Decompression Sickness: Adjunctive Therapy

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.

General care

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.

Drug therapy

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).