Management of Intercranial Pressure


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Management of Intercranial Pressure

  1. 1. Intracranial Pressure and Cerebral Edema Neuro-ICU 2009 PJ Papadakos MD FCCM Director CCM Professor Anesthesiology, Surgery and Neurosurgery Rochester NY USA
  2. 2. Is there a debate?
  3. 3. HOW DO PATIENTS PRESENT ? • Obvious--motor vehicle accident, car vs pedestrian, fall from height, etc • Less obvious--sports injuries (football), delayed deterioration (epidural) • Hidden--shaken baby syndrome, older child maltreatment • Inter cranial Hemorrhage • Stroke
  4. 4. CAVEATS IN BRAIN INJURY • Neurologic examination - the most important information you have • Accurate history is often unavailable or inaccurate • Potential for associated injuries or illness (cardiovascular, respiratory, cervical spine)
  5. 5. CEREBRAL RESUSCITATION • Primary survey - airway, breathing, and circulation • Neurologic evaluation • Secondary survey - “head to toe” • Neuroradiologic evaluation • Ongoing evaluation and transport
  6. 6. MECHANISMS OF INJURY-PRIMARY • Impact: epidural, subdural, contusion, intracerebral hemorrhage, skull fractures • Inertial: concussion, diffuse axonal injury • Hypoxic Ischemic
  7. 7. MECHANISMS OF 2nd INJURY • Global – Hypoxia and ischemia of brain – Decreased cerebral blood flow due to increased intracranial pressure • Local – impairment of cerebral blood flow or extra cellular milieu due to the presence of injured brain
  8. 8. PATHOPHYSIOLOGY • Primary damage – the only treatment is by prevention. • Secondary damage – multifactorial and time dependent.
  9. 9. SOME of the SECONDARY EVENTS IN TRAUMATIC BRAIN INJURY diffuse axonal inflammation injury BBB disruption apoptosis necrosis edema formation ischemia Brain trauma energy failure cytokines Eicosanoids Calcium polyamines Acetyl ROS endocannabinoids Choline Shohami, 2000 Green – pathophysiological processes; Yellow – various mediators
  10. 10. Time is Important
  11. 11. Dynamic Changes Following Brain Injury Days Weeks / Months Hours Weeks/Mont hs 2 7 8 hrs 14 Ca , Na+ Glut, ROS I Necrosis Apoptosis N J Inflammation U R Repair Remodeling Y Plasticity Functional Recovery Barone &Feuerstein JCBF, 1999
  12. 12. Physiology
  13. 13. The Lund Concept • January 1989, Lund University Hospital Department of Neurosurgery • Protocol aimed at non- surgical reduction of ICP • Bedside measurements of CBF and vasoreactivity identified subgroup of patients with severe TBI, intractable ICP, and 100% mortality
  14. 14. Lund concept • Volume-targeted therapy • Reduction of capillary hydrostatic pressure • Maintenance of colloid osmotic pressure and control of fluid balance • Reduction of cerebral blood volume • Controlled ICP
  15. 15. Blood Brain Barrier in Trauma
  16. 16. The Lund Concept • Avoid hyperglycemia and hyperthemia. • Avoid hypovolemia and stress response: increased baroreceptor reflex and cathacholamine release • Avoid hyperosmotic therapy: transient effects with adverse rebound and renal effects • Avoid vasopressors: vasoconstriction increases BP and CPP but may compromise brain microcirculatory perfusion (esp. pericontusional) and other organ system perfusion (ARDS)
  17. 17. The Lund Concept • Stress reduction: sedatives midazolam and thiopental (0.5-3.0 mg/kg/h) combined with alpha- 2 agonism and beta-1 blockade. Avoid propofol. • Normovolemia: by normalizing plasma oncotic pressure via RBC infusion to normal S-Hb (125- 140 g/L) and albumin transfusion (20-25%) • Normalize BP: Clonidine (0.3-1.0 ug/kg X 4-6) and Metoprolol (0.04-0.08 mg/kg). Refrain from using vasopressors. Dihydroergotamine induce venous vasoconstriction with great volume in venous side. No fixed limits for CPP
  18. 18. MONRO-KELLIE DOCTRINE Vintracranial vault=Vbrain+Vblood +Vcsf
  19. 19. BRAIN: CEREBRAL EDEMA-VASOGENIC (Caused mainly by activation of NMDA receptors by glutamate)
  20. 20. BRAIN: CEREBRAL EDEMA-CYTOTOXIC (Caused mainly by activation of cytokines, ROS and other pro-inflammatory mediators)
  21. 21. BLOOD: CEREBRAL BLOOD FLOW o The brain has the ability to control its blood supply to match its metabolic requirements o Chemical or metabolic byproducts of cerebral metabolism can alter blood vessel caliber and behavior
  22. 22. BLOOD: CEREBRAL BLOOD FLOW (VOLUME) • Increases in cerebral metabolic rate – Hyperthermia – Seizures – Pain, anxiety
  23. 23. CSF: CEREBROSPINAL FLUID • 10% of intracranial volume • Initial displacement of CSF from ventricles • Ventriculostomy to drain CSF
  24. 24. Intracranial Compliance • Calvarium is composed of three fluid compartments: Cerebral Blood Volume, CSF, and cerebral parenchyma
  25. 25. GUIDELINES – GENERAL ASPECTS • Standards: accepted principles of patient management that reflect a high degree of clinical certainty • Guidelines: strategies that reflect moderate clinical certainty • Options: unclear clinical certainty
  26. 26. Prehospital
  27. 27. Basic Principles: Airway • Resuscitation ABCs • Rapid sequence intubation • Retrospective studies report increased mortality: skill and optimal ventilation • Bag-valve-mask or LMA
  28. 28. PREHOSPITAL AIRWAY MANAGEMENT • Hypoxia must be avoided, and correct immediately . 13%-27% O2 • Supplemental oxygen should be administered • No advantage of ETI (ET intubation) Vs. BVM (Bag / valve / mask) ventilation for the pre- hospital airway in pediatric TBI 420 TBI; 115 BVM; 177 ETIno change (Gausche, JAMA 2000) • TBI + ETI  ETCO2
  29. 29. RESUSCITATION OF BP AND O2 AND PREHOSPITAL BRAIN- SPECIFIC TX’S FOR SPTBI PATIENTS • Hypotension should be identified and corrected as rapidly as possible with fluid resuscitation. (G) • Hypotension on arrival to ER (Pigula, J Ped Surg 1993) 18% ER: mortality 61% Vs. 22%, ↓BP+↓O2 – mortality  85% ! • Levine (Neurosurg 1992): TBI 0-4y ↓BP – 32% poor outcome. • Laurssen (J Neurosurg 1988):↑BP ↓EX; White (CCM 2001): syst BP > 135  X19 in survival !
  30. 30. PREHOSPITAL TREATMENTS • No evidence of efficacy: sedation, NMB, Mannitol, saline 3%, hyperventilation. • The prophylactic administration of mannitol is not recommended. • Mannitol may be considered for use in euvolemic patients who show signs of cerebral herniation or acute neurological deterioration.
  31. 31. PREHOSPITAL TREATMENTS • Mild prophylactic hyperventilation is not recommended. • Hyperventilation may be considered in patients who show signs of – Imminent cerebral herniation or – acute neurological deterioration • After correcting hypotension or hypoxemia
  32. 32. Pathophysiology of TBI • Primary injury • Secondary Injury • Ischemia/hypoxia • Excitotoxicity • Energy/Mitochondrial failure • Proinflammatory mediators • Free radical release • Neuronal death cascades
  33. 33. How do we Image
  34. 34. Imaging/ Diagnosis of Head Injury • CT scan remains imaging of choice • Regional heterogeneity of brain metabolism • Need information on brain function: CBF, perfusion and metabolism in TBI • Xenon-enhanced CT in the ED setting
  35. 35. Need for Portable Imaging • Transport risk of critical trauma patients • Portable CT with helical scanning capability, low radiation exposure, wireless links to imaging network, user-friendly, ability to perform perfusion studies.
  36. 36. Magnetoencephalography
  37. 37. MRI • As Field Strength increases (up to 7T) see more abnormaities • Diffusion tensor imaging (DTI) • Based on fractional anisotropic movement of water molecules • Non-invasive measurement of fiber pathway structure
  38. 38. CT SCANS and X-rays
  39. 39. Skull fracture
  40. 40. Coup-Contrecoup • focal injury consisting of contusions and hematoma at the site of the blow, opposite side of the brain
  41. 41. Hemorrage
  42. 42. Intracranial Hemorrhage
  43. 43. Cerebral Edema
  44. 44. Reversible high T2 signal abnormalities in pre-eclampsia
  45. 45. Monitoring
  46. 46. INDICATIONS FOR ICP MONITORING IN PATIENTS WITH SEVERE TBI • ↑ICP ≡↓Outcome; Aggressive Tx ≡↑Outcome • Intra-cranial pressure monitoring (ICP) is appropriate in all patients with severe traumatic brain injury (TBI) (Glasgow Coma [GCS] score ≤8) • The presence of open fontanels and/or sutures in an infant with severe TBI does not preclude the development of intracranial hypertension or negate the utility of ICP monitoring.
  47. 47. INTRACRANIAL PRESSURE MONITORING • STBI (GCS≤8) + Abnormal CT ≡ 53-63% ↑ICP (adult data). • Intra-cranial pressure monitoring is not routinely indicated in infants and children with mild or moderate head injury. • However, a physician may choose to monitor ICP in certain conscious patients with • traumatic mass lesions or – serial neurological examination is precluded by sedation, neuromuscular blockade, or anesthesia.
  48. 48. INTRACRANIAL PRESSURE MONITORING TECHNOLOGY • ICP monitoring: a ventricular catheter; external strain gauge transducer (??); catheter tip pressure transducer device  All accurate & reliable (O) • Ventricular cath. device most accurate, reliable, low cost + enables therapeutic (CSF) drainage. • No report of meningitis  ICP monitoring. Jensen: 7% +tip; positive > 7.5 days
  49. 49. THRESHOLD FOR TREATMENT OF INTRA- CRANIAL HYPERTENSION • ICP>20-40mmHg ≡ Mort. 28%; ICP>40mmHg ≡ 100% • Treatment for intracranial hypertension, defined as a pathologic elevation in intracranial pressure (ICP), should begin at an ICP ≥20 mm Hg. (O) • Patients may herniate at ICP < 20-25mmHg. • Is there a lower ICP threshold for younger children ? • Interpretation and treatment of ↑ICP based on any ICP threshold should be corroborated by frequent – clinical examination – monitoring of physiologic variables (CPP, Compliance) – cranial imaging.
  50. 50. CEREBRAL PERFUSION PRESSURE (CPP) • A cerebral perfusion pressure (CPP) >40 mm Hg
  51. 51. THE ROLE OF CSF DRAINAGE • Cerebrospinal fluid (CSF) drainage can be considered as an option in the management of elevated ICP Drainage: Ventriculostomy Lumber puncture.
  52. 52. Near-infrared spectroscopy • Measures complex IV cytocrome c • Mito redox state • Can detect changes in PO2/ lactate-pyruvate ratio • Potential tool for measuring cerebral aerobic metabolism
  53. 53. EEG/ Bispectral Index Analysis • Continuous EEG monitoring shows that 20% of TBI patients have seizures w/in 2 wks • EEG Power spectrum analysis to monitor sedation and prevent oversedation
  54. 54. Microdialysis • Measures biochemical changes in brain tissue • Increased lactate, EAA, glycerol • Decreased glucose, pyruvate • Need to collect dialysate q30 minutes for 5 days (240 samples) • Future role in target delivery of agents
  55. 55. Brain Oxygen Tension Monitoring • Direct measurement of cerebral oxygen metabolism • Interpretation of PbtO2 threshold 10-20 mmHg • Placement in uninjured versus injured brain
  56. 56. Treatment
  57. 57. Osmotic gradient created between Osmotic • Brain and blood (intact BBB) or theory • ICF and ECF (impaired BBB) Water moves out of the brain to re-establish osmotic equilibrium Brain volume is reduced ICP falls
  58. 58. Lower viscosity Rheologic and/or raise BP theory CBF rises Muizelaar JP et al: Mannitol Reflex causes compensatory vasoconstriction cerebral vasoconstriction and vasodilation in response to blood viscosity changes. J Reduced cerebral blood Neurosurg 59:822-828, 1983 volume (CBV) ICP falls
  59. 59. USE OF HYPEROSMOLAR THERAPY • Mannitol (2 X Class III) Vs. Hypertonic Saline (3 X Class II; 1 X Class III). • Mannitol is effective. • Euvolemia + Folly catheter • Accepted osmolarity: Mannitol < 320mOsm/L; Hyper NS < 360mOsm/L • Mannitol blood viscosity  arteriolar diameter and  osmotic effect. • Hyper NS  Osmolar grad; membrane pot.; cellular volume; ANP; Inflammation; C.O.
  60. 60. HYPEROSMOLAR THERAPY • Hypertonic saline is effective for control of increased ICP after severe head injury • Effective doses: cont. infusion of 3% saline 0.1 - 1.0 ml/kg/h, a sliding scale. • Goal minimum dose maintain ICP <20 mmHg. • Mannitol bolus dose: 0.25g/Kg – 1g/Kg.
  61. 61. Hypertonic saline • Efficacy in concentrations of 3%-7.5%- 23.4% in lowering ICP • Therapeutic action more effective (53.9% vs 35%) and longer lasting than mannitol • Attenuates microcirculatory disturbances (prevent secondary cerebral small vessel diameter increases and aggregation of WBCs by 90%)
  62. 62. Hypertonic saline • Clinical studies show decreases in mean number and duration of intracranial hypertensive episodes • Vasoregulatory effects: prevents vasospasm • Lowers rate of clinical failure • Theoretical concerns of CPM and rapid brain shrinkage/SDH
  63. 63. USE OF HYPERVENTILATION in the ACUTE MANAGEMENT • Mild or prophylactic hyperventilation (paco2 <35 mm hg) should be avoided. • Mild hyperventilation (paco2 30-35 mm hg) may be considered for longer periods for intra- cranial hypertension refractory to – Sedation and analgesia – Neuromuscular blockade – Cerebrospinal fluid drainage – hyperosmolar therapy
  64. 64. HYPERVENTILATION • Aggressive hyperventilation (Paco2 < 30 mm Hg) may be considered as a second tier option in the setting of refractory hypertension (O). • Cerebral blood flow (CBF), jugular venous oxygen saturation, or brain tissue oxygen monitoring is suggested to help identify cerebral ischemia in this setting. • Aggressive hyperventilation therapy titrated to clinical effect may be necessary for BRIEF PERIODS in cases of cerebral herniation or acute neurologic deterioration.
  65. 65. High dose barbiturate therapy • For refractory intracranial hypertension • Lower cerebral metabolic rate for O2 and modulate vascular tone • Membrane stabilization and reduced lipid peroxidation • Controversial evidence as to efficacy in severe TBI • Differential effects noted between thiopental, methohexital and pentobarbital
  66. 66. THE USE of BARBITURATES in the CONTROL of INTRA-CRANIAL HYPERTENSION • High-dose barbiturate therapy may be considered in hemodynamically stable patients with salvageable severe head injury and refractory intracranial hypertension. • If high-dose barbiturate therapy is used, then appropriate hemodynamic monitoring (CVP, Swan- Ganz, repeated ECHOs) and cardiovascular support (Dopamine, Adrenaline) are essential.
  67. 67. THE USE of BARBITURATES in the CONTROL of INTRA-CRANIAL HYPERTENSION • Gold standard – continuous EEG to achieve a state of burst suppression. • Serum barbiturate levels are NOT GOOD for monitoring that therapy. • Prophylactic therapy is not recommended (side effects).
  68. 68. Neuromuscular blockade • For mechanically ventilated to prevent cough reflex in initial 24-48 hours • Muscle relaxants cross BBB and can activate cerebral Ach receptors causing autonomic dysfunction, weakness and seizures • Resistance due to receptor up-regulation often present so need monitoring with peripheral nerve stimulator
  69. 69. Temperature Control
  70. 70. Concept: Brain Thermo-Pooling Dr. Nariyuki Hayashi
  71. 71. Hypothermia • Dr. Hugh Rosomoff : NIH Clinical Center 1955
  72. 72. Brain Thermo-Pooling Phenomenon • Brain thermo-pooling (elevation of brain tissue temperature) with damage of blood-brain barrier (BBB). • Risk: Blood temperature higher than 38.C., systolic blood pressure lower than 90-100mmHg, and cerebral perfusion pressure (CPP) lower than 70mmHg hinders washout of brain tissue temperature by cerebral blood flow. • Recorded brain tissue temperature of 40-44 degrees Celsius.
  73. 73. Temperature Control in TBI • Systemic and cerebral hyperthermia is detrimental to outcome • Up to 80% of TBI patients in ICU setting with reactive hyperthermia • Monitoring of core temperature, pyrexia identified and treated • In refractory cases electrical surface cooling blankets to prevent brain hyperthermia
  74. 74. Temperature Control in TBI • Surface cooling is problematic: access, time constraints, imprecision • Multi-trauma patients with splinting • Shivering increases O2 consumption and increases ICP
  75. 75. Intravascular Cooling Devices
  76. 76. Alsius Cooling Catheter • Saline-filled Polyethylene balloon catheter • Combines cooling capabilities with central venous access • Products may be used with femoral, subclavian or jugular access
  77. 77. InnerCool Catheters • Metallic coil heating element • Very Rapid rate of cooling (6 degrees Celsius per hour) • FDA approval for Neurosurgical ICU and recovery
  78. 78. Radiant Cooling Catheter • Triple-helical coil design • Expandable to 27 Fr in IVC to increase heat exchange • 37 to 33 degrees Celsius in less than 1 hour
  79. 79. Transcranial Cooling
  80. 80. Intranasal cooling
  81. 81. Therapeutic Hypothermia • Hypothermia neuroprotective in TBI models by decreasing EAAs, augment antioxidant activity and reduction of inflammatory markers • Randomized controlled trials have shown conflicting results • Clifton et al., showed possible outcome benefit with mild hypothermia in patients with GCS of 5-7
  82. 82. Therapeutic Hypothermia • NABIS H1 (National Acute Brain Injury Study: Hypothermia): 492 patients at 5 Centers • Failed to show beneficial outcome • Intercenter variability in treatment, delay in reaching target core temp, inconsistent fluid therapy • Subgroup analysis showed beneficial effects in patients age 16-45, normotensive, GCS>4 with initial core body temp less than 35 degrees Celsius and maintained core temperature
  83. 83. Neuroprotective agents • • Selfotel DCppene • • Cerestat Trilizad • • Cp101-606 PEG-SOD • • Bradycor IGF-1/GH • • Dexabinol Nimodipine • • SNX-111 Anticonvulsants • Steroids
  84. 84. Neuroprotective agents • • Selfotel DCppene • • Cerestat Trilizad • • Cp101-606 PEG-SOD • • Bradycor IGF-1/GH • • Dexabinol Nimodipine • • SNX-111 Anticonvulsants • Steroids
  85. 85. Calcium Channel Blockers
  86. 86. Ca2+ influx Plasma membrane channels Ligand-Operated Voltage-Operated Receptor-Operated Ca2+/Cation Ca2+ specific Ca2+ / Cation Ca2+ Mitochondrial Sarco-/Endo-plasmic Ca Uptake reticulum Ca Uptake Ca/Mg pump Na-Ca exchg.
  87. 87. Calcium Channel blockers • May be membrane protective • Affect Vasospasm
  88. 88. Coronary/Cerebral Steal The detrimental redistribution of blood flow in patients with atherosclerotic disease from underperfused areas toward better perfused areas Stenosis Before Vasodilator After Vasodilator
  89. 89. Dexabinol • Cannabinoid and non-competitive NMDA- receptor antagonist • Safely decreases mean time of ICP elevation above 25 mmHg and MAP <90 • Also acts as antioxidant and cytokine inhibitor • Phase III trials promising
  90. 90. Anti-inflammatory agents • Anti-ICAM-1 (Enlimomab) • Anti IL1-alpha • Anti a4 integrin Ab • Chemokine inhibitor (CXC/CC types) • MEK 1 /2 (MAP/ERK kinase) inhibitor U0216 • P38 MAP kinase inhibitor SB239063 • Selective PKC inhibitor Go6976 • Caspase inhibition • Naloxone • Proteosome inhibitor PS519 • Indomethicin • Celecoxib (COX-2 selective) • Cyclosporin A • Epoeitin A
  91. 91. Failure of Translational research • • Rx w/in 1 hour Rx w/in 8 hours • • Single dose Multiple dosages • • Lesion/infarct size GOS • • Outcome days/wks Outcome mos/yrs • • No adjunct therapy Multiple Rx • • Inbred rodents/male Variable population • • Single mechanism of Multiple mechanisms injury
  92. 92. Future Trends in Preclinical Research • Multiple models/ complexity (secondary injury) • Different species/gender/age • Timing of interventions • Range of severities • Physiological dosages • Drug interactions (antiepileptics) • Multifaceted treatment cocktails • Surrogate biomarkers (animal ICU): ICP, SjvO2, imaging, microdialysis, etc.
  93. 93. Surgical Decompression
  94. 94. DECOMPRESSIVE CRANIECTOMY • Decompressive craniectomy appears to be less effective in patients who have experienced extensive secondary brain insults • Patients who experience – Secondary deterioration on the Glasgow coma scale (GCS) and/or evolving cerebral herniation syndrome within the first 48 hrs after injury may represent a favorable group – Unimproved GCS of 3 may represent an unfavorable group
  95. 95. THE USE OF CORTICOSTEROIDS IN THE TREATMENT TBI • With the lack of sufficient evidence for beneficial effect and the potential for increased complications and suppression of adrenal production of cortisol, the routine use of steroids is not recommended for patients following severe traumatic brain injury.
  96. 96. NUTRITIONAL SUPPORT • Replace 130-160% of resting metabolism expenditure after TBI in patients. Weight- specific resting metabolic expenditure guidelines can be found in Talbot's tables. • Based on the adult guidelines, nutritional support should – begin by 72 hrs – with full replacement by 7 days.
  97. 97. THE ROLE of ANTI-SEIZURE PROPHYLAXIS FOLLOWING STBI • Prophylactic anti-seizure therapy may be considered as a treatment option to prevent increased oxygen utilization
  98. 98. Questions ?