
What is the India ink stain for cryptococcal meningitis?
A negative staining technique for Cryptococcus neoformans – the yeast appears as a clear halo (capsule) against a dark background. Sensitivity is 50-80% in CSF. Cryptococcal antigen (CrAg) test is more sensitive (>95%).
89
What is the treatment for cryptococcal meningitis in HIV?
Induction: IV amphotericin B (0.7-1 mg/kg/day) + oral flucytosine (100 mg/kg/day) for 2 weeks. Consolidation: oral fluconazole (400 mg/day) for 8 weeks. Maintenance: fluconazole (200 mg/day) until CD4 >100 for >6 months. Flucytosine is often unavailable in resource-limited settings.
90
What is the CSF opening pressure in cryptococcal meningitis and why is it important?
Often markedly elevated (>300 mm H₂O). High pressure is associated with worse outcomes and requires therapeutic lumbar puncture (removing CSF to lower pressure).
91
What is the most common cause of parasitic meningitis?
Naegleria fowleri – causes primary amebic meningoencephalitis (PAM). Acquired from warm freshwater (lakes, hot springs, poorly chlorinated swimming pools). Enters through the nasal mucosa and cribriform plate. Rapidly fatal (mortality >97%). CSF shows motile trophozoites.
92
What is the most common cause of eosinophilic meningitis?
Angiostrongylus cantonensis (rat lungworm) – transmitted by ingestion of intermediate hosts (snails, slugs, freshwater shrimp, or contaminated vegetables). Presents with severe headache, paresthesias, and CSF eosinophilia (>10% eosinophils). Treatment: supportive (steroids may help).
93
What is the most common cause of meningitis in a patient with a cochlear implant?
Streptococcus pneumoniae – due to the implant providing a pathway from the middle ear to the cochlea and then to the subarachnoid space. Vaccination against pneumococcus is strongly recommended before implantation.
94
What is the most common cause of meningitis following head trauma with CSF rhinorrhea?
Streptococcus pneumoniae (pneumococcus) – most common. Recurrent episodes suggest an anatomical defect that requires surgical repair.
95
What is the most common cause of neonatal meningitis?
Group B streptococci (GBS – Streptococcus agalactiae) – most common in developed countries. E. coli (especially K1 strain) – most common in developing countries. Listeria monocytogenes (associated with contaminated food).
96
What is the prevention strategy for neonatal group B streptococcal meningitis?
Maternal screening for GBS rectovaginal colonization at 35-37 weeks gestation. Intrapartum antibiotic prophylaxis (IV penicillin G or ampicillin) for colonized mothers, those with preterm labor, prolonged rupture of membranes (>18 hours), or intrapartum fever.