IELTS Academic Reading Practice Test 369

During the first millennium BCE, the city of Varanasi on the Ganges was one of the great centres of learning in India, and it was there, according to tradition, that a physician named Sushruta taught and practised his craft. His name is attached to the Sushruta Samhita, a Sanskrit compendium of medicine that devotes more attention to surgery than any other text to survive from the ancient world.

The date of its composition is disputed. Some of its material may go back to around 600 BCE, but the version that has come down to us was evidently revised and enlarged over many centuries, and scholars place its final form somewhere in the early centuries of the first millennium CE.

Surgery, known in the text as shalya, is treated as one of eight branches of medicine, but it is plainly the author's chief concern. The Samhita sorts operations into eight kinds, among them cutting, puncturing, probing, extracting and stitching, and it lists more than a hundred instruments, many of them described in detail. Just as striking is the attention paid to training. Before a student approached a patient he was expected to rehearse on other materials: to practise incisions on gourds and similar plants, to learn puncturing on the stretched skin of an animal, and to master the draining of fluid from a bag filled with liquid.

Knowledge of the body's interior is a further theme. Direct dissection was evidently difficult or unacceptable, so the text describes a different method. A body was to be wrapped in grass or cloth, placed in a running stream and left until the tissues had softened; the layers could then be separated and examined one by one. Whatever the practical difficulties of such a procedure, the description suggests that its author regarded anatomy as the foundation of good surgery, and that a serious effort was made to learn it.

The operation for which the text is best known is the reconstruction of the nose. A person whose nose had been cut off — a punishment, and a common injury in warfare — could have it rebuilt with a flap of skin taken from the cheek, left attached at one edge so that it kept its blood supply, turned down over the missing part and stitched in place. The Samhita also describes the repair of torn earlobes by a similar method. These were not curiosities. They addressed injuries that were frequent, and they show an understanding of how living tissue with its own supply of blood can be moved and made to heal.

Much of the text is concerned with the ordinary business of wounds. Wounds are classified, the fluid that comes from them is described, and instructions are given for cleaning them and for dressing them with honey, clarified butter and other substances. Cauterisation, using a hot iron or a heated liquid, was employed to stop bleeding and to destroy abnormal tissue, and the text discusses it at length. Rules are also set out for the patient's diet and rest during recovery, subjects to which ancient Indian medicine gave considerable importance.

Among the operations described is one for a clouded lens in the eye. A fine needle was passed into the eye and used to push the lens out of the line of sight, a technique later known in Europe as couching. It relieved the blindness, though it left the patient without a lens and unable to focus. Operations for hernia and for stones in the bladder, and the setting of broken bones, are among the many other procedures the Samhita discusses.

The text did not remain in India. During the Abbasid caliphate, when scholars in Baghdad translated a great range of Greek, Persian and Indian learning into Arabic, a version of the Samhita was among the works rendered into that language, and from Arabic it entered the medical tradition of the Islamic world. The routes by which such knowledge travelled westwards are complex and are still debated. What is not in doubt is that the Arabic compendia studied in medieval European universities drew on Indian as well as Greek sources.

European awareness of Indian surgery was renewed at the end of the eighteenth century. In 1794, a London periodical published a letter from two British surgeons in Bombay describing how a man whose nose had been cut off during a military campaign had been given a new one by an Indian practitioner, using skin from the forehead. The account was read widely, and the operation it described, sometimes called the Indian method, influenced surgeons in Britain and elsewhere. It is a striking example of practical knowledge moving between medical cultures.

Modern admiration for the Samhita can easily tip into exaggeration. It is sometimes claimed that its author performed operations that belong to modern medicine, and that Indian surgeons understood ideas that were not established elsewhere for another two thousand years. Such claims should be treated with caution. The text is a product of its time, containing much that is rational and observant and much that is magical, religious and merely traditional, the two woven together so tightly that separating them is difficult. Its importance lies elsewhere: in the fact that surgery was studied, taught and written about systematically, and in the influence of its methods on practitioners far beyond the Ganges.

A heart attack usually happens when a clot blocks one of the coronary arteries, the vessels that supply the heart muscle itself. The event appears sudden, but in most cases it is the final act of a process that has been developing silently for decades. That process is atherosclerosis, the gradual build-up of fatty material within the walls of arteries. Almost everyone living in an industrialised country has some degree of it by middle age, and it is the underlying cause of most heart attacks and of many strokes as well.

An artery is not a simple pipe. Its wall has three coats: an inner lining of endothelial cells, a middle layer of smooth muscle, and an outer sheath of connective tissue. The endothelial lining, only one cell thick, is far from passive. It senses the speed and pressure of the blood, releases nitric oxide, which relaxes the muscle beneath it, and controls what passes between the bloodstream and the wall. In a healthy vessel the inner layer is smooth and the passage of cholesterol-bearing particles into the wall is limited.

The disease begins with cholesterol. Cholesterol does not dissolve in blood, so it travels inside particles coated with proteins, the most abundant of which are low-density lipoproteins, or LDL. When LDL particles linger in the blood at high concentration, they can cross the endothelium and become trapped in the tissue beneath it. There they are exposed to oxygen and other chemicals and are chemically modified — oxidised, in the language of the laboratory. This modification is the crucial step, because the body treats oxidised LDL as a foreign intruder rather than as a normal constituent of blood.

The response is inflammation. Cells of the endothelial lining display adhesion molecules that catch white blood cells called monocytes, which roll along the surface and then squeeze between the endothelial cells into the wall. Once inside, a monocyte matures into a macrophage, a cell whose normal task is to engulf bacteria and debris. The macrophage swallows the oxidised LDL, but it cannot break the cholesterol down. It becomes engorged with fat droplets, takes on a foamy appearance under the microscope, and is then known as a foam cell. Collections of these cells form the earliest visible lesion, a fatty streak, which can be found in the arteries of children.

As the lesion grows, the artery remodels. Smooth muscle cells migrate from the middle layer into the inner layer and begin to produce collagen and other fibrous proteins, which form a cap over the growing core of fat, foam cells and dead cell remains. The vessel widens outwards to accommodate the plaque, so the channel through which blood flows may stay almost normal for years. This explains why a person can have advanced disease without symptoms, and why an examination carried out before any complaint appears may reveal nothing. Calcium is also deposited in older plaques, making them stiff.

The dangerous moment comes when the cap thins and ruptures. Macrophages release enzymes that digest collagen, and the cap can weaken until it tears. Blood then meets the contents of the plaque, material that never normally leaves the artery wall, and a clot forms within minutes. The clotting protein fibrin and cell fragments called platelets are central to this. If the clot blocks the artery, the tissue it supplies dies: heart muscle in a heart attack, brain tissue in a stroke. The plaques most likely to rupture are not necessarily the largest, but those with thin caps and a rich population of inflammatory cells.

Why some people develop these plaques faster than others is partly understood. Smoking, high blood pressure, diabetes and a high concentration of LDL are established causes, and all of them can be modified. Age and family history cannot. Researchers have also examined markers of inflammation such as C-reactive protein, which can be measured in a blood sample and which tends to be raised in people at higher risk, although whether it adds much to the standard risk factors is still debated. None of these factors, on its own, explains why two people of the same age can be affected so differently.

Treatment has two aims: to lower the amount of cholesterol in the blood, and to deal with narrowed arteries. Statins block an enzyme that the liver uses to make cholesterol, so the liver takes up more LDL from the blood. Other drugs, including injections given every few weeks, work by helping the liver clear LDL more efficiently. Where a coronary artery is already narrowed, a stent can hold it open, or coronary bypass surgery can carry blood around it using a piece of vein taken from the leg. These procedures relieve the blockage but do not remove the disease from the rest of the arteries.

Important questions remain. No one can yet predict which plaque will rupture, and millions of people carry plaques that will never cause trouble. Attempts to raise HDL, the particle that carries cholesterol away from tissues, have repeatedly failed to reduce heart attacks in large trials, which suggests that the picture is more complex than a simple balance between good and bad cholesterol. Attention has turned to inflammation itself: in a large trial reported in 2017, an anti-inflammatory drug reduced heart attacks, though it also made serious infection more likely. Other particles, such as lipoprotein(a), are being studied as targets.

It is a familiar scene in teaching hospitals at the end of a long shift: a young doctor, twenty hours into the working day, struggling to remember which of thirty patients has had which drug. For forty years, hospitals in Europe and North America have been reducing the hours that doctors in training are expected to work, and for forty years the arguments about those reductions have generated more heat than light. My own view is that limits on hours are necessary and long overdue, but that the number of hours is a poor guide to the safety of care.

The modern debate began with a tragedy. In 1984 a student named Libby Zion died in a New York hospital while junior doctors working long shifts were caring for her. Her father campaigned for an explanation, and the case led to an inquiry which reported in 1987 and recommended that doctors in training should work no more than eighty hours a week and no more than twenty-four hours at a stretch. The recommendations became law in New York State in 1989, and the campaign had become a national cause long before anyone had produced firm evidence that shorter hours would save lives. American training programmes adopted an eighty-hour limit in 2003 and tightened it in 2011.

Europe moved in a similar direction. Under the European Working Time Directive, doctors in training across the European Union became subject to an average limit of forty-eight hours a week, a rule that hospitals in the United Kingdom were given until 2009 to meet in full. Some senior surgeons complained that the change would destroy the craft of surgery, since a trainee who is not in the hospital cannot be in the operating theatre. The direction of travel was right, even if the rules were sometimes crude and applied without much thought about how the remaining hours were used.

The case for shorter shifts rests on a simple observation. A tired brain learns badly, forgets instructions and reacts slowly, and these effects are well documented in people who have been kept awake for long periods. It would be strange if a doctor who has been awake for twenty-four hours made the same decisions as one who has slept. Drivers who have been awake that long perform worse than those over the legal alcohol limit, and clinicians are unlikely to differ. The shifts of the past, when a doctor might be on duty for a hundred hours a week, are now widely regarded as dangerous for patients and doctors alike.

The evidence that shorter hours have produced safer care is, nevertheless, surprisingly thin. Analyses of large numbers of American hospitals have generally failed to find a clear fall in deaths among patients after the 2003 rules took effect. It is tempting to conclude that fatigue does not matter after all. That conclusion does not follow. What the studies suggest, rather, is that shortening shifts is not the same as reducing tiredness, and that something in the way the new rotas operate has offset the benefit.

The most likely culprit is the handover. Each change of shift requires one doctor to transfer the essential facts about each patient to another, and in a busy ward that conversation may be brief, interrupted or incomplete. Shortening shifts increases the number of handovers, so that a patient may be assessed by four or five doctors in a week, none of whom sees the whole picture. The work itself does not shrink; it is compressed into fewer hours, and a doctor covering the same number of patients in twelve hours rather than twenty-four is under greater pressure, not less. Continuity of care, which matters most in complicated long-term illness, is easily lost.

Training raises a further problem, particularly in surgery. A trainee who leaves the hospital after eight hours will miss many of the operations carried out overnight, and the number of procedures a surgeon performs before qualifying has fallen in several countries. Yet the loss may be smaller than it appears. A tired trainee who stands at the edge of an operating theatre at two in the morning may learn very little, and the time saved can be used deliberately: simulators, recorded operations and structured practice can replace some of what the old apprenticeship provided, provided that hospitals organise it. What is indefensible is to shorten hours and then leave training to chance.

The argument, however, has been framed in the wrong way. Hours are a crude measure of what a job does to the person doing it. A forty-eight-hour week on a ward that is short of nurses is more exhausting than a sixty-hour week with proper support, and a twelve-hour shift with no opportunity to eat or rest is not obviously humane. What matters is how many patients a doctor is responsible for, how much supervision is available, and whether a tired doctor can say so without being thought weak. Rota design, naps and clear rules about cover do more for safety than a headline figure.

Hours limits, then, are necessary but not sufficient. Few people would now argue that the shifts of the 1970s should return. But a cap on hours is only a starting point, and it can be actively harmful if it is introduced without extra staff, better handovers and a serious plan for training. The question worth asking is not how many hours a young doctor works, but what happens during them, and who is responsible when the shift ends.