Transcript Case Presentation

Case Presentation
NSS SGD
Ontok.Rodriguez.Salongcay.Samson.Bautista
General Data
 T.A. 43 year old female
 Laguna
 Right-handed
 Married
 Roman Catholic
 Beautician in Brunei
 Date of admission: October 6, 2009
 On her 8th hospital day
Source of History
 Informant: patient
 Reliability: good
Chief Complaint
Headache
History of Present Illness
Patient is apparently well, with no known co-morbidity.
2 months PTA, while cleaning the toilet
(+) Headache – VAS 10/10, sudden onset, fronto-parietal
area, throbbing, non-radiating
(+) Weakness and numbness – both lower extremities
(+) Loss of consciousness – lasted for 3 days allegedly
(+) Diaphoresis
(-) Nausea / Vomiting
History of Present Illness
 admitted at local hospital in Brunei
 Blood pressure was 160 / 100 mmHg
 CT scan - subarachnoid hemorrhage
- Right PCOM aneurysm, infundibular type
 Nimodipine 60 mg x 21 days, other meds unrecalled
History of Present Illness
 advised surgery for clipping of aneurysm - deferred
 Preferred to be further treated in the Philippines
 Patient allegedly discharged with normal neurologic findings
 Patient admitted at PGH for further management
Review of Systems
 (-) fever, weight loss, anorexia
 (-) dyspnea, cough, colds
 (-) palpitations, chest pain, easy fatigability
 (-) abdominal pain, mass, tenderness, bowel movement
changes
 (-) dysuria, hematuria, tea-colored urine
 (-) muscle or joint pain, tenderness, swelling
Past Medical History
(-) Diabetes mellitus
(-) Tuberculosis
(-) Cardiovascular disease
(-) Bronchial asthma
(-) Allergy to food or medication
(-) Connective tissue disease
(-) Substance abuse
(-) Previous surgical operations or hospitalizations
Family History
(-) similar illness
(+) Hypertension – mother
(+) Stroke – uncle, maternal side
(-) Diabetes mellitus
(-) Tuberculosis
(-) Cardiovascular disease
(-) Bronchial asthma
(-) Allergy to food or medication
(-) Connective tissue disease
(-) Substance abuse
Personal and Social History
 Vocational course graduate
 Works as a beautician in Brunei
 Married with 2 children
 Denies use of cigarette, alcoholic beverage, or illicit drugs
 Eats fatty, salty, and sweet foods regularly
 No regular physical exercise
Physical Examination
General Survey: Patient is awake, coherent, ambulatory and not in
cardiorespiratory distress
Vital Signs: BP 130/90 mmHg HR 90 beats/min RR 20 breaths/min T 37.3˚C
Head, Eyes, Ears, Nose, Throat: Pink palpebral conjunctivae, anicteric sclerae, (-)
anterior neck mass, (-) cervical lymphadenopathy, (-) neck vein engorgement,
(-) bruits
Chest/Lungs: Equal chest expansion, clear breath sounds, (-) rales, (-) crackles, (-)
wheezes
Cardiovascular: Adynamic precordium, distinct heart sounds, normal rate, regular
rhythm, (-) murmurs
Abdomen: Flat, normoactive bowel sounds, soft, (-) masses or tenderness
Genitourinary: Deferred
Skin/Extremities: Pink nail beds, full and equal pulses, (-) cyanosis, (-) edema, (-)
clubbing, (-) skin lesion
Physical Examination
Neurologic:
GCS 15 (E4 V5 M6)
Patient presently awake, conversant, oriented to time, place
and person
Physical Examination
Neurologic:
Cranial Nerves
I – can smell
II – can read fine print
III – pupils 3 mm, equally briskly reactive to light; EOM’s full and equal
IV – EOM’s full and equal
V – can clench jaw, intact light touch sensation on face, brisk corneal reflex
VI – EOM’s full and equal
VII – can raise eyebrow, smile, frown, (-) facial asymmetry
VIII – can hear grossly
IX – symmetrical uvula and soft palate, (+) gag reflex
X – can taste, (+) gag reflex
XI – good shoulder shrug
XII – tongue midline
Physical Examination
Neurologic:
Sensory – intact light touch, temperature, vibration, pain
sensation
Motor - Muscle strength 5/5 in all extremities
Deep tendon reflex ++ (triceps, biceps, brachioradialis, patella,
Achilles’)
Cerebellar – (-) dysdiadochokenisia, dysmetria, nystagmus,
tandem walk, heel-to-shin test
(-) Brudzinski sign, Kernig’s sign, nuchal rigidity
Summary of hx and PE
This is a case of a 43 year old female with no known comorbidity presenting with acute onset of severe headache,
bilateral lower extremity weakness and numbness, loss of
consciousness for three days, allegedly resolving after several
days. Physical examination upon admission revealed essentially
normal systemic and neurologic findings.
CT scan
Differentials
Differentials
 Intracranial Hemorrhage (Subarachnoid Hemorrhage)
- Rule In
- Acute onset
- Severe headache
- Focal neurologic deficits
- Loss of consciousness
- Patient’s age
- Patient is hypertensive
- Family history of stroke
- Patient’s diet preferences (increased cholesterol)
- Patient was doing household chores during onset
- Rule Out
- Cannot be ruled out
Differentials
 Ischemic Stroke
 Rule In
 Acute onset
 Focal neurologic deficits
 Patient’s age
 Family history of stroke
- Patient’s diet preferences – fatty, salty and sweet foods
 Rule Out
 Cannot be completely ruled out (without CT Scan)
Differentials
 Brain Tumor
 Rule In
 Headache
 Focal neurologic deficits
 Rule Out
 Onset of symptoms is acute
Differentials
 Brain Abscess
 Rule In
 Headache
 Focal neurologic deficits
 Rule Out
 Onset of symptoms is acute
 No evidence of infection (afebrile, no cough/colds, no previous head
surgery, etc.)
Differentials
 Migraine
 Rule In
 Headache
 Patient’s sex
 Rule Out
 First episode
 No perceived “aura” prior to onset
 Focal neurologic deficits rarely occurs with migraine
Assessment
 Subarachnoid Hemorrhage
Course in the
Wards
Course in the Wards
10/6/09
S> Patient admitted at ACU ER. Patient seen by the treatment officer,
(+) HA, VAS 2/10 fronto-temporal.(-) fever, coughs, dyspnea, chest pains, epigastric pain, urinary or bowel
changes
O> BP: 120/70
HR: 80
RR: 20
E/N systemic PE findings
Neuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerebellar/ meningeal signs
CT scan:
A> SAH
P>Dx: Blood typing, CBC, Blood Chem, CT scan (plain and with contrast)
TX:Tramadol 50mg/cap q8 prn for HA, Captopril 2mg TID, Lactulose 30cc HS
Patient was referred to Neurology
Course in the Wards
10/07/09
S> Seen by the Neurology service.No new symptoms/ complaints, no neurological deficits. (-) headache, () dizziness, (-) nausea, (-) vomiting, (-) nape pain (-) blurring of vision
O> BP: 120/80
HR: 80
RR: 20
E/N systemic PE findings
Neuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerabellar/ meningeal sigins
A> SAH secondary to cerebral aneurysm
P> For repeat 4V angiography
Patient transferred to NSS
WOF: decrease in sensorium, severe headache,seizures, new onset neurological deficits
Course in the Wards
10/09/09
S> Patient admitted at W6B17. (-) headache, (-) dizziness, (-) nausea, (-) vomiting, (-) nape pain. No other
neurologic complaint.
O> BP: 120/70
HR: 80
RR: 20
E/N systemic PE findings
Neuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerebellar/ meningeal signs
A> SAH
P> Tx: Tramadol 50mg/cap was shifted to Etorocoxib 120mg/tab
For 4V angiography
For possible craniotomy, clipping of the aneurysm
Course in the Wards
10/10/09
S> Patient had headache, VAS 5/10 (fronto-temporal), (+) nape pain, (+) dipahoresis, (+) vomiting (3x,
non-bloody, non bilous, non-mucoid, about 3 tablespoons per episode), (+) chest pain, non radiating,
‘described as mabigat’ , (point tenderness)
O> BP: 140/90
HR: 105
RR: 20
Neuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerabellar/ meningeal signs
A> t/c costohondritis r/o ACE
P> for stat ECG
for Na, K, Cl
Encourage deep breathings
Captopril 20mg/tab BID
Etoricoxib 120mg/tab for headache
Referred to Gen MeD
Course in the Wards
10/11/09
S> Patient seen by Gen Med. At that time (-) chest pain, (-) headache,(-) blurring of vision, (-)nape
pain, (-) nausea,
(-)vomiting, (-)fever, (+) palpitations
0> BP 90/60
HR 100
RR 20
E/N systemic PE findings
Neuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerabellar/ meningeal signs
ECG: ST, NA, NSSTTWC
A> SAH
Hypertension most probably secondary (reactive)
Chest pain not anginal
P> Suggest decrease Captopril to ½ tab for BP >160/100
Course in the Wards
10/12/09
S> Patient seen by SAPOD for clearance for 4v angiography and possible clipping of the aneurysm. (-)
chest pain, (-) headache, (-)nape pain, (-) nause, (-)vomiting, (-)fever, (+) palpitations, (-) orthopnea, (-)
PND, (-) exertional dyspnea
O> > BP: 120/70
HR: 80
RR: 20
E/N systemic PE findings
Neuro Exam : intact cranial nerves, (-) sensory and motor deficits, (-) cerabellar/ meningeal signs
A> SAH
Hypertension St. II
P> Shift Captopril to Metoprolol 50mg/tab, ½ tab BID
LABS
 ECG: ST, NA, NSSTTWC
 PT 11.8/11.6/>1.0/ 1.10
APTT/ 35.5/30.9
 Blood Chemis try : FBS: 5.81
BUN 3.34
Crea: 6.4
 Hemoglobin: 123
Hematocrit: 0.38
WBC:5.7
Platelet : 302
Na: 141
K: 3.6
Subarachnoid hemorrhage
Discussion
RELEVANT ANATOMY
saccular aneurysms - bifurcations of vessels of circle of
Willis.
Circle of Willis
• close proximity to ventral surface of diencephalon
• adjacent to optic nerves and tracts.
• important anastomosis for the 4 arteries that supply the brain
- 2 vertebral and the 2 internal carotid arteries
• divided into anterior and posterior sections
Anterior portion of the
circle of Willis
• Consists of:
1. internal carotid
arteries
2. anterior cerebral
artery
3. anterior
communicating
artery
Posterior portion of the
circle of Willis
• consists of:
1. posterior cerebral
arteries
2. posterior
communicating
arteries, paired
Location of aneurysm rupture
anterior circulation - 85% of saccular aneurysms
most common sites of rupture are as follows:
1. internal carotid artery,
including posterior communicating junction (41%)
2. anterior communicating artery/
anterior cerebral artery (34%)
3. middle cerebral artery (20%)
4. vertebral-basilar arteries (4%)
5. other arteries (1%)
Subarachnoid hemorrhage DISCUSSION
DEFINITION:
extravasation of blood into the subarachnoid space between
the pial and arachnoid membranes
detrimental effect on both local and global brain function
and leads to high morbidity and mortality rates.
Subarachnoid hemorrhage DISCUSSION
Subarachnoid hemorrhage DISCUSSION
Subarachnoid hemorrhage:
1. Traumatic: head trauma
2. Non-traumatic (spontaneous):
a. ruptured cerebral aneurysm
b. arteriovenous malformation (AVM)
Subarachnoid hemorrhage DISCUSSION
FREQUENCY
Age
• Incidence increases with age
• peaks at age 50 years
• 80% of SAH cases: 40-65 years
Sex
• women to men ratio (3:2)
• risk of SAH from aneurysmal rupture - maternal deaths in pregnancy
• AVM rupture during pregnancy.
Race
• different ethnic groups develop intracranial aneurysms
Subarachnoid hemorrhage DISCUSSION
ETIOLOGY
Nontraumatic subarachnoid hemorrhage (SAH)
- caused by extravasation of blood from abnormal blood vessels
onto the surface of brain
- result of:
1. aneurysmal ("berry," or saccular)
2. AVM leakage or rupture – 10 %
Subarachnoid hemorrhage DISCUSSION
Less common causes of SAH:
• Fusiform and mycotic aneurysms
• Fibromuscular dysplasia
• Blood dyscrasias
• Moyamoya disease
• Infection
• Neoplasm
• Trauma (fracture at the base of the skull leading to internal
carotid aneurysm)
• Amyloid angiopathy (especially in elderly people)
• Vasculitis
• Idiopathic SAH
Subarachnoid hemorrhage DISCUSSION
Etiology Of Cerebral Aneurysms - unknown
Congenital defects in the muscle and elastic tissue of the
arterial media in the vessels of the circle of Willis
• familial cerebral aneurysm - 10%
• multiple aneurysms in patients with SAH 15%
• congenital diseases
coarctation of the aorta
Marfan syndrome
Ehlers-Danlos syndrome
fibromuscular dysplasia
polycystic kidney disease
Subarachnoid hemorrhage DISCUSSION
Aneurysmal formation - Acquired factors
 Atherosclerosis
 Hypertension
 Hemodynamic stress
Subarachnoid hemorrhage DISCUSSION
RISK FACTORS
 Smoking
 heavy alcohol consumption
 hypertension and SAH – conflicting evidence
hypertension has been identified as a risk factor for aneurysm formation, the
data with respect to rupture are conflicting
hypertensive states (stimulants e.g. cocaine) - promote aneurysm growth and
earlier rupture
Subarachnoid hemorrhage DISCUSSION
The following do not appear to be significant risk factors for
SAH:
• Use of oral contraceptives
• Hormone replacement therapy
• Hypercholesterolemia
• Vigorous physical activity
• The risk of AVM rupture is greater during pregnancy
Subarachnoid hemorrhage DISCUSSION
PATHOPHYSIOLOGY
• Aneurysms - occur at branching sites on large cerebral arteries of circle of Willis.
defects in media of arteries
small outpouchings
↓
expand due to hydrostatic pressure
1. pulsatile blood flow
2. blood turbulence
(greatest at the arterial bifurcations)
↓
mature aneurysm
paucity of media
replaced by connective tissue
diminished or absent elastic lamina
Subarachnoid hemorrhage DISCUSSION
Law of La Place:
‘tension is determined by the radius of the aneurysm and the pressure
gradient across the wall of the aneurysm’
probability of rupture ~ aneurysm wall tension
Subarachnoid hemorrhage DISCUSSION
rate of rupture is directly related to the
size of the aneurysm
< 5 mm diameter - 2% risk of rupture
6-10 mm diameter - 40% risk of rupture
Subarachnoid hemorrhage DISCUSSION
aneurysm ruptures
↓
blood extravasation
(under high arterial pressure)
↓
1. local tissue damage
2. global increase in intracranial pressure (ICP)
3. meningeal irritation
Subarachnoid hemorrhage DISCUSSION
PRESENTATION
signs and symptoms:
subtle prodromal events to
classic presentation of catastrophic headache
clinical history
physical examination
- neurologic examination
Subarachnoid hemorrhage DISCUSSION
Cause of prodromal signs and symptoms:
1. sentinel leaks
2. mass effect of aneurysm expansion
3. emboli
Subarachnoid hemorrhage DISCUSSION
1. Sentinel (‘warning’) leaks
• produce minor blood leakage
• symptoms:
head pain - sudden focal or generalized, severe
nausea, vomiting
photophobia
malaise
neck pain
• not elevated ICP
• not in setting of AVM
Subarachnoid hemorrhage DISCUSSION
2. Mass effect
• characteristic features based upon aneurysm location.
a. Posterior communicating artery/internal carotid artery
Focal, progressive retro-orbital headaches
oculomotor nerve palsy
(Just posterior and superior to the cavernous sinus, the oculomotor nerve crosses the terminal portion of the internal
carotid artery at its junction with the posterior communicating artery.)
b. Middle cerebral artery
Contralateral face or hand paresis
aphasia (left side)
contralateral visual neglect (right side)
c. Anterior communicating artery
Bilateral leg paresis
bilateral Babinski sign
d. Basilar artery apex
Vertical gaze, paresis, and coma
e. Intracranial vertebral artery/posterior inferior cerebellar artery
Vertigo, components of lateral medullary syndrome
Subarachnoid hemorrhage DISCUSSION
3. Emboli:
 transient ischemic attacks from intra-aneurysmal thrombus formation.
 classic symptoms and signs of aneurysmal rupture:
 Headache - sudden onset, severe, ‘worst headache of my life’
 Nausea, vomiting
 meningeal irritation
 nuchal rigidity and pain
 back pain
 bilateral leg pain
 Photophobia and visual changes
 sudden loss of consciousness (LOC)
 Transient or comatose for several days
 Seizures
Subarachnoid hemorrhage DISCUSSION
Physical Examination Findings
normal or consistent with the following:
a. Focal neurologic abnormalities - hemiparesis, aphasia,
hemineglect, cranial nerve palsies, and memory loss
b. Motor neurologic deficits - middle cerebral artery
aneurysms
c. Ophthalmologic examination - subhyaloid retinal
hemorrhages, papilledema
d. Blood pressure elevation
e. Temperature elevation - chemical meningitis from
subarachnoid blood products
f. Tachycardia
Subarachnoid hemorrhage DISCUSSION
CLINICAL GRADING SCALES
• Clinical scales:
1. Hunt and Hess grading system
2. World Federation of Neurological Surgeons
(WFNS) grading system
• Imaging scale:
Fischer scale
CT scan appearance
subarachnoid blood quantification
Subarachnoid hemorrhage DISCUSSION
HUNT AND HESS GRADING SYSTEM
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 hemiparesis
Grade 5
Comatose and/or decerebrate rigidity
Subarachnoid hemorrhage DISCUSSION
WFNS SCALE
Grade 1
Glasgow Coma Score (GCS) of 15, motor deficit absent
Grade 2
GCS of 13-14, motor deficit absent
Grade 3
GCS of 13-14, motor deficit present
Grade 4
GCS of 7-12, motor deficit absent or present
Grade 5
GCS of 3-6, motor deficit absent or present
Subarachnoid hemorrhage DISCUSSION
FISCHER SCALE (CT SCAN APPEARANCE)
Grade 1
No blood detected
Grade 2
Diffuse deposition of subarachnoid blood, no clots, and no layers of blood
greater than 1 mm
Grade 3
Localized clots and/or vertical layers of blood 1 mm or greater in thickness
Grade 4
Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots
are present
Subarachnoid hemorrhage DISCUSSION
Hunt and Hess and WFNS grading systems
- correlation with patient outcome.
Fischer classification
- predict likelihood of symptomatic cerebral vasospasm,
All 3 grading systems are useful in determining the
indications for and timing of surgical management.
Subarachnoid hemorrhage DISCUSSION
‘For an accurate assessment of SAH severity, these grading systems
must be used in concert with the patient's overall general medical
condition and the location and size of the ruptured
aneurysm.’
Management
Work-up
Work-up
 CBC count - For evaluation of possible infection or hematologic





abnormality
Prothrombin time (PT) and activated partial thromboplastin
time (aPTT) - For evaluation of possible coagulopathy
Serum electrolytes - To establish a baseline for detection of future
complications
Blood type and screen - In case intraoperative transfusion is required
or in the setting of massive hemorrhage
Cardiac enzymes - For evaluation of possible myocardial ischemia
Arterial blood gas (ABG) - Assessment is necessary in cases with
pulmonary compromise
Imaging
 CT scan: The diagnosis of SAH usually depends on a
high index of clinical suspicion combined with
radiographic confirmation via CT scan without contrast.
 CT scan has a sensitivity of 98% within the first 12 hours
of the ictus and 93% within 24 hours;
 sensitivity decreases to approximately 80% at 72 hours
and 50% at 1 week.
 CT scan findings are positive in 92% of patients who
have SAH.
Lumbar Puncture
LP should be performed when strong clinical suspicion of SAH
exists with a negative finding on CT scan or when a CT scan
is not available.
 If possible, a CT scan should be performed before LP to
exclude significant intracranial mass effect, elevated ICP,
obstructive hydrocephalus, or obvious intracranial bleed.
 LP findings often are negative within 2 hours of the ictus, and
LP is most sensitive 12 hours after the bleed.
Lumbar Puncture
 LP should not be performed if the CT scan demonstrates an
SAH because of the (small) risk of further intracranial bleeding
associated with a drop in ICP.
 SAH often can be distinguished from traumatic LP by
comparing the red blood cell count of the first and last tubes of
CSF. The RBC count usually will not decrease between the first
and last tubes in the setting of SAH; however, case reports of
this phenomenon do exist.
 The most reliable method of differentiating SAH from a
traumatic tap is to spin down the CSF and examine the
supernatant fluid for the presence of xanthochromia, a pink or
yellow coloration of the CSF supernatant caused by the
breakdown of RBCs and subsequent release of heme pigments.
Cerebral angiography
 Cerebral angiography is particularly useful in cases of diagnostic
uncertainty
 Cerebral angiography can provide the following important
surgical information in the setting of SAH:
 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)
Medical Therapy
Medical therapy
 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.
Medical therapy
Therapeutic goals of subarachnoid hemorrhage:
1. blood pressure control
2. prevention of seizures
3. treatment of nausea
4. management of ICP
5. prevention of vasospasm
6. control of pain
7. maintenance of cerebral perfusion
Medical therapy
 The traditional treatment of ruptured cerebral
aneurysms included strict blood pressure control,
with fluid restriction and antihypertensive
therapy.
 This approach was associated with a high rate of
morbidity and mortality from the ischemic
complications of hypovolemia and hypotension.
Medical 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.
Medical therapy
Calcium channel blocker
 calcium - involved in the generation of the action potential.
calcium channel blockers - inhibit movement of calcium
ions across the cell membrane, depressing both impulse
formation (automaticity) and conduction velocity.
Nimodipine (Nimotop) - 60 mg PO q4h x 21 d
 For improvement of neurological impairments resulting
from spasms following SAH caused by ruptured congenital
intracranial aneurysm in patients who are in good postictal
neurological condition.
Medical therapy
therapeutic interventions for increased ICP include the
following:
• Osmotic agents (eg, mannitol), which can decrease ICP
dramatically (50% after 30 min postadministration)
• Loop diuretics (eg, furosemide) also can decrease ICP
• The use of IV steroids (eg, Decadron) is controversial but is
recommended by some authors.
Prophylaxis and treatment of
complications
Common complications of SAH:
 Rebleeding
 Vasospasm
 Hydrocephalus
 Hyponatremia
 Seizures
 Pulmonary complications
 Cardiac complications
Rebleeding
 Rebleeding is the most dreaded early
complication of SAH.
 The greatest risk of rebleeding occurs within the
first 24 hours of rupture (4.1%).
 The cumulative risk of rebleeding is 19% at 14
days. The overall mortality rate from rebleeding is
reported to be as high as 78%.
Measures to prevent rebleeding
 Bedrest
 Analgesia. Pain is associated with a transient elevation
in blood pressure and increased risk of rebleeding.
 Sedation
 Stool softeners
 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.
Vasospasm
 Cerebral vasospasm, the delayed narrowing of the large capacitance
vessels at the base of the brain
 leading cause of morbidity and mortality in survivors of
nontraumatic SAH.
 Vasospasm is reported to occur in as many as 70% of patients with
SAH and is clinically symptomatic in as many as 30% of patients.
 Most commonly, this occurs 4-14 days after the hemorrhage.
Risk factors for vasospasm
 Larger volumes of blood in the subarachnoid space
 Clinically severe SAH
 Female sex
 Young age
 Smoking
Measures used for prevention of
vasospasm
 Maintenance of normovolemia, normothermia, and normal
oxygenation are paramount to vasospasm prophylaxis.
 Volume status should be monitored closely
 Prophylaxis with oral nimodipine: Calcium channel
blockers have been shown to reduce the incidence of ischemic
neurological deficits

nimodipine has been shown to improve overall outcome within 3
months of aneurysmal SAH
Measures used for prevention of
vasospasm
 Some evidence indicates that subarachnoid clot removal
achieved via intracisternal injections of recombinant
tissue plasminogen activator (rTPA) may dramatically
reduce the risk of vasospasm.
 Aspiration and irrigation of the subarachnoid clot at the time
of aneurysmal clipping associated with a significant risk of
iatrogenic trauma to pial surfaces and small vessels.
Surgical therapy
Surgical Clipping
 introduced by Walter Dandy of the Johns Hopshins Hospital
in 1937.
 It consists of performing a craniotomy, exposing the
aneurysm, and closing the base of the aneurysm with a
clip.
 The aneurysmal neck is obliterated via application of a clip
that occludes blood flow to the aneurysmal dome without
compromising flow to the parent artery.
Surgical Clipping
 Surgical clipping has a lower rate of aneurysm
recurrence after treatment.
 Direct aneurysmal clipping is still considered
first-line treatment in the United States.
 Clips are available in various sizes and shapes.
Endovascular coiling
 Endovascular coiling was introduced by Guido Guglielmi at
UCLA in 1991.
 It consists of passing a catheter into the femoral artery in the
groin, through the aorta, into the brain arteries, and finally
into the aneurysm itself.
 Once the catheter is in the aneurysm, platinum coils are
pushed into the aneurysm and released.
 These coils initiate a clotting or thrombotic reaction
within the aneurysm that, if successful, will eliminate the
aneurysm.
Endovascular coiling
 Guglielmi detachable coil system (GDC) is the
first-line therapy in Europe.
 They are soft, flexible, and can be contoured to the
configuration of the aneurysm. Sizes range from 2-20
mm in diameter and 2-30 cm in length.
 In limited clinical trials, GDCs have been reported to
achieve excellent rates of aneurysmal occlusion
combined with a low complication rate in appropriate
patients.
Surgical clipping vs. Endovascular coiling
 the risks associated with surgical clipping and endovascular
coiling, in terms of stroke or death from the procedure,
are the same .
 The major problem associated with endovascular coiling
is a higher aneurysm recurrence rate.
 Although endovascular coiling is associated with a shorter
recovery period as compared to surgical clipping, it is also
associated with a significantly higher recurrence rate after
treatment.
Other surgical options
 Proximal ligation of the parent artery or trapping of
aneurysms with or without bypass.
 Proximal ligation is effective for giant aneurysms.
 Wrapping or coating of aneurysms may be the only
option in rare cases of dissecting or fusiform aneurysms
Timing of surgical intervention
Advantages of early surgery (0-3 d) :
 Prevention of rebleeding, which is associated with a high




mortality rate
Possible prophylaxis against vasospasm by removal of
subarachnoid clot
Prevention and treatment of ischemic complications
Prevention of medical complications
Decreased duration of hospitalization
Timing of surgical intervention
Disadvantages of early surgery for SAH :
 Technical problems associated with edematous brain
tissue
 High risk of intraoperative rupture of
fragile aneurysm
 Higher surgical morbidity and mortality rates
Timing of surgical intervention
Advantages of delayed surgery for SAH (>10 d
posthemorrhage)
 Brain tissue is less edematous.
 Lower risk of intraoperative aneurysm rupture
 Lower surgical morbidity and mortality rates
 Flexibility of scheduling
The disadvantages of delayed surgery:
 Increased rate of morbidity and mortality due to rebleeding
 Technical difficulties due to adhesions around the aneurysm
Complications of surgical clipping
 Hemorrhagic complications
 Ischemic complications
 Damage to parent artery or perforating arteries
 Acute or delayed neurological deficits from iatrogenic
trauma
 Meningitis
 Cellulitis and wound infection
 Nonspecific postsurgical syndrome similar to
postconcussive syndrome
Common complications of
endovascular therapy
 Aneurysm rupture (GDCs, balloons)
 Thromboembolism (GDCs) with acute or delayed
neurologic deficit
 Balloon rupture or deflation
Prognosis
 Despite advances in medical and surgical therapy, the mortality
rate for aneurysmal SAH remains 50% at 1 year.
 Survival is inversely proportional to SAH grade upon
presentation.
 Hunt and Hess Grading and Survival Rate
Grade 1 – 70%
Grade 2 – 60%
Grade 3 – 50%
Grade 4 – 20%
Grade 5 – 10%
Prognosis
 Approximately 25% of survivors have persistent
neurologic deficits.
 Most survivors have either a transient or a permanent
cognitive deficit.
 Mortality and morbidity are influenced by:
magnitude of the bleed
age of the patient
co-morbid conditions
medical complications.
Sentinel Headache and the Risk of
Rebleeding After Aneurysmal
Subarachnoid Hemorrhage
Stroke, Journal of the American Heart
Association
(Sep 28, 2008)
INTRODUCTION
 The presence of a severe, sudden headache, often referred to
as a warning leak, minor leak, or sentinel headache (SH),
during the days or weeks before subarachnoid hemorrhage
(SAH) has been reported in 15% to 60% of all patients
eventually admitted with an SAH
 Pathophysiology of an SH: changes in the wall of the
aneurysm without rupture or rupture of an intracranial
aneurysm causing minor SAH
INTRODUCTION
 The current mainstay of treatment of acute SAH consists of
prevention of another bleed, because the rebleeding rate and
associated mortality are exceedingly high
 Most protocols favor early treatment in 48 to 72 hours after
the ictus
INTRODUCTION
 Because the rebleeding rate may be highest immediately after
SAH, some investigators have suggested a general policy of
“ultraearly” surgery, which is unlikely to gain wide
acceptance, because it does not provide treatment with the
best team under the optimum circumstances for many
patients
INTRODUCTION
 It would be of important clinical value to identify a
subgroup of patients that is more likely than others
to experience rebleeding
 The hypothesis of this study was that there is a causal relation
between the aneurysm or SAH and the clinical sign of an SH;
ie, patients with an SH may have more fragile aneurysms
INTRODUCTION
 This hypothesis was prospectively tested by investigating
whether patients who presented with an SH before the index
SAH indeed had a higher rate of rebleeding compared with
those without an SH
SUBJECTS AND METHODS
Patient Population
 237 consecutive patients with SAH proven by computed
tomography (CT) or lumbar puncture
 Patient characteristics, treatment, radiological features, the
presence of an SH, and rebleeding, was prospectively entered
in an SPSS database
SUBJECTS AND METHODS
General Patient Management
 Early surgery strategy (24 to 48 hours) was done in patients
of all clinical grades unless the patients were
hemodynamically unstable or moribund
 Routine surveillance included daily transcranial Doppler
measurements and, in selected cases, multimodal monitoring
of brain tissue O2, regional cerebral blood flow, and
interstitial metabolites
SUBJECTS AND METHODS
General Patient Management
 All patients received Nimodipine from the day of admission
 Fludrocortisone was administered as an adjunct in case of
hyponatremia
 Desmopressin was used to control excessive diuresis
 Outcome was assessed according to a modified Rankin Scale
(mRS) after 6 months
SUBJECTS AND METHODS
Sentinel Headache
 Thorough history was taken of patients, relatives,
accompanying persons, general practitioners, and emergency
or admitting doctors
 Inquired about a sudden, severe headache of unknown
character and intensity lasting at least 1 hour in the last 4
weeks before the index SAH that had never been experienced
before
 There had to have been an improvement before the index
SAH or another deterioration that led to a diagnosis of SAH
SUBJECTS AND METHODS
Rebleeding
 Only included CT-proven episodes of rebleeding
(neuroradiologist was blinded to a history of SH)
 Cases with a high clinical suspicion of rebleeding but without
confirmation by at least 2 subsequent CT scans were not
included
SUBJECTS AND METHODS
Rebleeding
 All patients underwent CT scanning after
clipping/intervention within 48 hours as well as at day 14 or
at discharge
 Rebleeding after aneurysm obliteration was not included
SUBJECTS AND METHODS
Data Analysis
 To test for an association with rebleeding, categorical
variables were tested with Fisher exact test or x2 test
 Continuous variables were subjected to the Mann-Whitney U
test or a t-test
 Binary logistic-regression model for the prediction of
rebleeding was used to find the most important baseline
predictors
 Results with P<0.05 were considered statistically significant
RESULTS
Patient Population
RESULTS
Rebleeding
 Overall rebleeding rate - 9.7% (23 of 237)
 SH before the index SAH - 17.3% (41 of 237)
 Univariate analysis revealed that the presence of an SH,
maximum aneurysm size, and the number of aneurysms an
individual patient presented with were significantly
associated with rebleeding
RESULTS
Rebleeding
 Trend for an association with less rebleeding for aneurysms
of the anterior circulation
 No association between the frequency of rebleeding and
patient age, sex, smoking habits, or findings on the initial CT
scan
RESULTS
Rebleeding
 The odds of eventually experiencing a rebleeding
episode for a patient with an SH compared with a
patient without an SH was 13.6 (P<0.0001) in the
univariate model
RESULTS
Rebleeding
 Relative risk was 9.0
 Sensitivity was 65.2%
 Specificity 87.9%
 Positive predictive value was 36.6%
 Negative predictive value was 95.9%
RESULTS
Rebleeding
 In a binary logistic-regression model,the presence of an SH
remained a very statistically significant and independent
predictor of rebleeding after controlling for age, aneurysm
size, number of aneurysms, and the time at risk
RESULTS
Outcome
 Overall outcome at 6 months was available for 212 patients
 Rebleeding significantly increased the odds of death, reduced
the odds of survival with good outcome, and reduced the
odds of survival with functional independence
RESULTS
Outcome
CONCLUSION
 The presence of an SH is strongly related to an increased
frequency of rebleeding before aneurysm obliteration
 Therefore, a history of SH might be used to identify a
subgroup of patients with a high risk for rebleeding and who
could benefit from ultraearly aneurysm obliteration or
immediate clot-stabilizing drug treatment
Thank you vey much!!!!!
Block_U_lala