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Blast injuries
COLLECTIVE REVIEW blast injury; trauma, blast injury
Blast Injuries [Stapczynski JS: Blast injuries. Ann Emerg Med 11:687-694, December 1982.]
d. Stephan Stapczynski, MD Harbor City, California
INTRODUCTION "Blast injury" is a general term to describe the harmful effects m animals or man produced by a sudden change in environmental pressure originating from an explosion. While first described as a specific entity in 1924,1 it was not until the Second World War that studies in England ~-5 and Germany 6,7 established the clinical and pathological features of this syndrome. After the war, work with experimental animals continued to add knowledge to this field. 812 These injuries were once rare in peacetime, but the worldwide spread of terrorism has made no country immune from the potential for civilian blast injuries. The pathophysiology of blast injuries differs significantly from other forms of trauma, and thus we will stress the key differences in the approach to these patients in the emergency department.
From the Department of Emergency Medicine, Harbor-UCLA Medical Center, Torrance, California. Address for reprints: J. S. Stapczynski, MD, 26416 Zephyr Avenue, Harbor City, California 90710.
TERMINOLOGY Injuries produced by explosions can be divided into four categories. 11,13 Primary blast injuries describe the damage inflicted by the sudden changes in environmental pressure (the "blast wave") itself. The effects are greatest at or near the interface between gas and liquid, and thus organs containing air are most easily injured. In secondary blast injuries the damage results from the victim being struck by flying debris. Tertiary blast injuries are those sustained when the victim is thrown against stationary objects. Both secondary and tertiary blast injuries result from the ability of the blast wave to accelerate loose objects outward from an explosion. 11 Miscellaneous blast injuries include exposure to dust (both radioactive and nonradioactive), direct thermal bums from the explosion, and bums from blast-ignited fires.
BLAST PHYSICS Detonation is a high-speed chemical decomposition of a solid or liquid explosive into a gas. 1517 The space previously occupied by the explosive is filled with a gas under high pressure and temperature. There are two principal types of explosives. High explosives (HE) detonate rapidly; the chemical reaction is triggered by a mechanical shock wave that travels at high speed (10,000 to 30,000 meters/sec) through the explosive. A typical HE is T N T (trinitrotoluene), one gram of which can release 1,120 calories of blast energy and, at the moment of detonation, generate pressures of approximately 106 psi within the initial gas. 17 HE possess brisance (that is, shattering power). The energy is released so rapidly and the pressures generated rise so quickly that nearby objects can be shattered by the force of the explosion. Ordinary explosives, like gunpowder, release their energy slowly by either burning or deflagratmg, and therefore do not possess brisance. The very high pressure within the gaseous products of detonation is transmitted to the surrounding medium and is propagated as a shock wave that travels out radially from the explosion.17 The idealized shock wave is a steep 11:12 December 1982
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BLAST INJURIES Stapczynski
Fig. 1. An idealized s h o c k w a v e (pressure v time).
Fig. 2. M e c h a n i s m s of p r i m a r y blast injuries. fronted pressure pulse that rises rapidly to a m a x i m u m and then decays over a longer period to a m i n i m u m less than the previous ambient pressure (Figure 1). Afterward, the environmental pressure returns to the previous baseline. Idealized shock waves are found only in free-field explosions; the presence of reflecting or absorbing barriers may radically alter the wave form and peak pressure. 16 The velocity of the shock wave and the duration of the positive pressure component is determined by three factors: 1) The size of the explosive charge: A bigger explosion produces shock waves of faster velocity and longer duration; 21 The surrounding medmm: Denser media (like water, as opposed to air) propagate the shock wave faster and with a longer positive pressure duration; and 3) The distance from the explosion: The further from the charge, the slower the shock wave velocity and the longer the duration. Shock waves initially travel faster than the speed of sound, but as they expand, the velocity decreases to the speed of sound and thereafter the shock wave is propagated as an acoustical wave. For the common HE detonated in air, this distance is roughly 50 to 60 charge radii from the initial charge. 16 The peak pressure of the shock wave decreases as the shock wave expands. Because the peak pressure is a prime determinant of the potential for primary blast injuries, the military has performed experiments with different explosives to measure the pressures produced at various distances. The peak pressure at any distance is a function of the initial charge mass and the distance from the explosion. Experimental data usually fit the followhag equation: 16 Peak pressure = A/z + B/z 2 + C/z 3 where: z = R (distance)/3X/Q (charge mass). For explosions in air, the experimentally derived constants A, B, and C are such that close to an explosion (less than 10 charge radii) the last term of the equation dominates, with the peak pressure varying as the inverse of 74/688
P
the distance cubed; far from an explosion (more than 50 to 60 charge radii) the first term dominates, with the d0eak4~re-.~,qllre~vak-yJ/lgasthe inverse of the distance. The distance of 50 to 60 charge radii also correlates with the approximate distance where the peak pressure of an explosion in air is about 15 psi above ambient pressure. The threshold for lung damage from primary blast injuries from typical HE is roughly 15 psi, and therefore primary blast injuries are seen only when the v i c t i m is close to the explosion. Secondary and tertiary blast injuries, however, can occur at much greater distances. Transient winds (the "displacement wave") accompany the pressure variations produced by the shock wave) ° The low density of air means that high velocity winds can be produced by even small changes in pressure: a peak pressure of 0.25 psi corresponds to a wind velocity of 125 mph. Loose objects can be accelerated by the shock wave, but their ultimate velocity is determined by corresponding wind velocity. The high velocity of the displacement wave means that small, light objects can be accelerated rapidly over short distances, and reach a high speed even at low peak pressures. The instantaneous acceleration for large objects is less, but close to an explosion may still be significant. For a typical adult of 165 lb, a peak pressure of 15 psi from an explosion can produce an instantaneous acceleration of about 450 ft/sec 2, or approximately 14 gravities. For common terrorist bombs, this acceleration would last only a few Annals of Emergency Medicine
milliseconds, and the ultimate velocity reached by the victim would be quite low. For explosions from nuclear devices, however, the very long duration of the positive pressure component of the shock wave means a significant time exists in which to accelerate the victim. 11 In this circumstance, even low peak pressures can hurl the victim with significant velocity. The instantaneous acceleration is usually within the tolerable range, but damage may be done if the victim impacts a hard, stationary object. The potential for tertiary blast injuries does not exist in the process of acceleration, but rather in the sudden deceleration when the victim impacts a hard surface.
UNDERWATER EXPLOSIONS Explosions in water produce shock waves of greater peak pressure and longer durationA4, is The shock wave travels at the corresponding speed of sound, which in water is about five times faster than in air. Because of the greater peak pressures, the distance at which primary blast injuries can occur is much greater than for explosions in air. And because water is denser than air, the displacement wave is very low in velocity and rarely produces significant damage. The gaseous products of an underwater explosion produce a bubble which rises toward the surface. When it reaches the surface, the bubble produces the characteristic explosive plume as particles of water are hurled high into the air.14 It is difficult to predict the damage that may result from underwater blasts because the initial shock wave may reflect off the 11:12 December 1982
Spalling Implosion Acceleration-deceleration (inertial) Pressure differentials 2
TABLE. Expected primary blast
injuries
Injury
Pressure (psi)
Ear drum rupture 5 Lung damage threshold 15 Lethality threshold 30-42 LD50 (50% fatal) 42-57 95-100% fatal 58-80
POTENTIAL FOR INJURY
surface or bottom and onto the target. The target may feel the effects of the initial shock wave and any reflected ones - - all with the possibility of summating to produce a higher peak pressure.
MECHANISMS OF INJURY
i,
The sudden change in pressure caused by the shock wave can damage living tissue by four mechanisms is (Figure 2). When a shock wave reaches an interface between media of different densities, reflections create turbulence and cavitation. This can throw particles of fluid from the more dense to the less dense medium ("spalling"). In animal tissues, as the shock wave travels through an organ containing both liquid and gas, particles of liquid are "spalled" into the gaseous compartment. As a shock wave travels through an organ containing pockets of gas, each pocket of gas can be compressed by the pressure of the surrounding fluid. Once the shock wave has passed, the rebound expansion of each gas pocket is then a miniature internal "secondary" explosion. As the victim is either accelerated away from an explosion or impacted against a stationary object, the possibility of acceleration-deceleration (inertial) injury exists. In this situation, organs of different densities, masses, or attachments may be accelerated at different rates relative to one another,
11:12 December 1982
and the shearing motion that can develop tears or disrupts the tissues. This is significant in causing tertiary blast injuries. Finally, at the moment of impact of the shock wave upon the victim, a difference in pressure may evolve between the outer surface of the body and the intemal organs. Because water is e s s e n t i a l l y incompressible, the pressure on the exterior and within the fluid-containing tissues and vascular system remains equal. However, because gas within the alveoli is easily compressible, at the moment of impact of the shock wave, a pressure differential may exist between the vascular system and the alveoli. This drives blood from the pulmonary capillaries into the alveolar spaces, and contributes to the pulmonary hemorrhage seen in primary blast injuries. The potential for primary blast injuries varies according to the peak pressure and duration of that pressure. ]°A1 Animal experiments also document the protection offered by barriers, like foxholes or furniture, as they markedly reduce the peak pressure the protected animal experiences. For the common HE used in civilian terrorist bombs, the duration of the positive pressure is 2 and 10 ms for charges of 50 and 4,000 lb, respectively. For a human being exposed to this type of blast, the potential injuries vary with the peak pressure 1° (Table}. Rapid acceleration of small fragments by an explosion is a major factor in secondary blast injuries. Small missiles are commonly accelerated to velocities of several hundred feet per second. At velocities of 50 ft/sec skin is easily lacerated, and at velocities of 400 ft/sec serious wounds involving penetration of body cavities are seen in most cases, n These velocities are c o m m o n l y produced from terrorist bombs, and it is the secondary injuries caused by flying glass, shrapnel, and debris that produce much of the morbidity from these explosions, is The acceleration of a human victim by an explosion may be tolerable, but it is the sudden impact against a hard surface that can be lethal. Extrapolation of animal experiments to a 70-kg man predicts a 50% mortality from a vertical impact against a flat, concrete surface at a velocity of 26 ~t/sec or 18 mph. TM This estimate agrees with data in the literature on the ability of human beings to survive deceleration in-
Annals of Emergency Medicine
juries. Impacts of 10 ft/sec appear to be the limit of voluntary tolerance of human beings in both the sitting and standing positions. 19 Impacts of 11 to 16 ft/sec onto hard surfaces with the knees locked can produce fractures in the lower extremities. 11 Impacts of 15 to 23 ft/sec can cause skull fractures. 2° And finally, motor vehicle accidents at velocities of less than 41 ft/sec are associated with up to 70% mortality. 1~ Thus if the v i c t i m is accelerated to a velocity greater than 15 to 20 ft/sec and impacts a hard surface, serious injuries can be expected.
PATHOPHYSIOLOGY The organs most commonly affected by primary blast injuries are the lungs, ears, bowel, central nervous system, and cardiovascular system, t2 In the lungs, primary blast injury produces damage to alveolar parenchyma producing edema and hemorrhage into the interstitial and intra-alveolar spaces.2! ~s Lacerations can occur in m a n y locations, rupturing alveolar walls, tearing the visceral pleura, and creating fistulae between the alveolar spaces and the pulmonary veins. Primary blast injury to the ear produces rupture of the tympanic membrane, usually a linear perforation involving the pars tensa. ~9'3° Occasionally there may be dislocation of the ossicles. The inner ear may also be damaged, producing tinnitus and sensorineural hearing loss affecting all frequencies. Primary blast damage to the bowel produces serosal hemorrhages and perforations) 1'2~ The large bowel is more often injured than the small bowel due to the presence of pockets of gas within the colonic lumen as opposed to the small intestineY ,22 Injuries to the bowel are more common in immersion blasts than in air blasts, and often the damage is in multiple locations. Primary blast injury to the nervous system usually produces a concussion syndrome, al Intracranial hematomas in survivors who reach the hospital are unusual. 32 Because of the formation of alveolar-venous fistulae, air may be forced into the pulmonary venous system and may travel through the left side of the heart into the systemic circulation. 6,33,34 These air bubbles can embolize to such critical a r e a s o f the circulation as the brain and heart. Systemic air emboli are a likely cause of abnormal neurologic findings z4'35 and/ 689/75
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Fig. 3. A six-person decompression chamber capable of greater than 6 ATA. or myocardial ischemia 22,36 in a blastinjured victim. Solid organs without a gas/liquid interface are surprisingly protected from primary blast injuries. However, the victim may also be affected by either penetrating or crush wounds that result from secondary or tertiary blast injuries. C L I N I C A L PRESENTATION The clinical presentation of primary-blast-injured victims is the result of damage to lungs, ears, bowel, and brain. ~5,37,3s Common respiratory symptoms include dyspnea, chest pain, and hemoptysis. 27 Chest examination will show tales or rhonchi and, possibly, evidence of pneumothorax or pneumomediastinum. In victims with severe lung damage, cyanosis is present. Rupture of the tympanic membrane produces decreased auditory acuity. Fortunately, when the external canal is kept clean and dry, up to 80% of these perforations heal spontaneously. 30'37 Although there may be initial severe sensorineural deafness and tinnitus, rapid i m p r o v e m e n t usually occurs during the~first few hours. 8° Much of the recent information about primary blast" injuries to the bowel comes f r o m a report of 32 Israeli sailors injured while in the water after abandoning their sinking destroyerY Nineteen sustained both abdominal and pulmonary injuries, and an additional five had only abdominal injuries. All 24 presented with acute abdominal pain, tenderness, and/or rebound tenderness. Nausea, vomiting, and an urge to defecate were common. One patient had bright red rectal bleeding. Nervous system findings are, generally, the minor mental status changes of the concussion syndrome. Focal neurological findings may be due to systemic air emboli. When the victim is exposed to an i m m e r s i o n blast, transient weakness of the lower extremities lasting a few seconds to minutes may be seen. 2z The h y p o t e n s i o n seen in blastinjured victims is due to decreased cardiac output resulting from blood loss, myocardial ischemia from air emboli, or acute cor pulmonale, z2,z4 Systemic air emboli can be difficult to 76/690
detect; the diagnosis depends on clinical suspicion. Occasionally air emboli can be visualized in the retinal vessels, and this is a helpful clue as to the etiology of the patient's abnormal neurological status. 24 Air emboli may also be seen on computerized axial tomography of the brain. 39
FREQUENCY OF INJURY The frequency with which these injuries are seen varies with the severity of damage sustained by the victim. A review of 305 fatalities from civilian terrorist bombs 3s found brain damage in 60%, skull fractures in 51%, diffuse lung contusions in 47%, liver lacerations in 34%, splenic lacerations in 29%, and frequent fractures and traumatic amputations in the victims. These patients experienced a severe force, as reflected by the fact that 237 (78%) were dead on arrival to the hospital, and another 40 (13%) died during the next 24 hours. Fortunately most blast-injured victims are not so severely wounded. In a review of 1,532 victims (all but nine Of whom survived) 37 the most common injuries were lacerations (619), abrasions (276), bruises (203), fractures (62), and bums (50). Most lacerations involved the head and neck, pointing out the protective effect of ordinary clothing. Fractures were frequently multiple, often compound, and more l i k e l y affecting the l o w e r limbs. Traumatic amputations were seen in 20 patients, 13 above the knee] Annals of Emergency Medicine
LABORATORY Chest radiographic changes can be divided into signs of hemorrhage, laceration, and cardiac impairment. 21 H e m o r r h a g e and e d e m a produces linear, patchy, or diffuse infiltrates that may be seen as early as 2 to 4 hours after the explosion. 21'17 Pulmonary lacerations are manifested by radiographic signs of pneumothorax, hemothorax, p n e u m o m e d i a s t i n u m , interstitial emphysema, and pneumatoceles. Cardiac impairment may be reflected in an enlarged cardiac shadow and dilated azygos vein, which is admittedly difficult to evaluate on a s u p i n e AP f i l m . ~1 R a d i o g r a p h i c changes usually worsen during the first 24 to 48 hours, and then initially clear during the next 2 to 4 daysY Resolution of the infiltrates takes about one week, and healing of interstitial emphysema or pneumatoceles takes a week or two longer. In severely injured blast victims, the electrocardiogram usually shows sinus tachycardia, and occasionally Q waves or ST-T wave changes of ischemia.22 '36 T h e i s c h e m i a is presumably not a direct effect of the blast, but results f r o m secondary effects such as air embolization to the coronary arteries.
EMERGENCY TREATMENT Victims need initial evaluation, resuscitation, and supportive care. Patients should be on s u p p l e m e n t a l oxygen because the damage to the pulmonary parenchyma may not initially 11:12 December 1982
Fig. 4. A monoplace hyperbaric cham-
ber capable of 3 ATA.
be apparentY y Because of the danger of fluid accumulation in injured tissue, fluid therapy should be closely monitored to avoid exacerbating respiratory problemsY -28 Pneumo- and hemothoraces should be treated with chest tubesY The use of prophylactic chest tubes in severely injured victims on ventilators has been mentioned, 23 but most would opt for careful monitoring and use of tubes should the need arise. 27 A stable, patent airway is a must. 2s P a t i e n t s w i t h o u t a d e q u a t e spontaneous respirations should be intubated and mechanically ventilated. However, the risk of positive pressure ventilation (PPV) is great because of the potential for producing or exacerbating pneumothorax or systemic air emboli. 24 ' 27 In animal experime n t s, the use of mechanical ventilation during the early recovery period increased mortality from blast injuries, presumably from systemic air emboli. 4° Systemic air emboli may be a major problem when high ventilation pressures are used in normal lungs or lungs damaged by penetrating injury. 41'42 If hypoxemia is not improved with supplemental oxygen and PPV, then positive end expiratory pressure (PEEP) will often help. 24,26,2z As with PPV, PEEP carries the risk of air embolism or pneumothorax, and in addition can decrease cardiac output. The decision to use PPV or PEEP is a difficult one. They should be used if necessary to support life, and they should not be 11:12 December 1982
used unless absolutely needed. Maintaining spontaneous respirations is clearly best. In the patient with systemic air emboli, hyperbaric therapy is the treatment of choice. 43"46 It is dramatically effective for cerebral air emboli, even up to 11 hours after the acute event. 44 A recent a d v a n c e m e n t in hyperbaric therapy has been the use of intermittent 100% oxygen during the decompression phase. 43 The US Navy regimen is to rapidly compress the patient to 6 atmospheres absolute (ATA) using air, and decompress according to the relief of s y m p t o m s and other guidelines. At 2.8 ATA, 100% oxygen is begun and used intermittently during the remainder of decompression. This regimen reduces the time required for decompression, improves tissue oxygenation, and reduces the incidence of decompression sickness. The use of 100% oxygen does carry the risk of acute oxygen toxicity. The s y m p t o m s are primarily neurologic and result from sudden, intense CNS vasoconstriction. This syndrome may develop abruptly, and is manifested by muscle twitching, paresthesias, dizziness, visual changes, and seizures. Keeping the'partial pressure of oxygen below 2.8 ATA (1,520 m m Hg) reduces this risk. There are two types of hyperbaric chambers in civilian use [Figures 3 and 4). The first, a "decompression chamber;' is a large, multiperson device capable of holding a patient, Annals of Emergency Medicine
attendants, and equipment. It can be pressurized to 6 ATA. This type of chamber is theoretically better for treating systemic air emboli because 6 ATA would compress air embolic bubbles to one-sixth their previous size, and would restore circulation. The second type of chamber, more commonly available in hospitals, is the "hyperbaric chamber," a singleperson device designed for 100% oxygen at 2 to 3 ATA. Hyperbaric chambers are used to improve tissue oxygenation as an adjunctive treatment of various diseases, and are not specifically designed to treat decompression sickness or s y s t e m i c air emboli. However, these small, low pressure chambers may be useful for patients with severe respiratory distress from blast injuries, and might improve arterial oxygenation without resorting to positive pressure ventilation or PEEP (with their attendant risks). 22'24,47 Even though 3 ATA is theoretically and experimentally less effective than 6 ATA, the widespread availability of these chambers m a y make them just as effective in treating systemic air emboli. Air embolism resulting from cardiac surgery has been successfully treated in 3 ATA monoplace chambers. 48 Intravenous tubing, ventilator tubing, and other lines can be run through gaskets in these devices so that patients can be monitored and treated. Mannitol may also be used as an adjunctive drug in the treatment of air embolism, but should not delay or replace recompression. 49 General anesthesia is poorly tolerated during the first 24 to 48 hours in victims with primary blast injuries of the lungs,'6 22 ' 36 possibly because of the risk of systemic air emboli during surgery. Of the 16 Israeli sailors who were operated on during the first 24 hours, three died suddenly. 2z If possible, surgery should be delayed for 24 to 48 hours, or another method of anesthesia should be used. The surgical procedure should be as brief as possible. Because gas bubbles expand as the surrounding pressure decreases, lowering the ambient pressure by ascending in altitude increases the potential for damage for air emboli in the blastinjured victim. Therefore, if these patients must be transferred by helicop691/77
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Figs. 5, 6 & 7. Examples of penetrating fragment w o u n d s in a blast-injured victim. ter, low altitude is necessary. Primary blast injuries m a y not be evident at first, and all patients should be observed, for injuries have been detected several hours after the explosion. 2s The treatment of lacerations, abrasions, fractures, a m p u t a t i o n s , and other wounds produced by blast injuries is not different from treatment for injuries resulting from other forms of trauma. Terrorist bombs commonly produce high-velocity penetrating fragment wounds that require careful evaluation 13,3s (Figures 5, 6, and 7). Delayed primary closure should be the rule, with the possible exception of wounds to the head, neck, external genitalia and occasionally the chest, where debridement and primary closure can be done. 38
REFERENCES 1. Hooker DR: Physiological effects of air concussion. Am J Physio167:219-274, 1924. 2. Logan DD: Detonation of high explosives in shells and bombs and its effects. Br Med J 2:864-866, 1939. 3. Zuekerman S: Experimental study of blast injuries to the lungs. Lancet 2:219224, 1940. 4. Dean DM, Thomas AR, Allison RS: Effects of high-explosives blasts on lungs. Lancet 2:224-226, 1940. 5. Hadfield G, Ross JM, Swain RHA, et al: Blast from high explosive. Preliminary report on ten fatal cases. Lancet 2:478-481, 1940. 6. Desaga H: Blast injuries, in German Aviation Medicine, World War II, vol 2. Washington DC, US Government Printing Office, 1950, p 1274-1293. 7. Benzinger T: Physiological effects of blast in air and water, in German Aviation Medicine, World War II, vol 2. Washington DC, US Government Printing Office, 1950, p 1225-1259. 8. Corey EL: Medical aspects of blast. US Naval Med Bull 46:623-651, 1946. 9. Clemedson CJ: An experimental study on air blast injuries. Acta Physiol Scand 18(suppl 61):1-200, 1949. 10. White CS: Biological blast effects. US Atomic Energy Commission Technical Report TID-5564. Albuquerque, Lovelace Foundation for Medical Education and Research, 1959. 11. White CS: Biological effects of blast. Defense Atomic Support Agency Report DASA-1271. Albuquerque, Lovelace Foun78/692
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problem and its treatment. Israeli J Med Sci 11:268-274, 1975. 25. Gray RC, Coppel DL: Surgery of violence III. Intensive care of patients with bomb blast and gunshot injuries. Br Med l 1:502-504, 1975. 26. Coppel DL: Blast injuries of the lungs. Br J Surg 63:735-737, 1976. 27. Caseby NG, Porter MF: Blast injuries of the lungs; clinical presentation, management and course. Injury 8:1-12, 1976. 28. Fishman AP, Pietra GG: Stretched pores, blast injury, and neurohemodynamic pulmonary edema. Physiologist 23:53-56, 1980. 29. Pahor AL: Blast injuries to the ear: An historical and literary review. J Laryngol Otol 93:225-251, 1979. 30. Kerr AG: Trauma and the temporal bone. The effects of blast on the ear. l Laryngol Otol 94:107-110, 1980. 31. Cramer F, Paster S, Stephenson C: Cerebral injuries due to explosion waves - cerebral blast concussion. Arch NeuroI Psychiatry 61:1-20, 1949. 32. Murthy JMK, Chopra JS, Gulati DR: Subdural hematoma in an adult following blast injury. Case report. J Neurosurg 50: 260-261, 1979. 33. Gouze FJ, Hayter R: Air embolism in immersion blast. US Naval Med Bull 43: 871-877, 1944.
dation for Medical Education and Research, 1961. 12. Chiffelle TL: Pathophysiology of direct air-blast injury. Defense Atomic Support Agency Report DASA-1778. Albuquerque, Lovelace Foundation for Medical Education and Research, 1966. 13. de Candole CA: Blast injury. Can Med Assoc J 96:207-214, 1967. 14. Rawlins JSP: Physical and pathophysiological effects of blast. Injury 9:313-320, 1978. 15. Schardin H: The physical principles of the effects of detonation, in German Aviation Medicine, World War II, vol 2. Washington DC, US Govemment Printing Office, 1950, p 1207-1224. 16. Cook M_A:Shock waves in gaseous and condensed media, in The Sciences of High Explosives. New York, Reinhold Publishing Corp, 1958, chap 13, p 322-352. 17. Kinney GA: Explosive Shocks in Air. 11:12 December 1982
New York, The MacMillan Co, 1962. 18. Richmond DR, Bowen IG, White CS: Tertiary blast effects: Effects of impact on mice, rats, guinea pigs, and rabbits. Aerospace Med 32:789-805, 1961. 19. Swearingen JJ, McFadden EB, Garner JD, et al: Human tolerance to vertical impact. Aerospace Med 31:989-998, 1960. 20. Gurdjian ES: Deformation studies of the skull: Mechanisms of skull fracture, in Impact Head Injur~. Springfield, Charles C. Thomas, 1975, p 113-138. 21. Hirsch M, Bazini J: Blast injury of the chest. Clin Raddol 20:362-370, 1969. 22. Huller T, Bazini Y: Blast injuries of the chest and abdomen. Arch Srtrg 100:24-30, 1970. 23. McCaughey W, Coppel DL, Dundee JW: Blast injuries to the lungs. A report of two cases. Anaesthesia 28:2-9, 1973. 24. Weiler-Ravell D, Adatto R, Borman JB: Blast injury of the chest. A review of the Annals of Emergency Medicine
34. Clemedson CJ, Hultman HI: Air embolism and the cause of death in blast injury. Milit Surg 114:424-437, 1954. 35. Menkin M, Schwartzman RJ: Cerebral air embolism. Report of five cases and review of the literature. Arch Neurol 34:168170, 1977. 36. Leavetl BS: Acute heart failure following blast injury. War Med 7:162-167, 1945. 37. Hadden WA, Rutherford WH, Merrett JD: The injuries of terrorist bombing: A study of 1532 consecutive patients. Br J Surg 65:525-531, 1978. 38. Hill JF: Blast injury with particular reference to recent terrorist bombing incidents. Ann Roy Cell Surg Engl 61:4-11, 1979. 39. Matz S, Segal A, Nemesh L, et al: Diagnosis of air embolism to the brain by computerized axial tomography. Comput Tomogr 4:107-110, 1980. 40. Damon EG, Henderson EA, Jones RK: The effect of intermittent positive pressure respiration on occurrence of air embolism and mortality following primary blast injury. Defense Nuclear Agency Report DNA-2989E Washington DC, US Government Printing Office, 1973. 41. Kao DK, Tiemey DF: Air embolism with positive-pressure ventilation of rats. J Appl Physiol 42:368-371, 1977. 42. Meier GH, Wood WJ, Symbas PN: Sys693/79
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temic air embolization from penetrating lung injury. Ann Thorac Surg 27:161-168~ 1979. 43. Van Genderen L, Waite CL: Evaluation of the rapid decompression high pressure oxygenation approach for the treatment of traumatic cerebral air embolism. Aerospace Med 39:709-713, 1968. 44. Kindwall EP: Massive surgical air embolism treated with brief recompression
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to six atmospheres followed by hyperbaric oxygen. Aerospace Med 44:663-666, 1973. 45. Bond GF: Arterial gas embolism, in David JC, Hunt TK (eds): Hyperbaric Oxygen Therapy. Bethesda, Undersea Medical Society, 1977, p 141-152. 46. Pierce EC: Specific therapy for arterial gas embolism. Ann Thorac Surg 29:300304, 1980. 47. Damon EG, Jones RK: Comparative
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effects of hyperbaric pressure in treatment of- primary blast injury. Defense Atomic Support Agency Report DASA-270. Washington DC, US Government Printing Ofrice, 1973. 48. Hart GB: Treatment of decompression illness and air embolism with hyperbaric oxygen. Aerospace Med 45:1190-1193, 1974. 49. Kizer KW: Manni¢ol in dysbarism. West f Med 132:86, 1980.
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Blast Injuries [Stapczynski JS: Blast injuries. Ann Emerg Med 11:687-694, December 1982.]
d. Stephan Stapczynski, MD Harbor City, California
INTRODUCTION "Blast injury" is a general term to describe the harmful effects m animals or man produced by a sudden change in environmental pressure originating from an explosion. While first described as a specific entity in 1924,1 it was not until the Second World War that studies in England ~-5 and Germany 6,7 established the clinical and pathological features of this syndrome. After the war, work with experimental animals continued to add knowledge to this field. 812 These injuries were once rare in peacetime, but the worldwide spread of terrorism has made no country immune from the potential for civilian blast injuries. The pathophysiology of blast injuries differs significantly from other forms of trauma, and thus we will stress the key differences in the approach to these patients in the emergency department.
From the Department of Emergency Medicine, Harbor-UCLA Medical Center, Torrance, California. Address for reprints: J. S. Stapczynski, MD, 26416 Zephyr Avenue, Harbor City, California 90710.
TERMINOLOGY Injuries produced by explosions can be divided into four categories. 11,13 Primary blast injuries describe the damage inflicted by the sudden changes in environmental pressure (the "blast wave") itself. The effects are greatest at or near the interface between gas and liquid, and thus organs containing air are most easily injured. In secondary blast injuries the damage results from the victim being struck by flying debris. Tertiary blast injuries are those sustained when the victim is thrown against stationary objects. Both secondary and tertiary blast injuries result from the ability of the blast wave to accelerate loose objects outward from an explosion. 11 Miscellaneous blast injuries include exposure to dust (both radioactive and nonradioactive), direct thermal bums from the explosion, and bums from blast-ignited fires.
BLAST PHYSICS Detonation is a high-speed chemical decomposition of a solid or liquid explosive into a gas. 1517 The space previously occupied by the explosive is filled with a gas under high pressure and temperature. There are two principal types of explosives. High explosives (HE) detonate rapidly; the chemical reaction is triggered by a mechanical shock wave that travels at high speed (10,000 to 30,000 meters/sec) through the explosive. A typical HE is T N T (trinitrotoluene), one gram of which can release 1,120 calories of blast energy and, at the moment of detonation, generate pressures of approximately 106 psi within the initial gas. 17 HE possess brisance (that is, shattering power). The energy is released so rapidly and the pressures generated rise so quickly that nearby objects can be shattered by the force of the explosion. Ordinary explosives, like gunpowder, release their energy slowly by either burning or deflagratmg, and therefore do not possess brisance. The very high pressure within the gaseous products of detonation is transmitted to the surrounding medium and is propagated as a shock wave that travels out radially from the explosion.17 The idealized shock wave is a steep 11:12 December 1982
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Fig. 1. An idealized s h o c k w a v e (pressure v time).
Fig. 2. M e c h a n i s m s of p r i m a r y blast injuries. fronted pressure pulse that rises rapidly to a m a x i m u m and then decays over a longer period to a m i n i m u m less than the previous ambient pressure (Figure 1). Afterward, the environmental pressure returns to the previous baseline. Idealized shock waves are found only in free-field explosions; the presence of reflecting or absorbing barriers may radically alter the wave form and peak pressure. 16 The velocity of the shock wave and the duration of the positive pressure component is determined by three factors: 1) The size of the explosive charge: A bigger explosion produces shock waves of faster velocity and longer duration; 21 The surrounding medmm: Denser media (like water, as opposed to air) propagate the shock wave faster and with a longer positive pressure duration; and 3) The distance from the explosion: The further from the charge, the slower the shock wave velocity and the longer the duration. Shock waves initially travel faster than the speed of sound, but as they expand, the velocity decreases to the speed of sound and thereafter the shock wave is propagated as an acoustical wave. For the common HE detonated in air, this distance is roughly 50 to 60 charge radii from the initial charge. 16 The peak pressure of the shock wave decreases as the shock wave expands. Because the peak pressure is a prime determinant of the potential for primary blast injuries, the military has performed experiments with different explosives to measure the pressures produced at various distances. The peak pressure at any distance is a function of the initial charge mass and the distance from the explosion. Experimental data usually fit the followhag equation: 16 Peak pressure = A/z + B/z 2 + C/z 3 where: z = R (distance)/3X/Q (charge mass). For explosions in air, the experimentally derived constants A, B, and C are such that close to an explosion (less than 10 charge radii) the last term of the equation dominates, with the peak pressure varying as the inverse of 74/688
P
the distance cubed; far from an explosion (more than 50 to 60 charge radii) the first term dominates, with the d0eak4~re-.~,qllre~vak-yJ/lgasthe inverse of the distance. The distance of 50 to 60 charge radii also correlates with the approximate distance where the peak pressure of an explosion in air is about 15 psi above ambient pressure. The threshold for lung damage from primary blast injuries from typical HE is roughly 15 psi, and therefore primary blast injuries are seen only when the v i c t i m is close to the explosion. Secondary and tertiary blast injuries, however, can occur at much greater distances. Transient winds (the "displacement wave") accompany the pressure variations produced by the shock wave) ° The low density of air means that high velocity winds can be produced by even small changes in pressure: a peak pressure of 0.25 psi corresponds to a wind velocity of 125 mph. Loose objects can be accelerated by the shock wave, but their ultimate velocity is determined by corresponding wind velocity. The high velocity of the displacement wave means that small, light objects can be accelerated rapidly over short distances, and reach a high speed even at low peak pressures. The instantaneous acceleration for large objects is less, but close to an explosion may still be significant. For a typical adult of 165 lb, a peak pressure of 15 psi from an explosion can produce an instantaneous acceleration of about 450 ft/sec 2, or approximately 14 gravities. For common terrorist bombs, this acceleration would last only a few Annals of Emergency Medicine
milliseconds, and the ultimate velocity reached by the victim would be quite low. For explosions from nuclear devices, however, the very long duration of the positive pressure component of the shock wave means a significant time exists in which to accelerate the victim. 11 In this circumstance, even low peak pressures can hurl the victim with significant velocity. The instantaneous acceleration is usually within the tolerable range, but damage may be done if the victim impacts a hard, stationary object. The potential for tertiary blast injuries does not exist in the process of acceleration, but rather in the sudden deceleration when the victim impacts a hard surface.
UNDERWATER EXPLOSIONS Explosions in water produce shock waves of greater peak pressure and longer durationA4, is The shock wave travels at the corresponding speed of sound, which in water is about five times faster than in air. Because of the greater peak pressures, the distance at which primary blast injuries can occur is much greater than for explosions in air. And because water is denser than air, the displacement wave is very low in velocity and rarely produces significant damage. The gaseous products of an underwater explosion produce a bubble which rises toward the surface. When it reaches the surface, the bubble produces the characteristic explosive plume as particles of water are hurled high into the air.14 It is difficult to predict the damage that may result from underwater blasts because the initial shock wave may reflect off the 11:12 December 1982
Spalling Implosion Acceleration-deceleration (inertial) Pressure differentials 2
TABLE. Expected primary blast
injuries
Injury
Pressure (psi)
Ear drum rupture 5 Lung damage threshold 15 Lethality threshold 30-42 LD50 (50% fatal) 42-57 95-100% fatal 58-80
POTENTIAL FOR INJURY
surface or bottom and onto the target. The target may feel the effects of the initial shock wave and any reflected ones - - all with the possibility of summating to produce a higher peak pressure.
MECHANISMS OF INJURY
i,
The sudden change in pressure caused by the shock wave can damage living tissue by four mechanisms is (Figure 2). When a shock wave reaches an interface between media of different densities, reflections create turbulence and cavitation. This can throw particles of fluid from the more dense to the less dense medium ("spalling"). In animal tissues, as the shock wave travels through an organ containing both liquid and gas, particles of liquid are "spalled" into the gaseous compartment. As a shock wave travels through an organ containing pockets of gas, each pocket of gas can be compressed by the pressure of the surrounding fluid. Once the shock wave has passed, the rebound expansion of each gas pocket is then a miniature internal "secondary" explosion. As the victim is either accelerated away from an explosion or impacted against a stationary object, the possibility of acceleration-deceleration (inertial) injury exists. In this situation, organs of different densities, masses, or attachments may be accelerated at different rates relative to one another,
11:12 December 1982
and the shearing motion that can develop tears or disrupts the tissues. This is significant in causing tertiary blast injuries. Finally, at the moment of impact of the shock wave upon the victim, a difference in pressure may evolve between the outer surface of the body and the intemal organs. Because water is e s s e n t i a l l y incompressible, the pressure on the exterior and within the fluid-containing tissues and vascular system remains equal. However, because gas within the alveoli is easily compressible, at the moment of impact of the shock wave, a pressure differential may exist between the vascular system and the alveoli. This drives blood from the pulmonary capillaries into the alveolar spaces, and contributes to the pulmonary hemorrhage seen in primary blast injuries. The potential for primary blast injuries varies according to the peak pressure and duration of that pressure. ]°A1 Animal experiments also document the protection offered by barriers, like foxholes or furniture, as they markedly reduce the peak pressure the protected animal experiences. For the common HE used in civilian terrorist bombs, the duration of the positive pressure is 2 and 10 ms for charges of 50 and 4,000 lb, respectively. For a human being exposed to this type of blast, the potential injuries vary with the peak pressure 1° (Table}. Rapid acceleration of small fragments by an explosion is a major factor in secondary blast injuries. Small missiles are commonly accelerated to velocities of several hundred feet per second. At velocities of 50 ft/sec skin is easily lacerated, and at velocities of 400 ft/sec serious wounds involving penetration of body cavities are seen in most cases, n These velocities are c o m m o n l y produced from terrorist bombs, and it is the secondary injuries caused by flying glass, shrapnel, and debris that produce much of the morbidity from these explosions, is The acceleration of a human victim by an explosion may be tolerable, but it is the sudden impact against a hard surface that can be lethal. Extrapolation of animal experiments to a 70-kg man predicts a 50% mortality from a vertical impact against a flat, concrete surface at a velocity of 26 ~t/sec or 18 mph. TM This estimate agrees with data in the literature on the ability of human beings to survive deceleration in-
Annals of Emergency Medicine
juries. Impacts of 10 ft/sec appear to be the limit of voluntary tolerance of human beings in both the sitting and standing positions. 19 Impacts of 11 to 16 ft/sec onto hard surfaces with the knees locked can produce fractures in the lower extremities. 11 Impacts of 15 to 23 ft/sec can cause skull fractures. 2° And finally, motor vehicle accidents at velocities of less than 41 ft/sec are associated with up to 70% mortality. 1~ Thus if the v i c t i m is accelerated to a velocity greater than 15 to 20 ft/sec and impacts a hard surface, serious injuries can be expected.
PATHOPHYSIOLOGY The organs most commonly affected by primary blast injuries are the lungs, ears, bowel, central nervous system, and cardiovascular system, t2 In the lungs, primary blast injury produces damage to alveolar parenchyma producing edema and hemorrhage into the interstitial and intra-alveolar spaces.2! ~s Lacerations can occur in m a n y locations, rupturing alveolar walls, tearing the visceral pleura, and creating fistulae between the alveolar spaces and the pulmonary veins. Primary blast injury to the ear produces rupture of the tympanic membrane, usually a linear perforation involving the pars tensa. ~9'3° Occasionally there may be dislocation of the ossicles. The inner ear may also be damaged, producing tinnitus and sensorineural hearing loss affecting all frequencies. Primary blast damage to the bowel produces serosal hemorrhages and perforations) 1'2~ The large bowel is more often injured than the small bowel due to the presence of pockets of gas within the colonic lumen as opposed to the small intestineY ,22 Injuries to the bowel are more common in immersion blasts than in air blasts, and often the damage is in multiple locations. Primary blast injury to the nervous system usually produces a concussion syndrome, al Intracranial hematomas in survivors who reach the hospital are unusual. 32 Because of the formation of alveolar-venous fistulae, air may be forced into the pulmonary venous system and may travel through the left side of the heart into the systemic circulation. 6,33,34 These air bubbles can embolize to such critical a r e a s o f the circulation as the brain and heart. Systemic air emboli are a likely cause of abnormal neurologic findings z4'35 and/ 689/75
BLAST INJURIES Stapczynski
Fig. 3. A six-person decompression chamber capable of greater than 6 ATA. or myocardial ischemia 22,36 in a blastinjured victim. Solid organs without a gas/liquid interface are surprisingly protected from primary blast injuries. However, the victim may also be affected by either penetrating or crush wounds that result from secondary or tertiary blast injuries. C L I N I C A L PRESENTATION The clinical presentation of primary-blast-injured victims is the result of damage to lungs, ears, bowel, and brain. ~5,37,3s Common respiratory symptoms include dyspnea, chest pain, and hemoptysis. 27 Chest examination will show tales or rhonchi and, possibly, evidence of pneumothorax or pneumomediastinum. In victims with severe lung damage, cyanosis is present. Rupture of the tympanic membrane produces decreased auditory acuity. Fortunately, when the external canal is kept clean and dry, up to 80% of these perforations heal spontaneously. 30'37 Although there may be initial severe sensorineural deafness and tinnitus, rapid i m p r o v e m e n t usually occurs during the~first few hours. 8° Much of the recent information about primary blast" injuries to the bowel comes f r o m a report of 32 Israeli sailors injured while in the water after abandoning their sinking destroyerY Nineteen sustained both abdominal and pulmonary injuries, and an additional five had only abdominal injuries. All 24 presented with acute abdominal pain, tenderness, and/or rebound tenderness. Nausea, vomiting, and an urge to defecate were common. One patient had bright red rectal bleeding. Nervous system findings are, generally, the minor mental status changes of the concussion syndrome. Focal neurological findings may be due to systemic air emboli. When the victim is exposed to an i m m e r s i o n blast, transient weakness of the lower extremities lasting a few seconds to minutes may be seen. 2z The h y p o t e n s i o n seen in blastinjured victims is due to decreased cardiac output resulting from blood loss, myocardial ischemia from air emboli, or acute cor pulmonale, z2,z4 Systemic air emboli can be difficult to 76/690
detect; the diagnosis depends on clinical suspicion. Occasionally air emboli can be visualized in the retinal vessels, and this is a helpful clue as to the etiology of the patient's abnormal neurological status. 24 Air emboli may also be seen on computerized axial tomography of the brain. 39
FREQUENCY OF INJURY The frequency with which these injuries are seen varies with the severity of damage sustained by the victim. A review of 305 fatalities from civilian terrorist bombs 3s found brain damage in 60%, skull fractures in 51%, diffuse lung contusions in 47%, liver lacerations in 34%, splenic lacerations in 29%, and frequent fractures and traumatic amputations in the victims. These patients experienced a severe force, as reflected by the fact that 237 (78%) were dead on arrival to the hospital, and another 40 (13%) died during the next 24 hours. Fortunately most blast-injured victims are not so severely wounded. In a review of 1,532 victims (all but nine Of whom survived) 37 the most common injuries were lacerations (619), abrasions (276), bruises (203), fractures (62), and bums (50). Most lacerations involved the head and neck, pointing out the protective effect of ordinary clothing. Fractures were frequently multiple, often compound, and more l i k e l y affecting the l o w e r limbs. Traumatic amputations were seen in 20 patients, 13 above the knee] Annals of Emergency Medicine
LABORATORY Chest radiographic changes can be divided into signs of hemorrhage, laceration, and cardiac impairment. 21 H e m o r r h a g e and e d e m a produces linear, patchy, or diffuse infiltrates that may be seen as early as 2 to 4 hours after the explosion. 21'17 Pulmonary lacerations are manifested by radiographic signs of pneumothorax, hemothorax, p n e u m o m e d i a s t i n u m , interstitial emphysema, and pneumatoceles. Cardiac impairment may be reflected in an enlarged cardiac shadow and dilated azygos vein, which is admittedly difficult to evaluate on a s u p i n e AP f i l m . ~1 R a d i o g r a p h i c changes usually worsen during the first 24 to 48 hours, and then initially clear during the next 2 to 4 daysY Resolution of the infiltrates takes about one week, and healing of interstitial emphysema or pneumatoceles takes a week or two longer. In severely injured blast victims, the electrocardiogram usually shows sinus tachycardia, and occasionally Q waves or ST-T wave changes of ischemia.22 '36 T h e i s c h e m i a is presumably not a direct effect of the blast, but results f r o m secondary effects such as air embolization to the coronary arteries.
EMERGENCY TREATMENT Victims need initial evaluation, resuscitation, and supportive care. Patients should be on s u p p l e m e n t a l oxygen because the damage to the pulmonary parenchyma may not initially 11:12 December 1982
Fig. 4. A monoplace hyperbaric cham-
ber capable of 3 ATA.
be apparentY y Because of the danger of fluid accumulation in injured tissue, fluid therapy should be closely monitored to avoid exacerbating respiratory problemsY -28 Pneumo- and hemothoraces should be treated with chest tubesY The use of prophylactic chest tubes in severely injured victims on ventilators has been mentioned, 23 but most would opt for careful monitoring and use of tubes should the need arise. 27 A stable, patent airway is a must. 2s P a t i e n t s w i t h o u t a d e q u a t e spontaneous respirations should be intubated and mechanically ventilated. However, the risk of positive pressure ventilation (PPV) is great because of the potential for producing or exacerbating pneumothorax or systemic air emboli. 24 ' 27 In animal experime n t s, the use of mechanical ventilation during the early recovery period increased mortality from blast injuries, presumably from systemic air emboli. 4° Systemic air emboli may be a major problem when high ventilation pressures are used in normal lungs or lungs damaged by penetrating injury. 41'42 If hypoxemia is not improved with supplemental oxygen and PPV, then positive end expiratory pressure (PEEP) will often help. 24,26,2z As with PPV, PEEP carries the risk of air embolism or pneumothorax, and in addition can decrease cardiac output. The decision to use PPV or PEEP is a difficult one. They should be used if necessary to support life, and they should not be 11:12 December 1982
used unless absolutely needed. Maintaining spontaneous respirations is clearly best. In the patient with systemic air emboli, hyperbaric therapy is the treatment of choice. 43"46 It is dramatically effective for cerebral air emboli, even up to 11 hours after the acute event. 44 A recent a d v a n c e m e n t in hyperbaric therapy has been the use of intermittent 100% oxygen during the decompression phase. 43 The US Navy regimen is to rapidly compress the patient to 6 atmospheres absolute (ATA) using air, and decompress according to the relief of s y m p t o m s and other guidelines. At 2.8 ATA, 100% oxygen is begun and used intermittently during the remainder of decompression. This regimen reduces the time required for decompression, improves tissue oxygenation, and reduces the incidence of decompression sickness. The use of 100% oxygen does carry the risk of acute oxygen toxicity. The s y m p t o m s are primarily neurologic and result from sudden, intense CNS vasoconstriction. This syndrome may develop abruptly, and is manifested by muscle twitching, paresthesias, dizziness, visual changes, and seizures. Keeping the'partial pressure of oxygen below 2.8 ATA (1,520 m m Hg) reduces this risk. There are two types of hyperbaric chambers in civilian use [Figures 3 and 4). The first, a "decompression chamber;' is a large, multiperson device capable of holding a patient, Annals of Emergency Medicine
attendants, and equipment. It can be pressurized to 6 ATA. This type of chamber is theoretically better for treating systemic air emboli because 6 ATA would compress air embolic bubbles to one-sixth their previous size, and would restore circulation. The second type of chamber, more commonly available in hospitals, is the "hyperbaric chamber," a singleperson device designed for 100% oxygen at 2 to 3 ATA. Hyperbaric chambers are used to improve tissue oxygenation as an adjunctive treatment of various diseases, and are not specifically designed to treat decompression sickness or s y s t e m i c air emboli. However, these small, low pressure chambers may be useful for patients with severe respiratory distress from blast injuries, and might improve arterial oxygenation without resorting to positive pressure ventilation or PEEP (with their attendant risks). 22'24,47 Even though 3 ATA is theoretically and experimentally less effective than 6 ATA, the widespread availability of these chambers m a y make them just as effective in treating systemic air emboli. Air embolism resulting from cardiac surgery has been successfully treated in 3 ATA monoplace chambers. 48 Intravenous tubing, ventilator tubing, and other lines can be run through gaskets in these devices so that patients can be monitored and treated. Mannitol may also be used as an adjunctive drug in the treatment of air embolism, but should not delay or replace recompression. 49 General anesthesia is poorly tolerated during the first 24 to 48 hours in victims with primary blast injuries of the lungs,'6 22 ' 36 possibly because of the risk of systemic air emboli during surgery. Of the 16 Israeli sailors who were operated on during the first 24 hours, three died suddenly. 2z If possible, surgery should be delayed for 24 to 48 hours, or another method of anesthesia should be used. The surgical procedure should be as brief as possible. Because gas bubbles expand as the surrounding pressure decreases, lowering the ambient pressure by ascending in altitude increases the potential for damage for air emboli in the blastinjured victim. Therefore, if these patients must be transferred by helicop691/77
BLAST INJURIES Stapczynski
Figs. 5, 6 & 7. Examples of penetrating fragment w o u n d s in a blast-injured victim. ter, low altitude is necessary. Primary blast injuries m a y not be evident at first, and all patients should be observed, for injuries have been detected several hours after the explosion. 2s The treatment of lacerations, abrasions, fractures, a m p u t a t i o n s , and other wounds produced by blast injuries is not different from treatment for injuries resulting from other forms of trauma. Terrorist bombs commonly produce high-velocity penetrating fragment wounds that require careful evaluation 13,3s (Figures 5, 6, and 7). Delayed primary closure should be the rule, with the possible exception of wounds to the head, neck, external genitalia and occasionally the chest, where debridement and primary closure can be done. 38
REFERENCES 1. Hooker DR: Physiological effects of air concussion. Am J Physio167:219-274, 1924. 2. Logan DD: Detonation of high explosives in shells and bombs and its effects. Br Med J 2:864-866, 1939. 3. Zuekerman S: Experimental study of blast injuries to the lungs. Lancet 2:219224, 1940. 4. Dean DM, Thomas AR, Allison RS: Effects of high-explosives blasts on lungs. Lancet 2:224-226, 1940. 5. Hadfield G, Ross JM, Swain RHA, et al: Blast from high explosive. Preliminary report on ten fatal cases. Lancet 2:478-481, 1940. 6. Desaga H: Blast injuries, in German Aviation Medicine, World War II, vol 2. Washington DC, US Government Printing Office, 1950, p 1274-1293. 7. Benzinger T: Physiological effects of blast in air and water, in German Aviation Medicine, World War II, vol 2. Washington DC, US Government Printing Office, 1950, p 1225-1259. 8. Corey EL: Medical aspects of blast. US Naval Med Bull 46:623-651, 1946. 9. Clemedson CJ: An experimental study on air blast injuries. Acta Physiol Scand 18(suppl 61):1-200, 1949. 10. White CS: Biological blast effects. US Atomic Energy Commission Technical Report TID-5564. Albuquerque, Lovelace Foundation for Medical Education and Research, 1959. 11. White CS: Biological effects of blast. Defense Atomic Support Agency Report DASA-1271. Albuquerque, Lovelace Foun78/692
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problem and its treatment. Israeli J Med Sci 11:268-274, 1975. 25. Gray RC, Coppel DL: Surgery of violence III. Intensive care of patients with bomb blast and gunshot injuries. Br Med l 1:502-504, 1975. 26. Coppel DL: Blast injuries of the lungs. Br J Surg 63:735-737, 1976. 27. Caseby NG, Porter MF: Blast injuries of the lungs; clinical presentation, management and course. Injury 8:1-12, 1976. 28. Fishman AP, Pietra GG: Stretched pores, blast injury, and neurohemodynamic pulmonary edema. Physiologist 23:53-56, 1980. 29. Pahor AL: Blast injuries to the ear: An historical and literary review. J Laryngol Otol 93:225-251, 1979. 30. Kerr AG: Trauma and the temporal bone. The effects of blast on the ear. l Laryngol Otol 94:107-110, 1980. 31. Cramer F, Paster S, Stephenson C: Cerebral injuries due to explosion waves - cerebral blast concussion. Arch NeuroI Psychiatry 61:1-20, 1949. 32. Murthy JMK, Chopra JS, Gulati DR: Subdural hematoma in an adult following blast injury. Case report. J Neurosurg 50: 260-261, 1979. 33. Gouze FJ, Hayter R: Air embolism in immersion blast. US Naval Med Bull 43: 871-877, 1944.
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New York, The MacMillan Co, 1962. 18. Richmond DR, Bowen IG, White CS: Tertiary blast effects: Effects of impact on mice, rats, guinea pigs, and rabbits. Aerospace Med 32:789-805, 1961. 19. Swearingen JJ, McFadden EB, Garner JD, et al: Human tolerance to vertical impact. Aerospace Med 31:989-998, 1960. 20. Gurdjian ES: Deformation studies of the skull: Mechanisms of skull fracture, in Impact Head Injur~. Springfield, Charles C. Thomas, 1975, p 113-138. 21. Hirsch M, Bazini J: Blast injury of the chest. Clin Raddol 20:362-370, 1969. 22. Huller T, Bazini Y: Blast injuries of the chest and abdomen. Arch Srtrg 100:24-30, 1970. 23. McCaughey W, Coppel DL, Dundee JW: Blast injuries to the lungs. A report of two cases. Anaesthesia 28:2-9, 1973. 24. Weiler-Ravell D, Adatto R, Borman JB: Blast injury of the chest. A review of the Annals of Emergency Medicine
34. Clemedson CJ, Hultman HI: Air embolism and the cause of death in blast injury. Milit Surg 114:424-437, 1954. 35. Menkin M, Schwartzman RJ: Cerebral air embolism. Report of five cases and review of the literature. Arch Neurol 34:168170, 1977. 36. Leavetl BS: Acute heart failure following blast injury. War Med 7:162-167, 1945. 37. Hadden WA, Rutherford WH, Merrett JD: The injuries of terrorist bombing: A study of 1532 consecutive patients. Br J Surg 65:525-531, 1978. 38. Hill JF: Blast injury with particular reference to recent terrorist bombing incidents. Ann Roy Cell Surg Engl 61:4-11, 1979. 39. Matz S, Segal A, Nemesh L, et al: Diagnosis of air embolism to the brain by computerized axial tomography. Comput Tomogr 4:107-110, 1980. 40. Damon EG, Henderson EA, Jones RK: The effect of intermittent positive pressure respiration on occurrence of air embolism and mortality following primary blast injury. Defense Nuclear Agency Report DNA-2989E Washington DC, US Government Printing Office, 1973. 41. Kao DK, Tiemey DF: Air embolism with positive-pressure ventilation of rats. J Appl Physiol 42:368-371, 1977. 42. Meier GH, Wood WJ, Symbas PN: Sys693/79
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temic air embolization from penetrating lung injury. Ann Thorac Surg 27:161-168~ 1979. 43. Van Genderen L, Waite CL: Evaluation of the rapid decompression high pressure oxygenation approach for the treatment of traumatic cerebral air embolism. Aerospace Med 39:709-713, 1968. 44. Kindwall EP: Massive surgical air embolism treated with brief recompression
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Annals of Emergency Medicine
effects of hyperbaric pressure in treatment of- primary blast injury. Defense Atomic Support Agency Report DASA-270. Washington DC, US Government Printing Ofrice, 1973. 48. Hart GB: Treatment of decompression illness and air embolism with hyperbaric oxygen. Aerospace Med 45:1190-1193, 1974. 49. Kizer KW: Manni¢ol in dysbarism. West f Med 132:86, 1980.
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