Diagnostic Tests for Nystagmus
Nystagmus Tests: Book Excerpts
Home Diagnostic Testing
These home medical tests may be relevant to Nystagmus:
- Vision & Eye Health: Home Testing:
Nystagmus Diagnosis: Book Excerpts
Diagnostic Tests for Nystagmus: Online Medical Books
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for more information about the diagnostic tests for Nystagmus.
EYE PAIN:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The primary care specialist may want to treat cases of obvious conjunctivitis without a culture and sensitivity. However, a smear and culture is useful especially if
Neisseria
is suspected. A smear may also reveal eosinophils suggesting allergic conjunctivitis. The primary care specialist may also use fluorescein dye to diagnose a foreign body. Most primary care physicians feel competent to use tonometry to diagnose glaucoma and may feel competent to use a slit lamp. However, when there is any doubt about the diagnosis, the most cost-effective approach is to refer the patient to an ophthalmologist.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
NYSTAGMUS:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The basic diagnostic workup includes visual acuity, visual fields, audiogram, caloric testing, and x-rays of the skull, mastoids, and petrous bones. If these are negative or indefinite, a CT scan or MRI of the brain will be necessary. A spinal fluid analysis will help diagnose central nervous system lues and multiple sclerosis. A BSEP or VEP study may be needed to diagnose multiple sclerosis. The help of a neurologic specialist should be sought before ordering expensive diagnostic tests. Cisternography, tomography, and vertebral basilar angiography are occasionally necessary to establish the diagnosis. Magnetic resonance angiography is an excellent noninvasive means of visualizing the vertebral-basilar circulation.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Eye pain:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient's eye pain doesn't result from a chemical burn, take a complete history. Have the patient describe the pain fully. Is it an ache or a sharp pain? How long does it last? Is it accompanied by burning, itching, or discharge? Find out when it began. Is it worse in the morning or late in the evening? Ask about recent trauma or surgery, especially if the patient complains of sudden, severe pain. Does he have headaches? If so, find out how often and at what time of day they occur.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Ocular deviation:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
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 a headache? Also, ask if he’s noticed associated motor or sensory changes or a 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.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Nystagmus:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
Begin by asking the patient how long he’s had nystagmus. Does it occur intermittently? Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract, and about head trauma and cancer. Does the patient or anyone in his family have a history of stroke? Then explore associated signs and symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness, bladder dysfunction, and fever.
Begin the physical examination by assessing the patient’s level of consciousness (LOC) and vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary changes, drowsiness, elevated systolic pressure, and an altered respiratory pattern. Next, assess nystagmus fully by testing extraocular muscle function: Ask the patient to focus straight ahead and then to follow your finger up, down, and in an “X” across his face. Note when nystagmus occurs as well as its velocity and direction. Finally, test reflexes, motor and sensory function, and the cranial nerves.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Ocular deviation:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
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 any 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 visual acuity, then evaluate extraocular muscle function by testing the six cardinal fields of gaze.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Nystagmus:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Begin by asking the patient how long he has had nystagmus. Does it occur intermittently? Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract, and about head trauma and cancer. Does the patient or anyone in his family have a history of stroke? Then explore associated signs and symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness, bladder dysfunction, and fever.
Begin the physical examination by assessing the patient’s level of consciousness (LOC) and vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary changes, drowsiness, elevated systolic pressure, and altered respiratory pattern. Next, assess nystagmus fully by testing extraocular muscle function: Ask the patient to focus straight ahead and then to follow your finger up, down, and in an “X” across his face. Note when nystagmus occurs, as well as its velocity and direction. Finally, test reflexes, motor and sensory function, and the cranial nerves.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Eye pain [Ophthalmalgia]:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient’s eye pain doesn’t result from a chemical burn or from acute angle-closure glaucoma, take a complete history. Have the patient describe the pain fully. Is it an ache or a sharp pain? How long does it last? Is it accompanied by burning, itching, or a discharge? Find out when it began. Is it worse in the morning or late in the evening? Ask about recent trauma or surgery, especially if the patient complains of severe pain that developed suddenly. Does he have headaches? If so, find out how often and at what time of day they occur.
During the physical examination, don’t manipulate the eye if you suspect trauma. Carefully assess the eyelids and conjunctivae for redness, inflammation, and swelling. Then examine the eyes for ptosis or exophthalmos. Finally, test visual acuity with and without correction, and assess extraocular movements. Characterize any discharge. (See Examining the external eye, page 322.)
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Nystagmus:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Visual acuity. Visual acuity is more depressed in acquired sensory nystagmus than in congenital nystagmus.
B. Ocular motility. The direction, plane, and amplitude of the eye movement are described. Nystagmus is conjugate if both eyes demonstrate the same movement and dissociated if they have different movements. Look for a null zone (field of gaze in which the nystagmus is minimal) or a neutral zone (field of gaze where nystagmus reverses direction).
C. Eye examination. Evaluate for any cause of poor vision that will help confirm sensory nystagmus. Look for aniridia (absence of iris) or iris transillumination as seen in albinism; both are associated with poor vision and nystagmus at an early age. Congenital cataracts or corneal opacities will have poor red reflexes. Analyze the optic nerve to assess for hypoplasia or atrophy. Latent nystagmus (seen only when one eye is covered) is present in congenital esotropia.
D. Other examinations. Head bobbing is usually present with congenital motor nystagmus and spasmus nutans (see below). A complete neurologic assessment should be done to screen for associated signs seen in cerebellar disease, multiple sclerosis, and so on.
Diagnostic assessment
(3,4). An accurate description of the nystagmus will help to categorize the type of eye movement disorder and to determine if any further diagnostic testing is needed.
A. Congenital nystagmus. The nystagmus develops at birth or in the perinatal period with small binocular and conjugate pendular eye movements. Over the first year of life, a jerk nystagmus develops with a null point. The nystagmus decreases with convergence and is abolished during sleep. Head nodding develops at any point up to age 20 years. Any cause of poor vision can cause sensory nystagmus. Two forms of acquired nystagmus when seen in the young merit concern.
1. Opsoclonus. Repetitive, irregular, and multidirectional (“dancing eyes” or saccadomania), opsoclonus is associated with cerebellar or brainstem disease, postviral meningitis, or neuroblastoma.
2. Spasmus nutans. Triad of head turn, nystagmus, and head bobbing that begins between 6 months to 3 years is seen in spasmus nutans. The nystagmus can be monocular or binocular and dissociated; of low amplitude and high frequency; and with horizontal or vertical pendular movements. This usually resolves between age 2 and 8 years. An identical clinical picture can be produced by a glioma of the optic chiasm.
B. Acquired nystagmus. The following are acquired forms of nystagmus with localized pathology.
1. See-saw. One eye rises and rotates in whereas the other descends and rotates out. Movements are pendular. This is frequently seen with lesions of the chiasm or third ventricle.
2. Downbeating. The fast phase of the nystagmus beats down and localizes the lesion at the cervicomedullary junction at the level of the foramen magnum. Arnold-Chiari malformation is the most common cause but spinocerebellar degeneration, brainstem stroke, multiple sclerosis, and platybasia will induce this type of nystagmus.
3. Upbeat. The fast phase beats up and can be of large or small amplitude. The lesion commonly involves the brainstem or vermis of the cerebellum.
4. Convergence-retraction. Here, is seen convergence of the eyes with jerk nystagmus and retraction of the globe on upgaze. Eyelid retraction, limitation in upgaze, and large unreactive pupils are associated with the nystagmus. Papilledema may be present. This is caused by midbrain abnormalities loosely correlated with age 10 years, pinealoma; 20 years, head trauma; 30 years, brainstem vascular malformation; 40 years, multiple sclerosis; 50 years, basilar artery stroke.
5. Periodic alternating. Jerk nystagmus has the fast phase in one direction with a head turn for 60 to 90 seconds, then reverses direction (neutral zone). The cycles repeat continuously with the nystagmus being horizontal throughout. This can be seen with vestibulocerebellar disease (stroke, multiple sclerosis, spinocerebellar degeneration), severe bilateral visual loss (optic atrophy, dense vitreous hemorrhage), or it can be congenital.
6. Gaze-evoked. Jerk nystagmus is present only when eyes look to the side. This is most commonly seen with alcohol or other central nervous system depressants. Cerebellar disease and brainstem disease can be associated with this nystagmus.
7. Vestibular. Nystagmus is caused by dysfunction of inner ear, nerve, or central nuclear complex. Peripheral vestibular disease produces unidirectional jerk nystagmus with fast phase opposite the lesion and usually horizontal. This is commonly associated with vertigo, tinnitus, and deafness (Chapters 6.8 and 6.9). It is caused by labyrinthitis, Ménière’s disease, neuronitis, vascular ischemia, trauma, or toxicity. Central (nuclear) disease is characterized by uni- or bidirectional nystagmus that may be purely horizontal jerk, vertical, or rotatory. Vertigo, tinnitus, and deafness are mild, if present, and symptoms are not relieved with eye fixation as in peripheral disease. This implies bilateral brainstem disease including demyelinating tumor, trauma, or stroke.
8. Latent nystagmus. As discussed, latent nystagmus is found in congenital esotropia.
9. Dissociated. The nystagmus in one eye is different than the other. This is seen in posterior fossa lesions; if an abduction nystagmus is present with an internuclear ophthalmoplegia, multiple sclerosis is likely.
C. Other ocular oscillations
1. Ocular bobbing is characterized by fast, conjugate, downward movement of the eye followed by a slow drift to primary position of gaze. This is seen in comatose patients with large pontine lesions (hemorrhage, stroke, or tumor). Obstructive hydrocephalus or metabolic encephalopathy can cause this type of eye movement.
2. Superior oblique myokymia is present with small unilateral, vertical, and rotatory movements of one eye. Symptoms of oscillopsia worsen when looking down and in. This is usually benign and self-limited, but has been noted with multiple sclerosis.
Testing
A. Laboratory. Urine drug screening for alcohol or barbiturates can be helpful in gaze-evoked nystagmus. High serum levels of phenytoin or lithium produce a gaze-evoked nystagmus. Ocular albinism can be associated with a bleeding disorder secondary to platelet dysfunction (Hermansky-Pudlak syndrome) or white blood cell dysfunction with increased susceptibility to infection and lymphoma (Chediak-Higashi syndrome). A bleeding time and a polymorphonuclear leukocyte function test should be ordered in consultation with a pathologist. Urinary vanillylmandelic acid should be obtained in an opsoclonus patient to look for by-products of neuroblastoma.
B. Imaging studies. Magnetic resonance imaging (MRI) scan must be obtained for any nystagmus having localized pathology. A child with spasmus nutans must have glioma of the chiasm ruled out by computed tomography (CT) or MRI. For vertical nystagmus, especially downbeating, order an MRI with sagittal views to look for cerebellar vermis herniating through the foramen magnum as seen in Arnold-Chiari malformations. An abdominal or a head CT or MRI should be done to look for neuroblastoma in the adrenal glands or brain in a patient with opsoclonus. Abdominal ultrasound or CT is needed to evaluate the kidneys in aniridia, for which a significant incidence of Wilm’s tumor is seen.
References
1. Friedberg MA, Rapuano CJ. Wills Eye Hospital office and emergency room diagnosis and treatment of eye disease. Philadelphia: JB Lippincott, 1990:268–271.
2. Bajandas FJ, Kline LB. Neuro-ophthalmology review manual. Thorofare, NJ: Slack Inc., 1988:67–75.
3. Vaughn D, Asbury T, Tabbara KF. General ophthalmology. Norwalk: Appleton & Lange, 1989:270–272.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Eye Pain:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
A foreign body sensation occurs with a foreign body, corneal abrasion, or keratoconjunctivitis sicca. Itching is associated with allergic and vernal conjunctivitis. Photophobia occurs with iritis and herpes simplex keratitis. Deep pain suggests acute glaucoma or posterior scleritis. Pain on eye movement is found with optic neuritis, sinusitis, and influenza.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Diplopia/Nystagmus:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
The direction of gaze with the most prominent diplopia reflects the action of the paretic muscle. Binocular diplopia is due to ocular misalignment, and the patient will usually close one eye to compensate. Acute monocular diplopia can occur with corneal aberrations, cataract, or foveal traction.
CN III paresis: The lateral rectus and superior oblique are unopposed, turning the eye outward and downward. An acute lesion may be peripheral (diabetic or ischemic) or central (posterior communicating artery aneurysm or
cavernous sinus lesion). Both have ptosis, absent eye elevation, and adduction, but a peripheral lesion has normal pupil size and movement (“pupillary sparing”). A central lesion produces a pupil that is dilated and unresponsive to light or accomodation. Causes include tumor, aneurysm, or severe trauma. Unilateral third nerve palsy with contralateral superior rectus palsy and bilateral partial ptosis, and bilateral third nerve palsy always represents a central lesion. Unilateral external ophthalmoplegia with normal contralateral superior rectus function, unilateral internal ophthalmoplegia, and unilateral ptosis represents a peripheral lesion.
CN IV paresis: Superior oblique weakness produces vertical diplopia. The patient tilts his or her head to the opposite side to lessen the displacement. Typical causes are a relatively minor head blow, and idiopathic.
CN VI paresis: Lateral rectus palsy produces weakness in abduction and horizontal diplopia that is better in near than in distant vision. When CN V is also affected (reduced facial sensation around the upper face and cornea), a cavernous sinus lesion should be suspected. Papilledema should also be looked for, as it indicates a mass lesion displacing the brainstem.
If the patient has an isolated lesion of one of the cranial nerves, pain will be localized to just above the eyebrow on the weak side. Intraorbital pathology is indicated by pain in the eye itself or on eye movement. The worst headache of the patient’s life raises concern for intracranial aneurysm.
True nystagmus is characterized by rapid regular oscillations around a fixed point not just with lateral gaze but also when the eyes are looking forward. A few beats of nystagmus at extremes of gaze are not pathologic. Nystagmus of ocular causes has a pendular motion whereas disease in the central nervous system produces fast and slow components. Irregular bursts of rapid eye movements (saccadic intrusions) almost always indicate a cerebellar lesion.
Internuclear ophthalmoplegia occurs when the oculomotor and abducens nerves (CN III and VI) are disconnected at the medial longitudinal fasciculus. When conjugate gaze is attempted, one eye will not adduct medially and the abducting eye (lateral gaze) will show nystagmus. This finding is seen in persons with multiple sclerosis and pontine vascular lesions.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Involuntary Weight Loss:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Cachexia is accelerated loss of lean body mass in the context of a chronic inflammatory response, caused by a combination of decreased intake (with decreased appetite) and increased metabolic rate. The cause of the weight loss will usually be evident, based on concurrent symptoms. If not, first document that weight loss has occurred by using prior records of measured weights or the discovery of loose-fitting clothes (tightening belt notches) or dentures. If the cause is not found on the first pass, document the weight and re-examine several weeks later.
Weight loss in patients with congestive heart failure, cirrhosis, and
uremia may be masked by fluid retention, but temporalis and limb wasting will be prominent. Weight loss in malignancy of more than 5% of body mass prior to treatment portends a poor prognosis.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Eye pain:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
During the physical examination, don’t manipulate the eye if you suspect trauma. Carefully assess the lids and conjunctivae for redness, inflammation, and swelling. Then examine the eyes for ptosis or exophthalmos. Finally, test visual acuity with and without correction, and assess extraocular movements. Characterize any discharge. (See Examining the external eye, page 272.)
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Ocular deviation:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Perform a complete neurologic assessment, including a complete eye assessment. During the physical assessment, 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 visual acuity; then evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing the six cardinal positions of gaze.)
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Nystagmus:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Begin the physical assessment by evaluating the patient’s level of consciousness (LOC) and vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary changes, drowsiness, elevated systolic pressure, and altered respiratory pattern. Next, assess nystagmus fully by testing extraocular muscle function: Ask the patient to focus straight ahead and then to follow your finger up, down, and in an “X” across his face. Note when nystagmus occurs as well as its velocity and direction. Finally, test reflexes, motor and sensory function, and the cranial nerves.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Nystagmus:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Nystagmuscan usually be detected by simple observation, and type, direction,amplitude, frequency, and gaze should be determined.Whether nystagmus is physiologic orpathologic can usually be determined by history and physical exam.Careful eye exam can diagnose eye disordersassociated with nystagmus. If results of eye exam are normal, aneurologic disorder including a vestibular disturbance should beinvestigated.Association of nystagmus with hearingloss and vertigo suggests disturbance of peripheral vestibular system.Nystagmus associated with ataxia withouttinnitus and hearing loss suggests disturbance in brainstem or cerebellarfunction.CT and MRI are useful in diagnosisof neurologic disorders that may be associated with nystagmus.When considering causes of gaze-evokednystagmus, positive drug history may be diagnostic.Idiopathic congenital nystagmus isdiagnosis of exclusion.
» READ BOOK EXCERPT ONLINE »
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Involuntary Movements:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Movementdisorders generally must be identified by clinical features, incontext of history, family history, and careful physical exam. Oncespecific type of movement is recognized, specific cause should beinvestigated.In absence of any associated neurologicdeficits, neuroimaging and electroencephalography are not routinelyuseful for childhood-onset movement disorders.
» READ BOOK EXCERPT ONLINE »
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Ocular deviation:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
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.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Nystagmus:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Begin by asking the patient how long he has had nystagmus. Does it occur intermittently? Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract, and about head trauma and cancer. Does the patient or anyone in his family have a history of stroke? Then explore associated signs and symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness, bladder dysfunction, and fever.
Begin the physical examination by assessing the patient's level of consciousness (LOC) and vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary changes, drowsiness, elevated systolic pressure, and an altered respiratory pattern. Next, assess nystagmus fully by testing extraocular muscle function: Ask the patient to focus straight ahead and then to follow your finger up, down, and in an “X” across his face. Note when nystagmus occurs as well as its velocity and direction. Finally, test reflexes, motor and sensory function, and the cranial nerves.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Eye pain [Ophthalmalgia]:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient's eye pain doesn't result from a chemical burn, take a complete history. Have the patient describe the pain fully. Is it an ache or a sharp pain? How long does it last? Is it accompanied by burning, itching, or discharge? Find out when it began. Is it worse in the morning or late in the evening? Ask about recent trauma or surgery, especially if the patient complains of sudden, severe pain. Does the patient wear contact lenses? How often are they removed or replaced if they're disposable? Does he have headaches? If so, find out how often and at what time of day they occur.
During the physical examination, don'tmanipulate the eye if you suspect trauma. Carefully assess the lids and conjunctiva for redness, inflammation, and swelling. Then examine the eyes for ptosis or exophthalmos. Finally, test visual acuity with and without correction, and assess extraocular movements. Characterize any discharge. (See Examining the external eye.)
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
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