HYPERBARIC OXYGEN REDUCES EDEMA AND NECROSIS OS SKELETAL MUSCLE IN COMPARTMENT SYNDROMES ASSOCIATED WITH HEMORRHAGIC HYPOTENSION

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 1986;68:1218-1224. J Bone Joint Surg Am.
MJ Skyhar, AR Hargens, MB Strauss, DH Gershuni, GB Hart and WH Akeson 
 
 compartment syndromes associated with hemorrhagic hypotension
Hyperbaric oxygen reduces edema and necrosis of skeletal muscle in
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The Journal of Bone and Joint Surgery
Copyright 966 by The Journal ol Bone and Jou:t Surgery. Incorporated
1218 THE JOURNAL OF BONE AND JOINT SURGERY
Hyperbaric Oxygen Reduces Edema and Necrosis of Skeletal
Muscle in Compartment Syndromes Associated
with Hemorrhagic Hypotension*
BY M. J. SKYHAR, M.D.t, A. R. HARGENS, PH.D.t, SAN DIEGO, M. B. STRAUSS, M.D4, LONG BEACH, D. H.
GERSHUNI, M.D.t, SAN DIEGO, G. B. HART, M.D4, LONG BEACH, AND W. H. AKESON, MD.I’, SAN DIEGO, CALIFORNIA
From the Division of Orthopaedics and Rehabilitation. Veterans Administration and University of Cal(ftirnia Medical Centers, San Diego.
and the Baromedical Department. Memorial Hospital Medical Center ofLong Beach, Long Beach
ABSTRACT: This study examined the effect of ex-
posures to hyperbaric oxygen on the development of the
edema and necrosis of muscle that are associated with
compartment syndromes that are complicated by hem-
orrhagic hypotension . A compartment syndrome
(twenty millimeters of mercury for six hours) was in-
duced by infusion of autologous plasma in the antero-
lateral compartment of the left hind limb of seven
anesthetized dogs while the mean arterial blood pressure
was maintained at sixty-five millimeters of mercury after
30 per cent loss of blood volume. These dogs were treated
with hyperbaric oxygen (two atmospheres of pure oxy-
gen) and were compared with six dogs that had an iden-
tical compartment syndrome and hypotensive condition
but were not exposed to hyperbaric oxygen Forty-eight
hours later, edema was quantified by measuring the
weights of the muscles (the pressurized muscle compared
with the contralateral muscle), and necrosis of muscle
was evaluated by measuring the uptake of technetium-
99m stannous pyrophosphate. The ratio for edema was
significantly (p = 0.01) greater in dogs that had not been
exposed to hyperbaric oxygen (1 . 15 ± 0.01) than in the
dogs that had been treated with hyperbaric oxygen (1.01
± 0.03), and the ratio for necrosis of muscle was also
significantly (p = 0.04) greater in dogs that had not had
hyperbaric oxygen (1 .96 ± 041) than in those that had
been treated with hyperbaric oxygen (1.05 ± 0.11).
Comparisons were also made with the muscles of four
normal control dogs and separately with the muscles of
six normotensive dogs that had an identical compart-
‘ment syndrome and normal blood pressure and were not
treated with hyperbaric oxygen. The water content and
absolute uptake of technetium-99m stannous pyrophos-
* No benefits in any form have been received or will be received from
a commercial party related directly or indirectly to the subject of this article.
Funds were received in total or partial support of the research or clinical
study presented in this article. The funding sources were Veterans Admin-
istration and National Institutes of Health Grants GM-24901 . AM-26344,
and RCDA AM 00602 to Dr. Hargens.
1� Division of Orthopaedics and Rehabilitation (V- I S 1 ). Veterans
Administration and University of California Medical Centers, San Diego.
California 92161.
� Baromedical Department. Memorial Hospital Medical Center of
Long Beach, Long Beach, California 90801.
phate in the contralateral control muscles of the four
groups ofdogs were not significantly different, indicating
that the treatment with hyperbaric oxygen primarily
reduced the edema and necrosis that are associated with
compartment syndromes combined with hemorrhagic
hypotension.
CLINICAL RELEVANCE: The results of this study sug-
gest that hyperbaric oxygen may be helpful in treating
patients who have borderline compartment syndrome
(twenty to fifty millimeters of mercury and no neuro-
logical deficit) that is associated with hemorrhagic hy-
potension but that such treatment should be considered
only as an adjunct to the standard treatment of fluid
replacement and fasciotomy. We are now evaluating the
efficacy and indications for hyperbaric oxygen in the
treatment of borderline compartment syndrome in hu-
mans.
Compartment syndrome of skeletal muscle develops
when the intracompartmental pressure is elevated suffi-
ciently to reduce capillary perfusion to the extent that the
intracompartmental tissues become ischemic , non-func-
tional, and necrotic9. We employ a threshold pressure of
thirty millimeters of mercury as one indication for surgical
decompression of a compartment syndrome in the normo-
tensive patient’6. Factors that lower the threshold pressure
for development of compartment syndromes include local
injury to blood vessels, coagulopathy, and systemic
hypotension23. For a model canine hind-limb compartment
syndrome with hemorrhagic hypotension, an intracompart-
mental pressure of twenty millimeters of mercury for six
hours produces a degree of necrosis as great as that produced
by an intracompartmental pressure of forty to fifty milli-
meters of mercury for eight hours in a normotensive dog23.
Trauma to skeletal muscle sometimes leads to an acute
compartment syndrome’6, and severe blood loss also occurs
frequently in patients who have multiple injuries. The hem-
orrhagic shock causes peripheral vascular insufficiency’3,
decreased blood pressure, and reduced blood flow to skeletal
muscle78. Metabolic and respiratory alterations also accom-
pany hemorrhagic shock. These alterations produce resis-
tance to insulin and abnormalities of the metabolism of
HYPERBARIC OXYGEN REDUCES EDEMA AND NECROSIS OF SKELETAL MUSCLE 1219
VOL. 68-A, NO. 8. OCTOBER 1986
amino acid and glucose in skeletal muscle2’9. A study in-
volving injection of xenon- 133 and iodine- 13 1 into skeletal
muscle showed that the transport of nutritive substances and
metabolic products through the interstitial space is impaired
in the presence of hemorrhagic hypotension’4. These
changes lower the threshold pressure for the development
of compartment syndrome23.
Once a compartment has been decompressed, perfusion
is usually improved, but fasciotomy may not be all that is
required to restore function to marginally viable tissues be-
cause edema and ischemia of the tissue do not always resolve
immediately, particularly in the presence of hypotension.
Better and more effective methods for the treatment of com-
partment syndromes are needed.
Strauss et al. determined that intermittent treatment
with hyperbaric oxygen reduced the edema and necrosis of
skeletal muscle significantly in experimentally induced com-
partment syndromes in normotensive animals. The reduction
of edema and necrosis was reflected by ratios of the weight
of muscle and of the uptake of technetium-99m pyrophos-
phate in experimental and control limbs, comparing treated
and untreated dogs. Histological criteria were also used in
grading necrosis of muscle. Histological evidence of ne-
crosis of muscle was reduced in the experimental limbs of
the dogs that received hyperbaric oxygen as compared with
those of the dogs that had an identical compartment syn-
drome but were not treated with hyperbaric oxygen2’.
The purpose of this study was to determine if similar
beneficial effects could be achieved using intermittent
administration of hyperbaric oxygento treat experimentally
induced compartment syndromes in the hind limbs of dogs
that had hemorrhagic hypotension.
Materials and Methods
Preparation of the Animals
Twenty-three conditioned mongrel dogs weighing sev-
enteen to thirty kilograms were divided into four groups
(Table I). Group 1 consisted of four normal dogs that had
normal blood pressure and in which a compartment syn-
drome was not produced. Group 2 consisted of six dogs that
also had normal blood pressure, but in each of them an
anterolateral compartment syndrome (twenty millimeters of
mercury for six hours) was produced. Group 3 consisted of
six hypotensive dogs that had a compartment syndrome that
was identical to the one produced in the dogs in Group 2.
Group 4 consisted of seven hypotensive dogs that had the
same compartment syndrome as that produced in Groups 2
and 3, and these dogs were treated with hyperbaric oxygen.
One week before production of the compartment syn-
drome in Groups 2, 3, and 4, 250 milliliters of blood was
withdrawn from thejugular vein. The blood was centrifuged
and the plasma was decanted. The red blood cells were
diluted with an appropriate volume of 0.9 per cent sodium
chloride solution and then were returned to the animal. One
day before production of the compartment syndrome, the
dogs were denied food but water intake was not restricted.
Xylazine hydrochloride (one milligram per kilogram of body
weight) was administered intramuscularly as a pre-anes-
thetic agent, followed by intravenous pentobarbital sodium
(twenty milligrams per kilogram ofbody weight). Once they
were anesthetized, the dogs were intubated and connected
to a Harvard respirator. Bicillin (penicillin G benzathine)
(1.2 million units) was administered intramuscularly and
Ancef (cefazolin sodium) (one gram), injected into one liter
of lactated Ringer solution, was infused through the right
brachial vein at a rate of two milliliters per minute during
the compartment syndrome. The right brachial artery was
cannulated for continuous monitoring of the mean central
arterial blood pressure, using a strain-gauge pressure-trans-
ducer and four-channel strip-chart recorder (Hewlett-Pack-
ard). In the dogs that were to undergo hemorrhagic
hypotension (Groups 3 and 4), the left jugular vein was
cannulated with K-SO tubing and was ligated distally. The
tubing was tunneled subcutaneously to an exit incision dor-
sally on the dog’s neck and then was anchored with sutures
to serve as permanent access to the central venous system.
The patency of this central venous line was maintained by
intermittent flushing with heparinized saline. The left carotid
artery was cannulated with silicone-treated PE-240 tubing
(Clay Adams) and was ligated distally for the initiation of
hemorrhage. Heparmn (5,000 units) was given intravenously
at the time of cannulation, with hourly supplements of 500
units during the hypotensive period. The dog’s core tem-
perature was maintained at 38 degrees Celsius by a heating
pad placed beneath the animal, and the temperature of the
gastrocnemius muscle was maintained at 34 degrees Celsius
using an infrared lamp. Both temperatures were monitored
continuously with probes and a thermistor thermometer
(Rochester Electro-Medical, model B-2).
Hemorrhagic Shock
Shock was induced by a slow hemorrhage in the dogs
in Groups 3 and 4 (Table I); approximately 30 per cent of
the calculated blood volume was allowed to flow from the
cannulated left carotid artery into a reservoir over a period
of twenty minutes. The mean arterial blood pressure was
monitored and the hemorrhage was continued, if necessary,
until an arterial pressure of sixty-five millimeters of mercury
was obtained. The average volume of blood that was with-
drawn was fifty-six milliliters per kilogram of body weight.
The arterial pressure was maintained by adjusting the res-
ervoir to an appropriate height above the level of the heart
So that the open catheter and tubing produced a hydrostatic
column of blood that maintained the animal’s arterial pres-
sure constant at sixty-five millimeters of mercury. Further
adjustments in height usually were not necessary. After six
hours of compartment syndrome under hypotensive blood-
pressure conditions, the blood was warmed to 38 degrees
Celsius and returned to the animal.
Model Compartment Syndrome
Autologous plasma was warmed to 37 degrees Celsius,
filtered, and infused intramuscularly into the anterolateral
muscle compartment of the left hind limb through a 19-
1220 M. J. SKYHAR ET AL.
THE JOURNAL OF BONE AND JOINT SURGERY
TABLE I
AMPLITUDE AND D URATION OF INTR ACOMPARTMENTAL PRESSURE IN TH E EXPERIMENTAL HIND LIMBS
Mean Arterial Blood
No. of Pressure during
Group Dogs Compartment Syndrome
(mm Hg)
Amplitude Duration
(mm Hg) (Hrs.)
Groupl: 4 95±5 0 0
normal controls (no compartment syndrome)
Group2: 6 98±6 20 6
no hyperbaric
oxygen, normal
blood pressure
Group 3: 6 65 20 6
no hyperbaric
oxygen. reduced
blood pressure
Group 4: 7 65 20 6
hyperbaric
oxygen, reduced
blood pressure
gauge needle. The rate and volume (approximately seven
to nine milliliters) of plasma that was injected was sufficient
to elevate intracompartmental pressure to twenty millimeters
of mercury in Groups 2, 3, and 4 (Table I). This pressure
was maintained for six hours by adjusting the height of the
reservoir of autologous plasma above the site of the infusion.
In the dogs in Group 1 , an infusion needle was placed in
the left anterolateral compartment but no plasma was in-
fused. Intramuscular pressures were monitored continuously
by strain-gauge transducers at proximal and distal sites in
the left anterolateral compartment of each dog using slit
catheters”, and the pressures were recorded on a strip-chart
recorder. In each animal, the left anterolateral compartment
was pressurized and the contralateral compartment served
as the control. An infusion needle and slit catheters were
placed in an identical fashion into the control leg to nor-
malize their effects on the formation of edema and uptake
of technetium-99m stannous pyrophosphate in each leg.
Protocols for Animals in Groups 3 and 4
For dogs in Groups 3 and 4 (Table I), at the completion
of six hours of hemorrhagic shock with pressurization of
the left anterolateral compartment (twenty millimeters of
mercury for six hours), normal blood pressure was restored
by transfusion with autologous whole blood. If necessary,
saline solution was also infused to restore the normal base-
line blood pressure. Each dog was allowed to recover par-
tially from the anesthesia so that intubation and the Harvard
respirator were no longer necessary . The intracompartmen-
tal catheters, carotid and brachial artery catheters, and tem-
perature probes were removed, but the jugular-vein infusion
site was maintained with a heparin lock. The dogs were
taken to the vivarian recovery room, where they were mon-
itored until they were fully awake. They were given one to
two milligrams per kilogram of body weight of meperidine
intramuscularly for analgesia.
During the twelve hours after the six-hour episode of
compartment syndrome, the dogs in Group 3 were confined
to a recovery cage, where they usually slept. Forty-eight
hours after onset of the compartment syndrome , the amounts
of necrosis of muscle and edema were determined for Group
3 exactly as will be described for the dogs in Groups 1 , 2,
and 4.
Within fifteen minutes after removal of the intracom-
partmental catheters, each dog in Group 4 was put in a
monoplace hyperbaric chamber (Vickers clinical hyperbaric
oxygen system, CHS/3) for a one-hour exposure to pure
oxygen at two atmospheres of absolute pressure while the
animal breathed spontaneously. Access to the jugular-vein
catheter from outside the chamber was established by con-
necting the tubing to an intravenous-line portin the bulkhead
of the chamber. The line was occasionally flushed with
heparinized normal saline solution. The dog was kept lightly
sedated with intravenous pentobarbital sodium (ten milli-
grams per kilogram of body weight) as necessary during
treatment with hyperbaric oxygen. After the first one-hour
exposure to hyperbaric oxygen, the dog was returned to its
cage. Four hours later, a second one-hour treatment with
hyperbaric oxygen was administered, and after four more
hours a third treatment was given, so that each dog had
three one-hour exposures to hyperbaric oxygen over an
eleven-hour period. The amounts of swelling and tenseness
of the experimental and control anterolateral compartments
were observed and compared before and after each exposure
to hyperbaric oxygen.
Quantification of Necrosis of Muscle and Edema
Intracompartmental skeletal necrosis of muscle was
quantified by uptake of technetium-99m stannous pyro-
phosphate, as described by Hargens et ‘ ‘ . Forty-eight
hours after the onset of pressurization of the compartment,
each animal was sedated by an intramuscular injection of
xylazine (fifty milligrams). A bolus of five millicuries of
technetium-99m pyrophosphate was then injected intrave-
nously into the brachial vein. The dog remained sedated
and was held upright by a cloth sling under the abdomen
GROUP 3
120
100
80
I
GROUP 4
60
:t:
E
E
I
I I
80 \�
-1 0 1 2 3 4 5
TIME (hrs)
FIG. 1
0 1 2 3 4 5 6
TIME (hrs)
VOL. 68-A, NO. 8. OCTOBER 1986
HYPERBARIC OXYGEN REDUCES EDEMA AND NECROSIS OF SKELETAL MUSCLE 1221
to equalize circulation of the blood in the two hind limbs.
Three hours after injection of the isotope, the dog was killed
with an overdose of intravenous pentobarbital sodium. The
three major muscles of the anterolateral compartment (tib-
ialis cranialis, extensor digitorum longus, and fibularis lon-
gus) were removed from both limbs simultaneously by two
operating teams.
The three muscles comprising the muscle groups from
each side were weighed individually for the evaluation of
edema, as previously described2’ . An index for edema was
calculated as the ratio of the weight of muscle on the ex-
perimental side to that on the control side. Experimental
and control muscle groups from each animal were cut into
one-centimeter-thick segments for studies of radioactivity.
Each segment that was obtained in this fashion was weighed,
and its uptake of technetium-99m stannous pyrophosphate
was determined in a gamma well-counter (Chicago Nuclear,
model 1 185). Triplicate standard samples, each diluted iO�
times from the original injection solution of technetium-
99m pyrophosphate, were used to determine the absolute
uptake and to permit comparison between the different dogs.
Each segment was counted for gamma radioactivity, and
the data for all segments of muscle and standard samples
were corrected for decay of radioactivity. The percentage
of the total dose of technetium-99m pyrophosphate in each
sample was then calculated. Ratios of the uptake in the
experimental limb to that in the control limb were deter-
mined using the sum of the uptake of isotope in the segments
from the pressurized muscles and the sum of the uptake in
the segments from the contralateral control muscles of each
dog.
Two other groups of dogs (Groups 1 and 2) were in-
cluded to rule out the possible systemic effects of hemor-
rhagic hypotension or hyperbaric oxygen, or both, on
absolute uptake of technetium-99m pyrophosphate in the
contralateral control muscles. The ratios of uptake for the
dogs that were treated with hyperbaric oxygen (Group 4)
were then compared with the ratios for the six dogs that
were treated in an identical manner but were not exposed
to hyperbaric oxygen (Group 3). The results for uptake of
technetium-99m pyrophosphate from our previous study,
done without hyperbaric oxygen23, were included for pur-
poses of comparison with animals that were treated with
hyperbaric oxygen in the present study. Using paired and
(I)
� 100
(I)
w
ci�
w
I-
w
U-
0
uJ
Condensed plots of the maximum range of mean arterial pressure (indicated by bars above and below the median) for four representative dogs in
Group 3 and four representative dogs in Group 4. The mean arterial pressures are presented for the hour preceding hemorrhage and for each hour
during the period of hemorrhagic hypotension. During the hypotensive period. the arterial pressures of some dogs changed abruptly from sixty-five
millimeters of mercury, but immediate adjustments were made to restabilize the pressure at sixty-five millimeters of mercury. The data points that are
marked with an asterisk indicate essentially no variation of mean arterial pressure for the given hour.
60
1222 M. J. SKYHAR El AL.
1.50
��1
0
I-
� 1.00
C.)
-I
Li
LU .
><
Lii
I�4A��
GROUP I GROUP 2 GROUP 3 GROUP 4
FIG. 2
Comparison of weights of the muscles of the anterolateral compartment of the normal dogs and of the three groups of dogs with compartment
syndrome. Group 1 consisted of normal controls; Group 2, dogs that had compartment syndrome, normal blood pressure, and no treatment with
hyperbaric oxygen; Group 3, dogs that had compartment syndrome, hypotension, and no treatment with hyperbaric oxygen; and Group 4, dogs that
had compartment syndrome, hypotension, and treatment with hyperbaric oxygen. The results (mean and standard error) are expressed as ratios of the
weight of the experimental anterolateral compartment to that of the contralateral anterolateral compartment. The Group-4 dogs had significantly less
edema than did the Group-3 dogs (p = 0.01). Two days after pressurization, the Group-2 dogs did not have significant edema as compared with the
Group- I dogs. The water content of the contralateral compartment was not different in the four groups of animals.
-J
0
0
GROUP I GROUP 2 GROUP 3 GROUP 4
FIG. 3
Comparison of ratios of uptake of technetium-99m stannous pyrophosphate of the muscles of the anterolateral compartment of the normal dogs and
of the three groups of dogs that had compartment syndrome. Group 1 consisted of normal controls; Group 2, dogs that had compartment syndrome,
normal blood pressure, and no treatment with hyperbaric oxygen; Group 3, dogs that had compartment syndrome, hypotension, and no treatment with
hyperbaric oxygen; and Group 4, dogs that had compartment syndrome, hypotension, and treatment with hyperbaric oxygen. The results (mean and
standard error) are expressed as ratios of the uptake in the experimental anterolateral compartment to that in the contralateral anterolateral compartment.
Group-4 dogs had significantly less necrosis of muscle (uptake of pyrophosphate in the experimental leg) than did Group-3 dogs (p = 0.04). For
purposes of comparison, results for uptake from a previous study of hypotensive dogs that had an identical compartment syndrome and were not treated
with hyperbaric oxygen23 are included in this figure only. The Group-2 dogs did not have significant necrosis as compared with the Group-i dogs. The
uptake of pyrophosphate in the contralateral compartment was not different in the four groups of animals.
unpaired Student t tests, the statistical significance was set in four representative animals from Groups 3 and 4 during
at p < 0.05. the experimental period demonstrated that the blood pres-
sures of these hypotensive dogs were maintained at essen-
Results tially the same levels during the six-hour compartment
Plots of the mean and range of arterial blood pressures syndrome (Fig. 1). After this period, the intracompartmental
ThE JOURNAL OF BONE AND JOINT SURGERY
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HYPERBARIC OXYGEN REDUCES EDEMA AND NECROSIS OF SKELETAL MUSCLE 1223
VOL.68-A, NO. 8. OCTOBER 1986
catheters were removed and the blood pressure of the ani-
mals was restored to normal. Group-4 animals were then
treated with hyperbaric oxygen and Group-3 animals were
not.
Qualitatively, there was reduction of tenseness and
swelling in the experimental compartments of the dogs that
were exposed to intermittent hyperbaric oxygen. All dogs
in Groups 3 and 4 recovered uneventfully from the hypo-
tensive period. All dogs were killed two days after the
episode of compartment syndrome (sham compartment syn-
drome for Group 1).
The effect of hyperbaric oxygen on edema of muscle
is reflected by the muscle-weight ratios of the experimental
and contralateral control limbs (Fig. 2). The mean ratio for
the dogs that were treated with hyperbaric oxygen (Group
4) was unity and was significantly less (p = 0.01) than the
ratio of 1 . 15 for the dogs that were not exposed to hyperbaric
oxygen (Group 3). Necrosis of muscle, as quantified by
uptake of technetium-99m pyrophosphate, was significantly
reduced (p = 0.04) in Group-4 dogs as compared with
Group-3 dogs (Fig. 3). Accumulation ofthis radionucleotide
indicates irreversible ischemic injury, since pyrophosphate
is absorbed by the calcium deposits of necrotic and severely
injured cells’ ‘ . The mean ratio for the dogs that were not
exposed to hyperbaric oxygen was 1 .96, indicating in-
creased uptake of technetium-99m pyrophosphate and ver-
ifying necrosis in the experimental limb. However, the mean
ratio for the dogs that were treated with hyperbaric oxygen
was 1 .05, reflecting significantly less damage to muscle in
the experimental limb.
As compared with normal control dogs (Group I ), ra-
tios of uptake of technetium-99m pyrophosphate for dogs
in Group 4 (compartment syndrome with hypotension and
treatment with hyperbaric oxygen) and Group 2 (compart-
ment syndrome with normal blood pressure and no treatment
with hyperbaric oxygen) were not significantly different
(p = 1 .00 and p = 0.66, respectively). These results in-
dicate that the experimental muscles of the dogs in Groups
1 , 2, and 4 were essentially normal, with uptake of tech-
netium-99m pyrophosphate about equal to that in the con-
tralateral muscles. Also, the absolute water content and
absolute uptake of technetium-99m pyrophosphate per gram
of tissue were not different in the contralateral control mus-
des of the four groups of dogs in this study (minimum p
= 0.68). This is important because our comparisons of
ratios for the experimental and control sides for weight and
uptake of pyrophosphate assumed that the contralateral (con-
trol) muscle remains normal in terms of water content and
uptake of pyrophosphate despite exposure of the animal to
hemorrhagic hypotension or hyperbaric oxygen, or both.
Discussion
As has been previously demonstrated in the normoten-
sive state2’ , in the hypotensive state hyperbaric oxygen also
significantly reduces edema and necrosis of muscle after an
induced compartment syndrome. This is reflected by re-
ductions in the edema and necrosis of muscle in the dogs
that were treated with hyperbaric oxygen compared with the
dogs that were not treated with hyperbaric oxygen. The
mechanisms by which hyperbaric oxygen reduces necrosis
of skeletal muscle in compartment syndromes associated
with hemorrhagic hypotension are probably similar to those
elucidated by Strauss et al. for the normotensive state:
namely, hyperoxygenation and vasoconstriction.
Hyperoxygenation increases the amount of physically
dissolved oxygen in the fluids of plasma and tissue and is
directly proportional to the partial pressure of inhaled
oxygen’ . Breathing pure oxygen at three atmospheres gen-
erates a fifteenfold increase in dissolved oxygen. This is
sufficiently high to meet the requirements for basal oxy-
genation of tissue in the absence of hemoglobin-borne
oxygen5. Hyperoxygenation also helps to drive oxygen
across partial barriers’7 such as the intracellular and inter-
stitial edema that is associated with compartment syndrome.
The administration of hyperbaric oxygen causes va-
soconstriction by direct action of the increased partial pres-
sure of oxygen on the blood vessels, reducing blood flow
by approximately 20 per cent3. This vasoconstrictive effect
may seem undesirable; however, the net effect is mainte-
nance of oxygenation of the tissues, reduced capillary blood
pressure, and decreased transudation and diapedesis3’5. De-
creased capillary blood pressure causes a shift in the trans-
capillary flow of fluid to promote greater resorption of
extravascular fluid and decreased interstitial-fluid pressure,
thus improving local microcirculation ‘�.
There are two general forms of shock associated with
trauma. The shock that is associated with massive damage
to tissue alters vascular permeability, resulting in intracel-
lular and diffuse protein-rich interstitial edema. Failure of
multiple organs is likely to occur�. The shock that is as-
sociated with soft-tissue injury (as in our model) rarely
precipitates organ-failure syndromes and is primarily as-
sociated with the shift of fluid from interstitial to intra-
cellular spaces2#{176}.The pathophysiology of acute compart-
ment syndrome includes intracellular or interstitial edema,
or both, depending on the etiology, resulting in compromise
of the microcirculation9. When shock and compartment syn-
drome occur concomitantly in the clinical setting, the de-
crease in blood pressure and shifts in fluid decrease the
microcirculatory perfusion in the compartment and increase
the intracompartmental pressure. These factors combine to
lower the threshold of intracompartmental pressure for the
development of ischemia and necrosis. For this reason, im-
proper application or prolonged use of military anti-shock
trousers for the treatment of acute hypovolemia may cause
a compartment syndrome in the lower extremity even in the
absence of injury to the extremity622.
Clinical experience has indicated that there are three
main untoward effects of treatment with hyperbaric
oxygen’2. They are, in order of importance, cerebral oxygen
toxicity, barotrauma to the middle ear, and anxiety due to
confinement within the chamber. These effects are virtually
eliminated by the use of oxygen pressures below the thresh-
old for seizures, appropriate pre-treatment evaluation, and
1224 M. J. SKYHAR ET AL.
judicious use ofproper medications’2. Untoward side effects have trauma to a single extremity, both without and with
of hyperbaric oxygen were not a problem in this study in concomitant hypovolemic shock, followed by appropriate
animals. resuscitation with fluid. The results to date have been en-
The efficacy and indications for the use of hyperbaric couraging. However, hyperbaric chambers are not widely
oxygen in the treatment of patients who have so-called bor- available, and their use in treating patients with compart-
derline compartment syndrome (twenty to fifty millimeters ment syndrome must still be considered adjunctive in nature.
of mercury without a neurological deficit) are presently un-
der investigation at the University of California at San NOTE: The authors thank B. R. Thompson. K. Freestone, R. C. OHara. A. Crenshaw, and
. . . . . . . C. Johansson for their expert technical assistance. They also thank J. Robison for her assistance
Diego. This randomized clinical study includes patients who w�#{252}�tie preparation of the manuscript.
References
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