Barotraumas occur whenever increasing pressure is exerted to air-filled spaces of the human body and efforts to equalize pressure from the diver fail. Barotraumas’ emergence is explained by Boyle’s law. According to that law, volume of air contained in these spaces will be reduced when descending and expanded when ascending. Equalization is achieved by means of introducing or releasing air when pressure (depth) increases or decreases respectively. Failure of equalization will result to damage of involved spaces or/and surrounding tissues.
Middle & Inner Ear
Barotraumas occur, more commonly, in the middle ear. Middle ear is the cavity lying between the Eustachian tube and tympanic membrane (eardrum). Failure to equalize through the Eustachian tube during descent or ascent will result to middle ear barotraumas felt as ear pain. Severity may range from mild irritation and “feeling of fullness” persisting after the dive, to fluid or blood accumulation in the middle ear. Rupture of the tympanic membrane is the extreme consequence of middle ear barotrauma.
Inner ear barotrauma presents with hearing loss, tinnitus, vertigo and vomiting. History of difficulty equalizing the ears or a forceful equalization may help distinguishing inner ear barotrauma from inner ear decompression sickness. Inner ear barotrauma may need surgery to heal. However, onsite identification of the true cause of symptoms may some times be difficult and need specialist’s examination to get appropriate medical help.
Sinus equalization problems appear when sinus openings are obstructed by nasal congestion & discharge, polyps or deviated nasal septum. During descent, volume of air in the sinuses is reduced. Failure to equalize will lead to fluid or/and blood accumulation, usually accompanied with sharp pain to the sinus/es involved. During ascent, expansion of air within the blocked sinus may worsen pain or lead to nasal discharge, usually mucus mixed with traces of blood.
Pulmonary barotrauma (Pulmonary Over-Inflation Syndrome) is the consequence of air overexpansion in the lungs, consistent with Boyle’s law, during rapid uncontrolled ascent or when lung pathology is present. It results to alveolar wall rupture and air entering the circulation or spread to surrounding tissues. Its consequences may be the following: Arterial Gas Embolism (AGE), Pneumothorax, Subcutaneous Emphysema, Mediastinal Emphysema or Pneumopericardium.
AGE is important to recognize and the situation that will demand treatment in the decompression chamber (recompression) as soon as possible. It appears with various symptoms, clinical picture and severity depending on the organ mainly involved. The brain is most commonly injured (cerebral embolism) and various neurological findings appear: weakness/paralysis, ataxia, loss of consciousness, convulsions etc. Distinguishing AGE from Decompression Sickness (DCS) occasionally may be difficult, but for both, medical management in general follows the same principles. However, important difference is that symptoms in AGE appear immediately after surfacing or within the first 10 minutes. It’s very rare for symptoms to begin later than 15 minutes after surfacing. And, pulmonary barotraumas with resulting AGE have been reported from uncontrolled ascent from as shallow as 1,5 meters (5 feet).
Relatively rare situations may be the result of pressure on other air-filled spaces of the body, such as the intestine, a cavity in a tooth or air-filled spaces between the diving equipment and the human body. During descent, compression of air inside a dry suit may cause visible painful skin irritation, unless the diver introduces additional air to the suit. Likewise, failure to equalize pressure in the mask during descent, will lead to mask squeeze (negative pressure in the mask due to reduced volume of air between the mask and the face) resulting to swelling of the face and subconjunctival hemorrhages (bloodshot eyes). Those conditions do not demand special care, but may cause concern to the diver and confusion regarding their cause. They will also need variable abstinence from diving activities for them to heal.
Gases under pressure
In conditions of increased environmental pressure, “innocent” gases may become toxic. When diving at depth, total pressure of gas mixture the diver breathes will increase in proportion to the increased pressure at depth. The same is true for the (partial) pressure of each one of the gases of the breathing mixture (oxygen & nitrogen when using air), according to Dalton’s law. This means that while percentage proportion of gases remain the same, environmental pressure determined by the depth of diving will lead to increased amount of each gas reaching the human body through the lungs. In that way, pressure may cause normally non-toxic gases to reach toxic levels (e.g. Oxygen, Nitrogen). It can also assist normally “toxic” gases accidentally confounding the breathing mixture in sub-toxic levels (when in surface) to reach toxic levels (e.g. Carbon Monoxide or Dioxide).
Pulmonary oxygen toxicity may be seen in prolonged dives breathing pure Oxygen, mainly used in military diving. It is very unlikely to occur in recreational diving and happens when breathing Oxygen of partial pressure above 0.5 bar. Difficulty breathing, cough, retrosternal chest burning sensation with progressive increase, are some of its features. It may progress to pulmonary edema.
Central Nervous System (CNS) oxygen toxicity is the reason why there is a universal depth limit of 6 meters when diving with 100% Oxygen using closed-circuit breathing devices. Transferring this to other types of diving, the limit concerning oxygen is set for its partial pressure not to exceed 1.6 ATA. In recreational and technical diving, CAUTION should be taken with oxygen-enriched breathing mixtures used during decompression and appropriate percentage of oxygen in Nitrox for depth used. CNS oxygen toxicity extreme manifestation is convulsions which may lead to loss of consciousness and drowning while underwater. Other than that, an unconscious diver brought to the surface by his buddy will likely suffer from pulmonary barotrauma. CNS oxygen toxicity in diving is life-threatening and should be avoided by all means. A person’s cerebral or systematic pathology predisposing to CNS toxicity is reason for cessation of all diving activities
Oxygen toxicity (mainly to the lungs) is of more concern for therapeutic “dives” with hyperbaric oxygen, where sessions for as long as a couple of hours every day to pure oxygen and for duration up to 6-8 weeks, expose the patients to much larger amounts of oxygen comparing to SCUBA diving. Air-breaks during sessions and weekend breaks are used to eliminate the occurrence of such phenomena.
Carbon Dioxide toxicity (poisoning)
It occurs, more often, in diving with closed or semi-closed breathing circuits due to malfunction of carbon dioxide retention mechanism. Accumulation of excess exhaled carbon dioxide leads to symptoms, from increased respiratory rate and dyspnoea to confusion, convulsions and loss of consciousness.
Nitrogen Narcosis («Martini effect»)
Nitrogen has anesthetic (narcotic) properties and affects cognitive and physical performance. Its narcotic effects are proportional to its partial pressure which is depth-dependant. Susceptibility to nitrogen narcosis may vary from dive to dive and between individuals but in some divers, especially novice divers with little experience, it may substantially affect short-term memory and decision-making ability. When diving with air, nitrogen narcosis will become noticeable at 30 meters depth. It gradually causes impairment of multi-tasking, memory and focus. At 50 – 70 meters, it produces impaired judgment and severe delay in response to signals, instructions and other stimuli. It is completely reversed in a few minutes by ascending to shallower depth. Nitrogen Narcosis itself is not harmful and has no long-term effects, but may compromise dive safety by leading to risky behavior under its influence.
Carbon Monoxide toxicity (poisoning)
Compressed air in diving cylinders, normally, does not contain carbon monoxide. However, it is a possibility in the case of compressor’s filtering malfunction or fumes mixed with compressed air due to faulty exhaust proximity to inlet air. Carbon monoxide concentration may be not enough to cause intoxication if breathing on the surface. When breathing the same gas mixture at depth, its partial pressure will increase similarly with oxygen & nitrogen, reaching “toxic” levels. Caution must be taken for appropriate compressor’s maintenance, regular air filters’ replacement and procedure of cylinders’ refilling.
Decompression sickness or illness (DCS or DCI)
DCS includes a variety of clinical manifestations of disease that comes as the result of decompression. This happens at the end of a diving activity, when the diver returns to the reduced pressure at the surface, after staying for some time at increased pressure undersea. It can also happen to caisson workers and fighter pilots. The cause of DCS is the formation of bubbles from inert gas supersaturation due to excess inert gas absorption during staying at depth undersea, a phenomenon explained by the gas laws. Bubbles block vessels and obstruct blood flow. Moreover, they cause complex biochemical interactions and initiate complex inflammatory responses that involve blood and its cells (platelets, white blood cells) and the blood vessels wall. These responses lead to microcirculation damage with resulting thrombosis, edema, ischemia/hypoxia and organ/system dysfunction
For DCS to occur, accumulation of a critical quantity of inert gas is needed. When diving at certain depths for a certain time (what matters is the maximum depth), it may be safe to return to the surface without the need for decompression stop (no-D dives). In deeper and longer dives, the need to stop at certain depths for some time to allow gradual elimination of excess inert gas (decompression stops) is important, in order to prevent occurrence of DCS. Decompression schedule for a given dive profile are dependent on depth and duration at depth, and instructions about rate of ascent and decompression stops (depth & duration of each stop) are found in decompression tables (e.g. US Navy diving tables) or related software used in diving computers. In the vast majority of dives, these procedures lead to safe release of inert gas from the body tissues. Rarely, due to other factors, there may be a case of DCS even after the use of the most conservative & safe decompression schedules. It is generally considered safer for someone to dive well within the limits of a decompression schedule. Increased physical load during diving, diving in very cold water, repetitive dives and flying shortly after diving are additive risk factors for DCS. Spear-fishing using SCUBA is a situation that produces cases of DCS and in some countries it is illegal.
Which activity exposes a person to the possibility of DCS? Certainly, diving activities. Exclusively? No, fighter pilots are susceptible too. Also, astronauts, people working under increased environmental pressure (caisson workers, tunnel workers, even workers responsible for repairing parts at the anterior pressurized compartment of a TBM – this machine was also used for the construction of Athens metro lines after the very first part). In USA, there are approximately 1000 DCS cases every year. In Greece, for the last few years, the Department of Hyperbaric & Diving Medicine of the Athens Naval Hospital (serving 65-70% of the country) has been treating approximately 30 emergencies annually. Clearly, actual number of DCS sufferers is underestimated.
Theoretically, whenever there is a SCUBA dive there is a possibility for DCS, regardless of the profile used (there is a saying: if you want to be absolutely sure that you won’t get DCS, then don’t dive). Don’t get scared, diving is extremely safe and DCS very rare when adhering to safety rules. It’s just that besides the inert gas load that transforms to bubbles, there are other factors known and unknown that predispose to DCS manifestation. Conclusively, when evaluating a person for possible DCS, it is important to assess symptoms and clinical findings and secondarily the diving profile (depth, duration etc).
DCS is caused by bubbles in the blood and tissues, formed by inert gas coming out of solution under the influence of reduction in ambient pressure. French physiologist Paul Bert was the first to discover this causal relation in 1878 studying caisson workers. He noticed that while staying in the pressurized environment, workers did not experience any symptoms. When pressure decreased quickly at the end of the shift, bubbles were formed throughout the body. He concluded that bubbles were responsible for the wide range of symptoms workers experienced
During the dive and stay at some depth, human tissues absorb nitrogen which is the main ingredient of the air the diver breathes. Amount of nitrogen absorbed is analogous to ambient pressure (and thus, the depth) and increases according to length of stay until a state of saturation is reached. After that, no more nitrogen is absorbed. As long as the diver stays at that depth, nothing occurs and absorbed nitrogen stays in solution in the tissues. When ambient pressure is reduced (ascent) excess nitrogen is released from the body. If sufficient amount of nitrogen has been absorbed and pressure reduction is fast, it forms bubbles in the blood and tissues, as a big quantity of gas is forced to leave the body in a short time. Increasing amount of nitrogen lead to increasing number and size of bubbles that act as small emboli, until they become capable of causing obstructive phenomena. Besides causing thrombosis, tissue ischemia/hypoxia and edema, bubbles interact with endothelial cells and initiate the inflammation cascade that increases tissue injury and result in clinical manifestation of DCS. Bubbles around or/and in the joints are responsible for the symptoms of “bends” (musculoskeletal DCS). Numbness and weakness (sensory and motor deficit) are signs of spinal cord or brain involvement (spinal cord – cerebral DCS). Bubble-induced injury to pulmonary circulation produces the “chokes” (pulmonary DCS). Massive bubble formation may lead to extensive embolization of small vessels resulting to shock.
For simplicity, only nitrogen is mentioned above as inert gas, assuming the diver undersea breathes air which is known to contain approximately 79% nitrogen & 21% oxygen. In the vast majority of dives globally, air is used as the breathing mixture. When other (artificial) gas mixtures are used, bubbles will contain the inert gas/gases used – usually helium. Although there are differences between inert gases, interaction of corresponding bubbles with human body and the pathology caused share similar features.
The widely used, Golding etal. classification, describes 2 types of DCS based on organ involved: 1. Type I – mild: joint pain (musculoskeletal form), skin involvement & lymphatic system involvement. 2. Type II – severe: CNS involvement (brain, spinal cord), cardio-respiratory (pulmonary) involvement & audio-vestibular (inner ear) involvement
It is possible for the two types to co-exist and so, pain in the elbow (type I) to be combined with motor deficit due to neurologic involvement (type II). Moreover, some cutaneous manifestations maybe the first signs of severe form of DCS.
Both types will basically need treatment in a decompression chamber. Treatment schedule and possible extra care DCS type dependant, and so is prognosis and course of disease. It is useful to consider that type II DCS involves noble and sensitive tissues carrying higher possibility of residual injury.
Unusual (or not corresponding to level of activity) fatigue – itching – joint pain – soreness of extremities or torso – dizziness – vertigo – tingling, numbness – muscle weakness, paralysis – dyspnoea/difficulty breathing
Skin discoloration/rash – motor deficit – urine retention – anxiety, confusion, agitation – memory deficit – tremor – gait disorders – ataxia – vomiting – hemoptysis – loss of consciousness – shock – convulsions – coma
Onset of symptoms
In most cases, symptoms begin within the first hour after reaching the surface and rarely, it takes more than 24 to appear. There are some differences depending on the type: more than 90% of the severe neurologic form of DCS will have manifested within the first 3 hours after surfacing – it takes 6 hours for the same proportion suffering from the mild musculoskeletal form to appear. Rarely, severe cases and usually diving at bigger depths may have onset of symptoms in-water while ascending, or at the time of surfacing. In any case, any symptom or condition appearing within hours after a dive is considered possible DCS unless proven otherwise. On the other hand, as previously mentioned, AGE produces symptoms almost exclusively within the first 10 minutes after surfacing.
Most common symptoms of DCS are joint pain, tingling and sensory abnormalities. Constitutional symptoms like generalized weakness, feeling unwell or unexplained fatigue are also common and appear first but may also be present at the end of a strenuous dive that does not produce DCS. Other symptoms include weakness of an arm or leg, or difficulty urinating. Severe DCS produces obvious, clear signs and symptoms. However, in most of these severe cases initial symptoms are mild (tingling, pain) and gradually progress within minutes to a few hours.
Symptoms may be attributed to various causes, like overexertion or a tight diving suit. It’s not unusual for someone to seek medical help only when symptoms insist for hours, or worsen. Thus, treatment schedule may need to be prolonged to achieve complete recovery or worse, lead to residual disease. For example, in the case of musculoskeletal type of DCS left untreated until symptoms subside, relapse may occur on subsequent dives, and in the long term such injuries may to lead to e.g. diver’s aseptic necrosis, called Dysbaric Osteonecrosis. This particular condition however, may present after years of uneventful diving activities.
Immediate seek for medical help and recompression therapy is of critical importance when symptoms appear in order to timely and effectively treat DCS. Delay to treatment may result to residual disease and permanent deficit, especially in the case of the severe neurological DCS.
In the minds of most people involved with diving, the term Arterial Gas Embolism is synonymous with “brain air embolism” and the latter is usually reported. The reason behind this is that the brain is injured in the majority of AGE cases, although embolisms of coronary vessels and elsewhere in the body have been reported. Moreover, as the vast majority of dives are using air as the breathing gas, it is air that enters the bloodstream after alveolar wall rupture due to pulmonary over inflation. Thus, gas emboli contain air. Clarifications: 1. Fundamentals of therapeutic schedule are the same with DCS and are described in the same “chapter” of diving medicine. 2. It may coexist with DCS, if rapid uncontrolled ascent started at the end of a deep dive with excess nitrogen load (residual nitrogen). Neuman & Bove proposed in 1990 the term type III DCS to describe AGE coexisting with DCS. 3. AGE may result from very shallow dives – does not require excess nitrogen load. 4. It may occur in dives breathing 100% Oxygen (DCS does not) – if it does, it will be “brain oxygen embolism”.
AGE is a consequence of pulmonary over inflation – pulmonary barotrauma, occurring during ascent with unequivalent (less) release of air from the lungs. Air (or other breathing mixture that fills the lungs) expands during ascent, until the point it causes rupture of the pulmonary tissues and air entry to the circulation. The resulting bubbles distribute all over the body through the bloodstream, but more often (for various reasons) the brain is affected due to respective embolism of the cerebral vessels. It is a severe form of diving incident
It is caused by breath-hold during ascent to an inexperienced, panicked or unconscious diver. Also, it may be due to rapid uncontrolled ascent (blow-up). Rarely, it may occur after normal controlled ascent when pathology of the lungs is present causing air-trapping. People known to suffer from obstructive pulmonary disease, like asthma, should be assessed extensively for diving fitness, in order to have appropriate directions, medical treatment if needed and follow-up tests.
The case of a diver surfacing unconscious or losing consciousness within first 10 minutes is a medical emergency and actions for prompt (but safely) transport to an appropriate facility with decompression chamber should be taken. In other cases, AGE may have milder course accompanied with dizziness, “tingling”, weakness but no profound paralysis, confusion and other mental dysfunctions. Action should secure treatment availability, although time for conducting careful examination is allowed.
Like in DCS, cases with mild symptoms may be incorrectly attributed to other causes and delay proper treatment, until delayed deterioration or reoccurence.
Dizziness – blurred vision – sensory disturbance – pain – disorientation – weakness
Sputum mixed with blood – paresis (motor deficit) – convulsions – unconsciousness – arrest