Neurocritical care for retrieval medicine

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Neurocritical care for retrieval medicine

• Stuart Lane

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Overview

• Traumatic Brain Injury TBI
• Subarachnoid haemorrhage SAH
• Arteriovenous Malformation AVM
• Intracranial Haemorrhage ICH
• Ischaemic stroke
• Specific therapies e.g. vasospasm
• Monitoring and drains
• Extras

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TBI

• The leading cause of death and morbidity from
  ages 1- 44yrs old
• The latest Brain Trauma Foundation (BTF)
  guidelines 2007 are well accepted
• Prehospital
• Hypoxaemia and hypotension
• GCS used in pre-hospital setting DISCUSS GCS
• Non-use paralysis for intubation
• Hypertonic NaCl for GCS lt8 can be considered
• Hyperventilation for signs of herniation
• Penetrating injury also included
• Initial medical management no different
• Surgical management different
• Most likely to be blunt closed TBI

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Interhospital transfer

• Avoid hypotension and hypoxaemia
• Hypotension is worse than hypoxaemia
• Dramatically worsen outcome
• Intubation is assumed for this presentation
• Oxygen PaO2 gt 90mmHg / SpO2 gt 95
• PaCO2 35-40 mmHg / PETCO2 31-35 mmHg
• CPP cant be assessed without an ICP monitor
• MAP gt 8O mmHg if no monitor
• CPP 50-70 if monitor.
• What do we mean by CPP?
• What did the trials really show / ?ARDS

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Interhospital transfer

• Phenytoin only if witnessed seizure
• Resuscitation to euvolaemia with isotonic
  crystalloids, then use noradrenaline to augment
  MAP FLUIDS
• NGT / OGT
• Normothermic
• If spine cleared, then sit 30 head up
• Brown tape vs.. white tape
• Remove collar and use sandbags venous
  congestion
• Avoid hyperglycaemia not really a retrieval
  issue
• Paralyse for transfer
• No evidence of improving ICP
• Significant amount of movement for retrieval
• BTF not in retrieval patients
• Paralysis not evidenced, not worried about CIPMN
  at this time
• May make the patient more CVS stable

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ICP monitoring and EVDs
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ICP monitoring and EVDs
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ICP monitoring and EVDs

• The transducer is fixed at a reference level
• Foramen magnum / external auditory meatus.
• The system is connected to a drainage chamber
• Allows drainage of CSF into the collecting bag or
  chamber.
• The height of this drainage chamber can be
  adjusted relative to the reference point
• When the EVD is unclamped and the stopcock is
  opened it allows drainage of CSF
• When the ICP is more than the set height of the
  draining chamber.
• The drainage will continue until
• The ICP falls to a value less than the chamber
  height
• The EVD is clamped.

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ICP monitoring and EVDs

• P1- Percussion wave
• Created by systolic blood pulsation transmitted
  through choroid plexus)
• P2- Tidal wave
• Reflects brain compliance
• Exceeds P1 in noncompliant brain
• P3- Dicrotic wave
• Produced due to aortic valve closure

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ICP monitoring and EVDs

• A waves - plateau waves
• Lasting 520 min
• 50 100 mmHg high
• B wave
• Frequency of 0.52 min-1
• Up to 50mmHg
• C waves
• Last 45 min-1
• Up to 20mmHg
• Intervention is required for A and B waves
• C waves may be
• Normal
• Due to a change in the vasomotor tone.

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Closed vs open EVD

• Limit clamping of EVDs
• Administration of intrathecal antibiotics
• Assessment for removal
• Getting the patient into a chair / back into bed
• Clamp it whilst transferring the patient from bed
  to stretcher
• Avoid loss of csf if the drain goes below the
  level of required drainage
• Open it again and leave open for transfer
• For a long transfer, if known ICP problems, then
  measure ICP and check pupils at intervals
• Clamp it again when transferring the patient from
  stretcher to bed

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What if the ICP goes up

• Recheck everything
• ABC and glucose
• Monitoring equipment including waveform
• Deepen sedation
• Paralyse, if not already done
• Deepen sedation further
• Consider CSF drainage / open drainage system
• Osmotherapy
• Mannitol vs. hypertonic saline
• Manual hyperventilation in an emergency

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Second line ICP therapy

• ABC again
• Recheck the waveform if you have one
• If ICP remains gt 20 mmHg for 15 minutes despite
  the above treatment
• More sedation
• Optimise fluids.
• Consider diuresis
• EVD left open
• Mild hypothermia
• More paralysis
• Thiopentone bolus
• Maintain MAP with noradrenaline

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Forget about..

• Transcranial Doppler
• Jugular bulb monitoring
• Brain oxygen content monitor
• Cerebral microdialysis
• Corticosteroids

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SAH

• 5 of all strokes
• 1015 die before reaching hospital
• Pathophysiology
• 80 aneurysmal,
• 15 AVM
• 5 other e.g. clotting abnormalities / drugs
• Rebleeding risk
• 8 in the first 48 hours
• 1 per day thereafter
• Reasonable to delay surgery
• Poor grade
• Established vasospasm

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Grading systems
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Aneurysmal SAH

• Management different if aneurysm is secured or
  unsecured
• Much extrapolation of TBI data
• Oxygen PaO2 gt 90mmHg / SpO2 gt 95
• PaCO2 35-40 mmHg / PETCO2 31-35 mmHg
• Fluid resuscitation to euvolaemia with isotonic
  crystalloid
• Noradrenaline to maintain MAP gt70mmHg
• EVD for hydrocephalus ?CLOT DISRUPTION
• Debatable for prevention of hydrocephalus
• ICP monitoring for severe cases
• OGT / NGT

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Surgery

• Surgery within 48hrs if possible
• Clipping vs.. coiling still a big debate
• Improved mortality with coiling
• Rebleeding slightly higher in coiling group
• Clipping still favoured in the US
• Discussion between neurosurgeon and
  neuroradiologist
• Can still Transfer to any neurosurgical centre
• Coiling favoured
• Patients with poor clinical grade
• Patients who are medically unstable
• In situations where aneurysm location imparts an
  increased surgical risk
• cavernous sinus
• basilar tip aneurysms
• Small-neck aneurysms in the posterior fossa
• Patients with early vasospasm
• Cases where the aneurysm lacks a defined surgical
  neck
• Patients with multiple aneurysms in different
  arterial territories if surgical risk is high
• It is falling out of favour once again in some
  groups

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Transfer of aneurysmal SAH

• MAP 70 if aneurysm not secured
• 30 head up
• Keep normothermic
• Avoid hyperglycaemia
• Nimodipine can wait TRIALS
• Magnesium can wait TRIALS
• Monitoring and access
• CVC and arterial lines discussed later

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Vasospasm

• Delayed narrowing of the large capacitance
  vessels at the base of the brain
• Poorly understood (DOES IT EXIST)
• Normally 7-10 days post SAH
• 70 of SAH patients have angiographic evidence
• 30 have significant clinical sequelae
• Impaired autoregulation
• Cerebral ischaemia
• Cerebral infarction
• Prevention and treatment are different entities
• Prevention
• Nimodipine
• Magnesium
• No other agents
• HHH therapy is therapy not treatment
• Illogical
• Not supported

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Vasospasm

• Treatment
• Fluids to euvolaemia
• Try to avoid excess hypervolaemia
• Imaging to rule out other possible problems
• Titrate MAP to neurological improvement with
  noradrenaline
• MAP 90-100 if unconscious
• Angiography
• Verapamil / papaverine injections
• Angioplasty

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AVM

• The direct connection between the arterial and
  venous systems supplies a low-resistance shunt
  for arterial blood and exposes the venous system
  to abnormally high pressures
• Use systolic BP limitations
• Lots of sedation and paralysis for transfer

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ICH

• 10 of all strokes
• Surgical intervention becoming less common
• Posterior fossa lesions gt 3cm
• Young patients with lobar haemorrhage
• Association with a structural vascular lesion
• STITCH trial
• Craniotomy for superficial clots (lt10mm from the
  skull) with clinical deterioration
• Aspiration for deep clots

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rFVIIa for ICH CHANGE CLIPS
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rFVIIa for ICH
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rFVIIa for ICH
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Transfer of ICH

• Specific guidelines
• MAP lt130mmHg in chronic hypertension
• No use of rVIIa
• Extrapolation of TBI data once again
• Sedate
• Paralyse

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Ischaemic stroke

• 85 of all strokes
• Thrombosis
• Embolism
• Hypoperfusion
• Venous occlusion
• Clinical presentation
• Decreased conscious level
• CT showing
• No haemorrhage
• No significant MCA territory involvement

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Thrombolysis?

• Severe neurological impairment with NIH stroke
  scale gt22
• CT evidence of extensive MCA territory infarct
• Sulcal effacement
• Loss of GW differentiation
• Greater than 1/3 MCA territory

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NIH stroke scale

• Total score out of 44
• Level of consciousness
• Best gaze
• Visual
• Facial palsy
• Motor arm
• Motor leg
• Limb ataxia
• Sensory
• Language
• Dysarthria
• Extinction and inattention
• If retrieval required
• Likely to be greater than 22
• Unable to assess accurately

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Thrombolysis

• Within the first 3 hours
• substantial net benefits for virtually all
  patients with potentially disabling deficits.
• Within 3-4.5 hours
• moderate net benefits when applied to all
  patients with potentially disabling deficits.
• MRI of the extent of the infarct core
• can likely increase the therapeutic yield of
  lytic therapy, especially in the 3 to 9 hour
  window.
• Intra-arterial fibrinolytic therapy in 3 to 6
  hours
• moderate net benefits when applied to all
  patients with potentially disabling deficits and
  large artery cerebral thrombotic occlusions.
• Based on NINDS 1 and NIND 2 rt-PA trials

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For transfer

• Have the primary hospital discuss this with the
  receiving hospital
• IV rt-PA
• Aspirin if no haemorrhage on CT
• Anticoagulation not indicated unless suggestion
  of venous infarction
• Dose of clexane for transfer
• Specialist interventional radiology centre for
  intra-arterial thrombolysis
• New techniques

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Other possibilities..

• Hemicraniectomy for significant MCA infarct
• Treat as for raised ICP
• Surgery is definitive treatment
• 18-60 years within 48 hours
• More likely to be called when thrombolysis has
  caused haemorrhagic transformation
• Cryoprecipitate infusion
• Platelet transfusion
• Primary centre to arrange pre-arrival

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Other conditions

• Cerebral tumours
• Consider steroids for raised ICP
• Mannitol is effective
• Cerebral abscess
• Consider steroids for raised ICP

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Monitoring

• Arterial line
• Desirable
• Not if delaying treatment
• Central Venous Catheter
• Desirable
• For multiple infusions (Not in retrieval
  medicine)
• For catacholamines
• CVP measurement is wasting time and useless
• Not if delaying treatment
• Dont delay treatment
• Heavy sedation, may require catacholamines
• Paralysis may help here

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Clinical monitoring of possible cerebral
herniation

• Difficult if sedated / paralysed
• Pupils need to be seen
• So do not tape
• Clinical examination remains paramount
• Emergency measures
• Hyperventilation
• Osmotherapy
• Burr hole

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Clinical monitoring of possible cerebral
herniation

• Can occur at ICPs lt25mmHg
• ICP threshold is not uniform
• Depends on the location of the mass lesion
• Abnormal posturing on presentation
• Pupillary abnormalities

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Brain herniation syndromes

• Supratentorial herniation
• 1 Uncal
• 2 Central (transtentorial)
• 3 Cingulate (subfalcine)
• 4 Transcalvarial
• Infratentorial herniation
• 1Upward (upward cerebellar)
• 2 Tonsillar (downward cerebellar)

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Summary

• Keep it simple for transfer
• Maintain brain perfusion
• Use MAPs appropriate to pathology
• Most specific therapies can wait
• Monitoring remains clinical, with assistance from
  numbers
• Avoid delays with primary patholgies

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Questions?
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Questions?