Decompression sickness, is also called divers’ disease, the bends, aerobullosis, and caisson disease, is a medical condition caused by dissolved gases emerging from solution as bubbles inside the body tissues during decompression.
In recreational scuba diving the incidence of decompression sickness is low ranging from 0.4 to 1 case per 10,000 dives.
The risk however is higher for deeper, longer dives and for dives in which decompression requirements are violated.
DCS is caused by a reduction in ambient pressure that results in the formation of bubbles of inert gases within tissues of the body.
Bubble formation is the primary mechanism of injury in decompression sickness.
Divers absorb inert gas into tissues when breathing compressed gas during a dive, with more gas absorbed on deeper or longer dives.
During ascent the partial pressure of dissolved gas in tissues may exceed ambient pressure, causing supersaturation, which leads to the formation of bubbles in those tissues or in the blood passing through them.
It may happen when leaving a high-pressure environment, ascending from depth, or ascending to altitude.
DCS most commonly occurs during or soon after a decompression ascent from underwater diving, but can also result from other causes of depressurisation, such as emerging from a caisson, decompression from saturation, flying in an unpressurised aircraft at high altitude, and extravehicular activity from spacecraft.
This may also occur with rapid from sea level to high altitude resulting in venous gas emboli with small, but, extremely common after driving for rapid altitude exposure:they are usually filtered by pulmonary capillaries and are asymptomatic.
Venous gas emboli can reach the arterial circulation by overwhelming the filtering capacity of the pulmeriary capillary network or through pulmonary or intracardiac right to left shunts, such as is atrial septal defect and patent foramen ovale.
The presence of a patent foramen ovale increases the probability of cerebral, spinal cord, inner ear decompression sickness, presumably because tiny arterialized venous gas emboli arriving in the capillaries of supersaturated tissues after a dive grow through inward diffusion of gas.
The brains vulnerability probably arises from exposure to high numbers of small, arterialized gas embolize, perhaps coalesce the form larger bubbles.
Bubble formation within tissue because mechanical disruption and focal hemorrhage, particularly in white matter.
Intravascular bubbles may have physical effects with inflammatory and thrombogenic responses.
Small amounts of arterial gas can initiate a progressive decline in cerebral blood flow, strip endothelial cells from underlying basement membrane resulting in impaired regulation of vascular tone, plasma leak and hypovolemia.
By similar mechanisms hi load of venous gas emboli can injure pulmonary capillaries and induced pulmonary edema.
Most modern diving is recreational with breathing through a self-contained, underwater breathing apparatus.
Exhaled gas is expelled into the water, but gas can be conserved with the use of rebreathing units.
Rebreathers combine oxygen and a diligent gas to maintain a constant partial pressure of inspired oxygen, irrespective of the depth.
DCS and arterial gas embolism are collectively referred to as decompression illness.
Since bubbles can form in or migrate to any part of the body, DCS can produce many symptoms, and its effects may vary from joint pain and rashes to paralysis and death.
Individual susceptibility can vary from day to day, and different individuals under the same conditions may be affected differently or not at all.
The classification of types of DCS by its symptoms has evolved since its original description in the 19th century.
The severity of symptoms varies from barely noticeable to rapidly fatal.
Decompression sickness manifestations can occur singly or in combinations, but the most severe cases typically have multiple manifestations.
The inner ear decompression sickness is more common after deeper diving, and musculoskeletal pain is the most prevalent form after saturation diving and in altitude induced decompression sickness.
Manifestations may rise during decompression from long, deep exposures but typically rise after the return to surface pressure.
DCS caused by diving can be managed through proper decompression procedures.
Contracting DCS is now uncommon.
Divers almost universally use dive tables or dive computers to limit their exposure and to monitor their ascent speed.
DCS is treated by hyperbaric oxygen therapy in a recompression chamber.
Recompression in a hyperbaric chamber is the definitive treatment for decompression sickness, and arterial gas embolism.
Recompression reduces symptoms caused by mechanical disruption of tissue, and relieving ischemia by promoting the redistribution of intravascular bubbles and reducing bubble volume.
Diagnosis confirmation is bye by a positive response to treatment.
If treated early, there is a significantly higher chance of successful recovery.
DCS is classified by symptoms.
Type I is for symptoms involving only the skin, musculoskeletal system, or lymphatic system.
Type II refers tosymptoms where other organs, such as the central nervous system) are involved.
Type II DCS is considered more serious and usually has worse outcomes.
Type I and Type II DCS have the same initial management.
DCS and arterial gas embolism are treated similarly: both the result of gas bubbles in the body.
The symptoms from arterial gas embolism are generally more severe because they often arise from an infarction of blood supply and tissue death.
DCS is most frequently observed in the shoulders, elbows, knees, and ankles: Joint pain accounts for about 60% to 70% of all altitude DCS cases, with the shoulder being the most common site for altitude and bounce diving, and the knees and hip joints for saturation and compressed air work.
Neurological symptoms of headache and visual disturbance are present in 10% to 15% of DCS cases.
Skin manifestations in DCs are present in about 10% to 15% of cases.
Pulmonary DCS is very rare in divers and has been observed much less frequently in aviators since the introduction of oxygen pre-breathing protocols.
Decompression sickness can occur during rapid decompression to a high altitude in unpressurized aircraft, typically more than 5500 m:in this context it is referred to as chokes and is associated with chest pain, cough, cyanosis, and syncope.
By reducing tissue nitrogen levels by pre-breathing 100% oxygen attenuates the risk and it is now routine for high altitude aircraft crews so it reduces severe decompression.
Signs and symptoms of decompression sickness:
Musculoskeletal bubble location: Mostly large joints of the limbs;
elbows, shoulders, hip, wrists, knees, ankles.
Localized deep pain, ranging from mild to excruciating.
Sometimes a dull ache, more rarely a sharp pain.
Active and passive motion of the joint may aggravate the pain.
The pain may be reduced by bending the joint to find a more comfortable position.
If caused by altitude, pain can occur immediately or up to many hours later.
Cutaneous:
Itching, usually around the ears, face, neck, arms, and upper torso.
Sensation of tiny insects crawling over the skin.
Mottled skin usually around the shoulders, upper chest and abdomen, with itching.
Swelling of the skin, accompanied by pitting edema.
Neurologic/Brain
Altered sensation, paresthesias,increased sensitivity
Confusion or memory loss
Visual abnormalities
Unexplained mood or behavior changes
Seizures, unconsciousness
Neurologic;Spinal cord
Ascending weakness or paralysis in the legs
Urinary and fecal incontinence
Girdling sensation around the abdominal region and/or chest
Constitutional
Headache
Unexplained fatigue
Generalized malaise, poorly localized aches
Inner ear
Loss of balance
Dizziness, vertigo, nausea, vomiting
Hearing loss
Pulmonary
Dry persistent cough
Burning chest pain under the sternum, aggravated by breathing
Shortness of breath
Symptoms Frequency
local joint pain 89%
arm symptoms 70%
leg symptoms 30%
dizziness 5.3%
paralysis 2.3%
shortness of breath 1.6%
extreme fatigue 1.3%
collapse/unconsciousness 0.5%
DCS can occur rapidly after a dive,
In more than half of all cases symptoms do not begin to appear for at least an hour after a dive.
Rarely, symptoms OF DCS may occur before the dive has been completed.
Time to onset of symptoms percentage of cases
within 1 hour 42%
within 3 hours 60%
within 8 hours 83%
within 24 hours 98%
within 48 hours 100%
In a series of 5278 cases of decompression sickness symptoms develop within one hour after the diver resurfaced in 73% of mild cases, and 98% of severe cases, and 99% of all symptoms appeared within six hours.
The risk of DCS increases when diving for extended periods or at greater depth, without ascending gradually and making the decompression stops needed to slowly reduce the excess pressure of inert gases dissolved in the body.
Rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis, which can develop from a single exposure to rapid decompression.
The most common health risk on ascent to altitude is altitude sickness, or acute mountain sickness (AMS).
AMS results not from the formation of bubbles from dissolved gasses in the body but from exposure to a low partial pressure of oxygen and alkalosis.
Passengers in unpressurized aircraft at high altitude may also be at some risk of DCS.
Commercial aircraft are required to maintain the cabin at or below a pressure altitude of 2,400 m (7,900 ft) even when flying above 12,000 m (39,000 ft).
Divers who drive up a mountain or fly shortly after diving are at particular risk even in a pressurized aircraft because the regulatory cabin altitude of 2,400 m (7,900 ft) represents only 73% of sea level pressure.
The higher the altitude the greater the risk of altitude DCS but there is no specific, maximum, safe altitude below which it never occurs.
There are very few symptoms at or below 5,500 m (18,000 ft) unless patients had predisposing medical conditions or had dived recently.
A correlation exists between increased altitudes above 5,500 m (18,000 ft) and the frequency of altitude DCS.
Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism.
Environmental factors increase the risk of DCS:
the magnitude of the pressure reduction ratio
repetitive exposures – repetitive dives within a short period of time increase the risk of developing DCS; Repetitive ascents to altitudes above 5,500 metres (18,000 ft) within similar short periods increase the risk of developing altitude DCS.
Ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DCS.
Recreational dive tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute.
A rapid decompression with high rate of ascent above 5,500 metres (18,000 ft) has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.
The longer the duration of the dive, the greater is the risk of DCS.
Longer flights, especially to altitudes of 5,500 m (18,000 ft) and above, carry a greater risk of altitude DCS.
Underwater diving before flying increases the risk of developing DCS even if the dive itself was within the dive table safe limits.
Dive tables suggest post-dive time at surface level before flying to allow any residual excess nitrogen to dissipate.
DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving.
An atrial septal defect may allow bubbles to pass into the arterial circulation.
Factors that possibly contribute to increased risk of DCS:
dehydration
patent foramen ovale
age – there are some reports indicating a higher risk of altitude DCS with increasing age.
recent joint or limb injuries may predispose individuals to developing decompression-related bubbles.
Individual exposure to very cold ambient temperatures may increase the risk of altitude DCS.
Decompression sickness risk is reduced by increased ambient temperature during decompression following dives in cold water.
Patients with a high body fat content have a greater risk of DCS, due to nitrogen’s five times greater solubility in fat than in water, leading to greater amounts of total body dissolved nitrogen during time at pressure.
Fat represents about 15–25 percent of a healthy adult’s body, but stores about half of the total amount of nitrogen at normal pressures.
There is no evidence that alcohol consumption increases the incidence of DCS.
To avoid decompression sickness after long or deep bounce dives, the
surfacing diver must enter a decompression chamber for surface decompression.
Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body: bubbles produce the symptoms of decompression sickness.
On ascent from a dive, inert gas comes out of solution in a process called outgassing.
Under normal conditions, most offgassing occurs by gas exchange in the lungs.
Astronauts performing extravehicular activity undergo substantial decompression to space suit pressure, and the risk of decompression sickness is reduced by prolong oxygen prebreathing combined with mild exercise to denitrogenate the astronaut before staged decompression.
If inert gas comes out of solution too quickly to allow outgassing in the lungs, bubbles may form in the blood or within the solid tissues of the body.
The bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage.
DCS could damage: spinal cord function, leading to paralysis, sensory dysfunction, or death.
In the presence of a right-to-left shunt of the heart, such as a patent foramen ovale, venous bubbles may enter the arterial system, resulting in an arterial gas embolism.
Ebullism, may occur during explosive decompression, when water vapour forms bubbles in body fluids due to a dramatic reduction in environmental pressure.
Breathing gas mixtures that include helium, can also cause decompression sickness.
Helium enters and leaves the body faster than nitrogen, and is preferred over nitrogen in gas mixtures for deep diving.
Any inert gas that is breathed under pressure can form bubbles when the ambient pressure decreases.
DCS can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas:
isobaric counterdiffusion, and is problematic for very deep dives.
The location of where bubbles initially form is not known.
Once microbubbles form, they grow by either a reduction in pressure or by diffusion into surroundings.
Such bubbles may be located within tissues or carried along with the bloodstream.
It is the speed of blood flow within a blood vessel and its rate of delivery of perfusion that are the main factors that determine whether dissolved gas is taken up by tissue bubbles or circulation bubbles for bubble growth.
Vascular bubbles formed in the systemic capillaries may be trapped in the lung capillaries, resulting in a temporarily blockage.
A severe blockage is called chokes.
If the diver has a patent foramen ovale bubbles may pass through it and bypass the pulmonary circulation to enter the arterial blood.
These bubbles, if not absorbed in the arterial plasma and lodge in systemic capillaries they will block the flow of oxygenated blood to the tissues supplied by those capillaries.
The evidence suggests that the risk of serious neurological disease increased in divers with a resting right-to-left shunt through a patent foramen ovale.
Inert gas can diffuse into bubble nuclei between tissues, distorting and permanently damaging the tissues.
Inert gas bubbles may also compress nerves, causing pain, and extravascular bubbles usually form in slow tissues such as joints, tendons and muscle sheaths.
Direct expansion causes tissue damage, release of histamines and their associated affects.
Biochemical damage may be as important as, or more important than mechanical effects.
Bubble size and growth are affected by gas exchange with adjacent tissues, the presence of surfactants, coalescence and disintegration by collision.
Vascular bubbles may cause direct blockage, platelets activation, and trigger the coagulation process, causing clotting.
Arteries may be blocked by intravascular fat aggregation.
Platelets accumulate in the vicinity of bubbles.
Endothelial damage may be a mechanical effect of bubble pressure on the vessel walls, a toxic effect of platelet aggregates and possibly toxic effects due to the association of lipids with the air bubbles.
Protein molecules may be denatured by a cascade of pathophysiological events with consequent production of clinical signs of decompression sickness.
A sudden release of pressure in saturated tissue results in a complete disruption of cellular organelles.
A more gradual reduction in pressure may allow accumulation of a smaller number of larger bubbles, some of which may not produce clinical signs.
While gas is dissolved in all tissues, decompression sickness is only clinically recognized in the central nervous system, bone, ears, teeth, skin and lungs.
Necrosis has frequently been reported with decompression sickness in the lower cervical, thoracic, and upper lumbar regions of the spinal cord.
A drastic pressure reduction from saturation produces explosive mechanical disruption of cells by local effervescence.
With a more gradual pressure loss discrete bubbles are accumulated in the white matter, surrounded by a protein layer.
Treatment: approach varies by the severity of the clinical findings on presentation and circumstances.
Standard resuscitation intervention should be performed, if needed.
A diver is placed in the supine or recovery position to maintain and protect the airway.
Horizontal positioning helps maintain arterial blood pressure in the presence of hypovolemia but is associated with the higher intracranial pressure, than with head up.
The highest possible fraction of inspired oxygen is administered.