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EVB in Hospitalized Cirrhotic Patients
Cirrhosis is a leading cause of death in the United States. In 2010, cirrhosis resulted in an estimated 49,500 deaths, which represented a significant increase from 35,500 deaths 2 decades ago.[1] Cirrhotic patients are susceptible to numerous disease‐specific complications including ascites, esophageal varices, hepatic encephalopathy (HE), and hepatorenal syndrome (HRS).[2]
Esophageal varices develop in approximately 50% of patient with cirrhosis, and their presence correlates with the severity of liver disease.[3] In cirrhotic patients, esophageal variceal bleeding (EVB) occurs at an annual rate of 5% to 15% and results in substantial morbidity and mortality.[3] Utilizing US national data, Jamal et al. reported a decline in the rate of hospitalizations related to EVB from 1988 to 2002.[4] However, recent large‐scale studies relating to the epidemiology of EVB are lacking. We conducted a retrospective analysis using a national US database to study the differences in demographic characteristics, rate of complications, outcomes, and temporal trends in hospitalized cirrhotic patients with and without EVB.
METHODS
We utilized biennial data (20022012) from the Healthcare Cost and Utilization Project Nationwide Inpatient Sample using methods described earlier.[5] Initially, we extracted all entries with any discharge diagnosis of cirrhosis (International Classification of Diseases, Ninth Revision, Clinical Modification [ICD‐9‐CM] codes: 571.2, 571.5, 571.6) in adult patients ages 18 years and older.[6] Within this cirrhotic population, we next extracted all entries with any discharge diagnosis of EVB (ICD‐9‐CM codes: 456.0., 456.20).[6] Population‐based rates relating to hospital discharges were reported as per 100,000 population/year.
The outcome variables of interest were in‐hospital mortality, total charges (rounded to the nearest $1000) and length of stay (LOS). Demographic details and hospital characteristics were also extracted. Cases were queried for complications well recognized in cirrhotic patients. These included urinary tract infection (UTI) (ICD‐9‐CM codes: 1122, 59010‐11, 5902‐03, 59080‐81, 5950, 5970, 5990), skin and subcutaneous tissue infections (SSCI) (ICD‐9‐CM codes: 680‐82, 684, 686), spontaneous bacterial peritonitis (SBP) (ICD‐9‐CM codes: 56723, 5672), Clostridium difficile infection (ICD‐9‐CM code: 00845), or pneumonia (ICD‐9‐CM codes: 480‐83, 487).[6] Also queried were HE (ICD‐9‐CM code: 572.2)[7] and HRS (ICD‐9‐CM code: 572.4).[8] Comorbid conditions were assessed using the Elixhauser comorbidity index minus the presence of liver disorders but including alcohol abuse.[9]
Statistical analyses were performed using SAS version 9.3 (SAS Institute, Cary, NC). To determine the independent association of EVB on outcome variables, we performed case‐control matching (EVB vs no EVB). We used high‐dimensional propensity scores in a 1:5 matching ratio with a greedy matching algorithm generated by regression analysis of patients with EVB based on demographics details (age, gender, insurance status), comorbid conditions, alcohol abuse, infections as detailed above, HE, and HRS. The 2 test and the Mann‐Whitney U test compared categorical and continuous variables. For trend analysis, we used the Cochrane‐Armitage test. The threshold for significance for all analyses was P0.01.
RESULTS
In 2012, there were 570,020 hospital discharges related to cirrhosis in patients 18 years of age and older. Within this cohort, EVB occurred in 32,945 discharges (5.78%). Table 1 details differences between cirrhotic patients with and without EVB. Comparatively, patients with EVB were younger (median age 55 years, interquartile range [IQR] 13 years vs median age 58 years, IQR 15 years; P0.01), more likely to be male (70.1% vs 60.4%; P0.01), and without health insurance (21.0% vs 12.50%; P0.01). Minor differences between the 2 groups were observed in respect to hospital region, location, teaching status, and household income quartile. There was no difference in the number of comorbid conditions (median 4 comorbid conditions in each group).
| Study Group | P Value | ||
|---|---|---|---|
| Cirrhosis Without Variceal Bleeding | Cirrhosis With Variceal Bleeding | ||
| |||
| Total 570,220 (100%) | 537,275 (94.22%) | 32,945 (5.78%) | |
| Age, y, median (IQR) | 58 (15) | 55 (13) | |
| Gender | |||
| Male | 60.40% | 70.10% | |
| Female | 39.60% | 29.90% | |
| Mortality | 5.80% | 9.90% | |
| Insurance | |||
| Private | 19.70% | 22.40% | |
| Medicare/Medicaid | 67.80% | 56.60% | |
| None | 12.50% | 21.00% | |
| Length of stay, median (IQR) | 4 (5) | 4 (4) | |
| Hospital charges, median (IQR) | 28 (39) | 41 (49) | |
| Associated comorbidities, median (IQR) | 4 (2) | 4 (3) | |
| Alcohol consumption | 48.80% | 63.90% | |
| Infections | |||
| Overall | 24.10% | 13.50% | |
| UTI | 13.10% | 6.90% | |
| Pneumonia | 1.50% | 1.40% | 0.03 |
| SBP | 3.40% | 3.40% | 0.45 |
| SSCI | 6.30% | 1.70% | |
| CDI | 2.20% | 1.40% | |
| Hepatic encephalopathy | 17.70% | 18.80% | |
| Hepatorenal syndrome | 3.70% | 4.30% | |
| EVL | 66.40% | ||
| TIPS | 4.90% | ||
| Blood transfusions | 56.90% | ||
Patients with EVB suffered a significantly higher rate of alcohol abuse (63.90% vs 48.80%; P0.01). EVB was also associated with an overall lower incidence of infection (13.50% vs 24.10%; P0.01). Specifically, the greatest difference in rates of infection were observed for UTI (6.90% vs 13.10%; P0.01) and SSCI (1.70% vs 6.30%; P0.01). Also, patients with EVB demonstrated a small, yet significant increased incidence of HE (18.80% vs 17.70%; P0.01) and HRS (4.30% vs 3.70%; P0.01).
Cirrhotic patients with EVB demonstrated worse overall outcomes compared to their counterparts without EVB. This manifested in an unadjusted higher mortality rate (9.90% vs 5.80%; P0.01) and increased hospital charges (median $41,000 [IQR $49,000] vs $28,000 [IQR $39,000]; P0.01). LOS between the 2 groups did not differ (median 4 days). After adjusting for demographic differences, complications, and comorbid conditions, EVB in patients with cirrhosis continued to be independently associated with a higher mortality rate (10.00% vs 5.00%; P0.01) and increased hospital charges (median $41,000 [IQR $49,000] vs $26,000 [IQR $34,000]; P0.01). Again, LOS was similar for the 2 groups (median 4 days).
Between the years 2002 and 2012, the number of hospital discharges related to cirrhosis increased from 337,956 to 570,220 (P0.01). Concurrently, the incidence of EVB in this population declined from 8.60% to 5.78% (Figure 1), representing an overall decrease of 33.0% with a significant decreased trend (P0.01).
We also calculated population‐adjusted hospitalization rates for discharges related to cirrhosis and EVB. The rate of cirrhosis‐related discharges continued to demonstrate an increased trend from 157.42/100,000 population in 2002 to 237.43/100,000 population in 2012 (P0.01). However, no significant trend was observed for EVB‐related hospital discharges in the same period of time (13.60/100,000 population in 2002 to 13.72/100,000 population in 2012; P=0.91).
DISCUSSION
Our results indicated a significantly higher rate of alcohol abuse in cirrhotic patients with EVB. Alcohol consumption is an independent risk factor for esophageal variceal bleeding.[10, 11] Continued alcohol consumption not only increases the risk for development of varices but may also precipitate variceal rupture.[10] Other risk factors associated with EVB in this study (younger age, male, lower economic status) are likely related to a higher incidence of alcohol abuse in this demographic.[12]
Patients with EVB were also noted to have a lower overall incidence of infection, especially UTI and SSCI. The use of broad‐spectrum antibiotics decreases mortality from secondary infection and improves the prognosis of cirrhotic patients with EVB.[13, 14] The American Association for the Study of Liver Diseases recommends the use of third‐generation cephalosporins in the setting of EVB.[3] The widespread adoption of this in clinical practice may have contributed to a decreased rate of infection in patients with EVB. The difference in the incidence rates of HE and HRS, although statistically significant, were small, and likely the consequence of the large numbers involved in our study.
Our results also indicate that cirrhotic patients with EVB were twice as likely to die compared to matched counterparts without EVB. The increased mortality associated with EVB could be related to hemorrhagic/hypovolemic shock and cardiovascular collapse, aspiration into airway, multiorgan dysfunction due to poor perfusion, infections including SBP, and HE. Although prior studies have demonstrated the relationship between EVB and increased mortality, typically they have been restricted to small single‐center studies involving fewer than 200 patients.[6, 7, 8, 9] Cirrhotic patients with EVB also incurred significantly higher hospital charges compared to matched counterparts. Interestingly, the hospital LOS did not differ between the 2 groups. Intensive care and procedural costs were likely a major contributor to the higher charges; cirrhotic patients with EVB underwent a median of 3 procedures (IQR 2) during their hospital stay compared to a median of 1 procedure (IQR 3) for cirrhotic patients without EVB (P0.01; data not shown).
In contrast to trends from earlier decades,[4] the population‐adjusted rate of EVB‐related hospital discharges did not change significantly from 2002 to 2012. However, these data are confounded in their interpretation by a substantial increase in the prevalence of cirrhosis in the United States during the same time period.[15] Therefore, it may be more meaningful to state that there was a contemporaneous decline in EVB‐related hospital discharges when considered in the context of a complicating rate in hospitalized cirrhotic patients. These results are consistent with a recent single‐center study[16] and are very likely the fruition of intensive screening programs with primary and secondary prophylaxis for EVB involving esophageal variceal ligation and pharmacotherapy (‐blockers) as well as the increased acceptance of transjugular intrahepatic portosystemic shunt placement.[17, 18, 19]
There are limitations to our study. First, we relied exclusively on ICD‐9‐CM codes for case identification. Second, there is a nonavailability of data pertaining to Model for End‐Stage Liver Disease score calculations, medication, and antibiotic usage. Third, the Nationwide Inpatient Sample database does not allow for distinguishing individual patients with repeat admissions. Finally, our results represent a weighted estimate of national data.
CONCLUSION
EVB in cirrhotic patients was associated with significantly higher mortality and increased hospital charges. Also, the rate of EVB‐related hospital discharges as a complicating factor in patients with cirrhosis declined significantly during the decade 2002 to 2012. This likely reflects the ongoing effectiveness of primary and secondary prophylaxis.
Acknowledgements
The authors acknowledge the Healthcare Cost and Utilization Project (HCUP) Nationwide Inpatient Sample, sponsored by the Agency for Healthcare Research and Quality, which contributes to HCUP (
Disclosures: C.P., the first author and corresponding author, conceptualized the study, and with A.D. gathered and analyzed the data. C.P. and M.D. wrote, edited, and proofread the manuscript as well as created the bibliography and formulated the table and figure. R.G., R.T., and M.O. edited, commented on, and reviewed the manuscript. All of the authors reviewed and agreed on the final version of the manuscript for submission. The authors report no conflicts of interest.
- US Burden of Disease Collaborators. The state of US health, 1990‐2010: burden of diseases, injuries, and risk factors. JAMA. 2013;310(6):591–608.
- , Complications of cirrhosis. Curr Opin Gastroenterol. 2012;28(3):223–229.
- , , , , Practice Guidelines Committee of the American Association for the Study of Liver Diseases, Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46(3):922–938.
- , , , Declining hospitalization rate of esophageal variceal bleeding in the United States. Clin Gastroenterol Hepatol. 2008;6(6):689–695; quiz 605.
- , , , , , Association of Clostridium difficile infection with outcomes of hospitalized solid organ transplant recipients: results from the 2009 Nationwide Inpatient Sample database. Transpl Infect Dis. 2012;14(5):540–547.
- , , Prevalence and in‐hospital mortality trends of infections among patients with cirrhosis: a nationwide study of hospitalised patients in the United States. Aliment Pharmacol Ther. 2014;40(1):105–112.
- , , Racial disparities in the management of hospitalized patients with cirrhosis and complications of portal hypertension: a national study. Hepatology. 2007;45(5):1282–1289.
- , Protein‐calorie malnutrition as a prognostic indicator of mortality among patients hospitalized with cirrhosis and portal hypertension. Liver Int. 2009;29(9):1396–1402.
- , , , Comorbidity measures for use with administrative data. Med Care. 1998;36(1):8–27.
- , , , , , Potential precipitating factors of esophageal variceal bleeding: a case‐control study. Am J Gastroenterol. 2011;106(1):96–103.
- , , , et al. Effects of ethanol consumption on hepatic hemodynamics in patients with alcoholic cirrhosis. Gastroenterology. 1997;112(4):1284–1289.
- , , , Prevalence, correlates, disability, and comorbidity of DSM‐IV alcohol abuse and dependence in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Arch Gen Psychiatry. 2007;64(7):830–842.
- , , Role of prophylactic antibiotics in cirrhotic patients with variceal bleeding. World J Gastroenterol. 2014;20(7):1790–1796.
- , , , et al. Meta‐analysis: antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding—an updated Cochrane review. Aliment Pharmacol Ther. 2011;34(5):509–518.
- , , , et al. The epidemiology of cirrhosis in the United States: a population‐based study [published online ahead of print October 8, 2014]. J Clin Gastroenterol. doi: 10.1097/MCG.0000000000000208.
- , , , Hospitalization for variceal hemorrhage in an era with more prevalent cirrhosis. World J Gastroenterol. 2014;20(32):11326–11332.
- , Banding ligation versus beta‐blockers for primary prevention in oesophageal varices in adults. Cochrane Database Syst Rev. 2012;8:CD004544.
- , , , et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med. 2010;362(25):2370–2379.
- , , , Meta‐analysis: banding ligation and medical interventions for the prevention of rebleeding from oesophageal varices. Aliment Pharmacol Ther. 2012;35(10):1155–1165.
Cirrhosis is a leading cause of death in the United States. In 2010, cirrhosis resulted in an estimated 49,500 deaths, which represented a significant increase from 35,500 deaths 2 decades ago.[1] Cirrhotic patients are susceptible to numerous disease‐specific complications including ascites, esophageal varices, hepatic encephalopathy (HE), and hepatorenal syndrome (HRS).[2]
Esophageal varices develop in approximately 50% of patient with cirrhosis, and their presence correlates with the severity of liver disease.[3] In cirrhotic patients, esophageal variceal bleeding (EVB) occurs at an annual rate of 5% to 15% and results in substantial morbidity and mortality.[3] Utilizing US national data, Jamal et al. reported a decline in the rate of hospitalizations related to EVB from 1988 to 2002.[4] However, recent large‐scale studies relating to the epidemiology of EVB are lacking. We conducted a retrospective analysis using a national US database to study the differences in demographic characteristics, rate of complications, outcomes, and temporal trends in hospitalized cirrhotic patients with and without EVB.
METHODS
We utilized biennial data (20022012) from the Healthcare Cost and Utilization Project Nationwide Inpatient Sample using methods described earlier.[5] Initially, we extracted all entries with any discharge diagnosis of cirrhosis (International Classification of Diseases, Ninth Revision, Clinical Modification [ICD‐9‐CM] codes: 571.2, 571.5, 571.6) in adult patients ages 18 years and older.[6] Within this cirrhotic population, we next extracted all entries with any discharge diagnosis of EVB (ICD‐9‐CM codes: 456.0., 456.20).[6] Population‐based rates relating to hospital discharges were reported as per 100,000 population/year.
The outcome variables of interest were in‐hospital mortality, total charges (rounded to the nearest $1000) and length of stay (LOS). Demographic details and hospital characteristics were also extracted. Cases were queried for complications well recognized in cirrhotic patients. These included urinary tract infection (UTI) (ICD‐9‐CM codes: 1122, 59010‐11, 5902‐03, 59080‐81, 5950, 5970, 5990), skin and subcutaneous tissue infections (SSCI) (ICD‐9‐CM codes: 680‐82, 684, 686), spontaneous bacterial peritonitis (SBP) (ICD‐9‐CM codes: 56723, 5672), Clostridium difficile infection (ICD‐9‐CM code: 00845), or pneumonia (ICD‐9‐CM codes: 480‐83, 487).[6] Also queried were HE (ICD‐9‐CM code: 572.2)[7] and HRS (ICD‐9‐CM code: 572.4).[8] Comorbid conditions were assessed using the Elixhauser comorbidity index minus the presence of liver disorders but including alcohol abuse.[9]
Statistical analyses were performed using SAS version 9.3 (SAS Institute, Cary, NC). To determine the independent association of EVB on outcome variables, we performed case‐control matching (EVB vs no EVB). We used high‐dimensional propensity scores in a 1:5 matching ratio with a greedy matching algorithm generated by regression analysis of patients with EVB based on demographics details (age, gender, insurance status), comorbid conditions, alcohol abuse, infections as detailed above, HE, and HRS. The 2 test and the Mann‐Whitney U test compared categorical and continuous variables. For trend analysis, we used the Cochrane‐Armitage test. The threshold for significance for all analyses was P0.01.
RESULTS
In 2012, there were 570,020 hospital discharges related to cirrhosis in patients 18 years of age and older. Within this cohort, EVB occurred in 32,945 discharges (5.78%). Table 1 details differences between cirrhotic patients with and without EVB. Comparatively, patients with EVB were younger (median age 55 years, interquartile range [IQR] 13 years vs median age 58 years, IQR 15 years; P0.01), more likely to be male (70.1% vs 60.4%; P0.01), and without health insurance (21.0% vs 12.50%; P0.01). Minor differences between the 2 groups were observed in respect to hospital region, location, teaching status, and household income quartile. There was no difference in the number of comorbid conditions (median 4 comorbid conditions in each group).
| Study Group | P Value | ||
|---|---|---|---|
| Cirrhosis Without Variceal Bleeding | Cirrhosis With Variceal Bleeding | ||
| |||
| Total 570,220 (100%) | 537,275 (94.22%) | 32,945 (5.78%) | |
| Age, y, median (IQR) | 58 (15) | 55 (13) | |
| Gender | |||
| Male | 60.40% | 70.10% | |
| Female | 39.60% | 29.90% | |
| Mortality | 5.80% | 9.90% | |
| Insurance | |||
| Private | 19.70% | 22.40% | |
| Medicare/Medicaid | 67.80% | 56.60% | |
| None | 12.50% | 21.00% | |
| Length of stay, median (IQR) | 4 (5) | 4 (4) | |
| Hospital charges, median (IQR) | 28 (39) | 41 (49) | |
| Associated comorbidities, median (IQR) | 4 (2) | 4 (3) | |
| Alcohol consumption | 48.80% | 63.90% | |
| Infections | |||
| Overall | 24.10% | 13.50% | |
| UTI | 13.10% | 6.90% | |
| Pneumonia | 1.50% | 1.40% | 0.03 |
| SBP | 3.40% | 3.40% | 0.45 |
| SSCI | 6.30% | 1.70% | |
| CDI | 2.20% | 1.40% | |
| Hepatic encephalopathy | 17.70% | 18.80% | |
| Hepatorenal syndrome | 3.70% | 4.30% | |
| EVL | 66.40% | ||
| TIPS | 4.90% | ||
| Blood transfusions | 56.90% | ||
Patients with EVB suffered a significantly higher rate of alcohol abuse (63.90% vs 48.80%; P0.01). EVB was also associated with an overall lower incidence of infection (13.50% vs 24.10%; P0.01). Specifically, the greatest difference in rates of infection were observed for UTI (6.90% vs 13.10%; P0.01) and SSCI (1.70% vs 6.30%; P0.01). Also, patients with EVB demonstrated a small, yet significant increased incidence of HE (18.80% vs 17.70%; P0.01) and HRS (4.30% vs 3.70%; P0.01).
Cirrhotic patients with EVB demonstrated worse overall outcomes compared to their counterparts without EVB. This manifested in an unadjusted higher mortality rate (9.90% vs 5.80%; P0.01) and increased hospital charges (median $41,000 [IQR $49,000] vs $28,000 [IQR $39,000]; P0.01). LOS between the 2 groups did not differ (median 4 days). After adjusting for demographic differences, complications, and comorbid conditions, EVB in patients with cirrhosis continued to be independently associated with a higher mortality rate (10.00% vs 5.00%; P0.01) and increased hospital charges (median $41,000 [IQR $49,000] vs $26,000 [IQR $34,000]; P0.01). Again, LOS was similar for the 2 groups (median 4 days).
Between the years 2002 and 2012, the number of hospital discharges related to cirrhosis increased from 337,956 to 570,220 (P0.01). Concurrently, the incidence of EVB in this population declined from 8.60% to 5.78% (Figure 1), representing an overall decrease of 33.0% with a significant decreased trend (P0.01).
We also calculated population‐adjusted hospitalization rates for discharges related to cirrhosis and EVB. The rate of cirrhosis‐related discharges continued to demonstrate an increased trend from 157.42/100,000 population in 2002 to 237.43/100,000 population in 2012 (P0.01). However, no significant trend was observed for EVB‐related hospital discharges in the same period of time (13.60/100,000 population in 2002 to 13.72/100,000 population in 2012; P=0.91).
DISCUSSION
Our results indicated a significantly higher rate of alcohol abuse in cirrhotic patients with EVB. Alcohol consumption is an independent risk factor for esophageal variceal bleeding.[10, 11] Continued alcohol consumption not only increases the risk for development of varices but may also precipitate variceal rupture.[10] Other risk factors associated with EVB in this study (younger age, male, lower economic status) are likely related to a higher incidence of alcohol abuse in this demographic.[12]
Patients with EVB were also noted to have a lower overall incidence of infection, especially UTI and SSCI. The use of broad‐spectrum antibiotics decreases mortality from secondary infection and improves the prognosis of cirrhotic patients with EVB.[13, 14] The American Association for the Study of Liver Diseases recommends the use of third‐generation cephalosporins in the setting of EVB.[3] The widespread adoption of this in clinical practice may have contributed to a decreased rate of infection in patients with EVB. The difference in the incidence rates of HE and HRS, although statistically significant, were small, and likely the consequence of the large numbers involved in our study.
Our results also indicate that cirrhotic patients with EVB were twice as likely to die compared to matched counterparts without EVB. The increased mortality associated with EVB could be related to hemorrhagic/hypovolemic shock and cardiovascular collapse, aspiration into airway, multiorgan dysfunction due to poor perfusion, infections including SBP, and HE. Although prior studies have demonstrated the relationship between EVB and increased mortality, typically they have been restricted to small single‐center studies involving fewer than 200 patients.[6, 7, 8, 9] Cirrhotic patients with EVB also incurred significantly higher hospital charges compared to matched counterparts. Interestingly, the hospital LOS did not differ between the 2 groups. Intensive care and procedural costs were likely a major contributor to the higher charges; cirrhotic patients with EVB underwent a median of 3 procedures (IQR 2) during their hospital stay compared to a median of 1 procedure (IQR 3) for cirrhotic patients without EVB (P0.01; data not shown).
In contrast to trends from earlier decades,[4] the population‐adjusted rate of EVB‐related hospital discharges did not change significantly from 2002 to 2012. However, these data are confounded in their interpretation by a substantial increase in the prevalence of cirrhosis in the United States during the same time period.[15] Therefore, it may be more meaningful to state that there was a contemporaneous decline in EVB‐related hospital discharges when considered in the context of a complicating rate in hospitalized cirrhotic patients. These results are consistent with a recent single‐center study[16] and are very likely the fruition of intensive screening programs with primary and secondary prophylaxis for EVB involving esophageal variceal ligation and pharmacotherapy (‐blockers) as well as the increased acceptance of transjugular intrahepatic portosystemic shunt placement.[17, 18, 19]
There are limitations to our study. First, we relied exclusively on ICD‐9‐CM codes for case identification. Second, there is a nonavailability of data pertaining to Model for End‐Stage Liver Disease score calculations, medication, and antibiotic usage. Third, the Nationwide Inpatient Sample database does not allow for distinguishing individual patients with repeat admissions. Finally, our results represent a weighted estimate of national data.
CONCLUSION
EVB in cirrhotic patients was associated with significantly higher mortality and increased hospital charges. Also, the rate of EVB‐related hospital discharges as a complicating factor in patients with cirrhosis declined significantly during the decade 2002 to 2012. This likely reflects the ongoing effectiveness of primary and secondary prophylaxis.
Acknowledgements
The authors acknowledge the Healthcare Cost and Utilization Project (HCUP) Nationwide Inpatient Sample, sponsored by the Agency for Healthcare Research and Quality, which contributes to HCUP (
Disclosures: C.P., the first author and corresponding author, conceptualized the study, and with A.D. gathered and analyzed the data. C.P. and M.D. wrote, edited, and proofread the manuscript as well as created the bibliography and formulated the table and figure. R.G., R.T., and M.O. edited, commented on, and reviewed the manuscript. All of the authors reviewed and agreed on the final version of the manuscript for submission. The authors report no conflicts of interest.
Cirrhosis is a leading cause of death in the United States. In 2010, cirrhosis resulted in an estimated 49,500 deaths, which represented a significant increase from 35,500 deaths 2 decades ago.[1] Cirrhotic patients are susceptible to numerous disease‐specific complications including ascites, esophageal varices, hepatic encephalopathy (HE), and hepatorenal syndrome (HRS).[2]
Esophageal varices develop in approximately 50% of patient with cirrhosis, and their presence correlates with the severity of liver disease.[3] In cirrhotic patients, esophageal variceal bleeding (EVB) occurs at an annual rate of 5% to 15% and results in substantial morbidity and mortality.[3] Utilizing US national data, Jamal et al. reported a decline in the rate of hospitalizations related to EVB from 1988 to 2002.[4] However, recent large‐scale studies relating to the epidemiology of EVB are lacking. We conducted a retrospective analysis using a national US database to study the differences in demographic characteristics, rate of complications, outcomes, and temporal trends in hospitalized cirrhotic patients with and without EVB.
METHODS
We utilized biennial data (20022012) from the Healthcare Cost and Utilization Project Nationwide Inpatient Sample using methods described earlier.[5] Initially, we extracted all entries with any discharge diagnosis of cirrhosis (International Classification of Diseases, Ninth Revision, Clinical Modification [ICD‐9‐CM] codes: 571.2, 571.5, 571.6) in adult patients ages 18 years and older.[6] Within this cirrhotic population, we next extracted all entries with any discharge diagnosis of EVB (ICD‐9‐CM codes: 456.0., 456.20).[6] Population‐based rates relating to hospital discharges were reported as per 100,000 population/year.
The outcome variables of interest were in‐hospital mortality, total charges (rounded to the nearest $1000) and length of stay (LOS). Demographic details and hospital characteristics were also extracted. Cases were queried for complications well recognized in cirrhotic patients. These included urinary tract infection (UTI) (ICD‐9‐CM codes: 1122, 59010‐11, 5902‐03, 59080‐81, 5950, 5970, 5990), skin and subcutaneous tissue infections (SSCI) (ICD‐9‐CM codes: 680‐82, 684, 686), spontaneous bacterial peritonitis (SBP) (ICD‐9‐CM codes: 56723, 5672), Clostridium difficile infection (ICD‐9‐CM code: 00845), or pneumonia (ICD‐9‐CM codes: 480‐83, 487).[6] Also queried were HE (ICD‐9‐CM code: 572.2)[7] and HRS (ICD‐9‐CM code: 572.4).[8] Comorbid conditions were assessed using the Elixhauser comorbidity index minus the presence of liver disorders but including alcohol abuse.[9]
Statistical analyses were performed using SAS version 9.3 (SAS Institute, Cary, NC). To determine the independent association of EVB on outcome variables, we performed case‐control matching (EVB vs no EVB). We used high‐dimensional propensity scores in a 1:5 matching ratio with a greedy matching algorithm generated by regression analysis of patients with EVB based on demographics details (age, gender, insurance status), comorbid conditions, alcohol abuse, infections as detailed above, HE, and HRS. The 2 test and the Mann‐Whitney U test compared categorical and continuous variables. For trend analysis, we used the Cochrane‐Armitage test. The threshold for significance for all analyses was P0.01.
RESULTS
In 2012, there were 570,020 hospital discharges related to cirrhosis in patients 18 years of age and older. Within this cohort, EVB occurred in 32,945 discharges (5.78%). Table 1 details differences between cirrhotic patients with and without EVB. Comparatively, patients with EVB were younger (median age 55 years, interquartile range [IQR] 13 years vs median age 58 years, IQR 15 years; P0.01), more likely to be male (70.1% vs 60.4%; P0.01), and without health insurance (21.0% vs 12.50%; P0.01). Minor differences between the 2 groups were observed in respect to hospital region, location, teaching status, and household income quartile. There was no difference in the number of comorbid conditions (median 4 comorbid conditions in each group).
| Study Group | P Value | ||
|---|---|---|---|
| Cirrhosis Without Variceal Bleeding | Cirrhosis With Variceal Bleeding | ||
| |||
| Total 570,220 (100%) | 537,275 (94.22%) | 32,945 (5.78%) | |
| Age, y, median (IQR) | 58 (15) | 55 (13) | |
| Gender | |||
| Male | 60.40% | 70.10% | |
| Female | 39.60% | 29.90% | |
| Mortality | 5.80% | 9.90% | |
| Insurance | |||
| Private | 19.70% | 22.40% | |
| Medicare/Medicaid | 67.80% | 56.60% | |
| None | 12.50% | 21.00% | |
| Length of stay, median (IQR) | 4 (5) | 4 (4) | |
| Hospital charges, median (IQR) | 28 (39) | 41 (49) | |
| Associated comorbidities, median (IQR) | 4 (2) | 4 (3) | |
| Alcohol consumption | 48.80% | 63.90% | |
| Infections | |||
| Overall | 24.10% | 13.50% | |
| UTI | 13.10% | 6.90% | |
| Pneumonia | 1.50% | 1.40% | 0.03 |
| SBP | 3.40% | 3.40% | 0.45 |
| SSCI | 6.30% | 1.70% | |
| CDI | 2.20% | 1.40% | |
| Hepatic encephalopathy | 17.70% | 18.80% | |
| Hepatorenal syndrome | 3.70% | 4.30% | |
| EVL | 66.40% | ||
| TIPS | 4.90% | ||
| Blood transfusions | 56.90% | ||
Patients with EVB suffered a significantly higher rate of alcohol abuse (63.90% vs 48.80%; P0.01). EVB was also associated with an overall lower incidence of infection (13.50% vs 24.10%; P0.01). Specifically, the greatest difference in rates of infection were observed for UTI (6.90% vs 13.10%; P0.01) and SSCI (1.70% vs 6.30%; P0.01). Also, patients with EVB demonstrated a small, yet significant increased incidence of HE (18.80% vs 17.70%; P0.01) and HRS (4.30% vs 3.70%; P0.01).
Cirrhotic patients with EVB demonstrated worse overall outcomes compared to their counterparts without EVB. This manifested in an unadjusted higher mortality rate (9.90% vs 5.80%; P0.01) and increased hospital charges (median $41,000 [IQR $49,000] vs $28,000 [IQR $39,000]; P0.01). LOS between the 2 groups did not differ (median 4 days). After adjusting for demographic differences, complications, and comorbid conditions, EVB in patients with cirrhosis continued to be independently associated with a higher mortality rate (10.00% vs 5.00%; P0.01) and increased hospital charges (median $41,000 [IQR $49,000] vs $26,000 [IQR $34,000]; P0.01). Again, LOS was similar for the 2 groups (median 4 days).
Between the years 2002 and 2012, the number of hospital discharges related to cirrhosis increased from 337,956 to 570,220 (P0.01). Concurrently, the incidence of EVB in this population declined from 8.60% to 5.78% (Figure 1), representing an overall decrease of 33.0% with a significant decreased trend (P0.01).
We also calculated population‐adjusted hospitalization rates for discharges related to cirrhosis and EVB. The rate of cirrhosis‐related discharges continued to demonstrate an increased trend from 157.42/100,000 population in 2002 to 237.43/100,000 population in 2012 (P0.01). However, no significant trend was observed for EVB‐related hospital discharges in the same period of time (13.60/100,000 population in 2002 to 13.72/100,000 population in 2012; P=0.91).
DISCUSSION
Our results indicated a significantly higher rate of alcohol abuse in cirrhotic patients with EVB. Alcohol consumption is an independent risk factor for esophageal variceal bleeding.[10, 11] Continued alcohol consumption not only increases the risk for development of varices but may also precipitate variceal rupture.[10] Other risk factors associated with EVB in this study (younger age, male, lower economic status) are likely related to a higher incidence of alcohol abuse in this demographic.[12]
Patients with EVB were also noted to have a lower overall incidence of infection, especially UTI and SSCI. The use of broad‐spectrum antibiotics decreases mortality from secondary infection and improves the prognosis of cirrhotic patients with EVB.[13, 14] The American Association for the Study of Liver Diseases recommends the use of third‐generation cephalosporins in the setting of EVB.[3] The widespread adoption of this in clinical practice may have contributed to a decreased rate of infection in patients with EVB. The difference in the incidence rates of HE and HRS, although statistically significant, were small, and likely the consequence of the large numbers involved in our study.
Our results also indicate that cirrhotic patients with EVB were twice as likely to die compared to matched counterparts without EVB. The increased mortality associated with EVB could be related to hemorrhagic/hypovolemic shock and cardiovascular collapse, aspiration into airway, multiorgan dysfunction due to poor perfusion, infections including SBP, and HE. Although prior studies have demonstrated the relationship between EVB and increased mortality, typically they have been restricted to small single‐center studies involving fewer than 200 patients.[6, 7, 8, 9] Cirrhotic patients with EVB also incurred significantly higher hospital charges compared to matched counterparts. Interestingly, the hospital LOS did not differ between the 2 groups. Intensive care and procedural costs were likely a major contributor to the higher charges; cirrhotic patients with EVB underwent a median of 3 procedures (IQR 2) during their hospital stay compared to a median of 1 procedure (IQR 3) for cirrhotic patients without EVB (P0.01; data not shown).
In contrast to trends from earlier decades,[4] the population‐adjusted rate of EVB‐related hospital discharges did not change significantly from 2002 to 2012. However, these data are confounded in their interpretation by a substantial increase in the prevalence of cirrhosis in the United States during the same time period.[15] Therefore, it may be more meaningful to state that there was a contemporaneous decline in EVB‐related hospital discharges when considered in the context of a complicating rate in hospitalized cirrhotic patients. These results are consistent with a recent single‐center study[16] and are very likely the fruition of intensive screening programs with primary and secondary prophylaxis for EVB involving esophageal variceal ligation and pharmacotherapy (‐blockers) as well as the increased acceptance of transjugular intrahepatic portosystemic shunt placement.[17, 18, 19]
There are limitations to our study. First, we relied exclusively on ICD‐9‐CM codes for case identification. Second, there is a nonavailability of data pertaining to Model for End‐Stage Liver Disease score calculations, medication, and antibiotic usage. Third, the Nationwide Inpatient Sample database does not allow for distinguishing individual patients with repeat admissions. Finally, our results represent a weighted estimate of national data.
CONCLUSION
EVB in cirrhotic patients was associated with significantly higher mortality and increased hospital charges. Also, the rate of EVB‐related hospital discharges as a complicating factor in patients with cirrhosis declined significantly during the decade 2002 to 2012. This likely reflects the ongoing effectiveness of primary and secondary prophylaxis.
Acknowledgements
The authors acknowledge the Healthcare Cost and Utilization Project (HCUP) Nationwide Inpatient Sample, sponsored by the Agency for Healthcare Research and Quality, which contributes to HCUP (
Disclosures: C.P., the first author and corresponding author, conceptualized the study, and with A.D. gathered and analyzed the data. C.P. and M.D. wrote, edited, and proofread the manuscript as well as created the bibliography and formulated the table and figure. R.G., R.T., and M.O. edited, commented on, and reviewed the manuscript. All of the authors reviewed and agreed on the final version of the manuscript for submission. The authors report no conflicts of interest.
- US Burden of Disease Collaborators. The state of US health, 1990‐2010: burden of diseases, injuries, and risk factors. JAMA. 2013;310(6):591–608.
- , Complications of cirrhosis. Curr Opin Gastroenterol. 2012;28(3):223–229.
- , , , , Practice Guidelines Committee of the American Association for the Study of Liver Diseases, Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46(3):922–938.
- , , , Declining hospitalization rate of esophageal variceal bleeding in the United States. Clin Gastroenterol Hepatol. 2008;6(6):689–695; quiz 605.
- , , , , , Association of Clostridium difficile infection with outcomes of hospitalized solid organ transplant recipients: results from the 2009 Nationwide Inpatient Sample database. Transpl Infect Dis. 2012;14(5):540–547.
- , , Prevalence and in‐hospital mortality trends of infections among patients with cirrhosis: a nationwide study of hospitalised patients in the United States. Aliment Pharmacol Ther. 2014;40(1):105–112.
- , , Racial disparities in the management of hospitalized patients with cirrhosis and complications of portal hypertension: a national study. Hepatology. 2007;45(5):1282–1289.
- , Protein‐calorie malnutrition as a prognostic indicator of mortality among patients hospitalized with cirrhosis and portal hypertension. Liver Int. 2009;29(9):1396–1402.
- , , , Comorbidity measures for use with administrative data. Med Care. 1998;36(1):8–27.
- , , , , , Potential precipitating factors of esophageal variceal bleeding: a case‐control study. Am J Gastroenterol. 2011;106(1):96–103.
- , , , et al. Effects of ethanol consumption on hepatic hemodynamics in patients with alcoholic cirrhosis. Gastroenterology. 1997;112(4):1284–1289.
- , , , Prevalence, correlates, disability, and comorbidity of DSM‐IV alcohol abuse and dependence in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Arch Gen Psychiatry. 2007;64(7):830–842.
- , , Role of prophylactic antibiotics in cirrhotic patients with variceal bleeding. World J Gastroenterol. 2014;20(7):1790–1796.
- , , , et al. Meta‐analysis: antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding—an updated Cochrane review. Aliment Pharmacol Ther. 2011;34(5):509–518.
- , , , et al. The epidemiology of cirrhosis in the United States: a population‐based study [published online ahead of print October 8, 2014]. J Clin Gastroenterol. doi: 10.1097/MCG.0000000000000208.
- , , , Hospitalization for variceal hemorrhage in an era with more prevalent cirrhosis. World J Gastroenterol. 2014;20(32):11326–11332.
- , Banding ligation versus beta‐blockers for primary prevention in oesophageal varices in adults. Cochrane Database Syst Rev. 2012;8:CD004544.
- , , , et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med. 2010;362(25):2370–2379.
- , , , Meta‐analysis: banding ligation and medical interventions for the prevention of rebleeding from oesophageal varices. Aliment Pharmacol Ther. 2012;35(10):1155–1165.
- US Burden of Disease Collaborators. The state of US health, 1990‐2010: burden of diseases, injuries, and risk factors. JAMA. 2013;310(6):591–608.
- , Complications of cirrhosis. Curr Opin Gastroenterol. 2012;28(3):223–229.
- , , , , Practice Guidelines Committee of the American Association for the Study of Liver Diseases, Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46(3):922–938.
- , , , Declining hospitalization rate of esophageal variceal bleeding in the United States. Clin Gastroenterol Hepatol. 2008;6(6):689–695; quiz 605.
- , , , , , Association of Clostridium difficile infection with outcomes of hospitalized solid organ transplant recipients: results from the 2009 Nationwide Inpatient Sample database. Transpl Infect Dis. 2012;14(5):540–547.
- , , Prevalence and in‐hospital mortality trends of infections among patients with cirrhosis: a nationwide study of hospitalised patients in the United States. Aliment Pharmacol Ther. 2014;40(1):105–112.
- , , Racial disparities in the management of hospitalized patients with cirrhosis and complications of portal hypertension: a national study. Hepatology. 2007;45(5):1282–1289.
- , Protein‐calorie malnutrition as a prognostic indicator of mortality among patients hospitalized with cirrhosis and portal hypertension. Liver Int. 2009;29(9):1396–1402.
- , , , Comorbidity measures for use with administrative data. Med Care. 1998;36(1):8–27.
- , , , , , Potential precipitating factors of esophageal variceal bleeding: a case‐control study. Am J Gastroenterol. 2011;106(1):96–103.
- , , , et al. Effects of ethanol consumption on hepatic hemodynamics in patients with alcoholic cirrhosis. Gastroenterology. 1997;112(4):1284–1289.
- , , , Prevalence, correlates, disability, and comorbidity of DSM‐IV alcohol abuse and dependence in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Arch Gen Psychiatry. 2007;64(7):830–842.
- , , Role of prophylactic antibiotics in cirrhotic patients with variceal bleeding. World J Gastroenterol. 2014;20(7):1790–1796.
- , , , et al. Meta‐analysis: antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding—an updated Cochrane review. Aliment Pharmacol Ther. 2011;34(5):509–518.
- , , , et al. The epidemiology of cirrhosis in the United States: a population‐based study [published online ahead of print October 8, 2014]. J Clin Gastroenterol. doi: 10.1097/MCG.0000000000000208.
- , , , Hospitalization for variceal hemorrhage in an era with more prevalent cirrhosis. World J Gastroenterol. 2014;20(32):11326–11332.
- , Banding ligation versus beta‐blockers for primary prevention in oesophageal varices in adults. Cochrane Database Syst Rev. 2012;8:CD004544.
- , , , et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med. 2010;362(25):2370–2379.
- , , , Meta‐analysis: banding ligation and medical interventions for the prevention of rebleeding from oesophageal varices. Aliment Pharmacol Ther. 2012;35(10):1155–1165.
Letter to the Editor
The recently published article by Schouten et al.[1] showed no difference in measured patient outcomes with the use of face‐to‐face handoffs. The authors bring several potential explanations for this observation, all of which might be relevant. Another potential explanation could be the human brain's very predisposition for cognitive biases, and face‐to‐face interaction only increases this possibility. The "framing effect" is a cognitive bias when people make decisions differently depending how information is presented, and "anchoring" describes the human tendency to rely heavily on the first piece of information provided. In our case, the daytime physicians who received face‐to‐face handoffs could have been biased with additional information provided and how this information was provided, and this could have increased the rate of measured adverse patient outcome for this group, eliminating the between group difference. More research is needed to study the influence of the cognitive biases in the medical field.
- , , , , . Association of face‐to‐face handoffs and outcomes of hospitalized internal medicine patients. J Hosp Med. 2015;10(3):137–141.
The recently published article by Schouten et al.[1] showed no difference in measured patient outcomes with the use of face‐to‐face handoffs. The authors bring several potential explanations for this observation, all of which might be relevant. Another potential explanation could be the human brain's very predisposition for cognitive biases, and face‐to‐face interaction only increases this possibility. The "framing effect" is a cognitive bias when people make decisions differently depending how information is presented, and "anchoring" describes the human tendency to rely heavily on the first piece of information provided. In our case, the daytime physicians who received face‐to‐face handoffs could have been biased with additional information provided and how this information was provided, and this could have increased the rate of measured adverse patient outcome for this group, eliminating the between group difference. More research is needed to study the influence of the cognitive biases in the medical field.
The recently published article by Schouten et al.[1] showed no difference in measured patient outcomes with the use of face‐to‐face handoffs. The authors bring several potential explanations for this observation, all of which might be relevant. Another potential explanation could be the human brain's very predisposition for cognitive biases, and face‐to‐face interaction only increases this possibility. The "framing effect" is a cognitive bias when people make decisions differently depending how information is presented, and "anchoring" describes the human tendency to rely heavily on the first piece of information provided. In our case, the daytime physicians who received face‐to‐face handoffs could have been biased with additional information provided and how this information was provided, and this could have increased the rate of measured adverse patient outcome for this group, eliminating the between group difference. More research is needed to study the influence of the cognitive biases in the medical field.
- , , , , . Association of face‐to‐face handoffs and outcomes of hospitalized internal medicine patients. J Hosp Med. 2015;10(3):137–141.
- , , , , . Association of face‐to‐face handoffs and outcomes of hospitalized internal medicine patients. J Hosp Med. 2015;10(3):137–141.
Letter to the Editor/
As a practicing hospitalist, I enjoyed the recently published research article by Schouten et al.[1] Their findings are not surprising to our hospitalist group. We evolved over the years from mandatory face‐to‐face or verbal handoffs to secured e‐mail communications. The night physician transfers care through a secured hospital‐provided email by 7 am. This information is supplemented by a phone call, originating from the day hospitalist on an as‐needed basis. This system works best for most community hospitalist programs, because it provides flexibility, improved communication, and saves a lot of time. In the era of electronic medical records and constantly updated tests results, a face‐to‐face communication is less important. We used to spend 45 to 60 minutes on the handoffs, sometimes even longer due to people being late or not answering phone calls right away. It squeezed time out of patient encounters. The accepting day hospitalist needed to review electronic records (including dictated history and physical information if completed) during the course of the day regardless of the sign out from the night physician. Now, the information flow is smoother and it leaves more time for patient encounters. The day hospitalist keeps printed e‐mail with him or her so that information is readily accessible.
For the relatively smaller community hospitalist groups, it is difficult to ensure that all hospitalists will be available for the face‐to‐face handoffs. The hospitalist who is supposed to take sign‐outs could also be on call for the admissions or responsible for codes or rapid responses, which may interrupt or delay the sign‐out process. The Society of Hospital Medicine recommends both written and verbal sign‐outs.[2] This goal could be achieved more efficiently by the model followed by our group as discussed above. The verbal component could be over the phone rather than face‐to‐face meetings.
- , , , , . Association of face‐to‐face handoffs and outcomes of hospitalized internal medicine patients. J Hosp Med. 2015;10(3):137–141.
- , , , , , . Hospitalist handoffs: a systematic review and task force recommendations. J Hosp Med. 2009;4(7):433–440.
As a practicing hospitalist, I enjoyed the recently published research article by Schouten et al.[1] Their findings are not surprising to our hospitalist group. We evolved over the years from mandatory face‐to‐face or verbal handoffs to secured e‐mail communications. The night physician transfers care through a secured hospital‐provided email by 7 am. This information is supplemented by a phone call, originating from the day hospitalist on an as‐needed basis. This system works best for most community hospitalist programs, because it provides flexibility, improved communication, and saves a lot of time. In the era of electronic medical records and constantly updated tests results, a face‐to‐face communication is less important. We used to spend 45 to 60 minutes on the handoffs, sometimes even longer due to people being late or not answering phone calls right away. It squeezed time out of patient encounters. The accepting day hospitalist needed to review electronic records (including dictated history and physical information if completed) during the course of the day regardless of the sign out from the night physician. Now, the information flow is smoother and it leaves more time for patient encounters. The day hospitalist keeps printed e‐mail with him or her so that information is readily accessible.
For the relatively smaller community hospitalist groups, it is difficult to ensure that all hospitalists will be available for the face‐to‐face handoffs. The hospitalist who is supposed to take sign‐outs could also be on call for the admissions or responsible for codes or rapid responses, which may interrupt or delay the sign‐out process. The Society of Hospital Medicine recommends both written and verbal sign‐outs.[2] This goal could be achieved more efficiently by the model followed by our group as discussed above. The verbal component could be over the phone rather than face‐to‐face meetings.
As a practicing hospitalist, I enjoyed the recently published research article by Schouten et al.[1] Their findings are not surprising to our hospitalist group. We evolved over the years from mandatory face‐to‐face or verbal handoffs to secured e‐mail communications. The night physician transfers care through a secured hospital‐provided email by 7 am. This information is supplemented by a phone call, originating from the day hospitalist on an as‐needed basis. This system works best for most community hospitalist programs, because it provides flexibility, improved communication, and saves a lot of time. In the era of electronic medical records and constantly updated tests results, a face‐to‐face communication is less important. We used to spend 45 to 60 minutes on the handoffs, sometimes even longer due to people being late or not answering phone calls right away. It squeezed time out of patient encounters. The accepting day hospitalist needed to review electronic records (including dictated history and physical information if completed) during the course of the day regardless of the sign out from the night physician. Now, the information flow is smoother and it leaves more time for patient encounters. The day hospitalist keeps printed e‐mail with him or her so that information is readily accessible.
For the relatively smaller community hospitalist groups, it is difficult to ensure that all hospitalists will be available for the face‐to‐face handoffs. The hospitalist who is supposed to take sign‐outs could also be on call for the admissions or responsible for codes or rapid responses, which may interrupt or delay the sign‐out process. The Society of Hospital Medicine recommends both written and verbal sign‐outs.[2] This goal could be achieved more efficiently by the model followed by our group as discussed above. The verbal component could be over the phone rather than face‐to‐face meetings.
- , , , , . Association of face‐to‐face handoffs and outcomes of hospitalized internal medicine patients. J Hosp Med. 2015;10(3):137–141.
- , , , , , . Hospitalist handoffs: a systematic review and task force recommendations. J Hosp Med. 2009;4(7):433–440.
- , , , , . Association of face‐to‐face handoffs and outcomes of hospitalized internal medicine patients. J Hosp Med. 2015;10(3):137–141.
- , , , , , . Hospitalist handoffs: a systematic review and task force recommendations. J Hosp Med. 2009;4(7):433–440.
Treatment differences between urban and rural women with hormone receptor-positive early-stage breast cancer based on 21-gene assay recurrence score result
Symptom-related emergency department visits and hospital admissions during ambulatory cancer treatment
Background People with cancer experience symptoms related to the disease and treatments. Symptom distress has a negative impact on quality of life (QoL). Attending to symptoms and side effects of treatment promotes safe and effective delivery of therapies and may prevent or reduce emergency department visits (EDVs) and unplanned hospital admissions (HAs). There is limited evidence examining symptom-related EDVs or HAs (sx-EDV/HAs) and interventions in ambulatory oncology patients.
Objective To examine factors associated with sx-EDV/HAs in ambulatory oncology patients receiving chemotherapy and/or radiation.
Methods This secondary analysis used data from a randomized controlled trial of ambulatory oncology patients (n = 663) who received the web-based Electronic Self-Report Assessment – Cancer intervention (symptom self-monitoring, tailored education, and communication coaching) or usual care with symptom self-monitoring alone. Group differences were described by summary statistics and compared by t test. Factors associated with the odds of at least 1 sx-EDV/HA were modeled using logistic regression.
Results 98 patients had a total of 171 sx-EDV/HAs with no difference between groups. Higher odds of at least 1 sx-EDV/HA were associated with socioeconomic and clinical factors. The multivariable model indicated that work status, education level, treatment modality, and on-treatment Symptom Distress Scale-15 scores were significantly associated with having at least 1 sx-EDV/HA.
Limitations This is a secondary analysis not sized to determine cause and effect. The results have limited generalizability.
Conclusion Most patients did not experience a sx-EDV/HA. Demographic and clinical factors predicted a sx-EDV/HA.
Funding National Institute of Nursing Research, National Institutes of Health, R01 NR008726; 2008-2011
Click on the PDF icon at the top of this introduction to read the full article.
Background People with cancer experience symptoms related to the disease and treatments. Symptom distress has a negative impact on quality of life (QoL). Attending to symptoms and side effects of treatment promotes safe and effective delivery of therapies and may prevent or reduce emergency department visits (EDVs) and unplanned hospital admissions (HAs). There is limited evidence examining symptom-related EDVs or HAs (sx-EDV/HAs) and interventions in ambulatory oncology patients.
Objective To examine factors associated with sx-EDV/HAs in ambulatory oncology patients receiving chemotherapy and/or radiation.
Methods This secondary analysis used data from a randomized controlled trial of ambulatory oncology patients (n = 663) who received the web-based Electronic Self-Report Assessment – Cancer intervention (symptom self-monitoring, tailored education, and communication coaching) or usual care with symptom self-monitoring alone. Group differences were described by summary statistics and compared by t test. Factors associated with the odds of at least 1 sx-EDV/HA were modeled using logistic regression.
Results 98 patients had a total of 171 sx-EDV/HAs with no difference between groups. Higher odds of at least 1 sx-EDV/HA were associated with socioeconomic and clinical factors. The multivariable model indicated that work status, education level, treatment modality, and on-treatment Symptom Distress Scale-15 scores were significantly associated with having at least 1 sx-EDV/HA.
Limitations This is a secondary analysis not sized to determine cause and effect. The results have limited generalizability.
Conclusion Most patients did not experience a sx-EDV/HA. Demographic and clinical factors predicted a sx-EDV/HA.
Funding National Institute of Nursing Research, National Institutes of Health, R01 NR008726; 2008-2011
Click on the PDF icon at the top of this introduction to read the full article.
Background People with cancer experience symptoms related to the disease and treatments. Symptom distress has a negative impact on quality of life (QoL). Attending to symptoms and side effects of treatment promotes safe and effective delivery of therapies and may prevent or reduce emergency department visits (EDVs) and unplanned hospital admissions (HAs). There is limited evidence examining symptom-related EDVs or HAs (sx-EDV/HAs) and interventions in ambulatory oncology patients.
Objective To examine factors associated with sx-EDV/HAs in ambulatory oncology patients receiving chemotherapy and/or radiation.
Methods This secondary analysis used data from a randomized controlled trial of ambulatory oncology patients (n = 663) who received the web-based Electronic Self-Report Assessment – Cancer intervention (symptom self-monitoring, tailored education, and communication coaching) or usual care with symptom self-monitoring alone. Group differences were described by summary statistics and compared by t test. Factors associated with the odds of at least 1 sx-EDV/HA were modeled using logistic regression.
Results 98 patients had a total of 171 sx-EDV/HAs with no difference between groups. Higher odds of at least 1 sx-EDV/HA were associated with socioeconomic and clinical factors. The multivariable model indicated that work status, education level, treatment modality, and on-treatment Symptom Distress Scale-15 scores were significantly associated with having at least 1 sx-EDV/HA.
Limitations This is a secondary analysis not sized to determine cause and effect. The results have limited generalizability.
Conclusion Most patients did not experience a sx-EDV/HA. Demographic and clinical factors predicted a sx-EDV/HA.
Funding National Institute of Nursing Research, National Institutes of Health, R01 NR008726; 2008-2011
Click on the PDF icon at the top of this introduction to read the full article.
Asymptomatic carotid stenosis and central sleep apnea linked
More than two-thirds of patients with asymptomatic carotid stenosis are likely have sleep apnea, according to an observational study.
The polysomnography results of 96 patients with asymptomatic extracranial carotid stenosis revealed that 69% had sleep apnea. Obstructive sleep apnea was present in 42% of patients and central sleep apnea in 27%.
Stenosis severity was significantly associated with central sleep apnea, but not with obstructive sleep apnea. Researchers found that central sleep apnea, but not obstructive sleep apnea, was associated with arterial hypertension and diabetes mellitus in those patients with asymptomatic carotid stenosis (CHEST 2015;147:1029-1036 [doi:10.1378/chest.14-1655]).
The patients ranged in age from 39 to 86 years (mean age, 70 years); 64 were men. Of the 96 patients, 21 had mild/moderate stenosis and 75 had severe carotid stenosis. Patients with severe stenosis were older, average age 67 years, than were those with mild/moderate stenosis, average age 61 years. The frequency of arterial hypertension and diabetes mellitus was higher in the severe stenosis group than in the mild/moderate stenosis group.
The prevalence of sleep apnea was 76% in patients with severe stenosis compared with 29% in those with mild/moderate carotid stenosis. Total apnea-hypopnea index was higher in the severe stenosis group compared with the mild/moderate stenosis group (P less than or equal to .009). Increase in sleep apnea severity was based on an increase in central apnea-hypopnea index (P less than or equal to .001) but not in obstructive apnea-hypopnea index, reflecting an augmentation of central sleep apnea and not of obstructive sleep apnea in patients with severe compared with mild/moderate carotid stenosis.
“This vascular risk constellation seems to be more strongly connected with CSA [central sleep apnea] than with OSA [obstructive sleep apnea], possibly attributable to carotid chemoreceptor dysfunction,” wrote Dr. Jens Ehrhardt and colleagues at Jena University Hospital, Germany.
No conflicts of interest were declared.
More than two-thirds of patients with asymptomatic carotid stenosis are likely have sleep apnea, according to an observational study.
The polysomnography results of 96 patients with asymptomatic extracranial carotid stenosis revealed that 69% had sleep apnea. Obstructive sleep apnea was present in 42% of patients and central sleep apnea in 27%.
Stenosis severity was significantly associated with central sleep apnea, but not with obstructive sleep apnea. Researchers found that central sleep apnea, but not obstructive sleep apnea, was associated with arterial hypertension and diabetes mellitus in those patients with asymptomatic carotid stenosis (CHEST 2015;147:1029-1036 [doi:10.1378/chest.14-1655]).
The patients ranged in age from 39 to 86 years (mean age, 70 years); 64 were men. Of the 96 patients, 21 had mild/moderate stenosis and 75 had severe carotid stenosis. Patients with severe stenosis were older, average age 67 years, than were those with mild/moderate stenosis, average age 61 years. The frequency of arterial hypertension and diabetes mellitus was higher in the severe stenosis group than in the mild/moderate stenosis group.
The prevalence of sleep apnea was 76% in patients with severe stenosis compared with 29% in those with mild/moderate carotid stenosis. Total apnea-hypopnea index was higher in the severe stenosis group compared with the mild/moderate stenosis group (P less than or equal to .009). Increase in sleep apnea severity was based on an increase in central apnea-hypopnea index (P less than or equal to .001) but not in obstructive apnea-hypopnea index, reflecting an augmentation of central sleep apnea and not of obstructive sleep apnea in patients with severe compared with mild/moderate carotid stenosis.
“This vascular risk constellation seems to be more strongly connected with CSA [central sleep apnea] than with OSA [obstructive sleep apnea], possibly attributable to carotid chemoreceptor dysfunction,” wrote Dr. Jens Ehrhardt and colleagues at Jena University Hospital, Germany.
No conflicts of interest were declared.
More than two-thirds of patients with asymptomatic carotid stenosis are likely have sleep apnea, according to an observational study.
The polysomnography results of 96 patients with asymptomatic extracranial carotid stenosis revealed that 69% had sleep apnea. Obstructive sleep apnea was present in 42% of patients and central sleep apnea in 27%.
Stenosis severity was significantly associated with central sleep apnea, but not with obstructive sleep apnea. Researchers found that central sleep apnea, but not obstructive sleep apnea, was associated with arterial hypertension and diabetes mellitus in those patients with asymptomatic carotid stenosis (CHEST 2015;147:1029-1036 [doi:10.1378/chest.14-1655]).
The patients ranged in age from 39 to 86 years (mean age, 70 years); 64 were men. Of the 96 patients, 21 had mild/moderate stenosis and 75 had severe carotid stenosis. Patients with severe stenosis were older, average age 67 years, than were those with mild/moderate stenosis, average age 61 years. The frequency of arterial hypertension and diabetes mellitus was higher in the severe stenosis group than in the mild/moderate stenosis group.
The prevalence of sleep apnea was 76% in patients with severe stenosis compared with 29% in those with mild/moderate carotid stenosis. Total apnea-hypopnea index was higher in the severe stenosis group compared with the mild/moderate stenosis group (P less than or equal to .009). Increase in sleep apnea severity was based on an increase in central apnea-hypopnea index (P less than or equal to .001) but not in obstructive apnea-hypopnea index, reflecting an augmentation of central sleep apnea and not of obstructive sleep apnea in patients with severe compared with mild/moderate carotid stenosis.
“This vascular risk constellation seems to be more strongly connected with CSA [central sleep apnea] than with OSA [obstructive sleep apnea], possibly attributable to carotid chemoreceptor dysfunction,” wrote Dr. Jens Ehrhardt and colleagues at Jena University Hospital, Germany.
No conflicts of interest were declared.
FROM CHEST
Key clinical point: More than two-thirds of patients with asymptomatic carotid stenosis are likely to have sleep apnea.
Major finding: The prevalence of sleep apnea was 76% in patients with severe stenosis compared with 29% in those with mild/moderate carotid stenosis.
Data source: Study of 96 patients with asymptomatic extracranial carotid stenosis.
Disclosures: No conflicts of interest were declared.
Spacing out
The number of parents asking their pediatricians to stray from the recommended immunization schedule by spreading out the vaccines is increasing, and so is the number of pediatricians who are agreeing to follow these spaced-out schedules.
One of the two reasons most often given by pediatricians for agreeing to the less than optimal immunization schedules is that by showing a willingness to compromise, that physician may be helping to build a trusting relationship with these families. The other reason is a concern – let’s be honest and call it a fear – that a dissatisfied family will move its care to another physician/provider.
When we scratch the surface of these two rationales, neither seems to make much sense. The conflict over immunization spacing comes to a head at the 2-month well-child visit recommended call for six injections. If the infant has had an unremarkable neonatal course, there may not have been any situation in which the physician was forced to demonstrate her trustworthiness. As long as she has dressed professionally, showed up on time for appointments, washed her hands, and appeared genuinely interested in the child’s well-being, that’s about all she has had to do.
The physician may give the impression that she can be trusted, but real trust is usually something that must accumulate over time, in monthly – or more likely yearly – increments. Occasionally a crisis allows the physician to behave so heroically that her route to a trusting relationship is compressed to just a few hours, but fortunately these crises are rare.
Does agreeing to an unnecessary and unsubstantiated diversion from the recommended immunization schedule play a role in trust building? It may signal that the physician is willing to compromise, which in some situations may not be a bad attribute. For example, the mother who has struggled and failed at breastfeeding her 6 weeks despite everyone’s best efforts will appreciate her pediatrician’s willingness to compromise. But should compromise of scientifically validated practices really be one of the cornerstones of a physician-patient relationship?
I have never had a family request that the immunization schedule be spread out for their second child because they have seen for themselves that the process is not what they have feared. I gave all the immunizations myself, and my administration style was quick and matter-of-fact. The problem, of course, is getting hesitant parents up to and over that hurdle of the 2-month visit. Unfortunately, the evidence seems to be that education and extra time and reassurance are of little value in getting them to that point of trust.
The more difficult issue is a physician’s fear that by failing to agree to a spaced-out schedule, she will open a spigot and families will flow out of her practice to other more compromising providers. Is this just an ego thing? No one likes to feel rejected. Will the feared patient exodus seriously depress the physician’s income or will it be merely a trickle that can be ignored? Obviously, the answer varies from community to community. Do families have so many options that they will easily be able to find a provider who is eager to grow his or her practice, and is less concerned about the immunization level of the community? Or, is the pediatrician so busy that a firm adherence to the standard schedule might provide a welcome opportunity to have a more manageable panel size, and at the same time shift the patient mix toward families that don’t require the extra time in fruitless “educational” discussions?
These are questions that don’t seem to be getting asked. What are the numbers? Is the loss of patients just an irrational fear for physicians created by an irrational fear of a small segment of the population? If the physician practices in a group, could her fear of patient loss be eased if the entire group committed itself to following the standard immunization schedule? Are group members discussing this issue among themselves and with their practice managers? Or, is everyone just spacing out?
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com. Scan this QR code to read similar articles or go to pediatricnews.com.
The number of parents asking their pediatricians to stray from the recommended immunization schedule by spreading out the vaccines is increasing, and so is the number of pediatricians who are agreeing to follow these spaced-out schedules.
One of the two reasons most often given by pediatricians for agreeing to the less than optimal immunization schedules is that by showing a willingness to compromise, that physician may be helping to build a trusting relationship with these families. The other reason is a concern – let’s be honest and call it a fear – that a dissatisfied family will move its care to another physician/provider.
When we scratch the surface of these two rationales, neither seems to make much sense. The conflict over immunization spacing comes to a head at the 2-month well-child visit recommended call for six injections. If the infant has had an unremarkable neonatal course, there may not have been any situation in which the physician was forced to demonstrate her trustworthiness. As long as she has dressed professionally, showed up on time for appointments, washed her hands, and appeared genuinely interested in the child’s well-being, that’s about all she has had to do.
The physician may give the impression that she can be trusted, but real trust is usually something that must accumulate over time, in monthly – or more likely yearly – increments. Occasionally a crisis allows the physician to behave so heroically that her route to a trusting relationship is compressed to just a few hours, but fortunately these crises are rare.
Does agreeing to an unnecessary and unsubstantiated diversion from the recommended immunization schedule play a role in trust building? It may signal that the physician is willing to compromise, which in some situations may not be a bad attribute. For example, the mother who has struggled and failed at breastfeeding her 6 weeks despite everyone’s best efforts will appreciate her pediatrician’s willingness to compromise. But should compromise of scientifically validated practices really be one of the cornerstones of a physician-patient relationship?
I have never had a family request that the immunization schedule be spread out for their second child because they have seen for themselves that the process is not what they have feared. I gave all the immunizations myself, and my administration style was quick and matter-of-fact. The problem, of course, is getting hesitant parents up to and over that hurdle of the 2-month visit. Unfortunately, the evidence seems to be that education and extra time and reassurance are of little value in getting them to that point of trust.
The more difficult issue is a physician’s fear that by failing to agree to a spaced-out schedule, she will open a spigot and families will flow out of her practice to other more compromising providers. Is this just an ego thing? No one likes to feel rejected. Will the feared patient exodus seriously depress the physician’s income or will it be merely a trickle that can be ignored? Obviously, the answer varies from community to community. Do families have so many options that they will easily be able to find a provider who is eager to grow his or her practice, and is less concerned about the immunization level of the community? Or, is the pediatrician so busy that a firm adherence to the standard schedule might provide a welcome opportunity to have a more manageable panel size, and at the same time shift the patient mix toward families that don’t require the extra time in fruitless “educational” discussions?
These are questions that don’t seem to be getting asked. What are the numbers? Is the loss of patients just an irrational fear for physicians created by an irrational fear of a small segment of the population? If the physician practices in a group, could her fear of patient loss be eased if the entire group committed itself to following the standard immunization schedule? Are group members discussing this issue among themselves and with their practice managers? Or, is everyone just spacing out?
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com. Scan this QR code to read similar articles or go to pediatricnews.com.
The number of parents asking their pediatricians to stray from the recommended immunization schedule by spreading out the vaccines is increasing, and so is the number of pediatricians who are agreeing to follow these spaced-out schedules.
One of the two reasons most often given by pediatricians for agreeing to the less than optimal immunization schedules is that by showing a willingness to compromise, that physician may be helping to build a trusting relationship with these families. The other reason is a concern – let’s be honest and call it a fear – that a dissatisfied family will move its care to another physician/provider.
When we scratch the surface of these two rationales, neither seems to make much sense. The conflict over immunization spacing comes to a head at the 2-month well-child visit recommended call for six injections. If the infant has had an unremarkable neonatal course, there may not have been any situation in which the physician was forced to demonstrate her trustworthiness. As long as she has dressed professionally, showed up on time for appointments, washed her hands, and appeared genuinely interested in the child’s well-being, that’s about all she has had to do.
The physician may give the impression that she can be trusted, but real trust is usually something that must accumulate over time, in monthly – or more likely yearly – increments. Occasionally a crisis allows the physician to behave so heroically that her route to a trusting relationship is compressed to just a few hours, but fortunately these crises are rare.
Does agreeing to an unnecessary and unsubstantiated diversion from the recommended immunization schedule play a role in trust building? It may signal that the physician is willing to compromise, which in some situations may not be a bad attribute. For example, the mother who has struggled and failed at breastfeeding her 6 weeks despite everyone’s best efforts will appreciate her pediatrician’s willingness to compromise. But should compromise of scientifically validated practices really be one of the cornerstones of a physician-patient relationship?
I have never had a family request that the immunization schedule be spread out for their second child because they have seen for themselves that the process is not what they have feared. I gave all the immunizations myself, and my administration style was quick and matter-of-fact. The problem, of course, is getting hesitant parents up to and over that hurdle of the 2-month visit. Unfortunately, the evidence seems to be that education and extra time and reassurance are of little value in getting them to that point of trust.
The more difficult issue is a physician’s fear that by failing to agree to a spaced-out schedule, she will open a spigot and families will flow out of her practice to other more compromising providers. Is this just an ego thing? No one likes to feel rejected. Will the feared patient exodus seriously depress the physician’s income or will it be merely a trickle that can be ignored? Obviously, the answer varies from community to community. Do families have so many options that they will easily be able to find a provider who is eager to grow his or her practice, and is less concerned about the immunization level of the community? Or, is the pediatrician so busy that a firm adherence to the standard schedule might provide a welcome opportunity to have a more manageable panel size, and at the same time shift the patient mix toward families that don’t require the extra time in fruitless “educational” discussions?
These are questions that don’t seem to be getting asked. What are the numbers? Is the loss of patients just an irrational fear for physicians created by an irrational fear of a small segment of the population? If the physician practices in a group, could her fear of patient loss be eased if the entire group committed itself to following the standard immunization schedule? Are group members discussing this issue among themselves and with their practice managers? Or, is everyone just spacing out?
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at pdnews@frontlinemedcom.com. Scan this QR code to read similar articles or go to pediatricnews.com.
Acne Scarring: A Review of Cosmetic Therapies
Acne vulgaris is one of the most common inflammatory dermatoses affecting nearly all adolescents and a large proportion of adults.1 Incidence rates trend downward with age, but prevalence has been reported to be as high as 51% in individuals aged 20 to 29 years.2 Notably, recent evidence suggests there is an increasing incidence rate of acne among postadolescent women, with the severity associated with the menstrual cycle.3,4 Scarring is a common result of acne and may even occur in the setting of appropriate medical therapy. In particular, some form of facial scarring has been reported to occur in up to 95% of acne patients, with severe scarring in 30% of these patients.5 The detrimental effects of acne scarring are not only limited to impaired cosmetic appearance, as it also has been associated with depression symptoms, suicidal ideation, mental health problems, and general social impairment.6 Given the negative impact of acne scarring on overall health and well-being as well as its permanent nature, early and effective treatment is essential to maximize cosmetic outcomes and minimize long-term deleterious effects.
Acne scarring can be broadly divided into 2 major categories: atrophic and hypertrophic. Atrophic scarring is more common and is characterized by an overall localized reduction in collagen content. Clinically, atrophic scars present as depressions in the skin secondary to inflammatory fibrous contractions induced by acne. This type of scarring can be further divided into various subtypes based on morphologic criteria (eg, size, depth), such as boxcar, ice pick, and rolling scars.7 Conversely, hypertrophic scarring is characterized by an overall increase in collagen content and presents as firm raised lesions. Hypertrophic scars should be distinguished from keloid scars, as the former will not outgrow the margins of the original wound while the latter will.8 Treatment of acne scarring is based on scar type and can be accomplished through a variety of medical and surgical modalities (Table). In this article, we review some of the most commonly utilized therapies for both atrophic and hypertrophic acne scarring with a focus on cosmetic outcomes. It is important to keep in mind, however, that the best treatment is to prevent the occurrence of acne scarring through early and proactive treatment of acne.9
Dermabrasion
Dermabrasion is a decades-old technique that employs the use of a motorized device equipped with an abrasive material to physically remove the superficial layers of the skin, thus inducing the wound-healing process with subsequent formation of new collagen.10 In the same vein, microdermabrasion utilizes aluminum oxide crystals ejected from a nozzle to induce superficial microlacerations.11 This technique is most successful when used to soften scar edges in superficial atrophic scars of the rolling or boxcar subtypes.12 Dermabrasion has been shown to be equally as effective as laser therapy in the treatment of facial scars but is reported to have a much greater risk for adverse effects (AEs)(eg, erythema, edema) that may last for several weeks posttherapy.13,14 Dermabrasion is a particularly operator-dependent technique for which outcomes may vary depending on operator experience. As such, it is not generally recommended as a first-line therapy given its risks and relatively modest results; however, dermabrasion can be a useful adjunct when performed in the right setting. This technique, in addition to laser resurfacing, should be used with caution in patients who have recently taken or currently are taking isotretinoin, as several case series have reported postprocedural development of hypertrophic or keloid scars,15-17 but these findings subsequently were questioned in the literature.18
Laser Therapy
Laser technology has advanced tremendously over the last few decades and there are now a multitude of available lasers that are capable of variable depth penetration and energy delivery patterns. Common to all, however, is the ability to induce localized thermal damage with eventual collagen remodeling. Lasers can be divided into 2 major categories: ablative and nonablative. Ablative lasers cause epidermal destruction, while nonablative lasers are able to selectively target dermal layers without disrupting the overlying epithelium. Generally speaking, ablative lasers are more effective than nonablative lasers in the treatment of atrophic scars, with reported mean improvements of up to 81%.19 This increased efficacy comes with an increased risk for AEs such as postinflammatory hyperpigmentation, prolonged posttreatment erythema, and formation of additional scarring.20 Both ablative and nonablative lasers can be applied in the more recently developed technology of fractional photothermolysis. With this method, noncontiguous microscopic columns of thermal injury surrounded by zones of viable tissue are created, which is in contrast to the traditional manner of inducing broad thermal injury. Fractional ablative lasers can achieve efficacy rates similar to traditional ablative lasers with a reduced risk for permanent scarring or dispigmentation.21 Notably, recent studies have shown promising results for the use of fractional ablative lasers as a mechanism to enhance drug delivery of topically applied medications such as poly-L-lactic acid and triamcinolone acetonide in the treatment of atrophic and hypertrophic scars, respectively.22,23
Lasers also play a role in the treatment of hypertrophic acne scars with the use of nonablative pulsed dye lasers. These lasers cause selective thermolysis of dermal vasculature, and average clinical improvements in hypertrophic scars of 67.5% after a single treatment have been reported.24 Temporary postoperative purpura and long-term hyperpigmentation are reported outcomes of this therapy.20
Radiofrequency
Nonablative radiofrequency (RF) is a relatively novel technique that creates an electric current in the dermis at preset depths to induce thermal damage and eventual collagen synthesis. There are a variety of modalities for which RF can be applied, but microneedle bipolar RF and fractional bipolar RF treatments offer the best results for atrophic acne scars. Improvements in scar appearance of 25% to 75% have been reported after several treatment sessions.25 Better results have been reported in the treatment of ice pick scars as compared to more superficial scars,26 but additional studies will be necessary to validate this claim. Adverse effects are largely limited to temporary erythema and posttreatment scabbing.27
Subcision
Subcision is a more physically intensive technique useful for treatment of superficial atrophic acne scars. This method involves the use of a small needle that is inserted into the periphery of a scar before being moved in a back-and-forth manner underneath the base of the scar to loosen the fibrotic adhesions that result in the depressed appearance of the scar. Additionally, loosening of the tissue and resultant bleeding creates a potential space for future collagen deposition during the subsequent wound-healing phase. Subcision has a reported success rate of 50% to 60% in the treatment of rolling scars, and prospective, randomized, split-face trials have indicated that the short-term outcomes of subcision are superior to dermal fillers while being equally effective long-term.28,29 Of note, a small percentage of patients may develop a localized nodule at the site of treatment, which can be resolved with intralesional steroids.11
Skin Needling
Skin needling, also referred to as collagen induction therapy, utilizes vertical needle punctures rather than the horizontally directed punctures that are used in subcision and can be used to treat rolling and boxcar scars. Traditionally, a small roller equipped with rows of small needles typically ranging in size from 0.5 to 3.0 mm in length is passed over the skin using gentle pressure, puncturing the superficial layers of the skin to loosen fibrotic adhesions and induce collagen synthesis. This procedure may be repeated several times within a single session or over multiple sessions depending on the depth and quality of the scars. This technique has been reported to reduce scar depth up to 25% after 2 sessions.30
Punch Techniques
Punch techniques are useful for treatment of deeper atrophic acne scarring, for which most other treatment modalities are not particularly effective. A punch excision approximately equal to the scar size is first performed, which may then be followed by either removal of the scar tissue with subsequent suturing, graft replacement of the removed tissue, or elevation of the already established scar tissue to the level of surrounding skin where it is then held in place by sutures or adhesive skin closure material. Success rates with this method are largely limited to case series, but punch techniques are reported to be efficacious, especially for treatment of ice pick scars. Risks for this method include graft failure, graft depression, and formation of sinus tracts.31
Chemical Peels
Chemicals peels traditionally employ the use of acidic compounds to strip away the outer layers of skin to variable depths depending on the concentration of the agent being applied. Chemical peels are not generally recommended for application in a nonspecific manner in the treatment of acne scars given the relatively mild cosmetic improvements seen and the high rate of AEs such as pigmentary alterations and additional scar formation.12 Rather, clinicians should employ the CROSS (chemical reconstruction of skin scars) technique, in which peel agents such as trichloroacetic acid are applied in high concentrations only to areas of atrophic scarring. Use of this method can minimize AEs while simultaneously achieving high success rates, with excellent results in 100% (32/32) of patients after 5 to 6 treatment sessions.32 This method has been successful for hard-to-treat ice pick scars.33
Soft-Tissue Augmentation
Soft-tissue augmentation is another effective treatment of superficial atrophic acne scarring that utilizes injections of collagen fillers such as hyaluronic acid, calcium hydroxylapatite, poly-L-lactic acid, silicone, and even autologous fat to replace lost tissue volume while simultaneously inducing collagen production via stretching of dermal fibroblasts.34 These treatments may require multiple sessions for cosmetic improvement but have shown considerable efficacy in the treatment of atrophic acne scars. Hyaluronic acid has been reported to be particularly effective for rolling scars.12 However, these compounds only provide temporary results, thus requiring repeated treatments to maintain cosmetic outcomes. Permanent options include the recently US Food and Drug Administration–approved polymethylmethacrylate microspheres suspended in bovine collagen as well as the novel technique of autologous fibroblast transfer. These options are relatively new, but initial double-blind, randomized, controlled trials have shown minimal AEs with substantial improvements in 64% to 100% of atrophic scars treated.35,36
Intralesional Therapy
Intralesional corticosteroid injections are a mainstay treatment of hypertrophic acne scarring and are believed to exert their effects by decreasing fibroblast proliferation and promoting collagen degradation.37 Treatment with steroids generally is effective, with reported improvement in 75% (6/8) of patients and complete flattening in 50% (4/8) of lesions according to one study.38 Development of hypopigmentation, dermal atrophy, and telangiectasia are potential sequelae of this treatment.37
5-Fluorouracil, bleomycin, and verapamil also have been used with good results as intralesional treatments of hypertrophic scars, but these agents typically are reserved for cases of corticosteroid failure. Such compounds are thought to mediate their effects through inhibition of dermal fibroblast proliferation.39 Results with these therapies are varied, but greater than 75% improvement is seen in most cases. Adverse effects include injection-site ulceration and hyperpigmentation.39
Cryotherapy
Contact cryotherapy has been studied as treatment of hypertrophic acne scars. The exact mechanism through which scars are reduced is unclear, but it is hypothesized that the physical damage caused by freezing and thrombosis lead to collagen restructuring. According to one study, cryotherapy was reported to achieve good or excellent results in 76% (29/38) of cases.40 Permanent pigmentary alterations are a possible AE.
Silicone Dressings
Silicone dressings are a reasonable treatment option for hypertrophic acne scarring given their proven efficacy and minimal risk for AEs. Thin sheets of silicone gels or membranes are applied daily in a topical manner to acne scars and are believed to be therapeutic through a combination of pressure and hydration, which subsequently inhibits fibroblast production of collagen. Notable reductions in scar appearance and size are seen in 60% to 80% of individuals using this method.41 Adverse effects are limited to pruritus and local skin maceration. Patient noncompliance may be an issue, as the silicone dressings may be applied on highly visible areas such as the face. Patients may apply the dressings at night, but efficacy may be reduced.
Conclusion
When determining which treatment options to use in a patient with acne scarring, it is important to first determine the patient’s treatment goals while simultaneously establishing realistic expectations. Important factors to consider are the patient’s preferences regarding treatment risk, duration, and permanence, as well as budget and social or work requirements. As such, treatment plans for each patient should be determined on a case-by-case basis. It also is important to note that a combination of different treatment modalities often is necessary and superior to monotherapy in achieving satisfactory cosmetic outcomes.
1. Ghodsi SZ, Orawa H, Zouboulis CC. Prevalence, severity, and severity risk factors of acne in high school pupils: a community-based study. J Invest Dermatol. 2009;129:2136-2141.
2. Collier CN, Harper JC, Cafardi JA, et al. The prevalence of acne in adults 20 years and older. J Am Acad Dermatol. 2008;58:56-59.
3. Kim GK, Michaels BB. Post-adolescent acne in women: more common and more clinical considerations. J Drugs Dermatol. 2012;11:708-713.
4. Geller L, Rosen J, Frankel A, et al. Perimenstrual flare of adult acne. J Clin Aesthet Dermatol. 2014;7:30-34.
5. Layton AM, Henderson CA, Cunliffe WJ. A clinical evaluation of acne scarring and its incidence. Clin Exp Dermatol. 1994;19:303-308.
6. Halvorsen JA, Stern RS, Dalgard F, et al. Suicidal ideation, mental health problems, and social impairment are increased in adolescents with acne: a population-based study. J Invest Dermatol. 2011;131:363-370.
7. Jacob CI, Dover JS, Kaminer MS. Acne scarring: a classification system and review of treatment options. J Am Acad Dermatol. 2001;45:109-117.
8. Rivera AE. Acne scarring: a review and current treatment modalities. J Am Acad Dermatol. 2008;59:659-676.
9. Goodman GJ. Acne and acne scarring: why should we treat? Med J Aust. 1999;171:62-63.
10. Frank W. Therapeutic dermabrasion. back to the future. Arch Dermatol. 1994;130:1187-1189.
11. Goodman GJ. Postacne scarring: a review of its pathophysiology and treatment. Dermatol Surg. 2000;26:857-871.
12. Hession MT, Graber EM. Atrophic acne scarring: a review of treatment options. J Clin Aesthet Dermatol. 2015;8:50-58.
13. Levy LL, Zeichner JA. Management of acne scarring, part II: a comparative review of non-laser-based, minimally invasive approaches. Am J Clin Dermatol. 2012;13:331-340.
14. Christophel JJ, Elm C, Endrizzi BT, et al. A randomized controlled trial of fractional laser therapy and dermabrasion for scar resurfacing. Dermatol Surg. 2012;38:595-602.
15. Katz BE, McFarlane DF. Atypical facial scarring after isotretinoin therapy in a patient with previous dermabrasion. J Am Acad Dermatol. 1994;30:852-853.
16. Bernestein LJ, Geronemus RG. Keloid formation with the 585-nm pulsed dye laser during isotretinoin treatment. Arch Dermatol. 1997;133:111-112.
17. Zachariae H. Delayed wound healing and keloid formation following argon laser treatment or dermabrasion during isotretinoin treatment. Br J Dermatol. 1988;118:703-706.
18. Wootton CI, Cartwright RP, Manning P, et al. Should isotretinoin be stopped prior to surgery? a critically appraised topic. Br J Dermatol. 2014;170:239-244.
19. Alster TS, West TB. Resurfacing of atrophic facial acne scars with a high-energy, pulsed carbon dioxide laser. Dermatol Surg. 1996;22:151-155.
20. Sobanko JF, Alster TS. Management of acne scarring, part I: a comparative review of laser surgical approaches. Am J Clin Dermatol. 2012;13:319-330.
21. Cho SB, Lee SJ, Oh SH, et al. Non-ablative 1550nm erbium-glass and ablative 10,600nm carbon dioxide fractional lasers for acne scar: a randomized split-face study with blinded response evaluation. J Eur Acad Dermatol Venereol. 2010;24:921-925.
22. Rkein A, Ozog D, Waibel JS. Treatment of atrophic scars with fractionated CO2 laser facilitating delivery of topically applied poly-L-lactic acid. Dermatol Surg. 2014;40:624-631.
23. Waibel JS, Wulkan AJ, Shumaker PR. Treatment of hypertrophic scars using laser and laser assisted corticosteroid delivery. Lasers Surg Med. 2013;45:135-140.
24. Alster TS, McMeekin TO. Improvement of facial acne scars by the 585-nm flashlamp-pumped pulsed dye laser. J Am Acad Dermatol. 1996;35:79-81.
25. Simmons BJ, Griffith RD, Falto-Aizpurua LA, et al. Use of radiofrequency in cosmetic dermatology: focus on nonablative treatment of acne scars. Clin Cosmet Investig Dermatol. 2014;7:335-339.
26. Ramesh M, Gopal M, Kumar S, et al. Novel technology in the treatment of acne scars: the matrix-tunable radiofrequency technology. J Cutan Aesthet Surg. 2010;3:97-101.
27. Johnson WC. Treatment of pitted scars; punch transplant technique. J Dermatol Surg Oncol. 1986;12:260-265.
28. Alam M, Omura N, Kaminer MS. Subcision for acne scarring: technique and outcomes in 40 patients. Dermatol Surg. 2005;31:310-317.
29. Sage R, Lopiccolo M, Liu A, et al. Subcuticular incision versus naturally sourced porcine collagen filler for acne scars: a randomized split-face comparison. Dermatol Surg. 2011;37:426-431.
30. Fabbrocini G, Annunziata MC, D’arco V, et al. Acne scars: pathogenesis, classification and treatment [published online ahead of print October 14, 2010]. Dermatol Res Pract. 2010;2010:893080.
31. Johnson WC. Treatment of pitted scars: punch transplant technique. J Dermatol Surg Oncol. 1986;12:260-265.
32. Lee JB, Chung WG, Kwahck H, et al. Focal treatment of acne scars with trichloroacetic acid: chemical reconstruction of skin scars method. Dermatol Surg. 2002;28:1017-1021.
33. Bhardwaj D, Khunger N. An assessment of the efficacy and safety of CROSS technique with 100% TCA in the management of ice pick acne scars. J Cutan Aesthet Surg. 2010;3:93-96.
34. Wang F, Garza LA, Kang S, et al. In vivo stimulation of de novo collagen production caused by cross-linked hyaluronic acid dermal filler injections in photodamaged human skin. Arch Dermatol. 2007;143:155-163.
35. Karnik J, Baumann L, Bruce S, et al. A double-blind, randomized, multicenter, controlled trial of suspended polymethylmethacrylate microspheres for the correction of atrophic facial acne scars. J Am Acad Dermatol. 2014;71:77-83.
36. Munavalli GS, Smith S, Maslowski JM, et al. Successful treatment of depressed, distensible acne scars using autologous fibroblasts: a multi-site, prospective, double blind, placebo-controlled clinical trial. Dermatol Surg. 2013;39:1226-1236.
37. Leventhal D, Furr M, Reiter D. Treatment of keloids and hypertrophic scars: a meta-analysis and review of the literature. Arch Facial Plast Surg. 2006;8:362-368.
38. Darzi MA, Chowdri NA, Kaul SK, et al. Evaluation of various methods of treating keloids and hypertrophic scars: a 10-year follow-up study. Br J Plast Surg. 1992;45:374-379.
39. Ledon JA, Savas J, Franca K, et al. Intralesional treatment for keloids and hypertrophic scars: a review. Dermatol Surg. 2013;39:1745-1757.
40. Zouboulis CC, Blume U, Büttner P, et al. Outcomes of cryosurgery in keloids and hypertrophic scars. a prospective consecutive trial of case series. Arch Dermatol. 1993;129:1146-1151.
41. Puri N, Talwar A. The efficacy of silicone gel for the treatment of hypertrophic scars and keloids. J Cutan Aesthet Surg. 2009;2:104-106.
Acne vulgaris is one of the most common inflammatory dermatoses affecting nearly all adolescents and a large proportion of adults.1 Incidence rates trend downward with age, but prevalence has been reported to be as high as 51% in individuals aged 20 to 29 years.2 Notably, recent evidence suggests there is an increasing incidence rate of acne among postadolescent women, with the severity associated with the menstrual cycle.3,4 Scarring is a common result of acne and may even occur in the setting of appropriate medical therapy. In particular, some form of facial scarring has been reported to occur in up to 95% of acne patients, with severe scarring in 30% of these patients.5 The detrimental effects of acne scarring are not only limited to impaired cosmetic appearance, as it also has been associated with depression symptoms, suicidal ideation, mental health problems, and general social impairment.6 Given the negative impact of acne scarring on overall health and well-being as well as its permanent nature, early and effective treatment is essential to maximize cosmetic outcomes and minimize long-term deleterious effects.
Acne scarring can be broadly divided into 2 major categories: atrophic and hypertrophic. Atrophic scarring is more common and is characterized by an overall localized reduction in collagen content. Clinically, atrophic scars present as depressions in the skin secondary to inflammatory fibrous contractions induced by acne. This type of scarring can be further divided into various subtypes based on morphologic criteria (eg, size, depth), such as boxcar, ice pick, and rolling scars.7 Conversely, hypertrophic scarring is characterized by an overall increase in collagen content and presents as firm raised lesions. Hypertrophic scars should be distinguished from keloid scars, as the former will not outgrow the margins of the original wound while the latter will.8 Treatment of acne scarring is based on scar type and can be accomplished through a variety of medical and surgical modalities (Table). In this article, we review some of the most commonly utilized therapies for both atrophic and hypertrophic acne scarring with a focus on cosmetic outcomes. It is important to keep in mind, however, that the best treatment is to prevent the occurrence of acne scarring through early and proactive treatment of acne.9
Dermabrasion
Dermabrasion is a decades-old technique that employs the use of a motorized device equipped with an abrasive material to physically remove the superficial layers of the skin, thus inducing the wound-healing process with subsequent formation of new collagen.10 In the same vein, microdermabrasion utilizes aluminum oxide crystals ejected from a nozzle to induce superficial microlacerations.11 This technique is most successful when used to soften scar edges in superficial atrophic scars of the rolling or boxcar subtypes.12 Dermabrasion has been shown to be equally as effective as laser therapy in the treatment of facial scars but is reported to have a much greater risk for adverse effects (AEs)(eg, erythema, edema) that may last for several weeks posttherapy.13,14 Dermabrasion is a particularly operator-dependent technique for which outcomes may vary depending on operator experience. As such, it is not generally recommended as a first-line therapy given its risks and relatively modest results; however, dermabrasion can be a useful adjunct when performed in the right setting. This technique, in addition to laser resurfacing, should be used with caution in patients who have recently taken or currently are taking isotretinoin, as several case series have reported postprocedural development of hypertrophic or keloid scars,15-17 but these findings subsequently were questioned in the literature.18
Laser Therapy
Laser technology has advanced tremendously over the last few decades and there are now a multitude of available lasers that are capable of variable depth penetration and energy delivery patterns. Common to all, however, is the ability to induce localized thermal damage with eventual collagen remodeling. Lasers can be divided into 2 major categories: ablative and nonablative. Ablative lasers cause epidermal destruction, while nonablative lasers are able to selectively target dermal layers without disrupting the overlying epithelium. Generally speaking, ablative lasers are more effective than nonablative lasers in the treatment of atrophic scars, with reported mean improvements of up to 81%.19 This increased efficacy comes with an increased risk for AEs such as postinflammatory hyperpigmentation, prolonged posttreatment erythema, and formation of additional scarring.20 Both ablative and nonablative lasers can be applied in the more recently developed technology of fractional photothermolysis. With this method, noncontiguous microscopic columns of thermal injury surrounded by zones of viable tissue are created, which is in contrast to the traditional manner of inducing broad thermal injury. Fractional ablative lasers can achieve efficacy rates similar to traditional ablative lasers with a reduced risk for permanent scarring or dispigmentation.21 Notably, recent studies have shown promising results for the use of fractional ablative lasers as a mechanism to enhance drug delivery of topically applied medications such as poly-L-lactic acid and triamcinolone acetonide in the treatment of atrophic and hypertrophic scars, respectively.22,23
Lasers also play a role in the treatment of hypertrophic acne scars with the use of nonablative pulsed dye lasers. These lasers cause selective thermolysis of dermal vasculature, and average clinical improvements in hypertrophic scars of 67.5% after a single treatment have been reported.24 Temporary postoperative purpura and long-term hyperpigmentation are reported outcomes of this therapy.20
Radiofrequency
Nonablative radiofrequency (RF) is a relatively novel technique that creates an electric current in the dermis at preset depths to induce thermal damage and eventual collagen synthesis. There are a variety of modalities for which RF can be applied, but microneedle bipolar RF and fractional bipolar RF treatments offer the best results for atrophic acne scars. Improvements in scar appearance of 25% to 75% have been reported after several treatment sessions.25 Better results have been reported in the treatment of ice pick scars as compared to more superficial scars,26 but additional studies will be necessary to validate this claim. Adverse effects are largely limited to temporary erythema and posttreatment scabbing.27
Subcision
Subcision is a more physically intensive technique useful for treatment of superficial atrophic acne scars. This method involves the use of a small needle that is inserted into the periphery of a scar before being moved in a back-and-forth manner underneath the base of the scar to loosen the fibrotic adhesions that result in the depressed appearance of the scar. Additionally, loosening of the tissue and resultant bleeding creates a potential space for future collagen deposition during the subsequent wound-healing phase. Subcision has a reported success rate of 50% to 60% in the treatment of rolling scars, and prospective, randomized, split-face trials have indicated that the short-term outcomes of subcision are superior to dermal fillers while being equally effective long-term.28,29 Of note, a small percentage of patients may develop a localized nodule at the site of treatment, which can be resolved with intralesional steroids.11
Skin Needling
Skin needling, also referred to as collagen induction therapy, utilizes vertical needle punctures rather than the horizontally directed punctures that are used in subcision and can be used to treat rolling and boxcar scars. Traditionally, a small roller equipped with rows of small needles typically ranging in size from 0.5 to 3.0 mm in length is passed over the skin using gentle pressure, puncturing the superficial layers of the skin to loosen fibrotic adhesions and induce collagen synthesis. This procedure may be repeated several times within a single session or over multiple sessions depending on the depth and quality of the scars. This technique has been reported to reduce scar depth up to 25% after 2 sessions.30
Punch Techniques
Punch techniques are useful for treatment of deeper atrophic acne scarring, for which most other treatment modalities are not particularly effective. A punch excision approximately equal to the scar size is first performed, which may then be followed by either removal of the scar tissue with subsequent suturing, graft replacement of the removed tissue, or elevation of the already established scar tissue to the level of surrounding skin where it is then held in place by sutures or adhesive skin closure material. Success rates with this method are largely limited to case series, but punch techniques are reported to be efficacious, especially for treatment of ice pick scars. Risks for this method include graft failure, graft depression, and formation of sinus tracts.31
Chemical Peels
Chemicals peels traditionally employ the use of acidic compounds to strip away the outer layers of skin to variable depths depending on the concentration of the agent being applied. Chemical peels are not generally recommended for application in a nonspecific manner in the treatment of acne scars given the relatively mild cosmetic improvements seen and the high rate of AEs such as pigmentary alterations and additional scar formation.12 Rather, clinicians should employ the CROSS (chemical reconstruction of skin scars) technique, in which peel agents such as trichloroacetic acid are applied in high concentrations only to areas of atrophic scarring. Use of this method can minimize AEs while simultaneously achieving high success rates, with excellent results in 100% (32/32) of patients after 5 to 6 treatment sessions.32 This method has been successful for hard-to-treat ice pick scars.33
Soft-Tissue Augmentation
Soft-tissue augmentation is another effective treatment of superficial atrophic acne scarring that utilizes injections of collagen fillers such as hyaluronic acid, calcium hydroxylapatite, poly-L-lactic acid, silicone, and even autologous fat to replace lost tissue volume while simultaneously inducing collagen production via stretching of dermal fibroblasts.34 These treatments may require multiple sessions for cosmetic improvement but have shown considerable efficacy in the treatment of atrophic acne scars. Hyaluronic acid has been reported to be particularly effective for rolling scars.12 However, these compounds only provide temporary results, thus requiring repeated treatments to maintain cosmetic outcomes. Permanent options include the recently US Food and Drug Administration–approved polymethylmethacrylate microspheres suspended in bovine collagen as well as the novel technique of autologous fibroblast transfer. These options are relatively new, but initial double-blind, randomized, controlled trials have shown minimal AEs with substantial improvements in 64% to 100% of atrophic scars treated.35,36
Intralesional Therapy
Intralesional corticosteroid injections are a mainstay treatment of hypertrophic acne scarring and are believed to exert their effects by decreasing fibroblast proliferation and promoting collagen degradation.37 Treatment with steroids generally is effective, with reported improvement in 75% (6/8) of patients and complete flattening in 50% (4/8) of lesions according to one study.38 Development of hypopigmentation, dermal atrophy, and telangiectasia are potential sequelae of this treatment.37
5-Fluorouracil, bleomycin, and verapamil also have been used with good results as intralesional treatments of hypertrophic scars, but these agents typically are reserved for cases of corticosteroid failure. Such compounds are thought to mediate their effects through inhibition of dermal fibroblast proliferation.39 Results with these therapies are varied, but greater than 75% improvement is seen in most cases. Adverse effects include injection-site ulceration and hyperpigmentation.39
Cryotherapy
Contact cryotherapy has been studied as treatment of hypertrophic acne scars. The exact mechanism through which scars are reduced is unclear, but it is hypothesized that the physical damage caused by freezing and thrombosis lead to collagen restructuring. According to one study, cryotherapy was reported to achieve good or excellent results in 76% (29/38) of cases.40 Permanent pigmentary alterations are a possible AE.
Silicone Dressings
Silicone dressings are a reasonable treatment option for hypertrophic acne scarring given their proven efficacy and minimal risk for AEs. Thin sheets of silicone gels or membranes are applied daily in a topical manner to acne scars and are believed to be therapeutic through a combination of pressure and hydration, which subsequently inhibits fibroblast production of collagen. Notable reductions in scar appearance and size are seen in 60% to 80% of individuals using this method.41 Adverse effects are limited to pruritus and local skin maceration. Patient noncompliance may be an issue, as the silicone dressings may be applied on highly visible areas such as the face. Patients may apply the dressings at night, but efficacy may be reduced.
Conclusion
When determining which treatment options to use in a patient with acne scarring, it is important to first determine the patient’s treatment goals while simultaneously establishing realistic expectations. Important factors to consider are the patient’s preferences regarding treatment risk, duration, and permanence, as well as budget and social or work requirements. As such, treatment plans for each patient should be determined on a case-by-case basis. It also is important to note that a combination of different treatment modalities often is necessary and superior to monotherapy in achieving satisfactory cosmetic outcomes.
Acne vulgaris is one of the most common inflammatory dermatoses affecting nearly all adolescents and a large proportion of adults.1 Incidence rates trend downward with age, but prevalence has been reported to be as high as 51% in individuals aged 20 to 29 years.2 Notably, recent evidence suggests there is an increasing incidence rate of acne among postadolescent women, with the severity associated with the menstrual cycle.3,4 Scarring is a common result of acne and may even occur in the setting of appropriate medical therapy. In particular, some form of facial scarring has been reported to occur in up to 95% of acne patients, with severe scarring in 30% of these patients.5 The detrimental effects of acne scarring are not only limited to impaired cosmetic appearance, as it also has been associated with depression symptoms, suicidal ideation, mental health problems, and general social impairment.6 Given the negative impact of acne scarring on overall health and well-being as well as its permanent nature, early and effective treatment is essential to maximize cosmetic outcomes and minimize long-term deleterious effects.
Acne scarring can be broadly divided into 2 major categories: atrophic and hypertrophic. Atrophic scarring is more common and is characterized by an overall localized reduction in collagen content. Clinically, atrophic scars present as depressions in the skin secondary to inflammatory fibrous contractions induced by acne. This type of scarring can be further divided into various subtypes based on morphologic criteria (eg, size, depth), such as boxcar, ice pick, and rolling scars.7 Conversely, hypertrophic scarring is characterized by an overall increase in collagen content and presents as firm raised lesions. Hypertrophic scars should be distinguished from keloid scars, as the former will not outgrow the margins of the original wound while the latter will.8 Treatment of acne scarring is based on scar type and can be accomplished through a variety of medical and surgical modalities (Table). In this article, we review some of the most commonly utilized therapies for both atrophic and hypertrophic acne scarring with a focus on cosmetic outcomes. It is important to keep in mind, however, that the best treatment is to prevent the occurrence of acne scarring through early and proactive treatment of acne.9
Dermabrasion
Dermabrasion is a decades-old technique that employs the use of a motorized device equipped with an abrasive material to physically remove the superficial layers of the skin, thus inducing the wound-healing process with subsequent formation of new collagen.10 In the same vein, microdermabrasion utilizes aluminum oxide crystals ejected from a nozzle to induce superficial microlacerations.11 This technique is most successful when used to soften scar edges in superficial atrophic scars of the rolling or boxcar subtypes.12 Dermabrasion has been shown to be equally as effective as laser therapy in the treatment of facial scars but is reported to have a much greater risk for adverse effects (AEs)(eg, erythema, edema) that may last for several weeks posttherapy.13,14 Dermabrasion is a particularly operator-dependent technique for which outcomes may vary depending on operator experience. As such, it is not generally recommended as a first-line therapy given its risks and relatively modest results; however, dermabrasion can be a useful adjunct when performed in the right setting. This technique, in addition to laser resurfacing, should be used with caution in patients who have recently taken or currently are taking isotretinoin, as several case series have reported postprocedural development of hypertrophic or keloid scars,15-17 but these findings subsequently were questioned in the literature.18
Laser Therapy
Laser technology has advanced tremendously over the last few decades and there are now a multitude of available lasers that are capable of variable depth penetration and energy delivery patterns. Common to all, however, is the ability to induce localized thermal damage with eventual collagen remodeling. Lasers can be divided into 2 major categories: ablative and nonablative. Ablative lasers cause epidermal destruction, while nonablative lasers are able to selectively target dermal layers without disrupting the overlying epithelium. Generally speaking, ablative lasers are more effective than nonablative lasers in the treatment of atrophic scars, with reported mean improvements of up to 81%.19 This increased efficacy comes with an increased risk for AEs such as postinflammatory hyperpigmentation, prolonged posttreatment erythema, and formation of additional scarring.20 Both ablative and nonablative lasers can be applied in the more recently developed technology of fractional photothermolysis. With this method, noncontiguous microscopic columns of thermal injury surrounded by zones of viable tissue are created, which is in contrast to the traditional manner of inducing broad thermal injury. Fractional ablative lasers can achieve efficacy rates similar to traditional ablative lasers with a reduced risk for permanent scarring or dispigmentation.21 Notably, recent studies have shown promising results for the use of fractional ablative lasers as a mechanism to enhance drug delivery of topically applied medications such as poly-L-lactic acid and triamcinolone acetonide in the treatment of atrophic and hypertrophic scars, respectively.22,23
Lasers also play a role in the treatment of hypertrophic acne scars with the use of nonablative pulsed dye lasers. These lasers cause selective thermolysis of dermal vasculature, and average clinical improvements in hypertrophic scars of 67.5% after a single treatment have been reported.24 Temporary postoperative purpura and long-term hyperpigmentation are reported outcomes of this therapy.20
Radiofrequency
Nonablative radiofrequency (RF) is a relatively novel technique that creates an electric current in the dermis at preset depths to induce thermal damage and eventual collagen synthesis. There are a variety of modalities for which RF can be applied, but microneedle bipolar RF and fractional bipolar RF treatments offer the best results for atrophic acne scars. Improvements in scar appearance of 25% to 75% have been reported after several treatment sessions.25 Better results have been reported in the treatment of ice pick scars as compared to more superficial scars,26 but additional studies will be necessary to validate this claim. Adverse effects are largely limited to temporary erythema and posttreatment scabbing.27
Subcision
Subcision is a more physically intensive technique useful for treatment of superficial atrophic acne scars. This method involves the use of a small needle that is inserted into the periphery of a scar before being moved in a back-and-forth manner underneath the base of the scar to loosen the fibrotic adhesions that result in the depressed appearance of the scar. Additionally, loosening of the tissue and resultant bleeding creates a potential space for future collagen deposition during the subsequent wound-healing phase. Subcision has a reported success rate of 50% to 60% in the treatment of rolling scars, and prospective, randomized, split-face trials have indicated that the short-term outcomes of subcision are superior to dermal fillers while being equally effective long-term.28,29 Of note, a small percentage of patients may develop a localized nodule at the site of treatment, which can be resolved with intralesional steroids.11
Skin Needling
Skin needling, also referred to as collagen induction therapy, utilizes vertical needle punctures rather than the horizontally directed punctures that are used in subcision and can be used to treat rolling and boxcar scars. Traditionally, a small roller equipped with rows of small needles typically ranging in size from 0.5 to 3.0 mm in length is passed over the skin using gentle pressure, puncturing the superficial layers of the skin to loosen fibrotic adhesions and induce collagen synthesis. This procedure may be repeated several times within a single session or over multiple sessions depending on the depth and quality of the scars. This technique has been reported to reduce scar depth up to 25% after 2 sessions.30
Punch Techniques
Punch techniques are useful for treatment of deeper atrophic acne scarring, for which most other treatment modalities are not particularly effective. A punch excision approximately equal to the scar size is first performed, which may then be followed by either removal of the scar tissue with subsequent suturing, graft replacement of the removed tissue, or elevation of the already established scar tissue to the level of surrounding skin where it is then held in place by sutures or adhesive skin closure material. Success rates with this method are largely limited to case series, but punch techniques are reported to be efficacious, especially for treatment of ice pick scars. Risks for this method include graft failure, graft depression, and formation of sinus tracts.31
Chemical Peels
Chemicals peels traditionally employ the use of acidic compounds to strip away the outer layers of skin to variable depths depending on the concentration of the agent being applied. Chemical peels are not generally recommended for application in a nonspecific manner in the treatment of acne scars given the relatively mild cosmetic improvements seen and the high rate of AEs such as pigmentary alterations and additional scar formation.12 Rather, clinicians should employ the CROSS (chemical reconstruction of skin scars) technique, in which peel agents such as trichloroacetic acid are applied in high concentrations only to areas of atrophic scarring. Use of this method can minimize AEs while simultaneously achieving high success rates, with excellent results in 100% (32/32) of patients after 5 to 6 treatment sessions.32 This method has been successful for hard-to-treat ice pick scars.33
Soft-Tissue Augmentation
Soft-tissue augmentation is another effective treatment of superficial atrophic acne scarring that utilizes injections of collagen fillers such as hyaluronic acid, calcium hydroxylapatite, poly-L-lactic acid, silicone, and even autologous fat to replace lost tissue volume while simultaneously inducing collagen production via stretching of dermal fibroblasts.34 These treatments may require multiple sessions for cosmetic improvement but have shown considerable efficacy in the treatment of atrophic acne scars. Hyaluronic acid has been reported to be particularly effective for rolling scars.12 However, these compounds only provide temporary results, thus requiring repeated treatments to maintain cosmetic outcomes. Permanent options include the recently US Food and Drug Administration–approved polymethylmethacrylate microspheres suspended in bovine collagen as well as the novel technique of autologous fibroblast transfer. These options are relatively new, but initial double-blind, randomized, controlled trials have shown minimal AEs with substantial improvements in 64% to 100% of atrophic scars treated.35,36
Intralesional Therapy
Intralesional corticosteroid injections are a mainstay treatment of hypertrophic acne scarring and are believed to exert their effects by decreasing fibroblast proliferation and promoting collagen degradation.37 Treatment with steroids generally is effective, with reported improvement in 75% (6/8) of patients and complete flattening in 50% (4/8) of lesions according to one study.38 Development of hypopigmentation, dermal atrophy, and telangiectasia are potential sequelae of this treatment.37
5-Fluorouracil, bleomycin, and verapamil also have been used with good results as intralesional treatments of hypertrophic scars, but these agents typically are reserved for cases of corticosteroid failure. Such compounds are thought to mediate their effects through inhibition of dermal fibroblast proliferation.39 Results with these therapies are varied, but greater than 75% improvement is seen in most cases. Adverse effects include injection-site ulceration and hyperpigmentation.39
Cryotherapy
Contact cryotherapy has been studied as treatment of hypertrophic acne scars. The exact mechanism through which scars are reduced is unclear, but it is hypothesized that the physical damage caused by freezing and thrombosis lead to collagen restructuring. According to one study, cryotherapy was reported to achieve good or excellent results in 76% (29/38) of cases.40 Permanent pigmentary alterations are a possible AE.
Silicone Dressings
Silicone dressings are a reasonable treatment option for hypertrophic acne scarring given their proven efficacy and minimal risk for AEs. Thin sheets of silicone gels or membranes are applied daily in a topical manner to acne scars and are believed to be therapeutic through a combination of pressure and hydration, which subsequently inhibits fibroblast production of collagen. Notable reductions in scar appearance and size are seen in 60% to 80% of individuals using this method.41 Adverse effects are limited to pruritus and local skin maceration. Patient noncompliance may be an issue, as the silicone dressings may be applied on highly visible areas such as the face. Patients may apply the dressings at night, but efficacy may be reduced.
Conclusion
When determining which treatment options to use in a patient with acne scarring, it is important to first determine the patient’s treatment goals while simultaneously establishing realistic expectations. Important factors to consider are the patient’s preferences regarding treatment risk, duration, and permanence, as well as budget and social or work requirements. As such, treatment plans for each patient should be determined on a case-by-case basis. It also is important to note that a combination of different treatment modalities often is necessary and superior to monotherapy in achieving satisfactory cosmetic outcomes.
1. Ghodsi SZ, Orawa H, Zouboulis CC. Prevalence, severity, and severity risk factors of acne in high school pupils: a community-based study. J Invest Dermatol. 2009;129:2136-2141.
2. Collier CN, Harper JC, Cafardi JA, et al. The prevalence of acne in adults 20 years and older. J Am Acad Dermatol. 2008;58:56-59.
3. Kim GK, Michaels BB. Post-adolescent acne in women: more common and more clinical considerations. J Drugs Dermatol. 2012;11:708-713.
4. Geller L, Rosen J, Frankel A, et al. Perimenstrual flare of adult acne. J Clin Aesthet Dermatol. 2014;7:30-34.
5. Layton AM, Henderson CA, Cunliffe WJ. A clinical evaluation of acne scarring and its incidence. Clin Exp Dermatol. 1994;19:303-308.
6. Halvorsen JA, Stern RS, Dalgard F, et al. Suicidal ideation, mental health problems, and social impairment are increased in adolescents with acne: a population-based study. J Invest Dermatol. 2011;131:363-370.
7. Jacob CI, Dover JS, Kaminer MS. Acne scarring: a classification system and review of treatment options. J Am Acad Dermatol. 2001;45:109-117.
8. Rivera AE. Acne scarring: a review and current treatment modalities. J Am Acad Dermatol. 2008;59:659-676.
9. Goodman GJ. Acne and acne scarring: why should we treat? Med J Aust. 1999;171:62-63.
10. Frank W. Therapeutic dermabrasion. back to the future. Arch Dermatol. 1994;130:1187-1189.
11. Goodman GJ. Postacne scarring: a review of its pathophysiology and treatment. Dermatol Surg. 2000;26:857-871.
12. Hession MT, Graber EM. Atrophic acne scarring: a review of treatment options. J Clin Aesthet Dermatol. 2015;8:50-58.
13. Levy LL, Zeichner JA. Management of acne scarring, part II: a comparative review of non-laser-based, minimally invasive approaches. Am J Clin Dermatol. 2012;13:331-340.
14. Christophel JJ, Elm C, Endrizzi BT, et al. A randomized controlled trial of fractional laser therapy and dermabrasion for scar resurfacing. Dermatol Surg. 2012;38:595-602.
15. Katz BE, McFarlane DF. Atypical facial scarring after isotretinoin therapy in a patient with previous dermabrasion. J Am Acad Dermatol. 1994;30:852-853.
16. Bernestein LJ, Geronemus RG. Keloid formation with the 585-nm pulsed dye laser during isotretinoin treatment. Arch Dermatol. 1997;133:111-112.
17. Zachariae H. Delayed wound healing and keloid formation following argon laser treatment or dermabrasion during isotretinoin treatment. Br J Dermatol. 1988;118:703-706.
18. Wootton CI, Cartwright RP, Manning P, et al. Should isotretinoin be stopped prior to surgery? a critically appraised topic. Br J Dermatol. 2014;170:239-244.
19. Alster TS, West TB. Resurfacing of atrophic facial acne scars with a high-energy, pulsed carbon dioxide laser. Dermatol Surg. 1996;22:151-155.
20. Sobanko JF, Alster TS. Management of acne scarring, part I: a comparative review of laser surgical approaches. Am J Clin Dermatol. 2012;13:319-330.
21. Cho SB, Lee SJ, Oh SH, et al. Non-ablative 1550nm erbium-glass and ablative 10,600nm carbon dioxide fractional lasers for acne scar: a randomized split-face study with blinded response evaluation. J Eur Acad Dermatol Venereol. 2010;24:921-925.
22. Rkein A, Ozog D, Waibel JS. Treatment of atrophic scars with fractionated CO2 laser facilitating delivery of topically applied poly-L-lactic acid. Dermatol Surg. 2014;40:624-631.
23. Waibel JS, Wulkan AJ, Shumaker PR. Treatment of hypertrophic scars using laser and laser assisted corticosteroid delivery. Lasers Surg Med. 2013;45:135-140.
24. Alster TS, McMeekin TO. Improvement of facial acne scars by the 585-nm flashlamp-pumped pulsed dye laser. J Am Acad Dermatol. 1996;35:79-81.
25. Simmons BJ, Griffith RD, Falto-Aizpurua LA, et al. Use of radiofrequency in cosmetic dermatology: focus on nonablative treatment of acne scars. Clin Cosmet Investig Dermatol. 2014;7:335-339.
26. Ramesh M, Gopal M, Kumar S, et al. Novel technology in the treatment of acne scars: the matrix-tunable radiofrequency technology. J Cutan Aesthet Surg. 2010;3:97-101.
27. Johnson WC. Treatment of pitted scars; punch transplant technique. J Dermatol Surg Oncol. 1986;12:260-265.
28. Alam M, Omura N, Kaminer MS. Subcision for acne scarring: technique and outcomes in 40 patients. Dermatol Surg. 2005;31:310-317.
29. Sage R, Lopiccolo M, Liu A, et al. Subcuticular incision versus naturally sourced porcine collagen filler for acne scars: a randomized split-face comparison. Dermatol Surg. 2011;37:426-431.
30. Fabbrocini G, Annunziata MC, D’arco V, et al. Acne scars: pathogenesis, classification and treatment [published online ahead of print October 14, 2010]. Dermatol Res Pract. 2010;2010:893080.
31. Johnson WC. Treatment of pitted scars: punch transplant technique. J Dermatol Surg Oncol. 1986;12:260-265.
32. Lee JB, Chung WG, Kwahck H, et al. Focal treatment of acne scars with trichloroacetic acid: chemical reconstruction of skin scars method. Dermatol Surg. 2002;28:1017-1021.
33. Bhardwaj D, Khunger N. An assessment of the efficacy and safety of CROSS technique with 100% TCA in the management of ice pick acne scars. J Cutan Aesthet Surg. 2010;3:93-96.
34. Wang F, Garza LA, Kang S, et al. In vivo stimulation of de novo collagen production caused by cross-linked hyaluronic acid dermal filler injections in photodamaged human skin. Arch Dermatol. 2007;143:155-163.
35. Karnik J, Baumann L, Bruce S, et al. A double-blind, randomized, multicenter, controlled trial of suspended polymethylmethacrylate microspheres for the correction of atrophic facial acne scars. J Am Acad Dermatol. 2014;71:77-83.
36. Munavalli GS, Smith S, Maslowski JM, et al. Successful treatment of depressed, distensible acne scars using autologous fibroblasts: a multi-site, prospective, double blind, placebo-controlled clinical trial. Dermatol Surg. 2013;39:1226-1236.
37. Leventhal D, Furr M, Reiter D. Treatment of keloids and hypertrophic scars: a meta-analysis and review of the literature. Arch Facial Plast Surg. 2006;8:362-368.
38. Darzi MA, Chowdri NA, Kaul SK, et al. Evaluation of various methods of treating keloids and hypertrophic scars: a 10-year follow-up study. Br J Plast Surg. 1992;45:374-379.
39. Ledon JA, Savas J, Franca K, et al. Intralesional treatment for keloids and hypertrophic scars: a review. Dermatol Surg. 2013;39:1745-1757.
40. Zouboulis CC, Blume U, Büttner P, et al. Outcomes of cryosurgery in keloids and hypertrophic scars. a prospective consecutive trial of case series. Arch Dermatol. 1993;129:1146-1151.
41. Puri N, Talwar A. The efficacy of silicone gel for the treatment of hypertrophic scars and keloids. J Cutan Aesthet Surg. 2009;2:104-106.
1. Ghodsi SZ, Orawa H, Zouboulis CC. Prevalence, severity, and severity risk factors of acne in high school pupils: a community-based study. J Invest Dermatol. 2009;129:2136-2141.
2. Collier CN, Harper JC, Cafardi JA, et al. The prevalence of acne in adults 20 years and older. J Am Acad Dermatol. 2008;58:56-59.
3. Kim GK, Michaels BB. Post-adolescent acne in women: more common and more clinical considerations. J Drugs Dermatol. 2012;11:708-713.
4. Geller L, Rosen J, Frankel A, et al. Perimenstrual flare of adult acne. J Clin Aesthet Dermatol. 2014;7:30-34.
5. Layton AM, Henderson CA, Cunliffe WJ. A clinical evaluation of acne scarring and its incidence. Clin Exp Dermatol. 1994;19:303-308.
6. Halvorsen JA, Stern RS, Dalgard F, et al. Suicidal ideation, mental health problems, and social impairment are increased in adolescents with acne: a population-based study. J Invest Dermatol. 2011;131:363-370.
7. Jacob CI, Dover JS, Kaminer MS. Acne scarring: a classification system and review of treatment options. J Am Acad Dermatol. 2001;45:109-117.
8. Rivera AE. Acne scarring: a review and current treatment modalities. J Am Acad Dermatol. 2008;59:659-676.
9. Goodman GJ. Acne and acne scarring: why should we treat? Med J Aust. 1999;171:62-63.
10. Frank W. Therapeutic dermabrasion. back to the future. Arch Dermatol. 1994;130:1187-1189.
11. Goodman GJ. Postacne scarring: a review of its pathophysiology and treatment. Dermatol Surg. 2000;26:857-871.
12. Hession MT, Graber EM. Atrophic acne scarring: a review of treatment options. J Clin Aesthet Dermatol. 2015;8:50-58.
13. Levy LL, Zeichner JA. Management of acne scarring, part II: a comparative review of non-laser-based, minimally invasive approaches. Am J Clin Dermatol. 2012;13:331-340.
14. Christophel JJ, Elm C, Endrizzi BT, et al. A randomized controlled trial of fractional laser therapy and dermabrasion for scar resurfacing. Dermatol Surg. 2012;38:595-602.
15. Katz BE, McFarlane DF. Atypical facial scarring after isotretinoin therapy in a patient with previous dermabrasion. J Am Acad Dermatol. 1994;30:852-853.
16. Bernestein LJ, Geronemus RG. Keloid formation with the 585-nm pulsed dye laser during isotretinoin treatment. Arch Dermatol. 1997;133:111-112.
17. Zachariae H. Delayed wound healing and keloid formation following argon laser treatment or dermabrasion during isotretinoin treatment. Br J Dermatol. 1988;118:703-706.
18. Wootton CI, Cartwright RP, Manning P, et al. Should isotretinoin be stopped prior to surgery? a critically appraised topic. Br J Dermatol. 2014;170:239-244.
19. Alster TS, West TB. Resurfacing of atrophic facial acne scars with a high-energy, pulsed carbon dioxide laser. Dermatol Surg. 1996;22:151-155.
20. Sobanko JF, Alster TS. Management of acne scarring, part I: a comparative review of laser surgical approaches. Am J Clin Dermatol. 2012;13:319-330.
21. Cho SB, Lee SJ, Oh SH, et al. Non-ablative 1550nm erbium-glass and ablative 10,600nm carbon dioxide fractional lasers for acne scar: a randomized split-face study with blinded response evaluation. J Eur Acad Dermatol Venereol. 2010;24:921-925.
22. Rkein A, Ozog D, Waibel JS. Treatment of atrophic scars with fractionated CO2 laser facilitating delivery of topically applied poly-L-lactic acid. Dermatol Surg. 2014;40:624-631.
23. Waibel JS, Wulkan AJ, Shumaker PR. Treatment of hypertrophic scars using laser and laser assisted corticosteroid delivery. Lasers Surg Med. 2013;45:135-140.
24. Alster TS, McMeekin TO. Improvement of facial acne scars by the 585-nm flashlamp-pumped pulsed dye laser. J Am Acad Dermatol. 1996;35:79-81.
25. Simmons BJ, Griffith RD, Falto-Aizpurua LA, et al. Use of radiofrequency in cosmetic dermatology: focus on nonablative treatment of acne scars. Clin Cosmet Investig Dermatol. 2014;7:335-339.
26. Ramesh M, Gopal M, Kumar S, et al. Novel technology in the treatment of acne scars: the matrix-tunable radiofrequency technology. J Cutan Aesthet Surg. 2010;3:97-101.
27. Johnson WC. Treatment of pitted scars; punch transplant technique. J Dermatol Surg Oncol. 1986;12:260-265.
28. Alam M, Omura N, Kaminer MS. Subcision for acne scarring: technique and outcomes in 40 patients. Dermatol Surg. 2005;31:310-317.
29. Sage R, Lopiccolo M, Liu A, et al. Subcuticular incision versus naturally sourced porcine collagen filler for acne scars: a randomized split-face comparison. Dermatol Surg. 2011;37:426-431.
30. Fabbrocini G, Annunziata MC, D’arco V, et al. Acne scars: pathogenesis, classification and treatment [published online ahead of print October 14, 2010]. Dermatol Res Pract. 2010;2010:893080.
31. Johnson WC. Treatment of pitted scars: punch transplant technique. J Dermatol Surg Oncol. 1986;12:260-265.
32. Lee JB, Chung WG, Kwahck H, et al. Focal treatment of acne scars with trichloroacetic acid: chemical reconstruction of skin scars method. Dermatol Surg. 2002;28:1017-1021.
33. Bhardwaj D, Khunger N. An assessment of the efficacy and safety of CROSS technique with 100% TCA in the management of ice pick acne scars. J Cutan Aesthet Surg. 2010;3:93-96.
34. Wang F, Garza LA, Kang S, et al. In vivo stimulation of de novo collagen production caused by cross-linked hyaluronic acid dermal filler injections in photodamaged human skin. Arch Dermatol. 2007;143:155-163.
35. Karnik J, Baumann L, Bruce S, et al. A double-blind, randomized, multicenter, controlled trial of suspended polymethylmethacrylate microspheres for the correction of atrophic facial acne scars. J Am Acad Dermatol. 2014;71:77-83.
36. Munavalli GS, Smith S, Maslowski JM, et al. Successful treatment of depressed, distensible acne scars using autologous fibroblasts: a multi-site, prospective, double blind, placebo-controlled clinical trial. Dermatol Surg. 2013;39:1226-1236.
37. Leventhal D, Furr M, Reiter D. Treatment of keloids and hypertrophic scars: a meta-analysis and review of the literature. Arch Facial Plast Surg. 2006;8:362-368.
38. Darzi MA, Chowdri NA, Kaul SK, et al. Evaluation of various methods of treating keloids and hypertrophic scars: a 10-year follow-up study. Br J Plast Surg. 1992;45:374-379.
39. Ledon JA, Savas J, Franca K, et al. Intralesional treatment for keloids and hypertrophic scars: a review. Dermatol Surg. 2013;39:1745-1757.
40. Zouboulis CC, Blume U, Büttner P, et al. Outcomes of cryosurgery in keloids and hypertrophic scars. a prospective consecutive trial of case series. Arch Dermatol. 1993;129:1146-1151.
41. Puri N, Talwar A. The efficacy of silicone gel for the treatment of hypertrophic scars and keloids. J Cutan Aesthet Surg. 2009;2:104-106.
Practice Points
- Scarring is a common and undesirable outcome of acne vulgaris that can occur even in the setting of appropriate medical management.
- Acne scars can be classified into several different types based on scar quality and appearance. The choice of treatment with medical or surgical measures should be made with respect to the type of scar present.
- A combination of therapeutic modalities often is necessary to achieve optimal cosmetic outcomes in the treatment of both atrophic and hypertrophic acne scars.
Portulaca oleracea (purslane)
Portulaca oleracea, also known as purslane, has long been used in various traditional medicine systems to relieve pain and edema.1Portulaca oleracea is a warm-climate annual plant originally found in the Middle East, North Africa, and the Indian subcontinent and now cultivated in the Arabian peninsula; Japan, where it is an abundant garden plant from spring to fall;2,3 and throughout the world.
The use of P. oleracea, a member of the Portulacaceae family, as a vegetable as well as herbal medicine dates back several centuries.4 In modern times, purslane has been found to be rich in antioxidants, particularly omega-3 fatty acids, vitamins C and E, beta-carotene, melatonin, and glutathione, as well as several minerals.5,6,7 Currently, it is considered one of the top ten most common plants in the world, and one of the most-used medical plants according to the World Health Organization.6 It is considered a weed in the United States, but is eaten in many parts of the world.
Antioxidant activity
Using two different assays, Uddin et al. determined in 2012 that P. oleracea cultivars exhibited significant antioxidant activity through various growth stages. In addition, the researchers suggested that purslane could provide multiple minerals as well as antioxidants in the context of nutraceutical products and functional food.7 Early this year, Silva et al. studied the antioxidant activity of P. oleracea leaves, flowers, and stems from two different locations in Portugal, with assays revealing significantly greater antioxidant activity in the stems of both samples compared to the leaves and flowers. However, the phenolic extracts of all three plant sections from both samples were found to protect DNA against hydroxyl radicals. The investigators concluded that their findings, particularly related to high antioxidant activity, support the potential benefits of purslane consumption to human health.8
A 2014 analysis of 13 collected purslane accessions revealed significant mineral content (particularly potassium, followed by nitrogen, sodium, calcium, magnesium, phosphorus, iron, zinc, and manganese) and showed that antioxidant activity was more strongly associated with ornamental as opposed to common purslane, the latter of which was richer in mineral content.6
Anti-inflammatory activity
In 2000, Chan et al. found that a 10% ethanolic extract of the dried leaves and stem of a P. oleracea cultivar displayed significant anti-inflammatory and analgesic properties after topical and intraperitoneal, but not oral, administration in comparison to diclofenac sodium, a synthetic drug used as active control. They added that these activities corresponded to the reputed effects of the traditional uses of the wild species.9
Wound healing activity
Rashed et al. reported in 2003 that a crude extract of P. oleracea accelerates wound healing. They used Mus musculus JVI-1 to show that fresh homogenized crude aerial parts of the plant topically applied on excision wound surfaces reduced wound surface areas and increased tensile strength. The best documented contraction was associated with a single dose of 50 mg, followed by two doses of 25 mg each.10
Oral lichen planus treatment
In 2010, Agha-Hosseini et al. conducted a randomized double-blind placebo-controlled 3-month study to assess the effectiveness of purslane in the treatment of oral lichen planus. Thirty-seven symptomatic patients (confirmed by biopsy) were divided into a purslane treatment group (n = 20) and a placebo group (n = 17). The investigators reported that partial to complete clinical improvement was observed in 83% of the treatment group, with no response in the remaining 17%, whereas partial improvement was seen in 17% of the placebo group, 73% had no response, and the condition was aggravated in 10% of the placebo group. No adverse side effects were reported in either group, and the researchers concluded that purslane was clinically effective in treating oral lichen planus and warrants consideration as a treatment option for the disorder.5
Other activities
In 2001, Radhakrishnan et al. identified several neuropharmacological actions, particularly anti-nociceptive and muscle-relaxing activity, with a range of effects on the central and peripheral nervous system observed in animal studies.1 The betacyanins found in P. oleracea have subsequently been found to confer a protective effect against neurotoxicity, specifically, ameliorating the D-galactose-induced cognitive deficits in senescent mice.11P. oleracea also has been shown to efficiently eliminate the endocrine-disrupting chemical bisphenol A from a hydroponic solution.12
In 2012, Yan et al. showed that three newly isolated homoisoflavonoids, known as portulacanones, and the compound 2,2’-dihydroxy-4’,6’-dimethoxychalcone selectively exhibited in vitro cytotoxic activities against four human cancer cell lines.2
Conclusions
This antioxidant-rich plant is found throughout the world and has long been associated with traditional health care. Modern research into its potential dermatologic uses is ongoing, but the evidence is relatively scarce. There are indications that the antioxidant, anti-inflammatory, and wound healing activity reportedly exhibited by purslane may be harnessed for various cutaneous applications. However, much more research is necessary to determine how extensive a role purslane may play in skin care.
References
1.J. Ethnopharmacol. 2001;76:171-6
2.Phytochemistry 2012;80:37-41
3.J. Biosci. Bioeng. 2007;103:420-6
4.J. Ethnopharmacol. 2000;73:445-51
5.Phytother. Res. 2010;24:240-4
6.Biomed. Res. Int. 2014;2014:296063
7.Int. J. Mol. Sci. 2012;13:10257-67
8.Nat Prod. Commun. 2014;9:45-50
9. J. Ethnopharmacol. 2000;73:445-51
10. J. Ethnopharmacol. 2003;88:131-6
11. Phytomedicine. 2010 Jun;17:527-32
12. Biosci. Biotechnol. Biochem. 2012;76:1015-7
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever.
Portulaca oleracea, also known as purslane, has long been used in various traditional medicine systems to relieve pain and edema.1Portulaca oleracea is a warm-climate annual plant originally found in the Middle East, North Africa, and the Indian subcontinent and now cultivated in the Arabian peninsula; Japan, where it is an abundant garden plant from spring to fall;2,3 and throughout the world.
The use of P. oleracea, a member of the Portulacaceae family, as a vegetable as well as herbal medicine dates back several centuries.4 In modern times, purslane has been found to be rich in antioxidants, particularly omega-3 fatty acids, vitamins C and E, beta-carotene, melatonin, and glutathione, as well as several minerals.5,6,7 Currently, it is considered one of the top ten most common plants in the world, and one of the most-used medical plants according to the World Health Organization.6 It is considered a weed in the United States, but is eaten in many parts of the world.
Antioxidant activity
Using two different assays, Uddin et al. determined in 2012 that P. oleracea cultivars exhibited significant antioxidant activity through various growth stages. In addition, the researchers suggested that purslane could provide multiple minerals as well as antioxidants in the context of nutraceutical products and functional food.7 Early this year, Silva et al. studied the antioxidant activity of P. oleracea leaves, flowers, and stems from two different locations in Portugal, with assays revealing significantly greater antioxidant activity in the stems of both samples compared to the leaves and flowers. However, the phenolic extracts of all three plant sections from both samples were found to protect DNA against hydroxyl radicals. The investigators concluded that their findings, particularly related to high antioxidant activity, support the potential benefits of purslane consumption to human health.8
A 2014 analysis of 13 collected purslane accessions revealed significant mineral content (particularly potassium, followed by nitrogen, sodium, calcium, magnesium, phosphorus, iron, zinc, and manganese) and showed that antioxidant activity was more strongly associated with ornamental as opposed to common purslane, the latter of which was richer in mineral content.6
Anti-inflammatory activity
In 2000, Chan et al. found that a 10% ethanolic extract of the dried leaves and stem of a P. oleracea cultivar displayed significant anti-inflammatory and analgesic properties after topical and intraperitoneal, but not oral, administration in comparison to diclofenac sodium, a synthetic drug used as active control. They added that these activities corresponded to the reputed effects of the traditional uses of the wild species.9
Wound healing activity
Rashed et al. reported in 2003 that a crude extract of P. oleracea accelerates wound healing. They used Mus musculus JVI-1 to show that fresh homogenized crude aerial parts of the plant topically applied on excision wound surfaces reduced wound surface areas and increased tensile strength. The best documented contraction was associated with a single dose of 50 mg, followed by two doses of 25 mg each.10
Oral lichen planus treatment
In 2010, Agha-Hosseini et al. conducted a randomized double-blind placebo-controlled 3-month study to assess the effectiveness of purslane in the treatment of oral lichen planus. Thirty-seven symptomatic patients (confirmed by biopsy) were divided into a purslane treatment group (n = 20) and a placebo group (n = 17). The investigators reported that partial to complete clinical improvement was observed in 83% of the treatment group, with no response in the remaining 17%, whereas partial improvement was seen in 17% of the placebo group, 73% had no response, and the condition was aggravated in 10% of the placebo group. No adverse side effects were reported in either group, and the researchers concluded that purslane was clinically effective in treating oral lichen planus and warrants consideration as a treatment option for the disorder.5
Other activities
In 2001, Radhakrishnan et al. identified several neuropharmacological actions, particularly anti-nociceptive and muscle-relaxing activity, with a range of effects on the central and peripheral nervous system observed in animal studies.1 The betacyanins found in P. oleracea have subsequently been found to confer a protective effect against neurotoxicity, specifically, ameliorating the D-galactose-induced cognitive deficits in senescent mice.11P. oleracea also has been shown to efficiently eliminate the endocrine-disrupting chemical bisphenol A from a hydroponic solution.12
In 2012, Yan et al. showed that three newly isolated homoisoflavonoids, known as portulacanones, and the compound 2,2’-dihydroxy-4’,6’-dimethoxychalcone selectively exhibited in vitro cytotoxic activities against four human cancer cell lines.2
Conclusions
This antioxidant-rich plant is found throughout the world and has long been associated with traditional health care. Modern research into its potential dermatologic uses is ongoing, but the evidence is relatively scarce. There are indications that the antioxidant, anti-inflammatory, and wound healing activity reportedly exhibited by purslane may be harnessed for various cutaneous applications. However, much more research is necessary to determine how extensive a role purslane may play in skin care.
References
1.J. Ethnopharmacol. 2001;76:171-6
2.Phytochemistry 2012;80:37-41
3.J. Biosci. Bioeng. 2007;103:420-6
4.J. Ethnopharmacol. 2000;73:445-51
5.Phytother. Res. 2010;24:240-4
6.Biomed. Res. Int. 2014;2014:296063
7.Int. J. Mol. Sci. 2012;13:10257-67
8.Nat Prod. Commun. 2014;9:45-50
9. J. Ethnopharmacol. 2000;73:445-51
10. J. Ethnopharmacol. 2003;88:131-6
11. Phytomedicine. 2010 Jun;17:527-32
12. Biosci. Biotechnol. Biochem. 2012;76:1015-7
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever.
Portulaca oleracea, also known as purslane, has long been used in various traditional medicine systems to relieve pain and edema.1Portulaca oleracea is a warm-climate annual plant originally found in the Middle East, North Africa, and the Indian subcontinent and now cultivated in the Arabian peninsula; Japan, where it is an abundant garden plant from spring to fall;2,3 and throughout the world.
The use of P. oleracea, a member of the Portulacaceae family, as a vegetable as well as herbal medicine dates back several centuries.4 In modern times, purslane has been found to be rich in antioxidants, particularly omega-3 fatty acids, vitamins C and E, beta-carotene, melatonin, and glutathione, as well as several minerals.5,6,7 Currently, it is considered one of the top ten most common plants in the world, and one of the most-used medical plants according to the World Health Organization.6 It is considered a weed in the United States, but is eaten in many parts of the world.
Antioxidant activity
Using two different assays, Uddin et al. determined in 2012 that P. oleracea cultivars exhibited significant antioxidant activity through various growth stages. In addition, the researchers suggested that purslane could provide multiple minerals as well as antioxidants in the context of nutraceutical products and functional food.7 Early this year, Silva et al. studied the antioxidant activity of P. oleracea leaves, flowers, and stems from two different locations in Portugal, with assays revealing significantly greater antioxidant activity in the stems of both samples compared to the leaves and flowers. However, the phenolic extracts of all three plant sections from both samples were found to protect DNA against hydroxyl radicals. The investigators concluded that their findings, particularly related to high antioxidant activity, support the potential benefits of purslane consumption to human health.8
A 2014 analysis of 13 collected purslane accessions revealed significant mineral content (particularly potassium, followed by nitrogen, sodium, calcium, magnesium, phosphorus, iron, zinc, and manganese) and showed that antioxidant activity was more strongly associated with ornamental as opposed to common purslane, the latter of which was richer in mineral content.6
Anti-inflammatory activity
In 2000, Chan et al. found that a 10% ethanolic extract of the dried leaves and stem of a P. oleracea cultivar displayed significant anti-inflammatory and analgesic properties after topical and intraperitoneal, but not oral, administration in comparison to diclofenac sodium, a synthetic drug used as active control. They added that these activities corresponded to the reputed effects of the traditional uses of the wild species.9
Wound healing activity
Rashed et al. reported in 2003 that a crude extract of P. oleracea accelerates wound healing. They used Mus musculus JVI-1 to show that fresh homogenized crude aerial parts of the plant topically applied on excision wound surfaces reduced wound surface areas and increased tensile strength. The best documented contraction was associated with a single dose of 50 mg, followed by two doses of 25 mg each.10
Oral lichen planus treatment
In 2010, Agha-Hosseini et al. conducted a randomized double-blind placebo-controlled 3-month study to assess the effectiveness of purslane in the treatment of oral lichen planus. Thirty-seven symptomatic patients (confirmed by biopsy) were divided into a purslane treatment group (n = 20) and a placebo group (n = 17). The investigators reported that partial to complete clinical improvement was observed in 83% of the treatment group, with no response in the remaining 17%, whereas partial improvement was seen in 17% of the placebo group, 73% had no response, and the condition was aggravated in 10% of the placebo group. No adverse side effects were reported in either group, and the researchers concluded that purslane was clinically effective in treating oral lichen planus and warrants consideration as a treatment option for the disorder.5
Other activities
In 2001, Radhakrishnan et al. identified several neuropharmacological actions, particularly anti-nociceptive and muscle-relaxing activity, with a range of effects on the central and peripheral nervous system observed in animal studies.1 The betacyanins found in P. oleracea have subsequently been found to confer a protective effect against neurotoxicity, specifically, ameliorating the D-galactose-induced cognitive deficits in senescent mice.11P. oleracea also has been shown to efficiently eliminate the endocrine-disrupting chemical bisphenol A from a hydroponic solution.12
In 2012, Yan et al. showed that three newly isolated homoisoflavonoids, known as portulacanones, and the compound 2,2’-dihydroxy-4’,6’-dimethoxychalcone selectively exhibited in vitro cytotoxic activities against four human cancer cell lines.2
Conclusions
This antioxidant-rich plant is found throughout the world and has long been associated with traditional health care. Modern research into its potential dermatologic uses is ongoing, but the evidence is relatively scarce. There are indications that the antioxidant, anti-inflammatory, and wound healing activity reportedly exhibited by purslane may be harnessed for various cutaneous applications. However, much more research is necessary to determine how extensive a role purslane may play in skin care.
References
1.J. Ethnopharmacol. 2001;76:171-6
2.Phytochemistry 2012;80:37-41
3.J. Biosci. Bioeng. 2007;103:420-6
4.J. Ethnopharmacol. 2000;73:445-51
5.Phytother. Res. 2010;24:240-4
6.Biomed. Res. Int. 2014;2014:296063
7.Int. J. Mol. Sci. 2012;13:10257-67
8.Nat Prod. Commun. 2014;9:45-50
9. J. Ethnopharmacol. 2000;73:445-51
10. J. Ethnopharmacol. 2003;88:131-6
11. Phytomedicine. 2010 Jun;17:527-32
12. Biosci. Biotechnol. Biochem. 2012;76:1015-7
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever.
NASPAG: Obesity raises unique contraceptive concerns in teens
ORLANDO – The data with respect to the effects of obesity on the efficacy of contraceptives in adolescents are limited, but the general consensus is that if efficacy is reduced, it isn’t by enough to make a real difference, according to Dr. Alene Toulany.
The effect of obesity is likely to be very small, and studies that have looked at pharmacokinetics in obesity have estimated that body weight accounts for only about 10%-20% of the variability of hormone levels, Dr. Toulany said at the North American Society for Pediatric and Adolescent Gynecology annual meeting.
“We know that this is within the normal range for individuals who are not obese, she said.
The concerns regarding efficacy in obese patients are understandable, as obesity increases the metabolic rate, increases clearance of hepatically metabolized drugs, increases circulating blood volume, and affects the absorption of contraceptive steroids through the adipose tissue, she said, adding that “it makes sense that the serum drug levels may be insufficient to maintain contraceptive effects, but the data are very limited and inconsistent.”
That’s not to say obesity isn’t a concern, added Dr. Toulany, an adolescent medicine specialist at the Hospital for Sick Children, Toronto, and the University of Toronto.
“Without fail, all of us will be seeing patients with obesity,” she said. The rate of adolescent obesity has quadrupled in the last 3 decades, increasing from 5% among those aged 12-19 years in 1980 to more than 20% now. A third are currently overweight or obese.
Further, sexually active obese women, regardless of age, are significantly less likely to use contraception, and obese teens are more likely to engage in risky sexual behaviors than are nonobese teens.
For these reasons, it is important to find the most effective contraceptive method, taking into account other risk factors and the likelihood of compliance, she said, noting that obesity is an independent risk factor for venous thromboembolism (VTE) and that studies suggest the risk is additive in users of estrogen-containing contraceptives.
However, she said, the benefits outweigh the risks of pregnancy in obesity – especially of unintended pregnancy.
The absolute risk of VTE in healthy women of reproductive age is small, and in adolescents it’s even smaller, she explained.
“The presence of risk factors for VTE should be taken into account when we see these youth in our clinics, but we can and should offer estrogen-containing contraceptives as long as there are no other risk factors,” she said.
Contraceptive options in young obese patients include:
• Intrauterine devices. There is no evidence that either copper IUDs or progestin-releasing IUDs have reduced efficacy in obese adolescents.
• Implants. These are highly effective in obese women, and even though the concentrations may be 30%-60% lower in obese women, they do remain above the contraceptive threshold for at least the first 3 years, Dr. Toulany said.
• Depot medroxyprogesterone acetate. There is some concern about weight gain with this injectable progestin-only contraceptive, particularly in those who are already obese, but it remains an option, as the levels do remain above what is needed to prevent ovulation. Interestingly, the persistence of ovulation suppression following discontinuation is different in obese women, and may be prolonged, compared with nonobese women; it is important to counsel patients about this, she said.
“So although randomized, controlled trials report no significant weight gain, we do agree with these observational studies that show that overweight and obese teens gain more weight with Depo-Provera than with oral contraceptives or with no contraceptives,” she said.
• Oral contraceptive pills. Although these may be less effective in obese adolescents, they remain an option and may be the best option in a given patient. Combined oral contraceptives are believed to be generally effective for pregnancy prevention, but “may be less forgiving of imperfect use,” and thus may not be the best choice in those who may have problems with adherence, for example.
The contraceptive patch is probably not a good option, because efficacy may be diminished as a result of absorption through the adipose tissues in those weighing more than 90 kg, Dr .Toulany said. Evidence is insufficient regarding the use of contraceptive rings in obese patients.
Bariatric surgery is increasingly being performed in adolescents, and this raises unique concerns with respect to contraception, Dr. Toulany said.
“We recommend discontinuing estrogen-containing contraceptives 1 month before surgery to reduce the risk of VTE postoperatively,” she said.
After bariatric surgery, those who undergo a restrictive procedure such as gastric banding or a gastric sleeve procedure that reduces the volume of the stomach can use oral contraceptives, but postsurgery vomiting and diarrhea could increase the risk of complications. In those who undergo surgery using a technique that involves a significant malabsorption component, such as Roux-en-Y gastric bypass, nonoral contraceptives are the best option.
“Most patients going for bariatric surgery have an IUD inserted at the time of surgery, and that’s what we would recommend,” Dr. Toulany said.
She reported having no relevant financial disclosures.
ORLANDO – The data with respect to the effects of obesity on the efficacy of contraceptives in adolescents are limited, but the general consensus is that if efficacy is reduced, it isn’t by enough to make a real difference, according to Dr. Alene Toulany.
The effect of obesity is likely to be very small, and studies that have looked at pharmacokinetics in obesity have estimated that body weight accounts for only about 10%-20% of the variability of hormone levels, Dr. Toulany said at the North American Society for Pediatric and Adolescent Gynecology annual meeting.
“We know that this is within the normal range for individuals who are not obese, she said.
The concerns regarding efficacy in obese patients are understandable, as obesity increases the metabolic rate, increases clearance of hepatically metabolized drugs, increases circulating blood volume, and affects the absorption of contraceptive steroids through the adipose tissue, she said, adding that “it makes sense that the serum drug levels may be insufficient to maintain contraceptive effects, but the data are very limited and inconsistent.”
That’s not to say obesity isn’t a concern, added Dr. Toulany, an adolescent medicine specialist at the Hospital for Sick Children, Toronto, and the University of Toronto.
“Without fail, all of us will be seeing patients with obesity,” she said. The rate of adolescent obesity has quadrupled in the last 3 decades, increasing from 5% among those aged 12-19 years in 1980 to more than 20% now. A third are currently overweight or obese.
Further, sexually active obese women, regardless of age, are significantly less likely to use contraception, and obese teens are more likely to engage in risky sexual behaviors than are nonobese teens.
For these reasons, it is important to find the most effective contraceptive method, taking into account other risk factors and the likelihood of compliance, she said, noting that obesity is an independent risk factor for venous thromboembolism (VTE) and that studies suggest the risk is additive in users of estrogen-containing contraceptives.
However, she said, the benefits outweigh the risks of pregnancy in obesity – especially of unintended pregnancy.
The absolute risk of VTE in healthy women of reproductive age is small, and in adolescents it’s even smaller, she explained.
“The presence of risk factors for VTE should be taken into account when we see these youth in our clinics, but we can and should offer estrogen-containing contraceptives as long as there are no other risk factors,” she said.
Contraceptive options in young obese patients include:
• Intrauterine devices. There is no evidence that either copper IUDs or progestin-releasing IUDs have reduced efficacy in obese adolescents.
• Implants. These are highly effective in obese women, and even though the concentrations may be 30%-60% lower in obese women, they do remain above the contraceptive threshold for at least the first 3 years, Dr. Toulany said.
• Depot medroxyprogesterone acetate. There is some concern about weight gain with this injectable progestin-only contraceptive, particularly in those who are already obese, but it remains an option, as the levels do remain above what is needed to prevent ovulation. Interestingly, the persistence of ovulation suppression following discontinuation is different in obese women, and may be prolonged, compared with nonobese women; it is important to counsel patients about this, she said.
“So although randomized, controlled trials report no significant weight gain, we do agree with these observational studies that show that overweight and obese teens gain more weight with Depo-Provera than with oral contraceptives or with no contraceptives,” she said.
• Oral contraceptive pills. Although these may be less effective in obese adolescents, they remain an option and may be the best option in a given patient. Combined oral contraceptives are believed to be generally effective for pregnancy prevention, but “may be less forgiving of imperfect use,” and thus may not be the best choice in those who may have problems with adherence, for example.
The contraceptive patch is probably not a good option, because efficacy may be diminished as a result of absorption through the adipose tissues in those weighing more than 90 kg, Dr .Toulany said. Evidence is insufficient regarding the use of contraceptive rings in obese patients.
Bariatric surgery is increasingly being performed in adolescents, and this raises unique concerns with respect to contraception, Dr. Toulany said.
“We recommend discontinuing estrogen-containing contraceptives 1 month before surgery to reduce the risk of VTE postoperatively,” she said.
After bariatric surgery, those who undergo a restrictive procedure such as gastric banding or a gastric sleeve procedure that reduces the volume of the stomach can use oral contraceptives, but postsurgery vomiting and diarrhea could increase the risk of complications. In those who undergo surgery using a technique that involves a significant malabsorption component, such as Roux-en-Y gastric bypass, nonoral contraceptives are the best option.
“Most patients going for bariatric surgery have an IUD inserted at the time of surgery, and that’s what we would recommend,” Dr. Toulany said.
She reported having no relevant financial disclosures.
ORLANDO – The data with respect to the effects of obesity on the efficacy of contraceptives in adolescents are limited, but the general consensus is that if efficacy is reduced, it isn’t by enough to make a real difference, according to Dr. Alene Toulany.
The effect of obesity is likely to be very small, and studies that have looked at pharmacokinetics in obesity have estimated that body weight accounts for only about 10%-20% of the variability of hormone levels, Dr. Toulany said at the North American Society for Pediatric and Adolescent Gynecology annual meeting.
“We know that this is within the normal range for individuals who are not obese, she said.
The concerns regarding efficacy in obese patients are understandable, as obesity increases the metabolic rate, increases clearance of hepatically metabolized drugs, increases circulating blood volume, and affects the absorption of contraceptive steroids through the adipose tissue, she said, adding that “it makes sense that the serum drug levels may be insufficient to maintain contraceptive effects, but the data are very limited and inconsistent.”
That’s not to say obesity isn’t a concern, added Dr. Toulany, an adolescent medicine specialist at the Hospital for Sick Children, Toronto, and the University of Toronto.
“Without fail, all of us will be seeing patients with obesity,” she said. The rate of adolescent obesity has quadrupled in the last 3 decades, increasing from 5% among those aged 12-19 years in 1980 to more than 20% now. A third are currently overweight or obese.
Further, sexually active obese women, regardless of age, are significantly less likely to use contraception, and obese teens are more likely to engage in risky sexual behaviors than are nonobese teens.
For these reasons, it is important to find the most effective contraceptive method, taking into account other risk factors and the likelihood of compliance, she said, noting that obesity is an independent risk factor for venous thromboembolism (VTE) and that studies suggest the risk is additive in users of estrogen-containing contraceptives.
However, she said, the benefits outweigh the risks of pregnancy in obesity – especially of unintended pregnancy.
The absolute risk of VTE in healthy women of reproductive age is small, and in adolescents it’s even smaller, she explained.
“The presence of risk factors for VTE should be taken into account when we see these youth in our clinics, but we can and should offer estrogen-containing contraceptives as long as there are no other risk factors,” she said.
Contraceptive options in young obese patients include:
• Intrauterine devices. There is no evidence that either copper IUDs or progestin-releasing IUDs have reduced efficacy in obese adolescents.
• Implants. These are highly effective in obese women, and even though the concentrations may be 30%-60% lower in obese women, they do remain above the contraceptive threshold for at least the first 3 years, Dr. Toulany said.
• Depot medroxyprogesterone acetate. There is some concern about weight gain with this injectable progestin-only contraceptive, particularly in those who are already obese, but it remains an option, as the levels do remain above what is needed to prevent ovulation. Interestingly, the persistence of ovulation suppression following discontinuation is different in obese women, and may be prolonged, compared with nonobese women; it is important to counsel patients about this, she said.
“So although randomized, controlled trials report no significant weight gain, we do agree with these observational studies that show that overweight and obese teens gain more weight with Depo-Provera than with oral contraceptives or with no contraceptives,” she said.
• Oral contraceptive pills. Although these may be less effective in obese adolescents, they remain an option and may be the best option in a given patient. Combined oral contraceptives are believed to be generally effective for pregnancy prevention, but “may be less forgiving of imperfect use,” and thus may not be the best choice in those who may have problems with adherence, for example.
The contraceptive patch is probably not a good option, because efficacy may be diminished as a result of absorption through the adipose tissues in those weighing more than 90 kg, Dr .Toulany said. Evidence is insufficient regarding the use of contraceptive rings in obese patients.
Bariatric surgery is increasingly being performed in adolescents, and this raises unique concerns with respect to contraception, Dr. Toulany said.
“We recommend discontinuing estrogen-containing contraceptives 1 month before surgery to reduce the risk of VTE postoperatively,” she said.
After bariatric surgery, those who undergo a restrictive procedure such as gastric banding or a gastric sleeve procedure that reduces the volume of the stomach can use oral contraceptives, but postsurgery vomiting and diarrhea could increase the risk of complications. In those who undergo surgery using a technique that involves a significant malabsorption component, such as Roux-en-Y gastric bypass, nonoral contraceptives are the best option.
“Most patients going for bariatric surgery have an IUD inserted at the time of surgery, and that’s what we would recommend,” Dr. Toulany said.
She reported having no relevant financial disclosures.
EXPERT ANALYSIS FROM THE NASPAG ANNUAL MEETING