16 - Meningitis and Subarachnoid Haemorraghe Flashcards

1
Q

What are the main differences between the three types of extracerebral haemorraghe? e.g mechanism, CT appearance, presentation, risk factors and management

A
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2
Q

What is the function of the subarachnoid space?

A
  • Between arachoid and pia mater and contains CSF
  • CSF can compensate when there is an increase in ICP by decreasing in volume
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3
Q

How does CSF drain from the ventricular system and spinal canal back to the blood?

A

Cilliary action of ependymal cells and vascular pulsations cause it to move and then reabsorbed into the sagittal sinuses via arachnoid granulations

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4
Q

What layer of the brain is the Circle of Willis situated in?

A

SUBARACHNOID

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5
Q

What is the epidemiology of subarachnoid haemorraghes?

A
  • 6% of all strokes
  • More prevalent in females 1.6:1
  • Most under 50 (50-55)
  • More common in black and Finnish
  • 50% mortality, 60% long term problems after
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6
Q

What are some risk factors for a subarachnoid haemorraghe?

A
  • Smoking
  • Hypertension
  • Excess alcohol consumption
  • Predisposition to aneurysm formation e.g EDS
  • Family history
  • CKD, Marfan’s, Neurofibromatosis
  • Trauma
  • Cocaine use
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7
Q

How does a subarachnoid haemorraghe present?

A

- Thunderclap headache (sudden onset and severe, diffuse and sentinel can start up to a week before)

  • Loss of consciousness and confusion
  • Meningism (neck stiffness, photophobia, headache)

- Focal neurology

- History of sentinel bleed (previous headache)

- May present as cardiac arrest due to Cushing’s after bleed

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8
Q

What is the general pathophysiology of a subarachnoid haemorraghe?

A

- Rupture of a berry aneurysm or AVM in the circle of Willis and 80% non-traumatic

  • Risk factors for developing aneurysms are the same as CVS e.g hypertension, genetic predisposition
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9
Q

Where do berry aneurysms in the cerebral circulation normally occur?

A

- ACA (30%): can compress optic chiasm and frontal lobe/pituitary

- PCA (25%): can compress occulomotor nuclei so ipsilateral third nerve palsy

- Bifurcation of MCA into superior and inferior (20%)

  • Most in anterior circulation as lots of birfurcations and these are weaker
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10
Q

Why are large cerebral arteries affected by aneurysms more than the smaller ones?

A
  • Small ones are less likely to rupture
  • Intracranial large communicating arteries lack external elastic lamina and have thin adventitia so are weaker
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11
Q

Why may someone have sentinel headaches in the months before a subarachnoid haemorraghe and why do they get meningism when the aneurysm ruptures?

A
  • Minor leaks from the aneurysm
  • Blood gets into the subarachnoid space which is irritant
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12
Q

What happens when there is a bleed into the subarachnoid space that causes the early brain injury?

A

- Microthrombi can be released and occlue smaller distal arteries

- Vasoconstriction due to irritation by blood

- Cerebral oedema due to general inflammatory response of tissue hypoxia

- Apoptosis of brain cells

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13
Q

What are some cellular changes that occur when there is a subarachnoid haemorraghe?

A

- Oxidative stress due to reperfusion

- Release of inflammatory mediators activating microglia/paths

- Platelet activation so formation of thrombi

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14
Q

What are some systemic complications with a subarachnoid haemorraghe?

A

- Sympathetic activation due to Cushing’s response

- Myocardial necrosis due to sympathetic activation so appears as MI on ECG

- Systemic inflammatory response

  • Can also get early rebleeding, acute hydrocephalus by blood blocking CSF drainage, global cerebral ischaemia
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15
Q

What imaging investigations do we do into a suspected subarachnoid haemorraghe and what signs would we see on the images?

A

- CT head without contrast as contrast will look like blood

  • Filling of basal cisterns in five point star pattern
  • May be blood in the ventricles
  • Once confirmed do angiography to confirm location and do surgical planning
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16
Q

Apart from doing a CT scan, what other investigation do you need to do to confirm a subarachnoid haemorraghe and what is the technique for this?

A

Lumbar Puncture (AFTER 6 HOURS)

  • Identify iliac crest (L4/L5)
  • Give local anaesthetic
  • Insert LP needle between spinous process and punch through supra and interspinous ligaments and then lig flavum and dura
  • Remove needle and allow CSF to drip (DONT ASPIRATE)
17
Q

What findings would there be in the lumbar puncture of someone with a SAH?

A
  • Increased opening pressure due to raised ICP
  • Frank blood or xanthochromia (after 12 hours)
  • High protein
  • Normal glucose and WBC
  • High red cell count
18
Q

Why is it better to do a lumbar puncture 6-12 hours after an SAH?

A
  • Can see xanthochromia due to metabolism of haemoglobin to bilirubin in the CSF
  • Helps exclude a traumatic tap
19
Q

How is an SAH treated?

A

- ABC: check airway support, give oxygen, give fluids, give nimodipine to stop cerebral vasospasm and secondary ischaemia

- Neurological observations: check signs to see if ICP rising

- Neurosurgery to prevent re-bleeding and treat

20
Q

What are some surgical options after a subarachnoid haemorraghe?

A
  • Decompressive craniectomy
  • Coiling: platinum wire into the aneurysm sac, which causes thrombosis of blood within the aneurysm itself. done by neuroradiologists

- Clipping: spring clip around the neck of the aneurysm, causing it to lose blood supply and shrivel up. done by neurosurgeons

21
Q

What is the prognosis of someone with a subarachnoid haemorraghe?

A
  • 10-15% die before hospital
  • 25% die within 24 hours
  • 40% mortality in first month from rebleeding and intraventricular blood is an indicator of this

DELAYED ISCHAEMIA FROM CEREBRAL VASOPSPASM IS MOST COMMONEST CAUSE OF DEATH

22
Q

What are some risk factors for meningitis?

A
  • Mainly bacterial but can be viral, fungal or non-infective
  • Pyogenic inflammation of leptomeninges and this can then lead to encephalitis
  • <5 and >65 affected the most
23
Q

What organisms are the most common cause of meningitis?

A

Neonates: E.Coli, Group B Streptococcus, Listeria monocytogenes

Children: HiB, Neisseria Meningitidis (vaccines)

Elderly: Strep Pneumoniae (vaccine available), Listeria monocytogenes

24
Q

What are the clinical features of meningitis in adults and babies?

A

- Meningism Triad: photophobia, neck stiffness, headache

- Seizures

- Meningococcal rash

- Drowsiness

- Shock

25
Q

Why does a rash occur in meningitis?

A
  • Occurs in meningococcal (N.Meningitidis)
  • Bleeding into skin or mucosa causing non-blanching petechiae rash that can join to become purpuric
  • Microvascular thrombi
26
Q

What is the pathophysiology of bacteria causing meningitis getting to the meninges?

A
  • Colonisation of nasopharynx the ascent of bacteria through ET to middle ear and infection can spread into CSF e.g mastoid sinus

OR

  • Colonisation of nasopharynx, seeding to lower respiratory tract causes pneumonia, lung inflammation allows bacteria to enter blood (bacteraemia) and bacteria invades CSF by destroying capillaries over choroid plexus so can get into subarachnoid space

OR

Neonates can get pathogens from placenta or reprodutive tract

27
Q

Once bacteria has reached the meninges, how do the bacteria cause meningitis?

A

- 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
  • Maculopapular rash seen in meningococcal septicaemia by microvascular thrombosis due to:

o Sluggish circulation
o Impaired fibrinolysis
o Increased tissue factor expression in endothelialcells

28
Q

What investigations do we do in suspected meningitis?

A
  • Blood cultures with sepsis screen and PCR
  • CXR or midstream urine if suspected septic focus
  • Lumbar puncture (check ICP as don’t want to cause herniation)
29
Q

What findings would be on a lumbar puncture from viral and bacterial meningitis?

A

Bacterial:

  • Cloudy (lots of WBCs like neutrophils)
  • Elevated protein due to immune proteins
  • Low glucose as bacteria and immune cells metabolis it
  • +ve gram stain

Viral (more common but treatment supportive)

  • Clear or cloudy
  • Normal or raised protein
  • Normal glucose
  • High WBCs but mainly lymphocytes because of adaptive immune response
30
Q

When should we delay a lumbar puncture due to suspected raised ICP (as you don’t want to cause a herniation)?

A
  • Decreasing consciousness
  • Brainstem signs
  • Recent seizure
  • Can do CT but normal CT doesn’t mean safe to do LP
31
Q

How do we treat meningitis?

A

Supportive: analgesia, antipyretics, fluids if shock, oxygen, airway support

Specific: IV Ceftriaxone ASAP (bacterial) or Aciclovir (viral herpes) or Ganiclovir (CMV).

  • Dexamethasone to prevent hearing loss due to swelling of vestibulocochlear nerve or cochlea
32
Q

What are some complications of meningitis?

A
33
Q

A four year old boy develops visual disturbance over a period of three months, accompanied by headache and vomiting. A tumour in the left hemisphere is suspected, what other clinical signs may there be?

A
34
Q

The boy’s parents are told that without surgical intervention, his condition will deteriorate. Focusing on the movement of fluid within the cranial cavity in the context of raised intracranial pressure, give an account of the pathophysiology of how his condition may progress

A