Subarachnoid Haemorrhage - Slide 1

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  • Subarachnoid hemorrhage (SAH). There is high-attenuation blood in the Sylvian fissures (blue arrows) and the interhemispheric fissure (red arrow) seen on this non-contrast enhanced CT of the brain. Do not confuse normal, physiologic calcifications (white and black arrows) for blood.
  • Subarachnoid Haemorrhage - Slide 1

    1. 1. Subarachnoid HaemorrhageSubarachnoid Haemorrhage
    2. 2. SAHSAH • What is it?What is it? – Bleeding into the subarachnoid space (spaceBleeding into the subarachnoid space (space between the pia & arachnoid meningeal layers) wherebetween the pia & arachnoid meningeal layers) where blood vessels lie & CSF flowsblood vessels lie & CSF flows • Where does the blood come from?Where does the blood come from? – An aneursym on a blood vessel in the subarachnoidAn aneursym on a blood vessel in the subarachnoid space has ruptured (~70%)space has ruptured (~70%) – Unknown (~15%)Unknown (~15%) – AVM (~10%)AVM (~10%) – Rare causes (e.g. tumour) (~5%)Rare causes (e.g. tumour) (~5%) • Where does the blood go?Where does the blood go? – Anywhere where CSF goes, may get hydrocephalus ifAnywhere where CSF goes, may get hydrocephalus if into ventricle & causes obstruction of CSF circulationinto ventricle & causes obstruction of CSF circulation
    3. 3. SAHSAH • Incidence = 1/7000 peopleIncidence = 1/7000 people • Higher chance if:Higher chance if: – FemaleFemale – 33rdrd trimester of pregnancytrimester of pregnancy – Middle-agedMiddle-aged – Abuse of stimulant drugsAbuse of stimulant drugs – Connective tissue disorderConnective tissue disorder – Family historyFamily history
    4. 4. What causes aneurysms to form?What causes aneurysms to form? • Defects in the media of the arteriesDefects in the media of the arteries • Defects are thought to expand as a resultDefects are thought to expand as a result of hydrostatic pressure from pulsatileof hydrostatic pressure from pulsatile blood flow and blood turbulence, which isblood flow and blood turbulence, which is greatest at the arterial bifurcationsgreatest at the arterial bifurcations
    5. 5. What causes aneurysms toWhat causes aneurysms to rupture?rupture? • The probability of rupture is related to the tension on theThe probability of rupture is related to the tension on the aneurysm wallaneurysm wall • The law of La Place states that tension is determined byThe law of La Place states that tension is determined by the radius of the aneurysm and the pressure gradientthe radius of the aneurysm and the pressure gradient across the wall of the aneurysmacross the wall of the aneurysm • Therefore, the rate of rupture is directly related to theTherefore, the rate of rupture is directly related to the size of the aneurysmsize of the aneurysm • Aneurysms with a diameter of 5 mm or less have a 2%Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas 40% of those 6-10 mm haverisk of rupture, whereas 40% of those 6-10 mm have already ruptured upon diagnosisalready ruptured upon diagnosis
    6. 6. SAH – The ProblemSAH – The Problem • They occur in young peopleThey occur in young people – 80% in 40-65 year olds80% in 40-65 year olds – 15% in 20-40 year olds15% in 20-40 year olds • It can kill quicklyIt can kill quickly – 25% die within 24 hours25% die within 24 hours – 50% will be dead at 6 months50% will be dead at 6 months • It causes significant disabilityIt causes significant disability – Cognitive impairmentCognitive impairment – Neurological disability depending on size of bleed &Neurological disability depending on size of bleed & complications encounteredcomplications encountered
    7. 7. How do they present?How do they present? • HeadacheHeadache – sudden onset & severesudden onset & severe – small leak may cause minor headache & may besmall leak may cause minor headache & may be warning sign of rupturewarning sign of rupture • Reduced consciousnessReduced consciousness • MeningismMeningism – VomitingVomiting – Neck stiffnessNeck stiffness – PhotophobiaPhotophobia • SeizuresSeizures
    8. 8. What causes symptoms & signs?What causes symptoms & signs? • Blood leaking from the aneurysmBlood leaking from the aneurysm • Local pressure effects of the aneurysmLocal pressure effects of the aneurysm • Associated ICHAssociated ICH • EmboliEmboli
    9. 9. What causes symptoms & signs?What causes symptoms & signs? • Blood leaking from the aneurysmBlood leaking from the aneurysm – HeadacheHeadache – MeningismMeningism
    10. 10. What causes symptoms & signs?What causes symptoms & signs? • Local pressure effects of the aneurysmLocal pressure effects of the aneurysm – AcomAcom • Visual symptoms due to optic chiasm compressionVisual symptoms due to optic chiasm compression • Positive babinskiPositive babinski • Bilateral lower limb paresisBilateral lower limb paresis – MCAMCA • Contralateral hand & face paresisContralateral hand & face paresis • Contralateral visual neglectContralateral visual neglect • Aphasia (dominant side)Aphasia (dominant side) – ICA/PcomICA/Pcom
    11. 11. What causes symptoms & signs?What causes symptoms & signs? • Associated ICHAssociated ICH – The aneurysm usually lies within the subarachnoidThe aneurysm usually lies within the subarachnoid cisternscisterns – It can become adherent to adjacent brain due toIt can become adherent to adjacent brain due to adhesions (e.g. from a previous leak)adhesions (e.g. from a previous leak) – The bleed therefore can also extend into the brainThe bleed therefore can also extend into the brain • MCA = TL causing hemiparesis & aphasia (if dominant)MCA = TL causing hemiparesis & aphasia (if dominant) • Acom = mutismAcom = mutism – AVM is more likely to cause ICH as they usually lieAVM is more likely to cause ICH as they usually lie somewhat in brain parenchymasomewhat in brain parenchyma
    12. 12. HeadacheHeadache • A sudden onset severe headacheA sudden onset severe headache ISIS caused by a SAHcaused by a SAH untiluntil you have doneyou have done investigations which prove otherwiseinvestigations which prove otherwise
    13. 13. Sudden onset severe headacheSudden onset severe headache
    14. 14. Sudden onset severe headacheSudden onset severe headache
    15. 15. InvestigationsInvestigations • CT scan without contrastCT scan without contrast • Lumbar punctureLumbar puncture • CT COWCT COW • Cerebral angiogramCerebral angiogram • MRI/MRAMRI/MRA 98% sensitive @ 12 hours 80% at day 3 50% at day 7 Also good to see if any associated ICH or hydrocephalus. May help localise the location of the aneurysm if there is more than 1 & may also see AVM
    16. 16. Where is the aneurysm? • Where is the blood on the CT scan? – Basal cisterns – COW aneurysm – Sylvian fissure – ICA, Pcom, MCA – Interhemispheric or intraparenchymal - Acom
    17. 17. • A cistern where the arachnoid extends across between the two temporal lobes, and encloses the cerebral peduncles including the structures contained in the interpeduncular fossa . MCA stroke - Emergency neuroradiology. Axial CT scan at the level of the basal cisterns shows the "hyperdense middle cerebral artery (MCA) sign" (arrow) representing acute clot within the right middle cerebral artery, accounting for the patient's clinical symptoms
    18. 18. SAH & LP • CT & LP are critical to diagnosing SAH • No need for LP if obvious blood in subarachnoid space on CT • Blood may not be evident on CT, especially if it is performed > few days after bleed • LP should only be performed after 12
    19. 19. SAH & LP • When blood enters the CSF (e.g. from SAH or during LP) the red cells are broken down & oxyhaemoglobin is released • It then takes 12 hours for the oxyhaemoglobin to be converted into bilirubin – conversion is via an enzyme found in the brain. • Bilirubin in the CSF, therefore, tells us that blood must have been in the subarachnoid space for at least 12 hours • Blood which entered the CSF during the LP would not encounter the enzyme & could not produce bilirubin • The CSF will look xanthochromic (yellowish discolouration) if bilirubin is present which they will look for with spectroscopy in the lab
    20. 20. What may I find on examination?What may I find on examination? • Normal examNormal exam • Confusion/memory lossConfusion/memory loss • AphasiaAphasia • CN abnormalitesCN abnormalites – CNII – papilloedema, usually mild initially & retinalCNII – papilloedema, usually mild initially & retinal haemorrhageshaemorrhages – CNIII – palsyCNIII – palsy • Hemiparesis/neglectHemiparesis/neglect • Obs – HTN, tachycardic, febrileObs – HTN, tachycardic, febrile
    21. 21. TreatmentTreatment • Main aim is damage control – want toMain aim is damage control – want to prevent further bleeding & try to avoid theprevent further bleeding & try to avoid the complications that SAH patients getcomplications that SAH patients get • SAH patients will vary greatly from GCSSAH patients will vary greatly from GCS 15/15 to GCS 3/1515/15 to GCS 3/15
    22. 22. To coil or clip? • Coiling – Endovascular technique done in angiography by interventional radiologists under GA – May be best if small necked aneurysm – Used in particularly sensitive areas e.g. basilar tip – Must be able to access the aneurysm (e.g. any stenosis or tortuous vessels) – Like dome:neck ratio to be 2:1 or greater • Clipping – Craniotomy & careful dissection using microscope to reach aneurysm & clip usually at neck – May be performed after failed clipping – If aneurysm can’t be reached by the endovascular root
    23. 23. That’s DandyThat’s Dandy • First to clip anFirst to clip an aneursymaneursym successfully in 1937successfully in 1937 • Walter DandyWalter Dandy
    24. 24. Operative microscope •
    25. 25. Complications with SAHComplications with SAH 1.1. Re-bleedingRe-bleeding 2.2. HydrocephalusHydrocephalus 3.3. VasospasmVasospasm 4.4. HyponatraemiaHyponatraemia 5.5. SeizuresSeizures
    26. 26. Complications with SAHComplications with SAH • Re-bleedingRe-bleeding – 80% mortality if re-bleed80% mortality if re-bleed – Greatest risk is in the first 24 hours after theGreatest risk is in the first 24 hours after the initial bleedinitial bleed – Aim to prevent by controlling BP to avoidAim to prevent by controlling BP to avoid dramatic changes & isolate the aneurysmdramatic changes & isolate the aneurysm from the circulation (coil or clip)from the circulation (coil or clip)
    27. 27. Complications with SAH • Hydrocephalus – Obstructive • Blood enters the ventricles & can block the flow of CSF e.g. at the aqueduct or outlet of the 4th ventricle – Communicating • Due to blood blocking reabsorption of CSF through the arachnoid granules – May need an extraventricular drain to treat – Keep head of bed at 300 (promote CSF flow & venous return)
    28. 28. Complications with SAH • Vasospasm – Blood vessel goes into spasm causing ischaemia - stroke – To prevent keep them filled with at least 3L fluid day & nimodipine IV/PO & insert central line to monitor central venous pressure – aiming for 8-10 – Suspected with deteriorating GCS/new neurological deficit – Treatment – Urgent CT brain to rule out a bleed as a cause of the deterioration then urgent angiogram to diagnose & treat vasospasm – Greatest risk of vasospasm is days 4-7 but significant risk for first 3 weeks after bleed, therefore will use preventative measures for at least 3 weeks
    29. 29. Complications with SAH • Hyponatraemia – Susceptible due to being fluid loaded & cerebral salt wasting – Cerebral salt wasting = renal loss of sodium due to intracranial pathology ? Cause. Loss of water & salt (whereas SIADH is loss of salt & retention of water) – Treat with normal or hypertonic saline – If refractory may need a mineralocorticoid e.g. fludrocortisone to stimulate renal reabsorption – but this should only be used under instructions from consultant endocrinologist
    30. 30. Complications with SAH • Seizures – A seizure is a disturbance of sensation, movement or consciousness – All seizures originate from the surface of the brain – cortex – Blood is an irritant to the cortex – Prophylaxis with phenytoin or levetiracetam – Ensure phenytoin levels are therapeutic – Treat as seizure from any cause & suspect re-bleed
    31. 31. Complications with SAH • VTE – On bed rest – TEDS – Prophylactic enoxaparin as soon as consultant sees fit – Always keep VTE in the back of your mind
    32. 32. How are SAH graded?How are SAH graded? GCS 15, onlyGCS 15, only CN deficit if anyCN deficit if any Grade 1Grade 1 No bloodNo blood GCS 13-14, noGCS 13-14, no deficitdeficit Grade 2Grade 2 Diffuse blood,Diffuse blood, no clots &no clots & <1mm<1mm GCS 13-14,GCS 13-14, with deficitwith deficit Grade 3Grade 3 Clots & bloodClots & blood 1mm or more1mm or more GCS 7-12, +/-GCS 7-12, +/- deficitdeficit Grade 4Grade 4 ICH orICH or intraventricularintraventricular clotsclots GCS 3-6 +/-GCS 3-6 +/- deficitdeficit Grade 5Grade 5 World Federation Neurosurgeons Fischer grading
    33. 33. Subdural HaematomaSubdural Haematoma
    34. 34. Extra-dural haematomaExtra-dural haematoma
    35. 35. Extra-dural haemtomaExtra-dural haemtoma
    36. 36. Intra-parenchymal haematomaIntra-parenchymal haematoma

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