Transcript Neurovascular Emergencies Victor Politi, M.D., FACP Medical Director, SVCMC,

Neurovascular
Emergencies
Victor Politi, M.D., FACP
Medical Director, SVCMC,
School of Allied Health,
Physician Assistant Program
Anatomy

Skull
 closed

system/ unable to expand
Brain- 3 parts
 cerebellum
 cerebrum
 brain
stem
Spinal column
 Nerves

Anatomy

Cerebrum
 controls
higher mental function;
personality, memory, reason, senses

Cerebellum
 small
posterior portion of brain; coordinates
muscle movements and balance

Brainstem
 top
of the spinal cord, base of the brain;
controls vital functions like heart rate,
breathing, gag reflex
Anatomy

Meninges the
covering around the brain and spinal cord
 Three
layers
dura mater
arachnoid
pia mater
Anatomy

Cerebrospinal fluid
 fluid
that cushions the brain and spine and
helps circulate nutrients

Spinal cord
 Attached
to brainstem and carries information
between the body and brain
Neurological Changes

Neurological changes come from
 Hypoxia
 Pressure
Brain Injury - Hypoxia

Ischemia
 mismatch
between needed cerebral blood
flow and the amount of perfusion supplied

Injury
 After
a period of ischemia, the brain becomes
damaged

Infarction
 Irreversible
death of brain tissue
Neurological Changes

Reasons for increased ICP (pressure)
 Bleeding
 Edema
 Inflammation
 Tumor
Neurological Changes Bleeding

Bleeding
 aneurysm
 trauma
 CVA
 subdural
(SDH) - bleeding below the Dura
 Epidural- bleeding above the Dura
 Subarachnoid (SAH)
 Intracerebral- bleeding within the brain
Neurological Changes-EDEMA

Edema  general
swelling of brain tissue in response to
 trauma (injury)
 hypoxia (cellular death)
Neurological Changes 
Inflammation  infection

of brain tissue
Tumor  cancer
 arteriovenous
malformation (AVM)
Assessment of Neurological
Function

Level of consciousness
 Glasgow
Coma Scale (GCS) the standard
measure used to quantify level of
consciousness in head injury patients

Widely used in scoring systems, treatment
protocols and general clinical decision-making in
critically ill patients
Glasgow Coma Score
The GCS is scored between 3 and 15, 3
being the worst, 15 the best
 GCS is composed of 3 parameters: Best
Eye Response, Best Verbal Response,
Best Motor Response
 A GCS of 13 or higher correlates with a
mild brain injury, 9-12 is moderate injury
and 8 or less a severe brain injury

Glasgow Coma Scale


E (eye)+ M (motor) + V (verbal) = 3 to 15

90% less than or equal to 8 are in coma

Greater than or equal to 9 not in coma

8 is the critical score

Less than or equal to 8 at 6 hours - 50% die

9-11 = moderate severity

Greater than or equal to 12 = minor injury
Coma is defined as: (1) not opening eyes, (2) not
obeying commands, and (3) not uttering understandable
words.
Glasgow Coma Scale (GCS)

Measures best response
 Eyes
 Verbal
 Motor

scaled 1-4
scaled 1-5
scaled 1-6
Total 3-15
Glasgow Coma Scale (GCS)Eyes:
Score
Response
4
3
Eyes open
spontaneously
Eyes open to verbal
2
Eyes open to painful
1
Eyes do not open
Glasgow Coma Scale (GCS)Verbal:
Score
Response
5
Oriented
4
Confused
3
Incomprehensible
2
Moans
1
No verbal or Tubed
Glasgow Coma Scale (GCS)Motor:
Score
6
5
4
3
2
1
Response
Obeys commands
Localizes pain
Withdraws to painful stimuli
Posturing Flexion
Posturing Extension
No motor response
Assessment of Neurological Function
Decorticate Posturing
Seen when there is lesion of corticospinal
tract superior to level of brainstem
 indicated in comatose patient who
responds to sternal rub by full flexion of
the elbows, wrists, fingers, as well as
plantar flexion of feet with extension and
internal rotation of legs

Assessment of Neurological Function Decerebrate posturing
Seen in patients with lesions of brainstem
 patients exhibit extension of the arms,
flexion of the wrists, jaw-clenching, backarching, plantar flexion, neck extension,
either spontaneously or in response to
sternal rub

Assessment of Neurological Function Disability
Severe headache
 Confusion, disorientation, memory loss
 Abnormal or slurred speech
 Loss of vision or partial vision (one or both
eyes)
 Poor balance or lack of coordination
 Seizures
 Nausea/emesis

Assessment of Neurological Function Disability

Numbness, weakness, clumsiness or
paralysis of an arm, leg or side of the face
Cushing Triad
Increased BP
Decreased HR
Irregular Respirations
Cushing Triad

Increase in BP to overcome the increase
of pressure inside the skull
 Brain
trying to prevent infarct
Decreased HR to allow the heart to pump
more effectively and increase BP
 Cheyne-Stokes respirations to try to blow
off CO2

 CO2 is
a potent vasodilator
Cushing Triad

CO2 is a potent vasodilator
 Increase

of CO2 in the blood
Causes increase in blood volume intracranially
 Decrease

in CO2 in the blood
Causes decrease in blood volume intracranially
Cushing Triad

The body may attempt to decrease ICP by
reducing the blood volume in the skull
 this
is done by regulating the respiratory rate
Herniation
The increased ICP is forcing the brain
through the Foramen Magnum
 Signs and Symptoms:

 worsening
GCS
 sudden change in pupil response (dilation or
no responsiveness)
 Change in VS indicating Cushing's response
 General demise of patient
 (generally all must be occurring)
Herniation

Suspected herniation is the only time it is
acceptable to hyperventilate your patient
Treatment

Airway
 Increased
ICP may diminish or paralyze the
gag reflex

- allowing aspiration
 Suction
 Positioning

- C Spine ?
Treatment

Breathing
 severe
brain injury may interfere with
breathing center of the brain
be ready to BVM patient if necessary
 High flow oxygen (10-15 lpm)

Treatment

Circulation
 Treat

 IV
for shock
prevent hypotension - hypoxia and infarct of brain
tissue
initiate
assist with BP control
 med line if seizure

Treatment

Positioning
 What

can be done to assist flow into the skull
maintain blood pressure
 What
can be done to assist flow out of the
skull
HOB elevated to 30
 C-collar removed

Treatment

Communicate with the patient
 whether
they respond or not
 They may be awake and cannot communicate
Neurovascular Emergencies
TIA (transient ischemic attack)
 Stroke
 Hemorrhage
 Aneurysm
 Tumor
 Seizure
 Headache (“worst of life”)

Headache
Epidemiology





1-2% of visits to the emergency department
4% of visits to the physician’s office
Most have primary headache disorders
Among all patients with headache in an ED,
1% will have SAH
In patients with the worst ever headache of
their life, and normal neurological exam, 12%
will have SAH
Working classification of headache

Migraine (10% prevalence)

Tension-type headache(30-80%
prevalence) (CTH-2%)

Other headache (includes cluster HA and
secondary headaches)
Secondary headache disorders







Stroke, SAH
Tumour
Infection
Systemic disorders- thyroid disease, HT,
pheochromocytoma.
Temporal arteritis
Ophthalmological and ENT causes.
Traumatic
Danger signals





First or worst headaches
Headache on exertion, early morning, or
nocturnal
Progressive headache
New onset headache in adult >50 years old
Abnormal physical or neurological findings
(fever, stiff neck)
History

Past history of headaches
 “first,

Age of onset
>

worst, different, progressive, persistent”
50 years
Headache characteristics





Palliative
Quality
Region
Severity (0-10)
Timing
History

Associated Symptoms







Fever/Chills/Nightsweats
Nausea/Vomiting
Photophobia & Phonophobia
Neck pain or stiffness
Alterations in level of consciousness
Focal neurologic symptoms
Family History
Physical Examination

General Exam
 Vital
Signs
 General Appearance
 HEENT (Trauma, dentition, sinus/temples)
 Neck (ROM, Kernig’s and Brudzinski’s sign)
 Skin (Rash, bruising, hemorrhages)
 Lymph Nodes
Physical Examination

Neurologic Exam
 Mental
Status: LOC, Orientation, Language,
mood/thoughts
 Cranial









Nerves
I: Not tested unless history suggestive
II: Reading VA each eye, VF by confrontation with double
simultaneous stimulation, fundoscopy
III, IV, VI: Lateral and vertical eye mvts, pupillary light response
V: Pinprick and touch sensation on face
VII: Close eyes, show teeth
VIII: Whispered voice each ear
IX, X: Palate lifts in midline, gag present
XI: Shrug shoulders
XII: Protrude tongue
Physical Examination

Neurologic Exam (cont.)
 Limbs:









Each limb tested separately
Tone
Power of main muscle groups (0-5 MRC Scale)
Coordination: finger-to-nose, heel-to-shin
Tendon reflexes
Plantar response
Pinprick and light touch on hands and feet
Double simultaneous stimulation on hands and feet
Joint position sense in hallux and index finger
Vibration sense at ankle and index finger
 Gait
 Romberg’s
test
Laboratory Studies

Blood
 CBC
 Chemistry
panel
 ESR
 PT/PTT
(Consider hypercoagulable profile)
 TSH
 ABG
(if clinically indicated)
 Drug screen

Urinalysis
Imaging

X-rays
 CXR
 Cervical

Spine X-ray
Cranial computed tomography (CT)
 preferred
initial imaging study for acute headache
Cranial magnetic resonance imaging
(MRI)
 Magnetic resonance angiography
(MRA)
 Cerebral angiography

Other Studies

Lumbar puncture (LP)
 indicated
if acute or chronic meningitis, SAH,
pseudotumor cerebri (IIT) or low CSF
pressure headache suspected
 preferable to perform CT before LP

Electroencephalogram (EEG)
 indicated
if seizures are suspect
Differential Diagnosis

Primary headache
 Migraine
 Tension-type
headache
 Cluster headache
 Indomethacin-responsive headache
syndromes

Secondary headache
Secondary Headache DDx

Subarachnoid Hemorrhage (SAH)
 “first
or worst headache”
physicians consistently misdiagnose SAH
 pts with the greatest potential tx benefits are most
often misdiagnosed
 early complications develop in patients with an
incorrect dx


Meningitis
 associated
confusion
with fever, neck stiffness,
Secondary Headache DDx

Subdural hematoma


recent trauma (+/-)
Stroke (Ischemic or Hemorrhagic)
 occurs

Cervicocephalic arterial dissection
 trauma

with focal neurologic sx
hx (+/-), neck pain, ipsilateral Horner’s
Giant cell arteritis
>
50 yrs, visual loss, temporal pain,  ESR
Secondary Headache DDx

Dental: abscesses/TMJ


Sinusitis


sharp unilateral pain usually over maxillary distribution
Low CSF pressure headache


overdiagnosed, dx more likely with fever/purulent nasal
discharge
Trigeminal neuralgia


oral or jaw pain initially
sx resolve in supine position and recur when upright
Acute Glaucoma

periorbital pain, conjuntival injection, lens clouding
Subhyaloid hemorrhage
Physical findings in SAH






Nuchal rigidity
Altered consciousness,
Papilledema, retinal and subhyaloid
hemorrhage, 3rd and 6th nerve palsy,
Bilateral leg weakness, abulia,
Nystagmus, ataxia,
Aphasia, hemiparesis, left-sided visual
neglect
Diagnosis of SAH
25-51% of patients receive an incorrect
diagnosis
 91% of those with correct diagnosis
have a favorable outcome at 6 weeks
Vs 53% with an incorrect diagnosis
 Median delay in diagnosis(4 studies):
3 - 14 days

Reasons for misdiagnosis of
SAH
Failure to appreciate the spectrum of
clinical presentation
 Failure to understand the limitations of CT
 Failure to perform and correctly interpret
the results of LP

Indications for neuroimaging






First or worst headache
Progressive or CDH
Side-locked headache
Headaches not responding to treatment
New onset headache in patients with cancer,
HIV infection, or age >50 yrs
Associated fever, stiff neck, neurological
deficits
CT

versus
MRI
Preferred in

SAH

ICH



Posterior fossa
lesions
CVT
Meningeal disease
Cerebritis and
abscess
Pituitary pathology
SAH
L.P in evaluation of headache




Suspected SAH if CT is negative
(Deterioration after LP in patients with
clots on CT or a dilated pupil)
Start antibiotics in patients with suspected
meningitis, while waiting for CT
CSF pressure should be measured
Distinguish traumatic tap from true
hemorrhage
L.P in evaluation of headache
First or worst headache - SAH,
meningitis
 Headache with features s/o infectionmeningitis /encephalitis
 CVT - elevated CSF opening pressure

Probability of detecting
xanthochromia in CSF with
spectrophotometry after SAH
 12
hours
 1 week
 2 weeks
 3 weeks
 4 weeks
100%
100%
100%
>70%
>40%
Angiography
In proven SAH- 4 vessel angio to
identify source and r/o multiple
aneurysms
 Initial arteriogram negative in up
to 16% of SAH
 MRA detects 90% of saccular
aneurysms of >5mm
 Spiral CT angio detects 85% of
saccular aneurysms

Thunderclap headache
 Sudden
severe headache with
max intensity within 1 minute
 Normal CT scan
 Normal CSF study
 180 patients followed up for 1- 3
years. None developed SAH.
Wijdicks 1988, Markus 1991,
Linn 1994
Thunderclap headache
 Primary
causes- Migraine, benign
thunderclap headache, benign
orgasmic headache
 Secondary-unruptured saccular
aneurysm, cerebral vasospasm, CVT,
arterial dissection, pituitary apoplexy,
occipital neuralgia
Evans RW 2000
Cerebral Aneurysm
Cerebral aneurysm

The brain has many arterial blood vessels that
supply blood pumped by the heart. When the
wall of a blood vessel becomes weak and/or
thin, it forms a bulge or a bubble. This bulge or
bubble is called an aneurysm.

Aneurysms may also rupture, causing bleeding
in the brain. This bleeding results in
Subarachnoid Hemorrhage
Symptoms

Often asymptomatic

Focal neurological deficits depending on
location; for example, if the aneurysm
compresses the area of brain controlling the left
leg, then left leg weakness will occur.

Mild headaches

Nausea

Neck stiffness

Severe "thunderclap" headaches if the
aneurysm ruptures (Subarachnoid
Hemorrhage)
Causes

Genetic predisposition in persons
with polycystic kidney disease or
coarctation of the aorta

Cause often unknown
Exam

Focal neurological deficits

Neck stiffness if aneurysm has ruptured
Imaging

Cerebral Angiography (dye is injected into
the carotid artery to get an image of the
blood vessels of the brain)

CT scan will usually show bleeding after
an aneurysmal rupture

MRI
Laboratory Studies

Lumbar puncture (spinal tap) -cerebrospinal fluid will show blood after an
interval of time if there is aneurysm
rupture.

ECG- may cause EKG abnormalities

Subarachnoid hemorrhage may cause
heart abnormalities
Treatment

Unruptured aneurysms:
 Large Aneurysms are surgically
clipped at their bases to prevent
rupture.
 Small (less than 1/2 centimeter) ones
without symptoms are usually
followed with repeated cerebral
angiographies
Treatment

Ruptured aneurysms:
 Surgical clip placed at the base of the
aneurysm
 Aminocaproic acid may be
considered, but has complications
 Calcium channel blockers such as
Nimodipine may prevent spasm of the
artery where the aneurysm ruptured
STROKE
Stroke
3rd Leading cause of death in the United
States
 The mortality from the acute event is about
20%
 Leading cause of disability

Three Types of Stroke
Temporary or partially occluded blood flow
(TIA)
 Hemorrhagic stroke
 Ischemic (infarct) stroke

Stroke - Type 1

Temporary partial occlusion of blood flow
 TIA or
Transient ischemic attack
 nonpermanent deficits
 30% will have a stroke
Management of TIA
ASA
 Dipyridamole (Persantine)
 Ticlid
 Plavix
 Carotid Endarterectomy

Stroke - Type 2

Hemorrhage Stroke
 bleeding
in skull or brain (subarachnoid or
intracerebral)
 blood must be removed
 burst aneurysm

(the “worst headache of my life”)
Hemorrhagic Stroke




Only 1 out of every 5 strokes
30-day mortality of 30-50%
Occur in younger patient population
Two major categories  intracerebral
 subarachnoid hemorrhage
ICH

Majority of hemorrhagic strokes

Leading risk factors - increasing age,hx of prior stroke
Associated with




Chronic HTN
Amyloidosis
Other causes 
bleeding diathesis due to iatrogenic anticoagulation, vascular
malformation and cocaine use
SAH

Half as common as ICH

Half of all SAH due to berry aneurysm rupture
most commonly occurring at arterial bifurcations
or branchings

Arteriovenous malformations make up another
6% of all SAH
Stroke - Type 3

Ischemic (infarct) stroke
 70-80%
of all strokes
 can be reversed with “clot busters”
 occlusion or blockage
embolization (primarily from the carotid artery or
the heart)
 thrombosis
 low flow state

Ischemic Stroke

Three Major Categories
 Thrombotic
 Embolic
 Hypoperfusion
Ischemic Stroke
Stroke

Arteriosclerosis  what
occurs in the heart can occur in the brain
as well...
CAROTID ATHEROSCLEROSIS

The proximal internal carotid artery and the
carotid bifurcation are most frequently involved

Ulceration frequently occurs, placing the patient
at higher risk for embolization or thrombosis
Risk Factors




Hypertension
Hypercholesterolemia
Smoking



Diabetes mellitus
Obesity
Family history
The risk of stroke from carotid disease is highest
in patients who have recently sustained a
reversible neurologic event, such as a transient
ischemic attack
Clinical syndromes





Persistent, disabling neurologic deficit
Non-disabling strokes
Transient ischemic attacks (TIAs)
Reversible ischemic neurologic deficits
(RINDs)
Less commonly, patients present with
vertebrobasilar symptoms such as diplopia,
dizziness, dysarthria, visual loss, dysphagia,
or ataxia
RIND
Reversible Ischemic Neurological Deficit
(RIND)
 Admit and observe for signs of neurologic
changes
 Seizure precautions
 Repeat neuro exam and further studies
I.e. repeat ct/MRI/ Doppler

Evaluation of carotid artery stenosis
Carotid duplex ultrasonography
 Transcranial Doppler
 Computed tomographic angiography
 Magnetic resonance angiography (MRA)
 Carotid angiography (the gold standard)

ACUTE phase care
Turn to affected side
 Elevate HOB with neutral head alignment
 O2
 Anticoagulants
 Possibly anticonvulsants

ACUTE phase care
prevent straining
 prevent agitation/restlessness
 BP management

Diagnostics
Look for risk factors
 Carotid Doppler
 Complete cardiac work-up
 LP
 CT Scan
 MRI
 EEG

Differential Diagnosis of Acute Stroke











Hypoglycemia
Postictal paralysis (Todd’s paralysis)
Bell’s palsy
Hypertensive encephalopathy
Epidural/Subdural hematoma
Brain tumor/abscess
Complicated migraine
Encephalitis
Diabetic ketoacidosis
Hyperosmotic coma
Meningoencephalitis
What initial support should be given?
Oxygen
 BP management
 Cardiac Evaluation

What are the initial aids to dx and management ?
Blood tests (blood sugar)
 ECG
 Pulse Ox
 non-contrast CT scan
 Lumbar puncture when CT normal and
SAH suspect

Other Tests/Studies
MRI
 PET
 Doppler Study

Early Management

Ischemic Disease
 Consideration
of thrombolysis
 Consideration of anticoagulation
Early Management

Primary intracerebral hemorrhage
 Consideration
of operative intervention
ventricular shunt
 Hematoma evacuation

Early Management

Subarachnoid hemorrhage
 Consideration
of angiography
 Consideration of early operation
T.P.A. - Thrombolytics for CVA

When to Use

Time to Drug From Onset of Symptoms

Exclusion Criteria
Tissue Plasminogen Activator (TPA)

Medication approved by FDA for acute treatment
of stroke

Must be given within 3 hours of neurologic
symptoms(numbness, tingling, weakness, speech problems,
language difficulties), while awake
Tissue Plasminogen Activator (TPA)

IV r-TPA given in a dose of 0.9mg/kg up to a maximum
of 90mg - 10% of the dose in a bolus and the remainder
infused over one hour


improves outcome after stroke when given very early and within
3 hours on onset of stroke in carefully selected persons.
The benefit persists over the long term (3 months)
Tissue Plasminogen Activator (TPA)
Contraindications

Patient selection and timing of symptoms are critical!

Symptoms not rapidly improving or resolved

No currently active internal bleeding

No illness predisposing to an increased risk of bleed
Tissue Plasminogen Activator (TPA)
Contraindications

No history of prior brain hemorrhage

No significant GI or GU bleeding in past 3 months

No known stroke, serious head trauma, or brain surgery
in past 3 months

No lumbar puncture or arterial puncture in past week
Tissue Plasminogen Activator (TPA) Contraindications






No pregnancy
Diastolic BP < or = 110 and systolic BP of < or = 185
Platelet count less than 100,000/mm3
No Major surgery within preceding 14 days
Blood glucose <50mg/dl or > 400mg/dl
recent MI
Unconsciousness


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A: Alcohol or acidosis
E: Epilepsy/environment
I: Infection
O: Overdose
U: Uremia
T: Trauma
I: Insulin
P: Psychosis
S: Stroke/Seizures
Seizures
Seizures
A short circuit of the brains electrical
energy
 Effects vary depending what part of the
brain is affected

Seizures
Epilepsy
 Head Injuries
 Hypoglycemia
 Hypoxia
 Poisoning
 Withdrawal

Seizures

Seizure Types (4 types)
 Grand
mal
 Focal motor
 Petit mal
 Febrile
Grand Mal

Three phases
 Tonic
- muscle rigidity
 Clonic-violent, rhythmic, jerking of extremities
 Postictal - decreased LOC
Grand mal signs
Loss of consciousness
 loss of bowel and bladder
 cyanosis or dusky appearance

 hypoxia
from diaphragm seizing too
Grand mal seizure emergencies
Seizure lasts more than 5 minutes
 recovery from seizure is slow
 second seizure follows immediately (status
epilepticus)
 person having seizure is pregnant
 Signs of illness or injury are present

Focal Seizure

Focal seizure (temporal lobe)
 1-2
minute loss of consciousness
 bizarre behavior
smacking of lips
 picking at things
 swallowing

 postictal
like episode after
Petit mal seizures
Start with children 6-12
 Brief, sudden lapses in consciousness
 Small jerks of face or arms
 No post ictal period

Febrile seizures
High temperature
 5% of children (6 months to 6 years)
 Can run in families
 Tylenol/Motrin
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What is the most appropriate
work-up ?

Most patients present with a motor
convulsion - and are initially evaluated in
the ED
History

Once it is determined that the patient had
a seizure  In
case of a previously documented &
evaluated seizure disorder - typical attack little further evaluation is required
 Is patient taking anticonvulsant medications
? Any change in medication
 ? Missed dose,etc.

History

If there is no previous history of seizures a
much more detailed hx is needed
 Any
symptoms of previously unrecognized
seizures?
 Any other neurologic symptoms?
 Any systemic illness ?
 Any drug ingestion/alcohol use?
 Family Hx?
Neurologic Exam
Evaluate patients level of consciousness
and mentation - serial exams
 Any signs of increased intracranial
pressure?
 Any focal weakness or reflex change?

Neurologic Dysfunction

Shortly after a seizure, this dysfunction
can be identified which represents Todd’s
paralysis (postictal focal cerebral
dysfunction) and localizes seizure onset;

it resolves within minutes to hours
Treatment
ED treatment will vary depending upon the
specific clinical situation
 Four scenarios

 The
acute seizure
 Patient with previous epilepsy had a recent
seizure
 Patient with first seizure
 Patient in status epilepticus
Treatment
Protect patient from harm (do not forcibly
restrain)
 Roll patient on their side
 Do not put anything in their mouth

 they
will not swallow their tongue
 bite it - maybe but not swallow it
Treatment
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Protect patient from injury
IV line established
Endotracheal intubation -if necessary
Nasogastric tube -if necessary
Initial blood work blood
glucose, electrolytes, where indicated serum toxicology screens and anticonvulsant
levels
 In cases of prolonged seizure - CK levels and
urine myoglobin should be done
Treatment

Lumbar puncture -rarely indicated (difficult)
 If
bacterial meningitis suspect - empiric antibiotic
therapy should be started

Radiographic studies
 CT

scan (delayed until seizure controlled)
Thiamine /glucose given IV is hypoglycemia
suspected/confirmed