When considering a return to diving after an episode of DCS, it is important to consider the following:
Has there been a good response to treatment?
Are there any residual symptoms and signs attributable to DCS?
Was the development of DCS consistent with the diving exposure?
Does the individual have an increased susceptibility to DCS?
Was there any evidence of associated pulmonary barotrauma?
Evidence supports the existence of bubbles for some days or weeks after DCS and recompression therapy – a function of the slower rate of gas elimination, especially in the presence of bubbles. For this reason, the authors of this text recommend a minimum period of 4 weeks before a return to diving. Bubble micronuclei may exist indefinitely within the tissues only to re-expand with an exposure to an inert gas load.
Patients with incomplete recovery after recompression should be followed up clinically with appropriate investigations, e.g. brain imaging techniques, electroencephalography (EEG), bone scans and neuropsychological testing as indicated by the clinical condition.
If there has been a less than complete recovery following neurological DCS, the recommendation of the authors of this text is that the individual not dive again. Autopsy evidence suggests that DCS may involve greater areas of the brain and spinal cord than are detected clinically – a characteristic of some degree of neurological redundancy. A further insult may result in this subclinical damage extending to become clinically evident. Therefore, the second episode of neurological DCS may result in a significantly worse outcome.
If the episode of DCS occurs after a relatively trivial exposure, a cause for this increased susceptibility should be actively sought (e.g. pulmonary barotrauma, patent foramen ovale). Evidence of pulmonary barotrauma (see Chapter 6) usually renders the individual permanently unfit to dive.
Many episodes of DCS result from a complete disregard for decompression schedules or from simply stretching accepted computer algorithms to their limits. Rapid and frequent ascents and multiday repetitive diving are commonly reported. Before a return to diving, the patient with DCS should be counseled on safe diving practices. Diving according to published dive tables (e.g. the PADI tables) is now exceedingly rare, and almost all diving is controlled by a personal diving computer. Although greeted with some initial skepticism by dive physicians, these computers do not seem to have been associated with a higher incidence of DCS – if anything, quite the reverse, with DCS numbers falling across most jurisdictions.
Safe diving practices
Use a decompression schedule that has been tested and has a known and acceptable risk of DCS (e.g. Canadian Defence and Civil Institute of Environmental Medicine [DCIEM] tables; see Appendix A) or a reputable personal diving computer.
Add a depth/time penalty for future diving; i.e. for a dive to 16 metres for 35 minutes use the decompression limits for a 40-minute, 18-metre dive. With a computer, stay well within the no decompression limit rather than dive to that limit.
Restrict diving to two dives a day, with a long surface interval.
Have a rest day after each 3 days of diving.
Perform slow ascent rates.
Incorporate a ‘safety stop’ of 3 to 5 minutes at 3 to 5 metres on every dive.
Ensure conservative flying after any diving exposure.
Consider substituting nitrox (oxygen enriched air) for air, but dive according to the air tables.
There is a lack of good scientific data on when it is safe to fly or ascend to altitude following an episode of DCS. Recommendations vary from 24 hours to 42 days. The bubble micronuclei discussed earlier may expand with altitude exposure, with a resultant return of symptoms. Because many diving destinations are in remote tropical areas, divers with DCS are usually very reluctant and financially inconvenienced if they cannot return home for 4 to 6 weeks, so this is a very real practical problem.
It is the policy of the authors of this text to recommend to these divers that they delay flying or ascending to altitude for 2 weeks if possible, with a preferred minimum of 1 week. These times should be extended for divers with continuing symptoms after recompression.
In rare situations one may attempt to remove asymptomatic bubbles and micronuclei by exposing the symptom-free diver to a few 2-hour sessions of breathing 100 per cent oxygen, before flying, and a further possibility is to charter an aircraft whose cabin pressures are kept at 1 ATA (not within many people’s capability!).
General medical treatment is required during the recompression sessions. Patients should not be left unattended in RCCs, particularly while they are breathing increased oxygen concentrations.
First aid and resuscitation techniques are often required, as are accurate clinical assessments – and for these reasons it is desirable to have a trained medical attendant in the chamber. Most hospital-based hyperbaric facilities require their hyperbaric workers to have undergone a formal training program. It is necessary to consider the possibility that DCS may occur in the attendants, and hyperbaric attendants have an entire Australian Standard devoted to ensuring that facilities are aware of appropriate safety and training for these workers13. It is embarrassing to produce DCS in attendants during recompression therapy.
The advantages of oxygen over air tables include increasing nitrogen elimination gradients, avoiding extra nitrogen loads, increasing oxygenation to tissues, decreasing the depths required for the reduced exposure time and improving overall therapeutic efficiency. The same caveats about organization, resources and sea conditions are applicable when comparing underwater air and underwater oxygen treatment.
Minimum requirements for the safe conduct of in-water oxygen tables Equipment
At least one G-sized (7000 litres) oxygen cylinder – medical grade.
Regulator and hoses (minimum 12 metres – marked in 1-metre intervals) rated as ‘oxygen-safe’ and maintained appropriately.
Suitable method for weighting diver and attendant to avoid unwanted changes in depth.
Hookah air supply for attendant diver.
Suitable diving platform (boat or wharf) above column of water to >9-metre depth.
Appropriate thermal protection for prolonged immersion.
A suitable communication system with divers.
Appropriately trained individuals to oversee the procedures.
Attendant diver (breathing air).
Suitably trained attendant(s) to ensure appropriate decompression rate and gas supply.
Ability of the patient diver to be safely immersed for the duration of the table (e.g. not having seizures or unconscious).
Protected site with calm water.
Freedom from unacceptable tidal fluctuation and current.
Water temperature compatible with thermal protection available.
Beginning in 1970, this option has been applied to the underwater treatment of DCS. The procedures were developed in response to an urgent need for management of cases in remote localities – remote in both time and distance from hyperbaric facilities. As a result of the success of this treatment, and its ready availability, it is now practised even when experts are not available to supervise it.
The physiological principles on which this treatment is based are well known and not contentious, although the indications for treatment have caused some confusion. As for conventional oxygen therapy tables, underwater oxygen was first applied mainly for minor cases of DCS, but it was subsequently found to be of considerable value in serious cases.
The techniques and equipment for underwater oxygen therapy are designed to make for safety, ease and ready availability, even in medically unsophisticated countries. Although accurate estimates are problematic, it is likely this approach is now in widespread use in the Pacific Islands and remote parts of Australia.
Hawaiians have included a deep air ‘dip’ before underwater oxygen treatment, in an attempt to force bubbles back into solution or to allow bubbles trapped in arteries to transfer to the venous system.
Oxygen is supplied at maximum depth of 9 metres from a surface supply. Ascent is commenced after 30 minutes in mild cases, or 60 minutes in severe cases, if significant improvement has occurred. These times may be extended for another 30 minutes if there has been no improvement. The ascent is at the rate of 12 minutes/metre. After surfacing, the patient should be given periods of oxygen breathing, interspersed with air breathing, usually on a 1 hour on, 1 hour off basis, with respiratory volume measurements and chest x-ray examination if possible.
No equipment should be used with oxygen unless it is assessed ‘oxygen safe’ or if it is contaminated, dirty or lubricated with oil.
An air breathing diver attendant should always be present, and the ascent should be controlled by the surface tenders. The duration of the three tables is 2 hours 6 minutes, 2 hours 36 minutes and 3 hours 6 minutes. The treatment can be repeated twice daily, if needed.
The underwater oxygen treatment table is not meant to replace formal recompression therapy in chambers. It is an emergency procedure, able to be applied with equipment usually found in remote localities, and is designed to reduce the many hazards associated with conventional underwater air treatments. The customary supportive and pharmacological adjuncts to the treatment of recompression sickness should still be used, if available, and the superiority of experienced personnel and comprehensive hyperbaric facilities is not being challenged. Underwater oxygen treatment is considered as a first aid regimen, not superior to portable RCCs, but sometimes surprisingly effective and rarely, if ever, detrimental.
The relative value of proposed first aid regimens (underwater oxygen, underwater heliox, an additional deep descent and surface oxygen treatment) needs to be clarified.
Use of Underwater Oxygen Treatment
Because this treatment is applied in remote localities, many cases are not well documented. Twenty-five cases were well supervised before this technique increased suddenly in popularity. Two such cases are described (Case Report 13.3 and Case Report 13.4).
CASE REPORT 13.3: A 68-year-old male salvage diver performed two dives to 30 metres for 20 minutes each, with a surface interval of 1.5 hours, while searching for the wreck of HMS Pandora about 100 miles from Thursday Island in the Torres Strait.
No decompression staging was possible, allegedly because of the increasing attentions of a tiger shark. A few minutes after surfacing, the diver developed paraesthesiae, back pain, progressively increasing incoordination and paresis of the lower limbs.
Two attempts at underwater air recompression were unsuccessful when the diving boat returned to its base moorings. The National Marine Operations Centre was contacted for assistance.
It was about 36 hours after the dive before the patient was flown to the regional hospital on Thursday Island.
Both the Air Force and the Navy had been involved in the organization, but because of very hazardous air and sea conditions, and very primitive airstrip facilities, another 12 hours would be required before the patient could have reached an established recompression centre (distance, 3000 km [2000 miles]).
On examination at Thursday Island, the patient was unable to walk, with evidence of both cerebral and spinal involvement. He had marked ataxia, slow and slurred speech, intention tremor, severe back pain, generalized weakness, difficulty in micturition, severe weakness of lower limbs with impaired sensation, increased tendon reflexes and equivocal plantar responses.
An underwater oxygen unit was available on Thursday Island for use by the pearl divers, and the patient was immersed to 8 metres of depth (the maximum depth off the wharf). Two hours were allowed at that lesser depth, and the patient was then decompressed. There was total remission of all symptoms and signs, except for small areas of hypoaesthesia on both legs.
CASE REPORT 13.4: A 23-year-old female sports diver was diving with a 2000-litre (72 cubic feet) scuba cylinder in the Solomon Islands (nearest recompression chamber was 3500 km away and prompt air transport was not available); the dive depth was 34 metres and the duration approximately 20 minutes, with 8 minutes of decompression. Within 15 minutes of surfacing, she developed respiratory distress, then numbness and paraesthesiae, very severe headaches, involuntary extensor spasms, clouding of consciousness, muscular pains and weakness, pains in both knees and abdominal cramps. The involuntary extensor spasms recurred every 10 minutes or so.
The patient was transferred to the hospital, where neurological DCS was diagnosed, and she was given oxygen via a facemask for 3 hours without significant change. During that time an underwater oxygen unit was prepared, and the patient was accompanied to a depth of 9 metres (30 feet) off the wharf. Within 15 minutes she was much improved, and after 1 hour she was asymptomatic. Decompression at 12 minutes/meter was uneventful, and a commercial aircraft subsequently flew the patient to Australia.
There have now been many hundreds of cases of underwater air and underwater oxygen treatments recorded12. Apart from the relative paucity of complications, the major lesson learned was that prompt re-immersion of the diver allowed shorter duration of treatment and complete resolution of DCS manifestations. Many divers so treated resumed diving within days.
By far the most traditional of the non-chamber treatments of DCS is underwater recompression therapy. In this situation the water, instead of an RCC, exerts the pressure. Air supply is usually from compressors sited on the diving boat. Although this treatment is frequently disparaged, it has often been the only therapy available to severely injured divers, and it has had many successes, most of which have never been reported. This was certainly so in those remote localities such as Northern Australia, in the pearl fishing areas, where long periods were spent under water and standard diving equipment was used.
The failure of DCS to respond to recompression therapy is often related directly to the delay in treatment. Sometimes chambers are not readily available. For this reason, underwater air recompression was effectively used in Hawaii, with good results, within minutes of symptoms developing. This was also the experience of professional shell divers of Australia, at least until underwater oxygen therapy became available.
Despite the value of underwater air recompression therapy, many problems may be encountered, and this treatment should not be entered into without appropriate planning and resources.
Most amateurs or semi-professionals do not carry the compressed air supplies or compressor facilities necessary for the extra decompression. Most have only scuba cylinders or simple portable compressors that will not reliably supply divers (the patient and the attendant) for the depths and durations required. Environmental conditions are not usually conducive to underwater treatment. Often the depths required can be achieved only by returning to the open ocean. The advent of night, inclement weather, rising seas, tiredness and exhaustion and boat safety requirements make the return to the open ocean a very serious decision. Because of the considerable depth required, hypothermia becomes likely. Seasickness in the injured diver, the diving attendants and the boat tenders is a significant problem. Nitrogen narcosis produces added difficulties in the diver and the attendant.
The treatment often has to be aborted because of these difficult circumstances, thereby producing DCS in the attendants and aggravating it in the diver. Although in the absence of an RCC it may be the only treatment available to prevent death or severe disability, it should never be undertaken without careful consideration of the resources available and the environmental conditions.
General medical treatment is required. This will vary according to the manifestations.
Previously a head-down or Trendelenburg position was recommended for patients suspected of having CAGE to prevent re-embolization. The head-down position was originally used to divert emboli from the brain, given that the bubbles would preferentially rise to the higher vessels through the effect of buoyancy. This practice is no longer recommended because the increased venous pressure may cause increasing intracranial pressure and decreasing cerebral perfusion, thus aggravating the neurological disorder. In addition, increased venous return from the lower limbs may increase the possibility of paradoxical gas embolism through a patent foramen ovale. For the same reasons, the legs should not be raised. The patient should be supine or in the coma position and advised not to strain or perform Valsalva manoeuvres.
The haematological effects of DCS may aggravate dehydration from immersion and cold-induced diuresis. This increases blood viscosity and reduces blood flow to the major organs. Rehydration is important, whether orally or intravenously, with a target of urinary output of 1 to 2 ml/kg per hour. Patients with serious cases should be intravenously hydrated with non–sugar-containing electrolyte fluids.
Hartman’s solution, Ringer’s lactate or physiological saline is preferable until the serum electrolytes and plasma osmolarity can be determined. Intravenous colloids are rarely used but may be of value, and low-molecular-weight dextran in saline has been used in the past to prevent rouleaux formation, expand the blood volume rapidly and reduce the likelihood of intravascular coagulation. Problems with using colloids include fluid overload, anaphylaxis, renal failure and bleeding – to date no advantage over crystalloids has been reported.
Glucose and other carbohydrate fluids must be avoided because cerebral injury may be exacerbated by hyperglycemia.
Urinary catheterization will be required for most patients with spinal DCS, as will careful skin and body maintenance.
During treatment, vital signs should be monitored, including an electrocardiogram (ECG), and this should not cause difficulties in most chambers.
Surface oxygen administration
One area that has been relatively overlooked recently is the administration of oxygen at normobaric pressure.
Albert R. Behnke – July 1990
The administration of 100 per cent oxygen will often relieve symptoms, if sometimes only temporarily, and it may reduce the likelihood that other symptoms will develop (a Divers Alert Network report suggests up to 50 per cent symptom resolution)5. This approach is particularly of value before subjecting the patient to altitude.
Oxygen has been demonstrated to:
Enhance inert gas elimination.
Prevent venous gas emboli, as detected by Doppler.
Reduce the size of inert gas bubbles.
Prevent development of DCS.
Treat developed DCS.
Prevent recurrences of DCS.
Possibly improve oxygenation of damaged tissues.
In one series6, surface oxygen was shown to be an effective treatment for DCS. Although this was a highly selected population, the series did demonstrate the value of surface oxygen, given early and for some hours, in remote areas where recompression facilities are not readily available. When it is used in transit, the DAN report of 1996 suggested that oxygen will result in some DCS cures and a reduction of DCS sequelae after recompression5.
Although the value of administering 100 per cent oxygen with intermittent air breaks is unquestioned, problems do arise with inexperienced personnel. Commonly, an inadequate mask is used. Most available masks do not readily produce 40 per cent oxygen in the inspiratory gas even at very high flows. Other risks involve the inflammable nature of oxygen and the contribution to oxygen toxicity.
Some diving physicians prefer to use 100 per cent oxygen after recompression therapy to prevent the recurrence of DCS symptoms and avoid repeated treatments; however this practice is now unusual, and current practice tends toward repeated treatments for residual symptoms.
Many classes of drugs have been tried to improve both symptoms and outcome from DCS. Few have stood the test of time. Drug use has often been based on the results of animal experimentation using extreme exposures and/or very rapid decompressions, and therefore of limited applicability. Some agents may be of value if they are administered before the actual decompression accident. There is some logic in the use of pharmacological agents to reduce, for example, platelet aggregation, microthrombi and neurological oedema. Other drugs proposed include those that increase tissue perfusion and/or expedite inert gas elimination. The clinical value of most drugs is less than remarkable.
Lidocaine (formerly lignocaine in the United Kingdom) is recommended with caution, in the same dosage as used for cardiac dysrrhythmias, for severe cerebral and spinal DCS. There have been a couple of hopeful case reports and some experimental evidence to support this recommendation. A beneficial effect of lidocaine has been demonstrated in animal models of air embolism7,8, and this benefit seemed confirmed when the drug was associated with a cerebral protective effect when it was used prophylactically in patients undergoing left-sided heart valve surgery9. Later studies did not confirm these findings, however, and many practitioners have abandoned this approach after unsuccessful use in their own practice.
NSAIDS have been advocated because of both their inhibitory effect on platelet aggregation and their wider anti-inflammatory and analgesic actions. On the one hand, the effect on platelet activation may modify the activation of the coagulation pathway by bubbles if given early enough after diving, and on the other, NSAIDS will temporarily relieve many of the symptoms of DCS and may hasten the resolution of those symptoms following recompression. The one double-blind randomized controlled study of these agents suggested that the results of recompression were similar with or without the NSAID tenoxicam, but on average one less recompression session was required10. Currently, many diving physicians recommend the adjunctive use of an NSAID for 5 to 7 days, beginning during or after the first recompression table.
There is evidence that antiplatelet agents such as aspirin or dipyridamole, when given prophylactically, modify platelet action following decompression. However, there are no controlled studies to support the use of these drugs in the treatment of DCS. There are more arguments against the use of aspirin than for it, with the increased likelihood of aggravating inner ear or spinal cord haemorrhagic disease. Aspirin has a variety of other negative influences on susceptible individuals, such as bronchospasm, and there are reports in animal studies linking aspirin with an increased risk of dysbaric osteonecrosis.
Aminophylline, and probably other sympathomimetic drugs, may be contraindicated in dysbaric diving accidents. It results in the dilatation of the pulmonary vasculature and a profuse release of bubbles trapped in the pulmonary circulation into the systemic circulation.
Heparin and coumarin derivatives have been advocated because of their effect on the coagulation pathway. They were said to be indicated in cases of disseminated intravascular coagulation that had no evidence of systemic infarction and bleeding. These drugs are now rarely, if ever, used in DCS. Correction of specific coagulation defects seems a more logical approach to the rare complication of disseminated intravascular coagulation in DCS. It can be harmful following the haemorrhagic disorders of the spinal cord and inner ear and other DCS manifestations.
The use of corticosteroids has previously been justified on the belief that this class of drugs may reduce cerebral oedema and modify the inflammatory process. This experience came not from treating DCS but from treating cerebral oedema associated with traumatic and vascular brain injury. Just as the use of corticosteroids has been discredited in brain injury, there are no definitive studies to support its use in DCS-related brain injury.
Although high-dose methylprednisolone initiated within 8 hours of traumatic spinal injury resulted in a significantly greater neurological recovery in a large randomized trial (the second National Acute Spinal Cord Injury Study [NASCIS 2]11), there was no clinically significant improvement in function, and this practice has been abandoned because of serious side effects in some cases. In DCS there are no published trials supporting methylprednisolone use, and corticosteroids are no longer recommended. Some of the disadvantages of include severe sepsis, hemorrhage, hyperglycemia, anaphylaxis and an increased susceptibility to oxygen toxicity.
Diazepam (Valium) has been recommended for use in DCS. It may be of considerable value in reducing the incidence and degree of oxygen toxicity, especially in patients with serious cases who require extensive exposure to oxygen under pressure. It may also be useful in the occasional patient with a toxic-confusional state as a result of involvement of the neurological system from either DCS or CAGE. These patients can be very difficult to handle in the RCC, and they may not tolerate the oronasal mask without an anxiolytic. The dosage must be regulated according to the clinical state of the patient, but otherwise a 10-mg initial dose may be supplemented by 5 mg every few hours, without causing any significant drowsiness, respiratory depression or interference with the clinical picture.
Vestibular DCS may require suppressants, such as diazepam, to help control vertigo.
These fascinating compounds have been developed in the efforts to produce an artificial blood substitute and to enable liquid respiration in patients with very poor lung function when they are acutely unwell in an intensive care setting. These compounds have the ability to absorb enormous volumes of oxygen and nitrogen and present several exciting possibilities for use in diving medicine. At this time, these agents are experimental only, and the authors of this text are not aware of any reported use in diving humans. This is likely to change, however, because several groups are interested in further investigation.
Potential uses include the treatment of DCS, in which the intravenous administration of a modest volume of perfluorocarbon may rapidly denitrogenate the tissues and eliminate any intravascular bubbles. Also of interest are the potential to increase the blood oxygen-carrying capacity with the administration of modest amounts of increased oxygen administration, the prevention of DCS by administration before diving and the extension of deep diving limits by the utilization of liquid breathing techniques (see the famous sequence in the movie The Abyss).
Although recompression treatment of CAGE traditionally involved a deep excursion to 50 metres followed by a standard USN Table 6, diving physicians now use a standard 18-metre oxygen table such as USN Table 6.
If the CAGE is not caused by DCS and is a manifestation of pulmonary barotrauma,
then the following other factors should be considered:
The possibility of little or no inert gas loading in the tissues (thus making long saturation type treatments inappropriate and brief deep excursions more valuable).
The presence of pulmonary tissue damage.
The possibility of pneumothorax.
Fitness for further diving and its investigations.
The fact that some authority has promulgated a therapeutic table does not make it effective, and there have been many modifications and deletions made to these tables during the professional lives of these authors.
As a good general rule, if symptoms recur during treatment, both the recompression schedule and the clinical management should be questioned. The physician should ensure that there has been adequate recompression and supportive therapy, including correct positioning, rehydration and so forth. The diagnosis should be reassessed, considering the following:
Pulmonary barotrauma and each of its clinical manifestations (see Chapter 6).
Complications of DCS, affecting target organs.
Non-diving general medical diseases.
Nevertheless, patients with DCS do sometimes deteriorate during recompression therapy. The composition of the breathing mixture should be confirmed, as should the efficiency of the mask seal.
One air table (USN 4, RN 54) frequently caused DCS in attendants who did not even have a nitrogen load to start with. It is difficult to understand how it could then improve patients at the shallow stops. Oxygen is now used by both patient and attendant from 18 metres to prevent this problem. The short air embolism Table 5A, which many of us believed to be a contributor to deaths during treatment, has been removed from the US Navy Manual.
If similar and significant symptoms recur, they must be presumed to represent a reexpansion of a bubble, which was not completely removed, and treated accordingly.
Occasionally, there may be other explanations, such as:
The inflammatory tissue reaction to the bubble.
Lipid, platelet or fibrin deposits or emboli.
Redistribution of gas emboli.
Although redistribution could be expected to respond to recompression therapy, it would be a great coincidence if it were to reproduce the same symptoms as the original lesion.
Recurrences of the original symptoms or the development of other serious symptoms should be seen as resulting from inadequate treatment or caused by aggravation of the problem by re-exposure to nitrogen at depth or on the surface. Recurrence of symptoms requires surface oxygen (if mild), hyperbaric oxygenation or a conventional therapy table.
Paraesthesia and other symptoms developing while undergoing recompression therapy may reflect the development of oxygen toxicity (see Chapter 17) and therefore are not necessarily an indication to extend the therapy.
It is not necessary to recompress repeatedly for minor and fluctuating symptoms, unless these symptoms have some ominous clinical significance. Minor residual musculoskeletal or peripheral nerve disease is very common, and chasing these symptoms to obtain a complete ‘cure’ becomes demoralizing and exhausting for both patient and attendants. It has become common practice to follow a formal recompression table with an ‘oxygen soak’ (typically a 9- to 14-metre oxygen table for 1 to 2 hours) on the following day, to reduce the incidence of minor persistent symptoms. It is probable that most of these symptoms are transient and more anxiety provoking than functionally important.
With spinal cord or cerebral damage, it is common practice to continue with intermittent hyperbaric oxygen therapy until all subjective and objective improvement has ceased. These authors use standard oxygen tables, as described earlier, on a daily schedule. Other regimens may be applied, but the use of repeated diving therapeutic tables, such as extended Table 6 (USN) with its hyperbaric ‘air breaks’, is illogical and has increased complications to both attendant and patient. It is very unusual for even a patient with serious case to receive more than five or six treatment tables.
Both recompression and altitude exposure alter blood gases (oxygen, carbon dioxide and pH) and may affect these minor symptoms, presumably by affecting marginal ischaemia or nerve irritability from myelin sheath damage. Patients should be reassured that such minor symptoms – often persisting for weeks to months after DCS – are not uncommon and do not require intervention.
No-one who has seen the victim of compressed air illness, gravely ill or unconscious, put back into a chamber and brought back to life by the application of air pressure, will forget the extraordinary efficiency of recompression, or will be backward in applying it to a subsequent case of illness.
—— Robert Davis, 1935
This chapter deals with the definitive management of decompression sickness (DCS). For information on the first aid management of the diving accident victim, see Chapter 48. DCS takes many forms, and although recompression is often the treatment of choice, the optimal treatment varies with circumstance. Consider the following cases:
Saturation DCS as the diver very slowly approaches the surface.
The same diver subjected to an extreme excursion from saturation.
Inner ear DCS after helium breathing.
A cerebrovascular incident after a short bounce to 50 metres.
A joint bend developing hours after a long shallow dive.
A dramatic crisis involving pulmonary, haematological and neurological systems after explosive decompression from saturation or from gross omitted decompression.
Respiratory symptoms followed by the rapid development of paraplegia.
Mild joint pain DCS after a shallow dive in a diver who has remained well within the established tables.
These cases cannot be managed optimally by a single regimen, yet the approach to their management is similar.
The guiding principle of treatment for DCS is recompression followed by a slow decompression back to atmospheric pressure, with the patient hopefully devoid of symptoms and signs. Oxygen breathing is used to increase the washout of inert gas and promote bubble resolution. Fluid replacement is recommended because divers are often dehydrated as a consequence of cold water diuresis, seasickness and bubble-induced fluid shifts out of the intravascular compartment. Many adjuvant therapies have been tried, most with little evidence of effect, including antiplatelet agents, corticosteroids, heparin and dextrans, whereas non-steroidal anti-inflammatory drugs (NSAIDs) and lidocaine have shown some promise.
If left untreated, the pain of joint DCS resolves spontaneously, usually within days or weeks. There have been reports of spontaneous resolution of cases of neurological DCS without recompression therapy; however, most patients require treatment or remain symptomatic. It is not known whether untreated DCS increases the likelihood of dysbaric osteonecrosis or subclinical neurological injury.
Care should be taken to avoid circumstances that will aggravate the ‘bubbling’ of DCS. These include excessive movement of the patient, exposure to altitude and the breathing of certain gases (e.g. nitrous oxide anesthesia).
Appropriate manipulation of the depth-time profile as discussed in the preceding section on decompression planning is obviously important in managing the risk of DCS. In addition, certain known or suspected risk factors for DCS, some of which have already been mentioned, can be manipulated or managed to reduce risk further.
Patent foramen ovale
The role of the patent foramen ovale (PFO) in the pathophysiology of DCS is discussed in Chapter 10, in which it was pointed out that PFO appears associated with an increased risk of cerebral, spinal, vestibulocochlear and cutaneous DCS. The most plausible explanation for this increase in risk is that a right-to-left shunt allows VGE to enter the arterial circulation, and these small bubbles can then distribute widely in the body and cause harm, as previously described. The degree of shunt facilitated by the PFO has consistently been found to be significant; with large and spontaneous shunts being important and very small shunts seemingly unimportant. The crucial question is this: ‘How should this knowledge be applied to reducing risk of DCS?’
One obvious strategy would be to screen divers for PFO after an episode of neurological, inner ear or cutaneous DCS and, possibly, to repair large PFOs in divers who wish to continue diving. Another more radical strategy would be to screen all prospective divers before entry to the sport. Many divers have enthusiastically embraced such ideas. When participants on Internet diving discussion forums report an episode of DCS, a chorus of advice to check for a PFO inevitably follows, even if the event involved a form of DCS that has never been associated with a PFO (e.g. musculoskeletal DCS). However, decisions to screen divers for PFO or to repair any lesion that is discovered are not straightforward.
As pointed out in Chapter 10, PFO is very common (around 30 per cent of divers or diving candidates can be expected to have one) and so is the formation of VGE after diving; yet cerebral, spinal and inner ear DCS cases remain rare. There are clearly factors beyond merely having a PFO and producing venous bubbles that are involved in the chain of events leading to the relevant forms of DCS, and at this time we are not certain what they are. Screening all prospective divers by using an expensive invasive test (see Chapter 10), which would detect the target lesion in about 30 per cent of subjects (and potentially exclude them from diving), with the aim of preventing an event that occurs perhaps once in 10 000 dives (even in an unscreened population), is neither sensible nor justified.
In contrast, it may be appropriate to test divers who have had one of the relevant forms of DCS, particularly if there have been multiple events or if the event(s) followed dives that seem unprovocative in terms of decompression stress. It is also inevitable that the diving physician will be approached by enthusiasts who have never had DCS but who are aware of the association of serious DCS with PFO and who wish to be tested for this heart condition. Referring for testing may be appropriate under these circumstances, but the following points should always be explained to the diver before testing is undertaken.
The bubble contrast echocardiographic test is relatively safe, but there are some risks. Transient symptoms of cerebral arterial gas embolism have been reported following tests with strongly positive results for right-to-left shunt.
The test result is likely to be positive in at least 30 per cent of cases (or more depending on the context), and the diver may then have some difficult options to choose from (see later). If the diver does not intend to take one of those options, then there is little practical point in having the test.
A positive test result after an episode of DCS does not guarantee that the PFO was the cause of the DCS.
As a corollary to point 3, repairing a PFO discovered after an episode of DCS does not guarantee that another event will not occur.
A negative test result does not mean that the diver is ‘resistant’ to DCS, as many seem to believe.
If screening for a PFO is undertaken and the result is positive, the response should take account of the size or shunting behaviour of the lesion. There are data suggesting that a grade 1 PFO (see Chapter 10) is of little or no consequence and can be ignored. In contrast, a spontaneously shunting (grade 3) PFO is likely to confer increased risk and merits a response.
To mitigate the risk implied by a large PFO, the diver effectively has three options: cease diving, modify diving practice in an attempt to reduce VGE production or have the PFO repaired. The option to cease diving is self-explanatory and unpalatable to many. Modification of diving practice to reduce VGE production is an imprecise business, but the general aim is to reduce the provocation for bubble formation on arrival at the surface. Options for achieving this include diving well within no decompression limits, ensuring that safety stops are completed, using nitrox (see Chapter 62) but planning the dive as though using air and, if decompression diving using gradient factors, lowering the GF-High to force longer shallow decompression stops at the end of the dive. Breathing oxygen during those stops would also help. In a related vein, advice could also include avoidance of any heavy exercise that could open a pulmonary shunt, or manoeuvres that could encourage right-to-left shunting across a PFO (e.g. lifting or straining), over the typical 2-hour period of maximum VGE formation after a dive.
Having a PFO repaired involves the use of a transvenous catheter technique that leaves an occluder device across the atrial septum. It is an effective treatment, although repair may be incomplete in up to 10 per cent of cases. It is also an invasive procedure, and like many medical procedures considered ‘safe’, it nevertheless has significant risks, some of which are life-threatening. These risks include formation of blood clots on the device, loosening of the occluder from its position, the appearance of new heart rhythm disturbances and new mild aortic regurgitation. Patients are routinely required to take a potent antiplatelet agent for 6 months after placement. Occasionally, open heart surgery is required for explantation of devices that are causing complications. Despite these concerns, most procedures have satisfactory results, and the PFO is closed without complications. It is not known how many divers have taken this option to mitigate the risk of PFO in diving, but anecdotally the numbers are growing. Other than the potential for harm during and after the procedure, one of the concerns about the repair option is that data demonstrating that repair reduces subsequent risk of DCS are incomplete. There is one comparative study that followed divers with large PFOs discovered after DCS who self-selected into groups undergoing repair or not4. The study and its results are summarized in Figure 12.8.
In this study, divers who continued diving without repair had a markedly higher rate of DCS than those who had a repair, but caution is required in interpreting these data because the numbers of DCS cases arising after the repair decision were so small, and the divers were not randomized. Notwithstanding this concern, the study does provide some reassurance that there is a positive return on the risk exposure associated with having a repair. Many diving enthusiasts may well be prepared to take this risk for the apparent benefit of eliminating their anatomical right-to-left shunt. This may be particularly true of those conducting deep technical dives who may see little practical potential for improving the conservatism of their dives.
The relationship between DCS risk and exercise is a complex and evolving issue, and exercise needs to be considered in multiple contexts, specifically exercise before diving, exercise during diving and exercise after diving.
Until the early 2000s, little attention had been given to the issue of exercise before diving and its relationship with risk of DCS, other than general speculation that being physically fit was probably a good thing. Things changed with the publication of a remarkable series of experiments demonstrating that a single bout of heavy exercise approximately 20 hours before diving markedly reduced mortality in a rodent model of severe DCS. By 48 hours after exercise, the protective effect seemed to wear off. Translation of this finding into human research is incomplete, but there have been several studies demonstrating that heavy exercise between 2 and 20 hours before diving reduces VGE counts after diving. The mechanism for this protective effect is unclear. Early speculation that it was mediated by nitric oxide seemed disproved when protection persisted in the presence of a nitric oxide synthase inhibitor, although as a sidebar to this line of research it was discovered that exogenously administered nitric oxide also appeared to reduce post-dive VGE. It has been suggested that exercise produces some sort of endothelial conditioning effect that results in fewer suitable sites for micronuclei to grow when the surrounding tissue becomes supersaturated. Similarly, exercise may disturb stable micronuclei so that they subsequently involute, thus reducing the population transiently. Restoration of micronuclei numbers by whatever process is responsible for producing them would explain the decay in benefit over time following the exercise episode. There are no widely recommended practical strategies designed to take advantage of this phenomenon. Perhaps the best that can be said is that going for a run (or something similar) between 2 and 24 hours before diving may help reduce the risk of DCS.
The effect of exercise during diving may depend on its timing. The typical pattern is that activity during the bottom time sees the diver exercising moderately, and then ascent and decompression (if any) are largely done at rest. This is probably a disadvantageous pattern of exercise because it will result in increased perfusion and inert gas uptake (in some tissues at least) during the bottom phase of the dive and then decreased perfusion and inert gas elimination during the decompression. It is widely accepted that this explains the perception that dives involving hard work at the bottom are associated with greater risk of DCS. A reduction in risk may therefore be achieved by reducing work at depth and maintaining gentle levels of exercise during decompression. There is some evidence in support of these notions. Although a reduction in work at depth can be impractical in occupational diving, in recreational diving it is afforded by, for example, use of diver propulsion vehicles. Similarly, in a decompression diving situation, to maintain gentle exercise during decompression it is usually possible to fin gently against the resistance of the down line or decompression stage. In diving where hard work at the bottom cannot be avoided, the use of a longer safety stop (for a no decompression dive) or lengthening of the prescribed shallow stops in a decompression dive would be an appropriate precaution. There are no universally accepted guidelines for ‘padding’ decompression in this way.
Exercise after diving has generally been considered unwise, although the timing is unclear. Several concerns are noted, not the least of which is that there are many reports of symptoms of DCS arising during periods of work soon after diving. This, of course, may be coincidental, but there are plausible reasons to believe that exercise may have a causative role in such cases. First, exercise may promote the passage of VGE across pulmonary shunts into the arterial system, where they may be more harmful, as described in Chapter 10. Second (and similarly), exercise (particularly that involving lifting or straining) may promote right-to-left shunting of VGE across a PFO with the same result. Finally, it is speculated that where there are micronuclei in tissues supersaturated with inert gas, exercise may contribute to their excitation into growth, thus producing bubbles. This would be analogous to shaking an open bottle of carbonated drink, but the validity of this concern is unknown. At a practical level, mitigation of this risk involves refraining from exercise or lifting for a period after diving. This ‘period’ should definitely extend for at least several hours because this corresponds to the peak and duration of VGE formation after typical dives. Longer would be better, but how long is unknown.
Hydration (or more correctly, dehydration) is one of the most widely recognized of the alleged risk factors for DCS among divers. For all the attention given to the matter, there is remarkably little proof that dehydration actually imputes increased risk.
There is one study in which pigs deprived of water and administered a diuretic during a saturation pressure exposure had more severe DCS than normally hydrated pigs after decompression. In addition, limited human data have shown that supplemental hydration just before diving reduces VGE numbers after diving, especially in subjects who appear prone to VGE formation. This finding is encouraging but falls short of proving that good hydration is protective in humans. Nevertheless, the proposition makes sense. There is evidence that divers are prone to dehydration through factors such as exposure to hot conditions, poor availability of water on boats, sea sickness and immersion diuresis. There is also evidence that realistic levels of ‘dehydration’ reduce regional tissue perfusion during exercise, and because perfusion is important for inert gas washout, it seems plausible that dehydration could impair this process. It is certainly true to say that no one has ever demonstrated dehydration to be beneficial.
It follows that maintenance of hydration can probably only be good. As a somewhat arbitrary guide, the supplementation of normal fluid intake with a litre of water over the hour before diving would make sense.
It has long been observed that the risk of DCS seems higher when diving is conducted in cold conditions. The potentially dramatic effect of temperature on risk of DCS was demonstrated in a landmark study performed by the US NEDU5. It is a complicated study with multiple arms and profiles, but the most important observation was the comparison of outcomes when divers undertook a 120-foot for 30-minute dive with decompression as prescribed by a US Navy dive table under two different thermal conditions. In one set of dives (referred to as cold/warm), the divers were immersed in water at a temperature of 26°C for the bottom phase of the dive and 36°C for the decompression. In the second set of dives (referred to as warm/cold), the temperature conditions were reversed between the bottom and decompression phases. The divers wore no thermal protection. In the cold/warm series, there were no cases of DCS in 80 dives (0 per cent), whereas in the warm/cold series, there were 7 cases of DCS in 32 dives (22 per cent).
The water temperatures and the lack of exposure protection make the conditions difficult to interpret in real-world terms, but the dramatic change in DCS risk between the cold/warm and warm/cold conditions is highly relevant. It can be argued that the condition most analogous to real diving would be the markedly more hazardous warm/cold situation. Thus, divers tend to start a dive warm and become progressively colder during the dive. If there is a lesson to be learned from the NEDU temperature study it is that becoming cold during a dive should be avoided as much as possible.
Practical strategies to mitigate the risk of diving in cold water include optimizing exposure protection, which would include the use of drysuits with state of the art undergarments and possibly even active heating systems, which are now widely available. The ideal time to turn these heating systems on would be during decompression. Extreme divers in cold water caves have even established underwater habitats where the diver can remain under pressure, but not immersed, thus giving an opportunity to reduce conductive heat loss into the water and to take hot fluids orally. As previously, there is always the option of ‘padding’ or extending decompression for decompression dives conducted in cold water.
Some data suggest that remaining warm after diving (despite a cold environment) may reduce production of VGE and the incidence of DCS. It is therefore probably sensible to avoid becoming cold early after a dive, especially one that was provocative from a decompression point of view. Almost paradoxically, however, there is a report of two cases of DCS arising in temporal relation to exposure to hot water in a shower early after diving. This single report has achieved considerable penetration into the diving community and is the cause of much anxiety about showers after diving. It is plausible that sudden warming of supersaturated superficial tissue could decrease gas solubility and precipitate symptomatic bubble formation. However, many divers take showers early in the post-diving period with no problems, and the risk of such events seems very low.
It has long been believed that obesity is a risk factor for DCS, based largely on the ‘first principle’ belief that because nitrogen is highly soluble in fat, an obese person can absorb more nitrogen. Whether this is a practically relevant consideration is controversial. There is conflict in the literature with some studies (probably the majority of those that have addressed this issue) purporting to show an association between risk of DCS and obesity, whereas others have not. Whatever the truth of this matter, obesity is a condition that is often associated with reduced functional capacity and other health problems. Obese divers would benefit from losing weight for multiple reasons.
There are some data suggesting that older divers are at higher risk of DCS and perhaps at higher risk of an incomplete recovery if they suffer serious event. However, once again, there is conflict in the literature on this subject. The fact that older divers are likely to have a lower functional capacity and a higher risk of cardiac events is probably of greater importance than concern about the risk of DCS.
As alluded to earlier, multiple dives in a single day are common in recreational diving. Sequential dives conducted while dissolved inert gas in tissue remains after a previous dive are referred to as ‘repetitive dives’. The definition of repetitive diving differs according to which table or decompression algorithm is used because there is variability in assumptions about total outgassing time. For example, the Professional Association of Diving Instructors, Inc. considers that complete outgassing occurs after 6 hours, whereas the Canadian Defence and Civil Institute of Environmental Medicine (DCIEM) table works on a much longer total outgassing time of 18 hours.
Irrespective of the definition, it is clear that if a second dive takes place in the presence of residual dissolved inert gas remaining after a previous one, then tissue gas loading during the second will compound on that remaining from the first. Perhaps for this reason it has frequently been taught that repetitive diving is a risk factor for DCS, although it is not clear why it should be, provided residual inert gas is adequately accounted for in calculation of no decompression limits or decompression protocols for subsequent dives. One argument that is sometimes advanced in this regard is that bubble formation after the first dive alters inert gas kinetics on the second dive, or those bubbles may undergo further growth after the second dive. There are no convincing data that clearly identify repetitive dives per se as being associated with increased risk. Indeed, the situation is made even less clear by the existence of an acclimatization phenomenon reported from occupational environments in which the incidence of DCS among a cohort of workers undertaking diving or compressed air work is reliably noted to fall over a multiday sequence of exposures. These exposures frequently differ (e.g. in being once daily) from the typical repetitive dives undertaken by recreational divers that may involve up to four or more short exposures per day. Nevertheless, the truth relating to risk in these situations is unclear. Part of the problem relates to the fact that so much of the diving undertaken by recreational divers is repetitive, so it is not surprising that many of the DCS cases arise in repetitive diving.
One particular form of repetitive diving that is associated with considerable controversy is so-called ‘reverse profile’ diving. This is the performance of a repetitive dive deeper than the previous dive (or than another dive in the repetitive sequence). In this sense, the term ‘reverse profile’ is a misnomer because what is really being discussed is reverse depth diving. The origins of the edict that reverse profile diving is hazardous are unclear. Cursory manipulation of the repetitive function of common dive tables reveals that avoidance of reverse profiles results in more allowable bottom time over the sequence. That alone could be reason enough to avoid reverse profiles, but as in repetitive diving itself, it is not clear why reverse profile diving should be considered more hazardous provided residual inert gas from the previous shallower dive(s) is adequately accounted for in calculation of no decompression limits or decompression protocols for the subsequent deeper excursion.
As described earlier, gas content models regulate ascent and impose decompression stops to maintain tissue supersaturation below empirically derived thresholds across the range of tissues with different kinetic behaviour. Such models have been very successful, but are not invariably so; that is, DCS can certainly still occur even when divers decompress according to the model. The occurrence of such events always results in interest in alternative approaches that may (potentially) be more successful. Moreover, as discussed in Chapter 10, it has long been known that even decompressions performed in accordance with established guidelines frequently result in the formation of venous gas emboli (VGE), whose numbers can be correlated (albeit imprecisely) with the risk of DCS. Much of the early research that revealed this VGE phenomenon took place when the use of gas content models to control decompression was almost ubiquitous. Thus, the emerging recreational technical diving world of the late 1990s and early 2000s was fertile ground for well-meaning advocates of alternative approaches to decompression.
A school of thought that had been around for some time, but came to prominence during this period, was the so-called ‘bubble-model’ approach. Bubble model advocates had taken note of the frequently high VGE counts after decompression conducted according to gas content models and advanced the notion that, at least in part, the failure of these models to control bubble formation effectively could increase the risk of DCS even when the diver did everything right. Moreover, they proposed that initiation of bubble formation probably occurred during exposure to the relatively large supersaturations allowed by gas content models during the long ascent to the first decompression stop. Using advanced physics, bubble modellers purported to be able to quantify bubble formation from micronuclei (see Chapter 10) of a given size for a given level of supersaturation, and their calculations suggested that shorter initial ascents (and therefore smaller initial supersaturations) than allowed by gas content models would result in ‘excitation’ of smaller populations of micronuclei and therefore help prevent initiation of bubble formation. It was even suggested that by imposing deeper initial decompression stops a diver could reduce the requirement for the shallow decompression stops later in the ascent because initiation of bubble formation would have been controlled earlier. A stylized comparison between these two approaches to decompression using the same format as previous figures is shown in Figure 12.5.
As in Figures 12.3 and 12.4, line A in Figure 12.5 represents descent to the bottom depth indicted at point 1, and line B represents the increase in tissue gas pressure as inert gas is absorbed during the time spent at that depth (bottom time). By the end of the bottom time the illustrated tissue has reached the ambient pressure line (grey dot at point 2) and is thus saturated with inert gas. As in Figure 12.4, the supersaturation limit or M-value line as prescribed by a gas content model is depicted, and if the diver was following such a model, then direct ascent (line C) would proceed until the tissue gas pressure equalled the maximum allowed (point 3), at which time the first decompression stop would be imposed at a depth corresponding to point 4. After the tissue has off-gassed sufficiently, the ascent would be resumed with stops imposed each time the maximum supersaturation is approached.
In contrast, the ascent prescribed by a typical bubble model (depicted by the grey arrows) involves shorter initial ascents, deeper initial decompression stops and smaller initial supersaturations. A bubble model could also (as depicted) allow surfacing with a tissue gas supersaturation greater than the maximum allowed by the gas content model, based on the belief that the process of bubble initiation had been controlled earlier and that this allowed exposure to greater supersaturation later in the ascent.
There was a compelling theoretical attraction to the concept of using ‘deep stops’ to ‘control bubble formation early in the ascent’. There were also some widely discussed anecdotal observations from several prominent divers that insertion of deep stops into their ascents seemed to result in feeling less fatigued after dives. In the early 2000s these factors, combined with the burgeoning influence of Internet communication, became an article of faith among deep recreational technical divers that bubble model approaches to decompression were superior even though no formal testing of the algorithms had been undertaken. There was widespread adoption of the two most readily available bubble model algorithms (the varying permeability model [VPM] and the reduced gradient bubble model [RGBM]). It largely went unnoticed when VPM was revised into VPM-B to increase shallow stop time after reports of DCS began to emerge. Gas content models with their relatively rapid early ascents and longer shallow stops were derided as being a recipe for ‘bending and mending’ (an allusion to causing bubble formation with supersaturation of fast tissues early in the ascent and then fixing the problem with long shallow stops late in the ascent).
The use of gas content models did persist, perhaps because they were easier to understand or to program for use in computers, but even users of these algorithms began to manipulate them to make them behave more like bubble models. One technique for such a manipulation that became and remains popular is the use of so-called ‘gradient factors’. This involves limiting supersaturation to less than permitted by the conventional supersaturation limit by redefining maximal permissible supersaturation as a fraction of the difference between ambient pressure and the limit. These fractions have come to be known as gradient factors. Thus, if a diver elects to limit supersaturation to 80 per cent of the usual difference between ambient pressure and the supersaturation limit, this is referred to as ‘gradient factor 80’ or ‘GF 80’. Typical implementations of the gradient factor method require the diver to select two gradient factors: the first (often referred to as GF-Low) notionally controls supersaturation in the fast tissues early in the ascent, and the second (often referred to as GF-High) controls supersaturation in the slower tissues at the point of surfacing. The algorithm then interpolates a series of modified M-values in between these two user-specified points. Not surprisingly, lowering the first gradient factor limits supersaturation in the fast tissues early in the ascent by imposing deeper decompression stops, and lowering the second will produce longer shallower stops to reduce supersaturation in the slower tissues at the point of surfacing. Choosing a low GF-Low and a higher GF-High produces a decompression profile that resembles a bubble model decompression. This is illustrated in Figure 12.6 for a GF-Low of 20 per cent and a GF-High of 90 per cent (in common use this terminology would be abbreviated to ‘GF 20/90’).
As in previous figures, line A in Figure 12.6 represents descent to the bottom depth indicted at point 1, and line B represents the increase in tissue gas pressure as inert gas is absorbed during the time spent at that depth (bottom time). By the end of the bottom time the illustrated tissue has reached the ambient pressure line (grey dot at point 2) and is thus saturated with inert gas. At the start of decompression, the initial ascent (line C) is allowed to proceed until the tissue reaches 20 per cent of the supersaturation limit, at which point a stop is imposed at the depth corresponding to point 3. The ascent then continues with further stops imposed when the tissue supersaturation approaches the modified supersaturation limit defined by a line joining the chosen GF-Low (black dot labelled 20 per cent) and the chosen GF-High (black dot labelled 90 per cent). If this approach is compared with the two profiles shown in Figure 12.5, it is clear that it is now very different from the unmodified gas content model decompression and substantially similar to the bubble model decompression. For obvious reasons, the use of gradient factors with a low GF-Low and bubble model decompressions are collectively referred to as ‘deep stop’ approaches to decompression.
The ZH-L Buhlmann gas content model that forms the basis for most tables and computers designed to guide decompression diving by recreational divers was subjected to some human testing; albeit minimal for the trimix diving and depth range for which it is now implemented. The bubble models and gradient factor manipulations of gas content models have had essentially no testing. It is acknowledged that the preceding discussion of bubble model theory represents a gross oversimplification of a complicated matter, but the fact remains, no matter how attractive the theory, it has never been tested in a practical sense. Advocates frequently cite the ubiquitous nature of deep stop approaches as some sort of proof that they are optimal, but this is an invalid argument in the absence of comparative outcome data. These approaches clearly work in the majority of dives, but whether they are optimal is an unresolved question.
Debate over this issue has been rekindled with the publication of several studies that have suggested that the emphasis on deep stop approaches to decompression may need to be reconsidered. Several of these studies have focussed on measuring VGE after diving and suggest that deep stops may not reduce the appearance of VGE as previously widely assumed. However, by far the most significant development has been the 2011 publication of a study performed by the US Navy Experimental Diving Unit (NEDU) at Panama City in Florida3. The investigators compared outcomes after air dives to 170 feet for 30 minutes with same-duration decompression on air prescribed by either a gas content model or a bubble model. Both decompression protocols are US Navy models that are not used by recreational divers, but they nevertheless have characteristics that reflect the respective approaches; the gas content model allows greater supersaturation in faster tissues early in the ascent and distributes decompression time shallower, and the bubble model imposes deeper stops early in the ascent and thereby distributes decompression time deeper. The remarkable feature of this study was that the primary outcome measure was DCS in human subjects. The divers performed a standardized workload during the bottom time, and temperature effects were standardized across the groups by having all divers wear no thermal protection in water at a temperature of 30°C. There were 11 cases of DCS in 198 dives in the deep stops group and 3 cases in 192 dives in the shallow stops group. The trial was ceased at this point because the difference became significant on sequential analysis.
This result was not the outcome expected or hypothesized by the investigators. Attempts to explain it have focussed on the likelihood that protection of fast tissues from supersaturation early in the ascent does not seem to be as effective as thought, and it comes at the expense of increased supersaturation in the slow tissues later in the ascent because they are continuing to absorb gas during deep stops. This principle is illustrated in Figure 12.7. As in previous figures, line A in Figure 12.7 represents descent to the bottom depth (indicted at point 1), and line B represents the increase in tissue gas pressure as inert gas is absorbed during the time spent at that depth (bottom time). By the end of the bottom time the tissue represented by the grey dot at point 2 has reached the ambient pressure line and is thus saturated with inert gas, whereas the slower tissue represented by the grey dot at point 3 is still absorbing inert gas. At the start of decompression, gas content model decompression allows an the initial ascent (line C) to proceed until the faster controlling tissue reaches the maximum supersaturation limit, where the first decompression stop is imposed at a depth indicated by point 4. In contrast, the bubble model allows a shorter ascent (line D) to the first stop at a depth indicated by point 5. In the slower tissue, whose tissue gas pressure at the beginning of ascent is indicated by point 3, the gas content model decompression gives the tissue little more time to absorb inert gas as illustrated by line E because absorption ceases and outgassing begins once the tissue reaches then crosses the ambient pressure line. In contrast, the deep stops prescribed by the bubble model will result in further inert gas absorption by this tissue (line F).
The NEDU study forces us to question whether the proposed benefit of using a bubble model (protection of fast tissues early in the ascent) is worth the disadvantage of the increased gas loading that occurs in slower tissues as a result. Bubble model advocates have tried to portray the study as irrelevant because the experiments involved air diving and used a deep stop profile that is not exactly the same as that prescribed by VPM-B. Nevertheless, analyses of ‘real-world’ VPM-B profiles prescribed for dives using accelerated decompression on oxygen (such as are typically undertaken by technical divers) suggest that the same disadvantageous pattern of protecting fast tissue from supersaturation early in the ascent at the expense of slower tissue supersaturation later still occurs.
It is clear that the optimal approach to decompression from the deep bounce dives undertaken by recreational technical divers is not established; however, it seems plausible to suggest that we have evolved an approach that risks overemphasizing deep stops. One trend that is emerging as this book goes to press is the use of gradient factors to reduce the emphasis on deep stops (by increasing the GF-Low) and re-emphasizing shallow stops (by decreasing the GF-High). Thus, whereas gradient factor combinations such as 10/90 were popular during the height of belief in deep stops, it is increasingly common to see combinations such as 40/70 or 50/70 now.