Neuro-Ophthalmologic Emergencies

Educational Objectives

The goal of this program is to improve the awareness of current practice for diagnosis and management of neuro-ophthalmologic emergencies. After hearing and assimilating this program, the clinician will be better able to:

1. Identify the non-vascular causes of visual loss.
2. Describe the categories of vascular causes of visual loss.
3. Recognize the clinical and pathophysiological phenomenology of pituitary apoplexy.
4. Understand the important elements of history and diagnostic work-up.

Summary

Non-vascular causes of visual loss: if visual loss is only for seconds, it is likely not vascular; for example, if a blur improves with blinking, likely a surface disease such as dry eye; if vision grays or blacks out, consider transient visual obscurations such as papilledema; papilledema can be unilateral and asymmetric; consider increased intracranial pressure with bilateral or unilateral transient visual obscurations; if visual loss is long, lasting 20-40 minutes, or up to 60 minutes, consider migraine; positive signs for migraine include classic symptoms such as zig-zag lines that sparkle and shimmer, or wavy lines or sparkles; migraine symptoms should be a binocular phenomenon, although this is sometimes difficult to determine

Vascular causes of vision loss: typically considered if visual loss does not above demonstrate characteristics of unusually short or long length

Amaurosis fugax: defined as visual loss lasting several minutes, though can last up to 24 hours; should be monocular

Differential versus cerebral stroke or transient ischemic attack (TIA): amaurosis fugax demonstrates more migraine-related mechanisms as compared to symptoms of cardiac emboli — important differentiating factor; amaurosis fugax has a younger age distribution than cerebral stroke — affects more people under age 65; if both sets of patients are examined, those with amaurosis fugax are more likely to have carotid stenosis than those with cerebral TIA, but less likely to have a cardiac source; atrial fibrillation is 25 times less common in amaurosis fugax than cerebral TIA; patients with amaurosis fugax are more likely to have visual episodes on a recurrent basis and 50% less likely to have a cerebral stroke (Oscar Benevente’s data); both diseases are the same in the rate of death and heart attack; so, if amaurosis fugax carries lower stroke risk, is carotid endarterectomy indicated? note that amaurosis fugax patients also have 50% lower perioperative risk of stroke; patients with amaurosis fugax have better prognosis, are typically younger and therefore with less carotid disease, more migraine-related issues

Management: old age, male, a history of stroke, claudication, or stenosis >80%, or three or more episodes warrants a carotid endarterectomy; decision is more complex in younger patients — must do a careful review of the history for young stroke factors — presence of cardiac disease, hypercoagulability, vasculitis, dissection, or drug use; then evaluate to determine if there is a presence of other manifestations of migraine

Central retinal artery occlusion: presents as visual loss that does not resolve; central retinal artery comes out of the optic disk, spreads out over the retina and supplies the inner neural elements of the retina (not the photoreceptors or the choroid); central retinal artery occlusion generally presents with painless visual loss — patient may or may not have a history of preceding amaurosis fugax; more important is history of giant cell temporal arteritis; if examined within 7 days of onset, an ischemic retina should be present; ischemic retina — pale and fuzzy, details are blurry; may be gray or yellow, and the middle should show a cherry red spot — this is shine-through of the choroid circulation at the fovea, because there is diminished inner retina at that spot; if no red spot is seen, may mean the choroid circulation has also been compromised, which is a sign of an ophthalmic artery occlusion further behind, which gives rise to both the choroid and the central retinal artery; emboli may be seen, especially with a partial artery occlusion such as a branch retinal artery occlusion; may not be evident because occlusion may be behind the dural sheath; if occlusion not observed within 7 days, then ischemia will drain and clear out; cherry red spot no longer visible, but optic atrophy will be present, and arterioles will be attenuated because of limited living retina; 15-50% of patients may have a cilioretinal artery; when examining the optic disk on fundoscopy, may visualize a vessel in a fish hook shape coming from the edge of the optic disk and around toward the macular fovea area; this vessel is a posterior ciliary artery coming from the choroidal circulation, not the central retinal artery; if this vessel supplies part of the macular bundle, it will not be affected in a central retinal artery occlusion and macular function will be preserved

Risk factors and diagnosis: similar risk factors to stroke — hypertension, diabetes, hyperlipidemia, previous stroke, heart attack, smoking, family history of vascular disease; if the patient is young, consider young stroke risk factors, look at C-reactive protein (CRP) and platelet count, which may suggest giant cell arteritis; two-thirds of patients will have an undiagnosed component of a metabolic syndrome — hypertension, diabetes or hyperlipidemia; need to obtain imaging to examine the carotids, and obtain an echocardiogram

Treatment: in the acute stage, goal is to get back lost vision; standard treatments include nitrates to increase blood flow, hyperbaric oxygen to improve oxygenation, ocular massage to try to move the clot, anterior chamber paracentesis to reduce intraocular pressure, acetazolamide, and steroids; limited evidence that any of the above treatments are more effective than placebo; new data suggests that intraarterial or intravenous tPA (tissue plasminogen activator) may be effective; studies are complicated, because they include long time windows of up to 24 hours, whereas studies done in monkeys show that treatment within 100 minutes is needed for full recovery; ischemia lasting >4 hours typically does not see any recovery; tPA studies suggest that there may be some meaningful benefit (more than 3 lines of acuity in recovery) if tPA is administered within 6 hours; consider using stroke protocols — if the patient comes in within the window for stroke with a central retinal artery occlusion, manage similarly to stroke

Follow up: after initial treatment is complete, must consider short and long term management; in the subacute stage, neovascularization from ocular ischemia can occur, which can lead to severe glaucoma; patients need to be monitored by an ophthalmologist for the first 4 months; over the long term, must manage vascular risk factors for stroke and MI prevention and even consider carotid endarterectomy

Central retinal vein occlusion: typically managed by a retina expert — important to diagnose and arrange referral for treatment; this also presents with painless visual loss, but without associated amaurosis fugax; on examination, patient may have decreased acuity or variable degrees of field loss; key differentiating sign is blood everywhere in the back of the eye; blood and fluid have leaked; typically leak will be along the veins with flame and blotch hemorrhages; may demonstrate a slightly swollen disk and macular edema

Differential diagnosis and risk factors: if symptoms are seen in one eye, consider central retinal vein occlusion; if presentation is in both eyes, consider hypertensive retinopathy; blood in one eye with a central retinal vein occlusion will typically be diffuse, but can be segmental due to a branch retinal vein occlusion, which is more common than a central occlusion; risk factors include hypertension, diabetes, hyperlipidemia, hyperviscosity; in young patients, consider inflammatory disorders like Behçet’s and other vasculitis, hypercoagulability, and ocular disease (patients with glaucoma are at higher risk)

Pathophysiology: thrombosis in the vein increases venous pressure in the eye; leads to increased vascular permeability and an increase in vascular endothelial growth factor (VEGF); result is macular edema, which is why acuity decreases; patients then develop ischemia and neovascularization which can lead to neovascular glaucoma

Treatment: typically managed by a retina specialist; standard treatment typically used to include laser photocoagulation; newer therapy includes intraocular injections of steroids or intraocular injections of anti-VEGF antibodies; metareviews have shown these are equally effective, although steroids may have more adverse effects

Anterior ischemic optic neuropathy: classic presentation: patient wakes up in the morning and finds they have lost vision in one eye, it is painless; in the ER, examination shows no cherry red spot, no retinal hemorrhages; the retina appears normal, but the disk is swollen; fields of vision are impaired and acuity may or may not be decreased, depending on whether the macular region is involved; this suggests a diagnosis of anterior ischemic optic neuropathy; anterior because the optic disk is swollen; over the first 2 months, as the disk edema resolves, about 20-40% of patients will show some modest improvement in either acuity or fields of vision

Management: initial therapy appears to be mostly ineffective; treatments tried have included aspirin, heparin, steroids, and phenytoin; optic nerve sheath fenestration appears to make the situation worse; steroids have some data supporting use, but only from one large, retrospective, nonrandomized, observational study that has not been duplicated; main goal of management is to prevent either another episode of visual loss or some other ischemic deficit in the brain or heart

Importance of distinguishing giant cell arteritis from non-arteritis in anterior ischemic optic neuropathy: must consider whether initial presentation is consistent with giant cell arteritis, which is 7 times less common than non-arteritic form; if non-arteritic, median time for involvement of the second eye is 7 years; with arteritis, median time is 2 weeks; (reminder: central retinal artery occlusion can also be secondary to giant cell arteritis)

Age of patient: if patient is <50 years old, not likely to be arteritis; between the ages of 55-59, there is a 2:10,000 chance of having giant cell arteritis, whereas the prevalence I patients >85 years old is 1:100

Signs and symptoms: classic systemic features indicating arteritis include jaw claudication (or even trismus) or temporal artery pain with tenderness on exam; other symptoms may include the presence of headache, scalp tenderness, weight loss, myalgias, or a history of polymyalgia rheumatica; ophthalmic features suggesting giant cell arteritis versus non-arteritis include a history of amaurosis fugax or presence of severe vision loss; when examining the fundus, the appearance of a chalky white disk suggests giant cell arteritis; fluorescein angiogram showing that the choroid is not filling would also suggest an occlusive problem, which is the mechanism in giant cell arteritis, rather than a watershed pathology

Laboratory tests: most useful positive results are an erythrocyte sedimentation rate (ESR) >100 mm/h or platelets >400,000; a CRP <2.45 mg/L or platelets <400,000 would indicate a low likelihood of giant cell arteritis

Biopsy of temporal artery: gold standard for diagnosis, but is not completely accurate; sensitivity of the biopsy is about 86%, meaning 14% of patients will have a negative first biopsy; consider a biopsy of the other side if suspicion is high; biopsy may be negative due to multiple factors; specimen may have been too small — at least 1-2 cm of artery is needed, because involvement can be patchy; another cause of negative biopsy is steroid treatment; steroids should be started immediately for suspicion of giant cell arteritis, ie, likely before the biopsy; most data, however, suggests that the pathology may be unaffected by duration of steroid treatment of up to one month

Treatment: for giant cell arteritis, patients should be started immediately on steroids; either 80-100 mg of prednisone orally or intravenous methylprednisolone; no strong evidence favoring use of IV over oral prednisone

Posterior ischemic optic neuropathy: similar to anterior ischemic optic neuropathy, but no visible disk swelling; consider two potential causes, giant cell arteritis or shock; for example, recent cardiac surgery or lumbar spine surgery are situations in which the patient may wake up exhibiting these symptoms; also could occur with hypotension and sepsis; if the patient does not have either giant cell arteritis or a blood pressure-related perfusion issue, consider other diagnoses, such as optic neuritis, which would cause pain with eye movement, or a tumor of the optic nerve; if the eye appears atrophic, probably not sudden onset visual loss but rather suddenly noticed visual loss

Pupils: most important thing to recognize when evaluating the pupil is that it is a muscle; if trying to identify a weakness, make the muscle work; with the pupils, to make the constrictors work, turn the lights on; to make the dilators work, examine pupils in the dark; if a patient exhibits anisocoria that is more obvious in the dark, this indicates that the smaller pupil is the abnormal one; the pupil is not dilating, which could be a sign of Horner syndrome; if the anisocoria is worse in bright light, then the constrictors are not working, so consider the parasympathetic pathway

Horner syndrome: many diseases may cause Horner syndrome, including lung cancer, cervical myelopathy, neuroblastoma in children; most often in emergency room cause is vascular; likely either carotid dissection or vertebral dissection; carotid dissection now usually treated with aspirin; Horner’s syndrome not likely to be an isolated sign in a vertebral dissection but part of a lateral medullary syndrome; look for other signs of lateral medullary syndrome; if pathology is not clear, can obtain an MRI and MR angiogram from the aortic arch to the circle of Willis to differentiate from other conditions

Enlarged pupils: warning signs of increased intracranial pressure, which may lead to a “blown” pupil, include a patient who is drowsy, may have focal neurologic defects; the back of the eye may exhibit papilledema; should also consider other causes of an enlarged pupil, such as whether the muscle could be affected, known as traumatic mydriasis; if the pupil sphincter has been damaged or torn, the pupil will become enlarged, and will have an irregular shape; will be history of trauma to eye; conditions affecting the synapse between the nerve and the muscle may also lead to an enlarged pupil; major consideration should be pharmacologic causes; a sympathetic stimulator, such as adrenaline or phenylephrine, or a glaucoma drop like brimonidine can cause an enlarged pupil, although will generally not cause a very large pupil; for really large pupil will need parasympathetic blockade with atropine or atropine-like drug; scopolamine patch can cause enlarged pupil; diagnosis can be made by instilling 2-4% pilocarpine drops in the eye — if no constriction occurs, this confirms the diagnosis; consider botulism if the patient presents with ocular myasthenia and enlarged pupils on both sides

Adie’s pupil: benign condition with an enlarged pupil in the acute phase, may exhibit a small pupil in the chronic phase; Adie’s pupil is a ciliary ganglionitis and may be part of a more widespread subtle peripheral neuropathy (check for absent ankle jerks), or could be part of ciliary ganglion damage from eye surgery; in the acute phase, it may be difficult to determine definitive features because these neurogenic changes take time to develop; three important neurogenic changes are light-near dissociation, which requires reinnervation; segmental constriction where some parts of the pupil constrict and others do not, also related to reinnervation; and supersensitivity, where extremely low doses of pilocarpine, eg, 0.1% (too low to affect normal eye, so test both eyes), will constrict the denervated eye; these issues take a few weeks to develop

Third nerve palsy: in addition to an enlarged pupil, these patients demonstrate ptosis, have difficulty moving the eye up, down, or in; a unilateral dilated pupil in drowsy patient could indicate impending uncal herniation and death; this could be caused by head trauma or mass lesion like blood or tumor in head; other signs could include focal neurologic deficits and papilledema; unilateral dilated pupil could be caused by compression of third nerve by uncus; bilateral fixed and dilated pupils could be a sign of hemorrhage into the midbrain that affects the third nerve structures before they leave the midbrain; a lesser-known sign of uncal herniation may be hemianopia from compression of the posterior cerebral artery, hard to assess in drowsy or comatose patient; important to remember to also look for other signs of herniation such as posturing, bradycardia, hypertension, or respiratory depression

Oculomotor conditions:

Painful third nerve palsy: primary concern with a painful third nerve palsy is for an aneurysm; aneurysm may rupture within 1-2 weeks and cause death; important to differentiate between aneurysm and a more benign microvascular palsy, which will resolve in 12-14 weeks; aneurysmal third nerve palsy mainly occurs in adults; approximately 1 in 6 adult third nerve palsies will be associated with an aneurysm; in children only occurs in approximately 2% of patients; both ischemic and aneurysmal palsies will have pain, but in an ischemic palsy, the pain typically diminishes in 7-10 days; “pupil rule” — complete pupil sparing in an otherwise complete third nerve palsy indicates absence of posterior communicating artery (PCOM) aneurysm; note that partial pupil sparing and partial extraocular muscle involvement do not count for this rule; aneurysms of concern are those at the junction of the internal carotid (ICA) and the posterior communicating artery (PCOM), the ICA-PCOM aneurysm; with this type of aneurysm, the dorsal and medial surfaces of the nerve are compressed, which is where the pupil fibers run; an aneurysm in a different location, such as a basilar tip aneurysm, might have a different relationship to the nerve and may produce pupil-sparing third nerve palsy

Partial pupil sparing: should be evaluated for potential aneurysm; obtain a CT angiogram — better than MR angiogram because it can detect aneurysms as small as 2 mm; typically, an aneurysm will need to be at least that size to compress the third nerve; may rarely consider a conventional angiogram if the CT angiogram is normal and there is still reason for suspicion; also consider other signs suggesting compression by an aneurysm or a mass; first, aberrant regeneration, if patient tries, eg, to adduct eye, but eye goes up instead, or pupil constricts, or lid lowers, ie, some other part of the third nerve is activated, this is sign of compression until proven otherwise; second is if other nerves are involved, such as the sixth or fourth nerve, in addition to the third nerve, consider a mass; third sign of compression is divisional palsy; the superior division of the third nerve supplies the levator and the superior rectus (moving the eye or the lid up), and the inferior division supplies everything else — if divisional signs are present, consider cavernous sinus mass

Fourth nerve palsy: majority of these are benign; if it is symptomatic, almost always there is something atypical involved, such as pain, partial ptosis, or third nerve involvement; an isolated fourth nerve palsy is probably not a cause for concern

Sixth nerve palsy: can have significant consequences; key is to consider possibility of a false localizing sign; look for a sixth nerve palsy with increased intracranial pressure, decreased intracranial pressure, abnormal CSF, or something in the skull base; it is typically similar to fourth nerve; isolated sixth nerve palsy with nothing else affected has a lower incidence of serious disease; but, must assess for long-tract signs, check neighboring cranial nerves, look for partial numbness of face (numbness in any division of trigeminal nerve suggests skull-base problem); in summary, look carefully for signs of larger problem than sixth nerve palsy and image accordingly

Sella-related disorders: may be neuro-ophthalmologic emergency

Cavernous sinus fistula: arterial-to-venous shunting problem; artery involved could be the carotid or a meningeal artery, venous structure involved is the cavernous sinus; if the carotid is the origin of the shunt, results in a high-flow situation; major volume of blood is being dumped at high pressure into a low-pressure venous sinus, resulting in a high-flow fistula; typically caused by either head trauma causing rupture of the carotid in the cavernous sinus, or rupture of a giant carotid aneurysm in the cavernous sinus; meningeal branches are much smaller, which will create a low-flow fistula; could occur with trauma, but can also occur spontaneously and is more common in the elderly

High-flow fistula: symptoms are typically obvious; patient may come in with severe pain; eye will be red and bulging, possibly pulsatile, and all the orbital tissues will be severely swollen; visual loss may also be present; may hear a bruit; because the cavernous sinuses are connected, this high pressure may also be transmitted to the other side, resulting in bilateral signs; most important risk with a high-flow fistula is death; death may be due to a hemorrhage intracranially and subarachnoid, or from a bleed into the nose or ear causing exsanguination; death can occur in up to one-third of patients within the first week

Low-flow fistula: not as severe as high-flow fistula; patients present more subtly; patients typically have about 2-3 weeks of some ache or pain in the eye; the eye will be red and condition may be mistaken for conjunctivitis or pink eye; on exam, on looking carefully, may notice a little proptosis; intraocular pressure will be elevated; over time, cranial neuropathies may develop; typically affects cranial nerves six or three, possibly a Horner syndrome, but that may not be present initially; not a life-threatening problem similar to a high-flow fistula, but is a situation with potential for vision loss from secondary glaucoma

Treatment: for a high-flow fistula, typically managed with balloon embolization, or even tying off the carotid artery to defer the bleeding; get neuroradiologist and neurosurgeon involved right away; low-flow fistula has several management options; these can spontaneously resolve in about 10-60% of patients, so one option is to do nothing; obtaining an angiogram to try to confirm the diagnosis is sometimes in itself curative; could consider trying to embolize with glue or particles; radiotherapy is another option, but may have long-term side effects such as accelerated atherosclerosis in the carotid, optic neuropathy, maybe even cerebral necrosis or hypothalamic dysfunction; also will need to arrange for follow up with ophthalmologist for glaucoma monitoring; fistula-related glaucoma often does not respond to drops, so surgical procedure may be needed

Cavernous sinus thrombosis: patient will typically present with headache; headache will often be periorbital with facial pain and will last for several days; patient will then begin to notice orbital swelling, which after several days can affect both eyes; double vision can develop; on examination, patients may have third, fourth, or sixth nerve involvement as well as facial numbness in the V1 or V2 distribution; patients may start to notice visual loss in one eye, due to optic nerve involvement; at this point, called supraorbital fissure syndrome; after more time patients can develop altered mental status as well as, fever, proptosis, chemosis, ptosis, and extraocular motility defects; the back of the eye may demonstrate a swollen disk and dilated retinal veins

Causes: may be caused by facial infections in the central part of the face around the eye and the nose, because these drain to the cavernous sinus; most commonly see small nasal furuncles; may also be caused by sinusitis from the ethmoid or the sphenoids, which are very close to the cavernous sinus; may rarely be related to dental work; 70% of the time staph organisms are involved; could be strep or anaerobes, especially if sinusitis or a dental procedure is involved; if the patient is immunosuppressed (eg, HIV infection, idiopathic CD4 lymphopenia, on chemotherapy), consider mucormycosis or aspergillus

Diagnosis and treatment: tests for diagnosis include MRI or CT with venogram; lumbar puncture with cultures may also be helpful — may mimic meningitis or parameningeal focus; treatment will include antibiotics, most likely vancomycin or ceftriaxone; will need course of about 3 weeks; addition of anticoagulants or steroids might improve the recovery of any neuropathy that is present; if the patient has sphenoid sinusitis, can consider asking an ENT surgeon to drain the sinus; mortality is down from about 70% to 30% if the patient is treated promptly with antibiotics, but about half of the survivors will have some sort of residual cranial neuropathy

Pituitary apoplexy: if the patient has a known pituitary tumor, diagnosis is simple; however, approximately 4 out of every 5 patients present with apoplexy as the initial presentation of the tumor; patients typically present with sudden severe headache, vomiting, and perhaps fever, which can mimic other diseases such as subarachnoid hemorrhage or meningitis; pituitary adenomas are 5 times more likely that any other kind of brain tumor to bleed; no clear reason for this; some suggest that the blood supply is rather fragile and tenuous in the parasellar area; apoplexy can develop in other tumor types, such as meningiomas, but is unusual; rarely, apoplexy can develop in a non-tumorous pituitary, such as Sheehan syndrome in the postpartum state

Symptoms: other symptoms may be present in addition to bad headache, vomiting, and fever; if pituitary tumor expands upwards, it can affect the optic apparatus; this could affect the optic nerve intracranially, the optic chiasm or the optic tract, which can lead to monocular visual loss, a bi-temporal hemianopia, or a homonymous hemianopia; up to about 50% of people with apoplexy will have some sort of visual deficit; if the tumor expands sideways, it will impact the structures in the cavernous sinus region, which will cause double vision; this will be a third nerve palsy, a sixth nerve palsy, or a combination of both; if the tumor expands backwards, it may affect the hypothalamus and the midbrain, which will lead to fever and altered consciousness; it may even break into the subarachnoid space, which would lead to a subarachnoid hemorrhage; if the tumor expands downwards into the sphenoid sinus, the patient may present with epistaxis; this may cause a fatal nosebleed that will not stop when the front of the nose is packed, because the bleeding is at the back

Risk factors and diagnosis: with a pituitary tumor, some of the provoking factors may be major surgery with hypotension and blood loss; anticoagulation, including aspirin, is another risk factor; lumbar puncture spinal anesthesia can also provoke apoplexy; a patient with a known pituitary tumor on hormonal treatment is another risk factor; for example if the patient is taking bromocriptine to treat a prolactinoma, and they suddenly stop the medication, that is a risk situation for pituitary apoplexy; these patients will have an elevated white blood count, may have hyponatremia, will not often be symptomatic from hormonal deficiency yet, but pituitary hormone levels will often demonstrate some sort of deficiency; major concern is for acute Addisonian crisis, which may be fatal; consider in presence of hypotension with severe headache; because this mimics subarachnoid hemorrhage and meningitis, many of these patients have imaging done, which shows a pituitary mass; then need to make the connection that maybe that mass is the problem, not meningitis or subarachnoid hemorrhage; a CT scan with axial cuts only may not pick up a pituitary tumor; often more apparent on coronal images, which should always be obtained; mass can be seen on CT in about 75% of patients; signs of apoplexy may not be obvious in the CT scan, are only visible in about 25% of cases; best way to see the apoplectic signs of hemorrhage or necrosis is with MRI, which is positive in 90% of cases

Treatment: first must manage adrenal insufficiency and volume problems, which are the main sources of mortality and morbidity; this includes steroid replacement and fluid management; if there is severe visual loss or life-threatening complications, then consider surgery; if the patient is stable and has only minor visual signs, then the benefits of surgery are far less clear; spontaneous improvement of the neurologic deficits can occur after several weeks, so some suggest that the most common-sense way to approach this condition is to observe the patient carefully in the hospital; if neurologic deficits fail to improve or are getting worse over several days, then consider surgery

Readings

Brune AJ, Gold DR: Acute visual disorders — what should the neurologist know? Semin Neurol 2019 Feb;39(1):53-60; Pyrgelis ES, Mavridis I, Meliou M: Presenting symptoms of pituitary apoplexy. J Neurol Surg A Cent Eur Neurosurg 2018 Jan;79(1):52-59.

Disclosures

For this activity, the faculty and planning committee reported nothing to disclose.

Acknowledgements

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

NEBR190107

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.