Introduction
Decompression sickness (DCS), often referred to as “the bends,” is a serious condition that arises from the formation of gas bubbles in the blood and tissues. This occurs when dissolved gases, typically nitrogen, come out of solution due to a rapid decrease in ambient pressure. Individuals who experience sudden pressure changes, such as scuba divers ascending too quickly, aviators at high altitudes, and workers in compressed air environments, are most susceptible to DCS.
During deep-sea dives or pressurized activities, the body’s tissues absorb gases like nitrogen at higher pressures. A gradual ascent or decompression allows these gases to be released slowly and safely. However, a rapid reduction in pressure can cause these dissolved gases to form bubbles. These bubbles can obstruct blood vessels, leading to inflammation and tissue damage, which are the hallmarks of DCS. Recognizing the signs and symptoms of DCS and understanding its diagnosis are crucial for timely intervention and management.
Preventive measures, including adherence to safe diving protocols, controlled ascent rates, and decompression schedules, are paramount in minimizing the risk of DCS. Treatment for DCS typically involves administering high-concentration oxygen and, in more severe cases, hyperbaric oxygen therapy (HBOT). Early diagnosis and prompt treatment, along with effective coordination among healthcare professionals, significantly improve patient outcomes in DCS cases.
Etiology of DCS
The fundamental cause of DCS is a rapid decrease in ambient pressure, leading to the formation of gas bubbles within the body. Nitrogen, the most abundant gas in the atmosphere and commonly used in diving air mixtures, is the primary culprit. While inert under normal conditions, excessive nitrogen in the bloodstream can cause significant problems.
As divers descend deeper into the sea, the partial pressure of nitrogen increases, forcing more of the gas to dissolve into body tissues. Conversely, at higher altitudes, the partial pressure of nitrogen decreases. A slow ascent allows for the gradual release of nitrogen from tissues in a gaseous state, which is then safely exhaled. However, a rapid ascent or decompression overwhelms the body’s capacity to eliminate nitrogen, resulting in the rapid formation of nitrogen gas bubbles in tissues and circulation. This same phenomenon can affect aviators in unpressurized aircraft and astronauts during spacewalks.
Certain individual factors can heighten the risk of DCS. Dehydration, the presence of a patent foramen ovale (PFO), pre-existing injuries, exposure to cold temperatures, higher body fat percentage, and recent alcohol consumption are all recognized risk enhancers. Type I DCS, characterized by skin, lymphatic, or musculoskeletal symptoms, is the most common form. Type II DCS, which involves the nervous system, is often linked to the shunting of venous bubbles from the right to the left side of the heart through a PFO.
Epidemiology of Decompression Sickness
Thanks to advancements in technology and stringent diving safety regulations, DCS is now considered a relatively rare condition. In recreational diving, estimates suggest an incidence of about 3 cases per 10,000 dives. However, the incidence is higher among commercial divers, ranging from 1.5 to 10 cases per 10,000 dives, reflecting the more demanding nature of their work. Dive depth and duration are directly correlated with the likelihood of DCS. Statistically, males are about 2.5 times more likely to experience DCS compared to females.
Pathophysiology of DCS
The symptoms of DCS are a direct result of vascular obstruction and inflammation caused by the formation of gas bubbles. These bubbles induce ischemia and inflammation, damaging various tissues throughout the body. In the skin, this can manifest as pruritic, net-like, red lesions known as cutis marmorata. Bone and joint damage can lead to necrosis and significant pain in the affected areas. Lymph nodes may also become swollen and painful as part of the inflammatory response.
In milder cases of DCS affecting the nervous system, transient edema can occur. Severe DCS, however, can result in permanent lesions in both the white and gray matter of the brain and spinal cord.
Isolated inner-ear DCS, where the inner ear is affected without overt brain damage, is believed to occur due to slower inert gas elimination from the inner ear compared to the brain. This slower washout allows more gas to accumulate and form bubbles within the inner ear structures. Individuals who switch from breathing helium-oxygen mixes to nitrogen-rich mixes, often to reduce costs, are at increased risk. Even without changing gas mixtures, a PFO can predispose individuals to isolated inner-ear DCS.
Abdominal organs can also be affected in DCS, particularly in cases of rapid and significant gas decompression in the abdominal area. Bubble formation in the tissues and portal and mesenteric vessels can lead to gut necrosis, pancreatic edema, and liver damage.
History and Physical Examination for DCS Diagnosis
Approximately 75% of DCS patients develop symptoms within the first hour following the pressure change event. Rapid and focused assessment is crucial, and initial stabilization measures should be implemented immediately. High-flow oxygen should be administered to anyone suspected of DCS, even if their oxygen saturation levels appear normal, as it helps to reduce nitrogen bubble size.
The patient’s history will typically reveal rapid decompression, followed by symptoms affecting the skin, muscles, bones, joints, inner ear, brain, spinal cord, and, less frequently, the lungs, appearing within minutes to hours. In Type I DCS, the shoulder is the most commonly affected joint, although any joint can be involved. Cutis marmorata may be localized or widespread. Patients may also report swollen and painful lymph nodes.
Type II DCS may present with the symptoms described above, along with additional neurological symptoms such as headache, visual and hearing disturbances, nausea, tinnitus, and impaired coordination. Some patients may also exhibit altered mental status.
In rare cases, DCS can involve the abdominal organs, mediastinum, or lungs, leading to symptoms like abdominal pain, chest pain, or dyspnea. Pulmonary DCS, also known as “the chokes,” can mimic conditions like pulmonary embolism, asthma exacerbation, or myocardial infarction and is potentially fatal if not promptly managed.
Physical examination of a DCS patient may initially show normal vital signs and no apparent distress. Skin examination may reveal localized or generalized lesions. An eye exam might detect scotomas, and otoscopy may show signs of barotrauma. A significant PFO might produce audible murmurs. Musculoskeletal examination can reveal joint or muscle tenderness. Nystagmus may be present if the inner ear is involved. Neurological deficits, depending on the affected areas of the brain or spinal cord, can manifest as sensorimotor weakness and altered deep tendon reflexes. The patient’s level of consciousness can range from fully conscious to unconscious, depending on the severity of neurological damage. Pulmonary DCS may present with crackles or rales due to pulmonary edema, and patients with pre-existing lung conditions like asthma may exhibit wheezing. Absent breath sounds could indicate pneumothorax, a complication of pulmonary DCS.
Dcs Diagnosis is primarily clinical. Recompression therapy, if available, can provide immediate symptom relief and serve as a diagnostic confirmation. After initial stabilization, a more detailed history, including diving history and details of the incident, should be obtained, and assessment for other injuries like wounds or fractures should be conducted.
Evaluation and Diagnostic Process for DCS
DCS diagnosis is fundamentally clinical. Extensive diagnostic workups are usually unnecessary and can be detrimental due to the potentially rapid progression of the condition. However, in patients presenting with dyspnea and suspected pulmonary DCS, an immediate chest X-ray is mandatory to rule out pneumothorax, as untreated pneumothorax is a contraindication for HBOT.
Imaging and laboratory tests are typically non-specific in DCS. Chest radiographs are often normal but may show infiltrates or lung collapse in pulmonary DCS. Bone X-rays may reveal gas bubbles in joints acutely. However, chronic bone and joint necrosis may be evident in long-term divers or those with frequent compression-decompression cycles. Gas inclusions in abdominal and thoracic structures might be visible on CT or MRI scans. Brain and spinal CT and MRI can show edema, infarcts, hemorrhages, or gas pockets in CSF spaces. Echocardiography may reveal a PFO.
Laboratory findings may reflect renal, hepatic, and pancreatic damage if abdominal organs are involved. Elevated C-reactive protein and white blood cell counts may also be present, indicating inflammation.
Treatment and Management Strategies for DCS
For unconscious patients without pulse or respiration, immediate cardiovascular resuscitation is paramount, irrespective of the suspected cause. Patients suspected of DCS should receive 100% oxygen until HBOT can be administered. Intravenous fluid resuscitation and continuous cardiac monitoring should be initiated. A chest X-ray should be obtained urgently to rule out pneumothorax before HBOT. Recompression via HBOT should be started as soon as possible, ideally following U.S. Navy treatment protocols.
For patients requiring transfer to a definitive treatment center, pressurized aircraft evacuation is recommended. If a helicopter or unpressurized aircraft is used, altitude should be limited to 300 meters (1000 feet).
Conscious patients can receive oral fluids and electrolytes unless abdominal or thoracic surgery is being considered. HBOT can still benefit patients with delayed neurological, pulmonary, or dermatological symptoms. Low molecular weight heparin may be used to prevent deep vein thrombosis and thrombotic pulmonary embolism in non-ambulatory patients. Other anticoagulants, NSAIDs, and steroids are no longer recommended for routine DCS treatment. Aspirin should be avoided as it can mask pain and other DCS symptoms.
Vomiting patients should be positioned upright or with their head elevated to prevent aspiration. Trendelenburg and left lateral decubitus positions are no longer recommended for prolonged periods due to the increased risk of cerebral edema.
Differential Diagnosis of DCS
DCS Type I, characterized by musculoskeletal pain, skin rashes, and lymph node swelling, needs to be differentiated from:
- Systemic viral illnesses
- Systemic lupus erythematosus
- Acute leukemia
- Bacterial infections such as gonorrhea and syphilis
- Lymphoma
- Lyme disease
- Dehydration
DCS Type II, with neurological involvement, may be confused with:
- Inner ear barotrauma
- Stroke
- Drowning
- Thermal stress
- Nitrogen narcosis
- Meningococcemia
- Intracranial and intraspinal masses
- Multiple sclerosis
- Hypoglycemia
- Acute coronary syndrome
- Marine life toxin exposure
- Oxygen toxicity
A rapid, focused clinical assessment is the most critical tool for differentiating DCS from these conditions and initiating timely treatment.
Pertinent Studies and Ongoing Research in DCS
Ongoing research focuses on improving DCS risk prediction models. Enhancements in these models, integrated into dive computers and decompression tables, aim to reduce DCS incidence and improve outcomes.
Dive computers now monitor depth, time, and dive profiles, and incorporating advanced predictive models allows for real-time nitrogen uptake and elimination calculations. These advanced computers offer more precise decompression profiles and can alert divers to potential DCS risks.
Decompression tables, which guide ascent rates and decompression stops, are also continuously refined with improved predictive models to create safer dive profiles.
Treatment Planning and On-site Interventions for DCS
When delays in reaching a recompression facility are anticipated, on-site interventions are crucial. Immediate oxygen administration, especially within 4 hours of surfacing, improves outcomes and reduces the need for extensive recompression therapy. In-water recompression (IWR) with oxygen at a depth of 9 meters is an option that has shown success. However, IWR carries risks, including oxygen-induced neurotoxicity, seizures, and drowning, so it must be performed by highly trained personnel.
The US Navy Treatment Table 6, using oxygen at 18 meters, is the standard of care for DCS. Specific HBOT protocols may vary based on patient presentation and oxygen availability.
Prognosis of DCS
The prognosis for DCS varies based on symptom severity, the timeliness and appropriateness of treatment, and the individual’s overall health. Generally, patients with mild symptoms who receive prompt and appropriate treatment and are in good health prior to the incident have a favorable prognosis. Symptoms may resolve within days with high-flow oxygen and rest.
Factors associated with a poorer prognosis include severe systemic symptoms, delays in treatment, and poor baseline health. Delayed or inadequate recompression can lead to long-term neurological complications or even death.
Potential Complications of DCS
DCS can affect multiple organ systems, leading to various complications. While dermatological lesions may heal without lasting effects, more serious complications include:
- Osteonecrosis, potentially leading to bone fractures and chronic arthritis, commonly affecting the femur, humerus, and tibia.
- Permanent neurological deficits, ranging from sensorimotor weakness to incontinence and coma, resulting from severe nervous system damage.
- Pulmonary fibrosis in survivors of pulmonary DCS.
- Damage to abdominal organs, including pancreatic, hepatic, and renal impairment, and gastrointestinal strictures that can cause obstruction.
Early and effective treatment with high-flow oxygen and HBOT is crucial to minimize the severity of these complications.
Postoperative and Rehabilitation Care for DCS
Rehabilitation following DCS is tailored to address the residual complications, which vary depending on the severity of the condition, the patient’s general health, and treatment response. Most DCS cases are Type I, with about 85% of patients recovering fully. These patients may benefit from medical follow-up, education on DCS prevention, and ongoing monitoring. Psychological support can be provided if needed.
Patients with more severe or widespread DCS may require comprehensive rehabilitation, including physical therapy to improve mobility, strength, and flexibility; neurorehabilitation to regain motor skills, coordination, and sensory functions; occupational therapy to enhance functional independence; and nutritional guidance. Counseling can also aid in psychological recovery and coping with any lasting complications.
Deterrence and Patient Education for DCS Prevention
DCS prevention requires a multi-faceted approach. Individuals must adhere to safe diving and flying protocols, plan dives and flights appropriately, and respect training limits. Inexperienced divers and pilots should only undertake challenging activities under expert supervision. Maintaining hydration, physical fitness, adequate rest, avoiding alcohol, and ensuring proper gear maintenance are also crucial for staying alert and maintaining muscle control.
Healthcare providers play a vital role in educating patients about DCS risks and preventive measures. Clinicians should emphasize the importance of seeking immediate medical help if any unusual symptoms appear after diving or altitude exposure. Medical screening to identify predisposing conditions like PFO or pre-existing lung disease is also important.
Dive center operators can contribute by maintaining diving equipment and computers, requiring medical clearances for divers, having medical teams on site, and establishing protocols for transporting DCS patients to appropriate medical facilities. Community efforts in disseminating information and promoting safe diving and flying practices are also essential.
Key Points in DCS Management
- Prevention is the most effective strategy against DCS, involving individuals, healthcare providers, dive operators, and the community.
- Early recognition is critical for effective management. Patients must be educated to seek immediate medical attention if they experience symptoms after rapid decompression.
- Initial management includes high-flow oxygen, with HBOT as definitive treatment. Associated injuries should also be identified and treated.
- Recovery and prognosis depend on the extent of organ involvement, treatment timing and adequacy, and the patient’s baseline health.
DCS is a clinical emergency that requires prompt diagnosis and treatment to avoid potentially severe complications. It should be considered a medical emergency until ruled out.
Enhancing Healthcare Team Outcomes in DCS Management
Effective DCS management requires a multidisciplinary team of healthcare professionals trained to rapidly recognize and treat the condition and support patient recovery. This team includes:
- Emergency medical technicians as first responders.
- Emergency medicine and hyperbaric therapy physicians.
- Medical intensivists for critically ill patients requiring intensive care.
- Specialists such as neurologists, pulmonologists, surgeons, gastroenterologists, nephrologists, hepatologists, and cardiologists for specific complications.
- Radiologists for image interpretation.
- Nurses for care coordination and patient education.
- Respiratory therapists for respiratory support.
- Pharmacists for medication management.
- Rehabilitation teams including physical therapists, occupational therapists, neurorehabilitation specialists, nutritionists, and psychological therapists for comprehensive recovery.
- Primary care providers for outpatient follow-up.
For facilities lacking DCS management resources, the Divers’ Alert Network (DAN) offers referrals to hyperbaric facilities and 24/7 consultation with hyperbaric medicine experts. DAN’s emergency hotline is +1-919-684-9111.
Review Questions
Figure: Gas in Portal System in DCS Diagnosis
Computed tomography scan showing gas filling the portal venous system, indicative of severe decompression sickness affecting abdominal organs.
Figure: Thickened Esophageal Walls in DCS Evaluation
Computed tomography scan showing thickened esophageal walls (indicated by arrow), a potential sign of esophageal involvement in decompression sickness.
Figure: Ulcerated Esophagus in DCS Complications
Endoscopic view revealing multiple ulcers in the distal esophagus with erythematous and friable mucosa, a complication of severe decompression sickness.
Figure: Esophageal Biopsies for DCS Pathology
Microscopic view of esophageal biopsies showing acute inflammatory infiltrates with hemosiderin and fibrinopurulent exudate, confirming esophageal damage in DCS.
Figure: Esophageal Stricture Post-DCS
Repeat endoscopy 8 weeks post-initial presentation revealing an esophageal stricture, a long-term complication following esophageal decompression sickness.
Figure: Abdominal Rash in Decompression Sickness Diagnosis
Photograph illustrating the mottled, tender, pruritic rash on a patient’s torso, a characteristic skin manifestation of Type I decompression sickness.
Figure: DCS Rash Close-Up
Closer view photograph of the rash on a patient’s torso, highlighting the typical appearance of a decompression sickness-related skin eruption.
References
[References]
1.Livingstone DM, Smith KA, Lange B. Scuba diving and otology: a systematic review with recommendations on diagnosis, treatment and post-operative care. Diving Hyperb Med. 2017 Jun;47(2):97-109. [PMC free article: PMC6147252] [PubMed: 28641322]
2.Clarke JR, Moon RE, Chimiak JM, Stinton R, Van Hoesen KB, Lang MA. Don’t dive cold when you don’t have to. Diving Hyperb Med. 2015 Mar;45(1):62. [PubMed: 25964043]
3.Geng M, Zhou L, Liu X, Li P. Hyperbaric oxygen treatment reduced the lung injury of type II decompression sickness. Int J Clin Exp Pathol. 2015;8(2):1797-803. [PMC free article: PMC4396314] [PubMed: 25973070]
4.Hall J. The risks of scuba diving: a focus on Decompression Illness. Hawaii J Med Public Health. 2014 Nov;73(11 Suppl 2):13-6. [PMC free article: PMC4244896] [PubMed: 25478296]
5.Pollock NW, Buteau D. Updates in Decompression Illness. Emerg Med Clin North Am. 2017 May;35(2):301-319. [PubMed: 28411929]
6.Sun Q, Gao G. Decompression Sickness. N Engl J Med. 2017 Oct 19;377(16):1568. [PubMed: 29045210]
7.Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving Hyperb Med. 2015 Jun;45(2):105-10. [PubMed: 26165533]
8.Lindfors OH, Räisänen-Sokolowski AK, Hirvonen TP, Sinkkonen ST. Inner ear barotrauma and inner ear decompression sickness: a systematic review on differential diagnostics. Diving Hyperb Med. 2021 Dec 20;51(4):328-337. [PMC free article: PMC8923696] [PubMed: 34897597]
9.King AE, Andriano NR, Howle LE. Trinomial decompression sickness model using full, marginal, and non-event outcomes. Comput Biol Med. 2020 Mar;118:103640. [PubMed: 32174319]
10.Howle LE, Weber PW, Hada EA, Vann RD, Denoble PJ. The probability and severity of decompression sickness. PLoS One. 2017;12(3):e0172665. [PMC free article: PMC5351842] [PubMed: 28296928]
11.Madden D, Thom SR, Dujic Z. Exercise before and after SCUBA diving and the role of cellular microparticles in decompression stress. Med Hypotheses. 2016 Jan;86:80-4. [PubMed: 26804603]
12.Honěk J, Šrámek M, Honěk T, Tomek A, Šefc L, Januška J, Fiedler J, Horváth M, Novotný Š, Brabec M, Veselka J. Screening and Risk Stratification Strategy Reduced Decompression Sickness Occurrence in Divers With Patent Foramen Ovale. JACC Cardiovasc Imaging. 2022 Feb;15(2):181-189. [PubMed: 34419390]
13.Lee HJ, Lim DS, Kang YC. Recurrent Decompression Illness Even After the Closure of Patent Foramen Ovale in a Diver. JACC Case Rep. 2023 Jan 04;5:101687. [PMC free article: PMC9830462] [PubMed: 36636504]
14.Chin W, Joo E, Ninokawa S, Popa DA, Covington DB. Efficacy of the U.S. Navy Treatment Tables in treating DCS in 103 recreational scuba divers. Undersea Hyperb Med. 2017 Sept-Oct;44(5):399-405. [PubMed: 29116694]
15.Kohshi K, Denoble PJ, Tamaki H, Morimatsu Y, Ishitake T, Lemaître F. Decompression Illness in Repetitive Breath-Hold Diving: Why Ischemic Lesions Involve the Brain? Front Physiol. 2021;12:711850. [PMC free article: PMC8446421] [PubMed: 34539434]
16.Kohshi K, Tamaki H, Lemaître F, Morimatsu Y, Denoble PJ, Ishitake T. Diving-related disorders in commercial breath-hold divers (Ama) of Japan. Diving Hyperb Med. 2021 Jun 30;51(2):199-206. [PMC free article: PMC8426123] [PubMed: 34157736]
17.Mitchell SJ, Bennett MH, Bryson P, Butler FK, Doolette DJ, Holm JR, Kot J, Lafère P. Consensus guideline: Pre-hospital management of decompression illness: expert review of key principles and controversies. Undersea Hyperb Med. 2018 May-Jun;45(3):273-286. [PubMed: 30028914]
18.Walker, III JR, Murphy-Lavoie HM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 1, 2023. Diving in Water Recompression. [PubMed: 29630272]
19.Smart D. Five consecutive cases of sensorineural hearing loss associated with inner ear barotrauma due to diving, successfully treated with hyperbaric oxygen. Diving Hyperb Med. 2024 Dec 20;54(4):360-367. [PubMed: 39675746]
