Subarachnoid hemorrhage is bleeding into the subarachnoid space surrounding the brain. It accounts for 5% of strokes but has high mortality and disability rates. The main causes are aneurysms (85%) and hypertension is a major risk factor. Patients present with sudden severe headache, vomiting, and possible loss of consciousness. Grading systems assess severity based on symptoms and imaging findings. Management involves stabilizing the patient, treating complications, and potentially clipping or coiling the aneurysm to prevent rebleeding. Anesthesia aims to control blood pressure rises during intubation and carefully monitor the patient.

1. SUBARACHNOID HAEMORRHAGE:
PATHOPHYSIOLOGY, GRADING,
ASSESSMENT, COMPLICATION AND
ICU MANAGEMENT
Presented by Baby Pegu

2. Definition
Clinical features
Risk factor
Pathophysiology
Grading
Anesthetic considerations

3. Subarchnoid hemorrhage (SAH) is an acute
cerebrovascular disorder that encompasses various
sources of usually diffuse bleeding into the
subarachnoid space.
SAH accounts for only 5% of all strokes but is a
worldwide health burden with high rates of fatality
and permanent disability rates.
In most population the incidence is 6-7 per 100000
person –years with regional variation. It is around 20
per 100000 in Finland and Japan.

4. ETIOLOGY
1.Aneurysm (85 %)
2. Non aneurysmal perimesencephalic
hemorrhage (10%)
3. Rare causes (5%)
• Inflammatory causes of cerebral arteries
• Non inflammatory lesions of intracerebral vessels
• Tumours
• Drugs : cocaine abuse , anticoagulant drugs.

5. RISK FACTORS
• Hypertension
• Smoking
• Chronic alcohol abuse
• Female sex
• Family history of intracranial aneurysm in first
degree relatives.
• Inherited diseases: autosomal dominant polycystic
kidney disease,marfan syndrome, neurofibromatosis type
1, ehler danols syndrome, fibromuscular dysplasia

6. CLINICAL FEATURES
1. Sudden severe headache, sentinal headache
2. Nausea and vomiting.
3. Stiff neck and photophobia
4. A brief loss of consciousness , seizure episode.
5. Focal neurological deficit including cranial
nerve palsy, hemiparesis and even coma.
7. Systemic features include severe
hypertension, hypoxemia, neurogenic pulmonary
edema, cardiac manifestations including ecg
changes mimicking acute MI.

7. Clinical features of intracranial
aneurysms based on location
Location of Aneurysm Clinical features
Anterior communicating artery Bilateral temporal hemianopia
Bilateral lower extrimity weakness
Posterior communicating artery Third nerve palsy
Intercavernous internal carotid artery Facial or orbital pain
Progressive vision loss or opthalmoplegia
Posterior circulation aneurysms Brainstem dysfunction, occipital or
posterior cervical pain

9. PATHOPHYSIOLOGY
Aneurysmal SAH is a neurological
syndrome with complex
complication. The hemorrhage
triggers a cascade of complex events
which can result in early brain injury ,
delayed cerebral ischaemia and
systemic complication.

11. Early brain injury

12. Delayed cerebral ischaemia

13. Systemic effects
Cardiac effects : The effects of SAH on the
mycardium can range from alteration in the ecg , to
leakage of cardiac troponins, to wall motion
abnormalities. The mechanism of myocardial
dysfunction is due to increased release of localised
catecholamine in the mycardium. This intense
stimulation leads to contraction band necrosis and
subsequent myocardial dysfunction. However the
prognosis of SAH induced ventricular dysfuction is
good and generally reversible.

14. ECG changes: ECG abnormalities occur in 40%
to 100% of patients with SAH. These
abnormalites include sinus bradycardia , sinus
tacchycardia. AV dissociation to ventricular
tachycardia and fibrillation.
Morphological changes include t wave
inversion, depression of st segment,
appearance of U wave , prolongation of QT
interval.

15. Respiratory system
Pulmonary edema has been observed to accompany SAH in 8%
to 28% of cases which correlate closely with clinical grades.
Aspiration and peumonia are potential complication.
Intravascular volume status and electrolyt
abnormalities.
The intravascular volume status has been found to be abnormally
low in 36% to 100% of patients with SAH and correlates with the
clinical grading.
Hyponatremia is observed in 30% to 57% of cases with SAH.
Hyponatremia is related to SIADH and cerebral salt wasting
syndrome.
Other significant electrolyte abnormality include hypokalemia and
hypocalcemia

16. GRADING OF SAH
1. Botterells clinical grading
2. Modified hunt and hess clinical
grades for patient with SAH
3. World Federation of Neurological
Surgeons’s Grades
4. Fisher Grades for Computed
Tomography (CT) Findings in SAH.

17. Botterell’s clinical grades for patients
with SAH
GRADE CRITERIA
I Conscious with or without meningeal signs
II Drowsy without significant neurologicac deficit
III Drowsy with neurologic deficit and probable cerebral
clot
IV Major neurologic deficit present
V moribund with failing vital centres and extensor rigidity

18. Modified Hunt and Hess Clinical
Grades for patients with SAH
GRADE CRITERIA MORTALITY(%) MORBIDITY(%
)
0 Unruptured aneurysm 0 - 2 0 - 2
I Asymptomatic or minimal headache
,and slight nuchal rigidity
2 - 5 0 - 2
II Moderate to severe headache, nuchal
rigidity, but no neurolgic deficit other
than cranial nerve palsy
5 - 10 7
III Drowsiness , confusion, or mild focal
deficit.
5 - 10 25
IV Stupor ,mild or severe hemiparesis,
possible early decerebrate rigidity,
vegetative disturbance
20 -30 25
V Deep coma , decerebrate rigidity,
moribund appearance
30-40 35 - 45

19. World Federation of Neurological
Surgeon’s Grades for Pattients with
SAH
GRADE GLASSGOW COMA SCALE MOTOR DEFICIT
I 15 ABSENT
II 14 - 13 ABSENT
III 14 - 13 PRESENT
IV 12 - 7 PRESENT OR ABSENT
V 6 - 3 PRESENT OR ABSENT

20. Fisher Grades for Computed
Tomography findings in SAH
GRADE CT finding (s)
1 No bleed detected
2 Diffuse thin layer of subarchnoid blood ( vertical layer < 1 mm thick)
3 Localised clot or thick layer of subarchnoid blood ( vertical layers >1
mm thick)
4 Intracerebral or intraventricular blood with diffuse or no subarchnoid
blood.

21. DIAGNOSIS
CT SCAN : non contrast CT is the first investigation
if SAH is suspected. The ability to detect SAH is
dependent on the amount of subarchnoid blood ,
the interval after symptoms onset, the resolution
of the scanner.
The probability of detecting a hemorrhage is
proportional to clinical grades and the time from
hemorrhage. In the first 12 hour the sensitivity of
CT for SAH is 98- 100% , declining to 93% at
24hours and 57%- 85% 6 days after SAH.

22. LUMBAR PUNCTURE : a lumbar puncture is
necessary in any patient with sudden onset
headache and a normal head CT scan. Csf include
cell count , the presence of xanthochromia and
detection of bilirubun.
MRI : after the initial days when hyperdensity on CT
scan decreases MR is better for detecting blood with
fluid attenuation inversion recovery.
ANGIOGRAPHY: angiographic study serve to identify
one or more aneurysm and also anatomical
configuration of the aneurysm in relation to
adjoining arteries.

23. MANAGEMENT
PHARMACOLOGICAL NONPHARMACOLICAL
1.Calcium channel blockers 1. Surgical
2.Magnesium sulphate 2. Reduction of ICP
3.Endothelin receptor 3. Hypervolumic,
antagonist hypertensive and
4.Tirilazide hemodilution
5.Nicaraven therapy

24. Hypervolemic, hypertensive, and
hemodilution therapy (triple H
therapy)
The ischaemic areas of the brain have impaired autoregulation and
thus CBF depends on perfusion pressure which partly depends on
intravascular volume and mean arterial pressure.
Hypervolumia is achieved with infusion of crystalloids as well as
colloids . Although iv fluid loading is sufficient to raise BP
,vasopressors such as dopamine , dobutamine and phenylephrine
etc can also be added.
The BP is titrated to a level necessary to reverse signds and symptoms
of vasospasm or a max of 160 to 200mmhg in patients whose
aneurysm has been clipped.or 120 to 150mmhg in unclipped
patients.
S/E : Worsening of cerebral edema , increase ICP , hemorrhage into an
infarcted area, pulmonary edema , myacardial infarction, dilutional
hyponatremia, and coagulopathy.

25. Hemodilution is the last componentt of triple H
therapy, is based on correlation of hematocrit and
whole blood viscosity. As the hematocrit and
viscosity diminishes, the cerebrovascular
resistance correspondently decreases and CBF
increases. Hematocrit of 33% (27% to 30%)
provide an optimal balance between viscocity and
oxygen carrying capacity.
S/E : oxygen carrying capacity is reduced by
hemodilution.

26. SURGERY
CLIP vs COIL
The ISAT ( International subarchnoid Aneurysm trial
) a prospective multicentric RCT.
ISAT reported that outcome ( death or dependency
ratio ) was better with coiling group compared
with surgical clipping .
However rate of rebleeding was higher in coiling
group as compared to clipping group.
Also risk of seizure was less in coiling as compared
to clilpping.

28. ANESTHETIC MANAGEMENT
PREMEDICATION : premedication should be
individualised. Patients with a good cliniical grade
may receive Morphine 1 to 5 mg or Midazolam 1
to 5 mg for sedation.
Intraoperative consideration and induction of
anaesthesia.
Monitorings requirements:
Ecg tracings, NIBP , pulse oximetry, capnoghraphy,
neuromuscular monitoring, intra areterial blood
pressure monitoring,central venous pressure
catheter and pulmonary artery catheter.

29. Induction
Induction consist of two phases
Induction to achieve loss of consciouness
 prophylaxis to prevent rise in blood pressure
in response to laryngoscopy and intubation.
Achieving loss of consciousness
propofol ( 1.5 -2 mg/kg) or thiopental (3-
5mg/kg) in combination with fentanyl or
remifentanyl is suitable.
Etomidate (.3 to0.4mg/kg) and midazolam ( 0.1
-0.2 mg/kg) are other alternative.

30. Prophylactic against a rise In ICP
during laryngoscopy