Inner ear decompression sickness

Last updated
Inner ear decompression sickness
Other namesAudiovestibular decompression sickness
Specialty Diving and hyperbaric medicine
Symptoms Vertigo, nystagmus, nausea, ataxia, hearing loss
CausesGas bubbles forming in inner ear and associated vascular system from supersaturation
Risk factors Deep diving, long decompressions, gas switching with helium mixtures, right-to-left shunt
Diagnostic method By symptoms, inner ear involvement
Differential diagnosis Decompression and dive history
TreatmentHyperbaric oxygen therapy
Frequencyrare

Inner ear decompression sickness, (IEDCS) or audiovestibular decompression sickness is a medical condition of the inner ear caused by the formation of gas bubbles in the tissues or blood vessels of the inner ear. Generally referred to as a form of decompression sickness, it can also occur at constant pressure due to inert gas counterdiffusion effects. [1]

Contents

Usually only one side is affected, and the most common symptoms are vertigo with nystagmus, loss of balance, and nausea. The symptoms are similar to those caused by some other diving injuries and differential diagnosis can be complicated and uncertain if several possible causes for the symptoms coexist.

First aid is breathing the highest practicable concentration of normobaric oxygen. Definitive treatment is recompression with hyperbaric oxygen therapy. Anti-vertigo and anti-nausea drugs are usually effective at suppressing symptoms, but do not reduce the tissue damage. Hyperbaric oxygen may be effective for reducing oedema and ischaemia even after the most effective period for reducing the injury has passed.

IEDCS is often associated with relatively deep diving, relatively long periods of decompression obligation, and breathing gas switches involving changes in inert gas type and concentration. Onset may occur during the dive or afterwards. IEDCS is a relatively uncommon manifestation of decompression sickness, occurring in about 5 to 6% of cases. The most commonly used decompression models do not appear to accurately model IEDCS, and therefore dive computers based on those models alone are not particularly effective at predicting it, or avoiding it. There are a few rule of thumb methods which have been reasonably effective for avoidance, [2] but they have not been tested under controlled conditions.

Classification

DCS is classified by symptoms. The earliest descriptions of DCS used the terms: "bends" for joint or skeletal pain; "chokes" for breathing problems; and "staggers" for neurological problems. [3] In 1960, Golding et al. introduced a simpler classification using the term "Type I ('simple')" for symptoms involving only the skin, musculoskeletal system, or lymphatic system, and "Type II ('serious')" for symptoms where other organs (such as the central nervous system) are involved. [3] Type II DCS is considered more serious and usually has worse outcomes. [4] This system, with minor modifications, may still be used today. [5] Following changes to treatment methods, this classification is now much less useful in diagnosis, [6] since neurological symptoms may develop after the initial presentation, and both Type I and Type II DCS have the same initial management. [7]

Decompression illness and dysbarism

The term dysbarism encompasses decompression sickness, arterial gas embolism, and barotrauma, whereas decompression sickness and arterial gas embolism are commonly classified together as decompression illness when a precise diagnosis cannot be made. [8] DCS and arterial gas embolism are treated very similarly because they are both the result of gas bubbles in the body. [7] The U.S. Navy prescribes identical treatment for Type II DCS and arterial gas embolism. [9] Their spectra of symptoms also overlap, although the symptoms from arterial gas embolism are generally more severe because they often arise from an infarction (blockage of blood supply and tissue death).

Signs and symptoms

The usual symptoms are tinnitus, ataxia, difficulty with coordination, vertigo, nausea, vomiting, and hearing loss. [10] [11] It is not unusual for other symptoms of decompression sickness to be present simultaneously, which can make diagnosis easier, but sometimes only vestibular symptoms manifest.

Causes

Incompletely understood, but probably caused by nucleation and development of one or more inert gas bubbles which affect the function of the inner ear, either directly in the endolymphatic and perilymphatic spaces [11] or by way of the perfusion or innervation of the inner ear.

It has been hypothesized that in divers with a right-to-left shunt shunt, gas embolism of the labyrinthine artery may be a cause. [11]

Predisposing factors

Several factors are considered likely to increase the risk of IEDCS:

Mechanism

The inner ear, particularly the vestibule, is poorly perfused, and when saturated can take a relatively long tine to off-gas, which may be described as a slow tissue compartment. Supersaturated total inert gases loading may be due to decompression or to Isobaric counterdiffusion of gases after a switch in which the new gas mixture contains a relatively high partial pressure of a gas with higher diffusivity than the gas replaced, causing a net ingassing of the affected tissues and a consequently excessive combined inert gas supersaturation. The tissues may remain supersaturated for some time, which may trigger autochthonous bubble formation and growth from pre-existing bubble nuclei, and if venous gas bubbles concurrently pass through a shunt and reach the supersaturated area, the high local inert gas concentration may cause intravascular bubble growth. [14] [1]

Pathophysiology

The primary provoking agent in decompression sickness is bubble formation from excess dissolved gases. The earliest bubble formation detected is subclinical intravascular bubbles detectable by doppler ultrasound in the venous systemic circulation. The presence of these "silent" bubbles is no guarantee that they will persist and grow to be symptomatic. [16] Gas bubble formation in blood vessels causes obstruction and inflammation, and platelet aggregation may occur. [11] In more solid tissues there may be mechanical damage, and the presence of mobile bubbles in the fluids of the inner ear may cause abnormal stimuli. The pathogenesis remains elusive, [13] and may have more than one mechanism. Development of the inner ear injury has been attributed to a vascular mechanism. [13]

Diagnosis

IEDCS and inner ear barotrauma (IEBt) are the inner ear injuries associated with ambient pressure diving, both of which manifest as cochleovestibular symptoms. The similarity of symptoms makes differential diagnosis difficult, which can delay appropriate treatment or lead to inappropriate treatment. [17]

Distinguishing between IEDCS and IEBt can be difficult, and both can be present at the same time. While IEDCS is more likely to cause vertigo, and IEBt is more likely to cause hearing loss, these are not reliable distinguishing factors. [14] Lindfors et al 2021 [17] report that the most useful variables they found for distinguishing between IEBt and IEDCS are dive mode, (scuba versus freediving), breathing gas type (compressed air versus mixed gas), dive profile (deep or shallow), symptom onset (descending versus ascending or at surface), distribution of cochleovestibular symptoms (vestibular versus cochlear) and presence or absence of other DCS symptoms. It is considered appropriate in the presence of any symptom typical of DCS, to assume and treat for DCS with recompression. [14]

Symptom comparison between inner ear barotrauma and inner ear decompression sickness [19]
BarotraumaDecompression sickness
Conductive or mixed hearing lossSensorineural hearing loss
Occurs during descent or ascentOnset during ascent or after surfacing
Cochlear symptoms (ie hearing loss) predominateVestibular symptoms (vertigo) predominant; right sided
History of difficult ear clearing or forced Valsalva manoeuvreNo history of eustachian tube dysfunction
Low-risk dive profileDepth >15 m, helium mixtures, helium to nitrogen gas switches, repetitive dives
Isolated inner ear symptoms, or inner and middle ear on the same sidesOther neurological or dermatological symptoms suggestive of DCS

Prevention

IEDCS caused by inert gas counterdiffusion can be avoided by avoiding gas switches where the relative concentration of inert gas diluents with dissimilar diffusivity is large. [2]

Treatment

Early recompression treatment with hyperbaric oxygen is more likely to prevent permanent inner ear damage. [11] Recompression increases ambient pressure which returns gases into solution and hyperbaric oxygen improves oxygenation of ischaemic tissues while facilitating inert gas elimination. Slow decompression to normal atmospheric pressure allows controlled outgassing of residual inert gas to avoid re-formation of bubbles. U.S. Navy treatment table 6 has been successfully used, [10] but multiple exposures of hyperbaric oxygen therapy may be necessary if symptoms are not resolved in the initial treatment or if symptoms return. [11] Repeat treatments are focused on resolving sequelae as the initial bubbles will already have been resorbed during adequate initial treatment.

First aid treatment of 100% oxygen, or the highest available oxygen fraction is recommended for several hours or until recompression is available, as this establishes the highest possible ambient pressure oxygen window which induces a maximum inert gas gradient between the lungs and gases in the tissues, resulting in faster inert gas removal, while providing the greatest relief for ischaemic tissues. Rehydration is also indicated. [11] Anti-inflammatory drugs may help, but could also increase leakage of fluids through damaged tissue.[ citation needed ]

The symptoms of IEDCS are not easily discriminated from symptoms of inner ear barotrauma, and a possible necessity for bilateral myringotomy should be assessed before hyperbaric oxygen therapy is started. In practice, if there is uncertainty about a diagnosis of barotrauma, recompression does not appear to cause harm. [11]

Ameliorative: Anti-nausea drugs may be administered for short term relief. They should not mask vertigo, nystagmus, tinnitis or hearing deficits.

Prognosis

A minority of cases recover completely. About 90% of cases of diving-related vestibular dysfunction have mild to moderate long term residual symptoms. Vestibulocochlear assessment and exclusion of a right-to-left vascular shunt prior to continuing scuba diving is recommended. [15] [19] Recent experience in Finland reports a higher rate of complete recovery, of about 65 to 70% in technical and recreational divers respectively. [15]

Epidemiology

Otological injuries account for about 2/3 of all diving related injuries, but about 50% of all presentations are middle ear barotrauma. Decompression sickness is much less common, and IEDCS is rare, [19] with an estimated incidence rate of 0.01–0.03% in recreational dives. [12] It is becoming more frequently reported, bur epidemiological data remain limited to small case series. [13] The condition is usually associated with deep diving on mixed gas, and is frequently accompanied by other central nervous system symptoms of decompression sickness. [10] However it has also been known to occur as the only manifestation of decompression sickness following moderate or short and shallow scuba dives on air. [10] [15]

See also

Related Research Articles

<span class="mw-page-title-main">Decompression sickness</span> Disorder caused by dissolved gases forming bubbles in tissues

Decompression sickness is a medical condition caused by dissolved gases emerging from solution as bubbles inside the body tissues during decompression. DCS most commonly occurs during or soon after a decompression ascent from underwater diving, but can also result from other causes of depressurisation, such as emerging from a caisson, decompression from saturation, flying in an unpressurised aircraft at high altitude, and extravehicular activity from spacecraft. DCS and arterial gas embolism are collectively referred to as decompression illness.

<span class="mw-page-title-main">Hyperbaric medicine</span> Medical treatment at raised ambient pressure

Hyperbaric medicine is medical treatment in which an ambient pressure greater than sea level atmospheric pressure is a necessary component. The treatment comprises hyperbaric oxygen therapy (HBOT), the medical use of oxygen at an ambient pressure higher than atmospheric pressure, and therapeutic recompression for decompression illness, intended to reduce the injurious effects of systemic gas bubbles by physically reducing their size and providing improved conditions for elimination of bubbles and excess dissolved gas.

<span class="mw-page-title-main">Air embolism</span> Vascular blockage by air bubbles

An air embolism, also known as a gas embolism, is a blood vessel blockage caused by one or more bubbles of air or other gas in the circulatory system. Air can be introduced into the circulation during surgical procedures, lung over-expansion injury, decompression, and a few other causes. In flora, air embolisms may also occur in the xylem of vascular plants, especially when suffering from water stress.

<span class="mw-page-title-main">Barotrauma</span> Injury caused by pressure

Barotrauma is physical damage to body tissues caused by a difference in pressure between a gas space inside, or in contact with, the body and the surrounding gas or liquid. The initial damage is usually due to over-stretching the tissues in tension or shear, either directly by an expansion of the gas in the closed space or by pressure difference hydrostatically transmitted through the tissue. Tissue rupture may be complicated by the introduction of gas into the local tissue or circulation through the initial trauma site, which can cause blockage of circulation at distant sites or interfere with the normal function of an organ by its presence. The term is usually applied when the gas volume involved already exists prior to decompression. Barotrama can occur during both compression and decompression events.

Decompression Illness (DCI) comprises two different conditions caused by rapid decompression of the body. These conditions present similar symptoms and require the same initial first aid. Scuba divers are trained to ascend slowly from depth to avoid DCI. Although the incidence is relatively rare, the consequences can be serious and potentially fatal, especially if untreated.

In-water recompression (IWR) or underwater oxygen treatment is the emergency treatment of decompression sickness (DCS) by returning the diver underwater to help the gas bubbles in the tissues, which are causing the symptoms, to resolve. It is a procedure that exposes the diver to significant risk which should be compared with the risk associated with the available options and balanced against the probable benefits. Some authorities recommend that it is only to be used when the time to travel to the nearest recompression chamber is too long to save the victim's life; others take a more pragmatic approach and accept that in some circumstances IWR is the best available option. The risks may not be justified for case of mild symptoms likely to resolve spontaneously, or for cases where the diver is likely to be unsafe in the water, but in-water recompression may be justified in cases where severe outcomes are likely if not recompressed, if conducted by a competent and suitably equipped team.

<span class="mw-page-title-main">Diving medicine</span> Diagnosis, treatment and prevention of disorders caused by underwater diving

Diving medicine, also called undersea and hyperbaric medicine (UHB), is the diagnosis, treatment and prevention of conditions caused by humans entering the undersea environment. It includes the effects on the body of pressure on gases, the diagnosis and treatment of conditions caused by marine hazards and how relationships of a diver's fitness to dive affect a diver's safety. Diving medical practitioners are also expected to be competent in the examination of divers and potential divers to determine fitness to dive.

Diving disorders, or diving related medical conditions, are conditions associated with underwater diving, and include both conditions unique to underwater diving, and those that also occur during other activities. This second group further divides into conditions caused by exposure to ambient pressures significantly different from surface atmospheric pressure, and a range of conditions caused by general environment and equipment associated with diving activities.

<span class="mw-page-title-main">Vertigo</span> Type of dizziness where a person has the sensation of moving or surrounding objects moving

Vertigo is a condition in which a person has the sensation of movement or of surrounding objects moving when they are not. Often it feels like a spinning or swaying movement. It may be associated with nausea, vomiting, perspiration, or difficulties walking. It is typically worse when the head is moved. Vertigo is the most common type of dizziness.

In physiology, isobaric counterdiffusion (ICD) is the diffusion of different gases into and out of tissues while under a constant ambient pressure, after a change of gas composition, and the physiological effects of this phenomenon. The term inert gas counterdiffusion is sometimes used as a synonym, but can also be applied to situations where the ambient pressure changes. It has relevance in mixed gas diving and anesthesiology.

<span class="mw-page-title-main">Decompression (diving)</span> Pressure reduction and its effects during ascent from depth

The decompression of a diver is the reduction in ambient pressure experienced during ascent from depth. It is also the process of elimination of dissolved inert gases from the diver's body which accumulate during ascent, largely during pauses in the ascent known as decompression stops, and after surfacing, until the gas concentrations reach equilibrium. Divers breathing gas at ambient pressure need to ascend at a rate determined by their exposure to pressure and the breathing gas in use. A diver who only breathes gas at atmospheric pressure when free-diving or snorkelling will not usually need to decompress, Divers using an atmospheric diving suit do not need to decompress as they are never exposed to high ambient pressure.

<span class="mw-page-title-main">Decompression practice</span> Techniques and procedures for safe decompression of divers

To prevent or minimize decompression sickness, divers must properly plan and monitor decompression. Divers follow a decompression model to safely allow the release of excess inert gases dissolved in their body tissues, which accommodated as a result of breathing at ambient pressures greater than surface atmospheric pressure. Decompression models take into account variables such as depth and time of dive, breathing gasses, altitude, and equipment to develop appropriate procedures for safe ascent.

<span class="mw-page-title-main">History of decompression research and development</span> Chronological list of notable events in the history of diving decompression.

Decompression in the context of diving derives from the reduction in ambient pressure experienced by the diver during the ascent at the end of a dive or hyperbaric exposure and refers to both the reduction in pressure and the process of allowing dissolved inert gases to be eliminated from the tissues during this reduction in pressure.

<span class="mw-page-title-main">Decompression theory</span> Theoretical modelling of decompression physiology

Decompression theory is the study and modelling of the transfer of the inert gas component of breathing gases from the gas in the lungs to the tissues and back during exposure to variations in ambient pressure. In the case of underwater diving and compressed air work, this mostly involves ambient pressures greater than the local surface pressure, but astronauts, high altitude mountaineers, and travellers in aircraft which are not pressurised to sea level pressure, are generally exposed to ambient pressures less than standard sea level atmospheric pressure. In all cases, the symptoms caused by decompression occur during or within a relatively short period of hours, or occasionally days, after a significant pressure reduction.

Brian Andrew Hills, born 19 March 1934 in Cardiff, Wales, died 13 January 2006 in Brisbane, Queensland, was a physiologist who worked on decompression theory.

<span class="mw-page-title-main">Physiology of decompression</span> The physiological basis for decompression theory and practice

The physiology of decompression is the aspect of physiology which is affected by exposure to large changes in ambient pressure, and involves a complex interaction of gas solubility, partial pressures and concentration gradients, diffusion, bulk transport and bubble mechanics in living tissues. Gas is breathed at ambient pressure, and some of this gas dissolves into the blood and other fluids. Inert gas continues to be taken up until the gas dissolved in the tissues is in a state of equilibrium with the gas in the lungs,, or the ambient pressure is reduced until the inert gases dissolved in the tissues are at a higher concentration than the equilibrium state, and start diffusing out again.

<span class="mw-page-title-main">Built-in breathing system</span> System for supply of breathing gas on demand within a confined space

A built-in breathing system is a source of breathing gas installed in a confined space where an alternative to the ambient gas may be required for medical treatment, emergency use, or to minimise a hazard. They are found in diving chambers, hyperbaric treatment chambers, and submarines.

Middle ear barotrauma (MEBT), also known to underwater divers as ear squeeze and reverse ear squeeze, is an injury caused by a difference in pressure between the external ear canal and the middle ear. It is common in underwater divers and usually occurs when the diver does not equalise sufficiently during descent or, less commonly, on ascent. Failure to equalise may be due to inexperience or eustachian tube dysfunction, which can have many possible causes. Unequalised ambient pressure increase during descent causes a pressure imbalance between the middle ear air space and the external auditory canal over the eardrum, referred to by divers as ear squeeze, causing inward stretching, serous effusion and haemorrhage, and eventual rupture. During ascent internal over-pressure is normally passively released through the eustachian tube, but if this does not happen the volume expansion of middle ear gas will cause outward bulging, stretching and eventual rupture of the eardrum known to divers as reverse ear squeeze. This damage causes local pain and hearing loss. Tympanic rupture during a dive can allow water into the middle ear, which can cause severe vertigo from caloric stimulation. This may cause nausea and vomiting underwater, which has a high risk of aspiration of vomit or water, with possibly fatal consequences.

The US Navy has used several decompression models from which their published decompression tables and authorized diving computer algorithms have been derived. The original C&R tables used a classic multiple independent parallel compartment model based on the work of J.S.Haldane in England in the early 20th century, using a critical ratio exponential ingassing and outgassing model. Later they were modified by O.D. Yarborough and published in 1937. A version developed by Des Granges was published in 1956. Further developments by M.W. Goodman and Robert D. Workman using a critical supersaturation approach to incorporate M-values, and expressed as an algorithm suitable for programming were published in 1965, and later again a significantly different model, the VVAL 18 exponential/linear model was developed by Edward D. Thalmann, using an exponential ingassing model and a combined exponential and linear outgassing model, which was further developed by Gerth and Doolette and published in Revision 6 of the US Navy Diving Manual as the 2008 tables.

References

  1. 1 2 3 Doolette, David J.; Mitchell, Simon J. (June 2003). "Biophysical basis for inner ear decompression sickness". Journal of Applied Physiology. 94 (6): 2145–50. doi:10.1152/japplphysiol.01090.2002. PMID   12562679.
  2. 1 2 Burton, Steve (December 2004). "Isobaric Counter Diffusion". ScubaEngineer. Retrieved 10 January 2010.
  3. 1 2 Francis & Mitchell, Manifestations, p. 578.
  4. Pulley, Stephen A. (27 November 2007). "Decompression Sickness". Medscape. Retrieved 15 May 2010.
  5. Marx, p. 1908.
  6. Francis & Mitchell, Manifestations, p. 579.
  7. 1 2 Francis, T James R; Smith, D.J. (1991). "Describing Decompression Illness". 42nd Undersea and Hyperbaric Medical Society Workshop. 79(DECO)5–15–91. Archived from the original on 27 July 2011. Retrieved 23 May 2010.{{cite journal}}: CS1 maint: unfit URL (link)
  8. Francis & Mitchell, Manifestations, p. 580.
  9. U.S. Navy Supervisor of Diving (2008). "Chapter 20: Diagnosis and Treatment of Decompression Sickness and Arterial Gas Embolism". U.S. Navy Diving Manual (PDF). SS521-AG-PRO-010, revision 6. Vol. 5. U.S. Naval Sea Systems Command. p. 37. Archived from the original (PDF) on 5 March 2011. Retrieved 15 May 2010.
  10. 1 2 3 4 Reissman, P; Shupak, A; Nachum, Z; Melamed, Y. (June 1990). "Inner ear decompression sickness following a shallow scuba dive". Aviat Space Environ Med. 61 (6): 563–6. PMID   2369397.
  11. 1 2 3 4 5 6 7 8 9 Boyd, K.L.; Wray, A.A. (8 May 2022). "Inner Ear Decompression Sickness". StatPearls [Internet]. Treasure Island, FL.: StatPearls Publishing. PMID   32491626.
  12. 1 2 Vann, R.D.; Butler, F.K.; Mitchell, S.J.; Moon, R.E. (8 January 2011). "Decompression illness". Lancet. 377 (9760): 153–64. doi:10.1016/S0140-6736(10)61085-9. PMID   21215883. S2CID   7242178.
  13. 1 2 3 4 5 Gempp, E.; Louge, P. (May 2013). "Inner ear decompression sickness in scuba divers: a review of 115 cases". European Archives of Otorhinolaryngology. 270 (6): 1831–7. doi:10.1007/s00405-012-2233-y. PMID   23100085. S2CID   9474902.
  14. 1 2 3 4 5 Meier, Matthew (5 November 2021). "Inner-Ear Barotrauma vs. DCS". xray-mag.com. X-Ray Magazine. Retrieved 26 July 2022.
  15. 1 2 3 4 Lindfors, O.H.; Lundell, R.V.; Arola, O.J.; Hirvonen, T.P.; Sinkkonen, S.T.; Räisänen-Sokolowski, A.K. (Fourth Quarter 2021). "Inner ear decompression sickness in Finland: a retrospective 20-year multicenter study". Undersea Hyperb Med. 48 (4): 399–408. doi:10.22462/07.08.2021.4. PMID   34847303. S2CID   249142535.
  16. Calder 1986, pp. 241–245.
  17. 1 2 Lindfors, O.H.; Räisänen-Sokolowski, A.K.; Hirvonen, T.P.; Sinkkonen, S.T. (20 December 2021). "Inner ear barotrauma and inner ear decompression sickness: a systematic review on differential diagnostics". Diving and Hyperbaric Medicine. 51 (4): 328–337. doi:10.28920/dhm51.4.328-337. PMC   8923696 . PMID   34897597.
  18. Marx, John (2010). Rosen's emergency medicine: concepts and clinical practice (7th ed.). Philadelphia, PA: Mosby/Elsevier. ISBN   978-0-323-05472-0.
  19. 1 2 3 4 Nofz, Lyndon; Porrett, Jemma; Yii, Nathan; De Alwis, Nadine. "Diving related otological injuries". www1.racgp.org.au. Reprinted from AJGP vol 49, no 8, August 2020 The Royal Australian College of General Practitioners 2020

Sources

D'Aoust, B. G.; White, R.; Swanson, H.; Dunford, R. G.; Mahoney, J. (1982). "Differences in Transient and Steady State Isobaric Counterdiffusion" (PDF). Report to the Office of Naval Research. Retrieved 10 January 2010.

Calder, Ian M. (1986). "Dysbarism. A Review". Forensic Science International. 30 (4): 237–266. doi:10.1016/0379-0738(86)90133-7. PMID   3519392.

Francis, T James R; Mitchell, Simon J (2003). "10.6: Manifestations of Decompression Disorders". In Brubakk, Alf O; Neuman, Tom S (eds.). Bennett and Elliott's physiology and medicine of diving (5th Revised ed.). United States: Saunders. pp. 578–599. ISBN   978-0-7020-2571-6. OCLC   51607923.

Graves, D.J.; Idicula, J.; Lambertsen, Christian J.; Quinn, J.A. (February 1973). "Bubble formation in physical and biological systems: a manifestation of counterdiffusion in composite media". Science. 179 (4073): 582–584. Bibcode:1973Sci...179..582G. doi:10.1126/science.179.4073.582. PMID   4686464. S2CID   46428717.

Graves, D.J.; Idicula, J.; Lambertsen, Christian J.; Quinn, J.A. (March 1973). "Bubble formation resulting from counterdiffusion supersaturation: a possible explanation for isobaric inert gas 'urticaria' and vertigo". Physics in Medicine and Biology. 18 (2): 256–264. Bibcode:1973PMB....18..256G. CiteSeerX   10.1.1.555.429 . doi:10.1088/0031-9155/18/2/009. PMID   4805115. S2CID   250737144 . Retrieved 10 January 2010.

Lambertson, Christian J. (1 June 1989). Vann, R.D. (ed.). Relations of isobaric gas counterdiffusion and decompression gas lesion diseases. The Physiological Basis of Decompression. 38th Undersea and Hyperbaric Medical Society Workshop. UHMS Publication Number 75 (Phys) (Report).