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Diving Medicine

Course Authors

Dipak Chandy, M.D., and E. Neil Schachter, M.D.

Dr. Chandy is a third-year Fellow in Pulmonary Medicine
at The Mount Sinai School of Medicine.

Drs. Chandy and Schachter report no commercial conflict of interest.

Estimated course time: 1 hour(s).

Albert Einstein College of Medicine – Montefiore Medical Center designates this enduring material activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

In support of improving patient care, this activity has been planned and implemented by Albert Einstein College of Medicine-Montefiore Medical Center and InterMDnet. Albert Einstein College of Medicine – Montefiore Medical Center is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.

 
Learning Objectives

Upon completion of this Cyberounds®, you should be able to:

  • Discuss the physiology of scuba diving

  • List major medical complications of scuba diving

  • Discuss the basis for prevention and therapy of barotrauma in divers.

 

In the United States, there are more than five million recreational scuba divers and each year another several hundred thousand people take up the sport. Accordingly, the incidence of diving-related disorders has increased. More than a thousand diving-related injuries are recorded annually, of which almost 10% are fatal.

Diving-related disorders can be classified as:

  • Nitrogen narcosis
  • Decompression sickness
  • Barotrauma

Two laws of physics, on the behavior of gases under varying pressures, govern the pathophysiology of diving-related disorders. Henry's law states that, at a constant temperature, the amount of a gas dissolved in a liquid is directly proportional to the partial pressure of that gas. Boyle's law states that, at a constant temperature, the volume of a gas varies inversely with the pressure to which it is subjected. As we shall see, Henry's law helps to explain the principles behind nitrogen narcosis and decompression sickness, while Boyle's law provides the explanation for barotrauma.

Nitrogen Narcosis

Nitrogen narcosis usually occurs at depths greater than 100 feet (30 metres) as the result of a raised partial pressure of nitrogen in nervous system tissue. It is also known as the "rapture of the depths" because nitrogen narcosis induces symptoms and signs similar to benzodiazepine or alcohol intoxication. Changes in personality and behavior and impairment of neuromuscular and intellectual performance are characteristic. At depths greater than 300 feet (100 metres), hallucinations and loss of consciousness can occur. Divers recover rapidly so long as they ascend to a shallower depth. The main danger of this condition stems from the impairment of the diver's judgment, which can lead to drowning accidents.

Decompression Sickness

The condition is also called "caisson disease," as it was first recognized among tunnel workers returning to atmospheric pressure after working in the compressed environment of caissons. The term "bends" is frequently associated with this illness because laborers with decompression sickness sometimes walked with a slight stoop. This habitus resembled a posture affected by women socialites during the era in which New York's Brooklyn Bridge was being built and was known as the Grecian Bend.

As predicted by Henry's law, when a diver descends and breathes air under increased pressure, the tissues get loaded with increased quantities of nitrogen and oxygen. As the diver returns to the surface, the sum of the gas tensions in the tissues may exceed the ambient pressure and lead to the liberation of free gas from these tissues as bubbles. The location and volume of these bubbles determine whether symptoms occur.

Approximately 75% of patients developing decompression sickness will experience symptoms within one hour of diving and almost everyone affected will present within the first 24 hours. Since commercial aircraft are not pressurized to sea level, air travel within 24 hours of diving can precipitate decompression sickness in a diver who has a subclinical bubble load. Prodromal manifestations include fatigue, malaise, headache, anorexia and a sense of foreboding.

Decompression sickness is classified into two types based on the clinical manifestations:

Type I presents with mild complaints and typically affects the following systems:

Musculoskeletal - Localized joint pain is the most common manifestation of decompression sickness.(1) Symptoms are believed to be caused by the stretching of noncompliant tissues and impairment of blood flow because bubbles are present in the periarticular tissues.

Cutaneous - Pruritus, usually over the upper torso, is thought to be caused by the presence of small bubbles in the skin and is relatively common. Even without treatment, the itching generally resolves within 30 minutes. Localized erythema, which may evolve into mottled areas of cyanosis, can also be seen.

Lymphatic - Though rare, obstruction by bubbles can lead to pain, lymphadenopathy and localized edema, usually with follicular depressions, a peau d'orange effect.(2) These symptoms are seen, primarily, on the torso and chest.

Type II is more severe and can lead to permanent injury and even death. The following systems are typically affected:

Neurological - About 60% of divers with decompression sickness will have symptoms and signs of nervous system involvement. Most of these neurological manifestations are thought to occur as inert gas bubbles coalesce and then occlude venous outflow. Most of these cases are characterized by damage to the spinal cord. Paresthesias and weakness may progress to paraplegia. Cerebral manifestations include visual disturbances, loss of memory and changes in affect, personality and speech.(3)

Pulmonary - In about 5% of decompression sickness cases, the bubble load is sufficient to precipitate a pulmonary air embolism.

Audiovestibular - The primary manifestations are severe hearing loss, tinnitus, vertigo, nausea, vomiting and nystagmus.

Treatment

First aid includes hydration, administration of oxygen and positioning in the left lateral recumbent and mild Trendelenburg position in an effort to trap air bubbles in the right atrium.

Definitive treatment includes hyperbaric therapy as soon as possible since one of the main determinants of outcome is the time to initiation of treatment.(4) Recompression treatment should never be withheld, even after a long delay, because there remains a chance of favorable results.(5) Complete resolution of symptoms in Type II decompression sickness is seen in almost 75% of cases.

Barotrauma

This is the most common form of diving-related injury and develops when an air-filled body space fails to equalize its pressure to changing ambient pressures. During ascent, increasing air volume in a space that also contains tissue provokes tissue disruption, while during descent, decreasing air volume in a similar space causes mucosal edema, vascular engorgement and hemorrhage.

Ear barotrauma - The involvement of the middle ear during descent is the most common disorder among divers.(6) Normally, pressure in the middle ear equilibrates with ambient pressure through the Eustachian tube. However, if on descent, this equalization is prevented by mucosal edema or anatomical variations, the negative pressure in the middle ear may cause the inner ear to fill with serous fluid or blood and rupture of the tympanic membrane may result.(7)

Treatment of middle-ear barotrauma consists of decongestants, analgesics and antihistaminics. Antibiotics should be used if purulent otorrhea is seen.(8) Inner-ear barotrauma is a fairly uncommon injury but should be ruled out in all cases of middle-ear barotrauma.

Sinus barotrauma - This is the second most common disorder among divers and is related to blockage of the sinus ostia from congestion of the nasal mucosa or the presence of a mass. The frontal sinus is commonly affected because its duct's course is relatively long and tortuous.(9) During descent, increase in ambient pressure can produce mucosal engorgement, edema and inflammation. Common symptoms include headache, epistaxis and localized sinus pain.

Treatment includes the use of decongestants and antibiotics if a purulent nasal discharge is seen.

Pulmonary barotrauma - This is the second leading cause of death among divers (drowning is the first). As a diver descends, the air in the lungs is compressed. When lung volume decreases below residual volume, pulmonary edema and hemorrhage occur. As a diver ascends, overexpansion injury, in the form of alveolar rupture, can occur when transalveolar pressure exceeds 20-80 mmHg.(10) Divers who hold their breath as they ascend, as well as those with obstructive airway disease, including asthma, are at increased risk. Alveolar rupture can lead to the following conditions:

Pneumomediastinum - Following alveolar rupture, air can dissect along the perivascular sheath into the mediastinum. The diagnosis can be confirmed by chest and neck films.

No specific treatment is required but breathing 100% oxygen is recommended to hasten recovery.

Pneumothorax - This is relatively uncommon (10% of barotrauma) and develops when air ruptures into the pleural space. A chest radiograph establishes the diagnosis. If life-threatening, immediate chest decompression is usually accomplished by inserting a large-bore needle into the second intercostal space in the midline of the affected hemithorax followed by tube thoracostomy.

Arterial air embolism - This is the most serious sequela of pulmonary barotrauma. It results from the passage of air into the pulmonary veins and from there into the systemic circulation. Paradoxical arterial embolism, usually across a cardiac septal defect, can arise in a situation where only venous emboli should occur. In the systemic circulation, bubbles typically break up as they reach vascular branch points and ultimately lodge in vessels with diameters ranging from 30-60 mm. Symptoms and signs are dependent on the final location of these bubbles. The most serious clinical events arise with embolization to the cerebral and coronary arteries. Manifestations of cerebral emboli range from focal sensory, motor or visual deficits to seizures, loss of consciousness, apnea and death. Air in the coronary circulation can lead to myocardial infarction, dysrhythmias and cardiac arrest.

Emergency treatment includes hydration and breathing 100% oxygen. These can be expected to ameliorate some of the acute symptoms of cerebral air embolism. Patients should be transferred to the nearest hyperbaric facility as soon as possible. Prognosis is generally good, especially for early treatment of cerebral air emboli, but decreased clinical efficacy is seen after a 4-5 hour delay.(11) The treatment for patients with residual deficits is repeated hyperbaric treatments and improvements are often seen over several days.

Diving and Co-existing Conditions

Pregnancy - Though not an absolute contraindication to diving, all pregnant women should probably be discouraged from taking the risks associated with diving.(12) The fetus is not protected from decompression sickness and is at greater risk of embolization and malformations because it lacks the pulmonary filter. However, should a pregnant woman dive during early pregnancy, an abortion is not recommended, as several normal pregnancies have been reported, even among women who continued diving throughout their pregnancy.

Lung disease - The presence of COPD, cystic fibrosis, bronchiectasis, interstitial lung disease and a history of thoracic surgery or prior pneumothorax from any cause should be considered absolute contraindications to diving. A patient with active asthma should also be strongly discouraged from diving, even if they have normal pulmonary function tests, since individual lung units, the physiological term for the lobule (terminal bronchiole and the areas distal to it), have prolonged time constants. However, asthmatics with normal pulmonary function and easily controlled airway reactivity during exercise are probably not at increased risk of diving-related barotrauma.(13)

Cardiovascular disease - A patient with a history of arrhythmias should undergo a cardiac stress test before being allowed to dive. An intracardiac shunt should also be considered a contraindication as venous air emboli can lead to arterial embolization.


Footnotes

1Green, RD, Leitch, DR. Twenty years of treating decompression sickness. Aviat Space Environ Med 1987; 58:362.
2Edmonds, C, Thomas, RL. Medical aspects of diving: IV. Med J Aust 1972; 2: 1367.
3Dick, PK, Massey, EW. Neurologic presentation of decompression sickness and air embolism in sports divers. Neurology 1985; 35:667.
4Melamed, Y, Sherman, D, Wiler-Ravell, D, et al. The transportable recompression rescue chamber as an alternative to delayed treatment in serious diving accidents. Aviat Space Environ Med 1981; 52:480.
5Myers, RAM, Bray, P. Delayed treatment of serious decompression sickness. Ann Emerg Med 1985; 14:254.
6Neblett, LM. Otolaryngology and sport scuba diving: Update and guidelines. Ann Otol Rhinol Laryngol Suppl 1985; 115:1.
7Farmer, JC Jr. Eustachian tube function and otologic barotrauma. Ann Otol Rhinol Laryngol suppl 1985; 120:45.
8Melamed, Y, Shupak, A, Bitterman, H. Medical problems associated with underwater diving. N Engl J Med 1992; 326:30.
9Fagan, P, McKenzie, B, Edmonds, C. Sinus barotrauma in divers. Ann Otol Rhinol Laryngol 1976; 85:61.
10Hardy, KR. Diving-related emergencies. Emer Med Clin of North Am 15:223.
11Leitch, DR, Green, RD. Pulmonary barotrauma in divers and the treatment of cerebral arterial gas embolism. Aviat Space Environ Med 1986; 57:931.
12Camporesi, EM. Diving and pregnancy. Semin Perinatol 1996; 20:292.
13Bove, AA. Pulmonary barotrauma in divers: Can prospective pulmonary function testing identify those at risk? Chest 1997; 112:576.