Moderate to severe DI

Moderate to severe DI includes those categories traditionally assigned to Type II (and III) in the Golding Classification 26. The criteria for moderate to severe DI are met if at any stage DI presents with more than simple limb pain and cutaneous features:

Pulmonary DI

This relatively uncommon syndrome usually presents with a patho-

gnomonic triad of:

* If a wet dive took place in a dry suit, then there may be direct absorption of gas into the skin as for a chamber dive. This should be distinguished from dives resulting in cutaneous lesions where no skin-gas contact occurred.

* Cutis marmorata is associated with systemic decompensation, paradoxical embolism (e.g., via a PFO, ASD or intra-pulmonary shunt) and high spinal, cerebral and audiovestibular forms of DI. Therefore while the condition itself is not particularly serious, its associations prompt attention to the other systems of greater vulnerability and justify urgent recompression.

• Substernal pain: usually burning and progressively increasing. Initially the pain may be noted only when coughing. Over time the pain may become constant.

• Cough: initially intermittent and easily provoked by cigarette smoking (Behnke's sign). Paroxysms of coughing may become uncontrollable.

• Progressive respiratory distress and dyspnea.

The manifestations of pulmonary DI are believed to result from the combined effects of gas emboli in the pulmonary artery and obstruction of the vascular supply to the bronchial mucosa. Untreated Pulmonary DI may be fatal.

Neurological DI

The neurological manifestations of Dysbaric Illness are unpredictable: They range from minor sensory abnormalities to loss of consciousness and death. Clinically they may resemble acute stroke or an acute exacerbation of multiple sclerosis. Although an increasing number of mild sensory changes are being assigned to peripheral nerve and nerve root lesions (some of which may not necessarily be related to DI), the clinical prerogative is to assume a central origin until proven otherwise and to manage these presentations promptly.

Cerebral DI: Brain involvement in DI appears to be especially common in aviators. However it is not known if this is due to paradoxical embolization of large volumes of venous gas; the release vasoactive mediators; hypoxemia due to a disruption of pulmonary circulation in conditions of marginal oxygenation at extreme altitude or something else entirely. In this group a migraine like headache often accompanies visual disturbances. When there is brain involvement in divers a common presentation is hemiparesis which is different to the clinical presentation in aviators. Collapse with unconsciousness are rare presentations of DI and more likely to be due to injected gas than bubble evolution from supersaturated tissues.

Spinal Cord DI: Paraplegia is a 'classic' symptom of DI in divers and almost invariably represents spinal cord involvement x. Bladder paralysis with urinary retention and fecal incontinence frequently accompany paraplegia. In the last few years, cases of serious paralysis in recreational divers dropped from 13.4 percent in 1987 to only 2.9 percent in 1997, and the number of cases of divers losing consciousness dropped from 7.4 percent to 3.9 percent of total injuries during the same period. The incidence of loss of bladder function, another sign of neurological DI, dropped from 2.2 percent to 0.4 percent during this period (DAN Diving Accident Reports) 119.

x A notable exception is embolization of the anterior cerebral arteries which can also present with bilateral lower extremity paralysis and loss of bladder function.

However this change in incidence has not been balanced by an equivalent rise in the frequency of pain only or skin DI. On the contrary, there seems to be a trend towards an increased incidence of milder neurological manifestations. Paresthesias, some with well and other with less clearly defined presentations (including ubiquitous numbness and/or tingling) as well as vague, ambiguous and ill-defined symptoms now predominate recreational DI. The diagnostic ambiguity is compounded by the fact that many of these manifestations appear to respond to normobaric oxygen and recompression. However, while suggestive, response to recompression cannot be considered diagnostic in these conditions. Certain non-diving related nerve damage also appears to respond to hyperoxygenation so that one of the greatest clinical challenges in DI lies in unraveling true diving injuries from a myriad of other transient peripheral neuropathies 124.

Inner Ear DI

Cochlear and/or vestibular DI was previously almost exclusively associated with saturation and experimental diving and - accordingly - quite rare. In recent times the incidence has been increasing due to an escalation in deep recreational technical diving involving mixed gas and gas switching on decompression. Either or both cochlear and vestibular apparatus may be involved presenting with tinnitus, deafness, vertigo, nausea, and vomiting. Nystagmus may be present on physical examination. The mechanisms remain unclear (refer section 4.2.4.). Inner ear DI is a serious medical emergency and must be treated immediately to avoid permanent damage. Since the nutrient arteries of the inner ear are very small, rapid reduction in bubble diameter, with immediate 100% oxygen administration and prompt recompression are essential.

Shock

Shock occasionally occurs in DI and is usually associated with serious pulmonary and cardiovascular manifestations. Fatalities are usually the result of shock or pulmonary forms of DI and resuscitation and immediate recompression are of paramount importance.

Girdle Pain: Back, Abdominal, or Chest Pain

Unlike limb pain, pain in these areas should be considered carefully as it is frequently associated with progressive spinal cord DI.

Extreme Fatigue

Fatigue disproportionate to the amount of preceding activity has long been regarded as an evolving serious manifestation of DI. The biochemical and pathophysiological mechanisms are unknown although there is increasing evidence that it may be the result of vasoactive mediators and cytokines released due to venous gas embolization.

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