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Home > RNJ > 2009 > September/October > Challenges of Diffuse Axonal Injury Diagnosis

Challenges of Diffuse Axonal Injury Diagnosis
Margaret Thomas, BS RN CRRN Linda Dufour, MSN RN CRRN

“This can’t be right. Jay is in a vegetative state following a severe traumatic brain injury (TBI), but his computed tomography scan is essentially normal. How am I going to explain this to his mom?”

This is a conversation I overhear among my rehabilitation nurse colleagues from time to time. Jay has a type of brain trauma called diffuse axonal injury (DAI). Recent statistics from the National Centers for Injury Prevention and Control (NCIPC, 2006) indicate 1.4 million people sustain a TBI each year in the United States. The leading causes of TBI are falls (28%), motor vehicle accidents (20%), being struck by or against an object (19%), and assaults (11%; NCIPC). DAI, one of the most important causes of cognitive dysfunction after TBI (Sugiyama et al., 2007), occurs in a more widespread pattern in certain regions of the brain than the localized zone of focal injuries. It is one of the most devastating forms of TBI and a common cause of vegetative state and severe disability. DAI occurs in 40%–50% of all patients who are hospitalized from TBI (Meythaler, Peduzzi, Eleftheriou, & Novack, 2001).

Significance

Diffused axonal injury (DAI) can affect consciousness, alertness, speed of information processing, and basic bodily functions. DAI rarely results in death; however, a high percentage of patients remain in a vegetative state (Wasserman & Koenigsberg, 2007). DAI diagnosis is a challenge because it is not well detected on computed tomography (CT) scans. DAI also is noted to be a progressive injury, with the majority of axon damage occurring hours to days postinjury (Newcombe et al., 2007). Meythaler and colleagues (2001) found that initial CT scans and magnetic resonance imaging (MRI) often are normal and that about 10% of cases will show classic CT findings that are associated with hemorrhagic punctate lesions in certain regions of the brain. Other changes may appear within weeks after the injury. DAI often is referred to as a diagnosis of exclusion because traditional imaging techniques are unable to detect the brain pathology despite obvious clinical symptoms such as prolonged disorders of consciousness (Smith, Meaney, & Shull, 2003).

Because of DAI’s severe neurologic consequences, rehabilitation nurses must be aware of this often “invisible” TBI to coordinate care of affected patients and explain the diagnostic challenges to family members and caregivers. When families have questions about unremarkable scan reports, rehabilitation nurses are the ideal resource to explain the pathophysiology of “cellular trauma,” the ways in which it translates into the current clinical situation, and the reasons why the condition is unclear on scans. It also is critical for rehabilitation nurses to be aware that although scan results help to diagnose conditions, DAI care provision largely is based on patient presentation.

Nature of Injury

Unlike brain trauma occuring from direct impact and localized deformation, DAI results from shearing forces to the brain. Think of DAI as an injury of “velocity” because it can occur without direct impact to the head. The main factors associated with DAI are rotational forces from sudden acceleration and deceleration of the brain (Smith et al., 2003; Wasserman & Koenigsberg, 2007). A motor vehicle crash involving high speeds could produce such an effect. Severe blows to the head, sports injuries, or shaken-baby syndrome also can cause DAI. As a result of the acceleration and deceleration of the brain itself, the axon on the neuron shears, stretches, and may disconnect. The axon pathology often is associated with tissue tears located in the junctional areas of the gray-white matter. The injury is noted to be more prevalent in areas in which tissue density difference is greatest (Wasserman & Koenigsberg). The damage may be conceptualized as one that occurs at a “microscopic” level versus damage that is evident to the naked eye, and therein lies some of the difficulty with diagnoses.

The injury typically is widespread and bilateral. Injury is most severe along midline structures (Meythaler et al., 2001; Wasserman & Koenigsberg, 2007). Microscopic examination of brain tissue reveals swelling of the cell, an axon that has split in two, and the formation of a retraction ball. Wasserman and Koenigsberg call this a “pathological hallmark” of shearing injury. The pathology of axonal damage rarely is seen at the time of initial injury (with the exception of tissue tearing), but rather during the course of hours to days postinjury (Smith et al., 2003). The actual cellular injury is thought to be significantly worse than what can be seen using traditional imaging techniques.

Diagnosing DAI

Traditional imaging techniques such as CT scans are not sensitive to the level of cellular detail necessary to diagnose DAI. About 50%–80% of patients with DAI have an initial normal CT scan. Among the scans that are positive, common findings are small petechial hemorrhages at the gray-white matter junctions within the corpus callosum and brainstem. There may be small areas of low density that may correlate to areas of edema and shearing of tissue (Wasserman & Koenigsberg, 2007). Both CT and MRI can produce false negatives in the early period postinjury. There also may be a poor correlation between scan findings and clinical symptoms. MRI is more sensitive than CT in detecting DAI. Several new imaging and spectroscopic techniques currently are available, and many are under study (Newcombe et al., 2007; Okamoto, Hashimoto, Aoki, & Ohashi, 2007; Sugiyama et al., 2007; Wasserman & Koenigsberg; Zheng, Liu, Li, & Wu, 2007). There is emerging literature on new and promising techniques such as MRI with T1 weighted, T2 weighted, gradient echo sequences, and diffusion tensor imaging. Some of these techniques are used alone or in combination with other techniques, such as functional MRI (Mao, Polensek, Goldstein, Holder, & Ni, 2007) or single-photon emission computed tomography (Okamoto et al.). Other technologies include magnetic resonance spectroscopy and magnetization transfer imaging (Smith et al., 2003). The ultimate goal is earlier and accurate DAI diagnosis, and, in some cases, prognosis.

Nursing Implications

Rehabilitation nurses have strong standards for evidence in clinical practice. It will be important to monitor the literature for new studies related to diagnostic accuracy for patients with suspected DAI. A clear understanding of DAI’s cellular pathology is imperative to provide education and support to caregivers who will question the dichotomy between their loved one with a severe disorder of consciousness and an essentially normal CT scan. Reassuring family members that evidence-based care is being delivered according to best practices despite the existence of a scan that may only offer a diagnosis of exclusion is critical. A patient with a severe brain injury will need certain elements of care such as airway management, skin and positioning, nutrition, bowel and bladder management, pulmonary hygiene, deep vein thrombosis prevention and management, seizure prophylaxis or monitoring, and organized cognitive and behavioral care. Levels of care and rehabilitation interventions may change as a patient recovers.

Because brain injury presentations vary from person to person, an accurate diagnosis is important; however, care delivery should remain individualized according to behavioral, cognitive, and physical needs. The healthcare industry is on the cutting edge of new diagnostic imaging capabilities. It will be nursing’s challenge to learn about the latest imaging techniques used to diagnose this often “invisible” type of brain injury, coordinate individualized rehabilitative care, and educate loved ones regarding the current state of the science.

About the Authors

Margaret Thomas, BS RN CRRN, is a staff nurse at Shepherd Center in Atlanta, GA. Address correspondence to her at margaret_thomas@shepherd.org.

Linda Dufour, MSN RN CRRN, is a clinical nurse specialist at Shepherd Center in Atlanta, GA.

References

Mao, H., Polensek, S. H., Goldstein, F. C., Holder, C. A., & Ni, C. (2007). Diffusion tensor and functional magnetic resonance imaging of diffuse axonal injury and resulting language impairment. Journal of Neuroimaging, 17, 292–294.

Meythaler, J. M., Peduzzi, J. D., Eleftheriou, E., & Novack, T. A. (2001). Current concepts: Diffuse axonal injury-associated traumatic brain injury. Archives of Physical Medicine and Rehabilitation, 82(10), 1461–1471.

National Centers for Injury Prevention and Control. (2006). Heads up: Brain injury in your practice tool kit. Retrieved May 30, 2009, from www.cdc.gov/ncipc/pub-res/
tbi_toolkit/toolkit.htm.

Newcombe, V. F. J., Williams, G. B., Nortje, J., Bradley, P. G., Harding, S.G., Smielewski, P., et al. (2007). Analysis of acute traumatic axonal injury using diffusion tensor imaging. British Journal of Neurosurgery, 21(4), 340–348.

Okamoto, T., Hashimoto, K., Aoki, S., & Ohashi, M. (2007). Cerebral blood flow in patients with diffuse axonal injury—examination of the easy Z score imaging system utility. European Journal of Neurology, 14, 540–547.

Smith, D., Meaney, D., & Shull, W. (2003). Diffuse axonal injury in head trauma. Journal of Head Trauma Rehabilitation, 18(4), 307–316.

Sugiyama, K., Kondo, T., Higano, S., Endo, M., Watanabe, H., Shindo, K., et al. (2007). Diffusion tensor imaging fiber tractography for evaluating diffuse axonal injury. Brain Injury, 21(4), 413–419.

Wasserman, J., & Koenigsberg, R. (2007). Diffuse axonal injury. Retrieved May 30, 2009, from www.emedicine.com/radio/topic216.htm.

Zheng, W. B., Liu, G. R., Li, L. P., & Wu, R. H. (2007). Prediction of recovery from a post-traumatic coma state by diffusion-weighted imaging (DWI) in patients with diffuse axonal injury. Neuroradiology, 49, 271–279.