Diving Injuries and
Diving Injuries and Decompression Sickness
Sailing and voyaging the oceans of the world is truly an adventure in itself. Sport diving has been a naturally adjunct to cruising for many years and evermore increasing. If you are the captain of a vessel, in many cases you are the designated medical officer and responsible for the health and well being of your crew and guests.
In 1975, there were an estimated 213,000 divers in the U.S., in 1987, 500,000 people became certified. It is estimated that there were as many as 2.45-3.1 million divers by 1990.1 Due to the increased interest in recreational SCUBA diving, all ships medical officers need to be aware of the spectrum of diving injuries. Divers often seek help hours after diving injuries occur and in emergency departments far from the dive location.2
There are a variety of injuries associated with scuba diving. These injuries make up a group referred to as barotrauma or trauma to the soft tissues of the body as caused by pressure. Most of these injuries are not life-threatening. Examples include: sinus squeeze, ear squeeze, reverse ear squeeze and tooth squeeze. Squeeze injuries can cause mild to severe pain and may damage the related soft tissue structures. If pain persists after the dive or blood presents after an ear or sinus squeeze, the patient should be evaluated to ensure proper treatment of the injury and prophylactic treatment of infection.
Divers may also incur bites, stings and contact irritations, as well as more common injuries like abrasions, lacerations and fractures. Bites and stings should be evaluated based on severity, and anaphylaxis should always be a concern. Many stings and irritations can be neutralized with warm water or vinegar. If present, SCUBA instructors or divemasters may be familiar with various remedies for specific envenomations. If the remedies do not contradict your local treatment protocol, heed their advice.
The two most significant and often life-threatening SCUBA-related injuries are decompression sickness (DCS) and arterial gas embolism (AGE). These injuries are often referred to as decompression illness.2,3 Although this article focuses on decompression sickness, arterial gas embolism is mentioned because it is often difficult to differentiate the two. Keep in mind, however, if you are summoned more than one hour after the dive or far from the dive site, you are most likely dealing with decompression sickness.
Significant symptoms of arterial gas embolism will be apparent within moments of surfacing from a dive. Therefore, this ailment will be seen primarily by medical officers who work near diving destinations. Decompression sickness can occur hours after a dive and range in severity from discomfort to life-threatening. Because it may occur far from a dive site, symptoms should be recognizable to all medical officers.
Arterial Gas Embolism
Arterial gas embolism is caused by an overexpansion of the lungs, which results in torn alveoli and release of air into the pulmonary capillaries.2 The air bubbles then travel through the heart and may find their way to the brain, where they cause symptoms similar to those of a stroke. AGE may present severely, causing the divers immediate collapse and death upon surfacing, or it may mimic the neurologic symptoms of decompression sickness.2,5 Some reports attribute 10%-30% of all SCUBA-related deaths to AGE.2
Though the differential diagnosis may be difficult, treatment of AGE is the same as for decompression sickness. Often, the patient suffering AGE has a history of uncontrolled ascent from his last dive. Additionally, symptoms of AGE manifest within minutes of surfacing.
Decompression sickness, also known as the bends or Caissons Disease, is a function of Henrys Law which states: The amount of gas dissolved in a liquid is proportional to the partial pressure of the gas in contact with the liquid.4,5
As a diver descends deeper, atmospheric pressure increases, allowing the blood and body tissues to absorb a greater volume of inert gas, such as nitrogen. Nitrogen is not metabolized by the body; therefore, whatever is absorbed must eventually be released from the body.4 The amount of nitrogen absorbed is determined by the depth (increasing depth=increased pressure) and duration (increased duration=increased time to absorb) of the dive.1,4 Conversely, as the diver ascends, pressure is decreased and absorbed nitrogen is released or off-gassed.4 In most cases, if safety precautions have been followed, the nitrogen will be released and cleared from the body through normal respiration. However, if the diver ascends too quickly or bottom time is too long, and the diver does not take proper precautions (such as safety stops), nitrogen can come out of absorption and form bubbles in the blood and body tissues that interfere with normal physiologic function. Even if a diver does everything correctly, the risk of developing DCS is always present. Risk factors associated with DCS include dehydration, alcohol consumption, fatigue, hypothermia and obesity.2,5
Dehydration. Dehydration results in decreased blood volume, thereby lowering the amount of blood available to absorb nitrogen and lowering the threshold DCS.5
Alcohol Consumption. Alcohol consumption prior to a dive is known to contribute to dehydration, impaired decision-making and performance, and increased heat loss.
Heavy Exercise/Fatigue. As a diver works harder, a concurrent increase occurs in the rate of circulation, thereby carrying nitrogen to body tissues at a faster rate. At the end of a dive, the divers circulation slows, decreasing the rate at which the nitrogen can be eliminated.5 It is suggested that heavy exercise (such as weight lifting, running, etc.) be avoided for four to six hours after a dive.
Age/Hypothermia/Injury/Illness. Each of these conditions affects the efficiency of circulation and can decrease the bodys effectiveness in eliminating excess nitrogen.5
Fat Tissue. Fat tissue is capable of absorbing high levels of nitrogen; however, it is unable to off-gas as quickly as other tissues and may predispose a diver to DCS.5 Additionally, the myelin sheath, which protects nerve cells, is made up of excess fatty tissue. This makes the central nervous system very susceptible to DCS.4
While most risk factors occur before or during a dive, one important factor may occur after a dive. As seen in the opening scenario, flying after diving may induce or exacerbate DCS. When a diver returns to the waters surface, the body is under normal pressure of approximately 1 atmosphere (14.7 psi at sea level). At this pressure, the body will off-gas until it reaches a point of equilibrium.6 If the ambient pressure decreases, nitrogen will come out of absorption faster. The most common causes of decreased ambient pressure are: "ascent over mountains, aircraft flight, spacecraft flights and altitude chamber flights."6 Current guidelines (based upon multiple studies) recommend a minimum 12-hour interval prior to flying after a simple single-day dive. Twenty-four hours is preferred, especially after multiday, multiple dives.5-7
Just as there are risk factors for DCS, there are factors that can decrease the risk. A diver who is in good physical condition is less likely to fall victim than one who is not. In one study using exercise-conditioned swine, the authors concluded that exercise conditioning appears to decrease the risk of neurologic DCS, regardless of other factors such as weight, age, or body fat.8 Another study suggests that "aerobically trained runners appeared to be at lower risk of venous bubbling and bends than weightlifters or sedentary subjects."
Divers Alert Networks Report on Decompression Illnesses and Fatalities 1997 yields a high percentage of divers affected by DCS to be physically fit; however, they note that this information is based on self-evaluation, and specific fitness programs are not documented.9 It stands to reason that the physically fit diver who avoids the risk factors mentioned previously and dives a conservative profile is at a significantly lower risk for decompression illness.
Signs & Symptoms of DCS
At least half of all DCS cases will occur within 90 minutes of breaking surface at the end of a dive; and 95% will occur within 48 hours. While rare, there are cases that dont present for more than 48 hours.9 Once signs and symptoms develop, they will progress over the course of a few hours. In the time it takes for symptom onset and recognition, a diver may travel far from the dive site. This illustrates the need for all medical officers to be familiar with DCS.
Type I DCS9
Pruritis (itching)If the only symptom, will usually resolve on its own.
RashRed rash patches, usually over shoulders and upper chest.5, 10, 11
Cutis marmorata (skin marbling)Usually a sign of impending worsening of DCS. This condition may be preceded by a burning sensation and itching over the shoulders and torso.4
Localized pitting edema.3
Pain may occur in joints and be exacerbated with movement. Usually, larger joints, shoulders or elbows are affected.3 Most often, the pain is steady, though it will sometimes throb. Pain may occur by itself or with other forms of DCS.4 Pain, which is present in over 75% of cases, may occur in joints and worsen with movement.5,10,11
Type II DCS9
Paralysis/hemiphlegia (paralysis affecting one side of the body)
Visual disturbancesDiplopia (double vision), tunnel vision, blurred vision, scotomas (blind spots in the field of vision)4
Vestibular disturbances (auditory problems)
Genitourinary-urinary dysfunction, pripasm (sustained, often painful erection)
Nausea & vomiting
Dysarthria (speech difficulty)
Back pain, abdominal pain12
Neurologic DCS is most often a result of effects on the spinal cord and correlates with hemorrhagic infarcts, axonal degeneration (damage to the impulse-generating region of nerve cells) and severe demyelination (damage to the protective fatty layer of nerve cells) in affected areas.2
The "chokes" or pulmonary DCS, can resemble Adult Respiratory Distress Syndrome (ARDS).2 If this occurs, it will happen within minutes of breaking surface.
Pulmonary DCS is caused by bubbles becoming trapped in pulmonary circulation, or more specifically, in the capillaries that surround the alveoli. The obstructive damage caused by such bubbles will result in pulmonary edema (causing pink frothy sputum) and fluid buildup in the alveoli. This will severely restrict gas exchange, causing irreversible hypoxia and death.
The chokes present with substernal chest pain (usually described as burning and pleuritic), cough and dyspnea.2,4 Hemoptysis and frothy sputum may also be present.12 Without immediate in-hospital treatment, prognosis is poor, and respiratory failure and shock will ensue.2,4 While rare, pulmonary DCS is considered to be remarkably severe and will most often result in death.
Also rare is inner ear DCS, causing vertigo, staggers, nausea, vomiting, deafness, tinnitus and nystagmus. This must be treated urgently, as it can cause permanent damage.4 Inner ear DCS is caused by inert gas bubbles forming in the internal auditory vascular system.2
Acute Carpal Tunnel Syndrome may also develop as a result of DCS.13
Treatment of DCS
Type I DCS: Skin and Pain Only
Type I DCS often resolves by itself; however, most physicians recommend observation for at least 24 hours to ensure symptoms do not progress.2 For this reason, all cases of suspected DCS must be evaluated. It must be stressed to these patients that they should seek immediate care. Even though the condition may be self-correcting, proper diagnosis and treatment are essential to prevent permanent damage or reoccurence.
Type II DCS: Neurologic & Cardiorespiratory
Definitive treatment for DCS of any type is recompression in a hyperbaric facility.2,4,15 Aggressive oxygen therapy is imperative and should be the most important field treatment. Divers and dive boats often carry their own oxygen, and treatment may have already begun when you arrive.
Provide 100% O2 via non-rebreather face mask for the conscious patient, or intubation and ventilation with 100% O2 for unconscious patients (Note: While some EMS systems no longer permit carrying demand valve O2 devices, Divers Alert Network recommends this device for use on conscious patients.)
Place the patient in a position of comfort if no spinal injury is suspected or airway compromise present.
Provide intravenous fluid: Ringers lactate or normal saline.
Reassure the patient.
Transport to a facility with hyperbaric capabilities. A facility with a multiplace chamber is recommended, however, it may be necessary to transport injured divers to the nearest facility for stabilization of life-threatening problems prior to transport to a hyperbaric chamber. If possible, choose a trauma center.
If medevac is utilized as the transport medium, DAN recommends maintaining cabin pressure at sea level or flying as low as possible, preferably under 1,000 feet in an unpressurized cabin (helicopter).
It is imperative to obtain the following data (to assist in evaluation and treatment at a recompression site): maximum depth dived; bottom time; any safety stops; time since reaching surface; whether the dive was single or multiple dives were done.
If there were multiple dives, the above information must be obtained for each dive, adding surface intervals between dives. (You dont have to understand the meaning of each of these numbers, but you must obtain it.)
Divers are taught to send an injured divers equipment along with the diver, so anticipate this. You may need to secure the equipment and pass it on to the hospital, or leave it with a law enforcement officer. At a minimum, take the divers computer and dive buddy. The dive buddy can usually supply critical information to the receiving facility or hyperbaric chamber staff.
When possible, contact medical control or the receiving hospital to notify them of the patients condition and your impending arrival. Always consider calling Divers Alert Network or having the receiving hospital know they can make contact. Call 919/684-8111 or collect 919/684-4DAN, state that you have a diving emergency and need to speak with the person on call. DANs experts will consult with you and/or your medical control to assist with coordination of resources and proper diagnosis and treatment of the patient.
Rapid transport to a recompression chamber is imperative. Studies have shown that increased time to recompression has a negative effect on prognosis.16
The definitive treatment for DCS is Hyperbaric Oxygen Therapy (HBO) in a pressurized chamber.14,15 It is generally accepted that the advantage to this treatment is enhanced oxygenation of ischemic tissue under pressure. Recompression shrinks bubbles and hyperoxygenation enhances the rate of inert gas elimination from the body.14 HBO can be provided in either a multiplace or monoplace chamber.
The multiplace chamber can accommodate 2-14 patients and has room for medical personnel to enter and exit the chamber without sacrificing chamber pressure. This allows for treatment of other acute problems without interrupting HBO therapy. Monoplace chambers can accommodate one patient in a supine position. Other treatment cannot take place in this chamber. Additionally, the multiplace chamber can reach pressures of up to 6 atmospheres (ATA) while the monoplace can attain only 3 ATA.14
Standard HBO therapy for divers in the United States is based on the U.S. Navy Treatment Tablesa set of clinical tables that vary in rate and pressure that a diver must undergo.
Do Nots of treating DCS:
Dont ever allow a diver to descend back to depth for the purpose of recompression.
Do not discontinue oxygen if/when symptoms subside.
Do not use IV solutions containing dextrose, especially if neurologic involvement is suspected
Do not use the head down/feet up position. (Note: You will find that many EMT and paramedic texts in print today recommend raising the injured divers feet. Divers Alert Network is the foremost authority in the field of SCUBA accidents, and their current recommendation is not to raise the legs. The head down/feet up position used to be recommended, as it was thought that bubbles could be trapped in the right atrium, thereby not making it into the general circulation. New evidence shows that this position has two disadvantages: 1) It is generally uncomfortable for the patient, and 2) it may lead to cerebral edema. Research also indicates that if bubbles are in circulation, they are not successfully trapped in the right atrium.)
The number of recreational divers is increasing rapidly. While many programs exist to make the sport safer, the potential for a ships captain to deal with cases of DCS and AGE increases.
There is a clear need for marine personnel in all areas to be aware of the signs, symptoms and treatment of diving-related injuries and decompression illness. The important thing is acquiring a basic ability to recognize DCS and AGE and provide treatment to injured divers. Initial recognition and proper treatment of an injured diver can save a life.
Dovenberger J. Recreational scuba injuries. J Fla Med Assoc 79(9):616-619, 1992.
Clenney TL, Lassen LF. Recreational scuba diving injuries. AM Fam Physician 53: 1761-1774, 1996.
Dive & Travel Medical Guide. Divers Alert Network, 1996.
Jerrard DA. Diving medicine. Emerg Med Clin North Am 10:329-338, 1992.
The Encyclopedia of Recreational Diving. Santa Ana, CA: International PADI, Inc., 1991.
Shefield, PJ. Flying after diving guidelines. Aviat Space Environ Med 61:1130-1138, 1990.
Vann RD, Denoble P, Emmerman MN, et al. Flying after diving and decompression sickness. Aviat Space Environ Med 64:801-807, 1993.
Broome JR, Dutka AJ, McNamee A. Exercising conditioning reduces the risk of neurologic decompression illness in swine. Undersea Hyperb Med 22:73-85, 1995.
Report on Decompression Illness and Diving Fatalities. Divers Alert Network, 1997.
PADI Rescue Diver Manual. Santa Ana, CA: International PADI, Inc., 1987.
PADI Divemaster Manual. Santa Ana, CA: International PADI, Inc., 1990.
Bledsoe BE, Porter RS, Shade BR. Paramedic Emergency Care, 2nd ed. Englewood Cliffs, NJ: Prentice-Hall, Inc., 1994.
Isakov AP, Broome JR, Dutka AJ. Acute carpal tunnel syndrome in a diver. Evidence of peripheral nervous system involvement in decompression illness. Ann Emerg Med 28:90-93, 1996.
Grim PS, et al. Hyperbaric oxygen therapy. JAMA 263:2216-2220, 1990.
Broome JR. Aspects of neurologic decompression illness. A review from Bethesda. J Roy Nav Med Serv 81:120-126, 1995.
Ball R. Effect of severity, time to recompression with oxygen, and re-treatment on outcome in forty-nine cases of spinal cord decompression sickness. Undersea Hyperb Med 20(2):133-145, 1993.
Domenic A. Sammarco, R.Ph., EMT
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