Advanced monitoring in the intensive care unit: brain tissue oxygen tension <ul><li>Current Opinion in Critical Care Volum...
patients with acute intracranial disorders   <ul><li>Cerebral monitoring  </li></ul><ul><li>1.intracranial pressure  </li>...
Technical aspects of brain tissue oxygen tension measurements  <ul><li>In 1956, Clark described the principles of an elect...
Other methods of brain oxygenation monitoring  <ul><li>1.  Jugular bulb oximetry   </li></ul><ul><li>Intermittent or conti...
Near-infrared spectroscopy  <ul><li>noninvasive technique  </li></ul><ul><li>hemoglobin is a strong absorber of near-infra...
intraparenchymally introduced Po 2  sensor <ul><li>Continuous measurement of cerebral oxygenation  </li></ul><ul><li>a tec...
Brain tissue oxygen guided treatment supplementing ICP/CPP therapy after traumatic brain injury   <ul><li>Journal of Neuro...
<ul><li>Secondary brain damage is a major factor in determining patient outcome following traumatic brain injury. </li></u...
METHODS  <ul><li>93 severe traumatic brain injury (Glasgow coma score (GCS)≦8) </li></ul><ul><li>Neuromonitoring:   </li><...
Treatment protocols <ul><li>ICP/CPP guided group :  40pts </li></ul><ul><li>intracranial pressure (ICP) below 20 mm Hg </l...
P ti o 2  guided group   :  53pts   <ul><li>treatment targets were the same as group1 </li></ul><ul><li>but in addition, t...
RESULTS  ~D10   <ul><li>No significant differences : age, GCS, pupillary response, injury type, treatment intensity level,...
Outcome <ul><li>after six months, both treatment groups were divided into a  poor  outcome (GOS = 1–3) and a  good   outco...
DISCUSSION  <ul><li>In the first 24 hours after the impact, P ti O 2  values are lowest </li></ul><ul><li>did not translat...
Cerebral perfusion and metabolism in resuscitated patients with severe post-hypoxic encephalopathy  <ul><li>Journal of the...
positron emission tomography (PET) <ul><li>8 patients with severe post-hypoxic encephalopathy </li></ul><ul><li>caused by ...
<ul><li>Using this method, we aimed to identify regional vulnerability, which was hypothesized to provide : </li></ul><ul>...
Results <ul><li>10 patients, Ages mean 60 </li></ul><ul><li>All patients were unconscious (Glasgow Coma Scale, GCS, 2–4–2 ...
Results
Results <ul><li>The [O-15]-water scans were obtained  without arterial sampling , and therefore only qualitatively assesse...
Results <ul><li>CT and MRI scanning did not show any major change with respect to the hypoxic injury </li></ul><ul><li>all...
Cerebral Circulation and Prognosis of the Patient with Hypoxic Encephalopathy <ul><li>Keio Journal of Medicine. 49 Suppl 1...
Early prediction of cerebral prognosis  is important to optimize the management of these patients <ul><li>21 pts,all with ...
<ul><li>1.Low hemispheric CBF (30 ml/100 g/min),  </li></ul><ul><li>2.poor reactivity of acetazolamide challenge test (10 ...
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Advanced monitoring in the intensive care unit brain tissue ...

  1. 1. Advanced monitoring in the intensive care unit: brain tissue oxygen tension <ul><li>Current Opinion in Critical Care Volume 8(2)  April 2002               </li></ul>
  2. 2. patients with acute intracranial disorders <ul><li>Cerebral monitoring </li></ul><ul><li>1.intracranial pressure </li></ul><ul><li>2.cerebral perfusion pressure </li></ul><ul><li>new techniques: for cerebral oxygenation and metabolism. </li></ul><ul><li>Brain tissue oxygen pressure measurement for evaluation of cerebral oxygenation </li></ul>
  3. 3. Technical aspects of brain tissue oxygen tension measurements <ul><li>In 1956, Clark described the principles of an electrode that could measure oxygen tension polarographically in blood or tissue. </li></ul><ul><li>Two companies developed this type of electrode for application in cerebral monitoring. </li></ul><ul><li>1.Licox system </li></ul><ul><li>2.Paratrend catheter </li></ul>
  4. 4. Other methods of brain oxygenation monitoring <ul><li>1. Jugular bulb oximetry </li></ul><ul><li>Intermittent or continuous of jugular oxygen saturation </li></ul><ul><li>global measurement of oxygenation in cerebrovenous blood </li></ul><ul><li>P br O 2 :a very local measurement in the brain tissue. </li></ul>
  5. 5. Near-infrared spectroscopy <ul><li>noninvasive technique </li></ul><ul><li>hemoglobin is a strong absorber of near-infrared light </li></ul><ul><li>the amount of absorption varies with the degree of hemoglobin oxygenation </li></ul><ul><li>too much uncertainty about the validity of observed values to recommend routine application in adult patients with acute cerebral disorders. </li></ul>
  6. 6. intraparenchymally introduced Po 2 sensor <ul><li>Continuous measurement of cerebral oxygenation </li></ul><ul><li>a technically reliable, clinically applicable, safe technique </li></ul><ul><li>In relatively undamaged part of the brain: the more global balance between oxygen offer and demand </li></ul><ul><li>In the penumbra or vascular territory: emphasize the importance of saving potentially viable tissue </li></ul>
  7. 7. Brain tissue oxygen guided treatment supplementing ICP/CPP therapy after traumatic brain injury <ul><li>Journal of Neurology Neurosurgery and Psychiatry 2003; 74 :760-764 </li></ul>
  8. 8. <ul><li>Secondary brain damage is a major factor in determining patient outcome following traumatic brain injury. </li></ul><ul><li>Cerebral hypoxia has been identified as a principal cause of secondary brain damage </li></ul><ul><li>impaired autoregulation, systemic hypotension, hypoxia, and intracranial hypertension </li></ul>
  9. 9. METHODS <ul><li>93 severe traumatic brain injury (Glasgow coma score (GCS)≦8) </li></ul><ul><li>Neuromonitoring: </li></ul><ul><li>we used intracranial pressure catheters and PtiO2 catheters (Licox Systems) </li></ul><ul><li>The PtiO2 probes were implanted into normal tissue (on CT examination) at a depth of 22 to 27 mm subdurally. </li></ul>
  10. 10. Treatment protocols <ul><li>ICP/CPP guided group : 40pts </li></ul><ul><li>intracranial pressure (ICP) below 20 mm Hg </li></ul><ul><li>cerebral perfusion pressure (CPP) above 70 mm Hg </li></ul><ul><li>All patients were sedated, intubated, and ventilated to maintain PaO2 at 100 to 120 mm Hg and PaCO2 ~35 mm Hg </li></ul><ul><li>Mannitol, vasopressors, volume expansion, and barbiturates were given </li></ul><ul><li>Surgical options: evacuation of haematomas and intractably raised intracranial pressure (decompressive craniectomy) </li></ul>
  11. 11. P ti o 2 guided group : 53pts <ul><li>treatment targets were the same as group1 </li></ul><ul><li>but in addition, the avoidance of hypoxic P ti O 2 levels of less than 10 mm Hg was attempted </li></ul><ul><li>by increasing the CPP </li></ul><ul><li>by increasing vasopressor and fluid intake </li></ul><ul><li>increasing the FiO 2 was not used to raise the P ti O 2 </li></ul>
  12. 12. RESULTS ~D10 <ul><li>No significant differences : age, GCS, pupillary response, injury type, treatment intensity level, and incidence of initial hypoxia or initial hypotension </li></ul><ul><li>no differences for median ICP and CPP between the two treatment groups </li></ul><ul><li>In contrast, median P ti O 2 values in the P ti O 2 guided group (median = 26.6 mm Hg) were significantly higher than in the ICP/CPP guided group (median = 23.0 mm Hg); p = 0.03). </li></ul>
  13. 13. Outcome <ul><li>after six months, both treatment groups were divided into a poor outcome (GOS = 1–3) and a good outcome group (GOS = 4–5). </li></ul><ul><li>an increased proportion of patients with a good outcome in the P ti O 2 guided group (65% v 54%) </li></ul>
  14. 14. DISCUSSION <ul><li>In the first 24 hours after the impact, P ti O 2 values are lowest </li></ul><ul><li>did not translate into a statistically significant improvement six months after the trauma </li></ul><ul><li>There was a tendency for a better outcome in the P ti O 2 guided group(65% good outcome v.s. 54%) </li></ul>
  15. 15. Cerebral perfusion and metabolism in resuscitated patients with severe post-hypoxic encephalopathy <ul><li>Journal of the Neurological Sciences 210 (2003) 23-30 </li></ul>
  16. 16. positron emission tomography (PET) <ul><li>8 patients with severe post-hypoxic encephalopathy </li></ul><ul><li>caused by cardiac arrest and resulting in a coma lasting for at least 24 h </li></ul><ul><li>The radiotracers 15-oxygen labeled water ([O-15]-water) for regional cerebral perfusion </li></ul><ul><li>18-Fluor deoxyglucose ([F-18]-FDG) for the measurement of metabolism </li></ul>
  17. 17. <ul><li>Using this method, we aimed to identify regional vulnerability, which was hypothesized to provide : </li></ul><ul><li>(i) insight in pathogenic mechanisms </li></ul><ul><li>(ii) early prognostic parameters. </li></ul>
  18. 18. Results <ul><li>10 patients, Ages mean 60 </li></ul><ul><li>All patients were unconscious (Glasgow Coma Scale, GCS, 2–4–2 or less) </li></ul><ul><li>nine patients were intubated and artificially ventilated, one breathed spontaneously. </li></ul><ul><li>2 were excluded. 8 patients were scanned at day 1 following resuscitation. </li></ul>
  19. 19. Results
  20. 20. Results <ul><li>The [O-15]-water scans were obtained without arterial sampling , and therefore only qualitatively assessed. </li></ul><ul><li>In contrast to the distribution of [F-18]-FDG, most of the perfusion scans still showed a clear demarcation of gray and white matter . </li></ul>
  21. 21. Results <ul><li>CT and MRI scanning did not show any major change with respect to the hypoxic injury </li></ul><ul><li>all patients had a poor outcome. </li></ul><ul><li>The comparison between survivors and nonsurvivors did not reveal obvious differences in PET data </li></ul><ul><li>suggesting that this technique does not provide major prognostic clues adding to the prognostic information </li></ul>
  22. 22. Cerebral Circulation and Prognosis of the Patient with Hypoxic Encephalopathy <ul><li>Keio Journal of Medicine. 49 Suppl 1:A109-11, 2000 Feb . </li></ul>
  23. 23. Early prediction of cerebral prognosis is important to optimize the management of these patients <ul><li>21 pts,all with hypoxic encephalopathy </li></ul><ul><li>Xe-CT and MRI were carried out 3 weeks after the onset </li></ul><ul><li>Cerebral blood flow (CBF) of the patients was measured at rest and 15 minutes after intravenous administration of acetazolamide (1 g). </li></ul><ul><li>The prognosis was evaluated 3 months after the onset in accordance with Glasgow Outcome Scale (GOS). </li></ul>
  24. 24. <ul><li>1.Low hemispheric CBF (30 ml/100 g/min), </li></ul><ul><li>2.poor reactivity of acetazolamide challenge test (10 ml/100 g/min), </li></ul><ul><li>3.presence of hyperintensity areas in the basal ganglia in T1 weighted images (T1WI) and T2 weighted images (T2WI) </li></ul><ul><li>are the factors associated with poor outcome in hypoxic encephalopathy. </li></ul>

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