Monday, May 20, 2019




Ajmal Khan Tibbiya College
Aligarh Muslim University
Aligarh, India


Corticosteroids are a double-edged sword. While they are useful in the management of various conditions, they also have multiple ocular and systemic side effects which may even be life threatening at times. 

In certain countries steroids are easily available over-the-counter while online pharmacies are also responsible for the unmonitored accessibility of these agents.

Ocular side effects include: increased susceptibility or reactivation of certain infections, cataract and increase in intra-ocular pressure (IOP).

Prolonged elevation of IOP can cause damage to the optic nerve leading to the development of steroid-induced glaucoma (SIG).  


SIG is a form of open angle glaucoma.

The exact mechanism responsible for elevated IOP after steroid intake is not clear.

It is most likely associated with reduced facility of aqueous outflow.

Other theories include:
Stabilization of lysosomal membranes and accumulation of polymerized glycosaminoglycans (GAGs) in the trabecular meshwork (TM). Hydration of GAGs leads to biological edema in the TM and consequently reduced aqueous outflow. Corticosteroids, which stabilize lysosomal membranes, could reduce the release of lysosomal hyaluronidase resulting in a relative inhibition of hyaluronate depolymerization.

Ultra-structurally, accumulation of basement membrane like material staining for type IV collagen is also seen in SIG. Extracellular deposition of extracellular matrix material in the TM shows 2 patterns: Fingerprint-like deposition of material in the uveal meshwork and accumulation of fine fibrillar material in the juxtacanalicular region. 

Corticosteroids cause inhibition of phagocytic properties of endothelial cells lining the TM leading to accumulation of aqueous debris.

Glucocorticoids decrease synthesis of prostaglandins, which regulate aqueous outflow. They also inhibit TM cell arachidonic acid metabolism and reduce phagocytic activity of TM cells. Dexamethasone also causes cross-linked actin network formation. However, the effect of such an alteration of cellular cytoskeleton on TM cell function is not clear. 

There is some genetic influence in the development of SIG, as several genes have been found to be associated with protective as well as damaging glucocorticoid treated TM cells. A number of genes are suspected though not yet proven to have a role in the development of SIG. These include: MYOC (previously called trabecular meshwork induced glucocorticoid response [TIGR]) gene and genes regulating alpha1 chymotrypsin, pigment epithelium derived factor, cornea-derived transcript 6, prostaglandin D2 synthetase, growth arrest specific 1, decorin, insulin like growth factor binding protein 2, ferritin light chain, fibulin-1C and others.


Steroid induced IOP elevation can occur at any age.

Children may have a severe ocular hypertensive response to topical steroids.

In a study SIG was responsible for 1/4th of all cases of acquired glaucoma in children.

According to Becker and also Armaly, individuals can be categorized into high, intermediate and low responders to topical steroids. 

HIGH RESPONDERS: Had IOP increase above 31 mmHg or 15 mmHg above baseline.
INTERMEDIATE RESPONDERS: Had IOP increase between 20-31 mmHg or between 6-15 mmHg above baseline.
LOW (NON) RESPONDERS: Had IOP less than 20 mmHg or rise of less than 6 mmHg from baseline.


Factors which increase the risk of SIG include=

1. Patient related factors: Glaucoma or glaucoma suspects have marked rise in IOP levels after several weeks of topical corticosteroid therapy. First degree relatives of POAG patients have higher risk of being steroid responders. 

2. High myopia, patients with H/O penetrating keratoplasty or refractive surgeries may have a high IOP response which gets masked due to low central corneal thickness, Ocular rigidity changes, Corneal edema and fluid accumulation beneath the LASIK flap.

3. Extremes of age: Children below 10 years of age and elderly individuals show higher steroid responsiveness.

4. Type I Diabetes mellitus and connective tissue disease (specially rheumatoid arthritis).

5. Pigment dispersion syndrome and traumatic angle recession.

6. Systemic disorders such as adrenal adenoma.


Topical: IOP elevation is more common by this route compared to systemic administration.

Periocular therapy: Long-acting repository steroids are most liable to cause rise in IOP. A patient’s previous response to topical steroids does not predict their response to periocular steroids.

Intravitreal injections: Injections of triamcinolone or depot steroids such as ozurdex can cause elevation of IOP within 2-4 weeks of the procedure.

Systemic therapy: Injections, tablets (oral), Skin preparations, Inhalational agents and other systemic steroid use is less commonly associated with rise in IOP. Use of steroids for muscle building is another danger for SIG.

The potency and strength of the steroid used are related to the IOP response which occurs. Often the response does not correlate to the dosage or duration of treatment.


Raised IOP in susceptible individuals usually occurs in a few weeks after commencement (average: 4 weeks). However, it may occur within hours or several years later.


Signs and symptoms vary with the age of the patients. Infants present with features of congenital glaucoma such as watering and photophobia. Adults show features of open angle glaucoma. SIG may be accompanied with other complications such as mydriasis and ptosis.


Primary open angle glaucoma 
Normal tension glaucoma 
Juvenile open angle glaucoma 
Uveitic glaucoma 
Glaucomatocyclitic crisis


First line of management is discontinuation of the steroid. Usually IOP returns to normal in a few days or weeks. Patients require pharmacological IOP lowering during this period.

If steroids cannot be stopped in the patient, they can be substituted with non adrenal steroids such as: rimexolone, loteprednol etabonate, fluoromethalone & medrysone.

Depot steroids need to removed by excision and clearing all steroid deposits in the area.

Intravitreal steroids may require vitrectomy to remove them.

Steroids can possibly be replaced with non-steroidal anti-inflammatory agents such as: flurbiprofen, bromfenac, ketorolac and nepafenac.

If IOP does not respond to medical treatment then Argon laser trabeculolasty can be tried. It may control IOP until the steroid-induced hypertensive effect disappears. 

Ultimately glaucoma filtering procedures or even glaucoma drainage devices are required in intractable cases.


SIG is an avoidable condition which is aggravated by factors such as easy accessibility, risk factors for IOP elevation and poor monitoring. Increasing awareness regarding this condition can lead to a reduction in the prevalence of SIG.

Thursday, May 16, 2019





Bhopal, India


Sunday, May 5, 2019

A rethink of 10-2 visual fields in early glaucoma

Conventionally, the utilization of visual field programs for analysis of the central retina, such as the 10-2 test, has been confined to patients with advanced glaucoma.  However, over the recent past, a number of studies have shown that Humphrey visual field programs for testing the retinal periphery, such as the 30-2 or 24-2, often miss central defects. A subgroup of patients has been identified which present with central visual field defects during the early course of the disease while retaining normal peripheral visual fields. The diagnosis in these patients will be missed on 24-2 or 30-2 programs unless tested on strategies focused on the central retina. This is leading to a new awareness regarding performing of 10-2 tests early during the disease process. 

To address the issue of the current role of this test in our clinical practice and whether a rethink is required regarding the application of the 10-2 test in early stages of glaucoma a review was undertaken. This review has recently been published by the US Ophthalmic Review journal.

Kindly take a look if it interests you,

With best wishes

The article is available at the following link:

Friday, May 3, 2019

Abu al-Hasan Ali Ibn Sahl Rabbani al-Tabari : A visionary

Guest author

Birjis Fatma
Ajmal Khan Tibbiya College


By 2020 India is projected to become second overall in the world with respect to the number of individuals having glaucoma. In 2010 more than 60 million people worldwide were suspected of suffering from glaucoma. This number is projected to increase to nearly 80 million by 2020. Nearly 8.4 million people were blind due to this disease in 2010 and model calculations estimate the number of those who will become bilaterally blind from glaucoma to increase to more than 11 million by 2020. 

Glaucoma is a disease known to mankind since antiquity. The term glaucoma is derived from the Greek word “glaukos” (greenish or bluish hue of the pupil). Hippocrates, in his aphorisms believed to be presented in 400 BC, used the term to describe “a kind of blindness which came with aging and was associated with a glazed look of the pupil”. However, when we critically analyze the definition of “glaukos” we can conclude that this glazed look of the pupil could be due to glaucoma but equally well possible from cataract. 

Life history of Al-Tabari:

For many years ophthalmology, like other branches of medicine, languished during the Dark Ages. Finally, in the 11th century AD, an Islamic scholar, Abu al-Hasan Ali Ibn Sahl Rabbani al-Tabari, demystified glaucoma and presented succinct clinical features which form the basis of this disease till today. This article sheds some light on this doyen of Medieval Islamic medicine. 

Just as a candle cannot burn without fire, a doctor’s zeal to treat is fueled by his spiritual core. This spiritual strength develops by devotion and concentration towards one’s field. A legendary figure who epitomizes the balance between spirituality and medicine is the great physician Al-Tabari. His contributions have left an indelible footprint in the history of medicine. His writings are a treasure which cannot be estimated for their value. His work has illuminated the world like the warm rays of the winter sun. 

Al-Tabari was born in the 8th or 9th century (usually mentioned as 838 but also 810, 808 or 783 AD) in an influential Syriac family of Merv in present day Turkmenistan. In his book Al-Radd ala al-Nasara, he wrote that he was Christian until the age of 70 and then converted to Islam. He has mentioned this in another book: Kitab-al-din wa-al-dawla. His father Sahl Ibn Bishr was a state official, highly educated and a well respected member of the Syriac community. It is mentioned that Al-Tabari’s father was a physician whose pre-eminence earned him the Syriac title of “Rabbān” which translates to “Our Master” or “Our teacher”. Sahl was the first translator of Ptolemy’s Almagest into Arabic (800). His uncle Abu Zakkār Yahyā Bin Al-Nuumaan was also a distinguished scholar and a leader of the Syriac society. 

At 10 years of age Al-Tabari accompanied his family to Tabristan (hence the suffix Al-Tabari). His early youth was spent in that region studying philosophy, medicine, religious and other aspects of natural sciences. On completing his education he subsequently moved to Iraq in 813, around the age of 30 years. In 825 he returned to Tabarīstān and became royal scribe of the Governor Māzyār Bin Qārin. He also started writing his treatise Firdaus al-Hikma (Paradise of Wisdom) at this time.

Later Māzyār was executed and Al-Tabari went back to Iraq. In Samarra he completed the Firdaus al-Hikma around 850 AD. While he was in Iraq,the Abbasid caliph Al-Mu’tasim appointed him as his divan scribe. Al-Tabari continued to work there until the death of the Caliph, upon which he returned to Samarra.

During the reign of the new Caliph al-Mutawakkil (847-861) Al-Tabari joined the court service again as a physician and courtier. Under the Caliph’s patronage Al-Tabari embraced Islam around the period of 849-850. The Caliph gave him the title of Mawla Amir Al-Muminin. Just like his birth, it is not clear in which year and at what place did Al-Tabari pass away. It is conjectured to be around 864 AD.

Al-Tabari wrote a large number of books, the exact number is unknown as some his works are no more extant. Some of his famous works include the following:
Kitab al-Ain fi al-Mualajaat (The book on Ophthalmology treatments): An enormous treatise exclusively on ophthalmology. In his own words “I have authored a distinct book completely and exclusively on ophthalmology in which I have mentioned all ocular diseases including important and unimportant, each for each temper”. Unfortunately, this book is lost.

Firdaus al-hikma (Paradise of wisdom), also known as al-Kunnāsh al-hadra, it incorporated Syriac, Greek and Indian medical systems and compendiums to form the World’s first Medical Encyclopaedia. In Book 3 (Chapter 12) of Part IV, he described ocular anatomy and diseases. 

Firdaus Al-Hikma

Al-Mu’alajat al-Buqratiya (The Hippocratic Treatments) an important book, which also deals with ophthalmology. He devoted the 4th article of the book on “Ocular diseases and their categories, benefits, creation and treatments”. In this book he mentioned “Migraine of Eye” (shaqiqat al-ayn). The condition was characterized by eye pain, a pressure sensation, opacification of ocular fluids and a dilated pupil. Apparently, this was the first reference of raised intra-ocular pressure in glaucoma. He also described 2 novel types of “ramad” (conjunctivitis). 

He also wrote: Maqala fi tib al-ain (A paper on Ophthalmology). A copy of this is presumably present in Aleppo Library in Syria.

In the Firdaus-al-Hikmat he also described the Islamic codes of ethics as personal characters of the physician which are very much contemporaneous in this era of moral degradation. This code of ethics describe the physicians obligations towards his patients, community, colleagues and assistants.

In conclusion, Al-Tabari was a visionary medieval physician who used his teachings and works to spread his extensive knowledge regarding medicine in general and ophthalmology in particular.