PPT

1. DEFINITIONS

2. A stroke
* Acute neurologic injury that occurs as a result of ischemic cerebral
infarction (80%) or brain hemorrhage (20% ).
Transient ischemic attack (TIA)
*modern tissue-based definitions is defined as a transient episode of
neurologic dysfunction caused by focal brain, spinal cord, or retinal
ischemia, without acute infarction.(ischemic stroke is defined as an
infarction of CNS tissue).
*classic time-based definitions of TIA
sudden onset of a focal neurologic symptom and/or sign lasting less
than 24 hours, presumably brought on by a transient decrease in blood
supply, which rendered the brain ischemic in the area producing the
symptom.
*Stroke, also known as cerebrovascular accident (CVA), cerebrovascular
insult (CVI), or brain attack

3. 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.

4. CLASSIFICATION

5. STROKE
(CVA or CVI
or
BRAIN
ATTACK)
ISCHEMIC
(80%)
THROMBOTIC
large V & small V (lacunars)
EMBOLIC
HYPOPERFUSION
HEMORRHAGIC
(20% )
INTRA-
AXIAL.H
(blood inside the
brain)
INTRAPARENCHYMAL
INTRAVENTRICULAR
EXTRA-
AXIAL.H
(bl outside the
brain, but still inside
the cranium)
EPIDURAL
SUBDURAL
SUBARACHNOID

6. Differentiation between stroke subtypes

7. Stroke type Clinical course Risk factors Other clues
ICH
Gradual
progression during
minutes or hours
HTN, trauma, bleeding
diatheses, illicit drugs (e g,
amphetamines, cocaine),
vascular malformations.
More common in blacks
and Asians than in whites.
precipitated by sex
or other physical
activity.
Patient may have
reduced alertness.
SAH
Abrupt onset of
sudden, severe
headache.
Focal Brain
dysfunction less
common than with
othertypes
Smoking, HTN, genetic
susceptibility
(eg, polycystic kidney
disease, family history of
SAH) and sympathomimetic
drugs (eg, cocaine)
precipitated by sex
or other physical
activity.
Patient
may have reduced
alertness.

8. Stroke type Clinical course Risk factors Other clues
Thrombotic
Stroke
Stuttering progression
with periods of
improvement.
Lacunes develop over
hours or at most a few
days.
Large artery ischemia
may evolve over
longer periods.
Atherosclerotic risk factors
(age, smoking, DM, etc.).
Men affected more than
women.
May have history of TIA.
May have
neck
bruit.
Embolic Stroke
Sudden onset with
deficit maximal at
onset.
Clinical findings may
improve quickly.
Atherosclerotic risk factors
as above.
Men more women. History
of heart disease (valvular,
AF, endocarditis).
ppt by getting
up at night to
urinate, or
sudden
coughing
or sneezing.

9. Clinical diagnosis of stroke subtypes
RISK FACTORS
ACTIVITY AT THE ONSET OR JUST BEFORE THE STROKE
ASSOCIATED SYMPTOMS
General physical examination
Neurologic examination
SILENT BRAIN INFARCTS
UMNL&LMNL
Cortical or subcortical stroke

10. UNMODIFIABLE
Prior stroke Male sex Older age Family history of stroke
MODIFIABLE FACTORS
Hypertension Cigarette smoking Dyslipidemia Diabetes
Abdominal obesity Alcoholism Lack of physical activity
High-risk diet (eg, high in saturated fats, and calories)
Psychosocial stress (eg, depression) Heart disorders (MI,AF,IE)
Hypercoagulability (thrombotic stroke only) Vasculitis
Intracranial aneurysms (subarachnoid hemorrhage only)
Use of certain drugs (eg, cocaine, amphetamines)
RISK FACTORS

11. DIFFERENTIAL DIAGNOSIS
 SPACE OCCUPYING LESION(TUMOR)
 SEIZURE
 MIGRAINE
 SUBDURAL HAEMATOMA
 METABOLIC DISTURBANCE LIKE HYPOGLYCAEMIA

12. Hypoglycemia
 That transient hypoglycemia may produce
a stroke like picture with hemiplegia and
aphasia has been known for years.
 The wide use of bedside rapid laboratory
testing for glucose now makes this easily
detectable and treatable. The hemiplegia
may resolve immediately with the
administration of intravenous glucose but
resolution over a hours is also reported

13. Space Occupying Lesions
 Subacute or chronic duration of symptoms,
however some patients may present with
acutely probably due to bleeding into a
tumour
 Associated with deep seated bursting
headache, projectile vomiting due raised ICT

14. SEIZURES AND POST ICTAL
STATES
 Traditional thought is that these postictal
symptoms are manifestations of seizure-
induced alterations in neuronal function
that are reversible; structural neuronal
alterations are not present. The postictal
weakness or Todd’s paralysis usually
follows partial motor seizures but may
follow generalized seizures as well.
Duration is usually brief but may last 48
hours

15. MIGRAINE
 Migraine may actually precipitate a stroke, but
there is also a variant of migraine, hemiplegic
migraine, where unilateral hemiparesis outlasts
the headache. This is difficult if not impossible to
diagnose correctly at first presentation when it
must be regarded as a diagnosis of exclusion; only
with recurrent, stereotypic attacks can this be
suspected. Cases with alternating hemiplegia
have been reported. At times this disorder has
been shown to be familial.

16. ACTIVITY AT THE ONSET OR JUST BEFORE THE STROKE
HEMORRHAGIC
STROKE
Physical activity
Sex
Trauma
ISCHEMIC STROKE
Morning hours
Sudden coughing and sneezing
Getting up during the night to urinate

17. ASSOCIATED SYMPTOMS

18. HEADACHE
*Severe headache at the onset of neurologic symptoms favors
SAH.
*Headache after symptom onset that is accompanied by
gradually increasing neurologic signs, decreased consciousness,
and vomiting is most often indicative of ICH.
*Headaches in the prodromal period before thrombotic strokes.
*A prior history of intermittent severe headaches that are
instantaneous in onset, persist for days, and prevent daily
activities often reflects the presence of an aneurysm.

19. VOMITING
*Vomiting is common in patients with ICH, SAH, and posterior
circulation large artery ischemia.
FEVER & INFECTIONS
*Fever raises the suspicion of endocarditis and resulting embolic
stroke.
*Infections activate acute phase blood reactants, predisposing to
thrombosis.
SEIZURES
*Seizures in the acute phase of stroke are more common in
hemorrhagic than ischemic stroke.

20. ALTERD MENTAL STATUS
*Hemorrhagic strokes.
*Thrombotic and embolic strokes that are large or involve the
posterior circulation large arteries.
*Ischemia involving the tegmentum of the pons.
*Large hemispheric infarcts are typically followed by edema that
can progress to coma.
Focal Signs
*Focal neurologic signs are suggestive of ICH, while the absence of
focal signs suggests SAH.

21. GENERAL PHYSICAL EXAMINATION

22. General physical examination
*Absent pulses (inferior extremity, radial, or carotid) favors a diagnosis
of atherosclerosis with thrombosis.
*Sudden onset of a cold, blue limb favors embolism.
*Occlusion of the common carotid artery in the neck can be diagnosed
by the absence of a carotid pulse.
*The presence of a neck bruit suggests the presence of, occlusive
extracranial disease.
*Cardiac findings, especially A F, murmurs and cardiac enlargement,
favor cardiac-origin embolism.
*Subhyaloid hemorrhages in the eye suggest a suddenly developing
brain or SAH.

23. NEUROLOGIC EXAMINATION

24. NEUROLOGIC EXAMINATION
*Weakness of the face, arm, and leg on one side of the body
unaccompanied by sensory, visual, or cognitive abnormalities (pure
motor stroke) favors the presence of a thrombotic stroke involving
penetrating arteries or a small ICH.
*Large focal neurologic deficits that begin abruptly or progress quickly
are characteristic of embolism or ICH.
*Abnormalities of language suggest anterior circulation disease, as
does the presence of motor and sensory signs on the same side of the
body .
*Vertigo, staggering, diplopia, deafness, crossed symptoms (one side
of the face and other side of the body), bilateral motor and/or sensory
signs, and hemianopsia suggest involvement of the posterior
circulation.
* The sudden onset of impaired consciousness in the absence of focal
neurologic signs is characteristic of SAH.

25. SILENT BRAIN INFARCTS
*Silent brain infarcts are infarcts identified only by neuroimaging.
*There is no accompanying clinical history of stroke or TIA.
*This relationship is somewhat clouded because a more detailed
history may elicit symptoms to suggest that a lesion is not truly silent.
*In addition, these lesions seem to be associated with cognitive
deficits.
*More appropriate to refer to these clinically unrecognized lesions as
covert brain infarcts.
*Patients with TIA and minor stroke appear to have a high risk of
covert infarcts as well as clinically symptomatic infarcts.

26. UPPER AND LOWER MOTOR NEURON LESION
(UMNL&LMNL )

27. UMNL LMNL
Paralysis Spastic- clasp knife-affect
movement-hypertonic
Flaccid- affect
muscles-hypotonic
weakness Without Atrophy ( only
Disuse)
With Atrophy
D T R Hyperreflexia often with
clonus
Hyporeflexia or
absent
Babinski Sign extensor planter
Superficial Reflex Absent( abd reflex abscent) Present
Fasciculation
&Fibrillation
Present Absent

28. Spasticity
*Spasticity is a state of sustained increase in muscle tension in
response to muscle lengthening, in particular, with passive
movements.
*Increased resistance to passive movement in antigravity muscle
(flexor in arm, extensor in leg).
*Clasp Knife Phenomenon.
*Sign of Upper Motor Neuron Syndrome, especially IC lesion.
Rigidity
*Increased muscle tone, no increased DTR.
*Cogwheel Phenomenon
*Symptom of basal ganglia .

29. PSEUDOBULBAR PALSY BULBAR PALSY
LESION upper motor neuron lesion of
cranial nerves IX, X and XII.
lower motor neuron lesion
of cranial nerves IX, X and
XII.
BULBAR SYMPTOMS Dysphagia-Nasal regurgitation- dysarthria.
hoarseness of voice
QUADRIPLEGIA Present(Spastic) Absent
TONGUE (WASTED
&FASCICULATIONS)
Absent Present
PALATAL AND
PHARYNGEAL REFLEXES
Exaggerated Absent
JAW REFLEX Exaggerated(if the lesion is
above the pons).
Absent
EMOTIONAL&MOOD
CHANGES
may be present Absent

30. Causes
Bulbar palsy Pseudobulbar palsy
Motor neurone disease cause is bilateral CVAs affecting
the IC( commonest).
Brainstem CVA Multiple sclerosis
Guillain-Barre syndrome Motor neurone disease
Poliomyelitis High brainstem tumours
Subacute menignitis (carcinoma,
lymphoma)
Head injury
Neurosyphilis
Syringobulbia

31. Differentiating features between ant and post.
circulation stroke
Clinical features Post.circ Ant. circ
Vertigo Present Absent
Unsteadiness Present Absent
Crossed hemiplegia Present Absent
Bilateral deficits Present Absent
Cerebellar signs Present Absent
Ocular Present Absent
Dissociated sensory loss Present Absent
Horners syndrome Present Absent

32. CORTICAL OR SUBCORTICAL STROKE
Patient with any of the following signs may have a cortical
stroke, not subcortical stroke:
*gaze preference or gaze deviation
*expressive or receptive aphasia
*visual field deficits
*visual or spatial neglect

43. LABORATORY STUDIES

44. All patients
*Noncontrast brain CT or brain MRI.
*Serum glucose. *Oxygen saturation. *ECG
*Serum electrolytes, urea nitrogen, creatinine.
*CBC *Cardiac enzymes and troponin. *Coagulation profile.
SELECTED PATIENTS
*ABG if hypoxia is suspected.
*EEG if seizures are suspected.
*Chest radiograph if lung disease is suspected.
*Pregnancy test in women of child-bearing potential.
*Liver function tests *Toxicology screen *Blood alcohol level
BIOMARKER (Serum D-dimer )
*Useful in separating stroke subtypes.
*highest in those with cardioembolic strokes and cerebral venous thrombosis
*lowest in those with brain ischemia due to penetrating artery disease.
*In patients with large artery thromboembolism, D-dimer levels are lower than in
patients with cardiogenic embolism but higher than in those with penetrating
artery disease.

45. ACUTE STROKE MANAGEMENT

46. MAIN GOALS
*Ensure medical stability.
*Quickly reverse conditions that are contributing to the pt's
problem.
*Determine if pt with acute ischemic stroke are candidates for
thrombolytic therapy.
Evaluation and management
*Vital signs and ABC stabilization.
*Obtaining a rapid but accurate history and ex to help distinguish
between ischemic and hemorrhage stroke, and DD of acute stroke.
*Obtaining emergent brain CT or MRI and other important lab,
cardiac monitoring during the first 24 hours after the onset of
ischemic stroke .

47. *Assessing swallowing and preventing aspiration .
Position of the pt
*for patients in the acute phase of stroke who are at risk for
elevated intracranial pressure, aspiration, cardiopulmonary
decompensation, or oxygen desaturation, we recommend keeping
the head in neutral alignment with the body and elevating the head
of the bed to 30 degrees;
*for patients in the acute phase of stroke who are not at risk for
elevated intracranial pressure, aspiration, or worsening
cardiopulmonary status, we suggest keeping the head of bed flat (0
to 15 degree head-of-bed position)
Fever
*Evaluating and treating the source of fever; for patients with acute
stroke, we suggest maintaining normothermia for at least the first
several days after an acute stroke .

48. VOLUME DEPLETION AND ELECTROLYTE DISTURBANCES
* Intravascular volume depletion is frequent in the setting of acute
stroke, particularly in older adult patients, and may worsen cerebral
blood flow.
*For most patients with acute stroke and volume depletion, isotonic
saline without dextrose is the agent of choice for intravascular fluid
repletion and maintenance fluid therapy.
*Avoid excess free water (eg, as in ½ isotonic saline) because
hypotonic fluids may exacerbate cerebral edema in acute stroke and
are less useful than isotonic solutions for replacing intravascular
volume.
*Avoid fluids containing glucose, which may exacerbate
hyperglycemia.
* Fluid management must be individualized on the basis of
cardiovascular status, electrolyte disturbances, and other conditions
that may perturb fluid balance,In particular, hyponatremia following
SAH may be due to SIADH.

49. SERUM GLUCOSE
*Checking serum glucose.
* Low serum glucose (<60 mg/dL or 3.3 mmol/L) should be
corrected rapidly.
*Normoglycemia is the desired goal.
*Treatment with insulin if serum glucose concentrations >180
mg/dL (>10 mmol/L).

50. Management of blood pressure
Acute ischemic stroke
*For patients who will receive thrombolytic therapy,
antihypertensive treatment is recommended so that systolic blood
pressure is ≤185 mmHg and diastolic blood pressure is ≤110 mmHg.
*For patients who are not treated with thrombolytic therapy, we
suggest treating high blood pressure only if
1- Hypertension is extreme (systolic blood pressure >220 mmHg or
diastolic blood pressure >120 mmHg) OR
2- If the patient has another clear indication (active ischemic
coronary disease, heart failure, aortic dissection, hypertensive
encephalopathy, acute renal failure, or pre-eclampsia/eclampsia) .

51. *When treatment is indicated, we suggest cautious lowering of
blood pressure by approximately 15 percent during the first 24
hours after stroke onset.
Hemorrhagic stroke
*In both (ICH) and SAH, the approach to blood pressure lowering
must account for the potential benefits (eg, reducing further
bleeding) and risks (eg,reducing cerebral perfusion).
*Recommendations for blood pressure management in acute ICH
and SAH are discussed in detail separately.

52. Thrombolytic therapy (Alteplase)
*For eligible patients with acute ischemic stroke, we recommend
intravenous alteplase therapy(0.9mg /kg ivi over 60 min), provided
that treatment is initiated within three hours of clearly defined
symptom onset.
Inclusion criteria
*Clinical diagnosis of ischemic stroke causing measurable
neurologic deficit.
*Onset of symptoms <4.5 hours before beginning treatment; if the
exact time of stroke onset is not known, it is defined as the last
time the patient was known to be normal.
*Age ≥18 years.
*no contraindication .

53. Antithrombotic therapy
*there are two major classes of antithrombotic drugs that can be
used to treat acute ischemic stroke:
1- Antiplatele 2- Anticoagulants
ASPIRIN (160 to 325 mg daily)
*STARTING within 48 hours of presumed ischemic stroke onset.
*Reduce the risk of early recurrent ischemic stroke without a
major risk of early hemorrhagic complications and improved long-
term outcome.
* Although aspirin, clopidogrel, and the combination of aspirin-
extended-release dipyridamole are all acceptable options for
secondary stroke prevention, aspirin is the only antiplatelet agent
that has been established as effective for the very early treatment
of acute ischemic stroke.

54. *Clopidogrel is alternatives for patients intolerant to aspirin,
although the effectiveness of these antiplatelets in acute stroke is
not established.
*The use of dual antiplatelet therapy remains largely unproven,
with the exception that short-term treatment with clopidogrel
plus aspirin appears to be beneficial for high-risk TIA and minor
stroke in Asian populations .
*We recommend early dual antiplatelet treatment with
clopidogrel plus aspirin for 21 days, followed by clopidogrel
monotherapy through at least day 90, for Asian patients with
high-risk TIA (ie, ABCD2 score of ≥4) or minor stroke.

55. *Beyond the acute phase of ischemic stroke and TIA, long-term
antiplatelet therapy for secondary stroke prevention should be
continued with aspirin, clopidogrel, or the combination of aspirin-
extended-release dipyridamole.
*Aspirin and other antiplatelet agents may be used in
combination with subcutaneous heparin and low molecular
weight heparin for D V T prophylaxis.
*The available evidence suggests that early anticoagulation with
heparin or low molecular weight heparin is associated with a
higher mortality and worse outcomes compared with aspirin
treatment initiated within 48 hours of ischemic stroke onset .

56. *Antiplatelet agents should be started as early as possible after
the diagnosis of ischemic stroke is confirmed.
*Aspirin and other antithrombotic agents should not be given
alone or in combination for the first 24 hours following
treatment with intravenous alteplase.
*While parenteral anticoagulation is not recommended during
the first 48 hours after acute ischemic stroke, oral
anticoagulation is recommended for secondary stroke
prevention in patients with atrial fibrillation and other high risk
sources of cardiogenic embolism.
*The timing of its initiation for such patients is mainly
dependent on the size of the infarct, which is presumed to
correlate with the risk of hemorrhagic transformation.

57. • For medically stable patients with a small or moderate-sized
infarct, warfarin can be initiated soon (after 24 hours) after
admission with minimal risk of transformation to hemorrhagic
stroke, while withholding anticoagulation for two weeks is
generally recommended for those with large infarctions,
symptomatic hemorrhagic transformation, or poorly controlled
hypertension.
*Urgent anticoagulation is not recommended for the treatment of
patients with acute ischemic stroke . Statin therapy .
*For patients receiving statin therapy prior to stroke onset, we
suggest continuing statin treatment.

58. SAH
*The optimal therapy of hypertension in SAH is not clear.
*While lowering blood pressure may decrease the risk of
rebleeding, this benefit may be offset by an increased risk of
infarction.
*A decrease in systolic blood pressure to <160 mm Hg in the
setting of an unsecured aneurysm is reasonable.
*Agents such as labetalol, nicardipine, and enalapril are preferred.
*Nimodipine (60 mg po or NGT /4h) improve neurologic outcomes
in SAH.
* Nimodipineis started within four days of onset and is continued
for 21 days.

59. *Prophylactic antiepileptic drug (AED) therapy is not required in
all patients, but may be considered in some with unsecured
aneurysms and large concentrations of blood at the cortex.
*Seizures should be treated promptly.
*Continuation of AED therapy may not be necessary in patients
without acute seizures after the aneurysm is secured.
*AEDs are usually continued for approximately six months in
patients who have experienced an acute seizure (within seven
days) following SAH.

60. ACUTE ICH
Patients with acute ICH should be managed in an ICU.
1- General management issues include:
*D/C of all anticoagulant and antiplatelet drugs, and immediate
reversal of anticoagulant effects with the appropriate agents.
*Maintenance of normothermia and evaluation and treatment of
fever source.
*Normal saline initially should be used for maintenance and
replacement fluids.
*Treating hyperglycemia (elevated serum glucose >185 mg/dL
(>10.3 mmol/L) with insulin; hypoglycemia should be avoided.

61. *NPO until swallowing function is evaluated to prevent aspiration .
2-Management of of elevated ICP
*includes elevating the head of the bed to 30 degrees and use of
analgesia and sedation.
*Suggested iv agents for sedation are propofol, etomidate, or
midazolam.
*Suggested agents for analgesia and antitussive effect are
morphine or alfentanil.
*Invasive monitoring and treatment of ICP should be
considered for patients with GCS <8, those with clinical
evidence of transtentorial herniation, or those with
significant IVH or hydrocephalus.

62. *More aggressive therapies for reducing elevated ICP include
osmotic diuretics (eg, mannitol), ventricular catheter drainage of
cerebrospinal fluid, and neuromuscular blockade .
3-Blood pressure
*Severe elevations in blood pressure may worsen ICH by
representing a continued force for bleeding.
*Labetalol, esmolol, hydralazine, nitroprusside, and nitroglycerin
are useful iv agents for controlling BP.
*For patients with systolic blood pressure (SBP) >200 mmHg or
MAP >150 mmHg, we suggest aggressive reduction of B P with
continuous intravenous infusion of medication accompanied by
blood pressure monitoring every five minutes.

63. *For patients with SBP >180 mmHg or MAP >130 mmHg and
evidence or suspicion of elevated ICP, we suggest monitoring
ICP and reducing B P using intermittent or continuous
intravenous medication to keep cerebral perfusion pressure in
the range of 61 to 80 mmHg .
*For patients with SBP >180 mmHg or MAP >130 mmHg and no
evidence or suspicion of elevated ICP, we suggest a modest
reduction of B P to a target MAP of 110 mmHg or target blood
pressure of 160/90 mmHg using intermittent or continuous
intravenous medication accompanied by reexamination of the
patient every 15 minutes.

64. 4- antiepileptic treatment
*Appropriate iv antiepileptic treatment should be used to quickly
control seizures for patients with ICH and clinical seizures.
5-Cerebellar hemorrhages
*For patients with cerebellar hemorrhages >3 cm in diameter who
are deteriorating or who have brainstem compression and/or
hydrocephalus due to ventricular obstruction, we recommend
surgical removal of hemorrhage .
6- Treating hypertension is the most important step to reduce the
risk of ICH, and probably recurrent ICH.
7-Stopping smoking, heavy alcohol use, and cocaine use are also
recommended.

65. HAEMORRHAGIC LESION

66. ISCHAEMIC LESION