Stroke or Cerebrovascular incident, is defined as an abrupt onset of a neurological deficit that is attributable to a focal vascular cause. The clinical manifestations of stroke are highly variable because of the complex anatomy of the brain

1. STROKE
Vivek Dev
College of Medicine
Virgen Milagrosa University
Foundation

2. STROKE
• Stroke or Cerebrovascular incident, is defined as an abrupt onset of a
neurological deficit that is attributable to a focal vascular cause.
• The clinical manifestations of stroke are highly variable because of the
complex anatomy of the brain.

3. Risk Factors
• Age
• Gender (women more
likely to die)
• Race (African
Americans)
• Heredity
Non-modifiable

4. Risk Factors
• Asymptomatic carotid
stenosis
• Diabetes mellitus
• Heart disease, atrial
fibrillation
• Heavy alcohol
consumption
• Hypercoagulability
• Hyperlipidemia
• Hypertension
• Obesity
• Oral contraceptive use
• Physical inactivity
• Sickle cell disease
• Smoking
Modifiable

5. Etiology & Pathophysiology
• Brain requires constant supply of glucose and oxygen,
delivered by blood.
• Brain receives 15% of resting output and accounts for 20% of
total body oxygen consumption.
• Cerebral blood flow is maintained via auto regulation. Thus
the brain is highly aerobic tissue where oxygen is limiting
factor.

6. Etiology & Pathophysiology
• If blood flow is interrupted
– Neurologic metabolism is altered in 30 seconds
– Metabolism stops in 2 minutes
– Cell death occurs in 5 minutes

7. Etiology & Pathophysiology
• Atherosclerosis is a
major cause of stroke
– Can lead to
thrombus
formation and
contribute to
emboli

8. Etiology & Pathophysiology
• Around the core area of ischemia is a border zone
of reduced blood flow where ischemia is
potentially reversible
• If adequate blood flow can be restored early (<3
hours) and the ischemic cascade can be interrupted
– less brain damage and less neurologic function
lost

9. Transient Ischemic Attacks (TIA)
• Temporary focal loss of neurologic function caused by
ischemia (analogous to angina in CAD)
• Most resolve within 3 hours
• May be due to micro-emboli that temporarily block
blood flow
• A warning sign of progressive cerebrovascular disease

10. Types of Stroke
• Classification based on underlying
pathophysiologic findings
– Ischemic
• Thrombotic
• Embolic
– Hemorrhagic

11. Major Types of Stroke

12. Ischemic Stroke
• Result of inadequate blood flow to brain due to partial
or complete occlusion of an artery
• Constitute 85% of all strokes
• Most patients with ischemic stroke do not have a
decreased level of consciousness in the first 24 hours
• Symptoms often worsen during first 72 hours d/t
cerebral edema

13. Ischemic Stroke
• Thrombotic stroke
– Thrombosis occurs in relation to injury to a blood
vessel wall → blood clot
– Result of thrombosis or narrowing of the blood vessel
– Most common cause of stroke

14. Ischemic Stroke
• Thrombotic stroke
– Two-thirds are associated with HTN and diabetes
– Often preceded by a TIA

15. Ischemic Stroke
• Embolic stroke
– Embolus lodges in and occludes a cerebral artery
– Results in infarction and edema of the area supplied
by the vessel
– Second most common cause of stroke

16. Ischemic Stroke
• Embolic stroke
– Majority of emboli originate in heart, with plaque
breaking off from the endocardium and entering
circulation
– Associated with sudden, rapid occurrence of severe
clinical symptoms

17. Ischemic Stroke
• Embolic stroke
– Patient usually remains conscious although may have
a headache
– Recurrence is common unless the underlying cause is
aggressively treated

18. Hemorrhagic Stroke
• Account for approximately 15% of all strokes
• Result from bleeding into the brain tissue itself or
into the subarachnoid space or ventricles

19. Hemorrhagic Stroke
• Intracerebral hemorrhage
– Bleeding within the brain caused by a rupture of a vessel
– Hypertension is the most important cause
– Commonly occurs during activity

20. Hemorrhagic Stroke
• Intracerebral hemorrhage
– Often a sudden onset of symptoms that progress
over minutes to hours b/c of ongoing bleeding
– Manifestations include neurologic deficits,
headache, N & V, decreased levels of
consciousness, and HTN

21. Hemorrhagic Stroke
• Subarachnoid hemorrhage
– Bleeding into cerebrospinal space between the
arachnoid and pia mater
– Commonly caused by rupture of a cerebral
aneurysm

22. Manifestations of Stroke

23. Manifestations of Stroke
• Ischemic stroke
- Deficit at maximal onset
- Atherothrombotic stroke, usually occurs during sleep.
- Cardioembolic stroke, sudden onset of maximal deficit (< 5mins.)
with rapid improvement of initially massive symptoms.
• Hemorrhagic stroke
- Headache, vomiting, SBP >220 mmHg, impaired consciousness and
evolution of focal deficits over minutes to hours.

24. Manifestations of Stroke
(Anterior vs. Posterior circulation)

25. Manifestations of Stroke
Arterial Involvement

26. Manifestations of Stroke
(Lacunar Syndrome)
• < 1.5 cm in size
• Infarct involving deep brain structures: cerebral subcortical white
matter, basal ganglia, thalamus, pons and cerebellum.
• Intact higher cortical functions.
• Risk factors are diabetes and hypertension.
• Syndromes: pure motor, pure sensory, sensorimotor, dysarthria or
clumsy hand, ataxic hemiparesis.

27. Manifestations of Stroke
Manifestations of Right-Brain and Left-Brain Stroke

29. Diagnostic work-ups
1. Cranial CT Scan
• Gold standard
• initial diagnostic of choice to differentiate ischemic and hemorrhagic stroke
• Highly sensitive in detecting hemorrhage
2. CRANIAL MRI
• Higher sensitivity and specificity
• Better imaging for POSTERIOR circulation ischemic strokes
3. EEG
• Results show changes in brain activity that may be useful in diagnosing brain conditions after
an injury , stroke or brain tumor .

30. Diagnostic work-ups
4.Blood Chemistry
✓CBC – level of hemoglobin or presence of anemia
✓Urinalysis – presence of infection
✓FBS
✓Lipid Profile
✓Liver enzymes
✓Creatinine
✓Serum Electrolytes – Na, K, Ca
5. ECG – underlying cause for ischemic stroke such as embolic source in atrial fibrillation , ongoing myocardial ischemia ,
chronic myocardial injury and valvular abnormalities.
6. Chest X-ray – rule out pneumonia secondary to CoVID-!9
7. RTPCR – To check for the presence of the virus causing CoVID-19
8. Stool exam – To determine the cause of the diarrhea

31. Management
• Pharmacologic & Non-pharmacologic
• Impact of illness to the family
• Community awareness

34. The National Institutes
of Health Stroke Scale
(NIHSS)

37. Motor- Left
Arm
2 (some effort
against gravity)
Motor- Left Leg 2 (some effort
against gravity)
Best Language 2 (severe
Aphasia)
6 (Moderate
stroke)

38. EARLY SPECIFIC MANAGEMENT OF ISHEMIC STROKE
A.THROMBOLYTIC THERAPY
B.ANTITHROMBOTIC THERAPY
C.NEUROPROTECTION

39. THROMBOLYTIC THERAPY
• IV Recombinant Tissue Plasminogen Factor (r-tPA)
• Mechanism of Action:
• catalyzes the conversion of plasminogen to plasmin, the major enzyme
responsible for clot breakdown
• Plasmin remodels the thrombus and limits its extension by proteolytic digestion
of fibrin
• Give within 3 hours of stroke onset at 0.9 mg/kg (max of 90 mg)
• 10 % of total dose given as IV bolus
• Rest given as infusion over 60 minutes
• Patients given r-tPA should not receive antiplatelets or anticoagulants within 24 hours
of treatment

40. ANTITHROMBOLYTIC THERAPY
Aspirin
– Mechanism of Action:
• Aspirin irreversibly inhibits platelet COX so that aspirin’s antiplatelet effect lasts 8–10 days (the
life of the platelet).
– Clinical Uses:
• Aspirin decreases the incidence of transient ischemic attacks, unstable angina, coronary artery
thrombosis with myocardial infarction, and thrombosis after coronary artery bypass grafting
– Adverse Effects:
• Gastric upset (intolerance) and Gastric and duodenal ulcers. Hepatotoxicity, asthma, rashes, GI
bleeding, and renal toxicity rarely if ever occur at antithrombotic doses.
– Start ASA 160-325 mg/day as early as possible and continue for 14 days
– Long – term ASA 80-100 mg/day monotherapy for secondary stroke prevention

41. NEUROPROTECTION
THE 5 “H” PRINCIPLE
Avoid Hypotension • Target mean arterial pressure (MAP): 110-130
mmHg
Avoid Hypoxemia • Target O2 Sat: >94%
• Monitor O2 saturation via pulse oximeter and/or
check ABGs
Avoid Hypoglycemia or Hyperglycemia • Target CBG: 140-180 mg/dL
• No benefit with intensive glycemic control after
stroke
• Use isotonic saline (0.9% NaCl) and avoid glucose-
containing (D5) IV fluids
Avoid Hyperthermia • Target: normothermia
• Relative risk of death or disability increases
twofold for every 1°C increase in body
temperature
• Treat fever with antipyretics and cooling blankets;
work-up for source of fever

42. NEUROPROTECTIVE
• Citicoline
• Mechanism of Action:
– naturally occurring endogenous nucleoside involved in the biosynthesis of lecithin.
– increases the synthesis of phosphatidylcholine (main neuronal membrane
phospholipid) and enhances acetylcholine production
– is claimed that it increases blood flow and oxygen consumption in the brain
• Dosage/Direction for Use
• Adult :
– PO Cerebrovascular disorders; Head injury; Parkinson’s disease; Cognitive disorder As
tab: 500 mg once daily or bid, or 1,000 mg once daily. As solution: 100-200 mg bid or
tid.
– IV/IM Cerebrovascular disorders; Head injury; Parkinson’s disease; Cognitive
disorder 500-1,000 mg/day.

43. NEUROPROTECTIVE
• Citicoline
• Adverse Reactions
Cardiac disorders: Bradycardia, tachycardia
Gastrointestinal disorders: Diarrhoea, epigastric discomfort, stomach pain.
General disorders and admin site conditions: Fatigue.
Nervous system disorders: Dizziness, headache.
Skin and subcutaneous tissue disorders: Rashes.
Vascular disorders: Hypotension

44. Impact of illness to the family
• Asses if the patient can cope with disclosure of his diagnosis
• Get the patient’s directives
• Ask the patient or legal guardian for the preferred management
• Open up possible palliative management
• Get informed consent

45. PSYCOSOCIAL ISSUES
• Fear of COVID
• Death and Dying
• Prime the patient and family
• Possible Palliative Care
• Financial
• Caregiver Fatigue

46. Community awareness
• Will there be advocacies for family and community?
- Patients with acute stroke often do not seek medical assistance on
their own because they may lose appreciation that something is wrong
(anosognosia) or lack the knowledge that acute treatment is
beneficial.
- Public awareness campaigns, to help raise awareness about the impact
of stroke and cancer and the importance of good healthcare system for
stroke and cancer.

47. Social Relevance

48. Social Relevance
• How should you conduct these?
- Develop population based policies that will reduce stroke
▪ Screening for blood pressure over the age of 40
▪ Healthy diets policy
▪ Physical activity policy
▪ Tobacco use policy
▪ Alcohol consumption policies.
- Cancer Medical Assistance
▪ DOH
▪ PCSO
▪ PWD Benefits
▪ SSS members
- Ensure better access to evidence based stroke and cancer treatments.
- Secure resources to develop stroke rehabilitation and support services.
Source: https://www.pfizer.com/Global_Stroke_Prevention_Policies.pdf

49. Collaborative Management
• If there was a need for referral, how would you prepare the patient?
- Determine and document the reason for the referral in the patient's medical
record.
- Explain to the patient why a referral is necessary, including what the patient
should expect from their visit with the specialist.
- Allow time for questions, and encourage the patient to ask questions during
the referral appointment.
- Contact the specialist directly to discuss the referral.
- Provide information on the patient’s current situation, as well as other medical records, test
results, and documents to avoid duplicate effort.
- Create a method for monitoring referrals.

50. Collaborative Management
• To what discipline shall you refer?
✓ Neurologist
✓ Oncologist
✓ Pulmonologist
✓ Palliative Care
✓ Geriatric Care

51. Research / EBM

53. CONCLUSIONS
Infection during hospitalization was not only associated with an increased risk of
recurrent stroke but also related to hemorrhagic transformation, combined
vascular events, and all-cause death during hospitalization. Ischemic stroke
patients with infection had a higher risk of hemorrhagic transformation and
intracerebral hemorrhage during hospitalization. Tissue ischemia and reperfusion
injury following AIS may increase vulnerability of cerebral vessels. Also, increased
inflammatory cytokinesand proteins following infection may intensify vascular
injurybypromoting endothelial dysfunction anddisrupture of blood-brainbarrier
and,therefore,maycontributetomorehemorrhagicevents.

55. Conclusions
Preclinical studies have suggested a large number of therapies that may have
to improve recovery from stroke. These are in various stages of translation,
with most at an early point of clinical trials. Principles of promoting
neuroplasticity in a clinical setting are emerging and have been reviewed
elsewhere. Issues unique to stroke recovery and rehabilitation studies are
increasingly being recognized and are important to effective clinical research
in this area. Many patients do not reach the hospital in time to receive
interventions that can reverse a stroke, and half of those who do receive such
therapies still show significant long-term disability. Restorative therapies that
aim to harness clinical neuroplasticity may be accessible by a large fraction of
patients with stroke and so hold the promise to reduce deficits and improve
function for a majority stroke survivors.

56. REFERENCES
• Harrison’s Principles of internal Medicine . 20th edition .
2018.
• Bates’ Guide to Physical Examination and History taking.
Bickley , Lynn. 11th edition . 2013
• IM Platinum 3rd edition .2018
• ACLS Acute Stroke Algorithm
• Basic & Clinical Pharmacology, 14th edition . Bertram G.
Katzung.
• American Heart Association
• https://www.ahajournals.org/doi/pdf/10.1161/STROKEAHA.1
20.029898
• https://www.j-stroke.org/upload/pdf/jos-2017-02796.pdf
• https://www.mims.com/philippines
• Pubmed.ncbi.nlm.nih.gov