European
Course Trauma Care
THORACIC TRAUMA
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EPIDEMIOLOGY
The 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 injury. It is
estimated that thoracic trauma are 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 secondary to cardiac tamponade airway obstruction and aspiration.
Two thirds of these patients reach the hospital prior to die. Only 10-15% of blunt trauma
require thoracic surgery, and 15-30% of the penetrating chest trauma require open
thoracotomy. 85% of patients with thoracic trauma, can be managed by simple lifesaving
manoeuvre that do not require surgical treatment.
Thoracic injury occurs in the chest wall, lungs and pleura, thoracic great. vessels,
diaphragm heart, trachea, bronchus and oesophagus. The magnitude of those problems and the
significance of the associated injuries serve to underscore the importance of complete
evaluation and timely intervention in the management of thoracic trauma.
Many patients can be successfully treated with or without tube thoracostomy, respiratory
support and in a few cases with emergency thoracotomy. Endotracheal intubation support and
treats post-traumatic respiratory insufficiency. Although some of the complex and
potentially fatal traumatic thoracic injuries require emergent surgical intervention, most
of them can be treated nonoperatively by the proper application of certain fundamental
principles of initial trauma management. These principles can substantially reduce the
morbidity and mortality. Appropriate early management of the rapidly fatal and potentially
fatal thoracic injuries can also significantly decrease the late complications. Optimal
treatment requires a through knowledge of the ethiology and pathophysiology of the thorax
and expertise the therapeutic interventions. Improved prehospital care and rapid
transportation have increased the survival, but the lethality remains high.
Pathophysiology
Thoracic trauma can induce two serious derangement:
1 Respiratory insufficiency due to:
pneumothorax tension pneumothorax open pneumothorax flail chest pulmonary contusion
aspiration
2. Hemorrhagic shock due to:
hemothorax hemomediastinum
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.
Penetrating wound of the chest (gunshot or stab wound) may cause comminuted fractures of a
rib, with bone fragments driven into the lung substance.
The most common manifestation of penetrating trauma to the visceral and parietal pleura is
disruption of normal negative intrapleural pressure resulting in pneumothorax. Penetrating
wounds cause both direct injury to structures encountered by the weapon and indirect
injury.
The extent of internal injuries cannot be judge by the appearance of a skin wound.
Blunt forces applied to the chest wall cause injury by three mechanisms: rapid
deceleration, direct impact and compression. Rapid deceleration is the usual force
involved in high speed motor vehicle accidents and falls from height. The degree of
external trauma may not fully predict the severity of internal injuries and clinical
suspicion of cardiac and vascular trauma should be heightened.
Direct impact by a blunt object can cause localised fractures of the ribs, sternum or
scapula with underlying lung parenchyma injury, cardiac contusion or pneumothorax.
Compression of the chest by a very heavy object, which prevents respiration and causes
marked increases in blood pressure within veins of the upper thorax, may result in
traumatic asphyxia. Anterior-posterior compression forces place indirect pressure on the
ribs, causing lateral, mid-shaft fractures. Lateral compression forces applied to the
shoulder are common causes of sternoclavicular joint dislocation and clavicle fractures.
Massive blunt injury to the chest wall may comprise elements of deceleration, direct
impact, and compression to yield multiple adjacent rib fractures is in more than one
location. In this setting, a free-floating segment of the chest wall can more
paradoxically with respiration causing ineffective ventilation.
Moreover than respiratory insufficiency thorax trauma can cause hemorrhagic shock due to
hemothorax and rarely to hemomediastinum. 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.
Goal of the chapter
At the end of this chapter the student must be able to identify and treat the
chest trauma and to understand and avoid the most common mistakes and complications in the
treatment. The initial management of the patients with thoracic trauma is frequently the
responsibility of the emergency physician who is not a thoracic surgeon but a general
surgeon. It is therefore imperative that emergency physician is able to recognise the
thoracic injuries that are or will be dramatic if not treated properly.
In unstable and critical circumstances, quick decisions and adequate manoeuvres based on
recordings of vital signs and a right interpretation of clinical and diagnostic pattern
are required.
The purpose of this chapter is to establish the right guidelines in the treatment of
thoracic injuries.
Thoracic injury: priorities
The evaluation of the patient's chest trauma is only a part of the total
assessment; furthermore because thoracic injuries are severe and potentially lethal, the
diagnosis and therapy go hand in hand.
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.
The airway can be occluded by foreign bodies present in the month or by a fall of the
tongue backwards as occurs in unconscious patients.
Patency of the airway must be retarded by a simple manoeuvre to remove foreign body from
the month or to correct backwards fall of the tongue (Chap. AIRWAY AND VENTILATION).
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.
Remember that cyanosis appears very late in hypoxia due to a thoracic trauma because in
shocky patients the skin blood flaw depends on blood redistribution in the body.
Circulation: the state of the circulation is evaluated by ossessing patient's pulses
(radial, carotideal 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 control the neck veins that are flat in hypodermia; are distended when there
is cardiac tamponade. But if cardiac tamponade is associated with hypovolemic shock
distension of the neck veins may be absent.
In thoracic trauma patients there are the following life-threatening lesions that must immediately identified and treated.
Open pneumothorax: usually results from a penetration wound of the chest
that may create a communication between the pleural space and external environment. As the
size of this defect approaches two thirds the size of the tracheal diameter, air passes
preferentially through the lower resistance injury tract rather than through the normal
airways. This severely compromises oxygenation and ventilation and is immediately
life-threating. In an open or "sucking" wound of the chest wall, the lung on the
affected side is exposed to atmospheric pressure, which results in the lung's collapse and
a shift of the mediastinum to the uninvolved side. Because of the severe degree of
venoarterial shunting that occurs in both lungs, resulting in profound
ventilation-perfusion inequality, the patient becomes cyanotic and has serious respiratory
distress.
The open pneumothorax must be treated rapidly using one of two approaches. In the
spontaneously ventilating patient, application of a sterile occlusive dressing with
vaseline gauze large enough to cover the wound entirely taped securely on three sides is
the treatment of choice. Tube thoracotomy at a remote site should be placed.
If the chest wall defect is relatively small, the pleura may soon seal and no further
intervention is necessary. A second approach is to simply intubate the patient and
initiate positive pressure ventilation.
Often surgical repair is required.
Tension pneumothorax: develops when air enters the pleural space but
cannot exit. The consequence is 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 valvelike 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 hyperresonance 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.
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 (500-1500 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.
Cardiac tamponade: penetrating cardiac injuries 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-calibre 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.
The following lesions are life-threatening but give to the physician more time to diagnose and treat them.
Thoracic cage injuries: with severe trauma, fractures of any rib or
combination of ribs and fractures in this area are likely. However, the fracture usually
occurs at the point of impact, often laterally such fractures are hard to see on X-ray
films. Crushing injuries may produce multiple eggshell fractures, the sites being
dependent on the direction of the compressing forces. For example, impaling the anterior
chest on a steering wheel as in an automobile accident, often fractures the sternum and
several ribs anteriorly on both sides. Besides rib fractures, costovertebral dislocation
may occur at any level, as may occur costochondral and chondrosternal separations.
Fractures may be transverse or oblique and the fragments may override or a pointed
fragment may be pushed inward, tearing the pleura and underlying lung.
In the elderly patient with atrophic, decalcified ribs, fractures may result from simple
trauma, coughing or any severe muscle pull. Fractures of the rib or sternum or
costovertebral separations are diagnosed from movement of fragments, ecchymosis and
crepitus, as well as by X-ray examination. Since pain characteristically occurs with
inspiration, the patient tends to splint the chest wall and therefore, hypoventilates.
A chest X-ray film must be performed, not only to identify the number and the extent of
rib fractures, but also to determine whether there is an associated pneumothorax,
hemothorax and pleural effusion. Rib fractures usually heal readily if complications are
handled properly. However, the pain associated with the fracture can prevent proper
ventilation and coughing, leading to atelectasis, retained secretions and pneumonia,
especially in the elderly. Damage to the underlying lung may cause hemothorax,
pneumothorax or pulmonary contusion, multiple rib fractures may produce paradoxical
movement of the chest wall, with a flail segment. Pain from a rib fracture can be treated
by intercostal or paravertebral block; this promptly relieves the pain and quiets the
laboured respiration which may be accentuating paradoxical motion of the chest. The major
problem with a block are increased reflex bronchial secretions; these must be removed if
patients are to avoid an obstructive type of pneumonia which is particularly dangerous in
the elderly.
If coughing is inadequate, tracheal aspiration on by catheter or by broncoscopy and
occasionally by endotracheal intubation may be necessary.
The ribs usually become fairly stable within 10 days to two weeks. Firm healing with
callus formation is seen after about six weeks.
Flail chest: A segment of chest wall does not have continuity with the
rest of thoracic cage because multiple risk fractures causing serious respiratory
distress.
In flail chest injury, the unstable segment wall moves separately and in ,an opposite
direction from the rest of the thoracic cage during the respiration cycle. In politrauma
patients flail chest injury is quite common. Thirty-one percent of 50.000 trauma patients
included in the Major Trauma Outcome study had chest injuries. Five percent of these
patients had flail chest injury.
Flail chest injury usually results from direct impact. If the crushing force is from the
lateral direction, the injury usually consists of fractures in at least two sites in
multiple adjacent ribs on the involved side, resulting in a "floating" central
portion of the chest wall, which goes in and out with respiration in a reverse or
paradoxical manner to the rest of the chest wall. This type of respiration markedly
decreases the efficiency of ventilation, and is usually accompanied by severe pain that
makes the coughing mechanism ineffectual.
If the crushing blow is directly over the sternum, as often happens in steering wheel
injuries, fractures of the sternum may occur. Such an injury is most frequently associated
with bilateral costochondral fractures usually from the first rib down resulting in
extreme flailing of the anterior portion of the chest wall.
The physiopathologic effects of flail chest are an important decrease in vital capacity,
reduction in functional residual capacity. Often there are ventilation-perfusion
imbalance, hypoxemia, decreased compliance, increased airway resistance and increased
breathing effort. The diagnosis of flail chest injury is made by physical examination.
adequate examination after blunt chest trauma must include inspection of an unclothed
patient from anterior, posterior and both lateral angles. Clinically, the unsupported
portion of the chest wall is seen to move paradoxically with respiration. On inspiration,
the flail area moves in; on expiration or coughing it moves outward. If the flail segment
is large, the important effect are those of inadequate ventilation, inadequate perfusion
resulting in progressive hypoxia and hypercapnia and inefficient coughing with retained
secretions, radiographs can document multiple rib fractures. The treatment of flail chest
involves selective use of endotracheal intubation and mechanical ventilation. Not all
patients require intubation. Flail chest patient without respiratory impairment generally
do well without ventilatory assistance. The primary indication for endotracheal intubation
and mechanical ventilation is respiratory decompensation. Aggressive pulmonary
physiotherapy with suctioning, incentive spirometry, early mobilisation, and umidification
of air is appropriate for all patients. Intermittent positive pressure breathing, postural
drainage, cupping or clapping and therapeutic fiberoptic broncoscopy to suction retained
secretions and treat atelectasis are often necessary.
Further than internal fixation effected by endotracheal tube or tracheostomy the
stabilisation of the chest wall may be performed by external surgical fixation.
Pneumothorax: lung laceration or bronchial lesion permit air entry into pleural
space. That results in collapse of the lung, increase of endopleural pressure and
compression of controlateral lung by mediastinum dislocation. In this case a severe
alteration of ventilation perfusion ratio may occur because blood circulation in non
ventilated pulmonary area. Chest percussion in patient with pneumothorax shows
hyperresonance and breath-sounds decrease or absence confirmation of the diagnosis is
obtained by chest X-ray.
In the absence; of hemodynamic compromise, even large pneumothoraces rarely require
emergent management. However, any post-traumatic pneumothorax should be treated as
expeditiously as possible. A chest tube is inserted after cardiologic evaluation and lung
reexpansion carefully and repeatedly assessed with follow-up chest X-rays. Placement of an
intercostal tube or catheter can be readily accomplished under local or intercostal nerve
block anaesthesia, or both.
It may be done at the bedside, but strict aseptic precautions need to be observed. The
site for tube insertion should be one that is away from adherent lung. Generally preferred
is the second or third anterior intercostal space in the midclavicular line or the fourth
or fifth intercostal space in the midaxillary line. To help select the optimal point of
entry, chest X-ray films should be reviewed unless the clinical situation is an of extreme
urgency.
Pulmonary contusion: is of primary importance in the field of major
trauma to the chest. It is a potential life-threatening condition mainly because the onset
of symptoms is insidious.
Also, since the force required to produce a lung contusion must be great, the lesion is
likely to occurs principally in cases of high speed accidents, falls from great heights
and injuries by high-velocity bullets.
Patients suffering such accidents often have so many other obvious injuries that detection
of a chest lesion may escape. After seemingly negligible initial signs and symptoms, the
outcome may be fatal. Symptoms and signs of pulmonary contusion are: dispnea, hypoxemia,
cyanosis, tachycardia, rare or absent breath sounds, rib fractures.
Hemorrhage, oedema and microatelectasis are the morphologic consequences of pulmonary
contusion. A prompt diagnosis is the main factor in initiating management and determining
whether treatment will be effective. The diagnosis is first suspected from history of
major trauma.
The chest X-ray film is very important, and may show patchy, undefined densities or
homogenous consolidation. Patients who sustain pulmonary contusion have to be treated with
intubation, mechanical ventilatory support and antibiotic therapy chest CAT scan permits
to evaluate exactly the extension of pulmonary contusion
Rupture of trachea or major bronchi: the trachea and major bronchi because of their similar anatomic position are subject to the same mechanisms of injury for either blunt or penetrating trauma. Rupture of the trachea or major bronchi is usually secondary to an injury of the chest as a result of an automobile accident. It is a serious injury with an estimated mortality of 30%. More than 80% of the ruptures of bronchi are within 2.5 cm of the carina. Injuries to the main bronchi and intrathoracic trachea are more prevalent than those to the cervical trachea because the latter is protected by the mandible and sternum anteriorly and by vertebrae posteriorly. The intimate anatomical relationship of the trachea to the great vessels, lungs and heart explain the high incidence of serious associated injuries in blunt and penetrating trauma. The clinical picture appears in two patterns, depending on whether or not there is free communication between the rupture of the trachea-bronchial tree and the pleural cavity. If there is free communication, a large pneumothorax results. The usual signs of tracheobronchial disruption are the followings:
hemoptysis dyspnea subcutaneous and mediastinal emphysema occasionally cyanosis.
Tube thoracostomy shows continuos bubbling of air in the water seal, and suction fails
to reexpand the lung. The chest X-ray demonstrate pneumothorax, pleural effusion,
pneumomediastinum or subcutaneous air. Overall 90% of these patients will have an abnormal
chest X-ray on admission.
Bronchoscopy should be carried out promptly when tracheobronchial rupture is suspected,
since it is the most reliable means of establishing the diagnosis.
The bronchoscopy has a role not only in diagnosis of tracheobronchial disruption, but also
may be an invaluable tool in resuscitation.
Tracheal and selective bronchial intubation may allow ventilation of the intact lung while
is performed on the controlateral bronchial rupture.
Bronchoscopy should be carried out promptly; if it indicates that the bronchial tear
involves less than one-third of the lumen, the patient is stable and if the thoracostomy
tube under-water-seal drainage results in complete expansion of the lung, treatment may be
conservative. However in all other types of tracheobronchial injury, thoracotomy should be
performed as soon as possible.
In this situation, ventilatory support with high frequency ventilation has not been shown
to be useful, whereas success has followed the use of double lumen tubes and selective
bronchial intubation followed by early surgical repair, with mucosal - to - mucosal
closure with interrupted sutures.
Heart injuries (cardiac contusion): myocardial contusion is associated,
in chest blunt trauma, with fractures of the sternum or ribs.
The diagnosis is based on electrocardiogram abnormalities and elevation of serial cardiac
enzymes.
Cardiac contusion can simulate a frank myocardial infarction. Electrocardiographic
findings are multiple, premature ventricular contractions, atrial fibrillation, right
branch block and changes in ST.
Patient must be submitted to observation with cardiac monitoring.
Thoracic great vessels injuries: is principally a civilian phenomenon an
currently accounts of 8-9% of vascular injuries seen in trauma centers. It may be result
of penetrating or blunt trauma.
The patient with chest trauma may present with respiratory distress due to hemothorax. An
initial "rush" of a large volume of blood after tube thoracostomy may indicate
great vessels injury. The classic signs of pericardial tamponade may be present.
Suggestive radiological signs include presence of hemothorax, pneumothorax or the foreign
bodies, widening of the superior mediastinum more than 8 cm and depression of the left
mainstem bronchus more than 140 degrees.
Aortography should be performed in the patient with moderate to severe injuries that is
stable hemodynamics. CAT and MR have not been shown to be as diagnostic as aortography.
The patient with signs of respiratory distress and suspected pneumothorax should undergo
immediate tube thoracostomy. As mentioned above, if blood loss is greater than 1 L, with
continued bleeding must be performed a thoracotomy and repair of the rupture of the
vessel.
Trauma to oesophagus: in trauma patients rupture of oesophagus is very
rare. More frequent is the perforation of the oesophagus for penetrating trauma.
Oesophagus trauma is lethal if unrecognised because mediastinitis due to contamination
mediastinal space by oesophageal content with very high concentration of necrosis
bacteria. The patient's complain of sudden excruciating pain in the epigastrium, which
lasts and radiates to the chest, to the back or both. Dyspnea, cyanosis and shock soon set
in and dominate the clinical picture. Emphysema and pneumo - or hydropneumothorax,
especially in the left mediastinum develop and become visible radiologically. Esophagogram
may be performed when the patient is stable.
Esophagoscopic visualisation of localised blood in the oesophagus or an actual laceration
is diagnostic.
Operation is advocated when the patient is unstable and when are present major injuries.
The principles in the management of major oesophageal injuries are those of early
operation, two - layer surgical closure when possible and wide mediastinal drainage.
Extensive tissue destruction or associated major mediastinal contamination, such as occurs
when repair is delayed by more than 12-16 hours, are indications to consider a closure
with a T-tube or an exclusion technique.
Diaphragmatic injuries: once relatively uncommon, injuries of the
diaphragm are occurring more frequently, paralleling the rise of frequency of automobile
accidents. The diagnosis is often missed because of associated intraabdominal injuries.
Diaphragmatic injuries may also be caused by penetrating or blunt trauma. Diaphragmatic
injury is suspected in any penetrating thoracic wound (gunshot, stab or accidental
perforation) at or below 4th intercostal space anteriorly, 6th interspace laterally, or
8th interspace posteriorly, although sharply oblique wounds or missiles deflected by ribs
may also penetrate diaphragm. Stomach and other abdominal viscera may herniate into left
thorax; left lung may collapse, right lung may be compressed, mediastinum my be shifted
and trachea deviated to the right.
Symptoms are related to the quantity of herniated viscera in to the thorax. The usual
clinical manifestations are: dyspnea, chest or shoulder pain and cyanosis. If the
herniated organ is stomach, the dyspnea can be relieved dramatically by introduction of a
nasogastric tube. The diagnosis is performed or suspected by chest X-ray that may
demonstrate: atelectasis with silhouetting of the ipsilateral diaphragm, evidence of an
air-filled or soled viscus in the thorax and abnormal curvilinear shadow above the
diaphragm. A contrast stomach X-ray may visualise the stomach herniated into thorax.
Ultrasound and CAT scan will confirm the diagnosis.
The most common errors in diaphragmatic trauma are failure to inspect the leaflets
adequately during operative exploration or penetrating injury and failure to suspect the
possibility of diaphragmatic injury.
The treatment is always surgery by an abdominal approach.
The decision to repair an isolated diaphragmatic rupture in an acutely injured patient
should depend on how the patient tolerates the loss of normal, negative intrathoracic
pressure.
Gross signs of cardiorespiratory distress or shock are indication for immediate
repair.
Thoracic aorta rupture: rupture of the thoracic aorta is a common cause
of sudden death in roctures of unrestrained frontal collision and in a fall from a great
height.
Laceration of the thoracic aorta supervenes near the aortic legamentum arteriosum.
If the aorta is non completely interrupted and there is an intact adventitial layer it is
possible to operate on the patient and to repair the lesion. If the patient is not
diagnosed and not adequately treated will die in few hours or days.
The dynamic of the collision, fractures of the scapula, the first and second ribs and the
medial third of the clavicle, all suggest severe trauma and should lead to a suspicion of
a laceration of the thoracic aorta.
The chest X-ray can show a widening of mediastinum, right tracheal shift, elevation and
rightward shift of the right bronchus, depression of the left bronchus, aortic knob
outline, deviation of the oesophagus to the right,. Transesophageal U.S. scan is a useful
diagnostic tool if available. CAT scan is mandatory as well as aortography. The treatment
is immediate surgery by qualified surgeon.
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