Selected Abstracts from Medline on Diving Medicine

Returned from

Search performed April, 2000

scroll down to review



TITLE: Computed chest tomography in an animal model for decompression
sickness: radiologic, physiologic, and pathologic findings [In
Process Citation]
AUTHORS: Reuter M; Tetzlaff K; Brasch F; Gerriets T; Weiher M
Struck N; Hirt S; Hansen J; Muller KM; Heller M
This study was conducted to investigate the early pulmonary effects of
acute decompression in an animal model for human decompression
sickness by CT and light microscopy. Ten test pigs were exposed to
severe decompression stress in a chamber dive. Three pigs were kept
at ambient pressure to serve as controls. Decompression stress was
monitored by measurement of pulmonary artery pressure and arterial
and venous Doppler recording of bubbles of inert gas. Chest CT was
performed pre- and postdive and in addition the inflated lungs were
examined after resection. Each lung was investigated by light
microscopy. Hemodynamic data and bubble recordings reflected severe
decompression stress in the ten test pigs. Computed tomography
revealed large quantities of ectopic gas, predominantly
intravascular, in three of ten pigs. These findings corresponded to
maximum bubble counts in the Doppler study. The remaining test pigs
showed lower bubble grades and no ectopic gas by CT. Sporadic
interstitial edema was demonstrated in all animals--both test and
control pigs--by CT of resected lungs and on histologic examination.
A severe compression-decompression schedule can liberate large
volumes of inert gas which are detectable by CT. Despite this severe
decompression stress, which led to venous microembolism, CT and light
microscopy did not demonstrate changes in lung structure related to
the experimental dive. Increased extravascular lung water found in
all animals may be due to infusion therapy.
SOURCE: Eur Radiol 2000;10(3):534-41


TITLE: Escape from a disabled submarine: decompression sickness risk
AUTHORS: Parker EC; Ball R; Tibbles PM; Weathersby PK
Individual crewmember escape from a disabled U.S. Navy nuclear
submarine has never been necessary, but remains an important
contingency. Decompression sickness (DCS) is one of the foreseeable
risks and a robust mathematical model of DCS incidence has been used
to estimate the magnitude of this risk under a variety of escape
scenarios. The model was calibrated with over 3000 well-controlled
human pressure exposures, less than 2% of which simulated pressure
profiles of submarine escape. For disabled submarine depths < 300
ft of sea water (fsw) and internal submarine pressures of <11 fsw
(arguably the most likely conditions), the DCS risks are comparable
to those routinely undertaken by U.S. Navy divers--less than 5%. For
progressively deeper depths and especially for higher submarine
internal pressures, the risk of DCS becomes much greater, including
unknown chances of permanent injury and death. Variations from the
baseline escape procedure are explored, including equipment
differences, delays in exiting the submarine and changes in the
oxygen content of the breathing mix.
SOURCE: Aviat Space Environ Med 2000 Feb;71(2):109-14


TITLE: Inner ear decompression sickness following altitude chamber operation.
AUTHORS: Nachum Z; Shupak A; Spitzer O; Sharoni Z; Ramon Y
Abramovich A; Shahal B
Decompression sickness (DCS) is a known hazard of altitude chamber
operation. The musculoskeletal, dermal, neurological and pulmonary
manifestations of DCS are well recognized, but inner ear injury has
not been reported. We present the unusual case of a medical corpsman
suffering from vestibular DCS after an altitude chamber exposure to
25,000 ft. The patient had a good clinical response to hyperbaric
treatment, but there was laboratory evidence of mild residual
vestibular damage with full compensation. This case suggests that
aviation medical personnel should be more aware of the possible
occurrence of inner ear DCS among subjects exposed to altitude.
SOURCE: Aviat Space Environ Med 1999 Nov;70(11):1106-9


TITLE: [Cerebellar hemorrhage--a rare, but serious complication in
decompression disease]
Since 1978, five conferences on diving-related illness have failed to
conclude that diving could lead to brain damage. We present a case
history of a diver with decompression disease who also experienced
brain damage. He performed a normal dive down to a depth of ten
metres, when suddenly he had to go up to the surface. The patient was
brought to the nearest hospital with a decompression chamber and
treated according to standard procedure, yet his condition did not
improve as expected. A CT scan showed bilateral, cerebellar bleeding
and a secondary hydrocephalus. A CT scan one year after the accident
showed a normalisation. The changes in the cerebellum could be
related to decompression disease. Neurosurgery may be necessary in
some cases of decompression disease.
SOURCE: Tidsskr Nor Laegeforen 1999 Oct 30;119(26):3901-2


TITLE: Magnetic resonance signal abnormalities and neuropsychological
deficits in elderly compressed-air divers.
AUTHORS: Tetzlaff K; Friege L; Hutzelmann A; Reuter M; Holl D
Leplow B
We investigated the association between MR signal abnormalities of the
central nervous system, neuropsychologic performance and exposure
indices in 20 experienced elderly compressed-air divers who had no
history of neurological decompression illness (DCI). Results of MRI
of the brain and psychometric testing were compared with 20 matched
healthy commercial employees who never dived: 60% of the divers and
45% of the controls had hyperintense MR abnormalities. Among divers,
both the number and the size of abnormalities correlated with hours
diving in the deep air-diving range of 40-60 m (p < 0.05). Divers'
mental flexibility and visual tracking performance were decreased in
comparison with controls (p < 0.05 and p < 0.01). Divers thus
are at risk of detrimental long-term effects of compressed-air diving
on the central nervous system even in the absence of a history of
neurological DCI. Copyright 1999 S. Karger AG, Basel
SOURCE: Eur Neurol 1999;42(4):194-9


TITLE: Circulating venous bubbles in recreational diving: relationships with
age, weight, maximal oxygen uptake and body fat percentage.
AUTHORS: Carturan D; Boussuges A; Burnet H; Fondarai J
Vanuxem P; Gardette B
Decompression sickness (DCS) is recognized as a multifactorial
phenomenon depending on several individual factors, such as age,
adiposity, and level of fitness. The detection of circulating venous
bubbles is considered as a useful index for the safety of a
decompression, because of the relationship between bubbles and DCS
probability. The aim of this work was to study the effects of
individual variables which can be assessed non invasively, on the
grades of bubbles detected 60 min, after diving by means of Doppler
monitoring, in a sample of 40 male recreational scuba divers. The
variables investigated were: age, weight, maximal oxygen uptake
(VO2max) and percentage of body fat (%BF). Bubble signals were graded
according to the code of Spencer. The relationships between the
bubble grades (BG) and the variables investigated were studied using
two methods: the differences between the average values of each
variable at each BG were analyzed by the Scheffe test. Then we
performed the non-parametric Spearman correlation analysis.
Significant differences (P < 0.05) were found (Scheffe test)
between average values of the variables at grade 0 and 3 (age: P =
0.0323; weight: P = 0.0420; VO2max: P = 0.0484), except for %BF (P =
0.1697). Relationships with P < 0.01 were found (Spearman
correlation) between BG and the variables: age: p = 0.486, P =
0.0024; weight: p = 0.463, P = 0.0039; VO2max: p = -0.481, P =
0.0027; except for %BF: p = 0.362, P = 0.0237. This work showed that
bubble production after hyperbaric exposures depends on several
individual factors. The effects of age, weight and VO2max are more
significant than the effect of %BF. We concluded that to take into
account such variables in decompression tables and diving computer
programs should allow to adapt the decompression procedures to
individual risk factors and reduce the DCS probability.
SOURCE: Int J Sports Med 1999 Aug;20(6):410-4


TITLE: Electroencephalography and magnetic resonance imaging after diving and decompression incidents: a controlled study.
AUTHORS: Sipinen SA; Ahovuo J; Halonen JP
Electroencephalography and magnetic resonance imaging after diving and
decompression incidents: a controlled study. Undersea Hyper Med
1999.; 26(2):61-65.--Diving incidents with symptoms of decompression
sickness (DCS) and/or arterial gas emboli (AGE) might increase the
degree of pathologic change in the electroencephalogram (EEG) or
magnetic resonance imaging (MRI) of the supraspinal central nervous
system (CNS). Diving itself, even without known symptoms of DCS
and/or AGE, has been proposed to increase the number of CNS lesions
using either EEG or MRI. In the first part of a two-part study we
examined the effects of recompression treatment on EEG in
decompression incidents in a group of sport and professional divers
compared with a control group of healthy naval divers. In the second
part we recorded brain MRI from three groups of volunteers: 1) divers
who were treated for DCS in pressure chamber, 2) divers who had never
had symptoms of DCS (and/or AGE), and 3) healthy normal controls who
were not divers. Our results indicate that DCS increases the
incidence of pathologic EEG recordings, whereas recompression
treatment decreases them. The results of MRI do not verify evidence
of increased numbers of CNS lesions in normal divers as compared to
non-diving, healthy control subjects, whereas some of the divers
treated for DCS in a pressure chamber had hyperintense lesions in
brain white matter. None of them had any abnormalities in EEG,
neurologic performance, or psychologic behavior. Both EEG and MRI are
sensitive and non-specific methods for judging suspected evidence of
brain lesions from diving or diving accidents.
SOURCE: Undersea Hyperb Med 1999 Summer;26(2):61-5


TITLE: Endothelial damage by bubbles in the pulmonary artery of the pig.
AUTHORS: Nossum V; Koteng S; Brubakk AO
A method for measuring endothelial damage caused by decompression was
developed for vessels with a large radius. Segments of the pulmonary
artery from pigs (8-12 wk old) were tested for endothelium damage
using a system for recording changes in the tension in the vessel
wall. Substance P (SP) was used as an endothelial-dependent dilation
agonist. A significant decrease was found in the total response
(Tmax) for SP as a result of endothelium damage, and the reduction in
response was related to the number of bubbles. Furthermore, the
sensitivity of the vessels to the agonist was significantly reduced
after exposure to bubbles. Staining the endothelium with silver
nitrate and light microscopy confirmed mechanical endothelium damage.
SOURCE: Undersea Hyperb Med 1999 Spring;26(1):1-8


TITLE: Outcome after treatment of neurological decompression illness is
predicted by a published clinical scoring system.
AUTHORS: Pitkin AD; Benton PJ; Broome JR
BACKGROUND: After recompression therapy, some cases of neurological
decompression illness (DCI) have a significant residual deficit.
Boussuges et al. report a scoring system to predict sequelae using
weighted historical and clinical indices at presentation which we
applied to the British Hyperbaric Association (BHA) database of UK
diving accidents, held at the Institute of Naval Medicine (INM).
METHODS: A database search identified 234 cases of neurological DCI
from the 2 yr, 1995-6. Of these, 217 case records contained
sufficient data to apply the scoring system. Outcome was classified
as severe sequelae (i.e., causing a functionally important deficit)
or as mild/no sequelae. RESULTS: The median score in UK cases with
severe sequelae was 13 (95% C.I. 11.5 to 14.5) and in cases with
mild/no sequelae, 6 (95% C.I. 5.5 to 6.5). Significantly more cases
with scores > 7 had severe sequelae than cases with scores < or
= 7 (chi2, p < 0.0001). The sensitivity of a score > 7 (for
severe sequelae) was 94% and the specificity was 65%. The positive
predictive value of a score > 7 (for severe sequelae) was 18% and
the negative predictive value of a score < or = 7 was 99%.
CONCLUSIONS: When applied to the INM/BHA database a score of > 7
by this scoring system has a higher sensitivity and lower specificity
for severe sequelae than reported by Boussuges et al. It has a higher
predictive accuracy for successful outcome of treatment (99% vs. 89%)
but a much lower predictive value for severe sequelae (18% vs. 86%).
Convergence between this and other published scoring systems may
allow derivation of a generic scoring system that could then be
evaluated prospectively in multiple centers.
SOURCE: Aviat Space Environ Med 1999 May;70(5):517-21


TITLE: Three cases of spinal decompression sickness treated by U.S. Navy
Treatment Table 7.
AUTHORS: Ito M; Domoto H; Tadano Y; Itoh A
For patients of type 2 decompression sickness, recompression therapy
using U.S. Navy Treatment Table 6 (TT6) and its extensions is the
most common means of treatment. However, some cases are resistant to
the recompression therapy, and the outcome of TT6 is not always
satisfactory. Although a new table, the U.S. Navy Treatment Table 7
(TT7) was described in 1985 in the U.S. Navy Diving Manual, to date
few cases who were treated using TT7 have been reported. Here, we
report three cases of spinal decompression sickness who received
treatment according to TT7. Two were sports scuba divers, and the
other a commercial diver. TT7 was applied later than 4 d after onset
in all three cases; two patients were remarkably improved during the
recompression therapy, while the other improved to a certain extent
after additional repetitive TT6. Mild impairment of lung function,
probably due to pulmonary oxygen toxicity, was observed on lung
function testing in one case. In all cases, after additional TT6
and/or rehabilitation, patients were able to return to active daily
SOURCE: Aviat Space Environ Med 1999 Feb;70(2):141-5


TITLE: Arterial gas embolism after decompression: correlation with
right-to-left shunting.
AUTHORS: Ries S; Knauth M; Kern R; Klingmann C Daffertshofer M; Sartor K; Hennerici M
Paradoxical gas embolism is a possible cause of neurologic sequelae
after decompression in divers. The authors detected arterial bubbles
after decompression from chamber dives in two of six divers using
transcranial Doppler sonography (TCD). Arterial bubbles correlated
with the size of right-to-left shunting as diagnosed by contrast TCD.
The pathway of spontaneous paradoxical embolism was tracked for the
first time, supporting the concept of paradoxical gas embolism as a
cause of early neurologic sequelae after decompression in at-risk
SOURCE: Neurology 1999 Jan 15;52(2):401-4


TITLE: Cytokine response after acute hyperbaric exposure in the rat.
AUTHORS: Ersson A; Linder C; Ohlsson K; Ekholm A
Intravascular gas has earlier been shown to activate leukocytes and
platelets, enhance cell adhesion, and promote secretion of vasoactive
substances from platelets. Since decompression is known to release
gas bubbles in the bloodstream, the present study was undertaken to
investigate the effect of a standardized decompression trauma on
inflammatory mediators. Two series of experiments were performed in
which male Wistar rats were subjected to a sublethal decompression
trauma using a dry pressure chamber. Postdive measurements of
cytokine levels were performed to look for signs of an inflammatory
reaction. All animals subjected to a decompression trauma showed
postdive signs of mild to severe decompression illness (DCI) and
measurements of interleukin-6 (IL-6) indicated a postdive increase in
the majority of these animals. Our finding of a postdive increase in
IL-6 suggests that an inflammatory response, probably created by a
blood-gas interface, may be a factor in the process leading to DCI.
SOURCE: Undersea Hyperb Med 1998 Winter;25(4):217-21


TITLE: Presumed venous infarction in spinal decompression sickness.
AUTHORS: Manabe Y; Sakai K; Kashihara K; Shohmori T
We describe the serial MR imaging findings in a patient with spinal
decompression sickness. In the acute phase, the spinal cord was
swollen, with increased T2 signal in the posterior part of the
column; 1 month later, marked contrast enhancement was noted in the
same location; and 2 months later, the swelling and T2 signal had
decreased. MR imaging may facilitate the early diagnosis of spinal
decompression sickness.
SOURCE: AJNR Am J Neuroradiol 1998 Sep;19(8):1578-80


TITLE: Decompression sickness risk in rats by microbial removal of dissolved
AUTHORS: Kayar SR; Miller TL; Wolin MJ; Aukhert EO; Axley MJ
Kiesow LA
We present a method for reducing the risk of decompression sickness
(DCS) in rats exposed to high pressures of H2. Suspensions of the
human colonic microbe Methanobrevibacter smithii were introduced via
a colonic cannula into the large intestines of the rats. While the
rats breathed H2 in a hyperbaric chamber, the microbe metabolized
some of the H2 diffusing into the intestine, converting H2 and CO2 to
methane and water. Rate of release of methane from the rats, which
was monitored by gas chromatography, varied with chamber H2 pressure.
This rate was higher during decompression than during compression,
suggesting that during decompression the microbe was metabolizing H2
stored in the rats' tissues. Rats treated with M. smithii had a 25%
(5 of 20) incidence of DCS, which was significantly lower (P <
0.01) than the 56% (28 of 50) incidence of untreated controls,
brought on by a standardized compression and decompression sequence.
Thus using a microbe in the intestine to remove an estimated 5% of
the body burden of H2 reduced DCS risk by more than one-half. This
method of biochemical decompression may potentially facilitate human
SOURCE: Am J Physiol 1998 Sep;275(3 Pt 2):R677-82


TITLE: Decompression sickness presenting as forearm swelling and peripheral neuropathy: a case report.
AUTHORS: Ball R; Auker CR; Ford GC; Lawrence D
Neurological symptoms after decompression from a dive are usually
thought to be manifestations of central nervous system (CNS)
decompression sickness (DCS). We present a case of DCS in which
neurological symptoms are present but which the clinical findings,
magnetic resonance imaging and electroneuromyographic studies suggest
were caused by muscle injury and exacerbation of an existing
peripheral neuropathy. This finding supports the alternative
hypothesis that some neurological symptoms and signs in DCS are due
to effects on peripheral nerves rather than the CNS.
SOURCE: Aviat Space Environ Med 1998 Jul;69(7):690-2


TITLE: Cutaneous lesions in swine after decompression: histopathology and
AUTHORS: Buttolph TB; Dick EJ Jr; Toner CB; Broome JR
Williams R; Kang YH; Wilt NL
A detailed histopathologic description of skin lesions from a porcine
model of decompression sickness (DCS) is presented. Pigs were dived
in a dry chamber on a variety of profiles over an 11-mo period, with
a 0.1-0.6 (10-60%) incidence of cutaneous lesions. The clinical
appearance of the lesions evolved from irregular, sharply demarcated
areas of erythema to violaceous and, eventually, darkly mottled
macules. The lesions were biopsied under deep, sedative anesthesia.
Histologic abnormalities were found in 91% (20/22) of the biopsies
from clinically apparent cutaneous lesions. Vascular congestion was
the most common finding. Focal areas of vasculitis were noted in 45%
(10/22) of the lesions. Perivascular neutrophil infiltrates, edema,
and occasionally, hemorrhage were also noted. Ultrastructural
abnormalities were found in all of the lesions studied. Acute
inflammation affecting the dermal vasculature was the most common
finding. Platelets were rarely observed aggregating within vessels.
The clinical and histologic features of cutaneous lesions in pigs
after decompression are compared with previous accounts in humans.
The model provides a useful tool for the study of cutaneous lesions
in DCS and may be a means of exploring interventions in the disease.
SOURCE: Undersea Hyperb Med 1998 Summer;25(2):115-21


TITLE: Patent foramen ovale and decompression sickness in sports divers.
AUTHORS: Germonpre P; Dendale P; Unger P; Balestra C
Patency of the foramen ovale (PFO) may be a cause of unexplained
decompression sickness (DCS) in sports divers. To assess the
relationship between PFO and DCS, a case-control study was undertaken
in a population of Belgian sports divers. Thirty-seven divers who
suffered from neurological DCS were compared with matched control
divers who never had DCS. All divers were investigated with
transesophageal contrast echocardiography for the presence of PFO.
PFO size was semiquantified on the basis of the amount of contrast
passage. Divers with DCS with lesions localized in the high cervical
spinal cord, cerebellum, inner ear organs, or cerebrum had a
significantly higher prevalence of PFO than divers with DCS
localizations in the lower spinal cord. For unexplained DCS (DCS
without commission of any diving procedural errors), this difference
was significant for large PFOs only. We conclude that PFO plays a
significant role in the occurrence of unexplained cerebral DCS, but
not of spinal DCS. We further stress the importance of
standardization and semiquantification of future PFO studies that use
transesophageal contrast echocardiography.
SOURCE: J Appl Physiol 1998 May;84(5):1622-6


TITLE: [Analysis of decompression safety during extravehicular activity of
astronauts in the light of probability theory]
Objectives of the study were comparative assessment of the risk of
decompression sickness (DCS) in human subjects during shirt-sleeve
simulation of extravehicular activity (EVA) following Russian and
U.S. protocols, and analysis of causes of the difference between real
and simulated EVA decompression safety. To this end, DCS risk during
exposure to a sing-step decompression was estimated with an original
method. According to the method, DCS incidence is determined by
distribution of nucleation efficacy index (z) in the worst body
tissues and its critical values (zm) as a function of initial
nitrogen tension in these tissues and final ambient pressure post
decompression. Gaussian distribution of z values was calculated
basing on results of the DCS risk evaluation on the U.S. EVA protocol
in an unsuited chamber test with various pre-breath procedures
(Conkin et al., 1987). Half-time of nitrogen washout from the worst
tissues was presumed to be 480 min. Calculated DCS risk during
short-sleeve EVA simulation by the Russian and U.S. protocols with
identical physical loading made up 19.2% and 23.4%, respectively.
Effects of the working spacesuit pressure, spacesuit rigidity,
metabolic rates during operations in EVA space suit, transcutaneous
nitrogen exchange in the oxygen atmosphere of space suit,
microgravity, analgesics, short compression due to spacesuit leak
tests on the eye of EVA are discussed. Data of the study illustrate
and advocate for high decompression safety of current Russian and
U.S. EVA protocols.
SOURCE: Aviakosm Ekolog Med 1998;32(1):50-4


TITLE: Effect of saturated air and nitrox diving on selected parameters of
AUTHORS: Olszanski R; Sicko Z; Baj Z; Czestochowska E
Konarski M; Kot J; Radziwon P; Raszeja-Specht A; Winnicka A
The objective of the study was to evaluate decompression stress after
air and nitrox saturated divings on the basis of the parameters of
haemostasis. Before and after each diving the following examinations
were performed: blood platelet count, aggregation, fibrinogen level
and coagulation factors VII, X and XII. After the air saturated dives
a slight reduction of factor X and XII and of fibrinogen was
observed. Evaluation of haemostatis may be one of the basic elements
in the assessment of decompression sickness risk.
SOURCE: Bull Inst Marit Trop Med Gdynia 1997;48(1-4):75-82


TITLE: The physiological basis of diving to depth: birds and mammals.
AUTHORS: Kooyman GL; Ponganis PJ
There is wide diversity in the animals that dive to depth and in the
distribution of their body oxygen stores. A hallmark of animals
diving to depth is a substantial elevation of muscle myoglobin
concentration. In deep divers, more than 80% of the oxygen store is
in the blood and muscles. How these oxygen stores are managed,
particularly within muscle, is unclear. The aerobic endurance of four
species has now been measured. These measurements provide a standard
for other species in which the limits cannot be measured. Diving to
depth requires several adaptations to the effects of pressure. In
mammals, one adaptation is lung collapse at shallow depths, which
limits absorption of nitrogen. Blood N2 levels remain below the
threshold for decompression sickness. No such adaptive model is known
for birds. There appear to be two diving strategies used by animals
that dive to depth. Seals, for example, seldom rely on anaerobic
metabolism. Birds, on the other hand, frequently rely on anaerobic
metabolism to exploit prey-rich depths otherwise unavailable to them.
SOURCE: Annu Rev Physiol 1998;60:19-32


TITLE: Probabilistic models of the role of oxygen in human decompression
AUTHORS: Parker EC; Survanshi SS; Massell PB; Weathersby PK
Probabilistic models of human decompression sickness (DCS) have been
successful in describing DCS risk observed across a wide variety of
N2-O2 dives but have failed to account for the observed DCS incidence
in dives with high PO2 during decompression. Our most successful
previous model, calibrated with 3,322 N2-O2 dives, predicts only 40%
of the observed incidence in dives with 100% O2 breathing during
decompression. We added 1,013 O2 decompression dives to the
calibration data. Fitting the prior model to this expanded data set
resulted in only a modest improvement in DCS prediction of O2 data.
Therefore, two O2-specific modifications were proposed: PO2-based
alteration of inert gas kinetics (model 1) and PO2 contribution to
total inert gas (model 2). Both modifications statistically
significantly improved the fit, and each predicts 90% of the observed
DCS incidence in O2 dives. The success of models 1 and 2 in improving
prediction of DCS occurrence suggests that elevated PO2 levels
contribute to DCS risk, although less than the equivalent amount of
N2. Both models allow rational optimization of O2 use in accelerating
decompression procedures.
SOURCE: J Appl Physiol 1998 Mar;84(3):1096-102


TITLE: Activation of coagulation in decompression illness.
AUTHORS: Boussuges A; Succo E; Juhan-Vague I; Sainty JM
In animal studies, many authors have observed coagulation activation
in decompression illness (DCI). These hemostasis modifications have
been attributed to circulating bubbles. We have studied molecular
hemostasis markers in 25 consecutive divers, victims of DCI admitted
to our hyperbaric center, and in 15 control divers. There was no
significant difference in parameters studied in the patients and the
control group (platelet, fibrinogen, antithrombin III, Thrombin
Antithrombin III complexes, and D-Dimers). An activation of
coagulation (D-Dimer > 500 was noted in three divers with
neurologic troubles. However, such signs of coagulation activation
were not correlated with the risk of sequeals. No control or study
patient with an osteoarticular or vestibular accident presented signs
of coagulation activation. Thus, there does not seem to be a
correlation between the severity of the accident and the level of
coagulation activation. Further studies will be necessary to evaluate
the responsibility of hemostasis modifications in the physiopathology
of decompression accidents in sports divers.
SOURCE: Aviat Space Environ Med 1998 Feb;69(2):129-32


TITLE: Effect of oxygen tension and rate of pressure reduction during
decompression on central gas bubbles.
AUTHORS: Reinertsen RE; Flook V; Koteng S; Brubakk AO
Reduction in ascent speed and an increase in the O2 tension in the
inspired air have been used to reduce the risk for decompression
sickness. It has previously been reported that decompression speed
and O2 partial pressure are linearly related for human decompressions
from saturation hyperbaric exposures. The constant of proportionality
K (K = rate/partial pressure of inspired O2) indicates the incidence
of decompression sickness. The present study investigated the
relationship among decompression rate, partial pressure of inspired
O2, and the number of central gas bubbles after a 3-h dive to 500 kPa
while breathing nitrox with an O2 content of 35 kPa. We used
transesophageal ultrasonic scanning to determine the number of
bubbles in the pulmonary artery of pigs. The results show that, for a
given level of decompression stress, decompression rate and O2
tension in the inspired air can be traded off against each other by
using pulmonary artery bubbles as an end point. The results also seem
to confirm that decompressions that have a high K value are more
SOURCE: J Appl Physiol 1998 Jan;84(1):351-6


TITLE: Information about venous gas emboli improves prediction of hypobaric decompression sickness.
AUTHORS: Conkin J; Powell MR; Foster PP; Waligora JM
HYPOTHESIS: Information about venous gas emboli (VGE) detected in the
pulmonary artery such as the occurrence of VGE, Grade of VGE, the
time when VGE first appear, and the time course of the Grade or
occurrence of VGE, could be used to better assess the probability of
decompression sickness [P(DCS)] in any hypobaric decompression. We
hypothesized that these data would improve the estimate of P(DCS)
since objective measurements of the decompression stress are
available for the individual. METHODS: A binary correlation and
survival analysis approach were used on information from 1,322
hypobaric chamber exposures to establish the relationships between
VGE and DCS. RESULTS: Based on the correlation analysis, the absence
of VGE is highly correlated with the absence of a DCS symptom, as
evident from a negative predictive value of 0.98. However, the
presence of VGE in the pulmonary artery is not highly correlated with
a subsequent DCS symptom, as evident from a positive predictive value
of 0.39 for Grades III and IV VGE. The correlation results suggest
the presence of VGE in the pulmonary artery is a necessary, but not
sufficient, condition for DCS. Based on the survival analysis, the
log logistic survival model, a one-variable model with two parameters
gave a log likelihood (LL) of -757. This model was expanded to
include seven additional variables, including four about VGE, and the
nine-parameter model gave a better LL of -481. CONCLUSION:
Information about VGE plus other variables known to influence DCS is
useful to better assess the P(DCS) for hypobaric decompressions.
SOURCE: Aviat Space Environ Med 1998 Jan;69(1):8-16


TITLE: Circulating bubbles and breath-hold underwater fishing divers: a
two-dimensional echocardiography and continuous wave Doppler study.
AUTHORS: Boussuges A; Abdellaoui S; Gardette B; Sainty JM
Since the 1960s, decompression illness after breath-hold diving has
been widely debated. The aim of this study was to detect circulating
bubbles after breath-hold diving in underwater fishing divers. We
used continuous Doppler (DUG, COMEX Pro) and transthoracic
two-dimensional (2D) echocardiography (Kontron Sigma 1). This study
was conducted during a training course organized by the French
Federation of Subaquatic Sports at Minorca (Balearic Islands). Ten
breath-hold divers performed repeated breath-hold dives for periods
ranging from 2 to 6 h [mean maximum depth 35 meters of seawater
(msw)]. A dive computer (Maestro Pro Beuchat, analyst PC interface)
was used to record diving patterns. No circulating bubbles were
detected in the right heart cavities (2D echocardiography) or in the
pulmonary artery (continuous Doppler). However, this study had some
limits: only 10 subjects were studied and the earliest detection was
3 min after immersion, further studies will thus be required.
SOURCE: Undersea Hyperb Med 1997 Winter;24(4):309-14


TITLE: Recompression treatments during the recovery of TWA Flight 800 [see
AUTHORS: Leffler CT; White JC
After the crash of TWA flight 800, U.S. Navy (USN) and civilian divers
recovered the aircraft and the victims' remains from 117 feet of sea
water (fsw). Safety information was gathered from observations,
interviews, and medical and diving records. Of 752 dives employing
surface decompression using oxygen (SDO2), 10 divers required
recompression treatments, mainly for type 2 decompression sickness
(DCS). When using hot water heating, the DCS risk was high until the
dive profiles were modified. Divers made nearly 4,000
no-decompression scuba dives. In eight scuba divers and one tender
treated with recompression, the diagnoses included DCS (3), arterial
gas embolism (AGE) (1), and vascular headache (2). All USN divers
recovered fully. The experience is consistent with previous work
suggesting an increase in DCS risk in warmer SDO2 divers. The USN
SDO2 tables can be made safer by limiting bottom time and extending
decompression. Even under stressful conditions, rapid ascents
resulting in AGE are uncommon. Vascular headaches can mimic DCS by
responding to oxygen.
SOURCE: Undersea Hyperb Med 1997 Winter;24(4):301-8


TITLE: Probabilistic gas and bubble dynamics models of decompression sickness
occurrence in air and nitrogen-oxygen diving.
AUTHORS: Gerth WA; Vann RD
Probabilistic models of the occurrence of decompression sickness (DCS)
with instantaneous risk defined as the weighted sum of bubble volumes
in each of three parallel-perfused gas exchange compartments were fit
using likelihood maximization to the subset of the USN Primary Air
and N2-O2 database [n = 2,383, mean P(DCS) = 5.8%] used in
development of the USN LE1 probabilistic models. Bubble dynamics with
one diffusible gas in each compartment were modeled using the Van
Liew equations with the nucleonic bubble radius, compartmental
volume, compartmental bulk N2 diffusivity, compartmental N2
solubility, and the N2 solubility in blood x compartmental blood flow
as adjustable parameters. Models were also tested that included the
effects of linear elastic resistance to bubble growth in one, two, or
all three of the modeled compartments. Model performance about the
training data and separate validation data was compared to results
obtained about the same data using the LE1 probabilistic model, which
was independently implemented from published descriptions. In the
most successful bubble volume model, BVM(3), diffusion significantly
slows bubble growth in one of the modeled compartments, whereas
mechanical resistance to bubble growth substantially accelerates
bubble resolution in all compartments. BVM(3) performed generally on
a par with LE1, despite inclusion of 12 more adjustable parameters,
and tended to provide more accurate incidence-only estimates of DCS
probability than LE1, particularly for profiles in which high
fractional O2 gas mixes are breathed. Values of many estimated BVM(3)
parameters were outside of the physiologic range, indicating that the
model emerged from optimization as a mathematical descriptor of
processes beyond bubble formation and growth that also contribute to
DCS outcomes. Although incomplete as a mechanistic description of DCS
etiology, BVM(3) remains applicable to a wider variety of
decompressions than LE1 and affords a conceptual framework for
further refinements motivated by mechanistic principles.
SOURCE: Undersea Hyperb Med 1997 Winter;24(4):275-92


TITLE: Neurological manifestation of arterial gas embolism following standard
altitude chamber flight: a case report.
AUTHORS: Rios-Tejada F; Azofra-Garcia J; Valle-Garrido J
Pujante Escudero A
In the course of a decompression at flight level 280 (28,000 ft) in an
altitude chamber flight, a 45-yr-old cabin air traffic controller
developed sudden numbness in his left upper and lower extremities
and, soon after, complete paralysis in the left side, dysarthria and
left facial palsy. A presumptive diagnosis of arterial gas embolism
(AGE) was made and hyperbaric oxygen therapy (HBO) was given after
airevac of the patient to the closest compression facility. Complete
resolution of the symptoms was obtained after treatment Table VI-A
(extended), plus 3 consecutive HBO treatments (90 min of Oxygen at
2.0 ATA). AGE is a rare event in the course of regular altitude
chamber flight and diagnosis should be done in the context of the
barometric pressure changes and an acute cerebral vascular injury.
Risk factors and follow-up diagnostic procedures are discussed.
SOURCE: Aviat Space Environ Med 1997 Nov;68(11):1025-8


TITLE: Dysbaric osteonecrosis in divers and caisson workers. An animal model.
AUTHORS: Lehner CE; Adams WM; Dubielzig RR; Palta M
Lanphier EH
Dysbaric osteonecrosis was induced successfully in adult sheep after
12 to 13, 24-hour exposures to compressed air (2.6-2.9 atmospheres
absolute) during a 2-month period. All exposed sheep had
decompression sickness and extensive bone and marrow necrosis in
their long bones. Radiographic analysis of these progressive lesions
showed mottled to distinct medullary opacities and endosteal
thickening characteristic of dysbaric osteonecrosis. Six months after
the last hyperbaric exposure, neovascularization of once ischemic
fatty marrow was centripetal from the diaphyseal cortex.
Proliferating endosteal new bone, fatty marrow calcification, and
appositional new bone formation were widespread. Juxtaarticular
osteonecrosis involved marrow fibrosis and loss of osteocytes in
subchondral cortical bone. Tidemark reduplication in juxtaarticular
bone and cartilage thinning suggested possible early osteoarthritis
induction by recurrent episodes of transient ischemia after multiple
hyperbaric exposures. Dysbaric osteonecrosis appears to involve a
bone compartment syndrome of elevated intramedullary pressure
initiated by decompression induced N2 bubble formation in the fatty
marrow of the long bones. An animal model that can be used to
investigate the pathogenesis, diagnosis, and treatment of dysbaric
osteonecrosis is discussed.
SOURCE: Clin Orthop 1997 Nov;(344):320-32


TITLE: MR imaging of the central nervous system in diving-related
decompression illness.
AUTHORS: Reuter M; Tetzlaff K; Hutzelmann A; Fritsch G
Steffens JC; Bettinghausen E; Heller M
PURPOSE: This investigation was conducted to determine whether MR
imaging showed cerebral or spinal damage in acute diving-related
decompression illness, a term that includes decompression sickness
(DCS) and arterial gas embolism (AGE). MATERIAL AND METHODS: A total
of 16 divers with dysbaric injuries were examined after the
initiation of therapeutic recompression. Their injuries comprised:
neurological DCS II n = 8; AGE n = 7; combined
cerebral-AGE/spinal-DCS n = 1. T1- and T2-weighted images of the
brain were obtained in 2 planes. In addition, the spinal cord was
imaged in 7 subjects. The imaging findings were correlated with the
neurological symptoms. RESULTS: MR images of the head showed ischemic
cerebrovascular lesions in 6/8 patients with AGE but showed focal
hyperintensities in only 2/8 divers with DCS. Spinal cord involvement
was detected in 1/7 examinations, which was the combined
cerebral-AGE/spinal-DCS case. There was agreement between the
locations of the documented lesions and the clinical manifestations.
CONCLUSION: MR readily detects cerebral damage in AGE but yields low
sensitivity in DCS. A negative MR investigation cannot rule out AGE
or DCS. However, MR is useful in the examination of patients with
decompression illness.
SOURCE: Acta Radiol 1997 Nov;38(6):940-4


TITLE: Nature and incidence of bubbles in the spinal cord of decompressed
The nature of so-called autochthonous bubbles was investigated. Their
presence in compressed/decompressed goats was compared with that in
animals killed before decompression and in controls. Ten goats (group
1) were subjected to compression/decompression in air. Clinical signs
of spinal decompression sickness usually occurred. Within 35 min of
surfacing, the animals were given a lethal dose of thiopentone
sodium, i.v.. Spinal cords were fixed by immersion in 10% formol
saline. Histologically autochthonous bubbles appeared to arise from
rupture of over-distended blood vessels. The incidence of grossly
dilated empty vessels (GDEV) was recorded. Seven goats (group 2) were
similarly compressed but killed before decompression. In five animals
of group 1 there was a greater number of GDEV than in controls (group
3, seven animals) but in the other five animals the incidence was
similar to the controls. The incidence of GDEV in group 2 was greater
than in the controls (P < 0.05). The percentage of sections of
spinal cord in which the meninges also contained GDEV was assessed.
In all except two animals in group 1, the percentage was higher than
in the controls, whereas in group 2 the percentage was higher than in
the controls. The experiments show that autochthonous bubbles arise
as an artifact and that intravascular bubbles arise in situ.
SOURCE: Undersea Hyperb Med 1997 Sep;24(3):193-200


TITLE: Magnetic resonance findings in scuba diving-related spinal cord
decompression sickness.
AUTHORS: Sparacia G; Banco A; Sparacia B; Midiri M
Brancatelli G; Accardi M; Lagalla R
Scuba diving is associated with risk of severe decompression sickness
(DCS type II), which results from rapid reduction of the
environmental pressure sufficient to cause the formation into tissue
or blood of inert gas bubbles previously loaded within tissues as a
soluble phase. DCS type II constitutes a unique subset of ischemic
insults to the central nervous system (CNS) with primarily
involvement of the spinal cord. Ten patients with diving-related
barotrauma underwent neurologic examination. Two of them presented
progressive sensory and motor loss in the extremities at admission
and were presumed affected by spinal cord DCS. Magnetic resonance
imaging (MRI) demonstrated abnormalities in the white-matter tracts
of the spinal cord in these patients, in each case corresponding to
an area of the cord believed to be clinically involved. After a
course of therapeutic recompressions, one patient was able to stand
and walk a short distance, and MRI revealed a decreased extension of
areas of spinal cord abnormalities. MRI has proved to be reliable in
the detection of pathologic changes of spinal cord decompression
sickness that were previously undetectable by other neuroimaging
methods and also has proved to be useful in the follow-up during
therapeutic hyperbaric recompressions.
SOURCE: MAGMA 1997 Jun;5(2):111-5


TITLE: Exercise during decompression reduces the amount of venous gas emboli.
AUTHORS: Jankowski LW; Nishi RY; Eaton DJ; Griffin AP
To determine the effects of moderate, intermittent exercise during
decompression on the Doppler detectable amount of venous gas emboli
(VGE), 29 healthy male volunteers performed 44 wet (8 degrees +/- 2
degrees C) dives to 45 msw (450 kPa) for 30 min with standard air
decompression. During compression and the bottom period, all subjects
were inactive; during decompression, 28 remained inactive, 11
performed leg exercise, and 5 did arm exercise. Intermittent exercise
was controlled at approximately 50% of each subject's arm or leg
aerobic capacity. At 30-min intervals after surfacing, subjects were
monitored with a Doppler ultrasonic bubble detector. The Doppler
scores were used to calculate the Kisman Integrated Severity Score
(KISS). The KISS were log transformed (with zeroes being equivalent
to log 0.01) and analyzed with a one-way analysis of variance. No
significant differences (P < or = .05) between mean KISS scores
after arm or leg exercise were observed, thus these data were pooled
and compared to those of the inactive controls. The mean pooled KISS
after exercising during decompression were significantly lower than
those of the inactive controls. Moderate, intermittent exercise
during decompression apparently reduces the amount of
Doppler-detectable VGE after diving. The incidence rate of
decompression sickness in both groups was not significantly different
(P < 0.05).
SOURCE: Undersea Hyperb Med 1997 Jun;24(2):59-65


TITLE: Abnormal serum biochemistries in association with arterial gas
AUTHORS: Smith RM; Neuman TS
Although diving-associated arterial gas emboli have been thought to
embolize the cerebral circulation preferentially, more recent
evidence suggests that gas bubbles disseminate widely and may cause
dysfunction in multiple organ systems. We performed a retrospective
survey of the records of patients presenting with diving-associated
gas embolism over a 10-yr period to determine the maximal levels of
serum transaminases and lactate dehydrogenase after a diving
accident. Twenty-nine subjects with arterial gas embolism were
identified whose dive profiles suggested that decompression sickness
was unlikely. Maximal transaminase levels (aspartate amino
transaminase = 442 +/- 187 IU/L; alanine amino transaminase = 315 +/-
205 IU/L) and lactate dehydrogenase level (800 +/- 227 IU/L) were
significantly greater in the gas embolism patients than those levels
measured in a group of normal individuals undergoing training dives
of similar depth and duration. These preliminary studies suggest that
arterial gas embolism frequently produces significant abnormalities
in serum enzyme activity in sport divers whose dives would not be
expected to produce decompression sickness. Arterialized gas bubbles
may circulate widely, causing injury outside of the cerebral
SOURCE: J Emerg Med 1997 May-Jun;15(3):285-9


TITLE: A case of spinal cord decompression sickness presenting as partial
Brown-Sequard syndrome.
AUTHORS: Kimbro T; Tom T; Neuman T
Type II decompression sickness (DCS) usually manifests as myelopathy;
however, there are no reports of Brown-Sequard syndrome in
association with diving accidents. We report a 35-year-old man who
developed type II DCS presenting as partial Brown-Sequard syndrome.
MRI of the thoracic spine revealed two punctate foci of increased
signal intensity in the right T6 spinal cord.
SOURCE: Neurology 1997 May;48(5):1454-6


TITLE: Activation of complement and neutrophils increases vascular
permeability during air embolism.
Pulmonary air embolism occurs in diving and aviation during acute
pressure reductions and in clinical complications. Undoubtedly
physical obstructions play a role, but bubbles in blood can produce a
number of indirect effects leading to tissue injury. In the present
study, we investigated the involvement of the complement system and
polymorphonuclear leukocytes (PMN) in altering segmental vascular
resistance, lung weight gain, and filtration coefficient (Kf), by
using isolated and perfused rat lungs. After establishing ventilation
with air and 5% CO2, the lung was removed en bloc and suspended in a
humidified chamber at 37 degrees C. Lung weight and arterial and
venous pressures were monitored continuously. The buffered salt
perfusate contains 4% Ficoll for osmotic balance. We used four series
of perfusates containing 20% of: a) normal plasma; b) decomplemented
plasma (from donor rats pretreated with a cobra venom factor); c)
normal plasma and PMN at 2 x 10(6).ml-1; and d) decomplemented plasma
and PMN at 2 x 10(6).ml-1. Pulmonary air embolism, air bubbles
introduced through the pulmonary artery, increased pulmonary arterial
resistance and pulmonary arterial blood pressure. The lung weight and
lung water content were greater than those in the control groups. Air
embolism increased vascular permeability, which was shown by an
elevated Kf after air infusion. After air embolism, Kf was 0.63 +/-
0.05 H2O-1.100 g-1 in lungs perfused with both PMN and
plasma, which was significantly greater than those in lungs perfused
with either plasma (0.49 +/- 0.04), decomplemented plasma (0.44 +/-
0.03), or PMN and decomplemented plasma (0.47 +/- 0.03). These
results demonstrated that air embolism increases vascular
permeability of the lung by pulmonary hypertension, activation of the
complement, and activation of PMN.
SOURCE: Aviat Space Environ Med 1997 Apr;68(4):300-5


TITLE: Helium and oxygen treatment of severe air-diving-induced neurologic
decompression sickness.
AUTHORS: Shupak A; Melamed Y; Ramon Y; Bentur Y; Abramovich A
Kol S
BACKGROUND: The use of helium and oxygen recompression treatment of
neurologic decompression sickness (DCS) has several theoretical
advantages over the traditionally used air and oxygen recompression
tables that have been confirmed by findings from recent animal
experiments. OBJECTIVES: To evaluate the outcome of patients with
neurologic DCS who had been treated with a helium-oxygen protocol and
to compare it with that of a retrospective control group that was
treated with air-oxygen tables. DESIGN: The study and control groups
included 16 and 17 diving casualties, respectively. The severity of
neurologic DCS was estimated according to a 9-point scale weighting
motor, sensory, and sphincter control functions. The study group was
treated with a helium-oxygen decompression protocol, and the control
group was treated with the US Navy air-oxygen Table 6 or 6A.
Persistent residual dysfunction was treated in both groups with daily
hyperbaric oxygen sessions, at 2.5 absolute atmospheres for 90
minutes, until no further clinical improvement was noted. SETTING:
The Israel Naval Medical Institute (Israel's national hyperbaric
referral center), Haifa. RESULTS: Significant clinical score
increments were found for both the helium-oxygen- and
air-oxygen-treated groups: 2.8 +/- 2.4 (mean +/- SD) and 7.4 +/- 1.1
at presentation vs 7.6 +/- 2.1 and 8.1 +/- 1.5 at discharge,
respectively (P < .001 and P = .005, respectively). Although the
score at presentation was significantly lower for the
helium-oxygen-treated group (P < .001), no difference was found
between the groups' average outcome scores. While most of the
improvement in the patients in the study group could be attributed to
the helium-oxygen treatment and not to the supplemental hyperbaric
oxygen, in the control group, no significant difference could be
demonstrated between the scores at presentation and at completion of
the air-oxygen recompression table. In 5 patients who were treated
with the use of the air-oxygen tables, deterioration was observed
after recompression. No deterioration or neurologic DCS relapse
occurred in the helium-oxygen-treated group. CONCLUSION: The results
suggest an advantage of helium-oxygen recompression therapy over
air-oxygen tables in the treatment of neurologic DCS.
SOURCE: Arch Neurol 1997 Mar;54(3):305-11


TITLE: Utility of Doppler-detectable microbubbles in the diagnosis and
treatment of decompression sickness.
AUTHORS: Kumar VK; Billica RD; Waligora JM
BACKGROUND: Doppler-detectable microbubbles (DMB) are frequently used
to evaluate altitude decompression stress. However, the role of DMB
in the therapy of decompression sickness (DCS) has not been examined.
HYPOTHESIS: The ability of Doppler to detect microbubbles during
decompression (Doppler test) may be used in the diagnosis of DCS, and
to aid clinical decisions about treatment options for DCS. METHODS:
We examined the data on DMB and symptoms from NASA Database on DCS (n= 516). The accuracy of Doppler test was obtained from the Receiver
Operating Characteristic (ROC) for DMB (grades I through IV), and
efficacy was obtained by calculating predictive or post-test
probabilities. Threshold analysis was used to obtain the
probabilities for testing and/or treatment decisions. RESULTS: The
Doppler test was useful for both screening and confirming DCS, when
different criteria (grade I for screening; grade IV for confirming)
were used for a positive test. Calculation of predictive values and
threshold analysis showed that: 1) early recompression was the
therapy of choice when post-test probability of disease was > 0.25
in individuals with non-specific pain at altitude, and early
recompression with 100% oxygen for 2 h at site level was optimal
therapy when this probability was > 0.33; 2) hyperbaric therapy
was optimal when post-test probability was > 0.04 in individuals
with uncertain symptoms post-flight. CONCLUSIONS: The Doppler test
was of greater utility in excluding DCS than confirming its presence,
and was useful in making therapeutic decisions on DCS when confronted
with non-specific symptoms at altitude.
SOURCE: Aviat Space Environ Med 1997 Feb;68(2):151-8


TITLE: Acute neurologic decompression illness in pigs: lesions of the spinal
cord and brain.
AUTHORS: Dick EJ Jr; Broome JR; Hayward IJ
A detailed histopathologic description of central nervous system
lesions from a porcine model of neurologic decompression illness is
presented. Pigs were dived in a dry chamber to 200 feet of seawater
for 24 min before the start of decompression. Of 120 pigs, 40 (33.3%)
were functionally unaffected and 80 (66.6%) developed neurologic
decompression illness; 16 died, 64 survived. Petechial hemorrhages
were grossly visible in the spinal cord of 73% of the survivors, 63%
of the fatalities, and 3% of the clinically unaffected pigs. The
thoracic part of the cord was most commonly involved. Histologic cord
lesions were found in 75 (63%) pigs: 83% of decompression illness
survivors, 81% of the fatalities, and 23% of those clinically
unaffected. Morphologically, hemorrhagic lesions were the most common
(54%). Other common findings included spongiosis (48%), axonal
swelling and loss (39%), and myelin degeneration (35%). White matter
hemorrhages in the spinal cord were generally more numerous and
extensive than those affecting the gray matter; however, gray matter
hemorrhage was associated with increasing disease severity. Brain
lesions were present in 23% of pigs and were most frequent in
fatalities. Cerebellar and brain stem hemorrhages were the most
common brain lesions; the molecular layer of the cerebellum appeared
particularly susceptible. Pigs were chosen because of their
cardiovascular and gas exchange similarities to humans. The clinical
and histopathologic features of the pig model were compared with
previous accounts in animals and humans; the model was judged
analogous to severe human decompression illness. The finding of
occult brain and cord lesions in clinically unaffected pigs is
discussed. The model provides a useful tool for the study of dysbaric
lesions of the central nervous system. Its noninvasive nature may
facilitate the study of nervous system injury and repair processes.
SOURCE: Lab Anim Sci 1997 Feb;47(1):50-7


TITLE: Intravenous lidocaine as adjunctive therapy in the treatment of
decompression illness.
Two cases of severe decompression illness for which IV lidocaine was
used as adjunctive therapy to recompression and hyperbaric oxygen
therapy are described. The first patient demonstrated improvement
only after lidocaine was added to her treatment; the second had
essentially complete recovery after only a single treatment despite
severe symptoms and a significant delay in presentation. These cases
support the need for a controlled clinical trial of lidocaine as an
adjunct to hyperbaric therapy in decompress on illness.
SOURCE: Ann Emerg Med 1997 Feb;29(2):284-6

TITLE: Late deterioration after decompression illness affecting the spinal
AUTHORS: Dyer J; Millac P
A former amateur diver presented with a progressive paraparesis.
Thirteen years previously he had developed acute spinal cord
dysfunction immediately after dry hyperbaric exposure. He had
completely recovered motor function in the intervening period. No
alternative reason for the later decline emerged from detailed
SOURCE: Br J Sports Med 1996 Dec;30(4):362-3


TITLE: Haemoconcentration in neurological decompression illness.
AUTHORS: Boussuges A; Blanc P; Molenat F; Bergmann E
Sainty JM
Decompression illness (DCI) is attributed to the formation of bubbles,
resulting from the reduction of the ambient pressure. Circulating
bubbles lead to capillary leak syndrome, extravasation of plasma and
haemoconcentration. Experimental model on animals has shown that a
haemoconcentration carried a poor prognosis. We measured the
haematocrit level in fifty-eight consecutive sport divers, victims of
neurological DCI, admitted to our hyperbaric center, and in sixteen
control divers. No significant difference was found in the
haematocrit values between the divers with neurological DCI (median
42.5%) and the controls (median 41.75%). The median haematocrit level
was significantly higher for divers with neurological sequelae when
compared with control (p = 0.01) or with divers without sequelae (p
< 0.05). A haematocrit level > or = 48% was correlated with
persistent neurological sequelae one month after the accident (p =
0.01). However, a haematocrit < 48% had no prognostic value.
SOURCE: Int J Sports Med 1996 Jul;17(5):351-5