Hyperbaric Oxygen Therapy
Questions and Answers
Pred skoraj 15. leti sem zasledil 102 strani teksta na temo hiperbarična medicina. Celotni tekst sem shranil in ga objavljam:
first, be sure you read how hyperbaric oxygenation works
The following document highlights current thought in some medical
circles regarding hyperbaric
oxygenation. To search
for topics use your web browser "edit" function, pull down to "find" and type in your
search
term.
This
manuscript
has
research
data
from
published
work,
some unpublished articles and some email discussion.
' Q: W4y i
.QJ!:Yg :n
pounds of water and almost 6 pounds of oxygen. People need about
the same amount
of oxygen
by weight
compared to food and water
combined! From that 6 pounds of oxygen
about 2 pounds gets into the blood for transport to tissue cells. We need this oxygen for the energy
cycle that
<. sustains life. When we do not have enough oxygen in our body tissues
a series of events occur that
\. )\ if
not corrected lead to disease
conditions, either infection, tissue destruction or both.
If there is
low oxygen in tissues (hypoxia) there
is a short window of opportunity to correct it. An excellent method to correct tissue
hypoxia is by using a hyperbaricchamber.
This web site is dedicated to making complex
physiology easier to understand so we can make informed
choices about health care.
What do you feel
inside
a
hyperbaric
chamber? Chamber atmosphere pressurization
occurs
7!owly allowing yoadjust ear
pres;ure changes. Yawning; swallowing or "blow the nose" clears ear pressure
changes.
Other
than
this
ear
pressure
there
are
no
unusual
or
different sensations.
What difference does extra pressure create? Hemoglobin (in red blood
cells) holds 97% of its
'maxiiiUii:ilamOuiiiOf oxygen from al air or holds 100% when breathing pure oxygen. One gram of hemoglobin
can only combine with 1.34 rn1 of
oxygen. Therefore, red blood cells can
only deliver
a limited level of oxygen
to tissue cells, a p02 of
39 mmHg or less.
This is called oxygen tension•(or oxygen
partial pressure, "p02") and is measured in units labeled
"mmHg" (the amount
of
pressure
able
to raise the equivalent weight of a liquid
mercury
column. Injuries,• infections and diseases can drop this vital tissue oxygen level down to almost zero! As we age we. can loose vital lung capacity and the ability
to effectively obtain
adequate oxygen; Some disease conditions impair oxygen utilizatiom Also, injuries or conditions with swelling can cause pressure that cuts off circulation flow. This loss of blood flow, called ischemia, cuts off oxygen circulation to the affected
areas of the body. This problem drops the p02-gravely low, destroys tissue, and slows healingResearch has shown optimal
tissue healing occurs
if p02 rises to between 50 and
80 mmHg. Oxygen given in a normal room is not sufficient to raise tissue
oxygen levels to that level
because red blood
cells cannot carry the extra oxygen. The answer is to deliver
the oxygen in a pressurized chamber to raise oxygen tension
beyond red blood cell saturation.
How does
eing_inside .!!.pressurized chlil!lber give l!Lm XYJl .n? When we are inside achamber pressurized at twice
the normal air pressure it may not feel different, but we l;>reathe double the number of molecules. Breathing
pure oxygen in such a chamber gives us 10 tinies the regular amount of oxygen. In one hour we can inhale about 2.4 pounds of oxygen. The extra oxygen dissolves directly into the blood fluid. In a few minutes this extra oxygen builds up tissue oxygen levels far above normal. This action has been
scientifically proven to stimulate healing. In order to raise
tissue oxygen tension
above 50mmHg for optimal healing
one must have oxygen delivered under increased atmospheric conditions. Look at the hyperbaric chart and observe
the venous oxygen
tension,
which
closely
represents
the final tissue oxygen tension,
rise
as
we
|
|||||||||||||||||||||||||||||||||||||||||||||||||
oxygenation has attracted interest
lately -·antil ic thte11i.r>Y-9l!Lf<Yl
to clear today's resista,nItI.\
.f-i:') strains of pathogens. Treatable
infections include such diverse situations
\J teomyelitis, diabeti grene. and related
deadlye infecti()_J.?S· In the last four
'-. ...--..._-----...,
-......,__ ...... ------ - --- .
deCiiaesn)'perbaric oxygenation research iias raised the value of
this unique ther y. Doctors
used
to ask, "Can
it work?" now they ask, "How much
is needed to completely work?" r I
How
does hyperbaric q_"ygenatio!Lhelp_in_pain_managemeut?
Related to crush injuries, pain results from swelling around.
sensory nerves. Hyperbaric oxygenation acts internally to reduce swelling. Swelling causes ischemia,
lack of oxygen circulation. When ischemia is severe and persistent it may lead to an anaerobic form of tissue
metabolism that perpetuates the entire ischemic process. Reference: W. Boyd A Textbook of Pathology 8th edition
pg. 69. Irritation of nerve roots with
muscle spasms
along the segmental distribution of nerve
roots can create ischemic changes
that can lead to serious
impairment. Reference: R. Jackson The Cervical
(_ . Syndrome 4th edition pg 148. A major cause of musculoskeletal pain originates from ischemia, that compares with the pain experienced in angina. Reference: T. Lewis "Pain in muscular
ischemia" Archives Internal Medicine 1932;49(5):713-27. Many conditions of
the central nervous system stem from vascular
ischemia. Reference: N.A. Hood "Diseases of the central
nervous system" British Medical
Journall975;3:398-400. It has been well known
for several decades
that ischemia has a depressant effect on nerve conduction, especially in the more sensitive afferent fibers. Reference: J.W. Magladery,et al
"Electrophysiological studies of nerve and reflex activity in normal man" Bulletin
John Hopkins Hospital 1950;86:291-312. Ischemic
changes in nerve root microcirculation often leads
to intraneural edema that worsens
the trouble. Reference: B.Rydevik, M.D.Brown, "Pathoanatomy and
pathophysiology of nerve root compression" Spine
1984;9 (1):7- 15. Recovery of nerve (and other tissue)
depends on eliminating ischemia in the
• affected tissue. Reference: F.H.Bentley, W.Schlapp "Experiments on
the blood supply
of nerves" Journal Physiology (London) 1943;102:62-71. Hyperbaric oxygenation has proven
benefits in reversing the effects of ischemia. References: J.D.Yeo "A
study of the effects of hyperbaric
oxygen on the experimental spinal cord injury" July 30, 1977 The Medical Journal of Australia
pg.l45-147. I.Eltorai "Hyperbaric oxygen in the management of pressure
sores in patients
with injuries to the spinal cord" Journal Dermatological Surgical
Oncology 7:9 Sept 1981; 737-739.
A.Sirsjii et a!"Hyperbaric oxygen
treatment enhances the recovery of blood flow and functional capillary density in post-ischemic striated muscle" 1993 Circulatory Shock 40:9-13.
Oxygen in Medical Practice: Oxygen is the most essential substrate for metabolism. We only function by oxidative metabolism and the reason for restoring blood flow to the brain with CPR is
to establish
an. oxygen supply. See: OlesonSP. Brain Res
1986;368:24- 29 also, JamesPB CalderiM JRSM 1991;84:493-495. Hypoxia
(low oxygen levels in tissue)
hinders healing. The sooner that tissue hypoxia
is corrected the better the outcome. Many hypoxic tissues
require hyperbaric pressure to achieve a significant increase
in oxygen delivery
because of poor oxygen
solubility in blood. Despite thousands
of publications, including
controlled trials, attesting
to the value of higher dosage oxygen, it is not widely practiced because:
I Oxygen
transport is determined by the percentage respired and the barometric pressure:
In normal hospital practice
barometric pressure is ignored and it is assumed that patients receiving I
00% are being given the same amount. In Denver Colorado which is at an altitude
of over 5000 feet, the partial
pressure is significantly lower than at sea level and a hyperbaric chamber is
needed to give the same amount of oxygen as at sea level.
II Tissue hypoxia may be present
in the absence of cyanosis: Oxygen supplementation is accepted in the alleviation of cyanosis, where the absolute
level of deoxygenated hemoglobin exceeds
5g
/100 ml of blood.
However, the presence of cyanosis requires
blood to be present in the
microcirculation of a tissue and there can be significant hypoxemia without cyanosis
when the
hematocrit is low or when there is microcirculatory closure.
III Plasma oxygen transport is not limited
by the saturation of hemoglobin: It is common for
physicians to argue that blood is saturated
with oxygen when a normal oxygen partial
pressure (0.21 atm abs) is breathed
at sea level. However it is not blood that is
saturated, it is hemoglobin. The transport
of oxygen by hemoglobin is finite as each of the ferrous
receptor sites on the
molecule can only bind one oxygen molecule.
However, the plasma oxygen content
increases directly as a function of the inspired
partial pressure of oxygen. Breathing pure oxygen at twice
atmospheric pressure, the plasma oxygen content is ten times
the value of breathing air at sea level
and life can be sustained
without hemoglobin (continued consciousness may need higher pressure).
()!
IV Oxygen
transport to tissue
depends on the tension of oxygen in plasma: Severe
tissue hypoxia can be present when arterial oxygen
tensions are normal if local circulatory factors, such as
arterial occlusion, closure of the microcirculation and edema are present. An increase in the
water content of tissue limits oxygen transport. If inflammation, edema and the invasion of metabolically active inflammatory cells occur at the same time, we
can have hypoxia even when
the blood flow per unit volume of tissue is increased, hence hyperemic hypoxia.
In hyperbaric conditions the oxygen plasma tension increases
from values of 95mm Hg to over 2000 mm Hg
increasing
the gradient or the transfer of oxygen into tissues by 20 fold.
V Normal blood
flow does not ensure normal
oxygenation: Oxygen delivery requires blood flow, although blood
flow may be normal and the tissue
still hypoxic. The only tissue that does not need
blood flow for oxygenation is the lung.
VI
Oxygen is not "Hyperbaric": The use of the term "hyperbaric" may appear to imply that the
oxygen delivered is different to the molecular oxygen available from the air. People
may think of it as singlet oxygen 01 or ozone 03, perhaps some regard
hyperbaric oxygen as 04. The correct
terminology is hyperbaric oxygena!ion q;r hyperoxia. The psychology of the word "hyperbaric"
._,.,- - ''i ·w
indicates a potential marketing
problem. '
VII The adjunctive nature of most oxygen supplementation: Oxygen may be a primary
treatment in some instances,
but the impression is often given that oxygen therapy
replaces other treatment.
In most cases this is incorrect, other therapy is needed and optimal care is not a competition between therapies. ·---·------------
VIII
Hypoxia, not oxygen, causes oxygen free radicals: Here is an important, often misunderstood point. Contrary to prevailing misinformation it is hypoxia that mediates the release of oxygen free radicals.
An inadequate oxygen supply to tissue results
in the catabolism of ATP
to adenosine and the creation
of an electron donor, xanthine. When oxygen is made available the electron is accepted
to form the superoxide anion 02. It is
important to recognize
that hypoxia causes a cascade of interactions
that generate hydroxyl ions which damage membranes and draws
calcium into the cell. Correcting hypoxia
will limit this free radical
formation. Many physicians fr&'''"' 1,k, k
tend to think oxygen causes oxidative damage, quite the contrary, it is the lack'" of oxygen that
causes the damage. Reperfusion injury occurs when circulation is cut then returned with poorly
oxygenated blood flow. Somehow oxygen gets blamed for this, yet
if one has benefit of hyperbaric oxygenation we see a dramatic reduction in reperfusion damage.
IX
Hyperoxia and oxygen
toxicity: It is
well known that exposure to pure oxygen
for a prolonged perioa;that is;-Iil excess of 24 hours at 1 atm abs causes reversible damage
to the endothelium of pulmonary capillaries. Short term ex_!JSl§!!r.e to _very high oxy _ressures, for example, ov_3
ATA :[ oms-mcauseeonvlilsions resembling grande mal epil-;;psy. The time to convulsion
i'sreduced by exercise or an increased
metabolic rate. However, cllniciiluse of hyperbaric oxygen
uses a well-defmed exposure limit that prevents
this. The sites where autoregulation may fail to
limit blood flow are the ends of fingers and toes. This is because
arteriovenous shunts are present to return blood in vasodilatation and results in blood flow which is greatly in excess of tissue
requirements. Toxicity to peripheral
nerve endings is often manifest
as parasthesia. Pre-existing epilepsy does not lower
the threshold to oxygen toxicity.
In fact, epilepsy
can be treated with
hyperbaric oxygenation and many of the 12,000 patients in our UK MS charity have epilepsy. We have
not had a convulsion in our 16 years of operation. See: Qibiao W, et al. Treatment of children's epilepsy by hyperbaric oxygenation; analysis of 100 cases. Proc 11th International
Congress on Hyperbaric Medicine. Best Publishers. 79- 81. We have looked
at trancutaneous values and they are linear to 2 atm abs but there is a wide distribution
after that. No long term sequelae have been described
after oxygen convulsions. Oxygen c9n':;!lsions were used in place of
electric shock therapy
in the 1950's in the USA. 'i/R't
|
X
Unfamiliar technology: Hyperbaric medicine
is not generally familiar to most
physicians because it is rarely taught in medical schools.
Those who are involved have generally come from
the fields of aviation or diving. As both of these disciplines use high technology, it is not surprising that hyperbaric oxygen
itself is viewed
in this light. However, the pressures used clinically, up to a maximum of 2.5 ATA, are very modest in comparison to the maximum human experimental pressnrisation of 71 atm
abs.
Unfortunately,
even
physicians
familiar
with hyperbaric medicine refer to "fitness to go under pressure," forgetting that we are all subject
to normal atmospheric pressure. Also, it is outside
our pharmaceutical paradigm in the west. In other cultures it has been more readily
accepted. The HB02 approach has largely come after the tablet/injection approach
was developed and therefore to take a place in healthcare, HB02 must produce
proof of improvement above that already
obtained. HB02 has to jump higher
"proof'
hurdles.
XI
Finance: The pressure against a 30" hyperbaric
chamber hatch at 2 atmospheres is 5 tons! This requires a chamber
certified to safely
hold the high pressure. The use of increased pressure requires a hyperbaric chamber and therefore
some financial investment. In the case of a walk-in multiplace chamber this can be considerable and there are usually building
modifications required. Plus, there is no commercial promotion of
oxygen in the pharmaceutical sense to make physicians aware of hyperbaric oxygenation's value. This will not change and is a major reason for the slow
growth of oxygen as a therapy. No promotion without a patent!
No matter how much scientific
evidence we produce we need marketing and no one will make that investment
without a return.
We have more scieritific v!deil:l5eab ut" actions and mechanisms supporting the correction of ( f
tissue hypoxia
than any pharmaceutical product. l
|
XII
Misunderstandings: It is very clear there is a general failure
to understand the fundamental
importan o{o fn human physiology. If this were not the
case, HB02 would already have ( become just another tool used in the day-to-day
practice of medicine
as are pills, surgical knives
and injections. Perhaps a major
barrier
to
gaining
greater
acceptance within the medical community at large is the persistencein referring to clinical HB02 treatments as "dives". Diving and clinical hyperbaric medicine are not the same thing. Diving relates to underwater
military, commercial or amateur
activities, recompression is necessary when things go wrong, it is not a choice
if you wish to resolve a DCS problem. In clinical applications patients do not go anywhere
near the water (in my experience a lot of people think they do), they are pressurized for the
specific purpose· of increasing tissue
oxygen
tensions in order restore or assist the healing process. The term "fitness to dive" is another diving
term and relates to the ability of an individual to deal with the physiological stress of deep diving and working underwater. The whole objective
of pressurizing a clinical patient is to increase
tissue oxygen tensions
in conditions where
HB02 is beneficial. This would not be necessary if
they were "fit". A patient in a chamber
breathing 100% oxygen is under less physiological stress rather than more because of the benefits derived from the oxygen. Someone raised the point about pneumothorax expanding on decompression - this does not apply because
breathing oxygen actually reduces
the volume of a pneumothorax by increasing
the
inherent unsaturation and gradient for nitrogen elimination.
The risk of ear squeeze
associated
with hyperbaric treatment is manageable, just slow down rate of pressure
change or insert grommets. It is not "fitness to dive" that is the issue, just responsible medical
practice. Our rate of impending or actual aural barotrauma (ear pain) requiring aborting
of a treatment on compression is about 3% of total attempted
treatments. This at least in part reflects our patient population. We have a high proportion
of people with a history of head and neck irradiation and eustachian tube dysfunction, complex
head and neck surgery and those with residual CNS depression from drugs.
Calling hyperbaric sessions "dives" contributes to the underuse of HB02 and reflects the involvement with those of us who have entered
the field from diving. Diving
is entering water,
we are not immersing patients in water! Many talk about delivering
oxygen under pressure
- being a gas it is impossible to deliver without pressure. We deliver
oxygen with INCREASED pressure. Also, the use of a pretreatment radiograph of
the chest is urmecessary -
it is not even predictive in submarine escape
training where the decompression rate can be 0.25 atm a second. I must say that I despair
when physicians have difficulty accepting the
idea that the sooner we correct hypoxia the
better the outcome.
The excellent studies of Zamboni's
group indicate the importance of a very large oxygen
concentration in modifYing
the
changes ·induced by ischemic hypoxia.
In our
experience of over 1.25 million sessions
in the last sixteen years the specific
pressure does not . appear to be so critical.
I cannot [see the basis of fears about pressure distinctions]. One patient
I rotEf''""!{i
treated in 1981 had a massive
leg injury in Borneo
and arrived back in
the UK after eleven weeks ' 1
in
the Shell base hospital in Penaga. There were 17 bone fragments between
his knee and ankle( ret ;I(_I
and
a large amount of soft tissue damage. I used 2 ata for 90 miJ!ll.! §_,mice daily. The space' ------.. .
between the tibial fragments
after fl:':a.tion was f:Zs-inches and new bone bridged this in f<:JlJI'_
weekof therap)'_:_He had a total osessions of HB02 and thirteen operations. The key issue in
fractures is - what are the tissueoxygen tensigns? Nilssmt and co- workers in
Gothenburg used 2.8 atm for two hours daily in their study bone healing>in rat mandibular osteotomies. They found twice the rate of healing in the HBEJi'grou:p·thwas also reduced
damage
inthe incisor pulp, odontoblasts and enamel
organ. The successful Marx protocol uses 2.4 atm
abs.- Dr. Philip James,
Wolfson Hyperbaric Medicine Unit, University of Dundee, Ninewalls
Medical School.
Brief biography
of Dr. Philip James: trained in general medicine,
involved in vascular
research before specializing in occupational meilicine. Over the last 25 years has been involved
in the study
of acute neurological syndromes
associated with decompression sickness. He became
interested in the effects on the nervous system after witnessing them first hand in decompression trials and then being involved
in the acute treatment of divers working
in the North Sea. He worked with Prof. Brian
Hills the biomedical scientist now living in Brisbane.
In persuing this area in the University of Texas and in
Texas A&M University they
researched
a number of aspects
of spinal cord function and pathophysiological mechanisms including
microembolism. They
also did research
into the blood-
brain barrier and its stabilization
by
adsorbed
surfactant
and
meqhanisms
of disruption. The message is that although blood-
brain barrier function
is well understood by the drug industry
it
has
been
ignored
by
neurologists
who
are
rarely
in
a
position
to
do
any
fundamental research. If tissue barriers
are disrupted then the secondary
effect is the activation of aseptic inflammation due
the
extravasation
of
protein
and
an
immune
response
- directed at damaged host tissue - the so- called "auto- immune" response. Over the last ten years
they have looked at experimental inflammation in a human model and the role of hypoxia and hyperoxia. The focus centers on treatment ofmicroembolism with hyperbaric oxygenation.
|
For most physicians hemoglobin saturation has become a constant
and a clinical endpoint. Oxygen saturation and oxygen tension
have similar numbers
attached- 100% (saturation) and 100 mm Hg (tension) . This is is re-inforced by statements which draw attention to the small volume of gas
carried in physical solution. In the
reference text Scientific Tables, published by JR Geigy SA Basle, the section on blood gases states: "The
oxygen in physical
solution is often ignored and the oxygen capacity equated with
the
amount
capable
of
being
bound
by the hemoglobin." The quantities for 100 ml of blood breathing air at sea level with an arterial
oxygen tension of about 95 mm Hg are 19 ml bound as oxyhemoglobin and 0.3 ml in physical solution. However it is only
the oxygen in physical sofuti'On that is available for transport to the tissues.and although the volume of oxygen
bound to hemoglobin is large it is not all readily available. The normal arterial
- venous difference is only about 5rnl per 1OOml of
blood at rest, which means that about 14 ml per 100 ml of blood is still present
after blood has circulated. The ability of tissues to remain viable
depends on a minimum level of oxygen
availability. Itnot possible to maintain normal
brain function as
the plasma oxygen tension
falls below 4.0 mm Hg, but at this tension
the arterial saturation is 75%
and artenal blood
still contains IT.8ml per 100 mi blood. Philip James
- Reference:
Haldane JS,
Meakins JC, Priestly JG. J Physiol1918-19;lii::420
|
Question about possible complication: Someone raised
the point about
pneumothorax expanding on decompression - this does not apply
because breathing oxygen actually reduces the volume of a pneumothorax
by increasing the inherent unsaturation and gradient for nitrogen elimination. (Just breathe 100% oxygen during
decompression.)
. Why
HB02
chambers are not in every doctor's clinipc_,
It is very clear there is a general
failure to understand the fundamental importance of oxygen in human physiology. If this were not the case, HB02 would already have become
just another tool used in the day-to-day practice of medicine.
Perhaps a major barrier to gaining greater acceptance within
the medical community
at large is the persistence in referring to clinical
HB02 treatments
as "dives". Diving and clinical
hyperbaric medicine are not the same thing. Diving relates to
underwater military, commercial or amateur activities, recompression is necessary when things go wrong, it is not a choice if you wish to resolve a decompression
sickness problem.
In clinical hyperbaric applications patients do not go anywhere near the water (in my experience a lot of people think they do), they are pressurized for the specific purpose of increasing tissue oxygen tensions in order restore
or assist the healing process. The term "fitness to dive" is another diving
term and relates to the ability of an individual
to deal with the physiological stress of deep diving and working underwater. The whole objective
of pressurizing a clinical patient
is to increase tissue oxygen
tensions in conditions where HB02 is beneficial.
This would
not be necessary if they were "fit". A patient in a chamber
breathing
100% oxygen
is under less physiological stress
rather than more because of the benefits
derived
from the oxygen. A simple risk analysis suggests
to me that the risk of ear squeeze
associated with
hyperbaric treatment, is considerably less than risk associated with radical surgery,
limb loss or death from multiple organ failure. There are many precautions that can be taken
to reduce the risk associated with treatment in any medical
modality, clinical HB02 is no different.
Slow down rate of pressure change, insert grommets and give vitamin E are just a representative sample.
It is not "fitness to dive" that is the issue, just responsible medical
practice. Our rate of impending or actual aural barotrauma (ear pain) requiring aborting of a treatment on compression is about 3% of
total attempted treatments. This at least in part reflects our patient population. We have a high proportion of people with a history of head and neck irradiation and eustachian tube dysfunction, complex head and neck surgery and those with residual CNS depression from drugs. Calling hyperbaric sessions
"dives" does contribute to the underuse of HB02 and reflects the involvement with those of us who have entered the field from diving. Diving
is entering water, we are not
immersing patients in water! Many talk about delivering oxygen
under pressure - being a gas it is impossible to deliver without pressure. We deliver oxygen
with INCREASED pressure.
Also, the use of pretreatment chest radiograph is unnecessary - it is not even predictive in submarine escape training where the decompression rate can be 0.25 atm a second. I
must say that I despair when physicians have difficulty accepting
the idea that the sooner
we correct hypoxia
the better the outcome. The excellent studies
of Zamboni's group indicate
the importance of a very large oxygen concentration in modifying the changes induced by ischemic
hypoxia. In our
experience of over
1.25 million sessions
in the last sixteen years the specific
pressure does not appear to be so critical. I cannot [see the basis of fears about pressure distinctions]. One patient I treated in 1981 had a massive leg injury in Borneo and arrived back in the UK after eleven weeks in the Shell
base hospital in Penaga. There were
17 bone fragments between his knee and ankle and a large amount of soft tissue damage. I used 2 ata for 90 minutes
twice daily. The space between
the tibial fragments after fixation was 1.25 inches and new bone bridged
this in four weeks of therapy. He had
a total of 254 sessions
of HB02 and thirteen operations. The key issue in fractures
is - what are the tissue and bone oxygen tensions?
Nilsson and co-workers in Gothenburg used 2.8 atm for
two hours daily in their study of bone healing
in rat mandibular osteotomies. They found twice the
rate of healing in the HB02 group there was also reduced damage in the incisor pulp,
odontoblasts and enamel organ.
The successful Marx protocol uses 2.4 atm abs.
Philip James, Wolfson Hyperbaric Medicine Unit
|
Q:
Most times my
child's ears are fine but last week she quickly developed
great pain in her cheek and we had to quit the session.
What do you think was going on there? A: It would appear likely that
the rate of compression was too fast - as indicated by your phrase "quickly developed
great pain in her cheek." A minor ear "squeeze" - that is as with the sinuses,
because of a failure to equalize quickly enough causes a serous discharge into the middle ear. This is because
the tissue damage releases inflammatory mediators which increase
the permeability of the blood vessels and they leak. If
this is severe then protein
molecules leave in the exudate.
Unfortunately proteins are glues
and so trie next pressurisation becomes
more difficult because
the swelling and stickiness of the exudate in middle ear and sinus cavities makes it more difficult to equalise. A decongestant given orally about 30 minutes before
treatment may help. It may also help to breathe
the pure oxygen for say ten minutes at atmospheric pressure
before attempting pressurisation, because the swelling is reduced by the high plasma oxygen tension. (the amount of oxygen dissolved
in the plasma). It is now essential
for her to use a slower compression rate. If discomfort
occurs the best course of action is to reduce
the chamber pressure
a small amount
quickly asking the child to signal when she is comfortable and then resume
pressurisation. By the way no one sbould operate
a chamber who is not used to being in one! It is the OJJ!y way thiit qperators can fully understand a
patient's problems. -Philip James
J! klkS!in D.&.!lJ!gTreated 1:Yifu_Hw.erbMic
O
_genation: A close cousin of stroke
can happen to scuba divers from bubbles. The problem is also
encountered in military
aircraft flying at very
high altitude and in extravehicular activity
on space missions. The pathophysiology of circulating bubbles is relevant
to many other areas of medicine. Bubbles
can enter the circulation
of
divers in two ways. If the
lung tears on a rapid
ascent, because of the expansion
of trapped gas, large bubbles can enter the systemic
arterial circulation. If they reach the brain they may cause
death or may result in stroke. Similar problems occur from bubbles
in cardiopulmonary bypass surgery in the "post-pump syndrome." Although
air bubbles have been regarded
as occlusive agents simply obstructing blood flow,
their effects are much more complex. Tissue necrosis may be caused by the ischaemia, but it is now known that, as in stroke,
a much larger volume of brain
tissue is affected. This zone, identified as the ischemic
penumbra, is associated with oedema, because of increased permeability of the blood- brain barrier. This may be severe enough to be associated with diapedetic hemorrhage. Brain lesions may evolve over many years and a pathological study of a gunshot wound to the brain after a survival
of 22 years has shown changes
still continuing with damaged, but preserved, neurons
present. Hyperbaric therapy is well
established as the defmitive treatment for air embolism and was originally based simply on reducing the size of bubbles by increasing barometric pressure. Since 1966, pure oxygen has been introduced in hyperbaric therapy with greater
success. It has now been recognised
that the improved outcome is due to the greatly
increased plasma oxygen content constricting dilated blood vessels and restoring the blood-brain barrier.
A high plasma oxygen concentration reduces leucocyte adhesion and improves endothelial function. In the second mechanism where gas enters
the circulation in divers it is derived from an excess nitrogen
content or supersaturation on decompression and so is known as decompression sickness. Most dives of any significance form some bubbles which are generally microscopic. They arise on the venous side of the circulation pass through the right
heart and are normally filtered
by the lung. However, transpulmonary passage may occur and transfer to the systemic arterial circulation is also possible via an atrial septal defect. In transit through the vasculature of the CNS microbubbles
cause an immediate focal disturbance of the blood brain barrier which, paradoxically, affects
the veins principally of the white
matter.
In very severe
cases this may present clinically as an acute
leucoencephalomyelitis, but decompression sickness can also mimic the individual neurological syndromes, such as transverse myelitis, Bell's palsy, or optic neuritis, which collectively are known
as multiple sclerosis
(MS). The associated
edema causes a reduction in oxygen transport because of the increased tissue water content and the extravasation of proteins
causes inflammation. The presence
of hypoxia has been found in acute plaques in MS using magnetic
resonance spectroscopy. The well-
established success of hyperbaric oxygen
therapy in the
inunediate treatment of the focal CNS lesions of decompression sickness is relevant to the
treatment of other neurological diseases associated with
disturbance ofthe blood-brain barrier.
Q: " a! U!). !Q§_and CQ £.f HB02_for treating decompression sickness
Type II patients in the 'long term, ie. months
after the initial
incident. A: There are two reasons
for immediately using an increase
in pressure and an increase
in the level of oxygen
in acute decompression
sickness. The pressure reduces the volume of any gas present and oxygen increases
the gradient for nitrogen elimination and relieves hypoxia.
Gas can cause physical damage by tearing tissue and/or damage to the endothelium of blood vessels.
The repair in both
mechanisms can be prolonged. The endothelium damage is the same as multiple sclerosis with focal breakdown
of the blood- brain barrier
and can result
in focal demyelination which is indistinguishable from the natural disease.
Reference: James PB. Evidence for subacute fat embolism as the
cause of multiple sclerosis. Lancet 1982;i:380-386. Current treatment protocols
such as US Navy allow for
serial trt;'atment when the initial treatment
does not result in
complete resolution. The protocol to be followed
- as with the protocols
for immediate treatment such as Table 7 - are vague and poorly researched. The only clinical
account of treatment
which gives a fascinating insight
into USN practice is in the following reference:
Curley MD, et al. Neuropsychologic
assessment of cerebral decompression sickness
and gas embolism. Undersea Biomed Res 1988;15:223-236. However "they" have never debated
the rationale for their approach
- despite invitations to do so at many international meetings
over the years and they only recommend a small number of additional
sessions. The inference
from the Manual is that thye are treating
just gas bubbles
but it is abundantly clear from the account by Curley et al that they are treating blood-
brain barrier
disturbance and edema. However
to admit this is to admit that edema in the CNS can be treated
which is not "approved" by the Undersea
and Hyperbaric Medical Society's Hyperbaric Oxygen Committee. A number of physicians around the World - myself included - have used prolonged
courses of HB02 after
delays in resolution in DCS 2 patients. Dr Harch in New Orleans
has followed the results using SPECT imaging, but only in the brain, because the spinal cord cannot
be imaged using
this technology. I arranged treatment
last year for a patient with the most profound neurological damage I have ever seen in a diver - poor vision quadriplegia etc. This started about a year post-event and was encouraged by improvement in vision in the chamber actually during oxygen breathing. He is making slow progress
after being static
for over nine months. I have also arranged treatment
for a four year old girl with spastic quadriplegia and she has regained
bladder and bowel function.The Russsians reported such and effect in spinal cord injured patients in the 1970's. - Philip James, Wolfson Hyperbaric
Medicine Unit, University
of Dundee
|
Q:
Can HB02 be used to help hip deg enerl!!_ign_? A: There are several reports of the successful use--;;nm021n t iillen.tof cartilage degeneration of the
femoral head asociated with aseptic necrosis, followed by magnetic
resonance imaging so it is reasonable to
assume that HB02 will be helpful in disc disease.
I have found HB02 of value in the acute inflammation associated with
herniation of the disc. As disc degeneration is
associated with the formation of gas in the nucleons pulposus there can sometimes be some slight
discomfort on compression.
Q2 risky? A: Dr. Philip James' notes
in 1999 their hyperbaric facilities have safely done over 1.2 million patient
sessions without incident.
He says that, "Engineering standards
are of primary importance but adequate training
for the operation of chambers in a non- acute setting requires only basic information. There is no maximum number of treatments - a treatment
every day would probably
keep all of us a good deal healthier.
Q: Is it safe enough for children? A: Our charity in the UK is collecting data on CP children
tre'itled\V,i.lliHB02 fly only the Chinese experience
with brain damage
and epilepsy is published. It is sensible
to supplement the growth period in children
having brain damage
as there is a syndrome
of delayed deterioration after birth injury." The current attitude
of pediatricians and obstetricians to deny a relationship between birth events, brain damage and cerebral palsy evidence is in the Consensus Statement
published in the British Medical
Journal. (1998 vol
|
319:1054-59.) There is an urgent need to clarify
the issues involved,
as I am sure EVERY parent
with a
brain
damaged child will
agree. As discussed already
the key to
understanding the development of brain injury
is to follow events as closely as possible in real time and imaging of
the nervous system is now providing
such evidence. Epidemiological studies simply muddy the
waters. At the eud of 1999 this article appeared
about the relationship between birth and brain
damage: Pavlakis SG, Kingsley PB, Harpur R, et a!. Correlation of basal
ganglia magnetic resonance spectroscopy with Apgar score in perinatal
asphyxia. Arch Neurol1999;56:1476-1481.
It establishes 1. A relationship between birth "asphyxia," low Apgar scores, lesions in the brain and
the later development.of cerebral palsy in TERM infants. 2. The presence
of lactate as an
indicator of poor outcome.
Cf Ashwal S, Holshouser BA, Tomasi
LG, Shu S, et a!. IH-magnetic
resonance spectroscopy- determined cerebral
lactate and poor neurological outcomes
in children with central
nervous system disease.
Ann Neurol 1997;41:470-81. 3. The vulnerability
of mid brain areas of the neonate. This has been already been discussed by Johnston of Johns Hopkins University, Baltimore, Johnston MV. Selective vulnerability in the neonatal
brain. Ann Neurol
1998;44:155-156. This editorial
discusses a paper in the same issue of the journal: Roland eta! Perinatal hypoxic- ischemic thalamic
injury: clinical features
and neuroimaging. Ann Neurol
1998;44:161-166. The
authors presented data on 20 term infants
with mid- brain changes who
"had a poor outcome with 35% dying and the rest surviving
with cerebral palsy." Johnston comments "The precise mechanisms for such 'surgical' selectivity in the face of a global insult
remain unclear." However he fails to discuss
the blood-brain barrier and the venous nutrition of
the
areas of white matter involved.- Philip James
Q: Is there any reason
to believe that the beneficial effects of HB02 would
continue beyond treatment endpoint?
If so, approximately how long and why? A: Barr and Perrins published some observations on this matter in the Proc.llth International Congress
1995 (ISBN 0-941332-44-6).
Briefly, they showed tissue oxygen
partial pressure measurements that rose from near zero to 50 mmHg after
some months long course of HB02
were retained
without further treatment
for at least three years! They thought they were witnessing a vascular 'medical
disobliteration'. Whether this is due to recanalization of atrophied vessels
or in- growth of neovasculature is open to question.
|
Dear List, I need some advice again. I took little Wyatt to the orthopedist and the neurosurgeon
today. In regards to HB02, the orthopedist is suggesting that HB02 has no lasting effects and if
it were going to be effective
at all it should have been administered as close to the ischemic
event as possible. BUT.. he says I would like little
Wyatt to try Botox injections for Wyatt's
tight abductors and maybe Baclofen for his high tone. He was happy to give me a referral for the Botox
and Baclofen consultation, but would not give me one for the possibility of seeking HB02. When I asked
why, he said that a lot of people were making money on people's
hopes (i.e. the HB02 centers) with no guaranteed
outcome and besides it is not without
risks . He s'ays that it presents a risk for corneal damage.
Has anyone heard that?
[At pressures
of 2 ata and higher there is some temporary myopia
in people inclined
toward hyperopia. This is not considered cornea
damage.] I went to the neorosurgeon for a consultation on Botox. He tells me that the only
place it might be helpful for Wyatt is in his abductors since
all of his other muscle
groups are in good shape,
but he says that it may NOT work because
the abductors are least responsive to
Botox!
Nevertheless, we should try it
anyway at least once because
if it does work it will be good for him. He said we did
not need the baclofen because
Wyatt does not have a really horrible
overall tone problem.
Is this logical?? Try a poison
(Botox) that may not work, but has some known serious side effects. Do not try 100% oxygen at greater than atmospheric pressures because it may not work,
but has very few if any side effects.
Maura Hawkins Mom to Stu (13), Eli (8) and Little
Wyatt (PVL, etc..)
Dear Maura, My twins, Luke and Zachary, 3, are starting
HB02 next
month. I spoke to our neurologist today, and he said he has had about 20 CP patients
try HB02. He said 60% of them had
definite improvements with nothing to attribute it to but the HB02. And, that was from a neurologist! Subsequently, one of my boys had the Botox injections about 2 mos. ago in his
(J abductors. It lasted about 2 wks on him, and even the effects were not that great. Our doctor also
told us that Baclofen
can sometimes intensify
seizure problems. Hope this helps, alittle!
Kerri,
mom to twins, Luke and Zach, 3yrs, Quad CP, PVL
·Dear List, I am finally getting
around to tell you of our experience with HB02 down in North
Carolina. These people
including their tech supports were fantastic. They helped to make my children feel at ease and are very caring people who arbecause of the great changes
they have seen in their own grandchild who has gone thru the treatments many times. I would
h!YJe.c.o.rnmend their prog!]!p.. My son Dalton has spastic quad CP (severe) and my d r also
went who has developmental delays due to her prematurity. These are two of my triplets.
Cheyenne spent 6.6 months in the NICU, came home on 02 24/7
and walked at 2.6years old. She
attends a regular Kindergarten program
with supports of OT, PT speech, and special ed. The
changes with her were subtle at first. She seemed to have longer sentences
and was able to follow thought processes better. She is now in 1st grade and doing very well. Attention
still is an issue for her but she is responding
to things like most other kids in her class. We also were able to tie the HB02 in with AIT (Auditory Integration Therapy, which my kids loved!).
Cheyenne's overall body movements and coordination have improved to the point
that she climbed
a McDonald jungle gym for
the first Jime.ever! Dalton's changes
were also subtle
but he is very physically involved. After abzyt<ffi sessionsj)oticed when I held him on
my hip that he was better able
('-- - •' .
Ni komentarjev:
Objavite komentar