Chapter 5: Factors Contributing to Decompression Stress

“A number of factors contribute to your individual susceptibility to DCS and can even alter your susceptibility from day to day.”

The most significant risk factor is your exposure profile — that is, the time, depth and ascent rate of your dives. Some degree of exposure intensity is required to initiate a decompression insult, regardless of the presence of other predisposing factors.

There are a host of factors, however, that can play a role in your outcome if you experience an exposure sufficient to make DCS a possibility. Several common risk factors are outlined in this chapter.

In this chapter, you’ll learn about:

Workload
Thermal Stress
Optimal Practices
Postdive Air Travel
Medical and Physical Fitness
State of Hydration
Breathing Gas Mixture
Carbon Dioxide Level
Patent Foramen Ovale
Additional Factors

Workload

During the Dive

The timing and intensity of exercise during a dive can substantially affect your risk of DCS. A high workload during the descent and bottom phase of a dive will increase your inert gas uptake, effectively increasing the subsequent decompression stress. And exertion near the end of or immediately after a dive, particularly if it involves high joint forces, can stimulate bubble formation and increase the likelihood of bubbles passing through the lungs without being filtered out of the circulation.

You should keep your exercise intensity as low as possible during the bottom phase of a dive. Mild exercise — on the order of no more than two to three times resting effort, and with very low joint forces — is appropriate during the upper ascent and stop phases of a dive. However, any exercise, particularly exercise involving high joint forces, should be avoided as long as possible after a dive. If you are unable to avoid postdive exercise, you should keep your dive profiles very conservative to minimize your overall risk.

Thermal Stress

A diver’s thermal status has long been known to influence decompression risk. The impact is best appreciated by considering the two fundamental phases of every dive: the descent and bottom phase, when gas uptake occurs, and the ascent and stop phase, when gas elimination occurs.

Two Phases

During the descent and bottom phase of a dive, a relatively warm state results in increased inert gas uptake; this is equivalent to conducting a deeper and/or longer dive. On the other hand, if you can maintain a cool or thermoneutral state during your descent and bottom phase, you will effectively reduce your inert gas uptake. This beneficial effect will be further magnified if you exert yourself as little as possible during this phase.

During the ascent and stop phase of your dive, a relatively warm state will promote inert gas elimination, thus reducing overall decompression stress. On the other hand, a cool or cold state during this phase will reduce inert gas elimination, effectively prolonging and possibly increasing decompression stress.

The decompression hazard associated with hot water suits — which effectively establish a warm condition in both phases of a dive — was established in a study of North Sea divers conducted 30 years ago (Shields and Lee 1986). The impact of thermal status on decompression stress was even more elegantly demonstrated in a recent study conducted by the U.S. Navy (Gerth et al. 2007). The controlled conditions of a research study cannot be directly correlated with everyday diving practices, but the key message from these studies is the importance of thoughtful thermal status. Keeping neutral on your way down — certainly avoiding unnecessary overheating — and warm on your way up (approaching a cool-warm pattern) will reduce the risk of DCS in comparison to being warmer on your way down and cool on your way up (a warm-cool pattern).

Optimal Practices

The difficulty comes in reconciling optimal practices for decompression safety with divers’ desires and normal practices. It is understandable for divers to want to warm themselves before the start of a dive, in anticipation of getting colder as the dive proceeds. Historically, divers did this by pouring warm water into their wetsuits or gloves before a dive. Then some divers began to place chemical hot packs in their suits. Modern divers have even more choices available to them, due to today’s array of active heating garments suitable for use with either wetsuits or drysuits. The problem, though, remains the same: warming the body’s peripheral tissues enhances circulation and increases the delivery of inert gases, particularly if the heating is applied early in a dive, when inert gas uptake is typically at its highest level. Furthermore, both warm water and chemical hot packs lose their effectiveness over time, potentially creating the warm-cool pattern shown to generate the greatest risk of DCS. Even active heating garments — which are able to keep the diver warm throughout a dive — involve a somewhat elevated risk. As shown with hot water suits, a warm-warm pattern, while associated with less DCS than a warm-cool pattern, remains more hazardous than a cool-warm pattern. Practically, divers should maintain adequate thermal protection to ensure clear thinking and physical capability. Excessive warming during dives should be avoided.

Divers must also keep in mind that postdive warming can also influence decompression risk. Indulging in rapid postdive warming, such as by taking a hot shower or getting into a hot tub, decreases the solubility of inert gas in tissues. This will promote the formation of bubbles in local tissues, often before perfusion increases sufficiently to remove the gas. Skin symptoms, fortunately often mild and transient — not cutis marmorata — can develop with rapid warming of the skin postdive. The challenge is to get divers to prioritize safe decompression over pure comfort. If an active heating system is to be used, this means leaving it off or on its lowest setting during your descent and bottom phase, and then turning it up a modest amount during your ascent and stop phase. It also means delaying the postdive pleasure of jumping into a hot shower or hot tub. If delayed gratification is not your style, then you should use more conservative dive profiles to reduce your overall risk.

Postdive Air Travel

Modern air travel has made distant dive locations easily accessible. Flying to a destination near sea level before diving engenders virtually no risk (outside the possibility of mild dehydration or impairment due to long periods of relative immobility). Since flights end with compression, the tissues of plane passengers will be undersaturated upon landing and subsequently accumulate inert gases to re-establish equilibrium with the ambient pressure.

Flying after diving, however, increases decompression stress, since the pressure in an aircraft cabin is lower than that of ground-level atmospheric pressure. Commercial aircraft must have the capability of maintaining cabin pressure at an equivalent of 8,000 feet (2,438 meters), approximately 0.76 ATA. This does not mean that cabin pressure is always maintained at higher pressures. A recent study found that 10 percent of the commercial flights tested had cabin pressures exceeding 8,000 ft (Hampson et al. 2013). Now imagine that you have just completed a dive to 66 feet (20 meters), where you experienced an underwater pressure of 3.0 ATA. Your return to the surface, and the 1.0 ATA pressure of sea level, has already subjected your body to a threefold reduction in pressure (3.0:1.0). If you then get on a plane that has a cabin altitude of 8,000 feet, you would be subjecting yourself to a fourfold reduction (3.0:0.76) and thus to even greater decompression stress. Furthermore, should your plane suffer an unlikely but not impossible cabin depressurization, you would be subjected to a much greater decompression stress.

DAN and the Undersea and Hyperbaric Medical Society (UHMS) held a workshop in 2002 to review the available data regarding the decompression stress of flying after diving and develop consensus guidelines (Sheffield and Vann 2004). There were two important stipulations regarding the guidelines: first, adhering to them will reduce your risk but offers no guarantee that you will avoid DCS, and second, observing even longer surface intervals than the recommended minimums will reduce your DCS risk further still. Keeping in mind these caveats, these are the guidelines:

After a single no-decompression dive, a minimum preflight surface interval of 12 hours is suggested.
After multiple dives per day or multiple days of diving, a minimum preflight surface interval of 18 hours is suggested.
After dives requiring decompression stops, there was little evidence on which to base a recommendation, but a preflight surface interval substantially longer than 18 hours is considered to be prudent.

There are two further factors of note regarding the DAN-UHMS flying after diving guidelines:

They apply to flights at altitudes of between 2,000 and 8,000 feet (610 and 2,438 meters). The effect of a flight at an altitude below 2,000 feet was considered mild enough not to warrant special consideration — giving divers the flexibility to engage in modest postdive air travel, such as a short, low-altitude, inter-island flight.
They apply only to divers who have experienced no DCS symptoms. It is essential that a diver who is experiencing any symptoms consistent with DCS seek treatment prior to flying.

It is important to remember that any postdive ascent to a higher altitude — even using ground transportation — increases your decompression stress. Taking a cautious approach in such a case, by keeping your final dive profiles more conservative and/or delaying your travel to the higher altitude, is always advisable. The U.S. Navy has generated detailed tables and procedures that allow computation of exposure limits to a greater range of altitudes and with more time flexibility than the DAN-UHMS guidelines (USN 2008). It is important to appreciate, though, that these are simply mathematical constructs based on the same data used in developing the DAN-UHMS guidelines. Furthermore, they require the computation of repetitive groups for planning, something that is done with dive tables but not dive computers. Despite these limitations, they can be useful, particularly for a regular pattern of altitude diving.

Medical and Physical Fitness

Poor medical and physical fitness can compromise your safety in general and may increase your risk of DCS. Definitive data are limited, but there is no question that it is prudent to maintain a high level of physical fitness and to dive progressively more conservatively as your fitness level declines. Safe diving is possible throughout much of a normal life span, but it is important for all divers to seek regular, objective evaluation of their capabilities and to adapt their diving practices accordingly. But even for divers who have transitioned from independent to more dependent forms of diving, in which they increasingly rely on the support of others, there will ultimately be a point at which they should hang up their fins.

Physical Activity Recommendations

Adults need two types of regular activity to maintain or improve their health—aerobics and strength training. The Centers for Disease Control and Prevention’s 2008 Physical Activity Guidelines for Americans recommends at least two and a half hours a week of moderate-intensity aerobic exercise to achieve health benefits, and five hours a week to achieve additional fitness benefits. And just as important as engaging in aerobic exercise is doing muscle-strengthening activities at least two days a week.

While good health and physical fitness will not solve all problems, the foundation is an important one. An adequate physical reserve can allow a quick response to keep a small problem from becoming a serious one. Relevant scenarios can be easily imagined for almost any dive.

Regular aerobic exercise has many positive benefits. Cardiac reserve is the difference between the rate at which the heart pumps blood at rest and its maximum capacity. An increase in this reserve may make it easier to meet the physical demands of diving activity and stress. Blood values of cholesterol can improve, reducing susceptibility to heart disease. Insulin sensitivity can improve, reducing the risk of developing diabetes. While the data specific to diving are much more preliminary, there is also some evidence that higher levels of aerobic fitness may contribute to a reduced decompression stress.

Most individuals are aware that being fit can improve quality of life. A major problem, however, is that time takes a toll on us. The ease with which we maintain our fitness level in our 20s can be very different from the reality as decades pass. Aerobic fitness typically declines on an average of one percent per year after age 30. The important point is that while some decline may be unavoidable due to a gradual loss of muscle mass and a reduction in the metabolic activity of aging muscle, the rate can be slowed and the reserve range broadened by adopting healthy lifestyles as early as possible.

The physical fitness needed for diving will vary with the demands of the environment, the equipment, and the nature of the dive. The best strategy is to incorporate regular physical activity into your life to improve or preserve your capabilities, and to prolong your diving life. Do not count on diving to keep you physically fit. If done properly, it should be your relaxing time in the water. To maintain or build aerobic capacity and strength, swim, cycle, run, or do whatever other physical activities you can enjoy. The more fit you are, the longer you get to play.

Detailed physical activity recommendations can be found at cdc.gov/physicalactivity/everyone/guidelines.

State of Hydration

Dehydration gets a substantial amount of attention in the lay diving community as a risk factor for DCS, but probably more than is warranted. Sound hydration is important for good health, both for general and for diving health, but for your dive profile, thermal stress and exertion level are far more important risk factors for DCS. The undue focus on dehydration is probably a result of two issues. The first is that substantial fluid shifts can result from DCS, often creating a need for substantial fluid therapy and creating an impression that this was a cause, rather than a consequence, of the disease. The second issue is human nature — the understandable desire to assign blame for a condition that is capricious. DCS is fickle. A diver may adhere to a similar dive profile many times without incident but then develop DCS while following the very same profile. It is comforting to try and identify a single causal agent, even if this is more wishful than factual. It is important for divers to realize that a multitude of factors can subtly affect the risk on any one dive and that there is a probabilistic nature to the disease. Focusing on a range of strategies to reduce risk is more effective than trying to put all the blame on one.

Breathing Gas Mixture

The particular breathing gas mixture you use, and how you use it, can play a role in the development of DCS. A mixture known as enriched air nitrox, or simply nitrox, is increasingly popular for recreational diving. The percentage of oxygen in the mix is increased, reducing the nitrogen fraction. This means that there is less nitrogen uptake at a given depth. The decompression effect of nitrox, compared to that of air, can be calculated by computing what is known as equivalent air depth (EAD). The risk of DCS when diving with nitrox to the EAD table limits is not appreciably different than diving with air to the air table limits. It is possible to achieve a decompression safety buffer by using nitrox with air table limits, since this will reduce your inert gas uptake compared to using air.

The critical caveat with nitrox is that its higher oxygen content means that a diver breathing nitrox is at risk of developing oxygen toxicity at a shallower depth than a diver breathing air. The recommended maximum partial pressure of oxygen — partial pressure being the portion of the total gas pressure represented by a single gas — is 1.4 ATA for recreational diving. When diving with air (21 percent oxygen), this level is reached at a seawater depth of 187 feet (57 meters) — beyond the usual recreational diving limit (187 feet of seawater = 6.6 ATA * 0.21 ATA oxygen in air = 1.4 ATA). When diving with a 32 percent nitrox mixture, this level is reached at a seawater depth of 111 feet (34 meters), and with 36-percent nitrox at just 95 feet (29 meters) — depths commonly reached by recreational divers.

Carbon Dioxide Level

Elevated levels of carbon dioxide can increase the risk of DCS and lower the threshold for oxygen toxicity. Carbon dioxide is a potent vasodilator, meaning it causes the blood vessels to widen, increasing blood flow and the delivery of gases to tissues. Factors that can raise divers’ carbon dioxide levels include the increased dead space of breathing equipment (gas volume that must be moved but does not take part in gas exchange), the additional work of breathing dense gas underwater, and exercise. Using a well-designed and well-maintained breathing system, minimizing physical effort and remaining relaxed while underwater can minimize carbon dioxide increase.

Patent Foramen Ovale

Patent foramen ovale (PFO), literally, open ovale window, is a persistent opening between the left and right atria of the heart. In fetal circulation, a major opening between the atria allows blood to largely bypass the lungs that are not yet being used for gas exchange. A flap normally closes over the opening after birth and is sealed by tissue. In approximately 25 percent of the population, a partial opening remains, the PFO. The opening can range in size from functionally irrelevant to physiologically significant, the latter allowing a substantial portion of blood to be shunting from the right heart to the left heart, bypassing gas exchange and filtration in the lungs. PFOs typically produce no symptoms and individuals are unaware of their status unless they are incidentally discovered through medical tests. However, the presence of a large PFO may increase the risk of DCS in divers who develop significant bubble loads. The correlation between PFO and DCS risk is not a clear one, since the frequency of PFO in the population is fairly high while DCS is relatively rare. The safest strategy — even if you have not been diagnosed with a PFO, but most certainly if you have — is to dive in a manner calculated to keep your bubble load low; this effectively eliminates any concern that bubbles might pass through a PFO and bypass the lungs, where they would normally be filtered out.

The most commonly held consensus is that screening all divers for PFO is probably not warranted. And even in divers who have been diagnosed with a PFO, deciding whether it warrants surgical closure is a choice that each individual should consider carefully with a well-informed medical team.

Additional Factors

A host of other factors may also contribute to any given individual’s risk of DCS. Some probably play minor roles, and some potentially play important roles that have not yet been fully defined. Nutritional status, for example, plays a major role in one’s general health and often in one’s physical fitness, too. While research on the subject of nutrition and diving is limited, it is possible that it also affects decompression safety. For example, one study assessed the relationship between cholesterol levels and decompression-induced bubbles. Doppler ultrasound was used to classify the 30 subjects as either “bubble-prone” or “bubble-resistant.” Among the study’s findings was that, on average, bubble-prone subjects had higher total blood cholesterol levels than the bubble-resistant subjects (Webb et al. 1988). Additional research into this and many other areas is needed.

Sex

There is little evidence in the diving medicine literature that sex plays a role in the development of DCS. Even if women do have a slightly elevated risk, as is suggested in the aviation medicine literature, it is possible that making safer choices with regard to your diving practices can compensate for any slightly elevated physiological susceptibility.

Age

Advancing age is sometimes suggested to increase DCS risk, but it may simply reflect typical patterns of compromised physical and medical fitness.

Next: Chapter 6 – Summary and Closing Thoughts >

Chapter 6: Summary and Closing Thoughts

“Prolonging shallow stops — either safety or obligatory — is cheap insurance. Stay long, breathe easy.”

The best way to avoid DCS is to be well informed and to dive conservatively, with good control. Acknowledging and accommodating any factors that may predispose you to DCS, setting reasonable limits for yourself, and then following those limits can confer a reasonable expectation of safety.

Ensure Your Safety

Most diving is now guided by dive computers. It is important to understand, however, that simply diving within the limits of your computer’s algorithm will not ensure your safety. Dive computers provide guidance based on your time-depth profile. They are unable to consider additional conditions or individual factors that can dramatically influence your risk — and thus they must be used thoughtfully. Many dive computers allow users to make adjustments in the algorithm’s computations, with the aim of adding safety buffers. It is important that divers know the conservative measures that are available, know how to employ them and are encouraged to employ them — and still dive with caution in mind. As a general rule, multilevel dives progressing from deep to shallow, with increasingly longer steps in the shallowest stages, will likely reduce your decompression risk.

DCS is a major concern for divers because of the potential severity of the condition. But without dismissing that concern, divers must also remember that DCS is a relatively rare disease and just one of many diving-related health concerns.

Fortunately, all the measures you can take to diminish your likelihood of suffering DCS will enhance your overall diving safety as well. These are the key measures:

Take small steps that favor conservatism in a variety of areas, to substantially improve your overall likelihood of a safe outcome while diving.
Acquire enough knowledge to permit you to appreciate both the hazards of diving and likely solutions.
Attain sufficient skill, particularly with regard to buoyancy control, to ensure that all your dives can be conducted as planned.
Practice good buddy selection, so your plans and actions are compatible with those of your diving companions and with safe diving practices.
Maintain good communication with your buddies, to address problems quickly, when they are likely to be most manageable. Informed and thoughtful collective action on the part of all divers in a group is critical to ensuring a good outcome.

Next: References >

References

Ainsworth BE, Haskell WL, Herrmann SD, Meckes N, Bassett DR Jr., Tudor-Locke C, Greer JL, Vezina J, Whitt-Glover MC, Leon AS. Compendium of physical activities: a second update of codes and MET values. Med Sci Sports Exerc. 2011; 43 (8):1575–81.

Gerth WA, Ruterbusch VL, Long ET. The influence of thermal exposure on diver susceptibility to decompression sickness. NEDU Report TR 06-07. November, 2007; 70 pp.

Hampson NB, Kregenow DA, Mahoney AM, Kirtland SH, Horan KL, Holm JR, Gerbino AJ. Altitude exposures during commercial flight: a reappraisal. Aviat Space Environ Med. 2013; 84(1): 27-31.

Longphre JM, Denoble PJ, Moon RE, Vann RD, Freiberger JJ. First aid normobaric oxygen for the treatment of recreational diving injuries. Undersea Hyperb Med. 2007; 34(1): 43-9.

Pollock NW. REMO₂ — an oxygen rebreather for emergency medical applications. Alert Diver. 2004; July/Aug: 50-5.

Pollock NW, Natoli MJ. Chemical oxygen generation: evaluation of the Green Dot Systems, Inc. portable non-pressurized emOx device. Wilderness Environ Med. 2010; 21(3): 244-9.

Pollock NW, Natoli MJ. Performance characteristics of the second-generation remote emergency medical oxygen closed-circuit rebreather. Wilderness Environ Med. 2007; 18(2): 86-92.

Sheffield PJ, Vann RD, eds. Flying After Recreational Diving Workshop Proceedings. Durham, NC: Divers Alert Network, 2004.

Shields TG, Lee WB. The Incidence of Decompression Sickness Arising from Commercial Offshore Air-Diving Operations in the UK Sector of the North Sea during 1982/83. Dept of Energy and Robert Gordon’s Institute of Technology: UK, 1986.

U.S. Navy Diving Manual, Revision 6, Volume 2. Published by Direction of Commander, Naval Sea Systems Command; 2008; Washington, D.C.

Vann RD, Butler FK, Mitchell SJ, Moon RE. Decompression illness. Lancet. 2011; 377(9760): 153-64.

Webb JT, Smead KW, Jauchem JR, Barnicott PT. Blood factors and venous gas emboli: surface to 429 mmHg (8.3 psi). Undersea Biomed Res. 1988; 15(2): 107-21.

Guidelines for Diabetes and Recreational Diving

Proceedings Summary | DAN/UHMS Diabetes and Recreational Diving Workshop

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Introduction

Diabetes is a major chronic disease that affects millions of people worldwide with an increasing trend. In the United States, more than 14 percent of adults are affected. Insulin-dependent diabetes mellitus (IDDM) affects up to half a million people of all ages, out of which 150,000 are younger than 19 years old. Many people continue to be productive members of the community and pursue various interests and careers despite having diabetes. However, when it comes to diving, the diving medicine community has long maintained the conservative position that IDDM is an absolute contraindication for diving. Recognizing that a substantial number of divers are diving successfully (either openly or surreptitiously) with diabetes in spite of the restriction has led many to believe that it is time to acknowledge this fact and re-examine the position concerning diabetes in diving.

A workshop addressing the issues of diabetes and recreational diving was jointly sponsored by the Undersea and Hyperbaric Medical Society (UHMS) and Divers Alert Network (DAN) on June 19, 2005 in Las Vegas, Nevada. They brought together experts and interested parties from within and beyond the international diving community. At the workshop, participants reviewed the existing data, discussed concerns, and finally developed consensus guidelines to address diabetes and recreational diving. The issues concerning professional diving require future, separate deliberations.

The consensus guidelines were released with the clear statement that it is a set of guidelines, not rules and with an understanding that various interest groups must have the flexibility to use the guidelines as they best serve their community’s needs.

This consensus reflects a more inclusive approach and provides guidelines on how to individually evaluate fitness to dive and how to keep it safe for those who qualify. Not everybody with diabetes who wishes to dive will be able to do so; there are various conditions and states of diabetes that would make diving with the condition too risky for divers and for those diving with them.

The guidelines are designed for individual divers who are primarily responsible for their own health and safety. They should adhere to these guidelines developed to improve their protection and that of their dive partners. The guidelines aim to also assist primary physicians and diving physicians evaluating and monitoring divers with diabetes. Other divers should be aware of the guidelines too, and be mindful of special considerations when buddied or leading dives with divers with diabetes.

Who may qualify for recreational scuba diving and how should they be monitored?

Individuals with diabetes who wish to dive must undergo the same medical fitness evaluation as other candidates to ensure first, that no other exclusionary conditions (e.g., epilepsy, pulmonary disease, heart disease, etc.) exist; and second, that there are no complications of diabetes that may increase the risk of injury while diving.

They should be 18 years or older (≥16 years if in special training program), with a well-established treatment, well maintained plasma glucose level and the ability to sustain those levels efficiently in the course of changing demands of daily activities. Candidates and divers with diabetes have to undergo mandatory medical examination annually, and if over 40 years old, they should be regularly evaluated for silent cardiovascular disease.

How to dive with diabetes

Candidates who pass the fitness evaluation and master regular scuba training, must also learn and adhere to the diabetic diving protocol. They should dive only in comfortable environmental conditions, with no overhead. Their dive should not exceed the depth 30 meters of sea water (100 fsw), duration of one hour nor involve compulsory decompression stops.

Divers with diabetes should dive with a buddy who is informed of their condition and is aware of the appropriate response in the event of a hypoglycemic episode. It is recommended that the buddy does not have diabetes.

Glucose management on the day of diving

Divers with diabetes whose medication may put them at risk of hypoglycemia, should use a protocol to manage their health on the day of diving.

Divers with diabetes should carry oral glucose in a readily accessible and ingestible form at the surface and during all dives. It is strongly recommended that parenteral glucagon is available at the surface. The dive buddy or another person at the surface should be knowledgeable in the use of glucagon. If symptoms or indications of hypoglycemia are noticed underwater, the diver should surface, establish positive buoyancy, ingest glucose and leave the water. An informed buddy should be in a position to assist throughout this process. Use of an “L” signal with the thumb and index finger of either hand is recommended as a signal for suspected hypoglycemia.

Blood glucose levels should be checked at the end of every dive. Appropriate response to the measured level can be determined by the individual mindful of his or her plans for the rest of the day. It should be noted that the requirements for blood glucose status remain the same for any subsequent dive. In view of the recognized potential for late decrements in blood glucose levels following diving, it is strongly recommended that the level is checked frequently for 12-15 hours after diving.

Divers with diabetes are strongly recommended to pay particular attention to adequate hydration on days of diving. Elevated blood glucose will lead to increased diuresis. While the data are limited, there is some evidence from divers with diabetes that an increase in hematocrit observed post-dive (suggesting dehydration) can be avoided by deliberate ingestion of fluid.

Divers with diabetes should log all dives, associated diabetic interventions and results of all blood glucose level tests conducted in association with diving. This log can be used to refine future planning in relation to diving.

Guidelines for recreational diving with diabetes

Selection and Surveillance

Age ≥18 years (≥16 years if in special training program)
Delay diving after start/change in medication:
- Three months with oral hypoglycemic agents (OHA)
- One year after initiation of insulin therapy
No episodes of hypoglycemia or hyperglycemia requiring intervention from a third party for at least one year
No history of hypoglycemia unawareness
HbA1c ≤9% no more than one month prior to initial assessment and at each annual review
- values >9% indicate the need for further evaluation and possible modification of therapy
No significant secondary complications from diabetes
Physician/Diabetologist should carry out annual review and determine that diver has good understanding of disease and effect of exercise
- in consultation with an expert in diving medicine, as required
Evaluation for silent ischemia for candidates >40 years of age
- after initial evaluation, periodic surveillance for silent ischemia can be in accordance with accepted local/national guidelines for the evaluation of diabetics
Candidate documents intent to follow protocol for divers with diabetes and to cease diving and seek medical review for any adverse events during diving possibly related to diabetes

Scope of diving

Diving should be planned to avoid
- depths >100 fsw (30 msw)
- durations >60 minutes
- compulsory decompression stops
- overhead environments (e.g., cave, wreck penetration)
- situations that may exacerbate hypoglycemia (e.g., prolonged cold and arduous dives)
Dive buddy/leader informed of diver’s condition and steps to follow in case of problem
Dive buddy should not have diabetes

Glucose management on the day of diving

General self-assessment of fitness to dive
Blood glucose (BG) ≥150 mg·dL-1 (8.3 mmol·L-1), stable or rising, before entering the water
- complete a minimum of three pre-dive BG tests to evaluate trends
Sixty minutes, 30 minutes and immediately prior to diving
- alterations in dosage of OHA or insulin on evening prior or day of diving may help
Delay dive if BG
- <150 mg·dL-1 (8.3 mmol·L-1)
- >300 mg·dL-1 (16.7 mmol·L-1)
Rescue medications
- carry readily accessible oral glucose during all dives
- have parenteral glucagon available at the surface
If hypoglycemia noticed underwater, the diver should surface (with buddy), establish positive buoyancy, ingest glucose and leave the water
Check blood sugar frequently for 12-15 hours after diving
Ensure adequate hydration on days of diving
Log all dives (include BG test results and all information pertinent to diabetes management)

Pollock NW, Uguccioni DM, Dear GdeL, eds. Diabetes and recreational diving: guidelines for the future. Proceedings of the UHMS/DAN 2005 June 19 Workshop. Durham, NC: Divers Alert Network; 2005.

Diabetes & Diving Infographic

Medical Examination of Diving Fatalities

Proceedings Summary | DAN and UHMS Medical Examination of Diving Fatalities Symposium

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Introduction

The DAN/ Undersea & Hyperbaric Medical Society (UHMS) sponsored Medical Examination of Diving Fatalities Symposium was held on June 18, 2014 in St. Louis, Missouri. Although the symposium was geared towards medical examiners, many of the issues discussed in the workshop are pertinent to dive professionals.

Why It May Not Be Drowning

A large number of deaths in scuba ascribed to drowning are in fact due to other causes: specifically, sudden cardiac death (SCD), and to a lesser extent, arterial gas embolism (AGE).

Some cases which have been labeled as “immersion” or “drowning” have subsequently been found to be due to other causes. Some of the more unusual causes include inhalation of inert gas (nitrogen), air hose entanglement (entrapment), and cuttlefish attack that caused perforated tympanic membrane, leading to panic, rapid ascent and gas embolism; there were also other causes labeled drowning.

Most medical examiners would call it drowning, simply because someone was in the water.

Cardiac Conditions Are Common Causes

Sudden cardiac death (SCD): two most common causes of SCD sudden causes in adults are coronary artery disease and left ventricle hypertrophy (LVH).
Atherosclerotic heart disease: it is not the heart attack that kills the person instantly, heart attacks and subsequent damage to the myocardium kill people over a time course of hours to days. It is the dysrhythmia that kills people instantly.
You can’t see an arrhythmia on autopsy.
Left Left ventricular hypertrophy (LVH): atherosclerotic disease often co-exists with another risk factor for SCD and that LVH. If you don’t recognize it, you are missing a huge risk factor for sudden death.
LVH may play a significant role in SCD in divers due to the stress on the body from diving may precipitate arrhythmias and death.
If we know what risk factors to look for, we may be able to improve our fitness to dive screenings and potentially prevent some of these deaths.

Looking for Preventable Causes of Death

Fatality investigation: in most cases investigation usually ends with establishing proximal cause of death. Unintentional or natural cause of death investigation usually stops short of pursuing root causes.

Injury research depends on the quality of data pro vided by investigation. Legal investigation may provide answers on questions of how it happened but often not concerned with “why”. The medical examination may answer what were the cause of death and the mode of death.

Field Investigations: Preserving the Evidence

Three general patterns to a diver’s death:

First, death occurs underwater with no rescue or resuscitation attempted. Disadvantage by possible delay in between when the diver dies and is recovered – autopsy info can be altered or affected.
Second, diver has a triggered even in the water and is brought to shore or boat for attempted rescue but dies prior to transportation to medical facility. Usually provides a witness to describe what happened.
Third, diver is transported to a medical facility and survives for a few hours or days. Advantages are that imaging and lab tests may guide determination of the cause of death, however autopsy findings may be altered by the survival interval and medical intervention.

Diving conditions and diving equipment may cause or contribute to a diver’s death. Information may be lost as witnesses leave, forget equipment, or worse, equipment is returned to the family.

Field investigation is categorized into six parts:

History
Antemortem events
The environment
Body recovery
Medical care administered before death
Body and equipment recovery and documentation and preservation of evidence

Post Mortem: How-To

Very few forensic pathologists have significant experience with the investigation of fatalities involving divers who were breathing compressed gas.
Fewer than 100 combined deaths occurring in the US, Canada, and the Caribbean each year.
Pathologists should be aware of the circumstances surrounding the fatal dive mishap, but the diver’s past medical and surgical history, recent health status, and any medications taken on a regular basis and on the day of the mishap need to be known.
Cardiovascular disease in particular is a frequent factor in a diving related fatality, especially in older divers.

What Medical Examiners Need to Know About Rebreathers

Three main root causes of fatal accidents with rebreathers:
- Diver error (the most common)
- Mechanical problems
- Electronic problems
An autopsy cannot reveal hypoxia, hyperoxia, or hypercapnia (the three most common causes of rebreather fatalities). In most cases, the medical examiner cannot detect the root cause of a rebreather fatality.

Expert Panel Review of Investigation and Autopsy Findings

Guidelines identified by common trends seen in diver death:

Ensure physical fitness to dive: train for your sport and be sure that you exercise regularly and follow a healthy diet.
Use the buddy system.
Follow your training: check your gauges often, respect depth and time restrictions, and do not dive beyond your training limits.
Weight yourself properly and remember to release your weights when appropriate.
Ensure that your skill level and familiarity are appropriate for conditions.
Have your equipment serviced and maintained regularly.
Account for all divers (a physical, individual response should be received from every diver before entering/after exiting).
Avoid overhead environments unless properly trained and equipped.
Breath-hold divers should remember to use the buddy system and be aware of the dangers of shallow-water blackout.

Denoble PJ (editor). Medical Examination of Diving Fatalities Symposium Proceedings. Durham, NC, Divers Alert Network, 2015, 64 pp.

Appendix F in the Recreational Diving Fatalities Workshop Proceedings is the Autopsy Protocol for Recreational Diving Fatalities by Dr. James Caruso

Vann RD, Lang MA, eds. Recreational Diving Fatalities. Proceedings of the Divers Alert Network 2010 April 8-10 Workshop. Durham, NC: Divers Alert Network, 2011. IBSN#978-0615-54812-8.

History

This is absolutely the most important part of the evaluation of a recreational diving fatality. Ideally, one should obtain significant past medical history with a special focus on cardiovascular disease, seizure disorder, diabetes, asthma and chronic obstructive pulmonary disease. Medications taken on a regular basis as well as on the day of the dive should be recorded, and information regarding how the diver felt prior to the dive should be obtained. Any history of drug or alcohol use must also be noted.

The dive history is extremely important. If possible, the investigator should find out the diver’s experience and certification level. The most important part of the history will be the specific events related to the dive itself. The dive profile (depth, bottom time) is an essential piece of information, and if the diver was not diving alone, eyewitness accounts will be invaluable. With the near-universal use of dive computers, the computer used by the deceased diver should be interrogated, and if it has a download function all recent dives should be reviewed.

Not only will the last dive or dive series be invaluable to the investigation, much can be learned about the diver by looking at previous dives made, including frequency, depth, ascent habits and with certain computers even breathing gas usage. Written dive logs are also a valuable source of information related to the diver’s experience level and dive habits.

Questions Include:

When did the diver begin to have a problem (predive, descent, bottom, ascent, postdive)?
Did the diver ascend rapidly (a factor in air embolism and pulmonary barotrauma)?
Was there a history of entrapment, entanglement or trauma?
If resuscitation was attempted, what was done, and how did the diver respond?

External Examination and Preparation

A thorough external examination including documentation of signs of trauma or animal bites or envenomation should be carried out. Palpate the area between the clavicles and the angles of the jaw for evidence of subcutaneous emphysema. X-rays of the head, neck, thorax and abdomen should be taken to look for free air. Postmortem CT imaging can be obtained as an alternative.

Modify the initial incision over the chest to make a “tent” or “pocket” out of the soft tissue (an “I” shaped incision) and fill this area with water. A large bore needle can be inserted into the second intercostal spaces on each side; if desired, any escaping air can be captured in an inverted, water-filled, graduated cylinder for measurement and analysis. As the breast-plate is removed, note any gas escaping from vessels. An alternative test for pneumothorax consists of teasing through the intercostal muscles with a scalpel and observing the relationship between the visceral and parietal pleura as each pleural cavity is entered. If the two pleural layers are still adjacent until the pleural cavity is breached, there is no evidence of a pneumothorax. If a pneumothorax had occurred during the final dive, the lung would already be at least partially deflated and not up against the parietal pleura.

The pericardial sac can be filled with water and the chambers of the heart may be incised with a scalpel to look for any intracardiac gas. As was possible for the pleural cavities, escaping gas may be captured and analyzed, but most medical examiner offices do not have the resources for such endeavors. After the mediastinum, heart and great vessels have been examined under water for the presence of gas, the water may be evacuated and a standard autopsy may be performed.

Carefully examine the lungs for bullae, emphysematous blebs and hemorrhage.

Note any interatrial or interventricular septal defects. Carefully check for evidence of cardiovascular disease and any changes that would compromise cardiac function.

Toxicology: Obtain blood, urine, vitreous, bile, liver and stomach contents. Not all specimens need to be run, but at least look for drugs or abuse. If an electrolyte abnormality is suspected or if the decedent is a diabetic, the vitreous fluid may prove useful for analysis.

Prior to opening the skull, tie off all the vessels in the neck to prevent artifactual air from entering the intracranial vessels. Tie the vessels at the base of the brain once the skull is opened. Disregard bubbles in the superficial veins or venous sinuses. Examine the meningeal vessels and the superficial cortical vessels for the presence of gas. Carefully examine the Circle of Willis and middle cerebral arteries for bubbles.

Have an expert evaluate the dive gear. Are the cylinders empty? If not, the gas should be analyzed for purity (a little carbon monoxide goes a long way at depth). All gear should be in good working order with accurate functioning gauges.

Possible Findings

Air Embolism

Intra-arterial and intra-arteriolar air bubbles in the brain
and meningeal vessels, petechial hemorrhages in gray and
white matter, evidence of COPD or pulmonary barotrauma (pneumothorax, pneumomediastinum, subcutaneous emphysema), signs of acute right heart failure, pneumopericardium, air in coronary and retinal
arteries.

Carbon Monoxide Poisoning

Deaths due to carbon monoxide poisoning are rare in recreational diving, but they do occur. Autopsy findings are similar to carbon-monoxide-related deaths in other settings, with the classic finding of a cherry red color to the organs and blood. A carboxy-hemoglobin measurement should be obtained as routine toxicology in all diving- related deaths to exclude the contribution of contaminated breathing gas.

Decompression Sickness

Lesions in the white matter in the middle third of the spinal cord including stasis infarction, if there is a patent foramen ovale (or other potential right to left heart shunt) a paradoxical air embolism can occur due to significant venous bubbles entering the arterial circulation.

Drowning

While drowning essentially remains a diagnosis of exclusion, there are some anatomic findings that are observed with considerable frequency. The lungs usually appear hyperinflated and can even meet at the midline when the anterior chest wall is removed. Lungs are typically heavy and edematous, and pleural effusions may be present. A moderate amount of water and even some plant material may be present, not only in the airway but also in the esophagus and stomach. Dilatation of the right ventricle of the heart is commonly observed as is engorgement of the large central veins. Fluid is also often found in the sphenoid sinus.

Venomous Stings or Bites

A bite or sting on any part of the body, unexplained edema on any part of the body, evidence of anaphylaxis or other severe allergic reaction.

Interpretation

The presence of gas in any organ or vessel observed at the autopsy of someone who breathed compressed gas just prior to death is not conclusive evidence of decompression sickness or air embolism. During a dive, especially one of considerable depth or bottom time, inert gas dissolves in the tissues, and the gas will come out of solution when the body returns to atmospheric pressure. This, combined with postmortem gas production, will produce bubbles in tissue and vessels. The phenomenon has caused many experienced pathologists to erroneously conclude that a death occurred due to decompression sickness or air embolism.

Intravascular bubbles present predominantly in arteries and observed during an autopsy performed soon after the death occurred is suspicious for air embolism. The dive history will help support or refute this theory.

Gas present only in the left ventricle or if analysis shows the gas in the left ventricle has a higher oxygen content than that present on the right side would also be supportive for the occurrence of an air embolism.

Intravascular gas from decomposition or off-gassing from the dive would contain little oxygen and be made up of mostly nitrogen and carbon dioxide.

Deeper, longer dives can cause decompression sickness and significant intravascular (mostly venous) gas. Decompression sickness is rarely fatal and more commonly causes significant morbidity (illness and injury) in severe cases. Rapid ascents and pulmonary barotrauma are associated with air embolism.

Diving Fatalities Infographic

Guidelines for Flying After Diving

Proceedings Summary | DAN Flying After Diving Workshop

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Introduction

This workshop on flying after recreational diving was organized by Divers Alert Network (DAN) to bring together representatives from the recreational diving industry with experts from other diving communities. The workshop had two purposes: (a) to review the guidelines and experimental data developed since the first flying after diving workshop in 1989; and (b) to debate a consensus for new flying after recreational diving guidelines.

Previous consensus advised to wait 12 hours after a single no-stop dive, 24 hours after multi-day repetitive dive, and 48 hours after dives that required decompression stops. This was considered overly conservative. Subsequently, DAN proposed a simpler 24-hour wait after any and all recreational diving. There were objections to this on the grounds that the decompression sickness (DCS) risks of flying after diving (FAD) were too low to warrant such a long delay and would result in lost business for island diving resorts.

DAN flying after diving trials

Because little human experimental data could be found that was relevant to flying after recreational diving, DAN funded a series of trials at the Duke University Center for Hyperbaric Medicine and Environmental Physiology that were conducted from 1992-1999. Dry, resting volunteers tested nine single and repetitive dive profiles that were near the recreational diving no-decompression limits. The dives were followed by four-hour simulated flights at 8,000 feet (2,438 meters). In 802 trials, there were 40 DCS incidents during or after flight. For single no-stop dives to 60 fsw (feet of sea water; 18 msw, or meters of sea water) or deeper, there was no DCS for surface intervals of 11 hours or longer. For repetitive, no-stop dives, DCS occurred for surface intervals of less than 17 hours. The results of the study were used by the US Navy in 1999 to revise its rules for ascent to altitude following air diving. The new procedures were based on the diver’s repetitive group upon surfacing from a dive and on the expected post-dive altitude. While they were not formally tested in the laboratory prior to issue, no DCS cases have been reported to the Naval Safety Center to date. However, the number of times the new procedures have been used in the field was unknown.

Flying with DCS symptoms

The workshop reviewed recent FAD trials and available field data regarding flying after diving and flying with DCS symptoms. There were potentially important differences between field and chamber studies. Diving in the field involved immersion, exercise, and multiple days of diving, while the chamber trials occurred on a single day with dry resting divers. Thus, the chamber trials might not adequately simulate flying after diving as it actually occurs. As more divers fly with symptoms than develop symptoms during or after flight, flying with symptoms may be a greater health problem than symptoms that occur during or after flight. This is an educational issue, not a scientific issue. Divers need to be taught to seek medical advice rather than to fly if they note signs and symptoms consistent with decompression illness.

Diving nitrox and pre-breathing oxygen reduces risk of DCS in flying after diving

The benefits of oxygen pre-breathing after air diving were confirmed by trials conducted by the Special Operations Command (SOCOM). This organization was concerned with high-altitude parachute operations that might occur after air diving. Flying after diving trials were conducted with dry, resting divers who breathed air while exposed for 60 minutes at 60 fsw (18 msw). Dives were followed by simulated flights of two- or three-hour duration at an altitude of 25,000 feet (7,620 meters). It was demonstrated that this flight may cause DCS even without previous diving. When the dive was followed by a 24-hour surface interval and a three-hour flight, with divers breathing oxygen for 30 minutes immediately preceding flight, during ascent, and while at altitude there was no DCS in 23 trials. The study indicated that: (a) DCS risk was low for these flying after diving exposures, at least for dry resting divers; and (b) preflight oxygen might be an effective means for reducing DCS risk.

Considering possible impact of flying after diving rules on dive operations

One generally thinks of diving guidelines as based on medical safety, but safety is not the only yardstick humans use in establishing rules for living. Economics also has a major impact, albeit one not always articulated with comfort in the medical community. Economics was a primary issue in the 1991 discussion about the impact of DAN’s proposed 24-hour flying after diving guideline. Offshore diving operations felt they would needlessly lose business with a single 24-hour guideline. With this in mind, it was useful to approach the problem of flying after diving with an economic model in which the optimal preflight surface interval was determined by the economic interests of society as represented by divers, resorts, and insurers. Models of this nature depend on their assumptions, and no model can represent all situations, but economic modeling can differentiate between important and unimportant factors. In the model presented, for example, important factors included cost of a dive, number of days diving, aggressiveness of the dive and the DCS risk due to flying after diving. Unimportant factors included the probability of evacuation, the cost of treatment, the diver’s salary and the number of dives per day.

The consensus process

Science is a quantitative activity, while the determination
of safety is a social process that considers the probability,
severity and the costs of injury. Ultimately, the
knowledgeable representatives of society make decisions
about safety for society at large based on available
information. The workshop participants were asked to
reach consensus concerning:

a. whether flying after diving guidelines were needed for recreational diving; (b) whether the current guidelines were adequate;
b. what the longest needed guideline might be; and
c. if shorter guidelines were appropriate
for short dives.

The ensuing discussion determined that guidelines were
needed, and the evidence that had been presented
demonstrated that existing guidelines were inadequate.
After some debate it was decided that unless dive
computers were used, written guidelines for recreational
diving should be simple and unambiguous without the
need for reference to tables such as the U.S. Navy
procedures required. Three groups of divers were
proposed for consideration:

a. uncertified individuals who took part in a “resort” or introductory scuba experience;
b. certified divers who made an unlimited number of no-decompression air or nitrox dives over multiple days; and
c. technical divers who made decompression dives or used helium breathing mixes.

Consensus recommendations for flying after diving

A minimum of 12-hour surface interval was recommended for the single no-decompression dive.
A minimum of 18-hour surface interval for multi-day repetitive diving.
Substantially longer than 18 hours after diving involving compulsory decompression, or using heliox and trimix.

Limitations

It was stressed that as the experimental trials described in the workshop had been conducted in a dry hyperbaric chamber with resting volunteers, longer guidelines might be needed for divers who were immersed and exercising. The effects of exercise and immersion on preflight surface intervals were seen to require experimental study. Additional studies were conducted since and the results will be published soon.

Vann RD. Executive Summary. In: Flying After Diving Workshop. Vann RD, ed. 2004. Durham: Divers Alert Network. ISBN 0-9673066-4-7. 16-19.

Flying After Diving Infographic

Guidelines for Patent Foramen Ovale and Diving

Proceedings Summary | DAN/UHMS PFO and Fitness to Dive Workshop

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Introduction

Prior to birth, oxygenated blood flows from the mother through the placenta to the heart of the fetus via the opening in the wall separating the left and right atrium (foramen ovale) into the fetal circulation. The foramen ovale has a “trap door” feature which opens due to the pressure of blood flow from the mother’s placenta entering the right atrium, and lets the blood pass to the left atrium. At birth, the lungs expand and the pressure in the left atrium increases and “slams shut” the foramen ovale. Shortly after birth the “door” fuses together, but in about 27 percent of people, it fails to fuse completely and results in a patent foramen ovale (PFO) also called persistent foramen ovale.

In people with PFO, if the pressure in the right atrium rises above the pressure in the left atrium, blood can flow from the right to the left atrium. The direct flow of blood from the right to the left atrium which bypasses the lungs is called right-to-left shunt (RLS). The RLS is known to let blood clots pass to the arterial side which can cause a stroke (brain trombo-embolism). Similarly, the PFO in divers may let gas bubbles from the venous blood — venous gas emboli (VGE) — pass the arterial side and cause decompression sickness.

Epidemiological studies have shown an association between PFO and certain types of neurological and cutaneous decompression sickness (DCS). The DCS risk in recreational divers has been reported at 3.6 cases per 10,000 dives, with 0.84 cases of neurological DCS per 10,000 dives and four-fold increase in risk with PFO. The overall risk of neurological DCS is low, even in the presence of a PFO. However, for some individuals, PFO seems to be a greater risk than predicted. Guidelines for PFO testing are aimed at identifying such individuals and managing their DCS risk.

The following guidelines were developed from the joint position statement on PFO and diving published by the South Pacific Underwater Medicine Society (SPUMS) the United Kingdom Sports Diving (UKSDMC), and the DAN sponsored workshop held in conjunction with the UHMS Annual Scientific Meeting in Montreal, Canada, June 2015.

Who Should Be Tested for PFO?

Routine screening for PFO at the time of dive medical fitness assessment (either initial or periodic) is not indicated. Consideration should be given to testing for PFO when there is a history of more than one episode of decompression sickness (DCS) with cerebral, spinal, vestibulocochlear or cutaneous manifestations.

Non-cutaneous manifestations of “mild DCI” as defined in the Remote DCI Workshop Proceedings [Consensus Statements, In: Management of Mild or Marginal Decompression Illness in Remote Locations, Workshop Proceedings (May 24-25, 2004). Mitchell SJ, Doolette DJ, Wachholz CJ, Vann RD, Eds. Divers Alert Network, Durham, NC, 2005, pp. 6-9.] are not indications for PFO investigation. Headache as an isolated symptom after diving is not an indication for PFO investigation.

PFO Testing and Evaluation Recommendations

PFO Testing

Testing is undertaken by centers well practiced in the technique.
The testing must include bubble contrast, ideally combined with trans-thoracic echocardiogram (TTE). Use of two-dimensional and color-flow echo cardiography without bubble contrast is not adequate.
The testing must include the use of provocation maneuvers to promote right-to-left shunt including Valsalva release or sniffing as described in the supporting references (both undertaken when the right atrium is densely opacified by bubble contrast).

What Does a Positive Test Mean?

A spontaneous shunt without provocation or a large, provoked shunt following diving when venous gas emboli are present is recognized as a risk factor for those forms of DCS with cerebral, spinal, vestibulocochlear or cutaneous manifestations.
Smaller shunts are associated with a lower but poorly defined risk of DCS. The significance of minor degrees of shunting needs to be interpreted in the clinical setting that led to testing.
Detection of a PFO after an episode of DCS does not guarantee that the PFO contributed to causation.

What Are the Options for Divers to Test Positive?

Following a diagnosis of PFO considered likely to be associated with increased DCS risk, the diver may consider the following options in consultation with a diving physician:

Stop diving.

Dive more conservatively. There are various strategies that might be employed to reduce the risk of significant venous bubble formation after diving, or the subsequent right-to-left shunting of such bubbles across a PFO. The appropriateness of this approach, and the strategies chosen, need to be considered on an individual basis, and in discussion with a diving medicine expert. Examples include: reducing dive times to well inside accepted no-stop limits; performing only one dive per day; use of nitrox with air dive planning tools; intentional lengthening of a safety stop or decompression time at shallow stops; avoidance of heavy exercise and unnecessary lifting or straining for at least three hours after diving.

Close the PFO. It is emphasized, however, that closing a PFO after an episode of DCS cannot be considered to provide assurance that DCS will not occur again. The options outlined above require careful consideration of the risks and benefits and the clinical setting that led to screening.

When Can Divers Who Undergo Closure Return to Diving?

Following closure of a PFO and before returning to diving, the diver requires a repeat bubble contrast echocardiogram demonstrating shunt closure, a minimum of three months after the closure. Diving should not be resumed until satisfactory closure of the PFO is confirmed, and the diver has ceased potent antiplatelet medication (aspirin is acceptable).

CAUTION
Venous bubbles can also enter the systemic circulation through intrapulmonary shunts, although the role of this pathway in the pathogenesis of decompression sickness is not as well established as PFO. These shunts are normally closed at rest. They tend to open with exercise, hypoxia and beta adrenergic stimulation, and close with hyperoxia. It is therefore plausible that exercise, hypoxia and adrenergic stimulation after a dive could precipitate decompression sickness when it might not otherwise have occurred, while supplemental oxygen is likely to minimize this effect.

Facts About Divers With PFO

Divers with PFO have 2.5 times greater overall risk of DCS than divers without a PFO and four times greater risk of neurological DCS. However, the absolute incidence of neurological DCS in divers with PFO is estimated at 4.7 DCS cases per 10,000 dives.
A major study at the Mayo Clinic by Dr. Hagen and colleagues determined there is a large prevalence of PFO in young people, however it declines and levels off at approximately 27 percent. They also found that in each of the decade intervals, there is no difference in prevalence of PFOs between men and women.
Four studies were compared, determining the prevalence of RLS or large PFO in divers with spinal DCI is 44 percent compared to 14.2 percent in controls, those without prevalence of RLS or large PFO.
Half of the divers in the studies with RLS related DCI have a PFO that is a centimeter in diameter or larger, therefore the greatest risk of DCI is in those with the largest PFOs (six percent), not all divers with a PFO.
Cerebral, spinal, cutaneous and inner ear DCS have been associated with PFO, however the link between PFO and cutaneous and inner ear DCS is the strongest. In approximately 74 percent of cases present with isolate inner ear symptoms (no other symptoms of hyperbaric related issues), 80 percent of the cases had a large spontaneously shunting PFO.
There are factors necessary for PFO to contribute to DCS: you need to have a large PFO; venous gas emboli must form; bubble must cross the PFO (provocative factor to open PFO needed) to arterial circulation; and the bubbles must reach a target tissue while it is still supersaturated and vulnerable.

Denoble PJ, Holm JR, eds. Patent Foramen Ovale and Fitness to Dive Consensus Workshop Proceedings. Durham, NC, Divers Alert Network, 2015, 146 pp.

Patent Foramen Ovale (PFO) Infographic

Chapter 2: Risk Factors for Cardiovascular Disease

“Coronary heart disease is a leading cause of morbidity and mortality among adults in both North America and Europe.”

It behooves divers to be aware of the risk factors for cardiovascular disease, especially atherosclerosis, and of specific measures they can take to mitigate them. Atherosclerosis — popularly known as “hardening of the arteries” — is the most common affliction of the heart. Its prevalence increases with age, and it causes premature death in many people. Indeed, it is often assumed to be associated with normal aging. However, the disorder can be prevented — or at least slowed down — and a physically active lifestyle extended well into older age.

In this chapter, you’ll learn about:

Overview of Cardiovascular Risk Factors
Hypertension
Hyperlipidemia
Overweight and Obesity
Metabolic Syndrome

Overview of Cardiovascular Risk Factors

The most common manifestations of acquired (rather than congenital) cardiovascular disease are coronary heart disease, stroke and peripheral artery disease. Coronary heart disease is a leading cause of morbidity and mortality among adults in both North America and Europe.

The likelihood that a given individual will acquire cardiovascular disease and suffer a life-threatening cardiovascular event depends on many risk factors. Some risk factors — such as family history, gender, ethnicity and age — cannot be changed. Other risk factors are modifiable — including some involuntary health conditions and some lifestyle-related factors. Involuntary conditions such as high blood pressure, high cholesterol and diabetes can be treated with medication as well as with diet and lifestyle adjustments. Lifestyle-related risk factors include tobacco use, an unhealthy diet, physical inactivity and excessive alcohol consumption — all of which can be voluntarily changed.

It is important to understand that having any of these risk factors does not mean that you will definitely develop cardiovascular disease. However, the more risk factors you have, the greater is the likelihood that you will develop cardiovascular disease — unless you control your involuntary health conditions and adopt a healthy lifestyle.

The following percentages of deaths caused by cardiovascular disease can be attributed to these specific risk factors:

High blood pressure: 13%
Tobacco use: 9%
High blood sugar: 6%
Physical inactivity: 6%
Overweight and obesity: 5%

Hypertension

Hypertension, or high blood pressure, is a common medical condition in the general population as well as among divers. Blood pressure is a measure of the force with which blood pushes outward on the arterial walls. A blood-pressure reading is a ratio of two numbers. The top number is the systolic pressure, when your heart is beating, and the bottom number is the diastolic pressure, when your heart is resting between beats. The unit of measurement for a blood-pressure reading is millimeters of mercury, which is abbreviated as “mmHg”; a normal reading is 120/80 mmHg, often referred to as “120 over 80.”

The criteria for a diagnosis of hypertension vary slightly from country to country and even from one reference to another. The table below shows the most common criteria used in the United States.

Statistics

78 million American adults (or 31% — almost 1 in 3) have hypertension.
69% of those who have a first heart attack, 77% of those who have a first stroke, and 74% of those with chronic heart failure have hypertension; it is also a major risk factor for kidney disease.
348,000 American deaths in 2009 were attributed, as either a primary or contributing cause, to hypertension.
$47.5 billion annually is spent on direct medical expenses related to hypertension.
$3.5 billion annually is lost in productivity due to hypertension.
Only 47% (less than half) of those with hypertension have the condition under control.
30% of American adults have prehypertension.

Sources: U.S. Centers for Disease Control and Prevention; and American Heart Association

Two kinds of complications face a person with hypertension: short term and long term. Short-term complications generally result from extremely high blood pressure; the most significant is the risk of a stroke (also called a “cerebrovascular accident”) due to the rupture of a blood vessel in the brain. Long-term detrimental effects are more common; they include coronary artery disease, kidney disease, congestive heart failure, eye problems and cerebrovascular disease.

Mild hypertension can often be controlled with diet and exercise; however, medication may be necessary to keep blood pressure within tolerable limits. Many classes of drugs are used to treat hypertension, and they have varying side effects. Some individuals must change medications after one drug appears to be or becomes ineffective. Others might need to take more than one drug at a time to keep their blood pressure under control.

A class of antihypertensive drugs known as beta blockers may cause a decrease in maximum exercise tolerance and may also have some effect on the airways. These side effects normally pose no problem for the average diver. Another class of antihypertensives, known as angiotensin-converting enzyme (ACE) inhibitors, may be preferred for divers, though a persistent cough is a possible side effect of ACE inhibitors. Calcium channel blockers are another choice, but a potential side effect of these drugs is lightheadedness upon going from a sitting or supine to a standing position.

Diuretics — drugs that promote the production of urine — are also frequently used to treat hypertension. Their use requires careful attention to maintaining adequate hydration and to monitoring electrolyte levels in the blood.

Effect on Diving

As long as an individual’s blood pressure is under control, the main concerns regarding fitness to dive are side effects of any medication(s) and evidence of damage to the major organs. Most antihypertensive drugs are compatible with diving as long as side effects are minimal and the diver’s performance in the water is not significantly compromised. In addition, a diver with long-standing hypertension should be monitored for evidence of associated damage to the heart and kidneys.

Divers who demonstrate adequate control of their blood pressure and who show no significant decrease in their performance in the water due to drug side effects should be able to dive safely. However, it is important that such divers have regular physical examinations, including screening for long-term consequences of hypertension, such as coronary artery disease.

Hyperlipidemia

Cholesterol — a soft, waxy substance — is one of the lipids found in the blood and, indeed, in all the cells of the body. Important to the healthy functioning of our bodies, cholesterol is a part of our cells’ membranes and is used in the production of hormones.

The cholesterol in the human body may originate from foods rich in cholesterol — such as meat, eggs and diary products — or it can be made internally by our bodies. The body can also produce cholesterol from foods that do not themselves contain cholesterol but that do contain saturated fat — such as palm oil and coconut oil — or from trans fats — such as fried food in restaurants and commercial cakes or cookies. Cholesterol by itself does not dissolve in blood; it has to be combined with proteins to form soluble lipoprotein particles. Lipoproteins come in two forms: low-density lipoprotein (LDL) and high-density lipoprotein (HDL).

LDL is considered “bad cholesterol” because too much of it leads to a narrowing and stiffening of the arteries due to a buildup of cholesterol, which accumulate in deposits called “plaques” on the arteries’ inner walls. This condition is called atherosclerosis. It contributes to hypertension and causes peripheral artery disease, coronary artery disease, heart attack and stroke — as well as erectile dysfunction in men.

In contrast, HDL cholesterol is considered “good cholesterol” because it reduces the risk of cardiovascular disease by transporting cholesterol away from the bloodstream and back to the liver, which facilitates its removal from the body. HDL thus helps to prevent the buildup of cholesterol plaques on the walls of the arteries. An individual’s HDL cholesterol level is to some extent a factor of one’s genetic makeup. But HDL levels can be lowered by type 2 diabetes; certain drugs, such as beta blockers and anabolic steroids; smoking; being overweight; and being sedentary. On the other hand, estrogen, a female hormone, raises HDL levels, partially explaining why cardiovascular disease is less prevalent in premenopausal women.

Triglycerides are another factor in hyperlipidemia. Triglyceride is the most common type of fat in the body. Normal triglyceride levels vary by age and sex. High triglyceride levels combined with high levels of LDL cholesterol increase one’s risk of cardiovascular disease.

Your cholesterol level is a composite measure of all these lipids, in either milligrams per deciliter of blood (mg/dL) or millimoles per liter of blood (mmol/L).

Many American experts recommend the following cholesterol levels:

Total cholesterol: 200 mg/dL (5.2 mmol/L)
LDL cholesterol: from below 70 mg/dL (1.8 mmol/L) to 129 mg/dL (3.3 mmol/L), depending on your health status
HDL cholesterol: above 60 mg/dL (1.6 mmol/L)
Triglycerides: below 150 mg/dL (3.9 mmol/L)

Source: American Heart Association

The American Heart Association recommends that all adults age 20 and older have their cholesterol and other risk factors for hyperlipidemia checked every four to six years and also work with their health-care providers to determine their risk for cardiovascular disease and stroke.

Overweight and Obesity

The terms overweight and obesity refer to a body weight in relation to height that is greater than is considered healthy; both conditions often (but not necessarily) result in a higher proportion of body fat, known as adipose tissue, compared with lean muscle mass. Overweight is applied to those with a somewhat elevated weight, and obesity to those who are extremely overweight.

Statistics

69% of adult Americans (more than two-thirds) are either overweight or obese.
Adult obesity rates have more than doubled in just over 30 years, from 15% in 1976–1980 to 36% percent in 2009–2010.
10 years ago, the obesity rate was significantly higher among women than men; currently, the rates are essentially the same — within a few decimal places of 36% for both men and women.

Body mass index (BMI) is a common way of expressing the ratio between weight and height. The following equations are used to calculate BMI:

BMI is an important measure for understanding population trends, but it does have some limitations, as follows:

It may overestimate the proportion of body fat in athletes and others with a muscular build.
It may underestimate the proportion of body fat in older persons and others who have lost muscle mass.

Accordingly, BMI is just one of many factors that should be considered in evaluating whether an individual is at a healthy weight — along with waist size, waist-to-hip ratio and a measurement known as “skin-fold thickness.”

Metabolic Syndrome

Metabolic syndrome is a disorder that affects how the body uses and stores energy. According to the American Heart Association, a diagnosis of metabolic syndrome requires the presence of three or more of these conditions:

Abdominal obesity — defined as a waist circumference of 40 inches (102 centimeters) or above for men and 35 inches (89 centimeters) or above for women).
A triglyceride level equal to or greater than 150 mg/dL (3.9 mmol/L).
An HDL cholesterol level below 40 mg/dL (1.0 mmol/L) for men and below 50 mg/dL (1.3 mmol/L) for women.
A blood pressure equal to or greater than 130/85 mmHg or the use of medication for hypertension.
A fasting blood glucose level equal to or greater than 100 mg/dL (5.6 mmol/L) or the use of medication for hyperglycemia.

Metabolic syndrome is associated with an elevated risk of cardiovascular disease. Other disorders associated with metabolic syndrome include endothelial dysfunction and chronic low-grade inflammation.

Measuring the circumference of your waist to detect abdominal obesity, meaning more fat is at your waist than at your hips, is a good start in assessing whether you may have metabolic syndrome. This is important because abdominal obesity represents a higher risk for heart disease and type 2 diabetes, and the risk increases progressively as waist size increases beyond the dimensions noted above. The implications of these factors are shown in the chart below.

Next: Chapter 3 – Structural Anomalies >

Chapter 3: Structural Anomalies of the Heart

“Divers who suffer decompression sickness have a patent foramen ovale (PFO) prevalence twice that of the population in general.”

Having healthy heart valves is essential if your heart is to properly pump and circulate blood throughout your body. Some people are born with structural anomalies in their heart valves or in the walls. Many such disorders are diagnosed early in life and corrected, restoring the affected individuals’ exercise capacity and enabling them to dive safely. However, some inborn structural disorders, like a condition known as patent foramen ovale, may not become obvious until after an affected individual has taken up diving — and may result in an increased risk of certain diving injuries. In addition, some people are impacted later in life by acquired valvular damage that may affect their fitness to dive.

In this chapter, you learn about:

Valvular Disorders
Mitral Valve Prolapse
Patent Foramen Ovale

Overview of Valvular Disorders

The heart has four main valves that facilitate the pumping activity of the heart:

The tricuspid valve, between the right atrium and the right ventricle.
The pulmonary valve, between the right ventricle and the pulmonary artery.
The mitral valve, between the left atrium and the left ventricle.
The aortic valve, between the left ventricle and the aorta.

Each valve consists of a set of flaps (also called “leaflets” or “cusps”) that open and close to enable blood to flow in the correct direction. The function of the valves may be compromised by either congenital or acquired abnormalities. Damage to the valves can occur due to infection, rheumatic fever or aging. For example, the opening in a valve may narrow (a condition known as “stenosis”), meaning the heart has to work harder to get blood through the opening; this generates higher pressure within the heart and eventually causes the cardiac muscle to overdevelop. Another common valvular problem is incomplete closure, which allows the blood to flow backward through the valve (a condition known as “regurgitation”); this overloads the heart with blood, eventually resulting in enlargement (or “dilatation”) of the heart’s cavities.

The two most common valvular disorders in older adults are aortic stenosis and mitral regurgitation. The symptoms of valvular disorders vary depending on which valve is affected as well as on the type and severity of the change. Mild changes may cause no symptoms; a heart murmur — detected when the heart is examined with a stethoscope — is often the first sign of valve damage. In aortic stenosis, however, exertion can cause chest pain (known as “angina”) or a feeling of tightness in the chest, shortness of breath, fainting or heart palpitations. Sudden death in otherwise healthy athletes is sometimes caused by aortic stenosis. Regurgitation can also cause detectable symptoms, such as shortness of breath or wheezing when lying down; these complaints may be intensified by exercise, increased resistance to breathing and immersion.

Treatment for valvular disorders generally involves surgery. Defective valves may be either repaired or replaced by prosthetic valves.

Preventing valvular damage is, of course, the best approach. Routine physical exams may uncover evidence of early valvular disease. In such cases, close, regular medical surveillance is advised to identify, and hopefully slow, progression of the damage.

Effect on Diving

Significant valvular anomalies may preclude diving until they can be corrected. Even after corrective surgery, there must be an assessment of such factors as exercise capacity, the presence of any residual regurgitation and the need for anticoagulation. Such an assessment should include a detailed examination of the heart and of the individual’s ability to exercise at a level consistent with diving, without evidence of ischemia, wheezing, cardiac dysfunction or a problem known as “right-to-left shunting.”

Mitral Valve Prolapse

Mitral valve prolapse (MVP) may also be referred to as “click-murmur syndrome” or “floppy-valve syndrome.” It is a common condition, especially in women. The problem arises as a result of excess tissue and loose connective tissue in the heart’s mitral valve, so that part of the valve protrudes down into the left ventricle during each contraction of the heart.

An individual with MVP may have absolutely no symptoms or may exhibit symptoms ranging from occasional palpitations or an unusual feeling in the chest when the heart beats, to chest pain or a myocardial infarction (or heart attack). MVP is also associated with a slightly increased risk of small strokes (known as “transient ischemic attacks”) or a transient loss of consciousness.

Beta blockers — drugs commonly used to treat high blood pressure — are occasionally prescribed for mitral valve prolapse. They often cause a drop in maximum exercise capacity and may also affect the airways. These side effects normally pose no problem for the average diver, but they may be significant in emergency situations.

Effect on Diving

Frequently, MVP results in no changes in blood flow that would prevent an individual from diving safely. A diver with MVP who has no symptoms (that is, no chest pain, alteration in consciousness, palpitations or abnormal heartbeats) and who takes no medication for the problem should be able to safely participate in diving. But anyone with MVP who exhibits an abnormal cardiac rhythm, which can produce palpitations, should not dive unless the palpitations can be controlled with a low dose of antiarrhythmic medication.

Patent Foramen Ovale

Patent foramen ovale (PFO) is a fairly common, congenital, generally benign hole between the heart’s left and right atria (see illustration).

While a fetus is developing in utero, the wall separating the left and right atria of the heart develops from the septum primum, which grows up, and septum secundum, which grows down. The septa overlap, creating a sort of trap door (known as the “foramen ovale”), which allows oxygenated blood from the mother’s placenta that has entered the fetus’ right atrium to pass through to its left atrium. At birth, the baby’s lungs expand, and the resulting pressure in the left atrium closes the foramen ovale. Typically, shortly after birth, this former opening fuses shut — but in about 27 percent of babies, it fails to fuse completely and results in a PFO.

A PFO often causes no symptoms, and most people who have one are never aware of the fact. PFO is diagnosed by injecting a small amount of air into a vein and observing its passage through the heart using echocardiography. There are two methods of echocardiography. Transthoracic echocardiography (TTE) is easy and noninvasive — it involves simply placing an ultrasound probe on the outer wall of chest — but it detects a PFO in only 10 percent to 18 percent of the population — about half of those who probably have one. Transesophageal echocardiography (TEE) — which involves local anesthesia and intravenous sedation, so the probe can be passed into the esophagus — detects a PFO in 18 percent to 33 percent of the population. However, even though TEE is more sensitive than TTE, there are still many false-negative results with both techniques; a properly conducted TTE may in fact be more reliable than a TEE.

One of the most common treatments for PFO is a procedure called transcatheter closure; it involves threading a catheter through the groin and up the femoral vein into the heart, where a device called an occluder is implanted across the PFO. Occluders come in various shapes and forms, but most act like a double umbrella that opens on each side of the atrial wall and seals the hole. With time, tissue grows over the occluder and completely covers its surface. The implantation is performed under local anesthesia and intravenous sedation, and the patient remains conscious. It takes less than an hour and can be performed on an outpatient or one-night-stay basis. Most patients can return to their normal activities in two days, but they must take anticoagulant and/or antiplatelet drugs for three to six months. Other postoperative restrictions include no elective dental care (such as cleanings) for three months, no contact sports for three months and no heavy lifting for one week. A diver who undergoes a transcatheter PFO closure must abstain from diving for three to six months.

No data is available on the outcome of PFO closure in divers. But the following outcomes were recorded in patients who underwent PFO closure for the prevention of stroke (note, however, that these patients have underlying medical conditions that may contribute to a greater than average risk of adverse outcomes):

Efficacy: Complete closure of the opening was achieved in 95 percent of cases and incomplete closure in 4 to 5 percent of cases; no improvement was shown in only 1 percent of cases.
Complications: Overall mortality was less than 1/10th of 1 percent (0.093 percent). The need for a follow-up operation due to an adverse event associated with the device was less than 1 percent (0.83 percent).
Serious complications: The incidence of death, stroke, infection, bleeding or blood vessel injury was 0.2 percent; of device movement or dislodgement, 0.25 percent; of clot formation on the device, 0.3 percent; of major complications in the perioperative period, 1.2 percent; and of minor midterm complications, 2.4 percent.

Effect on Diving

Divers who suffer decompression sickness (DCS) have a PFO prevalence twice that of the population in general. And in divers who exhibit neurological DCS symptoms, PFO prevalence is four times greater. The risk of DCS seems to increase with the size of the PFO. Based on these facts, it is assumed that divers with a PFO are at greater risk of DCS than those without a PFO; however, the only prospective study designed to directly measure the relative risk of DCS in divers with a PFO is still ongoing.

Next: Chapter 4 – Ischemic Heart Disease >

Beat the Squeeze: Equalize Like a Pro

DAN’s Smart Guide to Ear Equalization

The purpose of this Smart Guide is to help you understand how your ears respond to pressure and the best ways to protect them while scuba diving.

Download this guide (PDF)