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Decompression Illness (DCI) comprises two different conditions caused by rapid decompression of the body. These conditions present similar symptoms and require the same initial first aid. Scuba divers are trained to ascend slowly from depth to avoid DCI. Although the incidence is relatively rare, the consequences can be serious and potentially fatal, especially if untreated. [1]
DCI can be caused by two different mechanisms, which result in overlapping sets of symptoms. The two mechanisms are:
In any situation that could cause decompression sickness, there is also potentially a risk of arterial gas embolism, and as many of the symptoms are common to both conditions, it may be difficult to distinguish between the two in the field, and first aid treatment is the same for both mechanisms. [2]
Approximately 90 percent of patients with DCS develop symptoms within three hours of surfacing; only a small percentage become symptomatic more than 24 hours after diving. [3]
Below is a summary comparison of the signs and symptoms of DCI arising from its two components: Decompression Sickness and Arterial Gas Embolism. Many signs and symptoms are common to both maladies, and it may be difficult to diagnose the actual problem. The dive history can be useful to distinguish which is more probable, but it is possible for both components to manifest at the same time following some dive profiles.
| Decompression sickness | Arterial Gas Embolism |
|---|---|
| Signs | |
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| Symptoms | |
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Decompression sickness is caused by the formation and growth of inert gas bubbles in the tissues when a diver decompresses faster than the gas can be safely disposed of through respiration and perfusion. [4]
Arterial gas embolism is caused by gas in the lungs getting into the pulmonary venous circulation through injuries to the capillaries of the alveoli caused by lung overpressure injury. These bubbles are then circulated to the tissues via the systemic arterial circulation, and may cause blockages directly or indirectly by initiating clotting. [5]
The mechanism of decompression sickness is different from that of arterial gas embolism, but they share the causative factor of depressurization.
Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body. These bubbles produce the symptoms of decompression sickness. [6] [7] Bubbles may form whenever the body experiences a reduction in pressure, but not all bubbles result in DCS. [8] The amount of gas dissolved in a liquid is described by Henry's Law, which indicates that when the pressure of a gas in contact with a liquid is decreased, the amount of that gas dissolved in the liquid will also decrease proportionately.
On ascent from a dive, inert gas comes out of solution in a process called "outgassing" or "offgassing". Under normal conditions, most offgassing occurs by gas exchange in the lungs. [9] [10] If inert gas comes out of solution too quickly to allow outgassing in the lungs then bubbles may form in the blood or within the solid tissues of the body. The formation of bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage. [11] The most severe types of DCS interrupt — and ultimately damage — spinal cord function, leading to paralysis, sensory dysfunction, or death. In the presence of a right-to-left shunt of the heart, such as a patent foramen ovale, venous bubbles may enter the arterial system, resulting in an arterial gas embolism. [12] [13] A similar effect, known as ebullism, may occur during explosive decompression, when water vapour forms bubbles in body fluids due to a dramatic reduction in environmental pressure. [14]
When a diver holds their breath during an ascent the reduction in pressure will cause the gas to expand and the lungs will also have to expand to continue to contain the gas. If the expansion exceeds the normal capacity of the lungs, they will continue to expand elastically until the tissues reach their tensile strength limit, after which any increase in pressure difference between the gas in the lungs and the ambient pressure will cause the weaker tissues to rupture, releasing gas from the lungs into any permeable space exposed by the damaged tissue. This could be the pleural space between the lung and the chest walls, between the pleural membranes, and this condition is known as pneumothorax. The gas could also enter the interstitial spaces within the lungs, the neck and larynx, and the mediastinal space around the heart, causing interstititial or mediastinal emphysema, or it could enter the blood vessels of the venous pulmonary circulation via damaged alveolar capillaries, and from there reach the left side of the heart, from which they will be discharged into the systemic circulation. On the way out through the aorta the gas may be entrained in blood flowing into the carotid or basilar arteries. If these bubbles cause blockage in blood vessels, this is arterial gas embolism. Vascular obstruction and inflammation caused by gas bubbles causes end organ damage to most tissues. [15] Sufficient pressure difference and expansion to cause this injury can occur from depths as shallow as 1.2 metres (3.9 ft). [16]
Definitive diagnosis is difficult, as most of the signs and symptoms are common to several conditions and there are no specific tests for DCI. The dive history is important, if reliable, and the sequence and presentation of symptoms can differentiate between possibilities. Most doctors do not have the training and experience to reliably diagnose DCI, so it is preferable to consult a diving medicine specialist, as misdiagnosis can have inconvenient, expensive and possibly life-threatening consequences. Prior to 2000, there was a tendency to under-diagnose DCI, and as a result a number of cases did not get the treatment that could have produced a better result, while since 2000, there has been a swing to over-diagnosis, with consequent expensive and inconvenient treatments, and expensive inconvenient and risky evacuations that were not necessary. [2] The presence of symptoms of pneumothorax, mediastinal or interstitial emphysema would support a diagnosis of arterial gas embolism if symptoms of that condition are also present, but AGE can occur without symptoms of other lung overpressure injuries. Most cases of arterial gas embolism will present symptoms soon after surfacing, but this also happens with cerebral decompression sickness. [2]
Numbness and tingling are associated with spinal DCS, but can also be caused by pressure on nerves (compression neurapraxia). In DCS the numbness or tingling is generally confined to one or a series of dermatomes, while pressure on a nerve tends to produce characteristic areas of numbness associated with the specific nerve on only one side of the body distal to the pressure point. [2] A loss of strength or function is likely to be a medical emergency. A loss of feeling that lasts more than a minute or two indicates a need for immediate medical attention. It is only partial sensory changes, or paraesthesias, where this distinction between trivial and more serious injuries applies. [17]
Large areas of numbness with associated weakness or paralysis, especially if a whole limb is affected, are indicative of probable brain involvement and require urgent medical attention. Paraesthesias or weakness involving a dermatome indicate probable spinal cord or spinal nerve root involvement. Although it is possible that this may have other causes, such as an injured intervertebral disk, these symptoms indicate an urgent need for medical assessment. In combination with weakness, paralysis or loss of bowel or bladder control, they indicate a medical emergency. [17]
Almost all arterial gas embolism is avoidable by not diving with lung conditions which increase the risk and not holding the breath during ascent. These conditions will usually be detected in the diving medical examination required for professional divers. Recreational divers are not all screened at this level. Complete emptying of the lungs is not recommended in emergency swimming ascents as this is thought to increase the risk by collapsing small air passages and trapping air in parts of the lung. Rate of ascent is not usually an issue for AGE.
Decompression sickness is usually avoidable by following the requirements of decompression tables or algorithms regarding ascent rates and stop times for the specific dive profile, but these do not guarantee safety, and in some cases, unpredictably, there will be decompression sickness. Decompressing for longer can reduce the risk by an unknown amount. Decompression is a calculated risk where some of the variables are not well defined, and it is not possible to define the point at which all residual risk disappears. Risk is also reduced by reducing exposure to ingassing and taking into account the various known and suspected risk factors. Most, but not all, cases are easily avoided.
Treatment for the Decompression Sickness and the Arterial Gas Embolism components of DCI may differ significantly, but that depends mostly on the symptoms, as both conditions are generally treated based on the symptoms. [2] Refer to the separate treatments under those articles.
Urgency of treatment depends on the symptoms. Mild symptoms will usually resolve without treatment, though appropriate treatment may accelerate recovery considerably. Failure to treat severe cases can have fatal or long term effects. Some types of injuries are more likely to have long lasting effects depending on the organs involved. [2]
First aid is common for both DCS and AGE:
The prognosis of the DCS is generally favorable for patients with mild symptoms, given timely and appropriate treatment, and in excellent health before the dive. Symptoms may resolve within days after prompt administration of high-flow oxygen and rest. [15]
The outcome for cerebral arterial gas embolism largely depends on severity and the delay before recompression. Most cases which are recompressed within two hours do well. Recompression within six hours often produces improvement and sometimes full resolution. Delays to recompression of more than 6 to 8 hours are not often very effective, and are generally associated with delays in diagnosis and delays in transfer to a hyperbaric chamber. [18]
Xu et al. reported a 99.3% effectiveness rate of treating decompression illness with immediate recompression in a study of 5,278 cases across 2000-2010 in China. The initial symptom occurred within 6 hours after surfacing in 98.9% of cases. [19]
Long term complications can arise as end organ damage from air embolisms. In bones, dysbaric osteonecrosis leads to pathological fractures and chronic arthritis, particularly in the proximal femur, humerus, and tibia. In the brain and spinal cord, depending on the area and severity of damage there can be neurological deficits ranging from becoming comatose, having sensorimotor weakness, incontinence, and other effects. The lungs can develop pulmonary fibrosis. The pancreas, kidneys, and liver are also vulnerable, and reginal necrosis in the gastrointestinal tract can cause strictures leading to obstruction. [15]
Roughly 3 to 7 cases per 10,000 dives are diagnosed, of which about 1 in 100,000 dives are fatal. [2]
Decompression sickness is a medical condition caused by dissolved gases emerging from solution as bubbles inside the body tissues during decompression. DCS most commonly occurs during or soon after a decompression ascent from underwater diving, but can also result from other causes of depressurisation, such as emerging from a caisson, decompression from saturation, flying in an unpressurised aircraft at high altitude, and extravehicular activity from spacecraft. DCS and arterial gas embolism are collectively referred to as decompression illness.
An air embolism, also known as a gas embolism, is a blood vessel blockage caused by one or more bubbles of air or other gas in the circulatory system. Air can be introduced into the circulation during surgical procedures, lung over-expansion injury, decompression, and a few other causes. In flora, air embolisms may also occur in the xylem of vascular plants, especially when suffering from water stress.
Barotrauma is physical damage to body tissues caused by a difference in pressure between a gas space inside, or in contact with, the body and the surrounding gas or liquid. The initial damage is usually due to over-stretching the tissues in tension or shear, either directly by an expansion of the gas in the closed space or by pressure difference hydrostatically transmitted through the tissue. Tissue rupture may be complicated by the introduction of gas into the local tissue or circulation through the initial trauma site, which can cause blockage of circulation at distant sites or interfere with the normal function of an organ by its presence. The term is usually applied when the gas volume involved already exists prior to decompression. Barotrama can occur during both compression and decompression events.
In-water recompression (IWR) or underwater oxygen treatment is the emergency treatment of decompression sickness (DCS) by returning the diver underwater to help the gas bubbles in the tissues, which are causing the symptoms, to resolve. It is a procedure that exposes the diver to significant risk which should be compared with the risk associated with the available options and balanced against the probable benefits. Some authorities recommend that it is only to be used when the time to travel to the nearest recompression chamber is too long to save the victim's life; others take a more pragmatic approach and accept that in some circumstances IWR is the best available option. The risks may not be justified for case of mild symptoms likely to resolve spontaneously, or for cases where the diver is likely to be unsafe in the water, but in-water recompression may be justified in cases where severe outcomes are likely if not recompressed, if conducted by a competent and suitably equipped team.
Dysbarism refers to medical conditions resulting from changes in ambient pressure. Various activities are associated with pressure changes. Underwater diving is the most frequently cited example, but pressure changes also affect people who work in other pressurized environments, and people who move between different altitudes.
Diving medicine, also called undersea and hyperbaric medicine (UHB), is the diagnosis, treatment and prevention of conditions caused by humans entering the undersea environment. It includes the effects on the body of pressure on gases, the diagnosis and treatment of conditions caused by marine hazards and how relationships of a diver's fitness to dive affect a diver's safety. Diving medical practitioners are also expected to be competent in the examination of divers and potential divers to determine fitness to dive.
Diving disorders, or diving related medical conditions, are conditions associated with underwater diving, and include both conditions unique to underwater diving, and those that also occur during other activities. This second group further divides conditions caused by exposure to ambient pressures significantly different from surface atmospheric pressure, and a range of conditions caused by general environment and equipment associated with diving activities.
The decompression of a diver is the reduction in ambient pressure experienced during ascent from depth. It is also the process of elimination of dissolved inert gases from the diver's body which accumulate during ascent, largely during pauses in the ascent known as decompression stops, and after surfacing, until the gas concentrations reach equilibrium. Divers breathing gas at ambient pressure need to ascend at a rate determined by their exposure to pressure and the breathing gas in use. A diver who only breathes gas at atmospheric pressure when free-diving or snorkelling will not usually need to decompress. Divers using an atmospheric diving suit do not need to decompress as they are never exposed to high ambient pressure.
Hypobaric decompression is the reduction in ambient pressure below the normal range of sea level atmospheric pressure. Altitude decompression is hypobaric decompression which is the natural consequence of unprotected elevation to altitude, while other forms of hypobaric decompression are due to intentional or unintentional release of pressurization of a pressure suit or pressurized compartment, vehicle or habitat, and may be controlled or uncontrolled, or the reduction of pressure in a hypobaric chamber.
To prevent or minimize decompression sickness, divers must properly plan and monitor decompression. Divers follow a decompression model to safely allow the release of excess inert gases dissolved in their body tissues, which accommodated as a result of breathing at ambient pressures greater than surface atmospheric pressure. Decompression models take into account variables such as depth and time of dive, breathing gasses, altitude, and equipment to develop appropriate procedures for safe ascent.
Decompression in the context of diving derives from the reduction in ambient pressure experienced by the diver during the ascent at the end of a dive or hyperbaric exposure and refers to both the reduction in pressure and the process of allowing dissolved inert gases to be eliminated from the tissues during this reduction in pressure.
Decompression theory is the study and modelling of the transfer of the inert gas component of breathing gases from the gas in the lungs to the tissues and back during exposure to variations in ambient pressure. In the case of underwater diving and compressed air work, this mostly involves ambient pressures greater than the local surface pressure, but astronauts, high altitude mountaineers, and travellers in aircraft which are not pressurised to sea level pressure, are generally exposed to ambient pressures less than standard sea level atmospheric pressure. In all cases, the symptoms caused by decompression occur during or within a relatively short period of hours, or occasionally days, after a significant pressure reduction.
Haldane's decompression model is a mathematical model for decompression to sea level atmospheric pressure of divers breathing compressed air at ambient pressure that was proposed in 1908 by the Scottish physiologist, John Scott Haldane, who was also famous for intrepid self-experimentation.
Hyperbaric treatment schedules or hyperbaric treatment tables, are planned sequences of events in chronological order for hyperbaric pressure exposures specifying the pressure profile over time and the breathing gas to be used during specified periods, for medical treatment. Hyperbaric therapy is based on exposure to pressures greater than normal atmospheric pressure, and in many cases the use of breathing gases with oxygen content greater than that of air.
The physiology of decompression is the aspect of physiology which is affected by exposure to large changes in ambient pressure. It involves a complex interaction of gas solubility, partial pressures and concentration gradients, diffusion, bulk transport and bubble mechanics in living tissues. Gas is breathed at ambient pressure, and some of this gas dissolves into the blood and other fluids. Inert gas continues to be taken up until the gas dissolved in the tissues is in a state of equilibrium with the gas in the lungs, or the ambient pressure is reduced until the inert gases dissolved in the tissues are at a higher concentration than the equilibrium state, and start diffusing out again.
A built-in breathing system is a source of breathing gas installed in a confined space where an alternative to the ambient gas may be required for medical treatment, emergency use, or to minimise a hazard. They are found in diving chambers, hyperbaric treatment chambers, and submarines.
Inner ear decompression sickness, (IEDCS) or audiovestibular decompression sickness is a medical condition of the inner ear caused by the formation of gas bubbles in the tissues or blood vessels of the inner ear. Generally referred to as a form of decompression sickness, it can also occur at constant pressure due to inert gas counterdiffusion effects.
The US Navy has used several decompression models from which their published decompression tables and authorized diving computer algorithms have been derived. The original C&R tables used a classic multiple independent parallel compartment model based on the work of J.S.Haldane in England in the early 20th century, using a critical ratio exponential ingassing and outgassing model. Later they were modified by O.D. Yarborough and published in 1937. A version developed by Des Granges was published in 1956. Further developments by M.W. Goodman and Robert D. Workman using a critical supersaturation approach to incorporate M-values, and expressed as an algorithm suitable for programming were published in 1965, and later again a significantly different model, the VVAL 18 exponential/linear model was developed by Edward D. Thalmann, using an exponential ingassing model and a combined exponential and linear outgassing model, which was further developed by Gerth and Doolette and published in Revision 6 of the US Navy Diving Manual as the 2008 tables.
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