Decompression sickness

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2] Jaspinder Kaur, MBBS[3]

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Synonyms and keywords: Decompression illness; DCS; the diver's disease; the bends; Caisson disease; aerobullosis

Overview

Decompression sickness (DCS) is a multi-system condition characterized by a variety of clinical manifestations resulting from exposure to reduced barometric pressures that causes normally dissolved inert gases (mainly nitrogen) in body fluids and tissues to come out of physical solution, and develops a free gas phase by forming an intravascular and extravascular bubbles. The likelihood of DCS is related to the extent of bubble formation which results in minor symptoms from a few bubbles formation to a large bubble causing multiorgan failure and death. The severity and nature of the DCS injury vary from mild systemic, musculoskeletal and cutaneous manifestations to severe, life-threatening central nervous and cardiorespiratory symptoms. It is mostly observed in underwater decompression diving activities (e.g SCUBA) and depressurisation events such as emerging from a caisson, flying in an unpressurised aircraft at altitude, and extravehicular activity from spacecraft. The clinical presentation can show an individual susceptibility by varying from day to day and under the same conditions. The classification of types of DCS by its symptoms has evolved since its origin and research done to prevent it. It is uncommon if the divers follow the appropriate procedures by using dive tables or dive computers to limit their exposure and control their ascent speed. If DCS is suspected, it is treated by airway stabilization, oxygen, and hyperbaric therapy in a recompression chamber. An early treatment ensures a significantly higher chance of successful recovery.

Historical Perspective

• 1670: Sir Robert Boyle performed an experiment with a viper in a vacuum. A bubble was observed in its eye and it displayed signs of extreme discomfort. This was the first recorded description of DCS in animals.
• 1841: Jacques Triger documented the first cases of DCS in humans when two miners involved in pressurised caisson work developed symptoms.
• 1847: The effectiveness of recompression for the treatment of DCS in caisson workers was described by B. Pol and T.J. Watelle.
• 1857: Felix Hoppe-Seyler repeated Boyle's experiments and suggested that sudden death in compressed air workers was caused by bubble formation, and recommended recompression therapy.
• 1861: Bucquoy proposed the hypothesis that the blood gases return to the free state under the influence of decompression and cause accidents comparable to those of an injection of air in the veins".
• 1868: Alfred Le Roy de Méricourt described DCS as an occupational illness of sponge divers.
• 1873: Dr. Andrew Smith first used the terms "caisson disease" and "compressed air illness", describing 110 cases of DCS as the physician in charge during construction of the Brooklyn Bridge. The nickname "the bends" was used after workers emerging from pressurized construction on the Brooklyn Bridge adopted a posture similar to fashionable ladies of the period "the Grecian Bend".
• 1878: Paul Bert determined that DCS is caused by nitrogen gas bubbles released from tissues and blood during or after decompression, and showed the advantages of breathing oxygen after developing DCS.
• 1889–90 - Ernest William Moir builds the first medical airlock when he noticed that about 25% of the workforce digging the Hudson River Tunnel were dying from DCS and realised that the solution was recompression.
• 1908 – John Scott Haldane prepared the first recognised decompression table for the British Admiralty. This table was based on experiments performed on goats using an end point of symptomatic DCS.
• 1912 – Chief Gunner George D. Stillson of the United States Navy created a program to test and refine Haldane's tables.This program ultimately led to the first publication of the United States Navy Diving Manual and the establishment of a Navy Diving School in Newport, Rhode Island.

Classification

In 1960, The Golding Classification was introduced and categorized DCS into type 1 DCS and type 2 DCS .

Table 1 shows the Golding classification of DCS:

FEATURES	TYPE 1	TYPE 2
Systems involved	Joints, skin, and lymphatics	Neurological, inner ear, and cardiopulmonary
Onset of symptoms	Build in intensity	Gradual or abrupt
Severity	Mild	Severe

Following advancement to the treatment protocols and variable presentations, this classification is now much less useful in making the diagnosis. All the manifestations, whether DCS or arterial gas embolism (AGE), were categorized under the general designation “decompression illness (DCI)” when the precise diagnosis cannot be made because they both results from the gas bubbles in the body, have overlapping of their spectra of symptoms, and similar treatment methods.

Pathophysiology

The pathophysiology of DCS is in accordance with Henry’s law. It states that the solubility of a gas in a liquid is directly proportional to the pressure exerted on the gas and liquid. Thus, the amount of inert gases (eg, nitrogen, helium) dissolved in the blood and tissues increases at higher pressure, and hence depends on the depth and the duration of the dive.

During a dive, the partial pressure of nitrogen and oxygen increases resulting in a diffusion gradient favoring uptake of nitrogen into the bloodstream and tissues. Under normal circumstances, the lungs functions as a vehicle for the gaseous exchange and elimination from the body. As the atmospheric pressure decrease during the ascent, more nitrogen precipitates from the tissues into the bloodstream and then diffuses back into the alveoli for exhalation process. If ascent occurs too rapidly or the elimination gradient is so steep, the gas quickly dissipates from the tissues and blood forming small air bubbles. This process is called “out gassing” or “off gassing”. Slow ascent, on the other hand, allows for equilibrium to be gradually achieved, and prevents the rapid changes in partial pressure of nitrogen in the bloodstream. Hence, the amount of bubble formation depends on the depth and duration of the dive, and the rate of the ascent.

Venous bubbles may form de novo or result from the intravascular release of tissue bubbles. The venous gas emboli usually get filtered at arteriole level on reaching the lungs. However, the bubbles may pass directly into the arterial circulation if the pulmonary arterial pressure (PAP) rises after underwater diving.

• Bubbles primarily travel to vital organs such as the nervous system; and get lodged in arterioles and capillary beds causing mass effect. These bubbles obstruct venous outflow and occlude arteries, as well as cause a shearing force on endovascular surfaces and impairs vascular integrity during their transit. The disturbed vascular permeability further leads to hemoconcentration, disturbance of microvascular flow, and a breakdown in the blood brain barrier.
• Bubbles cause secondary multiple biochemical effects by activating platelets, complement, leucocytes and the clotting cascade; and hence resulting in an inflammatory response in the affected tissues.
• Autochthonous or extravascular bubbles arise spontaneously, and are more likely to form in tissues with high gas content and poor perfusion because the large amount of gas in the tissues such as spinal cord white matter, adipose tissue, and periarticular tissue cannot be removed by the low perfusing blood volume.

Bubbles are responsible for the proximate cause of injury, whereas the several pro-inflammatory activated pathways leads to the progression of injury. Thus, DCS can have an evolving course with inflammatory mediated symptoms worsening over time.

Clinical Features/presentation

The presentation of DCS is frequently idiosyncratic as its "typical" pattern gives an atypical presentation. Symptoms of DCS (listed in decreasing order of overall prevalence) observed by the U.S. Navy are as follows in Table 2:

Symptoms	Features in %
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

Onset: The median time to symptom/sign onset is 30 minutes and severe neurologic symptoms tend to present within 10 minutes; and majority of them experience symptoms/signs within 24 to 48 hours of emerging from the water. The U.S. Navy and Technical Diving International have published a table that documents time to onset of first symptoms. The table does not differentiate between types of DCS, or types of symptom.

Table 3 shows the time of onset of symptoms among DCS suspected cases:

Time to onset	Percentage of cases
Within 1 hour	42%
Within 3 hour	60%
Within 8 hour	83%
Within 24 hour	98%
Within 48 hour	100%

While bubbles can originate in any part of the body, DCS is most frequently observed in the joints namely shoulders, elbows, knees, and ankles. Shoulder is the most common site for altitude and bounce diving; and the knees and hip joints for saturation and compressed air work. The symptoms of limb bends arises from increased intermedullary pressure in the ends of long bones; and gas phase separation along ligaments and tendon sheaths, and thus presenting painful discomfort from the simple mechanical distention and movement. Dermatological manifestations are due to the blood extravasated from the cutaneous vessels as a consequence of bubble induced endothelial injury. Pulmonary DCS ("the chokes") is rarely reported in divers; and believed to arise from an extremely huge load of venous bubbles in the pulmonary artery which results in an elevated pulmonary artery and right ventricular pressures, and further increasing the interstitial fluid and hence, leads to the development of the chokes or difficult breathing. Spinal cord DCS have two interrelated mechanisms. The first is obstruction of venous outflow of the spinal cord in the epidural plexus which is a series of blood vessels having a relatively slow blood flow. Once this process develops, it results in an ongoing and progressive diminution of blood flow to the cord, and thereafter, the second process either begins with the in-situ bubble formation within the tissue of the spinal cord.

Table 4 shows symptoms and signs of different DCS types:

DCS type	Bubble location	Signs and symptoms
Musculoskeletal: BENDS	Mostly large joints (elbows, shoulders, hip, wrists, knees, ankles)	Characteristics: Localized deep pain, ranging from mild to excruciating; dull ache (sometimes); sharp pain (rarely) Aggravating factor: Active and passive motion of the joint Relieving factor: bending the joint to a comfortable position Onset: immediately or few hours later in case of altitude induced DCS
Cutaneous: SKIN BENDS	Skin	Site: Itching around the ears, face, neck, arms, and upper torso Formication: Sensation of tiny insects crawling over the skin Cutis Marmorata: Mottled or marbled skin usually around the shoulders, upper chest and abdomen, with itching Pitting edema: Swelling of the skin, accompanied by tiny scar-like skin depressions
Neurologic	Brain	Most common: Headache and visual disturbances Visual changes: Spots in visual field (scotoma), tunnel vision, double vision (diplopia), or blurry vision Confusion or memory loss Unexplained extreme fatigue or behavior changes Seizures, dizziness, vertigo, nausea, vomiting and unconsciousness may occur
Neurologic	Spinal cord	Abnormal sensations such as burning, stinging, and tingling around the lower chest and back Symptoms may spread from the feet up and may be accompanied by ascending weakness or paralysis Girdling abdominal or chest pain
Neurologic	Peripheral Nerves	Urinary and rectal incontinence Abnormal sensations, such as numbness, burning, stinging, tingling and paresthesia Muscle weakness or twitching
Constitutional	Whole body	Headache Unexplained fatigue Generalised malaise, poorly localised aches
Audiovestibular	Inner ear	Loss of balance Dizziness, vertigo, nausea, vomiting Hearing loss
Pulmonary CHOKES	Lungs	Dry persistent cough Burning chest pain under the sternum, aggravated by breathing Shortness of breath
Dysbaric osteonecrosis	Bones	Late manifestation and often occurs without any previous symptoms An insidious form caused by prolonged or closely repeated exposures to increased pressure Typically found in people working in compressed air and in deep commercial rather than recreational divers Deterioration of shoulder and hip articular surfaces cause chronic pain and severe joint disability

Differential Diagnosis

Differential diagnosis is the process by which medical personnel figure out which of the potential condition is most likely responsible for the symptoms when two or more conditions have overlapping symptoms among the many diving-related injuries. An alternative diagnosis should also be suspected if severe symptoms begin more than six hours following decompression without an altitude exposure or if any symptom occurs more than 24 hours after surfacing.

The table 5 below shows various different medical conditions mimicking the DCS:

Medical condition	Clinical characteristics
Arterial Gas Embolism (AGE)	Pulmonary Barotrauma: usually occurs when the air expands to cause the lung rupture and releases gas bubbles directly into the arterial circulation. Typical presentation: a diver who surfaces unconscious and remains so, or who loses consciousness within minutes of surfacing. A true medical emergency condition Rapid evacuation to a treatment facility is paramount.
Inner-ear barotrauma	Usually occurs during descent Tinnitus, hearing loss, and persistent vertigo Middle-ear barotraumas: Conductive hearing loss seen Both inner-ear and middle-ear barotrauma are usually preceded by difficulty in equalizing middle-ear pressure Alternobaric vertigo: transient vertigo during compression or decompression arises because of asymmetric middle-ear pressure equilibration
Middle-ear or maxillary sinus overinflation	It is caused by gas expansion during ascent and an obstructed eustachian tube or sinus ostium Compresses the facial nerve and causes unilateral upper and lower facial weakness, or Compression of branches of the trigeminal nerve causing hypoaesthesia of the face
Contaminated diving gas and oxygen toxic effects	Carbon monoxide poisoning: contaminated breathing gas can cause encephalopathy and convulsions. Oxygen toxicity: most common in divers using enriched oxygen breathing mixtures; and can cause convulsions at depth.
Musculoskeletal strains or trauma sustained	Time of onset (e.g.: before, during, or after diving) and history of trauma or strain are helpful. Pain is usually accompanied by tenderness or position-related or motion-related exacerbation on physical examination.
Seafood toxin ingestion	Ingestion of toxins (e.g.: ciguatera, puffer fish, paralytic shellfish poisoning ) Often associated with gastrointestinal symptoms, and can cause neurological manifestations within hours after ingestion
Immersion pulmonary edema	This disorder usually begins during descent or at depth, whereas the onset of cardiorespiratory DCS occurs after the dive They might get confused since both cause dyspnea and cough
Water aspiration	Water aspiration could be mistaken for cardiorespiratory DCS Both can cause pulmonary edema, although the diver is usually aware of aspiration
Coincidental, unrelated acute neurological disorder	Diagnosis of stroke, hypothermia, hypoglycemia, and spinal hematoma is made with conventional techniques
Thermal stress	Usually occur due to cold exposure but sometimes excessive heat can be responsible

Epidemiology and Demographics

The incidence of DCS, fortunately, is rare. It is estimated in about 2 to 4/10,000 dives among recreational divers. The incidence among commercial divers, who often have minor musculoskeletal injuries, can be higher ranging from 1.5-10 per 10,000 dives. As explained, the incidence depends on the length and depth of the dive. The risk for DCS is 2.5 times greater for males than females.

Risk Factors

Various demographic, environmental, and dive style factors are associated with the predisposition to DCS. A statistical study published in 2005 tested potential multiple risk factors such as age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations of DCS were found with asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased diving depth, previous DCS episodes, multiple consecutive days of diving and being male were all associated with the higher risk. On the other hand, a lower risk was reported among nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification possibly as indicators of more extensive training and experience.

Environmental: The following environmental factors have been shown to increase the risk of DCS:

• Magnitude of the pressure reduction ratio: A large pressure reduction ratio is more likely to cause DCS than a small one.
• Repetitive exposures: Repetitive dives and ascents to altitudes above 5,500 metres (18,000 ft) within similar short periods increase the risk of developing DCS because excessive nitrogen remains dissolved in body tissues for at least 12 hours after each dive, and hence, repeated dives within 1 day are more likely to cause it.
• Rate of ascent: the faster the ascent, the greater the risk of developing DCS. The U.S. Navy Diving Manual indicates that ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute. An individual exposed to a rapid decompression (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.
• Duration of exposure: 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.
• Post dive air travel: Divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits.
• Diving before travelling to altitude: DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at 2,400 m (7,900 ft) increase their risk of DCS.
• Diving at altitude: Diving in water whose surface altitude is above 300 m (980 ft); for example, Lake Titicaca is at 3,800 m (12,500 ft) and diving in it without using versions of decompression tables or dive computers that are modified for high-altitude.

Individual: The following individual factors have been identified as possibly contributing to increased risk of DCS:

• Dehydration: DCS could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline, and the high surface tension of water is generally regarded as helpful in controlling bubble size. Therefore, maintaining adequate hydration is recommended.
• Patent foramen ovale (PFO): A hole between the atrial chambers of the heart in the fetus is normally closed by a flap with the first breaths at birth. In about 20% of adults the flap does not completely seal, however, allowing blood through the hole when coughing or during activities that raise chest pressure. In diving, this can allow venous blood with microbubbles of inert gas to bypass the lungs, where the bubbles would otherwise be filtered out by the lung capillary system, and return directly to the arterial system (including arteries to the brain, spinal cord and heart). In the arterial system, bubbles are far more dangerous because they block circulation and cause infarction. In the brain, infarction results in stroke, and in the spinal cord, it may predispose to paralysis.)
• Age: A higher risk of altitude DCS with increasing age (especially >42 years of age) has been reported.
• Previous injury: Recent joint or limb injuries may predispose individuals to developing decompression-related bubbles.
• Ambient temperature: An individual exposure to very cold ambient temperatures may increase the risk of altitude DCS which can be reduced by increasing ambient temperature during decompression following the dives in cold water.
• Body type: A person who has a high body fat content which stores about the half the total amount of the nitrogen is at greater risk of DCS. This is due to nitrogen's five times greater solubility in fat than in water, leading to greater amounts of total body dissolved nitrogen during high atmospheric pressure.
• Alcohol consumption: It increases dehydration and inhibits pituitary release of antidiuretic hormone (ADH); and therefore may increase susceptibility to DCS. Contrarily, another study found no evidence that alcohol consumption increases the incidence of DCS.
• Work and exercise: Work or exercise at depth or shortly after diving is strongly associated with DCS, as it promotes increased inert gas uptake. Light exercise during ascent or stop phase can promote gas excretion, but strenuous exercise will promote bubble formation.
• Temperature: Warm conditions may favor nitrogen uptake, and places a patient at higher risk of “out gassing” during ascent as more nitrogen has been dissolved. On the other hand, cold conditions slow the process, but no definitive studies have demonstrated a causal relationship between thermal conditions and development of DCS.
• Asthma: They are generally advised not to dive due to a theoretical risk of bronchospasm triggered by cold or changing environments, inability to quickly respond to an asthma attack while submerged, and supposed increased barotrauma during ascent. However, there is limited data to support preventing asthmatics from diving, so more studies are warranted. Well-controlled asthmatics with normal PFTs can occasionally be permitted to dive, but this should be assessed on a case-by-case basis.

Diagnosis

DCS is primarily a clinical diagnosis assessed with a very thorough and detailed dive history and the clinical examination, including the neurologic examination. Time of onset and the specific symptoms/signs (table 4) aid in establishing the diagnosis. 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. Hence, there should be no delay in treatment for further diagnostic workup.

Diagnostic criteria: In 2004 Freiberger identified important diagnostic factors using simulated diving injury cases. The top five diagnostic factors in order of importance were: (1) a neurologic symptom as the primary presenting symptom, (2) onset time to symptoms, (3) joint pain as a presenting symptom, (4) any relief after recompression treatment, and (5) maximum depth of the last dive.

Laboratory findings: No laboratory studies make a definitive diagnosis of DCS. However, an elevation in serum CK is associated with severe AGE, and hemoconcentration is associated with DCS.

Imaging findings: No imaging study can confirm the diagnosis of DCS. However, studies may rule out other causes of the patient’s symptoms. These studies should be performed rapidly as prompt intervention is important in managing DCS successfully. CXR should always be performed to evaluate for pneumothorax, pneumomediastinum, pulmonary overexpansion injury, or pulmonary edema. Bubbles are rarely detectable with radiography in joints affected by pain. Skeletal x-rays are not diagnostic for dysbaric osteonecrosis which may show joint degeneration; and cannot differentiate it from the other joint disorders.

Other diagnostic studies:

MRI or CT can occasionally identify bubbles in DCS, but they are not sensitive in determining the diagnosis and certainly is not the best method to rule out DCS. CT and MRI may be helpful to rule out other differential disorders that causes similar signs and symptoms (eg, herniated intervertebral disk, ischemic stroke, central nervous system hemorrhage).

A head CT scan should be strongly considered in any patient who has altered mental status in order to evaluate alternative diagnoses, such as subdural or epidural hematoma. A “normal” head CT is not useful in excluding DCS as it is not common to see vascular gas on a head CT under circumstances of suspected DCS.

MRI is not useful for detection of abnormalities of the spinal cord or brain related to DCS and hence, can often be falsely reassuring. However, it can pick up ischemic lesions of the brain or spinal cord.

Chest CT: It is sensitive for the detection of an extrapulmonary air, but is unnecessary because of its high radiation exposure.

Doppler ultrasonography and echocardiography can be done to rule out right to left shunt and for research purposes into venous gas emboli but not for diagnosis of DCS.

Specific neurophysiological tests (eg, audiometry and electronystagmography for inner-ear decompression sickness) can usually be delayed until after recompression.

Other Non invasive pulmonary diagnostic test in making or excluding the diagnosis: NONE

Other Diagnostic procedures (e.g.: Bronchoscopy) in making or excluding the diagnosis: NONE

Pathology/Cytology/Genetics Study in making or excluding the diagnosis: NONE

Although laboratory and radiological analyses are useful for detection of DCS related abnormalities in some cases; however, these studies are not considered as the deciding factor for the start of the recompression therapy, and hence, recompression should be given without any delay unless there is a strong suspicion of a non-diving related cause (eg, cerebral hemorrhage).

Treatment

The several elements to the effective management of DCS consist of initial treatment including on-the-scene evaluation and first aid; transportation; and definitive medical treatment.

On the scene first aid: The foundation of first aid is basic life support. 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). All DCS suspected cases should have initial treatment with high flow oxygen at 15ltr/min via a non-rebreathe mask or pocket masks regardless of their oxygen saturations. This high-flow 100% oxygen enhances nitrogen washout by widening the nitrogen pressure gradient between the lungs and the circulation, thus accelerating reabsorption of embolic bubbles.

Decompression sickness

Mild Symptoms: •Inhalation of oxygen with FiO2 1.0; •Fluid administration (i.v. if possible,otherwise oral in unconscious patient)

Severe Symptoms with pain, neurological and/or pulmonary impairment

Complete relief of symptoms within 30 minutes

Emergency treatment: •Flat supine position; •CPR if necessary; •Insufflation of 100% inspired Oxygen; •Intubation when unconscious; •Intravenous line; •Infusion therapy; •HBOT as soon as possible

If no

Hyperbaric Oxygen Therapy: •Treatment protocol most widespread: Table 6 USN; •When intubated: paracentesis recommended; •Lung ventilated at both sides?; •Pneumothorax?

If yes

Further drug therapy (scientifically not finally proven); •Corticosteroids, Aspirin, Lidocaine

Further measures: •Foley catheters; •Renal protection; •Early rehabilitation measures; •Physiotherapeutic excercise between treatments

Hospitalisation for 24h

Fluid administration is indicated to restore lost intravascular volume and minimize the dehydration. Oral resuscitation fluid (or plain water) is indicated for alert patients with mild manifestations. Isotonic IV fluid resuscitation and maintenance IV fluids should be administered to those with serious manifestations in order to counteract interstitial fluid shifts and decreases in plasma volume arising from endothelial injury.

It is essential that the suspected cases should be stabilized at the nearest medical facility before transportation to a recompression chamber. Insert a catheter if there is any suspicion of the patient having the urinary retention.

Early oxygen first aid is important and may reduce symptoms substantially, but this should not change the treatment plan. Symptoms of air embolism and serious DCS often clear after initial oxygen breathing, but they may reappear later. Because of this, always contact DAN at +1-919-684-9111 or a dive physician in cases of suspected DCI, even if the symptoms and signs appear to have resolved.

Positioning and transportation: The supine position or the recovery position should be preferred if vomiting occurs. The Trendelenburg position and the left lateral decubitus position (Durant's maneuver) have beneficial effect if air emboli are suspected, however these positions are no longer recommended for extended duration due to concerns regarding cerebral edema.

Patients with more severe symptoms need an evacuation to a suitable recompression facility because time to treatment and severity of the injury are important determinants of outcome and hence, transport should not be delayed for the performance of nonessential procedures. In case of aeromedical transport, pressurized aircraft with 1 atmosphere internal pressure is preferred. 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 and oxygen should be given continuously. Instructions to fly the patient “as low as safely possible” should be given to helicopter transport. Commercial aircraft, although pressurized, typically have a cabin pressure equivalent to 2438 m (8000 ft) at normal cruise altitude, which may precipitate symptoms.

Definitive treatment: Hyperbaric Oxygen Therapy (HBOT)

The definitive treatment is hyperbaric oxygen (HBOT) therapy which delivers the pure 100% oxygen at a pressure substantially higher than that of atmospheric pressure in recompression chambers. It should be initiated as soon as possible. Delays of > 4 hours from the time of injury to recompression correlate with a marked elevation in the incidence of residual symptoms following therapy.

Indication: All the patients except those whose symptoms are limited to itching, skin mottling, and fatigue which may be treated with oxygen therapy alone; however these patients should be observed for any kind of deterioration.

Effects of Recompression therapy:

• Bubble crushing: as per Boyles law, increasing pressure decreases the volume of bubbles
• Flushing out the nitrogen bubbles with oxygen delivery by improving gradient
• Healing damaged tissue with hyperbaric oxygen

Equipment: It is conducted in an acrylic tube sized monoplace chamber to hold just one patient, or in a multiplace chamber which is sized to accommodate one or more patients with one or more technicians or other medical personnel. Multilock chambers are designed to allow patients, tenders or equipment to be transferred into and out of the chamber while treatment is ongoing.

Regimen: A common HBO regimen is the U.S. Navy Treatment Table 6 (USN 2008). According to this regimen, HBOT chamber is brought to 2.8 atmospheres absolute (ATA), (equivalent of depth of 60 feet/18 meters) over a few minutes and then 100% FiO2 is initiated. 100% FiO2 is used for 20 minutes at a time, alternating with 5 minute intervals of room air breathing to reduce the risk of oxygen toxicity. Upon completion, the pressure is increased by no more than 1 foot/minute, with a prolonged period of equilibration at 30 feet. The total therapy time is about 5 hours. The therapy can be continued daily for several days until no further improvement is seen in the patient's symptoms.

Mechanism of action: The mechanism of HBOT is twofold. First, elevated atmospheric pressure in the chamber increases the partial pressure of gases and dissolution of nitrogen back into liquid (Henry’s law), and the increased pressure also decreases the volume of gas present in the body (Boyle’s law). Second, increased FiO2 results in decreased partial pressure of nitrogen in inspired gas. This enhances the diffusion gradient of nitrogen out of body tissues, favoring exhalation and elimination from the body, and blunting the neutrophillic response to injured endothelium.

Risks:

• Barotrauma:
  • Middle ear barotrauma: most common adverse effect of HBOT; generally requires supportive care. Bilateral tympanostomy tubes may be required in severe cases.
  • Pulmonary barotrauma: risk of pneumothorax; chest tube can be inserted
  • Pneumomediastinum: managed conservatively
  • Similar mechanism and management as barotrauma caused by diving
• Oxygen toxicity:
  • Pulmonary toxicity: small airways dysfunction observed on exceeding the treatment duration and pressure beyond the recommended therapeutic protocols
  • CNS toxicity: generalized tonic-clonic seizures occur with an incidence of approximately 1-4 per 10,000 patient treatments. Risk is higher in patients who are hypercapnic, acidemia and/or septic.
• Seizures: mechanisms not well-understood
  • CNS toxicity: managed by decreased FiO2 with same elevated atmospheric pressure
  • Ocular toxicity: myopia can be seen in those who undergo prolonged daily therapy
• Confinement anxiety: Managed with anxiolytics
• Fire: due to elevated FiO2

In-water recompression (IWR) therapy: It is practical only with a substantial amount of planning, support, equipment and personnel; appropriate water conditions; and suitable patient status. Critical challenges can arise due to changes in the patient's consciousness, oxygen toxicity, gas supply, and even thermal stress. An unsuccessful in-water recompression may leave the patient in worse shape than had the attempt not been made. Hence, it would only be suitable for an organized and disciplined group of divers with suitable equipment and practical training in the procedure.

Common pressure reductions that cause DCS

The main cause of DCS is a reduction in the pressure surrounding the body. Common ways in which the required reduction in pressure occur are:* leaving a high atmospheric pressure environment* rapid ascent through the water during a dive* ascent to altitude while flying

Leaving a high pressure environment

The original name for DCS was caisson disease; this term was used in the 19th century, when large engineering excavations below the water table, such as with the piers of bridges and with tunnels, had to be done in caissons under pressure to keep water from flooding the excavations. Workers who spend time in high-pressure atmospheric pressure conditions are at risk if they leave that environment and reduce the pressure surrounding them.DCS was a major factor during the construction of Eads Bridge when 15 workers died from what was then a mysterious illness, and later during construction of the Brooklyn Bridge, where it incapacitated the project leader Washington Roebling.

Ascent during a dive

DCS is best known as an injury that affects scuba divers. The pressure of the surrounding water increases as the diver descends and reduces as the diver ascends. The risk of DCS increases by diving long or deep without slowly ascending and making the decompression stops needed to eliminate the inert gases normally, although the specific risk factors are not well understood. Some divers seem more susceptible than others under identical conditions. There have been known cases of bends in snorkellers who have made many deep dives in succession. DCS may be the cause of the disease taravana which affects South Pacific island natives who for centuries have dived without equipment for food and pearls.Two linked factors contribute to divers' DCS, although the complete relationship of causes is not fully understood:* deep or long dives: inert gases in breathing gases, such as nitrogen and helium, are absorbed into the tissues of the body in higher concentrations than normal (Henry's Law) when breathed at high pressure.* fast ascents: reducing the ambient pressure, as happens during the ascent, causes the absorbed gases to come back out of solution, and form "microbubbles" in the blood. Those bubbles will safely leave the body through the lungs if the ascent is slow enough that the volume of bubbles does not rise too high. The physiologist John Haldane studied this problem in the early 20th century, eventually devising the method of staged, gradual decompression, whereby the pressure on the diver is released slowly enough that the nitrogen comes gradually out of solution without leading to DCS. Bubbles form after every dive: slow ascent and decompression stops simply reduce the volume and number of the bubbles to a level at which there is no injury to the diver. Severe cases of decompression sickness can lead to death. Large bubbles of gas impede the flow of oxygen-rich blood to the brain, central nervous system, and other vital organs. Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON) "bone cell death from bad pressure". DON can develop from a single exposure to rapid decompression. DON is diagnosed with lesions visible in X-ray images of the bones. Unfortunately, X-rays appear normal for at least 3 months after the permanent damage has occurred; it may take 4 years after the damage has occurred for its effects to become visible in the X-ray images. [4]

Avoidance

Decompression tables and dive computers have been developed that help the diver choose depth and duration of decompression stops for a particular dive profile at depth. Avoiding decompression sickness is not an exact science. Accidents can occur after relatively shallow and short dives. To reduce the risks, divers should avoid long and deep dives and should ascend slowly. Also, dives requiring decompression stops and dives with less than a 16-hour interval since the previous dive increase the risk of DCS. There are many additional risk factors, such as age, obesity, fatigue, use of alcohol, dehydration, and a patent foramen ovale. In addition, flying at a high altitude less than 24 hours after a deep dive can be a precipitating factor for decompression illness.Astronauts aboard the International Space Station preparing for Extra-vehicular activity "camp out" at low atmospheric pressure (approximately 10 psi = 700 mbar) spending 8 sleeping hours in the airlock chamber before their spacewalk. Their spacesuits can operate at 4.7 psi = 330 mbar for maximum flexibility.

Helium

Nitrogen is not the only breathing gas that causes DCS. Gas mixtures such as trimix and heliox include helium, which can also be implicated in decompression sickness. Helium both enters and leaves the body faster than nitrogen, and for dives of three or more hours in duration, the body almost reaches saturation of helium. For such dives, the decompression time is shorter than for nitrogen-based breathing gases such as air. There is some debate as to the decompression effects of helium for shorter duration dives. Most divers do longer decompressions, whereas some groups like the WKPP have been pioneering the use of shorter decompression times by including deep stops. Decompression time can be significantly shortened by breathing rich nitrox (or pure oxygen in very shallow water) during the decompression phase of the dive. The reason is that the nitrogen outgases at a rate proportional to the difference between the ppN₂ (partial pressure of nitrogen) in the diver's body and the ppN₂ in the gas that he or she is breathing, but the likelihood of bubbles is proportional to the difference between the ppN₂ in the diver's body and the total surrounding air or water pressure.

Ascent to altitude

People flying in un-pressurized aircraft at high altitude, such as stowaways, or passengers in a cabin that has experienced rapid decompression, or pilots in an open cockpit, can suffer from decompression sickness. Even Lockheed U-2 pilots experienced altitude DCS in the mid-'50s during the Cold War flying over their targets. Divers who dive and then fly in aircraft are at risk even in pressurized aircraft because the cabin air pressure is less than the air pressure at sea level. The same applies to divers going into higher elevations by land after diving. Altitude DCS became a commonly observed problem associated with high-altitude balloon and aircraft flights in the 1930s. In present-day aviation, technology allows civilian aircraft (commercial and private) to fly higher and faster than ever before. Though modern aircraft are safer and more reliable, occupants are still subject to the stresses of high-altitude flight and the unique problems that go with these lofty heights. A century-and-a-half after the first DCS case was described, our understanding of DCS has improved and a body of knowledge has accumulated; however, this problem is far from being solved. Altitude DCS is still a risk to the occupants of modern aircraft. There is no specific altitude threshold that can be considered safe for everyone below which it can be assured that no one will develop altitude DCS. However, there is very little evidence of altitude DCS occurring among healthy individuals at pressure altitudes below 18,000 feet who have not been scuba diving. Individual exposures to pressure altitudes between 18,000 and 25,000 feet have shown a low occurrence of altitude DCS. Most cases of altitude DCS occur among individuals exposed to pressure altitudes of 25,000 feet or higher. A US Air Force study of altitude DCS cases reported that only 13 percent occurred below 25,000 feet The higher the altitude of exposure, the greater the risk of developing altitude DCS. It is important to clarify that although exposures to incremental altitudes above 18,000 feet show an incremental risk of altitude DCS they do not show a direct relationship with the severity of the various types of DCS (see Table 1).Arterial gas embolism and DCS have very similar treatment because they are both the result of gas bubbles in the body. Their spectra of symptoms also overlap, although those from arterial gas embolism are more severe because they often cause infarction and tissue death as noted above. In a diving context, the two are joined under the general term of decompression illness. Another term, dysbarism, encompasses decompression sickness, arterial gas embolism, and barotrauma.Ascent to altitude can happen without flying in places such as the Ethiopia and Eritrea highland (8000 feet = about 1.5 miles above sea level) and the Peru and Bolivia altiplano and Tibet (2 to 3 miles above sea level).

Medical treatment

Mild cases of the "bends" and skin bends (excluding mottled or marbled skin appearance) may disappear during descent from high altitude but still require medical evaluation. If the signs and symptoms persist during descent or reappear at ground level, it is necessary to provide hyperbaric oxygen treatment immediately (100-percent oxygen delivered in a high-pressure chamber). Neurological DCS, the "chokes," and skin bends with mottled or marbled skin lesions (see Table 1) should always be treated with hyperbaric oxygenation. These conditions are very serious and potentially fatal if untreated.

Effects of breathing pure oxygen

One of the most significant breakthroughs in altitude DCS research was oxygen pre-breathing. Breathing pure oxygen before exposure to a low-barometric pressure decreases the risk of developing altitude DCS. Oxygen pre-breathing promotes the elimination or washout of nitrogen from body tissues. Pre-breathing pure oxygen for 30 minutes before starting the ascent to altitude reduces the risk of altitude DCS for short exposures (10 to 30 minutes only) to altitudes between 18,000 and 43,000 feet. However, oxygen pre-breathing has to be continued without interruption with in-flight, pure oxygen to provide effective protection against altitude DCS. Furthermore, it is very important to understand that breathing pure oxygen only during the flight (ascent, en route, descent) does not decrease the risk of altitude DCS, and should not be used instead of oxygen pre-breathing. Although pure oxygen pre-breathing is an effective method to protect against altitude DCS, it is logistically complicated and expensive for the protection of civil aviation flyers, either commercial or private. Therefore, it is only used now by military flight crews and astronauts for their protection during high altitude and space operations.

Breathing pure oxygen to remove nitrogen from the bloodstream

Scuba diving before flying

The rule about decompression sickness risk on ascending to lower surrounding pressure does not stop at sea level (even though decompression tables stop at sea level), but continues when a diver soon after diving goes into air pressure much less than at sea level. Altitude DCS can occur during exposure to altitudes as low as 5,000 feet or less. This can happen:# In an airliner at high altitude the cabin pressure is usually not at full sea level pressure, but like the air pressure at approx. 8,000 feet altitude.# At high altitudes on land: e.g. if you scuba dive in Eritrea, and then go onto the Asmara plateau (where Eritrea's main airport is), which is about 8000 feet or 1.5 miles or 2400 meters above sea level.# Occasionally in cave diving, "Torricellian chambers" are found; they are full of water at less than atmospheric pressure. They arise when the water level drops and there is no way for air to get into the chamber.

What to do if altitude DCS occurs

• Put on your oxygen mask immediately and switch the regulator to 100% oxygen.* Begin an emergency descent and land as soon as possible. Even if the symptoms disappear during descent, you should still land and seek medical evaluation while continuing to breathe oxygen.* If one of your symptoms is joint pain, keep the affected area still; do not try to work the pain out by moving the joint around.* Upon landing seek medical assistance from an aviation authority medical officer, aviation medical examiner (AME), military flight surgeon, or a hyperbaric medicine specialist. Be aware that a physician not specialized in aviation or hypobaric medicine may not be familiar with this type of medical problem. Therefore, be your own advocate.* Definitive medical treatment may involve the use of a hyperbaric chamber operated by specially trained personnel.* Delayed signs and symptoms of altitude DCS can occur after return to ground level whether or not they were present during flight.

Things to remember

• Altitude DCS is a risk every time you fly in an un-pressurized aircraft above 18,000 feet (or at a lower altitude if you scuba dive prior to the flight).* Be familiar with the signs and symptoms of altitude DCS (see Table 1). Monitor all aircraft occupants, including yourself, any time you fly an unpressurized aircraft above 18,000 feet.* Avoid unnecessary strenuous physical activity prior to flying an un-pressurized aircraft above 18,000 feet, and for 24 h after the flight.* Even if you are flying a pressurized aircraft, altitude DCS can occur as a result of a sudden loss of cabin pressure (in-flight rapid decompression).* After exposure to an in-flight rapid decompression, do not fly for at least 24 h. In the meantime, stay vigilant for the possible onset of delayed symptoms or signs of altitude DCS. If you present delayed symptoms or signs of altitude DCS, seek medical attention at once.* Keep in mind that breathing 100% oxygen during flight (ascent, en route, descent) without oxygen pre-breathing before take-off does not prevent altitude DCS.* Do not ignore any symptoms or signs that go away during the descent. This could confirm that you are suffering altitude DCS. You should be medically evaluated as soon as possible.* If there is any indication that you may have experienced altitude DCS, do not fly again until you are cleared to do so by an aviation authority medical officer, an aviation medical examiner, a military flight surgeon, or a hyperbaric medicine specialist.* Allow at least 24 hours to elapse between scuba diving and flying.* Be prepared for a future emergency by finding where hyperbaric chambers are available in your area of operations. However, keep in mind that not all of the available hyperbaric treatment facilities have personnel qualified to handle altitude DCS emergencies. To obtain information on the locations of hyperbaric treatment facilities capable of handling altitude DCS emergencies, call the Diver's Alert Network at (USA phone number) (919) 684-8111.

Decompression sickness in popular culture

• In the 1880s, Decompression sickness became known as The Bends because afflicted individuals characteristically arched their backs in a manner reminiscent of a then-popular women's fashion called the Grecian Bend.* A diver with decompression sickness flying in an aircraft was part of the plot in the episode Airborne of House, M.D., first aired Tuesday April 11, 2007.* Rock band Radiohead released an album entitled The Bends, a reference to decompression sickness.* Decompression sickness played a part in the anime visual novel "Ever 17"* A character in the series "Dive" by Gordan Korman experiences a case of Decompression sickness.* In an episode of "Jackie Chan Adventures" titled Clash of the Titanics, Jackie experienced decompression sickness* Roger Bochs, a character in the Marvel Comics series Alpha Flight, experiences decompression sickness after battling alongside the Avengers in Atlantis.== References ==

External links

• Decompression Sickness: Prevention, Risks, Exercise, PFO, References, Links* What causes the bends?* Whales Suffer From Bends* UK Sport Diving Medical Committee: Bone Necrosis* Divers Alert Network: diving medicine articles* Dive Tables from the NOAATemplate:Consequences of external causescs:Dekompresní nemocda:Trykfaldssygede:Dekompressionserkrankungit:Malattia da decompressionehu:Keszon-betegségnl:Caissonziektefi:Sukeltajantautisv:Tryckfallssjukauk:Кесонна хворобаTemplate:WikiDoc Sources