Transcript Hypertensive angiosclerosis

Lecture 6
THE CHANGES OF VISUAL ORGAN
IN SYSTEMIC DISEASES
Lecture is delivered by
Ph. D., assistant of professor Tabalyuk T.A.
FUNDUS CHANGES IN ARTERY HYPERTENSION
(Krasnov M., 1948)
Hypertensive angiopathy – mild generalized arteriolar narrowing,
tortuosity and dilation of veins, Gvists’ symptom (tortuosity of small
venuls around macula).
Hypertensive angiosclerosis – thickening of arteriolar walls, «cooper
wiring», «silver wiring», symptom of arteriovenous crossing:
Salus-Gun-Relman I - conic narrowing of vein in arteriovenous crossing;
Salus-Gun-Relman II - arc bending of vein in arteriovenous crossing;
Salus-Gun-Relman III - absence of vein picture in arteriovenous crossing.
Hypertensive retinopathy – all above changes plus retinal haemorrhages,
cotton wool spots and hard exudates.
Hypertensive neuroretinopathy – all above changes plus optic disc
swelling.
Management:
 control of blood pressure and treatment by general practitioner;
 regular review if treatment is not indicated;
 vitaminotherapy, tissue therapy and proteolitic ferments to dissolve retinal
haemorrhages and exudates.
Salus-Gun-Relman I
Salus-Gun-Relman III
Hypertensive retinopathy
(Kanski Jack)
Grade 1 – mild generalized arteriolar narrowing
Grade 2 – focal as well as marked generalized
arteriolar constriction
Grade 3 – as Grade 2 plus retinal haemorrhages,
cotton wool spots and hard exudates
Grade 4 – as Grade 3 plus optic disc swelling
Retinal artery occlusion (RAO)
Aetiology: embolization from a carotid or cardiac source,
or vazoobliteration by atheroma or arteritis.
Clinical features: acute loss of vision; may be permanent
or transient (amaurosis fugax). Retinal pallor
corresponding to the involved area (central or branch) is
seen, and in central RAO a «cherry red spot» at the
fovea is typically present. Segmentation of the arteriolar
blood column («cattle trucking») may be seen. Later the
arterioles become attenuated and the optic disc pale.
Emmergency: s/l nitroglicerini, validoli, euphyllini i/v, nospa or acidi nicotinici i/m, diacarbi per os.
Acute RAO may be relieved by lowering IOP by nassage,
intravenous acetaxolamide, anterior chamber
paracentesis
Central retinal artery occlusion with
«cherry-red spot»
Retinal vein occlusion (RVO)
Predisposing factors include increasing age, hypertension,
hyperviscosity, trombophilic disorders, and raised IOP.
Presents with sudden mild to severe loss of vision in one
eye. Acute signs include haemorrhages, cotton wool
spots, venous tortuosity, optic dics and retinal oedema.
Fundus picture in RVO is called picture of «pressed
tomato» or «red ischaemia».
Classification:
Branch RVO – usually involves a retinal quatrant;
Hemiretinal veib occlusion;
Central RVO (ischaemic or non-ischaemic).
Emmergency: anticoagulants (heparini), trombolytics
(streptodekesa), and antiagregants (pentoxiphillini)
systemically.
Central retinal vein occlusion
Branch retinal vein occlusion
Peculiarities of renal hypertension – exudative syndrome,
retinal oedema, a lot of cotton wool spots on gray background,
optic disc swelling, «star figure» in macula.
Peculiarities of atherosclerosis - exudative syndrome is not
typical, the primary are thickening of arteriolar walls, «cooper
wiring» «silver wiring».
Fundus picture in pregnancy toxicosis is like changes in
hypertensive angiopathy, retinopathy, neuroretinopathy
(arteriolar narrowing, its tortuosity, haemorrhages, cotton wool
spots, optic disc swelling, «star figure» in macula). Despite
artery hypertension in arteriolar spasm caused by pregnancy
toxicosis, symptoms of arteriovenous crossing are not marked.
In severe retinal swelling on background of pregnancy toxicosis
transsudative retinal detachment or retinal vein occlusion may
happen.
Retinopathy in renal hypertension.
A color fundus photograph that shows optic disk swelling,
cotton-wool spots (blue arrow), hemorrhages (white
arrow), retinal exudation and a macular star (green arrow).
Diabetic retinopathy (DR) is the most common cause of blidness
in the working-age population. The incidence of severity of DR are
strongly related to duration of diabetes: good control of blood
glucose and hypertension are very important.
Fundus picture in diabetic angiopathy - tortuosity
and dilation of veins, microaneurysms;
nonproliferative DR – dot and blot haemorrhages and hard
exudates in retina;
proliferative DR – new vessel formation at the optic disk or
elsewhere on the retina. Severe visual loss may occur as a
result of vitreous haemorrhage or tractional retinal detachment
due to constriction of fibrovascular tissue.
diabetic maculopathy is the most common cause of visual
impairment in patients with diabetes. Loss of visual functions is
usually caused by oedema, typically accompanied by exudates.
Less commonly, the macula becomes ischemic, often with
severe deterioration in central vision.
Nonproliferative diabetic retinopathy
Management of DR:
Regular review if treatment is not indicated,
frequency dependent on severity of DR;
Panretinal laser photocoagulation for proliferative DR;
Grid or focal laser photocoagulation for macular
oedema fitting certain criteria (clinically significant macular
oedema);
.
Vitrectomy for persistant vitreous haemorrhage or
tractional retinal detachment involving the centre of the
macula.
Fundus photo showing scatter laser
surgery for diabetic retinopathy.
The complex of hyperthyroidism (Graves’ disease) consists of
the following eye signs:
Proptosis due to abnormal fluid infiltration of orbital
contents;
Retraction of the upper lid due to overaction of the levator
muscle (Dalrimple’s symptom);
Diplopia due to malfunction of the extrinsic ocular muscle;
Visual loss due to the effects of corneal exposure or of
pressure on the optic nerve;
Infrequent blinking (Shtelfag’s sign);
Convergence weakness (Mebius sign);
Hyperpigmentation of upper eyelid (Ellinek’s sign);
Graefe’s sign is lid lag; failure to follow the eyeball on
down gaze;
Joffroi’s sign is excessive retraction of the upper lid on
looking upwards.
Thyroid orbitopathy
The ear diseases, i.e. purulent processes in it may be a source
of purulent methastasis into the orbit and eyeball. As a result
orbital cellulitis, choroiditis, panuveitis, panophthalmitis, optic
neuritis may occur.
The nose diseases may cause conjunctivitis, blepharitis,
chronic dacriocyctitis.
The stomatological diseases may result in orbital periostitis or
cellulitis, keratitis or iridocyclitis.
The brain tumours are assosiated with papilloedema,
hemianopsia, paralysis of oculomotor muscles, visual
disturbances of cortical genesis.
In rheumatoid diseases usually uvea is involved. Iridocyclitis,
choroiditis or panuveitis may occur.
Orbital cellulitis
Signs:
 eyelids oedema
 chemosis
 proptosis
 limiting of eye movements
 decreasing of visual acuity
 general intoxication (headacke,
increased temperature, brain
signs).
Optic neuritis, papilloedema, central
vein occlusion may occur with
outcome in optic atrophy.
OPTIC NEURITIS – inflammation of the optic nerve, with a
range of causes, the most important being multiple sclerosis.
Clinical features: presents with subacute, usually unilateral,
impairment of central vision that may be associated with pain,
especially on eye movement. The optic disc is usually normal
(retrobulbar neuritis) and occasionally swollen and red
(papillitis). Severe or recurrent attacks may lead to optic
atrophy.
PAPILLOEDEMA – disc swelling caused by raised intracranial
pressure.
Clinical features: symptoms of raised intracranial pressure
including headaches and nausea. Transient visual obscuration
lasting a few seconds are common but visual acuity is normal
until late.
Signs: early – hyperaemia with indistinct margins;
established – obvious elevation, peripapillary
haemorrhages and cotton wool spots;
long-standing – markedly elevated «champagne
cork» appearance;
Optic neuritis
Papilloedema
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