Airway & Respiratory, Cardiac & Resuscitation, Patient Care

Recognizing and Treating Injuries Caused by SCUBA Diving

Issue 8 and Volume 40.

Recreational diving is a popular sport with more than a million divers worldwide. Although recreational SCUBA diving is most popular in warm climates, dive shops and divers can be found anywhere there’s a significant body of water, including quarries, lakes and rivers. EMS providers must have a basic understanding of diving physiology and dive injuries to handle these emergencies and to support public safety dive teams. Considering the ease of vacation travel, EMS providers may be called to assess diving-related injuries that occurred far from their service area, making it important for the provider to recognize these injuries and make the correct triage and transport decisions.


Although diving injuries can occur after being exposed to increased pressure in caissons or hyperbaric chambers, the underwater environment is the most common cause. Common physiologic stressors while diving include the cardiovascular and respiratory effects of immersion, pressure effects on gas spaces in the body, and the effect of gasses breathed at higher-than-normal pressure during compression and their elimination during decompression.

The most common form of recreational diving utilizes self-contained underwater breathing apparatus (SCUBA). Breathing air is contained in a steel or aluminum cylinder mounted to the back of a vest device known as a buoyancy compensator. The diver typically wears weights to produce negative buoyancy, however, the diver can inflate the buoyancy compensator with breathing air to become neutrally buoyant and float in the water. Incorrectly inflating the buoyancy compensator can result in a too-rapid ascent or descent, resulting in pressurization injuries.

The typical SCUBA apparatus is an open-circuit system in which the diver exhales through a regulator that exits into the water, which creates the characteristic stream of bubbles. Although previously only used by the military and commercial divers, closed-circuit and semi-closed-circuit breathing apparatus are becoming more popular in the recreational diving community. The exhaled breath is captured and carbon dioxide (CO2) is removed with a chemical agent to recycle the oxygen. Additional oxygen may be added into the breathing loop by the apparatus to maintain composition. These “rebreathers” are smaller and produce little-to-no bubbles in the water when the diver exhales.

One of the principal challenges of being underwater is the temperature gradient from the skin to the environment. An unclothed person at rest is thermal neutral (will neither gain nor lose heat) between 77 degree F (25 degrees C) and 86 degrees F (30 degrees C). The conductive properties of water (about 20 times higher) raise the thermal neutral point for an immersed individual to approximately 95 degrees F (35 degrees C). Although the exercising muscles will generate some heat during diving, most divers wear some form of wetsuit to help conserve heat. The thickness of these suits will vary based upon the environmental conditions. Wetsuits worn in cool water tend to have full-length arms and legs while those worn in warmer regions may only cover the torso and upper thigh. The wetsuit allows a thin layer of water between the suit and the diver’s skin. The diver’s body heat warms that layer of water and slows the conductive heat loss. While it’s possible to suffer hyperthermia when diving in very warm water, most dives result in some heat loss.

Ambient pressure decreases with altitude and increases with depth. While the falling pressures associated with altitude aren’t usually noticed until ascending many thousands of feet, the rise in pressure with immersion is dramatic. By convention, sea-level pressure is noted as one atmosphere absolute (ATA). The properties of gasses under pressure change with increasing depth. Of principal importance to the diver descending into the water is the reduced volume of gas, increased partial pressure, and increased solubility with rising ambient pressure. The pressure increases one full ATA with every 33 feet of depth in sea water (fsw) or approximately 10 meters of sea water (msw). (See Figure 1.) If a diver takes a 500 mL breath at the surface and then descends to 33 fsw, the same 500 mL tidal volume contains twice as many molecules of air because of the doubled pressure (2 ATA). If the diver held his breath while ascending back to the surface, the air in his lungs would double in volume as the pressure returns to 1 ATA and traumatic injury would occur.

Another prominent physiologic effect of immersion is the shift of body fluids from the extremities to the central circulation. The compressive effects of water during immersion displace blood volume from the arms and legs centrally. When diving in cold water, reflexive vasoconstriction magnifies the effect. The increased fluid in the lung vasculature decreases the gas spaces, reducing tidal volume. Greater central blood volume stretches the right atrium to release atrial natriuretic factor, which results in a diuresis. Divers returning to land after a multi-hour immersion (common among military and commercial divers) may be mildly hypovolemic when blood redistributes into the extremities.

Figure 1: Efect of pressure and depth on air volume

The increased hydrostatic pressure and breathing resistance cause an increase in the work and energy cost of breathing. In addition, the position of the diver in the water can create a difference in the gas pressure between the lung centroid and the SCUBA regulator pressure, causing a static lung load that also affects breathing. In some divers, increased central volume can result in pulmonary edema, especially during exercise in cold water where arterial pressure can increase, although the mechanism isn’t clear.

Diving that follows the recommended tables is a very safe activity with few incidences of barotrauma or decompression sickness. The exact “triggers” for diving accidents where standard procedures are followed aren’t fully understood, however, violating the safety procedures and dive tables can result in accidents.


Barotrauma is physical damage to tissues caused by unequal pressure between a gasfilled space and an adjacent fluid and ambient pressure. It can occur in divers during descent or ascent. The most common type of barotrauma during descent is an overpressurization injury of the middle/inner ear or paranasal sinuses. Divers will perform a Valsalva’s maneuver during descent to equalize pressure in the ears but middle ear barotrauma can occur when the diver can’t successfully equalize the pressure. This may happen if the diver descends too rapidly or there’s congestion in the eustachian tube that prevents the diver from equalizing the ear with the rising external water pressure. In severe cases, the eardrum may rupture, causing bleeding and admitting water into the inner ear, which may lead to infections.

Ear barotrauma will cause dizziness and vertigo. Divers who continue to dive without allowing time for the injury to heal may suffer permanent damage to the eardrum and serious ear infections. Failure to equalize the paranasal sinuses during descent may cause blood vessels in the sinus to enlarge and rupture. When this happens, blood will appear inside the diver’s mask.

Divers are cautioned to never hold their breath while under water. Extra-alveolar air injuries may occur if a diver ascends against a closed glottis. Air in the lungs expands as pressure decreases. The expanding alveoli may rupture, allowing air to enter the pleural space (pneumothorax, tension pneumothorax) or mediastinum (pneumomediastinum). In some cases, the escaping gas enters the arterial circulation as a gas embolism and will likely become trapped in the brain. Over-pressurization of the lungs may also cause subcutaneous emphysema, which will be felt at the base of the neck and upper thorax. (See Figure 2.) The symptoms of these injuries usually appear immediately after the diver surfaces, which can help distinguish this type of injury from other forms of decompression illness.


The appearance of bubbles in the blood or body tissues after being exposed to greater-thannormal pressure was originally termed “the bends” or “caisson disease” and, later, “decompression sickness” (DCS). Although the disease has been described throughout history, the association between bubble appearance and inappropriate decompression wasn’t initially understood. In older texts and articles, DCS is typically classified as Type 1 (joint pain, skin symptoms) or Type 2 (central nervous system and cardiovascular symptoms), but the inconsistent use of these terms has led the hyperbaric and dive medicine community to collectively refer to these injuries as decompression illness (DCI).

Figure 2: Lung overpressure injuries

Bubbles occur in the body during the ascent as pressure decreases and the volume of a gas increases. Most divers don’t realize that nearly every dive results in subclinical bubble formation. After most dives, these small bubbles are contained in the venous circulation, filtered by the lungs, and don’t cause signs or symptoms. If the bubbles created during ascent become too numerous, too large, or cross to the arterial circulation, they’ll likely manifest as some form of DCI. Once lodged in smaller vessels, platelets will adhere to the bubbles and a small clot will form, further aggravating the tissue ischemia.

In most cases, DCI occurs because the diver violated the dive tables or failed to plan their dive correctly. Dive tables were created by the U.S. Navy and adapted by the National Association of Underwater Instructors and the Professional Association of Diving Instructors for civilian use. The dive tables provide the diver with the maximum time that can be spent at a depth without having to make decompression stops in the water when they rise to the surface and to control their assent rate.

In cases where the depth-time decompression isn’t safe without stops, the diver is required to ascend at a specific rate and stop at intervals that are recommend by the dive tables. In recent years, dive tables have been supplemented or replaced by dive computers worn on the diver’s buoyancy compensator that will record the dive profile and inform the diver if they have violated the nodecompression limits.

DCI typically occurs within 30–60 minutes of returning to the surface, although minor presentations may not appear for many hours. The poor vascularity of connective tissue slows the exit of compressed gasses when ascending, so bubble formation commonly occurs in or adjacent to joints where the connective tissue density is highest. The pain in a joint can range from mild to severe and in some cases is transient. However, this type of DCI pain doesn’t radiate. Other mild forms of DCI include itching, painful pitting edema, and red or purplish-blue mottling of the skin, commonly called the “skin bends.” (See photo, p. 49.) One particularly ominous form of skin DCI is abdominal pain. This may indicate a bubble has formed in the spinal cord and is pressing on a ventral spinal nerve causing a referred pain in the abdominal skin.

Life-threatening versions of DCI include air bubbles that enter the arterial circulation and become lodged in the spinal cord or brain. Signs and symptoms of cerebral gas embolism include paralysis, coma, seizure and cardiovascular instability. Spinal cord involvement may be subtle and gradual in onset but ultimately results in severe motor deficits, and in the worst cases, paralysis.

The most serious cardiopulmonary form of DCI is called “the chokes.” The chokes usually follow a rapid, uncontrolled ascent to the surface. There’s massive bubble formation in the venous circulation that clogs the pulmonary arteries and reduces blood oxygenation. The primary symptom of the chokes include a dry persistent cough that becomes progressively worse. In severe cases there can be frothing at the mouth. Signs of hypoxia and cyanosis signal impending cardiopulmonary collapse.


Routine BLS and ALS protocols should be applied when treating any diver for a traumatic injury and extra-alveolar air injury, or suspected DCI. Every diving injury should be treated with 100% oxygen. Signs of DCI may be delayed as much as 24 hours, and therefore 100% oxygen delivered by nonrebreather mask should be given to any symptomatic patient who’s been diving in the past 24 hours—even for minor presentations such as visual disturbances, mild pain and extreme unexplained fatigue. Inhaling pure oxygen will wash most inert gas from the lungs, creating the highest possible concentration gradient to remove dissolved nitrogen and nitrogen bubbles from the blood and tissues. Maximizing oxygen concentration in the blood will also minimize tissue damage from bubble formation.

Maintain the airway and treat respiratory threats throughout transport. Extra-alveolar air resulting in a tension pneumothorax should be treated with needle decompression unless a hyperbaric chamber is immediately available. Immediately recompressing the patient should resolve the pneumothorax. Slow decompression using the U.S. Navy treatment tables may allow you to bring the diver back to normal pressure without recreating the air in the intrapleural space and avoid the need for placing a chest tube during the hospital stay.

Diving normally results in mild hemoconcentration, so an infusion of IV normal saline is appropriate. Avoid glucose-containing solutions and hypotonic solutions when treating dive-related injury and illness. Multiple medications including lidocaine, antiinflammatories and aspirin have been suggested for treating decompression illness, but none are currently supported with clinical evidence.

The appearance of bubbles in the blood or body tissues after being exposed to greater-than-normal pressure was originally termed “the bends,” as seen here. Photo courtesy Neal Pollock

Diving injuries related to ascent (extraalveolar air, arterial gas embolism, DCI) should be transported to a hyperbaric facility, preferably a center operating a multiplace hyperbaric chamber. Recompressing the patient within the chamber may resolve the symptoms of DCI by forcing the bubbles back into solution, following a slow ascent back to surface pressure while breathing oxygen. Although there’s no time limit to begin recompression, transport to the hyperbaric facility shouldn’t be delayed. Air transport will further reduce pressure around the diver and worsen DCI so ground transport is preferred.

If the transport time by ground is unacceptably long, a helicopter evacuation at the lowest safe altitude or a fixed wing transport with the cabin pressurized to 1 ATA is preferred. If possible, bring the diver’s equipment, dive computer and logbook to the hospital so the treating physician can recreate the recent dive profiles and select the appropriate recompression protocol. Don’t provide pain medication for suspected DCI. Masking the symptoms will make it impossible for a physician to gauge the success of recompression therapy. If analgesia is required to treat associated trauma, short-acting agents such as nitrous oxide are preferred.


The rarity of DCI and other diving injuries can make it challenging for EMS providers to correctly diagnose and treat these injuries. Providing 100% oxygen and rapid transport to a hyperbaric facility should be the starting point for any suspected dive-related injury.

Medical advice for treating dive injuries can be obtained 24 hours a day from the Divers Alert Network emergency hotline at 919-684-9111.

Acknowledgments: Special thanks to David Pendergast, PhD, from State University of New York at Buffalo; Dick Rutkowski, DMT, at Hyperbarics International; and the staff at Dip ’N Dive, Buffalo, N.Y., for their thoughtful comments on this article.


  • Bove AA. Diving medicine. Am J Respir Crit Care Med. 2014;189(12):1479–1486.
  • Levett DZ, Millar IL. Bubble trouble: A review of diving physiology and disease. Postgrad Med J.2008;84(997):571–578.
  • Rutkowski D: Diving Accident Management Manual. Hyperbarics International: Key Largo, Fla., 2012.
  • Vann RD, Butler FK, Mitchell SJ, et al. Decompression illness. Lancet. 2001;377(9760):153–164.