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

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 ? mm 3 WBC increased in proportion to red cells Glucose N Proteins high (for 1000 RBC 1. 5 Gm /dl proteins)

CT negative SAH CSF 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 angiog ram • 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 -op Post-op

PRE - OP Moya disease 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 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 C 2

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 activity Benign 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