1. Learning Objectives Understand basic statistics of thoracic trauma
Recognize potential pitfalls in the acute management of thoracic injuries
Recognize the types and mechanisms of life threatening thoracic injuries
Comprehend initial assessment and management of various thoracic injuries
Understand secondary management of thoracic injuries and some unique challenges they can impose
There are 4 major objectives to this module:
The first is to understand that statistics of the epidemiology and incidence of thoracic injuries in the US
The second objective is to recognize that there are various types of thoracic injuries that are a function of the nature and mechanism of the inflicting agent. We will cover thoracic trauma divided into sub-categories of blunt trauma – which can be further divided into deceleration injury such as sustained in falls and MVA and penetrating trauma which is sub-divided by injuring agent also into GSW and stab wounds.
The third objective is to comprehend the initial assessment and management of thoracic injuries with a special understanding that there are unique problems associated with thoracic trauma that is different from abdominal trauma and the cause of similar hemodynamic parameters can be different with thoracic injuries.
The fourth objective is to understand secondary management of the various thoracic injuries with a special emphasis on imaging, work-up and definitive surgery.

2. Key Questions?
What are some of the unique challenges and pitfalls posed by thoracic injuries?
How can we identify acute life threatening thoracic injuries early and treat them appropriately to assure patient survivorship?
When do thoracic injuries take precedence over other injuries in the primary survey?
Which thoracic injuries can be treated during the secondary survey after other issues have been addressed?
We will address several key questions during this module. These questions focus on the unique challenges that are posed by thoracic injuries and how we can identify and treat the life threatening injuries within the golden time period that will save lives. Other questions we will address are how to prioritize thoracic trauma in the multiple injury patients – which need to come first and which can be put off until the secondary survey issues are addressed.

3. Statistics
Thoracic trauma accounts for 20-25% deaths due to injury in US
16,000 deaths per year due to chest injury
Rate of thoracic injuries 12 per million population per day (~30/day in Miami- Dade County)
About 50% fatalities of MVA have sustained some chest injury
Ratio penetrating/non penetrating variable usually about 75-85% blunt injuries
The approximate rate of thoracic trauma in the United States is 12 per million population per day - and 20-25% of deaths due to trauma are attributed to thoracic injuries. It is estimated that thoracic trauma is responsible of approximately 16,000 deaths per year in the United States. The incidence has increased rapidly in this century of high-speed vehicular travel. Immediate deaths are usually due to major disruption of the heart or of great vessels. Early deaths due to thoracic trauma occurring within 30 minutes to 3 hours after the injury are usually secondary to cardiac tamponade, airway obstruction and aspiration, or rupture of thoracic aortic tears that have been temporarily contained. Two thirds of these patients reach the hospital prior to death. Only 10-15% of blunt trauma require thoracic surgery, and 15-30% of the penetrating chest trauma require open thoracotomy. Overall, about 85% of patients with thoracic trauma can be managed without surgical treatment.

4. Management – Primary Survey Always consider mechanical factors
Airway/spinal stabilization
Trachea, bronchial disruption
Breathing
Chest wall integrity, pneumothorax, flail
Pulmonary contusions, 02 diffusion block
Circulation
Tamponade, hemothorax, tension pneumothorax
Cardiac, great vessel injury
The evaluation of the patient's chest trauma is only a part of the total assessment and the basic ABC’s of the primary survey and resuscitation cannot be overlooked. It is important to keep several special factors in mind when dealing with a patient with potential thoracic injuries because thoracic injuries are severe and potentially lethal and the diagnosis and therapy go hand in hand as there can be unique mechanical factors that cause the alterations in vital signs. Injuries such as tension pneumothorax can be rapidly fatal if missed but treated and cured in a matter of moments when recognized.
In unstable and critical patients quick decisions based on check of the following vital signs are required. Airway patency: in the initial survey is mandatory to control the airway patency. Patency of the airway does not necessarily assure adequate ventilation in patients with chest injuries unless the airway is in continuity with the lungs. Patients may be ventilated without oxygenating their blood with chest injuries due to pulmonary contusions or airway disruption. All the airway manipulations must be performed with respect to potential cervical spinal injuries. Breathing: in order to know if patient is breathing is necessary to check respiratory movement, and their extension which can be compromised by chest wall integrity. Cyanosis appears very late in hypoxia due to a thoracic trauma because in shocky patients the skin blood flow depends on blood redistribution in the body. Circulation: the state of the circulation is evaluated by assessing patient's pulses (radial, carotid or femoral). The blood pressure is evaluated by width of pulse. In hypovolemic shock radial pulse becomes small; may be absent when blood pressure is below 60 mm/Hg. In thoracic trauma is important to assess the neck veins that are flat in hypovolemia are distended when there is cardiac tamponade. But if cardiac tamponade is associated with hypovolemic shock distension of the neck veins may be absent. Thoracic cavity is constituted from two structures: the first, rigid, comprehending the rib cage, clavicle, sternum, scapula and the second comprehending respiratory muscles. Adequate ventilation and oxygenation depends on an intact chest wall. Significant injury with fracture and muscular disruption may allow direct injury to the underlying lungs, heart, great vessels and upper abdominal viscera. In addition, respiration may be seriously impaired by effective or paradoxical motion of a portion of the thoracic cage (as in flail chest) and the result is respiratory insufficiency.

5. Immediate Life Threatening Thoracic Injuries: Cardiac Tamponade
Pathophysiology – intra-pericardial pressure exceeds filling pressure of right heart
Impairs venous return and cardiac filling leading to hypotension, narrow pulse pressure, PEA
“Beck’s Triad” - hypotension, neck vein distension, distant/absent heart tones
Signs and symptoms masked by hypovolemia
Treat with immediate volume replacement to ↑ CVP, pericardial decompression
This patient is a young man who presented with a penetrating knife wound to the left second interspace in a parasternal location. This is a great x-ray
Cardiac tamponade is usually due to penetrating cardiac injuries and are a leading cause of traumatic death in urban areas and are generally more severe than blunt injuries. Patients with penetrating wounds of the heart can be classified in 3 general groups:
1. patients who have received extensive lacerations or large-caliber gunshot wounds, that die almost immediately, as a result of rapid and voluminous blood loss;
2. patient with small wounds of the heart, caused by ice picks, knives or other small agents who because of the development of cardiac tamponade, reach the hospital alive. Cardiac tamponade, by bringing pressure to bear on the bleeding heart wall, also plays an important role in controlling the hemorrhage;
3. patient with associated serious injuries in the chest and/or elsewhere in the body which, in themselves, may contribute to death.
The condition of the patient, when he is admitted to the hospital, must not be used as an index of the severity of the injury. There are moribund patients with no blood pressure and nonperceptible pulse, who survive operation and recover; on the other hand there are patients in fair condition, with a systolic blood pressure ranging from 70 mmHg to normal and fair-to-good pulse, who die before surgery. The immediate cause of death is either exanguination, cardiac tamponade or interference with the conduction mechanism. Diagnosis generally is easy if the physician maintains a high degree of suspicion of heart injury in every chest wound he encounters. The safest approach is to remove the patient's clothing and survey the entire body surface quickly for evidence of multiple injuries. Auscultation of the thorax is performed specifically to evaluate the clarity of heart tones and breath sounds. Muffled heart tones are an indication of blood in the pericardium. A systolic - to diastolic gradient of less then 30 mmHg, associated with hypotension is consistent with cardiac tamponade. Neck veins are distended. Central venous pressure is elevated. The X-ray film may demonstrate a widening of the cardiac silhouette. The ultrasound scan shows presence of blood in pericardial space. Electrocardiograph is not particularly helpful. Prompt definitive therapy is imperative. This includes antishock therapy, pericardiocentesis (possibly under U.S. guide), emergency thoracotomy and suture of the wound.
Treat with VOLUME immediately to raise the CVP greater than the intrapericardial pressure and shock trousers then proceed with percutaneous and ultimately surgical decompression of the pericardium.
Cardiac tamponade requires prompt recognition and treatment. Signs and symptoms range from rarely stable to Beck’s triad of hypotension, CVP above 12cc of water and muffled heart sounds – all three findings are present in fewer than 40% of patients with tamponade. An elevated CVP is the most significant diagnostic finding. Only 60ml of haemopericardium is necessary for a tamponade to occur in adults. A vicious cycle is set in motion i.e.
 LVEDV   S.V.   CO  compensatory tachycardia   cardiac work   O2 demand  hypoxia and lactic acidosis.
An enlarged cardiac silhouette on CXR and / pericardial effusion as demonstrated by echocardiography help to confirm the clinical suspicion and diagnosis.

6. Immediate Life Threatening Thoracic Injuries: Tension Pneumothorax
Suspect with any injury
High intra-thoracic, extra- pulmonary pressure
Absent breath sounds, shift of trachea, hypotension
Can be worsened with intubation and + pressure
Treat symptoms → immediate decompression
Tension pneumothorax develops when air enters the pleural space but cannot exit and as a result there is a progressively increasing intrathoracic pressure in the affected hemithorax resulting in impaired central venous return and mediastinal shift. Air enters pleural cavity through lung wound or ruptured bleb (or occasionally via penetrating chest wound) with valve like opening. Ipsilateral lung collapse and mediastinum shifts to opposite side compressing controlateral lung and impairing its ventilating capacity. Clinically, the patient experiences dyspnea, complains of chest pains, and becomes cyanotic because of shunting in the collapse of lung and has hemodynamic instability because decrease is venous return for endopleural hypertension. The presence of hyper-resonance and the absence of breath sounds, together with X-ray examination, should be useful in confirming the cause of the emergency. A chest X-ray film indicates that the trachea and mediastinum are deviated to the side opposite the tension pneumothorax, while on the ipsilateral side intercostal spaces are widened and the diaphragm is pushed downward. The emergency require immediate thoracostomy with underwater-seal drainage. If the lung does not fully re-expand after tube thoracostomy and there is a large ongoing air leak the airways should be evaluated bronchoscopically to exclude a major injury. However, in most cases, no further treatment for tension pneumothorax will be required after chest tube insertion.

7. Crucial 1° Survey Differential Dx: Cardiac Tamponade vs
Crucial 1° Survey Differential Dx: Cardiac Tamponade vs. Tension Pneumothorax
Clinical Sign
Cardiac Tamponade
Tension Pneumothorax
Blood Pressure
Cardiac Tones
Breath Sounds
Neck Veins
Respirations
Treatment
Low (PEA)
Low 
Muffled
Normal 
Normal
Absent - collapsed side
Identifying cardiac tamponade vs. tension pneumothorax is a critical differential diagnosis that must be made accurately and almost instantaneously since both are treatable and curable injuries. Both present with low or absent blood pressure (PEA) but the physiology is opposite since tamponade is due to compression of the right heart and tension pneumothorax is due to absent filling of the right heart. The major differentials relate to etiology – the neck veins are distended in tamponade since blood is trying to enter the heart and cant and flat in tension pneumothorax since there is no blood in the right heart. An important pitfall in this differential finding is that in hypovolemic patients neck veins can be flat in both injuries. Cardiac tones are usually muffled in tamponade but this can be difficult to appreciate in the noisy trauma areas and breath sounds are usually absent on the affected side in tension pneumothorax but this can also be had to hear. Generally patients are very tachypnic when alert with a tension pneumothorax but patients in shock are all tachypnic so this can also be an unreliable indicator. Both can be worsened by positive pressure ventilation since both are functions of right heart physiology and the treatment for both is a needle – one into the chest the other into the pericardium. 
Distended (flat in hypovolemia)
Flat
± Normal
Tachypnea
Needle/drain pericardium
Needle/tube chest

8. Immediate Life Threatening Thoracic Injuries: Primary Survey
This is a list of the immediate causes of death following chest injuries. Each will be discussed in more detail on the following slides.

9. Immediate Life Threatening Thoracic Injuries: Primary Survey
Cardiac disruption/tamponade
Tracheal disruption
Open pneumothorax
Tension pneumothorax
Massive hemothorax (great vessels, pulmonary vessels)
This is a list of the immediate causes of death following chest injuries. Each will be discussed in more detail on the following slides.

10. Immediate Life Threatening Thoracic Injuries: Cardiac Trauma
This patient is a young man who presented with a penetrating knife wound to the left second interspace in a parasternal location. This is a great x-ray
Cardiac tamponade is usually due to penetrating cardiac injuries and are a leading cause of traumatic death in urban areas and are generally more severe than blunt injuries. Patients with penetrating wounds of the heart can be classified in 3 general groups:
1. patients who have received extensive lacerations or large-caliber gunshot wounds, that die almost immediately, as a result of rapid and voluminous blood loss;
2. patient with small wounds of the heart, caused by ice picks, knives or other small agents who because of the development of cardiac tamponade, reach the hospital alive. Cardiac tamponade, by bringing pressure to bear on the bleeding heart wall, also plays an important role in controlling the hemorrhage;
3. patient with associated serious injuries in the chest and/or elsewhere in the body which, in themselves, may contribute to death.
The condition of the patient, when he is admitted to the hospital, must not be used as an index of the severity of the injury. There are moribund patients with no blood pressure and nonperceptible pulse, who survive operation and recover; on the other hand there are patients in fair condition, with a systolic blood pressure ranging from 70 mmHg to normal and fair-to-good pulse, who die before surgery. The immediate cause of death is either exanguination, cardiac tamponade or interference with the conduction mechanism. Diagnosis generally is easy if the physician maintains a high degree of suspicion of heart injury in every chest wound he encounters. The safest approach is to remove the patient's clothing and survey the entire body surface quickly for evidence of multiple injuries. Auscultation of the thorax is performed specifically to evaluate the clarity of heart tones and breath sounds. Muffled heart tones are an indication of blood in the pericardium. A systolic - to diastolic gradient of less then 30 mmHg, associated with hypotension is consistent with cardiac tamponade. Neck veins are distended. Central venous pressure is elevated. The X-ray film may demonstrate a widening of the cardiac silhouette. The ultrasound scan shows presence of blood in pericardial space. Electrocardiograph is not particularly helpful. Prompt definitive therapy is imperative. This includes antishock therapy, pericardiocentesis (possibly under U.S. guide), emergency thoracotomy and suture of the wound.
Treat with VOLUME immediately to raise the CVP greater than the intrapericardial pressure and shock trousers then proceed with percutaneous and ultimately surgical decompression of the pericardium.
Cardiac tamponade requires prompt recognition and treatment. Signs and symptoms range from rarely stable to Beck’s triad of hypotension, CVP above 12cc of water and muffled heart sounds – all three findings are present in fewer than 40% of patients with tamponade. An elevated CVP is the most significant diagnostic finding. Only 60ml of haemopericardium is necessary for a tamponade to occur in adults. A vicious cycle is set in motion i.e.
 LVEDV   S.V.   CO  compensatory tachycardia   cardiac work   O2 demand  hypoxia and lactic acidosis.
An enlarged cardiac silhouette on CXR and / pericardial effusion as demonstrated by echocardiography help to confirm the clinical suspicion and diagnosis.

11. Immediate Life Threatening Thoracic Injuries: Cardiac Tamponade
The first chest film is a great x-ray to show all the classic examples of cardiac tamponade with the huge mediastinal shadow of the pericardium, displaced trachea (note clavicles are aligned so the endotracheal tube is truly pushed off to the right) and opacity of the left hemithorax. But DON’T get fooled but this – life threatening tamponade can present with an x-ray that doesn’t show much at all and as a matter of fact the next patient was moribund and virtually DOA.
The x-ray on the right is a young man who presented with a penetrating knife wound to the left second interspace in a parasternal location. Cardiac tamponade is usually due to penetrating cardiac injuries and are a leading cause of traumatic death in urban areas and are generally more severe than blunt injuries. Patients with penetrating wounds of the heart can be classified in 3 general groups:
1. patients who have received extensive lacerations or large-caliber gunshot wounds, that die almost immediately, as a result of rapid and voluminous blood loss;
2. patient with small wounds of the heart, caused by ice picks, knives or other small agents who because of the development of cardiac tamponade, reach the hospital alive. Cardiac tamponade, by bringing pressure to bear on the bleeding heart wall, also plays an important role in controlling the hemorrhage;
3. patient with associated serious injuries in the chest and/or elsewhere in the body which, in themselves, may contribute to death.
The condition of the patient, when he is admitted to the hospital, must not be used as an index of the severity of the injury. There are moribund patients with no blood pressure and non-perceptible pulse, who survive operation and recover such as the young guy in the x-ray on the right; on the other hand there are patients in fair condition, with a systolic blood pressure ranging from 70 mmHg to normal and fair-to-good pulse, who die before surgery. The immediate cause of death is either exsanguinations, cardiac tamponade or interference with the conduction mechanism. Diagnosis generally is easy if the physician maintains a high degree of suspicion of heart injury in every chest wound he encounters. The safest approach is to remove the patient's clothing and survey the entire body surface quickly for evidence of multiple injuries. Auscultation of the thorax is performed specifically to evaluate the clarity of heart tones and breath sounds. Muffled heart tones are an indication of blood in the pericardium. A systolic - to diastolic gradient of less then 30 mmHg, associated with hypotension is consistent with cardiac tamponade. Neck veins are distended. Central venous pressure is elevated. The X-ray film may demonstrate a widening of the cardiac silhouette. The ultrasound scan shows presence of blood in pericardial space. Electrocardiograph is not particularly helpful. Prompt definitive therapy is imperative. This includes antishock therapy, pericardiocentesis (possibly under ultrasound guide), emergency thoracotomy and suture of the wound.

12. Distribution of Penetrating Cardiac Trauma

13. ED Thoracotomy (EDT)

14. Rationale for EDT
Resuscitate agonal patient with penetrating cardiothoracic injuries
Evacuation of pericardial tamponade
Control intra-thoracic hemorrhage
Perform open CPR
Repair cardiac injuries
Apply x-clamp to thoracic aorta
Apply hilar x-clamp to lung
Aspirate air embolism
Asensio JA, et.al. An evidence-based critical appraisal of emergency department thoracotomy, Evidence-Based Surgery 2003: 1(1)

15. Indications for ED Thoracotomy
1. Salvageable post-injury cardiac arrest:
 Patients sustaining witnessed penetrating trauma with < 15 minutes of pre-hospital CPR
 Patients sustaining witnessed blunt trauma with < 5 minutes of pre-hospital CPR
Persistent severe post-injury hypotension (SBP<60mmHg) due to:
 Cardiac tamponade
 Hemorrhage – intra-thoracic, intra-abdominal, extremity, cervical
 Air embolism
     
C Clay Cothren and Ernest E Moore Emergency department thoracotomy for the critically injured patient: Objectives, indications, and outcomes Department of Surgery, Denver Health Medical Center and the University of Colorado Health Sciences Center, Denver, CO, USA World Journal of Emergency Surgery 2006, 1:4 

16. Contra-indications for ED Thoracotomy
1. Penetrating trauma: CPR >15 minutes and no signs of life (pupillary response, respiratory effort, motor activity:
2. Blunt trauma: CPR > minutes and no signs of life or asystole
     
C Clay Cothren and Ernest E Moore Emergency department thoracotomy for the critically injured patient: Objectives, indications, and outcomes Department of Surgery, Denver Health Medical Center and the University of Colorado Health Sciences Center, Denver, CO, USA World Journal of Emergency Surgery 2006, 1:4 

17. Emergency Department Thoracotomy: Outcomes Review of 42 published series
Survivors/ Total EDT
Survivors/ Penetrating Trauma
Survivors/ Blunt Trauma
537/8744 (6.1%)
500/8619 (5.8%)
35/7945 (0.44%)
Asensio JA, et.al. An evidence-based critical appraisal of emergency department thoracotomy, Evidence-Based Surgery 2003: 1(1)

18. Application of Aortic Cross Clamp

19. Esophagus
Aorta
Spine
Diaphragm

20. Vertical Pericardial Incision
LIMA

21. Internal Paddles for Direct Cardioversion

22. Laceration Adjacent to Coronary Artery

23. Laceration Adjacent to Coronary Artery

24. Coronary Artery Laceration

25. Ventricular Lacerations and Repairs

26. Ventricular Lacerations and Repairs

27. Ventricular Lacerations and Repairs

28. Atrial Lacerations and Repairs

29. Sub-xyphoid Trans-diaphragmatic Pericardial Window

30. Sub-xyphoid Trans-diaphragmatic Pericardial Window

31. Blunt Cardiac Injuries

32. Blunt Thoracic Trauma: Cardiac Contusions
Blunt anterior chest trauma
Acute injury pattern (anterior wall: ↑ST’s I, aVL, V2-V4, ↓II,III, aVF), AF, BBB
W/U & Rx acute myocardial infarction, inotropes
Watch for & treat PVC’s aggressively (K+, temp)
Cardiac echo to assess wall motion, valves

33. Immediate Life Threatening Thoracic Injuries: Massive Hemothorax
Can be due to blunt or penetrating injuries
Immediate volume replacement, compression suit and OR
Caution with CVP lines
Massive hemothorax is common in both penetrating and blunt chest injuries. Patients who sustain acute hemothorax are at risk for hemodynamic instability due to loss of intravascular volume and compromised central venous return due to increased intrathoracic pressure. Lung compression due to massive blood accumulation may also cause respiratory compromise. Sources of hemothorax are: lung, intercostal vessels, internal mammary artery, thoracicoacromial artery, lateral thoracic artery, mediastinal great vessels, heart, abdominal structures (liver, spleen) when diaphragmatic hernia. The diagnosis is readily made from the clinical picture and X-ray evidence of fluid in the pleural space. Primary thoracentesis is carried out to confirm the diagnosis. Optimal therapy consists of the placement of a large (36 French) chest tube. A moderate size hemothorax ( ml) that stops bleeding after thoracostomy can generally be treated by closed drainage alone. However, a hemothorax of greater than 1500 to 2000 ml as with continued bleeding of more than 100 to 200 ml per hour is an indication for emergency thoracotomy or thoracoscopy. A small percentage of hemothoraces proceed to clot and cannot be evacuated by thoracentesis. Massive clots may lead to respiratory difficulty and infection, and should be evacuated surgically. Small clots will probably be resorbed and do not require operative removal.
Hemothorax is common in both penetrating and non-penetrating injures to the chest. If the hemorrhage is severe, it may not only cause hypovolemic shock but also dangerously reduces vital capacity by compressing the lung on the involved side. Persistent hemorrhage usually arises from an intercostal or internal thoracic (internal mammary) artery and less frequently from the major hylar vessels. Bleeding from the lung generally stops within a few minutes, although initially it may be profuse. In some cases hemothorax may come from a wound of the heart or from abdominal structures such as the liver or spleen if the diaphragm has been lacerated. Hypovolemic shock and hemomediastinum can derive from a thoracic great vessels injury that may be result of penetrating or blunt trauma. The most common etiology is penetrating trauma; however, the descending thoracic aorta, the innominate artery, the pulmonary veins, and the vena cavae are susceptible to rupture for blunt trauma. 

34. Application of Pulmonary Hilar Cross Clamp

35. Pulmonary Tractotomy
Lung-Sparing Surgery After Penetrating Trauma Using Tractotomy, Partial Lobectomy, and Pneumonorrhaphy
George C. Velmahos, MD, PhD; Craig Baker, MD; Demetrios Demetriades, MD, PhD; Jeremy Goodman; James A. Murray, MD; Juan A. Asensio, MD
Arch Surg. 1999;134:

36. Pulmonary Tractotomy
Lung-Sparing Surgery After Penetrating Trauma Using Tractotomy, Partial Lobectomy, and Pneumonorrhaphy
George C. Velmahos, MD, PhD; Craig Baker, MD; Demetrios Demetriades, MD, PhD; Jeremy Goodman; James A. Murray, MD; Juan A. Asensio, MD
Arch Surg. 1999;134:

37. Immediate Life Threatening Thoracic Injuries: Tracheal Disruption
Massive subcutaneous emphysema in chest wall – displaced trachea
Cervical, facial sub- cutaneous emphysema
Hemoptysis
Blunt injuries almost always within 1” carina
Most tracheal injuries are cervical and range from crush injuries to compete tracheal separation. CXR don’t make the diagnosis but there are some things of note on this x-ray such as the massive emphysema in the neck and chest wall and even sub-diaphragmatic regions and also not the separation of the tracheal shadow – note ETT – from the esophagus – note NG tube. · If endotracheal intubation is not possible, a surgical airway should be obtained · Primary repair of tracheal lacerations or separation should be performed, if possible · Blunt trauma typically causes a circumferential laceration of either main bronchus with complete separation · Only 50% of patients will have a pneumothorax with this injury, and hemothorax is uncommon · Only 1/3 of patients are diagnosed in the first 24 hours, and only 1/2 within the first month · Early repair is the preferred treatment if the diagnosis is made, and requires thoracotomy with intubation of the uninjured bronchus · Late strictures from incomplete tears or parenchymal isolation from complete tears can be repaired with bronchoplastic procedures, but may require pulmonary resection.
Laryngotracheal injuries constitute only a small fraction of admissions in a major trauma centre. The frequency has been reported to be as low as 0.3 percent. However, mortality is reported as high as 24 percent. Complete disruption of trachea is amongst the rarest injuries with only a few cases reported in literature. Seuvre (cited by Papamicheal is credited with the first description of traumatic tracheal disruption. Direct blows are more likely to be associated with fractures of cartilaginous frame work of the larynx(7). The signs and symptoms are often subtle even in complete transections of trachea. The two ends may be held in close approximation by peritracheal connective tissue and soft tissues of the neck.
Clinical features include subcutaneous surgical emphysema, pneumothorax, respiratory distress, hemoptysis and loss of palpable landmarks8. Most of these features were present in our cases except pneumothorax which was seen only in the first case. The signs and symptoms are non specific and correlate poorly with the severity of the underlying injury(9). Therefore, a high degree of suspicion and a more aggressive approach towards diagnosis and management is required as delayed treatment may prove fatal as in our second case.
Neck and chest radiographs though essential cannot be completely relied upon. CT scan or MRI if available can give accurate diagnosis, otherwise direct laryngoscopy and bronchoscopy can be utilized to confirm the diagnosis as delay leads to a poor prognosis.
Management includes, tracheostomy and early surgical repair. The best results are obtained with a complete repair of the larynx and trachea with end to end anastomosis of disrupted trachea which avoids a permanent tracheostomy and patient retains a good voice. The second best option is a permanent tracheostomy which means a loss of voice.

38. Blunt Thoracic Trauma: Tracheobronchial Injury
2° Blunt injury
Persistent pneumothorax
Huge air leak
Rare injury 2-3% of survivors MVA
Definitive repairs with pleural flap
Tracheobronchial tear can be caused by the following:
Shearing forces between the fixed carina or proximal bronchus and the mobile distal bronchi/lungs in a deceleration injury
Rapid anteroposterior compression of the chest causing lateral traction on the lungs and tearing of the bronchus from the fixed carina
Rupture resulting from an abrupt increase in pressure against a closed glottis
Compression of the trachea between the sternum and spinal column
Blunt trauma to the cervical trachea
Necrosis resulting from compromised mucosal blood flow after overinflation of an endotracheal tube cuff
Perforation by a stylet or endotracheal tube
Other penetrating injury
Tracheobronchial injury occurs in % of major blunt trauma patients and is found in % of trauma-related autopsies. Tracheobronchial tear also has been reported in 18% of autopsies after emergency intubation; however, since minor injuries often are not identified, the actual frequency of tracheobronchial tear may remain unknown. Death occurs in approximately 30% of patients with tracheobronchial tears, with 50% of fatalities occurring within the first hour. Mortality may be related to an inadequate airway, tension pneumothorax, occlusion of the airway by protrusion of the esophagus into the tear, or accompanying injuries. In two thirds of survivors, diagnosis is delayed, occasionally for many years, resulting in complications such as airway stenosis, atelectasis, pneumonia, mediastinitis, sepsis, and decreased pulmonary capacity. Blunt trauma accounts for the preponderance of all tracheobronchial injuries. Tracheobronchial injury from blunt trauma is 3 times more common in males, because blunt trauma involves males much more often than females. Women have a greater chance of iatrogenic injury from endotracheal tubes, because their tracheas are smaller.
Clinical signs of tracheobronchial tear include the following:
Dyspnea
Cough
Hemoptysis
Cyanosis
Cervical subcutaneous emphysema
Tracheal shift
Persistent pneumothorax following satisfactory placement of a thoracostomy tube
Signs of airway obstruction
Immediate treatment depends on the patient's condition and associated injuries. At a minimum, emergency bronchoscopic confirmation of the diagnosis and location is important if tracheobronchial tear is suggested. This may aid in placing the endotracheal tube cuff beyond the injury or selectively intubating the unaffected bronchus.

39. Immediate Life Threatening Thoracic Injuries: Tracheal Disruption
Most tracheal injuries are cervical and range from crush injuries to compete tracheal separation. CXR don’t make the diagnosis but there are some things of note on this x-ray such as the massive emphysema in the neck and chest wall and even sub-diaphragmatic regions and also not the separation of the tracheal shadow – note ETT – from the esophagus – note NG tube. · If endotracheal intubation is not possible, a surgical airway should be obtained · Primary repair of tracheal lacerations or separation should be performed, if possible · Blunt trauma typically causes a circumferential laceration of either main bronchus with complete separation · Only 50% of patients will have a pneumothorax with this injury, and hemothorax is uncommon · Only 1/3 of patients are diagnosed in the first 24 hours, and only 1/2 within the first month · Early repair is the preferred treatment if the diagnosis is made, and requires thoracotomy with intubation of the uninjured bronchus · Late strictures from incomplete tears or parenchymal isolation from complete tears can be repaired with bronchoplastic procedures, but may require pulmonary resection.
Laryngotracheal injuries constitute only a small fraction of admissions in a major trauma centre. The frequency has been reported to be as low as 0.3 percent. However, mortality is reported as high as 24 percent. Complete disruption of trachea is amongst the rarest injuries with only a few cases reported in literature. Seuvre (cited by Papamicheal is credited with the first description of traumatic tracheal disruption. Direct blows are more likely to be associated with fractures of cartilaginous frame work of the larynx(7). The signs and symptoms are often subtle even in complete transections of trachea. The two ends may be held in close approximation by peritracheal connective tissue and soft tissues of the neck.
Clinical features include subcutaneous surgical emphysema, pneumothorax, respiratory distress, hemoptysis and loss of palpable landmarks8. Most of these features were present in our cases except pneumothorax which was seen only in the first case. The signs and symptoms are non specific and correlate poorly with the severity of the underlying injury(9). Therefore, a high degree of suspicion and a more aggressive approach towards diagnosis and management is required as delayed treatment may prove fatal as in our second case.
Neck and chest radiographs though essential cannot be completely relied upon. CT scan or MRI if available can give accurate diagnosis, otherwise direct laryngoscopy and bronchoscopy can be utilized to confirm the diagnosis as delay leads to a poor prognosis.
Management includes, tracheostomy and early surgical repair. The best results are obtained with a complete repair of the larynx and trachea with end to end anastomosis of disrupted trachea which avoids a permanent tracheostomy and patient retains a good voice. The second best option is a permanent tracheostomy which means a loss of voice.

40. Immediate Life Threatening Thoracic Injuries: Tracheal Disruption
Most tracheal injuries are cervical and range from crush injuries to compete tracheal separation. CXR don’t make the diagnosis but there are some things of note on this x-ray such as the massive emphysema in the neck and chest wall and even sub-diaphragmatic regions and also not the separation of the tracheal shadow – note ETT – from the esophagus – note NG tube. · If endotracheal intubation is not possible, a surgical airway should be obtained · Primary repair of tracheal lacerations or separation should be performed, if possible · Blunt trauma typically causes a circumferential laceration of either main bronchus with complete separation · Only 50% of patients will have a pneumothorax with this injury, and hemothorax is uncommon · Only 1/3 of patients are diagnosed in the first 24 hours, and only 1/2 within the first month · Early repair is the preferred treatment if the diagnosis is made, and requires thoracotomy with intubation of the uninjured bronchus · Late strictures from incomplete tears or parenchymal isolation from complete tears can be repaired with bronchoplastic procedures, but may require pulmonary resection.
Laryngotracheal injuries constitute only a small fraction of admissions in a major trauma centre. The frequency has been reported to be as low as 0.3 percent. However, mortality is reported as high as 24 percent. Complete disruption of trachea is amongst the rarest injuries with only a few cases reported in literature. Seuvre (cited by Papamicheal is credited with the first description of traumatic tracheal disruption. Direct blows are more likely to be associated with fractures of cartilaginous frame work of the larynx(7). The signs and symptoms are often subtle even in complete transections of trachea. The two ends may be held in close approximation by peritracheal connective tissue and soft tissues of the neck.
Clinical features include subcutaneous surgical emphysema, pneumothorax, respiratory distress, hemoptysis and loss of palpable landmarks8. Most of these features were present in our cases except pneumothorax which was seen only in the first case. The signs and symptoms are non specific and correlate poorly with the severity of the underlying injury(9). Therefore, a high degree of suspicion and a more aggressive approach towards diagnosis and management is required as delayed treatment may prove fatal as in our second case.
Neck and chest radiographs though essential cannot be completely relied upon. CT scan or MRI if available can give accurate diagnosis, otherwise direct laryngoscopy and bronchoscopy can be utilized to confirm the diagnosis as delay leads to a poor prognosis.
Management includes, tracheostomy and early surgical repair. The best results are obtained with a complete repair of the larynx and trachea with end to end anastomosis of disrupted trachea which avoids a permanent tracheostomy and patient retains a good voice. The second best option is a permanent tracheostomy which means a loss of voice.

41. Immediate Life Threatening Thoracic Injuries: Tracheal Disruption
Blunt or penetrating trauma (extrinsic compression from hematoma)
Intra/extra thoracic location (supraglotic, glotic, subglotic
Presentation
• Massive, sometimes uncontrollable air leak
Stridor, acute respiratory distress, Δ voice
Neck, upper chest subcutaneous emphysema – often massive and disfiguring
Acutely manage with deep intubation (beyond injury), scope, sometimes tracheostomy
Most tracheal injuries are cervical and range from crush injuries to compete tracheal separation · If endotracheal intubation is not possible, a surgical airway should be obtained · Primary repair of tracheal lacerations or separation should be performed, if possible · Blunt trauma typically causes a circumferential laceration of either main bronchus with complete separation · Only 50% of patients will have a pneumothorax with this injury, and hemothorax is uncommon · Only 1/3 of patients are diagnosed in the first 24 hours, and only 1/2 within the first month · Early repair is the preferred treatment if the diagnosis is made, and requires thoracotomy with intubation of the uninjured bronchus · Late strictures from incomplete tears or parenchymal isolation from complete tears can be repaired with bronchoplastic procedures, but may require pulmonary resection.
Laryngotracheal injuries constitute only a small fraction of admissions in a major trauma centre. The frequency has been reported to be as low as 0.3 percent. However, mortality is reported as high as 24 percent. Complete disruption of trachea is amongst the rarest injuries with only a few cases reported in literature. Seuvre (cited by Papamicheal is credited with the first description of traumatic tracheal disruption. Direct blows are more likely to be associated with fractures of cartilaginous frame work of the larynx(7). The signs and symptoms are often subtle even in complete transections of trachea. The two ends may be held in close approximation by peritracheal connective tissue and soft tissues of the neck.
Clinical features include subcutaneous surgical emphysema, pneumothorax, respiratory distress, hemoptysis and loss of palpable landmarks8. Most of these features were present in our cases except pneumothorax which was seen only in the first case. The signs and symptoms are non specific and correlate poorly with the severity of the underlying injury(9). Therefore, a high degree of suspicion and a more aggressive approach towards diagnosis and management is required as delayed treatment may prove fatal as in our second case.
Neck and chest radiographs though essential cannot be completely relied upon. CT scan or MRI if available can give accurate diagnosis, otherwise direct laryngoscopy and bronchoscopy can be utilized to confirm the diagnosis as delay leads to a poor prognosis.
Management includes, tracheostomy and early surgical repair. The best results are obtained with a complete repair of the larynx and trachea with end to end anastomosis of disrupted trachea which avoids a permanent tracheostomy and patient retains a good voice. The second best option is a permanent tracheostomy which means a loss of voice.

42. Immediate Life Threatening Thoracic Injuries: Open Pneumothorax
“Sucking” chest wound
Respiratory distress
Preferential path of air when hole ≥ ⅔ diameter of trachea
Cover 3 sides
Chest tube drainage and auto-transfusion when available
An open pneumothorax occurs when there is a pneumothorax associated with a chest wall defect, such that the pneumothorax communicates with the exterior.
During inspiration, when a negative intra-thoracic pressure is generated, air is entrained into the chest cavity not through the trachea but through the hole in the chest wall. This is because the chest wall defect is much shorter than the trachea, and hence provides less resistance to flow. Once the size of the hole is more than 0.75 times the size of the trachea, air preferentially enters through the thoracic cavity.
This results in inadequate oxygenation and ventilation, and a progressive build-up of air in the pleural space. The pneumothorax may tension if a flap has been created that allows air in, but not out.
Diagnosis should be made clinically during the primary survey. A wound in the chest wall is identified that appears to be 'sucking air' into the chest and may be visibly bubbling - this is diagnostic.
Breathing is rapid, shallow and laboured. There is reduced expansion of the hemithorax, accompanied by reduced breath sounds and an increased percussion note. One or all of these signs may not be appreciated in the noisy trauma room.
100% oxygen should be delivered via a facemask. Consideration should be given to intubation where oxygenation or ventilation is inadequate. Intubation should not delay placement of a chest tube and closure of the wound.
The definitive management of the open pneumothorax is to place an occlusive dressing over the wound and immediately place an intercostal chest drain.
Rarely, if a chest drain is not available and the patient is far from a definitive care facility, a bandage may be applied over the wound and taped on 3 sides. This, in theory, acts as a flap-valve to allow air to escape from the pneumothorax during expiration, but not to enter during inspiration. This dressing may be difficult to apply to a large wound and it's effect is very variable. As soon as possible a chest drain should be placed and the wound closed.

43. Immediate Life Threatening Mediastinal Trauma : Zone 1 Penetrating Injuries
Between mid-clavicular lines → sternal notch to xyphoid and posterior infra-scapular
35% unstable → OR (½ of unstable patients die in ED)
65% stable on arrival to ED
TEE, CT scan, endoscopy
20% stable patients have major injury on work up
An excellent review of penetrating mediastinal trauma was presented by Burrack from King’s County Hospital (Joshua H. Burack, MD, Emad Kandil, MD, Ahmed Sawas, BS, Patricia A. O’Neill, MD, Salvatore J. A. Sclafani, MD, Robert C. Lowery, MD, and Michael E. Zenilman, MD. Ann Thorac Surg 2007;83:377– 82). This retrospective study was conducted detailing an experience with 207 patients admitted with mediastinal penetrating trauma (MPT). Seventy-two (35%) were unstable (45 gun shot wounds, 27 stab wounds) and 19 died in the emergency department. Fifty-three had emergent intervention and 32 survived. Work-up was done on 135 stable patients (65%)
consisting of 46 gunshot wounds and 89 stab wounds, of which 5 had a positive TTE result and underwent a repair
of a cardiac injury. CTA evaluation was normal in almost 80% of patients, who subsequently did not require further
evaluation or treatment. In the stable patients, endoscopy or esophagography confirmed one tracheal injury and no esophageal injury. In the entire group, 10 patients (7%) had occult injury, and there were no deaths or missed injuries.
Methods. Unstable patients underwent emergent operative
intervention, and stable patients underwent chest
roentgenogram, transthoracic echocardiography (TTE),
and CTA. Further testing (angiogram, bronchoscopy,
esophagoscopy, esophagogram) was done only if one of
these studies revealed evidence of a trajectory in the
vicinity of major vasculature or viscera.
Results. Between 1997 and 2003, Conclusions. In cases of MPT, unstable patients require
surgery, and in stable patients, TTE and chest CTA are
effective screening tools. Patients with a negative TTE
and CTA results can be observed and may not require
further testing or endoscopy, whereas patients with positive
TTE or CTA results require further assessment to
exclude occult injury.

44. Triage and Outcome of Patients with Mediastinal Penetrating Trauma
The Annals of Thoracic Surgery Burack JH Volume 83, Issue 2, February 2007, Pages
Stable vs. Unstable Hemodynamic State
1. Traumatic cardiac arrest or near arrest and an EDT
2. Cardiac tamponade
3. Persistent ATLS class III shock despite fluid resuscitation (blood loss 1500–2000 mL, pulse rate > 120, blood pressure decreased)
4. Chest Tube output > 1500 mL of blood on insertion
5. Chest Tube output > 500 mL/hour for the initial hour
6. Massive hemothorax after chest tube drainage

45. Mechanism of Initial Clinical Presentation
Total
Stable (%)
Unstable (%)
Death (%) SW
116
89 (77%)
27 (23%)
8 (7%)
GSW 91
46 (51%)
45 (49%)
38 (42%)

46. Mediastinal Injury Location and Initial Clinical Presentation
M1= left para-sternal
M2 = right trans-mediastinal
M3 = mid-sternal (anterior and/or posterior)
M4 = lower trans-mediastinal
Total
Stable
Unstable
Death M1
16 
10 (63%)
6 (37%)
2 (13%) M2
34 
26 (76%)
8 (24%)
5 (15%) M3
137 
92 (67%)
45 (33%)
28 (20%) M4
20 
7 (35%)
13 (65%)
12 (60%)

47. Management Algorithm for Penetrating Mediastinal Trauma
(72)

48. Occult Injury in Stable Patients
Angiographic Findings
Treatment 1
Injury (thrombosis) to 4th Intercostal artery
Observation 2
Injury to the vertebral artery at the thoracic inlet
Coil embolization 3
Injury to the Internal Mammary artery 4
Injury to the left Subclavian artery
Sternotomy/thoracotomy and interposition graft of the subclavian artery 5
Inominate artery pseudoaneurysm and thoracic tracheal injury
Endovascular stent graft, thoracotomy, and tracheal resection

49. Distribution of Arterial Injuries with Penetrating Mediastinal Trauma
Artery
Injuries
Patients
Deaths
Innominate
23(38%)
18(35%)
1(10%)
Aortic Arch
17(28%)
13(25%)
3(30%)
L Common Carotid
11(18%)
8(15%)
2(20%)
Ascending Aorta
4(7%)
4(8%)
L Subclavian
5(8%)
Combined/multiple
Total
60(100%)
52(100%)
10(19%)
K. Buchan and J.V. Robbs, Surgical management of penetrating mediastinal arterial trauma, European Journal of Cardio-Thoracic Surgery Volume 9, Issue 2, 1995, Pages Dept Surgery University of Natal, South Africa

50. Traumatic Aortic-Innominate Vein Fistula

51. Immediate Life Threatening Thoracic Injuries: Aortic Disruption
Most common at ligamentum arteriosum but can be multiple (pendulum effect)
~⅓ fatal on site due to free rupture (uncontained)
Hypotension, exsanguination
MVA, falls from height
Up to 15% of all deaths following motor vehicle collisions are due to injury to the thoracic aorta. Many of these patients are dead at scene from complete aortic transection. Patients who survive to the emergency department usually have small tears or partial-thickness tears of the aortic wall with pseudoaneurysm formation.
Most blunt aortic injuries occur in the proximal thoracic aorta, although any portion of the aorta is at risk. The proximal descending aorta, where the relatively mobile aortic arch can move against the fixed descending aorta (ligamentum arteriousm), is at greatest risk from the shearing forces of sudden deceleration. Thus the aorta is a greatest risk in frontal or side impacts, and falls from heights. Other postulated mechanisms for aortic injury are compression between the sternum and the spine, and sudden increases in intra-luminal aortic pressure at the moment of impact.

52. Contained Injuries to the Aorta
Widened mediastinum (53% sensitivity, 59% specificity and 83% negative predictive value)
Obliteration of aortic knob
Rightward deviation of trachea
(compare NG tube to trachea)
Depression of left main stem bronchus
Pleural/apical cap
Left hemothorax (can be bilateral)
Fractures of 1st and/or 2nd ribs
On chest x-ray look for these signs but they are VERY unreliable on a portable AP CXR and diagnosis requires a high index of suspicion often based on nature of injury. mediastinal width of more than 8cm at the level of the aortic arch is considered abnormal and an indication for further imaging. A widened mediastinum is reported as having a 53% sensitivity, 59% specificity and 83% negative predictive value for traumatic aortic injury.
To maintain spinal precautions in blunt trauma patients, most AP chest radiographs are taken in the supine position. This will lead to fluid shifts that may cause a widened mediastinum. Some authors recommend repeating the radiograph with the patient erect, if the spine can be cleared prior to this. Around 40% of widened mediastinums will 'normalize' with the patient in the erect position.
Other less sensitive signs of mediastinal great vessel injury include depression of the left main-stem bronchus, deviation of the naso-gastric tube to the right, apical pleural haemoatoma (cap), disruption of the calcium ring in the aortic knob (broken-halo). None of these 'classic' signs have any useful sensitivity to use them as a screening for blunt aortic injury. Thus the 'funny-looking' mediastinum remains the best indicator of the need for further imaging and should be examined with these other findings to judge the risk of aortic injury:
Widened mediastinum (least reliable)
Obliteration of aortic knob
Rightward deviation of trachea
Rightward deviation of esophagus (look for NG tube)
Depression of left main stem bronchus
Pleural/apical cap
Left hemothorax (can be bilateral)
Fractures of 1st and/or 2nd rib(s)
On CT scan the diagnosis is correct 97% of the time look for peri-aortic hematoma, pleural effusions and aortography is correct in about 97-98% of the time.

53. Contained Injuries to the Aorta
On chest x-ray look for these signs but they are VERY unreliable on a portable AP CXR and diagnosis requires a high index of suspicion often based on nature of injury. mediastinal width of more than 8cm at the level of the aortic arch is considered abnormal and an indication for further imaging. A widened mediastinum is reported as having a 53% sensitivity, 59% specificity and 83% negative predictive value for traumatic aortic injury.
To maintain spinal precautions in blunt trauma patients, most AP chest radiographs are taken in the supine position. This will lead to fluid shifts that may cause a widened mediastinum. Some authors recommend repeating the radiograph with the patient erect, if the spine can be cleared prior to this. Around 40% of widened mediastinums will 'normalize' with the patient in the erect position.
Other less sensitive signs of mediastinal great vessel injury include depression of the left main-stem bronchus, deviation of the naso-gastric tube to the right, apical pleural haemoatoma (cap), disruption of the calcium ring in the aortic knob (broken-halo). None of these 'classic' signs have any useful sensitivity to use them as a screening for blunt aortic injury. Thus the 'funny-looking' mediastinum remains the best indicator of the need for further imaging and should be examined with these other findings to judge the risk of aortic injury:
Widened mediastinum (least reliable)
Obliteration of aortic knob
Rightward deviation of trachea
Rightward deviation of esophagus (look for NG tube)
Depression of left main stem bronchus
Pleural/apical cap
Left hemothorax (can be bilateral)
Fractures of 1st and/or 2nd rib(s)
On CT scan the diagnosis is correct 97% of the time look for peri-aortic hematoma, pleural effusions and aortography is correct in about 97-98% of the time.

54. Contained Injuries to the Aorta
Not a source of multiple hypotensive episodes in survivors - look for other injuries
Salvageable tear when hematoma contained
~⅓ die per 24 hours without treatment
Widened mediastinum very unreliable sign on portable x-ray
TEE, helical contrast CT scan, MRI, aortogram
Consider percutaneous stent placement
Address after life threatening injuries stabilized
Most blunt aortic injuries surviving to hospital are partial-transections, and should be managed with blood pressure control until the defintivie repair. Thus the priority in the management of hemodynamically unstable patients with potential aortic injury is to rapidly identify and control on-going hemorrhage from other sites, and to avoid over-resuscitation. Sites of concealed hemorrhage are identified with Chest and Pelvis radiographs and FAST ultrasound or Diagnostic Peritoneal Lavage.
The caveat to these cases is the patient with and aortic tear and impending rupture. These patients classically present as 'meta-stable' - ie they respond to fluid resuscitation and then drop their blood pressure in a cyclical manner. It is important to recognize this futile cycle early and avoid aggressive cyclical resuscitation, as this will ultimately lead to free rupture of the aorta and an iatrogenic hypothermia & coagulopathy. Beware the 'meta-stable' patient with a widened mediastinum and a left-sided hemothorax!

55. Summary Life ending thoracic injuries are common
Survival depends on proper and immediate diagnosis and appropriate management
ED thoracotomy can save lives but expected survivorship is <10%
Don’t forget ABC’s of trauma and damage control principles