Anterior Ischemic Optic Neuropathy Discharge Summary Sample



1.  Anterior ischemic optic neuropathy.
2.  Left cavernous internal carotid artery aneurysm and left anterior coronary artery aneurysm.

CONSULTATIONS:  Ophthalmology.

1.  MRI of the brain with and without contrast and diffusion as well as MRI of the orbits with and without contrast.
2.  MRA of the head and neck.
3.  Transthoracic echocardiogram with bubble study.
4.  Four-vessel cerebral angiogram.
5.  CT without contrast of the abdomen and pelvis.

HOSPITAL COURSE:  This is a (XX)-year-old female who presented with a chief complaint of decreased visual acuity for one week. The patient reportedly saw a neurologist who did an MRA of the brain and LP. By verbal report, the MRI showed white matter disease, and the results of the LP were unknown at the time the patient was initially evaluated.

The patient was also started on Plavix by Dr. John Doe at that time. The patient was noted to have an inferior altitudinal field defect in her left eye as well as a scotoma. The remainder of the patient’s exam was essentially normal. However, the patient gave report that she has a significant family history with a brother, who presented very similarly with acute visual loss. They suspected that the patient may have had an embolic event or an anterior ischemic optic neuropathy.

Subsequently, the patient had an MRI of the brain and orbit and MRA of the head and neck for evaluation. In addition, she had a transthoracic echocardiogram to rule out possible cardioembolic stroke. The patient was also asked to be seen by Ophthalmology to rule out other etiologies of acute visual loss. The patient was also started on aspirin in addition to the Plavix the patient was already on.

In addition, the patient had genetic tests to rule out possible mitochondrial disorder (Leber optic neuropathy). The patient revealed scattered punctate T2 abnormalities in the periventricular subcortical white matter area, which is nonspecific for small vessel disease versus demyelinating. There are no abnormalities noted at the optic nerve. The MRA of the head and neck, however, did show two small atherosclerotic aneurysms in the cavernous segment of left internal carotid artery, while the transthoracic echocardiogram was negative for any valid pathology with a negative bubble study.

Due to the presence of possible aneurysm on the MRA, we suspect this may be possible source of embolisms. It was decided that cerebral angiogram would be done for better characterization of the vasculature. The cerebral angiogram once again revealed a 4 mm left cavernous internal carotid aneurysm as well as a smaller 1-2 mm left anterior coronary artery aneurysm, both without evidence of clots.

Ophthalmology, as previously noted, was asked to see the patient for further evaluation, and they also felt that patient’s visual loss was secondary to anterior ischemic optic neuropathy and were agreeable for an embolic workup as well as vasculitic workup. As noted, the cerebral angiogram did not show any evidence of any vasculitic process and the patient had a normal sed rate. They too were also agreeable to the use of antiplatelet agent unless an embolic source was found or requiring patient to require anticoagulation.

Based on the patient’s studies, it was decided that the patient should be placed on double antiplatelet therapy, namely Plavix and aspirin, as she was started on admission. The patient’s hospital course was generally uncomplicated with the exception of an episode following the cerebral angiogram where the patient was hypotensive with a blood pressure of 86/40 at which time the patient was symptomatic, feeling nauseous and cold and clammy. The patient’s blood pressure responded to fluids, and the patient remained hemodynamically stable with an H&H of 12.8 and 37.8 respectively.

However, with the patient’s recent cerebral angiogram, there was concern that during the patient’s episode of hypotension, she may have had retroperitoneal bleed. Subsequently, abdominal and pelvic CT without contrast was done to rule out hematoma; although, it was somewhat limited but asked not to receive any contrast. There was no evidence for retroperitoneal hemorrhage. In fact, the patient had no further episodes of hypotension the remainder of her hospitalization.

VITAL SIGNS:  Stable. Afebrile.
GENERAL:  The patient is awake, alert, and oriented x4.
NEURO/OPTICAL EXAM:  Cranial Nerves: Pupils are reactive on the right with an afferent defect on the left. Left inferior field cut on confrontational testing. Funduscopic exam was well visualized. Extraocular muscles are intact. Face is symmetric. Tongue is midline.
LUNGS:  Clear to auscultation bilaterally.
HEART:  Regular rate and rhythm without murmurs, rubs or gallops.
RECTAL:  Deferred.
BACK:  Specifically nontender.
EXTREMITIES:  Motor is 5/5 in the upper and lower extremities bilaterally.
NEUROLOGICAL:  Sensation is grossly intact to light touch and proprioception. DTRs are 2+ and symmetric throughout. Toes are downgoing bilaterally. Gait is normal. Cerebellar function intact on finger-to-nose and rapid alternating movement.

DISCHARGE MEDICATIONS:  Plavix 75 mg p.o. daily and aspirin 81 mg p.o. daily.

DISCHARGE CONDITION:  The patient was discharged in stable condition.

DISCHARGE INSTRUCTIONS:  The patient is to follow up with Dr. John Doe. It was recommended that the patient have a followup MRA to evaluate her aneurysms in approximately six months for any further change. Because of the size of the patient’s aneurysm, it was discussed with the patient and her husband, more than likely the patient would not require any neurosurgical intervention at this time unless there has been a change in the size of the aneurysm. The patient is to follow up with Ophthalmology.

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