Family physicians who care for infants and young children are often asked to diagnose growth lags and failure to meet parents’ expectations for reaching developmental milestones: Why isn’t my child gaining weight? Why isn’t he talking? The other kids in the day-care center ride tricycles—why can’t he? Will he catch up? My mother thinks he’s funny looking. Do you?

Simple reassurance is all that most of these worried families need. But for families with children whose growth or developmental milestones are sufficiently outside the usual parameters, more than reassurance is called for. As you consider whether the lags that worry parents are signs of a serious disability, it’s important to make a place for fetal alcohol syndrome (FAS) in your differential.

FAS, a congenital disorder caused by alcohol exposure during pregnancy, is characterized by growth deficiency before and after birth, distinctive facial features, and central nervous system (CNS) dysfunctions. The cognitive and developmental effects of FAS persist throughout life and are severe enough to limit employment and independent living.^1,2

A spectrum of severity. FAS is the most severe expression of prenatal alcohol exposure. The term fetal alcohol spectrum disorders (FASD) is a nondiagnostic umbrella term that includes FAS as well as ARND (alcohol-related neurobehavioral disorder) and ARBD (alcohol-related birth defects). Children with ARND and ARBD fail to meet the full FAS diagnostic criteria but still exhibit the negative effects of gestational alcohol exposure. Centers for Disease Control and Prevention (CDC) diagnostic criteria for FAS are summarized in TABLE 1. Studies by the CDC have reported FAS prevalence rates from 0.2 to 1.5 cases per 1000 live births, with a higher prevalence among minority (Native American and African American) and impoverished groups.¹

An opportunity—and a challenge. As a family physician, you have a unique opportunity to modify the impact of FAS by recognizing the disorder in infancy or early childhood, actively engineering appropriate referrals, and supporting families in the difficult task of parenting a child with disabilities. Correctly diagnosing a child with FAS before age 6 can have a protective influence, decreasing the odds that he or she will suffer severe secondary disabilities in adolescence and adulthood. You can also help prevent FAS by screening for potentially harmful drinking patterns and helping sexually active female patients decrease alcohol consumption and use contraception successfully.

Providing these supportive and preventive services can be challenging. A recent survey of pediatricians revealed that only 34% felt prepared to manage and coordinate the treatment of children with FASD, and only 13% routinely counseled adolescent patients about the risks of drinking and pregnancy.³ Th is article will help you surmount the difficulties these tasks present and perform vital functions for alcohol-affected families you may encounter in your practice.

TABLE 1
Diagnostic criteria for fetal alcohol syndrome

The place to start: Spotting mothers at risk

Recognizing an infant with FAS starts by asking the baby’s mother about her pattern of drinking while she was pregnant. Most studies on the effects of gestational exposure to alcohol have emphasized moderate to high levels of exposure. In 1 study, children who were exposed to binge drinking were 1.7 times as likely to have IQ scores in the mentally retarded range and 2.5 times more likely to have clinically significant levels of delinquent behavior.⁴ Binge drinking is defined by the National Institute of Alcohol Abuse and Alcoholism as a pattern of drinking that brings blood alcohol concentration to 0.8% or above, which typically happens in women who consume 4 or more drinks in a period of about 2 hours.⁵

But a pregnant woman doesn’t have to be a binge drinker to put her fetus at risk. Even low levels of prenatal alcohol use—as low as 1 drink per week—have been associated with adverse behavioral changes in children, including increased aggressive behaviors documented at school age.⁶,⁷ The research documenting effects at these low levels has led the American Academy of Pediatrics (AAP) and the American Congress of Obstetricians and Gynecologists (ACOG) to recommend total abstinence from alcohol throughout pregnancy.⁸,⁹ Patterns of “at risk” drinking for women include binge drinking or persistent regular use (>7 drinks in 1 week). If a mother provides a history of that level of prenatal exposure, her child should be referred for multidisciplinary evaluation at an FAS center, even in the absence of the characteristic facial features.¹

The face of FAS

Without a history of prenatal alcohol exposure, the cardinal features of facial dysmorphia (short palpebral fissures, smooth philtrum, and thin vermillion border) plus deficits in height and weight are the main physical findings of FAS. Evaluating height and weight percentiles is a routine part of well-child care, requiring minimal training. Height or weight or both at or below the 10th percentile, adjusted for age, sex, gestational age, and race or ethnicity, meet part of the CDC diagnostic criteria for FAS, but must be accompanied by at least 1 of the typical facial features associated with FAS to meet referral guidelines.¹ The diagnostic guidelines are more restrictive, requiring all 3 facial features to meet the threshold for an FAS diagnosis, vs another diagnosis, such as alcohol-related neurodevelopmental disorders (TABLE 1).

Learning to measure faces. Examining a child for the facial characteristics of FAS requires a set of skills that can be learned in a relatively short time, with moderate interrater reliability when compared with dysmorphologists, according to 1 study.¹⁰

Tools for measuring. Palpebral fissure length (PFL) can be measured with a clear plastic ruler pressed onto the child’s cheek to determine the distance from the endocanthion to the exocanthion while the child is gazing upward.¹¹ To meet the CDC criteria for FAS, this distance should be at or below the 10th percentile compared to norms. The shape of the lips and the nature of the philtrum are then compared to preestablished comparison photographs available on the University of Washington Lip-Philtrum Guides (see URL that follows).¹² The vermillion border and the philtrum must both receive a rank of 4 or 5 to meet FAS criteria.¹¹

Tools available online for physicians include Lip-Philtrum Guides (www.depts.washington.edu/fasdpn/htmls/lip-philtrum-guides.htm) and an instructional video depicting PFL measurement techniques (www.depts.washington.edu/fasdpn/htmls/photo-face.htm), both from the University of Washington FAS Diagnostic and Prevention Network. In addition, a physical evaluation summary form, with reference data for PFL in Caucasian, black, and Hispanic children, is available at http://www.fas.academicedge.com/documents/phyevaln.pdf.

The Astley-Clarren criteria. The 4-digit diagnostic code developed by Astley and Clarren for diagnosis of FAS and employed at some FAS referral centers uses very strict criteria.¹³ Centers using these criteria define “abnormal” as ≥2 standard deviations below the mean or its equivalent, ≤2.5th percentile.¹³ Th is applies to the 3 facial features and CNS dysfunction (low IQ, eg). If all 3 facial features are identified in the Astley-Clarren system as abnormal (PFL ≤2.5th percentile, lip philtrum 5, vermillion 5), the sensitivity of the facial features is 100% and specificity is 99.8% for a diagnosis of FAS.¹³

The CDC criteria, developed with increased surveillance by providers as a goal, uses relaxed criteria of ≤10th percentile of PFL and 4 or 5 on the philtrum/vermillion border guide to identify abnormal facial features and <10th percentile in CNS dysfunctions. Sensitivity and specificity data for those CDC criteria are not available.¹

CNS abnormalities may be noted early enough to trigger a referral for complete evaluation, but must be present in some degree to confirm a diagnosis of FAS. Abnormalities may include microcephaly with head circumference below the 10th percentile; clinically significant brain abnormalities observable through imaging, especially a small or absent corpus callosum; and functional deficits in any of a multitude of domains. In an infant, these deficits may be expressed in global developmental delays, sleep cycle problems, poor muscle tone, and feeding problems with poor suck and texture aversion.¹

Evaluation may not confirm the diagnosis. Children referred for more extensive evaluation may or may not be confirmed to have FAS. In 2 demographically similar counties in New York state, only 5% of children initially identified in 1 county (10 of 208) and 13% (53 of 420) of children in the other county were confirmed to have FAS.¹² The FAS diagnosis is complicated and the CNS and growth deficiencies may not be expressed until a later age.¹⁴ (See “Fetal alcohol syndrome across the lifespan”^1,15)

Providers may feel reluctant to alarm or stigmatize families when they are unsure of the diagnosis, but the long-term benefit of confirming the diagnosis early on may be significant for the child and family. The case on page 341 (Tanya) illustrates the complexity of diagnosing FASD.

The encouraging news for family physicians is that the odds of escaping adverse life outcomes are increased 2- to 4-fold by receiving a diagnosis of FAS before age 6 and by being raised in a stable environment.¹⁶ Early diagnosis can be protective by helping with eligibility requirements for support services and by opening the door to medical management of FAS-associated conditions such as ADHD and depression. In addition, the diagnosis can alert family physicians to the family’s need for help with ongoing problems with alcohol use. The case on page 341 (Brianna) illustrates the complex secondary problems a teen with FAS may face.

Putting families in touch with resources
Multidisciplinary FAS teams may include physicians (a geneticist or developmental pediatrician), psychologists, speech pathologists, educational specialists, social workers, and occupational therapists. These groups typically have in-depth intake and evaluation processes, including neurodiagnostic studies that help clarify the cognitive and functional domains that are affected.

You can locate the nearest FAS evaluation team and other resources for providers and families on the National and State Resource Directory for the National Organization on Fetal Alcohol Syndrome. Go to www.nofas.org, click on Resources, then on National and State Resources Directory in the box on the left side of the page. There may be a waiting list for evaluation, but under Part C of the Individuals with Disabilities Education Act (IDEA), FAS is considered a “presumptive eligibility” diagnosis. Presumptive diagnoses allow children under age 3 at risk of later developmental delay to be served without meeting particular eligibility criteria.¹ Physicians may refer these children for developmental assessment services and early intervention services while waiting for the more complete FAS evaluation.

After the age of 3, children and families are referred to preschool programs for children with disabilities that are administered through IDEA Part B, with no “presumptive eligibility” diagnoses. Eligibility for educational services under this program is entirely based on functional criteria.

Your best bet: Prevention

The key to preventing FAS is to find out whether your patient’s drinking patterns and contraceptive habits put her at risk for an alcohol-exposed pregnancy. Make it routine practice to ask women, in a way that encourages honest reporting, about both of these aspects of their lives. The US Preventive Services Task Force recommends screening and counseling intervention in primary care settings to reduce alcohol misuse in adults, including pregnant women.¹⁷ The case on page 341 (Clarice) illustrates how screening and brief intervention can be used to prevent alcohol-exposed pregnancy.

Screening should include simple quantity and frequency questions developed by the National Institute on Alcohol Abuse to clarify a patient’s current drinking patterns. The questions include the numbers of days per week of any drinking, the average number of drinks per day, and the maximum number of drinks consumed in 1 day during the past month. Determining that a woman drinks more than 7 drinks per week has a 29% sensitivity, but a 90% specificity for identifying lifetime risk of alcohol abuse or dependence.¹⁸

Other tools include TWEAK (Tolerance, Worry, Eye-opener, Amnesia, (K)Cut down), T-ACE (Tolerance, Annoyed, Cut down, Eye opener), and AUDIT (Alcohol Use Disorder Identification Test). They are detailed below and available online at Project Cork. Go to www.projectcork.org, and click on “clinical tools.”

The 5-item TWEAK tool (TABLE 2) appears to be the optimal screening questionnaire for identifying women in racially mixed populations with heavy drinking or alcohol abuse and dependence, but a score of 2 points should be the threshold for identifying female problem drinkers.^19,20 Using the lower cutoff of 2, the sensitivity of TWEAK is in the 87% to 91% range for women, with a specificity of 77% to 90%.¹⁸

The T-ACE tool is a set of 4 questions, with the question addressing tolerance weighted more heavily than the others. With a score of 2 or more, the sensitivity of T-ACE is 70% to 88%; the specificity is 79% to 85%.¹⁸

The AUDIT tool is a self-administered screen that consists of a series of 10 questions that are each scored on a scale of 0 to 4. The maximum score is 40. A score of 2 indicates some harmful use of alcohol, but a score of 8 or more has a sensitivity of 59% to 66%, with a specificity of 93% to 97% in women.¹⁸

TABLE 2
TWEAK your patients for alcohol use

When your patient is at risk

Brief interventions are recommended for nonpregnant and pregnant women who have exhibited a pattern of at-risk or problem drinking.²¹TABLE 3 summarizes patterns of drinking in women, from not drinking at all through various degrees of risk to alcohol dependency. Referral to an addiction specialist is recommended for women with alcohol dependence.

Brief interventions for alcohol abuse can be single-session encounters from 5 to 15 minutes’ duration, or multi-contact brief sessions, including possible phone follow-up contacts. Project TrEAT (Trial for Early Alcohol Treatment) provided two 15-minute sessions with the primary care physician (either a family physician or internist in community-based practice) scheduled 1 month apart, with nurse follow-up phone calls 2 weeks after each appointment.²²

TABLE 3
Drinking patterns in women

Patients received general information regarding adverse effects of alcohol and the prevalence of problem drinking, in addition to tools to help them identify drinking triggers and track their consumption. The patient and physician developed a “drinking agreement” in the form of a rescription. Men and non pregnant women were included in this study.

Women reduced their alcohol use by 47% and their frequency of binge drinking by 56%, as noted at a 6-month follow-up, with changes well maintained at 12 months. The reductions for female patients were actually slightly higher than for male participants.²²

Chang and colleagues provided a 25-minute single session brief intervention to pregnant women who had screened positive on the T-ACE questionnaire with a score of 2 or more, and were identified as being at risk for prenatal alcohol use.²³ Participants were randomly assigned to the intervention group or a control group. Both the control group and the brief intervention group decreased their use of alcohol after enrolling in the study and undergoing the initial detailed assessment.

For women who were heavier drinkers, the brief interventions for prenatal alcohol use were statistically more effective in reducing their frequency of alcohol consumption, vs the initial assessment alone. In addition, the effects of the brief intervention were significantly enhanced when a support partner of the woman’s choice also participated.²³

The Project Choices Intervention Research Group studied an intervention that included 4 sessions of motivational interviewing regarding alcohol habits, and a contraception counseling session.²⁴ Study participants were recruited from 6 community-based settings with high proportions of women at risk for an alcohol-exposed pregnancy, including a jail and 2 drug and alcohol treatment centers. Among the 143 women who completed the 6-month follow-up, 68.5% were no longer at risk of having an alcohol-exposed pregnancy.

These participants successfully lowered their risk by reducing alcohol use only (12.9%), adopting appropriate contraception use only (23.1%), or by changing both risk factors (32.9%). Even if all the study participants who were lost to follow-up were assumed to have been unsuccessful at eliminating their risk of alcohol-exposed pregnancy, more than half of the women (51.6%) successfully changed.²⁴

Take advantage of opportunities
FAS is the most severe consequence of alcohol-exposed pregnancy, leaving the affected child with a lifelong disability. As a family physician, you have access to easy-touse, cost-effective clinical tools to screen for at-risk drinking behaviors and have sufficient rapport with your patients to encourage effective contraceptive practices. You also have effective tools for helping patients reduce their alcohol consumption.

Within the context of your long-term relationships with patients, you can provide brief interventions that include factual information and opportunities for goal setting. You can assist families with an FAS child to access services, manage medically related complications, and plan for special education and vocational skills training.

Recognition that 1 child in a family is affected by prenatal alcohol exposure gives you another window of opportunity to address the underlying substance use issues in the mother and the family, increasing the odds that future pregnancies will not be alcohol exposed.

CORRESPONDENCE Mary C. Boyce, MD, Wesley Family Medicine Residency, 850 N. Hillside, Wichita, KS 67214; [email protected]

Family physicians who care for infants and young children are often asked to diagnose growth lags and failure to meet parents’ expectations for reaching developmental milestones: Why isn’t my child gaining weight? Why isn’t he talking? The other kids in the day-care center ride tricycles—why can’t he? Will he catch up? My mother thinks he’s funny looking. Do you?

Simple reassurance is all that most of these worried families need. But for families with children whose growth or developmental milestones are sufficiently outside the usual parameters, more than reassurance is called for. As you consider whether the lags that worry parents are signs of a serious disability, it’s important to make a place for fetal alcohol syndrome (FAS) in your differential.

FAS, a congenital disorder caused by alcohol exposure during pregnancy, is characterized by growth deficiency before and after birth, distinctive facial features, and central nervous system (CNS) dysfunctions. The cognitive and developmental effects of FAS persist throughout life and are severe enough to limit employment and independent living.^1,2

A spectrum of severity. FAS is the most severe expression of prenatal alcohol exposure. The term fetal alcohol spectrum disorders (FASD) is a nondiagnostic umbrella term that includes FAS as well as ARND (alcohol-related neurobehavioral disorder) and ARBD (alcohol-related birth defects). Children with ARND and ARBD fail to meet the full FAS diagnostic criteria but still exhibit the negative effects of gestational alcohol exposure. Centers for Disease Control and Prevention (CDC) diagnostic criteria for FAS are summarized in TABLE 1. Studies by the CDC have reported FAS prevalence rates from 0.2 to 1.5 cases per 1000 live births, with a higher prevalence among minority (Native American and African American) and impoverished groups.¹

An opportunity—and a challenge. As a family physician, you have a unique opportunity to modify the impact of FAS by recognizing the disorder in infancy or early childhood, actively engineering appropriate referrals, and supporting families in the difficult task of parenting a child with disabilities. Correctly diagnosing a child with FAS before age 6 can have a protective influence, decreasing the odds that he or she will suffer severe secondary disabilities in adolescence and adulthood. You can also help prevent FAS by screening for potentially harmful drinking patterns and helping sexually active female patients decrease alcohol consumption and use contraception successfully.

Providing these supportive and preventive services can be challenging. A recent survey of pediatricians revealed that only 34% felt prepared to manage and coordinate the treatment of children with FASD, and only 13% routinely counseled adolescent patients about the risks of drinking and pregnancy.³ Th is article will help you surmount the difficulties these tasks present and perform vital functions for alcohol-affected families you may encounter in your practice.

TABLE 1
Diagnostic criteria for fetal alcohol syndrome

The place to start: Spotting mothers at risk

Recognizing an infant with FAS starts by asking the baby’s mother about her pattern of drinking while she was pregnant. Most studies on the effects of gestational exposure to alcohol have emphasized moderate to high levels of exposure. In 1 study, children who were exposed to binge drinking were 1.7 times as likely to have IQ scores in the mentally retarded range and 2.5 times more likely to have clinically significant levels of delinquent behavior.⁴ Binge drinking is defined by the National Institute of Alcohol Abuse and Alcoholism as a pattern of drinking that brings blood alcohol concentration to 0.8% or above, which typically happens in women who consume 4 or more drinks in a period of about 2 hours.⁵

But a pregnant woman doesn’t have to be a binge drinker to put her fetus at risk. Even low levels of prenatal alcohol use—as low as 1 drink per week—have been associated with adverse behavioral changes in children, including increased aggressive behaviors documented at school age.⁶,⁷ The research documenting effects at these low levels has led the American Academy of Pediatrics (AAP) and the American Congress of Obstetricians and Gynecologists (ACOG) to recommend total abstinence from alcohol throughout pregnancy.⁸,⁹ Patterns of “at risk” drinking for women include binge drinking or persistent regular use (>7 drinks in 1 week). If a mother provides a history of that level of prenatal exposure, her child should be referred for multidisciplinary evaluation at an FAS center, even in the absence of the characteristic facial features.¹

The face of FAS

Without a history of prenatal alcohol exposure, the cardinal features of facial dysmorphia (short palpebral fissures, smooth philtrum, and thin vermillion border) plus deficits in height and weight are the main physical findings of FAS. Evaluating height and weight percentiles is a routine part of well-child care, requiring minimal training. Height or weight or both at or below the 10th percentile, adjusted for age, sex, gestational age, and race or ethnicity, meet part of the CDC diagnostic criteria for FAS, but must be accompanied by at least 1 of the typical facial features associated with FAS to meet referral guidelines.¹ The diagnostic guidelines are more restrictive, requiring all 3 facial features to meet the threshold for an FAS diagnosis, vs another diagnosis, such as alcohol-related neurodevelopmental disorders (TABLE 1).

Learning to measure faces. Examining a child for the facial characteristics of FAS requires a set of skills that can be learned in a relatively short time, with moderate interrater reliability when compared with dysmorphologists, according to 1 study.¹⁰

Tools for measuring. Palpebral fissure length (PFL) can be measured with a clear plastic ruler pressed onto the child’s cheek to determine the distance from the endocanthion to the exocanthion while the child is gazing upward.¹¹ To meet the CDC criteria for FAS, this distance should be at or below the 10th percentile compared to norms. The shape of the lips and the nature of the philtrum are then compared to preestablished comparison photographs available on the University of Washington Lip-Philtrum Guides (see URL that follows).¹² The vermillion border and the philtrum must both receive a rank of 4 or 5 to meet FAS criteria.¹¹

Tools available online for physicians include Lip-Philtrum Guides (www.depts.washington.edu/fasdpn/htmls/lip-philtrum-guides.htm) and an instructional video depicting PFL measurement techniques (www.depts.washington.edu/fasdpn/htmls/photo-face.htm), both from the University of Washington FAS Diagnostic and Prevention Network. In addition, a physical evaluation summary form, with reference data for PFL in Caucasian, black, and Hispanic children, is available at http://www.fas.academicedge.com/documents/phyevaln.pdf.

The Astley-Clarren criteria. The 4-digit diagnostic code developed by Astley and Clarren for diagnosis of FAS and employed at some FAS referral centers uses very strict criteria.¹³ Centers using these criteria define “abnormal” as ≥2 standard deviations below the mean or its equivalent, ≤2.5th percentile.¹³ Th is applies to the 3 facial features and CNS dysfunction (low IQ, eg). If all 3 facial features are identified in the Astley-Clarren system as abnormal (PFL ≤2.5th percentile, lip philtrum 5, vermillion 5), the sensitivity of the facial features is 100% and specificity is 99.8% for a diagnosis of FAS.¹³

The CDC criteria, developed with increased surveillance by providers as a goal, uses relaxed criteria of ≤10th percentile of PFL and 4 or 5 on the philtrum/vermillion border guide to identify abnormal facial features and <10th percentile in CNS dysfunctions. Sensitivity and specificity data for those CDC criteria are not available.¹

CNS abnormalities may be noted early enough to trigger a referral for complete evaluation, but must be present in some degree to confirm a diagnosis of FAS. Abnormalities may include microcephaly with head circumference below the 10th percentile; clinically significant brain abnormalities observable through imaging, especially a small or absent corpus callosum; and functional deficits in any of a multitude of domains. In an infant, these deficits may be expressed in global developmental delays, sleep cycle problems, poor muscle tone, and feeding problems with poor suck and texture aversion.¹

Evaluation may not confirm the diagnosis. Children referred for more extensive evaluation may or may not be confirmed to have FAS. In 2 demographically similar counties in New York state, only 5% of children initially identified in 1 county (10 of 208) and 13% (53 of 420) of children in the other county were confirmed to have FAS.¹² The FAS diagnosis is complicated and the CNS and growth deficiencies may not be expressed until a later age.¹⁴ (See “Fetal alcohol syndrome across the lifespan”^1,15)

Providers may feel reluctant to alarm or stigmatize families when they are unsure of the diagnosis, but the long-term benefit of confirming the diagnosis early on may be significant for the child and family. The case on page 341 (Tanya) illustrates the complexity of diagnosing FASD.

The encouraging news for family physicians is that the odds of escaping adverse life outcomes are increased 2- to 4-fold by receiving a diagnosis of FAS before age 6 and by being raised in a stable environment.¹⁶ Early diagnosis can be protective by helping with eligibility requirements for support services and by opening the door to medical management of FAS-associated conditions such as ADHD and depression. In addition, the diagnosis can alert family physicians to the family’s need for help with ongoing problems with alcohol use. The case on page 341 (Brianna) illustrates the complex secondary problems a teen with FAS may face.

Putting families in touch with resources
Multidisciplinary FAS teams may include physicians (a geneticist or developmental pediatrician), psychologists, speech pathologists, educational specialists, social workers, and occupational therapists. These groups typically have in-depth intake and evaluation processes, including neurodiagnostic studies that help clarify the cognitive and functional domains that are affected.

You can locate the nearest FAS evaluation team and other resources for providers and families on the National and State Resource Directory for the National Organization on Fetal Alcohol Syndrome. Go to www.nofas.org, click on Resources, then on National and State Resources Directory in the box on the left side of the page. There may be a waiting list for evaluation, but under Part C of the Individuals with Disabilities Education Act (IDEA), FAS is considered a “presumptive eligibility” diagnosis. Presumptive diagnoses allow children under age 3 at risk of later developmental delay to be served without meeting particular eligibility criteria.¹ Physicians may refer these children for developmental assessment services and early intervention services while waiting for the more complete FAS evaluation.

After the age of 3, children and families are referred to preschool programs for children with disabilities that are administered through IDEA Part B, with no “presumptive eligibility” diagnoses. Eligibility for educational services under this program is entirely based on functional criteria.

Your best bet: Prevention

The key to preventing FAS is to find out whether your patient’s drinking patterns and contraceptive habits put her at risk for an alcohol-exposed pregnancy. Make it routine practice to ask women, in a way that encourages honest reporting, about both of these aspects of their lives. The US Preventive Services Task Force recommends screening and counseling intervention in primary care settings to reduce alcohol misuse in adults, including pregnant women.¹⁷ The case on page 341 (Clarice) illustrates how screening and brief intervention can be used to prevent alcohol-exposed pregnancy.

Screening should include simple quantity and frequency questions developed by the National Institute on Alcohol Abuse to clarify a patient’s current drinking patterns. The questions include the numbers of days per week of any drinking, the average number of drinks per day, and the maximum number of drinks consumed in 1 day during the past month. Determining that a woman drinks more than 7 drinks per week has a 29% sensitivity, but a 90% specificity for identifying lifetime risk of alcohol abuse or dependence.¹⁸

Other tools include TWEAK (Tolerance, Worry, Eye-opener, Amnesia, (K)Cut down), T-ACE (Tolerance, Annoyed, Cut down, Eye opener), and AUDIT (Alcohol Use Disorder Identification Test). They are detailed below and available online at Project Cork. Go to www.projectcork.org, and click on “clinical tools.”

The 5-item TWEAK tool (TABLE 2) appears to be the optimal screening questionnaire for identifying women in racially mixed populations with heavy drinking or alcohol abuse and dependence, but a score of 2 points should be the threshold for identifying female problem drinkers.^19,20 Using the lower cutoff of 2, the sensitivity of TWEAK is in the 87% to 91% range for women, with a specificity of 77% to 90%.¹⁸

The T-ACE tool is a set of 4 questions, with the question addressing tolerance weighted more heavily than the others. With a score of 2 or more, the sensitivity of T-ACE is 70% to 88%; the specificity is 79% to 85%.¹⁸

The AUDIT tool is a self-administered screen that consists of a series of 10 questions that are each scored on a scale of 0 to 4. The maximum score is 40. A score of 2 indicates some harmful use of alcohol, but a score of 8 or more has a sensitivity of 59% to 66%, with a specificity of 93% to 97% in women.¹⁸

TABLE 2
TWEAK your patients for alcohol use

When your patient is at risk

Brief interventions are recommended for nonpregnant and pregnant women who have exhibited a pattern of at-risk or problem drinking.²¹TABLE 3 summarizes patterns of drinking in women, from not drinking at all through various degrees of risk to alcohol dependency. Referral to an addiction specialist is recommended for women with alcohol dependence.

Brief interventions for alcohol abuse can be single-session encounters from 5 to 15 minutes’ duration, or multi-contact brief sessions, including possible phone follow-up contacts. Project TrEAT (Trial for Early Alcohol Treatment) provided two 15-minute sessions with the primary care physician (either a family physician or internist in community-based practice) scheduled 1 month apart, with nurse follow-up phone calls 2 weeks after each appointment.²²

TABLE 3
Drinking patterns in women

Patients received general information regarding adverse effects of alcohol and the prevalence of problem drinking, in addition to tools to help them identify drinking triggers and track their consumption. The patient and physician developed a “drinking agreement” in the form of a rescription. Men and non pregnant women were included in this study.

Women reduced their alcohol use by 47% and their frequency of binge drinking by 56%, as noted at a 6-month follow-up, with changes well maintained at 12 months. The reductions for female patients were actually slightly higher than for male participants.²²

Chang and colleagues provided a 25-minute single session brief intervention to pregnant women who had screened positive on the T-ACE questionnaire with a score of 2 or more, and were identified as being at risk for prenatal alcohol use.²³ Participants were randomly assigned to the intervention group or a control group. Both the control group and the brief intervention group decreased their use of alcohol after enrolling in the study and undergoing the initial detailed assessment.

For women who were heavier drinkers, the brief interventions for prenatal alcohol use were statistically more effective in reducing their frequency of alcohol consumption, vs the initial assessment alone. In addition, the effects of the brief intervention were significantly enhanced when a support partner of the woman’s choice also participated.²³

The Project Choices Intervention Research Group studied an intervention that included 4 sessions of motivational interviewing regarding alcohol habits, and a contraception counseling session.²⁴ Study participants were recruited from 6 community-based settings with high proportions of women at risk for an alcohol-exposed pregnancy, including a jail and 2 drug and alcohol treatment centers. Among the 143 women who completed the 6-month follow-up, 68.5% were no longer at risk of having an alcohol-exposed pregnancy.

These participants successfully lowered their risk by reducing alcohol use only (12.9%), adopting appropriate contraception use only (23.1%), or by changing both risk factors (32.9%). Even if all the study participants who were lost to follow-up were assumed to have been unsuccessful at eliminating their risk of alcohol-exposed pregnancy, more than half of the women (51.6%) successfully changed.²⁴

Take advantage of opportunities
FAS is the most severe consequence of alcohol-exposed pregnancy, leaving the affected child with a lifelong disability. As a family physician, you have access to easy-touse, cost-effective clinical tools to screen for at-risk drinking behaviors and have sufficient rapport with your patients to encourage effective contraceptive practices. You also have effective tools for helping patients reduce their alcohol consumption.

Within the context of your long-term relationships with patients, you can provide brief interventions that include factual information and opportunities for goal setting. You can assist families with an FAS child to access services, manage medically related complications, and plan for special education and vocational skills training.

Recognition that 1 child in a family is affected by prenatal alcohol exposure gives you another window of opportunity to address the underlying substance use issues in the mother and the family, increasing the odds that future pregnancies will not be alcohol exposed.

CORRESPONDENCE Mary C. Boyce, MD, Wesley Family Medicine Residency, 850 N. Hillside, Wichita, KS 67214; [email protected]

Family physicians who care for infants and young children are often asked to diagnose growth lags and failure to meet parents’ expectations for reaching developmental milestones: Why isn’t my child gaining weight? Why isn’t he talking? The other kids in the day-care center ride tricycles—why can’t he? Will he catch up? My mother thinks he’s funny looking. Do you?

Simple reassurance is all that most of these worried families need. But for families with children whose growth or developmental milestones are sufficiently outside the usual parameters, more than reassurance is called for. As you consider whether the lags that worry parents are signs of a serious disability, it’s important to make a place for fetal alcohol syndrome (FAS) in your differential.

FAS, a congenital disorder caused by alcohol exposure during pregnancy, is characterized by growth deficiency before and after birth, distinctive facial features, and central nervous system (CNS) dysfunctions. The cognitive and developmental effects of FAS persist throughout life and are severe enough to limit employment and independent living.^1,2

A spectrum of severity. FAS is the most severe expression of prenatal alcohol exposure. The term fetal alcohol spectrum disorders (FASD) is a nondiagnostic umbrella term that includes FAS as well as ARND (alcohol-related neurobehavioral disorder) and ARBD (alcohol-related birth defects). Children with ARND and ARBD fail to meet the full FAS diagnostic criteria but still exhibit the negative effects of gestational alcohol exposure. Centers for Disease Control and Prevention (CDC) diagnostic criteria for FAS are summarized in TABLE 1. Studies by the CDC have reported FAS prevalence rates from 0.2 to 1.5 cases per 1000 live births, with a higher prevalence among minority (Native American and African American) and impoverished groups.¹

An opportunity—and a challenge. As a family physician, you have a unique opportunity to modify the impact of FAS by recognizing the disorder in infancy or early childhood, actively engineering appropriate referrals, and supporting families in the difficult task of parenting a child with disabilities. Correctly diagnosing a child with FAS before age 6 can have a protective influence, decreasing the odds that he or she will suffer severe secondary disabilities in adolescence and adulthood. You can also help prevent FAS by screening for potentially harmful drinking patterns and helping sexually active female patients decrease alcohol consumption and use contraception successfully.

Providing these supportive and preventive services can be challenging. A recent survey of pediatricians revealed that only 34% felt prepared to manage and coordinate the treatment of children with FASD, and only 13% routinely counseled adolescent patients about the risks of drinking and pregnancy.³ Th is article will help you surmount the difficulties these tasks present and perform vital functions for alcohol-affected families you may encounter in your practice.

TABLE 1
Diagnostic criteria for fetal alcohol syndrome

The place to start: Spotting mothers at risk

Recognizing an infant with FAS starts by asking the baby’s mother about her pattern of drinking while she was pregnant. Most studies on the effects of gestational exposure to alcohol have emphasized moderate to high levels of exposure. In 1 study, children who were exposed to binge drinking were 1.7 times as likely to have IQ scores in the mentally retarded range and 2.5 times more likely to have clinically significant levels of delinquent behavior.⁴ Binge drinking is defined by the National Institute of Alcohol Abuse and Alcoholism as a pattern of drinking that brings blood alcohol concentration to 0.8% or above, which typically happens in women who consume 4 or more drinks in a period of about 2 hours.⁵

But a pregnant woman doesn’t have to be a binge drinker to put her fetus at risk. Even low levels of prenatal alcohol use—as low as 1 drink per week—have been associated with adverse behavioral changes in children, including increased aggressive behaviors documented at school age.⁶,⁷ The research documenting effects at these low levels has led the American Academy of Pediatrics (AAP) and the American Congress of Obstetricians and Gynecologists (ACOG) to recommend total abstinence from alcohol throughout pregnancy.⁸,⁹ Patterns of “at risk” drinking for women include binge drinking or persistent regular use (>7 drinks in 1 week). If a mother provides a history of that level of prenatal exposure, her child should be referred for multidisciplinary evaluation at an FAS center, even in the absence of the characteristic facial features.¹

The face of FAS

Without a history of prenatal alcohol exposure, the cardinal features of facial dysmorphia (short palpebral fissures, smooth philtrum, and thin vermillion border) plus deficits in height and weight are the main physical findings of FAS. Evaluating height and weight percentiles is a routine part of well-child care, requiring minimal training. Height or weight or both at or below the 10th percentile, adjusted for age, sex, gestational age, and race or ethnicity, meet part of the CDC diagnostic criteria for FAS, but must be accompanied by at least 1 of the typical facial features associated with FAS to meet referral guidelines.¹ The diagnostic guidelines are more restrictive, requiring all 3 facial features to meet the threshold for an FAS diagnosis, vs another diagnosis, such as alcohol-related neurodevelopmental disorders (TABLE 1).

Learning to measure faces. Examining a child for the facial characteristics of FAS requires a set of skills that can be learned in a relatively short time, with moderate interrater reliability when compared with dysmorphologists, according to 1 study.¹⁰

Tools for measuring. Palpebral fissure length (PFL) can be measured with a clear plastic ruler pressed onto the child’s cheek to determine the distance from the endocanthion to the exocanthion while the child is gazing upward.¹¹ To meet the CDC criteria for FAS, this distance should be at or below the 10th percentile compared to norms. The shape of the lips and the nature of the philtrum are then compared to preestablished comparison photographs available on the University of Washington Lip-Philtrum Guides (see URL that follows).¹² The vermillion border and the philtrum must both receive a rank of 4 or 5 to meet FAS criteria.¹¹

Tools available online for physicians include Lip-Philtrum Guides (www.depts.washington.edu/fasdpn/htmls/lip-philtrum-guides.htm) and an instructional video depicting PFL measurement techniques (www.depts.washington.edu/fasdpn/htmls/photo-face.htm), both from the University of Washington FAS Diagnostic and Prevention Network. In addition, a physical evaluation summary form, with reference data for PFL in Caucasian, black, and Hispanic children, is available at http://www.fas.academicedge.com/documents/phyevaln.pdf.

The Astley-Clarren criteria. The 4-digit diagnostic code developed by Astley and Clarren for diagnosis of FAS and employed at some FAS referral centers uses very strict criteria.¹³ Centers using these criteria define “abnormal” as ≥2 standard deviations below the mean or its equivalent, ≤2.5th percentile.¹³ Th is applies to the 3 facial features and CNS dysfunction (low IQ, eg). If all 3 facial features are identified in the Astley-Clarren system as abnormal (PFL ≤2.5th percentile, lip philtrum 5, vermillion 5), the sensitivity of the facial features is 100% and specificity is 99.8% for a diagnosis of FAS.¹³

The CDC criteria, developed with increased surveillance by providers as a goal, uses relaxed criteria of ≤10th percentile of PFL and 4 or 5 on the philtrum/vermillion border guide to identify abnormal facial features and <10th percentile in CNS dysfunctions. Sensitivity and specificity data for those CDC criteria are not available.¹

CNS abnormalities may be noted early enough to trigger a referral for complete evaluation, but must be present in some degree to confirm a diagnosis of FAS. Abnormalities may include microcephaly with head circumference below the 10th percentile; clinically significant brain abnormalities observable through imaging, especially a small or absent corpus callosum; and functional deficits in any of a multitude of domains. In an infant, these deficits may be expressed in global developmental delays, sleep cycle problems, poor muscle tone, and feeding problems with poor suck and texture aversion.¹

Evaluation may not confirm the diagnosis. Children referred for more extensive evaluation may or may not be confirmed to have FAS. In 2 demographically similar counties in New York state, only 5% of children initially identified in 1 county (10 of 208) and 13% (53 of 420) of children in the other county were confirmed to have FAS.¹² The FAS diagnosis is complicated and the CNS and growth deficiencies may not be expressed until a later age.¹⁴ (See “Fetal alcohol syndrome across the lifespan”^1,15)

Providers may feel reluctant to alarm or stigmatize families when they are unsure of the diagnosis, but the long-term benefit of confirming the diagnosis early on may be significant for the child and family. The case on page 341 (Tanya) illustrates the complexity of diagnosing FASD.

The encouraging news for family physicians is that the odds of escaping adverse life outcomes are increased 2- to 4-fold by receiving a diagnosis of FAS before age 6 and by being raised in a stable environment.¹⁶ Early diagnosis can be protective by helping with eligibility requirements for support services and by opening the door to medical management of FAS-associated conditions such as ADHD and depression. In addition, the diagnosis can alert family physicians to the family’s need for help with ongoing problems with alcohol use. The case on page 341 (Brianna) illustrates the complex secondary problems a teen with FAS may face.

Putting families in touch with resources
Multidisciplinary FAS teams may include physicians (a geneticist or developmental pediatrician), psychologists, speech pathologists, educational specialists, social workers, and occupational therapists. These groups typically have in-depth intake and evaluation processes, including neurodiagnostic studies that help clarify the cognitive and functional domains that are affected.

You can locate the nearest FAS evaluation team and other resources for providers and families on the National and State Resource Directory for the National Organization on Fetal Alcohol Syndrome. Go to www.nofas.org, click on Resources, then on National and State Resources Directory in the box on the left side of the page. There may be a waiting list for evaluation, but under Part C of the Individuals with Disabilities Education Act (IDEA), FAS is considered a “presumptive eligibility” diagnosis. Presumptive diagnoses allow children under age 3 at risk of later developmental delay to be served without meeting particular eligibility criteria.¹ Physicians may refer these children for developmental assessment services and early intervention services while waiting for the more complete FAS evaluation.

After the age of 3, children and families are referred to preschool programs for children with disabilities that are administered through IDEA Part B, with no “presumptive eligibility” diagnoses. Eligibility for educational services under this program is entirely based on functional criteria.

Your best bet: Prevention

The key to preventing FAS is to find out whether your patient’s drinking patterns and contraceptive habits put her at risk for an alcohol-exposed pregnancy. Make it routine practice to ask women, in a way that encourages honest reporting, about both of these aspects of their lives. The US Preventive Services Task Force recommends screening and counseling intervention in primary care settings to reduce alcohol misuse in adults, including pregnant women.¹⁷ The case on page 341 (Clarice) illustrates how screening and brief intervention can be used to prevent alcohol-exposed pregnancy.

Screening should include simple quantity and frequency questions developed by the National Institute on Alcohol Abuse to clarify a patient’s current drinking patterns. The questions include the numbers of days per week of any drinking, the average number of drinks per day, and the maximum number of drinks consumed in 1 day during the past month. Determining that a woman drinks more than 7 drinks per week has a 29% sensitivity, but a 90% specificity for identifying lifetime risk of alcohol abuse or dependence.¹⁸

Other tools include TWEAK (Tolerance, Worry, Eye-opener, Amnesia, (K)Cut down), T-ACE (Tolerance, Annoyed, Cut down, Eye opener), and AUDIT (Alcohol Use Disorder Identification Test). They are detailed below and available online at Project Cork. Go to www.projectcork.org, and click on “clinical tools.”

The 5-item TWEAK tool (TABLE 2) appears to be the optimal screening questionnaire for identifying women in racially mixed populations with heavy drinking or alcohol abuse and dependence, but a score of 2 points should be the threshold for identifying female problem drinkers.^19,20 Using the lower cutoff of 2, the sensitivity of TWEAK is in the 87% to 91% range for women, with a specificity of 77% to 90%.¹⁸

The T-ACE tool is a set of 4 questions, with the question addressing tolerance weighted more heavily than the others. With a score of 2 or more, the sensitivity of T-ACE is 70% to 88%; the specificity is 79% to 85%.¹⁸

The AUDIT tool is a self-administered screen that consists of a series of 10 questions that are each scored on a scale of 0 to 4. The maximum score is 40. A score of 2 indicates some harmful use of alcohol, but a score of 8 or more has a sensitivity of 59% to 66%, with a specificity of 93% to 97% in women.¹⁸

TABLE 2
TWEAK your patients for alcohol use

When your patient is at risk

Brief interventions are recommended for nonpregnant and pregnant women who have exhibited a pattern of at-risk or problem drinking.²¹TABLE 3 summarizes patterns of drinking in women, from not drinking at all through various degrees of risk to alcohol dependency. Referral to an addiction specialist is recommended for women with alcohol dependence.

Brief interventions for alcohol abuse can be single-session encounters from 5 to 15 minutes’ duration, or multi-contact brief sessions, including possible phone follow-up contacts. Project TrEAT (Trial for Early Alcohol Treatment) provided two 15-minute sessions with the primary care physician (either a family physician or internist in community-based practice) scheduled 1 month apart, with nurse follow-up phone calls 2 weeks after each appointment.²²

TABLE 3
Drinking patterns in women

Patients received general information regarding adverse effects of alcohol and the prevalence of problem drinking, in addition to tools to help them identify drinking triggers and track their consumption. The patient and physician developed a “drinking agreement” in the form of a rescription. Men and non pregnant women were included in this study.

Women reduced their alcohol use by 47% and their frequency of binge drinking by 56%, as noted at a 6-month follow-up, with changes well maintained at 12 months. The reductions for female patients were actually slightly higher than for male participants.²²

Chang and colleagues provided a 25-minute single session brief intervention to pregnant women who had screened positive on the T-ACE questionnaire with a score of 2 or more, and were identified as being at risk for prenatal alcohol use.²³ Participants were randomly assigned to the intervention group or a control group. Both the control group and the brief intervention group decreased their use of alcohol after enrolling in the study and undergoing the initial detailed assessment.

For women who were heavier drinkers, the brief interventions for prenatal alcohol use were statistically more effective in reducing their frequency of alcohol consumption, vs the initial assessment alone. In addition, the effects of the brief intervention were significantly enhanced when a support partner of the woman’s choice also participated.²³

The Project Choices Intervention Research Group studied an intervention that included 4 sessions of motivational interviewing regarding alcohol habits, and a contraception counseling session.²⁴ Study participants were recruited from 6 community-based settings with high proportions of women at risk for an alcohol-exposed pregnancy, including a jail and 2 drug and alcohol treatment centers. Among the 143 women who completed the 6-month follow-up, 68.5% were no longer at risk of having an alcohol-exposed pregnancy.

These participants successfully lowered their risk by reducing alcohol use only (12.9%), adopting appropriate contraception use only (23.1%), or by changing both risk factors (32.9%). Even if all the study participants who were lost to follow-up were assumed to have been unsuccessful at eliminating their risk of alcohol-exposed pregnancy, more than half of the women (51.6%) successfully changed.²⁴

Take advantage of opportunities
FAS is the most severe consequence of alcohol-exposed pregnancy, leaving the affected child with a lifelong disability. As a family physician, you have access to easy-touse, cost-effective clinical tools to screen for at-risk drinking behaviors and have sufficient rapport with your patients to encourage effective contraceptive practices. You also have effective tools for helping patients reduce their alcohol consumption.

Within the context of your long-term relationships with patients, you can provide brief interventions that include factual information and opportunities for goal setting. You can assist families with an FAS child to access services, manage medically related complications, and plan for special education and vocational skills training.

Recognition that 1 child in a family is affected by prenatal alcohol exposure gives you another window of opportunity to address the underlying substance use issues in the mother and the family, increasing the odds that future pregnancies will not be alcohol exposed.

CORRESPONDENCE Mary C. Boyce, MD, Wesley Family Medicine Residency, 850 N. Hillside, Wichita, KS 67214; [email protected]

CASE 1 Vincent B, a 33-year-old executive, visits his family physician for an evaluation of chronic orchialgia. Although his testicular pain has waxed and waned for several years, it has recently worsened, making it increasingly difficult for him to exercise or to sit for extended periods of time. In fact, this visit was prompted by a lengthy meeting during which he developed a “dull ache” that did not let up until he left the meeting and walked around.

CASE 2 Jason H, a 42-year-old married father of 3 who had a vasectomy 2 years ago, has had progressively worsening testicular pain ever since. He also has occasional pain after ejaculation, but no known hematospermia. Recently, the pain has become so bad that it limits both his physical and sexual activities and is having a negative effect on his relationship with his wife. Jason is sexually monogamous, has no significant medical history, and takes no prescription medications.

These 2 cases are based on actual patients we have seen in our practices. If Vincent and Jason (not their real names) were your patients, how would you initiate a work-up for testicular pain? What treatments would you offer? And at what point would you consider a referral to a urologist?

Chronic orchialgia is a complex urogenital focal pain syndrome in which neurogenic inflammation is the principal mediator. This debilitating condition is associated with substantial anxiety and frustration, and is characterized by intermittent or constant unilateral or bilateral testicular pain, occurring for at least 3 months, that has a significant negative impact on activities of daily living and physical activity.¹

A variety of procedural and surgical options may help to minimize or alleviate chronic orchialgia. But which approach is best? There are no evidence-based guidelines for the treatment of this condition, and no randomized controlled trials to demonstrate the superiority of 1 modality over another. All diagnostic and treatment recommendations are based on expert opinion derived from small cohort studies.

With that in mind, we conducted a systematic review of the literature evaluating medical and surgical therapies for chronic testicular pain—and developed an algorithm (FIGURE 1), along with the text and TABLE that follow, for family physicians (FPs) to use as a guide.

FIGURE 1
Chronic orchialgia: A diagnosis and treatment algorithm^1,3,4,6,10

CASE 1 Vincent B
Over the last few years, Vincent has had similar episodes of bilateral testicular pain. He denies any history of direct trauma to the testicles, and he works out regularly by lifting weights and running. When the pain becomes unbearable, he takes acetaminophen or ibuprofen and takes a few days off from exercising, which provides modest—but temporary—relief.

Vincent reports that he has had about a dozen lifetime sexual partners and had chlamydia over a decade ago as a college student. He is currently engaged and sexually monogamous, and tested negative for Chlamydia trachomatis, Neisseria gonorrhoeae, hepatitis, syphilis, and human immunodeficiency virus (HIV) at his annual health maintenance examination last month. Shortly before that, Vincent was treated empirically for epididymitis with a 4-week course of ciprofloxacin, with no significant improvement in symptoms. He has no significant past medical history, denies depression, and takes no prescription medications.

Physical examination reveals mild to moderate diffuse tenderness to palpation throughout the scrotum, including both testicles and spermatic cords. There is no erythema of the scrotum. Nor are there any palpable scrotal masses, varicoceles, or hydroceles; testicular, scrotal, or penile lesions; inguinal masses; or lymph nodes. His urethral meatus is patent. The prostate is smooth, nonnodular, and non-tender. The remainder of the physical exam is unremarkable.

Determining a cause can be a challenge

There are numerous possible causes of testicular pain (TABLE), including an inguinal hernia, torsion of the testicle, trauma, and a history of chlamydia or gonorrhea, to name a few.

TABLE
Causes of acute and chronic orchialgia^1,3,4

Chronic testicular pain can also be psychogenic, often relating to a history of sexual abuse or relationship stress. One study examining comorbid psychological conditions in men with chronic orchialgia identified a somatization disorder in 56% of the patients, nongenital chronic pain syndromes in 50%, and major depression or chemical dependency in 27%.² Overall, however, estimates suggest that in about 25% of patients with chronic orchialgia, no identifiable etiology is found. ¹

Establish a baseline with a physical exam
Conduct a physical examination of the scrotum, testes, spermatic cords, penis, inguinal region, and prostate as a baseline measurement in a patient who presents with chronic orchialgia.^3,4 An initial urinalysis should be performed to rule out infection or identify microscopic hematuria, which may prompt a more targeted work-up and therapeutic plan. Take a thorough medical and psychosocial/ sexual history, as well.

Order an ultrasound of the scrotum and testes, the accepted gold standard to highlight structural abnormalities of the testicles. The addition of color Doppler makes it possible to find areas of hypervascularity, an indication of inflammation in the testicle and epididymis (FIGURES 2A AND B).

FIGURE 2
Well-circumscribed extratesticular mass

Epididymal cysts are common findings on scrotal ultrasound; they are frequently incidental, but may relate to the patient’s pain, depending on the size of the cyst. Smaller cysts that do not correlate with pain do not require treatment. Larger, painful cysts can be treated with aspiration or injection with a sclerosing agent—or with surgical excision, which offers the highest potential cure rate.^3,4 A computed tomography (CT) scan without contrast is the best way to find genitourinary system calculi, which could be the source of referred renal pain to the groin and scrotum. A contrast-enhanced CT is best to evaluate for solid renal masses.

Start with the most conservative treatment

In the absence of any findings that require surgical intervention, start conservatively.

Initiate a trial of nonsteroidal anti-inflammatory drugs (NSAIDs) for at least 1 month. Although this is the standard first-line treatment, NSAIDs have been shown to help only a small percentage of patients with chronic orchialgia, and only on a short-term basis.^1,3,4

Recommend scrotal elevation with supportive undergarments to decrease venous congestion. Tell the patient, too, that modifying his seated posture to avoid scrotal pressure may alleviate pain and poses no discernible risk of worsening orchialgia.⁵

Treat suspected STIs. The Centers for Disease Control and Prevention report that in men 14 to 35 years of age, epididymitis is most commonly caused by chlamydia or gonorrhea.⁶ In males younger than 14 or older than 35, epididymitis is most commonly caused by urinary coliform pathogens, including Eschericia coli.

If epididymitis is suspected to be due to chlamydia or gonorrhea, treatment should include either doxycycline 100 mg orally twice daily for 10 days or a single dose of azithromycin 1 g orally (for chlamydia eradication) and a single dose of ceftriaxone 125 mg intramuscularly (for gonorrhea eradication).^6,7 If coliform bacteria is suspected, order a standard dose of a quinolone (eg, ciprofloxacin or levofloxacin 500 mg/d) for 10 days.⁶ For refractory cases, treatment with a standard dose of a quinolone for 4 weeks is recommended.⁶

It is generally reasonable to treat most patients empirically for suspected epididymitis with antibiotics if no other identifiable etiology can be determined. Multiple antibiotic treatments should be avoided, however, in the absence of either an identifiable urogenital infection or ultrasound findings consistent with epididymitis (eg, congestion and enlargement). Antibiotics have not been shown to decrease the severity of chronic orchialgia and their use, unless clearly indicated, may lead to drug resistance.³

Consider a tricyclic antidepressant or gabapentin
Both tricyclic antidepressants (TCAs) and gabapentin have demonstrated benefit in the treatment of chronic pelvic and neuropathic pain.^8,9 Doses should be titrated to achieve a maximal therapeutic benefit while avoiding anticholinergic and neurologic side effects.

A cohort study using a multidisciplinary team consisting of a psychologist, an anesthetist, a physiotherapist, and an occupational therapist found >50% symptomatic improvement in 62% of men with chronic orchialgia treated with gabapentin up to 1800 mg per day, and 67% of men treated with nortriptyline up to 150 mg per day.¹⁰

However, a subgroup of patients who reported postvasectomy testicular pain did not achieve a 50% symptomatic improvement rate with either TCA or gabapentin therapy.

CASE 1 Vincent B
The FP reassured Vincent that his physical examination was normal and recommended a 1-month trial of ibuprofen (600 mg every 6 hours), and regular use of supportive briefs. Since the patient had been treated with antibiotics in the past with no change in symptoms—and because he was thought to be at low risk for an STI—the physician did not prescribe another empiric trial of antibiotics. He did send the patient for an ultrasound evaluation of the scrotum and testes, which revealed only a 0.5 × 0.4 × 0.6-cm right epididymal cyst that was not palpable on examination.

The patient returned after 1 month, noting that his symptoms had neither improved nor worsened. The FP suggested that he stop taking the ibuprofen and begin a trial of gabapentin 100 mg daily, titrating up to 3 times daily for the first month, then to 300 mg 3 times daily in the second month.

When he returned 3 months later, Vincent reported that his symptoms had improved by about 50%. He has since been able to increase both the intensity and frequency of physical activity. Vincent is not interested in further increasing the dose of gabapentin and declined a referral to a urologist for consideration of procedural and surgical therapeutic options, but agreed to follow up as needed if his testicular pain worsened.

Postvasectomy pain is not unusual

Several years after a vasectomy, the diameter of a man’s ejaculatory ducts often doubles in size to counteract the increase in fluid pressure.¹¹ The specific cause of long-term post-vasectomy pain syndrome, or congestive epididymitis, is unknown, but has been reported in 5% to 43% of men who have undergone this procedure.^12-14 Sperm granulomas or spermatoceles represent the body’s effort to spare the testicle from damage secondary to increasing fluid pressure. While these granulomas are benign lesions, their presence may predispose a man to postvasectomy pain syndrome.^15-17

CASE 2 Jason H
Two months before Jason’s visit to the FP, his testicular pain had become so excrutiating that he went to the ED seeking treatment. He was given an ultrasound with color Doppler and found to have postvasectomy surgical changes consistent with bilateral spermatoceles, but no evidence of epididymitis or a mass. Before leaving the ED, Jason received ceftriaxone (125 mg IM) as gonorrhea prophylaxis. He was discharged home with prophylactic antibiotics for chlamydia, as well as ibuprofen. He was advised to avoid strenuous physical activity and told to follow-up with his FP if his symptoms did not improve.

During several months of conservative medical therapy, including trials of NSAIDs, quinolone antibiotics, TCAs, and gabapentin, Jason did not experience any significant pain relief. He was frustrated by the dull, aching pain in his scrotum that continued to limit his physical and sexual activities.

Finally, the FP recommended a urologic consultation.

Consider these minimally invasive procedures
When conservative medical management fails, minimally invasive techniques are the next step. There are 2 commonly used procedures, both of which can be performed by a urologist in an outpatient setting.

Spermatic cord blocks with lidocaine and methylprednisolone have been shown to provide relief for weeks up to several months in small case studies, and may be repeated at intervals of several months if modest relief is achieved.^18,19

Transrectal ultrasound-guided periprostatic anesthetic injections, another microinvasive option, offers minimal risk and may provide some short-term relief. However, data on long-term benefit and resolution of pain and disability are lacking.²⁰

Consider surgery only after all else fails

If all medical and conservative therapies have been tried and the patient continues to have debilitating pain, surgical options should be considered. Because current surgical therapies are not always effective and are not reversible (and research on the various options is limited), it is important to initiate a detailed discussion with the patient. Such conversations should be held in consultation with a urologist.

Highlight risks and benefits and provide realistic expectations of short- and long-term postsurgical outcomes. It is also important to address psychological factors and social stressors that often contribute to chronic pelvic pain syndromes, which can improve long-term outcomes regardless of the chosen treatment. For this reason, a referral to a psychiatrist may be indicated.

Microsurgical denervation of the spermatic cord. Removal of the afferent nerve stimulus to the testicle is believed to result in the downregulation of the peripheral and central nervous systems, so the patient no longer has the perception of testicular pain. Several small trials have yielded favorable symptomatic pain relief scores in up to 71% of patients, with reported adverse outcomes including rare testicular atrophy—but no complaints of hypoesthesia or hyperesthesia of the scrotum, penile shaft, inguinal, or medial thigh skin.^21,22 This treatment should be considered only in patients who have experienced a significant degree of temporary relief from spermatic cord injection.

Epididymectomy is recommended only when pain is localized to the epididymis, as this is a testicle-sparing procedure. Unilateral or bilateral epididymectomy is a viable option for the treatment of chronic orchialgia related to postvasectomy pain syndrome or chronic epididymitis. Reports highlighting symptomatic improvement based on small case series range from 43% to 74%, with the highest success rate found during a 5½-year follow-up.^23-25 In 1 study, 90% of patients reported that they were satisfied with their choice to undergo the procedure.²⁵

Vasectomy reversal (vasovasostomy) and inguinal or scrotal orchiectomy should be considered only after all other treatment modalities have failed. Vasovasostomy has the potential to restore fertility in up to 98% of cases,²⁶ which may or may not be desirable. One study of men who experienced post-vasectomy pain syndrome and underwent microsurgical vasovasostomy found that after nearly 2½ years, 84% experienced complete pain resolution.²⁷

The goal of orchiectomy is to relieve orchialgia by releasing the entrapped ipsilateral genitofemoral and/or ilioinguinal nerves. One study determined that 90% of men who underwent unilateral epididymectomy for chronic orchialgia required an orchiectomy to resolve pain.¹ Another study found that 80% of patients continued to suffer both short- and long-term debilitating orchialgia postorchiectomy.²⁸

CASE 2 Jason H
Jason saw a urologist, who initially offered him bilateral spermatic cord blocks. They provided Jason with moderate symptom relief on most days of the week and allowed him to increase his physical and sexual activities. Three months later, Jason went back to the urologist for evaluation because he felt that the effects of the spermatic cord blocks had worn off. In the next 6 months, he had 2 additional bilateral blocks.

Nearly a year after a series of spermatic cord blocks, most of it spent in persistent discomfort, Jason returned to his FP with a request for narcotic pain medication. The FP tried to be supportive, but told Jason that chronic narcotic therapy was not an ideal choice—and referred him back to the urologist to discuss surgical options.

The urologist recommended a bilateral epididymectomy and the patient, who was desperate to obtain some pain relief and now regretted undergoing a vasectomy, agreed. Within the first few weeks after his surgery, he noticed a reduction in pain, and he slowly increased his physical activity. A year later, Jason reported only minimal testicular and scrotal discomfort that did not limit his physical or sexual activities—and he continues to be pleased with the outcome of his treatment.

CORRESPONDENCE Joel J. Heidelbaugh, MD, FAAFP, Ypsilanti Health Center, 200 Arnet, Suite 200, Ypsilanti, MI 48198; [email protected]

CASE 1 Vincent B, a 33-year-old executive, visits his family physician for an evaluation of chronic orchialgia. Although his testicular pain has waxed and waned for several years, it has recently worsened, making it increasingly difficult for him to exercise or to sit for extended periods of time. In fact, this visit was prompted by a lengthy meeting during which he developed a “dull ache” that did not let up until he left the meeting and walked around.

CASE 2 Jason H, a 42-year-old married father of 3 who had a vasectomy 2 years ago, has had progressively worsening testicular pain ever since. He also has occasional pain after ejaculation, but no known hematospermia. Recently, the pain has become so bad that it limits both his physical and sexual activities and is having a negative effect on his relationship with his wife. Jason is sexually monogamous, has no significant medical history, and takes no prescription medications.

These 2 cases are based on actual patients we have seen in our practices. If Vincent and Jason (not their real names) were your patients, how would you initiate a work-up for testicular pain? What treatments would you offer? And at what point would you consider a referral to a urologist?

Chronic orchialgia is a complex urogenital focal pain syndrome in which neurogenic inflammation is the principal mediator. This debilitating condition is associated with substantial anxiety and frustration, and is characterized by intermittent or constant unilateral or bilateral testicular pain, occurring for at least 3 months, that has a significant negative impact on activities of daily living and physical activity.¹

A variety of procedural and surgical options may help to minimize or alleviate chronic orchialgia. But which approach is best? There are no evidence-based guidelines for the treatment of this condition, and no randomized controlled trials to demonstrate the superiority of 1 modality over another. All diagnostic and treatment recommendations are based on expert opinion derived from small cohort studies.

With that in mind, we conducted a systematic review of the literature evaluating medical and surgical therapies for chronic testicular pain—and developed an algorithm (FIGURE 1), along with the text and TABLE that follow, for family physicians (FPs) to use as a guide.

FIGURE 1
Chronic orchialgia: A diagnosis and treatment algorithm^1,3,4,6,10

CASE 1 Vincent B
Over the last few years, Vincent has had similar episodes of bilateral testicular pain. He denies any history of direct trauma to the testicles, and he works out regularly by lifting weights and running. When the pain becomes unbearable, he takes acetaminophen or ibuprofen and takes a few days off from exercising, which provides modest—but temporary—relief.

Vincent reports that he has had about a dozen lifetime sexual partners and had chlamydia over a decade ago as a college student. He is currently engaged and sexually monogamous, and tested negative for Chlamydia trachomatis, Neisseria gonorrhoeae, hepatitis, syphilis, and human immunodeficiency virus (HIV) at his annual health maintenance examination last month. Shortly before that, Vincent was treated empirically for epididymitis with a 4-week course of ciprofloxacin, with no significant improvement in symptoms. He has no significant past medical history, denies depression, and takes no prescription medications.

Physical examination reveals mild to moderate diffuse tenderness to palpation throughout the scrotum, including both testicles and spermatic cords. There is no erythema of the scrotum. Nor are there any palpable scrotal masses, varicoceles, or hydroceles; testicular, scrotal, or penile lesions; inguinal masses; or lymph nodes. His urethral meatus is patent. The prostate is smooth, nonnodular, and non-tender. The remainder of the physical exam is unremarkable.

Determining a cause can be a challenge

There are numerous possible causes of testicular pain (TABLE), including an inguinal hernia, torsion of the testicle, trauma, and a history of chlamydia or gonorrhea, to name a few.

TABLE
Causes of acute and chronic orchialgia^1,3,4

Chronic testicular pain can also be psychogenic, often relating to a history of sexual abuse or relationship stress. One study examining comorbid psychological conditions in men with chronic orchialgia identified a somatization disorder in 56% of the patients, nongenital chronic pain syndromes in 50%, and major depression or chemical dependency in 27%.² Overall, however, estimates suggest that in about 25% of patients with chronic orchialgia, no identifiable etiology is found. ¹

Establish a baseline with a physical exam
Conduct a physical examination of the scrotum, testes, spermatic cords, penis, inguinal region, and prostate as a baseline measurement in a patient who presents with chronic orchialgia.^3,4 An initial urinalysis should be performed to rule out infection or identify microscopic hematuria, which may prompt a more targeted work-up and therapeutic plan. Take a thorough medical and psychosocial/ sexual history, as well.

Order an ultrasound of the scrotum and testes, the accepted gold standard to highlight structural abnormalities of the testicles. The addition of color Doppler makes it possible to find areas of hypervascularity, an indication of inflammation in the testicle and epididymis (FIGURES 2A AND B).

FIGURE 2
Well-circumscribed extratesticular mass

Epididymal cysts are common findings on scrotal ultrasound; they are frequently incidental, but may relate to the patient’s pain, depending on the size of the cyst. Smaller cysts that do not correlate with pain do not require treatment. Larger, painful cysts can be treated with aspiration or injection with a sclerosing agent—or with surgical excision, which offers the highest potential cure rate.^3,4 A computed tomography (CT) scan without contrast is the best way to find genitourinary system calculi, which could be the source of referred renal pain to the groin and scrotum. A contrast-enhanced CT is best to evaluate for solid renal masses.

Start with the most conservative treatment

In the absence of any findings that require surgical intervention, start conservatively.

Initiate a trial of nonsteroidal anti-inflammatory drugs (NSAIDs) for at least 1 month. Although this is the standard first-line treatment, NSAIDs have been shown to help only a small percentage of patients with chronic orchialgia, and only on a short-term basis.^1,3,4

Recommend scrotal elevation with supportive undergarments to decrease venous congestion. Tell the patient, too, that modifying his seated posture to avoid scrotal pressure may alleviate pain and poses no discernible risk of worsening orchialgia.⁵

Treat suspected STIs. The Centers for Disease Control and Prevention report that in men 14 to 35 years of age, epididymitis is most commonly caused by chlamydia or gonorrhea.⁶ In males younger than 14 or older than 35, epididymitis is most commonly caused by urinary coliform pathogens, including Eschericia coli.

If epididymitis is suspected to be due to chlamydia or gonorrhea, treatment should include either doxycycline 100 mg orally twice daily for 10 days or a single dose of azithromycin 1 g orally (for chlamydia eradication) and a single dose of ceftriaxone 125 mg intramuscularly (for gonorrhea eradication).^6,7 If coliform bacteria is suspected, order a standard dose of a quinolone (eg, ciprofloxacin or levofloxacin 500 mg/d) for 10 days.⁶ For refractory cases, treatment with a standard dose of a quinolone for 4 weeks is recommended.⁶

It is generally reasonable to treat most patients empirically for suspected epididymitis with antibiotics if no other identifiable etiology can be determined. Multiple antibiotic treatments should be avoided, however, in the absence of either an identifiable urogenital infection or ultrasound findings consistent with epididymitis (eg, congestion and enlargement). Antibiotics have not been shown to decrease the severity of chronic orchialgia and their use, unless clearly indicated, may lead to drug resistance.³

Consider a tricyclic antidepressant or gabapentin
Both tricyclic antidepressants (TCAs) and gabapentin have demonstrated benefit in the treatment of chronic pelvic and neuropathic pain.^8,9 Doses should be titrated to achieve a maximal therapeutic benefit while avoiding anticholinergic and neurologic side effects.

A cohort study using a multidisciplinary team consisting of a psychologist, an anesthetist, a physiotherapist, and an occupational therapist found >50% symptomatic improvement in 62% of men with chronic orchialgia treated with gabapentin up to 1800 mg per day, and 67% of men treated with nortriptyline up to 150 mg per day.¹⁰

However, a subgroup of patients who reported postvasectomy testicular pain did not achieve a 50% symptomatic improvement rate with either TCA or gabapentin therapy.

CASE 1 Vincent B
The FP reassured Vincent that his physical examination was normal and recommended a 1-month trial of ibuprofen (600 mg every 6 hours), and regular use of supportive briefs. Since the patient had been treated with antibiotics in the past with no change in symptoms—and because he was thought to be at low risk for an STI—the physician did not prescribe another empiric trial of antibiotics. He did send the patient for an ultrasound evaluation of the scrotum and testes, which revealed only a 0.5 × 0.4 × 0.6-cm right epididymal cyst that was not palpable on examination.

The patient returned after 1 month, noting that his symptoms had neither improved nor worsened. The FP suggested that he stop taking the ibuprofen and begin a trial of gabapentin 100 mg daily, titrating up to 3 times daily for the first month, then to 300 mg 3 times daily in the second month.

When he returned 3 months later, Vincent reported that his symptoms had improved by about 50%. He has since been able to increase both the intensity and frequency of physical activity. Vincent is not interested in further increasing the dose of gabapentin and declined a referral to a urologist for consideration of procedural and surgical therapeutic options, but agreed to follow up as needed if his testicular pain worsened.

Postvasectomy pain is not unusual

Several years after a vasectomy, the diameter of a man’s ejaculatory ducts often doubles in size to counteract the increase in fluid pressure.¹¹ The specific cause of long-term post-vasectomy pain syndrome, or congestive epididymitis, is unknown, but has been reported in 5% to 43% of men who have undergone this procedure.^12-14 Sperm granulomas or spermatoceles represent the body’s effort to spare the testicle from damage secondary to increasing fluid pressure. While these granulomas are benign lesions, their presence may predispose a man to postvasectomy pain syndrome.^15-17

CASE 2 Jason H
Two months before Jason’s visit to the FP, his testicular pain had become so excrutiating that he went to the ED seeking treatment. He was given an ultrasound with color Doppler and found to have postvasectomy surgical changes consistent with bilateral spermatoceles, but no evidence of epididymitis or a mass. Before leaving the ED, Jason received ceftriaxone (125 mg IM) as gonorrhea prophylaxis. He was discharged home with prophylactic antibiotics for chlamydia, as well as ibuprofen. He was advised to avoid strenuous physical activity and told to follow-up with his FP if his symptoms did not improve.

During several months of conservative medical therapy, including trials of NSAIDs, quinolone antibiotics, TCAs, and gabapentin, Jason did not experience any significant pain relief. He was frustrated by the dull, aching pain in his scrotum that continued to limit his physical and sexual activities.

Finally, the FP recommended a urologic consultation.

Consider these minimally invasive procedures
When conservative medical management fails, minimally invasive techniques are the next step. There are 2 commonly used procedures, both of which can be performed by a urologist in an outpatient setting.

Spermatic cord blocks with lidocaine and methylprednisolone have been shown to provide relief for weeks up to several months in small case studies, and may be repeated at intervals of several months if modest relief is achieved.^18,19

Transrectal ultrasound-guided periprostatic anesthetic injections, another microinvasive option, offers minimal risk and may provide some short-term relief. However, data on long-term benefit and resolution of pain and disability are lacking.²⁰

Consider surgery only after all else fails

If all medical and conservative therapies have been tried and the patient continues to have debilitating pain, surgical options should be considered. Because current surgical therapies are not always effective and are not reversible (and research on the various options is limited), it is important to initiate a detailed discussion with the patient. Such conversations should be held in consultation with a urologist.

Highlight risks and benefits and provide realistic expectations of short- and long-term postsurgical outcomes. It is also important to address psychological factors and social stressors that often contribute to chronic pelvic pain syndromes, which can improve long-term outcomes regardless of the chosen treatment. For this reason, a referral to a psychiatrist may be indicated.

Microsurgical denervation of the spermatic cord. Removal of the afferent nerve stimulus to the testicle is believed to result in the downregulation of the peripheral and central nervous systems, so the patient no longer has the perception of testicular pain. Several small trials have yielded favorable symptomatic pain relief scores in up to 71% of patients, with reported adverse outcomes including rare testicular atrophy—but no complaints of hypoesthesia or hyperesthesia of the scrotum, penile shaft, inguinal, or medial thigh skin.^21,22 This treatment should be considered only in patients who have experienced a significant degree of temporary relief from spermatic cord injection.

Epididymectomy is recommended only when pain is localized to the epididymis, as this is a testicle-sparing procedure. Unilateral or bilateral epididymectomy is a viable option for the treatment of chronic orchialgia related to postvasectomy pain syndrome or chronic epididymitis. Reports highlighting symptomatic improvement based on small case series range from 43% to 74%, with the highest success rate found during a 5½-year follow-up.^23-25 In 1 study, 90% of patients reported that they were satisfied with their choice to undergo the procedure.²⁵

Vasectomy reversal (vasovasostomy) and inguinal or scrotal orchiectomy should be considered only after all other treatment modalities have failed. Vasovasostomy has the potential to restore fertility in up to 98% of cases,²⁶ which may or may not be desirable. One study of men who experienced post-vasectomy pain syndrome and underwent microsurgical vasovasostomy found that after nearly 2½ years, 84% experienced complete pain resolution.²⁷

The goal of orchiectomy is to relieve orchialgia by releasing the entrapped ipsilateral genitofemoral and/or ilioinguinal nerves. One study determined that 90% of men who underwent unilateral epididymectomy for chronic orchialgia required an orchiectomy to resolve pain.¹ Another study found that 80% of patients continued to suffer both short- and long-term debilitating orchialgia postorchiectomy.²⁸

CASE 2 Jason H
Jason saw a urologist, who initially offered him bilateral spermatic cord blocks. They provided Jason with moderate symptom relief on most days of the week and allowed him to increase his physical and sexual activities. Three months later, Jason went back to the urologist for evaluation because he felt that the effects of the spermatic cord blocks had worn off. In the next 6 months, he had 2 additional bilateral blocks.

Nearly a year after a series of spermatic cord blocks, most of it spent in persistent discomfort, Jason returned to his FP with a request for narcotic pain medication. The FP tried to be supportive, but told Jason that chronic narcotic therapy was not an ideal choice—and referred him back to the urologist to discuss surgical options.

The urologist recommended a bilateral epididymectomy and the patient, who was desperate to obtain some pain relief and now regretted undergoing a vasectomy, agreed. Within the first few weeks after his surgery, he noticed a reduction in pain, and he slowly increased his physical activity. A year later, Jason reported only minimal testicular and scrotal discomfort that did not limit his physical or sexual activities—and he continues to be pleased with the outcome of his treatment.

CORRESPONDENCE Joel J. Heidelbaugh, MD, FAAFP, Ypsilanti Health Center, 200 Arnet, Suite 200, Ypsilanti, MI 48198; [email protected]

CASE 1 Vincent B, a 33-year-old executive, visits his family physician for an evaluation of chronic orchialgia. Although his testicular pain has waxed and waned for several years, it has recently worsened, making it increasingly difficult for him to exercise or to sit for extended periods of time. In fact, this visit was prompted by a lengthy meeting during which he developed a “dull ache” that did not let up until he left the meeting and walked around.

CASE 2 Jason H, a 42-year-old married father of 3 who had a vasectomy 2 years ago, has had progressively worsening testicular pain ever since. He also has occasional pain after ejaculation, but no known hematospermia. Recently, the pain has become so bad that it limits both his physical and sexual activities and is having a negative effect on his relationship with his wife. Jason is sexually monogamous, has no significant medical history, and takes no prescription medications.

These 2 cases are based on actual patients we have seen in our practices. If Vincent and Jason (not their real names) were your patients, how would you initiate a work-up for testicular pain? What treatments would you offer? And at what point would you consider a referral to a urologist?

Chronic orchialgia is a complex urogenital focal pain syndrome in which neurogenic inflammation is the principal mediator. This debilitating condition is associated with substantial anxiety and frustration, and is characterized by intermittent or constant unilateral or bilateral testicular pain, occurring for at least 3 months, that has a significant negative impact on activities of daily living and physical activity.¹

A variety of procedural and surgical options may help to minimize or alleviate chronic orchialgia. But which approach is best? There are no evidence-based guidelines for the treatment of this condition, and no randomized controlled trials to demonstrate the superiority of 1 modality over another. All diagnostic and treatment recommendations are based on expert opinion derived from small cohort studies.

With that in mind, we conducted a systematic review of the literature evaluating medical and surgical therapies for chronic testicular pain—and developed an algorithm (FIGURE 1), along with the text and TABLE that follow, for family physicians (FPs) to use as a guide.

FIGURE 1
Chronic orchialgia: A diagnosis and treatment algorithm^1,3,4,6,10

CASE 1 Vincent B
Over the last few years, Vincent has had similar episodes of bilateral testicular pain. He denies any history of direct trauma to the testicles, and he works out regularly by lifting weights and running. When the pain becomes unbearable, he takes acetaminophen or ibuprofen and takes a few days off from exercising, which provides modest—but temporary—relief.

Vincent reports that he has had about a dozen lifetime sexual partners and had chlamydia over a decade ago as a college student. He is currently engaged and sexually monogamous, and tested negative for Chlamydia trachomatis, Neisseria gonorrhoeae, hepatitis, syphilis, and human immunodeficiency virus (HIV) at his annual health maintenance examination last month. Shortly before that, Vincent was treated empirically for epididymitis with a 4-week course of ciprofloxacin, with no significant improvement in symptoms. He has no significant past medical history, denies depression, and takes no prescription medications.

Physical examination reveals mild to moderate diffuse tenderness to palpation throughout the scrotum, including both testicles and spermatic cords. There is no erythema of the scrotum. Nor are there any palpable scrotal masses, varicoceles, or hydroceles; testicular, scrotal, or penile lesions; inguinal masses; or lymph nodes. His urethral meatus is patent. The prostate is smooth, nonnodular, and non-tender. The remainder of the physical exam is unremarkable.

Determining a cause can be a challenge

There are numerous possible causes of testicular pain (TABLE), including an inguinal hernia, torsion of the testicle, trauma, and a history of chlamydia or gonorrhea, to name a few.

TABLE
Causes of acute and chronic orchialgia^1,3,4

Chronic testicular pain can also be psychogenic, often relating to a history of sexual abuse or relationship stress. One study examining comorbid psychological conditions in men with chronic orchialgia identified a somatization disorder in 56% of the patients, nongenital chronic pain syndromes in 50%, and major depression or chemical dependency in 27%.² Overall, however, estimates suggest that in about 25% of patients with chronic orchialgia, no identifiable etiology is found. ¹

Establish a baseline with a physical exam
Conduct a physical examination of the scrotum, testes, spermatic cords, penis, inguinal region, and prostate as a baseline measurement in a patient who presents with chronic orchialgia.^3,4 An initial urinalysis should be performed to rule out infection or identify microscopic hematuria, which may prompt a more targeted work-up and therapeutic plan. Take a thorough medical and psychosocial/ sexual history, as well.

Order an ultrasound of the scrotum and testes, the accepted gold standard to highlight structural abnormalities of the testicles. The addition of color Doppler makes it possible to find areas of hypervascularity, an indication of inflammation in the testicle and epididymis (FIGURES 2A AND B).

FIGURE 2
Well-circumscribed extratesticular mass

Epididymal cysts are common findings on scrotal ultrasound; they are frequently incidental, but may relate to the patient’s pain, depending on the size of the cyst. Smaller cysts that do not correlate with pain do not require treatment. Larger, painful cysts can be treated with aspiration or injection with a sclerosing agent—or with surgical excision, which offers the highest potential cure rate.^3,4 A computed tomography (CT) scan without contrast is the best way to find genitourinary system calculi, which could be the source of referred renal pain to the groin and scrotum. A contrast-enhanced CT is best to evaluate for solid renal masses.

Start with the most conservative treatment

In the absence of any findings that require surgical intervention, start conservatively.

Initiate a trial of nonsteroidal anti-inflammatory drugs (NSAIDs) for at least 1 month. Although this is the standard first-line treatment, NSAIDs have been shown to help only a small percentage of patients with chronic orchialgia, and only on a short-term basis.^1,3,4

Recommend scrotal elevation with supportive undergarments to decrease venous congestion. Tell the patient, too, that modifying his seated posture to avoid scrotal pressure may alleviate pain and poses no discernible risk of worsening orchialgia.⁵

Treat suspected STIs. The Centers for Disease Control and Prevention report that in men 14 to 35 years of age, epididymitis is most commonly caused by chlamydia or gonorrhea.⁶ In males younger than 14 or older than 35, epididymitis is most commonly caused by urinary coliform pathogens, including Eschericia coli.

If epididymitis is suspected to be due to chlamydia or gonorrhea, treatment should include either doxycycline 100 mg orally twice daily for 10 days or a single dose of azithromycin 1 g orally (for chlamydia eradication) and a single dose of ceftriaxone 125 mg intramuscularly (for gonorrhea eradication).^6,7 If coliform bacteria is suspected, order a standard dose of a quinolone (eg, ciprofloxacin or levofloxacin 500 mg/d) for 10 days.⁶ For refractory cases, treatment with a standard dose of a quinolone for 4 weeks is recommended.⁶

It is generally reasonable to treat most patients empirically for suspected epididymitis with antibiotics if no other identifiable etiology can be determined. Multiple antibiotic treatments should be avoided, however, in the absence of either an identifiable urogenital infection or ultrasound findings consistent with epididymitis (eg, congestion and enlargement). Antibiotics have not been shown to decrease the severity of chronic orchialgia and their use, unless clearly indicated, may lead to drug resistance.³

Consider a tricyclic antidepressant or gabapentin
Both tricyclic antidepressants (TCAs) and gabapentin have demonstrated benefit in the treatment of chronic pelvic and neuropathic pain.^8,9 Doses should be titrated to achieve a maximal therapeutic benefit while avoiding anticholinergic and neurologic side effects.

A cohort study using a multidisciplinary team consisting of a psychologist, an anesthetist, a physiotherapist, and an occupational therapist found >50% symptomatic improvement in 62% of men with chronic orchialgia treated with gabapentin up to 1800 mg per day, and 67% of men treated with nortriptyline up to 150 mg per day.¹⁰

However, a subgroup of patients who reported postvasectomy testicular pain did not achieve a 50% symptomatic improvement rate with either TCA or gabapentin therapy.

CASE 1 Vincent B
The FP reassured Vincent that his physical examination was normal and recommended a 1-month trial of ibuprofen (600 mg every 6 hours), and regular use of supportive briefs. Since the patient had been treated with antibiotics in the past with no change in symptoms—and because he was thought to be at low risk for an STI—the physician did not prescribe another empiric trial of antibiotics. He did send the patient for an ultrasound evaluation of the scrotum and testes, which revealed only a 0.5 × 0.4 × 0.6-cm right epididymal cyst that was not palpable on examination.

The patient returned after 1 month, noting that his symptoms had neither improved nor worsened. The FP suggested that he stop taking the ibuprofen and begin a trial of gabapentin 100 mg daily, titrating up to 3 times daily for the first month, then to 300 mg 3 times daily in the second month.

When he returned 3 months later, Vincent reported that his symptoms had improved by about 50%. He has since been able to increase both the intensity and frequency of physical activity. Vincent is not interested in further increasing the dose of gabapentin and declined a referral to a urologist for consideration of procedural and surgical therapeutic options, but agreed to follow up as needed if his testicular pain worsened.

Postvasectomy pain is not unusual

Several years after a vasectomy, the diameter of a man’s ejaculatory ducts often doubles in size to counteract the increase in fluid pressure.¹¹ The specific cause of long-term post-vasectomy pain syndrome, or congestive epididymitis, is unknown, but has been reported in 5% to 43% of men who have undergone this procedure.^12-14 Sperm granulomas or spermatoceles represent the body’s effort to spare the testicle from damage secondary to increasing fluid pressure. While these granulomas are benign lesions, their presence may predispose a man to postvasectomy pain syndrome.^15-17

CASE 2 Jason H
Two months before Jason’s visit to the FP, his testicular pain had become so excrutiating that he went to the ED seeking treatment. He was given an ultrasound with color Doppler and found to have postvasectomy surgical changes consistent with bilateral spermatoceles, but no evidence of epididymitis or a mass. Before leaving the ED, Jason received ceftriaxone (125 mg IM) as gonorrhea prophylaxis. He was discharged home with prophylactic antibiotics for chlamydia, as well as ibuprofen. He was advised to avoid strenuous physical activity and told to follow-up with his FP if his symptoms did not improve.

During several months of conservative medical therapy, including trials of NSAIDs, quinolone antibiotics, TCAs, and gabapentin, Jason did not experience any significant pain relief. He was frustrated by the dull, aching pain in his scrotum that continued to limit his physical and sexual activities.

Finally, the FP recommended a urologic consultation.

Consider these minimally invasive procedures
When conservative medical management fails, minimally invasive techniques are the next step. There are 2 commonly used procedures, both of which can be performed by a urologist in an outpatient setting.

Spermatic cord blocks with lidocaine and methylprednisolone have been shown to provide relief for weeks up to several months in small case studies, and may be repeated at intervals of several months if modest relief is achieved.^18,19

Transrectal ultrasound-guided periprostatic anesthetic injections, another microinvasive option, offers minimal risk and may provide some short-term relief. However, data on long-term benefit and resolution of pain and disability are lacking.²⁰

Consider surgery only after all else fails

If all medical and conservative therapies have been tried and the patient continues to have debilitating pain, surgical options should be considered. Because current surgical therapies are not always effective and are not reversible (and research on the various options is limited), it is important to initiate a detailed discussion with the patient. Such conversations should be held in consultation with a urologist.

Highlight risks and benefits and provide realistic expectations of short- and long-term postsurgical outcomes. It is also important to address psychological factors and social stressors that often contribute to chronic pelvic pain syndromes, which can improve long-term outcomes regardless of the chosen treatment. For this reason, a referral to a psychiatrist may be indicated.

Microsurgical denervation of the spermatic cord. Removal of the afferent nerve stimulus to the testicle is believed to result in the downregulation of the peripheral and central nervous systems, so the patient no longer has the perception of testicular pain. Several small trials have yielded favorable symptomatic pain relief scores in up to 71% of patients, with reported adverse outcomes including rare testicular atrophy—but no complaints of hypoesthesia or hyperesthesia of the scrotum, penile shaft, inguinal, or medial thigh skin.^21,22 This treatment should be considered only in patients who have experienced a significant degree of temporary relief from spermatic cord injection.

Epididymectomy is recommended only when pain is localized to the epididymis, as this is a testicle-sparing procedure. Unilateral or bilateral epididymectomy is a viable option for the treatment of chronic orchialgia related to postvasectomy pain syndrome or chronic epididymitis. Reports highlighting symptomatic improvement based on small case series range from 43% to 74%, with the highest success rate found during a 5½-year follow-up.^23-25 In 1 study, 90% of patients reported that they were satisfied with their choice to undergo the procedure.²⁵

Vasectomy reversal (vasovasostomy) and inguinal or scrotal orchiectomy should be considered only after all other treatment modalities have failed. Vasovasostomy has the potential to restore fertility in up to 98% of cases,²⁶ which may or may not be desirable. One study of men who experienced post-vasectomy pain syndrome and underwent microsurgical vasovasostomy found that after nearly 2½ years, 84% experienced complete pain resolution.²⁷

The goal of orchiectomy is to relieve orchialgia by releasing the entrapped ipsilateral genitofemoral and/or ilioinguinal nerves. One study determined that 90% of men who underwent unilateral epididymectomy for chronic orchialgia required an orchiectomy to resolve pain.¹ Another study found that 80% of patients continued to suffer both short- and long-term debilitating orchialgia postorchiectomy.²⁸

CASE 2 Jason H
Jason saw a urologist, who initially offered him bilateral spermatic cord blocks. They provided Jason with moderate symptom relief on most days of the week and allowed him to increase his physical and sexual activities. Three months later, Jason went back to the urologist for evaluation because he felt that the effects of the spermatic cord blocks had worn off. In the next 6 months, he had 2 additional bilateral blocks.

Nearly a year after a series of spermatic cord blocks, most of it spent in persistent discomfort, Jason returned to his FP with a request for narcotic pain medication. The FP tried to be supportive, but told Jason that chronic narcotic therapy was not an ideal choice—and referred him back to the urologist to discuss surgical options.

The urologist recommended a bilateral epididymectomy and the patient, who was desperate to obtain some pain relief and now regretted undergoing a vasectomy, agreed. Within the first few weeks after his surgery, he noticed a reduction in pain, and he slowly increased his physical activity. A year later, Jason reported only minimal testicular and scrotal discomfort that did not limit his physical or sexual activities—and he continues to be pleased with the outcome of his treatment.

CORRESPONDENCE Joel J. Heidelbaugh, MD, FAAFP, Ypsilanti Health Center, 200 Arnet, Suite 200, Ypsilanti, MI 48198; [email protected]

[email protected]

When children or adolescents present complaining of heart palpitations, first determine just what they are describing. “Heart palpitation” is a very vague term and could mean anything: Patients might say their “heart is racing,” they feel like they “skipped a heartbeat,” or it could just be a greater awareness of their heart beating.

A comprehensive history is important in determining the possibility of a significant arrhythmia. Every child walking in with a history of palpitation does not have a cardiac arrhythmia.

Significant arrhythmias are far fewer in children than adults. More common in children are noncardiac issues, such as heart palpitations associated with anxiety and panic attacks or minor arrhythmias such as premature atrial and ventricular beats.

Normal heart rhythm is sinus rhythm, and sinus tachycardia is not a problem most of the time. Sinus tachycardia has many possible etiologies. It can occur when a child or adolescent exercises, feels anxious, or is running a fever. Fortunately, sinus tachycardia is not something we normally worry about. Children are easily excited and may experience their heart racing. They may report that they feel short of breath during an episode, which may point to anxiety. In some cases, excessive caffeine intake may be responsible for these symptoms.

Ask about onset and duration of symptoms during history taking. For example, patients who report a rapid heartbeat that lasts a half-hour or longer are more of a concern than those who report a few minutes or seconds of symptoms where it feels like “their heart is popping out of their chest.” Also inquire about dizziness, which could indicate their blood pressure falls during an episode.

Pediatricians who feel comfortable addressing cardiac issues should try to differentiate benign sinus tachycardia from the more concerning forms: supraventricular tachycardia and ventricular tachycardia.

If parents report the child's heart was racing and it was 120 beats per minute (bpm), you can reassure them. If the heart rate is 120, 130, 140, 150, or even 160, it is generally nothing to worry about—it is bound to be sinus tachycardia. Even very fast sinus tachycardia may be normal given the circumstances. For example, a 16-year-old athlete at the peak of physical activity might have a heart rate closer to 190 or 200 bpm. That is fast, but it is appropriate for the age and level of activity.

More worrisome is supraventricular tachycardia (SVT), which has an entirely different mechanism in terms of electrophysiology of the heart, reentry being responsible for most. The electrical conduction system of the heart may have a bypass tract or a dual atrioventricular node which allows for reentry to occur. In general, the heart rate of 200 bpm or higher is likely to be SVT and warrants referral to a cardiac specialist.

Patients with heart rates falling in the in-between range (170-200 bpm) may have sinus tachycardia or SVT and should also have a work-up. Attempting to document the rhythm during episodes becomes important in these children.

SVT can occur in children of any age, including newborns and infants. It usually starts abruptly and unpredictably—out of the blue, the heart starts racing. The child can be completely inactive at the time. For a minority, exercise may be the trigger. The rapid heartbeat may be short or last for many hours, and then the episode stops as suddenly as it started. It is not life threatening unless the child is in incessant SVT for hours.

A routine ECG can sometimes help pediatricians with their differential diagnosis. Markers, such as a bypass tract, can show up on the ECG tracing. If a pre-excitement pattern is seen, further work-up may be needed, even in asymptomatic children incidentally discovered on routine testing for other reasons. Unequivocal diagnosis of SVT requires ECG documentation of the abnormal rhythm during an episode.

Because episodes of SVT tend to be unpredictable, trying to record the rhythm during the episode is not an easy exercise. One solution is to ask parents to record the child's pulse rate or heart rate during an episode, while the patient is complaining of symptoms. Going to the nearest emergency department increases the possibility of ECG identification of the SVT.

A pediatrician can also prescribe 24-hour Holter monitoring to try to catch an episode. If a patient is referred to a pediatric cardiologist, the patient is often monitored for a longer period of time in an attempt to catch the arrhythmia, such as 48-72 hours. Another helpful device is a loop recorder, which is worn constantly; it records and erases the ECG data after each half-hour. Parents are instructed to save the data after the episode by pushing a button. The data can then be transmitted to the monitoring company via telephone. The signal is turned into an ECG rhythm strip and sent to the physician for further analysis and necessary action.

The most worrisome arrhythmia in children is ventricular tachycardia (VT). It is a life-threatening arrhythmia. Fortunately, it is the most uncommon. Nonetheless, people who treat children have to be aware of conditions that are a setup for this kind of arrhythmia.

Hypertrophic cardiomyopathy is one such condition. It is a genetic condition leading to abnormality of the ventricular muscle. The abnormality produces a structural change with thickening of the heart muscle in an asymmetric fashion. The thickness may cause obstruction of the left ventricular outflow tract. In addition, such an individual is prone to VT. The presenting symptom for such individuals tends to be loss of consciousness or a fainting episode with the arrhythmia, generally occurring in the setting of vigorous physical activity. It can be a silent condition, fainting or collapse being the first symptom for some patients. Diagnosis is made by a combination of tests, including echocardiogram and ECG. Genetic testing is now available for the condition but does not help with practical management issues.

If a child is reporting other problems, such as constant fatigue and/or symptoms with minor daily activities, it suggests the possibility of myocarditis, usually related to viral infections. The heart of a child with such an infection becomes dilated and does not contract well. These patients are prone to VT. While some children with myocarditis recover, others may suffer permanent damage. The heart may remain dilated and prone to VT.

Another rare condition to include in your differential diagnosis is prolonged QT interval syndrome. The condition is genetic in nature and tends to run in families. The mechanism involves gates or ion channels in cell membranes that normally regulate the influx of sodium, potassium, and calcium. In a child with the syndrome, the gates remain open too long, thereby allowing too much sodium or calcium to enter the cells, and VT can ensue. ECG tracings and a history of syncope can be diagnostic. Genetic testing is available and helpful.

Ventricular tachycardia is very worrisome because it can be fatal within minutes. Therefore, VT is an emergency in most instances, although there are some benign forms that are well tolerated. The distinction can sometimes require an electrophysiology study. The placement of automatic external defibrillators in public places has enhanced the chances of survival in patients who experience rapid VT.

[email protected]

When children or adolescents present complaining of heart palpitations, first determine just what they are describing. “Heart palpitation” is a very vague term and could mean anything: Patients might say their “heart is racing,” they feel like they “skipped a heartbeat,” or it could just be a greater awareness of their heart beating.

A comprehensive history is important in determining the possibility of a significant arrhythmia. Every child walking in with a history of palpitation does not have a cardiac arrhythmia.

Significant arrhythmias are far fewer in children than adults. More common in children are noncardiac issues, such as heart palpitations associated with anxiety and panic attacks or minor arrhythmias such as premature atrial and ventricular beats.

Normal heart rhythm is sinus rhythm, and sinus tachycardia is not a problem most of the time. Sinus tachycardia has many possible etiologies. It can occur when a child or adolescent exercises, feels anxious, or is running a fever. Fortunately, sinus tachycardia is not something we normally worry about. Children are easily excited and may experience their heart racing. They may report that they feel short of breath during an episode, which may point to anxiety. In some cases, excessive caffeine intake may be responsible for these symptoms.

Ask about onset and duration of symptoms during history taking. For example, patients who report a rapid heartbeat that lasts a half-hour or longer are more of a concern than those who report a few minutes or seconds of symptoms where it feels like “their heart is popping out of their chest.” Also inquire about dizziness, which could indicate their blood pressure falls during an episode.

Pediatricians who feel comfortable addressing cardiac issues should try to differentiate benign sinus tachycardia from the more concerning forms: supraventricular tachycardia and ventricular tachycardia.

If parents report the child's heart was racing and it was 120 beats per minute (bpm), you can reassure them. If the heart rate is 120, 130, 140, 150, or even 160, it is generally nothing to worry about—it is bound to be sinus tachycardia. Even very fast sinus tachycardia may be normal given the circumstances. For example, a 16-year-old athlete at the peak of physical activity might have a heart rate closer to 190 or 200 bpm. That is fast, but it is appropriate for the age and level of activity.

More worrisome is supraventricular tachycardia (SVT), which has an entirely different mechanism in terms of electrophysiology of the heart, reentry being responsible for most. The electrical conduction system of the heart may have a bypass tract or a dual atrioventricular node which allows for reentry to occur. In general, the heart rate of 200 bpm or higher is likely to be SVT and warrants referral to a cardiac specialist.

Patients with heart rates falling in the in-between range (170-200 bpm) may have sinus tachycardia or SVT and should also have a work-up. Attempting to document the rhythm during episodes becomes important in these children.

SVT can occur in children of any age, including newborns and infants. It usually starts abruptly and unpredictably—out of the blue, the heart starts racing. The child can be completely inactive at the time. For a minority, exercise may be the trigger. The rapid heartbeat may be short or last for many hours, and then the episode stops as suddenly as it started. It is not life threatening unless the child is in incessant SVT for hours.

A routine ECG can sometimes help pediatricians with their differential diagnosis. Markers, such as a bypass tract, can show up on the ECG tracing. If a pre-excitement pattern is seen, further work-up may be needed, even in asymptomatic children incidentally discovered on routine testing for other reasons. Unequivocal diagnosis of SVT requires ECG documentation of the abnormal rhythm during an episode.

Because episodes of SVT tend to be unpredictable, trying to record the rhythm during the episode is not an easy exercise. One solution is to ask parents to record the child's pulse rate or heart rate during an episode, while the patient is complaining of symptoms. Going to the nearest emergency department increases the possibility of ECG identification of the SVT.

A pediatrician can also prescribe 24-hour Holter monitoring to try to catch an episode. If a patient is referred to a pediatric cardiologist, the patient is often monitored for a longer period of time in an attempt to catch the arrhythmia, such as 48-72 hours. Another helpful device is a loop recorder, which is worn constantly; it records and erases the ECG data after each half-hour. Parents are instructed to save the data after the episode by pushing a button. The data can then be transmitted to the monitoring company via telephone. The signal is turned into an ECG rhythm strip and sent to the physician for further analysis and necessary action.

The most worrisome arrhythmia in children is ventricular tachycardia (VT). It is a life-threatening arrhythmia. Fortunately, it is the most uncommon. Nonetheless, people who treat children have to be aware of conditions that are a setup for this kind of arrhythmia.

Hypertrophic cardiomyopathy is one such condition. It is a genetic condition leading to abnormality of the ventricular muscle. The abnormality produces a structural change with thickening of the heart muscle in an asymmetric fashion. The thickness may cause obstruction of the left ventricular outflow tract. In addition, such an individual is prone to VT. The presenting symptom for such individuals tends to be loss of consciousness or a fainting episode with the arrhythmia, generally occurring in the setting of vigorous physical activity. It can be a silent condition, fainting or collapse being the first symptom for some patients. Diagnosis is made by a combination of tests, including echocardiogram and ECG. Genetic testing is now available for the condition but does not help with practical management issues.

If a child is reporting other problems, such as constant fatigue and/or symptoms with minor daily activities, it suggests the possibility of myocarditis, usually related to viral infections. The heart of a child with such an infection becomes dilated and does not contract well. These patients are prone to VT. While some children with myocarditis recover, others may suffer permanent damage. The heart may remain dilated and prone to VT.

Another rare condition to include in your differential diagnosis is prolonged QT interval syndrome. The condition is genetic in nature and tends to run in families. The mechanism involves gates or ion channels in cell membranes that normally regulate the influx of sodium, potassium, and calcium. In a child with the syndrome, the gates remain open too long, thereby allowing too much sodium or calcium to enter the cells, and VT can ensue. ECG tracings and a history of syncope can be diagnostic. Genetic testing is available and helpful.

Ventricular tachycardia is very worrisome because it can be fatal within minutes. Therefore, VT is an emergency in most instances, although there are some benign forms that are well tolerated. The distinction can sometimes require an electrophysiology study. The placement of automatic external defibrillators in public places has enhanced the chances of survival in patients who experience rapid VT.

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When children or adolescents present complaining of heart palpitations, first determine just what they are describing. “Heart palpitation” is a very vague term and could mean anything: Patients might say their “heart is racing,” they feel like they “skipped a heartbeat,” or it could just be a greater awareness of their heart beating.

A comprehensive history is important in determining the possibility of a significant arrhythmia. Every child walking in with a history of palpitation does not have a cardiac arrhythmia.

Significant arrhythmias are far fewer in children than adults. More common in children are noncardiac issues, such as heart palpitations associated with anxiety and panic attacks or minor arrhythmias such as premature atrial and ventricular beats.

Normal heart rhythm is sinus rhythm, and sinus tachycardia is not a problem most of the time. Sinus tachycardia has many possible etiologies. It can occur when a child or adolescent exercises, feels anxious, or is running a fever. Fortunately, sinus tachycardia is not something we normally worry about. Children are easily excited and may experience their heart racing. They may report that they feel short of breath during an episode, which may point to anxiety. In some cases, excessive caffeine intake may be responsible for these symptoms.

Ask about onset and duration of symptoms during history taking. For example, patients who report a rapid heartbeat that lasts a half-hour or longer are more of a concern than those who report a few minutes or seconds of symptoms where it feels like “their heart is popping out of their chest.” Also inquire about dizziness, which could indicate their blood pressure falls during an episode.

Pediatricians who feel comfortable addressing cardiac issues should try to differentiate benign sinus tachycardia from the more concerning forms: supraventricular tachycardia and ventricular tachycardia.

If parents report the child's heart was racing and it was 120 beats per minute (bpm), you can reassure them. If the heart rate is 120, 130, 140, 150, or even 160, it is generally nothing to worry about—it is bound to be sinus tachycardia. Even very fast sinus tachycardia may be normal given the circumstances. For example, a 16-year-old athlete at the peak of physical activity might have a heart rate closer to 190 or 200 bpm. That is fast, but it is appropriate for the age and level of activity.

More worrisome is supraventricular tachycardia (SVT), which has an entirely different mechanism in terms of electrophysiology of the heart, reentry being responsible for most. The electrical conduction system of the heart may have a bypass tract or a dual atrioventricular node which allows for reentry to occur. In general, the heart rate of 200 bpm or higher is likely to be SVT and warrants referral to a cardiac specialist.

Patients with heart rates falling in the in-between range (170-200 bpm) may have sinus tachycardia or SVT and should also have a work-up. Attempting to document the rhythm during episodes becomes important in these children.

SVT can occur in children of any age, including newborns and infants. It usually starts abruptly and unpredictably—out of the blue, the heart starts racing. The child can be completely inactive at the time. For a minority, exercise may be the trigger. The rapid heartbeat may be short or last for many hours, and then the episode stops as suddenly as it started. It is not life threatening unless the child is in incessant SVT for hours.

A routine ECG can sometimes help pediatricians with their differential diagnosis. Markers, such as a bypass tract, can show up on the ECG tracing. If a pre-excitement pattern is seen, further work-up may be needed, even in asymptomatic children incidentally discovered on routine testing for other reasons. Unequivocal diagnosis of SVT requires ECG documentation of the abnormal rhythm during an episode.

Because episodes of SVT tend to be unpredictable, trying to record the rhythm during the episode is not an easy exercise. One solution is to ask parents to record the child's pulse rate or heart rate during an episode, while the patient is complaining of symptoms. Going to the nearest emergency department increases the possibility of ECG identification of the SVT.

A pediatrician can also prescribe 24-hour Holter monitoring to try to catch an episode. If a patient is referred to a pediatric cardiologist, the patient is often monitored for a longer period of time in an attempt to catch the arrhythmia, such as 48-72 hours. Another helpful device is a loop recorder, which is worn constantly; it records and erases the ECG data after each half-hour. Parents are instructed to save the data after the episode by pushing a button. The data can then be transmitted to the monitoring company via telephone. The signal is turned into an ECG rhythm strip and sent to the physician for further analysis and necessary action.

The most worrisome arrhythmia in children is ventricular tachycardia (VT). It is a life-threatening arrhythmia. Fortunately, it is the most uncommon. Nonetheless, people who treat children have to be aware of conditions that are a setup for this kind of arrhythmia.

Hypertrophic cardiomyopathy is one such condition. It is a genetic condition leading to abnormality of the ventricular muscle. The abnormality produces a structural change with thickening of the heart muscle in an asymmetric fashion. The thickness may cause obstruction of the left ventricular outflow tract. In addition, such an individual is prone to VT. The presenting symptom for such individuals tends to be loss of consciousness or a fainting episode with the arrhythmia, generally occurring in the setting of vigorous physical activity. It can be a silent condition, fainting or collapse being the first symptom for some patients. Diagnosis is made by a combination of tests, including echocardiogram and ECG. Genetic testing is now available for the condition but does not help with practical management issues.

If a child is reporting other problems, such as constant fatigue and/or symptoms with minor daily activities, it suggests the possibility of myocarditis, usually related to viral infections. The heart of a child with such an infection becomes dilated and does not contract well. These patients are prone to VT. While some children with myocarditis recover, others may suffer permanent damage. The heart may remain dilated and prone to VT.

Another rare condition to include in your differential diagnosis is prolonged QT interval syndrome. The condition is genetic in nature and tends to run in families. The mechanism involves gates or ion channels in cell membranes that normally regulate the influx of sodium, potassium, and calcium. In a child with the syndrome, the gates remain open too long, thereby allowing too much sodium or calcium to enter the cells, and VT can ensue. ECG tracings and a history of syncope can be diagnostic. Genetic testing is available and helpful.

Ventricular tachycardia is very worrisome because it can be fatal within minutes. Therefore, VT is an emergency in most instances, although there are some benign forms that are well tolerated. The distinction can sometimes require an electrophysiology study. The placement of automatic external defibrillators in public places has enhanced the chances of survival in patients who experience rapid VT.

Peter Pronovost, MD, PhD, an intensivist and patient-safety researcher at Johns Hopkins University School of Medicine in Baltimore, has been widely profiled as the “checklist doctor” for his celebrated five-step checklist to reduce the incidence of central-line infections. But he objects to the label.

Just handing doctors and nurses a piece of paper is not likely to improve patient safety without two other essential steps: “We must also measure the results and give clinicians feedback, and we must change the culture so that they work collaboratively together,” he explains.

Dr. Pronovost shares his personal story as a safety expert who borrowed from aviation in developing his first checklist in 2001 in a Johns Hopkins surgical ICU in his new book, Safe Patients, Smart Hospitals, co-authored with Eric Vohr (New York: Hudson Street Press, 2010).

Dr. Pronovost says he still encounters resistance to the checklist in many U.S. hospitals. “Nobody debates that we should be doing the things on the checklist,” he says. “The evidence is strong. The barrier is culture or medical hierarchy. In what other industry would there be an accepted standard that failure to comply with it kills, in this case, 30,000 people per year, and yet we’re not comfortable having one worker question another about compliance with it?”

Hospitalists have a huge role in hospital quality and safety, he adds.

“I envision that they could take almost any practice guideline that’s out there and convert it into a checklist,” he says, emphasizing that hospitalists should appoint an interdisciplinary team to work on the project and make the checklists specific to one time and place. It also is important for hospitals to support hospitalists with dedicated time to work on such projects. “But in return, the hospitalists have to commit measuring safety performance and producing positive results,” he says.

Peter Pronovost, MD, PhD, an intensivist and patient-safety researcher at Johns Hopkins University School of Medicine in Baltimore, has been widely profiled as the “checklist doctor” for his celebrated five-step checklist to reduce the incidence of central-line infections. But he objects to the label.

Just handing doctors and nurses a piece of paper is not likely to improve patient safety without two other essential steps: “We must also measure the results and give clinicians feedback, and we must change the culture so that they work collaboratively together,” he explains.

Dr. Pronovost shares his personal story as a safety expert who borrowed from aviation in developing his first checklist in 2001 in a Johns Hopkins surgical ICU in his new book, Safe Patients, Smart Hospitals, co-authored with Eric Vohr (New York: Hudson Street Press, 2010).

Dr. Pronovost says he still encounters resistance to the checklist in many U.S. hospitals. “Nobody debates that we should be doing the things on the checklist,” he says. “The evidence is strong. The barrier is culture or medical hierarchy. In what other industry would there be an accepted standard that failure to comply with it kills, in this case, 30,000 people per year, and yet we’re not comfortable having one worker question another about compliance with it?”

Hospitalists have a huge role in hospital quality and safety, he adds.

“I envision that they could take almost any practice guideline that’s out there and convert it into a checklist,” he says, emphasizing that hospitalists should appoint an interdisciplinary team to work on the project and make the checklists specific to one time and place. It also is important for hospitals to support hospitalists with dedicated time to work on such projects. “But in return, the hospitalists have to commit measuring safety performance and producing positive results,” he says.

Peter Pronovost, MD, PhD, an intensivist and patient-safety researcher at Johns Hopkins University School of Medicine in Baltimore, has been widely profiled as the “checklist doctor” for his celebrated five-step checklist to reduce the incidence of central-line infections. But he objects to the label.

Just handing doctors and nurses a piece of paper is not likely to improve patient safety without two other essential steps: “We must also measure the results and give clinicians feedback, and we must change the culture so that they work collaboratively together,” he explains.

Dr. Pronovost shares his personal story as a safety expert who borrowed from aviation in developing his first checklist in 2001 in a Johns Hopkins surgical ICU in his new book, Safe Patients, Smart Hospitals, co-authored with Eric Vohr (New York: Hudson Street Press, 2010).

Dr. Pronovost says he still encounters resistance to the checklist in many U.S. hospitals. “Nobody debates that we should be doing the things on the checklist,” he says. “The evidence is strong. The barrier is culture or medical hierarchy. In what other industry would there be an accepted standard that failure to comply with it kills, in this case, 30,000 people per year, and yet we’re not comfortable having one worker question another about compliance with it?”

Hospitalists have a huge role in hospital quality and safety, he adds.

“I envision that they could take almost any practice guideline that’s out there and convert it into a checklist,” he says, emphasizing that hospitalists should appoint an interdisciplinary team to work on the project and make the checklists specific to one time and place. It also is important for hospitals to support hospitalists with dedicated time to work on such projects. “But in return, the hospitalists have to commit measuring safety performance and producing positive results,” he says.

An author of a recent study that found improved results for depressed alcohol-dependent patients when they were treated for both diagnoses says hospitalists are positioned to help push increased usage of the dual-medication approach.

“This could change the way people treat these patients,” says first author Helen Pettinati, PhD, professor of psychiatry and director of the Addiction Treatment & Medication Development Division at the University of Pennsylvania School of Medicine’s Treatment Research Center in Philadelphia.

The study in the American Journal of Psychiatry tracked 170 patients, with some treated with 14 weeks of sertraline (200 mg/day, n=40), naltrexone (100 mg/day, n=49), both drugs (n=42), or double placebo (n=39). All groups received weekly counseling as well. Patients treated with both medications produced a higher alcohol abstinence rate (53.7%) and demonstrated a longer delay before relapse to heavy drinking (median delay=98 days) than the naltrexone (abstinence rate: 21.3%; delay=29 days), sertraline (abstinence rate: 27.5%; delay=23 days), and placebo (abstinence rate: 23.1%; delay=26 days) groups. In addition, patients treated with both medications “reported fewer serious adverse events, and tended to not be depressed by the end of treatment,” the authors wrote.

Pettinati says it is uncommon for hospitalists and other physicians to consider treating hospitalized patients with medication for alcohol dependence. She hopes hospitalists see this study as a spotlight on that approach. In past years, Pettinati suggests, medication for alcohol dependence might have been viewed as unnecessary because patient lengths-of-stay (LOS) were longer. Today, HM leaders are pushing for ever-shorter LOS.

“Now when a person comes in,” Pettinati says, “you have to make an immediate decision what kind of medication you want to treat this person with.”

An author of a recent study that found improved results for depressed alcohol-dependent patients when they were treated for both diagnoses says hospitalists are positioned to help push increased usage of the dual-medication approach.

“This could change the way people treat these patients,” says first author Helen Pettinati, PhD, professor of psychiatry and director of the Addiction Treatment & Medication Development Division at the University of Pennsylvania School of Medicine’s Treatment Research Center in Philadelphia.

The study in the American Journal of Psychiatry tracked 170 patients, with some treated with 14 weeks of sertraline (200 mg/day, n=40), naltrexone (100 mg/day, n=49), both drugs (n=42), or double placebo (n=39). All groups received weekly counseling as well. Patients treated with both medications produced a higher alcohol abstinence rate (53.7%) and demonstrated a longer delay before relapse to heavy drinking (median delay=98 days) than the naltrexone (abstinence rate: 21.3%; delay=29 days), sertraline (abstinence rate: 27.5%; delay=23 days), and placebo (abstinence rate: 23.1%; delay=26 days) groups. In addition, patients treated with both medications “reported fewer serious adverse events, and tended to not be depressed by the end of treatment,” the authors wrote.

Pettinati says it is uncommon for hospitalists and other physicians to consider treating hospitalized patients with medication for alcohol dependence. She hopes hospitalists see this study as a spotlight on that approach. In past years, Pettinati suggests, medication for alcohol dependence might have been viewed as unnecessary because patient lengths-of-stay (LOS) were longer. Today, HM leaders are pushing for ever-shorter LOS.

“Now when a person comes in,” Pettinati says, “you have to make an immediate decision what kind of medication you want to treat this person with.”

An author of a recent study that found improved results for depressed alcohol-dependent patients when they were treated for both diagnoses says hospitalists are positioned to help push increased usage of the dual-medication approach.

“This could change the way people treat these patients,” says first author Helen Pettinati, PhD, professor of psychiatry and director of the Addiction Treatment & Medication Development Division at the University of Pennsylvania School of Medicine’s Treatment Research Center in Philadelphia.

The study in the American Journal of Psychiatry tracked 170 patients, with some treated with 14 weeks of sertraline (200 mg/day, n=40), naltrexone (100 mg/day, n=49), both drugs (n=42), or double placebo (n=39). All groups received weekly counseling as well. Patients treated with both medications produced a higher alcohol abstinence rate (53.7%) and demonstrated a longer delay before relapse to heavy drinking (median delay=98 days) than the naltrexone (abstinence rate: 21.3%; delay=29 days), sertraline (abstinence rate: 27.5%; delay=23 days), and placebo (abstinence rate: 23.1%; delay=26 days) groups. In addition, patients treated with both medications “reported fewer serious adverse events, and tended to not be depressed by the end of treatment,” the authors wrote.

Pettinati says it is uncommon for hospitalists and other physicians to consider treating hospitalized patients with medication for alcohol dependence. She hopes hospitalists see this study as a spotlight on that approach. In past years, Pettinati suggests, medication for alcohol dependence might have been viewed as unnecessary because patient lengths-of-stay (LOS) were longer. Today, HM leaders are pushing for ever-shorter LOS.

“Now when a person comes in,” Pettinati says, “you have to make an immediate decision what kind of medication you want to treat this person with.”

A recent study that associates lower 30-day readmission rates for heart failure patients who receive followups within one week might be a jumpstart to new incentives for fewer readmissions, says the report’s author.

“In a way, [hospitalists] are central to all this,” says Adrian F. Hernandez, MD, MHS, an assistant professor at Duke University School of Medicine and a cardiologist at Duke University Medical Center in Durham, N.C. “During the hospital stay, they are quarterbacking that patient’s care. They have a central responsibility to make sure that patient discharge is seamless.”

The study tracked 30,136 patients who were seen at 225 hospitals from January 2003 to December 2006. It reported that in the first 30 days after discharge, 6,428 patients (21.3 percent) were readmitted (JAMA. 2010;303(17):1716-1722).

At the hospital level, the median rate of early followup was 38.3 percent. According to the study, patients whose index admission was in a hospital in the lowest quartile of early followup had a 23.3% 30-day readmission rate. The rates of 30-day readmission were 20.5% among patients in the second quartile, 20.5% among patients in the third quartile, and 20.9% among patients in the fourth quartile.

Dr. Hernandez says the next step is for hospitals and their staffs to commit to more streamlined transitional-care techniques that include immediate followup with patients, be it via teleconferencing with doctors or phone calls with nonphysician providers (NPPs) or clinical pharmacists. He adds that incentivizing doctors to reduce readmissions is a logical next step to improving the discharge process.

“Now that 30-day readmissions are publicly reported and hospitals are being held accountable for that, they need to invest in systems that will enhance that transitional period,” Dr. Hernandez says.

A recent study that associates lower 30-day readmission rates for heart failure patients who receive followups within one week might be a jumpstart to new incentives for fewer readmissions, says the report’s author.

“In a way, [hospitalists] are central to all this,” says Adrian F. Hernandez, MD, MHS, an assistant professor at Duke University School of Medicine and a cardiologist at Duke University Medical Center in Durham, N.C. “During the hospital stay, they are quarterbacking that patient’s care. They have a central responsibility to make sure that patient discharge is seamless.”

The study tracked 30,136 patients who were seen at 225 hospitals from January 2003 to December 2006. It reported that in the first 30 days after discharge, 6,428 patients (21.3 percent) were readmitted (JAMA. 2010;303(17):1716-1722).

At the hospital level, the median rate of early followup was 38.3 percent. According to the study, patients whose index admission was in a hospital in the lowest quartile of early followup had a 23.3% 30-day readmission rate. The rates of 30-day readmission were 20.5% among patients in the second quartile, 20.5% among patients in the third quartile, and 20.9% among patients in the fourth quartile.

Dr. Hernandez says the next step is for hospitals and their staffs to commit to more streamlined transitional-care techniques that include immediate followup with patients, be it via teleconferencing with doctors or phone calls with nonphysician providers (NPPs) or clinical pharmacists. He adds that incentivizing doctors to reduce readmissions is a logical next step to improving the discharge process.

“Now that 30-day readmissions are publicly reported and hospitals are being held accountable for that, they need to invest in systems that will enhance that transitional period,” Dr. Hernandez says.

A recent study that associates lower 30-day readmission rates for heart failure patients who receive followups within one week might be a jumpstart to new incentives for fewer readmissions, says the report’s author.

“In a way, [hospitalists] are central to all this,” says Adrian F. Hernandez, MD, MHS, an assistant professor at Duke University School of Medicine and a cardiologist at Duke University Medical Center in Durham, N.C. “During the hospital stay, they are quarterbacking that patient’s care. They have a central responsibility to make sure that patient discharge is seamless.”

The study tracked 30,136 patients who were seen at 225 hospitals from January 2003 to December 2006. It reported that in the first 30 days after discharge, 6,428 patients (21.3 percent) were readmitted (JAMA. 2010;303(17):1716-1722).

At the hospital level, the median rate of early followup was 38.3 percent. According to the study, patients whose index admission was in a hospital in the lowest quartile of early followup had a 23.3% 30-day readmission rate. The rates of 30-day readmission were 20.5% among patients in the second quartile, 20.5% among patients in the third quartile, and 20.9% among patients in the fourth quartile.

Dr. Hernandez says the next step is for hospitals and their staffs to commit to more streamlined transitional-care techniques that include immediate followup with patients, be it via teleconferencing with doctors or phone calls with nonphysician providers (NPPs) or clinical pharmacists. He adds that incentivizing doctors to reduce readmissions is a logical next step to improving the discharge process.

“Now that 30-day readmissions are publicly reported and hospitals are being held accountable for that, they need to invest in systems that will enhance that transitional period,” Dr. Hernandez says.

Clinical question: Do rapid-response teams (RRTs) reduce the rates of cardiopulmonary arrest and hospital mortality?

Background: RRTs are charged with prompt evaluation and treatment of inpatients with clinical deterioration to prevent cardiopulmonary arrest and its attendant mortality. Though hundreds of hospitals have implemented these teams as part of their quality-improvement (QI) initiatives, previous studies on RRTs have reported mixed results on the clinically meaningful outcome of hospital mortality.

Study design: Meta-analysis and systematic review.

Setting: Randomized, controlled trials and prospective studies on RRTs from multiple databases, including PubMed, EMBASE, and CINAHL.

Synopsis: Eighteen studies (13 adult and five pediatric) with a total sample size of nearly 1.3 million admissions were analyzed. Of these, 15 reported on the primary outcome of in-hospital mortality; 16 reported on the secondary outcome of cardiopulmonary arrest. All of the studies exhibited extensive heterogeneity of outcomes, but six studies were deemed to be of high quality.

In adults, RRT implementation reduced non-ICU cardiopulmonary arrest by 33.8%, without an effect on hospital mortality (pooled RR, 0.96; 95% CI, 0.84-1.09). Interestingly, the inclusion of recent evidence neutralized positive results from initial studies in the overall pooled analysis.

In children, apart from reduction in arrest (37.7%), a weak association with lower mortality rates (pooled RR, 0.79; 95% CI, 0.63-0.98) was noticed. This did not hold on sensitivity analysis, but that could be explained by their higher likelihood to survive cardiac arrest than adults.

The discordance between the primary and secondary outcomes could be due to pre-arrest transfer to ICU or establishment of DNR status by RRT, hence excluding them from mortality analysis.

Bottom line: Although RRTs reduce rates of cardiopulmonary arrest outside the ICU, no consistent evidence shows RRTs improve survival to discharge.

Citation: Chan PS, Jain R, Nallmothu BK, Berg RA, Sasson C. Rapid response teams: a systematic review and meta-analysis. Arch Intern Med. 2010;170(1):18-26.

Reviewed for TH eWire by Rubin Bahuva, MD, Chadi Alraies, MD, Anuradha Ramaswamy, MD, Sudhir Manda, MD, Maria Giselle Velez, MD, and Mital Patel, MD, Department of Hospital Medicine, Cleveland Clinic

For more physician reviews of HM-related research, visit our website.

Clinical question: Do rapid-response teams (RRTs) reduce the rates of cardiopulmonary arrest and hospital mortality?

Background: RRTs are charged with prompt evaluation and treatment of inpatients with clinical deterioration to prevent cardiopulmonary arrest and its attendant mortality. Though hundreds of hospitals have implemented these teams as part of their quality-improvement (QI) initiatives, previous studies on RRTs have reported mixed results on the clinically meaningful outcome of hospital mortality.

Study design: Meta-analysis and systematic review.

Setting: Randomized, controlled trials and prospective studies on RRTs from multiple databases, including PubMed, EMBASE, and CINAHL.

Synopsis: Eighteen studies (13 adult and five pediatric) with a total sample size of nearly 1.3 million admissions were analyzed. Of these, 15 reported on the primary outcome of in-hospital mortality; 16 reported on the secondary outcome of cardiopulmonary arrest. All of the studies exhibited extensive heterogeneity of outcomes, but six studies were deemed to be of high quality.

In adults, RRT implementation reduced non-ICU cardiopulmonary arrest by 33.8%, without an effect on hospital mortality (pooled RR, 0.96; 95% CI, 0.84-1.09). Interestingly, the inclusion of recent evidence neutralized positive results from initial studies in the overall pooled analysis.

In children, apart from reduction in arrest (37.7%), a weak association with lower mortality rates (pooled RR, 0.79; 95% CI, 0.63-0.98) was noticed. This did not hold on sensitivity analysis, but that could be explained by their higher likelihood to survive cardiac arrest than adults.

The discordance between the primary and secondary outcomes could be due to pre-arrest transfer to ICU or establishment of DNR status by RRT, hence excluding them from mortality analysis.

Bottom line: Although RRTs reduce rates of cardiopulmonary arrest outside the ICU, no consistent evidence shows RRTs improve survival to discharge.

Citation: Chan PS, Jain R, Nallmothu BK, Berg RA, Sasson C. Rapid response teams: a systematic review and meta-analysis. Arch Intern Med. 2010;170(1):18-26.

Reviewed for TH eWire by Rubin Bahuva, MD, Chadi Alraies, MD, Anuradha Ramaswamy, MD, Sudhir Manda, MD, Maria Giselle Velez, MD, and Mital Patel, MD, Department of Hospital Medicine, Cleveland Clinic

For more physician reviews of HM-related research, visit our website.

Clinical question: Do rapid-response teams (RRTs) reduce the rates of cardiopulmonary arrest and hospital mortality?

Background: RRTs are charged with prompt evaluation and treatment of inpatients with clinical deterioration to prevent cardiopulmonary arrest and its attendant mortality. Though hundreds of hospitals have implemented these teams as part of their quality-improvement (QI) initiatives, previous studies on RRTs have reported mixed results on the clinically meaningful outcome of hospital mortality.

Study design: Meta-analysis and systematic review.

Setting: Randomized, controlled trials and prospective studies on RRTs from multiple databases, including PubMed, EMBASE, and CINAHL.

Synopsis: Eighteen studies (13 adult and five pediatric) with a total sample size of nearly 1.3 million admissions were analyzed. Of these, 15 reported on the primary outcome of in-hospital mortality; 16 reported on the secondary outcome of cardiopulmonary arrest. All of the studies exhibited extensive heterogeneity of outcomes, but six studies were deemed to be of high quality.

In adults, RRT implementation reduced non-ICU cardiopulmonary arrest by 33.8%, without an effect on hospital mortality (pooled RR, 0.96; 95% CI, 0.84-1.09). Interestingly, the inclusion of recent evidence neutralized positive results from initial studies in the overall pooled analysis.

In children, apart from reduction in arrest (37.7%), a weak association with lower mortality rates (pooled RR, 0.79; 95% CI, 0.63-0.98) was noticed. This did not hold on sensitivity analysis, but that could be explained by their higher likelihood to survive cardiac arrest than adults.

The discordance between the primary and secondary outcomes could be due to pre-arrest transfer to ICU or establishment of DNR status by RRT, hence excluding them from mortality analysis.

Bottom line: Although RRTs reduce rates of cardiopulmonary arrest outside the ICU, no consistent evidence shows RRTs improve survival to discharge.

Citation: Chan PS, Jain R, Nallmothu BK, Berg RA, Sasson C. Rapid response teams: a systematic review and meta-analysis. Arch Intern Med. 2010;170(1):18-26.

Reviewed for TH eWire by Rubin Bahuva, MD, Chadi Alraies, MD, Anuradha Ramaswamy, MD, Sudhir Manda, MD, Maria Giselle Velez, MD, and Mital Patel, MD, Department of Hospital Medicine, Cleveland Clinic

For more physician reviews of HM-related research, visit our website.

The IRS has sided with medical residents and their employers who for years have argued that they should have always been eligible for the “student exemption”—but don’t count on any money just yet.

By mid-June, the IRS expects to have contacted hospitals, universities, and individual residents who filed Social Security and Medicare payroll tax refund claims as of April 1, 2005. The date is significant because it is when the IRS ruled that employees who work 40 hours or more at a school, college, or university are eligible for student exemptions.

The IRS’ administrative decision in early March affects taxes paid before 2005.

The IRS has only taken the first step and says instructions on how to further process claims will be forthcoming. For now, the federal agency says, “employers and individuals with pending claims do not need to take any action at this time.”

Still, Joseph Ming-Wah Li, MD, SFHM, assistant professor of medicine at Harvard Medical School and director of the hospital medicine division at Beth Israel Deaconess Medical Center in Boston, urges hospitalists to pay attention to the refund; over three years of residency, it could amount to several thousand dollars per physician.

“The government ruling recently was that residents should be treated more like students instead of employees,” says Dr. Li, SHM's president-elect.

Hospitals, medical schools, and residents themselves have been filing so-called “FICA refund claims” since the 1990s. A series of legal challenges led to opposing interpretations of tax codes, leading the IRS to suspend all claims until a ruling was made.

And while pending claims will now be processed, it is too late for new claims to be filed. However, residents who did not file individual claims in what the IRS calls a “timely fashion” should check with their residency institution to determine if a claim was filed on their behalf.

Read "Dr. Hospitalist's" take on this topic in this month's issue of The Hospitalist.

For more details, visit the IRS website.

The IRS has sided with medical residents and their employers who for years have argued that they should have always been eligible for the “student exemption”—but don’t count on any money just yet.

By mid-June, the IRS expects to have contacted hospitals, universities, and individual residents who filed Social Security and Medicare payroll tax refund claims as of April 1, 2005. The date is significant because it is when the IRS ruled that employees who work 40 hours or more at a school, college, or university are eligible for student exemptions.

The IRS’ administrative decision in early March affects taxes paid before 2005.

The IRS has only taken the first step and says instructions on how to further process claims will be forthcoming. For now, the federal agency says, “employers and individuals with pending claims do not need to take any action at this time.”

Still, Joseph Ming-Wah Li, MD, SFHM, assistant professor of medicine at Harvard Medical School and director of the hospital medicine division at Beth Israel Deaconess Medical Center in Boston, urges hospitalists to pay attention to the refund; over three years of residency, it could amount to several thousand dollars per physician.

“The government ruling recently was that residents should be treated more like students instead of employees,” says Dr. Li, SHM's president-elect.

Hospitals, medical schools, and residents themselves have been filing so-called “FICA refund claims” since the 1990s. A series of legal challenges led to opposing interpretations of tax codes, leading the IRS to suspend all claims until a ruling was made.

And while pending claims will now be processed, it is too late for new claims to be filed. However, residents who did not file individual claims in what the IRS calls a “timely fashion” should check with their residency institution to determine if a claim was filed on their behalf.

Read "Dr. Hospitalist's" take on this topic in this month's issue of The Hospitalist.

For more details, visit the IRS website.

The IRS has sided with medical residents and their employers who for years have argued that they should have always been eligible for the “student exemption”—but don’t count on any money just yet.

By mid-June, the IRS expects to have contacted hospitals, universities, and individual residents who filed Social Security and Medicare payroll tax refund claims as of April 1, 2005. The date is significant because it is when the IRS ruled that employees who work 40 hours or more at a school, college, or university are eligible for student exemptions.

The IRS’ administrative decision in early March affects taxes paid before 2005.

The IRS has only taken the first step and says instructions on how to further process claims will be forthcoming. For now, the federal agency says, “employers and individuals with pending claims do not need to take any action at this time.”

Still, Joseph Ming-Wah Li, MD, SFHM, assistant professor of medicine at Harvard Medical School and director of the hospital medicine division at Beth Israel Deaconess Medical Center in Boston, urges hospitalists to pay attention to the refund; over three years of residency, it could amount to several thousand dollars per physician.

“The government ruling recently was that residents should be treated more like students instead of employees,” says Dr. Li, SHM's president-elect.

Hospitals, medical schools, and residents themselves have been filing so-called “FICA refund claims” since the 1990s. A series of legal challenges led to opposing interpretations of tax codes, leading the IRS to suspend all claims until a ruling was made.

And while pending claims will now be processed, it is too late for new claims to be filed. However, residents who did not file individual claims in what the IRS calls a “timely fashion” should check with their residency institution to determine if a claim was filed on their behalf.

Read "Dr. Hospitalist's" take on this topic in this month's issue of The Hospitalist.

For more details, visit the IRS website.

Clinical question: Does remote ICU monitoring improve mortality and length of stay?

Background: A shortage of intensivists has led to increased use of remote ICU monitoring or telemedicine technology to allow intensivists to remotely and simultaneously care for patients in multiple ICUs. Data evaluating this practice have been limited.

Study design: Pre- and postintervention observational study.

Setting: Open and closed medical-surgical ICUs in community, urban, and tertiary-care teaching U.S. hospitals.

Synopsis: This observational study in six ICUs aimed to assess the association of a telemedicine intervention with clinical outcomes. The intervention consisted of a remote office with real-time audiovisual monitoring, vital signs, early warning signals, and other electronic data. Comparing preintervention (n=2,034) and postintervention (n=2,108) groups, there were no differences in mortality, LOS, or complications.

Overall, the general limitation of the study was that integration of the tele-ICU and actual ICUs was limited. Physicians for nearly two-thirds of the patients chose “minimal delegation” to the tele-ICU physician. Tele-ICU involvement was particularly limited in “closed” units, which were already staffed by on-site intensivists. Furthermore, despite access to various real-time data, critical elements of the record such as physician order entry and progress notes were not shared in real time; notes, for example, required daily faxing.

While it is unfortunate that the study could not evaluate the full potential of the adjunctive tele-ICU, it illustrates the real-world obstacles of integrating such technology into clinical practice. In future studies, a standardized telemedicine approach might facilitate evaluation efforts.

Bottom line: While this study demonstrated no benefit of telemedicine, study limitations preclude conclusions. Further studies are needed.

Citation: Thomas EJ, Lucke JF, Wueste L, Weavind L, Patel B. Association of telemedicine for remote monitoring of intensive care patients with mortality, complications, and length of stay. JAMA. 2009;302(24):2671-2678.

Dr. Kim is a hospitalist at Brigham and Women's Hospital in Boston, and an instructor at Harvard Medical School.

For more reviews of HM-related research, visit our website.

Clinical question: Does remote ICU monitoring improve mortality and length of stay?

Background: A shortage of intensivists has led to increased use of remote ICU monitoring or telemedicine technology to allow intensivists to remotely and simultaneously care for patients in multiple ICUs. Data evaluating this practice have been limited.

Study design: Pre- and postintervention observational study.

Setting: Open and closed medical-surgical ICUs in community, urban, and tertiary-care teaching U.S. hospitals.

Synopsis: This observational study in six ICUs aimed to assess the association of a telemedicine intervention with clinical outcomes. The intervention consisted of a remote office with real-time audiovisual monitoring, vital signs, early warning signals, and other electronic data. Comparing preintervention (n=2,034) and postintervention (n=2,108) groups, there were no differences in mortality, LOS, or complications.

Overall, the general limitation of the study was that integration of the tele-ICU and actual ICUs was limited. Physicians for nearly two-thirds of the patients chose “minimal delegation” to the tele-ICU physician. Tele-ICU involvement was particularly limited in “closed” units, which were already staffed by on-site intensivists. Furthermore, despite access to various real-time data, critical elements of the record such as physician order entry and progress notes were not shared in real time; notes, for example, required daily faxing.

While it is unfortunate that the study could not evaluate the full potential of the adjunctive tele-ICU, it illustrates the real-world obstacles of integrating such technology into clinical practice. In future studies, a standardized telemedicine approach might facilitate evaluation efforts.

Bottom line: While this study demonstrated no benefit of telemedicine, study limitations preclude conclusions. Further studies are needed.

Citation: Thomas EJ, Lucke JF, Wueste L, Weavind L, Patel B. Association of telemedicine for remote monitoring of intensive care patients with mortality, complications, and length of stay. JAMA. 2009;302(24):2671-2678.

Dr. Kim is a hospitalist at Brigham and Women's Hospital in Boston, and an instructor at Harvard Medical School.

For more reviews of HM-related research, visit our website.

Clinical question: Does remote ICU monitoring improve mortality and length of stay?

Background: A shortage of intensivists has led to increased use of remote ICU monitoring or telemedicine technology to allow intensivists to remotely and simultaneously care for patients in multiple ICUs. Data evaluating this practice have been limited.

Study design: Pre- and postintervention observational study.

Setting: Open and closed medical-surgical ICUs in community, urban, and tertiary-care teaching U.S. hospitals.

Synopsis: This observational study in six ICUs aimed to assess the association of a telemedicine intervention with clinical outcomes. The intervention consisted of a remote office with real-time audiovisual monitoring, vital signs, early warning signals, and other electronic data. Comparing preintervention (n=2,034) and postintervention (n=2,108) groups, there were no differences in mortality, LOS, or complications.

Overall, the general limitation of the study was that integration of the tele-ICU and actual ICUs was limited. Physicians for nearly two-thirds of the patients chose “minimal delegation” to the tele-ICU physician. Tele-ICU involvement was particularly limited in “closed” units, which were already staffed by on-site intensivists. Furthermore, despite access to various real-time data, critical elements of the record such as physician order entry and progress notes were not shared in real time; notes, for example, required daily faxing.

While it is unfortunate that the study could not evaluate the full potential of the adjunctive tele-ICU, it illustrates the real-world obstacles of integrating such technology into clinical practice. In future studies, a standardized telemedicine approach might facilitate evaluation efforts.

Bottom line: While this study demonstrated no benefit of telemedicine, study limitations preclude conclusions. Further studies are needed.

Citation: Thomas EJ, Lucke JF, Wueste L, Weavind L, Patel B. Association of telemedicine for remote monitoring of intensive care patients with mortality, complications, and length of stay. JAMA. 2009;302(24):2671-2678.

Dr. Kim is a hospitalist at Brigham and Women's Hospital in Boston, and an instructor at Harvard Medical School.

For more reviews of HM-related research, visit our website.

When and how the national focus on reducing hospital readmissions will hit hospitals’ bottom lines is not clear, but it’s more a matter of when, not if, says Eric Coleman, MD, MPH, AGSF, FACP, director of the Care Transitions Program at the University of Colorado Denver.

Reducing readmissions “jumps off the page as an area where we could see enormous savings in national health expenditures,” Dr. Coleman told participants in an SHM webinar last month. The challenge, he said, is to align incentives with quality and safety for a moving target that also happens to be highly politicized. “We’re generally pretty good at identifying who’s at risk of readmission, but it’s harder to say who’s at modifiable risk,” he explained.

Evidence shows that hospitalists already reduce costs through improved length of stay. “Can hospitalists demonstrate the ability to reduce readmission rates as well?” Dr. Coleman asked.

Bundling payment for hospital stays with various post-hospital providers is a major focus of national efforts to reduce healthcare costs. Bundling gives providers on the healthcare continuum strong motivation to work together, Dr. Coleman said. The government won’t tell providers how to divide bundled payments, but Dr. Coleman predicts that consulting firms offering ideas for divvying up the money will emerge.

The Medicare Payment Advisory Commission (MEDPAC) has signaled its interest in changing payment incentives by reducing reimbursement for readmissions as well as several provisions that directly address readmissions in the healthcare reform package signed by President Obama in March. These include:

- A national pilot program on payment bundling;

- A hospital readmissions reduction program with financial penalties starting in October 2012 for select conditions; and

- A QI program to help hospitals with high severity-adjusted readmission rates.

When and how the national focus on reducing hospital readmissions will hit hospitals’ bottom lines is not clear, but it’s more a matter of when, not if, says Eric Coleman, MD, MPH, AGSF, FACP, director of the Care Transitions Program at the University of Colorado Denver.

Reducing readmissions “jumps off the page as an area where we could see enormous savings in national health expenditures,” Dr. Coleman told participants in an SHM webinar last month. The challenge, he said, is to align incentives with quality and safety for a moving target that also happens to be highly politicized. “We’re generally pretty good at identifying who’s at risk of readmission, but it’s harder to say who’s at modifiable risk,” he explained.

Evidence shows that hospitalists already reduce costs through improved length of stay. “Can hospitalists demonstrate the ability to reduce readmission rates as well?” Dr. Coleman asked.

Bundling payment for hospital stays with various post-hospital providers is a major focus of national efforts to reduce healthcare costs. Bundling gives providers on the healthcare continuum strong motivation to work together, Dr. Coleman said. The government won’t tell providers how to divide bundled payments, but Dr. Coleman predicts that consulting firms offering ideas for divvying up the money will emerge.

The Medicare Payment Advisory Commission (MEDPAC) has signaled its interest in changing payment incentives by reducing reimbursement for readmissions as well as several provisions that directly address readmissions in the healthcare reform package signed by President Obama in March. These include:

- A national pilot program on payment bundling;

- A hospital readmissions reduction program with financial penalties starting in October 2012 for select conditions; and

- A QI program to help hospitals with high severity-adjusted readmission rates.

When and how the national focus on reducing hospital readmissions will hit hospitals’ bottom lines is not clear, but it’s more a matter of when, not if, says Eric Coleman, MD, MPH, AGSF, FACP, director of the Care Transitions Program at the University of Colorado Denver.

Reducing readmissions “jumps off the page as an area where we could see enormous savings in national health expenditures,” Dr. Coleman told participants in an SHM webinar last month. The challenge, he said, is to align incentives with quality and safety for a moving target that also happens to be highly politicized. “We’re generally pretty good at identifying who’s at risk of readmission, but it’s harder to say who’s at modifiable risk,” he explained.

Evidence shows that hospitalists already reduce costs through improved length of stay. “Can hospitalists demonstrate the ability to reduce readmission rates as well?” Dr. Coleman asked.

Bundling payment for hospital stays with various post-hospital providers is a major focus of national efforts to reduce healthcare costs. Bundling gives providers on the healthcare continuum strong motivation to work together, Dr. Coleman said. The government won’t tell providers how to divide bundled payments, but Dr. Coleman predicts that consulting firms offering ideas for divvying up the money will emerge.

The Medicare Payment Advisory Commission (MEDPAC) has signaled its interest in changing payment incentives by reducing reimbursement for readmissions as well as several provisions that directly address readmissions in the healthcare reform package signed by President Obama in March. These include:

- A national pilot program on payment bundling;

- A hospital readmissions reduction program with financial penalties starting in October 2012 for select conditions; and

- A QI program to help hospitals with high severity-adjusted readmission rates.