Scuba Diving Medical - Health

dyspnea, hypoxemia, and characteristic chest radiographic findings. All cases occurred in cold water. All scuba divers were treated with complete resolution, and three have returned to diving without further episodes. Mechanisms that would contribute to a raised capillary transmural pressure or to a reduced blood-gas barrier function or integrity are discussed. Pulmonary edema in scuba divers is multifactorial, and constitutional factors may play a role. Physicians should be aware of this potential, likely underreported, problem in scuba divers. (CHEST 2001; 120:1686-1694)

Key words: altitude sickness; diving; hypoxia; immersion; pulmonary edema; respiratory distress syndrome; swimming



Abbreviations: ECM = extracellular matrix; fsw = feet of sea water; HAPE = high-altitude pulmonary edema; msw = meters of sea water; scuba = self-contained underwater breathing apparatus

**********

Acute pulmonary edema has been described previously in swimmers and divers using a self-contained underwater breathing apparatus (scuba). (1-6) The prevalence of pulmonary edema during scuba diving and surface swimming is unknown but is probably underreported. In a survey (4) of 1,250 divers, of the 460 responders, 5 (1.1%) had a history suggestive of pulmonary edema. With > 3 million scuba divers currently in the United States alone, literally thousands of divers could be at risk for developing pulmonary edema.

Acute pulmonary edema occurs when the pulmonary capillary permeability is increased (noncardiogenic), when the pulmonary capillary hydrostatic pressure exceeds the plasma oncotic pressure (cardiogenic), or both. In swimmers and divers, an increased transalveolar pressure gradient due to a combination of factors has been implicated in the pathogenesis of the condition. The final common pathway appears to be stress failure of pulmonary capillaries manifested by leaks in the capillary endothelial layer and the alveolar epithelial layer, and sometimes the breakdown of the full thickness of the alveolar wall leading to high-permeability pulmonary edema or even frank hemorrhage. (7) The exact nature of the stress in scuba divers and immersion victims is not clear but may be due to raised pulmonary capillary pressure from systemic sympathetic discharge, the development of high negative intrathoracic pressure due to multiple factors, or as-yet undefined biochemical or adrenergic responses to conditions encountered during swimming and diving.

As in high-altitude pulmonary edema (HAPE), constitutional factors may predispose a subgroup of individuals to the development of pulmonary edema with scuba diving or water immersion. The occurrence of hypoxemia or severe acid-base abnormalities make prompt recognition and treatment important. (8)

MATERIALS AND METHODS

Information was collected on scuba divers from 1986 to 1999, who were referred to the Pacific Grove Hyperbaric Facility in Monterey, CA, the John Muir Medical Center in Walnut Creek, CA, or Doctors Medical Center in San Pablo, CA, for the evaluation of pulmonary edema that developed during diving. Data regarding patient diving history, details of incident dives, medications, medical history including prior episodes, laboratory and radiograph evaluations, treatments, and outcomes were reviewed and are summarized in Table 1.

DISCUSSION

The pathophysiologic mechanisms for the development of acute pulmonary edema in apparently otherwise healthy scuba divers are not clear. In most divers, the pulmonary edema occurs without an obvious precipitating cause, can occur in shallow or deep dives and in cold or warm water, and has been reported in swimmers. (2-4) Patients may have arterial blood gas findings of acidosis and hypoxemia, chest radiographic abnormalities, rarely have evidence of heart failure, and survivors respond completely to conventional therapy for pulmonary edema. Water aspiration may be a contributing or causative factor and should be considered.

In our series of eight patients, the only obvious factor common to all was the history of scuba diving. Other possible contributing factors included but were not limited to, poor physical conditioning, cold water exposure, immersion effects, strenuous exertion, tight-fitting wet suit, anxiety, malfunctioning regulators or other equipment, aspiration, and hypertension.

All the patients in this report were middle-aged (age range, 46 to 61 years) people of average fitness. The water temperature was 50 to 55 [degrees] F for six of the divers, in the low 80s for one, and was recorded as "cold" for one. None of the patients reported having strenuous exertion during the dive. One diver (case 5) had a wet suit that was too tight and was considerably apprehensive during her dive. There were no reports of equipment malfunction, but one diver (case 2) ran out of air on the day prior to his incident dive, had to "buddy-breathe" with his diving instructor, and complained of significant postdive fatigue that evening. The fatigue had resolved by the next morning when he developed pulmonary edema during his first scuba dive that day. Aspiration is included in the differential diagnosis of one diver (case 4) but is unlikely because she became symptomatic during ascent at about 20 feet of seawater (fsw), which was clearly before the apparent surface aspiration. Three of the eight patients had histories of hypertension, and four reported histories suggestive of asthma, which points to a possible role for these conditions.

Six of the eight divers had prior diving experience, one was a new diver, and for one experience was not documented. Interestingly, three of the patients reported histories of similar episodes on previous scuba dives. One diver (case 1) had 20 years of diving experience, had suffered a similar episode 1 week prior, and subsequently resumed diving. One diver (case 4) also had prior diving experience. One diver (case 6) was a relatively new diver and resumed scuba following this episode. The onset of symptoms occurred while at depth, during ascent, or shortly after surfacing. Pulmonary edema occurred in water as shallow as 15 fsw (4.6 m of sea water [msw]), and as deep as 110 fsw (34 msw), with an average of 54 fsw (17 msw). Depth was not reported for one diver. There was a variable time of onset as well. In five of the divers, the onset of symptoms occurred during the first dive of the day. None of the divers were current cigarette smokers, although two had a history of tobacco use.

Medical Problems in Scuba Diving

We read with great interest the Roentgenogram of the Month by Hamad et al[1] in a recent issue of CHEST. Concerning the anamnesis and the chest radiograph, we agree with the diagnosis but not with some of the explanations regarding medical problems encountered during scuba diving or any other hyperbaric exposure (hyperbaric chambers, etc). There are a number of inaccuracies in the text.

The authors mention barotrauma, decompression sickness, and nitrogen narcosis as common complications of scuba diving, going on to state that "the mechanism in all these complications is the same." Indeed, all of these phenomena may result from breathing compressed gas under water, but the mechanisms are different.[2] Barotrauma is due to a failure to equalize pressures between different compartments, or doing so at an insufficient rate, with the result that during descent there is a relative underpressure in these compartments. In this case, there is no relation to Henry's law but rather to Boyle's law. It is therefore erroneous to state that "compressed gases cause a negative pressure on the walls of the body cavities." Common complications are middle ear and sinus barotrauma. Stomach rupture due to barotrauma is a rare event, in contrast to what may be understood from the text.[3,4]

At every depth, the pressure of the air (which is the breathing mixture in most sport diving) in the lung must be equivalent to the ambient pressure. If the diver holds his breath during ascent, when the ambient pressure drops by one atmosphere for every 10 m, according to Boyle's law the lung will expand to a point of rupture, resulting in subcutaneous emphysema, pneumothorax, cerebral gas embolism, and pneumocardia, as in the presented ease. Again, there is no relation to Henry's law. The gas involved is whatever gas is breathed during the dive, and not "expanding nitrogen" as mentioned by the authors.

It is our impression that the authors have confused barotrauma with decompression sickness. In the latter, nitrogen bubbles form in the tissues and blood after a certain nitrogen load is formed in the lipid-rich tissues during the dive, and supersaturation occurs during an uncontrolled ascent due to the rapid decrease in ambient pressure. This is not the mechanism in the case described.

Finally, the US Navy protocols were not developed to prevent subcutaneous emphysema, pneumothorax, or pneumocardia, as may be understood from the text. They are designed to prevent decompression sickness, by restricting the rate of ascent and by instructing the diver to interrupt his/her ascent at certain depths for certain lengths of time. This allows a more gradual release of nitrogen into the blood and avoids supersaturation of nitrogen in the tissues, so that there is less possibility of nitrogen bubbles forming in the tissues and the blood.

Amir Abramovich, MD
Yoav Yanir, MD
Avi Shupak, MD
Israel Naval Medical Institute
Haifa, Israel
Correspondence to: Amir Abramovich, MD, Israel Naval Medical Institute, PO Box 8040, 31 080 Haifa, Israel

Letter to the Editor
CHEST, Sept, Amir Abramovich, Yoav Yanir, Avi Shupak, Abdullah Hamad, Adnan Alghadban, Laurie Ward To the Editor:

REFERENCES

[1] Hamad A, Alghadban A, Ward L. Seizure in a scuba diver. Chest 2001; 119:285-286

[2] Melamed Y, Shupak A, Bitterman H. Medical problems associated with underwater diving. N Engl J Med 1992; 326:30-35

[3] Halpern P, Sorkine P, Leykin Y, et al. Rupture of the stomach in a diving accident with attempted resuscitation: a case report. Br J Anaesth 1986; 58:1059-1061

[4] Cramer FS, Heimbach RD. Stomach rupture as a result of gastrointestinal barotrauma in a scuba diver, J Trauma 1982; 22:238-240

Medical Problems of Recreational Scuba Diving

Recreational scuba diving is defined as pleasure diving to a depth of up to 130 feet without decompression stops. Recreational scuba diving has become very popular in the past 20 years. There are almost 9 million certified divers in the United States alone.

Several scuba certifying agencies offer training for divers, from beginners to experts. Three of these agencies are the Professional Association of Diving Instructors (PADI), the National Association of Underwater Instructors (NAUI) and Scuba Schools International (SSI). Basic classes involve classroom instruction and training in a pool and in open water settings. The most popular courses last from 4 to 8 weeks.

What are the common medical problems of scuba diving?

The most common medical problems are simple "squeezes." These can affect your middle ear or face mask during descent. Squeezes cause pain in your ears. The pain is caused by the difference in pressure between the air spaces of your ears and mask, and higher water pressure as you go deeper in the water. Squeezes that affect the inner ear or sinuses are less common.

Cuts, scrapes and other injuries to the arms and legs can be caused by contact with fish and other marine animals, certain species of coral and hazards such as exposed sharp metal on wrecks or fishing line. Can I be seriously hurt while scuba diving?

Yes. The most dangerous medical problems are barotrauma to the lungs and decompression sickness, also called "the bends."

Barotrauma occurs when you are rising to the surface of the water (ascent) and gas inside the lungs expands, hurting surrounding body tissues. In some divers, these lung injuries can be bad enough to cause lung collapse (pneumothorax). The injuries may also allow free air bubbles to escape into the blood stream. This is called arterial gas embolism. Arterial gas embolism often causes chest pain, breathing trouble and neurologic problems such as stroke.

Decompression sickness occurs during ascent and on the surface of the water. Inert nitrogen gas that is dissolved in body tissues and blood comes out of solution and forms bubbles in the blood. The bubbles can injure various body tissues and may block blood vessels. The most common signs of severe decompression sickness are dysfunction of the spinal cord, brain and lungs.

How common are medical problems in scuba diving?

Fortunately, serious medical problems are not common in recreational scuba divers. While there are millions of dives each year in the United States, only about 90 deaths are reported each year worldwide. In addition, fewer than 1,000 divers worldwide require recompression therapy to treat severe dive-related health problems.

How can I lower my risk of medical problems?

Most severe dive-related injuries and deaths happen to beginning divers. To be safe, you must dive within the limits of your experience and level of training.

NEVER try any dive you're not comfortable with. During descent, you should gently equalize your ears and mask. At depth, never dive outside the parameters of the dive tables or your dive computer.

NEVER hold your breath while ascending. You should always ascend slowly while breathing normally. Become familiar with the underwater area and its dangers. Learn which fish, coral and other hazards to avoid so that injuries do not occur.

NEVER panic underwater. If you become confused or afraid during a dive, stop, try to relax and think the problem through. You can also get help from your dive buddy or dive master.

What should I do in a scuba diving emergency?

If you or one of your dive buddies has had an accident while diving, or if you would like to discuss a potential diving-related health problem, call the Divers Alert Network (DAN) emergency telephone line (1-919-684-8111). DAN is located at Duke University Medical Center in Durham, N.C. Doctors, emergency medical technicians and nurses are available 24 hours a day to answer your questions. If needed, they will direct you to the nearest hyperbaric chamber or other appropriate medical facility. A hyperbaric chamber is a facility where they can place you under increased pressure, similar to being underwater. This can often help injury from arterial gas embolism or decompression sickness by shrinking bubbles and allowing them to pass through your blood vessels.

American Family Physician,What is recreational scuba diving?

Where can I get more information about recreational scuba diving and dive medicine?

Several Web sites and e-mail addresses offer information about recreational scuba diving, dive medicine and dive-related health issues:

Web sites:
DAN: http://www.diversalertnetwork.org
Scubamed, sponsored by Underwater Medicine Associates:
http://www.scubamed.com
Diving Medicine Online: http://www.gulftel.com/~scubadoc
Undersea & Hyperbaric Medical Society: http://www.uhms.org
Association of Commercial Diving Educators: http://www.diveweb.com/acde/
National Association of Underwater Instructors: http://www.naui.org
PADI: http://www.padi.com
Scuba Schools International: http://www.ssiusa.com
E-mail addresses:
DAN: dan@diversalertnetwork.org
NAUI: nauihq@nauiww.org
PADI: TNE@padi.com
SSI: admin@ssiusa.com

COPYRIGHT American Academy of Family Physicians
COPYRIGHT Gale Group

Neurologic Complications of Scuba Diving

Recreational scuba diving has become a popular sport in the United States, with almost 9 million certified divers. When severe diving injury occurs, the nervous system is frequently involved. In dive-related barotrauma, compressed or expanding gas within the ears, sinuses and lungs causes various forms of neurologic injury. Otic barotrauma often induces pain, vertigo and hearing loss. In pulmonary barotrauma of ascent, lung damage can precipitate arterial gas embolism, causing blockage of cerebral blood vessels and alterations of consciousness, seizures and focal neurologic deficits. In patients with decompression sickness, the vestibular system, spinal cord and brain are affected by the formation of nitrogen bubbles. Common signs and symptoms include vertigo, thoracic myelopathy with leg weakness, confusion, headache and hemiparesis. Other diving-related neurologic complications include headache and oxygen toxicity. (Am Fam Physician 2001;63:2211-8,2225-6.)

Recreational scuba diving, which is defined as pleasure diving without mandatory decompression to a maximum depth of 130 ft, has become a popular activity in the past 20 years. In the United States alone, there are almost 9 million certified divers.(1) Although divers are concentrated along coastal regions, many others dive in inland lakes, streams, quarries and reservoirs, or fly to distant dive sites. Physicians practicing almost anywhere in the United States may see a patient with a dive-related injury or complaint.

In general, severe injury and death are uncommon in recreational diving accidents.(1-5) The Divers Alert Network(1) reports an average rate of 90 fatalities per year since 1980. Each year, between 900 and 1,000 divers are treated with recompression therapy for severe dive-related complications. In many of these patients, one or more of the major symptoms are neurologic in origin. The nervous system is frequently involved in dive-related complications and fatalities.(5) Physicians need to be aware of the broad spectrum of neurologic injuries that can occur during dive accidents to ensure early recognition, accurate diagnosis and appropriate therapy.

Dive-Related Barotrauma

During descent and ascent in the water, the diver is constantly exposed to alterations of ambient pressure. Barotrauma refers to tissue damage that occurs when a gas-filled body space (e.g., lungs, middle ear) fails to equalize its internal pressure to accommodate changes in ambient pressure.(2-4) The behavior of gasses at depth is governed by Boyle's law: the volume of a gas varies inversely with pressure.(6) During descent, as ambient pressure increases, the volume of gas-filled spaces decreases unless internal pressure is equalized. If the pressure is not equalized by a larger volume of gas, the space will be filled by tissue engorged with fluid and blood. This process underlies the common "squeezes" of descent that affect the middle ear, external auditory canal, mask, sinuses and teeth.

OTIC AND SINUS BAROTRAUMA

Barotrauma to the middle or inner ear can occur during the descent or ascent phases of the dive and may cause vertigo and other neurologic symptoms.(2-5,7) Middle ear barotrauma of descent is the most common type of diving injury and may involve hemorrhage and rupture of the tympanic membrane. Symptoms include the acute onset of pain, vertigo and conductive hearing loss that lateralizes to the affected side during the Weber's test. In severe cases (usually during ascent), increased pressure in the middle ear can cause reversible weakness of the facial nerve and Bell's palsy (facial baroparesis).(8)

Vertigo can also be induced if barotrauma differentially affects the two vestibular organs (alternobaric vertigo). The vertigo resolves after pressure equalization occurs. Treatment of middle ear barotrauma involves decongestants (e.g., intranasal oxymetazoline, oral pseudoephedrine), antihistamines, analgesics and antibiotics (amoxicillin-clavulanate [Augmentin] in a dosage of 500/125 mg three times per day or clindamycin [Cleocin] in a dosage of 300 mg three times per day for 10 to 14 days) in patients with otorrhea and perforation.(2,4,7)

Inner ear barotrauma also can develop in patients with middle ear barotrauma.(2-5,7) A pressure gradient between the perilymph of the inner ear and the middle ear cavity can occur, causing rupture of the labyrinthine windows (round and oval) and leakage of perilymph into the middle ear (i.e., fistula). Symptoms include the acute onset of vertigo, sensorineural hearing loss, tinnitus, nausea and emesis. The Weber's test will lateralize to the unaffected side in this group of patients. Reducing intracranial and perilymphatic pressures through bed rest, head elevation and with stool softeners can help. Surgical exploration may be necessary for repair of the fistula if conservative treatment is ineffective within five to 10 days (i.e., the symptoms persist or worsen).

PULMONARY BAROTRAUMA

Pulmonary barotrauma is the most severe form of barotrauma and occurs during ascent.(2-4,9) In accordance with Boyle's law, as the ambient pressure is reduced during ascent, gas inside the lungs will expand in volume.(6) If the expanding gas is not allowed to escape by exhalation, the alveoli and surrounding tissues will tear. The most common cause of pulmonary barotrauma among recreational divers is breath holding. Other causes are related to pulmonary obstructive diseases, such as asthma or bronchitis, which can lead to the trapping of gas. Several forms of pulmonary barotrauma can develop, including mediastinal emphysema, subcutaneous emphysema, pneumothorax and arterial gas embolism. Arterial gas embolism is the most dangerous form of pulmonary barotrauma and accounts for nearly one fourth of fatalities per year among recreational divers.(3) In addition, it is the only form in which neurologic symptoms predominate over pulmonary symptoms.(9)
Arterial gas embolism develops when free air enters the pulmonary vasculature and is carried to the heart and arterial circulation.(9,10) A large proportion of air bubbles can reach the brain, occlude blood vessels and cause stroke-like events. The most common signs and symptoms of arterial gas embolism are neurologic (Table 1(2,4,6,7)), although pulmonary symptoms may also be present. In more than 80 percent of patients, symptoms develop within five minutes of reaching the surface, but they also can occur during ascent or after a longer surface interval.

TABLE 1

Presenting Signs and Symptoms
in Patients with Arterial Gas Embolism

Sign or symptom Percentage

Stupor or confusion 24
Coma without seizures 22
Coma with seizures 18
Unilateral motor deficits 14
Visual disturbances 9
Vertigo 8
Unilateral sensory deficits 8
Bilateral motor deficits 8
Collapse 4

Information from references 2,4,6 and 7.
Almost two thirds of patients with arterial gas embolism have alterations of consciousness (i.e., coma or obtundation). Seizures, focal motor deficits, visual disturbances, vertigo and sensory changes are also common. Spinal cord lesions occur less frequently. Many patients show initial improvement within minutes to hours, secondary to partial clearance of air emboli. Magnetic resonance imaging (MRI) may demonstrate focal lesions in the brain after arterial gas embolism.(10) Arterial gas embolism can mimic decompression sickness, and the presentation of the two syndromes may be clinically indistinguishable (Table 2(1-5,7-10).2,4,6) Arterial gas embolism and decompression sickness can develop simultaneously in some patients. In fact, the air emboli of arterial gas embolism may act as a nidus, or "seed," to precipitate decompression sickness. Therefore, the two syndromes are often described and treated together using the more global term, decompression illness.(4)
TABLE 2

American Family Physician, by Herbert B. Newton

Clinical Features, Dive Profile and Treatment of the Neurologic
Complications of Scuba Diving

Disorder Clinical features

Middle ear Acute pain, vertigo, hearing barotrauma loss, rupture or hemorrhage of descent of tympanic membrane

Facial baroparesis Ipsilateral facial paralysis, resolves within hours

Inner ear Acute vertigo, nausea, emesis, barotrauma tinnitus, sensorineural hearing loss; often associated with middle ear barotrauma

Arterial gas Stupor, confusion, coma, embolism seizures, focal weakness, visual loss

Inner ear DCS Acute vertigo, nausea, emesis, nystagmus, tinnitus, sensorineural hearing loss

Cerebral DCS Confusion, focal weakness, fatigue, visual loss, diplopia, speech dysfunction, gait abnormality, headache

Spinal cord DCS Paresthesias/sensory loss in trunk and/or extremities, leg weakness,
loss of bowel/bladder function

Headache (arterial Severe generalized headache gas embolism associated with alteration of
or DCS) consciousness and other signs

Headache Pounding, throbbing pain; (migraine) nausea, emesis, photophobia

Oxygen toxicity Focal seizures, visual constriction, nausea, emesis, vertigo,
paresthesias, rare generalized seizures

Disorder Treatment

Middle ear Improved equalization techniques, barotrauma oral and nasal decongestants;
of descent with otorrhea use antibiotics

Facial baroparesis No treatment

Inner ear ENT evaluation, bed rest, head barotrauma elevation, stool softeners; consider surgical exploration if symptoms persist

Arterial gas 100 percent oxygen, United embolism States Navy Table 6 algorithm
recompression, supportive care

Inner ear DCS Same as above

Cerebral DCS Same as above

Spinal cord DCS Same as above

Headache (arterial Same as above; analgesics gas embolism or DCS)

Headache Avoid precipitating stimuli, (migraine) dive conservatively, consider prophylactic therapy

Oxygen toxicity Reduce depth and oxygen exposure, supportive care, seizure
management; see arterial gas embolism treatment

ENT = ear, nose and throat; DCS = decompression sickness.

Information from references 1 through 5 and 7 through 10.
Treatment of arterial gas embolism consists of basic or advanced cardiac life support, 100 percent oxygen, rehydration and transport to a recompression facility.(2,4,9,10) Oxygen reduces ischemia in affected tissues and accelerates the dissolution of air emboli. Seizures, arrhythmias, shock, hyperglycemia and pulmonary dysfunction should be treated, if present. Recompression therapy should be initiated immediately, using the United States Navy (USN) Table 6 algorithm.(2-5,10,11) Recompression therapy reduces the size of air bubbles by increasing ambient pressure, expedites passage of emboli through the vasculature and re-establishes blood flow to ischemic tissues.

Decompression Sickness

Decompression sickness is caused by the release of inert gas bubbles (usually nitrogen) into the bloodstream and tissues after ambient pressure is reduced.(2-5,10) At depth, the partial pressures of gasses in the breathing mixture increase in proportion to the ambient pressure, according to Dalton's law.(6) Although oxygen is actively metabolized, nitrogen is inert and becomes dissolved in body tissues until saturation, proportional to the ambient pressure as defined by Henry's law.(6) The propensity for the formation of nitrogen bubbles depends on the depth of the dive, the length of time at depth and the rate of ascent. If ambient pressure is released too quickly, the dissolved nitrogen gas that cannot remain in solution will form air bubbles within the blood, interstitial fluids and organs (Figure 1).

Decompression sickness is traditionally classified into type I and type II. In type I decompression sickness, symptoms are usually mild and may manifest as fatigue or malaise (i.e., constitutional decompression sickness) or may be more specific, involving the muscles, joints and skin.(10) Type II decompression sickness is more severe and can affect the lungs, vestibular apparatus and the nervous system.

In inner ear and neurologic decompression sickness, the formation of bubbles affects the brain, spinal cord, cranial and peripheral nerves, and the neural vasculature. Nitrogen bubbles can injure neural tissues by mechanical disruption, compression, vascular stenosis or obstruction, and activation of inflammatory pathways (e.g., cytokines, complement).(4,10) Cerebral decompression sickness (30 to 40 percent of cases) usually involves arterial circulation, while spinal cord decompression sickness (50 to 60 percent of cases) involves obstruction of venous drainage and the formation of bubbles within the cord parenchyma.(12)

The incidence of decompression sickness among recreational scuba divers is estimated to be one case per 5,000 to 10,000 dives.(1) Diving within the limits of dive tables is no guarantee against decompression sickness, because more than 50 percent of cases of decompression sickness occur after no-decompression dives. In addition to the dive profile and rate of ascent, other factors may influence the risk of decompression sickness, including hypothermia, fatigue, increased age, dehydration, alcohol intake, female gender, obesity and patent foramen ovale.(2-5,13)
In type II neurologic decompression sickness, more than 50 percent of patients develop symptoms within one hour of ascent; within six hours, 90 percent of divers are symptomatic.(1,4,14) Inner ear decompression sickness presents with acute vertigo, nausea, emesis, nystagmus and tinnitus. The pathophysiology remains unclear; one mechanism is bubble rupture of the intraosseous membranes in the semicircular canals. In many cases, inner ear decompression sickness is clinically indistinguishable from otic barotrauma, although the dive profile and timing of symptoms may help to clarify the diagnosis (Table 2).(2-5,7,10)

Neurologic decompression sickness can present with a wide spectrum of symptoms (Table 3). The most severe presentation is partial myelopathy referable to the thoracic spinal cord.(10,15) Patients complain of paresthesias and sensory loss in the trunk and extremities, a tingling or constricting sensation around the thorax, ascending leg weakness ranging from mild to severe, pain in the lower back or pelvis and loss of bowel and/or bladder control. The neurologic examination will often reveal monoparesis or paraparesis, a sensory level and sphincter disturbances. However, neurologic examination also may be normal.

TABLE 3

Presenting Signs and Symptoms
in Patients with Decompression Sickness

Sign or symptom Percentage

Numbness 59
Pain 55
Dizziness 27
Extreme fatigue 25
Headache 24
Weakness 23
Nausea 14
Gait abnormality 12
Hypoesthesia 10
Visual disturbance 8
Itching 5

Information from references 1,2,4,5 and 9.
Pathologic features within the spinal cord include hemorrhagic infarctions, edema, bubble defects, axonal degeneration and demyelination (Figure 2).(12,15) Cerebral decompression sickness can occur alone or in combination with spinal decompression sickness and manifests as an alteration of mentation or confusion, weakness, headache, gait disturbance, fatigue, diplopia or visual loss. The neurologic examination may show hemiparesis, dysphasia, gait ataxia, hemianopsia and other focal signs. Behavioral and cognitive aspects of cerebral decompression sickness may be persistent or slow to improve.(10,16) The pathologic features are similar to those of spinal decompression sickness, although not as pronounced.(10,17)

The diagnosis of neurologic decompression sickness is clinical and should be suspected in any patient with a recent history of diving who has a consistent presentation. Neuroimaging studies may further clarify the diagnosis but should not delay treatment. MRI demonstrates high-signal lesions of the brain and spinal cord in 30 to 55 percent of cases (Figure 3), which suggests ischemia, edema and swelling. The lesions do not enhance with contrast. However, images on MRI are often normal.(5,10,16)

The initial management of neurologic decompression sickness is similar to that of arterial gas embolism and decompression illness, and requires transport to a recompression facility.(2-5,10,16) If transport by helicopter is necessary, the patient should be flown at an altitude of less than 1,000 ft to minimize exacerbation of symptoms. The definitive treatment is recompression therapy using the USN Table 6 algorithm.(11) USN Table 6 consists of initial recompression to 60 ft of salt water with 100 percent oxygen for 60 minutes. The patient is then decompressed to 30 ft of salt water for two additional periods each of breathing pure oxygen and air. Recompression therapy reduces the size of bubbles, allowing easier reabsorption and dissipation, and increases the nitrogen gradient to expedite off-gassing. The majority of recreational divers with neurologic decompression sickness have an excellent recovery after prompt recompression therapy.
The Divers Alert Network (DAN) at Duke University Medical Center, Durham, N.C., is available 24 hours a day to discuss arterial gas embolism or decompression sickness and provide divers a referral to the nearest recompression facility, if necessary. The emergency hotline number is 919-684-8111. For nonemergency medical questions, call DAN at 919-684-2948.

Headache

Headache is a common symptom in divers. There are numerous benign causes, including exacerbation of tension or migraine headaches, exposure to cold, mask or sinus barotrauma, sinusitis and a tight face mask. Migraines are not often precipitated by diving, but can be severe when they occur. If a migraine develops, the dive should be terminated because of the potential for nausea, emesis and alteration of consciousness. Dangerous causes of headache include cerebral decompression sickness, contamination of the breathing gas with carbon monoxide, arterial gas embolism, severe otic or sinus barotrauma with rupture, and oxygen toxicity.(2-5,10) If headache occurs in a patient with potential arterial gas embolism or decompression sickness, it should be considered an emergency, because it suggests the presence of intracerebral bubbles. This type of headache usually develops within minutes of ascent. Immediate use of 100 percent oxygen and of recompression therapy is indicated.

Oxygen Toxicity

In the recreational diver, the most likely cause of oxygen toxicity is diving with oxygen enriched air (i.e., Nitrox). Nitrox is a breathing mixture that contains more than 21 percent oxygen (usually 32 to 36 percent), and allows extended bottom time. When diving with Nitrox, the diver is at risk of oxygen toxicity if the maximum oxygen depth limit and/or the oxygen time limit is exceeded. In general, the higher the oxygen content in the Nitrox mixture, the shallower the dive to minimize the potential for oxygen toxicity. Symptoms develop at depth without warning and consist of focal seizures (e.g., facial or lip twitching occurs in 50 to 60 percent of patients), vertigo, nausea and emesis, paresthesias, visual constriction and respiratory changes.(18) Generalized seizures or syncope can also occur in 5 to 10 percent of patients. Although uncommon, generalized seizures at depth are often fatal, because divers may drown or arterial gas embolism may be precipitated during rescue to the surface.(4) The cause of oxygen toxicity to the nervous system mainly involves oxygen-free radical formation, as well as reduction of the inhibitory neurotransmitter, gamma-aminobutyric acid. Treatment consists of reducing oxygen exposure and dive depth and, if necessary, managing seizures.

In: Bennett PB, Elliott DH, eds. The physiology and medicine of diving. 4th ed. London: Saunders, 1993;17:481-505.
Dr. Newton received support in part from a National Cancer Institute grant, CA 16058.

The author thanks Harrison Weed, M.D., for critical review of the manuscript and David Carpenter for his editorial expertise.

REFERENCES

(1.) Divers Alert Network. Report on decompression illness and diving fatalities: DAN's annual review of recreational scuba diving injuries and fatalities based on 1998 data. Durham, NC: Divers Alert Network, 2000.

(2.) Melamed Y, Shupak A, Bitterman H. Medical problems associated with underwater diving. N Engl J Med 1992;326:30-5.

(3.) Clenney TL, Lassen LF. Recreational scuba diving injuries. Am Fam Physician 1996;53:1761-74.

(4.) Moon RE. Treatment of diving emergencies. Crit Care Clin 1999;15:429-56.

(5.) Dick AP, Massey EW. Neurologic presentation of decompression sickness and air embolism in sport divers. Neurology 1985;35:667-71.


(6.) Brylske A. The gas laws. A guide for the mathematically challenged. Dive Training 1997;September:26-34.

(7.) Farmer JC. Otological and paranasal sinus problems in diving. In: Bennett PB, Elliott DH, eds. The physiology and medicine of diving. 4th ed. London: Saunders, 1993;11:267-300.

(8.) Molvaer OI, Eidsvik S. Facial baroparesis: a review. Undersea Biomed Res 1987;14:277-95.

(9.) Neuman TS. Pulmonary barotrauma. In: Bove AA, ed. Bove and Davis' Diving medicine. 3d ed. Philadelphia: Saunders, 1997;13:176-83.

(10.) Greer HD, Massey EW. Neurologic injury from undersea diving. Neurol Clin 1992;10:1031-45.

(11.) U.S. Navy. Recompression treatments when chamber available. U.S. Navy Diving Manual Vol. 1 (Air Diving). Revision 1, ch. 8, rev. 15. February 1993; Naval Sea Systems Command Publication NAVSEA 0994-LP-001-9110.

(12.) Francis TJ, Pezeshkpour GH, Dutka AJ, Hallenbeck JM, Flynn ET. Is there a role for the autochthonous bubble in the pathogenesis of spinal cord decompression sickness? J Neuropathol Exp Neurol 1988;47:475-87.

(13.) Knauth M, Ries S, Pohimann S, Kerby T, Forsting M, Daffertshofer M, et al. Cohort study of multiple brain lesions in sport divers: role of a patent foramen ovale. BMJ 1997;314:701-5.

(14.) Francis TJ, Pearson RR, Robertson AG, Hodgson M, Dutka AJ, Flynn ET. Central nervous system decompression sickness: latency of 1070 human cases. Undersea Biomed Res 1988;15:403-17.

(15.) Aharon-Peretz J, Adir Y, Gordon CR, Kol S, Gal N, Melamed Y. Spinal cord decompression sickness in sport diving. Arch Neurol 1993;50:753-6.

(16.) Levin HS, Goldstein FC, Norcross K, Amparo EG, Guinto FC, Mader JT. Neurobehavioral and magnetic resonance imaging findings in two cases of decompression sickness. Aviat Space Environ Med 1989;60:1204-10.

(17.) Palmer AC, Calder IM, Yates PO. Cerebral vasculopathy in divers. Neuropathol Appl Neurobiol 1992;18:113-24.

(18.) Clark JM, Thom SR. Toxicity of oxygen, carbon dioxide, and carbon monoxide. In: Bove AA, ed. Bove and Davis' Diving medicine. 3d ed. Philadelphia: Saunders, 1997;10:131-45.

HERBERT B. NEWTON, M.D., is associate professor of neurology and director of the division of neuro-oncology at Ohio State University Medical Center and Arthur G. James Cancer Hospital and Solove Research Institute, Columbus, Ohio. He graduated from the State University of New York at Buffalo School of Medicine and Biomedical Sciences, Buffalo. Dr. Newton received his neurology training at the University of Michigan Medical School, Ann Arbor. He completed a fellowship in neuro-oncology at Memorial Sloan-Kettering Cancer Center, New York City. Dr. Newton is certified by the Professional Association of Diving Instructors (PADI) as a DiveMaster and Instructor in dive medicine (PADI 162347) and is a member of the Diver's Alert Network and the Undersea & Hyperbaric Medical Society.

Address correspondence to Herbert B. Newton, M.D., Department of Neurology, Ohio State University Medical Center, 465 Means Hall, 1654 Upham Dr., Columbus, OH 43210 (e-mail: newton.12@osu.edu). Reprints are available from the author.

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Open water, open mouths: scuba divers face infection risks

Circling sharks and empty air tanks may haunt scuba divers' imaginations, but ordinary microbes are a far more probable hazard. A new study takes a stab at quantifying the risks that waterborne bacteria and viruses pose to divers.

While scientists regularly measure bacterial concentrations in waters used by beachgoers, they don't test all the sites visited by divers, surfers, and kayakers. What's more, researchers don't know how much of the water these people swallow, says microbiologist and mathematical modeler Jack Schijven of the National Institute of Public Health and the Environment in Bilthoven, the Netherlands.

To begin measuring the microbial risk to divers, Sehijven and his institute colleague Ana Maria de Roda Husman provided a questionnaire to 233 professional divers and posted a similar survey online for about 26,000 recreational divers in the Netherlands. Thirty-seven pros--who do underwater-construction or search-and-rescue work, for example--and 483 amateurs responded. They supplied data on illnesses they'd had in the past year, how many dives they'd made in various aquatic environments, and what volume of water they'd swallowed on a typical dive.

The researchers focused on skin, ear, eye, respiratory, or gastrointestinal symptoms, which might have been caused by infections acquired during dives. Most respondents said that they'd had at least one such illness. Diarrhea and ear problems topped the list.

"Only 20 percent of the divers stated that they did not have any complaint at all," Schijven says. "We were really astonished."

The study didn't include a comparison group of nondivers, so it's unclear what portion of the ailments resulted from diving, he cautions.

Other data from the questionnaires suggest that recreational divers face a gastrointestinal infection risk of up to 1.1 percent per marine dive and 1.5 percent per freshwater dive.

The recreational divers tended either to swallow no water or to swallow about the volume of a shot glass. Professional divers, who often wear full face masks, generally swallowed a few drops of water or less. From the survey information and data on pathogen abundance, the researchers estimate in the May Environmental Health Perspectiws that professionals face the highest risks.

The pros "have to dive in any kind of water, even wastewater," Schijven says.

Overall, divers reported more ear complaints during the summer months than the winter months. That's "a strong hint" that diving is to blame, Schijven says, because the bacterial suspects in such infections prefer warm water. By contrast, gastrointestinal problems, which are caused by pathogens that survive longer in cold water, are most frequent during winter.

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