Clinical Review

Abuse of prescription drugs has been a national problem for decades, but recently the number of young Americans using prescription drugs for nonmedical purposes has been increasing at an alarming rate. Between 1999 and 2006, the US Department of Health and Human Services reports, the number of surveyed 12- to 17-year-olds who reported nonmedical use of a psychotherapeutic medication within the previous year increased by more than 60%.¹

High-profile cases have thrust the problem into public view. In July 2007, the son of former Vice President Al Gore was arrested on suspicion of illegal possession of Vicodin^®, Xanax^®, Valium^®, and Adderall^®.² And in January 2008, the 28-year-old actor Heath Ledger was found dead of acute intoxication resulting from the combined effects of oxycodone, hydrocodone, diazepam, temazepam, alprazolam, and doxylamine.³

Recent public awareness campaigns have taken up the fight against prescription drug abuse, as demonstrated in television ads from the Partnership for a Drug-Free America (www.drugfree.org). Their clear message is that abuse of prescription drugs can be as dangerous as that of illicit drugs like cocaine or heroin.

In 2005, an estimated 1.4 million US emergency department (ED) visits were related to substance abuse—in 37% of cases, abuse of prescription drugs. Prescription drug overdose is common among 12- to 17-year-olds, with more than 13,000 ED visits per year attributed to overmedication.⁴ The prescription drugs that are most commonly abused have potentially serious adverse effects and can cause accidental disability or death. They are also frequently implicated in suicide attempts: 45% involve prescription pain medication and 56%, sedatives or stimulants.⁴

It is imperative for clinicians, especially emergency medicine providers (EMPs), to appreciate the magnitude of prescription drug abuse among adolescents so that overdoses or chronic abuse can be identified appropriately, and treatment and prevention strategies can be implemented. An understanding of the basic pharmacology and toxicology of commonly abused prescription medications is especially helpful.

Awareness of the current trends and demographics of prescription drug abuse will enable EMPs to reevaluate their prescribing practices. The challenge is to maximize safe and effective treatment while minimizing the diversion of prescription drugs and the development of substance abuse disorders.

Defining the Problem
Using the three behavioral variables of intent, practice, and consequences, this definition can be established: Prescription drug abuse is the use of a controlled substance for reasons other than that for which it was prescribed, often in dosages different from those prescribed, resulting in disability or dysfunction and often involving illegal activity and risk of harm to the abuser.⁵

The National Institute on Drug Abuse⁶ designates prescription drugs with potential for abuse as psychotherapeutics. Classes of psychotherapeutics, in descending order of prevalence of abuse, are pain relievers, tranquilizers, stimulants, and sedatives.¹

Increasing Prevalence
The most recent National Survey on Drug Use and Health (NSDUH) showed use of illicit drugs and overall teen drug use at a five-year low. Since 2002, current illicit drug use among 12- to 17-year-olds has declined by 16%, including an 18% decrease in current marijuana use and a marked 25% decrease in marijuana use among teenage boys.^1,7,8

Yet these promising findings are overshadowed by the alarming number of young people who report misusing prescription drugs. More youth now initiate drug use with prescription pain relievers than with marijuana.¹ In two recent studies, 5.2 million respondents 12 or older had used prescription pain relievers nonmedically in the previous month—a 10% increase since 2005. Concurrently, overall nonmedical use of prescription drugs among 12- to 17-year-olds increased by 12%.^1,7 (See figure.¹)

Among adolescents, pain relievers are the most commonly abused prescription drugs. On an average day in 2006, 2,517 adolescents used pain relievers nonmedically for the first time.¹ The wide availability of these drugs contributes significantly to the problem. A recent analysis of Drug Enforcement Administration (DEA) data shows that in 1996, Americans purchased more than 200,000 pounds of codeine, hydrocodone, meperidine, morphine, and oxycodone. Between 1997 and 2007, the volume of five major painkillers distributed in the US rose by 90%. Sales of oxycodone alone rose nearly 600% between 1997 and 2005^9,10 (see Table 1^9-11).

The simultaneous decline in use of illicit drugs and increase in prescription drug abuse may be explained in part by teenagers' perception that abusing prescriptions is less harmful and less risky than using illicit street drugs. Widespread direct-to-consumer advertising for pain relievers, psychotropics, and sedatives may also lead teens to rationalize their use of prescriptions.

What Demographics Tell Us
Prevalence of prescription drug abuse by adolescents varies by region, ethnicity, and gender. It is highest in small cities and the Western states and lowest in urban areas of the Northeast. Prevalence rates are highest among American Indians or Alaska Natives (17%) and lowest among adolescents of Asian descent (7%). In general, Caucasian youths are more likely to misuse prescription psychotherapeutics than are African-Americans or Asian-Americans.¹

Notably, rates of nonmedical prescription use among 12- to 17-year-olds were higher in girls than in boys for pain relievers, stimulants, and tranquilizers.¹ In all other age-groups, prescription drug abuse is more prevalent among males.

Several risk factors correlate significantly with adolescent nonmedical prescription use, including mental health treatment, use of illicit drugs, female gender, and binge drinking. Self-reported lack of religiosity, high rates of family conflict, and presence of sensation-seeking behaviors are also considered risk factors.^11,12

Diversion of Prescription Psychotherapeutics
Diversion, the most common means of obtaining medications for unintended purposes, encompasses a number of inappropriate or illegal activities, including selling, trading, or sharing legitimately prescribed medications. Patients trying to obtain greater quantities than would ordinarily be prescribed (for primary or secondary purposes) may resort to doctor-shopping, falsely claiming a lost prescription, seeking escalating dosing from the provider, or forgery.

In addition to the long-established routes of diversion (eg, theft, doctor-shopping, malingering), prescription exchange among teenagers is a growing trend. Opioids and other agents are increasingly available to young patients through family members, because rising numbers of prescriptions are being written. These startling increases may reflect a fear of litigation for undertreating patients' pain or a concern to score well in patient satisfaction surveys. Other possible factors are a paradigm shift in pain management, the ever-increasing use of EDs by patients with chronic pain, or influence from the pharmaceutical industry. Nevertheless, the result is a flood of available drugs complicating a system that is already fraught with abuse.

Despite the rise in prescriptions for opioids, only about 14% of those used by teenagers are prescribed for them. Most teens who abuse prescription medications obtain them from peers or family members with legitimate prescriptions. About one-third of those who use prescription opioids rely on Internet no-prescription Web sites (NPWs) or drug dealers.⁸

In a 2005 Web-based survey of 1,086 high school students, 49% had been prescribed a sleeping aid, sedative, stimulant, or pain medication at least once.¹⁰ Among these students, 24% (27.5% of girls; 17.4% of boys) reported having lent their prescriptions or given them to other students.¹⁰ Having their medications stolen or being forced to give them away were often cited as significant problems.

Internet NPWs offer teenagers nearly unlimited opportunities to buy psychotherapeutics privately. The Government Accountability Office estimates that some 400 Internet pharmacies (200 based overseas) were selling drugs illegally in 2003.¹³ Identification beyond a credit card is rarely required, and search engines facilitate purchasing: Using search terms like "no prescription vicodin," Gordon et al¹⁴ reported a hit rate of 80% to 90% for NPWs but no links to addiction help–related sites. Buying psychotherapeutics from drug dealers is less discreet but often more expensive (see Table 2^15,16).

Identifying and Managing Abuse and Overdose
Three drug classes account for the majority of prescription medication abuse among teenagers: opioids, stimulants, and sedative-hypnotics (see Table 3^1,17). Dose-response curves suggest their anticipated effects, but individual responses vary; anyone willing to take a prescribed medication for nonmedical purposes is at risk for adverse effects. The following is a brief review of presenting signs and symptoms, appropriate intervention, and long-term complications of prescription drug abuse and overdose.¹⁸

Opioids
Of the three psychotherapeutic classes mentioned, opioids are most commonly used for nonmedical purposes. This class comprises naturally derived opiates (eg, heroin, morphine, codeine), semisynthetic opioids (eg, hydrocodone, oxycodone), and synthetically made opioids (eg, fentanyl, methadone, meperidine).

After ingestion, the initial effect is relaxation and blunted response to pain. With increasing doses, drowsiness ensues, with a reduction in pulse rate and blood pressure. Other common findings include muscle flaccidity, pupillary miosis, bradypnea, and decreased bowel sounds. (NOTE: Among the opioids, meperidine does not cause miosis.) Significant overdose results in the classic presentation of central nervous system (CNS) and respiratory depression and miosis; the episode may culminate in coma, apnea, and even death.

Treatment of a patient who pre-sents with opioid overdose consists of airway and ventilatory support, with special consideration given to opioid antagonists (eg, naloxone) that competitively inhibit the binding of opioid agonists. The goal of naloxone therapy is to elicit appropriate spontaneous ventilation, not necessarily complete arousal. Precipitation of withdrawal symptoms should be avoided, and clinicians should be aware that the half-life of naloxone is relatively short (especially compared with methadone); resedation may follow initial improvement.

Oxycodone (OxyContin^®) is of particular concern, in part due to its potency—and its subsequent prevalence. According to Monitoring the Future,¹⁹ a remarkable 5.3% prevalence of oxycodone use was reported in 12th graders in 2007.

Ordinarily, an 80-mg dose of oxycodone is slowly released over 12 hours, but numerous methods are used to circumvent the pill's time-release matrix; these uses are associated with high morbidity and mortality rates. Crushed oxycodone—hillbilly heroin—is immediately available for systemic absorption. Insufflation, too, results in relatively immediate effects. Slower absorption can be achieved by parachuting—a method of rolling or folding powdered or crushed drugs in toilet paper or other thin paper and ingesting it.¹⁸

Oxycodone injection requires more preparation. After the wax coating is removed, the pill is crushed into a fine powder, mixed with water, and liquefied over heat; any remaining wax is extracted, and the liquid is filtered through cotton and injected. Residual impurities can cause significant intravascular complications.

Stimulants
These agents include amphetamines and amphetamine-like drugs, such as phendimetrazine and benzphetamine, which are marketed as weight-loss medications. Methamphetamine is the most commonly abused drug in this class, with a lifetime use rate, throughout the US population, of 4.9%.⁷ However, only a small proportion is derived from the prescription forms used to treat attention-deficit/hyperactivity disorder or narcolepsy.

The two most commonly abused individual stimulants are methylphenidate (Ritalin^®) and dextroamphetamine (Dexedrine^®), with US lifetime use rates of 1.7% and 1.1%, respectively.⁷ As a class, prescription diet pills have a higher rate of nonmedical US lifetime use, 3.4%.

Despite amphetamines' low therapeutic index, persons who use them are known to develop high tolerance with ongoing use.¹⁸ Clinical response to amphetamines can be described as sympathomimetic effects, with CNS signs and symptoms ranging from anxiety and euphoria to severe agitation, hyperthermia, and seizures. Tachycardia, hypertension, diaphoresis, and tremors are classic symptoms. Potentially lethal complications include tachyarrhythmias, myocardial infarction, rhabdomyolysis, status epilepticus, and intracranial hemorrhage. Chronic use can lead to cardiomyopathy, dental decay, paranoia, and pulmonary hypertension.

The mainstays of treatment include blunting the sympathomimetic response with benzodiazepines and addressing the secondary complications of stimulant use. Managing agitation, hyperthermia, rhabdomyolysis, seizures, and tachydysrhythmias are critical following severe toxicity.¹⁸

Sedative-Hypnotic Medications
Under the umbrella of sedative-hypnotic agents fall benzodiazepines, barbiturates, skeletal muscle relaxants, antidepressants, and antihistamines. Certainly, benzodiazepines dominate this assortment, but several other medications pose serious risk when used nonmedically. Despite their preponderance, benzodiazepines cause relatively few deaths (compared with barbiturates), especially when they are used alone.

Although the clinical presentation of a patient with benzodiazepine overdose varies according to the specific agent ingested, common features include drowsiness, CNS depression, stupor, nystagmus, hypothermia, respiratory depression, and coma.¹⁸ Occasionally, ataxia is the only presenting sign of accidental benzodiazepine ingestion in the pediatric patient, but CNS depression is usually present. Cardiovascular instability can result directly, from depression of myocardial contractility, medullary depression, and vasodilation; or indirectly, from respiratory compromise. Ancillary signs, such as barbiturate blisters, may facilitate the diagnosis.

Primary treatment remains airway support with symptomatic and supportive care. Though rarely indicated following benzodiazepine poisoning, flumazenil is a competitive inhibitor of benzodiazepine receptors. It should be considered only in patients previously naive to benzodiazepines (as in the case of accidental pediatric ingestion) or following iatrogenic sedation. Use of flumazenil after long-term benzodiazepine therapy or in patients with a lowered seizure threshold may precipitate an acute withdrawal state, arrhythmias, and seizures. With proper airway support and monitoring, most patients improve clinically as the drugs are metabolized.¹⁸

Preventive Strategies for Emergency Medicine Clinicians
Although data involving emergency PAs and NPs are not readily available, fewer than 40% of physicians receive formal medical school training in recognizing prescription drug abuse or diversion.⁴ According to the Center on Addiction and Substance Abuse (CASA) survey, 43% of physicians neglect to ask about prescription drug abuse during the patient history.²⁰

Because continuity of care is inherently lacking in emergency medicine, certain active interventions are recommended during the patient encounter to limit nonmedical use of prescription drugs. Three particularly important techniques are recognizing cardinal features of patients who seek to obtain psychotherapeutic medications for nonmedical purposes; adapting prescription writing habits to provide safe, appropriate interventions; and educating patients.

In a limited time, EMPs must obtain as much information as possible about a patient's illness and personal situation without appearing to be suspicious or judgmental; confrontations may prompt some patients to resort to verbal aggression. Many EMPs pride themselves on their aptitude for "reading" patients and gaining their trust during the initial encounter.

Patterns in the medical records may indicate a history of prescription drug abuse. A more detailed history might elicit other relevant risk factors: a history of chronic pain, psychiatric disorders—even smoking within one hour of waking in the morning.^4,20 In the presence of two or more risk factors, strong consideration should be given to nonnarcotic treatment of pain and referral to a primary care clinician for multidisciplinary intervention.

Several available screening tools can increase sensitivity while standardizing the process; examples are the Screener and Opioid Assessment for Patients in Pain (see www.painedu.org) and the Screening Instrument for Substance Abuse Potential.²¹ These may be more useful in the primary care or outpatient setting than in the ED with its time constraints.

The manner in which EMPs write prescriptions can have direct impact on medication diversion. In the ED, prescriptions are more commonly written for opioid pain medications than for sedatives or stimulants. While addressing pain adequately is important, it is often appropriate to prescribe lower-potency opioids or even nonnarcotic pain relievers. EMPs should limit the total number of pills specified in proportion to the immediate diagnosis, and refills should not be provided—if for no other reason than to encourage timely follow-up.

Delayed-release opioids, because they lack the protective measures built into delayed-release stimulants, should be avoided in the ED for treatment of acute pain; research is under way to develop oxycodone in viscous gel form that is immune to injection.²² In other efforts, opioids are being combined with the antagonist naloxone to blunt the opioids' immediate euphoric effects.²⁰ Writing out the number of pills on hand-written prescriptions and using watermark paper for computer-generated prescriptions can also diminish forgery and diversion.

Patient Education
Educating patients—especially teenagers—about the potential for drug tolerance, dependence, and abuse plays an integral role in combating this problem. With most diverted prescription psychotherapeutic medications coming from family or friends, convincing parents to safeguard prescriptions in the household is critical. A huge discrepancy exists between what parents perceive about their children's prescription drug use and what actually occurs. Although 21% of teenagers admit to using prescription pain medications for their psychotherapeutic effects, only 1% of parents consider it "extremely likely" or "very likely" that their child has done so.²³

When parents actively address this important issue—teaching their children about the dangers of drug and prescription drug abuse—these practices can be reduced by nearly half.23 Impressing on parents the importance of their role in preventing prescription drug abuse may be the single most important way for EMPs to further the cause.

Resources for Concerned Clinicians
The DEA and the FDA rely on a complex set of databases to monitor prescription drug abuse. The Drug Abuse Warning Network (DAWN)²⁴ and the NSDUH,⁸ administered by the Department of Health and Human Services, are two examples. DAWN is a public health surveillance system that monitors drug-related visits to hospital EDs through chart review and drug-related deaths investigated by medical examiners and coroners. By joining DAWN, EDs can gain access to real-time data and receive payments to participate in data collection.²⁴ NSDUH gathers data by administering in-home, face-to-face questionnaires to a representative sample of the population. Both programs publish reports on the Internet and make findings available to the general public.^8,24

Also in the arena of prescription drug abuse monitoring is an industry-initiated database known as RADARS (Researched Abuse, Diversion and Addiction-Related Surveillance), developed by Purdue Pharma to address diversion and abuse of OxyContin^®. RADARS' goal is to develop proactive, timely, geographically sensitive methods to detect abuse and diversion of OxyContin and other scheduled prescription medications.²⁵ This program acquires high-quality data from drug abuse experts, law enforcement agencies, and regional Poison Control Centers, covering more than 80% of the nation's zip codes. Regionally specific risk-minimization strategies are RADARS' next goal.

Conclusion
Clinicians who provide emergency care are in a position to slow, or even reverse, the escalating misuse of prescription medications by teenage patients. Primary care providers, too, are called on to keep abreast of emerging reports on this trend, to reconsider how they write prescriptions for psychotherapeutic agents, and to be vigilant to the signs of abuse in their adolescent patients.           

Abuse of prescription drugs has been a national problem for decades, but recently the number of young Americans using prescription drugs for nonmedical purposes has been increasing at an alarming rate. Between 1999 and 2006, the US Department of Health and Human Services reports, the number of surveyed 12- to 17-year-olds who reported nonmedical use of a psychotherapeutic medication within the previous year increased by more than 60%.¹

High-profile cases have thrust the problem into public view. In July 2007, the son of former Vice President Al Gore was arrested on suspicion of illegal possession of Vicodin^®, Xanax^®, Valium^®, and Adderall^®.² And in January 2008, the 28-year-old actor Heath Ledger was found dead of acute intoxication resulting from the combined effects of oxycodone, hydrocodone, diazepam, temazepam, alprazolam, and doxylamine.³

Recent public awareness campaigns have taken up the fight against prescription drug abuse, as demonstrated in television ads from the Partnership for a Drug-Free America (www.drugfree.org). Their clear message is that abuse of prescription drugs can be as dangerous as that of illicit drugs like cocaine or heroin.

In 2005, an estimated 1.4 million US emergency department (ED) visits were related to substance abuse—in 37% of cases, abuse of prescription drugs. Prescription drug overdose is common among 12- to 17-year-olds, with more than 13,000 ED visits per year attributed to overmedication.⁴ The prescription drugs that are most commonly abused have potentially serious adverse effects and can cause accidental disability or death. They are also frequently implicated in suicide attempts: 45% involve prescription pain medication and 56%, sedatives or stimulants.⁴

It is imperative for clinicians, especially emergency medicine providers (EMPs), to appreciate the magnitude of prescription drug abuse among adolescents so that overdoses or chronic abuse can be identified appropriately, and treatment and prevention strategies can be implemented. An understanding of the basic pharmacology and toxicology of commonly abused prescription medications is especially helpful.

Awareness of the current trends and demographics of prescription drug abuse will enable EMPs to reevaluate their prescribing practices. The challenge is to maximize safe and effective treatment while minimizing the diversion of prescription drugs and the development of substance abuse disorders.

Defining the Problem
Using the three behavioral variables of intent, practice, and consequences, this definition can be established: Prescription drug abuse is the use of a controlled substance for reasons other than that for which it was prescribed, often in dosages different from those prescribed, resulting in disability or dysfunction and often involving illegal activity and risk of harm to the abuser.⁵

The National Institute on Drug Abuse⁶ designates prescription drugs with potential for abuse as psychotherapeutics. Classes of psychotherapeutics, in descending order of prevalence of abuse, are pain relievers, tranquilizers, stimulants, and sedatives.¹

Increasing Prevalence
The most recent National Survey on Drug Use and Health (NSDUH) showed use of illicit drugs and overall teen drug use at a five-year low. Since 2002, current illicit drug use among 12- to 17-year-olds has declined by 16%, including an 18% decrease in current marijuana use and a marked 25% decrease in marijuana use among teenage boys.^1,7,8

Yet these promising findings are overshadowed by the alarming number of young people who report misusing prescription drugs. More youth now initiate drug use with prescription pain relievers than with marijuana.¹ In two recent studies, 5.2 million respondents 12 or older had used prescription pain relievers nonmedically in the previous month—a 10% increase since 2005. Concurrently, overall nonmedical use of prescription drugs among 12- to 17-year-olds increased by 12%.^1,7 (See figure.¹)

Among adolescents, pain relievers are the most commonly abused prescription drugs. On an average day in 2006, 2,517 adolescents used pain relievers nonmedically for the first time.¹ The wide availability of these drugs contributes significantly to the problem. A recent analysis of Drug Enforcement Administration (DEA) data shows that in 1996, Americans purchased more than 200,000 pounds of codeine, hydrocodone, meperidine, morphine, and oxycodone. Between 1997 and 2007, the volume of five major painkillers distributed in the US rose by 90%. Sales of oxycodone alone rose nearly 600% between 1997 and 2005^9,10 (see Table 1^9-11).

The simultaneous decline in use of illicit drugs and increase in prescription drug abuse may be explained in part by teenagers' perception that abusing prescriptions is less harmful and less risky than using illicit street drugs. Widespread direct-to-consumer advertising for pain relievers, psychotropics, and sedatives may also lead teens to rationalize their use of prescriptions.

What Demographics Tell Us
Prevalence of prescription drug abuse by adolescents varies by region, ethnicity, and gender. It is highest in small cities and the Western states and lowest in urban areas of the Northeast. Prevalence rates are highest among American Indians or Alaska Natives (17%) and lowest among adolescents of Asian descent (7%). In general, Caucasian youths are more likely to misuse prescription psychotherapeutics than are African-Americans or Asian-Americans.¹

Notably, rates of nonmedical prescription use among 12- to 17-year-olds were higher in girls than in boys for pain relievers, stimulants, and tranquilizers.¹ In all other age-groups, prescription drug abuse is more prevalent among males.

Several risk factors correlate significantly with adolescent nonmedical prescription use, including mental health treatment, use of illicit drugs, female gender, and binge drinking. Self-reported lack of religiosity, high rates of family conflict, and presence of sensation-seeking behaviors are also considered risk factors.^11,12

Diversion of Prescription Psychotherapeutics
Diversion, the most common means of obtaining medications for unintended purposes, encompasses a number of inappropriate or illegal activities, including selling, trading, or sharing legitimately prescribed medications. Patients trying to obtain greater quantities than would ordinarily be prescribed (for primary or secondary purposes) may resort to doctor-shopping, falsely claiming a lost prescription, seeking escalating dosing from the provider, or forgery.

In addition to the long-established routes of diversion (eg, theft, doctor-shopping, malingering), prescription exchange among teenagers is a growing trend. Opioids and other agents are increasingly available to young patients through family members, because rising numbers of prescriptions are being written. These startling increases may reflect a fear of litigation for undertreating patients' pain or a concern to score well in patient satisfaction surveys. Other possible factors are a paradigm shift in pain management, the ever-increasing use of EDs by patients with chronic pain, or influence from the pharmaceutical industry. Nevertheless, the result is a flood of available drugs complicating a system that is already fraught with abuse.

Despite the rise in prescriptions for opioids, only about 14% of those used by teenagers are prescribed for them. Most teens who abuse prescription medications obtain them from peers or family members with legitimate prescriptions. About one-third of those who use prescription opioids rely on Internet no-prescription Web sites (NPWs) or drug dealers.⁸

In a 2005 Web-based survey of 1,086 high school students, 49% had been prescribed a sleeping aid, sedative, stimulant, or pain medication at least once.¹⁰ Among these students, 24% (27.5% of girls; 17.4% of boys) reported having lent their prescriptions or given them to other students.¹⁰ Having their medications stolen or being forced to give them away were often cited as significant problems.

Internet NPWs offer teenagers nearly unlimited opportunities to buy psychotherapeutics privately. The Government Accountability Office estimates that some 400 Internet pharmacies (200 based overseas) were selling drugs illegally in 2003.¹³ Identification beyond a credit card is rarely required, and search engines facilitate purchasing: Using search terms like "no prescription vicodin," Gordon et al¹⁴ reported a hit rate of 80% to 90% for NPWs but no links to addiction help–related sites. Buying psychotherapeutics from drug dealers is less discreet but often more expensive (see Table 2^15,16).

Identifying and Managing Abuse and Overdose
Three drug classes account for the majority of prescription medication abuse among teenagers: opioids, stimulants, and sedative-hypnotics (see Table 3^1,17). Dose-response curves suggest their anticipated effects, but individual responses vary; anyone willing to take a prescribed medication for nonmedical purposes is at risk for adverse effects. The following is a brief review of presenting signs and symptoms, appropriate intervention, and long-term complications of prescription drug abuse and overdose.¹⁸

Opioids
Of the three psychotherapeutic classes mentioned, opioids are most commonly used for nonmedical purposes. This class comprises naturally derived opiates (eg, heroin, morphine, codeine), semisynthetic opioids (eg, hydrocodone, oxycodone), and synthetically made opioids (eg, fentanyl, methadone, meperidine).

After ingestion, the initial effect is relaxation and blunted response to pain. With increasing doses, drowsiness ensues, with a reduction in pulse rate and blood pressure. Other common findings include muscle flaccidity, pupillary miosis, bradypnea, and decreased bowel sounds. (NOTE: Among the opioids, meperidine does not cause miosis.) Significant overdose results in the classic presentation of central nervous system (CNS) and respiratory depression and miosis; the episode may culminate in coma, apnea, and even death.

Treatment of a patient who pre-sents with opioid overdose consists of airway and ventilatory support, with special consideration given to opioid antagonists (eg, naloxone) that competitively inhibit the binding of opioid agonists. The goal of naloxone therapy is to elicit appropriate spontaneous ventilation, not necessarily complete arousal. Precipitation of withdrawal symptoms should be avoided, and clinicians should be aware that the half-life of naloxone is relatively short (especially compared with methadone); resedation may follow initial improvement.

Oxycodone (OxyContin^®) is of particular concern, in part due to its potency—and its subsequent prevalence. According to Monitoring the Future,¹⁹ a remarkable 5.3% prevalence of oxycodone use was reported in 12th graders in 2007.

Ordinarily, an 80-mg dose of oxycodone is slowly released over 12 hours, but numerous methods are used to circumvent the pill's time-release matrix; these uses are associated with high morbidity and mortality rates. Crushed oxycodone—hillbilly heroin—is immediately available for systemic absorption. Insufflation, too, results in relatively immediate effects. Slower absorption can be achieved by parachuting—a method of rolling or folding powdered or crushed drugs in toilet paper or other thin paper and ingesting it.¹⁸

Oxycodone injection requires more preparation. After the wax coating is removed, the pill is crushed into a fine powder, mixed with water, and liquefied over heat; any remaining wax is extracted, and the liquid is filtered through cotton and injected. Residual impurities can cause significant intravascular complications.

Stimulants
These agents include amphetamines and amphetamine-like drugs, such as phendimetrazine and benzphetamine, which are marketed as weight-loss medications. Methamphetamine is the most commonly abused drug in this class, with a lifetime use rate, throughout the US population, of 4.9%.⁷ However, only a small proportion is derived from the prescription forms used to treat attention-deficit/hyperactivity disorder or narcolepsy.

The two most commonly abused individual stimulants are methylphenidate (Ritalin^®) and dextroamphetamine (Dexedrine^®), with US lifetime use rates of 1.7% and 1.1%, respectively.⁷ As a class, prescription diet pills have a higher rate of nonmedical US lifetime use, 3.4%.

Despite amphetamines' low therapeutic index, persons who use them are known to develop high tolerance with ongoing use.¹⁸ Clinical response to amphetamines can be described as sympathomimetic effects, with CNS signs and symptoms ranging from anxiety and euphoria to severe agitation, hyperthermia, and seizures. Tachycardia, hypertension, diaphoresis, and tremors are classic symptoms. Potentially lethal complications include tachyarrhythmias, myocardial infarction, rhabdomyolysis, status epilepticus, and intracranial hemorrhage. Chronic use can lead to cardiomyopathy, dental decay, paranoia, and pulmonary hypertension.

The mainstays of treatment include blunting the sympathomimetic response with benzodiazepines and addressing the secondary complications of stimulant use. Managing agitation, hyperthermia, rhabdomyolysis, seizures, and tachydysrhythmias are critical following severe toxicity.¹⁸

Sedative-Hypnotic Medications
Under the umbrella of sedative-hypnotic agents fall benzodiazepines, barbiturates, skeletal muscle relaxants, antidepressants, and antihistamines. Certainly, benzodiazepines dominate this assortment, but several other medications pose serious risk when used nonmedically. Despite their preponderance, benzodiazepines cause relatively few deaths (compared with barbiturates), especially when they are used alone.

Although the clinical presentation of a patient with benzodiazepine overdose varies according to the specific agent ingested, common features include drowsiness, CNS depression, stupor, nystagmus, hypothermia, respiratory depression, and coma.¹⁸ Occasionally, ataxia is the only presenting sign of accidental benzodiazepine ingestion in the pediatric patient, but CNS depression is usually present. Cardiovascular instability can result directly, from depression of myocardial contractility, medullary depression, and vasodilation; or indirectly, from respiratory compromise. Ancillary signs, such as barbiturate blisters, may facilitate the diagnosis.

Primary treatment remains airway support with symptomatic and supportive care. Though rarely indicated following benzodiazepine poisoning, flumazenil is a competitive inhibitor of benzodiazepine receptors. It should be considered only in patients previously naive to benzodiazepines (as in the case of accidental pediatric ingestion) or following iatrogenic sedation. Use of flumazenil after long-term benzodiazepine therapy or in patients with a lowered seizure threshold may precipitate an acute withdrawal state, arrhythmias, and seizures. With proper airway support and monitoring, most patients improve clinically as the drugs are metabolized.¹⁸

Preventive Strategies for Emergency Medicine Clinicians
Although data involving emergency PAs and NPs are not readily available, fewer than 40% of physicians receive formal medical school training in recognizing prescription drug abuse or diversion.⁴ According to the Center on Addiction and Substance Abuse (CASA) survey, 43% of physicians neglect to ask about prescription drug abuse during the patient history.²⁰

Because continuity of care is inherently lacking in emergency medicine, certain active interventions are recommended during the patient encounter to limit nonmedical use of prescription drugs. Three particularly important techniques are recognizing cardinal features of patients who seek to obtain psychotherapeutic medications for nonmedical purposes; adapting prescription writing habits to provide safe, appropriate interventions; and educating patients.

In a limited time, EMPs must obtain as much information as possible about a patient's illness and personal situation without appearing to be suspicious or judgmental; confrontations may prompt some patients to resort to verbal aggression. Many EMPs pride themselves on their aptitude for "reading" patients and gaining their trust during the initial encounter.

Patterns in the medical records may indicate a history of prescription drug abuse. A more detailed history might elicit other relevant risk factors: a history of chronic pain, psychiatric disorders—even smoking within one hour of waking in the morning.^4,20 In the presence of two or more risk factors, strong consideration should be given to nonnarcotic treatment of pain and referral to a primary care clinician for multidisciplinary intervention.

Several available screening tools can increase sensitivity while standardizing the process; examples are the Screener and Opioid Assessment for Patients in Pain (see www.painedu.org) and the Screening Instrument for Substance Abuse Potential.²¹ These may be more useful in the primary care or outpatient setting than in the ED with its time constraints.

The manner in which EMPs write prescriptions can have direct impact on medication diversion. In the ED, prescriptions are more commonly written for opioid pain medications than for sedatives or stimulants. While addressing pain adequately is important, it is often appropriate to prescribe lower-potency opioids or even nonnarcotic pain relievers. EMPs should limit the total number of pills specified in proportion to the immediate diagnosis, and refills should not be provided—if for no other reason than to encourage timely follow-up.

Delayed-release opioids, because they lack the protective measures built into delayed-release stimulants, should be avoided in the ED for treatment of acute pain; research is under way to develop oxycodone in viscous gel form that is immune to injection.²² In other efforts, opioids are being combined with the antagonist naloxone to blunt the opioids' immediate euphoric effects.²⁰ Writing out the number of pills on hand-written prescriptions and using watermark paper for computer-generated prescriptions can also diminish forgery and diversion.

Patient Education
Educating patients—especially teenagers—about the potential for drug tolerance, dependence, and abuse plays an integral role in combating this problem. With most diverted prescription psychotherapeutic medications coming from family or friends, convincing parents to safeguard prescriptions in the household is critical. A huge discrepancy exists between what parents perceive about their children's prescription drug use and what actually occurs. Although 21% of teenagers admit to using prescription pain medications for their psychotherapeutic effects, only 1% of parents consider it "extremely likely" or "very likely" that their child has done so.²³

When parents actively address this important issue—teaching their children about the dangers of drug and prescription drug abuse—these practices can be reduced by nearly half.23 Impressing on parents the importance of their role in preventing prescription drug abuse may be the single most important way for EMPs to further the cause.

Resources for Concerned Clinicians
The DEA and the FDA rely on a complex set of databases to monitor prescription drug abuse. The Drug Abuse Warning Network (DAWN)²⁴ and the NSDUH,⁸ administered by the Department of Health and Human Services, are two examples. DAWN is a public health surveillance system that monitors drug-related visits to hospital EDs through chart review and drug-related deaths investigated by medical examiners and coroners. By joining DAWN, EDs can gain access to real-time data and receive payments to participate in data collection.²⁴ NSDUH gathers data by administering in-home, face-to-face questionnaires to a representative sample of the population. Both programs publish reports on the Internet and make findings available to the general public.^8,24

Also in the arena of prescription drug abuse monitoring is an industry-initiated database known as RADARS (Researched Abuse, Diversion and Addiction-Related Surveillance), developed by Purdue Pharma to address diversion and abuse of OxyContin^®. RADARS' goal is to develop proactive, timely, geographically sensitive methods to detect abuse and diversion of OxyContin and other scheduled prescription medications.²⁵ This program acquires high-quality data from drug abuse experts, law enforcement agencies, and regional Poison Control Centers, covering more than 80% of the nation's zip codes. Regionally specific risk-minimization strategies are RADARS' next goal.

Conclusion
Clinicians who provide emergency care are in a position to slow, or even reverse, the escalating misuse of prescription medications by teenage patients. Primary care providers, too, are called on to keep abreast of emerging reports on this trend, to reconsider how they write prescriptions for psychotherapeutic agents, and to be vigilant to the signs of abuse in their adolescent patients.           

Abuse of prescription drugs has been a national problem for decades, but recently the number of young Americans using prescription drugs for nonmedical purposes has been increasing at an alarming rate. Between 1999 and 2006, the US Department of Health and Human Services reports, the number of surveyed 12- to 17-year-olds who reported nonmedical use of a psychotherapeutic medication within the previous year increased by more than 60%.¹

High-profile cases have thrust the problem into public view. In July 2007, the son of former Vice President Al Gore was arrested on suspicion of illegal possession of Vicodin^®, Xanax^®, Valium^®, and Adderall^®.² And in January 2008, the 28-year-old actor Heath Ledger was found dead of acute intoxication resulting from the combined effects of oxycodone, hydrocodone, diazepam, temazepam, alprazolam, and doxylamine.³

Recent public awareness campaigns have taken up the fight against prescription drug abuse, as demonstrated in television ads from the Partnership for a Drug-Free America (www.drugfree.org). Their clear message is that abuse of prescription drugs can be as dangerous as that of illicit drugs like cocaine or heroin.

In 2005, an estimated 1.4 million US emergency department (ED) visits were related to substance abuse—in 37% of cases, abuse of prescription drugs. Prescription drug overdose is common among 12- to 17-year-olds, with more than 13,000 ED visits per year attributed to overmedication.⁴ The prescription drugs that are most commonly abused have potentially serious adverse effects and can cause accidental disability or death. They are also frequently implicated in suicide attempts: 45% involve prescription pain medication and 56%, sedatives or stimulants.⁴

It is imperative for clinicians, especially emergency medicine providers (EMPs), to appreciate the magnitude of prescription drug abuse among adolescents so that overdoses or chronic abuse can be identified appropriately, and treatment and prevention strategies can be implemented. An understanding of the basic pharmacology and toxicology of commonly abused prescription medications is especially helpful.

Awareness of the current trends and demographics of prescription drug abuse will enable EMPs to reevaluate their prescribing practices. The challenge is to maximize safe and effective treatment while minimizing the diversion of prescription drugs and the development of substance abuse disorders.

Defining the Problem
Using the three behavioral variables of intent, practice, and consequences, this definition can be established: Prescription drug abuse is the use of a controlled substance for reasons other than that for which it was prescribed, often in dosages different from those prescribed, resulting in disability or dysfunction and often involving illegal activity and risk of harm to the abuser.⁵

The National Institute on Drug Abuse⁶ designates prescription drugs with potential for abuse as psychotherapeutics. Classes of psychotherapeutics, in descending order of prevalence of abuse, are pain relievers, tranquilizers, stimulants, and sedatives.¹

Increasing Prevalence
The most recent National Survey on Drug Use and Health (NSDUH) showed use of illicit drugs and overall teen drug use at a five-year low. Since 2002, current illicit drug use among 12- to 17-year-olds has declined by 16%, including an 18% decrease in current marijuana use and a marked 25% decrease in marijuana use among teenage boys.^1,7,8

Yet these promising findings are overshadowed by the alarming number of young people who report misusing prescription drugs. More youth now initiate drug use with prescription pain relievers than with marijuana.¹ In two recent studies, 5.2 million respondents 12 or older had used prescription pain relievers nonmedically in the previous month—a 10% increase since 2005. Concurrently, overall nonmedical use of prescription drugs among 12- to 17-year-olds increased by 12%.^1,7 (See figure.¹)

Among adolescents, pain relievers are the most commonly abused prescription drugs. On an average day in 2006, 2,517 adolescents used pain relievers nonmedically for the first time.¹ The wide availability of these drugs contributes significantly to the problem. A recent analysis of Drug Enforcement Administration (DEA) data shows that in 1996, Americans purchased more than 200,000 pounds of codeine, hydrocodone, meperidine, morphine, and oxycodone. Between 1997 and 2007, the volume of five major painkillers distributed in the US rose by 90%. Sales of oxycodone alone rose nearly 600% between 1997 and 2005^9,10 (see Table 1^9-11).

The simultaneous decline in use of illicit drugs and increase in prescription drug abuse may be explained in part by teenagers' perception that abusing prescriptions is less harmful and less risky than using illicit street drugs. Widespread direct-to-consumer advertising for pain relievers, psychotropics, and sedatives may also lead teens to rationalize their use of prescriptions.

What Demographics Tell Us
Prevalence of prescription drug abuse by adolescents varies by region, ethnicity, and gender. It is highest in small cities and the Western states and lowest in urban areas of the Northeast. Prevalence rates are highest among American Indians or Alaska Natives (17%) and lowest among adolescents of Asian descent (7%). In general, Caucasian youths are more likely to misuse prescription psychotherapeutics than are African-Americans or Asian-Americans.¹

Notably, rates of nonmedical prescription use among 12- to 17-year-olds were higher in girls than in boys for pain relievers, stimulants, and tranquilizers.¹ In all other age-groups, prescription drug abuse is more prevalent among males.

Several risk factors correlate significantly with adolescent nonmedical prescription use, including mental health treatment, use of illicit drugs, female gender, and binge drinking. Self-reported lack of religiosity, high rates of family conflict, and presence of sensation-seeking behaviors are also considered risk factors.^11,12

Diversion of Prescription Psychotherapeutics
Diversion, the most common means of obtaining medications for unintended purposes, encompasses a number of inappropriate or illegal activities, including selling, trading, or sharing legitimately prescribed medications. Patients trying to obtain greater quantities than would ordinarily be prescribed (for primary or secondary purposes) may resort to doctor-shopping, falsely claiming a lost prescription, seeking escalating dosing from the provider, or forgery.

In addition to the long-established routes of diversion (eg, theft, doctor-shopping, malingering), prescription exchange among teenagers is a growing trend. Opioids and other agents are increasingly available to young patients through family members, because rising numbers of prescriptions are being written. These startling increases may reflect a fear of litigation for undertreating patients' pain or a concern to score well in patient satisfaction surveys. Other possible factors are a paradigm shift in pain management, the ever-increasing use of EDs by patients with chronic pain, or influence from the pharmaceutical industry. Nevertheless, the result is a flood of available drugs complicating a system that is already fraught with abuse.

Despite the rise in prescriptions for opioids, only about 14% of those used by teenagers are prescribed for them. Most teens who abuse prescription medications obtain them from peers or family members with legitimate prescriptions. About one-third of those who use prescription opioids rely on Internet no-prescription Web sites (NPWs) or drug dealers.⁸

In a 2005 Web-based survey of 1,086 high school students, 49% had been prescribed a sleeping aid, sedative, stimulant, or pain medication at least once.¹⁰ Among these students, 24% (27.5% of girls; 17.4% of boys) reported having lent their prescriptions or given them to other students.¹⁰ Having their medications stolen or being forced to give them away were often cited as significant problems.

Internet NPWs offer teenagers nearly unlimited opportunities to buy psychotherapeutics privately. The Government Accountability Office estimates that some 400 Internet pharmacies (200 based overseas) were selling drugs illegally in 2003.¹³ Identification beyond a credit card is rarely required, and search engines facilitate purchasing: Using search terms like "no prescription vicodin," Gordon et al¹⁴ reported a hit rate of 80% to 90% for NPWs but no links to addiction help–related sites. Buying psychotherapeutics from drug dealers is less discreet but often more expensive (see Table 2^15,16).

Identifying and Managing Abuse and Overdose
Three drug classes account for the majority of prescription medication abuse among teenagers: opioids, stimulants, and sedative-hypnotics (see Table 3^1,17). Dose-response curves suggest their anticipated effects, but individual responses vary; anyone willing to take a prescribed medication for nonmedical purposes is at risk for adverse effects. The following is a brief review of presenting signs and symptoms, appropriate intervention, and long-term complications of prescription drug abuse and overdose.¹⁸

Opioids
Of the three psychotherapeutic classes mentioned, opioids are most commonly used for nonmedical purposes. This class comprises naturally derived opiates (eg, heroin, morphine, codeine), semisynthetic opioids (eg, hydrocodone, oxycodone), and synthetically made opioids (eg, fentanyl, methadone, meperidine).

After ingestion, the initial effect is relaxation and blunted response to pain. With increasing doses, drowsiness ensues, with a reduction in pulse rate and blood pressure. Other common findings include muscle flaccidity, pupillary miosis, bradypnea, and decreased bowel sounds. (NOTE: Among the opioids, meperidine does not cause miosis.) Significant overdose results in the classic presentation of central nervous system (CNS) and respiratory depression and miosis; the episode may culminate in coma, apnea, and even death.

Treatment of a patient who pre-sents with opioid overdose consists of airway and ventilatory support, with special consideration given to opioid antagonists (eg, naloxone) that competitively inhibit the binding of opioid agonists. The goal of naloxone therapy is to elicit appropriate spontaneous ventilation, not necessarily complete arousal. Precipitation of withdrawal symptoms should be avoided, and clinicians should be aware that the half-life of naloxone is relatively short (especially compared with methadone); resedation may follow initial improvement.

Oxycodone (OxyContin^®) is of particular concern, in part due to its potency—and its subsequent prevalence. According to Monitoring the Future,¹⁹ a remarkable 5.3% prevalence of oxycodone use was reported in 12th graders in 2007.

Ordinarily, an 80-mg dose of oxycodone is slowly released over 12 hours, but numerous methods are used to circumvent the pill's time-release matrix; these uses are associated with high morbidity and mortality rates. Crushed oxycodone—hillbilly heroin—is immediately available for systemic absorption. Insufflation, too, results in relatively immediate effects. Slower absorption can be achieved by parachuting—a method of rolling or folding powdered or crushed drugs in toilet paper or other thin paper and ingesting it.¹⁸

Oxycodone injection requires more preparation. After the wax coating is removed, the pill is crushed into a fine powder, mixed with water, and liquefied over heat; any remaining wax is extracted, and the liquid is filtered through cotton and injected. Residual impurities can cause significant intravascular complications.

Stimulants
These agents include amphetamines and amphetamine-like drugs, such as phendimetrazine and benzphetamine, which are marketed as weight-loss medications. Methamphetamine is the most commonly abused drug in this class, with a lifetime use rate, throughout the US population, of 4.9%.⁷ However, only a small proportion is derived from the prescription forms used to treat attention-deficit/hyperactivity disorder or narcolepsy.

The two most commonly abused individual stimulants are methylphenidate (Ritalin^®) and dextroamphetamine (Dexedrine^®), with US lifetime use rates of 1.7% and 1.1%, respectively.⁷ As a class, prescription diet pills have a higher rate of nonmedical US lifetime use, 3.4%.

Despite amphetamines' low therapeutic index, persons who use them are known to develop high tolerance with ongoing use.¹⁸ Clinical response to amphetamines can be described as sympathomimetic effects, with CNS signs and symptoms ranging from anxiety and euphoria to severe agitation, hyperthermia, and seizures. Tachycardia, hypertension, diaphoresis, and tremors are classic symptoms. Potentially lethal complications include tachyarrhythmias, myocardial infarction, rhabdomyolysis, status epilepticus, and intracranial hemorrhage. Chronic use can lead to cardiomyopathy, dental decay, paranoia, and pulmonary hypertension.

The mainstays of treatment include blunting the sympathomimetic response with benzodiazepines and addressing the secondary complications of stimulant use. Managing agitation, hyperthermia, rhabdomyolysis, seizures, and tachydysrhythmias are critical following severe toxicity.¹⁸

Sedative-Hypnotic Medications
Under the umbrella of sedative-hypnotic agents fall benzodiazepines, barbiturates, skeletal muscle relaxants, antidepressants, and antihistamines. Certainly, benzodiazepines dominate this assortment, but several other medications pose serious risk when used nonmedically. Despite their preponderance, benzodiazepines cause relatively few deaths (compared with barbiturates), especially when they are used alone.

Although the clinical presentation of a patient with benzodiazepine overdose varies according to the specific agent ingested, common features include drowsiness, CNS depression, stupor, nystagmus, hypothermia, respiratory depression, and coma.¹⁸ Occasionally, ataxia is the only presenting sign of accidental benzodiazepine ingestion in the pediatric patient, but CNS depression is usually present. Cardiovascular instability can result directly, from depression of myocardial contractility, medullary depression, and vasodilation; or indirectly, from respiratory compromise. Ancillary signs, such as barbiturate blisters, may facilitate the diagnosis.

Primary treatment remains airway support with symptomatic and supportive care. Though rarely indicated following benzodiazepine poisoning, flumazenil is a competitive inhibitor of benzodiazepine receptors. It should be considered only in patients previously naive to benzodiazepines (as in the case of accidental pediatric ingestion) or following iatrogenic sedation. Use of flumazenil after long-term benzodiazepine therapy or in patients with a lowered seizure threshold may precipitate an acute withdrawal state, arrhythmias, and seizures. With proper airway support and monitoring, most patients improve clinically as the drugs are metabolized.¹⁸

Preventive Strategies for Emergency Medicine Clinicians
Although data involving emergency PAs and NPs are not readily available, fewer than 40% of physicians receive formal medical school training in recognizing prescription drug abuse or diversion.⁴ According to the Center on Addiction and Substance Abuse (CASA) survey, 43% of physicians neglect to ask about prescription drug abuse during the patient history.²⁰

Because continuity of care is inherently lacking in emergency medicine, certain active interventions are recommended during the patient encounter to limit nonmedical use of prescription drugs. Three particularly important techniques are recognizing cardinal features of patients who seek to obtain psychotherapeutic medications for nonmedical purposes; adapting prescription writing habits to provide safe, appropriate interventions; and educating patients.

In a limited time, EMPs must obtain as much information as possible about a patient's illness and personal situation without appearing to be suspicious or judgmental; confrontations may prompt some patients to resort to verbal aggression. Many EMPs pride themselves on their aptitude for "reading" patients and gaining their trust during the initial encounter.

Patterns in the medical records may indicate a history of prescription drug abuse. A more detailed history might elicit other relevant risk factors: a history of chronic pain, psychiatric disorders—even smoking within one hour of waking in the morning.^4,20 In the presence of two or more risk factors, strong consideration should be given to nonnarcotic treatment of pain and referral to a primary care clinician for multidisciplinary intervention.

Several available screening tools can increase sensitivity while standardizing the process; examples are the Screener and Opioid Assessment for Patients in Pain (see www.painedu.org) and the Screening Instrument for Substance Abuse Potential.²¹ These may be more useful in the primary care or outpatient setting than in the ED with its time constraints.

The manner in which EMPs write prescriptions can have direct impact on medication diversion. In the ED, prescriptions are more commonly written for opioid pain medications than for sedatives or stimulants. While addressing pain adequately is important, it is often appropriate to prescribe lower-potency opioids or even nonnarcotic pain relievers. EMPs should limit the total number of pills specified in proportion to the immediate diagnosis, and refills should not be provided—if for no other reason than to encourage timely follow-up.

Delayed-release opioids, because they lack the protective measures built into delayed-release stimulants, should be avoided in the ED for treatment of acute pain; research is under way to develop oxycodone in viscous gel form that is immune to injection.²² In other efforts, opioids are being combined with the antagonist naloxone to blunt the opioids' immediate euphoric effects.²⁰ Writing out the number of pills on hand-written prescriptions and using watermark paper for computer-generated prescriptions can also diminish forgery and diversion.

Patient Education
Educating patients—especially teenagers—about the potential for drug tolerance, dependence, and abuse plays an integral role in combating this problem. With most diverted prescription psychotherapeutic medications coming from family or friends, convincing parents to safeguard prescriptions in the household is critical. A huge discrepancy exists between what parents perceive about their children's prescription drug use and what actually occurs. Although 21% of teenagers admit to using prescription pain medications for their psychotherapeutic effects, only 1% of parents consider it "extremely likely" or "very likely" that their child has done so.²³

When parents actively address this important issue—teaching their children about the dangers of drug and prescription drug abuse—these practices can be reduced by nearly half.23 Impressing on parents the importance of their role in preventing prescription drug abuse may be the single most important way for EMPs to further the cause.

Resources for Concerned Clinicians
The DEA and the FDA rely on a complex set of databases to monitor prescription drug abuse. The Drug Abuse Warning Network (DAWN)²⁴ and the NSDUH,⁸ administered by the Department of Health and Human Services, are two examples. DAWN is a public health surveillance system that monitors drug-related visits to hospital EDs through chart review and drug-related deaths investigated by medical examiners and coroners. By joining DAWN, EDs can gain access to real-time data and receive payments to participate in data collection.²⁴ NSDUH gathers data by administering in-home, face-to-face questionnaires to a representative sample of the population. Both programs publish reports on the Internet and make findings available to the general public.^8,24

Also in the arena of prescription drug abuse monitoring is an industry-initiated database known as RADARS (Researched Abuse, Diversion and Addiction-Related Surveillance), developed by Purdue Pharma to address diversion and abuse of OxyContin^®. RADARS' goal is to develop proactive, timely, geographically sensitive methods to detect abuse and diversion of OxyContin and other scheduled prescription medications.²⁵ This program acquires high-quality data from drug abuse experts, law enforcement agencies, and regional Poison Control Centers, covering more than 80% of the nation's zip codes. Regionally specific risk-minimization strategies are RADARS' next goal.

Conclusion
Clinicians who provide emergency care are in a position to slow, or even reverse, the escalating misuse of prescription medications by teenage patients. Primary care providers, too, are called on to keep abreast of emerging reports on this trend, to reconsider how they write prescriptions for psychotherapeutic agents, and to be vigilant to the signs of abuse in their adolescent patients.           

Dr. Goldstein serves on the advisory boards of Eli Lilly, Pfizer, GlaxoSmithKline, Novo Nordisk, Novartis, Procter & Gamble, Upsher Smith, and Wyeth; is a consultant for Cook ObGyn and Ackrad Labs (a Cooper Co.); and is a speaker for Eli Lilly, Novo Nordisk, Procter & Gamble, and Wyeth.

FRAX tool makes it possible to direct therapy to women who need it most

The World Health Organization (WHO) has finally released the FRAX risk-assessment tool, which enables clinicians to calculate a woman’s 10-year risk of developing a hip fracture or any major osteoporotic fracture. The tool (at www.shef.ac.uk/FRAX) should, ultimately, be available as part of all dual-energy x-ray absorptiometry (DXA) software so that, when bone mass is measured, the patient’s 10-year risk of hip fracture and overall osteoporotic fracture is reported along with bone density.

FRAX has different thresholds for treatment from country to country, depending on resources available. The tool uses age, weight, height, fracture history, parental fracture history, smoking status, glucocorticoid use, history of rheumatoid arthritis, alcohol consumption, and bone mineral density (BMD) of the femoral neck to determine a woman’s risk of fracture.

In many respects, this tool is a welcome change from the use of BMD measurements alone. I have long been concerned that many clinicians base treatment decisions solely on T-scores. Compare, for example, a 51-year-old newly menopausal woman who has a T-score of -2.0 at the hip with a 67-year-old woman who has the same T-score but who entered menopause at age 48 with a T-score of 0. These women have the same bone mass but very different degrees of bone quality and fracture risk.

Nevertheless, use of an arbitrary threshold (i.e., 3% risk of hip fracture and 20% risk of any osteoporotic fracture over the next 10 years) to determine who gets treatment has limitations. Virtually all bone experts would agree that a pharmacotherapeutic agent that reduces hip fracture by 50% is a “home run.” However, if we deny treatment until a woman’s 10-year risk of hip fracture reaches 3%, that is the same as saying that, for every 100 women who are treated, only 1.5 will fracture a hip instead of three. The health establishment may call that cost-effective, but it will not be acceptable to all patients.

Moreover, patients do not always understand the difference between risk reduction and prevention. It pays to remember these facts when counseling women.

NOF uses new risk-assessment tool to refine treatment guidelines

National Osteoporosis Foundation. Clinician’s Guide to Prevention and Treatment of Osteoporosis. Available at: www.nof.org/professionals/clinicians_guide_landing_pg.htm. Accessed October 8, 2008.

Dawson-Hughes B, Tosteson ANA, Melton LJ 3rd, et al, for the National Osteoporosis Foundation Guide Committee. Implications of absolute fracture risk assessment for osteoporosis practice guidelines in the USA. Osteoporos Int. 2008;19:449–458.

Siris E, Delmas PD. Assessment of 10-year absolute fracture risk: a new paradigm with worldwide application [editorial]. Osteoporos Int. 2008;19:383–384.

In February, the National Osteoporosis Foundation (NOF) updated its Clinician’s Guide to Prevention and Treatment of Osteoporosis, first published in 1999 and last revised (with minor changes) in 2003. The guidelines are available at www.nof.org/professionals/clinicians_guide_landing_pg.htm, along with a link to the WHO fracture risk-assessment tool, FRAX (www.shef.ac.uk/FRAX).

The previous NOF guidelines applied only to postmenopausal white women and based recommendations for intervention entirely on a patient’s T-score, with some modification of the level of intervention with the presence of clinical risk factors. The new guidelines make use of FRAX to focus recommendations on those at highest risk of fracture.

When to begin treatment

The new NOF guidelines advise the practitioner to:

• check for secondary causes of osteoporosis
• recommend BMD testing for women 65 years and older, for younger postmenopausal women when the risk-factor profile raises concern, and when there is a history of fracture
• initiate treatment in women who have had hip or vertebral fracture
• initiate treatment in women who have a DXA-based T-score ≤-2.5 at the femoral neck, total hip, or spine
• initiate treatment in postmenopausal women who have low bone mass (T-score >-2.5 but <-1.0) and a 10-year risk of hip fracture ≥3% or a 10-year probability of any major osteoporosis-related fracture >20%, based on the US-adopted WHO absolute fracture risk model
• measure BMD in DXA centers that use accepted quality assurance measures appropriate for monitoring bone loss every 2 years. For patients on pharmacotherapy, DXA BMD testing is typically performed 2 years after initiating therapy and at 2-year intervals thereafter.

New determinants of treatment

These guidelines replace earlier ones in which all postmenopausal women who had a T-score <-2.0 and those who had a T-score <-1.5 “with risk factors” were candidates for therapy.

Treatment shifts to older population

The new guidelines will probably shift some treatment from younger patients who have a modestly reduced BMD to an older population more likely to have a higher risk of fracture.

For example, consider the following patient—a 52-year-old Caucasian woman who:

• is 5 ft 4 in tall and weighs 130 lb
• has no family or personal history of fracture
• doesn’t smoke or use alcohol excessively
• doesn’t use glucocorticoids
• has no rheumatoid arthritis
• has a femoral-neck T-score of -2.1.

She has a 10-year risk of hip fracture of 1.5% and an 8.5% risk of any major osteoporotic fracture. Therefore, she is no longer a candidate for pharmacotherapy. (Under the previous guidelines, she was.)

Conversely, a 77-year-old woman who has the same height, weight, and history and a T-score of the femoral neck of -1.4, has a 10-year risk of hip fracture of 2.7% and a 23% risk of any major osteoporotic fracture. She is now a candidate for pharmacotherapy. (Under the previous guidelines, she was not a candidate.)

How to counsel the patient

The updated guidelines also include a range of recommendations on what information to include in patient counseling:

• the risk of osteoporosis and related fracture
• the need to get adequate calcium (1,200 mg/day) and vitamin D (800 to 1,000 IU/day)
• the importance of regular weight-bearing and muscle-strengthening exercise to reduce the risk of fall and fracture
• the need to avoid smoking and excess alcohol intake.

Oral bisphosphonates and atrial fibrillation—is there a link?

Heckbert SR, Li G, Cummings SR, Smith NL, Psaty BM. Use of alendronate and risk of incident atrial fibrillation in women. Arch Intern Med. 2008;168:826–831.

Black DM, Delmas PD, Eastell R, et al, for the HORIZON Pivotal Fracture Trial. Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. N Engl J Med. 2007;356:1809–1822.

Sørensen HT, Christensen S, Mehnert F, et al. Use of bisphosphonates among women and risk of atrial fibrillation and flutter: population-based case-control study. BMJ. 2008;336:813–816.

Postmenopausal women who have osteoporosis and are treated with once-yearly IV zoledronic acid have a higher risk of serious atrial fibrillation than nonusers do, according to a recent publication from the Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) trial. This finding was unexpected and had not been recognized previously. But does it indicate elevated risk with oral bisphosphonate use?

In the Fracture Intervention Trial (FIT) of alendronate for patients who have osteoporosis, the risk of serious atrial fibrillation was higher in alendronate recipients (1.5%, n=47) than in nonusers (1.0%, n=31).¹ However, this difference did not quite reach statistical significance (p=.07).

One case-control study points to 3% risk

The findings in regard to annual infusion of zoledronic acid prompted further evaluation of oral bisphosphonates. Heckbert and colleagues conducted a population-based case-control study at Group Health, an integrated health-care delivery system in Washington state, and estimated that 3% of incident atrial fibrillation might be explained by alendronate use.

Over 3 years, they identified 719 women who had a confirmed history of atrial fibrillation and 966 controls who did not, selected at random from the Group Health enrollment but matched for age and presence or absence of treated hypertension. More atrial fibrillation case patients than controls had ever used alendronate (6.5% [n=47] vs 4.1% [n=40]; p=.03).

Compared with never users of any bisphosphonate, those who had used alendronate had a higher risk of incident atrial fibrillation (odds ratio, 1.86; 95% confidence interval [CI], 1.09–3.15) after adjustment for matching variables, a diagnosis of osteoporosis, and history of cardiovascular disease.

Second case-control study finds no elevated risk

Sørensen and associates conducted a case-control study using medical databases in Denmark and concluded that there is no increased risk of atrial fibrillation and flutter with use of an oral bisphosphonate. They identified 13,586 patients who had atrial fibrillation and flutter and 65,054 patients who did not. Of these, 435 cases (3.2%) and 1,958 controls (2.9%) were current users of a bisphosphonate for osteoporosis. Etidronate and alendronate were used with almost the same frequency among cases and controls. The adjusted relative risk of atrial fibrillation with current use of a bisphosphonate, compared with nonuse, was 0.95 (95% CI, 0.84–1.07). New users had a relative risk of 0.75 (95% CI, 0.49–1.16), broadly similar to the estimate for continuing users (relative risk, 0.96; 95% CI, 0.85–1.09).

Bottom line? There is no compelling evidence that oral bisphosphonates cause an increase in atrial fibrillation. Even in the smaller case-control study that found a suggestion of elevated risk, the authors think that, at most, 3% of cases of atrial fibrillation might be attributable to oral alendronate.

An approach to osteonecrosis of the jaw among bisphosphonate users

Khan AA, Sándor GK, Dore E, et al. Canadian consensus practice guidelines for bisphosphonate-associated osteonecrosis of the jaw. J Rheumatol. 2008;35:1391–1397.

Since 2003, when the first reports of osteonecrosis of the jaw (ONJ) in patients receiving bisphosphonates were published, there has been widespread uncertainty among patients, physicians, and oral surgeons about diagnosis, identification of individuals at risk, prevention, and management of this troubling disorder (FIGURE 1).

To address these concerns, a multidisciplinary task force was convened by the Canadian Association of Oral and Maxillofacial Surgeons to systematically review the data. The task force included representatives from national and international societies representing the disciplines of oral surgery, dentistry, oral pathology, oral medicine, endocrinology, rheumatology, and oncology.

After reviewing the data, the task force made the following recommendations:

• In all oncology patients, a thorough dental examination, including radiographs, should be completed before IV bisphosphonate therapy is initiated. In this population, any invasive dental procedure is ideally completed before the start of high-dose bisphosphonate therapy. For nonurgent procedures in current users of bisphosphonate therapy, the drug should be discontinued 3 to 6 months before the dental treatment.
• Nononcology patients who are starting oral or IV bisphosphonate therapy do not require a dental examination beforehand, provided dental care is appropriate and oral hygiene is good.
• All patients taking a bisphosponate should be encouraged to stop smoking, limit alcohol use, and maintain good oral hygiene.
• Patients who have already been diagnosed with ONJ are best managed with supportive care, including pain control, treatment of secondary infection, and removal of necrotic debris. Aggressive debridement is contraindicated.

These recommendations are extremely helpful, especially because they make it clear that the average patient who has osteoporosis does not need to discontinue therapy before undergoing a dental procedure. Nor do patients who are about to embark on therapy—oral or IV—need any special dental examination as long as they maintain good oral hygiene and dental self-care.

Task force members were identified on the basis of their knowledge and expertise in the diagnosis and management of ONJ.

FIGURE 1 Osteonecrosis of the jaw

Blood flow to bone tissue is decreased in osteonecrosis of the jaw, leading to death of that tissue and the eventual collapse of bone.
ILLUSTRATIONS BY ROB FLEWELL FOR OBG MANAGEMENT

Distinctive fracture pattern linked to long-term alendronate

Neviaser AS, Lane JM, Lenart BA, Edobor-Osula F, Lorich DG. Low-energy femoral shaft fractures associated with alendronate use. J Orthop Trauma. 2008;22:346–350.

Patients who sustain a fracture of the proximal femoral shaft after minimal or no trauma are likely to be long-term users of alendronate, according to a recent study. These fractures are characterized by a simple transverse pattern, “beaking” of the cortex on one side, and hypertrophy of the diaphyseal cortex (FIGURE 2).

In a retrospective study, Neviaser and colleagues blindly reviewed both radiographs and medical records of 59 patients who had femoral-shaft fractures. Among the 25 users of alendronate, 19 had experienced low- or no-trauma fractures with this distinctive pattern; only one nonuser had (odds ratio, 139.33; 95% CI, 19.0–939.4; p<.0001). This fracture pattern was 98% specific to alendronate use.

The average duration of alendronate use in patients who had this fracture pattern was significantly longer than in those who did not (6.9 years vs 2.5 years, respectively; p=.002). Only one patient with this fracture pattern had been taking alendronate for less than 4 years.

FIGURE 2 Low-impact femoral fracture

Simple transverse fractures of the proximal femur after low or no trauma have been linked to long-term alendronate use.

First reports came in 2005

Neviaser and associates mention case reports from 2005 that described nine patients who sustained spontaneous nontraumatic, nonpathologic fractures while on prolonged alendronate therapy (>3 years).² In 2007, Goh and colleagues reported 13 subtrochanteric fractures, nine of which occurred in patients treated with alendronate. Of the nine, eight had a pattern associated with cortical hypertrophy.³

Cause-and-effect relationship remains unproven

The proximal femoral shaft is normally subjected to high stress, Neviaser and colleagues observe, and would not be expected to fracture from minimal trauma without underlying bone pathology.

In their study, 11 patients who had untreated osteoporosis had femoral-shaft fractures, but none had this specific pattern (unicortical beak, hypertrophied diaphyseal cortex). The authors hypothesize that adynamic metabolism from impaired resorption may be the underlying pathophysiology that leads to these fractures. They also point out that, although the pattern was 98% specific to alendronate users, this does not necessarily prove cause and effect—only an association. Clearly, further study is necessary.

Dr. Goldstein serves on the advisory boards of Eli Lilly, Pfizer, GlaxoSmithKline, Novo Nordisk, Novartis, Procter & Gamble, Upsher Smith, and Wyeth; is a consultant for Cook ObGyn and Ackrad Labs (a Cooper Co.); and is a speaker for Eli Lilly, Novo Nordisk, Procter & Gamble, and Wyeth.

FRAX tool makes it possible to direct therapy to women who need it most

The World Health Organization (WHO) has finally released the FRAX risk-assessment tool, which enables clinicians to calculate a woman’s 10-year risk of developing a hip fracture or any major osteoporotic fracture. The tool (at www.shef.ac.uk/FRAX) should, ultimately, be available as part of all dual-energy x-ray absorptiometry (DXA) software so that, when bone mass is measured, the patient’s 10-year risk of hip fracture and overall osteoporotic fracture is reported along with bone density.

FRAX has different thresholds for treatment from country to country, depending on resources available. The tool uses age, weight, height, fracture history, parental fracture history, smoking status, glucocorticoid use, history of rheumatoid arthritis, alcohol consumption, and bone mineral density (BMD) of the femoral neck to determine a woman’s risk of fracture.

In many respects, this tool is a welcome change from the use of BMD measurements alone. I have long been concerned that many clinicians base treatment decisions solely on T-scores. Compare, for example, a 51-year-old newly menopausal woman who has a T-score of -2.0 at the hip with a 67-year-old woman who has the same T-score but who entered menopause at age 48 with a T-score of 0. These women have the same bone mass but very different degrees of bone quality and fracture risk.

Nevertheless, use of an arbitrary threshold (i.e., 3% risk of hip fracture and 20% risk of any osteoporotic fracture over the next 10 years) to determine who gets treatment has limitations. Virtually all bone experts would agree that a pharmacotherapeutic agent that reduces hip fracture by 50% is a “home run.” However, if we deny treatment until a woman’s 10-year risk of hip fracture reaches 3%, that is the same as saying that, for every 100 women who are treated, only 1.5 will fracture a hip instead of three. The health establishment may call that cost-effective, but it will not be acceptable to all patients.

Moreover, patients do not always understand the difference between risk reduction and prevention. It pays to remember these facts when counseling women.

NOF uses new risk-assessment tool to refine treatment guidelines

National Osteoporosis Foundation. Clinician’s Guide to Prevention and Treatment of Osteoporosis. Available at: www.nof.org/professionals/clinicians_guide_landing_pg.htm. Accessed October 8, 2008.

Dawson-Hughes B, Tosteson ANA, Melton LJ 3rd, et al, for the National Osteoporosis Foundation Guide Committee. Implications of absolute fracture risk assessment for osteoporosis practice guidelines in the USA. Osteoporos Int. 2008;19:449–458.

Siris E, Delmas PD. Assessment of 10-year absolute fracture risk: a new paradigm with worldwide application [editorial]. Osteoporos Int. 2008;19:383–384.

In February, the National Osteoporosis Foundation (NOF) updated its Clinician’s Guide to Prevention and Treatment of Osteoporosis, first published in 1999 and last revised (with minor changes) in 2003. The guidelines are available at www.nof.org/professionals/clinicians_guide_landing_pg.htm, along with a link to the WHO fracture risk-assessment tool, FRAX (www.shef.ac.uk/FRAX).

The previous NOF guidelines applied only to postmenopausal white women and based recommendations for intervention entirely on a patient’s T-score, with some modification of the level of intervention with the presence of clinical risk factors. The new guidelines make use of FRAX to focus recommendations on those at highest risk of fracture.

When to begin treatment

The new NOF guidelines advise the practitioner to:

• check for secondary causes of osteoporosis
• recommend BMD testing for women 65 years and older, for younger postmenopausal women when the risk-factor profile raises concern, and when there is a history of fracture
• initiate treatment in women who have had hip or vertebral fracture
• initiate treatment in women who have a DXA-based T-score ≤-2.5 at the femoral neck, total hip, or spine
• initiate treatment in postmenopausal women who have low bone mass (T-score >-2.5 but <-1.0) and a 10-year risk of hip fracture ≥3% or a 10-year probability of any major osteoporosis-related fracture >20%, based on the US-adopted WHO absolute fracture risk model
• measure BMD in DXA centers that use accepted quality assurance measures appropriate for monitoring bone loss every 2 years. For patients on pharmacotherapy, DXA BMD testing is typically performed 2 years after initiating therapy and at 2-year intervals thereafter.

New determinants of treatment

These guidelines replace earlier ones in which all postmenopausal women who had a T-score <-2.0 and those who had a T-score <-1.5 “with risk factors” were candidates for therapy.

Treatment shifts to older population

The new guidelines will probably shift some treatment from younger patients who have a modestly reduced BMD to an older population more likely to have a higher risk of fracture.

For example, consider the following patient—a 52-year-old Caucasian woman who:

• is 5 ft 4 in tall and weighs 130 lb
• has no family or personal history of fracture
• doesn’t smoke or use alcohol excessively
• doesn’t use glucocorticoids
• has no rheumatoid arthritis
• has a femoral-neck T-score of -2.1.

She has a 10-year risk of hip fracture of 1.5% and an 8.5% risk of any major osteoporotic fracture. Therefore, she is no longer a candidate for pharmacotherapy. (Under the previous guidelines, she was.)

Conversely, a 77-year-old woman who has the same height, weight, and history and a T-score of the femoral neck of -1.4, has a 10-year risk of hip fracture of 2.7% and a 23% risk of any major osteoporotic fracture. She is now a candidate for pharmacotherapy. (Under the previous guidelines, she was not a candidate.)

How to counsel the patient

The updated guidelines also include a range of recommendations on what information to include in patient counseling:

• the risk of osteoporosis and related fracture
• the need to get adequate calcium (1,200 mg/day) and vitamin D (800 to 1,000 IU/day)
• the importance of regular weight-bearing and muscle-strengthening exercise to reduce the risk of fall and fracture
• the need to avoid smoking and excess alcohol intake.

Oral bisphosphonates and atrial fibrillation—is there a link?

Heckbert SR, Li G, Cummings SR, Smith NL, Psaty BM. Use of alendronate and risk of incident atrial fibrillation in women. Arch Intern Med. 2008;168:826–831.

Black DM, Delmas PD, Eastell R, et al, for the HORIZON Pivotal Fracture Trial. Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. N Engl J Med. 2007;356:1809–1822.

Sørensen HT, Christensen S, Mehnert F, et al. Use of bisphosphonates among women and risk of atrial fibrillation and flutter: population-based case-control study. BMJ. 2008;336:813–816.

Postmenopausal women who have osteoporosis and are treated with once-yearly IV zoledronic acid have a higher risk of serious atrial fibrillation than nonusers do, according to a recent publication from the Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) trial. This finding was unexpected and had not been recognized previously. But does it indicate elevated risk with oral bisphosphonate use?

In the Fracture Intervention Trial (FIT) of alendronate for patients who have osteoporosis, the risk of serious atrial fibrillation was higher in alendronate recipients (1.5%, n=47) than in nonusers (1.0%, n=31).¹ However, this difference did not quite reach statistical significance (p=.07).

One case-control study points to 3% risk

The findings in regard to annual infusion of zoledronic acid prompted further evaluation of oral bisphosphonates. Heckbert and colleagues conducted a population-based case-control study at Group Health, an integrated health-care delivery system in Washington state, and estimated that 3% of incident atrial fibrillation might be explained by alendronate use.

Over 3 years, they identified 719 women who had a confirmed history of atrial fibrillation and 966 controls who did not, selected at random from the Group Health enrollment but matched for age and presence or absence of treated hypertension. More atrial fibrillation case patients than controls had ever used alendronate (6.5% [n=47] vs 4.1% [n=40]; p=.03).

Compared with never users of any bisphosphonate, those who had used alendronate had a higher risk of incident atrial fibrillation (odds ratio, 1.86; 95% confidence interval [CI], 1.09–3.15) after adjustment for matching variables, a diagnosis of osteoporosis, and history of cardiovascular disease.

Second case-control study finds no elevated risk

Sørensen and associates conducted a case-control study using medical databases in Denmark and concluded that there is no increased risk of atrial fibrillation and flutter with use of an oral bisphosphonate. They identified 13,586 patients who had atrial fibrillation and flutter and 65,054 patients who did not. Of these, 435 cases (3.2%) and 1,958 controls (2.9%) were current users of a bisphosphonate for osteoporosis. Etidronate and alendronate were used with almost the same frequency among cases and controls. The adjusted relative risk of atrial fibrillation with current use of a bisphosphonate, compared with nonuse, was 0.95 (95% CI, 0.84–1.07). New users had a relative risk of 0.75 (95% CI, 0.49–1.16), broadly similar to the estimate for continuing users (relative risk, 0.96; 95% CI, 0.85–1.09).

Bottom line? There is no compelling evidence that oral bisphosphonates cause an increase in atrial fibrillation. Even in the smaller case-control study that found a suggestion of elevated risk, the authors think that, at most, 3% of cases of atrial fibrillation might be attributable to oral alendronate.

An approach to osteonecrosis of the jaw among bisphosphonate users

Khan AA, Sándor GK, Dore E, et al. Canadian consensus practice guidelines for bisphosphonate-associated osteonecrosis of the jaw. J Rheumatol. 2008;35:1391–1397.

Since 2003, when the first reports of osteonecrosis of the jaw (ONJ) in patients receiving bisphosphonates were published, there has been widespread uncertainty among patients, physicians, and oral surgeons about diagnosis, identification of individuals at risk, prevention, and management of this troubling disorder (FIGURE 1).

To address these concerns, a multidisciplinary task force was convened by the Canadian Association of Oral and Maxillofacial Surgeons to systematically review the data. The task force included representatives from national and international societies representing the disciplines of oral surgery, dentistry, oral pathology, oral medicine, endocrinology, rheumatology, and oncology.

After reviewing the data, the task force made the following recommendations:

• In all oncology patients, a thorough dental examination, including radiographs, should be completed before IV bisphosphonate therapy is initiated. In this population, any invasive dental procedure is ideally completed before the start of high-dose bisphosphonate therapy. For nonurgent procedures in current users of bisphosphonate therapy, the drug should be discontinued 3 to 6 months before the dental treatment.
• Nononcology patients who are starting oral or IV bisphosphonate therapy do not require a dental examination beforehand, provided dental care is appropriate and oral hygiene is good.
• All patients taking a bisphosponate should be encouraged to stop smoking, limit alcohol use, and maintain good oral hygiene.
• Patients who have already been diagnosed with ONJ are best managed with supportive care, including pain control, treatment of secondary infection, and removal of necrotic debris. Aggressive debridement is contraindicated.

These recommendations are extremely helpful, especially because they make it clear that the average patient who has osteoporosis does not need to discontinue therapy before undergoing a dental procedure. Nor do patients who are about to embark on therapy—oral or IV—need any special dental examination as long as they maintain good oral hygiene and dental self-care.

Task force members were identified on the basis of their knowledge and expertise in the diagnosis and management of ONJ.

FIGURE 1 Osteonecrosis of the jaw

Blood flow to bone tissue is decreased in osteonecrosis of the jaw, leading to death of that tissue and the eventual collapse of bone.
ILLUSTRATIONS BY ROB FLEWELL FOR OBG MANAGEMENT

Distinctive fracture pattern linked to long-term alendronate

Neviaser AS, Lane JM, Lenart BA, Edobor-Osula F, Lorich DG. Low-energy femoral shaft fractures associated with alendronate use. J Orthop Trauma. 2008;22:346–350.

Patients who sustain a fracture of the proximal femoral shaft after minimal or no trauma are likely to be long-term users of alendronate, according to a recent study. These fractures are characterized by a simple transverse pattern, “beaking” of the cortex on one side, and hypertrophy of the diaphyseal cortex (FIGURE 2).

In a retrospective study, Neviaser and colleagues blindly reviewed both radiographs and medical records of 59 patients who had femoral-shaft fractures. Among the 25 users of alendronate, 19 had experienced low- or no-trauma fractures with this distinctive pattern; only one nonuser had (odds ratio, 139.33; 95% CI, 19.0–939.4; p<.0001). This fracture pattern was 98% specific to alendronate use.

The average duration of alendronate use in patients who had this fracture pattern was significantly longer than in those who did not (6.9 years vs 2.5 years, respectively; p=.002). Only one patient with this fracture pattern had been taking alendronate for less than 4 years.

FIGURE 2 Low-impact femoral fracture

Simple transverse fractures of the proximal femur after low or no trauma have been linked to long-term alendronate use.

First reports came in 2005

Neviaser and associates mention case reports from 2005 that described nine patients who sustained spontaneous nontraumatic, nonpathologic fractures while on prolonged alendronate therapy (>3 years).² In 2007, Goh and colleagues reported 13 subtrochanteric fractures, nine of which occurred in patients treated with alendronate. Of the nine, eight had a pattern associated with cortical hypertrophy.³

Cause-and-effect relationship remains unproven

The proximal femoral shaft is normally subjected to high stress, Neviaser and colleagues observe, and would not be expected to fracture from minimal trauma without underlying bone pathology.

In their study, 11 patients who had untreated osteoporosis had femoral-shaft fractures, but none had this specific pattern (unicortical beak, hypertrophied diaphyseal cortex). The authors hypothesize that adynamic metabolism from impaired resorption may be the underlying pathophysiology that leads to these fractures. They also point out that, although the pattern was 98% specific to alendronate users, this does not necessarily prove cause and effect—only an association. Clearly, further study is necessary.

Dr. Goldstein serves on the advisory boards of Eli Lilly, Pfizer, GlaxoSmithKline, Novo Nordisk, Novartis, Procter & Gamble, Upsher Smith, and Wyeth; is a consultant for Cook ObGyn and Ackrad Labs (a Cooper Co.); and is a speaker for Eli Lilly, Novo Nordisk, Procter & Gamble, and Wyeth.

FRAX tool makes it possible to direct therapy to women who need it most

The World Health Organization (WHO) has finally released the FRAX risk-assessment tool, which enables clinicians to calculate a woman’s 10-year risk of developing a hip fracture or any major osteoporotic fracture. The tool (at www.shef.ac.uk/FRAX) should, ultimately, be available as part of all dual-energy x-ray absorptiometry (DXA) software so that, when bone mass is measured, the patient’s 10-year risk of hip fracture and overall osteoporotic fracture is reported along with bone density.

FRAX has different thresholds for treatment from country to country, depending on resources available. The tool uses age, weight, height, fracture history, parental fracture history, smoking status, glucocorticoid use, history of rheumatoid arthritis, alcohol consumption, and bone mineral density (BMD) of the femoral neck to determine a woman’s risk of fracture.

In many respects, this tool is a welcome change from the use of BMD measurements alone. I have long been concerned that many clinicians base treatment decisions solely on T-scores. Compare, for example, a 51-year-old newly menopausal woman who has a T-score of -2.0 at the hip with a 67-year-old woman who has the same T-score but who entered menopause at age 48 with a T-score of 0. These women have the same bone mass but very different degrees of bone quality and fracture risk.

Nevertheless, use of an arbitrary threshold (i.e., 3% risk of hip fracture and 20% risk of any osteoporotic fracture over the next 10 years) to determine who gets treatment has limitations. Virtually all bone experts would agree that a pharmacotherapeutic agent that reduces hip fracture by 50% is a “home run.” However, if we deny treatment until a woman’s 10-year risk of hip fracture reaches 3%, that is the same as saying that, for every 100 women who are treated, only 1.5 will fracture a hip instead of three. The health establishment may call that cost-effective, but it will not be acceptable to all patients.

Moreover, patients do not always understand the difference between risk reduction and prevention. It pays to remember these facts when counseling women.

NOF uses new risk-assessment tool to refine treatment guidelines

National Osteoporosis Foundation. Clinician’s Guide to Prevention and Treatment of Osteoporosis. Available at: www.nof.org/professionals/clinicians_guide_landing_pg.htm. Accessed October 8, 2008.

Dawson-Hughes B, Tosteson ANA, Melton LJ 3rd, et al, for the National Osteoporosis Foundation Guide Committee. Implications of absolute fracture risk assessment for osteoporosis practice guidelines in the USA. Osteoporos Int. 2008;19:449–458.

Siris E, Delmas PD. Assessment of 10-year absolute fracture risk: a new paradigm with worldwide application [editorial]. Osteoporos Int. 2008;19:383–384.

In February, the National Osteoporosis Foundation (NOF) updated its Clinician’s Guide to Prevention and Treatment of Osteoporosis, first published in 1999 and last revised (with minor changes) in 2003. The guidelines are available at www.nof.org/professionals/clinicians_guide_landing_pg.htm, along with a link to the WHO fracture risk-assessment tool, FRAX (www.shef.ac.uk/FRAX).

The previous NOF guidelines applied only to postmenopausal white women and based recommendations for intervention entirely on a patient’s T-score, with some modification of the level of intervention with the presence of clinical risk factors. The new guidelines make use of FRAX to focus recommendations on those at highest risk of fracture.

When to begin treatment

The new NOF guidelines advise the practitioner to:

• check for secondary causes of osteoporosis
• recommend BMD testing for women 65 years and older, for younger postmenopausal women when the risk-factor profile raises concern, and when there is a history of fracture
• initiate treatment in women who have had hip or vertebral fracture
• initiate treatment in women who have a DXA-based T-score ≤-2.5 at the femoral neck, total hip, or spine
• initiate treatment in postmenopausal women who have low bone mass (T-score >-2.5 but <-1.0) and a 10-year risk of hip fracture ≥3% or a 10-year probability of any major osteoporosis-related fracture >20%, based on the US-adopted WHO absolute fracture risk model
• measure BMD in DXA centers that use accepted quality assurance measures appropriate for monitoring bone loss every 2 years. For patients on pharmacotherapy, DXA BMD testing is typically performed 2 years after initiating therapy and at 2-year intervals thereafter.

New determinants of treatment

These guidelines replace earlier ones in which all postmenopausal women who had a T-score <-2.0 and those who had a T-score <-1.5 “with risk factors” were candidates for therapy.

Treatment shifts to older population

The new guidelines will probably shift some treatment from younger patients who have a modestly reduced BMD to an older population more likely to have a higher risk of fracture.

For example, consider the following patient—a 52-year-old Caucasian woman who:

• is 5 ft 4 in tall and weighs 130 lb
• has no family or personal history of fracture
• doesn’t smoke or use alcohol excessively
• doesn’t use glucocorticoids
• has no rheumatoid arthritis
• has a femoral-neck T-score of -2.1.

She has a 10-year risk of hip fracture of 1.5% and an 8.5% risk of any major osteoporotic fracture. Therefore, she is no longer a candidate for pharmacotherapy. (Under the previous guidelines, she was.)

Conversely, a 77-year-old woman who has the same height, weight, and history and a T-score of the femoral neck of -1.4, has a 10-year risk of hip fracture of 2.7% and a 23% risk of any major osteoporotic fracture. She is now a candidate for pharmacotherapy. (Under the previous guidelines, she was not a candidate.)

How to counsel the patient

The updated guidelines also include a range of recommendations on what information to include in patient counseling:

• the risk of osteoporosis and related fracture
• the need to get adequate calcium (1,200 mg/day) and vitamin D (800 to 1,000 IU/day)
• the importance of regular weight-bearing and muscle-strengthening exercise to reduce the risk of fall and fracture
• the need to avoid smoking and excess alcohol intake.

Oral bisphosphonates and atrial fibrillation—is there a link?

Heckbert SR, Li G, Cummings SR, Smith NL, Psaty BM. Use of alendronate and risk of incident atrial fibrillation in women. Arch Intern Med. 2008;168:826–831.

Black DM, Delmas PD, Eastell R, et al, for the HORIZON Pivotal Fracture Trial. Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. N Engl J Med. 2007;356:1809–1822.

Sørensen HT, Christensen S, Mehnert F, et al. Use of bisphosphonates among women and risk of atrial fibrillation and flutter: population-based case-control study. BMJ. 2008;336:813–816.

Postmenopausal women who have osteoporosis and are treated with once-yearly IV zoledronic acid have a higher risk of serious atrial fibrillation than nonusers do, according to a recent publication from the Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) trial. This finding was unexpected and had not been recognized previously. But does it indicate elevated risk with oral bisphosphonate use?

In the Fracture Intervention Trial (FIT) of alendronate for patients who have osteoporosis, the risk of serious atrial fibrillation was higher in alendronate recipients (1.5%, n=47) than in nonusers (1.0%, n=31).¹ However, this difference did not quite reach statistical significance (p=.07).

One case-control study points to 3% risk

The findings in regard to annual infusion of zoledronic acid prompted further evaluation of oral bisphosphonates. Heckbert and colleagues conducted a population-based case-control study at Group Health, an integrated health-care delivery system in Washington state, and estimated that 3% of incident atrial fibrillation might be explained by alendronate use.

Over 3 years, they identified 719 women who had a confirmed history of atrial fibrillation and 966 controls who did not, selected at random from the Group Health enrollment but matched for age and presence or absence of treated hypertension. More atrial fibrillation case patients than controls had ever used alendronate (6.5% [n=47] vs 4.1% [n=40]; p=.03).

Compared with never users of any bisphosphonate, those who had used alendronate had a higher risk of incident atrial fibrillation (odds ratio, 1.86; 95% confidence interval [CI], 1.09–3.15) after adjustment for matching variables, a diagnosis of osteoporosis, and history of cardiovascular disease.

Second case-control study finds no elevated risk

Sørensen and associates conducted a case-control study using medical databases in Denmark and concluded that there is no increased risk of atrial fibrillation and flutter with use of an oral bisphosphonate. They identified 13,586 patients who had atrial fibrillation and flutter and 65,054 patients who did not. Of these, 435 cases (3.2%) and 1,958 controls (2.9%) were current users of a bisphosphonate for osteoporosis. Etidronate and alendronate were used with almost the same frequency among cases and controls. The adjusted relative risk of atrial fibrillation with current use of a bisphosphonate, compared with nonuse, was 0.95 (95% CI, 0.84–1.07). New users had a relative risk of 0.75 (95% CI, 0.49–1.16), broadly similar to the estimate for continuing users (relative risk, 0.96; 95% CI, 0.85–1.09).

Bottom line? There is no compelling evidence that oral bisphosphonates cause an increase in atrial fibrillation. Even in the smaller case-control study that found a suggestion of elevated risk, the authors think that, at most, 3% of cases of atrial fibrillation might be attributable to oral alendronate.

An approach to osteonecrosis of the jaw among bisphosphonate users

Khan AA, Sándor GK, Dore E, et al. Canadian consensus practice guidelines for bisphosphonate-associated osteonecrosis of the jaw. J Rheumatol. 2008;35:1391–1397.

Since 2003, when the first reports of osteonecrosis of the jaw (ONJ) in patients receiving bisphosphonates were published, there has been widespread uncertainty among patients, physicians, and oral surgeons about diagnosis, identification of individuals at risk, prevention, and management of this troubling disorder (FIGURE 1).

To address these concerns, a multidisciplinary task force was convened by the Canadian Association of Oral and Maxillofacial Surgeons to systematically review the data. The task force included representatives from national and international societies representing the disciplines of oral surgery, dentistry, oral pathology, oral medicine, endocrinology, rheumatology, and oncology.

After reviewing the data, the task force made the following recommendations:

• In all oncology patients, a thorough dental examination, including radiographs, should be completed before IV bisphosphonate therapy is initiated. In this population, any invasive dental procedure is ideally completed before the start of high-dose bisphosphonate therapy. For nonurgent procedures in current users of bisphosphonate therapy, the drug should be discontinued 3 to 6 months before the dental treatment.
• Nononcology patients who are starting oral or IV bisphosphonate therapy do not require a dental examination beforehand, provided dental care is appropriate and oral hygiene is good.
• All patients taking a bisphosponate should be encouraged to stop smoking, limit alcohol use, and maintain good oral hygiene.
• Patients who have already been diagnosed with ONJ are best managed with supportive care, including pain control, treatment of secondary infection, and removal of necrotic debris. Aggressive debridement is contraindicated.

These recommendations are extremely helpful, especially because they make it clear that the average patient who has osteoporosis does not need to discontinue therapy before undergoing a dental procedure. Nor do patients who are about to embark on therapy—oral or IV—need any special dental examination as long as they maintain good oral hygiene and dental self-care.

Task force members were identified on the basis of their knowledge and expertise in the diagnosis and management of ONJ.

FIGURE 1 Osteonecrosis of the jaw

Blood flow to bone tissue is decreased in osteonecrosis of the jaw, leading to death of that tissue and the eventual collapse of bone.
ILLUSTRATIONS BY ROB FLEWELL FOR OBG MANAGEMENT

Distinctive fracture pattern linked to long-term alendronate

Neviaser AS, Lane JM, Lenart BA, Edobor-Osula F, Lorich DG. Low-energy femoral shaft fractures associated with alendronate use. J Orthop Trauma. 2008;22:346–350.

Patients who sustain a fracture of the proximal femoral shaft after minimal or no trauma are likely to be long-term users of alendronate, according to a recent study. These fractures are characterized by a simple transverse pattern, “beaking” of the cortex on one side, and hypertrophy of the diaphyseal cortex (FIGURE 2).

In a retrospective study, Neviaser and colleagues blindly reviewed both radiographs and medical records of 59 patients who had femoral-shaft fractures. Among the 25 users of alendronate, 19 had experienced low- or no-trauma fractures with this distinctive pattern; only one nonuser had (odds ratio, 139.33; 95% CI, 19.0–939.4; p<.0001). This fracture pattern was 98% specific to alendronate use.

The average duration of alendronate use in patients who had this fracture pattern was significantly longer than in those who did not (6.9 years vs 2.5 years, respectively; p=.002). Only one patient with this fracture pattern had been taking alendronate for less than 4 years.

FIGURE 2 Low-impact femoral fracture

Simple transverse fractures of the proximal femur after low or no trauma have been linked to long-term alendronate use.

First reports came in 2005

Neviaser and associates mention case reports from 2005 that described nine patients who sustained spontaneous nontraumatic, nonpathologic fractures while on prolonged alendronate therapy (>3 years).² In 2007, Goh and colleagues reported 13 subtrochanteric fractures, nine of which occurred in patients treated with alendronate. Of the nine, eight had a pattern associated with cortical hypertrophy.³

Cause-and-effect relationship remains unproven

The proximal femoral shaft is normally subjected to high stress, Neviaser and colleagues observe, and would not be expected to fracture from minimal trauma without underlying bone pathology.

In their study, 11 patients who had untreated osteoporosis had femoral-shaft fractures, but none had this specific pattern (unicortical beak, hypertrophied diaphyseal cortex). The authors hypothesize that adynamic metabolism from impaired resorption may be the underlying pathophysiology that leads to these fractures. They also point out that, although the pattern was 98% specific to alendronate users, this does not necessarily prove cause and effect—only an association. Clearly, further study is necessary.

The author reports that he is president of Shoulder Dystocia Litigation Consultants, working with defense lawyers, insurance company case managers, and hospital risk managers in shoulder dystocia-related injuries and litigation.

CASE

You are a defendant in a malpractice case, and your lawyer has just finished questioning you—the “direct” part of your testimony. She asked you straightforward questions and you answered fully and without interruption. You were able to explain, at length, your account of what happened during the events in question. This is the first time you’ve been sued; you’re nervous, but things have gone well so far, you feel.

Cross-examination by the plaintiff’s attorney comes next. He starts aggressively, questioning the quality of your training and experience. Have any disciplinary actions ever been taken against you by your hospital or the state licensing board? Did you have specialty fellowship training? He makes it seem that, if you didn’t, you have no business taking care of patients.

He drills in: Have you taken courses in the specific area at question in the case—as if whole courses are given routinely on the narrow topics that are often the subject of litigation, whether shoulder dystocia, placental abruption, damage to a ureter, or other bad outcomes.

He moves on to ask about details of the case but cuts you off when you try to flesh out your answers. He admonishes you: Listen to the question and answer “Yes” or “No”!

He begins to raise his voice.

The attorney attacks your notes in the medical record; he makes them seem incomplete and inadequate. He tells members of the jury that they can assume that you did not take a specific action, despite your claim to the contrary, because it’s not in the record: “If it wasn’t written down, it didn’t happen.”

His demeanor becomes more confrontational. The increasingly abusive questioning goes on and on, and your sense that things are going well has evaporated.

How, you ask yourself as the assault continues, did all this rancor and accusation come on so fast and so unexpectedly?

This scenario, or versions close to it, occurs all too often to physicians in courtrooms across the United States. Defendant physicians who are vilified and goaded feel angry, frustrated, and helpless. No wonder—the courtroom environment is alien to us. We trained for years to become competent, knowledgeable practitioners of our specialty; we work hard every day to provide the best possible care; and we diligently keep up with advances in ObGyn medicine by reading the literature and attending continuing medical education conferences. But in the courtroom, attorneys make a pointed attempt to paint us as incompetent and uncaring—even malicious.

Moreover, customary rules of argumentation don’t apply. We can’t answer questions fully or correct misstatements that are implicit in certain questions. Judges often limit what we can say and what the jury is allowed to hear. Not only is the medical care we gave questioned—we are subject to attempts to discredit us personally. We’re asked questions about the most private aspects of our life: “What’s your income?” “Why were you divorced?” “What is the financial arrangement between you and your partners?” “Are you seeing—have you ever seen—a psychiatrist?”

The playing field has been set at a tilt

Perhaps your greatest disadvantage when you are sued is that, most likely, this is going to be your first time in a courtroom. You haven’t had the chance to become familiar with the venue—the courtroom—or the tactics of cross-examination used by plaintiff attorneys.

Combine an accusation of malpractice and the need to defend yourself in an alien environment with rules made by and favoring lawyers that are foreign to you and that you cannot control—what a daunting prospect! Plaintiff attorneys take advantage of the situation to prey on defendants.

There are ways to defend yourself!

Did you go into an operating room or a delivery room for the first time without preparation or training? No! Likewise, don’t go into a courtroom unprepared.

You may be surprised to learn that you do have advantages over lawyers for plaintiffs:

• You know more medicine than they ever will, no matter how many malpractice cases they have tried.
  
• You were there when the actions under dispute took place. You can speak from direct experience about those actions, with authority, as a knowledgeable eyewitness.
  
• Despite how it may appear, you have the right to defend your actions and your statements vigorously.
  

Plaintiff lawyers routinely employ a standard repertoire of tricks and traps, which I have seen used time and again. My goals here are to describe them to you so that you can see them coming and to tell you how to defend yourself against them. You’ll then be in a position to counter these tricks by 1) giving them a name, 2) confronting the lawyer—in front of the judge and the jury—with what he or she is attempting to do, and 3) employing defensive tactics.

A note about language in this article: For simplicity, when I say “he” when referring to a physician or lawyer, I mean “he” or “she.” And I mean “plaintiff attorney” when I say just “lawyer” or “attorney,” unless I am referring explicitly to your (the defendant’s) representation.

First, three little words to set the stage

Always keep in mind that, for you to be found guilty of malpractice, the plaintiff attorney has to prove beyond a reasonable doubt that the actions you did, or did not, take violated what is known in the medicolegal arena as standard of care. Because this standard is what you are being judged against, it is vital that you understand—and, in turn, that the jury understands—exactly what the term means.

Standard of care is defined as care generally given by well-trained physicians in your own specialty under similar circumstances. Standard of care does not mean “ideal” care, as may be recommended in a medical textbook or other kinds of professional communication. The standard of care is, essentially, generally accepted practice: The level and degree of care most often used by your contemporary peers. You are guilty of malpractice only if the care that you gave fell below the care that would generally have been given to a patient by others, in your specialty, under the circumstances you faced.

Inside an attorney’s bulging bag of tricks

What tactics might an attorney use to harass and intimidate you?

He’ll bully you. Imagine this: A plaintiff lawyer is brought into a surgical suite for the first time. He is asked to participate in an operation but isn’t allowed to speak unless spoken to. He is allowed to answer direct questions only in a format dictated by the senior surgeon. That lawyer would not know what was going on, would be continuously on the defensive, and would feel totally in over his head—if he didn’t faint first!

What I just described is the equivalent of what happens to you in a courtroom. An attorney is allowed great leeway over the types of questions that he can ask and the manner in which they can be posed. He often attempts to intimidate you with harsh language, a raised voice, physical gestures, and sarcasm. He might ask questions with implied premises that aren’t true. His behavior might be confrontational. He might try to cut you off. And he might insist that your answers be solely “Yes” or “No.”

He’ll troll through your CV. Every educational activity in which you have participated, and every professional position you have ever held, is subject to inquiry. In addition to being asked if you have ever been sued or had disciplinary action taken against you, an attorney will review your education, step by step. He might imply that, if you were educated abroad or went to a less-than-well-known medical school, you are poorly trained or somehow not “of high quality.” He will likely ask you how many times you took the specialty board exam before you passed it. You might even be asked how high you finished in your medical school class, or if you were given your first choice of residency program in a match.

He’ll create artificial standards in the minds of jury members. You might be asked if you have published in your field or if you have an academic appointment—the assumption being that, if your answer is “No,” your opinion about issues being discussed at the trial are not as authoritative as (he will claim) those of the plaintiff’s expert witness, who may be well known in the specialty.

He’ll take statements out of context. Articles that you published (even if years ago), previous depositions or trial testimony you have given, and even PowerPoint presentations you made to nurses on your labor and delivery unit may be probed and quoted. Usually, the attorney presents only brief snippets of these works, which are likely to be read to the jury out of context.

He’ll ask for specific references. Often, when an attorney asks about facts that you’ve mentioned or opinions you hold regarding issues that bear on the case in your trial, he will attempt to embarrass you by asking you to name the specific text, article, or author from which you obtained that information. Here’s an example: You know that the threshold for macrosomia in a shoulder dystocia case is 4,500 g, and that random late decelerations in a fetal monitor strip marked by otherwise excellent variability do not demand immediate C-section—but you may not be able to cite, off the top of your head, exactly in which textbook or journal article you read this or the information can be found. You might also be asked what an ACOG Bulletin or your hospital’s policy book says about a certain subject or aspect of care.

He’ll drag in the medical record and informed consent. An attorney might try to convince a jury that “if it isn’t written down, it didn’t happen.” He might cite a lack of an extensive written description of what occurred during the events in question as evidence of sloppy charting or poor care. He might claim that lack of a detailed note replicating a conversation that took place during the consent process displays a lack of concern for the patient’s right to know.

He’ll imply the existence of a standard of care. Lawyers often try to convince a jury that a defendant physician committed malpractice by claiming that she should have taken certain actions, when, in fact, these actions would have been unnecessary or inappropriate under the circumstances. Examples: Asking whether clinical pelvimetry was documented in the chart of a multiparous woman who came in actively laboring, or asking if fundal height was measured in the office during a patient’s last three prenatal visits.

Here are two other examples:

• In a case involving vacuum extraction delivery: “Doctor, have you ever read the vacuum device’s product safety manual?”
  
• When a plaintiff has testified that she told you at her first prenatal visit that her previous pregnancies were uncomplicated: “Did you call for, or read, the record from any of her previous pregnancies?”
  

He’ll create a false impression. A common attorney’s tactic is to pose questions to you that imply that certain things are true, when they are not. A common example of this tactic occurs in shoulder dystocia cases, when putative risk factors are addressed.

Consensus in the shoulder dystocia literature is that there are only three or four statistically consistent risk factors for this condition: shoulder dystocia in a prior delivery, macrosomia, gestational diabetes, and (possibly) mid-vacuum or forceps delivery. Often, however, attorneys imply to the jury that many other risk factors exist—and that your patient had any number of them and that you should have been aware of them.

You might be asked if your patient underwent oxytocin induction, had a long first stage of labor, had an epidural anesthetic placed, or was post-dates—none of which have a proven association with shoulder dystocia. You’ll be given little leeway, in answering questions posed to you, to try to refute the lawyer’s false assumptions. The impression may thus be left by this concatenation of nonproven factors that your patient was at high risk of shoulder dystocia, that this was foreseeable, and that you were negligent in not having performed a C-section to prevent it.

Likewise, lawyers often deliberately misuse statistics—such as when they discuss sonographic variability in the estimation of fetal weight: “Don’t you acknowledge, Doctor, that ultrasound estimates of fetal weight can vary by 15% of the actual weight? So why didn’t you take into account that the 4,300 g estimate you were given could, in fact, have been as high as 4,700 g?” Given the rules that restrict how you can answer, you are rarely allowed to explain to a jury that, first, the 15% variability applies only to a baby whose weight is more than one standard deviation from average and, second, the weight-estimate variability can be on the low side as well as on the high side.

How should you respond to interrogation?

Although you face disadvantages as a defendant physician in a courtroom, there are ways to fight back—to stick up for yourself and respond to the techniques that attorneys perpetrate. You aren’t as defenseless as it might appear!

Never allow an attorney to bully you in the courtroom or at a deposition. If the attorney begins to use such behavior, call it by its name and demand that it be stopped. Your lawyer will likely have raised an objection before you do; if she does not, protest such inappropriate behavior yourself. Never allow an attorney who is questioning you to raise his voice or speak to you sarcastically or rudely.

You don’t necessarily have to play by the rules for answering questions, despite any admonition by a plaintiff lawyer that you do so. Unless you are advised otherwise by the judge or by your lawyer, answer questions the way you want to, as long as your answer is a reply to the question that was asked. You are never obliged to answer a question with just “Yes” or “No.” If an attorney tries to impose such a limitation on you, declare that you cannot answer the question under those terms. If your answers are being cut off, don’t hesitate to tell the jury that you are not being allowed to tell the whole story.

If questions posed to you contain false premises, point that out. For example, you might be asked, “Given the obvious fetal distress that was present, why did you apply forceps?” If there was no fetal distress, or if that is one of the issues in dispute, you can respond that the question contains incorrect information or an unwarranted assumption, and therefore cannot be answered as asked.

Prepare to be asked about your background and training. Have your lawyer ask you preemptively, during her questioning, about anything in your professional life that might appear the least bit negative. This allows you to explain the matter fully without being cut off by the plaintiff attorney. Have your lawyer ask questions that show how your background and training compare with those of other physicians in your hospital and community. If you have been sued in the past, have your lawyer ask you about how many times an ObGyn is sued, on average, in her career (“three” is the answer), and use this fact to show the jury that being sued is not an anomaly but the rule in ObGyn practice.

Never answer a question about something you wrote in the past or about prior testimony without demanding to read it yourself, on the stand, in context. (The same is true for quotations from the medical literature read to you by the plaintiff attorney: You have a right to know the source and date of publication of quoted material, and you should insist on being able to read the quotation for yourself so that you can understand it in context.)

If asked from what text or article you learned a specific piece of information, point out the absurdity of being asked to remember such specifics from among the tens of thousands of things you have learned and read over your training and career.

When asked about your notes in the medical record and why you did or did not write a particular item, point out that the medical record is not a document that is intended to be used to prosecute or defend medical cases years down the road but rather is meant to convey important clinical information among health-care providers. Tell the jury what sorts of notes are routinely written and how much information is generally put into a note. If the notes you wrote are appropriate, even if brief, be sure and explain to the jury that what you did is, in fact, the standard of care—not an idealized conception taken from a textbook or an expert’s talk as to how notes should be written. Don’t agree with a lawyer’s contention that “if it isn’t written down, it didn’t happen.” That may be a lawyer’s rule; it is not a medical rule. Do not let the jury go into the jury room thinking that it is.

Know the specifics of your case. It is true that, as a defendant witness, several factors are out of your control. But don’t forget what you do have under your control: Knowledge of obstetrics and gynecology and experience in the field. You know the medical issues involved in the litigation better than anyone else in the courtroom.

Still, do your homework. Make sure that you know the specifics of your case, inside and out. Study the medical record of the case carefully and read all the depositions your lawyer provides for you. Know what the relevant ACOG Bulletin, major texts (such as Williams Obstetrics), and the literature say about the issues that are involved. Know who the experts are in this area of care and be prepared to quote pertinent articles that they have written. Work to never let yourself be surprised by the facts of the case or the medical information presented by the plaintiff’s side. Treat your testimony as a very important final examination. Do that, and you will be in an excellent position to successfully answer questions and refute incorrect statements.

Preempt questions about informed consent. Ask your lawyer to have you explain, during the direct portion of your testimony, about informed consent conversations, how they are usually held, and how they are documented. Tell the jury the difference between a calm consent discussion in the office before a routine medical procedure and a consent discussion in an urgent situation. By the way: The general rule about informed consent is that a physician is obliged to discuss with a patient any significant risk greater than 1%. This is a documented standard.¹

Don’t let incorrect claims go unchallenged. Consider this scenario: A plaintiff attorney states that, given the circumstances of a certain clinical situation, you should have taken a particular action. This is often the case in fetal asphyxia cases, when experts for the plaintiff often testify that they can tell, from looking at the fetal heart rate monitoring strip, the exact moment at which a fetus was in trouble and should have been delivered by C-section. Consider having your lawyer issue an in-court challenge to an expert witness who makes such a claim to perform a blind reading of five fetal monitor strips for which the outcomes are known and to see if his predictions are correct. A plaintiff attorney will never take you up on such a challenge—and that refusal will be noted and appreciated by the jury.

This isn’t your backyard but you can play here

Amid what is often hostile treatment, it can be difficult to remember who you are: A highly trained, hard-working physician who has given most of your professional life to providing superb care. A plaintiff attorney is out to make you appear incompetent, and his motive is clear: He’ll earn one-quarter to one-third of any award that he wins for his client.

You are obviously convinced of the correctness of what you did in the case—or you wouldn’t have gone to court to defend yourself. You know the medicine better than the plaintiff lawyer does and, having been the caregiver, you can discuss all aspects of the case with much greater authority than he ever can. His only advantage? You’re in his backyard and he controls many of the rules.

But if you’re meticulously prepared, if you work with your lawyer and follow her advice, and if you are aware of the plaintiff attorneys’ tricks and techniques that I’ve described, you can neutralize much of the disadvantage you’re under in the legal system and defend your case on a greatly leveled playing field.

The author reports that he is president of Shoulder Dystocia Litigation Consultants, working with defense lawyers, insurance company case managers, and hospital risk managers in shoulder dystocia-related injuries and litigation.

CASE

You are a defendant in a malpractice case, and your lawyer has just finished questioning you—the “direct” part of your testimony. She asked you straightforward questions and you answered fully and without interruption. You were able to explain, at length, your account of what happened during the events in question. This is the first time you’ve been sued; you’re nervous, but things have gone well so far, you feel.

Cross-examination by the plaintiff’s attorney comes next. He starts aggressively, questioning the quality of your training and experience. Have any disciplinary actions ever been taken against you by your hospital or the state licensing board? Did you have specialty fellowship training? He makes it seem that, if you didn’t, you have no business taking care of patients.

He drills in: Have you taken courses in the specific area at question in the case—as if whole courses are given routinely on the narrow topics that are often the subject of litigation, whether shoulder dystocia, placental abruption, damage to a ureter, or other bad outcomes.

He moves on to ask about details of the case but cuts you off when you try to flesh out your answers. He admonishes you: Listen to the question and answer “Yes” or “No”!

He begins to raise his voice.

The attorney attacks your notes in the medical record; he makes them seem incomplete and inadequate. He tells members of the jury that they can assume that you did not take a specific action, despite your claim to the contrary, because it’s not in the record: “If it wasn’t written down, it didn’t happen.”

His demeanor becomes more confrontational. The increasingly abusive questioning goes on and on, and your sense that things are going well has evaporated.

How, you ask yourself as the assault continues, did all this rancor and accusation come on so fast and so unexpectedly?

This scenario, or versions close to it, occurs all too often to physicians in courtrooms across the United States. Defendant physicians who are vilified and goaded feel angry, frustrated, and helpless. No wonder—the courtroom environment is alien to us. We trained for years to become competent, knowledgeable practitioners of our specialty; we work hard every day to provide the best possible care; and we diligently keep up with advances in ObGyn medicine by reading the literature and attending continuing medical education conferences. But in the courtroom, attorneys make a pointed attempt to paint us as incompetent and uncaring—even malicious.

Moreover, customary rules of argumentation don’t apply. We can’t answer questions fully or correct misstatements that are implicit in certain questions. Judges often limit what we can say and what the jury is allowed to hear. Not only is the medical care we gave questioned—we are subject to attempts to discredit us personally. We’re asked questions about the most private aspects of our life: “What’s your income?” “Why were you divorced?” “What is the financial arrangement between you and your partners?” “Are you seeing—have you ever seen—a psychiatrist?”

The playing field has been set at a tilt

Perhaps your greatest disadvantage when you are sued is that, most likely, this is going to be your first time in a courtroom. You haven’t had the chance to become familiar with the venue—the courtroom—or the tactics of cross-examination used by plaintiff attorneys.

Combine an accusation of malpractice and the need to defend yourself in an alien environment with rules made by and favoring lawyers that are foreign to you and that you cannot control—what a daunting prospect! Plaintiff attorneys take advantage of the situation to prey on defendants.

There are ways to defend yourself!

Did you go into an operating room or a delivery room for the first time without preparation or training? No! Likewise, don’t go into a courtroom unprepared.

You may be surprised to learn that you do have advantages over lawyers for plaintiffs:

• You know more medicine than they ever will, no matter how many malpractice cases they have tried.
  
• You were there when the actions under dispute took place. You can speak from direct experience about those actions, with authority, as a knowledgeable eyewitness.
  
• Despite how it may appear, you have the right to defend your actions and your statements vigorously.
  

Plaintiff lawyers routinely employ a standard repertoire of tricks and traps, which I have seen used time and again. My goals here are to describe them to you so that you can see them coming and to tell you how to defend yourself against them. You’ll then be in a position to counter these tricks by 1) giving them a name, 2) confronting the lawyer—in front of the judge and the jury—with what he or she is attempting to do, and 3) employing defensive tactics.

A note about language in this article: For simplicity, when I say “he” when referring to a physician or lawyer, I mean “he” or “she.” And I mean “plaintiff attorney” when I say just “lawyer” or “attorney,” unless I am referring explicitly to your (the defendant’s) representation.

First, three little words to set the stage

Always keep in mind that, for you to be found guilty of malpractice, the plaintiff attorney has to prove beyond a reasonable doubt that the actions you did, or did not, take violated what is known in the medicolegal arena as standard of care. Because this standard is what you are being judged against, it is vital that you understand—and, in turn, that the jury understands—exactly what the term means.

Standard of care is defined as care generally given by well-trained physicians in your own specialty under similar circumstances. Standard of care does not mean “ideal” care, as may be recommended in a medical textbook or other kinds of professional communication. The standard of care is, essentially, generally accepted practice: The level and degree of care most often used by your contemporary peers. You are guilty of malpractice only if the care that you gave fell below the care that would generally have been given to a patient by others, in your specialty, under the circumstances you faced.

Inside an attorney’s bulging bag of tricks

What tactics might an attorney use to harass and intimidate you?

He’ll bully you. Imagine this: A plaintiff lawyer is brought into a surgical suite for the first time. He is asked to participate in an operation but isn’t allowed to speak unless spoken to. He is allowed to answer direct questions only in a format dictated by the senior surgeon. That lawyer would not know what was going on, would be continuously on the defensive, and would feel totally in over his head—if he didn’t faint first!

What I just described is the equivalent of what happens to you in a courtroom. An attorney is allowed great leeway over the types of questions that he can ask and the manner in which they can be posed. He often attempts to intimidate you with harsh language, a raised voice, physical gestures, and sarcasm. He might ask questions with implied premises that aren’t true. His behavior might be confrontational. He might try to cut you off. And he might insist that your answers be solely “Yes” or “No.”

He’ll troll through your CV. Every educational activity in which you have participated, and every professional position you have ever held, is subject to inquiry. In addition to being asked if you have ever been sued or had disciplinary action taken against you, an attorney will review your education, step by step. He might imply that, if you were educated abroad or went to a less-than-well-known medical school, you are poorly trained or somehow not “of high quality.” He will likely ask you how many times you took the specialty board exam before you passed it. You might even be asked how high you finished in your medical school class, or if you were given your first choice of residency program in a match.

He’ll create artificial standards in the minds of jury members. You might be asked if you have published in your field or if you have an academic appointment—the assumption being that, if your answer is “No,” your opinion about issues being discussed at the trial are not as authoritative as (he will claim) those of the plaintiff’s expert witness, who may be well known in the specialty.

He’ll take statements out of context. Articles that you published (even if years ago), previous depositions or trial testimony you have given, and even PowerPoint presentations you made to nurses on your labor and delivery unit may be probed and quoted. Usually, the attorney presents only brief snippets of these works, which are likely to be read to the jury out of context.

He’ll ask for specific references. Often, when an attorney asks about facts that you’ve mentioned or opinions you hold regarding issues that bear on the case in your trial, he will attempt to embarrass you by asking you to name the specific text, article, or author from which you obtained that information. Here’s an example: You know that the threshold for macrosomia in a shoulder dystocia case is 4,500 g, and that random late decelerations in a fetal monitor strip marked by otherwise excellent variability do not demand immediate C-section—but you may not be able to cite, off the top of your head, exactly in which textbook or journal article you read this or the information can be found. You might also be asked what an ACOG Bulletin or your hospital’s policy book says about a certain subject or aspect of care.

He’ll drag in the medical record and informed consent. An attorney might try to convince a jury that “if it isn’t written down, it didn’t happen.” He might cite a lack of an extensive written description of what occurred during the events in question as evidence of sloppy charting or poor care. He might claim that lack of a detailed note replicating a conversation that took place during the consent process displays a lack of concern for the patient’s right to know.

He’ll imply the existence of a standard of care. Lawyers often try to convince a jury that a defendant physician committed malpractice by claiming that she should have taken certain actions, when, in fact, these actions would have been unnecessary or inappropriate under the circumstances. Examples: Asking whether clinical pelvimetry was documented in the chart of a multiparous woman who came in actively laboring, or asking if fundal height was measured in the office during a patient’s last three prenatal visits.

Here are two other examples:

• In a case involving vacuum extraction delivery: “Doctor, have you ever read the vacuum device’s product safety manual?”
  
• When a plaintiff has testified that she told you at her first prenatal visit that her previous pregnancies were uncomplicated: “Did you call for, or read, the record from any of her previous pregnancies?”
  

He’ll create a false impression. A common attorney’s tactic is to pose questions to you that imply that certain things are true, when they are not. A common example of this tactic occurs in shoulder dystocia cases, when putative risk factors are addressed.

Consensus in the shoulder dystocia literature is that there are only three or four statistically consistent risk factors for this condition: shoulder dystocia in a prior delivery, macrosomia, gestational diabetes, and (possibly) mid-vacuum or forceps delivery. Often, however, attorneys imply to the jury that many other risk factors exist—and that your patient had any number of them and that you should have been aware of them.

You might be asked if your patient underwent oxytocin induction, had a long first stage of labor, had an epidural anesthetic placed, or was post-dates—none of which have a proven association with shoulder dystocia. You’ll be given little leeway, in answering questions posed to you, to try to refute the lawyer’s false assumptions. The impression may thus be left by this concatenation of nonproven factors that your patient was at high risk of shoulder dystocia, that this was foreseeable, and that you were negligent in not having performed a C-section to prevent it.

Likewise, lawyers often deliberately misuse statistics—such as when they discuss sonographic variability in the estimation of fetal weight: “Don’t you acknowledge, Doctor, that ultrasound estimates of fetal weight can vary by 15% of the actual weight? So why didn’t you take into account that the 4,300 g estimate you were given could, in fact, have been as high as 4,700 g?” Given the rules that restrict how you can answer, you are rarely allowed to explain to a jury that, first, the 15% variability applies only to a baby whose weight is more than one standard deviation from average and, second, the weight-estimate variability can be on the low side as well as on the high side.

How should you respond to interrogation?

Although you face disadvantages as a defendant physician in a courtroom, there are ways to fight back—to stick up for yourself and respond to the techniques that attorneys perpetrate. You aren’t as defenseless as it might appear!

Never allow an attorney to bully you in the courtroom or at a deposition. If the attorney begins to use such behavior, call it by its name and demand that it be stopped. Your lawyer will likely have raised an objection before you do; if she does not, protest such inappropriate behavior yourself. Never allow an attorney who is questioning you to raise his voice or speak to you sarcastically or rudely.

You don’t necessarily have to play by the rules for answering questions, despite any admonition by a plaintiff lawyer that you do so. Unless you are advised otherwise by the judge or by your lawyer, answer questions the way you want to, as long as your answer is a reply to the question that was asked. You are never obliged to answer a question with just “Yes” or “No.” If an attorney tries to impose such a limitation on you, declare that you cannot answer the question under those terms. If your answers are being cut off, don’t hesitate to tell the jury that you are not being allowed to tell the whole story.

If questions posed to you contain false premises, point that out. For example, you might be asked, “Given the obvious fetal distress that was present, why did you apply forceps?” If there was no fetal distress, or if that is one of the issues in dispute, you can respond that the question contains incorrect information or an unwarranted assumption, and therefore cannot be answered as asked.

Prepare to be asked about your background and training. Have your lawyer ask you preemptively, during her questioning, about anything in your professional life that might appear the least bit negative. This allows you to explain the matter fully without being cut off by the plaintiff attorney. Have your lawyer ask questions that show how your background and training compare with those of other physicians in your hospital and community. If you have been sued in the past, have your lawyer ask you about how many times an ObGyn is sued, on average, in her career (“three” is the answer), and use this fact to show the jury that being sued is not an anomaly but the rule in ObGyn practice.

Never answer a question about something you wrote in the past or about prior testimony without demanding to read it yourself, on the stand, in context. (The same is true for quotations from the medical literature read to you by the plaintiff attorney: You have a right to know the source and date of publication of quoted material, and you should insist on being able to read the quotation for yourself so that you can understand it in context.)

If asked from what text or article you learned a specific piece of information, point out the absurdity of being asked to remember such specifics from among the tens of thousands of things you have learned and read over your training and career.

When asked about your notes in the medical record and why you did or did not write a particular item, point out that the medical record is not a document that is intended to be used to prosecute or defend medical cases years down the road but rather is meant to convey important clinical information among health-care providers. Tell the jury what sorts of notes are routinely written and how much information is generally put into a note. If the notes you wrote are appropriate, even if brief, be sure and explain to the jury that what you did is, in fact, the standard of care—not an idealized conception taken from a textbook or an expert’s talk as to how notes should be written. Don’t agree with a lawyer’s contention that “if it isn’t written down, it didn’t happen.” That may be a lawyer’s rule; it is not a medical rule. Do not let the jury go into the jury room thinking that it is.

Know the specifics of your case. It is true that, as a defendant witness, several factors are out of your control. But don’t forget what you do have under your control: Knowledge of obstetrics and gynecology and experience in the field. You know the medical issues involved in the litigation better than anyone else in the courtroom.

Still, do your homework. Make sure that you know the specifics of your case, inside and out. Study the medical record of the case carefully and read all the depositions your lawyer provides for you. Know what the relevant ACOG Bulletin, major texts (such as Williams Obstetrics), and the literature say about the issues that are involved. Know who the experts are in this area of care and be prepared to quote pertinent articles that they have written. Work to never let yourself be surprised by the facts of the case or the medical information presented by the plaintiff’s side. Treat your testimony as a very important final examination. Do that, and you will be in an excellent position to successfully answer questions and refute incorrect statements.

Preempt questions about informed consent. Ask your lawyer to have you explain, during the direct portion of your testimony, about informed consent conversations, how they are usually held, and how they are documented. Tell the jury the difference between a calm consent discussion in the office before a routine medical procedure and a consent discussion in an urgent situation. By the way: The general rule about informed consent is that a physician is obliged to discuss with a patient any significant risk greater than 1%. This is a documented standard.¹

Don’t let incorrect claims go unchallenged. Consider this scenario: A plaintiff attorney states that, given the circumstances of a certain clinical situation, you should have taken a particular action. This is often the case in fetal asphyxia cases, when experts for the plaintiff often testify that they can tell, from looking at the fetal heart rate monitoring strip, the exact moment at which a fetus was in trouble and should have been delivered by C-section. Consider having your lawyer issue an in-court challenge to an expert witness who makes such a claim to perform a blind reading of five fetal monitor strips for which the outcomes are known and to see if his predictions are correct. A plaintiff attorney will never take you up on such a challenge—and that refusal will be noted and appreciated by the jury.

This isn’t your backyard but you can play here

Amid what is often hostile treatment, it can be difficult to remember who you are: A highly trained, hard-working physician who has given most of your professional life to providing superb care. A plaintiff attorney is out to make you appear incompetent, and his motive is clear: He’ll earn one-quarter to one-third of any award that he wins for his client.

You are obviously convinced of the correctness of what you did in the case—or you wouldn’t have gone to court to defend yourself. You know the medicine better than the plaintiff lawyer does and, having been the caregiver, you can discuss all aspects of the case with much greater authority than he ever can. His only advantage? You’re in his backyard and he controls many of the rules.

But if you’re meticulously prepared, if you work with your lawyer and follow her advice, and if you are aware of the plaintiff attorneys’ tricks and techniques that I’ve described, you can neutralize much of the disadvantage you’re under in the legal system and defend your case on a greatly leveled playing field.

The author reports that he is president of Shoulder Dystocia Litigation Consultants, working with defense lawyers, insurance company case managers, and hospital risk managers in shoulder dystocia-related injuries and litigation.

CASE

You are a defendant in a malpractice case, and your lawyer has just finished questioning you—the “direct” part of your testimony. She asked you straightforward questions and you answered fully and without interruption. You were able to explain, at length, your account of what happened during the events in question. This is the first time you’ve been sued; you’re nervous, but things have gone well so far, you feel.

Cross-examination by the plaintiff’s attorney comes next. He starts aggressively, questioning the quality of your training and experience. Have any disciplinary actions ever been taken against you by your hospital or the state licensing board? Did you have specialty fellowship training? He makes it seem that, if you didn’t, you have no business taking care of patients.

He drills in: Have you taken courses in the specific area at question in the case—as if whole courses are given routinely on the narrow topics that are often the subject of litigation, whether shoulder dystocia, placental abruption, damage to a ureter, or other bad outcomes.

He moves on to ask about details of the case but cuts you off when you try to flesh out your answers. He admonishes you: Listen to the question and answer “Yes” or “No”!

He begins to raise his voice.

The attorney attacks your notes in the medical record; he makes them seem incomplete and inadequate. He tells members of the jury that they can assume that you did not take a specific action, despite your claim to the contrary, because it’s not in the record: “If it wasn’t written down, it didn’t happen.”

His demeanor becomes more confrontational. The increasingly abusive questioning goes on and on, and your sense that things are going well has evaporated.

How, you ask yourself as the assault continues, did all this rancor and accusation come on so fast and so unexpectedly?

This scenario, or versions close to it, occurs all too often to physicians in courtrooms across the United States. Defendant physicians who are vilified and goaded feel angry, frustrated, and helpless. No wonder—the courtroom environment is alien to us. We trained for years to become competent, knowledgeable practitioners of our specialty; we work hard every day to provide the best possible care; and we diligently keep up with advances in ObGyn medicine by reading the literature and attending continuing medical education conferences. But in the courtroom, attorneys make a pointed attempt to paint us as incompetent and uncaring—even malicious.

Moreover, customary rules of argumentation don’t apply. We can’t answer questions fully or correct misstatements that are implicit in certain questions. Judges often limit what we can say and what the jury is allowed to hear. Not only is the medical care we gave questioned—we are subject to attempts to discredit us personally. We’re asked questions about the most private aspects of our life: “What’s your income?” “Why were you divorced?” “What is the financial arrangement between you and your partners?” “Are you seeing—have you ever seen—a psychiatrist?”

The playing field has been set at a tilt

Perhaps your greatest disadvantage when you are sued is that, most likely, this is going to be your first time in a courtroom. You haven’t had the chance to become familiar with the venue—the courtroom—or the tactics of cross-examination used by plaintiff attorneys.

Combine an accusation of malpractice and the need to defend yourself in an alien environment with rules made by and favoring lawyers that are foreign to you and that you cannot control—what a daunting prospect! Plaintiff attorneys take advantage of the situation to prey on defendants.

There are ways to defend yourself!

Did you go into an operating room or a delivery room for the first time without preparation or training? No! Likewise, don’t go into a courtroom unprepared.

You may be surprised to learn that you do have advantages over lawyers for plaintiffs:

• You know more medicine than they ever will, no matter how many malpractice cases they have tried.
  
• You were there when the actions under dispute took place. You can speak from direct experience about those actions, with authority, as a knowledgeable eyewitness.
  
• Despite how it may appear, you have the right to defend your actions and your statements vigorously.
  

Plaintiff lawyers routinely employ a standard repertoire of tricks and traps, which I have seen used time and again. My goals here are to describe them to you so that you can see them coming and to tell you how to defend yourself against them. You’ll then be in a position to counter these tricks by 1) giving them a name, 2) confronting the lawyer—in front of the judge and the jury—with what he or she is attempting to do, and 3) employing defensive tactics.

A note about language in this article: For simplicity, when I say “he” when referring to a physician or lawyer, I mean “he” or “she.” And I mean “plaintiff attorney” when I say just “lawyer” or “attorney,” unless I am referring explicitly to your (the defendant’s) representation.

First, three little words to set the stage

Always keep in mind that, for you to be found guilty of malpractice, the plaintiff attorney has to prove beyond a reasonable doubt that the actions you did, or did not, take violated what is known in the medicolegal arena as standard of care. Because this standard is what you are being judged against, it is vital that you understand—and, in turn, that the jury understands—exactly what the term means.

Standard of care is defined as care generally given by well-trained physicians in your own specialty under similar circumstances. Standard of care does not mean “ideal” care, as may be recommended in a medical textbook or other kinds of professional communication. The standard of care is, essentially, generally accepted practice: The level and degree of care most often used by your contemporary peers. You are guilty of malpractice only if the care that you gave fell below the care that would generally have been given to a patient by others, in your specialty, under the circumstances you faced.

Inside an attorney’s bulging bag of tricks

What tactics might an attorney use to harass and intimidate you?

He’ll bully you. Imagine this: A plaintiff lawyer is brought into a surgical suite for the first time. He is asked to participate in an operation but isn’t allowed to speak unless spoken to. He is allowed to answer direct questions only in a format dictated by the senior surgeon. That lawyer would not know what was going on, would be continuously on the defensive, and would feel totally in over his head—if he didn’t faint first!

What I just described is the equivalent of what happens to you in a courtroom. An attorney is allowed great leeway over the types of questions that he can ask and the manner in which they can be posed. He often attempts to intimidate you with harsh language, a raised voice, physical gestures, and sarcasm. He might ask questions with implied premises that aren’t true. His behavior might be confrontational. He might try to cut you off. And he might insist that your answers be solely “Yes” or “No.”

He’ll troll through your CV. Every educational activity in which you have participated, and every professional position you have ever held, is subject to inquiry. In addition to being asked if you have ever been sued or had disciplinary action taken against you, an attorney will review your education, step by step. He might imply that, if you were educated abroad or went to a less-than-well-known medical school, you are poorly trained or somehow not “of high quality.” He will likely ask you how many times you took the specialty board exam before you passed it. You might even be asked how high you finished in your medical school class, or if you were given your first choice of residency program in a match.

He’ll create artificial standards in the minds of jury members. You might be asked if you have published in your field or if you have an academic appointment—the assumption being that, if your answer is “No,” your opinion about issues being discussed at the trial are not as authoritative as (he will claim) those of the plaintiff’s expert witness, who may be well known in the specialty.

He’ll take statements out of context. Articles that you published (even if years ago), previous depositions or trial testimony you have given, and even PowerPoint presentations you made to nurses on your labor and delivery unit may be probed and quoted. Usually, the attorney presents only brief snippets of these works, which are likely to be read to the jury out of context.

He’ll ask for specific references. Often, when an attorney asks about facts that you’ve mentioned or opinions you hold regarding issues that bear on the case in your trial, he will attempt to embarrass you by asking you to name the specific text, article, or author from which you obtained that information. Here’s an example: You know that the threshold for macrosomia in a shoulder dystocia case is 4,500 g, and that random late decelerations in a fetal monitor strip marked by otherwise excellent variability do not demand immediate C-section—but you may not be able to cite, off the top of your head, exactly in which textbook or journal article you read this or the information can be found. You might also be asked what an ACOG Bulletin or your hospital’s policy book says about a certain subject or aspect of care.

He’ll drag in the medical record and informed consent. An attorney might try to convince a jury that “if it isn’t written down, it didn’t happen.” He might cite a lack of an extensive written description of what occurred during the events in question as evidence of sloppy charting or poor care. He might claim that lack of a detailed note replicating a conversation that took place during the consent process displays a lack of concern for the patient’s right to know.

He’ll imply the existence of a standard of care. Lawyers often try to convince a jury that a defendant physician committed malpractice by claiming that she should have taken certain actions, when, in fact, these actions would have been unnecessary or inappropriate under the circumstances. Examples: Asking whether clinical pelvimetry was documented in the chart of a multiparous woman who came in actively laboring, or asking if fundal height was measured in the office during a patient’s last three prenatal visits.

Here are two other examples:

• In a case involving vacuum extraction delivery: “Doctor, have you ever read the vacuum device’s product safety manual?”
  
• When a plaintiff has testified that she told you at her first prenatal visit that her previous pregnancies were uncomplicated: “Did you call for, or read, the record from any of her previous pregnancies?”
  

He’ll create a false impression. A common attorney’s tactic is to pose questions to you that imply that certain things are true, when they are not. A common example of this tactic occurs in shoulder dystocia cases, when putative risk factors are addressed.

Consensus in the shoulder dystocia literature is that there are only three or four statistically consistent risk factors for this condition: shoulder dystocia in a prior delivery, macrosomia, gestational diabetes, and (possibly) mid-vacuum or forceps delivery. Often, however, attorneys imply to the jury that many other risk factors exist—and that your patient had any number of them and that you should have been aware of them.

You might be asked if your patient underwent oxytocin induction, had a long first stage of labor, had an epidural anesthetic placed, or was post-dates—none of which have a proven association with shoulder dystocia. You’ll be given little leeway, in answering questions posed to you, to try to refute the lawyer’s false assumptions. The impression may thus be left by this concatenation of nonproven factors that your patient was at high risk of shoulder dystocia, that this was foreseeable, and that you were negligent in not having performed a C-section to prevent it.

Likewise, lawyers often deliberately misuse statistics—such as when they discuss sonographic variability in the estimation of fetal weight: “Don’t you acknowledge, Doctor, that ultrasound estimates of fetal weight can vary by 15% of the actual weight? So why didn’t you take into account that the 4,300 g estimate you were given could, in fact, have been as high as 4,700 g?” Given the rules that restrict how you can answer, you are rarely allowed to explain to a jury that, first, the 15% variability applies only to a baby whose weight is more than one standard deviation from average and, second, the weight-estimate variability can be on the low side as well as on the high side.

How should you respond to interrogation?

Although you face disadvantages as a defendant physician in a courtroom, there are ways to fight back—to stick up for yourself and respond to the techniques that attorneys perpetrate. You aren’t as defenseless as it might appear!

Never allow an attorney to bully you in the courtroom or at a deposition. If the attorney begins to use such behavior, call it by its name and demand that it be stopped. Your lawyer will likely have raised an objection before you do; if she does not, protest such inappropriate behavior yourself. Never allow an attorney who is questioning you to raise his voice or speak to you sarcastically or rudely.

You don’t necessarily have to play by the rules for answering questions, despite any admonition by a plaintiff lawyer that you do so. Unless you are advised otherwise by the judge or by your lawyer, answer questions the way you want to, as long as your answer is a reply to the question that was asked. You are never obliged to answer a question with just “Yes” or “No.” If an attorney tries to impose such a limitation on you, declare that you cannot answer the question under those terms. If your answers are being cut off, don’t hesitate to tell the jury that you are not being allowed to tell the whole story.

If questions posed to you contain false premises, point that out. For example, you might be asked, “Given the obvious fetal distress that was present, why did you apply forceps?” If there was no fetal distress, or if that is one of the issues in dispute, you can respond that the question contains incorrect information or an unwarranted assumption, and therefore cannot be answered as asked.

Prepare to be asked about your background and training. Have your lawyer ask you preemptively, during her questioning, about anything in your professional life that might appear the least bit negative. This allows you to explain the matter fully without being cut off by the plaintiff attorney. Have your lawyer ask questions that show how your background and training compare with those of other physicians in your hospital and community. If you have been sued in the past, have your lawyer ask you about how many times an ObGyn is sued, on average, in her career (“three” is the answer), and use this fact to show the jury that being sued is not an anomaly but the rule in ObGyn practice.

Never answer a question about something you wrote in the past or about prior testimony without demanding to read it yourself, on the stand, in context. (The same is true for quotations from the medical literature read to you by the plaintiff attorney: You have a right to know the source and date of publication of quoted material, and you should insist on being able to read the quotation for yourself so that you can understand it in context.)

If asked from what text or article you learned a specific piece of information, point out the absurdity of being asked to remember such specifics from among the tens of thousands of things you have learned and read over your training and career.

When asked about your notes in the medical record and why you did or did not write a particular item, point out that the medical record is not a document that is intended to be used to prosecute or defend medical cases years down the road but rather is meant to convey important clinical information among health-care providers. Tell the jury what sorts of notes are routinely written and how much information is generally put into a note. If the notes you wrote are appropriate, even if brief, be sure and explain to the jury that what you did is, in fact, the standard of care—not an idealized conception taken from a textbook or an expert’s talk as to how notes should be written. Don’t agree with a lawyer’s contention that “if it isn’t written down, it didn’t happen.” That may be a lawyer’s rule; it is not a medical rule. Do not let the jury go into the jury room thinking that it is.

Know the specifics of your case. It is true that, as a defendant witness, several factors are out of your control. But don’t forget what you do have under your control: Knowledge of obstetrics and gynecology and experience in the field. You know the medical issues involved in the litigation better than anyone else in the courtroom.

Still, do your homework. Make sure that you know the specifics of your case, inside and out. Study the medical record of the case carefully and read all the depositions your lawyer provides for you. Know what the relevant ACOG Bulletin, major texts (such as Williams Obstetrics), and the literature say about the issues that are involved. Know who the experts are in this area of care and be prepared to quote pertinent articles that they have written. Work to never let yourself be surprised by the facts of the case or the medical information presented by the plaintiff’s side. Treat your testimony as a very important final examination. Do that, and you will be in an excellent position to successfully answer questions and refute incorrect statements.

Preempt questions about informed consent. Ask your lawyer to have you explain, during the direct portion of your testimony, about informed consent conversations, how they are usually held, and how they are documented. Tell the jury the difference between a calm consent discussion in the office before a routine medical procedure and a consent discussion in an urgent situation. By the way: The general rule about informed consent is that a physician is obliged to discuss with a patient any significant risk greater than 1%. This is a documented standard.¹

Don’t let incorrect claims go unchallenged. Consider this scenario: A plaintiff attorney states that, given the circumstances of a certain clinical situation, you should have taken a particular action. This is often the case in fetal asphyxia cases, when experts for the plaintiff often testify that they can tell, from looking at the fetal heart rate monitoring strip, the exact moment at which a fetus was in trouble and should have been delivered by C-section. Consider having your lawyer issue an in-court challenge to an expert witness who makes such a claim to perform a blind reading of five fetal monitor strips for which the outcomes are known and to see if his predictions are correct. A plaintiff attorney will never take you up on such a challenge—and that refusal will be noted and appreciated by the jury.

This isn’t your backyard but you can play here

Amid what is often hostile treatment, it can be difficult to remember who you are: A highly trained, hard-working physician who has given most of your professional life to providing superb care. A plaintiff attorney is out to make you appear incompetent, and his motive is clear: He’ll earn one-quarter to one-third of any award that he wins for his client.

You are obviously convinced of the correctness of what you did in the case—or you wouldn’t have gone to court to defend yourself. You know the medicine better than the plaintiff lawyer does and, having been the caregiver, you can discuss all aspects of the case with much greater authority than he ever can. His only advantage? You’re in his backyard and he controls many of the rules.

But if you’re meticulously prepared, if you work with your lawyer and follow her advice, and if you are aware of the plaintiff attorneys’ tricks and techniques that I’ve described, you can neutralize much of the disadvantage you’re under in the legal system and defend your case on a greatly leveled playing field.

Some 200,000 women in the United States are diagnosed with breast cancer each year. Among them, 15% to 20% have a family history of breast cancer and/or other cancers, and an additional 5% to 10% have a hereditary form of the disease.¹ Although great strides are being taken in the early detection and treatment of breast cancer, this disease remains the second leading cause of cancer deaths among women.

Equally important to early detection and improved treatment options is an understanding of factors that increase women’s risk for breast cancer, and the identification and management of women at increased risk—as well as identifying women who should be referred for high-risk evaluation and management. Interventions that limit the risk, whether offered by the primary care provider or a breast cancer specialist, can ultimately prevent some breast cancers from developing.

Risk assessment for breast cancer and an overview of high-risk evaluation and management provide the basis for this article.

Risk Factors
A variety of factors—some modifiable, some not—increase a woman’s risk for breast cancer (see Table 1²). Factors associated with particularly increased risk include:

• Family history of breast cancer in a first-degree relative or of breast or ovarian cancer in two or more close relatives^1-3

• Prior breast biopsy findings that revealed atypical ductal hyperplasia (ADH), atypical lobular hyperplasia (ALH), or lobular carcinoma in situ (LCIS)

• Personal or family history of a BRCA1 or BRCA2 mutation

• Having undergone radiation to the chest wall between ages 10 and 30

• Personal or family history of other rare hereditary breast cancer syndromes,⁴ such as Cowden syndrome, Li-Fraumeni syndrome, or Peutz-Jeghers syndrome.^5-7

To understand high-risk factors in the overall context of breast cancer, it is important to understand the differences between sporadic, familial, and hereditary cancers. The majority of breast cancers, approximately 70%, occur sporadically.⁸ Sporadic cancers may be caused by random events occurring among or within cells, radiation exposure, or environmental or other unknown factors.

Among breast cancers, 15% to 20% are familial^8,9—ie, a recognized pattern of cancers occurs in the patient’s family, but affected members have tested negative for known genetic mutations. Familial cancers may be influenced by not-yet-identified genetic mutations or by environmental factors. As families usually share the same environment, dietary habits, and lifestyles, there may be an association between those factors and families with a cancer history. 

Anyone who has a personal or family history of a mutation in either of the breast or ovarian cancer susceptibility genes, BRCA1 and BRCA2, has a significant risk for breast cancer. These are hereditary autosomal dominant mutations, inherited from an affected parent. Hereditary cancer syndromes, such as those associated with BRCA1 or BRCA2, are relatively rare. Only 5% to 10% of breast cancers are considered hereditary; of those, approximately 80% are related to mutations in BRCA1 or BRCA2.¹⁰

Several “red flags” suggest the possibility of a hereditary type of breast cancer syndrome. Genetic risk is primarily identified through thorough history taking, which must address both the maternal and paternal sides of the family—over three generations, if possible.¹⁰ Table 2^10-14 identifies these red flags.

Atypical cells identified on breast biopsy also increase breast cancer risk. The presence of ADH or ALH increases a woman’s risk four to five times higher than the average.² LCIS is associated with a 10-fold increase in breast cancer risk.⁹ The overall incidence of breast cancer in women with LCIS is estimated at 22.3%.³

Radiation exposure to the chest wall, particularly when administered between ages 10 and 30, also increases the risk for breast cancer. This usually occurs in female patients who have undergone mantle-field radiation treatment for another cancer, such as Hodgkin’s disease or non-Hodgkin’s lymphoma.^15,16 Risk associated with this type of treatment can be as great as 12 times the normal risk. Patients treated before or during adolescence appear to be at highest risk.² Persons exposed to other types of radiation (eg, survivors of atomic weapons) also have increased breast cancer risk.¹

Rare genetic syndromes not associated with BRCA1 or BRCA2 have been associated with breast cancer as well. Cowden, Li-Fraumeni, and Peutz-Jeghers syndromes are all known hereditary breast cancer syndromes.^4-7 Although these syndromes account for less than 1% of all breast cancers,¹⁰ it is important to be able to identify a patient who is at risk for harboring a genetic mutation that causes one of these syndromes—and to understand how to manage a woman who is already affected. 

Cowden syndrome is an autosomal dominant disorder caused by a mutation in the PTEN gene.^4,17 This syndrome carries a 25% to 50% risk for breast cancer.¹⁸ Other findings associated with Cowden syndrome include facial or buccal lesions, fibrocystic breast disease, benign thyroid conditions (eg, goiter), nonmedullary thyroid cancer, endometrial cancer, macrocephaly, uterine fibroids, and gastrointestinal hamartomas.^3,10

Li-Fraumeni syndrome is a highly penetrant, autosomal dominant disorder caused by a mutation in the TP53 gene.^4,6,19,20 Affected women’s overall cancer risk is 50% by age 35 and 90% lifelong. Breast cancer risk is estimated at 50% by age 50.³ Multiple primary cancers, including early-onset breast cancer (ie, before age 40), sarcoma, leukemia, childhood brain tumors, and adrenocortical carcinoma, are all associated with Li-Fraumeni.^6,10,19,21

Peutz-Jeghers syndrome is also an autosomal dominant condition, caused by a mutation in the STK11 gene.^3,22,23 The mean age of breast cancer diagnosis in affected women is 44. Hallmark features of Peutz-Jeghers include gastrointestinal hamartomas (often discovered during childhood²⁴) and cancers of the colon, small bowel, pancreas, uterus, thyroid, lung, and breast. The most commonly reported malignancies in patients with Peutz-Jeghers syndrome are breast cancer and colon cancer. Associated phenotypic features include pigmented spots on the lips, buccal mucosa, and skin.^10,24

Risk Assessment Tools
Women with any of the identified high-risk factors should be referred to a provider experienced in high-risk breast cancer assessment and management. Many comprehensive breast centers are adding high-risk programs to their array of services. Researching those programs in your area will facilitate the process of referral for women in your practice who are identified as high risk.

In efforts to identify patients at high risk for breast cancer, the importance of thorough history taking cannot be overstated. It is imperative that both the maternal and paternal sides of the family be assessed, as genetic mutations can be acquired through the patient’s mother or father.¹⁰

A variety of tools to assess breast cancer risk are available. The one most commonly used is the Gail risk assessment model,²⁵ which was developed at the National Cancer Institute. A modified version, validated during the Breast Cancer Prevention Trial,²⁶ calculates five-year and lifetime risk based on the following criteria:

• Current age

• Age at menarche

• Age at first live birth

• Race

• Number of first-degree relatives with a history of breast cancer

• Number of previous breast biopsies

• History of atypical cells on previous breast biopsy.

The Gail model has certain limitations. It cannot be used to assess women younger than 35²⁷ or older than 85. Also, age at breast cancer diagnosis, non–first-degree relatives with breast cancer, paternal cancer history, ovarian cancer history, and ethnicity are not included among its considerations.³

The Claus model²⁸ assesses risk in women with a family history of breast cancer more accurately than the Gail model, but it does not incorporate male breast cancer, ovarian cancer, or ethnicity.⁹

Several models are available to predict the risk for carrying a BRCA1 or BRCA2 mutation. The Myriad Genetic Laboratories database,²⁹ the BRCAPRO model,^30,31 the Manchester scoring system,^32,33 the Tyrer-Duffy-Cuzick (IBIS) model,³⁴ and the BOADICEA model³⁵ all provide probability data, but each has its limitations. Breast specialists who provide high-risk assessment services calculate risk using a variety of models and choosing the most appropriate model(s) for each patient.^36,37 Women with a high probability of carrying a mutation, based on history and findings from the risk assessment model, are referred for genetics counseling and testing.

Reducing the Risk
Risk reduction is an integral component of high-risk breast cancer management, and several strategies are currently recommended, including these:

• Exercise for 45 to 60 minutes at least five times per week.^2,38 In women who engage in at least five hours of vigorous exercise each week, a 0.62 relative risk for breast cancer has been reported.^38,39

• Limit alcohol intake to fewer than one to two drinks per day. A number of studies have documented a 30% to 50% increase in the incidence of breast cancer among women who consume alcohol in greater quantities.^38,40

• Avoid obesity. Compared with women who have maintained their weight since age 18, those who gain 55 lb or more by menopause onset have a 1.45 relative risk for breast cancer.^38,41

• Breastfeed infants. Lactation for two years or longer decreases the lifetime risk for breast cancer by 50%.³

• Follow a low-fat, high-fiber diet, rich in fresh fruits and vegetables. Increasing fruit and vegetable intake by even one serving per day has been associated with a 9% decrease in breast cancer incidence.^38,42

Chemoprevention for At-Risk Women
Another risk reduction strategy for women at particularly high risk for breast cancer is chemoprevention. Currently, two medications, tamoxifen and raloxifene, are FDA approved for breast cancer risk reduction in women at high risk. These agents are offered to women with specific high-risk factors, including:

• Findings of LCIS, ADH, or ALH on previous breast biopsy

• A five-year probability of breast cancer exceeding 1.7%, based on a validated risk assessment model (eg, the Gail model, BRCAPRO)

• Presence of the BRCA1 or BRCA2 mutation.

Tamoxifen is a selective estrogen receptor modulator (SERM) that blocks the effects of estrogen on breast tissue.⁴³ Often referred to as an “antiestrogen,” it is approved for use in both premenopausal and postmenopausal women. In the Breast Cancer Prevention Trial,⁴⁴ women at high risk for breast cancer who took tamoxifen for five years had about a 50% risk reduction for invasive breast cancer and a 30% risk reduction in noninvasive breast cancer. The usual dose of tamoxifen is 20 mg/d.

Adverse effects associated with tamoxifen use, however, include blood clots, stroke, and uterine cancer. Women should not take tamoxifen if they have a history of cataracts, are current hormone therapy users, are planning a pregnancy or have the potential for becoming pregnant, or have a history of stroke, deep venous thrombosis, or pulmonary embolus. Less serious adverse effects include menopausal symptoms, menstrual irregularities, headache, fatigue, nausea, and skin irritation.⁴³

Raloxifene, though more commonly prescribed to prevent and treat osteoporosis, has been shown to reduce the risk for invasive breast cancer by 56% to 72%, compared with placebo^45,46; it exerts estrogenic effects on bone and antiestrogenic effects on breast and endometrial tissue.⁴⁷ This SERM is approved for breast cancer risk reduction only in postmenopausal women.⁴⁸ Recommended use is 60 mg/d for five years.

Although raloxifene provides a risk reduction benefit comparable to that of tamoxifen against invasive breast cancer (ie, incidence rates of 4.4 and 4.3, respectively, per 1,000 women per year⁴⁹), it does not appear to reduce the risk for noninvasive breast cancer (ie, ductal carcinoma in situ).⁵⁰ Potential major complications attributed to raloxifene use include blood clots, stroke, and uterine cancer, although the risk for uterine cancer is lower than with tamoxifen use.⁴⁹ Minor adverse effects include leg cramps, menopausal symptoms, edema of the extremities, and flulike symptoms. Contraindications are comparable to those associated with tamoxifen.⁴⁸

Screening Recommendations
Combined with mammography and breast ultrasound, the use of MRI to screen high-risk women is now being recommended, according to guidelines published in March 2007 by the American Cancer Society.²⁰ Patient factors suggesting greatest benefit from annual MRI screening (combined with mammography) are listed in Table 3.^4,20,51-55

In addition to patient-driven reduction strategies and the provider-initiated interventions for surveillance and management, monthly breast self-examination is encouraged, as are clinical breast examinations every six months.

Even with the most aggressive risk reduction program, not all breast cancers can be prevented. A key objective of high-risk screening and management is to identify patients with breast cancer at the earliest possible stage so that a cure is more likely to be achieved.

Conclusion
Identifying and screening women at high risk for breast cancer are essential skills for all primary care providers. Maintaining a comprehensive list of referral sources for high-risk management and genetic counseling services in your area will allow you to partner with other professionals to provide patients with the best possible care. Women feel empowered by education, particularly the newly acquired knowledge about breast cancer risk reduction—and reassured, knowing that their providers are interested and well informed in this complex area of women’s health.

Some 200,000 women in the United States are diagnosed with breast cancer each year. Among them, 15% to 20% have a family history of breast cancer and/or other cancers, and an additional 5% to 10% have a hereditary form of the disease.¹ Although great strides are being taken in the early detection and treatment of breast cancer, this disease remains the second leading cause of cancer deaths among women.

Equally important to early detection and improved treatment options is an understanding of factors that increase women’s risk for breast cancer, and the identification and management of women at increased risk—as well as identifying women who should be referred for high-risk evaluation and management. Interventions that limit the risk, whether offered by the primary care provider or a breast cancer specialist, can ultimately prevent some breast cancers from developing.

Risk assessment for breast cancer and an overview of high-risk evaluation and management provide the basis for this article.

Risk Factors
A variety of factors—some modifiable, some not—increase a woman’s risk for breast cancer (see Table 1²). Factors associated with particularly increased risk include:

• Family history of breast cancer in a first-degree relative or of breast or ovarian cancer in two or more close relatives^1-3

• Prior breast biopsy findings that revealed atypical ductal hyperplasia (ADH), atypical lobular hyperplasia (ALH), or lobular carcinoma in situ (LCIS)

• Personal or family history of a BRCA1 or BRCA2 mutation

• Having undergone radiation to the chest wall between ages 10 and 30

• Personal or family history of other rare hereditary breast cancer syndromes,⁴ such as Cowden syndrome, Li-Fraumeni syndrome, or Peutz-Jeghers syndrome.^5-7

To understand high-risk factors in the overall context of breast cancer, it is important to understand the differences between sporadic, familial, and hereditary cancers. The majority of breast cancers, approximately 70%, occur sporadically.⁸ Sporadic cancers may be caused by random events occurring among or within cells, radiation exposure, or environmental or other unknown factors.

Among breast cancers, 15% to 20% are familial^8,9—ie, a recognized pattern of cancers occurs in the patient’s family, but affected members have tested negative for known genetic mutations. Familial cancers may be influenced by not-yet-identified genetic mutations or by environmental factors. As families usually share the same environment, dietary habits, and lifestyles, there may be an association between those factors and families with a cancer history. 

Anyone who has a personal or family history of a mutation in either of the breast or ovarian cancer susceptibility genes, BRCA1 and BRCA2, has a significant risk for breast cancer. These are hereditary autosomal dominant mutations, inherited from an affected parent. Hereditary cancer syndromes, such as those associated with BRCA1 or BRCA2, are relatively rare. Only 5% to 10% of breast cancers are considered hereditary; of those, approximately 80% are related to mutations in BRCA1 or BRCA2.¹⁰

Several “red flags” suggest the possibility of a hereditary type of breast cancer syndrome. Genetic risk is primarily identified through thorough history taking, which must address both the maternal and paternal sides of the family—over three generations, if possible.¹⁰ Table 2^10-14 identifies these red flags.

Atypical cells identified on breast biopsy also increase breast cancer risk. The presence of ADH or ALH increases a woman’s risk four to five times higher than the average.² LCIS is associated with a 10-fold increase in breast cancer risk.⁹ The overall incidence of breast cancer in women with LCIS is estimated at 22.3%.³

Radiation exposure to the chest wall, particularly when administered between ages 10 and 30, also increases the risk for breast cancer. This usually occurs in female patients who have undergone mantle-field radiation treatment for another cancer, such as Hodgkin’s disease or non-Hodgkin’s lymphoma.^15,16 Risk associated with this type of treatment can be as great as 12 times the normal risk. Patients treated before or during adolescence appear to be at highest risk.² Persons exposed to other types of radiation (eg, survivors of atomic weapons) also have increased breast cancer risk.¹

Rare genetic syndromes not associated with BRCA1 or BRCA2 have been associated with breast cancer as well. Cowden, Li-Fraumeni, and Peutz-Jeghers syndromes are all known hereditary breast cancer syndromes.^4-7 Although these syndromes account for less than 1% of all breast cancers,¹⁰ it is important to be able to identify a patient who is at risk for harboring a genetic mutation that causes one of these syndromes—and to understand how to manage a woman who is already affected. 

Cowden syndrome is an autosomal dominant disorder caused by a mutation in the PTEN gene.^4,17 This syndrome carries a 25% to 50% risk for breast cancer.¹⁸ Other findings associated with Cowden syndrome include facial or buccal lesions, fibrocystic breast disease, benign thyroid conditions (eg, goiter), nonmedullary thyroid cancer, endometrial cancer, macrocephaly, uterine fibroids, and gastrointestinal hamartomas.^3,10

Li-Fraumeni syndrome is a highly penetrant, autosomal dominant disorder caused by a mutation in the TP53 gene.^4,6,19,20 Affected women’s overall cancer risk is 50% by age 35 and 90% lifelong. Breast cancer risk is estimated at 50% by age 50.³ Multiple primary cancers, including early-onset breast cancer (ie, before age 40), sarcoma, leukemia, childhood brain tumors, and adrenocortical carcinoma, are all associated with Li-Fraumeni.^6,10,19,21

Peutz-Jeghers syndrome is also an autosomal dominant condition, caused by a mutation in the STK11 gene.^3,22,23 The mean age of breast cancer diagnosis in affected women is 44. Hallmark features of Peutz-Jeghers include gastrointestinal hamartomas (often discovered during childhood²⁴) and cancers of the colon, small bowel, pancreas, uterus, thyroid, lung, and breast. The most commonly reported malignancies in patients with Peutz-Jeghers syndrome are breast cancer and colon cancer. Associated phenotypic features include pigmented spots on the lips, buccal mucosa, and skin.^10,24

Risk Assessment Tools
Women with any of the identified high-risk factors should be referred to a provider experienced in high-risk breast cancer assessment and management. Many comprehensive breast centers are adding high-risk programs to their array of services. Researching those programs in your area will facilitate the process of referral for women in your practice who are identified as high risk.

In efforts to identify patients at high risk for breast cancer, the importance of thorough history taking cannot be overstated. It is imperative that both the maternal and paternal sides of the family be assessed, as genetic mutations can be acquired through the patient’s mother or father.¹⁰

A variety of tools to assess breast cancer risk are available. The one most commonly used is the Gail risk assessment model,²⁵ which was developed at the National Cancer Institute. A modified version, validated during the Breast Cancer Prevention Trial,²⁶ calculates five-year and lifetime risk based on the following criteria:

• Current age

• Age at menarche

• Age at first live birth

• Race

• Number of first-degree relatives with a history of breast cancer

• Number of previous breast biopsies

• History of atypical cells on previous breast biopsy.

The Gail model has certain limitations. It cannot be used to assess women younger than 35²⁷ or older than 85. Also, age at breast cancer diagnosis, non–first-degree relatives with breast cancer, paternal cancer history, ovarian cancer history, and ethnicity are not included among its considerations.³

The Claus model²⁸ assesses risk in women with a family history of breast cancer more accurately than the Gail model, but it does not incorporate male breast cancer, ovarian cancer, or ethnicity.⁹

Several models are available to predict the risk for carrying a BRCA1 or BRCA2 mutation. The Myriad Genetic Laboratories database,²⁹ the BRCAPRO model,^30,31 the Manchester scoring system,^32,33 the Tyrer-Duffy-Cuzick (IBIS) model,³⁴ and the BOADICEA model³⁵ all provide probability data, but each has its limitations. Breast specialists who provide high-risk assessment services calculate risk using a variety of models and choosing the most appropriate model(s) for each patient.^36,37 Women with a high probability of carrying a mutation, based on history and findings from the risk assessment model, are referred for genetics counseling and testing.

Reducing the Risk
Risk reduction is an integral component of high-risk breast cancer management, and several strategies are currently recommended, including these:

• Exercise for 45 to 60 minutes at least five times per week.^2,38 In women who engage in at least five hours of vigorous exercise each week, a 0.62 relative risk for breast cancer has been reported.^38,39

• Limit alcohol intake to fewer than one to two drinks per day. A number of studies have documented a 30% to 50% increase in the incidence of breast cancer among women who consume alcohol in greater quantities.^38,40

• Avoid obesity. Compared with women who have maintained their weight since age 18, those who gain 55 lb or more by menopause onset have a 1.45 relative risk for breast cancer.^38,41

• Breastfeed infants. Lactation for two years or longer decreases the lifetime risk for breast cancer by 50%.³

• Follow a low-fat, high-fiber diet, rich in fresh fruits and vegetables. Increasing fruit and vegetable intake by even one serving per day has been associated with a 9% decrease in breast cancer incidence.^38,42

Chemoprevention for At-Risk Women
Another risk reduction strategy for women at particularly high risk for breast cancer is chemoprevention. Currently, two medications, tamoxifen and raloxifene, are FDA approved for breast cancer risk reduction in women at high risk. These agents are offered to women with specific high-risk factors, including:

• Findings of LCIS, ADH, or ALH on previous breast biopsy

• A five-year probability of breast cancer exceeding 1.7%, based on a validated risk assessment model (eg, the Gail model, BRCAPRO)

• Presence of the BRCA1 or BRCA2 mutation.

Tamoxifen is a selective estrogen receptor modulator (SERM) that blocks the effects of estrogen on breast tissue.⁴³ Often referred to as an “antiestrogen,” it is approved for use in both premenopausal and postmenopausal women. In the Breast Cancer Prevention Trial,⁴⁴ women at high risk for breast cancer who took tamoxifen for five years had about a 50% risk reduction for invasive breast cancer and a 30% risk reduction in noninvasive breast cancer. The usual dose of tamoxifen is 20 mg/d.

Adverse effects associated with tamoxifen use, however, include blood clots, stroke, and uterine cancer. Women should not take tamoxifen if they have a history of cataracts, are current hormone therapy users, are planning a pregnancy or have the potential for becoming pregnant, or have a history of stroke, deep venous thrombosis, or pulmonary embolus. Less serious adverse effects include menopausal symptoms, menstrual irregularities, headache, fatigue, nausea, and skin irritation.⁴³

Raloxifene, though more commonly prescribed to prevent and treat osteoporosis, has been shown to reduce the risk for invasive breast cancer by 56% to 72%, compared with placebo^45,46; it exerts estrogenic effects on bone and antiestrogenic effects on breast and endometrial tissue.⁴⁷ This SERM is approved for breast cancer risk reduction only in postmenopausal women.⁴⁸ Recommended use is 60 mg/d for five years.

Although raloxifene provides a risk reduction benefit comparable to that of tamoxifen against invasive breast cancer (ie, incidence rates of 4.4 and 4.3, respectively, per 1,000 women per year⁴⁹), it does not appear to reduce the risk for noninvasive breast cancer (ie, ductal carcinoma in situ).⁵⁰ Potential major complications attributed to raloxifene use include blood clots, stroke, and uterine cancer, although the risk for uterine cancer is lower than with tamoxifen use.⁴⁹ Minor adverse effects include leg cramps, menopausal symptoms, edema of the extremities, and flulike symptoms. Contraindications are comparable to those associated with tamoxifen.⁴⁸

Screening Recommendations
Combined with mammography and breast ultrasound, the use of MRI to screen high-risk women is now being recommended, according to guidelines published in March 2007 by the American Cancer Society.²⁰ Patient factors suggesting greatest benefit from annual MRI screening (combined with mammography) are listed in Table 3.^4,20,51-55

In addition to patient-driven reduction strategies and the provider-initiated interventions for surveillance and management, monthly breast self-examination is encouraged, as are clinical breast examinations every six months.

Even with the most aggressive risk reduction program, not all breast cancers can be prevented. A key objective of high-risk screening and management is to identify patients with breast cancer at the earliest possible stage so that a cure is more likely to be achieved.

Conclusion
Identifying and screening women at high risk for breast cancer are essential skills for all primary care providers. Maintaining a comprehensive list of referral sources for high-risk management and genetic counseling services in your area will allow you to partner with other professionals to provide patients with the best possible care. Women feel empowered by education, particularly the newly acquired knowledge about breast cancer risk reduction—and reassured, knowing that their providers are interested and well informed in this complex area of women’s health.

Some 200,000 women in the United States are diagnosed with breast cancer each year. Among them, 15% to 20% have a family history of breast cancer and/or other cancers, and an additional 5% to 10% have a hereditary form of the disease.¹ Although great strides are being taken in the early detection and treatment of breast cancer, this disease remains the second leading cause of cancer deaths among women.

Equally important to early detection and improved treatment options is an understanding of factors that increase women’s risk for breast cancer, and the identification and management of women at increased risk—as well as identifying women who should be referred for high-risk evaluation and management. Interventions that limit the risk, whether offered by the primary care provider or a breast cancer specialist, can ultimately prevent some breast cancers from developing.

Risk assessment for breast cancer and an overview of high-risk evaluation and management provide the basis for this article.

Risk Factors
A variety of factors—some modifiable, some not—increase a woman’s risk for breast cancer (see Table 1²). Factors associated with particularly increased risk include:

• Family history of breast cancer in a first-degree relative or of breast or ovarian cancer in two or more close relatives^1-3

• Prior breast biopsy findings that revealed atypical ductal hyperplasia (ADH), atypical lobular hyperplasia (ALH), or lobular carcinoma in situ (LCIS)

• Personal or family history of a BRCA1 or BRCA2 mutation

• Having undergone radiation to the chest wall between ages 10 and 30

• Personal or family history of other rare hereditary breast cancer syndromes,⁴ such as Cowden syndrome, Li-Fraumeni syndrome, or Peutz-Jeghers syndrome.^5-7

To understand high-risk factors in the overall context of breast cancer, it is important to understand the differences between sporadic, familial, and hereditary cancers. The majority of breast cancers, approximately 70%, occur sporadically.⁸ Sporadic cancers may be caused by random events occurring among or within cells, radiation exposure, or environmental or other unknown factors.

Among breast cancers, 15% to 20% are familial^8,9—ie, a recognized pattern of cancers occurs in the patient’s family, but affected members have tested negative for known genetic mutations. Familial cancers may be influenced by not-yet-identified genetic mutations or by environmental factors. As families usually share the same environment, dietary habits, and lifestyles, there may be an association between those factors and families with a cancer history. 

Anyone who has a personal or family history of a mutation in either of the breast or ovarian cancer susceptibility genes, BRCA1 and BRCA2, has a significant risk for breast cancer. These are hereditary autosomal dominant mutations, inherited from an affected parent. Hereditary cancer syndromes, such as those associated with BRCA1 or BRCA2, are relatively rare. Only 5% to 10% of breast cancers are considered hereditary; of those, approximately 80% are related to mutations in BRCA1 or BRCA2.¹⁰

Several “red flags” suggest the possibility of a hereditary type of breast cancer syndrome. Genetic risk is primarily identified through thorough history taking, which must address both the maternal and paternal sides of the family—over three generations, if possible.¹⁰ Table 2^10-14 identifies these red flags.

Atypical cells identified on breast biopsy also increase breast cancer risk. The presence of ADH or ALH increases a woman’s risk four to five times higher than the average.² LCIS is associated with a 10-fold increase in breast cancer risk.⁹ The overall incidence of breast cancer in women with LCIS is estimated at 22.3%.³

Radiation exposure to the chest wall, particularly when administered between ages 10 and 30, also increases the risk for breast cancer. This usually occurs in female patients who have undergone mantle-field radiation treatment for another cancer, such as Hodgkin’s disease or non-Hodgkin’s lymphoma.^15,16 Risk associated with this type of treatment can be as great as 12 times the normal risk. Patients treated before or during adolescence appear to be at highest risk.² Persons exposed to other types of radiation (eg, survivors of atomic weapons) also have increased breast cancer risk.¹

Rare genetic syndromes not associated with BRCA1 or BRCA2 have been associated with breast cancer as well. Cowden, Li-Fraumeni, and Peutz-Jeghers syndromes are all known hereditary breast cancer syndromes.^4-7 Although these syndromes account for less than 1% of all breast cancers,¹⁰ it is important to be able to identify a patient who is at risk for harboring a genetic mutation that causes one of these syndromes—and to understand how to manage a woman who is already affected. 

Cowden syndrome is an autosomal dominant disorder caused by a mutation in the PTEN gene.^4,17 This syndrome carries a 25% to 50% risk for breast cancer.¹⁸ Other findings associated with Cowden syndrome include facial or buccal lesions, fibrocystic breast disease, benign thyroid conditions (eg, goiter), nonmedullary thyroid cancer, endometrial cancer, macrocephaly, uterine fibroids, and gastrointestinal hamartomas.^3,10

Li-Fraumeni syndrome is a highly penetrant, autosomal dominant disorder caused by a mutation in the TP53 gene.^4,6,19,20 Affected women’s overall cancer risk is 50% by age 35 and 90% lifelong. Breast cancer risk is estimated at 50% by age 50.³ Multiple primary cancers, including early-onset breast cancer (ie, before age 40), sarcoma, leukemia, childhood brain tumors, and adrenocortical carcinoma, are all associated with Li-Fraumeni.^6,10,19,21

Peutz-Jeghers syndrome is also an autosomal dominant condition, caused by a mutation in the STK11 gene.^3,22,23 The mean age of breast cancer diagnosis in affected women is 44. Hallmark features of Peutz-Jeghers include gastrointestinal hamartomas (often discovered during childhood²⁴) and cancers of the colon, small bowel, pancreas, uterus, thyroid, lung, and breast. The most commonly reported malignancies in patients with Peutz-Jeghers syndrome are breast cancer and colon cancer. Associated phenotypic features include pigmented spots on the lips, buccal mucosa, and skin.^10,24

Risk Assessment Tools
Women with any of the identified high-risk factors should be referred to a provider experienced in high-risk breast cancer assessment and management. Many comprehensive breast centers are adding high-risk programs to their array of services. Researching those programs in your area will facilitate the process of referral for women in your practice who are identified as high risk.

In efforts to identify patients at high risk for breast cancer, the importance of thorough history taking cannot be overstated. It is imperative that both the maternal and paternal sides of the family be assessed, as genetic mutations can be acquired through the patient’s mother or father.¹⁰

A variety of tools to assess breast cancer risk are available. The one most commonly used is the Gail risk assessment model,²⁵ which was developed at the National Cancer Institute. A modified version, validated during the Breast Cancer Prevention Trial,²⁶ calculates five-year and lifetime risk based on the following criteria:

• Current age

• Age at menarche

• Age at first live birth

• Race

• Number of first-degree relatives with a history of breast cancer

• Number of previous breast biopsies

• History of atypical cells on previous breast biopsy.

The Gail model has certain limitations. It cannot be used to assess women younger than 35²⁷ or older than 85. Also, age at breast cancer diagnosis, non–first-degree relatives with breast cancer, paternal cancer history, ovarian cancer history, and ethnicity are not included among its considerations.³

The Claus model²⁸ assesses risk in women with a family history of breast cancer more accurately than the Gail model, but it does not incorporate male breast cancer, ovarian cancer, or ethnicity.⁹

Several models are available to predict the risk for carrying a BRCA1 or BRCA2 mutation. The Myriad Genetic Laboratories database,²⁹ the BRCAPRO model,^30,31 the Manchester scoring system,^32,33 the Tyrer-Duffy-Cuzick (IBIS) model,³⁴ and the BOADICEA model³⁵ all provide probability data, but each has its limitations. Breast specialists who provide high-risk assessment services calculate risk using a variety of models and choosing the most appropriate model(s) for each patient.^36,37 Women with a high probability of carrying a mutation, based on history and findings from the risk assessment model, are referred for genetics counseling and testing.

Reducing the Risk
Risk reduction is an integral component of high-risk breast cancer management, and several strategies are currently recommended, including these:

• Exercise for 45 to 60 minutes at least five times per week.^2,38 In women who engage in at least five hours of vigorous exercise each week, a 0.62 relative risk for breast cancer has been reported.^38,39

• Limit alcohol intake to fewer than one to two drinks per day. A number of studies have documented a 30% to 50% increase in the incidence of breast cancer among women who consume alcohol in greater quantities.^38,40

• Avoid obesity. Compared with women who have maintained their weight since age 18, those who gain 55 lb or more by menopause onset have a 1.45 relative risk for breast cancer.^38,41

• Breastfeed infants. Lactation for two years or longer decreases the lifetime risk for breast cancer by 50%.³

• Follow a low-fat, high-fiber diet, rich in fresh fruits and vegetables. Increasing fruit and vegetable intake by even one serving per day has been associated with a 9% decrease in breast cancer incidence.^38,42

Chemoprevention for At-Risk Women
Another risk reduction strategy for women at particularly high risk for breast cancer is chemoprevention. Currently, two medications, tamoxifen and raloxifene, are FDA approved for breast cancer risk reduction in women at high risk. These agents are offered to women with specific high-risk factors, including:

• Findings of LCIS, ADH, or ALH on previous breast biopsy

• A five-year probability of breast cancer exceeding 1.7%, based on a validated risk assessment model (eg, the Gail model, BRCAPRO)

• Presence of the BRCA1 or BRCA2 mutation.

Tamoxifen is a selective estrogen receptor modulator (SERM) that blocks the effects of estrogen on breast tissue.⁴³ Often referred to as an “antiestrogen,” it is approved for use in both premenopausal and postmenopausal women. In the Breast Cancer Prevention Trial,⁴⁴ women at high risk for breast cancer who took tamoxifen for five years had about a 50% risk reduction for invasive breast cancer and a 30% risk reduction in noninvasive breast cancer. The usual dose of tamoxifen is 20 mg/d.

Adverse effects associated with tamoxifen use, however, include blood clots, stroke, and uterine cancer. Women should not take tamoxifen if they have a history of cataracts, are current hormone therapy users, are planning a pregnancy or have the potential for becoming pregnant, or have a history of stroke, deep venous thrombosis, or pulmonary embolus. Less serious adverse effects include menopausal symptoms, menstrual irregularities, headache, fatigue, nausea, and skin irritation.⁴³

Raloxifene, though more commonly prescribed to prevent and treat osteoporosis, has been shown to reduce the risk for invasive breast cancer by 56% to 72%, compared with placebo^45,46; it exerts estrogenic effects on bone and antiestrogenic effects on breast and endometrial tissue.⁴⁷ This SERM is approved for breast cancer risk reduction only in postmenopausal women.⁴⁸ Recommended use is 60 mg/d for five years.

Although raloxifene provides a risk reduction benefit comparable to that of tamoxifen against invasive breast cancer (ie, incidence rates of 4.4 and 4.3, respectively, per 1,000 women per year⁴⁹), it does not appear to reduce the risk for noninvasive breast cancer (ie, ductal carcinoma in situ).⁵⁰ Potential major complications attributed to raloxifene use include blood clots, stroke, and uterine cancer, although the risk for uterine cancer is lower than with tamoxifen use.⁴⁹ Minor adverse effects include leg cramps, menopausal symptoms, edema of the extremities, and flulike symptoms. Contraindications are comparable to those associated with tamoxifen.⁴⁸

Screening Recommendations
Combined with mammography and breast ultrasound, the use of MRI to screen high-risk women is now being recommended, according to guidelines published in March 2007 by the American Cancer Society.²⁰ Patient factors suggesting greatest benefit from annual MRI screening (combined with mammography) are listed in Table 3.^4,20,51-55

In addition to patient-driven reduction strategies and the provider-initiated interventions for surveillance and management, monthly breast self-examination is encouraged, as are clinical breast examinations every six months.

Even with the most aggressive risk reduction program, not all breast cancers can be prevented. A key objective of high-risk screening and management is to identify patients with breast cancer at the earliest possible stage so that a cure is more likely to be achieved.

Conclusion
Identifying and screening women at high risk for breast cancer are essential skills for all primary care providers. Maintaining a comprehensive list of referral sources for high-risk management and genetic counseling services in your area will allow you to partner with other professionals to provide patients with the best possible care. Women feel empowered by education, particularly the newly acquired knowledge about breast cancer risk reduction—and reassured, knowing that their providers are interested and well informed in this complex area of women’s health.