SAEM Clinical Images Series: My Mom Could Not See

retinal

An 87-year-old female with a history of hypertension, hyperlipidemia, chronic kidney disease stage IIIB, type 2 diabetes mellitus, and schizophrenia presented for evaluation due to sudden visual loss in her right eye, which began 12 hours before she arrived at the emergency department. She has experienced a sudden loss of vision in her right eye for more than six hours. She reports no eye pain or redness, nor has she experienced any flashing lights. Additionally, there have been no symptoms of numbness, tingling, headache, double vision, facial droop, slurred speech, temporal tenderness, jaw claudication, or localized weakness/numbness. Over the past one to two months, the patient has lost 30 pounds and has noted increasing weakness over the last several weeks.

Vitals: BP 136/46; Temp 97.2°F; HR 54; RR 16; SpO2 96% RA

Constitutional: Alert but doses off frequently, no acute distress, appeared weak.

Neuro: No facial droop, no tongue deviation, no dysarthria, strength 4+/5 throughout, normal finger to nose

HEENT: Normocephalic/atraumatic. No mass palpable. Conjunctiva normal on both eyes. EOMI. Decreased right eye light flex compared to the left eye, visual acuity on the left side can count fingers on the right side only seeing a light. No orbital swelling. Normal ear canal bilaterally, normal TM both sides. Septum midline. Oropharynx is clear and moist and mucous membranes are normal. No lymphadenopathy, no bruit.

CV: Regular rate and rhythm with normal S1 and S2, no murmurs.

MSK: Moves all extremities, no deformity, normal muscle tone.

Skin: Warm and dry. No skin rash.

CBC: WBC 9

Hgb: 8.8

Hct: 29.5

Plt: 394

CMP: Na 137, K 4.7, Cl 101, CO2 25, BUN 25, Cr 1.56

PT: 14.2

INR: 1.1

The fundoscopy of the right eye reveals a Central Retinal Artery Occlusion (CRAO), characterized by a pale retina with a cherry-red macula and “box-carring” of the blood vessels.

The potential causes of CRAO in elderly patients include Giant Cell Arteritis (GCA), atherosclerosis, or embolism. It is advisable to measure inflammatory markers, such as the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), particularly in patients over the age of 50. Despite the absence of temporal tenderness and jaw claudication, this patient’s non-specific systemic symptoms like weight loss and weakness, combined with elevated ESR (105) and CRP (6.8), heighten the suspicion of GCA as the etiology of the CRAO. Consultations with ophthalmology and rheumatology are warranted. Administering high-dose pulse steroids is crucial for preventing further complications, such as CRAO in the left eye. Additionally, evaluating non-arteritic causes of CRAO, including carotid artery imaging and echocardiography, should also be considered.

Take-Home Points

  • With acute painless vision loss, fundoscopy can aid in determining the differential diagnosis and further workup.
  • In CRAO, remember arteritic and non-arteritic causes.
  • Age cut off in CRAO will help to guide further work up.

  • Diagnosis and management of Central Retina Artery Occlusion. (2017). American Academy of Ophtalmology Eyenet magazine. [Online] Available at: https://www.aao.org/eyenet/ article/diagnosis-and-management-of-crao [Accessed 22 Dec 2023]
  • Guluma K, Lee JE. Ophtalmology. Rosen’s Emergency Medicine: Concepts and Clinical Practice 10th-ed. Edited by Ron Walls. Elsevier. 2023. 57, 750-780.e4

By |2024-12-02T21:51:58-08:00Dec 13, 2024|Ophthalmology, SAEM Clinical Images|

SAEM Clinical Images Series: A Rash with Cranial Nerve Deficits

rash

A 48-year-old male with no significant past medical history presented to the Emergency Department with a left-sided facial rash and associated burning left eye pain that started four days prior. He was seen at an ophthalmology clinic when his symptoms started and given oral valacyclovir which he took for three days without improvement. He also endorsed left-sided facial weakness and diplopia for the last eight days. He denied fevers, chills, nausea, vomiting, ear pain, tinnitus, hearing changes, blurry vision, photophobia, history of malignancy or HIV, history of stroke. He reported remote use of tobacco nine months prior, cocaine use that stopped three weeks prior, and alcohol use only on weekends.

Vitals: Temp 36.8°C; BP 148/85; HR 80; RR 18; O2 Sat 96% on room air

General: Alert, no acute distress.

Skin: Healed vesicular rash along V2 distribution of trigeminal nerve.

Head: Normocephalic, atraumatic.

Eye: Visual acuity – right 20/40, left 20/70 without correction (at baseline per patient). Left eye viewed with fluorescein showing dendritic lesions. EOM: right intact, impaired abduction of left eye. Unable to close the left lid. Pupils: R pupil 3mm, briskly reactive to light, L pupil 3mm not briskly reactive

Ears: Without vesicular lesions bilaterally

Cardiovascular: Normal peripheral perfusion.

Respiratory: Respirations are non-labored.

Neurological: Alert and oriented to person, place, time, and situation. Cranial nerves: CN II grossly intact, CN III: left pupil reactive to light but sluggish, CN V: facial sensation to light touch intact, CN VI: impaired abduction of left eye, CN VII: left facial droop with left forehead involved, CN VIII – XII intact. 5/5 motor strength to bilateral upper and lower extremities, no sensory deficits, has a steady gait.

CBC, BMP, and ESR all within normal limits.

The patient has a left-sided painful vesicular rash in the V2 distribution of the trigeminal nerve and dendrites on fluorescein-stained exam of the left eye, concerning for herpes zoster ophthalmicus. Hutchinson sign (involvement of the tip or side of the nose, as seen in the images) indicates involvement of the nasociliary branch of the trigeminal nerve, and patients with this finding have an increased risk of ocular involvement [1]. Although this patient did not have auditory canal involvement, Ramsay Hunt Syndrome is also important to consider. The image also shows impaired abduction of the left eye, concerning for a CN VI palsy, and the physical exam showed sluggish left pupil reactivity to light, concerning for a CN III palsy. Given the patient reported diplopia and had multiple cranial nerve deficits, cavernous sinus syndrome was also a differential diagnosis.

The recommended treatment for herpes zoster ophthalmicus is oral Valacyclovir, however, if there is any concern for disseminated zoster (3 or more dermatomes involved, CNS involvement, or other extradermal complications), patients should be treated with IV Acyclovir 10 mg/kg based on ideal body weight every 6 hours [1]. Since this patient underwent a trial of Valacyclovir without improvement and there was concern for possible CNS involvement with multiple cranial nerve deficits on exam, the patient was started on IV Acyclovir. Consultation with ophthalmology is also recommended for management of zoster ophthalmicus. The presence of diplopia, CN III and CN VI palsies was also concerning for possible cavernous sinus syndrome, which can be caused by a broad range of infectious, inflammatory, neoplastic, and vascular pathologies. It can have varying presentations based on the affected neurovascular structures however the constellation of symptoms includes diplopia, ophthalmoplegia, Horner syndrome, facial sensory loss, and CN III, VI, and VI deficits. If it is suspected, MRI with and without contrast is the preferred imaging modality to determine the location and extent of disease [2]. Neurology consultation is also helpful in co-management.

Take-Home Points

  • In a patient with a facial vesicular rash, it is important to perform a full cranial nerve exam to evaluate for deficits that may indicate CNS involvement, inspect the anterior chamber to evaluate for zoster ophthalmicus, and examine the ears to evaluate for Ramsay Hunt Syndrome.
  • Start antivirals early if zoster ophthalmicus is suspected since this disease process can be vision-threatening.

  • Anderson Erik, Do-Nguyen Amy. Varicella-Zoster Virus (VZV). In: Mattu A and Swadron S, ed. CorePendium. Burbank, CA: CorePendium, LLC. https://www.emrap.org/ corependium/chapter/recV6PonFTQbz5R9c/Varicella-Zoster-Virus-VZV#h.q140vny9bkbo. Updated August 16, 2023. Accessed January 11, 2024.
  • Munawar K, Nayak G, Fatterpekar GM, et al. Cavernous sinus lesions. Clinical Imaging. 2020;68:71-89. doi:https://doi.org/10.1016/ j.clinimag.2020.06.029

SAEM Clinical Images Series: Didn’t See That Coming

hyphema

A 23-year-old healthy male presented to the emergency department with left eye pain, soreness, and blurry vision after being hit in the left eye with a Nerf gun bullet two days prior. He had no prior ophthalmologic history and does not wear corrective lenses.

Left eye: Visual acuity 20/30. Intraocular Pressure 17. Pupil 3mm, irregular, minimally reactive. Slit lamp exam revealing 3+ RBCs, vertical layering of blood along the nasal aspect.

Vertical hyphema

Blunt trauma induces shearing forces upon the vasculature of the ciliary body and iris, resulting in the accumulation of red blood cells (RBCs) in the anterior chamber. This space normally contains only clear, aqueous humor. RBCs slowly settle to the bottom of the anterior chamber in a gravity-dependent manner. Classically this develops in a horizontal pattern, but patients who subsequently sleep on their side may experience vertical hyphema formation. Although trauma is the most common etiology, hyphema can occur due to any hematologic abnormality. It is a frequent complication of sickle cell disease. As in all cases of ocular trauma, globe rupture must be immediately ruled out before proceeding with a comprehensive ophthalmologic examination.

The patient had a Grade I hyphema.

Grade 0: No visible layering, but red blood cells within the anterior chamber (microhyphema)

Grade I: Layered blood occupying less than one-third of the anterior chamber

Grade II: Blood filling one-third to one-half of the anterior chamber

Grade III: Layered blood filling one-half to less than total of the anterior chamber

Grade IV: Total filling of the anterior chamber with blood (also known as 8-ball hyphema)

Take-Home Points

  • A hyphema is a collection of blood in the anterior chamber of the eye.
  • Before measuring intraocular pressure, remember to inspect the anterior ocular anatomy with consideration for globe rupture. If this is not excluded, avoid tonometry as it can cause extrusion of aqueous humor and further damage to the globe.
  • Blunt trauma is the most common cause of hyphema. However, non-traumatic hyphema should prompt investigation for hematologic disorders such as Sickle cell disease.

  • Brandt MT, Haug RH. Traumatic hyphema: a comprehensive review. J Oral Maxillofac Surg. 2001 Dec;59(12):1462-70. doi: 10.1053/joms.2001.28284. PMID: 11732035.
  • Gragg J, Blair K, Baker MB. Hyphema. 2022 Dec 26. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 29939579.

By |2024-09-28T21:19:11-07:00Sep 30, 2024|Ophthalmology, SAEM Clinical Images|

SAEM Clinical Images Series: What’s Coming Out of Your Eye?

open globe

A 32-year-old male with no significant past medical history presented to the emergency department (ED) from an outside hospital for further management of right eye pain and vision loss sustained after he was struck by a metal wire while at work. The patient presented to an outside “eye doctor” and was told to go to the nearest hospital for evaluation. At the outside hospital, he was given analgesia, antiemetics, and a tetanus booster, and transferred to our hospital for ophthalmologic evaluation. On arrival to our emergency department, the patient expressed continued eye pain with bloody discharge as well as blurry vision from his right eye. He had no other complaints and denied any other trauma or loss of consciousness during the event.

Right Eye: 12 mm corneoscleral laceration with superior iris prolapse through the laceration at the 12 o’clock position, approximately 6 mm in length. Pupil 3 mm, teardrop shaped, and reactive without relative afferent pupillary defect. Seidel test positive on fluorescein stain. Conjunctival injection superiorly. Visual acuity: able to count fingers. Extraocular movements intact. Ocular pressure deferred. 1 mm superior eyelid laceration.

CT Orbits/Sella w/ IV Contrast: No acute orbital fracture. No evidence of retrobulbar hematoma or emphysema. Intraconal and extraconal fat planes are preserved. Extraocular muscles are symmetric and normal in position. The globes are grossly unremarkable. Absent right lens.

Open Globe Injury

In the photo, you can see the teardrop shape of the pupil, conjunctival injection, corneal laceration, and superior iris prolapse.

Tonometry and ocular ultrasound (US) are generally not recommended as you could squeeze more liquid out of the eye or increase the intraocular pressure even more, pushing the iris further out. An emergent ophthalmology consult is needed to plan for operative repair. The patient should be given an eye shield, IV antibiotics, and tetanus prophylaxis. Avoid increasing intraocular pressure by using anti-emetics, analgesia, and bed elevation. Recommended antibiotics are vancomycin and a third-generation cephalosporin to prevent endophthalmitis. Postoperatively, these patients need IV antibiotics x 48 hours, steroid eye drops, antibiotic ointment, an eyepatch, and recommendations for no heavy lifting, bending, or strenuous activity, and head of bed should be elevated at 45 degrees.

Take-Home Points

  • Open globe injuries present as eye pain, vision loss, teardrop pupil, afferent pupillary defect, and a corneal laceration.
  • Avoid ocular US or tonometry in these patients as these could increase intraocular pressure further and worsen the injury.
  • Management includes an eye shield, head of bed elevation, avoiding ocular manipulation, analgesia, and antiemetics. Update tetanus and start IV antibiotics – vancomycin and a third-generation cephalosporin. Consult ophthalmology emergently.
  • Open globe injury: Assessment and preoperative management. American Academy of Ophthalmology. (2023, March 23). https://www.aao.org/eyenet/article/open- globe-injury
  • Ahmed Y, Schimel AM, Pathengay A, Colyer MH, Flynn HW Jr. Endophthalmitis following open-globe injuries. Eye (Lond). 2012 Feb;26(2):212-7. doi: 10.1038/eye.2011.313. Epub 2011 Dec 2. PMID: 22134598; PMCID: PMC3272210.

By |2024-09-06T22:03:57-07:00Sep 13, 2024|Ophthalmology, SAEM Clinical Images|

SAEM Clinical Images Series: An Interesting Case of Ocular Trauma

ocular trauma

A 27-year-old male with no past medical history presents to the Emergency Department with right eye pain. He states that approximately one week prior, he was working on a wire fence when he lost hold of a wire under tension, and it subsequently hit him in his right eye. He had immediate pain in his affected eye and was unable to see anything but light for the next three days. His vision slowly improved though it never normalized. He continued to have pain, so he presented for evaluation. He also reported seeing floaters and denied pain with eye movement, increased light sensitivity, or eye discharge.

Eyes: Lids without injury. Visual acuity was 20/50 OD, 20/30 OS. Intact visual fields to finger confrontation. Extraocular muscle movements were intact and without pain. Right pupil was oval-shaped and reactive, and an evident defect at the iris from the 9 to 11 o’clock position was noted. On fluorescein stain, there was no uptake, with a negative Seidel sign. Tonometry was normal (13 OD, 12 OS). On slit lamp examination, the patient had a clear cornea, an appropriately deep anterior chamber with no hyphema or hypopyon, and 1+ mixed cells. The lens was clear, with no movement or vibration (phacodonesis) noted. A vitreous hemorrhage OD was also identified on bedside ultrasound.

Non-contributory

Iridodialysis

Traumatic iridodialysis is an uncommon ocular emergency with very distinct findings that we can encounter in the Emergency Department. It is most commonly seen with blunt trauma but can also occur with penetrating injury to the eye. This injury appears as a crescent-shaped defect at the peripheral area of the iris. Blunt trauma causes an acute globe compression, which temporarily increases intraocular pressure. This increased pressure is dissipated throughout the eye, leading to forceful fluid shifts that cause increased tension along the pupillary sphincter muscle. The weaker area of the sphincter muscle can subsequently tear, resulting in separation of the iris from the ciliary body.

Iridodialysis can be managed conservatively if it is asymptomatic and uncomplicated. Complicating factors, which include elevated intraocular pressures refractory to medical therapy, the presence of a large hyphema, rupture from blunt trauma, or the need for exploration secondary to penetrating trauma, require an Ophthalmology consult and may require emergent surgical repair.

Take-Home Points

  • Patients with iridodialysis are at risk for globe rupture, so a fluorescein exam must be performed prior to measuring intraocular pressure.
  • Ophthalmology should be consulted if the patient has complicating factors, which include elevated intraocular pressures refractory to medical therapy, the presence of a large hyphema, rupture from blunt trauma, or the need for exploration secondary to penetrating trauma.
  • Knoop, K. J., Knoop, K. J., & Stack, L. B. (n.d.). Chapter 2: Ophthalmic Conditions. In The Atlas of Emergency Medicine (p. 89). essay, McGraw-Hill Medical.
  • Pujari, A., Agarwal, D., Kumar Behera, A., Bhaskaran, K., & Sharma, N. (2019). Pathomechanism of iris sphincter tear. Medical hypotheses, 122, 147–149. https:// doi.org/10.1016/j.mehy.2018.11.013

By |2024-08-19T10:01:53-07:00Aug 26, 2024|Ophthalmology, SAEM Clinical Images|

SAEM Clinical Images Series: Seeing Double

ophthalmoplegia

A 53-year-old woman with no significant past medical history presented to the emergency department with a 3-day history of double vision on leftward gaze. She initially presented to urgent care with a chief complaint of chest heaviness and concern that her blood pressure was too high, but was sent to the emergency department for further cardiac and neurological evaluation after her urgent care provider noticed abnormal eye movement. She endorsed mild, intermittent headaches associated with diplopia when looking to the left. However, she denied any blurry vision when looking forward. She denied any trauma or falls.

Vitals: Temp 36.7°C; Heart rate 86 beats/min; Respirations 18 breaths/min; BP 150/82 mmHg; O2 Saturation: 100%

General: No acute distress and appears comfortable. She is alert and oriented.

Eyes: Equal, round and reactive pupils and severely limited adduction of the right eye, all other extraocular movements are normal.

Neuro: All other cranial nerves are intact, normal tone in bilateral upper and lower extremities, normal sensation bilaterally to light touch and pinprick except for mildly decreased sensation to pinprick over right ulnar distribution.

CBC, CMP, EKG, and Troponins were normal.

Lipid panel: Cholesterol 241 (H)

CSF: No oligoclonal bands, Protein 197 (H), Albumin 57 (H), IgG 16.3 (H)

Internuclear ophthalmoplegia (INO) is defined as the inability to adduct the eye due to a lesion in the medial longitudinal fasciculus (MLF) and can be accompanied by nystagmus in the same eye. The two main causes of internuclear ophthalmoplegia are demyelination of the medial longitudinal fasciculus (MLF) from multiple sclerosis (MS) and ischemic cranial nerve damage from stroke. However, a comprehensive list of causes of INO includes: infarction (ischemic stroke), demyelination (MS), tumor, encephalitis, hemorrhage, hydrocephalus, Chiari malformation, infection (Lyme Disease), and trauma. Usually, MS is seen in younger patients where both eyes are affected whereas strokes occur more often in older patients and only one eye is affected.

The therapeutic approach focuses on treating the underlying cause and hence determining the etiology is of immense importance. A brain MRI should be ordered to evaluate for ischemia and demyelination. Proton density imaging is beneficial in identifying MLF lesions in multiple sclerosis. A lumbar puncture can also help rule out infections. A kappa-free light chain antibody test is a faster and less expensive way to test for multiple sclerosis than looking for oligoclonal bands in the CSF.

Given this patient’s relatively young age and vascular risk factors, stroke is highest on the differential. Her brain MRI showed areas of restricted diffusion in the right dorsal medial pons correlating with her exam. It also showed periventricular and subcortical white matter changes which is a non-specific finding in chronic small vessel ischemic changes vs underlying demyelinating disease. This was followed up with an MRI of her spine that demonstrated C5-6 stenosis with associated cord edema and an additional enhancing C3-4 lesion concerning for demyelinating disease. Her lumbar puncture revealed 3 nucleated cells and a protein of 197 but was deemed a traumatic tap. There were no oligoclonal bands. The initial brain MRI findings favored stroke for which she underwent a stroke work-up and was ultimately discharged on aspirin and atorvastatin for secondary prevention. However, due to concern for demyelinating disease, she was also treated with a 3-day course of IV methylprednisolone. Ultimately, she was discharged and asked to come back for a follow-up for repeat brain imaging and evaluation. A recent study showed that patients with unilateral or bilateral INO who experienced symptomatic diplopia were commonly managed by uniocular occlusion. Another case report showed that a young man who presented with acute INO responded rapidly to treatment with IV alteplase when administered within 2 hours of the onset of symptoms and resolution within 15 minutes. A case series revealed that 1 in 5 patients failed to recover from an INO. Hence, it is critical that a definitive workup is carried out to determine the etiology of the INO.

Take-Home Points

  • Brain MRI including DWI is a useful diagnostic tool for INO.
  • Unilateral INO is more frequently related to ischemic/vascular causes whereas bilateral INO is associated with MS.
  • Kim SS, Lee MH, Ji C. Unilateral Internuclear Ophthalmoplegia Following Minor Head Injury. Korean J Neurotrauma. 2022 Oct 24;18(2):329-334. doi: 10.13004/kjnt.2022.18.e64. PMID: 36381451; PMCID: PMC9634317.
  • Mahawish KM, Aravind A. Acute onset internuclear ophthalmoplegia responsive to treatment with intravenous alteplase. N Z Med J. 2020 May 22;133(1515):119-121. PMID: 32438384.
  • Simmons J, Rhodes M. Conservative and Surgical Management of Unilateral and Bilateral Internuclear Ophthalmoplegia (INO)-A Retrospective Analysis. Br Ir Orthopt J. 2022 Nov 7;18(1):152-158. doi: 10.22599/bioj.280. PMID: 36420121; PMCID: PMC9650975.

By |2024-03-16T21:53:50-07:00Mar 22, 2024|Neurology, Ophthalmology, SAEM Clinical Images|

SAEM Clinical Images Series: Workout Gone Wrong

hyphema

A 28-year-old male presented to the ED for evaluation of an injury to his right eye. While working out with an exercise band, it snapped back, hitting the patient in the right eye. He experienced blurry vision and excess eye tearing immediately after the incident occurred. The patient also developed gross blood over the front of the eye.

Vitals: Temp 98°F, HR 73, BP (135/77), RR 16, SpO2 99%

HEENT: Gross blood in the anterior portion of the right eye (grade I). The right pupil is dilated with minimal responsiveness to light. Visual Acuity: OD 20/70, OS 20/10, Both 20/10. Pressure: OD (21), OS (16). Decreased visual field on the right when compared to the left. Staining with tetracaine and fluorescein did not reveal any evidence of corneal abrasion or ulceration. Left eye is atraumatic in appearance.

Neurologic: Alert and oriented x3

Non-contributory

A Hyphema is a collection of blood in the anterior chamber of the eye due to the tearing of the iris root vessels.

The most common cause is blunt trauma to the eye. Spontaneous hyphemas can also occur and are often associated with sickle cell disease. It can be caused by ocular surgery and neoplastic disease, as well.

Take-Home Points

  • Hyphemas are an ocular emergency and should prompt immediate consultation with an ophthalmologist.
  • Patients should elevate the head of the bed to 45 degrees since layering of the blood is gravity-dependent.
  • Treatment usually involves the administration of steroidal and cycloplegic ophthalmic drops.
  • Cline, D., Ma, O. J., Meckler, G. D., Stapczynski, J. S., Thomas, S. H., Tintinalli, J. E., & Yealy, D. M. (2020). 241. In Tintinalli’s emergency medicine: A comprehensive study guide. essay, McGraw-Hill Education.
  • Traumatic Hyphema. Wikem. (2020, March 18). Retrieved January 11, 2023, from https://www.wikem.org/wiki/Main_Page

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