Trauma of rapid decompression

Trauma

of Rapid

Decompression

LT. COL. ANDRES I. KARSTENS, M.c., u.s.A.F.,

From tbe School of Aviation Medicine, dolpb Air Force Base, Texas.

U.S.A.F.,

Ran-

APID decompression, frequently termed “explosive” decompression in the past, is the sudden and complete accidenta failure of pressurization of crew space and passenger space in aircraft fhght. The probability of accidenta cabin decompression and the associated disadvantages must be weighed against the advantages of pressurization. Cabin pressurization is used in both military and civilian aircraft for the folIowing reasons: (I) prevention of hypoxia and dysbarism in crew and/or passengers; (2) reduction of persona equipment and impediments to crew mobility; (3) comfort for passengers and crew; and (4) protection of physicaIIy unsound passengers and/or patients. The relative importance of the above factors will vary, depending on the purpose of the flight, true altitude attained, duration of the flight, passenger demands for comfort and the like. In military aircraft, the accomplishment of the mission will be the genera1 controlling factor; in civihan aircraft, passenger safety and business success of the airline wiI1 be the general controlling factor. In miIitary combat aircraft, when flying from 30,000 feet to 40,000 feet, clysbarism is probabIy the most compelling reason for pressurization, since bends are the most likely unavoidabIe cause of aborting a mission at those ahitudes. At aItitudes significantly above 40,000 feet both hypoxia and bends dictate an absolute need of some form of pressurization. In view of the above, we can see that cabin pressurization will always be with us. It can also be stated axiomatically that the possibility of accidental rapid decompressions wi11 aln-ays be with us in some form, if not due to unavoidable structural weaknesses of the aircraft, then due to enemy action, error on the part of the operator or unforseeabIe stresses.

R

Randolph

Air Force Base, Texas

In the past the most common cause of sudden accidental cabin decompression has been structural or mechanica faiIures. These have most often been separation of a window or observation blister, such as the astrodome, or the accidenta opening of a norma exit. Occurrences of sudden accidenta decompressions are psychoIogicaIIy disturbing and detrimental to organizationa moraIe. This applies equally to either miIitary operations or civilian passenger operations. Consequently, a fuIl understanding of any potentia1 hazards which may exist, as well as understanding of the measures needed to eliminate such hazards, is necessary. The United States Air Force has found it advisable to familiarize all flying personnel with rapid decompression and the methods for eliminating potential hazards associated therewith. This is accompIished by having a11 personnel experience actuaI rapid decompression in indoctrination chambers as part of their altitude training. Th e potential hazards to crewmen and passengers in rapid decompression may be summarized as foIIows: (I) traumatic injury due to accidental ejection by wind bIast, or aircraft deceleration; (2) non-traumatic hazards of hypoxia, bends, gas and vapor ebullition at high aItitudes, and expansion of gases trapped in body cavities; and (3) puImonary injury syndrome due to expansion of intrapulmonary gases. The principal hazards to flyers in the past have been in the first two categories. WhiIe hypoxia is regarded as the major hazard in flying aircraft at high aItitude, accidenta ejection has led to more morbidity to date, and aircraft deceleration and/or disintegration due to major cabin disruption has contributed to a number of deaths in two instances as reported by Armstrong et al. [I]. Since such injuries are simply due to external blows and not peculiar to decompression, we shah not dweII upon them,

Karstens cabin. These are: (I) an elastic and compliant walled thorax and abdomen, of variabIe thickness and Tveight; (2) a pulmonary decompression orifice of variable size; and (3) lungs which are limited in their capacity for elastic expansion under positive intrapulmonary pressure. Gases which are trapped in a body cavity during a decompression tend to expand in

but wil1 rather consider the possibiIities and nature of the puImonary injuries which, although rare, are peculiar to decompression. PULMONARY

TRAUMA

In order to discuss the occurrence, and mechanism of pulmonary injury, consider the etioIogic forces first.

nature Iet us

DECOMPRESSION ORIFICE

ALTITUDE IN FEET -

-----Ii------

IMBIENT 150mm.Hg ABSOLUTE ----,-

63

PRtSSURE IN ATMOSPHERES

000

CABIN 600 milwg ABSOLUTE PRESSURE 450mm.Hg DIFFERENTIAL PRESSURE

WET

/

DRY

m

SEA LEVEL

FIG. 2. Relative voIumes of wet and dry gases versus pressure altitude at body temperature.

FIG. I. Diagrammatic representation of a pressurized

cabin.

accordance with the physica Iaws relating pressure and voIume of gases. Because the surfaces of the fungs are wet, the gases in the lungs are kept saturated with water vapor. Therefore, the voIume of trapped intrapulmonary gases is not exactly inversely proportiona1 to the absoIute intrapuImonary pressure, but is inversely proportional to absolute pressure minus the vapor pressure. Consequently, reIative Iung voIumes before and after a decomprovided no gas escapes, are expression, pressed by the formuIa

In Figure I we have depicted a schematic pressurized cabin with certain important physical variabIes. These are: I. Size of the cabin: Variation in size influences the time of decompression. 2. Size of the decompression orifice: Variations in the size of this orifice influence the time of decompression, as does also the initial and final pressure. 3. Ambient pressure: This is also the final cabin pressure foIlowing a decompression. 4. Cabin pressure: This is also the initial intrapulmonary pressure. 3. DifferentiaI pressure: This is the difference between ambient pressure and initial cabin pressure; this Iimits the highest attainable transthoracic pressure following a decompression. These five factors determine the time duration of decompression, the maximum intrapuImonary pressure attainabIe, and the relative voIume of intrapuImonary gases before and after a decompression. In addition to the physica variabIes of the pressurized cabin, we have the physical and physioIogic variables of the men sitting in the

where V1 = Vz = PZ = P1 = 47 =

V1 -=

P2 -

V?

PI - 47

47

initia1 Iung voIume fina Iung volume fina intrapuImonary pressure initia1 intrapuImonary pressure vapor pressure in mm. Hg at temperature

body

Figure 2 iIIustrates the gas expansion ratios of dry and wet gases at body temperature and at various aItitudes. Note that these gas exratios are based on expansion to pansion 742

Trauma

of Rapid

Decompression celIs and fibers might be unable to elongate at the speed required, with consequent tearing of capillaries and alveolar walls and other tissues of the lung. Additionally, theories of excessive expenditure of energy on the lungs and/or bIast Iike effects have been proposed [r,~]. At autopsy the rat lungs in question manifested extensive, diffuse hemorrhage, best described as “hepatization.” Work must first be cIone on Iarger animals at these exceedingly rapid decompression rates before extrapoIation of the results to human beings. Such extremeIy rapid decompressions continue to be of interest, since very rapid decompression couId theoretically occur where cabin volume is very smaI1 and a Iarge potential decompression orifice exists. Sweeney [4j approached what he considered to be the Iimits of human toIerance to very rapid decompression with decompression times of 3 miIIiseconds through 30 mm. Hg differentials, from 140 mm. Hg to 90 mm. Hg. AnimaIs exposed to 5 miIIisecond decompressions to 40,000 feet through wide ranges of pressure toIerate the exposure well [r3], although autopsies on such animals show patchy areas of hemorrhage and ateIectasis. In addition, there is evidence that a reflex effect on respiration and blood pressure is produced through reflex action initiated by the stretch receptors of the lung. Returning for a moment to our diagram, Figure I, we may consider what might happen if the respiratory passages were completely blocked during a cabin decompression. In spite of extensive research in rapid decompression to altitude, we have IittIe specific experimenta data on rapid decompression to aItitude with occIuded respiratory passages. The hazards precIude such experiments in human beings, and animal trials have nearIy a11 been with no artificial respiratory obstruction. However, some pertinent information is avaiIabIe on the subject as discussed herein. Theoretic considerations, supported by reIated experiences in submarine escape training and ascent from depth in underwater swimming, indicate that grave damage could occur if complete obstructions of the respiratory passages were associated with rapid decompression at altitude. CIosure of the glottis by iIIadvised voluntary breath holding, incIuding VaIsaIva maneuvers, is the most IikeIy means for such respiratory obstruction. If, in Figure I, cIosure of the glottis were

ambient pressure, a situation which does not actually obtain in gases enclosed in body cavities. Both theoretic considerations and experience will indicate that there are essentially two conditions which must be considered as the most hazardous and most Iikely to produce pulmonary injury. These are: (I) conditions which produce overdistention of the Iungs, and (2) exceedingly rapid decompressions which produce intolerable rates of distention. We shall see that the hazards of the first condition are well-demonstrated and understood, whiIe in the second condition they are not as well understood and are difficult to demonstrate experimentaIly. One may visualize several possibIe combinations of the factors depicted in Figure I in an accidental decompression. If cabin decompression is reIativeIy slow and the glottis remains open, the lungs decompress through the mouth or nose aImost as rapidIy as the cabin decompresses and very Iittle differential pressure is buiIt up across the chest wall with little consequent expansion of the chest. If cabin decompression is reIativeIy faster, the discharge of air from the Iungs is speeded up also, but a Iarger differential pressure and more distention of the Iungs occurs. This is due to the inability of gases to escape through the respiratory orifices with sufficient speed. A hypothetic instantaneous decompression would exert an initial pressure across the Iung and chest waI1 which wouId be equal to the initial cabin differentia1 pressurization. ActuaI operation experience supported by laboratory experiment has shown, however, that if the airway to the Iungs remains open, the fastest cabin decompression IikeIy to be attained, except under very specia1 conditions, will not resuIt in sufficient distention of the Iungs to produce either injury or symptoms. Even with the oxygen mask on, partIy obstructing the expiratory passage of air, no injury has been encountered with chamber decompression as rapid as 300 milliseconds, from 20,000 feet to 47,000 feet [2]. To date we have IittIe data on exceedingIy rapid decompressions, i.e., of the order of I miIIisecond, with the exception of some recently reported work on rats [3]. Theoretically, such decompressions couId tear Iung tissue by distending the Iungs faster than the time required for puImonary compIiance. IndividuaI 743

Karstens compIete during the decompression with an initia1 Iung volume of 3,000 cc (one-haIf the tota Iung capacity at fuII inspiration), even disregarding the effect of water vapor, the gas in the lungs could expand to 6,000 cc whiIe retaining a residual transthoracic pressure of

may be associated with the hemorrhages, as we11 as frothy blood-stained fluid at the nose or mouth. There are a few cases in which experimental or indoctrinationa rapid decompressions have led to near disaster by the aforementioned DEPTH UNDER WATER IN FEET

PERCENT OF TOTAL LUNG CAPACITY

PRESSURE IN mm&l

140

700

INITIAL

600

PRESSURE IN ATMOSPHERES

PRESSURE

RESIDUAL ’ DIFFERENTIAL

-

60

-

40

-160 20

000 D

.I

j .2

.3

.4

.5

.6

.7

.8

.S

1.0.

-224L

SECONDS

FIG. 3. Graphic iIIustration of significant pressures and lung volumes in a rapid decompression from 600 mm. Hg cabin pressure to ISO mm. Hg ambient pressure with a closed gIottis. An initia1 Iung volume of 30 per cent of tota1 lung capacity was assumed for iIIustration. The reIationship of fina Iung voIume to fins1 intrapulmonary pressure is caIcuIated from the formuIa V1 p:! 47 _= -~. The residual differentia1 at maximum V, PI - 47 lung volume is the damaging factor producing pulinterstitial emphysema, mediastina1 emmonary physema and air embolism.

9J.m

cs;;:;; UNITS

FIG. 4. Dry gas volumes surface of water.

150 mm. Hg (300 mm. Hg, intrapuImonary; 150 mm. Hg, ambient); if the effect of water vapor is added to the caIcuIation, the fina lung volumes and pressures are as iIIustrated in experimentations indicate Figure 3. AnimaI that marked trauma and pathophysioIogic sequences would foIIow such a distention. As shown by PoIak and Adams [f] in anesthetized dogs, pulmonary distention produced by IOO air pressure wiI1 mm. Hg intrapuImonary produce peribronchia1 tearing of aIveoIi, capillaries and smaI1 veins, followed by peribronchial hemorrhage, peribronchial interstitial emphysema, and mediastina1 emphysema; air emboh appear in the pulmonary veins, heart coronary vessels, and systemic chambers, vasculature. Patchy ateIectasis and emphysema 744

OF VOLUME

versus pressure

depth below

mechanism. AI1 were associated with breath hoIding. Benzinger [6] described two cases in Germany during W’orld War II; both were due to breath hoIding. An Air Force officer in 1944, misunderstood instructions prior to a familiarization decompression and suffered interstitial mediastina1 emphysema which was manifested by marked interstitia1 emphysema of the tissues of the neck, as a consequence of hoIding his breath during the decompression 171. A second simiIar case was observed; both subjects recovered uneventfuhy. Both cases were associated with breath hoIding during the decompression. In fact, no cases have occurred which were not associated with breath hoIding. A considerabIy Iarger number of cases of simiIar pathophysiology have resuIted from training in underwater submarine escape, as described by Behnke [8] and others [9-121. WhiIe the injuries have not usualIy been severe, severa deaths have occurred in underwater escape training. More recentIy underwater swimming, with breathing apparatus

Trauma

of Rapid

Decompression with overdistention does this uniform expansion fai1, and the peribronchia1 aIveoIi are torn away from the adjacent bronchi; simultaneously the aIveoIi are ruptured and smaI1 veins are torn. These torn vessels are heId open by the elastic recoi1 of a11 the surrounding pulmonary tissue; aIveoIar air is allowed to escape into the peribronchia1 areas and along the pressure gradient into the pulmonary veins, as well as along the peribronchia1 interstitial routes to the mediastinum. After the distention is reIieved, simiIar movements of air probably continue during subsequent respirations, especially if positive and negative intrathoracic pressures are enhanced by partiaIIy obstructed airways, painfu1 “grunting” breathing, improper use of fuI1 body respirators, or completeIy ilI-advised use of positive pressure resusitation. The symptoms of such an event vary with the severity of the distention and damage and massiveness of the interstitia1 emphysema and embolism. A massive embolism wiI1 result in air in the Ieft heart with cessation of cardiac output, cerebra1 ischemia, coronary emboIism and ischemia, and probabIe cardiac death. Less massive emboIism wiI1 result in chest or abdominal pain, either from lungs, mediastinum, or heart, with symptoms of faintness and shock. The majority of such cases described in Navy diver personne1 strongIy suggest the acute myocardial ischemia syndrome. Recovery is frequentIy compIete folIowing such mild symptoms in divers. ShouId rapid decompression occur at aItitudes signiticantIy higher than 65,000 feet, vapor-thorax might ensue after a number of seconds to compIicate any pre-existing injury. This induces additiona ateIectasis as has been shown in dogs decompressed to 30 mm. Hg (72,000 feet), Hitchcock [I?], [r4]. However, in actua1 flight, hypoxia of an intoIerabIy severe degree wouId have preceded the vaporthorax; the emergency protection measures necessary to prevent the hypoxia, (pressure suit activation) would automaticalIy prevent the vapor-thorax, as we11 as vapor emphysema or vapor embolism.

from which the swimmer can inspire whiIe at depth, has added another cause for such injury. Gas voIume heId in the Iungs whiIe under water varies with depth as iIIustrated in Figure 4, disregarding water vapor effect and assuming no change in transthoracic pressure. Thus a person who started from a depth of g6 feet with 2,500 cc. of gas in his Iungs would, if he held his breath without voIuntariIy compressing his chest, have about 5,000 cc. lung volume when he reached the 32 foot IeveI. If he continued to hoId his breath until he reached the surface, the air couId potentially doubIe in volume again; since this is impossibIe, a high transthoracic pressure would buiId up with littIe more expansion; the pathophysiology described above wouId ensue. If he took a maximum from his breathing inspiration apparatus, he might suffer such injury when surfacing from a few feet of depth, such as the bottom of a swimming ~001, provided he did not continue to breathe during the ascent. The pathophysioIogy described is the consequence of the physical nature of the puImonary and intrathoracic structures. Positive intrapulmonary pressure aIone without chest and/or abdominal expansion does not physicaIIy injure the Iungs or produce air emboIism or interstitial puImonary emphysema. Since the chest and abdomen are essentially isobaric regions, no change in relative pressures occurs within these regions and no additiona physical stress is pIaced on any of the contained structures if the thoracic and abdomina1 cavities are not aIlowed to expand. (Such positive pressures do dispIace blood to the periphery, and thereby may cause a diminution in cardiac output.) However, high positive intrapuImonary pressure with distention of the lungs beyond their eIastic Iimits produces injury which is characterized by tearing of puImonary tissues especialIy in peribronchia1 areas. The reason for this seIective site of tearing is pureIy anatomic and functiona1. When expanded within the ordinary Iimits of vital capacity the lungs expand uniformIy in a11 directions, the bronchia tree Iengthening aIong its entire length, the smaIIer bronchioIes and aIveoIi expanding “toward” the Iarger divisions, as well as peripheraIIy, to fil1 in the peribronchia1 spaces, aIthough maintaining a pressure negative, relative to intrapulmonary pressure, in the extra-aIveoIar peribronchial areas. OnIy

PREVENTION

The danger of a crew member hoIding his breath during an accidenta decompression in flight is remote. Prevention of injury from ordinary rapid decompression in flight Iies 745

Karstens tentionally cIose the gIottis or VaIsaIva, at the wrong moment. The mechanism of injury and the sequelae are identica1 with those of injury whiIe surfacing from depth under water, where opportunity to inspire at depth existed, and the gIottis was cIosed during the ascent. Experience to date would indicate that unintentiona cIosure of the glottis at the time of an unpredictabIe accidenta decompression in an aircraft is extremeIy unlikely, and the hazard of puImonary injury exceedingIy remote. The probIem of exceedingly rapid decompressions, of the order of I to 5 miIIiseconds is briefly discussed.

in well known and effective measures for avoiding accidenta ejection and hypoxia, as we11 as engineering to reduce the chances of hazardous decompression to an insignificant minimum. Prevention of injury in indoctrination chambers requires understanding and carefuI expIanation regarding the hazards of breath holding during an anticipated decompression. The experience gained in submarine escape training and underwater swimming may be used to good advantage in such famiIiarization. TREATMENT

Should accidenta puImonary injury occur during a decompression, treatment wouId depend on avaiIabIe facilities, circumstances and severity of injury. In flight one couId do Iittle eIse than give the subject IOO per cent oxygen and place him in a horizontal position, administering such supportive therapy as is indicated and feasibIe. If an injury shouId occur during an indoctrination decompression in a chamber, immediate recompression to ground Ievel is the first step. Diagnostic, monitoring, and therapeutic aids shouId aIways be avaiIabIe at any altitude chamber. If symptoms of air emboIism are present, compression to severa atmospheres, using 100 per cent oxygen, folIowed by sIow decompression to one atmosphere, in accordance with Navv treatment tabIes for divers, is probabIy indicated. AI1 necessary diagnostic and therapeutic aids shouId be avaiIabIe in such a chamber. Pulmonary edema, depressed respiration, and symptoms of shock may compIicate the picture in varying degrees and modify therapy. If pneumothorax is present, it shouId be reIieved by aspiration through an intercosta1 space.

REFERENCES

r. ARMSTKONG,J. A., FRYER, D. I., STEWART, W. K. and WHITTINGHAM, H. E. Interpretation of injuries in the comet aircraft disasters: an experimenta1 approach. Lancet, 268: 6875, 1955. 2. LUFT. U. C.. BANCROFT. R. W. and CARTER. E. T. Rapid decompression with pressure-demand oxygen equipment. School of Aviation Medicine, U.S.A.F. Project 21-1201-0008, Report No. 2, 1953. 3. KOLDER, H. Explosive low pressure decompression. Abstracts of Communication, XX International PhysioIogicaI Congress, p. 5 14, BrusseIs, BeIgium, 1956. 4. SWEENEY, H. M. ExpIosive decompression. Air S. Bull., I : I, x944. 5. POLAK, B. and ADAMS, H. Traumatic air emboIism in submarine escape training. U.S. Nav. M. Bull., 30: 165, 1932. 6. German aviation medicine in WorId War II, vo1. I. U.S. Government Printing Of&e. 7. SWEENEY, H. M. Personal communication. 8. BEHNKE, A. R. AnaIysis of accidents occurring in trainine. with the submarine “Iune.” U.S. Nav. Mu. Bull., 30: 177, 1932. g. ADAMS, B. H. and POLAK, I. B. Traumatic Iung Iesions produced in dogs by simuIating submarine escape. U.S. Nav. M. Bull., 31: 18, 1933. IO. KINSEY, J. L. A neuroIogic syndrome occurring during treatment of air embolism. U.S. Armed Forces M. J., 1762, 1955. I I. MACCLATCHIE, L. K. Medical aspects of submarine “Iung” training. U.S. Nav. M. Bull., 29: 357366, 1931. 12. BROWN, E. W. Shock due to excessive distension of the Iungs during training with escape apparatus. U.S. Nav. M. Bull., 29: 366-370, 1931. 13. HITCHCOCK, F. A. Physiologica and pathoIogica1 effects of expIosive decompression. J. Aviation Med., 25: 578-586, 1954. _ 14. COLE, C. R., CHAMBERLAIN, D. M., BURCH, B. H., KEMPH, J. P. and HITCHCOCK,F. A. PathoIogicaI effects of explosive decompression to 30 mm Hp. J. Appl. Pbysiol., 6: 96, 1953.

SUMMARY

The hazards of rapid decompression in fIight Iie chiefly in ensuing hypoxia, accidenta ejection, and associated physical injuries. Proper equipment and operating procedures can circumvent a11 these hazards. During chamber indoctrination runs, rapid decompression can produce pulmonary injury if persons anticipating the decompression in-

746