the pupillary response in traumatic brain injury: a...

October–December 2007 Journal of Trauma Nursing • Volume 14, Number 4 191

The Pupillary Response inTraumatic Brain Injury: A Guide for Trauma Nurses

Andrea Adoni, BSN, RN, CCRN, CEN, EMT

Molly McNett, PhD(c), MSN, RN

■ ABSTRACTTraumatic brain injuries (TBIs) affect more than 1.4 mil-lion Americans annually. Trauma nurses caring for thesepatients routinely perform serial neurologic assessments,including pupillary examinations. While trauma nursesare likely familiar with basic components of the pupil-lary examination, some confusion about more specificaspects of the examination and the physiologic basis ofthe pupillary response may still remain, particularly as itpertains to patients with TBI. Therefore, the purpose ofthis article is to identify the key components of a pupil-lary examination and its associated physiologicresponse. A case study is provided to illustrate the appli-cation of this information among patients with TBI.

■ KEY WORDSBrain injury, Pupil, Trauma

Traumatic brain injury (TBI) affects more than 1.4 mil-lion Americans annually.1 These injuries, defined as a

blow or penetrating injury to the head that disrupts normalbrain function,2 occur as a result of falls (28%), motorvehicle crashes (20%), being struck by or against a moving

Andrea Adoni, BSN, RN, CCRN, CEN, EMT, is Flight NurseSpecialist, Cleveland Metro LifeFlight; MetroHealth MedicalCenter, and ACNP student, Frances Payne Bolton School ofNursing, Case Western Reserve University; and Molly McNett,MSN, RN, is Research Coordinator, Department of NursingResearch, MetroHealth Medical Center, Cleveland, Ohio.

Corresponding Author: Andrea Adoni, BSN, RN, CCRN,CEN, EMT, Cleveland Metro Lifeflight Office, 4th FloorHamann, MetroHealth Medical Center, 2500 MetroHealth Dr,Cleveland, OH 44109 ([email protected]).

or stationary object (19%), and assaults (11%).3 Injuries tothe 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 sus-tained TBIs may change quickly and evidence of deteriora-tion may be subtle, trauma nurses must be adept atperforming astute neurologic assessments.

A key component of any neurologic assessment is thepupillary examination.4 Trauma nurses at all levels ofcare routinely perform pupillary assessments on patientsand are likely to be familiar with the basic componentsof the pupillary examination. However, some confusionmay still remain about more specific aspects of the exam-ination and the physiologic basis of the pupillaryresponse, particularly as it pertains to patients who havesustained TBIs. Therefore, the purpose of this article is toidentify the key components of the pupillary examina-tion, explain the physiologic basis of the pupillaryresponse, and illustrate the application of this informa-tion in patients with TBI through a case study.

■ CASE STUDYAn 18-year-old woman was a restrained driver of a vehi-cle that was T-boned (lateral) at a high speed on the dri-ver’s side of the car. The car subsequently rolled over ontoits roof. Emergency medical services arrived to find thevictim conscious but with a Glasgow Coma Scale (GCS)Score of 13 (Table 1). The victim’s pupils were noted tobe equal and reactive. The victim’s level of consciousnesscontinued to deteriorate while the emergency medicalservices worked to free her from the wreckage. Shearrived at the regional emergency department after 40-minute extrication with a GCS Score of 8: she was givena 2 for opens eyes to painful stimuli, a 2 for unintelligibleverbal response, and a 4 for withdraws to pain. Herpupils were now unequal. The right pupil measured 5 mmand was nonreactive to a direct light, whereas her leftpupil measured 2 mm and displayed a sluggish reaction

C L I N I C A L C A R E

192 Journal of Trauma Nursing • Volume 14, Number 4 October–December 2007

to direct light. She was noted to have a small foreheadlaceration with surrounding ecchymosis. She wassedated, paralyzed, and intubated by the emergencydepartment staff to ensure airway protection. A comput-erized tomography (CT) scan of the patient’s head wasperformed, which revealed a large subdural hematoma.The patient’s neurologic status continued to deteriorate,and, therefore, the local air medical service was immedi-ately dispatched to transport the patient to a level Itrauma center. She was transported to a level I traumacenter for further evaluation of her head injury. Upon herarrival to the trauma center, her trauma evaluation wascompleted, and she was transferred to the surgical inten-sive care unit. Her pupils were found nonreactive on herinitial trauma evaluation at the trauma center. In the sur-gical intensive care unit, a neurosurgical consultation forthe treatment of an acute subdural hematoma and possi-ble surgical evacuation was obtained.

■ IDENTIFYING TBIIdentifying an acute brain injury in patients with traumarequires serial neurologic examinations, including pupil-lary assessments, a CT scan, and possibly a magnetic reso-nance imaging. As depicted in the case study, evidence ofTBI may be present in the initial neurologic examinationperformed at the scene. Victims may have altered GCSscores or impaired level of consciousness ranging from sub-tle to severe. The initial pupillary examinations may appearbenign, and pupillary changes may not surface until hoursafter the occurrence of the injury. Performing serial neuro-logic examinations, including pupillary assessments, aids inidentifying subtle changes in a patient’s neurologic status.These subtle changes can indicate the presence of TBIand/or an acute deterioration in a patient’s condition.4 Thepresence of TBI is confirmed with a CT and/or a magneticresonance imaging once a patient arrives in a healthcarefacility. The CT scan can quickly aid in differentiatingbetween a focal and a diffuse brain injury.

Subdural hematomas are one type of focal brain injuryoccurring in approximately 30% of patients with TBI.4 Anacute subdural hematoma occurs usually after a decelera-tion injury in which cerebral veins rupture because ofeither a linear or rotational shearing force.5 Rupture ofthese vessels causes bleeding into the subdural space. Thisbleeding may exert additional pressure onto the surround-ing brain tissue, causing shifting of the tissue or masseffect. Because the subdural space is not limited by the cra-nial sutures, this bleeding can potentially spread along theentire cerebral hemisphere.6 As the size of the bleed andthe mass effect on the brain increases, the patient’s neuro-logic status declines, and pupillary changes often appear.As bleeding continues, the likelihood of a poor prognosisalso increases: mortality rates as high as 50% have beenreported among the patients who present with a subduralhematoma requiring immediate surgical evacuation.6

■ THE PUPILLARY EXAMINATIONThe standard of care for any patient with TBI includesserial neurologic examinations. These examinationsinclude a pupillary assessment and are often performedby trauma nurses at the scene, in the emergency depart-ment, and in the acute and critical care units.7 Unlikeother components of the neurologic examination thatrequire patients to be conscious, the pupillary examina-tion is one of the few neurologic signs that can beassessed in an unconscious patient or in a patient receiv-ing neuromuscular blocking agents and sedation. Thepupillary examination is a minimally invasive assessment,which provides valuable information about the severityand progression of the brain injury, as well as brainstemfunction. Thus, it is important for trauma nurses to per-form pupillary examinations thoroughly and understandthe physiologic basis of the pupillary response.

TABLE 1

The Glasgow

Coma Scale

Eye opening

Spontaneous 4

Response to verbal command 3

Response to pain 2

No response 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Best motor response

Obeys commands 6

Locales to pain 5

Withdraws to pain 4

Flexion to pain 3

Extension to pain 2

No motor response 1


When performing a pupillary examination in patientswith TBI, a trauma nurse should make the consciouspatient focus on a distant object straight ahead. In thecomatose patient, pupils are assessed per the positionthey are found in. A pupil assessment should include theexamination of size and equality of pupils, pupillaryshape, and reactivity to light.

Pupil Size and EqualityPupil size is reported as the width or diameter of eachpupil in millimeters. A standardized pupil gauge shouldbe used to report the pupil size in millimeters. The use ofthis gauge aids in decreasing subjectivity, particularlywhen serial assessments are performed. The normaldiameter of the pupil is between 2 and 5 mm, with theaverage pupil measuring 3.5 mm. Although both pupilsshould be equal in size, a 1-mm discrepancy is consid-ered a normal deviation. This condition is known asanisocoria and is present in 15% to 17% of the popula-tion without any known clinical significance.6 Pupil sizeshould be assessed both before and after the pupilresponds to direct light.

Pupil ShapePupil shape is reported as round, irregular, or oval. Thenormal shape of the pupil is round. An irregular-shapedpupil may be the result of ophthalmological proceduressuch as cataract surgery or lens implants, and this shouldbe noted on the initial assessment and confirmed with thepatient or family. A pupil that is oval in shape may indi-cate the early compression of cranial nerve III due toincreased intracranial pressure (ICP), and thus should beaddressed immediately. If an oval pupil is detected, meas-ures should be taken to decrease ICP. As ICP is reduced,the oval-shaped pupil should resolve. However, if ICPcontinues to rise or is not treated, the oval-shaped pupilwill become further dilated and will eventually becomenonreactive to light.

Reactivity to LightPupil reactivity is reported as the response or reflex ofeach pupil to direct light. Reactivity is assessed byshining a low-beam flashlight inward from the outercanthus of each eye. Each eye should be checked sepa-rately. The light should not shine directly into thepupil because the glare or reflection may obscure visu-alization.6 The reaction that each pupil has to the lightstimulus should be recorded. The speed of pupillaryreactivity is recorded as brisk, sluggish, or nonreactive.Normally, pupils should constrict briskly in responseto light. A sluggish or slow pupillary response mayindicate increased ICP, and nonreactive pupils areoften associated with severe increases in ICP and/orsevere brain damage.

A complete pupillary reactivity examination alsoincludes assessment of the consensual pupillary responseand accommodation. The consensual pupillary responseis the constriction that normally occurs in a pupil whenlight is shown into the opposite eye.6 Because of thisresponse, the trauma nurse should wait for several sec-onds before assessing pupillary light reflex in the secondeye, as that pupil may be temporarily constricted.Accommodation is the constriction of pupils that occurswhen a conscious patient is focusing on a close object.Pupils should normally constrict bilaterally when anobject is held within 4 to 6 inches of a patient’s nose.6

■ PHYSIOLOGICAL BASIS OF THE PUPILLARY RESPONSEThe pupil is a small hole in the center of the iris, whichallows light to enter in the lens of the eye. The diame-ter of the pupil is controlled by smooth muscle withinthe iris; and pupillary size, shape, and reactivity tolight are regulated by the autonomic nervous system.6

The diameter of the iris is controlled by 2 muscles: thepupilloconstrictor, which is a sphincter muscle con-trolled by the parasympathetic nervous system; andthe pupillodilator, which has sympathetic nervous sys-tem control.8

Parasympathetic Response: Pupillary ConstrictionNormally, when light is shone into the eye, the rods andcones of the retina serve as sensory receptors and send theimpulse via afferent nerve pathways through axons in theoptic nerve, optic chiasm, and optic tract.6 This impulsereaches the Edinger–Westphal nuclei in the midbrain. Theparasympathetic response originates in these nuclei, andefferent nerve pathways transmit the impulse via cranialnerve III to the pupilloconstrictor muscle.4 Both the ipsi-lateral and the contralateral Edinger–Westphal nucleireceive identical afferent input, which causes the consen-sual light reflex.8 The neurotransmitter responsible forthe synaptic response in pupillary constriction is acetyl-choline.

Sympathetic Response: Pupillary DilationThe sympathetic pathway responsible for pupil dilationoriginates in the posterior-lateral hypothalamus andinvolves 3 neurons.4 The first ipsilateral preganglioniccentral neuron travels through the lateral brainstem tothe spinal cord. The second preganglionic neuron crossesthe lung apex and ascends the neck where it synapses inthe cervical ganglion. The third postganglionic neuronaccompanies the internal carotid into the skull base to thetrigeminal ganglion and joins the nerve fibers of theabducens as it passes through the inferior orbital fissure.This neuron then continues through the trigeminal nerveuntil it reaches the pupillodilator muscle in the iris. The


TABLE 2

Abnormal Pupils Observed in Patients With TBIa

Pupillary Abnormality Pupillary Response/Assessment Findings Causes

Unequal pupils

Constricted pupils

Mydriasis: One pupil is dilated

and nonreactive to light. Other

pupil is of normal size and

reacts to light.

Adie’s pupil: One pupil is larger

than the other. The affected

(larger) pupil does not

immediately respond to direct

or consensual light reflex;

however, if light stimulus is

prolonged, this pupil will

slowly constrict to light and

slowly dilate in the dark.

Accommodation in the

affected pupil is sluggish.

The other pupil is of normal

size and reacts to light.

Horner’s syndrome: One pupil is

smaller than the other. The

affected (smaller) pupil has an

impaired response to light and

accommodation. There is

ptosis of the eyelid on the side

of the affected pupil. There is a

loss of sweating on the

affected side.

Miosis: Pupils are pinpoint

bilaterally and too small to

observe reaction to light.

Defect in efferent pathway

Compression of cranial nerve III

Uncal herniation

Compression of posterior

communicating artery

Damage to nerve endings in

sphincter muscle of iris from

direct trauma


Loss of parasympathetic nerve

supply to sphincter muscle in

iris (frequently caused by viral

infection)

Sensitivity to cholinergic drugs


Total or partial loss of

sympathetic innervation to

pupil (due to lesion in

sympathetic fibers in

brainstem or spinal cord)

Damage to hypothalamus


Disruption in sympathetic

pathway (can be due to

intraocular inflammation

from trauma/direct orbital

injury)

Irritation of parasympathetic

pathways

Pontine hemorrhage

Drug induced: opiates/narcotics,

pilocarpine, acetylcholine

(continues)


TABLE 2

Abnormal Pupils Observed in Patients With TBIa

Pupillary Abnormality Pupillary Response/Assessment Findings Causes

aFrom Hickey4 and Barker.6

Dilated pupils

Equal pupils with abnormal

response

Argyll–Robertson: Pupils are

small and irregular in shape,

and may be unequal. Pupils do

not respond to light stimulus,

but do constrict with

accommodation. May dilate

minimally in the dark.

Drug-induced mydriasis: Pupils

are dilated bilaterally. Pupils

may or may not have reaction

to light stimulus.

Anoxia mydriasis: Pupils are

dilated bilaterally and do not

respond to light stimulus.

There is no consensual

response or accommodation.

Hippus: Pupils may be equal in

size. Pupils initially react briskly

to light, but then alternate

between dilation and

constriction.

Marcus Gunn pupil: Pupils are

equal in size, but one pupil

has an abnormal response to

light. When direct light is

shone into the affected eye,

there is a sluggish reaction.

When direct light is shone

into the normal eye, the

affected eye will constrict

(normal consensual reaction),

but when the light is then

directed back to the affected

eye, the pupil in the affected

eye will dilate.

Defect in afferent pathway

Usually due to viral infection

(neurosyphilis, encephalitis)


Sympathetic stimulants or

parasympathetic blocking

agents cause pupillary dilation.

Caused by hallucinogens,

antihistamines, amphetamines,

anticholinergics, dopamine,

and barbiturates

May be caused by ophthalmic

mydriatics that are administered

for intraocular examinations

(atropine, scopolamine)


Transtentorial herniation

Anoxia

Brain death


Early compression of cranial nerve III

Lesion/injury to midbrain

Barbiturate toxicity

Defect in afferent pathway

Lesion or atrophy of the retina

or optic nerve causes damage

to afferent nerve fibers

Retinal detachment

Occlusion in retinal vasculature

(Continued)


neurotransmitter responsible for this synaptic reaction isnorepinephrine.

Cranial NervesThe 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 parasympa-thetic response of the pupil, causing pupillary constric-tion.6 Cranial nerves III, IV, and VI innervate the musclessurrounding the eye and are responsible for extraoculareye movements (EOMs). Assessment of EOM is appro-priate in the conscious trauma patient and can be partic-ularly important when caring for patients with facialtrauma. However, assessment of EOMs in the uncon-scious patient with TBI is not always possible or indi-cated. When caring for this type of patient, it is necessaryto assess only cranial nerve III by testing the pupillaryresponse to light.

■ ABNORMAL PUPILLARY RESPONSE IN TBI PATIENTSWhen performing pupillary examinations in patients withTBI, trauma nurses may detect abnormalities, such as anirregular pupil size, shape, or a sluggish or nonreactivepupil. When an abnormality is detected, the trauma nurseshould first identify whether the abnormality was presenton the previous pupillary examination. If an abnormalpupil is present on the initial pupillary examination, itshould be clearly documented, and a physician should beimmediately notified. Immediate notification of a physi-cian should occur with changes in pupillary response.Comparing the current examination with the previous toprovide time-oriented data for the physician is wise butshould never delay immediate physician notification.

A complete neurologic examination should be per-formed and any changes in the patient’s condition shouldbe noted and reported to a physician. An abnormal pupilin a patient with TBI is often indicative of increasing ICPdue to progression of the hematoma/hemorrhage or cere-bral edema. However, the trauma nurse should be awareof other clinical factors that may cause an abnormal pupilresponse. Table 2 highlights abnormal pupils that may beseen in TBI patients and identifies both physiologic andclinical factors contributing to the abnormalities.Regardless of the cause of an abnormal pupil, the traumanurse should always notify a physician immediately whenan abnormal pupil is detected. A CT scan and continuous

ICP monitoring will aid in definitively identifying thecause of the abnormal pupil.

■ CONCLUSIONSInterdisciplinary care for patients with TBI is oftenextremely complex, and trauma nurses have an integralrole in early detection and monitoring of changes inpatient status. The pupillary examination is a crucialcomponent of the serial neurologic assessments routinelyperformed by trauma nurses at all levels of care delivery.The pupillary examination can be quickly and easily per-formed in the unconscious or minimally responsivepatient when a TBI is suspected, and can provide valuableinformation about the degree of initial or progressingbrain injury. As evidenced in the case study, a specific typeof TBI, the subdural hematoma, may cause pupillarychanges, which indicate the need for rapid interventionsto decrease ICP and/or cerebral bleeding and edema. Bygaining a better understanding of the physiologic basis ofthe pupillary response and the particular components ofthe pupillary examination, trauma nurses are in a keyposition to detect early changes in a patient’s conditionand administer or advocate for immediate interventions.

REFERENCES

1. Centers for Disease Control and Prevention, Division of Injury andDisability Outcomes and Progress. Traumatic brain injury in theUnited States: emergency department visits, hospitalizations, anddeaths. www.cdc.gov/ncipc/pub-res/TBI_in_US_04/TBI-USA_Book-Oct1.pdf. Accessed March 10, 2006.

2. Centers for Disease Control and Prevention, National Center for InjuryPrevention and Control. Injury topics and fact sheets: traumatic braininjury. http://www.cdc.gov/ncipc/factsheets/tbi.htm. Accessed January5, 2007.

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

4. Hickey J. The Clinical Practice of Neurological and NeurosurgicalNursing. 5th ed. Philadelphia: Lippincott Williams & Wilkins;2003:132–135, 170–176.

5. Davis AE. Mechanisms of traumatic brain injury: biomechanical, struc-tural and cellular considerations. Crit Care Nurs Q. 2000;23:1–13.

6. Barker E. Neuroscience Nursing. St Louis, MO: Mosby;2001;45:60–78, 334–335.

7. March K, Wellwood J, Lovasick D, Madden L, Criddle L, HenricksonS. Craniocerebral trauma. In: Bader M, Littlejohns L, eds. AANN CoreCurriculum for Neuroscience Nurses. 4th ed. St Louis, MO: Saunders;2004:277–334.

8. Gilman S, Newman S. Manter and Gatz’s Essentials of ClinicalNeuroanatomy and Neurophysiology. Philadelphia: FA Davis; 2003.

the pupillary response in traumatic brain injury: a...

Documents