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Pulmonary Contusion
Pulmonary Contusion Glenn H. Shepard, M.D., Joe L. Ferguson, B.S., and John H. Foster, M.D.
P
hysical forces acting on an intact chest wall may produce a variety of lesions, including pneumothorax, hemothorax, flail chest, rib fractures, cardiac contusion, great vessel laceration, and pulmonary contusion. Recently, there has been interest in pulmonary contusion, especially the difficulties in early recognition and its contribution to disturbances in pulmonary function [l, 4, 213. In civilian practice, pulmonary contusion is most commonly encountered in automobile accident victims 141 whose chests violently strike steering wheels and dashboards. Falls, athletic injuries, and industrial accidents also produce this injury [6]. In military practice, pulmonary contusion may be caused by nonpenetrating wounds from high-velocity missiles, blows from blunt objects, and the blast of high-explosive shells [18]. Blast injuries were formerly regarded as a unique form of injury. They were thought to result from the passage of positive and negative pressure waves through the pulmonary parenchyma and by direct passage of the pressure wave via the trachea to the alveoli [l 1, 241. Zuckerman [24] demonstrated that the injury was caused instead by rapidly moving gases forcefully striking the chest wall, causing pulmonary contusion in the same manner a blunt object does. Regardless of etiology, the pathological picture of pulmonary contusion is one of rupture of blood vessels and alveoli with interstitial and alveolar hemorrhage. Gas diffusion across the alveolocapillary membrane is mechanically blocked. T h e severity of the lesion depends upon the amount of lung tissue contused and the pulmonary reserve. T h e lesions may range from clinically undetectable areas of hemorrhage to fatal, massive, bloody consolidation of one or both lungs. Two clinical cases in the authors’ experience illustrate the difficulty of early diagnosis of pulmonary contusion and the rapid deterioration of patients with serious injuries. CASE
1
A 54-year-old female was admitted to the Nashville General Hospital following an automobile accident. Her blood pressure on admission was 100/60and the From the S. R. Light Laboratory for Surgical Research, Department of Surgery, and the Department of Physics, Vanderbilt University and Medical Center, Nashville, Tenn. Presented at the Fifteenth Annual Meeting of the Southern Thoracic Surgical Association, San Juan, P.R., Nov. 14-16, 1968. Address reprint requests to Dr. Shepard, Duval Medical Center, Jacksonville, Fla. 32206.
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Pulmonary Contusion pulse rate was 80 per minute. A flail chest was noted. Lung fields were clear to auscultation. Moderate upper abdominal tenderness was present. A chest x-ray showed several small infiltrates in the left upper lobe, but no serious injury was suspected initially. The ECG was normal. Tracheotomy was performed, and controlled positive pressure breathing stabilized the chest wall. Thirty minutes after admission the blood pressure dropped to 80160. Abdominal paracentesis produced no blood. Four units of blood were transfused with further fall in blood pressure. Venous pressure was 5 cm.H,O. Abdominal tenderness suggested the necessity for laparotomy in unexplained hypotension, but cyanosis developed followed by cardiac arrest. T h e patient died one hour following admission. Autopsy showed massive contusion of the left upper and lower lobes of the lung with no abdominal visceral or other injury. Comment. Abdominal rigidity and tenderness occur not infrequently with pulmonary contusion, which at times produces diagnostic difficulties [ 131. CASE
2
A 35-year-old Army sergeant was admitted to the Second Surgical Hospital, the Republic of Vietnam, shortly after being accidentally shot by an M-16 rifle from close range in the region of the third rib anterolaterally. Vital signs were stable on admission, with a pulse rate of 70. Auscultation of the lungs revealed a few rhonchi in the left upper lobe. The patient complained of shortness of breath, but no serious problems were evident initially. Hypotension developed while x-rays were being made twenty minutes following admission. Great vessel laceration was suspected. Four units of blood were rapidly infused in preparation for a thoracotomy, but the patient’s condition rapidly deteriorated. He died 45 minutes after admission. Autopsy showed the missile still in the chest wall, with no pleural penetration. The left upper and lower lobes were massively contused from the nonpenetrating high-velocity missile wound. No other lesions were noted.
EXPERIMENTAL METHODS A N D MATERIALS T h e paucity of early clinical findings to support a diagnosis of a major pulmonary lesion and the rapid demise of these two patients stimulated an interest in the early physiological and pathological changes that occur with pulmonary contusion. Earlier work in this laboratory suggested an experimental model, using the blast of blank cartridges, to consistently produce localized areas of pulmonary contusion [201. By being able to control the size of the lesion with this experimental technique, objective appraisal of the lesions was made possible. Further studies were made to determine the effects of hydrocortisone in the acute blast injury. GROUP I
Eight mongrel dogs weighing 10 to 15 kg. were deeply anesthetized with intravenous sodium pentobarbital. Intravenous and intraarterial cutdowns were attached to manometers. Modified Carlin tubes were positioned through tracheotomies. A 3 x 5 x 0.3 cm. lead plate was placed subcutaneously in the left anterolateral chest wall over the fourth to eighth rib in half of the animals to prevent penetrating wounds. A piezoelectric transducer (Kistler Model 603L) in a %-inch nylon sleeve was introduced through a stab wound into the thoracic cavity 4 cm. superior to the site selected for wounding. It was secured with silk sutures perpendicular to the chest wall to prevent introduction of air into the thoracic cavity. A second piezoelectric transducer (Massa Model M-213) was placed in the left bronchial limb of the Carlin tube in nonocclusive fashion. Number 8 ureteral catheters, with tips 2 inches distal to the ends of the bronchial VOL.
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SHEPARD, FERGUSON, AND FOSTER limbs of the Carlin tubes, were used for collection of alveolar gas samples and measurement of intrabronchial pressures. Each animal was wounded on maximum inspiration in the sixth intercostal space anterolaterally with a .38 police special caliber blank fired from a Smith and Wesson revolver. Wounds were centered over the lead plates in 4 animals, while the remaining 4 dogs were wounded on an unprotected chest wall. Penetrating wounds, when produced, were sutured immediately, and the air was aspirated from the pleural space. Intrathoracic pressures (in 8 animals) and left intrabronchial pressures (in 4 animals) were recorded at the moment of wounding on an oscilloscope (Textronic 502 dual beam). Venous and arterial pressures were continually monitored from immediately prior to wounding until the time of sacrifice 4 hours after wounding. Aliquots of air from both bronchi and blood samples were examined at hourly intervals for pH, PO,, and pC0,. Right and left intrabronchial and intrapleural pressures were measured at the same intervals. Anteroposterior chest x-rays were taken hourly. Two pathologists independently examined the postmortem findings. GROUP I1
Four mongrel dogs weighing 12 to 15 kg. were anesthetized with intravenous sodium pentobarbital. Piezoelectric transducers (Kistler Model 603L) were placed in the pleural space as described earlier. All animals were wounded without shields and were sacrificed 15 minutes after wounding. GROUP I11
T e n mongrel dogs weighing 10 to 12 kg. were anesthetized with intravenous sodium pentobarbital. A 3 x 5 x 0.3 cm. lead shield, centered over the left seventh intercostal space anterolaterally, was placed subcutaneously in all animals. Wounds were inflicted using the same method as described for the Group I dogs. Five of the animals were given hydrocortisone in doses of 40 mg. per kilogram of body weight immediately following wounding and every 12 hours until the time of sacrifice. Twenty-four hours postwounding, 3 treated and 3 untreated animals were sacrificed. Seventy-two hours postwounding, 2 treated and 2 untreated animals were sacrificed. Autopsies were performed by two pathologists. Gross and microscopic studies of the tissues were performed using a double-blind technique. RESULTS GROUP I
Table 1 shows the intrabronchial and intrathoracic pressures recorded at the moment of injury. T h e positive phase of the intrathoracic blast wave averaged 70 mm. H g in the 4 lead-shielded animals and 212 mm. H g in those animals not shielded. T h e duration of the blast wave was 4 msec. in each of the shielded dogs and 2 msec. in each of the unshielded ones, contrasting with a duration of 0.2 msec. in air (Fig. 1). Endobronchial pressures were 26 and 30 mm. H g for 2 shielded dogs and 126 and 130 mm. H g for 2 unshielded dogs at the time of wounding. Figure 2 shows simultaneous recordings of intrathoracic and intrabronchial pressures. A time lag appeared between the appearance of the intrapleural pressure wave and the bronchial pressure wave, which in each case was calculated to approximate the speed of sound. Blood pressure depressions were observed in every animal within 20 seconds of wounding and averaged 24 mm. Hg. A slowing of the pulse an average of 27 beats per minute occurred in all animals. Venous pressures remained constant in the immediate postwounding period, but rose an average of 2.2 cm. H,O 3 hours after wounding. Figure 3 shows a representative recording of pulse, blood pressure, and venous pressure.
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THE ANNALS OF THORACIC SURGERY
Pulmonary Contusion TABLE 1.
INTRABRONCHIAL AND INTRATHORACIC PRESSURES (POSITIVE PHASE) A T MOMENT OF INJURY
Intrapleural Pressure Dog No.
Intrabronchial Pressure
Intensity (mm. Hg)
Duration (msec.)
88
4 4 4 4 2
la 2a 3a
100
62 31 220 250 127 250
4a
5 6 7 8
Intensity (mm. Hg)
Duration (msec.)
4
30
-
-
26
4
-
-
2 2 2
-
126
2
-
-
130
2
'Lead shield used.
mmHg I50 I00 50 0
- 50
-100 -150
20 18 16 14 12 10 8 6 4 2 0
20 18 16 14 I2 10 8 6 4 2 0
f Wounding
m SEC.
A
mSEC.
B
fI
Wounding
20 1 8 I6 1 4 I2 10 8 6 4 2 0
C
~SEC. Wounding
FIG. 1. Comparison of blast waves in shielded animals (A), in unshielded animals (B), and in air (C). VOL.
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FIG. 2. Simultaneous recordings of intrathoracic (upper scale) and intrabronchial (lower scale) pressures. Note lag in appearance of intrabronchial pressure wave. In 6 of the 7 animals followed for 4 hours, a diminution of left intrabronchial pressures occurred, approximating zero, while the right intrabronchial and right and left intrapleural pressures remained unchanged. At the conclusion of the experiment, the Carlin tubes were removed and the intrabronchial pressures checked at bronchoscopy to be certain of the placement of the catheter tip. This study confirmed the observed reduction of intrabronchial pressures in the injured side. Results of the alveolar and blood gas studies showed no change from baseline levels except in Dog 6, which died 2 hours after wounding. (Blood gases taken just prior to expiration showed pH 6.9, pCOz 100, pOz 25. These changes were due to an uncorrected tension pneumothorax.) There were likewise no differences in alveolar samples of the injured side when compared to the uninjured side. No x-ray changes were detectable until 3 hours after injury. Four of the surviving 7 dogs showed circumscribed densities in the left lung field (Fig. 4) corresponding in location to those of the injured segments found at autopsy. Pathological study at autopsy showed that pulmonary contusion was produced in 7 of the 8 animals. The uninjured animal (Dog 4)showed intrapleural pressure at the moment of wounding (31 mm. Hg) considerably below that of the other animals. Consistent 2 x 1 x 1 cm. lesions were produced. These lesions were purple VENOUS PRESSURE mm.Hp
20 10 0 Pulse 96/min
Pulse 80/min
Pulse 80/min
Pulse 84/min
PHRS.
4HRS.
BLOOD PRESSURE
I)ASELINE
WOUNDING
FIG. 3 . Representative recordings of venous pressure, pulse, and blood pressure at wounding and 2 and 4 hours later.
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Pulmonary Contusion
FIG. 4 . X-ray 3 hours after wounding. Note density in left hemithorax near cardiac border. in color with a distinct border separating them from surrounding lung tissue. Larger wounds were produced in the unshielded group, with penetrating wounds occurring in 2 of the 4 animals. Microscopic study showed circumscribed parenchymal and alveolar hemorrhage with normal tissues around the injured area. GROUP I1
Intrapleural pressures of 200 to 258 mm. Hg were recorded at the moment of wounding. A penetrating wound occurred in one animal. Autopsies performed 15 minutes after wounding showed a faint bluish blush with indistinct borders in the areas wounded. Microscopic study showed alveolar and interstitial hemorrhage. When compared macroscopically and microscopically to the Group I lesions (sacrifice performed 4 hours after wounding), the amount of hemorrhage was much greater in the Group I animals. GROUP I11
Gross pathological examination showed consistent 2 x 1 x 1 cm. lesions produced in the superior segment of the lower lobes in all animals. No macroscopic or microscopic differences could be detected between hydrocortisone-treated and untreated groups at either 24 or 72 hours. At 24 hours, active fibroplasia was evident, along with a small amount of edema fluid confined to the contused area. At 72 hours, a greater number of fibroblasts were present. No resolution of hemorrhagic exudate was observed. No inflammatory reaction was seen.
DISCUSSION
T h e blast wave created by an explosion (as in the firing of a blank cartridge) is a single pulse of increased pressure followed by a wave of VOL.
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suction. The positive phase lasts up to 5 msec. (depending on the nature of the explosion) and the negative phase up to 30 msec. The amplitude (intensity) decreases as the distance from the blast increases and with the placement of protective shields. Energies in the magnitude of 7% pounds per square inch (473 mm. Hg) are required to produce pulmonary contusion [12]. With blast injuries caused by detonation of explosives, these pressures may envelop the entire chest with multilobar injury. In blunt trauma as seen in automobile accidents, the pressures are distributed over a smaller area. In the reported experiment, lead shields were used to diminish the amplitude of the blast wave. Impressions in the lead shield created by the discharge of the blank showed the forces of the blast to be distributed over an area 2 cm. in diameter. This corresponded to the size of the pulmonary contusion. Blast waves measured intrapleurally 4 cm. from the point of wounding in this experiment were of insufficient magnitude to produce injury, as evidenced by an absence of pulmonary hemorrhage in this region. This shows a rapid dissipation of energy at the point of impact. When comparing blast waves in air, in the unshielded pleural space, and in the shielded pleural space, one sees a progressive decrease in amplitude (intensity) and increase in duration of the blast wave. These differences between the shielded and unshielded groups demonstrate the degree of protection given by the shields and supports Zuckerman’s studies [25] showing that protective shields can diminish the amount of injury caused by blast waves. A consistent diminution of intrabronchial pressures was recorded from the time of wounding to the time of sacrifice in the Group I dogs. T h e depth of anesthesia precluded splinting originating from somatic nerve stimulation. With the generous supply of autonomic nerves in the parietal pleura and pulmonary blood vessels, a plausible explanation would be an autonomic reflex mediated through the vagus nerve [7]. Retention of bronchial secretions due to an inadequate expansion of the lung could hypothetically result in a traumatic wet lung. De Takats et al. [5] experimentally demonstrated that a similar vagal reflex mechanism was responsible for increased production of bronchial secretions. This was proposed as the mechanism for the traumatic wet lung. Daniel and Gate [2] showed diminution of secretions with thoracic sympathectomy, which gives support to theories of autonomic reflexes. In four of the Group I11 animals (2 treated and 2 untreated), increased secretions were noted in the injured lung, suggesting that one or both of the proposed reflex mechanisms may have been operational. Diminution of blood pressure and slowing of the pulse appeared in all animals moments after wounding in spite of the extremely small relative size of the pulmonary contusion. With blood and alveolar gases
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Pulmonary Contusion
showing no hypoxia or hypercarbia and in the absence of significant blood loss, autonomic reflexes again provide the most reasonable explanation. Hooker [9] made similar observations and labeled this occurrence “concussion shock.” He explained this on the basis of nervous factors. Hypotension appearing in the two clinical case reports similarly were not explained by blood loss. Volume expansion only added to the pulmonary edema and worsened rather than improved the pathological process. Gross comparisons of pulmonary wounds 15 minutes, 4 hours, and 24 hours following wounding showed a progressive amount of hemorrhage occurring with passage of time. T h e greatest difference appeared between the 15-minute and the 4-hour groups. While the former group showed a faint bluish blush, the 4-hour group showed a definite circumscribed hemorrhagic area. Microscopic findings substantiated these impressions. Little change was noted grossly between the one- and threeday lesions, while an increased fibroplasia was the only microscopic difference. T h e initial x-ray changes appearing at 3 hours correlate well with these pathological findings. Hadfield and Christie [8] have observed that with pulmonary contusion in man, bleeding may continue up to 48 hours. Delayed appearance of x-ray findings has also been reported in man [l, 211. Contrecoup injuries were noted in 3 animals, all found adjacent to the vertebral column. Clinical reports show that in man, contrecoup injuries occur only in the fixed, posterior regions adjacent to the vertebral column after blows on the anterolateral chest wall [lo, 141. Hydrocortisone has been used clinically for treatment of pulmonary contusion [4]. T h e rationale for its use is in the inhibition of the inflammatory response and the relief of bronchospasm [19]. In the present study, no inflammatory response was noted in the contused area up to 72 hours after wounding. In man there have been no inflammatory components described in the region of pulmonary contusion [1, 3, 4, 12, 16, 17, 21, 231. While the term traumatic pneumonitis was proposed as an entity resulting from pulmonary contusion [15], this concept has been disregarded, as no infectious process is involved in the pathogenesis of pulmonary contusion [21, 223. No changes appeared in the treated group to support any beneficial effects of hydrocortisone. Retained secretions were noted equally often in treated and untreated animals. T h e lesions produced by the technique herein described lend themselves to such critical studies as the evaluation of the effects of drugs. T h e ability to predictably produce lesions of like size in the same region of the lung (Fig. 5 ) estabhhes blank cartridge wounding as a useful tool in the laboratory investigation of trauma.
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FIG. 5 . Control and hydrocortisone-treated lesions at 7 2 hours. Note that all lesions are similar in size and location. SUMMARY
Small, circumscribed, “minimal” pulmonary contusions were produced in dogs. Physiological changes noted were hypotension with slowing of the pulse rate. Diminished intrabronchial pressures were recorded on the side of injury. In the absence of changes in alveolar and blood gases and in the absence of significant blood or plasma loss, reflex mechanisms are suspected. The extravasation of blood in the contused area occurs gradually over a 24-hour period. No x-ray changes were noted until 3 hours after injury. Pathological studies showed no evidence of any inflammatory reaction in these experimental pulmonary contusions. No pathological differences were noted between control and hydrocortisone-treated dogs. Retained bronchial secretions were noted in an equal number of control and hydrocortisone-treated animals. Physical studies of the blast waves causing the injury are presented. REFERENCES 1 . Alfano, G. S., and Hale, H. W. Pulmonary contusion. J. Trauma 5:647, 1965. 2. Daniel, R. A., and Cate, W. R. Wet lung-an experimental study. Ann. Surg. 127:836, 1948. 118
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Pulmonary Contusion 3. Dean, D. M., Thomas, A. R., and Allison, R. S. Effects of explosion blast on lungs. Brit. Med. J . 2:224, 1940. 4. Demuth, W. E., and Smith, J. M. Pulmonary contusion. Amer. J . Surg. 109: 819, 1965. 5 . De Takats, G., Fenn, G. K., and Jenkenson, E. L. Reflex pulmonary atelectasis. J.A.M.A. 120:686, 1942. 6. Fallon, M. Lung injury in the intact thorax. Brit. J . Surg. 28:39, 1940. 7. Gillian, L. A. Clinical Aspects of the Autonomic Neruous System. Boston: Little Brown, 1954. P. 170. 8. Hadfield, G., and Christie, R. V. A case of pulmonary concussion (“blast”) due to high explosive. Brit. Med. J . 1:77, 1941. 9. Hooker, D. R. Physiological aspects of air concussion. Amer. J . Physiol. 67:239, 1924. 10. Klubs, K. Lunge und Trauma. Arch. Ex@ Path. Pharm. 62:39, 1909. 11. Lockwood, A. L. Some experiences in the last war. Brit. Med. J . 1:357, 1940. 12. Lung injuries in air raids-discussion on pathology and diagnosis. Panel discussion. Brit. Med. J . 2:239, 1941. 13. O’Reilly, J. N., and Gloyne, S. R. Blast injury of the lung. Lancet 2:423, 1941. 14. Osborn, G. R. Findings in 262 fatal accidents. Lancet 2:277, 1943. 15. Phillips, C. Pneumonia following nonpenetrating pulmonary injuries. J.A.M.A. 133:161, 1947. 16. Ross, J. M. Hemorrhage into the lungs in cases of death due to trauma. Brit. Med. J . 1:79, 1941. 17. Savage, 0. Pulmonary concussion (“blast”) in non-thoracic bottle wounds. Lancet 1:424, 1945. 18. Sealy, W. C. Contusions of the lung from nonpenetrating injuries to the thorax. Arch. Surg. 59:882, 1949. 19. Sealy, W. C., Young, G. W., Hauck, W. S., and Stephen, R. C. T h e use of steroids for the control and prevention of serious respiratory embarrassment during and after thoracic operations. J . Thorac. Cardiovasc. Surg. 39: 109, 1960. 20. Shepard, G. H. Blank cartridge wounds: Clinical and experimental studies. J . Trauma. I n press. 21. Stevens, E., and Templeton, A. W. Traumatic nonpenetrating lung contusion. Radiology 85:247, 1965. 22. Williams, J. R., and Stembridge, V. A. Pulmonary contusion secondary to nonpenetrating chest trauma. Amer. J . Roentgen. 91:284, 1964. 23. Wilson, J. V. The pathology of closed injuries of the chest. Brit. Med. J . 1:470, 1943. 24. Zuckerman, S. Experimental studies of blast injury of the lung. Lancet 2: 219, 1940. 25. Zuckerman, S. Discussion on the problem of blast injuries. Proc. Roy. SOC. Med. 34:171, 1941.
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iig
P
hysical forces acting on an intact chest wall may produce a variety of lesions, including pneumothorax, hemothorax, flail chest, rib fractures, cardiac contusion, great vessel laceration, and pulmonary contusion. Recently, there has been interest in pulmonary contusion, especially the difficulties in early recognition and its contribution to disturbances in pulmonary function [l, 4, 213. In civilian practice, pulmonary contusion is most commonly encountered in automobile accident victims 141 whose chests violently strike steering wheels and dashboards. Falls, athletic injuries, and industrial accidents also produce this injury [6]. In military practice, pulmonary contusion may be caused by nonpenetrating wounds from high-velocity missiles, blows from blunt objects, and the blast of high-explosive shells [18]. Blast injuries were formerly regarded as a unique form of injury. They were thought to result from the passage of positive and negative pressure waves through the pulmonary parenchyma and by direct passage of the pressure wave via the trachea to the alveoli [l 1, 241. Zuckerman [24] demonstrated that the injury was caused instead by rapidly moving gases forcefully striking the chest wall, causing pulmonary contusion in the same manner a blunt object does. Regardless of etiology, the pathological picture of pulmonary contusion is one of rupture of blood vessels and alveoli with interstitial and alveolar hemorrhage. Gas diffusion across the alveolocapillary membrane is mechanically blocked. T h e severity of the lesion depends upon the amount of lung tissue contused and the pulmonary reserve. T h e lesions may range from clinically undetectable areas of hemorrhage to fatal, massive, bloody consolidation of one or both lungs. Two clinical cases in the authors’ experience illustrate the difficulty of early diagnosis of pulmonary contusion and the rapid deterioration of patients with serious injuries. CASE
1
A 54-year-old female was admitted to the Nashville General Hospital following an automobile accident. Her blood pressure on admission was 100/60and the From the S. R. Light Laboratory for Surgical Research, Department of Surgery, and the Department of Physics, Vanderbilt University and Medical Center, Nashville, Tenn. Presented at the Fifteenth Annual Meeting of the Southern Thoracic Surgical Association, San Juan, P.R., Nov. 14-16, 1968. Address reprint requests to Dr. Shepard, Duval Medical Center, Jacksonville, Fla. 32206.
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T H E ANNALS OF THORACIC SURGERY
Pulmonary Contusion pulse rate was 80 per minute. A flail chest was noted. Lung fields were clear to auscultation. Moderate upper abdominal tenderness was present. A chest x-ray showed several small infiltrates in the left upper lobe, but no serious injury was suspected initially. The ECG was normal. Tracheotomy was performed, and controlled positive pressure breathing stabilized the chest wall. Thirty minutes after admission the blood pressure dropped to 80160. Abdominal paracentesis produced no blood. Four units of blood were transfused with further fall in blood pressure. Venous pressure was 5 cm.H,O. Abdominal tenderness suggested the necessity for laparotomy in unexplained hypotension, but cyanosis developed followed by cardiac arrest. T h e patient died one hour following admission. Autopsy showed massive contusion of the left upper and lower lobes of the lung with no abdominal visceral or other injury. Comment. Abdominal rigidity and tenderness occur not infrequently with pulmonary contusion, which at times produces diagnostic difficulties [ 131. CASE
2
A 35-year-old Army sergeant was admitted to the Second Surgical Hospital, the Republic of Vietnam, shortly after being accidentally shot by an M-16 rifle from close range in the region of the third rib anterolaterally. Vital signs were stable on admission, with a pulse rate of 70. Auscultation of the lungs revealed a few rhonchi in the left upper lobe. The patient complained of shortness of breath, but no serious problems were evident initially. Hypotension developed while x-rays were being made twenty minutes following admission. Great vessel laceration was suspected. Four units of blood were rapidly infused in preparation for a thoracotomy, but the patient’s condition rapidly deteriorated. He died 45 minutes after admission. Autopsy showed the missile still in the chest wall, with no pleural penetration. The left upper and lower lobes were massively contused from the nonpenetrating high-velocity missile wound. No other lesions were noted.
EXPERIMENTAL METHODS A N D MATERIALS T h e paucity of early clinical findings to support a diagnosis of a major pulmonary lesion and the rapid demise of these two patients stimulated an interest in the early physiological and pathological changes that occur with pulmonary contusion. Earlier work in this laboratory suggested an experimental model, using the blast of blank cartridges, to consistently produce localized areas of pulmonary contusion [201. By being able to control the size of the lesion with this experimental technique, objective appraisal of the lesions was made possible. Further studies were made to determine the effects of hydrocortisone in the acute blast injury. GROUP I
Eight mongrel dogs weighing 10 to 15 kg. were deeply anesthetized with intravenous sodium pentobarbital. Intravenous and intraarterial cutdowns were attached to manometers. Modified Carlin tubes were positioned through tracheotomies. A 3 x 5 x 0.3 cm. lead plate was placed subcutaneously in the left anterolateral chest wall over the fourth to eighth rib in half of the animals to prevent penetrating wounds. A piezoelectric transducer (Kistler Model 603L) in a %-inch nylon sleeve was introduced through a stab wound into the thoracic cavity 4 cm. superior to the site selected for wounding. It was secured with silk sutures perpendicular to the chest wall to prevent introduction of air into the thoracic cavity. A second piezoelectric transducer (Massa Model M-213) was placed in the left bronchial limb of the Carlin tube in nonocclusive fashion. Number 8 ureteral catheters, with tips 2 inches distal to the ends of the bronchial VOL.
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111
SHEPARD, FERGUSON, AND FOSTER limbs of the Carlin tubes, were used for collection of alveolar gas samples and measurement of intrabronchial pressures. Each animal was wounded on maximum inspiration in the sixth intercostal space anterolaterally with a .38 police special caliber blank fired from a Smith and Wesson revolver. Wounds were centered over the lead plates in 4 animals, while the remaining 4 dogs were wounded on an unprotected chest wall. Penetrating wounds, when produced, were sutured immediately, and the air was aspirated from the pleural space. Intrathoracic pressures (in 8 animals) and left intrabronchial pressures (in 4 animals) were recorded at the moment of wounding on an oscilloscope (Textronic 502 dual beam). Venous and arterial pressures were continually monitored from immediately prior to wounding until the time of sacrifice 4 hours after wounding. Aliquots of air from both bronchi and blood samples were examined at hourly intervals for pH, PO,, and pC0,. Right and left intrabronchial and intrapleural pressures were measured at the same intervals. Anteroposterior chest x-rays were taken hourly. Two pathologists independently examined the postmortem findings. GROUP I1
Four mongrel dogs weighing 12 to 15 kg. were anesthetized with intravenous sodium pentobarbital. Piezoelectric transducers (Kistler Model 603L) were placed in the pleural space as described earlier. All animals were wounded without shields and were sacrificed 15 minutes after wounding. GROUP I11
T e n mongrel dogs weighing 10 to 12 kg. were anesthetized with intravenous sodium pentobarbital. A 3 x 5 x 0.3 cm. lead shield, centered over the left seventh intercostal space anterolaterally, was placed subcutaneously in all animals. Wounds were inflicted using the same method as described for the Group I dogs. Five of the animals were given hydrocortisone in doses of 40 mg. per kilogram of body weight immediately following wounding and every 12 hours until the time of sacrifice. Twenty-four hours postwounding, 3 treated and 3 untreated animals were sacrificed. Seventy-two hours postwounding, 2 treated and 2 untreated animals were sacrificed. Autopsies were performed by two pathologists. Gross and microscopic studies of the tissues were performed using a double-blind technique. RESULTS GROUP I
Table 1 shows the intrabronchial and intrathoracic pressures recorded at the moment of injury. T h e positive phase of the intrathoracic blast wave averaged 70 mm. H g in the 4 lead-shielded animals and 212 mm. H g in those animals not shielded. T h e duration of the blast wave was 4 msec. in each of the shielded dogs and 2 msec. in each of the unshielded ones, contrasting with a duration of 0.2 msec. in air (Fig. 1). Endobronchial pressures were 26 and 30 mm. H g for 2 shielded dogs and 126 and 130 mm. H g for 2 unshielded dogs at the time of wounding. Figure 2 shows simultaneous recordings of intrathoracic and intrabronchial pressures. A time lag appeared between the appearance of the intrapleural pressure wave and the bronchial pressure wave, which in each case was calculated to approximate the speed of sound. Blood pressure depressions were observed in every animal within 20 seconds of wounding and averaged 24 mm. Hg. A slowing of the pulse an average of 27 beats per minute occurred in all animals. Venous pressures remained constant in the immediate postwounding period, but rose an average of 2.2 cm. H,O 3 hours after wounding. Figure 3 shows a representative recording of pulse, blood pressure, and venous pressure.
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Pulmonary Contusion TABLE 1.
INTRABRONCHIAL AND INTRATHORACIC PRESSURES (POSITIVE PHASE) A T MOMENT OF INJURY
Intrapleural Pressure Dog No.
Intrabronchial Pressure
Intensity (mm. Hg)
Duration (msec.)
88
4 4 4 4 2
la 2a 3a
100
62 31 220 250 127 250
4a
5 6 7 8
Intensity (mm. Hg)
Duration (msec.)
4
30
-
-
26
4
-
-
2 2 2
-
126
2
-
-
130
2
'Lead shield used.
mmHg I50 I00 50 0
- 50
-100 -150
20 18 16 14 12 10 8 6 4 2 0
20 18 16 14 I2 10 8 6 4 2 0
f Wounding
m SEC.
A
mSEC.
B
fI
Wounding
20 1 8 I6 1 4 I2 10 8 6 4 2 0
C
~SEC. Wounding
FIG. 1. Comparison of blast waves in shielded animals (A), in unshielded animals (B), and in air (C). VOL.
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FIG. 2. Simultaneous recordings of intrathoracic (upper scale) and intrabronchial (lower scale) pressures. Note lag in appearance of intrabronchial pressure wave. In 6 of the 7 animals followed for 4 hours, a diminution of left intrabronchial pressures occurred, approximating zero, while the right intrabronchial and right and left intrapleural pressures remained unchanged. At the conclusion of the experiment, the Carlin tubes were removed and the intrabronchial pressures checked at bronchoscopy to be certain of the placement of the catheter tip. This study confirmed the observed reduction of intrabronchial pressures in the injured side. Results of the alveolar and blood gas studies showed no change from baseline levels except in Dog 6, which died 2 hours after wounding. (Blood gases taken just prior to expiration showed pH 6.9, pCOz 100, pOz 25. These changes were due to an uncorrected tension pneumothorax.) There were likewise no differences in alveolar samples of the injured side when compared to the uninjured side. No x-ray changes were detectable until 3 hours after injury. Four of the surviving 7 dogs showed circumscribed densities in the left lung field (Fig. 4) corresponding in location to those of the injured segments found at autopsy. Pathological study at autopsy showed that pulmonary contusion was produced in 7 of the 8 animals. The uninjured animal (Dog 4)showed intrapleural pressure at the moment of wounding (31 mm. Hg) considerably below that of the other animals. Consistent 2 x 1 x 1 cm. lesions were produced. These lesions were purple VENOUS PRESSURE mm.Hp
20 10 0 Pulse 96/min
Pulse 80/min
Pulse 80/min
Pulse 84/min
PHRS.
4HRS.
BLOOD PRESSURE
I)ASELINE
WOUNDING
FIG. 3 . Representative recordings of venous pressure, pulse, and blood pressure at wounding and 2 and 4 hours later.
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FIG. 4 . X-ray 3 hours after wounding. Note density in left hemithorax near cardiac border. in color with a distinct border separating them from surrounding lung tissue. Larger wounds were produced in the unshielded group, with penetrating wounds occurring in 2 of the 4 animals. Microscopic study showed circumscribed parenchymal and alveolar hemorrhage with normal tissues around the injured area. GROUP I1
Intrapleural pressures of 200 to 258 mm. Hg were recorded at the moment of wounding. A penetrating wound occurred in one animal. Autopsies performed 15 minutes after wounding showed a faint bluish blush with indistinct borders in the areas wounded. Microscopic study showed alveolar and interstitial hemorrhage. When compared macroscopically and microscopically to the Group I lesions (sacrifice performed 4 hours after wounding), the amount of hemorrhage was much greater in the Group I animals. GROUP I11
Gross pathological examination showed consistent 2 x 1 x 1 cm. lesions produced in the superior segment of the lower lobes in all animals. No macroscopic or microscopic differences could be detected between hydrocortisone-treated and untreated groups at either 24 or 72 hours. At 24 hours, active fibroplasia was evident, along with a small amount of edema fluid confined to the contused area. At 72 hours, a greater number of fibroblasts were present. No resolution of hemorrhagic exudate was observed. No inflammatory reaction was seen.
DISCUSSION
T h e blast wave created by an explosion (as in the firing of a blank cartridge) is a single pulse of increased pressure followed by a wave of VOL.
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suction. The positive phase lasts up to 5 msec. (depending on the nature of the explosion) and the negative phase up to 30 msec. The amplitude (intensity) decreases as the distance from the blast increases and with the placement of protective shields. Energies in the magnitude of 7% pounds per square inch (473 mm. Hg) are required to produce pulmonary contusion [12]. With blast injuries caused by detonation of explosives, these pressures may envelop the entire chest with multilobar injury. In blunt trauma as seen in automobile accidents, the pressures are distributed over a smaller area. In the reported experiment, lead shields were used to diminish the amplitude of the blast wave. Impressions in the lead shield created by the discharge of the blank showed the forces of the blast to be distributed over an area 2 cm. in diameter. This corresponded to the size of the pulmonary contusion. Blast waves measured intrapleurally 4 cm. from the point of wounding in this experiment were of insufficient magnitude to produce injury, as evidenced by an absence of pulmonary hemorrhage in this region. This shows a rapid dissipation of energy at the point of impact. When comparing blast waves in air, in the unshielded pleural space, and in the shielded pleural space, one sees a progressive decrease in amplitude (intensity) and increase in duration of the blast wave. These differences between the shielded and unshielded groups demonstrate the degree of protection given by the shields and supports Zuckerman’s studies [25] showing that protective shields can diminish the amount of injury caused by blast waves. A consistent diminution of intrabronchial pressures was recorded from the time of wounding to the time of sacrifice in the Group I dogs. T h e depth of anesthesia precluded splinting originating from somatic nerve stimulation. With the generous supply of autonomic nerves in the parietal pleura and pulmonary blood vessels, a plausible explanation would be an autonomic reflex mediated through the vagus nerve [7]. Retention of bronchial secretions due to an inadequate expansion of the lung could hypothetically result in a traumatic wet lung. De Takats et al. [5] experimentally demonstrated that a similar vagal reflex mechanism was responsible for increased production of bronchial secretions. This was proposed as the mechanism for the traumatic wet lung. Daniel and Gate [2] showed diminution of secretions with thoracic sympathectomy, which gives support to theories of autonomic reflexes. In four of the Group I11 animals (2 treated and 2 untreated), increased secretions were noted in the injured lung, suggesting that one or both of the proposed reflex mechanisms may have been operational. Diminution of blood pressure and slowing of the pulse appeared in all animals moments after wounding in spite of the extremely small relative size of the pulmonary contusion. With blood and alveolar gases
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showing no hypoxia or hypercarbia and in the absence of significant blood loss, autonomic reflexes again provide the most reasonable explanation. Hooker [9] made similar observations and labeled this occurrence “concussion shock.” He explained this on the basis of nervous factors. Hypotension appearing in the two clinical case reports similarly were not explained by blood loss. Volume expansion only added to the pulmonary edema and worsened rather than improved the pathological process. Gross comparisons of pulmonary wounds 15 minutes, 4 hours, and 24 hours following wounding showed a progressive amount of hemorrhage occurring with passage of time. T h e greatest difference appeared between the 15-minute and the 4-hour groups. While the former group showed a faint bluish blush, the 4-hour group showed a definite circumscribed hemorrhagic area. Microscopic findings substantiated these impressions. Little change was noted grossly between the one- and threeday lesions, while an increased fibroplasia was the only microscopic difference. T h e initial x-ray changes appearing at 3 hours correlate well with these pathological findings. Hadfield and Christie [8] have observed that with pulmonary contusion in man, bleeding may continue up to 48 hours. Delayed appearance of x-ray findings has also been reported in man [l, 211. Contrecoup injuries were noted in 3 animals, all found adjacent to the vertebral column. Clinical reports show that in man, contrecoup injuries occur only in the fixed, posterior regions adjacent to the vertebral column after blows on the anterolateral chest wall [lo, 141. Hydrocortisone has been used clinically for treatment of pulmonary contusion [4]. T h e rationale for its use is in the inhibition of the inflammatory response and the relief of bronchospasm [19]. In the present study, no inflammatory response was noted in the contused area up to 72 hours after wounding. In man there have been no inflammatory components described in the region of pulmonary contusion [1, 3, 4, 12, 16, 17, 21, 231. While the term traumatic pneumonitis was proposed as an entity resulting from pulmonary contusion [15], this concept has been disregarded, as no infectious process is involved in the pathogenesis of pulmonary contusion [21, 223. No changes appeared in the treated group to support any beneficial effects of hydrocortisone. Retained secretions were noted equally often in treated and untreated animals. T h e lesions produced by the technique herein described lend themselves to such critical studies as the evaluation of the effects of drugs. T h e ability to predictably produce lesions of like size in the same region of the lung (Fig. 5 ) estabhhes blank cartridge wounding as a useful tool in the laboratory investigation of trauma.
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FIG. 5 . Control and hydrocortisone-treated lesions at 7 2 hours. Note that all lesions are similar in size and location. SUMMARY
Small, circumscribed, “minimal” pulmonary contusions were produced in dogs. Physiological changes noted were hypotension with slowing of the pulse rate. Diminished intrabronchial pressures were recorded on the side of injury. In the absence of changes in alveolar and blood gases and in the absence of significant blood or plasma loss, reflex mechanisms are suspected. The extravasation of blood in the contused area occurs gradually over a 24-hour period. No x-ray changes were noted until 3 hours after injury. Pathological studies showed no evidence of any inflammatory reaction in these experimental pulmonary contusions. No pathological differences were noted between control and hydrocortisone-treated dogs. Retained bronchial secretions were noted in an equal number of control and hydrocortisone-treated animals. Physical studies of the blast waves causing the injury are presented. REFERENCES 1 . Alfano, G. S., and Hale, H. W. Pulmonary contusion. J. Trauma 5:647, 1965. 2. Daniel, R. A., and Cate, W. R. Wet lung-an experimental study. Ann. Surg. 127:836, 1948. 118
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Pulmonary Contusion 3. Dean, D. M., Thomas, A. R., and Allison, R. S. Effects of explosion blast on lungs. Brit. Med. J . 2:224, 1940. 4. Demuth, W. E., and Smith, J. M. Pulmonary contusion. Amer. J . Surg. 109: 819, 1965. 5 . De Takats, G., Fenn, G. K., and Jenkenson, E. L. Reflex pulmonary atelectasis. J.A.M.A. 120:686, 1942. 6. Fallon, M. Lung injury in the intact thorax. Brit. J . Surg. 28:39, 1940. 7. Gillian, L. A. Clinical Aspects of the Autonomic Neruous System. Boston: Little Brown, 1954. P. 170. 8. Hadfield, G., and Christie, R. V. A case of pulmonary concussion (“blast”) due to high explosive. Brit. Med. J . 1:77, 1941. 9. Hooker, D. R. Physiological aspects of air concussion. Amer. J . Physiol. 67:239, 1924. 10. Klubs, K. Lunge und Trauma. Arch. Ex@ Path. Pharm. 62:39, 1909. 11. Lockwood, A. L. Some experiences in the last war. Brit. Med. J . 1:357, 1940. 12. Lung injuries in air raids-discussion on pathology and diagnosis. Panel discussion. Brit. Med. J . 2:239, 1941. 13. O’Reilly, J. N., and Gloyne, S. R. Blast injury of the lung. Lancet 2:423, 1941. 14. Osborn, G. R. Findings in 262 fatal accidents. Lancet 2:277, 1943. 15. Phillips, C. Pneumonia following nonpenetrating pulmonary injuries. J.A.M.A. 133:161, 1947. 16. Ross, J. M. Hemorrhage into the lungs in cases of death due to trauma. Brit. Med. J . 1:79, 1941. 17. Savage, 0. Pulmonary concussion (“blast”) in non-thoracic bottle wounds. Lancet 1:424, 1945. 18. Sealy, W. C. Contusions of the lung from nonpenetrating injuries to the thorax. Arch. Surg. 59:882, 1949. 19. Sealy, W. C., Young, G. W., Hauck, W. S., and Stephen, R. C. T h e use of steroids for the control and prevention of serious respiratory embarrassment during and after thoracic operations. J . Thorac. Cardiovasc. Surg. 39: 109, 1960. 20. Shepard, G. H. Blank cartridge wounds: Clinical and experimental studies. J . Trauma. I n press. 21. Stevens, E., and Templeton, A. W. Traumatic nonpenetrating lung contusion. Radiology 85:247, 1965. 22. Williams, J. R., and Stembridge, V. A. Pulmonary contusion secondary to nonpenetrating chest trauma. Amer. J . Roentgen. 91:284, 1964. 23. Wilson, J. V. The pathology of closed injuries of the chest. Brit. Med. J . 1:470, 1943. 24. Zuckerman, S. Experimental studies of blast injury of the lung. Lancet 2: 219, 1940. 25. Zuckerman, S. Discussion on the problem of blast injuries. Proc. Roy. SOC. Med. 34:171, 1941.
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