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Jules Eden - experienced diving medicine specialist, and founder of e-med.co.uk - gives a free guide to Decompression Sickness (DCS), answering many of typical questions asked by divers:


The increasing popularity of SCUBA diving and growth of commercial diving has increased the incidence of decompression sickness (DCS). As more people of varying ages and fitness dive more often, helped by developments in technology to go deeper and for longer then doctors will see more cases of this condition.

At our Hyperbaric Chamber in London we have seen many cases of DCS in divers who have observed all the rules and stayed within their tables or computer algorithms, but still develop DCS.

Here we explain how it can develop, how it is diagnosed and how it is treated.


Effects of increasing pressure occur only on compressible substances in the body. The human body is primarily made of water, which is non-compressible; however, the gases of hollow spaces, bowels, and those dissolved in the blood are at the mercy of pressure changes.

 Physical characteristics of gases are described by the following 4 gas laws that quantify the physics and problems involved in descending under water.

To understand how DCS can occur and how it is treated then a diver needs to understand these 4 laws.

Boyle's law

The volume of a gas is directly proportional to the pressure it is under.

Every 33 feet of decent increases the pressure by one atmosphere (atm). Therefore, lung volume during a breath-hold dive at 33 feet is one-half that at the surface. At 66 feet it is 1/3, at 99 feet it is 1/4 and at 132 feet it is one-fifth. Similarly, going from 99 feet to the surface without venting (exhaling) would cause the lungs, with minimal ability to further expand, to increase pressure to three times normal with the greatest change occurring in the last 33 feet where it would double. This is the key law for this chapter to explain pressurisation issues and injuries.

Dalton's law

As an individual descends, total pressure of breathing air increases; therefore, the partial pressures of the individual components of breathing air in the body will increase proportionally. As the individual descends deeper under water, an increasing amount of nitrogen dissolves in the blood. Nitrogen at higher partial pressures alters the electrical properties of cerebral cellular membranes, causing an anaesthetic effect termed nitrogen narcosis. Every 50 feet of depth is equivalent to one alcoholic drink. Thus, at 150 feet divers may experience alterations in reasoning, memory, response time, and other problems such as idea fixation, overconfidence, and calculation errors.

Descending deeper increases the amount of dissolved oxygen. Breathing 100% oxygen at 2 atm (33 feet) may cause  oxygen toxicity in as little as 30-60 minutes. At 300 feet, the normal 21% oxygen in compressed air can become toxic, because the partial pressure of oxygen is approximately equal to 100% at 33 feet. For these reasons deep divers (usually professional or military, but increasingly sport divers as well) use specialised mixtures that replace nitrogen with helium and allow for varying percentages of oxygen depending on depth.

Henry's law

With increasing depth, nitrogen in compressed air equilibrates through the alveoli of the lungs into the blood. Over time, increasing amounts of nitrogen dissolve in the lipid or fat component of tissues, where it accumulates. As an individual ascends, there is a lag before saturated tissues start to release nitrogen back into the blood. It is this delay that creates problems.

When a critical amount of nitrogen is dissolved in the tissues, ascending too quickly causes the dissolved nitrogen to return to gas form while still in the blood or tissues, causing bubbles to form. Further reductions in pressure through flying or ascending to a higher altitude also contribute to bubble formation. The average airline cabin is pressurised only to 8000 feet to save fuel costs. If a person flies too soon after diving, this additional decrease in pressure may be enough to precipitate bubbling. If the bubbles are still in the tissue, they can cause local problems; or if they are in the blood embolization may result.



A reduction in pressure while ascending at the end of a dive can release dissolved gas (principally nitrogen) from solution in the tissues and blood and consequently form bubbles in the body.

DCS results from the effects of these bubbles on organ systems. The bubbles may disrupt cells and cause loss of function. They may act as emboli and block circulation, as well as cause mechanical compression and stretching of the blood vessels and nerves.

Additionally, the blood-bubble interface acts as a foreign surface, activating the early phases of blood coagulation and the release of  substances from the cells lining the blood vessels causing vasoconstriction which can worsen the effects of a blocked vessel.

 DCS may be divided into 3 categories:

(1) Type I (mild),

(2) Type II (serious) and

(3) Arterial gas embolization (AGE).

Type I DCS

Type I DCS is characterised by

(1) mild pains that begin to resolve within 10 minutes of onset (niggles);

(2) "skin bends" that cause itching or burning sensations of the skin; or

skin rash, which generally is a mottled rash causing marbling of the skin or a violet coloured rash which is most often seen on the chest and shoulders. On rare occasions, skin has an orange peel appearance.

It is important that this is not confused with other causes of a rash whilst diving. A suit squeeze will generally have a different pattern and look more like bruising, whilst a neoprene contact dermatitis will be in areas where a suit rubs, such as the neck or cuffs.

(4) Lymphatic involvement is uncommon and usually is signalled by painless pitting oedema which is a swelling of the lower limbs that a thumb when pressed in will leave an impression. The mildest cases involve the skin or the lymphatics. Some authorities consider anorexia and excessive fatigue after a dive as manifestations of Type I DCS.

(5) Pain (the bends) occurs in the majority (70-85%) of patients with DCS. Pain is the most common symptom of DCS and is often described as a dull, deep, throbbing, toothache-type pain, usually in a joint or tendon area but also in tissue. The shoulder is the most commonly affected joint in most divers after a shallower than 40 metre dive, whereas the knees are affected more in deep divers. The pain is initially mild and slowly becomes more intense. Because of this, many divers attribute early DCS symptoms to overexertion or a pulled muscle.

Upper limbs are affected about 3 times as often as lower limbs. The pain of Type I DCS may mask neurological signs that are hallmarks of the more serious Type II DCS.


Type II DCS is characterised by nervous system involvement pulmonary, lung symptoms and circulatory problems such as hypovolaemic shock. Pain is reported in only about 30% of cases. Because of the anatomical complexity of the central and peripheral nervous systems, signs and symptoms are variable and diverse. Symptom onset is usually immediate but may be delayed as long as 36 hours.

Nervous system

The spinal cord is the most common site for Type II DCS; symptoms mimic spinal cord trauma. Low back pain may start within a few minutes to hours after the dive and may progress to paresis, paralysis, paraesthesia, loss of sphincter control, and girdle pain of the lower trunk.

DCS can be dynamic and does not follow typical peripheral nerve distribution patterns. This strange shifting of symptoms confuses the diagnosis, differentiating DCS from traumatic nerve injuries.

Other common symptoms include headaches or visual disturbances, dizziness, tunnel vision, and changes in mental status. Labyrinthine or inner ear DCS (the staggers) causes a combination of nausea, vomiting, vertigo, and nystagmus in addition to tinnitus and partial deafness.


Pulmonary DCS (the chokes) is characterised by (1) inspiratory burning and substernal discomfort, (2) non-productive coughing that can become paroxysmal like a coughing fit, and (3) severe respiratory distress. This occurs in about 2% of all DCS cases and can end in death. Symptoms can start up to 12 hours after a dive and persist for 12-48 hours.

Circulatory system

Hypovolaemic shock commonly is associated with other symptoms. For reasons not yet fully understood, fluid shifts from intravascular to extravascular spaces. The problems of tachycardia (rapid heart beat) and postural hypotension (dizziness when you suddenly sit or stand up) are treated by oral rehydration, if the patient is conscious or via an IV if unconscious. The treatment of DCS is less effective if dehydration is not corrected.

Thrombi or clots may form from activation of the early phases of blood coagulation and the release of vasoactive substances from cells lining the blood vessels. The blood-bubble interface may act as a foreign surface causing this effect.

AGE (Arterial Gas Embolization)

Pulmonary overpressurization, for example during a breath holding ascent, can cause large gas embolization when rupture into the pulmonary vein allows alveolar gas to enter systemic or arterial circulation. Gas emboli can lodge in coronary, cerebral, and other systemic arterioles. These gas bubbles continue to expand as ascending pressure decreases, thus increasing the severity of clinical signs. Symptoms and signs depend on where the emboli travel to. Coronary artery embolization can lead to myocardial infarction or abnormal rhythms. Cerebral artery emboli can cause stroke or seizures.

Differentiating cerebral AGE from Type II neurologic DCS is usually based upon suddenness of symptoms.

AGE symptoms typically occur within 10-20 minutes after surfacing. Multiple systems may be involved. Clinical features may occur suddenly or gradually, beginning with dizziness, headache, and profound anxiousness. More dramatic symptoms of unresponsiveness, shock, and seizures can occur quickly. Neurologic symptoms vary, and death can result. CNS DCS is clinically similar to AGE; since the treatment of either requires recompression, differentiating between them is not of great importance.


History: When you feel unwell after a dive is essential to remember that symptoms or signs that appear during or following a dive are pressure-related until proven otherwise by a diagnostic or therapeutic recompression. Therefore, the doctors will ask you about pressure exposure as an aid to the diagnosis. The following specifics about the dive will be elicited:

  • Where was the dive location (e.g. ocean, lake, river, quarry or cave)?
  • What was the timing of events over the prior 72 hours (e.g. time dives occurred, length of dives, surface intervals, safety stops, flying, and type of timing used [e.g. watch with tables, dive computer])?
  • What was the rate of ascent and the depth that you dove to?

  • What were the approximate times spent at specific depths?
  • What work did you do during the dive (consider currents, distance swam, water temperature, and primary activity [e.g. wreck diving, artefact recovery])?
  • What gases did you use (compressed air, rebreathing equipment, mixed gases)?
  • Did you encounter any problems (violation of no-decompression limit dive tables, equipment, entanglement, dizziness, marine bites or stings)?
  • What was your physical condition before, during and after the dive (e.g. fatigue, alcohol intake, fever, vertigo, nausea, overexertion, pulled muscles)?
  • Was first aid delivered (e.g. oxygen, positioning, medications, fluids)?
  • You will be asked about the following symptoms:
    • General symptoms of profound fatigue or heaviness, weakness, sweating, malaise, or anorexia
    • Musculoskeletal symptoms of joint pain, tendonitis, back pain, or heaviness of extremities
    • Mental status symptoms of confusion, unconsciousness, changes in personality
    • Eye and ear symptoms of loss of vision in a particular area, double vision, tunnel vision, blurring, tinnitus, or partial hearing loss
    • Skin symptoms of itching or mottling
    • Lung symptoms of shortness of breath, non-productive cough, or blood in your sputum
    • Cardiac symptoms of inspiratory, substernal, or sharp or burning chest pain
    • Gastrointestinal symptoms of abdominal pain, faecal incontinence, nausea, or vomiting
    • Genitourinary symptoms of urinary incontinence or urinary retention
    • Neurological symptoms of loss of sensation (general or over a joint), paresis, paralysis, migrainous headache, vertigo, abnormal verbalisation, or unsteady gait
    • Lymphatic symptoms of swollen lower limbs

Physical: Physical exam findings will include the following:

  • General - fatigue, shock
  • Mental status - disorientation, mental dullness
  • Eyes - visual field deficit, pupillary changes, air bubbles in the retinal vessels, or nystagmus
  • Mouth - Liebermeister's sign (a sharply defined area of pallor in the tongue)
  • Pulmonary - rapid respiratory rate, respiratory failure, respiratory distress, or haemoptysis (blood in the sputum)
  • Cardiac - rapid heart beat, low blood pressure, abnormal cardiac rhythms, or Hamman's sign (crackling sound heard over the heart during ventricular contraction)
  • Gastrointestinal - vomiting
  • Genitourinary - urinary bladder distension, decreased urinary output
  • Neurologic - loss of sensation, loss of power, anal sphincter weakness, fitting, or poor co-ordination and wobbly gait, especially on heel to toe walking.
  • Musculoskeletal - subjective joint pain without objective findings, or decreased range of motion (ROM) due to muscle splinting of involved joint or tendon
  • Lymphatic - lymphoedema where there is swelling of the tissues due to the blocking of the lymphatic system.
  • Skin - itching, mottling/marbling, violet colour, cyanosis, or pallor
  • Diagnostic techniques - Pain, frequently musculoskeletal, is present in 57.8% of DCS cases. Two specific techniques that can aid the practitioner in diagnosing DCS are:
    • Placing a large BP cuff over the area of pain and inflating it to 150-250 mm Hg. In the patient with nitrogen bubbling in the joint or tendons, this increase can force some of the nitrogen back into solution, resulting in a temporary decrease in pain.
    • Milking the muscle toward the affected joint may increase pain by pushing more nitrogen bubbles toward the joint.
  • Differentiating between AGE and DCS
    • AGE - (1) Any type of dive can cause AGE, (2) onset is immediate (< 10-120 min), and (3) neurological deficits manifest in brain only.
    • DCS - (1) Dive must be of sufficient duration to saturate tissues, (2) onset is latent (0-36 h), and (3) neurological deficits manifest in spinal cord and brain.


  • Predisposing causes for DCS
    • Inadequate decompression or surpassing no-decompression limits
    • Inadequate surface intervals (failure to decrease accumulated nitrogen)
    • Flying or going to higher altitude soon (12-24 hours) after diving. This increases the pressure gradient.
  • Individual physiological differences
    • Obesity (nitrogen is lipid or fat soluble)
    • Fatigue
    • Age
    • Poor physical condition
    • Dehydration
    • Illness affecting lung or circulatory efficiency
    • Prior musculoskeletal injury (scar tissue decreases diffusion)
  • Environmental factors
    • Cold water (vasoconstriction decreases nitrogen off-loading)
    • Heavy work (vacuum effect in which tendon use causes gas pockets)
    • Rough sea conditions
    • Heated diving suits (leads to dehydration)
  • Divers who have been chilled on decompression dives (or dives near the no-decompression limit) and take very hot baths or showers may stimulate bubble formation.
  • Decompression tables: Decompression sickness may occur even if the decompression tables and no-decompression limits are strictly observed. The decompression tables and no-decompression limits list the maximum time allowed for a dive based upon the maximum depth achieved. The limits take into consideration nitrogen saturation of lipid tissues. Once nitrogen has saturated tissues, a standard ascent to the surface with decreasing ambient pressure can allow nitrogen to bubble out of solution according to Henry's law. Once the no-decompression limit has been passed, one or more decompression stops are required during ascent to allow delayed diffusion of nitrogen out of the lipid tissues back into the blood. Nitrogen is then exhaled through the lungs.

These tables also include calculations based upon the surface interval between dives and residual nitrogen off-loading during the time between dives. The original tables have 3 problems:

    1. The tables are based on young, healthy, and fit, Navy volunteers. Since many civilian divers do not fit this profile, the tables have limitations.
    2. The rapidly expanding use of dive computers takes into account the actual time spent at each depth. This allows for more time under water and removes a built-in factor that helps keep divers in the conservative range.
    3. There is an increasing number of casual divers.
  • The best defence against DCS is diving conservatively. However, divers may still develop DCS.
  • Today, diving experts recommend a safety stop at 15 feet for 3-5 minutes. For no-decompression dives, this is essentially a decompression stop. Since the largest change in pressure per foot occurs in the 15 feet just under the surface, this stop allows for additional nitrogen equilibration and off-loading.


Prehospital Care:

  • Extricate from water and immobilise if trauma is suspected.

  • Administer 100% oxygen, intubate if necessary, and administer IV saline.

  • If the diver is conscious then they should rehydrate with non alcoholic fluids at a rate of  1 litre each hour.

  • Perform CPR and ACLS if required as well as needle decompression of the chest if tension pneumothorax is suspected.

  • Keep the patient lying flat, and DO NOT put them in the head down position as this can worsen brain swelling.

  •  Transport to nearest emergency department and hyperbaric facility, if feasible, and try to keep all diving gear with diver. Diving gear may provide clues as to why the diver had trouble (e.g., faulty air regulator, hose leak, carbon monoxide contamination of compressed air).

Emergency Department Care:

  • Administer 100% oxygen to wash nitrogen out of the lungs and set up an increased diffusion gradient to increase nitrogen off-loading from the body.
  • Keep lying flat.
  • Perform intubation, aggressive resuscitation, and chest tube thoracotomy, if indicated.
  • Administer IV fluids for rehydration until urinary output is 1-2 mL/h. Rehydration improves circulation and perfusion.
  • Administer aspirin for antiplatelet activity if there is no active bleeding. Treat patients for nausea, vomiting, pain, and headache.
  • Contact closest hyperbaric facility (or DAN for referral) to arrange transfer and try to keep all diving gear with the diver. The diving gear may provide clues as to why the diver had trouble (e.g., faulty air regulator, hose leak, carbon monoxide contamination of the compressed air).
  • Patients with Type I or mild Type II DCS can have dramatic improvement and complete resolution. This improvement should not dissuade the practitioner from HBO referral or transfer as relapses have occurred with worse outcomes.
  • HBO treatment
    • Patients with mild Type I DCS probably do not require treatment other than breathing pure oxygen at sea level for a short time. Diver with Type I DCS symptoms, however, require close observation as symptoms may portend the onset of more serious problems requiring hyperbaric recompression. Consult a diving medicine or HBO specialist for all diving-related injuries. The only effective treatment for gas embolism is recompression; other treatments are merely symptomatic.

    • There are several types of hyperbaric chambers, which range from small monoplace (single person) chambers to complex multiple place, multiple lock-out chambers large enough for multiple patients and attendants. All chambers have the ability to maintain critical care monitoring and mechanical ventilation.

    • The basic theory behind HBO therapy is to first repressurize the patient to a depth where the bubbles from nitrogen or air are redissolved into the body tissues and fluids. Then, by breathing intermittent higher concentrations of oxygen, a larger diffusion gradient is established. The patient is slowly brought back to surface atmospheric pressure. This allows gases to diffuse gradually out of the lungs and body.

    • The exact combination of timing and depths is governed by treatment tables. These were developed primarily by the US Navy with some minor modifications by the US Air Force. In the UK we use the Tables devised by the Royal Navy. The commonest table to initiate treatment on is called Table 62. This takes 4 ˝  hours to complete. With early recognition and treatment over 75% of patients improve. If  there are still symptoms after the first treatment then retreatment is indicated. This is called a Table 60 and only takes 1 ˝ hours to complete. Retreatment continues on a daily basis until there is full symptom resolution or there is what we call a plateau in treatment where there seems to be no more change in symptoms from one retreat to the next.

    • Even with significant delays in recognition and treatment of DCS, positive results are obtained.

    • An important issue is transport of the patient to the closest hyperbaric facility. This is frequently accomplished by land transport; however, occasionally air transportation is required. Helicopter transport necessitates the pilot maintaining altitude at < 1000 feet. Fixed-wing transport should be limited to aircraft that can maintain cabin pressure at surface 1 atm (e.g., Lear Jet, Cessna Citation, military C-130 Hercules).


Admission is only indicated at an institution with HBO capability.


  • Residual paralysis, myocardial necrosis, and other ischaemic injuries may occur if recompression is not carried out immediately. These may occur even in adequately treated patients.


  • Early symptom recognition, prompt diagnosis, and appropriate treatment are keys to a positive outcome with DCS. With these, a success rate of greater than 75-85% can be achieved.


What happens next?

Flying after recompression:

Patients with joint pain, skin or lymphatic DCS who have completely resolved all symptoms after recompression can fly 24 hours after exiting the chamber.

Patients with neurological or multisystem DCS who have complete resolution should not fly for 48 hours after recompression.

If a longer recompression than a Table 62 has been used then 72 hours is the limit.

If there are still residual symptoms after finishing treatment then 72 hours is the limit and then only after consultation with a diving medical specialist.

Diving after recompression:

Divers who have had a successfully treated Type 1 DCS can return back to the water from 7 days after treatment has finished, however we do recommend that these are guidelines for fit Naval divers, and we suggest that in others that they leave diving for at least 4 weeks after treatment of mild DCS.

Divers who have had mild tingling or numbness, fully treated on a Table 62 should wait for at least 4 weeks after recompression. This is the time, though, for Sport divers, professionals could dive again after 14 days.

If there has been incomplete recovery after recompression, or the DCS was more serious there should be a period of 4 weeks for fit professionals and 6 weeks for Sport divers.

If there has been a serious AGE there may be doubt over whether a diver should ever dive again, and that decision should be left to a diving medical specialist.


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