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Multimodal Monitoring in Head Injured Patients - Management of CPP: Detection and Treatment of optimal CPP

Multimodal Monitoring in Head Injured Patients - Management of CPP: Detection and Treatment of optimal CPP. Jürgen Meixensberger Department of Neurosurgery. 1. Why? 2. Critical Border ? 3. Time Course ? 4. Individual optimized CPP ? 5. Therapy.

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Multimodal Monitoring in Head Injured Patients - Management of CPP: Detection and Treatment of optimal CPP

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  1. Multimodal Monitoring in Head Injured Patients -Management of CPP:Detection and Treatment of optimal CPP Jürgen Meixensberger Department of Neurosurgery

  2. 1. Why? 2. Critical Border ? 3. Time Course ? 4. Individual optimized CPP ? 5. Therapy CPP = index of input pressure determining CBF and perfusion Effect of reduced CBF ml/100g/min Edema, Lactate Ischemia Loss of electric activity Penumbra Loss of Na/K Pump, ATP Infarction Cell death

  3. Risk to secondary ischemic brain damage • Traumatic brain injury diffuse focal, multiple • Subarachnoid Hemorrhage Vasospasm • Ischemic Stroke Penumbra

  4. Guideline German Society of Neurosurgery Traumatic Brain Injury in Adults CPP „Adequate cerebral perfusion pressure is necessary to provide a sufficient cerebral blood flow. The question, whether to treat increased ICP or maintainance of CPP as first treatment goal, is still controversial in the literature.“ AWMF – Leitlinien – Register Nr. 008/001

  5. Definition Cerebral Perfusion Pressure*is a surrogate of cerebral blood flow CBF. CBF = CPP (MAP – ICP*)/CVR * Referenced to the Foramen of Monroi Cerebral Perfusion Pressure CPP

  6. Induced Hypertension Jaeger M, Acta Neurochir 2005 Meixensberger J, JNNP 2003 CPP and Cerebral Oxygenation Valadka A, Acta Neurochir 2002 Menzel M, J Neurosurg Anesthesiol 1999 Doppenberg E, Surg Neurol 1998 Individual increasing of CPP guided by PtiO2 >10 mmHg decreased significantly amount of hypoxic episodes after TBI.

  7. CPP=70 mmHg CPP=90 mmHg Coles JP, Brain 2004 1. Why? 2.Critical Border ? 3. Time Course ? 4. Individual optimized CPP ? 5. Causes 6. Therapy

  8. The optimal CPP in patients suffering from TBI is unclear. • Recommendations: From CPP>50, > 60 mmHg to CPP>90 mmHg • Reduced as well as high CPP influenced Outcome in a negative manner. • Robertson et al. Crit Care Med 1999, Contant et al. J Neurosurg 2001 (n=189) • Balestreri et al. Neurocrit Care 2006 (n=429)

  9. Outcome - Function of ICP and CPP Balestreri et al Neurocritical Care 2006 N = 429

  10. Meixensberger J, Acta Neurochir 1993 Optimal CPP Brain Trauma Foundation, J Neurotrauma 2003,2007 CPP < 70 mmHg • Robertson C, Crit Care Med 1999Robertson et al., • Contant et al. J Neurosurg 2001 (n=189) • Balestreri et al. Neurocrit Care 2006 (n=429) CPP > 60 mmHg Avoid CPP < 50 mmHg Intact Autoregulation: CPP > 70 mmHg EBIC, Acta Neurochir 1997 CPP 60–70 mmHg

  11. Optimized CPP - Therapy * TBI N = 30 * Episode > 10 min

  12. 1. Why? 2. Critical Border ? 3. Time Course ? 4. Individual optimized CPP ? 5. Causes 6. Therapy % ptiO2 < 10 mmHg % ptiO2 < 10 mmHg F R E Q U E N C Y Day 1-2 Day 3-5 Day 6-8 CPP mmHg

  13. 1. Why? 2. Critical Border ? 3. Time Course ? 4. Individual optimized CPP ? 5. Causes 6. Therapy Effect of reduced CBF ml/100g/min Edema, Lactate Ischemia Loss of electric activity Penumbra Loss of Na/K Pump, ATP Infarction Cell death

  14. Concept individual optimized CPP (CPPopt) Steiner et al. Crit Care Med 2002 (n=114) • Based on continous monitoring of cerebrovascular pressure reactivity index PRX • PRx = moving correlation coefficient MAP / ICP Czosnyka et al. Neurosurgery 1997

  15. PRx CPPopt CPP Individual optimized CPP Steiner et al. Crit Care Med 2002

  16. PRx CPPopt CPP Individual optimized CPP + PtiO2 Steiner et al. Crit Care Med 2002

  17. TBI n=33 • Continous Monitoring(ICM-plus Software) • MAP • ICP [Codman] • CPP • PtiO2 [Licox] • PRx = moving correlationcoefficient MAP / ICP • Czosnyka et al. Neurosurgey 1997 • Data analysis CPP vs. PRx CPP vs. PtiO2 CPP-class of 5 mmHg

  18. PRx CPP Results: • CPPopt n=28/33 (85 %) • CPPopt n=7 60-65 mmHg n=1 65-70 mmHg n=8 70-75 mmHg n=1 75-80 mmHg n=6 80-85 mmHg n=3 85-90 mmHg n=2 90-95 mmHg

  19. CPPopt PRx CPP

  20. PtiO2 PRx CPPopt CPP

  21. CPPopt PRx CPP

  22. PtiO2 PRx CPPopt CPP

  23. CPPopt PtiO2 PRx n=28 CPP Jaeger et al Crit Care Med 2010

  24. Therapeutic Options: CPP > 60, < 70 mmHg * Induced hypervolemia with cristalloids Cave: heart insufficience No body/head – elevation 0° Inotropica – infusion Cave: acute coronary syndrome, arrhythmia Diuretics – Reduction of centralvenous pressure Ventilation - „best PEEP“ - concept * Option; Prognostic value only given by case reports;

  25. Management of CPP after TBI Recommendations: Avoid CPP < 50 mmHg – tominimize edema formation CPP > 70 – 80 mmHg – can improve perfusion if autoregulation is intact Class II evidence CPP of 60 mmHg – sufficient CBF and cerebral perfusion in most cases Ancillary monitoring is helpful to target CPP

  26. Management of CPP after TBI Recommendations: Need for more data Individualized optimal CPP based on hemodynamic monitoring/ pressure autoregulation indices Randomized outcome studies

  27. Thank You for Your Attention !

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