POTD: Idiopathic Intracranial Hypertension

POTD: Idiopathic intracranial hypertension

 

Idiopathic intracranial hypertension (IIH) aka pseudotumor cerebri and benign intracranial hypertension

·      rare condition

·      presents with gradual onset and chronic headache, vision changes, nausea, vomiting, and tinnitus

·      + papilledema/ swelling of the optic disc on fundoscopy

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·      optic sonography

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  • ONSDs should be measured 3 mm behind the papilla, an average of less than 5 mm is considered normal.

  • ONSD > 5 mm has been shown to be 90% sensitive and 85% specific for ICP > 20.

·      Classic presentation: young, obese female

·      + association has been found with this diagnosis and the use of oral contraceptive medications, tetracycline, anabolic steroids, and vitamin A

·      Pathophysiology is not well understood but thought to be caused by an imbalance in CSF production and reabsorption

·      Diagnostic criteria include an alert patient with either a normal neurologic examination or findings consistent with papilledema, visual field defect, or an enlarged blind spot

·      Definitive dx: Lumbar puncture

  • done in a recumbent position reveals an elevated CSF opening pressure of more than 20 mm Hg in an obese patient (normal being up less than 20 mm Hg).

  • normal CSF analysis.

·      CT head may show “slit like” or normal ventricles without mass effect

·      DDx: glaucoma, venous sinus thrombosis, ICH, IC mass.

·      Treatment

  • Repeat LPs  

  • Acetazolamide

  • Surgical shunt if severe and refractory

  • offending agents such as oral contraceptive medications should be discontinued.

·      Permanent loss of vision can occur in up to 10% of patients, and higher if left untreated

 

Sources:

 

  • Dubourg J, Javouhey E, Geeraerts T, Messerer M, Kassai B. Ultrasonography of optic nerve sheath diameter for detection of raised intracranial pressure: a systematic review and meta-analysis. Intensive Care Med. 2011;37(7):1059-68. [pubmed]

  • Blaivas M, Theodoro D, Sierzenski PR. Elevated intracranial pressure detected by bedside emergency ultrasonography of the optic nerve sheath. Acad Emerg Med. 2003;10(4):376-81. [PDF]

  • https://www.ultrasoundoftheweek.com/uotw-5-answer/

  • Peer IX

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POTD: Trauma Tuesday: Lateral Canthotomy

When to perform it?

·      To release orbital compression syndrome, most commonly due to retrobulbar hematoma.

·      IOP > 40, the pressure that indicated that you need to cut and release the compartment syndrome.

·      Without decompression, irreversible vision loss due to increasing orbital pressure may occur in as little as 90-120 minutes.

Clinical situation: trauma to the head/face.

Physical exam:

https://www.emra.org/emresident/article/emergency-department-evaluation-of-blunt-orbital-trauma/

https://www.emra.org/emresident/article/emergency-department-evaluation-of-blunt-orbital-trauma/

CT head and face

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familiarize yourself with the anatomy

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Before starting, highly consider sedation.

Steps:

1)    Generously inject 1% Lidocaine with epi to numb that lateral canthus to the orbital rim.

  • Do this by directing the needle away from the globe itself

  • Helps with bleeding and with pain.

2)    Using the needle driver as your hemostat, advance from the lateral canthus to outer orbit rim. Clamp down and hold for 1- 2 minutes.

3)    Using your small scissors, cut the lateral canthus to the orbital rim.

4)    Then cut inferiorly to cut the inferior crus of the lateral canthus (you may need to probe around to feel the structures)

5)    Repeat IOP. If the IOP is not immediately lower, then cut the superior crus of the lateral canthus and recheck pressure.

Pearls:

·      There is a lot of swelling. It can be hard to fit your hemostat in place and to feel your landmarks. Use you instruments to feel/probe around.

·      Also, do not worry about cutting too much. You are doing this to save this patient’s vision. After discussing this with optho, these are repaired quite easily days/weeks later. For example, Dr. Tome Levy performed this once on a patient that I later followed up with in split flow about 2 weeks later. There was no physical evidence on physical exam that this had ever happened. At first I thought I had the wrong patient in front of me… but the patient confirmed that a week and half ago he had in fact had the optho plastic surgery to repair it.  

Sources:

https://emedicine.medscape.com/article/82812-overview

http://www.tamingthesru.com/blog/annals-of-b-pod/ocular-emergency

This is an excellent emrap video that reviews the procedure: https://www.youtube.com/watch?v=tgQaKVGynFA

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Do you see what eye see?

Do you see what eye see?

Eye complaints can be abundant in the ED - so what should we focus on? Today's pearl is going to focus on the diagnoses of atraumatic vision loss.

Let's break it down by symptoms: Painless or painful?

Good physical exam must include: visual acuity, visual fields, pupillary exam, fluorescein woods lamp, slit lamp and of course - a head to toe complete physical exam. 


Painless Vision Loss: 

  1. TIA/stroke: sudden vision loss usually from embolic or thrombotic event, can often be from carotid artery occlusion. If transient, often called amaurosis fugax but that can apply to any cause of transient vision loss. Risk factors: it is a stroke/TIA of the eye, so same cardiovascular risk factors. Testing: MRI, ECG, Echo, Carotid US. ED role: Don't miss it - this is a stroke and should admitted to a monitored stroke unit.

2. Central retinal artery occlusion: Sudden, permanent typically unilateral vision loss (permanent damage ~90 minutes of occlusion). Risk factors: atherosclerosisdisease (HTN, DM, Smoking, etc.) and treatment involves treating risk factors (varied success with laser treatment of pressure decreasing eye drops); or secondary to Giant cell arteritis (+/- headache, pain with hair burshing or chewing)  in which case rapid high dose corticosteroids can prevent vision loss. PE: decreased visual acuity, asymmetric red reflex, "Cherry red spot" on the macula on fundoscopy. ED role: urgent/emergent optho referral or ED consult. Recognize if cause is giant cell arteritis (CRP, ESR) and treat with high dose steroids. Consider timolol 0.5% topical drops but no strong evidence. Will need PCP to address concurrent risk factors. 

3. Central retinal vein occlusion: often times sudden but occasional gradual (days-weeks) vision loss due to swelling of the macula. Risk factors: same as above and glaucoma. Think of this as a DVT for the eye. PE: decreased visual acuity. "Blood and thunder" on fundoscopy. ED role: Evaluate for cause or presence of other pathologies secondary to a hypercoagulable state (DVT, PE, sickle cell, etc.). Refer to optho and will need PCP to address concurrent risk factors. 

retinal vein occlusion image-full.png

4. Retinal Detachment: Sudden, spontaneous "flasher and floaters" or "spots or stars" or loss of vision that is like a "curtain closing." Usually loss of peripheral vision. Risk factors: recent eye injury or surgery, severe nearsightedness (think elderly). ED Role: POCUS - look for a delicate floating line in the anechoic eyeball space. If their is no macular separation, their vision can be saved! This is an optho emergency. Unless you're Errel, err on the side of caution and call optho for all of these since we might not be able to definitively determine if the macula is involved.

5. Vitreous Hemorrhage and Posterior Vitreous Detachment: Floaters, strings, or cobwebs in their vision that change with eye movement. Flashes of light. Risk factors: retinal damage (surgery, trauma, prior retinal tear), Diabetic Retinopathy, trauma, sickle. ED role: POCUS: swirling cloud-like opacity at moves with ocular movement and is not tethered to the optic disk or retina "washing machine sign". ED role: Avoid Anticoagulation, elevate head of bed, optho referral.

6. Optic Neuritis/papillitis: painless vision loss over hours to days, typically unilateral. +/- prior episodes. +/- other neuro symptoms. May worsen with eye movement. Risk factors: typically females 18-45, multiple sclerosis. Viral: mono, zoster, encephalitis, TB. Physical exam: decreased acuity, relative afferent pupil defect, often normal fundoscopy; requires complete neuro exam. ED role: MRI brain. Diagnose underlying cause. Often required admission for continued IV high dose steroids. 

Painful Vision Loss:

1. Acute angle glaucoma: sudden, usually form bright to dark environment (movie theater). Often with headache, N/V, and light sensitivity/halos. PE: midsize, nonreactive pupil. Must include tonometry, IOP>20! Risk factors: Asian, femaile, shallow anterior chamber. ED role: timolol  0.05% 1-2 drops (beta blocker, watch for systemic absorption SE) eye drops and brimonidine (alpha agonist) eye drops to reduce IOP. Miotic agent pilocarpine (2-4% 1-2 drops q15 m). Titrate until symptoms improve, IOP decreases. Systemic carbonic anhydrase inhibitors like acetazolamide 500 mg IV. Elevate head of bed. Treat nausea and headache, too! Urgent optho referral.

2. Corneal Ulcer: foreign body sensation, red eye. PE: injected conjunctiva, gray patch on cornea. Increased fluorescein uptake on Woods lamp. Possible hypopyon purulent collection. ED role: Evaluate for foreign body. Consider HSV keratitis. Start opthalmic antibiotic drops, must have pseudomonas coverage for contact lens wearers (tobramycin), consider antifungal. **Admit for IV ceftriaxone for suspected gonococcal infection. Will need optho evaluation and ulcer culture. 

cornealulcer.jpg
Corneal-Abrasion.jpg

3. Uveitis/Iritis: painful, progressing red eye worse with eye movement, +photophobia suggests anterior. Floaters suggests posterior, often no pain. Can be panuveitis. Causes can be inflammatory (HLA B-27 usually bilateral, eg. reactive arthritic, psoriasis, IBD, ankylosing spondylitis; sarcoid, Kawasaki), traumatic, infectious (toxoplasmosis, CMV, HSV, adeno, measles, mumps, TB, syphilis, Lyme), or secondary to medications(sulfa). PE: injected conjunctiva with ciliary flush (erythema around the iris). Sluggish, constricted, or irregular pupils. Slit lamp shows cloudy anterior chamber and "cell and flare." ED role: evaluate for underlying cause (STD screen, CXR for TB, etc.) and refer to optho urgently and appropriate f/u. 

I am certain that this is not a comprehensive list, so please - learn on!

Buzzword pearls to part with: 

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Not a we problem, an eye problem.

Here is a light visual sampling of eye pathology.

Pterygium:  no acute intervention, follow up pmd +/- opthomology, if impinging on pupil patient will require surgical removal of this benign growth.

Teardop pupil: indicates globe rupture and intraocular foreign body until proven otherwise,  protect globe from any external pressure with eye shield, reduce and prevent IOP elevation- elevate head of bed 30 degrees, analgesia, control hypertension, no valsalva maneuvers, prevent vomiting, EMERGENT optho OR

Hordeolum/Chalazion:  no acute intervention, warm packs, no antibiotics indicated, pcp follow up

Hyphema: blood in the anterior chamber can be traumatic or spontaneous only needs urgent ophthalmology follow up if up to the pupil. no ED intervention unless signs of intraocular infection then this is an emergency.

Hypopyon: sign of wide range pathology, can be secondary to trauma, perform woods lamp exam for ulceration, slit lamp exam look for uveitis, urgent opthomology follow up, if infectious etiology suspected systemic antibiotics,

Corneal abrasion: seen on woods lamp exam, raise suspicion for eyelid foreign body be sure to evert both eyelids,  flush eye with saline to remove small foreign body, if abrasion is overlying the pupil antibiotic and urgent ophthalmology follow up.  patient should not wear contacts on injured eye until healed

Dedritic ulceration:  Herpetic keratitis treat with po acyclovir or opthalmic antiviral, Urgent opthalmology follow up.

Corneal ulceration: ensure no sign perforation-seidel sign,  opthalmic antibiotics, urgent optho follow up, if patient wears contacts add coverage for Pseudomonas,  do not wear contacts until healed.

Seidel sign: vitreous flowing from site of globe perforation, emergent optho consult in the ER.  protect globe from any external pressure with eye shield, reduce and prevent IOP elevation- elevate head of bed 30 degrees, analgesia, control hypertension, no valsalva maneuvers, prevent vomiting,

Exopthalmos: if in setting of trauma with increased intraocular pressure perform lateral canthotomy,   suspect retrobulbar hematoma or orbital cellulitis,  CT scan emergent optho consult,

Corneal foreign body with rust ring: remove foerign body, urgent follow up for rust ring removal which should be done after 24 hours from initial injury, this is because reepithelialization makes removal easier.

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Pearl of the Day: Periorbital Infections

Periorbital Infections Periorbital Cellulitis - infection of eyelids and periocular tissues anterior to orbital septum - average age: 2 years; most patients < 10 years - spreads from local infection (e.g., conjunctivitis, dacryoadenitis, dacryocystitis, hordeolum), paranasal sinusitis, hematogenous spread from nasopharyngeal pathogens, upper respiratory tract infections - most common pathogens: S. pneumoniae, Streptococcus pyogenes, H. influenzae, Moraxella catarrhalis

Signs/Symptoms - erythematous, tender, swollen, warm eyelid and periorbital area - excessive tearing - no limitation in extraocular muscles, proptosis, pain with eye movement, normal visual acuity - may have difficulty opening eyelid

Management - may require CT scan of orbits to rule out orbital cellulitis - well-appearing, afebrile -> oral antibiotic therapy (e.g., amoxicillin-clavulanate, cephalexin) - severe periorbital cellulitis -> IV antibiotic therapy (e.g., ceftriaxone + vancomycin)

Blepharitis - inflammation of lid margins - anterior blepharitis: inflammation of eyelid where eyelashes attach, usually infectious in nature - posterior belpharitis: inflammation of inner portion of eyelid margin in contact with eye, usually due to dysfunction of meibomian gland - average age: 40 - 50 years - most common etiology: reaction to deltalike toxin from overgrowth of S. epidermidis - symptoms: conjunctival injection, crusting, pruritic eyelids, photophobia, occasionally eye pain - treatment: daily cleansing of edges of eyelids and eyelashes, warm compresses; severe cases require erythromycin or bacitracin-polymyxin ointment

Dacryocele - small bluish-hued palpable mass at nasolacrimal duct without conjunctival erythema or discharge - due to obstruction at valve of Hasner and common canaliculus - treatment: urgent referral to ENT or ophthalmology for possible marsupialization

Dacryoadenitis - inflammation of lacrimal gland - chronic dacryoadenitis is caused by noninfectious inflammatory disorders (e.g., Sjogren's, sarcoidosis, thyroid disesase) - acute dacryoadenitis is usually infectious (from EBV, mumps virus, coxsackievirus, CMV, VZV, S. aureus, streptococci, Neisseria gonorrhea, Chlamydia trachomatis, Brucella melitensis) - viral dacryoadenitis causes less intense discomfort and erythema - treatment: mild infections can be treated with oral first-generation cephalosporin (e.g., cephalexin) or trimethoprim/sulfamethoxazole if MRSA is suspected; severe infections require IV antibiotics (e.g., nafcillin, vancomycin)

Dacryocystitis - inflammation of lacrimal duct or sac usually caused from obstruction - common pathogens:  Streptococcus pneumoniae, staphylococci, Haemophilus influenzae - initial chronic mucopurulent discharge that progresses to erythema and swelling to inframedial eye - usually secondary bacterial infection following viral upper respiratory infection - diagnosis: applying gentle pressure with finger or cotton swab applied to nasolacrimal sac causes reflux of mucopurulent material (should be cultured) - if improperly treated, can lead to periorbital and orbital cellulitis - treatment: usually requires hospital admission with IV antibiotics (e.g., cefuroxime, cefazolin, clindamycin, +/- vancomycin)

Resources Tintinalli's Emergency Medicine, 8th Edition Periorbital Infections, Medscape, https://emedicine.medscape.com/article/798397-overview

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