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Neuroscience > Session 10 Subarachnoid Haemorhage And Meningitis > Flashcards

Session 10 Subarachnoid Haemorhage And Meningitis Flashcards

1
Q

What are the risk factors for subarachnoid haemorrhage?

A 
Hypertension 
Smoking 
Excess alcohol consumption 
Predisposition to aneurism formation 
Family history 
Associated conditions: CDK (resultant effect on vessel wall), Marfan’s syndrome (effect on connective tissues of vessels), Neurofibromatosis
Trauma 
Cocaine use
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2
Q

Why do subarachnoid haemorrhages usually occur?

A

Following rupture of an aneurism in the circle of Willis

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3
Q

What is an aneurism?

A

A weakness in a vessel (usually artery) wall which can cause an abnormal bulge

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4
Q

What causes aneurisms?

A

Genetic predisposition

Haemodynamic effects at branch points in the circle of Willis(e.g. higher resulting flow rate in progressively smaller branches, turbulence)

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5
Q

What type are most aneurisms?

A

Berry aneurisms

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6
Q

What are the common sites all aneurisms?

A

anterior communicating artery / proximal anterior cerebral artery (30%)
- these can compress the optic chiasm and may affect frontal lobe or pituitary

Posterior communicating artery (25%)
- can compress the adjacent oculomotor nerve causing an ipsilateral third nerve palsy

Bifurcation of the middle cerebral artery as it splits into superior and inferior divisions (20%)

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7
Q

What does bleeding into the subarachnoid space cause? 3 key points

A

Early brain injury

Cellular changes

Systemic complications

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8
Q

Early brain injury is caused by bleeding into the subarachnoid space. How does this occur?

A

Microthombi may occlude more distal branches

Vasoconstriction: as a result of blood in the CSF irritating cerebral arteries

Cerebral oedema: general inflammatory response to tissue hypoxia and extravasated blood

Apoptosis of brain cells

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9
Q

Cellular changes occur due to bleeding into the subarachnoid space. Why does this occur?

A

oxidative stress - could be 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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10
Q

What systemic complications can occur due to bleeding into subarachnoid space?

A

Sympathetic activation (early cushing response)

Myocardial necrosis (due to sympathetic activation)

Systemic inflammatory response that can affect multiple symptoms

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11
Q

What are the clinical features of subarachnoid haemorrhage?

A

Thunderclap headache

  • explosive in onset and SEVERE
  • diffuse pain
  • can last from 1 hr to a week

Frequently loss of consciousness and confusion

Meningism

  • neck stiffness
  • photophobia
  • headache

Focal neurology

History of sentinel bleed (previous headache)

May present as cardiac arrest if intracranial pressure rises rapidly following bleed leading to profound cushing’s response

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12
Q

What investigations would you perform if you suspected subarachnoid haemorrhage?

A

CT head

  • prominent filling of the basal cisterns in a five pointed star pattern
  • blood may be seen within the ventricles (maybe due to reflex from subarachnoid space)

CT angiogram if bleed confirmed

  • allows direct visualisation of bleeding aneurysm of aneurysm sac
  • vital for planning surgery

Lumbar puncture

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13
Q

Describe the technique of performing a lumbar puncture

A
  1. Identify iliac crest (L4-L5 level)
  2. Give local anaesthetic
  3. Insert needle between spinous processes and through the supraspinous and interspinous ligaments
  4. Feel give as pass through ligamentum flavum and dura
  5. Remove needle styles and collect CSF in sterile containers (allow to drip - don’t aspirate!)
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14
Q

What would LP findings show in SAH?

A

Increased opening pressure (as there is now additional volume in the subarachnoid space)

Frank blood or xanthochromia seen

High protein (blood constituents and Hb)

High red cell count

NB:
White cells are often normal
Glucose not affected

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15
Q

What is xanthochromia?

When would this be seen ?

Why is this useful?

A

Yellow colouring of the CSF due to metabolism of Hb to bilirubin within the subarachnoid space

Seen at least 12 hours POST bleed

More specific than frank blood for SAH (helps exclude a bloody or traumatic tap)

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16
Q

Treatment of SAH in 3 main points?

A

ABC approach

  • support airway if diminished conscious level
  • give oxygen
  • support circulation: fluids, nimodipine to alleviate cerebral vasospasm

Neurological observations - look for trends which may be suggestive of increasing ICP

Neurosurgery

17
Q

What are the types of surgery you can perform to treat SAH?

A

Decrompressive surgery (craniectomy)

Coiling: insertion of a platinum wire into the aneurism sac which causes thrombosis of blood within the aneurism itself
(Neuroradiologist)

Clipping: placement of a spring clip around the neck of the aneurism, causing it to lose blood supply and shrivel up
(Neurosurgeons)

18
Q

What typical organisms cause meningitis in neonates?

A

E.coli

Group B streptococcus

Listeria monocytogenes

19
Q

What typical organisms cause meningitis in children?

A

Haemophilus influenzae type B (HiB vaccine)

Neisseria meningitidis

20
Q

What typical organisms cause meningitis in the elderly?

A

Streptococcus pneumoniae

Listeria monocytogenes

21
Q

What are the risk factors for meningitis?

A

CSF defects (e.g. spina bifida)

Spinal produced results

Endocarditis

Diabetes

Alcoholism

Splenectomy

Crowded housing

22
Q

What is the triad of meningism with fever?

A

Headache

Neck stiffness

Photophobia

23
Q

What are some associated symptoms of meningitis?

A 
Flu-like symptoms 
Joint pains and stiffness
Seizure 
Meningococcal rash (non blanching) 
Drowsiness
Shock 
Babies: inconsolable crying, rigidity, bulging fontanelle (late sign)
24
Q

How does meningitis occur (pathophysiology)?

A

Bugs that normally live in the NOSE gain entry to the circulation and cause a bacteraemia

This bacteraemia causes damage to vessel walls in the brain and meninges, allowing pathogen to enter the subarachnoid space

Once in this space, pathogens multiply rapidly causing purulent CSF and severe meningeal inflammation

Vasospasm of cerebral vessels can cause cerebral infarction

Oedema of brain parenchyma can cause raised ICP

25
Q

Maculopapular rash seen in meningococcal septicaemia. What is this caused by?

A

Caused by microvascular thrombosis due to many factors including:

Sluggish circulation
Impaired fibrinolysis
Increased tissue factor expression in endothelial cells

26
Q

What investigations would you carry out if you suspected meningitis?

A

Bloods: sepsis screen and PCR
Chest X ray or mid stream urine: if you suspect a particular septic focus

LP findings - need to compare bloods to these

27
Q

Compare LP findings of bacterial meningitis with viral meningitis

A

Bacterial

  • CSF = cloudy
  • high protein (immune proteins etc)
  • high white cells, primarily neutrophils (phagocytose bacteria)
  • low glucose as bacteria and white cells metabolise it

Viral

  • CSF = clear (but can be cloudy!)
  • protein level = normal or raised
  • high white cells, primarily lymphocytes to mount an adaptive response
  • normal glucose (>60% plasma)

Main differences are neutrophils vs lymphocytes and low glucose vs normal glucose

28
Q

Outline the treatment for meningitis

A

Supportive

  • analgesia
  • antipyretics
  • fluids is shocked

Medical

  • IV ceftriaxone
  • dexamethasone to prevent hearing loss (due to swelling of Vestibulocochlear nerve or effect on cochlea)
  • if viral: acyclovir (herpes) or ganciclovir (Cytomegalovirus)
29
Q

What are the complications of meningitis and what are they due to?

A

Septic shock - due to bacteraemia

DIC - due to bacteraemia

Coma - due to raised ICP

Cerebral oedema - due to cerebral inflammation

Raised ICP

Death - brain herniation or sepsis

Seizures - due to irritation of brain parenchyma

SIADH - may direct effect on Hypothalamus and pituitary

Hearing loss - due to swelling of Vestibulocochlear nerve or cochlea itself - perilymph is continuous with subarachnoid space!

Hydrocephalus - due to interruption of CSF drainage pathways and effect on arachnoid granulations

Focal paralysis - maybe due to cerebral abscess

Neuroscience (17 decks)

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