stroke and unconsciousness

7/29/2019 Stroke and Unconsciousness

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Abdul Gofir

Stroke Unit Sardjito Hospital/Department ofNeurology Faculty of Medicine

Universitas Gadjah Mada


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Anatomy and Physiology


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Brain Death Current Consensus

Absent Cerebral Function

Absent Brainstem Function

Apnea


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Normal Brain Anatomy


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Normal Brain Anatomy

Cerebral Cortex

Brain Stem

Reticular

Activating

System


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Cerebral Cortex Cognition

Voluntary Movement

Sensation


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Brain Stem


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Brain Stem

Midbrain

Cranial Nerve III

pupillary function

eye movement


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Brain Stem

Pons

Cranial Nerves IV, V, VI

conjugate eye movement

corneal reflex


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Brain Stem

Medulla

Cranial Nerves IX, X

Pharyngeal (Gag) Reflex

Tracheal (Cough) Reflex

Respiration


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Reticular Activating

System

Receives multiplesensory inputs

Mediates

wakefulness


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Causes of Brain Death

Normal Cerebral Anoxia


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Normal Cerebral Hemorrhage


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Normal Subarachnoid Hemorrhage


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Normal Trauma


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Normal Meningitis


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Mechanism of Cerebral Death

Neuronal Injury

Decreased IntracranialBlood Flow

Neuronal Swelling

Increased Intracranial

Pressure

ICP>MAP is

incompatible

with life


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Conditions Distinct From Brain

Death

Persistent Vegetative State

Locked-in Syndrome

Minimally Responsive State


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Persistent Vegetative State

Normal Sleep-Wake Cycles

No Response to Environmental Stimuli

Diffuse Brain Injury with Preservation of Brain

Stem Function


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Locked-in SyndromeVentral Pontine Infarct

Complete Paralysis

Preserved Consciousness

Preserved Eye Movement


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Minimally Responsive State

Diffuse or Multi-Focal Brain Injury

Preserved Brain Stem Function

Variable Interaction with Environmental Stimuli

Static Encephalopathy


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Intracerebral HemorrhageA 50-years-old American woman arrives at the hospital

with the abrupt onset of a left hemiparesis and rightgaze preference. Initially she is alert but becomes

increasingly obtunded. Her blood pressure is 220/110mmHg


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The HistoryAge

Sudden onset focal neurologic deficit

Specific vascular territory Seizure at onset of Sx: 5%

Headache at onset: 10-30%

Fall or trauma at onset


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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


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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 vasculardistribution


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Stroke Scales Severity NIH stroke scale 0-42, 0 = normal

valid, reproducible, assists in patient selection, facilitatescommunication

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


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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


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Diagnostic Testing Laboratory studies

CBC, differential, platelets

electrolyte profile, glucose (finger stick)

INR, aPTT

Troponin

EKG

CXR


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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


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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 signsof ischemia are present


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ECT2 hours

24 hours


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Other Imaging Modalities MRI standard

DWI/PWI

Xenon CT

Perfusion CT

CT Angiography


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Differential Diagnosis Deciphered by history, PE, diagnostics

DDx:

TIA vascular disordersseizure infections (endocarditis)

trauma complex migraine

mass lesions metabolic abnormalities


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Stroke Vital SignsAirway

Breathing

CirculationC-spine

Glucose

Temperature


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Airway ManagementUpper airway patency

Maintain C-Spine precautions

Asses level of consciousness

Inspect for loose dentures, foreign bodies

Suction secretionsAssess gag reflex, tongue control


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Oxygenation and

Ventilation

Respiratory rate and depth

Signs of fatigue - Paradoxical respirations

Breath sounds - (CHF, pneumonia,COPD)

Supplemental O2 with O2sat > 95%

Support with Basic airway techniques

Ventilatory support as required


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Basic airway techniques

Foreign body removal

Suction with rigidsuction device

Positioningjaw thrust

chin lift

Nasal airway Bag valve mask


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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 respiratorydistress: CHF, MI, etc.


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Monitoring of oxygenation

Pulse oximetry indicator of oxygenation not ventilation

falsely high in CO poisoning

falsely low in PVOD, hypotension, peripheralvasoconstriction

ABG pCO2 allows eval of ventilation

obtain from compressible site

Supernormal oxygenation not of proven benefit


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Circulation Goal: maintain cerebral perfusion

Optimize cardiovascular status

Monitor and reevaluate


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Circulation

Evaluate cardiac history and status

Cardiac output

preload afterload

contractility

stroke volume


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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


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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


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Vascular Access

Two peripheral IVs

Use .9NS or .45 NS unlesshypotensive

Use .9NS if hypotensive

Replace blood products as indicated


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Autoregulation The ability of the vasculature in the brain tomaintain a constant blood f low across a wide rangeof blood pressures

Autoregulation - impaired or lost in the area of theinfarction

Ischemic tissues are perfusion dependant

Autoregulation is shifted to higher pressure

patients with a history of HTN


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0

20

40

60

80

100

0 50 100

150

200

250

MAP mm Hg

CBF

ml/100

mg/min Ischemic

Normotensive

Hypertensive

Autoregulation

of Cerebral Blood Flow


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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


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Hypertension - Ischemic Stroke Drugs - short acting, titrate

Labetalol

IV: 10-20 mg increments, double dose Q 20 min, maxcumulative 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


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Hypertension -Ischemic

Stroke Nitroglycerine

Paste: 1-2 inches to skin

IV Drip: 5mcg/min, increase in increments of 5-10mcgevery 3-5 min

NitroprussideIV Drip: 0.3 - 10 mcg/min/kg

Continuos BP monitoring

check thiocyanate levels

AVOID NIFEDIPINE


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Hypertension

Intracerebral Hemorrhage Treat aggressively

Elevate head of bed

Use labetalol, nitroglycerine, nitroprusside or lasixAVOID NIFEDIPINE

Keep systolic < 160 mm Hg

diastolic < 100 mm Hg


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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


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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


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GlucoseWorse 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


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GlucoseAvoid any IV fluids with D5

instruct prehospital personnel not to give D50 as part ofthe coma cocktail to acute stroke patients

Check a finger stick ASAP

treat only if low (< 50)

Use insulin to establish euglycemia


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Temperature Fever worsens outcome:

for every 1C rise in temp, risk of pooroutcome 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


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Seizures

Occur in 5% of acute strokes

Usually generalized tonic-clonic

Possible causes:

severe strokescortical involvement

unstable tissue at risk

spreading depolarizationshx of seizure disorder


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Primary treatment of

AcuteIschemic Stroke Supportive care

Aspirin

IV thrombolysis No role for antithrombotics


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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


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SummaryEvaluation History with time of symptom onset

Physical exam

trauma, NIHSS score

Laboratory evaluation

Non-contrast CT head


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Supportive CareSupportive 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
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Neurologic InfectionYou are called to ER to see a 46-year-old woman for

altered mental status. On arrival, you find an Asianwoman complaining of headache, nausea and

vomiting. Her examination is notable for fever,lethargy, papilledema, and nuchal rigidity.


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History Time course of symptoms

History of, risk factors for, and prior testing humanimmunodefisiency virus (HIV)

If HIV positive : CD4 count, hightly activeantiretroviral treatment history, opportunistic history,and prophylaxis medication complience

Other immunocompromised states


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History Travel history

Exposure

Vaccinations/inoculations

Time of year

Port de entry of infection : pulmo, ears, nose, headtrauma, lumbal puncture


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Physical ExaminationVital signs : full set, including accurate rectal

temperature

Head, eyes, ears, nose, and throat : be attentive for

facial rash, ear canal vesicles, thrush, parotitis, dentalabscess, mastoid tenderness

Evaluate carefull for nuchal rigidity, meningismus andrange of motion

Dematologic


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Neurologic ExaminationAssess level of consciousness

Assess of cranial nerve include Brainstem reflex

Assess of meningeal signs

Assess motor skills and reflex

Assess gag reflex, tongue control


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Diagnostic Evaluation Complete blood count, chemistry panel, Liver functiontest, PTT, APTT, HIV, Lyme antibody, Tuberculin skintest

Blood culture, urinalysis and toxicology, sputumculture

Chest x-ray, ECG, cardiac monitoring, considertransesophageal echocardiogram

Lumbal puncture

Imaging

EEG


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Treatment Treat immediately for bacterial meningitis

Consider dexamethasone IV 10 mg every 6 hours for 4days

Virulent pathogens such as gram-negative bacterialmeningitis and Staphylococcus aureus meningitisshould be treated for minimum of 21 days andsometimes longer depending on clinical response

stroke and unconsciousness

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