Emergency in neurology

Emergency in Neurology

Narongrit Kasemsap, MD Neurology unit, Internal Medicine Department,

Khonkaen University

Objectives

Localization Patient with Coma.

Evaluation and Management TIA and Ischemic Stroke Patient.

Management Patient with Status Epilepticus.

Approach to Patient with Coma

Consciousness

Awareness (content of consciousness)

Arousal (level of consciousness )

“ State of awareness of self and the environment ”

Reticular activating system

Neuroanatomical Basis of Coma

Diffuse

Extensive bilateral hemisphere

Bilateral thalamic lesion

Hypothalamus

Categorized Coma Coma without focal signs or meningism

Anoxic-ischemic, metabolic, toxic, drug-induced, infection, post-ictal state

Coma with meningism

SAH, meningitis, meningoencephalitis

Coma with focal signs

Intracranial hemorrhage, infarction, tumour, abscess

Multifocal Lesion Mimic toxic or metabolic causes

Venous sinus thrombosis

Bilateral subdural hematoma

Vasculitis

Meningitis

Causes of Alteration of Conscious

Structural causes

Metabolic causes

Assesment History

General examination

Neurological examination

Where is the lesion ?

What is the nature ?

History Difficult and sometime impossible.

Patient past health and illness.

seizure, diabetes, hypertension

substance abuse

depression, suicide attempts

etc..

Current medication.

Physical Examination General examination

General Neurological examination

Level of consciousness

Motor function

Brain stem function

Respiratory pattern

Abnormal Respiratory Pattern

Cheyne-Stroke

Central NeurogenicHyperventilation

Apneusis

Ataxic breathing

Cluster breathing

lower pons

middle pons

low midbrain and upper pons

RAS at medulla

Pupillary Finding in Comatose

Lesions above the thalamus and below the pons preserve pupillary reactions

Ocular motility Resting position.

Spontaneous eye movements.

If blinking is present : intact pontine reticular formation.

Bell’s phenomenon : intact pons and midbrain.

Reflex eye movements.

Eye deviation

Disconjugate eye movement : CN III, CN VI, brainstem lesion.

Upward deviation : poor localising value

Downward deviation : poor localising value

Skew deviation : posterior fossa lesion

Disconjugate eye

CN IIICN VI

Brainstem

Spontaneous Eye Movement

Purposeful eye movements : locked-in syndrome, catatonia, and pseudo-coma.

Roving eye movements : toxic, metabolic, bilateral hemisphere.

Contralateral conjugate eye deviation : epilepsy.

Normal / Metabolic encephalopathy

Bilateral CN VI palsy

Oculocephalic (Doll’s eye)

Right CN III, INO

Absent response

Oculocephalic (Doll’s eye)

RightLeft

MLF

Caloric response

COWS : Cold Opposite Warm Same

Check tympanic membrane before testing

Fast phase nystagmus

Painful Stimuli

Motor Response

to PainDecerebrate rigidity

Decorticate posture

Clinico-Anatomical Correlation in Coma

Bilateral hemisphere damage/dysfunction

Symmetrical signs

May have fits or myoclonus

Normal brain stem reflexes

Normal oculocephalic and calorics response

Normal pupils

Supratentorial mass lesion with secondary brain stem compression

ipsilateral third nerve palsy

contralateral hemiplegia

Brain stem lesion Abnormal OCR, calorics

Asymmetrical motor responses

Toxic/metabolic Normal pupils: single most important criterion

(except opiate poisoning)

Ocular motility: rove randomly in mild coma and come to rest in primary position with deepening coma

Absent OCR and calorics

Decorticate and decerebrate rigidity or flaccidity, multifocal myoclonus

Mimic of Coma

Maintain airway, breathing, and circulation (ABC’s)

Urgently correct any hypothermia, if profound.

If trauma has occurred or is strongly suspected

Stability of the cervical spine before moving the head.

Initial Management of Coma

Initial Management of Coma

Rule out hypoglycemia esp DM.

Check basic blood work (blood count, E’lyte, BS, BUN, Cr, LFT, PT, PTT, ABG, possibly CO level if suspected) and urine drug screen.

Coma Cocktail

50 ml of 50%glucose IV

100 mg of thiamine IV

Naloxone or Flumazenil for opiate or BZP overdose.

Comatose patient with suspected SAH

Rule out SAH : brain CT scan without contrast.

Lumbar puncture if SAH is still strongly suspected but not seen on brain CT scan.

If SAH : neurosurgical consultation and urgent cerebral angiography.

Generally delay CSF examination in CT-negative patients with sudden headache by 12 h from the onset to ‘allow’ the yellow colour to develop.

Comatose patient with fever or septic syndrome Examine for any likely systemic focus (abscess,

peritonitis) of infection.

Panculture blood and urine, CXR.

Perform LP to exclude meningitis and begin initial broad-spectrum antibiotic coverage.

If LP is contraindicated : brain CT scan with and without contrast.

Brain MRI if suspect Herpes simplex encephalitis

CT brain of Increased ICP

Lateral midline shift

Loss of suprachiasmatic or basal cisterns

Fourth ventricle effacement

Obliteration of supracerebellar or quadrigeminal plate cisterns with patent ambient cisterns

Cerebrovascular disease

Transient Ischemic Attack

(TIA)

“A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal

ischemia, without acute infarction”

Stroke. 2009;40:2276-2293.

Risk Stratification• ABCD2 score

• Age >60 years (1)

• BP>140/ 90 mmHg (1)

• Clinical symptoms :

• focal weakness with the spell (2)

• speech impairment without weakness (1)

• Duration

• <60 minutes (2)

• 10 to 59 minutes (1)

• Diabetes (1)

The 2-day risk of stroke Score Risk

0-1 0%2-1 1.3%4-5 4.1%6-7 8.1%

Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals. Stroke. 2009 Jun;40(6):2276–93.

Risk Stratification

Johnston SC, Rothwell PM, Nguyen-Huynh MN, Giles MF, Elkins JS, Bernstein AL, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007 Jan 27;369(9558):283–92.

Stroke

“Sudden loss of blood circulation to an area of the brain, resulting in a corresponding

loss of neurologic function”

Etiology Diagnosis

Baseline laboratory

FBS, CBC, Lipid, BUN, Cr, Electrolytes,

Coagulogram ,Urine exam

Cardiac work up : CXR, EKG

Non-contrast CT brain

Work up for Etiology of Stroke

Cardio-embolic stroke

Echocardiogram : TTE, TEE

Holter monitoring : paroxysmal AF

Work up for Etiology of Stroke

Stroke in the young <45 yr No evidence of Cardio-embolism or

atherosclerosis risk factor

ESR, ANA, anti-HIV, VDRL, LFT.

Protein C, Protein S, Antithrombin III, factor V laiden, prothrombin gene, Homocysteine.

Antiphospholipid syndrome : anticardiolipin, Lupus anticoagulant

Suspected of intra or extra-cranial artery stenosis

Carotid bruit, Amouroxis fugax

Lacunar infarction with mRS>2

Vascular Work up

Carotid duplex ultrasonography

Transcranial Doppler ultrasonography

Vascular Work up

Magnetic resonance angiography

Computerized angiography

Vascular Work up

Onset of stroke

Sudden onset of focal neurological deficit

Basic life support and capillary blood glucose to exclude hypoglycaemia

Onset <4.5 hr

Stroke Fast Track

Emergency LabCBC, BS, BUN, Cr

Cogulogram, E’lyte, EKG

Emergency Non-Contrast CT

Acute Ischemic Stroke

Start Thrombolytic Treatment within 4.5 hr of Stroke onset

Normal or Hypodensity

Onset 4.5-72 hr

Emergency Lab and Non-Contrast CT

Acute Ischemic Stroke Treatment

N Engl J Med 1995;333:1581-7

Treatment with iv t-PA within 3 hours of the onset of ischemic stroke improved clinical outcome at 3 months.

National Institute of Neurological Disorders and Stroke (NINDS) study group

Significantly improved clinical outcomes in patients with acute ischemic stroke

N Engl J Med 2008;359:1317-29.

ECASS III

mRS

Inclusion Criteria

&Exclusion

Criteria (0-3 hr)

Inclusion Criteria

Exclusion Criteria

Stroke 2013

ExclusionCriteria (0-3 hr)

Relative Exclusion Criteria

Stroke 2013

Additional Exclusion Criteria for IV rtPA Within 3 to 4.5 Hours

Stroke 2013

Intravenous Thrombolytic Therapy

Indication

• Onset < 4.5 hours.

• Age >18 yrs.

• CT brain : no intracerebral / subarachnoid haemorrhage.

0.9 mg/kg (ไม่เกิน 90 mg) แบ่งให้ 10% iv in 1 นาที ส่วนที่

เหลือ drip ใน 60 นาที

ขวดละ 50 mg

ตัวอย่างการคำนวน• น้ำหนัก 62.5 kgs x 0.9 mg = 56.25 mg

• ให้ 5.6 mg in 1 min then 50.6 mg in 60 mins.

• ใช้ยา 2 ขวด

• น้ำหนัก 58 kgs x 0.9 mg = 52.2 mg

• ให้ 5 mg in 1 min then 45 mg in 60 mins.

• ใช้ยา 1 ขวด (ไม่เกิน 55 mg ใช้ 50 mg แทนได้)

• น้ำหนัก 120 kgs x 0.9 mg = 108 mg

• ให้ไม่เกิน 90 mg : 9 mg then 81 mg in 60 mins.

Acute Treatment

Anti-platelets

• Aspirin 160-325 mg/d ภายใน 48 ชั่วโมง

• กรณีที่ได้รับ thrombolytic therapy ห้ามให้ anti-platelets ภายใน 24 ชั่วโมง

Acute TreatmentAnticoagulants

แนะนำให้ใน Cardio-embolic stroke ยกเว้นมีข้อห้าม ได้แก่

Large infarction size, Brain edema.

กรณีอื่นๆ ยังมีหลักฐานไม่เพียงพอ เช่น crescendo TIA, extracranial arterial dissection, basilar artery thrombosis

INR 2-3, 2.5-3.5 (mechanical prosthetic heart valve)

AF, AMI with LV thrombus, Cardiomyopathy,

Rheumatic MV diseaseMechanical Prosthetic heart valve

Massive MCA territory

Ischemic Stroke

Anticoagulant in AIS

Early administration of UFH or LMWH does not lower the risk of early recurrent stroke including among people with cardioembolic sources.

Not recommended for treatment of patients with acute ischemic stroke (Class III; Level of Evidence A).

General ManagementNPO : drowsiness, large infarction

Swallowing evaluation

Early mobilization

General Management1. ควรให้ยาลดความดันโลหิตเมื่อ

• SBP>220 หรือ DBP>120 mmHg

• SBP <220 หรือ DBP <120 mmHg ร่วมกับ

• SBP>180 หรือ DBP>105 (thrombolytic treatment)

2. Anti-hypertensive

• Captropril, Nicardipine, Nitroglycerine, Nitroprusside

3. ในกรณีที่ความดันโลหิต <100/70 mmHg ให้หาสาเหตุและแก้ไข

Congestive heart failureAortic dissectionAcute Myocardial InfarctionAcute renal failure

Don’t Use Nifedipine sublingual or oral

ป้องกันภาวะ hypoxemia (keep O2sat>92%)

ควบคุมระดับน้ำตาลในเลือดที่ 80-140 mg/dl และ 140-180 mg/dl ในรายที่เป็นเบาหวาน

ควรให้สารน้ำเป็น 0.9%NaCl, หลีกเลี่ยงการใช้ free water หรือสารน้ำที่มีน้ำตาล

ควบคุมอุณหภูมิร่างกายให้ปกติ ถ้ามีไข้ให้หาสาเหตุและรักษา

ให้ยากันชักเมื่อมีอาการ ไม่ควรให้เพื่อป้องกัน

General Management

Management of Stroke Complication

ICH after Thrombolytic treatment

Suspect : acute neurological deterioration, acute headache, severe hypertension, nausea/vomiting

Stop thrombolytic + CT brain Emergency.

Check PT, aPTT, platelet count.

Cross match for FFP 10 mg/kg

Management of Stroke Complication

Increased Intracranial Pressure

Intubation and Hyperventilation if alteration of consciousness.

Avoid hypervolemia, hypotonic solution, dextrose in iv fluid.

Osmotherapy

20% mannitol

10% glycerol

Consult Neurosurgeon : decompressive craniectomy.

Secondary Stroke Prevention

Drugs DosageAspirin 60-325 mg/d

Clopidogrel 75 mg/d

Cilostazol 200 mg/d

Aspirin + dipyridamole 25+200 mg/d

Antiplatelet drugs

Secondary Stroke PreventionAnticoagulant : use in cardio-embolic stroke.

Warfarin

New oral anticoagulant :

Dabigatran

Apixaban

Rivaroxaban

Asesment Stroke Risk : CHA2DS2-VASc

0 : Low risk 1 : Moderate risk 2 : High risk

Better at identifying “truly low-risk”

Assessing Bleeding Risk : HAS-BLED 0-2 : Low risk

>3 : High risk

Stroke. 2011

Secondary Stroke PreventionCarotid endarterectomy

Carotid stenosis 70-99% ในรายที่มีอาการไม่มาก

ควรทำภายใน 2 สัปดาห์ หรือกรณีที่อาการคงที่อาจพิจารณาผ่าตัดภายในระยะเวลาไม่เกิน 6 เดือน

Secondary Stroke Prevention ความดันโลหิตสูง: keep BP <140/90 mmHg, <130/80 (DM)

เบาหวาน : goal HbA1C <7.0%

ไขมันในเลือดสูง : LDL <100 mg/dl, <70 mg/dl (DM), HDL >40 (male), HDL>50 (female), TG<150 mg/dl

ดัชนีมวลกาย (BMI) <23

รอบเอวชาย <36 นิ้ว (90 เซนติเมตร), รอบเอวหญิง <32 นิ้ว (80 เซนติเมตร)

แนะนำเลิกสูบบุหรี่, งดดื่มสุราและให้ออกกำลังกาย

Status Epilepticus

≥ 5 minutes of continuous seizures

≥2 discrete seizures between which there is incomplete recovery of consciousness

Definition

Neurocrit Care (2012) 17:3–23

Convulsive Status Epilepticus

Focal motor SE and EPC not included in these definition

Non-Convulsive Status Epilepticus (NCSE)

Electrographic seizure without clinical GCSE

Two distinct phenotype : “Wandering confused”, “Subtle status”

Classified by Semiology


Cause of SE : Acute Process


Metabolic disturbances: E’lyte, hypoglycemia, renal failure

Sepsis

CNS infection: meningitis, encephalitis, abscess

Stroke: ischemic stroke, ICH,SAH, CVST

Head trauma with or without epidural or subdural hematoma

Drug : toxicity, withdrawal (opioid, BZP, barbiturate, alcohol), Non-compliance with AEDs

Hypoxia, cardiac arrest

Hypertensive encephalopathy, PRES

Autoimmune encephalitis : anti-NMDA, anti-VGKC, paraneoplastic syndrome

Cause of SE : Chronic Process


Preexisting epilepsy: breakthrough seizures or discontinuation of AEDs

Chronic ethanol abuse in setting of ethanol intoxication or withdrawal

CNS tumors

Remote CNS pathology (stroke, abscess, TBI, cortical dysplasia)

Diagnostic Work up


Monitor vital signs.

CT scan of brain.

DTx, BS, CBC, basic metabolic panel, Ca, Mg, AED levels.

Continuous EEG monitoring

Consider : Brain MRI, CSF study, toxicology (INH, TCA, CsA, theophylline, cocaine, sympathomimetics, alcohol, organophosphates)

Complication of Status Epilepticus

Metabolic acidosis

Brain edema

Hypoglycemia

Others : arrhythmia, hyperthermia/hypothermia, hyperkalemia, DIC, rhabdomyolysis, myoglobinuria, renal failure

Stage of Status Epilepticus

Current Opinion in Neurology 2011, 24:165–170

Rapid action, Parenteral, Lipid soluble

Early 0 - 30 min Lorazepam, Diazepam

Establish 30 - 60 min Phenytoin, Phenobarbital, Valproate, Levetiracetam

Refractory > 60 min Propofol, Thiopental, Midazolam

Drugs use in Stage of Early Status Epilepticus

Route of administration Adult dose

Diazepam i.v. bolus ( <2-5 mg/min) 10-20 mg

Lorazepam i.v. bolus 4 mg

Midazolam Buccal or intranasal, i.m. 5-10 mg

Clonazepam i.v. bolus (<2 mg/min) 1-2 mg at 2 mg/min


Drugs use in Stage of Established Status Epilepticus

Route of administration Loading Dose Continuous dose

Phenytoin i.v. bolus (<50 mg/min) 15-20 mg/kg after 8 hr 300-500

mg/d q8h

Fosphenytoin i.v. bolus (<100 mg PE/min) 15-20 mg PE/kg after 8 hr 300-500

mg/d q8 h

Phenobarbital i.v. bolus (<100 mg/min) 10-20 mg/kg after 8 hr 180-240

mg/d q12h

Valproate i.v. bolus (<50mg/min) 15-30 mg/kg 1-2 mg/kg/hr

Levetiracetam i.v. bolus in 15 min

Optimal dose not known, often use 2000-4000 mg 10-30 mg/kg q12h

Topiramate * naso / orogastric 500 mg q 12h x 2days150-750 q 12h usual effective

300-1600

Current Opinion in Neurology 2011, 24:165–170 แนวทางรักษาโรคลมชัก* small report

Drugs use in Stage of Established Refractory Epilepticus

Route of administration

Midazolam Bolus : 0.1–0.3mg/kg at 4mg/min Infusion : 0.05–0.4mg/kg/h

ThiopentoneBolus : 100–250 mg bolus over 20s then further 50mg boluses every 2–3min until controlled Infusion : 3–5mg/kg/h to maintain burst suppression

PentobarbitalBolus : 10–20mg/kg bolus at 25mg/min Infusion : 0.5–1mg/kg/h increasing to 1–3mg/kg/h to maintain burst suppression

Propofol Bolus : 2mg/kg Infusion : 5–10mg/kg/h to maintain burst suppression


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Emergency in neurology

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