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Pupillary changes

Pupillary changes include nonreactive pupils or pupils that are sluggish. Nonreactive (fixed) pupils fail to constrict in response to light or to dilate when the light is removed. The development of a unilateral or bilateral nonreactive response indicates an important change in the patient’s condition and may signal a life-threatening emergency and possibly brain death. It also occurs with the use of certain optic drugs.

A sluggish pupillary reaction is an abnormally slow pupillary response to light. It can occur in one pupil or both, unlike the normal reaction, which is always bilateral. A sluggish reaction accompanies degenerative disease of the central nervous system and diabetic neuropathy. It can occur normally in the elderly, whose pupils become smaller and less responsive with age.

Act Now: Ifthe patient is unconscious and develops unilateral or bilateral nonreactive pupils, quickly take his vital signs. Stay alert for decerebrate or decorticate posture, bradycardia, elevated systolic blood pressure, widened pulse pressure, and the development of other untoward changes in the patient’s condition. Remember, a unilateral dilated, nonreactive pupil may be an early sign of uncal brain herniation. Emergency surgery to decrease intracranial pressure (ICP) may be necessary. If the patient isn’t already being treated for increased ICP, insert an I.V. line to administer a diuretic, an osmotic, or a corticosteroid. You may also need to start the patient on controlled hyperventilation.

Assessment

History

Ifthe patient is conscious, obtain a brief history. Does he use eyedrops? If so, what type and when did he last instill them? Also ask if he’s experiencing pain and, if so, try to determine its location, intensity, and duration.

Physical examination

Check the patient’s visual acuity in both eyes. Then test the pupillary reaction to accommodation: Normally, both pupils constrict equally as the patient shifts his glance from a distant to a near object.

Next, hold a penlight at the side of each eye and examine the cornea and iris for abnormalities. Measure intraocular pressure (IOP) with a tonometer, or estimate IOP by placing your second and third fingers over the patient’s closed eyelid. If the eyeball feels rock-hard, suspect elevated IOP. Ophthalmoscopic and slit-lamp examinations of the eye will need to be performed. If the patient has experienced ocular trauma, don’t manipulate the affected eye. After the examination, be sure to cover the affected eye with a protective metal shield, but don’t let the shield rest on the globe.

To assess pupillary reaction to light, first test the patient’s direct light reflex. Darken the room, and cover one of the patient’s eyes while you hold open the opposite eyelid. Using a bright penlight, bring the light toward the patient from the side and shine it directly into his opened eye. If normal, the pupil will promptly constrict. Next, test the consensual light reflex. Hold both of the patient’s eyelids open, and shine the light into one eye while watching the pupil of the opposite eye. If normal, both pupils will promptly constrict. Repeat both procedures to test light reflexes in the opposite eye. A sluggish reaction in one or both pupils indicates dysfunction of cranial nerves (CNs) II and III, which mediate the pupillary light reflex. (See Innervation of direct and consensual light reflexes, page 250.)

Pediatric pointers

Children have nonreactive and sluggish pupils for the same reasons as adults. The most common cause is oculomotor nerve palsy from increased ICP.

Medical causes

Adie’s syndrome

Adie’s syndrome produces an abrupt onset of unilateral mydriasis along with a sluggish or nonreactive pupillary response. It may also produce blurred vision and cramplike eye pain. Eventually, both eyes may be affected. Musculoskeletal assessment reveals hypoactive or absent deep tendon reflexes (DTRs) in the arms and legs.

Botulism

Bilateral mydriasis and nonreactive pupils usually appear 12 to 36 hours after ingestion of tainted food. Other early findings include blurred vision, diplopia, ptosis, strabismus, and extraocular muscle palsies, along with anorexia, nausea, vomiting, diarrhea, and dry mouth. Vertigo, deafness, hoarseness, nasal voice, dysarthria, and dysphagia follow. Progressive muscle weakness and absent DTRs usually evolve over 2 to 4 days, resulting in severe constipation and paralysis of respiratory muscles with respiratory distress.

Diabetic neuropathy

A patient with long-standing diabetes mellitus may have a sluggish pupillary response. Additional findings include orthostatic hypotension, syncope, dysphagia, episodic constipation or diarrhea, painless bladder distention with overflow incontinence, retrograde ejaculation, and impotence.

Encephalitis

As encephalitis progresses, initially sluggish pupils become dilated and nonreactive. Decreased accommodation and other symptoms of cranial nerve palsies, such as dysphagia, develop. Within 48 hours after onset, encephalitis causes a decreased level of consciousness, high fever, headache, vomiting, and nuchal rigidity. Aphasia, ataxia, nystagmus, hemiparesis, and photophobia may occur with seizures.

Familial amyloid polyneuropathy

Familial amyloid polyneuropathy produces sluggish or nonreactive pupils and miosis. Corneal opacities may affect visual acuity. The patient may also experience anhidrosis, orthostatic hypotension, alternating diarrhea and constipation, and impotence. Initially, he’ll experience paresthesia and possibly pain in the feet and lower legs; later, absent DTRs and thinning legs will develop.

Glaucoma (acute angle-closure)

An ophthalmic emergency, examination reveals a moderately dilated, nonreactive pupil in the affected eye. Conjunctival injection, corneal clouding, and decreased visual acuity also occur. The patient experiences a sudden onset of blurred vision, followed by excruciating pain in and around the affected eye. He commonly reports seeing halos around white lights at night. Severely elevated IOP commonly induces nausea and vomiting.

Herpes zoster

The patient with herpes zoster affecting the nasociliary nerve may have a sluggish pupillary response. Examination of the conjunctiva reveals follicles. Additional ocular findings include a serous discharge, absence of tears, ptosis, and extraocular muscle palsy.

Iris disease (degenerative or inflammatory)

Iris disease causes pupillary nonreactivity in the affected eyes. Visual acuity may also decrease.

Midbrain lesions

Although rare, midbrain lesions produce bilateral midposition nonreactivepupils.Other findings include loss of upward gaze, coma, central neurogenic hyperventilation, bradycardia, hemiparesis or hemiplegia, and decorticate or decerebrate posture.

Multiple sclerosis (MS)

MS may produce small, irregularly shaped pupils that react better to accommodation than to light. Additional ocular findings may include ptosis, nystagmus, diplopia, and blurred vision. In most cases, vision problems and sensory impairment, such as paresthesia, are the earliest indications along with weakness, numbness, tingling, and unsteadiness. Features that may occur later include intention tremor, spasticity, hyperreflexia, and gait ataxia as well as muscle weakness and paralysis, dysphagia and dysarthria, constipation, and urinary urgency, frequency, and incontinence. The patient may also develop impotence and emotional instability.

Ocular trauma

Severe damage to the iris or optic nerve may produce a nonreactive, dilated pupil in the affected eye (traumatic iridoplegia). This sign is usually transitory but can be permanent. Slit-lamp examination commonly reveals a V-shaped notch in the pupillary rim, indicating a tear in the iris sphincter muscle. The patient usually experiences eye pain and may also develop eye edema and ecchymoses.

Oculomotor nerve palsy

The first signs of this oculomotor ophthalmoplegia commonly include a dilated, nonreactive pupil and loss of the accommodation reaction. These findings may occur in one eye or both, depending on whether the palsy is unilateral or bilateral. Among the causes of total third cranial nerve palsy is life-threatening brain herniation. Central herniation causes bilateral midposition nonreactive pupils, whereas uncal herniation initially causes a unilateral dilated, nonreactive pupil. Other common findings include diplopia, ptosis, outward deviation of the eye, and inability to elevate or adduct the eye. Additional findings depend on the underlying cause of the palsy.

Tertiary syphilis

A sluggish pupillary reaction (especially in Argyll Robertson pupils) occurs in the late stage of neurosyphilis, along with marked weakness of the extraocular muscles, visual field defects and, possibly, cataractous changes in the lens. The patient may complain of orbital rim pain that worsens at night. He may also exhibit lid edema, decreased visual acuity, and exophthalmos. Tertiary lesions appear on the skin and mucous membranes. Liver, respiratory, cardiovascular, and additional neurologic dysfunction may also occur.

Uveitis

A small, nonreactive pupil that appears suddenly with severe eye pain, conjunctival injection, diminished vision, and photophobia typifies anterior uveitis. With posterior uveitis, similar features develop insidiously, along with blurred vision and a distorted pupil shape.

Wernicke’s disease

Initially, Wernicke’s disease produces an intention tremor accompanied by a sluggish pupillary reaction. Later, pupils may become nonreactive. Additional ocular findings include diplopia, gaze paralysis, nystagmus, ptosis, decreased visual acuity, and conjunctival injection. The patient may also exhibit orthostatic hypotension, tachycardia, ataxia, apathy, and confusion.

Other causes

Drugs

Instillation of a topical mydriatic and a cycloplegic may induce a temporarily nonreactive pupil in the affected eye. Opiates, such as heroin and morphine, cause pinpoint pupils with a minimal light response that can be seen only with a magnifying glass. And atropine poisoning produces widely dilated, nonreactive pupils.

Nursing considerations

If the patient is conscious, monitor his pupillary light reflex to detect changes. If he’s unconscious, close his eyes to prevent corneal exposure. (Use tape to secure the eyelids, if needed.) A sluggish pupillary reaction isn’t diagnostically significant, although it occurs with various disorders.

Patient teaching

Stress the importance of regular ophthalmologic examinations. Provide information and techniques to use to reduce photophobia. Teach the patient self-care techniques related to diabetes. Provide information on maintaining a safe home environment.

Pictures

Pupillary changes - 4966.png

Book Source Details

  • Book Title: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series
  • Author(s): Springhouse
  • Year of Publication: 2007
  • Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2007 Lippincott Williams & Wilkins.

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Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2008 Williams & Wilkins.

More About Causes of Skin color changes




More About This Book:
Title: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2007
ISBN: 1-58255-624-5

 » Next page: Papular rash (Signs & Symptoms: A 2-in-1 Reference for Nurses)

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