Management of SAH and their

complication
El noamany abo nar
 Initial evaluation
• Admission to SAH center or neurocritical unit
why ?
better monitoring , detection of complication ,
early management of complication.
 Initial evaluation

Confirm diagnosis
Avoid misdiagnosis

History Lumber
CT brain puncture
History
Complete history
Overeliance on classic presentation
Appreciate that headache can improve spontaneously
Focus on ECG , blood pressure
Assuming symptoms may related to other disorder ( viral meningitis , migrain ,
sinus related headache , psychiatric disorder)
 Ct brain
Sensitivity decrease with time
False negative with small volume of blood
Lack of thin cuts , motion artifact

Lumber puncture
Failure to distinguish a traumatic tap from true SAH
Failure to recognize xanthochromia ( absent less than 12 hours and later
than 2 weeks )
Assessment of SAH severity

Modified fisher scale

 Rebleeding Hydrocephalus Seizures

Systemic Delayed cerebral

medical complications ischemia ( vasospasm )
complication

Cardio-pulmonary
Systemic Glycemic
dysfunction Venous thrombo-
inflammatory dysfunction
Fever embolism
response syndrome

Hypo-natremia Anemia
 Rebleeding
1st 6- 72 hrs
Mortality rate -20 to 60 %

Risk factors
Poor grade
HTN
Large aneurysm
Use antiplatelet
 Rebleeding
Control blood pressure and avoid
fluctuation and peak
SBP< 160 mmhg
Nicardipine 5-15 mg/hr
Labetelol 5-20 mg /hr Anti-fibrinolytics :
( tranexamic acid ,aminocaproic
acid)
Pain control For Short time ( up to 72 hrs)
Short acting opiates ( oxycodone ,
Hydrocodone /acetaminophen
Pethidine )
Aneurysm management

Surgical clipping
OR Endovascular coiling

Aneurysm with wide Old age ,poor clinical

neck to body ratio grade ,multiple
Middle cerebral artery comorbidities , top of
aneurysm basilar aneurysm , high
Aneurysm with large surgical risk
parenchymal hge

Aneurysmal repair is with in 72 hours

 Vasospasm
( delayed cerebral ischemia)
30% of SAH patients

It is a Clinical diagnosis

Any neurologic deterioration that persist for more than 1

hour and cant be explained by any other neurologic or
systemic conditions
 Vasospasm
( delayed cerebral ischemia)
Vasospasm is not simply due to vascular smooth muscle contraction, and changes
in vessel caliber develop slowly over several days. Inflammatory arteriopathic
changes are seen in the vessel wall, including subintimal edema and infiltration of
leukocytes.

The prevailing view is that substances released from the blood clot interact with
the vessel wall to cause inflammatory arterial spasm. Putative mediators with
intrinsic vasoconstrictive properties include oxyhemoglobin, hydroperoxides and
leukotrienes, free radicals, prostaglandins, thromboxane A2, serotonin, endothelin,
platelet derived growth factor, and other inflammatory mediators. Cortical
spreading depression may further contribute to DCI after SAH by creating
prolonged neuronal depolarization in conjunction with a paradoxical reduction in
local cerebral blood flow
 Vasospasm
( delayed cerebral ischemia)
Occur at 3rd day up to 14th day then resolve over 2 to 4 weeks

Potential signs of incipient delayed cerebral ischemia

New focal neurological deficit
Decline in GCS 2 points or more , unexplained
Increase in main arterial pressure unexplained
Increase in TCD velocities
EEG signs of new focal ischemia
 Vasospasm
( delayed cerebral ischemia)
Diagnosis :
1- TCD
2- DSA /CTA /CTP
3- brain tissue oxygenation , cerebral blood flow and micro
dialysis monitoring
4- continuous scalp EEG
 Vasospasm
( delayed cerebral ischemia)
TCD
Monitoring with TCD every other day between 3rd and 14th day
Adequate sensitivity and specificity for ICA , MCA

Thresholds for vasospasm :

Normal Mean MCA velocities < 120 cm/s
Consider vasospasm :
Mean MCA velocities > 200 cm /s
Lindgaard ratio >3
Rapid rise in velocities more than 50 cm/s
 Vasospasm
( delayed cerebral ischemia)
Limitations of TCD :

Operator dependent.
Low sensitivity and specificity for ACA and post. Circulation
Cerebral blood flow may increase due to other causes ( fever ,
HTN ,anemoa
 Vasospasm
( delayed cerebral ischemia)
DSA / CTA / CTP :

Gold standard for large and middle artery vasospasm

CTA + CTP
 Vasospasm
( delayed cerebral ischemia)
Prevention :

Ca channel blocker :
Nimodipine
FDA approved
Dose : 60 mg / 4hours for 21 days

SE: hypotension
 Vasospasm
( delayed cerebral ischemia)
Prevention :

Maintain euvolemia :

Fluid Input and output monitoring

CVP 10-20
Daily weight
Pulmonary wedge pressure 12-18 mmhge
Avoid prophylaxis hypervolemia
Maintain MAP 10-20% above base line
 Vasospasm
( delayed cerebral ischemia)
Treatment :

HHT
Hypertension and mild hypervolemic therapy

IV fluid bolus then maintain euvolemia

Hypertension:
α 1 agonist ( phenylephrine )
Induction blood pressure 20-40 mmhg above the base line
• if cardiomyopathy – dobutamine
 Vasospasm
( delayed cerebral ischemia)
If neurological deficit still present :

CT to rule out hydrocephalus

CTA
DSA ( angioplasty or inject intraarterial ( nicardipine ) )
 Seizures

If early seizure before aneurysm repair - early rebleeding

Long term epilepsy -- 2% SAH

Nonconvulsive seizure - 7-18 %

Nonconvulsive status epilepticus - 3-13%

Continuous EEG monitoring

Levetiracetam
 Hydrocephalus
26 % of SAH

CP :

Mild hydrocephalus :
lethargy, psychomotor slowing, and impaired short-term memory.
Additional findings may include limitation of upward gaze, sixth
cranial nerve palsies.

severe cases
acute obstructive hydrocephalus leads to elevated intracranial
pressure and stupor or coma. Progressive brain stem herniation
 Hydrocephalus
•Risk factor for development of hydrocephalus include :
• Older age
• IVH
• Posterior circulation aneurysms
• Treatment with antifibrinolytic agents
• Low GCS on presentation
 Hydrocephalus
Diagnosis :
CT brain
 Hydrocephalus

Treatment :
Resolve spontaneously 30%
Insertion EVD or lumber drain
Weaning of drain after aneurysmal repair or 48
hours after insertion if pt is stable

Failure of drain - VP shunt

 Cardiopulmonary dysfuncti on
Can range from minor ECG changes to severe stress cardiomyopathy
 Cardiopulmonary dysfuncti on

Forms of cardiopulmonary dysfunction :

• ECG changes : inverted T wave , QT interval prolongation , arrythmia ( AF,

bradycardia , VT, VF )
 Cardiopulmonary dysfuncti on
• Takotsubo cardiomyopathy :
Definition of Takotsubo cardiomyopathy involve several criteria which
involve :
• Transient regional wall motion abnormalities (RWMAs) of the LV
and/or RV after a stressful trigger e.g. emotional.
• RWMAs extend beyond the distribution of a single coronary artery.
• New and reversible ECG abnormalities e.g. ST elevation, diffuse T-
wave inversion (note that ECG can’t reliably differentiate Takotsubo
cardiomyopathy versus occlusive MI).
• Troponin elevation (relatively small rise compared to magnitude of
wall motion abnormality).
Echocardiography may show classic pattern of
akinesia of the apex, with hypercontractility of the
base. ( apical ballooning )
 Cardiopulmonary dysfuncti on
• Neurogenic pulmonary edema :
• Pulmonary edema may occur either as a result from the acute left
ventricular dysfunction or independently as neurogenic pulmonary edema
from substantial increases in pulmonary capillary pressures from the
sympathetic surge.
•Neurogenic pulmonary edema should be on differential diagnosis if there is
unexplained early hypoxemia in a patient with severe, high-grade SAH.

DD?
•atrogenic volume overload
•Cardiogenic pulmonary edema primarily due to
Takotsubo cardiomyopathy.
•Aspiration pneumonitis or pneumonia.
 Venous thrombo-embolism
Deep vein thrombosis after SAH is common, with rates between 2% and 20%

•Prior to aneurysm protection

• Chemical DVT prophylaxis is contraindicated.
• Pneumatic compression devices should be used for DVT prophylaxis.

•After aneurysm protection

When to initiate DVT prophylaxis:
• After aneurysm coiling: chemical DVT prophylaxis may usually be started
immediately (but confirm this with the neurointerventional team).
• After surgical clipping: chemical DVT prophylaxis may usually be started after
>24 hours (but confirm this with the neurosurgery team).
•Agent:
• Heparin-induced thrombocytopenia is relatively common in this context, with
some series reporting rates of 6%. The use of low-molecular-weight heparin may
be preferable in patients with adequate renal function, because low-molecular-
weight heparin causes less heparin-induced thrombocytopenia than unfractionated
heparin
 Fever
• Central fever (neurogenic) is the most common medical complication after SAH,
occurring in up to 70% of patients and is more likely to occur in patients with high-grade
SAH and poor neurologic status

• hypothalamic irritation from blood products

• evaluation and exclusion for infection. Evaluation may include cultures of blood,
sputum, and cerebrospinal fluid (for patients with external ventricular drains).

• Management :
antipyretics - surface cooling
strict avoid and manage shivering

Leads to : delayed cerebral ischemia and poor clinical outcome

 Hyponatremia
• Hyponatremia is the most common electrolyte disorder after SAH and can occur in up to
30% of patients

Causes of hyponatremia :

• Cerebral salt wasting: Caused by excessive secretion of brain natriuretic peptide (BNP)
with subsequent suppression of aldosterone synthesis .
• Syndrome of inappropriate secretion of antidiuretic hormone (SIADH)

•In both cerebral salt wasting and SIADH, the laboratory findings are similar as:
• Low serum sodium (<134 mEq/mL)
• Low serum osmolality (<274 mmol/L)
• High urine sodium (>20 mmol/L)
• High urine osmolality (>100 mmol/L).

•The only differentiating finding is the patient’s intravascular volume status:

• Cerebral salt wasting is a hypovolemic state.
• SIADH is an euvolemic or even hypervolemic state.
 Hyponatremia
• Treatment :
SIADH :
diuretic ( loop diuretics ) + limit free water
intake

Cerebral salt wasting syndrome

fluid intake and

fludrocortisone (0.1-0.3 mg PO BID)
Hypertonic saline infusion
 Anemia
• Due to :
excessive blood draw
blood loss
systemic inflammation

Maintain HB level > 10 gm /dl

Hb levels < 9 gm /dl associated with delayed

cerebral ischemia and poor outcome
 Hyperglycemia
•Glycemic dysfunction is very common after SAH because
of stress and has been associated with delayed cerebral
ischemia and poor clinical outcome. However, it remains
unclear whether this is merely an association or causative.

•In the absence of clinical trials of glucose control in

patients with SAH, current recommendations are to
maintain a blood glucose level between 80 mg/dL and 200
mg/dL.
 Analgesia
•SAH may be painful, with ongoing meningeal irritation causing
headache.
•Management
• NSAIDs should generally be avoided due to risks of
coagulopathy and renal dysfunction (at least until the aneurysm is
secured).
•Scheduled acetaminophen may be helpful (e.g. 1 gram
q6hrs).
•Dexamethasone: Meningeal chemical irritation from the SAH
often responds to one or several single doses of dexamethasone (2
mg to 10 mg) .
•Opioid should be minimized as they are not effective for
meningeal pain (e.g. by using boluses for breakthrough pain only).
Short-acting opiates (e.g. fentanyl) are preferred
 Neurological worsening in patients with known
SAH
There are several causes of neurological decompensation including :
•Aneurysm rebleeding.
• Repeat noncontrast head CT is diagnostic.
•Seizure.
• EEG is diagnostic especially in nonconvulsive seizures and status epilepticus in
comatose patients.
•Vasospasm and delayed cerebral ischemia.
• CTA and CTP are diagnostic.
•Worsening hydrocephalus
• Repeat non-contrast head CT is diagnostic
•Hyponatremia
•High fever (e.g. central fever).
•Cardiopulmonary causes (Takotsubo cardiomyopathy, neurogenic pulmonary edema).
• Echocardiography and coronary angiography is diagnostic.
•Medication effect (e.g. sedation).
•Infection (e.g. ventriculitis following ventricular drain placement).