16. Subarachnoid haemorrhage and meningitis Flashcards

1
Q

what are the 3 layers of the meninges?

A
  • Dura mater
  • Arachnoid mater
  • Pia mater
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2
Q

function of dura mater and two divisions?

A
  • (Tough mother)- surround and supports dural sinuses
  • Endosteal layer
  • Meningeal layer
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3
Q

which two layers make the Leptomeninges?

A
  • Arachnoid mater

* Pia mater

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4
Q

what are dural folds?

A

The two dura mater layers are firmly adhered to each other except
where they split:
•To enclose venous sinuses
•To form dural septa

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5
Q

what are the 4 important dural septa?

A
  1. Falx cerebri (between cerebral hemispheres)
  2. Falx cerebelli (between cerebellar hemispheres)
  3. Tentorium cerebelli
  4. Diaphragma sella
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6
Q

where does extradural bleeds occur and what can cause it?

A
  • Between endosteal layer and skull
  • Trauma
  • Middle meningeal artery
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7
Q

presentation and imaging of extardural bleed?

A
  • LOC, consciousness, LOC (lucid interval)

* CT scan- biconvex bleed (lemon)

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8
Q

where does subdural bleeds occur and what can cause it?

A
  • Between meningeal layer and arachnoid
  • Trauma
  • Torn bridging veins
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9
Q

imaging of subdural bleed?

A

• Concave towards brain (banana)

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10
Q

what is the subarachnoid space?

A

Located between arachnoid and pia

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11
Q

what are enlarged areas of subarachnoid space called and what do they contain?

A
  • enlarged regions called cisterns
  • Occur where brain moves away from skull
  • Filled with CSF
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12
Q

function of CSF?

A
  • Physical support of neural structures
  • Excretion (of brain metabolites)
  • Intracerebral transport (hormone releasing factors)
  • Control of chemical environment
  • Volume changes reciprocally with volume of intracranial contents to control ICP
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13
Q

where is CSF produced?

A
  • Formed by choroid plexuses (and extra-choroidal structures)
  • choroid plexuses are capillaries and loose connective tissue that filter plasma from blood to form CSF
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14
Q

describe flow of CSF

A
  • 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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15
Q

What percent of strokes are subarachnoid haemorrhages?

A

6% of all strokes

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16
Q

What is the mortality of subarachnoid haemorrhage?

A

50% mortality, 60% suffer some longer term morbidity following the event

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17
Q

who are subarachnoid haemorrhages more common in?

A

• More likely in females (1.6:1)
• More likely in black, Finnish and Japanese
populations
• Average age of onset is 50-55 yrs

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18
Q

What are the risk factors for subarachnoid haemorrhage?

A
  • Hypertension
  • Smoking
  • Excess alcohol consumption
  • Predisposition to aneurysm formation
  • Family history
  • Associated conditions
  • Trauma
  • Cocaine use
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19
Q

what are the associated conditions that increase risk of SAH?

A

o Chronic kidney disease (resultant effect on vessel
wall)
o Marfan’s syndrome (effect on connective tissues of
vessels)
o Neurofibromatosis (unclear mechanism, if any link)

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20
Q

What usually cause SAH?

A
  • Rupture of aneurysms (80% of non-traumatic cases)

- Rupture of AVMs (arteriovenous malformations) -10%

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21
Q

What causes aneurysm to develop?

A

Aneurysms develop due to pressures on the arterial wall (vessels in subarachnoid space)
• Usually at bifurcation points
• Large cerebral arteries in anterior circle of Willis most affected
• genetic predisposition
• haemodynamic effects at branch points in the circle of Willis (e.g. higher resulting flow rate in progressively smaller branches, turbulence)
- cerebral arteries lack elastic lamina and have thin adventitia

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22
Q

What are the risk factors for developing aneurysms?

A
  • Same as cardiovascular- hypertension, smoking etc

* Alcohol++

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23
Q

Where are the common site for aneurysms to develop?

A
  • Anterior communicating (30%)
  • posterior communicating (25%)
  • bifurcation of MCA into superior and inferior divisions (20%)
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24
Q

What can an aneurysm at the anterior communicating artery cause?

A

Can compress the nearby optic chiasm and may affect frontal lobe or even pituitary

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25
Q

What can an aneurysm at the posterior communicating artery cause?

A

Can compress the adjacent oculomotor nerve causing an ipsilateral third nerve palsy

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26
Q

4 things that bleeding into SAS cause that lead to early brain injury?

A
  • microthrombi: occlude more distal branches
  • vasoconstriction
  • cerebral oedema: general inflammatory response to tissue hypoxia and extravasated blood
  • apoptosis of brain cells
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27
Q

Why does vasoconstriction

A

As a result of blood in CSF irritating cerebral arteries

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28
Q

WHat are the cellular changes after SAH? (3)

A
  • oxidative stress (related to reperfusion)
  • release of inflammatory mediators
  • platelet activation (form thrombi)
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29
Q

What are the systemic complications after a SAH? (3)

A
  • sympathetic activation (cushings response)
  • myocardial necrosis (due to sympathetic activity)
  • systemic inflammatory response
  • Acute hydrocephalus (blood in subarachnoid space may block normal drainage of CSF)
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30
Q

What are the clinical features of SAH?

A
  • Thunderclap headache
  • Frequently loss of consciousness and confusion
  • meningism
  • may be focal neurology
  • history of sentinel headaches/bleed - Minor leaks from aneurysm
  • may present as cardiac arrest
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31
Q

Describe the headache in SAH.

A

Thunderclap headache
• Explosive in onset and severe, often reported as worst headache ever or even ‘like being hit on the head with a cricket bat’
• Diffuse pain
• Can last from an hour to a week

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32
Q

What are the features of meningism?

A

• Neck stiffness • Photophobia • Headache

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33
Q

what may SAH patient present with?

A
  • Headache (48%)
  • Dizziness
  • Orbital pain
  • Diplopia
  • Visual loss (anterior communicating artery aneurysm)
  • Nausea and vomiting
34
Q

WHat focal neurological signs may be present?

A
  • compression of optic chiasm (bitemporal hemianopia)

- compression of third nerve (down and out and open)

35
Q

WHat is the first line investigation for SAH?

A

CT head

36
Q

What is seen in CT of SAH?

A
  • Prominent filling of the basal cisterns in a five pointed ‘star’ pattern
  • Blood may be seen within the ventricles (maybe due to reflux from subarachnoid space)
37
Q

WHat are cisterns?

A
  • Large, expanded subarachnoid spaces, between arachnoid and pia mater
38
Q

If bleeding is confirmed what should be done?

A

CT angiogram if bleed confirmed
• Will allow direct visualisation of bleeding aneurysm of aneurysm sac
• Vital for planning surgery

39
Q

If the CT is negative with convincing history what should be done?

A

lumbar puncture

40
Q

WHat is the technique for LP?

A
  • Identify iliac crests (giving L4-L5 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 containers (allow to drip, don’t aspirate!)
41
Q

WHat are the typical findings of a LP in SAH?

A
  • Increased opening pressure
  • Frank blood or xanthochromia may be seen
  • High protein (blood constituents and haemoglobin)
  • White cells often not raised
  • Glucose not affected
  • High red cell count
42
Q

What is xanthochromia, how long after SAH presentation is it seen?

A

Yellow colouring of the CSF due to metabolism of haemoglobin to bilirubin within the subarachnoid space
• Seen at least 12 hours post bleed

43
Q

Why is presence of xanthochromia better than frank blood?

A

More specific than frank blood for SAH - helps exclude a bloody/traumatic tap

44
Q

how long should you wait before LP and why?

A
  • Should wait at least 6 hours (12+ is preferable)
  • Need time for lysis of red blood cells to take place (release of bilirubin)
  • This gives the CSF a yellow tinge after centrifuging (this can differentiate this from traumatic tap)
  • Xanthochromia
45
Q

What is the initial (non-surgical) treatment for SAH? (3)

A

ABC approach
• Support airway if diminished conscious level
• Give oxygen
• Support circulation

46
Q

What can be given to support circulation?

A
  • Fluids

- Maybe nimodipine to alleviate cerebral vasospasm

47
Q

What neurosugical treatment is available?

A
  • decompressive surgery (craniectomy)
  • coiling
  • clipping
48
Q

WHat is involved in clipping in SAH, who is it performed by?

A
  • Placement of a spring clip around the neck of the aneurysm, causing it to lose blood supply and ‘shrivel up’
  • Performed by neurosurgeons
49
Q

WHat is involved in coiling in SAH, who is it performed by?

A
  • Insertion of (frequently) a platinum wire into the aneurysm sac, which causes thrombosis of blood within the aneurysm itself
  • Performed by neuroradiologists
50
Q

within how many hours should patients be operated and why?

A

Operate on patients who have good neurological status within 48 hours
• To prevent re-bleeding

51
Q

How often does rebleeding occur after SAH?

A

30% within 2 weeks in unoperated patients

52
Q

What is the most common cause od death following aneurysmal SAH?

A

Delayed ischaemia from cerebral vasospasm

53
Q

compare encephalitis and meningitis

A
  • Infections focused on parenchyma (encephalitis)

* Infections focused on the meninges (meningitis)

54
Q

which parts of the meninges are affected in meningitis?

A

• Inflammation of the dura (rare)
• Inflammation of the Leptomeninges (essentially arachnoid tissue
and subarachnoid space) more common

55
Q

Most common cause of meningitis?

A

infection (bacterial or viral)

•Can occasionally be caused by fungal disease or non infectious modalities (trauma/surgery)

56
Q

What are the typical organisms that cause meningitis in neonates?

A
  • E. coli
  • Group B streptococcus (ahalactiae)
  • Listeria monocytogenes
57
Q

What are the typical organisms that cause meningitis in children?

A
  • Haemophilus influenzae type B (HiB vaccine given, ‘meningococcus’)
  • Neisseria meningitidis (vaccines given for some strains
58
Q

What are the typical organisms that cause meningitis in elderly?

A
  • Streptococcus pneumoniae (vaccines now given)

- Listeria monocytogenes

59
Q

What are the typical organisms that cause meningitis in adults?

A
  • Streptococcus pneumonia (pneumococcal meningitis)
  • Neisseria meningitides (meningococcal meningitis)
  • Haemophilus influenza (Hib meningitis)
60
Q

What are the risk factors for meningitis?

A
  • CSF defects (e.g. spina bifida)
  • Spinal procedures (e.g. surgery, lumbar puncture)
  • Endocarditis (as a focus of bacteraemia)
  • Diabetes (immunosuppression)
  • Alcoholism
  • Splenectomy (immunosuppression)
  • Crowded housing (students at risk)
  • Cochlear implants
61
Q

what is The triad of ‘meningism’ with fever associated with meningitis?

A
  • Headache
  • Neck stiffness (nuchal rigidity)
  • Photophobia
62
Q

What symptoms are associated with meningitis?

A
• Flu-like symptoms
• Joint pains and stiffness
• Seizure
• Meningococcal rash (non blanching)
• Drowsiness
• Patient may be in shock
• Babies: 
o Inconsolable crying / off feeds
o Rigidity / floppiness
o Bulging fontanelle (late sign)
63
Q

How might bacteria reach the CNS?

A
  • colonisation of the nasopharynx
  • ascent through eustachian tube to middle ear and then into CSF through mastoid air cells

or
• Colonisation of nasopharynx
• Seeding to lower respiratory tract (pneumonia)
• Lung inflammation allows bacteria to enter blood (bacteraemia)
• Invasion of CSF via capillaries that traverse choroid plexus or Subarachnoid space

64
Q

describe the pathophysiology of meningitis

A
  • The bacteraemia causes damage to vessel walls in the brain and meninges, allowing pathogen to enter the subarachnoid 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 intracranial pressure
65
Q

when is Maculopapular rash seen in ?

A

meningococcal septicaemia

66
Q

Why is a maculopapular rash seen in meningococcal septicaemia?

A

Caused by microvascular thrombosis ( bleeding into skin or mucosa) due to many factors, including

  • Sluggish circulation
  • Impaired fibrinolysis
  • Increased tissue factor expression in endothelial cells
67
Q

describe the features of rash in meningitis

A

a non blanching rash
• Larger lesions called termed purpuric
• Smaller lesions (1-2 mm) termed petechia

68
Q

where is the rash commonly found and who?

A
  • A petechial or purpuric rash usually is found on the trunk, legs, mucous membranes, and conjunctivae. Occasionally, it is on the palms and soles
  • Older patients have rash less commonly than younger
69
Q

What are the complications of meningitis?

A

▪ Septic shock (due to bacteraemia)
▪ DIC (due to bacteraemia)
▪ Raised ICP
▪ Coma (due to raised ICP)
▪ Cerebral oedema (due to cerebral inflammation)
▪ Death (due to brain herniation, sepsis)
▪ SIADH (maybe direct effect on hypothalamus/pituitary?)
▪ Seizures (due to irritation of brain parenchyma)
▪ Hearing loss (due to swelling of vestibulocochlear nerve or cochlea itself. Perilymph is continuous with subarachnoid space)
▪ Intellectual deficits (due to direct brain damage)
▪ Hydrocephalus (due to interruption of CSF drainage pathways and effect on arachnoid granulations)
▪ Focal paralysis (maybe due to cerebral abscess)

70
Q

What signs may be present on physical examination?

A
  • Kernig sign

- Brudzinsk

71
Q

What is Kernig sign?

A
  • Supine patient With thigh flexed to 90 degrees
  • Extension of knee is met with resistance
  • More common in children (up to 53%)
72
Q

What is brudzinsk sign?

A
  • When neck is Flexed there is an involuntary flexion of knees and hips
  • More common in children (up to 66%)
73
Q

What is the most important investigation for meningitis?

A

lumbar puncture

74
Q

What is the most important investigation for meningitis?

A
  • Cloudy CSF
  • High protein (immune proteins etc.)
  • High white cells, primarily neutrophils (which phagocytose bacteria)
  • Low glucose as bacteria (and white cells) metabolise it
75
Q

What is seen in LP in a viral meningitis?

A
  • Maybe clear but can be cloudy (due to immune cells and proteins)
  • Protein level may be normal or raised (as above)
  • High white cells, primarily lymphocytes to mount an adaptive response
  • Normal glucose (>60% plasma)
76
Q

When may doing a LP be dangerous?

A

When there is raised ICP

77
Q

What may happenn by doing an LP while there is raised ICP?

A

Precipitates the risk of brain herniation

78
Q

What are the best predictors to delay doing an LP?

A

Signs of raised ICP:
• Decreasing consciousness
• Brainstem signs
• Recent seizure

CT head may be useful

79
Q

What other investigations are done for meningitis?

A
  • bloods (compare to LP)
  • blood culture
  • PCR (from blood and CSF)
  • sepsis screen:
  • CXR and mid stream urine for septic focus
80
Q

What supportive treatment is given for meningitis?

A
  • Oxygen
  • Intubation in altered consciousness
  • Analgesia
  • Antipyretics
  • Fluids if shocked
81
Q

When should there be caution when giving fluids in meningitis?

A

Raised ICP

82
Q

What medical treatment is given for meningitis, what is given if viral cause?

A
  • IV Vancomycin + (Ceftriaxone or Cefotaxime)
  • Dexamethasone to prevent hearing loss (due to swelling of vestibulocochlear nerve or effect on cochlea
  • If viral: Aciclovir for Herpes, Ganciclovir for CMV