Decompression sickness

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Template:DiseaseDisorder infobox

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]

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 ^[1].

Historical Perspective

Template:Wikisource1911Enc

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 ^[2].
1841: Jacques Triger documented the first cases of DCS in humans when two miners involved in pressurised caisson work developed symptoms ^[2].
1847: The effectiveness of recompression for the treatment of DCS in caisson workers was described by B. Pol and T.J. Watelle ^[2] ^[3]
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 ^[4].
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" ^[5].
1868: Alfred Le Roy de Méricourt described DCS as an occupational illness of sponge divers ^[3].
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.^[4] ^[6]. 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" ^[2].
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 ^[7].
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 ^[8] ^[9].
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 ^[2] ^[10].
1912 – Chief Gunner George D. Stillson of the United States Navy created a program to test and refine Haldane's tables ^[11].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 ^[12].

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 ^[13]. 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 ^[14].

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 ^[15].

Venous bubbles may form de novo or result from the intravascular release of tissue bubbles ^[16]. The venous gas emboli usually get filtered at arteriole level on reaching the lungs. However, the bubbles may pass directly into the arterial circulation ^[17] 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 ^[18].
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 ^[19].
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 ^[16].

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 ^[20]:

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 ^[21] ^[22].

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 ^[20] ^[23].

Table 4 shows symptoms and signs of different DCS types ^[13]:

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 ^[24]	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 ^[25].

Table 5 below shows various different medical conditions mimicking the DCS ^[26]:

Medical condition	Clinical characteristics
Arterial Gas Embolism (AGE) ^[15]	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 ^[27]. 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 ^[28]
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 ^[29], or Compression of branches of the trigeminal nerve causing hypoaesthesia of the face ^[30]
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 ^[30]	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 ^[31].
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 ^[32]
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 ^[33].

Risk Factors

Various demographic, environmental, and diving factors are related to the predisposition of DCS. DeNoble et al in 2005 studied various multiple risk factors such as age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous history of DCI, number of the years since certification, number of 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 correlation of DCS were found with asthma, diabetes, cardiovascular disease, smoking, or body mass index. Variable such as increased diving depth, previous DCS episodes, multiple consecutive days of diving and being male were found to be associated with an increased incidence of DCS. Contrarily, a lower risk was reported among nitrox and drysuit use, higher frequency of diving in the past year, increasing age, and years since certification possibly as indicators of more extensive training and experience. ^[34]

Environmental factors

Magnitude of the pressure reduction ratio: A large pressure reduction ratio is more likely to cause DCS than a small one ^[35].
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 ^[35].
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 ^[36]. 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 ^[35].
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 ^[35].
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 ^[37].
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 ^[36].
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 ^[37].

Individual factors

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 ^[38]. Therefore, maintaining adequate hydration is recommended ^[36].
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) ^[39]. 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 ^[36].
Age: A higher risk of altitude DCS with increasing age (especially >42 years of age) has been reported ^[38].
Previous injury: Recent joint or limb injuries may predispose individuals to developing decompression-related bubbles ^[40].
Ambient temperature: An individual exposure to very cold ambient temperatures may increase the risk of altitude DCS ^[38]. which can be reduced by increasing ambient temperature during decompression following the dives in cold water ^[41].
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 ^[38].. 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 ^[42].
Alcohol consumption: It increases dehydration and inhibits pituitary release of antidiuretic hormone (ADH); and therefore may increase susceptibility to DCS ^[38].. Contrarily, another study found no evidence that alcohol consumption increases the incidence of DCS ^[43].
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 ^[15].
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 ^[15].
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 ^[15].

Diagnosis

DCS is primarily a clinical diagnosis which can be assessed with a very thorough and detailed dive history from a conscious patient and the clinical examination, including the neurologic examination. The specific symptoms/signs and their particular time of onset (table 3 and 4) aid in suspecting and establishing the diagnosis. However, the relief of symptoms by recompression will make the definitive confirmation of the probable diagnosis. Hence, an immediate treatment should be begun with no delay for further diagnostic investigation.

Diagnostic criteria

In 2004 Freiberger identified important five diagnostic factors in their order of importance using simulated diving injury cases:^[44]

(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

DCS is associated with hemoconcentration, and elevated serum CK is seen in severe AGE. However, none of the laboratory studies make a definitive diagnosis of DCS. ^[15]

Radiological findings

No imaging study can confirm the diagnosis of DCS. Bubble formation can occasionally be identified on MRI or CT scans; however, they are not considered the best method to rule out DCS due to their low sensitivity level in making the diagnosis. Although, they might be used to rule out the other differential disorders that presents with the similar signs and symptoms (eg, herniated intervertebral disk, ischemic stroke, central nervous system hemorrhage). These studies should be performed with no delay as prompt intervention is important in the successful management of the DCS.

Chest and Joints Radiography

Pneumothorax, pneumomediastinum, pulmonary overexpansion injury, or pulmonary edema should always be ruled out with chest radiographs. Radiographs rarely detect bubble formation in joints affected by pain. Skeletal x-rays are not considered diagnostic for dysbaric osteonecrosis which may show joint degeneration;and hence cannot be used to differentiate between different joint disorders. ^[15] ^[26]

Computed Tomography Scan

Head CT: A “normal” head CT is not helpful in excluding DCS due to the very low chances of visibility of vascular gas bubbles on a head CT in the cases of suspected DCS. However, it should be strongly considered in any patient who presented with an altered mental status in order to evaluate alternative diagnoses, such as subdural or epidural hematoma. ^[15] ^[45]

Chest CT: An extrapulmonary air can be detected on it, but it can be avoided due to its high radiation exposure. ^[26].

Magnetic Resonance Imaging

MRI can be falsely reassuring for detecting the spinal cord or brain abnormalities related to DCS. However, it can diagnose ischemic lesions of the brain or spinal cord due to the etiologies other than DCS. ^[46].

Other diagnostic studies

Doppler ultrasonography and Echocardiography: They are not considered the diagnostic tests for DCS; but done to rule out right to left shunt and for research purposes into venous gas emboli. ^[47]

Neurophysiological tests (eg, audiometry and electronystagmography for inner-ear decompression sickness): They can usually be delayed until after recompression. ^[26]

Non invasive pulmonary diagnostic test: None of them are used in making or excluding the diagnosis. ^[15]

Pulmonary diagnostic procedures (e.g.: Bronchoscopy): None is required in making or excluding the diagnosis. ^[15]

Pathology/Cytology/Genetics Study: None is considered in making or excluding the diagnosis. ^[15]

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). ^[26]

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 ^[24].

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

Figure 1: Treatment algorithm of Decompression Sickness (DCS)^[48]

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 ^[24].

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 ^[49].

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 ^[50].

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 ^[33] 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 ^[15] ^[24].

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 ^[15].

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 ^[24].

Effects of Recompression therapy^[51]:

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 ^[49] ^[52].

Regimen: A common HBOT 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 ^[49] ^[53].

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 ^[15].

Risks^[15] ^[54]:

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 ^[50] ^[49].

Breathing pure oxygen to remove nitrogen from the bloodstream

Adjuvant treatment: Aspirin, NSAIDs, and corticosteroids have all been studied and not shown to have benefit in DCS. These drugs may mask the symptoms and can exacerbate micro-haemorrhages caused by DCS leading to a permanent sequelae. Opiates should also be avoided as they can increase the risk of oxygen toxicity. Oxygen is usually sufficient to control pain ^[15] ^[51].

Follow-up evaluation and return to diving:

If the DCI was severe, significant residual neurological dysfunction may be present, even after the most aggressive treatment. In these cases, there may be follow-up treatments, along with physical therapy.

Clearing a diver after DCS to return to diving is a complex undertaking with potential medical and legal risks. A careful risk/benefit assessment to ensure that the diver is completely asymptomatic and back to his or her pre-dive baseline function must be conducted by both the diver and the physician. Given the potential life-threatening implications of improperly clearing a diver to return to diving, referral of the patient to a diving medicine specialist is appropriate. In cases in which the risks clearly outweigh the benefits, divers should be instructed to refrain from diving for the remainder of their lives. Furthermore, a diver who has had multiple bouts of DCS even if symptoms were not severe and resolves completely must take special considerations. In these cases, a Diving Medical Specialist must be consulted to determine if diving can be resumed safely.

The physician must also consider when it is safe for a patient to fly home or drive at altitude. A retrospective review of 126 DCS cases demonstrated that those who flew home on commercial flights < 72 hours after recompression had a higher likelihood of recurrence of symptoms and signs of DCS. Similarly, physicians should be wary if patients must drive through high-altitude areas, as the drop in atmospheric pressure could, at least theoretically, potentiate a recurrence^[15].

The U.S. Navy has set down the following rules for returning to diving after treatment for professionals where time off must be minimized so operations are not compromised ^[55].

For pain-only DCI where there are no neurological symptoms, divers may begin diving two to seven days after treatment
If there are neurological symptoms, the diver may resume diving two to four weeks after treatment, depending on symptom severity.
For very severe symptoms, the diver must be reevaluated three months after treatment and cleared by a Diving Medical Officer.

For recreational divers, where diving is not a livelihood, a more conservative approach is called for to further minimize the chance that a diving injury will recur {{cite web ^[55]

After pain-only DCI where there are no neurological symptoms, a minimum of two weeks without diving is recommended.
If there are minor neurological symptoms, six weeks without diving is recommended.
If there are severe neurological symptoms or any residual symptoms, no further diving is recommended.

Prognosis

Prognosis is severity dependent. It also depends upon on other factors such as the time to recompression, availability and time to surface oxygen, previous episode, and supportive care ^[50].

Prevention

Significant bubble formation can usually be avoided by limiting the depth and duration of dives to a range that does not need decompression stops during ascent (called no-stop limits) or by ascending with decompression stops as specified in published guidelines (eg, the decompression table in the US Navy Diving Manual) ^[53] ^[56].

Many divers wear a portable dive computer that continually tracks depth and time at depth and calculates a decompression schedule. Computer divers should be cautious in approaching no-decompression limits, especially when diving deeper than 100 feet (30 meters).

In addition to suggested guidelines ^[56], many divers make a safety stop for a few minutes at about 4.6 m (15 ft) below the surface. However, cases can occur after appropriately identified no-stop dives and despite widespread use of dive computers.

Recreational divers should dive conservatively, whether they are using dive tables or computers.

Experienced divers often select a table depth (versus actual depth) of 10 feet (3 meters) deeper than called for by standard procedure. This practice is highly recommended for all divers, especially when diving in cold water or under strenuous conditions ^[55].

Avoiding the risk factors noted above (deep / long dives, exercise at depth or after a dive) will decrease the chance of DCS occurring.

Altitude DCS: 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. 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).
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.
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 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.
If there is any indication that you may have experienced altitude DCS, do not fly again until you are cleared to do so.
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) 684-9111.

MORE INFORMATION:

Divers Alert Network: www.diversalertnetwork.org 24-hour emergency hotline, 919-684-9111
Duke Dive Medicine: www.dukedivemedicine.org Physician-to-physician consultation, 919-684-8111
Undersea and Hyperbaric Medical Society
US Navy Diving Manual