Abdul Gofir

Stroke Unit Sardjito Hospital/Department of

Neurology Faculty of Medicine
Universitas Gadjah Mada
Anatomy and Physiology
 Brain Death Current Consensus

 Absent Cerebral Function

 Absent Brainstem Function

 Apnea
Normal Brain Anatomy
 Normal Brain Anatomy

Cerebral Cortex

Reticular
Activating
Brain Stem System
 Cerebral Cortex
 Cognition
 Voluntary Movement
 Sensation
Brain Stem
Brain Stem

Midbrain
Cranial Nerve III
 pupillary function
 eye movement
Brain Stem

Pons
Cranial Nerves IV, V, VI
 conjugate eye movement
 corneal reflex
Brain Stem

Medulla
Cranial Nerves IX, X
 Pharyngeal (Gag) Reflex
 Tracheal (Cough) Reflex
Respiration
 Reticular Activating
System

 Receives multiple
sensory inputs

 Mediates
wakefulness
Causes of Brain Death

Normal Cerebral Anoxia

Causes of Brain Death

Normal Cerebral Hemorrhage

Causes of Brain Death

Normal Subarachnoid Hemorrhage

Causes of Brain Death

Normal Trauma
Causes of Brain Death

Normal Meningitis
 Mechanism of Cerebral Death

Neuronal Injury Neuronal Swelling

ICP>MAP is
incompatible
with life

Decreased Intracranial Increased Intracranial

Blood Flow Pressure
Conditions Distinct From Brain
Death
 Persistent Vegetative State

 Locked-in Syndrome

 Minimally Responsive State

 Persistent Vegetative State

 Normal Sleep-Wake Cycles

 No Response to Environmental Stimuli

 Diffuse Brain Injury with Preservation of Brain

Stem Function
Locked-in Syndrome
Ventral Pontine Infarct

 Complete Paralysis

 Preserved Consciousness

 Preserved Eye Movement

Minimally Responsive State
Static Encephalopathy

 Diffuse or Multi-Focal Brain Injury

 Preserved Brain Stem Function

 Variable Interaction with Environmental Stimuli

Intracerebral Hemorrhage
 A 50-years-old American woman arrives at the hospital
with the abrupt onset of a left hemiparesis and right
gaze preference. Initially she is alert but becomes
increasingly obtunded. Her blood pressure is 220/110
mmHg
The History
 Age
 Sudden onset focal neurologic deficit
 Specific vascular territory
 Seizure at onset of Sx: 5%
 Headache at onset: 10-30%
 Fall or trauma at onset
Time of Symptom Onset
 Most difficult portion of the history
 Start when patient “was last seen normal”
 Work forward in time (TV guide)
 Patients that awake with symptoms -
onset = time of sleep
 Confirm with family, friends, care taker
 EMS - bring family along in ambulance
Physical Exam
 Vital signs are vital,
 but occasionally inaccurate
 C-Spine tenderness, pain
 BP in both arms,
symmetry of pulses
 Signs of trauma,
associated injuries
 Neurologic deficit -
characteristic vascular
distribution
Stroke Scales
 Severity
 NIH stroke scale 0-42, 0 = normal
valid, reproducible, assists in patient selection, facilitates
communication
 Functional Scales
 m-Rankin 0-5, 0 = normal
 Barthel index 100, 100 = normal
 Glasgow outcome 0-5, 5= normal
 in NINDS t-PA stroke trial, 0 = normal
Stroke Scales
 NIH stroke scale 0-42
0-5 mild/minor in most patients
5-15 moderate
15-20 moderately severe
> 20 very severe
underestimates volume of infarct in non-dominant (R)
hemispheric strokes
Diagnostic Testing
 Laboratory studies
 CBC, differential, platelets
 electrolyte profile, glucose (finger stick)
 INR, aPTT
 Troponin
 EKG
 CXR
Non-contrast CT of the Head
 Initial imaging study of choice
 Readily available
 Very sensitive for blood in the acute phase
 blood - 50-85 Hounsfield Units
 bone- 120 (70-200) Hounsfield Units
 Not sensitive for acute ischemic stroke
 nearly 100% sensitive by 7 days
 Posterior fossa structures - bone artifact
Non-contrast CT of the Head
 May shows early signs of ischemia in the 1st 3 hours
 loss of gray/white matter distinction
 hypodensity
 mass effect, edema
 hyperdense middle cerebral artery sign
 Re-evaluate the time of symptom onset, if early signs
of ischemia are present
ECT
2 hours

24 hours
Other Imaging Modalities
 MRI
 standard
 DWI/PWI
 Xenon CT
 Perfusion CT
 CT Angiography
Differential Diagnosis
 Deciphered by history, PE, diagnostics
 DDx:
TIA vascular disorders
seizure infections (endocarditis)
trauma complex migraine
mass lesions metabolic abnormalities
Stroke Vital Signs
Airway
Breathing
Circulation
C-spine
Glucose
Temperature
Airway Management
Upper airway patency

 Maintain C-Spine precautions

 Asses level of consciousness
 Inspect for loose dentures, foreign bodies
 Suction secretions
 Assess gag reflex, tongue control
Oxygenation and
Ventilation
 Respiratory rate and depth
 Signs of fatigue - Paradoxical respirations
 Breath sounds - (CHF, pneumonia,
COPD)
 Supplemental O2 with O2 sat > 95%
 Support with Basic airway techniques
 Ventilatory support as required
Basic airway techniques
 Foreign body removal
 Suction with rigid
suction device
 Positioning
 jaw thrust
 chin lift
 Nasal airway
 Bag valve mask
Advanced Airway
Management
 Rapid sequence intubation, orotracheal
 sedation and paralysis prevent increase in ICP
 Most common indications
 inability to maintain airway
 depressed level of consciousness
 need for hyperventilation to manage ICP
 Treat the underlying cause of respiratory
distress: CHF, MI, etc.
Monitoring of oxygenation
 Pulse oximetry
 indicator of oxygenation not ventilation
 falsely high in CO poisoning
 falsely low in PVOD, hypotension, peripheral
vasoconstriction
 ABG
 pCO2 allows eval of ventilation
 obtain from compressible site
 Supernormal oxygenation
 not of proven benefit
Circulation
 Goal: maintain cerebral perfusion
 Optimize cardiovascular status
 Monitor and reevaluate
Circulation
 Evaluate cardiac history and status
 Cardiac output
 preload
 afterload
 contractility
 stroke volume
Circulation
 Monitor vital signs Q 15 min in acute phase
 pulse (palpate in all 4 extremities)
 heart rate
 rhythm
 blood pressure (both arms)
 central venous pressure
ECG
 Cardiac Arrhythmia: 5% -30%
 Acute MI: 1%-2%
 ECG abnormalities
 more common with hemorrhagic
infarct
 T-Wave inversions
 nonspecific ST and T-wave changes
 Vascular Access
 Two peripheral IVs
 Use .9NS or .45 NS unless
hypotensive
 Use .9NS if hypotensive
 Replace blood products as indicated
Autoregulation
 The ability of the vasculature in the brain to
maintain a constant blood flow across a wide range
of blood pressures
 Autoregulation - impaired or lost in the area of the
infarction
 Ischemic tissues are perfusion dependant
 Autoregulation is shifted to higher pressure
patients with a history of HTN
Autoregulation
of Cerebral Blood Flow
100
CBF ml/100mg/min

Ischemic
80
Normotensive
60
Hypertensive
40

20

0
0

0
0

50

10

15

20

25

MAP mm Hg
Hypertension
Ischemic Stroke
 Loss of autoregulation
 Treat judiciously if at all
 Treatment guidelines - not receiving rt-PA
 AHA: MAP > 130 or Sys BP > 220
 MAP= [(2x DP)+SP]B3
 NSA: 220/115
Hypertension - Ischemic Stroke
 Drugs - short acting, titrate
 Labetalol
IV: 10-20 mg increments, double dose Q 20 min, max
cumulative dose 300mg
 Enalapril
Oral: 2.5 - 5.0 mg/day, max 40mg/day
IV : 0.625-1.25 mg IV Q 6hrs, max 5.0 Q 6 hrs
Hypertension -Ischemic
Stroke
 Nitroglycerine
Paste: 1-2 inches to skin
IV Drip: 5mcg/min, increase in increments of 5-10mcg
every 3-5 min
 Nitroprusside
IV Drip: 0.3 - 10 mcg/min/kg
Continuos BP monitoring
check thiocyanate levels
 AVOID NIFEDIPINE
Hypertension
Intracerebral Hemorrhage
 Treat aggressively
 Elevate head of bed
 Use labetalol, nitroglycerine, nitroprusside or lasix
 AVOID NIFEDIPINE
 Keep systolic < 160 mm Hg
diastolic < 100 mm Hg
 Hypotension
 More detrimental than hypertension
 Seek cause and treat aggressively
 CVP monitoring may be necessary
 Use .9 NS first to ensure adequate preload
 Then add vasopressors if needed
Hypertension: rt-PA Candidate
 Exclude for persistent BP > 185/110
 Check BP q 15 min
 May not aggressively lower BP to meet entry criteria
 Use Labetolol or Nitropaste
 Avoid Nifedipine
Glucose
 Worse outcome after stroke:
 diabetics
 acute hyperglycemia at time of infarct
 Mechanism uncertain
 increase in lactate in area of ischemia
 gene induction,
 increased number of spreading depolarizations
 Insulin is a neuroprotective
Glucose
 Avoid any IV fluids with D5
 instruct prehospital personnel not to give D50 as part of
the “coma cocktail” to acute stroke patients
 Check a finger stick ASAP
 treat only if low (< 50)
 Use insulin to establish euglycemia
Temperature
 Fever worsens outcome:
 for every 1°C rise in temp, risk of poor
outcome doubles (Reith, Lancet 1996)
 Greatest effect in the first 24 hours
 Brain temp is generally higher than core
 Treat aggressively with acetaminophen,
ibuprofen, or both
 Search for underlying cause
 Hypothermia currently under investigation
Seizures
 Occur in 5% of acute strokes
 Usually generalized tonic-clonic
 Possible causes:
severe strokes
cortical involvement
unstable tissue at risk
spreading depolarizations
hx of seizure disorder
Primary treatment of
AcuteIschemic Stroke
 Supportive care
 Aspirin
 IV thrombolysis
 No role for antithrombotics
Seizures
 Protect patient from injury during ictus
 Maintain airway
 Benzodiazepines:
 lorazepam (1-2 mg IV)
 diazepam (5-10 mg IV)
 Phenytoin:
 18 mg/kg loading dose, at 25-50 mg/min infusion
with cardiac monitor
 No need for prophylaxis
Summary
Evaluation
 History with time of symptom onset
 Physical exam
 trauma, NIHSS score
 Laboratory evaluation
 Non-contrast CT head
Supportive Care
Supportive Care
 Secure airway; basic and advanced methods
 Protect C-spine
 Assure oxygenation and ventilation
 Maximize perfusion, IV fluids
 Blood pressures (both arms), treat carefully
 Normalize the temperature and glucose
 Treat seizure if occurs
 Reevaluate
Neurologic Infection
 You are called to ER to see a 46-year-old woman for
“altered mental status”. On arrival, you find an Asian
woman complaining of headache, nausea and
vomiting. Her examination is notable for fever,
lethargy, papilledema, and nuchal rigidity.
History
 Time course of symptoms
 History of, risk factors for, and prior testing human
immunodefisiency virus (HIV)
 If HIV positive : CD4 count, hightly active
antiretroviral treatment history, opportunistic history,
and prophylaxis medication complience
 Other immunocompromised states
History
 Travel history
 Exposure
 Vaccinations/inoculations
 Time of year
 Por’t de entry of infection : pulmo, ears, nose, head
trauma, lumbal puncture
Physical Examination
 Vital signs : full set, including accurate rectal
temperature
 Head, eyes, ears, nose, and throat : be attentive for
facial rash, ear canal vesicles, thrush, parotitis, dental
abscess, mastoid tenderness
 Evaluate carefull for nuchal rigidity, meningismus and
range of motion
 Dematologic
Neurologic Examination
 Assess level of consciousness
 Assess of cranial nerve include Brainstem reflex
 Assess of meningeal signs
 Assess motor skills and reflex
 Assess gag reflex, tongue control
Diagnostic Evaluation
 Complete blood count, chemistry panel, Liver function
test, PTT, APTT, HIV, Lyme antibody, Tuberculin skin
test
 Blood culture, urinalysis and toxicology, sputum
culture
 Chest x-ray, ECG, cardiac monitoring, consider
transesophageal echocardiogram
 Lumbal puncture
 Imaging
 EEG
Treatment
 Treat immediately for bacterial meningitis
 Consider dexamethasone IV 10 mg every 6 hours for 4
days
 Virulent pathogens such as gram-negative bacterial
meningitis and Staphylococcus aureus meningitis
should be treated for minimum of 21 days and
sometimes longer depending on clinical response