Thursday, October 21, 2010

Bruno’s Eyes: Little poison, little ignorance --- and not at all little SARD

Our family pet, Bruno, lost his eye sight suddenly. When one does not know what the sudden blindness is due to one calls it Sudden Aquired Retinal Degeneration (SARD). So Bruno has a name for the illness but he has no cure.

That is not good enough.

We are hoping it will be temporary. The prognosis is not too good. The treatment is uncertain. The diagnosis is undecided. The end is not surprising.

This blog (click on pictures to expand) appears on the internet with the hope that someone somewhere could suggest something which could be useful. It does not claim at all to be right in its analysis.

This blog is also meant to point to precautionors to be taken in this increasingly complex world. The technical parts and images connected with the eye is taken from the internet and summarized in section 4. I dont think I will be correct throughout. This blog is only to alert.

Should one read this blog, the reader could comment and make suggestions.

1. Bruno

Bruno came home from a local kennel as a thoroughbred. There seemed to be considerable in-breeding as seen from his breeding certificate. When my daughter Surabhi went to pick him up she was in love with him at first sight. The four-week-old pup seemed to be the weakest of the litter.

When Surabhi brought him home his health collapsed immediately. After considerable concern over his life and spoon-feeding he survived.

Bruno grew up to be surprisingly and considerably bigger (at least by a third) than his siblings. He looked a perfect fox terrier except that he was considered to be too big to ever win a medal in a dog show. He became every bit a happy and friendly fox terrier, who loved playing with the ball and could play for hours.

Bruno was brought up mainly a vegetarian. He occasionally (about once a week) got his meat and fish and meat. His carnivorous instinct saw him snapping at insects and eating them up.

His first brush with ill health happened when he was about five years old when he had a rather sever attack of mange (probably from a rare neighbourhood mangy dog). This attack coincided with a serious fatal illness of a dear family member. He was not given as much attention as he should have been given perhaps- Bruno was treated by a vet only after two months. He recovered well.

Bruno then had an attack of babesia in 2009 which was not diagnosed properly by two experienced vets. A dedicated vet who learnt her trade under the nearly legendary vet, the late Dr. Balakrishnan of Pune, examined Bruno’s blood under the microscope personally and obtained an image of the parasite that confirmed the disease. The babesia was treated successfully.

In spite of a seemingly good health he seemed to have (what we thought) was a relapse of babesia, mainly because he had symptoms similar to the first attack. The parasite was not seen directly in the blood this time though. We thought that this was because we started the treatment of berenil at an early stage as his haemoglobin count had decreased to a very low level of 5,000. As a further precaution he was given a 28 day course of doxycycline antibiotic because of prevalent opinion among doctors. It was thought that babesia will be knocked out forever.


2. Ride from Pune in Maharashtra to Rewa in Madhya Pradesh


Bruno became blind in Rewa where my wife, Lalitha, had driven us from Pune through Ahmednagar, Paithan, Jalna, Lonar, Malegaon, Nagpur, and Jabalpur to Rewa mostly by National Highways 6 and 7 (NH 6 and 7). Because the road was very bad we had to drive very slowly almost all the way from Ahmednagar to Rewa (~ 1200 km) on very bumpy roads at an average speed of 35 km/hr. So we drove long and bumpy being shaken and stirred most of the time in the atmosphere.

Maharshtra, under the patronage of Sharad Pawar, the Union Minister for food and agriculture, is now a capital for genetically modified crops (mainly of the Bt variety). Rewa is in Madhya Pradesh. Its capital city, Bhopal, is now identified as the city with the worst environmental disaster and with the Bhopal eye syndrome which followed the release of methyl isocyante (MIC) by Union Carbide (now owned by Dow Chemicals) and other chemicals including hydrogen cyanide, monomethyl amine into the environment.

Because of our genetically modified coloniality we treated thes american companies with utmost consideration and as a reward Dow Chemicals has introduced, for example, Dursban. In June 2000 Dow was forced to withdraw one its main products, Dursban from the American market following a mass of scientific information about this brain damaging chlorpyrifos insecticide (an organophosphate widely used as pesticide in agriculture and as nerve gas agents in chemical warfare in world war II).

Since October 2000 Dow is promoting Dursban in India as a household chemical "safe for humans and pets" and has set up factories for production of this hazardous chemical. Homeowners are advised to keep pets and children off the grass for a time after the lawn has been treated for insects by pesticides such as Dursban. In a July 28, 2010, netsay we find the following: “According to a report in the Hindustan Times, a Dow subsidiary could be blacklisted for allegedly bribing Indian officials to allow sales of Dursban there”.

I found out about this much later after the incident.

We found out during our many stops between Pune and Rewa, that the land on either side of the road has GM crops of the Bt cotton variety almost all the way, when there were no stretches of forests.

We stopped some times in this GM-crop-fested landscape. During one of these stops a man was seen spraying pesticide. I asked him if the pesticide spraying had decreased, because Bt cotton is supposed to reduce the use of pesticides by nearly 50%. To my surprise, the man answered that the pesticided he sprayed had increased more than five times. He said that the Bt cotton plants of the new variety were much larger than the earlier non Bt varieties. They had more leaves and so they required more pesticide.

That was news to me and everyone else (except perhaps official bodies), I guess.

I later learnt that 50% of the Bt cotton crop is not approved by the government.

I also learnt that 50% of the pesticides being used were of unknown composition. For instance, it is not known whether Dursban could have been used in another avatar from.

What could be correct is that use of pesticides specific for bollworm is reduced as claimed by the propagators of Bt crops; it is the farmer who uses his discretion to use other pesticides for the other pests who have probably benefitted by the absence of the regular cotton pests.

It turns out that one of the first things one learns from netsay is that pesticides don’t have to be ingested (as in directly eating or drinking) to be absorbed in the body. They can be inhaled (just as opium, I guess) and carried to the blood and thereby throughout the body without actually hurting the respiratory system. They also cause acute eye effects including permanent blindness. More importantly the pesticide can pass through the eyes and into the body without irritating the eyes.

When we were finally in the living quarters of a cement factory complex in Rewa (in Madhya Pradesh) the most dominant first impression at nights were the large number of stink bugs, which made the residents close the windows, put off the lights and sit outside well into the night. These stink bugs feed on soya bean crops which are mainly of the GM (Bt) kind and is the main crop around.

In order to control these bugs there are many common household pesticides that are used. The exact identity of these pesticides could not be known (bureaucratic indifference?) . They could have been the natural environment-friendly or green chrysanthemum-based pyrethrin. Its synthetically derived products are pyrethroid instecticides which are also conveniently presumed to be green unless proved otherwise. Industry does not fund research for such proofs. Articles are now appearing that the pyrethroid insects are not that green.

It also seems that insecticides usually require to be bound for long term protection to the agricultural product. These are called inert products and the companies manufacturing them are not required to disclose their identity. Among these inert products that could lead to blindness (as per netsay) is ethylene glycol.

3. Bruno’s Loss of Eye Sight

Bruno loved playing with a ball. He especially loved catching the ball after it was bounced off a wall. The sure way to cheer Bruno up would be to play “catch” with him. If we did not play he would bring the ball and urge you to play.

On the night of the third day of our stay Lalitha and my sister Sagorika along with Lalitha noticed during the afternoon of 05/10 that he was not seeing the ball and relying on his senses to catch the ball. He started bumping into objects. He could see a bit as he jumped over obstacles. By the evening Bruno was totally blind as far as we could tell.

Bruno’s eyes seemed to be bulging out a bit and seemed to have a bluish colour. It made him look loveable.

We got private and prompt help from the driver of the company vehicle. My sister and her husband were catching a train on the evening of 05/10/10. The driver, Shivakumar, found an address of a vet at Satna about 50 kms away from Rewa. We drove down to a medical shop at Satna and found the vet waiting for us there. Standing by the roadside that evening he looked at the dog in the dim streetlight, with his hand on his hips. He gave instructions to his compounder about the injections to be given. It was a mixture of a steroid (dexamethasone) and an antibiotic (gentamicin). The shot was to be repeated the next day he said. He also gave an intravenal injection of AD3E (consisting of vitamin A some vitamin A mixture).

Vitamin AD3E is a combination of vitamins in preparation has a significant part for maintenance of many life processes in an organism. Vitamin A, which is essential for normal structure and activity of eptihelial cells, an integral part of sight pigments of rhodopsin and iodopsin, Vitamin D3 which regulates metabolism of calcium and phosphorus and vitamin E which among other things enhances the resorption and improves exploitation of retinol, stabilizes cellular membranes and has effect on metabolism of proteins, carbohydrates, fats, mineral substances and water. Besides, Vitamin E is necessary for normal function of endocrine glands, especially suprarenal glands. This is to be supplemented by eye drops and vitamin tablets-

The next morning Bruno seemed to have recovered some sight as he jumped over some small ditches and stepped over obstacles without bumping into them. The bulging in his eyes had reduced a bit.

Among the first thing that we confirmed the next morning was that the pupil of Bruno’s eyes were extremely dilated.

The next day (06/10/10) thanks especially to the efforts of the Katoch family in Rewa, we were able to visit an ophthalmologist. Human-eye doctors have a reluctance to examine dogs in Rewa or anywhere else, for that matter, because it would seem to be an insult to other human patients who resent being treated in the same footing as animals. Fortunately one doctor agreed. He examined Bruno’s eyes. The first thing he exclaimed was “How can it be?. I cannot see the retina!”

The retina is detached was his diagnosis. His prognosis was that the Bruno would be blind.

That evening I took some photographs and some videos for future reference

I tried to look for reasons to indicate why Bruno should be so suddenly blind. As is usual in the highest levels of knowledge, when one is faced with an unknown phenomenon, one gives the phenomenon a name, preferably an acronym. In Bruno’s case net-say would use the acronym SARD (Sudden Appearance of Retinal Disorder). It did not help at all to know that Bruno had a name for his blindness as the prognosis for SARD is that he will be totally blind. That knowledge does not help.

I tried to look at the cause (etiology?)

When I took Bruno out for his morning walk the obvious place to walk him was the patch of grass by the side of the road outside the large park in the residential complex of the cement factory. During the time we went there were always a large number of white birds (seemingly cattle egrets) which moved around the grass. The grass itself was long. There were a large number of moth-like insects in the grass which will fly around in dense clusters when disturbed by Bruno and settle elsewhere. The cattle egrets would be roaming on the grass probably feeding on these insects or dead or dying stink bugs from the previous night’s invasion of the colony by these bugs.

Bruno would step unusually warily and gingerly on it. He would walk very slowly on the grass sniffing hestitantly. Then sometimes he would shove his nose into the roots of the grass making literally snorting noises. He would then take his face out with a dazed look that seemed to me to be typical of people literally snorting “grass”. I did not take this reaction to be dangerous as I thought there should be no danger in a place that were not hostile to birds and insects. The possibility of a bird-flu-like virus appearing because of the close proximity to the bird droppings did occur to me. There was no direct indicators for a bird flu epidemic in the colony.

The only illness which could be close to epidemic proportions in Rewa was conjunctivitis.

Because of this reaction of Bruno, I tried to walk Bruno on another patch of grass which is the lawn in front of the bungalows. This patch of grass was unusually dry. Bruno would hesitate much more to walk on this grass and seemed to be more scared of it. I was later told that some spray had been used on the lawn and it became brown overnight. On later further investigation I was told that the same spray would be used on cattle fodder and nothing seems to happen to the cattle.

When we contacted our doctor in Pune, she told us that if it was due to some organophosphate poisoning because of pesticide, we could try an injection of atrophine sulphate. We found a doctor (a Dr. Mishra) who was surprised that we should give atropine when the eyes were dilated. However, after discussions with Pune he agreed and gave the shot. Bruno took it sportingly. This was around noon of 7/10/10.

We had located a veterinary hospital in Rewa in a new and open campus, a little outside Rewa city. This hospital was newly started and it had a bunch of young and enthusiastic doctors. We were referred to one Dr. Manish Shukla and a Dr. Anita. They treated us very well. They seemed to be a set of enthusiastic faculty who interacted very well with their students. They accepted the disgnosis of retinal detatchment after talking to the ophthalmologist. They recommended a subcutaneous injection of a steroid and an antibiotic. After consultations with Pune we decided not to inject the steroid. They prescribed some medicines.

We went back to Rewa to get the medicine. We went in for lunch keeping Bruno in a jeep in the shade. He looked fine (Fig 2). This was the best he would get.

When we came back from lunch we (I and Sivaram the driver) found that Bruno was seeing better. He followed my hand movement. He also jumped down readily from the jeep although he might have misjudged the height and fell rather awkwardly. This was the best he got (Fig 2). On the evening (23.00 hrs) of 07/10 the dilation in his right eye had increased again.

We went back to the hospital. They gave him one AD3E injection. There was some interest in giving a subcutaneous steroid injection. It was thought, after consultation with Pune that it could be a bit dangerous. We gave Bruno some eyedrops containing a steroid and an antibioitic.

I have shown in Fig 3 some shots of Bruno’s eyes. The first two photos were taken in June 2008 when Bruno should have been healthy. Bruno was then a proud owner of a collar given to him by Surabhi. The second picture from top is just to highlight artefacts that could arise when using a flash and also to show the normal size of the pupil at night.

It is evident from Fig 3 that the pupils of both the eyes were considerably dilated. In addition both the eyes on 6/10 at 19.30 hours had an haze in the eyes. This haze indicated corneal damage. I also felt that the eyes were sort of bulging out. I later found that one could identify such features with keratitis and corneal edema (section 4. 3) which happens because of stromal damage (see section 4. 2).

In the images of 07/10 in Fig 3 it is seen that the haze on the cornea is not there in the morning (07.00 hrs) of 07/10. The hazy feature coincided with the image from the internet for posterior stromal edema (section 4.4). The right eye shows some particle-like features which is absent in the left eye. By the afternoon of 07/10 the dilation of the pupil of both the eyes had considerably reduced. This is when Bruno looked the best (Fig 2). The left eye did not have these features.

After the opthalmological investigation the doctor had said that the left eye is less damaged than the right eye and that there could be a faint hope for the left eye.

Further search of the internet got me to the Descemet’s membrane (section 4. 5.) in the cornea. I got to one paper (section 4.5) on the effect of toxic detergents on the corneal endothelium (section 4.6). Much of what is written there is ophthalmology (greek) for me. However, other discussions on posterior polymorphous corneal dystrophy (section 4. 7) suggested damage to the cornea. For instance, the figure on top right of section 4.6 could give optical images that has features corresponding to the right eye in 07/10 images of Fig 3.

Stromal opacities in the central cornea could also give rise to the appearance of particle-like (if that is the correct word) features in the right eye as in macular corneal dystrophy (sec 4.8).

The left eye, on the other hand had no granular features except on the night of 6/10. The feature of the left eye seemed to be similar to some images of corneal dystrophy (sec 4.9).

The sequence of changes in the right and left eyes are given in Figs 4 and 5, respectively.

The problem with dystrophy (progressive degeneration of a body tissue such as muscle, caused by inadequate nourishment of the affected part, as a result of some unknown cause) of any kind is that it is usually associated with a slow genetic cause. It cannot be associated with a sudden blindness unless a genetic weakness triggers the catastrophe.

The triggering factor in Bruno’s case could have been a toxin. He could have sniffed it from the grass.

I did not take pictures of Bruno’s eyes for some time as I disliked the idea of using a flash on his poor eyes.

Since Bruno seemed to be weak we decided to delay our return trip from Rewa to Pune and started on 09/10/10.

We chose a different route on which we could maintain an average speed of 45-50 km per hour. Bruno took the trip well enough. But by the evening he had become tired. His right eyelid had swollen. After we reached our home in Pune on 10/10/10 late (11.00 pm) in the night Bruno was extremely tired. His right eye had collapsed and some liquid had come out (Fig 4. 10/10, 23.32). As a result the dilation in his right eye had reduced (Fig 4, 11/10 15.44) markedly the next day as compared to his left eye (Fig 4, 11/10 15.44 left). There was some evidence (sec 4.9) for a corneal dystrophy, though.

The features of the left eye (Fig 5) did not seem to change much. The pupil were always dilated and the features seemed to be similar to corneal dystrophy.

Serious examination of Bruno started on 11/10 in Pune. A no-nonsense ophthalmologist examined. She gave us the first hope. She said not seeing the retinal attachment does not necessarily mean that there is retinal detatchment. There could be, for example, an haemorrage or some other cause that blocks the features of the optic fibre. She suggested an ultrasound examination and treatment with steroid and antibiotic to reduce any haemorrage. Prior to this a blood examination had to be done.

The blood examination turned out to give a disastrous result. Parameters such as haemoglobin (cyanmeth), R.B.C. count, P. C. V. (packed cell volume), and W.B.C. count were a quarter of their normal values. The platelet count was still worse being at best 1/25 of the normal value. It

seemed logical to rule out ehrliochosis or other tick-borne disease since Bruno was already on doxycycline for four weeks. Most vets (except one) ruled out treatment with doxycycline since he was already on doxycycline for four weeks. The blood cells showed anisocytosis (excessive inequality in the size of red blood cells). There was evidence for leucopenia.

Bruno is a weak child. His spirit keeps him buoyant and lively. Has the inbreeding in his kennel causing him the troubles he is now facing.

We took Bruno for his songraph scan on 13/10 in the afternoon. There was a power failure. He had to climb up three floors to the sonograph machine which he willingly did. But he was tired.

He took the sonogram well.

The good thing about the report was that his retina was in place.

The diagnosis of most likely posterior hemorrhage seemed consistent with prior studies (top left of Fig 6). This could be treated only with a steroid it was concluded and steroid treatment was advised as eye-drops six times a day, one drop at a time. This was started.

Steroid injection was to be started. The first shot was to be a prednisolone injection. It was to be followed by oral administration of the drug.

The first injection on the morning of 14/10 Bruno took well. He was given an oral administration of the steroid in the evening. That night I took a photograph and analyzed it the next day. I noticed a peculiar swelling on the cornea of both the eyes as seen in Fig 7. The peculiar feature I notices is I marked out by yellow circles in the figure. The closest that I could come to on searching the net is that it could be keratoconus (sec 4. 10).

This also suggested that the corneal endothelium was affected (sec 4. 11).

He was given another intramuscular prednisolone injection on his right leg on the morning of 15/10.

Bruno did not take well to the steroids. By the evening of 15/10 he was vomiting and he spent the whole of 16/10 retching violently. He drank a lot of water and vomited it all. His food would come out as it was even after 12 hours as it had been taken without any smell. By the morning of 17th he had stabilized. He was nursed slowly back to some sort of a normal self. We relied on ragi (finger millet) mixed with home-made yogurt from organic milk as his main nutrition at this stage. He would not eat meat or even eggs.

The dilation of both his eyes had increased.

The right eye (Fig 8) developed a red colour and I thought that the red colour (seen prominently from a particular angle, see pictures of right eye on 20/10 with and without flash) was on the cornea in a circular spot, corresponding roughly to that in Fig 7, which moved with time. The left eye did not change much. The dilation of the pupil may have marginally decreased at best.

It seemed strange that despite all the treatment the dilation of the eyes remained unaffected. I thought of mydriasis (sec 4. 12) or a third nerve palsy (sec 4. 13). The use of pilocarpine eye-drop treatment came to mind and coincided with our ophthalmologists idea to try 1% pilocarpine eye-drop for a day. The pharmacy had only a 2% pilocarpine eye-drop solution. We started using that.

On examining his sonogram (Fig 6) I thought the sonogram of the left eye in particular had features similar to that of Ciliochoroidal Detatchment (sec 4.14).

I thought of many other things such as macular hole (was the reddish spot a reflection of the macular hole?; section 4.15), macular edema (sec 4.16) and retinal vein occlusion (sec 4.17)


4. About the Eye


Before Bruno, a seven year old smooth-haired fox-terrier, lost his eye-sight suddenly I did not know anything about eyes and their functioning.

When one does not know much about the eye, one treats blindness as a general feature of the strengths and weaknesses of the total body.

One should not look at the eye alone and hope to find a treatment for blindness. It is like a man taking the pendulum of a clock for repair when the clock has stopped working.

Yet one continues. Eye specialists are there for the purpose.

Our fault is to recognize that when we visit the eye-specialist we should not present the eye to the doctor as we would present the pendulum of a clock to a clock-repair shop. We should treat the whole body and its environment. The same is expected from the eye doctor. The majority of us fail in this count.

Perhaps one should know about the eyes in a way which will help one to understand the rest of the body which caused the affliction to the eye.

I still do not know about eyes.

I am, however, beginning to be familiar with some of the jargon used. I suspect that the general reader is also unfamiliar with the terms used. This report will use the most familiar documented objects from the internet (which I will write as internet-say).

4. 1. The parts of the eye we may be dealing with are shown in the figure below.


4. 2. There are words such as epithelium (tissue composed of cells that line the cavities and surfaces of structures throughout the body), and endothelium (a layer of cells that lines the inside of some body cavities, e.g. blood vessels; the endothelium for the cornea is shown below)and stroma (The supportive framework of an organ, usually composed of connective tissue; for the cornea the stroma is between the epithelium and the endothelium. For the cornea, they are illustrated below

The corneal endothelium is the innermost layer of the cornea responsible for the maintenance of the osmotic balance of the cornea. It pumps excess fluid out of the stroma, which has the danger of swelling with water. A compromised function can result in edema, loss of transparency, and hence a decrease in visual acuity. Endothelial cells are essential in keeping the cornea clear. Once endothelium cells are destroyed by disease or trauma, they cannot be recovered. Too much damage to endothelial cells can lead to corneal edema (swelling caused by excess fluid) and blindness ensues, with corneal transplantation the only available therapy.

4. 3. Keratitis is a condition in which the cornea becomes inflamed. There is painful inflammation and swelling of the cornea that sometimes occurs with infection after bacteria or fungi enter the cornea, trauma, chemical exposure, or thermal injury. Vision is usually impaired.

(a) Stromal infiltration and corneal edema in patient with acute-onset of interstitial keratitis. No underlying etiology (the philosophical investigation of causes and origins) was found and appears to be an idiopathic case (describes a disease or disorder that has no known cause).(b) Patient who developed interstitial keratitis showing chronic phase with dense scarring(from http://www.clspectrum.com/article.aspx?article=100635)

Vascular keratitis is caused by neovascularization-the process by which the transparency of the cornea is lost due to an ingrowth of blood vessels and connective tissue.

4.4. Posterior stromal edema (cloudy diffuse opacity)

Left: Beagle cornea showing corneal alterations of posterior stromal edema. Right: Polymorphic stromal infiltrates or endothelial swelling in region of Descemet’s membrane

4. 5. Descemet's membrane lies between the stroma, and the endothelial layer of the cornea. It has a different kind of collagen than the stroma. Significant damage to the membrane may require a corneal transplant as the endothelial cells depend on it for support and cannot re-grow after injury without it.

4.6. Toxic Effects of Detergents on the Corneal Endothelium
R. M. M. A. Nuyts, MD; H. F. Edelhauser, E. Pels, A. C. Breebaart, Arch. Opthalmol. 106, 1158 (1990)

Top left, Scanning electron micrograph of human corneal endothelium after 3 minutes of perfusion with balanced salt solution plus. The mosaic pattern of endothelial cells is intact. Top right, Scanning electron micrograph of human corneal endothelium after 3 minutes of perfusion with a 1% detergent solution. Many endothelial cells are detached from
Descemet's membrane. Remaining cells show degenerative changes, such as cell shrinkage, junctional separation, and gaps between cells. Bottom left, Transmission electron micrograph of human corneal endothelium after 3 minutes of perfusion with balanced salt solution plus. There is a smooth posterior surface with normal intracellular organelles and a few cytoplasmic vacuoles. Bottom right, Transmission electron micrograph of human corneal endothelium after 3 minutes of perfusion with a 1% detergent solution. Only remnants of endothelial cells are attached to Descemet's membrane. The outer plasma membrane is ruptured with extensive dilation of the endoplasmic reticulum, cytoplasmic vacuolization, and severe mitochondrial swelling. Note the pyknotic nucleus with the clumping of the nuclear chromatin.

4. 7. Posterior polymorphous corneal dystrophy (PPCD) is autosomal (a chromosome other than one that determines sex) dominant and bilateral, and it is characterized by transition of the corneal endothelium to an epithelial phenotype (the visible characteristics of an organism resulting from the interaction between its genetic makeup and the environment), hyperplasia (unusual growth in a part of the body, caused by an excessive multiplication of cells)of the endothelium, disrupted Descemet membrane, opacities, iridocorneal adhesions, corneal edema, corectopia (the positioning of the pupil of the eye other than in the center of the iris), and secondary glaucoma.

4. 8. Macular Corneal Dystrophy

Stromal opacities in the central cornea in Macular Corneal Dystrophy. (http://www.reviewofcontactlenses.com/content/c/21310/)

Macula (a small yellowish spot in the middle of the retina that provides the greatest visual acuity and color perception)
I am not sure at this stage whether macular corneal dystrophy (MCD) has anything to do directly with the macula of the retina. It is considered to be an hereditary disease. It is the least common of the major corneal stromal dystrophies, but thought to be the most severe. Gray-white anterior stromal lesions similar to GCD appear in the cornea. in the first decade of life. There is stromal haze between the deposits, and the entire cornea is often involved. Patients typically develop severe visual loss. The stromal deposits in MCD are composed of mucopolysaccharides that accumulate within the endoplasmic reticulum of keratocytes of the corneal stroma, extracellularly between stromal lamellae, and underneath and within the corneal epithelium.
The retina is the seeing part of the eye and the macula is the central part of that, which is responsible for the greatest detail vision. Macular dystrophy could certainly cause legal blindness, which means one can’t see any better than 20/200 out of both eyes.

4. 9. Corneal dystrophy is a degenerative change of the cornea in which cholesterol is deposited between the epithelium and the stroma of the cornea. Although the deposits are usually right in the center of the cornea, deposits can occur elsewhere depending on the cause of the degeneration. (The term “corneal dystrophy” has been used to refer to a group of inherited corneal diseases that are typically bilateral, symmetric, slowly progressive and without relationship to environmental or systemic factors.1 But, not every disorder labeled as a “corneal dystrophy” meets the criteria set forth by the definition.)

http://www.wellsphere.com/pet-health-article/corneal-dystrophy-image/366289

4. 10. Keratoconus is a weakening and thinning of the central cornea. The cornea develops a cone-shaped deformity. Progression can be rapid, gradual or intermittent. Keratoconus usually occurs in both eyes, but can occur in only one eye.


4. 11. Endothelium damage

C, cornea; EL, eyelid; I, iris; LE, lens epithelium; R, retina;

The important role of the endothelium in maintaining normal corneal thickness by pumping fluid out of the stroma by an active transport process. In rabbits corneal thickness is maintained by a sodium bicarbonate pumping mechanism within the endothelium.

4. 12. Mydriasis is an excessive dilation of the pupil due to disease, trauma or the use of drugs. Normally, the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A mydriatic pupil will remain excessively large even in a bright environment and is sometimes colloquially referred to as a "blown pupil".

Pupillary dilation (mydriasis) indicates unopposed sympathetic activity due to impaired parasympathetic axons. This may reflect compression or distortion of the oculomotor nerve by either primary injury or herniation. Mydriasis also may be an effect of adrenergic stimuli such as epinephrine, anticholinergics, cocaine, PCP, and drug withdrawal.

4. 13. Third Nerve Palsy
One needs to examine ocular motility (motile : capable of movement) as well as ptosis (a drooping of the upper eyelid, resulting from muscle weakness or an inability to move muscles). In the absence of those findings, it would be extremely rare for an ambulatory patient to present with a third nerve palsy manifested solely as an isolated dilated pupil. If there is a suspicion that the patient has instilled an atropine-like substance into the eye one can confirm this by instilling 1% pilocarpine solution into the dilated eye. If there is no constriction than one may assume that a mydriatic has previously been in contact with that eye. In a third nerve palsy, the pupil will constrict to the pilocarpine. If the above techniques fail to provide the diagnosis, the patient should be referred to an ophthalmologist in order to inspect the iris with a slit lamp and measure the intraocular pressure.

4.14. Ciliochoroidal Detatchment. B-scan ultrasonography is especially useful when the fundus (the part of a hollow organ of the body farthest from its opening, e.g. the part of the eye's retina opposite the pupil) is not easily visualized. It can help in determining the size and the extent of ciliochoroidal detachment, choroidal hemorrhage, and retinal detachment. An example is shown in the image below.

B-scan ultrasound of choroidal effusions before and after surgical drainage.

4. 15. Macular hole
A condition in which there is a partial or full thickness absence of the retina in the macular area. It may occur as a result of trauma, degeneration, old age, preretinal macular fibrosis or pathological myopia. It appears ophthalmoscopically as a round or oval, well defined, reddish spot at the macula. There is metamorphopsia, loss of visual acuity and a central scotoma. An operculum of retinal tissue may overlie the hole. The vitreous in front of the hole eventually condenses and separates from the retina. In partial macular hole a layer of photoreceptors may still be attached to the retinal pigment epithelium (lamellar hole), as in cystoid macular oedema. Treatment usually consists of reattaching the retina, if detached, and possibly vitrectomy.

4. 16. Macular Edema : swelling or thickening occurs of the central retina (macula) associated among others with uveitis, eye injury, retinal vein occlusion, or drug toxicity.


The big news today is injections of anti-vegf agents -ramibizumab -is a big one may reduce swelling and give significent vision improvement. Some of the drugs have been used in test for a number of years with huge debate over their use for DME. But it appears more doctors are using them. Maybe kenelog is one. There or others. A big problem is that the steroids need to be replaced as they are used. Basically the drugs are "wrapped" in a small pellet that slowly disolves. This form of treatment use to take frequent injections but today the time is much longer between pellet replacement.

4. 17. Retinal vein occlusion (RVO) is essentially a blockage of a portion of the venous circulation that drains the retina. With blockage, a pressure build up occurs in the capillaries, leading to hemorrhages and leakage of fluid and blood. This can lead to macular edema with leakage near the macula. Macular ischemia occurs when these capillaries, which supply oxygen to the retina, manifest leakage and nonperfusion. Neovascularization is the most devastating pathologic complication with the development of abnormal blood vessel growth.

5. The tail of the Tale


The photo of Bruno’s eyes (Fig 9) was taken after a day (20/10) of severe distress around midnight. The gentle eyes remained gentle. The kerytoconus (sec 4.10) bulge still seemed to be there. The redness of the right eye (not shown) seemed to have spread.

My final diagnosis is that Bruno was affected by environmental poisoning brought about by the injudicious and reckless use of pesticides in farms and public places. It was brought about by the long and taxing ride through an environmentally polluted zone caught up in an uncivilized (by European standards, at least) socio-economic game plan, far removed from (what we ideally imagine to be) our own native ethos which we (the modern civilized people) dismiss as jadi-buti see the net) tribal witch doctor jingo.

The proper people to address these concerns are environmentalists. They themselves (many of them are NGOs, the few rare ones are genuine but they seem to be effectively camouflaged in the internet) are so flippant, worrying about pesticides in the coca-cola rather rather than, for example, the pesticide management of their food. The industrial lobby is very happy with them because of the many diverse views they express which helps in not pointing to the culprits specifically.

Bruno could have been a weak dog, finally. His blindness was sparked by the environment. There was no environmental awareness among the people who mattered. This must include the doctors.

The problem with Bruno’s eyes could open other eyes to the symptoms of death in the environment we should love and embrace and not exploit. I think that was the original practice of shinto religion (a Japanese religion in which devotees worship and make offerings to numerous gods and spirits associated with the natural world). It is the original belief in another name in India and the far east. The Shinto religion was blacklisted in the Western mind because of the refusal of the Japanese to give up on their traditional thinking, even after the “civilized” stom bomb was dropped on them.

I felt after all the analysis that some less sophisticated but environmentally alert people such as those in the shepherd tribe would have diagnosed Bruno’s illness much faster and treated him quicker with available leaves or bark of plants and herbs. I have seen it happen a few times. The homeopathic medical system is an outcome of such approaches where technical names for particular illnesses or body parts are not important and the body and the illness is treated in holistic (taking into account all of somebody's physical, mental, and social conditions in the treatment of illness) terms. We all know what the allopathic system does.

This article is written mainly with the interest to animal lovers and student of allopathic medicine in mind so that they may be prepared for such contingencies. The doctors have no experience to handle such incidents.

The financially successful (usually westernized) environmentalists have far less insights and clues to such local problems because of their obsession with western recognition for western funding.

I am certain that in India and indeed all over the world these accidents are noticed and dismissed as a fatalistic SARD.

Postscript.

Bruno passed away at 20.40 of 21/10. His body started oozing seral juices the previous day. He was alert and responsive till 14.00 hrs of 21/10. No doctor was free to attend to him on that day. Our Pune doctor had to go to Bangalore. Other doctors were otherwise active with their professional work or lectures. In any case holistic Bruno would not have benefited from specialist quick treatments. Before going he sought solace in Lalitha’s lap and his last response was to recognize my daughter’s voice on the phone.

He was buried that night at a spot (Fig 10 right) in amitaboni where Bruno had once speculated (Fig 10 left) upon as a final resting place with foresight I am sure (Fig 10).

We will not miss Bruno. How can we not miss him?

I would have put up the blog yesterday 20/10/10. However, thanks to the UPS (Uninterrupted Power Supply) manufactorer's lobby I suspect, there was no electric power during the whole day time which coincided with the critical period of Bruno's death.

2 comments:

hrushikesh said...

I am sorry to read that your dog died. I really appreciate the effort that you have made to analyse the cause of death. This blog will really crate an awareness in the minds of people. :)

Surabhi said...

very difficult to read this - he didnt deserve this