Neuro: Emergencies Flashcards
Why is spinal cord compression an emergency?
Neurones in the spinal cord have a limited ability to regenerate so delays in management can result in irreversable cord damage and potential life long loss of function
Aetiology of spinal cord compression?
Trauma
Prolapsed intravertical disc
Atlantoaxial subluxation (RA)
Infection (discitis in IVDU)
Boney mets
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
What is Cauda Equina and how might it present?
Cauda equina syndrome is compression of the nerve roots caudal to termination of the cord (cornus medullas, usually at level of L2/3 in most adults) resulting in characteristic symptoms:
Saddle anaesthesia (loss of sensation in the perineum – around the genitals and anus)
Loss of sensation in the bladder and rectum (not knowing when they are full)
Urinary retention (compression sufficient to cause UR overflow incontinence) or incontinence (due to loss of sensation)
Faecal incontinence
Bilateral sciatica
Bilateral or severe motor weakness in the legs
Reduced anal tone on PR examination
Sexual dysfunction
Less consistent: loss of lower limb reflexes, loss of anal tone, lower limb weaknes and sensory deficit (often symetrical)
Cord compression above what level can lead to tetrapegia/quadraplegia?
T1
What type of paralysis can an impingement below T1 cause?
Paraplegia
Red flag symptoms of spinal cord compression?
Weakness
Paraesthesia
Ataxia
Urinary retention
UMN signs (clonus, hyperreflexia)
What do the nerves of the cauda equina supply?
Sensation to the lower limbs, perineum, bladder and rectum
Motor innervation to the lower limbs and the anal and urethral sphincters
Parasympathetic innervation of the bladder and rectum
CES complications
Even with early surgery, patients can be left with bladder, bowel or sexual dysfunction. Leg weakness and sensory impairment
CES management
Immediate hospital admission
Emergency MRI scan to confirm or exclude cauda equina syndrome (CT myelogram if contraindicated)
Neurosurgical input to consider lumbar decompression surgery WITHIN 48 HOURS
What tumours commonly metastisie to bone?
Breast
Thryoid
Kidney
Prostate
Lung
What is MSCC and how does it present?
When a metastatic lesion compresses the spinal cord (before the end of the spinal cord and the start of the cauda equina), this is called metastatic spinal cord compression (MSCC). This is different to cauda equina, which specifically refers to compression of the cauda equina.
MSCC presents similarly to cauda equina, with back pain and motor and sensory signs and symptoms. A key feature is back pain that is worse on coughing or straining.
MSCC is an oncological emergency and requires rapid imaging and management. There are specialist MSCC coordinators who should be involved early to coordinate the imaging and treatment of patients with MSCC.
MSCC management?
Treatments will depend on individual factors. They may include:
High dose dexamethasone (to reduce swelling in the tumour and relieve compression)
Analgesia
Surgery
Radiotherapy
Chemotherapy
Which intravertabrsal discs most commonly cause CES?
L4/5 L5/S1
What type of motor neurone picture will CES cause?
Lower motor neruone signs
What type of motor neurone picture will cord compression at the cervical spine cause?
UMN
Over what timeframe should surgical decompression be performed in CES?
Within 48 hours of onset of symptoms
How does hyperventilating play a role in management of raised ICP?
Aims to keep CO2 within its normal limits as hypercapnea will cause vasodilation of cerebral vessels and further increase ICP
What is cushings triad
Bradycardia
Hyperventilation
Hypertension
Sign of raised ICP
Extradural haemorrhage
This is a haemorrhage between the skull and dura mater of the meninges. Commonly caused by trauma to the pterion, with subsequent tearing of the middle meningeal artery, patients present with:
acute severe headache,
contralateral hemiplegia,
and a rapid deterioration in GCS following a lucid period. On CT, a
biconvex hematoma is diagnostic. This occurs as the haemorrhage stops expanding at the sutures of the
skull, where the dura meets the skull, causing the haemorrhage to expand towards the brain. Neurosurgical
intervention is usually needed.
DSM 5 classification of delerium?
- Due to another medical condition
- Substance intoxication
- Substance withdrawal
- Delirium due to multiple eiteologies
- Medication related
Further specifiers:
Time: Acute - hours/days Persistent: weeks/months
Level of activity:
Hyperactive (increased psychomotor activity - e.g. myocolonus)
Hypoactive (psychomotor retardation)
Mixed (fluctuations between both0
What might delerium be otherwise called?
Acute confusional state
Encephalopathy
Acute brain failure
ITU psychosis
Acute reversible psychosis
Acute mental status change
Organic brain syndrome
Highest prevalence of delirium?
In increasing order:
Post repair of fractured hip
Post CABG
Nursing homes
ICU elderly
Terminally ill patients
What should always be considered when there is an acute or subacute deterioration in behavior, cognition or function?
Delerium
Consequences of missed delerium?
Increased mortality
Increased morbiditiy: poor functional recovery, possible future cognitive decline, increased institutionalisation, depresssion, PTSD
Risk factors for delerium?
Elderly: imapaired Ach neurotransmission, vascular changes, pharmacokenitic changes
CNS disorders: major neurocognitive disorders represents one of the greatest risk factors
New medications (including starting more than 3-5 new meds)
Burns patients
Low serum albumin
Drug and alcohol abuse
Clinical course of delerium?
Abrupt of acute onset - within days
FLuctuation in symptom severity:
Waxinag and waning, worse at night, may result in diagnostic uncertainty
Symptoms of hyperactive delirium?
Acting disorientated
Anxiety
Hallucinations
Rambling
Rapid changes in emotion
Restlessness
Cognitive defects
Hypoactive delerium symptoms?
Apathy
Decreased responsiveness
Flat affect
Laziness
Withdrawal
Cognitive defects
Differential diagnosis of delerium?
Delerium: abrupt, fluctuating, hours to weeks, alertness increased or decreased, activity increased or decreased, attention impaired, orientation impaired
Dementia: slow and incidious, usually stable daily course, lasts years, clear conciousnes, alertness normal, acitivty variable, attention usually normal and orientation is impaired
Depression: Variable onset, stable daily course, variable length, conciousness is clear, alertness normal, acitvity is variable, attention is usually normal, orientation is normal
What factors can contribute to neurotransmitter imbalance and disruption of synaptic communication leading to delirium?
Systemic inflammation causing activation of primed microgila increase cytokine activity levels in the brain
Hypoxemia, metabolic derangements impair cerebral metabolism leading to decreased synthesis and release of neurotransmitters
Drugs
How might you investigate an acute confusion?
Capillary Blood Glucose
CT head
FBC
LFT
TSH, B12, Folate
RPR
ABG
Levels of any drugs if appropriate (e.g. digoxin)
Urine dip +/- culture
MRI brain (focal neyroloigcal signs, head trauma, no clear cause found)
ECG
EEG (usually generalised slowing, low voltage fast activity in alcohol or sedative hypotonic withdrawal)
Cardiac enzymes
HIV
CXR
ANA RF CRP
Life threatening causes of delerium?
Wernicke’s encephalopathy, withdrawal (alcohol of benzos)
Hypoglycemia, hypoperfusion of CNS, hypertensive crisis, hyper or hypothermia
Infections, intracranial pressure
Metabolica derangements, menigitis/encephalitis
Posions
Seziures (status epilepticus)
WHIMPS
Causes of viral meningitis?
Enteroviruses
HSV
Mumps
Viral menigitis vs bacteria
Viral: rarely life threatening, vs life threatening
Viral: requires pain relief, fluid, rest vs admission and IVABx
Viral: not considered to be contagious vs can be contagious and may req public health cation
Viral: Aftereffects of headaches, tiredness, memory loss vs deafness, aquired brain injury and limb loss (septicemia)
Headache in menitgitis?
Jolt accentuation of headache
Brain imaging is unnecessary in most patient with suspected meningitis, except for under which circumstances?
Focal neurological deficits
Altered mental statu/coma
Papiledema
Seizures
Trauma
In which case do CT before LP but not before abx
When will CSF have a fibrin web appearence?
Fungal/TB meningitis
Empirical antibiotic therapy of menitgitis?
Vancomycin plus
CEFTRIAXON
Ampicillin if over 50 or immunocompromised,
cefotaxime +ampicillin in neonates
Management of viral meningitis?
Acyclovir
What type of meningitis does amphotericin B treat?
Fungal
For which type of meningitis should dexamethasone 10mg IV QDS be used?
pneumococcal menigitis (for 4 days)
Chemoprophylaxis in menigitis?
Rifampicin x4 doses in household contacts
Ciprofloxacin 500mg x1 dose in direct contact
What is a subarachnoid haemorrhage?
Extravasation of the blood into the subarachnoid space
Causes of SAH?
Spontaneous: aneurysmal, AVN, cryptogenic
Traumatic
Prognosis for SAH?
1/3 die
1/3 disability
1/3 complete recovery
Signs in SAH?
Kernig sign
Brudzinki sign
Neck stiffness
Photphobia
Back pain
(signs of menigism)
Focal neurological signs: hemiperisis, occulomotor nerve plasy, abducens nerve palsy
Papillodema, retinal haemorrhage
Syncope (half)
Decreased conciousness
Seizures
How quickly does a thunderclap headache become severe?
Within 5 minuites
SAH invetigations
CT brain - disrubution of blood may indicate site of aneurysm, detect early hyrdrocephelus - 10% negative (sensitivity decreases with time of headache onset)
LP/CSF - xanthochromia 100% sensitive for nearly a week after 12 hours post onset (don’t do it before) - no need if CT positive
MRI - more sensitive than CT after 3 days, may remain positive up to 6 weeks (echo gradient sequences -looking for hemosiderin conspicuous with ‘susceptibility artifact’
Angiography - invasive or non invasive, CT or MRI, directly visualise, in invasive can perform endovascular coiling at the same time.
When might delayed vasospasam occur following an SAH?
4-14 days
What is high fever, altered mental status and seizures in the ABSENCE of neck stiffness suggestive of?
Enecphalitis
How is encephalitis managed?
Empirical involving broad spectrum antimicrobial cover with
2g IV ceftriaxone BD and 10mg/kg TDS for two weeks
Supportive management of complications including prompt termination of seizure activity with anticonvulsantw
Standard workup for enecephalitis?
Routine panel of blood tests
Blood cultures
Viral PCR
CSF for viral PCR
Malaria blood films if exposure suspected
CNS imaging - HSV has a predilection for the temporal lobes and bilateral multifocal haemorrhage is typical
Causes of encephalopathy?
Hypoglycemia
Hepatic encephalopathy
DKA
Drug induced encephalopathy
Beri Beri
Uremic encephalopathy
SLE
Hypoxic encephalopathy
Criteria for CT head following injury
As recommended by nice, the criteria for head CT after head injury include:
Clinical evidence of skull fracture.
More than 30 minutes retrograde amnesia.
Focal neurological deficit or seizure.
GCS <13 at any time (or <15 2 hours after injury).
More than 1 episodes of vomiting.
Loss of consciousness and any amnesia in patients who:
Are >65 years
Suffered a dangerous mechanism of injury (great height, road traffic accident)
Have evidence of coagulopathy (including anticoagulation with warfarin).
Fever and altered mental state should immediately suggest what, and what is the most important treatment to initiate
Encephalitis
HSV
IV IV Aciclovir
What’s the distribution of acute encephalitis and what is therefore seen on imaging
HSV has a predilection for the temporal lobes and bilateral multifocal haemorrhage is typical.
Low level burning thigh pain worsening over period of days with well demarcated area of loss of sensation but no other abnormalities on neurological examination
meralgia paraesthetica; a condition that classically arises due to compression of the lateral cutaneous nerve of the thigh
What is a bulbar palsy?
A bulbar palsy is a ‘lower motor neurone’ lesion affecting cranial nerves 9, 10 and 12.
This causes impairments in speech and swallowing.
How might a bulbar palsy present?
Clinical signs include an absent or normal jaw jerk reflex, an absent gag reflex, a flaccid fasciculating tongue, nasal quiet speech, and signs suggestive of the cause e.g. limb fasciculations of motor neurone disease.
Causes of bulbar palsy?
Causes of bulbar palsy include motor neurone disease (in particular the progressive bulbar palsy variant), myasthenia gravis, Guillain-Barré syndrome, brainstem stroke (the lateral medullary syndrome), and syringobulbia.
Bulbar palsy is most commonly caused by a brainstem stroke or tumor.
Acute bulbar palsy is a rare varient of GBS
How might bulbar palsy be fatal?
Bulbar palsy can prove to be fatal in progressive cases. Death from progressive bulbar palsy often occurs 1 to 3 years from the start of the disorder, however, it is often attributed to the development of associated aspiration pneumonia (infection of the lungs). Aspiration pneumonia often occurs in individuals with bulbar palsy as they may have difficulty swallowing and as a result, a large amount of material, or food, may enter the lungs and lead to infection.
Extensive bulbar damage may also damage the respiratory center in the brainstem, which is involved in signaling and controlling breathing. This can lead to a life threatening inability to breathe properly.
Additionally, progressive bulbar palsy may advance to ALS, or amyotrophic lateral sclerosis, and prognosis is usually poor. With ALS, death of motor neurons interferes with an individual’s ability to breathe and can ultimately result in fatality.
Aetiology of encephalitis?
Encephalitis is usually of viral aetiology, with herpes simplex virus type 1 as the most common culprit. This said, HSV-2, cytomegalovirus, epstein barr virus, varicella zoster virus, HIV and the arboviruses (including west nile virus) can also cause a similar picture.
Bacterial pathogens that cause meningitis (with the addition of lyme disease and mycoplasma) may sometimes progress to cause a meningoencephalitis, and uncommonly severe falciparum malaria may be the cause.
Autoimmune encephalitis, including the NMDA-receptor-antibody associated encephalitis should also enter the differential diagnosis.
Patients with generalised disease of the brain not attributable to inflammation are often said to be “encephalopathic”.
Clinical features of encephallitis?
Clinical criteria have been devised which allow clinicians to suspected a diagnosis, the cardinal feature of which is altered mental status (not as prominent in meningitis). Other suggestive features include fever, a flu-like prodromal illness, and early seizures.
What is encephalopathy and why might it occur?
Encephalopathy is a broader term, of which encephalitis may be included.
Causes of encephalopathy include:
hypoglycaemia,
hepatic encephalopathy,
DKA,
drug-induced encephalopathy,
uremic encephalopathy,
SLE,
hypoxic encephalopathy, and
Beri-Beri.
How should suspected encephalitis be treated?
Treatment of suspected encephalitis is empirical and should involve broad spectrum antimicrobial cover with 2g IV ceftriaxone BD and 10 mg/kg aciclovir TDS for two weeks.
Supportive management of complications including prompt termination of seizure activity with anticonvulsants (such as phenytoin) also important.
Side affects of aciclovir, often used to manage encephalitis?
Generalised fatigue/malaise (common)
Gastrointestinal disturbance (common)
Photosensitivity and urticarial rash (common)
Acute renal failure
Haematological abnormalities
Hepatitis
Neurological reactions
