The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at The Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.
Diving
Medicine
The most common diving related injury involves middle ear barotrauma. The incidence of vestibular symptoms reaches about 20% among divers in some studies. Most importantly for this talk, as an otolaryngologist we are considered the diving experts. So it is quite probable that sometime in our career we will all see a patient who is a scuba diver. In literature there are many referrals to breath-hold divers used by kings to recover treasures for their wealth and fame. In the 17th century an open diving bell was documented, which was an air-holding chamber that prolonged possible diving times. In 1810 a copper helmet was designed, which was sealed to a watertight canvas. This allowed air to be pumped down from the surface. Today we have a modification of this original design for very deep hard-hat diving. In early 1940 Jacques Cousteu designed what was then referred to as the aqua-lung. Today it is known as the scuba device. Scuba is an acronym for self-contained underwater breathing apparatus. These were actually initially used in World War II, but because of their relatively low cost and their reliability, the apparatus was made available to the everyday diver and for recreational purposes. For those unfamiliar with scuba diving, the basic set up involves a tank, which the diver wears on his back, that delivers pressurized air via a hose and a mouthpiece, which is known as a regulator. The pressure is comparable to the aquatic depth that the diver obtains. A demand regulator either at the tank or at the mouthpiece controls the differential on the pressure from the tank air to the ambient pressure. The duration of the dive is limited to the amount of air in the tank as well as to the physiology of the diver. The weight of the air at sea level is one atmosphere, so atmospheric pressure is sea level, which is described as one square inch of air for as far as the atmosphere extends. Atmospheric pressure is also recorded as 14.7 lb. per square inch or 760 tore. One atmosphere under water is 33 feet of seawater, which is the equivalent of 34 feet of fresh water. So, there is one-foot difference in the amount of an atmospheric pressure. Probably the most important concept to understand is that when a body is submerged in water, it not only experiences the pressure from the water, but it also experiences the pressure from the air, which is called absolute pressure - atmospheric plus water pressure. As divers, we refer to the gauge pressure, which is really the pressure that is important to us and is the pressure that is exerted by the water alone. Just for comparison, 18,000 feet into the atmosphere in an airplane is the equivalent of a half of atmosphere. This gives a perspective as to what we are looking at from a diving standpoint. As you descend to deeper depths, 33 feet, 66 feet, your absolute pressure is the air pressure plus the water pressure. Basic laws govern scuba diving. Probably the most important law to us as otolaryngologists and divers is Boyle's Law. This law says that at constant temperature, volume and pressure are inversely related. Since we deal with air-filled cavities, this is clearly the most common law relating to us as otolaryngologists. Remember that soft tissue is mostly made of water and is relatively incompressible compared to air-filled spaces. However the sinuses and the middle ears are all affected by pressure changes. Again, a scuba diver breathes air through his tank, through his glottis, which is delivered to him at one atmosphere pressure. As the diver descends deeper into the ocean, the pressure increases but the lung volume remains constant. However, even at deeper depths, inspiration becomes more difficult because as the density of the molecules changes, it becomes more difficult to breathe the air. As the diver descends, the pressure increases in the lungs because depth pressure increases. However, the volume stays the same. The volume is constant, the density changes and the pressure changes. The fact that the lung volume stays the same is what protects the lungs while we are diving. Breath-hold diving or free diving is a very common sport especially in Hawaii and along the West Coast. Even snorkeling involves diving using only mask, fins, and a snorkel. Most of these divers are limited to 1-2 atmospheres of gauge pressure in their depth. Again the thing to remember with these divers is that their lung volumes will be changing because they are not using a scuba apparatus to equalize their pressures. At one atmosphere, the lung volume goes down by ½ and at two atmospheres their lung volume is reduced by 1/3 again. Those are important concepts to remember. The second law is Dalton's Law, which basically says that in a gas mixture, pressure exerted by each gas is the same as it would exert if it alone occupied the same volume. So, as you increase the total pressure, the relative contributions of each gas in the mixture remain the same. If oxygen is one-third of the mixture at sea level, even if you decrease or descend to three atmospheres pressure, it still would have an equal contribution. The contribution of oxygen triples to the total mixture. This is extremely important with the biological effects of gas. The partial pressures of each individual gas in the tank determine the tissue diffusion and the amount of gas that is ultimately dissolved in the body tissues and in the blood stream. Remember that oxygen delivery depends on PO2 and not on total gas pressure. A good example to illustrate this is that at sea level the PO2 is 16 tore, which is 21% of 760 tore. At 132 feet of seawater, which is four atmospheres, the PO2 is equivalent to breathing 100% air at sea level. This shows that even though it has the same amount of concentration at that depth and the relative contribution is the same, because the pressure is so much greater, the effects are quite different. This can lead to oxygen toxicity, because breathing the equivalent of 100% oxygen is very difficult and very damaging to the body over long periods of time. The last law
of Physics to consider is Henry's Law, which basically says that given
temperature, the mass of the gases dissolved, and the given volume
of solvent is proportional to the pressure of the gas with which it
is at equilibrium. Basically, this law dictates how much of a gas
is absorbed at a given pressure. This is important when we discuss
things like nitrogen narcosis and decompression sickness. Again, this
is most important when applied with nitrogen solubility in the body
tissues during descent and then the relative insolubility when ascent
is performed. Divers themselves refer to another law: Martini's Law. This law states for every 50 feet of descent, a diver breathing tank air experiences the equivalent of drinking one martini on an empty stomach. At dives of 100 feet of seawater, or even down to close to 150 feet of seawater, the effect can be like drinking three mixed drinks with no food in your stomach. This can become extremely dangerous especially when the diver needs to make quick decisions and needs to determine exactly what his dive bottom times should be. Commercial divers who dive much deeper than recreational divers, often substitute helium in their gas mixtures for nitrogen in order to limit the anesthetic effect and to allow them to dive deeper without intoxicating effects. Ears, sinuses, and the neighboring structures are all susceptible to injury during diving. The ear and the Eustachian tube are considered to be the weak links in our body's ability to tolerate diving situations. The nasopharyngeal opening of the Eustachian tube is usually closed. As we all know, it opens with positive nasopharyngeal pressure or by contracture of a number of muscles: tensor vallee palantini, lavatar palantini, and the palato pharyngeus muscles contract and open the nasopharyngeal orifice of the Eustachian tubes. In 1937 Armstrong and his colleagues did a very interesting study of something that is probably obvious to us now. Upon descent with divers he found that the Eustachian tube acts as a flutter valve and actually is closed and only opens if the diver equalizes. The Eustachian tube will not open on its own under these pressures to equalize middle ear pressure. It has to be reflexive or voluntary, an act made by the diver himself to ensure that his middle ear pressure is equalized throughout his dive. If pressure is not equalized, the diver experiences what is commonly called a middle ear squeeze, which refers to barotrauma of the middle ear. A Valsalva, which involves holding the nose, closing the mouth and exhaling against a closed glottis, is one of the techniques used to re-inflate or auto-inflate the middle ear and equalize the pressures. If divers have upper respiratory infections, allergies, nasal polyposis or septal deviation, they increase their risk of middle ear squeeze because of their inability to equalize their pressures. The most common or simple problem that can occur is occlusion of the EAC, which can be related to cerumen, ear plugs, or a hood used in cold water diving. The diver experiences pain during descent because of the pressure build-up due to the occlusion. On examination of these patients, we see congestion of the external auditory canal skin and often of the TM as well, with edema in the canal. There may be rupture of the skin and even a tympanic membrane perforation from this problem, which will cause hemorrhage and severe, severe pain. Treatment is conservative: stay out of the water and do not scuba dive until the area is completely healed. Probably the most common problem involving the EAC with scuba divers is otitis externa. This is often due to the water exposure or divers drying their ears excessively with cotton after a dive. It is a fairly simple problem, and for a mild case, the patient should use acidified alcohol solution after dives, often called Swim Ear. There are also silicone oil sprays that divers can apply to the EAC skin before dives, providing a protective coat. The most common problem in the middle ear is barotrauma, also known as aerotitis media or middle ear squeeze. When scuba divers make their descent, the most critical time is within the first atmosphere. It is most important that pressure is equalized properly. If pressures are not equalized, the diver will experience severe otalgia. This can lead to subsequent tympanic membrane rupture. This can actually occur at even just a few feet of water and in pressure differences as low as 5 pounds per square inch. With a tympanic membrane rupture, there is often otorrhea and the diver frequently experiences dizziness and some form of a mild hearing loss. At surface pressure all pressures are equalized. As a diver descends, the ambient pressure increases and the pressure in the middle ear should be equalized through the Eustachian tubes. However, if there is a block in the Eustachian tubes, the diver can no longer equalize his pressures. If he continues to submerge or to descend, this pressure will increase and eventually the weak link in the system will give, which means that the tympanic membrane will likely rupture. If the diver chooses to return to the surface he can do so. However, he will continue to experience the problem and the situation is often even worsened because small amounts of oxygen are actually absorbed through the middle ear, further increasing the negative pressure differential in the middle ear and causing further pressure. Mucosa edema of the middle ear occurs and there is hemorrhage into the small capillaries. Treatment involves the use of systemic decongestants and mucolytic agents plus or minus an antihistamine for patients experiencing allergy. The otolaryngologist should also instruct the diver to perform periodic auto-inflation if he is not having pain without movement. If continued pain occurs, it usually indicates a middle ear infection. At that time, a decision needs to be made whether the patient would benefit from a myringotomy or PE tube and certainly antibiotics. With a tympanic membrane perforation, the original treatment is the same as always: with oral hygiene and ototopical agents, these usually close non-surgically. However, tympanoplasty is indicated for persistent perforation. Divers should
be encouraged to concentrate on prevention of these injuries. A nasal
decongestant before a dive can help prevent this sort of problem.
When these medicines are applied to the nose, the position of the
head is very important. The diver should actually have his head down
so that the medicine can reach the Eeustachian tube ostium more easily.
Some divers use systemic decongestants, such as Sudafed, and often
add an antihistamine for allergy. It is very important to remember
that these should be non-sedating medicines and that no new medicines
should be given before a dive unless that have already been tried
on the surface. Some divers begin Valsalva and auto-inflation in the middle ear before they even begin their dive. With a very forceful Valsalva, a diver can experience barotrauma. This is related to an increased intrathoracic and abdominal pressure, which ultimately increases the CSF pressure via engorged spinal veins, which can be transmitted to the endolymph, the cochlea, perilymph, and eventually to the round window and oval window membranes. This leads to tinnitus and usually a unilateral high frequency hearing loss. Another preventative measure is the Frenzel maneuver, which involves holding the nose, closing the glottis and contracting the pharyngeal muscles. This also forces air into the Eustachian tubes. Some people are able to perform this to equalize pressure and don't have to use a Valsalva technique. Other preventive measures include using a feet-first descent. Multiple studies have shown that it is easier to inflate the middle ear with the head up, as this causes less hyperemia of the Eustachian tubes and mucosa. The diver is also less distracted with his head up, and it may help him to remember to continuously auto-inflate his middle ear every 2-3 feet as he makes his descent. An anchor line on the boat should also be used to verify exactly how deep the diver is. If a diver experiences middle ear squeeze, he should ascend a few feet and attempt to auto-inflate, and then begin the redescent. It is also important to have a form-fitting mask, so that nasal compression is easier to perform. Jaw and head movements from side to side are often used to facilitate middle ear inflation. One of the more uncommon problems seen in divers is what is known as ultinebaric facial paralysis. This is extremely uncommon. This is due to dehiscent portions of the facial nerve, which are vulnerable to barometric trauma. It is usually seen in normal people who descend during a dive, but when they ascend and get to the surface, they have a facial paralysis. This is almost always a transient paralysis and is related to barotrauma. These divers almost always resume normal function of the facial nerve over time. Inner ear problems in divers are usually related to middle ear barotrauma. As we have discussed, middle ear negative pressure causes a depression of the tympanic membrane. This can be transmitted to the ossicle of the stapes and cause significant and rapid foot plate depression, which can tear the sensitive inner ear membranes and lead to the types of hearing losses we have discussed. The second thing that can occur in the inner ear is sudden pressure equalization, which can cause a rush of air up the Eustachian tube, putting an outward force on the tympanic membranes and the ossicles and pulling the stapes footplate up. This can cause a pressure wave in the inner ear and distort the inner ear membranes. All these membranes are extremely fragile. There are multiple theories as to how the trauma occurs. But it is thought that either Ricener's membrane or the basilar membranes are involved or the vestibule and semi-circular canals are involved. The shearing force of this rapid fluid movement is transmitted to the labyrinth and cochlea and can cause tears in the membranes and hemorrhage from the small torn vessels. Round window implosion is a well-described problem in the literature from inner ear trauma during diving. This involves a pull on the stapes footplate and a shock wave through the scala vestibuli to the scala tympani. It causes a bulging inward from a rapid pull on the stapes footplate and it causes an inward pull on the round window membrane, which causes an implosion injury and the leakage of perilymph into the middle ear. A sudden pull on the stapes footplate can also lead to a tear of the annular ligament of the oval window, leading to a crack in the footplate and also leakage. Frequently when divers are having a difficult time auto-inflating, their first inclination is to try harder to equalize the pressure. This can lead to the elevation of the CSF pressure that can be transmitted directly through a patent cochlear aqueduct into the internal meatus, raising intracochlear pressure to dangerous levels. The difference between the middle ear and the perilymph space can cause an explosive outward rupture of the round window membranes. It is the opposite of the implosion injury, an outward injury, which can cause perilymph leakage and a perilymph fistula. Dr. Healy and his colleagues did a study that looked at 40 cases of perilymph fistula in divers. The patients' chief complaints with this problem were episodic positional vertigo. They did not have as many complaints of hearing loss or tinnitus. These patients all underwent surgical exploration. At exploration, 31 out of 40 of these patients (75% of them) had oval window leaks, 5 of them had round window leaks, and 4 of them had both oval window and round window leaks. None of these patients had a hearing loss for longer than 3 weeks. They regained any significant hearing in those ears. If the suspicion is high for a perilymph fistula, early exploration leads to the best hearing restoration. Healy felt that the most important factors during these procedures were proper magnification, and patience. He commented that after blotting in the middle ear, it often took 5 to 10 minutes for perilymph to build back up or for a leak to be revisualized. In two patients he had to perform bilateral jugular vein compression to enhance the perilymph leakage. To summarize, hearing loss and dizziness are indicative of inner ear barotrauma and require immediate treatment. Depending on the etiology, or presumed etiology, treatment involves strict bedrest and convalescence, no coughing, no sneezing, auto inflating or straining. These patients all deserve an audiogram to determine whether this is a middle ear or an inner ear problem. With inner ear problems with a cochlear etiology, you will see a non-progressive centrally neural hearing loss. And, as I said, with a perilymph fistula one way to distinguish it is that there is often a progressive and fluctuating hearing loss. In the study by Healy, he also found that posturography with EAC pressure changes have a 97% sensitivity for diagnosing a perilymph fistula. Antonelli and his colleagues did a study looking at 18 temporal bones examined from 11 divers who died from complications during diving, either from rapid ascent or drowning. He found that bleeding into the middle ear and mastoid air cells was nearly universal in all these divers. The most common damage seen was bleeding around Ricener's membrane and the round window membrane. He also found that a number of these divers, usually the ones who had rapid ascent injuries, had rupture of both the utricle and saccule and that tympanic membrane rupture from rapid ascent was far more common in people who dive than had been presumed. The other interesting point was that most of the inner ear damage was not surgically treatable. Other than for the perilymph fistula, most of these injuries do not have surgical treatments. Lastly, Zannini and his colleagues followed 160 professional divers with serial audiograms. He found that these 160 divers had significantly worse hearing than control divers. The greatest loss was in the group with the longest diving times. He found that their hearing losses were in the highest frequencies, usually in the 8 kilohertz. Divers who reported difficulty auto inflating their middle ears had even worse hearing or the most central hearing loss. Zannini also commented that perilymph fistula demands early surgical exploration and that inner ear barotrauma is managed medically with vasodilators, steroids, histamines, and Carbogen. There is a different set of problems that divers can experience during descent which involve the sinuses. This is called aerosinusitis or sinus squeeze and involves osteomuculuson and pressure equalization. It is really infrequently an issue in the sinuses but if you have a demitasse mucosa with an upper respiratory infection, an allergy, a polyp occluding the ostium or a septal deviation, this can cause a problem and mimic what happens in the middle ear. You get a negative pressure in the sinuses because of the inability for the pressures to equalize. This causes a vacuum, which can lead to mucosal edema, hemorrhage and severe pain. Management includes sinus irrigation and either endoscopic sinus surgery, if it is a polyp, or septoplasty to straighten the septum. Tooth squeeze or aerodontalgia is a very uncommon problem. The most common cause of tooth pain in the diver is from aerosinusitis. But aerodontalgia can be caused by an air pocket underneath the tooth cap or filling. It causes severe pain when the diver descends and the pressure changes. To treat this condition, dental work should be done and the filling or cap should be replaced. Facemask squeeze is failure to equalize pressure changes in the facemask. It can lead to tissue damage from the pressure differential in the mask along the soft tissues. The most common areas of injury are around the eyeball and the lining of the eyelids where the mucosa is quite sensitive. Exhaling through the nose and into the facemask and equalizing the pressure that way easily prevents facemask squeeze. Epistaxis is bleeding from the nose into the mask underwater. It is a very common problem. The bleeding is due to pressure changes on Keisselbach's plexus. Oftentimes the diver will not even recognize that he has had a nosebleed. As you move underwater, the selective absorption of color by the blue green seawater makes blood appear blue green. So oftentimes the diver will ascend to the surface and then realize that his mask is full of blood. There is no treatment required. Almost all of these invariably resolve within minutes of reaching the surface just through external compression on the nose. Alternobaric vertigo is another problem seen in divers. This is transient vestibular dyfunction due to dysequilibrium of pressures in the two middle ears. It can lead to vertiginous feeling and has been seen in up to 15% to 16% of divers in some series. When you are underwater, any sort of incoordination or change in equilibrium can be extremely dangerous. These patients usually have poor auto-inflation and don't usually have any hearing loss or tinnitus. To correct this problem, the diver should reverse the direction of movement, allowing the vestibular system to equilibrate. Another way to correct this involves auto-inflating the middle ear to equalize the pressures. Finally, unequal caloric stimulation vertigo is a problem seen when cold water enters only one ear (due to either an external canal obstruction or a hood). It is like a caloric stimulation test. The best way to treat this is by removing the obstruction so that both of the ears are sensing the cold water at the same time. Anxiety is the most common cause of dizziness in the diver. It is actually not due to the vestibular system. There are multiple studies that say that greater than 50% of all scuba deaths are due to panic or anxiety in the diver. Treatment would include educating yourself properly before you scuba dive. Go through proper certification and never dive alone. TMJ syndrome is caused by forcefully biting down on the regulator. This is frequently seen in novice divers who become anxious and excited and then bite down. It is treated just like any other treatment of TMJ, with reassurance, heat, NSAIDS and a soft diet There are other problems that divers may encounter that are associated with ascent. These are pulmonary rather than pressure accidents and these are very serious problems. These are all caused by holding of the breath during ascent and can be predisposed in patients with obstructive lung disease. At the surface, the pressures are all equal. As we descend, the ambient pressure increases and the lung pressure increases as well. As we are breathing, the pressures all stay equal because of our scuba apparatus. However, if we don't breath during the ascent, the pressure in the lungs stays high and the pressure on the outside stays low. The lung pressures are higher than ambient pressure and this pressure has to go somewhere.
The second thing is pneumothorax, which is caused by air from alveoli rupturing into the pleural cavity. It is sudden and rapid and causes shortness of breath and labored breathing and can actually be life-threatening underwater. The treatment is a chest tube. On a boat, or out in the water when a chest tube is not available, a large bore needle with a condom or a piece of plastic can substitute as a one way air valve to ventilate the air pressures. These patients need to be put on 100% oxygen immediately and, for this type of pneumothorax, patients should undergo chamber recompression. The most serious problem that occurs in diving is an air embolism, a devastating problem that can lead to neurologic complications. This occurs when alveoli and pulmonary blood vessels rupture and air bubbles get to the blood stream and then track to the body. If these end up in the cerebral circulation they can coalesce to form larger bubbles and actually entirely block the cerebral circulation. These divers usually experience loss of consciousness after surfacing. Frequently, while still in the water, they have frothy, bloody sputum and complain of chest pain, confusion, and blurry vision. These patients need to be transferred immediately to recompression chambers and frequently need treatment in these chambers intermittently for up to 2 weeks. If you are ever with a diver and suspect air embolism, the diver needs to be transported in the left lateral decubitus position. Air rises, so we want them in the left lateral decubitus to prevent a bubble from blocking the left ventricular outflow track. They also need 100% oxygen. Another issue is air evacuation, since flying in an airplane or at elevation can cause an increased bubble formation in the body. However, if the issue is getting the patient to a recompression chamber as quickly as possible, then the risk is usually warranted, as opposed to taking them by ground. Not holding the breath, and just breathing normally as the ascent is made will prevent air embolism. Also, make sure that patients with obstructive lung disease do not scuba dive. Case Presentation The patient is a 25-year-old male with extensive SCUBA diving experience who was on a dive with friends. The patient was nearing the end of his dive and noted his gauge air pressure to be at 500 psi. He began to surface when, at 50 fsw depth, he begun to breathe 'heavy air', indicating a lack of adequate remaining air in his scuba tank. He emergently descended to his dive buddy at 80 fsw depth and began to share his companion's air. During his emergent re-descent, he noted severe otalgia while failing to equalize his middle ear pressure. Upon reaching the surface, the patient noted left-sided bloody otorrhea and rhinorrhea. He also experienced mild dizziness. On subsequent otolaryngologic exam, the patient had a 25% left tympanic membrane perforation. His dizziness had completely resolved. 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©2001,
The Bobby R. Alford Department of Otorhinolaryngology and Communicative Sciences,
Baylor College of Medicine
One Baylor Plaza, NA102, Houston, TX 77030 oto@bcm.tmc.edu
URL: http://www.bcm.tmc.edu/oto (Modified: 12/11/01)