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Pertinent History,
Physical Examination, Neurologic
Examination
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
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
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
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
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
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
Source:
Next
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.
Intracranial hypertension
following aneurysmal rupture occurs
secondary to:
subarachnoid blood,
parenchymal hematoma,
acute hydrocephalus,
or loss of vascular autoregulation.