CASE IV

40 year old male came in at ER due to sudden severe

generalized headache described as worst headache ever in my
life
Accompanied by vommiting 2x. No other symptoms
History: Known Hypertensive with irregular intake of
medication
Neurologic examnination: BP: 140/100, Positive Kernings and
Brudzinki signs no other pertinent exam
CT scan: Diffuse subarachnoid hemmorhage, basal and sylvian
cisterns with concentration in the aterior interhemispheric
fissure

Pertinent History,
Physical Examination, Neurologic
Examination

Reburon, Eva Maricon R.

Pertinent History
40 year old male came in at ER due to sudden severe
generalized headache described as worst headache ever in
my life
Accompanied by vommiting 2x. No other symptoms
History: Known Hypertensive with irregular intake of
medication
Neurologic examnination: BP: 140/100, Positive Kernings
and Brudzinki signs no other pertinent exam
CT scan: Diffuse subarachnoid hemmorhage, basal and
sylvian cisterns with concentration in the aterior
interhemispheric fissure

Predisposing Factors
o
o
o
o
o
o
o
o
o
o

Young adults (40 years old)

Both genders are equally affected
Hypertension
Cigarette smoking
Atherosclerosis
Trauma
Infection
Inflammation
Binge drinking
Illicit drugs,
phenylpropanolamine, and other
sympathomimetic agents

Clinical Manifestations
o rapidly developing,
o severe headache, typically called the
worst headache of my life, that is
sometimes accompanied by a stiff neck
o nausea or vomiting
o Hemipharesis (weakness of one side of
the body)
o Hemisensory defects
o Dysphagia (difficulty of swallowing)
o Visual defects ( Diplopia, Ptosis, Dilated
pupils and Difficult to rotate the eye)
o Loss of consciousness
o Neck pain or stiffness

History

Physical Examination
BP may become labile as ICP increases.

BP: 140/100

Temperature elevation, secondary to chemical meningitis from subarachnoid

blood products, is common after the fourth day following bleeding.
Tachycardia may be present for several days after the occurrence of a hemorrhage.
Funduscopy may reveal papilledema.
Subhyaloid retinal hemorrhage (small round hemorrhage, perhaps with visible
meniscus, near the optic nerve head) is evident in 20-30% of patients. Other
retinal hemorrhages may be seen.
Seizures may occur.

Guidelines for a Screening Neurologic Examination from

the American Academy of Neurology
Sensory Systemone modality at toescan be light
touch, pain/temperature, or proprioception
Reflexes
Deep tendon reflexesbiceps, patellar, Achilles
Plantar responses
SIGNS OF MENINGEAL
IRRITATION/AFFECTATION
Brudzinskis
Kernigs

Note: If there is reason to suspect neurologic disease

based on the patients history or the results of any
components of the screening examination, a more
complete neurologic examination is necessary.

Neurologic examination

Neurologic Examination

Positive
Kernings and
Brudzinki signs

Cranial nerve palsies, along with memory loss, are present in 25% of
patients. The most frequent is oculomotor nerve palsy with or without
ipsilateral mydriasis, which results from rupture of a posterior
communicating artery aneurysm. Abducens nerve palsy is usually due
to increased ICP rather than a true localizing sign. Monocular vision
loss can be caused by an ophthalmic artery aneurysm compressing the
ipsilateral optic nerve.
Hemiparesis results from middle cerebral artery (MCA) aneurysm,
ischemia or hypoperfusion in the vascular territory, or intracerebral
clot. Patients may also have aphasia, hemineglect, or both. Leg
monoparesis or paraparesis with or without akinetic mutism/abulia
points to anterior communicating aneurysm

CLASSIFY/SPECIFIC
HEADACHE
SYNDROME

 HEADACHE +
POSTIVE NEUROLOGIC EXAMINATION
+
SIGN OF SYSTEMIC DISEASE =

SECONDARY HEADACHE

CLASSIFICATION

 ACUTE NON RECURRENT

HEADACHE
SPECIFIC HEADACHE
SYNDROME

PATHOPHYSIOLOGY
Saccular
aneurysms
occur at the bifurcations
of the large- to mediumsized intracranial arteries

As an aneurysm develops,
it typically forms a neck
with a dome.

Approximately 85% of
aneurysms occur in
the
anterior
circulation, mostly on
the circle of Willis.
About 20% of patients
have
multiple
aneurysms, many at
rupture
is
into
the
mirror sites bilaterally.
subarachnoid space in the
basal cisterns and often
into the parenchyma of
the adjacent brain
Aneurysm size and site are important in
predicting risk of rupture.
>7 mm in diameter and those at the top of
the basilar artery and at the origin of the
posterior communicating artery are at
greater risk of rupture.

arterial
internal
elastic
lamina
disappears
at
the
base of the neck
media
thins,
and
connective
tissue
replaces
smoothAtmuscle
the site cells
of rupture (most
often the dome) the wall
thins, and the tear that
allows bleeding is often
0.5 mm long.

TYPICAL PRESENTATION
Severe headache with nausea and vomiting
Diminished level of consciousness
ATYPICAL PRESENTATION
thunderclap headache
Seizure
Confusional state
Associated head trauma

the yellow discoloration of cerebrospinal

fluid (CSF) caused by hemoglobin
catabolism

Main Diagnosis

Differential Diagnosis

Hypertensive intraparenchymal
hemorrhage
Hypertensive intraparenchymal
hemorrhage (hypertensive
hemorrhage or hypertensive
intracerebral hemorrhage) usually
results from spontaneous rupture of a
small penetrating artery deep in the
brain.

Patient Condition

Pertinent Positive

Pertinent Negative

Male
40 years old
Headache
Vomiting
Hypertension
(+) Brudzinksi sign
(+) Kernigs sign

Headache
Vomiting
Hypertension
(+) Brudzinksi sign
(+) Kernigs sign

Decrease consciousness
Difficulty speaking
Difficulty swallowing
Loss of coordination
Loss of balance
Seizures
Sensation changes
Decerase in sensation
-Numbness
-Tingling
Weakness
Vision change

Cushing Disease
Cushings disease pituitary
adrenocoticotropic hormone (ACTH)
oversecretion includes bilateral
adenocortical hyperplasia and excess
production of cortisol and adrenal
androgens which together provoke the
clinical and biologic features of the
disease.

Patient Condition

Pertinent Positive

Pertinent Negative

Male
40 years old
Headache
Vomiting
Hypertension
(+) Brudzinksi sign
(+) Kernigs sign

Headache
Hypertention

Headache
Increased thirst and
urination
Trunk obesity
Moon face
Buffalo hump
Acne
Weak muscles
Mental changes

DIAGNOSTICS

Laboratory and
Radiographic Approach
Stephen A. Ujano

Sources:

Approach to Diagnosis
The diagnosis of subarachnoid
hemorrhage (SAH) usually depends
on a high index of clinical
suspicion combined with
radiologic confirmation via
urgent computed tomography
(CT) scan without contrast.
Source

Ok

Neuroimaging
Computed
Tomography Scan
(Non-Contrast) Brain
- most sensitive
imaging study in SAH
- 100% sensitivity and
specificity within 6
hours
- 93% sensitivity within
24 hours

Next

Next

EDH

ICH
Next

SDH

Result for SAH

Diffused subarachnoid
hemorrhage, basal and
sylvian cisterns with
concentration in the
interhemispheric fissure

Next

Neuroimaging
Digital-subtraction Cerebral Angiography
- criterion standard for the detection of
cerebral aneurysms
- useful in cases of diagnostic uncertainty
Cerebrovascular anatomy
Aneurysm location and source of bleeding
Aneurysm size and shape, as well as
orientation of the aneurysm dome and neck
Relation of the aneurysm to the parent
artery and perforating arteries
Presence of multiple or mirror aneurysms
(identically placed aneurysms in both the
left and right circulations)

Next

Neuroimaging
Computed Tomography Scan
(Contrast) Brain or
Multidetector CT
Angiography
- Injection of iodine-rich
contrast material and CT
scanning to help diagnose
and evaluate blood vessel
disease
- Alternative method for
locating aneurysm and
useful in planning of
definitive therapy

Next

Laboratory Studies
Serum chemistry panel - To establish a
baseline for detection of future complications
Creatinine To assess renal function for
possible contrast administration in CT
Complete blood count - For evaluation of
possible infection or hematologic abnormality
Prothrombin time (PT) and activated partial
thromboplastin time (aPTT) - For evaluation of
possible coagulopathy

Next

Laboratory Studies
Blood typing/screening - To prepare for
possible intraoperative transfusions
Cardiac enzymes - For evaluation of
possible myocardial ischemia
Arterial blood gas (ABG) - Necessary in
patients with pulmonary compromise
Serum electrolytes Hyponatremia and
hypovolemia can occur in SAH

Next

Others
Electrocardiography (ECG)
- Can show ST segment and T wave changes
- SAH patients can have myocardial ischemia due to the
increased level of circulating catecholamines or to
autonomic stimulation from the brain
Nonspecific ST and T wave changes, Decreased PR
intervals, Increased QRS intervals, Increased QT intervals,
Presence of U waves, Dysrhythmias, including premature
ventricular contractions (PVCs), supraventricular
tachycardia (SVT), and bradyarrhythmias
Chest X-ray
- baseline chest radiograph to serve as a reference point
for evaluation of possible pulmonary complications

Next

Others
Lumbar Puncture
- The hallmark of aneurysmal
rupture is blood in the CSF.
- Indicated only if CT Scan is
unavailable or if CT scan
failed to establish SAH
diagnosis in the absence of
mass or obstructive
hydrocephalus
- SAH result: xanthochromia
and inc. RBC

Normal CSF

Color: Colorless, clear,

like water
Opening pressure:
10-20 cm H2O
Glucose: 40-70 mg/dL
Proteins: 15-50 mg/dL
RBC: Adult: 0 /mm3
WBC: Adult: 0-5/mm 3

Source:

Next

Harrisons IM 18th Ed.

Others
MRI (Magnetic Resonance Imaging)
- performed if no lesion is found on
angiography
- sensitivity in detecting blood is considered
equal or inferior to that of CT scan
- useful tool to diagnose AVMs that are not
detected by cerebral angiography or spinal
AVMs causing SAH
- more costly and not sensitive for SAH within
the first 48 hours

Next

Management of SAH
Upano, Celimar Monette A.

Neurosurgical clipping
Surgical repair involves placing a metal clip across the
aneurysm neck, thereby immediately eliminating the
risk of rebleeding.
This approach requires craniotomy and brain retraction,
which is associated with neurologic morbidity.

Endovascular coiling
Endovascular techniques involve placing
platinum coils, or other embolic material, within
the aneurysm via a catheter that is passed from
the femoral artery.
The aneurysm is packed tightly to enhance
thrombosis and over time is walled off from
the circulation.

Neurosurgical clipping vs Endovascular coiling

The International Subarachnoid Aneurysm Trial (ISAT), was
terminated early when 24% of patients treated with
endovascular therapy were dead or dependent at 1 year
compared to 31% treated with surgery, a significant 23%
relative reduction.
After 5 years, risk of death was lower in the coiling group,
although the proportion of survivors who were
independent was the same in both groups. Risk of
rebleeding was low, but more common in the coiling
group. Also, because some aneurysms have a morphology
that is not amenable to endovascular treatment, surgery
remains an important treatment option.
Centers that combine both endovascular and
neurosurgical expertise likely offer the best outcomes for
patients

Medical management of SAH

focuses on:
protecting the airway,
managing blood pressure before and
after aneurysm treatment,
preventing rebleeding prior to treatment,
Managing vasospasm,
treating hydrocephalus,
treating hyponatremia, and
preventing pulmonary embolus.

Intracranial hypertension
following aneurysmal rupture occurs
secondary to:

subarachnoid blood,
parenchymal hematoma,
acute hydrocephalus,
or loss of vascular autoregulation.

 Patients who are stuporous should

undergo emergent ventriculostomy to
measure ICP and to treat high ICP in order
to prevent cerebral ischemia.
Medical therapies designed to combat
raised ICP (e.g., mild hyperventilation,
mannitol, and sedation) can also be used
as needed.
High ICP refractory to treatment is a
poor prognostic sign.

 Prior to definitive treatment of the ruptured

aneurysm, care is required to maintain
adequate cerebral perfusion pressure while
avoiding excessive elevation of arterial
pressure.
If the patient is alert, it is reasonable to lower
the blood pressure to normal using
nicardipine, labetolol, or esmolol.
If the patient has a depressed level of
consciousness, ICP should be measured and
the cerebral perfusion pressure targeted to 60
70 mmHg.

 If headache or neck pain is

severe, mild sedation and
analgesia are prescribed.
Extreme sedation is avoided
because it can obscure changes in
neurologic status.
Adequate hydration is necessary
to avoid a decrease in blood
volume predisposing to brain
ischemia.

 Anticonvulsants are sometimes given as prophylactic

therapy since a seizure could theoretically promote
rebleeding.
Glucocorticoids may help reduce the head and neck ache
caused by the irritative effect of the subarachnoid blood.
There is no good evidence that they reduce cerebral
edema, are neuroprotective,or reduce vascular injury, and
their routine use therefore is not recommended.
Antifibrinolytic agents are not routinely prescribed but
may be considered in patients in whom aneurysm
treatment cannot proceed immediately. They are
associated with a reduced incidence of aneurysmal
rerupture but may also increase the risk of delayed cerebral
infarction and deep-vein thrombosis (DVT).

 Vasospasm remains the leading cause of

morbidity and mortality following aneurysmal
SAH.
Treatment with the calcium channel antagonist
nimodipine (60 mg PO every 4 h) improves
outcome, perhaps by preventing ischemic
injury rather than reducing the risk of vasospasm.
Symptomatic cerebral vasospasm can also
be treated by increasing the cerebral perfusion
pressure by raising mean arterial pressure
through plasma volume expansion and the
judicious use of IV vasopressor agents, usually
phenylephrine or norepinephrine.

 Treatment with induced hypertension and

hypervolemia generally requires monitoring of
arterial and central venous pressures; it is best to
infuse pressors through a central venous line as well.
Volume expansion helps prevent hypotension,
augments cardiac output, and reduces blood
viscosity by reducing the hematocrit. This method is
called triple-H (hypertension, hemodilution, and
hypervolemic) therapy.
If symptomatic vasospasm persists despite
optimal medical therapy, intraarterial vasodilators and
percutaneous transluminal angioplasty are considered.

 Acute hydrocephalus can cause stupor or coma.

It may clear spontaneously or require temporary
ventricular drainage.
If Chronic hydrocephalus develops, ventricular
shunting is the treatment of choice.
Free-water restriction is contraindicated in
patients with SAH at risk for vasospasm because
hypovolemia and hypotension may occur and
precipitate cerebral ischemia.
Supplemental oral salt coupled with normal saline
will mitigate hyponatremia, but often patients also
require hypertonic saline.
Care must be taken not to correct serum
sodium too quickly in patients with marked
hyponatremia of several days duration, as central
pontine myelinolysis may occur.

 Pneumatic compression stockings

applied to prevent pulmonary embolism.
Unfractionated heparin administered
subcutaneously for DVT prophylaxis can be
initiated immediately following endovascular
treatment and within days following
craniotomy and surgical clipping and is a
useful adjunct to pneumatic compression
stockings.
Treatment of pulmonary embolus depends on
whether the aneurysm has been treated and
whether or not the patient has had a
craniotomy.

 Systemic anticoagulation with heparin is

contraindicated in patients with ruptured
and untreated aneurysms.
It is a relative contraindication following
craniotomy for several days, and it may
delay thrombosis of a coiled aneurysm.
Following craniotomy, use of inferior vena
cava filters is preferred to prevent further
pulmonary emboli, while systemic
anticoagulation with heparin is preferred
following successful endovascular treatment.