Chest trauma is a significant source
of morbidity and mortality in the
Blunt injury to the chest can affect any one or all components of the chest wall and thoracic cavity. These components include the bony skeleton (ribs, clavicles, scapulae, sternum), lungs and pleurae, tracheobronchial tree, esophagus, heart, great vessels of the chest, and the diaphragm. In the subsequent sections, each particular injury and injury pattern resulting from blunt mechanisms is discussed. The pathophysiology of these injuries is elucidated, and diagnostic and treatment measures are outlined.
Trauma is responsible for more than
100,000 deaths annually in the
The major pathophysiologies encountered in blunt chest trauma involve derangements in the flow of air, blood, or both in combination. Blunt trauma commonly results in chest wall injuries (eg, rib fractures). The pain associated with these injuries can make breathing difficult, and this may compromise ventilation.
Direct lung injuries, such as pulmonary contusions, are frequently associated with major chest trauma and may impair ventilation by a similar mechanism.
Space-occupying lesions, such as pneumothoraces, hemothoraces, and hemopneumothoraces, interfere with oxygenation and ventilation by compressing otherwise healthy lung parenchyma. A situation of special concern is tension pneumothorax in which pressure continues to build in the affected hemithorax as air leaks from the pulmonary parenchyma into the pleural space. This can push mediastinal contents toward the opposite hemithorax. Distortion of the superior vena cava by this mediastinal shift can result in decreased blood return to the heart, circulatory compromise, and shock.
The thorax is bordered superiorly by the thoracic inlet, just cephalad to the clavicles. The major arterial blood supply to and venous drainage from the head and neck pass through the thoracic inlet.
The thoracic outlets form the superolateral borders of the thorax and transmit branches of the thoracic great vessels that supply blood to the upper extremities. The nerves that comprise the brachial plexus also access the upper extremities via the thoracic outlet. The veins that drain the arm, most importantly the axillary vein, empty into the subclavian vein, which returns to the chest via the thoracic outlet.
Inferiorly, the pleural cavities are separated from the peritoneal cavity by the hemidiaphragms. Communication routes between the thorax and abdomen are supplied by the diaphragmatic hiatuses, which allow egress of the aorta, esophagus, and vagal nerves into the abdomen and ingress of the vena cava and thoracic duct into the chest.
The chest wall is composed of layers of muscle, bony ribs, costal cartilages, sternum, clavicles, and scapulae. In addition, important neurovascular bundles course along each rib, containing an intercostal nerve, artery, and vein. The inner lining of the chest wall is the parietal pleura. The visceral pleura invests the lungs. Between the visceral and parietal pleurae is a potential space, which, under normal conditions, contains a small amount of fluid that serves mainly as a lubricant.
The lungs occupy most of the volume of each hemithorax. Each is divided into lobes. The right lung has 3 lobes, and the left lung has 2 lobes. Each lobe is further divided into segments.
The trachea enters through the thoracic inlet and descends to the carina at thoracic vertebral level 4, where it divides into the right and left mainstem bronchi. Each mainstem bronchus divides into lobar bronchi. The bronchi continue to arborize to supply the pulmonary segments and subsegments.
The heart is a mediastinal structure contained within the pericardium. The right atrium receives blood from the superior vena cava and inferior vena cava. Right atrial blood passes through the tricuspid valve into the right ventricle. Right ventricular contraction forces blood through the pulmonary valve and into the pulmonary arteries. Blood circulates through the lungs, where it acquires oxygen and releases carbon dioxide. Oxygenated blood courses through the pulmonary veins to the left atrium. The left heart receives small amounts of nonoxygenated blood via the thebesian veins, which drain the heart, and the bronchial veins. Left atrial blood proceeds through the mitral valve into the left ventricle.
Left ventricular contraction propels blood through the aortic valve into the coronary circulation and the thoracic aorta, which exits the chest through the diaphragmatic hiatus into the abdomen. A ligamentous attachment (remnant of ductus arteriosus) exists between the descending thoracic aorta and pulmonary artery just beyond the take-off of the left subclavian artery.
The esophagus exits the neck to enter the posterior mediastinum. Through much of its course, it lies posterior to the trachea. In the upper thorax, it lies slightly to the right with the aortic arch and descending thoracic aorta to its left. Inferiorly, the esophagus turns leftward and enters the abdomen through the esophageal diaphragmatic hiatus. The thoracic duct arises primarily from the cisterna chyli in the abdomen. It traverses the diaphragm and runs cephalad through the posterior mediastinum in proximity to the spinal column. It enters the neck and veers to the left to empty into the left subclavian vein.
The clinical presentation of patients with blunt chest trauma varies widely and ranges from minor reports of pain to florid shock. The presentation depends on the mechanism of injury and the organ systems injured.
Obtaining as detailed a clinical history as possible is extremely important in the assessment of a patient with a blunt thoracic trauma. The time of injury, mechanism of injury, estimates of MVA velocity and deceleration, and evidence of associated injury to other systems (eg, loss of consciousness) are all salient features of an adequate clinical history. Information should be obtained directly from the patient whenever possible and from other witnesses to the accident if available.
The closed damages of the chest are divided:
². According to the injury of other organs:
1. Isolated trauma.
2. Combined trauma (craniocerebral, with damage of abdominal organs, with damage of bones).
²². According to the mechanism of trauma:
²II. According to the character of the chest viscerae damage:
1. Without damage of viscerae.
2. With damage of viscerae (lungs, trachea, bronchi, esophagus, heart, vessels, diaphragm etc.).
IV. According to the character of complications:
1) Early (pneumothorax, hemothorax, subcutaneous, mediastinal emphysema floative rib fracture, traumatic shock, asphyxia);
2) Late (posttraumatic pneumonia, posttraumatic pleurisy, suppurative diseases of lungs and pleura).
V. According to the state of cardiopulmonary system:
1. Without phenomena of respiratory failure.
2. Acute respiratory failure (of ², ²², ²²² degree).
3. Without phenomena of cardiovascular failure.
4. Acute cardiovascular failure (of ², ²², ²²² degree).
V². According to the gravity of a trauma:
Simple rib fractures are the most common injury sustained following blunt chest trauma, accounting for more than half of thoracic injuries from nonpenetrating trauma. Approximately 10% of all patients admitted after blunt chest trauma have one or more rib fractures. These fractures are rarely life-threatening in themselves but can be an external marker of more severe visceral injury inside the abdomen and the chest.
The most common mechanism of injury for rib fractures in elderly persons is a fall from height or from standing. In adults, motor vehicle accident (MVA) is the most common mechanism. Youths sustain rib fractures most often secondary to recreational and athletic activities.
Rib fractures may compromise ventilation by a variety of mechanisms. Pain from rib fractures can cause respiratory splinting, resulting in atelectasis and pneumonia. Multiple contiguous rib fractures (ie, flail chest) interfere with normal costovertebral and diaphragmatic muscle excursion, potentially causing ventilatory insufficiency. Fragments of fractured ribs can also act as penetrating objects leading to the formation of a hemothorax or a pneumothorax. Ribs commonly fracture at the point of impact or at the posterior angle (structurally their weakest area). Ribs four through nine (4-9) are the most commonly injured.
Rib fractures are the most common blunt thoracic injuries. Ribs 4-10 are most frequently involved. Patients usually report inspiratory chest pain and discomfort over the fractured rib or ribs. Physical findings include local tenderness and crepitus over the site of the fracture. If a pneumothorax is present, breath sounds may be decreased and resonance to percussion may be increased. Rib fractures may also be a marker for other associated significant injury, both intrathoracic and extrathoracic. In one report, 50% of patients with blunt cardiac injury have rib fractures. Fractures of ribs 8-12 should raise the suggestion of associated abdominal injuries. Lee and colleagues reported a 1.4- and 1.7-fold increase in the incidence of splenic and hepatic injury, respectively, in those with rib fractures.
Paradoxical chest wall excursion with inspiration is seen with flail chest. A flail chest occurs when a large segment of ribs is not attached to the spine. These ribs are broken in at least 2 places on each rib. The paradoxical movement occurs because the middle section of the rib between the 2 fracture sites moves in response to intrathoracic pressure changes not intercostal muscle contractions.
Specific signs of ventilatory insufficiency include cyanosis, tachypnea, retractions, and use of accessory muscles for ventilation.
If fracture of the lower ribs is suspected, assess the patient for abdominal tenderness and costal margin tenderness, which could raise suspicion for injury to intra-abdominal organs.
Anteroposterior (AP) and lateral chest films are used routinely to assist in the diagnosis of rib fractures, yet sensitivity as low as 50% has been reported. Delayed or follow-up radiographs can be very helpful.
Chest radiographs are much more useful in the diagnosis of underlying injuries, including hemothorax, pneumothorax, lung contusion, atelectasis, pneumonia, and vascular injuries.
Findings of sternal fracture or scapular fracture should increase suspicion for rib fractures.
A chest CT scan is more sensitive than plain radiographs for detecting rib fractures. The modality can also provide information regarding the number of ribs involved.
If complications from rib fractures are suspected clinically or diagnosed by plain radiographs, a chest CT scan may be helpful to document specific injuries, to characterize extent of injury, and to plan for definitive management.
An associated CT scan of the abdomen with intravenous contrast should be considered in cases involving lower rib fractures with suspected or known injury to the liver and/or the spleen.
The fracture of the VI-VIII left ribs
First and second rib fractures are considered a separate entity from other rib fractures because of the excessive energy transfer required to injure these sturdy and well-protected structures. First and second rib fractures are harbingers of associated cranial, major vascular, thoracic, and abdominal injuries. The clinician should aggressively seek to exclude the presence of these other injuries.
Pain control and pulmonary toilet are the specific treatment measures for rib fractures. First and second rib fractures do not require surgical therapy. An exception to this would be the need to excise a greatly displaced bone fragment.
Elderly patients with 3 or more rib fractures have been shown to have a 5-fold increased mortality rate and a 4-fold increased incidence of pneumonia. Effective pain control is the cornerstone of medical therapy for patients with rib fractures. For most patients, this consists of oral or parenteral analgesic agents. Intercostal nerve blocks may be feasible for those with severe pain who do not have numerous rib fractures. A local anesthetic with a relatively long duration of action (eg, bupivacaine) can be used. Patients with multiple rib fractures whose pain is difficult to control can be treated with epidural analgesia.
Adjunctive measures in the care of these patients include early mobilization and aggressive pulmonary toilet. Rib fractures do not require surgery. Pain relief and the establishment of adequate ventilation are the therapeutic goals for this injury. Rarely, a fractured rib lacerates an intercostal artery or other vessel, which requires surgical control to achieve hemostasis acutely. In the chronic phase, nonunion and persistent pain may also require an operation.
The direct force of traumatizing factor on the chest wall results in rib fracture.
The pain localized in the zone of damage, is the chief clinical manifestation. The pain intensifies at respiration, cough and change of a body position of the patient. The overwhelming majority of the patients complain of crepitation of ribs in the fracture site.
At examination the respiratory lag on affected side is observed.
Crepitating of osseous fragment revealed by palpation, and depending on number of injured ribs diminished breathing sounds by auscultation.
On chest roentgenograms the break in continuity of bone fragments of ribs is observed.
This is one of the most severe complication of the closed trauma of the chest. The floation arises from fracture of three and more ribs along two anatomic lines. The multiple rib fractures produce an unstable segment of chest wall that moves paradoxically inward upon inspiration and balloons outward during expiration (flail chest). Thereby the respiration disturbed not only in the area of a floating segment, but also in all lungs. The permanent movement of flail chest result in rocking shift of mediastinum, which causes deviation of its organs. As a result the respiratory failure is associated with cardiovascular.
A flail chest, by definition, involves 3 or more consecutive rib fractures in 2 or more places, which produces a free-floating, unstable segment of chest wall. Separation of the bony ribs from their cartilaginous attachments, termed costochondral separation, can also cause flail chest. Patients report pain at the fracture sites, pain upon inspiration, and, frequently, dyspnea. Physical examination reveals paradoxical motion of the flail segment. The chest wall moves inward with inspiration and outward with expiration. Tenderness at the fracture sites is the rule. Dyspnea, tachypnea, and tachycardia may be present. The patient may overtly exhibit labored respiration due to the increased work of breathing induced by the paradoxical motion of the flail segment.
A significant amount of force is required to produce a flail segment. Therefore, associated injuries are common and should be aggressively sought. The clinician should specifically be aware of the high incidence of associated thoracic injuries such as pulmonary contusions and closed head injuries, which, in combination, significantly increase the mortality associated with flail chest.
All of the treatment modalities mentioned above for patients with rib fractures are appropriate for those with flail chest. Respiratory distress or insufficiency can ensue in some patients with flail chest because of severe pain secondary to the multiple rib fractures, the increased work of breathing, and the associated pulmonary contusion. This may necessitate endotracheal intubation and positive pressure mechanical ventilation. Intravenous fluids are administered judiciously because fluid overloading can precipitate respiratory failure, especially in patients with significant pulmonary contusions.
In an attempt to stabilize the chest wall and to avoid endotracheal intubation and mechanical ventilation, various operations have been devised for correcting flail chest. These include pericostal sutures, the application of external fixation devices, or the placement of plates or pins for internal fixation. With improved understanding of pulmonary mechanics and better mechanical ventilatory support, surgical therapy has not been proven superior to the supportive and medical measures discussed. However, most authors would agree that stabilization is warranted if a thoracotomy is indicated for another reason.
1. Central floative segment a multiple rib fracture along parasternal or midclavicular lines.
2. Anterolateral floative segment a multiple rib fracture along parasternal and anteaxillary lines.
3. Lateral floative segment a multiple rib fracture along anterior and posterior axillary lines.
4. Posterior floative segment a multiple rib fracture along postaxillary and paravertebral lines.
The patients state is grave or extremely grave. The expressed pain syndrome frequently results in traumatic shock. The patient is restless. Observed the cyanosis of skin, tachypnea, and tachycardia to 120-160 beat/min of weak filling and tension. Arterial pressure at first elevated, then its decrease observed. At examination characteristic paradoxical respiratory movements of chest, inward upon inspiration and outward during expiration, crepitus of bone fragments by palpation are revealed. Breathing sounds diminished on the side of damage by auscultation.
In case of floative rib fracture the chest X-ray examination reveals multiple, double rib fracture with deformity of the chest.
In 75 % of cases the multiple rib fracture is the cause of injury of lungs, pneumothorax or pneumohemothorax.
Pain relief in closed trauma of the chest is achieved by means of different blocks:
1. Vagosympathetic block;
2. Alcohol - novocaine block of the site of fracture;
3. Paravertebral block.
Alcohol - novocaine block of the site of fracture
Except blocks, in some cases analgesics and opiates are instituted. On 2-3 day desirable the administration of electrophoresis with novocaine. For prophylaxis of congested phenomena in a pulmonary tissue used respiratory gymnastics, forced ventilation of lungs, inhalations.
The methods of reduction of the skeleton of the flail chest are divided onto three groups:
1. External fixation of a movable segment by means of suturing for intercostal muscles and traction during 2-3 weeks;
2. Intrmedullary costal osteosynthesis;
3. Mechanical ventilation (often with positive end-expiratory pressure).
Most sternal fractures are caused by MVAs. The upper and middle thirds of the bone are most commonly affected in a transverse fashion. Patients report pain around the injured area. Inspiratory pain or a sense of dyspnea may be present. Physical examination reveals local tenderness and swelling. Ecchymosis is noted in the area around the fracture. A palpable defect or fracture-related crepitus may be present.
Associated injuries occur in 55-70% of patients with sternal fractures. The most common associated injuries are rib fractures, long bone fractures, and closed head injuries. The association of blunt cardiac injuries with sternal fractures has been a source of great debate. Blunt cardiac injuries are diagnosed in fewer than 20% of patients with sternal fractures. Caution should be used before completely excluding myocardial injury. The workup should begin with an ECG.
Most sternal fractures require no therapy specifically directed at correcting the injury. Patients are treated with analgesics and are advised to minimize activities that involve the use of pectoral and shoulder girdle muscles. The most important aspect of the care for these patients is to exclude blunt myocardial and other associated injuries. Patients who are experiencing severe pain related to the fracture and those with a badly displaced fracture are candidates for open reduction and internal fixation. Various techniques have been described, including wire suturing and the placement of plates and screws. The latter technique is associated with better outcomes.
The fracture of breastbone is commonly caused by direct forces at the site of the sternum. Usually it is the outcome of compression or result of trauma to vehicle helm.
The fracture in most cases located in the upper and medial thirds of breastbone.
The patients complain of severe pain in the site of fracture, which intensifies at respiration and movements. The pain behind the sternum and in the heart area follows the contusion of lungs and heart. Sometimes hemoptysis is observed.
Examination reveals the deformity of breastbone in the site of fracture. Displaced fragments are palpated here, that accompanied by severe pain syndrome.
By auscultation, if there are no intrapleural complications, the respiration in the first 2-3 days is vesicular from both sides. Then the fine bubbling rales are auscultated which is the first objective manifestation of a posttraumatic pneumonia.
The complete fracture of breastbone is characterized by a break in continuity of both cortical plates with a local dislocation of fragments.
Fracture of breastbone
1. Complaints and history of the disease.
2. Physical findings.
3. Chest roentgenograms in two planes.
The sternal fracture without displacement of fragments requires conservative treatment. The fracture of the corpus of breastbone with dislocation of fragments quite often requires operative treatment with performance of osteosynthesis.
Pneumothorax is defined as the presence of air or gas in the pleural cavity, that is, in the potential space between the visceral and parietal pleura of the lung. The result is collapse of the lung on the affected side. Air can enter the intrapleural space through a communication from the chest wall (ie, trauma) or through the lung parenchyma across the visceral pleura.
Spontaneous pneumothorax is a commonly encountered problem with approaches to treatment that can vary from observation to aggressive intervention. Spontaneous pneumothorax occurs in people without underlying lung disease and in the absence of an inciting event. In other words, air is present in the intrapleural space without preceding trauma and without underlying clinical or radiologic evidence of lung disease. However, many patients whose condition is labeled as spontaneous pneumothorax have subclinical lung disease. Patients are typically between age 18 and 40 years.
Spontaneous pneumothoraces in most patients occur from the rupture of blebs and bullae. Although primary spontaneous pneumothorax (PSP) is defined as a lack of underlying pulmonary disease, these patients have asymptomatic blebs and bullae detected on computed tomography scans or upon thoracotomy. PSP is typically observed in tall, young people without parenchymal lung disease and is thought to be related to increased shear forces in the apex.
Traumatic pneumothorax results from injury, typically blunt trauma or penetrating trauma that disrupts the parietal or visceral pleura (see the images below). The mechanisms of injury are secondary to medical or surgical procedures. Pneumothoraces due to trauma are relatively straightforward and usually require tube thoracostomy.
The pleural space has a negative pressure, with the chest wall tending to spring outward and the lung's elastic recoil tending to collapse. If the pleural space is invaded by gas from a ruptured bleb, the lung collapses until equilibrium is achieved or the rupture is sealed. As the pneumothorax enlarges, the lung becomes smaller. The main physiologic consequence of this process is a decrease in vital capacity and partial pressure of oxygen.
Tension pneumothorax occurs anytime a disruption involves the visceral pleura, parietal pleura, or the tracheobronchial tree. This condition develops when injured tissue forms a 1-way valve, allowing air inflow into the pleural space and prohibiting air outflow. The volume of this nonabsorbable intrapleural air increases with each inspiration because of the 1-way valve effect. In addition to this mechanism, the positive pressure used with mechanical ventilation therapy can cause air trapping. As a result, pressure rises within the affected hemithorax.
As the pressure increases, the ipsilateral lung collapses and causes hypoxia. Further pressure build-up causes the mediastinum to shift toward the contralateral side and impinge on and compress both the contralateral lung and the vasculature entering the right atrium of the heart. Hypoxia results as the collapsed lung on the affected side and the compressed lung on the contralateral side compromise effective gas exchange. This hypoxia and decreased venous return caused by compression of the relatively thin walls of the atria impair cardiac function. The inferior vena cava is thought to be the first to kink and restrict blood flow back to the heart. It is most evident in trauma patients who may be hypovolemic with reduced venous blood return to the heart.
Arising from numerous causes, this condition rapidly progresses to respiratory insufficiency, cardiovascular collapse, and, ultimately, death if unrecognized and untreated.
². According to extension of process:
²². According to degree of a lung collapse:
1. Partial (collapse of lung to 1/3 of its volume).
2. Subtotal (collapse of lung to 2/3 of its volume).
3. Total (collapse of lung exceeding 2/3 of its volume).
Estimating the size of the pneumothorax
In evaluating the chest radiograph, first impressions of pneumothorax size can be misleading. The following methods may be used to estimate the size of the pneumothorax:
Calculate the ratio of the transverse radius of the pneumothorax (cubed) to the transverse radius of the hemithorax (cubed). To express the pneumothorax size as a percentage, multiply the fractional size by 100. This formula assumes a constant shape of the lung when it collapses and is invalid if pleural adhesions are present. The ratio of lung size to hemithorax size to estimate pneumothorax size avoids the subjective underestimation of pneumothorax expressed as a percentage of previous lung volume.
A 2.5-cm margin of gas peripheral to the collapsing lung corresponds to a pneumothorax of about 30%. Complete collapse of the lung is a 100% pneumothorax.
A simple approach involves measuring
the distance from the apex of the lung to the top margin of the visceral pleura
(thoracic cupola) on the upright chest radiograph, such that a small
pneumothorax is a distance to the apex that measures less than
²²². According to the mechanism of occurrence:
The closed pneumothorax is the complication, which arises from the damage of visceral pleural membrane, which results in entry of air in a pleural space and atelectasis of lung. In chest trauma the cause of occurrence of the closed pneumothorax is the perforation of a visceral pleura and pulmonary tissue by the fragment of fractured rib.
The open pneumothorax results from formation of hole in a chest wall at massive trauma and free entry of air during inspiration inward a pleural space, and during expiration outward.
The valvular pneumothorax occurs at damage of a pulmonary tissue or chest wall with formation of the valve, when the air during inspiration enters a pleural space, and during expiration, due to valve closure, does not exits outside. It is the most dangerous form of pneumothorax, which results in a complete pulmonary collapse, shift of mediastinum, inflection of major vessels and cardiac arrest.
The chief clinical manifestation of posttraumatic pneumothorax, which results from a pulmonary collapse, is the rest dyspnea, which amplifies at a minor exertion. This sign arises due to atelectasis of lung and its exclusion from breathing. On the background of collapsed lung only the main and lobar bronchi and pleural space are ventilated. The oxygenation of blood in collapsed lungs does not occur, therefore the shunting of a venous blood arise.
The chest pain is more characteristic manifestation for trauma with the damage of ribs, however pulmonary collapse also can associate with a pain syndrome. Nevertheless the patients promptly adapt for it and the dyspnea finally remains the basic clinical manifestation of such complication.
On the background of severe trauma of the chest the signs of damage dominate in clinical manifestation on inappreciable entry of air in a pleural space. Pneumothorax mostly revealed during X-ray examination. Progressing of air entry in a pleural space and pulmonary collapse cause the respiratory lag on affected side. By palpation the vocal fremitus is absent. It indicates the origin of the complication rib fracture.
Percussion obtains bandbox sound, or pulmonary sound with tympanitis. By auscultation - weak or absent breathing sounds, sometimes amphoric respiration. The expressiveness of clinical pattern depends on degree of a pulmonary collapse.
Pulmonary atelectasis and presence of air in a pleural space are the X-ray findings that enable to establish the final diagnosis.
1. Complaints and history of the disease.
The presentation of patients with pneumothorax varies depending on the type of pneumothorax.
Spontaneous and iatrogenic pneumothorax
Despite descriptions of Valsalva maneuvers and increased intrathoracic pressures as inciting factors, spontaneous pneumothorax usually develops at rest. By definition, spontaneous pneumothorax is not associated with trauma or stress. Symptoms of iatrogenic pneumothorax are similar to those of a spontaneous pneumothorax and, depend on the age of the patient, the presence of underlying lung disease, and the extent of the pneumothorax.
Until a bleb ruptures and causes pneumothorax, no clinical signs or symptoms are present in primary spontaneous pneumothorax (PSP). Young and otherwise healthy patients can tolerate the main physiologic consequences of a decrease in vital capacity and partial pressure of oxygen fairly well, with minimal changes in vital signs and symptoms, but those with underlying lung disease may have respiratory distress. The most common underlying abnormality in secondary spontaneous pneumothorax is chronic obstructive pulmonary disease (COPD), and cystic fibrosis carries one of the highest associations, with more than 20% reporting spontaneous pneumothorax.
In one series, acute onset of chest pain and shortness of breath were present in all patients in one series; typically, both symptoms are present in 64-85% of patients. The chest pain is described as severe and/or stabbing, radiates to the ipsilateral shoulder and increases with inspiration (pleuritic). In PSP, chest often improves over the first 24 hours, even without resolution of the underlying air accumulation. Well-tolerated primary pneumothorax can take 12 weeks to resolve. In secondary pneumothorax (SSP), the chest pain is more likely to persist with more significant clinical symptoms.
Shortness of breath/dyspnea in PSP is generally of sudden onset and tends to be more severe with secondary spontaneous pneumothoraces (SSPs) because of decreased lung reserve. Anxiety, cough, and vague presenting symptoms (eg, general malaise, fatigue) are less commonly observed.
A history of previous pneumothorax is important, as recurrence is common, with rates reported between 15% and 40%. Up to 15% of recurrences can be on the contralateral side. Secondary pneumothoraces are often more likely to recur, with cystic fibrosis carrying the highest recurrence rates at 68-90%. No study has shown that the number or size of blebs and bullae found in the lung can be used to predict recurrence.
Signs and symptoms of tension pneumothorax are usually more impressive than those seen with a simple pneumothorax, and clinical interpretation of these is crucial for diagnosing and treating the condition. Unlike the obvious patient presentations oftentimes used in medical training courses to describe a tension pneumothorax, actual case reports include descriptions of the diagnosis of the condition being missed or delayed because of subtle presentations that do not always present with the classically described clinical findings of this condition.
Symptoms of tension pneumothorax may include chest pain (90%), dyspnea (80%), anxiety, fatigue, or acute epigastric pain (a rare finding).
2. Physical examination.
The general appearance of the patient with pneumothorax may vary from asymptomatic to respiratory distress. It may include diaphoresis, splinting chest wall to relieve pleuritic pain, and cyanosis (in the case of tension pneumothorax). Findings on lung auscultation also vary depending on the extent of the pneumothorax. Affected patients may also reveal altered mental status changes, including decreased alertness and/or consciousness (a rare finding).
Respiratory findings may include the following:
· Respiratory distress (considered a universal finding) or respiratory arrest
· Tachypnea (or bradypnea as a preterminal event)
· Asymmetric lung expansion: A mediastinal and tracheal shift to the contralateral side can occur with a large tension pneumothorax.
· Distant or absent breath sounds: Unilaterally decreased or absent lung sounds is a common finding, but decreased air entry may be absent even in an advanced state of the disease.
· Lung sounds transmitted from the unaffected hemithorax are minimal with auscultation at the midaxillary line
· Hyperresonance on percussion: This is a rare finding and may be absent even in an advanced state of the disease.
· Decreased tactile fremitus
Adventitious lung sounds (crackles, wheeze; an ipsilateral finding)
· Cardiovascular findings may include the following:
· Tachycardia: This is the most common finding. If the heart rate is faster than 135 beats per minute (bpm), tension pneumothorax is likely.
· Pulsus paradoxus
· Hypotension: This should be considered as an inconsistently present finding; although hypotension is typically considered a key sign of a tension pneumothorax, studies suggest that hypotension can be delayed until its appearance immediately precedes cardiovascular collapse.
· Jugular venous distention: This is generally seen in tension pneumothorax, although it may be absent if hypotension is severe.
· Cardiac apical displacement: This is a rare finding.
3. Chest X-radiography in 2 planes.
Portable chest radiography should always be included in the initial radiographic evaluation of major trauma, as significant chest injuries carry an estimated 10-50% risk of associated pneumothorax. Chest computed tomography (CT) scanning should always be performed for significant chest injuries, because they carry an estimated risk of associated pneumothorax as high as 50% and about half of these pneumothoraces may be occult.
When evaluating the chest radiograph for pneumothorax, assess rotation, which can obscure a pneumothorax and mimic a mediastinal shift. Compare the symmetry and shape of the clavicles, and look at the relative lengths of the ribs in the middle lung fields on each side on the anteroposterior (AP) or posteroanterior (PA) views. On an image with rotation, the ribs on each side often have unequal lengths.
In a nonloculated pneumothorax, air rises to the nondependent portion of the pleural cavity. Therefore, carefully examine the apices of an upright chest radiograph, and scrutinize the costophrenic and cardiophrenic angles on a supine chest radiograph.
Finding of pneumothorax on chest radiographs may include the following:
· A linear shadow of visceral pleura with lack of lung markings peripheral to the shadow may be observed, indicating collapsed lung.
· An ipsilateral lung edge may be seen parallel to the chest wall.
· In supine patients, deep sulcus sign (very dark and deep costophrenic angle) with radiolucency along costophrenic sulcus may help to identify occult pneumothorax. The anterior costophrenic recess becomes the highest point in the hemithorax, resulting in an unusually sharp definition of the anterior diaphragmatic surface due to gas collection and a depressed costophrenic angle
· Small pleural effusions commonly are present and increase in size if the pneumothorax does not reexpand.
· Mediastinal shift toward the contralateral lung may also be apparent.
· Airway or parenchymal abnormalities in the contralateral lung suggest causes of secondary pneumothorax. Evaluation of the parenchyma in the collapsed lung is less reliable.
Although expiratory images are thought to better depict subtle pneumothoraces (the volume of the pneumothorax is constant and hence proportionally higher on expiratory images), a randomized controlled trial revealed no difference in the ability of radiologists to detect pneumothoraces on inspiratory and expiratory images after procedures with the potential to cause pneumothoraces.
Computed tomography (CT) scanning is the most reliable imaging study for the diagnosis of pneumothorax, but it is not recommended for routine use in pneumothorax. This imaging modality can help to accomplish the following:
· Distinguish between a large bulla and a pneumothorax
· Indicate underlying emphysema or emphysemalike changes (ELCs)
· Determine the exact size of the pneumothorax, especially if it is small
· Confirm the diagnosis of pneumothorax in patients with head trauma who are mechanically ventilated
· Detect occult/small pneumothoraces and pneumomediastinum (although the clinical significance of these occult pneumothoraces is unclear, particularly in the stable nonintubated patient)
CT scanning is widely used in actual clinical practice to assess the possibility of associated concurrent pulmonary disease because of the inherent superiority of CT scans to visualize the details of lung parenchyma and pleura, as can be seen in the images below.
When performed on primary spontaneous pneumothorax patients, CT detects multiple blebs and bullae in the setting of negative chest radiographic findings. This may not impact management, as there has been no correlation between number of blebs and recurrence. However, CT scanning may have a role in secondary spontaneous pneumothorax, especially to differentiate from giant bullous emphysema.
CT scanning can detect occult pneumothorax in patients who will require mechanical ventilation in trauma and emergency surgery settings. This modality has also been shown to be more sensitive than radiography for hemothorax and pulmonary contusion.
Collapse of the lung, air in the pleural cavity, and deviation of mediastinal structures are present in tension pneumothorax.
A chest trauma, which complicated by pneumothorax with a partial pulmonary collapse (to 1/3 of volume) is indication to aspiration of air by means of thoracentesis. The cases, if the negative pressure in a pleural space is not obtained, and also subtotal, and total pneumothorax require closed drainage of a pleural space.
Under the local anesthesia by solution of novocaine in ²² intercostal space in the midclavicular line by means of a trocar in a pleural space inserted a plastic tube, which fixed to skin. The drainage connects to aspirative system or according to method of Bulau. In the majority of patients the pneumothorax liquidates in some hours, or during 1-2 days.
The absence of effect (incomplete expansion of lung) of active aspiration, and also valvular closed pneumothorax is the indications to operative management suturing of the pulmonary wound. In some cases a segmental resection of lung, or lobectomy is carried out.
Tension pneumothorax is a life-threatening condition that demands urgent management. If this diagnosis is suspected, do not delay treatment in the interest of confirming the diagnosis (ie, before radiologic evaluation).
The basic principle or emergent needle decompression is to introduce a catheter into the pleural space, thus producing a pathway for the air to escape and relieving the built-up pressure. Although this procedure is not the definitive treatment for tension pneumothorax, emergent needle decompression does arrest its progression and serves to restore cardiopulmonary function slightly. Needle length in persons with large pectoral muscles may be an issue, and long needles or angiocatheters may be necessary.
Immediately place the patient on 100% oxygen, ventilate the patient if necessary, and evaluate the patient for evidence of respiratory compromise, hemodynamic instability, or clinical deterioration.
Essentially, a large-bore (16 or 18 gauge) angiocatheter is introduced in the midclavicular line at the second intercostal space. Use large-bore catheters, because hemothorax can be associated with pneumothorax, and the patient may, therefore, require immediate intravenous (IV) infusion. Upright positioning, if not inappropriate due to cervical spine or trauma concerns, may be beneficial. This serves as a bridge until the definitive treatment of tube thoracostomy. The catheter is left in place until the chest tube is placed.
The procedure is as follows:
· Locate the anatomic landmarks and quickly prepare the area to be punctured with an iodine-based solution (eg, Betadine).
a large-bore needle with a catheter into the second intercostal space, just
superior to the third rib at the midclavicular line, 1-
· Once the needle is in the pleural space, listen for the hissing sound of air escaping to confirm the diagnosis of tension pneumothorax (note this finding on the patient's chart). In an area with high ambient noise, the escape of air may not be detected. Remove the needle while leaving the catheter in place.
· Secure the catheter in place, and install a flutter valve.
After needle decompression, immediately begin preparation to insert a thoracostomy tube. Then, reassess the patient, paying careful attention to the ABCs (ie, airway, breathing, circulation) of trauma management.
Nonemergent needle aspiration can be used to treat a small primary spontaneous pneumothorax (PSP) or an iatrogenic pneumothorax.
The procedure is as follows:
· Palpate the rib and intercostal space intended for needle aspiration. For needle aspiration, the anterior approach at the second or third intercostal space at the midclavicular line or a lateral approach at the fifth or sixth intercostal space at the midaxillary line is appropriate. For catheter aspiration, the lateral approach is preferred.
· Prepare the skin with povidone-iodine (Betadine), alcohol scrubs, or both, and cover with sterile drapes.
· Instill a local anesthetic (eg, 1% Xylocaine solution) to skin and soft tissue down to the pleura, directing the needle over the top of the rib into the desired intercostal space.
· Insert a large-bore Angiocath (14-gauge in an adult, 18- or 20-gauge in an infant) or ready-to-use aspiration kit into the chosen intercostal space over the top of the rib and perpendicular to the chest wall.
· For simple needle aspiration, withdraw air once the pleural cavity is entered, and when resistance is felt, withdraw the needle.
· For catheter aspiration, once the pleural cavity is entered, a soft pigtail catheter is advanced over the needle into the pleural space. A scalpel may be necessary to enlarge the entry site at the skin. Remove the needle once the pleural cavity is entered, and attach the catheter to a 3-way stopcock and large syringe (eg, 60-mL syringe) to evacuate air.
no more air can be aspirated (discontinue if resistance is felt, if the patient
coughs excessively, or if more than
· Close the stopcock, and secure the catheter to the chest wall.
· Obtain a chest radiograph to assess the degree of success, and obtain another radiograph 4 hours later to confirm the absence of recurring accumulation.
· If no recurrence is present, remove the catheter and massage the insertion site with sterile gauze to seal the channel into the pleural space.
· Discharge the patient with appropriate return instructions. (Some authors suggest observation for an additional 2 h after catheter removal.)
· If the pneumothorax persists, attach a Heimlich valve or a water seal and admit the patient.
Potential complications associated with needle aspiration includes pneumothorax (with potential to later tension pneumothorax), cardiac tamponade, hemorrhage (which can be life threatening), loculated intrapleural hematoma, atelectasis, pneumonia, arterial air embolism (when needle thoracostomy is performed and no tension pneumothorax is present), and pain to the patient.
Tube thoracostomy is the definitive treatment for secondary spontaneous pneumothorax (SSP) (see the following image) and tension pneumothorax. Needle decompression mandates an immediate follow up with a tube thoracostomy.
The procedure is as follows:
· If the patient is hemodynamically stable, consider conscious sedation with careful titration of a short-acting narcotic and benzodiazepine.
· Place the patient in a 30-60° reverse Trendelenburg position.
· Scrub the site (centered around the fifth or sixth rib in the midaxillary line) with povidone-iodine (Betadine), alcohol, or both.
· Locally anesthetize the site with lidocaine. (Use a generous amount, and anesthetize all the way down to the pleura.)
· Create a 3- to 4-cm horizontal incision over the fifth or sixth rib in the midaxillary line.
· Use a curved hemostat, and dissect (in a controlled manner) through the soft tissue and down to the rib.
· Push the hemostat just over the superior portion of the rib, avoiding the intercostal neurovascular bundle that runs under the inferior portion of the next most superior rib. Then, puncture the intercostal muscles and parietal pleura. Spread the hemostat wide to create an adequate opening.
· Maintain the intrapleural position by inserting a finger along side of the hemostat. Assess the presence and location of pulmonary adhesions. Sweep the finger in all directions, and feel for the diaphragm and possible intra-abdominal structures. Remove the hemostat. To avoid losing the desired tract, some authors recommend keeping the finger in place until the tube is inserted.
· Insert the chest tube over the finger into the pleural space. A clamp may suffice for guiding the thoracostomy tube into place on the proximal end.
the chest tube posteriorly, and insert it until it is at least
· Look for condensation in the tube as a sign of correct placement and air evacuation.
· Attach the tube to a water seal and vacuum device (eg, Pleur-Evac). Look for respiratory variation of the water seal and bubbling of air through the water seal. Document the amount of blood or other fluids drained.
· Connect the thoracostomy tube to an underwater seal apparatus and suction.
· Suture the tube in place, dress the wound, and tape the tube to the chest. Cover the site with Vaseline-impregnated gauze, and apply a suitable dressing. A variety of anchoring and closure techniques exist, all of which are probably equivalent
· Obtain a follow-up chest x-ray to assess tube positioning and lung reexpansion.
Complications of tube thoracostomy include death, injury to lung or mediastinum, hemorrhage (usually from intercostal artery injury), neurovascular bundle injury, infection, bronchopleural fistula, and subcutaneous or intraperitoneal tube placement.
· Surgical decompression (vacuum-assisted thoracostomy [VATS], open thoracotomy, etc) is indicated for the following:
· Persistent air leak for longer than 5-7 days with a chest tube in place
· Recurrent, ipsilateral pneumothorax
· Contralateral or bilateral pneumothorax
· First-time presentation in a patient with a high-risk occupation (eg, diver, pilot)
· Patients with acquired immunodeficiency syndrome (AIDS) (often because of extensive underlying necrosis)
· Unacceptable risk of recurrent pneumothorax for patients with plans for extended stays at remote sites
· Lymphangiomyomatosis, a condition causing a high risk of pneumothorax.
Accumulation of blood within the chest, or hemothorax, is a relatively common problem, most often resulting from injury to intrathoracic structures or the chest wall. Hemothorax unrelated to trauma is considerably less common and can result from various causes. Prompt identification and treatment of traumatic hemothorax is an essential part of the care of the injured patient. In cases of hemothorax unrelated to trauma, a careful investigation for the underlying source must be performed while treatment is occurring.
Bleeding into the pleural space can occur with virtually any disruption of the tissues of the chest wall and pleura or the intrathoracic structures.
The physiologic response to the development of a hemothorax is manifested in 2 major areas: hemodynamic and respiratory. The degree of hemodynamic response is determined by the amount and rapidity of blood loss.
Normal respiratory movement may be hampered by the space-occupying effect of a large accumulation of blood within the pleural space. In trauma cases, abnormalities of ventilation and oxygenation may result, especially if associated with injuries to the chest wall. In some cases of nontraumatic origin, especially those associated with pneumothorax and a limited amount of bleeding, respiratory symptoms may predominate.
Hemodynamic changes vary depending on the amount of bleeding and the rapidity of blood loss. Blood loss of up to 750 mL in a 70-kg man should cause no significant hemodynamic change. Loss of 750-1500 mL in the same individual will cause the early symptoms of shock, ie, tachycardia, tachypnea, and a decrease in pulse pressure.
Significant signs of shock with signs of poor perfusion occur with loss of blood volume of 30% or more (1500-2000 mL). Because the pleural cavity of a 70-kg man can hold 4 or more liters of blood, exsanguinating hemorrhage can occur without external evidence of blood loss.
Blood occupying the pleural cavity takes up space that the lung would fill in normal respiratory excursion. A large enough collection causes the patient to complain of dyspnea and may produce the clinical finding of tachypnea. The volume of blood required to produce these symptoms in a given individual varies depending on a number of factors, including organs injured, severity of injury, and underlying pulmonary and cardiac reserve.
Dyspnea is a common symptom in cases in which hemothorax develops in an insidious manner, such as those secondary to metastatic disease. Blood loss in such cases is not acute as to produce a visible hemodynamic response, and dyspnea is often the predominant complaint.
Two pathologic states are associated with the later stages of hemothorax. These include empyema and fibrothorax.
Empyema results from bacterial contamination of the retained hemothorax. If undetected or improperly treated, this can lead to bacteremia and septic shock.
Fibrothorax results when fibrin deposition develops in an organized hemothorax and coats both the parietal and visceral pleural surfaces, trapping the lung. The lung is fixed in position by this adhesive process and is unable to fully expand. Persistent atelectasis of portions of the lung and reduced pulmonary function result from this process.
². According to extent:
²². According to degree of hemorrhage:
1. Small (the loss less 10 % of volume of circulating blood).
2. Moderate (loss of 10-20 % of volume of circulating blood).
3. Great (loss of 20-40 % of volume of circulating blood).
4. Total (exceeds 40 % of volume of circulating blood).
²²². According to duration of bleeding:
1. With persistent hemorrhage.
2. With the stopped bleeding.
²V. According to the presence of clots in a pleural space:
2. No- coagulated.
V. According to the presence of infection:
1. Not infected.
2. Infected (suppurative).
If hemothorax is the complication of blunt chest trauma, the clinical manifestations depend on the gravity of trauma and degree of hemorrhage. Also hemothorax by itself results in pulmonary compression and shift of mediastinum.
In case of small hemothorax clinical manifestations of hemorrhage are slightly expressed or absent at all.
Dyspnea, cough, general malaise and dizziness are obvious in moderate hemothorax. The skin is pale. The hemodynamic disturbances tachycardia and decreased arterial pressure are observed.
The great and total hemothorax are associated with extremely grave condition. The patients are troubled with expressed general malaise, dizziness, dyspnea and difficult breathing. In some cases they enter medical hospitals in a terminal state. The skin is sharply pale. The peripheral pulse impaired or absent. Tachycardia, weak cardiac tones, low arterial pressure are obvious.
By percussion the dullness is revealed. On auscultation - the breathing over the site of hemothorax is sharply diminished or is not heard.
The X-ray picture of hemothorax is rather specific. The intensive homogeneous shadow on the side of the lesion with oblique upper contour (Damuaso' line) is observed. The costal sinus does not visualized. In small hemothorax, depending on the degree of intrapleural bleeding, the shadow observed only in the region of sinus. In moderate hemothorax it achieves a scapular angle (on the back surface) or V rib on anterior surface of the chest wall. In great hemothorax this shadow achieves ²²² rib, and total hemothorax characterized by complete shadow of a pleural space, and in some cases mediastinal shift to the healthy side.
Left side small hemothorax
Left side moderate hemothorax
Right side great hemothorax
Left side total hemothorax
1. Complaint and anamnesis of the disease.
2. Physical examination.
Symptoms and physical findings associated with hemothorax in trauma vary widely depending on the amount and rapidity of bleeding, the existence and severity of underlying pulmonary disease, the nature and degree of associated injuries, and the mechanism of injury.
Hemothorax is rarely a solitary finding in blunt trauma. Associated chest wall or pulmonary injuries are nearly always present.
Simple bony injuries consisting of one or multiple rib fractures are the most common blunt chest injuries. A small hemothorax may be associated with even single rib fractures but often remains unnoticed during the physical examination and even after chest radiography. Such small collections rarely need treatment.
Complex chest wall injuries are those in which either 4 or more sequential single rib fractures are present or a flail chest exists. These types of injuries are associated with a significant degree of chest wall damage and often produce large collections of blood within the pleural cavity and substantial respiratory impairment. Pulmonary contusion and pneumothorax are commonly associated injuries. Injuries resulting in laceration of intercostal or internal mammary arteries may produce a hemothorax of significant size and significant hemodynamic compromise. These vessels are the most common source of persistent bleeding from the chest after trauma.
Delayed hemothorax can occur at some interval after blunt chest trauma. In such cases, the initial evaluation, including chest radiography, reveals findings of rib fractures without any accompanying intrathoracic pathology. However, hours to days later, a hemothorax is seen. The mechanism is believed to be either rupture of a trauma-associated chest wall hematoma into the pleural space or displacement of rib fracture edges with eventual disruption of intercostal vessels during respiratory movement or coughing.
Large hemothoraces are usually related to injury of vascular structures. Disruption or laceration of major arterial or venous structures within the chest may result in massive or exsanguinating hemorrhage.
Hemodynamic manifestations associated with massive hemothorax are those of hemorrhagic shock. Symptoms can range from mild to profound, depending on the amount and rate of bleeding into the chest cavity and the nature and severity of associated injuries.
Because a large collection of blood will compress the ipsilateral lung, related respiratory manifestations include tachypnea and, in some cases, hypoxemia.
A variety of physical findings such as bruising, pain, instability or crepitus upon palpation over fractured ribs, chest wall deformity, or paradoxical chest wall movement may lead to the possibility of coexisting hemothorax in cases of blunt chest wall injury. Dullness to percussion over a portion of the affected hemithorax is often noted and is more commonly found over the more dependent areas of the thorax if the patient is upright. Decreased or absent breath sounds upon auscultation are noted over the area of hemothorax.
3. Chest roentgenograms in 2 planes.
The upright chest radiograph is the ideal primary diagnostic study in the evaluation of hemothorax.
In the normal unscarred pleural space, a hemothorax is noted as a meniscus of fluid blunting the costophrenic angle or diaphragmatic surface and tracking up the pleural margins of the chest wall when viewed on the upright chest x-ray film. This is essentially the same chest radiographic appearance found with any pleural effusion.
In cases in which pleural scarring or symphysis is present, the collection may not be free to occupy the most dependent position within the thorax, but will fill whatever free pleural space is available. This situation may not create the classic appearance of a fluid layer on a chest x-ray film.
As much as 400-500 mL of blood is required to obliterate the costophrenic angle as seen on an upright chest radiograph.
In the acute trauma setting, the portable supine chest radiograph may be the first and only view available from which to make definitive decisions regarding therapy. The presence and size of a hemothorax is much more difficult to evaluate on supine films. As much as 1000 mL of blood may be missed when viewing a portable supine chest x-ray film. Only a general haziness of the affected hemithorax may be noted.
In blunt trauma cases, hemothorax is frequently associated with other chest injuries visible on the chest radiograph, such as rib fractures (see below), pneumothorax, or a widening of the superior mediastinum.
Additional studies such as ultrasonography or CT scan may sometimes be required for identification and quantification of a hemothorax noted on a plain chest radiograph
5. Investigation of a pleural content.
6. Test by Revilour-Greguar.
7. General blood analysis.
Hematocrit of pleural fluid. Measurement of the hematocrit is virtually never needed in a patient with a traumatic hemothorax.
This study may be needed for the analysis of a bloody effusion from a nontraumatic cause. In such cases, a pleural effusion with a hematocrit value of more than 50% of that of the circulating hematocrit is considered a hemothorax.
8. Biochemical blood analysis.
9. Determining of the blood group and Rh factor.
The coagulated hemothorax. The patient's late apply for medical aid or major bleeding results in formation of clots in a pleural space, and in some cases all blood, which has accumulated in a pleural space, forms by itself a major entire clot.
Depending on degree of bleeding and, consequently, size of clot, the patients complain of chest pain, which intensifies at respiration, dyspnea, general malaise, and dizziness. As a rule, on 3-5 day the fever to 37,5-38°Ñ is observed.
The physical findings (diminishing and absence of vocal fremitus by palpation, dullness by percussion and sharply diminished or absent breathing by auscultation) suggest the presence of pathological process in a pleural space.
Chest roentgenogram reveals the intensive shadow, sometimes heterogeneous (with enlightenments and multiple levels).
The needle aspiration obtains small amount of a liquid hemolyzed blood and small bloody thrombi (according to inner diameter of the needle).
Suppurative hemothorax. The coagulated hemothorax in overwhelming majority is infected, that results in occurrence of a pleural empyema (clinical manifestations, diagnostics and treatment look in chapter " pleural empyema").
A treatment of small hemothorax requires needle aspiration or drainage of pleural space and elimination of blood. The manipulation is carried out in V²-V²² intercostal spaces in the postaxillary or scapular lines.
Total, great or moderate hemothorax with persistent bleeding (positive test by Revilour-Greguar) requires thoracotomy for liquidation of a bleeding source.
The bleeding wounds of lungs are sewed up by twist suture. If the pleural space contains liquid blood, the surgeon carries out its reinfusion. The clots are removed from pleural space.
Tube thoracostomy drainage is the
primary mode of treatment for hemothorax. In adult patients, large-bore chest
tubes, usually 36-
Thoracostomy tube placement for hemothorax should ideally be in the sixth or seventh intercostal space at the posterior axillary line. In the supine trauma victim, a common error in chest tube insertion is placement too anteriorly and superiorly, making complete drainage very unlikely.
After tube thoracostomy is performed, a repeat chest radiograph should always be obtained. This helps identify chest tube position, helps determine completeness of the hemothorax evacuation, and may reveal other intrathoracic pathology previously obscured by the hemothorax. If drainage is incomplete as visualized on the postthoracostomy chest radiograph, placement of a second drainage tube should be considered. Preferably, a video-assisted thoracic surgery (VATS) operative procedure should be undertaken to evacuate the pleural space.
In cases of hemopneumothorax, 2 chest tubes may be preferred, with the tube draining the pneumothorax placed in a more superior and anterior position.
Surgical exploration in cases of traumatic hemothorax should be performed in the following circumstances:
Greater than 1000 mL of blood is evacuated immediately after tube thoracostomy. This is considered a massive hemothorax.
Bleeding from the chest continues, defined as 150-200 mL/h for 2-4 hours.
Persistent blood transfusion is required to maintain hemodynamic stability.
In the majority of trauma cases requiring chest exploration, the bleeding source is from the chest wall, most commonly intercostal or internal mammary arteries. Once identified, these can be easily controlled with suture ligatures in most cases. After control of obvious bleeding and evacuation of clot and blood, a rapid but thorough exploration of the entire chest cavity should be performed.
Unstable rib fractures found at the time of surgery may require some debridement of sharp rib edges to prevent further injury to the lung or adjacent chest wall structures. At some centers, flail segments or extensive rib fractures are stabilized with wires or other types of support in an attempt to improve postoperative chest wall mechanics.
A thoracic surgeon should be present or immediately available at the time of emergency thoracic exploration because control of bleeding from difficult areas such as the hilum of the lung, the heart, or the great vessels may require a surgeon with expertise in that field.
Adequate drainage of the chest after control of bleeding is very important. Because chest drainage tubes are placed under direct vision, the complication of retained hemothorax should occur with extreme infrequency. A minimum of 2 large-bore chest tubes should be used, with one positioned posteriorly and the other positioned anteriorly. Some surgeons prefer the addition of a right-angled chest tube positioned over the diaphragm.
The late sequelae of hemothorax, including residual clot, infected collections, and trapped lung, require additional treatment and, most often, surgical intervention.
The cause of this complication of blunt chest trauma is the damage by edge of the broken rib of parietal and visceral pleural membranes with the following entering of air from a pulmonary tissue into a pleural space and through damaged chest wall (ruptured intercostal muscles) into subcutaneous fat.
In overwhelming majority the subcutaneous emphysema is the outcome of a valvular pneumothorax and pneumothorax in obliterated pleural space.
Subcutaneous emphysema is divided on:
As the subcutaneous emphysema is the outcome of trauma complicated by a rib fracture and posttraumatic pneumothorax, the chief complaints are of chest pain and dyspnea, which intensify at respiration, movements and minor physical activity.
In localized subcutaneous emphysema the patients the complaints of the chest trauma are predominant in symptomatology. On examination observed a swelling of a chest wall in the place of damage. By palpation a subcutaneous crepitation is felt over this region. Percussion reveals a bandbox sound or tympanitis. Auscultation of lungs over subcutaneous emphysema is usually impossible.
The widespread and total subcutaneous emphysema represents a serious moral problem for the patient. Owing to extent of air all over the chest, abdominal wall, neck (wide-spread emphysema), and also face, arms and legs (total emphysema), the patients has a specific appearance: swelling face, thick neck, enlargement of the chest, arms, and legs. Subcutaneous emphysema by itself usually causes no respiratory and cardiovascular disturbances. However the patients note the change of the quality of voice. By palpation the subcutaneous emphysema is felt in whole body ("crisping snow").
It is necessary to note, that in widespread and total emphysema the auscultation is impossible. However the presence of subcutaneous emphysema at the closed trauma of the chest enables to suspect the presence of posttraumatic pneumothorax.
On the chest roentgenogram the enlightenment of a subcutaneous fat (presence of air) is observed.
1. Complaint and history of the disease.
2. Physical findings.
3. Chest X-radiography.
Widespread and total subcutaneous emphysema requires the draining of subcutaneous space by plastic tubes in infra- and supraclavicular region, and also in the zone of the most expressed emphysema. Also performed the drainage of a pleural space.
The subcutaneous emphysema resolves depending on its extent from several days to 2-3,5 weeks.
The isolated injuries of trachea and bronchi as the result of blunt trauma of the chest occur rarely and located mainly in a cervical part.
The main causes of tearing of trachea and bronchi are:
1) shearing forces, which arises at the moment of trauma owing to a sudden rise of intraluminal pressure against a closed glottis when the airway is compressed against the spine.;
2) compressing of a bronchial tree between a breastbone and vertebral column;
3) shift of lungs in sudden and rapid deceleration or acceleration of a body occurs with greater amplitude, than fixed bifurcation of trachea.
Such disruptions most often occurs as a result of vehicular impacts, falls from great heights, direct blows to the chest. In most cases disruption of trachea and bronchi are accompanied with the other visceral damages: lungs, skull and brain, heart, liver and flail chest.
². According to degree of disruption:
· without damage of cartilaginous rings (I degree);
· with fracture of cartilaginous rings (II degree).
2. Partial disruption of all layers (²²² degree).
3. Complete transverse disruption of all walls without disjunction of the of trachea, (bronchus) (²V degree).
4. Abruption with disjunction of the edges of trachea (bronchus) (V degree).
²². According to direction of rupture:
²²². According to localization of the damage:
²V. According to the size of injury:
1. Combined damages of trachea (bronchi) and adjacent organs.
2. Damage of trachea (bronchi) and other segments of the body.
3. Damage of a trachea (bronchi). adjacent organs and other segments of the body.
The clinical manifestations of the injury of trachea depend on the type of disruption, its degree and presence of concomitant damages.
Incomplete isolated disruption of trachea commonly manifests by cough and hemoptysis. Respiration is not disturbed as a rule.
The small disruptions are characterized by various clinics. If the hole is occluded by clot and mediastinal tissues, the signs, which had appeared earlier (cough, hemoptysis, mediastinal emphysema), can disappear. Nevertheless the repeated occurrence of cough, as a rule, leads to severe aggravation of the patient state.
Major and circular disruptions of trachea cause a grave state of the patients. They manifest except difficult breathing by such signs:
1) mediastinal emphysema or pneumothorax;
2) compression syndrome compression and inflection of major vessels due to tension pneumothorax or mediastinal emphysema with transmission into acute cardiopulmonary failure;
3) hemorrhage syndrome;
4) aspiration syndrome, which is the outcome of bleeding into airways or aspirations of the gastric content;
5) traumatic shock.
The injuries of bronchi occur in the way of abruption of main bronchi or their disruption in the zone of bifurcation. In the zone of a tracheal bifurcation observed multiple (2-4) disruptions, which can be longitudinal, transversal or oblique.
Depending on the character of trauma, it is necessary to distinguish direct and secondary disruptions of bronchi. The direct injuries arise from the gunshot and knife wounds, penetration of rib fragments or other subjects in mediastinum or endoscopic manipulations.
The overwhelming majority of bronchial disruption is the part of blunt trauma of the chest. By the way, the damage of vessels of a lung root occurs in 41,3 %.
The predominant clinical signs of a bronchial disruption are the respiratory disturbance, gas syndrome, hemoptysis and hemothorax. However these signs may be observed only in isolated injuries of lungs.
The patients state is grave. Rest dyspnea and acute pain behind a breastbone are the most troubling manifestations. The difficult swallowing, hoarseness, swelling face and subcutaneous crepitation are observed. Auscultatory on the side of trauma the breathing sounds are weak or absent at all.
The sequence of examination of the patients with injuries of trachea and bronchi depends on the character and gravity of trauma, clinical signs and concomitant damages, which threatening life.
If the state of the patient allows, a chest X-radiography is performed. Commonly it is possible to find out mediastinal emphysema, sometimes the sign of discontinuing of trachea.
The injuries of bronchi manifest by the distension of mediastinum and presence of air strips along its borders, and in some cases total or tension pneumothorax observed.
Final and most informative diagnostic method is the tracheobronchoscopy, which can be also the therapeutic method. However it is necessary to carry out decompression of a mediastinal emphysema and pneumothorax before such investigation.
Before examination the clots and liquid blood are aspirated from airways, then adjusted the localization and character of disruption. The incomplete disruptions are usually longitudinal and oblique and located on the line of membranous and cartilaginous part, circular mainly in a cervical part of trachea. Except disruption of the wall, observed the absence of cartilaginous rings in this region and filled by blood parabronchial fat.
The open damages of trachea take place mainly in a cervical part and rarely - in thoracic. In all cases of neck trauma it is necessary always suspect the opportunity of damage of trachea and esophagus.
Such variants of clinical course are distinguished:
- acute course (first 30 days after operation);
- chronic course (complication of trauma).
Acute course is divided onto three stages:
1. The initial stage (lasts during 2 days after the trauma with typical signs of disruption; the urgent resuscitation measures are required).
2. The stage of temporary compensation (lasts during 2 weeks; at this time it is possible to carry out diagnostic examination).
3. The stage of persistent compensation (lasts during 30 days; during this time a stenosis and other persistent complications of disruption of trachea and bronchi develops).
1. Complaint and the history of disease.
2. Physical findings.
3. Chest X-radiography.
4. Diagnostic thoracentesis.
5. General blood and urine analyses.
6. Biochemical blood analysis.
There are primary operations in acute stage (first two days after the trauma) and late repairing operations (in 1 month after the trauma). The operation is based in resection of injured tissues, edges of bronchus with the further suturing of disruption, or wedge-like or circular resection with following anastomosis. In series of cases lobe-, bilobe- or pneumonectomy is performed.
Mediastinal emphysema is the complication of the blunt trauma of the chest, which is characterized by entering and accumulation of air in mediastinum.
The causes of mediastinal emphysema is partial (damage of a membranous part) or complete disruptions of trachea, bronchi, esophagus and in some cases tension pneumothorax.
The entry of air in mediastinum leads to compressing of superior cava vein and right atrium, which results in the expressed discirculation.
The patients complain of difficult breathing and swallowing, pain behind breastbone, hoarseness, cough attacks. As a rule, the patient's position is forced semi-sitting. The neck and face are thickened, cervical veins distended, the skin is cyanotic. By palpation the crepitation of neck, face, and shoulder area. By auscultation heart tones are diminished with tachycardia.
On X-ray film on the background of enlightenment observed well-defined contour of a mediastinal pleura. If there is the damage of mediastinal pleural membrane a pneumothorax (mainly total or intense) is revealed.
Mediastinal emphysema with left-side pneumothorax
1. Complaint and history of the disease.
2. Physical findings.
3. Examination X-radiography of organs of the chest.
4. Definition of central venous pressure.
5. Control of hemodynamic data.
Progressing mediastinal emphysema requires the urgent drainage of a forward mediastinum in order to prevent external cardiac tamponade.
Tension mediastinal emphysema resulting from disruption of trachea or bronchus operative management, pneumothorax, etc., requires the treatment, which is described in previous chapters.
Drainage of anterior mediastinum
Circulatory shock, commonly known as just shock, is a serious, life-threatening medical condition where insufficient blood flow reaches the body tissues. As the blood carries oxygen and nutrients around the body, reduced flow hinders the delivery of these components to the tissues, and can stop the tissues from functioning properly. The process of blood entering the tissues is called perfusion, so when perfusion is not occurring properly this is called a hypoperfusional (hypo = below) state.
Circulatory shock should not be confused with the emotional state of shock, as the two are not related. Medical shock is a life-threatening medical emergency and one of the most common causes of death for critically-ill people. Shock can have a variety of effects, all with similar outcomes, but all relate to a problem with the body's circulatory system. For example, shock may lead to hypoxemia (a lack of oxygen in arterial blood) or cardiac arrest (the heart stopping
Fig. Classes of hemorragical shock
Effects of inadequate perfusion on cell function.
There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next.
During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate (ATP). Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extra-cellular fluid, and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent.
This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline.
Fig. Compensatory mecanisms
Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin-angiotensin axis is activated and arginine vasopressin is released to conserve fluid via the kidneys.
Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin-angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock .
Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.
At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death have occurred. Death will occur imminently.
A medical emergency is an injury or illness that is acute and poses an immediate risk to a person's life or long term health. These emergencies may require assistance from another person, who should ideally be suitably qualified to do so, although some of these emergencies can be dealt with by the victim themselves. Dependent on the severity of the emergency, and the quality of any treatment given, it may require the involvement of multiple levels of care, from a first aider to an emergency physician through to specialist surgeons.
Any response to an emergency medical situation will depend strongly on the situation, the patient involved and availability of resources to help them. It will also vary depending on whether the emergency occurs whilst in hospital under medical care, or outside of medical care (for instance, in the street or alone at home).
For emergencies starting outside of medical care, a key component of providing proper care is to summon the emergency medical services (usually an ambulance), by calling for help using the appropriate local emergency telephone number, such as 999, 911, 112 or 000 or 111. After determining that the incident is a medical emergency (as opposed to, for example, a police call), the emergency dispatchers will generally run through a questioning system such as AMPDS in order to assess the priority level of the call, along with the caller's name and location.
Those trained to perform first aid can act within the bounds of the knowledge they have, whilst awaiting the next level of definitive care. Those who are not able to perform first aid can also assist by remaining calm and staying with the injured or ill person. A common complaint of emergency service personnel is the propensity of people to crowd around the scene of victim, as it is generally unhelpful, making the patient more stressed, and obstructing the smooth working of the emergency services. If possible, first responders should designate a specific person to ensure that the emergency services are called. Another bystander should be sent to wait for their arrival and direct them to the proper location. Additional bystanders can be helpful in ensuring that crowds are moved away from the ill or injured patient, allowing the responder adequate space to work.
Many states of the
The principles of the chain of survival apply to medical emergencies where the patient has an absence of breathing and heartbeat. This involves the four stages of Early access, Early CPR, Early defibrillation and Early advanced life support
Unless the situation is particularly hazardous, and is likely to further endanger the patient, evacuating an injured victim requires special skills, and should be left to the professionals of the emergency medical and fire service.
Within hospital settings, an adequate staff is generally present to deal with the average emergency situation. Emergency medicine physicians have training to deal with most medical emergencies, and maintain CPR and ACLS certifications. In disasters or complex emergencies, most hospitals have protocols to summon on-site and off-site staff rapidly.
Both emergency room and inpatient medical emergencies follow the basic protocol of Advanced Cardiac Life Support. Irrespective of the nature of the emergency, adequate blood pressure and oxygenation are required before the cause of the emergency can be eliminated. Possible exceptions include the clamping of arteries in severe hemorrhage.
While the golden hour (medicine) is a trauma treatment concept, two emergency medical conditions have well-documented time-critical treatment considerations: stroke and myocardial infarction (heart attack). In the case of stroke, there is a window of three hours within which the benefit of clot-busting drugs outweighs the risk of major bleeding. In the case of a heart attack, rapid stabilization of fatal arrhythmias can prevent sudden cardiac death. In addition, there is a direct relationship between time-to-treatment and the success of reperfusion (restoration of blood flow to the heart), including a time dependent reduction in the mortality and morbidity.In 1972 Hinshaw and Cox suggested the following classification which is still used today. It uses four types of shock: hypovolemic, cardiogenic, distributive and obstructive shock:
Hypovolemic shock This is the most common type of shock and based on insufficient circulating volume. Its primary cause is loss of fluid from the circulation from either an internal or external source. An internal source may be haemorrhage. External causes may include extensive bleeding, high output fistulae or severe burns.