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The beginning of diving activities stems from humane need and desire to explore. As a result, reports of diving experiences date back to the ancient years. Skyllias (500 BC) and even Alexander the Great (320 BC) are some of the first divers – the latter is reported as the first using diving equipment (a glass barrel).

While free (breath-hold) diving is being used for centuries practically without significant changes, autonomous (SCUBA) diving evolved greatly in the previous century, together with relevant technological advances that allowed that to happen.

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Historically, diving has served energy, construction, technology, research, military, food supply, search & rescue and recreation. In Greece, diving has been historically linked to Kalymnos and sponge diving. Nowadays, it prevails occupational (aquaculture, underwater works), research (underwater archaeology), military training and touristic activities (recreational diving, diving tourism). Diving training (diving schools) has expanded accordingly.

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Let’s take a closer look on the types of diving, on the basis of influence on the human body and physiology.

1. Free (or skin) diving: in this case, the person “travels” underwater without the use of a breathing device. This dive depends on the person’s physical status and endurance, lasting no more than a few minutes. It is also called breath-hold diving

2. Autonomous diving: in this case, a source of breathing gas is used by the person underwater. The diver has the autonomy to travel underwater using tanks of compressed gas (usually air). This way he has the ability to stay underwater as long as a couple of hours, depending on the depth and some other factors. This is what we call SCUBA diving (S.C.U.B.A.: Self-Contained Underwater Breathing Apparatus)

3. Diving when the source of breathing gas is on the surface and given to the diver through an air-line is, obviously, not autonomous. However, on the basis of human physiology and effects it has on the diver, we consider it the same type of diving

4. Submarines (and their crews) “dive” into various depths. However, pressure inside the submarine does not change, while external pressure (applied on the submarine’s hull) increases in proportion to the depth. As a result, submarine crews normally do not count as divers (unless, in the unfortunate case of damage of the pressure hull that leads to flooding and pressure increase-or during procedures for crew escape)

Diving (or Undersea) Medicine studies, treats and manages disorders resulting from autonomous diving (as well as other cases of exposure to non-diving pressure variations – caisson workers, subway construction etc). Inert gas bubbles and the resulting Decompression Illness (DCI) constitute the landmark of Diving Medicine, and in the vast majority of cases it originates from this type of diving. Rarely, breath-hold diving has been reported to lead to DCI, under certain extreme conditions, which are far from the average breath-hold diver’s performance. The basic difference is that the SCUBA diver stays and breathes underwater. For the most of the following text, the term diving will refer to autonomous diving.

Diving Medicine has evolved through the years in parallel with SCUBA diving development and nowadays, the average autonomous diver’s physical profile is very different from what it used to be a couple of decades ago. And although Decompression (hyperbaric) Chambers and use of Treatment Tables are still based on the same basic principles and philosophy, it’s the physical variability of people participating in recreational diving that makes this field of medicine increasingly interesting. Conditions that used to preclude someone from diving are now considered compatible with diving, either with limitations and precautions or not. Customization or even individualization of diving activities is now a possibility, following appropriate tests, specialist opinion and surveillance. We are aware now, of diving aspects that influence long-term health of an individual – of special interest for professional divers. Of course, health and safety first. Persons that should avoid this outstanding activity must be identified. Studying and examining conditions and symptoms that used to be answered by “problem” or “no problem” is not sufficient anymore. Appropriately informed diving training and plethora of diagnostic testing coupled with development of Diving Medicine specialization in Greece, give the ability of specialized consulting services that guide diagnostic & treatment strategy. The next step forward is augmentation of diving tourism. Presence of respective specialists is important to all the above-mentioned, as well as the very important part – prevention of diving incidents.

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Humane efforts to stay underwater have been through many stages. From the use of inflated goatskin floats and the diving bells around 1500 AD, it was in 1715 that Lethbridge invented the first personal diving “suit”: a wooden barrel fit with a glass (to allow vision) and two holes for the arms. He reported dives having autonomy of 34 minutes duration and 20 meters depth. In 1828, the Deane brothers constructed the first diving dress that had a helmet (copper) and air was supplied from a hose. The helmet was loosely attached to the suit and so the diver could only work in a full vertical position, otherwise water entered the helmet. Augustus Siebe modified that dress, fitting the helmet with a full length watertight diving suit and thus, correcting that. Siebe’s standard diving dress was used by the salvage team on the wreck of «HMS Royal George» outside Portsmouth, around 1840. Interestingly, after concluding salvage, an official commented that, of those having made frequent dives, “not a man escaped the repeated attacks of rheumatism and cold”!!!! Divers at this project were working in most instances at 20-25 MSW depth, for 6-7 hours every day. At that time, evolution and increasing use of tunnel / compressed-air working took place. During that time, with the construction of large projects and corresponding increased duration of compressed-air working, presentation and identification of Decompression Sickness became clear. It was then named “caisson disease” or “bends”. The same condition that we now call Decompression Sickness (type Ι) and, during works at «HMS Royal George» wreck, was characterized as “rheumatism”.

In 1905, US Navy designed and started using an advanced helmet (MK-V) that offered both natural protection and increased mobility to the diver. This helmet (with modifications) is still in use in many parts of the world.

The SCUBA era

The majority of diving activities worldwide today, are of the type previously described as SCUBA diving. SCUBA is an acronym for Self Contained Underwater Breathing Apparatus. The diver carries his own source of breathing gas and so, he does not rely on breath-hold, or on air provided from the surface. This form is used exclusively in recreational diving and in the vast majority of professional and scientific diving.

SCUBA dives with closed-circuit rebreathers have been performed since 1880, especially during World Wars for military use. However, the big change resulted from work of Jacques-Yves Cousteau and Emile Gagnan during WW II, when they managed to combine an advanced demand regulator for breathing with cylinders filled with compressed air and carried on the back. This way, they built the first effective and safe open-circuit SCUBA, known as Aqua-Lung (In open-circuit SCUBA, the diver inhales gas from the cylinders he carries and exhales in the water. In closed-circuit SCUBA, exhaled gas is recycled and after CO2 scrubbing is reused by the diver).

Development of Aqua-Lung was outcome of the progress that took place for over 100 years. Cousteau used his equipment successfully at 60 meters, without adversities and so, after the end of WW II, Aqualung became quickly a commercial success. It still remains the most widely used SCUBA device and it contributed remarkably to the fact that undersea world is open to anyone to explore – of course following appropriate training and fulfillment of medical criteria of fitness to dive.

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Air that we breathe consists almost completely of Oxygen (21%) and Nitrogen (79%). The composition of the diver’s breathing gas is the same when his cylinders are filled with compressed air – that’s the case with the majority of diving activities. But what changes during diving is the PRESSURE exercised on the diver, depending on the depth he is at each instance (pressure increases by 1 Atmosphere Absolut every 10 meters of sea water). Pressure change and the rate of this change is the main determinant of effects of diving on human physiology. Understanding how gases respond to pressure changes is crucial and offers the explanation for diving induced conditions. It is also the basic science behind the effective management of these conditions, as well as prevention so as to establish safe diving rules and habits. Let’s take a closer look at the peculiarities of the undersea environment, starting with the gas laws.

Pressure (symbol: P) is the ratio of force to the area over which that force is distributed. Pressure is the main environmental change on human while diving and is the sum of: a. the pressure exerted by water/sea (Hydrostatic Pressure – the weight of the water), b. the pressure exerted by earth’s atmosphere on water/sea surface (Atmospheric Pressure – the weight of atmosphere’s mass). Main units of measurement for pressure are: Atm (ATA) – Psi – mmHg – Torr – msw – fsw – bar – Pascal. Atmospheric Pressure at sea level is considered fixed, equal to 760mmHg or 1Atm. On the other hand, Hydrostatic Pressure increases in proportion to depth by 1 ATA every 10,08 meters of sea water (msw) or 33,07 feet of sea water (fsw). Simplified: 1 ATA is added every 10msw or 33fsw.

Pressure and its variations influence human physiology to such an extent that we consider undersea environment as a high-pressure (hyperbaric) environment, depending on the depth and governed by the well-known gas laws. Gases under pressure store increased energy amounts. On the other hand, small changes in the percentage proportion of gases are maximized when environmental pressure increases and resulting physiological effects vary greatly. For better understanding of the effects of pressure variations, knowledge of these laws is necessary

Ideal Gas Law or General Gas Law: It shows the relationship between pressure-volume-temperature for a fixed mass of gas. P x V = n x R x T , where </>

P = pressure,  V = volume,  n = number of moles in the gas,  R = universal gas constant,  Τ = temprature (°Κ), όπου°Κ = 273+°C.

The General Gas Law encloses the following gas laws when gas mass is constant (n and R are constant)

Boyle’s law: the volume of a given mass of gas is inversely proportional to its pressure, if the temperature remains constant

P1 xV1 = P2xV2   ή   V2 = (P1xV1) / P2

In diving practice, since every 10m of descent total pressure increases by 1 ATA, at the depth of 10m volume of gases is halved comparing to the volume at surface (V1/2). Descent from 20 to 30 meters leads to volume change from V1/3 to V1/4. It appears that greater volume changes while diving occur at the beginning of descent and the end of ascent

Charles’s law: for a gas at constant pressure, the volume is directly proportional to its absolute temperature

Ρ1/Τ1 = Ρ2/Τ2   ή   Ρ2 = Ρ1 x Τ2/Τ1.

Partial pressure of gases

In a mixture of gases, each gas has a partial pressure equal to the fraction of the particular gas times the total pressure of the gas mixture. It is the hypothetical pressure of that gas if it alone occupied the volume of the mixture at the same temperature. The total pressure of an ideal gas mixture is the sum of the partial pressures of each individual gas in the mixture

PGAS= FGASxPB    , where:

PGAS  where:

FGAS  : fraction

PB: total pressure = (D+10)/10 ,

and so, partial pressure of a gas in a breathing gas mixture, at the depth of D meters is equal to : PGAS=FGASx(D+10)/10.

Example : How much is Ο2 partial pressure (Po2) in air breathing at the depth of 30 meters?

*Fo2 = 0,21

Po2 = 0,21 x (30+10)/10 = 0,84 ATA

In conclusion, partial pressure of Ο2 and Ν2 increase when breathing air as the diving gas in proportion to the depth of diving (the same is true with any other gas present in the breathing gas eg helium in heliox). It should be emphasized that percentage proportion (fraction) of each gas doesn’t increase. Increase of surrounding pressure (depth) alone results in increase of the amount of gas getting in touch with the human body, as explained by the gas laws

Dalton’s law: the total pressure of a mixture of gases is the sum of the partial pressures of the individual gases

Pascal’s law (principle of transmission of fluid-pressure): pressure exerted anywhere in a confined incompressible fluid is transmitted equally in all directions throughout the fluid-filled spaces, such that the pressure variations remain the same. That explains why the diver’s body does not smash when going deeper. Human body (except some air-filled spaces) is a complex of vascularised, watery tissues – consists of more than 60% water

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Barotraumas

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.

Paranasal sinuses

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 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).

Oxygen toxicity

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)

General 

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).

Etiology

Cause

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

Pathogenesis

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.

Classification

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.

Symptoms

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

Signs

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.

Arterial Embolism

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.

Symptoms

Dizziness – blurred vision – sensory disturbance – pain – disorientation – weakness

Signs

Sputum mixed with blood – paresis (motor deficit) – convulsions – unconsciousness – arrest

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First Aid

As in any occasion, basic life support comes first. Unconscious diver must be safely brought to land as soon as possible and then check for signs of life. Cardiopulmonary resuscitation should be initiated in the unfortunate occasion of a comatose unresponsive diver. This a very rare occasion though.

Pure Oxygen provision is very important and should be initiated when oxygen becomes available in any case with possible DCS. High flow through a face mask is used, covering the holes with adhesive tape. Oxygen is able to slow-down DCS progression, reduce or even eliminate symptoms. Its beneficial properties include increased oxygenation of injured tissues and edema reduction.

CAUTION: Even in the case of symptoms relief with the use of oxygen at surface, treatment in a decompression chamber may be necessary. Recurrence with persisting symptoms will require prolonged treatment. It is safe practice for any incident related with diving to communicate with respective staff of the decompression chamber, in order to establish contact and receive appropriate instructions regardless of the need of transfer or not.

Fluid replacement is another necessary regimen, and this may begin onsite. A conscious diver that doesn’t vomit is able to drink water. Drinking approximately 2 liters within 2 hours is an easy rule to follow. Fluid replacement is necessary because of dehydration caused both by DCS (if present) and diving itself. If the diver is transferred to a health center or nearby hospital, fluid replacement will be accomplished intravenously (placement of iv catheter). There, if needed, other supportive measures will include urinary catheterization, medications etc in coordination with respective Diving & Hyperbaric department.

Treatment in the decompression (hyperbaric) chamber – Recompression & Hyperbaric Oxygen Therap

Recompression & hyperbaric oxygen therapy is the treatment of choice for both DCS & AGE. Recompression reduces bubbles’ size and hyperbaric oxygen leads to elimination of inert gas, normalization of tissue oxygenation and reduction of tissue edema. Evacuation of the patient-diver to the nearest hyperbaric facility should be prompt, with no delay unless required for patient’s safety (in Greece, geographical characteristics implies that necessity-other cases should be carefully monitored and treated locally awaiting for air-transfer, while others should better be immediately evacuated by road). Emergency Services (EKAB) take all the above into account when arranging a sick diver’s transport (air transport with a pressurized cabin aircraft, or if a helo is available it will fly below 300 meters or 1000 feet, transport with continuous oxygen provision). If however, there is no advice available when facing a sick diver, transport to the nearest health center is a safe and good choice. On the other hand, placing a semi-conscious diver in a car to have a 3-hour trip to the nearest decompression chamber could be very risky and should be avoided. In any case, calling the department of hyperbaric & diving medicine is beneficial in order to resolve all such issues and get appropriate instructions. The diving buddy should also be prepared to provide some info concerning the diving profile, breathing mixture, repetitive dives, time of symptoms onset, change of symptoms, medical history, diving location and telephone number.

Treatment in the decompression (hyperbaric) chamber includes recompression and depending on the case and response, gradual pressure reduction until the “depth” where 100% oxygen breathing through a specifically designed mask begins (= hyperbaric oxygen). In some cases, hyperbaric oxygen is provided promptly after compression to the desired pressure, and duration and “depth” of treatment are largely individualized. Symptoms may not resolve after the initial treatment and it’s very common for the patient to undergo further hyperbaric oxygen sessions the following days. However, the usual result is resolution of disease and associated symptoms. Emergency DCS commonly necessitates admission for medications and monitoring, not forgetting that initially, other treatment modalities may be required (urinary catheter).

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Τα μέτρα πρόληψης αφορούν την κατάδυση και το σχεδιασμό της, τον άνθρωπο – δύτη και τις δραστηριότητες πριν-κατά τη διάρκεια-μετά την κατάδυση.

Πρώτα απ’ όλα ΕΚΠΑΙΔΕΥΣΗ. Θεωρείται δεδομένο αλλά πρέπει να το επαναλαμβάνουμε και να το τονίζουμε. Για την κατάδυση υπάρχουν αρκετά ρητά, ένα εκ των οποίων “planyourdive, diveyourplan”. Ο σχεδιασμός ενός ασφαλούς προφίλ κατάδυσης χρησιμοποιώντας το πιο συντηρητικό μοντέλο δε θα περιορίσει τη χαρά και την ευχαρίστηση σε ένα δύτη αναψυχής. Καλό είναι να μένει κάποιος μακριά από τα όρια των no-Dlimits των πινάκων και προσοχή σε καταδύσεις βαθύτερες των 30 μέτρων όπου στατιστικά αυξάνουν τα ποσοστά της Νόσου. Αποφυγή των παραγόντων κινδύνου ελαττώνει τις πιθανότητες νόσησης και αυτοί είναι: βαθιές και μεγάλης διάρκειας καταδύσεις, άσκηση/κούραση κατά τη διάρκεια ή αμέσως μετά την κατάδυση, επαναληπτικές καταδύσεις. Οι γιο-γιο καταδύσεις θα πρέπει να αποφεύγονται καθώς έχουν ενοχοποιηθεί για αρτηριοποίηση φλεβικών «σιωπηλών» φυσαλίδων και εμφάνιση Νόσου σε περιπτώσεις όχι αντίστοιχα μεγάλου φορτίου Αζώτου. Το ίδιο και το ανάστροφο προφίλ σε άτομα που κάνουν επαναληπτικές καταδύσεις. Μην ξεχάσουμε πως το ψαροντούφεκο με ελεύθερη κατάδυση μετά από αυτόνομη κατάδυση μπορεί να οδηγήσει σε εκδήλωση Νόσου που δε θα εμφανιζόταν αν ο δύτης επέτρεπε, χωρίς τις αυξομειώσεις της πίεσης λόγω βάθους, την ομαλή εξάλειψη του Αζώτου από τον οργανισμό. Η προσθήκη της λεγόμενης «προληπτικής» στάσης αποσυμπίεσης σε όλες τις no-D καταδύσεις παρέχει περαιτέρω ασφάλεια – καλύτερα στα 5 μέτρα. Είναι σωστό η κατάδυση να γίνεται σε μέρα όπου έχει προηγηθεί ένας καλός ύπνος και όχι κακή χρήση αλκοόλ. Η άφθονη λήψη υγρών προ της κατάδυσης έχει δείξει πως οδηγεί σε ελαττωμένο αριθμό φυσαλίδων και αφού η κατάδυση προκαλεί σχετική αφυδάτωση, να προσέχουμε στη ζεστή μας χώρα το καλοκαίρι να μην ξεκινάμε την κατάδυσή μας αφυδατωμένοι. Γενικώς, το μπάνιο με ζεστό νερό μετά την κατάδυση καλό είναι να αποφεύγεται. Όχι άνοδος σε υψόμετρο ή πτήση μετά από κατάδυση. Ειδικά για την πτήση μετά από κατάδυση και για τις ανάγκες του καταδυτικού τουρισμού, υπάρχουν οδηγίες – ενδεικτικά, από τη DAN και ειδικός «πίνακας» στο καταδυτικό εγχειρίδιο του Αμερικάνικου Ναυτικού. Η κατάδυση να γίνεται πάντα με «ζευγάρι» και αν απέχουμε καιρό από τις καταδύσεις να γίνεται σταδιακή επανένταξη: είτε με τη μορφή αρχικά ρηχών – μικρής διάρκειας καταδύσεων, είτε με κατάδυση με εκπαιδευτή – οργανωμένη ομάδα. Το αίσθημα ασφάλειας περιορίζει την κατανάλωση αέρα και επιτρέπει την ευχαρίστηση της κατάδυσης. Και για να βάλουμε τα πράγματα στη θέση τους, η αυτόνομη κατάδυση είναι ασφαλής δραστηριότητα. Σύμφωνα με τις εκτιμήσεις της DAN, έχουμε 3 – 4 καταδυτικά προβλήματα ανά 10.000 καταδύσεις και η πλειονότητα αυτών είναι ήπιας βαρύτητας.

Όσον αφορά τον άνθρωπο – δύτη τώρα, μια πρώτη ιατρική εκτίμηση είναι καλό να γίνεται στον υποψήφιο δύτη. Αναλόγως του σκοπού της κατάδυσης για κάθε άνθρωπο, οι απαιτήσεις είναι διαφορετικές. Για τους επαγγελματίες είναι υποχρεωτική η ετήσια εξέταση και ιατρική πιστοποίηση της καταδυτικής καταλληλότητας. Ακόμα περισσότερο, για τις στρατιωτικές καταδύσεις στη χώρα μας, τα στάνταρντ είναι καλά καθορισμένα και αυστηρά ενώ το πρόγραμμα ιατρικού ελέγχου συγκεκριμένο. Μιλώντας λοιπόν για τις καταδύσεις αναψυχής, δεν υπάρχει νομική απαίτηση ιατρικής εξέτασης προ της εκπαίδευσης για τις καταδύσεις. Για κάποιον υποψήφιο αυτοδύτη, η ιατρική εκτίμηση από καταδυτικό ιατρό μπορεί να είναι η πρώτη γενική κλινική εξέταση που γίνεται από ιατρό στην ενήλικη ζωή του. Εξετάζοντας ειδικότερα τα συστήματα του οργανισμού που ενδιαφέρουν για την επαφή με την κατάδυση (ακρόαση, δυνατότητα εξίσωσης κλπ) και το ιατρικό ιστορικό – ερωτηματολόγιο, διασφαλίζεται πως δεν ξεκινά την κατάδυση με μειονέκτημα που μπορεί να φέρει κινδύνους για τον ίδιο και την καταδυτική του παρέα. Κάποιες παθήσεις μπορεί να είναι αντένδειξη για καταδύσεις και αυτό πρέπει να συζητιέται. Ακόμα και αν ένα πρόβλημα υγείας είναι υπό καλό έλεγχο στην εκτός νερού ζωή, μπορεί να δημιουργήσει κινδύνους για το δύτη. Υπάρχουν και καταστάσεις που ανακαλύπτονται τυχαία σε τσεκάπ που δεν προκαλούν συμπτώματα / δεν απαιτούν θεραπεία, αποτελούν όμως αντένδειξη για καταδύσεις. Από την άλλη πλευρά, παθήσεις που παλαιότερα αποτελούσαν απόλυτη αντένδειξη για καταδύσεις, είναι σήμερα αποδεκτές από τη διεθνή καταδυτική ιατρική κοινότητα πως επιτρέπουν στον άνθρωπο να καταδύεται με περιορισμούς και την κατάλληλη παρακολούθηση. Κάποιες παθήσεις μπορεί να μην επιτρέπουν σε κάποιον να καταδύεται για επαγγελματικούς λόγους, αλλά να είναι επιτρεπτές για καταδύσεις αναψυχής και χωρίς να σημαίνει πως διακινδυνεύει την ασφάλεια και την υγεία του. Τέλος, ιδιαιτερότητες που μπορεί να υπάρχουν σε ανθρώπους είναι καλό να αναγνωρίζονται και να δίνονται κατάλληλες κατευθύνσεις.

Παράγοντες κινδύνου που αφορούν το δύτη και αναγνωρίζονται ευρέως, είναι η παχυσαρκία (λιπώδης ιστός αποθηκεύει αλλά και αποδεσμεύει αργά και μεγάλες ποσότητες Αζώτου), η ηλικία που είναι σταθερός παράγοντας κινδύνου στις περισσότερες νοσολογικές οντότητες, το ιστορικό νόσησης από Νόσο εξ Αποσυμπίεσης (που μπορεί να κρύβει μέσα της τη ροπή του ατόμου για παράτολμες συμπεριφορές και ακραία καταδυτικά προφίλ), η αφυδάτωση, η παρουσία μεσοκολπικής επικοινωνίας και η φυσική κατάσταση. Το φύλο, σαν παράγοντας κινδύνου (οι άνδρες κινδυνεύουν περισσότερο), μπορεί να εξαλειφθεί στο μέλλον καθώς όλο και περισσότερες γυναίκες καταδύονται πια. Μια και το είπαμε, η εγκυμοσύνη αποτελεί λόγο διακοπής (προσωρινώς) των καταδύσεων, ώστε να μην παραβλαπτεί η εμβρυο-μητρική κυκλοφορία και άρα το έμβρυο. Γενικότερα, καλή υγεία και φυσική κατάσταση είναι παράγοντες που μπορεί να προστατεύσουν από συμβάματα σε μια κατάδυση. Ο δύτης δε θα πρέπει να πάσχει από κατάσταση που επηρεάζει το επίπεδο διανοητικής κατάστασης και εγρήγορσης, επιδεινώνεται από την κατάδυση ή οδηγεί σε Νόσο εξ Αποσυμπίεσης. Η λήψη φαρμάκων σε σχέση με την κατάδυση είναι ένα άλλο κεφάλαιο. Ενδιαφέρει ο λόγος για τον οποίο κάποιος παίρνει φάρμακα και αν αυτό είναι κάτι που θα προδιαθέσει σε καταδυτικό ατύχημα ή αν η κατάδυση θα επηρεάσει αρνητικά αυτό το πρόβλημα. Κάποια φάρμακα μπορεί να προδιαθέσουν σε Νόσο, ενώ κάποια άλλα μπορεί να προκαλούν συμπτώματα που μπορεί να μοιάζουν με τα πρώτα γενικά συμπτώματα της Νόσου. Δεν υπάρχει εγκεκριμένη επίσημη λίστα φαρμάκων που επιτρέπονται στην κατάδυση, όπως υπάρχει για τους χειριστές αεροσκαφών. Αυτό που είναι σημαντικό είναι το φάρμακο να μην προκαλεί προβλήματα/συμπτώματα, και σε αυτό βοηθά αν ο δύτης είναι εξοικειωμένος με το συγκεκριμένο φάρμακο. Σχετικά ασφαλή είναι τα κοινά αναλγητικά (η ασπιρίνη προτείνεται συχνά σαν «προληπτικό» μέτρο προ της κατάδυσης), τα αντιισταμινικά νεότερης γενιάς, τα τοπικώς δρώντα (κρέμες, αλοιφές), τα αντισυλληπτικά και τα αποσυμφορητικά (εφόσον δεν χρησιμοποιούνται αμέσως πριν την κατάδυση για να καταφέρει κάποιος με σοβαρή δυσκολία να εξισώσει). Κάθε καινούριο φάρμακο πάντως θα πρέπει να συζητιέται, καθώς και αυτά που λαμβάνονται χρονίως.

Σε αλλαγή της κατάστασης υγείας θα πρέπει να γίνεται συζήτηση με κάποιο ειδικό. Μετά από κάποιο χειρουργείο ή εισαγωγή σε νοσοκομείο για άλλο λόγο, θα πρέπει να παρέλθει χρόνος για να αναρρώσει ο οργανισμός και αυτό μπορεί να διαφέρει από άνθρωπο σε άνθρωπο. Το πότε θα επανέλθει κάποιος στις καταδύσεις ή αν κάποιο νέο-διαγνωσθέν θέμα υγείας αλλάζει τη δυνατότητα για κατάδυση, θα πρέπει πάντα να προβληματίζει. Επίσης, υποτροπιάζον πρόβλημα υγείας που αναγκάζει σε πολλαπλές επισκέψεις και θεραπείες κάποιον δύτη θα πρέπει να δημιουργεί προβληματισμό τόσο για τον προαναφερθέντα λόγο, όσο για το αν η κατάδυση μπορεί να σχετίζεται με αυτό, ακόμα και αν χρονικά δεν συνδέονται μεταξύ τους.

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Vasileios N. Kalentzos MD, MPH
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Συμβεβλήμενοι με τον ΕΟΠΥΥ

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Δεκτές όλες οι κάρτες

Πιστωτικές ή Χρεωστικές
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