pre-extern tutorial, 12

8/2/2019 Pre-Extern Tutorial, 12

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Tutorial for Pre-Extern

Emergency Neurology

Surat Tanprawate, MD, MSc(London), FRCP(T)Division of Neurology, Chiang Mai University

Friday, March 16, 2012


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Neurology extern should know

Medical coma

Acute stroke

Tonic-clonic seizure and statusepilepticus



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COMA

andACUTE CONFUSIONAL

STATE



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Wakefulness and ascending

reticular activating system(ARAS)

drowsiness

stuporous

semi-coma

coma

>> level


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2 component of consciousness: arousal and awarenesscoma, vegetative state, minimally conscious state, and locked-in syndrome.

VARIOUS STATE OF CONSCIOUSNESS



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Practical approach

History taking as the patient can not talk, then ask their relative or witness

underlying disease is important (DM, atherosclerotic risk,HIV)

symptoms before and during coma(neurological complain)

Physical examination

evaluate location and cause

evaluate severity

clinical classification

coma with localizing sign

coma without localizing signbut with meningeal sign

coma without both localizing

and meningeal signCPOMRGCSFriday, March 16, 2012


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CPOMR can help us to

localize the lesion

Conscious: drowsy, stupor, semi-coma, coma

Pupil: dilate, constrict, response to light, uni-bilateralabnormality

Ocular movement: dolls eye, eye deviation,nystagmus

Respiratory pattern:

ARAS is located

mainly at the

brainstem, and

both hemisphere



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The pupil

Parasympathetic control Sympathetic control



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Pupillary pattern



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Dolls eye

Oculocephalic reflex



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Motor response and

Posture in comaDecerebrate rigiditybilateral upper and lower limb

extensor posture, usually the

consequence of bilateral mid-brainlesions

Decorticate posture

bilateral flexion of the upper limbs andextension of the lower limbs, usually theconsequence of an diencephalic lesion

(late)



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the Respiratory pattern

Cheyne-Srokes

Central neurogenic hyperventilation

Apneusis

Clustering breathing

Ataxic breathing



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Where is it?



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COMALocalizing sign-no

Meningeal sign-yes

Severe meningitisor

Meningitis with complication;hydrocephalus, vasculitis, infarct

Encephalitis

Subarachnoid

hemorrhage

-CTBrainwithcontrast

-Lumbar

puncture

CT with CM in bacterialmeningitis

CT without CM in SAH

MRI Brain in viral encephalitis



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Non-structural lesion caused

coma

Exogenous- drug, toxin (lead,

thallium, cyanide, methanol,CO), addict substance (heroin,amphetamine)

Endogenous- metabolic; Ca,Na, glucose, hypoxemia,hypercapnia, hypothyroid :::

internal toxin; uremia, hepaticencephalopathy

Thesecausesarereversible;ifnolocalizingsign;labscreenfirstGlucose,

CBC

with

Plt,

BUN,

Cr,

Elyte,

Ca,

Mg,

PO,

Oxygen

sat



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Keep in Externs Mind

Alter mental state1. Ask history; if obvious history suggest cause, treat

immediately (hypoglycemia in DM patient, toxin

ingestion)

2. Restore vital signs (Oxygen, BP)...then taking lab

(glucose immediately, and other basic lab)

3. Physical exam: CPOMR + Meningeal sign

-) if coma with no both focal or meningeal sign: metabolic, toxic,drug, diffuse intracranial lesion, SAH, brain stem stroke, stroke with

brain herniation

-) if coma with meningeal sign; do CT brain emergency

-) if coma with focal sign; do CT brain emergency



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Acute stroke



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when we suspect stroke

when the patient has sudden neurological deficit;symptoms depend on where is the brain is

involved

weak, numb

brain stem sign

cerebellar sign

cortical sign

alter mental state



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Stroke can be...

Ischemic 75%

Hemorrhagic

(25%);subarachnoid,intracerebral

Large-artery atherosclerosis(emboli/thrombosis)

Cardioembolism(high-risk/medium-risk)

Small-vessel occlusion(lacune) Stroke of other determine etiology

Stroke of undetermined etiology

TOAST,TrialofOrg10172inAcuteStrokeTreatment.HP Adams, Jr, BH Bendixen,Stroke 1993;24;35-41

TOAST classification



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HP Adams, Jr, BH Bendixen,Stroke 1993;24;35-41

FeaturesofTOASTClassificationof

SubtypesofIschemicStroke



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Anterior vs Posterior

circulation



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Lacunar stroke syndrome

Pure motor stroke/hemiparesis Ataxic hemiparesis Dysarthria/clumsy hand syndrome

Pure sensory stroke Mixed sensorimotor stroke



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3.1%

3.6%

18.2%

0.0% 5.0% 10.0% 15.0% 20.0% 25.0% 30.0%

seizures

toxic/metabolic

PN palsy

tumour

SDH

confusional state

migraine

psychogenic

dementia

syncope/presyncope

MS

vertigo

TGA

SAH

miscellaneous

% of all stroke mimics (n=670)

Condition that mimic stroke



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Acute brain attack

ABCD, Neuro signw/u stroke mimicker; speciallyhypoglycemia in DM, post-seizureEKGIV NSS, Lab (CBC plt, PT,PTT, INR, BUN/Cr/elyte

CT Brain non-contrast

emergency

clinical strokewithin 2-3.5 hours

Activate Fast tract forrt-PA

CT Brain normal or evidence of acute ischemic stroke

IV rtPA if indicated



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CT brain,

non-contrast

Ischemic stroke

Hemorrhagic stroke

sensitivity 100%

Minor or subtle signs : loss oflentiform nucleus, loss of insularribbon, loss of gray-whitedifferentiation and sulcaleffacement



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Problems of clinical diagnosis

within 6 hours of onset

Do you need a neurologist?

Approximately 75% of conditions mimicking stroke areneurological

How many of these can be identified by CT?

~15% of non-stroke disorders (e.g. subdural) found by CT

rest diagnosed clinically/with other tests

CT < 6hrs of ischemic stroke often normal

If CT is normal Often need stroke specialist or neurologist to confirm clinical

diagnosis of stroke before thrombolysis:

avoid thrombolysis for migraine, focal epilepsy, functionalweakness, ischemic deficit after subarachnoid hemorrhage!



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Standard treatment in acute

ischemic stroke

IV rtPA within 3 hrs : NNT=10 (now 3-4.5hrs)

Stroke unit : NNT = 30-40

ASA within 48 hrs : NNT 140

Early decompressive surgery for malignantMCA infarction : NNT =2 for death prevent



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3-4.5



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Anti-platelet in acute

ischemic stroke Aspirin 160-325 mg 48 ( rtPA 24

)

Every 1000 patients treated

13 more patients alive/independent

7 less recurrent ischemic stroke

2 increase symptomatic ICH

acute phase aspirin secondary prevention ( > 2 weeks)



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Anti-coagulant in acute

ischemic stroke :heparinIVdrip,LMWH(enoxaparin)SC acute ischemic stroke

Extracranial carotid or vertebral dissection

Cerebral venous sinus thrombosis

Unstable large vessel infarction

Cardioembolic clot

Arterial dissection



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Brain herniation

Subfalcine (A)

Uncal (B) Central (C)

Extradural (D)

Tonsillar (E)



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Herniation syndrome



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Treatment IICP

20-30

(Jugular vein)

osmotherapy: Mannitol* 0.25-0.5 g/kg 20

4-6

10% Glycerol 250 ml 30-60 4

50% Glycerol 50 ml 4

/ Furosemide 1 mg/Kg



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Treatment IICP

hypotonic solution

Hyperventilation Pco2 30-35 mmHg

steroid



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Hemicraniectomy in malignant

middle cerebral artery infarction

Malignant MCA infarction : MCA brain herniation

Signs

Contralateral weakness

Eye deviate to ipsilateral lesion

Global aphasia in dominant hemisphere

Hemispatial neglect in nondominant hemisphere

Signs of IICP, brain herniation



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Hemicraniectomy in

malignant MCA infarction



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Keep in Externs mind

Stroke1. when the sudden neurological deficit occur;

suspect stroke...every case

2. check time and onset (eligible for rt-PA??) and

exclude mimicker cause (hypoglycemia, seizure)

3. if within 4.5 hours; call resident/neurologist

activate FAST TRACT can request CT brain

emergency

4. check v/s, assess severity, check and follow up

neurological signs



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Tonic-clonic seizureand status epilepticus



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Seizure and Epilepsy

Seizure

the clinical manifestation of an abnormal andhypersynchronous discharge of a population of corticalneurones

Epilepsy

a tendency toward recurrent seizures unprovoked bysystemic or neurologic insults

least two unprovoked seizures at least 24 hours apart.

Acute symptomatic seizure

a seizure occurring after identifiable cause (metabolic,stroke, traumatic brain injury or infection)



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Seizure or Not seizure

Seizure mimicker

pseudo-seizure

convulsive syncope movement disorder: myoclonus,

chorea

hipnic jerk



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Convulsive syncope

Convulsive movements due to syncope

Myoclonic, tonic, eye movement

Very common,

normal blood donors (12-42%)

Not an epileptic seizure arising in an ischemic cortex-cortex is silent

Originates in brainstem-ischemic decortication

Does not require AEDs



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Identify cause of

seizureAcute processes

Stroke Metabolic

disturbances

CNS infection

Trauma

Drug Toxicity

Hypoxia

Chronic processes

Pre-existing epilepsy Ethanol abuse

Old CVA

Relatively long-standing tumors



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What should we do?

Evaluate ABCD, and check basic lab,intubation or oxygen therapy if indicate

Clarify: is it seizure?? If seizure is not stop; consider AEDs

Complete general, and neuro-exam Brain imaging if indicate



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How to define

status... 1981, ILAE (International League against

Epilepsy)

a seizure that persists for a sufficient lengthof time or is repeated frequently enough that

recovery between attacks does not occur

Premonitory status: increase in the usualfrequency or severity of their seizures may

precede status epilepticus need for

emergency management

Status

Epilepticus



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Compensated Decompensated



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Premonitory tonic-clonic status

epilepticus

Buccal midazolam 10 mg(0.15-0.3 mg/kg inchildren)Rectal diazepam 10- 30 mg(0.2-0.3 mg/kg in

children), repeated if necessary

Early tonic-clonic status epilepticus

! IV lorazepam, 4 mg bolus(0.07 mg/kg in children), repeated ifnecessary

! Basic life support airway intubation! Monitoring : regular neurological observationECG, pulse

oximetry

! Investigation: ABG, urea, elyte, glucose, liver enz, ca, mg, fullblood count, AED level, blood sam ple for storage, ECG

Upto

30min

NICE (2004), SIGN (2003) and the Royal College of Physicians Consensus Statement (2003)



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Established tonic-clonic status epilepticus

! IV phenobarbitone, 20 mg/kg, 100 mg/minor

! IV PHT 10-15 mg/kg, 50 mg/ minor

! Phosphenytoin, 15mg phenytoin equivalent/kg

Refractory tonic-clonic status epilepticus Get an anaesthetist

! Thiopentone 100-250 mg iv bolus, further 50 mg bolus every 2-3minutes until seizure are controlled, then 3-5 mg/kg/hours to

maintain a burst suppression pattern on the EEG

or

! Propofol 2 mg/kg iv bolus, repeated if necessary, then 5-10mg.kg/hrs, reducing to 1-3 mg/kg/hrs

or

! midazolam., 0.1-0.2 mg/kg bolus to control seizure, repeated ifnecessary, then 0.05-0.5 mg/kg/hrs

After30min

After30-60min

NICE (2004), SIGN (2003) and the Royal College of Physicians Consensus Statement (2003)


K i E t Mi d


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Keep in Externs Mind

Seizure1. Seizure or not seizure: history, neuro exam

2. Identify cause, ABCD management

3.Start AEDs if seizure tend to be recurrent

4. if seizure is going to be status; need to bequick, and follow up the status epilepticus

guideline therapy



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openneurons

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