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