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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5771_Библиотеки_им_академика_М_И_Перельмана.pdf
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A B
Ocular Inflammatory Diseases
C D
E
Figure 12.7 Sarcoidosis. Fundus photograph showing pale peripapillary choroidal lesion with extensive disk congestion, edema, and dilated retinal vessels
(A). Transverse B-scan showing an irregularly shaped peripapillary choroidal lesion (arrow) overlying the optic disc and extending around the retrobulbar
optic nerve. Note low reflective widening (asterix) (B). Diagnostic A-scan showing regular internal structure with medium reflectivity (arrows) (C). Posttreatment fundus photograph showing regression of choroidal lesion with normalization of optic disc and retinal changes (D). Chest CT scan demonstrating
mediastinal lymphadenopathy that on biopsy was confirmatory for sarcoidosis (E).
137
Ophthalmic Ultrasonography
12
Figure 12.8 Toxocariasis. Transverse B-scan demonstrating a taut
membrane (arrow) extending across the vitreous and adherent to an
irregularly shaped, highly reflective granuloma that is causing shadowing of
the orbit (arrowhead).
Taban M, Lowder CY. Ocular inflammatory diseases. Ultrasound Clin 2008; 3:245–255.
Reproduced with permission from: Ventura ACM, Hayden BC,
A
Hypotony
Uveitic hypotony may be acute or chronic. Acute hypotony is often related to an active inflammatory process,
due to prostaglandin-mediated increased uveoscleral
outflow, impaired secretory function of the ciliary body,
or supraciliary or suprachoroidal effusion.
Chronic hypotony, defined as intraocular pressure of
less than 6 mmHg, may occur as a result of chronic
uveitis, and may or may not be associated with active
inflammation (Figure 12.11). Other causes of hypotony
include long-standing retinal detachment, ocular trauma
and previous vitreous surgery. Hypotony in uveitis is
multifactorial. Chronic inflammation may lead to the
formation of ciliary membranes, damage to the secretory
ciliary epithelium and tractional ciliary body detachment,
resulting in decreased aqueous production and hypotony.
Atrophy of the ciliary processes may cause permanent
damage to the aqueous secretory mechanism.
Uveitic patients with chronic hypotony and patients
with opaque media, are among those that most benefited
from UBM examination in a study by Tran et al, demonstrating great clinical value and improving the management in a significant manner.17 The length of ciliary
processes may be measured by UBM. Patients with diffuse
and recurrent uveitis have been shown to have a significant loss of the ciliary processes, particularly in the inferior quadrant. Patients who are found to have atrophic
changes may need a more aggressive treatment approach
for any signs of inflammation, to prevent further damage
and eventual hypotony (Figure 12.12).18 Findings that
have been described by UBM examination in chronic
hypotony include epiciliary membranes, supraciliary
effusion, ciliary traction and detachment, massive
16
B
C
Figure 12.9 Toxoplasmosis. Marked vitreous haze with toxoplasmosis
lesions of the fundus (A). Longitudinal B-scan at a low gain demonstrating a
posterior vitreous detachment (arrowhead) and a dome-shaped, elevated
lesion of the fundus (arrow) (B). Diagnostic A-scan demonstrating the
regularly structured, medium-high reflectivity of the lesion (arrows) (C).
138
12
Figure 12.10 Vogt–Koyanagi–Harada syndrome. Axial B-scan showing
marked choroidal thickening (arrow) and a serous retinal detachment
(arrowhead).
Lowder CY. Ocular inflammatory diseases. Ultrasound Clin 2008; 3:245–255.
Reproduced with permission from: Ventura ACM, Hayden BC, Taban M,
thickening of the anterior uvea and ciliary atrophy (Figure
12.13
). The proliferating tissue covering or causing traction on the ciliary processes is a potentially reversible
cause of chronic hypotony. The location and thickness of
epiciliary membranes may guide the surgical approach.
The absence of ciliary process atrophy may suggest a
better surgical prognosis. In the setting of atrophy, surgery
alone may not lead to a significant rise in intraocular
pressure or improvement in vision.
16,19–20
Ocular Inflammatory Diseases
A
B
Scleral inflammatory disease
Episcleritis
Episcleritis is an inflammatory condition that affects the
episcleral tissue, which lies between the sclera and conjunctiva. Most cases are idiopathic, although up to a third
may be related to an underlying systemic disorder, such
as collagen vascular diseases or infectious entities. Most
patients with episcleritis complain of an acute onset mild
to moderate ocular discomfort, associated with a sectorial
or diffuse injection. A freely mobile nodule may be noted
in cases of nodular episcleritis. The diagnosis is primarily
clinical, based on slit-lamp examination. When episcleritis is severe, UBM may be performed to demonstrate episcleral thickening and distinction of the low-to-medium
reflective episcleral tissue from the underlying highly
reflective scleral tissue (Figure 12.14).
21
Scleritis
Scleritis is an inflammatory condition affecting the sclera
and can occur in any age group, but typically presents
between ages 30 and 50, affecting females more commonly than males. The prevalence in the general population is estimated to be 6 per 100 000 people.
22
C
Figure 12.11 Chronic hypotony secondary to uveitis. Fundus photo
showing vitreous haze (A). Axial B-scan at a low gain showing marked
thickening of the posterior fundus (arrows) (B). Transverse B-scan at a high
gain showing dense, clumped vitreous opacities adjacent to the thickened
choroid (arrows) (C).
139
Ophthalmic Ultrasonography
12
A
C
Figure 12.12 Chronic hypotony causing loss of ciliary body processes. Transverse UBM of a normal eye showing normal length ciliary body processes (A).
Transverse UBM in eyes with chronic hypotony demonstrating mild (B), moderate (C), and marked truncation of the ciliary body processes (D).
B
D
Figure 12.13 Epiciliary membrane. Radial UBM shows a cyclitic membrane
(arrow) adherent to the ciliary body (small arrows).
140
The disorder can be divided into anterior or posterior,
based on the anatomic distribution of the disease.
Anterior scleritis
Anterior scleritis is further subdivided into diffuse,
nodular, necrotizing with inflammation and necrotizing
without inflammation. Presenting symptoms of anterior
scleritis typically include ocular pain poorly responsive to
analgesics, associated with redness, which persists after
application of topical phenylephrine. Ultrasonography in
anterior scleritis can demonstrate thickening of the anterior sclera, as well as the presence of shallow ciliochoroidal detachments. UBM can be important in the evaluation
and differentiation of anterior scleritis by defining the
involved area and recognizing areas of scleral thinning,
nodular lesions and regions of necrosis (Figure 12.15).
Focal areas with decreased reflectivity and thickening
can typically be detected, probably representing the
Ocular Inflammatory Diseases
12
A
Figure 12.14 Episcleritis. External photograph showing conjunctival and episcleral congestion (A). Radial UBM showing a low reflective dome-shaped
elevation (white arrow) and clearly distinct scleral borders (black arrows) (B).
A B
B
C
Figure 12.15 Anterior scleritis. External photograph showing marked scleral congestion (A). UBM shows scleral thickening (arrow) and areas of low
reflectivity (asterix) (B). Associated inflammation may cause enlargement of ciliary body (small arrows) (C).
141
Ophthalmic Ultrasonography
12
Figure 12.16 Necrotizing scleritis. Longitudinal UBM demonstrates marked
thickening and diffuse, hyporeflective areas within sclera (asterix).
perivascular or scleral infiltration and edema.23 Onset of
necrosis has been characterized by the presence of lowreflectivity pockets by UBM (Figure 12.16). Necrotizing
scleritis can be followed by marked tissue loss, but slitlamp examination may be limited to determine the extent
of scleral thinning. UBM examination can quantify the
scleral thickness with a high degree of accuracy.
23
Specific entities
Intraocular tumor masquerading as scleritis
In rare circumstances, choroidal melanoma and metastatic carcinoma can masquerade as scleritis, confounding
the diagnosis. Inflammation is usually secondary to
tumor necrosis. Careful evaluation by ophthalmoscopy
and ultrasonography is necessary to establish the correct
diagnosis (Figure 12.19).
25
Endophthalmitis
Infectious endophthalmitis is a potentially devastating
condition that may result as a major complication of
surgery or trauma or may develop from an endogenous
source elsewhere in the body. Ultrasonography can be
used to determine the extent and severity of the condition. Reported findings include dense vitreous opacities
and membranes, posterior vitreous detachment, hyaloid
thickening, large endovitreal vacuoles, choroidal thickening, macular edema, choroidal abscess or granuloma,
optic nerve head swelling, choroidal detachment, retinal
traction and detachment (Figure 12.20).
26–27
Postoperative non-infectious
inflammation after cataract surgery
Posterior scleritis
The diagnosis of posterior scleritis may be more challenging due to its non-specific clinical features. Certain
patients can present with minimal clinical findings.
Ocular examination may be entirely normal or may disclose the presence of exudative retinal detachment, chorioretinal lesions, optic nerve edema, subretinal mass,
choroidal effusion and vasculitis. B-scan ultrasonography
is an essential tool for an accurate diagnosis of posterior
scleritis. The most important finding is thickening of the
sclera, which can vary in degree and can be either diffuse
or localized. Usually, the thickened sclera is highly reflective, with regular internal structure. Thickening of the
retinochoroid layer can also be observed. There may be
an associated inflammatory reaction in the episcleral
region (Figure 12.17). In the peripapillary region, episcleral inflammation results in distention of sub-Tenon’s
space, and may produce the echographic “T-sign”
(Figure 12.18).
Nodular posterior scleritis can present as an elevated
choroidal mass and mimic an intraocular tumor (Chapter
11). The thickened sclera in these nodular lesions demonstrates high reflectivity with regular internal structure
on ultrasonography. Choroidal and ciliary body detachments, as well as ciliochoroidal effusion syndrome may
also occur in the setting of posterior scleritis and can be
confirmed by ultrasonography (Figure 12.5).
24
The breakdown of the blood–aqueous barrier and release
of inflammatory agents, due to excessive surgical manipulation or irritation of ocular tissue by an intraocular lens
(IOL) is the major cause of postoperative noninfectious
inflammation in pseudophakic eyes. An IOL that erodes
into tissues may lead to chronic inflammation. A case
series by Ozdal et al showed misplacement of one or both
haptics by UBM in 68.5% of cases of chronic postoperative inflammation. Clinically relevant lens remnants were
present in 11.1% of patients. Edematous ciliary body
processes and thickened ciliary bodies were observed in
20.4% of cases. Treatment with anti-inflammatory agents
or surgical repositioning or removal of IOL can be considered according to UBM findings (Figure 12.21).
28
Inflammatory orbital diseases
Inflammatory orbital diseases can be either infectious or
non-infectious. Frequently the inflammation is idiopathic
and referred to as “orbital pseudotumor” or “non-specific
orbital inflammation”. Both children and adults may be
affected. Symptoms depend on the involved tissue and
can include proptosis, extraocular muscle restriction, conjunctival inflammation and chemosis, and soft tissue
edema. Imaging studies with orbital computerized tomography (CT) scan, magnetic resonance imaging (MRI)
and ultrasonography are important in the diagnosis.
Pain associated with ocular rotations suggests myositis.
142
12
A B
Ocular Inflammatory Diseases
C D
E F
Figure 12.17 Posterior scleritis. External photograph demonstrating marked injection of anterior sclera (A). Longitudinal (B) and transverse (C) B-scan
demonstrating marked, diffuse thickening of the posterior fundus and sclera (arrows) with a thin band of low reflectivity in Tenon’s space (black arrows)
indicative of posterior scleritis. Diagnostic A-scan showing highly reflective thickening of the posterior fundus and sclera (D). Note bullous choroidal
detachments (arrows) with moderate, clumped opacities beneath (asterix) on transverse B-scan (E) of the peripheral fundus and corresponding fundus
photograph (F).
143
Ophthalmic Ultrasonography
12
A
Figure 12.18 “T-sign” in posterior scleritis. Axial B-scan shows posterior scleral thickening and low reflective infiltrate behind the peripapillary sclera and
optic nerve creating the classical “T-sign” (A, arrows). Axial B-scan showing marked thickening of the sclera with only a very thin band of low reflectivity
behind the peripapillary sclera (B, arrows).
2008; 3:245–255.
A B
Reproduced with permission from: Ventura ACM, Hayden BC, Taban M, Lowder CY. Ocular inflammatory diseases. Ultrasound Clin
B
C D
Figure 12.19 Melanoma of the choroid mimicking scleritis. Slit lamp photograph shows anterior scleritis (A). Fundus photograph showing elevated
pigmented ciliochoroidal mass (B). Modified immersion B-scan longitudinal (C) and transverse (D) shows an irregularly shaped, shallowly elevated lesion in
the cilio-choroidal region (arrows).
144
Ocular Inflammatory Diseases
12
Figure 12.20 Endophthalmitis. Transverse B-scan showing marked
membrane formation (arrow) throughout the vitreous space and marked,
irregular fundus thickening (small arrows).
A
Figure 12.21 Displaced IOL eroding iris. Radial UBM showing grossly
centered IOL (arrowhead) with haptic (arrow) adjacent to thinned iris (small
arrow).
B
C
Figure 12.22 Orbital myositis. External photograph demonstrating exotropia of the left eye (A). B-scan shows marked enlargement of the medial rectus
muscle (arrow) and its inserting tendon (small arrow), longitudinal view (B) and transverse view (C). A-scan demonstrating regular structure and low
reflectivity of the lesion (D).
D
145
Ophthalmic Ultrasonography
12
E
G
Figure 12.22, cont’d
left medial rectus.
F
Orbital CT scan (E, axial view), post contrast MRI (F, T1 axial view), and pre contrast (G, T1 coronal view) confirming enlargement of the
Imaging shows enlargement of one or more extraocular
muscles, involving the tendinous insertions (Figure
12.22
). In contrast, Graves’ orbitopathy is characterized
by enlargement of muscles but sparing of the muscle
tendons. Orbital CT scan or MRI are the preferred imaging
modalities for evaluation of the orbital muscles.
Ultrasonographic diagnosis of Graves’ orbitopathy is
based on the following features: absence of mass lesion,
enlargement of orbital tissues with a heterogeneous
reflectivity, thickening of the bellies of at least two
extraocular muscles, and thickened periorbital tissue
(Figure 12.23).
29
Figure 12.23 Graves ophthalmopathy. Longitudinal B-scan shows marked
enlargement of the lateral rectus muscle (arrows) with an inserting tendon
of normal thickness (arrowhead).
Hayden BC, Taban M, Lowder CY. Ocular inflammatory diseases. Ultrasound Clin 2008;
3:245–255.
146
Reproduced with permission from: Ventura ACM,