17 Methods of Tertiary Prevention
In practice, tertiary prevention resembles treatment of established disease. The difference is in perspective. Whereas treatment is expressly about “fixing what is wrong,” tertiary prevention looks ahead to potential progression and complications of disease and aims to forestall them. Thus, although treatment and tertiary prevention often share methods, their motives and goals diverge.
Methods of tertiary prevention are designed to limit the physical and social consequences of disease or injury after it has occurred or become symptomatic. There are two basic categories of tertiary prevention. The first category, disability limitation, has the goal of halting the progress of the disease or limiting the damage caused by an injury. This category of tertiary prevention can be described as the “prevention of further impairment.” The second category, called rehabilitation, focuses on reducing the social disability produced by a given level of impairment. It aims to strengthen the patient’s remaining functions and to help the patient learn to function in alternative ways. Disability limitation and rehabilitation usually should be initiated at the same time (i.e., when the disease is detected or the injury occurs), but the emphasis on one or the other depends on factors such as the type and stage of disease, the type of injury, and available methods of treatment. This chapter discusses opportunities for tertiary prevention and provides specific clinical examples of disability limitation and rehabilitation.
I Disease, Illness, Disability, and Disease Perceptions
Although sometimes used interchangeably, there are important distinctions among disease, disability, and illness. Typically, disease is defined as the medical condition or diagnosis itself (e.g., diabetes, heart disease, chronic obstructive lung disease). Disability is the adverse impact of the disease on objective physical, psychological, and social functioning. For example, although stroke and paralytic polio are different diseases, both can result in the same disability: weakness of one leg and inability to walk. Illness is the adverse impact of a disease or disability on how the patient feels. One way to distinguish these terms is to specify that disease refers to the medical diagnosis, disability to the objective impact on the patient, and illness to the subjective impact.
Disability and illness obviously derive from the medical disease. However, illness is also powerfully influenced by patients’ perceptions of their disease, its duration and severity, and their expectations for a recovery; together, these beliefs are called illness perceptions. Disease and illness interact; a patient’s illness perceptions strongly predict recovery, loss of work days, adherence, and health care utilization.1,2 To be successful, tertiary prevention and rehabilitation must not only improve patients’ physical functioning, but also influence their illness perceptions. Although there is some evidence of effective psychological interventions on illness perceptions,3 a recent systematic review of interventions of illness perceptions in cardiovascular health found too much heterogeneity among studies to allow for general conclusions.4 Despite the mixed quality of the data, the practicing clinician should consider the patients’ illness perceptions, if only to understand which patients are at high risk of poor outcomes.
II Opportunities for Tertiary Prevention
The first sign of an illness provides an excellent opportunity to initiate methods of tertiary prevention. The sooner disability limitation and rehabilitation are begun, the greater the chance of preventing significant impairment. In the case of infectious diseases, such as tuberculosis and sexually transmitted diseases, early treatment of a disease in one person may prevent its transmission to others, making treatment of one person the primary prevention of that disease in others. Similarly, early treatment of alcoholism or drug addiction in one family member may prevent social and emotional problems, including codependency, from developing in other family members.
Symptomatic illness can identify individuals most in need of preventive efforts. In this sense, the symptoms function similar to screening, by defining individuals especially in need. When they feel well, people may not be convinced by health promotion and disease prevention messages. When they become ill, however, they may understand for the first time the value of changing their diet, behavior, or environment. For example, a person at risk for coronary artery disease who has experienced no symptoms will generally be less open to changes in diet and exercise than someone who has experienced chest pain. The onset of symptoms may provide a window of opportunity for health promotion aimed at preventing progression of the disease (“teachable moment”). Cardiovascular disease is used here to illustrate the approach to prevention after the disease has made its presence known. However, almost any hospitalization or major life event (e.g., pregnancy, birth of a grandchild) can be a teachable moment for patients, and the prognosis for most diseases improves with better diet, exercise, and adherence.
III Disability Limitation
Disability limitation includes therapy as well as attempts to halt or limit future progression of the disease, called symptomatic stage prevention. Most medical or surgical therapy of symptomatic disease is directed at preventing or minimizing impairment over the short-term and long-term. For example, both coronary angioplasty and coronary artery bypass are aimed at both improving function and extending life. These are attempts to undo the threat or damage from an existing disease, in this case, coronary artery disease (CAD). The strategies of symptomatic stage prevention include the following:
In this section, CAD, hyperlipidemia, hypertension, and diabetes mellitus are used to illustrate how methods of disability limitation can be applied to patients with chronic diseases. The emphasis is on symptomatic stage prevention.
A Cardiovascular Disease
Cardiovascular disease encompasses coronary artery disease, cerebrovascular accident (CVA, stroke), heart failure, and peripheral artery disease (PAD). If cardiovascular disease has already occurred, the clinician’s immediate goal is to prevent death and permanent damage. Beyond that, the clinician’s goal is to slow, stop, or even reverse the progression of the disease process.
1 Risk Factor Modification
When cardiovascular disease becomes symptomatic (e.g., with a heart attack), the acute disease needs to be addressed with interventions, such as thrombolysis, rhythm stabilization, and perhaps stents or surgical bypass. When a patient is stabilized, the risk factors to be addressed to slow or reverse disease progression are generally similar to those for primary prevention, but the urgency for action is increased. The following modifiable risk factors are important to address when cardiovascular disease has already occurred: hypertension, smoking, dyslipidemia, diabetes, diet, and exercise.
In practice, which risk factor to address first should be negotiated between clinician and patient. The most important risk factor to modify should be the one the patient is actually motivated and able to change. Any change there will improve risk, and successful behavior change in one area can provide motivation for further change later.
Cigarette Smoking
Smoking accelerates blood clotting, increases blood carbon monoxide levels, and causes a reduction in the delivery of oxygen. In addition, nicotine is vasoconstrictive (causes blood vessels to tighten). The age-related risk of myocardial infarction (MI) in smokers is approximately twice that in nonsmokers. For individuals who stop smoking, the excess risk declines fairly quickly and seems to be minimal after 1 year of nonsmoking. Smoking cessation is probably the most effective behavioral change a patient can make when cardiovascular disease is present. Smoking cessation also helps to slow related smoking-induced problems most likely to complicate the cardiovascular disease, such as chronic obstructive pulmonary disease (COPD).
Diabetes Mellitus
Type 2 diabetes mellitus increases the risk of repeat MI or restenosis (reblockage) of coronary arteries. Keeping the level of glycosylated hemoglobin (a measure of blood sugar control; e.g., Hb A1c) at less than 7% significantly reduces the effect of diabetes on the heart, kidneys, and eyes. Many authorities advocate treating diabetes as a coronary heart disease equivalent, based on a Finnish study that showed that patients with diabetes (who had not had a heart attack) had a similar risk of MI as patients with established CAD.5 Even though this study’s methods and results are in dispute, the management of diabetes mellitus has shifted. The approach no longer focuses only on sugar control, but instead aims for multifactorial strategy to identify and target patients’ broader cardiovascular risk factors.6 This approach includes treating lipids and controlling blood pressure (BP).
Hypertension
Any hypertension increases the risk of cardiovascular disease, and severe hypertension (systolic BP ≥195 mm Hg) approximately quadruples the risk of cardiovascular disease in middle-aged men.7,8 Effects of hypertension are direct (damage to blood vessels) and indirect (increasing demand on heart). Control of hypertension is crucial at this stage to prevent progression of cardiovascular disease.
Sedentary Lifestyle
It seems that at least 30 minutes of moderate exercise (e.g., fast walking) at least three times per week reduces the risk of cardiovascular disease. There is increasing evidence that sitting itself, independent of the amount of exercise, increases the risk of MI.9 The uncertainty occurs partly because it is difficult to design observational studies that completely avoid the potential bias of self-selection (e.g., people with incipient heart disease may have cues that tell them to avoid exercise). Nevertheless, there is increasing emphasis on the potential benefits of even modest physical activity, which has direct effects on lipids and also helps to keep weight down, which itself improves the blood lipid profile. Conversely, there is a growing appreciation for adverse health effects of “sedentariness.”9
Excess Weight
In people who are overweight, the risk for cardiovascular disease partly depends on how the body fat is distributed. Fat can be distributed in the hips and legs (peripheral adiposity, giving the body a pear shape) or predominantly in the abdominal cavity (central adiposity, giving the body an apple shape, more common in men than women.) Fat in the hips and legs does not seem to increase the risk of cardiovascular disease. In contrast, fat in the abdominal cavity seems to be more metabolically active, and the risk of cardiovascular disease is increased. This is not surprising, because fat mobilized from the omentum goes directly to the liver, which is the center of the body’s lipid metabolism. Centrally located body fat is implicated in the insulin resistance syndrome and is associated with increased sympathetic tone and hypertension.
Weight loss ameliorates some important cardiac risk factors, such as hypertension and insulin resistance. Some studies suggest that alternating dieting and nondieting, called weight cycling, is a risk factor in itself,10 but other studies question this conclusion.11 The most recent findings in this area suggest that weight gain and loss may result in lasting hormonal and cytokine alterations that facilitate regaining weight.12 Although weight cycling may have specific associated risks, whether any such risks are truly independent of obesity itself remains unclear.13–16 At present, expert opinion generally supports a benefit from weight loss, with greater benefit clearly attached to sustainable weight loss17 (http://www.nwcr.ws/). Achieving sustained weight loss remains a considerable challenge (see Chapter 19).
Dyslipidemia
The risk of progression of cardiovascular disease is increased in patients with dyslipidemia (abnormal levels of lipids and the particles that carry them), which can act synergistically with other risk factors (see later and also Chapter 5, especially Table 5-2, and Chapter 19). Disease progression can be slowed by improving blood lipid levels or by addressing other modifiable risk factors (e.g., hypertension, diabetes) that benefit from diet and exercise.
2 Therapy
The immediate care and long-term care of patients with symptomatic CAD depend on the extent to which the disease has progressed when the patient comes under medical care. Even in the presence of severe CAD, there may be little or no warning before MI occurs. After acute medical and surgical therapy (tertiary prevention) is provided, the provider should initiate efforts directed at symptomatic stage prevention (also tertiary prevention in this case).
3 Symptomatic Stage Prevention
Every patient with symptomatic cardiac disease needs evaluation for risk factors and a plan to reduce the risk of adverse cardiac events. If the patient already has had an MI or undergone revascularization (opening up blocked arteries) through percutaneous transluminal coronary angioplasty (cardiac catheterization) or coronary artery bypass surgery, the goals include preventing restenosis and slowing the progression of atherosclerosis elsewhere.
Behavior Modification
Patients should be questioned about smoking, exercise, and eating habits, all of which affect the risks of cardiovascular disease. Smokers should be encouraged to stop smoking (see Chapter 15 and Box 15-2), and all patients should receive nutrition counseling and information about the types and appropriate levels of exercise to pursue. Hospitalized patients with elevated blood lipids should be placed on a “heart healthy” diet (see Chapter 19) and encouraged to continue this type of diet when they return home. This change in diet requires considerable coaching, often provided by a specialized cardiac rehabilitation nurse, dietitian, or both.
B Dyslipidemia
Dyslipidemia, sometimes imprecisely called “hyperlipidemia,” is a general term used to describe an abnormal elevation in one or more of the lipids or lipid particles found in the blood. The complete lipid profile provides information on the following:
High-density lipoprotein (HDL) cholesterol
Low-density lipoprotein (LDL) cholesterol
Very-low-density lipoprotein (VLDL) cholesterol, which is associated with triglycerides (TGs)
The TC level is equal to the sum of the HDL, LDL, and VLDL levels:
The “good cholesterol,” HDL, is actually not only cholesterol but rather a particle (known as apoprotein) that contains cholesterol and acts as a scavenger to remove excess cholesterol in the body (also known as reverse cholesterol transport). HDL is predominantly protein, and elevated HDL levels have been associated with decreased cardiovascular risk. LDL, the “bad cholesterol,” is likewise not just cholesterol but a particle that contains it. Elevated LDL levels have been associated with increased cardiovascular risk. A high level of certain LDL particles may be a necessary precursor for atherogenesis (development of fatty arterial plaques). Much of the damage may be caused by oxidative modification of the LDL, making it more atherogenic.12 VLDL, another “bad cholesterol,” is actually a precursor of LDL. The particle is predominantly triglyceride.
1 Assessment
A variety of index measures have been proposed to assess the need for intervention and to monitor the success of preventive measures. The most frequently used guidelines are those of the Third National Cholesterol Education Program (NCEP),18 as modified based on more recent research.19 This discussion and Table 17-1 indicate the levels of blood lipids suggested by the widely accepted NCEP recommendations for deciding on treatment and follow-up. New NCEP recommendations are expected in 2012.
Table 17-1 Evaluation of Blood Lipid Levels in Persons without and with Coronary Risk Factors or Coronary Artery Disease (CAD)
Total Cholesterol Level
Some screening programs measure only the total cholesterol (TC) level. In adults without known atherosclerotic disease, a TC level less than 200 mg/dL does not require the need for action, although the level should be checked every 5 years. A level between 200 and 239 mg/dL is considered borderline high, and a fasting lipid profile is recommended, with action determined on the basis of the findings. If TC level is 240 mg/dL or greater, diagnosis based on a fasting lipid profile is needed, and dietary and lifestyle changes should be initiated; in addition, lipid-lowering drugs should be considered.
The TC level may be misleading and is a poor summary measure of the complicated lipoprotein-particle distributions that more accurately define risk. In insulin resistance, for example, TC tends to be normal, but there is an adverse pattern of lipoproteins—high triglycerides and low HDL. This pattern originally was discerned in the Framingham Heart Study and is sometimes referred to as syndrome X. In the Helsinki Heart Study, primary dyslipidemia was defined as the presence of a non-HDL cholesterol level 200 mg/dL or greater on two successive measurements.20 Many clinicians find this index useful because it uses the total contribution of cholesterol fractions currently considered harmful. Some specialists pay attention to the ratio of the TC level to the HDL level, as discussed later.
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