Disability - neuro Flashcards
Outline GCS scoring?
Eyes: 4 = spontaneously open 3 = open to voice 2 = open to pain 1 = won't open
Verbal: 5 = coherent 4 = inappropriate words 3 = confused 2 = sounds incomprehensible 1 = nothing
motor:
6 = spontaneous
5 = Localise to pain
4 = withdraw from pain
3 = Flex or decorticate response to pain
2 = extensor decerebrate response to pain
1 = no response
Classes of analgesia?
Via WHO step ladder:
Step 1 = non opioid e.g. NSAID
Step 2 = Weak opioid e.g. codeine
Step 3 = Strong opioid = morphine
Give examples of common opioids and whether they are synthetic or non-synthetic?
Synthetic = Pethidine, fentanyl Semi-synthetic = dihydrocodeine, diamorphine Noun-Synthetic = morphine, codeine
what receptors do morphine act upon, and the effect?
Mu = analgesia and miosis, reduced gut motility K = analgesia and dissociative Delta = Analgesia and anti-depressant
Systemic effects of morphine?
Pain - analgesia of moderate to severe pain, not good for neuropathic pain
Respiratory depression - blunt the chemoreceptor affect to PaCO2
neurological sedation
GI = N+V, reduced motility - stimulate chemoreceptor trigger zone in area postrema
Psychiatric = euphoria, dependance and tolerance
Immuno = histamine release = pruritus
Why not morphine in biliary pain?
Causes sphincteric contraction (Sphicnter of oddi) plus it stimulates gall bladder contraction = exacerbate pain
Which drug for opiate overdose?
Naloxone
Partial mu receptor antagonist
Short half life
How does paracetamol cause OD?
normally paracetamol metabolised in liver to n-acetylbenzoquinoneimine. This is the toxic metabolite, but is normally mopped up by glutathione.
Inn paracetamol OD to much for glutathione to deal with = hepatocyte injury.
NAC is a precursor of glutathione
How do NSAIDs work?
Inhibit COX, reducing prostaglandin formation.
Systemic SE’s of NSAIDs?
GI - dyspepsia, gastritis, peptic ulceration. Causes direct secretion of acid from parietal cells, and causes reduced mucus + bicarb production.
renal - Can precipitate AKI
Coagulopathy - inhibits thromboxane A2 on platelets, meaning cannot aggregate to form a platelet plug. This effect stays until new platelets made.
Bronchospasm - Inhibition of COX leads to arachidonic acid being metabolised down leukotriene pathway = bronchospasm.
How do NSAIDs cause renal injury?
Inhibition of compensatory PGI2 and PGE2. These normally vasodilate kidney when there is reduced renal perfusion, so without them cannot increase blood flow and offset the ATN.
When is epidural commonly used?
Postoperatively
Why is epidural often not used in ITU?
often have septic patients or patients with coagulopathy which are contraindications.
Also have hypovolaemic patients so giving epidural can cause further hypovolaemia.
systemic effects of epidural?
Hypotension: due to the block of sympathetic outflow = reduced SVR and CO.
Attenuates surgical stress response
Respiratory - Reduced FRC
Coagulopathy - reduces number of post-op DVT’s
what is CSF volume
150ml
Where is CSF produced?
70% in chord plexus of 3rd, 4th and lateral ventricle
remaining 30% comes directly from vessels lining ventricular wall .
Circulation of CSF?
Begins in lateral ventricle.
Travels to 3rd ventricle via foramen of Monro
Travels to nth ventricle via aqueduct of Sylvius
Travels to subarachnoid space of spinal cord via foramen of Luschka and magendie.
Then enters cranial cavity via foramen magnum and flows around brain in subarachnoid space
What are arachnoid villi composed of?
Fusion of arachnoid membrane and endothelium of dural venous sinus it has bulged into
Where is CSF absorbed?
80% is arachnoid villi
20% spinal nerve roots
What structures form BBB?
Tight junctions between endothelial cells of cerebral capillaries
Astrocytic foot processes applied to basal membrane of cerebral capillaries
What can pass through BBB?
Lipids and lipid soluble substances e.g. GA, opiates
protons (H+)
Which three parts of the brain lie outside the BBB?
Neurohypophysis = posterior lobe of pituitary gland - produces ADH and oxytocin
Circumventricular organs = around 3rd and 4th ventricles
Median eminence of hypothalamus
What. pathologies can affect the BBB?
Infection
Trauma
Tumours
Ischaemia
What is cerebral blood flow?
750ml/min = 15% CO
This flow is maintained by auto regulation, between systolic of 50mmHg and 150mmHg
Mechanism of auto regulation?
- myogenic: Increase in wall tension due to raised MAP stimulates a reactive contraction of smooth muscle, maintaining flow
- Metabolic: If blood flow is increased due to rise in arterial pressure, the normal vasodilators produces are washed away, leading to increased vascular resistance and normal flow
- Neurogenic - sympathetic stimulation can affect arteriolar tone.
What the factors play a role in cerebral flow regulation>
PaCO2 - if increases have increased vasodilation of cerebral arterioles increasing blood flow
Low CO2 causes vasoconstriction and decreased flow
PaO2 - Brain has very high demand for oxygen. Any acute hypoxia causes vasodilation to rapidly increase flow
What is CPP?
MAP - ICP
Must remain above 70mmHg for adequate perfusion
What is Cushings reflex?
in raised ICP, you get a hypertension to maintain CPP and a resultant bradycardia
What is Monroe-Kelly Doctrine?
Cranial cavity is a fixed space, with non-compressible contents
Draw a graph showing relationship between intracranial volume and ICP?
draw
Give some causes of raised ICP?
- CSF - hydrocephalus:
a) Increased production (RARE) Choroid tumour / hyperplasia
b) Decreased absorption - Pseudotumor cerebri syndrome
c) Blockage - tumour, scarring from infection - Blood = SDH, EDH, SAH, intracerebral bleed
- Brain e.g. tumour, cerebral oedema
Signs. and symptoms of raised ICP?
Headache and N+V = worse In morning
B/L papillodema - shows chronic
Reduced GCS
How to control ICP?
Conservative:
Bed position and fluid restrict
Controlled ventilation - specifically CO2
medical:
Diuretics = mannitol 0.25-1g/kg over 30 mins IV
Barbiturates e.g. thiopentone
Surgical:
Drainage of CSF from ventricular catheter
Surgery - Decompressive craniectomy
Most important complication of raised ICP?
Cerebral herniation
Different types of herniation?
Subfalcine = cingulate gyrus herniating under the falx cerebri . Can compress ACA = coma and contralateral weakness
Tonsillar - displacement of cerebellar tonsils via foramen magnum = cerebellar signs and Resp depression
Transtentorial = Uncus of temporal lobe passes via tectorial hiatus. Compresses midbrain and PCA
Also compresses ipsilateral occulomotor = blown pupil
Name a flash localising sign in herniation?
Abducens nerve palsy means cannot abduct eye.
Think this is because motor nucleus affected and is site of lesion, BUT actually herniation causes kinking of CNN6 on its long intracranial course.
When CT?
Reduced GCS, or new neurology
Persisting symptoms e.g. headache or meningism
Management of neurological compromised patient?
Generally - ABCDE
Tight ventilatory control
Careful fluid and electrolyte balance
Manage cause:
1. CSF = Ventriculoperitoneal shunt. But acutely may require external ventricular drain.
- Blood = EDH needs immediate evacuation. SDH = burr holes. SAH = coil or clipping.
- Brain = Steroids, PPI, laxatives and eventual debunking if possible.
Types of spinal injury?
Central cord = motor weakness mainly affecting UL
Anterior cord = motor weakness and spinothalamic. Dorsal tract unaffected = Fine touch, proprioception and vibration.
Brown sequard = hemisection:
Ipsilateral motor loss and dorsal column. Contralateral spinothalamic
Why can spinal cord trauma cause bradycardia?
- Loss of sympathetic outflow
- Increase in parasympathetic stimulation due to procedures such. as suctioning / intubation
- Cushing reflex
Why can spinal cord lesion cause hypotension?
Sympathetic loss leads to reduced vascular tone
Often miss occult blood loss e.g. blunt abdo trauma
Dangers of autonomic dysfunction in these situations?
Occult blood loss can be missed, and hypotension ascribed to neurogenic shock.
Overload with fluids - pulmonary oedema
Reduced CPP due to hypotension
Hypothermia
What is spinal shock?
Temporary flaccid paralysis immediately after injury.
Can recover after one month.
What drug is key in spinal cord injury?
High dose IV methyl Prednisolone.
Reduces free radical production causing secondary spinal cord injury.
Important issues during long term management?
Rehab Prevention of ulcers Chest physio Feeding - line insertion Psychological therapy
LP purpose?
Diagnostic:
Infection
SAH
Hydrocephalus
Therapeutic - hydrocephalus
Pre-procedure checks for LP?
Lab = platelets and PT Radiology = CT often done before
If suspect SAH, LP must be 12 hours after
Equipment and procedure?
Sterile pack, LP needle, manometer, LA, 4 universal pots.
- Position - on side knees up
- Mark between L3/L4 = iliac crests
- Prep and drape.
4, LA
- Insert LP needle
- Take out needle, leave catheter in and insert manometer
- 4 universal samples - Virology, cytology, protein and glucose, cultures
SE’s of LP?
Minor = headache, pain, paraesthsia
Major = haematoma, infection, paraplegia
