Decompression sickness (DCS) occurs when dissolved gasses (usually nitrogen or helium, used in mixed gas diving) exit solution and form bubbles inside the body on depressurization. DCS occurs from underwater diving decompression (ascent), working in a caisson, flying in an unpressurized aircraft, and extra-vehicular activity from spacecraft. Proper decompression procedures during diving can help decrease DCS. Experts have classified DCS as Type I with symptoms involving only the skin, musculoskeletal system, or lymphatic systems; and Type II with symptoms that involve the central nervous system.
DCS is bubble formation, growth, and elimination caused by a reduction in ambient pressure that results in inert gasses, usually nitrogen, that is dissolved in solution within tissues of the body. Individuals that breath air in a pressurized environment reach a state of equilibrium/saturation of of gas. This dissolved gas will be driven out of solution when leaving a higher-pressure environment to a lower pressure environment, such as ascending from depth during SCUBA diving, leaving a caisson work site, or ascending to altitude in an unpressured aircraft. There are individual factors identifid as possibly contributing to an increased risk of DCS. These include dehydration, patent foramen ovale, previous injury, cold ambient temperature, high body fat content, and alcohol consumption. Type II decompression sickness (neurological symptoms) is thought to occur from right-to-left shunting of venous bubbles.
The incidence of decompression sickness, fortunately, is rare. Estimates for sports diving are three cases per 10,000 dives. The incidence among commercial divers can be higher ranging from 1.5-10 per 10,000 dives. As expected, the incidence depends on the length and depth of the dive. The risk for DCS is 2.5 times greater for males than females.
The pathophysiology of DCS is due directly to the formations of bubbles coming out of solution. Tissue damage results from multiple mechanisms including blockage of blood flow and vascular spasm. Gas bubbles also cause endothelial damage resulting in activation of the intrinsic clotting cascade with platelet activation. Inflammatory mediators are released and with increased endothelial permeability development of edema, which leads to tissue ischemia.
Initial evaluation of a patient suspected of DCS should include a detailed history and physical exam. For a conscious patient get the details of exposure, including onset, duration, and progression of symptoms. For a diver with DCS, it is vital to determine the patient's dive profile and gas mix. Ear exam should look for signs of barotrauma. The patient should have a detailed neurological exam.
DCS occurs most frequently in the shoulders, elbows, knees, and ankles. Joint pain ("the bends") accounts for most cases, with the shoulder being the most prevalent site. Neurological symptoms present in 10% to 15% of DCS cases with a headache and visual disturbances being the most common symptoms. Skin manifestations are a feature in about 10% to 15% of DCS cases. Pulmonary DCS ("the chokes") is quite rare in divers and much less frequently seen in aviators because of oxygen pre-breathing protocols. Bubbles in the skin or joints result in mild symptoms, larger numbers of bubbles in the venous blood may cause lung damage, and bubbles involving spinal cord function may lead to paralysis, sensory dysfunction, or death. If there is a cardiac right-to-left shunt, (e.g., a patent foramen ovale), venous bubbles could potentially enter the arterial circulation, resulting in an arterial gas embolism.
DCS should be suspected if related symptoms occur following a drop in pressure within 24 hours of diving. The diagnostic confirmation is if the symptoms are relieved by recompression. MRI or CT can occasionally identify bubbles in DCS, but they are not good at determining the diagnosis and certainly cannot be used to rule out DCS.
As the goal for treating all patient's with symptomatic DCS is Hyperbaric Oxygen (HBO), with emphasis placed on recompression. There should be no delay in treatment for further diagnostic workup. The one exception is a chest x-ray, as untreated pneumothoraces are an absolute contraindication for HBO.
All decompression sickness cases should have initial treatment with 100% oxygen until HBO therapy is available. Neurological, pulmonary, and mottled skin lesions should be treated with HBO therapy even if seen several days after development. Fluid administration is indicated, as this helps minimize dehydration. The recommendation to administer aspirin is no longer valid, as analgesics may mask symptoms. Patient placement is in the supine position or the recovery position if vomiting occurs. The Trendelenburg position and the left lateral decubitus position (Durant's maneuver) have potentially beneficial if air emboli are suspected, but these positions are no longer recommended for extended periods, owing to concerns regarding cerebral edema. If the patient experiences an altered mental status or is unconscious, initial management should focus on the treatment and stabilization of ABC's, (airway, breathing, and circulation). Patient's should receive HBO treatment as soon as possible.
Patients that need evacuation to a definitive treatment center by aeromedical transport should fly on pressurized aircraft. If unpressurized aircraft, such as helicopters, are the only means of transport then flight altitude should be limited to 300 m or 1000 ft if possible.
Vertigo can indicate inner ear or vestibular decompression sickness wherein bubbles form in the perilymph fluid of the cochlea. However, other diving related causes merit consideration, as recompression and hyperbaric oxygen can cause worsening of some of these conditions. Inner ear barotrauma, in particular, would be a contraindication to compression as high-pressure gas may be forced into the cochlea causing further trauma on decompression. Alternobaric and caloric vertigo should be differentiated from decompression sickness by history. Cerebral arterial gas embolism affecting the midbrain or cerebellum can also present as inner ear decompression sickness but receives similar treatment.
The differential diagnosis for divers should also consider that the stress of diving can exacerbate chronic medical problems. Consider cardiac disease for patients with chest pain and exacerbation of intrinsic lung disease for shortness of breath. Other considerations include pain from previous musculoskeletal injury and stroke and hypoglycemia for altered mental status. Further concerns include drowning or near-drowning and thermal stress.
There are a variety of hyperbaric chamber treatment protocols for decompression sickness. These differences are based on such things as the severity of the insult, the availability of oxygen. There are also in water recompression protocols. The usual US treatment protocol is a US Navy Treatment Table 6 done with oxygen at pressurized to 2.8 atmospheres absolute (ATA). In water, recompression is a relatively high risk but is a consideration if there would otherwise be significant delays to treatment, logistical difficulties or other problems. It requires appropriate training, equipment, and pre-planning. Immediate treatment at the surface with oxygen is beneficial for improving outcomes and decreasing recompression treatments.
Treatment of DCS employing the US Navy Treatment Table 6 with oxygen at 18m is the standard of care. Significant delay to treatment, transportation difficulties, and facilities with limited experience may lead one to consider on-site treatment. Surface oxygen for first aid is shown to improve the efficacy of recompression and decreased the number of recompression treatments required when administered less than four hours post dive. In water recompression (IWR) to 9m, breathing oxygen is one option that has shown success over the years. IWR is not without risk and requires certain precautions. IWR would only be suitable for an organized and disciplined group of divers with suitable equipment and practical training in the procedure.
Having had decompression sickness may place one at increased risk for future similar events. Prognosis is severity dependent and also dependent on such factors as the time to recompression, availability and time to surface oxygen, and supportive care.
Decompression sickness can cause long-term damage. Central nervous system lesions in the spine and brain may occur.
The risk of decompression sickness is reducible in several ways. Divers should avoid flying within 24 hours after their last dive and longer no-fly periods may be required based on dive profiles and guided by decompression tables or computers. The use of oxygen-enriched gas can also ameliorate risk if used on "air tables." Using a more conservative dive table or dive computer setting will likewise reduce risk. Isobaric decompression, breathing oxygen at depth, likewise can lessen the inert gas burden and reduce decompression sickness risk.
Cold exposure, heavy exercise, recent alcohol use, and dehydration all increase risk and should be avoided. Preliminary research also shows that exercise several hours before diving may be protective while exercise after diving may increase the risk of DCS.
Treatment is with 100% oxygen, followed by recompression in a hyperbaric chamber. In most cases, this will prevent long-term effects. However, permanent injury from DCS is possible. To prevent the excess formation of bubbles leading to decompression sickness, divers limit their ascent rate. The recommended ascent rate used by popular decompression models is about 10 meters (33 ft) per minute.
Early identification and referral to a hyperbaric center are important for good outcomes from serious decompression sickness. In water, treatments need a well-trained and organized team approach. Divers should have oxygen for immediate administration in the case of DCS. The Divers' Alert Network provides referrals to hyperbaric facilities and 24/7 consultation with hyperbaric trained physicians and other providers.