The role of Hyperbaric-Oxygen Therapy for intracranial
pathology in Intensive Care
GV. Sparacia, B. Sparacia, A. Sansone
Cerebral oedema represents the main aggravating factor to be predicted
in various forms of brain ailments. Oedema is initially produced at a threshold
of cerebral blood flow (CBF) lower than 20 ml/100 gr/min., so an early
stage of cytotoxic oedema is followed by a vasogenic-oedema stage coincident
with reperfusion.
After reperfusion circulatory and metabolic
changes persist in the period following ischemic attack, yet the brain
metabolism's special nature makes the neuronal cell more resistant to hypoxia
than was previously supposed by clinical experience. Most of the ischemic
penumbra zones may thus make a full recovery if appropriate therapy is
applied at the right time. Consideration of this kind have led to proposals
of various therapies all with the scope of lowering brain consumption of
O2, improving perfusion in the brain and
relieving nerve tissue from all mechanical pressure. However, no suggested
treatment seems without disadvantages and risks, so there is no agreed
consensus of opinion. Actually the only effective treatment, in having
no contra-indications or paradoxical results, seems to be mechanical ventilation
with timely checks on PaCO2 values.
In treating encephalic lesions with hyperbaric
oxygen our experience springs from over a decade's descriptions by various
authors who worked at appraising feasible therapies using it experience
both clinical and experimental (3,4,5,6,7,9). Recalling the ischemic penumbra
zone's physiopathology, HBO administration offers a restriction of post-ischemic
perfusional damage both directly through improved bio-availability of oxygen
in ischemic areas, and indirectly through regulatory action of cerebral
flow that improves perfusion in "critical" areas.
It logically follows - as epiphenomenon of
what we sketched out, and subject matter of our previous notes - our aim
is reduction of oedema and of PIC with overall improvement of cell perfusion.
We always gave prominence to testing clinically how useful a tool HBO may
be in conjunction with conventional treatments by now applied everywhere,
assessing results so as to suggest conditions where such treatment might
be indeed effective and where, on the contrary, useless or, worse, contra-indicated.
Without dwelling on the problems of metabolism and perfusion that follow
cerebral lesions, we can take for certain that:
- a) HBO improves oxygen diffusibility both above and beneath tentorial
level, encouraging in affected areas metabolic and
ATP action by lowering lactates and raising ATP (2,3,7);
- b) improves glucose metabolisation by lowering production of substances,
like aspartate and glutamate, responsible for over-response
of the receptors (2);
- c) due to improved metabolic processes and well-timed perfusional flow
redistribution with suitably controlled treatment, the generation
of radicals in the intracranial area is brought under greater control;
- d) as therapy can act only on areas not irreversibly damaged (1), treatment
must occur as early as possible;
- e) HBO's antioedemigenic action, though theoretically of the greatest
use, however needs active support therapy to avoid
or check risks of rebound effects, by planning different treatment
cycles together with precise morpho-functional
monitoring of the encephalon.
In line with our experience of nearly 4 years we thought it especially
useful to study HBO's effects on subjects with focal brain damage involving
(or not) altered consciousness states due to ischemia, thrombosis and/or
having a small site of haemorrhage not relevant to neurosurgery but
leading in any case to an asymmetry of measured flow between the to hemisphere,
but excluding:
- a) generalised cerebral oedema and practically irreversible damage;
- b) subjects with high level of carotid stenosis.
For comparative data we used morphofunctional features and their development,
metabolic features connected with brain oxygen flow, and finally the prognosis
of possible improvement both quoad vitam for life quality and in relation
to the results. So monitoring was by means of: CT at admission and 6 hours
after first treatment, then every 24-36 hours; auditory and somatosensory
evoked potentials every 8 hours; EEG 3 hours after end of treatment; Echo-Doppler
of epiaortic vessels at admission and after HBO therapy; haemogasanalysis;
Glasgow Coma Scale; CMRO2 assessment and,
where possible, measurement of liquor pressure by lumbar puncture before
and 3 hours after wards. Lastly, brain bloodflow measure with INHAMATIC
33 SYSTEM (Medimatic) 6 hours after first treatment, repeated 24 hours
later. In line with this plan 26 subjects of both sexes, aged between 48
and 64, were studied: patients admitted to our Reanimation Centre for encephalic
disorders of vascular or traumatic origin (Table 1), divided into 2 groups
of 13 patients each: the first (Group A), after we had consent, were given
HBO in conjunction with usual therapies. HBO treatment was applied with
bathymetry of 1.5-1.8 ATA for 66 minutes subdivided into three 20 minute
oxygen-breathing cycles (FiO2 = 1) using
facial mouth-mask or intubation in the trachea and mechanical ventilation,
with 3 minute intervals of air breathing. Treatment was repeated every
12 hours for the first 4 days, then at daily intervals for 8-10 days. The
second group was treated instead with routine therapies (either for absence
of consent or because of late transfer from other departments) and taken
as control (Group B). data are given as mean + DS. Statistical analysis
was made using variance analysis for multiple values (ANOVA).
Table 1
|
Group A
|
Number
of cases
|
CGS
|
CGS
(after 8 days)
|
H.B.O.
(days)
|
Deaths |
|
Ischemic focus-site
Cranial/encephalic trauma
Haemorrhagic stroke (non-neurosurgical)
|
4
6
3
|
6.5 + 2
7.1 + 1.5
7.4 + 1.8
|
11.3 + 1.2
13.5 + 1.8
9.5 + 2
|
10
9
8
|
1
-
1
|
|
Group B
|
|
|
|
|
|
|
Ischemic focus-site
Cranial/encephalic trauma
Haemorrhagic stroke(non-neurosurgical)
|
2
5
6
|
7.5 (n.v)
7.3 + 0.8
6.8 + 1.2
|
10.2 + 1.4
10.1 + 0.9
8.5 + 2.4
|
|
1
1
2
|
Commenting straightaway on these data, there is clearly lower death-rate,
though not significant, in subject treated with HBO, just as function recovery
is also favoured, both morphological aspects and metabolic (CNRO2)
and clinical (CGS) ones. On the other hand, improved prognosis is dramatically
higher both for life quality/quoad vitam and for functioning, in the patient
group in post-traumatic coma, with or without focus-site lesions. This
is effective therapeutics, confirmed by improved evoked potential responses
but mainly by measured bloodflow data that always showed a tendency to
redistribute and homogenise flow, with vasoconstriction persisting at the
check after 6 hours. There was no case of increased oedema around the lesion
after treatment nor diametrical growth of focus-site. Summing up, in agreement
with the most recent biochemical, clinical and therapeutic observations
already reported in connexion with post-anoxic brain lesion treatment (8),
HBO's usefulness can be confirmed, as long as it is applied rigorously
with suitable monitoring, even for ever more refined researches into phisiopathology
and brain damage. Improved perfusion treatment plus activating of inverse
haematic (stealing" phenomenon and oxygen bioavailability brought
into penumbra area, all explain the positive effects on metabolism of nerve-cells
and glia, lowering or eliminating oedemigenic effects of a histotoxic and
angiogenic kind, with outcomes visible with CT and bloodflow measurement.
Indeed it is the bringing of dissolved oxygen up to glial level that is
truly the new fact to be attributed to HBO in treating brain damage. And
precisely where the phenomenon of blood redistribution from non-ischemic
areas to tissues around the lesions is to be taken into account, which
is affected by the vasoconstriction effect to which unharmed areas are
notoriously more susceptible, with evident result lowering, "stealing"
and intracranial pressure and raising tissue oxygen flow.
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