Neurocritical care for retrieval medicine

1. Neurocritical care for retrieval medicine Stuart Lane

2. 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

3. 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 <8 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

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

5. 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

6. ICP monitoring and EVD’s

7. ICP monitoring and EVD’s

8. ICP monitoring and EVD’s • 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.

9. ICP monitoring and EVD’s • 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

10. ICP monitoring and EVD’s • A waves - plateau waves • Lasting 5–20 min • 50 –100 mmHg high • B wave • Frequency of 0.5–2 min-1 • Up to 50mmHg • C waves • Last 4–5 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.

11. Closed vs open EVD • Limit clamping of EVD’s • 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

12. 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

13. Second line ICP therapy • ABC again • Recheck the waveform if you have one • If ICP remains > 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

14. Forget about.. • Transcranial Doppler • Jugular bulb monitoring • Brain oxygen content monitor • Cerebral microdialysis • Corticosteroids

15. SAH • 5% of all strokes • 10–15% 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

16. Grading systems

17. Aneurysmal SAH • Management different if aneurysm is secured or unsecured • Much extrapolation of TBI data • Oxygen PaO2 > 90mmHg / SpO2 > 95% • PaCO2 35-40 mmHg / PETCO2 31-35 mmHg • Fluid resuscitation to euvolaemia with isotonic crystalloid • Noradrenaline to maintain MAP >70mmHg • EVD for hydrocephalus ?CLOT DISRUPTION • Debatable for prevention of hydrocephalus • ICP monitoring for severe cases • OGT / NGT

18. 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

19. 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

20. 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

21. 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

22. 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

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

24. rFVIIa for ICH CHANGE CLIPS

25. rFVIIa for ICH

26. rFVIIa for ICH

27. Transfer of ICH • Specific guidelines • MAP <130mmHg in chronic hypertension • No use of rVIIa • Extrapolation of TBI data once again • Sedate • Paralyse

28. 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

29. Thrombolysis? • Severe neurological impairment with NIH stroke scale >22 • CT evidence of extensive MCA territory infarct • Sulcal effacement • Loss of GW differentiation • Greater than 1/3 MCA territory

30. 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

31. 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

32. 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

33. 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

34. Other conditions • Cerebral tumours • Consider steroids for raised ICP • Mannitol is effective • Cerebral abscess • Consider steroids for raised ICP

35. 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 • Don’t delay treatment • Heavy sedation, may require catacholamines • Paralysis may help here

36. 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

37. Clinical monitoring of possible cerebral herniation • Can occur at ICP’s <25mmHg • ICP threshold is not uniform • Depends on the location of the mass lesion • Abnormal posturing on presentation • Pupillary abnormalities

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

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

40. Questions?

41. Questions?