What is decompression sickness. How does it occur. What are the types of decompression sickness. What are the risk factors for developing decompression sickness. How is decompression sickness diagnosed and treated. What are the long-term effects of decompression sickness. How can decompression sickness be prevented.

Understanding the Basics of Decompression Sickness

Decompression sickness (DCS), colloquially known as “the bends,” is a condition that occurs when dissolved gases in the body form bubbles during rapid decompression. This phenomenon typically affects divers, caisson workers, and individuals exposed to sudden changes in atmospheric pressure. To fully grasp the complexities of DCS, it’s crucial to understand its underlying mechanisms and manifestations.

What exactly causes decompression sickness? DCS results from the formation, growth, and elimination of gas bubbles in the body’s tissues and bloodstream. These bubbles primarily consist of nitrogen, which is normally dissolved in the body’s fluids under high pressure. When a person rapidly ascends from a high-pressure environment to a lower-pressure one, the dissolved nitrogen can come out of solution, forming potentially harmful bubbles.

Types of Decompression Sickness

Decompression sickness is typically classified into two main types:

• Type I DCS: This form affects the skin, musculoskeletal system, and lymphatic systems.
• Type II DCS: This more severe form involves the central nervous system.

Why is this classification important? Understanding the type of DCS a patient is experiencing helps medical professionals determine the appropriate treatment approach and assess the potential severity of the condition.

The Science Behind Bubble Formation in DCS

To comprehend the intricacies of decompression sickness, it’s essential to delve into the science of bubble formation. When divers or other individuals breathe pressurized air, their bodies reach a state of equilibrium, with inert gases like nitrogen dissolving into their tissues. As they ascend or move to a lower-pressure environment, this dissolved gas can form bubbles if the pressure change occurs too rapidly.

How do these bubbles cause damage? The bubbles can obstruct blood flow, cause vascular spasm, and trigger an inflammatory response. They may also lead to endothelial damage, activating the intrinsic clotting cascade and causing platelet activation. This cascade of events can result in tissue ischemia and various symptoms associated with DCS.

Factors Influencing Bubble Formation

Several factors can influence the likelihood and severity of bubble formation in DCS:

1. Depth and duration of dive
2. Rate of ascent
3. Individual physiology
4. Dehydration
5. Body fat content
6. Alcohol consumption
7. Previous injuries
8. Ambient temperature

Why do these factors matter? Understanding these influences can help divers and other at-risk individuals take appropriate precautions to minimize their risk of developing DCS.

Recognizing the Symptoms of Decompression Sickness

Identifying the symptoms of decompression sickness is crucial for prompt diagnosis and treatment. The manifestations of DCS can vary widely, ranging from mild discomfort to life-threatening conditions. What are the most common symptoms of DCS?

• Joint pain (especially in shoulders, elbows, knees, and ankles)
• Skin rashes or itching
• Fatigue
• Dizziness
• Numbness or tingling sensations
• Difficulty breathing (“the chokes”)
• Neurological symptoms (headaches, visual disturbances, confusion)
• Paralysis (in severe cases)

It’s important to note that symptoms can appear immediately after surfacing or may be delayed for several hours. How quickly do symptoms typically onset? In most cases, symptoms manifest within 6 hours of decompression, but in rare instances, they may appear up to 24 hours later.

The “Bends”: Joint Pain in DCS

Why is decompression sickness often referred to as “the bends”? This nickname originates from the characteristic joint pain experienced by many DCS sufferers. The pain, typically described as a deep ache, most commonly affects the shoulders but can occur in any joint. What causes this pain? It’s believed to result from bubbles forming in or around the joints, leading to inflammation and discomfort.

Diagnosing Decompression Sickness: Challenges and Approaches

Diagnosing decompression sickness can be challenging due to the wide range of potential symptoms and their similarity to other conditions. How do medical professionals diagnose DCS? The process typically involves a combination of the following:

1. Detailed patient history, including recent diving or pressure exposure
2. Physical examination, with particular attention to neurological signs
3. Ear examination to check for signs of barotrauma
4. Imaging studies (in some cases) to rule out other conditions

Why is obtaining a detailed dive profile crucial in diagnosing DCS? The dive profile provides essential information about the depth, duration, and decompression procedures used, which can help assess the likelihood of DCS and guide treatment decisions.

Differential Diagnosis: Ruling Out Other Conditions

What other conditions might mimic the symptoms of decompression sickness? Medical professionals must consider several alternatives when evaluating a patient with suspected DCS:

• Arterial gas embolism
• Pulmonary barotrauma
• Inner ear barotrauma
• Contaminated air (carbon monoxide poisoning)
• Marine life envenomation
• Musculoskeletal injuries
• Neurological conditions unrelated to diving

How do doctors differentiate between these conditions and DCS? A thorough history, physical examination, and sometimes additional tests are crucial in making an accurate diagnosis.

Treatment Strategies for Decompression Sickness

Once diagnosed, prompt treatment of decompression sickness is essential to prevent long-term complications. What is the primary treatment for DCS? The mainstay of treatment is recompression therapy using a hyperbaric chamber. How does recompression therapy work? By exposing the patient to increased atmospheric pressure, the therapy helps reduce bubble size and drive the excess gas back into solution, alleviating symptoms and preventing further tissue damage.

First Aid and Emergency Response

What immediate steps should be taken when DCS is suspected? The initial response to suspected decompression sickness includes:

1. Administering 100% oxygen
2. Ensuring proper hydration
3. Positioning the patient horizontally
4. Contacting emergency services or the nearest hyperbaric facility
5. Avoiding further exposure to low pressure (such as air travel)

Why is 100% oxygen administration crucial? Breathing pure oxygen helps accelerate the elimination of nitrogen from the body and can provide symptomatic relief while awaiting definitive treatment.

Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy (HBOT) is the definitive treatment for decompression sickness. How is HBOT administered? Patients are placed in a pressurized chamber and breathe 100% oxygen at pressures greater than sea level. What are the benefits of HBOT? This therapy helps reduce bubble size, improve tissue oxygenation, and promote healing. How long does treatment typically last? Treatment protocols vary but often involve initial sessions lasting 4-8 hours, followed by shorter daily sessions as needed.

Prevention Strategies: Minimizing the Risk of DCS

While treatment options for decompression sickness have improved, prevention remains the best approach. How can divers and others at risk reduce their chances of developing DCS? Several strategies can help minimize the risk:

• Adhering to proper decompression procedures and dive tables
• Using dive computers to monitor depth and time
• Ascending slowly and making safety stops
• Avoiding alcohol consumption before and after diving
• Staying well-hydrated
• Maintaining good physical fitness
• Avoiding hot showers or exercise immediately after diving
• Allowing adequate surface intervals between dives

Why is gradual ascent so important in preventing DCS? A slow, controlled ascent allows dissolved gases to be eliminated from the body more safely, reducing the risk of bubble formation.

Specialized Prevention Techniques

What additional measures can be taken to prevent DCS in high-risk situations? For technical divers, astronauts, and others exposed to extreme pressure changes, specialized techniques may be employed:

1. Use of mixed gas diving (replacing some nitrogen with helium)
2. Oxygen pre-breathing before decompression
3. Utilization of advanced decompression algorithms
4. Implementation of saturation diving techniques for prolonged exposures

How do these techniques help? By reducing nitrogen loading, enhancing gas elimination, and optimizing decompression profiles, these methods can significantly lower the risk of DCS in challenging environments.

Long-Term Effects and Complications of Decompression Sickness

While many cases of decompression sickness resolve completely with prompt treatment, some individuals may experience long-term effects. What are the potential long-term complications of DCS? Chronic issues may include:

• Residual joint pain or stiffness
• Neurological deficits
• Cognitive impairment
• Dysbaric osteonecrosis (bone tissue death)
• Increased susceptibility to future DCS episodes

Why do some individuals experience long-term effects while others recover fully? The severity and duration of the initial DCS episode, the timeliness of treatment, and individual factors all play a role in determining long-term outcomes.

Monitoring and Follow-up Care

How should individuals who have experienced DCS be monitored? Follow-up care typically involves:

1. Regular medical check-ups
2. Neurological assessments
3. Bone scans (in cases of suspected osteonecrosis)
4. Psychological support if needed
5. Guidance on future diving or pressure exposure activities

Why is ongoing monitoring important? Regular follow-up allows for early detection and management of any lingering or developing complications related to the DCS episode.

The Role of Research in Advancing DCS Understanding and Treatment

Ongoing research plays a crucial role in improving our understanding of decompression sickness and developing more effective prevention and treatment strategies. What are some current areas of research in DCS? Key focus areas include:

• Advanced bubble detection techniques
• Genetic factors influencing DCS susceptibility
• Novel decompression algorithms
• Pharmacological interventions to reduce bubble formation
• Improved recompression protocols
• Long-term effects of multiple DCS exposures

How might these research efforts benefit divers and others at risk of DCS? By enhancing our understanding of the underlying mechanisms of DCS and developing more targeted prevention and treatment approaches, research has the potential to significantly reduce the incidence and severity of decompression sickness.

Emerging Technologies in DCS Management

What new technologies are being developed to address DCS? Several innovative approaches are currently under investigation:

1. Wearable devices for real-time bubble detection
2. AI-powered decompression planning tools
3. Portable hyperbaric chambers for remote locations
4. Gene therapy to enhance decompression tolerance
5. Nanotechnology-based gas elimination enhancers

How might these technologies transform DCS prevention and treatment? By providing more accurate risk assessment, personalized decompression strategies, and rapid intervention capabilities, these advancements could significantly improve outcomes for individuals at risk of DCS.

In conclusion, decompression sickness remains a significant concern for divers, astronauts, and others exposed to rapid pressure changes. Understanding its causes, recognizing its symptoms, and implementing effective prevention and treatment strategies are crucial for minimizing its impact. As research continues to advance our knowledge of DCS, we can look forward to improved methods for managing this potentially serious condition, ensuring safer experiences for those who venture into high-pressure environments.

Decompression Sickness – StatPearls – NCBI Bookshelf

Jeffrey S. Cooper; Kenneth C. Hanson.

Author Information and Affiliations

Last Update: September 2, 2022.

Continuing Education Activity

Decompression sickness (DCS) occurs when dissolved gasses (usually nitrogen or helium, used in mixed gas diving) exit solution and form bubbles inside the body on depressurization. DCS occurs from underwater diving decompression (ascent), working in a caisson, flying in an unpressurized aircraft, and extra-vehicular activity from spacecraft. Proper decompression procedures during diving can help decrease DCS. Experts have classified DCS as Type I with symptoms involving only the skin, musculoskeletal system, or lymphatic systems; and Type II with symptoms that involve the central nervous system. This activity reviews the presentation of decompression sickness and highlights the role of the interprofessional team in its management.

Objectives:

• Review the etiology of decompression sickness.

• Describe the presentation of decompression sickness.

• Summarize the treatment of decompression sickness.

• Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by decompression sickness.

Access free multiple choice questions on this topic.

Introduction

Decompression sickness (DCS) occurs when dissolved gasses (usually nitrogen or helium, used in mixed gas diving) exit solution and form bubbles inside the body on depressurization. DCS occurs from underwater diving decompression (ascent), working in a caisson, flying in an unpressurized aircraft, and extra-vehicular activity from spacecraft. Proper decompression procedures during diving can help decrease DCS. Experts have classified DCS as Type I with symptoms involving only the skin, musculoskeletal system, or lymphatic systems; and Type II with symptoms that involve the central nervous system.

Etiology

DCS is bubble formation, growth, and elimination caused by a reduction in ambient pressure that results in inert gasses, usually nitrogen, that are dissolved in solution within tissues of the body. Individuals that breathe air in a pressurized environment reach a state of equilibrium/saturation of gas. This dissolved gas will be driven out of solution when leaving a higher-pressure environment to a lower pressure environment, such as ascending from depth during self-contained underwater breathing apparatus (SCUBA) diving, leaving a caisson worksite, or ascending to altitude in an unpressured aircraft. There are individual factors identified as possibly contributing to an increased risk of DCS. These include dehydration, patent foramen ovale,[1] previous injury, cold ambient temperature, high body fat content, and alcohol consumption. Type II decompression sickness (neurological symptoms) is thought to occur from right-to-left shunting of venous bubbles.[2]

Epidemiology

The incidence of decompression sickness, fortunately, is rare. Estimates for sports diving are three cases per 10,000 dives. The incidence among commercial divers can be higher ranging from 1.5-10 per 10,000 dives. As expected, the incidence depends on the length and depth of the dive.[3] The risk for DCS is 2.5 times greater for males than females.

Pathophysiology

The pathophysiology of DCS is due directly to the formations of bubbles coming out of solution. Tissue damage results from multiple mechanisms including blockage of blood flow and vascular spasm.[4] Gas bubbles also cause endothelial damage resulting in activation of the intrinsic clotting cascade with platelet activation. Inflammatory mediators are released and with increased endothelial permeability development of edema, which leads to tissue ischemia.[5]

History and Physical

The initial evaluation of a patient suspected of DCS should include a detailed history and physical exam. For a conscious patient, get the details of exposure, including onset, duration, and progression of symptoms. For a diver with DCS, it is vital to determine the patient’s dive profile and gas mix.[3] An ear exam should look for signs of barotrauma. The patient should have a detailed neurological exam. 

DCS occurs most frequently in the shoulders, elbows, knees, and ankles. Joint pain (“the bends”) accounts for most cases, with the shoulder being the most prevalent site. Neurological symptoms present in 10% to 15% of DCS cases with a headache and visual disturbances being the most common symptoms. Skin manifestations are a feature in about 10% to 15% of DCS cases. Pulmonary DCS (“the chokes”) is quite rare in divers and much less frequently seen in aviators because of oxygen pre-breathing protocols. Bubbles in the skin or joints result in mild symptoms, larger numbers of bubbles in the venous blood may cause lung damage, and bubbles involving spinal cord function may lead to paralysis, sensory dysfunction, or death. If there is a cardiac right-to-left shunt, (e.g., a patent foramen ovale), venous bubbles could potentially enter the arterial circulation, resulting in an arterial gas embolism.

DCS should be suspected if related symptoms occur following a drop in pressure within 24 hours of diving. The diagnostic confirmation is if the symptoms are relieved by recompression. Magnetic resonance imaging (MRI) or computed tomography (CT) can occasionally identify bubbles in DCS, but they are not good at determining the diagnosis and certainly cannot be used to rule out DCS.

Evaluation

DCS is a clinical diagnosis. As the goal for treating all patients with symptomatic DCS is hyperbaric oxygen (HBO), with emphasis placed on recompression, there should be no delay in treatment for further diagnostic workup. The one exception is a chest x-ray, as untreated pneumothoraces are an absolute contraindication for HBO.[3]

Treatment / Management

All decompression sickness cases should have initial treatment with 100% oxygen until HBO therapy is available. Neurological, pulmonary, and mottled skin lesions should be treated with HBO therapy even if seen several days after development. Fluid administration is indicated, as this helps minimize dehydration. The recommendation to administer aspirin is no longer valid, as analgesics may mask symptoms. Patient placement is in the supine position or the recovery position if vomiting occurs. The Trendelenburg position and the left lateral decubitus position (Durant’s maneuver) may be potentially beneficial if air emboli are suspected, but these positions are no longer recommended for extended periods, owing to concerns regarding cerebral edema. If the patient experiences an altered mental status or is unconscious, initial management should focus on the treatment and stabilization of ABCs, (airway, breathing, and circulation). Patients should receive HBO treatment as soon as possible.

Patients that need evacuation to a definitive treatment center by aeromedical transport should fly on pressurized aircraft. If unpressurized aircraft, such as helicopters, are the only means of transport then flight altitude should be limited to 300 m or 1000 ft if possible. [3]

Differential Diagnosis

Vertigo can indicate inner ear or vestibular decompression sickness wherein bubbles form in the perilymph fluid of the cochlea.[6] However, other diving-related causes merit consideration, as recompression and hyperbaric oxygen can cause worsening of some of these conditions. Inner ear barotrauma, in particular, would be a contraindication to compression as high-pressure gas may be forced into the cochlea causing further trauma on decompression. Alternobaric and caloric vertigo should be differentiated from decompression sickness by history. Cerebral arterial gas embolism affecting the midbrain or cerebellum can also present as inner ear decompression sickness but receives similar treatment.[1]

The differential diagnosis for divers should also consider that the stress of diving can exacerbate chronic medical problems. Consider cardiac disease for patients with chest pain and exacerbation of intrinsic lung disease for shortness of breath. Other considerations include pain from previous musculoskeletal injury and stroke and hypoglycemia for altered mental status.  Further concerns include drowning or near-drowning and thermal stress.[3]

Treatment Planning

There are a variety of hyperbaric chamber treatment protocols for decompression sickness. These differences are based on such things as the severity of the insult and the availability of oxygen. There are also in water recompression protocols. The usual US treatment protocol is a US Navy Treatment Table 6 done with oxygen pressurized to 2.8 atmospheres absolute (ATA). In water, recompression is a relatively high risk but is a consideration if there would otherwise be significant delays to treatment, logistical difficulties, or other problems. It requires appropriate training, equipment, and pre-planning. Immediate treatment at the surface with oxygen is beneficial for improving outcomes and decreasing recompression treatments.   

Treatment of DCS employing the US Navy Treatment Table 6 with oxygen at 18m is the standard of care. Significant delay to treatment, transportation difficulties, and facilities with limited experience may lead one to consider on-site treatment.  Surface oxygen for first aid is shown to improve the efficacy of recompression and decreased the number of recompression treatments required when administered less than four hours post-dive. In-water recompression (IWR) to 9m, breathing oxygen is one option that has shown success over the years. IWR is not without risk and requires certain precautions. IWR would only be suitable for an organized and disciplined group of divers with suitable equipment and practical training in the procedure.

Prognosis

Having had decompression sickness may place patients at increased risk for future similar events. Prognosis is severity dependent and also dependent on such factors as the time to recompression, availability and time to surface oxygen, and supportive care.

Complications

Decompression sickness can cause long-term damage. Central nervous system lesions in the spine and brain may occur.

Deterrence and Patient Education

The risk of decompression sickness is reducible in several ways. Divers should avoid flying within 24 hours after their last dive and longer no-fly periods may be required based on dive profiles and guided by decompression tables or computers. The use of oxygen-enriched gas can also ameliorate risk if used on “air tables.” Using a more conservative dive table or dive computer setting will likewise reduce risk. Isobaric decompression, breathing oxygen at depth, likewise can lessen the inert gas burden and reduce decompression sickness risk. 

Cold exposure, heavy exercise, recent alcohol use, and dehydration all increase risk and should be avoided. Preliminary research also shows that exercise several hours before diving may be protective while exercise after diving may increase the risk of DCS.[7]

Pearls and Other Issues

The treatment of DCS is with 100% oxygen, followed by recompression in a hyperbaric chamber.[8] In most cases, this will prevent long-term effects. However, permanent injury from DCS is possible. To prevent the excess formation of bubbles leading to decompression sickness, divers limit their ascent rate. The recommended ascent rate used by popular decompression models is about 10 meters (33 ft) per minute.

Enhancing Healthcare Team Outcomes

The management of patients with decompression sickness best done with an interprofessional team. Early identification and referral to a hyperbaric center are important for good outcomes from serious decompression sickness. In water, treatments need a well-trained and organized team approach.[9][10] Divers should have oxygen for immediate administration in the case of DCS. The Divers’ Alert Network provides referrals to hyperbaric facilities and 24/7 consultation with hyperbaric trained physicians and other providers.

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

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.

Pollock NW, Buteau D. Updates in Decompression Illness. Emerg Med Clin North Am. 2017 May;35(2):301-319. [PubMed: 28411929]

4.

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]

5.

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]

6.

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]

7.

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]

8.

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]

9.

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]

10.

Walker, III JR, Murphy-Lavoie HM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 1, 2023. Diving in Water Recompression. [PubMed: 29630272]

Disclosure: Jeffrey Cooper declares no relevant financial relationships with ineligible companies.

Disclosure: Kenneth Hanson declares no relevant financial relationships with ineligible companies.

Decompression Sickness – StatPearls – NCBI Bookshelf

Jeffrey S. Cooper; Kenneth C. Hanson.

Author Information and Affiliations

Last Update: September 2, 2022.

Continuing Education Activity

Decompression sickness (DCS) occurs when dissolved gasses (usually nitrogen or helium, used in mixed gas diving) exit solution and form bubbles inside the body on depressurization. DCS occurs from underwater diving decompression (ascent), working in a caisson, flying in an unpressurized aircraft, and extra-vehicular activity from spacecraft. Proper decompression procedures during diving can help decrease DCS. Experts have classified DCS as Type I with symptoms involving only the skin, musculoskeletal system, or lymphatic systems; and Type II with symptoms that involve the central nervous system. This activity reviews the presentation of decompression sickness and highlights the role of the interprofessional team in its management.

Objectives:

• Review the etiology of decompression sickness.

• Describe the presentation of decompression sickness.

• Summarize the treatment of decompression sickness.

• Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by decompression sickness.

Access free multiple choice questions on this topic.

Introduction

Decompression sickness (DCS) occurs when dissolved gasses (usually nitrogen or helium, used in mixed gas diving) exit solution and form bubbles inside the body on depressurization. DCS occurs from underwater diving decompression (ascent), working in a caisson, flying in an unpressurized aircraft, and extra-vehicular activity from spacecraft. Proper decompression procedures during diving can help decrease DCS. Experts have classified DCS as Type I with symptoms involving only the skin, musculoskeletal system, or lymphatic systems; and Type II with symptoms that involve the central nervous system.

Etiology

DCS is bubble formation, growth, and elimination caused by a reduction in ambient pressure that results in inert gasses, usually nitrogen, that are dissolved in solution within tissues of the body. Individuals that breathe air in a pressurized environment reach a state of equilibrium/saturation of gas. This dissolved gas will be driven out of solution when leaving a higher-pressure environment to a lower pressure environment, such as ascending from depth during self-contained underwater breathing apparatus (SCUBA) diving, leaving a caisson worksite, or ascending to altitude in an unpressured aircraft. There are individual factors identified as possibly contributing to an increased risk of DCS. These include dehydration, patent foramen ovale,[1] previous injury, cold ambient temperature, high body fat content, and alcohol consumption. Type II decompression sickness (neurological symptoms) is thought to occur from right-to-left shunting of venous bubbles.[2]

Epidemiology

The incidence of decompression sickness, fortunately, is rare. Estimates for sports diving are three cases per 10,000 dives. The incidence among commercial divers can be higher ranging from 1.5-10 per 10,000 dives. As expected, the incidence depends on the length and depth of the dive.[3] The risk for DCS is 2.5 times greater for males than females.

Pathophysiology

The pathophysiology of DCS is due directly to the formations of bubbles coming out of solution. Tissue damage results from multiple mechanisms including blockage of blood flow and vascular spasm.[4] Gas bubbles also cause endothelial damage resulting in activation of the intrinsic clotting cascade with platelet activation. Inflammatory mediators are released and with increased endothelial permeability development of edema, which leads to tissue ischemia.[5]

History and Physical

The initial evaluation of a patient suspected of DCS should include a detailed history and physical exam. For a conscious patient, get the details of exposure, including onset, duration, and progression of symptoms. For a diver with DCS, it is vital to determine the patient’s dive profile and gas mix.[3] An ear exam should look for signs of barotrauma. The patient should have a detailed neurological exam. 

DCS occurs most frequently in the shoulders, elbows, knees, and ankles. Joint pain (“the bends”) accounts for most cases, with the shoulder being the most prevalent site. Neurological symptoms present in 10% to 15% of DCS cases with a headache and visual disturbances being the most common symptoms. Skin manifestations are a feature in about 10% to 15% of DCS cases. Pulmonary DCS (“the chokes”) is quite rare in divers and much less frequently seen in aviators because of oxygen pre-breathing protocols. Bubbles in the skin or joints result in mild symptoms, larger numbers of bubbles in the venous blood may cause lung damage, and bubbles involving spinal cord function may lead to paralysis, sensory dysfunction, or death. If there is a cardiac right-to-left shunt, (e.g., a patent foramen ovale), venous bubbles could potentially enter the arterial circulation, resulting in an arterial gas embolism.

DCS should be suspected if related symptoms occur following a drop in pressure within 24 hours of diving. The diagnostic confirmation is if the symptoms are relieved by recompression. Magnetic resonance imaging (MRI) or computed tomography (CT) can occasionally identify bubbles in DCS, but they are not good at determining the diagnosis and certainly cannot be used to rule out DCS.

Evaluation

DCS is a clinical diagnosis. As the goal for treating all patients with symptomatic DCS is hyperbaric oxygen (HBO), with emphasis placed on recompression, there should be no delay in treatment for further diagnostic workup. The one exception is a chest x-ray, as untreated pneumothoraces are an absolute contraindication for HBO.[3]

Treatment / Management

All decompression sickness cases should have initial treatment with 100% oxygen until HBO therapy is available. Neurological, pulmonary, and mottled skin lesions should be treated with HBO therapy even if seen several days after development. Fluid administration is indicated, as this helps minimize dehydration. The recommendation to administer aspirin is no longer valid, as analgesics may mask symptoms. Patient placement is in the supine position or the recovery position if vomiting occurs. The Trendelenburg position and the left lateral decubitus position (Durant’s maneuver) may be potentially beneficial if air emboli are suspected, but these positions are no longer recommended for extended periods, owing to concerns regarding cerebral edema. If the patient experiences an altered mental status or is unconscious, initial management should focus on the treatment and stabilization of ABCs, (airway, breathing, and circulation). Patients should receive HBO treatment as soon as possible.

Patients that need evacuation to a definitive treatment center by aeromedical transport should fly on pressurized aircraft. If unpressurized aircraft, such as helicopters, are the only means of transport then flight altitude should be limited to 300 m or 1000 ft if possible. [3]

Differential Diagnosis

Vertigo can indicate inner ear or vestibular decompression sickness wherein bubbles form in the perilymph fluid of the cochlea.[6] However, other diving-related causes merit consideration, as recompression and hyperbaric oxygen can cause worsening of some of these conditions. Inner ear barotrauma, in particular, would be a contraindication to compression as high-pressure gas may be forced into the cochlea causing further trauma on decompression. Alternobaric and caloric vertigo should be differentiated from decompression sickness by history. Cerebral arterial gas embolism affecting the midbrain or cerebellum can also present as inner ear decompression sickness but receives similar treatment.[1]

The differential diagnosis for divers should also consider that the stress of diving can exacerbate chronic medical problems. Consider cardiac disease for patients with chest pain and exacerbation of intrinsic lung disease for shortness of breath. Other considerations include pain from previous musculoskeletal injury and stroke and hypoglycemia for altered mental status.  Further concerns include drowning or near-drowning and thermal stress.[3]

Treatment Planning

There are a variety of hyperbaric chamber treatment protocols for decompression sickness. These differences are based on such things as the severity of the insult and the availability of oxygen. There are also in water recompression protocols. The usual US treatment protocol is a US Navy Treatment Table 6 done with oxygen pressurized to 2.8 atmospheres absolute (ATA). In water, recompression is a relatively high risk but is a consideration if there would otherwise be significant delays to treatment, logistical difficulties, or other problems. It requires appropriate training, equipment, and pre-planning. Immediate treatment at the surface with oxygen is beneficial for improving outcomes and decreasing recompression treatments.   

Treatment of DCS employing the US Navy Treatment Table 6 with oxygen at 18m is the standard of care. Significant delay to treatment, transportation difficulties, and facilities with limited experience may lead one to consider on-site treatment.  Surface oxygen for first aid is shown to improve the efficacy of recompression and decreased the number of recompression treatments required when administered less than four hours post-dive. In-water recompression (IWR) to 9m, breathing oxygen is one option that has shown success over the years. IWR is not without risk and requires certain precautions. IWR would only be suitable for an organized and disciplined group of divers with suitable equipment and practical training in the procedure.

Prognosis

Having had decompression sickness may place patients at increased risk for future similar events. Prognosis is severity dependent and also dependent on such factors as the time to recompression, availability and time to surface oxygen, and supportive care.

Complications

Decompression sickness can cause long-term damage. Central nervous system lesions in the spine and brain may occur.

Deterrence and Patient Education

The risk of decompression sickness is reducible in several ways. Divers should avoid flying within 24 hours after their last dive and longer no-fly periods may be required based on dive profiles and guided by decompression tables or computers. The use of oxygen-enriched gas can also ameliorate risk if used on “air tables.” Using a more conservative dive table or dive computer setting will likewise reduce risk. Isobaric decompression, breathing oxygen at depth, likewise can lessen the inert gas burden and reduce decompression sickness risk. 

Cold exposure, heavy exercise, recent alcohol use, and dehydration all increase risk and should be avoided. Preliminary research also shows that exercise several hours before diving may be protective while exercise after diving may increase the risk of DCS.[7]

Pearls and Other Issues

The treatment of DCS is with 100% oxygen, followed by recompression in a hyperbaric chamber.[8] In most cases, this will prevent long-term effects. However, permanent injury from DCS is possible. To prevent the excess formation of bubbles leading to decompression sickness, divers limit their ascent rate. The recommended ascent rate used by popular decompression models is about 10 meters (33 ft) per minute.

Enhancing Healthcare Team Outcomes

The management of patients with decompression sickness best done with an interprofessional team. Early identification and referral to a hyperbaric center are important for good outcomes from serious decompression sickness. In water, treatments need a well-trained and organized team approach.[9][10] Divers should have oxygen for immediate administration in the case of DCS. The Divers’ Alert Network provides referrals to hyperbaric facilities and 24/7 consultation with hyperbaric trained physicians and other providers.

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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]

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Pollock NW, Buteau D. Updates in Decompression Illness. Emerg Med Clin North Am. 2017 May;35(2):301-319. [PubMed: 28411929]

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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]

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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]

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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]

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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]

8.

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]

9.

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]

10.

Walker, III JR, Murphy-Lavoie HM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 1, 2023. Diving in Water Recompression. [PubMed: 29630272]

Disclosure: Jeffrey Cooper declares no relevant financial relationships with ineligible companies.

Disclosure: Kenneth Hanson declares no relevant financial relationships with ineligible companies.

Decompression sickness. What is decompression sickness?

IMPORTANT
The information in this section should not be used for self-diagnosis or self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

Decompression sickness is a complex of symptoms that develops when gas bubbles form in vessels and tissues against the background of a rapid decrease in atmospheric pressure. Pathology can be acute or chronic. Manifested by pain in the joints, muscles, Meniere’s syndrome, dyspepsia, signs of CNS damage, acute pulmonary and cardiovascular insufficiency. When making a diagnosis, anamnestic data and the results of an objective examination are used; radiography, ultrasound, MRI, and CT are used to assess the condition of various organs. Treatment – recompression followed by slow decompression, symptomatic drug therapy.

ICD-10

T70.3 Decompression sickness

• Causes
• Pathogenesis
• Classification
• Symptoms of decompression sickness
• Complications
• Diagnostics
• Treatment of decompression sickness
• Prognosis and prevention
• Prices for treatment

General

Decompression sickness (decompression sickness, DCS) is a complex of changes that develop during the transition from high atmospheric pressure to normal, less often from normal to low. Pathology got its name from the word “caisson”, denoting a chamber created in the 40s of the 19th century and intended for work under water or in conditions of water-saturated soils. DCS is considered an occupational disease of divers and specialists working in caisson chambers; in some cases, it is diagnosed in pilots. In recent years, due to the widespread use of diving, it has been identified in other populations. According to statistics, the incidence of the disease is 2-4 cases per 10,000 dives.

decompression sickness

Causes

The immediate cause of decompression sickness is a rapid decrease in atmospheric pressure with a change in the depth of immersion in water, less often – when the aircraft is raised to a considerable height. The faster the atmospheric pressure changes, the greater the risk of this pathology. Factors that increase the likelihood of developing the disease are:

• Aging of the body. As we age, the condition of all organs deteriorates. This causes a decrease in the compensatory capabilities of the lungs and heart during a period of pressure changes.
• Hypothermia. It is accompanied by a slowdown in blood flow in the peripheral vessels. Blood from distant parts of the body enters the pulmonary vessels more slowly, gas is released from the blood in a physiological way to a lesser extent.
• Dehydration. The viscosity of the blood in this condition increases, which provokes a slowdown in blood circulation. With a change in external pressure on the periphery, stasis occurs, which is aggravated by the formation of bubbles that block the lumen of the vessels.
• Physical activity. Potentiates a violation of the uniformity of blood flow, as a result of which conditions are created for the intensive dissolution of gases in the blood, followed by the appearance of “silent” bubbles. A characteristic feature is the deposition of microbubbles in the joints and an increase in the likelihood of pathology on subsequent dives.
• Lipidemia, overweight. Fats have increased hydrophobicity, therefore, with their high content, bubbles form more actively. Adipose tissue cells intensively dissolve the inert gases that are part of the respiratory mixtures.
• Hypercapnia. It develops with a low quality of the respiratory mixture or attempts to “save” it by holding your breath. An increase in the amount of CO2 provokes a shift in the acid-base state to the acid side. Because of this, more inert gases dissolve in the blood.
• Alcohol intoxication. Drinking alcohol causes dehydration. In addition, alcohol molecules cause small bubbles to coalesce into larger ones and become centers around which large bubbles form, blocking blood vessels.

Pathogenesis

At elevated pressure, the gases of the respiratory mixture, due to diffusion, dissolve in significant quantities in the blood of the capillaries of the lung tissue. When the pressure is reduced, the opposite phenomenon is observed – gases “come out” of the liquid, forming bubbles. The faster the pressure changes, the more intense the process of back diffusion becomes. With a rapid rise, the patient’s blood “boils”, the gases released form many large bubbles that can block vessels of various calibers and damage various organs.

Large bubbles connect with small ones, platelets “stick” to the formed bubbles, blood clots are formed that attach to the walls of small vessels and block their lumen. Part of the thrombi comes off with fragments of the vascular wall, migrates through the bloodstream and blocks other vessels. With the accumulation of a large number of such formations, a gas embolism develops. With significant damage to the walls, the integrity of the arterioles is violated, hemorrhages occur.

The appearance of bubbles and the formation of their complexes with platelets triggers a cascade of biochemical reactions, as a result of which various mediators are released into the blood, intravascular coagulation occurs. Bubbles also form outside the vascular bed, in the articular cavities and soft tissue structures. They increase in volume and compress the nerve endings, causing pain. Pressure on soft tissue formations causes damage to them with the formation of foci of necrosis in muscles, tendons and internal organs.

Classification

Due to the possibility of damage to various organs, significant differences in severity and prognosis, the most rational from a practical point of view is the systematization of the types of decompression sickness based on the prevailing manifestations. The clinical classification of M. I. Yakobson is a detailed version of the allocation of degrees of the disease, taking into account the symptoms. There are four forms of pathology:

• Light. Arthralgia, myalgia, neuralgia, caused by compression of nerve endings by gas bubbles, prevail. A number of patients revealed livedo, itching, greasiness of the skin caused by blockage of small superficial veins, ducts of the sebaceous and sweat glands.
• Medium. Disorders of the vestibular apparatus, eyes and gastrointestinal tract, resulting from embolism of capillaries and arterioles of the labyrinth, accumulation of gas bubbles in the vessels of the mesentery and intestines, and transient spasm of the retinal arteries predominate.
• Heavy. It is manifested by rapidly growing symptoms of damage to the spinal cord, usually at the level of the midthoracic segments, which is due to the tendency of myelin to absorb nitrogen and weak vascularization of the midthoracic region, due to which the actively forming vesicles do not migrate with blood, but compress the nervous tissue. Signs of brain involvement are much less common. Disorders of cardiac and respiratory activity are possible.
• Lethal. Occurs with a total cessation of blood circulation in the lungs or medulla oblongata, the development of acute heart failure. It is provoked by the formation of a large number of large bubbles, simultaneously blocking many vessels.

To assess the threat to the patient’s life and determine the optimal treatment tactics in traumatology and orthopedics, a simplified classification is also used, which includes two types of acute DCS. The first type is characterized by damage to peripheral structures (skin, musculo-articular system). The second is accompanied by changes in the nervous, respiratory, cardiovascular, digestive systems, in the absence of treatment, a fatal outcome is possible. In addition, there is a chronic variant of decompression sickness, which can develop in the presence of an acute pathology in history or without previous acute events; It is diagnosed in people who have worked in caissons for a long time.

Symptoms of decompression sickness

In the case of a severe injury, manifestations can occur already in the first minutes after ascent, but more often the clinical picture of decompression sickness develops gradually. In half of patients, symptoms are detected within an hour. After 6 hours, signs of pathology are detected in 90% of patients. There is rarely a delayed onset of symptoms (over 1-2 days). With a mild form, pain in the joints, bone structures, muscle tissue, and back area is noted. The pain syndrome is usually more pronounced in the area of ​​the shoulder and elbow joints. Patients describe sensations as “drilling”, “deep”, aggravated by movement. Often there is a rash, itching of the skin, increased greasiness, marbling of the color of the skin. There may be an increase in lymph nodes.

With moderate decompression sickness, Meniere’s syndrome is observed, caused by damage to the organ of balance and including dizziness, headache, pallor, sweating, nausea, and vomiting. Gastrointestinal disorders are manifested by pain, vomiting and diarrhea. Spasm of the retinal vessels is accompanied by the appearance of photomorphopsia, “flies” and “fog” before the eyes. The severe form is characterized by lower spastic paraplegia, pelvic disorders, impaired sensitivity in the lower half of the body according to the conduction type. Sometimes there are hemiparesis or hemiplegia, headaches, speech disorders, psychotic disorders that are transient.

Cardiovascular and respiratory symptoms are found in the severe form and reach the greatest severity in the lethal variant of the disease. Weakness, pallor, shortness of breath, intense chest pain, cough, drop in blood pressure are determined. With the progression of symptoms, pulmonary edema develops, breathing becomes frequent, shallow, the pulse slows down, the skin becomes bluish or pale gray. Possible pulmonary and myocardial infarctions. The lethal form is accompanied by acute heart failure, asphyxia due to blockade of the pulmonary circulation or impaired regulation of breathing by the medulla oblongata.

The most common manifestation of chronic decompression sickness is deforming arthrosis, caused by the repeated impact of small bubbles on the bone and joint structures. The opinions of scientists regarding myodegeneration of the heart, early atherosclerosis and frequent diseases of the middle ear in people engaged in work in the caisson way, differ. Some experts consider the listed pathologies to be the result of recurring subclinical DCS, others – the result of other factors that occur when staying at great depths.

Complications

The type and severity of complications are determined by the form of the disease, the timeliness and adequacy of therapeutic measures. The most common sequelae of acute decompression sickness are chronic Meniere’s syndrome and aeropathic myelosis. Other possible complications are pneumonia, myocarditis, endocarditis, cardiodystrophy, cardiosclerosis, paresis, paralysis, sensory disturbances, aseptic osteonecrosis.

Diagnosis

The acute form of decompression sickness is diagnosed on the basis of the patient’s complaints, anamnestic data and the results of an external examination. On radiographs, gas bubbles can be detected in the joints, muscle tissue, fascia, tendon sheaths. To determine the state of the central nervous system, tomographic studies of the spinal cord and brain are prescribed. Confirmation of the diagnosis is the improvement of the patient’s condition during recompression. The examination program for the development of complications is determined by the nature of the alleged pathology, may include ECG, echocardiography, radiography, ultrasound, MRI and CT of various organs.

Treatment of decompression sickness

Therapy of the disease, depending on the form, severity of symptoms of complications, is carried out by resuscitators, traumatologists, occupational pathologists and other specialists. With unsharply expressed skin, muscle and joint manifestations, observation in dynamics is permissible. In other cases, urgent recompression in a pressure chamber is indicated. First, the pressure is increased to indicators corresponding to the depth of the patient’s immersion. In a serious condition of the victim, apply pressure higher than the initial one. The minimum duration of recompression is 30 minutes, if symptoms persist, the procedure is continued until the patient’s condition returns to normal. Then slow decompression is carried out, reducing the pressure by 0.1 atmosphere every 10 minutes. After reducing the pressure to 2 atmospheres, inhalation of oxygen is used to accelerate the process of nitrogen removal. If signs of DCS appear after pressure normalization, repeated recompression is performed.

According to the indications, symptomatic therapy is prescribed. Carry out infusion of glucose solution, plasma, saline solutions. Pharmaceutical preparations are used to normalize and stimulate the activity of the cardiovascular system. If necessary, vasodilators are included in the treatment plan. With intense pain syndrome, non-narcotic analgesics are used. Narcotic pharmaceuticals are not indicated due to a possible inhibitory effect on the respiratory center. With myalgia and arthralgia, local warming and analgesic drugs are recommended. After leaving the pressure chamber, physiotherapy is carried out: sollux, diathermy, therapeutic baths.

Prognosis and prevention

The outcome of DCS is determined by the severity of the lesion and the time of initiation of recompression. In 80% of patients there is a complete recovery. Fatal outcomes are observed quite rarely, usually with an emergency rise or lack of specialized assistance. Prevention of decompression sickness includes the use of quality equipment for diving and professional work at depth, strict adherence to the rules of ascent, taking into account the data of specially designed tables, regular medical examinations, and the elimination of factors that increase the risk of DCS. Preventive measures also involve the establishment of a sufficient time interval between the first and subsequent dives or flights in air transport, limiting the time spent in high pressure conditions for divers and caisson workers.

Sources

1. Occupational diseases: Diagnosis, treatment, prevention / Skepyan N.A. – 2013
2. Occupational diseases / Artamonova V.G., Shatalov N.N. – 1988
3. Decompression sickness / Shitov A. – 2011
4. diagnostics and self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.

   causes, symptoms, risk group, treatment

   1. How does decompression sickness occur?
   2. Consequences of decompression sickness
   3. Severity of decompression sickness
   4. Chronic decompression sickness
   5. Symptoms of diving illness
   6. Complications of DCS
   7. Diagnostics
   8. Treatment

   Image by chayanuphol on Shutterstock

   Decompression sickness is a pathological condition in which gas bubbles form in the vessels and tissues of the body. This is due to the rapid decrease in atmospheric pressure. Otherwise, the disease is called decompression sickness (DCS).

   The name “caisson” comes from the word “caisson”. This device was invented in the XIX century for underwater work. The design was a chamber in which a person descended into the water. First, decompression sickness was diagnosed by specialists in underwater work. Over time, its distribution has become wider. Sometimes this condition occurs in pilots who, when changing flight altitude, are exposed to changes in atmospheric pressure. However, divers are more susceptible to this disease than others. Diving enthusiasts cannot always cope with the transition from high pressure to normal, which is why they develop “diver’s disease”. According to statistics, up to 4 cases of decompression sickness are recorded per 10 thousand dives. It can be not only acute, but also chronic.

   To prevent the disease, you should use high-quality breathing mixtures when diving, avoid a sharp rise from the depth to the surface, observe the intervals between dives or flights, and undergo preventive examinations if a person works underwater.

   How decompression sickness occurs

   The main reason for the formation of air bubbles in organs and tissues is a sharp decrease in atmospheric pressure when ascending to a height or water surface after diving. However, there are factors that increase the risk of developing “diver’s disease”:

   • age changes. With age, the heart and lungs have a harder time coping with stress, so decompression sickness is more common in middle-aged and mature people than in young people;

   • hypothermia. Cold impairs the blood supply to organs and tissues. This is especially true for peripheral vessels. Because of this, the pulmonary vessels receive less blood, which leads to gas retention and the formation of bubbles;

   • increased blood viscosity. This condition occurs when you are dehydrated. The blood flow slows down, there is stagnation of blood in the peripheral vessels;

   • intoxication. Drinking alcohol before diving is life-threatening. Alcohol provokes dehydration, and with the content of alcohol in the blood, air bubbles become larger and can clog the lumen of the vessel;

   • overweight. If the body contains a large percentage of adipose tissue, bubbles form faster due to the hydrophobicity of fat. In addition, fats tend to dissolve inert gases from the breathing mixtures used by divers;

   • increase in carbon dioxide concentration. This condition is called hypercapnia. It occurs when using poor-quality mixtures or when breathing improperly under water. With an increase in the concentration of CO2 in the blood, more inert gases are dissolved;

   • exercise stress. Under load, blood flow becomes uneven. Gases in the blood dissolve more rapidly and air bubbles appear. As a rule, they are very small in size and are localized in the area of ​​​​the joints. On subsequent dives, decompression sickness may become more pronounced.

   Consequences of decompression sickness

   When immersed in water, atmospheric pressure rises. Because of this, the gases of the respiratory mixtures dissolve in the blood of the capillaries of the tissues of the lungs. After ascent, when the pressure returns to normal limits, the opposite occurs. Gases dissolved in the blood form bubbles. If the diver ascends quickly, that is, the body does not have time to adapt. If the rate of ascent is not observed, the blood seems to “boil”. At this point, not only small, but also large bubbles are formed. They attract platelets to themselves, increasing in size. These compounds can cause thromboembolism – blockage of the lumen of the vessel.

   When a large number of such bubbles with platelets appear in the blood, a gas embolism develops. Circulating through the bloodstream, these compounds can damage the walls of blood vessels, provoking hemorrhage.

   In addition to vessels, bubbles can be found in the joint cavities and soft tissues. Gas compounds compress the nerve endings, cause pain throughout the body. In addition, there may be foci of necrosis in the muscles and internal organs, which is also caused by compression.

   Severity of decompression sickness

   Depending on the symptoms, three degrees of severity of the disease are distinguished:

   • light. With a mild degree of pathology, the patient experiences pain in the muscles and joints, which is associated with pressure on the nerve endings of air bubbles. Due to blockage of superficial vessels and sweat glands, itching of the skin begins, it becomes more oily;

   • average. Pathology of moderate severity causes a deterioration in coordination of movements, visual impairment, and a disorder in the functioning of the digestive tract. This is due to the accumulation of gases in the vessels of the mesentery and intestines;

   • heavy. The main symptom of pathology is damage to the spinal cord due to compression of the nervous tissue. In some cases, the brain is involved in the pathological process. This is manifested by disorders in the work of the heart and respiratory system. In addition, in a particularly severe stage, air bubbles block vital vessels, which leads to a cessation of the blood supply to the lung tissue, a person develops acute heart failure.

   Even with moderate severity of pathology, acute “diver’s disease” can lead to severe damage to organs and systems. If left untreated, these conditions are life threatening.

   Chronic decompression sickness

   This type of pathology is quite rare. It affects people who perform professional work at depth every day or regularly go in for scuba diving.

   Symptoms of diving illness

   Beginners are not always able to recognize the symptoms of decompression sickness, because they increase gradually. The exceptions are the most severe degrees of the disease, in which a person feels unwell from the first minutes after surfacing. In most people, the first signs of pathology appear within an hour and gradually increase over five to six hours. The least common is delayed decompression sickness. It appears 1-2 days after the dive.

   Symptoms depend on the degree of the disease. Patients with a mild form of pathology feel pain in the back and joints. Usually, the shoulders and elbows hurt the most, and the pain gets worse with movement. A rash or “marble” pattern may appear on the skin. Changes are accompanied by itching. Some people have enlarged lymph nodes.

   If the degree of damage is more severe, the patient is dizzy and has a headache, hearing deteriorates, sweating appears, and the skin turns pale. A person cannot engage in habitual activities due to flies and fog before his eyes. There are also pains in the abdomen, which are accompanied by nausea and vomiting, loose stools.

   In patients with severe decompression sickness, the sensitivity of the lower body is disturbed, spasms, problems with urination and defecation are observed. If the brain is involved in the pathological process, headaches appear, a temporary speech disorder develops, and hearing deteriorates.

   Patients with severe DCS require urgent treatment due to impaired respiratory and cardiac function. The disease manifests itself as weakness and shortness of breath, chest pain, and a decrease in pressure. In the absence of medical care, acute oxygen deficiency develops, pulmonary edema may also develop, and the risk of myocardial infarction increases. Breathing becomes superficial, the skin turns pale, becomes cyanotic.

   In the lethal form of the disease, death occurs due to severe heart failure, which is caused by impaired blood circulation in the lungs or depression of the respiratory center located in the brain.

   If the disease proceeds in a chronic form, the joints and bones primarily suffer. This leads to the development of deforming arthrosis. Divers may experience irregularities in the work of the heart. The opinions of experts about cardiac pathologies against the background of decompression sickness diverge. Many are sure that regular stay at depth contributes to the earlier development of atherosclerosis, myodegeneration of the heart.

   Complications of DCS

   Most often, patients suffer from chronic Meniere’s syndrome, in which the pathology affects the middle ear. The person experiences dizziness, hearing gradually worsens. Another possible disorder is aeropathic myelosis, which is a lesion of bone marrow cells.

   In moderate and severe variants of the disease, all kinds of cardiac pathologies of an inflammatory and degenerative nature occur. Among the most common are endocarditis and myocarditis, cardiosclerosis. On the part of the respiratory system, pneumonia may develop. Of the neurological manifestations of the disease, paresis, muscle paralysis, loss of sensitivity are most often noted.

   Diagnostics

   With signs of DCS, you should contact a traumatologist. Depending on the form of the disease and its manifestations, cardiologists and neurologists are also involved in treatment. The doctor examines the patient, collects an anamnesis. Of the hardware procedures, ECG, X-ray, ultrasound of internal organs, CT and MRI are prescribed.

   Without fail, the doctor evaluates the work of the heart and lungs, the condition of the spinal cord and brain. When examining an x-ray, you can see gas bubbles in the tissues and joints, which confirms decompression sickness.

   Treatment

   With minor manifestations of the disease, the patient is at home or in the hospital under the supervision of a doctor. With moderate and severe degrees, it is necessary to carry out recompression, which takes place in the pressure chamber and allows you to normalize the patient’s condition.

   Recompression consists of several stages. First, the pressure rises, as if the person is again at depth. In such conditions, a person is from half an hour or more. After normalization of the state, the pressure is gradually reduced, simulating the rise to the surface of the water. Oxygen is also supplied, which will displace nitrogen from the blood. In some cases, the procedure has to be repeated.

   If the patient has developed complications, then symptomatic treatment, physiotherapy are prescribed.