Advanced monitoring in the intensive care unit brain tissue ...
Transcript of Advanced monitoring in the intensive care unit brain tissue ...
Advanced monitoring in the intensive care unit: brain tissue oxygen tension
Current Opinion in Critical Care Volume 8(2) April 2002
patients with acute intracranial disorders Cerebral monitoring 1.intracranial pressure 2.cerebral perfusion pressure new techniques: for cerebral oxygenat
ion and metabolism. Brain tissue oxygen pressure measure
ment for evaluation of cerebral oxygenation
Technical aspects of brain tissue oxygen tension measurements In 1956, Clark described the principles
of an electrode that could measure oxygen tension polarographically in blood or tissue.
Two companies developed this type of electrode for application in cerebral monitoring.
1.Licox system 2.Paratrend catheter
Other methods of brain oxygenation monitoring 1. Jugular bulb oximetry Intermittent or continuous of jugular
oxygen saturation global measurement of oxygenation i
n cerebrovenous blood PbrO2 :a very local measurement in the
brain tissue.
Near-infrared spectroscopy noninvasive technique hemoglobin is a strong absorber of near-inf
rared light the amount of absorption varies with the de
gree of hemoglobin oxygenation too much uncertainty about the validity of
observed values to recommend routine application in adult patients with acute cerebral disorders.
intraparenchymally introduced Po2 sensor Continuous measurement of cerebral oxyge
nation a technically reliable, clinically applicable, s
afe technique In relatively undamaged part of the brain: t
he more global balance between oxygen offer and demand
In the penumbra or vascular territory: emphasize the importance of saving potentially viable tissue
Brain tissue oxygen guided treatment supplementing ICP/CPP therapy after traumatic brain injury
Journal of Neurology Neurosurgery and Psychiatry 2003;74:760-764
Secondary brain damage is a major factor in determining patient outcome following traumatic brain injury.
Cerebral hypoxia has been identified as a principal cause of secondary brain damage
impaired autoregulation, systemic hypotension, hypoxia, and intracranial hypertension
METHODS 93 severe traumatic brain injury (Glas
gow coma score (GCS)≦8) Neuromonitoring: we used intracranial pressure cathete
rs and PtiO2 catheters (Licox Systems) The PtiO2 probes were implanted into
normal tissue (on CT examination) at a depth of 22 to 27 mm subdurally.
Treatment protocols ICP/CPP guided group : 40pts intracranial pressure (ICP) below 20 mm Hg cerebral perfusion pressure (CPP) above 70 mm Hg All patients were sedated, intubated, and ventilate
d to maintain PaO2 at 100 to 120 mm Hg and PaCO2 ~35 mm Hg
Mannitol, vasopressors, volume expansion, and barbiturates were given
Surgical options: evacuation of haematomas and intractably raised intracranial pressure (decompressive craniectomy)
Ptio2 guided group : 53pts treatment targets were the same as group1 but in addition, the avoidance of hypoxic Pti
O2 levels of less than 10 mm Hg was attempted
by increasing the CPP by increasing vasopressor and fluid intake increasing the FiO2 was not used to raise th
e PtiO2
RESULTS ~D10 No significant differences : age, GCS, pupilla
ry response, injury type, treatment intensity level, and incidence of initial hypoxia or initial hypotension
no differences for median ICP and CPP between the two treatment groups
In contrast, median PtiO2 values in the PtiO2 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).
Outcome after six months, both treatment grou
ps were divided into a poor outcome (GOS = 1–3) and a good outcome group (GOS = 4–5).
an increased proportion of patients with a good outcome in the PtiO2 guided group (65% v 54%)
DISCUSSION In the first 24 hours after the impact, P
tiO2 values are lowest did not translate into a statistically sig
nificant improvement six months after the trauma
There was a tendency for a better outcome in the PtiO2 guided group(65% good outcome v.s. 54%)
Cerebral perfusion and metabolism in resuscitated patients with severe post-hypoxic encephalopathy
Journal of the Neurological Sciences 210 (2003) 23-30
positron emission tomography (PET)
8 patients with severe post-hypoxic encephalopathy
caused by cardiac arrest and resulting in a coma lasting for at least 24 h
The radiotracers 15-oxygen labeled water ([O-15]-water) for regional cerebral perfusion
18-Fluor deoxyglucose ([F-18]-FDG) for the measurement of metabolism
Using this method, we aimed to identify regional vulnerability, which was hypothesized to provide :
(i) insight in pathogenic mechanisms (ii) early prognostic parameters.
Results 10 patients, Ages mean 60 All patients were unconscious (Glasgo
w Coma Scale, GCS, 2–4–2 or less) nine patients were intubated and artif
icially ventilated, one breathed spontaneously.
2 were excluded. 8 patients were scanned at day 1 following resuscitation.
Results
Results The [O-15]-water scans were obtained
without arterial sampling, and therefore only qualitatively assessed.
In contrast to the distribution of [F-18]-FDG, most of the perfusion scans still showed a clear demarcation of gray and white matter.
Results CT and MRI scanning did not show any majo
r change with respect to the hypoxic injury all patients had a poor outcome. The comparison between survivors and non
survivors did not reveal obvious differences in PET data
suggesting that this technique does not provide major prognostic clues adding to the prognostic information
Cerebral Circulation and Prognosis of the Patient with Hypoxic Encephalopathy
Keio Journal of Medicine. 49 Suppl 1:A109-11, 2000 Feb.
Early prediction of cerebral prognosis is important to optimize the management of these patients
21 pts,all with hypoxic encephalopathy Xe-CT and MRI were carried out 3 weeks aft
er the onset Cerebral blood flow (CBF) of the patients w
as measured at rest and 15 minutes after intravenous administration of acetazolamide (1 g).
The prognosis was evaluated 3 months after the onset in accordance with Glasgow Outcome Scale (GOS).
1.Low hemispheric CBF (30 ml/100 g/min), 2.poor reactivity of acetazolamide challeng
e test (10 ml/100 g/min), 3.presence of hyperintensity areas in the ba
sal ganglia in T1 weighted images (T1WI) and T2 weighted images (T2WI)
are the factors associated with poor outcome in hypoxic encephalopathy.