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Clinical Neuroscience > Session 10: Subarachnoid Haemorrhage and Meningitis > Flashcards

Session 10: Subarachnoid Haemorrhage and Meningitis Flashcards

1
Q

Epidemiology of SAH.

A

6% of all strokes.

More common in females than males 1.6:1

Most are under 50

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2
Q

Prognosis of SAH.

A

50% mortality

60% suffer some longer term morbidity following the event if they survive.

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3
Q

Risk factors of SAH.

A

Hypertension

Smoking

Excess alcohol consumption

Predisposition aneurysm formation

FH

Trauma

Cocaine use

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4
Q

Give associated conditions with SAH.

A

CKD

Marfan’s syndrome

Neurofibromatosis

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5
Q

What is the most common pathophysiology of an SAH?

A

A rupture of an aneurysm in the circle of Willis.

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6
Q

Why might there be an aneurysm in the circle of Willis?

A

Genetics

Haemodynamic effects at branch point in the circle of Willis leading to turbulent flow.

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7
Q

What are the most common type of aneurysm in SAH?

A

Berry aneurysm

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8
Q

Common sites of aneurysm in circle of willis leading to SAH.

A

Anterior communicating artery/proximal ACA (30%)

Posterior communicating artery (25%)

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

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9
Q

Specific structures at risk of Anterior communicating artery/proximal ACA aneurysm.

A

Can compress nearby optic chiasm leading to bitemporal hemianopia.

May affect frontal lobe or even pituitary.

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10
Q

Specific structures at risk of posterior communicating artery aneurysm.

A

Compression of CN III leading to ipsilateral third nerve palsy.

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11
Q

What will bleeding into the subarachnoid space cause?

A

Early brain injury

Cellular changes

Systemic complications

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12
Q

What causes early brain injury due to bleeding into subarachnoid space?

A

Microthrombi which can occlude more distal branches.

Also vasoconstriction as a result of blood in the CSF irritating cerebral arteries.

Cerebral oedema due to general inflammatory response.

Apoptosis of brain cells.

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13
Q

Explain the cellular changes in bleeding into subarachnoid space.

A

Oxidative stress

Release of inflammatory mediators and activation of microglia.

Platelet activation which will lead to formation of thrombi.

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14
Q

Systemic complications of bleeding into subarachnoid space.

A

Sympathetic activation and early cushing response.

Myocardial necrosis due to sympathetic activation.

Systemic inflammatory response.

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15
Q

Clinical features of SAH.

A

Thunderclap headache

Frequently loss of consciousness and confusion

Meningism

Can have focal neurology

Can have a history of sentinel bleed

May present as cardiac arrest (profound Cushing response)

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16
Q

Features of thunderclap headache.

A

Explosive in onset and severe commonly described as being hit on the head with a cricket bat.

Diffuse pain

Can last from an hour to a week.

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17
Q

Features of meningism.

A

Neck stiffness

Photophobia

Headache

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18
Q

Investigations of SAH

A

CT head

CT angiogram if a bleed is confirmed

Lumbar puncture

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19
Q

What will a CT head look like in SAH?

A

Five pointed star pattern

Blood may be seen within the ventricles

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20
Q

Why is a CT angiogram performed if the bleed is confirmed?

A

To allow direct visualisation of bleeding aneurysm of aneurysm sac.

This is important for planning surgery

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21
Q

Explain LP technique.

A

Feel for iliac crests at around L4/L5

Give local anaesthetics

Insert LP needle between spinous processes and through the supraspinous and interspinous ligaments.

Feel the give as you pass through the ligamentum flavum and dura.

Remove needle and collect CSF in sterile containers.

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22
Q

LP findings in SAH.

A

Increased opening pressure

Frank blood or xanthochromia

HIgh protein

White cells often not raised

Glucose not affected

High red cell count

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23
Q

What is xanthochromia?

A

A yellow colouring of the CSF due to metabolism of haemoglobin to bilirubin.

24
Q

When is xanthochromia seen?

A

At least 12 hours post bleed and is more specific than frank blood.

25
Q

Treatment of SAH. (ABC)

A

ABC approach

Support airways

Give O2

Support circulation by fluids and also nimodipine to alleviate cerebral vasospasms.

26
Q

Other treatments of SAH.

A

Neurological observations

Neurosurgery

27
Q

Explain neurosurgery of SAH.

A

Decompressive surgery (craniectomy)

Coiling

Clipping

28
Q

Explain coiling in neurosurgery for SAH

A

Insertion of a platinum wire into the aneurysm sac.

This causes thrombosis of blood within the aneurysm itself and will stop the bleed.

29
Q

Explain clipping in neurosurgery for SAH.

A

A spring clip is placed around the neck of the aneurysm. This causes loss of blood supply to the aneurysm and it will shrivel up.

30
Q

Pathogens of meningitis (very broad)

A

Bacterial

Viral

Fungal

Or even non-infective

31
Q

Typical organism in neonates.

A

E. Coli

Group B strep

Listeria monocytogenes

32
Q

Typical organism in children

A

HiB

N. meningitidis

33
Q

Typical organism in elderly.

A

S. pneumoniae

Listeria monocytogenes

34
Q

Risk factors of meningitis.

A

CSF defects such as spina bifida

Spine procedures like surgery or LP

Endocarditis (vegetation ends up in brain)

Diabetes

Alcoholism

Splenectomy (lots of encapsulated bacteria innit)

Crowded housing (beware students!)

35
Q

Triad of meningitis

A

Headache

Neck stiffness

Photophobia

With a fever!

36
Q

Associated symptoms of menigitis.

A

Flu-like

Joint pains and stiffness

Seizure

Meningococcal rash (non-blanching)

Drowsiness

Shock

37
Q

Associated symptoms of meningitis in babies.

A

Inconsolable crying

Rigidity or floppiness

Bulging fontanelle

38
Q

Pathophysiology of meningitis.

A

Usually gain entry from nose into circulation. This leads to a bacteraemia.

Bacteraemia causes damage to vessel walls in brain and meninges.

This damage allows pathogen to enter subarachnoid space.

Once in there the pathogen can rapidly multiply and cause a purulent CSF + severe meningeal inflammation.

There are vasospasms of cerebral vessels. This can cause cerebral infarction.

Oedema of brain parenchyma -> raised ICP.

39
Q

Why is a maculopapula rash seen in meningitis?

A

More specifically seen in meningococcal septicaemia and this is due to microvascular thrombosis.

40
Q

What causes the microvascular thrombosis?

A

Sluggish circulation

Impaired fibrinolysis

Increased tissue factor

41
Q

Investigations of meningitis.

A

Bloods

Sepsis screen

PCR

CXR or mid stream urine might be done

Lumbar puncture

42
Q

LP findings in bacterial meningitis.

A

Cloudy CSF

High protein

High white cells (neutrophils primarily)

Low glucose (due to bacteria)

43
Q

LP findings in viral meningitis.

A

May be clear, may be cloudy

Protein levels are normal or raised

Hight white cells (lymphocytes primarily)

Normal glucose

44
Q

Supportive treatment of meningitis.

A

Analgesia

Antipyretics

Fluids

45
Q

Medical specific treatments of bacterial meningitis.

A

IV ceftriaxone.

Dexamethasone to prevent hearing loss

46
Q

Medical specific treatments of viral meningitis.

A

Aciclovir if Herpes

Ganciclovir for CMV

47
Q

Complications of meningitis.

A

Septic shock (bacteraemia)

DIC (bacteraemia)

Coma (ICP)

Cerebral oedema

Raised ICP

Seizures

Epilepsy

Death

48
Q

Less common complications of meningitis

A

SIADH

Hearing loss (swelling of CN VIII or cochlea itself)

Intellectual deficits

Hydrocephalus (obstruction of CSF drainage)

Focal paralysis

49
Q

Physical examinations of meningitis.

A

Kernig sign where you flex the patients thigh to 90 degrees.

When there is extension of knee it is met with resistance.

Brudzinski sign when the neck is flexed leading to an involuntary flexion of knees and hips.

50
Q

Explain how pneumococcus bacteria can end up in the meninges.

A

Colonisation of nasopharynx which is normal.

There is then ascent of bacteria through the eustachian tube to middle ear leading to otitis media.

This can then travel further into CSF through the mastoid sinuses succeeding mastoiditis.

51
Q

When we say that the leptomeninges are inflamed in meningitis. Which structures do we mean?

A

Arachnoid tissue and subarachnoid space.

52
Q

Why is it important to give nimodipine in an SAH?

A

Because there is a risk of delayed ischaemia from cerebral vasospasm.

This is the most common cause of death following an SAH.

Nimodipine prevents cerebral vasospasms!

53
Q

Common complication of SAH.

A

Rebleeding

54
Q

Why are intracranial arteries susceptible to aneurysm?

A

Because they lack the external elastic lamina.

They also have thin adventitia.

55
Q
A

Clinical Neuroscience (22 decks)

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