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Managing Type 2 Diabetes in Men
Managing the Multiple Symptoms of Benign Prostatic Hyperplasia — CME
Managing Type 2 Diabetes in Men
Meeting New Challenges with Antiplatelet Therapy in Primary Care
Dr. Aguilar has disclosed that he has ongoing relationships with the following companies: Amylin Pharmaceuticals; Eli Lilly; Janssen Pharmaceuticals, Inc; Novo Nordisk, Inc; and Takeda Pharmaceuticals USA, Inc.
SUPPORT
This program is sponsored by the PCEC and is supported by funding from Novo Nordisk, Inc.
The prevalence of type 2 diabetes mellitus (T2DM) is similar in men and women (11.8% vs 10.8%, respectively), however there are gender differences that should be considered when developing a treatment plan (eg, cardiovascular risk, psychosocial factors, coping strategies, and the perception of benefit from self-care) when managing those diagnosed with this disease and those at risk for developing it.1 This article describes these differences in the context of two patients—one at risk for T2DM being seen by his health care provider for a routine physical examination, and one who has been treated for several years for T2DM and is being seen for a follow-up office visit. For each patient, the implications for treatment are discussed.
Men at Risk for Type 2 Diabetes Mellitus
JW is a 48-year-old white male being seen for a routine physical examination; he last saw a physician 6 years ago, also for a routine physical. He has no complaints and is taking no medications. Having divorced 7 years ago, he lives alone in an apartment and eats many of his meals at fast food restaurants. JW drinks 2 to 3 beers a night several times a week and more when he socializes with his friends 2 to 3 evenings per week. He smokes socially. His father has a 12-year history of T2DM. His mother has a 4-year history of essential hypertension and a 9-year history of chronic obstructive pulmonary disease.
Physical examination shows that JW is 5’11” tall, weighs 207 pounds (body mass index (BMI), 29 kg/m2), and has a 41” waist circumference; his blood pressure (BP) is 138/86 mm Hg and respiratory rate is 17 breaths/min. The remainder of his physical examination, including eye and neurologic exams, is normal. Laboratory results, including a screening glycated homoglobin (A1C), are pending.
Key Risk Factors for Type 2 Diabetes Mellitus in Men
This case is not an uncommon presentation of a middle-aged male who has several risk factors for diabetes (see Case Study 1 continued ). JW also has key risk factors for T2DM in men. The Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) Augsburg surveys identified 128 men and 85 women with T2DM.2 Increasing age and BMI, positive parental history of T2DM, and a low high-density lipoprotein cholesterol (HDL-C) level were independent risk factors predicting the development of T2DM in both men and women. However, several other factors posed a higher risk in men relative to women, including systolic BP (hazard ratio [HR], 1.16 per 10-mm Hg increase), regular smoking (HR, 1.75), and alcohol intake ≥ 40 g/d (HR, 1.95). (Note: 1 fluid ounce 80 proof alcohol ≈ 11 g ethanol; 12 fluid ounces beer [~5% alcohol] ≈ 14 g ethanol). After adjusting for these factors, a separate analysis (4424 men, 4380 women) showed that men who lived alone were more likely to develop T2DM than either men or women who did not live alone (HR, 1.69 in men vs 0.85 in women; P = .006).3 While the number of people with T2DM in MONICA was small, the results suggest that measuring BP, particularly systolic BP, and taking a smoking and alcohol history may be especially important in men.
With respect to alcohol intake, epidemiologic and randomized clinical trials have generally demonstrated an inverse relationship between moderate alcohol consumption (20 to 30 g/d) and the long-term risk of T2DM.2,4-7 Differences among studies in how patients were grouped preclude determination of the daily alcohol consumption that confers the greatest risk benefit, although one recent study conducted over 4 years indicates that the greatest benefit in diabetes risk reduction may occur when men who previously consumed 8
Other nutrition and lifestyle patterns also seem to be particularly beneficial in reducing the risk of T2DM in men. Survey data involving 22,921 Japanese men and 29,759 Japanese women followed over 5 years showed that fish and seafood intake was significantly associated with a decreased risk of T2DM in men but not in women.9 The odds ratio of developing T2DM for the highest quartile versus the lowest quartile of fish and seafood intake was 0.73 (P = .04 for trend). Additional analysis did not identify any significant association with the fat content of fish.
Results of the Health Professionals Follow-up Study provide evidence of benefit in lowering the risk of T2DM in men who consume high amounts of low-fat dairy products, whole grains, and magnesium ( TABLE 1 ). With respect to dairy food consumption, after 12 years of follow-up involving 1243 incident cases of T2DM, the relative risk (RR) of developing T2DM in men in the top quintile of dairy intake was 0.77 compared with those in the lowest quintile (P = .003 for trend).10 Men in the highest quintile consumed 4.1 servings of dairy food per day compared with 0.5 servings per day in the lowest quintile. Each serving-per-day increase in total dairy intake was associated with a 9% lower risk for T2DM, with a lower risk seen with consumption of low-fat vs high-fat dairy food. With respect to whole-grain intake, the RR of developing T2DM was 0.58 in men in the upper vs lower quintiles (3.2 vs 0.4 servings/d), although the effect was attenuated with BMI (P = .0006 for trend).11 Similar observations were made with respect to magnesium consumption; a RR of 0.76 for T2DM was observed in men with a median magnesium consumption of 457 mg/d compared with those who consumed 270 mg/d.12
TABLE 1
Suggestions for Men Who Are at Risk of or Have Been Diagnosed with Type 2 Diabetes Mellitus (T2DM)*
For men who are at risk:
|
For men who have been diagnosed:
|
| BP, blood pressure; HDL-C, high-density lipoprotein cholesterol. *These suggestions are in addition to developing and fostering a collaborative, patient-centered approach. |
JW has the following risk factors for T2DM:
- Overweight with central adiposity
- Physical inactivity
- First-degree relative with T2DM
- Possible cardiovascular disease (CVD; hypertension, smoking)
- High daily alcohol intake (10 to 20 g alcohol/beer x 2-3 beers/d = 20 to 60 g alcohol/d)
- Poor nutrition
- Lives alone
Plan:
- Discuss above risk factors with JW
- Repeat BP measurement at next visit; implement treatment if BP >140/90 mm Hg (130/80 mm Hg if T2DM is diagnosed)
- Consider evaluation for alcohol/substance abuse
- Evaluate for smoking cessation program
- Nutrition referral for lifestyle and dietary management intervention
Working with men to avoid the development of T2DM is an important objective for family physicians. It is essential to identify men who are at increased risk, including those with prediabetes, provide education about the disease and its risk factors, and implement appropriate risk reduction strategies. Risk reduction strategies should focus on modifiable factors, such as body weight, physical activity, BP, blood lipids, blood glucose, and smoking. With JW, his motivation to “get back into shape” will help move the conversation toward achievable goals that can be set and modified over time. Other strategies that may be helpful in reducing the risk of developing T2DM in men include a moderate daily alcohol intake and a diet high in fish and seafood, low-fat dairy products, whole grains, and magnesium ( TABLE 1 ).
Once diagnosed with T2DM, there are risk management strategies that can be particularly helpful in men. These include strategies that target cardiovascular health, as well as those that consider the psychosocial and coping behaviors of men.
Risk of Complications in Men With Type 2 Diabetes Mellitus
Physical examination: BP, 126/78 mm Hg; body weight, 183 pounds (a 13 to 17 pound increase since the knee injury); waist circumference, 38” (BMI, 28 kg/m2); grade 1 retinopathy bilaterally; neurologic exam normal.
Laboratory: A1C, 7.8%; lipids normal except triglyceride level, 219 mg/dL; creatinine clearance (calculated), 69 mL/min; urine, 45 mg albumin/g creatinine.
MR’s self-measured fasting plasma glucose (FPG) has ranged from 121 to 143 mg/dL over the past month; isolated postprandial glucose (PPG) measurements show 194 to 258 mg/dL.
MR works as a vocational teacher at the local high school, and he teaches driver education after school. Review of his pharmacy records suggests his adherence over the past year has been: metformin (88%), hydrochlorothiazide (72%), and lisinopril (72%).
Assessment:
- A1C level of 7.8% indicates an estimated average glucose (eAG) of 177 mg/dL13
- –Mildly elevated FPG and PPG
- –Evidence of microvascular disease (retinopathy, nephropathy)
- –Creatinine clearance 69 mL/min and microalbuminuria indicate stage 2 chronic kidney disease14
In addition to referring MR for physical rehabilitation of his knee, you discuss with MR the need and options for intensifying his diabetes therapy.
Does the fact that MR is male affect your management plan?
In people diagnosed with T2DM, there are differences between men and women with respect to risk for cardiovascular and other comorbid diseases, as well as in their psychosocial well-being and coping strategies.
Risk for Cardiovascular Disease in Type 2 Diabetes Mellitus
A systematic literature review shows that men with T2DM generally fare better than women with T2DM regarding their risk for CVD. Men with T2DM have a 2- to 3-fold increase in the risk of developing coronary heart disease (CHD) compared with men without T2DM, whereas women with T2DM have a 4- to 6-fold increase in risk compared with women without T2DM.15 Compared with women with T2DM, men with T2DM also have a better prognosis after myocardial infarction (MI) and a lower risk of death overall from CVD. Possible reasons for these differences include a lower risk of hypertension, a less severe form of dyslipidemia, and a lower prevalence of obesity in men with T2DM compared with women with T2DM.15 These same reasons for observed differences between men and women were seen in a meta-analysis of 29 studies, where the RR of fatal MI in men with T2DM compared with women with T2DM was 0.68.16 Similar findings were seen in the Skaraborg Project, which involved 1116 Swedish patients with hypertension and/or T2DM.17 Compared with a healthy population, the age-adjusted HR for fatal MI was 1.9 for men with T2DM and 5.0 for women with T2DM over 8.1 years of follow-up (RR, 0.38 for men vs women). Analysis of the data indicated that these results were not explained by the more favorable survival rate in women without T2DM than in men without T2DM.17
Somewhat different results have been reported by the Italian Diabetes and Informatics Study Group in a slightly different T2DM population. This investigation involved men and women with T2DM (N = 11,644) who could have microvascular but not macrovascular disease.18 After 4 years of follow-up, the age-adjusted incident rates for first CHD event (composite of acute MI, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty) were 28.8 per 1000 person-years in men and 23.3 per 1000 person-years in women. Incident rates (per 1000 person-years) of acute MI (10.3 vs 4.7), major CHD events (13.1 vs 5.8), and fatal CHD (2.6 vs 0.6) were all significantly more frequent in men than in women, respectively. Multivariate analysis showed that hypertension and A1C were additional risk factors for CHD in men; for each 20% increment above the A1C upper limit of normal, there was a 14% risk increase for CHD. The presence of microvascular complications increased risk by 20% in men and 35% in women. In this analysis, glycemic control and hypertension were found to be the predominant risk factors in men, while high triglyceride levels, low HDL-C levels, and microangiopathy were predominant in women.
Additional multivariate analyses provide greater insight into specific factors that affect the risk of CVD and outcomes in men with T2DM. One investigation compared men and women with T2DM who were normotensive without evidence of CVD but with microalbuminuria. After 4.7 years of follow-up, men were found to be at lower risk (RR, 0.12) for a composite of death, acute MI, unstable angina, coronary interventions, heart failure, cerebral ischemic stroke or transient ischemic attack, and peripheral artery disease.19 Other investigators have reported a lower risk of stroke, including fatal stroke, in men with T2DM compared with women with T2DM.20,21 For example, analysis of the General Practice Research Database identified 22,178 men and 19,621 women with T2DM between the ages of 35 and 89 years.20 The stroke rate per 1000 person-years across all ages was 10.82 (95% confidence interval (CI), 10.17-11.51) in men and 13.16 (95% CI, 12.40-13.97) in women. In men, the rate per 1000 person-years rose from 1.81 in the 35 to 44 year age group to 28.35 in men 85 years of age or older. Although the rate of stroke per 1000 person-years was lower in women than men in the 35 to 44 year age group (1.53 vs 1.81), the rate in women exceeded that of men in the 85 years of age or older group (32.20 vs 28.35).
Other Chronic Complications
Kidney disease is affected by blood lipids, specifically HDL-C, in men with T2DM. An investigation in men and women with T2DM with normoalbuminuria or microalbuminuria at baseline showed that a low HDL-C level was an independent predictor of progression to a more advanced stage of albuminuria over 4.3 years of follow-up (HR, 0.391 for men with normal HDL-C compared with men with low HDL-C). In women, no lipid parameters were associated with progression of albuminuria.22
While these investigations do not provide a clear picture of the differences regarding cardiovascular risk between men and women with T2DM, they suggest that men with T2DM have a lower risk of nonfatal and fatal CVD and stroke than do women with T2DM. However, the lower risk seen in men may be affected by the cardiovascular endpoints measured and the presence of microvascular disease. Possible independent risk factors for CVD in men with T2DM include hypertension, poor glycemic control, and low HDL-C.
Risk factors that place MR at greater risk for CVD compared with a woman with T2DM and therefore serve as key treatment targets include:
- Hypertension—although controlled (126/78 mm Hg) with hydrochlorothiazide and lisinopril
- Poor glycemic control—A1C, 7.8% (eAG, 177mg/dL)
- –Increase physical activity—refer for knee rehabilitation
- –Intensify glucose-lowering therapy by adding an additional glucose-lowering agent (eg, dipeptidyl peptidase-4 inhibitor, glucagon-like peptide-1 receptor agonist, thiazolidinedione, α-glucosidase inhibitor, sulfonylurea, glinide, or basal insulin)
- Microalbuminuria (45 mg urinary albumin/g creatinine)—encourage better adherence to lisinopril; monitor renal function
- Hypertriglyceridemia—initiate omega-3 fatty acid or extended-release niacin
Psychosocial Well-Being, Benefit of Self-Care, and Coping Strategies
Type 2 diabetes mellitus is a chronic disease with glycemic control largely determined by patient self-management, and the attitudes and beliefs of patients with T2DM are important factors to consider from diagnosis onward.23 There are important differences between men and women with T2DM regarding attitudes and beliefs. Published investigations provide some, although not entirely consistent, insight into these psychosocial differences between men and women with T2DM. These differences are summarized in TABLE 2 .24-32 Taking these differences into account when planning treatment and when communicating with and educating the patient is essential for improved patient self-management.
TABLE 2
Psychosocial and Coping Characteristics of Men with Type 2 Diabetes Mellitus (T2DM)24-32
Compared with women with T2DM, generally, men with T2DM:
|
Key interventions for MR:
- Maintain a dialogue and enhance collaboration with MR
- Establish shared goals that are customized to incorporate MR’s personal goals
- Problem solve with MR to identify ways he can better integrate the diabetes self-care objectives of dietary changes and blood glucose self-monitoring into his daily life
- Emphasize that enhanced or greater disease control can be achieved by good self-management, including better adherence to the management plan
- Remind MR that T2DM is a progressive disease that requires intermittent medication adjustments to keep pace with its progression
- Build upon the belief that T2DM can be controlled by reminding MR that the disease was well controlled before his knee injury
- –Focus on the importance of rehabilitating his knee
- –Develop a rehabilitation plan
- Provide informational support regarding options for intensifying diabetes therapy (eg, dipeptidyl peptidase-4 inhibitor, thiazolidinedione, glucagon-like peptide-1 receptor agonist, sulfonylurea, or insulin)
- –Discuss MR’s needs and concerns, as well as barriers for each treatment option, particularly hypoglycemia and weight gain
- –Provide instruction or educational materials regarding injection devices
- –Involve the healthcare team, as appropriate
- Keep the treatment regimen as simple as possible; consider pill combinations where appropriate
Summary
The growing epidemic of T2DM requires intervention to assist patients who have been diagnosed to better manage the disease, to reduce the risk of developing the disease in those who have not yet been diagnosed, and to manage the associated complications. In addition to individualizing interventions based on a patient’s needs, concerns, and capabilities, taking gender into account is necessary. In otherwise healthy people, several independent factors appear to pose a higher risk of T2DM in men relative to women, including systolic hypertension, regular smoking, and alcohol intake ≥ 40 g/d. At the same time, men achieve greater risk reduction from moderate daily alcohol intake and a diet high in fish and seafood, low-fat dairy products, whole grains, and magnesium.
Once diagnosed with T2DM, men generally fare better than women regarding the risk for CVD; they also have a better prognosis after MI and a lower risk of death overall from CVD. Possible independent risk factors for CVD in men with T2DM that are especially important may include hypertension, poor glycemic control, and low HDL-C levels. Psychosocial complications, such as depression, are less likely in men with T2DM. However, men expend less effort coping, are less likely to utilize healthcare services, and are less informed about treatment options. Although men have a lower expectation of the benefit of self-management, they find support from family and friends more helpful than do women, but they are fearful of losing control of their disease.
Taking these gender differences into account should prove helpful as family care physicians work with men to reduce their risk of developing T2DM and in helping men diagnosed with T2DM to better self-manage their disease.
1. Centers for Disease Control and Prevention. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Published 2011. Accessed May 2, 2011.
2. Meisinger C, Thorand B, Schneider A, Stieber J, Doring A, Lowel H. Sex differences in risk factors for incident type 2 diabetes mellitus: the MONICA Augsburg cohort study. Arch Intern Med. 2002;162(1):82-89.
3. Meisinger C, Kandler U, Ladwig KH. Living alone is associated with an increased risk of type 2 diabetes mellitus in men but not women from the general population: the MONICA/KORA Augsburg Cohort Study. Psychosom Med. 2009;71(7):784-788.
4. Baliunas DO, Taylor BJ, Irving H, et al. Alcohol as a risk factor for type 2 diabetes: a systematic review and meta-analysis. Diabetes Care. 2009;32(11):2123-2132.
5. Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovick D. Lifestyle risk factors and new-onset diabetes mellitus in older adults: the cardiovascular health study. Arch Intern Med. 2009;169(8):798-807.
6. Joosten MM, Grobbee DE, van der A DL, Verschuren WM, Hendriks HF, Beulens JW. Combined effect of alcohol consumption and lifestyle behaviors on risk of type 2 diabetes. Am J Clin Nutr. 2010;91(6):1777-1783.
7. Gigleux I, Gagnon J, St-Pierre A, et al. Moderate alcohol consumption is more cardioprotective in men with the metabolic syndrome. J Nutr. 2006;136(12):3027-3032.
8. Joosten MM, Chiuve SE, Mukamal KJ, Hu FB, Hendriks HF, Rimm EB. Changes in alcohol consumption and subsequent risk of type 2 diabetes in men. Diabetes. 2011;60(1):74-79.
9. Nanri A, Mizoue T, Noda M, et al. Fish intake and type 2 diabetes in Japanese men and women: the Japan Public Health Center-based Prospective Study. Am J Clin Nutr. 2011;94(3):884-891.
10. Choi HK, Willett WC, Stampfer MJ, Rimm E, Hu FB. Dairy consumption and risk of type 2 diabetes mellitus in men: a prospective study. Arch Intern Med. 2005;165(9):997-1003.
11. Fung TT, Hu FB, Pereira MA, et al. Whole-grain intake and the risk of type 2 diabetes: a prospective study in men. Am J Clin Nutr. 2002;76(3):535-540.
12. Lopez-Ridaura R, Willett WC, Rimm EB, et al. Magnesium intake and risk of type 2 diabetes in men and women. Diabetes Care. 2004;27(1):134-140.
13. Nathan DM, Kuenen J, Borg R, et al. Translating the A1C assay into estimated average glucose values. Diabetes Care. 2008;31(8):1473-1478.
14. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Ann Intern Med. 2003;139(2):137-147.
15. Legato MJ, Gelzer A, Goland R, et al. Gender-specific care of the patient with diabetes: review and recommendations. Gend Med. 2006;3(2):131-158.
16. Huxley R, Barzi F, Woodward M. Excess risk of fatal coronary heart disease associated with diabetes in men and women: meta-analysis of 37 prospective cohort studies. BMJ. 2006;332(7533):73-78.
17. Larsson CA, Gullberg B, Merlo J, Rastam L, Lindblad U. Female advantage in AMI mortality is reversed in patients with type 2 diabetes in the Skaraborg Project. Diabetes Care. 2005;28(9):2246-2248.
18. Avogaro A, Giorda C, Maggini M, et al. Incidence of coronary heart disease in type 2 diabetic men and women: impact of microvascular complications, treatment, and geographic location. Diabetes Care. 2007;30(5):1241-1247.
19. Zandbergen AA, Sijbrands EJ, Lamberts SW, Bootsma AH. Normotensive women with type 2 diabetes and microalbuminuria are at high risk for macrovascular disease. Diabetes Care. 2006;29(8):1851-1855.
20. Mulnier HE, Seaman HE, Raleigh VS, et al. Risk of stroke in people with type 2 diabetes in the UK: a study using the General Practice Research Database. Diabetologia. 2006;49(12):2859-2865.
21. Tuomilehto J, Rastenyte D, Jousilahti P, Sarti C, Vartiainen E. Diabetes mellitus as a risk factor for death from stroke. Prospective study of the middle-aged Finnish population. Stroke. 1996;27(2):210-215.
22. Hanai K, Babazono T, Yoshida N, et al. Gender differences in the association between HDL cholesterol and the progression of diabetic kidney disease in type 2 diabetic patients. Nephrol Dial Transplant. 2012;27(3):1070-1075.
23. Tuerk PW, Mueller M, Egede LE. Estimating physician effects on glycemic control in the treatment of diabetes: methods, effects sizes, and implications for treatment policy. Diabetes Care. 2008;31(5):869-873.
24. Rubin RR, Peyrot M, Siminerio LM. Health care and patient-reported outcomes: results of the cross-national Diabetes Attitudes, Wishes and Needs (DAWN) study. Diabetes Care. 2006;29(6):1249-1255.
25. McCollum M, Hansen LB, Ghushchyan V, Sullivan PW. Inconsistent health perceptions for US women and men with diabetes. J Womens Health (Larchmt). 2007;16(10):1421-1428.
26. Gucciardi E, Wang SC, DeMelo M, Amaral L, Stewart DE. Characteristics of men and women with diabetes: observations during patients’ initial visit to a diabetes education centre. Can Fam Physician. 2008;54(2):219-227.
27. Chiu CJ, Wray LA. Physical disability trajectories in older Americans with and without diabetes: the role of age, gender, race or ethnicity, and education. Gerontologist. 2011;51(1):51-63.
28. Nielsen AB, de Fine Olivarius N, Gannik D, Hindsberger C, Hollnagel H. Structured personal diabetes care in primary health care affects only women’s HbA1c. Diabetes Care. 2006;29(5):963-969.
29. Shalev V, Chodick G, Heymann AD, Kokia E. Gender differences in healthcare utilization and medical indicators among patients with diabetes. Public Health. 2005;119(1):45-49.
30. Kacerovsky-Bielesz G, Lienhardt S, Hagenhofer M, et al. Sex-related psychological effects on metabolic control in type 2 diabetes mellitus. Diabetologia. 2009;52(5):781-788.
31. Brown SA, Harrist RB, Villagomez ET, Segura M, Barton SA, Hanis CL. Gender and treatment differences in knowledge, health beliefs, and metabolic control in Mexican Americans with type 2 diabetes. Diabetes Educ. 2000;26(3):425-438.
32. Liburd LC, Namageyo-Funa A, Jack L, Jr. Understanding “masculinity” and the challenges of managing type-2 diabetes among African-American men. J Natl Med Assoc. 2007;99(5):550-552, 554–558.
Managing the Multiple Symptoms of Benign Prostatic Hyperplasia — CME
Managing Type 2 Diabetes in Men
Meeting New Challenges with Antiplatelet Therapy in Primary Care
Dr. Aguilar has disclosed that he has ongoing relationships with the following companies: Amylin Pharmaceuticals; Eli Lilly; Janssen Pharmaceuticals, Inc; Novo Nordisk, Inc; and Takeda Pharmaceuticals USA, Inc.
SUPPORT
This program is sponsored by the PCEC and is supported by funding from Novo Nordisk, Inc.
The prevalence of type 2 diabetes mellitus (T2DM) is similar in men and women (11.8% vs 10.8%, respectively), however there are gender differences that should be considered when developing a treatment plan (eg, cardiovascular risk, psychosocial factors, coping strategies, and the perception of benefit from self-care) when managing those diagnosed with this disease and those at risk for developing it.1 This article describes these differences in the context of two patients—one at risk for T2DM being seen by his health care provider for a routine physical examination, and one who has been treated for several years for T2DM and is being seen for a follow-up office visit. For each patient, the implications for treatment are discussed.
Men at Risk for Type 2 Diabetes Mellitus
JW is a 48-year-old white male being seen for a routine physical examination; he last saw a physician 6 years ago, also for a routine physical. He has no complaints and is taking no medications. Having divorced 7 years ago, he lives alone in an apartment and eats many of his meals at fast food restaurants. JW drinks 2 to 3 beers a night several times a week and more when he socializes with his friends 2 to 3 evenings per week. He smokes socially. His father has a 12-year history of T2DM. His mother has a 4-year history of essential hypertension and a 9-year history of chronic obstructive pulmonary disease.
Physical examination shows that JW is 5’11” tall, weighs 207 pounds (body mass index (BMI), 29 kg/m2), and has a 41” waist circumference; his blood pressure (BP) is 138/86 mm Hg and respiratory rate is 17 breaths/min. The remainder of his physical examination, including eye and neurologic exams, is normal. Laboratory results, including a screening glycated homoglobin (A1C), are pending.
Key Risk Factors for Type 2 Diabetes Mellitus in Men
This case is not an uncommon presentation of a middle-aged male who has several risk factors for diabetes (see Case Study 1 continued ). JW also has key risk factors for T2DM in men. The Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) Augsburg surveys identified 128 men and 85 women with T2DM.2 Increasing age and BMI, positive parental history of T2DM, and a low high-density lipoprotein cholesterol (HDL-C) level were independent risk factors predicting the development of T2DM in both men and women. However, several other factors posed a higher risk in men relative to women, including systolic BP (hazard ratio [HR], 1.16 per 10-mm Hg increase), regular smoking (HR, 1.75), and alcohol intake ≥ 40 g/d (HR, 1.95). (Note: 1 fluid ounce 80 proof alcohol ≈ 11 g ethanol; 12 fluid ounces beer [~5% alcohol] ≈ 14 g ethanol). After adjusting for these factors, a separate analysis (4424 men, 4380 women) showed that men who lived alone were more likely to develop T2DM than either men or women who did not live alone (HR, 1.69 in men vs 0.85 in women; P = .006).3 While the number of people with T2DM in MONICA was small, the results suggest that measuring BP, particularly systolic BP, and taking a smoking and alcohol history may be especially important in men.
With respect to alcohol intake, epidemiologic and randomized clinical trials have generally demonstrated an inverse relationship between moderate alcohol consumption (20 to 30 g/d) and the long-term risk of T2DM.2,4-7 Differences among studies in how patients were grouped preclude determination of the daily alcohol consumption that confers the greatest risk benefit, although one recent study conducted over 4 years indicates that the greatest benefit in diabetes risk reduction may occur when men who previously consumed 8
Other nutrition and lifestyle patterns also seem to be particularly beneficial in reducing the risk of T2DM in men. Survey data involving 22,921 Japanese men and 29,759 Japanese women followed over 5 years showed that fish and seafood intake was significantly associated with a decreased risk of T2DM in men but not in women.9 The odds ratio of developing T2DM for the highest quartile versus the lowest quartile of fish and seafood intake was 0.73 (P = .04 for trend). Additional analysis did not identify any significant association with the fat content of fish.
Results of the Health Professionals Follow-up Study provide evidence of benefit in lowering the risk of T2DM in men who consume high amounts of low-fat dairy products, whole grains, and magnesium ( TABLE 1 ). With respect to dairy food consumption, after 12 years of follow-up involving 1243 incident cases of T2DM, the relative risk (RR) of developing T2DM in men in the top quintile of dairy intake was 0.77 compared with those in the lowest quintile (P = .003 for trend).10 Men in the highest quintile consumed 4.1 servings of dairy food per day compared with 0.5 servings per day in the lowest quintile. Each serving-per-day increase in total dairy intake was associated with a 9% lower risk for T2DM, with a lower risk seen with consumption of low-fat vs high-fat dairy food. With respect to whole-grain intake, the RR of developing T2DM was 0.58 in men in the upper vs lower quintiles (3.2 vs 0.4 servings/d), although the effect was attenuated with BMI (P = .0006 for trend).11 Similar observations were made with respect to magnesium consumption; a RR of 0.76 for T2DM was observed in men with a median magnesium consumption of 457 mg/d compared with those who consumed 270 mg/d.12
TABLE 1
Suggestions for Men Who Are at Risk of or Have Been Diagnosed with Type 2 Diabetes Mellitus (T2DM)*
For men who are at risk:
|
For men who have been diagnosed:
|
| BP, blood pressure; HDL-C, high-density lipoprotein cholesterol. *These suggestions are in addition to developing and fostering a collaborative, patient-centered approach. |
JW has the following risk factors for T2DM:
- Overweight with central adiposity
- Physical inactivity
- First-degree relative with T2DM
- Possible cardiovascular disease (CVD; hypertension, smoking)
- High daily alcohol intake (10 to 20 g alcohol/beer x 2-3 beers/d = 20 to 60 g alcohol/d)
- Poor nutrition
- Lives alone
Plan:
- Discuss above risk factors with JW
- Repeat BP measurement at next visit; implement treatment if BP >140/90 mm Hg (130/80 mm Hg if T2DM is diagnosed)
- Consider evaluation for alcohol/substance abuse
- Evaluate for smoking cessation program
- Nutrition referral for lifestyle and dietary management intervention
Working with men to avoid the development of T2DM is an important objective for family physicians. It is essential to identify men who are at increased risk, including those with prediabetes, provide education about the disease and its risk factors, and implement appropriate risk reduction strategies. Risk reduction strategies should focus on modifiable factors, such as body weight, physical activity, BP, blood lipids, blood glucose, and smoking. With JW, his motivation to “get back into shape” will help move the conversation toward achievable goals that can be set and modified over time. Other strategies that may be helpful in reducing the risk of developing T2DM in men include a moderate daily alcohol intake and a diet high in fish and seafood, low-fat dairy products, whole grains, and magnesium ( TABLE 1 ).
Once diagnosed with T2DM, there are risk management strategies that can be particularly helpful in men. These include strategies that target cardiovascular health, as well as those that consider the psychosocial and coping behaviors of men.
Risk of Complications in Men With Type 2 Diabetes Mellitus
Physical examination: BP, 126/78 mm Hg; body weight, 183 pounds (a 13 to 17 pound increase since the knee injury); waist circumference, 38” (BMI, 28 kg/m2); grade 1 retinopathy bilaterally; neurologic exam normal.
Laboratory: A1C, 7.8%; lipids normal except triglyceride level, 219 mg/dL; creatinine clearance (calculated), 69 mL/min; urine, 45 mg albumin/g creatinine.
MR’s self-measured fasting plasma glucose (FPG) has ranged from 121 to 143 mg/dL over the past month; isolated postprandial glucose (PPG) measurements show 194 to 258 mg/dL.
MR works as a vocational teacher at the local high school, and he teaches driver education after school. Review of his pharmacy records suggests his adherence over the past year has been: metformin (88%), hydrochlorothiazide (72%), and lisinopril (72%).
Assessment:
- A1C level of 7.8% indicates an estimated average glucose (eAG) of 177 mg/dL13
- –Mildly elevated FPG and PPG
- –Evidence of microvascular disease (retinopathy, nephropathy)
- –Creatinine clearance 69 mL/min and microalbuminuria indicate stage 2 chronic kidney disease14
In addition to referring MR for physical rehabilitation of his knee, you discuss with MR the need and options for intensifying his diabetes therapy.
Does the fact that MR is male affect your management plan?
In people diagnosed with T2DM, there are differences between men and women with respect to risk for cardiovascular and other comorbid diseases, as well as in their psychosocial well-being and coping strategies.
Risk for Cardiovascular Disease in Type 2 Diabetes Mellitus
A systematic literature review shows that men with T2DM generally fare better than women with T2DM regarding their risk for CVD. Men with T2DM have a 2- to 3-fold increase in the risk of developing coronary heart disease (CHD) compared with men without T2DM, whereas women with T2DM have a 4- to 6-fold increase in risk compared with women without T2DM.15 Compared with women with T2DM, men with T2DM also have a better prognosis after myocardial infarction (MI) and a lower risk of death overall from CVD. Possible reasons for these differences include a lower risk of hypertension, a less severe form of dyslipidemia, and a lower prevalence of obesity in men with T2DM compared with women with T2DM.15 These same reasons for observed differences between men and women were seen in a meta-analysis of 29 studies, where the RR of fatal MI in men with T2DM compared with women with T2DM was 0.68.16 Similar findings were seen in the Skaraborg Project, which involved 1116 Swedish patients with hypertension and/or T2DM.17 Compared with a healthy population, the age-adjusted HR for fatal MI was 1.9 for men with T2DM and 5.0 for women with T2DM over 8.1 years of follow-up (RR, 0.38 for men vs women). Analysis of the data indicated that these results were not explained by the more favorable survival rate in women without T2DM than in men without T2DM.17
Somewhat different results have been reported by the Italian Diabetes and Informatics Study Group in a slightly different T2DM population. This investigation involved men and women with T2DM (N = 11,644) who could have microvascular but not macrovascular disease.18 After 4 years of follow-up, the age-adjusted incident rates for first CHD event (composite of acute MI, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty) were 28.8 per 1000 person-years in men and 23.3 per 1000 person-years in women. Incident rates (per 1000 person-years) of acute MI (10.3 vs 4.7), major CHD events (13.1 vs 5.8), and fatal CHD (2.6 vs 0.6) were all significantly more frequent in men than in women, respectively. Multivariate analysis showed that hypertension and A1C were additional risk factors for CHD in men; for each 20% increment above the A1C upper limit of normal, there was a 14% risk increase for CHD. The presence of microvascular complications increased risk by 20% in men and 35% in women. In this analysis, glycemic control and hypertension were found to be the predominant risk factors in men, while high triglyceride levels, low HDL-C levels, and microangiopathy were predominant in women.
Additional multivariate analyses provide greater insight into specific factors that affect the risk of CVD and outcomes in men with T2DM. One investigation compared men and women with T2DM who were normotensive without evidence of CVD but with microalbuminuria. After 4.7 years of follow-up, men were found to be at lower risk (RR, 0.12) for a composite of death, acute MI, unstable angina, coronary interventions, heart failure, cerebral ischemic stroke or transient ischemic attack, and peripheral artery disease.19 Other investigators have reported a lower risk of stroke, including fatal stroke, in men with T2DM compared with women with T2DM.20,21 For example, analysis of the General Practice Research Database identified 22,178 men and 19,621 women with T2DM between the ages of 35 and 89 years.20 The stroke rate per 1000 person-years across all ages was 10.82 (95% confidence interval (CI), 10.17-11.51) in men and 13.16 (95% CI, 12.40-13.97) in women. In men, the rate per 1000 person-years rose from 1.81 in the 35 to 44 year age group to 28.35 in men 85 years of age or older. Although the rate of stroke per 1000 person-years was lower in women than men in the 35 to 44 year age group (1.53 vs 1.81), the rate in women exceeded that of men in the 85 years of age or older group (32.20 vs 28.35).
Other Chronic Complications
Kidney disease is affected by blood lipids, specifically HDL-C, in men with T2DM. An investigation in men and women with T2DM with normoalbuminuria or microalbuminuria at baseline showed that a low HDL-C level was an independent predictor of progression to a more advanced stage of albuminuria over 4.3 years of follow-up (HR, 0.391 for men with normal HDL-C compared with men with low HDL-C). In women, no lipid parameters were associated with progression of albuminuria.22
While these investigations do not provide a clear picture of the differences regarding cardiovascular risk between men and women with T2DM, they suggest that men with T2DM have a lower risk of nonfatal and fatal CVD and stroke than do women with T2DM. However, the lower risk seen in men may be affected by the cardiovascular endpoints measured and the presence of microvascular disease. Possible independent risk factors for CVD in men with T2DM include hypertension, poor glycemic control, and low HDL-C.
Risk factors that place MR at greater risk for CVD compared with a woman with T2DM and therefore serve as key treatment targets include:
- Hypertension—although controlled (126/78 mm Hg) with hydrochlorothiazide and lisinopril
- Poor glycemic control—A1C, 7.8% (eAG, 177mg/dL)
- –Increase physical activity—refer for knee rehabilitation
- –Intensify glucose-lowering therapy by adding an additional glucose-lowering agent (eg, dipeptidyl peptidase-4 inhibitor, glucagon-like peptide-1 receptor agonist, thiazolidinedione, α-glucosidase inhibitor, sulfonylurea, glinide, or basal insulin)
- Microalbuminuria (45 mg urinary albumin/g creatinine)—encourage better adherence to lisinopril; monitor renal function
- Hypertriglyceridemia—initiate omega-3 fatty acid or extended-release niacin
Psychosocial Well-Being, Benefit of Self-Care, and Coping Strategies
Type 2 diabetes mellitus is a chronic disease with glycemic control largely determined by patient self-management, and the attitudes and beliefs of patients with T2DM are important factors to consider from diagnosis onward.23 There are important differences between men and women with T2DM regarding attitudes and beliefs. Published investigations provide some, although not entirely consistent, insight into these psychosocial differences between men and women with T2DM. These differences are summarized in TABLE 2 .24-32 Taking these differences into account when planning treatment and when communicating with and educating the patient is essential for improved patient self-management.
TABLE 2
Psychosocial and Coping Characteristics of Men with Type 2 Diabetes Mellitus (T2DM)24-32
Compared with women with T2DM, generally, men with T2DM:
|
Key interventions for MR:
- Maintain a dialogue and enhance collaboration with MR
- Establish shared goals that are customized to incorporate MR’s personal goals
- Problem solve with MR to identify ways he can better integrate the diabetes self-care objectives of dietary changes and blood glucose self-monitoring into his daily life
- Emphasize that enhanced or greater disease control can be achieved by good self-management, including better adherence to the management plan
- Remind MR that T2DM is a progressive disease that requires intermittent medication adjustments to keep pace with its progression
- Build upon the belief that T2DM can be controlled by reminding MR that the disease was well controlled before his knee injury
- –Focus on the importance of rehabilitating his knee
- –Develop a rehabilitation plan
- Provide informational support regarding options for intensifying diabetes therapy (eg, dipeptidyl peptidase-4 inhibitor, thiazolidinedione, glucagon-like peptide-1 receptor agonist, sulfonylurea, or insulin)
- –Discuss MR’s needs and concerns, as well as barriers for each treatment option, particularly hypoglycemia and weight gain
- –Provide instruction or educational materials regarding injection devices
- –Involve the healthcare team, as appropriate
- Keep the treatment regimen as simple as possible; consider pill combinations where appropriate
Summary
The growing epidemic of T2DM requires intervention to assist patients who have been diagnosed to better manage the disease, to reduce the risk of developing the disease in those who have not yet been diagnosed, and to manage the associated complications. In addition to individualizing interventions based on a patient’s needs, concerns, and capabilities, taking gender into account is necessary. In otherwise healthy people, several independent factors appear to pose a higher risk of T2DM in men relative to women, including systolic hypertension, regular smoking, and alcohol intake ≥ 40 g/d. At the same time, men achieve greater risk reduction from moderate daily alcohol intake and a diet high in fish and seafood, low-fat dairy products, whole grains, and magnesium.
Once diagnosed with T2DM, men generally fare better than women regarding the risk for CVD; they also have a better prognosis after MI and a lower risk of death overall from CVD. Possible independent risk factors for CVD in men with T2DM that are especially important may include hypertension, poor glycemic control, and low HDL-C levels. Psychosocial complications, such as depression, are less likely in men with T2DM. However, men expend less effort coping, are less likely to utilize healthcare services, and are less informed about treatment options. Although men have a lower expectation of the benefit of self-management, they find support from family and friends more helpful than do women, but they are fearful of losing control of their disease.
Taking these gender differences into account should prove helpful as family care physicians work with men to reduce their risk of developing T2DM and in helping men diagnosed with T2DM to better self-manage their disease.
Managing the Multiple Symptoms of Benign Prostatic Hyperplasia — CME
Managing Type 2 Diabetes in Men
Meeting New Challenges with Antiplatelet Therapy in Primary Care
Dr. Aguilar has disclosed that he has ongoing relationships with the following companies: Amylin Pharmaceuticals; Eli Lilly; Janssen Pharmaceuticals, Inc; Novo Nordisk, Inc; and Takeda Pharmaceuticals USA, Inc.
SUPPORT
This program is sponsored by the PCEC and is supported by funding from Novo Nordisk, Inc.
The prevalence of type 2 diabetes mellitus (T2DM) is similar in men and women (11.8% vs 10.8%, respectively), however there are gender differences that should be considered when developing a treatment plan (eg, cardiovascular risk, psychosocial factors, coping strategies, and the perception of benefit from self-care) when managing those diagnosed with this disease and those at risk for developing it.1 This article describes these differences in the context of two patients—one at risk for T2DM being seen by his health care provider for a routine physical examination, and one who has been treated for several years for T2DM and is being seen for a follow-up office visit. For each patient, the implications for treatment are discussed.
Men at Risk for Type 2 Diabetes Mellitus
JW is a 48-year-old white male being seen for a routine physical examination; he last saw a physician 6 years ago, also for a routine physical. He has no complaints and is taking no medications. Having divorced 7 years ago, he lives alone in an apartment and eats many of his meals at fast food restaurants. JW drinks 2 to 3 beers a night several times a week and more when he socializes with his friends 2 to 3 evenings per week. He smokes socially. His father has a 12-year history of T2DM. His mother has a 4-year history of essential hypertension and a 9-year history of chronic obstructive pulmonary disease.
Physical examination shows that JW is 5’11” tall, weighs 207 pounds (body mass index (BMI), 29 kg/m2), and has a 41” waist circumference; his blood pressure (BP) is 138/86 mm Hg and respiratory rate is 17 breaths/min. The remainder of his physical examination, including eye and neurologic exams, is normal. Laboratory results, including a screening glycated homoglobin (A1C), are pending.
Key Risk Factors for Type 2 Diabetes Mellitus in Men
This case is not an uncommon presentation of a middle-aged male who has several risk factors for diabetes (see Case Study 1 continued ). JW also has key risk factors for T2DM in men. The Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) Augsburg surveys identified 128 men and 85 women with T2DM.2 Increasing age and BMI, positive parental history of T2DM, and a low high-density lipoprotein cholesterol (HDL-C) level were independent risk factors predicting the development of T2DM in both men and women. However, several other factors posed a higher risk in men relative to women, including systolic BP (hazard ratio [HR], 1.16 per 10-mm Hg increase), regular smoking (HR, 1.75), and alcohol intake ≥ 40 g/d (HR, 1.95). (Note: 1 fluid ounce 80 proof alcohol ≈ 11 g ethanol; 12 fluid ounces beer [~5% alcohol] ≈ 14 g ethanol). After adjusting for these factors, a separate analysis (4424 men, 4380 women) showed that men who lived alone were more likely to develop T2DM than either men or women who did not live alone (HR, 1.69 in men vs 0.85 in women; P = .006).3 While the number of people with T2DM in MONICA was small, the results suggest that measuring BP, particularly systolic BP, and taking a smoking and alcohol history may be especially important in men.
With respect to alcohol intake, epidemiologic and randomized clinical trials have generally demonstrated an inverse relationship between moderate alcohol consumption (20 to 30 g/d) and the long-term risk of T2DM.2,4-7 Differences among studies in how patients were grouped preclude determination of the daily alcohol consumption that confers the greatest risk benefit, although one recent study conducted over 4 years indicates that the greatest benefit in diabetes risk reduction may occur when men who previously consumed 8
Other nutrition and lifestyle patterns also seem to be particularly beneficial in reducing the risk of T2DM in men. Survey data involving 22,921 Japanese men and 29,759 Japanese women followed over 5 years showed that fish and seafood intake was significantly associated with a decreased risk of T2DM in men but not in women.9 The odds ratio of developing T2DM for the highest quartile versus the lowest quartile of fish and seafood intake was 0.73 (P = .04 for trend). Additional analysis did not identify any significant association with the fat content of fish.
Results of the Health Professionals Follow-up Study provide evidence of benefit in lowering the risk of T2DM in men who consume high amounts of low-fat dairy products, whole grains, and magnesium ( TABLE 1 ). With respect to dairy food consumption, after 12 years of follow-up involving 1243 incident cases of T2DM, the relative risk (RR) of developing T2DM in men in the top quintile of dairy intake was 0.77 compared with those in the lowest quintile (P = .003 for trend).10 Men in the highest quintile consumed 4.1 servings of dairy food per day compared with 0.5 servings per day in the lowest quintile. Each serving-per-day increase in total dairy intake was associated with a 9% lower risk for T2DM, with a lower risk seen with consumption of low-fat vs high-fat dairy food. With respect to whole-grain intake, the RR of developing T2DM was 0.58 in men in the upper vs lower quintiles (3.2 vs 0.4 servings/d), although the effect was attenuated with BMI (P = .0006 for trend).11 Similar observations were made with respect to magnesium consumption; a RR of 0.76 for T2DM was observed in men with a median magnesium consumption of 457 mg/d compared with those who consumed 270 mg/d.12
TABLE 1
Suggestions for Men Who Are at Risk of or Have Been Diagnosed with Type 2 Diabetes Mellitus (T2DM)*
For men who are at risk:
|
For men who have been diagnosed:
|
| BP, blood pressure; HDL-C, high-density lipoprotein cholesterol. *These suggestions are in addition to developing and fostering a collaborative, patient-centered approach. |
JW has the following risk factors for T2DM:
- Overweight with central adiposity
- Physical inactivity
- First-degree relative with T2DM
- Possible cardiovascular disease (CVD; hypertension, smoking)
- High daily alcohol intake (10 to 20 g alcohol/beer x 2-3 beers/d = 20 to 60 g alcohol/d)
- Poor nutrition
- Lives alone
Plan:
- Discuss above risk factors with JW
- Repeat BP measurement at next visit; implement treatment if BP >140/90 mm Hg (130/80 mm Hg if T2DM is diagnosed)
- Consider evaluation for alcohol/substance abuse
- Evaluate for smoking cessation program
- Nutrition referral for lifestyle and dietary management intervention
Working with men to avoid the development of T2DM is an important objective for family physicians. It is essential to identify men who are at increased risk, including those with prediabetes, provide education about the disease and its risk factors, and implement appropriate risk reduction strategies. Risk reduction strategies should focus on modifiable factors, such as body weight, physical activity, BP, blood lipids, blood glucose, and smoking. With JW, his motivation to “get back into shape” will help move the conversation toward achievable goals that can be set and modified over time. Other strategies that may be helpful in reducing the risk of developing T2DM in men include a moderate daily alcohol intake and a diet high in fish and seafood, low-fat dairy products, whole grains, and magnesium ( TABLE 1 ).
Once diagnosed with T2DM, there are risk management strategies that can be particularly helpful in men. These include strategies that target cardiovascular health, as well as those that consider the psychosocial and coping behaviors of men.
Risk of Complications in Men With Type 2 Diabetes Mellitus
Physical examination: BP, 126/78 mm Hg; body weight, 183 pounds (a 13 to 17 pound increase since the knee injury); waist circumference, 38” (BMI, 28 kg/m2); grade 1 retinopathy bilaterally; neurologic exam normal.
Laboratory: A1C, 7.8%; lipids normal except triglyceride level, 219 mg/dL; creatinine clearance (calculated), 69 mL/min; urine, 45 mg albumin/g creatinine.
MR’s self-measured fasting plasma glucose (FPG) has ranged from 121 to 143 mg/dL over the past month; isolated postprandial glucose (PPG) measurements show 194 to 258 mg/dL.
MR works as a vocational teacher at the local high school, and he teaches driver education after school. Review of his pharmacy records suggests his adherence over the past year has been: metformin (88%), hydrochlorothiazide (72%), and lisinopril (72%).
Assessment:
- A1C level of 7.8% indicates an estimated average glucose (eAG) of 177 mg/dL13
- –Mildly elevated FPG and PPG
- –Evidence of microvascular disease (retinopathy, nephropathy)
- –Creatinine clearance 69 mL/min and microalbuminuria indicate stage 2 chronic kidney disease14
In addition to referring MR for physical rehabilitation of his knee, you discuss with MR the need and options for intensifying his diabetes therapy.
Does the fact that MR is male affect your management plan?
In people diagnosed with T2DM, there are differences between men and women with respect to risk for cardiovascular and other comorbid diseases, as well as in their psychosocial well-being and coping strategies.
Risk for Cardiovascular Disease in Type 2 Diabetes Mellitus
A systematic literature review shows that men with T2DM generally fare better than women with T2DM regarding their risk for CVD. Men with T2DM have a 2- to 3-fold increase in the risk of developing coronary heart disease (CHD) compared with men without T2DM, whereas women with T2DM have a 4- to 6-fold increase in risk compared with women without T2DM.15 Compared with women with T2DM, men with T2DM also have a better prognosis after myocardial infarction (MI) and a lower risk of death overall from CVD. Possible reasons for these differences include a lower risk of hypertension, a less severe form of dyslipidemia, and a lower prevalence of obesity in men with T2DM compared with women with T2DM.15 These same reasons for observed differences between men and women were seen in a meta-analysis of 29 studies, where the RR of fatal MI in men with T2DM compared with women with T2DM was 0.68.16 Similar findings were seen in the Skaraborg Project, which involved 1116 Swedish patients with hypertension and/or T2DM.17 Compared with a healthy population, the age-adjusted HR for fatal MI was 1.9 for men with T2DM and 5.0 for women with T2DM over 8.1 years of follow-up (RR, 0.38 for men vs women). Analysis of the data indicated that these results were not explained by the more favorable survival rate in women without T2DM than in men without T2DM.17
Somewhat different results have been reported by the Italian Diabetes and Informatics Study Group in a slightly different T2DM population. This investigation involved men and women with T2DM (N = 11,644) who could have microvascular but not macrovascular disease.18 After 4 years of follow-up, the age-adjusted incident rates for first CHD event (composite of acute MI, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty) were 28.8 per 1000 person-years in men and 23.3 per 1000 person-years in women. Incident rates (per 1000 person-years) of acute MI (10.3 vs 4.7), major CHD events (13.1 vs 5.8), and fatal CHD (2.6 vs 0.6) were all significantly more frequent in men than in women, respectively. Multivariate analysis showed that hypertension and A1C were additional risk factors for CHD in men; for each 20% increment above the A1C upper limit of normal, there was a 14% risk increase for CHD. The presence of microvascular complications increased risk by 20% in men and 35% in women. In this analysis, glycemic control and hypertension were found to be the predominant risk factors in men, while high triglyceride levels, low HDL-C levels, and microangiopathy were predominant in women.
Additional multivariate analyses provide greater insight into specific factors that affect the risk of CVD and outcomes in men with T2DM. One investigation compared men and women with T2DM who were normotensive without evidence of CVD but with microalbuminuria. After 4.7 years of follow-up, men were found to be at lower risk (RR, 0.12) for a composite of death, acute MI, unstable angina, coronary interventions, heart failure, cerebral ischemic stroke or transient ischemic attack, and peripheral artery disease.19 Other investigators have reported a lower risk of stroke, including fatal stroke, in men with T2DM compared with women with T2DM.20,21 For example, analysis of the General Practice Research Database identified 22,178 men and 19,621 women with T2DM between the ages of 35 and 89 years.20 The stroke rate per 1000 person-years across all ages was 10.82 (95% confidence interval (CI), 10.17-11.51) in men and 13.16 (95% CI, 12.40-13.97) in women. In men, the rate per 1000 person-years rose from 1.81 in the 35 to 44 year age group to 28.35 in men 85 years of age or older. Although the rate of stroke per 1000 person-years was lower in women than men in the 35 to 44 year age group (1.53 vs 1.81), the rate in women exceeded that of men in the 85 years of age or older group (32.20 vs 28.35).
Other Chronic Complications
Kidney disease is affected by blood lipids, specifically HDL-C, in men with T2DM. An investigation in men and women with T2DM with normoalbuminuria or microalbuminuria at baseline showed that a low HDL-C level was an independent predictor of progression to a more advanced stage of albuminuria over 4.3 years of follow-up (HR, 0.391 for men with normal HDL-C compared with men with low HDL-C). In women, no lipid parameters were associated with progression of albuminuria.22
While these investigations do not provide a clear picture of the differences regarding cardiovascular risk between men and women with T2DM, they suggest that men with T2DM have a lower risk of nonfatal and fatal CVD and stroke than do women with T2DM. However, the lower risk seen in men may be affected by the cardiovascular endpoints measured and the presence of microvascular disease. Possible independent risk factors for CVD in men with T2DM include hypertension, poor glycemic control, and low HDL-C.
Risk factors that place MR at greater risk for CVD compared with a woman with T2DM and therefore serve as key treatment targets include:
- Hypertension—although controlled (126/78 mm Hg) with hydrochlorothiazide and lisinopril
- Poor glycemic control—A1C, 7.8% (eAG, 177mg/dL)
- –Increase physical activity—refer for knee rehabilitation
- –Intensify glucose-lowering therapy by adding an additional glucose-lowering agent (eg, dipeptidyl peptidase-4 inhibitor, glucagon-like peptide-1 receptor agonist, thiazolidinedione, α-glucosidase inhibitor, sulfonylurea, glinide, or basal insulin)
- Microalbuminuria (45 mg urinary albumin/g creatinine)—encourage better adherence to lisinopril; monitor renal function
- Hypertriglyceridemia—initiate omega-3 fatty acid or extended-release niacin
Psychosocial Well-Being, Benefit of Self-Care, and Coping Strategies
Type 2 diabetes mellitus is a chronic disease with glycemic control largely determined by patient self-management, and the attitudes and beliefs of patients with T2DM are important factors to consider from diagnosis onward.23 There are important differences between men and women with T2DM regarding attitudes and beliefs. Published investigations provide some, although not entirely consistent, insight into these psychosocial differences between men and women with T2DM. These differences are summarized in TABLE 2 .24-32 Taking these differences into account when planning treatment and when communicating with and educating the patient is essential for improved patient self-management.
TABLE 2
Psychosocial and Coping Characteristics of Men with Type 2 Diabetes Mellitus (T2DM)24-32
Compared with women with T2DM, generally, men with T2DM:
|
Key interventions for MR:
- Maintain a dialogue and enhance collaboration with MR
- Establish shared goals that are customized to incorporate MR’s personal goals
- Problem solve with MR to identify ways he can better integrate the diabetes self-care objectives of dietary changes and blood glucose self-monitoring into his daily life
- Emphasize that enhanced or greater disease control can be achieved by good self-management, including better adherence to the management plan
- Remind MR that T2DM is a progressive disease that requires intermittent medication adjustments to keep pace with its progression
- Build upon the belief that T2DM can be controlled by reminding MR that the disease was well controlled before his knee injury
- –Focus on the importance of rehabilitating his knee
- –Develop a rehabilitation plan
- Provide informational support regarding options for intensifying diabetes therapy (eg, dipeptidyl peptidase-4 inhibitor, thiazolidinedione, glucagon-like peptide-1 receptor agonist, sulfonylurea, or insulin)
- –Discuss MR’s needs and concerns, as well as barriers for each treatment option, particularly hypoglycemia and weight gain
- –Provide instruction or educational materials regarding injection devices
- –Involve the healthcare team, as appropriate
- Keep the treatment regimen as simple as possible; consider pill combinations where appropriate
Summary
The growing epidemic of T2DM requires intervention to assist patients who have been diagnosed to better manage the disease, to reduce the risk of developing the disease in those who have not yet been diagnosed, and to manage the associated complications. In addition to individualizing interventions based on a patient’s needs, concerns, and capabilities, taking gender into account is necessary. In otherwise healthy people, several independent factors appear to pose a higher risk of T2DM in men relative to women, including systolic hypertension, regular smoking, and alcohol intake ≥ 40 g/d. At the same time, men achieve greater risk reduction from moderate daily alcohol intake and a diet high in fish and seafood, low-fat dairy products, whole grains, and magnesium.
Once diagnosed with T2DM, men generally fare better than women regarding the risk for CVD; they also have a better prognosis after MI and a lower risk of death overall from CVD. Possible independent risk factors for CVD in men with T2DM that are especially important may include hypertension, poor glycemic control, and low HDL-C levels. Psychosocial complications, such as depression, are less likely in men with T2DM. However, men expend less effort coping, are less likely to utilize healthcare services, and are less informed about treatment options. Although men have a lower expectation of the benefit of self-management, they find support from family and friends more helpful than do women, but they are fearful of losing control of their disease.
Taking these gender differences into account should prove helpful as family care physicians work with men to reduce their risk of developing T2DM and in helping men diagnosed with T2DM to better self-manage their disease.
1. Centers for Disease Control and Prevention. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Published 2011. Accessed May 2, 2011.
2. Meisinger C, Thorand B, Schneider A, Stieber J, Doring A, Lowel H. Sex differences in risk factors for incident type 2 diabetes mellitus: the MONICA Augsburg cohort study. Arch Intern Med. 2002;162(1):82-89.
3. Meisinger C, Kandler U, Ladwig KH. Living alone is associated with an increased risk of type 2 diabetes mellitus in men but not women from the general population: the MONICA/KORA Augsburg Cohort Study. Psychosom Med. 2009;71(7):784-788.
4. Baliunas DO, Taylor BJ, Irving H, et al. Alcohol as a risk factor for type 2 diabetes: a systematic review and meta-analysis. Diabetes Care. 2009;32(11):2123-2132.
5. Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovick D. Lifestyle risk factors and new-onset diabetes mellitus in older adults: the cardiovascular health study. Arch Intern Med. 2009;169(8):798-807.
6. Joosten MM, Grobbee DE, van der A DL, Verschuren WM, Hendriks HF, Beulens JW. Combined effect of alcohol consumption and lifestyle behaviors on risk of type 2 diabetes. Am J Clin Nutr. 2010;91(6):1777-1783.
7. Gigleux I, Gagnon J, St-Pierre A, et al. Moderate alcohol consumption is more cardioprotective in men with the metabolic syndrome. J Nutr. 2006;136(12):3027-3032.
8. Joosten MM, Chiuve SE, Mukamal KJ, Hu FB, Hendriks HF, Rimm EB. Changes in alcohol consumption and subsequent risk of type 2 diabetes in men. Diabetes. 2011;60(1):74-79.
9. Nanri A, Mizoue T, Noda M, et al. Fish intake and type 2 diabetes in Japanese men and women: the Japan Public Health Center-based Prospective Study. Am J Clin Nutr. 2011;94(3):884-891.
10. Choi HK, Willett WC, Stampfer MJ, Rimm E, Hu FB. Dairy consumption and risk of type 2 diabetes mellitus in men: a prospective study. Arch Intern Med. 2005;165(9):997-1003.
11. Fung TT, Hu FB, Pereira MA, et al. Whole-grain intake and the risk of type 2 diabetes: a prospective study in men. Am J Clin Nutr. 2002;76(3):535-540.
12. Lopez-Ridaura R, Willett WC, Rimm EB, et al. Magnesium intake and risk of type 2 diabetes in men and women. Diabetes Care. 2004;27(1):134-140.
13. Nathan DM, Kuenen J, Borg R, et al. Translating the A1C assay into estimated average glucose values. Diabetes Care. 2008;31(8):1473-1478.
14. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Ann Intern Med. 2003;139(2):137-147.
15. Legato MJ, Gelzer A, Goland R, et al. Gender-specific care of the patient with diabetes: review and recommendations. Gend Med. 2006;3(2):131-158.
16. Huxley R, Barzi F, Woodward M. Excess risk of fatal coronary heart disease associated with diabetes in men and women: meta-analysis of 37 prospective cohort studies. BMJ. 2006;332(7533):73-78.
17. Larsson CA, Gullberg B, Merlo J, Rastam L, Lindblad U. Female advantage in AMI mortality is reversed in patients with type 2 diabetes in the Skaraborg Project. Diabetes Care. 2005;28(9):2246-2248.
18. Avogaro A, Giorda C, Maggini M, et al. Incidence of coronary heart disease in type 2 diabetic men and women: impact of microvascular complications, treatment, and geographic location. Diabetes Care. 2007;30(5):1241-1247.
19. Zandbergen AA, Sijbrands EJ, Lamberts SW, Bootsma AH. Normotensive women with type 2 diabetes and microalbuminuria are at high risk for macrovascular disease. Diabetes Care. 2006;29(8):1851-1855.
20. Mulnier HE, Seaman HE, Raleigh VS, et al. Risk of stroke in people with type 2 diabetes in the UK: a study using the General Practice Research Database. Diabetologia. 2006;49(12):2859-2865.
21. Tuomilehto J, Rastenyte D, Jousilahti P, Sarti C, Vartiainen E. Diabetes mellitus as a risk factor for death from stroke. Prospective study of the middle-aged Finnish population. Stroke. 1996;27(2):210-215.
22. Hanai K, Babazono T, Yoshida N, et al. Gender differences in the association between HDL cholesterol and the progression of diabetic kidney disease in type 2 diabetic patients. Nephrol Dial Transplant. 2012;27(3):1070-1075.
23. Tuerk PW, Mueller M, Egede LE. Estimating physician effects on glycemic control in the treatment of diabetes: methods, effects sizes, and implications for treatment policy. Diabetes Care. 2008;31(5):869-873.
24. Rubin RR, Peyrot M, Siminerio LM. Health care and patient-reported outcomes: results of the cross-national Diabetes Attitudes, Wishes and Needs (DAWN) study. Diabetes Care. 2006;29(6):1249-1255.
25. McCollum M, Hansen LB, Ghushchyan V, Sullivan PW. Inconsistent health perceptions for US women and men with diabetes. J Womens Health (Larchmt). 2007;16(10):1421-1428.
26. Gucciardi E, Wang SC, DeMelo M, Amaral L, Stewart DE. Characteristics of men and women with diabetes: observations during patients’ initial visit to a diabetes education centre. Can Fam Physician. 2008;54(2):219-227.
27. Chiu CJ, Wray LA. Physical disability trajectories in older Americans with and without diabetes: the role of age, gender, race or ethnicity, and education. Gerontologist. 2011;51(1):51-63.
28. Nielsen AB, de Fine Olivarius N, Gannik D, Hindsberger C, Hollnagel H. Structured personal diabetes care in primary health care affects only women’s HbA1c. Diabetes Care. 2006;29(5):963-969.
29. Shalev V, Chodick G, Heymann AD, Kokia E. Gender differences in healthcare utilization and medical indicators among patients with diabetes. Public Health. 2005;119(1):45-49.
30. Kacerovsky-Bielesz G, Lienhardt S, Hagenhofer M, et al. Sex-related psychological effects on metabolic control in type 2 diabetes mellitus. Diabetologia. 2009;52(5):781-788.
31. Brown SA, Harrist RB, Villagomez ET, Segura M, Barton SA, Hanis CL. Gender and treatment differences in knowledge, health beliefs, and metabolic control in Mexican Americans with type 2 diabetes. Diabetes Educ. 2000;26(3):425-438.
32. Liburd LC, Namageyo-Funa A, Jack L, Jr. Understanding “masculinity” and the challenges of managing type-2 diabetes among African-American men. J Natl Med Assoc. 2007;99(5):550-552, 554–558.
1. Centers for Disease Control and Prevention. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Published 2011. Accessed May 2, 2011.
2. Meisinger C, Thorand B, Schneider A, Stieber J, Doring A, Lowel H. Sex differences in risk factors for incident type 2 diabetes mellitus: the MONICA Augsburg cohort study. Arch Intern Med. 2002;162(1):82-89.
3. Meisinger C, Kandler U, Ladwig KH. Living alone is associated with an increased risk of type 2 diabetes mellitus in men but not women from the general population: the MONICA/KORA Augsburg Cohort Study. Psychosom Med. 2009;71(7):784-788.
4. Baliunas DO, Taylor BJ, Irving H, et al. Alcohol as a risk factor for type 2 diabetes: a systematic review and meta-analysis. Diabetes Care. 2009;32(11):2123-2132.
5. Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovick D. Lifestyle risk factors and new-onset diabetes mellitus in older adults: the cardiovascular health study. Arch Intern Med. 2009;169(8):798-807.
6. Joosten MM, Grobbee DE, van der A DL, Verschuren WM, Hendriks HF, Beulens JW. Combined effect of alcohol consumption and lifestyle behaviors on risk of type 2 diabetes. Am J Clin Nutr. 2010;91(6):1777-1783.
7. Gigleux I, Gagnon J, St-Pierre A, et al. Moderate alcohol consumption is more cardioprotective in men with the metabolic syndrome. J Nutr. 2006;136(12):3027-3032.
8. Joosten MM, Chiuve SE, Mukamal KJ, Hu FB, Hendriks HF, Rimm EB. Changes in alcohol consumption and subsequent risk of type 2 diabetes in men. Diabetes. 2011;60(1):74-79.
9. Nanri A, Mizoue T, Noda M, et al. Fish intake and type 2 diabetes in Japanese men and women: the Japan Public Health Center-based Prospective Study. Am J Clin Nutr. 2011;94(3):884-891.
10. Choi HK, Willett WC, Stampfer MJ, Rimm E, Hu FB. Dairy consumption and risk of type 2 diabetes mellitus in men: a prospective study. Arch Intern Med. 2005;165(9):997-1003.
11. Fung TT, Hu FB, Pereira MA, et al. Whole-grain intake and the risk of type 2 diabetes: a prospective study in men. Am J Clin Nutr. 2002;76(3):535-540.
12. Lopez-Ridaura R, Willett WC, Rimm EB, et al. Magnesium intake and risk of type 2 diabetes in men and women. Diabetes Care. 2004;27(1):134-140.
13. Nathan DM, Kuenen J, Borg R, et al. Translating the A1C assay into estimated average glucose values. Diabetes Care. 2008;31(8):1473-1478.
14. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Ann Intern Med. 2003;139(2):137-147.
15. Legato MJ, Gelzer A, Goland R, et al. Gender-specific care of the patient with diabetes: review and recommendations. Gend Med. 2006;3(2):131-158.
16. Huxley R, Barzi F, Woodward M. Excess risk of fatal coronary heart disease associated with diabetes in men and women: meta-analysis of 37 prospective cohort studies. BMJ. 2006;332(7533):73-78.
17. Larsson CA, Gullberg B, Merlo J, Rastam L, Lindblad U. Female advantage in AMI mortality is reversed in patients with type 2 diabetes in the Skaraborg Project. Diabetes Care. 2005;28(9):2246-2248.
18. Avogaro A, Giorda C, Maggini M, et al. Incidence of coronary heart disease in type 2 diabetic men and women: impact of microvascular complications, treatment, and geographic location. Diabetes Care. 2007;30(5):1241-1247.
19. Zandbergen AA, Sijbrands EJ, Lamberts SW, Bootsma AH. Normotensive women with type 2 diabetes and microalbuminuria are at high risk for macrovascular disease. Diabetes Care. 2006;29(8):1851-1855.
20. Mulnier HE, Seaman HE, Raleigh VS, et al. Risk of stroke in people with type 2 diabetes in the UK: a study using the General Practice Research Database. Diabetologia. 2006;49(12):2859-2865.
21. Tuomilehto J, Rastenyte D, Jousilahti P, Sarti C, Vartiainen E. Diabetes mellitus as a risk factor for death from stroke. Prospective study of the middle-aged Finnish population. Stroke. 1996;27(2):210-215.
22. Hanai K, Babazono T, Yoshida N, et al. Gender differences in the association between HDL cholesterol and the progression of diabetic kidney disease in type 2 diabetic patients. Nephrol Dial Transplant. 2012;27(3):1070-1075.
23. Tuerk PW, Mueller M, Egede LE. Estimating physician effects on glycemic control in the treatment of diabetes: methods, effects sizes, and implications for treatment policy. Diabetes Care. 2008;31(5):869-873.
24. Rubin RR, Peyrot M, Siminerio LM. Health care and patient-reported outcomes: results of the cross-national Diabetes Attitudes, Wishes and Needs (DAWN) study. Diabetes Care. 2006;29(6):1249-1255.
25. McCollum M, Hansen LB, Ghushchyan V, Sullivan PW. Inconsistent health perceptions for US women and men with diabetes. J Womens Health (Larchmt). 2007;16(10):1421-1428.
26. Gucciardi E, Wang SC, DeMelo M, Amaral L, Stewart DE. Characteristics of men and women with diabetes: observations during patients’ initial visit to a diabetes education centre. Can Fam Physician. 2008;54(2):219-227.
27. Chiu CJ, Wray LA. Physical disability trajectories in older Americans with and without diabetes: the role of age, gender, race or ethnicity, and education. Gerontologist. 2011;51(1):51-63.
28. Nielsen AB, de Fine Olivarius N, Gannik D, Hindsberger C, Hollnagel H. Structured personal diabetes care in primary health care affects only women’s HbA1c. Diabetes Care. 2006;29(5):963-969.
29. Shalev V, Chodick G, Heymann AD, Kokia E. Gender differences in healthcare utilization and medical indicators among patients with diabetes. Public Health. 2005;119(1):45-49.
30. Kacerovsky-Bielesz G, Lienhardt S, Hagenhofer M, et al. Sex-related psychological effects on metabolic control in type 2 diabetes mellitus. Diabetologia. 2009;52(5):781-788.
31. Brown SA, Harrist RB, Villagomez ET, Segura M, Barton SA, Hanis CL. Gender and treatment differences in knowledge, health beliefs, and metabolic control in Mexican Americans with type 2 diabetes. Diabetes Educ. 2000;26(3):425-438.
32. Liburd LC, Namageyo-Funa A, Jack L, Jr. Understanding “masculinity” and the challenges of managing type-2 diabetes among African-American men. J Natl Med Assoc. 2007;99(5):550-552, 554–558.
Introduction
Managing the Multiple Symptoms of Benign Prostatic Hyperplasia — CME
Managing Type 2 Diabetes in Men
Meeting New Challenges with Antiplatelet Therapy in Primary Care
Dr. Brunton has disclosed that he is on the advisory boards and speakers’ bureaus for Boehringer Ingelheim, Eli Lilly, Kowa, Novo Nordisk, Inc, and Teva Pharmaceuticals, and is on the advisory boards for Abbott and Sunovion.
A decade ago, the World Health Organization suggested that “increasing the effectiveness of adherence interventions may have a far greater impact on the health of the population than any improvement in specific medical treatments.”1 A recent survey found that medication adherence rates over the course of 1 year were 24% for patients with depression, 36% with diabetes, 54% with epilepsy, 32% with dyslipidemia, and 42% with hypertension.2 Poor adherence rates such as these contribute to the low rates of disease control in patients with diabetes, dyslipidemia, hypertension, and other chronic diseases.3,4 Since chronic diseases are largely self-managed, effective patient self-management is critical to good health-related outcomes. To help patients self-manage their diseases, the family physician must work collaboratively with each patient to select, initiate, and modify therapy based upon the patient’s needs, interests, and capabilities. Just as there are important differences between children and adults, men and women often manifest diseases differently. In addition, men and women often deal with and manage their diseases in different ways. While “Men’s Health” is often considered to be a focus on the urogenital tract, we have sought to also focus on diseases that have a high prevalence in men, or where treatment in men may be different compared with women.
The first 2 articles in this supplement on men’s health concern 2 diseases increasingly encountered by men as they age. Dr. Martin Miner provides his thoughts about screening for and diagnosing benign prostatic hyperplasia, including strategies to promote patient report of symptoms and the role of the prostate specific antigen test. A case study is utilized to illustrate key considerations when selecting therapy and promoting patient self-management of benign prostatic hyperplasia. Dr. Gary Ruoff follows a patient from initial diagnosis of gout through selection of treatment for the acute flare and chronic treatment with urate-lowering therapy. A treatment plan is presented at each management step. In the next article, Dr. Richard Aguilar takes a case study approach to describe key risk factors for type 2 diabetes mellitus in men. He also discusses how men self-manage type 2 diabetes differently than women and provides insight as to how to address common psychosocial issues in men. Drs. Louis Kuritzky and José Díez review clinical experience with the two newest antiplatelet agents, prasugrel and ticagrelor. Answers are also provided to common questions and problems encountered with the use of antiplatelet agents in primary care. The next 2 articles focus on major modifiable risk factors contributing to cardiovascular disease. In the first, Dr. Michael Cobble focuses on patient assessment and treatment strategies to help men modify abnormal lipid levels and blood pressure for primary prevention of coronary heart disease. Finally, a more in-depth discussion of dyslipidemia is provided by Dr. Peter Toth, who begins by providing a brief overview of the current evidence regarding the long-term benefits of statin therapy, as well as his clinical perspective on the newest statin, pitavastatin. Dr. Toth also provides answers to many problems frequently encountered in the primary care management of patients with dyslipidemia using statin therapy.
It is my hope that the insights provided by these authors will be helpful to family physicians in managing their male patients with these common chronic diseases.
1. World Health Organization. Adherence to long-term therapies: evidence for action. http://www.who.int/chp/knowledge/publications/adherence_full_report.pdf. Published 2003. Accessed May 7, 2012.
2. Khanna R, Pace PF, Mahabaleshwarkar R, Basak RS, Datar M, Banahan BF. Medication adherence among recipients with chronic diseases enrolled in a state medicaid program [published online ahead of print March 8, 2012]. Popul Health Manag. doi:10.1089/pop.2011.0069.
3. Ford ES. Trends in the control of risk factors for cardiovascular disease among adults with diagnosed diabetes: findings from the National Health and Nutrition Examination Survey 1999-2008. J Diabetes. 2011;3(4):337-347.
4. Roger VL, Go AS, Lloyd-Jones DM, et al. American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012;125(1):e2-e220.
Managing the Multiple Symptoms of Benign Prostatic Hyperplasia — CME
Managing Type 2 Diabetes in Men
Meeting New Challenges with Antiplatelet Therapy in Primary Care
Dr. Brunton has disclosed that he is on the advisory boards and speakers’ bureaus for Boehringer Ingelheim, Eli Lilly, Kowa, Novo Nordisk, Inc, and Teva Pharmaceuticals, and is on the advisory boards for Abbott and Sunovion.
A decade ago, the World Health Organization suggested that “increasing the effectiveness of adherence interventions may have a far greater impact on the health of the population than any improvement in specific medical treatments.”1 A recent survey found that medication adherence rates over the course of 1 year were 24% for patients with depression, 36% with diabetes, 54% with epilepsy, 32% with dyslipidemia, and 42% with hypertension.2 Poor adherence rates such as these contribute to the low rates of disease control in patients with diabetes, dyslipidemia, hypertension, and other chronic diseases.3,4 Since chronic diseases are largely self-managed, effective patient self-management is critical to good health-related outcomes. To help patients self-manage their diseases, the family physician must work collaboratively with each patient to select, initiate, and modify therapy based upon the patient’s needs, interests, and capabilities. Just as there are important differences between children and adults, men and women often manifest diseases differently. In addition, men and women often deal with and manage their diseases in different ways. While “Men’s Health” is often considered to be a focus on the urogenital tract, we have sought to also focus on diseases that have a high prevalence in men, or where treatment in men may be different compared with women.
The first 2 articles in this supplement on men’s health concern 2 diseases increasingly encountered by men as they age. Dr. Martin Miner provides his thoughts about screening for and diagnosing benign prostatic hyperplasia, including strategies to promote patient report of symptoms and the role of the prostate specific antigen test. A case study is utilized to illustrate key considerations when selecting therapy and promoting patient self-management of benign prostatic hyperplasia. Dr. Gary Ruoff follows a patient from initial diagnosis of gout through selection of treatment for the acute flare and chronic treatment with urate-lowering therapy. A treatment plan is presented at each management step. In the next article, Dr. Richard Aguilar takes a case study approach to describe key risk factors for type 2 diabetes mellitus in men. He also discusses how men self-manage type 2 diabetes differently than women and provides insight as to how to address common psychosocial issues in men. Drs. Louis Kuritzky and José Díez review clinical experience with the two newest antiplatelet agents, prasugrel and ticagrelor. Answers are also provided to common questions and problems encountered with the use of antiplatelet agents in primary care. The next 2 articles focus on major modifiable risk factors contributing to cardiovascular disease. In the first, Dr. Michael Cobble focuses on patient assessment and treatment strategies to help men modify abnormal lipid levels and blood pressure for primary prevention of coronary heart disease. Finally, a more in-depth discussion of dyslipidemia is provided by Dr. Peter Toth, who begins by providing a brief overview of the current evidence regarding the long-term benefits of statin therapy, as well as his clinical perspective on the newest statin, pitavastatin. Dr. Toth also provides answers to many problems frequently encountered in the primary care management of patients with dyslipidemia using statin therapy.
It is my hope that the insights provided by these authors will be helpful to family physicians in managing their male patients with these common chronic diseases.
Managing the Multiple Symptoms of Benign Prostatic Hyperplasia — CME
Managing Type 2 Diabetes in Men
Meeting New Challenges with Antiplatelet Therapy in Primary Care
Dr. Brunton has disclosed that he is on the advisory boards and speakers’ bureaus for Boehringer Ingelheim, Eli Lilly, Kowa, Novo Nordisk, Inc, and Teva Pharmaceuticals, and is on the advisory boards for Abbott and Sunovion.
A decade ago, the World Health Organization suggested that “increasing the effectiveness of adherence interventions may have a far greater impact on the health of the population than any improvement in specific medical treatments.”1 A recent survey found that medication adherence rates over the course of 1 year were 24% for patients with depression, 36% with diabetes, 54% with epilepsy, 32% with dyslipidemia, and 42% with hypertension.2 Poor adherence rates such as these contribute to the low rates of disease control in patients with diabetes, dyslipidemia, hypertension, and other chronic diseases.3,4 Since chronic diseases are largely self-managed, effective patient self-management is critical to good health-related outcomes. To help patients self-manage their diseases, the family physician must work collaboratively with each patient to select, initiate, and modify therapy based upon the patient’s needs, interests, and capabilities. Just as there are important differences between children and adults, men and women often manifest diseases differently. In addition, men and women often deal with and manage their diseases in different ways. While “Men’s Health” is often considered to be a focus on the urogenital tract, we have sought to also focus on diseases that have a high prevalence in men, or where treatment in men may be different compared with women.
The first 2 articles in this supplement on men’s health concern 2 diseases increasingly encountered by men as they age. Dr. Martin Miner provides his thoughts about screening for and diagnosing benign prostatic hyperplasia, including strategies to promote patient report of symptoms and the role of the prostate specific antigen test. A case study is utilized to illustrate key considerations when selecting therapy and promoting patient self-management of benign prostatic hyperplasia. Dr. Gary Ruoff follows a patient from initial diagnosis of gout through selection of treatment for the acute flare and chronic treatment with urate-lowering therapy. A treatment plan is presented at each management step. In the next article, Dr. Richard Aguilar takes a case study approach to describe key risk factors for type 2 diabetes mellitus in men. He also discusses how men self-manage type 2 diabetes differently than women and provides insight as to how to address common psychosocial issues in men. Drs. Louis Kuritzky and José Díez review clinical experience with the two newest antiplatelet agents, prasugrel and ticagrelor. Answers are also provided to common questions and problems encountered with the use of antiplatelet agents in primary care. The next 2 articles focus on major modifiable risk factors contributing to cardiovascular disease. In the first, Dr. Michael Cobble focuses on patient assessment and treatment strategies to help men modify abnormal lipid levels and blood pressure for primary prevention of coronary heart disease. Finally, a more in-depth discussion of dyslipidemia is provided by Dr. Peter Toth, who begins by providing a brief overview of the current evidence regarding the long-term benefits of statin therapy, as well as his clinical perspective on the newest statin, pitavastatin. Dr. Toth also provides answers to many problems frequently encountered in the primary care management of patients with dyslipidemia using statin therapy.
It is my hope that the insights provided by these authors will be helpful to family physicians in managing their male patients with these common chronic diseases.
1. World Health Organization. Adherence to long-term therapies: evidence for action. http://www.who.int/chp/knowledge/publications/adherence_full_report.pdf. Published 2003. Accessed May 7, 2012.
2. Khanna R, Pace PF, Mahabaleshwarkar R, Basak RS, Datar M, Banahan BF. Medication adherence among recipients with chronic diseases enrolled in a state medicaid program [published online ahead of print March 8, 2012]. Popul Health Manag. doi:10.1089/pop.2011.0069.
3. Ford ES. Trends in the control of risk factors for cardiovascular disease among adults with diagnosed diabetes: findings from the National Health and Nutrition Examination Survey 1999-2008. J Diabetes. 2011;3(4):337-347.
4. Roger VL, Go AS, Lloyd-Jones DM, et al. American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012;125(1):e2-e220.
1. World Health Organization. Adherence to long-term therapies: evidence for action. http://www.who.int/chp/knowledge/publications/adherence_full_report.pdf. Published 2003. Accessed May 7, 2012.
2. Khanna R, Pace PF, Mahabaleshwarkar R, Basak RS, Datar M, Banahan BF. Medication adherence among recipients with chronic diseases enrolled in a state medicaid program [published online ahead of print March 8, 2012]. Popul Health Manag. doi:10.1089/pop.2011.0069.
3. Ford ES. Trends in the control of risk factors for cardiovascular disease among adults with diagnosed diabetes: findings from the National Health and Nutrition Examination Survey 1999-2008. J Diabetes. 2011;3(4):337-347.
4. Roger VL, Go AS, Lloyd-Jones DM, et al. American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012;125(1):e2-e220.
Sports concussion: A return-to-play guide
• Prohibit sports participation as long as a patient exhibits concussive symptoms after a head injury. C
• Evaluate a patient’s balance and cognitive function to help gauge the severity of concussion and the likely delay in a return to sports activity. C
• Use a stepwise protocol in returning an asymptomatic patient to full sports activity. C
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
CASE KD is an 18-year-old high school basketball player who was knocked backwards during a game, hitting her head on the floor. She had immediate head and neck pain but no loss of consciousness; she was transported by EMS to the local emergency department (ED) for further evaluation. Results of head and neck CT scans were normal, and she was discharged home. Four days later, KD’s parents brought her to our office because she was experiencing ongoing headache, phonophobia, nausea, light-headedness, poor balance, increased sleepiness, and irritability.
The Centers for Disease Control and Prevention estimate that approximately 300,000 sports concussions occur yearly in the United States,1 and that 135,000 of these cases are treated in EDs.2 These numbers have not gone unnoticed in the consumer press. Over the past 18 months, Sports Illustrated, Newsweek, and Time3-5 have published stories on sports-related concussion, helping to raise public awareness of its risks.
Recommendations for practitioners have changed. In 1997, the American Academy of Neurology6 published one-size-fits-all guidelines on managing concussion, using levels of symptomatology and loss of consciousness to grade the severity of concussion from 1 to 3. These guidelines were similar to the Cantu and Colorado guidelines of the early 1990s.7,8 Since then, however, the diagnostic criteria and expert opinion about treatment and return to physical activity have changed. Indeed, several medical organizations9-12 now recommend a more individualized approach to evaluation and management, which we describe here.
It begins with a definition
While there is no single agreed-upon characterization of “concussion,” the 3rd International Conference on Concussion in Sport (ICCS)12 provides this definition:
Concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. Several common features that incorporate clinical, pathologic, and biomechanical injury constructs that may be utilized in defining the nature of a concussive head injury include:
- Concussion may be caused either by a direct blow to the head, face, or neck or a blow elsewhere on the body with an ‘‘impulsive’’ force transmitted to the head.
- Concussion typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously.
- Concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury.
- Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course.… In a small percentage of cases, however, postconcussive symptoms may be prolonged.
- No abnormality on standard structural neuroimaging studies is seen in concussion.
Office evaluation
Obtain a thorough history and conduct a neurologic evaluation and musculoskeletal examination of the head and neck.
Clues to expected length of recovery
A patient with a concussion may lose consciousness after the impact, or have a brief convulsion that is not a seizure.13 In the periodimmediately after the injury, the patient may exhibit a constellation of such signs and symptoms as headache, confusion, a dazed look, dilated pupils, amnesia, poor balance, nausea, or vomiting. These features typically resolve over time, but may persist for weeks or months. Anterograde or retrograde amnesia may also occur. TABLE 1 details a more complete list of concussion symptoms. If the patient is a child or young adult, it is useful to have a parent present at the office visit to describe the patient’s mood, sleep, appetite, and overall health after the injury.
Factors that may portend a longer recovery include a previous concussion, retrograde or anterograde amnesia, younger age, and female sex.14
Dire problems beyond concussion. Complaints or historical elements inconsistent with concussion that should be considered red flags include any focal neurologic complaints, vomiting or headache that worsens after a period of improvement, or obtundation or disorientation that has worsened since the injury. With such findings, consider more serious head injuries and arrange for a more complete immediate neurologic work-up.
CASE Our neurologic examination yielded normal results. However, our patient was unable to balance correctly on one leg. The cognitive exam revealed a deficit in short-term memory. We diagnosed a concussion, advised her to refrain from sports, and prescribed cognitive rest. A return to school for half days would be considered once her symptoms began to resolve.
TABLE 1
Signs and symptoms commonly associated with concussion
| Headache “Pressure in head” Neck pain Nausea or vomiting Dizziness Blurred vision Balance problems | Sensitivity to light Sensitivity to noise Feeling slowed down Feeling like “in a fog” “Don’t feel right” Difficulty concentrating Difficulty remembering | Fatigue or low energy Confusion Drowsiness Trouble falling asleep Irritability Sadness Nervousness or anxiety |
| Adapted from SCAT2 in Appendix 1 of: McCrory P, Meeuwisse W, Johnston K, et al. Br J Sports Med. 2009;43(suppl 1):i76-i90.12 | ||
Options for the neurologic exam
With a simple concussion, expect a normal neurologic examination, with the possible exception of the ability to balance. Head imaging is not necessary in the setting of suspected concussion, because results of computed tomography (CT) and magnetic resonance imaging (MRI) will likely be normal.12
Balance testing can assist in the diagnosis of concussion and the monitoring of recovery from injury.15-17 The Balance Error Scoring System (BESS)15 is a validated and simple test that can be done in the office. The test involves 3 consecutive stances: (a) normal stance with feet comfortably apart and hands on hips, (b) with feet aligned heel to toe with the dominant leg in front, and (c) standing on the nondominant leg with the dominant leg flexed 30 degrees at the hip. Have the patient repeat each version of the test for 20 seconds with eyes closed, on a stable and then unstable surface (eg, foam mat).
It’s recommended that another staff member be present to spot the patient in case of a fall. A link to a complete description of the test and scoring details is provided in the Web resources box.
Assess cognitive function. One tool for assessing cognitive function is the Sports Concussion Assessment Tool 2 (SCAT2).12 SCAT2 includes newer, as yet unvalidated sections and several sections that have been independently studied and proven useful in diagnosing concussion. Validated sections are the Maddocks questions, used only at the time and place of injury18 ; the modified BESS15 ; and the Standardized Assessment of Concussion (SAC).19 The SCAT2 and the SAC (which may be used separately) include questions that assist in evaluating short-term memory and attention, and are useful in the physician’s office.
Do computer-based tools help? Another option for cognitive assessment is computer-based neuropsychologic testing developed specifically for use with suspected concussion. Any of these programs can be used in the office by a trained practitioner. Schools may also use the programs under the supervision of an athletic trainer or team physician. Available programs are ImPACT, developed by the University of Pittsburgh (http://impacttest.com); the Cognitive Stability Index (CSI), by HeadMinder (http://www.headminder.com/site/csi/home.html); and the Computerized Cognitive Assessment Tool (CCAT), by CogState/Axon Sports (http://www.axonsports.com). Multiple studies have shown such programs to be useful in diagnosing and monitoring recovery from sports concussion.20-23
However, among sports medicine practitioners, there seems to be a consensus that computer-based neuropsychologic testing is most useful when a baseline score exists. Baseline testing is usually done preseason on athletes in a healthy state. If a baseline score is not available, a patient’s postinjury score is compared with normative data produced by the developer of the individual test.
Few, if any, outcome studies have been conducted to determine whether computer-basedneuropsychologic testing provides any meaningful improvement in the care of athletes who have suffered concussions. There is also concern that few studies by independent sources have replicated the data disseminated by developers of the tests.24,25 The most recent guidelines by the 3rd ICCS recommend using neuropsychologic testing only as an aid to an overall medical evaluation, not as the sole determinant of recovery from concussion.12 Numerous studies now underway may help clarify the role of neuropsychologic testing in concussion.
CASE By the time of our follow-up exam 7 days later (11 days from injury), KD had returned to school for half days, but her phonophobia and headaches worsened at school and she had difficulty focusing on academic tasks. Neurologic, balance, and cognitive exams were all normal. We advised her to gradually return to school full time while abstaining from sporting activity.
At 16 days’ follow-up (20 days from injury), KD had returned to school full time and said she felt more like herself, although she continued to have daily headaches and phonophobia. All exam results were normal. Sports were still off limits, and we told her to expect at least 7 more days of respite before any return to exercise would be allowed.
At 23 days’ follow-up (27 days from injury), KD’s symptoms had completely resolved, and all exam results were normal. We prescribed a stepwise return to athletic activity over the next 10 days and discussed this plan with the school’s athletic trainer, who would supervise her return to play.
American Academy of Neurology (AAN). Position Statement on Sports Concussion. http://www.aan.com/globals/axon/assets/7913.pdf
American Academy of Pediatrics (AAP). Sports-Related Concussion in Children and Adolescents. http://pediatrics.aappublications.org/cgi/content/abstract/126/3/597
The Balance Error Scoring System (BESS). http://www.sportsconcussion.com/pdf/management/BESSProtocolNATA09.pdf
Centers for Disease Control and Prevention. Concussion and Mild TBI. http://www.cdc.gov/concussion/index.html
Sport Concussion Assessment Tool 2 (SCAT2). http://www.athletictherapy.org/en/pdf/SCAT2.pdf
3rd International Conference on Concussion in Sport. http://bjsm.bmj.com/content/43/Suppl_1/i76.full
Individualize management
The one-size-fits-all approach previously recommended6 is no longer the standard of care. In your initial encounter with the patient (and parents, as appropriate), explain the nature of the injury, expected course of recovery, and requirements for a return to play. Also discuss the possibility of postconcussive syndrome and the risk of rare sequelae such as second impact syndrome.
If the patient is symptomatic or exhibits examination findings consistent with concussion, recommend immediate cessation of sports activity.9-12 With a school-aged athlete, if symptoms reported by the patient or parents are significant, consider prescribing cognitive rest, which can be provided through quiet accommodations at school or perhaps even time off from school or exams.12,24 In the early period of recovery, increased cognitive or physical activity can cause symptoms to worsen. With improvement, the patient may return to school half time to lessen the chance of a significant return of symptoms. If half days are tolerated, the patient may transition to full days. Make sure the diagnosis and expectations for recovery are communicated to the appropriate school officials so that necessary accommodationscan be made. If symptoms after the initial office visit are mild, a one-week return to school is appropriate to evaluate the patient’s recovery.
Allowing a return to sports. Once the patient is asymptomatic, and physical and cognitive test results are normal, discuss a return-to-play protocol with the patient (and with parents and athletic trainer or coach, as appropriate). Multiple sources10,11,26 now recommend a stepwise return to play, as detailed by the 3rd ICCS ( TABLE 2 ).12 Increase or decrease the length of the protocol depending on the patient and the specifics of the case.
There is little science to guide the treatment of children with concussion. However, given that their brains are still developing, it’s prudent to be more conservative than with older adolescents or adults. Multiple sources apart from the 3rd ICCS agree with this recommendation. Several authors suggest more cognitive rest and a longer return-to-play protocol in all cases.10,27 In fact, the ICCS committee additionally recommends observing a symptom-free waiting period for pediatric athletes before even starting a return-to-play protocol.
McCrory et al26 suggest that children under age 15 be treated more conservatively than those 15 and older. They suggest treating those 15 and older with the protocol for older adolescents. Specifying an age at which one should always make a decision for or against conservative care can be problematic. However, based on the recommendations above, it would seem reasonable to provide conservative treatment for children younger than high school age and perhaps even those in the early years of high school.
Consider legal implications. Become familiar with state laws that require certain steps in managing sports concussion. The Web site http://www.sportsconcussions.org/laws.html28 lists states with sports concussion statutes, as well as states with bills working their way through the legislative system. Currently, 29 states are listed with laws; 14 more and the District of Columbia have pending legislation.
TABLE 2
Stepwise protocol for return to play
| If symptoms recur at any step, have patient return to prior level | |
| 1. Light aerobic activity | Walking, swimming, exercise bike; keeping exertion <70% of maximum heart rate |
| 2. Sport-specific exercises | Exertional drills in sport, eg, running drills in football/soccer, skating drills in hockey |
| 3. Noncontact training drills | Progression to more complex noncontact drills, eg, passing/catching drills in football, shooting/passing in basketball, hitting drills in volleyball |
| 4. Full-contact practice | Return to full practice if no recurrence of symptoms through first 3 steps and cleared by physician |
| 5. Game activity | Return to full sport participation if no recurrence of symptoms with above steps |
| Adapted from: McCrory P, Meeuwisse W, Johnston K, et al. Br J Sports Med. 2009;43(suppl 1):i76-i90.12 | |
Anticipate complications
Most patients with concussions who are managed appropriately do well. However, complications can occur. The most serious complication is second impact syndrome, which usually occurs when concussion is unrecognized or not well managed. While not well understood, this condition is thought to result from a sudden increase in intracranial pressure after a second head injury in an athlete already suffering from concussion symptoms. The injury typically results in serious long-term neurologic deficits, or even fatality.29 Second impact syndrome has been documented as occurring in the same game after an initial injury, as well as in subsequent games.29
A more common, but less serious, complication is postconcussion syndrome.30 This is an ill-defined condition in which the patient suffers from concussive symptoms for an extended period of time, generally for more than 3 months.30 As with acute concussion, the constellation of symptoms ranges from headache to cognitive impairment. In cases of postconcussion syndrome, it is appropriate to consult with neuropsychologists, psychiatrists, or neurologists for assistance with symptoms and associated mood disorders. Similar to acute concussion management, it is generally recommended that athletes not be cleared to resume play while struggling with the symptoms of postconcussion syndrome.30
There have also been recent reports of late-life sequelae in those who have sustained multiple concussions. Depression and dementia have been suggested in surveys of retired NFL players.31,32 There have also been studies both suggesting14 and questioning33,34 whether multiple concussions result in long-term cognitive deficits. While the evidence available at this time is not firm, there seems to be an increasing belief that multiple concussions can affect long-term cognitive abilities. For these reasons, use caution in making return-to-play decisions for patients with multiple concussions or concussions with long-lasting symptoms.
CORRESPONDENCE Aaron M. Lear, MD, 224 West Exchange Street, Suite 440, Akron, OH 44302; [email protected]
1. CDC. Sports-related recurrent brain injuries—United States. MMWR Morb Mortal Wkly Rep. 1997;46:224-227.
2. CDC. Brain injury awareness month—March 2010. MMWR Morb Mortal Wkly Rep. 2010;59:235.-
3. Epstein D. The damage done. Sports Illustrated. November 1, 2010:42. Available at: http://sportsillustrated.cnn.com/vault/article/magazine/MAG1176377/index.htm. Accessed May 16, 2012.
4. Kliff S. Heading off sports injuries. Newsweek. February 4, 2010. Available at: http://www.newsweek.com/2010/02/04/heading-off-sports-injuries.html. Accessed February 9, 2011.
5. Kluger J. Headbanger nation. Health special: kids and concussions. Time. February 3, 2011. Available at: http://www.time.com/time/specials/packages/article/0,28804,2043395_2043506_2043494,00.html. Accessed February 9, 2011.
6. American Academy of Neurology. Practice parameter: the management of concussion in sports (summary statement). Report of the quality standards subcommittee. Neurology. 1997;48:581-585.
7. Cantu R. Cerebral concussion in sport. Management and prevention. Sports Med. 1992;14:64-74.
8. Kelly J, Nichols J, Filley C, et al. Concussion in sports. Guidelines for the prevention of catastrophic outcome. JAMA. 1991;266:2867-2869.
9. American Academy of Neurology. Position statement on sports concussion. October 2010. AAN policy 2010-36. Available at: http://www.aan.com/globals/axon/assets/7913.pdf. Accessed February 23, 2011.
10. Halstead M, Walter K. Council on Sports Medicine and Fitness. American Academy of Pediatrics. Clinical report—sport-related concussion in children and adolescents. Pediatrics. 2010;126:597-615.
11. Herring SA, Cantu RC, Guskiewicz KM, et al. Concussion (mild traumatic brain injury) and the team physician: a consensus statement—2011 update. Med Sci Sports Exerc. 2011;43:2412-2422.Available at: http://journals.lww.com/acsm-msse/Fulltext/2011/12000/Concussion__Mild_Traumatic_Brain_Injury__and_the.24.aspx. Accessed February 23, 2011.
12. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport: the 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Br J Sports Med. 2009;43(suppl 1):i76-i90.
13. Ropper A, Gorson K. Clinical practice. Concussion. N Engl J Med. 2007;356:166-172.
14. Reddy C, Collins MW. Sports concussion: management and predictors of outcome. Curr Sports Med Rep. 2009;8:10-15.
15. Guskiewicz KM. Assessment of postural stability following sport-related concussion. Curr Sports Med Rep. 2003;2:24-30.
16. Broglio S, Sosnoff J, Ferrara M. The relationship of athlete-reported concussion symptoms and objective measures of neurocognitive function and postural control. Clin J Sport Med. 2009;19:377-382.
17. Reimann B, Guskiewicz K. Effects of mild head injury on postural stability as measured through clinical balance testing. J Athl Train. 2000;35:19-25.
18. Maddocks D, Dicker G, Saling M. The assessment of orientation following concussion in athletes. Clin J Sport Med. 1995;5:32-35.
19. McCrea M. Standardized mental status assessment of sports concussion. Clin J Sport Med. 2001;11:176-181.
20. Collie A, Maruff P, Makdissi M, et al. CogSport: reliability and correlation with conventional cognitive tests used in postconcussion medical evaluations. Clin J Sport Med. 2003;13:28-32.
21. Erlanger D, Saliba E, Barth J, et al. Monitoring resolution of postconcussion symptoms in athletes: preliminary results of a web-based neuropsychological test protocol. J Athl Train. 2001;36:280-287.
22. Schatz P, Pardini J, Lovell M, et al. Sensitivity and specificity of the ImPACT Test battery for concussion in athletes. Arch Clin Neuropsychol. 2006;21:91-99.
23. Schatz P, Putz B. Cross-validation of measures used for computer-based assessment of concussion. Appl Neuropsychol. 2006;13:151-159.
24. Kirkwood M, Randolph C, Yeates K. Returning pediatric athletes to play after concussion: the evidence (or lack thereof) behind baseline neuropsychological testing. Acta Pædiatr. 2009;98:1409-1411.
25. Randolph C. Baseline neuropsychological testing in managing sport-related concussion: does it modify risk? Curr Sports Med Rep. 2011;10:21-26.
26. McCrory P, Collie A, Anderson V, et al. Can we manage sport related concussion in children the same as in adults? Br J Sports Med. 2004;38:516-519.
27. d’Hemecourt P. Subacute symptoms of sports-related concussion outpatient management and return to play. Clin Sports Med. 2011;30:63-72.
28. Concussion laws. Available at: http://www.sportsconcussions.org/laws.html. Accessed July 5, 2011.
29. Wetjen N, Pichelmann M, Atkinson J. Second impact syndrome: concussion and second injury brain complications. J Am Coll Surg. 2010;211:553-557.
30. Jotwani V, Harmon KG. Postconcussion syndrome in athletes. Curr Sports Med Rep. 2010;9:21-26.
31. Guskiewicz K, Marshall S, Bailes J, et al. Association between recurrent concussion and late-life cognitive impairment in retired professional football players. Neurosurgery. 2005;57:719-726.
32. Guskiewicz K, Marshall S, Bailes J, et al. Recurrent concussion and risk of depression in retired professional football players. Med Sci Sports Exerc. 2007;39:903-909.
33. Belanger H, Spiegel E, Vanderploeg R. Neuropsychological performance following a history of multiple self-reported concussions: a meta-analysis. J Int Neuropsychol Soc. 2010;16:262-267.
34. Burce J, Echemendia R. History of multiple self-reported concussions is not associated with reduced cognitive abilities. Neurosurgery. 2009;64:100-106.
• Prohibit sports participation as long as a patient exhibits concussive symptoms after a head injury. C
• Evaluate a patient’s balance and cognitive function to help gauge the severity of concussion and the likely delay in a return to sports activity. C
• Use a stepwise protocol in returning an asymptomatic patient to full sports activity. C
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
CASE KD is an 18-year-old high school basketball player who was knocked backwards during a game, hitting her head on the floor. She had immediate head and neck pain but no loss of consciousness; she was transported by EMS to the local emergency department (ED) for further evaluation. Results of head and neck CT scans were normal, and she was discharged home. Four days later, KD’s parents brought her to our office because she was experiencing ongoing headache, phonophobia, nausea, light-headedness, poor balance, increased sleepiness, and irritability.
The Centers for Disease Control and Prevention estimate that approximately 300,000 sports concussions occur yearly in the United States,1 and that 135,000 of these cases are treated in EDs.2 These numbers have not gone unnoticed in the consumer press. Over the past 18 months, Sports Illustrated, Newsweek, and Time3-5 have published stories on sports-related concussion, helping to raise public awareness of its risks.
Recommendations for practitioners have changed. In 1997, the American Academy of Neurology6 published one-size-fits-all guidelines on managing concussion, using levels of symptomatology and loss of consciousness to grade the severity of concussion from 1 to 3. These guidelines were similar to the Cantu and Colorado guidelines of the early 1990s.7,8 Since then, however, the diagnostic criteria and expert opinion about treatment and return to physical activity have changed. Indeed, several medical organizations9-12 now recommend a more individualized approach to evaluation and management, which we describe here.
It begins with a definition
While there is no single agreed-upon characterization of “concussion,” the 3rd International Conference on Concussion in Sport (ICCS)12 provides this definition:
Concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. Several common features that incorporate clinical, pathologic, and biomechanical injury constructs that may be utilized in defining the nature of a concussive head injury include:
- Concussion may be caused either by a direct blow to the head, face, or neck or a blow elsewhere on the body with an ‘‘impulsive’’ force transmitted to the head.
- Concussion typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously.
- Concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury.
- Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course.… In a small percentage of cases, however, postconcussive symptoms may be prolonged.
- No abnormality on standard structural neuroimaging studies is seen in concussion.
Office evaluation
Obtain a thorough history and conduct a neurologic evaluation and musculoskeletal examination of the head and neck.
Clues to expected length of recovery
A patient with a concussion may lose consciousness after the impact, or have a brief convulsion that is not a seizure.13 In the periodimmediately after the injury, the patient may exhibit a constellation of such signs and symptoms as headache, confusion, a dazed look, dilated pupils, amnesia, poor balance, nausea, or vomiting. These features typically resolve over time, but may persist for weeks or months. Anterograde or retrograde amnesia may also occur. TABLE 1 details a more complete list of concussion symptoms. If the patient is a child or young adult, it is useful to have a parent present at the office visit to describe the patient’s mood, sleep, appetite, and overall health after the injury.
Factors that may portend a longer recovery include a previous concussion, retrograde or anterograde amnesia, younger age, and female sex.14
Dire problems beyond concussion. Complaints or historical elements inconsistent with concussion that should be considered red flags include any focal neurologic complaints, vomiting or headache that worsens after a period of improvement, or obtundation or disorientation that has worsened since the injury. With such findings, consider more serious head injuries and arrange for a more complete immediate neurologic work-up.
CASE Our neurologic examination yielded normal results. However, our patient was unable to balance correctly on one leg. The cognitive exam revealed a deficit in short-term memory. We diagnosed a concussion, advised her to refrain from sports, and prescribed cognitive rest. A return to school for half days would be considered once her symptoms began to resolve.
TABLE 1
Signs and symptoms commonly associated with concussion
| Headache “Pressure in head” Neck pain Nausea or vomiting Dizziness Blurred vision Balance problems | Sensitivity to light Sensitivity to noise Feeling slowed down Feeling like “in a fog” “Don’t feel right” Difficulty concentrating Difficulty remembering | Fatigue or low energy Confusion Drowsiness Trouble falling asleep Irritability Sadness Nervousness or anxiety |
| Adapted from SCAT2 in Appendix 1 of: McCrory P, Meeuwisse W, Johnston K, et al. Br J Sports Med. 2009;43(suppl 1):i76-i90.12 | ||
Options for the neurologic exam
With a simple concussion, expect a normal neurologic examination, with the possible exception of the ability to balance. Head imaging is not necessary in the setting of suspected concussion, because results of computed tomography (CT) and magnetic resonance imaging (MRI) will likely be normal.12
Balance testing can assist in the diagnosis of concussion and the monitoring of recovery from injury.15-17 The Balance Error Scoring System (BESS)15 is a validated and simple test that can be done in the office. The test involves 3 consecutive stances: (a) normal stance with feet comfortably apart and hands on hips, (b) with feet aligned heel to toe with the dominant leg in front, and (c) standing on the nondominant leg with the dominant leg flexed 30 degrees at the hip. Have the patient repeat each version of the test for 20 seconds with eyes closed, on a stable and then unstable surface (eg, foam mat).
It’s recommended that another staff member be present to spot the patient in case of a fall. A link to a complete description of the test and scoring details is provided in the Web resources box.
Assess cognitive function. One tool for assessing cognitive function is the Sports Concussion Assessment Tool 2 (SCAT2).12 SCAT2 includes newer, as yet unvalidated sections and several sections that have been independently studied and proven useful in diagnosing concussion. Validated sections are the Maddocks questions, used only at the time and place of injury18 ; the modified BESS15 ; and the Standardized Assessment of Concussion (SAC).19 The SCAT2 and the SAC (which may be used separately) include questions that assist in evaluating short-term memory and attention, and are useful in the physician’s office.
Do computer-based tools help? Another option for cognitive assessment is computer-based neuropsychologic testing developed specifically for use with suspected concussion. Any of these programs can be used in the office by a trained practitioner. Schools may also use the programs under the supervision of an athletic trainer or team physician. Available programs are ImPACT, developed by the University of Pittsburgh (http://impacttest.com); the Cognitive Stability Index (CSI), by HeadMinder (http://www.headminder.com/site/csi/home.html); and the Computerized Cognitive Assessment Tool (CCAT), by CogState/Axon Sports (http://www.axonsports.com). Multiple studies have shown such programs to be useful in diagnosing and monitoring recovery from sports concussion.20-23
However, among sports medicine practitioners, there seems to be a consensus that computer-based neuropsychologic testing is most useful when a baseline score exists. Baseline testing is usually done preseason on athletes in a healthy state. If a baseline score is not available, a patient’s postinjury score is compared with normative data produced by the developer of the individual test.
Few, if any, outcome studies have been conducted to determine whether computer-basedneuropsychologic testing provides any meaningful improvement in the care of athletes who have suffered concussions. There is also concern that few studies by independent sources have replicated the data disseminated by developers of the tests.24,25 The most recent guidelines by the 3rd ICCS recommend using neuropsychologic testing only as an aid to an overall medical evaluation, not as the sole determinant of recovery from concussion.12 Numerous studies now underway may help clarify the role of neuropsychologic testing in concussion.
CASE By the time of our follow-up exam 7 days later (11 days from injury), KD had returned to school for half days, but her phonophobia and headaches worsened at school and she had difficulty focusing on academic tasks. Neurologic, balance, and cognitive exams were all normal. We advised her to gradually return to school full time while abstaining from sporting activity.
At 16 days’ follow-up (20 days from injury), KD had returned to school full time and said she felt more like herself, although she continued to have daily headaches and phonophobia. All exam results were normal. Sports were still off limits, and we told her to expect at least 7 more days of respite before any return to exercise would be allowed.
At 23 days’ follow-up (27 days from injury), KD’s symptoms had completely resolved, and all exam results were normal. We prescribed a stepwise return to athletic activity over the next 10 days and discussed this plan with the school’s athletic trainer, who would supervise her return to play.
American Academy of Neurology (AAN). Position Statement on Sports Concussion. http://www.aan.com/globals/axon/assets/7913.pdf
American Academy of Pediatrics (AAP). Sports-Related Concussion in Children and Adolescents. http://pediatrics.aappublications.org/cgi/content/abstract/126/3/597
The Balance Error Scoring System (BESS). http://www.sportsconcussion.com/pdf/management/BESSProtocolNATA09.pdf
Centers for Disease Control and Prevention. Concussion and Mild TBI. http://www.cdc.gov/concussion/index.html
Sport Concussion Assessment Tool 2 (SCAT2). http://www.athletictherapy.org/en/pdf/SCAT2.pdf
3rd International Conference on Concussion in Sport. http://bjsm.bmj.com/content/43/Suppl_1/i76.full
Individualize management
The one-size-fits-all approach previously recommended6 is no longer the standard of care. In your initial encounter with the patient (and parents, as appropriate), explain the nature of the injury, expected course of recovery, and requirements for a return to play. Also discuss the possibility of postconcussive syndrome and the risk of rare sequelae such as second impact syndrome.
If the patient is symptomatic or exhibits examination findings consistent with concussion, recommend immediate cessation of sports activity.9-12 With a school-aged athlete, if symptoms reported by the patient or parents are significant, consider prescribing cognitive rest, which can be provided through quiet accommodations at school or perhaps even time off from school or exams.12,24 In the early period of recovery, increased cognitive or physical activity can cause symptoms to worsen. With improvement, the patient may return to school half time to lessen the chance of a significant return of symptoms. If half days are tolerated, the patient may transition to full days. Make sure the diagnosis and expectations for recovery are communicated to the appropriate school officials so that necessary accommodationscan be made. If symptoms after the initial office visit are mild, a one-week return to school is appropriate to evaluate the patient’s recovery.
Allowing a return to sports. Once the patient is asymptomatic, and physical and cognitive test results are normal, discuss a return-to-play protocol with the patient (and with parents and athletic trainer or coach, as appropriate). Multiple sources10,11,26 now recommend a stepwise return to play, as detailed by the 3rd ICCS ( TABLE 2 ).12 Increase or decrease the length of the protocol depending on the patient and the specifics of the case.
There is little science to guide the treatment of children with concussion. However, given that their brains are still developing, it’s prudent to be more conservative than with older adolescents or adults. Multiple sources apart from the 3rd ICCS agree with this recommendation. Several authors suggest more cognitive rest and a longer return-to-play protocol in all cases.10,27 In fact, the ICCS committee additionally recommends observing a symptom-free waiting period for pediatric athletes before even starting a return-to-play protocol.
McCrory et al26 suggest that children under age 15 be treated more conservatively than those 15 and older. They suggest treating those 15 and older with the protocol for older adolescents. Specifying an age at which one should always make a decision for or against conservative care can be problematic. However, based on the recommendations above, it would seem reasonable to provide conservative treatment for children younger than high school age and perhaps even those in the early years of high school.
Consider legal implications. Become familiar with state laws that require certain steps in managing sports concussion. The Web site http://www.sportsconcussions.org/laws.html28 lists states with sports concussion statutes, as well as states with bills working their way through the legislative system. Currently, 29 states are listed with laws; 14 more and the District of Columbia have pending legislation.
TABLE 2
Stepwise protocol for return to play
| If symptoms recur at any step, have patient return to prior level | |
| 1. Light aerobic activity | Walking, swimming, exercise bike; keeping exertion <70% of maximum heart rate |
| 2. Sport-specific exercises | Exertional drills in sport, eg, running drills in football/soccer, skating drills in hockey |
| 3. Noncontact training drills | Progression to more complex noncontact drills, eg, passing/catching drills in football, shooting/passing in basketball, hitting drills in volleyball |
| 4. Full-contact practice | Return to full practice if no recurrence of symptoms through first 3 steps and cleared by physician |
| 5. Game activity | Return to full sport participation if no recurrence of symptoms with above steps |
| Adapted from: McCrory P, Meeuwisse W, Johnston K, et al. Br J Sports Med. 2009;43(suppl 1):i76-i90.12 | |
Anticipate complications
Most patients with concussions who are managed appropriately do well. However, complications can occur. The most serious complication is second impact syndrome, which usually occurs when concussion is unrecognized or not well managed. While not well understood, this condition is thought to result from a sudden increase in intracranial pressure after a second head injury in an athlete already suffering from concussion symptoms. The injury typically results in serious long-term neurologic deficits, or even fatality.29 Second impact syndrome has been documented as occurring in the same game after an initial injury, as well as in subsequent games.29
A more common, but less serious, complication is postconcussion syndrome.30 This is an ill-defined condition in which the patient suffers from concussive symptoms for an extended period of time, generally for more than 3 months.30 As with acute concussion, the constellation of symptoms ranges from headache to cognitive impairment. In cases of postconcussion syndrome, it is appropriate to consult with neuropsychologists, psychiatrists, or neurologists for assistance with symptoms and associated mood disorders. Similar to acute concussion management, it is generally recommended that athletes not be cleared to resume play while struggling with the symptoms of postconcussion syndrome.30
There have also been recent reports of late-life sequelae in those who have sustained multiple concussions. Depression and dementia have been suggested in surveys of retired NFL players.31,32 There have also been studies both suggesting14 and questioning33,34 whether multiple concussions result in long-term cognitive deficits. While the evidence available at this time is not firm, there seems to be an increasing belief that multiple concussions can affect long-term cognitive abilities. For these reasons, use caution in making return-to-play decisions for patients with multiple concussions or concussions with long-lasting symptoms.
CORRESPONDENCE Aaron M. Lear, MD, 224 West Exchange Street, Suite 440, Akron, OH 44302; [email protected]
• Prohibit sports participation as long as a patient exhibits concussive symptoms after a head injury. C
• Evaluate a patient’s balance and cognitive function to help gauge the severity of concussion and the likely delay in a return to sports activity. C
• Use a stepwise protocol in returning an asymptomatic patient to full sports activity. C
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
CASE KD is an 18-year-old high school basketball player who was knocked backwards during a game, hitting her head on the floor. She had immediate head and neck pain but no loss of consciousness; she was transported by EMS to the local emergency department (ED) for further evaluation. Results of head and neck CT scans were normal, and she was discharged home. Four days later, KD’s parents brought her to our office because she was experiencing ongoing headache, phonophobia, nausea, light-headedness, poor balance, increased sleepiness, and irritability.
The Centers for Disease Control and Prevention estimate that approximately 300,000 sports concussions occur yearly in the United States,1 and that 135,000 of these cases are treated in EDs.2 These numbers have not gone unnoticed in the consumer press. Over the past 18 months, Sports Illustrated, Newsweek, and Time3-5 have published stories on sports-related concussion, helping to raise public awareness of its risks.
Recommendations for practitioners have changed. In 1997, the American Academy of Neurology6 published one-size-fits-all guidelines on managing concussion, using levels of symptomatology and loss of consciousness to grade the severity of concussion from 1 to 3. These guidelines were similar to the Cantu and Colorado guidelines of the early 1990s.7,8 Since then, however, the diagnostic criteria and expert opinion about treatment and return to physical activity have changed. Indeed, several medical organizations9-12 now recommend a more individualized approach to evaluation and management, which we describe here.
It begins with a definition
While there is no single agreed-upon characterization of “concussion,” the 3rd International Conference on Concussion in Sport (ICCS)12 provides this definition:
Concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. Several common features that incorporate clinical, pathologic, and biomechanical injury constructs that may be utilized in defining the nature of a concussive head injury include:
- Concussion may be caused either by a direct blow to the head, face, or neck or a blow elsewhere on the body with an ‘‘impulsive’’ force transmitted to the head.
- Concussion typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously.
- Concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury.
- Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course.… In a small percentage of cases, however, postconcussive symptoms may be prolonged.
- No abnormality on standard structural neuroimaging studies is seen in concussion.
Office evaluation
Obtain a thorough history and conduct a neurologic evaluation and musculoskeletal examination of the head and neck.
Clues to expected length of recovery
A patient with a concussion may lose consciousness after the impact, or have a brief convulsion that is not a seizure.13 In the periodimmediately after the injury, the patient may exhibit a constellation of such signs and symptoms as headache, confusion, a dazed look, dilated pupils, amnesia, poor balance, nausea, or vomiting. These features typically resolve over time, but may persist for weeks or months. Anterograde or retrograde amnesia may also occur. TABLE 1 details a more complete list of concussion symptoms. If the patient is a child or young adult, it is useful to have a parent present at the office visit to describe the patient’s mood, sleep, appetite, and overall health after the injury.
Factors that may portend a longer recovery include a previous concussion, retrograde or anterograde amnesia, younger age, and female sex.14
Dire problems beyond concussion. Complaints or historical elements inconsistent with concussion that should be considered red flags include any focal neurologic complaints, vomiting or headache that worsens after a period of improvement, or obtundation or disorientation that has worsened since the injury. With such findings, consider more serious head injuries and arrange for a more complete immediate neurologic work-up.
CASE Our neurologic examination yielded normal results. However, our patient was unable to balance correctly on one leg. The cognitive exam revealed a deficit in short-term memory. We diagnosed a concussion, advised her to refrain from sports, and prescribed cognitive rest. A return to school for half days would be considered once her symptoms began to resolve.
TABLE 1
Signs and symptoms commonly associated with concussion
| Headache “Pressure in head” Neck pain Nausea or vomiting Dizziness Blurred vision Balance problems | Sensitivity to light Sensitivity to noise Feeling slowed down Feeling like “in a fog” “Don’t feel right” Difficulty concentrating Difficulty remembering | Fatigue or low energy Confusion Drowsiness Trouble falling asleep Irritability Sadness Nervousness or anxiety |
| Adapted from SCAT2 in Appendix 1 of: McCrory P, Meeuwisse W, Johnston K, et al. Br J Sports Med. 2009;43(suppl 1):i76-i90.12 | ||
Options for the neurologic exam
With a simple concussion, expect a normal neurologic examination, with the possible exception of the ability to balance. Head imaging is not necessary in the setting of suspected concussion, because results of computed tomography (CT) and magnetic resonance imaging (MRI) will likely be normal.12
Balance testing can assist in the diagnosis of concussion and the monitoring of recovery from injury.15-17 The Balance Error Scoring System (BESS)15 is a validated and simple test that can be done in the office. The test involves 3 consecutive stances: (a) normal stance with feet comfortably apart and hands on hips, (b) with feet aligned heel to toe with the dominant leg in front, and (c) standing on the nondominant leg with the dominant leg flexed 30 degrees at the hip. Have the patient repeat each version of the test for 20 seconds with eyes closed, on a stable and then unstable surface (eg, foam mat).
It’s recommended that another staff member be present to spot the patient in case of a fall. A link to a complete description of the test and scoring details is provided in the Web resources box.
Assess cognitive function. One tool for assessing cognitive function is the Sports Concussion Assessment Tool 2 (SCAT2).12 SCAT2 includes newer, as yet unvalidated sections and several sections that have been independently studied and proven useful in diagnosing concussion. Validated sections are the Maddocks questions, used only at the time and place of injury18 ; the modified BESS15 ; and the Standardized Assessment of Concussion (SAC).19 The SCAT2 and the SAC (which may be used separately) include questions that assist in evaluating short-term memory and attention, and are useful in the physician’s office.
Do computer-based tools help? Another option for cognitive assessment is computer-based neuropsychologic testing developed specifically for use with suspected concussion. Any of these programs can be used in the office by a trained practitioner. Schools may also use the programs under the supervision of an athletic trainer or team physician. Available programs are ImPACT, developed by the University of Pittsburgh (http://impacttest.com); the Cognitive Stability Index (CSI), by HeadMinder (http://www.headminder.com/site/csi/home.html); and the Computerized Cognitive Assessment Tool (CCAT), by CogState/Axon Sports (http://www.axonsports.com). Multiple studies have shown such programs to be useful in diagnosing and monitoring recovery from sports concussion.20-23
However, among sports medicine practitioners, there seems to be a consensus that computer-based neuropsychologic testing is most useful when a baseline score exists. Baseline testing is usually done preseason on athletes in a healthy state. If a baseline score is not available, a patient’s postinjury score is compared with normative data produced by the developer of the individual test.
Few, if any, outcome studies have been conducted to determine whether computer-basedneuropsychologic testing provides any meaningful improvement in the care of athletes who have suffered concussions. There is also concern that few studies by independent sources have replicated the data disseminated by developers of the tests.24,25 The most recent guidelines by the 3rd ICCS recommend using neuropsychologic testing only as an aid to an overall medical evaluation, not as the sole determinant of recovery from concussion.12 Numerous studies now underway may help clarify the role of neuropsychologic testing in concussion.
CASE By the time of our follow-up exam 7 days later (11 days from injury), KD had returned to school for half days, but her phonophobia and headaches worsened at school and she had difficulty focusing on academic tasks. Neurologic, balance, and cognitive exams were all normal. We advised her to gradually return to school full time while abstaining from sporting activity.
At 16 days’ follow-up (20 days from injury), KD had returned to school full time and said she felt more like herself, although she continued to have daily headaches and phonophobia. All exam results were normal. Sports were still off limits, and we told her to expect at least 7 more days of respite before any return to exercise would be allowed.
At 23 days’ follow-up (27 days from injury), KD’s symptoms had completely resolved, and all exam results were normal. We prescribed a stepwise return to athletic activity over the next 10 days and discussed this plan with the school’s athletic trainer, who would supervise her return to play.
American Academy of Neurology (AAN). Position Statement on Sports Concussion. http://www.aan.com/globals/axon/assets/7913.pdf
American Academy of Pediatrics (AAP). Sports-Related Concussion in Children and Adolescents. http://pediatrics.aappublications.org/cgi/content/abstract/126/3/597
The Balance Error Scoring System (BESS). http://www.sportsconcussion.com/pdf/management/BESSProtocolNATA09.pdf
Centers for Disease Control and Prevention. Concussion and Mild TBI. http://www.cdc.gov/concussion/index.html
Sport Concussion Assessment Tool 2 (SCAT2). http://www.athletictherapy.org/en/pdf/SCAT2.pdf
3rd International Conference on Concussion in Sport. http://bjsm.bmj.com/content/43/Suppl_1/i76.full
Individualize management
The one-size-fits-all approach previously recommended6 is no longer the standard of care. In your initial encounter with the patient (and parents, as appropriate), explain the nature of the injury, expected course of recovery, and requirements for a return to play. Also discuss the possibility of postconcussive syndrome and the risk of rare sequelae such as second impact syndrome.
If the patient is symptomatic or exhibits examination findings consistent with concussion, recommend immediate cessation of sports activity.9-12 With a school-aged athlete, if symptoms reported by the patient or parents are significant, consider prescribing cognitive rest, which can be provided through quiet accommodations at school or perhaps even time off from school or exams.12,24 In the early period of recovery, increased cognitive or physical activity can cause symptoms to worsen. With improvement, the patient may return to school half time to lessen the chance of a significant return of symptoms. If half days are tolerated, the patient may transition to full days. Make sure the diagnosis and expectations for recovery are communicated to the appropriate school officials so that necessary accommodationscan be made. If symptoms after the initial office visit are mild, a one-week return to school is appropriate to evaluate the patient’s recovery.
Allowing a return to sports. Once the patient is asymptomatic, and physical and cognitive test results are normal, discuss a return-to-play protocol with the patient (and with parents and athletic trainer or coach, as appropriate). Multiple sources10,11,26 now recommend a stepwise return to play, as detailed by the 3rd ICCS ( TABLE 2 ).12 Increase or decrease the length of the protocol depending on the patient and the specifics of the case.
There is little science to guide the treatment of children with concussion. However, given that their brains are still developing, it’s prudent to be more conservative than with older adolescents or adults. Multiple sources apart from the 3rd ICCS agree with this recommendation. Several authors suggest more cognitive rest and a longer return-to-play protocol in all cases.10,27 In fact, the ICCS committee additionally recommends observing a symptom-free waiting period for pediatric athletes before even starting a return-to-play protocol.
McCrory et al26 suggest that children under age 15 be treated more conservatively than those 15 and older. They suggest treating those 15 and older with the protocol for older adolescents. Specifying an age at which one should always make a decision for or against conservative care can be problematic. However, based on the recommendations above, it would seem reasonable to provide conservative treatment for children younger than high school age and perhaps even those in the early years of high school.
Consider legal implications. Become familiar with state laws that require certain steps in managing sports concussion. The Web site http://www.sportsconcussions.org/laws.html28 lists states with sports concussion statutes, as well as states with bills working their way through the legislative system. Currently, 29 states are listed with laws; 14 more and the District of Columbia have pending legislation.
TABLE 2
Stepwise protocol for return to play
| If symptoms recur at any step, have patient return to prior level | |
| 1. Light aerobic activity | Walking, swimming, exercise bike; keeping exertion <70% of maximum heart rate |
| 2. Sport-specific exercises | Exertional drills in sport, eg, running drills in football/soccer, skating drills in hockey |
| 3. Noncontact training drills | Progression to more complex noncontact drills, eg, passing/catching drills in football, shooting/passing in basketball, hitting drills in volleyball |
| 4. Full-contact practice | Return to full practice if no recurrence of symptoms through first 3 steps and cleared by physician |
| 5. Game activity | Return to full sport participation if no recurrence of symptoms with above steps |
| Adapted from: McCrory P, Meeuwisse W, Johnston K, et al. Br J Sports Med. 2009;43(suppl 1):i76-i90.12 | |
Anticipate complications
Most patients with concussions who are managed appropriately do well. However, complications can occur. The most serious complication is second impact syndrome, which usually occurs when concussion is unrecognized or not well managed. While not well understood, this condition is thought to result from a sudden increase in intracranial pressure after a second head injury in an athlete already suffering from concussion symptoms. The injury typically results in serious long-term neurologic deficits, or even fatality.29 Second impact syndrome has been documented as occurring in the same game after an initial injury, as well as in subsequent games.29
A more common, but less serious, complication is postconcussion syndrome.30 This is an ill-defined condition in which the patient suffers from concussive symptoms for an extended period of time, generally for more than 3 months.30 As with acute concussion, the constellation of symptoms ranges from headache to cognitive impairment. In cases of postconcussion syndrome, it is appropriate to consult with neuropsychologists, psychiatrists, or neurologists for assistance with symptoms and associated mood disorders. Similar to acute concussion management, it is generally recommended that athletes not be cleared to resume play while struggling with the symptoms of postconcussion syndrome.30
There have also been recent reports of late-life sequelae in those who have sustained multiple concussions. Depression and dementia have been suggested in surveys of retired NFL players.31,32 There have also been studies both suggesting14 and questioning33,34 whether multiple concussions result in long-term cognitive deficits. While the evidence available at this time is not firm, there seems to be an increasing belief that multiple concussions can affect long-term cognitive abilities. For these reasons, use caution in making return-to-play decisions for patients with multiple concussions or concussions with long-lasting symptoms.
CORRESPONDENCE Aaron M. Lear, MD, 224 West Exchange Street, Suite 440, Akron, OH 44302; [email protected]
1. CDC. Sports-related recurrent brain injuries—United States. MMWR Morb Mortal Wkly Rep. 1997;46:224-227.
2. CDC. Brain injury awareness month—March 2010. MMWR Morb Mortal Wkly Rep. 2010;59:235.-
3. Epstein D. The damage done. Sports Illustrated. November 1, 2010:42. Available at: http://sportsillustrated.cnn.com/vault/article/magazine/MAG1176377/index.htm. Accessed May 16, 2012.
4. Kliff S. Heading off sports injuries. Newsweek. February 4, 2010. Available at: http://www.newsweek.com/2010/02/04/heading-off-sports-injuries.html. Accessed February 9, 2011.
5. Kluger J. Headbanger nation. Health special: kids and concussions. Time. February 3, 2011. Available at: http://www.time.com/time/specials/packages/article/0,28804,2043395_2043506_2043494,00.html. Accessed February 9, 2011.
6. American Academy of Neurology. Practice parameter: the management of concussion in sports (summary statement). Report of the quality standards subcommittee. Neurology. 1997;48:581-585.
7. Cantu R. Cerebral concussion in sport. Management and prevention. Sports Med. 1992;14:64-74.
8. Kelly J, Nichols J, Filley C, et al. Concussion in sports. Guidelines for the prevention of catastrophic outcome. JAMA. 1991;266:2867-2869.
9. American Academy of Neurology. Position statement on sports concussion. October 2010. AAN policy 2010-36. Available at: http://www.aan.com/globals/axon/assets/7913.pdf. Accessed February 23, 2011.
10. Halstead M, Walter K. Council on Sports Medicine and Fitness. American Academy of Pediatrics. Clinical report—sport-related concussion in children and adolescents. Pediatrics. 2010;126:597-615.
11. Herring SA, Cantu RC, Guskiewicz KM, et al. Concussion (mild traumatic brain injury) and the team physician: a consensus statement—2011 update. Med Sci Sports Exerc. 2011;43:2412-2422.Available at: http://journals.lww.com/acsm-msse/Fulltext/2011/12000/Concussion__Mild_Traumatic_Brain_Injury__and_the.24.aspx. Accessed February 23, 2011.
12. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport: the 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Br J Sports Med. 2009;43(suppl 1):i76-i90.
13. Ropper A, Gorson K. Clinical practice. Concussion. N Engl J Med. 2007;356:166-172.
14. Reddy C, Collins MW. Sports concussion: management and predictors of outcome. Curr Sports Med Rep. 2009;8:10-15.
15. Guskiewicz KM. Assessment of postural stability following sport-related concussion. Curr Sports Med Rep. 2003;2:24-30.
16. Broglio S, Sosnoff J, Ferrara M. The relationship of athlete-reported concussion symptoms and objective measures of neurocognitive function and postural control. Clin J Sport Med. 2009;19:377-382.
17. Reimann B, Guskiewicz K. Effects of mild head injury on postural stability as measured through clinical balance testing. J Athl Train. 2000;35:19-25.
18. Maddocks D, Dicker G, Saling M. The assessment of orientation following concussion in athletes. Clin J Sport Med. 1995;5:32-35.
19. McCrea M. Standardized mental status assessment of sports concussion. Clin J Sport Med. 2001;11:176-181.
20. Collie A, Maruff P, Makdissi M, et al. CogSport: reliability and correlation with conventional cognitive tests used in postconcussion medical evaluations. Clin J Sport Med. 2003;13:28-32.
21. Erlanger D, Saliba E, Barth J, et al. Monitoring resolution of postconcussion symptoms in athletes: preliminary results of a web-based neuropsychological test protocol. J Athl Train. 2001;36:280-287.
22. Schatz P, Pardini J, Lovell M, et al. Sensitivity and specificity of the ImPACT Test battery for concussion in athletes. Arch Clin Neuropsychol. 2006;21:91-99.
23. Schatz P, Putz B. Cross-validation of measures used for computer-based assessment of concussion. Appl Neuropsychol. 2006;13:151-159.
24. Kirkwood M, Randolph C, Yeates K. Returning pediatric athletes to play after concussion: the evidence (or lack thereof) behind baseline neuropsychological testing. Acta Pædiatr. 2009;98:1409-1411.
25. Randolph C. Baseline neuropsychological testing in managing sport-related concussion: does it modify risk? Curr Sports Med Rep. 2011;10:21-26.
26. McCrory P, Collie A, Anderson V, et al. Can we manage sport related concussion in children the same as in adults? Br J Sports Med. 2004;38:516-519.
27. d’Hemecourt P. Subacute symptoms of sports-related concussion outpatient management and return to play. Clin Sports Med. 2011;30:63-72.
28. Concussion laws. Available at: http://www.sportsconcussions.org/laws.html. Accessed July 5, 2011.
29. Wetjen N, Pichelmann M, Atkinson J. Second impact syndrome: concussion and second injury brain complications. J Am Coll Surg. 2010;211:553-557.
30. Jotwani V, Harmon KG. Postconcussion syndrome in athletes. Curr Sports Med Rep. 2010;9:21-26.
31. Guskiewicz K, Marshall S, Bailes J, et al. Association between recurrent concussion and late-life cognitive impairment in retired professional football players. Neurosurgery. 2005;57:719-726.
32. Guskiewicz K, Marshall S, Bailes J, et al. Recurrent concussion and risk of depression in retired professional football players. Med Sci Sports Exerc. 2007;39:903-909.
33. Belanger H, Spiegel E, Vanderploeg R. Neuropsychological performance following a history of multiple self-reported concussions: a meta-analysis. J Int Neuropsychol Soc. 2010;16:262-267.
34. Burce J, Echemendia R. History of multiple self-reported concussions is not associated with reduced cognitive abilities. Neurosurgery. 2009;64:100-106.
1. CDC. Sports-related recurrent brain injuries—United States. MMWR Morb Mortal Wkly Rep. 1997;46:224-227.
2. CDC. Brain injury awareness month—March 2010. MMWR Morb Mortal Wkly Rep. 2010;59:235.-
3. Epstein D. The damage done. Sports Illustrated. November 1, 2010:42. Available at: http://sportsillustrated.cnn.com/vault/article/magazine/MAG1176377/index.htm. Accessed May 16, 2012.
4. Kliff S. Heading off sports injuries. Newsweek. February 4, 2010. Available at: http://www.newsweek.com/2010/02/04/heading-off-sports-injuries.html. Accessed February 9, 2011.
5. Kluger J. Headbanger nation. Health special: kids and concussions. Time. February 3, 2011. Available at: http://www.time.com/time/specials/packages/article/0,28804,2043395_2043506_2043494,00.html. Accessed February 9, 2011.
6. American Academy of Neurology. Practice parameter: the management of concussion in sports (summary statement). Report of the quality standards subcommittee. Neurology. 1997;48:581-585.
7. Cantu R. Cerebral concussion in sport. Management and prevention. Sports Med. 1992;14:64-74.
8. Kelly J, Nichols J, Filley C, et al. Concussion in sports. Guidelines for the prevention of catastrophic outcome. JAMA. 1991;266:2867-2869.
9. American Academy of Neurology. Position statement on sports concussion. October 2010. AAN policy 2010-36. Available at: http://www.aan.com/globals/axon/assets/7913.pdf. Accessed February 23, 2011.
10. Halstead M, Walter K. Council on Sports Medicine and Fitness. American Academy of Pediatrics. Clinical report—sport-related concussion in children and adolescents. Pediatrics. 2010;126:597-615.
11. Herring SA, Cantu RC, Guskiewicz KM, et al. Concussion (mild traumatic brain injury) and the team physician: a consensus statement—2011 update. Med Sci Sports Exerc. 2011;43:2412-2422.Available at: http://journals.lww.com/acsm-msse/Fulltext/2011/12000/Concussion__Mild_Traumatic_Brain_Injury__and_the.24.aspx. Accessed February 23, 2011.
12. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport: the 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Br J Sports Med. 2009;43(suppl 1):i76-i90.
13. Ropper A, Gorson K. Clinical practice. Concussion. N Engl J Med. 2007;356:166-172.
14. Reddy C, Collins MW. Sports concussion: management and predictors of outcome. Curr Sports Med Rep. 2009;8:10-15.
15. Guskiewicz KM. Assessment of postural stability following sport-related concussion. Curr Sports Med Rep. 2003;2:24-30.
16. Broglio S, Sosnoff J, Ferrara M. The relationship of athlete-reported concussion symptoms and objective measures of neurocognitive function and postural control. Clin J Sport Med. 2009;19:377-382.
17. Reimann B, Guskiewicz K. Effects of mild head injury on postural stability as measured through clinical balance testing. J Athl Train. 2000;35:19-25.
18. Maddocks D, Dicker G, Saling M. The assessment of orientation following concussion in athletes. Clin J Sport Med. 1995;5:32-35.
19. McCrea M. Standardized mental status assessment of sports concussion. Clin J Sport Med. 2001;11:176-181.
20. Collie A, Maruff P, Makdissi M, et al. CogSport: reliability and correlation with conventional cognitive tests used in postconcussion medical evaluations. Clin J Sport Med. 2003;13:28-32.
21. Erlanger D, Saliba E, Barth J, et al. Monitoring resolution of postconcussion symptoms in athletes: preliminary results of a web-based neuropsychological test protocol. J Athl Train. 2001;36:280-287.
22. Schatz P, Pardini J, Lovell M, et al. Sensitivity and specificity of the ImPACT Test battery for concussion in athletes. Arch Clin Neuropsychol. 2006;21:91-99.
23. Schatz P, Putz B. Cross-validation of measures used for computer-based assessment of concussion. Appl Neuropsychol. 2006;13:151-159.
24. Kirkwood M, Randolph C, Yeates K. Returning pediatric athletes to play after concussion: the evidence (or lack thereof) behind baseline neuropsychological testing. Acta Pædiatr. 2009;98:1409-1411.
25. Randolph C. Baseline neuropsychological testing in managing sport-related concussion: does it modify risk? Curr Sports Med Rep. 2011;10:21-26.
26. McCrory P, Collie A, Anderson V, et al. Can we manage sport related concussion in children the same as in adults? Br J Sports Med. 2004;38:516-519.
27. d’Hemecourt P. Subacute symptoms of sports-related concussion outpatient management and return to play. Clin Sports Med. 2011;30:63-72.
28. Concussion laws. Available at: http://www.sportsconcussions.org/laws.html. Accessed July 5, 2011.
29. Wetjen N, Pichelmann M, Atkinson J. Second impact syndrome: concussion and second injury brain complications. J Am Coll Surg. 2010;211:553-557.
30. Jotwani V, Harmon KG. Postconcussion syndrome in athletes. Curr Sports Med Rep. 2010;9:21-26.
31. Guskiewicz K, Marshall S, Bailes J, et al. Association between recurrent concussion and late-life cognitive impairment in retired professional football players. Neurosurgery. 2005;57:719-726.
32. Guskiewicz K, Marshall S, Bailes J, et al. Recurrent concussion and risk of depression in retired professional football players. Med Sci Sports Exerc. 2007;39:903-909.
33. Belanger H, Spiegel E, Vanderploeg R. Neuropsychological performance following a history of multiple self-reported concussions: a meta-analysis. J Int Neuropsychol Soc. 2010;16:262-267.
34. Burce J, Echemendia R. History of multiple self-reported concussions is not associated with reduced cognitive abilities. Neurosurgery. 2009;64:100-106.
Community Oncology Podcast - Erwinia asparaginase for acute lymphoblastic leukemia
Join Community Oncology Editor-in Chief Dr David H. Henry for an audio tour of the May issue, featuring "Erwinia asparaginase for acute lymphoblastic leukemia in children with hypersensitivity to E. coli-derived asparaginase" and "Creating a community-based, patient-centered cancer survivorship program."
Join Community Oncology Editor-in Chief Dr David H. Henry for an audio tour of the May issue, featuring "Erwinia asparaginase for acute lymphoblastic leukemia in children with hypersensitivity to E. coli-derived asparaginase" and "Creating a community-based, patient-centered cancer survivorship program."
Join Community Oncology Editor-in Chief Dr David H. Henry for an audio tour of the May issue, featuring "Erwinia asparaginase for acute lymphoblastic leukemia in children with hypersensitivity to E. coli-derived asparaginase" and "Creating a community-based, patient-centered cancer survivorship program."
Statins Appear Safe, Even Beneficial, in Cirrhosis
SAN DIEGO – Statin therapy is not only safe for patients with cirrhosis, it may slow the progression of their liver disease to hepatic decompensation and help them live longer, a study has shown.
The findings, reported at the annual Digestive Disease Week, should help allay fears that decreased hepatic clearance of statins could lead to complications in patients with advanced liver disease, as was previously hypothesized, said lead investigator Dr. Sonal Kumar.
"In fact, it seems the opposite may be true," said Dr. Kumar of Brigham and Women’s Hospital, Boston, referring to the results of her retrospective study in which statin therapy in cirrhosis patients was associated with a decreased risk of hepatic decompensation, a delay in the time to decompensation, and reduced all-cause mortality, compared with cirrhosis patients not taking statins.
The investigators were aware that some clinicians either do not initiate statin therapy or discontinue statins in patients with advanced liver disease because of perceived safety concerns. Dr. Kumar and her colleagues sought to determine the actual effect of statin therapy on the risk of hepatic decomposition in cirrhosis.
They identified all patients with biopsy-proven cirrhosis who had taken statins for a minimum of 3 months for treatment of dyslipidemia. A control population of cirrhosis patients not on statins was matched 2:1 for age, gender, and Child-Pugh class from the Partners HealthCare System Research Patient Data Registry, which includes demographic and diagnostic information on patients treated at Massachusetts General Hospital and Brigham and Women’s Hospital.
The primary outcomes of the study were hepatic decompensation, defined as the development of ascites, jaundice (bilirubin greater than 2.5 mg/dL), hepatic encephalopathy, or variceal hemorrhage, and time to decompensation. Mortality was a secondary outcome, Dr. Kumar explained.
The investigators created a Cox proportional hazards model for decompensation to control for age, Child-Pugh class, diabetes, coronary artery disease, and hepatocellular carcinoma, and they used conditional logistic regression to assess mortality, she said.
Of 243 cirrhosis patients included in the analysis, 81 were statin users and 162 were matched controls. "In each group, approximately 70% of patients were Child-Pugh A and 30% were Child-Pugh B/C, and the MELD [Model for End-Stage Liver Disease] score, albumin, presence of varices, and beta-blocker use were similar between groups," Dr. Kumar noted. In the statin group, which was followed for a mean of 1,756 days, decompensation was reported in 31 patients (38.2%), compared with 80 patients (50.62%) in the control group.
The control patients were followed for a mean of 1,503 days, and on Cox analysis, "statin therapy was the only factor significantly associated with lower decompensation risk, with a hazard ratio of 0.46." Additionally, Kaplan-Meier curves showed a significantly longer time to decompensation in patients receiving statin therapy, she said. In subgroup analyses, significantly longer time to decompensation was observed in Child-Pugh A and Child-Pugh B/C patients.
Overall mortality was significantly lower in the statin group, at 37.0%, than in the control group, at 50.6%, said Dr. Kumar. Statin use remained significantly associated with decreased mortality in multivariate analysis, with an odds ratio of 0.36, while coronary artery disease and hepatocellular carcinoma were associated with increased mortality, with respective odds ratios of 3.6 and 4.9.
There were no statistically significant differences in cause of death between the two groups, "however it is important to note that cause of death was not documented for approximately one-third of the study patients, so we cannot make definitive statements about whether patients on statins were less likely to die of liver-related or cardiovascular causes than patients in the control group," said Dr. Kumar.
The apparent hepatoprotective effect of statin therapy in cirrhosis patients may be a function of previously observed hemodynamic and molecular effects of statins, Dr. Kumar hypothesized. Sinusoidal endothelial dysfunction with decreased nitric oxide production contributes to increased hepatic resistance in cirrhosis, she explained. Just as statins improve endothelial dysfunction in the peripheral vasculature, they may also improve the vascular disturbances that contribute to portal hypertension in cirrhosis by selectively increasing nitric oxide availability in the liver, thus reducing pressures, she said.
The retrospective design of the study limits the conclusions that can be taken from it. Specifically, "we can’t say that all patients with liver disease should be prescribed statins," Dr. Kumar said. "What we can say is that statin therapy is safe in this population, it may be beneficial for its effects on the liver as well as the cardiovascular system, and clinicians should not hesitate to prescribe it for appropriate cardiovascular indications in cirrhosis patients." The findings also indicate that prospective studies are warranted to clarify the role of statins in advanced liver disease, she stressed.
Dr. Kumar disclosed no relevant financial conflicts of interest.
SAN DIEGO – Statin therapy is not only safe for patients with cirrhosis, it may slow the progression of their liver disease to hepatic decompensation and help them live longer, a study has shown.
The findings, reported at the annual Digestive Disease Week, should help allay fears that decreased hepatic clearance of statins could lead to complications in patients with advanced liver disease, as was previously hypothesized, said lead investigator Dr. Sonal Kumar.
"In fact, it seems the opposite may be true," said Dr. Kumar of Brigham and Women’s Hospital, Boston, referring to the results of her retrospective study in which statin therapy in cirrhosis patients was associated with a decreased risk of hepatic decompensation, a delay in the time to decompensation, and reduced all-cause mortality, compared with cirrhosis patients not taking statins.
The investigators were aware that some clinicians either do not initiate statin therapy or discontinue statins in patients with advanced liver disease because of perceived safety concerns. Dr. Kumar and her colleagues sought to determine the actual effect of statin therapy on the risk of hepatic decomposition in cirrhosis.
They identified all patients with biopsy-proven cirrhosis who had taken statins for a minimum of 3 months for treatment of dyslipidemia. A control population of cirrhosis patients not on statins was matched 2:1 for age, gender, and Child-Pugh class from the Partners HealthCare System Research Patient Data Registry, which includes demographic and diagnostic information on patients treated at Massachusetts General Hospital and Brigham and Women’s Hospital.
The primary outcomes of the study were hepatic decompensation, defined as the development of ascites, jaundice (bilirubin greater than 2.5 mg/dL), hepatic encephalopathy, or variceal hemorrhage, and time to decompensation. Mortality was a secondary outcome, Dr. Kumar explained.
The investigators created a Cox proportional hazards model for decompensation to control for age, Child-Pugh class, diabetes, coronary artery disease, and hepatocellular carcinoma, and they used conditional logistic regression to assess mortality, she said.
Of 243 cirrhosis patients included in the analysis, 81 were statin users and 162 were matched controls. "In each group, approximately 70% of patients were Child-Pugh A and 30% were Child-Pugh B/C, and the MELD [Model for End-Stage Liver Disease] score, albumin, presence of varices, and beta-blocker use were similar between groups," Dr. Kumar noted. In the statin group, which was followed for a mean of 1,756 days, decompensation was reported in 31 patients (38.2%), compared with 80 patients (50.62%) in the control group.
The control patients were followed for a mean of 1,503 days, and on Cox analysis, "statin therapy was the only factor significantly associated with lower decompensation risk, with a hazard ratio of 0.46." Additionally, Kaplan-Meier curves showed a significantly longer time to decompensation in patients receiving statin therapy, she said. In subgroup analyses, significantly longer time to decompensation was observed in Child-Pugh A and Child-Pugh B/C patients.
Overall mortality was significantly lower in the statin group, at 37.0%, than in the control group, at 50.6%, said Dr. Kumar. Statin use remained significantly associated with decreased mortality in multivariate analysis, with an odds ratio of 0.36, while coronary artery disease and hepatocellular carcinoma were associated with increased mortality, with respective odds ratios of 3.6 and 4.9.
There were no statistically significant differences in cause of death between the two groups, "however it is important to note that cause of death was not documented for approximately one-third of the study patients, so we cannot make definitive statements about whether patients on statins were less likely to die of liver-related or cardiovascular causes than patients in the control group," said Dr. Kumar.
The apparent hepatoprotective effect of statin therapy in cirrhosis patients may be a function of previously observed hemodynamic and molecular effects of statins, Dr. Kumar hypothesized. Sinusoidal endothelial dysfunction with decreased nitric oxide production contributes to increased hepatic resistance in cirrhosis, she explained. Just as statins improve endothelial dysfunction in the peripheral vasculature, they may also improve the vascular disturbances that contribute to portal hypertension in cirrhosis by selectively increasing nitric oxide availability in the liver, thus reducing pressures, she said.
The retrospective design of the study limits the conclusions that can be taken from it. Specifically, "we can’t say that all patients with liver disease should be prescribed statins," Dr. Kumar said. "What we can say is that statin therapy is safe in this population, it may be beneficial for its effects on the liver as well as the cardiovascular system, and clinicians should not hesitate to prescribe it for appropriate cardiovascular indications in cirrhosis patients." The findings also indicate that prospective studies are warranted to clarify the role of statins in advanced liver disease, she stressed.
Dr. Kumar disclosed no relevant financial conflicts of interest.
SAN DIEGO – Statin therapy is not only safe for patients with cirrhosis, it may slow the progression of their liver disease to hepatic decompensation and help them live longer, a study has shown.
The findings, reported at the annual Digestive Disease Week, should help allay fears that decreased hepatic clearance of statins could lead to complications in patients with advanced liver disease, as was previously hypothesized, said lead investigator Dr. Sonal Kumar.
"In fact, it seems the opposite may be true," said Dr. Kumar of Brigham and Women’s Hospital, Boston, referring to the results of her retrospective study in which statin therapy in cirrhosis patients was associated with a decreased risk of hepatic decompensation, a delay in the time to decompensation, and reduced all-cause mortality, compared with cirrhosis patients not taking statins.
The investigators were aware that some clinicians either do not initiate statin therapy or discontinue statins in patients with advanced liver disease because of perceived safety concerns. Dr. Kumar and her colleagues sought to determine the actual effect of statin therapy on the risk of hepatic decomposition in cirrhosis.
They identified all patients with biopsy-proven cirrhosis who had taken statins for a minimum of 3 months for treatment of dyslipidemia. A control population of cirrhosis patients not on statins was matched 2:1 for age, gender, and Child-Pugh class from the Partners HealthCare System Research Patient Data Registry, which includes demographic and diagnostic information on patients treated at Massachusetts General Hospital and Brigham and Women’s Hospital.
The primary outcomes of the study were hepatic decompensation, defined as the development of ascites, jaundice (bilirubin greater than 2.5 mg/dL), hepatic encephalopathy, or variceal hemorrhage, and time to decompensation. Mortality was a secondary outcome, Dr. Kumar explained.
The investigators created a Cox proportional hazards model for decompensation to control for age, Child-Pugh class, diabetes, coronary artery disease, and hepatocellular carcinoma, and they used conditional logistic regression to assess mortality, she said.
Of 243 cirrhosis patients included in the analysis, 81 were statin users and 162 were matched controls. "In each group, approximately 70% of patients were Child-Pugh A and 30% were Child-Pugh B/C, and the MELD [Model for End-Stage Liver Disease] score, albumin, presence of varices, and beta-blocker use were similar between groups," Dr. Kumar noted. In the statin group, which was followed for a mean of 1,756 days, decompensation was reported in 31 patients (38.2%), compared with 80 patients (50.62%) in the control group.
The control patients were followed for a mean of 1,503 days, and on Cox analysis, "statin therapy was the only factor significantly associated with lower decompensation risk, with a hazard ratio of 0.46." Additionally, Kaplan-Meier curves showed a significantly longer time to decompensation in patients receiving statin therapy, she said. In subgroup analyses, significantly longer time to decompensation was observed in Child-Pugh A and Child-Pugh B/C patients.
Overall mortality was significantly lower in the statin group, at 37.0%, than in the control group, at 50.6%, said Dr. Kumar. Statin use remained significantly associated with decreased mortality in multivariate analysis, with an odds ratio of 0.36, while coronary artery disease and hepatocellular carcinoma were associated with increased mortality, with respective odds ratios of 3.6 and 4.9.
There were no statistically significant differences in cause of death between the two groups, "however it is important to note that cause of death was not documented for approximately one-third of the study patients, so we cannot make definitive statements about whether patients on statins were less likely to die of liver-related or cardiovascular causes than patients in the control group," said Dr. Kumar.
The apparent hepatoprotective effect of statin therapy in cirrhosis patients may be a function of previously observed hemodynamic and molecular effects of statins, Dr. Kumar hypothesized. Sinusoidal endothelial dysfunction with decreased nitric oxide production contributes to increased hepatic resistance in cirrhosis, she explained. Just as statins improve endothelial dysfunction in the peripheral vasculature, they may also improve the vascular disturbances that contribute to portal hypertension in cirrhosis by selectively increasing nitric oxide availability in the liver, thus reducing pressures, she said.
The retrospective design of the study limits the conclusions that can be taken from it. Specifically, "we can’t say that all patients with liver disease should be prescribed statins," Dr. Kumar said. "What we can say is that statin therapy is safe in this population, it may be beneficial for its effects on the liver as well as the cardiovascular system, and clinicians should not hesitate to prescribe it for appropriate cardiovascular indications in cirrhosis patients." The findings also indicate that prospective studies are warranted to clarify the role of statins in advanced liver disease, she stressed.
Dr. Kumar disclosed no relevant financial conflicts of interest.
FROM THE ANNUAL DIGESTIVE DISEASE WEEK
Major Finding: Among patients with advanced liver disease, the hepatic decompensation rate was 38.2% in patients on statin therapy and 50.6% in those not using statins.
Data Source: This was a retrospective analysis of medical record data for 243 patients with biopsy-proven cirrhosis: 81 taking statins for dyslipidemia and 162 controls.
Disclosures: Dr. Kumar disclosed no relevant financial conflicts of interest.
Banner Good Samaritan Battles VTE in Real Time
Banner Good Samaritan Medical Center in Phoenix is combating hospital-acquired VTE with a quality initiative that uses risk-assessment tools and order sets embedded in the electronic health record (EHR) and real-time interventions with physicians.
Cases of hospital-acquired VTE are identified as they occur and assessed for whether they were preventable, says Lori Porter, DO, academic hospitalist and team leader for Banner Good Samaritan's VTE Committee. "If we think the VTE was preventable, we will call the provider and say, 'Can you tell me why you think this happened?'" she says. (Check out more information about Banner Good Samaritan’s VTE program at the Institute for Healthcare Improvement website.)
The program emphasizes risk re-assessment, appropriate use of extended prophylaxis, and involvement of Banner's house staff. All four hospitalist services at Banner Good Samaritan have been receptive to using the order sets.
Banner Good Samaritan's results include a drop in preventable hospital-acquired VTEs to 25% in 2011 from 45% in 2009, along with a 29% relative risk reduction in DVT and 18% in pulmonary embolism.
The hospital belongs to SHM's VTE Prevention Collaborative, and works with mentor Gregory Maynard, MD, MSc, SFHM, senior vice president of SHM's Center for Healthcare Improvement and Innovation. It uses what Dr. Porter calls "a simple, three-bucket system" for assessing and classifying risk level, derived from the 2008 antithrombotic therapy guidelines from the American College of Chest Physicians (ACCP). However, in February, ACCP issued a new edition of the guidelines, which Dr. Porter has not been eager to embrace.
"They've gone back to a conservative point-scoring system for risk assessment, which seems cumbersome in clinical practice. If a simpler approach has proven to be effective for us, then why commit to making a complicated change?" says Dr. Porter.
Dr. Maynard agrees that the new antithrombotic guidelines have sparked differences of opinion. Dr. Porter's teams, for example, "use the simpler three-bucket model with good results: better prophylaxis, decrease in VTE, and no discernible increase in bleeding," he says. "Improvement teams that want to mimic these results should look at this model, in addition to the models outlined in the ninth edition, and see which models their doctors and nurses would actually use reliably."
Banner Good Samaritan Medical Center in Phoenix is combating hospital-acquired VTE with a quality initiative that uses risk-assessment tools and order sets embedded in the electronic health record (EHR) and real-time interventions with physicians.
Cases of hospital-acquired VTE are identified as they occur and assessed for whether they were preventable, says Lori Porter, DO, academic hospitalist and team leader for Banner Good Samaritan's VTE Committee. "If we think the VTE was preventable, we will call the provider and say, 'Can you tell me why you think this happened?'" she says. (Check out more information about Banner Good Samaritan’s VTE program at the Institute for Healthcare Improvement website.)
The program emphasizes risk re-assessment, appropriate use of extended prophylaxis, and involvement of Banner's house staff. All four hospitalist services at Banner Good Samaritan have been receptive to using the order sets.
Banner Good Samaritan's results include a drop in preventable hospital-acquired VTEs to 25% in 2011 from 45% in 2009, along with a 29% relative risk reduction in DVT and 18% in pulmonary embolism.
The hospital belongs to SHM's VTE Prevention Collaborative, and works with mentor Gregory Maynard, MD, MSc, SFHM, senior vice president of SHM's Center for Healthcare Improvement and Innovation. It uses what Dr. Porter calls "a simple, three-bucket system" for assessing and classifying risk level, derived from the 2008 antithrombotic therapy guidelines from the American College of Chest Physicians (ACCP). However, in February, ACCP issued a new edition of the guidelines, which Dr. Porter has not been eager to embrace.
"They've gone back to a conservative point-scoring system for risk assessment, which seems cumbersome in clinical practice. If a simpler approach has proven to be effective for us, then why commit to making a complicated change?" says Dr. Porter.
Dr. Maynard agrees that the new antithrombotic guidelines have sparked differences of opinion. Dr. Porter's teams, for example, "use the simpler three-bucket model with good results: better prophylaxis, decrease in VTE, and no discernible increase in bleeding," he says. "Improvement teams that want to mimic these results should look at this model, in addition to the models outlined in the ninth edition, and see which models their doctors and nurses would actually use reliably."
Banner Good Samaritan Medical Center in Phoenix is combating hospital-acquired VTE with a quality initiative that uses risk-assessment tools and order sets embedded in the electronic health record (EHR) and real-time interventions with physicians.
Cases of hospital-acquired VTE are identified as they occur and assessed for whether they were preventable, says Lori Porter, DO, academic hospitalist and team leader for Banner Good Samaritan's VTE Committee. "If we think the VTE was preventable, we will call the provider and say, 'Can you tell me why you think this happened?'" she says. (Check out more information about Banner Good Samaritan’s VTE program at the Institute for Healthcare Improvement website.)
The program emphasizes risk re-assessment, appropriate use of extended prophylaxis, and involvement of Banner's house staff. All four hospitalist services at Banner Good Samaritan have been receptive to using the order sets.
Banner Good Samaritan's results include a drop in preventable hospital-acquired VTEs to 25% in 2011 from 45% in 2009, along with a 29% relative risk reduction in DVT and 18% in pulmonary embolism.
The hospital belongs to SHM's VTE Prevention Collaborative, and works with mentor Gregory Maynard, MD, MSc, SFHM, senior vice president of SHM's Center for Healthcare Improvement and Innovation. It uses what Dr. Porter calls "a simple, three-bucket system" for assessing and classifying risk level, derived from the 2008 antithrombotic therapy guidelines from the American College of Chest Physicians (ACCP). However, in February, ACCP issued a new edition of the guidelines, which Dr. Porter has not been eager to embrace.
"They've gone back to a conservative point-scoring system for risk assessment, which seems cumbersome in clinical practice. If a simpler approach has proven to be effective for us, then why commit to making a complicated change?" says Dr. Porter.
Dr. Maynard agrees that the new antithrombotic guidelines have sparked differences of opinion. Dr. Porter's teams, for example, "use the simpler three-bucket model with good results: better prophylaxis, decrease in VTE, and no discernible increase in bleeding," he says. "Improvement teams that want to mimic these results should look at this model, in addition to the models outlined in the ninth edition, and see which models their doctors and nurses would actually use reliably."
Report: EHR Implementation Associated with Quality
Hospitals that have made it to the advanced stages of electronic health record (EHR) implementation are significantly more likely to set national benchmarks for quality and safety performance, according to the 2012 HIMSS Analytics Report.
The research (PDF), sponsored by Thomson Reuters and HIMSS Analytics, found a correlation between hospitals that are both ranked in the Thomson Reuters 100 Top Hospitals and at the upper end of the seven-stage HIMMS scale for EHR adoption.
While the link between electronic implementation and quality is important, William Bria, MD, chief medical information officer at Shriners Hospitals for Children in Philadelphia, cautions hospitalists and others from taking too much comfort in it. Simply implementing EHR and other technologies doesn't work, he says; the system has to be crafted in conjunction with its users.
"The best-led organizations in the country are using the metrics of safety and quality of care right alongside the implementation plan of their [health IT] programs," says Dr. Bria. "And the only way this occurs, of course, is if the partnering between executive and technological leadership and clinical leadership occurs."
Dr. Bria views research on the success of EHRs in improving hospital performance as an opportunity for hospitalists to get more involved in both the planning and implementation processes. He urges hospitalists to work with other physicians and IT staffers to learn how best to use their EHR, and not assume they can master complex software systems as easily as they understand smartphones and tablet computers.
"You can buy a piano and bang on it with your fist, and you won't really attract anybody to listen to your music," Dr. Bria says. "On the other hand, if you learn how to play, you study hard, and you learn the nuances of musicianship, you can become a Van Cliburn."
Hospitals that have made it to the advanced stages of electronic health record (EHR) implementation are significantly more likely to set national benchmarks for quality and safety performance, according to the 2012 HIMSS Analytics Report.
The research (PDF), sponsored by Thomson Reuters and HIMSS Analytics, found a correlation between hospitals that are both ranked in the Thomson Reuters 100 Top Hospitals and at the upper end of the seven-stage HIMMS scale for EHR adoption.
While the link between electronic implementation and quality is important, William Bria, MD, chief medical information officer at Shriners Hospitals for Children in Philadelphia, cautions hospitalists and others from taking too much comfort in it. Simply implementing EHR and other technologies doesn't work, he says; the system has to be crafted in conjunction with its users.
"The best-led organizations in the country are using the metrics of safety and quality of care right alongside the implementation plan of their [health IT] programs," says Dr. Bria. "And the only way this occurs, of course, is if the partnering between executive and technological leadership and clinical leadership occurs."
Dr. Bria views research on the success of EHRs in improving hospital performance as an opportunity for hospitalists to get more involved in both the planning and implementation processes. He urges hospitalists to work with other physicians and IT staffers to learn how best to use their EHR, and not assume they can master complex software systems as easily as they understand smartphones and tablet computers.
"You can buy a piano and bang on it with your fist, and you won't really attract anybody to listen to your music," Dr. Bria says. "On the other hand, if you learn how to play, you study hard, and you learn the nuances of musicianship, you can become a Van Cliburn."
Hospitals that have made it to the advanced stages of electronic health record (EHR) implementation are significantly more likely to set national benchmarks for quality and safety performance, according to the 2012 HIMSS Analytics Report.
The research (PDF), sponsored by Thomson Reuters and HIMSS Analytics, found a correlation between hospitals that are both ranked in the Thomson Reuters 100 Top Hospitals and at the upper end of the seven-stage HIMMS scale for EHR adoption.
While the link between electronic implementation and quality is important, William Bria, MD, chief medical information officer at Shriners Hospitals for Children in Philadelphia, cautions hospitalists and others from taking too much comfort in it. Simply implementing EHR and other technologies doesn't work, he says; the system has to be crafted in conjunction with its users.
"The best-led organizations in the country are using the metrics of safety and quality of care right alongside the implementation plan of their [health IT] programs," says Dr. Bria. "And the only way this occurs, of course, is if the partnering between executive and technological leadership and clinical leadership occurs."
Dr. Bria views research on the success of EHRs in improving hospital performance as an opportunity for hospitalists to get more involved in both the planning and implementation processes. He urges hospitalists to work with other physicians and IT staffers to learn how best to use their EHR, and not assume they can master complex software systems as easily as they understand smartphones and tablet computers.
"You can buy a piano and bang on it with your fist, and you won't really attract anybody to listen to your music," Dr. Bria says. "On the other hand, if you learn how to play, you study hard, and you learn the nuances of musicianship, you can become a Van Cliburn."
'The Talk' About PSA Screening Just Got Thornier
Nuance is not a commonly cited virtue of American discourse, as you well know if you’ve watched reality television of late, or, for that matter, any recent political debate. And that’s what makes me nervous about the recent decision by the U.S. Preventive Services Task Force (USPSTF) to recommend against routine screening for prostate cancer using prostate-specific antigen levels.
I’m neither a physician nor a biostatistician; rest assured, I won’t argue the science here. But I do worry about the psychological implications of a Grade D recommendation (considered "at least fair" evidence) that screening does more harm to men than good.
The task force’s report, published online May 21 in Annals of Internal Medicine (annals.org), makes some excellent points about the need for more reliable screening measures and real quality-of-life costs associated with false positive PSA results and aggressive treatment of what is, in many cases but not all, a slow-growing disease.
Its call for better research deserves special mention. Prostate cancer, in my opinion, has long been a neglected step-brother in cancer research funding, despite the fact that it kills more American men than does any other cancer, except lung cancer. Just because I was curious, I compared this week the number of hits on PubMed for the search terms "prostate cancer" and "screening" versus "breast cancer" and "screening." To be sure, it’s a crude measure of relative attention, but the disparate tally was striking: 55,758 to 129,451.
The task force report also offers physicians a brief, handy guide on how to talk with patients about the latest findings, including three generic "patient scenarios." I think that’s fine, as far as it goes, but what the guide fails to capture is the nuance of American attitudes toward screening, toward medicine in general (and especially large, impersonal task forces known by their acronyms), toward preventive health care, and toward prostate cancer itself.
It will be those attitudes physicians will encounter once patients, their partners, and families hear the recommendations in a 12-second sound bite, while channel-flipping on their way to an update on the Kardashian family.
There will be patients, I suspect, who will completely disregard the recommendations; a few, perhaps, because they’ve read of the scientific objections of many dubious urologists.
More, undoubtedly, will suspect a conspiracy between medicine and insurance companies bent on depriving patients of life-saving treatment in the interest of saving a few bucks.
Others won’t hear the word "screening," and will refuse to see the doctor when they suffer dysuria, hematuria, or pain, telling their annoying wives they heard on the news there’s no point in getting a test for that.
Some patients will insist on the PSA every year beginning in their 30s and will press for a biopsy if their numbers wobble a bit from year to year – a strategy they would have pursued regardless of recommendations to the contrary today, tomorrow, or in 10 years.
Unfortunately, black men will hear the news and may resist getting a PSA even in the face of a family history of prostate cancer and the deplorable under-representation of African American men in the studies on which the recommendation was made. (Just 4% of men enrolled in the U.S. Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (N. Engl. J. Med. 2009;360:1310-9) were non-Hispanic blacks; the ethnicity of those in the other trials wasn’t even reported, despite the fact that black men die of prostate cancer at a rate double that of white men.)
More than a few individuals will consider the recommendations against the backdrop of evidence that scientists call "anecdote" and regular folks call "Uncle Bill." If he died at 74, ravaged by bone pain, there’s a good bet that the nephews in the family will still be urging the doctor to check the box on the lab slip marked "PSA." If, on the other hand, Albert down the street had prostate surgery, and never regained the ability to urinate normally (or have an erection, it might be whispered), the new recommendations might be welcomed just fine.
My point is, the press conferences and headlines that trumpet controversial new cancer guidelines come and go, the acronym-laced logos repacked into boxes and the microphone cords looped into their cases. But the aftershocks ripple for months, as physicians in their small offices try to weigh in with their own beliefs and experiences, as they manage the fear, denial, and doubt that the patients bring in on their own.
Cost matters. Risks and benefits must be given appropriate weight. Medicine is, today as always, a journey negotiated in the partial fog of unknowns.
But when a recommendation is drastic and not universally agreed-upon by the medical community, my wish would be for a bit more nuance in the telling, to make more sense of it to us all.
Nuance is not a commonly cited virtue of American discourse, as you well know if you’ve watched reality television of late, or, for that matter, any recent political debate. And that’s what makes me nervous about the recent decision by the U.S. Preventive Services Task Force (USPSTF) to recommend against routine screening for prostate cancer using prostate-specific antigen levels.
I’m neither a physician nor a biostatistician; rest assured, I won’t argue the science here. But I do worry about the psychological implications of a Grade D recommendation (considered "at least fair" evidence) that screening does more harm to men than good.
The task force’s report, published online May 21 in Annals of Internal Medicine (annals.org), makes some excellent points about the need for more reliable screening measures and real quality-of-life costs associated with false positive PSA results and aggressive treatment of what is, in many cases but not all, a slow-growing disease.
Its call for better research deserves special mention. Prostate cancer, in my opinion, has long been a neglected step-brother in cancer research funding, despite the fact that it kills more American men than does any other cancer, except lung cancer. Just because I was curious, I compared this week the number of hits on PubMed for the search terms "prostate cancer" and "screening" versus "breast cancer" and "screening." To be sure, it’s a crude measure of relative attention, but the disparate tally was striking: 55,758 to 129,451.
The task force report also offers physicians a brief, handy guide on how to talk with patients about the latest findings, including three generic "patient scenarios." I think that’s fine, as far as it goes, but what the guide fails to capture is the nuance of American attitudes toward screening, toward medicine in general (and especially large, impersonal task forces known by their acronyms), toward preventive health care, and toward prostate cancer itself.
It will be those attitudes physicians will encounter once patients, their partners, and families hear the recommendations in a 12-second sound bite, while channel-flipping on their way to an update on the Kardashian family.
There will be patients, I suspect, who will completely disregard the recommendations; a few, perhaps, because they’ve read of the scientific objections of many dubious urologists.
More, undoubtedly, will suspect a conspiracy between medicine and insurance companies bent on depriving patients of life-saving treatment in the interest of saving a few bucks.
Others won’t hear the word "screening," and will refuse to see the doctor when they suffer dysuria, hematuria, or pain, telling their annoying wives they heard on the news there’s no point in getting a test for that.
Some patients will insist on the PSA every year beginning in their 30s and will press for a biopsy if their numbers wobble a bit from year to year – a strategy they would have pursued regardless of recommendations to the contrary today, tomorrow, or in 10 years.
Unfortunately, black men will hear the news and may resist getting a PSA even in the face of a family history of prostate cancer and the deplorable under-representation of African American men in the studies on which the recommendation was made. (Just 4% of men enrolled in the U.S. Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (N. Engl. J. Med. 2009;360:1310-9) were non-Hispanic blacks; the ethnicity of those in the other trials wasn’t even reported, despite the fact that black men die of prostate cancer at a rate double that of white men.)
More than a few individuals will consider the recommendations against the backdrop of evidence that scientists call "anecdote" and regular folks call "Uncle Bill." If he died at 74, ravaged by bone pain, there’s a good bet that the nephews in the family will still be urging the doctor to check the box on the lab slip marked "PSA." If, on the other hand, Albert down the street had prostate surgery, and never regained the ability to urinate normally (or have an erection, it might be whispered), the new recommendations might be welcomed just fine.
My point is, the press conferences and headlines that trumpet controversial new cancer guidelines come and go, the acronym-laced logos repacked into boxes and the microphone cords looped into their cases. But the aftershocks ripple for months, as physicians in their small offices try to weigh in with their own beliefs and experiences, as they manage the fear, denial, and doubt that the patients bring in on their own.
Cost matters. Risks and benefits must be given appropriate weight. Medicine is, today as always, a journey negotiated in the partial fog of unknowns.
But when a recommendation is drastic and not universally agreed-upon by the medical community, my wish would be for a bit more nuance in the telling, to make more sense of it to us all.
Nuance is not a commonly cited virtue of American discourse, as you well know if you’ve watched reality television of late, or, for that matter, any recent political debate. And that’s what makes me nervous about the recent decision by the U.S. Preventive Services Task Force (USPSTF) to recommend against routine screening for prostate cancer using prostate-specific antigen levels.
I’m neither a physician nor a biostatistician; rest assured, I won’t argue the science here. But I do worry about the psychological implications of a Grade D recommendation (considered "at least fair" evidence) that screening does more harm to men than good.
The task force’s report, published online May 21 in Annals of Internal Medicine (annals.org), makes some excellent points about the need for more reliable screening measures and real quality-of-life costs associated with false positive PSA results and aggressive treatment of what is, in many cases but not all, a slow-growing disease.
Its call for better research deserves special mention. Prostate cancer, in my opinion, has long been a neglected step-brother in cancer research funding, despite the fact that it kills more American men than does any other cancer, except lung cancer. Just because I was curious, I compared this week the number of hits on PubMed for the search terms "prostate cancer" and "screening" versus "breast cancer" and "screening." To be sure, it’s a crude measure of relative attention, but the disparate tally was striking: 55,758 to 129,451.
The task force report also offers physicians a brief, handy guide on how to talk with patients about the latest findings, including three generic "patient scenarios." I think that’s fine, as far as it goes, but what the guide fails to capture is the nuance of American attitudes toward screening, toward medicine in general (and especially large, impersonal task forces known by their acronyms), toward preventive health care, and toward prostate cancer itself.
It will be those attitudes physicians will encounter once patients, their partners, and families hear the recommendations in a 12-second sound bite, while channel-flipping on their way to an update on the Kardashian family.
There will be patients, I suspect, who will completely disregard the recommendations; a few, perhaps, because they’ve read of the scientific objections of many dubious urologists.
More, undoubtedly, will suspect a conspiracy between medicine and insurance companies bent on depriving patients of life-saving treatment in the interest of saving a few bucks.
Others won’t hear the word "screening," and will refuse to see the doctor when they suffer dysuria, hematuria, or pain, telling their annoying wives they heard on the news there’s no point in getting a test for that.
Some patients will insist on the PSA every year beginning in their 30s and will press for a biopsy if their numbers wobble a bit from year to year – a strategy they would have pursued regardless of recommendations to the contrary today, tomorrow, or in 10 years.
Unfortunately, black men will hear the news and may resist getting a PSA even in the face of a family history of prostate cancer and the deplorable under-representation of African American men in the studies on which the recommendation was made. (Just 4% of men enrolled in the U.S. Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (N. Engl. J. Med. 2009;360:1310-9) were non-Hispanic blacks; the ethnicity of those in the other trials wasn’t even reported, despite the fact that black men die of prostate cancer at a rate double that of white men.)
More than a few individuals will consider the recommendations against the backdrop of evidence that scientists call "anecdote" and regular folks call "Uncle Bill." If he died at 74, ravaged by bone pain, there’s a good bet that the nephews in the family will still be urging the doctor to check the box on the lab slip marked "PSA." If, on the other hand, Albert down the street had prostate surgery, and never regained the ability to urinate normally (or have an erection, it might be whispered), the new recommendations might be welcomed just fine.
My point is, the press conferences and headlines that trumpet controversial new cancer guidelines come and go, the acronym-laced logos repacked into boxes and the microphone cords looped into their cases. But the aftershocks ripple for months, as physicians in their small offices try to weigh in with their own beliefs and experiences, as they manage the fear, denial, and doubt that the patients bring in on their own.
Cost matters. Risks and benefits must be given appropriate weight. Medicine is, today as always, a journey negotiated in the partial fog of unknowns.
But when a recommendation is drastic and not universally agreed-upon by the medical community, my wish would be for a bit more nuance in the telling, to make more sense of it to us all.
Race, Sex Affect Congenital Heart Surgery Outcomes
FT. LAUDERDALE, FLA. – Sex and race appear to play a role in outcomes following congenital heart surgery in children and adolescents, according to a new analysis of data from almost 21,000 patients.
Black patients had significantly greater rates of mortality and complications and a significantly longer length of postoperative stay than other races, while female patients had a significantly shorter length of stay than males, Dr. Daniel J. DiBardino reported at the annual meeting of the Society of Thoracic Surgeons.
"The analysis of demographic and clinical data from nearly 21,000 patients in the congenital heart surgery database revealed important associations between gender, race, and outcome," said Dr. DiBardino, who is a cardiac surgeon at the Blair E. Batson Children’s Hospital in Jackson, Miss.
Dr. DiBardino’s study was chosen as a 2011 Richard E. Clark Paper by the Society of Thoracic Surgeons.
The researchers used data from the Society of Thoracic Surgeons Congenital Heart Surgery Database (STS-CHSD). Patients were included in the analysis if they were less than 18 years of age and had undergone cardiac surgery between 2007 and 2009.
Exclusion criteria included centers with more than 15% of data missing for key variables and centers with very small samples (less than five cases).
Data collection included demographics (age, sex, weight, and race) and preoperative data (noncardiac/genetic abnormalities and STS-defined risk factors). Race was classified as white, black, Hispanic, and other.
Operations were classified by STAT Mortality category, which is "a complexity stratification tool based on empiric data from 80,000 cases in STS and EACTS (European Association for Cardio-Thoracic Surgery) databases," said Dr. DiBardino.
The researchers looked at hospital mortality, postoperative length of stay, and complications. Multivariable analyses included dichotomous variables (mortality, complications) and a continuous variable (postoperative length of stay). Models were adjusted for age, weight, noncardiac/genetic abnormalities, any other STS preoperative risk factor, and STAT Mortality category.
In all, 20,399 patients were included from 49 centers. Of these, 54% were male. In terms of race, 55% were white, 17% were black, 16% were Hispanic, and 12% were other.
Based on unadjusted outcomes, there were no differences between the sexes for in-hospital mortality or complications. However, females had significantly shorter postoperative stays. In terms of race, white patients had significantly lower mortality, shorter length of stay, and fewer complications than any of the other racial groups.
In the adjusted multivariate analysis, there was no difference for mortality between the sexes. However, black patients had a significantly greater mortality risk with an odds ratio of 1.67.
Females did have a significantly shorter mean length of stay – 0.8 fewer days. In terms of race, black patients had a significantly longer mean length of stay by 2.4 hospital days, compared with white patients. Hispanic patients also had a significantly longer mean length of stay by almost 1 hospital day.
There was no difference between the sexes in terms of the occurrence of complications. In terms of race, "black patients experienced significantly more complications than other races with an odds ratio of 1.15," according to Dr. DiBardino.
The study is unique with the respect to the use of multivariable models. The researchers measured the association of sex and race with outcomes within each center and then combined the results, in order to mitigate the potential center effects.
"Our results cannot be explained by the possibility that patients of certain races might be disproportionately treated at centers with poorer outcomes in general."
The evaluation of complex relationships between clinical variables and socioeconomic and other factors affecting health care remains a significant challenge.
Since some pertinent socioeconomic data are not collected in the STS-CHSD, an analysis of a linked data set, which capitalizes on the strengths of both the CHSD and those of an administrative claims data set may be the next logical step, said Dr. DiBardino.
Dr. DiBardino and his coinvestigators reported that they have no relevant disclosures.
FT. LAUDERDALE, FLA. – Sex and race appear to play a role in outcomes following congenital heart surgery in children and adolescents, according to a new analysis of data from almost 21,000 patients.
Black patients had significantly greater rates of mortality and complications and a significantly longer length of postoperative stay than other races, while female patients had a significantly shorter length of stay than males, Dr. Daniel J. DiBardino reported at the annual meeting of the Society of Thoracic Surgeons.
"The analysis of demographic and clinical data from nearly 21,000 patients in the congenital heart surgery database revealed important associations between gender, race, and outcome," said Dr. DiBardino, who is a cardiac surgeon at the Blair E. Batson Children’s Hospital in Jackson, Miss.
Dr. DiBardino’s study was chosen as a 2011 Richard E. Clark Paper by the Society of Thoracic Surgeons.
The researchers used data from the Society of Thoracic Surgeons Congenital Heart Surgery Database (STS-CHSD). Patients were included in the analysis if they were less than 18 years of age and had undergone cardiac surgery between 2007 and 2009.
Exclusion criteria included centers with more than 15% of data missing for key variables and centers with very small samples (less than five cases).
Data collection included demographics (age, sex, weight, and race) and preoperative data (noncardiac/genetic abnormalities and STS-defined risk factors). Race was classified as white, black, Hispanic, and other.
Operations were classified by STAT Mortality category, which is "a complexity stratification tool based on empiric data from 80,000 cases in STS and EACTS (European Association for Cardio-Thoracic Surgery) databases," said Dr. DiBardino.
The researchers looked at hospital mortality, postoperative length of stay, and complications. Multivariable analyses included dichotomous variables (mortality, complications) and a continuous variable (postoperative length of stay). Models were adjusted for age, weight, noncardiac/genetic abnormalities, any other STS preoperative risk factor, and STAT Mortality category.
In all, 20,399 patients were included from 49 centers. Of these, 54% were male. In terms of race, 55% were white, 17% were black, 16% were Hispanic, and 12% were other.
Based on unadjusted outcomes, there were no differences between the sexes for in-hospital mortality or complications. However, females had significantly shorter postoperative stays. In terms of race, white patients had significantly lower mortality, shorter length of stay, and fewer complications than any of the other racial groups.
In the adjusted multivariate analysis, there was no difference for mortality between the sexes. However, black patients had a significantly greater mortality risk with an odds ratio of 1.67.
Females did have a significantly shorter mean length of stay – 0.8 fewer days. In terms of race, black patients had a significantly longer mean length of stay by 2.4 hospital days, compared with white patients. Hispanic patients also had a significantly longer mean length of stay by almost 1 hospital day.
There was no difference between the sexes in terms of the occurrence of complications. In terms of race, "black patients experienced significantly more complications than other races with an odds ratio of 1.15," according to Dr. DiBardino.
The study is unique with the respect to the use of multivariable models. The researchers measured the association of sex and race with outcomes within each center and then combined the results, in order to mitigate the potential center effects.
"Our results cannot be explained by the possibility that patients of certain races might be disproportionately treated at centers with poorer outcomes in general."
The evaluation of complex relationships between clinical variables and socioeconomic and other factors affecting health care remains a significant challenge.
Since some pertinent socioeconomic data are not collected in the STS-CHSD, an analysis of a linked data set, which capitalizes on the strengths of both the CHSD and those of an administrative claims data set may be the next logical step, said Dr. DiBardino.
Dr. DiBardino and his coinvestigators reported that they have no relevant disclosures.
FT. LAUDERDALE, FLA. – Sex and race appear to play a role in outcomes following congenital heart surgery in children and adolescents, according to a new analysis of data from almost 21,000 patients.
Black patients had significantly greater rates of mortality and complications and a significantly longer length of postoperative stay than other races, while female patients had a significantly shorter length of stay than males, Dr. Daniel J. DiBardino reported at the annual meeting of the Society of Thoracic Surgeons.
"The analysis of demographic and clinical data from nearly 21,000 patients in the congenital heart surgery database revealed important associations between gender, race, and outcome," said Dr. DiBardino, who is a cardiac surgeon at the Blair E. Batson Children’s Hospital in Jackson, Miss.
Dr. DiBardino’s study was chosen as a 2011 Richard E. Clark Paper by the Society of Thoracic Surgeons.
The researchers used data from the Society of Thoracic Surgeons Congenital Heart Surgery Database (STS-CHSD). Patients were included in the analysis if they were less than 18 years of age and had undergone cardiac surgery between 2007 and 2009.
Exclusion criteria included centers with more than 15% of data missing for key variables and centers with very small samples (less than five cases).
Data collection included demographics (age, sex, weight, and race) and preoperative data (noncardiac/genetic abnormalities and STS-defined risk factors). Race was classified as white, black, Hispanic, and other.
Operations were classified by STAT Mortality category, which is "a complexity stratification tool based on empiric data from 80,000 cases in STS and EACTS (European Association for Cardio-Thoracic Surgery) databases," said Dr. DiBardino.
The researchers looked at hospital mortality, postoperative length of stay, and complications. Multivariable analyses included dichotomous variables (mortality, complications) and a continuous variable (postoperative length of stay). Models were adjusted for age, weight, noncardiac/genetic abnormalities, any other STS preoperative risk factor, and STAT Mortality category.
In all, 20,399 patients were included from 49 centers. Of these, 54% were male. In terms of race, 55% were white, 17% were black, 16% were Hispanic, and 12% were other.
Based on unadjusted outcomes, there were no differences between the sexes for in-hospital mortality or complications. However, females had significantly shorter postoperative stays. In terms of race, white patients had significantly lower mortality, shorter length of stay, and fewer complications than any of the other racial groups.
In the adjusted multivariate analysis, there was no difference for mortality between the sexes. However, black patients had a significantly greater mortality risk with an odds ratio of 1.67.
Females did have a significantly shorter mean length of stay – 0.8 fewer days. In terms of race, black patients had a significantly longer mean length of stay by 2.4 hospital days, compared with white patients. Hispanic patients also had a significantly longer mean length of stay by almost 1 hospital day.
There was no difference between the sexes in terms of the occurrence of complications. In terms of race, "black patients experienced significantly more complications than other races with an odds ratio of 1.15," according to Dr. DiBardino.
The study is unique with the respect to the use of multivariable models. The researchers measured the association of sex and race with outcomes within each center and then combined the results, in order to mitigate the potential center effects.
"Our results cannot be explained by the possibility that patients of certain races might be disproportionately treated at centers with poorer outcomes in general."
The evaluation of complex relationships between clinical variables and socioeconomic and other factors affecting health care remains a significant challenge.
Since some pertinent socioeconomic data are not collected in the STS-CHSD, an analysis of a linked data set, which capitalizes on the strengths of both the CHSD and those of an administrative claims data set may be the next logical step, said Dr. DiBardino.
Dr. DiBardino and his coinvestigators reported that they have no relevant disclosures.
Major Finding: In adjusted multivariate analyses, black patients had a significantly greater mortality risk (67%), a significantly longer mean length of stay by 2.4 hospital days, and a significantly greater risk of complications (15%). Female patients had a significantly shorter mean length of stay – 0.8 fewer days.
Data Source: The retrospective review included 20,399 patients younger than 18 years from 49 centers, collected in the Society of Thoracic Surgeons Congenital Heart Surgery Database.
Disclosures: Dr. DiBardino and his coinvestigators reported that they have no relevant disclosures.
Race, Sex Affect Congenital Heart Surgery Outcomes
FT. LAUDERDALE, FLA. – Sex and race appear to play a role in outcomes following congenital heart surgery in children and adolescents, according to a new analysis of data from almost 21,000 patients.
Black patients had significantly greater rates of mortality and complications and a significantly longer length of postoperative stay than other races, while female patients had a significantly shorter length of stay than males, Dr. Daniel J. DiBardino reported at the annual meeting of the Society of Thoracic Surgeons.
"The analysis of demographic and clinical data from nearly 21,000 patients in the congenital heart surgery database revealed important associations between gender, race, and outcome," said Dr. DiBardino, who is a cardiac surgeon at the Blair E. Batson Children’s Hospital in Jackson, Miss.
Dr. DiBardino’s study was chosen as a 2011 Richard E. Clark Paper by the Society of Thoracic Surgeons.
The researchers used data from the Society of Thoracic Surgeons Congenital Heart Surgery Database (STS-CHSD). Patients were included in the analysis if they were less than 18 years of age and had undergone cardiac surgery between 2007 and 2009.
Exclusion criteria included centers with more than 15% of data missing for key variables and centers with very small samples (less than five cases).
Data collection included demographics (age, sex, weight, and race) and preoperative data (noncardiac/genetic abnormalities and STS-defined risk factors). Race was classified as white, black, Hispanic, and other.
Operations were classified by STAT Mortality category, which is "a complexity stratification tool based on empiric data from 80,000 cases in STS and EACTS (European Association for Cardio-Thoracic Surgery) databases," said Dr. DiBardino.
The researchers looked at hospital mortality, postoperative length of stay, and complications. Multivariable analyses included dichotomous variables (mortality, complications) and a continuous variable (postoperative length of stay). Models were adjusted for age, weight, noncardiac/genetic abnormalities, any other STS preoperative risk factor, and STAT Mortality category.
In all, 20,399 patients were included from 49 centers. Of these, 54% were male. In terms of race, 55% were white, 17% were black, 16% were Hispanic, and 12% were other.
Based on unadjusted outcomes, there were no differences between the sexes for in-hospital mortality or complications. However, females had significantly shorter postoperative stays. In terms of race, white patients had significantly lower mortality, shorter length of stay, and fewer complications than any of the other racial groups.
In the adjusted multivariate analysis, there was no difference for mortality between the sexes. However, black patients had a significantly greater mortality risk with an odds ratio of 1.67.
Females did have a significantly shorter mean length of stay – 0.8 fewer days. In terms of race, black patients had a significantly longer mean length of stay by 2.4 hospital days, compared with white patients. Hispanic patients also had a significantly longer mean length of stay by almost 1 hospital day.
There was no difference between the sexes in terms of the occurrence of complications. In terms of race, "black patients experienced significantly more complications than other races with an odds ratio of 1.15," according to Dr. DiBardino.
The study is unique with the respect to the use of multivariable models. The researchers measured the association of sex and race with outcomes within each center and then combined the results, in order to mitigate the potential center effects.
"Our results cannot be explained by the possibility that patients of certain races might be disproportionately treated at centers with poorer outcomes in general."
The evaluation of complex relationships between clinical variables and socioeconomic and other factors affecting health care remains a significant challenge.
Since some pertinent socioeconomic data are not collected in the STS-CHSD, an analysis of a linked data set, which capitalizes on the strengths of both the CHSD and those of an administrative claims data set may be the next logical step, said Dr. DiBardino.
Dr. DiBardino and his coinvestigators reported that they have no relevant disclosures.
FT. LAUDERDALE, FLA. – Sex and race appear to play a role in outcomes following congenital heart surgery in children and adolescents, according to a new analysis of data from almost 21,000 patients.
Black patients had significantly greater rates of mortality and complications and a significantly longer length of postoperative stay than other races, while female patients had a significantly shorter length of stay than males, Dr. Daniel J. DiBardino reported at the annual meeting of the Society of Thoracic Surgeons.
"The analysis of demographic and clinical data from nearly 21,000 patients in the congenital heart surgery database revealed important associations between gender, race, and outcome," said Dr. DiBardino, who is a cardiac surgeon at the Blair E. Batson Children’s Hospital in Jackson, Miss.
Dr. DiBardino’s study was chosen as a 2011 Richard E. Clark Paper by the Society of Thoracic Surgeons.
The researchers used data from the Society of Thoracic Surgeons Congenital Heart Surgery Database (STS-CHSD). Patients were included in the analysis if they were less than 18 years of age and had undergone cardiac surgery between 2007 and 2009.
Exclusion criteria included centers with more than 15% of data missing for key variables and centers with very small samples (less than five cases).
Data collection included demographics (age, sex, weight, and race) and preoperative data (noncardiac/genetic abnormalities and STS-defined risk factors). Race was classified as white, black, Hispanic, and other.
Operations were classified by STAT Mortality category, which is "a complexity stratification tool based on empiric data from 80,000 cases in STS and EACTS (European Association for Cardio-Thoracic Surgery) databases," said Dr. DiBardino.
The researchers looked at hospital mortality, postoperative length of stay, and complications. Multivariable analyses included dichotomous variables (mortality, complications) and a continuous variable (postoperative length of stay). Models were adjusted for age, weight, noncardiac/genetic abnormalities, any other STS preoperative risk factor, and STAT Mortality category.
In all, 20,399 patients were included from 49 centers. Of these, 54% were male. In terms of race, 55% were white, 17% were black, 16% were Hispanic, and 12% were other.
Based on unadjusted outcomes, there were no differences between the sexes for in-hospital mortality or complications. However, females had significantly shorter postoperative stays. In terms of race, white patients had significantly lower mortality, shorter length of stay, and fewer complications than any of the other racial groups.
In the adjusted multivariate analysis, there was no difference for mortality between the sexes. However, black patients had a significantly greater mortality risk with an odds ratio of 1.67.
Females did have a significantly shorter mean length of stay – 0.8 fewer days. In terms of race, black patients had a significantly longer mean length of stay by 2.4 hospital days, compared with white patients. Hispanic patients also had a significantly longer mean length of stay by almost 1 hospital day.
There was no difference between the sexes in terms of the occurrence of complications. In terms of race, "black patients experienced significantly more complications than other races with an odds ratio of 1.15," according to Dr. DiBardino.
The study is unique with the respect to the use of multivariable models. The researchers measured the association of sex and race with outcomes within each center and then combined the results, in order to mitigate the potential center effects.
"Our results cannot be explained by the possibility that patients of certain races might be disproportionately treated at centers with poorer outcomes in general."
The evaluation of complex relationships between clinical variables and socioeconomic and other factors affecting health care remains a significant challenge.
Since some pertinent socioeconomic data are not collected in the STS-CHSD, an analysis of a linked data set, which capitalizes on the strengths of both the CHSD and those of an administrative claims data set may be the next logical step, said Dr. DiBardino.
Dr. DiBardino and his coinvestigators reported that they have no relevant disclosures.
FT. LAUDERDALE, FLA. – Sex and race appear to play a role in outcomes following congenital heart surgery in children and adolescents, according to a new analysis of data from almost 21,000 patients.
Black patients had significantly greater rates of mortality and complications and a significantly longer length of postoperative stay than other races, while female patients had a significantly shorter length of stay than males, Dr. Daniel J. DiBardino reported at the annual meeting of the Society of Thoracic Surgeons.
"The analysis of demographic and clinical data from nearly 21,000 patients in the congenital heart surgery database revealed important associations between gender, race, and outcome," said Dr. DiBardino, who is a cardiac surgeon at the Blair E. Batson Children’s Hospital in Jackson, Miss.
Dr. DiBardino’s study was chosen as a 2011 Richard E. Clark Paper by the Society of Thoracic Surgeons.
The researchers used data from the Society of Thoracic Surgeons Congenital Heart Surgery Database (STS-CHSD). Patients were included in the analysis if they were less than 18 years of age and had undergone cardiac surgery between 2007 and 2009.
Exclusion criteria included centers with more than 15% of data missing for key variables and centers with very small samples (less than five cases).
Data collection included demographics (age, sex, weight, and race) and preoperative data (noncardiac/genetic abnormalities and STS-defined risk factors). Race was classified as white, black, Hispanic, and other.
Operations were classified by STAT Mortality category, which is "a complexity stratification tool based on empiric data from 80,000 cases in STS and EACTS (European Association for Cardio-Thoracic Surgery) databases," said Dr. DiBardino.
The researchers looked at hospital mortality, postoperative length of stay, and complications. Multivariable analyses included dichotomous variables (mortality, complications) and a continuous variable (postoperative length of stay). Models were adjusted for age, weight, noncardiac/genetic abnormalities, any other STS preoperative risk factor, and STAT Mortality category.
In all, 20,399 patients were included from 49 centers. Of these, 54% were male. In terms of race, 55% were white, 17% were black, 16% were Hispanic, and 12% were other.
Based on unadjusted outcomes, there were no differences between the sexes for in-hospital mortality or complications. However, females had significantly shorter postoperative stays. In terms of race, white patients had significantly lower mortality, shorter length of stay, and fewer complications than any of the other racial groups.
In the adjusted multivariate analysis, there was no difference for mortality between the sexes. However, black patients had a significantly greater mortality risk with an odds ratio of 1.67.
Females did have a significantly shorter mean length of stay – 0.8 fewer days. In terms of race, black patients had a significantly longer mean length of stay by 2.4 hospital days, compared with white patients. Hispanic patients also had a significantly longer mean length of stay by almost 1 hospital day.
There was no difference between the sexes in terms of the occurrence of complications. In terms of race, "black patients experienced significantly more complications than other races with an odds ratio of 1.15," according to Dr. DiBardino.
The study is unique with the respect to the use of multivariable models. The researchers measured the association of sex and race with outcomes within each center and then combined the results, in order to mitigate the potential center effects.
"Our results cannot be explained by the possibility that patients of certain races might be disproportionately treated at centers with poorer outcomes in general."
The evaluation of complex relationships between clinical variables and socioeconomic and other factors affecting health care remains a significant challenge.
Since some pertinent socioeconomic data are not collected in the STS-CHSD, an analysis of a linked data set, which capitalizes on the strengths of both the CHSD and those of an administrative claims data set may be the next logical step, said Dr. DiBardino.
Dr. DiBardino and his coinvestigators reported that they have no relevant disclosures.
Major Finding: In adjusted multivariate analyses, black patients had a significantly greater mortality risk (67%), a significantly longer mean length of stay by 2.4 hospital days, and a significantly greater risk of complications (15%). Female patients had a significantly shorter mean length of stay – 0.8 fewer days.
Data Source: The retrospective review included 20,399 patients younger than 18 years from 49 centers, collected in the Society of Thoracic Surgeons Congenital Heart Surgery Database.
Disclosures: Dr. DiBardino and his coinvestigators reported that they have no relevant disclosures.