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SKINT Workshop Glasgow 2005

SKINT Workshop Glasgow 2005. Intracranial Pressure Monitoring. Faculty. Dr Martin Walker Dr Carl Waldmann Prof Peter Andrews. Introduction. Dr Martin Walker. Traumatic Brain Injury. Raised ICP is a feature of most forms of brain injury

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SKINT Workshop Glasgow 2005

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  1. SKINT WorkshopGlasgow 2005 Intracranial Pressure Monitoring

  2. Faculty Dr Martin Walker Dr Carl Waldmann Prof Peter Andrews

  3. Introduction Dr Martin Walker ICP Monitoring SKINT Workshop ICS 2005

  4. Traumatic Brain Injury • Raised ICP is a feature of most forms of brain injury • SAH, ICH, Hydrocephalus etc are the in domain of neurosurgery • Unproven role in infective diagnoses • Traumatic Brain injury (TBI) is the area where ICP monitoring is usual practice and there is uncertainty over whether it should only occur in neurosurgical centres ICP Monitoring SKINT Workshop ICS 2005

  5. Blood Brain CSF 10% 80% 10% Monro-Kellie Doctrine Vintracranialvault = Vbrain + Vblood + Vcsf ICP Monitoring SKINT Workshop ICS 2005

  6. ICP-Volume Curve ICP mm Hg 100 80 Small volume marked ICP ICP controlled due to compensation 60 40 20 0 Volume ICP Monitoring SKINT Workshop ICS 2005

  7. ICP Ranges Normal -3 - 15 mm Hg Slight increase 16 - 20 Moderate increase 21 - 40 Severe increase > 40 Normal v Significant ICP Monitoring SKINT Workshop ICS 2005

  8. Pathophysiology of intracranial hypertension • Initial injury: • hypoperfusion & relative ischaemia • 24 - 48 hrs post trauma: • Some areas remain hypoperfused and infarcted • Other areas develop relative hyperemia despite no  in cerebral metabolic demands (uncoupling) • BBB injury results in cerebral edema • 48 - 72 hrs post trauma: •  CBF and  CBV  ICP • At any time: • Pain, agitation, seizures, pyrexia, BS abnormalities ICP ICP Monitoring SKINT Workshop ICS 2005

  9. Direct neuronal disruption Blood-brain barrier injury Vasogenic edema Cytotoxic edema Hyperemia Ischaemia Intracranial hypertension Increased cerebral blood volume Haematoma CSF volume ICP Monitoring SKINT Workshop ICS 2005

  10. Intracranial compensation • The brain is essentially non-compressible • Any increase in intracranial volume decreases CSF or CBV • CSF - primarily displaced into the spinal subarachnoid space • Blood - venoconstriction of CNS capacitance vessels displaces blood in jugular venous system ICP Monitoring SKINT Workshop ICS 2005

  11. Exhaustion of compensation • Once these limited homeostatic mechanisms are exhausted additional small increases in intracranial volume produce marked elevations in ICP • Raised ICP may decrease CBF resulting in vicious cycle ICP Monitoring SKINT Workshop ICS 2005

  12. Herniation • ICP rises are not equally distributed throughout the skull & pressure gradients develop • This may result in herniation • laterally (cingulate herniation) • downwards (transtentorial herniation) ICP Monitoring SKINT Workshop ICS 2005

  13. Schematic model for coning inferred force vector causing transtentorial herniation midline diencephalon midbrain pons temporal lobe uncus

  14. Schematic model for 3rd nerve palsy associated with raised ICP uncus cavernous sinuses third cranial nerves temporal lobe midbrain cistern obliterated

  15. The significance of raised ICP (1) • Rate of ICP rise • More important than actual value • Slow volume increases with tumours are well tolerated by decreasing CSF volume or brain tissue atrophy • Sustained elevations of ICP (above 20 mmHg) are associated with poor outcome • no direct proof that lowering ICP affects outcome • However some ICP values carry clinical significance ICP Monitoring SKINT Workshop ICS 2005

  16. The significance of raised ICP (2) • 40% of pts with altered mental status will have raised ICP • Significant rises occur in ~50% of severe TBI (GCS <9) • usually during first 72 hrs • Persistent and uncontrollable ICP elevations occur in 15% of HI and are usually fatal • CBF is disturbed if ICP > 40 mm Hg • Sustained ICP > 60 mm Hg is fatal • Usual Rx threshold is 20 or 25 mmHg ICP Monitoring SKINT Workshop ICS 2005

  17. ICP & CPP Normal intracranial pressure CPP = MAP – ICP 70 = 80 – 10 mm Hg ICP Monitoring SKINT Workshop ICS 2005

  18. ICP/CPP following brain injury Increased intracranial pressure 60 = 80 – 20 Low MAP 60 = 70 – 10 Increased ICP and low MAP 50 = 70 – 20 CPP = MAP - ICP ICP Monitoring SKINT Workshop ICS 2005

  19. History of ICP Measurement (1) • 1783 Monro & Kellie (1824) define closed box concept • 1866 Lyden measures ICP via trephine • 1866 Knoll produces graphic CSF pressure trace • 1870s Duret observes deleterious effects of injecting fluid in to dogs skulls ICP Monitoring SKINT Workshop ICS 2005

  20. History of ICP Measurement (2) • 1891 Quinke introduces LP allowing CSF sampling & measurement • 1900 Cushing describes the classic Triad seen with severely elevated ICP • systolic hypertension with widened pulse pressure • bradycardia • respiratory irregularities • 1960 Lundberg introduced long term continuous ICP monitoring via an indwelling intraventricular catheter. ICP Monitoring SKINT Workshop ICS 2005

  21. Therapeutic approaches tointracranial hypertension • 1918: tentorial incision (Cushing) • 1923: osmotic diuretics (Fay) • 1955: hypothermia (Sedzimir) • 1957: hyperventilation (Furness) • 1960: ventricular drainage (Lundberg) • 1961: steroids (Gailich and French) • 1971: decompressive craniectomy (Ransohoff Kjellberg) • 1973: barbiturates (Shapiro et al)

  22. Techniques for measuring ICP • EVD (aka ventriculostomy) • Extradural transducer • Subarachnoid bolt • Intra-parenchymal monitors • Fibreoptic (Camino) • Strain gauge (Codman) ICP Monitoring SKINT Workshop ICS 2005

  23. Driver Bolt Drill bit Benumof JL. Clinical Procedures in Anesthesia & Intensive Care, Lippincott, 1992 ICP Monitoring SKINT Workshop ICS 2005

  24. Case History Dr Carl Waldmann

  25. TYPICAL SCENARIO IN 1986 • CT scan if available sent by courier to Oxford. • Intubated, Sedated & Ventilated. • No monitoring in ambulance. • CT scan at Oxford - no neurosurgery required. • Send back to Reading gagging on tube and O2 in ambulance ran out. • Ventilated for two days on our ICU, then trial extubation. • Pneumonia, poor outcome- • SELF-FULFILLING PROPHECY. Surely we can do better ICP Monitoring SKINT Workshop ICS 2005

  26. Referrals to Oxford Neuro Unit • In one year 1756 referrals range 114-192/m • 21-58 admitted/month • 5-12 had to be referred out of region • Population served 2.4 million • needs 90 ward beds and 12 NSITU beds • in fact only 38 ward and 6 ITU • shared ITU beds with neurology,head&neck ICP Monitoring SKINT Workshop ICS 2005

  27. WHY THE DELAYS? • Lack of coordination at DGH end • lack of coordination at Regional Centre. • Poor communication between the two. • Lack of standardisation of Neurosurgical policy UK wide. • Lack of EBM. ICP Monitoring SKINT Workshop ICS 2005

  28. CASE HISTORY JC aged 15 • RTA hit by car at 30mph • GCS 4 V1 E1 M2 • Sedated, Intubated, Ventilated • Closed Head Injury no other injuries • CT imagelink to Oxford Neurosurgeons • No neurosurgery required, poor outlook ICP Monitoring SKINT Workshop ICS 2005

  29. ICP Monitoring SKINT Workshop ICS 2005

  30. OXFORD REGION ImlinkDermot Dobson • No loss of quality at receiving end • avert danger of unnecessary transfer • quicker decision • first 100 patients saved 3170 ambulance miles equivalent to £7000 the cost of an imagelink system ICP Monitoring SKINT Workshop ICS 2005

  31. play fair and repatriate asapbut doesn’t happen due to bed-managers and meeting targets ICP Monitoring SKINT Workshop ICS 2005

  32. IMLINK • No way of printing imlink scans • duty neurosurgeon must come to Xray to see the images • there is no link to the neuro theatres • dialogue often has been with the SHO neurosurgeon • if no bed who arranges the transfer • do neurosurgeons speak the same language ICP Monitoring SKINT Workshop ICS 2005

  33. Drawbacks of CT Scans • Inadequate Structural Diagnosis • Inadequate Prognosis • Poor assessment therapeutic response ICP Monitoring SKINT Workshop ICS 2005

  34. CASE HISTORY JC • Days 1-9 sedated, CPP and ICP directed therapy • Day 3 increased cerebral oedema on CT • Day 7 Percutaneous Tracheostomy • Day 10 ICP monitor removed • Day 34 Discharged home sitting unaided, no verbal response, right sided hemipegia ICP Monitoring SKINT Workshop ICS 2005

  35. TECHNOLOGY ASSESSMENT • Therapeutic v non-therapeutic • ICP monitoring is non-therapeutic • no direct effect on outcome • Does it alter the process of management of Head Injured patients and hence outcome? ICP Monitoring SKINT Workshop ICS 2005

  36. Resistance by Neurosurgeons • in1871 in BMJ:-‘using the sphygmomanometer we paralyse our senses and weaken clinical acuity’ PORTSMOUTH ICP Monitoring SKINT Workshop ICS 2005

  37. ICP Monitoring SKINT Workshop ICS 2005

  38. Addy, Waldmann and Collin Clinical Intensive Care 1996 87-91 ICP Monitoring SKINT Workshop ICS 2005

  39. CHEKARI, FIELDEN & KLUCNIKSBJA abstract from 2002 SOtA ICS • No clinical complications in 17 patients • safe use in DGH using Codman intraparenchymal device • 36% good/moderate recovery • 36% died • 24% severe disability and PVS ICP Monitoring SKINT Workshop ICS 2005

  40. ABC & stabilise neck ICP Monitoring SKINT Workshop ICS 2005

  41. Needs to be a government target and star rating ICP Monitoring SKINT Workshop ICS 2005

  42. NATIONAL NEUROSCIENCES PROJECT Belinda Crawford Should patients with closed head injury be managed with ICP monitoring in a DGH setting? ICP Monitoring SKINT Workshop ICS 2005

  43. effect outcome 4% risky procedure 14% not in DGH 21% NO Liase neuro 14% follow protocol 25% up to intensivist 2% YES RESULTS ICP Monitoring SKINT Workshop ICS 2005

  44. The discussion has moved from ‘Should DGHs put in ICP monitoring devices?’ to ‘Can DGHs interpret the data generated by this form of monitoring?’ ICP Monitoring SKINT Workshop ICS 2005

  45. COMMENTS • In ideal world should be in a neuro unit • We are not in an ideal world! • What if surgical intervention needed • What about interpretation • What about decompressive Ventriculostomy • What about decompressive Craniotomy • What is the alternative • If it aint broke don’t mend it ICP Monitoring SKINT Workshop ICS 2005

  46. DISTRICT GENERAL HOSPITAL GOOD INITIAL RESUS GOOD BASIC INTENSIVE CARE MONITORING ICP ICP/ CPP DIRECTED THERAPY MULTIMODAL MONITORING DECISION SUPPORT via IT LINKS GOOD FOLLOW-UP & REHAB ICP Monitoring SKINT Workshop ICS 2005

  47. Data interpretation and practical aspects of ICP monitoringDr Martin Walker Measurement to monitoring Sample waveforms Artefacts Remediable causes of raised ICP Management and treatment of raised ICP

  48. Methods of monitoring & charting • Stand alone monitor • With or without continuous trace • Monitor connected to patient monitor • Autocalculation of ICP • Standard versus high-low hourly charting CPP = MAP with transducer at EAM ICP Monitoring SKINT Workshop ICS 2005

  49. Normal ICP Waveform The normal ICP waveform contains three phases: • P1 (percussion wave) from arterial pulsations • P2 (rebound wave) reflects intracranial compliance • P3 (dichrotic wave) represents venous pulsations ICP Monitoring SKINT Workshop ICS 2005

  50. Intracranial compliance

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