4. Acute Ischemic Stroke
AIS is caused by the sudden loss of blood circulation to an
area of the brain resulting in ischemia and corresponding
loss of neurological function.
Within seconds to minutes of loss of perfusion, an
ischemic cascade is unleashed resulting in a central area
of irreversible infarction surrounded by an area of
potentially reversible ischemic penumbra.
Goal of treatment : To preserve the area of oligemia in the
ischemic penumbra. This is done by limiting the severity
of injury (neuronal protection) and by restoring blood flow
to the penumbra.
5. Presentation
No clinical feature reliably distinguishes AIS from
hemorrhagic stroke, though headache, N/V, and
altered mental status make hemorrhagic stroke more
likely.
Common symptoms of AIS include the abrupt onset
of hemiparesis, monocular visual loss, ataxia, vertigo,
aphasia, or sudden depressed level of
consciousness.
Establishing the onset of symptoms is essential when
considering possible thrombolytic therapy.
6. Transient Ischemic Attack
TIA’s are defined as a transient ischemic neurological
deficit that resolves within 24 hours
80% resolve within 60 minutes
TIA’s precede 30% of AIS
Left untreated, 30% of TIA’s progress to AIS (20%
within the first month and 50% within the first year)
7. Physical Exam.
Goal of PE is to look for extra cranial causes of AIS and
to distinguish AIS from stroke mimics (seizures, tumors,
toxic-metabolic disturbances, positional vertigo, etc).
HEENT: Look for trauma signs and nuchal rigidity, listen
for cranial or cervical bruits, evaluate pulse strength.
Fundoscopy to look for emboli, hemorrhage,
papilledema.
C/V: Signs of CHF, Atrial fibrillation, arrhythmias.
Ext: Signs of venous thrombosis and arterial emboli.
17. Neurologic exam: AIS
Goal is to establish baseline for monitoring response to
therapy and to determine size and location of AIS
MS, CN, Motor, Coordination, Sensory and Gait need to be
covered, however speed is of the essence!
MCA: Contralateral : Hemiparesis, Hemianopsia and
Sensory loss
Ipsilateral: Gaze preference.
Dominant Hemisphere: Aphasia
Non-Dominant Hemisphere: Hemi-neglect and
cortical sensory deficits
18. Neurologic exam: AIS
ACA: Disinhibition, primitive reflexes, contralateral
hemiparesis (legs>arms), urinary incontinence.
PCA: Contralateral hemianopsia, cortical blindness,
altered mental status, impaired memory.
Vertebrobasilar: Vertigo, nystagmus, ataxia.
Crossed findings (ipsilateral cranial nerve deficits
along with contralateral long track signs).
Lacunar Infarcts: Pure motor, pure sensory,
ataxia/hemiparesis.
19. Work up: AIS
Labs: CBC with platelets, CMP, PT, PTT, cardiac
biomarkers, EKG.
Imaging: Emergent non-contrast CT
Distinguishes hemorrhagic from ischemic stroke
Defines age and anatomic distribution of stroke
Large hypodense area seen within 3 hours brings into
question of timing of AIS and may predict poor outcome
Hyperdense MCA sign
24. Other imaging studies: AIS
CT Angiography
MRI:
Diffusion-Perfusion mismatch (correlates to the core area of
infarction and surrounding area of the ischemic penumbra)
More sensitive than CT to early ischemic changes
MR Angiography
Conventional Cerebral Angiography
Echocardiography: (CHF, akinetic wall, vegetation/clots,
septal defects, PFO)
Carotid Doppler Ultrasound: Carotid stenosis evaluation
25. Treatment
ABCD’s
Airway: Intubation for GCS < 8 or lack of airway
protective reflexes
Breathing: O2 if hypoxic. Keep PCO2 32-36 mmHg
Circulation: Maintain adequate CPP (MAP-ICP).
Do not treat HTN unless > 200/120
D = Dextrose. Maintain normoglycemia (even if insulin is
needed) as hyperglycemia worsens neurological
outcome
26. Coma cocktail - DONT
Dextrose
Oxygen
Naloxone
Thiamine
Flumazanil?
27. Treatment : AIS
Fever: Hyperthermia worsens ischemic injury
Cerebral edema: Peaks 72-96 hours. Hyperventilation
can decrease CPP.
Mannitol may leak across compromised BBB. No
evidence of benefit for steroids.
Decompressive craniectomy and resection of necrotic
tissue may be indicated, especially in the setting of
hemorrhagic transformation.
Seizure control: Prophylactic AED is not indicated unless
malignant elevated ICP is present
28. Acute Thrombolysis:AIS
Balance restoration of blood flow and hemorrhage risk
No evidence of hemorrhage on CT
Hypodensity on CT < 1/3 of hemisphere
Onset of symptoms within 3 hours of rTPA use
SBP < 185 DBP < 110
INR < 1.7, Platelets > 100,000, No ASA or
anticoagulation, No trauma or recent surgery
rTPA: 0.9 mg/kg IV over 60 minutes with 10% of
dose given over the 1st minute
31. Intraventricular Hemorrhage
Accounts for 3% of all non-traumatic ICH
Hypertension is the most common etiology
Often results from an intraparenchymal hemorrhage
that extends into the ventricular system
S/S: Headache, N/V, Progressive deterioration of
consciousness, raised ICP, Nuchal rigidity
Survivors may develop post-hemorrhagic
hydrocephalus
32. Intraparenchymal Hemorrhage
Basal Ganglia Hemorrhage
Contralateral hemiparesis, hemichorea, hemisensory loss, and
hemi-neglect are common neurological deficits
34. Intraparenchymal Hemorrhage
Pontine Hemorrhage
Abrupt onset of coma, pinpoint pupils, autonomic
instability, horizontal gaze paralysis, and
quadriparesis
The miotic pupils and depressed LOC may mimic
opiate overdose
36. Intracranial Hemorrhage
Cerebellar Hemorrhage
Sudden onset of vertigo, severe N/V, and ataxia
altered mental status and coma over a few hours
Obstructive hydrocephalus can contribute to brainstem
herniation
Urgent posterior fossa decompression is essential for survival
39. Etiology: Intraparenchymal Hemorrhage
Hypertension is the #1 cause in adults
Anticoagulation and Anti-Platelet Meds
Systemic anticoagulated states (eg. DIC)
Aneurysms, AVM’s, Cavernous Angiomas
40. Treatment: ICH
ABCD’s
Intubation??
Treat Hypertension to keep SBP < 160 mmHg
Fluid and Electrolyte Management
Use Normal Saline, avoid Dextrose
Watch for SIADH and Cerebral Salt Wasting
Prevent Hyperthermia
Seizure Prophylaxis
Correct Underlying Coagulopathy
FFP, platelet Infusions, Vitamin K
41. Treatment :ICH
Recombinant Factor VII
Dosing ranges between 40 and 160 micrograms
Beneficial if given within 4 hours of onset
Risk of myocardial infarction and AIS
Management of ICP
Hyperventilate to keep PaCO2 around 30 mmHg
Avoid Mannitol (can leak into hematoma)
External Ventricular Drain (if hydrocep0halus present)
Surgical Evacuation of Hematoma (controversial)
42. Subarachnoid Hemorrhage
Aneurysmal rupture accounts for 80% of cases
Risk Factors
Advancing age, Smoking, HTN, Cocaine use, Hypertension,
Heavy Alcohol use, Connective Tissue Disorders, Sickle Cell
Disease, First Degree Relatives with Aneurysms
Fatality rate is 50% within 2 weeks
30% of survivors require lifelong care
15% of patients will have > 1 aneurysm
Outcome largely dependent on clinical presentation
and CT findings
43. Subarachnoid Hemorrhage
• Sudden-Onset “Thunderclap
Headache”
• “Worst Headache of my life”
• CN III palsy (p. comm aneurysm)
• CN VI palsy (raised ICP)
• Retinal Hemorrhages
• Altered Mental Status
• Nuchal Rigidity
Clinical
presenting
signs
44. Diagnostic Work Up
CT Imaging
Will pick up > 90% SAH (get thin cuts through skull
base)
Sensitivity drops to < 50% after 2 weeks
Carefully evaluate basilar cisterns for hemorrhage
45.
46. Diagnostic Work Up
Lumbar Puncture
Perform if high index of suspicion and negative CT
Elevated Opening Pressure
Increased RBC count that does not “clear” between tubes one and tube four
Xanthochromia (rule of 2’s)
Starts at 2 hours, Peaks at 2 days, Clears by 2 weeks
47. Diagnostic Work Up
Angiography
Digital Subtraction Angiography is gold standard
CT Angiography
MR Angiography
Look for Multiple Aneurysms
52. Status Epilepticus
Definitions
A single seizure or back-to-back seizures
without return of consciousness lasting
> 45 minutes (primate studies)
>30 minutes (WHO definition)
>10 minutes (working definition)
53. Etiologies
Idiopathic (24%) No precipitating event, pt is
neurologically and developmentally normal
Febrile (24%) Includes “febrile seizures” and
seizures in the setting of a febrile illness
Prior neurological insult or developmental
brain malformation
54. Etiologies
Vascular
Stroke (Hemorrhagic > Ischemic)
Subarachnoid Hemorrhage
Hypoxic Ischemic Encephalopathy
Toxic
Cocaine and other sympathomimetics
Alcohol withdrawal
Various Medications (Isoniazid, TCA’s, various
chemotherapy agents)
AED non-compliance or withdrawal
56. Status Epilepticus
History
Fever, pre-existing epilepsy, trauma, baseline AED’s and their dosing
Physical Exam
Signs of trauma, nuchal rigidity, end organ injury
Subtle signs of seizures (tachycardia, pupil dilation and hippus, nystagmus,
irregular respirations)
Work Up
Lytes, glucose, AED levels, CPK, LFT’s, ABG, ammonia
CT of brain
LP (when stable) if indicated. Empiric antibiotics.
57. Treatment
ABCD’s
Airway: Risk of aspiration,
suction to bedside
Breathing: Give
supplemental O2
C/V: Initial tachycardia
giving way to hypotension
(especially when
Benzos or Barbiturates
are given)
Dextrose: Symptomatic
hypoglycemia is causing
irreversible brain
injury until corrected
60. Long-Acting Anticonvulsant Therapy
Phenytoin
20 mg/kg over 20 minutes (regardless of weight)
C/R monitor during load
No dextrose in line
Extravasation injuries are severe
61. Long-Acting Anticonvulsant Therapy
Phenobarbital
20 mg/kg over 20 minutes
Watch for respiratory suppression (especially if the patient has received
Benzodiazepines)
Watch for hypotension
Good for Febrile Status Epilepticus
62. Refractory Status
Secure airway
Transfer to ICU
Extra lines for hypotension treatment
EEG Monitoring (electrical-clinical dissociation)
Medications
Pentobarbital
Other agents (Midazolam drip, Propofol, Lidocaine,
inhalation anesthetics, other AED’s)
63. Guillan-Barre´Syndrome
Progressive ascending weakness along with
various cranial neuropathies
Areflexia
Minimal sensory deficits (though radicular pain is
common)
Progression over days to 4 weeks
Preceding infection or Immunization: 1 to 4
weeks prior to onset of weakness (C. jejuni,
CMV, Mycoplasma, dT, OPV, VZV)
64. Physical Exam
Bulbar and Respiratory Compromise
Relatively Symmetric Ascending Weakness
Diminished/Absent DTR’s
No Sensory Level
Radicular Pain/Paresthesias
Autonomic Dysfunction: Increased or Decreased SNS or
PNS Function (tachy-brady arrhythmias,
hyper/hypotension, urinary retention,
decreased GI mobility)
65. Laboratory workup
CSF: Albuminocytological Dissociation
Elevated Protein without Pleocytosis
Nerve Conduction:
66. Treatment
ABC’s
Airway/Breathing: (Serial Examinations)
Forced Vital Capacity: (want > 15 ml/kg)
Negative Inspiratory Force (want > - 40 mmHg)
ABG’s : Look for rising Pa CO2
Clinical Exam (accessory muscles, SOB, diminished exhalation strength)
Elective Intubation if Respiratory Insufficiency or significant Bulbar Weakness
67. ABC’s
Cardiovascular
BP Monitoring
Careful when treating hypo or hypertension
Excessive Vagal Response with GI pain, Intubation, Tracheal
Suctioning and other Procedures
ICU Monitoring Until Patient Reaches Nadir of Weakness
68. IVIG
5 day infusion of 0.4 g/kg per day
Plasmapharesis
5 exchanges (40-50 ml/kg) given on alternate days using saline and
albumin as replacement fluid
No Role for Steroids
69. Outcome-GBS
10% to 20% require mechanical ventilation
Mortality 2% to 5%
After nadir, plateau phase lasts 2-4 weeks
70% complete recovery within 1 yr, 82% by 2 yrs
3% will go on to have relapse (CIDP)
71. Definition
Syncope is a symptom, the defining clinical
characteristics of which are:
• transient
• self-limited loss of consciousness
• leads to falling
• onset is relatively rapid
• recovery is spontaneous, complete, and
usually prompt
The underlying mechanism is a transient global
cerebral hypoperfusion
72. Classification of Syncope
Syncope must be differentiated from other
“non-syncopal” conditions which also lead
to transient loss of consciousness.
Pathophysiological classification is based on
the principal causes of the transient loss of
consciousness.
73. Real or apparent transient loss of consciousness
Syncope Non-syncopal attacks
• With partial or complete
loss of consciousness
• Without any impairment of
consciousness
75. Loss of consciousness: II - Non-syncopal
Partial or complete loss of consciousness
Metabolic Hypoxia,hyperventilation,
hypoglycemia
Epilepsy
Intoxication
Vertebro-basilar TIA
Any impairment of consciousness
Falls
Cataplexy
Drop attacks
Psychogenic ‘pseudo-syncope’ Fictitious disorders, malingering
and conversion
Carotid TIA
77. Management strategy
• Initial evaluation
(history, physical exam, ECG & BP supine/upright)
• Laboratory investigations guided by the
initial evaluation
• Treatment
The diagnostic strategy based on the initial
evaluation
79. Initial evaluation
Question 1
• Syncope or non-syncopal attack ?
Question 2
• Is heart disease present or absent ?
Question 3
• Which history of syncope ?
3 key questions:
80. Initial evaluation
Important historical features
1 - Questions about circumstances just prior to attack
• Position (supine, sitting or standing)
• Activity (supine, during or after exercise)
• Situation (urination, defecation, cough or swallowing)
• Predisposing factors (e.g., crowded or warm places, prolonged
standing, post-prandial period)
• Precipitating events (e.g., fear, intense pain, neck movements)
2 - Questions about onset of attack
• Nausea, vomiting, feeling of cold, sweating, aura, pain in neck
or shoulders
3 - Questions about attack (eyewitness)
• Skin colour (pallor, cyanotic)
• Duration of loss of consciousness
• Movements (tonic-clonic, etc)
• Tongue biting
81. Initial evaluation
Important historical features
5 - Questions about end of attack
Nausea, vomiting, diaphoresis, feeling of cold, confusion,
muscle aches, skin colour, wounds
6 - Questions about background
• Number and duration of syncopes
• Family history of arrhythmogenic disease
• Presence of cardiac disease
• Neurological history (Parkinsonism, epilepsy, narcolepsy)
• Internal history (diabetes, etc.)
• Medication (hypotensive and antidepressant agents)
82. Initial evaluation
Diagnostic criteria
• Vasovagal syncope is diagnosed if precipitating
events such as fear, severe pain, emotional
distress, instrumentation and prolonged standing
are associated with typical prodromal symptoms.
• Situational syncope is diagnosed if syncope
occurs during or immediately after urination,
defaecation, cough or swallowing.
• Orthostatic syncope is diagnosed when there is
documentation of orthostatic hypotension
associated with syncope or presyncope.
83. Initial evaluation
ECG diagnostic criteria
Syncope due to cardiac arrhythmia is diagnosed
in case of:
• Symptomatic sinus bradycardia <40 beats/min
or repetitive sino-atrial blocks or
sinus pauses >3 s.
• Mobitz II 2nd or 3rd degree atrioventricular block.
• Alternating left and right bundle branch block.
• Rapid paroxysmal supraventricular tachycardia
or ventricular tachycardia.
• Pacemaker malfunction with cardiac pauses.
84. Initial evaluation
ECG diagnostic criteria
Syncope due to cardiac ischemia
is diagnosed when symptoms are present with
ECG evidence of acute myocardial ischaemia
with or without myocardial infarction,
independently of its mechanism (*).
85. Clinical and ECG features that suggest a cardiac syncope
Presence of severe structural heart disease
Syncope during exertion or supine
Palpitations at the time of syncope
Suspected VT (e.g. heart failure or NSVT)
BBB
Mobitz 1 second degree AVB
Sinus bradycardia <50 bpm
WPW
Long QT
ARVD or Brugada Syndrome
86. Clinical and ECG features that suggest a neurally-mediated
syncope
Absence of cardiac disease.
Long history of syncope.
After sudden unexpected unpleasant sight, sound,
or smell.
Prolonged standing or crowded, warm places.
Nausea, vomiting associated with syncope.
During or in the absorptive state after a meal.
After exertion.
With head rotation, pressure on carotid sinus.
88. Certain or suspected heart disease
yes no
Cardiac evaluation
-Echocardiogram
-ECG monitoring
-Exercise test
-EP study
-ILR
NM evaluation
-Carotid sinus massage
-Tilt testing
-ATP test
-ILR
90. Treatment of Syncope:
General Principles
Principal goals of treatment:
Prevent recurrences
Reduce risk of mortality
Additional goals:
Prevent injuries associated with recurrences
Improve quality of life
91. Neurally-mediated syndromes: therapy
Initial treatment:
Education and reassurance
Sufficient for most
No treatment Single syncope and no high
risk settings
Additional treatment High risk or high frequency
settings
Recommendations
92. Treatment of Orthostatic
Hypotension
CAUSE TREATMENT
Drug-induced
autonomic
failure
Eliminate the offending
agent
Primary &
secondary
autonomic
failure
Modify physical factors
that influence systemic
blood pressure*
93. Treatment of Cardiac Arrhythmias
as Primary Cause
Treatment Goals:
Prevention of symptom recurrence
Improvement of quality of life
Reduction of mortality risk
94. Treatment of Cardiac Arrhythmias
Cardiac pacemaker therapy is indicated
Elimination of drugs that may increase susceptibility to
bradycardia should be considered
Catheter ablation for control of atrial arrhythmias
Sinus node dysfunction
(including bradycardia/tachycardia syndrome)
95. Metabolic Disturbances:
Hyperventilation
Hyperventilation resulting in hypocapnia and
transient alkalosis may be responsible for
confusional states or behavioral disturbances.
Clearcut distinction between such symptoms and
syncope may be difficult .
Frequently associated with anxiety episodes
and/or ‘panic’ attacks.
Recurrent faints associated with hyperventilation
should justify a psychiatric consultation.