The most important consideration in any head injury is whether or not the brain is injured. Even seemingly minor injury can cause significant brain damage secondary to obstructed blood flow and decreased tissue perfusion. The brain cannot store oxygen and glucose to any significant degree. Because the cerebral cells need an uninterrupted blood supply to obtain these nutrients, irre-versible brain damage and cell death occur when the blood sup-ply is interrupted for even a few minutes. Clinical manifestations of brain injury are listed in Chart 63-2. Closed (blunt) braininjury occurs when the head accelerates and then rapidly decel-erates or collides with another object (eg, a wall or dashboard of a car) and brain tissue is damaged, but there is no opening through the skull and dura. Open brain injury occurs when an object penetrates the skull, enters the brain, and damages the soft brain tissue in its path (penetrating injury), or when blunt trauma to the head is so severe that it opens the scalp, skull, and dura to expose the brain.
A cerebral concussion after head injury is a temporary loss of neurologic function with no apparent structural damage. A con-cussion generally involves a period of unconsciousness lasting from a few seconds to a few minutes.
The jarring of the brain may be so slight as to cause only dizziness and spots before the eyes (“seeing stars”), or it may be severe enough to cause complete loss of consciousness for a time. If the brain tissue in the frontal lobe is affected, the patient may exhibit bizarre irrational behavior, whereas involvement of the temporal lobe can produce temporary amnesia or disorientation.
The patient may be hospitalized overnight for observation or discharged from the hospital in a relatively short time after a con-cussion. Treatment involves observing the patient for headache, dizziness, lethargy, irritability, and anxiety. The occurrence of these symptoms after injury is referred to as postconcussion syndrome. Giving the patient information, explanations, and encouragement may reduce some of the problems of postconcussion syndrome. The patient is advised to resume normal activities slowly, and the family is instructed to observe for the following signs and symp-toms and to notify the physician or clinic (or bring the patient to the emergency department) if they occur:
· Difficulty in awakening
· Difficulty in speaking
· Severe headache
· Weakness of one side of the body
A concussion was once thought of as a minor head injury without significant sequelae. However, studies have demonstrated that there are often disturbing and sometimes residual effects, in-cluding headache, lethargy, personality and behavior changes, attention deficits, difficulty with memory, and disruption in work habits (Ponsford et al., 1999).
Elderly patients must be assessed very carefully. Even given similar mechanisms of injury, an elderly person will often suffer more severe injury than a young person and will often recover more slowly and with more complications (Perdue et al., 1998). The elderly patient with confusion or behavioral disturbances should be assessed for head injury, because unrecognized “minor” head trauma may account for behavioral and confusional episodes in some elderly people (Walshaw, 2000). A misdiagnosed or un-treated episode of confusion in an elderly patient may result in long-term disability that might have been avoided if the injury had been detected and treated promptly.
Cerebral contusion is a more severe injury in which the brain is bruised, with possible surface hemorrhage. The patient is un-conscious for more than a few seconds or minutes. Clinical signs and symptoms depend on the size of the contusion and the amount of associated cerebral edema. The patient may lie motionless, with a faint pulse, shallow respirations, and cool, pale skin. Often there is involuntary evacuation of the bowels and the bladder. The patient may be aroused with effort but soon slips back into unconsciousness. The blood pressure and the temperature are subnormal, and the picture is somewhat similar to that of shock.
In general, patients with severe brain injury who have abnor-mal motor function, abnormal eye movements, and elevated ICP have poor outcomes—that is, brain damage, disability, or death. Conversely, the patient may recover consciousness but pass into a stage of cerebral irritability. In this stage, the patient is conscious and easily disturbed by any form of stimulation such as noises, light, and voices; he or she may become hyperactive at times. Gradually, the pulse, respirations, temperature, and other body functions return to normal, but full recovery can be delayed for months. Residual headache and vertigo are common, and im-paired mental function or seizures may occur as a result of irreparable cerebral damage.
Diffuse axonal injury involves widespread damage to axons in the cerebral hemispheres, corpus callosum, and brain stem. It can be seen in mild, moderate, or severe head trauma and results in axonal swelling and disconnection (Porth, 2002). Clinically, with severe injury, the patient has no lucid intervals and experiences imme-diate coma, decorticate and decerebrate posturing, and global cerebral edema. Diagnosis is made by clinical signs in conjunction with a CT scan or MRI. Recovery depends on the severity of the axonal injury.
Hematomas (collections of blood) that develop within the cra-nial vault are the most serious brain injuries (Porth, 2002). A hematoma may be epidural (above the dura), subdural (below the dura), or intracerebral (within the brain) (Fig. 63-3). Major symptoms are frequently delayed until the hematoma is large enough to cause distortion of the brain and increased ICP. The signs and symptoms of cerebral ischemia resulting from the compression by a hematoma are variable and depend on the speed with which vital areas are affected and the area that is injured. In general, a rapidly developing hematoma, even if small, may be fatal, whereas a larger but slowly developing collection of blood may allow compensation for increases in ICP.
After a head injury, blood may collect in the epidural (extradural) space between the skull and the dura. This can result from a skull fracture that causes a rupture or laceration of the middle meningeal artery, the artery that runs between the dura and the skull infe-rior to a thin portion of temporal bone. Hemorrhage from this artery causes rapid pressure on the brain.
Symptoms are caused by the expanding hematoma. Usually, there is a momentary loss of consciousness at the time of injury, followed by an interval of apparent recovery (lucid interval). Although the lucid interval is considered a classic characteristic of an epidural hematoma, no lucid interval has been reported in many patients with this lesion (Servadei, 1997), and thus it should not be considered a critical defining criterion. During the lucid interval, compensation for the expanding hematoma takes place by rapid absorption of CSF and decreased intravascular volume, both of which help maintain a normal ICP. When these mecha-nisms can no longer compensate, even a small increase in the volume of the blood clot produces a marked elevation in ICP. Then, often suddenly, signs of compression appear (usually dete-rioration of consciousness and signs of focal neurologic deficits such as dilation and fixation of a pupil or paralysis of an extremity), and the patient deteriorates rapidly.
An epidural hematoma is considered an extreme emergency; marked neurologic deficit or even respiratory arrest can occur within minutes. Treatment consists of making openings through the skull (burr holes) to decrease ICP emergently, remove the clot, and control the bleeding. A craniotomy may be required to remove the clot and control the bleeding. A drain is usually in-serted after creation of burr holes or a craniotomy to prevent reaccumulation of blood.
A subdural hematoma is a collection of blood between the dura and the brain, a space normally occupied by a thin cushion of fluid. The most common cause of subdural hematoma is trauma, but it may also occur from coagulopathies or rupture of an aneurysm. A subdural hemorrhage is more frequently venous in origin and is due to the rupture of small vessels that bridge the subdural space. A subdural hematoma may be acute, subacute, or chronic, depending on the size of the involved vessel and the amount of bleeding present.
Acute subdural hema-tomas are associated with major head injury involving contusion or laceration. Clinical symptoms develop over 24 to 48 hours. Signs and symptoms include changes in the level of consciousness (LOC), pupillary signs, and hemiparesis. There may be minor or even no symptoms with small collections of blood. Coma, in-creasing blood pressure, decreasing heart rate, and slowing respi-ratory rate are all signs of a rapidly expanding mass requiring immediate intervention.
Subacute subdural hematomas are the result of less severe con-tusions and head trauma. Clinical manifestations usually appear between 48 hours and 2 weeks after the injury. Signs and symp-toms are similar to those of an acute subdural hematoma.
If the patient can be transported rapidly to the hospital, an immediate craniotomy is performed to open the dura, allowing the subdural clot to be evacuated. Successful outcome also de-pends on the control of ICP and careful monitoring of respira-tory function. The mortality rate for patients with acute and sub-acute subdural hematomas is high because of associated brain damage.
Chronic subdural hematomas candevelop from seemingly minor head injuries and are seen most frequently in the elderly. The elderly are prone to this type of head injury secondary to brain atrophy, which is an expected con-sequence of the aging process. Seemingly minor head trauma may produce enough impact to shift the brain contents abnormally. The time between injury and onset of symptoms may be lengthy (eg, 3 weeks to months), so the actual insult may be forgotten.
A chronic subdural hematoma resembles other conditions and may be mistaken for a stroke. The bleeding is less profuse and there is compression of the intracranial contents. The blood within the brain changes in character in 2 to 4 days, becoming thicker and darker. In a few weeks, the clot breaks down and has the color and consistency of motor oil. Eventually, calcification or ossification of the clot takes place. The brain adapts to this for-eign body invasion, and the clinical signs and symptoms fluctu-ate. There may be severe headache, which tends to come and go; alternating focal neurologic signs; personality changes; mental de-terioration; and focal seizures. Unfortunately, the patient may be labeled neurotic or psychotic if the cause of the symptoms is over-looked.
The treatment of a chronic subdural hematoma consists of surgical evacuation of the clot. The procedure may be carried out through multiple burr holes, or a craniotomy may be performed for a sizable subdural mass that cannot be suctioned or drained through burr holes.
Intracerebral hemorrhage is bleeding into the substance of the brain. It is commonly seen in head injuries when force is exerted to the head over a small area (missile injuries or bullet wounds; stab injury). These hemorrhages within the brain may also result from systemic hypertension, which causes degeneration and rup-ture of a vessel; rupture of a saccular aneurysm; vascular anom-alies; intracranial tumors; systemic causes, including bleeding disorders such as leukemia, hemophilia, aplastic anemia, and thrombocytopenia; and complications of anticoagulant therapy.
The onset may be insidious, beginning with the development of neurologic deficits followed by headache. Management includes supportive care, control of ICP, and careful administration of fluids, electrolytes, and antihypertensive medications. Surgical intervention by craniotomy or craniectomy permits removal of the blood clot and control of hemorrhage but may not be possi-ble because of the inaccessible location of the bleeding or the lack of a clearly circumscribed area of blood that can be removed.
Assessment and diagnosis of the extent of injury are accomplished by the initial physical and neurologic examinations. CT and MRI are the primary neuroimaging diagnostic tools and are useful in evaluating soft tissue injuries. Positron emission tomography (PET scan) is available in some trauma centers; this method of scanning examines brain function rather than structure. A flow-chart developed by the Brain Trauma Foundation for the initial management of brain-injured patients is presented in Figure 63-4 (Brain Trauma Foundation, 2000).
Any individual with a head injury is presumed to have a cer-vical spine injury until proven otherwise. From the scene of the injury, the patient is transported on a board with the head and neck maintained in alignment with the axis of the body. A cervi-cal collar should be applied and maintained until cervical spine x-rays have been obtained and the absence of cervical spinal cord injury documented.
All therapy is directed toward preserving brain homeostasis and preventing secondary brain injury. “Secondary injury” is a term used to describe injury to the brain subsequent to the orig-inal traumatic event (Bader & Palmer, 2000). Common causes of secondary injury are cerebral edema, hypotension, and respi-ratory depression that may lead to hypoxemia and electrolyte imbalance. Treatments to prevent this include stabilization of cardiovascular and respiratory function to maintain adequate cerebral perfusion, control of hemorrhage and hypovolemia, and maintenance of optimal blood gas values (Wong, 2000).
As the damaged brain swells with edema or as blood collects within the brain, a rise in ICP occurs; this requires aggressive treatment. If the ICP remains elevated, it can decrease the CPP. Initial management is based on the principle of preventing secondary injury and maintaining adequate cere-bral oxygenation (see Fig. 63-4).
Surgery is required for evacuation of blood clots, débridement and elevation of depressed fractures of the skull, and suture of se-vere scalp lacerations. ICP is monitored closely; if increased, it is managed by maintaining adequate oxygenation, elevating the head of the bed, and maintaining normal blood volume. Devices to monitor ICP or drain CSF can be inserted during surgery or at the bedside using aseptic technique. The patient is cared for in the intensive care unit, where expert nursing care and medical treatment are readily available.
Treatment also includes ventilatory support, seizure prevention, fluid and electrolyte maintenance, nutritional support, and pain and anxiety management. Comatose patients are intubated and mechanically ventilated to ensure adequate oxygenation and pro-tect the airway.
Because seizures are common after head injury and can cause secondary brain damage from hypoxia, antiseizure agents may be administered. If the patient is very agitated, benzodiazepines may be prescribed to calm him or her without decreasing LOC. These medications do not affect ICP or CPP, making them good choices for the head-injured patient.
A nasogastric tube may be inserted because reduced gastric motility and reverse peristalsis are associated with head injury, making regurgitation and aspiration common in the first few hours.
When a patient has sustained a severe head injury incompatible with life, the nurse may assist in the clinical examination for determination of brain death and in the process of organ pro-curement. Since 1981, all 50 states have recognized the Uni-form Determination of Brain Death Act (Lovasik, 2000). This act states that death will be determined with accepted medical standards and that death will indicate irreversible loss of all brain function. The patient has no neurologic activity upon clinical examination; adjunctive tests such as EEG and cerebral blood flow (CBF) studies are often used to confirm brain death (Lovasik, 2000). Many of these patients are potential organ donors, and the nurse may provide information to the family and assist them with this decision-making process about organ donation.
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