clinical approach and management of SAH

1. SAH
By/Lobna Ahmed
Neurology resident-
Alexanderia university-Egypt

2. CAUSES:
• The most common cause for SAH is a ruptured cerebral aneurysm
(85%); however, 10% of SAHs may not reveal a bleeding source.
• (5%) may be due to other vascular causes:
Arteriovenous malformation.
Arteriovenous fistula.
Reversible cerebral vasoconstriction syndrome [RCVS] .. the presence
of high-convexity SAH, rather than SAH in the basal cisterns, in addition to
the typical “sausage shape” areas of constriction /vasodilation on vessel
imaging has been described.

3. RISK
FACTORS

5. SCREENING & GENETICS
• SAH is predominant in women, African Americans.
• The average age at aneurysm rupture is 53 years.
• Current guidelines recommend screening for aneurysms if the patient has two
or more first-degree relatives with aneurysms or SAH
• A meta-analysis of both unruptured and ruptured intracranial aneurysms
identified the interleukin-6 (IL6) gene polymorphism G572C (chromosome 7)
to have an elevated risk for aneurysm formation, but no predominant genetic
risk factor has been identified. Several other single -nucleotide polymorphisms
have been associated with aneurysm formation, with the strongest
associations on chromosome 9 (near CDKN2B antisense inhibitor gene),
chromosome 8 (near the SOX17 transcription regulator gene), and
chromosome 4 (near the EDNRA gene).

6. CLINICAL PRESENTATION
• Often accompanied by loss of consciousness, nausea, vomiting, photophobia, and
neck pain.
• A small proportion of patients may experience a headache without many or any of the
associated symptoms (sentinel headache).
• Other less typical presenting signs may be seizures, acute encephalopathy, and
concomitant subdural hematoma with or without associated head trauma (due to the
SAH-related syncope), which may make a diagnosis of aneurysmal SAH more difficult.
sudden and severe headache
“worst headache of life”

7. PHYSICAL EXAMINATION
• The level of consciousness and the patient’s GCS score.
• Evaluation for meningeal signs.
• Presence of focal neurologic deficits.
• In cases with unusual presentation or uncertainty,
funduscopic evaluation may be helpful.
• Intraocular hemorrhage associated with SAH (Terson
syndrome) is associated with increased mortality and may be
seen in 40% of patients with SAH.

8. DIAGNOSIS
The most rapidly available and appropriate initial diagnostic
test for patients with suspected SAH is a non-contrast head CT.
It is important to correlate head CT findings to the time of headache
onset, as the sensitivity of head CT changes over the first 7
days >>from 93% (1ST 6 hours), to close to 100% (1ST 12 hours),
to 93% (1ST day), to less than 60% (at 7 days).
HEAD CT
SCAN

9. The characteristic appearance of hyperdense blood
in:
-The basal cisterns,
-Sylvian,
-Interhemispheric,
-Interpeduncular fissures..
should immediately lead to the suspicion of an
aneurysmal etiology.

12. ACOM
MCA

13. Basilar

14. LUMBAR
PUNCTURE • If negative or equivocal head CT findings in which a
high suspicion for SAH still exists, a lumbar puncture is
the immediate next recommended step.
• Opening pressure should be measured routinely
• CSF should be collected in four consecutive tubes,
with red blood cell count measured in tubes one and
four.
• evaluation for xanthochromia (takes approximately 12
hours to develop) by visual inspection and, if available,
spectrophotometry.

15. MRI
• In the hyperacute first 6 hours after SAH, during
which head CT may miss a small proportion of
SAHs and MRI may be slightly superior.
• Hemosiderin-sensitive MRI sequences GRE and
SWI or FLAIR sequences have superior
sensitivity to detect subacute or chronic SAH
compared to head CT.
• Dx of alternative pathologies, such as AVM and
inflammatory, infectious, and neoplastic
etiologies.

16. The arrows indicate the interpeduncular cistern anteriorly
and the ambient cistern posteriorly.

18. GRE with
blooming

19. Identifying the
bleeding source
• The gold standard of vessel
imaging remains cerebral
digital subtraction
angiography (DSA).
• CT angiography (CTA) has
become the first-line
vascular imaging in many
institutions.
• CTA may miss aneurysms as small as 4 mm or less.
• Two dimensional and three-dimensional DSA is pursued as standard diagnostics for aneurysm
detection as soon as the diagnosis of SAH has been established

20. To search for a possible AVM of the
brain, brainstem, or spinal cord

22. Perimesencephalic SAH
• Approximately 15%of patients with SAH will have negative imaging
studies for a source of bleeding, of which approximately 38% have non
aneurysmal peri-mesencephalic SAH (CSF space anterior to the mid
brain).
• The clinical course has been reported to be more benign.
• DSA should still be performed >> rare cases of small aneurysms in the
posterior circulation, fenestration of the vertebral or basilar arteries, or
anterior spinal artery abnormalities.
• Some centers protocol is to do an MRI brain and cervical spine, as well
as a repeat DSA approximately 7 days after the initial tests.

24. Pattern recognition

25. Initial evaluation:

26. Re-bleeding:
Life-threatening complication, with a mortality rate of 20% to 60%, has its
highest rate (8%to 23%)within the first 72 hours after SAH, with the
majority of rebleeding (50% to 90%) occurring within the first 6 hours.
- Poor-grade SAH.
- Hypertension.
- A large aneurysm.
- Use of antiplatelet drugs.
Risk factors
blood pressure fluctuations and extreme blood pressure peaks

27. blood pressure
goals are to keep
systolic blood
pressure
<160 mm hg
• Continuous monitoring with an arterial line
is highly recommended.
• IV medications to control blood pressure
should preferably be continuous
infusions of antihypertensives
(nicardipine 5 mg/h to 15 mg/h)
(labetalol 5 mg/h to 20 mg/h)
• To prevent wide fluctuations of blood
pressure that may be as detrimental to
aneurysm rebleeding as high blood
pressure itself.
Hydralazine is avoided as it can cause rebound hypertension.

28. Other medications:
• Pain control is best achieved with short-acting opiates.
• Meningeal chemical irritation from the SAH often responds to one or several single doses of
dexamethasone (2 mg to 10 mg).
 Short-term use (up to a maximum of 72 hours until aneurysm securement ) of
antifibrinolytics (tranexamic acid or ε-aminocaproic acid) is recommended by guidelines
based on a RCT.
 short-term antifibrinolytic therapy was safe but did not reduce preprocedural rebleeding.
 SE >> prolonged infusion can result in DVT, venous thromboembolism, stroke, and MI ,
and should therefore not be applied .
Antifibrinolytics

29. Disease Severity Scoring:
The outcome and delayed cerebral ischemia are associated with clinical
and radiologic scales, respectively.
The two most commonly used clinical scales, the World Federation of
Neurological Surgeons Scale (WFNSS) and the Hunt and Hess Scale ,
are strong predictors of outcome.
The most reliable and validated radiologic scale is the modified Fisher
Scale, which is nearly linearly associated with worse cerebral vasospasm
and delayed cerebral ischemia.

32. Admission to High-volume Centers:
• Likely owing to lack of protocolized care and expertise,
admission of patients with SAH to low-volume centers is
associated with a higher 30-day mortality.
More than 35 SAH cases per year with experienced cerebrovascular surgeons, endovascular
specialists, and neurocritical care services)

33. Aneurysm treatment:
Shifted from clipping to endovascular coiling after the
publication of ISAT (international trail of SAH treatment).
Endovascular
coiling
Surgical clipping
 Higher odds of survival free
of disability 1 year after
SAH.
 Lower risk of epilepsy.
 Lower risk of rebleeding and
incomplete occlusion of the
aneurysm.

34. Choice of intervention:
Depends on:
- The patient’s age.
- The aneurysm location.
- Morphology.
- Relationship to adjacent vessels.

35. “Currently, endovascular coiling is preferred over surgical
clipping whenever possible.”
• With the introduction of newer techniques such as stent-
assisted or balloon-assisted coiling, even broad-neck
aneurysms can now be treated with endovascular coiling.
• Follow-up angiograms are necessary, as the recurrence rate
of aneurysms is higher when they are treated with
endovascular coiling.

36. Critical Care Management of SAH:
It is commonly associated with systemic inflammatory
response syndrome (SIRS) (75%), which is related to elevated
levels of inflammatory cytokines.
SIRS has been associated with long-term cognitive dysfunction
and has been linked to nonconvulsive seizures in SAH (SIRS
has been found to precede nonconvulsive seizures).
SAH is a systemic disease

37. Neurological complications:
 Rebleeding is the most immediately life-threatening neurologic
complication after SAH. The best measure to reduce the risk of
rebleeding is the early and rapid treatment of the unsecured,
ruptured aneurysm.
1- Rebleeding:

38.  Acute symptomatic hydrocephalus occurs in 20% of patients, Within
minutes to days after SAH onset.
 Clinical signs are decreased levels of consciousness, impaired up-
gaze, hypertension, and delirium.
 The diagnosis is made by repeat head CT and clinical symptoms.
 Can resolve spontaneously in 30% of patients.
2- Hydrocephalus

39.  Insertion of an external ventricular drain (EVD) can be lifesaving.
 Some centers insert a lumbar drain instead of an EVD in cases of
communicating hydrocephalus,
 Rapid weaning of the EVD is recommended after aneurysm obliteration or
within 48 hours of insertion if the patient is neurologically stable.
 In those for whom weaning is unsuccessful (approximately 40%),
placement of a chronic ventriculoperitoneal shunt may be required.

40.  If occurred prior to aneurysm securement, they are usually a sign of early
rebleeding.
 Long-term epilepsy develops in 2% of patients with SAH and is correlated to a
higher severity of SAH.
 Nonconvulsive seizures and nonconvulsive status epilepticus is more
common in patients with SAH who are comatose and has been associated with
delayed cerebral ischemia and worse outcomes.
 Continuous EEG monitoring should be considered in patients with high-grade
SAH.
3- Seizures

41.  Treatment with AED should be limited to the pre-aneurysm treatment
time frame only, considering the known negative effects of
anticonvulsants, particularly phenytoin, on neurocognitive recovery after
SAH.
 Stop the AED as soon as the aneurysm has been secured and not to
extend prophylaxis beyond 3 to 7 days unless the patient presented with a
seizure at the onset of SAH.
 Patients who are comatose and patients with poor-grade SAH are
continued on AED after the aneurysm has been secured given the high
risk for nonconvulsive seizures in these patients.

42.  The most feared neurologic complications after SAH, as cerebral
infarction from delayed cerebral ischemia is the leading cause for
morbidity in patients who survive the initial SAH.
 Monitoring for delayed cerebral ischemia is the main reason for the
recommended prolonged ICU stay for patients with SAH.
4- Delayed Cerebral Ischemia
Defined as: any neurologic deterioration that persists for more than 1 hour and
cannot be explained by any other neurologic or systemic condition, such as fever,
seizures, hydrocephalus, sepsis, hypoxemia, sedation, and other metabolic causes.

43. Pathophysiology:
Was thought to be caused by cerebral vasospasm. However,
evidence now indicates that the pathophysiology of delayed
cerebral ischemia includes an interaction of:
 Early brain injury.
 Micro-thrombosis.
 Cortical spreading depolarizations.
 Related ischemia.
 Cerebral vasospasm.
Supported by the negative
endothelin 1 antagonist
trials in patients with SAH
undergoing clipping or
coiling.

45. Who will develop delayed cerebral
ischemia?
 Occurs on average 3 to 14 days
after SAH.
 The risk increases with SAH
thickness and intraventricular
hemorrhage.
 Additional risk factors include:
 Poor clinical grade.
 Loss of consciousness at
ictus.
 Cigarette.
 Smoking.
 Cocaine use.
 SIRS.
 Hyperglycemia
 Hydrocephalus.
 Nonconvulsive seizures.

46. Prophylaxis
The strongest evidence of prophylactic interventions
for the prevention of delayed cerebral ischemia.
Calcium channel
blockers (nimodipine)
Maintenance of normal
intravascular volume
status

48.  In all cases, adequate maintenance of intravascular euvolemia is Recommended.
 Central venous pressure is a poor predictor of fluid responsiveness and intravascular volume.
 Measurements of pulse pressure variation or respiratory variability of the inferior vena cava diameter
using point-of-care bedside ultrasound are easy to perform and are much more reliable monitoring
techniques for fluid responsiveness of patients who are critically ill, including those with SAH.
 Prophylactic hypervolemia must be avoided, as this strategy has not been shown to improve cerebral
blood flow and increases adverse cardiopulmonary complications.
 In Cerebral salt wasting with significant diuresis and natriuresis, additional administration of
FLUDROCORTISONE can be helpful in maintaining intravascular volume and normal sodium values
(fludrocortisone 0.2 mg to 0.4 mg enterally every 12 hours)

49. Diagnosis and monitoring
Should be suspected if patients with SAH develop a focal or
global neurologic deficit or have a decrease of 2 or more points
on the GCS that lasts for at least 1 hour and cannot be explained
by another cause.
ICP, cerebral perfusion pressure, continuous EEG, and
transcranial Doppler (TCD) monitoring; DSA, CTA, and CT
perfusion (CTP) imaging.
Clinical
Monitoring

50. Monitoring modalities
TCD CTADSA CTP
 CTA is now widely available and is often applied for
vasospasm screening before DSA given its high
degree of specificity and lack of invasiveness.
 CTA, however, can overestimate cerebral vasospasm.
 CTP imaging with elevated mean transit time may be
of additional value to CTA to assess for decreased
cerebral perfusion, but further investigations on the
application of CTP in SAH are needed.

51. Angiographic/TCD vasospasm vs
clinical symptomatic vasospasm
 Majority of patients with SAH (70%) has vasospasm that is associated with
outcome after SAH.
 Only symptomatic vasospasm, occurring in 30% of patients with SAH, has
been associated with delayed cerebral ischemia and poor outcome after SAH.
 Given the risks of endovascular cerebral vasospasm treatment, experts
recommend such treatment only for patients with symptomatic
vasospasm, while angiographic /TCD vasospasm should be managed with a
careful watch and wait approach with a very low threshold to trigger DSA and
endovascular treatment.

52. Thromboembolism
Cardiopulmonary
Fever
Glycemic
dysfunction
Anemia
Hyponatremia
5-Medical complications:

53. 1-Cardiopulmonary:
 Cardiopulmonary dysfunction is a well-known complication of SAH
and can range from minor ECG changes to severe stress
cardiomyopathy and neurogenic pulmonary edema.
 ECG changes can include T-wave inversions and prolonged QTc
intervals and may be the culprit for arrhythmias such as
bradycardia, atrial fibrillation, ventricular tachycardia, and
ventricular fibrillation.
 Cardiopulmonary complications after SAH are usually transient
and resolve within several days to 2 weeks.

55. Baseline Ix
ECG
ECHO
CXR
All patients
• Excessive fluid intake is avoided with a goal of euvolemia and not hypervolemia.
• A repeat follow-up echocardiogram is performed 10 to 14 days after ictus to evaluate for
resolution of Takotsubo cardiomyopathy.

56. 2- Fever:
 Fever is the most common medical complication after SAH,
occurring in up to 70% of patients.
 More likely to occur in patients with high-grade SAH and poor
neurologic status.
 Fever has been associated with delayed cerebral ischemia and
worse clinical outcomes and is likely related to SIRS and
chemical meningitis rather than an infectious process

57. 3-Thromboembolism and Prophylaxis
Deep vein thrombosis after SAH is common, with rates between
2% and 20%.
Chemoprophylaxis with subcutaneous fractionated or
unfractionated heparin is usually initiated immediately after
endovascular aneurysm repair and within 24 hours after
craniotomy for clipping.

58. 4-Glycemic Dysfunction
 Glycemic dysfunction is very common after SAH because of
stress and has been associated with delayed cerebral ischemia
and poor clinical outcome.
 Hypoglycemia can lead to brain metabolic crisis and must be
vigilantly avoided.
 In the absence of clinical trials of glucose control in patients
with SAH, current recommendations are to maintain a blood
glucose level between 80:200 mg /dL.

59. 5-Hyponatremia
 Hyponatremia is the most common electrolyte disorder in SAH
and can occur in up to 30% of patients.
 Causes: can be either due to cerebral salt wasting or SIADH.
 It is of utmost importance to correctly differentiate these two
syndromes because treatment is opposite and an incorrect
diagnosis with improper treatment can lead to detrimental
effects.

60. Common in
both:
Low serum sodium
(<134 mEq/mL).
Low serum osmolality
(<274 mmol/L).
High urine sodium
(>20 mmol/L).
High urine osmolality
(>100 mmol/L).
only
differentiating
finding is
The patient’s intravascular
volume status.
• Hypovolemic.
Cerebral salt wasting
• Euvolemic or even hypervolemic.SIADH

61. Cerebral salt
wasting
SIADH
Continuous infusion
of hypertonic saline
(1.5% to 3%) +
fludrocortisone if
diuresis and natriuresis
impede maintenance of
adequate volume
status.
Fluid administration
Diuresis with
loop diuretics.
Fluid restriction

63. 6-Anemia:
Most patients with SAH will experience anemia during their
hospitalization, which is presumably due to excessive blood
draws, blood loss from other reasons, or systemic inflammation.
Anemia and hemoglobin concentrations of less than 9 g /dL
have been associated with delayed cerebral ischemia and poor
clinical outcomes.

64. Thank you