Ear Decompression Sickness Research Articles

The lifetimes of small arterial gas emboli, and their possible connection to Inner Ear Decompression Sickness

We solved both the Diffusion and Laplace equations which predicted very similar results for the problem of a dissolving small gas bubble suspended in a liquid medium. These bubbles dissolved both because of surface tension and solute concentration effects. We focused on predicting bubble lifetimes (“td”), and dissolution dynamics — radius vs time (R vs t) for these contracting bubbles. We also presented a direct comparison of the predicted results, obtained by applying either Dirichlet or Neumann boundary conditions, to the bubble/medium interface. To the best of our knowledge, this is the first direct comparison that has ever been published on the application of these different boundary conditions to a moving gas/liquid boundary. We found that the results obtained by applying either Dirichlet or Neumann boundary conditions were very similar for small, short-lived bubbles (R0<25μ,td<40s), but diverged considerably for larger, longer-lived bubbles. We applied our expressions to the timely problem of Inner Ear Decompression Sickness, where we found that our predictions were consistent with much of what is known about this condition.

Ear Problems and Injuries in Athletes

The ear is an unique organ--the principal structure involved in both hearing and balance. Although not common, problems with the ear may be encountered in specific sporting populations. Common conditions affecting the ear in the athlete include otitis externa, an infection of the external ear; external auditory canal exostoses, or abnormal bony growths in the canal; and otitis media, an infection of the middle ear. Given its position on the head, the ear is subject to trauma, often resulting in an auricular hematoma. Divers, due to pressure changes on descent and ascent, are subject to both ear barotrauma and ear decompression sickness. This article will discuss recognition, treatment, and prevention of these conditions affecting the ear in the athlete.

Benign Paroxysmal Positional Vertigo Caused By Swimming

Benign paroxysmal positional vertigo (BPPV) is characterized by mechanical dysfunction of the vestibular system in the inner ear. Displacement of otoconia from utricle to semicircular canals is held responsible for the development of BPPV. Etiologic factors are mostly classified as idiopathic. Head trauma, viral labyrinthitis and otologic surgery are also included [1, 2]. A 58 year old, female patient was admitted to Ear Nose Throat Clinic with sudden onset of vertigo and nausea. In her detailed history, she had had a long-term swimming activity just before the onset of symptoms. She reported that her house is on the seaside in Antalya, and she swims as a recreational activity for 3-5 days/week every summer. She had been using the freestyle swimming technique (front crawl) and rotating her head to the left for breathing. Different from previous swimming sessions, she had swam faster at the last session. She did not have a history of head injury, upper respiratory tract infection or drug usage that affect the vestibular system in the last 2-3 weeks. Otoscopic examination was normal. Head shake, head thrust and Romberg tests were positive. Dix-Hallpike test was positive on the right side. During the test, horizonto-rotatuar nystagmus with latency period was observed. Other neurological examination findings were normal. Pure tone audiometry and tympanometry tests showed normal values. There was no limited range of motion of the neck. The patient was diagnosed as BPPV. There was no need for imaging of central nervous system because the Dix-Hallpike test was positive (peripheral vertigo) and neurological examination was greatly normal. Right Epley maneuver was performed for therapeutic approach (1 session). The patient's symptoms dramatically declined after the particle repositioning maneuver. In addition, the patient was referred to Sports Medicine Clinic for recommendations about the swimming sport. In order to prevent the possible recurrence, it was recommended to mainly use the backstroke style in which the head is in a more fixed position. It was also told to her that she should avoid rapid head movements during stroke, and should breathe on both sides while swimming in freestyle. Additionally, “ear band” was advised to use. After two weeks, she was able to return to swimming. After 12 months, the patient was called by phone. There was no symptomatic recurrence in 1 year. She could continue swimming activity without any problem in the subsequent summer. There are various studies in the literature showing the relationship between water sports and inner ear disorders. However, the majority of these studies are focused on diving related (inner ear decompression sickness) and water skiing related (traumatic audiovestibular injury) problems [3–6]. There is limited information in the literature about vestibulopathies due to surface swimming. Among the surface swimming styles (freestyle, breaststroke, backstroke, butterfly etc.); the freestyle swimming requires the fast rotational movements of the head. Aksoy and Sennaroglu [7] showed that the freestyle swimming takes a place in the etiology of BPPV. They also reported that there is no correlation between BPPV with duration and frequency of swimming. However, in our case, the patient had increased the speed of swimming at the last swimming session. Her head movements had accelerated toward the left for breathing. For this reason, swimming speed may play a greater role in development of BPPV than swimming duration and frequency. In another study, Giacomini et al. described two cases of BPPV due to intense swimming activity [2]. Conditions different from BPPV can cause vertigo in swimmers. It has been reported that asymmetric thermal inputs following water exposure may cause vertigo in swimmers who had undergone mastoidectomy [8]. A swimmer was reported as a case of vertigo that had been induced by compression of the vertebral artery [9]. This vertigo was a part of the complex clinical picture due to cerebellar stroke. Therefore, treatment had become intensive. Heidenreich et al [10] described the abnormal afferent activity in the neck due to recurrent head movements while swimming as “cervicogenic dizziness“. Their patient had neck pain which was effectively treated with physiotherapy. We concluded that a detailed history will help to reduce the cases which are classified as idiopathic BPPV. Freestyle swimming should be noted in the etiology of BPPV because it contains repetitive rotational movements of the head. Increased swimming speed seems to trigger the development of BPPV in our case. However, extensive studies are needed to reveal the effects of speed, duration and frequency of swimming on the vestibular system. After diagnosis of BPPV, the Epley maneuver should be preferred in treatment because it is simple, safe, non-invasive and has a high success rate.

Severe Capillary Leak Syndrome after Inner Ear Decompression Sickness in a Recreational Scuba Diver

BackgroundPost-decompression shock with plasma volume deficit is a very rare event that has been observed under extreme conditions of hypobaric and hyperbaric exposure in aviators and professional divers. Case ReportWe report a case of severe hypovolemic shock due to extravasation of plasma in a recreational scuba diver presenting with inner ear decompression sickness. Impaired endothelial function can lead to capillary leak with hemoconcentration and hypotension in severe cases. This report suggests that decompression-induced circulating bubbles may have triggered the endothelial damage, activating the classic inflammatory pathway of increased vascular permeability. ConclusionThis observation highlights the need for an accurate diagnosis of this potentially life-threatening condition at the initial presentation in the Emergency Department after a diving-related injury. An elevated hematocrit in a diver should raise the suspicion for the potential development of capillary leak syndrome requiring specific treatment using albumin infusion as primary fluid replacement.

Susceptibility of the Inner Ear Structure to Shunt-Related Decompression Sickness

Decompression sickness (DCS) is caused by formation and growth of bubbles from excess dissolved gas in body tissues following reduction in ambient pressure. Inner ear decompression sickness (IEDCS) is a complex disorder involving the vestibulo-cochlear apparatus whose pathophysiology remains incompletely understood. The records of 662 consecutive DCS cases treated over a 7-yr period at 2 UK hyperbaric units were examined for symptoms suggesting IEDCS (nausea, vomiting, dizziness, and hearing loss arising within 2 h of surfacing). For IEDCS cases, demographics, dive, treatment, and outcome data were extracted with particular attention to the outcome of testing for a right-to-left shunt. Included were 31 men and 2 women with a mean age of 46 yr (range 31-61 yr). Of these, 16 patients had isolated IEDCS and 17 patients had associated symptoms ranging from joint pain to tingling and numbness. The depth of the dive leading to the incident ranged from 49-256 ft (15-78 m). As primary treatment, 21 patients received a U.S. Navy Treatment Table 6 (USN TT6) and 11 patients received a Comex 30. No difference in the speed of recovery or number of treatments needed was seen between the two tables. All patients were advised to have a right to left shunt (RLS) check, but only 30 complied with that, with 24 (80%) testing RLS positive. Our retrospective study confirms the correlation between IEDCS and the presence of a significant patent foramen ovale (PFO). In our series 48% of patients had an isolated IEDCS. IEDCS responds slowly to treatment irrespective of the initial table used. Recovery is thought to be mainly a central compensation process.

Inner ear decompression sickness in scuba divers: a review of 115 cases

Inner ear decompression sickness (IEDCS) in scuba divers is increasingly observed, but epidemiological data are limited to small case series and the pathogenesis remains elusive. We report our experience over a 13-year period. We also thought to demonstrate that the development of this injury is mainly attributed to a mechanism of vascular origin. Diving information, clinical data, presence of circulatory right-to-left shunt (RLS), and laboratory investigations of 115 recreational divers were retrospectively analyzed. A follow-up study at 3 months was possible with the last 50 consecutive cases. IEDCS (99 males, 44 ± 11 years) represented 24 % of all the patients treated. The median delay of onset of symptoms after surfacing was 20 min. Violation of decompression procedure was recorded in 3 % while repetitive dives were observed in 33 %. The median time to hyperbaric treatment was 180 min. Pure vestibular disorders were observed in 76.5 %, cochlear deficit in 6 % and combination of symptoms in 17.5 %. Additional skin and neurological disorders were reported in 15 % of cases. In 77 %, a large RLS was detected with a preponderant right-sided lateralization of IEDCS (80 %, P < 0.001). Incomplete recovery was found in 68 % of the followed patients. Time to recompression did not seem to influence the clinical outcome. IEDCS is a common presentation of decompression sickness following an uneventful scuba dive, but the therapeutic response remains poor. The high prevalence of RLS combined with a right-sided predominance of inner ear dysfunction suggests a preferential mechanism of paradoxical arterial gas emboli through a vascular anatomical selectivity.

International classification of diseases and diving illnesses

Post-decompression shock with plasma volume deficit is a very rare event that has been observed under extreme conditions of hypobaric and hyperbaric exposure in aviators and professional divers.We report a case of severe hypovolemic shock due to extravasation of plasma in a recreational scuba diver presenting with inner ear decompression sickness. Impaired endothelial function can lead to capillary leak with hemoconcentration and hypotension in severe cases. This report suggests that decompression-induced circulating bubbles may have triggered the endothelial damage, activating the classic inflammatory pathway of increased vascular permeability.This observation highlights the need for an accurate diagnosis of this potentially life-threatening condition at the initial presentation in the Emergency Department after a diving-related injury. An elevated hematocrit in a diver should raise the suspicion for the potential development of capillary leak syndrome requiring specific treatment using albumin infusion as primary fluid replacement.

Hearing loss in divers: a 6-year prospective study

Occupational diving is associated with hearing loss, but the cause is disputed. Our aim was to follow a cohort of divers through the first 6 years of their career in order to look for evidence of permanent threshold shift associated with diving activity, occupational noise exposure or acute injuries. Hearing was measured by pure tone audiometry in 67 participants at a basic course for working divers. Hearing thresholds were adjusted for age (ISO 7029). The subjects were examined and interviewed by an otologist. Additional medical and exposure data were recorded in questionnaires and personal logbooks. The procedure was repeated after 3 and 6 years. None of the subjects suffered inner ear barotrauma or inner ear decompression sickness during follow-up. Middle ear barotrauma was common. The prevalence of subjective hearing difficulties increased during follow-up, and there was a significant threshold shift at 4 kHz (mean 2.6 dB, 95% confidence interval 0.9-4.3 dB). Both subjective and objective hearing loss was associated with occupational noise exposure, but not with diving frequency or with a history of middle ear barotrauma. In the absence of manifest inner ear barotrauma or inner ear decompression sickness, noise seems to be the most important cause of long-term hearing loss in occupational divers. This study did not find evidence of long-term hearing loss caused by uneventful diving per se.

Selective vulnerability of the inner ear to decompression sickness in divers with right-to-left shunt: the role of tissue gas supersaturation

Inner ear decompression sickness has been strongly associated with the presence of right-to-left shunts. The implied involvement of intravascular bubbles shunted from venous to arterial circulations is inconsistent with the frequent absence of cerebral symptoms in these cases. If arterial bubbles reach the labyrinthine artery, they must also be distributing widely in the brain. This discrepancy could be explained by slower inert gas washout from the inner ear after diving and the consequent tendency for arterial bubbles entering this supersaturated territory to grow because of inward diffusion of gas. Published models for inner ear and brain inert gas kinetics were used to predict tissue gas tensions after an air dive to 4 atm absolute for 25 min. The models predict half-times for nitrogen washout of 8.8 min and 1.2 min for the inner ear and brain, respectively. The inner ear remains supersaturated with nitrogen for longer after diving than the brain, and in the simulated dive, for a period that corresponds with the latency of typical cases. It is therefore plausible that prolonged inner ear inert gas supersaturation contributes to the selective vulnerability of the inner ear to short latency decompression sickness in divers with right-to-left shunt.

Behandlung akuter kochleovestibul�rer Sch�digungen nach dem Tauchen

There has been a steady in-crease of recreational scuba divers in the last years. The majority of diving associated diseases involve otorhinolaryngology, the most important of which are cochleovestibular dysfunctions as these can lead to permanent inner ear failure. We discuss the origin and clinical symptoms, as well as the therapy, of both inner ear barotrauma and inner ear decompression illness. Our own experiences are considered together with a review of the literature from the last decade. Inner ear decompression illness seems to be a relatively common diving associated incident and is not as rare as previously thought. Hyperbaric oxygen therapy is the treatment of choice for patients with inner ear decompression sickness, but is contraindicated in patients with inner ear barotrauma. As long as an inner ear decompression illness can not be ruled out, we suggest that every patient should be treated using hyperbaric oxygen therapy but only after bilateral paracentesis.

Inner ear decompression sickness and inner ear barotrauma in recreational divers: a long-term follow-up.

The objectives were to report the authors' experience with the long-term follow-up of patients with diving-related inner ear decompression sickness and inner ear barotrauma and to discuss residual cochlear and vestibular damage in relation to the question of fitness to dive. Retrospective consecutive case series. Eleven recreational divers with inner ear decompression sickness and nine with inner ear barotrauma (IEB) were followed. A complete otoneurological physical examination and laboratory evaluation were carried out. The latter included audiometry, electronystagmography, a rotatory chair test using the sinusoidal harmonic acceleration protocol, and computerized dynamic posturography. Residual cochleovestibular deficits were found in 10 (91%) of the patients with inner ear decompression sickness and 3 (33%) of those with IEB (P <.02, Fisher's Exact test; odds ratio, 20). A significantly shorter follow-up period was required for the inner ear barotrauma group (P <.05, simple t test) because three patients (33%) recovered completely within 1 month of the diving accident. Eight patients had residual vestibular deficits on follow-up, but only one (12.5%) was symptomatic. However, five (56%) of the nine patients who had a cochlear insult, as documented by follow-up audiometry, complained of significant hearing loss and tinnitus. Inner ear decompression sickness carries a high risk for residual inner ear damage despite hyperbaric oxygen recompression therapy. A favorable prognosis might be anticipated for inner ear barotrauma. The finding that most patients with residual vestibular deficits were asymptomatic at the time of follow-up emphasizes the need for a complete vestibular evaluation, including specific bedside testing and laboratory examinations, before a return to diving activity may be considered.

Inner ear decompression sickness in sport compressed-air diving.

We report our experience over the past 12 years with recreational diving-related inner ear decompression sickness (IEDCS). Retrospective, consecutive case series. Twenty-four divers, representing 29 cases of IEDCS, are presented with regard to evaluation, treatment, and follow-up. These 29 cases represent 26% of the severe decompression sickness (DCS) cases treated in that period. The patient group includes 22 divers who had a single event of IEDCS, one diver who had two events, and one with five repeated episodes. The cause of injury in 23 cases (79%) was violation of the decompression schedule. The mean time from surfacing to appearance of symptoms was 47 +/- 65 minutes. In 83%, symptoms appeared within 1 hour of ascent, in 97% within 2 hours, and in only one diver after 5.5 hours. Ten divers (34%) had pure vestibular involvement, 4 (14%) had cochlear insult alone, and 15 (52%) had combined vestibulo-cochlear injury. Except for one patient who had central as well as peripheral vestibulo-cochlear DCS, all the remaining patients had end organ involvement only, as demonstrated by physical examination and laboratory test results. Fifteen (52%) had isolated IEDCS, whereas 14 had additional symptoms of DCS. Twenty-six cases were treated by hyperbaric oxygenation with supplementary daily hyperbaric sessions. Of the 25 cases with vestibular injury and the 19 with cochlear damage, only 7 (28%) and 6 (32%), respectively, made a full recovery, whereas the others remained with residual damage. Of the 17 treated within 6 hours of symptom appearance, 9 (53%) were cured, compared with one of the 9 treated later (P <.05). IEDCS related to compressed-air recreational diving is more common than previously thought, and might occur even when no decompression schedule violation took place. Prompt diagnosis leading to the early commencement of hyperbaric oxygen recompression therapy is the key to complete recovery of cochlear and vestibular function.

Medical aspects of diving in otorhinolaryngology. I. Barotrauma and decompression sickness

Recreational scuba diving has become immensely popular in recent years and is no longer restricted to individualists or adventurers. During a dive, the human body with its gas-filled cavities is exposed to an increased ambient pressure. In the present review article, aspects of diving and hyperbaric medicine related to the otolaryngology field are presented. The basics of physics, physiology and pathophysiology that are essential to understand the effects of an increased and varying ambient pressure are reviewed. Barotrauma of the outer, middle and inner ear, the paranasal sinuses, face, teeth and larynx are explained and classified in those during the compression and decompression phase. This is followed by a discussion of inner ear decompression sickness. The present article will provide a background and foundation for both, an adequate treatment of these diseases and a critical and responsible health education of the diver.

Diving‐related inner ear injuries

Diving-related inner ear barotrauma (IEB) and inner ear decompression sickness (IEDS) most often result in permanent severe cochleovestibular deficits, unless immediate diagnosis is reached and the correct treatment is commenced early. Nine cases of sport-diving-induced inner ear injuries that were referred to the Israeli Naval Hyperbaric Institute between October 1987 and September 1989 are presented with regard to evaluation, treatment, and follow-up. The diagnosis was IEB in five divers and IEDS in four. Explorative tympanotomy was carried out with remarkable results in two patients with IEB, while the remaining three were relieved by bed rest alone. Three of the four IEDS patients were recompressed according to the extended US Navy Table 6 with good short-term results. The role of complete otoneurological evaluation in the decision-making process leading to the correct diagnosis and treatment is emphasized.

Inner Ear Decompression Sickness Combined with a Fistula of the round Window

Inner ear barotrauma with rupture of the round or oval window secondary to diving and decompression sickness (DCS) of the inner ear can be a difficult diagnosis to differentiate. The dive profile or associated elements of DCS will often confirm the diagnosis. Occasionally, diagnosis is made during recompression or during operation. The differential diagnosis is important, since immediate recompression is indicated for inner ear DCS, while it is contraindicated in cases of inner ear barotrauma. We have found no cases reported in the world literature in which both diseases have been diagnosed and proven simultaneously. We present a case of a diver who developed DCS with inner ear manifestations complicated by a round window fistula. Treatment and clinical outcome are discussed along with a brief review of the suspected cause.

Inner ear decompression sickness

With recent increases in commercial, military, and sport diving to deeper depths, inner ear injuries during such exposures have been encountered more frequently and noted during several phases of diving: during compression, at stable deep depths, with excessive noise exposure in diving, and during decompression. The pathophysiology of these injuries differs, depending upon the phase of diving in which the injuries occur. In this report, 23 cases of hearing loss, tinnitus, and/or vertigo occurring during or shortly after decompression are presented. Thirteen of these cases occurred in helium-oxygen dives involving a change to air during the latter stages of decompression. A significant correlation is present between prompt recompression treatment, relief of symptoms, and lack of residual deficits. Current knowledge indicates that the management of otologic decompression sickness should include: 1. prompt recompression to at least 99 feet deeper than the symptom onset depth; 2. recompression using the previous helium-oxygen mixture when the injuries occur during or shortly after a switch from helium-oxygen to air during the latter stages of decompression; 3. the use of parenteral diazepam for symptom relief and cyclic inhalations of oxygen enriched treatment gases; and 4. the avoidance of further diving by divers who exhibit permanent inner ear injuries after the acute symptoms have subsided.