Blunt chest injuries
Blunt chest injuries: Excerpt from Professional Guide to Diseases (Eighth Edition)
Chest injuries, including blunt chest injuries, consist of myocardial contusion as well as rib and sternal fractures that may be simple, multiple, displaced, or jagged. Such fractures may cause potentially fatal complications, such as hemothorax, pneumothorax, hemorrhagic shock, and diaphragmatic rupture.
Causes and incidence
Motor vehicle accidents cause two-thirds of major chest injuries in the United States. Other common causes include sports and blast injuries and cardiopulmonary resuscitation. About 50% of these injuries affect the chest wall; 80% of those with significant blunt chest trauma also have extrathoracic injuries.
Chest injuries account for 70% of all trauma-related deaths in the United States.
Signs and symptoms
Rib fractures produce tenderness, slight edema over the fracture site, and pain that worsens with deep breathing and movement; this painful breathing causes the patient to display shallow, splinted respirations that may lead to hypoventilation. Sternal fractures, which are usually transverse and located in the middle or upper sternum, produce persistent chest pains, even at rest. If a fractured rib tears the pleura and punctures a lung, it causes pneumothorax. This usually produces severe dyspnea, cyanosis, agitation, extreme pain and, when air escapes into chest tissue, subcutaneous emphysema.
Multiple rib fractures within two or more places may cause flail chest, in which a portion of the chest wall “caves in,” causing a loss of chest wall integrity and preventing adequate lung inflation. (See Flail chest: Paradoxical breathing.)
Signs and symptoms of flail chest include bruised skin, extreme pain caused by rib fracture and disfigurement, paradoxical chest movements, tachycardia, hypotension, respiratory acidosis, cyanosis, and rapid, shallow respirations. Flail chest can also cause tension pneumothorax, a condition in which air enters the chest but can’t be ejected during exhalation. This life-threatening thoracic pressure buildup causes lung collapse and subsequent mediastinal shift. The cardinal symptoms of tension pneumothorax include severe dyspnea, absent breath sounds (on the affected side), agitation, jugular vein distention, tracheal deviation (away from the affected side), cyanosis, and shock.
Hemothorax occurs when a rib lacerates lung tissue or an intercostal artery, causing blood to collect in the pleural cavity, thereby compressing the lung and limiting respiratory capacity. It can also result from rupture of large or small pulmonary vessels.
Massive hemothorax is the most common cause of shock after a chest injury. Although slight bleeding occurs even with mild pneumothorax, such bleeding resolves very quickly, usually without changing the patient’s condition. Rib fractures may also cause pulmonary contusion (resulting in hemoptysis, hypoxia, dyspnea, and possible obstruction), large myocardial tears (which can be rapidly fatal), and small myocardial tears (which can cause pericardial effusion).
Myocardial contusions — actual bruising of the heart muscle — produce electrocardiographic (ECG) abnormalities. Laceration or rupture of the aorta is almost always immediately fatal. Because aortic laceration may develop 24 hours after blunt injury, patient observation is critical. Diaphragmatic rupture (usually on the left side) causes severe respiratory distress. Unless treated early, abdominal viscera may herniate through the rupture into the thorax (with resulting bowel sounds in the chest), compromising both circulation and the lungs' vital capacity.
Other complications of blunt chest trauma may include cardiac tamponade, pulmonary artery tears, ventricular rupture, and bronchial, tracheal, or esophageal tears or rupture.
Diagnosis
A history of trauma with dyspnea, chest pain, and other typical clinical features suggest a blunt chest injury. To determine its extent, a physical examination and diagnostic tests are needed.
❑ In hemothorax, percussion reveals dullness. In tension pneumothorax, it reveals tympany. Auscultation may reveal a change in position of the loudest heart sound.
❑ Chest X-rays may confirm rib and sternal fractures, pneumothorax, flail chest, pulmonary contusions, lacerated or ruptured aorta, tension pneumothorax, diaphragmatic rupture, lung compression, or atelectasis with hemothorax.
❑ With cardiac damage, the ECG may show abnormalities, including unexplained tachycardias, atrial fibrillation, bundle-branch block (usually right), ST-segment changes, and ventricular arrhythmias such as multiple premature ventricular contractions.
❑ Serial aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, creatine kinase (CK), and CK-MB levels are elevated. However, cardiac enzymes fail to detect up to 50% of patients with myocardial damage.
❑ Retrograde aortography and transesophageal echocardiography reveal aortic laceration or rupture.
❑ Contrast studies and liver and spleen scans detect diaphragmatic rupture.
❑ Echocardiography, computed tomography scans, and cardiac and lung scans show the injury’s extent.
Treatment
Blunt chest injuries call for immediate physical assessment, control of bleeding, patent airway maintenance, adequate ventilation, and fluid and electrolyte balance.
Special considerations
❑ Check all pulses and level of consciousness. Evaluate skin color and temperature, depth of respiration, use of accessory muscles, and length of inhalation compared to exhalation.
❑ Check pulse oximetry values for adequate oxygenation.
❑ Observe tracheal position. Look for distended jugular veins and paradoxical chest motion. Listen to heart and breath sounds carefully; palpate for subcutaneous emphysema (crepitation) or a lack of structural integrity of the ribs.
❑ Obtain a history of the injury. Unless severe dyspnea is present, have the patient locate the pain, and ask if he’s having trouble breathing. Obtain an order for laboratory studies (arterial blood gas analysis, cardiac enzyme studies, complete blood count, type, and crossmatch).
❑ For simple rib fractures, have the patient cough and breathe deeply to mobilize secretions while splinting to decrease pain. Give adequate analgesics, encourage bed rest, and apply heat. Don’t strap or tape the chest.
❑ For more severe fractures, assist with administration of intercostal nerve blocks. (Obtain X-rays before and after the nerve blocks to rule out pneumothorax.) Intubate the patient with excessive bleeding or hemopneumothorax. Chest tubes may be inserted to treat hemothorax and to assess the need for thoracotomy. To prevent atelectasis, turn the patient frequently and encourage coughing and deep-breathing exercises.
❑ For pneumothorax, assist during placement of a chest tube anterior to the midaxillary line at the fourth intercostal space to aspirate as much air as possible from the pleural cavity and to re-expand the lungs. When time permits, insert chest tubes attached to water-seal drainage and suction.
❑ For flail chest, place the patient in semi-Fowler’s position. Re-expanding the lung is the first definitive care measure. Administer oxygen at a high flow rate under positive pressure. Suction the patient frequently, as completely as possible. Maintain acid-base balance. Observe carefully for signs of tension pneumothorax. Start I.V. therapy, using lactated Ringer’s or normal saline solution. Beware of both excessive and insufficient fluid resuscitation.
Alert For hemothorax, treat shock with I.V. infusions of lactated Ringer’s or normal saline solution. Administer packed red blood cells for blood losses greater than 1,500 ml or circulating blood volume losses exceeding 30%. Autotransfusion is an option. Administer oxygen, and assist with insertion of chest tubes in the fourth intercostal space anterior to the midaxillary line to remove blood. Monitor and document vital signs and blood loss. Watch for and immediately report falling blood pressure, rising pulse rate, and hemorrhage — all require a thoracotomy to stop bleeding.
❑ For a pulmonary contusion, give limited amounts of colloids (such as salt-poor albumin, whole blood, or plasma) as ordered to replace volume and maintain oncotic pressure. Give analgesics, diuretics and, if necessary, corticosteroids as ordered. Monitor blood gas levels to ensure adequate ventilation; provide oxygen therapy, mechanical ventilation, and chest tube care.
❑ For suspected cardiac damage, close intensive care or telemetry may detect arrhythmias and prevent cardiogenic shock. Impose bed rest in semi-Fowler’s position (unless the patient requires shock position); administer oxygen, analgesics, and supportive drugs to control heart failure or supraventricular arrhythmias as needed. Watch for cardiac tamponade, which calls for pericardiocentesis. (Provide essentially the same care as you would for a patient with a myocardial infarction.)
Alert For myocardial rupture, septal perforation, and other cardiac lacerations, immediate surgical repair is mandatory. Less severe ventricular wounds require use of a digital or balloon catheter; atrial wounds require a clamp or balloon catheter.
Alert For patients with aortic rupture or laceration, immediate surgery is mandatory, using synthetic grafts or anastomosis to repair the damage. Give large volumes of I.V. fluids (lactated Ringer’s or normal saline solution) and whole blood, along with oxygen at very high flow rates; then transport the patient promptly to the operating room.
Alert For tension pneumothorax, expect to assist with insertion of a 14G to 16G angiocatheter in the second intercostal space at the midclavicular line to release pressure in the chest. After this, insert a chest tube to normalize pressure and re-expand the lung. Administer oxygen under positive pressure along with I.V. fluids.
❑ For a diaphragmatic rupture, insert a nasogastric tube to temporarily decompress the stomach, and prepare the patient for surgical repair.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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