The blow that causes a concussion is usually sudden and forceful. It occurs when the head strikes a stationary object (as in a fall to the ground) or when a moving object strikes the head (as in a punch to the head). Such blows may also result from automobile accidents, athletic injury, or child abuse. Significant jarring can lead to unconsciousness. Microscopic shearing of nerve fibers is thought to occur in the brain from sudden acceleration or deceleration from the head injury.

A concussion may produce vomiting and a short-term loss of consciousness. The patient may also suffer from anterograde and retrograde amnesia, in which the patient not only can’t recall what happened immediately after the injury, but also has difficulty recalling events that led up to the traumatic incident. The presence of anterograde amnesia and the duration of retrograde amnesia reliably correlate with the injury’s severity. The length of the unconsciousness may also relate to the concussion’s severity.

This type of injury commonly causes adults to be irritable or lethargic, to behave out of character, and to complain of dizziness, nausea, or severe headache. Some children have no apparent ill effects, but many grow lethargic and somnolent in a few hours. Postconcussion syndrome—characterized by headache, dizziness, vertigo, anxiety, and fatigue—may persist for several weeks after the injury.

A cerebral contusion results from coup-contrecoup or acceleration-deceleration injuries. Such injuries can occur directly beneath the site of impact when the brain rebounds against the skull from the force of a blow (such as in a beating with a blunt instrument), when the force of the blow drives the brain against the opposite side of the skull, or when the head is hurled forward and stopped abruptly (as in an automobile accident when a driver’s head strikes the windshield). The brain continues moving and slaps against the skull (acceleration) and then rebounds (deceleration). These injuries can also cause the brain to strike against bony prominences inside the skull (especially the sphenoidal ridges), causing intracranial hemorrhage or hematoma that may result in tentorial herniation. (See Hemorrhage, hematoma, and tentorial herniation.)

The patient with a cerebral contusion may have severe scalp wounds and labored respirations. He may lose consciousness for a few minutes or longer. If conscious, he may be drowsy, confused, disoriented, agitated, or even violent. He may display hemiparesis, unequal pupillary response, and decorticate or decerebrate posturing. Eventually, he should return to a relatively alert state, perhaps with temporary aphasia, slight hemiparesis, or unilateral numbness. A lucid period followed by rapid deterioration suggests epidural hematoma.

Skull fractures invariably result from a traumatic blow to the head. Motor vehicle accidents, bad falls, sports injuries, and physical assaults top the list of causes. The brain can be directly affected by damage to the nervous system and by bleeding.

Closed head injuries occur in 200 out of every 100,000 patients. Severe head trauma carries a 30% mortality rate.

Many skull fractures are accompanied by scalp wounds—abrasions, contusions, lacerations, or avulsions. If the scalp has been lacerated or torn away, bleeding may be profuse because the scalp contains many blood vessels. Occasionally, bleeding may be heavy enough to induce hypovolemic shock. The patient may also be in shock from other injuries or from medullary failure in severe head injuries.

Linear fractures that are associated only with concussion don’t produce loss of consciousness. They require evaluation, but not definitive treatment. A fracture that results in a cerebral contusion or laceration, however, may cause the classic signs of brain injury: agitation and irritability, loss of consciousness, changes in respiratory pattern (labored respirations), abnormal deep tendon reflexes, and altered pupillary and motor responses.

If the patient with a skull fracture remains conscious, he is apt to complain of a persistent, localized headache. A skull fracture may also result in cerebral edema, which may cause compression of the reticular activating system. This cuts off the normal flow of impulses to the brain and results in possible respiratory distress. The patient may experience alterations in level of consciousness (LOC), progressing to unconsciousness or even death.

When jagged bone fragments pierce the dura mater or the cerebral cortex, skull fractures may cause subdural, epidural, or intracerebral hemorrhage or hematoma. With the resulting spaceoccupying lesions, clinical findings may include hemiparesis, unequal pupils, dizziness, seizures, projectile vomiting, progressive unresponsiveness, and decreased pulse and respiratory rates. Sphenoidal fractures may also damage the optic nerve, causing blindness, whereas temporal fractures may cause unilateral deafness or facial paralysis. Symptoms reflect the head injury’s severity and extent. However, some elderly patients may have cortical brain atrophy, with more space for brain swelling under the cranium, and consequently may not show signs of increased intracranial pressure (ICP) until it’s very high.

Vault fractures commonly produce soft-tissue swelling near the fracture, making it difficult to detect without a computed tomography (CT) scan.

Basilar fractures commonly produce a hemorrhage from the nose, pharynx, or ears; blood under the periorbital skin (raccoon eyes) and under the conjunctiva; and Battle’s sign (supramastoid ecchymosis), sometimes with bleeding behind the eardrum (hemotympanum). This type of fracture may also cause cerebrospinal fluid (CSF) or even brain tissue to leak from the nose or ears.

Depending on the extent of brain damage, the patient with a skull fracture may suffer residual effects, such as seizures, hydrocephalus, and organic brain syndrome. Children may develop headaches, giddiness, easy fatigability, neuroses, and behavior disorders.

Nasal bone fractures usually result from direct trauma. The causative injury may be relatively minor, such as a fall, or more severe, such as a car accident.

Immediately after injury, a nosebleed may occur, and soft-tissue swelling may quickly obscure the break. Nasal fractures may cause significant blood loss. After several hours, pain, edema, periorbital ecchymoses, and nasal displacement and deformity are prominent. Possible complications include septal hematoma, which may lead to abscess formation, resulting in avascular septal necrosis and saddle nose deformity.

Simple fractures or dislocations are usually caused by a manual blow along the jawline; more serious compound fractures commonly result from automobile accidents. Other causes include industrial accidents, recreational or sports injuries, assaults, or other trauma. Recurrence of a dislocated jaw is common.

Malocclusion is the most obvious sign of a dislocation or fracture. Other signs include mandibular pain, swelling, ecchymosis, loss of
function, and asymmetry. In addition, mandibular fractures that damage the alveolar nerve produce paresthesia or anesthesia of the chin and lower lip. Maxillary fractures produce infraorbital paresthesia and commonly accompany fractures of the nasal and orbital complex.

The usual cause of perforated eardrum is trauma, such as the deliberate or accidental insertion of foreign objects (cotton swabs or bobby pins) or sudden excessive changes in pressure (explosion, a blow to the head, flying, or diving). The injury may also result from untreated otitis media and, in children, from acute otitis media.

Sudden onset of a severe earache and bleeding, clear drainage, or drainage of pus from the ear are the first signs of a perforated eardrum. Other symptoms include hearing loss, tinnitus, and vertigo. Purulent otorrhea within 24 to 48 hours of injury signals infection.

Whiplash commonly results from rear-end automobile accidents. A seat belt keeps a person’s body from being thrown forward, but the head may snap forward, then backward, causing a whiplash injury to the neck. Other causes include roller coasters or other amusement park rides, sports injuries, or punches or shoves.

Although symptoms may develop immediately, they’re often delayed 12 to 24 hours if the injury is mild. Whiplash produces moderate to severe anterior and posterior neck pain. Within several days, the anterior pain diminishes, but the posterior pain persists or even intensifies, causing patients to seek medical attention if they didn’t do so before. Whiplash may also cause dizziness, gait disturbances, vomiting, headache, nuchal rigidity, neck muscle asymmetry, and rigidity or numbness in the arms.

Most serious spinal injuries result from motor vehicle accidents, falls, dives into shallow water, and gunshot wounds. Less serious injuries result from heavy object lifting and minor falls. Spinal dysfunction may also result from hyperparathyroidism and neoplastic lesions.

Spinal cord injuries occur in 12,000 to 15,000 people per year in the United States. About 10,000 of these injuries cause permanent paralysis; many other patients die as a result of these injuries. Most spinal cord injuries occur in males between the ages of 15 and 35 years; about 5% occur in children. Mortality is higher in pediatric spinal cord injuries.

The most obvious symptoms of spinal injury are muscle spasm and back pain that worsen with movement. In cervical fractures, pain may produce point tenderness; in dorsal and lumbar fractures, it may radiate to other body areas such as the legs. After mild injuries, symptoms may be delayed for several days or weeks. If the injury damages the spinal cord, clinical effects range from mild paresthesia to quadriplegia and shock.

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.

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.

Stab wounds from a knife or an ice pick are the most common penetrating chest wounds; gunshot wounds are a close second. Wartime explosions or firearms fired at close range are the usual sources of large, gaping wounds.

Penetrating chest injuries cause one in every four deaths in the United States. Many patients with this type of injury die after reaching the hospital.

In addition to the obvious chest injuries, penetrating chest wounds can also cause:

Penetrating chest wounds may also cause lung lacerations (bleeding and substantial air leakage through the chest wall), arterial lacerations (loss of more than 100 ml blood/hour through the chest tube), exsanguination, pneumothorax (air in pleural space causes loss of negative intrathoracic pressure and lung collapse), tension pneumothorax (intrapleural air accumulation causes potentially fatal mediastinal shift), and hemothorax. Other effects may include arrhythmias, cardiac tamponade, mediastinitis, subcutaneous emphysema, esophageal perforation, bronchopleural fistula, and tracheobronchial, abdominal, or diaphragmatic injuries.

Blunt (nonpenetrating) abdominal injuries usually result from automobile accidents, falls from heights, or sports injuries; penetrating abdominal injuries, from stab and gunshot wounds.

The most commonly injured organs associated with penetrating abdominal trauma are the small intestine (29%), liver (28%), and colon (23%). Penetrating abdominal trauma affects 35% of those admitted to urban trauma centers and 1% to 12% of those admitted to suburban and rural centers.

Symptoms vary with the degree of injury and the organs damaged. Penetrating abdominal injuries cause obvious wounds (gunshots commonly produce both entrance and exit wounds) with variable blood loss, pain, and tenderness. They commonly result in pallor, cyanosis, tachycardia, shortness of breath, and hypotension. (See Projectile pathway.) Blunt abdominal injuries cause severe pain (which may radiate beyond the abdomen to the shoulders), bruises, abrasions, contusions, or distention. They may also result in tenderness, abdominal splinting or rigidity, nausea, vomiting, pallor, cyanosis, tachycardia, and shortness of breath. Rib fractures commonly accompany blunt injuries. (See Effects of blunt abdominal trauma.)

In both blunt and penetrating injuries, massive blood loss may cause hypovolemic shock. Damage to solid abdominal organs (liver, spleen,
pancreas, and kidneys) generally causes hemorrhage. Damage to hollow organs (stomach, intestine, gallbladder, and bladder) causes rupture and release of the organs’ contents (including bacteria) into the abdomen, which in turn produces inflammation and, possibly, infection.