Chest Trauma
The discussion of chest trauma is divided into two sections. The first deals with five conditions that may be rapidly fatal unless appreciated and therapeutic maneuvers instituted immediately; patients in this category will generally present with severe respiratory distress and/or evolving or established shock. The second section involves potentially serious or potentially fatal conditions, most of which will evolve less acutely and thus provide the physician with more of an opportunity for some degree of diagnostic evaluation. A number of relatively minor problems related to trauma to the chest and back are also discussed.
INITIAL ASSESSMENT
The initial assessment and management of the patient with serious chest trauma must include the early recognition of all of the following five conditions, any of which may be rapidly fatal unless appropriate therapeutic measures are instituted immediately.
These include:
Cardiac tamponade
Tension pneumothorax
Open or sucking pneumothorax
Flail or unstable chest wall associated with respiratory insufficiency
Massive hemothorax
Several general points relevant to the patient with serious chest trauma should be made:
Establishing a patent airway, including intubation and ventilation in patients with-out appropriate ventilatory function, and ascertaining the adequacy of air exchange within the chest are initial priorities, as with all seriously injured patients.
Two 14- or 16-gauge peripheral intravenous lines should be established immediately. Ringer lactate solution (or normal saline) is then infused. A central line should not be used initially for fluid resuscitation due to its length and narrow gauge.
A portable roentgenogram of the chest should be obtained as soon as possible in all patients with severe chest injuries.
The mechanism of injury is important to determine, because blunt and penetrating injuries to the chest are associated with specific disorders. For example, cardiac tamponade is unusual except in patients in whom penetration of the chest, back, or upper abdomen has occurred, whereas flail chest and pulmonary contusion occur most often in association with blunt trauma.
There is often no correlation between the external appearance of the chest wall and the extent of intrathoracic injury; this is particularly true in young children who, because of an extremely compliant and resilient chest wall, may have severe compressive or crushing trauma producing devastating intrathoracic injury while the external chest remains normal.
Many patients with serious trauma to the chest may have impressive or obvious extrathoracic injuries that are not life threatening; the acute treatment of these is obviously a secondary priority.
SPECIFIC DISORDERS
Cardiac Tamponade
Cardiac tamponade occurs in patients with lacerations or puncture wounds to the heart as a result of penetrating injuries to the anterior chest, upper abdomen, or back. The acute presentation of these patients is extremely variable and is determined by the extent and nature of the injury to the heart and to what extent bleeding is confined by the pericardium.
It is important to note that in patients with significant pericardial disruption, hemorrhage into the chest may occur, producing hemorrhagic shock and massive hemothorax; therefore, injuries to the heart should be suspected in patients presenting with hemothorax.
Frequently, pericardial continuity is sufficiently maintained to compromise the egress of blood from the pericardial sac, thereby producing cardiac tamponade. It is important initially to stress the following two points. First, progressive cardiac tamponade may be rapidly fatal unless treated in the emergency department with pericardiocentesis; and second, in patients with significant blood loss from whatever cause, many of the classic signs of tamponade will be absent or extremely subtle. The classic triad of Beck includes arterial hypotension, elevated venous pressure, and muffling of the heart sounds. It should be noted, however, that at least 30% of patients presenting with tamponade after penetrating injuries to the heart will not have initial evidence of increased venous pressure either clinically or by central venous pressure determination because of significant blood loss. Such patients will nevertheless manifest evidence of increasing venous pressure as fluid and blood replacement proceeds.
Diagnosis
Three very important diagnostic findings in patients with tamponade, which may also be seen in patients with tension pneumothorax, include tachycardia, hypotension, and a central venous pressure greater than 15 cm H2O.
Classically, patients with cardiac tamponade, if alert, report severe dyspnea, and many appear extremely anxious, restless, or agitated.
Breath sounds are normal bilaterally unless significant hemothorax or pneumothorax coexists.
Hypotension may be absent, mild, or marked as tamponade, bleeding, or both progress.
A reduced pulse pressure may be noted transiently, and pulsus paradoxus may be noted (pulsus paradoxus is a decline of more than 10 mm Hg in systolic pressure associated with inspiration).
Jugular venous distention, although frequently absent in volume-depleted patients, is an important finding if present, particularly when associated with hypotension. In addition, inspiratory filling of the jugular venous system or inspiratory increases in jugular venous pressure (Kussmaul sign) are additional findings.
Muffling of the heart sounds may be noted on physical examination, and electrocardiographic evidence of reduced voltage or the finding of electrical alternans points toward a diagnosis of tamponade.
Unless radiographs are available for comparison or hemothorax coexists, the chest roentgenogram is usually not particularly helpful.
Emergency transthoracic echocardiography is the diagnostic procedure of choice, because it documents the presence of the pericardial effusion and signs of tamponade physiology (e.g., right atrial collapse). When as little as 200 mL of blood acutely enters the intact pericardial space, tamponade may occur, and this amount of blood will not significantly distort the cardiac silhouette.
Treatment
Once a diagnosis of acute cardiac tamponade is confirmed or suspected, emergency pericardiocentesis should be performed. In addition and importantly, because hemodynamic function of the ventricle can be improved in patients with cardiac tamponade by increasing right-sided filling pressures, the rapid administration of crystalloids or blood can be helpful.
Have immediately available equipment for intubation and for cardiopulmonary resuscitation. Oxygen should be administered.
Optimally, position patients on the stretcher with the head and thorax elevated at approximately 45 to 55 degrees.
Prepare and drape the perixiphoid area.
Immediately inferior and to the left of the xiphoid process, anesthetize the skin with 1% lidocaine.
Connect a 16- or 18-gauge cardiac needle, 12 to 18 cm long, to a 50-mL syringe using a three-way stopcock.
If ultrasound is available, this procedure is ideally done with ultrasound guidance.
Alternatively, continuously record and closely observe a precordial or V-lead electrocardiogram while the needle is slowly advanced; this will signal cardiac penetration and prevent repeated cardiac puncture or laceration. If an alligator clip is available, this may be used to connect the pericardiocentesis needle to the V lead, which provides the most direct means of recording proximity to or contact with the epicardium during the procedure. If ventricular penetration occurs, then a typical “current-of-injury” pattern will be noted with elevation of the ST segment. If atrial penetration occurs, PR segment elevation may be noted. In addition, the occurrence of ectopic ventricular beats associated with needle advancement should also be noted and frequently signals cardiac penetration. When evidence of cardiac penetration occurs, the needle should be withdrawn several millimeters and this depth marked by attaching a snap or clip to the needle.
The most common method is the paraxiphoid approach, with the needle angled down approximately 45 degrees and directed toward the medial left clavicle; the needle should be felt to move under the interior aspect of the ribs. Advance the needle carefully, gently aspirating, under ultrasound guidance or observing the heart monitor for the above-mentioned perturbations.
One can occasionally feel the pericardium as it is entered, and if tamponade is present, blood is easily aspirated. As much blood as possible should be removed; however, clinical signs of improvement may occur after only a small volume is aspirated. Aspirated blood should be retained and, if it originates from within the pericardial space, may not clot. Blood that does clot may have originated from within the ventricle or atrium or, if from the pericardial space, may not have occupied that space for a long enough time for defibrination to occur.
At the point of entry of the pericardial space or the point at which aspiration is most successful, a Kelly clamp or snap should be secured to the needle at the skin surface; this will stabilize its position during aspiration and will serve as a marker for subsequent aspirations, should they be necessary. Alternatively, a small plastic catheter may be inserted into the pericardial space should tamponade recur and reaspiration be required.
Other Measures
Patients with cardiac tamponade are considered candidates for thoracotomy, and appropriate preparations must be initiated early. In the patient with minimal benefit from initial pericardiocentesis, other treatable causes that may be rapidly fatal and produce findings consistent with tamponade should be reconsidered; these include tension pneumothorax and shock secondary to massive hemothorax. Importantly, all patients must be closely monitored for signs of recurrence of the cardiac tamponade. This should be readily demonstrated upon repeat ultrasound.
Tension Pneumothorax
Simple pneumothorax is complicated by tension when the chest wall or lung is disrupted in such a fashion as to allow air to enter the pleural space during inspiration but not escape during expiration. Progressively forceful inspiratory efforts then accumulate air under increasing pressure within the pleural space. Oblique or flap-type lacerations of the lung, for example, may be tethered in an open position during inspiration when intrapleural pressures decrease, only to become compressed during expiration. Eventually, as pressure increases, mediastinal displacement develops away from the involved side, thereby leading to compression and distortion of perimediastinal venous structures. Reduced venous return to the right side of the heart on this basis and marked compression of adjacent pulmonary parenchyma result in severe and progressive shunting and hypoxemia. If venous compromise and pulmonary compression are not corrected, then profound hypotension, hypoxemia, and death rapidly ensue.
Diagnosis
On arrival, patients generally report or have evidence of penetrating trauma to the chest, back, or upper abdomen.
Evidence of ventilatory or circulatory compromise may be noted at the time of presentation.
“Sucking” or open wounds of the chest may be noted (and should immediately be treated).
The involved hemithorax may demonstrate decreased respiratory excursions, and breath sounds are generally reduced.
Subcutaneous emphysema may be present.
Deviation of the trachea away from the involved side and similar displacement of the cardiac apical impulse are late findings.
Jugular venous distention and hyperresonance to percussion on the involved side are also late findings.
A portable chest roentgenogram will demonstrate collapse of the involved lung with varying degrees of displacement of the mediastinal structures toward the opposite side. Tension pneumothorax should be a clinical diagnosis.
Treatment
Immediate percutaneous needle puncture-aspiration using a 14- or 16-gauge needle is indicated.
Place the needle in the second interspace along the midclavicular line.
The diagnosis is confirmed when air rushes out of the chest.
Open Pneumothorax
Sucking chest wounds are easily diagnosed when one hears air rushing in and out of the wound.
Pneumothorax associated with open defects of the chest wall, the single or collective diameters of which approach the diameter of the trachea, will effectively compete with the trachea for airflow during inspiration. In patients with large open defects, shunting of air away from the trachea and alveoli may result in rapidly evolving respiratory failure unless airflow is redirected.
Treatment
In patients with stable vital signs and adequate respiratory and circulatory function, the open wound should be covered with a sterile gloved hand, the surrounding area prepared in the usual sterile manner, and an occlusive dressing sterilely applied.
Petrolatum-impregnated gauze is an appropriate dressing and should be applied, so it extends 2 to 3 inches beyond the wound edge in all dimensions; two layers may be required, and these must be secured to the chest wall on three sides with several layers of adhesive tape.
A dry sterile dressing may then be applied. Occlusion of the dressing on three sides creates a flutter valve effect; closing the wound at all four sides could convert an open pneumothorax to a tension pneumothorax.
After the wound is closed in the aforementioned manner, preparations for chest tube placement should be undertaken immediately. Should deterioration in respiratory or circulatory status occur during the procedure, tension pneumothorax should be suspected and the dressing removed or percutaneous puncture of the involved pleural space undertaken immediately.
