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_Sem 4. CNS NOTES > S10 L3 The meninges and subarachnoid haemorrhage > Flashcards

S10 L3 The meninges and subarachnoid haemorrhage Flashcards

1
Q

What are the meninges?

A

Three layers surrounding the brains
- Dura mater
→ Tough, fibrous outer layer, supports and surrounds the dural sinuses
→ Two layer- endosteal and meningeal layer
- Arachnoid mater*
→ Arachnoid trabeculae pass through the space to blend with the pia
- Pia mater*
→ Thin layer that adheres closely to brain- pierced by blood vessels
*together called the leptomeninges

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2
Q

What are the dural folds?

A
  • Endosteal and meningeal layer normally closely adhered
  • Split to form the dural folds
  • Enclose the dural venous sinuses
    1. Falx cerebri → between the two cerebral hemispheres
    2. Falx cerebelli → between cerebellar hemispheres
    3. Tentorium cerebelli → supports occipital lobe, separate from cerebellum
    4. Diaphragma sella → covers superior surface of the pituitary gland with passageway for the pituitary stalk
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3
Q

What is dural bleed?

A

Different types
1. Extradural
→ Between endosteal layer and skull
→ Trauma - middle meningeal artery rupture
→ Lucid interval - LOC → Conscious → LOC
→ Lentiform appearance- CT scan (endosteal layer tightly adhered to the bone so blood can only collect up to the edge of the bone, then bulges inwards)
2. Subdural
→ Between the meningeal layer of dura and arachnoid mater
→ Trauma - bridging veins affected
→ Concave towards brain - collects along whole half of the hemisphere

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4
Q

What is the subarachnoid space?

A
  • Space between the arachnoid mater and pia mater

- Contain enlarged areas - cisterns (occurs where the brain moves away from the skull)

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5
Q

What is contained within the subarachnoid space?

A

Filled with CSF

  • Physical support of neural structures
  • Excretion (brain metabolites)
  • Intracerebral transport (hormone releasing factor)
  • Control of chemical environment
  • Volume changes reciprocally with volume of intracranial contents - blood
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6
Q

What is CSF?

A
  • Formed by choroid plexus (and extra-choroidal structures)
  • Flow
    → Lateral ventricles
    → 3rd ventricle (aqueduct of Sylvius)
    → 4th ventricle (median and lateral apertures)
    → Subarachnoid space (small amount into spinal cord)
    Propelled by newly formed fluid, ciliary action of ventricular ependyma, vascular pulsations
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7
Q

What is a subarachnoid haemorrhage?

A

Extravasation of blood into the subarachnoid space

Traumatic or spontaneous

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8
Q

What is the epidemiology of subarachnoid haemorrhage?

A
  • 6% of all strokes
  • F>M (1.6:1)
  • Most <50 years
  • 50% mortality
  • 60% suffer long term morbidity
  • More likely in black, Finnish and Japanese populations
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9
Q

What are the risk factors for subarachnoid haemorrhage?

A
  • Hypertension
  • Smoking
  • Excess alcohol consumption
  • Predisposition to aneurysm formation
  • Family history
  • Associated conditions
    → Chronic kidney disease (resultant effect on vessel wall)
    → Marfan’s syndrome (effect on connective tissue of vessel)
    → Neurofibromatosis (unclear mechanism, if any link)
  • Trauma
  • Cocaine use
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10
Q

What are the clinical features of subarachnoid haemorrhage?

A
  • Thunderclap headache
    → Sudden onset, worst headache they’ve ever had
    → Diffuse pain
    → Can last from an hour to a week
  • Frequent loss of consciousness and confusion
  • Meningism
    → Neck stiffness
    → Photophobia
    → Headache
  • Orbital pain
  • Diplopia
  • Visual loss (anterior communicating artery aneurysm)
  • Maybe focal neurology
  • Maybe history of sentinel bleed (previous headache)
  • Maybe presents as cardiac arrest (if ↑ICP following bleed causes Cushing response)
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11
Q

What is the pathophysiology of a subarachnoid haemorrhage?

A
  • Usually occurs following rupture of aneurysm in the circle of Willis - Berry aneurysm
  • Accounts for 80% of non-traumatic bleeds
  • Rupture of AVMs- 10% (arteriovenous malformation)
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12
Q

Why do aneurysm develop?

A
  • Weakness in the vessel wall (usually artery) can cause an abnormal bulge
  • Usually at a bifurcation point
  • Large cerebral arteries in the anterior circle of Willis most affected
  • Intracranial arteries lack external elastic lamina and have thin adventitia → slightly more prone
  • May be genetic predisposition
  • May be caused by haemodynamic effects at branch points in the circle of Willis
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13
Q

What are the common sites for aneurysm development?

A

Most are berry aneurysms → look like berries
Small aneurysms <5mm unlikely to rupture
- Anterior communicating artery or proximal anterior cerebral artery (30%) → compress optic chiasm, affect frontal or pituitary
- Posterior communicating artery (25%) → compress adjacent oculomotor nerve causing ipsilateral 3rd nerve palsy
- Bifurcation of the middle cerebral artery as it split into superior and inferior divisions (20%)

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14
Q

What are the early brain changes to subarachnoid haemorrhage?

A

→ Microthrombi - may occlude more distal branches
→ Vasoconstriction - result of blood in CSF irritating cerebral arteries
→ Cerebral oedema - general inflammatory response to tissue hypoxia and extravasated blood
→ Apoptosis of brain cells
→ Early rebleeding ↑risk of another bleed
→ Acute hydrocephalus (blood in subarachnoid space may block normal drainage of CSF)

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15
Q

What are the cellular changes to subarachnoid haemorrhage?

A

→ Oxidative stress - maybe related to reperfusion
→ Release of inflammatory mediators - can activate many pathways as well as activation of microglia
→ Platelet activation - formation of thrombi

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16
Q

What are the systemic complications of subarachnoid haemorrhage?

A

→ Sympathetic activation - early Cushing response
→ Myocardial necrosis - sympathetic activation, specific ECG changes seen
→ Systemic inflammatory response - can affect multiple systems

17
Q

What is the first investigation that you would request for suspected subarachnoid haemorrhage?

A

CT scan

  • Detect 93% if done within 24 hours
  • Small amount of blood can be difficult to see
  • Prominent bleeding of basal cistern in a five pointed ‘star’ pattern
  • Blood maybe seen in the ventricles due to reflux from subarachnoid space
18
Q

If the history is suggestive of subarachnoid haemorrhage but the CT scan is negative, what test would you request?

A

Lumbar puncture
- Should wait at least 6 hours (12+ preferable) from symptoms onset → allow time for lysis of RBC and release of bilirubin
- CSF will have a yellowish tinge after centrifuging (differentiate it from a traumatic tap)
→ Called Xanthochromia or Frank blood
- Also high protein (blood constituents and Hb), white cells often raised, glucose not affected, high red cell count

19
Q

How do you perform a lumbar puncture?

A
  • Identify the iliac crest → L4/5 level
  • Give local anaesthetic
  • Insert LP needle between spinous processes and through the supraspinous and interspinous ligaments
  • Feel give as pass through ligamentum flavum and dura
  • Remove needle stylet and collect CSF in sterile container (allow to drip, don’t aspirate)
    Traumatic tap → as you do a LP you go through blood vessels, so the blood you detect is from this instead of CSF itself, if you centrifuge it then you can differentiate between TT and SAH
20
Q

Once the subarachnoid haemorrhage is confirmed what investigations do you do?

A

CT angiogram

  • Direct visualisation of bleeding aneurysm
  • Vital for planning surgery
21
Q

What is the treatment for subarachnoid haemorrhage?

A
  1. Stabilisation - ABC approach
    → Support airway if diminished and unconscious
    → Give oxygen
    → Support circulation - monitor cardiovascular parameters - give fluids, calcium channel blocker (Nimodipine) to prevent vasospasm and secondary ischaemia
  2. Neurological observations
    → Look for trends which maybe suggestive of ↑ICP
  3. Neurosurgery
    → Operate on patients with good neurological status within 48hrs (prevent re-bleeding)
    → Decompressive surgery (craniectomy)
    → Clipping (surgery) - clamping of neck of aneurysm (with spring clip), loose blood supply, shrivels up
    → Coiling (neuro-radiologist) - insertion of wire into aneurysm sac which causes thrombosis of blood within aneurysm, stops it bleeding into subarachnoid space
22
Q

What is the prognosis of subarachnoid haemorrhage?

A

Not very good- poor prognosis

  • 10-15% die before reaching hospital
  • 25% die within 24hrs
  • 40% mortality within first month
  • 50% mortality within 6months
  • 33% survivors will have major neurological deficits
  • Re-bleeding occurs in 30% of first 2/52 weeks in unoperated patients
  • Delay ischaemia from cerebral vasospasm is commonest cause of death following aneurysmal SAH
  • Intraventricular haemorrhage (around 35% of cases) predicts poor outcome
23
Q

What are the different categories of infection in the CNS?

A
  • Infections focused on parenchyma (encephalitis)
  • Infections focused on meninges (meningitis)
    → inflammation of the dura - rare
    → inflammation of the leptomeninges (especially arachnoid tissue and subarachnoid space) more common
24
Q

What is meningitis?

A

Pyogenic inflammation of the meninges and underlying subarachnoid
Gain access from other parts of the body
Bacterial or viral
Occasionally caused by fungal disease or non infectious modalities (trauma/surgery)

25
Q

What are the signs and symptoms of meningitis?

A 
Triad of meningism with a fever (44%) 
→ Headache, neck stiffness, photophobia 
→ Develops over hours in bacterial cases, days in viral cases 
Other symptoms include
- Flu like
- Joint pains 
- Rash 
- Reduced GCS/seizures 
Babies 
- Inconsolable crying/ high pitched 
- Reduced feeds 
- Floppy 
- Bulging fontanelle
26
Q

Which type of meningitis is a rash most common in? Why does it occur?

A

Meningococcal meningitis
Bleeding into skin or mucosa (microvascular thrombosis)
- Produces a non blanching rash
- Larger lesion- purpuric
- Smaller lesion- 1-2mm - petechial
Normally found on trunk, legs, mucous membranes, and conjunctiva - occasionally on palms and soles

27
Q

What is the most common cause of meningitis?

A

Gain access from other parts of the body - mortality still high 25%
Prior to antibiotic was almost always fatal
Bacterial or viral
Most common bacterial causes
- Streptococcal pneumoniae (pneumococcal meningitis) → ↓32% since pneumococcal conjugate vaccine (PVC13)
- Neisseria meningitides (meningococcal meningitis) → rash causing, high mortality
- Haemophilus influenza (Hib meningitis) → Hib vaccine - before accounted for 45% bacteria meningitis

Specific for groups

  • Neonates → E.Coli, Group B streptococcus, Listeria monocytogenes
  • Children → Haemophilus influenza type B, Neisseria meningitidis
  • Elderly → Streptococcal pneumoniae, Listeria monocytogenes
28
Q

What are the risk factors for community acquired bacterial meningitis?

A
  • Young and old the most affected (<5 years, >65 years)
  • Crowding → bacterial disease spread more easily
  • Immune problems (non immunised infants, cancer, asplenia)
  • Cochlear implants → easier route for bacteria to colonise and enter the brain
  • CSF defects → spina bifida
  • Spina procedures → surgery, lumbar puncture
  • Endocarditis
  • Diabetes →immunosuppression
  • Alcoholism
29
Q

How does the bacteria reach the CNS?

A
  • Colonise nasopharynx (normal)
    → Ascent of bacteria through Eustachian tube to middle ear (otitis media)
    → Prolonged infection in this area can lead to bacteria to spread directly to the CSF (through mastoid sinuses)
  • Colonisation nasopharynx
    → Seeding to lower respiratory tract (pneumonia)
    → Lung inflammation allows bacteria to enter blood (bacteriaemia) → invasion of CSF via capillaries that traverse the choroid plexus or subarachnoid space
  • Neonates can get pathogens from a maternal source
    → placenta/reproductive tract secretions
30
Q

What is the pathophysiology of meningitis?

A
  1. Bugs which normally colonise the nose gain access to the circulation and cause bacteraemia
  2. The bacteraemia causes damage to vessel walls in the brain and meninges, allowing pathogens to enter the subarachnoid space
  3. Once in the subarachnoid space pathogens multiply rapidly causing purulent CSF and severe meningeal inflammation
  4. Vasospasm of cerebral vessels can cause cerebral infarction
  5. Oedema of brain parenchyma can cause raised intracranial pressure
  6. Maculopapular rash seen in meningococcal septicaemia cause by microvascular thrombosis due to many factors including sluggish circulation, impaired fibrinolysis, ↑tissue factor expression in endothelial cells
31
Q

What are the effects of meningitis?

A

Bacteria quickly multiply once in the subarachnoid space
→ Inflammatory mediators induced
→ Lots of leucocytes enter the CSF
Inflammatory cascade results in cerebral oedema and ↑ICP

32
Q

What are the complications of meningitis?

A
  1. Septic shock - bacteraemia
  2. Disseminated intravascular coagulation - bacteraemia
  3. Coma - ↑ICP
  4. Seizures - irritation of the meninges
  5. Hearing loss (Vestibulocochlear nerve/ cochlear swelling)
  6. Hydrocephalus (blockage of CSF drainage pathways)
  7. Focal paralysis (potentially due to cerebral abscess)
  8. Death - brain herniation and sepsis
  9. SIADH release
  10. Intellectual deficits
  11. Raised ICP
33
Q

How is meningitis diagnosed?

A

Symptoms/signs
Physical examination
Kernig sign
→ Supine patient with thigh flexed to 90 degrees
→ Extension of the knee is met with resistance
→ More common in children (up to 53%)
Brudzinski
→ When neck is flexed → involuntary flexion of the knees and hips
→ More common in children (up to 66%)

34
Q

What is the first line investigations for meningitis?

A
  • Lumbar puncture is most important investigation
  • PCR from bloods and CSF
  • Blood culture
  • Bloods with sepsis screen
35
Q

What findings would you expect on a lumbar puncture?

A

Bacterial meningitis
→ Cloudy CSF
→ High protein (immune cells etc…)
→ High white cells, primarily neutrophils (which can phagocytose bacteria)
→ Low glucose as bacteria (and white cells) metabolise it
Viral meningitis
→ Maybe clear but can be cloudy
→ Protein level may be normal or raised
→ High white cells, primarily lymphocytes to mount an adaptive response
→ Normal glucose >60% plasma

36
Q

What consideration needs to be made before lumbar puncture is carried out?

A

↑ICP could be brain herniation
(5% people with acute bacterial meningitis)
Performing and LP ↑chance of it occurring (sudden ↓ pressure (removal of CSF))
If suspected ↑ICP delay LP
CT scan maybe helpful- find contraindication to ding an LP - but normal CT may not mean LP is safe to perfom

37
Q

What are the clinical signs of brain herniation?

A

Decreasing consciousness
Brainstem herniation
Recent seizure

38
Q

What is the treatment for meningitis?

A
  • Admit to hospital
  • Empirical antibiotics → broad spectrum → vancomycin +(ceftriaxone (IV) or cefotaxime)
  • Supportive therapy → Intubation (if altered consciousness), fluids if shocked (caution with ↑ICP), oxygen, analgesics and antipyretics
  • Dexamethasone to prevent hearing loss → swelling of vestibulocochlear nerve
    If viral → aciclovir for herpes, ganciclovir for CMV (cytomegalovirus)

_Sem 4. CNS NOTES (21 decks)

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