Secondary injury is the biochemical and cellular response to the initial trauma that can exacerbate the primary injury and cause loss of brain tissue not originally damaged. Secondary injury can be caused by ischemia, hypercapnia, hypotension, cerebral edema, sustained hypertension, calcium toxicity, or metabolic derangements. Hypoxia or hypotension, the best known culprits for secondary injury, typically are the result of extracranial trauma.9 A detrimental cycle may develop causing a focal primary injury to expand as a result of uncontrolled, refractory secondary injury.

Tissue ischemia occurs in areas of poor cerebral perfusion as a result of hypotension or hypoxia. The cells in ischemic areas become edematous. Extreme vasodilation of the cerebral vasculature occurs in an attempt to supply oxygen to the cerebral tissue. This increase in blood volume increases intracranial volume and raises intracranial pressure (ICP).

Significant hypotension causes inadequate perfusion to neural tissue. Hypotension rarely is associated with TBI. Hypotension typically is not caused by brain injury unless terminal medullary failure occurs.¹⁰ If a trauma patient is unconscious and hypotensive, a detailed assessment of the chest, abdomen, and pelvis is performed to rule out internal injuries.

Hypercapnia (elevated CO₂) is a powerful vasodilator. Most often caused by hypoventilation in an unconscious patient, hypercapnia results in cerebral vasodilation and increased cerebral blood volume and ICP.

Cerebral edema occurs as a result of the changes in the cellular environment caused by contusion, loss of autoregulation, and increased permeability of the blood-brain barrier. Cerebral edema can be focal as it localizes around the area of contusion, or diffuse as a result of hypotension or hypoxia. Optimizing other aspects of secondary injury, such as oxygenation, ventilation, and perfusion can limit the extent of cerebral edema.

Initial hypertension in the patient with severe TBI is common. Because of the loss of autoregulation, increased blood pressure results in increased intracranial blood volume and ICP. The effects of increased ICP may be varied. As pressure increases inside the closed skull vault, cerebral perfusion decreases, which further compromises the brain. The combined effects of increasing pressure and decreasing perfusion precipitate a downward spiral of events.

Contusion, or bruising of the brain, usually is related to acceleration-deceleration injuries, which result in hemorrhage into the superficial parenchyma, often the frontal and temporal lobes. Frontal or temporal contusions are most common and can be seen in a coup-contrecoup mechanism of injury (see Figure 25-1). Coup injury affects the cerebral tissue directly under the point of impact. Contrecoup injury occurs in a line directly opposite the point of impact.

The clinical manifestations of contusion are related to the location of the contusion, the degree of contusion, and the presence of associated lesions. Contusions can be small, in which localized areas of dysfunction result in a focal neurological deficit. Larger contusions can evolve over 2 to 3 days after injury as a result of edema and further hemorrhaging. A large contusion can produce a mass effect that can cause a significant increase in ICP.

Contusions of the tips of the temporal lobe are a common occurrence and are of particular concern. Because the inner aspects of the temporal lobe surround the opening in the tentorium where the midbrain enters the cerebrum, edema in this area can cause rapid deterioration of the patient’s condition and can lead to herniation. Because of the location, this deterioration can occur with little or no warning at a deceptively low ICP.

Medical management of cerebral contusions may consist of medical or surgical therapies. Because a contusion can progress over 3 to 5 days after injury, secondary injury may occur. If contusions are small, focal, or multiple, they are treated medically with serial neurological assessments and possibly with ICP monitoring. Larger contusions that produce considerable mass effect require surgical intervention to prevent the increased edema and ICP as the contusion matures. Outcome of cerebral contusion varies, depending on the location and the degree of contusion.

Extravasation of blood creates a space-occupying lesion within the cranial vault that can lead to increased ICP. Three types of hematomas are discussed here (Figure 25-2). The first two, epidural and subdural hematomas, are extraparenchymal (outside of brain tissue) and produce injury by pressure effect and displacement of intracranial contents. The third type, intracerebral hematoma, directly damages neural tissue and can produce further injury as a result of pressure and displacement of intracranial contents.

Missile injuries penetrate the skull and produce significant focal damage, but little acceleration-deceleration or rotational injury. The injury may be depressed, penetrating, or perforating (Figure 25-3). Depressed injuries are caused by fractures of the skull, with penetration of bone into cerebral tissue. A low-velocity penetrating injury (knife) may involve only focal damage and no loss of consciousness. A high-velocity missile (bullet) can produce shock waves that are transmitted throughout the brain in addition to the injury caused by the bullet. Perforating injuries are missile injuries that enter and then exit the brain. Perforating injuries have much less ricochet effect but are still responsible for significant injury.

Risk of infection and cerebral abscess is a concern in cases of missile injuries. If fragments of the missile are embedded within the brain, careful consideration of the location and risk of increasing neurological deficit is weighed against the risk of abscess or infection. The outcome after missile injury is based on the degree of penetration, the location of the injury, and the velocity of the missile.

Most of the TBI management occurs in the ICU. Nonsurgical management includes management of ICP, maintenance of adequate cerebral perfusion pressure and oxygenation, and treatment of any complications (e.g., pneumonia, infection). ICP monitoring may be required for patients with a GCS score less than 8 and abnormal findings on a head CT scan.9

Axial loading—or vertical compression—injuries occur from vertical force along the spinal cord. This most commonly is seen in a fall from a height in which the person lands on the feet or buttocks. Compression injuries cause burst fractures of the vertebral body that often send bony fragments into the spinal canal or directly into the spinal cord (Figure 25-4).

Spinal shock is a condition that can occur shortly after traumatic injury to the spinal cord. Spinal shock is the complete loss of all muscle tone and normal reflex activity below the level of injury.4 Patients with spinal shock may appear completely without function below the area of the injury, although all of the area may not necessarily be destroyed.

Autonomic dysreflexia is a life-threatening complication that may occur with SCI. This condition is caused by a massive sympathetic response to any noxious stimuli (e.g., full bladder, line insertions, fecal impaction), which results in bradycardia, hypertension, facial flushing, and headache. Immediate intervention is needed to prevent cerebral hemorrhage, seizures, and acute pulmonary edema. Treatment is aimed at alleviating the noxious stimuli. A clinical algorithm for treatment of autonomic dysreflexia is provided in Box 25-7.¹² If symptoms persist, antihypertensive agents can be administered to reduce blood pressure. Prevention of autonomic dysreflexia is imperative and can be accomplished through the use of a comprehensive bowel and bladder program.

Assessment of breathing patterns and gas exchange is made after an airway has been secured. The level of injury dictates the degree of altered breathing patterns and gas exchange (Table 25-6). Because complete injuries above the C3 level result in paralysis of the diaphragm, patients with these injuries require mechanical ventilatory support.

The initial neurological assessment may not be an accurate indication of eventual motor and sensory loss. It focuses on the rapid and accurate identification of present, absent, or impaired functioning of the motor, sensory, and reflex systems that coordinate and regulate vital functions. A detailed motor and sensory examination includes the assessment of all 32 spinal nerves for evidence of dysfunction. Carefully mapped pathways for the sensory portion of the spinal nerves, called dermatomes, can assist in localizing the functional sensory level of injury. Motor function may be graded on a 6-point scale (Table 25-7). Initial assessment must be performed correctly and findings thoroughly documented in detail so that subsequent serial assessments can rapidly identify deterioration. The American Spinal Injury Association (ASIA) has developed a form that outlines the required assessments for initial and ongoing classification of SCIs (Figure 25-5). Ongoing spinal cord assessments must be documented during the critical care phase.

About 15% of trauma patients with an SCI have a cervical spine injury.10 Screening of the spinal cord for injury becomes an integral part of the assessment for all trauma patients. The degree of trauma, alteration in mentation, intoxication, and distracting injuries dictate the type and extent of examination required to clear the cervical spine. The Eastern Association of Surgeons in Trauma (EAST) developed guidelines for the clearance of the cervical spine (Table 25-8). In these guidelines, CT scan has replaced plain radiography as the principal modality for cervical spine assessment following trauma. On admission, the spine is palpated for obvious deformity, and the patient is assessed for the subjective response of pain to palpation. If the patient is intoxicated, has distracting injuries such as rib fractures, or has received analgesics, examination of the spinal cord may be deferred.¹⁰ MRI may be warranted to definitively diagnose an SCI when the patient is stabilized.

Methylprednisolone can improve neurological outcome after SCI, although it has been called into question because of the infection risk in these patients.12 Current guidelines cite the use of methylprednisolone as an option for the management of acute cervical spine injury.¹³ When it is used, patients receive a methylprednisolone bolus followed by a continuous infusion for at least 24 hours (preferably 48 hours) if their treatment began 3 to 8 hours after their injury.¹³ Although the exact mechanism is not completely understood, it is thought that methylprednisolone directly affects the changes that occur within the spinal cord after injury, primarily by preventing posttraumatic spinal cord ischemia, improving energy metabolism, restoring extracellular calcium, and improving nerve impulse conduction.

Blunt trauma to the chest most often is caused by MVCs or falls; thoracic injuries account for 20% of trauma deaths. The underlying mechanism of injury tends to be a combination of acceleration-deceleration injury and direct transfer mechanics, as in a crush injury. Various mechanisms of blunt trauma are associated with specific injury patterns. After head-on collisions, drivers have a higher frequency of injury than do backseat passengers because the driver comes in contact with the steering assembly. Severe thoracic injuries often are seen in patients who are unrestrained.14,15 Falls from greater than 20 feet are typically associated with thoracic injury.

The bedside ultrasound, called the focused assessment with sonography for trauma (FAST) examination is done at most trauma centers to evaluate the patient for the presence of intraabdominal blood.19 This is a quick and noninvasive means of rapid assessment, but success depends on the skill level of the operator.¹⁹ Bedside ultrasonography is used widely in the United States for the detection of abdominal free fluid and hemoperitoneum. Typically, the right and left upper abdominal quadrant areas are examined: the right upper quadrant (Morrison’s pouch), the left upper quadrant splenorenal area, the pericardial sac, and the pelvis (Douglas’ pouch). The primary disadvantage of FAST is the need for free intraperitoneal fluid to produce a positive study result.⁴ An initial negative FAST result may be followed by serial ultrasound examinations or abdominal CT.¹⁹

Although the FAST test has had good sensitivity and specificity, it is not intended to replace a CT scan. Obese abdomens and patients with ascites may have erroneous results, and further workup for these patients is warranted.²⁰ Ultrasound is also limited in its ability to diagnose diaphragmatic, intestinal, or pancreas injuries. Abdominal CT provides information about specific organ injury, pelvic injury, and retroperitoneal hemorrhage.

Invasive tests such as the diagnostic peritoneal lavage (DPL) can exclude or confirm the presence of intraabdominal injury.⁴ DPL is used only when the FAST exam or a CT scan is inconclusive. After the patient’s bladder has been emptied, a small incision is made in the abdomen through the skin and into the peritoneum. A small catheter is inserted (Figure 25-12). If frank blood is encountered, intraabdominal injury is evident, and the patient is taken immediately to the operating room. If gross blood is not initially encountered, a liter of fluid (lactated Ringer’s or 0.9% normal saline) is infused through the catheter into the abdomen. The intravenous bag is then placed in a dependent position, and abdominal fluid is allowed to drain into the intravenous bag. The drainage fluid is sent to the laboratory for analysis. Positive DPL results signal intraabdominal trauma and usually necessitate surgical intervention (Box 25-9). DPL is invasive, has been associated with complications, and cannot exclude retroperitoneal injuries.

The patient is assessed for additional complications, including ongoing hemorrhage, intraabdominal hypertension, and abdominal compartment syndrome. Abdominal compartment syndrome is defined as end-organ dysfunction caused by intraabdominal hypertension.22 Increased intraabdominal pressure can result from internal bleeding, visceral edema, or a noncompliant abdominal wall. Increased abdominal cavity pressure can impinge on diaphragmatic excursion and can affect ventilation. Clinical manifestations of abdominal compartment syndrome include decreased cardiac output, increased pulmonary vascular resistance, increased peak pulmonary pressures, increased ICP, decreased urine output, and hypoxia.²² Intraabdominal pressure can be measured through a bladder catheter after the injection of 25 mL of sterile saline.²²

Surgical decompression of the abdomen may be required for abdominal pressures greater than 20 to 25 mm Hg that are associated with other assessment findings such as decreased cardiac output, hypotension, elevated peak inspiratory pressures, and decreased urine output.²³ Surgical decompression involves opening the abdomen and then temporarily closing the abdomen with a sterile perforated plastic sheet, clips, vacuum-assisted techniques, and many other options.²³ The open abdomen is then covered with towels or dressings, and closed suction drains are placed over the top and brought out through a plastic drape over the entire wound. The wound is closed permanently several weeks later, or it is allowed to heal by second intention and eventual skin grafting.

After the patient is hemodynamically stable and the triad of hypothermia, coagulopathy, and acidosis has been corrected, the patient is taken back to the operating room for the definitive surgery, if required. During this phase, definitive repairs and wound closure are performed. Postoperatively, the patient is transported back to the ICU for continued care.

The liver is the primary organ injured in penetrating trauma and the second most often injured organ in blunt trauma. Abdominal CT is considered to be the most reliable diagnostic tool to identify and assess the severity of the injury to the liver.24 The severity of liver injuries is graded to provide a mechanism for determining the amount of trauma sustained by that organ, the care needed, and the possible outcomes (Table 25-9). Nonoperative management is considered the standard of care for hemodynamically stable patients with liver injury.²⁴ Patients are admitted to the ICU or a step-down unit and are monitored for signs of hemorrhage. Serial serum hematocrit and hemoglobin levels and vital signs are monitored over several days.

Patients with penetrating or blunt liver trauma who are hemodynamically unstable may require surgical intervention to correct the defect. Resection of the devitalized tissue is required for massive injuries. Hemorrhage is common with liver injuries, and ligation of the hepatic arteries or veins may be required to control hemorrhage. Drains may be placed intraoperatively to drain areas of blood and to prevent hematomas.

Care of the patient with severe liver injuries can be challenging for the critical care nurse. Lack of hemodynamic stability can result from hemorrhage and hypovolemic shock, leading to fluid volume deficit, decreased cardiac output, and decreased tissue perfusion. Combinations of crystalloid and colloid intravenous solutions may be used to correct hypovolemia. Fresh-frozen plasma, platelets, and cryoprecipitate may be administered to correct coagulopathies. A crucial nursing responsibility is to monitor the patient’s response to medical therapies. Continued hemodynamic instability (e.g., hypotension, decreased cardiac output) despite aggressive medical intervention may indicate continued hemorrhage, in which case an exploratory laparotomy may be required to determine and correct the source of bleeding. The patient’s postoperative ICU course may be complicated by coagulopathy, acidosis, and hypothermia. Jaundice may occur as a sign of hepatic dysfunction, but it may also be caused by reabsorption of hematomas or breakdown of transfused blood.

The spleen is the organ most commonly injured by blunt abdominal trauma and is second to the liver as a source of life-threatening hemorrhage. Spleen injuries, like liver injuries, are graded for the purpose of determining the amount of trauma sustained, the care needed, and the possible outcomes (Table 25-10). Hemodynamically stable patients may be monitored in the critical care unit by means of serial hematocrit values and vital signs. Progressive deterioration may indicate the need for operative management.²⁴

Patients who exhibit hemodynamic instability require operative intervention with splenectomy, partial splenectomy, or splenorrhaphy. Patients who have had a splenectomy are at risk for the development of overwhelming postsplenectomy sepsis with streptococcal pneumonia. These patients require polyvalent pneumococcal vaccine (Pneumovax) to help promote immunity against most pneumococcal bacteria. Patients with isolated spleen injuries that require surgical intervention rarely are admitted to the critical care unit. Complications after splenic trauma include wound infection, sepsis, subdiaphragmatic abscess, and fistulas of the colon, pancreas, and stomach.

Intestinal injuries can result from blunt or penetrating trauma. The diagnosis of small intestinal injuries is difficult. Surgical intervention is usually required in the presence of multiple CT findings (e.g., unexplained free fluid, pneumoperitoneum, bowel wall thickening, mesenteric fat streaking, mesenteric hematoma, intravenous contrast extravasation).25 Regardless of the mechanism of injury, intestinal contents (e.g., bile, stool, enzymes, bacteria) leak into the peritoneum and cause peritonitis. Surgical resection and repair are required. The patient’s postoperative course is dictated by the amount of spillage of intestinal contents. The patient is observed for signs of sepsis and for abscess or fistula formation.

Most renal trauma is caused by blunt trauma, resulting in contusions or lacerations without urinary extravasation. Injury to the kidneys may be reflected by flank ecchymosis and fracture of inferior ribs or spinous processes. Gross or microscopic hematuria may be present; however, the extent of kidney damage is often incongruous with the degree of hematuria.26 Gross hematuria can exist with minor injuries and usually clears within a few hours. CT is the most accurate modality available for diagnosing kidney injury because it can assess the extent of parenchymal laceration, urine extravasation, hemorrhage, and the presence of vascular injury.²⁶

Contusions and minor lacerations can usually be treated with observation. The success of nonoperative management may be enhanced by using angiographic embolization in those who are hemodynamically stable.²⁷ Operative interventions may be performed in patients with kidney injuries with a devascularized segment of the kidney. Postoperative and postinjury complications can include infection, hemorrhage, infarction, extravasation, calcification, acute tubular necrosis, and hypertension.

A large percentage of bladder injuries result from pelvic fractures.26 Physical findings may include lower abdominal bruising, distention, and pain. More definitive findings include difficulty voiding or incomplete recovery of irrigation fluids from catheterized patients.²⁶ Bladder injuries are classified as contusions, extraperitoneal ruptures, intraperitoneal ruptures, or combined injuries. The type of injury depends on the location and strength of the blunt force and volume of urine in the bladder at the time of injury. Extraperitoneal rupture of the bladder may be managed conservatively with catheterization and antibiotics for 7 to 10 days.²⁷ Unresolved extravasation may require surgical intervention.