Subarachnoid Hemorrhage is Extravasation of blood into the subarachnoid space. It occur mainly due to Ruptured aneurysm (75%).

1. Subarachnoid Hemorrhage
Ahmed M. Ibrahim

2. Introduction
• Definition:
Extravasation of blood into the
subarachnoid space.
• Incidence:
Spontaneous subarachnoid hemorrhage
(SAH) accounts for 2% to 7% of all
strokes but for a larger proportion of
morbidity and mortality from stroke due
to the younger mean age incidence and
high mortality. (Maher et al., 2020)

3. Etiology
1. Ruptured aneurysm (75%):
• F> M (2:1), 5th or 6th decade, with elevated BP.
• 2-3% mycotic aneurysm (especially infective endocarditis).
2. Arteriovenous Malformation (AVM) (10%):
• M>F, 2nd to 4th decades, or other vascular malformations
3. Coagulopathy.
4. Dissection of intracranial vessels.
5. Drug Induced.
6. Dural sinus thrombosis.
7. Hypertension or other small vessel disease.
8. Pituitary apoplexy.
9. Reperfusion following stroke.
10. Others: trauma, tumors, & vasculitis.

4. Etiology
Risk Factors:
a) Hypertension.
b) Smoking, alcohol.
c) Family history; 1" degree relatives..
d) Polycystic kidneys, Ehlers-Danlos Type IV,
pseudoxanthoma elasticum, fibromuscular dysplasia.

5. Distrubution of Congenital Cerebral Aneursyms

6. Clinical Picture
Headache:
• acute, paroxysmal, and sudden in
onset, "worst headache in my life"!
• Thunderclap Headache.
• Some of patients have a warning
leak (sentinel headaches are mild to
moderate in intensity, usually occur
within 2 weeks of overt SAH, and
are not accompanied by other
neurological symptoms).

7. Clinical Picture
• Transient or persistent alteration in
consciousness ranging from disorientation
to deep coma.
• Fever, sweating, vomiting, and tachycardia
are frequently present.

8. Clinical Picture
Meningeal irritation signs

9. Clinical Picture
Ocular Manifestations of Cerebral Aneurysms
• Cranial Neuropathies

10. Clinical Picture

11. • Visual Field

12. • Retinal Changes

13. Classification
Various classifications exist for SAH. These range from clinical grading systems to radiographic scales. The
most commonly used scales are Hunt & Hess, and World Federation of Neurological Surgeons (WFNS) scales

14. Investigations
Noncontrast CT Scan:
• If positive, perform cerebral angiagraphy.
•If negative, perform lumbar puncture.
•In the first 24 h, the sensitivity of a CT for
SAH is 92-95%, then declines to 57- 85%
on day 5 and 50% after 1 week.
•The pattern of blood identified on CT scan
can sometimes predict the bleeding sites.
A
B

15. CT scans of patients with aneurysmal subarachnoid haemorrhage from aneurysms of the
• Right middle cerebral artery (A)
• Right internal carotid artery (B)
• Anterior communicating artery (C)
• Left middle cerebral artery (D)
• Right superior cerebellar artery (E)

16. CT of patients with non-aneurysmal perimesencephalic subarachnoid
haemorrhage (F–H, J) resemble aneurysmal subarachnoid haemorrhage from
a basilar bifurcation aneurysm (I), showing that CT or catheter angiography
are necessary in all patients with this condition.

17. Case
• AS, Male patient, 32 years old presented by sudden
onset severe headache. Blood pressure was normal,
neck pain.
• CT brain was done: perimesencephalic SAH.
• CTA: free
• DSA: Cerebellar AVM supplied by left SCA & left
PICA + Venous drainage via straight sinus and left
transverse sinus
• Plan of Care: AVM embolization with Onyx

18. Cerebellar AVM supplied by left SCA & left PICA
+ Venous drainage via straight sinus and left transverse sinus

19. Non-aneurysmal subarachnoid haemorrhage due to
• Cerebral venous thrombosis (K, L)
• Trauma (M)
• Pituitary apoplexy (N)
• Pseudo-subarachnoid haemorrhage due to increased intracranial pressure, brain swelling, and
compression of th basal cisterns (O).

20. Magnetic Resonance Imaging (MRI) brain:
• Sensitivity varied among the five MR sequences studied from
50% to 94% in acute SAH and from 33% to 100% in subacute
SAH.
• The most sensitive sequences were FLAIR and T2* (gradient
echo) with T2* performing slightly better than FLAIR.
• The sensitivity of T2* was 94% under 4 days from the ictus and
100% between 4
and 14 days.

21. Angiography:
1) Conventional DSA.
3) CT Angiography.
2) 3D Digital Subtraction Angiography.
4) MR Angiography.

22. Lumbar Puncture
Indications
A classic history of SAH and negative non-contrast
CT.
Contraindications and risks of LP:
1) Infection at the site.
2) Coagulopathy, drug induced or otherwise.
3) Raised ICP particularly with posterior fossa
pathology.
4) Risks: herniation, rebleeding from aneurysm.
Deterioration occurs in ~10% of patients with
ruptured aneurysms following LP.

23. Lumbar Puncture
• Should never be done prior to CT scanning.
• "Three tube" test: should see a decrease in traumatic tap versus steady level of RBCS in true SAH.
• Elevated opening pressure (>20 cm H2O) seen in 60% of cases.
• Xanthochromia: Relates to the discoloration of the CSF from RBC breakdown (oxyhemoglobin and bilirubin)
subsequent to hemorrhage.
• Present as early as 4-6 hours after SAH and persist for 2-3 weeks.
• Detected by centrifugation or spectrophotometry which is more sensitive.

25. Treatment
Initial Resuscitation
and Triage
Treament of the cause
eg. Aneurysm Repair
Treament of the complications

26. Treatment
Patients with SAH should be managed at centers that treat many
patients and that have neurovascular teams and neurointensive care or
similar units. (Amato et al., 2017)
• Maintain adequate cerebral perfusion, adequate hydration
• Aggressive control of fever, hyperglycemia,
• Bed rest in a quiet room, avoid constipation,
• Prevent pulmonary embolism pneumatic compression stockings.
• Severe headache or neck pain: mild sedation and analgesia.
• Extreme sedation is avoided [obscure changes in neurological
status]

27. Surgical treatment
Early Aneurysm Repair: as early as feasible, Complete obliteration of the aneurysm is recommended
whenever possible
*Endovascular Technique (Coiling)
*Surgery (Clipping)
The benefits of early surgery are:
1) Reduced risk of re-bleeding .
2) Opportunity to clear blood from the subarachnoid space.
3) Ability to aggressively treat vasospasm.
4)  Vasospasm and ischemia.
5) prolonged bed rest.
6) Avoid need of long-term antifibrinolytics.
Complicatlons of aneurysm repair > occlusion of related arteries and intraprocedural rupture.
Coiling Clipping

28. AHA/ASA 2012
• Determination of aneurysm treatment, as judged by both experienced
cerebrovascular surgeons and endovascular specialists, should be a
multidisciplinary decision based on characteristics of the patient and the
aneurysm (Class I; Level of Evidence C).
• For patients with ruptured aneurysms judged to be technically amenable
to both endovascular coiling and neurosurgical clipping, endovascular
coiling should be considered (Class I; Level of Evidence B).

30. Case
• AA, 70 years old, male patient, hypertensive
presented by sudden sever headache.
• Brain CT:

31. CTA

32. • DSA:
Left
ICA
Left MCA
Left ACA
Lateral View A-P View
Left
ICA

34. Complications of SAH
Neurological Complications
1) Re-bleeding
2) Vasospasm or Delayed Cerebral Ischemia
3) Seizure
4) Hydrocephalus
5) Others:
- Brain edema.
- Intracerebral hematoma.

35. Systemic Complications
a. Neurogenic pulmonary edema.
b. Cardiac ECG changes:
- Prolonged QT, ST segment or T wave changes.
- Arrhythmias especially ventricular tachycardias.
c. Hypertension: due to pain, ↑↑ catecholamines.
d. Hyponatremia:
1-Syndrome of Inappropriate ADH Secretion
2-Cerebral salt-wasting syndrome
e.Hypomagnesemia (40%), hypakalemia (25 %) and hypernatremia
(20%) are

36. Re-bleeding (8- 23%)
• The risk of early re-bleeding is high (approximately 4% during the
first day and 1- 2% within the next two weeks).
• RFs; female, high BP, poor clinical grade.
• TTT:
1) Avoid  BP, cough, straining.
2) Mild sedation.
3) Short term anti-fibrinolytics (<72 hours), with tranexamic acid or
aminocaproic
4) Early surgical treatment. Guidelines suggest repairing the aneurysm
as early as feasible

37. • AHA/ASA 2012

38. Vasospasm or Delayed Cerebral Ischemia
• Segmental or generalized, according to amount
of blood.
• It is major cause of delayed morbidity and
death.
• Starts on day 3, maximum 5 to 14 days &
resolves on day 21.
• Causes infarction in 30% of patients.
• Spasm of major arteries  stroke syndromes.
• Detected by; angiography, CT angiography,
CT perfusion, or MRA, TCD ( BFV),
clinical (deteriorated conscious level & focal
deficit).

39. Vasospasm
(A) Computed tomography
angiography (CTA) and (B)
conventional angiogram of a patient
with subarachnoid hemorrhage
before
the occurrence of vasospasm. (C)
CTA and (D) conventional
angiogram of the same patient after
the occurrence of vasospasm
demonstrating severe vasospasm of
basilar trunk and proximal posterior
cerebral arteries.

40. Vasospasm or Delayed Cerebral Ischemia
Prophylaxis
a) Nimodipine (60 mg orally q.4 h) improves outcome until day 21(SE; hypotension).
b) Management of fluid and electrolyte balance especially hypomagnesemia.
c) Simvastatin 40-80 mg or pravastatin 40 mg daily until SAH day 14.
Management
a) Consider Trendelenburg position (head down).
b) Infusion of 500-1000 ml 0.9% saline or 5% albumin over 15 min.
c) "Triple-H" therapy (hypertension, hemodilution, and hypervolemia).
d) Start vasopressors (norepinephrine, or dopamine) to raise SBP to 160-220 mmHg (20 mmHg
above current) until deficits resolve.
e) MgSO4 inhibit vasospasm.
f) Endovascular: Refractory vasospasm
* Percutaneous transluminal angioplasty (balloon dilatation).
* Intraarterial vasodilator (papaverine, verapamil or nicardipine) infusion.

41. AHA/ASA 2012
• Oral nimodipine should be administered to all patients with aSAH (Class I;
Level of Evidence A). (It should be noted that this agent has been shown to
improve neurological outcomes but not cerebral vasospasm. The value of other
calcium antagonists, whether administered orally or intravenously, remains
uncertain.)
• Transcranial Doppler is reasonable to monitor for the development of
arterial vasospasm (Class IIa; Level of Evidence B).
• Induction of hypertension is recommended for patients with DCI unless
blood pressure is elevated at baseline or cardiac status precludes it (Class I;
Level of Evidence B).
• Cerebral angioplasty and/or selective intra-arterial vasodilator therapy is
reasonable in patients with symptomatic cerebral vasospasm, particularly
those who are not rapidly responding to hypertensive therapy (Class IIa;
Level of Evidence B).

42. Hypertension, Hemodilution, and Hypervolemia
• In 1976 Kosnik and Hunt described resolution of delayed neurologic deficits after aSAH with induction of
hypertension.
• This was followed by a description of aggressive volume administration (“hypervolemia”) to reverse the
neurologic deficits of DCI.
• Awad et al subsequently described the systematic use of “triple-H therapy”—hypertension, hypervolemia, and
hemodilution—to improve cerebral perfusion after aSAH. Triple-H therapy has not endured in its original
form.
• Hemodilution can decrease oxygen-carrying capacity and is no longer routinely performed.
• Randomized clinical trials have demonstrated that attempts to achieve “hypervolemia” do not improve
outcomes and may increase complications. Multiple studies have demonstrated, however, that an elevation in
mean arterial pressure (MAP) improves perfusion of ischemic regions of the brain.
• Despite decades of clinical use, hemodynamic augmentation for the treatment of DCI has, until recently, not
been evaluated in a clinical trial

43. Case
• WM, Female patient 33 years old, with no
previous history of chronic illness.
• Presented by Sudden falling attack with
disturbed conscious level, then she was
taken to the ER but she was diagnosed as a
conversion case as she regained
consciousness.
• 1 week later: She developed acute onset
Left sided weakness.
• The patient was prescribed to Xalerto

44. • CT Brain was done for follow up after 1 year

45. • CTA

46. • By asking about the past history
• Before the onset of the weakness when the patient had impaired
consciousness she also had headache and neck pain.

47. Aneurysm
Ophthalmic
Artery
A B

48. • Coils after Deployment

49. Seizure
Risk factors
a. Poor neurological grade.
b. MCA aneurysm ruptures.
c. Infarction due to vasospasm.

50. Seizure
long term use of anticonvulsants is not recommended except
with risk factors as;
• prior seizure
• intracerebral hematoma
• Intractable hypertension
• Infarction or MCA aneurysm.

51. Hydrocephalus
a. Immediate; within 3 days, due to intraventricular blood.
b. Delayed (subacute); develops aver a few days or weeks →
progressive drowsiness or slowed mentation (abulia) with
incontinence, due to subarachnoid blood

52. Hydrocephalus
- Acute hydrocephalus; may clear spontaneously or require
external ventricular drainage
- Chronic hydrocephalus; ventricular shunting.
Increased ICP:
Emergent ventriculostomy.
Medical therapies: mild hyperventilation, mannitol, and sedation.

53. Hyponatremia
• Hyponatremia in the setting of a central nervous system event is
a diagnostic challenge to physicians. Both SIADH and CSW
are likely etiologies, as they present with very similar
biochemical profiles.
• hyponatremia has been reported to occur in up to 30% of
patients with subarachnoid hemorrhage. (Momi et al., 2010)
• Serum Na < 135 mEq/l

54. Hyponatremia
SIADH:
• Brain injury  Stimulate Supraoptic/Paraventricular N of the
thalamus  release of ADH from pituitary neural lobe  Water
retention  Dilutional Hyponatemia
CSW:
• Brain injury  # adrenergic tone to the nephron   Renin in
juxtaglomerular cells  Aldosterone  Sodium Reabsorption in PCT.
• Brain injury  Release Natriuretic factors (including Brain natriuretic
peptide)  Sodium Reabsorption & inhibits Renin

55. Hyponatremia
Syndrome of Inappropriate ADH
Secretion
Cerebral salt-wasting syndrome
HR Normal
Dehydration signs, THR, 
intravascular volume
CVP Elevated central venous pressure Decreased central venous pressure
TTT
Fluid restriction (Limit free-water
intake)
Na & volume replacement± hypertonic
saline

58. Prevention [AHA/ASA 2012]
1. Treatment of high blood pressure with antihypertensive medication is recommended to prevent ischemic
stroke, intracerebral hemorrhage, and cardiac, renal, and other end-organ injury (Class I; Level of Evidence
A).
2. Hypertension should be treated, and such treatment may reduce the risk of a SAH (Class I; Level of
Evidence B).
3. Tobacco use and alcohol misuse should be avoided to reduce the risk of aSAH (Class I; Level of Evidence B).
4. In addition to the size and location of the aneurysm and the patient’s age and health status, it might be
reasonable to consider morphological and hemodynamic characteristics of the aneurysm when discussing the
risk of aneurysm rupture (Class IIb; Level of Evidence B).
5. Consumption of a diet rich in vegetables may lower the risk of aSAH (Class IIb; Level of Evidence B).
6. It may be reasonable to offer noninvasive screening to patients with familial (at least 1 first-degree relative)
aSAH and/or a history of aSAH to evaluate for de novo aneurysms or late regrowth of a treated aneurysm, but
the risks and benefits of this screening require further study (Class IIb; Level of Evidence B).
7. After any aneurysm repair, immediate cerebrovascular imaging is generally recommended to identify
remnants or recurrence of the aneurysm that may require treatment (Class I; Level of Evidence B).