By Domenic A. Sammarco, R.Ph., EMT
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 diver’s 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
Decompression sickness, also known as the ‘bends’ or Caisson’s Disease, is a function of Henry’s 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 diver’s 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 body’s 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 water’s 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 Network’s 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 don’t 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
Skin Bends
Pain
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
Cerebral Effects2-4,12
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
Pulmonary Effects
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.
Other Effects
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.
Do Nots of treating DCS:
Summary
The number of recreational divers is increasing rapidly. While many programs exist to make the sport safer, the potential for a ship’s 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.
References
Safe Travels!