Severe headache in a 54 year-old man
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Severe headache in a 54 year-old man
Coruña | Datukon | de Castro | de la LlanaApril 30, 2010 | Block G
NSS
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CLINICAL HISTORY
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General Data• I.B.• 54/M• Right-handed• Farmer• Abra
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Chief Complaint• Severe headache
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History of Present Illness• 1 month PTA (3/14/2010)– (+) dizziness, (+) syncope– (+) severe headache – piercing, graded 10/10 – (+) left-sided weakness– Brought to Abra Provincial Hospital treated as a
case of CVD– CT scan done in Vigan ten days post-event
revealed subarachnoid hemorrhage
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History of Present Illness• 1 month PTA– (-) sensorial changes– (+) minimal nape pain– (-) facial asymmetry– Advised transfer to PGH for further evaluation and
surgery– Opted not to consult due to financial constraints
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History of Present Illness• 2 weeks PTA– Patient was discharged asymptomatic
• 1 week PTA– (+) headache - sudden onset, persistent, no noted
aggravating or relieving factors, piercing, (-) radiations, graded 10/10, constant
– (-) medications taken
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History of Present Illness• 1 week PTA– Consulted again in Abra Provincial Hospital
admitted for three days given unrecalled medications with some pain relief
– Opted to take physician’s advice to seek consult in our institution
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Review of Systems• (-) fever• (-) cough• (-) colds• (-) dyspnea• (-) abdominal pain• (-) bowel changes• (-) dysuria
• (-) jaundice• (-) weight loss• (-) tinnitus• (-) blurring of vision• (-) rash• (-) orthopnea• (-) easy fatigability
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Past Medical History• (-) HPN but with note of occasionally elevated
BP on casual checking, no consults done• (-) DM, BA, PTB• (-) previous surgeries• (-) known allergies to food and medications
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Family Medical History• (+) HPN – siblings• (-) DM, BA, PTB, CA• (-) CVD
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Personal/Social History• (-) smoking• (-) alcoholic beverage consumption• denies illicit drug use• Married, with 3 biological children and 6
stepchildren• Farmer
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PHYSICAL EXAMINATION
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Physical Examination• Conscious, coherent, not in distress• VS: BP 130/80 HR 100 RR 20 T 36.7oC• HEENT: pink conjunctivae, anicteric sclerae, (-)
neck vein engorgement, (-) cervical lymphadenopathy, (-) masses
• Chest/Lungs: equal chest expansion, clear breath sounds, (-) rales, (-) wheezes
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Physical Examination• CVS: (-) heaves, (-) thrills, distinct heart
sounds, normal rate, regular rhythm, (-) murmurs
• Abdomen: flat, normoactive bowel sounds, soft, nontender, (-) masses, liver edge not palpable
• Extremities: pink nailbeds, (-) cyanosis, (-) edema, full & equal pulses
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Neurologic Examination• Awake, coherent, oriented to three spheres• GCS 15 (E4V5M6) • Cranial Nerves
I – grossly normalII, III – pupils 3mm briskly reactive to lightIII, IV, VI – full, equal EOMsV – intact sensation at V1-3
V, VII - brisk corneal reflexesVII – shallow R nasolabial fold
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Neurologic Examination• Cranial Nerves
VIII – intact gross hearingIX, X – intact gag, uvula midlineXI – good shoulder shrugXII – tongue midline
• Motor: good muscle tone, MMT 5/5 on all extremities
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Neurologic Examination• Sensory: 100% on all extremities• DTR’s ++, (-) Babinski, (-) clonus• Meningeals: supple neck, (-) Kernig’s sign, (-)
Brudzinski’s sign
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Summary• 54 y/o non-hypertensive male• Apparently well until he presented with
sudden-onset headache and left-sided weakness
• Initially managed as a case of CVD, but with findings of subarachnoid hemorrhage on CT scan done 10 days post event
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Summary• Seen in our institution 39 days post-ictus• With essentially normal physical examination
findings except right central facial nerve palsy
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ASSESSMENT
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Subarachnoid hemorrhage probably secondary to ruptured aneurysm, Grade 1
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DISCUSSION
Subarachnoid hemorrhageDifferential DiagnosesDiagnosticsManagementOutcome
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Subarachnoid hemorrhage• Extravasation of blood into the subarachnoid
space between the pial and arachnoid membranes
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Etiologies• Trauma– MOST COMMON cause of SAH
• Spontaneous– Ruptured aneurysms
(75-80%)– Cerebral AVMs– CNS vasculitides– Cerebral artery
dissection– Coagulation disorders– Dural sinus thrombosis– No cause determined
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Risk Factors• Hypertension• OCPs• Substance abuse—cigarette smoking, cocaine
abuse, alcohol consumption• Diurnal variation in BP• Pregnancy and parturition• During LT or cerebral angiography in those with
aneurysms• Advancing age
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Cerebral AneurysmsCerebral vs Extracranial blood vessels• Less elasticity of tunica media and adventitia• Tunica media has less muscle• Adventitia is thinner• More prominent internal elastic lamina• Subarachnoid space has very little supportive
tissue
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Cerebral Aneurysms• 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
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Cerebral AneurysmsEtiologies• Congenital (Medial gap: defect in muscular
layer of arterial wall)• Atherosclerotic or hypertensive• Embolic (atrial myxoma)• Infectious (mycotic aneurysms)• Traumatic• Associated with other conditions
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Cerebral AneurysmsLOCATION• Saccular aneurysms (berry aneurysms)– Located on major arteries at the apex of branch
points (site of maximum hemodynamic stress on a vessel)
• Fusiform aneurysms– More common in the vertebrobasilar system
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Cerebral Aneurysms• Saccular aneurysms location– 85-95% in carotid system, with the ff most
common locations• ACoA: 30%• P-comm: 25%• MCA: 20%
– 5-15% in the posterior circulation (vertebro-basilar)
– 20-30% would have multiple aneurysms
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Clinical Features: SymptomsMAJOR RUPTURE IS THE MOST FREQUENT PRESENTATION• Headache– Most common, present in 97% of cases– “Worst headache of my life”– Severe and sudden
• Vomiting• Syncope• Photophobia• Neck pain• Focal cranial nerve deficits (diplopia, ptosis)
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Clinical Features: Signs• (+) Kernig’s or Brudzinksi’s• Coma
– Increased ICP– Damage to brain tissue– Hydrocephalus– Diffuse ischemia– Seizure– Low blood flow
• Ocular hemorrhage– Due to compression of the central retinal vein and the
retinochoroidal anastomoses by elevated CSF pressure causing venoud HPN and disruption of retinal veins
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Aneurysmal Rupture• The probability of rupture is related to the
tension on the aneurysm wall• Law of La Place: tension is determined by the
radius of the aneurysm and the pressure gradient across the wall of the aneurysm
• The rate of rupture is directly related to the size of the aneurysm– < 5 mm: 2% risk of rupture– 6-10 mm: 40% have already ruptured upon diagnosis
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Aneurysmal Rupture• Blood extravasates under arterial pressure
into the subarachnoid space and quickly spreads through the CSF around the brain and spinal cord– Direct damage to local tissues– Increased ICP– Meningeal irritation
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Grading SAHHunt and Hess Classification of SAH
Grade Description
1 Asymptomatic or mild H/A and slight nuchal rigidity
2 CN palsy (III, VI), moderate to severe H/A, nuchal rigidity
3 Mild focal deficit, lethargy, confusion
4 Stupor, moderate to severe hemiparesis, early decerebrate rigidity
5 Deep coma, decerebrate rigidity, moribund appearance
Add one grade for serious systemic disease (HPN, DM, severe atherosclerosis, COPD), or severe vasospasm on arteriography.
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Grading SAH• Grades 1 & 2: operated ASAP as soon as an
aneurysm is diagnosed• Grade > 3 managed until condition improved
to grade 2 or 1• Exception: life threatening hematoma or
multiple bleeds (operated on regardless of grade)
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Grading SAHMORTALITY• Admission Grade 1 or 2: 20%• OR Grade 1 or 2: 14%• Rebleed: major cause of death for Grade 1 or
2• Signs of meningeal irritation increases surgical
risk
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Grading SAHWFNS SAH Grade
WFNSGrade
GCS Score Major Focal Deficit
0**1 15 -2 13-14 -3 13-14 +4 7-12 + or -5 3-6 + or -
*aphasia, hemiparesis or hemiplegia** intact anseurysm
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Grading SAHFischer Scale
(CT scan appearance)Grade Description
1 No blood detected2 Diffuse deposition of subarachnoid blood, no clots, and
no layers of blood greater than 1 mm3 Localized clots and/or vertical layers of blood 1 mm or
greater in thickness4 Diffuse or no subarachnoid blood, but intracerebral or
intraventricular clots are present
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SAH Grading• The Hunt and Hess and the WFNS grading
systems correlate well with patient outcome• The Fischer classification predicts the likelihood
of symptomatic cerebral vasospasm, one of the most feared complications of SAH
• All 3 grading systems are useful in determining the indications for and timing of surgical management
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DIFFERENTIAL DIAGNOSES
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Differential Diagnoses• Stroke• Aphasia• First Seizure in Adulthood• AVMs• Frontal Lobe Syndromes• Aseptic Meningitis• Hydrocephalus• Basilar Artery Thrombosis
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Differential Diagnoses• Intracranial Hemorrhage• Cerebellar Hemorrhage• Cerebral Aneurysms• Cerebral Venous Thrombosis• Meningococcal Meningitis• Epidural Hematoma• Migraine Headache
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DIAGNOSTICS
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Workup• Serum Chemistry Panel• CBC• PT PTT• Blood Typing/Screening tests• Imaging – CT without contrast is the most sensitive imaging
study in subarachnoid hemorrhage.
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Workup: CT Scan• Findings may be negative in 10-15% of
patients with SAH• Maximum sensitivity is within 24 hours post-
injury• Sensitivity is 80% at 3 days, 50% at 1 week
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Workup: CT Scan• Look for evidence of hydrocephalus– trapped temporal horns and "Mickey Mouse"
appearance of ventricular system• Intraparenchymal clot, intraventricular
hematoma, and interhemispheric hematoma• Degree and location of SAH are significant
prognostic factors.
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Workup: Cerebral Angiography• To assess the vascular anatomy• To determine site of bleed• To document presence or absence of other
aneurysms (about 20% have multiple aneurysms)
• For operative planning
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Workup: Cerebral Angiography• Negative angiographic findings do not rule out
aneurysm. • ~ 10-20% of patients with clinically diagnosed
SAH (CT and/or lumbar puncture) have negative angiographic findings.
• Repeat angiogram usually required in 10-21 days
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Four-Vessel Angiogram
• The gold standard for evaluation of cerebral aneurysms
• Four vessels: – R and L verterbral arteries– R and L carotid arteries
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Four-Vessel Angiogram
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Workup• MRI is inferior to CT in an acute setting to
detect SAH.• MR angiography (MRA) is less sensitive than
cerebral angiography to detect small aneurysms.
• CT angiography is beneficial in very unstable patients who cannot undergo angiography or in emergent settings prior to operative intervention for clot evacuation.
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Workup• ECG– Nonspecific ST and T changes, prolongation of QRS
segments or QT intervals, deeply inverted T waves, and U waves sometimes are seen in SAH
– Patients with SAH can have myocardial ischemia due to the increased level of circulating catecholamines or to autonomic stimulation from the brain.
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Workup• Lumbar puncture– Performed if CT scan shows no subarachnoid
hemorrhage presence of RBCs and xanthochromia
– Most sensitive 12 hours after onset of symptoms– Findings can be negative in ~10-15% of patients
with SAH.– Patients with negative CT and LP findings have a
favorable prognosis.
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MANAGEMENT
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General Symptomatic Treatment• Absolute bed rest in quiet, comfortable
environment• Cardiac monitoring and frequent assessment
of neuro-vital signs• Soft diet for alert patients, nasogastric-tube
(NGT) feedings if with impaired consciousness• Analgesics for headache. Avoid aspirin.
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General Symptomatic Treatment• Paracetamol and cooling blankets• Maintenance of euglycemia• Sedatives• Antiemetics• Stool softeners
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Early Specific Treatment• Nimodipine– Significant reduction in poor outcomes with
calcium antagonists.• Evidence rests mainly on one large trial with oral
nimodipine. – Uncertain whether acts through neuroprotection
or through reduction of the frequency of vasospasm, or both.
– 60 mg every 4 hours x 3 weeks
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Early Specific Treatment• Anticonvulsants– Short-term anticonvulsants recommended for
patients with documented seizures in the acute phase.
– In patients with significant cortical damage, thick cisternal clot, parenchymal hemorrhage, or those in coma
– Phenytoin 15 mg/kg LD then 3-5 mg/kg/day (100mg TID) in divided doses
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Early Specific Treatment• Steroids– Dexamethasone may help with headache and
nape pain.– Effect on edema controversial– Corticosteroids have no proven role and are not
recommended for use in SAH.
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Early Specific Treatment• Antifibrinolytic agents are NOT
recommended.– Reduce risk of rebleeding, BUT…– Associated with higher rate of cerebral ischemia
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Early Specific Treatment• Manage increased ICP• BP control– Best antihypertensive agent unsettled– IV nicardipine– Target SBP<150 mmHg in the pre-operative phase
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Management of Vasospasm
• Monitoring– Serial transcranial Doppler (TCD) recommended
for diagnosis and monitoring of vasospasm
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Management of Vasospasm
• Maintenance of euvolemia– Evidence on use of blood volume expansion alone
or in combination with induced hypertension and hemodilution (triple H therapy) in the prophylaxis and management of secondary ischemia (vasospasm) following aneurysmal SAH lacking
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Management of Vasospasm
• Endovascular angioplasty (chemical +/- mechanical) – Transluminal balloon angioplasty– Early intervention (before irreversible infarction
signs are noted)• CCB may provide neuroprotection• Magnesium sulfate and statins under
investigation
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Management• Main goal: excluding the aneurysm from the
circulation– “Nonsurgical” / endovascular: trapping (distal &
proximal arterial interruption, proximal ligation for giant aneurysms, endovascular coiling, balloon embolization
– Surgical: clipping (“gold standard”), wrapping or coating the aneurysm
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Timing of Surgery• Early surgery - performed within 72 hours
from ictus– Eliminates rebleeding risk if successful– Facilitates treatment of vasospasm– Lower mortality (but higher operative mortality)
• Late surgery - performed more than 3 days from ictus
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Timing of Surgery• Early, immediate surgery recommended for
good to moderate grade (Hunt and Hess I-III) aneurysmal SAH patients to minimize chance of devastating rebleed
• For poor grade patients (Grade IV-V), early surgery is recommended in the presence of:– Hematoma– Hydrocephalus
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Timing of Surgery• Surgery may be delayed in the presence of:– Ischemia or infarction– Severe angiographic vasospasm– Casted ventricles– Diffuse SAH (Fisher Grade III) Complex aneurysm
on angiography• Maximum cut-off age for early surgical
management (for the elderly) not recommended in the absence of organ failure
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Coiling• Can be performed early in both good- and
poor-grade patients.• Reduces rebleed rate for poor-grade patients
who would otherwise be treated conservatively.
• Vasospasm is not a contraindication and can be dealt with endovascularly during coiling.
• Can be performed under local anesthesia
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Where to Admit• Stroke Unit or Intensive Care Unit• In the absence of an ASU/ICU, may place
patient is a quiet, regular room with very close monitoring.
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Rehabilitation• Supportive rehabilitation done initially in the
pre-operative phase• Early rehabilitation recommended for all SAH
patients in postoperative period
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Outcome of Aneurysmal SAH• 10-15% die before reaching medical care• 45% overall mortality rate• NO SURGERY: Rebleeding is the major cause of
M&M in 15%• SURGERY: Vasospasm kills 7%• 66% who underwent clipping never return to
the same quality of life
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COURSE IN THE WARDS
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Course in the Wards
HD 1
•D39 post ictus•Admitted to the NSSCU•Labs: CBC, BT, PT/PTT, Na, K, Ca, Cl, BUN, Crea, FBS, CXR PA, 12L ECG, U/A, CT scan•Meds:•Amlodipine 5mg, 1 tab HS•Phenytoin 100mg/tab 1 tab q8•Simvastatin 20mg HS•Tramadol 50mg q8•Lactulose 30cc HS
HD 2
•D40 post ictus•Referred to Interventional Radiology for 4V angiography•Referred to SAPOD for clearance
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Laboratory Results• Blood Type: A+• CBC– 04/23/10: Hgb 163, Hct 0.458, WBC 5.8, Plt 266, L
0.615, N 0.263– 04/27/10: Hgb 115, Hct 0.321, WBC 9.41, Plt 248,
L 0.878, N 0.079
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Laboratory Results• PT/ PTT (04/23/10)– PT: 11.5/10.5/>1.0/1.01– aPTT: 34.7/34.4
• Blood Chemistry– 04/23/10: Glu 6.01, BUN 11.58, Crea 69, Na 132, K
3.7, Cl 90– 04/26/10: BUN 3.99, Crea 52, Na 196, K 3.4, Cl 112
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Laboratory Results• U/A– 04/24/10: yellow, turbid, pH 8.0, Sp Gr 1.010, CHO
(-), CHON (-), RBC 9, WBC 2, EC 2, Cast 0, Crystals 0, Bac 17
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Course in the Wards
HD 3
• D41 post ictus• E4V5M6• Scheduled for four-vessel
angiogram
HD 4
• D42 post ictus• s/p 4V angiogram• Phenytoin discontinued
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Patient’s 4VA Result• R transfemoral, B ICA, and L vertebral
angiograms were done using non-ionic contrast media (Ultravist – Lopromide)
• Saccular aneurym, L ACA – Acomm junction site, with slight vasospasm
• Aplastic A1 segment, R ACA, Patent Acomm
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Course in the Wards
HD 5
• D43 post-ictus• s/p clipping of aneurysm tolerated procedure well
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Course in the Wards• Presently on 8th hospital day• No subjective complaints• No neurologic deficits noted