Neurological Emergencies - ENC 2005 GI & Neuro Emergencies

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Transcript Neurological Emergencies - ENC 2005 GI & Neuro Emergencies

Emergency Nursing Course
Neurological Emergencies
Dr. Fu Tat Lee
(李富達醫生)
Princess Margaret Hospital
(瑪嘉烈醫院)
Outline
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Neurological assessment
Stroke
Seizure
Acute generalized weakness
Headache
Neurological assessment
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What is it?
Where is it?
The Neurological Assessment
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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
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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 Assessment
A. Mental Status
Glasgow Coma Scale
B. Cranial nerves (1st - 12th)
C.Upper & lower limbs
- motor
- sensory
- coordination
- reflexes
eye opening
motor response
verbal response
Decorticate posture
Decerebrate 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) nerve
Motor: Masseter
Sensory: ophthalmic, maxillary & mandibular divisions
VII nerve (Facial nerve)
Lower Motor Neuron lesion of VII nerve palsy
Bell’s palsy
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1st described by Dr Charles Bell in 1882
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Lower Motor neuron lesion of 7th nerve
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idiopathic etiology
- Dx on
i) no identifiable cause (viral/post viral Sx)
ii) peripheral
Symptoms
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Pain
Tearing
Drooling
Hypersensitivity to sound
Impairment of taste
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DDx:
Central 7th nerve palsy - sparing
ipsilateral frontalis muscle
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 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 nerve
Muscles for swallowing
10th Vagus nerve
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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 assessment
Motor
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Posture, Muscle wasting, Fasciculation
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Muscle Tone:
Hypertonic or Hypotonic
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Muscle power :
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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
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Coordination
Pastpointing, dysmetria, dysdiadochokinesia
Romberg testing
Gait
Tendon Reflex
Hyperreflexia or Hyporeflexia
Plantar Reflex
Upgoing or Downgoing
Line of Stroke
Normal Planter
reflex
Barbinski reflex
Signs of Upper Motor Neurone Lesions
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Little muscles wasting unless from disuse
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Spasticity + Clonus
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Hyperreflexia
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Extensor Plantar response
Signs of Lower Motor Neurone Lesions
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Wasting is prominent
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Fasciculation
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Hypotonia
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Hyporeflexia
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Normal or equivocal plantar reflex
Sensation
Temperature
Light touch
Temperature
Pain
Proprioception and vibration
Dermatone
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
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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
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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
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Major types of stroke
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Ischaemic (70%)
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Intracerebral haemorrhage (25%)
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Cortical
Subcortical
Posterior circulation
Lacunar infarction
Supratentorial
Infratentorial
Both
Subarachnoid haemorrhage (5%)
Mortality & Morbidity
Mortality at 1
month
Mortality at
1 year
Morbidity in
survivors
SAH
50%
Intracerebral
haemorrhage
40%
50%
Cortical infarct
20%
35%
Poor
<2%
Mild
Lacunar infarct
Severe
Circle of Willis
Principles of management
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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
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
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
Anticoagulation
Spontaneous haemorrhagic transformation of infarction
commonly occurs within 2-4 days
Clinical trials not support indiscriminate use of
anticoagulation
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Neurosurgery
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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
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febrile convulsion :
3 months to 5 years, rapidly rising fever
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
H3O
H ypotension due to hypovolemia, arrhythmia
H ypoxia
H ypoglycemia
O verdose & others
(Electrolyte disturbance,Intracranial SOL,
CVA, Infection)
mnemonics of “ A E I O U”
“T I PS”
A
Alcohol
withdrawal
T
Temperature, Trauma
E
Epilepsy
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Infection
I
Insulin
P
Psychogenic
O
Overdose &
S
drug withdrawal
U
Uraemia &
Metabolic
SOL, Shock
Status epileticus
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Traditional definition:
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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 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?
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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
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Spinal cord compression
Neuropathies
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Guillain-Barre syndrome
Metallic poisons (lead & arsenic)
Vitamin deficiencies (B12)
Systemic diseases (DM, Renal failure)
Drugs
Acute generalized weakness
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Motor end plate
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Myasthenia gravis
Botulism
Eatom-Lambert syndrome
Myopathies
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Acute periodic paralysis (Hyper, hypo or normokalemia)
Alcoholic myopathy
Polymyositis
Drug (steroid)
Guillain Barre Syndrome(GBS)
George Charles Guillain
Jean Alexandre Barre
Guillain Barre Syndrome
Pathology :
An autoimmune disease causing
acute demyelinating inflammatory
polyradiculopathy
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
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Investigation
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Nerve conduction test
CSF: high protein
Management (mainly supportive)
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ICU care
Ventilatory & circulatory support
Plasmaparesis
High dose Ig
Psychological support
GBS
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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
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Myasthenia Gravis
bimodal distribution in age and gender,
2nd/3rd decade female; 6th/7th decade
male
- associated with thymic
hyperplasia/thymoma
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complaints of muscle weakness, worsened by
prolonged activity and improved with rest
most common begin with ocular ptosis, diplopia and
blurred vision
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Respiratory failure
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Confirm by bedside Tensilon test (Endrophonium)
Headache
Headache
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Tension headache
Migraine
Cluster headache
Subarachnoid hemorrhage
Hypertension (DBP >130mmHg)
Meningitis
Space occupying lesion
Sinusitis
Acute Glaucoma
Postconcussion
Temporal arteritis
Trigeminal neuralgia
Possible causes
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Intracranial
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Hemorrhage
 SAH, Subdural, Intracerebral
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Tumour
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Meningitis
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Vessel
 Migraine, Hypertension
Extracranial
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Vessel
 Temporal arteritis
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Nerve
 Trigeminal neuralgia
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Muscle
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Tension
Referred pain
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Acute glaucoma, Sinusitis
Meningitis
Meningitis
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Viral
Bacterial
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Pneumococcus
Meningococcus
Haemophilus Influenzae Type B
Kernig’s sign
Brudzinski’s sign
Temporal arteritis
Trigeminal Neuralgia
Watch out !!!!
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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