Neurology Emergency Flashcards
Define Status Epilepticus
Recurrent seizures without recovering in between or a single seizure lasting more than 30 mins
Pathophysiology for status epilepticus
Mechanisms that abort seizure activity fail, either from excessive and abnormally persistent excitation, or ineffective inhibition
Accumulation of excitatory neurotransmitters (notably glutamate), hyperthermia, hypoxia, lactic acidosis and hypoglycaemia can cause cerebral injury
Presentation of status epilepticus
Types of seizures
- generalised tonic-clonic or focal evolving tonic-clonic
- focal aware motor
- impaired awareness cognitive
- absence
- focal impaired awareness
- focal aware
Ix for status eplipeticus
Anticonvulsant drug blood level
Toxicology screen
Comprehensive metabolic panel
FBC
- low platelets suggest intracranial bleed
- WCC indicates infection
ECG
- arrhythmias or cardiac ischaemia can occur after prolonged SE
EEG
- intermittent or continuous ictal discharges
ABG
- acidosis or alkalosis may be a complication
CT/MRI head
- rule out structural lesions
LP
- if meningitis or encephalitis suspected
Risk factors for status epilepticus
Hx of epilepsy Non-adherence to anticonvulsant drugs Chronic alcoholism Alcohol withdrawal Refractory epilepsy Electrolyte disturbances Previous cortical structural damage Drug use
Mx of status epilepticus
· 0 minutes – secure airway, give high flow oxygen
· 5 minutes – buccal midazolam (10mg)/IV lorazepam (4mg)
· 15 minutes – IV lorazepam (4mg) and call for a senior
· 25 minutes – Seek anaesthetic advice, rectal paraldehyde or IV phenytoin
Complications of status epilepticus
Focal neurological deficits
- may improve with time
Cognitive dysfunction
- most notably memory
DDx of status epilepticus
Psychogenic non-epileptic status epilepticus
- differentiate with video-EEG
- no epileptiform activity
Epidemiology of spinal cord compression
Trauma is the main cord Disc herniation Bony fracture - osteoporotic, metastases Spinal subluxation Penetrating injuries Tumour growth Infection
Pathophysiology of spinal cord compression
Spinal cord extends from foramen magnum to L1/L2
Cord and surrounded CSF wrapped by dura mater
- CSF acts as buffer to slight compression
Corticospinal (control of trunk and limb movements) and spinocerebellar (unconscious proprioception) tracts most vulnerable
Presentation of spinal cord compression
Back pain Numbness/paraesthesia Weakness/paralysis Bladder/bowel dysfunction Hyper-reflexia Loss of tone below level Hypotension and bradycardia - neurogenic shock Cauda equina syndrome - saddle anaesthesia - painless urinary retention - bilateral sciatica and weakness
Onset of spinal cord compression
Acute - traumatic compression - disc herniation Chronic - osteoporosis - osteomyelitis - malignancy
Ix for spinal cord compression
MRI spine - T2 weighted
- increased signal in disc compression and trauma
Gadolinium enhanced MRI spine
- assess for infection
Plain spine X-ray
- decreased disc space height - disc compression
- loss of bony detail - tumour, infection
- misalignment - trauma
- loss of end-plate definition - infection
Mx of spinal cord compression
Acute trauma
- immobilisation + decompression/stabilisation surgery
- IV dexamethasone
- supportive therapy - DVT prophylaxis, BP control, nutritional support
Epidural abscess
- vancomycin + metronidazole + cefotaxime
- consider decompression or CT-guided aspiration
- supportive
Cauda equina
- decompressive laminectomy
- supportive
Causes of brain damage in a head injury
Primary damage - focal cerebral contusions - diffuse axonal injury - extradural, subdural or subarachnoid haemorrhage Secondary damage - cerebral oedema - hypotension - hypoxia - seizures - hypoglycaemia - infection
Immediate CT criteria
· Loss of consciousness lasting more than 5 minutes (witnessed)
· Amnesia (anterograde or retrograde) lasting more than 5 minutes
· Abnormal drowsiness
· Three or more discrete episodes of vomiting
· Clinical suspicion of non-accidental injury
· Post-traumatic seizure but no history of epilepsy
· GCS < 14, or for a baby under 1 year GCS (paediatric) > 15
· Suspicion of open or depressed skull injury or tense fontanelle
· Any sign of basal skull fracture – haemotympanum, periorbital ecchymosis, CSF leakage from the ear or nose, Battle’s sign
· Focal neurological deficit
· If under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head
· Dangerous mechanism of injury – high-speed road traffic accident, fall from a height of greater than 3m
Clinical features of head injury
Head signs - haematoma - laceration - depressed fracture - anterior fontanelle depression CNS signs - decreased GCS - abnormal fundi/pupillary reflexes - focal neurological signs
Pupil light response in head injury
Unilaterally dilated pupils with sluggish or fixed light response
- 3rd nerve compression secondary to tentorial herniation
Bilaterally dilated pupils with sluggish or fixed light response
- poor CNS perfusion
- bilateral 3rd nerve palsy
Unilaterally dilated or equal pupils with cross reactive light response
- optic nerve injury
Bilaterally constricted pupils with difficult to assess light reflex
- opiates
- pontine lesions
- metabolic encephalopathy
Unilaterally constricted pupil and preserved light reflex
- sympathetic pathway disruption
Head injury mx
Call for senior help and neurology Nurse patient head up Give O2 Maintain tight control over BP Give adequate analgesia Avoid hypoglycaemia
Define acute respiratory distress
Non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness
Risk factors for ARDS
Critical illness - sepsis, aspiration, pneumonia, severe trauma, lung transplantation
Hx of alcohol abuse
Burns and smoke inhalation
Pathophysiology of ARDS
Diffuse alveolar damage leads to injury of alveolar-capillary membrane
Flooding of alveolar air spaces with oedema, inflammatory cells and oxidants
Epithelial injury - necrosis, fibrin deposition on exposed basement membrane and surfactant dysfunction
Presentation of ARDS
Low O2 sats - despite supplemental oxygen
Acute/progressively worsening resp failure
Critically ill patient
Dyspnoea/tachycardia
Pulmonary crepitations - diffuse
Low lung compliance
Fever, cough, pleuritic chest pain
Diagnostic criteria for ARDS
Acute onset - within 1 week
Bilateral opacities on x-ray
PaO2/FiO2 ratio of < 300 on PEEP or CPAP > 5cm H2O
Ix for ARDS
CXR - new onset bilateral opacities
ABG - low paO2
Blood/sputum/urine culture - sepsis most common cause of ARDS
Serum amylase/lipase - assess for pancreatitis as cause
Mx of ARDS
Oxygen and ventilation Prone positioning IV fluids Targeted antimicrobial therapy Supportive care - DVT prophylaxis - glucose control - beta-agonists to promote alveolar fluid clearance
Complications of ARDS
Multiple-organ failure
Persistent dyspnoea
Abnormal lung function
Define giant cell arteritis
Granulomatous vasculitis of large and medium sized arteries
- primarily affecting branches of external carotid
Epidemiology of giant cell arteritis
Typically over 50s
Peak between 70 and 80
F:M = 2:1
Pathophysiology of giant cell arteritis
Immune-mediated inflammation of walls of medium and large arteries
- presence of granulomas
Likely to be caused by environmental trigger (infection) in genetically predisposed individual
Presentation of giant cell arteritis
Headache and scalp tenderness
- over temporal or occipital areas
Polymyalgia rheumatica symptoms
- aching and neck stiffness, shoulders, hips, worsens after inactivity
Jaw claudication
- pain on chewing
Loss of vision
Superficial temporal artery tenderness of thickening
Fundoscopy - pallor and oedema of optic disc (ischaemia of optic nerve)
Ix for giant cell arteritis
ESR - raised
CRP - raised
FBC - normocytic, normochromic anaemia with normal WBC and elevated platelets
Temporal artery biopsy - granulomatous inflammation, multi-nucleated giant cells, focal and segmental inflammatory infiltrate
Temporal artery USS - wall thickening, stenosis or occlusion
Mx of giant cell arteritis
Prednisolone - orally for 4 weeks then tape over 6-12 months
Aspirin
Define Guillain-Barre Syndrome
Acute inflammatory neuropathy characterised by:
- motor difficulty
- absence of deep tendon reflexes
- paraesthesia without objective sensory loss
- increased CSF albumin with absence of cellular reaction
Epidemiology of Guillain-Barre Sydnrome
1 per 100,000
Mean onset 40 years old
Pathophysiology of Guillain-Barre Syndrome
Immune-mediated attack on Schwann cells of sensory and motor nerves
- usually triggered by preceding infection - CMV, EBV, hep B/C, HIV, campylobacter jejuni
Issues with propagation of nerve impulses
- conduction block and flaccid paralysis
When immune destruction stops, repair and remyelination occur
Presentation of Guillain-Barre Syndrome
Progressive symmetrical weakness - lower extremities and proximal muscles first Paraesthesia in feet and hands Resp distress Speech problems Back/leg pain Areflexia/hyporeflexia Extra-occular muscle weakness Facial droop Dysautonomia - sinus tachycardia - hypertension - postural hypotension Fixed and dilated pupils
Ix for Guillain-Barre Syndrome
Nerve conduction studies - slowed LP - elevated protein, normal/slightly raised lymphocytes LFTs - elevated Spirometry every 6 hours - monitoring for resp signs - reduced VC, mas inspiratory pressure Antiganglioside antibody
Mx of Guillain-Barre Syndrome
IV immunoglobulin - contraindicated in IgA deficiency and renal failure Plasma exchange Supportive -DVT prophylaxis - blood pressure control - intubation and ventilation if needed
Define acute bulbar palsy
Range of signs and symptoms linked to CN IX, X, XI and XII due to lower motor neurone lesion in medulla oblongata or lesions of lower cranial nerves outside brainstem
Presentation of acute bulbar palsy
Dysphagia Difficulty chewing Nasal regurgitation Slurring of speech Dysphonia Atrophic tongue with fasciculations Dribbling Weakness of soft palate Absent gag reflex Sparing of ocular muscles differentiates from myasthenia gravis
Causes of acute bulbar palsy
Genetic - Kennedy's disease - acute intermittent polyphoria Vascular - lateral or medial infarction Degenerative - Guillain-Barre Syndrome - poliomyelitis - Lyme disease Malignancy - brainstem glioma - malignant meningitis Toxic - botulism - venom Autoimmune - myasthenia gravis
DDx to acute bulbar palsy
Pseudobulbar palsy
- damage located in UMNs
- usually due to stroke
- presents with brisk jaw jerk, stiff and spastic tongue and labile affect
