General Ophthalmology

Script for eye examination and eye diseases

based on the chapter "Disorders of the Eye" from Harrison's Principles of Intern
al Medicine (17th edition)
Sebastian Kuepper
skuepper@uni-muenster.de
Content
Anatomy of the Eye General Eye Examination 3 5
Symptoms: red and painful eye corneal abrasion .................................
........ 8 .................................................. ..................
............ 8 subconjunctival hemorrhage ................. ....................
.............................. ............................. 8 .................
.. Blepharitis .................................................. ..............
.................................... ........ ..................................
...... 9 Dakrozystitis .................................................. 9 ....
............................. ............... conjunctivitis ...................
............................... ................................................
.. ...... .......................................... 10 Keratitis ..............
.................................... ..................................... 11 ..
........ herpes simplex .................................................. .....
............................................. ........ .........................
.............. 12 Herpes Zoster ................................................
.. ............................... 12 ................. uveitis ................
.................................. .............................................
..... .............. 13 acute angle-closure glaucoma ...........................
...... .................................................. Endophthalmitis ......
......... 13 ................................. .................................
................. ................................. 14 symptom: acute visual dis
turbance 15 Amaurosis fugax and Zentralarterienverschluss ....... ..............
.................................... .......... 15 anterior ischemic optic neuro
pathy (AION )................................. Optic neuritis ..................
............. 16 ................. .............................................
..... .................................................. .16 toxic optic neuropa
thy .............................................. .............................
..................... .17 papilledema ..........................................
..... .................................................. .................... 17
............................ vitreous detachment ..............................
.................... ............................... 17 ................. retina
l detachment .................................................. ................
.............................. 18 migraine with aura ...........................
....................... .................................................. strok
e and TIA ............... 18 ............................... ...................
............................... ............................. 18 symptom: chroni
c vision impairment 19 cataract (cataract ).......... ..........................
........................ ............................................... 19 glau
coma. .................................................. .......................
........................... ........................... 20 age-related macular d
egeneration (AMD )................. ............................................
...... ....... ........................................ 21 diabetic retinopathy
.................................................. Retinitis pigmentosa ........
.......................... ............. 22 ....................................
.............. melanoma and other tumors, 23 .......................... ........
........... .................................................. .................
........ 23 symptom: movement of the eyeball 24 endocrine ophthalmopathy .......
........ .................................................. ....................
.................... 24 pseudotumor orbit ....... ..............................
.................... .................................................. Horner's
 Syndrome ............................................ .. 25 ...................
............................... ...................... 25 symptom: drooping eyel
id ptosis congenita .................... 26 ....................................
.............. .............................................. 26 myogenic ptosis
. .................................................. ...........................
....................... ................ 26 neurogenic ptosis ..................
............. .................................................. ...............
................... 26 symptoms: double vision, motility disorders and nystagmus
27 myasthenia gravis ..... .................................................. .
................................................. 27 N. ........ oculomotor (thi
rd cranial nerve )............................................ .........N. .....
................................... 27 trochlear (cranial nerve IV )............
................................ ...............................................
... 28 ..... N. abducens (cranial nerve VI )....................................
........ .................................................. Strabismus .........
................................. ...... 29 ....................................
.............. ................................ 29 ................ nystagmus ..
................................................ ...............................
................... Literature ........ 30 31
2
ANATOMY
Structure of the eye
OF
EYE EYE
The visual system consists of eyeball, annex parts (lids, lacrimal apparatus, co
njunctiva), and visual pathway. The globe (eyeball) is composed of functionally
● ●
Refractive (cornea, lens, vitreous) and perceiving light units (retina).
The eyeball is surrounded by a three-layer wall. From outside to inside:
●
Tunica fibrosa:
○ ○
Sclera (sclera): design and resistance. Cornea (cornea) with a refraction lens d
iopters from 43rd Iris (Iris): optical aperture for the regulation of light. Cil
iary body (ciliary body): accommodation, suspension of the lens, the production
of aqueous humor. Choroid (choroidal) blood supply to the outer layer of the ret
ina. Pars caeca (stratum pigmentosum): Light filters and metabolism. Pars optica
(Str and Str pigmentosum nervosum): pay the photoreceptors.
Sclera choroid
●
Tunica vasculosa (= uvea):
○ ○ ○
●
Tunica interna (= retina): Conversion to optical neural signals.
○ ○
Schlemm canal Irisfortsätze Zonulafasern cornea iris pupil
anterior chamber, posterior chamber
Ciliary body, retina, vitreous, optic nerve Figure 1: Schematic cross section th
rough the eye.
Source: Wikipedia.de http://de.wikipedia.org/wiki/Bild:Eye_scheme.svg ()
Lens
3
The interior of the eye is divided into three functionally and anatomically sepa
rate rooms:
● ● ●
anterior chamber, posterior chamber and vitreous.
Anterior and posterior chamber containing the aqueous humor (nutrition of the le
ns and cornea, immune functions), which is formed in the posterior chamber by ci
liary body, passes through the pupil opening in the anterior chamber and from th
ere through the Schlemm's canal into the venous system. Through a balance of aqu
eous humor production and absorption is usually a constant intraocular pressure
of 12 will receive up to 20 mmHg upright. The vitreous is 98% water and is used
for light refraction (dpt 1.33). Visual pathway first Neuron: sensory cells of t
he retina (rods and cones). 2nd Neuron: bipolar cells. 3rd Neuron: ganglion cell
s, with their projections to the N. Optic (CN II) form. About optic chiasm and o
ptic tract to the geniculate body (Latin thalamus), where the results for the fo
urth Neuron is then over optic radiation to the visual cortex. Accommodation To
both distant and near objects can be reproduced sharply, then the refractive pow
er of the eye are adjusted accordingly. For this purpose the lens is distorted.
● ●
Distant view: By train the zonules (relaxed ciliary muscle), the lens is stretch
ed to an ellipse. The refractive power decreases. Nahblick: By discharge of zonu
le (ciliary muscle tense, parasympathetic fibers of the oculomotor nerve [III. C
N]) is the lens of their own elasticity and is replaced by a more "spherical" sh
ape. The refractive power increases (= accommodation).
Pupillary reflex goal: Constant light by adjusting the pupil size (part of the a
daptation).
●
Afferents: Retina → N. → Optic chiasm → Tr. opticus. Before the Latin corpus gen
release of fibers to praetectalis Area. Redirecting to Edinger-Westphal nuclei
on both sides (allows Isokorie and consensual light reaction). parasympathetic e
fference: Edinger-Westphal nucleus → N. oculomotor (III) → Ciliary ganglion → Nn
. short ciliary → M. pupil sphincter. sympathetic efference: hypothalamus, medul
la oblongata → → → sympathetic ganglion superior cervical ganglion → internal ca
rotid artery / A. ophthalmic (accompanying nerve plexus) → N. ciliary longi → pu
pil dilator.
● ●
Fremdreflex corneal reflex to protect the eye from drying out and debris by eyel
id closure.
● ●
Afferents: N. ophthalmicus (branch of trigeminal nerve V) Red nucleus → → → brai
nstem reticular formation (facial nucleus). Efference: N. facialis (CN VII) → M.
orbicularis oculi.
When strong light is also on the afferent nerve Optic (CN II).
4
GENERAL EYE EXAMINATION EYE EXAMINATION
Case history
● ● ● ● ●
Updated: red eye, pain (stabbing, dull, or eye movement), visual disturbance (ac
ute or chronic), double vision, injury? One or both sides? Eye History: glasses,
amblyopia, strabismus, surgery,€Trauma? Past history: if a general disease with
ocular involvement in such Diabetes mellitus, hypertension, infection, rheumati
c disease? Drugs History: e.g. Cortisone, Resochin, amiodarone, chlorpromazine?
Family history: refractive errors, strabismus, cataract, glaucoma, retinal detac
hment?
Visusprüfung The resolving power of the sound eye is an arc minute. For the diag
nosis of visual loss should first be ruled out a refraction. As a quick test, th
e "stenopaic gap" (a kind of punch cards are used): If the visual acuity improve
s as seen through the 2 mm pinhole, a refractive error is likely. A correction i
s done with plus glasses for hyperopia (farsightedness, the eyeball is too short
), with minus lenses in myopia (nearsightedness, the eyeball is too long). The m
easured and corrected visual acuity is known as "cum correctione visual acuity (
corrected visual acuity) called. The determination of visual acuity is carried o
ut separately for each eye. The exact test of visual acuity with refraction is d
one by the specialist. Orienting to the visual acuity with the Snellen table (6
m spacing) or the Rosenbaum card for the coat pocket (36 cm) can be determined.
The patient indicates which row he made six meters away (or 36 cm distance in th
e Rosenbaum card) can not read just yet. Visual acuity can then be read from the
table.
Myopia, hyperopia Snellen T-t ation
Figure 2: refractive errors and their correction. Snellen table for determinatio
n of visual acuity.
Source: Wikipedia.de (http://de.wikipedia.org/wiki/Bild:Myopia.svg, ... / Image:
Hypermetropia.svg, ... / Image: Snellen06.png)
Where: visual acuity =
Istentfernung Sollentfernung
Normal:
6 20 = 1.0 and (when given in ft). 6 20
If the visual acuity even after correction <1.0, this must be further clarified.
With a visual acuity below 5 / 50, the "counting fingers" at 1 m (possibly 30 c
m), with even poorer vision "hand movements" and finally "light a torch - the di
rection of recognized" documented.
Blindness is in visual acuity ≤ 0.02 or restriction of the visual field to ≤ 5 d
egrees.
5
The review of diagnostic pupillary pupillary reflex is one of them to any physic
al examination. They are being guided information on the functions of retina, N.
optic (II), midbrain and nerve oculomotor (III). A normal result does, however,
a partial damage of individual structures is not enough.
● ● ●
Miosis (small pupil): light, parasympathetic tone (sleep, fatigue, narcosis), op
ioids, Naheinstellungsreaktion (Konvergenzmiosis), Horner's syndrome. Mydriasis
(dilated pupil): dark, sympathetic (fear, joy, surprise: making "big eyes"), ocu
lomotor palsy, medications. Anisocoria (unequal dilated pupils): Note to efferen
t pupil defect, eg central paralysis, mass, intracranial pressure, head injury,
in various syndromes (eg, Adie's syndrome) but also idiopathic.
direct light reaction
Both eyes of the patient are covered. If one eye be released, the pupil narrows
to about 0.2 s (miosis) because of the incident light.
consensual (indirect) light reaction
By placing the edge of the hand to the nose of the patients examined eye is shie
lded from direct light. The other eye is now illuminated. The shielded, non-illu
minated pupil should constrict it too. A blinded eye shows no reaction in direct
lighting (amaurotic pupil). The consensual reaction to light when illuminated t
he healthy eye will remain.
"Swinging-flashlight test"
Used in diagnosis of discrete unilateral disorders of retinal or optic nerve. Ca
n e.g. be with retrobulbar neuritis and other optic neuropathies, the only refer
ence. If only a partial injury before the sensory structures, ranging mostly fro
m the residual function to allow a direct reaction to light. Only in (side) comp
arison of the pupils can have the disorder may be clinically apparent. These two
eyes are alternately with the same distance, lit the same time and same intensi
ty of light slanting down. Observed, the initial constriction and subsequent dil
ation of the pupil. A pathological finding, also known as "Marcus-Gunn pupil" me
ans (a relative afferent pupillary defect). Motilitätsprüfung patient is asked t
o follow an object with the eyes (eg, pen tip). In the nine main areas are exami
ned:
right top right bottom right top left top left bottom left straight down
Visual field testing (confrontation test) doctor and patient sit facing the same
amount. Both cover the opposite eye. The doctor takes an object from the outsid
e to the center line (all four quadrants).€In normal vision can see both the obj
ect simultaneously.
6
Direct ophthalmoscopy With direct ophthalmoscopy see an upright, 16 times magnif
ied image of the retina. This one goes with the electric ophthalmoscope as close
as possible to the patient's eye. It may not accommodate the examiner. One shou
ld recognize optic disc (where light reflected from temporal), and mean macular
periphery. The papilla (optic nerve head, outlet of artery and vein centralis, "
blind spot") is extremely sharp, vital colored (yellow-orange), in the retinal l
evel and possibly has a central depression (excavation).
1
2
The vessel caliber money Arte Source: National Eye Institute, National Institute
s of Health rie: vein is 2:3, spontaneous venous pulsation in the arterial pulse
Ggs. to normal. At intersections, the vessels are not constricted. The macula l
utea ("yellow spot") with the avascular fovea centralis has the greatest density
of photoreceptors and is the point of sharpest vision.
Figure 3: Fundus. (1) papilla, and V. A. centralis. (2) fovea centralis of the m
acula lutea.
papillae important pathological findings
● ● ●
fuzzy boundary (edge blurring): papilledema. Paleness: e.g. with optic atrophy.
enlarged cupping: glaucoma.
Assessment of intraocular pressure is with both index fingers probed with closed
eyes, the upper eyelid. The important thing is the page comparison. Palpation i
s only a stone-hard globe in acute angle-closure glaucoma is not detected a slig
ht increase in pressure would not. The tonometrische measurement of intraocular
pressure is performed by an ophthalmologist. There are various methods, most of
the Goldmann tonometer is used. Is a physiological intraocular pressure of 10 mm
Hg to 21. Slit lamp examination and gonioscopy with the slit lamp to lens, corne
a and anterior chamber can be assessed. The non-direct vision chamber angle can
be evaluated by the glaucoma diagnosis with the gonioscopy. Both studies will be
conducted by an ophthalmologist.
7
Symptom:
General
RED AND PAINFUL
EYE EYE
The symptoms "red eye" and "pain" may have a number of causes that need to be cl
arified by differential diagnosis. Grob are: for glaucoma, inflammation, hemorrh
age, trauma, and mechanical irritation. It is important to ask about side effect
s. A palpable hard eye can continue to think of a reaction-free pupil must glauc
oma (emergency, cause blindness!). In conjunctival injection, glued eyes in the
morning and secretion conjunctivitis is likely. A red eye without side effects c
an be with the appropriate local findings and medical history (such as heavy lif
ting, exertion, warfarin-dosing) on a bruising back.
Erosion
General
CORNEA
A corneal abrasion of the cornea is as erosion (English corneal abrasion refers)
. It is the result of a violation (eg, fingernail, branches), or foreign objects
from the left vertical scratches on the cornea. Strong clinical pain, tearing (
epiphora), foreign body sensation, blepharospasm, eyelid swelling and conjunctiv
al injection. Diagnosis of corneal staining with fluorescein, an epithelial defe
ct in the blue light is then visible. Always looking for a foreign body (eversio
n of the upper and lower eyelid)! Antibiotic ointment therapy union or hospitali
zation for recurrent erosion. The prognosis is good, it usually comes within a f
ew days for healing.
Subconjunctival
Hemorrhage hemorrhage
General A subconjunctival hemorrhage (syn. Hyposphagma) from rupture of small bl
ood vessels occurs either spontaneously (especially the elderly), trauma (histor
y), or by coughing, straining, bending, etc. before. Extensive clinical bleeding
under the conjunctiva, even with impressive local findings mostly harmless. Vis
ual acuity is not affected. Spontaneous regression therapy within two weeks. Whe
n thinking of recurrent hypertension or coagulation disorders!
8
Blepharitis
General An inflammation of the eyelid is known as blepharitis. Common causes: se
borrheic dermatitis (blepharitis squamosa) are, barley grain (Hordeolum, painful
bacterial infection of Zeis or Moll's glands) and Hailstone (chalazion, painles
s Chronic-granulomatous inflammation of the meibomian gland). Think For refracto
ry lesions in basal cell carcinoma or squamous cell carcinoma! Clinic
● ● ●
Blepharitis squamosa: low inflamed eyelid margins, scales, glued eyelashes, ofte
n accompanying chronic conjunctivitis. Hordeolum: painful nodules, pus central p
oint, the cause: often S. aureus. Chalazion: painless, coarse nodes.
Therapy
● ● ●
Blepharitis squamosa: warm compresses, strict hygiene, topical antibiotics. Good
prognosis, but often lengthy process. Hordeolum: antibiotic ointment, dry heat
(red light). Fast cure. Chalazion: Injection of corticosteroids, but are general
ly operative incision necessary.
DAKROZYSTITIS
General The most common disease of the lacrimal organs is the inflammation of th
e lacrimal sac (Dakrozystitis), mostly due to nasolacrimal outflow obstruction o
f the duct. Clinic
●
acute Dakrozystitis: highly flammable (pressure), painful swelling. Under pressu
re to drain pus. Pathogens are usually staphylococci, pneumococci and Pseudomona
s. chronic Dakrozystitis: epiphora, often lack signs of inflammation. Occurrence
in the context of Wegener's granulomatosis, and chronic. Nasenschleimhautentz.
●
After diagnosis of the acute symptoms: Rö. contrast for the representation of th
e outflow obstruction and surgical planning. Therapy
●
Dakrozystitis acute: acute: targeted antibiotic therapy (local and systemic), di
sinfecting envelopes, with abscess: incision. Later: most OP, e.g. nasolacrimal
by Toti: creation of a direct connection between the lacrimal sac and nasal muco
sa, bypassing the bile duct. chronic Dakrozystitis: Surgery after Toti or sac-ex
tirpation.
●
9
Conjunctivitis
General The most common cause of a "red eye", the conjunctival inflammation (con
junctivitis) is. This results in vasodilation, cellular infiltration and exudati
on. Pain is usually only minimally present, visual acuity is hardly restricted.
Differences are infectious (bacterial, viral, parasitic, mycotic) and non-infect
ious forms. Red Eye Clinic, sticky eyelids, eyelid swelling, foreign body sensat
ion, eyes burning. Possibly. Photophobia, and epiphora. In an allergic cause sev
ere itching is likely a blepharospasm suggests corneal involvement (keratoconjun
ctivitis). Diagnostic slit lamp (extent of vascular injection, nature of secreti
on, conjunctival swelling), Evert (follicle? Papillae? Foreign?), Smear (diagnos
tic agent) and Epithelabstrich (Ausstrichzytologie limit for the differential).
DD-conjunctivitis of the individual forms
●
infectious conjunctivitis:
○ ○
viral (most adenoviruses): watery discharge, epiphora and LK-swelling. In the Au
sstrichzytologie: lymphocytes and monocytes. bacteria (many poss. pathogen): pur
ulent discharge, hyperemia and conjunctival swelling (chemosis) are at the foref
ront. Granulocytes and bacteria in the Ausstrichzytologie. Chlamydia D-K: mucopu
rulent secretion, follicles in the tarsal conjunctiva. In the Ausstrichzytologie
: intracellular inclusion bodies. (The A-C, the chlamydia cause us not occurring
trachoma: in tropical countries leading cause of blindness!) Allergic conjuncti
vitis: viscous secretions, itching and papillae of the conjunctiva (cobblestone)
are typical. Eosinophils in the smear. Often, as part of "hay fever" (rhinoconj
unctivitis) or by triggering contact lenses (Riesenpapillenkonjunktivitis). nons
pecific conjunctivitis: caused by external stimuli or dry eye (keratoconjunctivi
tis sicca, such as Sjogren's syndrome. diagnosis: including the Schirmer test. C
omplete: corneal ulcer). Most foreign body sensation and epiphora.
○
●
non-infectious conjunctivitis:
○
○
Therapy
● ● ● ● ●
Viral: symptomatic with cool compresses. Prevention through hygiene (eg, no comm
on towels to use, do not rub the eyes). bacteria: antibiotic-containing ointment
, possibly in combination with cortisone (leads to faster relief, but only under
strict control). Chlamydia: tetracycline eye drops or ointment (4-6 wk). Danger
of "ping-pong infection, therefore mitbehandeln partner. allergy: desensitizati
on, possibly corticosteroid eye drops. non-specific: avoid artificial tears, the
triggering stimulus.
10
Keratitis
General In the investigation of the superficial cornea (keratoconjunctivitis) an
d deeper, ulcerative inflammation to be distinguished. The latter cause vision p
roblems due to possible scarring, opacity or perforation of the cornea and provi
de an ophthalmic emergency dar. The cause can be identified infectious and non-i
nfectious forms. Clinic
●
Infectious keratitis:
○
bacteria (90% of cases): purulent discharge, pain, photophobia, reduced visual a
cuity, epiphora, hypopyon (pus in the lower anterior chamber). Pathogens are v.a
. Staphylococci, pneumococci, Pseudomonas and Moraxella.
Hazardous-onset form is the ulcer serpens with rapid progression (a few hours!)
And intraocular involvement. Can lead to loss of the eye.
○ ○ ○ ●
Viral: watery discharge, often severe pain (especially in herpes simplex). Mycot
ic: slight discomfort.€Pathogen: Aspergillus and Candida albicans. Protozoa: sev
ere pain, photophobia, epiphora. Mostly in contact lens wearers (Acanthamoeba).
non-infectious keratitis: risk of erosion in the course of superinfection → → →
ulcer perforation. Among the non-infectious keratitis includes Superficial punct
ate keratitis (corneal punctate lesions due to wetting), keratitis sicca (dry ey
e), keratitis incomplete eyelid closure (eg facial paralysis) and keratitis neur
oparalytica (paralysis of the ophthalmic nerve, by loss of sensation of the corn
ea with reduced blinking frequency).
Rapid diagnosis diagnosis and treatment are crucial. Using slit lamp may epithel
ial, turbidity, cell and possibly pus are shown in the anterior chamber. Swabs f
or the detection of pathogens and resistance testing to perform! Therapy
●
bacteria: local antibiotics (broad spectrum are known to agents and resistance),
with hypopyon (anterior chamber involvement) shows therapeutic mydriasis of iri
s and ciliary body to immobilize ("Zykloplegie"). In advancing ulcer hospitaliza
tion. If necessary. OP (coverage of large epithelial defects with conjunctiva, c
ornea transplantation in perforated ulcer). Viral: local Antivirals for system w
ith varicella zoster (zoster ophthalmicus) possibly. Mycotic: local antifungal a
gents (for intraocular involvement systemic), if necessary, surgery. Acanthamoeb
a: Propamidin local, antibiotic eye drops and Zykloplegie. non-infectious: if po
ssible, treat the cause, artificial tears, infection prophylaxis. When paralysis
/ paresis possibly OP: lateral Lidvernähung (tarsorrhaphy).
● ● ● ●
11
HERPES
General
SIMPLEX
A primary infection with herpes simplex (usually Type I) runs on the eye as conj
unctivitis and blepharitis. An HSV keratitis is always a secondary infection (re
lapse by virus persistence in the ganglion gasseri), which can also lead to corn
eal ulcer. A primary infection can easily be confused with an adenovirus conjunc
tivitis, if the characteristic periocular vesicles (vesicles do not occur). Dend
ritic branching corneal epithelial lesions are pathognomonic for a secondary inf
ection. Clinic Very painful eye, photophobia, eyelid swelling, epiphora. Dependi
ng on the location and possible visual loss. Forms of HSV keratitis
● ● ●
Dendritica keratitis: epithelial branching tree-like, characteristic of HSV recu
rrence, repealed corneal sensitivity. Keratitis disciformis: central corneal dis
c. Vascularization, and iridocyclitis possible (especially if recurrent). endoth
elial keratitis: caused by viruses in the aqueous humor. Swelling of endothelial
cells, corneal opacity. In chamber angle involvement: sec. Glaucoma.
Diagnostic slit lamp, Fluoreszinfärbung shows corneal lesions. Topical antiviral
therapy agents (eg Trifluridin, acyclovir). In K. disciformis and intraocular i
nvolvement and systemic acyclovir. Cortisone is contraindicated in Hornhautläsio
n allowed with intact epithelium against. Cortisone prevents scarring, but it in
creases the risk for secondary glaucoma, corneal and prolonged course.
HERPES
General
Zoster
As with herpes simplex may occur in the varicella-zoster virus to an endogenous
relapse. To an eye involvement (zoster keratitis), it comes when the first Trige
minal branch (ophthalmic nerve) is concerned. Clinically, it shows an ocular inv
olvement by Hutchinson's sign: skin sores to go nose → N. nasociliaris affected
(including the inside of the eye care). Painful vesicular dermatitis clinic, lim
ited to one dermatome. Red eye, decreased sensitivity of the cornea. The corneal
lesions may resemble HSV keratitis. Later: anterior uveitis, secondary glaucoma
, scarring and neuralgia possible. Local therapy: acyclovir (mostly additional s
ystemic administration for the treatment of dermatitis). With intact epithelium
and cortisone allowed (see HSV keratitis).
12
Uveitis
General Depending on the affected section, we distinguish anterior uveitis (irit
is), uveitis intermedia (Zyklitis) and posterior uveitis (choroiditis). Mixed fo
rms are iridocyclitis and panuveitis. Clinic
●
Iridocyclitis: dull pain, visual loss, photophobia, Reizmiosis, epiphora, or mix
ed ciliary injection (conjunctiva is involved). Even chronic course possible. Ch
oroiditis: no pain, since choroid does not contain sensitive nerves. Visual loss
, visual disturbances (veil).
●
In contrast to iridocyclitis with glaucoma the anterior chamber of normal depth
and the pupil is narrow (Reizmiosis). Etiology and pathogenesis of uveitis is of
ten an immunological one (system) underlying disease, eg Ankylosing spondylitis,
M. Reiter, Crohn's disease, psoriasis (all HLA-B27-associated), sarcoidosis,€rh
eumatoid arthritis or Behçet M.. Acute anterior uveitis may also be infectious t
o conditions (rare), eg in herpes infection, syphilis, tuberculosis and leprosy.
A choroiditis may also be infectious due, for example, Cytomegalovirus (CMV), s
yphilis, brucellosis and toxoplasmosis. Diagnosis
●
Iridocyclitis: slit-lamp examination showed Tyndall phenomenon (protein accumula
tion and cellular infiltration of the anterior chamber → visual loss), and corne
al edema. Choroiditis: ophthalmoscopy shows whitish, ill-defined foci.
●
Therapy
●
Iridocyclitis: It is important to avoid synechiae (adhesions of the iris and len
s and iris and cornea): therapeutic mydriasis and steroid therapy.
In systemic erregerbedingter I.: antibiotic or antiviral therapy (if any).
●
Choroiditis: depending on the cause, steroids or antibiotics (local and systemic
).
ACUTE
ANGLE BLOCK BLOCK ANGLE GLAUCOMA GLAUCOMA
Rather rare and often misdiagnosed general cause of a red, painful eye. Suscepti
ble patients with flat anterior chamber (for example, are due to short bulb with
hyperopia or large pupil during cataract). A sudden blockage of aqueous outflow
, there is a paroxysmal increase in intraocular pressure to a multiple of the st
andard. Emergency, as threatened blindness in the affected eye!
13
Clinic
●
general: acute pain (possibly by projection misinterpreted as headache), nausea
and vomiting (by stimulation of the vagus). General symptoms can be so much in t
he foreground, that is first thought of appendicitis or brain tumor. Eye: mixed
injection, corneal edema, eye dull, flat anterior chamber entrundete, reactionle
ss pupil, rock hard eyeball, severe visual loss is (may not notice, because the
healthy eye laminated).
●
Diagnostic triad of red eye, pupil-free reaction on palpation and hard eyeball.
Treatment goals are the reduction in pressure within 6 hours, pain relief and cl
earing up of the cornea (the causal surgical treatment to enable).
●
drugs: osmotic reduction of vitreous volume (mannitol iv, glycerol oral), reduci
ng aqueous production (carbonic anhydrase inhibitors: acetazolamide iv; local be
ta-blockers, eg timolol) and extract the iris from the anterior chamber angle (l
ocal miotics: pilocarpine 1%). Mechanical: dent of the cornea with a glass rod (
aqueous pressed in the periphery, thereby opening the chamber angle). operativel
y: shunt between the front and back room, for example, Laser iridotomy.
● ●
Endophthalmitis
General After perforating trauma or endogenous infection via hematogenous spread
of pathogens (bacteria, viruses, fungi). Risk are v.a. chronically ill, immunos
uppressed or diabetic patients. It threatens the loss of the eye (within hours!)
. Hospital Deep, dull pain in the eye, acute visual loss, severe redness. Typica
l clinical history and diagnosis. Slit lamp: mixed injection, hypopyon. Ophthalm
oscopy: yellowish discoloration vitreous, whitish spots with hemorrhagic retinal
edge, possibly retinal detachment. Think For intravenous drug users and patient
s with indwelling catheter-visual defect on Candida endophthalmitis! Pathogen-sp
ecific antibiotic therapy (systemic, local and intravitreal). The course is vari
able.
14
Symptom:
General
ACUTE
Visual disorder visual disorder
The sudden loss of vision is always an emergency, even if it lasts only a few se
conds. differences have to be visual disturbances, emanating primarily from the
eye (eg, retinal detachment, Zentralarterienverschluss), and those who have a ne
urological cause (eg, cerebrovascular disease, migraine). Differential diagnosis
, the distinction is important in:
●
painless visual disturbance: for example at Zentralarterienverschluss, temporal
arteritis, retinal detachment, acute ischemic optic neuropathy, retrobulbar neur
itis, vitreous detachment. painful visual disturbance (often with "red eye"): ac
ute angle-closure glaucoma, acute iritis, verblitzung (photoelectrica keratitis)
, corneal ulcer, trauma.
●
Moreover, can be symptoms of groundbreaking diagnostic (eg, hard eyeball in glau
coma attack, Rußregen and black curtain to see in retinal detachment).
Amaurosis
General
Fugax AND
ZENTRALARTERIENVERSCHLUSS ZENTRALARTERIENVERSCHLUSS
Blindness in one eye by ischemia of the retina, eg in embolism of ipsilateral in
ternal carotid artery. When it comes to amaurosis fugax dissolution or washing o
ut of the embolus for full recovery of visual acuity within a short time. In con
trast, there is persistent occlusion after about an hour to irreversible retina
damage (infarction) with blindness in the affected eye. Rapid painless unilatera
l visual loss clinic ("falling curtain", "lights out") at Zentralarterienverschl
uss.€Visual loss or visual field loss when only one branch is affected. The dire
ct pupillary reflex is abolished. Ophthalmoscopy Diagnosis:
● ●
Amaurosis fugax: inconspicuous ophthalmoscopic findings. Zentralarterienverschlu
ss (infarction): narrow vessels, gray-white retina (edema). Only the fovea centr
alis appears as cherry stain.
Bulbusmassage therapy to flush the embolus in a peripheral retinal vessel. Hemod
ilution to improve blood flow. The prognosis is unfavorable, with complete Zentr
alarterienverschluss is the blindness of the eye to prevent almost never. Lysis
is due to the possible side effects and the low likelihood of success usually no
t carried out. More important is the search for the source of embolism (eg atria
l fibrillation), for example to prevent a stroke.
15
Anterior ischemic
Optic neuropathy (AION), optic neuropathy
General Acute ischemia of the optic disc, arteriosclerotic, or (rarely) arteriti
c due. The latter occurs as a complication of temporal arteritis (M. Horton befo
re). Hospital Sudden, unilateral, painless loss of vision (occasionally slow-pro
gressing) or visual field defects (wedge). Afferent pupil defect. In addition, t
emporal arteritis, headache, tender and pulseless temporal artery Kausch Merz. A
history of weight loss and Reduction. Allg.zustand. Diagnosis OPHTHALMOSCOPY pa
pilledema with sectoral accented edge blur. Therapy
● ●
AION: none. Hemodilution can be tried. AION in temporal arteritis: protect high-
dose systemic corticosteroids immediate (especially around the second eye).
Optic neuritis
General inflammation of the optic nerve in the (papillitis) or behind the eye (r
etrobulbar neuritis). Most younger patients are affected. Causes are infections
(eg Lyme disease), autoimmune diseases (eg lupus erythematosus, Crohn's disease,
M. Wegener), toxic injury (eg, methanol, lead, chloramphenicol) or idiopathic.
The retrobulbar neuritis is often a multiple sclerosis (encephalitis disseminata
advance). Hospital Sudden vision loss with central scotoma (often after exercis
e: Uhthoff's phenomenon), pain on eye movement and pressure on the eyeball. In a
ddition, afferent pupil defect and red-green color blindness-. Ophthalmoscopy Di
agnosis:
● ●
Papillitis: edema and hyperemia of the optic nerve head, blurred disc margin. Re
trobulbar neuritis: inconspicuous findings ("the patient sees nothing and the do
ctor does not").
Delayed latency visual evoked potentials (VEP) in demyelination. Therapy is ofte
n spontaneous improvement. If possible, treat underlying disease. To accelerate
the Visuserholung: steroid therapy (but does not affect the final result). The p
rognosis depends on the underlying disease.
16
TOXIC
Optic neuropathy
General Toxic damage of the optic nerve can lead to acute loss of vision by bila
teral swelling of the optic nerve head. Substances are, for example Ethambutol,
methanol, chloramphenicol, amiodarone, streptomycin, lead, arsenic, D-penicillam
ine, isoniazid and sulfonamide. At a similar picture can lead thiamin, vitamin B
12 and folic acid deficiency.
Papilledema
General Most-sided swelling of the optic nerve exit point (English papilledema),
eg with chronically elevated intracranial pressure. Because of the potentially
life-threatening increase in intracranial pressure for an immediate diagnosis is
necessary (neurosurgical, neurological, internist). Clinic Reversible darkening
phenomena (Obskurationen), enlarged blind spot, ongoing headache. Diagnosis
OPHTHALMOSCOPY randunscharfe papilla excavation is no longer distinguishable. Of
ten discrepancy between (good) and functional (pathological) ophthalmoscopic fin
dings.
Further diagnostics (eg imaging) to clarify the increase in pressure cause. Ther
apy to treat underlying disease. After normalization of intracranial pressure, p
apilledema is back, but it can remain an optic atrophy.
Vitreous detachment
General Partial or complete detachment of the vitreous from its base (English vi
treous detachment). At the age fluid-filled lacunae occur in the vitreous, which
may cause a collapse of the vitreous. This leads to densities that are perceive
d as free moving opacities (floaters). the vitreous from incomplete sets aside f
rom the retina, can develop on the remaining connections traction forces, which
in turn can lead to rupture or detachment of the retina. Clinic floaters ("float
ers"). Light flashes and chills indicate a retinal defect and must be clarified.
Ophthalmoscopy to exclude diagnosis of retinal damage.€Treatment vitreous detac
hment is not dangerous in itself, as long as the retina is not involved.
17
Retinal detachment
General elevation of the neurosensory retina from the retinal pigment epithelium
(syn. retinal detachment, Eng. Retinal detachment). Can cause retinal (rhegmato
genous retinal detachment), train through the vitreous strands (Traktionsamotio)
or liquid between the retina and retinal pigment epithelium (exudative retinal
detachment, such as M. Coats be).
Risk factors include high myopia, Z.n. Trauma and family history.
Clinic light flashes, floaters, Rußregen, shadows in the visual field (like a cu
rtain from top to bottom falling or ascending from below). For infestation of th
e retina center: rapid visual loss. Diagnosis
OPHTHALMOSCOPY bubble retinal detachment, possibly bright red retinal hole. Alwa
ys the other eye mituntersuchen because retinal holes can occur bds.
In therapy with low hole retinal detachment: Laser (attachment of the retina aro
und the hole). For more extensively findings: OP (Silikonplombe is sewn to the s
clera, the eyeball and to einzudellen so as to restore the contact between the r
etina and pigment epithelium). If necessary. Vitrectomy with replacement of the
vitreous by silicone oil to tampon to the eye from the inside. The rhegmatogenou
s retinal detachment is probably not a good prognosis, the other forms.
MIGRAINE
General
MIT
AURA AURA
In the 20-minute visual migraine aura, there is visual disturbances, such as vis
ion loss, flashes of light and perception of jagged colored lines (even with clo
sed eyes). Typically, the headache occurring after the aura. The described visua
l disturbances may be confused with amaurosis fugax in, come in contrast, howeve
r, on both sides and take longer.
STROKE
General
AND
TIA
An insufficiency of the posterior circulation can result in homonymous visual di
sturbances. A circulatory disorder of the visual cortex 'leads to hazy vision an
d possibly for the perception of flashes of light to those of a migraine aura ma
y be similar. Double vision, dizziness, weakness, dizziness, and dysarthria have
to think of a brainstem ischemia. When a heart attack in the area of the visual
cortex, "It is a homonymous visual field defect, which ends exactly on the vert
ical axis.
18
Symptom:
General
CHRONIC
Visual disorder visual disorder
The most common cause of chronic deterioration of vision in most age-related len
s opacity (cataract). Thus, the already known since ancient times "cataract surg
ery" one of the most frequently performed operations in general. In the cataract
and glaucoma family history is often positive. Differential importance of the d
istinction between central (eg macular degeneration), peripheral (eg for glaucom
a) and total loss of vision (eg cataract). Another possible cause of reduced vis
ion for a slow, which should not be forgotten, check the "old glasses (refractio
n and any new prescription).
Cataract (GREY STAR) (STAR GREY
General Creeping, clouding of the lens. Most age-related, but more frequently in
systemic diseases such as diabetes mellitus, renal insufficiency, and M. Wilson
, after trauma / surgery or iatrogenic (especially steroid, radiation). Rarely h
as a congenital cataract, e.g. inherited or due to intrauterine injury (rubella,
mumps, toxoplasmosis). The classification of senile cataract is based on morpho
logical criteria:
● ● ● ●
Nuclear cataract: hardening and discoloration of the lens nucleus, slow progress
ion.
Figure 4: cataract.
Source: Wikipedia.de (.../ Image: Cataract_in_human_eye.png)
Cortical cataract: cortical changes (vacuoles, water columns), is proceeding fas
ter than the nuclear cataracts. Special: rear shell opacity. Cataract matura: di
ffused white lens, shadowy yellow nucleus, visual acuity at light-dark perceptio
n reduced. Cataract hyper matura: complete liquefaction of the cortex, capsule s
inks, so that the upper edge is visible in the pupil, frequently secondary open
angle glaucoma (glaucoma phakolytisches).
Very independent variable clinic: insidious visual loss, graying ("all gray to g
ray) vision, blurred or distorted, altered color perception, glare. Diagnosis At
tenuated red reflex of the fundus ophthalmoscopy and at Spaltlampenunters. The o
nly effective therapy treatment: surgical removal of the opaque lens (usually an
outpatient basis under local anesthesia). Most inserting an artificial lens. Th
e posterior lens capsule remains in the OP i.d.R. (Received extracapsular catara
ct extraction, ECCE). This may deteriorate secondary (cataract, occurs in every
third patient). Treatment of cataract: clouded posterior chamber is cut by laser
in the optical axis. If no artificial lens used€may, at bilateral aphakia ("len
sless"), the refraction can be corrected with cataract glasses. This is now the
exception.
19
GLAUCOMA
General Creeping optic neuropathy, usually due to a chronically elevated intraoc
ular pressure. After the second leading cause of blindness diabetes mellitus in
industrialized nations. Differences are open-angle glaucoma (90%) and angle clos
ure glaucoma (see acute angle-closure glaucoma). Glaucoma is the previously heal
thy eye (primarily occur) and as a result of various eye diseases (secondary), e
g iridis in hyper mature cataract, rubeosis. Pathogenetically usually there is a
n increased outflow resistance, rarely increased aqueous humor production.
Figure 5: glaucoma.
Clinic
Source: Wikipedia.de (.../ Image: Glaukompapille2.jpg)
The open-angle glaucoma runs in Ggs. to angle-closure glaucoma insidious, painle
ss and often asymptomatic. Occasionally, nonspecific symptoms (headache, burning
eyes). In a symptomatic visual field defect of the optic nerve damage is alread
y advanced. The early diagnosis is so crucial! It is therefore recommended that
the first reading glasses prescribed by an ophthalmologist always allow to measu
re the opportunity in the eye pressure (glaucoma screening). Diagnosis
Slit lamp and gonioscopy: common shallow anterior chamber. Enger (with narrow-an
gle) or closed (with angle-closure glaucoma) chamber angle. OPHTHALMOSCOPY chara
cteristic is the crisp, faded, with enlarged papilla excavation and in the depth
kinked vessels. Tonometry: increased intraocular pressure (> 21 mmHg). Perimetr
y: paracentral nasal visual field defects (early sign).
Therapeutic goal of treatment of chronic glaucoma is the reduction of intraocula
r pressure in order to prevent the progression of optic atrophy and visual field
defects.
Drugs
Basically, there are the following possibilities of conservative treatment of gl
aucoma:
● ●
Inhibition of aqueous humor production and improving the aqueous outflow.
Be used as eye drops, alpha-2 agonists (eg clonidine), cholinergics (eg pilocarp
ine), beta blockers (eg timolol), carbonic anhydrase inhibitors (eg dorzolamide)
and prostaglandins (eg latanoprost), and combinations.
Operation
Laser trabeculoplasty (scar contraction in trabecular meshwork leading to dilata
tion of the spaces) with open anterior chamber angle or filtering surgery (aqueo
us humor is derived by Skleraöffnung under the conjunctiva) are available.
20
Age-
MACULAR DEGENERATION (AMD) MACULAR DEGENERATION
General Progressive, degenerative disease of the macula. Differences are exudati
ve (wet) and non-exudative (dry) macular degeneration. With over 65 years, the A
MD is a common cause of chronic, painless bilateral visual loss. Slow visual los
s clinic. In exudative form of macular edema and sudden loss of vision with poss
ible distortion of vision and micro-or macropsia. The peripheral vision usually
remains preserved, as a rule only the macula is affected. Etiology and pathogene
sis are the starting points of the action pigment epithelium and choroid. Aging
of the retinal pigment epithelium leading to increased deposition of products fr
om the photoreceptor metabolism (Druze): dry form. For perfusion of the choroid,
it is mediated by tissue hypoxia VEGF *- a vascular neoplasm with bleeding unde
r the retina: wet form. Diagnosis
Ophthalmoscopy: drusen, serous detachment of the retina. The choroidal neovascul
arization can be represented by means of fluorescein angiography.
If one patient before an Amsler card and see this instead of the checkerboard pa
ttern of wavy or distorted lines, this indicates a macular edema.
Figure 6: Amsler card (left: normal, right: AMD patient).
Source: National Eye Institute, National Institutes of Health.
Therapy
● ●
Dry AMD: No known effective therapy that can stop a possibly high-dose vitamin a
dministration (C, E, beta carotene) progression. wet AMD: laser or photodynamic
therapy can be deserted newly formed vessels. Monoclonal antibodies against VEGF
are currently in clinical trials.
* VEGF: vascular endothelial growth factor.
21
DIABETIC
RETINOPATHY RETINOPATHY
General Until 1921 this was a rare disease. After the discovery of insulin and t
he associated dramatically improved life expectancy of diabetic patients, diabet
ic retinopathy is now one of the most common causes of blindness in developed na
tions. We distinguish the following forms:
●
non-proliferative: microaneurysms, moderate bleeding, venous caliber changes. pr
oliferative: neovascularization or vitreous hemorrhage, rubeosis iridis. diabet.
Maculopathy: macular edema.
Figure 7: Diabetic retinopathy.
Source: National Eye Institute, NIH
● ●
In diabetes mellitus, it is inter alia to changes in small vessels (microangiopa
thy). With the invention of the ophthalmoscope by Hermann von Helmholtz (1850),
it was possible, small vessels in the living directly visualize and detect patho
logical changes. The regular examination of the fundus is an important measure t
o determine the extent of microangiopathy and to intervene early therapeutically
to further damage (not only for the eye) averted. Asymptomatic hospital. In the
late stage by participating in the macula, or vitreous hemorrhage sudden blindn
ess or visual loss. Blindness can occur through: rubeosis iridis (neovascularisa
tion on the iris), or diabetic macular edema Traktionsamotio. The etiology and p
athogenesis of diabetic retinopathy is a microangiopathy. With hyperglycemia it
comes to the vascular basement membrane thickening, capillary occlusions and ret
inal ischemia later with the formation of angiogenic factors (VEGF, IGF). The ne
wly formed blood vessels tend to be inferior microaneurysms, increased permeabil
ity and haemorrhage. Diagnosis
Ophthalmoscopy: microaneurysms, macular hemorrhages, yellow spots ("hard exudate
s" from the vessel leaked blood components, eg lipids).
Optimal glycemic control therapy (HbA1C <7%), laser treatment (with macular edem
a: centrally, in proliferative retinopathy: panretinal). When vitreous hemorrhag
e vitrectomy. Are important for each diabetic regular ophthalmological controls!
22
Retinitis
General
Pigmentosa
Heterogeneous group of (usually hereditary) diseases of the retina, where photor
eceptors are based. Despite the name, this is not an inflammatory process. The a
ge of onset depends on the mode of inheritance, most affected patients are young
. First clinic increased glare sensitivity and night blindness. Later, visual fi
eld defects (especially in the periphery: "Tunnel vision") and visual loss. Diag
nosis
OPHTHALMOSCOPY proliferations of the retinal pigment epithelium, optic atrophy,
close together arteries, relfexarmer fundus. Electroretinogram: greatly reduced
or abolished.
Treatment None. Optimization of Restsehvermögens through magnifying glasses.
MELANOMA
General
AND OTHER
Tumors Tumors
The most common primary intraocular malignant Uveamelanom is. Depending on locat
ion we distinguish iris melanoma (often without symptoms, possibly secondary gla
ucoma), Ziliarkörpermelanom (accommodation and refraction) and uveal melanoma (p
ossibly falls on by Begleitamotio in macular Participation: visual loss). In ord
er to determine position and expansion of the tumor, ultrasound and indocyanine
green angiography can be used. The metastasis is hematogenous, v.a. in the liver
.
Treatment options to remove the tumor, enucleation, radiotherapy and laser thera
py is possible.
More common than primary tumors are metastases that infect the eye, such as Mamm
a-Ca. Even leukemia and lymphoma can infiltrate the structures of the eye.
23
Symptom: LOCATION CHANGE LOCATION CHANGE
General
OF
Eyeball eyeball
Oculi
Asymmetrical appearance of the eyeballs is to first clarify what the eye is chan
ged, Is it a clear eye (exophthalmos) or is the other eye in the orbit sunken (e
nophthalmos)? Delineate the Pseudoexophthalmus (long eyeball with high myopia) a
nd the Pseudoenophthalmus (eyeball is smaller). By Exophthalmometer (by Hertel)
can be measured, how far the eyeball protrudes over the bony orbital rim and sid
e differences are observed. In diseases of the orbit usually is an interdiscipli
nary cooperation (otolaryngologist, neurosurgeon, internist) is required. Causes
of exophthalmos (protrusion of the eyeball) are:
● ● ● ●
thyroid eye disease (most frequently, such as Graves' disease), inflammatory cha
nges (eg, orbital cellulitis, Orbitaabszess, cavernous sinus thrombosis), vascul
ar changes (such as arteriovenous fistula, orbital hematoma) and tumors of the o
rbit (eg hemangioma dermoid, Optikusgliom, metastases ). Orbita (most common cau
se, such as blow-out fracture), neurogenic changes (such as Horner's syndrome) a
nd symmetrical wasting of the Orbitagewebes (eg, senile atrophy, dehydration).
Endocrine
Causes of enophthalmos are:
● ● ●
Eye disease eye disease
General autoimmune inflammatory disease with involvement of the orbit, eg with a
utoimmune thyroiditis. Most of asymmetric exophthalmos, sometimes even unilatera
lly. In adults the most common cause for both unilateral and for bds exophthalmo
s. Deposits of glycosaminoglycans in the orbit and inflammatory involvement of o
rbital fat tissue and muscles lead to exophthalmos. Clinic Reddened,€dry eyes, r
educed Bulbusmotilität, double images. Diagnosis
Clinical: exophthalmos, impaired convergence property (Möbius's sign), typical L
idzeichen (Dalrymple: retraction of the upper eyelid, from Gräfe: retraction of
the upper lid in lower view; Stellwag: blink less often; Cooker: Gaze; Gifford:
difficulty in eversion of the upper lid). Sonography thickened: extraocular eye
muscles.
Prednisone therapy (60 mg / d for 4 weeks), X-ray irradiation of the orbit. If n
ecessary. surgical Orbitadekompression to pressure injuries of the N. to prevent
optic.
24
PSEUDO TUMOR
General
ORBITA
Idiopathic, inflammatory with lymphocytic and eosinophilic infiltration Orbitasy
ndrom. A special case is the Tolosa-Hunt syndrome (granulomatous inflammation of
the orbital apex with painful ophthalmoplegia). Clinic Painful inflammation, ey
elid swelling, limited Bulbusmotilität. Diagnosis difficult. Sonographically are
the swollen eye muscles (myositis) with enlarged tendons. The MRI shows a diffu
se soft tissue swelling. The definitive diagnosis is confirmed by biopsy. High-d
ose therapy, systemic glucocorticoid administration (in the case of dramatic imp
rovement is based this finding, the diagnosis ex juvantibus).
HORNER SYNDROME SYNDROME
General Trias of (pseudo) enophthalmos (paralysis or paralysis of the orbital M.
rudimentary Lidretraktoren: lower is higher, the eye looks smaller), ptosis (pa
ralysis of the Müller M. tarsalis) and miosis (paralysis of the pupil dilator).
Cause is an injury in the course of the ipsilateral Sympathikusbahn:
● ● ●
central: e.g. Tumors, encephalitis, multiple sclerosis. preganglionic: e.g. Trau
ma, goiter, aneurysm, Pancoast tumor. postganglionic: e.g. Internal carotid aneu
rysm.
Diagnosis
Clinical: direct and consensual light reaction intact (in contrast to Parasympat
hikusschädigung), pupil is far slower (Dilatationsdefizit). Cocaine eye drops: p
upil on the affected side does not react with dilatation.
Therapy to treat underlying disease.
25
Symptom:
General
HANGING
LID LID
A (one-or two-sided), drooping of the eyelid is called ptosis. It can be made be
tween congenital and acquired ptosis. Unilateral ptosis rather indicates a neuro
genic, bilateral ptosis out more on a myogenic cause. By frown the patient attem
pts to extend the lids. Operational raising the upper eyelid
● ● ●
Fasanella-Servat operation for: v.a. to mild ptosis. Cut a portion of the rear v
ertical Lidblattes → Lidverkürzung. Levatorresektion: shortening of the levator
palpebrae M.. Frontalis suspension: Connect with the upper eyelid tissue in the
area of the brows using a sling (autologous fascia lata or plastic threads).
Ptosis
General
Congenital
Underdeveloped and hanging by congenital upper eyelid (usually unilateral) levat
or defect. If a pupil is masking Amblyopiegefahr! Case of bilateral ptosis recli
ned the baby's head so that both eyes can see. In Waardenburg syndrome is ptosis
, epicanthus and blepharophimosis. Surgical therapy raising the upper eyelid.
MYOG
Ptosis ptosis
General main cause of myogenic ptosis is myasthenia gravis. Usually both sides a
re affected, but not always equally strong. Typically, an increase of ptosis in
the course of the day (abnormal fatigue) is. This can be used diagnostically: En
trapment of ptosis by rapidly opening and closing of the eyelids or fatigue duri
ng prolonged looking up (Simpson-test). (The further diagnosis and treatment are
neurological.)
NEURO GENE
Ptosis ptosis
General Most-sided eyelid drooping due to damage to the innervation of the two e
ye-opener: Müller-muscle (sympathetic ptosis in Horner's syndrome) or LevatorMus
kel (paralytic ptosis with oculomotor injury). When Horner's syndrome is the pup
il is narrow and the Augenmotilität normal. When motility is disturbed oculomoto
r paralysis of the eye and affected the pupil normal width (external paralysis:
only external eye muscles) or extended (complete paralysis and ciliary muscle an
d sphincter pupil concerned, therefore absolute pupil, mydriasis, paralysis of a
ccommodation). Treatment depends on the underlying disease.
26
Symptom: DOUBLE IMAGE, DOUBLE IMAGE motility motility
General
AND
Nystagmus Nystagmus
First, must persist between monocular (double vision when one eye is covered, fo
r example, keratoconus, cataract or uncorrected refractive error) and disappear
binocular diplopia (double vision when one eye is covered, cause a deviation of
the eyes of Parallel stance can be distinguished). Binocular diplopia can neurog
enic (eg, sixth nerve palsy), myogenic (eg€with myasthenia) or by mechanical con
straint (eg blow-out fracture of the orbit, mass) may be caused. (Think mell If
nerve damage and diabetes.!)
Motility disorders can by nerve damage (eg, third nerve palsy) or by an imbalanc
e of the eye muscles (eg, caused in squint).
When nystagmus (eye tremor) occurs ruck or pendulum involuntary rhythmic eye mov
ements, which may be acquired or congenital.
Myasthenia
General
GRAVIS
In myasthenia gravis, it may not only to the drooping eyelid (see myogenic ptosi
s), but also to get double vision. Many myasthenia patients, only the eye muscle
s are affected, a systemic muscle weakness exists. Clinic Intermittent double vi
sion that can not be assigned to a single nerve. The pupils are always normal. I
f necessary. Accompanying myogenic ptosis. Diagnosis
Tensilon test (temporary improvement by administering a cholinesterase inhibitor
) and detection of acetylcholine receptor antibodies. DD: Botulinum toxin poison
ing.
Cholinesterase inhibitor therapy, glucocorticoids, azathioprine, and plasmaphere
sis in severe cases, immunoglobulin administration. If necessary. Thymectomy (th
ymoma is often a cause of antibody formation). The purely ocular form of myasthe
nia has a good prognosis.
N. Oculomotor (third cranial) nerve
General The (rare), oculomotor palsy is mainly by vascular disease (eg, aneurysm
) caused. The N. oculomotor muscles following supplies:
●
motor fibers → external eye muscles:
○ ○
M. rectus superior, inferior, and medial and inferior oblique eye movements → al
l down to the bottom lateral (N. IV) and lateral (N. VI). Levator palpebrae → le
vator.
M. ciliaris → accommodation. Sphincter pupil → miosis.
●
parasympathetic fibers → inner eye muscles:
○ ○
27
Clinic differences, the following diseases:
●
O.-complete paralysis: complete interior and almost all external eye muscles aff
ected (loss of motor function and pupil accommodation, mydriasis, ptosis). Becau
se of the ptosis, the patient has no diplopia. O. partial outer-paresis: isolate
d paralysis of the extraocular muscles supplied with squint to the outside botto
m. Because of the ptosis no double images. O. partial inner-paresis: paralysis o
f the isolated internal muscles supplied with mydriasis and lack of accommodatio
n. No double vision, since there is no squint.
● ●
V.a. participation of pupils in a motor diagnostic imaging is indicated to aneur
ysms, to exclude space-occupying processes and Clivuskantensyndrom. (More diagno
stics and therapy is neurosurgical, neurological and radiological.)
Figure 8: nerves of the eye area.
Source: Wikipedia.de http://de.wikipedia.org/wiki/Bild:Augennerven.jpg ()
N.
General
Trochlear
(IV CN) CN
The N. trochlear nerve supplies the superior oblique (moving laterally down and
internal rotation). An injury occurs v.a. after trauma. Vertical double vision c
linic, v.a. Looking down at the nasal (eg climbing stairs). Double images disapp
ear when looking upward. The patient attempts by compensatory head posture to av
oid double images (up to the ocular torticollis). Diagnosis
Bielschowsky Kopfneigetest: When inclination of the head on the side of the para
lyzed eye and fixation with the healthy eye deviates from the paralyzed eye upwa
rd. For slope on the healthy side produced no difference in the height.
28
N. Abducens (CN VI) nerve
General The N. abducens supplies the rectus lateralis (lateral motion). Causes o
f injury are vascular diseases (diabetes mell., Hypertension), meningitis, subar
achnoid hemorrhage, and tumors with increased intracranial pressure. The long co
urse at the base of the skull makes the nerve vulnerable to damage. A sixth nerv
e palsy can always have to think a brain booster! Clinic Einwärtsschielstellung,
horizontal double vision (largest in the attempted abduction), compensatory hea
d posture rotated toward the affected side. Occlusion therapy of the affected ey
e until the paralysis wears off. If no treatable underlying disease is found or
not the paralysis of regressing, may be a 1-year corrective eye muscle surgery.
Strabismus
General A deviation of the axis of vision in one eye from the normal is known as
squint (strabismus). In contrast to the paralysis squint (strabismus paralytic)
is the squint angle for accompanying squint (strabismus concomitant) the same f
or all eye movements. During early childhood strabismus syndrome is not fixating
eye is suppressed central nervous system, to avoid double vision. In children,
it can then come to amblyopia (visual acuity reduction in organically apparently
healthy eye,€to optical even with optimal correction persists). An untreated Am
bylopie can lead to a visual acuity <0.02 (one-eyed blindness), which mainly be
relevant is if the other eye illness (eg, trauma). The spatial vision is with on
e eye is not possible (relevance for certain professions, such as pilot). The cl
inic early childhood strabismus syndrome is asymptomatic, as caused by the suppr
ession of the non-fixating eye is no double images. More important, therefore, t
he routine eye examination, particularly one microstrabismus (due to the small a
ngle squint squint inconspicuous) to diagnose early. In the (rare) normosensoris
chen strabismus binocular vision is already well developed, not fixating eye can
no longer be suppressed and it is therefore of double images, which are avoided
by screw up of the eye. By early surgery, the binocular vision restored. Diagno
sis A squint of the eyes may be replaced by non-central corneal light reflex (ex
amination with a flashlight after Hirschberg) and pathological covered (at conce
aling one eye does not do an adjustment here covered eye) was diagnosed.
29
A latent strabismus (balance disorder of the eye muscles, which can lead under c
ertain circumstances, to squint, eg fatigue, alcohol, stress) is diagnosed by th
e revealed. The reaction of the just covered eye is still observed in Wiederaufd
ecken. Does that just covered eye, even a merger movement recording, the test is
pathological. Without symptoms no treatment of latent squint is necessary becau
se there is always a primary Parallel stance and full binocular vision. A more p
recise diagnosis (exact determination of squint angle, testing of binocular visi
on and stereopsis) is done by an ophthalmologist. During early childhood strabis
mus syndrome therapy is performed on the Prevention and Treatment of amblyopia i
n early childhood, the occlusion treatment. This mainly leading eye is covered i
ntermittently and poorly trained the seeing eye. It is important that while the
sehtüchtige eye loses vision. After the amblyopia treatment is completed success
fully, a surgical correction of squint to be done (strabismus surgery). By reduc
ing or relaxing the eye muscles, the position of the eyes is corrected at rest.
Nystagmus
General Sided, involuntary rhythmic nystagmus (jerk or a pendulum). Occur sponta
neously or provoked lagerungsabhängig. There are numerous causes, for example:
●
acquired:
○ ○ ○
Central nervous: inter alia Stroke, cancer, multiple sclerosis, encephalopathy.
toxic-metabolic, alcohol, lithium, barbiturates, benzodiazepines, ketamine. vest
ibular: M. Ménière, labyrinthitis. ocular: inter alia Albinism, cataracts, color
blindness. idiopathic: no identifiable cause.
●
: Congenital
○ ○
Differences are many different forms, including these are:
● ●
physiological: for example Optokinetic Nystagmus as seen from a moving train. Th
e direction of view-N.: Occurs when looking at in a certain direction, the expre
ssion of a brainstem or cerebellar damage (multiple sclerosis, stroke, tumor).
○ ○ ○
blickparetischer N. sudden blow by Blickhalteschwäche form, eg in stroke, trauma
, tumor (nothing to do with palsy!). dissociated nerve: both eyes affected in di
fferent ways, eg in internuclear ophthalmoplegia (lesion of the medial longitudi
nal fasciculus). Rebound-N.: After prolonged excessive turning of counter-regula
tion.
● ● ●
peripheral vestibular nerve: a horizontal spontaneous nystagmus in peripheral Ve
stibularisläsion (eg Menière), visible through Frenzel glasses. Central vestibul
ar nerve: "up-beat" - or "down-beat", eg with brain stem lesions. N storage.: Pr
ovoked by specific head position.
Treatment depends on the underlying disease, may help prism glasses.
30
LITERATURE
General Ophthalmology
● ●
Horton JC (2008): "Disorders of the Eye", in Kasper DL, Braunwald E, Fauci AS et
al.: Harrison's Principles of Internal Medicine. 17th Edition. New York: McGraw
-Hill. Lang GK (2004): Ophthalmology. 3rd Edition. Stuttgart: Thieme.
Special Ophthalmology
● ●
Augustin AJ (2007): Ophthalmology. 3rd Edition. Berlin: Springer. Kanski JJ (200
8): Clinical Ophthalmology. 6th Edition. London: Elsevier.
is the current version of this script are available for download at the address
http://www.harvey-semester.de/
31