Introduction

The word “cancer” brings a shiver down our spines despite profound advances in cancer diagnosis and management. When a person is diagnosed as having a “cancer” the first stumbling block that we surgeons usually face is the mental breakdown of the patient. A sense of fear looms within the patient that the days of life are now numbered and he or she then proceeds to an unknown destination!
In this world of ever increasing pollution and changing environmental conditions coupled with the increased knowledge about cancer genetics, cancer as a diagnosis would be more frequent in the coming years: so let us not be afraid of it, rather let us understand what we, as common persons can do to face a complex “cancerous” situation.
In this section, I am going to discuss briefly about breast cancer. Breast cancer is one of the leading cancer diagnoses in women although it has a low incidence in men. In fact, when considering the number of new cancer development in women, breast cancer stands out as the first one with over a million cases occurring worldwide every year. In the US, more than 200,000 new cases of invasive breast cancer is detected every year while around 60000 localized breast cancers occur. In India, the figure is somewhat more than 80000 per year. It is important to remember that these figures are on the rise!

Risk Factors for Breast Cancer

Several risk factors for breast cancer are known. As mentioned earlier, gender is an important risk factor with most cases occurring in women. Advanced age is the next most common risk and as the aged population increases due to improved healthcare, the number of breast cancers would also be on the rise. For example, while 1 out of 50 women have a risk of developing breast cancer at age 50, the same diagnosis can be expected in 1 out of 10 men at age 80! Women who begin their periods early and who achieve menopause later in life have an increased risk. Bearing the first child after 30 years of age is also an additional risk. Breast feeding is protective so that women who do not breast feed are subjected to increased risk. There is also a small risk in women who are on Oral Contraceptives and on Hormonal Replacement Therapy after menopause but the advantages conferred by these are so profound that the small risk that they confer can be safely ignored at present. A history of breast cancer in the family also increases the risk so also is alcohol consumption.
So, what can the common person do to counter these risks? The only factors that one can modify are possibly bearing a child before 30 and breast feed the child as well as abstaining from alcohol; you cannot modify the other factors! However, keeping in mind that a small element of risk always remains, it is important that in susceptible individuals an effort is made to detect the disease when it is in the localized state and before it becomes invasive because the chances of complete cure is possible in the former condition. There are a number of strategies to achieve this aim and I will focus on Self breast Examination, a simple method of examination that can be done by most women on a regular basis. If done properly, coupled with breast examination by a surgeon done on an annual basis, the chances of early detection of breast cancer are maximized.

This method of examining your breasts may appear a bit cumbersome in the beginning but with time you will know what is “normal” and what is not. It is important to know that the feel of the breasts vary with the stage of the menstrual period with the breasts appearing more firm and slightly nodular at the time of menses. Therefore, for best results, I would advice you to do this examination a few days after your periods when the tenderness has resolved. Please note that you can detect lumps more often adjacent to your armpits: do not be alarmed as these are not cancers in most instances!



STEP 1


In the beginning, have a LOOK at your breasts in the mirror with your shoulders straight and your arms on your hips.
Things to look out for:
*compare the two sides to see if the breasts have their usual size, shape, and color
*if there is visible distortion or swelling in either breast.
If you see any of the following changes, bring them to your doctor's attention:
*dimpling, puckering, or bulging of the skin of the breasts
*a nipple that has changed position compared to earlier or an inverted nipple (pushed inward instead of sticking out)
*redness, soreness, rash, or swelling in either breast especially when adjacent to the nipple.

STEP 2


Raise your arms and look out for the same things as in Step 1.

STEP 3

While you're still in front of the mirror, gently squeeze each nipple between your fingers and thumb and check for nipple discharge (this could be a milky or yellow fluid or blood or any other thick or thin clear fluid as well as greenish fluid). Please bring the same to the attention of the doctor.


STEP 4

Next, lie down and feel your breasts one at a time, using your right hand to feel your left breast and then your left hand to feel your right breast. While using one hand, keep the other below your head over a pillow for best results. Use a firm, smooth touch with the first few fingers of your hand, keeping the fingers flat and together.
Cover the entire breast from top to bottom, side to side—from your collarbone to the top of your abdomen, and from your armpit to your cleavage.
Follow a pattern to be sure that you cover the whole breast. You can begin at the nipple, moving in larger and larger circles until you reach the outer edge of the breast. You can also move your fingers up and down vertically, in rows, as if you were mowing a lawn. Be sure to feel all the breast tissue: just beneath your skin with a soft touch and down deeper with a firmer touch. Begin examining each area with a very soft touch, and then increase pressure so that you can feel the deeper tissue, down to your ribcage.

STEP 5


Finally, feel your breasts while you are standing or sitting. You can do this while in a shower. Cover your entire breast, using the same hand movements described in Step 4.
If you discover anything abnormal, it is imperative that you make an appointment with your surgeon as early as possible! Do not neglect: time is a critical factor in treatment!


Conclusion

Lastly, I would like to say a few things about screening mammography. Screening mammography is literally an X-ray of the breasts that is done to note anything suspicious within the breasts. This can be important in cancer detection but it is also important to note that it can miss 1 out of 5 cancers. It is of less use in younger women because they have dense breasts and therefore women in the age range 40-49 years should resort to a 2 yearly mammography while women above 50 years of age should opt for a yearly mammography.
To sum up, self breast examination is the most important part of screening for breast cancer and should be done by all women regardless of age supplemented by annual clinical examination by a surgeon or when abnormalities are detected by the patient herself during self examination. This is much more important in women who have a family history of breast cancer. Screening mammography is of most benefit to women above 40 years of age although it has the propensity of missing quite a few cancers.

Dealing With Back Pain in Pregnancy

During our prenatal exercise classes, we often ask if anyone is experiencing any physical discomforts. More often than not, the typical response is, "my lower back hurts!" How can we reduce the amount of back pain during pregnancy?

To begin with, we need to understand what is happening during pregnancy. The weight of a non-pregnant woman is centered in the middle of her pelvis. During pregnancy, the center shifts forward with the weight of the baby. Most women balance this weight by leaning back with the upper body, which increases the curve in her lower back, otherwise known as lordosis. This, coupled with the increased stress on the abdominal muscles leads to much of the discomfort she experiences.

Correcting this problem is fairly simple and requires only a few minutes and a mirror. You may notice your lower back tends to hollow inward. Pull your abdominal muscles up and in, tighten your buttocks, and press your lower back toward the wall behind you. Or, put another way, visualize your abdomen as a bowl of water. Tilt your pelvis so the "water" is level and cannot spill forward. With practice, this ?pelvic tilt? will feel comfortable and natural.

Remind yourself periodically throughout the day to check your posture and tilt your pelvis, especially if you feel tightness in your back.


There are a few other simple rules of body mechanics to remember as well:
· Wear flat or low-heeled shoes for increased comfort.
Higher heels make a pelvic tilt nearly impossible to
maintain.
· Avoid forward bending; try instead squatting or
lowering to one knee when getting up and down from
the floor or picking things up. The quadriceps muscles
in your thighs are stronger and meant for this purpose.
· Strengthen your abdominal muscles; they tend to
become less supportive during pregnancy, leading to
increased back pain. Ask your prenatal fitness
instructor or childbirth educator for a list of
appropriate abdominal exercises.
· Stretch your back! There are a variety of excellent
lower back stretches. Again, ask your instructor. Be
sure to try the pelvic tilt in the hands and knees
position.
Contract your abdominal muscles and press your middle and lower back toward the ceiling, tuck your tailbone down. When releasing this position, be sure to maintain a level spine, not allowing your back to sag or sway downward. Do these as often as necessary for relief.

· When all else fails, a back massage is a great way to relax and improve your sense of well-being!
Keep in mind that after the birth of your baby, you will still find it vital to maintain good posture, abdominal strength, and lower back flexibility. These are habits that will enable you to enjoy your baby and your body that much more!

How Does Your Baby Grow?

Nobody can tell exactly when your baby was conceived. But fertilization usually occurs about two weeks after the beginning of your last menstrual cycle.


Within a few hours after the egg is penetrated by the sperm in the fallopian tube, the egg begins to divide. In the next three to five days, a cluster of up to 50 cells floats down the fallopian tube to the uterus, where it continues to develop. By the tenth day, the ovum is firmly implanted in the uterine wall. Here it burrows little finger-like projections called "villi" into the blood supply of the uterine lining from which it will take its nourishment... and begins the miraculous growth that will make it a real live baby.


Second Week After FertilizationAs the cluster of cells begins to elongate, a water-tight sac forms around it, gradually filling with fluid. This will serve to cushion the growing life from shocks. Next to this, a tiny yolk sac forms, preparing to produce little blood vessels. Now the placenta--the round, flat membrane that will lie inside the uterine wall--begins to develop. Joined to the umbilical cord, it will take over the job of the more primitive villi, bringing food, water and minerals from the maternal blood to the fetus, and carrying fetal waste to the blood.

Third WeekThe cell cluster is now a hollow structure filled with fluid, measuring only about 1/100 of an inch in diameter (the thickness of a heavy pencil dot). But already there are primitive lung buds...a tube that will be your baby's heart...and a thickening that is the beginning of the central nervous system. The cluster begins to curl up now so that it will fit in its compact home as it grows.

Fourth WeekA primitive face is taking form, with large circles where eyes will appear. The mouth, lower jaw, and throat are developing. Little tubules foreshadow internal organs such as the gallbladder, liver, and stomach. Blood corpuscles are taking shape, and the circulation is beginning. The tiny "heart" tube will be beating 65 times a minute by the end of this week. The embryo as it is now called, will be 3/16 of an inch in length by the end of the week. In one month, the single fertilized egg has grown 10,000 times bigger than when it started.

Fifth WeekBy the end of this week, ears begin to develop from two folds of tissue, buds emerge that will become arms and legs, and your baby's eye lenses begin taking form. There is a tiny depression where the nose will be and an equally tiny thickening that will be the tongue. Eight to ten vertebrae of the backbone have been laid down. The brain, spinal cord, and nervous system are well established. Your baby's primitive blood vessels have begun to function.

Sixth WeekBy now the beating heart can be seen with special instruments. It is still outside the baby's body, but its four chambers are beginning to form. The mouth is still closed, but the digestive tract is developing downward from the mouth cavity. By the end of the sixth week, hollows appear where eyes and ears will form; the beginnings of testes or ovaries have appeared; the brain is growing rapidly; and the entire backbone has been laid down. There is even a skeleton, though it is mostly made up of cartilage, not yet real bone. A "tail" extends from the spinal cord; at this stage, the human embryo resembles that of a pig, rabbit, or elephant. It is now 1/4 of an inch in length.


Seventh WeekThe embryo has become a fetus. Its heart is now within its chest cavity. The tail has all but disappeared. Nasal openings are breaking through. Eyes can now be perceived through closed lids. Little buds signal the beginning of fingers and toes and delicate little muscle fibers are starting. The fetus is 1/2 an inch long and weights 1/1000 of an ounce.


Eighth WeekHuman facial features, particularly the jaws, are becoming well defined. Teeth are being formed. Fingers and toes are present, and external ears form elevations on either side of the head. In boys the penis begins to appear. The fetus is no 7/8 of an inch long and weighs 1/30 of an ounce.


Ninth WeekThe baby's face is now completely formed. The clitoris appears in girls. Your baby now resembles a miniature human, slightly more than one inch in length, weighing 1/5 of an ounce.


Tenth Week: Your baby's eyes have moved from the sides of its head, where they were originally, to the front. In males, the scrotum appears. Major blood vessels have almost reached final form. The heart waves are similar to those of an adult. The baby looks top-yeavy, for the head is almost half its entire size.


End of Third Month: Upper and lower eyelids have met and fused and tear glands are starting to appear. Primitive hair follicles are forming and so are the beginnings of vocal cords. Fingernails are already present and your baby can close his fingers to make tiny fists. He can also open his mouth, purse his lips, and squint up his face. He is now three inches long, and weights about one ounce.

Fourth Month : Your baby's heartbeat is now audible to the doctor's stethoscope. Its brain looks like a miniature adult brain. Sweat glands are forming on palms and soles, and the skin is thickening into various layers. Your baby now has eyebrows and eyelashes, has grown to six ounces, and is 8 1/2 inches in length. It is at this time that many babies start to such their thumbs.

Fifth Month: Your baby's muscles are active now, and by the midpoint of pregnancy, 20 weeks, you will probably have felt "quickening"--the baby's movements. There is hair on his head. He is skinny, but fat is beginning to be deposited under his translucent skin. Twelve inches in length, he weighs about one pound.

Sixth Month: Your baby's skin is wrinkled and has developed a cheese-like protective material called "vernix" which will remain right through birth. The eyes are open and will soon be sensitive to light (although color and form won't be perceived until long after birth). Your baby can now hear sounds. And wonder of wonders--with skin ridges fully formed on palms and soles, your baby now has finger- and footprints. Length, 14 inches. Weight, 2 pounds.


Seventh Month : Fine downy hair covers your baby's body. Taste buds have developed. The male's testicles have descended into the scrotum. By the end of this month, your baby is about 16 inches long, and 3 1/2 pounds in weight. Its organ systems are now adequately well developed so that even if born prematurely, it could probably survive. But the next two months will be periods of growth and maturation to ensure a healthy entry into the world.


Eighth Month: Baby is getting plumper and plumper, and the skin is somewhat less wrinkled as fat takes up the slack. He may now weight more than five pounds, and may be some 18 inches in length. His fingernails are long, extending beyond the fingertips.


Ninth Month: The baby's skin is red but smooth. It looks polished. The only downy hair remaining now is on arms and shoulders. On the head, the hair is about one inch long. Deposit of subcutaneous fat continues. By the end of this month, what was begun from you egg cell measuring 1/200 of an inch in diameter, and your husband's sperm cell, only 1/80,000 the size of the egg, will emerge as a bouncy little infant some 20 inches in length, and weighing an average of 7 pounds.

ANTIOXIDANTS IN OPHTHALMOLOGY
EVOLVING CONCEPTS

Prof Dr M R Jain, FAMS



ABSTRACT
As one ophthalmologist had mentioned way back a decade ago: ‘advocating antioxidants is like shooting in the dark’. It is no more now. Today the pathophysiology of free radical mediated eye degenerative diseases like age-related macular degeneration and cataract are well established, and so is the definite role of antioxidants, particularly carotenoids. As far as eye is concerned, lutein and zeaxanthin have a vital role to play, and these two carotenoids are a must for the eye to be well protected form developing macular degeneration as well as cataract. In addition, lycopene, another carotenoids has a special place in eye defense since it is the best quencher of singlet oxygen - a reactive oxygen species which causes havoc particularly in the eye.


INTRODUCTION
Free radical chemistry began in 1900s when they were determined as cause for fat spoilage. Importance of free radicals in human diseases pathophysiology was first recognized in 1969 when McCord & Fridovich isolated the first antioxidant enzyme superoxide dismutase.

The controversy as regards the use of antioxidants, particularly carotenoids, in ophthalmic diseases seems to be resolving due to advances made in measuring their levels in foods and tissues. There is consistent experimental and epidemiological evidence to substantiate the role of particularly lutein and zeaxanthin in prevention and, to a certain extent, cure of early age-related macular degeneration (ARMD) and cataract formation. Also clinical observations depending upon the recommended dietary modification and therapeutic supplementation presently are encouraging.



FREE RADICALS
DEFINITION
A free radical is defined as any species capable of independent existence and contains one or more unpaired electrons.



HOW FREE RADICALS ARE FORMED?
The various tissues in the human body are formed by innumerable molecules. Each molecule consists of two or more atoms joined together by chemical bonds. An atom, the smallest particle of an element, consists of a core which contains positively charged protons (or positrons) as well as neutral neutrons. In the orbit of each atom (referred to as orbital) are present the electrons (or negatrons). Each orbital can accommodate a maximum of two electrons both of which spin in opposite directions.

Most molecules are non-radical since they contain a paired set of electrons. But oxygen is always electronegative. As a consequence, it pulls electrons away from other atoms (including oxygen itself) and renders these as free radicals.
Oxygen-derived free radicals have a lifespan of only a few microseconds. Their concentration at any single site is miniscule. However the danger lies in their ability to combine with another nonradical to render the latter as free radical. Normally, bonds don’t split in a way that leaves a molecule with an odd, unpaired electron. But when weak bonds split, free radicals are formed. Free radicals are very unstable and react quickly with other compounds, trying to capture the needed electron to gain stability.

Fig: Serial formation of free radicals.



Generally, free radicals attack the nearest stable molecule, thereby "stealing" its electron. When the "attacked" molecule loses its electron, it becomes a free radical itself. This leads to a process of chain reaction. Once such a process has started, it can cascade, finally resulting in the disruption of a living cell.

Radicals can react with other molecules in a number of ways. If two radicals meet, they can combine their unpaired electrons symbolized by.) and join to form a covalent bond (a shared pair of electrons). The hydrogen atom, with one unpaired electron, is a radical and two atoms of hydrogen easily combine to form the diatomic hydrogen molecule:
H. + H.

Radicals react with nonradicals in several ways. A radical may donate its unpaired electron to a non-radical (a reducing radical) or it might take an electron from another molecule in order to form a pair (an oxidizing radical). A radical may also join onto a nonradical. Whichever of these three types of reaction occurs, the nonradical species becomes a radical. A feature of the reactions of free radicals with nonradicals is that they tend to proceed as chain reactions, where one radical begets another.



SOURCES OF FREE RADICALS
Some free radicals arise normally during metabolism. Sometimes the body’s cells or its immune system purposefully create them to neutralize viruses and bacteria. However, environmental factors such as pollution, radiation, cigarette smoke and herbicides can also generate free radicals. Free radicals causing structural damage (to proteins) resulting in aging changes such as cataract and ARMD.

An adult utilizes 3.5 ml oxygen per kg body weight per minute. Assuming a body weight of 70 kgs, this works out to 352.8 liters per day. Even if 1% of oxygen is converted to free radicals, this amounts to 1.72 kg of free oxygen radicals per year!



EXAMPLES SOURCES OF FREE RADICALS
Some free radicals well studied free radicals are:
• SUPEROXIDE ANION (O2.)
• HYDROXYL RADICAL (OH.)
It is important to note that free radicals such as hydroxyl radical differ from hydroxyl ions in their content of electrons.



REACTIVE OXYGEN SPECIES
These are partially reduced oxygen species which do not contain any unpaired electron. Examples of reactive oxygen species are:

• HYDROGEN PEROXIDE (H2O2)
• HYDROPEROXY RADICAL (HOO-)
• HYPOCHLOROUS ACID RADICAL (HOCl)

Under certain conditions reactive oxygen species have potential to enter free radical reactions to form the more toxic free radicals. Another reactive oxygen species, which is not a free radical, is singlet oxygen (O). In this, a rearrangement of electrons has occurred which allows it to react faster with biological molecules - as compared to ‘normal’ oxygen.



ANTIOXIDANTS
DEFINITION
Antioxidants can be defined as substances whose presence in relatively low concentrations significantly inhibits the rate of oxidation of the targets.



HOW ANTIOXIDANTS WORK?
Antioxidants serve as natural protectors in the body, mopping up free radicals and reactive oxygen species, which are potentially damaging. Antioxidants protect the tissues in 4 ways:

• Physically separating the free radicals / reactive oxygen species from the susceptible molecules of the human body.
• Providing molecules which effectively compete for oxygen.
• Rapidly repair the damage caused by free radicals / reactive oxygen species.
• Lyse the free radicals / reactive oxygen species and rapidly remove these.



CLASSIFICATION OF ANTIOXIDANTS
• ANTIOXIDANT ENZYMES
• Superoxide dismutase
• Catalase
• Glutathione peroxidase
• PREVENTIVE ANTIOXIDANTS
• Ceruloplasmin
• Transferrin
• Albumin
• CHAIN-BREAKING ANTIOXIDANTS
• Water-soluble*
• Uric acid (200-400 mmol/L)
• Ascorbate (25-100 mmol/L)
• Thiols (400-500 mmol/L)
• Bilirubin (10-20 mmol/L)
• Flavanoids
• Fat-soluble*
• Tocopherols (20-30 mmol/L)
• Ubiquinol-10 (<2 mmol/L)
• Beta-carotene (1-2 mmol/L)
• Estrogens
* optimal blood level given in brackets


The most important antioxidants are three vitamins and three minerals.

• ANTIOXIDANT VITAMINS
• CAROTENOIDS
• VITAMIN E
• VITAMIN C
• ANTIOXIDANT MINERALS
• SELENIUM
• ZINC
• MANGANESE
• COPPER




CAROTENOIDS
Carotenoids circulate in lipoproteins; 53% of beta carotene occurs in low density lipoproteins. Besides the well known beta carotene, the other carotenoids of human importance are:

• Lutein
• Zeaxanthin
• Lycopene
• Alpha carotene
• Beta cryptoxanthin

As far as the eye is concerned, Lutein and zeaxanthin are exclusively concentrated in the macula, lens and iris. The retina and choroids additionally contain lycopene, alpha- and beta carotene. In the ciliary body, all the carotenoids taken in foodstuff or as dietary supplement get accumulated.



VITAMIN E
Being a fat soluble vitamin, alpha tocopherol is abundant in all cell membranes as well as in lipoproteins. In the eye, vitamin E is present in retina and choroids, and balance in iris and ciliary body. It is important in protection of rods and cones in retina, and also for preventing free radical damage to lens. Vitamin E acts synergistically with vitamin C, beta carotene and selenium for better functioning of glutathione.



VITAMIN C
Vitamin C is protective for the cytoplasm & is also most important for plasma defense. It also occurs in certain cells like muscle, adrenals and eye. Vitamin C has the capacity to regenerate vitamin E. It is more significant in combating free radicals formed due to pollution and cigarette smoke. Vitamin C especially concentrates in ocular tissues and is the first antioxidant to tackle free radicals.



ZINC, MANGANESE & COPPER
Zinc (Zn), manganese (Mn) and copper (Cu) are constituents of superoxide dismutase (SOD) antioxidant enzyme. SOD is widely distributed in tissues as well as fluid compartments. CuZnSOD is present in cytoplasm and nucleus, MnSOD in operates mitochondria whilst CuSOD is most distributed in plasma. SOD attacks free radicals like hydroxyl radical to convert these into hydrogen peroxide.

Besides, Zn serves an important structural role, whilst Cu is necessary for functioning of another antioxidant enzyme called as catalases. Hydrogen peroxide is converted by catalases into harmless water and molecular oxygen.

In the retina, SOD plays an important role by scavenging free radicals to prevent the oxidative damage which plays a role in the development of drusen, an early sign of ARMD. Catalases, on the other hand, are vital for lens protection.


SELENIUM
Selenium (Se) is the most important dictator of glutathione peroxidase activity. Glutathione peroxidase is concentrated in various tissues, besides blood and synovial fluid. In tisues, it operates in the cytoplasm and mitochondria principally. Like catalases, glutathione peroxidase breaks down hydrogen peroxide, besides reducing lipid peroxidation like vitamin E and beta carotene.

Glutathione peroxidase and related enzymes in the retina, plus the precursor amino acids (N-acetylcysteine, L-glycine, and glutamine and selenium) are protective against damage to human retinal pigment epithelium cells. Glutathione peroxidase prevents free radical-induced apoptosis (cell suicide) and helps prevent or treat ARMD.



CAROTENOIDS
DEFINITION
More than 500 distinct compounds are today identified as naturally occurring carotenoids. They include cyclic hydrocarbon-carotenoids (carotenes), acyclic hydrocarbon carotenoids (lycopene), and oxygenated hydrocarbon carotenoids (xanthophylls like lutein and zeaxanthin).

Handelman and associates noted carotenoids concentration in the macula to be 5-fold higher compared to peripheral retina and 500 times more than the concentration in other tissues. Lutein is the major carotenoid in the peripheral retina, whereas zeaxanthin becomes more and more dominant as the foveal centre is approached. The proportion of lutein to zeaxanthin in macula is 1:2 and the proportion is reversed in the peripheral retina. The distribution of xanthophyll carotenoids suggests a possible role of lutein in protecting the rods and for zeaxanthin in protecting the cones that are concentrated in the central retina. The human lens carotenoids content is 10-20 ng/gm of wet tissue, and the ratio is 1.6:2.2 for Lutein and zeaxanthin.

Another most important dietary antioxidant of ocular significance is lycopene, which is however, conspicuous by its absence in macula. Due to its presence in high concentration in circulating blood in the eye, lycopene plays a prominent role in prevention of macular degeneration mainly by its very potent singlet oxygen quenching capacity.





FOCUS ON CAROTENOIDS IN ARMD
ARMD - INTRODUCTION
In developed countries, ARMD is the leading cause of blindness amongst the elderly (more than 60 years) with a prevalence ranging between 2 to 7% for severe (wet) form and a range of 12 to 30% for the dry form. The disease has caused irreversible visual impairment in an estimated 1.7 million Americans over the age of 65 years. The number of cases of ARMD has been predicted to increase from 2.7 million in 1970 to 7.5 million by the year 2030.

In India, the incidence of ARMD affects approximately 4-5 per cent of the population over the age of 50 years and may be affecting 19-20 per cent of people above 70 years of age. Early disease is characterized by yellowish-colored subretinal drusen. Late disease, which may be ‘dry’ or ‘wet’, may lead to significant loss of central vision. Wet form occurs only in 10 percent of population.



ARMD - PATHOPHYSIOLOGY
The light must pass the macular pigment, which contains abundance of zeaxanthin and lutein before striking the photoreceptors. If any damage to the rods and cones is to be prevented the short wave length of light rays (<500 nm range) must be filtered. This is accomplished as follows:

• 5-286 nm wavelength (ultraviolet C rays): filtered by the earth’s ozone layer.
• 286-320 nm wavelength (ultraviolet B rays): filtered by cornea.
• 320-400 nm wavelength (ultraviolet C rays): filtered by lens.
• 400-500 nm wavelength (visible blue light): filtered by lutein / zeaxanthin in macula.

The light entering the retina is between the wavelengths of 400 to 700 nm. The eye would be in perfect focus for daylight only at 560 nm, and even at night 500 nm wavelength of light is optimal for functioning of rods. Hence, filtering out 400-500 nm wavelength of light prevents damage to macula without affecting vision.
Thus macular pigments represent a significant filtering element and hence protect against the light–initiated cumulative oxidative damage. The macular pigment also removes much of the blurry, short wave blue and blue-green light that results from the eye’s chromatic aberration. Apart from this the earth’s atmosphere through which we view objects almost always contain small-suspended particles, which scatters short wave length light more than other wavelengths and results in a bluish veiling luminance.
The eye and skin are the only structures which have dual exposure to oxygen and light. In presence of blue light (400-500 nm wavelength) the oxygen will be split into singlet oxygen which is one of the most deadly reactive oxygen species as far as the eye is concerned. The blue light has potential to split molecular oxygen due to the high energy contained in it.

The singlet oxygen and other free radicals formed inside the eye initiate lipid peroxidation of photoreceptors. The polyunsaturated fatty acids in the outer membrane of rods and cones are attacked by free radicals and singlet oxygen species to result in damage of these photoreceptors. As a consequence, there is accumulation of lipofuscin by retinal pigment epithelium which then contributes in druse formation.



ARMD - MEDICAL MANAGEMENT
The damage to macula and formation of drusen can be prevented by filtering out the damaging blue light of the visible spectrum. This is possible by the macula, if its content of lutein and zeaxanthin are adequate. The additional available of lycopene in adequate amounts is of paramount importance in tackling the singlet oxygen single this carotenoids is the best antioxidant known for quenching this reactive oxygen species. In addition, glutathione peroxidase and SOD too have been shown to have preventive benefit in ARMD.



FOCUS OF CAROTENOIDS IN CATARACT
CATARACT - INTRODUCTION
Cataract is a multifactorial disease. Oxidative stress together with weakened antioxidant defense mechanism is attributed to the changes observed in human diabetic cataract. Oxidative damage to the lens has been recognized as a primary event in the pathogenesis of many forms of cataract. Consistent with this view, epidemiological reports have identified factors related to oxidative process that both increase (eg smoking and light exposure) and decrease (eg antioxidant intake) cataract risk.

Epidemiological studies provide evidence that nutritional antioxidants slow down the progression of cataract.



CATARACT - PATHOPHYSIOLOGY
Oxidative stress is high in the eye due to ultraviolet rays which promote liberation of free radicals and singlet oxygen. The epidemiological evidence to support the possibility that lutein and zeaxanthin have an important role in reducing the risk of cataract is somewhat consistent, and justifies the belief in free radical & reactive oxygen species mediated damage to the lens.

Few of the recent studies have stressed the significance of vitamin C, E and selenium in the etiology of cataract. Role of vitamin E has been more specifically stressed by several workers. Low blood levels of vitamin E are associated with approximately twice the risk of both cortical and nuclear cataracts, compared to median or high levels. Smokers are 2.6 times likely to develop posterior subcapsular cataracts more than nonsmokers. Patients with senile cataracts were found to have significantly lower blood and intraocular levels of the mineral selenium than control.



CATARACT - MEDICAL MANAGEMENT
Lower prevalence of nuclear cataract in women or men was associated with intake of lutein and zeaxanthin in high doses. Furthermore, in prospective cohort studies it was noted that people who consumed diet rich in lutein and zeaxanthin, had 20-25 percent lower risk of cataract extraction and 70 percent lower risk of cataract extraction under the age of 65 years.

Experimental study in human lens epithelial cells (HLEC) in culture was evaluated and it was concluded that addition of lycopene had a protective effect to prevent vacuolization of epithelial cells. It was observed that there was as positive effect of retardation of lens opacities due to lutein and zeaxanthin in the aging lenses.

In an 8 year prospective cohort study, Hankinson et al reported that an elevated intake of spinach, which is high in lutein and zeaxanthin (but low in beta carotene content) was most consistently associated with a lower risk of cataract extraction, whereas high beta carotene and vitamin E intakes alone had no beneficial effects against cataract prevention.

This study corroborated data from Jaques et al 1988 who demonstrated that persons with slightly elevated levels of plasma total carotenoids had a 25% lower risk for any type of cataract.



ANTIOXIDANTS IN RETINITS PIGMENTOSA
There is possibility that lutein may slow degeneration of vision in retinitis pigmentosa, a heterogeneous group of slow retinal degenerations. However, only preliminary data in a very small number of patients has been published in which lutein slowed vision loss associated with retinitis pigmentosa in one.






ANTIOXIDANTS IN DIABETIC RETINOPATHY
Several studies are in progress as regards role of antioxidants in diabetic retinopathy and glaucoma but as yet none is conclusive.



CONCLUSION
The overwhelming body of evidence points to significant beneficial effects of nutritional supplementation for most degenerative eye conditions. Important to remember is that most of the above studies used blood levels and food intakes associated with a normal diet. Taking supplements, specifically containing zeaxanthin, lutein and lycopene in adequate doses, which are theorized to provide protection to macula and lens with adequate doses, may have a much more protective effect than dietary levels alone. With so little risk, and the other potential health benefits from taking nutritional supplements, it would certainly seem prudent to try them, especially for macular degeneration where there are no real options.

Once the damage is done it cannot be reversed (except to a small degree), so prevention and early intervention is essential, especially if we have a family history of the disease. Of course, it's important to slow further progression at any stage of development. Prevention of lens and macula from the ultraviolet rays and hazard of smoking, however, needs to be over stressed.



























ANTIOXIDANTS IN OPHTHALMOLOGY
EVOLVING CONCEPTS

Prof Dr M R Jain, FAMS



ABSTRACT
As one ophthalmologist had mentioned way back a decade ago: ‘advocating antioxidants is like shooting in the dark’. It is no more now. Today the pathophysiology of free radical mediated eye degenerative diseases like age-related macular degeneration and cataract are well established, and so is the definite role of antioxidants, particularly carotenoids. As far as eye is concerned, lutein and zeaxanthin have a vital role to play, and these two carotenoids are a must for the eye to be well protected form developing macular degeneration as well as cataract. In addition, lycopene, another carotenoids has a special place in eye defense since it is the best quencher of singlet oxygen - a reactive oxygen species which causes havoc particularly in the eye.


INTRODUCTION
Free radical chemistry began in 1900s when they were determined as cause for fat spoilage. Importance of free radicals in human diseases pathophysiology was first recognized in 1969 when McCord & Fridovich isolated the first antioxidant enzyme superoxide dismutase.

The controversy as regards the use of antioxidants, particularly carotenoids, in ophthalmic diseases seems to be resolving due to advances made in measuring their levels in foods and tissues. There is consistent experimental and epidemiological evidence to substantiate the role of particularly lutein and zeaxanthin in prevention and, to a certain extent, cure of early age-related macular degeneration (ARMD) and cataract formation. Also clinical observations depending upon the recommended dietary modification and therapeutic supplementation presently are encouraging.



FREE RADICALS
DEFINITION
A free radical is defined as any species capable of independent existence and contains one or more unpaired electrons.



HOW FREE RADICALS ARE FORMED?
The various tissues in the human body are formed by innumerable molecules. Each molecule consists of two or more atoms joined together by chemical bonds. An atom, the smallest particle of an element, consists of a core which contains positively charged protons (or positrons) as well as neutral neutrons. In the orbit of each atom (referred to as orbital) are present the electrons (or negatrons). Each orbital can accommodate a maximum of two electrons both of which spin in opposite directions.

Most molecules are non-radical since they contain a paired set of electrons. But oxygen is always electronegative. As a consequence, it pulls electrons away from other atoms (including oxygen itself) and renders these as free radicals.
Oxygen-derived free radicals have a lifespan of only a few microseconds. Their concentration at any single site is miniscule. However the danger lies in their ability to combine with another nonradical to render the latter as free radical. Normally, bonds don’t split in a way that leaves a molecule with an odd, unpaired electron. But when weak bonds split, free radicals are formed. Free radicals are very unstable and react quickly with other compounds, trying to capture the needed electron to gain stability.

Fig: Serial formation of free radicals.



Generally, free radicals attack the nearest stable molecule, thereby "stealing" its electron. When the "attacked" molecule loses its electron, it becomes a free radical itself. This leads to a process of chain reaction. Once such a process has started, it can cascade, finally resulting in the disruption of a living cell.

Radicals can react with other molecules in a number of ways. If two radicals meet, they can combine their unpaired electrons symbolized by.) and join to form a covalent bond (a shared pair of electrons). The hydrogen atom, with one unpaired electron, is a radical and two atoms of hydrogen easily combine to form the diatomic hydrogen molecule:
H. + H.

Radicals react with nonradicals in several ways. A radical may donate its unpaired electron to a non-radical (a reducing radical) or it might take an electron from another molecule in order to form a pair (an oxidizing radical). A radical may also join onto a nonradical. Whichever of these three types of reaction occurs, the nonradical species becomes a radical. A feature of the reactions of free radicals with nonradicals is that they tend to proceed as chain reactions, where one radical begets another.



SOURCES OF FREE RADICALS
Some free radicals arise normally during metabolism. Sometimes the body’s cells or its immune system purposefully create them to neutralize viruses and bacteria. However, environmental factors such as pollution, radiation, cigarette smoke and herbicides can also generate free radicals. Free radicals causing structural damage (to proteins) resulting in aging changes such as cataract and ARMD.

An adult utilizes 3.5 ml oxygen per kg body weight per minute. Assuming a body weight of 70 kgs, this works out to 352.8 liters per day. Even if 1% of oxygen is converted to free radicals, this amounts to 1.72 kg of free oxygen radicals per year!



EXAMPLES SOURCES OF FREE RADICALS
Some free radicals well studied free radicals are:
• SUPEROXIDE ANION (O2.)
• HYDROXYL RADICAL (OH.)
It is important to note that free radicals such as hydroxyl radical differ from hydroxyl ions in their content of electrons.



REACTIVE OXYGEN SPECIES
These are partially reduced oxygen species which do not contain any unpaired electron. Examples of reactive oxygen species are:

• HYDROGEN PEROXIDE (H2O2)
• HYDROPEROXY RADICAL (HOO-)
• HYPOCHLOROUS ACID RADICAL (HOCl)

Under certain conditions reactive oxygen species have potential to enter free radical reactions to form the more toxic free radicals. Another reactive oxygen species, which is not a free radical, is singlet oxygen (O). In this, a rearrangement of electrons has occurred which allows it to react faster with biological molecules - as compared to ‘normal’ oxygen.



ANTIOXIDANTS
DEFINITION
Antioxidants can be defined as substances whose presence in relatively low concentrations significantly inhibits the rate of oxidation of the targets.



HOW ANTIOXIDANTS WORK?
Antioxidants serve as natural protectors in the body, mopping up free radicals and reactive oxygen species, which are potentially damaging. Antioxidants protect the tissues in 4 ways:

• Physically separating the free radicals / reactive oxygen species from the susceptible molecules of the human body.
• Providing molecules which effectively compete for oxygen.
• Rapidly repair the damage caused by free radicals / reactive oxygen species.
• Lyse the free radicals / reactive oxygen species and rapidly remove these.



CLASSIFICATION OF ANTIOXIDANTS
• ANTIOXIDANT ENZYMES
• Superoxide dismutase
• Catalase
• Glutathione peroxidase
• PREVENTIVE ANTIOXIDANTS
• Ceruloplasmin
• Transferrin
• Albumin
• CHAIN-BREAKING ANTIOXIDANTS
• Water-soluble*
• Uric acid (200-400 mmol/L)
• Ascorbate (25-100 mmol/L)
• Thiols (400-500 mmol/L)
• Bilirubin (10-20 mmol/L)
• Flavanoids
• Fat-soluble*
• Tocopherols (20-30 mmol/L)
• Ubiquinol-10 (<2 mmol/L)
• Beta-carotene (1-2 mmol/L)
• Estrogens
* optimal blood level given in brackets


The most important antioxidants are three vitamins and three minerals.

• ANTIOXIDANT VITAMINS
• CAROTENOIDS
• VITAMIN E
• VITAMIN C
• ANTIOXIDANT MINERALS
• SELENIUM
• ZINC
• MANGANESE
• COPPER




CAROTENOIDS
Carotenoids circulate in lipoproteins; 53% of beta carotene occurs in low density lipoproteins. Besides the well known beta carotene, the other carotenoids of human importance are:

• Lutein
• Zeaxanthin
• Lycopene
• Alpha carotene
• Beta cryptoxanthin

As far as the eye is concerned, Lutein and zeaxanthin are exclusively concentrated in the macula, lens and iris. The retina and choroids additionally contain lycopene, alpha- and beta carotene. In the ciliary body, all the carotenoids taken in foodstuff or as dietary supplement get accumulated.



VITAMIN E
Being a fat soluble vitamin, alpha tocopherol is abundant in all cell membranes as well as in lipoproteins. In the eye, vitamin E is present in retina and choroids, and balance in iris and ciliary body. It is important in protection of rods and cones in retina, and also for preventing free radical damage to lens. Vitamin E acts synergistically with vitamin C, beta carotene and selenium for better functioning of glutathione.



VITAMIN C
Vitamin C is protective for the cytoplasm & is also most important for plasma defense. It also occurs in certain cells like muscle, adrenals and eye. Vitamin C has the capacity to regenerate vitamin E. It is more significant in combating free radicals formed due to pollution and cigarette smoke. Vitamin C especially concentrates in ocular tissues and is the first antioxidant to tackle free radicals.



ZINC, MANGANESE & COPPER
Zinc (Zn), manganese (Mn) and copper (Cu) are constituents of superoxide dismutase (SOD) antioxidant enzyme. SOD is widely distributed in tissues as well as fluid compartments. CuZnSOD is present in cytoplasm and nucleus, MnSOD in operates mitochondria whilst CuSOD is most distributed in plasma. SOD attacks free radicals like hydroxyl radical to convert these into hydrogen peroxide.

Besides, Zn serves an important structural role, whilst Cu is necessary for functioning of another antioxidant enzyme called as catalases. Hydrogen peroxide is converted by catalases into harmless water and molecular oxygen.

In the retina, SOD plays an important role by scavenging free radicals to prevent the oxidative damage which plays a role in the development of drusen, an early sign of ARMD. Catalases, on the other hand, are vital for lens protection.


SELENIUM
Selenium (Se) is the most important dictator of glutathione peroxidase activity. Glutathione peroxidase is concentrated in various tissues, besides blood and synovial fluid. In tisues, it operates in the cytoplasm and mitochondria principally. Like catalases, glutathione peroxidase breaks down hydrogen peroxide, besides reducing lipid peroxidation like vitamin E and beta carotene.

Glutathione peroxidase and related enzymes in the retina, plus the precursor amino acids (N-acetylcysteine, L-glycine, and glutamine and selenium) are protective against damage to human retinal pigment epithelium cells. Glutathione peroxidase prevents free radical-induced apoptosis (cell suicide) and helps prevent or treat ARMD.



CAROTENOIDS
DEFINITION
More than 500 distinct compounds are today identified as naturally occurring carotenoids. They include cyclic hydrocarbon-carotenoids (carotenes), acyclic hydrocarbon carotenoids (lycopene), and oxygenated hydrocarbon carotenoids (xanthophylls like lutein and zeaxanthin).

Handelman and associates noted carotenoids concentration in the macula to be 5-fold higher compared to peripheral retina and 500 times more than the concentration in other tissues. Lutein is the major carotenoid in the peripheral retina, whereas zeaxanthin becomes more and more dominant as the foveal centre is approached. The proportion of lutein to zeaxanthin in macula is 1:2 and the proportion is reversed in the peripheral retina. The distribution of xanthophyll carotenoids suggests a possible role of lutein in protecting the rods and for zeaxanthin in protecting the cones that are concentrated in the central retina. The human lens carotenoids content is 10-20 ng/gm of wet tissue, and the ratio is 1.6:2.2 for Lutein and zeaxanthin.

Another most important dietary antioxidant of ocular significance is lycopene, which is however, conspicuous by its absence in macula. Due to its presence in high concentration in circulating blood in the eye, lycopene plays a prominent role in prevention of macular degeneration mainly by its very potent singlet oxygen quenching capacity.





FOCUS ON CAROTENOIDS IN ARMD
ARMD - INTRODUCTION
In developed countries, ARMD is the leading cause of blindness amongst the elderly (more than 60 years) with a prevalence ranging between 2 to 7% for severe (wet) form and a range of 12 to 30% for the dry form. The disease has caused irreversible visual impairment in an estimated 1.7 million Americans over the age of 65 years. The number of cases of ARMD has been predicted to increase from 2.7 million in 1970 to 7.5 million by the year 2030.

In India, the incidence of ARMD affects approximately 4-5 per cent of the population over the age of 50 years and may be affecting 19-20 per cent of people above 70 years of age. Early disease is characterized by yellowish-colored subretinal drusen. Late disease, which may be ‘dry’ or ‘wet’, may lead to significant loss of central vision. Wet form occurs only in 10 percent of population.



ARMD - PATHOPHYSIOLOGY
The light must pass the macular pigment, which contains abundance of zeaxanthin and lutein before striking the photoreceptors. If any damage to the rods and cones is to be prevented the short wave length of light rays (<500 nm range) must be filtered. This is accomplished as follows:

• 5-286 nm wavelength (ultraviolet C rays): filtered by the earth’s ozone layer.
• 286-320 nm wavelength (ultraviolet B rays): filtered by cornea.
• 320-400 nm wavelength (ultraviolet C rays): filtered by lens.
• 400-500 nm wavelength (visible blue light): filtered by lutein / zeaxanthin in macula.

The light entering the retina is between the wavelengths of 400 to 700 nm. The eye would be in perfect focus for daylight only at 560 nm, and even at night 500 nm wavelength of light is optimal for functioning of rods. Hence, filtering out 400-500 nm wavelength of light prevents damage to macula without affecting vision.
Thus macular pigments represent a significant filtering element and hence protect against the light–initiated cumulative oxidative damage. The macular pigment also removes much of the blurry, short wave blue and blue-green light that results from the eye’s chromatic aberration. Apart from this the earth’s atmosphere through which we view objects almost always contain small-suspended particles, which scatters short wave length light more than other wavelengths and results in a bluish veiling luminance.
The eye and skin are the only structures which have dual exposure to oxygen and light. In presence of blue light (400-500 nm wavelength) the oxygen will be split into singlet oxygen which is one of the most deadly reactive oxygen species as far as the eye is concerned. The blue light has potential to split molecular oxygen due to the high energy contained in it.

The singlet oxygen and other free radicals formed inside the eye initiate lipid peroxidation of photoreceptors. The polyunsaturated fatty acids in the outer membrane of rods and cones are attacked by free radicals and singlet oxygen species to result in damage of these photoreceptors. As a consequence, there is accumulation of lipofuscin by retinal pigment epithelium which then contributes in druse formation.



ARMD - MEDICAL MANAGEMENT
The damage to macula and formation of drusen can be prevented by filtering out the damaging blue light of the visible spectrum. This is possible by the macula, if its content of lutein and zeaxanthin are adequate. The additional available of lycopene in adequate amounts is of paramount importance in tackling the singlet oxygen single this carotenoids is the best antioxidant known for quenching this reactive oxygen species. In addition, glutathione peroxidase and SOD too have been shown to have preventive benefit in ARMD.



FOCUS OF CAROTENOIDS IN CATARACT
CATARACT - INTRODUCTION
Cataract is a multifactorial disease. Oxidative stress together with weakened antioxidant defense mechanism is attributed to the changes observed in human diabetic cataract. Oxidative damage to the lens has been recognized as a primary event in the pathogenesis of many forms of cataract. Consistent with this view, epidemiological reports have identified factors related to oxidative process that both increase (eg smoking and light exposure) and decrease (eg antioxidant intake) cataract risk.

Epidemiological studies provide evidence that nutritional antioxidants slow down the progression of cataract.



CATARACT - PATHOPHYSIOLOGY
Oxidative stress is high in the eye due to ultraviolet rays which promote liberation of free radicals and singlet oxygen. The epidemiological evidence to support the possibility that lutein and zeaxanthin have an important role in reducing the risk of cataract is somewhat consistent, and justifies the belief in free radical & reactive oxygen species mediated damage to the lens.

Few of the recent studies have stressed the significance of vitamin C, E and selenium in the etiology of cataract. Role of vitamin E has been more specifically stressed by several workers. Low blood levels of vitamin E are associated with approximately twice the risk of both cortical and nuclear cataracts, compared to median or high levels. Smokers are 2.6 times likely to develop posterior subcapsular cataracts more than nonsmokers. Patients with senile cataracts were found to have significantly lower blood and intraocular levels of the mineral selenium than control.



CATARACT - MEDICAL MANAGEMENT
Lower prevalence of nuclear cataract in women or men was associated with intake of lutein and zeaxanthin in high doses. Furthermore, in prospective cohort studies it was noted that people who consumed diet rich in lutein and zeaxanthin, had 20-25 percent lower risk of cataract extraction and 70 percent lower risk of cataract extraction under the age of 65 years.

Experimental study in human lens epithelial cells (HLEC) in culture was evaluated and it was concluded that addition of lycopene had a protective effect to prevent vacuolization of epithelial cells. It was observed that there was as positive effect of retardation of lens opacities due to lutein and zeaxanthin in the aging lenses.

In an 8 year prospective cohort study, Hankinson et al reported that an elevated intake of spinach, which is high in lutein and zeaxanthin (but low in beta carotene content) was most consistently associated with a lower risk of cataract extraction, whereas high beta carotene and vitamin E intakes alone had no beneficial effects against cataract prevention.

This study corroborated data from Jaques et al 1988 who demonstrated that persons with slightly elevated levels of plasma total carotenoids had a 25% lower risk for any type of cataract.



ANTIOXIDANTS IN RETINITS PIGMENTOSA
There is possibility that lutein may slow degeneration of vision in retinitis pigmentosa, a heterogeneous group of slow retinal degenerations. However, only preliminary data in a very small number of patients has been published in which lutein slowed vision loss associated with retinitis pigmentosa in one.






ANTIOXIDANTS IN DIABETIC RETINOPATHY
Several studies are in progress as regards role of antioxidants in diabetic retinopathy and glaucoma but as yet none is conclusive.



CONCLUSION
The overwhelming body of evidence points to significant beneficial effects of nutritional supplementation for most degenerative eye conditions. Important to remember is that most of the above studies used blood levels and food intakes associated with a normal diet. Taking supplements, specifically containing zeaxanthin, lutein and lycopene in adequate doses, which are theorized to provide protection to macula and lens with adequate doses, may have a much more protective effect than dietary levels alone. With so little risk, and the other potential health benefits from taking nutritional supplements, it would certainly seem prudent to try them, especially for macular degeneration where there are no real options.

Once the damage is done it cannot be reversed (except to a small degree), so prevention and early intervention is essential, especially if we have a family history of the disease. Of course, it's important to slow further progression at any stage of development. Prevention of lens and macula from the ultraviolet rays and hazard of smoking, however, needs to be over stressed.

What are vascular diseases and Vascular Surgery

“A surgeon's skills are measured by the way he handles the blood vessels”

These prophetic words of the great American surgeon William Halstead ushered in the era of one of the most skilful surgical specialties – Peripheral Vascular Surgery. This field has rapidly evolved over the last hundred years, with major advances occurring during the II World war and the Korean war. Endovascular interventions in the form of angioplasty and stenting have added an exciting new dimension for treatment of vascular diseases in the last two decades.

Vascular bypass operations in the leg preceded “heart bypass” operations by many years!

Vascular and Endovascular Surgery is a highly specialized field that deals with all the blood vessels in the body except those in the heart and the brain. Arteries that carry oxygenated blood from the heart to various organs and veins that return deoxygenated blood back to the heart, are the two main forms of blood vessels whose diseases are addressed by vascular surgeon. They are the life-lines of various body parts.The expression of vascular problems in different parts of the body is quite variable and this makes the specialty a complex, challenging field. A vascular surgeon is truly a “vascular specialist” since his expertise encompasses not only surgery, but also newer minimally invasive endovascular procedures (angioplasty, stenting) and vascular medicines. Hence vascular surgery remains one of the few “holistic” medical fields today which delivers complete, seamless care to patients with vascular disease.

How much is the problem?

What would be the magnitude of peripheral arterial disease of the legs in India? Since there are no specific data, we could extrapolate the available data to Indian population and the numbers thus obtained are quite staggering:

• Among 42 million diabetics – about 1000 per million will develop Critical Limb Ischemia, which usually means if some vascular procedure is not done they will lose the leg, which also makes them high risk for heart attack or stroke. If untreated this amounts to 42,000 amputations per year!
• Among rest of the population – about 500 per million (about 4,85,000) will develop critical limb ischemia needing a vascular correction or amputation!!
• In rest of the population about 38,00,000 (about 380 per 1,00,000 population) will develop peripheral vascular disease – these are the patients whose future vascular events can brought down significantly if proper medical care is given.

Venous diseases are far more common and include varicose veins, venous ulcers and deep vein thrombosis. All these problems affect a person’s quality of life and deep vein thrombosis is potentially life-threatening.

Causative factors
1. Smoking
2. Diabetes mellitus
3. High cholesterol
4. Lack of exercise
5. Obesity
6. Thrombophilia: tendency for blood to clot easily.
7. Heredity
8. Aging

Symptoms of vascular disease

Majority of vascular patients have one or more of the following three symptoms:

1. Painful extremity
2. Swollen extremity
3. Ulcerated extremity
Other problems include arterial aneurysms (dilated arteries) that have a potential for rupture, renovascular hypertension that is correctible, mesenteric ischemia that reduces blood supply to the intestines and has a higher fatality that heart attack, carotid artery stenosis that affects blood supply to the brain and results in paralytic attack which is preventable!
There has been an exponential increase of vascular problems in India due to unabated smoking and rapid increase in diabetic population (42 million or 4.2 crores), crossing all economic barriers. Peripheral vascular disease affects mostly the legs, which initially causes pain in the calf muscles while walking. The walking distance progressively reduces and if ignored will result in severe pain in the toes even at rest and eventually will result in gangrene of the toes and the foot, which might necessitate amputation. This “leg attack” is more dangerous than heart attack as it can endanger the limb and life of the patient. But this can be easily treated in the initial stages with appropriate medicines and simple life style modification programs. Unfortunately, these patients rarely reach a qualified vascular surgeon at this stage. One of the main reasons being lack of awareness among the public and also among many of the doctors about the vascular diseases and the role of vascular surgeon. There are only about 50 vascular surgeons in India, which results in these patients seen by other specialists, resulting in delayed referral to a vascular surgeon. In fact majority of these patients are not seen by vascular surgeon at all resulting in unnecessary limb and life loss. Even when a patient presents relatively late to a vascular surgeon, most of the limbs can be salvaged with a high success and low complication rate by vascular bypass or minimally invasive endovascular procedures like angioplasty and stenting if needed.

Blocked arteries in the leg mirrors rest of the body. Early diagnosis by good clinical examination and simple tests in patients with risks (smokers, diabetics, those over 50 years) will detect the disease even before they become symptomatic. It is well established now decreased blood flow in the legs is the biggest indicator of future hear attacks, strokes and amputation of legs or in other words the blocked arteries in the legs indicate a wide spread vascular disease in the body. When a patient has blocked arteries in the heart (cause of heart attack) it indicates that there is 30% chance that he/she has vascular disease else where, but a blocked artery in the leg indicates 60 to70% chance of diffuse vascular disease. Hence it is recommended in these risks groups should be examined peripheral arterial disease in the legs and if they do, they should be started on good medical treatment and life style modification program, which would markedly decrease the chance of future heart attacks, stroke or amputations.


Since poorly diagnosed and untreated vascular disease can lead to major limb and life threatening problems, it is of paramount importance that public and the medical profession is aware of early symptoms and the diagnostic methods. Early diagnoses and proper therapy will not only control the disease, but will markedly decrease the future complications and results in improved quality of life.

Vascular surgeon plays a pivotal role in diagnosing and treating these diseases, as our medical education imparts very little knowledge about vascular diseases to other specialties. Hence it is mandatory that any body suspected of these problems be evaluated by a vascular surgeon.

Patients with diabetic foot problems, which are the number one cause of admission in diabetic patients in India, usually are treated by vascular surgeon. These are of epidemic proportions, causing life and limb loss, though they can be easily prevented with proper foot care. Vascular surgeon plays a pivotal role in caring for the diabetic foot problems whether they are related to vasculopathy or neuropathy.

Vascular surgeon’s field is wide since it covers major portion of the human body. The next most important disease treated is stroke prevention surgery. Majority of strokes occur because of the narrowing of a blood vessel, called carotid artery, in the neck which carries blood to the brain. If diagnosed in time and treated with a highly successful surgical procedure called “Carotid Endarterectomy”, the chances of stroke is markedly reduced. In few, highly selected patients vascular surgeon may opt to perform “angioplasty and stenting”, but these cannot be applied to all patients at present, but might change in future. Again, it important to have these patients evaluated by a vascular surgeon, for proper diagnosis and treatment.

Vascular surgeons also deals with blood vessels in the upper limbs, those inside the abdomen supplying vital organs like the kidneys, liver intestines etc. Diseases of the veins, simplest of which is the varicose veins, also come under the purview of vascular surgeon.


Dr. P C Gupta, MS, FICA
Senior Consultant & Chief,
Vascular & Endovascular Surgery

Watch this space for disease specific articles.