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Penetrating injuries to the heart and great vessels result in significant prehospital mortality (50% to 75% for cardiac wounds), so the numbers of patients undergoing operations for such injuries are small even in the busiest civilian centers or wartime hospitals. The presentation is different for penetrating wounds to the nonhilar vessels of the lung parenchyma. With a systolic pressure of 25 mm Hg in the pulmonary artery and its branches, bleeding from injury to pulmonary parenchymal vessels requires thoracotomy in only 5% to 10% of patients. After blunt thoracic trauma, the majority of injuries involve the chest wall (i.e., fractured ribs) or lung (i.e., pneumothorax, hemothorax). As such, only 7% to 8% of patients with this injury pattern require thoracotomy or median sternotomy. In all patients with thoracic trauma, the most common indications for thoracotomy are hemorrhage from the lung, major arterial injury in the superior mediastinum or supraclavicular area, or a penetrating wound of the heart.
Penetrating wounds that injure the heart, the thoracic great vessels, or the hilum of the lung are often in a location referred to as the “cardiac box,” which is the area between the nipples from the sternal notch to the xiphoid process. Based on an autopsy study in 2017, this definition should be expanded to the posterior midline of the left hemithorax. Other penetrating wounds that increase the likelihood of injuries to these structures are those that traverse the mediastinum (i.e., transmediastinal wounds) and those to the thoracic outlet.
With blunt trauma to the chest, particularly from motor vehicle crashes, significant injuries to the heart and great vessels (and, occasionally, the lung) may occur whether or not the victim is restrained. Unrestrained victims with frontal or lateral impact can sustain all of the previously described deceleration or direct blunt injuries to the chest wall or intrathoracic structures. The most classic example of a deceleration injury is when the forward motion of the victim's thorax stops abruptly on contact with the hub of the steering wheel. This mechanism may cause varying degrees of traumatic disruption of the descending thoracic aorta, most commonly at the level of the ligamentum arteriosum. Depending on the position of any shoulder-harness restraint and the direction of impact, the innominate, carotid, subclavian, or vertebral arteries may also be prone to injury. Blunt thoracic vascular injury has also been reported as a result of air-bag inflation and is more prone to occur in women of small stature or in children.
Profoundly hypotensive patients with external hemorrhage at or near the thoracic outlet, those with hemorrhage into the pericardial sac or pleural cavity, or those with cardiac tamponade (diagnosis by ultrasound) should undergo rapid sequence or emergent endotracheal intubation in the emergency department. Awake patients with more normal hemodynamics with intrapleural blood or a pneumothorax, with or without tension physiology, should have a thoracostomy tube inserted in the 5th intercostal space at the midaxillary line. If this maneuver drains 1000 mL or more of blood in the first 15 minutes after tube insertion, the patient should be moved emergently to the operating room (OR). In this scenario, the patient should be placed on the operating table in the supine position with the anesthesiologist and operating team present. If another 200 mL of blood drains out of the thoracostomy tube in the next 15 minutes, the patient should be intubated in preparation for operation.
The decision as to whether the incision should be an anterolateral thoracotomy or a median sternotomy will depend on the entrance location and trajectory of any penetrating wound, the results of the thoracic and pericardial ultrasound, and the hemodynamic condition of the patient. If the amount of bloody drainage stops before 1200 mL and the patient has normal or near-normal hemodynamics, he or she should be moved to the intensive care unit (ICU) for close observation. Resumption of bleeding from the thoracostomy tube at a rate of 100 to 200 mL/h over the next 2 to 4 hours should prompt urgent thoracotomy or median sternotomy.
Any patient who is hypotensive from a pneumothorax, bleeding, or cardiac tamponade requires large-bore intravenous access for resuscitation, including placement of either 14-gauge extremity vein catheters, large-bore 7.5-Fr central venous catheter(s), or both. If there is concern about the original wounding mechanism having injured one of the subclavian veins, a contralateral upper extremity or subclavian vein should be used for venous access. Thoracic wounds in the expanded cardiac box or those with a transmediastinal trajectory that might have injured the superior vena cava should prompt placement of resuscitation lines into the common femoral veins.
Although the resuscitation fluid for patients with thoracic trauma was lactated Ringer's solution for many years, hypotensive patients (systolic blood pressure less than 90 mm Hg) are now managed with a strategy referred to as “damage control resuscitation” (DCR). In essence, this protocol involves avoiding administration of any crystalloid solutions if the patient is awake and has a recordable blood pressure. Initial application of this hypotensive resuscitation strategy allows for the fact that needless administration of any fluid aimed at achieving an arbitrary systolic blood pressure may lead to or worsen bleeding that has otherwise nearly stopped (i.e., “pop the clot” phenomenon).
Avoidance of crystalloid solutions such as normal saline or lactated Ringer's also stems from recognition that even small amounts of these fluids may dilute clotting factors and may lead to a condition referred to as dilutional coagulopathy. DCR is based on the early and balanced use of packed red blood cells (pRBC), thawed plasma, and platelets. Studies initiated from the wars in Iraq and Afghanistan demonstrated that the balanced use of pRBC, plasma, and platelets in a 1:1:1 ratio as part of a DCR strategy conveyed a mortality benefit to severely injured patients. Recent military studies have reported a mortality benefit with the use of the antifibrinolytic medication tranexamic acid (TXA), as well as administration of supplemental cryoprecipitate as part of the DCR strategy.
Resuscitative endovascular balloon occlusion of the aorta (REBOA) passed through the common femoral artery has replaced emergency center thoracotomy for resuscitation in patients with trauma isolated to the abdomen, pelvis, or lower extremities. Emergency center thoracotomy for resuscitation and bleeding control continues to be indicated in a highly selected group of patients. This maneuver with thoracic trauma, also referred to as resuscitative thoracotomy, is performed in hospitals that do not have an OR in or immediately adjacent to the emergency department. Algorithms, quality improvement data, and reviews of outcomes have helped refine the indications for this procedure. Reasonable indications to perform an emergency center thoracotomy in an injured patient are as follows :
Penetrating thoracic wound with agonal physiology or recent cardiac arrest
Uncontrolled bleeding from the thoracic inlet or a thoracostomy tube
Suspected subclavian vessel injury with intrapleural exsanguination
Need for open cardiac massage or occlusion of the descending thoracic aorta before laparotomy in the OR (REBOA not available)
Need for open cardiac massage or clamping of the descending thoracic aorta when countershock or closed-chest cardiac massage is ineffective (i.e., cardiopulmonary arrest)
Relative indications include a recent cardiac arrest associated with a flail or other chest wall abnormality (difficult external cardiac massage) or pregnancy (to save the child). Strong contraindications for the use of resuscitative thoracotomy include penetrating trauma with no signs of life in the field and blunt trauma with no signs of life on arrival in the emergency center.
A left anterolateral thoracotomy at the lower edge of the male nipple is performed when a penetrating left thoracic wound is present in an agonal or arrested patient. When a penetrating right thoracic wound is present and the patient is agonal on arrival, a bilateral anterolateral thoracotomy (i.e., clamshell thoracotomy) is performed. If intrapleural exsanguination from a suspected injury to a subclavian vessel is believed to be present, an anterolateral thoracotomy at a higher intercostal space is appropriate. The primary goals of either a unilateral anterolateral or a bilateral anterolateral thoracotomy are to control bleeding from a wound to the heart, a great vessel, or the lung, release a cardiac tamponade, or perform internal cardiac massage. Whether suture repair of the injured organ or vessel is appropriate in the emergency department will depend on the following factors: (1) magnitude of the injury; (2) success of temporary bleeding control maneuvers; (3) quality of lighting; and (4) availability of instruments and sutures.
An additional and important goal of resuscitative thoracotomy is to cross-clamp the descending thoracic aorta to maintain any remaining central aortic pressure and perfusion to the coronary and carotid arteries. One must be mindful in these scenarios that applying a cross-clamp to the descending thoracic aorta is more difficult through a higher left-sided thoracotomy incision. Thoracic aortic clamping is performed by first lifting the posterolateral edge of the left lung out of the hemithorax. Once the mediastinal pleura over the descending thoracic aorta and vertebral bodies is visualized, it is opened with scissors. Next, the descending thoracic aorta is encircled with the surgeon's left index finger before the cross clamp is applied. Subsequent maneuvers for cardiac massage or repair include a longitudinal pericardiotomy above the left phrenic nerve, exposure of the cardiac wound or rupture, and the use of fingers, staples, sutures, or balloons for bleeding control ( Figs. 16.1–16.4 ).
Because of the cost and low survivability of emergency center thoracotomy, the technique has been used more selectively in recent years. The reported survival rate of 7% to 10% is deceptive as it includes patients with a variety of injuries, while patients with penetrating cardiac wounds have significantly better outcomes. In an old report by Ivatury et al., 16 of 22 patients with penetrating cardiac injury who arrived in the emergency center without “detectable vital signs, cardiac activity, or spontaneous respirations” were able to have restoration of cardiac function with resuscitative thoracotomy. In this same report, eight patients (36%) survived without neurologic sequelae. A more recent (2009) report on 283 patients undergoing emergency center thoracotomy for penetrating injury to the heart and great vessels documented worse outcomes including a survival rate of 24% in those with stab wounds and only 3% in those with gunshot wounds. The injury scenario with the highest survival rate following emergency center thoracotomy is cardiac tamponade from an isolated, anterior cardiac stab wound in a patient presenting with measurable vital signs following a short prehospital transport.
For patients with penetrating wound(s) that may involve the heart, thoracic aorta, or great vessels and who are hemodynamically normal, it is appropriate to image the thorax to better characterize the presence and location of injury. This can be accomplished with a chest x-ray, which may demonstrate a hematoma in the superior mediastinum or in the supraclavicular area, a surgeon-performed ultrasound, or a contrast-enhanced CT scan or CT arteriography.
Asensio et al. have reviewed the unsuccessful attempts at cardiac repair by Cappelen in Norway and Farina in Italy that preceded Ludwig Rehn's successful repair of a wound to the right ventricle in 1896. L.L. Hill of Montgomery, Alabama, is credited with the first successful delayed repair of a stab wound to the left ventricle in the United States in 1902. In the modern era, the vast majority of cardiac injuries are from penetrating wounds and are treated in urban trauma centers. Blunt cardiac injuries occur mostly after head-on motor vehicle crashes, can be caused by air bags, and have a significant mortality that is often related to a delay in diagnosis.
Patients with penetrating cardiac injuries, especially from gunshot wounds, have a 50% to 75% mortality rate at the scene or on arrival at the hospital. This is secondary to acute cardiac tamponade if the lateral walls of the pericardial sac are intact or to exsanguination when there is communication with a pleural cavity. Only rapid transport to a trauma center or acute care hospital will save the lives of patients with repairable cardiac injuries and signs of life in the field. This is because therapeutic procedures such as pericardiocentesis, an open pericardial window, or an emergent anterolateral thoracotomy are not performed in the prehospital setting in the United States or during military conflicts.
In a review from the American College of Surgeons National Trauma Data Bank, blunt cardiac rupture had an incidence of 1/2400 admissions and occurred most commonly after motor vehicle crashes (73%) followed by automobile–pedestrian accidents (16%). In this study, blunt cardiac injury was determined to have an overall mortality of 89%. This is most commonly due to rupture of one or more cardiac chambers, tears at the right atrial-caval junctions, or a blunt coronary artery dissection or tear.
Patients with stab wounds to the heart may present with cardiac tamponade (60% to 90%), intrapleural hemorrhage (10% to 40%), or both. In contrast, patients with gunshot wounds present with cardiac tamponade (20%), intrapleural hemorrhage (80%), or both. Cardiac tamponade is caused by blood in an intact pericardial sac which compresses the atria and impairs venous return and cardiac filling. The cardiovascular response to decreased stroke volume is progressive tachycardia. Pulsus paradoxus is present in essentially all patients, as well. Whereas blood pressure decreases by as much as 10 mm Hg with inspiration secondary to a decrease in left ventricular stroke volume, this decrease may be 15 mm Hg or more in the setting of cardiac tamponade. In the setting of tamponade, there is a simultaneous progressive rise in central venous pressure secondary to the impaired venous return. In this scenario, patients often present with a dusky or deathlike appearance that is noticeable regardless of race. Alert patients express extreme anxiety (“Am I going to die?”) and frequently complain of a “heaviness” or pressure in the chest.
If the diagnosis of cardiac tamponade is delayed, myocardial ischemia and continued decreases in cardiac output occur. This spiral leads to cardiovascular collapse and cardiac arrest in minutes in patients with wounds or ventricular rupture. In patients with wounds or ruptures of the atria, compression of the hole by the extravasated blood in the pericardium may stop further hemorrhage and progressive tamponade. The main hemodynamic finding in such patients is the aforementioned progressive rise in central venous pressure to 20 to 30 mm Hg with profound hypotension or a cardiac arrest as the terminal event. The diagnosis of a compressed atrial wound may be delayed for 12 or more hours until clinical suspicion prompts a pericardial ultrasound, a pericardial window, a sternotomy, or a thoracotomy. In most reports, the classic Beck's triad of hypotension, distended cervical veins, and muffled heart sounds is present in less than 10% of patients with tamponade, whereas the incidence of Kussmaul's sign or jugular venous distension with inspiration is difficult to determine. Bleeding from the injured heart into a pleural cavity most often results from a gunshot wound, and the classic signs of hypovolemic shock are typically present. Depending on the patient’s hemodynamic status, an early resuscitative thoracotomy rather than a diagnostic test will be necessary.
Blunt cardiac injury (BCI) encompasses a spectrum of trauma including myocardial bruising (myocardial contusion), transmural infarction, or a rupture of the free wall or septum. The spectrum of cardiac injury is described in the American Association for the Surgery of Trauma's (AAST) Organ Injury Scale reported in 1994. Clinical manifestations that the trauma team must treat in rare patients include unexplained hypotension, new-onset arrhythmias, or cardiac tamponade. Mechanical problems that have occurred after a BCI include injury to papillary muscles, choradae tendineae, cardiac valves, and coronary arteries.
Other than the physical examination, diagnostic options for patients with penetrating injuries (or blunt ruptures) with secondary tamponade include the following: (1) an electrocardiogram to assess for a “J” wave; (2) measurement of central venous pressure; (3) pericardiocentesis; (4) subxiphoid pericardial window; (5) formal transthoracic (TTE) or transesophageal (TEE) ultrasound; and (6) surgeon-performed TTE as part of focused assessment for the sonographic evaluation of the trauma patient (FAST) examination.
A “J” wave (small positive reflection at the R-ST junction) as a sign of an occult cardiac injury after a penetrating thoracic wound was described by Nichol and Navsaria in 2014. In a group of 174 patients with penetrating thoracic wounds, the specificity to detect a hemopericardium was 85%, sensitivity 44%, and positive predictive value 91% ( P < .001).
Measurement of central venous pressure is invasive, time-consuming, and may not confirm the diagnosis of cardiac tamponade immediately. It is appropriate to use when there is no desire to anesthetize the stable patient to perform a diagnostic subxiphoid pericardial window or when the ultrasound machine is broken or unavailable. Any 10 mm Hg increase in central venous pressure over time in the relaxed supine patient receiving only maintenance intravenous fluids should prompt a subxiphoid pericardial window or median sternotomy or thoracotomy.
A pericardiocentesis may have a therapeutic effect in the patient with tamponade and hemodynamic instability; however, the diagnostic sensitivity of this maneuver in the stable patient with a small tamponade has always been questioned. To rule out aspiration of intracardiac blood mistaken as an early tamponade, the long spinal needle used for the pericardiocentesis should be attached to a monitor lead to rule out a current of injury as the cardiac wall is penetrated.
An open surgical subxiphoid pericardial window is performed under general anesthesia and mandates a bloodless operative approach. It is most helpful during an emergency laparotomy after a gunshot or stab wound when the track of the missile or knife appears to be in proximity to or appears to penetrate the pericardial sac. Also, it is used in many centers when non-surgeon or surgeon-performed ultrasound is unavailable or when there is not acceptable accuracy with the technique. The operative approach is through a 5- to 10-cm midline abdominal incision starting on the xiphoid process, which may be excised as needed for exposure. The linea alba is divided, and extraperitoneal dissection is performed bluntly in a superior direction toward the pericardium. Exposure is enhanced by lifting the xiphoid process (if still in place) and the lower sternum up with one medium Richardson retractor or two Navy-Army retractors. Once cardiac pulsations are palpated, the inferior pericardial sac is grasped with two long Allis clamps, and a 2-cm vertical pericardiotomy is made between the clamps. If this maneuver results in the release of blood from the pericardial sac, most surgeons transition to a median sternotomy followed by a longitudinal pericardiotomy, evacuation of the tamponade, and control of bleeding. Patients who manifest progressive hemodynamic deterioration during the subxiphoid pericardial window should undergo left anterolateral thoracotomy and opening of the pericardium through that approach.
Following the lead of the Trauma Centre faculty at the University of Cape Town, South Africa, some centers choose to wash blood out of the pericardial sac after a positive window in the reasonably stable patient and observe for further bleeding without opening the pericardial sac. The rationale for this is that pericardial wounds only or wounds that injure the cardiac wall superficially (epicardium and outer myocardium) may have stopped bleeding by the time the pericardial window has been performed. Should there be no further bleeding during a period of intraoperative observation with the pericardial sac open, a few groups around the world close the incision without performing a median sternotomy or anterolateral thoracotomy.
A formal TTE or TEE ultrasound performed by a cardiologist or anesthesiologist is an accurate technique to detect cardiac tamponade. This maneuver can also diagnose intracardiac lesions such as septal defects or valvular injuries and can calculate an ejection fraction. Unfortunately, the majority of penetrating cardiac injuries come to the emergency department on weeknights or weekends when the specialists who perform formal TTE or TEE ultrasound may not be available. Additionally, the sedation required to properly perform TEE would be contraindicated in the unstable patient with this injury scenario.
Over the past 25 years, reports have documented that limited TTE performed in the emergency center by surgeons or specialists in emergency medicine using a 3.5-MHz general access transducer is the diagnostic test of choice ( Fig. 16.5 ; Table 16.1 ). The FAST examination begins with a pericardial view in patients with either penetrating or blunt trauma. During the FAST, the probe is placed in a longitudinal direction in the subxiphoid area at an angle of 30 degrees off of the epigastrium with firm pressure. This usually results in a clear view of the apex of the heart, the pericardium, and the left lobe of the liver. The beating heart in this real-time ultrasound approach should lie immediately adjacent to the liver. Should tamponade be present, a black stripe will separate the beating heart from the liver. The black or anechoic stripe with an ultrasound density that is the same as blood in the inferior vena cava represents blood outside the heart, i.e., a tamponade. Failure to visualize an adequate sagittal view through the subxiphoid window is often secondary to the patient's complaining about pain or discomfort. Also, this cardiac window may be diminished in obese patients.
Author | Number of Patients | True-Positives | Accuracy |
---|---|---|---|
Rozycki et al., 1996 | 236 | 10 | 100% |
Rozycki et al., 1998 | 313 | 22 | 99.4% a |
Rozycki et al., 1999 | 261 | 29 | 97.3% b |
Nichol et al., 2015 | 172 | — | 86.7% c |
a Two false-positives, no false-negatives.
The ultrasound probe is next placed in a horizontal direction in the 4th or 5th left parasternal space to obtain a coronal view of the same cardiac structures. In the study by Rozycki et al., 246 patients with penetrating thoracic wounds were evaluated by surgeon-performed ultrasound. There were 236 true-negative results and 10 true-positive results. In the latter group, the mean time from ultrasound to operation was 12 minutes and all patients survived after repair of their cardiac wounds. A follow-up study by Rozycki et al. in 313 patients with penetrating precordial or transthoracic wounds resulted in 289 true-negative examinations, 2 false-positive examinations, and 22 true-positive examinations. In the latter group, all patients survived when surgery was immediately performed by the surgeon-sonographer. Finally, Rozycki et al. completed a multicenter study in which emergency pericardial sonograms were performed by ultrasound technicians, cardiologists, or surgeons. In a series of 261 patients with penetrating precordial or transthoracic wounds evaluated at five level I trauma centers, 29 (11%) had true-positive studies, and 28 survived after emergency cardiac repair. The accuracy (97%), specificity (97%), and sensitivity (100%) were equivalent to those reported in the previous study from Grady Memorial Hospital.
Some centers around the world have not had the same accuracy of surgeon-performed ultrasound in detecting intrapericardial blood, and all centers recognize the compromised accuracy of surgeon-performed pericardial ultrasound when a left hemothorax is present. Nichol et al., using a similar description of the expanded cardiac box as later described by Jhunjhunwala et al., offered a new management algorithm for the hemodynamically stable patient in 2015. First, a patient with a “screening ultrasound” positive for intrapericardial blood would be taken to the OR for a subxiphoid pericardial window under general anesthesia. Second, a patient with an equivocal screening ultrasound would undergo a pericardial window or a CT scan of the chest. And, third, a patient with a negative screening ultrasound should have an immediate CT scan of the chest or a repeat ultrasound in 24 hours.
As previously noted, 90% of blunt cardiac injuries are caused by precordial trauma sustained during motor vehicle or automobile–pedestrian crashes. Arrhythmias such as sinus tachycardia, premature atrial or ventricular contractions, and heart block are the most common manifestations of blunt cardiac injury. For this reason, the admission electrocardiogram (ECG) is the most logical diagnostic technique of choice. The usefulness of an ECG is often discounted by studies advocating radioisotope scanning, TTE, and TEE as diagnostic modalities for blunt cardiac injury. Multiple reports, however, have documented that an ECG is an excellent initial test when evaluating patients with blunt thoracic trauma. In essence, these studies have shown that a normal ECG in the emergency department effectively excludes significant blunt cardiac injury.
There is continued interest in using a measure of serum cardiac troponin I (TnI) in addition to the admission ECG to detect blunt cardiac injury. In one study from Los Angeles County Hospital, 27 of 80 patients (34%) with an abnormal ECG and TnI level after blunt chest trauma developed significant BCI. BCI in this and other studies is defined as arrhythmias requiring treatment or the presence of cardiogenic shock or cardiac structural injury. The authors concluded that a normal ECG and serum TnI on admission and 8 hours after injury excluded blunt cardiac injury. TTE or TEE may be used as an adjunct in patients with persistent ECG abnormalities or with unexplained hypotension after blunt chest trauma.
Admission to the hospital for a possible or likely BCI is justified when the following are present after thoracic trauma: (1) history of cardiac disease (i.e., angina pectoris, myocardial infarction, arrhythmias, coronary revascularization); (2) unexplained hypotension; and (3) new onset arrhythmia or conduction disturbance on an admission ECG. A patient with blunt thoracic trauma and a history of cardiac disease or the presence of non–life-threatening arrhythmias such as sinus tachycardia or atrial fibrillation should be admitted to a telemetry unit for monitoring and observation. When hypotension is present or when the ECG change is potentially lethal (i.e., ventricular tachycardia, ventricular fibrillation, third-degree heart block), treatment is initiated in the emergency center before transfer to the ICU.
When an operation for another injury is indicated in a patient with blunt cardiac injury, not including cardiac rupture, the prognosis is generally excellent. In a 1986 report by Flancbaum et al., 19 patients with BCI had an emergency operation, including 15 on the day of admission. Pulmonary artery catheters were placed in 12 patients, and inotropes were used in 11. The duration of anesthesia was 6 hours, and there were no cardiac-related complications or deaths.
As previously noted, a left or bilateral anterolateral thoracotomy (i.e., clamshell thoracotomy) is performed in the emergency department for release of suspected or documented tamponade, for control of cardiac hemorrhage, and for resuscitation. The same incision(s) would be used in the OR for agonal patients or for those in cardiac arrest. These incisions allow for expedited control of hemorrhage from cardiac perforation(s) and for cross-clamping of the descending thoracic aorta. The anterolateral thoracotomy approach may also be kept separate from any abdominal midline incision needed to address an intraabdominal injury. The median sternotomy is performed in the OR in patients who are more hemodynamically stable and who have solitary anterior stab wounds. In such patients, multiple cardiac perforations are unlikely and cross-clamping of the descending thoracic aorta is usually not needed.
Opening the left chest via an anterolateral thoracotomy and insertion of a Finochietto retractor are followed by a longitudinal left lateral pericardiotomy performed anterior to the left phrenic nerve. In obese patients where fat obscures the phrenic nerve, the accompanying pericardiacophrenic vessels mark the location. Even if the pericardium is difficult to grab with a forceps secondary to distention of the sac with blood, the surgeon should resist performing a pericardiotomy with a scalpel. This is a particularly dangerous as right-sided tamponade from a wound to the atrium or ventricle may push the heart to the left so that it lies immediately underneath or abuts the left pericardial sac. In this position, the left anterior descending coronary artery is at risk of injury if a scalpel is passed too deeply while opening the pericardium. A better technique is to lift the pericardium with a toothed forceps and to open the sac with the tip of a straight Mayo scissors. Once it has been opened, the pericardium generally lifts away from the surface of the heart allowing the incision to be extended in a superior direction until the pericardial fold on the great vessels is reached. The longitudinal left pericardiotomy is completed in an inferior direction until the left hemidiaphragm is reached. Exposure of the injured heart is enhanced by making a transverse pericardial incision to the right as well. This pericardial incision is made at a right angle to the left lateral pericardiotomy and extends to 1 cm anterior to the right phrenic nerve.
In patients undergoing bilateral anterolateral thoracotomy, either the pericardiotomy described previously or the midline pericardiotomy described later can be used. After a median sternotomy and insertion of a Finochietto retractor, the fat anterior to the pericardium and the anterior extensions of the parietal pleura are swept laterally with the fingers over laparotomy pads. This maneuver exposes the anterior surface of the pericardial sac which is grasped with toothed forceps and opened in a midline longitudinal direction from the great vessels to the diaphragm.
After the pericardiotomy is performed, blood and clots are removed from the pericardial sac manually and with irrigation and suction. Inspection of the anterior surface of the heart and great vessels is performed. If no anterior perforation or blunt rupture is noted, the surgeon should note the patient's blood pressure on the monitor. A profoundly hypotensive patient may not tolerate inspection of the posterior aspect of the heart, which requires elevation of the apex. Lifting the heart to inspect the underside compresses or kinks the vena cavae, restricting right-sided filling. This maneuver also carries with it a risk of sucking air into an open hypovolemic ventricle. With left ventricular perforation, air has the potential to rapidly move into the coronary arteries causing an air embolism and cardiac arrest. As such, manual palpation of the posterior surface of the heart without elevation of the apex is all that is advised until the patient is resuscitated with a relatively normal blood pressure. Palpation of a posterior defect or jet of blood as a ventricle contracts mandates leaving the finger in place for control of hemorrhage until the patient’s hypovolemia is corrected.
Finger | Atrium/ventricle |
Stapler | Atrium/ventricle |
Satinsky vascular clamp | Atrium |
Row of Allis clamps | Lateral atrium adjacent to pericardium |
Foley balloon catheter | Atrium/ventricle |
Crossed mattress sutures | Ventricle |
Inflow (superior vena cava/inferior vena cava) occlusion | Large ventricular hole or multiple chamber wounds |
3-mg intravenous adenosine to induce 10–20 s asystole | Large ventricular hole or multiple chamber wounds |
Once the patient has been stabilized and the surgeon is ready to lift the apex of the heart to inspect the posterior aspect, he or she should notify the anesthesia team so that they are aware and can assist in managing any associated hypotension. If there is bleeding from the posterior aspect of the heart that will require prolonged elevation and/or suturing, the surgeon should consider placing a cross-clamp on the descending thoracic aorta to preserve central pressure and cerebral circulation. This will, however, increase bleeding through the cardiac wound.
A finger or compression with fingers will control hemorrhage from a cardiac perforation or cardiac rupture in 95% of patients. This is because patients with larger defects die at the scene or in transit. Suture repair of a ventricular wound can be performed under the occluding finger. When a finger is not successful in controlling bleeding or when more definitive control is needed, the techniques in Table 16.2 may be applied. Disposable skin staplers with long rotating heads can be used to quickly close atrial or ventricular defects. Whether staple repair lines placed in the emergency department should be buttressed or replaced with sutures in the OR is controversial. The safest policy is to buttress any left ventricular repair with Teflon pledgets in the OR in patients who stabilize after the initial hemorrhage control and resuscitation maneuvers.
Elevation of an atrial wound with the fingers, forceps, or Allis clamps will frequently allow placement of a Satinsky vascular clamp under the perforation. Atrial wounds or ruptures in the lateral aspect adjacent to the pericardium cannot be controlled with a Satinsky clamp. With such injuries, Allis clamps grabbing both sides of the defect are placed in a row similar to the method described for wounds to the vena cava for the past 100 years. For atrial wounds adjacent to the ventricle or other difficult cardiac lacerations, use of a Foley balloon catheter to control hemorrhage was first described in 1966. Insertion of the tip and balloon of the catheter into the defect is followed by inflation of the balloon and gentle traction on the end of the catheter hanging out of the heart.
On rare occasions, the length of a ventricular laceration will lead to exsanguinating hemorrhage that will preclude the use of the stapler or the balloon catheter. With manual compression of the defect, a horizontal mattress suture is rapidly placed on either side of the defect, the two ends on each side are placed in the hands, and the hands holding the suture ends are crossed. This should prevent exsanguination as a continuous over-and-over suture row or a row of staples is placed. A temporary closure as described would then be buttressed with Teflon pledgets in the OR.
Because few surgeons are familiar with the manual technique for control of hemorrhage from the heart described over a century ago by Ernst Ferdinand Sauerbruch (1875–1951), the related technique of inflow occlusion is used occasionally to control major hemorrhage from the heart. Inflow occlusion slows the heart and improves one’s ability to control cardiac bleeding. With difficult-to-visualize cardiac wounds or in the case of large ventricular wounds, as described previously, application of vascular clamps to the superior and inferior vena cavae is appropriate. This maneuver decreases hemorrhage from the injured heart and rapidly causes a profound bradycardia which together allow for clamp or suture control of hemorrhage from complex cardiac wounds. Prior to tying down the last suture of a ventricular repair, the clamps on the cavae are removed to allow refilling of the ventricle. Evacuation of ventricular air is accomplished by elevation of the apex of the heart as refilling occurs and before the final suture of the repair is tied down. The exact time limit on inflow occlusion is unknown, but 1 to 2 minutes will usually allow for restoration of a cardiac rhythm after the repair has been completed.
There have been several reports about the administration of 3 mg of adenosine intravenously to aid in the repair of cardiac injuries. Approximately 20 seconds after administration of adenosine, the heart will stop beating (i.e., induced asystole) for 10 to 25 seconds allowing for initiation of a rapid suture repair. Further intravenous doses are given to complete the repair as needed. The annoying side effects associated with adenosine use, including facial flushing, thoracic discomfort, dyspnea, and headache, are not noticeable under general anesthesia.
After hemorrhage has been controlled, patients with preterminal bradycardia or new onset asystole need immediate cardiac resuscitation. If the heart feels empty, the descending thoracic aorta should be cross-clamped if this has not been performed previously. If a median sternotomy was the original approach, a left anterolateral thoracotomy will have to be performed to complete this maneuver. Cardiac resuscitation would then include administration of blood components as part of DCR, along with bimanual cardiac massage to perfuse the coronary and carotid arteries. It is critical not to lift the apex of the heart because this may cause impingement of the vena cavae or air embolism from the partially empty cardiac chamber with perforation if resuscitation has preceded repair.
When the heart does not respond to the infusion of volume and internal cardiac massage, cardioactive medications should be administered. These include 1 mg intravenous atropine for bradycardia, 1 to 3 mg intravenous epinephrine for bradycardia and hypotension, or 1 mg of intracardiac (into left ventricle) epinephrine for profound bradycardia or asystole. The onset of ventricular fibrillation is treated with internal electrical defibrillation using two paddles in contact with the heart anteriorly and posteriorly and 10 to 20 J as the initial electrical charge. After restoration of a satisfactory cardiac rhythm and blood pressure, suture repair of the cardiac perforation may be performed if not completed previously.
Suturing of the injured heart is often complicated by tachycardia and the side-to-side motion of the heart in the pericardial sac. A most helpful maneuver to stabilize the beating heart as repair is being performed is “clamp control of the right ventricular angle” as described at Temple University. To accomplish this maneuver, a Satinsky clamp is applied to the apex of the right ventricle, and an assistant holding this clamp will eliminate much of the side-to-side motion of the beating heart.
Repair of an atrial perforation or rupture above a Satinsky clamp is performed with a purse string or continuous 4-0 or 5-0 polypropylene suture. An alternate approach to a hole in the atrial appendage is to place a 2-0 silk tie under the Satinsky clamp much like in performing a decannulation maneuver following cardiopulmonary bypass. As noted, Allis clamps are used to control hemorrhage from atrial wounds in the lateral aspect adjacent to the pericardium. Repair is accomplished with a continuous or interrupted mattress technique using 4-0 polypropylene suture passed under the row of Allis clamps.
With a wound of the ventricle being controlled by the surgeon or the assistant's finger, horizontal mattress 3-0 or 4-0 polypropylene sutures can be placed under the finger and tied. When a Foley balloon catheter has been used to control hemorrhage from a ventricle, the surgeon must be mindful that placement of the sutures for the cardiac repair can rupture the underlying balloon. Therefore, as the continuous 3-0 or 4-0 polypropylene suture is placed around the controlled defect, the balloon must be temporarily pushed down into the ventricle with each passage of the needle. Hemorrhage will occur with this maneuver, but rupture of the balloon is prevented.
Teflon pledgets are used to buttress left ventricular repairs performed with sutures alone in the emergency department and any repairs performed in the OR. Commercially available pledgets or pledgets cut from Teflon strips may be used. When synthetic pledgets are not available, pieces of the pericardium may be used. The technique is to first pass the two needles of a 4-0 polypropylene suture through a pledget 6- to 10-mm long and 3- to 5-mm wide. The same needles are separately passed through both sides of the ventricular perforation under the surgeon or assistant's finger as described earlier. The two needles are then passed through another Teflon pledget of similar size and then cut off. As the two ends are pulled up tight, the second pledget is moved down to its side of the ventricular wound aided by ample irrigation on the monofilament sutures. Tying the polypropylene suture with appropriate tension will bring the Teflon pledgets in apposition, will seal the cardiac perforation, and prevent the sutures from tearing through edematous myocardium.
One technique for a cardiac surgeon to repair a wound is the use of a sutureless patch and bioglue. This technique appears to be most useful for small wounds in difficult-to-repair areas of the heart, such as the coronary sinus. Cardiac wounds adjacent to a coronary artery are repaired with pledgets as described previously, but the needles are passed through both sides of the ventricular perforation and under the adjacent coronary artery. Even with this modified technique, tying the pledgets together to control hemorrhage may cause compression of the coronary artery and ischemia of the distal myocardium. A direct, but limited, laceration of a proximal coronary artery may be repaired with interrupted single 6-0 or 7-0 polypropylene sutures on rare occasions. In contrast, a laceration of a distal coronary artery near the apex of the heart is treated with ligation and a 15-minute period of observation to assess myocardial ischemia.
The majority of patients who reach the hospital with signs of life despite a cardiac perforation or rupture have a limited injury that can be repaired by a general surgeon, trauma fellow, or a senior surgical resident. Approximately 1% to 3% of such patients have a more complex injury that can only be repaired by a cardiac surgeon using cardiopulmonary bypass ( Table 16.3 ; Fig. 16.6 ).
Acute |
|
Delayed |
|
If a left anterolateral or bilateral anterolateral thoracotomy has been performed, the superior and inferior transected ends of the internal mammary arteries should be clamped and ligated with 3-0 silk ties. If the heart is edematous after a repair, the pericardial sac is not closed. On occasion, there may appear to be a risk of postoperative cardiac herniation through a left lateral pericardiotomy performed through a left anterolateral thoracotomy. Closure of this lateral defect with interrupted 2-0 silk sutures would then be appropriate. The pericardial sac is drained with a right-angle 36-Fr thoracostomy tube inserted through the epigastric area of the abdominal wall. A second 36-Fr thoracostomy tube is placed anterior to the heart. If either pleural cavity has been opened, one or two 36-Fr thoracostomy tubes are placed through the 5th intercostal space between the ipsilateral anterior and middle axillary lines.
On occasion, epicardial pacing wires may have to be sewn to the heart when arrhythmias continue despite cardiac repair and resuscitation. An unstable patient who is not fully responsive to continuing resuscitation and inotropes may benefit from the transfemoral insertion of an intraaortic balloon pump before transfer to the ICU. For patients who will not tolerate wire closure of the sternum after a cardiac repair, a plastic silo (a genitourinary irrigation bag opened on three seams) should be sewn to the skin edges of the median sternotomy with continuous sutures of 2-0 nylon as a temporary closure maneuver. As the patient enters the diuretic phase of recovery in the subsequent 48 to 72 hours, the silo is removed, and the sternum is closed at a reoperation.
Cardiac failure after repair of a traumatic injury may require the use of inotropic medications and/or an intraaortic balloon pump. Possible causes of cardiac failure are: (1) tamponade from a coagulopathy, hemorrhage from the repair, or hemorrhage from a missed injury; (2) cardiac compression from closure of the sternum; (3) posttraumatic myocardial infarction without injury to a coronary artery ; (4) posttraumatic myocardial infarction with injury to a coronary artery; and (5) undiagnosed injury to a cardiac valve, a papillary muscle, the chordae tendineae, or the atrial or ventricular septum. An immediate ECG and TTE or TEE will assist in making the diagnosis. Cardiac compression from closure of the sternum is usually diagnosed at the completion of the first operation and is easily reversed by removing the sternal wires.
For more than 55 years, it has been recognized that patients who survive acute repair of a wound or rupture of the atrium or ventricle may also have an internal cardiac injury. Postoperative cardiac failure or the presence of a murmur on auscultation in a previously healthy patient is a clinical sign of such an internal injury. Other patients, particularly those with internal fistulas (i.e., right atrium to left ventricle) may be asymptomatic in the postoperative period. There is disagreement about studying all surviving patients with TTE before discharge. In the 2016 report from Grady Memorial Hospital, only 25 of 46 patients who survived after a penetrating cardiac wound from 2000 to 2010 had a post-repair two-dimensional TTE. All three of the patients who had “positive” echocardiograms (two ventricular septal defects; one cardiac failure) were symptomatic at the time.
An abnormal or inconclusive TTE would usually be followed by a TEE or cardiac catheterization. A patient with a hemodynamically significant injury to a valve, papillary muscle, chordae tendineae, or a septum should have delayed repair on cardiopulmonary bypass.
Survival after penetrating cardiac trauma depends on the mechanism of injury (stab vs. gunshot), the number of signs of life on admission (cardiovascular and respiratory components of trauma score), the location of the thoracotomy (emergency department vs. OR), the cardiac rhythm at the time of the pericardiotomy (rhythm vs. asystole), the number of chambers injured, and the associated injuries. Survival rates from two large series are listed in Table 16.4 .
Asensio et al. a | Morse et al. b | |||
---|---|---|---|---|
1994–96 | 1975–85 | 1986–96 | 2000–10 | |
Patients | 105 | 113 | 79 | 79 |
SW/GSW | 37/68 | 77/36 | 53/26 | 34/45 |
Survival SW | 24/37 (65%) | 59/77 (77%) | 47/53 (89%) | 26/34 (76%) |
Survival GSW | 11/68 (16%) | 23/36 (64%) | 15/26 (58%) | 20/45 (44%) |
Survival overall | 35/105 (33%) | 82/113 (73%) | 62/79 (78%) | 46/79 (58%) |
Survival EDT | 10/71 (14%) | 2/23 (9%) | 13/28 (46%) | 9/16 (56%) |
a Data from Asensio JA, Berne JD, Demetriades D, et al. One hundred five penetrating cardiac injuries: a 2-year prospective evaluation. J Trauma . 1998;144:1073–1082.
b Data from Morse BC, Carr JS, Dente CJ, et al. Penetrating cardiac injuries: a 36-year perspective at an urban, level I trauma center. J Trauma Acute Care Surg . 2016;81:623–631.
The great vessels in the chest and thoracic outlet are variously defined, but most consider this category to include the large vessels originating from the aortic arch and those in what is traditionally considered zone I of the neck. In this context, the terminology includes the ascending, transverse, and descending thoracic aorta as well as the innominate (brachiocephalic), common carotid, and subclavian arteries. Because of their sizes and proximal locations, the innominate and central jugular veins may also be included as great vessels of the chest. Table 16.5 provides the AAST Thoracic Vascular Organ Injury Scale for vascular trauma in this region.
Grade a | Injury Description b | ICD-9 | AIS-90 |
---|---|---|---|
I | Intercostal artery/vein | 901.81 | 2–3 |
Internal mammary artery/vein | 901.82 | 2–3 | |
Bronchial artery/vein | 901.89 | 2–3 | |
Esophageal artery/vein | 901.9 | 2–3 | |
Hemiazygos vein | 901.89 | 2–3 | |
Unnamed artery/vein | 901.9 | 2–3 | |
II | Azygous vein | 901.89 | 2–3 |
Internal jugular vein | 900.1 | 2–3 | |
Subclavian vein | 901.3 | 3–4 | |
Innominate vein | 901.3 | 3–4 | |
III | Carotid artery | 900.01 | 3–5 |
Innominate artery | 901.1 | 3–4 | |
Subclavian artery | 901.1 | 3–4 | |
IV | Thoracic aorta, descending | 901.0 | 4–5 |
Inferior vena cava (intrathoracic) | 902.10 | 3–4 | |
Pulmonary artery, primary intraparenchymal branch | 901.41 | 3 | |
Pulmonary vein, primary intraparenchymal branch | 901.42 | 3 | |
V | Thoracic aorta, ascending and arch | 901.0 | 5 |
Superior vena cava | 901.2 | 3–4 | |
Pulmonary artery, main trunk | 901.41 | 4 | |
Pulmonary vein, main trunk | 901.42 | 4 | |
VI | Uncontained total transection of thoracic aorta or pulmonary hilum | 901.0 | 5 |
901.41 | 4 | ||
901.42 | 4 |
a Increase one grade for multiple grade III or IV injuries if >50% circumference. Decrease one grade for grade IV and V injuries if <25% circumference.
b Based on most accurate assessment at autopsy, operation, or radiologic study.
Several authors have cited the repair of a stab wound of the ascending aorta in 1922 by Dfhanelidze in Russia as one of the earliest examples of a repair of a great vessel injury. Emergency ligation of injured great vessels and delayed repair of aneurysms and arteriovenous fistulas of the same were described in reports after World War II. The earliest civilian reports on techniques of exposure and repair of great vessel trauma (exclusive of blunt rupture of the thoracic aorta) were from Johns Hopkins and Baylor College of Medicine.
If wounds to the heart and coronary arteries (#553) are excluded from the 30-year review of 5760 cardiovascular injuries at Ben Taub Hospital in Houston, injuries to the great vessels accounted for approximately 10% of cases. The mechanism of these injuries is overwhelmingly penetrating (90%). Of patients who undergo emergent thoracotomy after penetrating thoracic injury, less than one-third have a great vessel injury as the cause of hemorrhage.
Blunt injuries to the great vessels (exclusive of the descending thoracic aorta, which will be described in Chapter 17 of this textbook), are uncommon. When they do occur, these injuries almost always involve the proximal innominate or subclavian artery. In an older series describing 43 patients with injury to the innominate artery from 1960 to 1992, a blunt mechanism was the cause in 17% of patients. Another even-older series on 93 patients with subclavian vascular trauma from 1955 to 1978 noted that only 2% of patients had a blunt mechanism of injury. Both of these reviews, however, included periods of time when shoulder-harness restraints either were not available on passenger vehicles or were not commonly used.
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