Pembahasan TO1 Part 2 PDF

PEMBAHASAN MATA
53.. DIAGNOSIS
MATA
ANAMNESIS
MATA MERAH
VISUS NORMAL
MATA TENANG MATA TENANG
• struktur yang MATA MERAH
VISUS TURUN VISUS TURUN
bervaskuler VISUS TURUN
MENDADAK PERLAHAN
sklera
konjungtiva mengenai media • uveitis posterior
• tidak refraksi (kornea, • perdarahan • Katarak
menghalangi uvea, atau vitreous • Glaukoma
media refraksi seluruh mata) • Ablasio retina • retinopati
• oklusi arteri atau penyakit
• konjungtivitis
• Keratitis vena retinal sistemik
murni
• Keratokonjungti • neuritis optik • retinitis
• Trakoma
vitis • neuropati optik pigmentosa
• mata kering,
• Ulkus Kornea akut karena obat • kelainan
xeroftalmia
• Uveitis (misalnya refraksi
• Pterigium
• glaukoma akut etambutol),
• Pinguekula
• Endoftalmitis migrain, tumor otak
• Episkleritis
• panoftalmitis
• skleritis
WWW.MEDSCAPE.COM www.wikipedia.org
Causes Etiology Clinical
Acute Glaucoma Pupilllary block Acute onset of ocular pain, nausea, headache, vomitting,
blurred vision, haloes (+), palpable increased of IOP(>21 mm
Hg), conjunctival injection, corneal epithelial edema, mid-
dilated nonreactive pupil
Acute Infection , Allergy itching and burning or a gritty, foreign-body sensation,

Conjunctivitis mucopurulent discharge, visual acuity is normal
Simpathetic Surgical, trauma to bilateral granulomatous uveitis, The ocular inflammation in the
Ophthalmia one eye, systemic fellow eye becomes apparent usually within 3 months after
disease injury.
acute anterior uveitis with mutton-fat keratic precipitates. The
posterior segment manifests moderate to severe vitritis,
usually accompanied by multiple yellowish-white choroidal
lesions
Floating spots, pain, photophobia
Acute uveitis Systemic disease; Pain, redness, photophoia, excessive tearing, decreased
psoriasis, syphilis vision, limbic injection, miosis, might be followed by glaucoma
Corneal Ulcer Infectious/systemic Mucopurulent discharge from eye, Foreign body sensation,
disease Light sensitivity, Pain
Inflammation eyelids
eyelids and conjunctiva, ciliary injection,
Fluorescein staining, Stromal melting,
melting, lagophtalmus,
lagophtalmus, hypopyon
54.
54. DIAGNOSIS
MATA
ANAMNESIS
MATA MERAH
VISUS NORMAL
MENDADAK PERLAHAN
sklera
• konjungtivitis
murni
• Trakoma
• mata kering,
xeroftalmia
• Pterigium
• Pinguekula
• Episkleritis
• panoftalmitis
• skleritis
WWW.MEDSCAPE.COM www.wikipedia.org
Disease Clinical
Cataract Decreased visual acuity, contours, shadows and color

vision are less vivid, Being sensitive to glare, Cloudy, fuzzy,
foggy, or filmy vision, Difficulty seeing at night or in dim
light, myopic shift, shadow test (+)
Glaukoma progressive visual field loss, and optic nerve changes
(increased cup-to-disc ratio on fundoscopic examination)
Macular loss of vision in the center of the visual field (the macula) ,
Degeneration difficult or impossible to read or recognize faces
Hypertensive Cooper wired shaped vessels, cotton wool spots, clear lens
retinopathy
Diabetic Blurred vision, progressive visual los, dot & blot

Retinopathy hemorrhage, neovascularization
www.wikipedia.org
CATARACT
Clouding that develops in the crystalline lens of the eye
or in its envelope (lens capsule)
Sign & symptoms:
Near-sightedness (myopia shift) Early in the development of
age-related cataract, the power of the lens may be increased
Reduce the perception of blue colorsgradual yellowing and
opacification of the lens
Gradual vision loss
Almost always one eye is affected earlier than the other
Shadow test +
Senile cataract
Elderly
Opacity in the lens
Subsequent swelling of the lens
Shrinkage with complete loss of transparency
www.wikipedia.org
Morgagnian cataract
The cataract cortex liquefies to form a milky white fluid
Cause severe inflammation if the lens capsule ruptures
and leaksphacomorphic glaucoma
Etiology:
Diabetes
Eye inflammation
Eye injury
Family history of cataracts
Long-term use of corticosteroids (taken by mouth) or
certain other medications
Radiation exposure
Smoking
Surgery for another eye problem
Too much exposure to ultraviolet light (sunlight)
www.wikipedia.org
CLASSIFICTION AGE-
RELATED CATARACT
Cortical senile cataract
Immature senile cataract (IMSC)
partially opaque lens, disc view
hazy
Shadow test +
Mature senile cataract (MSC)
completely opaque lens, no disc
view
Shadow test -
Hypermature senile cataract
(HMSC)
liquefied cortical
matterMorgagnian cataract
Senile nuclear cataract
Cataracta brunescens
Cataracta nigra
Cataracta rubra
eyescure.com
www.wikipedia.org
TREATMENT
Extracapsular cataract extraction (ECCE) and
Removing the lens, but leaving the majority of the
lens capsule intact
High frequency sound waves
(phacoemulsification)break up the lens before
extraction
Iintracapsular cataract extraction (ICCE)
Removing the lens and lens capsulerare
The cataractous lens is removed and replaced
with a plastic lens (an intraocular lens implant)
which stays in the eye permanently.
http://emedicine.medscape.com/article/798100
55. CORNEAL ULCER
An inflammatory or more seriously, infective condition of the
cornea involving disruption of its epithelial layer with
involvement of the corneal stroma
Causative Agent Feature Treatment
Fungal Fusarium & candida species, conjungtival Natamycin,
injection, satellite lesion,
lesion stromal infiltration, amphotericin B,
hypopion,
hypopion anterior chamber reaction Azole derivatives,
Flucytosine 1%
Protozoa infection associated with contact lens users swimming in
(Acanthamoeba) pools
Viral HSV is the most common cause, Dendritic lesion, Acyclovir
decrease visual accuity
Staphylococcus Rapid corneal destruction; 24-48 hour, stromal Tobramycin/cefazol
(marginal ulcer) abscess formation, corneal edema, anterior in eye drops,
segment inflammation. Centered corneal ulcers.
ulcers quinolones
Pseudomonas Traumatic events, contact lens, structural (moxifloxacin)
Streptococcus malposition
connective tissue RA, Sjögren syndrome, Mooren ulcer, or a
disease systemic vasculitic disorder (SLE)
Corneal diagnoses and systemic disease Mooren's ulcer vs. PUK: The difference can mean life or
death
PERIPHERAL ULCERATIVE KERATITIS (PUK)

Ulcer progressing slowly and easily, circumferentially,
and deeper toward the center of the cornea
Etiologyconnective tissue disease
rheumatoid arthritis (RA)
Sjögren syndrome
Mooren ulcer
systemic vasculitic disorder (eg, systemic lupus
erythematosus [SLE], Wegener granulomatosis,
polyarteritis nodosa).
Mooren ulcer
rapidly progressive, painful, ulcerative keratitis
initially affects the peripheral cornea, spread
circumferentially and then centrally
can only be diagnosed in the absence of an infectious or
systemic cause. http://emedicine.medscape.com/article/79810
0
56.
56. DIAGNOSIS
MATA
ANAMNESIS
MATA MERAH
VISUS NORMAL
MENDADAK PERLAHAN
sklera
• konjungtivitis
murni
• Trakoma
• mata kering,
xeroftalmia
• Pterigium
• Pinguekula
• Episkleritis
• panoftalmitis
• skleritis
GLAUCOMA
Disturbance of the structural or functional

integrity of the optic nerve that causes
characteristic atrophic changes in the optic
nerve, which may also lead to specific visual
field defects over time
Usually can be arrested or diminished by
adequate lowering of intraocular pressure (IOP)
JENIS GLAUKOMA :
1. Primer yaitu timbul pada mata yang

mempunyai bakat bawaan, biasanya
bilateral dan diturunkan.
2. Sekunder yang merupakan penyulit
penyakit mata lainnya (ada
penyebabnya) biasanya Unilateral
http://emedicine.medscape.com/article/1206147 www.wikipedia.org
TYPES OF GLAUCOMA
vomitting,
blurred vision, haloes (+), palpable increased of IOP(>21
IOP(>21 mm
Hg),
mid-
dilated nonreactive pupil,
pupil, elderly, suffer from hyperopia,
hyperopia, and
have no history of glaucoma
Open-angle Unknown History of eye pain or redness, Multicolored halos, Headache,
(chronic) IOP steadily increase, Gonioscopy Open anterior chamber
glaucoma angles, Progressive visual field loss
Congenital abnormal eye present at birth, epiphora, photophobia, and blepharospasm,
glaucoma development, buphtalmus (>12 mm)
congenital infection
Secondary Drugs Sign and symtoms like the primry one. Loss of vision
glaucoma (corticosteroids)
Eye diseases
(uveitis)
Systemic diseases
Trauma
Absolute end stage of all types of glaucoma, no vision, absence of
glaucoma pupillary light reflex and pupillary response, stony appearance.
Severe eye pain. The treatment destructive procedure like
cyclocryoapplication, cyclophotocoagulation,injection of 100%
alcohol
GLAUKOMA
glaucoma that develops

after the 3rd year of life
17
OPEN-ANGLE (CHRONIC) GLAUCOMA
Most common type
Chronic and progressive
acquired loss of optic nerve
fibers
Open anterior chamber angles
Visual field abnormalities
An increase in eye pressure
occurs slowly over
timepushes on the optic
nerve
Funduskopi: cupping and
atrophy of the optic disc
Risk factors
elevated intraocular pressure,
advanced age, black race, and
family history
TREATMENT
OP >28 mm Hg
Treated
Follow-up care in 1 month to assess treatment
The goal is reachedfollow-up care every 3-4 months
IOP 26-27 mm Hg
Follow-up care 2-3 weeks to recheck pressure
If IOP is still within 3 mm Hg of the initial readingfollow-up every 3-4 months
Visual field and dilated optic nerve evaluation once a year
If IOP is lower longer time to follow up
IOP 22-25 mm Hg
Follow-up care 2-3 months later for recheck of IOP at different times of the day
(ie, 8 am, 11 am, 1 pm, 4 pm)
If it is still within 3 mm Hg of the initial reading follow-up at 6 months
Humphrey visual field testing and dilated optic nerve evaluation, repeating it at
least yearly.
MEDICATION
Alpha-agonists
decreasing aqueous production
Beta-blockers
decrease aqueous humor production by the ciliary body
Carbonic anhydrase inhibitors
Reduce secretion of aqueous humor by inhibiting carbonic
anhydrase (CA) in the ciliary body
Miotic agents
contraction of the ciliary muscle, tightening the trabecular
meshwork and allowing increased outflow of aqueous through
traditional pathways
Prostaglandin analogs
Increase uveoscleral outflow of aqueous
ANGLE-CLOSURE (ACUTE) GLAUCOMA

The exit of the aqueous humor fluid is sud
At least 2 symptoms:
ocular pain
nausea/vomiting
history of intermittent blurring of vision with halos
AND at least 3 signs:
IOP greater than 21 mm Hg
conjunctival injection
corneal epithelial edema
mid-dilated nonreactive pupil
shallower chamber in the presence of occlusiondenly
blocked
TREATMENT
Aim:
IOP reduction
Acetazolamide 500 mg IV followed by 500 mg PO or 4 x 250 mg
topical beta-blocker (ie, carteolol, timolol) 0.25%-0.5% 1-2 dd
Sol.Glycerin 50% 4 x 100-150 ccHiperosmotic agent
Kcl 3 x 0,5 gr
suppression of inflammation
1-2 doses of topical steroids
reversal of angle closure
Pilocarpine (miotic) 2%1
2% 1 hour after beginning treatment,
administered every 15 minutes for 2 doses.then 3 times a day
Initial attackthe elevated pressure in the anterior chamber
causes a pressure-induced ischemic paralysis of the iris
pilocarpine ineffective
2% 3 times a day
Extraocular symptoms:
analgesics
antiemetics
Placing the patient in the supine position lens falls away
from the iris decreasing pupillary block
57. BUPHTHALMOS
Characterized by eye enlargement that results from
elevated IOP, which is often caused by primary
congenital glaucoma
Rarely present at birth
Primary congenital glaucoma
the result of abnormal formation of anterior chamber angle
(site of draining the eye fluid), causing obstruction of the
fluid outflow and elevated eye pressures
Develops within months after birth
Classic triad
Photophobia
Tearing
blepharospasm in bright light
blurred vision, haloes (+), palpable increased of IOP(>21 mm
dilated nonreactive pupil, elderly, suffer from hyperopia, and
have no history of glaucoma
Open-angle Unknown History of eye pain or redness, Multicolored halos, Headache,
(chronic) IOP steadily increase, Gonioscopy Open anterior chamber
glaucoma angles, Progressive visual field loss
Congenital abnormal eye present at birth, epiphora,
epiphora, photophobia, and blepharospasm,
blepharospasm,
glaucoma development, buphtalmus (>12
(>12 mm)
congenital infection
Secondary Drugs Sign and symtoms like the primry one. Loss of vision
glaucoma (corticosteroids)
Eye diseases
(uveitis)
Systemic diseases
Trauma
Absolute end stage of all types of glaucoma, no vision, absence of
glaucoma pupillary light reflex and pupillary response, stony appearance.
Severe eye pain. The treatment destructive procedure like
cyclocryoapplication, cyclophotocoagulation,injection of 100%
alcohol
58.
58. DIAGNOSIS
MATA
ANAMNESIS
MATA MERAH
VISUS NORMAL
MENDADAK PERLAHAN
sklera
• konjungtivitis
murni
• Trakoma
• mata kering,
xeroftalmia
• Pterigium
• Pinguekula
• Episkleritis
• panoftalmitis
• skleritis
www.wikipedia.org
Disorders Feature Correction
Myopia the light that comes in does not directly focus on the Concave lens. The
retina but in front of it
itimage at a distant object to smallest Dioptri to
be out of focus but in focus when looking at a close corret the visual
objec.
objec. aquity to 6/6
Hypermetropia imperfection in the eye (often when the eyeball is too Convex lenses. The
short or the lens cannot become round enough). largest Dioptri to
Difficult focusing on near objects corret the visual
aquity to 6/6
Astigmatisma Unspherical corneal structure; distorted image Lens correction,

laser ceratotomy
Presbyopia the eye exhibits a progressively diminished ability to Correction lens

focus on near objects with age, eyestrain, difficulty
seeing in dim light, problems focusing on small
objects
Anisometropia two eyes have unequal refractive power, leading to Iseikonic lenses
diplopia and asthenopia.
http://en.wikipedia.org/wiki/Myopia
MYOPIA
Classification:
Low myopia−3.00
diopters or less (i.e.
closer to 0.00).[6]
Medium myopia
−3.00 and −6.00
diopters
High myopia −6.00 or
more.[6] People with
high myopia
more likely to have retinal
detachments and
primary open angle
glaucoma
more likely to experience
floaters
http://www.aoa.org/documents/CPG-16.pdf www.wikipedia.org
HYPERMETROPIA
Classification:
Low hyperopia +2.00 diopters (D) or less
Moderate hyperopia+2.25 to +5.00 D
High hyperopia +5.00 D
Clinical categories:
Simple hyperopianormal biological variation, can be
of axial or refractive etiology
Pathological hyperopia abnormal ocular anatomy
due to maldevelopment, ocular disease, or trauma
Functional hyperopiaparalysis of accommodation
http://www.eyecarecontacts.com/optical_lenses.GIF
59.
59. http://www.nlm.nih.gov/medlineplus/ency/articl
e
Decreased visual acuity, contours, shadows and
CATARACT color vision are less vivid, Being sensitive to glare,
Cloudy, fuzzy, foggy, or filmy vision, Difficulty seeing
at night or in dim light, myopic shift, shadow test (+)
Test Fuction
Anel Test Determines the excretion function of the ductus
lacrimalis
Schimmer test determines whether the eye produces enough
tears to keep it moist. N : A negative (>10 mm of
moisture on the filter paper in 5 minutes)
Shadow test Detect immature cataract lens
Fluorescein test detect foreign bodies in the eye and detect
damage to the cornea
Humphrey visual Determine visual field
field test
60.
60. DIAGNOSIS
MATA
ANAMNESIS
MATA MERAH
VISUS NORMAL
MENDADAK PERLAHAN
sklera
• konjungtivitis
murni
• Trakoma
• mata kering,
xeroftalmia
• Pterigium
• Pinguekula
• Episkleritis
• panoftalmitis
• skleritis
http://emedicine.medscape.com/article/1217083 Optic_neuropathy.htm
60. OPTIC NEUROPATHY

Disease Etiology Clinical
Retrobulbar multiple demyelinating inflammation of optic nerve, young
neuritis sclerosis (MS) adults (30s), affects only one eye,decrease vision,
dyschromatopsia,
dyschromatopsia, ocular pain, exacerbated by
heat/exercise (Uhthoff
(Uhthoff phenomenon) and eye
movement.
Objects moving in a straight line may appear to have a
curved trajectory (Pulfrich
(Pulfrich phenomenon), Central
scotoma,
scotoma, headache, sudden color blindness,impaired
night vision,impaired contrast sensitivit
Compressive Tumors Asymetric,slowly progressive vision loss, proptosis,
optic neuropathy infections reduced visual acuity, dyschromatopsia, a relative
inflammatory afferent pupillary defect, visual field defect,(central
processes scotoma) and optic atrophy or optic disc swelling
Optic atrophy Axon degeneration, pale disc, reduced optic capillary,
Loss of vision, and loss of pupillary reaction
Etiology: vascular disturbances,degenerative retinal
disease,metabolic diseases, trauma, glaucoma, or
toxicity
Disease Etiology Clinical

Nutritional optic under-nutrition colors are not as vivid or bright as before , the color red
neuropathies (weight loss and is washed out, occurs in both eyes at the same time,no
wasting) eye pain, blur or fog, drop in vision, blind spots in the
center of their vision, preserved peripheral vision,
pupils respond normally to light
Central Retinal Atherosclerotic sudden, painless, unilateral blindness, pupil may
Artery Embolism plaques respond poorly to direct light but constricts briskly when
Endocarditis the other eye is illuminated (relative afferent pupillary
Fat defect), Neovascularization, Vitreous hemorrhage
http://www.cdc.gov/conjunctivitis/about/treatment.html
61. KONJUNGTIVITIS
Pathology Etiology Feature Treatment
Bacterial staphylococc Acute onset of redness, grittiness, topical antibiotics
istreptococci burning sensation, usually Artificial tears
, gonocci bilateral eyelids difficult to open
Corynebacte on waking, diffuse conjungtival
rium strains injection, mucopurulent
discharge, Papillae +
Viral Adenovirus Unilateral watery eye, redness, Days 3-3-5 of worst, clear
herpes discomfort, photophobia, eyelid up in 7–
7–14 days without
simplex virus edema & pre-
pre-auricular treatment
or varicella-
varicella- lymphadenopathy,
lymphadenopathy, follicular Artificial tears relieve
zoster virus conjungtivitis,
conjungtivitis, pseudomembrane dryness and inflammation
(+/-
(+/-) (swelling)
Antiviral herpes simplex
virus or varicella-
varicella-zoster
virus
Pathology Etiology Feature Treatment
Fungal Candida spp. can Not common, mostly occur in Topical antifungal
cause immunocompromised patient,
conjunctivitis after topical corticosteroid and
Blastomyces antibacterial therapy to an
dermatitidis inflamed eye
Sporothrix
schenckii
Vernal Allergy Chronic conjungtival bilateral Removal allergen
inflammation, associated atopic Topical antihistamine
family history, itching, Vasoconstrictors
photophobia, foreign body
sensation, blepharospasm,
cobblestone pappilae, Horner-
trantas dots
Inclusion Chlamydia several weeks/months of red, Doxycycline 100 mg
trachomatis irritable eye with mucopurulent PO bid for 21 days OR
sticky discharge, acute or Erythromycin 250 mg
subacute onset, ocular irritation, PO qid for 21 days
foreign body sensation, Topical antibiotics
watering, unilateral ,swollen
lids,chemosis ,Follicles
http://www.patient.co.uk/doctor/Contact-Lens-
62.
62. CONTACT LENS Problems.htm
Causes changes in the • Predisposing factors:

cornea • Dry eye
structure, turnover, tear • Blepharitis.
production and oxygen and
carbon dioxide levels • Atopic or allergic
Associted with: conjunctivitis.
type of lens used (eg soft, • Poor lens care or
rigid, gas-permeable) inexperienced CL user.
the frequency with which • Prolonged lens wear
the lenses are changed,
the cleaning systems including overnight wear.
Clinical manifestation: • Smoking.
pain and irritation or • Immunosuppression.
watering of the eye and a • Trauma or surgery.
red eye • Increasing age.
• Systemic disease.
Problems.htm
POOR LENS CARE
Accumulation of protein and lipid deposits on

the lens
cause irritation of the cornea and impaired visual
acuity
Bacteria, protozoa and fungi form a film over the
lens and the fungal filaments may invade the lens
itself
Ensure that the patient is using the lenses correctly
so as to prevent future deposit formation.
Problems.htm
ACANTHAMOEBA KERATITIS
Sign & symptom:
Pain
watery eyes
Irritation
photophobia ± red eye
usually unilateral
Initially present with a dendritic-type ulcer
anydendritic keratitis in a CL wearer should be assumed to
be caused by Acanthamoeba spp. until proved otherwise.
Treatment
combinations of anti-amoebic agents
63. ASTIGMATISM
Vision is blurred due to the inability of the optics of
the eye to focus a point object into a sharp focused
image on the retina
Cause:
irregular or toric curvature of the cornea or lens
Types
Regular
arising from either the cornea or crystalline lens
can be corrected by a toric lens
Irregular
caused by a corneal scar or scattering in the crystalline lens
cannot be corrected by standard spectacle lenses
can be corrected by contact lenses
CLASSIFICATION
Simple astigmatism
Simple hyperopic astigmatism
first
focal line is on retina, while the second is located
behind the retina.
Simple myopic astigmatism
firstfocal line is in front of the retina, while the second is
on the retina.
Compound astigmatism
Compound hyperopic astigmatism
both focal lines are located behind the retina.
Compound myopic astigmatism
both focal lines are located in front of the retina.
Mixed astigmatism
focal lines are on both sides of the retina (straddling
the retina).
http://www.improveeyesighthq.com/Corrective-Lens-Astigmatism.html
http://en.wikipedia.org www.medscape.com
64. CONGENITAL GLAUCOMA

Disorders Feature
Ambliopia Decrease of vision; disuse/inadequate foveal/peripheral retinal
stimulation and/or abnormal binocular interaction that cause
different visual input
Congenital abnormal eye development, congenital infection
glaucoma present at birth, epiphora,
epiphora, photophobia, and blepharospasm,
blepharospasm,
buphtalmus (>12
(>12 mm)
Retinoblastom rapidly developing cancer that develops in the cells of retina,
a amaurotic cat's eye reflex,deterioration of vision, a red and
irritated eye with glaucoma, and faltering growth or delayed
development,strabismus
Katarak clouding of the lens of the eye that is present at birth, Leukocoria
congenital or white reflex, nfant doesn't seem to be able to see,nystagmus
Peters anomaly anterior segment dysgenesis , may have an inherited pattern,
Central, paracentral, or complete corneal opacity,no
vascularization of this opacity occurs
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH000258
2/
Peters anomaly
Retinoblastoma
CONGENITAL
http://www.wrighteyecare.com/Peters_Anomaly.html
GLAUCOMA
http://www.stjude.org/Images/misc-retinoblastoma-0602.jpg
http://emedicine.medscape.com/article
CONGENITAL GLAUCOMA
Primary
Improper development of the eye's aqueous outflow
system, leading to increased intraocular pressure (IOP),
with consequent damage to ocular structures, resulting
in loss of vision
developmental abnormality that affects the trabecular
meshwork
Secondary
associated ocular or systemic anomalies
inflammation, trauma, and tumors
Exp:Peters anomaly, Rubella infection, Toxoplasma
infection
NEUROLOGI
PEMERIKSAAN SARAF KRANIALIS
No. 65
MIDBRAIN & CRANIAL NERVES
N. OLFACTORIUS (I)
Sensation of smell
Cara:
Kooperatif
Mata terpejam
Hidung bebas
hambatan
Dg kopi, tembakau,
teh
Lubang dites satu
persatu
N. OPTICUS (II)
Visus:
Snellen card (6/6)
Jari (../60)
Lambaian tangan (…/300)
Cahaya (…/~)
Warna (Ishihara)
Visual fields
Tes konfrontasi
Tes perimetri
Tes konfrontasi
perimetri
Pem fundus:
Discus (papil edema, atrofi)
Arteri & vena
Retina (perdarahan,
eksudat, tuberkel)
N. OCULOMOTORIUS (III)
Ptosis (klp mata jatuh)
Gerakan bola mata
Ke medial, atas, bawah
Refleks cahaya (+/-)
Ukuran pupil (mm):
Cahaya dari lateral mata
Bentuk pupil (isokor/anisokor)
Diplopia (pandangan dobel)
Nistagmus (gangg balans tonus
otot bola mata)
N. TROCHLEARIS (IV)
Gerak bola mata ke
lateral bawah
Diplopia (pandangan
dobel)
Nistagmus (gangg balans
tonus otot bola mata)
N. ABDUCENS (VI)
Gerak bola mata ke
lateral
Diplopia (pandangan
dobel)
Nistagmus (gangg balans
tonus otot bola mata)
N. TRIGEMINUS (V)
Fungsi:
Sensasi wajah
Gerakan mengunyah
Refleks cornea
Sentuhan kapas basah
pd limbus cornea
Bilateral blink (+)
Gerakan mengunyah:
Palpasi otot masseter
Buka mulut
Jaw jerk (sulit)
Saraf peka nyeri

N. FACIALIS (VII)
Fungsi:
Gerakan wajah
Pengecap 2/3 lidah
depan
Sekresi gld lacrimalis
& gld salivarius
Gerakan wajah:
Meringis
Tutup mata
Kerutkan dahi
Pengecap:
Gula, garam, cuka, kinina
Disentuh dg cottonbuds
Sekresi:
Inhalasi amonia (lakrimal)
Bumbu yg keras (saliva)
N. AUDITORIUS (VIII)
Fungsi:
Pendengaran (cochlear
nerve)
Keseimbangan (vestibular
nerve)
Pendengaran:
Garputala
Rinne’s test:
udara/tulang
Weber’s test: tulang
Schwabach’s test:
pt/examiner
Keseimbangan:
Rotational test:
Diputar di kursi 10x
selama 20 detik
Caloric test:
Irigasi dg air 250 ml
selama 40 dtk, suhu
30ºC & 44ºC
Romberg test:
Berdiri kaki rapat,
buka & tutup mata
N. GLOSSOPHARYNGEUS (IX)
Fungsi:
Mengatur otot
palatum & pharynx
Sensasi di pharynx,
tonsil, palatum, lidah
blkg
Refleks muntah
Pengecap 1/3 blkg
lidah
Saraf peka nyeri

N. VAGUS (X)
Fungsi:
Mengatur otot palatum &
pharynx
Refleks menelan
Disfagia
Sensasi di pharynx, tonsil,
palatum, lidah blkg
Mengatur otot pita suara
Saraf peka nyeri

N. ACCESSORIUS (XI)
Otot-otot leher
Otot-otot bahu
N. HYPOGLOSSUS (XII)
Otot lidah
Disartria (gangg
artikulasi)
Menjulurkan lidah:
mencong
Fasikulasi, tremor,
atrofi (tanda perifer)
TEKANAN TINGGI INTRAKRANIAL
No. 66
CSF PRESSURE
Normal
1-15 mmHg or <200mm H2O
Low pressure
Dehydration
Increased pressure
Valsalva,Tumor,
Subdural Hematoma,
Subarachnoid Hemorrhage, Infections,
Hydrocephalus
SYMPTOMS OF INCREASING ICP
Headache • Aniscoria
Visual changes • Hemiparesis
Nausea • Vital sign
Vomiting changes
Behavior changes
– Cushing
Triad
Changes in LOC
Seizures
CUSHING’S TRIAD
Vital Sign Changes in ICP :

1. Systolic pressure increases (widened pulse
pressure results).
2. Slowing of heart occurs—bradycardia (occurs as
result of reflexive slowing in response to
increased systolic pressure)
3. Respiration changes—becomes slowed
DIAGNOSIS OF INCREASED INTRACRANIAL
PRESSURE
Overt symptoms
Papilledema
Nuchal rigidity
COMMON CAUSES OF INCREASED-ICP
Vascular abnormalities
AV malformations, aneurisms, stroke
Diffuse cerebral ischemia
Closed head trauma, shaken baby, vasospasm
CNS infections
Tumors
Trauma
Obstruction of CSF flow
LOW BACK PAIN
No. 67
DIFFERENTIAL DIAGNOSIS OF LOW
BACK PAIN
Mechanical low back pain (97%)
Lumbar strain or sprain (≥ 70%) Diffuse pain in lumbar muscles; some radiation to buttocks
Degenerative disk or facet process (10%) Localized lumbar pain; similar findings to lumbar strain
Herniated disk (4%) Leg pain often worse than back pain; pain radiating below knee
Osteoporotic compression fracture (4%) Spine tenderness; often history of trauma
Spinal stenosis (3%) Pain better when spine is flexed or when seated, aggravated by
walking downhill more than uphill; symptoms often bilateral
Spondylolisthesis (2%) Pain with activity, usually better with rest; usually detected with
imaging; controversial as cause of significant pain
Nonmechanical spinal conditions (1%)

Neoplasia (0.7%) Spine tenderness; weight loss
Inflammatory arthritis (0.3%) Morning stiffness, improves with exercise
Infection (0.01%) Spine tenderness; constitutional symptoms
Nonspinal/visceral disease (2%)

Pelvic organs—prostatitis, pelvic inflammatory disease,
endometriosis
Lower abdominal symptoms common
Renal organs—nephrolithiasis, pyelonephritis Usually involves abdominal symptoms; abnormal urinalysis
Aortic aneurysm - Epigastric pain; pulsatile abdominal mass
Gastrointestinal system—pancreatitis, cholecystitis, peptic ulcer Epigastric pain; nausea, vomiting
Shingles - Unilateral, dermatomal pain; distinctive rash
*—Estimated percentage of patients with this condition among all adult patients with low back pain in primary care.
DIAGNOSES & RED FLAGS
Cancer Fracture
Age > 50 Age >50
History of Cancer Trauma
Weight loss Steroid use
Unrelenting night Osteoporosis
pain
Failure to improve Cauda Equina
Infection Syndrome
IVDU Saddle anesthesia
Steroid use Bowel/bladder
Fever
dysfunction
Loss of sphincter control
Unrelenting night
pain Major motor weakness
Failure to improve
HERNIATED NUCLEUS PULPOSUS
Clinical Features
Injury : history of falling, or lifting heavy

weights
Leg pain : Root irritation or compression
produces pain in the distribution of the
affected root. Coughing, sneezing or
straining aggravates the leg pan which is
more severe than backache
Parasthesia : Numbness or tingling
occurs in the distributing of affected root
Muscle weakness or fatigue in the
buttocks, legs and feet
Soreness or stiffness
NEUROLOGIC EXAMINATION
(L4 LEVEL)
Motor
Tibialis Anterior
Resisted inversion of ankle
Reflexes
Patellar Reflex (L2, L3, L4)
Sensory
Medial side of leg
(L5 LEVEL)
Motor
Extensor Hallicus Longus
Resisted dorsiflexion of great toe
Reflexes - none
Sensory
Dorsum of foot in midline
(S1 LEVEL)
Motor
Peroneus Longus and Brevis
Resisted eversion of foot
Reflexes
Achilles
Sensory
Lateral side of foot
STRAIGHT LEG RAISING (SLR) TEST
• L5 & S1 COMRPRESION CAUSES

LIMITATION TO LESS THAN 60O
FROM HORIZONTAL AND
PRODUCES PAIN DOWN THE
BACK OF LEG.
• DORSOFLEXION OF THE FOOT
WHILE THE LEG IS ELEVATED
AGGRAVATES THE PAIN.
• ELEVATION OF THE GOOD LEG
MAY PRODUCE PAIN IN THE
OTHER LEG.
OTHER INVESTIGATION
FEMORAL STRECH TEST
TEST FOR IRRITATION OF HIGHER NERVE ROOTS ( L4 AND
ABOVE) X- Ray Lumbosacral :
limited benefit, excluding
other pathology e.q
matastatic carcinoma
CT scan :
MRI :
best choice
Radiculography
HERNIATED NUCLEUS PULPOSUS
Nonoperative Care
Initial bed rest
Nonsteroidal anti-
inflammatory (NSAID)
medication
Physical therapy
Exercise/walking
Steroid injections
Operatitive Care
Reccurent attacks of leg
pain
Severe unremitting leg pain
The development of
neurological deficit
ACUTE MANAGEMENT
Medications
Pain control
Tylenol/NSAID’s
minimize narcotic use
Muscle relaxers
use Valium for short
term (1-2 days)
Corticosteroids
2mg/Kg burst for 5-7
days
PARESE NERVUS FASIALIS
No. 68
DIFFERENTIAL DIAGNOSIS
TIA
Ramsay Hunt Syndrome

Acoustic Neuromas
Heerfordt’s Syndrome
Melkersson-Rosenthal Syndrome
HERPES ZOSTER OTICUS
(RAMSAY HUNT SYNDROME)
10-15% of acute facial palsy cases

Lesions may involve the external ear, the skin of
EAC or soft palate
Associated symptoms – hearing loss, dysacusis
and vertigo
Additional involvement of CN V, IX and X and
cervical branches 2, 3 and 4
Pathogenesis – Neural injury due to edema at
point between the meatal foramen and the
geniculate fossa in the labyrinthe segment
MELKERSSON-ROENTHAL SYNDROME
Triad
Recurrent orofacial
edema
Recurrent facial palsy
(50-90%)
Lingua plicata (fissure
tongue) – 25%
Lips become chapped,
fissured and red-brown in
appearance
Biopies identify
granulomatous changes
Facial nerve decompression
may be indicated if facial
paralysis is severe and
recurrent
WHAT IS BELL’S PALSY?
Bell’s Palsy :
Is a paralysis
Causes weakness of
the muscles
Causes facial muscles
to droop
AFFECTS
Affects one side of the
face
The sense of taste
As well as the ability to
make tears and saliva
CAUSES
Cause is not clear,
clear some
cases are linked to the
herpes virus
Mostly caused by
inflammation of the
nerve that controls the
facial muscles
Some are linked to brain
tumors or lyme disease
But is NOT caused by a
stroke
SIGNS AND SYMPTOMS
Unilateral facial Pain behind the ear
paralysis Tearing
Inability to close the
Drooling
eye
Hyperacusis
Absence of the
nasolabial fold Sag of the eyebrow
May be loss of taste
on anterior tongue
DIAGNOSIS
Based on clinical findings
Imaging studies used to rule out other
pathology
Lyme titers, PCR testing may indicate
cause
TREATMENT
Corticosteroids (efficacy not proven)
Analgesics
Lubricating eye drops

Taping eye closed at night
Massage of the weakened muscles

PROGNOSIS
Generally very good
Most patients get significantly better in
about 2 weeks even without treatment
80-85% recover completely within 3
months
10% have permanent disfigurement or
other long term sequelae
PENYAKIT PARKINSON
No. 69
DIAGNOSTIC FEATURES
Four Cardinal Signs

T remor
R igidity
A kinesian and bradykinesia
P ostural instability
Clinical features of PD
Resting tremor: Most common first symptom, usually asymmetric and most
evident in one hand with the arm at rest.
Bradykinesia: Difficulty with daily activities such as writing, shaving, using a knife
and fork, and opening buttons; decreased blinking, masked facies, slowed chewing
and swallowing.
Rigidity: Muscle tone increased in both flexor and extensor muscles providing a
constant resistance to passive movements of the joints; stooped posture,
anteroflexed head, and flexed knees and elbows.
Additional clinical features of PD
Postural instability: Due to loss of postural reflexes.
Dysfunction of the autonomic nervous system: Impaired

gastrointestinal motility, bladder dysfunction, sialorrhea, excessive head and neck
sweating, and orthostatic hypotension.
Depression: Mild to moderate depression in 50 % of patients.
Cognitive impairment: Mild cognitive decline including impaired visual-spatial

perception and attention, slowness in execution of motor tasks, and impaired
concentration in most patients; at least 1/3 become demented during the course of
the disease.
STATUS EPILEPTIKUS
No. 70
DEFINITION
Two or more seizures without recovery or

consciousness in between.
Single seizure >20-30 min.
MANAGEMENT
First aid
Ensure airway patent
Give oxygen
Secure IV access
Draw blood for glucose, E/U& Cr, LFT, etc
Give diazepam 10 mg IV, repeat once only after

15mins, after 30mins give phenytoin 15mg/kg @
50mg/min, after 30-60mins intubate and give
general anaesthesia (propofol, thiopental)
NYERI KEPALA PRIMER
No. 71
PRIMARY, IDIOPATHIC HEADACHES
Tension type of
headache
Migraine
Cluster headache
Other, rare types
of primary
headaches
TERAPI MIGREN
ACUTE POLINEUROPATHY
No. 72
GBS DEFINITION
A variety of acute, acquired, immune- mediated,
often self-limiting polyneuropathies
• History of an inciting event, such as a diarrheal

illness or vaccination, recovering from a febrile illness
DIFFERENTIAL DIAGNOSIS OF NEUROPATHIES BY
CLINICAL COURSE
Acute onset Subacute onset Chronic Relapsing/
(a few days – 4 (weeks to months) course/ remitting
weeks) insidious course
onset
Guillain-Barré Maintained exposure to Hereditary motor Guillain-Barré
syndrome toxic sensory syndrome
agents/medications neuropathies
Acute intermittent Persisting nutritional Dominantly CIDP
porphyria deficiency inherited sensory
neuropathy
Critical illness Abnormal metabolic CIDP HIV/AIDS
polyneuropathy state
Diphtheric Paraneoplastic Toxic
neuropathy syndrome
Thallium toxicity CIDP Porphyria
CLASSIFICATION
A raised CSF protein concentration is present in
about 80% of patients
But CSF protein content is more likely to be
normal during the first days of the illness
CSF should be analysed before treatment with
intravenous immunoglobulin (IVIg), which can
cause aseptic meningitis
CLINICAL COURSE
In typical cases, the first symptoms
Numbness
Paraesthesia feet then hands
Pain : especially back pain
Weakness in the limbs
The weakness may initially be proximal, distal, or a
combination of both
Numbness and paraesthesia usually affect the
extremities and spread proximally
In 25% of cases, weakness of the respiratory
muscles requires artificial ventilation
Rapid progression
Bulbar palsy
Upper limb involvement
Autonomic dysfunction
Autonomic involvement is common
Urine retention
Ileus
Sinus tachycardia
Hypertension
Cardiac arrhythmia
Postural hypotension
The disease reaches its nadir by 2 weeks in most
cases and in 4 weeks in nearly all
Recovery begins with return of proximal,
followed by distal, strength over weeks or
months.
Between 4% and 15% of patients die
Up to 20% are disabled after a year despite

modern treatment
INVESTIGATION
SUPPORTIVE CARE
Monitor Resp status closely (follow NIFs), up

to 30% may req ventilatory support
In severe cases, intrarterial monitoring may
be necessary given the significant blood
pressure fluctuations
Neuropathic pain plagues most, often
managed w/ Gabapentin or Carbamazepine
DISEASE MODIFYING TREATMENT
IVIG : typically given for 5 d at 0.4 gram/kg/d (may
need to extend course depending on response)
Plasmapheresis: usually 4-6 treatments over 8-10
days
The choice b/w plasma exchange and IVIG is dep on

availability, pt contraindications, etc. Because of
ease of administration, IVIG is frequently preferred.
The cost and efficacy of the 2 treatments are
comparable.
Glucocorticoids have NO ROLE!!
HEAD INJURY
No. 73
SDH
Subdural hematomas
Most frequently from
tearing of a bridging vein
between the cerebral
cortex and a draining
venous sinus. Shape-
Crescent
- acute - <24hrs
- subacute – 24hrs-2wks
- chronic - >2wks
INTRA CEREBRAL HEAMATOMA
Formed within brain tissue & caused by shearing or tensile
forces that mechanically stretch and tear deep small caliber
arterioles
Most common in temporal and frontal regions
C/F depend on site involved
CONCUSSION
Temporary & brief interruption of neurological function after
minor head injury
Due to shearing / stretching of white matter fibres at the time
of impact or temporary neuronal dysfunction
C/o headache, confusion, amnesia
CT/MRI cannot detect
APPROACH TO A PATIENT WITH
HEAD INJURY
History
Initial Assessment
Primary Survey
Secondary Survey
PRIMARY SURVEY
Airway maintenance with cervical spine protection

INTUBATION WITH CERVICAL INLINE
STABILIZATION
Breathing and ventilation : Intubation precautions
Pre-medicate with Lidocaine, 1mg/kg IV 2 minutes
prior to attempt
Laryngoscopy produces an ICP Spike
CIRCULATION
Maintain MAP >90mmhg- adequate
Hematocrit >30%
Cushing reflex
INDICATIONS FOR CT SCAN / MRI
Skull fracture
Deteriorating GCS
Neurologic deficit
Amnesia, headache
Seizure
HERNIASI OTAK
No. 74
Brain herniations represent shift of the normal
brain through or across regions to another site due
to mass effect
Generally complications of mass effect whether
from tumor, trauma, or infection
4 large categories :
1. transtentorial
2. subfalcine
3. foramen magnum
4. alar or sphenoid herniation
UPPER LIMB MONONEUROPHATY
No. 75
BRACHIAL PLEXUS INJURIES
Loss of sensation will occur along the

medial side of the arm
Lower lesions can also be produced by a

presence of a cervical rib or malignant
metastases from the lungs in the lower
deep cervical lymph nodes
LONG THORACIC NERVE
( C5C6C7)
Supplies : Seratus anterior muscle Damaged by :
Carrying heavy object
Strapping the shoulder
Limited branchia neuritis
Diabetes melitus
Result in :
Winging of the scapula
Whe arms are streched in
front
AXILARY NERVE
( C5C6)
Supplies : deltoid & teres minor muscle Damaged by :
Shoulder dislocation
Limited bachial neuritis
Result in :
Weakness of abduction of
shoulder between 150-900
Sensory loss over the
outer aspect of the
shoulder
RADIAL NERVE
( C6C7C8)
Damaged by :
Fraktur of the humerus
Prolonged pressure
(satuday night palsy) :
Drunkard falling
asleep with one arm
over the back of a
chair.
Intramuscular injection
Lipoma,, fibroma,
Lipoma
neuroma
RADIAL NERVE
( C6C7C8)
Result in :
Weakness & wasting of
muscle supplied,
characterized by wrist
drop with flexed finger
(weak ekstensor).
Sensory loss of dorsum
hand n forearm.
Loss of triceps reflex
(when lession in the
axilaa) & supinator
reflexes
MUSCULOCUTANEUS NERVE
( C5C6)
Supply : Coracobrachialis, Damaged by :
biceps, brachialis Fraktur of the humerus
Systemic causes
Sensory supply : lateral border
of the arm
Result in :
Weakness of the elbow
flexion with
characterized sensory
loss
Absent
MEDIAN NERVE
( C7C8)
Sensory supply :
palmar surfaces of the
radial border of the
hand
Damaged by :
Injury in axilla
Compression at the
wirst (Carpal Tunnel
Syndrom)
MEDIAN NERVE
( C7C8)
Result in:
Weakness of abduction and apposition of thumb
Weakness of pronation of the forearm
Deviation of wrist to ulnar side on wrist flexion
Weakness of flexion of distal phalanx of thumb and index
finger
Wasting of thenar muscles is evident
Sensory loss is variable but most marked on index and
middle fingers
CARPAL TUNNEL SYNDROME
The carpal tunnel is formed by the

concave anterior surface of carpal bones
and closed by flexor retinaculum
Clinically, the syndrome consists of a
burning pain or pins & needles along the
distribution of the median nerve,
paresthesi
Lateral 3 & ½ fingers are involved
CARPAL TUNNEL SYNDROME
Condition is relieved
by decompressing
the tunnel by making
a longitudinal incision
through the flexor
retinaculum
ULNAR NERVE
( C7C8)
Sensory supply :
Both palmar and dorsal
surfaces of the ulnar
border of the hand
Damaged by :
Injury at elbow
Entrapment at elbow or
distal to the medial
epicondyle
Pressure on the nerve in
the palm
ULNAR NERVE
( C7C8)
Result in :
Ulnar claw hand
Sensory loss
ULNAR NERVE
( C7C8)
Sensory supply :
Both palmar and dorsal
surfaces of the ulnar
border of the hand
Damaged by :
Injury at elbow
Entrapment at elbow or
distal to the medial
epicondyle
Pressure on the nerve
in the palm
LOWER LIMB MONONEUROPHATY
No. 76
NERVES OF THE LOWER LIMB
Lumbar plexus T12-L5
Femoral nerve L2-L4 (VPR)
Obturator nerve L2-L4 (VPR)
Sacral plexus L4-S5

Sciatic nerve L4-S3
Tibial
L4-S3
Common peroneal/fibular L4-S2
Superficial peroneal L5-S2
Deep peroneal L4-S2
VPR – ventral primary rami
FEMORAL NERVE
( L1L2L3)
Damaged by : Result in :
Weakness of hip flexion
Fraktur of the upper
Weakness of knee extension with
femur wasting of thigh muscles
Congenital dislocation Sensory loss over the anterior and
medial aspect of thigh

of the hip
The knee jerk is lost
Neoplastic infiltration
Abses psoas muscle
Hematom iliopsoas
muscle
Diabetes melitus
FEMORAL NERVE INNERVATION
Anterior thigh muscles
Sartorius
Pectineus
Iliacus
Quadriceps
Cutaneous & proprioception
Hip & knee joint
Infrapatellar regoin
Medial femoral cutaneous
Intermediate femoral cutaneous
Saphenous-medial knee
OBTURATOR NERVE
( L2L3L4)
Medial thigh muscles
Adductors: brevis, longus,
½ magnus
Gracilis
Obturator externus
Hip & knee joint
Medial thigh
OBTURATOR NERVE
( L2L3L4)
Weakness of hip external rotation &
Same process as the adduction
femoral nerve Inability to cross the affected leg on the
During labour other

Sensory loss innermost aspect of the
Compression by hernia thigh
in the obturator canal Adductor reflex is absent
Sciatic Nerve
( L4,L5,S1,S2)
Lower limb muscles

Muscles of the posterior thigh
Muscles of the leg
Muscles of the feet
Hip, knee, & ankle
Posterior thigh & leg
Lateral leg
Plantar and dorsal foot
Sciatic Nerve
( L4,L5,S1,S2)
Weakness of hamstring muscles with
Congenital or traumatic loss of knee flexion
hip dislocation Distal foot and leg muscles are also
Penetrating injury affected

Sensory loss outer aspect of the leg
Misplaced Angkle reflex is absent
intramuscular injection
Entrapment at sciatic
notch
COMMON FIBULAR/PERONEAL N.
NEUROPATHY
At the region of the fibular head
ankle sprain
fibula fractures
habitual leg crossing
knee dislocations
total knee or hip arthroplasty
vaginal childbirth
Strawberry Picker’s Palsy
Signs & Symptoms :

Weakness dorsiflexion & eversion foot
Walks with “foot drop”
Sensory loss : dorsum & outer foot
*most often injured nerve of the lower limb

TIBIAL NERVE NEUROPATHY
Tibial nerve
Tarsal tunnel syndrome *
Burning pain in the sole foot
Weakness of toe flexion and athropy of small musle

of the foot
Prolonged sensory conduction velocity confirms in
diagnosis
Sergical decompresiion is often required
Signs & Symptoms

Weaknes of plantar flexion & inversion foot
Patient cannot stand on toes
Sensory loss : the sole of the foot
the ankle reflex is lost
•Most common entrapment neuropathy in the foot and ankle area

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PEMBAHASAN MATA

Causes Etiology Clinical

Acute Infection , Allergy itching and burning or a gritty, foreign-body sensation,

Cataract Decreased visual acuity, contours, shadows and color

Diabetic Blurred vision, progressive visual los, dot & blot

PERIPHERAL ULCERATIVE KERATITIS (PUK)

Disturbance of the structural or functional

1. Primer yaitu timbul pada mata yang

glaucoma that develops

ANGLE-CLOSURE (ACUTE) GLAUCOMA

Disorders Feature Correction

Astigmatisma Unspherical corneal structure; distorted image Lens correction,

Presbyopia the eye exhibits a progressively diminished ability to Correction lens

60. OPTIC NEUROPATHY

Disease Etiology Clinical

Causes changes in the • Predisposing factors:

POOR LENS CARE

Accumulation of protein and lipid deposits on

64. CONGENITAL GLAUCOMA

Saraf peka nyeri

Saraf peka nyeri

Saraf peka nyeri

Vital Sign Changes in ICP :

Nonmechanical spinal conditions (1%)

Nonspinal/visceral disease (2%)

Injury : history of falling, or lifting heavy

Resisted inversion of ankle

Resisted dorsiflexion of great toe

Resisted eversion of foot

• L5 & S1 COMRPRESION CAUSES

Ramsay Hunt Syndrome

10-15% of acute facial palsy cases

Lubricating eye drops

Massage of the weakened muscles

Four Cardinal Signs

A kinesian and bradykinesia

Dysfunction of the autonomic nervous system: Impaired

Depression: Mild to moderate depression in 50 % of patients.

Cognitive impairment: Mild cognitive decline including impaired visual-spatial

Two or more seizures without recovery or

Draw blood for glucose, E/U& Cr, LFT, etc

Give diazepam 10 mg IV, repeat once only after

• History of an inciting event, such as a diarrheal

Upper limb involvement

Up to 20% are disabled after a year despite

Monitor Resp status closely (follow NIFs), up

The choice b/w plasma exchange and IVIG is dep on

Airway maintenance with cervical spine protection

Loss of sensation will occur along the

Lower lesions can also be produced by a

The carpal tunnel is formed by the

Sacral plexus L4-S5

medial aspect of thigh

During labour other

Lower limb muscles

Penetrating injury affected

habitual leg crossing

total knee or hip arthroplasty

Strawberry Picker’s Palsy

Signs & Symptoms :

Walks with “foot drop”

Sensory loss : dorsum & outer foot

*most often injured nerve of the lower limb