Stroke (CVA)
Disease
Disclosure
The patient was admitted in another institution, but his case was presented
here at our institution for its educational value.
The presenter aimed to provide timely, updated, and informative insights that
could possibly guide and adopt for management practices.
Conference Objectives
GENERAL OBJECTIVES:
To present an exemplary Cerebrovascular Disease Acute Infarct, Left MCA
Territory and underwent rtPA (Thrombolysis)
SPECIFIC OBJECTIVES:
1. Discuss Cerebrovascular Accident Management:
Review clinical management as per the latest edition of Harrison’s.
2. Review Clinical Guidelines:
Discuss the 2024 guidelines by the Stroke Society of the Philippines.
3. Develop a Management Algorithm:
Create a guideline-based algorithm for stroke management tailored to our
institution’s resources.
Diagnostics &
MaNAGEMENT OF
STROKE
-
Aims to give recommendations on the aspects of
diagnosis and management in the acute phase of
the disease.
-
It is intended to be used by general physicians and
specialists, other healthcare professionals,
policymakers to improve stroke diagnosis and
acute stroke management.
-
Twenty-one (21) recommendations were
developed out of 17 clinical questions and their
corresponding evidence summaries.
Background, Clinical Practice Guidelines on the Management of Acute Ischemic Stroke and Intracerebral Hemorrhage in the Philippines, C 1 p.7
The case
GENERAL DATA
• FP
• 73/M/Married
• Bago City
Chief complaint
Right Sided Weakness
Unable to ride his Motorcycle
Light headedness
Generalized Weakness
Slurring of Speech
R Sided Weakness
Facial Asymmetry
~3H PTA
~2H PTA
Brought LDH
History
of
present
illness
LDH
AT THE ER
4/20/24 6:35pm
BP: 160/100
CR: 69 Irreg
T: 36
O2: 97%
Patient seen awake
(E3V2M6)
Decrease Regard
Slurred Speech
Right Sided Weakness
NIHSS 22 (Severe Stroke)
ASSESSMENT
To consider
Cerebrovascular Accident
Acute Infarct Left,
Probably Cardioembolic in
Origin 2’ to Chronic Atrial
Fibrillation 2’ to Severe
Mitral Stenosis 2’ to
Rheumatic Heart Disease
PLANS
IVF: PNSS 1L X 60CC/H
Labs:
• RBS Now (96mg/dL)
Therapeutics:
• Citicoline 1g IVTT Now
Orders:
• O2 @ 2LPM
• Immediate transfer to Stroke Center (TOT: 8:10pm)
National Institutes of Health Stroke Scale (NIHSS)
a systematic assessment tool used to evaluate the
severity of stroke-related neurological deficits.
It measures functions such as consciousness,
language, neglect, visual-field loss, motor strength,
and sensory loss.
The NIHSS scores range from 0 to 42
with higher scores indicating greater impairment.
American Stroke Association
NIHSS scale at ldh
0
2
0
2
1
2
0
1
3
0
2
4
0
3
0
4
NIHSS scale at ldh
0
0
2
1
2
0
4
1
1
2
2
22
3
0
4
0
4
1
1
0
2
2
22
0
22
STROKE SOCIETY OF THE PHILIPPINES HANDBOOK OF STROKE GUIDELINES FOR PREVENTION TREATMENT AND REHABILITATION, 6TH EDITION
History of present illness
Unable to ride his Motorcycle
Light headedness
Generalized Weakness
Slurring of Speech
R Sided Weakness
Facial Asymmetry
Transferred to a Stroke Center
~3H PTA
~2H PTA
Brought LDH
~1H PTA
Admitted
Past medical history
• Chronic Atrial Fibrillation w/ severe mitral stenosis
and tricuspid regurgitation previously appraised for
valve replacement surgery
• Hypertensive w/ good BP control
• Diabetes Mellitus Type 2 – Noninsulin dependent
• Chronic kidney disease sec to Hypertensive
nephrosclerosis & DM Nephropathy
• Benign Prostatic Hyperplasia
• Hepatitis B Infection
• Compliant to medications, lifestyle changes and with
regular follow up with his attendings
(CARDIO,NEPHRO, URO)
Personal social History
NON-SMOKER
Previously OCC’L ALCOHOL Beverage
Drinker
Retired Professional Mechanical Engineer
Diet:
• Usual diet include Eggplants and prefers
to eat Vegetables and Fish.
• Doesn’t Eat Pork, Chicken and Meat
since was advised by his Cardiologist
2018
• However he eats 4-5x a day
approximately 1-2cups of rice.
Family History
(+) Hypertension - mother, sibling
(+) Cerebrovascular Accident - sibling (still living)
(+) Younger sibling died at 40yo d/t Liver Cirrhosis
sec to Chronic Ethanol Intake
(-) Diabetes mellitus
(-) Asthma
(-) Cancer
(-) Known exposure to PTB
Review of systems
General
HEENT
Thorax and Lungs
(-) anorexia, (-) weight loss, (-) fatigue, (-) fever, (-) night sweats
(-) head injury (-) headache (-) dizziness (-) blurring of vision (-) diplopia
(-) decreased hearing (-) anosmia (-) pain (-) limitation of range of motion
(-) palpable masses (-) dysphagia (-) odynophagia
(-) cough (-) shortness of breath (-) difficulty of breathing (-) hemoptysis
CVS
(+) chest pain relieved by rest, (-) palpitations (+) 1 pillow orthopnea
(-) paroxysmal nocturnal dyspnea (-) chest heaviness (-) bipedal edema
GIT
(-) loss of appetite (-) hematemesis (-) nausea (-) vomiting (-) jaundice
(-) diarrhea (-) constipation
Review of systems
Genito
urinary
(-) pain upon urinating, (-) bloody/tea-colored urine, (-) decreased urination,
(-) excessive urination
Extremities
(-) edema (-) claudication (-) swelling
Musculo
skeletal
(-) muscle or joint pain (-) stiffness (-) swelling
Hema
(-) bleeding (-) easy bruising
Neuro
(-) seizure (-) loss of consciousness (-) headache (-) tremor (-) memory loss
Physical examination
Skin
warm and dry skin, (-) cyanosis, (-) jaundice, (-) pallor, (-) active dermatoses
HEENT
pink palpebral conjunctivae, anicteric sclerae, moist lips and buccal mucosa,
(+) flat right nasolabial fold, (-) carotid bruit, neck veins not distended,
thyroid gland not enlarged
Chest and Lungs
symmetrical chest expansion, bronchovesicular breath sounds, adynamic precordium, apex beat
at 5th LICS MCL, irregularly irregular rhythm, midsystolic ejection murmur heard best at the
right upper sternal border, no heaves, no lifts, no thrills
Abdomen
soft, non-distended, normoactive bowel sounds, non-tender on palpation,
(-) CVA tenderness
Extremities
Pulses full and equal, CRT <2 secs, (-) bipedal edema
Physical examination
Skin
warm and dry skin, (-) cyanosis, (-) jaundice, (-) pallor, (-) active dermatoses
HEENT
pink palpebral conjunctivae, anicteric sclerae, moist lips and buccal mucosa,
(+) flat right nasolabial fold, (-) carotid bruit, neck veins not distended,
thyroid gland not enlarged
Chest and Lungs
symmetrical chest expansion, bronchovesicular breath sounds, adynamic precordium, apex beat
at 5th LICS MCL, irregularly irregular rhythm, midsystolic ejection murmur heard best at the
right upper sternal border, no heaves, no lifts, no thrills
Abdomen
soft, non-distended, normoactive bowel sounds, non-tender on palpation,
(-) CVA tenderness
Extremities
Pulses full and equal, CRT <2 secs, (-) bipedal edema
Physical examination
CN I – not assessed
CN II – isocoric pupils 2-3 mm equally reactive to light
CN III, IV, VI – Preferential gaze to the Left
CN V – Not Assessed
Neuro
CN VII – flattened right nasolabial fold, facial asymmetry
CN VIII – reacts to voice on the left side of the body
CN IX- not tested
CN X- (+) Gag reflex
CN XI – Not tested
CN XII - Not tested
Physical examination
CN I – not assessed
CN II – isocoric pupils 2-3 mm equally reactive to light
CN III, IV, VI – Preferential gaze to the Left
CN V – Not Assessed
Neuro
CN VII – flattened right nasolabial fold, facial asymmetry
CN VIII – reacts to voice on the left side of the body
CN IX- not tested
CN X- (+) Gag reflex
CN XI – Not tested
CN XII - Not tested
Physical examination
Motors:
Neuro
1/5
Sensory:
Reflexes:
Localizes Pain
on L Extremities
5/5
1/5
5/5
Cerebellum: difficult to assess ataxia, dysmetria, dysdiadochokinesia
Reflexes: ++ on all extremities, (-) Babinski
Meningeal signs: (-) Brudzinski, (-) Kernig’s, (-) Nuchal rigidity
NIHSS: 22 (severe)
SALIENT FEATURES
•
•
•
73-year-old male
Weakness of right UE and LE
Right facial asymmetry
•
•
Known case of atrial fibrillation sec to
rheumatic heart disease
CAD-IHD, VHD, HTN, T2DM, CKD
•
Family history of stroke
•
•
•
•
•
•
•
•
•
(-) head trauma
(-) headache, visual disturbances
(-) nausea and vomiting
(-) loss of consciousness, confusion
GCS 11 (E4V1M6)
Incomprehensible
global aphasia
(+) flat right nasolabial fold
(+) Motor: 1/5 left UE and 1/5 left LE
Primary Impression
Acute Cereberovascular Infarct,
Left MCA Territory, (NIHSS 22)
probably Cardioembolic in Origin 2’ to Chronic Atrial
Fibrillation 2’ to Severe Mitral Stenosis 2’ to Rheumatic Heart
Disease
CHA₂DS₂-VASc Score for Atrial Fibrillation Stroke Risk
A clinical tool used to estimate the risk of stroke in
patients with atrial fibrillation (AF).
1.
2.
3.
4.
5.
6.
7.
Congestive heart failure (1 point)
Hypertension (1 point)
Age ≥ 75 years (2 points)
Diabetes mellitus (1 point)
Stroke/TIA/thromboembolism history (2 points)
Vascular disease (prior MI, peripheral artery disease,
or aortic plaque) (1 point)
Sex (female) (1 point)
American Heart Association (AHA)
CHA₂DS₂-VASc Score for Atrial Fibrillation
Stroke Risk
HAS-BLED Score for Major Bleeding Risk
The American Heart Association (AHA)
defines the HAS-BLED score as a clinical
tool used to estimate the risk of major
bleeding in patients with atrial fibrillation
(AF) who are on anticoagulation therapy.
The score evaluates seven factors, each
assigned a specific point value:
The score evaluates seven factors, each
assigned a specific point value:
A: Abnormal renal/liver function (1 point each)
H: Hypertension (uncontrolled, systolic blood
pressure >160 mmHg)
S: Stroke history
B: Bleeding history or predisposition
L: Labile INR (unstable/high INRs, time in
therapeutic range <60%)
E: Elderly (age >65)
D: Drugs/alcohol concomitantly (1 point each)
HAS-BLED Score for Major Bleeding Risk
STROKE SOCIETY OF THE PHILIPPINES. HANDBOOK OF STROKE: GUIDELINES FOR PREVENTION, TREATMENT, AND REHABILITATION. 6TH ED., STROKE SOCIETY OF THE PHILIPPINES, 2014.
STROKE SOCIETY OF THE PHILIPPINES. HANDBOOK OF STROKE: GUIDELINES FOR PREVENTION, TREATMENT, AND REHABILITATION. 6TH ED., STROKE SOCIETY OF THE PHILIPPINES, 2014.
36
FAUCI, ANTHONY S., ET AL., EDITORS. HARRISON'S PRINCIPLES OF INTERNAL MEDICINE. 21ST ED., MCGRAW-HILL EDUCATION, 2022.
Differential diagnosis
Differential Diagnosis
Intracranial Hemorrhage
Most likely due to
Least likely due to
High Blood Pressure
Rapid progressive onset of signs and
symptoms
Unilateral Symptoms
Speech impairment
Facial Droop
Unilateral Arm Weakness
Progressive neurologic deficit
No history of severe headache
No History of Anticoagulant Use
Differential Diagnosis
Subarachnoid Hemorrhage
Most likely due to
Unilateral Symptoms
Speech impairment
Facial Droop
Unilateral Arm Weakness
Least likely due to
Signs and symptoms not maximal
at onset
Rapid development of focal
neurological deficits (Progressive)
No history of sudden severe
Headache
Differential Diagnosis
Brain tumor
Most likely due to
Localized Neurological Deficits
Unilateral Symptoms
Speech impairment
Facial Droop
Unilateral Arm Weakness
Least likely due to
Neurodeficit was not progressive
over days / months
Signs and symptoms not maximal
at onset
No Headache
No History of Cancer
Course IN THE wards
STROKE CENTER
AT THE ER
BP: 150/70 mmHg
CR: 56 Irreg-Irreg
RR: 20 cpm
T: 36.5 C
SPO2: 98% RA
Pt seen awake, global aphasia
GCS 11 (E4V1M6)
isocoric pupils, EBRTL
(+) flat right nasolabial fold
SCE (-) rales (-) wheezes
AF irreg-irregular rhythm
soft abdomen
(-) edema, pulses 2+
(+) Motor: 1/5 L Extremities
NIHSS 22
ASSESSMENT
1. Cerebrovascular Disease
Acute Infarct, Left MCA
Territory, (NIHSS 22)
2. Atrial Fibrillation in Slow
Ventricular Response
secondary to Rheumatic
Heart Disease, Valvular
Heart Disease Secondary
3. Coronary Artery Disease Ischemic Heart Disease
4. Hypertensive
Cardiovascular Disease
5. Chronic Kidney Disease
secondary to DM
Nephropathy
6. Benign Prostatic
Hyperplasia
AT THE ER
IVF: PNSS 1l x 80 mL/h
Diet: NPO except meds
Labs:
Cranial CT angiogram STAT
CBC, serum Na, K, Mg, iCa, crea, BUN ALT, protime, aPTT, TSH, FT3, FT4 12L ECG, CXR AP view, urinalysis, CBG
monitoring q6h
Therapeutics:
•
Citicoline 1g now then q8h
•
Mannitol 75mL now then q6h
•
Trimetazidine 35mg/tab 1 tab BID
•
Atorvastatin 80mg/tab 1 tab ODHS
•
Fishoil 1 cap BID & Coenzyme Q10 1 tab OD
•
Empagliflozin 10mg/tab 1 tab ODPClunch
•
Tamsulosin 200mcg/tab 1 tab ODHS
•
Finasteride 5mg/tab 1 tab ODAM
•
Rebamipide 100mg/tab 1 tab TID
•
Lactulose 30mL ODHS, hold for >2 BM/day
•
Pantoprazole 40mg IV ODACBF
Orders:
•
Admit to ICU
•
For co-management with Interventional Radiology
•
For co-management with Cardiology
NIHSS scale at ldh
0
2
0
2
1
2
0
1
3
0
2
4
0
3
0
4
NIHSS scale at the er
0
0
2
1
2
0
4
1
1
2
2
22
3
0
4
0
4
1
1
0
2
2
22
0
22
Course IN THE wards
Atrial fibrillation with slow
ventricular response
Poor R-wave progression,
consider old anterior wall
infarction
Non-specific ST-T wave changes
Course IN THE wards
Suspicious densities are seen in both lung apices.
Apicolordotic view suggested.
The heart is enlarged. Cardiomegaly. The pulmonary
vessels are within normal limits.
Atherosclerotic aorta.
The diaphragm and costophrenic sulci are intact. A
gastric tube is seen coiled in the mid esophagus. Repositioning recommended. The rest of the included
chest structures are unremarkable.
Course IN THE wards
4/20
NV
Na
138.70
136.00-145.00
Mg
0.96
0.70-1.00
K
4.51
3.50-5.50
4.00 - 5.50 - x 10^12 L
iCa
1.09
1.05-1.3
90.90
80.00-100.00 fL
BUN
22.41
7.00-17.09
MCH
31.70
28.00-33.00 g/dL
Crea
1.80
0.80-1.50
WBC
4.8
5-10 x 10^9/L
ALT
38.00
Less than 50U/L
Uric acid
5.63
3.39-6.78
Neutrophil
0.67
0.50-0.70
aPTT
41.4
28.00-36.00
Lymph
0.02
0.20-0.70
Prothrombin
12.4
10.50-13.00
Eosinophil
0.02
0.00-0.05
INR
1.08
Mono
0.11
0.00-0.09
CT/BT
4 min / 1.15 min
2-5 min/ 1-3 min
Platelet
154
150.00 - 400.00 x 10 ^ 9/L
TSH
1.08
0.35-4.94
FT4
0.93
0.71-1.85
FT3
4.29
2.23-5.35
4/20
NV
Hgb
147
110 -150 g/L
Hct
0.42
0.38 - 0.47
RBC
4.63
MCV
Pale straw, pH 6.0, SG 1.010
2-4/HPF pus cells
Urinalysis
35-40/HPF RBC
Albumin negative
Bacteria Occasional/HPF
Initial plain CT scan shows hypodensities in the left thalamus and left external capsule (ASPECTS 8).
There are no other abnormal high or low density lesions in the cerebral hemispheres, cerebellum, brainstem and extra axial spaces.
Midline structures are in place.
The ventricles and subarachnoid cisterns are normal in size and configuration.
The calvarium and skull base structures are intact.
CT angiogram shows no evident vascular abnormality, aneurysm or arterio-venous malformation. The internal carotid, middle
cerebral, anterior cerebral, anterior communicating, vertebro-basilar, posterior cerebral, posterior communicating arteries are
patent and shows no evidence of occlusive disease. No large vessel occlusion present.
The left anterior cerebral artery is hypoplastic. The left vertebral artery terminates as the left posterior inferior cerebellar artery.
Wall calcifications seen in both internal carotid and right vertebral arteries. Venous phase is unremarkable.
Calcifications likewise present in the visualized aorta and coronary arteries.
IMPRESSION:
ACUTE INFARCTION, LEFT THALAMUS AND LEFT EXTERNAL CAPSULE (ASPECTS 8)
NO EVIDENT LARGE VESSEL OCCLUSION, ANEURYSM, OR VASCULAR MALFORMATION ATHEROSCLEROTIC INTERNAL CAROTID,
RIGHT VERTEBRAL, AORTA, AND CORONARY ARTERIES
The Alberta Stroke Program Early CT Score (ASPECTS)
a 10-point scale used to assess early
ischemic changes in the brain on a noncontrast CT (NCCT) scan. Here's how to
score it:
1.Start with a score of 10.
2.Subtract 1 point for each of the following regions if there is
evidence of early ischemic change:
• Caudate nucleus
• Lentiform nucleus
• Internal capsule
• Insular cortex
• M1: Anterior MCA cortex (frontal operculum)
• M2: MCA cortex lateral to the insular ribbon (anterior temporal
lobe)
• M3: Posterior MCA cortex (posterior temporal lobe)
• M4: Anterior MCA territory immediately superior to M1
• M5: Lateral MCA territory immediately superior to M2
• M6: Posterior MCA territory immediately superior to M3
https://www.stroke-manual.com/
Endovascular mechanical thrombectomy
A minimally invasive procedure to remove a stationary blood
clot (thrombus) from an artery using specialized
equipment.
Procedure: Involves inserting a catheter through a small
incision, usually in the groin, and guiding it to the clot
using imaging techniques. A device, such as a stent
retriever, is then used to capture and remove the clot2.
Applications: Primarily used to treat acute ischemic stroke by
restoring blood flow to the brain.
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3336
Endovascular mechanical thrombectomy
studied as an alternative or adjunctive treatment of acute
stroke in patients who are ineligible for, or have
contraindications to, thrombolytics or in those who
failed to achieve vascular recanalization with IV
thrombolytics
The outcomes from endovascular therapy are likely improved
with IV rtPA treatment prior to thrombectomy if the patient is
eligible for rtPA and it is safe to administer.
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3336
Middle cerebral artery anatomy
M1. The proximal MCA (M1 segment) gives rise to
penetrating branches (termed lenticulostriate
arteries) that supply the putamen, outer globus
pallidus, posterior limb of the internal capsule,
adjacent corona radiata, and most of the caudate
nucleus.
M2. MCA in most patients divides into superior and
inferior divisions “M2 branches”
M3. Cortical Branches
• Inferior division supply the inferior parietal and
temporal cortex
• Superior division supply the frontal and superior
parietal cortex
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3336
Middle cerebral artery anatomy
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3326
Harrison’s Algorithm
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3336
Rtpa
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3336
Rtpa
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3336
Tissue plasminogen activator
How does it work?
A protein/chemical/thrombolytic agent
used to dissolve blood clots in patients
experiencing an acute ischemic stroke.
www.ahajournals.org
https://www.mdpi.com, Direct-Acting Oral Anticoagulants and Their Reversal Agents—An Update,
Recombinant Tissue Plasminogen Activator (rtPA)
Administration
Alteplase 30mg:
3mg IV push then 27mg as IV drip
for 1 hour
AT THE ER
ASSESSMENT
S/P rTPA with Alteplase
1. Cerebrovascular Disease
Acute Infarct, Left MCA
Territory (NIHSS 5)
2. Atrial Fibrillation in SVR 2’
to Rheumatic Heart
Disease, Valvular Heart
Disease Secondary
3. Coronary Artery Disease Ischemic Heart Disease
4. Hypertensive
Cardiovascular Disease
5. Chronic Kidney Disease St
IIIB 2’ to DM Nephropathy
6. Benign Prostatic
Hyperplasia
BP: 140/80 mmHg
CR: 62 Irreg-Irreg
RR: 18 cpm
T: 36.6 C
SPO2: 99% RA
Pt seen awake,
mild dysarthria
GCS 14 (E4V4M6)
isocoric pupils, EBRTL
(-) Nasolabial fold
SCE (-) rales (-) wheezes
AP irregularly irregular rhythm
soft abdomen
(-) edema, pulses 2+
(+) Motor: 4/5 left UE and LE
NIHSS 2 (22)
AT THE ER
IVF: PNSS 1l x 100 mL/h
Diet: 1800 kcal/day, 50% CHO of low glycemic index, 56g CHON of HBV, low fat, low cholesterol,
800mg phosphorus, low purine
Labs:
CBG monitoring q6h
Therapeutics:
•
Alteplase 30mg: 3mg IV push then 27mg as IV drip for 1 hour
•
NAC 1.2g IV TID
•
Mannitol 75mL now then q6h
Orders:
•
For consult with Nephrology and continued monitoring
0
2
1
2
0
0
0
0
0
0
3
0
0
0
4
0
0
4
0
0
0
1
0
1
2
0
2
0
0
22
NIHSS scale at the er
0
0
0
0
1
1
0
2
2
0
2
1
2
0
0
0
0
0
0
3
0
0
0
4
0
0
4
1
0
0
0
1
0
2
1
2
1
0
0
22
2
Recombinant Tissue Plasminogen Activator (rtPA)
Recombinant Tissue Plasminogen Activator (rtPA), while effective
in treating acute ischemic stroke, can have several complications:
● Intracerebral Hemorrhage (ICH): The most serious
complication, leading to bleeding within the brain.
● Systemic Bleeding: Including gastrointestinal bleeding and
other sites.
● Oropharyngeal Angioedema: Swelling of the tongue and
throat, which can obstruct the airway.
● Reperfusion Injury: Tissue damage caused by the return of
blood flow.
● Seizures: Due to rtPA's neurotoxic effects.
● Neurological Worsening: Sudden deterioration in neurological
status.
● Reocclusion: The clot may reform after initial dissolution.
● Secondary Embolization: Pieces of the dissolved clot may
travel to other parts of the brain.
Course in the ward
The patient stayed at the ICU for 2 days and was trans out to
the room which he stayed for another 2 days and was
discharged
AT THE WARDS
D3-5
S/P rTPA with Alteplase D35
BP: 140/80 mmHg
CR: 62 bpm
RR: 18 cpm
T: 36.6 C
SPO2: 99% RA
Pt seen awake,
(-) Dysarthia
GCS 15 (E4V5M6)
isocoric pupils, EBRTL
SCE (-) rales (-) wheezes
AP irregularly irregular
rhythm
soft abdomen
(-) edema, pulses 2+
Motor: 5/5 R/L Extremities
NIHSS 0 (22)
ASSESSMENT
1. Cerebrovascular Disease
Acute Infarct, Left MCA
Territory (NIHSS 5)
2. Coronary Artery Disease
- Ischemic Heart Disease
3. Chronic Atrial Fibrillation
(CHADSVASC 3)
(HAS-BLED 4)
4. Hypertensive
Cardiovascular Disease
5. Chronic Kidney Disease
Stage IIIB secondary to
DM Nephropathy
6. Benign Prostatic
Hyperplasia
AT THE ER
Labs:
CBG monitoring q6h
Therapeutics:
•
Ampicillin-sulbactam 1.5g IV q8h
•
Rivaroxaban 15mg/tab 1 tab OD
•
Citicoline 1g q12h
•
Mannitol 50mL q8h then discontinue
Orders:
•
Refer to Rehabilitation Specialist
Modified rankin scale
A 7-level, clinician-reported measure of global disability.
It is widely used to assess the degree of disability or dependence in daily activities of individuals who
have suffered a stroke or other causes of neurological disability
Saver, et. Al, Standardized Nomenclature for Modified Rankin Scale Global Disability Outcomes. www.ahajournals.org
Final diagnosis
Cerebrovascular Disease Acute Infarct,
Left MCA Territory sp rTPA (NIHSS 0)
Coronary Artery Disease - Ischemic Heart Disease
Chronic Valvular Atrial Fibrillation (CHADSVASC 3) (HAS-BLED 4)
Secondary to Severe Mitral Stenosis
Secondary to Rheumatic Heart Disease
Hypertensive Cardiovascular Disease
Chronic Kidney Disease Stage IIIB secondary to DM Nephropathy
Benign Prostatic Hyperplasia
01
Cerebrovascular
accident / Stroke
nd
2
leading cause of death &
most common disabling condition in individuals
aged 50 or older
25%
2016, the lifetime global risk of
stroke from age 25 years onward
Smith, et. Al, Introduction to Cerebrovascular Disease, Harrison’s Principle of Internal Medicine, 21st Ed, p.3324
In the Philippines…
nd
2
leading cause of death in the Philippines
29th in the world
The Philippines has an age-adjusted death rate of
134.74 per 100,000 Population
DOH AO 2020-0059
NATIONAL POLICY FRAMEWORK ON THE PREVENTION
CONTROL AND MANAGEMENT OF ACUTE STROKE IN
THE PHILIPPINES
Clinical Practice Guidelines on the Management of Acute Ischemic Stroke and Intracerebral Hemorrhage in the Philippines, p.9
Cerebrovascular accident / Stroke
A Stroke, or a brain attack , happens when the blood supply to the brain
is suddenly blocked or when a blood vessel in the brain suddenly burst.
This caused the affected parts of the brain to become damaged or to die.
PNA STROKE COUNCIL
Types of stroke
Ischemic
An ischemic stroke occurs
when a vessel supplying blood
to the brain is obstructed.
Hemorrhagic
results from a weakened vessel that ruptures
and bleeds into the surrounding brain.
•
•
https://www.stroke.org/en/
Intracranial Hemorrhage
Subarachnoid Hemorrhage
Ischemic Stroke
● Accounts for 85% of all Strokes
● Acute occlusion of an intracranial vessel causes reduction
in blood flow to the brain region it supplies.
TRANSIENT ISCHEMIC ATTACK
-
A clinical syndrome wherein blood flow to ischemic tissue is
restored before significant infarction develops.
ISCHEMIC PENUMBRA
-
defined as the ischemic but reversibly dysfunctional tissue
surrounding a core area of infarction.
A Decrease in Cerebral Flow to zero causes death of brain tissue win 4-10mins
• < 16-18ml/100g Tissue per minute cause infarction w/in an hour
• < 20ml/100g tissue perminute cause ischemia without infarction unless prolonged several hours to days
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3335
ETIOLOGY OF ISCHEMIC STROKE
• Initial management of AIS often does not
depend on the etiology
• Establishing a cause is essential to reduce the
risk of recurrence.
• Nearly 30% of strokes remain unexplained
despite extensive evaluation.
• Focus should be on atrial fibrillation and carotid
atherosclerosis, because these etiologies have
proven secondary prevention strategies.
PATHOPHYSIOLOGY OF ISCHEMIC STROKE
FAUCI, ANTHONY S., ET AL., EDITORS. HARRISON'S PRINCIPLES OF INTERNAL MEDICINE. 21ST ED., MCGRAW-HILL EDUCATION, 2022.
ETIOLOGY OF ISCHEMIC STROKE
1.
2.
Cardioembolic Stroke
Artery-to Artery embolic Stroke
a. Carotid Atherosclerosis
b. Other Causes
c. Intracranial Atherosclerosis
d. Dissection
•
Intracranial
Do not cause hemorrhage
Thick Adventitia Layer
•
Extracranial
May Produce SAH
a. Trauma
MVA vs Sports Injury
Associated with vertebral
Artery dissection
a. Spinal Manipulative Therapy
Cardioembolic Stroke
•
•
•
Responsible for ~20% of all ischemic strokes.
Occur suddenly with maximum neurologic
deficit at onset
Thrombotic material from the atrial/ventricular
wall or left heart valves
1. TIA - lyse quickly
2. Stroke – Permanent
Cardioembolic Stroke
•
•
•
•
•
•
Nonrheumatic Atrial Fibrillation
- Thrombus formation in the atrium or
atrial appendage
- Average annual stroke risk: 5%
Myocardial infarction (MI)
Prosthetic valves
Rheumatic heart disease
Ischemic cardiomyopathy
Emboli
Paradoxical Embolization
Patent Foramen Ovale (PFO)
Atrial Septal Defect (ASD)
Fat and Tumor Emboli
Bacterial endocarditis
IV air
Amniotic fluid emboli
Cardioembolic Stroke
ETIOLOGY OF ISCHEMIC STROKE
1.
2.
Cardioembolic Stroke
Artery-to Artery embolic Stroke
a. Carotid Atherosclerosis
b. Other Causes
c. Intracranial Atherosclerosis
d. Dissection
•
Intracranial
Do not cause hemorrhage
Thick Adventitia Layer
•
Extracranial
May Produce SAH
a. Trauma
MVA vs Sports Injury
Associated with vertebral
Artery dissection
a. Spinal Manipulative Therapy
Artery-to-Artery Embolic Stroke
Cause: Thrombus on atherosclerotic plaques
embolizing to intracranial arteries.
Carotid Atherosclerosis
Common Sites: Bifurcation and proximal internal
carotid artery, carotid siphon.
Risk Factors: Male gender, older age, smoking,
hypertension, diabetes,hypercholesterolemia.
Prevalence: Causes ~10% of ischemic strokes.
Artery-to-Artery Embolic Stroke
Carotid Disease Classification
•
Symptomatic: Stroke or TIA
experienced, higher stroke risk.
•
Asymptomatic: Detected through
screening, lower stroke risk.
•
Degree of Stenosis: Higher
narrowing increases stroke risk,
except near occlusions.
Small-Vessel Stroke
Definition
•
Also known as lacunar infarction.
•
Results from occlusion of small
arteries in the brain due to
atherothrombotic or lipohyalinotic
processes.
•
Accounts for ~20% of all strokes.
Small-Vessel Stroke
Pathophysiology
•
Affected arteries: small branches
(30-300 μm) from the MCA stem,
circle of Willis, basilar, and vertebral
arteries.
•
Causes: atherothrombotic disease
at the origin or lipohyalinotic
thickening.
•
Infarcts (lacunes): range from 3 mm
to 2 cm in diameter.
•
Risk factors: hypertension and age.
Small-Vessel Stroke
Clinical Manifestations
•
Pure Motor Hemiparesis: Infarct in
posterior limb of internal capsule or pons.
•
Pure Sensory Stroke: Infarct in ventral
thalamus.
•
Ataxic Hemiparesis: Infarct in ventral pons
or internal capsule.
•
Dysarthria and Clumsy Hand/Arm:
Infarction in ventral pons or genu of
internal capsule.
•
Transient symptoms (small-vessel TIAs)
may precede infarcts.
•
Recovery: Often more rapid and complete
compared to large-vessel strokes; severe
permanent disability can still occur.
Small-Vessel Stroke
Evaluation and Prevention
•
Large-vessel sources of embolism
should be evaluated.
•
Secondary prevention: Focus on risk
factor modification, particularly
blood pressure reduction
TRANSIENT ISCHEMIC ATTACKS
Definition
• Episodes of stroke symptoms lasting briefly; typically
<1 hour, standard definition <24 hours.
• Brain imaging:
- Identified brain infarction reclassifies TIA as a
stroke.
- Normal imaging does not rule out TIA; clinical
syndrome is diagnostic.
Causes
•
Similar to ischemic stroke.
•
Can arise from emboli to the brain or in situ
thrombosis of an intracranial vessel.
•
With TIA, the occluded vessel reopens, restoring
neurologic function
TRANSIENT ISCHEMIC ATTACKS
Risk and Evaluation
•
Stroke Risk: ~10–15% within the first 3 months postTIA, most events in the first 2 days.
•
ABCD2 Score: Used to estimate stroke risk.
•
Urgent Evaluation and Treatment: Essential due to
high stroke risk.
•
Evaluation for TIA should parallel that of stroke due to
identical etiologies.
Types of stroke
Ischemic
An ischemic stroke occurs
when a vessel supplying blood
to the brain is obstructed.
Hemorrhagic
results from a weakened vessel that ruptures
and bleeds into the surrounding brain.
•
•
https://www.stroke.org/en/
Intracranial Hemorrhage
Subarachnoid Hemorrhage
intracerebral Hemorrhage
-
Accounts for ~10% of all strokes
-
~35–45% of patients die within the first
month
-
Incidence rates are particularly high in
Asians and blacks.
intracerebral Hemorrhage
Hypertensive ich
-
results from spontaneous rupture of a small
penetrating artery deep in the brain.
The most common sites are the basal ganglia
(especially the putamen), thalamus, cerebellum,
and pons.
CLINICAL MANIFESTATIONS
-
Generally presents as the abrupt onset of a focal
neurologic deficit.
intracerebral Hemorrhage
Cerebral amyloid angiopathy
-
a disease of the elderly in which
arteriolar degeneration occurs and
amyloid is deposited in the walls of the
cerebral arteries.
-
Amyloid angiopathy causes both
recurrent lobar hemorrhages
most common cause of lobar
hemorrhage in the elderly
-
-
accounts for some intracranial
hemorrhages associated with IV
thrombolysis given for myocardial
infarction.
intracerebral Hemorrhage
Cocaine and methamphetamine
-
Are frequent causes of stroke in young (age <45 years) patients.
ICH, ischemic stroke, and subarachnoid hemorrhage (SAH) are all associated with stimulant use.
anticoagulant therapy
-
Can occur at any location;
They are often lobar or subdural
continue to evolve over 24–48 h, especially if coagulopathy is insufficiently reversed
hematologic disorders
-
ICH associated with hematologic disorders (leukemia, aplastic anemia, thrombocytopenic purpura) can occur at
any site and may present as multiple ICHs.
-
Skin and mucous membrane bleeding may be evident and offers a diagnostic clue .
intracerebral Hemorrhage
neoplasm
-
Hemorrhage into brain tumor
May be the first manifestation of
neoplasm.
• Choriocarcinoma
• Glioblastoma
• Malignant Melanoma
multiforme
• Medulloblastoma
• Bronchogenic
carcinoma
• Renal Cell Carcinoma
Management of Acute Cerebral Ischemia
•
•
•
•
•
•
MEDICAL SUPPORT
IV THROMBOLYSIS
ENDOVASCULAR REVASCULARIZATION
ANTITHROMBOTIC TREATMENT
NEUROPROTECTION
STROKE CENTERS AND REHABILITATION
Smith, et. Al, Ischemic Stroke, Harrison’s Principle of Internal Medicine, 21st Ed, C 427 p.3337-3339
Diagnostics &
MaNAGEMENT OF
STROKE
-
Aims to give recommendations on the aspects of
diagnosis and management in the acute phase of
the disease.
-
It is intended to be used by general physicians and
specialists, other healthcare professionals,
policymakers to improve stroke diagnosis and
acute stroke management.
-
Twenty-one (21) recommendations were
developed out of 17 clinical questions and their
corresponding evidence summaries.
Background, Clinical Practice Guidelines on the Management of Acute Ischemic Stroke and Intracerebral Hemorrhage in the Philippines, C 1 p.7
Diagnosis
Diagnosis
Q1. Should we use non-contrast cranial computed tomography (NCCT)
compared to cranial magnetic resonance imaging (MRI) in diagnosing
patients suspected of having acute stroke within 6 hours?
RECOMMENDATION 1A:
Among adult patients suspected with acute stroke within 6 hours, we recommend using
either non-contrast computed tomography (NCCT) or cranial magnetic resonance
imaging (MRI) to rule out acute intracranial hemorrhage.
Overall Level of Certainty:
Strength of Recommendation:
Moderate
⨁⨁⨁◯
Strong
FOR INTRACRANIAL HEMORRHAGE, BOTH TESTS WERE 100%
SPECIFIC BUT NCCT HAD HIGHER SENSITIVITY (89%) THAN
CRANIAL MRI (81%).
RECOMMENDATION 1B:
Among adult patients suspected with acute stroke within 6 hours, we recommend using
cranial MRI to confirm the diagnosis of acute ischemic stroke.
Overall Level of Certainty:
Moderate
Strength of Recommendation:
⨁⨁⨁◯
Strong
CRANIAL MRI DEMONSTRATED HIGHER ACCURACY FOR
DIAGNOSING AN ACUTE STROKE (83% SENSITIVITY, 97%
SENSITIVITY) COMPARED TO NCCT (26% SENSITIVITY, 98%
SPECIFICITY).
Acute stroke unit
ACUTE STROKE UNIT
Q2. Should we routinely admit patients with acute stroke in a stroke
unit instead of a general ward?
RECOMMENDATION 2:
Among adult patients with acute stroke, we recommend admission in a stroke unit
compared to the general ward.
Overall Level of Certainty:
Low
Strength of Recommendation:
Strong
⨁⨁◯◯
Thrombolysis
Thrombolysis
Q3. Should we use intravenous thrombolysis with alteplase among
patients with acute ischemic stroke < 4.5 hours duration?
Thrombolysis
Q3. Should we use intravenous thrombolysis with alteplase among
patients with acute ischemic stroke < 4.5 hours duration?
RECOMMENDATION 3:
Among eligible patients with acute ischemic stroke <4.5 hours duration, we recommend
the use of intravenous thrombolysis with alteplase.
Overall Level of Certainty:
Strength of Recommendation:
Moderate
Strong
⨁⨁⨁◯
Thrombolysis
Q4. Should we use low-dose compared to standard-dose intravenous
alteplase thrombolysis among patients with acute ischemic stroke of
less than 4.5 hours duration from the onset of symptoms?
Thrombolysis
Q4. Should we use low-dose compared to standard-dose intravenous
alteplase thrombolysis among patients with acute ischemic stroke of
less than 4.5 hours duration from the onset of symptoms?
RECOMMENDATION 4:
Among patients with acute ischemic stroke with less than 4.5 hours from onset of
symptoms, we recommend the use of standard dose alteplase (0.9 mg/kg) over low dose
alteplase (less than 0.9 mg/kg).
Overall Level of Certainty:
Low
Strength of Recommendation:
Strong
⨁⨁◯◯
Thrombolysis
Q5. Should we do thrombolysis with tenecteplase as an alternative to
standard-dose alteplase for intravenous thrombolysis among patients
with acute ischemic stroke of less than 4.5 hours duration?
Thrombolysis
Q5. Should we do thrombolysis with tenecteplase as an alternative to
standard-dose alteplase for intravenous thrombolysis among patients
with acute ischemic stroke of less than 4.5 hours duration?
RECOMMENDATION 5:
Among patients with acute ischemic stroke of less than 4.5 hours duration, we
recommend the use of tenecteplase as an alternative to alteplase for intravenous
thrombolysis.
Overall Level of Certainty:
Low
Strength of Recommendation:
Strong
⨁⨁◯◯
Anti-thrombotic therapy
Anti-thrombotic therapy
Q6. Should we use dual antiplatelet therapy as first line treatment
over antiplatelet monotherapy among patients with acute minor noncardioembolic ischemic stroke or transient ischemic attack within 24
hours of symptom onset?
Anti-thrombotic therapy
Q6. Should we use dual antiplatelet therapy as first line treatment over antiplatelet
monotherapy among patients with acute minor non-cardioembolic ischemic stroke or
transient ischemic attack within 24 hours of symptom onset?
RECOMMENDATION 6A:
Among patients with acute minor non-cardioembolic acute ischemic stroke or high-risk
transient ischemic attack within 24 hours from symptom onset, we recommend
treatment with dual antiplatelet therapy using aspirin and clopidogrel for 21 days.
Overall Level of Certainty:
Strength of Recommendation:
Moderate
Strong
⨁⨁⨁◯
Anti-thrombotic therapy
Q6. Should we use dual antiplatelet therapy as first line treatment over antiplatelet
monotherapy among patients with acute minor non-cardioembolic ischemic stroke or
transient ischemic attack within 24 hours of symptom onset?
RECOMMENDATION 6B:
Among patients with acute minor non-cardioembolic ischemic stroke or high-risk
transient ischemic attack within 24 hours of symptom onset, we suggest against
treatment with dual antiplatelet therapy using aspirin and ticagrelor.
Overall Level of Certainty:
Strength of Recommendation:
Moderate
Weak
⨁⨁⨁◯
Early mobilization
Early mobilization
Q7. Should we do very early mobilization (24 hours) by trained staff (i.e.,
physical therapists, nurses) versus usual treatment among patients
with acute stroke?
RECOMMENDATION 7:
Among acute stroke patients, we recommend against very early mobilization within 24
hours by trained staff (i.e., physical therapists, nurses)
Overall Level of Certainty:
Low
Strength of Recommendation:
Strong
⨁⨁◯◯
Venous thromboembolism
(VTE) prophylaxis
Venous thromboembolism (VTE) prophylaxis
Q8. Should we use anticoagulants among immobile patients hospitalized
with acute ischemic stroke for deep vein thrombosis (DVT) prophylaxis?
RECOMMENDATION 8:
Among immobilized in-patients with acute ischemic stroke, we suggest the use of
anticoagulants (low-molecular-weight heparin or unfractionated heparin) versus no
anticoagulants for DVT prophylaxis.
Overall Level of Certainty:
Low
Strength of Recommendation:
Weak
⨁⨁◯◯
Venous thromboembolism (VTE) prophylaxis
Q9. Should we use graduated compression stockings (GCS) as add-on
therapy to standard of care among adult immobilized patients
hospitalized due to acute stroke?
RECOMMENDATION 9:
Among immobilized patients hospitalized with acute ischemic stroke or intracerebral
hemorrhage, we recommend against the use of graduated compression stockings.
Overall Level of Certainty:
Low
Strength of Recommendation:
Strong
⨁⨁◯◯
Venous thromboembolism (VTE) prophylaxis
Q10. Should we use intermittent pneumatic compression (IPC) among
immobilized patients hospitalized due to acute ischemic stroke?
RECOMMENDATION 10:
Among immobilized patients hospitalized with acute ischemic stroke, we suggest the use
of intermittent pneumatic compression.
Overall Level of Certainty:
Strength of Recommendation:
Moderate
Strong
⨁⨁⨁◯
Venous thromboembolism (VTE) prophylaxis
Q10. Should we use intermittent pneumatic compression (IPC) among
immobilized patients hospitalized due to acute ischemic stroke?
RECOMMENDATION 10:
Among immobilized patients hospitalized with acute ischemic stroke, we suggest the use
of intermittent pneumatic compression.
Overall Level of Certainty:
Strength of Recommendation:
Moderate
Strong
⨁⨁⨁◯
Venous thromboembolism (VTE) prophylaxis
Q11. Should we use intermittent pneumatic compression (IPC) as add-on
therapy to standard of care compared to non-use among immobilized
patients hospitalized with acute intracerebral hemorrhage (ICH)?
RECOMMENDATION 11:
Among immobilized patients hospitalized with acute ICH, we suggest the use of
intermittent pneumatic compression, compared to standard care alone (non-use).
Overall Level of Certainty:
Strength of Recommendation:
Moderate
Weak
⨁⨁⨁◯
Surgery for intracerebral hemorrhage
Surgery for intracerebral hemorrhage
Q12. Should we do surgery on top of best medical management versus
best medical management alone among patients with supratentorial
intracerebral hemorrhage (ICH)?
RECOMMENDATION 12:
Among adult patients with supratentorial spontaneous intracerebral hemorrhage and
signs of increased intracranial pressure, surgical evacuation of hematoma on top of
best medical management may be considered.
Overall Level of Certainty:
Low
Strength of Recommendation:
Weak
⨁⨁◯◯
Decompressive hemicraniectomy
Decompressive hemicraniectomy
Q13. Should we do surgery on top of best medical management versus
best medical management alone among patients with supratentorial
intracerebral hemorrhage (ICH)?
RECOMMENDATION 13A:
Among adult patients aged 60 years or younger with malignant MCA infarction,
surgical decompression on top of medical management may be considered.
Overall Level of Certainty:
Strength of Recommendation:
Moderate
Weak
⨁⨁⨁◯
Decompressive hemicraniectomy
Q13. Should we do surgery on top of best medical management versus
best medical management alone among patients with supratentorial
intracerebral hemorrhage (ICH)?
RECOMMENDATION 13B:
Among adult patients aged > 60 years with malignant MCA infarction, surgical
decompression on top of medical management may be considered.
Overall Level of Certainty:
Low
Strength of Recommendation:
Weak
⨁⨁◯◯
Neuroprotective agents
Neuroprotective agents
Q14. Should we routinely give edaravone as an add-on therapy among
patients with acute stroke?
RECOMMENDATION 14A:
Among patients with acute ischemic stroke, we do not recommend the routine use of
edaravone as add-on therapy.
Overall Level of Certainty:
Low
Strength of Recommendation:
Strong
⨁⨁◯◯
Neuroprotective agents
Q14. Should we routinely give edaravone as an add-on therapy among
patients with acute stroke?
RECOMMENDATION 14b:
Among patients with acute intracerebral hemorrhagic stroke, we do not recommend
the routine use of edaravone as add-on therapy.
Overall Level of Certainty:
Low
Strength of Recommendation:
Strong
⨁⨁◯◯
Neuroprotective agents
Q15. Should we give citicoline as an add-on therapy for adult patients
with acute stroke?
RECOMMENDATION 15:
Among patients with acute stroke, we do not recommend the use of citicoline as an addon therapy.
Overall Level of Certainty:
Strength of Recommendation:
Moderate
Strong
⨁⨁⨁◯
Neuroprotective agents
Q16. Should we give Cerebrolysin® as an add-on therapy for patients
with acute ischemic stroke?
RECOMMENDATION 16:
Among patients with acute ischemic stroke, we do not recommend the use of
Cerebrolysin® as an add-on therapy.
Overall Level of Certainty:
Low
Strength of Recommendation:
Strong
⨁⨁◯◯
Neuroprotective agents
Q17. Should we give NeuroAiDTM as an add-on therapy for adult patients
with acute ischemic stroke?
RECOMMENDATION 17:
Among patients with acute ischemic stroke, we do not recommend the use of NeuroAiDTM.
Overall Level of Certainty:
Very Low
Strength of Recommendation:
Strong
⨁◯◯◯
Referrences
Thank you.