I have to say that scuba injuries are not my strong suit. However, in doing this blog post, I have to say it’s not the worst thing to read about. For instance, you get a lot of random information like for some reason depth is measured in fathoms (which is just 2 yards, and seems completely unnecessary to have this). Also since a lot of these disorders were discovered in the 1800s, they have awesome nicknames like the bends, rapture of the deep, the chokes, and all the squeezes including face squeeze and ear squeeze.
For this blog post, I wanted to keep it simple and have it be a quick rundown of the things we need to know when looking at diving injuries as well as when our friends inevitably ask about if it’s okay for them to go diving. And as always, end on some fun history.
These are the more commonly seen injuries with diving. They occur from increasing pressure as the person dives deeper. Water is obviously far denser than air so submerging up to 30 feet can increase pressure significantly. For instance, a person would only need to dive to 33 feet to double atmospheric pressure, whereas a person would need to climb 18,000 feet from sea level to decrease atmospheric pressure 50%.
These injuries are all associated with barotrauma from the increasing pressure and include Middle Ear Barotrauma (most common disorder), Barosinusitis (2nd most common disorder), Facial Barotrauma (Face Squeeze), Inner Ear Barotruama, and External Ear Barotrauma.
The good news about these injuries is they are easily avoided with certain maneuvers that are taught to all divers. The maneuvers equalize pressures during descent preventing associated barotrauma. Furthermore, if these injuries do occur, they are often self-limited or treated in regular fashion (e.g. a perforated eardrum is still a perforated eardrum, no matter the cause)
These are the more serious conditions. These are the ones we associate with hyperbaric chambers. The literature likes to subdivide these into Decompression Sickness (DCS)–which can be further divided into Type I (MSK, skin, and lymphatics), Type II (neurologic)–and into Arterial Gas Embolus (AGE). However, there is a movement to lump these all together into “Decompression Illness,” which I think is fitting because they have the same etiology and same treatment.
The main thing to know about the above is that “Decompression Illness” occurs from nitrogen bubbles forming while a diver ascends. The nitrogen bubbles can deposit in any part of the body leading to joint pain, rash, lymphatic obstruction (edema), CNS (neurologic symptoms), or lead to embolus that can go to any tissue. Initial treatment is with 100% O2. The O2 displaces nitrogen gas in the lungs which increases the gradient allowing for the removal of nitrogen at higher rates. In addition, no matter the presentation, these pts should be sent for recompression therapy. The faster they can get to a hyperbaric chamber, the better their outcomes. However, no matter the timing, they should be transferred to a hyperbaric facility as there is evidence of improved mortality and morbidity at up to 24 hrs.
Pulmonary barotrauma can also occur during ascent. This is usually prevented by continuously breathing during ascent. For instance, if a diver took a full breath at 33 feet and held the breath during ascent, the lungs would need to double in size to accommodate the expansion of air. Although the lungs show great compliance, this could result in the rupture of alveoli and lead to pneumothorax, pneumomediastinum, subcutaneous emphysema, and/or alveolar hemorrhage. The great thing about this, though, is that it starts with the same treatment as above–with 100% FiO2. Furthermore, these pneumothoraces are often small and do not require a chest tube. (Of note, however, if a pt had concomitant DCS, then a chest tube should be placed prior to recompression therapy as could potentially lead to tension pneumothorax).
Differentiating These Disorders
Some of the above disorders can have similar presentations. For instance, ear barotrauma can lead to nausea, vomiting, vertigo, ataxia as can DCS with neurologic symptoms. However, these can be easily differentiated by the timing (e.g. ascent vs. descent) of the symptoms as well as the diving logs. All scuba divers are expected to keep a diving log (which includes duration and depth of diving). Based on these logs, you should be able to calculate the risk for DCS that a diver would have.
Differentiating pulmonary DCS from arterial gas embolus could also be difficult. However, arterial gas embolus is often more acute, occurring within 10 minutes of ascent, while DCS often has sporadic and progressive course, occurring >10 minutes after ascent. However, I would also argue that this really does not matter as you will still treat with 100% FiO2 and transfer to hyperbaric facility despite the etiology.
Who Can’t Dive
I mainly included this section because I think we were all curious as to whether Dr. Heinrich could dive. Also as doctors, we should be able to impress all our friends and family with answers to any medical question they could ever have.
- It is recommended that pts with recent sinusitis or URI abstain from diving for 2 weeks after resolution of symptoms. This is due to increased risk of ear and sinus barotrauma as they cannot equalize pressures adequately during descent. My roommate actually went diving with sinusitis (he didn’t want to delay his certification for his trip), and he ended up perforating his eardrum. It was the first time I saw nystagmus, and he ralphed everywhere–it was great. He had to get certified at another time.
- I felt like this goes without saying, but pregnant pts should also avoid scuba diving. This is actually due to the increased risk of the fetus developing DCS as the majority of fetal circulation bypasses the pulmonary bed (where nitrogen bubbles are expired). Scuba diving and pregnancy has been associated with low birth weight, prematurity, congenital malformation, and spontaneous abortions
- And then there is COPD and asthma… I read a few different guidelines on this, but Rosen’s has a nice section that combines all these recommendations. Essentially, asthma is only contraindicated if in active flare (which was defined as requiring rescue inhaler within previous 48 hrs). It was also advised to abstain from diving if asthma was cold-, exercise-, or emotion-induced as diving involves all of these. The reason for these recommendations is that asthmatics were at a 2-fold increased risk of pulmonary barotrauma (e.g. pneumothorax) than the general population.
Paul Bert (1833-1866) is credited for the discovery of oxygen toxicity (known as “the Paul Bert Effect”) as well as the implication of nitrogen in Decompression Syndrome. He was given the nickname “The Father of Aviation Medicine” as he worked on much of the physical effects seen on climbers and “balloonists” during that time. He also became interested in diving science after reading about Dr. Alphonse Gal’s first-hand experience of diving disorders. He not only helped to discover the cause of decompression sickness, but also posited that it could be prevented with slower ascents and treated with 100% FiO2 and recompression chambers.
Rosen’s Emergency Medicine : Concepts and Clinical Practice. St. Louis :Mosby, 2002. Print.
Dive-Tech, Mark Powell. Dive-Tech: Decompression Theory – Paul Bert and John Scott Haldane, www.dive-tech.co.uk/bert and haldane.htm.