Strani

petek, 15. marec 2019

STUDIJE IZ TUJE LITERATURE

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  This  manuscript  has  research  data  from  published  work,  some unpublished articles and some email discussion.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

































/I
breathe oxygen beginning at 1.5 atmospheres of increased pressure. This marks the start of true

hyperbaric pressure. Notice the phenomenal rise once atmospheric pressure increases twice above
normal. This hyperoxia, increased tissue oxygen, is useful in h {;;g·l/
What  is  the  difference  between saturation and  oxygen te ion?  The  problem we  face  in
advocating-proper usage oToxygen invciives confiision"tletWen  saturation and oxygen tension,
100% vs.. 100 mmHg. Only dissolved'oxygen contributes to the tension (or partial pressure).
Study  the  figures  for  oxygen  transported by  plasma  (liquid)  vs..  hemoglobin  (one  gram


I
hemoglobin can only combine with 1.34 m1 oxygen) - in 1OOml of healthy blood there is 19ml

f
oxygen as oxyhemoglobin and 0.3ml oxygen in liquid solution, here the hemoglobin is near


maximum saturation (98%) and the pressure or tension of oxygen in the liquid solution is


initially 95mmHg and downline tissue levels drop to 39mmHg or less. Breathing pure oxygen  t
2.5 times atmospheric pressure increases the amount of oxygen in (plasma) liquid solution to
t

about 6 m1 per lOOml  blood.  This increased oxygen volume measurably increases the oxygen
'

tension and downline tissue levels can rise upwards of200mmHg.



Oxygen given with increased pressure can correct many serious health problems. Hyperbaric


,-  \
oxygenation helps the body heal from conditions that have low oxygen in the tissues causing or


( /
complicating the outcome. Repetitive hyperbaric sessions can help many different conditions; let's



mention the first few ABC's such as anemia, burns and crush injuries. Compromised skin grafts



often improve with hyperbaric oxygemrtfon. Difficult toheaiiiif tions treated with hyperbaric



 
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


c,
 
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
                                                                     

c
 
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.


c
 
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


c
 
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


c)
 
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

c
 
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.


c\
 
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