This document presents a case report of a 75-year-old female patient who presented with right-sided body weakness and inability to speak for 1 hour. Her medical history includes hypertension for 25 years and ischemic heart disease for 10 years. On examination, she had right-sided facial weakness and numbness as well as aphasia. Diagnostic tests revealed an ischemic stroke likely due to an embolism. Her treatment plan included medications, oxygen therapy, and further tests such as echocardiography and carotid Doppler. The document then provides definitions and details on stroke types, risk factors, pathogenesis, management of ischemic and hemorrhagic strokes.

1. CASE PRESENTATION
Dr. Gauhar Mahmood Azeem
House Officer,
Medical Unit 4, Services Hospital Lahore.

2. Clinical History
• Biodata:
• A 75 year old female resident of Lahore presented to
Medical Emergency Services Hospital on the 1st of
December 2014 with complaints of
• Presenting Complaints:
• Right sided body weakness 1 hour
• Inability to talk 1 hour

3. Clinical History
• History of present illness:
Patient is a known hypertensive (25 years) and known
patient of IHD (10 years) and was relatively well 2 hours
back when while walking to the bathroom the patient fell
suddenly and after receiving help could not talk or move
the right arm or leg, there was also deviation of face to the
left…

4. Clinical History
• History of present illness:
…The weakness was sudden in onset, was not associated
with fits, up rolling of eyes, tongue bite, or urination. The
patient was previously mobile and has no history of
preceding fever, there is no history of vomiting, headaches,
or any such events before.

5. Clinical History
• Past History
• Hypertension 15 years
• Low ejection fraction 40% known for 6 months
• No history of diabetes, hepatitis, tuberculosis is there.

6. Clinical History
• Treatment History:
• Patient treated for an episode of shortness of breath 6
months back.
• Drug History:
• Patient taking
• Norvasc 5mg
• Ascard 75mg
• Loprin 75mg
• Drug compliance recently not good
• Patient not known allergic to any medication

7. Clinical History
• SocioEconomic History
• Higher Middle Class family.
• Owns own home.
• Occupational History
• Retired Professional banker.

8. Clinical History
• Family History
• Was positive for Hypertension, Diabetes and Ischemic
Heart Disease.

9. Examination
• Vitals
• Pulse: 118/min rate and rhythm irregularly irregular
• Blood Pressure: 160/80 mmHg
• Respiratory Rate: 16/min
• Temperature: 98’F
• Blood Sugar Random: 249 mg/dl

10. Examination
• Central Nervous System Examination
• GCS: M6 V1 E4 11/15
• Sensory loss not present.
• Right sided facial weakness, deviation to the left side.
• Patient has aphasia, dysphagia.
• Eye movement normal
• Power:
Right Arm 0/5 Left Arm 5/5
Right Leg 0/5 Left Leg 5/5

11. Examination
• Tone
• Increased in Right arm and leg. Normal in left arm and
leg.
• Reflexes
• Reflexes on the right side were exaggerated. Those on
left side were normal.
• Planters
• Right Plantar was up going.
• Left Plantar down going.

12. Examination
• Respiratory System
• Air entry equal on both sides, mild bilateral inspiratory
crepts.
• Gastrointestinal System
• Abdomen looks normal, no visceromegaly, no area of
tenderness, percussion note resonant, no shifting
dullness, bowel sounds present.

13. Examination
• Cardiovascular System
• Pulse Rate 118/min
• Pulse was irregularly irregular
• Mitral area 2 cm lateral to the mid-clavicular line.
• There was no abnormal heart sound appreciated and
finding on auscultation was irregularly irregular rhythm.

14. Investigations
• CBC
• Hb 8.6
• TLC 14.8
• Hct 28
• Platelets 351

15. Investigations
• LFT
• ALT 23 AST 19
• RFT
• Creatinine 0.6
• Serum Electrolytes
• Na+ 148 K+ 5.0
• PT 15 APTT 35

16. Investigations
• UCE
• Pus Cells 3-6
• Epithelial cells 1-2
• Cardiac Enzymes
• CPK 99 LDH 382 CKMB 15

17. ECG

18. CT Brain
• No areas of abnormal attenuation seen on CT scan.
• Normal Senile atrophic changes seen.
• Calcified Choroid Plexus.
• (60% of infarcts are seen within 3-6 hours and virtually all
are seen in 24 hours)

19. Differential Diagnosis
• Ischemic Stroke
• Hemorrhagic Stroke (CT scan rules this out)

20. Diagnosis
• Ischemic Stroke most likely due to Embolus

21. Treatment Plan
• INJ N/S x 1000CC x IV x BD
• INJ HEPARIN 1cc x SC x OD
• Tab ATORVA x 40mg x PO x OD
• Tab HERBESSER x 30mg x PO x TDS (diltiazem)
• Tab LOPRIN 75mg x 2 x PO x OD
• INJ RISEK x 40mg x IV x OD
• Oxygen inhalation to keep saturation O2 to 94-96%
• Ted Stocking, Chest Physio, Limb Physio.
• Planned CXR, Echocardiography, Carotic Doppler,
Fasting Lipid Profile.

22. STROKE

23. Definitions
• Stroke
• Clinical syndrome of rapid onset of focal deficits of brain function
lasting more than 24 hours or leading to death
• Transient Ischemic attack (TIA)
• Clinical syndrome of rapid onset of focal deficits of brain function
which resolves within 24 hours

24. Definitions
• Progressive Stroke
• A stroke in which the focal neurological deficits worsen with time
• Also called stroke in evolution
• Completed Stroke
• A stroke in which the focal neurological deficits persist and do not
worsen with time

25. Types of Stroke
• Ischemic
• Hemorrhagic

26. Risk Factors
• Ischemic Stroke
• Nonmodifiable risk factors include the
• Age
• Race
• Sex
• Ethnicity
• History of migraine headaches[21]
• Fibromuscular dysplasia
• Heredity: Family history of stroke or transient ischemic
attacks (TIAs)

27. Risk Factors
• Ischemic Stroke
• Modifiable Risk Factors
• Hypertension (the most important)
• Diabetes mellitus
• Cardiac disease: Atrial fibrillation, valvular disease, heart failure, mitral
stenosis, structural anomalies allowing right-to-left shunting (eg, patent
foramen ovale), and atrial and ventricular enlargement
• Hypercholesterolemia
• TIAs
• Carotid stenosis
• Hyperhomocystinemia
• Lifestyle issues: Excessive alcohol intake, tobacco use, illicit drug use,
physical inactivity[24]
• Obesity
• Oral contraceptive use/postmenopausal hormone use
• Sickle cell disease

28. Risk Factors
• Hemorrhagic Stroke
• Advanced age
• Hypertension (up to 60% of cases)
• Previous history of stroke
• Alcohol abuse
• Use of illicit drugs (eg, cocaine, other sympathomimetic
drugs)

29. Middle Cerebral Artery

30. Anterior Cerebral Artery

31. Posterior Cerebral Artery

32. Ischemic Stroke
• 80% of strokes
• Arterial occlusion of an intracranial vessel leads to
hypoperfusion of the brain region it supplies

33. Etiology
• Thrombotic
• Lacunar stroke
• Large vessel thrombosis
• Hypercoagulable
disorders
Systemic Hypoperfusion
Venous Thrombosis
• Embolic
• Artery to artery
• Carotid bifurcation
• Aortic arch
• Cardioembolic
• Atrial fibrillation
• Myocardial infarction
• Mural thrombus
• Bacterial endocarditis
• Mitral stenosis
• Paradoxical embolus

34. Thrombotic Stroke
• Atherosclerosis is the most common pathology leading
to thrombotic occlusion of blood vessels
• Hypercoagulable disorders – uncommon cause
• Antiphospholipid syndrome
• Sickle cell anemia
• Polycythemia vera
• Homocysteinemia
• Vasculitis: PAN, Wegener’s granulomatosis, giant cell
arteritis

35. Thrombotic Stroke
• Lacunar stroke
• Accounts for 20% of all strokes
• Results from occlusion of small deep penetrating arteries
of the brain
• Pathology: lipohyalinosis & microatheroma
• Thrombosis leads to small infarcts known as lacunes
• Clinically manifested as lacunar syndromes

36. Embolic Stroke
• Cardioembolic stroke
• Embolus from the heart gets lodged in intracranial vessels
• MCA most commonly affected
• Atrial fibrillation is the most common cause
• Others: MI, prosthetic valves, rheumatic heart disease
• Artery to artery embolism
• Thrombus formed on atherosclerotic plaques gets embolized to
intracranial vessels
• Carotid bifurcation atherosclerosis is the most comon source
• Others: aortic arch, vertebral arteries etc.

38. Pathophysiology of Ischemic Stroke
• Blood supply to the brain is auto-regulated
• Blood flow
• If zero leads to death of brain tissue within 4-10min
• <16-18ml/100g tissue/min infarction within an hour
• Ischemia leads to development of an ischemic core and
an ischemic penumbra

39. Ischemic Penumbra
• Tissue surrounding the core region of infarction which is
ischemic but reversibly dysfunctional
• Maintained by collaterals
• Can be salvaged if re-perfused in time
• Primary goal of revascularization therapies

40. Hemorrhagic Stroke
• Two types
• Intracerebral
hemorrhage(ICH)
• Subarachnoid
hemorrhage(SAH)
• Higher mortality rates
when compared to
ischemic stroke

41. Intracerebral Haemorrhage
• Result of chronic hypertension
• Small arteries are damaged due to hypertension
• In advanced stages vessel wall is disrupted and leads to
leakage
• Other causes: amyloid angiopathy, anticoagulant therapy,
cavernous hemangioma, cocaine, amphetamines

42. Subarachnoid Haemorrhage
• Most common cause is rupture of saccular or Berry
aneurysms
• Other causes include arteriovenous malformations,
angiomas, mycotic aneurysmal rupture etc.
• Associated with extremely severe headache

43. Pathophysiology of haemorrhagic stroke
• Explosive entry of blood into the brain parenchyma
structurally disrupts neurons
• White matter fibre tracts are split
• Immediate cessation of neuronal function
• Expanding hemorrhage can act as a mass lesion and
cause further progression of neurological deficits
• Large hemorrhages can cause transtentorial coning and
rapid death

44. Management

45. Management of Ischemic Stroke
• The central goal of therapy in acute ischemic stroke is to
preserve tissue in the ischemic penumbra, where
perfusion is decreased but sufficient to stave off infarction.
• ABC’s
• The goal for the emergent management of stroke is to
assess the patient’s airway, breathing, and circulation
(ABCs); stabilize the patient as necessary; and complete
initial evaluation and assessment, including imaging and
laboratory studies, within 60 minutes of patient arrival

46. Management of Ischemic Stroke
• Supplemental oxygen is recommended when the patient
has a documented oxygen requirement (ie, oxygen
saturation < 95%)
• In the small proportion of patients with stroke who are
relatively hypotensive, administration of IV fluid,
vasopressor therapy, or both may improve flow through
critical stenosis
• Hypoglycemia or hyperglycemia needs to be identified
and treated early in the evaluation.

47. Management of Ischemic Stroke
• Fibrinolytic Therapy
• With rtPA (alteplase) within 3-4.5 hours of symptoms
onset.
• Patient must meet the inclusion criteria and not have a
contraindication
Antiplatelet Therapy
• AHA/ASA guidelines recommend giving aspirin, 325 mg
orally, within 24-48 hours of ischemic stroke onset. The
benefit of aspirin is modest but statistically significant and
appears principally to involve the reduction of recurrent
stroke

48. Management of Ischemic Stroke
• Threshold for Blood Pressure lowering
Thresholds for antihypertensive treatment in acute
ischemic stroke patients who are not fibrinolysis
candidates, according to the 2013 ASA guidelines, are
systolic blood pressure higher than 220 mm Hg or diastolic
blood pressure above 120 mm Hg.
In those patients, a reasonable goal is to lower blood
pressure by 15% during the first 24 hours after onset of
stroke. Care must be taken to not lower blood pressure too
quickly or aggressively, since this could worsen perfusion in
the penumbra.

49. Management of Ischemic Stroke
• Fever Control
• Antipyretics are indicated for febrile stroke patients, since
hyperthermia accelerates ischemic neuronal injury.
Substantial experimental evidence suggests that mild
brain hypothermia is neuroprotective.
• Manage Cardiac Arrythmias eg in our case diltiazem was
given to manage AF
• In Cerebral Edema IV Mannitol can be given
• Pass NG tube if indicated, pass foleys.

50. Management of Ischemic Stroke
• Secondary prevention of stroke
• Platelet antiaggregants
• Antihypertensives
• Statins
• Lifestyle interventions
• Management of other conditions that may be contributing,
eg probable carotid endarterectomy for stenosis and
anticoagulation in valvular problems or AF
• Prevent pressure sores, aspirations, contractures, DVT

51. Management of Haemorrhagic Stroke
• The treatment and management of patients with acute
intracerebral hemorrhage depends on the cause and
severity of the bleeding. Basic life support, as well as
control of bleeding, seizures, blood pressure (BP), and
intracranial pressure, are critical.
• ICH is a neurological emergency and initial management
should be focused on assessing the patients airway,
breathing capability, blood pressure and signs of
increased intracranial pressure.

52. Management of Haemorrhagic Stroke
• The patient should be intubated based on risk of
aspiration, impending ventilatory failure (PaO2 < 60
mmHg or pCO2 > 50 mmHg), and signs of increased
intracranial pressure.
• Emergency measures for ICP control are appropriate for
stuporous or comatose patients, or those who present
acutely with clinical signs of brainstem herniation. The
head should be elevated to 30 degrees, 1.0–1.5 g/kg of
20% mannitol should be given by a rapid infusion, and the
patient should be hyperventilated to a pCO2 of 30–35
mmHg.

53. Management of Hemorrhagic Stroke
• In patients presenting with a systolic BP of 150 to 220 mm
Hg, acute lowering of systolic BP to 140 mm Hg is
probably safe.
• Management of seizures if any
• Acute management of seizures entail administering
intravenous lorazepam (0.05–0.10 mg/kg) followed by an
intravenous loading dose of phenytoin or fosphenytoin
(15–20 mg/kg), valproic acid (15–45 mg/kg), or
phenobarbital (15–20 mg/kg).

54. Management of Hemorrhagic Stroke
• If hemorrhage is due to anticoagulation, give Vitamin K,
FFP and PCC
• Fever should be treated aggressively because it is
independently associated with a poor outcome
• Neurosurgical Consultation