Archive for the ‘Eye Diseases’ Category

The Original OCT – First OCT Course anno 2003…old but not dusty!

Friday, February 7th, 2014

>English version find below

Es ist unglaublich und wunderschön zu sehen, wie OCT zum Segen der modernen Augenmedizin geworden ist. Die wirklich interessante Geschichte begann circa 2003, wo mit dem ersten kommerziell verfügbaren Time-Domain-OCT Stratus eine neue Epoche in der augenmedizinischen Diagnostik und Therapie eingeläutet wurde. Für den Patienten stand erstmals eine schonende und berührungsfreie Methode bereit, die ohne Nebenwirkungen beliebig oft wiederholt werden konnte.

Follow the first OCT presentation:

Download the first OCT presentation (113MB:  OCT anno 2003 Dr Maloca

OCT Original - the rey first presentation about OCT. Copyright © 2014 GETOCT™ Ltd. All rights reserved.

OCT Original – the very first presentation about OCT. Copyright © 2003-2014 GETOCT™ Ltd. All rights reserved.

Der Augenarzt betrat zuerst einen völlig neuen Mikrokosmos, obwohl aus histo-pathologischen Studien schon sehr viel bekannt war. Dennoch galt es mit Fleiss und Ausdauer, Erfahrungen zu sammeln, um die beste Diagnostik und Therapie zu finden. So haben beide Seiten von der heute etwas angestaubten, aber in den Grundzügen noch stets modernen Time-Domain-Technologie profitiert und viele Augen konnten gerettet werden.

Diabetes mellitus. Copyright © 2014 GETOCT™ Ltd. All rights reserved.

Diabetes mellitus. Copyright © 2003-2014 GETOCT™ Ltd. All rights reserved.

Als Erinnerung an diese “gute alte OCT-Zeit” wird hier der allererste Vortrag zu “OCT und Auge” veröffentlicht. Die Krankheiten haben in all den Jahren nichts an ihrer Aktualität und Gefährdung verloren. Doch gelingt es heute immer besser, die gefährliche Situation schneller und effektiver zu meistern. Schon 2003 zeigte sich eine neue Bildsprache, die mit den OCT-Geräten der neuesten Spectral-Domain-Technologie weiter verfeinert wurde. Dem Augenarzt erschliesst sich diese manchmal eigenwillige Sprache nicht sofort, sodass die “Originale OCT-Präsentation anno 2003″ auch heute Prinzipen zur richtigen Diagnostik aufzeigen kann. Viele interessante Minuten wünscht Dr. med. Peter Maloca, Luzern/University Basel.

Klassische Altersabhängige Makuladegeneration (AMD). Copyright © 2014 GETOCT™ Ltd. All rights reserved.

Klassische Altersabhängige Makuladegeneration (AMD). Copyright © 2003-2014 GETOCT™ Ltd. All rights reserved.

 

It’s amazing and wonderful to see how OCT has become a blessing of modern ophthalmology. The really interesting history began circa 2003, where it was heralded with the first commercially available time-domain OCT Stratus, a new era in eye care diagnostics and therapy. The eye doctor first entered a completely new microcosm, even though it was already very much known from histopathological studies. Nevertheless, it was hard work and perseverance to gain the top-experience to find the best diagnosis and treatment. So both sides have benefited from the “2003 modern time-domain technology” and many eyes were saved.

As a reminder to those “good old OCT-time” , the very first lecture will be published here in its original version. The diseases have lost in all the years none of their risks. But they can be defined today more quickly and effectively. In 2003 there was a new “visual language” introduced , which has been refined with the newer OCT devices as with the latest spectral domain technology. The eye doctor does not understand this sometimes idiosyncratic language immediately, so that the “Original OCT presentation from 2003″ can reveal principles for proper diagnosis even today. Many interesting minutes wishes Dr. Peter Maloca, Lucerne /University Basel.

Retinopathia centralis serosa. Copyright © 2014 GETOCT™ Ltd. All rights reserved.

Retinopathia centralis serosa. Copyright © 2003-2014 GETOCT™ Ltd. All rights reserved.

Diagnostic Atlas of Retinal Diseases offered by Optos (c)

Sunday, September 1st, 2013

A nice gesture from Optos  to realize rapidly which more eye diseases have to be discovered.

Download-> DE_Optos_Diagnostic_Atlas_A4 (PDF).

Diagnostic Atlas of Retinal Diseases. Copyright © 2013 Optos + GETOCT™ Ltd. All rights reserved.

Diagnostic Atlas of Retinal Diseases. Copyright © 2013 Optos + GETOCT™ Ltd. All rights reserved.

Stargardt’s Disease: what is it? Fundus flavimaculatus

Sunday, February 10th, 2013

Stargardt’s disease is a genetic disease of the retina. Morbus Stargardt ist eine genetische Krankheit der Netzhaut.                                                                                           ->English version below.


->View: case from GETOCT database enriched by Dr. med. Filippo Simona, Locarno, Switzerland and Dr. med. Peter Maloca, Lucerne, Switzerland. Register for more details at www.getoct.com.

Filippo Simona, MD, Locarno, Switzerland

Filippo Simona, MD, Locarno, Switzerland

Peter Maloca, MD

Peter Maloca, MD, Lucerne, Switzerland

 

 

 

 

 

 

 

 

 

 

Stargardt’s disease is a genetic disease of the retina. Morbus Stargardt ist eine genetische Krankheit der Netzhaut. Copyright © 2013 GETOCT™ Ltd. All rights reserved.

Stargardt’s disease is a genetic disease of the retina, most common by mutations in the ABCA4 gene. Morbus Stargardt ist eine genetische Krankheit der Netzhaut. Am häufigsten ist eine Mutation im ABCA4-Gen zu finden. Copyright © 2013 GETOCT™ Ltd. All rights reserved.

Die Netzhaut ist eine wichtige Gewebeschicht im Auge. Ein essentieller Teil der Netzhaut wird Makula genannt und ist der Ort des schärfsten Sehens. Nur mit der Makula können kleine Details gesehen werden. Lesen eines Buches ohne eine gesunde Makula ist nicht möglich.

Defektes Gen als Ursache des Morbus Stargardt: ABCA4-Gen

Der deutsche Augenarzt Karl Stargardt hat diese beidseitige Augenkrankheit 1901 in Marburg beschrieben. Der Begriff Fundus flavimaculatus wurde durch den Schweizer Augenarzt Adolphe Franceschetti 1963 eingeführt.

Die Netzhaut ist aufgebaut durch verschiedene Zellen, die in Schichten angeordnet sind. Beim Morbus Stargardt sterben lichtempfindliche Zellen vor allem in der Makula langsam ab (Makuladegeneration). Üblicherweise wird der Begriff Makuladegeneration heute vor allem für einen Verlust der zentralen Sehschärfe bei älteren Personen verwendet. Makuladegeneration entspricht aber eine Gruppe von verschiedenen Krankheiten, welche schlussendlich zu einem ähnlichen Resultat führen: den Verlust des schärfsten Sehens, der in jedem Lebensalter auftreten kann.

Die Ursache beim Morbus Stargartdt ist ein genetischer Defekt, der zu einer übermässigen Ansammlung von Lipofuszin vor allem in den Pigmentblattzellen führt. Liposfuszin wird als “Alterspigment” betrachtet.  Damit die Krankheit ausbrechen kann, müssen beide Eltern Träger des Defektes sein. Erhält ein Kind nur von einem betroffenen Elternteil den Gendefekt, so ist es wohl Träger, wird aber selber keine Krankheit entwickeln. Die Stargardt-Krankheit zeigt sich schon in der Kindheit und Jugend. Meistens ist der Verlauf um so langsamer, je später im Leben die ersten Symtome auftreten.

ABCA4-Gen und Rim Protein – Vitamin-A-Dimer-Theorie

Das ABCA4-Gen ist verantwortlich für die Herstellung eines relativ grossen Proteins (sogenanntes Rim Protein). Ein gesundes Rim-Protein ist wichtig den Transport von Vitamin A von den lichtempfindlichen Sehzellen (Photorezeptoren) zu den Pigmentblattzellen (Retinales Pigmentblatt, RPE). Im Pigmentepithel wird normalerweise das Vitamin A rezykliert und wieder genutzt. Beim Morbus Stargardt funktioniert der Vitamin-A-Transport nicht ausreichend, sodass sich Vitamin A-Produkte ansammeln und in der Menge toxisch wirken (“Vitamin-A-Dimer”). Auch bei gesunden Menschen erfolgt eine gewisse Vitamin-A-Dimer-Produktion, doch dauert die Anreicherung mehrere Jahrzehnte, bis eine toxische Schwelle erreicht wird.

Copyright © 2013 GETOCT™ Ltd. All rights reserved.

Beim Morbus Stargardt führt ein teilweise defektes ABCA 4-Gen zu einem unzureichenden Transport von Vitamin A durch das RIM-Transportprotein. Copyright © 2013 GETOCT™ Ltd. All rights reserved.

Morbus Stargard: eine Krankheit – verschiedene Namen

Verschiedene Namen werden für diese Krankheit verwendet:

-Juvenile Makuläre Degeneration (lat. juvenilis = jugendlich, zeitliches Auftreten schon im jugendlichen Alter)
-Makuläre Dytrophie mit Flecken, Typ 1  (Erscheinungsform beim Betrachten mit dem Augenspiegel)
-Fundus flavi-maculatus (lat. fundus = Boden/Hintergund eines Organs,  flavi = gelb, maculatus = befleckt, , beschrieben durch den Schweizer Augenarzt Adolphe Franceschetti 1963)
-”Schießscheibenmakulopathie”oder ” Ochsenaugen-Makulopathie” (deutsch, Erscheinungsform beim Betrachten mit dem Augenspiegel)
-”Bull’s eye” (engl., Erscheinungsform beim Betrachten mit dem Augenspiegel)
-Stargardt’s Disease (engl. disease =Erkrankung)
-SGD (als Abkürzung)

Woran entdeckt man einen Morbus Stargardt?

Es entstehen Probleme mit dem zentralen Sehen, welches verschwommen, verzogen sein kann und durch dunkle Stellen beeinträchtigt ist. Die Gewöhnung von Hell zu Dunkel kann verlangsamt sein. Mühe mit der Nachtsicht, wobei im Vergleich mit anderen Krankheiten das Sehen in der Dunkelheit dennoch relativ gut ist.  Das äussere Gesichtsfeld bleibt erhalten, indessen treten Störungen des Farben-Sehens auf. Das Fortschreiten der Krankheit ist sehr unterschiedlich und sehr individuell. Üblicherweise ist der Verlauf langsam, kombiniert mit schneller ablaufenden Episoden, sodass das Lesevermögen verloren gehen kann. Die Krankheit kann im Alter zwischen 6 bis 20 Jahren beginnen, wobei erste Einschränkungen häufig erst ab dem dreissigsten Lebensjahr auftreten.

Die gute Nachricht

Beim Morbus Stargardt bleiben der Sehnerv und die äusseren Bereiche der Netzhaut ohne Schädigung. Deshalb tritt eine vollständige Erblindung praktisch nie ein.

Lipofuszin – “Alterspigment”

Lipofuszin (gr. lipo = Fett, fuscus= dunkle Farbe) wird auch als “Alterspigment” betrachtet. Lipofuszin besteht aus oxidierten Eiweissen und Fetten und ist ein nicht weiter verwertbares oder abbaubares Abfallprodukt. Es zeigt sich als intrazelluläres,  gelbbraunes Granulat und ist typischerweise um den Zellkern angeordnet. Es ist in vielen gesunden Geweben wie Nervenzellen, Pigmentepithel des Auges, der Leber und Herzmuskel vorhanden. Die Akkumulation von Lipofuszin im retinalen Pigmentepithel kann ein Warnsignal für eine degenerative Erkrankung des Auges sein.

Selbst im gesunden Gewebe ist ein gewisser Lipofuszinanteil vorhanden, als ein Zeichen des normalen Stoffwechsels und Abbaus von Produkten, insbesondere der Fette (Lipide). Wenn es zu Störungen im Abbau von Lipofuszin kommt, dann sammelt sich Lipofuszin in der Zelle an (Lysosomen) und entwickelt dann seine toxischen Eigenschaften.

 

Lipofuscin (gr. lipo = fat) considered as "aging pigment". It shows as intracellular finely yellow-brown granules and is arranged around the nucleus.

Lipofuscin (gr. lipo = Fett) wird als “Alterspigment” betrachtet. Auch in gesunden Zellen (1) ist Lipofuszin (3) vorhanden, typischweise um den vitalen Zellkern (2) herum. Sammelt sich zu viel Lipofuszin an (4) entstehen toxische Effekte und die Zelle (5) stirbt ab (6). Copyright © 2013 GETOCT™ Ltd. All rights reserved.

Wie wird die Diagnose eines Morbus Stargardt gestellt?

Die sorgfältige Anamnese liefert bereits hilfreiche Hinweise. Eine Kontrolle beim Augenarzt zeigt in einem frühen Stadium oft keine krankhaften Veränderungen. Der Augenarzt überprüft das Auge darum mit diversen Hilfsmitteln:

Sehschärfe (Kurzsichtigkeit-Myopie, Weitsichtigkeit-Hyperopie, Hornhautverkrümmung-Astigmatismus):

Meistens besteht nur eine geringe Fehlsichtigkeit, die mit geeigneten Gläsern korrigiert werden kann.

Augenspiegel (Fundusuntersuchung)

Bei jüngeren Menschen findet sich normalerweise bei der Augenspiegelung ein sogenannter Foveolarreflex, der beim Morbus Stargardt fehlen kann. Im Pigmentblatt wird übermässig viel fetthaltiges, gelbliches Pigment (Lipofuscin) abglagert und zerstört langsam die Pigmentblattschicht, vor allem um das Lesezentrums (Fovea) herum. Diese Veränderung erinnert in der Form an eine Schiessscheibe oder an ein Ochsenauge (“Schießscheibenmakulopathie“, “Bull’s eye“). Zudem sind gelbliche, unregelmäßige Flecken sichtbar. Im Spätstadium können neugebildete Gefässe entstehen (subretinale Neovaskularisationen).

Netzhautfotografie (Fundusaufnahme, Autofluoreszenez AF, Fluoreszenz-Angiograhphie FA)

Zur Dokumentation ist eine Fotografie der Netzhaut geeignet. Weit wichtiger ist die Autofluoreszenz-Fotografie, die im Bereich der zerstörten Pigmentblattzellen dunkle Flecken nachweist. Die Fluoreszenzangiografie zeigt wegen der übermässigen Einlagerung von Lipofuszin in den verbleibenden Pigmentblattzellen eine Blockade der Aderhautfluoreszenz, sogenannte dunkle Aderhaut (“dark choroid”). Neovaskularisationen sind in der Fluoreszenzangiografie rasch erkennbar.

Elektrophysiologische Untersuchungen der Netzhaut

Ein Elektrookulogramms (EOG) bzw. ein Ganzfeld-Elektroretinogramm (ERG) sind im Frühstadium wenig hilfreich. Die elektrische Antwort der zentralen Sinneszellen (Zapfen) im multifokalen Elektroretinogramm (mfERG) sind aber schon früh reduziert.

Therapie:

Die Krankheit kann noch nicht geheilt werden, obwohl viele genetische Behandlungen erprobt werden. Wichtig ist der Schutz der verbleibenden Zellen:
-Nicht Rauchen
-Vitamin reiche Ernährung
-Sonnenschutz (Hut, Sonnenbrille mit Schutz vor UV-Licht und blauem Licht)
-gut korrigierte Brille
-Low vision Hilfen

->Download video Stargardt’s Disease by Dr. med. Filippo Simona, Locarno, Switzerland:
Morbus Stargardt Dr Simona & GETOCT

Defective ABCA4- gene as the cause of Stargardt’s Disease

A German ophthalmologist Karl Stargardt has described this bilateral disease in 1901 in Marburg. The retina is an important layer of the eye. An essential part of the retina is called the macula and is the site of sharpest vision. Only with the macula small details can be seen. Reading a book without a healthy macula is not possible. The retina itself is constructed by different cells. In Stargardt’s disease light-sensitive cells in the macula die slowly (macular degeneration). Usually, the term macular degeneration is now used primarily for a loss of central vision in the elderly. Macular degeneration is a group of different diseases, which ultimately lead to a similar result: the loss of central visual acuity, what can happen at any age.

The cause of Stargardt’s Disease is a genetic defect. Both parents must be carriers of the defect, that the disease can break out.  A child of only one affected parent is only carrier, but will not  develop the disease itself. Stargardt’s disease usually appears in childhood and adolescence.

ABCA4 gene and Rim protein – vitamin A dimer

The ABCA4 gene is responsible for the production of a relatively large protein (so-called rim protein). A healthy Rim-Protein is essential to transport vitamin A from the light-sensitive photoreceptor cells to the retinal pigment cells (Retinal pigment epithelium, RPE). In the RPE the vitamin A normally is recycled and reused. In Stargardt’s disease the vitamin A transport is insufficient, so that vitamin A products accumulate and toxic effects occur (“vitamin A dimer”). Even in healthy people a certain vitamin A dimer production is present, but the enrichment takes several decades until a toxic level is reached.

Copyright © 2013 GETOCT™ Ltd. All rights reserved.

In Stargardt’s Disease, a partially defective ABCA 4-gene leads to a lack of sufficiant vitamin A transport by the RIM-transport protein. Copyright © 2013 GETOCT™ Ltd. All rights reserved. Copyright © 2013 GETOCT™ Ltd. All rights reserved.

Stargard’s disease: one disease – different names

Different names are used for this disease:

-Juvenile Macular Degeneration (Latin juvenilis = teen, time occurrence even at a young age)
-Macular-Dytrophie with flecks, type 1 (appearance when viewed with an ophthalmoscope)
-Fundus flavi-maculatus (Latin fundus = bottom/the background of an organ, flavi = yellow, maculatus= with spots)
-”Schießscheibenmakulopathie” (German, appearance when viewed with the ophthalmoscope)
-“Bull’s eye” (appearance when viewed with the ophthalmoscope)
-Stargardt’s Disease (English disease = illness)
-SGD (abbreviation)

The term fundus flavimaculatus was introduced by the Swiss ophthalmologist Adolphe Franceschetti in 1963.

What are the signs of a Stargardt’s Disease?

There are problems with the central vision, which is blurred, can be warped and have dark spots. The adaptation from dark to light can be slowed down. Impaired night vision is detected, but compared to other diseases, night vision is still relatively good. The external visual field is maintained, however, disorders of color vision occur. The progression of the disease is very different and very individual. Usually,  the course is slower, the later in life, the first symptoms occur. The disease can begin at an age from 6 to 20 years, with first restrictions often occuring only from the age of thirty. The course is usually slow, combined with faster episodes leading often to legal blindness.

Good news about Stargardt

The optic nerve and the outer areas of the retina remain without damage. Therefore Stargardt almost never causes complete vision loss.

How is Stargardt’s disease diagnosed?

Careful medical history is already delivering useful informations. A visit at the eye doctor at an early stage often shows no pathological changes. The eye doctor checkes the eye therefore with various tools:

Visual acuity (myopia, hyperopia, astigmatism):

In most cases, there is a low refractive error that can be corrected with appropriate spectacles.

Ophthalmoscope (fundus examination)

In younger people a so-called “foveolar reflex” is visible,  that can be lacking in Stargardt disease. The pigment layer is excessively filed with a greasy, yellowish pigment (lipofuscin), and destroyed slowly, especially around the reading center (fovea). Lipofiscin is considered as an “aging pigment”. This change in the shape of a disk reminds to a bull’s eye (“bull’s eye maculopathy”). Moreover, yellowish, irregular flecks are visible. In the late stage newly formed vessels may arise (subretinal neovascularization).

Retinal photography (fundus imaging FI, autofluorescence AF, Fluorescence angiography FA)

To document a photograph of the retina is rational. Far more important is the autofluorescence photography, which in the area of ​​destroyed pigment cells proves dark spots or dark areas. Fluorescein angiography shows that because of the excessive storage of lipofuscin in the remaining leaf pigment cells block the choroidal fluorescence, called dark choroid (“dark choroid”). Neovascularization are quickly recognizable in the fluorescein angiography.

Electrophysiological studies of the retina

An elektrooculogram (EOG) and a full-field electroretinography (ERG) are not very helpful in the early stages. However, the electrical response of the central sensory cells (cones) in the multifocal electroretinogram (mfERG) are reduced early.

Therapy:

The disease can not be cured, although many genetic treatments are being tested. Important is the protection of the remaining cells:
-Non-Smoking
-Vitamin-rich diet
-Sun protection (hat, sunglasses with protection against UV light and blue light)
-Well-corrected spectacles
-Low-vision aids

Lipofuscin – “aging pigment”

Lipofuscin (gr. lipo = fat, fuscus= a swarthy or dark color) is considered as an “aging pigment”. Lipofuscin consists of oxidized proteins and fats, and is a further non-usable or degradable cellular waste product. It shows as intracellular, finely yellow-brown granules and is arranged around the nucleus. It is found in many healthy tissues as nerve cells, retinal pigment epithelium, the liver and heart muscle. Accumulation of lipofuscin in the retinal pigment epithelium may be a sign of a degenerative disease of the eye. Even in healthy tissue some degree of lipofuscin is present, as a sign of the normal metabolism and degradation of products, especially the lipids.  If there is interference of degradation, then the lipofuscin accumulates in the cell (lysosomes) and releases its toxic properties.

Stargardt GETOCT

Morbus Stargardt  GETOCT. Abnormal deposits of lipofuscin inside the pigment epitelium cells  (blue hexagons), lead to a slow destruction of the pigment cells. Normal pigment cells (above). Healthy pigment cells (light blue), diseased pigment cells inside in the macula (brown hexagons, below). Cause is a genetic disorder, a mutation of the ABCA4 gene, which leads to the accumulation of toxic metabolites (lipofuscin, considered as an “aging pigment”). Copyright © 2013 GETOCT™ Ltd. All rights reserved.

 

Lipofuscin (gr. lipo = fat) considered as "aging pigment". It shows as intracellular finely yellow-brown granules and is arranged around the nucleus.

Lipofuscin as “aging pigment”. Even in healthy cells (1) lipofuscin (yellow spheres, 3) is seen as a product of the metabolisme and a degradation of metabolites. Lipofuscin is typically arranged around the vital nucleus of the cell (2). In degeneration of retinal pigment epithelial cells (5), to much lipofuscin is stored (4), thus leading to a toxic reaction to the cell (6). The cell dies. Copyright © 2013 GETOCT™ Ltd. All rights reserved.

Vitreous floaters Glaskörpertrübungen Mouches volantes

Saturday, December 22nd, 2012

Intro:
-Vitreous floaters are very common, require no treatment, but are uncomfortable and accompanied by light flashes or peripheral vision loss, they may indicate a retinal detachment.

-Glaskörper-Trübungen (Mouches volantes) sind häufig, erfordern meist keine Behandlung, sind aber unangenehm, von Lichtblitzen-Begleitung oder peripherem Sehverlust begleitet sind sie ein Warnzeichen für eine Netzhautablösung.

What is the vitreous?
The vitreous body (humor) is a more or less clear gelatinous mass and occupies the entire space of the cavity of the eyeball between the posterior surface of the lens and the retina.  The vitreous is important in the first months of life in formation of the eye, but has no special function exept for maintenance of its transparency which is important for vision, intraocular pressure and providing a passage for metabolites. The vitreous occupies four fifths of the volume of the eye and weights about 4.0 g. It contains no vessels and no nerves. The vitreous body is composed of many small “bags” and communicating channels, convex posteriorly and to the sides, anteriorly there is a slight depression in which the lens is located. A central canal (Cloquet’s canal) with a diameter about 2 millimetres becomes wider as it approaches the optic nerve.  Peripherally it is very close with the inner retina, and is fixed to the anterior part of the eye, described as “vitreous base”.  The strength of fixation depends on the location: optic disc> macula> retinal vessels> retinal tissue. The vitreous is 99% water and 1% is formed bei special collagen fibers and hyaluronic acid.

Vitreous 1 GETOCT

Vitreous body. Schematic representation with an eye-model: the vitreous body is composed of many small "bags" and communicating channels, convex posteriorly and to the sides, anteriorly there is a slight depression in which the lens is located. Copyright © 2013 GETOCT™ Ltd. All rights reserved.

Is the vitreous important?
Yes! These fibers form a wondrous network. Over the years, or in special situations (myopia, inflammation, accidents) these delicate nets decompose, fibers clump together and liquid filled spaces arise. The fluid in theses spaces has no “shock absorbing vitreous network” around it, and moves without restriction leading to a stronger force development on the attached retina. The possibility of a retinal tear and a possible retinal detachment increases, particularly at the vitreous base.

Are changes of the vitreous important?
Sometimes. In every person, the vitreous body changes over the years. This is a normal process. Typically, the transparency is reduced and these fibrillar aggregates are seen as “dancing midges”. These opacities are seen only with sufficient light, for example, looking on a white wall, the snow or at the blue sky 90 degrees from the sun. However, one must never look at the sun. In the dark, these opacities are invisible. It is very disturbing when one moves from light into the fog, whene the eye is then illuminated diffusely and ” hundreds of flies” suddenly appear. This is not dangerous, but can interfere, especially in people who are very dependent on their eyes as photographers and illustrators.

Therapy against vitreous floaters?
In this situation “patience” helps as the cloudiness moves along the force of gravity and thus out the optical axis. This can unfortunately take months. In appropriate cases, a direct laser treatment of the floaters may be considered.
Uncomfortable it can be when suddenly extraordinarily many new floaters occur, associated with flashes or a  “lightning”. These flashes can be a sign of a more powerful traction of the vitreous to the retina. The retina is relatively tough and usually nothing happens. Nevertheless, a check carried out at an eye doctor is important. With excessive traction a tear in the retina may occur, opening an entry to the subretinal space. Sometimes these holes heal on their own. In critical situations, a hole is sealed off with a laser beam, so that the tear can not go further, but it takes up to two weeks untill the laser spots are strong enough. If the lesion is progressing only surgery can help: from the outside of the eye (scleral buckling) or inside (vitrectomy). These surgeries show very good results, so that today the onset of blindness due to retinal detachment is extremely rare.

Vitreous floaters Glaskoerpertrübung

My vitreous floaters

Strategies in Diabetes GETOCT 5

Sunday, September 2nd, 2012
Back from the summer holidays?
You are stored sun energy. GETOCT.

Try to catch the sun, the sun has taken you long before. Your body is stored sun energy! Sunset in Zadar at the adriatic coast 2012. »Zadar has the most beautiful sunset in the world, applauded at every evening.« Alfred Hitchcock, May 1964, from room 204, Zadar/Croatia. Copyright © 2012 GETOCT™ Ltd. All rights reserved.

You are stored sun energy!
Plants convert electromagnetic energy directed from the sun into biochemical energy and store it into sugar. Your body converts this chemically stored energy back into electrical power at a cellular level. You can stretch your hand to the sun to capture it, but from the first day of your life, you already have the solar energy in yourself. You are connected to the sun, your body is nothing more or less than a sun storage. In diabetes, the use and flow of this energy storage is disturbed. Yours Peter Maloca, MD.

What to do in diabetic retinopathy? by Martin K. Schmid, MD

The strategies change, new knowledge has to be evaluated and proofed. The findings of today may already be obsolete tomorrow. We can only show a snapshot of the current knowledge about diabetes. General recommendations must always be placed in the context of the affected patient. There is no standard diabetes patient, each person is different, everybody needs a customized procedure.

Basic frame:
It sounds simple but first of all: the basic frame of all diabetic problems, is the diabetes itself. Diabetic retinopathy represents “only” the complication of the underlying disease, called diabetes. Good interdisciplinary management of the underlying disease means control and treatment of the most important paramaters. Responsible for the treatment and control of the underlying disease are the internist and the patient together.

How should we monitor patients with diabetes?
It is important to know that after 20 years, more than 80 percent of affected patient develop a diabetic retinopathy. There are mainly the situations:

1. Pregnancy:

Pregnancy can be a source of danger in diabetes. Pregnancy can lead to a diabetes decompensation. A baseline checkup should already occur if a desire for pregnancy exists. During pregnancy the patient should be checked every three months, even monthly in special cases.

2. Type 1 diabetes:
Currently it is recommended in type 1 diabetes: annual check from the fifth year of manifestation, or from the age of eleven. In the presence of type 1 diabetes without retinopathy annual inspection should be performed. In the presence of type 1 diabetes with retinopathy, the procedure corresponds to the severity.

3. Type 2 diabetes:

In type 2 diabetes, it is different because at diagnosis 36 percent already show a retinopathy. If the retina is healthy in diabetes type 2, nevertheless the retina should be examined annually.
In diabetes with a healthy retina or only a few microaneurysms an annual inspection is recommended.
A moderate diabetic retinopathy means only a few hemorrhages, microaneurysms, beaded veines. In question of an ischemia a fluorescence angiography is worthwhile.  An OCT may be helpful in a decrease of visual acuity with looking for a macular edema.
The checks are carried out every 6 to 12 months depending on the situation.

An advanced diabetic retinopathy is characterized by the 4-2-1 – rule
-Presence of more than 20 microaneurysms in the four quadrants
-or venous beading in two quadrants and/or one quadrant with IRMA

View video Strategies in diabetes GETOCT 5:

Download video -> Strategies in Diabetes GETOCT5

Therapeutic strategies in macular edema:

Currently, the treatment of a macular edema is a most discussed topic. A proposal for control and treatment in diabetic macular edema is presented in this video.

A proposal for control and treatment:
In severe diabetic retinopathy a fluorescence angiography (FA) and OCT are performed. These two methods are the basis for the indication of a therapy. The laser is still an important tool, especially for the treatment of ischemia. After treatment, frequent monitoring is necessary.

Consider the morphology and function of the macula:
In a dry macula, good visual acuity and inconspicuous biomicroscopy, checks are carried out every year.
In borderline cases an OCT or fluorescence angiography (FA) should be performed, followed by an appropriate therapy.
In a clinically significant macular edeme, OCT and/or fluorescence angiography (FA) are the basis, followed by Laser and/or anti VEGF therapy. After treatment, a frequent monitoring is necessary in every case.

In cases with a thickened foveola a proposal may be:

If the edema is not located quite centrally, a focal laser may be sufficient. When this laser is not successful, we go back again in the proposed scheme.
If the foveola is thickened centrally, the anti-VEGF therapy is then possible.
If no stabilization occurs, the vision rises an additional laser treatment may be useful.
If therapy stabilized the situation, ​​a break and a close monitoring follows. If everything remains stable, the patient remains in the small control loop.
If the situation worsens, the patient returns to the top level of control.

This is not a fixed regimen, but must be customized and changed over time.

Quiz 2 on diabetes: what is a real retinal edema?

Sunday, July 1st, 2012

We put together some new trivia questions about diabetes and OCT. For interactive reasons questions are programmed in Flash.

 

Klick here to play Quiz 2 on diabetes in full size:

Quiz 2 on diabetes GETOCT

 

Strategies in Diabetes GETOCT 4

Sunday, July 1st, 2012

Diabetes damages the blood vessels and if untreated, can lead to blindness. The newest discoveries with anti-VEGF therapy in diabetes have their own requirements. One question is when should a macular edema be treated and when not?
So far, a clinically significant macular edema was the main criterion for therapy. There has been a shift from clinically significant macular edema towards the concept of  “center involving or central subfiled thickening”.  With OCT, the course over time can now be controlled much more accurately.

View video strategies in diabetes GETOCT 4 Youtube channel:

The question is, which concept is better: “clinically significant macular edema”  versus  “center involving”. In the label (package leaflet) of Lucentis is nothing written about retinal thickness. The single most important criterion is the visual acuity loss due to macular edema in diabetes. Monthly injections of Lucentis for three consecutive months until visual acuity is stable. Re-treatment, if the visual acuity is worse again. It is to discuss whether the visual acuity alone is a good parameter for treatment.
What is a “clinically significant macular edema”?
A GETOCT memory aid: important are two circles and a line (cross section papilla):
1. First inner circle with 500 microns around foveola
2. Second circle with one disc diameter around the the foveola
3. A line represents the disc diameter

The definition of clinically significant macular edema is important:
1.Retinal thickening within 500 microns of the center (foveola)
2.Hard exudates within 500 microns around the foveola with adjacent retinal thickening
3. Retinal thickening greater than one disc diameter in order to one disc area around foveola

The disadvantage of this arrangement is that the findings are not always clear.

Diabetes is a vascular disease
Diabetes affects vessels. Therefore, the assessment of the ischemic component is very important. Diabetes on the retina leads to a thinning of the peri foveolar capillary network. The normal fovelar avascular zone (FAZ) increases in size. Almost always, the lesions are irreversible. The capillary network is so badly damaged that swelling can not longer be caused, no edema is visible in advanced cases. In an avascular retina, OCT of the foveola shows completely thinner layers. The normal fine retinal layers are destroyed, but a few crumbs are visible. In very far-advanced stage, anti-VEGF and laser have no great benefit anymore for the visual acuity. The goal of therapy in very advanced situations is no longer the visual acuity, but to prevent vascular proliferations, thus bleeding and a secondary glaucoma or even blindness.

Download video:

Strategies in Diabetes GETOCT 4

Strategies in Diabetes GETOCT 3

Sunday, June 24th, 2012

OCT from third to the fourth dimension

Thanks OCT, we obtain information to the third dimension. Flurescence angiography allows only limited statements about the spatial extent of processes
The retinal thickness is measured precisely with OCT and an objective quantification is possible. The fourth dimension means a precise control over the course of years at exactly the same place.
The measurements are comparable with each other really well. With OCT is a synchronous mapping and comparison over time is possible and changes are shown. In some OCT devices the scanning area is permanently adjusted, no matter where the patient looks. This is advantageous because the patient can’t fix very well in advanced diseases. From these cross sections thicknesses maps can be produced, even differences over time can be calculated.

Anti-VEGF for diabetic macular edema?

Anti-VEGF for diabetic macular edema has been investigated in many studies.
The combination with ranibizumab turns to an increase in visual acuity. the sole laser therapy worsened the situation at the beginning rather. The number of injections in the combined group with a laser can be reduced.

Immediate or delayed laser?

Another study on laser: what impact does an immediate or delayed laser? If successful, the strategy with immediate laser, a significant gain is produced. When laser was carried out somewhat later, however, a similarly good progress is produced.  So it’s not a big difference whether immediate or slightly delayed laser is done.
The results with triamcinolone and laser show in the first 6 months of a profit, then drop due to cataract formation.  The number of injections in this study is also at eight to nine injections per year.

 

Youtoube Channel:


 

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Strategies in Diabetes GETOCT 3

 

Complication in diabetes facial nerve palsy

Wednesday, June 13th, 2012

(Bells palsy, Fazialisparese)  suddenly a “lopsided” face:

The facial nerve palsy (Bells palsy) is one of the most common injuries of affected cranial nerves. The paralysis affects all of its innervated facial muscles, so that the origin of the disorder is quickly visible. Most often there is no clear cause, it is often associated with infection.

Facial paralysis GETOCT

Facial paralysis right eye. Copyright © 2012 getoct™ Ltd. All rights reserved.

In diabetes a facial paralysis occurs more often, which fortunately is usually benign in course with spontaneous remission.
A major problem is due to paralysis of outer eye muscles resulting in an incomplete eyelid closing. The cornea can dry out, a visual loss occurs, even infection and scarring can permanently impair vision.
Therefore, a good humidification is important using eye drops, ointments and a monoculus (Uhrglasverband).

Problems of monoculus
The disadvantage of a monoculus is that older people show difficulties to change the monoculus themselves, withdrawal may be painful in a thin and sensitive skin,  allergies to adhesives occur soon, massive cosmetic restriction with grotesque appearance  interfere with the patient in his dealings with his social environment. Thus the patient may not feel very comfortable. GETOCT shows a nice trick to improve patient’s quality of life. Plese view the video:

Monoculus in facial paralysis GETOCT

Monoculus in facial paralysis. Copyright © 2012 getoct™ Ltd. All rights reserved.

 

View video (Recordings were made with the consent of the patient) :

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Trick in dry eye facial nerve paralysis GETOCT

Strategies in Diabetes GETOCT 1

Friday, March 30th, 2012

Diabetes is a vascular disease. The eye is composed of vessels.

Diabetes - too much energy at the wrong place

Diabetes - too much energy at the wrong place

Therefore, only the ophthalmologist can control the diabetic eye. What is the most asounding fact you can share about diabetes with us?

Strategies in Diabetes, OCT GETCOT Academy 2011

Strategies in Diabetes, OCT GETOCT Academy 2010-2011. Copyright © 2012 getoct™ Ltd. All rights reserved.

Even in a total decompensation of diabetes, hope will never die. We show you with informed consent a very impressive case between life and death.

 View Video Strategies in Diabetes part 1:

Download Video Strategies in Diabetes Part 1:

Strategies in Diabetes GETOCT 1