Clinical Practice Guideline

for

DECOMPRESSION SICKNESS and ARTERIAL GAS EMBOLISM

Developed for the

Aerospace Medical Association

by their constituent organization

American Society of Aerospace Medicine Specialists

 

Overview: Decompression sickness: Decompression sickness (DCS) can occur from decompression during flight, from altitude chamber exposure, from flying at high altitudes, from diving, from working in pressurized tunnels or caissons, or from hyperbaric chamber exposure.  The reported incidence of in-flight DCS is fortunately rather rare, possibly because of extremely reliable aircraft pressurization systems.  By contrast, DCS is much more commonly reported with altitude chamber operations employed for aircrew training and research (~3/1000 exposures per year).  DCS varies widely in its clinical presentation from minor skin itching, through joint or limb pain to serious neurologic, cardiopulmonary, and inner ear involvement.  Older classification systems, categorizing less severe DCS symptoms as Type I and more severe as Type II, have been dropped in favor of simple symptom descriptors.  Symptoms of severe DCS include any neurologic sign or symptom consistent with injury or dysfunction of the CNS including vertigo, headache, disorientation, slurred speech, incoordination; pulmonary symptoms (chokes) including chest pain, cough, and SOB; and circulatory collapse.  Since there are no pathognomonic signs or symptoms or definitive laboratory tests, diagnosis depends on a high index of suspicion and a very careful history for recent credible exposure.  Neurologic DCS presents in one of two forms: a peripheral form and a central nervous system form.  The central nervous system DCS includes spinal cord DCS and cerebral DCS.  The peripheral form often consists of paresthesias in upper or lower limbs (commonly in the same limb affected with musculoskeletal pain), which resolves quickly with treatment.  In some case of spinal DCS, what seems like peripheral neurologic symptoms on the trunk can progress rapidly to paraplegia, so caution (in the form of aggressive treatment) is warranted.  Involvement of the central nervous system can lead to permanent neurologic deficit if not recognized early and treated appropriately.  It is critical to perform a thorough neurologic exam to detect subtle findings including neurocognitive deficits.  Oftentimes patients judged to have only peripheral complaints prior to recompression will admit to a “haze” being lifted during recompression – this “haze” (mild disorientation, flat affect, personality change) should be considered a CNS symptom.  Current literature suggests it is rare for DCS symptoms to begin more than 24-48 hours following decompression exposure.  However, DCS should still be considered in the differential diagnosis for any individual presenting with DCS symptoms even beyond this period of time if they had a credible exposure (i.e. at or above 18,000 ft or hyperbaric exposure).  Three factors have been well established through both human use protocols and flight operations as predictors of altitude induced DCS.  These are altitude of exposure, duration of altitude exposure, and physical activity level while at altitude.  A fourth very important but not quantifiable factor is personal variability, i.e., some personnel are very susceptible whereas other personnel are highly resistant to developing DCS.  Exercise enhanced pre-breathing (EEP) with 100% oxygen prior to exposure is an effective countermeasure to developing DCS and is used routinely in U-2 operations.  Other factors commonly mentioned but less well validated include hypoxia, obesity, caffeine, smoking, alcohol consumption and recent injury or trauma.

 

The pathophysiology of decompression illness (both decompression sickness and arterial blood gas formation) is not entirely understood.  The pathophysiology behind neurologic DCS is likewise unknown as is the period of increased susceptibility (if any) to recurrent injury following an initial episode of neurologic DCS.  In general, inert gas bubbles (most commonly nitrogen) cause harm through vascular obstruction, ischemia, and stimulation of inflammatory processes following damage to the endothelium. Subsequent reperfusion injury may also occur.  The bubbles arise as a result of exposure to decreased ambient pressure either following hyperbaric exposure, e.g. SCUBA diving, prolonged exposure to underground environments, or by altitude exposure.  It is believed bubbles causing DCS almost exclusively arise within the venous system and are shunted to the arterial circulation through pulmonary shunts or more rarely atrial defects such as a patent foramen ovale (PFO) causing harm through mechanical distortion of tissues, pulmonary vascular obstruction, or stimulation of inflammatory processes that leads to tissue edema, hemoconcentration, and hypoxia.  Neurologic deficits may be transient or permanent.  Published studies on divers indicate a two-fold increased incidence of white matter hyperintensities (WMH) on brain MRI compared to controls even in the absence of a history of neurological DCS.  Similar WMH have been noted in 7 of 13 (54%) clinically evaluated high altitude U-2 military fliers that have experienced neurological DCS.  Preliminary research data on a very limited pilot sample at the USAF Aeromedical Consultation Service (AC) and Research Imaging Center (RIC) of the University of Texas at San Antonio Health Science Center revealed no lesions detected by 3.0 Tesla (T) MRI (research MRI) if the 1.5 T MRI (standard clinical MRI) did not detect lesions.  Additional lesions were, however, detected by the 3.0 T MRI when one or more lesions were noted on 1.5 T MRI.  Furthermore, these lesions were unique in their morphology and were not seen in the normative data base maintained by the RIC of the 133 age 20 to 40 year-old subjects with no history of neurologic insult, hypertension, hyperlipidemia, or diabetes mellitus nor in the entire study base population of 800 community-based subjects.  The clinical significance, both immediate and long term, of these lesions is currently unknown.

 

Recompression by hyperbaric oxygen therapy is the definitive treatment for DCS.  Symptoms of altitude related DCS often resolve upon descent to lower altitudes and/or the administration of 100% oxygen.  Less severe cases of DCS manifest as joint or limb pain.  When these symptoms of the “bends” resolve on descent or administration of 100% oxygen, they do not mandate hyperbaric therapy.  Specific guidelines for treatment of pain only DCS with ground level oxygen can be found in AFI 48-112.  However, DCS symptoms that persist or recur after initial recovery, and all cases of neurologic DCS (whether resolved with descent and oxygen or not) and chokes, require hyperbaric treatment as soon as possible.  Even in severe cases, expeditious treatment with hyperbaric oxygen has been associated with a high rate of recovery.

 

Arterial gas embolism: For an air embolism to occur there must be a direct communication between a source of air and the vasculature and a pressure gradient favoring the movement of air into the circulation.  Arterial gas embolism (AGE) is seen in trauma, the placement of central lines, surgery, positive pressure breathing, ascent in diving (breath holding), and rarely in aviation ascent (rapid decompression usually associated with positive pressure breathing and/or anti G-straining maneuver).  The symptoms may be difficult to separate from DCS; however in AGE the onset of symptoms is in general more rapid (within 10 minutes of ascent) and can be life-threatening with air bubbles obstructing the systemic or pulmonary arterial circulation.  Hyperbaric treatment is the only definitive treatment for AGE.

 

Aeromedical Concerns: DCS is a normal response to an abnormal condition.  If an individual is subjected to conditions sufficient to produce DCS often enough, he or she will eventually develop symptoms.  The major aeromedical concern is incapacitation in flight as well as any residual neurologic, neurocognitive, or neuropsychologic impairment.  The risk of recurrent injury or increased susceptibility to subsequent injury following an initial episode of DCS is unknown as is the short and long term risk of permanent neurocognitive impairment following repeated episodes of neurologic DCS.  Permanent subcortical dementia following a single episode of neurologic DCS in an aviator has been documented by US Air Force researchers.  The risk of seizures following altitudinal DCS is unknown.  In saturation divers 18% of divers were noted to have abnormal EEGs as compared to 5% of controls; however this study did not compare the incidence of seizures of divers compared to controls.  Furthermore it is unknown if data from saturation divers can be applied to altitudinal DCS.  Seizures are known to occur following stroke in young adults (~ 5-11% incidence over the first 3-years); whether the pathophysiology of DCS with presumed arterial occlusion and/or focal endothelium inflammatory change predisposes to subsequent seizures is unknown.   Additionally the MRI lesions noted following altitudinal DCS have a unique morphology and may not present the same risks of seizures as the typical stroke lesions.  Recent consensus statement from the 2010 DCS-AGE Workshop noted the risk of seizures is unknown with currently no medical evidence indicating increased risk of seizure.  This committee also concluded aspirin 81mg may potentially lessen the incidence of neurologic DCS secondary to its platelet inhibition effect.  Large vessel occlusion from AGE in the aviation environment is rare.  If it does occur, the pulmonary rupture that caused the AGE needs to heal before returning to flying duties.  Furthermore, a pulmonary pathologic condition, a predictor of recurrence, should be ruled out (chest x-ray).  While theoretically a PFO could also predispose the risk of DCS, there is no current evidence neurologic DCS is increased in the presence of a PFO in altitude induced DCS.  Current practice suggests closure of the PFO does not significantly decrease the risk of subsequent AGE or DCS.

 

Medical Work-up: The history of the DCS or AGE event is critical.  This needs to include risk factors, exposures, initial symptoms, treatment, residual symptoms (if any), and any functional limitations.  A good neurological exam will be important, and if there were initial neurological symptoms, neurocognitive testing will be very helpful.  For AGE cases, a chest X-Ray to rule out lung parenchymal pathology is necessary.

 

Aeromedical Disposition:

 

Air Force: An episode of DCS is disqualifying for all FCI, FCII, FCIIU, FCIII, ATC/GSB, SMOD, and altitude chamber personnel.  Waiver is required for any severe episode of DCS/AGE which would include any event that involves the central nervous system or spinal cord.  Any altitude-induced DCS/AGE episode that requires recompression therapy requires a waiver.  Altitude chamber induced DCS/AGE without residual symptoms or clinical findings following recompression treatment does not require a waiver but still requires evaluation. 

 

Current medical knowledge does not permit clear delineation of susceptibility to repeat DCS nor does it allow precise definition of risk of sudden incapacitation or of neurocognitive impairment.  As a consequence the Aeromedical Standards Working Group (ASWG) recommended the following pending acquisition of data that will permit further refinement of risks.  Current ASWG recommendations are a minimal 72-hours DNIF following a chamber exposure, a minimum 1-month DNIF following an altitudinal exposure with complete resolution of symptoms within 2-weeks of exposure and with acceptable, and a minimal 6-month DNIF following altitudinal exposure without complete resolution by 2-weeks or without acceptable studies.

 

Army: Decompression Sickness is not a large problem for Army aviation due to the flight profiles generally flown in the rotary wing environment.  Most cases in the Army occur during training in hypobaric chambers.  A single episode of Type I DCS (pain only) does not require a waiver and individuals can return to flying 72 hours after the symptoms have completely resolved.  Applicants have not been waivered who have had recurrent Type I DCS or Type II DCS (neurological involvement); however  waiver can be considered for rated personnel on a case by case basis one month after all symptoms have resolved.

 

Navy: Decompression sickness with full recovery is not considered disqualifying (NCD) for flying duties.  Type I or Type II DCS with residual symptoms after treatment is considered disqualifying (CD); however, waiver may be considered on a case-by-case basis.  Neurology (and possible neuropsychological examination) is required for waiver consideration.  The flight surgeon with a patient with suspected DCS should make an aeromedical disposition after consulting with Naval Aerospace Medical Institute (NAMI) Neurology, and document a normal evaluation by a neurologist, and a Diving Medical Officer (DMO) or Hyperbaric Medicine Officer (HMO) prior to returning a member to flight status.  Members with a history of DCS should be referred for hypoxic training using the Reduced Oxygen Breathing Device (ROBD) as it becomes available for use.  Bubble contrast echocardiogram is offered to patients only as an option.  Grounding requirements for Type I DCS are at least 3 days with no evidence of residual effects, and for Type II DCS are at least 14 days with no evidence of residual effects.  Treatment with recompression therapy is the standard; however, many Type I patients will respond completely to surface oxygen therapy and may not require hyperbaric oxygen.  The above recommendations adopt the policy used by the Navy diving community and consider DCS as a treatable occupational hazard that should have no adverse impact on a member's future career following full clinical recovery.

 

It has been postulated that patent foramen ovale (PFO) or atrial septal defect (ASD) predisposes to DCS.  NAMI has studied over 50 cases of altitude DCS with contrast echocardiography, and has been unable to demonstrate an increased prevalence of ASD in affected individuals.  Roughly 30% of the DCS cases had an ASD, corresponding closely to the expected prevalence in this age group.  Paradoxical embolism (from right to left) has been well documented in hospitalized patients, and theoretically gas bubbles can cross as well, leading to AGE.  The diving community is concerned about this possibility, and has excluded known ASD/PFO cases from diving duty.  Patients who have had repair of ASD may be more prone to arrhythmias.  The role of previously undiscovered ASD in the etiology of CNS decompression sickness is still controversial.

 

Civilian: Decompression sickness will initially be disqualifying for all classes until successfully treated.  Once treated the airman will need to provide the FAA with the pertinent medical records on the event and more than likely the airman will be returned to flight status.  A neurologic decompression event may require that the airman obtain a COGSCREEN-AE or complete neuropsychological testing prior to being considered for recertification of their medical certification. 

 

Waiver Experience:

 

Air Force: Review of AIMWTS showed 28 cases of decompression sickness; sixteen were FC II, seven were FC III and five were aerospace physiologist technicians (9C).  A total of four were disqualified; two FC II, and three aerospace physiologist technicians.  The two physiologist technicians were disqualified because of recurrent DCS during chamber flights, one of the FC II was disqualified due to severe residual neurological deficits and the other was disqualified for other medical problems.  AIMWTS review also showed one case of air embolism in a FC III aviator secondary to diving; waiver granted.

 

Army: Decompression sickness has been an uncommon diagnosis in this population.  In 2010, of the 16,852 rated aircrew who had a current flight physical, none carried this diagnosis.  Historically, there has been one rated aviators with this diagnosis, and six non-rated aircrew who have had DCS.  Of these six, two were waivered and four were disqualified.

 

Navy: Not available at this time.

 

Civilian: Statistical data is not kept for this condition. 

 

ICD 9 codes for Decompression sickness

993.3

Caisson disease

958.0

Air embolism

 

References:

 

Balldin UI, Pilmanis AA, Webb JT.  Central nervous system decompression sickness and venous gas emboli in hypobaric conditions.  Aviat Space Envir Med.  2004; 75:  969-972.

 

Elliot DH, Kindwall EP.  Decompression Sickness.  In: Kindwall EP, Whelan HT eds. Hyperbaric Medicine Practice, 2nd ed. rev. Flagstaff AZ:  Best Publishing Company, 2004; 433-487.

 

Rudge FW, Zwart BP.  Effects of decreased pressure:  Decompression sickness. Feb 2002  In:  Flight Surgeon’s Reference,

http://airforcemedicine.afms.mil/idc/groups/public/documents/afms/ctb_073676.pdf

 

Stepanek J.  Decompression sickness.  In: DeHart RL, Davis JR eds.  Fundamentals of Aerospace Medicine, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2002; 67-98.

 

USAFSAM Hyperbaric Medicine Division, Administrative treatment of DCS.

22 Feb 02.  At https://kx.afms.mil/kxweb/dotmil/kjPage.do?functionalArea=HBO_USAFSAM&cid=ctb_071714

 

Vann RD.  Mechanisms and Risks of Decompression.  In: Bove AA ed.  Bove and Davis’ Diving Medicine, 4th ed.  Philadelphia: Saunders, 2004; 127-164.

 

Bennett  MH, Lehm JP, Mitchell SJ, and Wasiak  J.  Recompression and Adjunctive Therapy for Decompression Illness: A Systematic Review of Randomized Controlled Trials. Anesth Analg, 2010;111:757–62.

 

Erdem I, Yildiz S, Uzun G, et al.  Cerebral White-Matter Lesions in Asymptomatic Military Divers. Aviat Space Environ Med, 2009; 80:2 – 4.

 

Reul J, Weis J, Jung A, et al.  Central nervous system lesions and cervical disc herniations in amateur divers.  Lancet, 1995;345:1403-05.

 

Jersey S, Baril R, Jesinger R, et al. The Role of Imaging in Aviation Neurological Decompression Sickness.  96th Annual Meeting Radiological Society of North America

 

Personal communication Peter Kochunov, Radiology Imaging Center, University of Texas Health Sciences Center, San Antonio, TX.

 

O’Dowd LC, Kelley MA.  Air embolism.  UpToDate.  Online version 18.2, May, 2010.

 

Todnem K, Skeidsvoll H, Svilus R, et.al.  Electroencephalography, evoked potentials and MRI brain scans in saturation divers.  An epidemiological study.  Electroencephalography and clinical.  Neurophysiology, 1991;79:322-329.

 

Burn J, Dennis M, Bamford J, et al.  Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project.  BMJ, 1997; 315:1582-7.

 

Naess H, Nyland HI, Thomassen L, et al.  Long-term outcome of cerebral infarction in young adults.  Acta Neurol Scand, 2004;110):107-12.

 

Lairez O, Cournot M, Minville V, Roncalli J, Austruy J, Elbaz M, Galinier M, Carrie D. Risk of neurological decompression sickness in the diver with a right-to-left shunt: literature review and meta-analysis. Clin J Sport Med 2009;19(6):512-3.

 

 

 

 

 

 

 

Developed by Dr. Steve McGuire, Dr. Rob Michaelson, and Dr. Dan Van Syoc

 

November 14, 2011