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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.

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emergency nursing course

Emergency Nursing Course

Neurological Emergencies

Dr. Fu Tat Lee

(李富達醫生)

Princess Margaret Hospital

(瑪嘉烈醫院)

outline
Outline
  • Neurological assessment
  • Stroke
  • Seizure
  • Acute generalized weakness
  • Headache
neurological assessment
Neurological assessment
  • What is it?
  • Where is it?
the neurological assessment
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 assessment1
The Neurological Assessment
  • Look for asymmetrical abnormalities
  • Tendon reflexes can be absent in health but may

indicate an abnormality in the sensory or motor system

  • An EXTENSOR PLANTAR REFLEX which is reproducible is never normal (except in infants)
the neurological assessment2
The Neurological Assessment

A. Mental Status

Glasgow Coma Scale eye opening

motor response

verbal response

B. Cranial nerves (1st - 12th)

C. Upper & lower limbs

- motor

- sensory

- coordination

- reflexes

slide10
Decorticate posture

Decerebrate posture

neurological examination
Neurological Examination

Cranial nerves

(1) 1st (olfactory) nerve

- anosmia (loss of smell)

slide13
2nd (optic) nerve

- visual acuity

- visual field

slide16
3rd (Oculomotor), 4th (Trochlear) and

6th (Abducent) nerves

- eye movements, upper eyelid & pupil size

5th trigeminal nerve
5th (Trigeminal) nerve

Motor: Masseter

Sensory: ophthalmic, maxillary & mandibular divisions

bell s 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
Symptoms
  • Pain
  • Tearing
  • Drooling
  • Hypersensitivity to sound
  • Impairment of taste
slide27
Other causes of LMN lesion of VII nerve:

Acoustic neuroma

Parotid gland tumour

Ramsey Hunt Syndrome:

facial nerve palsy due to Herpes Zoster

vesicles at the external auditory canal and ear.

bell s palsy1
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

slide30
8th (Acoustic) nerve

- balance

- deafness

Weber & Rinnie Test to distinguish conductive deafness

from sensory deafness

slide31
Rinnie test

Weber test

slide32
9th Glossopharyngeal nerve

Muscles for swallowing

10th vagus nerve
10th Vagus nerve
  • Smooth muscles of GI & respiratory tract
  • Pacemaker
  • Muscles of heart, pharynx & Larynx

gag reflex

(sensory 9th)

(motor 10th)

slide35
11th (accessory) nerve

- sternomastoid & trapezius muscle

neurological examination1
Neurological Examination

Upper & Lower limbs assessment

Motor

  • 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

excluded

III 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

slide38
Coordination

Pastpointing, dysmetria, dysdiadochokinesia

Romberg testing

Gait

  • Tendon Reflex

Hyperreflexia or Hyporeflexia

  • Plantar Reflex

Upgoing or Downgoing

slide39
Line of Stroke

Normal Planter reflex

Barbinski reflex

slide41
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
slide42
Sensation

Temperature

Light touch

Temperature

Pain

Proprioception and vibration

assessment of brainstem function
Assessment of Brainstem function

Brainstem reflex

pupillary reactions

corneal responses

spontaneous eye movements

oculocephalic 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
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
slide49
Major types of stroke
    • Ischaemic (70%)
      • Cortical
      • Subcortical
      • Posterior circulation
      • Lacunar infarction
    • Intracerebral haemorrhage (25%)
      • Supratentorial
      • Infratentorial
      • Both
    • Subarachnoid haemorrhage (5%)
principles of management
Principles of management
  • Assess vital signs
  • Confirm the diagnosis
  • Differentiate ischaemic from haemorrhagic stroke
  • Look out for clues for aetiology
  • Screen for early complications
specific management of ischaemic stroke
Specific management of Ischaemic Stroke

Stroke is an emergency

Acute therapy is available for ischaemic stroke within 3 hours of onset.

Tissue Plasminogen activator (TPA) 0.9mg/kg

10% as bolus and 90% infusion over 1 hour

within 3 hours increases the proportion of patients with minimal or no disability by 13-16%

6% risk of transforming infarction into symptomatic haemorrhagic

slide58
Antiplatelet therapy

Low dose Aspirin (160 to 300mg daily) within 48 hours

of onset prevents 11 recurrent ischaemic strokes or

deaths at the expense of 2 extra cases of haemorrhagic

transformation per thousand patients treated.

?? Glycoprotein IIb/IIIa inhibitor

slide59
Anticoagulation

Spontaneous haemorrhagic transformation of infarction

commonly occurs within 2-4 days

Clinical trials not support indiscriminate use of

anticoagulation

slide60
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
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

slide65
- Todd’s paralysis - focal weakness/paralysis after seizure lasting up to several days
  • febrile convulsion :

3 months to 5 years, rapidly rising fever

clinical evaluation
Clinical evaluation

ABCs

examine 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/clonic

H’stix

treat reversible causes
Treat reversible causes

H3O

H ypotension due to hypovolemia, arrhythmia

H ypoxia

H ypoglycemia

O verdose & others

(Electrolyte disturbance,Intracranial SOL,

CVA, Infection)

status epileticus
Status epileticus
  • Traditional definition:
    • 30 minutes of continuous seizure activity or a series of seizures without return to full consciousness between the seizures.
slide70
(D) Treatment

- support airway, IV, O2 and monitor

- treat reversible causes

1st line - Diazepam 0.25mg/kg IV or

0.5mg/kg PR

- Lorazepam 0.1mg/kg iv

- Midazolam 0.1 mg - 0.3 mg/Kg IVI

or 0.2mg/kg IMI

2nd line - Phenytoin 18 mg/Kg IV load at 50mg/min with cardiac monitoring

3rd line - Consider phenobarbitone (200mg=1ml=1 Ampule) imi, generalized anaesthesia

discharge
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
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 weakness1
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)
slide74
Guillain Barre Syndrome(GBS)

George Charles Guillain

Jean Alexandre Barre

guillain barre syndrome
Guillain Barre Syndrome

Pathology : An autoimmune disease causing

acute demyelinating inflammatory

polyradiculopathy

slide76
GBS

usually follow acute febrile illness, URTI, (days/weeks)

typical pattern : symmetrical ascending flaccid

motor paralysis, commonly with some sensory

Symptoms (tingling sensation)

Impaired breathing, BP and Heart rate

BEWARE !

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

investigations treatment
Investigations & treatment
  • Investigation
    • Nerve conduction test
    • CSF: high protein
  • Management (mainly supportive)
    • ICU care
    • Ventilatory & circulatory support
    • Plasmaparesis
    • High dose Ig
    • Psychological support
slide78
GBS
  • 90% weakest at the 3rd week
  • Most patients recover
myasthenia gravis
Myasthenia Gravis

- autoimmune disease

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

-

myasthenia gravis1
Myasthenia Gravis

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

- associated with thymic hyperplasia/thymoma

slide86
complaints of muscle weakness, worsened byprolonged 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
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
meningitis1
Meningitis
  • Viral
  • Bacterial
    • Pneumococcus
    • Meningococcus
    • Haemophilus Influenzae Type B
slide99
Kernig’s sign

Brudzinski’s sign

watch out
Watch out !!!!
  • The first or the worst headache of patient’s life, especially 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, papilloedema, and changes in conscious level and cognition
  • No obvious identifiable cause
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