pre-extern tutorial, 2013

7/29/2019 Pre-Extern Tutorial, 2013

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Tutorial for New-ExternSurvival Neurology

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


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Neurology extern should know

Medical coma andconfusional state

Acute stroke

Tonic-clonic seizure andstatus epilepticus


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COMA

andACUTE CONFUSIONAL

STATE


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Wakefulness and ascendingreticular 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 CONSCIOUSNESSDelirium

Acute confusional

state


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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 sign but withmeningeal sign

coma without both localizing andmeningeal sign

coma with seizureCPOMRGCS


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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-bilateral

abnormality

Ocular movement: dolls eye, eye deviation,nystagmus, ocular bobbbing

Respiratory pattern:

ARAS is locatedmainly at the

brainstem, and bothhemisphere


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The pupil

Parasympathetic control Sympathetic control


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Pupillary pattern


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Dolls eye

Oculocephalic reflexVestibulo-ocularreflex

Loss of VORindicatesbrainstem

dysfunction


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Motor response and

Posture in coma

Decerebrate rigiditybilateral upper andlower limbextensor posture, usually theconsequence of bilateral mid-brainlesions

Decorticate posturebilateral flexion ofthe upper limbs and extension of the

lower limbs, usually the consequence ofan 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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COMA

Localizing sign-noMeningeal sign-yes

Severe meningitisor

Meningitis with complication;hydrocephalus, vasculitis, infarct

Encephalitis

Subarachnoidhemorrhage

- CT Brain withcontrast

- 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

These causes are reversible; if no localizing sign; lab screen first

Glucose, 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, treatimmediately (hypoglycemia in DM patient, toxiningestion)

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 withbrain herniation-) if coma with meningeal sign; do CT brain emergency-) if coma with focal sign; do CT brain emergency-) if coma with sign suggesting to seizure: start AED


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Case exercise

A woman with sudden coma

complain vertigo, and then sudden coma C=coma, P=pupil 1.5 mm, O=multi-

directional nystagmus, and ocularbobbing, M=quadriplegia, R=apneusticbreathing

GCS=E1VTM1


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Hypodensity lesion at ponsand bilateral cerebellum

: Basilar artery thrombosis


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Delirium, Acute confusional state

- good wakefulness- impair orientation- fluctuation of consciousness(usually occur at night)

- broader cause than coma

Cause of delirium

- intracranial cause: stroke,

cerebritis, etc.- extracranial cause: elyteimbalance, deoxygenation etc.- multiple medical/surgical condition


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Please aware of aphasia that may mimic delirium

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Sensory aphasia


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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-arteryatherosclerosis(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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Anterior vs Posterior

circulation


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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-contrastemergency

clinical strokewithin 2-4.5 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 of lentiform nucleus, loss of insular ribbon, loss ofgray-white differentiation and sulcal effacement


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Standard treatment in acute

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

hrs)

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-coagulant in acute

ischemic stroke : heparin IV drip , 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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First case rt-PA in

CM

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5 Min


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25 Min


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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 30-35mmHg

steroid


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Hemicraniectomy in

malignant MCA infarction


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Keep in Externs mind

Stroke1. when the sudden neurological deficit occur; suspectstroke...every case

2. check time and onset (eligible for rt-PA??) andexclude mimicker cause (hypoglycemia, seizure)

3. if within 4.5 hours; call resident/neurologist activateFAST TRACT can request CT brain emergency

4. check v/s, assess severity, check and follow upneurological signs


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Seizure and statusepilepticus


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Seizure or Not seizure

Seizure mimicker pseudo-seizure convulsive syncope movement disorder: myoclonus,

chorea, paroxysmal dyskinesia hypnic jerk


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Id if f


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Identify cause of

seizure Acute processes

Stroke Metabolicdisturbances

CNS infection Trauma Drug Toxicity Hypoxia

Chronic processesPre-existing epilepsyEthanolabuseOld CVARelativelylong-standing tumors


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How to define

status...

The Epilepsy Foundation ofAmericas Working Group onSE (1993)

continuous seizure > 30 minutes

> 2 seizures with impairedconsciousness

Status

Epilepticus


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New proposed

definition of SE

Status Epilepticus Cooperative Studygroup (1998)

SE > 10 minutes

Lowenstein DH (1999) SE > 5 minutes


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Classification of status

epilepticus

1.Generalized convulsive statusepilepticus

2.Non-convulsive SE

3.Simple partial SE

(Treiman 1980)


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1. Overtgeneralizedconvulsive SE

2. Subtlegeneralizedconvulsive SE

3. Electricalgeneralizedconvulsive SE

(Treiman 1980)

Generalizedconvulsive

statusepilepticus


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Complication of SE

Acidosis

Cerebral edema Hypoglycemia Other: arrhythmia, hyperthermia,

hyperkalemia, DIC, rhabdomyolysis,myoglobinuria, renal failure


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Management of SE


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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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Key

treat early as possible

step up AED is depended on stage ofSE add on therapy is needed

monitor EEG regularly, even if noobvious seizure

D fi t f th


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Define stage of the

status epilepticus

Pre-monitory status(0-5 min) Early status(5-30 min)

Established status(30-60 min)

Refractory status(>60 min)


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Drug used

diazepam, phenytoin(Dilantin), valproicacid(Depakine), levetirazetam(Keppra)

Phenobarbital, propofol, midazolam,thiopental

Topiramate(feed)


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drug use depend on stage of status

stage of status AED treatment

Premonitory (0-5 min) Diazepam (i.v. bolus)

Early (5-30 min)

Diazepam (i.v. bolus) followed by

phenytoin (iv load) or sodium valproate(i.v. loading) or levetiracetam (i.v.)

Established (30-60 min)half dose i.v. load of previous drug, if

seizure dont stop, load another drug

Refractory ( > 60 min)Propofol (i.v.), or midazolam (i.v.), or

thiopental (i.v.) or phenobarbital (i.v.) ortopiramate (feed)


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Diazepam

diazepam 10 mg (2-5mg/min) max 10 mg per dose

can be repeated 2 doses


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Phenytoin

Vial: 250 mg/5 ml/vial 0.9% NaCl (dont use infusion pump)

starting dose: 20 mg/kg (rate < 1 mg/kg/min) maintenance: 5-8 mg/kg/day e.g. weight 50 kg

Dilantin 1000 mg+0.9%NSS 100 cc iv drip in20 min. then Dilantin 100 mg+0.9%NSS 100 cc

iv drip in 15 min


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Valproic acid

Vial: 400 mg/4 ml/vial 0.9% NaCl or 5% Dextrose

starting dose: 20-30 mg/kg (rate < 50 mg/min) maintenance: 1-2 mg/kg/hr (max 60 mg/kg/day) e.g. weight 50 kg

Depakine 1000 mg+0.9%NSS 100 cc iv drip in 30min. then Depakine 100 mg/hr (10 cc/hr)

warning: hepatotoxicity


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Midazolam

Vial: 1 mg/ml/vial, 5 mg/ml/vial, 15mg/ 3ml 0.9% NaCl or 5% Dextrose/w

starting dose: 0.1-0.3 mg/kg bolus (rate < 4 mg/min) maintenance: 0.05-0.4 mg/kg/hr e.g. weight 50 kg

Midazolam 5 mg iv bolus then + Midazolam(1:1)iv drip 5 cc/hr (0.1 mg/kg/hr)


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Levetiracetam

(Keppra) Vial: 500 mg/5 ml 0.9% NaCl or 5% Dextrose/w 100 ml starting dose: 2,000-4,000 mg/kg in 15 min maintenance: 10-30 mg/12 hr e.g. weight 50 kg

Keppra 2000 mg iv in 15 min then 1000 mg iv q12 hour


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Propofol

Vial: 10 mg/ml

5% Dextrose/w starting dose: 2 mg/kg bolus maintenance: 5-10 mg/kg/hr

e.g. weight 50 kg Propofol (2:1) iv 100 mg then 250 mg/hr

Consult is required


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Thiopentone

Vial: 1 g/vial starting dose: 100-250 mg in 20 min then 50 mg q 2-

3 min until seizure stop

maintenance: 3-5 mg/kg/hr

Consult is required


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Phenobarbital

Vial: 200 mg/4 ml in sterile water 10 ml 5% Dextose

starting dose: 20 mg/kg (rate < 100 mg/min)

maintenance: 1-4 mg/kg/day


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Topiramatefor SE

Clinical trial: 500 mg every 12 hoursnoso/orogastric feed for 2 days then150 mg-750 mg every 12 hours

Effective dose: 300-1600 mg/day


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Monitoring

Tapering off AED seizure stop > 24 hours Burst suppression on EEG > 24

hours

Slow tapering off AED if seizure recur, increase AED doseenough to control seizure

Keep in Externs Mind


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Keep in Extern s 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 epilepticusguideline therapy


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