IELTS Academic Reading Practice Test 328

Before 1948, medical care in Britain was provided by a patchwork of institutions with no overall plan. Voluntary hospitals, many of them founded by charitable donation, treated the sick poor but depended on subscriptions and fundraising events. Municipal hospitals, run by local authorities, had often begun as workhouse infirmaries and varied enormously in quality. General practitioners charged fees, and although some workers belonged to friendly societies and approved societies that helped to pay for treatment, the families of the poorest labourers frequently went without. The National Insurance Act of 1911 had given insured workers access to a doctor, but it covered neither their wives and children nor hospital treatment.

The Second World War changed the picture. Fearing heavy civilian casualties from bombing, the government took control of hospitals and created the Emergency Hospital Service, directing staff and beds from a single centre for the first time. The experience convinced many doctors and civil servants that organisation on a national scale was possible. It also gave political momentum to the report published in 1942 by the economist William Beveridge, which identified disease as one of five 'giants' blocking social progress and called for a comprehensive health service available to all.

When the Labour government took office in 1945, the new Minister of Health, Aneurin Bevan, was given the task of turning these ideas into a service. Bevan was a Welsh former miner and a formidable political fighter. His plan, embodied in the National Health Service Act of 1946, was radical: hospitals would be taken out of local authority and charitable hands and placed under regional boards responsible to the minister, and the service would be financed mainly from taxation rather than from insurance contributions or fees at the point of use.

The doctors were not persuaded. The British Medical Association, which spoke for many general practitioners, feared that a salaried service would turn them into civil servants and damage their independence, and a ballot of its members showed that most doctors opposed the Act. Negotiations continued for nearly two years. Bevan made two crucial concessions. General practitioners would not be salaried employees of the state but independent contractors paid according to the number of patients on their lists, and hospital consultants were allowed to keep their private patients and were offered merit awards on top of their salaries. Almost at the last moment, enough doctors agreed to join.

The service came into being on 5 July 1948. Bevan marked the occasion at Park Hospital in Davyhulme, near Manchester, a hospital originally built for the local Poor Law authority, where he met one of the first patients, a thirteen-year-old girl. The occasion was modest; the change was one of administration and principle, and many patients noticed only that they were no longer asked to pay.

Demand exceeded every expectation. People who had lived for years with poor eyesight or aching teeth queued for spectacles and dentures, and within a year the cost of the service far outstripped the government's estimates. The original estimates proved far too low, and by 1951 the Treasury was insisting on economies. Charges were introduced for spectacles and dental treatment, and Bevan resigned from the cabinet in protest. A prescription charge followed in 1952, under the Conservative government that had taken office in October 1951.

The rising cost prompted a committee of inquiry chaired by Claude Guillebaud, which reported in 1956. To the surprise of many, it found no evidence of widespread waste and concluded that, as a share of national income, its cost had actually fallen. Its report helped to quieten criticism and, more importantly, confirmed the principle that care should remain free at the point of use and financed from general taxation rather than from charges.

Staffing was a persistent difficulty. The new service inherited a nursing workforce depleted by the war, and hospitals recruited nurses from Ireland and the Caribbean, and later from the Philippines and other countries, creating a dependence on overseas training that has continued, with interruptions, ever since. Doctors were also in short supply, and the service relied heavily on graduates from the Commonwealth, particularly in the less popular specialties and in hospitals outside the big cities.

Yet the founding principles proved remarkably durable. The service was comprehensive, intended to cover every kind of care from cradle to grave; it was universal, offered to the whole population on the same terms; and it was free at the point of use, so that treatment depended on need rather than on ability to pay. Subsequent governments reorganised its structure repeatedly, and the balance between central control and local autonomy has never been settled, but no serious political party has proposed returning to a system of payment for care.

Seventy-five years after its launch, the National Health Service remains the largest employer in Britain and one of the largest in the world, and it is often named in opinion surveys as the institution of which the British are most proud. Its history also illustrates a lesson about reform. The 1946 Act succeeded not because its author got every detail right, but because he was willing to compromise about the means while holding firmly to the end.

When a blood vessel is cut, the body faces a problem that must be solved within minutes. Blood has to stay liquid while it is inside intact vessels, yet the moment a vessel is torn, it must be sealed before too much is lost. The sealing is achieved by a set of reactions known collectively as haemostasis, which normally proceed in three overlapping stages: the vessel narrows, cells called platelets gather to form a loose plug, and a mesh of protein fibres is laid down to strengthen and hold the plug in place. The system must also be fast and local, since a clot in the wrong place is as dangerous as no clot at all.

Once the vessel has narrowed, the platelets go to work. Platelets are small fragments of cells, produced in the bone marrow, that circulate in the blood in an inactive state. When the lining of a vessel is damaged, the tissue beneath it is exposed, including a protein called collagen and a substance known as von Willebrand factor. Platelets carry receptors that bind to these molecules, so they stick to the damaged patch and flatten out against it. Sticking is only the beginning: the attached platelets release chemical messengers, among them a substance called thromboxane, which attract more platelets to the site and make them clump together. The result, known as the platelet plug, is fragile, and it buys time for the next stage.

The next stage is chemical. The clotting factors are proteins made in the liver and released into the blood in an inactive state. When they are activated, they set off a sequence in which each factor switches on the next, and the sequence ends with the production of thrombin. Thrombin then converts a soluble protein called fibrinogen into fibrin, whose molecules join together into long threads that form a mesh across the wound, trapping red blood cells and producing what is recognised as a clot. Another factor cross-links the threads, making the mesh stronger and more resistant to being pulled apart.

For much of the twentieth century, this sequence was described as a cascade, and it was divided into two routes, one triggered by tissue damage and the other by contact with artificial surfaces. That account is still taught, but it is now regarded as an oversimplification based largely on what happens in a test tube. A newer description, known as the cell-based model, places the reactions on the surfaces of cells. Initiation occurs on cells that expose tissue factor; amplification takes place on the surface of activated platelets; and propagation, when most of the thrombin is generated, occurs on the platelets that have gathered at the wound.

Because clotting is dangerous if it spreads, several brakes are built into the system. Healthy endothelium, the layer of cells lining blood vessels, actively prevents clotting by releasing substances that inhibit platelets and the clotting factors. Antithrombin, a protein in the blood, neutralises several activated factors; proteins C and S switch off two of the most important ones; and a further inhibitor limits the tissue-factor route. The flow of blood also carries activated factors away from the site, so that the reactions can proceed only where they are anchored to a surface. This localisation is essential: without it, a small injury could set off clotting throughout the circulation.

Once the vessel has healed, the clot must be dismantled, and this is the work of the fibrinolytic system. A protein called plasminogen is converted into plasmin, an enzyme that cuts the fibrin mesh into small fragments. These fragments, one of which is measured in hospitals as D-dimer, can be detected in the blood. The test is useful because a negative result makes a clot unlikely, but because the fragments appear whenever any clot is broken down, a positive result is not specific: it does not show where the clot is. Researchers are trying to develop tests that reveal more.

Either direction of failure causes disease. Too little clotting produces bleeding disorders: haemophilia A and B arise from shortages of particular factors, and von Willebrand disease, the most common inherited bleeding disorder, affects the protein that platelets need in order to stick. Too much clotting produces thrombosis. In an artery, a clot may block the flow of blood to the heart muscle or the brain, causing a heart attack or a stroke; in a deep vein, particularly in the leg, it may form slowly and then break away and travel to the lungs, producing a pulmonary embolism. Immobility, surgery, cancer, pregnancy and inherited conditions such as factor V Leiden all raise the risk.

Treatment works at different points in the process. Heparin makes antithrombin far more effective; warfarin interferes with the recycling of vitamin K, which several clotting factors need; and newer drugs inhibit thrombin, or the factor that produces it, directly. Aspirin, given to many people at risk of heart disease, blocks an enzyme in platelets and makes them less willing to clump. Much remains unexplained. Researchers cannot yet say why clots form in vessels that show no sign of injury, and it is increasingly clear that inflammation and the immune system are involved. The part played by these processes in severe infections is the subject of intensive study.

Every doctor will, at some point, harm a patient by mistake. The mistake may be a missed diagnosis, a drug given in the wrong dose, or a procedure performed on the wrong side. When it happens, the doctor faces a choice that is far harder in practice than it looks from outside: whether to tell the patient, and if so, how much. The professional bodies that regulate medicine now say plainly that patients should be told. My own view is that they are right, but that the argument for telling them is more complicated than the simple claim that honesty is always best, and that the obligation needs to be defined with more care than campaigners usually allow.

The strongest reason for disclosure is not the relief of the doctor's conscience but respect for the patient. Patients are entitled to information that affects their health, and a mistake is such information. If a drug has been given in error, the patient may need tests; if a diagnosis has been delayed, the treatment may need to be changed. Withholding the fact of an error therefore deprives the patient of knowledge that is needed for decisions about their own care, and it does so at the very moment when their interests are most exposed. Trust, too, is at stake. Patients who discover later that something was concealed seldom regard the concealment as kindness.

How common such mistakes are is disputed. The report that put the subject on the political agenda, To Err Is Human, published by the Institute of Medicine in the United States in 1999, estimated that errors in American hospitals contributed to between 44,000 and 98,000 deaths each year. Some later analyses put the figure higher, but all such estimates depend on how deaths are attributed, and hospital records are an unreliable guide. What is not disputed is that most harmful errors are not the work of reckless individuals. They arise from the way work is organised: from unclear labels, tired staff, poor communication between teams and equipment that allows a mistake to be made.

Professionals have responded by changing their rules. In England, a statutory duty of candour now requires NHS organisations to tell patients when they have suffered harm, and the inquiry into failings at Mid Staffordshire, chaired by Robert Francis and published in 2013, made openness central to its recommendations. Regulators say that doctors must be honest with patients when things go wrong, must apologise and must explain what will be done to put matters right. Apology, they stress, is not an admission of legal liability; it is an acknowledgement that something has gone wrong.

Yet the case against full disclosure cannot simply be dismissed. Doctors fear, reasonably enough, that an admission will be used against them, and that fear has real effects: it encourages defensive behaviour, such as ordering unnecessary tests, and it can make clinicians reluctant to discuss a mistake with anyone at all, including colleagues who might prevent a repetition. There is also a genuine difficulty of definition. A patient who suffers a poor outcome has not necessarily been the victim of an error, and a doctor may sincerely believe that the care given was appropriate. Telling a patient that a mistake has occurred when the doctor is not sure that one has is not obviously honest either.

Evidence from hospitals that have adopted a policy of full disclosure is nevertheless encouraging. Several American health systems began in the early 2000s to investigate harmful events promptly, to explain them to patients, to offer compensation where it was due and to apologise. Their reported experience was that the number of claims fell and that legal costs were lower, not higher, than before. These results come from a small number of institutions with strong leadership and generous resources, and researchers have warned that they cannot be assumed to transfer everywhere. Many American states, meanwhile, have passed laws making an expression of sympathy inadmissible as evidence, though the protection these offer varies considerably.

The burden on the clinician is easily overlooked. The American physician Albert Wu coined the term 'second victim' in 2000 to describe health workers who are distressed by their own errors, and subsequent research has documented sleeplessness, shame and, in some cases, a decision to leave medicine altogether. A culture that responds to error only by finding someone to blame tends to produce silence, and silence is precisely what patients do not want. Support for the clinician and honesty towards the patient are therefore not competing goals; each depends on the other.

What, then, should the rule be? I would argue for a strong presumption of disclosure, applied promptly and in plain language, with an explanation of what happened, an apology, and a clear account of what will be done to prevent a recurrence. Patients should be told what is known and what is not, including the possibility that the harm was not caused by an error. Where an error has occurred, responsibility should ordinarily rest with the organisation, which designed the system, as well as with the individual. The duty to be open should not, however, extend to exposing a named clinician to public blame; that serves nobody's health. Honesty with patients and fairness to staff are both parts of the same reform.