Neurological Emergencies Flashcards
Describe the clinical features of raised ICP? (9)
- Headache
- Altered mental state (lethargy, irritability, slow decision making, abnormal behaviour)
- Papilloedma
- Vomiting (progresses to projectile)
- Pupil changes: irregular or dilated in one eye)
- Cranial nerve palsies (esp unilateral ptosis, III or IV lesions)
- Later changes: hemiparesis, raised BP, bradycardia
- Seizures, syncope if acute rise in ICP
- Cushings reflex
- visual changes: black spots, blurring, enlarged blind spot and reduced peripheral vision (subacute) or reduced central vision and visual acuity (acute advanced)
Describe the headache of raised ICP
nocturnal, starting on waking, worse on coughing/ moving
Describe what papillodema looks like
blurring of disc margins, loss of venous pulsations, flame haemorrhages
What is the cushings reflex and why does it occur?
hypertension + bradycardia + low resp rate due to: Ischaemia at medulla causing sympathetic activation so rise in BP + tachycardia// Baroreceptors detect increase in BP causing Bradycardia// Ischemia @ pons/ medulla resp centers so low resp rate
How should raised ICP be investigated?
- CT/ MRI for underlying lesions
- blood glucose, renal function and osmolality
- check for signs of CSF leak
- ICP monitoring can be done
Give 6 causes of raised ICP
- localised mass lesions (eg traumatic haematoma)
- neoplasms (glioma, meningioma, mets)
- abscesses
- focal odema secondary to trauma, infection or infarction
- disturbance of CSF circulation
- major venous sinus thombosis/ obstruction
- diffuse brain odema/ swelling
- idiopathic intracranial hypertension
Give 5 causes of diffuse brain odema/ swelling
- meningitis
- encephalitis
- diffuse brain injury
- sub arachnoid haemorrhage
- reyes syndrome
- water intoxication
- cerebral venous thrombosis
Describe the first line steps to management of raised ICP?
- stabilise ABC
- treat seizures with lorazepam +/- phenytoin
- Head CT if meets criteria
- assess C spine, immobilise and order neck CT if not cleared
- involve neurosurgery
- head elevation to 30 degrees
When should you intubate someone with a head injury/ raised ICP?
If: - sats <92% or - hypoxic on ABG or - GCS <8
Describe the further management of someone with raised ICP
- Analgesia with morphine and sedation w/ propofol if necessary
- mannitol (risk of hypovolaemia) or hypertonic saline if cerebral odema
- barbiturate coma
- hypothermia
- decompressive craniotomy and shunts
- treat cause (anticoag if venous outflow obstuction, diuretics then shunts if increased CSF, resections/ craniotomys/ steroids for SOLs)
- hyperventilation (causes hypercapnic vasoconstriction so decreases ICP)
Describe the clinical features of a subarachnoid haemorrhage?
- Sudden onset explosive headache (often occipital) lasting a few seconds or a fraction of a second then a diffuse headache which can last a week or so
- almost always have N+V
- altered mental status
- seizures
- neck stiffness/ meningism signs sometimes present around 6 hrs after
- intraocular haemorrhages seen on fundoscopy in 15%
- other signs of raised ICP
- 10-15% die before getting to hospital
What warning symptoms may occur prior to SAH as aneurysm expands and bleeds slightly (sentinel bleeds)?
- headache
- dizziness
- orbital pain
- diplopia
- ptosis
- sensory or motor disturbance
- seizures
- dysphagia
- bruits less common
Describe the investigation findings consistent with a subarachnoid haemorrhage? (4)
- CT scan without contrast: hyperdense blood vessel in basal cisterns (98% sensitive after 2 hrs and 100% after 6, sensitivity drops after 24hrs)
- cerebral panangiography then CT or MR angiography if aneurysm found
- LP if CT scan negative but suspect SAH- spectrophotometry should be able to detect xanthochromia if SAH occured (detected from 12hrs- 2weeks after bleed)
- ECG changes inc prolonged QT, Q waves, ST elevation
Describe the urgent and supportive management of a SAH? (4)
- stabilise pt and send straight to neurosurgical unit +/- intubation, ventilation, NG tube, analgesia and antiemetics
- endovascular obliteration by platinum spirals (coiling) or direct neurosurgical clipping to prevent rebleeding
- oral nimodipine given to prevent vasospasm which leads to cerebral ischaemia/ stroke
- hydrocephalus can occur as early or late complication, many will resolve on their own but some surgeons drain immediately
Describe the further management of an SAH? (3)
- secondary prevention (stop smoking etc)
- specialist rehab if lasting impairment
- antifibrinolytics reduce rate of rebleeding but doesnt improve overall outcomes
Describe the clinical features of meningitis
- Headache
- Fever
- Photophobia
- Neck stiffness
- Vomiting
- Muscle pains
- Non blanching purpuric rash
- seizures
- altered consciousness
- Fatigue, muscle pain
What signs require urgent senior review +/- critical care input when managing a meningitis pt? (9)
- rapidly progressive rash
- poor peripheral perfusion (cap refill >4/ BP >90mmhg)
- RR <8 or >30
- HR <40 or >140
- acidosis <7.3
- WBC <4
- lactate >4
- GCS <12 or drop of 2
- poor response to initial fluid resus
How should suspected meningitis (meningitis without signs of shock, severe sepsis or signs suggesting brain shift) be managed? (7)
- blood cultures
- bloods (FBC, renal function, glucose, lactate, clotting, viral PCR, blood gas)
- LP
- dexamethasone 10mg IV
- ceftriaxone IV 2g
- careful fluid resus
- throat swab for meningococal culture
- isolate until abx for 24 hrs, tell microbiology and PH
How should suspected meningitis with signs suggestive of brain shift/ raised ICP, severe sepsis or a rapidly evolving rash be managed? (9)
- critical care input
- secure airway, give O2
- take bloods, do cultures
- fluid resus (if shock/ sepsis/ rapidly evolving rash)
- ceftriaxone 2g IV
- Dexamethasone 10mg IV (omit if severe sepsis or rapdily evolving rash)
- Neuro imagine such as CT head if signs of raised ICP
- throat swab for meningococcal culture
- DELAY LP
What tests should be done on CSF when meningitis suspected? (7)
- glucose (w/ concurrent blood glucose)
- protein
- microscopy and culture
- lactate
- meningococcal and pneumococcal PCR
- enteroviral, HSV, VZV PCR
- consider investigations for TB meningitis
What are the criteria for delaying LP in meningitis?
- signs of severe sepsis
- rapidly evolving rash
- severe cario/ resp compromise
- significant bleeding rik
- signs suggestive of brain compartment shift (do CT first): focal neurosigns, presence of papillodema, continious or uncontrolled seizures, GCS <12
State 5 complications of meningitis
septic shock, DIC, septic arthiritis, haemolytic anamia, pericadial effusion, subdural effusion, SIADH, seizures, hearing loss, cranial nerve dysfunction
Describe the clinical features of encephalitis (5)
- bizarre behaviour or confusion
- decreased GCS or coma
- fever
- headache
- seizures
- focal neuro signs (weakness, visual disturbance, aphasia, cerebellar signs)
- history of travel or bite
Describe the key differences between meningitis and encephalitis?
- Seizures uncommon in meningitis but common in encephalitis
- photophobia, rash and neck stiffness much more common in meningitis
- focal neurological signs are a hallmark feature of encephalitis, but only occur in some and later in meningitis
- mental status is almost always altered in encephalitis, however is common but less so in meningitis
How should encephalitis be investigated?
How should encephalitis be investigated?
Give 3 common viral and 3 common non viral causes of encephalitis
Viral: HSV, arbovirus, EBV, CMv, VZV, HIB, mumps (paramyxo), measles, rabies, west nile
Non viral: any bacterial meningitis, lyme disease, TB, malaria, legionella, leptospirosis
How is encephalitis managed?
- start aciclovir within 30 mins or arrival- 10mg/ kg/ 8hrs IV for 14 days as empirical treatment
- specific therapies exist for CMV and toxoplasmosis
- supportive therapy in HDU/ ITU if necessary
- symptomatic treatment with phenytoin if necessary
Define status epilepticus
seizure lasting >30 mins or repeated seizures without intervening consciousness - usually in known epilepsy, if 1st presentation then high chance of structural brain lesion
How should status epilepticus be investigated/ assesed?
- bedside glucose (dont miss this as cause) early
- pulse oximetry and cardiac monitor while its happening
After treatment started: - consider anticonvulsant levels, toxicology, LP, blood cultures, urine cultures, EEG, CT and carbon monoxide levels
- CXR to evaluate for possible asipration
- lab glucose, ABG, u&e, ca, fbc, ecg
Describe management of status epilepticus (from start of seizure) (inc paeds and adult doses)
0 mins: ABC, high flow O2, check BM, make surroundings safe- (50ml 50% dextrose if hypo)
5 mins: give IV lorazepam 0.1mg/ kg (4mg) slow bolus or rectal diazepam 10-20mg
10-15 mins: (if no response) give 2nd bolus
20-25 mins: phenytoin infusion 20mg/kg (up to 2g) at 50mg/min w/ ECG monitoring AND seek ITU help for general anaesthetic with propofol/ thiopentone if still going at 45 mins
Give 5 causes of spinal cord/ cauda equina compression?
- neoplasms (breast, kindey, thyroid, lung, prostate mets, myeloma or primary bone tumours)
- trauma
- infections; abscesses
- spinal stenosis
- transverse myelitis
- disc prolapses (rare but lumbar disc herniations typically cause CES)
- post op haematoma
- spondylolithesis
Describe the locations and functions of the 2 main ascending sensory tracts and the main motor tract within the spinal cord
Describe the locations and functions of the 2 main ascending sensory tracts and the main motor tract within the spinal cord
What are the upper motor neurone signs?
- Weakness- esp of extensors in arms and flexors in legs
- Hyperreflexia, clonus, upgoing planters
- Hypertonia which is spastic (velocity dependent)- clasp knife
What are the lower motor neurone signs
- weakness (pattern consistent with neuronal distribution)
- muscle wasting
- fasiculation
- hypotonia/ flaccidity
- reflexed reduced or absent
- flexor planter reflex
Describe the type and distribution of motor and sensory deficit seen with cord lesions
- usually bilateral motor deficit from below level of lesion down- initially LMN signs then UMN over the next hrs.
- LMN signs + loss of reflexes at the level of the lesion
- Presence of a sensory level
- autonomic features may also be present & associated w/ worse prognosis (constipation, retention, incontinence)
Describe the MRC grading of muscle weakness
0= no contraction 1= flicker of contraction 2= some active movement 3= active movement against gravity 4= active movement against resistance 5= normal power (allowing for age)
Describe the classifications of head injuries?
- Focal (slit into haematoma (sub, extra or intracerebral) or contusion (coup vs contracoup)
vs - Diffuse (concussion vs diffuse axonal injury)
AND - traumatic (split into open/ penetrating vs closed)
vs - non traumatic (axonia, infection, CVA/ TIA, tumour etc)
Describe the pathophysiology of a concussion
- Stretching of axons causes impaired neurotransmission, ion regulation and reduced blood flow causing temporary brain dysfunction
Describe the clinical features of post concusion syndrome
Difficulty thinking clearly, slowed down, confusion, headache, N+V, balance problems, tired, light sensitive, irritable, sad, sleep disturbance, trouble falling asleep
Describe the pathophys of diffuse axonal injury
- Shearing of grey and white matter interface following traumatic acceleration/ deceleration or rotational forces
- Leads to axonal death so cerebral odema so raised ICP and death
- they get instate LOC with few recovering- v poor prognosis
State 5 signs of a basilar skull fracture
racoon eyes, CSF rhinorrhoea, CSF otorrhoea, battle sign, haemotympanum
Describe the differences in mechanism between extradural (EDH) and subdural (SDH) haemorrhage?
EDH: almost always traumatic
SDH: usually traumatic but less major trauma, can be spontaneous also
Describe the difference in presentation between EDH and SDH
EDH: young pt, LOC followed by lucid interval then rapid decline in consciousness, signs of raised ICP etc
SDH: acute bleeds can be any age, chronic bleeds seen in elderly, reduced GCS, neuro signs, or chronic bleeds= insidious neurological decline
Where is the bleed for EDH and SDH? What is the radiological appearance?
EDH: middle meningeal artery, lentiform shape, limited by suture lines
SDH: bridging veins, cresent shaped, not bound by suture lines but unable to cross midline due to falx cerebri, chronic bleeds appear hypodense- can have acute on chronic
What is the definitive management for EDH and SDH?
EDH: urgent craniotomy to relieve raised ICP, if small can just observe
SDH: acute- surgery to relieve raised ICP, if chronic and not causing symptoms then many are left alone
What are the criteria for a head CT within 1 hr of head injury?
- GCS <13 or <15 after 2 hrs
- focal neuro deficit
- suspected skull or C spine fracture
- seizure or vomiting >1 time
What are the criteria for head CT within 8 hrs of head injury?
- LOC or amnesia AND - age >65 (or) - coagulopathy (or) - high impact injury (or) - retrograde amnesia of > 30 mins
When is a CT neck NOT required to clear the neck and allow mobilisation?
- no posterior midline cervical tenderness
- no evidence of intoxication
- pt altert and orientated to person, place, time and event
- no focal neuro deficit
- no painful distracting injuries
How do acute bulbar and pseudobulbar palsies present differently?
- A bulbar palsy is one of the nuclei of CN IX- XII (medulla)
- A true bulbar palsy= LMN lesion (, flacid fassiculating tongue, normal or decreased jaw jerk and reduced gag reflex, quiet nasal speech)
- corticobulbar palsy/ pseudobulbar palsy is UMN (hot potato speech, increased jaw and palatine reflexes, mood incontinent giggling/ weeping, spastic tongue)
List causes of bulbar and a pseudobular palsies?
Bulbar: MND, guillian barre, polio, MG, syringobulbia, brainstem tumours or central pontine demyelinolysis
Pseudobulbar: MS, MND, BILATERAL stroke or centralpontine demyelinolysis
Subarachnoid Haemorrhage is bleeding between the arachnoid and pia mater. What are the two broad causes? Give some specifics.
Traumatic - eg RTA (may be other cranial bleeds as well)
Spontaneous - Rupture of cerebral aneurysm, AV malformation, Vasculitis
Give two modifiable and non modifiable risk factors for Subarachnoid Haemorrhage
Modifiable - Hypertension, Smoking
Non Modifiable - Female, ADPCKD
Where are Berry Aneurysms normally located?
Located at branching points of major blood vessels (points of maximum haemodynamic stress)
30-40% ACA
25% PCA
20% MCA
10% Bifurcation
Name four signs of Subarachnoid Haemorrhage
Neck Stiffness
Cranial Nerve Palsy
Reduced Consciousness
Diplopia
When is a Lumbar Puncture for Subarachnoid Haemorrhage required?
If more than 6 hours from onset
If strong clinical suspicion but no findings on CT
When should an LP be done for SAH? What would be a negative LP?
After 12 hours
If clear or if Oxyhaemaglobin alone (suggests trauma or traumatic tap)
Name four findings you would expect from a positive Lumbar Puncture for SAH
Opening Pressure (elevated)
Red Cell Count (elevated)
Xanthochromia
Bilirubin
Once an SAH has been diagnosed, what further investigation can be done?
CT Angiogram (to determine any underlying pathology, can be therapeutic - coil or clip at same time)
Name four medical managements of SAH
- IV fluids and monitoring
- GCS<8 requires intubation
- Nimodipine every 4h for 3w
- Analgesia and Antiemetics to prevent ValSalva
Name three possible surgical managements of SAH
Coiling
Clipping
External Ventricular Drain (if Hydrocephalus)
Name three complications of SAH
Rebleeding
Vasospasm
Hydrocephalus
Define Stroke
Clinical syndrome characterised by sudden onset of rapidly developing focal/global neurological disturbance, lasting more than 24h/leading to death (secondary to cerebral bloody supply disruption)
Strokes can be either Ischaemic or Haemorrhagic. How can Ischaemic strokes be classified?
By the Bamford/Oxford Classification
TACS, PACS, LAC, POC
Strokes can be either Ischaemic or Haemorrhagic. How can Haemorrhagic strokes be classified?
Intracerebral or Subarachnoid
Describe the pathophysiology of an Ischaemic Stroke
Either due to Thrombosis, Embolism or Dissection
Describe the pathophysiology of a Haemorrhagic Stroke
Usually due to Hypertension (but can also be due to vascular malformations, tumours, or bleeding disorders)
Describe the TAC classification of Ischaemic Stroke
Unilateral Sensory/Motor Weakness
Homonymous Hemianopia
Higher Cerebral Dysfunction
Requires 3/3
Describe the PAC classification of Ischaemic Stroke
Unilateral Sensory/Motor Weakness
Homonymous Hemianopia
Higher Cerebral Dysfunction
Requires 2/3
Describe the LAC classification of Ischaemic Stroke
Can be:
Pure Sensory, Pure Motor, Sensorimotor, Ataxic
Describe the POC classification of Ischaemic Stroke
One of the following: Brainstem Cerebellar Syndrome Conjugate Eye Movement Disorder Isolated Homonymous Hemianopia Bilateral Sensorimotor Loss Cranial Nerve Palsy and Contralateral Sensory/Motor
Name two Posterior Stroke Syndromes
Locked In Syndrome - Basilar Artery
Wallenberg Syndrome - Posteroinferior Cerebellar Artery (Nystagmus, Vertigo, Horners, Diplopia, Dysphagia)
FAST is the tool in the community used to screen for Stroke. What is the Hospital Tool called?
NIH Stroke Scale
- Good Score is <4
- Score>22 high risk of haemorrhagic transformation with thrombolysis
- Score>26 means thrombolysis is contraindicated
Name 5 investigations for a suspected stroke
CT head ECG Echo Bloods Carotid Doppler
How is a Haemorrhagic Stroke Managed?
Depends on the extent of the bleed and suitability for intervention
Large bleeds - decompressive hemicraniotomy or suboccipital craniotomy
How is an Ischaemic Stroke managed ideally?
Thrombolysis with Alteplase (synthetic tPA)
If within 4.5 hours and NIHSS is between 5 and 26
Name three contraindications to Thrombolysis
Ischaemic stroke within the past 3 months
Active Bleeding
Intracranial Neoplasm
Previous Haemorrhagic Stroke
If Thrombolysis is contraindicated in terms of Ischaemic Stroke management, what is the next line?
300mg Asparin for 2w followed by 75mg Clopidogrel lifelong
What is a Thrombectomy?
Removal of the thrombus done in specialist centres by interventional neuroradiology
Can be combined with Thrombolysis
Location specific and depends on brain tissue viability
Name two early and two late complications of Stroke
Early - Haemorrhagic transformation, Cerebral Oedema (eg Malignant MCA)
Late - Mobility and Sensory Issues, Fatigue
Raised ICP is initially compensated by shunting blood and CSF out. When it begins to decompensate, what are the symptoms?
Classic Triad - Headache (worse on waking), Papilloedema, Vomiting (projectile)
Pupillary changes, third nerve palsies, hypertension, bradycardia
Name 5 first line managements for raised ICP
Avoid Pyrexia Head Elevation at 30 degrees Sedation Mannitol (not if hyperosmotic or hypovolaemic) Analgesia
Name three second line managements of raised ICP
Barbiturate Coma
Hypothermia
Decompressive Hemicraniectomy
Name three complications of Status Epilepticus
Hyperthermia
Arrhythmia
Long term Neuro Damage
What is the first line management for Meningitis at UHL?
IV Ceftriaxone (Meropenem if PA) and Dexamethasone (unless immunosupressed)
Notify PHE
What is the first line management for Meningitis at UHL if over 60/immunocompromised?
Ceftriaxone + Amoxicillin + Dexamethasone
Name 5 causes of Spinal Cord Injury
Trauma Tumours Prolapsed Disc Haematoma Inflammatory DIsease
Other than insiduous progression, name five red flags for spinal cord injury
Gait Disturbance Loss of Bladder/Bowel Function L'hermitte's sign UMN signs in lower limbs LMN signs in upper limbs
How does a Spinal Cord Injury present?
Cervical Spine - Quadraplegia
Thoracic Spine - Paraplegia
Root pain in legs
May have loss of autonomic activity
Define Cauda Equina
Compression of nerve roots caudal to the level of spinal cord termination, causing one or more of: Bladder/Bowel Dysfunction, Saddle Anaesthesia, Sexual Dysfunction, Lower Limb Neuro Deficit
How can Cauda Equina be investigated?
Normally diagnosed from a good examination and history
MRI (40% show no abnormalities)
Urodynamic Studies (post surgery)
Name two differentials for Cauda Equina
Conus Medullaris Syndrome (less prominent pain, more urinary retention and constipation)
Mechanical Back Pain
How is Cauda Equina managed?
Urgent Surgical Decompression
Treat underlying cause
What is Cerebral Perfusion Pressure?
The available blood for brain tissue
CPP = MAP - ICP
Aim for >90
Describe a Subfalcine Herniation
Cingulate gyrus pushed under the free edge of the falx on the same side as mass
Can cause compression of the ACA
Describe a Tentorial Herniation
Uncus herniates through Tentorial Notch
Damages ipsilateral CNIII
Occludes blood flow in Posterior Cerebral and Superior Cerebellar
Can cause secondary brain stem haemorrhage (Duret)
Describe a Tonsilar Herniation
Cerebral Tonsils pushed through Foramen Magnum, compressing brainstem
Name 5 worrying features following a Head Injury
Vomiting Reduced GCS Confusion Signs of a Basal Skull Fracture Cushings triad
What are the three branches of GCS?
Eye Opening
Verbal Response
Motor
Best response out of each side is used
Describe the scoring of Eye Opening with GCS
4 - Spontaneously
3 - To Voice
2 - To Pain
1 - None
Describe the scoring of Verbal Response with GCS
5 - Conversation 4 - Confused 3 - Words 2 - Sounds 1 - None
Describe the scoring of Motor Response with GCS
6 - Obeys Commands 5 - Localises 4 - Withdraws 3 - Flexes 2 - Extends 1 - None
Name four indicaions for Head CT post Head Injury according to NICE
GCS<13 initially
Suspected Skull #
Focal Neurological Signs
>1 episode of vomiting
Describe the severity of Head Injury in terms of GCS
Mild (13-15)
Mod (9-12)
Severe (3-8)
Name four broad classifications of Bulbar Palsies
Muscle Disorders
Diseases of Motor Nuclei in Medulla and Lower Pons
Diseases of Intramedullary Nerves of Spinal Cord
Diseases of Peripheral Nerves supplying muscles
Name four presenting features of Bulbar Palsies
Weak and wasted tongue
Drooling
Absent palatal movements
Dysphonia
Name five causes of Bulbar Palsy
Diptheria Poliomyelitis MND Syringobulbia Guillaine Barre Syndrome
What is Pseudobulbar Palsy?
Disease of the corticobulbar tracts causing an UMN lesion
May have UMN signs in limbs
Name three causes of Pseudobulbar Palsy
MS
Internal Capsule Infarcts
Neurosyhphilis
How is Bulbar Palsy investigated?
Speech Assessment (Electromagnetic Articulography)
Routine Bloods
CT/MRI
How is Bulbar Palsy Managed?
Admission if dysphagia
Treat underling cause
Anticholinergics for drooling
Baclofen for Spasticity
Name four diseases affecting the NMJ and causing Respiratory Distress
Lambert Eaton
Myasthenia Gravis
Clostrodium Botulinim
Organophosphates
Name four diseases affecting the Muscle and causing Respiratory Distress
MND
Acid Maltase Deficiency
Electrolyte Disturbance (hypokalaemia)
Polymyositits
Name one diseases affecting the nerves and causing Respiratory Distress
Guillaine Barre Syndrome
