This document provides an overview of strokes, including definitions, classifications, clinical features, investigations, and management approaches. It defines different types of strokes such as transient ischemic attack, minor stroke, and stroke in evolution. Key points covered include: initial assessment focuses on ABCs and identifying candidates for reperfusion therapies; imaging helps determine etiology and guides management; factors like fever, blood pressure, and swallowing require attention; and prevention of complications like DVT is important. Management differs between ischemic versus hemorrhagic strokes, with the latter requiring reversal of anticoagulation and surgical intervention in some cases. Prognostic scoring systems can estimate mortality from intracerebral hemorrhage.

1. STROKE
DR NAVIN ADHIKARI

2. Introduction
• A stroke is defined as an abrupt onset of a neurologic deficit
that is attributable to a focal vascular cause.
• Transient ischaemic attack (TIA) means a sudden focal deficit,
e.g. a weak limb, aphasia or loss of vision lasting from seconds
to 24 hours with complete recovery.
• Minor stroke -Patients recover without significant deficit,
usually within a week.
• Stroke in evolution is a stroke in which the focal neurological
deficit worsens after the patient first presents. Such
worsening may be due to increasing volume of infarction,
haemorrhagic transformation or increasing cerebral oedema.

3. Relevant Anatomy

20. Presenting symptoms
Weakness
Unilateral weakness is the classical presentation of stroke and,
much more rarely, of CVT.
It is sudden, progresses rapidly and follows a hemiplegic
pattern
Reflexes are initially reduced but then become increased with a
spastic pattern of increased tone .
Upper motor neuron weakness of the face (7th cranial nerve) is
often present.

21. • Dysphasia and dysarthria are the most common presentations
of disturbed speech in stroke.
• Dysphasia indicates damage to the dominant frontal or
parietal lobe
• Dysarthia is speech disturbance may be isolated to disruption
of sound output.
• can occur in association with lesions of the cerebellum,
brainstem and lower cranial nerves, as well as in myasthenia
or myopathic disease
• Dysphonia describes hoarse or whispered speech. The most
common cause is laryngitis, but dysphonia can also result
from a lesion of the 10th cranial nerve or disease of the vocal
cords.

24. Visual loss
• Visual loss can be due to unilateral optic ischaemia (called
amaurosis fugax if transient)
• caused by disturbance of blood flow in the internal carotid
artery and ophthalmic artery, leading to monocular blindness.
• Ischaemia of the occipital cortex or post-chiasmic nerve tracts
results in a contralateral hemianopia

25. • Damage to the non-dominant cortex often results in
contralateral visuo-spatial dysfunction.
• e.g. sensory or visual neglect and
• apraxia (inability to perform complex tasks despite normal
motor, sensory and cerebellar function).
• sometimes misdiagnosed as delirium.

26. • Stroke causing damage to the cerebellum and its connections
can present as an acute ataxia and there may be associated
brainstem features such as diplopia and vertigo.
• Sudden severe headache is the cardinal symptom of SAH but
also occurs in intracerebral haemorrhage.
• Seizure is unusual in acute stroke but may be generalised or
focal (especially in cerebral venous disease).

27. CLASSIFICATION AND ETIOLOGY

30. Intracranial hemorrhages
• Eidural hemorrhage
• Subdural Hemorrhage
• Sub arachnoid hemorrhages
• Intracranial hemorrhage

31. Causes of hemorrhagic strokes

32. CLINCAL FEATURES

39. INITIAL ASSESSMENT
• Ensuring medical stability, with particular attention to airway,
breathing, and circulation.
• Quickly reversing any conditions that are contributing to the
patient's problem.
• Determining if patients with acute ischemic stroke are
candidates for intravenous thrombolytic therapy or
endovascular thrombectomy
• Moving toward uncovering the pathophysiologic basis of the
patient's neurologic symptoms

40. ABC evaluation
• Decreased consciousness or bulbar dysfunction may be
unable to protect their airway.
• Those with increased intracranial pressure due to
hemorrhage, vertebrobasilar ischemia, or bihemispheric
ischemia can present with vomiting, decreased respiratory
drive, or muscular airway obstruction.
• Hypoventilation, with a resulting increase in carbon dioxide,
may lead to cerebral vasodilation and elevate intracranial
pressure.

41. REVERSING ANY CONDITIONS
• Look for the differential of stroke mimics with if possible
reversing the possible causes immediately.
• Migraine aura
• Seizure with postictal paresis (Todd paralysis),
• Functional deficit (conversion reaction)
• Hypertensive encephalopathy
• Head trauma
• Spinal cord disorder (eg, compressive myelopathy, spinal dural
arteriovenous fistula)
• Subdural hematoma
• Syncope
• Toxic-metabolic disturbance (eg, hypoglycemia, exogenous
drug intoxication)

42. CANDIDATES FOR REPERFUSION
THERAPIES
• Intravenous thrombolysis (IVT)
• Mechanical thrombectomy (MT)

43. IVT
• Alteplase — is the mainstay of treatment for acute ischemic
stroke, provided that treatment is initiated within 4.5 hours of
clearly defined symptom onset.
• Benefit by time to treatment — IVT with alteplase improves
functional outcome at three to six months when given within
4.5 hours of ischemic stroke onset

44. IMAGING SELECTION
• For those who wake-up with stroke, more than 4.5 hours
after last known well, or unknown time of symptom onset
• Acute ischemic brain lesion detected on diffusion magnetic
resonance imaging (MRI) but no corresponding hyperintensity
on fluid-attenuated inversion recovery (FLAIR) MRI. This
mismatch (diffusion positive/FLAIR negative) correlates with a
stroke onset time of 4.5 hours or less.

45. Inclusion Criteria

46. Exclusion Criteria

51. Scoring Systems
• Different scoring systems
• FAST
• BE-FAST
• ROSIER
• NIHSS
• Modified NIHSS

53. IMMEDIATE INVESTIGATION
• Noncontrast brain CT or brain MRI
• Finger stick blood glucose
• Oxygen saturation

54. • Other immediate tests for the evaluation of ischemic and
hemorrhagic stroke include the following
• Electrocardiogram
• Complete blood count including platelets
• Troponin
• Prothrombin time and international normalized ratio
(INR)
• Activated partial thromboplastin time

57. Management
Key issues to be addressed in all tyes of stroke
• fluid management
• treatment of abnormal blood glucose levels
• swallowing assessment
• Head and body position
• treatment of fever and infection
• blood pressure control

58. Fever
• Occurs in patients with a primary central nervous system
infection such as meningitis, subdural empyema, brain
abscess.
• In addition, common etiologies of fever including aspiration
pneumonia and urinary tract infection should also be
excluded.
• Source of fever should be investigated and treated
• antipyretics should be used to lower temperature in febrile
patients with acute stroke
• Fever is associated with unfavorable outcomes in human
studies of stroke.

59. BLOOD PRESSURE MANAGEMENT
• Acute ischemic stroke is inherently different from the
approach in acute hemorrhagic stroke in BP management.
• In acute ischemic stroke, blood pressure should not be
treated acutely unless the hypertension is extreme (systolic
blood pressure >220 mmHg or diastolic blood pressure >120
mmHg).
• Before thrombolytic therapy is started, treatment is
recommended so that systolic blood pressure is ≤185 mmHg
and diastolic blood pressure is ≤110 mmHg .
• The blood pressure should be stabilized and maintained at or
below 180/105 mmHg for at least 24 hours after thrombolytic
treatment.
• labetalol, nicardipine, and clevidipine as first-line

60. Blood pressure in acute hemorrhagic stroke
• In both intracerebral hemorrhage (ICH) and subarachnoid
hemorrhage (SAH), the approach to blood pressure
management must take into account the potential benefits
(eg, reducing further bleeding) and risks (eg, reducing
cerebral perfusion) of blood pressure lowering.
• Severely elevated blood pressure can worsen ICH by inciting
continued or recurrent bleeding and by causing hemorrhage
expansion and potentially worse outcomes.
• Lowering blood pressure rapidly could cause further injury by
promoting cerebral and systemic hypoperfusion

61. • For patients with acute ICH who present with systolic blood
pressure (SBP) between 150 and 220 mmHg, lowering of SBP
to a target of 140 mmHg, ideally within the first one hour of
presentation.
• For patients with acute ICH who present with SBP >220
mmHg, rapid lowering of SBP to <220 mmHg . Thereafter, the
blood pressure is gradually reduced (over a period of hours)
to a target range of 140 to 160 mmHg.
• nicardipine, labetalol, clevidipine, esmolol, enalaprilat, and
fenoldopam (table 4). Nitroprusside and nitroglycerin are
typically avoided because they may increase intracranial
pressure.

62. Ischemic stroke management
• Antithrombotic therapy with aspirin within 48 hrs.
• Prophylaxis for deep venous thrombosis and pulmonary
embolism
• Antithrombotic therapy at discharge
• Lipid lowering with high intensity statin therapy
• Blood pressure reduction after the acute phase of ischemic
stroke has passed
• Behavioral and lifestyle changes including smoking cessation,
exercise, weight reduction for patients with obesity.

68. Venous thromboembolism (VTE)
prophylaxis
• with intravenous thrombolysis for acute ischemic stroke, IPC
should be started on admission, while anticoagulation should
be delayed until 24 hours after intravenous thrombolysis.
• not treated with intravenous thrombolysis, IPC should be
started on admission, and low-dose heparin (LMW or
unfractionated) can be added for patients who are not being
treated with DAPT for minor stroke.
• For patients who are receiving oral anticoagulant therapy at
the time of acute ischemic stroke, IPC is started on admission.
Low-dose heparin (LMW or unfractionated) can be used for
VTE prophylaxis

69. • contraindication to any anticoagulation (eg, gastrointestinal or
other major systemic bleeding, or symptomatic hemorrhagic
transformation of ischemic infarction), IPC is used alone for
VTE prophylaxis.

70. Lipid lowering agents
• treatment with hydroxymethylglutaryl (HMG) CoA reductase
inhibitors (statins) decreases the risk of stroke, while some
other lipid lowering interventions (eg, fibrates, resins, diet)
have no significant impact on stroke incidence
• high-intensity statin therapy, independent of the baseline low-
density lipoprotein cholesterol (LDL-C), to reduce the risk of
stroke and cardiovascular events.
• treating with atorvastatin 80 mg/day, since this was the agent
and dose used in the Stroke Prevention by Aggressive
Reduction in Cholesterol Levels (SPARCL) trial that showed a
benefit for secondary ischemic stroke prevention.

71. Antihyertensive at discharge
• ASA guidelines, recommend resumption of antihypertensive
therapy for previously treated, neurologically stable patients
with known hypertension
• In addition, initiation of antihypertensive therapy for
previously untreated, neurologically stable patients with any
type of stroke or transient ischemic attack (TIA) who have an
established blood pressure.
• Initiation of antihypertensive without delay.
• with acute ischemic stroke, elevated blood pressures are
typically tolerated (ie, "permissive hypertension") during the
first 24 to 48 hours (the acute phase of an ischemic stroke) to
theoretically augment cerebral blood flow and reduce
expansion of the ischemic infarct core

72. • neurologically unstable with fluctuating deficits or progressive
deterioration, delay starting or resuming antihypertensive
drug therapy until the stroke-related deficits have stabilized or
reached a nadir since blood pressure lowering may induce
ischemic symptoms.

73. Hemorraghic stroke management
• Reverse anticoagulation
• Blood Pressure Management
• Intracranial Pressure Management
• Cerebrospinal fluid drainage for obstructive hydrocephalus
• Surgical decompression

74. Raised ICP
Osmotic therapy
Hypertonic saline for patients with evidence of life-threatening
or progressive deterioration (including patients with
herniation syndromes and those awaiting emergent surgery),
use high-concentration (23.4 percent) saline as an
intermittent bolus via a central intravenous line, typically 15
to 30 mL every six hours.
Continuous infusion of 3 percent saline (via peripheral or central
intravenous line) titrated to a sodium goal of approximately
145 to 155 mEq/L.

75. • Initial therapy and for patients with evidence of life-
threatening or progressive deterioration (including patients
with herniation syndromes and those awaiting emergent
surgery), use mannitol 1 g/kg as a bolus via a central
intravenous line. For other patients, use mannitol at a dose of
0.25 to 0.5 g/kg every six hours.
• Glucocorticoids should not be used to lower the ICP in most
patients with ICH due to lack of benefit and risk of infection
and hyperglycemia.

76. Surgical decomression
• Evacuation of supratentorial hematomas does not appear to
improve outcome for most patients.
• cerebellar hematomas >3 cm in diameter will require surgical
evacuation.
• Patients with hematomas between 1 and 3 cm require careful
observation
• hematoma is < 1 cm in diameter, surgical removal is usually
unnecessary.

78. Thirty-day mortality rates increased steadily with ICH score. The
mortality rates were:
• ICH score 1 (13 percent)
• ICH score 2 (26 percent)
• ICH score 3 (72 percent)
• ICH score 4 (97 percent)
• ICH score 5 (100 percent)

79. CVT

81. Management of CVT
• MR venography demonstrates a filling defect in the affected
vessel.
• Anticoagulation, initially with heparin followed by warfarin, is
beneficial, even in the presence of venous haemorrhage.
• Management of underlying causes and complications, such as
persistently raised intracranial pressure, is important.
• About 10% of cerebral venous sinus thrombosis, particularly
cavernous sinus thrombosis, is associated with infection (most
commonly Staphylococcus aureus), needing antibiotic
treatment.

82. SAH
• SAH typically presents with a sudden, severe, ‘thunderclap’
headache (often occipital), which lasts for hours or even days,
often accompanied by vomiting, raised blood pressure and
neck stiffness or pain.
• On examination, the patient is usually distressed and irritable,
with photophobia. There may be neck stiffness due to
subarachnoid blood but this may take some hours to develop.
• Fundoscopy may reveal a subhyaloid haemorrhage, which
represents blood tracking along the subarachnoid space
around the optic nerve

85. References
• Harrison's Principles of Internal Medicine,
20th Edition
• Davidsons Principle and Practice of Medicine
• Kumar & Clark's Clinical Medicine, 7th Edition
• Uptodate 2020