Subarachnoid Haemorrhage When to screen? Whom to treat?
Subarachnoid Haemorrhage When to screen? Whom to treat?
ASHIS PATHAK
LEAD CONSULTANT for
VASCULAR NEUROSURGERY
HULL ROYAL INFIRMARY
ASHIS PATHAK
LEAD CONSULTANT for
VASCULAR NEUROSURGERY
HULL ROYAL INFIRMARY
SAH
• 9% of all strokes
• 75% caused by ruptured aneurysms
• 6% by AVMs
• 6% due to bleeding diathesis
• 13% no cause
Ruptured Intra-Cranial Aneurysms
Classical presentation• First described in Bible• Probably first mentioned in scientific literature by
Bonet 1679• Devastating headache, collapse, abrupt in onset,
incapacitating in severity• Diffuse, often radiates posteriorly & down to neck• Accompanied by blunting of consciousness, vomiting,
stiff neck, sometimes subhyaloid hges
• Headache remains for hours, more commonly days then clears off in few weeks, survival permitting
Pathogenesis of Headache in SAH• Initial pain
Stretching & tearing of distended vessel and adjacent
arachnoid
Sudden transmission of intra arterial pressure to the
rigid intracranial compartment
• Post-ictal pain
Chemical irritation of pain sensitive meninges by
blood
• Delayed pain
Chemical meningitis
Vasospasm
Hydrocephalus
Infarction
Sentinel bleed
• Less dramatic symptom - unusual sudden headaches, vomiting, dizziness• Up to 10% cases• Indicate small bleeds
CT negative SAH
• CT positivity depends on
Grade of SAH
Time after Hge
Quality of scan
• After few days SA blood becomes isodense
• Minor leak
• Blood localised around the aneurysm
CT negative SAH
• Lumbar Puncture
Contraindications: Abnormal clotting, Raised ICP,
Spinal AVM
• CSF Pressure normal to raised
RBC 10,000 to 50,0000 ?mm3
WBC increased in proportion to red cells
Glucose N
Proteins high (for 1000 RBC 1.5 Gm /dl proteins)
CT negative SAHCSF to be kept at 4 0 C & centrifuged immediately
Xanthochromia - Spectrophotometry appears within Hrs universal after 12 hours
Spectrophotometry – No haemoglobin or bilirubin after few hours further investigations not necessary unless strong history
After 3 weeks - History is most important angiography decisive
Warning leak / Bleed
Prerupture Manifestations• III N palsy 7% -12% of aneurysm pts III N palsy prior to rupture 20-30% of isolated IIIN palsy are due to aneurysm Mean time from onset of palsy to rupture - 29.6 days• Patient with oculomotor palsy with headaches is an
emergency, ideally needs CT & angiogram• Other features Hemiparesis Dysphasia Visual loss Field defect Seizures
Atypical presentation of aneurysmal SAH
D/D• Migraine
• Systemic infection
• Viral illness,
• Hypertensive crisis
• Cervical spinal disorders / arthritis
• Herniated disc
• Aseptic meningitis
• Brain tumours
• Sinusitis
• Alcohol intoxication
Migraine Vs
Aneurysmal SAH
Migraine Vs
Aneurysmal SAH
Head Injury & Aneurysmal SAH
Head Injury &
Aneurysmal SAH
Non Aneurysmal SAH
• 10% of SAH• No vascular cause detected on
angiogram• Course usually benign • Outcome good in 90% pts
Non –aneurysmal SAH
Non –aneurysmal SAH
Exertional activity & Aneurysmal SAH
• First co-operative study on 2288 ruptured aneurysms
One third ruptured in sleep
One third ruptured in unspecified circumstances
One third ruptured during exertional activity
e.g. Lifting, emotional strain, defaecation,
coitus, coughing, parturition
Post coital cephalgia or SAH
SAH Or Post-coital Headaches
• Duration of headache
• Vomiting
• Disturbance of consciousness
• Meningeal signs
• Demonstraion of blood in CSF
• Absence of prior sexually associated headaches
Paediatric SAH
Pre -opPost-op
Moya Moya diseasePRE - OP
POST- OP
Drug Abuse & Stroke
THREE WEEKS LATER
Headaches with
Incidental Aneurysms
Patient undecided - wants to think
Patient decides for image surveillance
Patient not concerned
Needs Intervention
Conclusion
• Awareness
• History is of paramount importance
• Neurological examination gives the clue
• Good investigative tools are a must
• Whenever in doubt – DO NOT HESITATE
• Remember - There are always exceptions
Sensitivity of Cerebral Blood vessels to pain
• Common, internal & external carotid vessels are sensitive to pain
• Main trunk of dural arteries & veinous sinuses are sensitive to pain Myelinated & unmyelinated nerve fibres project from dural arteries & veins to trigeminal nerve
• Larger areteies at Circle of Willis and upto first CM sensitive to pain.
• But substance P has been demonstrated in distal blood vessels also
Pattern of pain referral
• Pain from ICA is referred to ipsilateral sid eof head
• Pain from supratentorial structures is referred to the front of head
• Pain from infratentorial structures id referred to posterior aspect of head due to innervation of C2
Headaches of genereal physical exertion
• Primary ICH
• Embolism
• Thrombo-occlusive disease
Reversible cerebral vasoconstriction syndrome (RCVS)
• Orgasmic headache (OH) is an "explosive" headache that occurs at orgasm. Historically, it was considered benign with no treatment needed. Reversible cerebral vasoconstriction syndrome (RCVS) refers to a group of disorders characterized by recurrent thunderclap headache (TCH) and multifocal vasoconstriction.
Sudden catastrophic headache during sexual intercourse
• SAH due to rupture or expansion of intracranial aneurysm or AVM may need to be excluded
• Lundberg & Osterman (1974)reviewed 50 patents of SAH – 6 cases 12% SAH occured during coitus
• All cases residual pain lasted 24 hrs.
• 2 Pts became unconscious & 5 had vomiting
Physiology of sexual activity
• Increase in heart rate & BP
• Values reach maximum during orgasm
• Erratic respiratory pattern
• Valsalva with paroxysmal Increased intrathoracic pressure due to closed glottis
• Phenomenon similar to any severe exertional efforts with compartmental pressure changes
Physiology of sexual activityBenign Coital Cephalgia
• Raised intrathoracic pressure
• Transmitted intracranially
• Increased tension in dural matrix
• Tear in dural matrix leading to leakage of CSF
Physiology of sexual activity
• As sexual tension is elevated individual frowns, scowls, grimaces and facial muscles contract involuntarily in semispasm
• Jaw is clenched spastically, neck muscles contract rigidly as orgasm is imminent
• There is local and general vasodialtion during orgasm
• This mechanism can be cause of pre-orgasmal headaches.
• Primary migraine can be triggered with coitus but occurs following coitus but Benign Coital Cephalgia occurs during the act of intercourse
Physiology of sexual activity
• Gross vascular & autonomic changes during orgasm can be causes of vascular headaches.
• During orgasm there is abrupt increase in parasympathetic outflow.
• Sudden vasodiltion superadded with maximum cardiac output& extreme elevation of BP
• Unique intracranial context leading to sudden increase in intracranial blood volume or acute failure in intracranial autoregulation