Neurology Emergency Flashcards by Rosie Middleton

Define Status Epilepticus

Recurrent seizures without recovering in between or a single seizure lasting more than 30 mins

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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

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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

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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

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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

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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

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Complications of status epilepticus

Focal neurological deficits
- may improve with time
Cognitive dysfunction
- most notably memory

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DDx of status epilepticus

Psychogenic non-epileptic status epilepticus

differentiate with video-EEG
no epileptiform activity

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Epidemiology of spinal cord compression

Trauma is the main cord
Disc herniation
Bony fracture - osteoporotic, metastases
Spinal subluxation
Penetrating injuries
Tumour growth
Infection

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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

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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

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Onset of spinal cord compression

Acute
- traumatic compression
- disc herniation
Chronic
- osteoporosis
- osteomyelitis
- malignancy

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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

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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

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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

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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

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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

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Pupil light response in head injury

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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

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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

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Non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness

Risk factors for ARDS

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Critical illness - sepsis, aspiration, pneumonia, severe trauma, lung transplantation
Hx of alcohol abuse
Burns and smoke inhalation

Pathophysiology of ARDS

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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

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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

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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

Neurology Emergency Flashcards

(43 cards)