Subarachnoid hemorrhage

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1. SAH BY Dr Mohammud Ibraheem

2. Our points Anatomy of SA space Histology of cerebral vasculature Epidemiology Risk factors of SAH Types of SAH Classification cerebral aneurysm Grades of severity of SAH Clinical presentation Investigations

3. Anatomy

4. Histology

5. Intracranial arteries lack external elastic lamina, which in the anterior circulation disappears in the horizontal segment of the cavernous internal carotid arteries. Reduction and disappearance of the external elastic lamina and of elastic fibers in the tunica media occurs in the vertebral arteries as they enter the skull.

6. Epidemiology

7. Epidemiology SAH represent 1% - 6% of all strokes SAH constitutes 1% - 4% of all ED visits for acute headaches The most common cause of spontaneous SAH is a ruptured cerebral aneurysm (85%). The incidence of aSAH is 6.1/100,000 person-years worldwide. F emales affected 1.6 times more than males. aSAH is with a case-fatality rate up to 51% and long-term disability in 1/3 to 1/2 of all survivors. cognitive impairments in half of survivors 0.3% of all unruptured intracranial aneurysms rupture per year

8. Epidemiology Risk factors of rupture of an unruptured intracranial aneurysm: Hypertension Females Age (peaks in the 5 th and 6th d ecades) Larger aneurysm (6 mm-10 mm) Aneurysm location (bifurcations, posterior circulation) Aneurysm shape (irregular shape, with a daughter sac or multilobuations ) Ethnic origin (common in African American, Hispanic, Japanese and Finnish populations) Family history and past history of SAH Aneurysms that are growing or causing clinical symptoms

9. Epidemiology location in the ICA and larger neck are the protective factors against aneurysm rupture. 10% to 15% of patients with SAH do not have an identifiable bleeding source; of these, 38% have perimesencephalic SAH, which is a benign variant of SAH with excellent prognosis.

10. Epidemiology Over the past 2 to 3 decades, the SAH case-fatality rate has decreased by 17% - 50 % worldwide due to Advances in stroke systems of care Diagnostic accuracy Surgical techniques Critical care support Despite these, SAH remains a highly deadly and morbid disease, with 30-day mortality as high as 35 %. The overall mortality of SAH is underestimated.

11. Risk factors

12. Risk factors of SAH Modifiable Hypertension (90% in AC, 10% in PC) DM Tobacco smoking Cocaine use Bacterial endocarditis Fungal infection Tuberous sclerosis Coarctation of the aorta Pheochromocytoma Non modifiable Age Sickle cell anemia Neurofibromatosis type 1 C arotid- vertebrobasilar anastomoses AD inherited polycystic kidney disease Fibromuscular dysplasia Moyamoya syndrome Pseudoxanthoma elasticum α1- Antitrypsin deficiency SLE Ehlers- Danlos syndrome, vascular type (type IV )

13. Risk factors of SAH 10% of AD polycystic kidney disease have asymptomatic unruptured intracranial aneurysms. AD polycystic kidney disease accounts for 0.3% of all SAH. Although familial clustering is seen in SAH, variabilities in genetic loci account for 5% of the hereditary risk of SAH, suggesting that familial clustering may also be related to shared environmental risk factors.

14. Risk factors of SAH The risk in first-degree relatives of patients with SAH is 3 to 7 times higher than in the general population, but second-degree relatives have risks similar to that of the general population. the AHA/ASA SAH guidelines suggest screening is considered in those with two or more first-degree relatives with aneurysm or SAH .

15. Types of SAH

16. Primary SAH a SAH (85%): SAH due to rupture of intracerebral aneurysm Nonaneurysmal SAH ( perimesencephalic SAH) (10%): SAH with no evidence of cerebral aneurysm or other vascular malformations SAH due to other vascular malformations (5%): SAH due to bleeding from cerebral or spinal AVM, dural arteriovenous fistula, arterial dissection, moyamoya disease, or other malformation Secondary SAH Trauma RCVS PRES Cerebral amyloid angiopathy Pituitary apoplexy Cerebral vasculitis Primary ICH with 2nd extension to SA space Cerebral venous sinus thrombosis Tumor Coagulopathy Sympathomimetic drug use Alcohol use Endocarditis

17. Classification of Intracranial Aneurysms

18. By Morphology Saccular (90 %) Fusiform (associated with atherosclerosis). Dolichoectatic fusiform aneurysms is a variety of fusiform A Dissecting (associated with trauma or an underlying vasculopathy ) Mycotic (mortality of up to 80 %) By Size < 3 mm (small) 3–6 mm (small) 7–12 mm (small-medium) 13–25 mm (large) >25 mm (giant)

19. SAH Clinical and Radiographic Severity Scores

20. The initial clinical severity of SAH presentation varies from very mild to critical . SAH clinical severity is measured using: The Hunt and Hess Scale The World Federation of Neurological Surgeons Scale (WFNSS) Modified Fisher Scale

21. Hunt and Hess Scale GRAD Hunt and Hess Scale 1 Asymptomatic or mild headache, minimal or no nuchal rigidity 2 Moderate to severe headache, nuchal rigidity, and no neurologic deficit other than cranial nerve palsy 3 Mild alteration in mental status (confusion, lethargy), with or without mild focal neurologic deficit 4 Stupor and/or hemiparesis 5 Comatose and/or decerebrate rigidity and/or no motor response

22. World Federation of Neurological Surgeons Scale (WFNSS ) GRAD WFNSS 1 GCS score of 15, motor deficit absent 2 GCS score of 13-14, motor deficit absent 3 GCS score of 13-14, motor deficit present 4 GCS score of 7-12, motor deficit absent or present 5 GCS score of 3-6, motor deficit absent or present

23. Modified Fisher Scale GRADE CHARACTERS no SAH no IVH incidence of symptomatic vasospasm: 0% 1 focal or diffuse, thin SAH no IVH the incidence of symptomatic vasospasm: 24% 2 focal or diffuse, thin SAH IVH present the incidence of symptomatic vasospasm: 33% 3 thick SAH no IVH the incidence of symptomatic vasospasm: 33% 4 thick SAH IVH present the incidence of symptomatic vasospasm: 40%

24. Clinical presentation Neurological symptoms and signs N on-neurologic symptoms and signs

25. Symptoms Worst headache of life: sudden onset of severe headache, this presentation accounts for only 10–50% of patients with acute non-traumatic SAH Sentinel headache: a new headache without other associated SAH symptoms, leading to diagnosis of aSAH (40%) A change in headache characteristics Nausea , often with vomiting Sudden loss of consciousness, transient syncope Acute onset or progressive altered mental status

26. Neurologic examination findings Altered mental status Abnormal Glasgow Coma Scale score Focal cranial nerve palsies and ophthalmoplegia ( eg , 3 rd nerve palsy from PcomA aneurysm, 6 th nerve palsy from increased ICP) Meningismus : neck stiffness, photophobia Terson syndrome: intraocular extension of SA blood Focal neurologic deficits; Acute hemiparesis Bilateral leg weakness and abulia due to mass effect from hematoma in the interhemispheric fissure Seizure or seizurelike events Papilledema (18% of patients develop Terson syndrome)

27. Systemic manifestations Acute hypertension Cardiac dysrhythmia Cardiac arrest Hypotension/shock from neurogenic stunned myocardium Hypoxia from aspiration, respiratory depression, or neurogenic pulmonary edema

28. Ottawa SAH Rule Age ≥40 years Neck pain or stiffness Witnessed loss of consciousness Onset during exertion Thunderclap headache Limited neck flexion on examination Ottawa SAH Scale has 100% sensitivity (rule out test)

29. INVESTIGATIONS NCCT Lumbar puncture Vessel imaging Laboratory tests

30. Noncontrast head computed tomography (NCCT) NCCT is the most common modality that identifies the presence of acute blood in the SA space. It is most sensitive for SAH in the first 6 - 12h following vessel rupture, with a sensitivity of 93% - 100%. Diagnostic sensitivity by CT degrades over time, declining to 60% at 7 days post-SAH. For subacute or chronic SAH , MRI with GRE, SWI, or FLAIR sequences have superior sensitivity compared to NCCT Secondary SAH has different CT characteristics and tends to be present in the high cerebral convexity and not centered around the basal cisterns as in aSAH

31. Characteristic CT Appearance of a SAH CT features Aneurysmal location Preponderance of SA blood in the basal cisterns All SA blood along the sylvian fissure More common with MCA aneurysms SA blood in the interhemispheric fissure More common with AcoA or ACA aneurysms SA blood in the interpeduncular cistern All SA blood in prepontine area, 4th ventricular outlet, and foramen magnum Posterior circulation aneurysms Focal anterior temporal lobe intracerebral hematoma More common with MCA aneurysms Focal frontal lobe intracerebral hematoma More common with AcoA or ACA aneurysms Focal subarachnoid blood in the prepontine area Perimesencephalic SAH with no cerebrovascular malformations identified

32. Lumbar Puncture and CSF Analysis In cases of negative or equivocal imaging and high clinical suspicion for SAH, lumbar puncture for diagnostic CSF analysis can assist in the diagnosis of acute SAH , although the value of lumbar puncture has been questioned. The classic diagnostic criterion is presence of xanthochromia on laboratory spectrophotometry analysis . Lumbar puncture offers the opportunity to measure an opening pressure as a surrogate for ICP.

33. Lumbar Puncture and CSF Analysis Xanthochromia + headache ➡subarachnoid hemorrhage (SAH ) DD of xanthochromia hyperbilirubinemia previous traumatic tap hypercarotenemia Subarachnoid hemorrhage Excess protein (> 150mg/dl) free Hb

34. Vessel Imaging CTA is the 1 st-line vessel imaging modality. A negative CTA is insufficient to rule out the presence of an aneurysm, particularly when the aneurysm is < 4 mm Cerebral CTA has 90% - 97 % sensitivity compared to DSA with 3D reconstructions, which is the gold standard diagnostic modality for cerebral aneurysms. When cerebral aneurysms are detected on CTA, patients still proceed to DSA, which is also a potential therapeutic modality for endovascular treatment of the aneurysm .

35. CTA Advantages : Less cost and radiation , easy to perform, readily available Time saving Good sensitivity and specificity Can predict patients needing surgical clipping and avoid DSA Disadvantages : Poor sensitivity for small aneurysms (<3 mm) Poor detection of aneurysms near the base of the skull Poor negative predictive value, needing DSA for confirmation Poor detection of culprit aneurysm in cases with multiple aneurysm DSA Advantages: The gold standard to detect aneurysms Can reliably predict neck width 2 negative DSA 7 days apart exclude aneurysms Better modality in cases with a diffuse pattern of SAH Disadvantages : High radiation and iodine dose Invasive, involving risks of complications such as arterial puncture, emboli, dissection, hemorrhage and septicemia

36. Magnetic Resonance Imaging On FLAIR images, SAH appears as high signal-intensity (white) in normally low signal-intensity (black) CSF spaces . FLAIR and CT scanning have similar findings MRI is a useful to diagnose AVMs. MRI can detect aneurysms 5 mm and is useful for monitoring the status of small, unruptured aneurysms. MRI evaluate the degree of intramural thrombus in giant aneurysms.

37. Magnetic Resonance Imaging Magnetic resonance angiography offers benefits such as its lower cost and the absence of procedure-associated risk of stroke and arterial injury. MRA is an effective diagnostic procedure to detect cerebrovascular disease

38. Laboratory studies Serum chemistry panel Complete blood count PT/activated partial thromboplastin time ( aPTT ) Blood typing/screening Cardiac enzymes Arterial blood gas (ABG) determination

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