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Engage parents in treatment as part of family-based therapy for anorexia
SAN FRANCISCO – Parents have to stay level-headed if family-based therapy is going to work for anorexia nervosa, according to an expert on the technique, James Lock, MD, PhD, director of the Child and Adolescent Eating Disorder Program at Stanford (Calif.) University.
The idea of family-based therapy (FBT) is to guide parents to change behaviors – the patients’, but also their own – that undermine weight gain. Early on, the therapist has a meal with the family to observe dynamics that need to be addressed and encourage behaviors that help. It’s a nonauthoritarian approach, where the therapist helps families help themselves.
Heated emotion just opens the door to argument and resistance; patients aren’t rational when it comes to body image and eating, at least at first. Parents also have to learn not to be provoked by the child.
“You just have to ignore it. You don’t argue with the kids,” and “right now, ‘we love you’ just doesn’t go anywhere,” Dr. Lock said at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Instead, caregivers are simply supportive. The only messages that matter initially, when weight gain is critical, are along the lines of, “I know you need to eat this. You need to eat it.” Parents “need to support the behavior change and really be kind of neutral about everything else,” he said.
FBT is one of many therapeutic options for anorexia. It has a strong evidence base going back about 30 years. Dr. Lock and his colleagues have been involved in many of the more recent studies and reported a 12-month remission rate of 49% in one (Arch Gen Psychiatry. 2010 Oct; 67[10]:1025-32). There’s growing support for FBT in bulimia, as well.
The earliest goal is to engage the parents in treatment. They are complimented on what they are doing well and told not to blame themselves or their child for the illness. The seriousness of anorexia is also impressed upon the parents if they are in denial about the illness.
The family meal comes early, too. They’re stressful but necessary to learn what parents are trying to do to help and to coach them about what needs improvement. “You, as a therapist, need” to be at the meal and “join the family in their dilemmas,” Dr. Lock said.
Parents are responsible for weight restoration at first, but when steady weight gain occurs, they are taught to hand control of eating and weight back to the child. In time, therapists help with normal adolescent developmental issues and healthy family relationships.
There are maybe 20 sessions over 6-12 months, more or less depending on how it’s going; each one lasts an hour. Single-parent families seem to need more sessions, likely because there’s no spouse to share in the work. There are no meal plans in FBT, because meal plans “are not a normal way to eat. When you try to empower parents to make reasonable decisions about food, a 24-hour meal plan that the adolescent is aware of is just an opportunity for fighting over what it says,” Dr. Lock said.
Dr. Lock has coauthored a treatment manual on using FBT for anorexia.
SAN FRANCISCO – Parents have to stay level-headed if family-based therapy is going to work for anorexia nervosa, according to an expert on the technique, James Lock, MD, PhD, director of the Child and Adolescent Eating Disorder Program at Stanford (Calif.) University.
The idea of family-based therapy (FBT) is to guide parents to change behaviors – the patients’, but also their own – that undermine weight gain. Early on, the therapist has a meal with the family to observe dynamics that need to be addressed and encourage behaviors that help. It’s a nonauthoritarian approach, where the therapist helps families help themselves.
Heated emotion just opens the door to argument and resistance; patients aren’t rational when it comes to body image and eating, at least at first. Parents also have to learn not to be provoked by the child.
“You just have to ignore it. You don’t argue with the kids,” and “right now, ‘we love you’ just doesn’t go anywhere,” Dr. Lock said at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Instead, caregivers are simply supportive. The only messages that matter initially, when weight gain is critical, are along the lines of, “I know you need to eat this. You need to eat it.” Parents “need to support the behavior change and really be kind of neutral about everything else,” he said.
FBT is one of many therapeutic options for anorexia. It has a strong evidence base going back about 30 years. Dr. Lock and his colleagues have been involved in many of the more recent studies and reported a 12-month remission rate of 49% in one (Arch Gen Psychiatry. 2010 Oct; 67[10]:1025-32). There’s growing support for FBT in bulimia, as well.
The earliest goal is to engage the parents in treatment. They are complimented on what they are doing well and told not to blame themselves or their child for the illness. The seriousness of anorexia is also impressed upon the parents if they are in denial about the illness.
The family meal comes early, too. They’re stressful but necessary to learn what parents are trying to do to help and to coach them about what needs improvement. “You, as a therapist, need” to be at the meal and “join the family in their dilemmas,” Dr. Lock said.
Parents are responsible for weight restoration at first, but when steady weight gain occurs, they are taught to hand control of eating and weight back to the child. In time, therapists help with normal adolescent developmental issues and healthy family relationships.
There are maybe 20 sessions over 6-12 months, more or less depending on how it’s going; each one lasts an hour. Single-parent families seem to need more sessions, likely because there’s no spouse to share in the work. There are no meal plans in FBT, because meal plans “are not a normal way to eat. When you try to empower parents to make reasonable decisions about food, a 24-hour meal plan that the adolescent is aware of is just an opportunity for fighting over what it says,” Dr. Lock said.
Dr. Lock has coauthored a treatment manual on using FBT for anorexia.
SAN FRANCISCO – Parents have to stay level-headed if family-based therapy is going to work for anorexia nervosa, according to an expert on the technique, James Lock, MD, PhD, director of the Child and Adolescent Eating Disorder Program at Stanford (Calif.) University.
The idea of family-based therapy (FBT) is to guide parents to change behaviors – the patients’, but also their own – that undermine weight gain. Early on, the therapist has a meal with the family to observe dynamics that need to be addressed and encourage behaviors that help. It’s a nonauthoritarian approach, where the therapist helps families help themselves.
Heated emotion just opens the door to argument and resistance; patients aren’t rational when it comes to body image and eating, at least at first. Parents also have to learn not to be provoked by the child.
“You just have to ignore it. You don’t argue with the kids,” and “right now, ‘we love you’ just doesn’t go anywhere,” Dr. Lock said at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Instead, caregivers are simply supportive. The only messages that matter initially, when weight gain is critical, are along the lines of, “I know you need to eat this. You need to eat it.” Parents “need to support the behavior change and really be kind of neutral about everything else,” he said.
FBT is one of many therapeutic options for anorexia. It has a strong evidence base going back about 30 years. Dr. Lock and his colleagues have been involved in many of the more recent studies and reported a 12-month remission rate of 49% in one (Arch Gen Psychiatry. 2010 Oct; 67[10]:1025-32). There’s growing support for FBT in bulimia, as well.
The earliest goal is to engage the parents in treatment. They are complimented on what they are doing well and told not to blame themselves or their child for the illness. The seriousness of anorexia is also impressed upon the parents if they are in denial about the illness.
The family meal comes early, too. They’re stressful but necessary to learn what parents are trying to do to help and to coach them about what needs improvement. “You, as a therapist, need” to be at the meal and “join the family in their dilemmas,” Dr. Lock said.
Parents are responsible for weight restoration at first, but when steady weight gain occurs, they are taught to hand control of eating and weight back to the child. In time, therapists help with normal adolescent developmental issues and healthy family relationships.
There are maybe 20 sessions over 6-12 months, more or less depending on how it’s going; each one lasts an hour. Single-parent families seem to need more sessions, likely because there’s no spouse to share in the work. There are no meal plans in FBT, because meal plans “are not a normal way to eat. When you try to empower parents to make reasonable decisions about food, a 24-hour meal plan that the adolescent is aware of is just an opportunity for fighting over what it says,” Dr. Lock said.
Dr. Lock has coauthored a treatment manual on using FBT for anorexia.
EXPERT ANALYSIS FROM THE PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Congenital Hemangioma
Hemangiomas are the most common benign tumors of childhood. In recent years, subsets of hemangiomas that are fully formed at birth have been recognized as clinically and biologically distinct from the classic infantile hemangioma (IH). Congenital hemangiomas (CHs) are classified based on clinical course as rapidly involuting CHs (RICHs) or noninvoluting CHs (NICHs). The aim of this retrospective study was to describe the epidemiology, clinical aspects, and clinical outcome of CH over a 5-year period.
Methods
Using electronic medical records from the department of dermatology (Hedi Chaker Hospital, Sfax, Tunisia) for a 5-year period (2008-2012), we searched for hemangioma. After collecting those records, we identified patients with CHs. We studied the epidemiologic (eg, sex, age), clinical course (eg, location, size, number, color, surrounding skin), and evolutionary aspects in these patients.
Results
Twenty IHs were identified, 6 (30%) of which were considered CHs. The clinical characteristics of the 6 patients are summarized in the Table. We identified 2 females and 4 males aged 2 to 60 days (mean age, 16 days). Four patients had CHs involving the limbs (knee [n=2]; ankle [n=1]; elbow [n=1]) and 2 patients had CHs involving the trunk. Congenital hemangiomas were singular, oval shaped, and surrounded by a clear halo in all 6 patients. They presented as exophytic masses (n=3) or bossed plaques (n=3). A blue hue was noted in 5 patients and a purple hue in 1 patient. In some cases, telangiectasia (n=2) or small areas of necrosis (n=1) were noted at the center of the CHs. The CHs ranged in size from 3 to 6 cm (mean, 4 cm). Doppler ultrasonography was performed in 2 patients and showed fast blood flow. It is well known that manipulating a CH when it is ulcerative may cause a fatal hemorrhage. Thus, parents/guardians should be cautious when cleaning and dressing the lesions. Regular follow-up was recommended to all patients as noted in the medical records. The lesion involuted in4 patients after a mean period of 6 months, which allowed us to classify the lesions as RICHs (Figure, A). Two CHs were persistent after 2-year (Figure, B) and 4-year (Figure, C) follow-up, which was consistent with NICH classification.
Comment
Since 1996, vascular anomalies have been classified either as tumors or malformations.1 Infantile hemangioma is the most common vascular tumor and presents as an endothelial cellular proliferation that develops within days after birth. Congenital hemangiomas are fully developed at birth2,3 and are classified as RICHs and NICHs according to their clinical outcome.
As expected, our analysis revealed that CH usually is solitary and may present as a small lesion (eg, a few millimeters) but also may be large in size.4 Congenital hemangioma has an equal sex distribution and a predilection for the head and limbs near a joint. In contrast, IH exhibits female predilection and can occur anywhere on the body.4-6 In our study, CHs were more common in males and had a predilection for the limbs. Three patients presented with exophytic masses with a clear halo and overlying telangiectasia, which are commonly described features in CH.4,6
In the classification of vascular anomalies, RICHs and NICHs are fast-flow lesions that are indistinguishable at birth.7,8 Untreated, RICHs usually resolve in the first 14 months of life, often resulting in an area of atrophic or excess skin.8,9 Noninvoluting CHs persist and grow in proportion with the patient.10-12
When Doppler ultrasonography findings are inconsistent with a CH, an early biopsy from the periphery of the lesion may be performed to exclude an uncommon soft-tissue tumor such as infantile myofibromatosis or sarcoma.8,9,12 Because of the presence of a clear halo in all cases and mainly rapid involution of CHs, these differential diagnoses were dismissed. The histologic appearance of RICH differed from NICH and common IH, but some overlap was noted among the 3 lesions. Rapidly involuting CH was composed of small to large lobules of capillaries with moderately plump endothelial cells and pericytes; the lobules were surrounded by abundant fibrous tissue.9
Despite the notable differences in natural history between RICHs and NICHs, as RICHs regress within months while NICHs do not, both classes of CH share an important immunohistochemical phenotype; they do not express glucose transporter 1, the marker of IH.13 Tests for this marker were not performed in our study. The prognosis of CH generally is good, and special management is not required.
Conclusion
Rapidly involuting CHs and NICHs have many similarities, such as appearance, location, and sex distribution. The obvious differences in behavior serve to differentiate RICHs, NICHs, and common IHs. Infantile hemangiomas are not fully developed at birth and need many years to regress.
- Boon LM, Enjolras O, Mulliken JB. Congenital hemangioma: evidence of accelerated involution. J Pediatr. 1996;128:329-335.
- Neri I, Balestri R, Patrizi A. Hemangiomas: new insight and medical treatment. Dermatol Ther. 2012;25:322-334.
- Enjolras O, Mulliken JB. Vascular tumors and vascular malformations (new issues). Adv Dermatol. 1997;13:375-423.
- Mulliken JB, Enjolras O. Congenital hemangiomas and infantile hemangioma: missing links. J Am Acad Dermatol. 2004:50:875-882.
- Frieden IJ, Haggstrom AN, Drolet BA, et al. Infantile hemangiomas: current knowledge, future directions. proceedings of a research workshop on infantile hemangiomas, April 7-9, 2005, Bethesda, Maryland, USA. Pediatr Dermatol. 2005;22:383-406.
- Enjolras O, Picard A, Soupre V. Congenital haemangiomas and other rare infantile vascular tumours [in French]. Ann Chir Plast Esthet. 2006;51:339-346.
- Gorincour G, Kokta V, Rypens F, et al. Imaging characteristics of two subtypes of congenital hemangiomas: rapidly involuting congenital hemangiomas and non-involuting congenital hemangiomas. Pediatr Radiol. 2005;35:1178-1185.
- Rogers M, Lam A, Fischer G. Sonographic findings in a series of rapidly involuting congenital hemangiomas (RICH). Pediatr Dermatol. 2002;19:5-11.
- Berenguer B, Mulliken JB, Enjolras O, et al. Rapidly involuting congenital hemangioma: clinical and histopathologic features. Pediatr Dev Pathol. 2003;6:495-510.
- North PE, Waner M, James CA, et al. Congenital nonprogressive hemangioma: a distinct clinicopathologic entity unlike infantile hemangioma. Arch Dermatol. 2001;137:1607-1620.
- Chiavérini C, Kurzenne JY, Rogopoulos A, et al. Noninvoluting congenital hemangioma: 2 cases [in French]. Ann Dermatol Venerol. 2002;129:735-737.
- Enjolras O, Mulliken JB, Boon LM, et al. Noninvoluting congenital hemangioma: a rare cutaneous vascular anomaly. Plast Reconstr Surg. 2001;107:1647-1654.
- North PE, Waner M, Mizeracki A, et al. GLUT1: a newly discovered immunohistochemical marker for juvenile hemangiomas. Hum Pathol. 2000;31:11-22.
Hemangiomas are the most common benign tumors of childhood. In recent years, subsets of hemangiomas that are fully formed at birth have been recognized as clinically and biologically distinct from the classic infantile hemangioma (IH). Congenital hemangiomas (CHs) are classified based on clinical course as rapidly involuting CHs (RICHs) or noninvoluting CHs (NICHs). The aim of this retrospective study was to describe the epidemiology, clinical aspects, and clinical outcome of CH over a 5-year period.
Methods
Using electronic medical records from the department of dermatology (Hedi Chaker Hospital, Sfax, Tunisia) for a 5-year period (2008-2012), we searched for hemangioma. After collecting those records, we identified patients with CHs. We studied the epidemiologic (eg, sex, age), clinical course (eg, location, size, number, color, surrounding skin), and evolutionary aspects in these patients.
Results
Twenty IHs were identified, 6 (30%) of which were considered CHs. The clinical characteristics of the 6 patients are summarized in the Table. We identified 2 females and 4 males aged 2 to 60 days (mean age, 16 days). Four patients had CHs involving the limbs (knee [n=2]; ankle [n=1]; elbow [n=1]) and 2 patients had CHs involving the trunk. Congenital hemangiomas were singular, oval shaped, and surrounded by a clear halo in all 6 patients. They presented as exophytic masses (n=3) or bossed plaques (n=3). A blue hue was noted in 5 patients and a purple hue in 1 patient. In some cases, telangiectasia (n=2) or small areas of necrosis (n=1) were noted at the center of the CHs. The CHs ranged in size from 3 to 6 cm (mean, 4 cm). Doppler ultrasonography was performed in 2 patients and showed fast blood flow. It is well known that manipulating a CH when it is ulcerative may cause a fatal hemorrhage. Thus, parents/guardians should be cautious when cleaning and dressing the lesions. Regular follow-up was recommended to all patients as noted in the medical records. The lesion involuted in4 patients after a mean period of 6 months, which allowed us to classify the lesions as RICHs (Figure, A). Two CHs were persistent after 2-year (Figure, B) and 4-year (Figure, C) follow-up, which was consistent with NICH classification.
Comment
Since 1996, vascular anomalies have been classified either as tumors or malformations.1 Infantile hemangioma is the most common vascular tumor and presents as an endothelial cellular proliferation that develops within days after birth. Congenital hemangiomas are fully developed at birth2,3 and are classified as RICHs and NICHs according to their clinical outcome.
As expected, our analysis revealed that CH usually is solitary and may present as a small lesion (eg, a few millimeters) but also may be large in size.4 Congenital hemangioma has an equal sex distribution and a predilection for the head and limbs near a joint. In contrast, IH exhibits female predilection and can occur anywhere on the body.4-6 In our study, CHs were more common in males and had a predilection for the limbs. Three patients presented with exophytic masses with a clear halo and overlying telangiectasia, which are commonly described features in CH.4,6
In the classification of vascular anomalies, RICHs and NICHs are fast-flow lesions that are indistinguishable at birth.7,8 Untreated, RICHs usually resolve in the first 14 months of life, often resulting in an area of atrophic or excess skin.8,9 Noninvoluting CHs persist and grow in proportion with the patient.10-12
When Doppler ultrasonography findings are inconsistent with a CH, an early biopsy from the periphery of the lesion may be performed to exclude an uncommon soft-tissue tumor such as infantile myofibromatosis or sarcoma.8,9,12 Because of the presence of a clear halo in all cases and mainly rapid involution of CHs, these differential diagnoses were dismissed. The histologic appearance of RICH differed from NICH and common IH, but some overlap was noted among the 3 lesions. Rapidly involuting CH was composed of small to large lobules of capillaries with moderately plump endothelial cells and pericytes; the lobules were surrounded by abundant fibrous tissue.9
Despite the notable differences in natural history between RICHs and NICHs, as RICHs regress within months while NICHs do not, both classes of CH share an important immunohistochemical phenotype; they do not express glucose transporter 1, the marker of IH.13 Tests for this marker were not performed in our study. The prognosis of CH generally is good, and special management is not required.
Conclusion
Rapidly involuting CHs and NICHs have many similarities, such as appearance, location, and sex distribution. The obvious differences in behavior serve to differentiate RICHs, NICHs, and common IHs. Infantile hemangiomas are not fully developed at birth and need many years to regress.
Hemangiomas are the most common benign tumors of childhood. In recent years, subsets of hemangiomas that are fully formed at birth have been recognized as clinically and biologically distinct from the classic infantile hemangioma (IH). Congenital hemangiomas (CHs) are classified based on clinical course as rapidly involuting CHs (RICHs) or noninvoluting CHs (NICHs). The aim of this retrospective study was to describe the epidemiology, clinical aspects, and clinical outcome of CH over a 5-year period.
Methods
Using electronic medical records from the department of dermatology (Hedi Chaker Hospital, Sfax, Tunisia) for a 5-year period (2008-2012), we searched for hemangioma. After collecting those records, we identified patients with CHs. We studied the epidemiologic (eg, sex, age), clinical course (eg, location, size, number, color, surrounding skin), and evolutionary aspects in these patients.
Results
Twenty IHs were identified, 6 (30%) of which were considered CHs. The clinical characteristics of the 6 patients are summarized in the Table. We identified 2 females and 4 males aged 2 to 60 days (mean age, 16 days). Four patients had CHs involving the limbs (knee [n=2]; ankle [n=1]; elbow [n=1]) and 2 patients had CHs involving the trunk. Congenital hemangiomas were singular, oval shaped, and surrounded by a clear halo in all 6 patients. They presented as exophytic masses (n=3) or bossed plaques (n=3). A blue hue was noted in 5 patients and a purple hue in 1 patient. In some cases, telangiectasia (n=2) or small areas of necrosis (n=1) were noted at the center of the CHs. The CHs ranged in size from 3 to 6 cm (mean, 4 cm). Doppler ultrasonography was performed in 2 patients and showed fast blood flow. It is well known that manipulating a CH when it is ulcerative may cause a fatal hemorrhage. Thus, parents/guardians should be cautious when cleaning and dressing the lesions. Regular follow-up was recommended to all patients as noted in the medical records. The lesion involuted in4 patients after a mean period of 6 months, which allowed us to classify the lesions as RICHs (Figure, A). Two CHs were persistent after 2-year (Figure, B) and 4-year (Figure, C) follow-up, which was consistent with NICH classification.
Comment
Since 1996, vascular anomalies have been classified either as tumors or malformations.1 Infantile hemangioma is the most common vascular tumor and presents as an endothelial cellular proliferation that develops within days after birth. Congenital hemangiomas are fully developed at birth2,3 and are classified as RICHs and NICHs according to their clinical outcome.
As expected, our analysis revealed that CH usually is solitary and may present as a small lesion (eg, a few millimeters) but also may be large in size.4 Congenital hemangioma has an equal sex distribution and a predilection for the head and limbs near a joint. In contrast, IH exhibits female predilection and can occur anywhere on the body.4-6 In our study, CHs were more common in males and had a predilection for the limbs. Three patients presented with exophytic masses with a clear halo and overlying telangiectasia, which are commonly described features in CH.4,6
In the classification of vascular anomalies, RICHs and NICHs are fast-flow lesions that are indistinguishable at birth.7,8 Untreated, RICHs usually resolve in the first 14 months of life, often resulting in an area of atrophic or excess skin.8,9 Noninvoluting CHs persist and grow in proportion with the patient.10-12
When Doppler ultrasonography findings are inconsistent with a CH, an early biopsy from the periphery of the lesion may be performed to exclude an uncommon soft-tissue tumor such as infantile myofibromatosis or sarcoma.8,9,12 Because of the presence of a clear halo in all cases and mainly rapid involution of CHs, these differential diagnoses were dismissed. The histologic appearance of RICH differed from NICH and common IH, but some overlap was noted among the 3 lesions. Rapidly involuting CH was composed of small to large lobules of capillaries with moderately plump endothelial cells and pericytes; the lobules were surrounded by abundant fibrous tissue.9
Despite the notable differences in natural history between RICHs and NICHs, as RICHs regress within months while NICHs do not, both classes of CH share an important immunohistochemical phenotype; they do not express glucose transporter 1, the marker of IH.13 Tests for this marker were not performed in our study. The prognosis of CH generally is good, and special management is not required.
Conclusion
Rapidly involuting CHs and NICHs have many similarities, such as appearance, location, and sex distribution. The obvious differences in behavior serve to differentiate RICHs, NICHs, and common IHs. Infantile hemangiomas are not fully developed at birth and need many years to regress.
- Boon LM, Enjolras O, Mulliken JB. Congenital hemangioma: evidence of accelerated involution. J Pediatr. 1996;128:329-335.
- Neri I, Balestri R, Patrizi A. Hemangiomas: new insight and medical treatment. Dermatol Ther. 2012;25:322-334.
- Enjolras O, Mulliken JB. Vascular tumors and vascular malformations (new issues). Adv Dermatol. 1997;13:375-423.
- Mulliken JB, Enjolras O. Congenital hemangiomas and infantile hemangioma: missing links. J Am Acad Dermatol. 2004:50:875-882.
- Frieden IJ, Haggstrom AN, Drolet BA, et al. Infantile hemangiomas: current knowledge, future directions. proceedings of a research workshop on infantile hemangiomas, April 7-9, 2005, Bethesda, Maryland, USA. Pediatr Dermatol. 2005;22:383-406.
- Enjolras O, Picard A, Soupre V. Congenital haemangiomas and other rare infantile vascular tumours [in French]. Ann Chir Plast Esthet. 2006;51:339-346.
- Gorincour G, Kokta V, Rypens F, et al. Imaging characteristics of two subtypes of congenital hemangiomas: rapidly involuting congenital hemangiomas and non-involuting congenital hemangiomas. Pediatr Radiol. 2005;35:1178-1185.
- Rogers M, Lam A, Fischer G. Sonographic findings in a series of rapidly involuting congenital hemangiomas (RICH). Pediatr Dermatol. 2002;19:5-11.
- Berenguer B, Mulliken JB, Enjolras O, et al. Rapidly involuting congenital hemangioma: clinical and histopathologic features. Pediatr Dev Pathol. 2003;6:495-510.
- North PE, Waner M, James CA, et al. Congenital nonprogressive hemangioma: a distinct clinicopathologic entity unlike infantile hemangioma. Arch Dermatol. 2001;137:1607-1620.
- Chiavérini C, Kurzenne JY, Rogopoulos A, et al. Noninvoluting congenital hemangioma: 2 cases [in French]. Ann Dermatol Venerol. 2002;129:735-737.
- Enjolras O, Mulliken JB, Boon LM, et al. Noninvoluting congenital hemangioma: a rare cutaneous vascular anomaly. Plast Reconstr Surg. 2001;107:1647-1654.
- North PE, Waner M, Mizeracki A, et al. GLUT1: a newly discovered immunohistochemical marker for juvenile hemangiomas. Hum Pathol. 2000;31:11-22.
- Boon LM, Enjolras O, Mulliken JB. Congenital hemangioma: evidence of accelerated involution. J Pediatr. 1996;128:329-335.
- Neri I, Balestri R, Patrizi A. Hemangiomas: new insight and medical treatment. Dermatol Ther. 2012;25:322-334.
- Enjolras O, Mulliken JB. Vascular tumors and vascular malformations (new issues). Adv Dermatol. 1997;13:375-423.
- Mulliken JB, Enjolras O. Congenital hemangiomas and infantile hemangioma: missing links. J Am Acad Dermatol. 2004:50:875-882.
- Frieden IJ, Haggstrom AN, Drolet BA, et al. Infantile hemangiomas: current knowledge, future directions. proceedings of a research workshop on infantile hemangiomas, April 7-9, 2005, Bethesda, Maryland, USA. Pediatr Dermatol. 2005;22:383-406.
- Enjolras O, Picard A, Soupre V. Congenital haemangiomas and other rare infantile vascular tumours [in French]. Ann Chir Plast Esthet. 2006;51:339-346.
- Gorincour G, Kokta V, Rypens F, et al. Imaging characteristics of two subtypes of congenital hemangiomas: rapidly involuting congenital hemangiomas and non-involuting congenital hemangiomas. Pediatr Radiol. 2005;35:1178-1185.
- Rogers M, Lam A, Fischer G. Sonographic findings in a series of rapidly involuting congenital hemangiomas (RICH). Pediatr Dermatol. 2002;19:5-11.
- Berenguer B, Mulliken JB, Enjolras O, et al. Rapidly involuting congenital hemangioma: clinical and histopathologic features. Pediatr Dev Pathol. 2003;6:495-510.
- North PE, Waner M, James CA, et al. Congenital nonprogressive hemangioma: a distinct clinicopathologic entity unlike infantile hemangioma. Arch Dermatol. 2001;137:1607-1620.
- Chiavérini C, Kurzenne JY, Rogopoulos A, et al. Noninvoluting congenital hemangioma: 2 cases [in French]. Ann Dermatol Venerol. 2002;129:735-737.
- Enjolras O, Mulliken JB, Boon LM, et al. Noninvoluting congenital hemangioma: a rare cutaneous vascular anomaly. Plast Reconstr Surg. 2001;107:1647-1654.
- North PE, Waner M, Mizeracki A, et al. GLUT1: a newly discovered immunohistochemical marker for juvenile hemangiomas. Hum Pathol. 2000;31:11-22.
Practice Points
- Congenital hemangiomas (CHs) are fully developed hemangiomas that are present at birth.
- In our study, CHs were more common in males, with a predilection for the limbs.
- Infantile hemangiomas are not fully developed at birth and need many years to regress.
Cheap manufacture of generic cancer drugs is feasible, study shows
Photo courtesy of FDA
AMSTERDAM—New research suggests some generic cancer drugs could be manufactured for less than 1% of the prices currently charged in the US and UK.
For example, researchers calculated that manufacturing a 400 mg tablet of imatinib costs $0.92.
Charging $1.04 per tablet would cover costs and allow for a 10% profit margin.
However, the current price of imatinib is $84.36 per tablet in the UK and $247.74 per tablet in the US.
Melissa Barber, of the London School of Hygiene and Tropical Medicine in the UK, reported these findings at ECCO 2017: European Cancer Congress (abstract 1032).
Barber and her colleagues collected data on per-kilogram costs of exported active pharmaceutical ingredients (APIs) from an online database of Indian export logs.
The team then estimated generic prices for tablets through an established costing algorithm. They calculated per-dose API costs and added excipient costs of $2.63 per kg of finished pharmaceutical product and per-tablet costs of production of $0.01, plus a 10% profit margin accounting for a 26.6% average tax on profits (assuming manufacture in India.)
Finally, the researchers compared the calculated price to current unit prices in the US, UK, Spain, and India.
For imatinib, the team determined the cost of the API to be $2284 per kg and the API cost per tablet to be $0.91. They then added excipient cost ($0.002 per tablet), conversion cost ($0.01 per tablet), and a 10% profit margin accounting for a 26.6% tax on profits.
This resulted in the estimated generic price of $1.04 per tablet. The per-tablet price is below the estimated price in India ($0.22) but much higher than the estimated price in Spain ($57.53), the UK ($84.36), and the US ($247.74).
Barber noted that, according to her group’s calculations, imatinib could be produced for $54 a month.
Another drug that could be produced for a low cost is etoposide. Barber and her colleagues calculated a generic price for etoposide of $0.97 per 100 mg tablet.
However, the per-tablet price is $1.50 in India, $8.65 in Spain, $11.34 in the UK, and $87.14 in the US.
The researchers calculated a generic price for mercaptopurine of $0.03 per 50 mg tablet, which is the same as the per-tablet price in India. However, a 50 mg mercaptopurine tablet costs $3.14 in Spain, $2.56 in the UK, and $0.40 in the US.
“Showing that certain cancers could be treated for very low prices could transform the future of people with these cancers in very low-income countries where there are usually few or no treatment options,” Barber said. 
Photo courtesy of FDA
AMSTERDAM—New research suggests some generic cancer drugs could be manufactured for less than 1% of the prices currently charged in the US and UK.
For example, researchers calculated that manufacturing a 400 mg tablet of imatinib costs $0.92.
Charging $1.04 per tablet would cover costs and allow for a 10% profit margin.
However, the current price of imatinib is $84.36 per tablet in the UK and $247.74 per tablet in the US.
Melissa Barber, of the London School of Hygiene and Tropical Medicine in the UK, reported these findings at ECCO 2017: European Cancer Congress (abstract 1032).
Barber and her colleagues collected data on per-kilogram costs of exported active pharmaceutical ingredients (APIs) from an online database of Indian export logs.
The team then estimated generic prices for tablets through an established costing algorithm. They calculated per-dose API costs and added excipient costs of $2.63 per kg of finished pharmaceutical product and per-tablet costs of production of $0.01, plus a 10% profit margin accounting for a 26.6% average tax on profits (assuming manufacture in India.)
Finally, the researchers compared the calculated price to current unit prices in the US, UK, Spain, and India.
For imatinib, the team determined the cost of the API to be $2284 per kg and the API cost per tablet to be $0.91. They then added excipient cost ($0.002 per tablet), conversion cost ($0.01 per tablet), and a 10% profit margin accounting for a 26.6% tax on profits.
This resulted in the estimated generic price of $1.04 per tablet. The per-tablet price is below the estimated price in India ($0.22) but much higher than the estimated price in Spain ($57.53), the UK ($84.36), and the US ($247.74).
Barber noted that, according to her group’s calculations, imatinib could be produced for $54 a month.
Another drug that could be produced for a low cost is etoposide. Barber and her colleagues calculated a generic price for etoposide of $0.97 per 100 mg tablet.
However, the per-tablet price is $1.50 in India, $8.65 in Spain, $11.34 in the UK, and $87.14 in the US.
The researchers calculated a generic price for mercaptopurine of $0.03 per 50 mg tablet, which is the same as the per-tablet price in India. However, a 50 mg mercaptopurine tablet costs $3.14 in Spain, $2.56 in the UK, and $0.40 in the US.
“Showing that certain cancers could be treated for very low prices could transform the future of people with these cancers in very low-income countries where there are usually few or no treatment options,” Barber said.
Photo courtesy of FDA
AMSTERDAM—New research suggests some generic cancer drugs could be manufactured for less than 1% of the prices currently charged in the US and UK.
For example, researchers calculated that manufacturing a 400 mg tablet of imatinib costs $0.92.
Charging $1.04 per tablet would cover costs and allow for a 10% profit margin.
However, the current price of imatinib is $84.36 per tablet in the UK and $247.74 per tablet in the US.
Melissa Barber, of the London School of Hygiene and Tropical Medicine in the UK, reported these findings at ECCO 2017: European Cancer Congress (abstract 1032).
Barber and her colleagues collected data on per-kilogram costs of exported active pharmaceutical ingredients (APIs) from an online database of Indian export logs.
The team then estimated generic prices for tablets through an established costing algorithm. They calculated per-dose API costs and added excipient costs of $2.63 per kg of finished pharmaceutical product and per-tablet costs of production of $0.01, plus a 10% profit margin accounting for a 26.6% average tax on profits (assuming manufacture in India.)
Finally, the researchers compared the calculated price to current unit prices in the US, UK, Spain, and India.
For imatinib, the team determined the cost of the API to be $2284 per kg and the API cost per tablet to be $0.91. They then added excipient cost ($0.002 per tablet), conversion cost ($0.01 per tablet), and a 10% profit margin accounting for a 26.6% tax on profits.
This resulted in the estimated generic price of $1.04 per tablet. The per-tablet price is below the estimated price in India ($0.22) but much higher than the estimated price in Spain ($57.53), the UK ($84.36), and the US ($247.74).
Barber noted that, according to her group’s calculations, imatinib could be produced for $54 a month.
Another drug that could be produced for a low cost is etoposide. Barber and her colleagues calculated a generic price for etoposide of $0.97 per 100 mg tablet.
However, the per-tablet price is $1.50 in India, $8.65 in Spain, $11.34 in the UK, and $87.14 in the US.
The researchers calculated a generic price for mercaptopurine of $0.03 per 50 mg tablet, which is the same as the per-tablet price in India. However, a 50 mg mercaptopurine tablet costs $3.14 in Spain, $2.56 in the UK, and $0.40 in the US.
“Showing that certain cancers could be treated for very low prices could transform the future of people with these cancers in very low-income countries where there are usually few or no treatment options,” Barber said.
SSRI activation in children, adolescents often misdiagnosed as bipolar
SAN FRANCISCO – It’s not uncommon for children to arrive at the Western Psychiatric Institute and Clinic in Pittsburgh with selective serotonin reuptake inhibitor activation that was misdiagnosed as bipolar disorder, according to Boris Birmaher, MD.
“We get many kids into our clinic with a diagnosis of bipolar because of this, and they are not bipolar. You have to be careful,” he said during a talk about pediatric depression at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
SSRIs activate about 5%-10% of children. There might be sleep problems, fast speech, hyperactivity, agitation, aggression, and even suicidality, he said.
Younger children and those with autism or developmental disabilities are particularly at risk. Occasionally, a child might be a slow metabolizer so that even low SSRI doses cause problems. “Once in a blue moon,” Dr. Birmaher said he will screen for genetic cytochrome P450 deficiency, especially if a child doesn’t seem able to tolerate medications in general, not just psychiatric ones. He’s found a few slow metabolizers over the years.
Psychiatrists also have to be careful when children and adolescents are tagged as “treatment resistant.” It’s important to teach parents what treatment resistance would actually look like for their child, so they don’t jump to conclusions and misdirect therapy, he said.
For example, when a child has been prescribed an SSRI for anxiety, parents might come in and say it’s not helping, when in fact they’re concerned about homework not getting done and restlessness in class. “There’s no treatment resistance. You teach the parent how to measure improvement of anxiety” and tackle the ADHD if it’s truly a problem, said Dr. Birmaher, also professor of psychiatry at the University of Pittsburgh.
If there really is SSRI treatment resistance, he said he first ensures that a maximum dose of the drug has been tried, so long as it’s tolerated. If it doesn’t work after 4-6 weeks, he’ll switch to another SSRI or selective norepinephrine reuptake inhibitor, or combination treatment with, for instance, bupropion (Wellbutrin) or an atypical antipsychotic, which are particularly helpful for irritability, even in small doses. Atypicals seem to take the edge off, he said.
It’s trial and error, since there aren’t much data in children to guide treatment. “The only thing I highly recommend is to make one change at a time. Sometimes we see kids who’ve had two or three changes at the same time.” In those cases, he said, it’s impossible to know what to blame if there are side effects or what to credit if depression improves.
Dr. Birmaher said he had no pharmaceutical industry ties.
SAN FRANCISCO – It’s not uncommon for children to arrive at the Western Psychiatric Institute and Clinic in Pittsburgh with selective serotonin reuptake inhibitor activation that was misdiagnosed as bipolar disorder, according to Boris Birmaher, MD.
“We get many kids into our clinic with a diagnosis of bipolar because of this, and they are not bipolar. You have to be careful,” he said during a talk about pediatric depression at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
SSRIs activate about 5%-10% of children. There might be sleep problems, fast speech, hyperactivity, agitation, aggression, and even suicidality, he said.
Younger children and those with autism or developmental disabilities are particularly at risk. Occasionally, a child might be a slow metabolizer so that even low SSRI doses cause problems. “Once in a blue moon,” Dr. Birmaher said he will screen for genetic cytochrome P450 deficiency, especially if a child doesn’t seem able to tolerate medications in general, not just psychiatric ones. He’s found a few slow metabolizers over the years.
Psychiatrists also have to be careful when children and adolescents are tagged as “treatment resistant.” It’s important to teach parents what treatment resistance would actually look like for their child, so they don’t jump to conclusions and misdirect therapy, he said.
For example, when a child has been prescribed an SSRI for anxiety, parents might come in and say it’s not helping, when in fact they’re concerned about homework not getting done and restlessness in class. “There’s no treatment resistance. You teach the parent how to measure improvement of anxiety” and tackle the ADHD if it’s truly a problem, said Dr. Birmaher, also professor of psychiatry at the University of Pittsburgh.
If there really is SSRI treatment resistance, he said he first ensures that a maximum dose of the drug has been tried, so long as it’s tolerated. If it doesn’t work after 4-6 weeks, he’ll switch to another SSRI or selective norepinephrine reuptake inhibitor, or combination treatment with, for instance, bupropion (Wellbutrin) or an atypical antipsychotic, which are particularly helpful for irritability, even in small doses. Atypicals seem to take the edge off, he said.
It’s trial and error, since there aren’t much data in children to guide treatment. “The only thing I highly recommend is to make one change at a time. Sometimes we see kids who’ve had two or three changes at the same time.” In those cases, he said, it’s impossible to know what to blame if there are side effects or what to credit if depression improves.
Dr. Birmaher said he had no pharmaceutical industry ties.
SAN FRANCISCO – It’s not uncommon for children to arrive at the Western Psychiatric Institute and Clinic in Pittsburgh with selective serotonin reuptake inhibitor activation that was misdiagnosed as bipolar disorder, according to Boris Birmaher, MD.
“We get many kids into our clinic with a diagnosis of bipolar because of this, and they are not bipolar. You have to be careful,” he said during a talk about pediatric depression at a psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
SSRIs activate about 5%-10% of children. There might be sleep problems, fast speech, hyperactivity, agitation, aggression, and even suicidality, he said.
Younger children and those with autism or developmental disabilities are particularly at risk. Occasionally, a child might be a slow metabolizer so that even low SSRI doses cause problems. “Once in a blue moon,” Dr. Birmaher said he will screen for genetic cytochrome P450 deficiency, especially if a child doesn’t seem able to tolerate medications in general, not just psychiatric ones. He’s found a few slow metabolizers over the years.
Psychiatrists also have to be careful when children and adolescents are tagged as “treatment resistant.” It’s important to teach parents what treatment resistance would actually look like for their child, so they don’t jump to conclusions and misdirect therapy, he said.
For example, when a child has been prescribed an SSRI for anxiety, parents might come in and say it’s not helping, when in fact they’re concerned about homework not getting done and restlessness in class. “There’s no treatment resistance. You teach the parent how to measure improvement of anxiety” and tackle the ADHD if it’s truly a problem, said Dr. Birmaher, also professor of psychiatry at the University of Pittsburgh.
If there really is SSRI treatment resistance, he said he first ensures that a maximum dose of the drug has been tried, so long as it’s tolerated. If it doesn’t work after 4-6 weeks, he’ll switch to another SSRI or selective norepinephrine reuptake inhibitor, or combination treatment with, for instance, bupropion (Wellbutrin) or an atypical antipsychotic, which are particularly helpful for irritability, even in small doses. Atypicals seem to take the edge off, he said.
It’s trial and error, since there aren’t much data in children to guide treatment. “The only thing I highly recommend is to make one change at a time. Sometimes we see kids who’ve had two or three changes at the same time.” In those cases, he said, it’s impossible to know what to blame if there are side effects or what to credit if depression improves.
Dr. Birmaher said he had no pharmaceutical industry ties.
EXPERT ANALYSIS AT THE PSYCHOPHARMACOLOGY UPDATE INSTITUTE
The Pill: A pediatric perspective
Arguably, the introduction of the birth control pill has transformed female health more than any other drug in modern medicine. Although many of us practicing now do not know life without it, its history is not that long.
“The Pill” – as it is often referred to – was introduced in May of 1950.1 At that time, prevention of pregnancy was not listed as an indication, and promoting birth control was politically, socially, and legally unacceptable. In fact, the Comstock Law prohibited public discussion and research about contraception.1 Therefore, when the birth control pill was introduced, it was for cycle control and for married women only. It was not indicated for use as contraception in the United States until 1960.
Since that time, the birth control pill has evolved dramatically, not only in its formulation but in its indications as well. As pediatricians, we do not always find it easy to discuss with parents hormonal regulation and starting a patient on the birth control pill, particularly when it will not be used for contraception. There are many fears about using hormonal control, but there are many useful indications that improve the health and well-being of the pediatric patient.
Menorrhagia and dysmenorrhea are likely the most common reasons that hormonal therapy is started in adolescence. Beginning with the lowest estrogen dose to reduce side effects is prudent, adjusting accordingly if side effects should occur. Breakthrough bleeding is a common side effect that usually improves over time. Patients should continue treatment for at least 3 months before deciding if treatment is effective or not. If breakthrough bleeding continues, increasing the estrogen component or changing to a triphasic pill might reduce bleeding.
For a child with mental or significant physical disabilities, suppression of ovulation to prevent a menstrual cycle is very useful. Extended regimens can help to completely suppress ovulation, thereby avoiding withdrawal bleeding. There is anxiety about extended regimens, but there is no greater risk with using hormonal therapy continuously vs. intermittently.2 In fact, using it continuously reduces many of the unwanted side effects associated with the use of oral contraceptive pills (OCPs), for example, heavy bleeding, headaches, and nausea. Complete suppression is difficult, but the odds are better with continuous treatment. Using monophasic OCPs for 42-63 days on and 4-7 days off can be tried. The benefit of using monophasic pills is if a dose is missed, it is easy to make it up by just taking an extra pill. Companies have come out with extended-regimen packs, for example, Seasonale, Seasonique, Quartette, and Lybrel. There now is a chewable pill known as Femcon Fe, which would be useful in those patients who are not able to swallow pills.
Another indication for OCPs in the adolescent patient is acne. Although the exact mechanism is not completely understood, estrogen does decrease sebum by reducing the size of the gland4, and, therefore, all OCPs can reduce acne. Norgestimate combinations have the highest androgen to progesterone binding ratio, so they are more effective than OCPs that do not. A newer progestin, drospirenone, is a 17 alpha-spironolactone derivative that produces antiandrogenic activity.5 When used in a combination OCP, acne control appears to be even greater. Hormonal therapy should be considered whenever there has been limited improvement with topical treatment or if acne breakouts are associated with the onset of menses.
Another consideration is to add spironolactone 100 mg by mouth daily to the regimen. Studies have shown it can be safely used in women to reduce acne.6 Patients should be monitored frequently for hyperkalemia, and it should not be used in patients who are already pregnant.4 Lab work should be done to rule out other causes of hyperandrogenism; lab tests would include serum testosterone, androstenedione, dehydroepiandrosterone, sex hormone–binding globulin, and prolactin.4
Premenstrual syndrome (PMS) or premenstrual dysphoric disorder (PMDD) – which is the onset of depression, irritability, or anxiety in the second half of the menstrual cycle and remits with the onset of the menstrual cycle – also can be treated with hormonal therapy. This can be particularly helpful in teens with depression, as well as in those who are on treatment without significant resolution. PMS/PMDD appears to be best regulated with OCPs containing drospirenone,7 and using either a shortened course of the placebo phase or a continuous regimen appears to be the most beneficial.
Regardless of the indication for hormonal therapy, the initiation and management are essentially the same. Initiation can be on the first day of the menstrual cycle, on the Sunday after, or at the time of the visit. Initiation midcycle may result in breakthrough bleeding, but that will likely resolve over the next 3 months. No lab tests are required to start hormonal therapy, except for an HCG to rule out pregnancy. Weight and blood pressure should be documented so they can be monitored on follow-up visits. A detailed verbal explanation along with a handout should be provided on proper administration and side effects. Contraindications for the use of OCPs can be found on the Centers for Disease Control and Prevention’s website under medical criteria for the use of contraceptives.
Educating families and patients on their options for hormonal therapy can be life changing. Detailed questions about the menstrual cycle should be asked at every visit, and understanding the wide variety of indications for hormonal therapy can maximize treatment for a better outcome.
References
1. Can Fam Physician. 2012 Dec;58(12):e757–60.
2. J Midwifery Womens Health. 2012 Nov-Dec;57(6):585-92.
3. Obstet Gynecol. 2009;114:1428-31.
4. Semin Cutan Med Surg. 2008 Sep;27(3):188-96.
5. Pediatr Rev. 2008;29(11);386-97.
6. J Eur Acad Dermatol Venereol. 2005 Mar;19(2):163-6.
7. Obstet Gynecol. 2005 Sep;106(3):492-501.
Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures.
Arguably, the introduction of the birth control pill has transformed female health more than any other drug in modern medicine. Although many of us practicing now do not know life without it, its history is not that long.
“The Pill” – as it is often referred to – was introduced in May of 1950.1 At that time, prevention of pregnancy was not listed as an indication, and promoting birth control was politically, socially, and legally unacceptable. In fact, the Comstock Law prohibited public discussion and research about contraception.1 Therefore, when the birth control pill was introduced, it was for cycle control and for married women only. It was not indicated for use as contraception in the United States until 1960.
Since that time, the birth control pill has evolved dramatically, not only in its formulation but in its indications as well. As pediatricians, we do not always find it easy to discuss with parents hormonal regulation and starting a patient on the birth control pill, particularly when it will not be used for contraception. There are many fears about using hormonal control, but there are many useful indications that improve the health and well-being of the pediatric patient.
Menorrhagia and dysmenorrhea are likely the most common reasons that hormonal therapy is started in adolescence. Beginning with the lowest estrogen dose to reduce side effects is prudent, adjusting accordingly if side effects should occur. Breakthrough bleeding is a common side effect that usually improves over time. Patients should continue treatment for at least 3 months before deciding if treatment is effective or not. If breakthrough bleeding continues, increasing the estrogen component or changing to a triphasic pill might reduce bleeding.
For a child with mental or significant physical disabilities, suppression of ovulation to prevent a menstrual cycle is very useful. Extended regimens can help to completely suppress ovulation, thereby avoiding withdrawal bleeding. There is anxiety about extended regimens, but there is no greater risk with using hormonal therapy continuously vs. intermittently.2 In fact, using it continuously reduces many of the unwanted side effects associated with the use of oral contraceptive pills (OCPs), for example, heavy bleeding, headaches, and nausea. Complete suppression is difficult, but the odds are better with continuous treatment. Using monophasic OCPs for 42-63 days on and 4-7 days off can be tried. The benefit of using monophasic pills is if a dose is missed, it is easy to make it up by just taking an extra pill. Companies have come out with extended-regimen packs, for example, Seasonale, Seasonique, Quartette, and Lybrel. There now is a chewable pill known as Femcon Fe, which would be useful in those patients who are not able to swallow pills.
Another indication for OCPs in the adolescent patient is acne. Although the exact mechanism is not completely understood, estrogen does decrease sebum by reducing the size of the gland4, and, therefore, all OCPs can reduce acne. Norgestimate combinations have the highest androgen to progesterone binding ratio, so they are more effective than OCPs that do not. A newer progestin, drospirenone, is a 17 alpha-spironolactone derivative that produces antiandrogenic activity.5 When used in a combination OCP, acne control appears to be even greater. Hormonal therapy should be considered whenever there has been limited improvement with topical treatment or if acne breakouts are associated with the onset of menses.
Another consideration is to add spironolactone 100 mg by mouth daily to the regimen. Studies have shown it can be safely used in women to reduce acne.6 Patients should be monitored frequently for hyperkalemia, and it should not be used in patients who are already pregnant.4 Lab work should be done to rule out other causes of hyperandrogenism; lab tests would include serum testosterone, androstenedione, dehydroepiandrosterone, sex hormone–binding globulin, and prolactin.4
Premenstrual syndrome (PMS) or premenstrual dysphoric disorder (PMDD) – which is the onset of depression, irritability, or anxiety in the second half of the menstrual cycle and remits with the onset of the menstrual cycle – also can be treated with hormonal therapy. This can be particularly helpful in teens with depression, as well as in those who are on treatment without significant resolution. PMS/PMDD appears to be best regulated with OCPs containing drospirenone,7 and using either a shortened course of the placebo phase or a continuous regimen appears to be the most beneficial.
Regardless of the indication for hormonal therapy, the initiation and management are essentially the same. Initiation can be on the first day of the menstrual cycle, on the Sunday after, or at the time of the visit. Initiation midcycle may result in breakthrough bleeding, but that will likely resolve over the next 3 months. No lab tests are required to start hormonal therapy, except for an HCG to rule out pregnancy. Weight and blood pressure should be documented so they can be monitored on follow-up visits. A detailed verbal explanation along with a handout should be provided on proper administration and side effects. Contraindications for the use of OCPs can be found on the Centers for Disease Control and Prevention’s website under medical criteria for the use of contraceptives.
Educating families and patients on their options for hormonal therapy can be life changing. Detailed questions about the menstrual cycle should be asked at every visit, and understanding the wide variety of indications for hormonal therapy can maximize treatment for a better outcome.
References
1. Can Fam Physician. 2012 Dec;58(12):e757–60.
2. J Midwifery Womens Health. 2012 Nov-Dec;57(6):585-92.
3. Obstet Gynecol. 2009;114:1428-31.
4. Semin Cutan Med Surg. 2008 Sep;27(3):188-96.
5. Pediatr Rev. 2008;29(11);386-97.
6. J Eur Acad Dermatol Venereol. 2005 Mar;19(2):163-6.
7. Obstet Gynecol. 2005 Sep;106(3):492-501.
Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures.
Arguably, the introduction of the birth control pill has transformed female health more than any other drug in modern medicine. Although many of us practicing now do not know life without it, its history is not that long.
“The Pill” – as it is often referred to – was introduced in May of 1950.1 At that time, prevention of pregnancy was not listed as an indication, and promoting birth control was politically, socially, and legally unacceptable. In fact, the Comstock Law prohibited public discussion and research about contraception.1 Therefore, when the birth control pill was introduced, it was for cycle control and for married women only. It was not indicated for use as contraception in the United States until 1960.
Since that time, the birth control pill has evolved dramatically, not only in its formulation but in its indications as well. As pediatricians, we do not always find it easy to discuss with parents hormonal regulation and starting a patient on the birth control pill, particularly when it will not be used for contraception. There are many fears about using hormonal control, but there are many useful indications that improve the health and well-being of the pediatric patient.
Menorrhagia and dysmenorrhea are likely the most common reasons that hormonal therapy is started in adolescence. Beginning with the lowest estrogen dose to reduce side effects is prudent, adjusting accordingly if side effects should occur. Breakthrough bleeding is a common side effect that usually improves over time. Patients should continue treatment for at least 3 months before deciding if treatment is effective or not. If breakthrough bleeding continues, increasing the estrogen component or changing to a triphasic pill might reduce bleeding.
For a child with mental or significant physical disabilities, suppression of ovulation to prevent a menstrual cycle is very useful. Extended regimens can help to completely suppress ovulation, thereby avoiding withdrawal bleeding. There is anxiety about extended regimens, but there is no greater risk with using hormonal therapy continuously vs. intermittently.2 In fact, using it continuously reduces many of the unwanted side effects associated with the use of oral contraceptive pills (OCPs), for example, heavy bleeding, headaches, and nausea. Complete suppression is difficult, but the odds are better with continuous treatment. Using monophasic OCPs for 42-63 days on and 4-7 days off can be tried. The benefit of using monophasic pills is if a dose is missed, it is easy to make it up by just taking an extra pill. Companies have come out with extended-regimen packs, for example, Seasonale, Seasonique, Quartette, and Lybrel. There now is a chewable pill known as Femcon Fe, which would be useful in those patients who are not able to swallow pills.
Another indication for OCPs in the adolescent patient is acne. Although the exact mechanism is not completely understood, estrogen does decrease sebum by reducing the size of the gland4, and, therefore, all OCPs can reduce acne. Norgestimate combinations have the highest androgen to progesterone binding ratio, so they are more effective than OCPs that do not. A newer progestin, drospirenone, is a 17 alpha-spironolactone derivative that produces antiandrogenic activity.5 When used in a combination OCP, acne control appears to be even greater. Hormonal therapy should be considered whenever there has been limited improvement with topical treatment or if acne breakouts are associated with the onset of menses.
Another consideration is to add spironolactone 100 mg by mouth daily to the regimen. Studies have shown it can be safely used in women to reduce acne.6 Patients should be monitored frequently for hyperkalemia, and it should not be used in patients who are already pregnant.4 Lab work should be done to rule out other causes of hyperandrogenism; lab tests would include serum testosterone, androstenedione, dehydroepiandrosterone, sex hormone–binding globulin, and prolactin.4
Premenstrual syndrome (PMS) or premenstrual dysphoric disorder (PMDD) – which is the onset of depression, irritability, or anxiety in the second half of the menstrual cycle and remits with the onset of the menstrual cycle – also can be treated with hormonal therapy. This can be particularly helpful in teens with depression, as well as in those who are on treatment without significant resolution. PMS/PMDD appears to be best regulated with OCPs containing drospirenone,7 and using either a shortened course of the placebo phase or a continuous regimen appears to be the most beneficial.
Regardless of the indication for hormonal therapy, the initiation and management are essentially the same. Initiation can be on the first day of the menstrual cycle, on the Sunday after, or at the time of the visit. Initiation midcycle may result in breakthrough bleeding, but that will likely resolve over the next 3 months. No lab tests are required to start hormonal therapy, except for an HCG to rule out pregnancy. Weight and blood pressure should be documented so they can be monitored on follow-up visits. A detailed verbal explanation along with a handout should be provided on proper administration and side effects. Contraindications for the use of OCPs can be found on the Centers for Disease Control and Prevention’s website under medical criteria for the use of contraceptives.
Educating families and patients on their options for hormonal therapy can be life changing. Detailed questions about the menstrual cycle should be asked at every visit, and understanding the wide variety of indications for hormonal therapy can maximize treatment for a better outcome.
References
1. Can Fam Physician. 2012 Dec;58(12):e757–60.
2. J Midwifery Womens Health. 2012 Nov-Dec;57(6):585-92.
3. Obstet Gynecol. 2009;114:1428-31.
4. Semin Cutan Med Surg. 2008 Sep;27(3):188-96.
5. Pediatr Rev. 2008;29(11);386-97.
6. J Eur Acad Dermatol Venereol. 2005 Mar;19(2):163-6.
7. Obstet Gynecol. 2005 Sep;106(3):492-501.
Dr. Pearce is a pediatrician in Frankfort, Ill. She said she had no relevant financial disclosures.
What family physicians can do to combat bullying
CASE › Stacey, a 12-year-old girl with mild persistent asthma, presents to her family physician (FP) with her mother for her annual well visit. Stacey reports no complaints, but has visited twice recently for acute exacerbations of her asthma, which had previously been well-controlled. When reviewing her social history, Stacey reports that she started her second year of middle school 3 months ago. When asked if she enjoys school, Stacey looks down and says, “School is fine.” Her mother quickly adds that Stacey has quit the school cheerleading team—much to the coach’s dismay—and is having difficulty in her math class, a class in which she normally excels. Stacey appears embarrassed that her mother has brought these things up. Her mother says that at the beginning of the year, 2 girls began picking on Stacey, calling her names and making fun of her on social media and in front of other students.
For many years, bullying was trivialized. Some viewed it as a universal childhood experience; others considered it a rite of passage.1,2 It was not examined as a public health issue until the 1970s. In fact, no legislation addressing bullying or “peer abuse” existed in the United States until the mass shooting at Columbine High School in Littleton, Colo, in 1999. Within 3 years of the Columbine tragedy, the number of state laws that mentioned bullying went from zero to 15; within 10 years of Columbine, 41 states had laws addressing bullying,1 and by 2015, every state, the District of Columbia, and some territories had a bullying law in place.3
As research and advocacy regarding bullying has grown, its impact on the health of children, adolescents, and even adults has become more apparent. In a 2001 study of school-associated violent deaths in the United States between 1994 and 1999, the Centers for Disease Control and Prevention (CDC) found that among students, homicide perpetrators were more than twice as likely as homicide victims to have been bullied by peers.4 Given that homicide is the third leading cause of death in people ages 15 to 24,5 past exposure to bullying may be a significant contributing factor to mortality in this age group.4
In addition to a correlation with homicidal behavior, those involved in bullying—whether as the bully or victim—are at risk for a wide range of symptoms, conditions, and problems including poor psychosocial adjustment, depression, anxiety, suicide (the second leading cause of death in the 10-14 and 15-24 age groups5), academic decline, psychosomatic manifestations, fighting, alcohol use, smoking, and difficulty with the management of chronic diseases.6-10 Not only does being a victim of bullying have a direct impact on a child’s current mental and physical well-being, but it can have lasting psychological and behavioral effects that can follow children well into adulthood.7 The significant impact of bullying on individuals and society as a whole mandates a multifaceted approach that begins in your exam room. What follows is practical advice on screening, counseling, and working with schools and the community at large to curb the bullying epidemic.
Clarifying the problem: The CDC’s definition
Recognizing that varying definitions of bullying were being used in research studies that looked at violent or aggressive behaviors in youth, the CDC published a consensus statement in 2014 that proposed the following definition for bullying:11 any unwanted aggressive behavior by another youth or group of youths who are not siblings or current dating partners that involves an observed or perceived power imbalance and is repeated multiple times or is highly likely to be repeated. This expanded on an earlier definition by Olweus12,13 that also identified a longitudinal nature and power imbalance as key features.
Types of bullying. Direct bullying entails blatant attacks on a targeted young person, while indirect bullying involves communication with others about the targeted individual (eg, spreading harmful rumors). Bullying may be physical, verbal, or relational (eg, excluding someone from their usual social circle, denying friendship, the silent treatment, writing mean letters, eye rolling, etc.) and may involve damage to property. Boys tend toward more direct bullying behaviors, while girls more often engage in indirect bullying, which may be more challenging for both adults and other students to recognize.12,13 With increased use of technology and social media by adolescents, cyberbullying has become increasingly more prevalent, with its effects on adolescent health and academics being every bit as profound as those of traditional bullying.14
About 1 in 4/5 students suffer. The prevalence of bullying ranges by country and culture. The vast majority of early bullying research was conducted in Norway, which found that approximately 15% of students in elementary and secondary schools were involved in bullying in some capacity.12 In a study involving over 200,000 adolescents from 40 European countries, 26% of adolescents reported being involved in bullying, ranging from 8.6% to 45.2% for boys and 4.8% to 35.8% for girls.15 Variations in prevalence may be due to cultural differences in the acts of bullying or differences in interpretation of the term “bullying.”1,15
In the United States, a 2001 survey of more than 15,000 students in public and private schools (grades 6-10) asked the students about their involvement in bullying: 13% said they'd been a bully, 10.6% a victim, and 6.3% said they'd been both.6 There was no significant difference in the frequency of self-reported bullying among urban, suburban, or rural settings.
Despite efforts to educate the public about bullying and work with schools to intervene and prevent bullying, incidence remains largely unchanged. In 2013, the National Crime Victimization Survey reported that approximately 22% of adolescents ages 12 through 18 were victims of bullying.16 Similarly, the CDC's 2015 Youth Risk Behavior Surveillance System reported that 20.2% of high school students experienced bullying on school property.17
Screening: Best practices
The FP’s role begins with screening children at risk for bullying (TABLE 118-22) or those whose complaints suggest that they may be victims of bullying.
Start screening when children enter elementary school
Given that providers’ time is limited for every patient visit, it is important to address bullying at times that are most likely to yield impactful results. The American Academy of Pediatrics recommends that the topic of bullying be introduced at the 6-year-old well-child visit (a typical age for entry to elementary school).7 Views in the literature are inconsistent regarding when and how to address bullying at other time points. One approach is to pre-screen those with risk factors associated with bullying (TABLE 118-22), and to focus screening on those with warning signs of bullying, which include mood disorders, psychosomatic or behavioral symptoms, substance abuse, self-harm behaviors, suicidal ideation or a suicide attempt, a decline in academic performance, and reports of school truancy. Parental concerns, such as when a child suddenly needs more money for lunch, is having aggressive outbursts, or is exhibiting unexplained physical injuries, should also be regarded as cues to screen.9
Screen patients in high-risk groups
A number of groups of children are at high risk for bullying and warrant targeted screening efforts.
- Children with special health needs. Research has shown that children with special health needs are at increased risk for being bullied.18 In fact, the presence of a chronic disease may increase the risk for bullying, and bullying often negatively impacts chronic disease management. As a result, it’s important to have a high index of suspicion with patients who have a chronic disease and who are not responding as expected to medical management or who experience deterioration after being previously well-controlled.18
- Children who are under- or overweight. Similarly, bullying based on a child's weight is a phenomenon that has been recognized to have a significant impact on children’s emotional health.19
- Youth who identify as lesbian, gay, bisexual, transgender, or queer/questioning (LGBTQ+) are more likely than non-LGBTQ+ peers to attempt suicide when exposed to a hostile social environment, such as that created by bullying.20
Screening need not be complicated
One screening approach is simply to ask patients, “Are you being bullied?” followed by such questions as, “How often are you bullied?” or “How long have you been bullied?” Asking about the setting of the bullying (Does it happen at school? Traveling to/from school? Online?) and other details may help guide interventions and the provision of resources.9 Another approach is to provide patients with some type of written survey (see TABLE 223 for an example) to encourage responses that patients might be reluctant to disclose verbally.23,24 (See “Barriers to screening.")
SIDEBAR
Barriers to screeningScreening for any condition presupposes a response. Ideally, family physicians should be prepared to provide basic counseling, resources, and, if necessary, treatment, if a patient screens positive for bullying. But screening for violence or bullying can be difficult, and evidence-based guidelines for screening and intervention are lacking, leaving many primary care practitioners feeling ill-equipped to meaningfully respond.
One study of the use of a screening tool aimed at intimate partner violence (IPV) showed that even with the availability of a screening tool, health care providers’ use of the tool was inconsistent and referral practices were ineffective.1 Providers cited the following limiting factors in screening for IPV: 1) a lack of immediate referral availability, 2) a lack of time during the office visit, and 3) a lack of confidence in the ability to screen.1 These same issues may be barriers to screening for bullying.
1. Ramachandran DV, Covarrubias L, Watson C, et al. How you screen is as important as whether you screen: a qualitative analysis of violence screening practices in reproductive health clinics. J Community Health. 2013;38:856-863.
Provider and parental interventions
Interventions often entail counseling the patient and the family about bullying and its effects, empowering victims and their caregivers, and screening for bullying comorbidities and correlates.2 Refer patients to behavioral health specialists when there is evidence of pervasive effects on mood, behavior, or social development, but keep in mind that counseling can begin in your own exam room.
Effective discussion starters. Affirming the problem and its unacceptability, talking about the different types of bullying and where bullying may occur, and asking about patient perceptions of bullying can be effective discussion starters. FPs should help patients identify bullying, open lines of communication between children and their parents and between parents and other caregivers, and demonstrate respect and kindness in their approach to discussing the topic. Encourage children to speak with trusted adults when exposed to bullying. Talk to them about standing up to bullies (saying “stop” confidently or walking away from difficult situations) and staying safe by staying near adults or groups of peers when bullies are present (TABLE 325).
Empowering caregivers. Encourage parents to spend time each day talking with their child about the child’s time away from home (TABLE 325). Counsel parents/caregivers to expand their role. Knowing a child’s friends, encouraging the child academically, and increasing communication are all associated with lower risks of bullying.26 Similarly, parental oversight of Internet and social media use is associated with decreased participation in cyberbullying.27
In addition, the Positive Parenting telephone-based parenting education curriculum has been shown to decrease bullying, physical fighting, physical injuries, and victimization of children.28 The research-based, family strengthening program emphasizes 3 core elements of authoritative parenting: nurturance, discipline, and respect or granting of psychologic autonomy. The program entails 15- to 30-minute weekly phone conversations between parents and educators, as well as videos and a manual.
Are community programs in place—or are they needed?
Many schools have robust, state-mandated programs in place to identify bullying and provide support for students who are victims of bullying. (See “NJ’s harassment and bullying protocol: A case in point.”) Explaining this to victims and their families may help them come forward and seek assistance. FPs who want to advocate for their patients should start with local schools to support such programs and link students at risk with school counselors.
SIDEBAR
NJ's harassment and bullying protocol: A case in pointThere is no federal law that specifically applies to bullying, but all 50 states have some type of anti-bullying legislation on the books, and 40 of those states have additional detailed policies in place addressing the subject.1
New Jersey, for example, began enforcing one of the toughest harassment, intimidation, and bullying (HIB) protocols in the country back in September 20112 in the wake of the death of Rutgers University freshman Tyler Clementi, who committed suicide after his roommate allegedly shot a video of him with another man and posted it to the Internet.3 Among many other things, New Jersey’s legislation stipulates in its Anti-Bullying Bill of Rights4 that:
› Every school/district have plans in place that clearly define, prevent, prohibit, and promptly deal with acts of harassment, intimidation, or bullying, on school grounds, at school-sponsored functions, and on school buses.
› Plans must include a description of the type of behavior expected from each student and the consequences and remedial action for a person who commits an act of harassment, intimidation, or bullying. Student perpetrators may be suspended or expelled if convicted of any type of bullying, whether it be for teasing or something more severe.
› All school employees must act on any incidents of bullying reported to, or witnessed by, them and report such incidents on the same day to the school principal.
› Plans must include provisions and deadlines for investigating and resolving all matters in a timely fashion; investigations into allegations of bullying must be launched within one day.
› Every case of bullying must be reported to the state. Schools are graded by the state on their compliance with anti-bullying standards and policies and their handling of incidents.
› Schools must appoint safety teams made up of parents, teachers, and staff, and school personnel and students must receive extensive anti-bullying training.
1. US Department of Health and Human Services. Stopbullying.gov. Policies and laws. Available at: https://www.stopbullying.gov/laws/index.html.
Accessed January 5, 2017.
2. State of New Jersey Department of Education. An overview of amendments to laws on harassment, intimidation, and bullying. Available at: http://www.state.nj.us/education/students/safety/behavior/hib/overview.pdf. Accessed January 5, 2017.
3. Cohen A. Case study: Why New Jersey’s antibullying law should be a model for other states. Time. September 6, 2011. Available at: http://ideas.time.com/2011/09/06/why-new-jerseys-antibullying-law-should-be-a-model-for-other-states/. Accessed January 5, 2017.
4. New Jersey Legislature. Anti-bullying Bill of Rights Act. Available at: http://www.njleg.state.nj.us/2010/Bills/PL10/122.PDF. Accessed January 5, 2017.
If programs are lacking in your community, there is much you can do to educate yourself about successful programs and advise local community organizations and schools about them. Among the most successful and well-studied interventions for thwarting the bullying epidemic have been school-based community ones. The most studied of these is the Olweus Bullying Prevention Program (OBPP), which is based on 4 principles:1,29
- Adults both at home and at school should take a positive and encouraging interest in students.
- Unacceptable behavior should have strict and well-known limits.
- Sanctions should be applied consistently and should be non-hostile in nature.
- Adults both at home and in the educational environment should act as authorities.
In short, the program focuses on greater awareness and involvement on the part of adults, and employing measures at the school level (eg, surveys, better supervision during break and lunch times), the class level (eg, rules against bullying, regular class meetings with students), and the individual level (eg, serious talks with bullies, victims, parents of involved students).
Research has shown that the OBPP reduces bullying behaviors by as much as 50%, reduces vandalism and truancy, and reduces the number of new victims.12 Limits to the more widespread implementation of the OBPP have consisted mainly of the inability to appropriately train adults, including teachers and other school personnel in educational settings. Despite these limitations, the OBPP has been praised and endorsed by numerous groups, including the US Department of Justice.30
Other non-curricular, school-based programs exist, such as the School-Wide Positive Behavioral Interventions and Supports (SWPBIS). This program is a school-wide prevention strategy aimed at: 1) reducing behavior problems that lead to office discipline referrals and suspensions, and 2) changing perceptions of school safety. (For more information, see https://www.crimesolutions.gov/ProgramDetails.aspx?ID=385 and https://www.pbis.org/school/swpbis-for-beginners.)31
The research-based Second Step: Student Success Through Prevention (SS-SSTP) Middle School Program (http://www.cfchildren.org/second-step/middle-school)32 focuses on the often difficult middle school years. The program helps schools teach and model essential communication, coping, and decision-making skills to help adolescents navigate around common pitfalls such as peer pressure, substance abuse, and bullying (both in-person and online). The program aims to reduce aggression and provide support for a more inclusive environment that helps students stay in school, make good choices, and experience social and academic success.
The Positive Action Program (https://www.positiveaction.net/research/primer),33 which is predicated on the notion that we feel good about ourselves when we do positive things, features scripted lessons and kits of materials (eg, posters, games, worksheets, puzzles) appropriate for each grade level.
CASE › Stacey’s visit to her FP’s office has presented several clues that she may be a victim of bullying. Her mild persistent asthma appears to no longer be as well controlled as it was in the past. Direct questioning has revealed that 2 girls at school have been making fun of Stacey when she uses her inhaled corticosteroid in the morning before class, so she has stopped using it. These same students are on her cheerleading team, so she quit the team to avoid them. Her school-related anxiety is so great that she no longer pays attention in math class and is constantly worried that something is being posted about her online.
Stacy’s FP responds to this information with a multifaceted approach. In the exam room, he screens Stacy for depression. While she is negative and denies any suicidal ideation, Stacy is clearly having anxiety, so the FP refers Stacey to a counselor at a local mental health clinic. With Stacy’s permission, the FP discusses the issue with her mother and they decide together with Stacy that she should talk to a teacher at school about the ongoing bullying. Because this was not the first time that the FP has heard this from a child in the community, the FP plans to attend an upcoming school board meeting to advocate for an evidence-based bullying prevention program to help curb the ongoing problem facing his patients.
CORRESPONDENCE
Robert McClowry, MD, Department of Family and Community Medicine, Jefferson Family Medicine Associates, 833 Chestnut East, 3rd Floor, Suite 301, Philadelphia, PA, 19107-4414; Robert.McClowry@Jefferson.edu.
1. Olweus D, Limber SP. Bullying in school: evaluation and dissemination of the Olweus Bullying Prevention Program. Am J Orthopsychiatry. 2010;80:124-134.
2. Lyznicki JM, McCaffree MA, Robinowitz CB, et al. Childhood bullying: implications for physicians. Am Fam Physician. 2004;70:1723-1730.
3. Temkin D. All 50 states now have a bullying law. Now what? The Huffington Post. April 27, 2015. Available at: http://www.huffingtonpost.com/deborah-temkin/all-50-states-now-have-a_b_7153114.html. Accessed January 5, 2017.
4. Anderson M, Kaufman J, Simon TR, et al. School-associated violent deaths in the United States, 1994-1999. JAMA. 2001;286:2695-2702.
5. Centers for Disease Control and Prevention. Injury prevention and control: Data and statistics (WISQARS). Ten leading causes of death and injury. Available at: https://www.cdc.gov/injury/wisqars/leadingcauses.html. Accessed January 5, 2017.
6. Nansel TR, Overpeck M, Pilla RS, et al. Bullying behaviors among US youth: prevalence and association with psychosocial adjustment. JAMA. 2001;285:2094-2100.
7. Committee on Injury, Violence, and Poison Prevention. Policy statement—Role of the pediatrician in youth violence prevention. Pediatrics. 2009;124:393-402.
8. Klein DA, Myhre KK, Ahrendt DM. Bullying among adolescents: a challenge in primary care. Am Fam Physician. 2013;88:87-92.
9. Lamb J, Pepler DJ, Craig W. Approach to bullying and victimization. Can Fam Physician. 2009;55:356-360.
10. Spector ND, Kelly SF. Pediatrician’s role in screening and treatment: bullying, prediabetes, oral health. Curr Opin Pediatr. 2006;18:661-670.
11. Gladden RM, Vivolo-Kantor AM, Hamburger ME, et al. Bullying surveillance among youths: uniform definitions for public health and recommended data elements. National Center for Injury Prevention and Control, Centers for Disease Control and Prevention and US Department of Education; 2014. Available at: https://www.cdc.gov/violenceprevention/pdf/bullying-definitions-final-a.pdf. Accessed June 8, 2016.
12. Olweus D. Bullying at school: basic facts and effects of a school based intervention program. J Child Psychol Psychiatry. 1994;35:1171-1190.
13. Olweus D. Bully/victim problems in school: Facts and intervention. Eur J Psychol Educ. 1997;12:495-510.
14. Kowalski RM, Limber SP. Psychological, physical, and academic correlates of cyberbullying and traditional bullying. J Adolesc Health. 2013;53:S13-S20.
15. Craig W, Harel-Fisch Y, Fogel-Grinvald H, et al. A cross-national profile of bullying and victimization among adolescents in 40 countries. Int J Public Health. 2009;54(Suppl 2):216-224.
16. US Department of Education, National Center for Educational Statistics (2015). Student reports of bullying and cyberbullying: results from the 2013 School Crime Supplement to the National Victimization Survey. Available at: http://nces.ed.gov/pubsearch/pubsinfo.asp?pubid=2015056. Accessed November 9, 2016.
17. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance - United States, 2015. MMWR Morb Mortal Wkly Rep. 2016;65:1-174.
18. Van Cleave J, Davis MM. Bullying and peer victimization among children with special health care needs. Pediatrics. 2006;118:e1212-e1219.
19. Eisenberg ME, Neumark-Sztainer D, Story M. Associations of weight-based teasing and emotional well-being among adolescents. Arch Pediatr Adolesc Med. 2003;157:733-738.
20. Hatzenbuehler ML. The social environment and suicide attempts in lesbian, gay, and bisexual youth. Pediatrics. 2011;127:896-903.
21. Song LY, Singer MI, Anglin TM. Violence exposure and emotional trauma as contributors to adolescents’ violent behaviors. Arch Pediatr Adolesc Med. 1998;152:531-536.
22. Singer MI, Anglin TM, Song LY, et al. Adolescents’ exposure to violence and associated symptoms of psychological trauma. JAMA. 1995;273:477-482.
23. Glew GM, Fan MY, Katon W, et al. Bullying, psychosocial adjustment, and academic performance in elementary school. Arch Pediatr Adolesc Med. 2005;159:1026-1031.
24. Waseem M, Ryan M, Foster CB, et al. Assessment and management of bullied children in the emergency department. Pediatr Emerg Care. 2013;29:389-398.
25. US Department of Health and Human Services. stopbullying.gov. Available at: https//www.stopbullying.gov. Accessed January 5, 2017.
26. Shetgiri R, Lin H, Avila RM, et al. Parental characteristics associated with bullying perpetration in US children aged 10 to 17 years. Am J Public Health. 2012;102:2280-2286.
27. Hinduja S, Patchin JW. Social influences on cyberbullying behaviors among middle and high school students. J Youth Adolesc. 2013;42:711-722.
28. Borowsky IW, Mozayeny S, Stuenkel K, et al. Effects of a primary care-based intervention on violent behavior and injury in children. Pediatrics. 2004;114:e392-e399.
29. Olweus D. Bully/victim problems in school: Facts and intervention. Eur J Psychol Educ. 1997;12:495-510.
30. Mihalic SF. Blueprints for Violence Prevention: Report. US Department of Justice, Office of Justice Programs, Office of Juvenile Justice and Delinquency Prevention; 2004.
31. Waasdorp TE, Bradshaw CP, Leaf PJ. The impact of schoolwide positive behavioral interventions and supports on bullying and peer rejection: a randomized controlled effectiveness trial. Arch Pediatr Adolesc Med. 2012;166:149-156.
32. Espelage DL, Low S, Polanin JR, et al. The impact of a middle school program to reduce aggression, victimization, and sexual violence. J Adolesc Health. 2013;53:180-186.
33. Lewis KM, Schure MB, Bavarian N, et al. Problem behavior and urban, low-income youth: a randomized controlled trial of positive action in Chicago. Am J Prev Med. 2013;44:622-630.
CASE › Stacey, a 12-year-old girl with mild persistent asthma, presents to her family physician (FP) with her mother for her annual well visit. Stacey reports no complaints, but has visited twice recently for acute exacerbations of her asthma, which had previously been well-controlled. When reviewing her social history, Stacey reports that she started her second year of middle school 3 months ago. When asked if she enjoys school, Stacey looks down and says, “School is fine.” Her mother quickly adds that Stacey has quit the school cheerleading team—much to the coach’s dismay—and is having difficulty in her math class, a class in which she normally excels. Stacey appears embarrassed that her mother has brought these things up. Her mother says that at the beginning of the year, 2 girls began picking on Stacey, calling her names and making fun of her on social media and in front of other students.
For many years, bullying was trivialized. Some viewed it as a universal childhood experience; others considered it a rite of passage.1,2 It was not examined as a public health issue until the 1970s. In fact, no legislation addressing bullying or “peer abuse” existed in the United States until the mass shooting at Columbine High School in Littleton, Colo, in 1999. Within 3 years of the Columbine tragedy, the number of state laws that mentioned bullying went from zero to 15; within 10 years of Columbine, 41 states had laws addressing bullying,1 and by 2015, every state, the District of Columbia, and some territories had a bullying law in place.3
As research and advocacy regarding bullying has grown, its impact on the health of children, adolescents, and even adults has become more apparent. In a 2001 study of school-associated violent deaths in the United States between 1994 and 1999, the Centers for Disease Control and Prevention (CDC) found that among students, homicide perpetrators were more than twice as likely as homicide victims to have been bullied by peers.4 Given that homicide is the third leading cause of death in people ages 15 to 24,5 past exposure to bullying may be a significant contributing factor to mortality in this age group.4
In addition to a correlation with homicidal behavior, those involved in bullying—whether as the bully or victim—are at risk for a wide range of symptoms, conditions, and problems including poor psychosocial adjustment, depression, anxiety, suicide (the second leading cause of death in the 10-14 and 15-24 age groups5), academic decline, psychosomatic manifestations, fighting, alcohol use, smoking, and difficulty with the management of chronic diseases.6-10 Not only does being a victim of bullying have a direct impact on a child’s current mental and physical well-being, but it can have lasting psychological and behavioral effects that can follow children well into adulthood.7 The significant impact of bullying on individuals and society as a whole mandates a multifaceted approach that begins in your exam room. What follows is practical advice on screening, counseling, and working with schools and the community at large to curb the bullying epidemic.
Clarifying the problem: The CDC’s definition
Recognizing that varying definitions of bullying were being used in research studies that looked at violent or aggressive behaviors in youth, the CDC published a consensus statement in 2014 that proposed the following definition for bullying:11 any unwanted aggressive behavior by another youth or group of youths who are not siblings or current dating partners that involves an observed or perceived power imbalance and is repeated multiple times or is highly likely to be repeated. This expanded on an earlier definition by Olweus12,13 that also identified a longitudinal nature and power imbalance as key features.
Types of bullying. Direct bullying entails blatant attacks on a targeted young person, while indirect bullying involves communication with others about the targeted individual (eg, spreading harmful rumors). Bullying may be physical, verbal, or relational (eg, excluding someone from their usual social circle, denying friendship, the silent treatment, writing mean letters, eye rolling, etc.) and may involve damage to property. Boys tend toward more direct bullying behaviors, while girls more often engage in indirect bullying, which may be more challenging for both adults and other students to recognize.12,13 With increased use of technology and social media by adolescents, cyberbullying has become increasingly more prevalent, with its effects on adolescent health and academics being every bit as profound as those of traditional bullying.14
About 1 in 4/5 students suffer. The prevalence of bullying ranges by country and culture. The vast majority of early bullying research was conducted in Norway, which found that approximately 15% of students in elementary and secondary schools were involved in bullying in some capacity.12 In a study involving over 200,000 adolescents from 40 European countries, 26% of adolescents reported being involved in bullying, ranging from 8.6% to 45.2% for boys and 4.8% to 35.8% for girls.15 Variations in prevalence may be due to cultural differences in the acts of bullying or differences in interpretation of the term “bullying.”1,15
In the United States, a 2001 survey of more than 15,000 students in public and private schools (grades 6-10) asked the students about their involvement in bullying: 13% said they'd been a bully, 10.6% a victim, and 6.3% said they'd been both.6 There was no significant difference in the frequency of self-reported bullying among urban, suburban, or rural settings.
Despite efforts to educate the public about bullying and work with schools to intervene and prevent bullying, incidence remains largely unchanged. In 2013, the National Crime Victimization Survey reported that approximately 22% of adolescents ages 12 through 18 were victims of bullying.16 Similarly, the CDC's 2015 Youth Risk Behavior Surveillance System reported that 20.2% of high school students experienced bullying on school property.17
Screening: Best practices
The FP’s role begins with screening children at risk for bullying (TABLE 118-22) or those whose complaints suggest that they may be victims of bullying.
Start screening when children enter elementary school
Given that providers’ time is limited for every patient visit, it is important to address bullying at times that are most likely to yield impactful results. The American Academy of Pediatrics recommends that the topic of bullying be introduced at the 6-year-old well-child visit (a typical age for entry to elementary school).7 Views in the literature are inconsistent regarding when and how to address bullying at other time points. One approach is to pre-screen those with risk factors associated with bullying (TABLE 118-22), and to focus screening on those with warning signs of bullying, which include mood disorders, psychosomatic or behavioral symptoms, substance abuse, self-harm behaviors, suicidal ideation or a suicide attempt, a decline in academic performance, and reports of school truancy. Parental concerns, such as when a child suddenly needs more money for lunch, is having aggressive outbursts, or is exhibiting unexplained physical injuries, should also be regarded as cues to screen.9
Screen patients in high-risk groups
A number of groups of children are at high risk for bullying and warrant targeted screening efforts.
- Children with special health needs. Research has shown that children with special health needs are at increased risk for being bullied.18 In fact, the presence of a chronic disease may increase the risk for bullying, and bullying often negatively impacts chronic disease management. As a result, it’s important to have a high index of suspicion with patients who have a chronic disease and who are not responding as expected to medical management or who experience deterioration after being previously well-controlled.18
- Children who are under- or overweight. Similarly, bullying based on a child's weight is a phenomenon that has been recognized to have a significant impact on children’s emotional health.19
- Youth who identify as lesbian, gay, bisexual, transgender, or queer/questioning (LGBTQ+) are more likely than non-LGBTQ+ peers to attempt suicide when exposed to a hostile social environment, such as that created by bullying.20
Screening need not be complicated
One screening approach is simply to ask patients, “Are you being bullied?” followed by such questions as, “How often are you bullied?” or “How long have you been bullied?” Asking about the setting of the bullying (Does it happen at school? Traveling to/from school? Online?) and other details may help guide interventions and the provision of resources.9 Another approach is to provide patients with some type of written survey (see TABLE 223 for an example) to encourage responses that patients might be reluctant to disclose verbally.23,24 (See “Barriers to screening.")
SIDEBAR
Barriers to screeningScreening for any condition presupposes a response. Ideally, family physicians should be prepared to provide basic counseling, resources, and, if necessary, treatment, if a patient screens positive for bullying. But screening for violence or bullying can be difficult, and evidence-based guidelines for screening and intervention are lacking, leaving many primary care practitioners feeling ill-equipped to meaningfully respond.
One study of the use of a screening tool aimed at intimate partner violence (IPV) showed that even with the availability of a screening tool, health care providers’ use of the tool was inconsistent and referral practices were ineffective.1 Providers cited the following limiting factors in screening for IPV: 1) a lack of immediate referral availability, 2) a lack of time during the office visit, and 3) a lack of confidence in the ability to screen.1 These same issues may be barriers to screening for bullying.
1. Ramachandran DV, Covarrubias L, Watson C, et al. How you screen is as important as whether you screen: a qualitative analysis of violence screening practices in reproductive health clinics. J Community Health. 2013;38:856-863.
Provider and parental interventions
Interventions often entail counseling the patient and the family about bullying and its effects, empowering victims and their caregivers, and screening for bullying comorbidities and correlates.2 Refer patients to behavioral health specialists when there is evidence of pervasive effects on mood, behavior, or social development, but keep in mind that counseling can begin in your own exam room.
Effective discussion starters. Affirming the problem and its unacceptability, talking about the different types of bullying and where bullying may occur, and asking about patient perceptions of bullying can be effective discussion starters. FPs should help patients identify bullying, open lines of communication between children and their parents and between parents and other caregivers, and demonstrate respect and kindness in their approach to discussing the topic. Encourage children to speak with trusted adults when exposed to bullying. Talk to them about standing up to bullies (saying “stop” confidently or walking away from difficult situations) and staying safe by staying near adults or groups of peers when bullies are present (TABLE 325).
Empowering caregivers. Encourage parents to spend time each day talking with their child about the child’s time away from home (TABLE 325). Counsel parents/caregivers to expand their role. Knowing a child’s friends, encouraging the child academically, and increasing communication are all associated with lower risks of bullying.26 Similarly, parental oversight of Internet and social media use is associated with decreased participation in cyberbullying.27
In addition, the Positive Parenting telephone-based parenting education curriculum has been shown to decrease bullying, physical fighting, physical injuries, and victimization of children.28 The research-based, family strengthening program emphasizes 3 core elements of authoritative parenting: nurturance, discipline, and respect or granting of psychologic autonomy. The program entails 15- to 30-minute weekly phone conversations between parents and educators, as well as videos and a manual.
Are community programs in place—or are they needed?
Many schools have robust, state-mandated programs in place to identify bullying and provide support for students who are victims of bullying. (See “NJ’s harassment and bullying protocol: A case in point.”) Explaining this to victims and their families may help them come forward and seek assistance. FPs who want to advocate for their patients should start with local schools to support such programs and link students at risk with school counselors.
SIDEBAR
NJ's harassment and bullying protocol: A case in pointThere is no federal law that specifically applies to bullying, but all 50 states have some type of anti-bullying legislation on the books, and 40 of those states have additional detailed policies in place addressing the subject.1
New Jersey, for example, began enforcing one of the toughest harassment, intimidation, and bullying (HIB) protocols in the country back in September 20112 in the wake of the death of Rutgers University freshman Tyler Clementi, who committed suicide after his roommate allegedly shot a video of him with another man and posted it to the Internet.3 Among many other things, New Jersey’s legislation stipulates in its Anti-Bullying Bill of Rights4 that:
› Every school/district have plans in place that clearly define, prevent, prohibit, and promptly deal with acts of harassment, intimidation, or bullying, on school grounds, at school-sponsored functions, and on school buses.
› Plans must include a description of the type of behavior expected from each student and the consequences and remedial action for a person who commits an act of harassment, intimidation, or bullying. Student perpetrators may be suspended or expelled if convicted of any type of bullying, whether it be for teasing or something more severe.
› All school employees must act on any incidents of bullying reported to, or witnessed by, them and report such incidents on the same day to the school principal.
› Plans must include provisions and deadlines for investigating and resolving all matters in a timely fashion; investigations into allegations of bullying must be launched within one day.
› Every case of bullying must be reported to the state. Schools are graded by the state on their compliance with anti-bullying standards and policies and their handling of incidents.
› Schools must appoint safety teams made up of parents, teachers, and staff, and school personnel and students must receive extensive anti-bullying training.
1. US Department of Health and Human Services. Stopbullying.gov. Policies and laws. Available at: https://www.stopbullying.gov/laws/index.html.
Accessed January 5, 2017.
2. State of New Jersey Department of Education. An overview of amendments to laws on harassment, intimidation, and bullying. Available at: http://www.state.nj.us/education/students/safety/behavior/hib/overview.pdf. Accessed January 5, 2017.
3. Cohen A. Case study: Why New Jersey’s antibullying law should be a model for other states. Time. September 6, 2011. Available at: http://ideas.time.com/2011/09/06/why-new-jerseys-antibullying-law-should-be-a-model-for-other-states/. Accessed January 5, 2017.
4. New Jersey Legislature. Anti-bullying Bill of Rights Act. Available at: http://www.njleg.state.nj.us/2010/Bills/PL10/122.PDF. Accessed January 5, 2017.
If programs are lacking in your community, there is much you can do to educate yourself about successful programs and advise local community organizations and schools about them. Among the most successful and well-studied interventions for thwarting the bullying epidemic have been school-based community ones. The most studied of these is the Olweus Bullying Prevention Program (OBPP), which is based on 4 principles:1,29
- Adults both at home and at school should take a positive and encouraging interest in students.
- Unacceptable behavior should have strict and well-known limits.
- Sanctions should be applied consistently and should be non-hostile in nature.
- Adults both at home and in the educational environment should act as authorities.
In short, the program focuses on greater awareness and involvement on the part of adults, and employing measures at the school level (eg, surveys, better supervision during break and lunch times), the class level (eg, rules against bullying, regular class meetings with students), and the individual level (eg, serious talks with bullies, victims, parents of involved students).
Research has shown that the OBPP reduces bullying behaviors by as much as 50%, reduces vandalism and truancy, and reduces the number of new victims.12 Limits to the more widespread implementation of the OBPP have consisted mainly of the inability to appropriately train adults, including teachers and other school personnel in educational settings. Despite these limitations, the OBPP has been praised and endorsed by numerous groups, including the US Department of Justice.30
Other non-curricular, school-based programs exist, such as the School-Wide Positive Behavioral Interventions and Supports (SWPBIS). This program is a school-wide prevention strategy aimed at: 1) reducing behavior problems that lead to office discipline referrals and suspensions, and 2) changing perceptions of school safety. (For more information, see https://www.crimesolutions.gov/ProgramDetails.aspx?ID=385 and https://www.pbis.org/school/swpbis-for-beginners.)31
The research-based Second Step: Student Success Through Prevention (SS-SSTP) Middle School Program (http://www.cfchildren.org/second-step/middle-school)32 focuses on the often difficult middle school years. The program helps schools teach and model essential communication, coping, and decision-making skills to help adolescents navigate around common pitfalls such as peer pressure, substance abuse, and bullying (both in-person and online). The program aims to reduce aggression and provide support for a more inclusive environment that helps students stay in school, make good choices, and experience social and academic success.
The Positive Action Program (https://www.positiveaction.net/research/primer),33 which is predicated on the notion that we feel good about ourselves when we do positive things, features scripted lessons and kits of materials (eg, posters, games, worksheets, puzzles) appropriate for each grade level.
CASE › Stacey’s visit to her FP’s office has presented several clues that she may be a victim of bullying. Her mild persistent asthma appears to no longer be as well controlled as it was in the past. Direct questioning has revealed that 2 girls at school have been making fun of Stacey when she uses her inhaled corticosteroid in the morning before class, so she has stopped using it. These same students are on her cheerleading team, so she quit the team to avoid them. Her school-related anxiety is so great that she no longer pays attention in math class and is constantly worried that something is being posted about her online.
Stacy’s FP responds to this information with a multifaceted approach. In the exam room, he screens Stacy for depression. While she is negative and denies any suicidal ideation, Stacy is clearly having anxiety, so the FP refers Stacey to a counselor at a local mental health clinic. With Stacy’s permission, the FP discusses the issue with her mother and they decide together with Stacy that she should talk to a teacher at school about the ongoing bullying. Because this was not the first time that the FP has heard this from a child in the community, the FP plans to attend an upcoming school board meeting to advocate for an evidence-based bullying prevention program to help curb the ongoing problem facing his patients.
CORRESPONDENCE
Robert McClowry, MD, Department of Family and Community Medicine, Jefferson Family Medicine Associates, 833 Chestnut East, 3rd Floor, Suite 301, Philadelphia, PA, 19107-4414; Robert.McClowry@Jefferson.edu.
CASE › Stacey, a 12-year-old girl with mild persistent asthma, presents to her family physician (FP) with her mother for her annual well visit. Stacey reports no complaints, but has visited twice recently for acute exacerbations of her asthma, which had previously been well-controlled. When reviewing her social history, Stacey reports that she started her second year of middle school 3 months ago. When asked if she enjoys school, Stacey looks down and says, “School is fine.” Her mother quickly adds that Stacey has quit the school cheerleading team—much to the coach’s dismay—and is having difficulty in her math class, a class in which she normally excels. Stacey appears embarrassed that her mother has brought these things up. Her mother says that at the beginning of the year, 2 girls began picking on Stacey, calling her names and making fun of her on social media and in front of other students.
For many years, bullying was trivialized. Some viewed it as a universal childhood experience; others considered it a rite of passage.1,2 It was not examined as a public health issue until the 1970s. In fact, no legislation addressing bullying or “peer abuse” existed in the United States until the mass shooting at Columbine High School in Littleton, Colo, in 1999. Within 3 years of the Columbine tragedy, the number of state laws that mentioned bullying went from zero to 15; within 10 years of Columbine, 41 states had laws addressing bullying,1 and by 2015, every state, the District of Columbia, and some territories had a bullying law in place.3
As research and advocacy regarding bullying has grown, its impact on the health of children, adolescents, and even adults has become more apparent. In a 2001 study of school-associated violent deaths in the United States between 1994 and 1999, the Centers for Disease Control and Prevention (CDC) found that among students, homicide perpetrators were more than twice as likely as homicide victims to have been bullied by peers.4 Given that homicide is the third leading cause of death in people ages 15 to 24,5 past exposure to bullying may be a significant contributing factor to mortality in this age group.4
In addition to a correlation with homicidal behavior, those involved in bullying—whether as the bully or victim—are at risk for a wide range of symptoms, conditions, and problems including poor psychosocial adjustment, depression, anxiety, suicide (the second leading cause of death in the 10-14 and 15-24 age groups5), academic decline, psychosomatic manifestations, fighting, alcohol use, smoking, and difficulty with the management of chronic diseases.6-10 Not only does being a victim of bullying have a direct impact on a child’s current mental and physical well-being, but it can have lasting psychological and behavioral effects that can follow children well into adulthood.7 The significant impact of bullying on individuals and society as a whole mandates a multifaceted approach that begins in your exam room. What follows is practical advice on screening, counseling, and working with schools and the community at large to curb the bullying epidemic.
Clarifying the problem: The CDC’s definition
Recognizing that varying definitions of bullying were being used in research studies that looked at violent or aggressive behaviors in youth, the CDC published a consensus statement in 2014 that proposed the following definition for bullying:11 any unwanted aggressive behavior by another youth or group of youths who are not siblings or current dating partners that involves an observed or perceived power imbalance and is repeated multiple times or is highly likely to be repeated. This expanded on an earlier definition by Olweus12,13 that also identified a longitudinal nature and power imbalance as key features.
Types of bullying. Direct bullying entails blatant attacks on a targeted young person, while indirect bullying involves communication with others about the targeted individual (eg, spreading harmful rumors). Bullying may be physical, verbal, or relational (eg, excluding someone from their usual social circle, denying friendship, the silent treatment, writing mean letters, eye rolling, etc.) and may involve damage to property. Boys tend toward more direct bullying behaviors, while girls more often engage in indirect bullying, which may be more challenging for both adults and other students to recognize.12,13 With increased use of technology and social media by adolescents, cyberbullying has become increasingly more prevalent, with its effects on adolescent health and academics being every bit as profound as those of traditional bullying.14
About 1 in 4/5 students suffer. The prevalence of bullying ranges by country and culture. The vast majority of early bullying research was conducted in Norway, which found that approximately 15% of students in elementary and secondary schools were involved in bullying in some capacity.12 In a study involving over 200,000 adolescents from 40 European countries, 26% of adolescents reported being involved in bullying, ranging from 8.6% to 45.2% for boys and 4.8% to 35.8% for girls.15 Variations in prevalence may be due to cultural differences in the acts of bullying or differences in interpretation of the term “bullying.”1,15
In the United States, a 2001 survey of more than 15,000 students in public and private schools (grades 6-10) asked the students about their involvement in bullying: 13% said they'd been a bully, 10.6% a victim, and 6.3% said they'd been both.6 There was no significant difference in the frequency of self-reported bullying among urban, suburban, or rural settings.
Despite efforts to educate the public about bullying and work with schools to intervene and prevent bullying, incidence remains largely unchanged. In 2013, the National Crime Victimization Survey reported that approximately 22% of adolescents ages 12 through 18 were victims of bullying.16 Similarly, the CDC's 2015 Youth Risk Behavior Surveillance System reported that 20.2% of high school students experienced bullying on school property.17
Screening: Best practices
The FP’s role begins with screening children at risk for bullying (TABLE 118-22) or those whose complaints suggest that they may be victims of bullying.
Start screening when children enter elementary school
Given that providers’ time is limited for every patient visit, it is important to address bullying at times that are most likely to yield impactful results. The American Academy of Pediatrics recommends that the topic of bullying be introduced at the 6-year-old well-child visit (a typical age for entry to elementary school).7 Views in the literature are inconsistent regarding when and how to address bullying at other time points. One approach is to pre-screen those with risk factors associated with bullying (TABLE 118-22), and to focus screening on those with warning signs of bullying, which include mood disorders, psychosomatic or behavioral symptoms, substance abuse, self-harm behaviors, suicidal ideation or a suicide attempt, a decline in academic performance, and reports of school truancy. Parental concerns, such as when a child suddenly needs more money for lunch, is having aggressive outbursts, or is exhibiting unexplained physical injuries, should also be regarded as cues to screen.9
Screen patients in high-risk groups
A number of groups of children are at high risk for bullying and warrant targeted screening efforts.
- Children with special health needs. Research has shown that children with special health needs are at increased risk for being bullied.18 In fact, the presence of a chronic disease may increase the risk for bullying, and bullying often negatively impacts chronic disease management. As a result, it’s important to have a high index of suspicion with patients who have a chronic disease and who are not responding as expected to medical management or who experience deterioration after being previously well-controlled.18
- Children who are under- or overweight. Similarly, bullying based on a child's weight is a phenomenon that has been recognized to have a significant impact on children’s emotional health.19
- Youth who identify as lesbian, gay, bisexual, transgender, or queer/questioning (LGBTQ+) are more likely than non-LGBTQ+ peers to attempt suicide when exposed to a hostile social environment, such as that created by bullying.20
Screening need not be complicated
One screening approach is simply to ask patients, “Are you being bullied?” followed by such questions as, “How often are you bullied?” or “How long have you been bullied?” Asking about the setting of the bullying (Does it happen at school? Traveling to/from school? Online?) and other details may help guide interventions and the provision of resources.9 Another approach is to provide patients with some type of written survey (see TABLE 223 for an example) to encourage responses that patients might be reluctant to disclose verbally.23,24 (See “Barriers to screening.")
SIDEBAR
Barriers to screeningScreening for any condition presupposes a response. Ideally, family physicians should be prepared to provide basic counseling, resources, and, if necessary, treatment, if a patient screens positive for bullying. But screening for violence or bullying can be difficult, and evidence-based guidelines for screening and intervention are lacking, leaving many primary care practitioners feeling ill-equipped to meaningfully respond.
One study of the use of a screening tool aimed at intimate partner violence (IPV) showed that even with the availability of a screening tool, health care providers’ use of the tool was inconsistent and referral practices were ineffective.1 Providers cited the following limiting factors in screening for IPV: 1) a lack of immediate referral availability, 2) a lack of time during the office visit, and 3) a lack of confidence in the ability to screen.1 These same issues may be barriers to screening for bullying.
1. Ramachandran DV, Covarrubias L, Watson C, et al. How you screen is as important as whether you screen: a qualitative analysis of violence screening practices in reproductive health clinics. J Community Health. 2013;38:856-863.
Provider and parental interventions
Interventions often entail counseling the patient and the family about bullying and its effects, empowering victims and their caregivers, and screening for bullying comorbidities and correlates.2 Refer patients to behavioral health specialists when there is evidence of pervasive effects on mood, behavior, or social development, but keep in mind that counseling can begin in your own exam room.
Effective discussion starters. Affirming the problem and its unacceptability, talking about the different types of bullying and where bullying may occur, and asking about patient perceptions of bullying can be effective discussion starters. FPs should help patients identify bullying, open lines of communication between children and their parents and between parents and other caregivers, and demonstrate respect and kindness in their approach to discussing the topic. Encourage children to speak with trusted adults when exposed to bullying. Talk to them about standing up to bullies (saying “stop” confidently or walking away from difficult situations) and staying safe by staying near adults or groups of peers when bullies are present (TABLE 325).
Empowering caregivers. Encourage parents to spend time each day talking with their child about the child’s time away from home (TABLE 325). Counsel parents/caregivers to expand their role. Knowing a child’s friends, encouraging the child academically, and increasing communication are all associated with lower risks of bullying.26 Similarly, parental oversight of Internet and social media use is associated with decreased participation in cyberbullying.27
In addition, the Positive Parenting telephone-based parenting education curriculum has been shown to decrease bullying, physical fighting, physical injuries, and victimization of children.28 The research-based, family strengthening program emphasizes 3 core elements of authoritative parenting: nurturance, discipline, and respect or granting of psychologic autonomy. The program entails 15- to 30-minute weekly phone conversations between parents and educators, as well as videos and a manual.
Are community programs in place—or are they needed?
Many schools have robust, state-mandated programs in place to identify bullying and provide support for students who are victims of bullying. (See “NJ’s harassment and bullying protocol: A case in point.”) Explaining this to victims and their families may help them come forward and seek assistance. FPs who want to advocate for their patients should start with local schools to support such programs and link students at risk with school counselors.
SIDEBAR
NJ's harassment and bullying protocol: A case in pointThere is no federal law that specifically applies to bullying, but all 50 states have some type of anti-bullying legislation on the books, and 40 of those states have additional detailed policies in place addressing the subject.1
New Jersey, for example, began enforcing one of the toughest harassment, intimidation, and bullying (HIB) protocols in the country back in September 20112 in the wake of the death of Rutgers University freshman Tyler Clementi, who committed suicide after his roommate allegedly shot a video of him with another man and posted it to the Internet.3 Among many other things, New Jersey’s legislation stipulates in its Anti-Bullying Bill of Rights4 that:
› Every school/district have plans in place that clearly define, prevent, prohibit, and promptly deal with acts of harassment, intimidation, or bullying, on school grounds, at school-sponsored functions, and on school buses.
› Plans must include a description of the type of behavior expected from each student and the consequences and remedial action for a person who commits an act of harassment, intimidation, or bullying. Student perpetrators may be suspended or expelled if convicted of any type of bullying, whether it be for teasing or something more severe.
› All school employees must act on any incidents of bullying reported to, or witnessed by, them and report such incidents on the same day to the school principal.
› Plans must include provisions and deadlines for investigating and resolving all matters in a timely fashion; investigations into allegations of bullying must be launched within one day.
› Every case of bullying must be reported to the state. Schools are graded by the state on their compliance with anti-bullying standards and policies and their handling of incidents.
› Schools must appoint safety teams made up of parents, teachers, and staff, and school personnel and students must receive extensive anti-bullying training.
1. US Department of Health and Human Services. Stopbullying.gov. Policies and laws. Available at: https://www.stopbullying.gov/laws/index.html.
Accessed January 5, 2017.
2. State of New Jersey Department of Education. An overview of amendments to laws on harassment, intimidation, and bullying. Available at: http://www.state.nj.us/education/students/safety/behavior/hib/overview.pdf. Accessed January 5, 2017.
3. Cohen A. Case study: Why New Jersey’s antibullying law should be a model for other states. Time. September 6, 2011. Available at: http://ideas.time.com/2011/09/06/why-new-jerseys-antibullying-law-should-be-a-model-for-other-states/. Accessed January 5, 2017.
4. New Jersey Legislature. Anti-bullying Bill of Rights Act. Available at: http://www.njleg.state.nj.us/2010/Bills/PL10/122.PDF. Accessed January 5, 2017.
If programs are lacking in your community, there is much you can do to educate yourself about successful programs and advise local community organizations and schools about them. Among the most successful and well-studied interventions for thwarting the bullying epidemic have been school-based community ones. The most studied of these is the Olweus Bullying Prevention Program (OBPP), which is based on 4 principles:1,29
- Adults both at home and at school should take a positive and encouraging interest in students.
- Unacceptable behavior should have strict and well-known limits.
- Sanctions should be applied consistently and should be non-hostile in nature.
- Adults both at home and in the educational environment should act as authorities.
In short, the program focuses on greater awareness and involvement on the part of adults, and employing measures at the school level (eg, surveys, better supervision during break and lunch times), the class level (eg, rules against bullying, regular class meetings with students), and the individual level (eg, serious talks with bullies, victims, parents of involved students).
Research has shown that the OBPP reduces bullying behaviors by as much as 50%, reduces vandalism and truancy, and reduces the number of new victims.12 Limits to the more widespread implementation of the OBPP have consisted mainly of the inability to appropriately train adults, including teachers and other school personnel in educational settings. Despite these limitations, the OBPP has been praised and endorsed by numerous groups, including the US Department of Justice.30
Other non-curricular, school-based programs exist, such as the School-Wide Positive Behavioral Interventions and Supports (SWPBIS). This program is a school-wide prevention strategy aimed at: 1) reducing behavior problems that lead to office discipline referrals and suspensions, and 2) changing perceptions of school safety. (For more information, see https://www.crimesolutions.gov/ProgramDetails.aspx?ID=385 and https://www.pbis.org/school/swpbis-for-beginners.)31
The research-based Second Step: Student Success Through Prevention (SS-SSTP) Middle School Program (http://www.cfchildren.org/second-step/middle-school)32 focuses on the often difficult middle school years. The program helps schools teach and model essential communication, coping, and decision-making skills to help adolescents navigate around common pitfalls such as peer pressure, substance abuse, and bullying (both in-person and online). The program aims to reduce aggression and provide support for a more inclusive environment that helps students stay in school, make good choices, and experience social and academic success.
The Positive Action Program (https://www.positiveaction.net/research/primer),33 which is predicated on the notion that we feel good about ourselves when we do positive things, features scripted lessons and kits of materials (eg, posters, games, worksheets, puzzles) appropriate for each grade level.
CASE › Stacey’s visit to her FP’s office has presented several clues that she may be a victim of bullying. Her mild persistent asthma appears to no longer be as well controlled as it was in the past. Direct questioning has revealed that 2 girls at school have been making fun of Stacey when she uses her inhaled corticosteroid in the morning before class, so she has stopped using it. These same students are on her cheerleading team, so she quit the team to avoid them. Her school-related anxiety is so great that she no longer pays attention in math class and is constantly worried that something is being posted about her online.
Stacy’s FP responds to this information with a multifaceted approach. In the exam room, he screens Stacy for depression. While she is negative and denies any suicidal ideation, Stacy is clearly having anxiety, so the FP refers Stacey to a counselor at a local mental health clinic. With Stacy’s permission, the FP discusses the issue with her mother and they decide together with Stacy that she should talk to a teacher at school about the ongoing bullying. Because this was not the first time that the FP has heard this from a child in the community, the FP plans to attend an upcoming school board meeting to advocate for an evidence-based bullying prevention program to help curb the ongoing problem facing his patients.
CORRESPONDENCE
Robert McClowry, MD, Department of Family and Community Medicine, Jefferson Family Medicine Associates, 833 Chestnut East, 3rd Floor, Suite 301, Philadelphia, PA, 19107-4414; Robert.McClowry@Jefferson.edu.
1. Olweus D, Limber SP. Bullying in school: evaluation and dissemination of the Olweus Bullying Prevention Program. Am J Orthopsychiatry. 2010;80:124-134.
2. Lyznicki JM, McCaffree MA, Robinowitz CB, et al. Childhood bullying: implications for physicians. Am Fam Physician. 2004;70:1723-1730.
3. Temkin D. All 50 states now have a bullying law. Now what? The Huffington Post. April 27, 2015. Available at: http://www.huffingtonpost.com/deborah-temkin/all-50-states-now-have-a_b_7153114.html. Accessed January 5, 2017.
4. Anderson M, Kaufman J, Simon TR, et al. School-associated violent deaths in the United States, 1994-1999. JAMA. 2001;286:2695-2702.
5. Centers for Disease Control and Prevention. Injury prevention and control: Data and statistics (WISQARS). Ten leading causes of death and injury. Available at: https://www.cdc.gov/injury/wisqars/leadingcauses.html. Accessed January 5, 2017.
6. Nansel TR, Overpeck M, Pilla RS, et al. Bullying behaviors among US youth: prevalence and association with psychosocial adjustment. JAMA. 2001;285:2094-2100.
7. Committee on Injury, Violence, and Poison Prevention. Policy statement—Role of the pediatrician in youth violence prevention. Pediatrics. 2009;124:393-402.
8. Klein DA, Myhre KK, Ahrendt DM. Bullying among adolescents: a challenge in primary care. Am Fam Physician. 2013;88:87-92.
9. Lamb J, Pepler DJ, Craig W. Approach to bullying and victimization. Can Fam Physician. 2009;55:356-360.
10. Spector ND, Kelly SF. Pediatrician’s role in screening and treatment: bullying, prediabetes, oral health. Curr Opin Pediatr. 2006;18:661-670.
11. Gladden RM, Vivolo-Kantor AM, Hamburger ME, et al. Bullying surveillance among youths: uniform definitions for public health and recommended data elements. National Center for Injury Prevention and Control, Centers for Disease Control and Prevention and US Department of Education; 2014. Available at: https://www.cdc.gov/violenceprevention/pdf/bullying-definitions-final-a.pdf. Accessed June 8, 2016.
12. Olweus D. Bullying at school: basic facts and effects of a school based intervention program. J Child Psychol Psychiatry. 1994;35:1171-1190.
13. Olweus D. Bully/victim problems in school: Facts and intervention. Eur J Psychol Educ. 1997;12:495-510.
14. Kowalski RM, Limber SP. Psychological, physical, and academic correlates of cyberbullying and traditional bullying. J Adolesc Health. 2013;53:S13-S20.
15. Craig W, Harel-Fisch Y, Fogel-Grinvald H, et al. A cross-national profile of bullying and victimization among adolescents in 40 countries. Int J Public Health. 2009;54(Suppl 2):216-224.
16. US Department of Education, National Center for Educational Statistics (2015). Student reports of bullying and cyberbullying: results from the 2013 School Crime Supplement to the National Victimization Survey. Available at: http://nces.ed.gov/pubsearch/pubsinfo.asp?pubid=2015056. Accessed November 9, 2016.
17. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance - United States, 2015. MMWR Morb Mortal Wkly Rep. 2016;65:1-174.
18. Van Cleave J, Davis MM. Bullying and peer victimization among children with special health care needs. Pediatrics. 2006;118:e1212-e1219.
19. Eisenberg ME, Neumark-Sztainer D, Story M. Associations of weight-based teasing and emotional well-being among adolescents. Arch Pediatr Adolesc Med. 2003;157:733-738.
20. Hatzenbuehler ML. The social environment and suicide attempts in lesbian, gay, and bisexual youth. Pediatrics. 2011;127:896-903.
21. Song LY, Singer MI, Anglin TM. Violence exposure and emotional trauma as contributors to adolescents’ violent behaviors. Arch Pediatr Adolesc Med. 1998;152:531-536.
22. Singer MI, Anglin TM, Song LY, et al. Adolescents’ exposure to violence and associated symptoms of psychological trauma. JAMA. 1995;273:477-482.
23. Glew GM, Fan MY, Katon W, et al. Bullying, psychosocial adjustment, and academic performance in elementary school. Arch Pediatr Adolesc Med. 2005;159:1026-1031.
24. Waseem M, Ryan M, Foster CB, et al. Assessment and management of bullied children in the emergency department. Pediatr Emerg Care. 2013;29:389-398.
25. US Department of Health and Human Services. stopbullying.gov. Available at: https//www.stopbullying.gov. Accessed January 5, 2017.
26. Shetgiri R, Lin H, Avila RM, et al. Parental characteristics associated with bullying perpetration in US children aged 10 to 17 years. Am J Public Health. 2012;102:2280-2286.
27. Hinduja S, Patchin JW. Social influences on cyberbullying behaviors among middle and high school students. J Youth Adolesc. 2013;42:711-722.
28. Borowsky IW, Mozayeny S, Stuenkel K, et al. Effects of a primary care-based intervention on violent behavior and injury in children. Pediatrics. 2004;114:e392-e399.
29. Olweus D. Bully/victim problems in school: Facts and intervention. Eur J Psychol Educ. 1997;12:495-510.
30. Mihalic SF. Blueprints for Violence Prevention: Report. US Department of Justice, Office of Justice Programs, Office of Juvenile Justice and Delinquency Prevention; 2004.
31. Waasdorp TE, Bradshaw CP, Leaf PJ. The impact of schoolwide positive behavioral interventions and supports on bullying and peer rejection: a randomized controlled effectiveness trial. Arch Pediatr Adolesc Med. 2012;166:149-156.
32. Espelage DL, Low S, Polanin JR, et al. The impact of a middle school program to reduce aggression, victimization, and sexual violence. J Adolesc Health. 2013;53:180-186.
33. Lewis KM, Schure MB, Bavarian N, et al. Problem behavior and urban, low-income youth: a randomized controlled trial of positive action in Chicago. Am J Prev Med. 2013;44:622-630.
1. Olweus D, Limber SP. Bullying in school: evaluation and dissemination of the Olweus Bullying Prevention Program. Am J Orthopsychiatry. 2010;80:124-134.
2. Lyznicki JM, McCaffree MA, Robinowitz CB, et al. Childhood bullying: implications for physicians. Am Fam Physician. 2004;70:1723-1730.
3. Temkin D. All 50 states now have a bullying law. Now what? The Huffington Post. April 27, 2015. Available at: http://www.huffingtonpost.com/deborah-temkin/all-50-states-now-have-a_b_7153114.html. Accessed January 5, 2017.
4. Anderson M, Kaufman J, Simon TR, et al. School-associated violent deaths in the United States, 1994-1999. JAMA. 2001;286:2695-2702.
5. Centers for Disease Control and Prevention. Injury prevention and control: Data and statistics (WISQARS). Ten leading causes of death and injury. Available at: https://www.cdc.gov/injury/wisqars/leadingcauses.html. Accessed January 5, 2017.
6. Nansel TR, Overpeck M, Pilla RS, et al. Bullying behaviors among US youth: prevalence and association with psychosocial adjustment. JAMA. 2001;285:2094-2100.
7. Committee on Injury, Violence, and Poison Prevention. Policy statement—Role of the pediatrician in youth violence prevention. Pediatrics. 2009;124:393-402.
8. Klein DA, Myhre KK, Ahrendt DM. Bullying among adolescents: a challenge in primary care. Am Fam Physician. 2013;88:87-92.
9. Lamb J, Pepler DJ, Craig W. Approach to bullying and victimization. Can Fam Physician. 2009;55:356-360.
10. Spector ND, Kelly SF. Pediatrician’s role in screening and treatment: bullying, prediabetes, oral health. Curr Opin Pediatr. 2006;18:661-670.
11. Gladden RM, Vivolo-Kantor AM, Hamburger ME, et al. Bullying surveillance among youths: uniform definitions for public health and recommended data elements. National Center for Injury Prevention and Control, Centers for Disease Control and Prevention and US Department of Education; 2014. Available at: https://www.cdc.gov/violenceprevention/pdf/bullying-definitions-final-a.pdf. Accessed June 8, 2016.
12. Olweus D. Bullying at school: basic facts and effects of a school based intervention program. J Child Psychol Psychiatry. 1994;35:1171-1190.
13. Olweus D. Bully/victim problems in school: Facts and intervention. Eur J Psychol Educ. 1997;12:495-510.
14. Kowalski RM, Limber SP. Psychological, physical, and academic correlates of cyberbullying and traditional bullying. J Adolesc Health. 2013;53:S13-S20.
15. Craig W, Harel-Fisch Y, Fogel-Grinvald H, et al. A cross-national profile of bullying and victimization among adolescents in 40 countries. Int J Public Health. 2009;54(Suppl 2):216-224.
16. US Department of Education, National Center for Educational Statistics (2015). Student reports of bullying and cyberbullying: results from the 2013 School Crime Supplement to the National Victimization Survey. Available at: http://nces.ed.gov/pubsearch/pubsinfo.asp?pubid=2015056. Accessed November 9, 2016.
17. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance - United States, 2015. MMWR Morb Mortal Wkly Rep. 2016;65:1-174.
18. Van Cleave J, Davis MM. Bullying and peer victimization among children with special health care needs. Pediatrics. 2006;118:e1212-e1219.
19. Eisenberg ME, Neumark-Sztainer D, Story M. Associations of weight-based teasing and emotional well-being among adolescents. Arch Pediatr Adolesc Med. 2003;157:733-738.
20. Hatzenbuehler ML. The social environment and suicide attempts in lesbian, gay, and bisexual youth. Pediatrics. 2011;127:896-903.
21. Song LY, Singer MI, Anglin TM. Violence exposure and emotional trauma as contributors to adolescents’ violent behaviors. Arch Pediatr Adolesc Med. 1998;152:531-536.
22. Singer MI, Anglin TM, Song LY, et al. Adolescents’ exposure to violence and associated symptoms of psychological trauma. JAMA. 1995;273:477-482.
23. Glew GM, Fan MY, Katon W, et al. Bullying, psychosocial adjustment, and academic performance in elementary school. Arch Pediatr Adolesc Med. 2005;159:1026-1031.
24. Waseem M, Ryan M, Foster CB, et al. Assessment and management of bullied children in the emergency department. Pediatr Emerg Care. 2013;29:389-398.
25. US Department of Health and Human Services. stopbullying.gov. Available at: https//www.stopbullying.gov. Accessed January 5, 2017.
26. Shetgiri R, Lin H, Avila RM, et al. Parental characteristics associated with bullying perpetration in US children aged 10 to 17 years. Am J Public Health. 2012;102:2280-2286.
27. Hinduja S, Patchin JW. Social influences on cyberbullying behaviors among middle and high school students. J Youth Adolesc. 2013;42:711-722.
28. Borowsky IW, Mozayeny S, Stuenkel K, et al. Effects of a primary care-based intervention on violent behavior and injury in children. Pediatrics. 2004;114:e392-e399.
29. Olweus D. Bully/victim problems in school: Facts and intervention. Eur J Psychol Educ. 1997;12:495-510.
30. Mihalic SF. Blueprints for Violence Prevention: Report. US Department of Justice, Office of Justice Programs, Office of Juvenile Justice and Delinquency Prevention; 2004.
31. Waasdorp TE, Bradshaw CP, Leaf PJ. The impact of schoolwide positive behavioral interventions and supports on bullying and peer rejection: a randomized controlled effectiveness trial. Arch Pediatr Adolesc Med. 2012;166:149-156.
32. Espelage DL, Low S, Polanin JR, et al. The impact of a middle school program to reduce aggression, victimization, and sexual violence. J Adolesc Health. 2013;53:180-186.
33. Lewis KM, Schure MB, Bavarian N, et al. Problem behavior and urban, low-income youth: a randomized controlled trial of positive action in Chicago. Am J Prev Med. 2013;44:622-630.
PRACTICE RECOMMENDATIONS
› Suspect bullying when children with chronic conditions that were stable begin deteriorating for unexplained reasons or when children become non-adherent to medication regimens. C
› Empower not only patients, but also parents/caregivers, to take action and deter bullying behaviors. B
› Support school-based and community-oriented intervention programs, which have been shown to be among the most effective strategies for curbing bullying. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Steroids during late preterm labor: Better later than never
ILLUSTRATIVE CASE
A 21-year-old G1P0 at 35 weeks, 2 days of gestation presents to labor and delivery reporting a “gush of clear fluid.” On exam, you confirm she has preterm rupture of membranes. She is contracting every 3 minutes and has a cervix dilated to 3 cm. Is there any neonatal benefit to providing corticosteroids in this late preterm period?
Approximately 12% of all births in the United States are the result of preterm labor,2 and 8% are born in the late preterm period, defined as 34 to 36 weeks’ gestation.3 To reduce the risk of neonatal death and respiratory complications, both the American College of Obstetricians and Gynecologists and the National Institutes of Health recommend a course of corticosteroids between 24 and 34 weeks’ gestation for women at increased risk of preterm delivery.2,4 Due to a lack of evidence from randomized controlled trials (RCTs) on the benefit of corticosteroids in late preterm labor, there have not been recommendations to extend this period.5 However, multiple studies have shown that babies born during the late preterm period have more neonatal complications than term newborns.6-8
A retrospective chart review of more than 130,000 live births found newborns delivered between 34 and 36 weeks had higher rates of respiratory distress than those delivered at 39 weeks (ventilator use dropped from 3.3% at 34 weeks to 0.3% at 39 weeks and transient tachypnea decreased from 2.4% at 34 weeks to 0.4% at 39 weeks).6 Another retrospective review of more than 230,000 newborns, of which 19,000 were born in the late preterm period, revealed that more neonates born between 34 and 36 weeks’ gestation had respiratory distress syndrome than neonates delivered at 39 weeks (10.5% at 34 weeks, 6% at 35 weeks, 2.8% at 36 weeks vs 0.3% at 39 weeks; P<.001 for the trend).8
STUDY SUMMARY
Late preterm newborns breathe better with antenatal betamethasone
This randomized placebo-controlled trial examined the effectiveness of betamethasone in preventing neonatal respiratory complications for 2831 women at high probability of preterm delivery between 34 weeks and 36 weeks, 6 days of gestation. “High probability of preterm delivery” was defined as preterm labor with intact membranes and at least 3 cm dilation or 75% cervical effacement; spontaneous rupture of membranes; or anticipated preterm delivery for any other indication either through induction or cesarean section between 24 hours and 7 days after the planned randomization.
Patients were randomly assigned to receive either 2 intramuscular injections (12 mg each) of betamethasone or placebo, 24 hours apart. The 2 doses were successfully given in 60% of the betamethasone group and 59% of the placebo group. In 95% of the cases where the second dose was not given, it was because delivery occurred within 24 hours of the first dose.
The primary outcome was the need for respiratory support within 72 hours of birth, which was defined as one or more of the following: the use of continuous positive airway pressure (CPAP) or high-flow nasal cannula for at least 2 consecutive hours, supplemental oxygen for at least 4 continuous hours, extracorporeal membrane oxygenation (ECMO), or mechanical ventilation.
The median time to delivery from enrollment was 31 to 33 hours, and 31.4% underwent cesarean delivery. In the intention-to-treat analysis, the primary outcome was significantly lower in the betamethasone group than in the placebo group (11.6% vs 14.4%; relative risk [RR]=0.80; 95% CI, 0.66-0.97; P=.02; number needed to treat [NNT]=35). Secondary outcomes (severe complications, representing a composite of the use of CPAP or high-flow nasal cannula for at least 12 continuous hours, supplemental oxygen for at least 24 continuous hours, ECMO, mechanical ventilation, stillbirth, or neonatal death within 72 hours after delivery) were also lower in the betamethasone group (8.1% vs 12.1%; RR=0.67; 95% CI, 0.53-0.84; P<.001; NNT=25). The betamethasone group also had a lower risk of transient tachypnea of the newborn (6.7% vs 9.9%; RR=0.68; 95% CI, 0.53-0.87; P=.002).
There were no significant differences in the occurrence of maternal chorioamnionitis (about 2%) or endometritis (about 1%) between the groups. Hypoglycemia in the newborn occurred more in the betamethasone group (24% vs 15%; RR=1.6; 95% CI, 1.37-1.87; P<.001; number needed to harm [NNH]=11). The betamethasone group had 2 neonatal deaths: one from septic shock and the other from a structural cardiac anomaly and arrhythmia.
WHAT’S NEW
Betamethasone makes a difference even in the late, late preterm period
This study demonstrated clear benefit in neonatal respiratory outcomes when betamethasone vs placebo was used in the late preterm period. The findings were similar to those from the Antenatal Steroids for Term Elective Caesarean Section Research Team.9 Their trial showed a reduction in respiratory complications in term neonates delivered via elective cesarean section to mothers who received antenatal betamethasone (NNT=37 to prevent admission to a special care nursery with respiratory distress). The findings were also consistent with those of a recent meta-analysis (including this trial) evaluating the occurrence of respiratory complications with the use of antenatal betamethasone in women expected to deliver in the late preterm period or with a planned cesarean delivery at ≥37 weeks’ gestation.10
CAVEATS
Neonates may develop hypoglycemia
The authors of the study reported an increased risk of hypoglycemia in the neonates receiving antenatal betamethasone. The long-term implications of this are unclear, however, given that there was a reduction in intermediate care nursery and neonatal intensive care unit stays that were 3 days or longer in the betamethasone group. Also, there was no difference in hospital length of stay between the 2 groups. In addition, it’s not clear if there are any long-term neonatal complications of betamethasone use in the late preterm period.
CHALLENGES TO IMPLEMENTATION
Challenges are negligible since betamethasone is readily available
There are minimal challenges to implementing this strategy, as betamethasone is routinely used for preterm labor and is readily available on labor and delivery units.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
1. Gyamfi-Bannerman C, Thom EA, Blackwell SC, et al; NICHD Maternal–Fetal Medicine Units Network. Antenatal betamethasone for women at risk for late preterm delivery. N Engl J Med. 2016;374:1311-1320.
2. Practice Bulletin No. 159 Summary: Management of Preterm Labor. Obstet Gynecol. 2016;127:190-191.
3. Martin JA, Hamilton BE, Osterman MJ, et al. Births: final data for 2013. Natl Vital Stat Rep. 2015;64:1-65.
4. Effect of corticosteroids for fetal maturation on perinatal outcomes. NIH Consens Statement. 1994;12:1-24.
5. Society for Maternal-Fetal Medicine (SMFM) Publications Committee. Implementation of the use of antenatal corticosteroids in the late preterm birth period in women at risk for preterm delivery. Am J Obstet Gynecol. 2016;215:B13-B15.
6. McIntire DD, Leveno KJ. Neonatal mortality and morbidity rates in late preterm births compared with births at term. Obstet Gynecol. 2008;111:35-41.
7. Yoder BA, Gordon MC, Barth WH Jr. Late-preterm birth: does the changing obstetric paradigm alter the epidemiology of respiratory complications? Obstet Gynecol. 2008;111:814-822.
8. Consortium on Safe Labor, Hibbard JU, Wilkins I, Sun L, et al. Respiratory morbidity in late preterm births. JAMA. 2010;304:419-425.
9. Stutchfield P, Whitaker R, Russell I. Antenatal betamethasone and incidence of neonatal respiratory distress after elective caesarean section: pragmatic randomised trial. BMJ. 2005;331:662.
10. Saccone G, Berghella V. Antenatal corticosteroids for maturity of term or near term fetuses: systematic review and meta-analysis of randomized controlled trials. BMJ. 2016;355:i5044.
ILLUSTRATIVE CASE
A 21-year-old G1P0 at 35 weeks, 2 days of gestation presents to labor and delivery reporting a “gush of clear fluid.” On exam, you confirm she has preterm rupture of membranes. She is contracting every 3 minutes and has a cervix dilated to 3 cm. Is there any neonatal benefit to providing corticosteroids in this late preterm period?
Approximately 12% of all births in the United States are the result of preterm labor,2 and 8% are born in the late preterm period, defined as 34 to 36 weeks’ gestation.3 To reduce the risk of neonatal death and respiratory complications, both the American College of Obstetricians and Gynecologists and the National Institutes of Health recommend a course of corticosteroids between 24 and 34 weeks’ gestation for women at increased risk of preterm delivery.2,4 Due to a lack of evidence from randomized controlled trials (RCTs) on the benefit of corticosteroids in late preterm labor, there have not been recommendations to extend this period.5 However, multiple studies have shown that babies born during the late preterm period have more neonatal complications than term newborns.6-8
A retrospective chart review of more than 130,000 live births found newborns delivered between 34 and 36 weeks had higher rates of respiratory distress than those delivered at 39 weeks (ventilator use dropped from 3.3% at 34 weeks to 0.3% at 39 weeks and transient tachypnea decreased from 2.4% at 34 weeks to 0.4% at 39 weeks).6 Another retrospective review of more than 230,000 newborns, of which 19,000 were born in the late preterm period, revealed that more neonates born between 34 and 36 weeks’ gestation had respiratory distress syndrome than neonates delivered at 39 weeks (10.5% at 34 weeks, 6% at 35 weeks, 2.8% at 36 weeks vs 0.3% at 39 weeks; P<.001 for the trend).8
STUDY SUMMARY
Late preterm newborns breathe better with antenatal betamethasone
This randomized placebo-controlled trial examined the effectiveness of betamethasone in preventing neonatal respiratory complications for 2831 women at high probability of preterm delivery between 34 weeks and 36 weeks, 6 days of gestation. “High probability of preterm delivery” was defined as preterm labor with intact membranes and at least 3 cm dilation or 75% cervical effacement; spontaneous rupture of membranes; or anticipated preterm delivery for any other indication either through induction or cesarean section between 24 hours and 7 days after the planned randomization.
Patients were randomly assigned to receive either 2 intramuscular injections (12 mg each) of betamethasone or placebo, 24 hours apart. The 2 doses were successfully given in 60% of the betamethasone group and 59% of the placebo group. In 95% of the cases where the second dose was not given, it was because delivery occurred within 24 hours of the first dose.
The primary outcome was the need for respiratory support within 72 hours of birth, which was defined as one or more of the following: the use of continuous positive airway pressure (CPAP) or high-flow nasal cannula for at least 2 consecutive hours, supplemental oxygen for at least 4 continuous hours, extracorporeal membrane oxygenation (ECMO), or mechanical ventilation.
The median time to delivery from enrollment was 31 to 33 hours, and 31.4% underwent cesarean delivery. In the intention-to-treat analysis, the primary outcome was significantly lower in the betamethasone group than in the placebo group (11.6% vs 14.4%; relative risk [RR]=0.80; 95% CI, 0.66-0.97; P=.02; number needed to treat [NNT]=35). Secondary outcomes (severe complications, representing a composite of the use of CPAP or high-flow nasal cannula for at least 12 continuous hours, supplemental oxygen for at least 24 continuous hours, ECMO, mechanical ventilation, stillbirth, or neonatal death within 72 hours after delivery) were also lower in the betamethasone group (8.1% vs 12.1%; RR=0.67; 95% CI, 0.53-0.84; P<.001; NNT=25). The betamethasone group also had a lower risk of transient tachypnea of the newborn (6.7% vs 9.9%; RR=0.68; 95% CI, 0.53-0.87; P=.002).
There were no significant differences in the occurrence of maternal chorioamnionitis (about 2%) or endometritis (about 1%) between the groups. Hypoglycemia in the newborn occurred more in the betamethasone group (24% vs 15%; RR=1.6; 95% CI, 1.37-1.87; P<.001; number needed to harm [NNH]=11). The betamethasone group had 2 neonatal deaths: one from septic shock and the other from a structural cardiac anomaly and arrhythmia.
WHAT’S NEW
Betamethasone makes a difference even in the late, late preterm period
This study demonstrated clear benefit in neonatal respiratory outcomes when betamethasone vs placebo was used in the late preterm period. The findings were similar to those from the Antenatal Steroids for Term Elective Caesarean Section Research Team.9 Their trial showed a reduction in respiratory complications in term neonates delivered via elective cesarean section to mothers who received antenatal betamethasone (NNT=37 to prevent admission to a special care nursery with respiratory distress). The findings were also consistent with those of a recent meta-analysis (including this trial) evaluating the occurrence of respiratory complications with the use of antenatal betamethasone in women expected to deliver in the late preterm period or with a planned cesarean delivery at ≥37 weeks’ gestation.10
CAVEATS
Neonates may develop hypoglycemia
The authors of the study reported an increased risk of hypoglycemia in the neonates receiving antenatal betamethasone. The long-term implications of this are unclear, however, given that there was a reduction in intermediate care nursery and neonatal intensive care unit stays that were 3 days or longer in the betamethasone group. Also, there was no difference in hospital length of stay between the 2 groups. In addition, it’s not clear if there are any long-term neonatal complications of betamethasone use in the late preterm period.
CHALLENGES TO IMPLEMENTATION
Challenges are negligible since betamethasone is readily available
There are minimal challenges to implementing this strategy, as betamethasone is routinely used for preterm labor and is readily available on labor and delivery units.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
ILLUSTRATIVE CASE
A 21-year-old G1P0 at 35 weeks, 2 days of gestation presents to labor and delivery reporting a “gush of clear fluid.” On exam, you confirm she has preterm rupture of membranes. She is contracting every 3 minutes and has a cervix dilated to 3 cm. Is there any neonatal benefit to providing corticosteroids in this late preterm period?
Approximately 12% of all births in the United States are the result of preterm labor,2 and 8% are born in the late preterm period, defined as 34 to 36 weeks’ gestation.3 To reduce the risk of neonatal death and respiratory complications, both the American College of Obstetricians and Gynecologists and the National Institutes of Health recommend a course of corticosteroids between 24 and 34 weeks’ gestation for women at increased risk of preterm delivery.2,4 Due to a lack of evidence from randomized controlled trials (RCTs) on the benefit of corticosteroids in late preterm labor, there have not been recommendations to extend this period.5 However, multiple studies have shown that babies born during the late preterm period have more neonatal complications than term newborns.6-8
A retrospective chart review of more than 130,000 live births found newborns delivered between 34 and 36 weeks had higher rates of respiratory distress than those delivered at 39 weeks (ventilator use dropped from 3.3% at 34 weeks to 0.3% at 39 weeks and transient tachypnea decreased from 2.4% at 34 weeks to 0.4% at 39 weeks).6 Another retrospective review of more than 230,000 newborns, of which 19,000 were born in the late preterm period, revealed that more neonates born between 34 and 36 weeks’ gestation had respiratory distress syndrome than neonates delivered at 39 weeks (10.5% at 34 weeks, 6% at 35 weeks, 2.8% at 36 weeks vs 0.3% at 39 weeks; P<.001 for the trend).8
STUDY SUMMARY
Late preterm newborns breathe better with antenatal betamethasone
This randomized placebo-controlled trial examined the effectiveness of betamethasone in preventing neonatal respiratory complications for 2831 women at high probability of preterm delivery between 34 weeks and 36 weeks, 6 days of gestation. “High probability of preterm delivery” was defined as preterm labor with intact membranes and at least 3 cm dilation or 75% cervical effacement; spontaneous rupture of membranes; or anticipated preterm delivery for any other indication either through induction or cesarean section between 24 hours and 7 days after the planned randomization.
Patients were randomly assigned to receive either 2 intramuscular injections (12 mg each) of betamethasone or placebo, 24 hours apart. The 2 doses were successfully given in 60% of the betamethasone group and 59% of the placebo group. In 95% of the cases where the second dose was not given, it was because delivery occurred within 24 hours of the first dose.
The primary outcome was the need for respiratory support within 72 hours of birth, which was defined as one or more of the following: the use of continuous positive airway pressure (CPAP) or high-flow nasal cannula for at least 2 consecutive hours, supplemental oxygen for at least 4 continuous hours, extracorporeal membrane oxygenation (ECMO), or mechanical ventilation.
The median time to delivery from enrollment was 31 to 33 hours, and 31.4% underwent cesarean delivery. In the intention-to-treat analysis, the primary outcome was significantly lower in the betamethasone group than in the placebo group (11.6% vs 14.4%; relative risk [RR]=0.80; 95% CI, 0.66-0.97; P=.02; number needed to treat [NNT]=35). Secondary outcomes (severe complications, representing a composite of the use of CPAP or high-flow nasal cannula for at least 12 continuous hours, supplemental oxygen for at least 24 continuous hours, ECMO, mechanical ventilation, stillbirth, or neonatal death within 72 hours after delivery) were also lower in the betamethasone group (8.1% vs 12.1%; RR=0.67; 95% CI, 0.53-0.84; P<.001; NNT=25). The betamethasone group also had a lower risk of transient tachypnea of the newborn (6.7% vs 9.9%; RR=0.68; 95% CI, 0.53-0.87; P=.002).
There were no significant differences in the occurrence of maternal chorioamnionitis (about 2%) or endometritis (about 1%) between the groups. Hypoglycemia in the newborn occurred more in the betamethasone group (24% vs 15%; RR=1.6; 95% CI, 1.37-1.87; P<.001; number needed to harm [NNH]=11). The betamethasone group had 2 neonatal deaths: one from septic shock and the other from a structural cardiac anomaly and arrhythmia.
WHAT’S NEW
Betamethasone makes a difference even in the late, late preterm period
This study demonstrated clear benefit in neonatal respiratory outcomes when betamethasone vs placebo was used in the late preterm period. The findings were similar to those from the Antenatal Steroids for Term Elective Caesarean Section Research Team.9 Their trial showed a reduction in respiratory complications in term neonates delivered via elective cesarean section to mothers who received antenatal betamethasone (NNT=37 to prevent admission to a special care nursery with respiratory distress). The findings were also consistent with those of a recent meta-analysis (including this trial) evaluating the occurrence of respiratory complications with the use of antenatal betamethasone in women expected to deliver in the late preterm period or with a planned cesarean delivery at ≥37 weeks’ gestation.10
CAVEATS
Neonates may develop hypoglycemia
The authors of the study reported an increased risk of hypoglycemia in the neonates receiving antenatal betamethasone. The long-term implications of this are unclear, however, given that there was a reduction in intermediate care nursery and neonatal intensive care unit stays that were 3 days or longer in the betamethasone group. Also, there was no difference in hospital length of stay between the 2 groups. In addition, it’s not clear if there are any long-term neonatal complications of betamethasone use in the late preterm period.
CHALLENGES TO IMPLEMENTATION
Challenges are negligible since betamethasone is readily available
There are minimal challenges to implementing this strategy, as betamethasone is routinely used for preterm labor and is readily available on labor and delivery units.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
1. Gyamfi-Bannerman C, Thom EA, Blackwell SC, et al; NICHD Maternal–Fetal Medicine Units Network. Antenatal betamethasone for women at risk for late preterm delivery. N Engl J Med. 2016;374:1311-1320.
2. Practice Bulletin No. 159 Summary: Management of Preterm Labor. Obstet Gynecol. 2016;127:190-191.
3. Martin JA, Hamilton BE, Osterman MJ, et al. Births: final data for 2013. Natl Vital Stat Rep. 2015;64:1-65.
4. Effect of corticosteroids for fetal maturation on perinatal outcomes. NIH Consens Statement. 1994;12:1-24.
5. Society for Maternal-Fetal Medicine (SMFM) Publications Committee. Implementation of the use of antenatal corticosteroids in the late preterm birth period in women at risk for preterm delivery. Am J Obstet Gynecol. 2016;215:B13-B15.
6. McIntire DD, Leveno KJ. Neonatal mortality and morbidity rates in late preterm births compared with births at term. Obstet Gynecol. 2008;111:35-41.
7. Yoder BA, Gordon MC, Barth WH Jr. Late-preterm birth: does the changing obstetric paradigm alter the epidemiology of respiratory complications? Obstet Gynecol. 2008;111:814-822.
8. Consortium on Safe Labor, Hibbard JU, Wilkins I, Sun L, et al. Respiratory morbidity in late preterm births. JAMA. 2010;304:419-425.
9. Stutchfield P, Whitaker R, Russell I. Antenatal betamethasone and incidence of neonatal respiratory distress after elective caesarean section: pragmatic randomised trial. BMJ. 2005;331:662.
10. Saccone G, Berghella V. Antenatal corticosteroids for maturity of term or near term fetuses: systematic review and meta-analysis of randomized controlled trials. BMJ. 2016;355:i5044.
1. Gyamfi-Bannerman C, Thom EA, Blackwell SC, et al; NICHD Maternal–Fetal Medicine Units Network. Antenatal betamethasone for women at risk for late preterm delivery. N Engl J Med. 2016;374:1311-1320.
2. Practice Bulletin No. 159 Summary: Management of Preterm Labor. Obstet Gynecol. 2016;127:190-191.
3. Martin JA, Hamilton BE, Osterman MJ, et al. Births: final data for 2013. Natl Vital Stat Rep. 2015;64:1-65.
4. Effect of corticosteroids for fetal maturation on perinatal outcomes. NIH Consens Statement. 1994;12:1-24.
5. Society for Maternal-Fetal Medicine (SMFM) Publications Committee. Implementation of the use of antenatal corticosteroids in the late preterm birth period in women at risk for preterm delivery. Am J Obstet Gynecol. 2016;215:B13-B15.
6. McIntire DD, Leveno KJ. Neonatal mortality and morbidity rates in late preterm births compared with births at term. Obstet Gynecol. 2008;111:35-41.
7. Yoder BA, Gordon MC, Barth WH Jr. Late-preterm birth: does the changing obstetric paradigm alter the epidemiology of respiratory complications? Obstet Gynecol. 2008;111:814-822.
8. Consortium on Safe Labor, Hibbard JU, Wilkins I, Sun L, et al. Respiratory morbidity in late preterm births. JAMA. 2010;304:419-425.
9. Stutchfield P, Whitaker R, Russell I. Antenatal betamethasone and incidence of neonatal respiratory distress after elective caesarean section: pragmatic randomised trial. BMJ. 2005;331:662.
10. Saccone G, Berghella V. Antenatal corticosteroids for maturity of term or near term fetuses: systematic review and meta-analysis of randomized controlled trials. BMJ. 2016;355:i5044.
Copyright © 2017. The Family Physicians Inquiries Network. All rights reserved.
PRACTICE CHANGER
Use steroids in women at risk of preterm delivery, even if they are 36 weeks, 6 days’ pregnant, because steroids may reduce respiratory complications in the newborn with minimal risk for neonatal or maternal complications.
Gyamfi-Bannerman C, Thom EA, Blackwell SC, et al; NICHD Maternal–Fetal Medicine Units Network. Antenatal betamethasone for women at risk for late preterm delivery. N Engl J Med. 2016;374:1311-1320.1
STRENGTH OF RECOMMENDATION
A: Based on a good quality randomized controlled trial and consistent with a meta-analysis.
It’s time to screen for bullying
When I became a family physician (FP), it never crossed my mind that I would one day be asking school-aged children about bullying. Not so much because bullying didn’t exist, but because I wasn’t aware of the pervasiveness and seriousness of the problem and because there were no professional recommendations to do so.
That said, my family had some first-hand experience with the issue: One of my children was bullied in grade school. When my wife found out, she promptly visited the 2 boys’ homes and told them and their parents that the behavior would stop or else! (She may have used more colorful language.) And it did stop. But times have changed, and so has the nature of bullying, which can now extend beyond the hallway to an entire school body in seconds with a few taps on a cell phone. And the adverse consequences can be significant, as described by McClowry and colleagues.
The prevalence of bullying is discouragingly high, estimated to be about 20% in national surveys.1 Because bullying occurs so frequently, public health, community-based, and school-based approaches, rather than one-on-one office-based interventions, are likely to have the greatest overall impact on decreasing bullying. Randomized trials bear this out, showing that prevention programs in schools can effectively reduce the behavior.2,3
What is our responsibility as FPs? Screening is a reasonable first step, even in the absence of randomized trials demonstrating benefit. Because there have been no physician office-based trials of screening or interventions for bullying, we must rely on “expert opinion” at this time, with no assurance that what we do will actually help children. Absence of proof of benefit, however, does not mean absence of benefit, and doing nothing will definitely not help anyone. The authors recommend a single screening question: "Are you being bullied?"—especially for children who are at higher risk, such as those with disabilities/special health needs, LGBTQ+ status, and who are under- or overweight.
Clearly we need research to know which interventions truly help these children/adolescents and their parents. In the meantime, however, identifying the problem and offering emotional support are unlikely to harm—and may help. Opening the lines of communication, connecting children and their parents with available community resources, and supporting anti-bullying programs in your schools are additional ways we can make a difference today.
1. Kann L, McManus T, Harris WA, et al. Youth Risk Behavior Surveillance System – United States, 2015. MMWR Morb Mortal Wkly. 2016;65:1-174.
2. Waasdorp TE, Bradshaw CP, Leaf PJ. The impact of schoolwide positive behavioral interventions and supports on bullying and peer rejection: a randomized controlled effectiveness trial. Arch Pediatr Adolesc Med. 2012;166:149-156.
3. Espelage DL, Low S, Polanin JR, et al. The impact of a middle school program to reduce aggression, victimization, and sexual violence. J Adolesc Health. 2013;53:180-186.
Editor-in-Chief
Editor-in-Chief
Editor-in-Chief
When I became a family physician (FP), it never crossed my mind that I would one day be asking school-aged children about bullying. Not so much because bullying didn’t exist, but because I wasn’t aware of the pervasiveness and seriousness of the problem and because there were no professional recommendations to do so.
That said, my family had some first-hand experience with the issue: One of my children was bullied in grade school. When my wife found out, she promptly visited the 2 boys’ homes and told them and their parents that the behavior would stop or else! (She may have used more colorful language.) And it did stop. But times have changed, and so has the nature of bullying, which can now extend beyond the hallway to an entire school body in seconds with a few taps on a cell phone. And the adverse consequences can be significant, as described by McClowry and colleagues.
The prevalence of bullying is discouragingly high, estimated to be about 20% in national surveys.1 Because bullying occurs so frequently, public health, community-based, and school-based approaches, rather than one-on-one office-based interventions, are likely to have the greatest overall impact on decreasing bullying. Randomized trials bear this out, showing that prevention programs in schools can effectively reduce the behavior.2,3
What is our responsibility as FPs? Screening is a reasonable first step, even in the absence of randomized trials demonstrating benefit. Because there have been no physician office-based trials of screening or interventions for bullying, we must rely on “expert opinion” at this time, with no assurance that what we do will actually help children. Absence of proof of benefit, however, does not mean absence of benefit, and doing nothing will definitely not help anyone. The authors recommend a single screening question: "Are you being bullied?"—especially for children who are at higher risk, such as those with disabilities/special health needs, LGBTQ+ status, and who are under- or overweight.
Clearly we need research to know which interventions truly help these children/adolescents and their parents. In the meantime, however, identifying the problem and offering emotional support are unlikely to harm—and may help. Opening the lines of communication, connecting children and their parents with available community resources, and supporting anti-bullying programs in your schools are additional ways we can make a difference today.
When I became a family physician (FP), it never crossed my mind that I would one day be asking school-aged children about bullying. Not so much because bullying didn’t exist, but because I wasn’t aware of the pervasiveness and seriousness of the problem and because there were no professional recommendations to do so.
That said, my family had some first-hand experience with the issue: One of my children was bullied in grade school. When my wife found out, she promptly visited the 2 boys’ homes and told them and their parents that the behavior would stop or else! (She may have used more colorful language.) And it did stop. But times have changed, and so has the nature of bullying, which can now extend beyond the hallway to an entire school body in seconds with a few taps on a cell phone. And the adverse consequences can be significant, as described by McClowry and colleagues.
The prevalence of bullying is discouragingly high, estimated to be about 20% in national surveys.1 Because bullying occurs so frequently, public health, community-based, and school-based approaches, rather than one-on-one office-based interventions, are likely to have the greatest overall impact on decreasing bullying. Randomized trials bear this out, showing that prevention programs in schools can effectively reduce the behavior.2,3
What is our responsibility as FPs? Screening is a reasonable first step, even in the absence of randomized trials demonstrating benefit. Because there have been no physician office-based trials of screening or interventions for bullying, we must rely on “expert opinion” at this time, with no assurance that what we do will actually help children. Absence of proof of benefit, however, does not mean absence of benefit, and doing nothing will definitely not help anyone. The authors recommend a single screening question: "Are you being bullied?"—especially for children who are at higher risk, such as those with disabilities/special health needs, LGBTQ+ status, and who are under- or overweight.
Clearly we need research to know which interventions truly help these children/adolescents and their parents. In the meantime, however, identifying the problem and offering emotional support are unlikely to harm—and may help. Opening the lines of communication, connecting children and their parents with available community resources, and supporting anti-bullying programs in your schools are additional ways we can make a difference today.
1. Kann L, McManus T, Harris WA, et al. Youth Risk Behavior Surveillance System – United States, 2015. MMWR Morb Mortal Wkly. 2016;65:1-174.
2. Waasdorp TE, Bradshaw CP, Leaf PJ. The impact of schoolwide positive behavioral interventions and supports on bullying and peer rejection: a randomized controlled effectiveness trial. Arch Pediatr Adolesc Med. 2012;166:149-156.
3. Espelage DL, Low S, Polanin JR, et al. The impact of a middle school program to reduce aggression, victimization, and sexual violence. J Adolesc Health. 2013;53:180-186.
1. Kann L, McManus T, Harris WA, et al. Youth Risk Behavior Surveillance System – United States, 2015. MMWR Morb Mortal Wkly. 2016;65:1-174.
2. Waasdorp TE, Bradshaw CP, Leaf PJ. The impact of schoolwide positive behavioral interventions and supports on bullying and peer rejection: a randomized controlled effectiveness trial. Arch Pediatr Adolesc Med. 2012;166:149-156.
3. Espelage DL, Low S, Polanin JR, et al. The impact of a middle school program to reduce aggression, victimization, and sexual violence. J Adolesc Health. 2013;53:180-186.
Latuda receives FDA approval for adolescent schizophrenia treatment
Lurasidone HCl, marketed as Latuda, has received approval from the Food and Drug Administration for the treatment of schizophrenia in adolescents aged 13-17 years old, according to a press release from Sunovion Pharmaceuticals.
FDA approval of Latuda is based on results of a 6-week study in which adolescents with schizophrenia received either 40 mg of lurasidone per day, 80 mg per day, or a placebo. Patients who received lurasidone HCI showed statistical and clinical improvements in schizophrenia symptoms, compared with the placebo group. The drug was well tolerated with no significant adverse events reported.
“The impact on development and poor prognosis frequently associated with schizophrenia that begins in adolescence underscores the need for treatment that is both well tolerated and effective,” Robert L. Findling, MD, study investigator, and director of child and adolescent psychiatry at Johns Hopkins University, Baltimore, said in the press release. “The availability of Latuda provides health care providers with an important new option for helping adolescents with this illness that is chronic and severely disabling,” said Dr. Findling, also vice president of psychiatric services and research at the Kennedy Krieger Institute, Baltimore.
Find the full press release on the Sunovion Pharmaceuticals website.
Lurasidone HCl, marketed as Latuda, has received approval from the Food and Drug Administration for the treatment of schizophrenia in adolescents aged 13-17 years old, according to a press release from Sunovion Pharmaceuticals.
FDA approval of Latuda is based on results of a 6-week study in which adolescents with schizophrenia received either 40 mg of lurasidone per day, 80 mg per day, or a placebo. Patients who received lurasidone HCI showed statistical and clinical improvements in schizophrenia symptoms, compared with the placebo group. The drug was well tolerated with no significant adverse events reported.
“The impact on development and poor prognosis frequently associated with schizophrenia that begins in adolescence underscores the need for treatment that is both well tolerated and effective,” Robert L. Findling, MD, study investigator, and director of child and adolescent psychiatry at Johns Hopkins University, Baltimore, said in the press release. “The availability of Latuda provides health care providers with an important new option for helping adolescents with this illness that is chronic and severely disabling,” said Dr. Findling, also vice president of psychiatric services and research at the Kennedy Krieger Institute, Baltimore.
Find the full press release on the Sunovion Pharmaceuticals website.
Lurasidone HCl, marketed as Latuda, has received approval from the Food and Drug Administration for the treatment of schizophrenia in adolescents aged 13-17 years old, according to a press release from Sunovion Pharmaceuticals.
FDA approval of Latuda is based on results of a 6-week study in which adolescents with schizophrenia received either 40 mg of lurasidone per day, 80 mg per day, or a placebo. Patients who received lurasidone HCI showed statistical and clinical improvements in schizophrenia symptoms, compared with the placebo group. The drug was well tolerated with no significant adverse events reported.
“The impact on development and poor prognosis frequently associated with schizophrenia that begins in adolescence underscores the need for treatment that is both well tolerated and effective,” Robert L. Findling, MD, study investigator, and director of child and adolescent psychiatry at Johns Hopkins University, Baltimore, said in the press release. “The availability of Latuda provides health care providers with an important new option for helping adolescents with this illness that is chronic and severely disabling,” said Dr. Findling, also vice president of psychiatric services and research at the Kennedy Krieger Institute, Baltimore.
Find the full press release on the Sunovion Pharmaceuticals website.
Underdosing of Lorazepam in Children Is Associated With Increased Seizure Duration
HOUSTON—The first dose of lorazepam, when administered as a first-line antiepileptic drug (AED) for pediatric refractory status epilepticus, frequently is underdosed, and doses lower than 0.1 mg/kg are associated with increased seizure duration, according to research presented at the 70th Annual Meeting of the American Epilepsy Society (AES).
The results emphasize the importance of following AES status epilepticus guidelines, which call for lorazepam dosing of 0.1 mg/kg, said Dmitry Tchapyjnikov, MD, of Duke University School of Medicine in Durham, North Carolina, and colleagues.
“There is high variability in lorazepam dosing when used in the treatment of status epilepticus, but little is known about how this dosing variability affects seizure duration,” the researchers said. The investigators analyzed data from a multicenter prospective observational cohort of pediatric patients admitted with refractory status epilepticus (ie, status epilepticus did not resolve after two or more AEDs) between 2011 and 2016. The data were compiled by the Pediatric Status Epilepticus Research Group.
Researchers grouped patients by those who received a lower dose ( < 0.05 mg/kg), medium dose (0.05 mg/kg to < 0.1 mg/kg), and higher dose ( ≥ 0.1 mg/kg) of lorazepam. They used Cox proportional hazards models to assess the association between lorazepam dose and time to seizure resolution, adjusting for age, sex, presumed seizure cause, seizure duration prior to lorazepam administration, home AED use, prior neurologic conditions, and study site.
A total of 103 patients were included in the analysis. Patients had a median age of 4.5, and 48% were female. Lorazepam was administered at a median of 20 minutes after seizure onset. Twenty-eight percent of patients received a lower dose, 43% a medium dose, and 29% a higher dose. Individuals in the higher dose group were significantly more likely to experience seizure resolution sooner than patients in the medium and lower dose groups, with hazard ratios of 1.62 and 2.49, respectively. Median time to total seizure resolution following lorazepam administration was 93 minutes in the higher dose group, 160 minutes in the medium dose group, and 350 minutes in the lower dose group.
Among patients who had convulsive seizures, those in the higher dose group were more likely to experience convulsive seizure resolution sooner than those in the lower dose group (hazard ratio, 1.89). Median time to convulsive seizure resolution was 67 minutes in the higher dose group and 120 minutes in the lower dose group.
—Jake Remaly
HOUSTON—The first dose of lorazepam, when administered as a first-line antiepileptic drug (AED) for pediatric refractory status epilepticus, frequently is underdosed, and doses lower than 0.1 mg/kg are associated with increased seizure duration, according to research presented at the 70th Annual Meeting of the American Epilepsy Society (AES).
The results emphasize the importance of following AES status epilepticus guidelines, which call for lorazepam dosing of 0.1 mg/kg, said Dmitry Tchapyjnikov, MD, of Duke University School of Medicine in Durham, North Carolina, and colleagues.
“There is high variability in lorazepam dosing when used in the treatment of status epilepticus, but little is known about how this dosing variability affects seizure duration,” the researchers said. The investigators analyzed data from a multicenter prospective observational cohort of pediatric patients admitted with refractory status epilepticus (ie, status epilepticus did not resolve after two or more AEDs) between 2011 and 2016. The data were compiled by the Pediatric Status Epilepticus Research Group.
Researchers grouped patients by those who received a lower dose ( < 0.05 mg/kg), medium dose (0.05 mg/kg to < 0.1 mg/kg), and higher dose ( ≥ 0.1 mg/kg) of lorazepam. They used Cox proportional hazards models to assess the association between lorazepam dose and time to seizure resolution, adjusting for age, sex, presumed seizure cause, seizure duration prior to lorazepam administration, home AED use, prior neurologic conditions, and study site.
A total of 103 patients were included in the analysis. Patients had a median age of 4.5, and 48% were female. Lorazepam was administered at a median of 20 minutes after seizure onset. Twenty-eight percent of patients received a lower dose, 43% a medium dose, and 29% a higher dose. Individuals in the higher dose group were significantly more likely to experience seizure resolution sooner than patients in the medium and lower dose groups, with hazard ratios of 1.62 and 2.49, respectively. Median time to total seizure resolution following lorazepam administration was 93 minutes in the higher dose group, 160 minutes in the medium dose group, and 350 minutes in the lower dose group.
Among patients who had convulsive seizures, those in the higher dose group were more likely to experience convulsive seizure resolution sooner than those in the lower dose group (hazard ratio, 1.89). Median time to convulsive seizure resolution was 67 minutes in the higher dose group and 120 minutes in the lower dose group.
—Jake Remaly
HOUSTON—The first dose of lorazepam, when administered as a first-line antiepileptic drug (AED) for pediatric refractory status epilepticus, frequently is underdosed, and doses lower than 0.1 mg/kg are associated with increased seizure duration, according to research presented at the 70th Annual Meeting of the American Epilepsy Society (AES).
The results emphasize the importance of following AES status epilepticus guidelines, which call for lorazepam dosing of 0.1 mg/kg, said Dmitry Tchapyjnikov, MD, of Duke University School of Medicine in Durham, North Carolina, and colleagues.
“There is high variability in lorazepam dosing when used in the treatment of status epilepticus, but little is known about how this dosing variability affects seizure duration,” the researchers said. The investigators analyzed data from a multicenter prospective observational cohort of pediatric patients admitted with refractory status epilepticus (ie, status epilepticus did not resolve after two or more AEDs) between 2011 and 2016. The data were compiled by the Pediatric Status Epilepticus Research Group.
Researchers grouped patients by those who received a lower dose ( < 0.05 mg/kg), medium dose (0.05 mg/kg to < 0.1 mg/kg), and higher dose ( ≥ 0.1 mg/kg) of lorazepam. They used Cox proportional hazards models to assess the association between lorazepam dose and time to seizure resolution, adjusting for age, sex, presumed seizure cause, seizure duration prior to lorazepam administration, home AED use, prior neurologic conditions, and study site.
A total of 103 patients were included in the analysis. Patients had a median age of 4.5, and 48% were female. Lorazepam was administered at a median of 20 minutes after seizure onset. Twenty-eight percent of patients received a lower dose, 43% a medium dose, and 29% a higher dose. Individuals in the higher dose group were significantly more likely to experience seizure resolution sooner than patients in the medium and lower dose groups, with hazard ratios of 1.62 and 2.49, respectively. Median time to total seizure resolution following lorazepam administration was 93 minutes in the higher dose group, 160 minutes in the medium dose group, and 350 minutes in the lower dose group.
Among patients who had convulsive seizures, those in the higher dose group were more likely to experience convulsive seizure resolution sooner than those in the lower dose group (hazard ratio, 1.89). Median time to convulsive seizure resolution was 67 minutes in the higher dose group and 120 minutes in the lower dose group.
—Jake Remaly