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
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.
The aim of recompression treatment is to produce the following1:
An immediate reduction in bubble size, which will
Cause the surface tension acting on the bubble to increase and perhaps collapse the bubble.
Increase the surface area of the bubble relative to its volume, thus enhancing gas diffusion out of the bubble.
Reduce the length of any intravascular gas column and hence allow perfusion pressure to push bubbles out of the tissues into the venous circulation.
Reduce the compressive effect of bubbles on adjacent tissues.
Reduce the bubble-tissue and bubble-blood interfaces and the secondary inflammatory reactions that follow.
An increase in the diffusion gradient of gas out of the bubble (see Figure 10.3), which will
Relieve ischaemia and hypoxia.
Restore normal tissue function.
There are three factors to consider after deciding a diver needs recompression therapy:
The pressure (depth) required for therapy.
The gas mixture to be used.
The rate of decompression.
Depth of recompression
In deciding the depth of recompression, three different approaches are possible:
Recompress to a pressure (depth) dependent on the depth and duration of the original dive.
Recompress to a depth that produces clinical relief of symptoms and then tailor the gas mixtures for decompression from that depth.
Recompress to a predetermined fixed depth, i.e. according to standard tables of recompression therapy.
Only the third is in common practice these days, but each has some logic to it under certain circumstances.
RECOMPRESS TO A PRESSURE (DEPTH) DEPENDENT ON THE DEPTH AND DURATION OF THE ORIGINAL DIVE
This technique uses the principle that if a dive to 4 ATA produces DCS, then recompression to 4 ATA should relieve the symptoms. This approach was best typified by the now defunct concept of treating aviator DCS merely by descent to ground level.
This is not a particularly satisfactory technique because it is designed to cope with the total quantity of gas dissolved in the body during the original dive, irrespective of its distribution. Because DCS is the clinical manifestation of a gas bubble lodged in a vulnerable area, it is necessary to recompress to reduce the size of that particular bubble, irrespective of the total quantity of inert gas dissolved in the body. There is also evidence that once a bubble is formed, even compression to very high pressures may not completely eliminate that bubble, thus leaving bubble nuclei to re-expand on decompression.
The one advantage of this approach, apart from its simplicity, is evident when a diver develops DCS very soon after surfacing from a deep dive. Under these conditions, a prompt return to the original depth will ensure that there is no tissue-to-bubble pressure gradient that could cause bubble growth at a lesser depth.
RECOMPRESS TO A DEPTH OF RELIEF
This empirical approach was used first in underwater recompressions to reduce the depth exposure as far as possible. It is still applicable, both underwater and in chambers.
The freedom to be able to choose any depth to achieve an acceptable clinical result and then select an appropriate breathing gas is invaluable in serious cases (Figure 13.1).
As traditionally used for deep and saturation exposures, the patient is recompressed to the depth at which all major symptoms disappear, plus one additional atmosphere, based on the assumption that the additional pressure would result in a reduction bubble size and allow increased surface tension to promote bubble resolution.
This approach is not without difficulty because it requires a sound knowledge of saturation decompression and the ability to mix and administer different gas mixtures. Nitrogen narcosis and central nervous system and pulmonary oxygen toxicity become important considerations. A recompression chamber (RCC) should have a mixed gas capability to support such operations.
RECOMPRESSION USING STANDARD RECOMPRESSION SCHEDULES
This approach uses standard recompression tables roughly divided into the following groups:
Oxygen tables with deep excursions.
Helium-oxygen (heliox) tables.
Many such tables have been published by both commercial and military organizations around the world. Both air and heliox tables start at 30 and 50 metres, oxygen tables start at 9 to 18 metres, deep excursions are commonly to 30 metres and saturation treatments depend on the depth of symptom relief.
These tables clearly state the gas mixture to be used (usually oxygen or heliox), the periods to be spent at each depth and the rate of decompression. Standard air, oxygen and gas mixture tables for recompression are presented in Appendix B and Appendix C.
Standard recompression tables
A prudent diving physician will advise non-experts to adhere to strict treatment guidelines, as depicted in the manuals, but retain his or her own flexibility to treat patients who did not respond or in facilities that may not be appropriate to apply the guidelines. For this reason, this text covers more than one set of treatment techniques. The standard tables are as follows.
AIR TABLES (US NAVY 1A, 2A, 3 AND 4 AND ROYAL NAVY 52, 53, 54, 55, 71, 72 AND 73)
These tables are used increasingly rarely. The US Navy (USN) first published their air recompression Tables 1 to 4 in 1945, and these were the standard treatment tables for more than 20 years. What is remarkable about these tables is that they were never tested on subjects with DCS. The test subjects made normal dives, which required decompression, but were then subjected to a treatment table instead. The treatment tables were deemed satisfactory if the subjects did not surface with DCS after one of the treatment tables!
During the 1960s, reported failure rates of up to 50 per cent on the air tables resulted in the development of the shallow oxygen tables.
Many experienced clinicians today are reluctant to use air tables because of the problems they bring and their variable benefits. The difficulties with air tables include logistical problems with prolonged decompression, aggravation of symptoms during ascent, nitrogen narcosis and DCS in the attendants and respiratory distress caused by the increased density of air under pressure (particularly if pulmonary involvement is already present). The results are often not adequate unless the symptoms are mild, recent and not the result of gross omitted decompression.
However, if oxygen is unavailable and the RCC can logistically support a treatment table lasting up to 40 hours, air tables may be considered.
OXYGEN TABLES (US NAVY 5 AND 6, ROYAL NAVY 61 AND 62 AND COMEX 12)
The introduction of standard oxygen tables using 100 per cent oxygen interspersed with short air breathing ‘oxygen breaks’ gives more flexibility and improved results (Figure 13.2). These tables are shorter, needing only 2 to 5 hours, require compression only to 18 metres (2.8 ATA) and are therefore logistically achievable. Divers Alert Network (DAN) reports that about 80 per cent of all DCS is treated with these tables. The physiological advantages are in the speed of bubble resolution and increased oxygenation of tissues.
Disadvantages include the less immediate reduction in bubble size (i.e. to less than half the volume reduction achieved with the 50-metre standard air tables), increased fire hazard, oxygen toxicity and the occasional intolerance of a distressed patient to a mask. Although the pressure gradient of nitrogen in the intravascular bubble-to-blood interface is increased with oxygen breathing, if the diver has previously dived in excess of 18 metres, there could well be a gas pressure gradient from tissue-to-extravascular bubble during the early phase of recompression.
With the foregoing qualifications, the use of oxygen tables has received worldwide acceptance as the starting point for all standard recompression therapy. Although some authors have reported significant failures with these tables, the success rate is higher than with the air tables that preceded them, and no better-performing alternative has been identified. Success rates for complete resolution of symptoms vary with both severity and the time to recompression, but they are often reported at 80 to 90 per cent.
Whenever oxygen is used, attention must be paid to oxygen toxicity. Unless one is following established safe protocols, it is suggested that the oxygen parameters should not exceed those likely to result in neurological or pulmonary toxicity (see Chapter 17). In cases of potential death or disability, exceeding these parameters may be acceptable.
OXYGEN TABLES WITH DEEP EXCURSIONS (US NAVY 6A) AND HELIOX TABLES (COMEX 30)
USN Table 6A involves the addition of an initial period of breathing air at 50 metres followed by a standard Table 6. This table was initially introduced as a treatment of cerebral arterial gas embolism (CAGE) in submarine escape trainees (with a low nitrogen load), although later studies have not shown any benefit from this deep excursion over the shallow 18-metre oxygen tables in divers.
Most centres now recommend starting with a standard USN Table 6 at 18 metres; however, in severe cases of DCS or cases not responding, the option exists to go on to a deeper table using a mixed gas such as a Comex 30 (Figure 13.3, Plate 3). Although based on little evidence, some centres advocate initial use of the Comex 30-metre table for severe neurological DCS. Heliox mixtures (50/50) are substituted for oxygen at depths greater than 18 metres. In refractory cases, there is then the opportunity to go to 50 metres using a modified USN Table 6A, Royal Navy (RN) Table 64 or Comex 50 breathing heliox mixtures.
A 2011 workshop reviewed the evidence for the use of 30-metre heliox recompression and made some recommendations concerning the appropriate use of these more challenging treatment schedules2.
SATURATION TABLES (US NAVY 7)
Saturation treatments are used when divers have developed DCS during or just after decompression from saturation exposures. The customary treatment tables are inappropriate because of the extreme gas loads in ‘slow’ tissues and the often excessive oxygen exposures required. In general, increased pressure is applied, and the oxygen percentages are less. These tables may also be used after recompression to depth of relief in severe cases and when other tables have failed.
Recompression results in a reduction of bubble size, but it may also be associated with a further uptake of gas into the bubble. Ideally, a breathing mixture would be selected that diffuses into the bubble at a slower rate than the inert gas diffuses out, resulting in bubble shrinkage. This is one reason that the oxygen tables are preferred to the air tables because no further inert gas can be absorbed.
There is anecdotal evidence that recompression using heliox has been beneficial in treating DCS after air dives. Hyldegaard and associates3 demonstrated in a model of spinal DCS that, while breathing air, there is a steady increase in bubble size. When compression occurred while breathing oxygen, there was an initial increase and then decrease in bubble size, whereas with heliox there was a progressive shrinkage in bubble size.
The initial increase in bubble size with oxygen may be explained by the fact that at equal partial pressure differences the flux of oxygen in fat is twice that of nitrogen and four times that of helium3. This may explain the initial worsening of symptoms seen occasionally when patients with DCS are recompressed on oxygen.
There is little available evidence to suggest heliox tables are more effective than the oxygen tables, although many centres will move to a heliox table for the difficult or non-resolving acute case (Table 13.1). Heliox is also easier to breathe at depth than air – especially relevant to patients with respiratory ‘chokes’.
In determining which therapeutic table should be selected, remember:
The natural history of the disease:
The longer the surface interval before symptoms, the less likely they are to worsen over time.
Neurological symptoms have sequelae; many others do not.
The value of pressure: Recompression will prevent bubble growth and hasten resolution.
The depth effect of recompression is less important the longer the symptoms have been present.
Delay to recompression
Once a manifestation of DCS has developed, the subsequent progress may be related more to the time elapsed before recompression than to the specific treatment table selected. With prompt treatment the destructive tissue distension effects of bubbles are lessened, as are the effects of ischaemia and the chemical and cytological reactions to the bubble.
Even using air tables, Rivera4 demonstrated that if initial treatment was administered less than 30 minutes after symptoms developed, there was a 95 per cent probability of relief. This rate falls to 77 per cent if the delay exceeds 6 hours.
The delay among the dive, the development of symptoms and the presentation for treatment allows the clinician to assess the clinical importance and propose the most rational therapy.
To illustrate these principles, the approach to the patient who presents 30 minutes after a dive with an ascending paralysis is different from the patient who presents 48 hours after a dive with shoulder pain. The first patient’s neurological injury is likely to progress with time, whereas the shoulder pain will not and may undergo spontaneous resolution.
The first patient should be treated aggressively, commencing with an 18-metre oxygen table or even a 30-metre heliox table. If using the former, consideration should be given to the options of going deeper and changing gas mixtures if early or full recovery is not evident.
Patients who delay seeking medical assistance may benefit from recompression even up to 14 days after injury; however, most diving physicians would not consider deep or saturation tables for patients with these late presentations. Consider two illustrative case histories (Case Report 13.1 and Case Report 13.2).
CASE REPORT 13.1: The patient made a dive to 18 metres for 60 minutes on scuba. There had been no dives for a month before this. The isolated symptom of left shoulder pain developed 5 hours after the dive and had been present for 24 hours before the diver presented for medical treatment.
Comment: This is not only a mild case of DCS, it is not going to get significantly worse as long as the patient avoids further exposure to hypobaric or hyperbaric conditions. By the time the medical assessment was made (29 hours after the dive), the tissues will have equilibrated fully with the atmospheric pressure, and thus there will be no significant pressure gradient pushing nitrogen into the bubble. On the contrary, there will be a mild gradient in the opposite direction. The administration of 100 per cent oxygen will enhance this gradient further.
The authors’ approach to such a mild case would be to relieve the patient’s symptoms and perhaps to reduce the possibility of subsequent bone damage (although there is no clear evidence that this latter is really possible) by recompression on an oxygen treatment table – probably at 18 metres. If recompression was not feasible, then surface oxygen would be appropriate.
CASE REPORT 13.2: This patient has symptoms identical to those of the patient in Case Report 13.1, but this time the left shoulder symptoms followed 10 minutes after a 30-metre dive for 30 minutes with a rapid ascent and omitted decompression. The diver has presented for assistance immediately after the symptom developed.
Comment: This is a very different situation from Case Report 13.1. Even assuming that the left shoulder pain is musculoskeletal and not referred neurological or cardiac, the likelihood of progression from the theoretical ‘minor symptom’ to a major case of DCS is much higher.
First, because the symptom developed soon after the dive, it is likely to become worse. Second, more symptoms are likely to develop (remembering that DCS manifestations may continue to arise over the next 24 hours). Third, the tissues surrounding the bubbles may well have nitrogen supersaturation pressures of almost 4 ATA. The bubble, existing on the surface, will have a nitrogen pressure of approximately 1 ATA, as the bubble is at the same ambient pressure as the body. Under these conditions, there will be a gradient between the tissues and the bubbles, increasing the size of the latter until the tissue gas tension becomes equated with the bubble gas tension.
The therapeutic approach to this diver is to recompress him to the maximum depth at which 100 per cent oxygen can be used therapeutically, i.e. USN Table 6 at 18 metres, and if a satisfactory response is obtained and maintained, to decompress him from that depth. Recompression treatment at 18 metres will not rapidly reverse the tissue-to-bubble nitrogen gradient and, if other more serious symptoms develop, it may be necessary to recompress him deeper on heliox (or an oxygen and nitrogen mixture). The authors of this text would select a 30-metre 50 per cent heliox treatment schedule (e.g. Comex 30). At this depth there would be no tissue-to-bubble nitrogen gradient.
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).