GRANDROUNDS

Daryl Ann U. Baclay-Valdehuesa, M.D.

 General Data
• P. S.
• 57 year old
• Male
• Filipino
• Lupa, Sta. Barbara, Iloilo
 OBJECTIVES
• To present a case of Top of the
Basilar Syndrome.
• To present its clinical symptoms,
management and prognosis.
• To present its incidence in the
local setting.
Chief Complaint

Decreased in Sensorium
 History of Present
Illness
(+) Fever (+) Flank Pain
3 daysPTA (+) Cough
sought consult –
given unrecalled meds

ADMITTED
 History of Present
Illness

2 Hrs PTA
(+) Snoring
Unresponsive

ADMITTED
 Past Medical History
• Known Hypertensive
– Metoprolol – poorly compliant
• Non diabetic, Non asthmatic
• No known food or drug allergy
• Previous Hospitalization for
Pneumonia
 Personal History
• Smoker: 20 pack years
• Occasional Alcoholic Beverage
Drinker
• No known food or drug allergy
• Unemployed
 Family History
• Father – hypertensive
• Mother – diabetic
Physical Examination
• Unconscious, afebrile, not in
respiratory distress
• Vital Signs:
• Anicteric sclerae, pinkish
conjunctivae
• No neck vein engorgement, no
cervical lymphadenopathy
Physical Examination
• Symmetrical chest expansion,
harsh breath sounds, no wheeze,
no rales
• Adynamic precordium, PMI at 5th
ICS anterior axillary line, no
heaves, no thrills, normal rate,
regular rhythm, no murmur
• Flat abdomen, normoactive
bowel sounds, no mass palpated
• No bipedal edema, full pulses
Physical Examination
• NEUROLOGIC EXAMS
– GCS 6 (M4V1E1)
– Isocoric pupils equally reactive to
light and accomodation
– (+) Corneal reflex, OU
– No facial assymmetry
– No gag reflex
– No nystagmus, no Doll’s eye
Physical Examination

0/5 0/5
++ ++

++ ++

0/5 0/5 ++ ++
 ADMITTING
IMPRESSION
• T/C Cerebrovascular Disease,
prob Brainstem Infarct
• T/C Septic Encephalopathy sec
to Pneumonia
• Community Acquired
Pneumonia- Moderate Risk
• Hypertensive Cardiovascular
Disease
 At the ER
• CBG – 103mg%
• Venoclysis started : PNSS 1L x
80 cc/hr
• #ABG
• Intubation done
• Hook to mechanical ventilator
 At the ER
• Laboratories Requested
12 leads ECG
CBC, platelet count, CT, BT,
Protime
Na+, K+, creatinine, SGPT, uric
acid
Blood typing, Rh typing
ETA G/S, C/S, KOH
Chest x-ray PA
Urinalysis
 At the ER
• Medications
Citicholine 1 gm IVTT stat dose then
q12H
Tranexamic acid 500mg IVTT q 8H
Piperacillin-Tazobactam 4.5gm IV ANST
as loading dose then 2.25mg IVTT q
8H.
In line nebulization with Salbutmol 1
nebule q 8H
Ambroxol 1 amp IVTT q 8H
Ranitidine 50mg IVTT q8H
Lactulose 300cc OD at HS
 2 hours after
admission
• Problem : (+) Fever
• Temp : 38 C- 38.4 C
• Plan : Paracetamol 300mg
IVTT given then q4H
RTC
 3 hours after
• Problem
admission
: (+) Fever
• GCS 6 (m4v1e1) T: 38 C- 39 C
• (+) pinpoint pupils bilateral
• (-) corneal reflex, OU
• (+) Babinski reflex bilateral
• Cranial CT scan
• Referred to a neurologist
• Mannitol 150cc IV bolus given
then 100 cc q 8H
• Vitamin K 1 amp IV q 8H started
 3 hours after
admission
• A/I : Top of the Basilar Syndrome
P : Clopidogrel 75 mg/tab i tab OD
: Aspirin 80mg/tab i tab OD
Ideally for Intraarterial
Thrombolytics
Folks opted for no resuscitation
 10 hours after
admission
• GCS3 (m1v1e1)
• (-) Corneal reflex, OU
• T : >42 C
• Pronounced dead after 10 hrs and
30 minutes hospital stay
DISCUSSION
ANATOMY and PHYSIOLOGY
• BASILAR ARTERY
– Most important artery in the
posterior circulation
– Formed at the pontomedullary
junction by the confluence of both
vertebral arteries.
– Lies on the ventral surface of the
pons
Circle of Willis
ANATOMY and PHYSIOLOGY
• BASILAR ARTERY

– Branches
• Anterior Inferior Cerebellar Artery
• Posterior Cerebral Artery
• Superior Cerebellar Arteries
Circle of Willis
ANATOMY and PHYSIOLOGY
• BASILAR ARTERY
• Anterior Inferior Cerebellar Artery
– Lateral pontine tegmentum
– Brachium pontis or middle cerebellar
peduncle
– Flocculus, anterior cerebellum
• Posterior Cerebral Artery
– Terminal branch
– Midbrain, thalamus, medial aspect of the
temporal and occipital lobes
• Superior Cerebellar Arteries
– Lateral aspect of the pons and midbrain
– Superior surface of the cerebellum
Circle of Willis
TOP of the BASILAR SYNDROME

• Normally, blood flows in an

anterograde fashion from the
vertebral arteries to the basilar
artery up to its terminal
branches
ANATOMY and PHYSIOLOGY

• Normally, blood flows in an

anterograde fashion from the
vertebral arteries to the basilar
artery up to its terminal
branches
Circle of Willis
 III

IV

VI
VII

VII
HYPOTHALAMUS
Basilar Artery Stroke: Historical
Note
• 1868 – 1st clinicopathologic report of basilar
artery occlusion by Hayem
• 1882 – Leyden presented that patients with
sudden onset of bulbar signs,and were
presumed to have basilar thrombosis
• 1946 – Kubik & Adams’ classic report on
Basilar Artery Occlusion
• Early loss of consciousness
• Common bilateral involvement
• Combinations of pupillary disturbance, ocular and
other cranial nerve palsies, dysarthria, extensor
plantar reflexes,hemiplegia or quadriplegia and
often marked remission of symptoms.
Basilar Artery Stroke: Historical
Note

• 1980 – Caplan described the “

Top of the Basilar Syndrome”
which is the embolic occlusion of
the distal basilar artery
producing ischemia of the rostral
brainstem and the posterior
cerebral territories.
Top of the Basilar Syndrome
• Race
– African-American, Asian – more frequent
• Sex
– Male to Female Ratio: 2:1
• Age
– Most prevalent in the 6th and 7th decade
– Occlusion of the Distal Basilar Artery is
usually secondary to embolism – 4th
decade
– Women are typically older than men
Top of the Basilar Syndrome
• History
– Stuttering or progressive course of
symptoms or TIAs in the
vertebrobasilar territory is seen.

– 50% of patients- (+) TIAs or waxing

and waning of course over several
days to weeks prior to occlusion.
Top of the Basilar Syndrome
• History
– Heralding symptoms
• Motor deficits
(hemiparesis/tetraparesis or facial
paresis) – 40-67%
• Dysarthria and speech impairment -30
– 63%
• Vertigo, nausea or vomiting – 54 –
73%
• Headache – 40- 42%
• Visual disturbances – 21 – 33%
• Altered consciousness – 17 – 33%
Basilar Artery Occlusion
• Based on the temporal profile, may
manifest in 3 different ways:
1. Sudden onset of severe motor and
bulbar symptoms with reduced
consciousness.
2. Gradual or stuttering course of
posterior circulation symptoms that
finally become progressively disabling
or reduce consciousness
3. Prodromal symptoms including double
vision, dysarthria, vertigo and
paresthesia
Basilar Artery Occlusion

• Infrequent and catastrophic disease

• Gravest form of posterior circulation
strokes that account for about 20%
of ischemic strokes.
• Mortality : 85 to 85%
Basilar Artery Occlusion
• Locked-In-Syndrome
– Infarction of the basis pontis
secondary to occlusive disease of
the proximal and middle
segments of the basilar artery ->
QUADRIPLEGIA
– (+) Spared level of consciousness,
preserved vertical eye
movements and blinking
Basilar Artery Occlusion
• Top-of-the-Basilar Syndrome
– Manifestation of the upper
brainstem and diencephalic
ischemia.
– Occlusion of the rostral basilar
artery usually by an embolus.
– (+) changes in level of
consciousness,(+) 3rd nerve palsy
and pupillary abnormalities
 Laboratory Studies
• CBC
• Electrolytes
• BUN
• Creatinine
• Protime with INR and APTT
• Lipid profile.
 Imaging Studies
• CT-scan
– Sensitivity of nearly 95% for
identifying hemorrhage
– Low sensitivity for early ischemia
• MRI and MRA
– Are more sensitive
• Transcranial Doppler
– 72% sensitivity and 94%
specificity in patients with basilar
artery disease
 Other Tests
• Electrocardiography
– The prevalence of coronary disease is high
in patients with cerebrovascular disease.
– Of patients with acute stroke,5-20% have
an arrhythmia.
– 2-3% have a myocardial infarction.
– The presence of arrhythmias has an
impact on the long term management plan
for stroke prevention.
• Echocardiography
 Other Tests
• Catheter angiography
– Done to
• Establish the type of vascular lesion and
the mechanism of the stroke and, if
early enough.
• Establish if acute intervention is needed
to achieve recanalization.
Neuroprotection
Neuroprotection
Neuroprotection
Neuroprotection
Neuroprotectants
 Hemodynamic
Management
• Goal is to minimize ischemic
injury
• Cerebral ischemia results in
impaired autoregulation.
• MAP is critical in maintaining
cerebral blood flow.
• Treat if SBP is >220mmHg and
DBP is > 120 mmHg.
 Hemodynamic
Management
• Hypertension should not be
treated unless the patient has
evidence of acute end organ
damage such as:
– Hypertensive encephalopathy
– Unstable Angina
– Acute MI
– Heart Failure
– Acute Renal Failure
 Hemodynamic
Management
• Preferred anti-hypertensive
agents are Nicardepine and
Labetalol.
• Blood pressure treatment should
be considered when thrombolytic
therapy is to be administered
with target BP of DBP < 110
mmHg and SBP at less than 185
mmHg.
 Hemodynamic
Management
• Hypotension
– Maintain intravascular volume by
administering isotonic solutions.
– Use vasopressors if MAP continues
to be low.
– Vasopressors such as dopamine,
dobutamine or phenylephrine
should be used.
 Respiratory
Management
• Early assessment and
management of the airways is
vital, given the frequent
involvement of lower cranial
nerves and impairment of
consciousness in patients with
brainstem ischemia.
• Endotracheal intubation is
recommended in patients with a
decreased level of consciousness
 Thrombolysis
• Tissue Plasminogen activator
(tPA) is the only pharmaceutical
agent approved for treatment of
acute ischemic stroke within the
first 3 hours of onset.
• NINDS study revealed that there
is no statistically significant
difference in 3-month mortality
between the treatment group and
placebo group.
 Intravenous
Thrombolysis
• Intravenous tissue plasminogen
activator is the only approved
treaatment for acute ischemic
stroke with a number needed to
treat of 8 to cure one additional
stroke.
 Intraarterial
Thrombolysis
• Emerged as the therapeutic strategy
despite the absence of data from
randomized trials.
• Disadvantage : time delay for cerebral
angiography.
• Theoretical advantages include:
– Direct infusion of the medication into the
occluding thrombus with higher local drug
concentrations.
– Precise depiction of the arterial anatomy
including morphology of the thrombus.
– Assessment of treatment effect and extent of
collateral circulation
 Intraarterial
Thrombolysis
• Limited by the following:
– Availability of centers with an
interventional neuroradiology
service that operates 24 hours a
day, 7 days a week.
– Education of the public, general
practitioners and ER physicians that
newer therapies are currently
available will help expedite suitable
candidates to centers with
neurointerventional services and
stroke expertise.
 Intraarterial
Thrombolysis
• PROACT I Study
– First randomized, double-blinded,
multicenter trial in which safety,
recanalization, frequency and
clinical efficacy of direct IA infusion
of r-proUK was compared to
placebo.
– Partial or complete recanalization
was evident 120 minutes after
treatment onset in 58%(15/26) of r-
proUK group vs 14%(2/14) of
placebo group.
Intraarterial
Thrombolysis
 Intraarterial
Thrombolysis
• PROACT II Study
– Higher dose of r-proUK at 9mg
helped improved recanalization
efficiency by 26% but symptomatic
ICH rate increased by 4%.
– Good clinical outcomes at 90 days
with r-proUK group at 40% vs 25%
of control patients.
 Intraarterial vs
Intravenous
Thrombolysis
• IV thrombolysis appears to be better
suited to recanalization of smaller
distal emboli.
• IA thrombolysis can lyse better
intracranial large vessels.
• Morbidity and mortality of patients
treated with intra-arterial thrombolysis
is not at all different from the effect of
IV thrombolysis.
 Other treatments

• Avoiding systemic anticoagulation is

recommended for the first 24H after
thrombolysis
• Systemic anticoagulation may be an
alternative for patients with
contraindications for thrombolysis
 Other treatments
• Anticoagulation with heparin or
LMW heparanoids has been used,
but no evidence shows that this
has an impact on outcome.
• Clopidogrel, ASA + dipyridamole
– role not known
• Angioplasty with or without stent
placement is not known.
 CONCLUSIONS
• Recanalization of the basilar
artery is key to successful
treatmet and prognosis.
• Further investigations are needed
for the the time window for
treatment, patient selection and
best method for recanalization.
– Intra-arterial thrombolysis
– Mechanical thrombolysis
– Combination
 CONCLUSIONS
• In the absence of clear evidence,
treating patients in the context of
a clinical trial seems most
reasonable.
• If such an alternative is not
available and given the limited
time window, then IV
thrombolysis within 3 hrs
seem to be a reasonable
alternative.
 Intraarterial vs
Intravenous
Thrombolysis
• IV thrombolysis appears to be better
suited to recanalization of smaller
distal emboli.
• IA thrombolysis can lyse better
intracranial large vessels.
Characteristics of Patients
that can be treated with
rTPA
• Diagnosis of ischemic stroke causing
measurable neurologic deficit.
• The neurological signs should not be clearing
spontaneously.
• The neurological signs should not be minor
and limited.
• Caution should be exercised in treating
patient with a major deficit.
• The symptoms of stroke should not be
suggestive of SAH
Characteristics of Patients
that can be treated with
rTPA
• Onset of symptoms should be < 3 hrs before
beginning treatment.
• No head trauma or prior stroke in previous 3
months.
• No MI the previous 3 months.
• No GIT or urinary tract hemorrhage in
previous 27 days.
• No major surgery in the previous 14 days.
• No arterial puncture at a non compressible
site in the previous 7 days.
 Characteristics of Patients
that can be treated with
rTPA
• No history of previous intracranial
hemorrhage.
• BP not elevated (SBP < 185 mmHg,DBP <110
mmHg)
• No evidence of active bleeding and trauma
on examination.
• Not taking oral anticoagulant or
anticoagulant being taken with INR < 1.5.
• If receiving heparin, APTT must be in normal
range.
• Platelet count >100,000.
• Blood glucose > 50mg/dl.
Characteristics of Patients
that can be treated with
rTPA
• No seizure with no residual
impairments.
• CT does not showmultilobar
involvement (> 1/3 of cerebral
hemisphere).
• The family understands the
potential benefit and risks of the
management.
 ABG
• At 2lpm
– pH : 7.48
– pCO2 : 63.3
– pO2 : 70.1
– HCO3 : 48.1
– BE : + 23.6
– TCO2 : 50
 ABG
• At 100%
– pH : 7.44
– PCO2 : 52.9
– pO2 : 474.1
– HCO3 : 36.1
– BE : + 12
– TCO2 : 37.8
Cranial CT Scan
Cranial CT Scan
Cranial CT Scan
Chest X-ray
 ECG
• Sinus tachycardia
 Laboratory Results
• CBC
• Creatinine : 1.30mgs%
– Hgb : 161
• Uric acid : 667.67
– Hct : 0.48
• SGPT : 50.63
– WBC : 23.3
• Neu : 78%
• Na : 143.3
– Seg : 74% • K : 4.14
– Stab : 4%
• Albumin : 39.4
• Eos : 1%
• Protime activity :
• Lym : 18%
60.07%
• Mon : 3%
– INR : 1.57
 Laboratory Results
• Urinalysis
– Pale straw, acidic, slightly hazy, pH
1.020
– Pus cells: 4-5
– RBC : 8-10
– Sugar : negative
– Albumin : +