Emergency Nursing Course Neurological Emergencies Dr. Fu Tat Lee ( 李富達醫生 ) Princess...

Emergency Nursing Course

Neurological Emergencies

Dr. Fu Tat Lee( 李富達醫生 )

Princess Margaret Hospital( 瑪嘉烈醫院 )

Outline Neurological assessment Stroke Seizure Acute generalized weakness Headache

Neurological assessment

What is it? Where is it?

The Neurological Assessment

• History should direct the neurological examination to the most relevant areas.

• Symptoms may occur before signs can be detected.

• In the absence of symptoms, any signs are less likely to be important.

The Neurological Assessment

• Look for asymmetrical abnormalities

• Tendon reflexes can be absent in health but mayindicate an abnormality in the sensory or motor system

• An EXTENSOR PLANTAR REFLEX which is reproducible is never normal (except in infants)

The Neurological Assessment

A. Mental StatusGlasgow Coma Scale eye opening

motor responseverbal response

B. Cranial nerves (1st - 12th)C. Upper & lower limbs

- motor - sensory - coordination - reflexes

Decerebrate postureDecorticate posture

Neurological Examination

Cranial nerves(1) 1st (olfactory) nerve

- anosmia (loss of smell)

2nd (optic) nerve- visual acuity- visual field

Homonymous hemianopia

Bitemporal hemianopia

3rd (Oculomotor), 4th (Trochlear) and 6th (Abducent) nerves- eye movements, upper eyelid & pupil size

5th (Trigeminal) nerveMotor: MasseterSensory: ophthalmic, maxillary & mandibular divisions

VII nerve (Facial nerve)

Lower Motor Neuron lesion of VII nerve palsy

Bell’s palsy

- 1st described by Dr Charles Bell in 1882

- Lower Motor neuron lesion of 7th nerve

- idiopathic etiology

- Dx on i) no identifiable cause (viral/post viral Sx) ii) peripheral

Symptoms Pain Tearing Drooling Hypersensitivity to sound Impairment of taste

- DDx: Central 7th nerve palsy - sparing ipsilateral frontalis muscl

e

Other causes of LMN lesion of VII nerve:Acoustic neuromaParotid gland tumourRamsey Hunt Syndrome:

facial nerve palsy due to Herpes Zoster

vesicles at the external auditory canal and ear.

Bell’s palsy

Treatment : - Prednisolone 60 mg daily for 5 days- ? Acyclovir- physiotherapy- eyedrops and cover- refer medical or ENT if fail to recover

Prognosis : 80% recover completely within 3 months

8th (Acoustic) nerve- balance- deafness

Weber & Rinnie Test to distinguish conductive deafness

from sensory deafness

Rinnie test

Weber test

9th Glossopharyngeal nerveMuscles for swallowing

10th Vagus nerve Smooth muscles of GI &

respiratory tract Pacemaker Muscles of heart, pharynx & Larynx

gag reflex

(sensory 9th)

(motor 10th)

11th (accessory) nerve- sternomastoid & trapezius muscle

12th (hypoglossal) nerve- tongue

Neurological Examination

Upper & Lower limbs assessmentMotor Posture, Muscle wasting, Fasciculation Muscle Tone: Hypertonic or Hypotonic Muscle power : Grading : 0 complete paralysis

I flicker of contraction II movement is possible where gravity

excludedIII movement is possible against gravity

but not if any further resistance is added

IV movement is possible against gravity and some resistance

V normal power

CoordinationPastpointing, dysmetria, dysdiadochokinesia Romberg testingGait

Tendon ReflexHyperreflexia or Hyporeflexia

Plantar ReflexUpgoing or Downgoing

Line of Stroke Normal Planter reflex

Barbinski reflex

Signs of Upper Motor Neurone Lesions Little muscles wasting unless from disuse Spasticity + Clonus Hyperreflexia Extensor Plantar response

Signs of Lower Motor Neurone Lesions Wasting is prominent Fasciculation Hypotonia Hyporeflexia Normal or equivocal plantar reflex

SensationTemperatureLight touchTemperaturePainProprioception and vibration

Dermatone

Assessment of Brainstem function

Brainstem reflexpupillary reactionscorneal responsesspontaneous eye movementsoculocephalic responses (Doll’s eye reflex)oculo vesticular responses (Caloric test)respiratory patterns

Stroke

Stroke Stroke is a syndrome of rapidly developing clinical

symptoms and signs of focal or global disturbances of cerebral functions due to non-traumatic vascular causes, with symptoms lasting more than 24 hours.

Not a cerebrovascular “accident” but a consequence of cerebrovascular disease

Stroke is preventable Modifiable risk factors

History of stroke or TIA Hypertension Cardiac diseases Atrial fibrillation DM Internal carotid artery stenosis Smoking Alcohol abuse Hypercholesterolemia Obesity Lack of exercise Haematological diseases, coagulopathies

Major types of stroke Ischaemic (70%)

Cortical Subcortical Posterior circulation Lacunar infarction

Intracerebral haemorrhage (25%) Supratentorial Infratentorial Both

Subarachnoid haemorrhage (5%)

Mortality & Morbidity

Mortality at 1 month

Mortality at 1 year

Morbidity in survivors

SAH 50% Severe

Intracerebral haemorrhage

40% 50%

Cortical infarct 20% 35% Poor

Lacunar infarct <2% Mild

Circle of Willis

Principles of management Assess vital signs Confirm the diagnosis Differentiate ischaemic from haemorr

hagic stroke Look out for clues for aetiology Screen for early complications

Specific management of Ischaemic Stroke

Stroke is an emergencyAcute therapy is available for ischaemic stroke within 3 hours of onset.

Tissue Plasminogen activator (TPA) 0.9mg/kg10% as bolus and 90% infusion over 1 hourwithin 3 hours increases the proportion of patients with minimal or no disability by 13-16%

6% risk of transforming infarction into symptomatic haemorrhagic

Antiplatelet therapyLow dose Aspirin (160 to 300mg daily) within 48 hour

sof onset prevents 11 recurrent ischaemic strokes ordeaths at the expense of 2 extra cases of haemorrhag

ictransformation per thousand patients treated.

?? Glycoprotein IIb/IIIa inhibitor

AnticoagulationSpontaneous haemorrhagic transformation of infarct

ioncommonly occurs within 2-4 days

Clinical trials not support indiscriminate use ofanticoagulation

Neurosurgery Not needed in most cases Obstructive hydrocephalus Cerebellar haematoma or infarct Large superficial or lobar haematoma Markedly raised ICP

Seizure

Seizure

- Primary epilepsy, idiopathic, onset before 20

- Secondary epilepsy, symptomatic, by parenchymal abnormality e.g. tumor, AVM, aneurysm, contusion/hematoma

Different types of seizure- generalized/grand mal : witnessed LOC with

generalized activities

- minor/petit mal (absence) : prolonged unresponsive staring without LOC, + focal muscular activity

- focal : repetitive motor activity without LOC

- temporal lobe : hallucinations (visual, auditory, and olfactory), memory loss, and/or bizarre behavior which may progress to focal-generalized motor activity

- Todd’s paralysis - focal weakness/paralysis after seizure lasting up to several days

- febrile convulsion : 3 months to 5 years, rapidly rising fever

Clinical evaluationABCsexamine for trauma including head/facial abrasions, contusions, lacerations, tongue,buccal lacerations Is patient seizing? Is patient awake?Look for eye deviation and focal/generalized tonic/clonicH’stix

Treat reversible causes

H3OH ypotension due to hypovolemia, arrhythmiaH ypoxiaH ypoglycemiaO verdose & others (Electrolyte disturbance,Intracranial SOL, CVA, Infection)

mnemonics of “ A E I O U” “T I PS”

A Alcoholwithdrawal

T Temperature, Trauma

E Epilepsy I Infection

I Insulin P Psychogenic

O Overdose & drug withdrawal

S SOL, Shock

U Uraemia & Metabolic

Status epileticus Traditional definition:

30 minutes of continuous seizure activity or a series of seizures without return to full consciousness between the seizures.

(D) Treatment- support airway, IV, O2 and monitor- treat reversible causes1st line - Diazepam 0.25mg/kg IV or

0.5mg/kg PR- Lorazepam 0.1mg/kg iv- Midazolam0.1 mg - 0.3 mg/Kg IVI

or 0.2mg/kg IMI2nd line - Phenytoin 18 mg/Kg IV load at

50mg/min with cardiac monitoring3rd line - Consider phenobarbitone

(200mg=1ml=1 Ampule) imi, generalized anaesthesia

Discharge? Breakthrough seizure No underlying cause No head or other serious injury Good drug compliance No recent change on medication Escort by an responsible adult

Acute generalized weakness

Spinal cord compression Neuropathies

Guillain-Barre syndrome Metallic poisons (lead & arsenic) Vitamin deficiencies (B12) Systemic diseases (DM, Renal failure) Drugs

Acute generalized weakness

Motor end plate Myasthenia gravis Botulism Eatom-Lambert syndrome

Myopathies Acute periodic paralysis (Hyper, hypo or normokalemia) Alcoholic myopathy Polymyositis Drug (steroid)

George Charles Guillain Jean Alexandre Barre

Guillain Barre Syndrome(GBS)

Guillain Barre Syndrome

Pathology : An autoimmune disease causingacute demyelinating inflammatorypolyradiculopathy

GBSusually follow acute febrile illness, URTI,

(days/weeks)

typical pattern : symmetrical ascending flaccidmotor paralysis, commonly with some sensorySymptoms (tingling sensation)Impaired breathing, BP and Heart rate

BEWARE !A&E patient with lower extremity weakness and loss of lower extremity reflexes

Investigations & treatment Investigation

Nerve conduction test CSF: high protein

Management (mainly supportive) ICU care Ventilatory & circulatory support Plasmaparesis High dose Ig Psychological support

GBS 90% weakest at the 3rd week Most patients recover

What is the physical sign illustrated?

Myasthenia Gravis

- autoimmune disease

- antibodies against acetylcholine receptors at the neuromuscular junction of striated muscle

-

Myasthenia Gravis

bimodal distribution in age and gender, 2nd/3rd decade female; 6th/7th decade male

- associated with thymic hyperplasia/thymoma

- complaints of muscle weakness, worsened by prolonged activity and improved with rest

- most common begin with ocular ptosis, diplopia and blurred vision

- Respiratory failure

- Confirm by bedside Tensilon test (Endrophonium)

Headache

Headache Tension headache Migraine Cluster headache Subarachnoid hemorrhage Hypertension (DBP >130mmHg) Meningitis Space occupying lesion Sinusitis Acute Glaucoma Postconcussion Temporal arteritis Trigeminal neuralgia

Possible causes Intracranial

Hemorrhage SAH, Subdural, Intracerebral

Tumour Meningitis Vessel

Migraine, Hypertension Extracranial

Vessel Temporal arteritis

Nerve Trigeminal neuralgia

Muscle Tension

Referred pain Acute glaucoma, Sinusitis

Meningitis

Meningitis Viral Bacterial

Pneumococcus Meningococcus Haemophilus Influenzae Type B

Kernig’s sign

Brudzinski’s sign

Temporal arteritis

Trigeminal Neuralgia

Watch out !!!! The first or the worst headache of patient’s life, e

specially the onset is acute and associated with neurology

Progressively gets worse over days or weeks and subacute in onset

Associated with fever, nausea and vomit Associated with neck stiffness, focal neurology, pa

pilloedema, and changes in conscious level and cognition

No obvious identifiable cause