Decompression Sickness: Differential Diagnosis

The attribution of symptoms following diving to DCS is contingent on the symptoms being qualitatively consistent with one or more of those described. In addition, an evaluation of the ‘provocation’ of the dive is useful but not definitive. Thus, a dive that breached no decompression limits without adequate decompression (see Chapter 12), involved rapid ascent or involved risk factors (see Chapter 12) would be considered more provocative than one that, for example, was well inside the no decompression limits with no untoward events. The timing of symptom onset (discussed previously in this chapter) is also contributory to diagnosis, with DCS becoming less likely with greater symptom latencies after diving. Unfortunately, there is no formula in which these various factors can be integrated to give a definitive answer on diagnosis. There is no substitute for knowledge and experience in this regard. Diagnostic uncertainty and the non-specific nature of many DCS symptoms will inevitably result in recompression of divers with consistent symptoms caused by another disorder from time to time. Other disorders that may mimic DCS are briefly considered here. Although the authors of this text emphasize the fact that a temporal relationship between diving and symptom onset is compelling evidence of a diving-related problem, DCS has many non-specific symptoms, and there are often several differential diagnoses that should be considered, especially in respect of some of the mild symptoms. Some of the more common or important differential diagnoses for DCS symptoms are outlined in this section.

Musculoskeletal pain is the most common single symptom of DCS, and it may also be caused by many other problems. Muscular and soft tissue injuries are common events in the diving environment, where there is heavy lifting and ample opportunity for minor trauma. This should be considered, especially where the diver has a non-migratory monoarthropathy with a history consistent with a non-DCS cause. Examination findings such as bruising may help, although cutis marmorata can look a little like bruising, so care is needed in interpreting skin change. There have been a few cases of myocardial ischaemia manifesting after diving with left shoulder and arm pain and being diagnosed as musculoskeletal DCS.

Fatigue is extremely common after diving, and the diagnosis of DCS would never be made on the presence of fatigue alone. Malaise can occur in many systemic illnesses, and in particular, viral illness can induce significant malaise. Such illnesses are common on diving trips, especially where participants have travelled long distances on airplanes and have been exposed to many other travellers. The presence of other viral illness symptoms such as fever and coryza, which are not usually seen in DCS, can help with accurate diagnosis.

Patchy paraesthesiae and rash can occur as a result of contact exposures with irritants such as marine stingers (see Chapter 32) and soaps used to clean wetsuits. Other allergies can cause rash, and some toxic ingestions that may occur on dive trips (e.g. ciguatera fish poisoning) (see Chapter 33) can cause marked widespread paraesthesiae, as well as myalgias and malaise.

Pulmonary symptoms, such as chest pain and cough, can occur in many settings. The main clue to DCS as a cause would be early onset (usually within minutes) after diving. Nevertheless, this does not rule out other causes of diving-induced pulmonary irritation such as pulmonary barotrauma (rare) (see Chapter 6), immersion pulmonary oedema (rare) (see Chapter 30), oxygen toxicity (very rare) (see Chapter 17), near drowning (see Chapter 22) or salt water aspiration syndrome (see Chapter 24). Pulmonary barotrauma could be suspected if there was a history of rapid or panicked ascent, if the dive was unprovocative for DCS or if there were clear signs of pulmonary barotrauma such as haemoptysis, pneumothorax or subcutaneous emphysema in the supraclavicular area. Immersion pulmonary oedema can be a difficult differential diagnosis, although the symptoms often first appear at depth and force termination of the dive. Symptoms that appear at depth are not DCS. In addition, although some descriptions of pulmonary DCS refer to the possibility of pulmonary oedema, these may represent misdiagnoses. Pulmonary oedema has not been a feature of definite pulmonary DCS seen by these authors. Oxygen toxicity symptoms would be expected only at the end of very long periods of oxygen exposure in technical diving (see Chapter 62). Near drowning would almost certainly be indicated by a clear history of some sort of distress event and inhalation of water. Salt water aspiration syndrome usually has a longer latency than pulmonary DCS. Moreover, in all these differential diagnoses, the symptoms would be limited to pulmonary involvement. The appearance of other DCS manifestations would point strongly to DCS as the diagnosis.

Spinal symptoms following diving are almost invariably the result of DCS. It is possible that degenerative spinal disease (e.g. ‘sciatica’) could manifest for the first time early after diving, but the symptoms would be unilateral and frequently preceded by a history of previous problems. The abdominal and back pain that may be a feature of spinal DCS can also occur in the Irukandji syndrome (see Chapter 32). Nevertheless, spinal symptoms arising early after diving should never be rationalized to an alternative diagnosis without an extremely good reason.

The diagnosis of inner ear DCS involves one of the most difficult and troublesome differential diagnoses in diving medicine – the separation between DCS and inner ear barotrauma (IEBT) (see Chapter 7). Both disorders may manifest with vestibular and/or cochlear symptoms early after diving, but the diagnoses have significantly different implications for subsequent management. DCS mandates recompression therapy, whereas recompression is relatively contraindicated in IEBT and these patients may warrant referral for round window surgery. A key point that frequently resolves the problem is that IEBT often manifests first during descent, and frequently in association with difficulty equalizing pressures in the middle ears. Manifestation before decompression rules out DCS, and a clear history of difficulty with ear ‘clearing’ increases suspicion of IEBT. A dive that is very non-provocative for DCS would also tip the diagnostic suspicion toward IEBT, whereas a more provocative dive would tip suspicion the other way, particularly if the dive involved a gas switch from a high-helium to a high-nitrogen mix, or if other manifestations of DCS emerged. Nevertheless, not infrequently there is ambiguity around the diagnosis, and difficult decisions about treatment have to be made.

Transient vertigo (usually lasting seconds) can also occur during ascent if there is a difference in the rates at which the middle ears vent expanding gas through the Eustachian tubes. This is known as ‘alternobaric vertigo’. This phenomenon is relatively common, transitory and self-limiting. Alternobaric vertigo should never be used as an explanation for persistent vestibular symptoms after a dive.

As previously discussed in relation to classification of the bubble-induced dysbaric disorders, there is often diagnostic ambiguity around the appearance cerebral symptoms after diving where the competing diagnoses are CAGE secondary to pulmonary barotrauma or cerebral DCS caused by the left-to-right shunting of VGE across a PFO or pulmonary shunts. The circumstances of the dive may provide definitive clues. For example, CAGE would be plausible and cerebral DCS highly implausible as an explanation for the rapid onset of focal cerebral symptoms after a panic ascent during training in a swimming pool. In addition, irrespective of the circumstances of the dive, it is likely that gross focal symptoms are more compatible with a CAGE event, whereas dysexecutive symptoms are more likely to be caused by DCS. However, in respect of cerebral DCS versus CAGE, the diagnosis is almost irrelevant because recompression according to the same regimen is now the prevalent response to either diagnosis (see Chapter 13).

Another possible cause of gross focal symptoms is a cerebrovascular event coincident with completion of a dive. Such events have occurred, and on occasion, divers suffering cerebrovascular accidents have been recompressed before the misdiagnosis has been discovered. This is unlikely to be harmful, although it will delay access to therapies such as thrombolysis or clot retrieval. Equally, because most cerebral symptoms appearing early after diving are caused by either DCS or CAGE, the prioritization of recompression as first-line therapy without detailed investigation to exclude cerebrovascular accident is appropriate for most cases.

Dysexecutive symptoms arising after diving may also be caused by a gas toxicity such as carbon monoxide exposure. The related symptoms are often initially noticed at depth, and this provides a clue that something other than DCS is responsible. There may also be a history of foul-tasting breathing gas or multiple divers affected if they breathed gas from a common source.