Ocular Trauma, HA, Retinal Breaks Flashcards
Symptoms of corneal abrasion
pain, photophobia, tearing
Signs of corneal abrasion
corneal staining, without infiltration/opacification, injection, possible AC reaction
What does infiltration/opacification mean?
infectious process
What is an essential exam step with corneal abraison?
evert lids, consider double lid eversion with lid retraction
What are treatments of corneal abrasion?
antibiotic gtts/ung, cycloplegia, double pressure patch, bandange CL
When should you not pressure patch?
dirty wound: vegetative, fingernail, CL wearer
What pain meds can be given for corneal abrasion?
topical NSAIDs, oral opioids, gabapentin, Lyrica (pregabalin)
How can you debride for a corneal abrasion?
alger brush or golf spud
What are symptoms of foreign body?
FB sensation, pain, history
What are signs of foreign body?
FB, staining
What should you check with high velocity FB?
intraocular FB, double lid eversion, (-) seidel sign
What is treatment for foreign body?
remove FB with sped, needle, magnet, forceps… remove rust ring with alger brush then treat as corneal abrasion
What are signs of conjunctival laceration?
redness, with NaFl pooling in lacerated area
What is the treatment for conjunctival laceration?
push edges together with applicator and patch, laceration 5-7 mm or large may need suture
What investigation is warranted with intraorbital FB?
history of trauma, pupils, VA, seidel, CT imaging, OR consultation
ICD-10 for trauma
injury, how it happened, where it happened
With the injury code which character specifies the course of the disease?
7th character
What are the codes for the course of the disease in trauma coding?
A=initial D=subsequent S=sequelae/later recurrence
What is a primary headache?
that which cannot be attributed to known structural, toxic, or metabolic abnormalities
What are examples of primary headaches?
migraine, tension, cluster/trigeminal
What are secondary HA?
definable structural, toxic or metabolic abnormality causes the HA
What s/s indicate a secondary HA?
onset after 55 years, jaw/scalp/chewing pain, ONH swelling, fever, altered mental state, stiff neck, decreased vision, neurologic signs, pre-retinal hemes
What percent of HA are migraines?
up to 54%
What percent of the US is affected by migraines?
13%, 50% not diagnosed by medical provider
What gender has more migraines?
women, especially close to menstrual cycle
What is spreading depression associated with?
cortical vascular changes
Aura and migraine
classic has aura ~20%, no aura is common migraine
What are symptoms of migraine?
headache commonly localized to peri-orbital or retro-orbital region, may also have nausea, photophobia, phonophobia, rapid onset to peak time 20-60 mins
What is spreading depression?
wave of cortical excitation followed by wave of inhibition, commonly starting in the visual cortex
What is the vascular theory of migraine?
rapid constriction of cerebral arteries, secondary inflammation around vessels, release of chemotactic factors and inflammation around the brain = pain
Three pathophysiologies of migraines
neuropeptide release, pain signaling pathway, vessel dilation/contraction
What is neuropeptide release?
calcitonin gene-related peptide, vasoactive intestinal peptide, tx: inhibit the neuropeptide release
What is pain signaling pathway?
trigeminocervical complex-nociceptor signals to the thalamus
What is vessel dilation/contraction
vascular activity occurs, but may not actually play a direct role in migraine, dilation induced in non-migraineurs does not result in headache but does cause headache in migraineurs through peptide activation
What is ocular/retinal migraine?
affects only anterior visual pathways yielding monocular visual changes, possible vasospasm in retinal or posterior ciliary circulation resulting in ischemia to retina, choroid, ONH
What may be noted during ocular migrain attack?
arterial attenuations and subsequent arterial occlusions
What are the most common causes of TIA that must be excluded to yield diagnosis of ocular migraine?
embolus, vascular disease
What is the international headache society classification of ocular migraine?
at least 2 attacks, fully reversible monocular visual phenomena, HA begins during visual symptoms or within 60 mins, normal eye exam between attacks, no other disorder
Aura in the absence of HA are called
acephalgic migraines or typical aura without headache
Diseases that have been associated with misdiagnosis of retinal migraine
CRAO, CRVO, cilioretinal artery occlusion, focal retinal ischemia, ischemic optic neuropathy, optic atrophy
What is aura
scintillation building in intensity across the visual field, flurry of symptoms common
What is the most common HA?
tension 90%
What gender has more tension HA?
women
What are tension HAs?
unilateral or bilateral tightness or aching in frontal temporal and occipital regions, commonly features associated neck symptoms, abnormalities in sleep may result
When do tension HAs usually start?
between 4-8 am or 4-8 pm
What are cluster HA?
clusters of severe pain with remission periods, severe unilateral pain for 45-60 minutes, onset to peak is seconds, occur for 8-12 weeks with remission for 12-18 months
When do cluster HAs occur?
often at onset of sleep, symptoms peak in spring and fall
Who is affected by cluster HA?
men 20s-30s
How is cluster HA pain described?
unilateral retro-orbital to temporal, deep burning or boring, trigeminal autonomic symptoms may occur
What are trigeminal autonomic symptoms of cluster HA?
lacrimation, rhinorrhea ptosis, pupil constriction, facial flushing, conjunctival injection
What is WWOP?
gray/white appearance of peripheral retina, sharp demarcation from adjacent normal retinal, possible vitreoretinal interface
What is happening at a abnormal vitreoretinal interface?
hyper-reflectance of ellipsoid portion of photoreceptor inner segments
What is lattice degeneration?
8% of population, found midway between ora serrata and equator, thinning of inner retinal layers
What retinal layers are affected with lattice?
abnormal pigmentation/RPE hyperplasia with yellow/white surface flecks, associated vessels become attenuated and sheathed, loss of inner retinal layers down to outer nuclear layer with associated vitreous liquefaction
Where is a strong vitreal adhesion?
at the edge of lattice
What percent of lattice is associated with atrophic retinal holes?
25-35%
What percent of lattice is related to tractional retinal tears?
1%
What is snailtrack degeration?
degeneration of the neural elements of retina leading to an atrophy of the tissues with lipid deposits in the internal retinal layers, sharply demarcated, at or near equator
What is snailtracking made of?
microglial cells containing lipoproteins on the surface
Does snail tracking have a stronger or weaker vitreous traction than lattice?
weaker, less risk of retinal trauma
What are atrophic retinal holes?
a break in the retina not associated with traction forces, rather progressive retinal thinning, creases potetntial for liquified vitreous to invade and yield RD
What percent of the population has atrophic retinal holes
2-3% … 20% likelihood of presence in fellow eye
What is the red base in an atrophic retinal hole?
RPE-choroid showing
What surrounds an atrophic retinal hole?
often surrounded by cuff of intra-retinal edema or sub-clinical RD, pigment surrounding hole indicates it has been present 3+ months, this is reactive RPE hyperplasia
What possible causes atrophic holes?
focal vascular compromise
What are operculated holes?
vitreoretinal traction pulls a plug or operculum of retinal tissue away yielding a retinal hole, red area with overlying retinal floater that looks smaller than the hole
What is intrabasal
within vitreous bases, may be due to traction from lens zonules and are lower risk for RD because they are within strong adhesions of vitreous base
What is juxtabasal?
next to vitreous base and higher risk of RD when there’s a PVD because the cause is the VR traction
What amount of fluid with a hole should be referred?
> 2DD, symptomatic, aphakic or past Hx of hole consider phtocoagulation
What is retinoschisis?
splitting of internal layers of sensory retina, commonly bilateral and inferotemporal, usually asymptomatic
What is flat vs bullous retinoschisis?
flat: split occurs at outer plexiform layer, bullos: split occurs anterior to OPL leaving a very thin inner wall
How to distinguish retinoschisis from retinal detachment
schisis will not move with eye movement and when illuminated, schisis has honeycomb appearance
What is rhegmatogenous retinal detachment?
included retinal break, commonly starts as PVD yielding traction from vitrous at peripheral retina causing tear… leads to separation between photoreceptors and sensory retina
What is non-rhegmatogenous (traction/serous) detachment?
disease yielding tractional entities such as PDR allowing tension on retina giving away to RD, disease where fluid/hemorrhage develops between sensory retina and RPE
What are s/s of retinal detachment?
flashes and floaters, APD, reduced IOP, iritis, opaque or corrugated retina
Why do flashes occur?
retina moving resulting in stimulation of photoreceptors, phosphene effect
What is a greater emergency, macular on or off?
ON
What are signs an RD has been there for awhile?
pigmented demarcation line, taut surface of RD thinned retina, intraretinal exudates, intraretinal cysts and fixed retinal folds
What are preventative medications for migraine?
NSAIDs, TCAs, beta blockers, anti-depressants, botox
What medication are abortive for HA?
pain relievers, ergotamine and triptans
Retinotomy
incision to remove fluid from beneath the retinal detachment
pneumatic retinopexy
gas bubble placed in eye to place pressure against detachment area
cryo/photocoagulation
induce scars to seal edges of RD down
vitrectomy
removal of vitrous to relieve traction
fluid-gas exchange
outpatient fluid-gas exchange is a treatment option for patients suffering from post vitrectomy retinal detachment
scleral buckle
band around peripheral retina to relieve tension w/ elongation of axial lengs
Common adverse effect of RD surgery?
cataract
Ophthalmia nodosa
name for the nodular granulomatous inflammation reaction of the palpebral or bulbar conjunctiva to hair
What is management of ophthalmia nodosa?
ocular lubricants, topical steroids, removal of hairs if possible, surgical intervention if localized intense inflammation response
Caring for the patient with autism
social stories, describe what you are goin to do, distractors
