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Guy Jackson r.g.m.jackson at qmul.ac.uk
Tue Oct 11 16:50:18 BST 2005



      Maas AI. Fleckenstein W. de Jong DA. van Santbrink H.

Monitoring cerebral oxygenation: experimental studies and preliminary
clinical results of continuous monitoring of cerebrospinal fluid and brain
tissue oxygen tension.

      Acta Neurochirurgica - Supplementum. 59:50-7, 1993.


      Cerebral ischaemia is considered to be the central mechanism leading
to secondary brain damage in patients with severe head injury. It would
therefore seem appropriate to monitor cerebral oxygenation in these
patients. The possibilities of continuous monitoring of brain tissue and CSF
oxygen tension as parameters for cerebral oxygenation were evaluated. In
experimental studies the influence of changed oxygen offer and decreased
cerebral perfusion pressure on CSF and brain tissue pO2 were investigated.
Fast changes in CSF pO2 were observed in response to decreasing oxygen
offer. Slower changes were noted in response to hypo- and hyperventilation.
An autoregulatory mechanism regulating CSF pO2 is postulated. Reducing
cerebral perfusion pressure decreased both brain tissue and CSF pO2, but in
the reperfusion phase after complete ischaemia a dissociation occurred
between brain tissue and CSF pO2, CSF pO2 being restored, but brain tissue
pO2 remaining low or even decreasing further. From these studies it is
concluded that both CSF pO2 and brain tissue pO2 reflect changes in cerebral
oxygenation caused by changes in oxygen offer as well as by changes in
cerebral blood flow. Brain tissue pO2 is also sensitive to oxygen demand
from the tissue. Preliminary studies of continuous monitoring of brain
tissue pO2 in patients with severe head injury are reported.

Put simply the brain tissue O2 correlates to the CSF O2.

However, there is more: Responses to changes in FiO2 can differ in brain
injury. Differing vascular responses or different cellular/interstitial
conditions? Try:

van Santbrink H. vd Brink WA. Steyerberg EW. Carmona Suazo JA. Avezaat CJ.
Maas AI. Brain tissue oxygen response in severe traumatic brain injury.
[Journal Article] Acta Neurochirurgica. 145(6):429-38; discussion 438, 2003
van Santbrink H. vd Brink WA. Steyerberg EW. Carmona Suazo JA. Avezaat CJ.
Maas AI. Brain tissue oxygen response in severe traumatic brain injury.
[Journal Article] Acta Neurochirurgica. 145(6):429-38; discussion 438, 2003


OBJECTIVE: To investigate clinical relevance and prognostic value of brain
tissue oxygen response (TOR: response of brain tissue pO(2) to changes in
arterial pO(2)) in traumatic brain injury (TBI). PATIENTS AND METHODS: In a
prospective cohort study TOR was investigated in 41 patients with severe TBI
(Glasgow Coma Score < or =8) in whom continuous monitoring of brain tissue
oxygen pressure (PbrO(2)) was performed.TOR was investigated each day over a
five day period for 15 minutes by increasing FiO(2) on the ventilator
setting. FiO(2) was increased directly from baseline to 1.0 for a period of
15 minutes under stable conditions (145 tests). In 34 patients the effect of
decreasing PaCO(2) was evaluated on TOR by performing the same test after
increasing inspiratory minute volume on the ventilator setting to 20% above
baseline. Arterial blood gas analysis was performed before and after
changing ventilator settings. Multimodality monitoring, including PbrO(2)
was performed in all patients. Outcome at six months was evaluated according
to the Glasgow Outcome Scale. For statistical analysis the Mann-whitney
U-test was used for ordinally distributed variables, and the Chi-square test
for categorical variables. Predictive value of TOR was analyzed in a
multivariable model. RESULTS: 145 tests were available for analysis.
Baseline PbrO(2) varied from 4.0 to 50 mmHg at PaO(2) values of 73-237 mmHg.
At FiO(2) settings of 1.0, PbrO(2) varied from 9.1-200 mmHg and PaO(2) from
196-499 mmHg. Three distinct patterns of response were noted: response type
A is characterized by a sharp increase in PbrO(2), reaching a plateau within
several minutes; type B by the absence of a plateau, and type C by a short
plateau phase followed by a subsequent further increase in PbrO(2). Patterns
characterized by a stable plateau (type A), considered indicative of intact
regulatory mechanisms, were seen more frequently from 48 hours after injury
on. If present within the first 24 hours after injury such a response was
related to more favorable outcome (p = 0.06). Mean TOR of all tests was 0.73
+/- 0.59 with an median TOR of 0.58. Patients with an unfavourable outcome
had a higher TOR (1.03 +/- 0.60) during the first 24 hours, compared to
patients with a favorable outcome (0.61 +/- 0.51; p = 0.02). Multiple
logistic regression analysis supported the independent predictive value of
tissue oxygen response for unfavorable outcome (odds ratio 4.8). During
increased hyperventilation, mean TOR decreased substantially from 0.75 +/-
0.54 to 0.65 +/- 0.45 (p = 0.06; Wilcoxon test). Within the first 24 hours
after injury a decrease in TOR following hyperventilation was significantly
related to poorer outcome (p = 0.01). CONCLUSIONS: Evaluation of TOR affords
insight in (disturbances in) oxygen regulation after traumatic brain injury,
is of prognostic value and may aid in identifying patients at (increased)
risk for ischemia.



P.S. Sorry about the formatting, Ovid bit me!

----- Original Message ----- 
From: "Karim Brohi" <karim at trauma.org>
To: "'Trauma & Critical Care mailing list'" <trauma-list at trauma.org>
Sent: Tuesday, October 11, 2005 1:48 AM
Subject: RE: LICOX


You don't have to apologise :-)

I know the theory - but I'm not sure how much the pO2 of the interstitium
contributes to these measurements.  Animal models show
PbrO2 correlating well with cerebral blood flow and PaO2 and possibly the
cerebral metabolic rate for oxygen (though I have yet to
see convincing data on this) but not with much else.  Of course in vitro you
can get the electrode to equilibrate with interstitial
fluid - but I doubt this has much effect in vivo.

Also I'm sure you're not suggesting that the probe is able to measure O2
tension at different distances between the blood vessel
endothelium and the neuron, so I'm not sure how the diffusion distance will
come into play.   Neuronal O2 utilization will affect
the PvO2 which will pake up part (how much?) of the PbrO2 reading.
I can't find any work by Maas (or anyone else) that shows that brain tissue
oximetry readings are reflecting interstitial O2 and not
some venous/arterial mixture.


-----Original Message-----
From: trauma-list-bounces at trauma.org [mailto:trauma-list-bounces at trauma.org]
On Behalf Of Guy Jackson
Sent: 10 October 2005 12:08
To: Trauma & Critical Care mailing list
Subject: Re: LICOX


Sorry, but it is even more complex than this. What you have argued is true
at the capillary level, but the Licox samples the
interstitium. Thus local oedema can cause increase in what has been termed
'diffusion distance', thus reducing the levels of oxygen
the cells are exposed to; or the cells can become more active and reduce
local levels of oxygen by increased usage (with the failure
of coupling of supply and demand that can occur). This may be one of the
effects in spreading depression. All the factors you have
mentioned (SaO2, Hb, etc) are also relevant, and should be corrected first.
However, once you have done so you must conceder the
concept of 'diffusion distance', in which case providing more dissolved
oxygen (i.e.
over-pressure) might be of help. You can certainly raise interstitial levels
of oxygen this way (measured either by Licox or
Neurotrend), as evidenced by the work of Andreas Maas (and others). The
question that desperately needs to be answered is: Can you
improve outcome this way? The only interventional study I know of used a
rise in CPP as it's intervention, and used ten time too few
patients when you do the power analysis. It is no surprise that it reached a
p value of 0.1, but I am unsure what this means in this

Personally, I fully agree that Licox is a sensitive marker that something is
wrong, but I think it can tell us a little more than
this (compared to say CBF monitoring). The trouble comes when you try and
decipher the meaning from the data in front of you, given
the multiplicity of things that could be wrong. There are a lot of band
wagons being jumped on out there, and things are only going
to get worse with new modalities (microdialysis, etc) coming along. What is
needed is a system to organise the care of these often
complex patients. Here's the one I teach:

1. Sort out the ICU basics

2. Only when 1 is sorted, sort out the goal directed therapy (OK they can go

3. Sort out the extras.

4. Start again.



----- Original Message ----- 
From: "Karim Brohi" <karim at trauma.org>
To: "'Trauma & Critical Care mailing list'" <trauma-list at trauma.org>
Sent: Saturday, October 08, 2005 5:42 AM
Subject: RE: LICOX


The LICOX brain tissue oxygen electrode is a very interesting and
potentially very useful device, but as yet our understanding of it
is incomplete and it is very difficult to come up with protocols
incorporating it into clinical use (it's hard enough to get units
to follow even baseline brain injury management guidelines).  Mis-use of the
probe is rife and one potential misunderstanding of
what the probe is actually measuring is potentially very harmful (I'll
elaborate). Clearly ICP and CPP is not the full story for
brain injury management, just as maintaining blood pressure at the expense
of flow in shock has been shown to be detrimental at
certain times and in certain pathophysiological conditions.  What is clear
is that not all brain injuries are the same, and that the
same brain injury responds differently at different times in its management.

The short answer to your question is that patients should be managed along
standard traumatic brain injury guidelines.  When a
change in the PbrO2 (partial pressure of oxygen in the brain) is noted on
the LICOX, this should prompt a search for the cause:
recheck ABG, ICP & CPP, ventriculostomy catheter, consider repeat CT etc. DO
NOT simply turn up the FiO2.

What does the PbrO2 measure?  Well it is not measuring the neuronal PO2.

Here's my take on what PbrO2 is reflecting:  It IS measuring some ratio of
arteriolar, capillary and venous O2.  So although there
is some measure of local neuronal oxygen utilization from the venous
measurement, much of the measurement is derived from the PaO2.
ie.  PbrO2 = x.PaO2 + y.PvO2 (of that local area of the brain).  Thus while
the LICOX is showing you some degree of "tissue
oxygenation" from the venous measurement it is heavily weighted towards any
change in the PaO2.

But it's also not that simple, as data shows that PbrO2 is affected by flow
(ie. cardiac output) as well as the PaO2.  In essence
then, the PbrO2 is a surrogate measure for oxygen delivery to the brain (or
the area of brain tissue it is sitting in).  BUT, and
here is the important part, it is only measuring part of the story, and if
you don't understand that, then if you base your
treatment only on the PbrO2 you will make severe errors.

Here's the O2 delivery equation you know:
O2 delivery = Cardiac Output * Oxygen concentration of blood
= CO* [O2 bound to haemoglobin + O2 dissolved in the blood] (using CO really
to mean arterial flow in the brain) = CO *
[1.34*Hb*SaO2 + PaO2*0.0003] or = CO*[1.34*Hb*Sao2] + CO*[PaO2*0.0003]

and for the brain:
= CBF*[1.34*Hb*SaO2] + CBF*[PaO2*0.0003]

The PbrO2 is only measuring the right hand side of the equation -
CBF*[PaO2*0.0003].  For brain injured patients who are being
appropriately managed by guidelines their Hb is adequate and o2sats should
be in the 96-100% range - ie on the flat part of the Hb
dissociation curve. Increasing the PaO2 will have no effect on the SaO2.

Thus the left hand side of the equation is not reflected at all in the
PbrO2 - and yet the right hand side contributes nothing to
brain oxygenation (because of the 0.0003).

So...  you're patient with a LICOX probe in develops a drop in the LICOX
reading.  MANY people treat this by turning up the FiO2.
The LICOX reading will improve, because PaO2 will rise.  BUT brain
oxygenation will be unchanged because CBF*1.34*Hb*SaO2 will be
unchanged.  The REASON the LICOX reading fell is because CBF, Hb or SaO2
fell - and most usually that will be because cerebral blood
flow has reduced.  Increasing the FiO2 will have had NO effect except to
increase the LICOX reading.

So currently I believe the LICOX has a place, and that is as a sensitive
indicator that something is going wrong (a canary if you
like) with cerebral blood flow and oxygen delivery - and therefore a change
in the PbrO2 should prompt a search for this.  The LICOX
reading is not a number to be treated in exclusion.

Personally I also think it is difficult to evaluate the PbrO2 without a
jugular bulb catheter in place measuring global O2
utilization (despite the problems with these catheters).  Of course the
fundamental problem with all this is that can monitor the
hell out of the brain but we still only have about 5 possible therapeutic

Hope this is of value.  Be interested in other views on what PbrO2 measures
or how people are using these probes. Are there many
units out there who are routinely putting LICOX probes in their brain
injured patients?


-----Original Message-----
From: trauma-list-bounces at trauma.org [mailto:trauma-list-bounces at trauma.org]
On Behalf Of Lamb, Keith D.
Sent: 06 October 2005 03:04
To: 'Trauma & Critical Care mailing list'
Subject: LICOX

Anyone using LICOX to monitor brain tissue oxygenation in traumatic brain
injury. If so, what are you experiences, your standard
parameters, and any data that you have to support its use?


Keith D. Lamb RCP, RRT
Team Leader/Charge Therapist
Newark, Delaware

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