Ocular deviation refers to abnormal eye movement that may be conjugate (both eyes move together) or disconjugate (one eye moves separately from the other). This common sign may result from ocular, neurologic, endocrine, and systemic disorders that interfere with the muscles, nerves, or brain centers governing eye movement. Occasionally, it signals a life-threatening disorder such as a ruptured cerebral aneurysm. (See Ocular deviation: Its characteristics and causes in cranial nerve damage.)
Normally, eye movement is directly controlled by the extraocular muscles innervated by the oculomotor, trochlear, and abducens nerves (cranial nerves III, IV, and VI). Together, these muscles and nerves direct a visual stimulus to fall on corresponding parts of the retina. Disconjugate ocular deviation may result from unequal muscle tone (nonparalytic strabismus) or muscle paralysis associated with cranial nerve damage (paralytic strabismus). Conjugate ocular deviation may result from disorders that affect the centers in the cerebral cortex and brain stem responsible for conjugate eye movement. Typically, such disorders cause gaze palsy—difficulty moving the eyes in one or more directions.
If the patient displays ocular deviation, take his vital signs immediately and assess him for altered level of consciousness (LOC), pupil changes, motor or sensory dysfunction, and a severe headache. If possible, ask the patient's family about behavioral changes. Is there a history of recent head trauma? Respiratory support may be necessary. Also, prepare the patient for emergency neurologic tests such as a computed tomography (CT) scan.
If the patient isn't in distress, find out how long he has had the ocular deviation. Is it accompanied by double vision, eye pain, or headache? Also, ask if he has noticed associated motor or sensory changes or fever.
Check for a history of hypertension, diabetes, allergies, and thyroid, neurologic, or muscular disorders. Then obtain a thorough ocular history. Has the patient ever had extraocular muscle imbalance, eye or head trauma, or eye surgery?
During the physical examination, observe the patient for partial or complete ptosis. Does he spontaneously tilt his head or turn his face to compensate for ocular deviation? Check for eye redness or periorbital edema. Assess the patient's visual acuity, and then evaluate extraocular muscle function by testing the six cardinal fields of gaze.
Brain tumor.The nature of ocular deviation depends on the site and extent of the brain tumor. Associated signs and symptoms include headaches that are most severe in the morning, behavioral changes, memory loss, dizziness, confusion, vision loss, motor and sensory dysfunction, aphasia and, possibly, signs of hormonal imbalance. The patient's LOC may slowly deteriorate from lethargy to coma. Late signs include papilledema, vomiting, increased systolic blood pressure, widening pulse pressure, and decorticate posture.
Cavernous sinus thrombosis.With cavernous sinus thrombosis, ocular deviation may be accompanied by diplopia, photophobia, exophthalmos, orbital and eyelid edema, corneal haziness, diminished or absent pupillary reflexes, and impaired visual acuity. Other features include a high fever, headache, malaise, nausea and vomiting, seizures, and tachycardia. Retinal hemorrhage and papilledema are late signs.
Diabetes mellitus.A leading cause of isolated third cranial nerve palsy, especially in the middle-aged patient with long-standing mild diabetes, diabetes mellitus may cause ocular deviation and ptosis. Typically, the patient also complains of the sudden onset of diplopia and pain.
Encephalitis.Encephalitis causes ocular deviation and diplopia in some cases. Typically, it begins abruptly with fever, headache, and vomiting, followed by signs of meningeal irritation (for example, nuchal rigidity) and neuronal damage (for example, seizures, aphasia, ataxia, hemiparesis, cranial nerve palsies, and photophobia). The patient's LOC may rapidly deteriorate from lethargy to coma within 24 to 48 hours after onset.
Head trauma.The nature of ocular deviation depends on the site and extent of head trauma. The patient may have visible soft-tissue injury, bony deformity, facial edema, and clear or bloody otorrhea or rhinorrhea. Besides these obvious signs of trauma, he may also develop blurred vision, diplopia, nystagmus, behavioral changes, headache, motor and sensory dysfunction, and decreased LOC that may progress to coma. Signs of increased intracranial pressure—such as bradycardia, increased systolic pressure, and widening pulse pressure—may also occur.
Orbital blowout fracture.With an orbital blowout fracture, the inferior rectus muscle may become entrapped, resulting in limited extraocular movement and ocular deviation. Typically, the patient's upward gaze is absent; other directions of gaze may be affected if edema is dramatic. The globe may also be displaced downward and inward. Associated signs and symptoms include pain, diplopia, nausea, periorbital edema, and ecchymosis.
Orbital tumor.Ocular deviation occurs as the orbital tumor gradually enlarges. Associated findings include proptosis, diplopia and, possibly, blurred vision.
Stroke.Stroke, a life-threatening disorder, may cause ocular deviation, depending on the site and extent of the stroke. Accompanying features are also variable and include altered LOC, contralateral hemiplegia and sensory loss, dysarthria, dysphagia, homonymous hemianopsia, blurred vision, and diplopia. In addition, the patient may develop urine retention or incontinence or both, constipation, behavioral changes, headache, vomiting, and seizures.
Thyrotoxicosis.Thyrotoxicosis may produce exophthalmos—proptotic or protruding eyes—which, in turn, causes limited extraocular movement and ocular deviation. Usually, the patient's upward gaze weakens first, followed by diplopia. Other features are lid retraction, a wide-eyed staring gaze, excessive tearing, edematous eyelids and, sometimes, an inability to close the eyes. Cardinal features of thyrotoxicosis include tachycardia, palpitations, weight loss despite increased appetite, diarrhea, tremors, an enlarged thyroid, dyspnea, nervousness, diaphoresis, heat intolerance, and an atrial or a ventricular gallop.
▪ Monitor the patient's vital signs and neurologic status if you suspect an acute neurologic disorder.
▪ Take seizure precautions, if necessary.
▪ Prepare the patient for diagnostic tests, such as blood studies, orbital and skull X-rays, and a CT scan.
▪ Explain the disorder and its treatment.
▪ Discuss with the patient and his family changes in LOC that need to be reported.
▪ Talk about how to maintain a safe environment.
▪ Teach ways of reducing environmental stress.
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Copyright Details: Nursing: Interpreting Signs and Symptoms, Copyright © 2008 Williams & Wilkins.
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Title: Nursing: Interpreting Signs and Symptoms Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-58255-668-7 
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