eMedicine Specialties > Emergency Medicine > Environmental

Barotrauma

Author: Joseph Kaplan, MD, FACEP, Assistant Professor, Department of Emergency Medicine, Medical Center of Central Georgia
Coauthor(s): Marshall E Eidenberg, DO, Staff Emergency Physician, Via Christi Regional Medical Center
Contributor Information and Disclosures

Updated: Jun 23, 2008

Introduction

Background

Diving as a profession can be traced back more than 5000 years, yet diving-related disease was not described until Paul Bert wrote about caisson disease in 1878. Symptoms of caisson disease were noted among bridge workers after finishing their shifts underwater and coming back to the surface. These symptoms included dizzy spells, difficulty breathing, and sharp pain in the joints or abdomen. The caisson workers often noted that they felt better while working. This was usually attributed to their being rested at the beginning of the shift as opposed to being tired when the workday was through. The workers would often have severe back pain that left them bent over, which is how caisson disease earned the nickname "the bends."

Diving barotrauma can present with a variety of manifestations, from ear or mouth pain and headaches to major joint pain, paralysis, coma, and death. As a result of the wide variety of presentations, these disorders must be considered in any patient who has recently been exposed to a significant change in barometric pressure. The 3 major manifestations of barotrauma include the following: (1) sinus or middle ear effects, (2) decompression sickness (DCS), and (3) arterial gas emboli.

Barotrauma has also reportedly been caused by an air bag rupturing during deployment, forcing high-pressure gas into a person's lungs. It also reportedly has been associated with rapid ascent in military aircraft.

Recently, there has been a significant rise in articles dealing with combat-associated barotrauma. These articles deal mainly with blast injury patterns and ballistics. This is an extensive subject and will not be covered in this article.

Pathophysiology

Injuries caused by pressure changes are generally governed by the Boyle and Henry laws of physics.

The Boyle law states, "For any gas at a constant temperature, the volume of the gas will vary inversely with the pressure," or P1 X V1 = P2 X V2. Pressure rises by 1 atmosphere for every 33 ft (10 m) of seawater depth. This means that a balloon (or lungs) containing a volume of 1 cubic foot of gas at 33 ft of seawater depth will have a volume of gas of 2 cubic feet at the surface. If this air is trapped, as occurs when a person holds his or her breath during rapid ascent, it expands with great force against the walls of that space (reverse squeeze). During rapid ascent, incidents of pneumothorax and pneumomediastinum as well as sinus squeeze and inner ear injuries can occur. Sinus squeeze occurs with eustachian tube dysfunction, which may result in inner ear hemorrhage, tearing of the labyrinthine membrane, or perilymphatic fistula.

The Henry law states that the solubility of a gas in a liquid is directly proportional to the pressure exerted upon the gas and liquid. Thus, when the cap is removed from a bottle of soda pop, the soda begins to bubble as gas is released from the liquid. In addition, when nitrogen in a diver's air tank dissolves in the diver's fatty tissues or synovial fluids at depth, nitrogen will be released from those tissues as the diver ascends to a lower pressure environment. This occurs slowly and gradually if the diver ascends slowly and gradually, and the nitrogen enters the bloodstream to the lungs and is exhaled. However, should the diver ascend rapidly, nitrogen exits tissues rapidly and forms gas bubbles.

Decompression sickness

Decompression sickness (DCS) usually results from the formation of gas bubbles, which can travel to any part of the body, accounting for many disorders. A gas bubble forming in the back or joints can cause localized pain (the bends). In the spinal cord or peripheral nerve tissues, a bubble may cause paresthesias, neurapraxia, or paralysis. A bubble forming in the circulatory system can lead to pulmonary or cerebral gas emboli.

Some gases are more soluble in fats. Nitrogen, for example, is 5 times more soluble in fat than in water. Approximately 40-50% of serious DCS injuries involve the central nervous system (CNS). Women may be at an increased risk of DCS because they have more fat in their bodies. DCS also may occur at high altitudes. Those who dive in mountain lakes or combine diving with subsequent flying are at increased risk as well.

DCS is classified into 2 types. Type I is milder, is not life threatening, and is characterized by pain in the joints and muscles and swelling in the lymph nodes. The most common symptom of DCS is joint pain, which begins mildly and worsens over time and with movement. DCS type II is serious and life threatening. Manifestations may include respiratory, circulatory, and, most commonly, peripheral nerve and/or CNS compromise.

Arterial gas embolism (AGE) is the most dangerous manifestation of DCS type II. AGE occurs after a rapid ascent, when a gas bubble forms in the arterial blood supply and travels to the brain, heart, or lungs. This is immediately life threatening and can occur even after ascent from relatively shallow depths. However, AGE can also occur from iatrogenic causes.

Patients with a patent foramen ovale (up to 30% of the population) are at higher risk of gas passing from a right-to-left shunt and causing CNS injuries.

Frequency

United States

The average risk of severe (type II) DCS is 2.28 cases per 10,000 dives. The number of minor (type I) injures is not known because many divers do not seek treatment. Risk of DCS is increased in divers with asthma or pulmonary blebs. Risk of DCS type II is increased 2.5 times in patients with a patent foramen ovale. Deaths due to DCS in military aircraft have been reported to occur at a rate of 0.024 per million hours of flight time. Rates of decompression incidents for civilian aviation average about 35 per year, and less than half are significant.

International

No information is available on the incidence of diving barotrauma worldwide. The Australian defense force has averaged 82 incidents per million hours of flying time.

Race

No significant differences in the incidence of dive-related injuries have been associated with race.

Sex

Because of a generally greater percentage of body fat, females have a theoretically higher incidence of barotrauma injuries than males. However, no data support this hypothesis.

Age

Although no direct correlation exists with age and frequency of barotrauma, the most common group affected ranges between 21 and 40 years. However, direct correlation does exist between age and residual effects of barotrauma, which significantly rises after age 50 years.

Clinical

History

Patients with DCS present with a history of diving, generally within 24 hours of the onset of symptoms. Patients may also have a recent history of occupational pressurization or depressurization. For example, this occurs with aircraft mechanics who must test aircraft windows by working in pressurized aircraft. Air emboli have also occurred in mechanics who maintain training altitude chambers. Recently, military operations involving troops traveling from ground level to high-altitude environments in a relatively short time and operations involving soldiers doing strenuous activities at higher altitudes have resulted in many cases of DCS. Recent studies have indicated that aerobic exercise either prior to a dive or during decompression stops may decrease the post dive gas bubble formation.

  • Sinus squeeze
    • Patients usually present with complaints of facial or oral pain, nausea, vertigo, or headache.
    • Other important information to gather includes any history of recent upper respiratory infections, allergic rhinitis, sinus polyps, and sinus surgeries and whether the pain worsened during descent or ascent.
  • Middle ear squeeze
    • Patients often have a history of sudden vertigo, nausea, tinnitus, ear pain, deafness, or headache.
    • They may have a history of previous diving ear injury or a history of previous or current ear infection.
  • Decompression sickness type I
    • Patients often have a history of recent diving followed by a flight home. They may complain of slowly progressing pain or numbness in their limbs or back.
    • Patients present with joint, muscle, or back pain that worsens over time. The pain worsens with motion but is always present. The pain may range from mild (tickles) to severe (the bends).
    • Patients may have a history of previous decompression illness and multiple dives in the same day and frequently have not followed the dive tables closely. New dive computers that offer more "bottom time" do so by modifying the US Navy dive tables and possibly place divers at an increased risk for DCS injuries. Divers should be questioned as to the method of computing bottom and ascent times with safety stops. This information should be recorded as part of the medical record.
  • Decompression sickness type II
    • DCS type II usually presents sooner than DCS type I.
    • Patients may present with shortness of breath (the chokes), chest pain, severe headache, altered mental status, and shock. They also may complain of dizziness or weakness. Patients may rapidly deteriorate without emergent intervention.
    • Essential history to ascertain includes time since dive ended, the dive profile, when the symptoms began, and prior medical history. The dive profile consists of prior dives that day, depth of dive, bottom time, decompression stop depth, and length of stop.
    • Diver should be asked about his or her prior dive category.
    • Inquiry should be made specifically about previous decompression injuries, pulmonary blebs, Marfan syndrome, asthma, congenital pulmonary illnesses, HIV status, chronic obstructive pulmonary disease (COPD), lung tumors, histiocytosis X, cystic fibrosis, pregnancy, and any prior pulmonary injuries or surgeries.
  • Arterial gas embolism
    • AGE usually occurs shortly after ascending very rapidly, often from fairly shallow depths. People may be described to scream suddenly and lose consciousness. Onset of AGE often occurs within a few minutes of surfacing. Patients who experience AGE often die before reaching a medical facility. Air emboli have also recently been noted to occur iatrogenically in association with central venous monitoring during surgical procedures. Case reports have shown AGE occurring secondary to occupational rapid decompression in both aircraft maintenance and altitude-chamber maintenance personnel.
    • Obtaining a history from these patients can be difficult because they often present with altered mental status or are in shock.
    • Witnesses often report that divers experience a sudden or immediate loss of consciousness or collapse, usually within minutes of surfacing.
    • Ask the patient or dive partner about a history of patent foramen ovale.
  • Abdominal compartment syndrome: Divers can develop large amounts of intraperitoneal extraluminal gas, which can compress the intraperitoneal organs. This can lead to venous compression of these organs and secondary compartment syndrome.

Physical

The physical examination should be tailored to the patient's history.

  • Perform a general physical examination on all patients, with initial emphasis on ears, sinuses, and neck as well as on the pulmonary, cardiovascular, and neurologic systems. AGE often presents with signs and symptoms of acute stroke.
  • Inspect and palpate the extremities, and test range of motion in all joints.
  • Sinus squeeze
    • Inspect nasal mucosa for polyps, hemorrhage, or lesions.
    • Palpate and transilluminate sinuses to inspect for hemorrhage.
    • Percuss upper teeth with a tongue blade to inspect for severe sinus tenderness.
  • Ear squeeze
    • Carefully inspect the tympanic membrane (TM), looking in particular for the following signs:
      • Amount of congestion around the umbo
      • Percent of TM involvement
      • Amount of hemorrhage noted behind eardrum
      • Evidence of TM rupture
    • Palpate the eustachian tube for tenderness.
    • Test the patient's balance and hearing.
    • Evaluate the TM on the Teed scale:
      • Teed 0 - No visible damage, normal ear
      • Teed 1 - Congestion around the umbo, occurs with a pressure differential of 2 pounds per square inch (PSI)
      • Teed 2 - Congestion of entire TM, occurs with a pressure differential of 2-3 PSI
      • Teed 3 - Hemorrhage into the middle ear
      • Teed 4 - Extensive middle ear hemorrhage with blood bubbles visible behind TM; TM may rupture
      • Teed 5 - Entire middle ear filled with dark (deoxygenated) blood
  • Decompression sickness type I
    • Inspect for swelling or effusion in the affected joint.
    • Test for range of motion both actively and passively.
    • Palpate the affected area for crepitus and compartment tightness.
    • Evaluate neurovascular status by performing a complete neurologic examination. The examination should include testing motor and sensory functions, cerebellar function, and mental status. The findings from this examination must be recorded and used as a baseline to determine improvement in postdive chamber treatment.
  • Decompression sickness type II
    • Evaluate cardiovascular and pulmonary systems.
    • Note neck vein distention or petechiae on the head or neck.
    • Palpate the skin for crepitus.
    • Auscultate the lungs and heart for decreased breath sounds, muffled heart tones, or heart murmurs.
    • Evaluate neurologic status, including gross motor, sensory, and cerebellar examinations. Tandem walking (heel to toe, with eyes closed) is an excellent method of evaluation.
    • Document Glasgow Coma Scale and Mini Mental State Examination.
  • Arterial gas embolism: Use the same examination used for decompression sickness type II.

Causes

The causes of DCS are related to predisposing medical or genetic factors, as listed above, and to diver error. Diver error includes the following practices:

  • Multiple daily dives
  • Poor adherence to the dive tables
  • Breath holding (most common scenario for pulmonary barotrauma)
  • Rapid ascent - This can occur from relatively shallow depths. For example, pilots undergoing rapid ascent while performing underwater escape training after flight may experience DCS.
  • Flying or traveling to high altitudes within 24 hours after diving
  • Occupational causes - These causes include rapid depressurization by maintenance workers and mechanics after working in pressurized aircraft cabins. Reports of altitude chamber mechanics who have depressurized too quickly while working on the altitude chambers have also been documented. Pilots and crewmembers performing high-altitude air drops on military missions and special-operations soldiers involved in such missions have also reported instances of DCS.

More on Barotrauma

Overview: Barotrauma
Differential Diagnoses & Workup: Barotrauma
Treatment & Medication: Barotrauma
Follow-up: Barotrauma
Multimedia: Barotrauma
References

References

  1. Ball R, Auker CR, Ford GC, Lawrence D. Decompression sickness presenting as forearm swelling and peripheral neuropathy: a case report. Aviat Space Environ Med. Jul 1998;69(7):690-2. [Medline].

  2. Blatteau JE, Gempp E, Galland FM, et al. Aerobic exercise 2 hours before a dive to 30 msw decreases bubble formation after decompression. Aviat Space Environ Med. Jul 2005;76(7):666-9. [Medline].

  3. Bond JP, Kirschner DA. Spinal cord myelin is vulnerable to decompression. Mol Chem Neuropathol. Apr 1997;30(3):273-88. [Medline].

  4. Boussuges A, Blanc P, Molenat F, et al. Haemoconcentration in neurological decompression illness. Int J Sports Med. Jul 1996;17(5):351-5. [Medline].

  5. Bove AA. Risk of decompression sickness with patent foramen ovale. Undersea Hyperb Med. 1998;25(3):175-8. [Medline].

  6. Butler WP, Topper SM, Dart TS. USAF treatment table 8: treatment for altitude decompression sickness. Aviat Space Environ Med. Jan 2002;73(1):46-9. [Medline].

  7. Camporesi EM. Diving and pregnancy. Semin Perinatol. Aug 1996;20(4):292-302. [Medline].

  8. Cogar WB. Intravenous lidocaine as adjunctive therapy in the treatment of decompression illness. Ann Emerg Med. Feb 1997;29(2):284-6. [Medline].

  9. Colebatch HJ, Smith MM, Ng CK. Increased elastic recoil as a determinant of pulmonary barotrauma in divers. Respir Physiol. Feb 1976;26(1):55-64. [Medline].

  10. Colebatch HJ, Ng CK. Decreased pulmonary distensibility and pulmonary barotrauma in divers. Respir Physiol. Dec 1991;86(3):293-303. [Medline].

  11. Dujic Z, Palada I, Obad A. Exercise during a 3-min decompression stop reduces postdive venous gas bubbles. Med Sci Sports Exerc. Aug 2005;37(8):1319-23. [Medline].

  12. Evans DE, Kobrine AI, LeGrys DC, Bradley ME. Protective effect of lidocaine in acute cerebral ischemia induced by air embolism. J Neurosurg. Feb 1984;60(2):257-63. [Medline].

  13. Files DS, Webb JT, Pilmanis AA. Depressurization in military aircraft: rates, rapidity, and health effects for 1055 incidents. Aviat Space Environ Med. Jun 2005;76(6):523-9. [Medline].

  14. Germonpre P, Dendale P, Unger P, Balestra C. Patent foramen ovale and decompression sickness in sports divers. J Appl Physiol. May 1998;84(5):1622-6. [Medline].

  15. Goldenberg I, Shupak A, Shoshani O. Oxy-helium treatment for refractory neurological decompression sickness: a case report. Aviat Space Environ Med. Jan 1996;67(1):57-60. [Medline].

  16. Gustavsson LL, Hultcrantz E. [Medical aspects of diving--a sport for both women and men]. Lakartidningen. Feb 17 1999;96(7):749-53. [Medline].

  17. Hickey MJ, Zanetti CL. Delayed-onset cerebral arterial gas embolism in a commercial airline mechanic. Aviat Space Environ Med. Sep 2003;74(9):977-80. [Medline].

  18. Hyldegaard O, Madsen J. Influence of heliox, oxygen, and N2O-O2 breathing on N2 bubbles in adipose tissue. Undersea Biomed Res. May 1989;16(3):185-93. [Medline].

  19. Kieser J, Holborow D. The prevention and management of oral barotrauma. N Z Dent J. Dec 1997;93(414):114-6. [Medline].

  20. Kimbro T, Tom T, Neuman T. A case of spinal cord decompression sickness presenting as partial Brown-Sequard syndrome. Neurology. May 1997;48(5):1454-6. [Medline].

  21. Melamed Y, Shupak A, Bitterman H. Medical problems associated with underwater diving. N Engl J Med. Jan 2 1992;326(1):30-5. [Medline].

  22. Moon RE, de Lisle Dear G, Stolp BW. Treatment of decompression illness and latrogenic gas embolism. Respir Care Clin N Am. Mar 1999;5(1):93-135. [Medline].

  23. Moon RE, Sheffield PJ. Guidelines for treatment of decompression illness. Aviat Space Environ Med. Mar 1997;68(3):234-43. [Medline].

  24. Morgenstern K, Talucci R, Kaufman MS, et al. Bilateral pneumothorax following air bag deployment. Chest. Aug 1998;114(2):624-6. [Medline].

  25. Muehlberger PM, Pilmanis AA, Webb JT, Olson JE. Altitude decompression sickness symptom resolution during descent to ground level. Aviat Space Environ Med. Jun 2004;75(6):496-9. [Medline].

  26. Parell GJ, Becker GD. Inner ear barotrauma in scuba divers. A long-term follow-up after continued diving. Arch Otolaryngol Head Neck Surg. Apr 1993;119(4):455-7. [Medline].

  27. Payne SJ, Chappell MA. Automated determination of bubble grades from Doppler ultrasound recordings. Aviat Space Environ Med. Aug 2005;76(8):771-7. [Medline].

  28. Petri NM, Andric D. Differential diagnostic problems of decompression sickness--examples from specialist physicians' practices in diving medicine. Arch Med Res. Jan-Feb 2003;34(1):26-30. [Medline].

  29. Raymond LW. Pulmonary barotrauma and related events in divers. Chest. Jun 1995;107(6):1648-52. [Medline].

  30. Reuter M, Tetzlaff K, Warninghoff V, et al. Computed tomography of the chest in diving-related pulmonary barotrauma. Br J Radiol. May 1997;70(833):440-5. [Medline].

  31. Russi EW. Diving and the risk of barotrauma. Thorax. Aug 1998;53 Suppl 2:S20-4. [Medline].

  32. Segev Y, Landsberg R, Fliss DM. MR imaging appearance of frontal sinus barotrauma. AJNR Am J Neuroradiol. Mar 2003;24(3):346-7. [Medline].

  33. Sheffield PJ. Flying after diving guidelines: a review. Aviat Space Environ Med. Dec 1990;61(12):1130-8. [Medline].

  34. Sheridan MF, Hetherington HH, Hull JJ. Inner ear barotrauma from scuba diving. Ear Nose Throat J. Mar 1999;78(3):181, 184, 186-7 passim. [Medline].

  35. Shupak A, Melamed Y, Ramon Y, et al. Helium and oxygen treatment of severe air-diving-induced neurologic decompression sickness. Arch Neurol. Mar 1997;54(3):305-11. [Medline].

  36. Smerz RW. Age associated risks of recreational scuba diving. Hawaii Med J. May 2006;65(5):140-1, 153. [Medline].

  37. Tschopp S, Keel M, Schmutz J, Maggiorini M. Abdominal compartment syndrome after scuba diving. Intensive Care Med. Nov 2005;31(11):1595. [Medline].

  38. US Navy. US Navy Diving Manual. Rev 4. Vol 1-5. Claitor's Publishing Division; 1999: 1:1-5, 2:13-21, 3:19-31, 8:1-68, H:1-27.

  39. Webb JT, Pilmanis AA, Balldin UI, Fischer JR. Altitude decompression sickness susceptibility: influence of anthropometric and physiologic variables. Aviat Space Environ Med. Jun 2005;76(6):547-51. [Medline].

  40. Wherrett CG, Mehran RJ, Beaulieu MA. Cerebral arterial gas embolism following diagnostic bronchoscopy: delayed treatment with hyperbaric oxygen. Can J Anaesth. Jan 2002;49(1):96-9. [Medline].

Further Reading

Keywords

barotrauma, the bends, caisson disease, dive medicine, hyperbaric medicine, squeeze, sinus squeeze, decompression sickness, DCS, decompression sickness type I, decompression sickness type II, middle ear squeeze, arterial gas embolism, AGE, decompression chamber, recompression, diving-related disease, diving barotrauma

Contributor Information and Disclosures

Author

Joseph Kaplan, MD, FACEP, Assistant Professor, Department of Emergency Medicine, Medical Center of Central Georgia
Joseph Kaplan, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Marshall E Eidenberg, DO, Staff Emergency Physician, Via Christi Regional Medical Center
Marshall E Eidenberg, DO is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Dana A Stearns, MD, Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital
Dana A Stearns, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

David Eitel, MD, MBA, Associate Professor, Department of Emergency Medicine, York Hospital
David Eitel, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: eMedicine.com, Inc. Consulting fee Consulting

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.