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Sem 4: Nervous System > 10c.) Subarachnoid Haemorrhage & Meningitis > Flashcards

10c.) Subarachnoid Haemorrhage & Meningitis Flashcards

1
Q

What % of strokes do subarachnoid haemorrhages account for?

A

6%

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2
Q

Are subarachnoid haemorhages more common in males or females?

What age range are subarachnoid haemorrhages more common in?

A
  • Females (1.6:1)
  • <50yrs
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3
Q

Do subarachnoid haemorrhages carry a high mortality and morbidity?

A

Yes

  • Mortality= 50%
  • Morbidity=60% (most people suffer long term morbidity following event)
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4
Q

State 8 risk factors for subarachnoid haemorrhages

A
  • Hypertension
  • Smoking
  • Excess alcohol consumption
  • Predisposition to aneuryseum formation
  • Family history
  • Associated conditions (CKD, Marfan’s, neurofibromatosis)
  • Trauma
  • Cocaine use
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5
Q

Describe why CKD is a risk factor for subarachnoid haemorrhage

A
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6
Q

Describe why Marfan’s syndrome is a risk factor for subarachnoid haemorrhage

A
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7
Q

State some roles of CSF

A
  • Physical support of neural structures “render them weightless”
  • Excretion (of products from brain metabolism)
  • Intracerebral transport (hormone releasing factors)
  • Control of chemical environment
  • Volume changes reciprocally with volume of intracranil contents
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8
Q

Describe the pathophysiology behind subarachnoid haemorrhages

A

Rupture of aneurysm in circle of willis; most often is rupture of a berry aneurysm

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9
Q

What is an aneurysm?

A

Weakness in a vessel (usually an artery) leading to an abnormal bulge (dilation)

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10
Q

Aneurysms can have genetic predisposition but they can also be caused by haemodynamic effects; describe the hameodynamic effects that can lead to aneurysms

A

As smaller arteries branch off and turbulence is created it can put extra pressure on walls

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11
Q

Where are aneurysms most common in the circle of Willis?

A

Aneurysms in circle of Willis are usually at bifurcation points; the following places account for 75% of all aneurysms in circle of Willis:

  • Anterior communicating artery/proximal anterior cerebral artery (30%)
  • Posterior comminicating artery (25%)
  • Bifurcation of middle cerebral artery as it splits into superior & inferior divisons (20%)
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12
Q

What structures could an aneurysm in the anterior communicating artery/anterior cerebral artery compress?

A
  • Optic chiasm
  • Pituitary
  • Frontal lobe
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13
Q

What structure could an aneurysm of the posterior communicating artery compress?

A

Adjaent occulomotor nerve side leading to ipsilateral 3rd nerve palsy

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14
Q

Why are intracranial arteries susceptible to aneurysms?

A
  • Lack external elastic lamina
  • Thin adventitia
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15
Q

Describe what happens following a subarachnoid haemorrhage that can lead to early brain injury

A
  • Microthrombi form: occlude smaller distal arteries
  • Vasoconstriction: blood in CSF causes irritation of cerebral arteries
  • Cerebral oedema: brains response to hypoxia and extravasted blood
  • Apoptosis of brain cells
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16
Q

Alongside microthrombi, vasoconstriction, cerebral oedema and brain cell apoptosis; what other 3 cellular changes occur following a subarachnoid haemorrhage

A
  • Oxidative stress: perhaps related to reperfusion
  • Release of inflammatory mediators: can activate many pathways as well as activating microglia
  • Platelet actiavtion: formation of thrombi
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17
Q

State, and explain, 3 systemic complications following a subarachnoid haemorrhage

A
  • Sympathetic activation: early Cushing response as ICP increases
  • Myocardial necrosis: due to sympathetic activation (NOTE: SAH has typical ECG features)
  • Systemic inflammatory response:can affect multiple systems
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18
Q

State 3 local complications following a subarachnoid haemorrhage

A
  • Early re-bleeding
  • Acute hydrocephalus (if blood in subarachnoid space blocks normal CSF drainage)
  • Global cerebral ischaemia
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19
Q

What ECG changes may be seen on a patient who has had a subarachnoid haemorrhage?

A

ST elevation (providing myocardial necorsis has occured)

*NOTE: troponin would also be raised

20
Q

Describe the typical presentation of someone who has suffered a subarachnoid haemorrhage

A
  • Thunderclap headache
    • Sudden in onset, severe, worst headache ever, diffuse pain, can last an hour to a week
  • Loss of consciousness & confusion
  • Meningism
    • Neck stiffness
    • Photophobia
    • Headache
  • May be foacl neurology
  • May be history of sentinel headahces (due to prior minor leaks)
  • May present as cardiac arrest (if intracranilal pressure rises rapidly following a bleed leading to profound Cushing’s response)
  • Nausea/vomitting
21
Q

Describe the investigations that will be done for a suspected subarachnoid haemorrhage

A
  • CT scan
  • If convincing history, but negative CT do lumbar puncture *CAUTION: as can precipitate brain herniation if there is underlying brain patholgy such as in haemorrhage
  • Angiography: once diagnosis is confirmed to angiography to see where the aneruysm is
22
Q

Describe the appearance of a CT scan in someone who has had a subarachnoid haemorrhage

A
  • Prominent filling of basal cisterns in five pointed “star” pattern
  • Blood may be seen in ventricles
  • Ventricles may be compressed
23
Q

If you are performing a lumbar puncture due to suspected SAH and inconclusive CT, why must you wait at least 6 hours (ideally 12 hours)

A
  • When you do a lumbar puncture you could rupture some small vessels as you do this; this would lead to blood in CSF and hence a false positive result
  • If we wait at least 12 hours it gives time for lysis of RBCs in CSF and hence release of bilirubin; we can then test the CS for bilirubin as oppose to RBCs to determine if it is actually a SAH or just blood from the procedure
  • Centrifuging CSF will show xanthochromia (yellow-ish tinge to CSF due to bilirubin)
24
Q

What is xanthochromia?

A

Yellow-ish tinge to CSF due to bilirubin

25
Q

If you tested CSF following SAH what would each of the following levels be like:

  • Protein
  • WCC
  • Glucose
A
  • Protein= high (due to blood constituents & Hb)
  • WCC= normal (no infec)
  • Glucose= normal
  • RCC= high
26
Q

Describe the technique for doing a lumbar puncture

A
  • Identify iliac crests (gives you L4-L5 level)
  • Give local anaesthetic
  • Insert LP needle between spinous processes and through supraspinatous and interspinatous ligaments
  • As you then pass through ligamentum flavum & dura you should feel the needle ‘give’
  • Remove needle stylet and collect CSF in sterile containers
  • ALLOW TO DRIP, don’t aspirate
27
Q

In a SAH, what would the opening pressure on a lumbar puncture be?

A

Opening pressure would be increased/high due to additional volume in the subarachnoid space

28
Q

Describe the treatment for a SAH

A
  • ABC approach
    • Airway support if diminished conscious level
    • Give oxygen
    • Support circulation
      • Fluids
      • Nimodipine to alleviate cerebral vasospasm
  • Neurological observations
    • Looking for signs of increasing ICP
  • Neurosurgery
    • Decompressive surgery (craniectomy)
    • Coiling
      • Insertion of a (most often) platinum wire into aneurysm sac which causes thrombosis of blood within the aneurysm itself
    • Clipping
      • Put a spring clip around neck of anuerysm causign it to lose blood supply and ‘shrivel up’
29
Q

Discuss the mortality of SAH

A
  • Some die before they reach hosptial (10-15%)
  • Some die in 24 hours (25%)
  • 40% mortality in first month
  • 50% mortality in first 6 months
  • About a third of survivors have neurological deficits
30
Q

What is the most common cause of meningitis: viral, bacterial, fungal or non-infective?

A

Most common is bacterial or viral

  • *NOTE: bacterial is worse. Those with normal immune systems and viral meningitis usually get better on their own*
  • *Last two causes are rare*
31
Q

State the typical organisms causing bacterial meningitis in:

  • Neonates
  • Children
  • Adults
A
  • Neonates:
    • E.COli
    • Group B streptococcus
    • Listeria monocytogenes
  • Children
    • Hameophilius influenza type B
    • Neisseria meningitidis
  • Adults
    • Neisserie meningitidis
  • Elderly
    • Streptococcus pneumoniae
    • Listeria monocytogens
32
Q

Descirbe the symptoms of meningtis (include specific symptoms present in babies)

A

*NOTE: baby could be floppy or rigid

33
Q

State some risk factors for meningitis (state at least 5)

A
  • Diabetes (immunosupression)
  • CNS defects (e.g. spina bifida)
  • Splenectomy (immunosupression)
  • Crowded houses (e.g. students)
  • Endocarditis (source of bacteraemia)
  • Alcoholism
  • Spinal procedures (e.g. surgery, lumbar puncture)
34
Q

A rash is not always present in meningitis; with what bacteria is the rash most common?

A

Meningococcal meningitis

35
Q

Describe the rash which is sometimes seen in meningitis and why it occurs

A
  • NOTE: rash is indicative of sepsis so only see if you have sepsis & meningitis
  • Occurs due to disseminated intravascular coagulation (widespread activation of intravascular coagulation). Lots of small clots form using up coagulation factors, blood then has less clotting factors circulating. Damage to blood vessels results in bleeding from vessels. When bleed into skin this forms petechiae. Petechia can coalesce to form larger regions called ecchymoses.
  • Rahs is blud/purple, NON-BLANCHING (do Tumbler test) and is commonly seen on trunk, lower body and sometimes sclera/mucous membranes
36
Q

Describe the pathophysiology of meningitis

A
  • Pathogens which usually live in nose enter circulation and cause bacteraemia
  • Bacteraemia causes damage to blood vessel walls in brain and meninges- allowing pathogens to enter the subarachnoid space
  • Once in subarachnoid space, pathogens multiply rapidly producing purulent CSF & severe meningeal inflammation
  • Vasospasm of cerebral vessels can cause cereral infarction
  • Oedema of brain parenchyma can cause raised ICP
  • Maculopapular rash (DIC rash) seen in meningococcal septicaemia
37
Q

Discuss the prognosis of meningitis

A
  • Prior to antibiotics it was almost always fatal
  • Mortality still high (25%) even with antibiotics
  • Vaccines against Hameophilius influenza B (HiB), streptococcus pneumonia (PCV13) and Neisseria meningitidis (many vaccines against different strains) have also reduced incidence of meningitis
38
Q

State, and describe, 3 ways in which bacteria can reach the CNS

A

Remember, start with colonisation in nasopharynx

  • Eustachian tube
    • Ascent through Eustachian tube to reach middle eat (causing acute otitis media). Prolonged infection in middle ear can lead to spread, via mastoid air cells, into CSF
  • Via lower respiratory tract:
    • Seeding to lower respiratory tract (cause pneumonia)
    • Lung inflammation allows bacteria to enter blood
    • Bacteria invade CSF via capillaries that traverse choroid plexus or subarachnoid space
  • Neonates can get it from maternal source
    • E.g. placenta, reproductive tract secretions etc…
39
Q

State 4 investigations you might do if you suspect meningitis (highlight the most important of these investigations)

A
  • Bloods: sepsis screen & PCR
  • CXR: if you think they are septic
  • Mid stream urine: if you think they are septic
  • Lumbar puncture: can help differentiate between bacterial & viral (alongside blood tests)
40
Q

Describe CSF when someone has bacterial meningitis, include:

  • Appearance
  • Protein content
  • White cell content
  • Glucose
A
  • Cloudy CSF
  • High protein (due to immune proteins etc)
  • High white cells (primary neutrophils)
  • Low glucose (bacteria & white cells metabolise it)
41
Q

Describe CSF when someone has viral meningitis, include:

  • Appearance
  • Protein level
  • White cell level
  • Glucose
A
  • Maybe clear, maybe cloudy (due to immmune cells & proteins)
  • Protein level may be normal or raised (immune proteins etc..)
  • High white cells, primarily lymphocytes to mount an adpative response
  • Normal glucose (>60% plasma)
42
Q

State two physical examination findings/physical tests that are indicative of meningitis

NOTE: both these tests more commonly have +ve results in children

A
43
Q

If someone has raised ICP and you do a lumbar puncture you increase the chance of brain herniation; state 3 clinical signs that could indicate raised ICP and hence convince you to do a CT before doing lumbar puncture

A
  • Decreasing consciousness
  • Brainstem signs
  • Recent seizure

*NOTE: a normal CT does not necessarily mean it is safe to perform a LP

44
Q

Describe both the supportive and medical treatment for meningitis

A

Supportive:

  • Analgesia
  • Antipyretics
  • Fluids if shocked
  • Oxygen
  • Intuation if necessary

Medical if bacterial

  • IV ceftriaxone (may also give vancomycin)
  • Dexamethosone to prevent hearing loss (swelling of CNVIII or damage to cochlea can occur)

Medical if viral

  • Aciclovir for Herpes
  • Ganciclovir for cytomegalovirus
45
Q

State at least 6 complications of meningitis

A
  • Septic shock
  • Disseminated intravascular coagulation
  • Coma (due to raised ICP)
  • Death (brain herniation, sepsis)
  • SIADH (maybe direct effect on hypothalamus/pituitary)
  • Seizures (irritation of brain parenchyma)
  • Hearing loss (swelling of CNVIII or cochlea itself since perilymph is continous with subarachnoid space)
  • Intellectual deficits (direct damage to brain)
  • Hydrocephalus (interruption of CSF drainage pathways and effect on arachnoid granulations)
  • Focal paralysis (maybe due to cerebral abscess)

Sem 4: Nervous System (21 decks)

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