Dysbaric Illness (DI)
is a term that covers a broad range of complex
pathophysiological conditions associated with decompression. Although
much of the actual etiology of DI remains undefined, the primary cause is
believed to be separation and/or the appearance of gas within the body,
whether stationary or migratory, as result of decompression.
Gas bubbles form due to inert gas supersaturation or the traumatic
injection of gas into the arterial circulation following pulmonary barotrauma.
Its manifestations are protean which has led to the recommendation that any
signs and symptoms, observed in individuals recently exposed to a reduction
in environmental pressure, must be considered as being DI until proven
otherwise. This high index of suspicion should be extended to sub-acute and
chronic changes and to sub-clinical or ambiguous symptoms that may affect
the long bones, central nervous system and lungs.
Although primarily associated with compressed gas diving, DI also
occurs in association with altitude exposure and other sub-atmospheric
pressure reductions as well as in compressed air workers and health care
providers attending to patients while receiving hyperbaric oxygen therapy.
While the principles of management are similar, the environments in which
they may be applied vary greatly. This chapter focuses almost exclusively on
the consequences of compressed gas diving.
In understanding the study and classification of DI a technical distinction
needs be made between disease and disorder: Although often used
synonymously, the term disorder is usually assigned to physical
derangements, frequently slight and transitory in nature. A disease, on the
other hand, is usually a more serious, active, prolonged and deep-rooted
condition1
. Acute DI therefore begins as a disorder which, depending on its
pathophysiology and treatment, may become a disease 2-4
.
k
Although imperfect, the term Dysbaric Illness (DI) was chosen as the umbrella term for
decompression-related disorders and diseases. Although Dysbarism and Decompression
Illness have been proposed, these present linguistic challenges and their use is associated
with one particular descriptive classification. Although DI conceivably also includes
medical problems associated with compression its application in this chapter refers only to
those conditions that may develop upon decompression after breathing from a compressed
gas source.
2.2.1. Dysbaric Illness 175
- HISTORIC BACKGROUND
2.1 Discovery of Dysbaric Illness
Already in 1670, Robert Boyle demonstrated that Dysbaric Illness (DI)
could be produced in a reptile by the sudden lowering of atmospheric
pressure. Nearly two hundred years later the first case of DI was recorded in
compressed air workers: In 1845 Triger reported that two men had suffered
“very sharp pain” in the left arm and another had “pain in the knees and left
shoulder” thirty minutes after emerging from a seven hour exposure to a
pressure of between 2.4 atmospheres and 4.25 atmospheres 5
. As technology
advanced and supported longer exposures to greater pressures the incidence
of DI gradually increased until it became recognized as an occupational
illness in need of prevention and treatment.
2.2 Prevention and Treatment of DI
Prevention of DI could only follow an understanding of its cause.
Accordingly, the first measures were aimed at merely alleviating the
symptoms. Triger himself advocated “rubbing with spirits of wine” which,
he reported, “soon relieved this pain in both men and they kept working on
the following days”. Two years later, Pol and Watelle wrote that they felt
“justified in hoping that a sure and prompt means of relief would be to
recompress immediately, then decompress very carefully” 6
.
By the turn of the 19th century civil engineering had achieved proportions
of depth and complexity that DI became more than a trivial concern: On
15th May 1896 the Journal of the Society of Art described the landmark
work of E. W. Moir during the digging of the Hudson river tunnel in 1889 7
.
Facing a DI fatality rate of over 25% of the employed workers, Moir
installed a recompression chamber at the worksite. The result was a dramatic
reduction in mortality – only two deaths were recorded during the next 15
months out of a workforce of more than 120. Moir, who seemed almost
apologetic about this empirical therapy, wrote: “With a view to remedying
the state of things an air compartment like a boiler was made in which the
men could be treated homeopathically, or reimmersed in compressed air. It
was erected near the top of the shaft, and when a man was overcome or
paralyzed, as I have seen them often, completely unconscious and unable to
use their limbs, they were carried into the compartment and the air pressure
raised to about 1/2 or 2/3 of that in which they had been working, with
immediate improvement. The pressure was then lowered at the very slow
rate of one pound per minute or even less. The time allowed for equalization
being from 25 to 30 minutes, and even in severe cases the men went away
quite cured”.
176 A. Marroni et al.
Ironically Paul Bert in 1878 had already validated this concept 8
. He had
demonstrated that the cause of DI was nitrogen going into gas phase in the
tissues and that this bubble formation was responsible for symptoms. Bert
understood that prompt recompression was the key to effective treatment.
Remarkably, he already highlighted the existence of “silent bubbles” in the
venous blood; used oxygen at one atmosphere following very rapid
decompression; and observed that cardiopulmonary symptoms, but not
spinal cord paralysis, were relieved by normobaric oxygen breathing.
Since that time, prompt recompression followed by slow decompression
has been universally considered the standard of care in the treatment of DI.
Further developments delineated the best combinations of pressure, time, gas
composition and decompression rates as well as the addition of resuscitation
and adjunctive therapy (Fig. 2.2.1-1).
Treatment of DI
1900 1925 1950 1975 2000
No treatment
Hyperbaric air
Hyperbaric O2
Simple resuscitation
Neuroprotection
Year
Figure 2.2.1-1. Developments in the Treatment for DI over the past century (Courtesy of
Richard Moon, MD)
However, even though we are now gaining a better understanding of the
tools of therapy, we remain challenged by inconsistency and confusion in
terminology for DI and uncertainty of diagnosis. Clearly there is little
uncertainty in the case of severe neurological DI. However, minor forms
may manifest in very subtle ways. These are likely to be ignored or denied
by the affected diver unless there is an appropriate level of awareness.
Indeed, there is reason to believe that there is widespread underreporting of
symptoms that may cause an unquantified amount of morbidity. On the other
hand over-emphasis of risks and hazards may cause hypochondriacal
responses or deter pursuit of the activity altogether. It remains, therefore, an
ongoing challenge to achieve the correct balance between denial and hysteria
in the face of untoward symptoms following diving.
2.2.1. Dysbaric Illness 177
As far as prevention is concerned, the definitive contribution in the
context of diving was made by Boycott, Damant and Haldane in 1908 9
.
Their work, although based on speculative mechanisms, forever changed the
fate of those facing decompression after breathing compressed gas. For the
next 60 years refinements in modeling theory, mathematics and statistics
have suggested a variety of depth-time combinations followed by various
decompression stops strung together by empirical ascent rates. Unfortunately
the fundamental principles on which all of these systems are based are
empirical as are their progeny of tables and decompression algorithms. Their
limitations have become particularly evident in recreational diving where
one half of DI cases do not appear to be the consequence of overt dive
profile violations. These observations have led to a search for unique
physiological factors and other unique risk factors. Possibilities have
included pulmonary-systemic shunts (e.g., patent foramen ovale, atrial septal
defects, intra pulmonary shunts, etc.); endothelial morphological anomalies
and reactivity; activation of complement; and many more. The search for
these elusive risk factors continues, as does their ambiguity 2,10,11
.
The introduction of precordial Doppler in the 1970’s promised a solution
to the mystery of DI 12. Unfortunately the association between recordable
bubbles and DI symptoms did not prove to be particularly strong: high grade
bubbles correlated more closely with DI than lower grades, but DI has even
been observed in the absence of any detectable bubbles. Nevertheless, this
modality may again enjoy greater utility in the years to come: Recently there
has been an increasing emphasis on paradoxical embolism of venous gas and
a growing body of experimental and clinical evidence suggesting that large
quantities of asymptomatic or “silent” venous bubbles may in fact be causing
cellular and biological reactions and be releasing potentially damaging
biochemical substances in the blood 13-16
.
Current prevention theory for DI recommends that participants: (1)
possess and maintain an appropriate level of dive medical fitness (including
controlling daily physiological variables such as body temperature and
hydration status); (2) avoid / prevent air trapping with gas expansion (e.g.,
not diving with respiratory infections and untreated reactive airway
problems); and (3) observe appropriate decompression procedures for their
exposure (i.e., following the recommended combination of pressure and time
for their planned diving activities). Violation of one or more of these
parameters increases the risk of DI 2,3
.
In the future our improved ability to detect bubbles and – more recently –
to detect the biochemical injuries they cause, may ultimately generate more
physiological approaches to decompression. Accordingly, future
decompression safety is likely to focus on three areas of intervention: (1)
manipulating decompression (ascent) to reduce the appearance, quantities
and size of venous gas emboli; (2) reducing the propensity of the body to
178 A. Marroni et al.
form bubbles; and (3) preconditioning the body biochemically and/or
physically to reduce the pathophysiological impact of such bubbles 17-25
. - TERMINOLOGY FOR AND CLASSIFICATION
OF DYSBARIC ILLNESSES
DI has suffered from great inconsistency in terminology and
classification. There are many reasons for this, including wide variations in
latency, severity and diagnostic certainty. In addition, the boundaries
between arterial gas embolization and decompression sickness are blurred
due to possible arterialization of venous gas. These factors have confounded
research and remain an ongoing challenge.
There are many ways to classify medical conditions in general, e.g., by
diagnosis, prognosis, pathology, pathophysiology, clinical presentation, etc.
The objective for classification is usually for the purpose of simplification.
This may include improving communication between clinicians; determining
treatment guidelines; establishing prognosis; or conducting research and
analyzing epidemiological data.
Unlike most other diseases, there is no definitive test for DI. It is only the
causality to decompression and the prevalence of neurological involvement
that respectively provide epidemiological boundaries and clinical relevance
to defining and classifying the condition. To date no single system has
emerged that provides both clear pathological stratification and clinical
utility.
3.1 Terminology
Various clinical terms have emerged in an ongoing effort to describe and
classify DI. These have ranged from descriptions of a limited number of
distinct clinical syndromes (e.g., the “bends”, “chokes” and “staggers”); a
presumptive assignment of etiology and severity (e.g., type I decompression
sickness and arterial gas embolism); and the systematic capture of
descriptive clinical and causal factors associated with the condition (e.g.,
decompression illness or dysbarism, and gas bubble illness). Not only have
these terms proven to be ambiguous, but they have been applied
inconsistently and have introduced many linguistic challenges (e.g., the
differentiation between illness and sickness).
2.2.1. Dysbaric Illness 179
3.2 The Classification Systems
To date, three enduring systems have appeared for the classification of
DI:
x the traditional or Golding Classification 26
x the descriptive or Francis / Smith Classification 27-29
x the ICD-10 Classification
Each of these classification systems addresses different objectives and
accordingly has inherent strengths and weaknesses.
3.2.1 The Traditional / Golding Classification
The Golding classification, developed during the building of the Dartford
Tunnel, was based on the assumption that DI was bivariate 26: It was either
inert gas (decompression sickness or DCS) or embolic (arterial gas
embolism or AGE) related. DCS was either mild (Type I) or severe (Type II)
and each category had specific treatment recommendations. Then, in 1970 a
combined form of DCS and AGE was described. It was called “Type III
decompression sickness” in an effort to contain it within the existing
classification system, but it demolished the previously clearly defined
boundaries between DCS and AGE and illustrated the shortcomings of the
classification system 30. Also the Golding Classification made no provision
for the dynamic nature of DI (i.e., its tendency to present in one way but
evolve into another), nor could it account effectively for the wide range of
clinical severity and variability in prognosis contained within the given
category of ‘Type II DCS’.
The main benefit of the Golding classification remains its simplicity.
Unfortunately, while its application may indeed have been equally
uncomplicated in the days when commercial and military diving
predominated the sub aquatic realm, this is no longer applicable to the
nebulous world of recreational diving and its injuries. Recent comparisons
have also shown significant discordance in a retrospective application of the
Golding classification to cases relevant to the spectrum of DI encountered
today31-33
.
Table 2.2.1-1. Modified Golding Classification for Dysbaric Illness
x Arterial Gas Embolism
x Decompression Sickness
- Type I (Musculoskeletal Pain; Skin; Lymphatic; Extreme Fatigue; Peripheral Nervous
Symptoms) - Type II (Neurologic; Cardiorespiratory; Audiovestibular; Shock)
- Type III (Combined Decompression Sickness and Arterial Gas Embolism)
180 A. Marroni et al.
3.2.2 The Francis / Smith Classification
To solve the inherent problems of the Golding Classification, Francis and
Smith proposed a new descriptive classification system that focused on
clinical presentation rather than etiology of DI 27-29,33. It contained
descriptive categories that served a dual purpose of capturing actual clinical
manifestations (e.g., the dynamic evolution and organ systems involved) as
well as detailing factors relevant to etiological considerations (e.g., latency,
inert gas burden and evidence of pulmonary barotrauma). This system
offered flexibility, provided more relevant information and had a much
higher degree of concordance between clinicians (see Table 2.2.1-2.).
The greatest utility of this classification system is its ability to describe
and adapt to the evolving signs and symptoms of presumed DI in a diver.
However, it does not establish a diagnosis, only factors relevant to the
probability thereof within a descriptive matrix of an evolving clinical
presentation 34. However, a collection of these descriptions can be used for
clinical comparison and to examine trends. The latter can then be analyzed
in the pursuit of underlying pathophysiological mechanisms and – based on
they probability of diagnosis generated by the various determinants – a
specific diagnosis may be assigned with appropriate nomenclature or
descriptions of symptom-clusters. Kelleher has shown that useful predictions
regarding outcome can be made using such data 35
.
Table 2.2.1-2. The Francis & Smith Classification for Dysbaric Illness
x Evolution
o Spontaneously Recovery (Clinical improvement is evident)
o Static (No change in clinical condition)
o Relapsing (Relapsing symptoms after initial recovery)
x Progressive (Increasing number or severity of signs)
x Organ System:
o Neurological
o Cardiopulmonary
o Limb pain exclusively
o Skin
o Lymphatic
o Vestibular
x Time of onset:
o Time before surfacing
o Time after surfacing (or estimate)
x Gas Burden
o Low (e.g., within NDL)
o Medium (e.g., Decompression Dive)
o High (e.g., Violation of Dive Table)
2.2.1. Dysbaric Illness 181
x Evidence of Barotrauma
o Pulmonary (Yes / No)
o Ears
o Sinuses
x Other Comments
Unfortunately, although the Francis / Smith system has received
increasing acceptance, its strength has also remained its fundamental
deficiency – the inability to assign a specific diagnosis. Clinicians and
statisticians ultimately need to work with diagnoses or case definitions.
These have remained elusive. Nevertheless, the current recommendation of
the European Committee for Hyperbaric Medicine (Type 1 recommendation)
is to provisionally accept the Francis and Smith classification until a superior
system emerges 28,29,36
.
3.2.3 The ICD-10 Classification
In the International Classification of Diseases, 10th edition, there are
various codes related to decompression illness. These are broad categories
and do not serve the purpose of differentiating the clinical and etiological
subtleties of the conditions: There is no sub-classification for caisson’s
disease, although certain forms of barotrauma are sub-classified.
The ICD-10 codes most frequently used are:
x T70 (Effects of air pressure and water pressure)
x T70.0 (Otitic barotrauma)
x T70.1 (Sinus barotrauma)
x T70.3 (Caisson’s disease)
x T70.4 (Effects of high-pressure fluids)
x T70.8 (Other effects of air pressure and water pressure)
x T79.0 (Traumatic air embolism)
x T79.7 (Traumatic subcutaneous emphysema)
x M90.3 (Osteonecrosis in caisson disease – T70.3+)
While the ICD-10 has become the international standard for diagnostic
classification of general epidemiological data, its primary application is for
billing and national healthcare decision-making processes rather than
unraveling the intricacies of a given medical condition. In short the ICD-10
has function and value but contributes little to the sub specialty of diving
medicine.
3.2.4 Future classification systems
The present trend is towards developing clearly defined case definitions
for DCS, AGE and combined forms. The dilemma in developing these is that
182 A. Marroni et al.
there is disparity between epidemiological and clinical objectives. The
former requires specificity in favor of reliable diagnosis, the later sensitivity
in favor of avoiding under-treatment. It is likely that a scoring system will
ultimately be accepted which records risk-factors relevant to the exposure
and clinical features consistent with a diagnosis. Then, depending on the
objective the relative weighting of these factors will be adjusted respectively
for greater specificity or sensitivity. The ECHM has recommended the
development and acceptance of such an epidemiological classification
system which will allow multi-centre, multinational, retrospective analyses
derived from broad-based classifications that include the type of diving,
chronological data, clinical manifestations and outcome of a two-year follow
up for prognostic purposes.
- PATHOPHYSIOLOGY
Although DI is causally related to bubbles, there are a multitude of
pathophysiological mysteries between the physical appearance of bubbles
and the onset of biological injury or clinical illness. Various unknown
individual physical and physiological factors may contribute towards
individual variability in the production of, and response to, bubbles 37,38
.
Venous bubbles are commonly observed following routine and even
relatively shallow dives and appear to be largely asymptomatic. On the other
hand, the appearance of left ventricular or arterial bubbles are thought to be
of greater clinical importance; however these have rarely been observed,
even in a laboratory setting. Recently, ocular tear film bubbles have
generated some interest, but their persistence following decompression has
limited their reliability as a predictor of decompression stress 3,39
.
When it comes to actually diagnosing DI, we presently rely almost
exclusively on the diver’s history and an estimation of clinical probability
from an enormously divergent spectrum of signs and symptoms following
decompression. As yet, there are no specific biochemical markers for bubble
related injury 40-42. Also, the sensitivity of radiological and nuclear medical
examinations does not exceed that of clinical observation and, in the absence
of diagnostic uncertainty, these rarely affect management. We must
therefore accept that the best scientific case definition we have for DI at
present is one of exclusion, i.e. the appearance of unexplained pain,
cutaneous, cardiovascular or neurological abnormalities – chronologically
associated with compressed gas diving – upon the exclusion of other
etiologies. In a clinical setting, our index of suspicion should be high to
avoid under-treatment. Fortunately, the risk of injury remains relatively
2.2.1. Dysbaric Illness 183
small: in recreational diving, for example, DI occurs with an incidence of
one to three per 10,000 dives 43
.
4.1 The origin and destination of bubbles
With decreasing pressure, a threshold is eventually reached where
bubbles start to form in the body; this depends on the amount of inert gas
and the extent of decompression. At extreme altitudes, DI cannot be avoided,
even after prolonged oxygen pre-breathing 44
.
Although decompression bubbles are traditionally classified as intra- or
extravascular, this division may be misleading as it does not describe the
origin of bubbles but rather where they have been observed. In fact, there is
no proof that bubbles form directly in blood vessels. Rather, it is believed
that they may be admitted through endothelial gaps as they develop within
surrounding perivascular tissues 45. Another mechanism for the intravascular
appearance of bubbles is by traumatic introduction during pulmonary
barotrauma 46. As little as 10% overexpansion of the lungs is enough to
cause gas embolism 47,48. This would occur with an intratracheal pressure of
76-80 mm Hg (or 99.2-108 cm H2O), or during a breath-hold ascent (after
breathing compressed gas) from only 3 feet (~1 meter) of seawater to the
surface 48. Although traumatic injection of gas vs. bubbles released by inert
gas supersaturation represent two completely different etiological
mechanisms, they are often difficult to differentiate clinically: physical or
radiological evidence of pulmonary injury is often absent in AGE 49
,
whereas arterialization of inert venous gas emboli may result in arterial gas
embolization with clinically indistinguishable results.
Although the origin of bubbles may be ambiguous, their effects are more
distinct. Intravascular bubbles embolize tissue causing ischemia 50; they also
traverse the microvasculature (so-called “transbolism”) and injure
endothelium 51; they cause reperfusion injury and vasospasm 18. Bubbles can
cause venous stasis, hemorrhage and precipitate plasma protein interactions 52
.
Extravascular or tissue bubbles disrupt and tear delicate tissues and blood
vessels; they can also increase tissue compartment pressures i.e., cause
regional compartment syndromes 53
.
4.2 Effects of Bubbles on various Tissues and Organ
Systems
To consolidate the various mechanisms involved in DI into meaningful
clinical entities, it is useful to observe their effects on known target organs:
(1) blood and blood vessels; (2) the lungs; (3) the central and peripheral
184 A. Marroni et al.
nervous systems; (4) the inner ear; (5) the skin and lymphatics, and (6) bones
and joints.
4.2.1 Blood and blood vessels
Bubbles are biologically active. They interact with the cellular elements
in blood as well as plasma protein cascades – coagulation, complement,
kinin and plasmin. In addition, bubbles denature lipoproteins, liberating
blood lipids 54-57. Blood vessels, on the other hand, sustain damage through
physical contact. This may range from minimal damage to bleeding 51,58
.
Blood:
Upon appearance of a bubble in blood, the catalyzing event appears to be
the formation of a plasma-protein coat around the bubble. This bubble “skin”
is made up of plasma glycoproteins, fibrinogen and gamma globulins 59,60. It
is a biologically active interface that allows thrombocytes and white blood
cells to become attached 61
.
In time, activation of platelets leads to aggregation and coalescence
around bubbles with entrapment of other blood constituents. Cellular blood
elements – such as red blood cells – may become entangled in the growing
fibrin web. This thickening of the bubble “skin” may reduce diffusion
producing a mechanism for bubble stabilization and survival 62. General
platelet adhesiveness also increases in response to bubbles. Some studies
have reported platelet depletion following decompression, even in the
absence of symptoms 63. However, thrombocytopenia or anti-platelet
therapies do not appear to protect against DI. Also aggressive
anticoagulation runs the risk of precipitating hemorrhage in DI affecting the
spinal cord and inner ear 61,62,64,65. On the other hand, DI does induce a
hypercoagulable state with a high risk of thromboembolism aggravated by
paralysis. This should be actively prevented.
The activation of platelets and Hageman Factor also leads to activation of
inflammatory cascades. Leukotrienes are released while the presence of
gammaglobulin on the bubble skin, combined with the products of
complement activation, attract white blood cells to the area 66. Leukocytes
may interact directly with the bubble or with damaged endothelium. The
relevance of inflammation in DI underlies the recommended use of antiinflammatory agents and, more recently, of lidocaine 67. Lidocaine also has
leukocyte anti-adherent properties 68,69
.
DI has also been shown to result in elevations of blood lipid levels with
as yet undefined clinical implications 70
.
While the role of various elements in blood in DI has become
downplayed in recent literature, the significance has not disappeared: The
search continues to find safe and effective drugs or interventions that may
2.2.1. Dysbaric Illness 185
attenuate the various pathophysiological events following exposure to
bubbles. Recently research on nitric oxide donors and exercise have
suggested that they may have a modifying role in vivo 17
.
Blood vessels
The injection of 10-20µm bubbles into the carotid artery of a guinea pig
has been shown to cause visible damage to the luminal surface surfactant
layers of endothelial cells 71. This form of injury may result in alterations in
vasomotor tone, precipitate platelet or leukocyte adhesion, and cause failure
of the blood-brain barrier. In more extreme cases endothelial cells may
actually be stripped, exposing the basement membrane to plasma proteins
and platelets as well as adding bioactive cell remnants to the blood 61
.
4.2.2 The Lungs
Unlike pulmonary barotrauma, pulmonary DI is an intravascular
occlusive bubble disease. It results from the passage of venous gas emboli
through pulmonary capillaries. The peri-alveolar network of capillaries
serves as a trap for venous gas emboli. However, if the amount of gas is
excessive, it may cause cardiac air locking and pulmonary outflow
obstruction or microvascular obstruction with vasoconstriction, endothelial
damage, inflammation, capillary leak and pulmonary edema – “the chokes”.
The pulmonary “bubble trap” may also be overcome by massive
embolization or be bypassed via broncho-pulmonary shunts, arterio-venous
fistulae, or intra-cardiac shunts. A reduction in the diameter of circulating
bubbles – such as by repetitive diving or “yoyo” diving – may allow bubble
passage through the pulmonary capillary beds. All of these mechanisms may
lead to arterialization of bubbles – so-called paradoxical gas embolism. The
latter provides an attractive theoretical explanation for the poorly understood
associations between “chokes”, patent foramen ovale, and DI of the central
nervous system and skin 11,43
.
4.2.3 Nervous System
Approximately two thirds of DI affects the nervous system. Although
clinical features may be ambiguous a distinction is made between three
potential locations of injury: (1) the spinal cord, (2) cerebrum and (3)
peripheral nerves. In each case, the primary mechanism may be vascular
(embolic) or extra-vascular.
In a review of 1070 cases of neurological decompression sickness,
Francis et al discovered that 56% occurred within 10 minutes – some even
prior to surfacing 72. Even when considering the 768 cases of obvious spinal
cord injury in this series the majority still presented within 10 minutes of
186 A. Marroni et al.
surfacing. Therefore any mechanistic theory for DI would have to account
for this short latency. Conversely, there were 44% of cases that developed
clinical manifestations as long as 48 hours after surfacing. This supports the
probability of multiple mechanisms with varying latencies.
4.2.3.1 Spinal Cord
Four etiological theories have evolved to reconcile the varying
observations of onset time, severity, response to therapy, and histopathology.
They are (1) gas embolism; (2) venous infarction; (3) autochthonous (“in
situ”) bubbles; and (4) hemorrhage or inflammation.
Gas Embolism:
The first theory for DI of the spinal cord was developed by Boycott and
Damant. Lesions in the spinal cord of goats were found to consist, almost
entirely, of white matter lesions 9
. Indeed human pathology, although rarely
observed in this mostly non-fatal condition, has also shown similar punctate,
white matter lesions and hemorrhage. However, embolic injury to the spinal
cord is, generally speaking, very rare. This is believed to be due to the
relative difference in blood flow favoring embolization of the brain.
Experimental spinal cord embolism has also been shown to produce
ischemic grey matter pathology rather than white matter lesions 73. To
confuse the matter further a type of DI was identified that began as rapid
onset cerebral arterial gas embolism but then evolved into a particularly
resistant form of spinal injury. This has been called “combined”,
“concurrent” or “Type III decompression sickness” 30,74-76. Although the
exact mechanism is still unknown, the predominant theory is related to
growth of arterial gas emboli in tissues saturated with inert gas.
Venous Infarction:
In 1975, based on Batson’s experiments on tumor embolization via
epidural veins 77, Hallenbeck et al postulated that DI of the spinal cord was
due to bubble accumulation in the epidural venous plexus with subsequent
venous infarction of the spinal cord. Although confirmed in extreme
decompression 78-80, loss of function only occurred after several minutes and
therefore did not offer an explanation for ultra-short-latency disease. In
addition, the pattern of dysbaric injury was different to that observed in other
causes of venous infarction of the spinal cord that typically affects the
central grey matter 81
.
Autochthonous Bubbles:
Francis proposed that rapid-onset spinal cord damage may be related to
spontaneous bubble formation in the spinal cord white matter. He felt that
this was the only mechanism that could explain both the rapid onset and the
distribution of lesions observed in the spinal cord. In his classic experiment,
the spinal cord of decompressed dogs was rapidly perfusion-fixed at the
2.2.1. Dysbaric Illness 187
moment of maximal disruption of somatosensory evoked potentials. He
consistently found extravascular, white matter lesions – called
autochthonous bubbles 82,83. The puzzling piece is how these small, scattered
and isolated space occupying lesions (making up no more than 0.5% of the
spinal cord and being no more than 20-200um in diameter) are able to
produce such catastrophic clinical effects 84. It has been postulated that
autochthonous bubbles could account for loss of function if more than 30%
of the axons became dysfunctional due to direct injury, stretching or
compression, inflammation, biochemical injury or hemorrhage. In support of
this, Hills et al has also shown that small lesions (able to increase the spinal
cord volume by 14-31%) can cause an increase in tissue pressures with a
resulting spinal compartment syndrome 85
.
Hemorrhage and Inflammation:
In his studies on autochthonous bubbles, Francis made three important
additional observations 86: (1) animals that only developed abnormalities
after 30 minutes had no demonstrable space occupying lesions suggesting
another mechanisms for the dysfunction; (2) animals sacrificed some time
after the development of rapid-onset dysfunction no longer had bubbles
suggesting that they are temporary; and (3) the histological appearance of
spinal cords from dogs with late-onset spinal symptoms was similar to that
of spinal embolism or ischemic lesions 73. Interestingly in the animals
harvested some time after rapid onset illness, hemorrhage and inflammation
were observed in the same areas where autochthonous bubble injuries were
seen in those harvested early. This could explain why some cases of rapid
onset spinal cord DI appear resistant to recompression and would suggest
caution in the use of anti-coagulants in DI of the spinal cord.
Intriguingly, all of the mechanisms appear to converge within a particular
area: a c-shaped area around the spinal cord grey matter. This area represents
a watershed zone between the anterior and posterior spinal cord circulation
and would therefore be susceptible to both inert gas accumulation as well as
subsequent bubble-related ischemia. The cervical and lumbar enlargements
are particularly vulnerable and also correspond to the areas of greatest
clinical importance in DI.
It is unlikely that one single mechanism can account for the wide variety
of latencies and presentations of DI of the spinal cord and the decompression
schedules leading to them. Rather it is probably the result of several
interacting, compressive-ischemic mechanisms. DI of the spinal cord should
be thought of as a spectrum of cause-and-effect over a 48-hour timecontinuum. It is an interplay between a variety of distinct, yet synergistic
pathophysiological processes – some of which are amenable to
recompression and adjunctive medical therapy and some which,
unfortunately, are not.
188 A. Marroni et al.
Finally, in spite of the disturbing vulnerability of the spinal cord, it has a
remarkable capacity of recovery. Many divers with residual deficits after
recompression therapy continue to improve for years afterwards. However,
this does not indicate that the injury has been reversed, only that the body
has compensated for it 87,88
.
4.2.3.2 Cerebrum
Cerebral decompression disorders differ from those of the spinal cord in
that there is no experimental evidence suggesting autochthonous or venous
stasis mechanisms. Accordingly, greater emphasis is placed on embolic and
inflammatory mechanisms.
Cerebral DI has a very short latency. In the review by Francis, 75% of
the 311 cerebral DI cases became symptomatic within 10 minutes (even with
all cases of overt pulmonary barotrauma specifically excluded) 72. This
leaves paradoxical gas embolization as an attractive alternative possibility.
Clinical Features Systemic Gas Embolism (SGE):
Gas embolism is by its nature a systemic disease although clinically it
primarily affects the myocardium and the brain. While coronary embolism
may account for some diving fatalities, it is not associated with long term
morbidity. Cerebral events, on the other hand, are associated with both short
term mortality and long term morbidity.
SGE gain access to the cerebral circulation via the carotid and vertebral
arteries that converge at the base of the brain forming the circle of Willis.
Depending on the volume of gas and region of the brain involved the clinical
outcome of gas embolism ranges from instant death to spontaneous
uneventful recovery. Relapses have been reported in up to 30% of patients
with arterial gas embolism following submarine escape, irrespective of
preceding or concurrent recompression 89-91. A subset of patients may also
suffer subclinical damage only visualized by medical imaging 74
.
Irrespective of the cause, the ultimate outcome of cerebral gas
embolization appears to depend on the anatomical location, gas volume,
delivery rate, pre-embolic gas saturation as well as co-morbid factors such as
hypotension or dysfunction of vital centers.
4.2.3.3 Peripheral Nervous System
The peripheral nervous system may be affected by decompression
injuries anywhere from the posterior horn of the spinal cord, to the mixed
nerves, brachial or lumbar plexus, and cutaneous or muscular innervations.
The most important considerations are differential diagnosis and prognosis.
This area probably represents one of the areas of greatest clinical ambiguity.
However, even though the underlying pathophysiology remains obscure, the
prognosis is usually good.
2.2.1. Dysbaric Illness 189
4.2.4 Inner Ear
There are four dominant theories for the clinical and pathological
findings associated with DI of the inner ear. They are: (1) explosive /
hemorrhagic injuries; (2) counter diffusion; (3) gas induced osmosis; and (4)
vascular emboli 92,93
.
Explosive / hemorrhagic injuries
In 1980, Landolt et al found hemorrhage in the inner ear of squirrel
monkeys subjected to rapid decompression from saturation 94. Three years
later Venter was able to show an implosive injury of the semicircular canals
as the cause for the hemorrhage 95. The mechanism, they proposed, was one
of gas accumulation in temporal bone osteoclast pockets that then
explosively ruptured into the inner ear during decompression. Money
subsequently found evidence of the same type of injury in a diver who died
56 days after left inner ear DI 96. This mechanism is plausible for deep mixed
gas diving, but less convincing for inner ear DI following shallower dives.
Embolism
Blood supply to the inner ear is endarterial and consequently prone to
embolic or vascular injury. Embolic disturbance has been shown in cardiac
bypass surgery, but how this relates to diving remains uncertain 97
.
Counterdiffusion
This theory entertains the possibility that counterdiffusion can occur
under conditions where the inert gas in the middle ear differs from that in the
breathing mixture. Diffusion through the round or oval window could result
in accumulation of inert gas with bubbling, resulting in deafness or vertigo.
This theory has developed due to a high prevalence of inner ear DI in
helium-oxygen and mixed gas divers 27. Counterdiffusion may also occur
within the partitions of the inner ear itself. The vascularity of the inner ear is
not uniform: the stria vascularis supplies the endolymph directly and from
there inert gas would diffuse to the perilymph. Therefore, with gas
switching, it is possible that the endolymph could rapidly take up a new inert
gas, e.g. helium, before the perilymph has had time to eliminate the former
inert gas. Bubbles could then form within the endolymph with disruption of
function and even rupture 27
.
Gas-induced Osmosis
Finally, by a similar mechanism, inert gas accumulation in the
endolymph could result in gas-induced osmosis: an osmotic fluid shift
towards the endolymph resulting in a form of hydrops endolymphaticus
analogous to Meniere’s disease.
190 A. Marroni et al.
4.3 Skin
Skin bends or DI of the skin may present in a variety of ways with
varying etiologies and clinical significance.
Diver’s Lice
This erythematous rash usually presents in association with dry chamber
dives or the use of dry suits. The hypothesis is that inert gas enters the skin
directly and causes dermal bubbles with histamine release upon
decompression. The condition can be avoided by not having gas skin
contact, or by heating the skin during decompression. It is not considered
serious in the absence of other findings, and does not require recompression.
Cutis Marmorata
A more significant form of DI of the skin is called cutis marmorata or
skin marbling. Although the condition itself is benign, its association with
pulmonary and neurological DI requires careful consideration. Experimental
work in pigs has shown that this pattern of illness is associated with venous
congestion, inflammation, leukocyte adherence and endothelial damage 98
.
No bubbles have been visualized, but the manifestations usually resolve
promptly with recompression.
Counterdiffusion
A rare type of DI may result from exposure to different inert gases, such
as helium and nitrogen. Diffusion-related gas accumulation may occur when
one gas is in contact with the skin, while another is breathed 99,100
.
4.4 Musculoskeletal
Some of the first descriptions of DI or “the bends” involved painful joints - Even today, musculoskeletal pain it is the most common presenting
complaint 102
.
There are two bone and joint conditions associated with decompression:
acute muskuloskeletal DI and dysbaric osteonecrosis.
4.4.1 Acute Musculoskeletal DI
Although they have similar blood supply, joints, and musculo-tendinous
attachments, it is noteworthy that ‘bends’ pain only appears to affect long
bones of the appendicular skeleton – not the axial skeleton. Adult long bones
contain a fatty marrow cavity that could be a reservoir for inert gas and
predispose to DI. Axial bones largely contain haemopoietic tissue which
appears to be unaffected by decompression.
Another interesting feature of ‘bends’ pain is that it is influenced by premorbid hyperbaric activity. In a review of more than 19,000 cases, Sowden
2.2.1. Dysbaric Illness 191
found that bounce divers and pilots primarily developed shoulder pain,
whereas saturation divers and caisson workers developed knee pain 103
.
There are many theories but little evidence to explain this phenomenon.
There are four theories for bubble-related pain in bones and joints. They
involve stretching of nerve endings or inflammation occurring (1) within
joints; (2) around the joints, such as within tendons and muscle; (3) within
bone, due to gas expansion within fatty marrow, the medullary cavity and
bone sinusoids (a phenomenon also associated with cancer-pain), and; (4) as
a result of referred pain, either due to an injury to the nerves or nerve roots
associated with the joint, or due to a generalized release of inflammatory
modulators with flu-like symptoms and poliarthralgia.
Intra- and periarticular pain associated with decompression can usually
be localized and is of a non serious nature. There is a trend towards treating
these conservatively although they respond well and promptly to
recompression. Referred pain is part of the neurological spectrum of DI that
has been considered elsewhere. What remains, is medullary pain.
The discovery of sinusoid innervation has led to the concept of a venous
congestive mechanism for cancer and osteoarthritic bone pain 104,105. This
sinusoid congestion pain theory is also attractive as an explanation for
‘bends’ pain as it addresses several clinical phenomena: (1) the deep, poorly
localized, boring pain; (2) relief achieved by the local application of pressure
(e.g., a BP cuff); and (3) a gravity-related distribution of manifestations in
the various patient subgroups.
Although there is no scientific association between medullary pain and
dysbaric osteonecrosis, it is usually viewed as a more serious form of
musculoskeletal DI and recompression is recommended.
4.4.2 Dysbaric Osteonecrosis
Dysbaric osteonecrosis appears to affect predominantly saturation divers
and caisson workers. Again it appears to be the appendicular skeleton that is
at risk, particularly the humoral head, femoral head and juxta articular area
of the distal femur and proximal tibia. Lesions in proximity to the femoral
and humeral head may be symptomatic and may eventually become
disabling whereas femoral and tibial shaft lesions remain asymptomatic. The
question remains why it is only certain types of diving that predispose to this
disease, and why these areas are so uniquely vulnerable 106
.
192 A. Marroni et al.
4.5 Concluding Remarks on DI Mechanisms
The confusion and controversy regarding the pathophysiology of DI is
exemplified by the division that still exists in the use of two classification
systems: one pathological 107, and the other clinical 28,29
.
While we do not always know the cause of DI, we must not ignore
mechanisms altogether, thereby being unable to appreciate risk, determine
probability of injury and prescribe effective and rational treatment. Astute
clinical observation and focused research must remain the vital tools for
unraveling the mysteries of DI. - EPIDEMIOLOGY
There are five important epidemiological observations that have been
made regarding DI 2-4,14,21-24,108-123:
x The incidence is very low in general – in the order of 0.01-0.05 %
(1 to 5 per 10,000 dives).
x There is no demonstrable gender-specific predisposition to DI.
x Novice and experienced divers are at greatest risk for developing
DI.
x Dives in excess of 24 meters (80 feet) have a significantly greater
incidence of DI.
x Neurological involvement is by far the most common manifestation
in recreational divers.
5.1 Risk Factors
A variety of risk factors have been identified over the past century in an
effort to explain the variations in susceptibility to DI 2-4,14,21-24,108-123. These
include:
x Altitude Exposure: either diving at altitude or subsequent exposure
x Exercise: before, after or during the bottom phase of a dive
x Injury: previous DI or other acute injuries
x Omitted decompression: missed stops / errors of depth monitoring
x Uncontrolled ascents
x Personal traits (gender; physiognomy; level of fitness)
x Profiles: (variables of depth, multiple ascents, ascent rates and the
depth prior to final ascent to the surface within the same ‘squareprofile’ or depth-time envelope)
x Previous dives: residual nitrogen
x Hypoventilation: CO2 build-up
2.2.1. Dysbaric Illness 193
x Hypothermia: gas retention-release due to solubility changes
x Hypovolemia: dehydration and hemoconcentration
Although the relevance of individual factors is understood and – in some
cases – obvious, there is surprisingly little evidence on the relative
contributions of these factors towards the overall risk 38. The following are
discussed in more detail below:
5.1.1 Exercise: before, after or during the bottom phase of a dive
Exercise during exposure to increased ambient pressure (during the
bottom phase of the dive) appears to increase the incidence of DI. The
probable explanation of this is that the increased perfusion during exercise
leads to an increased uptake of inert gas that must be subsequently
eliminated during decompression. Conversely Vann et al have shown that
exercise during decompression stops may reduce the incidence of DI by an
opposite mechanism 25. Exercise prior to or following diving are risk factors
however and there are at least three reasons for this:
x Rapidly flowing blood, especially in the area of bifurcation of
vessels, may create foci of relative negative pressure through a
Venturi effect. Small numbers of molecules of gas from the
surrounding supersaturated blood may then diffuse into these foci
down a partial pressure gradient. The resulting localized collections
of small numbers of gas molecules are known as gas micronuclei and
are thought to act as a ‘nidus’ for bubble formation.
x Distraction between articulating joint surfaces causes extreme
reductions in ambient pressure and gradients of up to 270 atm. This
process – called tribonucleation – is thought to offer some
explanation for the variable incidence between different forms of
diving and compressed air activities vs. the ultra-low incidence of DI
during extravehicular activity in space. In the latter case it is thought
that the absence of gravity reduces articular shearing forces and in
the absence of ongoing production these micronuclei seem to
disappear.
x Increased local CO2 production in exercising muscle may play a role
since CO2 is a highly diffusible gas and might contribute to the
formation of gas micronuclei.
5.1.2 Injury: previous DI or other acute injuries
Recent local injury seems to lead to an increased incidence of DI
manifested by pain at or near the site of the injury. The mechanism
responsible for this phenomenon is unclear. Changes in local perfusion and
194 A. Marroni et al.
increased gas micronuclei formation in injured tissue are postulated
mechanisms.
5.1.3 Personal traits (gender; physiognomy; level of fitness)
There is no convincing evidence that gender affects DI risk in
recreational divers. Indirect measures of fitness and body mass have yet to
yield definitive answers on relative risk for DI. Advancing age is thought to
increase the incidence of DI for reasons that are not yet clearly known.
5.1.4 Hypoventilation: CO2 build-up
Even small increases in FiCO2 seem to increase the incidence of DI. The
mechanism of this effect is not clearly understood, although increased
availability of this highly diffusible gas for diffusion into gas micronuclei;
vasodilatation with increased inert gas uptake; and reduction in the ‘oxygen
window’ are all relevant factors.
5.1.5 Hypothermia: gas retention-release due to solubility changes
Diving in cold water tends to increase the incidence of DI. Inert gas
uptake is generally not affected since the exercising diver is usually warm
and has increased tissue perfusion because of exercise. However, when the
diver leaves the bottom and reaches his decompression stop where he
remains at rest he is likely to become cold. The resulting peripheral
vasoconstriction may then impair inert gas elimination.
5.1.6 Hypovolemia: dehydration and hemoconcentration
Dehydration was reported as a factor that increases the risk of DI during
studies on aviators during World War II, and it is still considered a
significant risk factor by the international diving and diving medical
communities. The mechanism is however again unclear and reliable
scientific evidence is missing. Changes in the surface tension in serum
favoring bubble formation has been postulated as a possible mechanism.
Alcohol ingestion prior to diving, also seems to be a risk factor – possibly
due to dehydration.
2.2.1. Dysbaric Illness 195 - CLINICAL MANIFESTATIONS 2,3,14
DI presents at various intervals following hyperbaric exposure 14: 50%
occur within 30 minutes of surfacing; 85% occur within one hour of
surfacing; 95% occur within 3 hours of surfacing; 1% delayed more than 12
hours. However, symptoms have been reported to appear as late as 24 hours
and more after surfacing and even longer if exposure to altitude follows the
hyperbaric excursion.
As far as manifestations are concerned, the clinical presentation of DI has
been divided into two broad categories based on severity of symptoms prior
to recompression. h
MILD DI
This category includes the following:
x Limb pain
x Lymphatic manifestations, or
x Cutaneous manifestations,
in the absence of any other systemic manifestations
MODERATE TO SEVERE DI
This includes the following:
x Pulmonary DI
x Central Nervous System DI (Brain; Spinal Cord; Inner Ear)
x Shock
x Girdle Pain (Abdominal; Thoracic; or Lumbar)
x Extreme fatigue
6.1
Mild DI includes those categories traditionally assigned to Type I in the
Golding Classification 26. Mild DI forms do not display any features of
moderate to severe DI and this should be confirmed by a competent health
care professional.
Pain
The upper extremities are involved 3 times more often than the lower
limbs in recreational and compressed air commercial diving. The situation is
reversed in caisson workers and in commercial saturation (Heliox) diving.
The pain can range from slight transient discomfort (‘niggle’) to a dull,
deep, boring and unbearable pain. It is usually not affected by movement and
h
As iterated in the preceding sections, DI does not present in watertight clinical
compartments, nor can the etiology always be confirmed. It should therefore be understood
that the clinical entities presented here may coincide or overlap with others across the
arbitrarily assigned boundaries of mild, moderate and severe DI.
Mild DI
196 A. Marroni et al.
there can occasionally be some degree of overlying local pitting edema and
subjective numbness (refer section 4.4.1).
Lymphatic Manifestations
The lymphatic manifestations of DI presumably result from obstruction
of lymphatic vessels by bubbles. The manifestations can include pain and
swelling of regional lymph nodes, with lymph edema of those tissues
drained by the obstructed lymph nodes.
Cutaneous Manifestations
Itching is commonly reported during decompression from dry chamber
dives where the skin is surrounded by chamber atmosphere rather than
water. It is thought to be the result of diffusion of gas from the chamber
atmosphere directly into the skin, followed by expansion during
decompression and a consequent itching sensation. This is not considered a
systemic form of DI and therefore need not be treated with recompression.
Itching with or without discoloration, signs of urticaria and/or blotchiness
occurring after in-water diving is considered to be systemic cutaneous DI i
.
Cutis Marmorata or marbling is thought to result from bubble-related
cutaneous venous obstruction. It usually presents as an area of erythema,
frequently affecting the upper back and chest. Lesions may migrate
spontaneously or with palpation and prominent linear purple markings are
frequently observed. These manifestations are considered to be an overt
manifestation of DI and should be promptly treated j
. Recompression often,
although not always, leads to prompt resolution.
6.2 Moderate to severe DI
Moderate to severe DI includes those categories traditionally assigned to
Type II (and III) in the Golding Classification 26. The criteria for moderate to
severe DI are met if at any stage DI presents with more than simple limb
pain and cutaneous features:
Pulmonary DI
This relatively uncommon syndrome usually presents with a
gnomonic triad of:
i
If a wet dive took place in a dry suit, then there may be direct absorption of gas into the skin
as for a chamber dive. This should be distinguished from dives resulting in cutaneous
lesions where no skin-gas contact occurred.
j
Cutis marmorata is associated with systemic decompensation, paradoxical embolism (e.g.,
via a PFO, ASD or intra-pulmonary shunt) and high spinal, cerebral and audiovestibular
forms of DI. Therefore while the condition itself is not particularly serious, its associations
prompt attention to the other systems of greater vulnerability and justify urgent
recompression.
patho-
2.2.1. Dysbaric Illness 197
x Substernal pain: usually burning and progressively increasing.
Initially the pain may be noted only when coughing. Over time
the pain may become constant.
x Cough: initially intermittent and easily provoked by cigarette
smoking (Behnke’s sign). Paroxysms of coughing may become
uncontrollable.
x Progressive respiratory distress and dyspnea.
The manifestations of pulmonary DI are believed to result from the
combined effects of gas emboli in the pulmonary artery and obstruction of
the vascular supply to the bronchial mucosa. Untreated Pulmonary DI may
be fatal.
Neurological DI
The neurological manifestations of Dysbaric Illness are unpredictable:
They range from minor sensory abnormalities to loss of consciousness and
death. Clinically they may resemble acute stroke or an acute exacerbation of
multiple sclerosis. Although an increasing number of mild sensory changes
are being assigned to peripheral nerve and nerve root lesions (some of which
may not necessarily be related to DI), the clinical prerogative is to assume a
central origin until proven otherwise and to manage these presentations
promptly.
Cerebral DI: Brain involvement in DI appears to be especially common
in aviators. However it is not known if this is due to paradoxical
embolization of large volumes of venous gas; the release vasoactive
mediators; hypoxemia due to a disruption of pulmonary circulation in
conditions of marginal oxygenation at extreme altitude or something else
entirely. In this group a migraine like headache often accompanies visual
disturbances. When there is brain involvement in divers a common
presentation is hemiparesis which is different to the clinical presentation in
aviators. Collapse with unconsciousness are rare presentations of DI and
more likely to be due to injected gas than bubble evolution from
supersaturated tissues.
Spinal Cord DI: Paraplegia is a ‘classic’ symptom of DI in divers and
almost invariably represents spinal cord involvement
. Bladder paralysis
with urinary retention and fecal incontinence frequently accompany
paraplegia. In the last few years, cases of serious paralysis in recreational
divers dropped from 13.4 percent in 1987 to only 2.9 percent in 1997, and
the number of cases of divers losing consciousness dropped from 7.4 percent
to 3.9 percent of total injuries during the same period. The incidence of loss
of bladder function, another sign of neurological DI, dropped from 2.2
percent to 0.4 percent during this period (DAN Diving Accident Reports) 119
.
A notable exception is embolization of the anterior cerebral arteries which can also present
with bilateral lower extremity paralysis and loss of bladder function.
198 A. Marroni et al.
However this change in incidence has not been balanced by an equivalent
rise in the frequency of pain only or skin DI. On the contrary, there seems to
be a trend towards an increased incidence of milder neurological
manifestations. Paresthesias, some with well and other with less clearly
defined presentations (including ubiquitous numbness and/or tingling) as
well as vague, ambiguous and ill-defined symptoms now predominate
recreational DI. The diagnostic ambiguity is compounded by the fact that
many of these manifestations appear to respond to normobaric oxygen and
recompression. However, while suggestive, response to recompression
cannot be considered diagnostic in these conditions. Certain non-diving
related nerve damage also appears to respond to hyperoxygenation so that
one of the greatest clinical challenges in DI lies in unraveling true diving
injuries from a myriad of other transient peripheral neuropathies 124
.
Inner Ear DI
Cochlear and/or vestibular DI was previously almost exclusively
associated with saturation and experimental diving and – accordingly – quite
rare. In recent times the incidence has been increasing due to an escalation in
deep recreational technical diving involving mixed gas and gas switching on
decompression. Either or both cochlear and vestibular apparatus may be
involved presenting with tinnitus, deafness, vertigo, nausea, and vomiting.
Nystagmus may be present on physical examination. The mechanisms
remain unclear (refer section 4.2.4.). Inner ear DI is a serious medical
emergency and must be treated immediately to avoid permanent damage.
Since the nutrient arteries of the inner ear are very small, rapid reduction in
bubble diameter, with immediate 100% oxygen administration and prompt
recompression are essential.
Shock
Shock occasionally occurs in DI and is usually associated with serious
pulmonary and cardiovascular manifestations. Fatalities are usually the
result of shock or pulmonary forms of DI and resuscitation and immediate
recompression are of paramount importance.
Girdle Pain: Back, Abdominal, or Chest Pain
Unlike limb pain, pain in these areas should be considered carefully as it
is frequently associated with progressive spinal cord DI.
Extreme Fatigue
Fatigue disproportionate to the amount of preceding activity has long
been regarded as an evolving serious manifestation of DI. The biochemical
and pathophysiological mechanisms are unknown although there is
increasing evidence that it may be the result of vasoactive mediators and
cytokines released due to venous gas embolization.
2.2.1. Dysbaric Illness 199