Traumatic brain injury (TBI) affects more than 1.4 million Americans annually.1 These injuries, defined as a blow or penetrating injury to the head that disrupts normal brain function,2 occur as a result of falls (28%), motor vehicle crashes (20%), being struck by or against a moving or stationary object (19%), and assaults (11%).3 Injuries to the brain are classified as focal, such as cerebral contusions, lacerations, and hematomas/hemorrhages, or diffuse, which include concussions and diffuse axonal injuries.4 Because the signs and symptoms of patients who have sustained TBIs may change quickly and evidence of deterioration may be subtle, trauma nurses must be adept at performing astute neurologic assessments.

A key component of any neurologic assessment is the pupillary examination.4 Trauma nurses at all levels of care routinely perform pupillary assessments on patients and are likely to be familiar with the basic components of the pupillary examination. However, some confusion may still remain about more specific aspects of the examination and the physiologic basis of the pupillary response, particularly as it pertains to patients who have sustained TBIs. Therefore, the purpose of this article is to identify the key components of the pupillary examination, explain the physiologic basis of the pupillary response, and illustrate the application of this information in patients with TBI through a case study.

CASE STUDY

An 18-year-old woman was a restrained driver of a vehicle that was T-boned (lateral) at a high speed on the driver's side of the car. The car subsequently rolled over onto its roof. Emergency medical services arrived to find the victim conscious but with a Glasgow Coma Scale (GCS) Score of 13 (Table 1). The victim's pupils were noted to be equal and reactive. The victim's level of consciousness continued to deteriorate while the emergency medical services worked to free her from the wreckage. She arrived at the regional emergency department after 40-minute extrication with a GCS Score of 8: she was given a 2 for opens eyes to painful stimuli, a 2 for unintelligible verbal response, and a 4 for withdraws to pain. Her pupils were now unequal. The right pupil measured 5 mm and was nonreactive to a direct light, whereas her left pupil measured 2 mm and displayed a sluggish reaction to direct light. She was noted to have a small forehead laceration with surrounding ecchymosis. She was sedated, paralyzed, and intubated by the emergency department staff to ensure airway protection. A computerized tomography (CT) scan of the patient's head was performed, which revealed a large subdural hematoma. The patient's neurologic status continued to deteriorate, and, therefore, the local air medical service was immediately dispatched to transport the patient to a level I trauma center. She was transported to a level I trauma center for further evaluation of her head injury. Upon her arrival to the trauma center, her trauma evaluation was completed, and she was transferred to the surgical intensive care unit. Her pupils were found nonreactive on her initial trauma evaluation at the trauma center. In the surgical intensive care unit, a neurosurgical consultation for the treatment of an acute subdural hematoma and possible surgical evacuation was obtained.

TABLE 1 The Glasgow Coma Scale

IDENTIFYING TBI

Identifying an acute brain injury in patients with trauma requires serial neurologic examinations, including pupillary assessments, a CT scan, and possibly a magnetic resonance imaging. As depicted in the case study, evidence of TBI may be present in the initial neurologic examination performed at the scene. Victims may have altered GCS scores or impaired level of consciousness ranging from subtle to severe. The initial pupillary examinations may appear benign, and pupillary changes may not surface until hours after the occurrence of the injury. Performing serial neurologic examinations, including pupillary assessments, aids in identifying subtle changes in a patient's neurologic status. These subtle changes can indicate the presence of TBI and/or an acute deterioration in a patient's condition.4 The presence of TBI is confirmed with a CT and/or a magnetic resonance imaging once a patient arrives in a healthcare facility. The CT scan can quickly aid in differentiating between a focal and a diffuse brain injury.

Subdural hematomas are one type of focal brain injury occurring in approximately 30% of patients with TBI.4 An acute subdural hematoma occurs usually after a deceleration injury in which cerebral veins rupture because of either a linear or rotational shearing force.5 Rupture of these vessels causes bleeding into the subdural space. This bleeding may exert additional pressure onto the surrounding brain tissue, causing shifting of the tissue or mass effect. Because the subdural space is not limited by the cranial sutures, this bleeding can potentially spread along the entire cerebral hemisphere.6 As the size of the bleed and the mass effect on the brain increases, the patient's neurologic status declines, and pupillary changes often appear. As bleeding continues, the likelihood of a poor prognosis also increases: mortality rates as high as 50% have been reported among the patients who present with a subdural hematoma requiring immediate surgical evacuation.6

THE PUPILLARY EXAMINATION

The standard of care for any patient with TBI includes serial neurologic examinations. These examinations include a pupillary assessment and are often performed by trauma nurses at the scene, in the emergency department, and in the acute and critical care units.7 Unlike other components of the neurologic examination that require patients to be conscious, the pupillary examination is one of the few neurologic signs that can be assessed in an unconscious patient or in a patient receiving neuromuscular blocking agents and sedation. The pupillary examination is a minimally invasive assessment, which provides valuable information about the severity and progression of the brain injury, as well as brainstem function. Thus, it is important for trauma nurses to perform pupillary examinations thoroughly and understand the physiologic basis of the pupillary response.

Pupil size is reported as the width or diameter of each pupil in millimeters. A standardized pupil gauge should be used to report the pupil size in millimeters. The use of this gauge aids in decreasing subjectivity, particularly when serial assessments are performed. The normal diameter of the pupil is between 2 and 5 mm, with the average pupil measuring 3.5 mm. Although both pupils should be equal in size, a 1-mm discrepancy is considered a normal deviation. This condition is known as anisocoria and is present in 15% to 17% of the population without any known clinical significance.6 Pupil size should be assessed both before and after the pupil responds to direct light.

Pupil Shape

Pupil reactivity is reported as the response or reflex of each pupil to direct light. Reactivity is assessed by shining a low-beam flashlight inward from the outer canthus of each eye. Each eye should be checked separately. The light should not shine directly into the pupil because the glare or reflection may obscure visualization.6 The reaction that each pupil has to the light stimulus should be recorded. The speed of pupillary reactivity is recorded as brisk, sluggish, or nonreactive. Normally, pupils should constrict briskly in response to light. A sluggish or slow pupillary response may indicate increased ICP, and nonreactive pupils are often associated with severe increases in ICP and/or severe brain damage.

A complete pupillary reactivity examination also includes assessment of the consensual pupillary response and accommodation. The consensual pupillary response is the constriction that normally occurs in a pupil when light is shown into the opposite eye.6 Because of this response, the trauma nurse should wait for several seconds before assessing pupillary light reflex in the second eye, as that pupil may be temporarily constricted. Accommodation is the constriction of pupils that occurs when a conscious patient is focusing on a close object. Pupils should normally constrict bilaterally when an object is held within 4 to 6 inches of a patient's nose.6

PHYSIOLOGICAL BASIS OF THE PUPILLARY RESPONSE

The pupil is a small hole in the center of the iris, which allows light to enter in the lens of the eye. The diameter of the pupil is controlled by smooth muscle within the iris; and pupillary size, shape, and reactivity to light are regulated by the autonomic nervous system.6 The diameter of the iris is controlled by 2 muscles: the pupilloconstrictor, which is a sphincter muscle controlled by the parasympathetic nervous system; and the pupillodilator, which has sympathetic nervous system control.8

Parasympathetic Response: Pupillary Constriction

Normally, when light is shone into the eye, the rods and cones of the retina serve as sensory receptors and send the impulse via afferent nerve pathways through axons in the optic nerve, optic chiasm, and optic tract.6 This impulse reaches the Edinger-Westphal nuclei in the midbrain. The parasympathetic response originates in these nuclei, and efferent nerve pathways transmit the impulse via cranial nerve III to the pupilloconstrictor muscle.4 Both the ipsilateral and the contralateral Edinger-Westphal nuclei receive identical afferent input, which causes the consensual light reflex.8 The neurotransmitter responsible for the synaptic response in pupillary constriction is acetylcholine.

Sympathetic Response: Pupillary Dilation

The sympathetic pathway responsible for pupil dilation originates in the posterior-lateral hypothalamus and involves 3 neurons.4 The first ipsilateral preganglionic central neuron travels through the lateral brainstem to the spinal cord. The second preganglionic neuron crosses the lung apex and ascends the neck where it synapses in the cervical ganglion. The third postganglionic neuron accompanies the internal carotid into the skull base to the trigeminal ganglion and joins the nerve fibers of the abducens as it passes through the inferior orbital fissure. This neuron then continues through the trigeminal nerve until it reaches the pupillodilator muscle in the iris. The neurotransmitter responsible for this synaptic reaction is norepinephrine.

Cranial Nerves

The eye is innervated by 3 cranial nerves (CN III, IV, VI), which work together to provide smooth eye movements. Cranial nerve III (oculomotor) controls the parasympathetic response of the pupil, causing pupillary constriction.6 Cranial nerves III, IV, and VI innervate the muscles surrounding the eye and are responsible for extraocular eye movements (EOMs). Assessment of EOM is appropriate in the conscious trauma patient and can be particularly important when caring for patients with facial trauma. However, assessment of EOMs in the unconscious patient with TBI is not always possible or indicated. When caring for this type of patient, it is necessary to assess only cranial nerve III by testing the pupillary response to light.

ABNORMAL PUPILLARY RESPONSE IN TBI PATIENTS

A complete neurologic examination should be performed and any changes in the patient's condition should be noted and reported to a physician. An abnormal pupil in a patient with TBI is often indicative of increasing ICP due to progression of the hematoma/hemorrhage or cerebral edema. However, the trauma nurse should be aware of other clinical factors that may cause an abnormal pupil response. Table 2 highlights abnormal pupils that may be seen in TBI patients and identifies both physiologic and clinical factors contributing to the abnormalities. Regardless of the cause of an abnormal pupil, the trauma nurse should always notify a physician immediately when an abnormal pupil is detected. A CT scan and continuous ICP monitoring will aid in definitively identifying the cause of the abnormal pupil.

TABLE 2 Abnormal Pupils Observed in Patients With TBI

TABLE 2

CONCLUSIONS

1. Centers for Disease Control and Prevention, Division of Injury and Disability Outcomes and Progress. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. http://www.cdc.gov/ncipc/pub-res/TBI_in_US_04/TBI-USA_Book-Oct1.pdf. Accessed March 10, 2006. [Context Link]

2. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Injury topics and fact sheets: traumatic brain injury. http://www.cdc.gov/ncipc/factsheets/tbi.htm. Accessed January 5, 2007. [Context Link]

3. Langlois J, Rutland-Brown W, Thomas K. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. http://www.cdc.gov/ncipc/pubres/TBI_in_US_04/TBI%20in%20the%20US_Jan_2006.pdf. Accessed January 5, 2007. [Context Link]

4. Hickey J. The Clinical Practice of Neurological and Neurosurgical Nursing. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2003:132-135, 170-176. [Context Link]

5. Davis AE. Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations. Crit Care Nurs Q. 2000;23:1-13. [Context Link]

6. Barker E. Neuroscience Nursing. St Louis, MO: Mosby; 2001;45:60-78, 334-335. [Context Link]

7. March K, Wellwood J, Lovasick D, Madden L, Criddle L, Henrickson S. Craniocerebral trauma. In: Bader M, Littlejohns L, eds. AANN Core Curriculum for Neuroscience Nurses. 4th ed. St Louis, MO: Saunders; 2004:277-334. [Context Link]

8. Gilman S, Newman S. Manter and Gatz's Essentials of Clinical Neuroanatomy and Neurophysiology. Philadelphia: FA Davis; 2003. [Context Link]