Aetiology

Though other aetiologies exist, the pathology of dysbarism is due to the body’s exposure to increased atmospheric pressure, which occurs most commonly while driving. Aviation decompression sickness and other aetiologies are rare and outside the scope of this topic. At sea level, the absolute pressure exerted by the atmosphere is termed 1 atmosphere absolute. Exposure to increased pressures increases the risk of dysbarism via two separate mechanisms: the increased dissolution of inert gases into tissues (decompression sickness) and the expansion of gas volume as the pressure decreases when the diver surfaces (barotrauma, arterial gas embolism [AGE]).

Risk factors for decompression sickness have been widely debated and, in general, definitive evidence is lacking. It should be noted that there is significant variability in individuals' tendency to form venous gas emboli (VGE). For a list of proposed risk factors, categorised by strength of evidence or general expert consensus, see Risk factors.

Pathophysiology

Barotrauma

  • Boyle's law states that the volume of a gas at constant temperature varies inversely with pressure. Barotrauma results from the application of this law to the gas-containing spaces within or adjacent to the body.[7][8]​

  • Local tissue damage is more frequent in relatively non-compliant structures such as the middle ear, sinuses, lungs, and teeth.[8]

  • The symptoms depend on the anatomical area affected.

  • The most common site is the middle ear. A descending diver 'equalises' middle-ear pressure with increasing external pressure by allowing air to pass through the eustachian tube. If equalisation is hindered (e.g., by tubal congestion or rapid descent), air contracting in the middle ear will draw in the tympanic membrane and mucosal lining. This leads to oedema and haemorrhage as a result of capillary damage. The tympanic membrane is fragile and will perforate if the pressure differential across it exceeds 2 metres (6.5 feet) of sea water.[8]

  • Plugging of sinus ostia by mucus can similarly cause epistaxis and pain over the affected sinus (commonly the frontal sinus).

  • External ear barotrauma may result from wax, earplugs, or a tight diving hood, again impeding compensatory changes in air volume with increasing depth. Failure of middle-ear equalisation can lead to an inner ear haemorrhage, labyrinthine membrane tears, and leakage of perilymph into the middle ear or mastoid via a fistula (most commonly in the round window). This causes hearing loss, vestibular disturbances, and tinnitus.[8]

  • On ascent, expanding gas trapped within the lungs may cause overdistension and rupture of pulmonary tissue, leading to mediastinal or subcutaneous emphysema, pneumopericardium, pneumothorax, or AGE.[1]

  • AGE occurs when overexpansion of the alveoli causes air to track into the pulmonary vasculature. Gas bubbles distribute themselves preferentially according to high cerebral blood flow, with cerebral AGE often presenting as stroke-like symptoms or loss of consciousness. Arrhythmias may arise from embolism of the coronary arteries. Although these may be the most commonly presenting symptoms, it should be noted that symptoms are not caused by a single obstructing bubble, but rather a shower of bubbles throughout the vasculature.​[1][9]

Decompression sickness

  • Henry's law states that gas enters into physical solution in direct proportion to the partial pressure exerted by that gas. Metabolically inert nitrogen will dissolve into blood and tissues with increasing depth. As a result of Henry's law, the reduction in ambient pressure on ascent after a dive causes gas to come out of the solution and bubbles to form in the intravascular space and/or the tissues.[7]​

  • Normally, bubbles enter into, or are generated within, the venous capillaries. These bubbles are eventually trapped and cleared by the lungs, which allow spontaneous bubble resolution in the 'pulmonary filter'. However, excessive numbers of bubbles may overwhelm this process, leading to bubbles passing as emboli into the left heart and the arterial circulation. Right-to-left shunts, such as occur in patent foramen ovale, atrial septal defect, or pulmonary arteriovenous malformations, may allow arterial gas embolisation to occur.[1][10]

  • Tissue or 'autochthonous' bubbles form, particularly in tissues with a rapidly attained high gas content (e.g., spinal cord white matter) and in tissues with relatively poor perfusion and slow saturation (e.g., adipose tissue).[11]​

  • Bubbles can cause local ischaemia and infarction, haemorrhage, endothelial damage, activation of the inflammatory cascade, and local stretching and compression.[1]​

  • It is thought that the diverse symptoms and signs of decompression sickness relate to the location and number of bubbles formed, although the considerable individual heterogeneity in susceptibility suggests that other mechanisms are involved.

  • The pathophysiology of decompression sickness is still incompletely understood. The presence of bubbles alone does not necessarily mean decompression sickness will occur. Many divers have been observed to develop VGE or bubbles after diving without symptoms.

Nitrogen narcosis

  • The precise mechanism of the narcosis has not been well elucidated. It appears to be a direct effect of gas dissolving into the lipid bi-layers of nerve-cell membranes. It is immediately reversible on returning to shallower depths. Any divers with persistent symptoms should be evaluated for an alternative cause of symptoms.[12]

Classification

Multiple systems of classification of decompression sickness have been proposed, some of which are described below. Practically, the diagnosis is a clinical one and treatment is the same, so classification is less relevant in the acute setting.

According to severity[3]

  • Decompression sickness, type I (mild):

    • Musculoskeletal

    • Skin

    • Lymphatic

  • Decompression sickness, type II (serious):

    • Neurological (cerebral, spinal, paraesthesias)

    • Cardiopulmonary ('the chokes': cough, retrosternal pain, collapse)

    • Inner ear (audiovestibular) ('the staggers': vertigo, tinnitus, dizziness)

According to evolution and manifestations[4]

  • Decompression sickness (DCS)

  • Evolution:

    • Progressive

    • Static

    • Spontaneously improving

    • Relapsing

  • Manifestations:

    • Pain (which may be limb pain or girdle pain)

    • Cutaneous

    • Musculoskeletal

    • Neurological

    • Audiovestibular

    • Pulmonary

    • Lymphatic

    • Constitutional

Decompression sickness and arterial gas embolism[3]

The Golding classification, developed during the construction of the Dartford Tunnel in the UK, grades decompression sickness by severity: type I (mild) and type II (serious).[5]​ The classification has been adopted for diving and later refined to its current form:[3]

  • Decompression sickness, divided into:

    • Type I (mild), including musculoskeletal, skin, and lymphatic manifestations

    • Type II (serious), including neurological, cardiopulmonary, and inner ear (audiovestibular) manifestations. Neurological manifestations include cerebral pathology, spinal pathology, and subjective paresthesia. Cardiopulmonary manifestations are also known as 'the chokes', and include cough and retrosternal pain; may lead to cardiovascular collapse. Inner ear (audiovestibular) manifestations are also known as 'the staggers', and include vertigo, tinnitus, and dizziness.

  • AGE

    • Is mechanistically different from decompression sickness. AGE occurs secondary to pulmonary overinflation or pulmonary barotrauma, resulting in a rapid embolisation of gas. Should be suspected in any diver who loses consciousness or develops focal neurological deficit within 15 minutes of surfacing.

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