Differential Diagnosis
Symptoms
Typical initial complaints are blurry vision, visual loss, and
sometimes complete blindness. In ION and retinal arterial occlusion (RAO), visual
loss is acute and painless. ION may be manifested as complete or partial loss of
light perception. A visual field deficit, sometimes with central visual field loss,
is present in ION or RAO. Retrobulbar hemorrhage and narrow-angle glaucoma, in contrast,
produce intense pain in the periorbital region.
One of the difficulties in diagnosing these conditions perioperatively
is that the symptoms can be subtle and are often unfamiliar to most anesthesiologists
and surgeons. The visual loss in all these conditions is frequently but not always
recognized within the first postoperative day and may be present when the patient
awakens from the anesthetic. However, with ION, the onset of ON edema may be slow,
and symptoms may not appear for several days. The diagnosis may sometimes be delayed
because of slow awakening from anesthesia and could be completely missed in a sedated,
mechanically ventilated patient. Visual symptoms could be misdiagnosed as delirium
on awakening from anesthesia, whereas blurry vision may be attributed to the anesthetics
or to the use of ointments in the eye. Focal neurologic complaints such as unilateral
weakness suggest a concomitant stroke, a frequent feature with cortical blindness.
Complete or incomplete cortical blindness is visual impairment
caused by damage to the visual pathway beyond the LGN or the visual cortex in the
occipital lobe. The optic disk and pupillary responses are normal, but patients
do not react to visual threat, or they show loss of optokinetic nystagmus with normal
eye motility.
Eye Examination
Ophthalmologic consultation is indicated for patients complaining
of postoperative visual loss or blurry vision. The initial evaluation includes examination
of pupil reactivity, ophthalmoscopy, and assessment of accommodation reflexes, IOP,
eye movement, and visual fields. Specialized studies include formal visual field
testing, fluorescein angiography, electroretinography (ERG), visual evoked potentials
(VEPs), computed tomography (CT), and magnetic resonance imaging (MRI). A detailed
neurologic examination is indicated if a cerebral cortical cause for the visual loss
is suspected or to rule it out.
Table 82-1
reviews findings on eye examination. An impaired direct pupillary
light reflex indicates an ipsilateral ON lesion. An afferent pupillary
defect may be seen in ION or RAO. A preserved consensual light
reflex indicates that the optic chiasm and the pretectal region are intact.
Impaired accommodation and fixation
reflexes indicate loss of the connection between the visual cortex, pretectal
region, and superior colliculus. Absence of optokinetic nystagmus and indifference
to visual threat indicate cortical damage. In cortical blindness, pupillary reflexes
and visual fields are preserved, but spatial perception and the sense of relationship
between sizes and distances are impaired. Restricted visual attention and an inability
to notice images formed on all parts of the retina at one time are also features.
Denial sometimes accompanies cortical blindness.
Pupil signs in the postoperative period are easily overlooked
or misdiagnosed, particularly after narcotic-based anesthetic techniques or with
the use of postoperative, parenterally administered analgesia. However, a unilateral
pupillary defect in a patient complaining of visual loss should trigger further evaluation.
Central (CRAO) or branch retinal artery occlusion (BRAO) may be
accompanied by extraocular muscle dysfunction (i.e., impaired eye movements). Facial
or periorbital edema may be present in patients with associated venous obstruction.
Ophthalmoscopy is critical in the differential diagnosis. In
patients with cortical damage, ophthalmoscopic findings
TABLE 82-1 -- Differential diagnosis: eye examination in retinal, optic nerve, or visual
cortex injury
|
AION |
PION |
Cortical Blindness |
CRAO |
BRAO |
|
Optic disk |
Pale swelling, peripapillary flame-shaped hemorrhages, edema
of ON head |
Normal (initially) |
Normal |
Normal |
Normal |
|
Retina |
Normal; attenuated arterioles, usually later |
Normal, attenuated arterioles later |
Normal |
Cherry-red macula,
*
pallor and edema, narrowed retinal arteries |
Emboli may be seen
†
partial retinal
whitening and edema |
|
Light reflex |
Absent or RAPD |
Absent or RAPD |
Normal |
Absent or RAPD |
Normal or RAPD |
|
Fixation and accommodation reflexes |
Normal |
Normal |
Impaired |
Normal |
Normal |
|
Response to visual threat |
Yes |
Yes |
No response |
Yes |
Yes |
|
Opticokinetic nystagmus |
Normal |
Normal |
Absent |
Normal |
Normal |
|
Tracking objects |
Normal |
Normal |
Absent |
Normal |
Normal |
|
Ocular muscle function |
Normal |
Normal |
Normal |
Sometimes impaired |
Normal |
|
Perimetry (gross) |
Altitudinal defect |
Altitudinal defect or blind eye |
Often hemianopia (depends on anatomy of lesion); periphery usually
affected |
Affected eye blind |
Scotoma; peripheral vision usually intact |
|
AION, anterior ischemic optic neuropathy; BRAO, branch retinal
arterial occlusion; CRAO, central retinal arterial occlusion; PION, posterior ischemic
optic neuropathy; RAPD, relative afferent pupillary defect. |
*Because
of a lack of overlying inner retinal cells in the fovea, the intact choroidal circulation
is visible as a cherry-red spot.
†Cholesterol,
platelet-fibrin emboli, calcified atheromatous material.
are normal; in RAO patients, characteristic temporal changes can be seen. Early
in the course of ischemia, opacification or whitening of the ischemic retina and
narrowing of retinal arterioles may be visible.[14]
[51]
BRAO is characterized by the findings of bright
yellowish, glistening cholesterol emboli, calcific (white, nonglistening), or migrant
pale emboli of platelet fibrin (dull, dirty white). A cherry-red macula with a white
ground-glass appearance of the retina and attenuated arterioles is a "classic" diagnostic
sign in CRAO with a preserved choriocapillaris ( Fig.
82-7
). The red appearance is due to pallor in the ischemic, overlying
retina, which allows the color of the intact, underlying choroidal circulation to
become visible.
In ION, the retina is normal, with no cherry-red spot. In the
acute stages, anterior ION (AION) is typically accompanied by pale swelling of the
optic disk and flame-shaped peripapillary hemorrhages. The disk is normal in posterior
ION (PION) because the pathology is retrolaminar and not accessible to external examination.
Later, optic atrophy appears in both AION and PION as the retinal ganglion cells
and axons die ( Fig. 82-8
);
these changes may include only a section of the optic nerve and disk.[14]
