Nonpenetrating Thoracic Injuries

Symposium on Trauma

Nonpenetrating Thoracic Injuries

Robert F. Wilson, MD.,* Charles Murray, MD.,t and David R. Antonenko, MD.!

Chest injuries are directly responsible for over 25 per cent of the 50,000 to 60,000 fatalities that result annually from automobile accidents and contribute significantly to another 25 per cent of these deaths.4.6 In most hospitals about two-thirds of the severe nonpenetrating thoracic injuries are due to traffic accidents. In trauma centers such as Detroit General Hospital, however, the frequency and severity of nonautomobile trauma is increased to about 50 per cent (Table 1). In addition to this increase in numbers of thoracic injuries, more rapid transportation by trained ambulance personnel is bringing many critically injured patients to the Emergency Department who previously would have died at the scene of the accident or en route to the hospital. Pathophysiology The basic pathologic mechanism involved in high speed accidents is the abrupt application of a shearing force to fixed and nonfixed contiguous intrathoracic structures as the patient rapidly decelerates. The mechanism underlying low speed accidents is the application of a more localized crushing type of injury to the thorax. The consequences of shearing and crushing associated with nonpenetrating thoracic trauma are less commonly seen in patients under the age of 7 years, due to the greater elasticity of the child's thorax. Initial Resuscitation Adequate ventilation must be provided immediately, particularly if there is any impairment of cardiovascular function. Of 340 patients admitted to Detroit General Hospital with nonpenetrating chest trauma

From the Department of Surgery, Wayne State University School of Medicine, Detroit, Michigan *Professor of Surgery tClinical Assistant Professor of Surgery tAssociate Professor of Surgery, University of Alberta Faculty of Medicine, Edmonton, Alberta, Canada; Formerly, Instructor of Surgery, Wayne State University School of Medicine

Surgical Clinics of North America- Vol. 57, No.1, February 1977

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R. F.

WILSON,

C.

MURRAY, AND

D. R.

ANTONENKO

Table 1. Etiology of Blunt Chest Trauma, Detroit General Hospital, 1974-1975 PER CENT

NUMBER

Falls Auto Beatings Motorcycle Other Unknown TOTAL

PATffiNTS

DEATHS

MORTALITY RATE

106 119 91 6 5 13

9 19 3

8.5 16.0 3.3 16.7

2

15.4

340

34

10.0

during 1974 and 1975, 19 (5.6 per cent) had both shock and acute respiratory distress when first seen in the Emergency Department and 16 of these 19 (84.2 per cent) died. If the patient is not breathing adequately, airway obstruction must be ruled out by checking for foreign bodies, such as dentures or vomitus in the upper airway, and for mandibular or laryngeal injuries. Where possible the airway should be restored immediately. If adequacy of the airway remains questionable, an endotracheal tube should be inserted. If an endotracheal tube cannot be inserted, a coniotomy (cricothyroidotomy) or tracheostomy is required. Persistent inadequate ventilation following intubation or tracheostomy is frequently the result of a hemothorax, pneumothorax, or hemopneumothorax which is best managed by chest tube(s) attached to waterseal drainage and 10 to 20 cm H 2 0 suction. If ventilation is still inadequate or questionable, ventilator assistance should be provided. Initially 40 to 70 per cent oxygen is usually adequate, but if cardiovascular function is impaired, 100 per cent oxygen should be administered. It must be emphasized that the great majority of patients with blunt chest injuries can be treated without major surgery. Emergency thoracotomy is needed in less than 5 per cent of patients with blunt thoracic

Table 2. Blunt Chest Injuries at Detroit General Hospital (1974-1975) With Frequency and Severity of Associated Extrathoracic Injuries* EXTRATHORACIC INJURffiS

THORACIC INJURIES

None

Mild

Moderate

Severe

Mild Moderate Severe

6 114(1) 13(4)

6 22(0) 11(1)

6<')

391 ' )

21(12) 23(13)

TOTAL

133(·)

391 ' )

21 81(1) 16(1) 118(2)

138(14) 63(19) 34()!34)

5()!'6)

Total

'The number in each block represents the number of patients in that category. The number in parentheses represents the number of deaths in that category.

19

NONPENETRATING THORACIC INJURIES

trauma, usually for control of severe continuing bleeding, massive air leak, or repair of a torn aorta or diaphragm. 23 In our series, only eight out of 340 (2.4 per cent) patients required thoracotomy on the day of admission, and in seven, this was done primarily to perform internal cardiac massage. Late thoracotomy may be required in another 1 to 2 per cent for decortication, bronchopleural fistula, a diaphragmatic injury which was not recognized initially, or drainage of a multiloculated empyema. During 1974 and 1975, isolated blunt thoracic injuries were associated with a mortality rate of 3.8 per cent (5/133). Over 50 per cent of our patients with severe blunt thoracic trauma requiring hospitalization had significant associated extrathoracic injuries (Table 2). If moderate to severe injuries of the chest were associated with severe extrathoracic injuries, the mortality rate jumped to 57 per cent (25/44).

INJURIES TO THE CHEST WALL SOFT TISSUES

Soft tissue damage is rarely the cause of major morbidity or mortality, but it is frequently a clue to severe life-threatening underlying injuries. In some patients, a chest wall contusion may be the only external evidence of severe thoracic trauma. In many instances, the paradoxical motion of a flail chest is minimal when the patient is first seen, especially if the rib fractures are posterior. Later, as pulmonary function deteriorates and more effort is required to ventilate the lungs, the flail becomes progressively more obvious. CLAVICULAR FRACTURES

Isolated clavicular fractures due to blunt trauma are usually not associated with major morbidity. Occasionally, however, direct trauma Table 3. Etiology of Shock and Acute Respiratory Failure on Admission (Detroit General Hospital, 1974-1975) in 340 Patients with Blunt Chest Trauma':' CRITICAL PROBLEM Shock and Respiratory Failure Res piratory Failure

SITE OF SEVERE INJURY

Shock

Thoracic Extrathoracic Both

1(1) 3(0) 4(0)

1(1) 5(4) 13(11)

13(3) 7(3) 17(7)

15(4) 15(7) 34(18)

TOTAL

8(0)

19(16)

37(13)

64(29)

TOTAL

"No one in this series of patients with blunt trauma to the chest was admitted in shock unless he had a severe extrathoracic injury. Whereas none of the seven patients with shock alone died, the mortality rate in the 17 patients who were admitted with both shock and acute respiratory failure was 88 per cent.

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R. F.

WILSON,

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MURRAY, AND

D. R.

ANTONENKO

Incidence of Injuries, Complications, and Death Following Nonpenetrating Thoracic Trauma Detroit General Hospital (1974-1975 Y

Table 4.

TYPES OF INJURIES RIB

NO.

FRACTURE

PATIENTS

None

37 102 109 55 37 340

1-2 3-4 5-6 7 or

more TOTAL

Intrathoracic

Abdominal

External Fracture

CATIONS

DEATHS

20%(22) 15%(8)

11%(4) 30%(31) 33%(36) 49%(21)

8%(3) 13%(13) 11 %(12) 24%(13)

16%(6) 15%(15) 18%(20) 36%(20)

11%(4) 28%(29) 17%(18) 38%(21)

3%(1) 10%(10) 5%(5) 11%(6)

30%(11) 20%(61)

68%(25) 33%(113)

16%(6) 14%(48)

43%(16) 23%(11)

46%(11) 26%(89)

32%(12) 10%(34)

Head 14%(5)

21%(21)

COMPLI-

"The number in parentheses represents the number of patients in that group.

Table 5. Thoracic Injuries Following Nonpenetrating Thoracic Trauma, Detroit General Hospital (1974-1975)" HEMOMYO-

THORAX AND/OR

LUNG

NO. OF RIB

NO. OF

PNEUMO-

CON-

FRACTURES

PATIENTS

THORAX

TUSIONS

None

37 102 109 55 37 340

5%(2) 29%(30) 27%(29) 38%(21) 57%(21) 31 %(105)

5%(2) 6%(6) 6%(1) 9%(5) 19%(1) 8%(21)

1-2 3-4 5-6 7 or more TOTAL

CARDIAL

ANY

CON-

THORACIC

PHRAGM

TUSIONS

INJURY

FLAIL

0 (0) 1%(1) 1%(1) 4%(2) 3%(1) 1%(5)

3%(1) 1%(1) 4%(4) 2%(1) 5%(2) 3%(9)

11%(4) 30%(31) 33%(36) 47%(26) 70%(26) 36%(123)

0 (0) 2%(2) 10%(11) 16%(9) 30%(11) 10%(33)

DIA-

*The number in parentheses represents the number of patients in that group. This included 30 patients with a hemothorax, 35 with a unilateral pneumothorax, five with a bilateral pneumothorax, and 32 with a hemopneumothorax.

Table 6. Abdominal Injuries Following Nonpenetrating Thoracic Trauma, Detroit General Hospital (1974-1975)", NUMBER OF PATIENTS

NUMBER OF

WITH

PATIENTS NUMBER OF RIB

WITH

FRACTURES

FRACTURES

Spleen

Liver

Bowel

Kidney

Other

INJURIES

0 1-2 3-4 5-6

37 102 109 55 37 340

0 7%(1) 6%(1) 11%(6) 5%(2) 6%(22)

0 4%(4) 3%(3) 9%(5)

0 2%(2) 1%(1) 7%(4) 3%(1) 2%(8)

3%(1) 3%(3) 1%(1) 4%(2)

3%(1) 2%(2) 2%(2) 5%(3)

0 2%(1)

0 2%(1)

8%(3) 13%(13) 11 %(12) 24%(13) 16%(6) 14%(48)

7 or more TOTAL

ABDOMINAL ORGAN INJURIES

8%(3) 4%(15)

ABDOMINAL

*The number in parentheses represents the number of patients in each group.

NONPENETRATING THORACIC INJURIES

21

produces sharp fragments which may injure the subclavian vein and produce a moderately large hematoma or venous thrombosis. With time, excess callus at the site of a clavicular fracture very rarely may cause pressure against the subclavian artery and/or brachial plexus, producing a thoracic outlet syndrome.

RIB FRACTURES

General PATHOPHYSIOLOGY. Rib injuries most frequently result from direct trauma but may be the result of rapid flexion or extension movements, particularly in the elderly. Even if they do not damage the underlying lung tissue or cause a hemopneumothorax, rib fractures can greatly interfere with ventilation because of pain produced either by motion of the bone fragments or from spasm of chest muscles attempting to splint that portion of the chest wall. If the patient cannot ventilate adequately because of chest pain, atelectasis often develops and progresses to severe pneumonitis. TREATMENT. Strapping the chest with adhesive tape to relieve the pain may be effective in young athletic individuals with few rib fractures, but in less vigorous patients, strapping may significantly reduce ventilation and cause progressive atelectasis. If one elects to use external support, rib-belts are more pleasant to use, do not blister the skin, and can be adjusted by the patient. Mild to moderate chest wall pain in many instances may be adequately treated by 30 to 60 mg of codeine every 3 to 4 hours. Since codeine and other narcotics may suppress the cough reflex, it is important to instruct the patient to cough and breathe deeply frequently. Severe pain from multiple rib fractures is best controlled with repeated intercostal nerve blocks, injecting 1 or 2 ml of 0.5-1.0 per cent Xylocaine with Adrenalin around the intercostal nerves at the lower borders of the involved ribs in the midscapular line. In many instances, to achieve adequate relief of pain, the intercostal block must include two intercostal nerves above and two below the ribs which are injured. This will often produce dramatic relief from pain for 12 to 24 hours. Since it is easy to puncture the lung while performing an intercostal block, it is wise to obtain a chest x-ray after the procedure to be sure the patient has not developed pneumothorax. Most rib fractures heal well after 3 to 6 weeks. A rare post-traumatic intercostal neuroma may require excisional therapy. Costochondral separation results in substantial morbidity since the relatively poor blood supply to a costal cartilage frequently results in delayed healing and an inordinate amount of pain. If attempts at nonoperative therapy are ineffective, surgical excision of the costal cartilage is usually curative. ASSOCIATED INJURIES. In a previous study of 783 patients admitted to Detroit General Hospital with blunt chest trauma,t it was found that if seven or more ribs were fractured, 50 per cent of the patients had an intrathoracic injury and 15 per cent had an injured intra-abdominal

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MURRAY, AND

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ANTONENKO

viscus. In the present series, the patients with seven or more rib fractures had a 68 per cent incidence of intrathoracic injury and 16 per cent had an intra-abdominal organ damage. If the patient with fractured ribs following blunt trauma becomes hypotensive and does not have a large hemothorax or pneumothorax to account for the fall in blood pressure, intra-abdominal bleeding must be suspected. In the current series of 340 patients, 40.7 per cent of those with shock had intra-abdominal injuries. In general, it is wise to admit any patient with two or more fractured ribs to the hospital for at least 24 to 48 hours, especially if the ninth, tenth, or eleventh ribs are involved. Such fractures are apt to be associated with splenic or hepatic injuries. In the present series, 15 (68.2 per cent) of the patients with an injured spleen had fractures of the left ninth, tenth, or eleventh ribs. During the hospitalization, the physician can observe the patient for such injuries that might not be apparent initially and determine what measures should be taken to provide adequate ventilation and relief of pain. First Rib Fractures First rib fractures have special significance because they are usually caused by severe trauma. They should make one look very closely for injuries to the thoracic aorta or major bronchi. In the previous study,l first rib fractures were found to be associated with a higher mortality rate (17 per cent) than any other rib fracture because of the frequent severe associated injuries. These fractures are also associated with an increased incidence of disruption of neurovascular structures of the upper extremity. Flail Chest PATHOPHYSIOLOGY. Segmental fractures (fracture in two or more locations on the same rib) of three or more adjacent ribs anteriorly or laterally often result in an unstable chest wall and the phenomenon known as flail chest. In the present series, a flail chest was noted in 10 per cent of the patients with three or four rib fractures and 30 per cent of those with seven or more rib fractures. A flail chest is characterized by a paradoxical inward movement during inspiration. The reduced ventilatory efficiency and increased ventilatory work which results, together with the underlying lung damage, is apt to cause progressive respiratory insufficiency. The flail or paradoxical chest wall motion may be especially severe if there is a transverse fracture of the sternum. Loss of bony support because of fractures occurring posteriorly near the sacrospinalis musculature is much less apt to result in an unstable chest wall because the splinting of these muscles provides good support for the underlying ribs. In the past, pendeluft, a ventilatory phenomenon referring to movement of a portion of the tidal volume back and forth between the lungs on the injured and uninjured sides with each breath, was considered to be an important cause of the physiologic derangement seen with flail chest. It was postulated that during inspiration the negative pressure in

NONPENETRATING THORACIC INJURIES

23

the chest caused the flailing segment of the chest wall to move inward ("paradoxically"). This reduces the negative pressure in the lung underlying the flailing chest wall and it was thought that this caused some air to move from the lung on the injured side to the lung on the uninjured side where there was more negative pressure. The reverse was assumed to occur during expiration. However, the underlying lung damage and hypoventilation from chest pain are much more important. Pendeluft is clinically significant only if partial obstruction of the trachea is also present. Immediately after injury, while lung compliance is still relatively normal and the pressure differential between the atmospheric and intrathoracic pressure is small, little flail may be apparent. Later, as lung compliance falls and more effort is needed to inflate the lungs, the differential between the intrathoracic and atmospheric pressures may overcome the resistance of the muscles attached to the fractured ribs, thereby allowing the involved chest wall to move paradoxically. In addition, the patient may fatigue rapidly because of decreased efficiency of ventilation and increasing muscle effort, beginning a vicious cycle of decreasing ventilation and increasing fatigue and oxygen need. TREATMENT. A flail chest can be most quickly managed initially by applying a sand bag or other type of pressure directly over the unstable portion of the chest wall. This is of particular value at the roadside where hospital facilities are not available. Although this reduces vital capacity, it increases the effective tidal volume and the efficiency of ventilation. Probably the major advance in the therapy of flail chest has been the increasing use of early ventilatory assistance to internally splint the chest wall and maintain optimal expansion. Although patients with a mild to moderate flail chest and little or no underlying pulmonary contusion or extrathoracic injury can often be managed well without ventilator assistance, careful selection and observation of such patients are extremely important. On the basis of our previous studies, we feel that a patient with a flail chest should be given ventilatory assistance immediately (even if he has relatively normal blood gases) if one or more of the following conditions are also present: shock, three or more associated injuries, severe head injury, previous pulmonary disease, fracture of eight or more ribs, or age greater than 65 years.22 Such patients require assisted ventilation for at least 7 and usually 10 to 14 days before they can be weaned from the respirator. Prophylactic ventilatory assistance in patients with a flail chest and moderate associated injuries was associated with a mortality of one-tenth (7 per cent vs 69 per cent) that of similar patients in whom ventilatory assistance was delayed until there was clinical evidence of acute respiratory failure. In the patient with flail chest who has marginal clinical indications for ventilatory assistance, any deterioration in pulmonary function as reflected by increasing tachypnea, restlessness or anxiety, decreased tidal volume, falling P a o 2 or rising P(A-aDo 2 ) or physiologic shunt (particularly if greater than 30 to 40 per cent27 ) should be considered as an indication for tracheal intubation and mechanical support.

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WILSON,

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MURRAY, AND

D. R.

ANTONENKO

Recently, Trinkle et al,24 sparked controversy by reporting a study which suggested that internal mechanical stabilization of the thorax has been overused and is not necessary in many patients with a flail chest. Nevertheless, these authors did provide ventilatory support when the arterial P0 2 was less than 60 mm Hg on supplemental oxygen. They also pointed out the underlying pulmonary contusion might be of more significance than the flail itself.

I

I ·11.i

!~

Ii:

Ii STERNAL FRACTURES

Sternal fractures are serious and are frequently associated with cardiovascular injury, particularly myocardial contusions. The fractures are usually transverse and so unstable that a significant flail is often present. Operative fixation is often unsatisfactory and treatment of these patients usually includes ventilator support for at least a few days. Painful pseudoarthrosis and permanent overlap deformities are not uncommon and may require later reconstruction.

THORACIC SPINE FRACTURES

Fractures of the thoracic spine are usually the result of direct trauma or compression due to acute flexion, particularly in the elderly. Avulsion of transverse processes by the sacrospinalis muscle group has also been reported. These patients frequently develop ventilatory problems and may occasionally have associated spinal cord injuries.

INJURIES TO THE LUNGS PARENCHYMAL INJURIES

Pulmonary Contusions Pulmonary contusion may result from high energy shock waves produced by explosions propagated through air or water or by high velocity missiles passing within a few centimeters of the lung. Most frequently, however, contusion follows rapid deceleration injuries. Three basic phenomena appear to be important in the etiology of pulmonary contusion: (1) the spalling effect in which the liquid-gas interface is disrupted by a shock wave moving in the liquid; (2) overexpansion of alveoli following the implosion effect caused by the pressure wave; and (3) the inertial effect as low-density alveolar tissue is stripped from heavier hilar structures.20 A distinction should be drawn both conceptually and clinically between pulmonary contusion and the adult respiratory distress syndrome (ARDS) with which it is often confused. Pulmonary contusions occur within minutes of injury, are usually fairly well localized to a segment or lobe, are usually seen on the initial chest x-ray, and tend to progress

NONPENETRATING THORACIC INJURIES

25

for 48 to 72 hours. In contrast, the acute respiratory distress syndrome, which is more frequent, occurs later (usually becoming apparent only 24 to 72 hours after the injury) and tends to be diffuse. Both problems are associated with an increased incidence of pulmonary infections as the extravasation of blood and fluid into the alveoli of the contused lung tissue provides an ideal site for severe pneumonitis and eventual abscess formation. These contusions, if they do not become infected, usually resolve within 2 to 5 days. The diagnosis of pulmonary contusion is usually made from the history and the finding of localized opacifications on the initial chest x-ray (Fig. 1). Interestingly, many of the worst contusions occur in patients without rib fractures. lO Treatment of pulmonary contusions includes maintenance of adequate ventilation to all parts of the lung, fluid restriction, diuretics (while maintaining adequate tissue perfusion), plasma or albumin to maintain normal plasma oncotic pressure, and prophylactic antibiotics. Although the use of colloids in these patients is controversial, there is an increasing tendency to give colloids so as to ensure that the plasma proteins do not fall below low normal levels. Although maintenance of adequate ventilation is extremely important, Ratcliff20 has cautioned that vigorous coughing, deep breathing, and positive pressure ventilation

Figure 1. Lung contusions are visualized as rather localized areas of opacification on chest x-rays taken soon after trauma. The lung infiltrates due to aspiration or the adult respiratory distress syndrome, including fat embolism, are usually not associated with any significant x-ray changes for the first 24 to 48 hours. The widening of the mediastinum on this patient was evaluated by a retrograde trans femoral aortogram and the aorta was found to be normal.

26

R. F.

WILSON,

C.

MURRAY, AND

D. R.

ANTONENKO

during the immediate postinjury phase should be kept to a minimum to reduce the chances of air embolism. The use of steroids is controversial and we do not use them except with smoke inhalation, aspiration of gastric contents, or severe progressive pulmonary insufficiency. One recent experimental report suggests that large doses of steroids will reduce the size of the contusion and the weight of the involved lung, presumably by lysosome preservation, decreased capillary permeability, and anti-inflammatory properties.s If the patient becomes septic and an abscess develops, resection of the involved tissue may be indicated, especially if there is a poor response to intensive antibiotic therapy and repeated bronchoscopy. Pulmonary Hematomas Pulmonary hematomas, which reflect a more severe disruption of pulmonary tissue, usually consist of a rather large extravasation of blood localized to a lobe or one or more segments. Most hematomas resolve spontaneously over a few weeks; however, if they become infected, they tend to cavitate and form lung abscesses which are difficult to manage. The optimal initial management of large pulmonary hematomas following chest trauma has recently been debated. Some feel that an immediate thoracotomy should be performed to remove the involved lung. The majority of surgeons still favor a much more conservative approach and will remove the injured lung tissue only in the presence of severe continuing hemorrhage, air leak, or infection. On the other hand, if a thoracotomy is required for some other reason, such as continued severe bleeding from an intercostal artery, some now feel that, because of the high incidence of severe persistent infection in these hematomas, the involved lobe should be resected. Further evaluation of this approach is required. Pulmonary Laceration with Hemopneumothorax Pulmonary lacerations following blunt trauma are usually mild and generally due to temporary inward protrusion of a fractured rib. However, lung lacerations may also be caused by avulsion of previous pleural adhesions as the lung moves away from the chest wall during rapid deceleration. In some instances, the adhesions themselves are quite vascular and bleeding from torn adhesions alone may be of a degree to cause shock. Lung lacerations can usually be handled satisfactorily by tube thoracostomy and suction drainage of the pleural cavity to relieve the hemopneumothorax. Small (20-24F) chest tubes can be used if only a pneumothorax is present. However, if the patient has a hemothorax, a large bore (36-40F) plastic chest tube is required. If the tube does not function adequately because of clots, it should be replaced rather than irrigated. Complete resolution of lung injuries with closed tube thoracostomy usually occurs, but thoracotomy with resection of a protruding rib fragment and/or closure of the parenchymal defect is occasionally necessary. In special circumstances, small collections of blood or air may be treated without a chest tube and carefully observed with serial chest x-

NONPENETRATING THORACIC INJURIES

27

rays. This may be done if the injury is already 24 to 48 hours old, the patient's condition is stable, and there are no other injuries. Major life-threatening lacerations of the lung following blunt trauma are quite uncommon and in one series occurred in only 4.4 per cent of patients admitted with thoracic trauma. 14 These patients generally have hemoptysis, multiple rib fractures with a flail, and a hemopneumothorax with pulmonary hematoma on the side of the injury. The laceration itself can be repaired in some patients if surgery is performed early but a majority require lobectomy to control the bleeding and air leak.

TRACHEOBRONCHIAL INJURIES

Patients with tracheal injuries in the chest have a much higher initial mortality rate than those with tracheal injuries in the neck, primarily because of the greater number of associated injuries, particularly to the heart and thoracic aorta. Lacerations of major branches of the tracheobronchial tree are uncommon but most frequently occur at the take-off of a main or upper lobe bronchus, particularly on the right side near the carina. Most of these injuries are due to rapid deceleration and shearing of the more mobile distal bronchi from the relatively fixed proximal structures. However, forced expiration against a closed glottis or compression against the vertebral column may also playa role. These lesions, frequently accompanied by severe tension pneumothorax and subcutaneous and mediastinal emphysema, require anatomic definition by bronchoscopy and/or bronchogram and surgical repair as soon as possible. Tension pneumothorax, increasing subcutaneous or mediastinal emphysema, or a massive air leak via the chest tubes should be considered due to a tracheobronchial injury until proven otherwise. Total atelectasis of a lung or lobe not responding to treatment should also make one suspect this injury. If bronchoscopy reveals no tear in such an individual, a bronchogram should be obtained. In a collected series,1 68 per cent of bronchial tears were not diagnosed until atelectasis and sepsis had developed. Interestingly, many of these patients had no extrathoracic injuries and up to 50 per cent had no rib fractures. 3 High tracheal injuries are usually best managed by a tracheal repair and a tracheostomy below it. Occasionally, if the patient's condition is precarious and the laceration is small, repair may not be necessary. Lower tracheal and bronchial lesions require thoracotomy and direct repair as soon as feasible. Any delay tends to increase the incidence of severe pulmonary infection and later stricture. The repair should be assessed by bronchoscopy or bronchogram in 3 months, or sooner if any obstructive symptoms follow. Lesions occurring in the distal tracheobronchial tree (segmental and subsegmental bronchi) may require resection of the involved bronchopulmonary segments. The temptation to oversew the torn parenchyma overlying these lesions should be avoided, and accurate isolation and control of the bronchovascular structures should be accomplished

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ANTONENKO

whenever possible. Failure to do this may result in systemic air embolism via open pulmonary veins, continued hemorrhage or air leak, or a localized pulmonary hematoma with or without secondary contamination and infection.

DIAPHRAGMATIC INJURIES INCIDENCE

The incidence of diaphragmatic injury in patients with multiple injuries following blunt trauma is estimated to be about 4 to 5 per cent and may be much greater if the pelvis is fractured.8 In the present series, only 5 (1.5 per cent) of the patients with blunt chest trauma had a diaphragmatic injury. Diaphragmatic rupture may occur with isolated blunt thoracic trauma but in at least two-thirds of the cases, blunt abdominal trauma (with or without thoracic injury) is the primary feature.28 The mechanisms whereby diaphragmatic injuries occur following blunt trauma are probably multiple and include a sudden increase in intrathoracic or intra-abdominal pressure while the diaphragm is fixed by a crushing force. 15 Because of the protection provided by the liver on the right and possible increased weakness of the left posterolateral diaphragm, the great majority of diaphragmatic injuries following blunt trauma occur on the left.2. 5, 13 In a large collected series of diaphragmatic injuries, 87.8 per cent occurred on the left, 11.0 per cent occurred on the right, and 1.2 per cent were bilateral.15

PATHOPHYSIOLOGY

Since 60 to 80 per cent of normal ventilation depends upon proper function of the diaphragm, extensive damage to this structure can cause serious respiratory problems. Penetrating injuries of the diaphragm are usually less than 2 cm in length, whereas the majority of diaphragmatic injuries caused by blunt trauma are more than 10 cm long.28 If the injury occurs on the left side, the abdominal contents may herniate into the chest, compressing the lungs and mediastinum, and reducing the vital capacity and venous return to the heart.

DIAGNOSIS

Diaphragmatic injuries may present in any of three phases.5 An early or acute phase is usually associated with cardiovascular or respiratory symptoms due to associated injuries, lung damage, or compression of the lung; a latent asymptomatic phase which may persist for days, months, or years; and a late phase associated with obstruction or strangulation of bowel, or occasionally with respiratory distress.9 Unless the diaphragmatic lesion is quite large, symptoms due to herniation of ab-

NONPENETRATING THORACIC INJURIES

29

dominal viscera into the thoracic cavity with obstruction or strangulation often occur late. An extremely scaphoid abdomen following blunt trauma should make one suspicious of a diaphragmatic hernia or injury (Gibson's sign). If the defect is small, the negative intrathoracic pressure may gradually pull the intraabdominal contents into the chest through the diaphragmatic wound over a period of several weeks, months, or years. Even after having been stable and asymptomatic for several years, a diaphragmatic hernia can suddenly enlarge causing either respiratory failure, or shock due to an impaired venous return or strangulation of the herniated bowel.9' 16If one does not suspect and look carefully for a diaphragmatic injury in all patients with chest or abdominal trauma, one is likely to miss the diagnosis during the initial hospitalization. About a third may have no related signs or symptoms, and the most frequent symptoms, dyspnea and abdominal pain, are rather nonspecific. The initial chest x-rays are also generally nonspecific; however, diaphragmatic injury should be suspected if any abnormal shadows are noted in the left lower lung field, if the left diaphragmatic outline is unclear or elevated, or if the mediastinum is pushed to the right (Fig. 2). If a nasogastric tube is inserted and the end of the tube passes from the abdomen up into the left chest, it is apparent that the stomach has herniated through the diaphragm. Upper and lower gastrointestinal x-rays can also provide a definitive diagnosis by demonstrating loops of bowel within the chest.

Figure 2. A, The posteroanterior chest x-rays on this 38-year-old male, who had been in an auto accident and had multiple fractured ribs with flail and a fractured clavicle, suggest diaphragmatic rupture. The left diaphragm is not clearly seen but appears to be elevated and there are some abnormal densities in the left lower lung field. B, On the left lateral film, however, the diaphragm is seen quite clearly. X-rays with barium later showed the gastrointestinal structures to be in proper relationship with one another within the abdomen and the final impression was left phrenic nerve paralysis.

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ANTONENKO

In some instances, the diagnosis is made by peritoneal lavage. Diaphragmatic injuries tend to bleed and cause a lavage to be positive. When a chest tube is in place on the involved side, aspiration of the lavage fluid through the chest tube is virtually diagnostic.

TREATMENT

Repair of diaphragmatic injuries via the transabdominal route is recommended for the acute injury because this allows complete exploration of the abdomen and repair of associated intraabdominal injuries, present in about three-quarters of the cases. If the diaphragmatic injury is not recognized for several weeks or if the hernia is on the right side, a transthoracic approach is preferred. In cases in which an abdominal approach is chosen and it is difficult to reduce the abdominal viscera, it may be helpful to slip a small catheter alongside the bowel into the hernia sac, thus allowing air to enter the sac and prevent the development of negative pressure as the bowel is reduced.

CARDIOV ASCULAR TRAUMA CARDIAC TRAUMA

Myocardial Contusion Myocardial contusion following blunt trauma is usually the result of direct impact of an automobile steering wheel over the precordium causing compression of the heart between the sternum and the vertebral column. This injury probably occurs far more frequently than is generally realized. In one series of cases, a 38 per cent incidence of cardiac injury was noted when routine EKG's were taken in 44 consecutive patients with severe chest trauma. 25 In another series, cardiac injury was found in eight out of 50 (16 per cent) consecutive patients dying of automobile accidents. In the present series, myocardial contusion was recognized in only 3 per cent. In some patients myocardial necrosis may occur and the resultant lesion may have EKG and enzyme changes very similar to those seen with an acute myocardial infarction. Myocardial Rupture Acute cardiac rupture following trauma is rarely seen except at the autopsy table but has been reportedP The circumstance during which this might occur apparently involves closure of the outflow tract of the ventricle and compression of the blood filled ventricle by a pressure sufficient to cause rupture of the free ventricular wall or the septum. Late rupture of contused myocardium and the late development of false aneurysms have likewise been documented. 19 These lesions seem to involve the left ventricle primarily and it is probable that the right ventricle is spared because of its greater compliance.

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Pericardial Injuries and Effusions Pericardial tamponade following blunt trauma is a rather rare but serious condition requiring early recognition and treatment. A rising venous pressure and falling blood pressure, particularly if there is no lung injury, should make one highly suspicious of this problem. The restriction of cardiac filling by the intrapericardial blood, resulting in a lifethreatening low output syndrome, can usually be resolved rapidly by needle aspiration of the intrapericardial fluid. In some instances, however, patient salvage requires surgical management of the underlying injury to the heart or ascending aorta. Chronic or recurrent effusions containing large quantities of cholesterol are not infrequent following pericardial injury and may cause later calcification with or without constrictive pericarditis.

RUPTURE OF THE THORACIC AORTA

Incidence and Prognosis Rupture of the thoracic aorta is much more frequent and serious than is generally appreciated. Approximately one out of every eight deaths due to traffic accidents is associated with rupture of the thoracic aorta. Of the approximately 8000 patients who have a traumatic rupture of their thoracic aorta annually, only about 10 to 20 per cent reach the hospital alive and even these patients have a poor prognosis. In one series, 30 per cent of such patients died in 6 hours and 49 per cent in 24 hoursP Early diagnosis and repair can be quite successful; unfortunately, the diagnosis is often not made until autopsy. Etiology and Location Rupture of the thoracic aorta is usually the result of rapid deceleration in high-speed auto aCci9-ents and most frequently occurs in tl:j.e isthmus, at or proximal to the ligamentum arteriosum and distal to the left subclavian artery. The ligamentum arteriosum and the descending thoracic aorta are relatively fixed structures whereas the transverse portion of the aortic arch from the innominate artery to the left subclavian artery is relatively mobile; thus, with rapid deceleration, shearing of the aortic wall at their junction may occur. The resultant tear may cause: (1) complete disruption of the circumference of the aorta with almost immediate exsanguinating hemorrhage; (2) incomplete disruption with an expanding hematoma contained by the adventitia of the aorta for a variable period of time; (3) laceration of a smaller portion of the aortic wall with gradual development of a false saccular aneurysm; or (4) in rare instances, dissection with partial aortic obstruction producing late findings similar to those found with coarctation of the aorta. The second most common site of deceleration injury of the thoracic aorta is the ascending aorta just above the aortic valve. Relative fixation of the base of the heart and the mobility of the ascending aorta cause the shearing in this area. Survival is rare with these injuries, which are seen most frequently in high falls from buildings or airplane crashes.

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C.

MURRAY, AND

D. R.

ANTONENKO

Subclavian artery injuries occur not infrequently in association with first and second rib fractures, but are less likely to be fatal and have attracted relatively little attention. Complete evaluation of all these vessels is essential when angiography is obtained to assess mediastinal widening. Subtraction films may be particularly helpful when the injury involves a branch of the aortic arch. Diagnosis CLINICAL. Early diagnosis of traumatic rupture of the thoracic aorta depends primarily upon a high index of suspicion. Although great force is usually needed to tear the aorta, up to a third of these patients may have little or no external evidence of chest trauma. Furthermore, the great majority of these patients have multiple severe extrathoracic injuries which tend to distract the physician. Consequently, if aortic transection is to be diagnosed early, it must be suspected in all patients who have been in an automobile accident at speeds exceeding 30 miles per hour. Findings which suggest the diagnosis of traumatic rupture of the aorta include: (1) a systolic murmur over the precordium or medial to the left scapula; (2) hoarseness or voice change because of pressure of the hematoma on the left recurrent laryngeal nerve; (3) hypertension in the upper extremities; or (4) hypotension or weak pulses in the lower extremities. In the rare instances in which the injury involves the ascending aorta and the patient reaches the hospital, the resulting aneurysm or hematoma may produce a clinical picture of superior vena caval obstruction. CHEST X-RAY. Although the circumstances of the accident and the physical findings are occasionally helpful, the diagnosis is usually made or suspected from findings on the routine chest roentgenogram. Since over 90 per cent of these injuries involve the aorta near the attachment of the ligamentum arteriosum, the characteristic x-ray finding is widening of the superior mediastinum adjacent to the aortic knob. Obliteration of the left apical cap is often present too and, occasionally, downward displacement of the left main stem bronchus is apparent. A left hemothorax is visible in many of these patients. Anteroposterior films, especially those taken at distances less than 6 feet, tend to magnify the heart and anterior mediastinum and are of much less value than upright posteroanterior films taken at the proper distance. Unfortunately, the mediastinal widening may not be apparent on the chest roentgenogram for several hours or days26 (Fig. 3). Consequently, serial x-rays should be taken in any patient with severe chest or upper abdominal trauma at 4 to 8 hour intervals during the first day and then daily for at least the next 3 days. AORTOGRAPHY Once an aortic rupture is suspected clinically or radiographically, an aortogram should be performed. Widening of the superior mediastinum does not always indicate disruption of the aorta or its branches. In ap-

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'I' I I !

.I : !

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Figure 3. A. Traumatic rupture of the aorta is usually suspected or diagnosed initially because widening of the superior mediastinum is noted on the chest x-ray. In some instances, however, the initial chest x-ray (A) may appear to be normal, whereas an x-ray taken a few hours later (B) may be remarkably different. In this instance, the mediastinal widening and opacification over the apex due to hematoma from the torn aorta are readily apparent on a chest x-ray taken about 5 hours later. The difference is somewhat exaggerated because the first film is taken in the posteroanterior direction, while the second film is taken in the anteroposterior projection. Anteroposterior films, particularly with the patient in the supine position and with poor lung inflation, may be somewhat deceptive because they tend to make the mediastinum appear rather wide, even in normal individuals.

proximately half our patients who had a widened mediastinum after blunt trauma, the aorta an~ its branches were normal on aortography. Where no major arterial injury has been found, disruption of venous structures in the mediastinum has been noted at surgery or autopsy. These venous injuries do not usually cause serious continuing intrapleural bleeding and generally resolve spontaneously. However, lesions of the superior vena cava or inferior vena cava, when diagnosed, have necessitated surgical repair. Aortography is generally performed using either a percutaneous right axillary or retrograde femoral arterial approach. Although concern has been expressed that the catheter or the pressure generated during injection of the contrast material might tear the remaining adventitia at the site of the aortic injury, the pressure of the injection is dissipated rapidly and no cases of catheter trauma to the damaged area have been reported. If it is difficult or impossible to obtain arterial aortograms, intravenous or forward aortograms using two large catheters in the superior vena cava can sometimes provide good visualization of the thoracic aorta (Fig. 4). We believe that aortography should be performed on all patients with suspected aortic injury. However, if the patient appears to be in shock from this injury or has a rapidly expanding mediastinal hematoma, the patient should be taken directly to the operating room.

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WILSON,

C.

MURRAY, AND

D. R.

ANTONENKO

Figure 4. Although a retrograde aortogram via the femoral artery is ideal for demonstrating thoracic aortic lesions, in some instances, a forward (venous) aortogram can show a traumatic rupture of the thoracic aorta rather clearly. The aortic tear distal to the subclavian artery was confirmed and repaired at surgery.

Treatment EXPECTANT. The chances of successful management of a rupture of the thoracic aorta depend largely on the number and severity of the associated injuries. The decision whether to repair the thoracic aorta immediately in the poor risk patient with multiple other severe injuries is difficult and must be individualized. It may be preferable in some poor risk patients with multiple severe injuries to improve their condition while observing them carefully until the risk of surgery is reasonable. SURGERY WITHOUT CARDIOPULMONARY BYPASS. On occasion a patient will require an operation because of a rapidly expanding hematoma or evidence of continuing blood loss into the left chest before cardiopulmonary bypass can be set up. Under such circumstances, an intravenous infusion of Arfonad may be used to reduce the blood pressure in the upper portion of the body and so diminish the chances of intracerebral hemorrhage or left heart failure while the aorta is clamped. The operation, however, must be rapid and precise because clamping of the descending aorta for more than 20 minutes without perfusion of the distal aorta invites serious risk of damage to the spinal cord and abdominal viscera. Another alternative to cardiopulmonary bypass is the use of a tube or graft to divert blood around the involved aorta. The proximal end of the tubing, filled with heparinized saline, can be inserted into the as c cending aorta or the aortic arch, and the distal end into the mid or lower descending thoracic aorta. Studies have shown that flow through a 7.5 mm cannula is about 2000 ml per min, while the flow through a 9 mm cannula is about 4000 ml per min,u If special heparin-coated polyvinyl

NONPENETRATING THORACIC INJURIES

35

tubing is used, the patient does not have to be exposed to the additional risks of systemic heparinization; this consideration is especially important in patients with severe intracranial injuries. SURGERY WITH CARDIOPULMONARY BYPASS. Cardiopulmonary bypass is not absolutely essential for repair of the thoracic aorta distal to the arch but it does allow increased time for a meticulous unhurried repair and does reduce the risk of ischemic damage to the spinal cord and abdominal viscera. If the patient's condition is stable, transfer to a hospital where cardiopulmonary bypass is available is wise. OTHER TECHNICAL CONSIDERATIONS. Interestingly, the aortic tear can be easily missed on direct visual exam or palpation since the aorta may look and feel surprisingly normal at surgery except for some subadventitial hemorrhage. Transverse incision into the suspected area after proximal and distal clamping may be required to confirm the diagnosis and the location and extent of injury. Although a recent incomplete tear of the aorta can usually be repaired directly, complete tears, particularly if more than 2 to 3 days old, may require a prosthetic graft. TRAUMATIC ANEURYSMS. Probably only about 1 to 2 per cent of patients who survive an acute rupture of the thoracic aorta for more than 30 minutes live long enough to form a chronic traumatic thoracic aortic aneurysmP Traumatic aneurysms of the thoracic aorta which are first noticed several weeks or months after the initial trauma are usually stable. However, even if they remain unchanged for several years, they always retain the potential for suddenly increasing in size and rupturing with fatal results. Once the diagnosis is confirmed by aortography, the aneurysm should be excised and the normal ends of the aorta anastomosed with a graft under left atrial-femoral or femoral artery-femoral vein cardiopulmonary bypass. Only a relatively small number of traumatic thoracic aneurysms have been reported, but elective resection appears to provide excellent resultsY. 26 SUMMARY In patients with nonpenetrating thoracic trauma, the rib fractures and other chest wall lesions may distract the physician from dangerous internal injuries in the chest or abdomen which may not be noted unless looked for very carefully. Early vigorous correction of any ventilatory problem is essential, particularly if there is any evidence of impaired tissue perfusion. Shock is frequently due to extrathoracic injuries, particularly intraabdominal bleeding. The flail associated with multiple rib fractures may seem mild initially, but severe underlying pulmonary contusion and/or associated extrathoracic injuries make early ventilatory assistance extremely important. Rupture of the thoracic aorta should be suspected in rapid deceleration injuries, but is often not considered unless there is widening of the superior mediastinum on the chest x-ray. Aortography to confirm· the aortic tear should be done if time permits, and early repair of the injury provides the best results.

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WILSON,

C.

MURRAY, AND

D. R.

ANTONENKO

REFERENCES 1. Bassett, J. S., Gibson, R D., and Wilson, R F.: Blunt injuries to the chest. J. Trauma, 8: 418,1968. 2. Bekassy, S. M., Dave, K. S., Wooler, G. H., and Ionescu, M. 1.: Spontaneous and traumatic rupture of the diaphragm. Ann. Surg., 177:320, 1973. 3. Bertelsen, S., and Howitz, P.: Injuries to the trachea and bronchi. Thorax, 27:188,1972. 4. Blair, E., Topuzulu, C., and Deane, R S.: Major blunt chest trauma. In Ravich, M. M. (ed.): Current Problems in Surgery. Chicago, Year Book Medical Publishers, 1969. 5. Carter, B. N., et al.: Traumatic diaphragmatic hernia. J. Roent., 65:56,1951. 6. Cohn, R.: Non-penetrating wounds of the lungs and bronchi. SURG. CLIN. N. AM., 52:585, 1972. 7. Collins, J. P., Ketharanathan, V., and McConchie, 1.: Rupture of major bronchi resulting from closed chest injuries. Thorax, 28:371,1973. 8. Franz, J. L., Fletcher, J. R, Kopriva, C. J., et al.: Effect of methylprednisolone sodium succinate on experimental pulmonary contusion. J. Thor. Cardiovasc. Surg., 68:842, 1974. 9. Fromm, S. H., and Lucas, C. E.: An unusual complication of chronic diaphragmatic hernia in the adult patient. J Thor. Cardiovasc. Surg., 61 :654, 1971. 10. Hankins, J. R, Attar, S., Turney, S. Z., et al.: Differential diagnosis of pulmonary parenchymal changes in thoracic trauma. Am. Surg., 39:309,1973. 11. Kirsh, M. M., Pellegrini, R V., and Sloan, H. E.: Treatment of blunt chest trauma. Surg. Ann., 4:51,1972. 12. Liedtke, A. J., and Demuth, W. E.: Nonpenetrating cardiac injuries: A collective review. Am. Heart J., 86:687,1973. 13. Lucido, J. L., and Wall, C. A.: Rupture of the diaphragm due to blunt trauma. Arch. Surg., 86:989, 1963. 14. Maghissi, K.: Laceration of the lung from blunt trauma. Thorax, 26:223, 1971. 15. Morley, J. E.: Traumatic diaphragmatic rupture. S. African Med. J., 48:325,1974. 16. Oringer, M. B., Dirsh, M. M., and Sloan, H.: Congenital and traumatic disphragmetic hernias exclusive of the hiatus. In Current Problems in Surgery. Chicago, Year Book Medical Publishers, March 1975. 17. Parmley, L. F., et al.: Non-penetrating traumatic injury to the aorta. Circulation, 17:1086, 1958. 18. Peltier, L. F.: Complications associated with fractures of the pelvis. J. Bone Joint Surg., 47:1060, 1965. 19. Pupello, D. F., Daily, P.O., Stinson, E. B., and Shumway, N. E.: Successful repair of left ventricular aneurysm due to trauma. J.A.M.A., 211 :826, 1970. 20. Ratcliff, J. L., et al.: Pulmonary contusion; a continuing management problem. J. Thor. Cardiovasc. Surg., 62:638, 1971. 21. Rodkey, G. V.: Management of abdominal injuries. SURG. CLIN. N. AM., 46:627,1966. 22. Sankaran, S., and Wilson, R F.: Factors affecting prognosis in patients with flail chest. J. Thor. Cardiovasc. Surg., 60:402, 1970. 23. Sturm, J. T.: Hemopneumothorax following blunt trauma of the thorax. Surg. Gynec. Obstet., 141 :539,1975. 24. Trinkle, J. K., Richardson, J. D., Franz, J. L., et al.: Management of flail chest without mechanical ventilation. Ann. Thor. Surg., 19:355, 1975. 25. Watson, J. H., and Bartholomac, W. M.: Cardiac injury due to non-penetrating chest trauma. Ann. Int. Med., 52:871, 1960. 26. Wilson, R. F., et al.: Acute mediastinal widening following blunt chest trauma. Arch. Surg., 104:551,1972. 27. Wilson, R. F., Larned, P. A., Corr, J. J., et al.: Physiologic shunting in the lung in critically ill and injured patients. J. Surg. Res., 12:571, 1970. 28. Wise, L., Connors, J., and Hwang, Y. H.: Traumatic injuries to the diaphragm. J. Trauma, 13:946,1973. Department of Surgery Wayne State University School of Medicine 540 E. Canfield Street Detroit, Michigan 48201

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