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Diabetes is a common disease throughout the world, with a prevalence that is expected to roughly double by the year 2030 to an estimated 366 million affected individuals globally.[1,2] This disease frequently causes microvascular complications of the eye, kidney, and nerve. As the fifth leading cause of blindness globally, diabetic retinopathy has a significant impact on patient quality of life. Although it is not clear exactly how diabetes leads to eye disease, hyperglycemia is a known risk factor for the incidence and progression of diabetic retinopathy. Three major classifications of diabetic retinopathy are recognized: DME, nonproliferative diabetic retinopathy (NPDR), and PDR. The principal features of DME include retinal swelling due to increased capillary leakage and deposits of hard exudates, especially at the borders of areas of edema.[16] Any lesion within a half disc diameter of the center of the macula is sight-threatening,[16] so DME is a potentially blinding disorder. Microaneurysms are the hallmark of NPDR (Figure 3), but cotton-wool spots (diffuse white patches representing areas of ischemia), venous dilation and beading (irregularities in the contour of the capillary walls resembling a string of pearls), intraretinal hemorrhages, and intraretinal microvascular abnormalities (IRMAs) may also be present.[16] It is particularly important for the ophthalmologist to be able to identify when NPDR is about to develop into PDR. For purposes of discussion with other healthcare providers, NPDR and PDR may be staged according to the International Clinical Diabetic Retinopathy Severity Scale, shown in Figure 5. Additional imaging techniques are available to resolve any lingering diagnostic uncertainty following fundus examination with slit-lamp biomicroscopy and examination of the peripheral retina with indirect ophthalmoscopy.
The American Academy of Ophthalmology (AAO) has issued evidence-based management recommendations for diabetic retinopathy. In summary, diabetic retinopathy is related to other DMC, and is a common complication of a highly prevalent endocrine disorder, diabetes mellitus.
Resnikoff S, Pascolini D, Etya'ale D, Kocur I, Pararajasegaram R, Pokharel GP, Mariotti SP. How does lymphedema arise?Damage, blockage or absence of lymph vessels leads to a reduced transport capacity of the lymph vessel system. How can lymphedema be treated?Combined Decongestive Therapy (CDT) is a successful method of treating lymphedema. Figure 2:(2a)The axial image demonstrates edema along the joint line in the posteromedial and posterior central knee (arrows). The posteromedial corner of the knee (PMC) is comprised of the structures between the posterior border of the superficial medial collateral ligament (SMCL) and the medial border of the posterior cruciate ligament (PCL).
The POL originates from the adductor tubercle of the medial femur, just posterior and proximal to the MCL and anterior and inferior to the medial head of the gastrocnemius. The semimembranosus tendon fans out distally with 5 insertions, attaching to bone, capsule, ligaments and the medial meniscus.
Figure 3:An axial plane illustration of the knee at the level of the menisci demonstrates the components of the posteromedial corner.
Many of the normal individual components of the PMC are difficult to see on MRI because of their complex anatomy, thinness and close association with other structures.4 The POL can be identified by location, as it forms the capsular layer posterior to the SMCL (Figures 4-7). Figure 4:Posterior to the SMCL, low signal intensity fibers representing the posterior oblique ligament (arrows) are evident adjacent to the medial epicondyle.
Figure 5:A T1-weighted sagittal image demonstrates the normal tendon origin of the medial head of the gastrocnemius along the posteromedial aspect of the medial femoral condyle (arrow). Figure 6:Above the level of the joint, the medial gastrocnemius tendon (arrow) and the semimembranosus tendon (arrowhead) lie in close proximity. Figure 7:Sequential axial images from proximal to distal demonstrate the fan like distal attachment of the semimembranosus (arrows).
Many injuries of the PMC can be identified by recognizing edema and soft-tissue thickening at the posteromedial knee, posterior to the MCL, in the expected location of the POL. Figure 8:An axial fat-suppressed proton density-weighted image in a 13 year old following a fall with twisting reveals soft tissue thickening and edema throughout the region of the POL (arrows). Figure 9:Axial and coronal fat-suppressed proton density images in a 15 year-old with medial pain demonstrate avulsive marrow edema within the medial epicondyle (asterisks), at the expected attachment site of the POL. Figure 10:Axial and sagittal fat-suppressed proton density-weighted images in a 28 year-old female with posteromedial pain reveals fluid and edema compatible with partial tearing at the tendon origin of the medial head of the gastrocnemius (arrows). Figure 11:An axial fat-suppressed proton density-weighted image in a 25 year-old who had a hyperextension injury with PCL disruption. Figure 12:A T2 weighted sagittal image in a 43 year-old with medial pain and swelling reveals lobulated fluid within the pes anserine bursa (arrows), compatible with bursitis. Clinical evaluation for PMC injuries includes testing for medial opening of the knee with valgus stress with the knee in full extension and in 30 degrees of flexion. Injuries of the posteromedial corner of the knee are easily overlooked but functionally significant. The retina is a layer of tissue at the back of the eye4 that processes objects in the visual field and sends signals to your brain.
If left untreated, people affected by CRVO can experience severe eye complications, which can cause significant vision loss. The retina consists of multiple layers that receive blood supply from two distinct systems of blood flow (dual circulation). The CRV shares a connective tissue with the CRA20 and generally runs the same course as the CRA. Two types of CRVO: Non-Ischemic & IschemicThe terminology used to describe CRVO traditionally has been inconsistent and controversial. CRVO is considered to be ischemic, or non perfuse, when blood flow in the retinal capillaries is more widely obstructed,30 a condition called capillary nonperfusion, causing an ischemic condition of the retina. Severity of vision loss, prognosis and response to treatment35 can be affected by the specific location and extent of the vein occlusion,36 as well as the degree of macula involvement in conditions of edema, ischemia or hemorrhage.37 Macular edema is a primary cause of vision loss in CRVO. The compression of the CRV causes the vein to narrow and leads to increased intravascular pressure, sluggish or turbulent blood flow, endothelial cell damage43 and, ultimately, occlusion of the central retinal vein.44 The occlusion obstructs blood flow and the extent of this obstruction determines whether the CRVO is ischemic or non-ischemic. Symptoms & Importance of Early DiagnosisVision loss or distortion in vision in CRVO patients is typically sudden and painless.60 61 If you experience any changes in vision, see an eye care specialist immediately.
That is why it is critical to be screened for CRVO if vision loss or distortions occur, and to begin treating the condition in its early stages. TestingThree common tests can detect and identify the extent of CRVO: funduscopy, fluorescein angiography and optical coherence tomography.



This test uses a hand-held ophthalmoscope to identify retinal hemorrhage or other abnormalities that indicate the presence of CRVO. If signs of CRVO are found, an eye care specialist will perform a fluorescein angiography (FA). If you have not been diagnosed with CRVO but suspect that some of the risk factors may apply to you, go see the appropriate doctors and get tested for hypertension, vascular disorders and glaucoma. If you are diagnosed with CRVO, get tested for systemic risk factors, such as hypertension or diabetes. Understanding VEGF & CRVOThe vascular endothelial growth factor (VEGF) is a glycoprotein that has been found to contribute significantly to the development of macular edema in people with CRVO.
This site has been determined by HON in Geneva, Switzerland to comply with standards for trustworthy health information. These diabetic microvascular complications, or DMC, manifest clinically as diabetic retinopathy, diabetic nephropathy, and diabetic neuropathy, respectively. Rapid increases in the number of microaneurysms, hemorrhages in all 4 quadrants, cotton-wool spots, and IRMAs adjacent to areas of capillary bed closure are all signs of high-risk NPDR. While direct ophthalmoscopy can detect microaneurysms and neovascularization, and may be useful in settings lacking better equipment, its lack of 3D capability means that it cannot accurately detect retinal thickening. DME can be classified more precisely by OCT than it can with ophthalmoscopy or biomicroscopy, so OCT may be used in the future to determine treatment recommendations for DME.[21,22] OCT images are color-coded representations of retinal thickness, so they do not replace fundus images obtained with standard biomicroscopy. DME is a potentially blinding complication that may occur at any stage of diabetic retinopathy. The rising global burden of diabetes and its complications: estimates and projections to the year 2010.
Prevalence of diabetic eye disease in patients entering a systematic primary care-based eye screening programme.
The prevalence of retinopathy in an unselected population of type 2 diabetes patients from Arhus County, Denmark.
Management of French patients with type 2 diabetes mellitus in medical general practice: report of the Mediab observatory. Prevalence of retinopathy in Caucasian type 2 diabetic patients from the South of Brazil and relationship with clinical and metabolic factors. The appearance of retinopathy and progression to proliferative retinopathy: the WHO multinational study of vascular disease in diabetes. Incidence of sight-threatening retinopathy in patients with type 2 diabetes in the Liverpool Diabetic Eye Study: a cohort study.
ICO international clinical guidelines: diabetic retinopathy (initial and follow-up evaluation). Proposed international clinical diabetic retinopathy and diabetic macular edema disease severity scales. International Clinical Classification of Diabetic Retinopathy Severity of Diabetic Macular Edema.
It can be caused by a deficiency of lymph vessels or nodes during fetal development and this type is called Primary Lymphedema.
Fluid and proteins can then not be removed properly and they start to accumulate in the tissues especially in the skin where many lymph vessels are found. It must be adapted to the specific requirements of each patient and treatment should only be attempted by a fully qualified therapist (hyperlink to Find a Therapist) who understands not only the pathology but also the most appropriate treatment.
This edema is in the expected location of the posterior oblique and oblique popliteal ligaments and the posterior joint capsule.
The SM flexes and internally rotates the knee and pulls the PHMM out of the joint during flexion, preventing impingement of the meniscus by apposing surfaces of the tibia and femur. At this level the semimembranosus (SM) can be seen contributing fibers to the oblique popliteal ligament (OPL) and to the posterior capsule. The medial gastrocnemius tendon and the semimembranosus can typically be directly visualized on either sagittal or axial images. Following trauma, injuries to the POL may be accompanied by marrow edema due to avulsive forces related to the strong proximal attachment of the POL at the adductor tubercle (Figures 8 and 9). There is diffuse posteromedial edema in the region of the POL(arrowheads), and the SM is thickened and edematous (arrow) compatible with partial tearing. Knowledge of the anatomy of this area is crucial as the imaging findings may consist of edema without clear visualization of the individual structures.
Anatomical reconstruction of the medial collateral ligament and posteromedial corner of the knee in patients with chronic medial collateral ligament instability. Regeneron Announces FDA Approval of EYLEA® (aflibercept) Injection For Macular Edema Following Central Retinal Vein Occlusion.
EYLEA® (aflibercept) Injection Approved For The Treatment of Macular Edema Following Central Retinal Vein Occlusion In Japan. FDA Approves Lucentis® (Ranibizumab Injection) for the Treatment of Macular Edema Following Retinal Vein Occlusion.
A small part of the retina, called the macula, is critical for seeing fine details clearly. This is a more severe form of CRVO in which vision is more likely to be poor and complications, such as neovascularization, are more likely to occur, depending on the degree of the ischemia.31 32 33 34 The degree of retinal ischemia depends on the extent of nonperfusion, so the greater the nonperfuse area, the greater the ischemia, and the greater the risk for complications. The condition can present with dilated or tortuous veins and intraretinal hemorrhage throughout the entire retina. FA is a test that takes images of the eye to evaluate the blood flow in the back of the retina.67 68 69 FA can identify the areas of capillary nonperfusion, leakage, and hemorrhage,70 which can affect treatment strategies. The increase in vascular permeability and weakened vessel wall cause blood vessels to leak fluid and blood into the retina, resulting in retinal edema.88 As fluid continues to accumulate in the retina, it ultimately reaches the macula and causes macular edema. Diabetic retinopathy is frequently underdiagnosed and studies have shown that early detection and treatment are key factors in delaying the progression of the disease. NPDR may progress to PDR with longer duration of diabetes, or poorer control of such risk factors as hyperglycemia and blood pressure.


As the vessels shear from normal motion of the vitreous gel, they bleed, and often develop a fibrous attachment to the vitreous that causes retinal traction. Indirect ophthalmoscopy, used with a dilated eye exam, allows a wide field of view and 3D retinal examination capability.
Additionally, since OCT measures the anatomic, but not the functional, status of the retina, it does not make FA an obsolete technique either. The 14-year incidence and progression of diabetic retinopathy and associated risk factors in type 1 diabetes. It can also be the result of an external cause such as the removal of lymph nodes, radiation, obstruction, trauma or injury to the lymph vessels. Vodder method of Manual Lymph Drainage and Combined Decongestive Therapy and to ensure the continuing competence of practitioners trained by the Dr. Fat-suppressed proton density axial (1a) and coronal (1b) images from the study are provided.
The central or tibial component is the most prominent and attaches strongly to the PHMM near the posterior tibial articular surface. The posterior oblique ligament (POL) is found between the superficial medial collateral ligament (SMCL) and the semimembranosus tendon on this view.
As the medial gastrocnemius tendon and SM tendon3,4 can be directly visualized, injuries to these structures can be specifically diagnosed by recognizing the intrinsic abnormalities of the affected regions (Figures 10 and 11). Proper identification of PMC injuries may lead to alterations in the treatment pathway, particularly in the setting of coexistent cruciate ligament disruption. Potential Anti-Vascular Endothelial Growth Factor Therapies for Central Retinal Vein Occlusion. The Prevalence of RVO: Pooled Data from Population Studies from the US, Europe, Asia and Australia. Management of Macular Edema Secondary to Branch Retinal Vein Occlusion: an Evidence-Based Update. Vascular Endothelial Growth Factor Promotes Progressive Retinal Nonperfusion in Patients with Retinal Vein Occlusion.
Ranibizumab for Macular Edema following Central Retinal Vein Occlusion Six-Month Primary End Point Results of a Phase III Study. Sustained benefits from ranibizumab for macular edema following central retinal vein occlusion: twelve-month outcomes of a phase III study.
Recurrence of macular edema in retinal vein occlusions after treatment with intravitreal ranibizumab (Lucentis).
Vascular Endothelial Growth Factor Trap-Eye for Macular Edema Secondary to Central Retinal Vein Occlusion Six-Month Results of the Phase 3 COPERNICUS Study.
VEGF Trap-Eye for macular oedema secondary to central retinal vein occlusion: 6-month results of the phase III GALILEO study.
Intravitreal Aflibercept Injection for Macular Edema Secondary to Central Retinal Vein Occlusion: 1-Year Results From the Phase 3 COPERNICUS Study.
Eighteen-Month Results of the GALILEO Study Evaluating Intravitreal Aflibercept Injection (IAI) for Macular Edema Secondary to Central Retinal Vein Occlusion (CRVO). Cotton-wool spots and edema of the optic disc may occur in some patients.50 Macular edema is often found in CRVO patients upon diagnosis51 and requires treatment to prevent severe or permanent vision loss.
Currently many FA instruments have digital imaging capability, permitting quantitative measurements to be made from the image series. Because diabetic retinopathy is frequently asymptomatic even in severe disease, periodic comprehensive eye examinations are recommended for all patients with diabetes. However all patients who have had damaged or deficient lymph systems are at risk of developing lymphedema (Foeldi E, Foeldi M, Kubik, S. The superior or capsular arm is most posterior and is continuous with the posterior joint capsule and the OPL, lying deep to the medial head of the gastrocnemius. The PMC is a primary stabilizer of the extended knee, the load-bearing position of the knee in gait. The medial head of the gastrocnemius muscle (MG), sartorius muscle (SA), gracilis tendon (G) and semitendinosus tendon (ST) are also indicated. This refers to anterior subluxation and external rotation of the medial tibial plateau with respect to the femur. Slit-lamp biomicroscopy permits 3D examination of both the retina and the anterior chamber, permitting diagnosis of NPDR, PDR, and DME, as well as cataract and other eye disorders that occur more frequently in patients with diabetes. Ultrasonography can be used in the presence of media opacities, and is therefore the most valuable imaging modality when vitreous hemorrhage is present. Recently, 20 MHz ophthalmic ultrasound probes have become available that permit high resolution imaging comparable to optical coherence tomography (OCT). Patients should consult with their physician regarding the use of medications for lymphedema. Other causes of posteromedial edema include a ruptured popliteal cyst, parameniscal cyst and pes anserine bursitis (Figure 12).
The POL is the primary stabilizer for internal rotation at all flexion angles and helps prevent posterior translation in extension.
In these cases the cruciate tear is repaired first, then the medial structures are repaired or reconstructed, from deepest to most superficial. The POL, with the SMCL, stabilizes valgus stress, internal and external rotation and anterior and posterior tibial motion. If a repair is performed, the POL and postermedial capsule are then sutured to the MCL and the lax SM attachments are retensioned to the POL or MCL.2 Reconstruction is frequently performed using the semitendinosus tendon which is released, leaving the pes anserinus insertion intact.



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