EM@3AM – Central Retinal Vein Occlusion

Author: Olivier Levac-Martinho, MD, BSc (@OlMartinho, Resident Physician, University of Ottawa) and Erica Simon, DO, MHA (@E_M_Simon, EMS Fellow, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 52-year-old male, with a previous medical history of CAD (CABG x3), HTN, DM, and smoking (30 pack years), presents to the emergency department following the painless loss of vision in his left eye. The patient denies headache, slurred speech, and motor and sensory deficits. He denies contact lens wear and denies a requirement for glasses. The man reports an eye examination within the previous year, stating “my eyes have been perfect.”

Initial VS: BP 123/76, HR 66, T 99.9F Oral, RR 12, SpO2 97% on room air.

Visual Acuity:
OD: 20/20
OS: 20/400
OU: 20/200

Pertinent physical exam findings:
HEENT: PERRLA, 2mm bilaterally, EOMI. OS: Tonometry: IOP 18 mmHg. Fundoscopy: retinal hemorrhages, cotton-wool spots, optic disc edema.
Cardiovascular: S1, S2, regular rate and rhythm. No carotid bruits.

What’s the next step in your evaluation and treatment?


 Answer: Central Retinal Vein Occlusion (CRVO)1-4

  • Epidemiology: CRVO typically occurs in persons > 65 years of age with a history of atherosclerotic disease. Risk factors include DM, HTN, vasculitis (systemic lupus erythematosus, HIV, syphilis, sarcoidosis, etc.), glaucoma (increased IOP = bowing of the lamina with subsequent impingement of the central retinal vein), and hypercoagulable states (hyperviscosity syndromes, protein C deficiency, protein S deficiency, etc.).1,2 Population studies report the prevalence of CRVO as 0.1-0.4% (incidence highest among African American individuals).1,2
  • Etiology: Occurs secondary to a thrombus occluding the lumen of the central retinal vein, compression of the central retinal vein by an atherosclerotic central retinal artery, or occlusion of the central retinal vein secondary to inflammation.1,3
  • Clinical Manifestations: Sudden onset, or progressively worsening, painless, monocular vision loss.1,4
  • Evaluation and Treatment:
    • Obtain visual acuity (vision often significantly reduced in the affected eye (> 20/200)).2,3
    • Perform a thorough H&P:
      • Question specifically regarding the aforementioned risk factors. Obtain a complete family history to include systemic thrombotic diseases and rheumatologic diseases.
    •  Ocular examination: pupillary exam may demonstrate an ipsilateral afferent pupillary deficit.2
      • Fundoscopic retinal exam: retinal hemorrhages in all quadrants of the fundus (“blood and thunder” appearance), optic nerve head swelling, splinter hemorrhages, cotton-wool spots, and macular edema +/- breakthrough vitreous hemorrhage.1,2
    • Consider a more extensive evaluation in persons < 65 years of age presenting without known risk factors for CRVO (e.g. blood dyscrasias: CBC, coags, etc.).
    •  Treatment => Emergent ophthalmology consult.
      • Available therapies include aspirin, anticoagulation, photocoagulation, and intravitreal injections (anti-vascular endothelial growth factors, steroids, etc.)1
      • Treatment of, or referral for, the management of CRVO systemic vascular risk factors (e.g. HTN, DM, etc.) is advised.
  • Pearls:
    • Nearly 7% of persons presenting with unilateral CRVO develop the condition in the contralateral eye within 5 years of onset of the first eye.1
    • The differential diagnosis of CRVO includes: stroke, TIA, amarosis fugax, temporal arteritis, retinal detachment, and posterior vitreous detachment.1

 

 References:

  1. Oellers P, Hahn P, Fekrat S. Central Retinal Vein Occlusion. In Ryan’s Retina. 6th ed. 2018. Philadelphia, Elsevier. 57; 1166-1179.
  2. Cugati S, Ten-year incidence of retinal vein occlusion in an older population: the Blue Mountains Eye Study, Arch Ophthalmol. 2006 May; 124(5):726-32.
  3. Klein R, The epidemiology of retinal vein occlusion: the Beaver Dam Eye Study; Trans Am Ophthalmol Soc. 2000;98:133-41
  4. Green WR, Central retinal vein occlusion: a prospective histopathologic study of 29 eyes in 28 cases, Trans Am Ophthalmol Soc. 1981; 79:371-422.

 

For Additional Reading:

Acute Visual Loss in the Emergency Department: Pearls and Pitfalls

Acute Visual Loss in the Emergency Department: Pearls and Pitfalls

The post EM@3AM – Central Retinal Vein Occlusion appeared first on emDOCs.net - Emergency Medicine Education.

EM@3AM – Carotid Artery Dissection

Author: Olivier Levac-Martinho, MD, BSc (@OlMartinho, Resident Physician, University of Ottawa) and Erica Simon, DO, MHA (@E_M_Simon, EMS Fellow, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 35-year-old male, with a history of Marfan syndrome, presents to the ED by EMS for diffuse headache, left-sided neck pain, and difficulty walking. The patient reports the onset of his symptoms immediately following chiropractic manipulation of his cervical spine. Per paramedics: field neurologic examination was notable for gait ataxia and right lower extremity weakness.

Initial VS: BP 145/82, HR 75, T 99.2F, RR 14, SpO2 97% on room air.

Upon ED evaluation, the patient denies slurred speech, he denies visual and cognitive deficits, and he denies additional motor/sensory symptoms.

Pertinent physical exam findings:
Neuro: GCS 15. CN II-XII intact. Left upper extremity: apraxia (unable to perform rapid alternating movement when verbally prompted x2).
Right lower extremity: motor 3/5; unable to perform heel-to-shin.  Absent two-point discrimination.
Positive Romberg. DTRs (triceps, biceps, patellar, achilles) 2+ bilaterally. No clonus.
Cardiovascular: regular rate and rhythm, no murmurs, rubs, or gallops.

What’s the next step in your evaluation and treatment?


Answer: Carotid Artery Dissection1-7

  • Epidemiology: Approximately 2.5% of all strokes in the U.S. occur secondary to carotid artery dissections. Carotid artery dissection is a common cause of stroke (nearly 20%) in the young adult and pediatric populations.1
  • Etiology: May occur spontaneously, or in the setting of major/minor neck trauma (MVC (classically a seat belt injury)) vs. chiropractic manipulation, retching, yoga, etc.).2
  • Risk Factors: Connective tissue diseases (Marfan syndrome, Ehlers Danlos), large vessel arteriopathy (fibromuscular dysplasia), and osteogenesis imperfecta (increased prevalence of spontaneous carotid artery dissection).2
  • Pathophysiology: Damage to the arterial wall => intimal bleeding and subsequent intramural hematoma => possible thrombus formation => potential for thromboembolic stroke.
  • Clinical Manifestations: Dissection of the cervical portion of a carotid artery is associated with unilateral headache, neck pain, facial pain, incomplete Horner’s syndrome (myosis, ptosis, absent anhydrosis), CN palsy (CN XII most common), amaurosis fugax, pulsatile tinnitus, and anterior cerebral stroke symptoms.
    • Note: symptoms may be transient or persistent.3
  •  Evaluation and Treatment:4-7
    • Assess the ABCs and obtain VS (+ accucheck).
    • Perform a thorough H&P:
      • Question specifically regarding recent MVCs, neck trauma, and the aforementioned risk factors.
    • Evaluation:4,5
      • Patients with symptoms consistent with cerebral ischemia: non-contrast CT head (evaluate for ischemic vs. hemorrhagic stroke).
      • To diagnose a cervical artery dissection: CT angiography of the neck or MR angiography appropriate for initial screening.5
        • Digital subtraction angiography is the gold standard (rarely required; consider in patients with a history suggestive of the diagnosis but initial CTA/MRA negative).5,6
    •  Treatment:5-7
      • Consult vascular surgery to discuss management:
        • Patients with extra-cranial carotid artery dissection, evidence of acute ischemic stroke, and symptom onset < 4.5 hours prior to arrival => consider thrombolysis if no contraindications.
          • Note: thrombolysis carries the potential risks of extending the intramural hematoma, dislocating an intraluminal thrombus with subsequent embolization, development of a subarachnoid hemorrhage due to leakage, or formation of a pseudoaneurysm.6
        • Patients with extra-cranial carotid artery dissection and evidence of ischemic stroke, presenting > 4.5 hours following symptom onset or thrombolysis contraindicated => antithrombotic therapy.
          • A 2012 randomized controlled trial (CADISS – Cervical Artery Dissection In Stroke Study) demonstrated no evidence of superiority in treatment with anticoagulation vs. antiplatelet therapy.7
          • Anticoagulation is preferred if severe stenosis, vessel occlusion, or pseudoaneurysm are present (assumed that anticoagulation more effectively prevents thromboembolic complications).5
          • Antiplatelet therapy is preferred if the patient is likely to have a poor prognosis (large infarct) or in individuals with a medical history pre-disposing to increased risk of bleeding (blood dycrasias, etc.).6
        • Patients with intra-cranial extension of the carotid artery dissection or dissection involving the aorta:
          • Thrombolysis is contraindicated (risk of SAH or aortic rupture) => requires antithrombotic therapy.6
        • For all patients, endovascular or surgical repair may be utilized in the setting of severe stenosis, expanding dissecting aneurysm, or persistent ischemia despite antithrombotic therapy.6
  •  Pearls:
    • In treating cervical artery dissection, the optimum duration of antithrombotic therapy is unclear (generally 3-6 months recommended). Follow-up imaging is required.6


References:

  1. Lee V. Incidence and outcome of cervical artery dissection: a population-based study. Neurology. 2006; 67(10): 1809-12.
  2. Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcomes. Lancet Neurol 2009; 8:668.
  3. Debette S. Differential features of carotid and vertebral artery dissections: the CADISP study. Neurology. 2011; 77(12):1174-1181
  4. Provenzale J. Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. Am J Roentgenol. 2009; 193(4): 1167-1174.
  5. Kwiatkowski T, Friedman B. Headache Disorders. In Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th Philadelphia, Elsevier. 2018; 93: 1265-1277.e2.
  6. Patel R, Adam R, Malkjian C, et al. Cervical carotid artery dissection: current review of diagnosis and treatment. Cardiology in Review. 2012; 20(3): 145-152.
  7. Zinkstok S, Vergouwen M, Engelter S, et al. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011; 42: 2515–2520.
  8. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015; 14: 361–367.

 

 

For Additional Reading:

Carotid Artery Dissection: Practice Update

Carotid Artery Dissection

 

 

The post EM@3AM – Carotid Artery Dissection appeared first on emDOCs.net - Emergency Medicine Education.