PEDIATRICS SLIDES ONLY > MENINGITIS > Flashcards

MENINGITIS Flashcards

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1
Q

What is meningitis?

A

Acute inflammation of the meninges (pia, arachnoid, and dura) covering the brain and spinal cord.

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2
Q

What layers are specifically involved in bacterial meningitis?

A

Pia mater and arachnoid mater (leptomeninges).

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3
Q

What space is primarily affected in bacterial meningitis?

A

Subarachnoid space.

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4
Q

Define bacterial meningitis.

A

Acute pyogenic inflammation of the leptomeninges and subarachnoid space caused by bacterial invasion of the CSF.

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5
Q

Why is bacterial meningitis considered a pediatric emergency?

A

Because it rapidly leads to cerebral edema, raised intracranial pressure, neurological damage, and death if untreated.

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6
Q

Where do most bacteria causing meningitis initially colonize?

A

The nasopharynx.

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7
Q

Name common organisms that colonize the nasopharynx before meningitis.

A

Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae.

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8
Q

Other sites of bacterial colonization before meningitis include which organs?

A

Skin, respiratory tract, gastrointestinal tract, genitourinary tract.

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9
Q

How do bacteria evade host immunity at mucosal surfaces?

A

Polysaccharide capsule and IgA protease production.

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10
Q

What is the function of the polysaccharide capsule?

A

Prevents phagocytosis by host immune cells.

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11
Q

What is the most common route of spread to the meninges?

A

Hematogenous spread.

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12
Q

What is direct contiguous spread?

A

Spread from nearby infections such as sinusitis, otitis media, or mastoiditis.

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13
Q

Give examples of direct CNS entry routes.

A

Skull base fracture, head trauma, neurosurgery.

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14
Q

How is meningitis transmitted in neonates?

A

Vertical transmission from maternal genital tract or horizontal transmission from caregivers.

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15
Q

How do bacteria cross the blood–brain barrier?

A

Endothelial penetration, tight junction disruption, or infected leukocytes (Trojan horse mechanism).

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16
Q

Why do bacteria multiply rapidly in CSF?

A

CSF has low immunoglobulins and complement.

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17
Q

Which bacterial components trigger inflammation in meningitis?

A

Endotoxin, peptidoglycan, lipoteichoic acid.

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18
Q

Which CNS cells are activated during meningitis?

A

Microglia, astrocytes, endothelial cells.

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19
Q

Which inflammatory cytokines are released?

A

TNF-α, IL-1, IL-6.

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20
Q

What effect do cytokines have on the blood–brain barrier?

A

Increase permeability.

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21
Q

What cells predominate in CSF during bacterial meningitis?

A

Neutrophils.

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22
Q

What type of exudate forms in bacterial meningitis?

A

Protein-rich purulent exudate.

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23
Q

Describe the gross appearance of meninges in bacterial meningitis.

A

Thickened, congested, opaque, covered with fibropurulent exudate.

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24
Q

Where is the exudate most prominent?

A

Cerebral convexities and base of the brain.

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25
What may be seen in ventricles and aqueduct?
Pus.
26
What inflammatory cells dominate microscopically?
Polymorphonuclear leukocytes.
27
What vascular change occurs in meningitis?
Vasculitis of meningeal and cerebral vessels.
28
What other microscopic features are seen?
Fibrin deposition and bacteria within exudate.
29
Name the three types of cerebral edema in meningitis.
Vasogenic, cytotoxic, interstitial.
30
What causes vasogenic edema?
Increased vascular permeability.
31
What causes cytotoxic edema?
Neuronal and glial cell injury due to ischemia and toxins.
32
What causes interstitial edema?
Obstruction of CSF outflow causing increased hydrostatic pressure.
33
What is the final consequence of cerebral edema?
Raised intracranial pressure.
34
What happens to cerebral vessels in meningitis?
Vasculitis, endothelial injury, thrombosis.
35
What results from reduced cerebral perfusion?
Ischemia, infarction, cortical necrosis.
36
What happens to CSF opening pressure?
It is increased.
37
Describe CSF appearance in bacterial meningitis.
Turbid or purulent.
38
Why is CSF protein increased?
Albumin leakage due to BBB disruption.
39
Why is CSF glucose reduced?
Increased bacterial metabolism and impaired glucose transport.
40
What type of pleocytosis occurs?
Neutrophilic pleocytosis.
41
Blockage of arachnoid villi leads to what?
Communicating hydrocephalus.
42
Blockage of ventricular pathways causes what?
Obstructive hydrocephalus.
43
Why are cranial nerves affected in meningitis?
Compression or inflammation by basal exudate.
44
Which cranial nerves are commonly involved?
II, III, VI, VIII.
45
What is the most common long-term sequel of bacterial meningitis?
Sensorineural hearing loss.
46
What causes hearing loss in meningitis?
Auditory neuritis, labyrinthitis, or central pathway damage.
47
What is nuchal rigidity?
Resistance to passive neck flexion.
48
Describe Kernig’s sign.
Pain and resistance on knee extension with hip flexed to 90°.
49
Describe Brudzinski’s sign.
Neck flexion causing involuntary hip and knee flexion.
50
Why are meningeal signs often absent in infants?
Immature nervous system and open sutures/fontanels.
51
Does absence of meningeal signs exclude meningitis in infants?
No.
52
What is the most important sign of raised ICP in infants?
Bulging anterior fontanel.
53
Name other signs of raised ICP in infants.
Increasing head circumference, high-pitched cry, vomiting, seizures, lethargy.
54
Why may the fontanel not bulge in dehydration?
Reduced CSF volume despite raised pressure.
55
How common is subdural effusion in infant meningitis?
Up to 50%.
56
Which organism is commonly associated with subdural effusion?
Haemophilus influenzae.
57
Clinical clues to subdural effusion include what?
Enlarging head circumference, bulging fontanel, failure to improve, focal deficits.
58
Why do seizures occur in meningitis?
Cerebritis, infarction, electrolyte imbalance.
59
What does deep coma indicate?
Poor prognosis.
60
Cutaneous signs of meningococcaemia include?
Petechiae and purpura.
61
What causes shock in meningococcaemia?
Endotoxin-mediated microvascular dysfunction.
62
Is Waterhouse–Friderichsen syndrome still used?
No, term is largely obsolete.
63
Mortality of meningococcal meningitis alone?
~8%.
64
Mortality with meningococcaemia?
~40%.
65
What age group is most commonly affected by meningitis?
Children under 5 years of age.
66
Which sex is more commonly affected by meningitis?
Males are more commonly affected than females.
67
In which season is meningitis more common in Africa?
Dry season.
68
What is the predominant cause of meningitis in Africa?
Neisseria meningitidis.
69
What serogroup of Neisseria meningitidis is common in Africa?
Serogroup A (also C, Y, W135 in newer outbreaks).
70
What is the African meningitis belt?
A region between 5°–15° North of the equator stretching from Gambia to Ethiopia.
71
How does head trauma predispose to meningitis?
Skull base fractures allow direct entry of organisms into the CNS.
72
Why does mastoiditis increase the risk of meningitis?
Due to contiguous spread from middle ear structures.
73
How does immunosuppressive therapy increase meningitis risk?
It impairs host immune response to infections.
74
Why are immunodeficiency states a risk factor?
Reduced ability to clear encapsulated organisms.
75
How does sickle cell disease predispose to meningitis?
Functional asplenia increases susceptibility to encapsulated bacteria.
76
Why does splenectomy increase meningitis risk?
Loss of splenic clearance of encapsulated organisms.
77
How does overcrowding increase meningitis risk?
Facilitates respiratory droplet transmission.
78
Why is otitis media a risk factor?
Direct contiguous spread to the meninges.
79
What is the most common presenting symptom of meningitis?
Fever.
80
Why is headache an important symptom?
Due to meningeal irritation and raised intracranial pressure.
81
Why does vomiting occur in meningitis?
Raised intracranial pressure stimulates the vomiting center.
82
Why is neck stiffness asked about in history?
It indicates meningeal irritation.
83
Why are seizures common in children with meningitis?
Due to cerebral edema, cerebritis, or metabolic derangements.
84
Why is loss of consciousness a poor prognostic sign?
It indicates severe cerebral involvement and raised ICP.
85
Why ask about immunization history?
Lack of vaccines increases risk of Hib, pneumococcal, and meningococcal meningitis.
86
Why ask about recent travel to northern Nigeria?
Increased exposure to meningitis belt outbreaks.
87
Why is herbal concoction use relevant?
May delay presentation or cause toxicity.
88
What does fever signify on examination?
Active infection.
89
Why assess hydration status?
Dehydration worsens cerebral perfusion and ICP.
90
What does irritability suggest in infants?
Early CNS involvement.
91
What does a bulging anterior fontanel indicate?
Raised intracranial pressure.
92
What does a positive Kernig’s sign indicate?
Meningeal irritation.
93
What does a positive Brudzinski sign indicate?
Meningeal irritation.
94
Why examine pupils?
To detect raised ICP or cranial nerve involvement.
95
Why examine cranial nerves?
Basal exudates can damage cranial nerves.
96
Why assess GCS?
Level of consciousness correlates with severity and prognosis.
97
Why is lumbar puncture essential in meningitis?
To confirm diagnosis and identify causative organism.
98
When is lumbar puncture contraindicated?
In raised intracranial pressure without prior imaging.
99
What CSF parameter reflects inflammation?
White blood cell count.
100
Why is CSF glucose reduced in bacterial meningitis?
Increased bacterial metabolism and impaired glucose transport.
101
Why is CSF protein increased?
Albumin leakage due to BBB breakdown.
102
What is the normal CSF WBC count?
<10 cells/mm³.
103
What is the predominant cell in normal CSF?
Lymphocytes.
104
What is normal CSF protein?
30–70 mg/dL.
105
What is the normal appearance of CSF?
Clear and colourless.
106
What is the CSF WBC count in bacterial meningitis?
400–100,000 cells/mm³.
107
What is the predominant cell type?
Neutrophils (>90%).
108
What happens to CSF protein?
Increased (80–500 mg/dL).
109
What happens to CSF glucose?
Reduced (<35 mg/dL).
110
What is the appearance of CSF?
Turbid, purulent, hazy.
111
What is CSF WBC count in viral meningitis?
5–500 cells/mm³.
112
Predominant cell?
Lymphocytes.
113
CSF glucose level?
Normal.
114
CSF protein level?
Normal or mildly increased.
115
What is characteristic CSF appearance in TB meningitis?
Slightly opaque with cobweb formation on standing.
116
How should meningitis be managed initially?
As a medical emergency.
117
Why elevate head of bed to 30°?
To reduce intracranial pressure.
118
Why place unconscious child in left lateral position?
To prevent aspiration.
119
Why restrict fluids to 2/3 maintenance?
To prevent SIADH and worsening cerebral edema.
120
Why give mannitol?
To reduce raised intracranial pressure.
121
Why give dexamethasone?
To reduce inflammation and prevent neurological sequelae.
122
First-line antibiotic for bacterial meningitis in children?
Ceftriaxone 100 mg/kg/day.
123
Duration of treatment for Neisseria meningitidis?
5–7 days.
124
Duration for Haemophilus influenzae?
7–10 days.
125
Duration for Streptococcus pneumoniae?
10–14 days.
126
Duration for Gram-negative meningitis?
21 days.
127
When does CSF become sterile after treatment?
Within 24–48 hours.
128
Most common long-term complication of bacterial meningitis?
Sensorineural hearing loss.
129
Early complications include?
Deafness, cortical blindness, hypoglycemia, SIADH.
130
Late complications include?
Hydrocephalus, cerebral palsy, seizure disorder.
131
What vaccines prevent meningitis?
Meningococcal, pneumococcal, Hib vaccines.
132
Drug used for chemoprophylaxis?
Rifampicin.
133
Who should receive chemoprophylaxis?
Household contacts.
134
What is aseptic meningitis?
Inflammation of meninges without bacterial growth on routine culture.
135
Most common cause of aseptic meningitis?
Enteroviruses.
136
CSF glucose in viral meningitis?
Normal.
137
Prognosis of viral meningitis?
Excellent; complete recovery in ~95%.
138
Why treat aseptic meningitis initially with antibiotics?
To exclude partially treated bacterial meningitis.
139
Is there a specific curative treatment for viral (aseptic) meningitis?
No. There is no specific antiviral treatment for most causes of viral meningitis.
140
What is the main aim of treatment in aseptic meningitis?
Supportive care, observation, and relief of symptoms.
141
Why should children with suspected aseptic meningitis be admitted?
For monitoring, observation, and to exclude bacterial meningitis.
142
What is the first-line drug for fever and pain in aseptic meningitis?
Paracetamol.
143
Why should aspirin be avoided in children with viral meningitis?
Because it can precipitate Reye’s syndrome.
144
Are opioids routinely required in aseptic meningitis?
No. Drugs such as codeine and morphine are rarely needed.
145
What supportive measures are commonly used in aseptic meningitis?
• Adequate hydration • Antipyretics • Observation • Analgesia
146
Should antibiotics be started in a child with suspected aseptic meningitis?
Yes, initially.
147
Why are antibiotics started in suspected aseptic meningitis?
To cover possible bacterial meningitis until it is definitively excluded.
148
When can antibiotics be stopped in aseptic meningitis?
When CSF culture and bacterial antigen tests are negative.
149
Why is this approach especially important in partially treated meningitis?
Because partially treated bacterial meningitis can mimic aseptic meningitis on CSF analysis.
150
When is acyclovir started in aseptic meningitis?
When herpes simplex virus (HSV) meningitis or encephalitis is suspected.
151
Why is acyclovir often started empirically?
Because HSV meningitis and encephalitis are serious and potentially fatal if untreated.
152
When can acyclovir be discontinued?
Once HSV infection is excluded.
153
What is the overall prognosis of viral meningitis?
Excellent.
154
What percentage of children recover completely from viral meningitis?
Approximately 95%.
155
Are long-term neurological sequelae common in viral meningitis?
No. They are uncommon.
156
What determines prognosis in non-viral aseptic meningitis?
The underlying cause.
157
How does prognosis compare between viral and bacterial meningitis?
Viral meningitis has a much better prognosis than bacterial meningitis.
158
What causes meningeal irritation signs?
Inflammation of the meninges causing pain when they are stretched.
159
In which conditions are meningeal signs seen?
• Meningitis • Subarachnoid haemorrhage
160
How is nuchal rigidity tested?
• Patient lies supine • Examiner gently flexes the neck forward • Attempts to bring the chin toward the chest
161
What is a positive nuchal rigidity sign?
• Resistance to passive neck flexion • Pain or discomfort • In severe cases, neck retraction
162
What is the mechanism behind neck stiffness?
Stretching of inflamed meninges causes reflex muscle spasm.
163
How is Kernig’s sign performed?
• Patient lies supine • Flex the hip to 90° • Then attempt to extend the knee
164
Which organism is commonly treated with chloramphenicol in meningitis?
Salmonella species.
165
When is chloramphenicol particularly useful?
In resource-limited settings or difficult circumstances.
166
What is the dose of Penicillin G in infants and older children?
250,000–400,000 units/kg/day given every 6 hours.
167
Which organisms are covered by Penicillin G in older children?
Group B Streptococcus and Neisseria meningitidis.
168
What is the dose of gentamicin in infants and older children?
7.5 mg/kg/day given every 8 hours.
169
Which organism is gentamicin used for in older children?
Listeria monocytogenes and sensitive Staphylococcus strains.
170
What is the dose of kanamycin in infants and older children?
30 mg/kg/day given every 8 hours.
171
Which organisms does kanamycin cover?
Escherichia coli, Proteus species.
172
What is the dose of amikacin in infants and older children?
30 mg/kg/day given every 8 hours.
173
Which organisms are targeted by amikacin?
Pseudomonas aeruginosa and Salmonella species.
174
What is the dose of cefotaxime in infants and older children?
200–300 mg/kg/day given every 6 hours.
175
Which organisms does cefotaxime cover?
Broad Gram-negative organisms including E. coli and Klebsiella.
176
What is the dose of ceftriaxone in infants and older children?
100 mg/kg/day given every 12 hours.
177
Which organisms are covered by ceftriaxone?
Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae, Staphylococcus, Salmonella.
178
What is the dose of ceftazidime in infants and older children?
125–150 mg/kg/day given every 8 hours.
179
Which organism is ceftazidime particularly useful for?
Pseudomonas aeruginosa.
180
What is the dose of vancomycin in infants and older children?
15 mg/kg/day given every 6 hours.
181
When is vancomycin indicated in meningitis?
When Streptococcus pneumoniae is resistant to beta-lactam antibiotics.
182
Is there a specific curative treatment for viral (aseptic) meningitis?
No. There is no specific antiviral treatment for most causes of viral meningitis.
183
What is the main aim of treatment in aseptic meningitis?
Supportive care, observation, and relief of symptoms.
184
Why should children with suspected aseptic meningitis be admitted?
For monitoring, observation, and to exclude bacterial meningitis.
185
What is the first-line drug for fever and pain in aseptic meningitis?
Paracetamol.
186
Why should aspirin be avoided in children with viral meningitis?
Because it can precipitate Reye’s syndrome.
187
Are opioids routinely required in aseptic meningitis?
No. Drugs such as codeine and morphine are rarely needed.
188
What supportive measures are commonly used in aseptic meningitis?
• Adequate hydration • Antipyretics • Observation • Analgesia
189
Should antibiotics be started in a child with suspected aseptic meningitis?
Yes, initially.
190
Why are antibiotics started in suspected aseptic meningitis?
To cover possible bacterial meningitis until it is definitively excluded.
191
When can antibiotics be stopped in aseptic meningitis?
When CSF culture and bacterial antigen tests are negative.
192
Why is this approach especially important in partially treated meningitis?
Because partially treated bacterial meningitis can mimic aseptic meningitis on CSF analysis.
193
When is acyclovir started in aseptic meningitis?
When herpes simplex virus (HSV) meningitis or encephalitis is suspected.
194
Why is acyclovir often started empirically?
Because HSV meningitis and encephalitis are serious and potentially fatal if untreated.
195
When can acyclovir be discontinued?
Once HSV infection is excluded.
196
What is the overall prognosis of viral meningitis?
Excellent.
197
What percentage of children recover completely from viral meningitis?
Approximately 95%.
198
Are long-term neurological sequelae common in viral meningitis?
No. They are uncommon.
199
What determines prognosis in non-viral aseptic meningitis?
The underlying cause.
200
How does prognosis compare between viral and bacterial meningitis?
Viral meningitis has a much better prognosis than bacterial meningitis.
201
What causes meningeal irritation signs?
Inflammation of the meninges causing pain when they are stretched.
202
In which conditions are meningeal signs seen?
• Meningitis • Subarachnoid haemorrhage
203
How is nuchal rigidity tested?
• Patient lies supine • Examiner gently flexes the neck forward • Attempts to bring the chin toward the chest
204
What is a positive nuchal rigidity sign?
• Resistance to passive neck flexion • Pain or discomfort • In severe cases, neck retraction
205
What is the mechanism behind neck stiffness?
Stretching of inflamed meninges causes reflex muscle spasm.
206
How is Kernig’s sign performed?
• Patient lies supine • Flex the hip to 90° • Then attempt to extend the knee
207
What constitutes a positive Kernig’s sign?
• Pain and resistance during knee extension • Patient may flex the knee reflexly
208
Why does Kernig’s sign occur?
Extension stretches inflamed meninges and nerve roots.
209
How is Brudzinski’s neck sign tested?
• Patient lies supine • Examiner passively flexes the neck
210
What is a positive Brudzinski’s neck sign?
• Involuntary flexion of hips and knees
211
What is the physiological basis of Brudzinski’s sign?
Reflex movement to reduce meningeal stretching.
212
How is Brudzinski’s leg sign elicited?
• Patient lies supine • Examiner flexes one hip and knee
213
What indicates a positive Brudzinski’s leg sign?
Involuntary flexion of the opposite leg
214
How is Lasègue’s sign performed?
Patient lies supine; Examiner raises the straight leg with knee extended
215
What is a positive Lasègue’s sign?
Pain radiating from lower back down the leg; Occurs before 60–70° hip flexion
216
What does Lasègue’s sign indicate?
Sciatic nerve or nerve root irritation.
217
Is Lasègue’s sign a true meningeal sign?
No. It is not specific for meningeal irritation.
218
How is Amoss sign tested?
Ask the patient to sit up from lying position
219
What is a positive Amoss sign?
Patient uses hands behind them for support; Avoids flexing the hips
220
JOLT ACCENTUATION OF HEADACHE
How is jolt accentuation tested? A. • Ask patient to rotate head horizontally 2–3 times per second
221
JOLT ACCENTUATION OF HEADACHE
What indicates a positive jolt accentuation test? A. • Worsening of headache
222
INFANTS ⚠️ IMPORTANT
Why are meningeal signs unreliable in infants under 18 months? A. • Immature neurological responses • Open sutures and fontanels • Inability to cooperate
223
INFANTS ⚠️ IMPORTANT
What replaces meningeal signs in infants with meningitis? A. • Bulging fontanel • Seizures • Irritability • Altered sensorium
224
🔑 FINAL EXAM PEARL
What must never be used to exclude meningitis in infants? A. Absence of meningeal signs.
PEDIATRICS SLIDES ONLY
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