3. SUB-ARACHNOID HAEMORRHAGE
Subarachnoid hemorrhage (SAH) refers to extravasation
of blood into the subarachnoid space between the pial and
arachnoid membranes.
It comprises half of spontaneous atraumatic intracranial
hemorrhages, the other half consist of bleeding that
occurs within the brain parenchyma.
NB the most common cause of SAH is head trauma.
However, the familiar medical use of the term SAH refers
to nontraumatic (or spontaneous) hemorrhage, which
usually occurs in the setting of a ruptured cerebral
aneurysm or arteriovenous malformation (AVM).
Its devastating condition with high morbidity and
mortality
Etiology
Rupture of “berry,” or saccular, aneurysms of the basal
vessels of the brain comprises 77% of nontraumatic SAH
cases
Aneurysms mostly arise from the terminal portion of the
internal carotid artery (ICA) and from the major branches
of the anterior portion of the circle of Willis.
Pathophysiology
Congenital and acquired factors are thought to play a role
in occurrence of aneurysm.
Aneurysms usually occur at the branching sites on the
large cerebral arteries of the circle of Willis. The early
precursors of aneurysms are small outpouchings through
defects in the media of the arteries.
These defects are thought to expand as a result of
hydrostatic pressure from pulsatile blood flow and blood
turbulence, which is greatest at the arterial bifurcations. A
mature aneurysm has a paucity of media, replaced by
connective tissue, and has diminished or absent elastic
lamina.
The rate of rupture is directly related to the size of the
aneurysm. Aneurysms with a diameter of 5 mm or less
have a 2% risk of rupture, whereas 40% of those 6-10 mm
have already ruptured upon diagnosis.
Brain injury from cerebral aneurysm formation can occur
in the absence of rupture via compressive forces that
cause injury to local tissues and/or compromise of distal
blood supply (mass effect).
When an aneurysm ruptures, blood extravasates under
arterial pressure into the subarachnoid space and quickly
spreads through the cerebrospinal fluid (CSF) around the
brain and spinal cord. Blood released under high pressure
may directly cause damage to local tissues. Blood
extravasation causes a global increase in intracranial
pressure (ICP). Meningeal irritation occurs.
Congenital defects in the muscle and elastic tissue of the
arterial media in the vessels. These defects lead to
microaneurysmal dilatation.
Aneurysms are acquired lesions related to hemodynamic
stress on the arterial walls at bifurcation points and bends.
AVMs are the second most identifiable cause of SAH,
accounting for 10% of cases of SAH
LOC often is transient; however some patients are
comatose for several days, depending on the location of
the aneurysm and the amount of bleeding.
6. Seizures during the acute phase
Risk factors for aneurismal SAH:
1.Hypertension - Fibromuscular dysplasia, polycystic
kidney disease, and aortic coarctation
2.Increased blood flow - Cerebral arteriovenous
malformation (AVM); persistent carotid-basilar
anastomosis; ligated, aplastic, or hypoplastic contralateral
vessel
3.Blood vessel disorders – Atherosclerosis ,Systemic
lupus erythematosus (SLE), Moyamoya disease, and
granulomatous angiitis
4.Genetic - Marfan syndrome, Ehlers-Danlos syndrome,
Osler-Weber-Rendu syndrome, pseudoxanthoma
elasticum, and Klippel-Trenaunay-Weber syndrome
5.Congenital - Persistent fetal circulation and
hypoplastic/absent arterial circulation
6.Metastatic tumors to cerebral arteries - Atrial myxoma,
choriocarcinoma, and undifferentiated carcinoma
7.Infectious - Bacterial, fungal
Use of oral contraceptives ,Hormone replacement therapy,
Hypercholesterolemia and alcohol consumtion may
contribute to HTN or atherosclerosis.
.Saccular or berry aneurysms are specific to the
intracranial arteries because their walls lack an external
elastic lamina and contain a very thin adventitia—factors
that may predispose to the formation of aneurysms. An
additional feature is that they lie unsupported in the
subarachnoid space.
Mortality/Morbidity:
As many as 60% of patients die in the first 30 days as the
result of SAH.
Sex: The incidence of SAH is slightly higher in women
than in men.
Age: The mean age for SAH is 50 years.
Clinical presentation
History
The signs and symptoms of SAH range from subtle
prodromal events, which often are misdiagnosed, to the
classic presentation of catastrophic headache.
A)Sentinel, or "warning," leaks that produce minor
blood leakage
Sentinel leaks produce sudden focal or generalized head
pain that may be severe. In addition to headaches, sentinel
leaks may produce nausea, vomiting, photophobia,
malaise, or, less commonly, neck pain.Signs of raised ICP
don’t occur
B)Aneurysmal rapture SAH
The classic symptoms and signs of aneurysmal rupture
into the subarachnoid space comprise one of the most
pathognomonic presentations in all of clinical medicine
1.A sudden onset of very severe headache, often
described as the “worst headache of my life”
2.Nausea and/or vomiting
3. Symptoms of meningeal irritation, including nuchal
rigidity and pain, back pain, and bilateral leg pain (but
may take several hours to manifest).
4. Photophobia and visual changes are common.
5. A sudden loss of consciousness (LOC) occurs at the
ictus in as many as 45% of patients as ICP exceeds
cerebral perfusion pressure
4. c)Mass effect
Expanding aneurysm or hemorrhage, characteristic
features based upon aneurysm location. 1.Posterior
communicating artery/internal carotid artery - Focal,
progressive retro-orbital headaches and oculomotor nerve
palsy
2.Middle cerebral artery - Contralateral face or hand
paresis, aphasia (left side), contralateral visual neglect
(right side)
3.Anterior communicating artery - Bilateral leg paresis
and bilateral Babinski sign
4.Basilar artery apex - Vertical gaze, paresis, and coma
5.Intracranial vertebral artery/posterior inferior cerebellar
artery - Vertigo, components of lateral medullary
syndrome.
Physical Examination
1.Focal neurologic signs hemiparesis, aphasia,
hemineglect, cranial nerve palsies, and memory loss
2. Ophthalmologic examination may reveal subhyaloid
retinal hemorrhages and papilledema.
3. Blood pressure elevation is observed in about .BPoften
becomes labile as ICP increases. Brabycardia may occur
4. Temperature elevation, secondary to chemical
meningitis.
Hunt and Hess grading system of SAH
Grade 1 - Asymptomatic or mild headache
Grade 2 - Moderate-to-severe headache, nuchal rigidity,
and no neurological deficit other than possible cranial
nerve palsy
Grade 3 - Mild alteration in mental status (confusion,
lethargy), mild focal neurological deficit
Grade 4 - Stupor and/or hemi paresis
Grade 5 - Comatose and/or decerebrate
MANAGEMENT
Indications for surgical management have been described
recently and include the following:
For patients with a mild- or intermediate-grade SAH
(Hunt and Hess 1-3), surgical treatment (Surgical
clipping) is strongly recommended because the risks of
SAH complications greatly exceed the risk of surgical
complications
For patients with a poor grade of SAH (Hunt and Hess
grades 4-5) The overall outcome is poor, with or without
surgical intervention.
Patients with a higher grade of SAH or poor medical
status that do not qualify for early surgery may be
candidates for delayed surgery or endovascular
obliteration of the aneurysm. Other indications of surgey
➢ Large and giant aneurysm
➢ Wide-necked aneurysms
➢ Vessels emanating from the aneurysm dome
➢ Mass effect or hematoma associated with the
aneurysm
➢ Recurrent aneurysm after coil embolization
Indications for endovascular treatment
Endovascular treatment with the Guglielmi detachable
coil system
➢ Patients with poor clinical grade
➢ Patients who are medically unstable
➢ In situations where aneurysm location imparts
an increased surgical risk, such as cavernous
sinus and many basilar tip aneurysms
➢ Small-neck aneurysms in the posterior fossa
➢ Patients with early vasospasm
➢ Cases where the aneurysm lacks a defined
surgical neck (although these are also difficult
to "coil")
➢ Patients with multiple aneurysms in different
arterial territories if surgical risk is high
Location of aneurysm rupture
Approximately 85% of saccular aneurysms occur in the
anterior circulation. The most common sites of rupture are
as follows:
-The internal carotid artery, including the posterior
communicating junction (41%)
-The anterior communicating artery/anterior cerebral
artery (34%)
-The middle cerebral artery (20%)
-The vertebral-basilar arteries (4%)
-Other arteries (1%)
Lab Studies:
1.CBC count - For evaluation of possible infection or
hematologic abnormality
2.Prothrombin time (PT) and activated partial
thromboplastin time (aPTT) - For evaluation of possible
coagulopathy
3.Serum electrolytes - To establish a baseline for
detection of future complications
4.Blood type and screen - In case intraoperative
transfusion is required or in the setting of massive
hemorrhage
5.Cardiac enzymes - For evaluation of possible
myocardial ischemia
6.Arterial blood gas (ABG) - Assessment is necessary in
cases with pulmonary compromise
Imaging Studies:
1. CT scan: the location of the hemorrhage and the mass
effects of the hemorrhage on the ventricles.
2. LP If diagnosis not clear, do lumbar puncture after
funduscopy to rule out raised ICP.
D-dimer assay: can be used to discriminate SAH from
traumatic LP.
After 24 hours, CSF samples may demonstrate a
polymorphonuclear and mononuclear polycytosis
secondary to chemical meningitis caused by the
degradation products of subarachnoid blood.
3. Cerebral angiography can provide the following
important surgical information in the setting of SAH:
a)Cerebrovascular anatomy
b)Aneurysm location and source of bleeding
c)Aneurysm size and shape, as well as orientation of the
aneurysm dome and neck
5. Other Tests
1. Transcranial Doppler studies are useful in the detection
and monitoring of arterial vasospasm.
2. Chest radiograph: All patients with SAH should have a
baseline chest radiograph to serve as a reference point for
evaluation of possible pulmonary complications.
3, Evaluation of ventricular wall motion via
echocardiogram may be necessary in cases with suspected
myocardial ischemia.
4.ECG- NonspecificST and T wave changes Decreased
PR intervals, Increased QRS intervals,Increased QT
intervals,Presence of U waves
Medical Management
The initial management of patients with SAH is directed
at patient stabilization. Assess the level of consciousness
and airway, as well as breathing and circulation (ABCs).
Endotracheal intubation should be performed for patients
presenting with coma, depressed level of consciousness,
inability to protect their airway, or increased ICP.
Intravenous (IV) access should be obtained, including
central and arterial lines. A short-acting benzodiazepine,
such as midazolam, should be administered prior to all
procedures
Hypertension control
The traditional treatment of ruptured cerebral aneurysms
included strict blood pressure control, with fluid
restriction and antihypertensive therapy.
The current recommendations advocate the use of
antihypertensive agents when the mean arterial pressure
(MAP) exceeds 130 mm Hg.
Intravenous beta-blockers, which have a relatively short
half-life, can be titrated easily and do not increase ICP.
Beta-blockers are the agents of choice in patients without
contraindications.
Most clinicians avoid the use of nitrates, such as
nitroprusside or nitroglycerin, which elevate ICP.
Hydralazine and calcium channel blockers have a fast
onset and lead to relatively less increase in ICP than do
nitrates.
Angiotensin-converting enzyme inhibitors have a
relatively slow onset and are not first-line agents in the
setting of acute SAH.
Increased ICP
1.Patients with signs of increased ICP or herniation
should be intubated and hyperventilated. Minute
ventilation should be titrated to achieve a PCO2 of 30-35
mm Hg. Avoid excessive hyperventilation, which may
potentiate vasospasm and ischemia.
2.Osmotic agents (eg, mannitol), which can decrease ICP
dramatically (50% after 30 min postadministration) Loop
diuretics (eg, furosemide) also can decrease ICP
3.The use of IV steroids (eg, Decadron) is controversial
d)Relation of the aneurysm to the parent artery and
perforating arteries
e) Presence of multiple or mirror aneurysms (identically
placed aneurysms in both the left and right circulations)
Additional medical management is directed to prevent
and treat the following common complications of SAH:
➢ Rebleeding
➢ Vasospasm
➢ Hydrocephalus
➢ Hyponatremia
➢ Seizures
➢ Pulmonary complications
➢ Cardiac complications
Rebleeding
Is the most dreaded early complication of SAH. The
greatest risk of rebleeding occurs within the first 24 hours
of rupture.The overall mortality rate from rebleeding is
reported to be as high as 78%.
Measures to prevent rebleeding include the following:
1.Bedrest in a quiet room
2. Analgesia, preferably with a short-acting and reversible
agent such as fentanyl: Pain is associated with a transient
elevation in blood pressure and increased risk of
rebleeding.
3.Sedation (used with caution to avoid distorting
subsequent neurologic evaluation) with a short-acting
benzodiazepine such as midazolam
4.Stool softeners
5.Antifibrinolytics have been shown to reduce the
occurrence of rebleeding.
However, outcome likely does not improve because of a
concurrent increase in the incidence of cerebral ischemia
2.Cerebral vasospasm
The delayed narrowing of the large capacitance vessels at
the base of the brain, is a leading cause of morbidity and
mortality in survivors of nontraumatic SAH.
-Vasospasm is reported to occur in as many as 70% of
patients .Most commonly, this occurs 4-14 days after the
hemorrhage.
-Vasospasm can lead to impaired cerebral auto regulation
and may progress to cerebral ischemia and infarction.
Measures used for prevention of vasospasm include the
following:
1.Maintenance of normovolemia, normothermia, and
normal oxygenation are paramount to vasospasm
prophylaxis. Volume status should be monitored closely,
with avoidance of volume contraction, which can
predispose to vasospasm.
2.Prophylaxis with oral nimodipine:
-Calcium channel blockers have been shown to reduce the
incidence of ischemic neurological deficits, and
nimodipine has been shown to improve overall outcome
within 3 months of aneurysmal SAH.
-Nimodipine may prevent the ischemic complications of
vasospasm by the neuroprotective effect of blockading the
influx of calcium into damaged neurons.
-Should be used cautiously to avoid the deleterious effects
of hypotension.
If vasospasm becomes symptomatic use of hypertensive,
hypervolemic, and hemodilutional (HHH) therapy.
There is demonstrated improved cerebral blood flow and
6. Initiation of HHH therapy requires placement of a
pulmonary artery catheter in order to guide volume
expansion and inotropic or vasopressor therapy.
This therapy should be reserved for patients with
aneurysms secured by surgical clipping or endovascular
techniques in order to reduce the risk of rebleeding.
Hypervolemia may be achieved by using packed
erythrocytes, isotonic crystalloid, and colloid and albumin
infusions in conjunction with vasopressin injection.
Corticosteroids may be of some benefit; however, such
treatment remains controversial.
The hematocrit should be maintained at 30-35% via
hemodilution or transfusion in order to optimize blood
viscosity and oxygen delivery.
Aggressive hypertensive therapy with inotropes and
vasopressors (eg, dobutamine) can be initiated, if
warranted
Hydrocephalus
Acute type Occurs within the first 24 hours after
hemorrhage. This condition can precipitate life-
threatening brainstem compression and occlusion of blood
vessels. Hydrocephalus presents as a relatively abrupt
mental status change, including lethargy, stupor, or coma.
CT scan differentiates hydrocephalus from rebleeding.
Treatment for acute hydrocephalus includes external
ventricular drainage, depending on the severity of clinical
neurologic dysfunction or CT scan findings.
Chronic hydrocephalus usually the communicating type
Hyponatremia
Elevated levels of atrial natriuretic factor (ANF) and
syndrome of inappropriate secretion of antidiuretic
hormone (SIADH) have been implicated in recent studies
of post-SAH hyponatremia. Use of slightly hypertonic
sodium chloride (1.5% sodium chloride) at rates above
maintenance requirements usually is efficacious for SAH-
induced hyponatremia. Avoid fluid restriction in patients
with SAH.
Seizures
Agents used for seizure prophylaxis include the
following:
Phenytoin, the agent of choice, can achieve rapid
therapeutic concentrations when loaded intravenously,
and it does not cause alterations in consciousness.
Phenobarbital produces a sedative effect, which may
mask the neurological evaluation; phenobarbital is used
less frequently than phenytoin.
Acute pulmonary edema and hypoxia
Are almost universal in severe SAH.
Neutrogenic in origin and unrelated to HHH therapy;
however, the latter is associated with an increased risk of
fluid overload.
Treatment of acute pulmonary edema may include the use
of gentle diuresis, dobutamine, and positive end-
expiratory pressure (PEEP).
resolution of the ischemic effects of vasospasm with this
therapy.
Cardiac dysfunction occurs in a significant number of
people with SAH. Neurogenic sympathetic hyperactivity,
as well as increased levels of systemic catecholamines,
has been implicated in SAH-associated cardiac
dysfunction. Arrhythmias occur in as many as 90% of
patients and most commonly include the following
-Premature ventricular complexes (PVCs)
-Bradyarrhythmias Supraventricular tachycardia
-Arrhythmias are most prevalent in the first 48 hours
following SAH. Only a small percentage of arrhythmias
(usually those associated with hypokalemia) are life
threatening
