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.