diffuse axonal injury(redirected from Diffused axonal injury)
diffuse axonal injury (DAI)
diffuse axonal injuryA form of post-traumatic brain injury which occurs over a broad swath of myelinated tracts of the CNS, resulting in significant neurologic effects ranging from loss of consciousness to persistent vegetative state.
MRI, if oedematous.
diffuse axonal injuryNeurology A form of post-traumatic brain damage which results in significant neurologic sequelae in survivors. See Retraction balls.
dif·fuse ax·o·nal in·jur·y(di-fyūs' ax'ŏn-ăl in'jŭr-ē)
Diffuse Axonal Injury
|Mean LOS:||2.8 days|
|Description:||MEDICAL: Traumatic Stupor and Coma, Coma > 1 Hour Without CC or Major CC|
|Mean LOS:||4.3 days|
|Description:||MEDICAL: Traumatic Stupor and Coma, Coma < 1 Hour With CC|
|Mean LOS:||11.5 days|
|Description:||SURGICAL: Craniotomy for Multiple Significant Trauma|
A diffuse axonal injury (DAI), the most severe of all brain injuries, occurs when nerve axons are stretched, sheared, or even torn apart. The severity and outcome of a DAI depend on the extent and degree of damage to brain structures and can be classified as mild, moderate, or severe DAI. All types of DAI are associated with an immediate and prolonged (> 6 hours) coma. Mild DAI is associated with a coma that lasts from 6 to 24 hours and has a 15% mortality rate; 80% of patients experience a good recovery. Moderate DAI, the most common form, is associated with a coma that lasts 24 hours or more, decerebration (extension posturing), and decortication (flexion posturing). Approximately 25% of patients with moderate DAI die. Severe DAI, which has a mortality rate of 50%, occurs when there is an extensive disruption of axons in the white matter of the central nervous system. People who emerge from coma usually do so in the first 3 months after injury, but many of those who live remain in a persistent vegetative state.
The pathophysiology of DAI is based on a model of shear injury; the brain trauma occurs because of sudden acceleration-deceleration impact, which can produce rotational forces that affect the brain. The injury to tissue is greatest in areas where the density difference in the brain is greatest, so most of DAI lesions occur at the junction of gray and white matter. Injury results in edema and axonal tearing, and the severity of injury depends on the distance from the center of rotation, the arc of rotation, and the duration and intensity of the force.
The predominant causes of injuries that lead to DAI are high-speed motor vehicle crashes (MVCs) and automobile-pedestrian crashes. The severity of the MVC is correlated with the severity of DAI.
No clear genetic contributions to susceptibility have been defined.
Gender, ethnic/racial, and life span considerations
Traumatic injuries are the leading cause of death in Americans aged 1 through 44 years and the fourth leading cause of death for all age groups. Head injury is the leading cause of all trauma-related deaths and is usually associated with MVCs. Head injuries from MVCs are more common in White/European Americans than other groups and more common in males than females.
Global health considerations
DAI is a diagnosis made primarily in Western nations radiographically. Few epidemiological data are available internationally or in developing countries.
If the patient has been in an MVC, determine the speed and type of the vehicle, the patient’s position in the vehicle, whether the patient was restrained, and whether the patient was thrown from the vehicle on impact. If the patient was injured in a motorcycle crash, determine if the patient was wearing a helmet. Determine if the patient experienced momentary loss of reflexes, momentary arrest of respiration, loss of consciousness, and the length of time the patient was unconscious. Determine if the patient has been experiencing excessive sweating (hyperhidrosis) or hypertension since the injury.
The primary symptom of DAI is decreased neurological status with loss of consciousness. The initial evaluation is centered on assessing the airway, breathing, circulation, and disability (neurological status). Exposure (undressing the patient completely) is incorporated as part of the primary survey. The secondary survey, a head-to-toe assessment, including vital signs, is then completed. Note a very high fever, hyperhidrosis, or hypertension. Observe posturing for flexion or extension.
The initial and ongoing neurological assessment includes monitoring of the vital signs, assessment of the level of consciousness, examination of pupil size and level of reactivity, and assessment of the Glasgow Coma Scale, which evaluates eye opening, best verbal response, and best motor response. Clinical findings may include a rapidly changing level of consciousness from confusion to coma, ipsilateral pupil dilation, hemiparesis, and abnormal posturing that includes flexion and extension. A neurological assessment is repeated at least hourly during the first 24 hours after the injury.
Examine the patient for signs of a basilar skull fracture: periorbital ecchymosis (raccoon’s eyes), subscleral hemorrhage, retroauricular ecchymosis (Battle’s sign), hemotympanum (blood behind the eardrum), and leakage of cerebrospinal fluid from ears (otorrhea) or nose (rhinorrhea). Gently palpate the entire scalp and facial bones, including the mandible and maxilla, for bony deformities or step-offs. Examine the oral pharynx for lacerations and check for any loose or fractured teeth.
DAI may alter an individual’s ability to cope effectively. It may lead to significant cognitive and behavioral disabilities. Although it is not possible to assess the comatose patient’s coping strategies, it is important to assist the family or significant others.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Magnetic resonance imaging||Normal brain and spinal cord||Cerebral edema, damage to brain structures||More valuable than CT scanning in diagnosing DAI; preferred method of diagnosis over other procedures, especially with gradient-echo sequences|
|Computed tomography (CT) scan||Normal brain and spinal cord||Cerebral edema, damage to brain structures||Identifies structural lesions in patients with head injuries|
Other Tests: Skull and cervical spine x-rays, arterial blood gases, complete blood count
Primary nursing diagnosis
DiagnosisIneffective airway clearance related to hypoventilation or airway obstruction.
OutcomesRespiratory status: Gas exchanges; Respiratory status: Ventilation; Comfort level
InterventionsAirway management; Oxygen therapy; Airway suctioning; Airway insertion and stabilization; Anxiety reduction; Cough enhancement; Mechanical ventilation; Positioning; Respiratory monitoring
Planning and implementation
Endotracheal intubation and mechanical ventilation are critical to ensure oxygenation and ventilation and to decrease the risk of pulmonary aspiration. A Pao2 greater than 100 mm Hg and a Paco2 between 28 and 33 mm Hg may be maintained to decrease cerebral blood flow and intracranial swelling. Fluid administration guided by intracranial pressure (ICP), cerebral perfusion pressure (CPP; calculated number CPP = MAP − I CP; MAP is mean arterial pressure), arterial blood pressure, and saturation of mixed venous blood (SvO2) is critical.
ICP monitoring may be used in patients with severe head injuries who have a high probability of developing intracranial hypertension. Some physicians use a Glasgow Coma Scale score of less than 7 as an indicator for monitoring ICP. The goal of this monitoring is to maintain the ICP at less than 10 mm Hg and the CPP at greater than 80 mm Hg. Management of intracranial hypertension can also be done by draining cerebrospinal fluid through a ventriculostomy.
Some patients may have episodes of agitation and pain, which can increase ICP. Sedatives and analgesics can be administered to control intermittent increases in ICP, with a resulting decrease in CPP. Additionally, some patients with severe head injuries may require chemical paralysis to improve oxygenation and ventilation. Other complications are also managed pharmacologically, such as seizures (by anticonvulsants), increased ICP (by barbiturate coma), infection (by antibiotics), and intracranial hypertension (by diuretics).
|Medication or Drug Class||Dosage||Description||Rationale|
|Sedatives and chemical paralytics||Varies by drug||Short acting: midazolam (Versed); propofol (Diprivan)||Control intermittent increases in ICP with a resultant decrease in CPP; improve oxygenation and ventilation|
|Analgesics||Varies by drug||Fentanyl (Sublimaze)||Control intermittent increases in ICP with a resultant decrease in CPP|
The highest priority is to maintain a patent airway, appropriate ventilation and oxygenation, and adequate circulation. Make sure the patient’s endotracheal tube is anchored well. If the patient is at risk for self-extubation, maintain him or her in soft restraints. Note the lip level of the endotracheal tube to determine if tube movement occurs. Notify the physician if the patient’s Pao2 drops below 80 mm Hg, if Paco2 exceeds 40 mm Hg, or if severe hypocapnia (Paco2 < 25 mm Hg) occurs.
Serial assessments of the patient’s neurological responses are of the highest importance. When a patient’s assessment changes, timely notification to the trauma surgeon or neurosurgeon can save a patient’s life. The patient with DAI is dependent on nurses and therapists for maintaining muscle tone, joint function, bowel and bladder function, and skin integrity. Consult the rehabilitation department early in the hospitalization for evaluation and treatment. Frequent turning, positioning, and use of a pressure-release mattress help prevent alterations in skin integrity. Keep skin pressure points clean and dry.
Provide simple educational tools about head injuries. Referrals to clinical nurse specialists, pastoral care staff, and social workers are helpful in developing strategies to increase education and support. Establish a visiting schedule that meets the needs of the patient and family while providing adequate time for patient care and rest. The mortality of patients with diffuse axonal injury ranges from 15% to 51%, with a wide variation in the level of cognitive functioning that the patient can reach through intensive rehabilitation. Education and support for the family are critical in assisting them in coping with the severity of this injury.
Evidence-Based Practice and Health Policy
Esbjornsson, E., Skoglund, T., Mitsis, M.K., Hofgren, C., Larsson, J., & Sunnerhagen, K.S. (2013). Cognitive impact of traumatic axonal injury (TAI) and return to work. Brain Injury, 27(5), 521–528.
- TAI can have severe and irreparable effects on cognition and the ability to return to normal daily functions, such as employment.
- A prospective study, in which 12 patients with traumatic brain injury (TBI) and suspected TA) were followed over a period of 12 months, revealed significant deterioration in cognitive performance. Using the Barrow Neurological Institute Screen for Higher Cerebral Functions (BNIS) in which a score < 47 indicates cognitive dysfunction, the median score among this sample of patients was 43 (range, 21 to 50) at 6 months and 43.5 (range, 18 to 49) at 12 months.
- During the follow-up period, improvements in reaction time (p = 0.028) were seen at 6 months; however, no further improvements were seen at 12 months. Although attention stabilized from the acute phase to 6 months (p = 0.034), a significant decline was noted among the patients at 12 months (p = 0.046).
- At 12 months, only four patients had returned to work and two were in vocational rehabilitation for 10 or fewer hours per week. All of the patients had been employed prior to sustaining TBI.
- Trauma history, description of the event, time elapsed since the event, whether or not the patient had a loss of consciousness, and if so, for how long
- Physical findings related to the site of head injury: Neurological assessment, presence of accompanying symptoms, presence of complications (decreased level of consciousness, unequal pupils, loss of strength and movement, confusion or agitation, nausea and vomiting), CPP, ICP, appearance, bruising or lacerations, drainage from the nose or ears
- Signs of complications: Seizure activity, infection (fever, purulent discharge from any wounds), aspiration pneumonia (shortness of breath, pulmonary congestion, fever, productive cough), increased ICP
- Response to medications used to control pain and increase ICP
Discharge and home healthcare guidelines
Teach the patient and significant others the purpose, dosage, schedule, precautions, and potential side effects, interactions, and adverse reactions of all prescribed medications. Teach the patient and family the strategies required to prevent complications of immobility. Encourage participation in physical, occupational, and speech therapy. Verify that the patient and family have demonstrated safety in performing the activities of daily living.
Review with the patient and family all follow-up appointments that are necessary. If outpatient or home therapies are needed, review the arrangements. If appropriate, assist the patient and family in locating ongoing psychosocial support to cope with this injury.