Vascular Mass on the Posterior Neck in a Newborn

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Vascular Mass on the Posterior Neck in a Newborn

The Diagnosis: Congenital Hemangioma

Surgical resection of the mass was performed at 4 months of age without complication (Figure 1). Histopathology revealed a lobular endothelial cell proliferation within a densely fibrotic stroma, multiple thin-walled vessels, and negative immunoreactivity to glucose transporter type 1 (GLUT-1)(Figures 2 and 3). Combined with the patient’s clinical history and findings on imaging (Figure 4), the most accurate diagnosis was a congenital hemangioma (CH). The mass was determined to be a noninvoluting congenital hemangioma (NICH).

A variety of vascular anomalies manifest in newborns and can be differentiated by the patient’s clinical history—particularly whether the lesion is present at birth or develops after birth. Imaging and histopathology of the lesion(s) may be utilized when clinical examination alone is not sufficient to make a diagnosis. Histopathology and immunohistochemistry further aid in differentiating the type of vascular lesion.

FIGURE 1. A congenital hemangioma in a newborn was surgically resected without complication.

FIGURE 2. Histopathology of a congenital hemangioma revealed a lobular endothelial cell proliferation within a densely fibrotic stroma as well as multiple thin-walled vessels (H&E, original magnification ×200).

Overall, vascular anomalies are classified broadly into 2 categories based on their pathogenesis: tumors and malformations. Vascular tumors are composed of proliferating endothelial cells that have the potential to resolve spontaneously over time. Examples include CH, infantile hemangioma (IH), kaposiform hemangioendothelioma (KHE), and tufted angioma (TA). In contrast, vascular malformations (ie, arteriovenous malformations) are composed of dysplastic vessels with normal endothelial cell turnover and do not resolve without intervention.1

Congenital hemangiomas are rare vascular tumors that are fully developed at birth. These tumors proliferate in utero, enabling prenatal detection via ultrasonography as early as 12 weeks’ gestation for large heterogeneous vascular masses.2-4 Congenital hemangiomas are described as solitary, well-circumscribed, raised, violaceous lesions most commonly located in the head and neck region.4-6 Histopathologically, they are characterized by lobules of proliferating capillaries surrounded by fibrous stroma and dysplastic vascular channels.6,7

Congenital hemangiomas are categorized based on their postnatal involution patterns.2 Fetally involuting CH both develops and begins regression in utero and often is completely regressed at birth.8 Rapidly involuting CH begins regression in the first few weeks of life and usually is completely involuted by 14 months of age.6,9-11 Conversely, NICH does not regress, often requiring surgical excision due to functional and cosmetic issues.12,13 Partially involuting CH is intermediary, beginning as rapidly involuting but not involuting completely and persisting as lesions that resemble NICH.14-16 Although generally benign and asymptomatic, these tumors can cause transient thrombocytopenia and coagulopathy at birth, as seen in our patient.17,18

FIGURE 3. Immunohistochemistry of a congenital hemangioma demonstrated negative immunoreactivity to glucose transporter type 1 (GLUT-1).

FIGURE 4. Magnetic resonance imaging of a congenital hemangioma demonstrated a well-circumscribed mass with avid arterial phase enhancement.

Infantile hemangioma is the most common vascular tumor of infancy.19-21 Although a precursor lesion may be present at birth, generally this tumor becomes apparent after the first few weeks of life as a solitary vascular plaque or nodule with a predilection for the head and neck.22-25 Once it arises, IH quickly enters a period of rapid growth, followed by a period of slower continued growth, with most reaching maximum size by 3 months.22 Thereafter, IH enters a slow period of involution (range, 3–9 years)26; more recent data suggest near resolution by 5 years of age.27 Infantile hemangioma is categorized based on its depth in the skin and subcutaneous tissues and can be classified as superficial, mixed, or deep.22,24,28,29 Superficial IH appears as a red plaque and may exhibit lobulation, while deep IH can be identified as flesh-colored or blue subcutaneous masses. Mixed IH may manifest with both superficial and deep features depending on the extent of its involvement in the dermal and subcutaneous layers. The pattern of involvement may be focal, segmental, or indeterminate.24 In contrast, CH typically is a solitary vascular mass with prominent telangiectases, nodules, and radiating veins.6 Histologically, IH is composed of proliferative plump endothelial cells that form capillaries, and the lesion stains positively for GLUT-1, whereas CH does not.30

Kaposiform hemangioendothelioma is classified as a locally aggressive vascular tumor that manifests either prenatally or in early infancy.31 It is described as a solitary, ill-defined, firm, purple plaque most commonly located on the extremities and retroperitoneum.32-34 Histopathologically, these lesions are characterized by dilated lymphatic channels and irregular sheets or lobules of spindle-shaped endothelial cells infiltrating the dermis and subcutaneous fat.33,35 In contrast to CH, KHE lesions show immunoreactivity to the markers podoplanin, lymphatic vessel endothelial receptor 1, and prospero homeobox 1 protein.36,37 Notably, 70% of these tumors are complicated by the presence of Kasabach-Merritt phenomenon, a potentially life-threatening emergency that occurs when platelets are trapped within a vascular tumor, leading to the consumption of clotting factors, intralesional bleeding, and rapid enlargement of the tumor.32 The Kasabach-Merritt phenomenon manifests clinically as microangiopathic hemolytic anemia, severe thrombocytopenia, and disseminated intravascular coagulation. 38 Although CH lesions also can be associated with thrombocytopenia and coagulopathy, they generally are mild and self-limited.18

Tufted angioma is a vascular tumor that arises within the first 5 years of life as firm violaceous papules or plaques, often with associated hyperhidrosis or hypertrichosis.39,40 Although TA grows slowly for a period of time, it eventually stabilizes and persists, rarely regressing completely.41 These tumors share many similarities with KHE, and it has been suggested that they may be part of the same spectrum. 42 As with KHE, TA lesions show immunoreactivity to the markers podoplanin, lymphatic vessel endothelial receptor 1, and prospero homeobox 1 protein, which are negative in CH.36,37 Although TA also can be complicated by Kasabach-Merritt phenomenon, the incidence is much lower (up to 38%).43,44 As such, TAs tend to be recognized as more superficial benign lesions. However, they still can cause notable cosmetic and functional impairment and should be monitored closely, especially in the presence of associated symptoms or complications.

Arteriovenous malformation is a vascular lesion that results from errors during the embryonic development of vascular channels.45 Although present at birth, it may not become clinically apparent until later in life. Arteriovenous malformations enlarge postnatally, and their growth is proportional to the developmental growth of the affected individual rather than the result of endothelial proliferation.46 In infants, AVM may manifest as a faint vascular stain that can evolve over time into a pink patch associated with a palpable thrill during adolescence. 4 On Doppler flow imaging, AVMs are identified as fast-flow anomalies arising from an abnormal communication between high-pressure arterial systems and low-pressure venous systems without the presence of a capillary bed.47 One of the differentiating factors between AVM and CH is that AVMs do not regress spontaneously and tend to have high recurrence rates, even with intervention. 48 In contrast, CH can be categorized based on its postnatal involution pattern. Another distinguishing factor is that AVMs tend to be larger and more invasive than CHs.46 Therefore, early diagnosis and intervention are crucial to prevent complications such as bleeding, seizures, or neurologic deficits associated with AVMs.1

References
  1. Enjolras O, Wassef M, Chapot R. Introduction: ISSVA Classification. In: Enjolras O, Wassef M, Chapot R, eds. Color Atlas of Vascular Tumors and Vascular Malformations. Cambridge University Press; 2007:3-11.
  2. Fadell MF, Jones BV, Adams DM. Prenatal diagnosis and postnatal follow-up of rapidly involuting congenital hemangioma (RICH). Pediatr Radiol. 2011;41:1057-1060.
  3. Feygin T, Khalek N, Moldenhauer JS. Fetal brain, head, and neck tumors: prenatal imaging and management. Prenat Diagn. 2020;40:1203-1219.
  4. Foley LS, Kulungowski AM. Vascular anomalies in pediatrics. Adv Pediatr. 2015;62:227-255.
  5. Bruder E, Alaggio R, Kozakewich HPW, et al. Vascular and perivascular lesions of skin and soft tissues in children and adolescents. Pediatr Dev Pathol. 2012;15:26-61.
  6. Berenguer B, Mulliken JB, Enjolras O, et al. Rapidly involuting congenital hemangioma: clinical and histopathologic features. Pediatr Dev Pathol. 2003;6:495-510.
  7. North PE, Waner M, James CA, et al. Congenital nonprogressive hemangioma: a distinct clinicopathologic entity unlike infantile hemangioma. Arch Dermatol. 2001;137:1607-1620.
  8. Maguiness S, Uihlein LC, Liang MG, et al. Rapidly involuting congenital hemangioma with fetal involution. Pediatr Dermatol. 2015;32:321-326.
  9. Keating LJ, Soares GM, Muratore CS. Rapidly involuting congenital hemangioma. Med Health R I. 2012;95:149-152.
  10. Schafer F, Tapia M, Pinto C. Rapidly involuting congenital haemangioma. Arch Dis Child Fetal Neonatal Ed. 2014;99:F422.
  11. Boon LM, Enjolras O, Mulliken JB. Congenital hemangioma: evidence of accelerated involution. J Pediatr. 1996;128:329-335.
  12. Liang MG, Frieden IJ. Infantile and congenital hemangiomas. Semin Pediatr Surg. 2014;23:162-167.
  13. Enjolras O, Mulliken JB, Boon LM, et al. Noninvoluting congenital hemangioma: a rare cutaneous vascular anomaly. Plast Reconstr Surg. 2001;107:1647-1654.
  14. Nasseri E, Piram M, McCuaig CC, et al. Partially involuting congenital hemangiomas: a report of 8 cases and review of the literature. J Am Acad Dermatol. 2014;70:75-79.
  15. Wassef M, Blei F, Adams D, et al. Vascular anomalies classification: recommendations from the International Society for the Study of Vascular Anomalies. Pediatrics. 2015;136:E203-E214.
  16. Boull C, Maguiness SM. Congenital hemangiomas. Semin Cutan Med Surg. 2016;35:124-127.
  17. Drolet BA, Frommelt PC, Chamlin SL, et al. Initiation and use of propranolol for infantile hemangioma: report of a consensus conference. Pediatrics. 2013;131:128-140.
  18. Baselga E, Cordisco MR, Garzon M, et al. Rapidly involuting congenital haemangioma associated with transient thrombocytopenia and coagulopathy: a case series. Br J Dermatol. 2008;158:1363-1370.
  19. Kanada KN, Merin MR, Munden A, et al. A prospective study of cutaneous findings in newborns in the United States: correlation with race, ethnicity, and gestational status using updated classification and nomenclature. J Pediatr. 2012;161:240-245.
  20. Munden A, Butschek R, Tom WL, et al. Prospective study of infantile haemangiomas: incidence, clinical characteristics and association with placental anomalies. Br J Dermatol. 2014;170:907-913.
  21. Léauté-Labrèze C, Harper JI, Hoeger PH. Infantile haemangioma. Lancet. 2017;390:85-94.
  22. Chang LC, Haggstrom AN, Drolet BA, et al. Growth characteristics of infantile hemangiomas: implications for management. Pediatrics. 2008;122:360-367.
  23. Hidano A, Nakajima S. Earliest features of the strawberry mark in the newborn. Br J Dermatol. 1972;87:138-144.
  24. Martinez-Perez D, Fein NA, Boon LM, et al. Not all hemangiomas look like strawberries: uncommon presentations of the most common tumor of infancy. Pediatr Dermatol. 1995;12:1-6.
  25. Payne MM, Moyer F, Marcks KM, et al. The precursor to the hemangioma. Plast Reconstr Surg. 1966;38:64-67.
  26. Bowers RE, Graham EA, Tomlinson KM. The natural history of the strawberry nevus. Arch Dermatol. 1960;82:667-680.
  27. Couto RA, Maclellan RA, Zurakowski D, et al. Infantile hemangioma: clinical assessment of the involuting phase and implications for management. Plast Reconstr Surg. 2012;130:619-624.
  28. Drolet BA, Esterly NB, Frieden IJ. Hemangiomas in children. N Engl J Med. 1999;341:173-181.
  29. Chiller KG, Passaro D, Frieden IJ. Hemangiomas of infancy: clinical characteristics, morphologic subtypes, and their relationship to race, ethnicity, and sex. Arch Dermatol. 2002;138:1567-1576.
  30. North PE, Waner M, Mizeracki A, et al. GLUT1: a newly discovered immunohistochemical marker for juvenile hemangiomas. Hum Pathol. 2000;31:11-22.
  31. Gruman A, Liang MG, Mulliken JB, et al. Kaposiform hemangioendothelioma without Kasabach-Merritt phenomenon. J Am Acad Dermatol. 2005;52:616-622.
  32. Croteau SE, Liang MG, Kozakewich HP, et al. Kaposiform hemangioendothelioma: atypical features and risks of Kasabach- Merritt phenomenon in 107 referrals. J Pediatr. 2013;162:142-147.
  33. Zukerberg LR, Nickoloff BJ, Weiss SW. Kaposiform hemangioendothelioma of infancy and childhood. an aggressive neoplasm associated with Kasabach-Merritt syndrome and lymphangiomatosis. Am J Surg Pathol. 1993;17:321-328.
  34. Mac-Moune Lai F, To KF, Choi PC, et al. Kaposiform hemangioendothelioma: five patients with cutaneous lesion and long follow-up. Mod Pathol. 2001;14:1087-1092.
  35. O’Rafferty C, O’Regan GM, Irvine AD, et al. Recent advances in the pathobiology and management of Kasabach-Merritt phenomenon. Br J Haematol. 2015;171:38-51.
  36. Le Huu AR, Jokinen CH, Rubin BP, et al. Expression of prox1, lymphatic endothelial nuclear transcription factor, in kaposiform hemangioendothelioma and tufted angioma. Am J Surg Pathol. 2010;34:1563-1573.
  37. Debelenko LV, Perez-Atayde AR, Mulliken JB, et al. D2-40 immuno-histochemical analysis of pediatric vascular tumors reveals positivity in kaposiform hemangioendothelioma. Mod Pathol. 2005;18:1454-1460.
  38. Haisley-Royster C, Enjolras O, Frieden IJ, et al. Kasabach-Merritt phenomenon: a retrospective study of treatment with vincristine. J Pediatr Hematol Oncol. 2002;24:459-462.
  39. Wilmer A, Kaatz M, Bocker T, et al. Tufted angioma. Eur J Dermatol. 1999;9:51-53.
  40. Herron MD, Coffin CM, Vanderhooft SL. Tufted angiomas: variability of the clinical morphology. Pediatr Dermatol. 2002;19:394-401.
  41. North PE. Pediatric vascular tumors and malformations. Surg Pathol Clin. 2010,3:455-494.
  42. Chu CY, Hsiao CH, Chiu HC. Transformation between kaposiform hemangioendothelioma and tufted angioma. Dermatology. 2003;206:334-337.
  43. Osio A, Fraitag S, Hadj-Rabia S, et al. Clinical spectrum of tufted angiomas in childhood: a report of 13 cases and a review of the literature. Arch Dermatol. 2010;146:758-763.
  44. Johnson EF, Davis DM, Tollefson MM, et al. Vascular tumors in infants: case report and review of clinical, histopathologic, and immunohistochemical characteristics of infantile hemangioma, pyogenic granuloma, noninvoluting congenital hemangioma, tufted angioma, and kaposiform hemangioendothelioma. Am J Dermatopathol. 2018;40:231-239.
  45. Christison-Lagay ER, Fishman SJ. Vascular anomalies. Surg Clin North Am. 2006;86:393-425.
  46. Liu AS, Mulliken JB, Zurakowski D, et al. Extracranial arteriovenous malformations: natural progression and recurrence after treatment. Plast Reconstr Surg. 2010;125:1185-1194.
  47. Young AE, Mulliken JB. Arteriovenous malformations. In: Mulliken JB, Young AE, eds. Vascular Birthmarks: Haemangiomas and Malformations. WB Saunders; 1988:228-245.
  48. Duggan EM, Fishman SJ. Vascular anomalies. In: Holcomb GW III, Murphy JP, St Peter SD, eds. Holcomb and Ashcraft’s Pediatric Surgery. 7th edition. Elsevier; 2019:1147-1170.
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Drs. Hesari, Alhajj, and Wang report no conflicts of interest. Dr. Shah has received royalties income from UpToDate.

Correspondence: Mandy Alhajj, DO, University Hospitals Cleveland Medical Center, Department of Dermatology, 11100 Euclid Ave, Cleveland, OH 44106 (Mandy.Alhajj2@UHhospitals.org).

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Dr. Hesari is from the Lake Erie College of Osteopathic Medicine, Bradenton, Florida. Dr. Alhajj is from the Department of Dermatology, University Hospitals Cleveland Medical Center, Ohio. Drs. Wang and Shah are from Rainbow Babies & Children’s Hospital, University Hospitals Cleveland Medical Center. Dr. Wang is from the Department of Pediatric Plastic Surgery and Dr. Shah is from the Department of Pediatric Dermatology.

Drs. Hesari, Alhajj, and Wang report no conflicts of interest. Dr. Shah has received royalties income from UpToDate.

Correspondence: Mandy Alhajj, DO, University Hospitals Cleveland Medical Center, Department of Dermatology, 11100 Euclid Ave, Cleveland, OH 44106 (Mandy.Alhajj2@UHhospitals.org).

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Dr. Hesari is from the Lake Erie College of Osteopathic Medicine, Bradenton, Florida. Dr. Alhajj is from the Department of Dermatology, University Hospitals Cleveland Medical Center, Ohio. Drs. Wang and Shah are from Rainbow Babies & Children’s Hospital, University Hospitals Cleveland Medical Center. Dr. Wang is from the Department of Pediatric Plastic Surgery and Dr. Shah is from the Department of Pediatric Dermatology.

Drs. Hesari, Alhajj, and Wang report no conflicts of interest. Dr. Shah has received royalties income from UpToDate.

Correspondence: Mandy Alhajj, DO, University Hospitals Cleveland Medical Center, Department of Dermatology, 11100 Euclid Ave, Cleveland, OH 44106 (Mandy.Alhajj2@UHhospitals.org).

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The Diagnosis: Congenital Hemangioma

Surgical resection of the mass was performed at 4 months of age without complication (Figure 1). Histopathology revealed a lobular endothelial cell proliferation within a densely fibrotic stroma, multiple thin-walled vessels, and negative immunoreactivity to glucose transporter type 1 (GLUT-1)(Figures 2 and 3). Combined with the patient’s clinical history and findings on imaging (Figure 4), the most accurate diagnosis was a congenital hemangioma (CH). The mass was determined to be a noninvoluting congenital hemangioma (NICH).

A variety of vascular anomalies manifest in newborns and can be differentiated by the patient’s clinical history—particularly whether the lesion is present at birth or develops after birth. Imaging and histopathology of the lesion(s) may be utilized when clinical examination alone is not sufficient to make a diagnosis. Histopathology and immunohistochemistry further aid in differentiating the type of vascular lesion.

FIGURE 1. A congenital hemangioma in a newborn was surgically resected without complication.

FIGURE 2. Histopathology of a congenital hemangioma revealed a lobular endothelial cell proliferation within a densely fibrotic stroma as well as multiple thin-walled vessels (H&E, original magnification ×200).

Overall, vascular anomalies are classified broadly into 2 categories based on their pathogenesis: tumors and malformations. Vascular tumors are composed of proliferating endothelial cells that have the potential to resolve spontaneously over time. Examples include CH, infantile hemangioma (IH), kaposiform hemangioendothelioma (KHE), and tufted angioma (TA). In contrast, vascular malformations (ie, arteriovenous malformations) are composed of dysplastic vessels with normal endothelial cell turnover and do not resolve without intervention.1

Congenital hemangiomas are rare vascular tumors that are fully developed at birth. These tumors proliferate in utero, enabling prenatal detection via ultrasonography as early as 12 weeks’ gestation for large heterogeneous vascular masses.2-4 Congenital hemangiomas are described as solitary, well-circumscribed, raised, violaceous lesions most commonly located in the head and neck region.4-6 Histopathologically, they are characterized by lobules of proliferating capillaries surrounded by fibrous stroma and dysplastic vascular channels.6,7

Congenital hemangiomas are categorized based on their postnatal involution patterns.2 Fetally involuting CH both develops and begins regression in utero and often is completely regressed at birth.8 Rapidly involuting CH begins regression in the first few weeks of life and usually is completely involuted by 14 months of age.6,9-11 Conversely, NICH does not regress, often requiring surgical excision due to functional and cosmetic issues.12,13 Partially involuting CH is intermediary, beginning as rapidly involuting but not involuting completely and persisting as lesions that resemble NICH.14-16 Although generally benign and asymptomatic, these tumors can cause transient thrombocytopenia and coagulopathy at birth, as seen in our patient.17,18

FIGURE 3. Immunohistochemistry of a congenital hemangioma demonstrated negative immunoreactivity to glucose transporter type 1 (GLUT-1).

FIGURE 4. Magnetic resonance imaging of a congenital hemangioma demonstrated a well-circumscribed mass with avid arterial phase enhancement.

Infantile hemangioma is the most common vascular tumor of infancy.19-21 Although a precursor lesion may be present at birth, generally this tumor becomes apparent after the first few weeks of life as a solitary vascular plaque or nodule with a predilection for the head and neck.22-25 Once it arises, IH quickly enters a period of rapid growth, followed by a period of slower continued growth, with most reaching maximum size by 3 months.22 Thereafter, IH enters a slow period of involution (range, 3–9 years)26; more recent data suggest near resolution by 5 years of age.27 Infantile hemangioma is categorized based on its depth in the skin and subcutaneous tissues and can be classified as superficial, mixed, or deep.22,24,28,29 Superficial IH appears as a red plaque and may exhibit lobulation, while deep IH can be identified as flesh-colored or blue subcutaneous masses. Mixed IH may manifest with both superficial and deep features depending on the extent of its involvement in the dermal and subcutaneous layers. The pattern of involvement may be focal, segmental, or indeterminate.24 In contrast, CH typically is a solitary vascular mass with prominent telangiectases, nodules, and radiating veins.6 Histologically, IH is composed of proliferative plump endothelial cells that form capillaries, and the lesion stains positively for GLUT-1, whereas CH does not.30

Kaposiform hemangioendothelioma is classified as a locally aggressive vascular tumor that manifests either prenatally or in early infancy.31 It is described as a solitary, ill-defined, firm, purple plaque most commonly located on the extremities and retroperitoneum.32-34 Histopathologically, these lesions are characterized by dilated lymphatic channels and irregular sheets or lobules of spindle-shaped endothelial cells infiltrating the dermis and subcutaneous fat.33,35 In contrast to CH, KHE lesions show immunoreactivity to the markers podoplanin, lymphatic vessel endothelial receptor 1, and prospero homeobox 1 protein.36,37 Notably, 70% of these tumors are complicated by the presence of Kasabach-Merritt phenomenon, a potentially life-threatening emergency that occurs when platelets are trapped within a vascular tumor, leading to the consumption of clotting factors, intralesional bleeding, and rapid enlargement of the tumor.32 The Kasabach-Merritt phenomenon manifests clinically as microangiopathic hemolytic anemia, severe thrombocytopenia, and disseminated intravascular coagulation. 38 Although CH lesions also can be associated with thrombocytopenia and coagulopathy, they generally are mild and self-limited.18

Tufted angioma is a vascular tumor that arises within the first 5 years of life as firm violaceous papules or plaques, often with associated hyperhidrosis or hypertrichosis.39,40 Although TA grows slowly for a period of time, it eventually stabilizes and persists, rarely regressing completely.41 These tumors share many similarities with KHE, and it has been suggested that they may be part of the same spectrum. 42 As with KHE, TA lesions show immunoreactivity to the markers podoplanin, lymphatic vessel endothelial receptor 1, and prospero homeobox 1 protein, which are negative in CH.36,37 Although TA also can be complicated by Kasabach-Merritt phenomenon, the incidence is much lower (up to 38%).43,44 As such, TAs tend to be recognized as more superficial benign lesions. However, they still can cause notable cosmetic and functional impairment and should be monitored closely, especially in the presence of associated symptoms or complications.

Arteriovenous malformation is a vascular lesion that results from errors during the embryonic development of vascular channels.45 Although present at birth, it may not become clinically apparent until later in life. Arteriovenous malformations enlarge postnatally, and their growth is proportional to the developmental growth of the affected individual rather than the result of endothelial proliferation.46 In infants, AVM may manifest as a faint vascular stain that can evolve over time into a pink patch associated with a palpable thrill during adolescence. 4 On Doppler flow imaging, AVMs are identified as fast-flow anomalies arising from an abnormal communication between high-pressure arterial systems and low-pressure venous systems without the presence of a capillary bed.47 One of the differentiating factors between AVM and CH is that AVMs do not regress spontaneously and tend to have high recurrence rates, even with intervention. 48 In contrast, CH can be categorized based on its postnatal involution pattern. Another distinguishing factor is that AVMs tend to be larger and more invasive than CHs.46 Therefore, early diagnosis and intervention are crucial to prevent complications such as bleeding, seizures, or neurologic deficits associated with AVMs.1

The Diagnosis: Congenital Hemangioma

Surgical resection of the mass was performed at 4 months of age without complication (Figure 1). Histopathology revealed a lobular endothelial cell proliferation within a densely fibrotic stroma, multiple thin-walled vessels, and negative immunoreactivity to glucose transporter type 1 (GLUT-1)(Figures 2 and 3). Combined with the patient’s clinical history and findings on imaging (Figure 4), the most accurate diagnosis was a congenital hemangioma (CH). The mass was determined to be a noninvoluting congenital hemangioma (NICH).

A variety of vascular anomalies manifest in newborns and can be differentiated by the patient’s clinical history—particularly whether the lesion is present at birth or develops after birth. Imaging and histopathology of the lesion(s) may be utilized when clinical examination alone is not sufficient to make a diagnosis. Histopathology and immunohistochemistry further aid in differentiating the type of vascular lesion.

FIGURE 1. A congenital hemangioma in a newborn was surgically resected without complication.

FIGURE 2. Histopathology of a congenital hemangioma revealed a lobular endothelial cell proliferation within a densely fibrotic stroma as well as multiple thin-walled vessels (H&E, original magnification ×200).

Overall, vascular anomalies are classified broadly into 2 categories based on their pathogenesis: tumors and malformations. Vascular tumors are composed of proliferating endothelial cells that have the potential to resolve spontaneously over time. Examples include CH, infantile hemangioma (IH), kaposiform hemangioendothelioma (KHE), and tufted angioma (TA). In contrast, vascular malformations (ie, arteriovenous malformations) are composed of dysplastic vessels with normal endothelial cell turnover and do not resolve without intervention.1

Congenital hemangiomas are rare vascular tumors that are fully developed at birth. These tumors proliferate in utero, enabling prenatal detection via ultrasonography as early as 12 weeks’ gestation for large heterogeneous vascular masses.2-4 Congenital hemangiomas are described as solitary, well-circumscribed, raised, violaceous lesions most commonly located in the head and neck region.4-6 Histopathologically, they are characterized by lobules of proliferating capillaries surrounded by fibrous stroma and dysplastic vascular channels.6,7

Congenital hemangiomas are categorized based on their postnatal involution patterns.2 Fetally involuting CH both develops and begins regression in utero and often is completely regressed at birth.8 Rapidly involuting CH begins regression in the first few weeks of life and usually is completely involuted by 14 months of age.6,9-11 Conversely, NICH does not regress, often requiring surgical excision due to functional and cosmetic issues.12,13 Partially involuting CH is intermediary, beginning as rapidly involuting but not involuting completely and persisting as lesions that resemble NICH.14-16 Although generally benign and asymptomatic, these tumors can cause transient thrombocytopenia and coagulopathy at birth, as seen in our patient.17,18

FIGURE 3. Immunohistochemistry of a congenital hemangioma demonstrated negative immunoreactivity to glucose transporter type 1 (GLUT-1).

FIGURE 4. Magnetic resonance imaging of a congenital hemangioma demonstrated a well-circumscribed mass with avid arterial phase enhancement.

Infantile hemangioma is the most common vascular tumor of infancy.19-21 Although a precursor lesion may be present at birth, generally this tumor becomes apparent after the first few weeks of life as a solitary vascular plaque or nodule with a predilection for the head and neck.22-25 Once it arises, IH quickly enters a period of rapid growth, followed by a period of slower continued growth, with most reaching maximum size by 3 months.22 Thereafter, IH enters a slow period of involution (range, 3–9 years)26; more recent data suggest near resolution by 5 years of age.27 Infantile hemangioma is categorized based on its depth in the skin and subcutaneous tissues and can be classified as superficial, mixed, or deep.22,24,28,29 Superficial IH appears as a red plaque and may exhibit lobulation, while deep IH can be identified as flesh-colored or blue subcutaneous masses. Mixed IH may manifest with both superficial and deep features depending on the extent of its involvement in the dermal and subcutaneous layers. The pattern of involvement may be focal, segmental, or indeterminate.24 In contrast, CH typically is a solitary vascular mass with prominent telangiectases, nodules, and radiating veins.6 Histologically, IH is composed of proliferative plump endothelial cells that form capillaries, and the lesion stains positively for GLUT-1, whereas CH does not.30

Kaposiform hemangioendothelioma is classified as a locally aggressive vascular tumor that manifests either prenatally or in early infancy.31 It is described as a solitary, ill-defined, firm, purple plaque most commonly located on the extremities and retroperitoneum.32-34 Histopathologically, these lesions are characterized by dilated lymphatic channels and irregular sheets or lobules of spindle-shaped endothelial cells infiltrating the dermis and subcutaneous fat.33,35 In contrast to CH, KHE lesions show immunoreactivity to the markers podoplanin, lymphatic vessel endothelial receptor 1, and prospero homeobox 1 protein.36,37 Notably, 70% of these tumors are complicated by the presence of Kasabach-Merritt phenomenon, a potentially life-threatening emergency that occurs when platelets are trapped within a vascular tumor, leading to the consumption of clotting factors, intralesional bleeding, and rapid enlargement of the tumor.32 The Kasabach-Merritt phenomenon manifests clinically as microangiopathic hemolytic anemia, severe thrombocytopenia, and disseminated intravascular coagulation. 38 Although CH lesions also can be associated with thrombocytopenia and coagulopathy, they generally are mild and self-limited.18

Tufted angioma is a vascular tumor that arises within the first 5 years of life as firm violaceous papules or plaques, often with associated hyperhidrosis or hypertrichosis.39,40 Although TA grows slowly for a period of time, it eventually stabilizes and persists, rarely regressing completely.41 These tumors share many similarities with KHE, and it has been suggested that they may be part of the same spectrum. 42 As with KHE, TA lesions show immunoreactivity to the markers podoplanin, lymphatic vessel endothelial receptor 1, and prospero homeobox 1 protein, which are negative in CH.36,37 Although TA also can be complicated by Kasabach-Merritt phenomenon, the incidence is much lower (up to 38%).43,44 As such, TAs tend to be recognized as more superficial benign lesions. However, they still can cause notable cosmetic and functional impairment and should be monitored closely, especially in the presence of associated symptoms or complications.

Arteriovenous malformation is a vascular lesion that results from errors during the embryonic development of vascular channels.45 Although present at birth, it may not become clinically apparent until later in life. Arteriovenous malformations enlarge postnatally, and their growth is proportional to the developmental growth of the affected individual rather than the result of endothelial proliferation.46 In infants, AVM may manifest as a faint vascular stain that can evolve over time into a pink patch associated with a palpable thrill during adolescence. 4 On Doppler flow imaging, AVMs are identified as fast-flow anomalies arising from an abnormal communication between high-pressure arterial systems and low-pressure venous systems without the presence of a capillary bed.47 One of the differentiating factors between AVM and CH is that AVMs do not regress spontaneously and tend to have high recurrence rates, even with intervention. 48 In contrast, CH can be categorized based on its postnatal involution pattern. Another distinguishing factor is that AVMs tend to be larger and more invasive than CHs.46 Therefore, early diagnosis and intervention are crucial to prevent complications such as bleeding, seizures, or neurologic deficits associated with AVMs.1

References
  1. Enjolras O, Wassef M, Chapot R. Introduction: ISSVA Classification. In: Enjolras O, Wassef M, Chapot R, eds. Color Atlas of Vascular Tumors and Vascular Malformations. Cambridge University Press; 2007:3-11.
  2. Fadell MF, Jones BV, Adams DM. Prenatal diagnosis and postnatal follow-up of rapidly involuting congenital hemangioma (RICH). Pediatr Radiol. 2011;41:1057-1060.
  3. Feygin T, Khalek N, Moldenhauer JS. Fetal brain, head, and neck tumors: prenatal imaging and management. Prenat Diagn. 2020;40:1203-1219.
  4. Foley LS, Kulungowski AM. Vascular anomalies in pediatrics. Adv Pediatr. 2015;62:227-255.
  5. Bruder E, Alaggio R, Kozakewich HPW, et al. Vascular and perivascular lesions of skin and soft tissues in children and adolescents. Pediatr Dev Pathol. 2012;15:26-61.
  6. Berenguer B, Mulliken JB, Enjolras O, et al. Rapidly involuting congenital hemangioma: clinical and histopathologic features. Pediatr Dev Pathol. 2003;6:495-510.
  7. North PE, Waner M, James CA, et al. Congenital nonprogressive hemangioma: a distinct clinicopathologic entity unlike infantile hemangioma. Arch Dermatol. 2001;137:1607-1620.
  8. Maguiness S, Uihlein LC, Liang MG, et al. Rapidly involuting congenital hemangioma with fetal involution. Pediatr Dermatol. 2015;32:321-326.
  9. Keating LJ, Soares GM, Muratore CS. Rapidly involuting congenital hemangioma. Med Health R I. 2012;95:149-152.
  10. Schafer F, Tapia M, Pinto C. Rapidly involuting congenital haemangioma. Arch Dis Child Fetal Neonatal Ed. 2014;99:F422.
  11. Boon LM, Enjolras O, Mulliken JB. Congenital hemangioma: evidence of accelerated involution. J Pediatr. 1996;128:329-335.
  12. Liang MG, Frieden IJ. Infantile and congenital hemangiomas. Semin Pediatr Surg. 2014;23:162-167.
  13. Enjolras O, Mulliken JB, Boon LM, et al. Noninvoluting congenital hemangioma: a rare cutaneous vascular anomaly. Plast Reconstr Surg. 2001;107:1647-1654.
  14. Nasseri E, Piram M, McCuaig CC, et al. Partially involuting congenital hemangiomas: a report of 8 cases and review of the literature. J Am Acad Dermatol. 2014;70:75-79.
  15. Wassef M, Blei F, Adams D, et al. Vascular anomalies classification: recommendations from the International Society for the Study of Vascular Anomalies. Pediatrics. 2015;136:E203-E214.
  16. Boull C, Maguiness SM. Congenital hemangiomas. Semin Cutan Med Surg. 2016;35:124-127.
  17. Drolet BA, Frommelt PC, Chamlin SL, et al. Initiation and use of propranolol for infantile hemangioma: report of a consensus conference. Pediatrics. 2013;131:128-140.
  18. Baselga E, Cordisco MR, Garzon M, et al. Rapidly involuting congenital haemangioma associated with transient thrombocytopenia and coagulopathy: a case series. Br J Dermatol. 2008;158:1363-1370.
  19. Kanada KN, Merin MR, Munden A, et al. A prospective study of cutaneous findings in newborns in the United States: correlation with race, ethnicity, and gestational status using updated classification and nomenclature. J Pediatr. 2012;161:240-245.
  20. Munden A, Butschek R, Tom WL, et al. Prospective study of infantile haemangiomas: incidence, clinical characteristics and association with placental anomalies. Br J Dermatol. 2014;170:907-913.
  21. Léauté-Labrèze C, Harper JI, Hoeger PH. Infantile haemangioma. Lancet. 2017;390:85-94.
  22. Chang LC, Haggstrom AN, Drolet BA, et al. Growth characteristics of infantile hemangiomas: implications for management. Pediatrics. 2008;122:360-367.
  23. Hidano A, Nakajima S. Earliest features of the strawberry mark in the newborn. Br J Dermatol. 1972;87:138-144.
  24. Martinez-Perez D, Fein NA, Boon LM, et al. Not all hemangiomas look like strawberries: uncommon presentations of the most common tumor of infancy. Pediatr Dermatol. 1995;12:1-6.
  25. Payne MM, Moyer F, Marcks KM, et al. The precursor to the hemangioma. Plast Reconstr Surg. 1966;38:64-67.
  26. Bowers RE, Graham EA, Tomlinson KM. The natural history of the strawberry nevus. Arch Dermatol. 1960;82:667-680.
  27. Couto RA, Maclellan RA, Zurakowski D, et al. Infantile hemangioma: clinical assessment of the involuting phase and implications for management. Plast Reconstr Surg. 2012;130:619-624.
  28. Drolet BA, Esterly NB, Frieden IJ. Hemangiomas in children. N Engl J Med. 1999;341:173-181.
  29. Chiller KG, Passaro D, Frieden IJ. Hemangiomas of infancy: clinical characteristics, morphologic subtypes, and their relationship to race, ethnicity, and sex. Arch Dermatol. 2002;138:1567-1576.
  30. North PE, Waner M, Mizeracki A, et al. GLUT1: a newly discovered immunohistochemical marker for juvenile hemangiomas. Hum Pathol. 2000;31:11-22.
  31. Gruman A, Liang MG, Mulliken JB, et al. Kaposiform hemangioendothelioma without Kasabach-Merritt phenomenon. J Am Acad Dermatol. 2005;52:616-622.
  32. Croteau SE, Liang MG, Kozakewich HP, et al. Kaposiform hemangioendothelioma: atypical features and risks of Kasabach- Merritt phenomenon in 107 referrals. J Pediatr. 2013;162:142-147.
  33. Zukerberg LR, Nickoloff BJ, Weiss SW. Kaposiform hemangioendothelioma of infancy and childhood. an aggressive neoplasm associated with Kasabach-Merritt syndrome and lymphangiomatosis. Am J Surg Pathol. 1993;17:321-328.
  34. Mac-Moune Lai F, To KF, Choi PC, et al. Kaposiform hemangioendothelioma: five patients with cutaneous lesion and long follow-up. Mod Pathol. 2001;14:1087-1092.
  35. O’Rafferty C, O’Regan GM, Irvine AD, et al. Recent advances in the pathobiology and management of Kasabach-Merritt phenomenon. Br J Haematol. 2015;171:38-51.
  36. Le Huu AR, Jokinen CH, Rubin BP, et al. Expression of prox1, lymphatic endothelial nuclear transcription factor, in kaposiform hemangioendothelioma and tufted angioma. Am J Surg Pathol. 2010;34:1563-1573.
  37. Debelenko LV, Perez-Atayde AR, Mulliken JB, et al. D2-40 immuno-histochemical analysis of pediatric vascular tumors reveals positivity in kaposiform hemangioendothelioma. Mod Pathol. 2005;18:1454-1460.
  38. Haisley-Royster C, Enjolras O, Frieden IJ, et al. Kasabach-Merritt phenomenon: a retrospective study of treatment with vincristine. J Pediatr Hematol Oncol. 2002;24:459-462.
  39. Wilmer A, Kaatz M, Bocker T, et al. Tufted angioma. Eur J Dermatol. 1999;9:51-53.
  40. Herron MD, Coffin CM, Vanderhooft SL. Tufted angiomas: variability of the clinical morphology. Pediatr Dermatol. 2002;19:394-401.
  41. North PE. Pediatric vascular tumors and malformations. Surg Pathol Clin. 2010,3:455-494.
  42. Chu CY, Hsiao CH, Chiu HC. Transformation between kaposiform hemangioendothelioma and tufted angioma. Dermatology. 2003;206:334-337.
  43. Osio A, Fraitag S, Hadj-Rabia S, et al. Clinical spectrum of tufted angiomas in childhood: a report of 13 cases and a review of the literature. Arch Dermatol. 2010;146:758-763.
  44. Johnson EF, Davis DM, Tollefson MM, et al. Vascular tumors in infants: case report and review of clinical, histopathologic, and immunohistochemical characteristics of infantile hemangioma, pyogenic granuloma, noninvoluting congenital hemangioma, tufted angioma, and kaposiform hemangioendothelioma. Am J Dermatopathol. 2018;40:231-239.
  45. Christison-Lagay ER, Fishman SJ. Vascular anomalies. Surg Clin North Am. 2006;86:393-425.
  46. Liu AS, Mulliken JB, Zurakowski D, et al. Extracranial arteriovenous malformations: natural progression and recurrence after treatment. Plast Reconstr Surg. 2010;125:1185-1194.
  47. Young AE, Mulliken JB. Arteriovenous malformations. In: Mulliken JB, Young AE, eds. Vascular Birthmarks: Haemangiomas and Malformations. WB Saunders; 1988:228-245.
  48. Duggan EM, Fishman SJ. Vascular anomalies. In: Holcomb GW III, Murphy JP, St Peter SD, eds. Holcomb and Ashcraft’s Pediatric Surgery. 7th edition. Elsevier; 2019:1147-1170.
References
  1. Enjolras O, Wassef M, Chapot R. Introduction: ISSVA Classification. In: Enjolras O, Wassef M, Chapot R, eds. Color Atlas of Vascular Tumors and Vascular Malformations. Cambridge University Press; 2007:3-11.
  2. Fadell MF, Jones BV, Adams DM. Prenatal diagnosis and postnatal follow-up of rapidly involuting congenital hemangioma (RICH). Pediatr Radiol. 2011;41:1057-1060.
  3. Feygin T, Khalek N, Moldenhauer JS. Fetal brain, head, and neck tumors: prenatal imaging and management. Prenat Diagn. 2020;40:1203-1219.
  4. Foley LS, Kulungowski AM. Vascular anomalies in pediatrics. Adv Pediatr. 2015;62:227-255.
  5. Bruder E, Alaggio R, Kozakewich HPW, et al. Vascular and perivascular lesions of skin and soft tissues in children and adolescents. Pediatr Dev Pathol. 2012;15:26-61.
  6. Berenguer B, Mulliken JB, Enjolras O, et al. Rapidly involuting congenital hemangioma: clinical and histopathologic features. Pediatr Dev Pathol. 2003;6:495-510.
  7. North PE, Waner M, James CA, et al. Congenital nonprogressive hemangioma: a distinct clinicopathologic entity unlike infantile hemangioma. Arch Dermatol. 2001;137:1607-1620.
  8. Maguiness S, Uihlein LC, Liang MG, et al. Rapidly involuting congenital hemangioma with fetal involution. Pediatr Dermatol. 2015;32:321-326.
  9. Keating LJ, Soares GM, Muratore CS. Rapidly involuting congenital hemangioma. Med Health R I. 2012;95:149-152.
  10. Schafer F, Tapia M, Pinto C. Rapidly involuting congenital haemangioma. Arch Dis Child Fetal Neonatal Ed. 2014;99:F422.
  11. Boon LM, Enjolras O, Mulliken JB. Congenital hemangioma: evidence of accelerated involution. J Pediatr. 1996;128:329-335.
  12. Liang MG, Frieden IJ. Infantile and congenital hemangiomas. Semin Pediatr Surg. 2014;23:162-167.
  13. Enjolras O, Mulliken JB, Boon LM, et al. Noninvoluting congenital hemangioma: a rare cutaneous vascular anomaly. Plast Reconstr Surg. 2001;107:1647-1654.
  14. Nasseri E, Piram M, McCuaig CC, et al. Partially involuting congenital hemangiomas: a report of 8 cases and review of the literature. J Am Acad Dermatol. 2014;70:75-79.
  15. Wassef M, Blei F, Adams D, et al. Vascular anomalies classification: recommendations from the International Society for the Study of Vascular Anomalies. Pediatrics. 2015;136:E203-E214.
  16. Boull C, Maguiness SM. Congenital hemangiomas. Semin Cutan Med Surg. 2016;35:124-127.
  17. Drolet BA, Frommelt PC, Chamlin SL, et al. Initiation and use of propranolol for infantile hemangioma: report of a consensus conference. Pediatrics. 2013;131:128-140.
  18. Baselga E, Cordisco MR, Garzon M, et al. Rapidly involuting congenital haemangioma associated with transient thrombocytopenia and coagulopathy: a case series. Br J Dermatol. 2008;158:1363-1370.
  19. Kanada KN, Merin MR, Munden A, et al. A prospective study of cutaneous findings in newborns in the United States: correlation with race, ethnicity, and gestational status using updated classification and nomenclature. J Pediatr. 2012;161:240-245.
  20. Munden A, Butschek R, Tom WL, et al. Prospective study of infantile haemangiomas: incidence, clinical characteristics and association with placental anomalies. Br J Dermatol. 2014;170:907-913.
  21. Léauté-Labrèze C, Harper JI, Hoeger PH. Infantile haemangioma. Lancet. 2017;390:85-94.
  22. Chang LC, Haggstrom AN, Drolet BA, et al. Growth characteristics of infantile hemangiomas: implications for management. Pediatrics. 2008;122:360-367.
  23. Hidano A, Nakajima S. Earliest features of the strawberry mark in the newborn. Br J Dermatol. 1972;87:138-144.
  24. Martinez-Perez D, Fein NA, Boon LM, et al. Not all hemangiomas look like strawberries: uncommon presentations of the most common tumor of infancy. Pediatr Dermatol. 1995;12:1-6.
  25. Payne MM, Moyer F, Marcks KM, et al. The precursor to the hemangioma. Plast Reconstr Surg. 1966;38:64-67.
  26. Bowers RE, Graham EA, Tomlinson KM. The natural history of the strawberry nevus. Arch Dermatol. 1960;82:667-680.
  27. Couto RA, Maclellan RA, Zurakowski D, et al. Infantile hemangioma: clinical assessment of the involuting phase and implications for management. Plast Reconstr Surg. 2012;130:619-624.
  28. Drolet BA, Esterly NB, Frieden IJ. Hemangiomas in children. N Engl J Med. 1999;341:173-181.
  29. Chiller KG, Passaro D, Frieden IJ. Hemangiomas of infancy: clinical characteristics, morphologic subtypes, and their relationship to race, ethnicity, and sex. Arch Dermatol. 2002;138:1567-1576.
  30. North PE, Waner M, Mizeracki A, et al. GLUT1: a newly discovered immunohistochemical marker for juvenile hemangiomas. Hum Pathol. 2000;31:11-22.
  31. Gruman A, Liang MG, Mulliken JB, et al. Kaposiform hemangioendothelioma without Kasabach-Merritt phenomenon. J Am Acad Dermatol. 2005;52:616-622.
  32. Croteau SE, Liang MG, Kozakewich HP, et al. Kaposiform hemangioendothelioma: atypical features and risks of Kasabach- Merritt phenomenon in 107 referrals. J Pediatr. 2013;162:142-147.
  33. Zukerberg LR, Nickoloff BJ, Weiss SW. Kaposiform hemangioendothelioma of infancy and childhood. an aggressive neoplasm associated with Kasabach-Merritt syndrome and lymphangiomatosis. Am J Surg Pathol. 1993;17:321-328.
  34. Mac-Moune Lai F, To KF, Choi PC, et al. Kaposiform hemangioendothelioma: five patients with cutaneous lesion and long follow-up. Mod Pathol. 2001;14:1087-1092.
  35. O’Rafferty C, O’Regan GM, Irvine AD, et al. Recent advances in the pathobiology and management of Kasabach-Merritt phenomenon. Br J Haematol. 2015;171:38-51.
  36. Le Huu AR, Jokinen CH, Rubin BP, et al. Expression of prox1, lymphatic endothelial nuclear transcription factor, in kaposiform hemangioendothelioma and tufted angioma. Am J Surg Pathol. 2010;34:1563-1573.
  37. Debelenko LV, Perez-Atayde AR, Mulliken JB, et al. D2-40 immuno-histochemical analysis of pediatric vascular tumors reveals positivity in kaposiform hemangioendothelioma. Mod Pathol. 2005;18:1454-1460.
  38. Haisley-Royster C, Enjolras O, Frieden IJ, et al. Kasabach-Merritt phenomenon: a retrospective study of treatment with vincristine. J Pediatr Hematol Oncol. 2002;24:459-462.
  39. Wilmer A, Kaatz M, Bocker T, et al. Tufted angioma. Eur J Dermatol. 1999;9:51-53.
  40. Herron MD, Coffin CM, Vanderhooft SL. Tufted angiomas: variability of the clinical morphology. Pediatr Dermatol. 2002;19:394-401.
  41. North PE. Pediatric vascular tumors and malformations. Surg Pathol Clin. 2010,3:455-494.
  42. Chu CY, Hsiao CH, Chiu HC. Transformation between kaposiform hemangioendothelioma and tufted angioma. Dermatology. 2003;206:334-337.
  43. Osio A, Fraitag S, Hadj-Rabia S, et al. Clinical spectrum of tufted angiomas in childhood: a report of 13 cases and a review of the literature. Arch Dermatol. 2010;146:758-763.
  44. Johnson EF, Davis DM, Tollefson MM, et al. Vascular tumors in infants: case report and review of clinical, histopathologic, and immunohistochemical characteristics of infantile hemangioma, pyogenic granuloma, noninvoluting congenital hemangioma, tufted angioma, and kaposiform hemangioendothelioma. Am J Dermatopathol. 2018;40:231-239.
  45. Christison-Lagay ER, Fishman SJ. Vascular anomalies. Surg Clin North Am. 2006;86:393-425.
  46. Liu AS, Mulliken JB, Zurakowski D, et al. Extracranial arteriovenous malformations: natural progression and recurrence after treatment. Plast Reconstr Surg. 2010;125:1185-1194.
  47. Young AE, Mulliken JB. Arteriovenous malformations. In: Mulliken JB, Young AE, eds. Vascular Birthmarks: Haemangiomas and Malformations. WB Saunders; 1988:228-245.
  48. Duggan EM, Fishman SJ. Vascular anomalies. In: Holcomb GW III, Murphy JP, St Peter SD, eds. Holcomb and Ashcraft’s Pediatric Surgery. 7th edition. Elsevier; 2019:1147-1170.
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Vascular Mass on the Posterior Neck in a Newborn
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A newborn male was delivered via cesarean section at 38 weeks 5 days’ gestation with a large vascular mass on the posterior neck. The mass previously had been identified on a 23-week prenatal ultrasound. Physical examination by dermatology at birth revealed a well-defined violaceous mass measuring 6×5 cm with prominent radiating veins, coarse telangiectases, and a pale rim. Magnetic resonance imaging demonstrated a well-circumscribed mass with avid arterial phase enhancement. The patient experienced transient thrombocytopenia that resolved following administration of methylprednisolone. No evidence of rapid involution was noted after 3 months of observation.

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The Future of Obesity

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I am not planning on having a headstone on my grave, or even having a grave for that matter. However, if my heirs decide to ignore my wishes and opt for some pithy observation chiseled into a tastefully sized granite block, I suspect they might choose “He always knew which way the wind was blowing ... but wasn’t so sure about the tides.” Which aptly describes both my navigational deficiencies they have observed here over my six decades on the Maine coast as well as my general inability to predict the future. Nonetheless, I am going to throw caution to the wind and take this opportunity to ponder where obesity in this country will go over the next couple of decades.

In March of last year the London-based World Obesity Federation published its World Obesity Atlas. In the summary the authors predict that based on current trends “obesity will cost the global economy of US $4 trillion of potential income in 2035, nearly 3% of current global domestic product (GDP).” They envision the “rising prevalence of obesity to be steepest among children and adolescents rising from 10% to 20% of the world’s boys during the period 2029 to 2035, and rising fro 8% to 18% of the world’s girls.”

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

These dire predictions assume no significant measures to reverse this trajectory such as universal health coverage. Nor do the authors attempt to predict the effect of the growing use of GLP-1 agonists. This omission is surprising and somewhat refreshing given the fact that the project was funded by an unrestricted grant from Novo Nordisk, a major producer of one of these drugs.

Unfortunately, I think it is unlikely that over the next couple of decades any large countries who do not already have a functioning universal health care system will find the political will to develop one capable of reversing the trend toward obesity. Certainly, I don’t see it in the cards for this country.

On the other hand, I can foresee the availability and ease of administration for GLP-1 agonists and similar drugs improving over the near term. However, the cost and availability will continue to widen the separation between the haves and the have-nots, both globally and within each country. This will mean that the countries and population subgroups that already experience the bulk of the economic and health consequences of obesity will continue to shoulder an outsized burden of this “disease.”

It is unclear how much this widening of the fat-getting-fatter dynamic will add to the global and national political unrest that already seems to be tracking the effects of climate change. However, I can’t imaging it is going to be a calming or uniting force.

Narrowing our focus from an international to an individual resource-rich country such as the United States, let’s consider what the significant growth in availability and affordability of GLP-1 agonist drugs will mean. There will certainly be short-term improvements in the morbidity and mortality of some of the obesity related diseases. However, for other conditions it may take longer than two decades for us to notice an effect. While it is tempting to consider these declines as a financial boon for the country that already spends a high percentage of its GDP on healthcare. However, as the well-known Saturday Night Live pundit Roseanne Roseannadanna often observed, ”it’s always something ... if it’s not one thing it’s another.” There may be other non-obesity conditions that surge to fill the gap, leaving us still with a substantial financial burden for healthcare.

Patients taking GLP-1 agonists lose weight because they feel full and eat less food. While currently the number of patients taking these drugs is relatively small, the effect on this country’s food consumption is too small to calculate. However, let’s assume that 20 years from now half of the obese patients are taking appetite blunting medication. Using today’s statistics this means that 50 million adults will be eating significantly less food. Will the agriculturists have gradually adjusted to produce less food? Will this mean there is more food for the those experiencing “food insecurity”? I doubt it. Most food insecurity seems to be a problem of distribution and inequality, not supply.

Physicians now caution patients taking GLP-1 agonists to eat a healthy and balanced diet. When the drugs are more commonly available, will this caution be heeded by the majority? Will we see a population that may no longer be obese but nonetheless malnourished because of bad choices?

And, finally, in a similar vein, will previously obese individuals suddenly or gradually begin to be more physically active once the appetite blunting medicines have helped them lose weight? Here, I have my doubts. Of course, some leaner individuals begin to take advantage of their new body morphology. But, I fear that old sedentary habits will die very slowly for most, and not at all for many. We have built a vehicle-centric society in which being physically active requires making a conscious effort. Electronic devices and sedentary entertainment options are not going to disappear just because a significant percentage of the population is no longer obese.

So there you have it. I suspect that I am correct about which way some of the winds are blowing as the obesity becomes moves into its treatable “disease” phase. But, as always, I haven’t a clue which way the tide is running.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

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I am not planning on having a headstone on my grave, or even having a grave for that matter. However, if my heirs decide to ignore my wishes and opt for some pithy observation chiseled into a tastefully sized granite block, I suspect they might choose “He always knew which way the wind was blowing ... but wasn’t so sure about the tides.” Which aptly describes both my navigational deficiencies they have observed here over my six decades on the Maine coast as well as my general inability to predict the future. Nonetheless, I am going to throw caution to the wind and take this opportunity to ponder where obesity in this country will go over the next couple of decades.

In March of last year the London-based World Obesity Federation published its World Obesity Atlas. In the summary the authors predict that based on current trends “obesity will cost the global economy of US $4 trillion of potential income in 2035, nearly 3% of current global domestic product (GDP).” They envision the “rising prevalence of obesity to be steepest among children and adolescents rising from 10% to 20% of the world’s boys during the period 2029 to 2035, and rising fro 8% to 18% of the world’s girls.”

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

These dire predictions assume no significant measures to reverse this trajectory such as universal health coverage. Nor do the authors attempt to predict the effect of the growing use of GLP-1 agonists. This omission is surprising and somewhat refreshing given the fact that the project was funded by an unrestricted grant from Novo Nordisk, a major producer of one of these drugs.

Unfortunately, I think it is unlikely that over the next couple of decades any large countries who do not already have a functioning universal health care system will find the political will to develop one capable of reversing the trend toward obesity. Certainly, I don’t see it in the cards for this country.

On the other hand, I can foresee the availability and ease of administration for GLP-1 agonists and similar drugs improving over the near term. However, the cost and availability will continue to widen the separation between the haves and the have-nots, both globally and within each country. This will mean that the countries and population subgroups that already experience the bulk of the economic and health consequences of obesity will continue to shoulder an outsized burden of this “disease.”

It is unclear how much this widening of the fat-getting-fatter dynamic will add to the global and national political unrest that already seems to be tracking the effects of climate change. However, I can’t imaging it is going to be a calming or uniting force.

Narrowing our focus from an international to an individual resource-rich country such as the United States, let’s consider what the significant growth in availability and affordability of GLP-1 agonist drugs will mean. There will certainly be short-term improvements in the morbidity and mortality of some of the obesity related diseases. However, for other conditions it may take longer than two decades for us to notice an effect. While it is tempting to consider these declines as a financial boon for the country that already spends a high percentage of its GDP on healthcare. However, as the well-known Saturday Night Live pundit Roseanne Roseannadanna often observed, ”it’s always something ... if it’s not one thing it’s another.” There may be other non-obesity conditions that surge to fill the gap, leaving us still with a substantial financial burden for healthcare.

Patients taking GLP-1 agonists lose weight because they feel full and eat less food. While currently the number of patients taking these drugs is relatively small, the effect on this country’s food consumption is too small to calculate. However, let’s assume that 20 years from now half of the obese patients are taking appetite blunting medication. Using today’s statistics this means that 50 million adults will be eating significantly less food. Will the agriculturists have gradually adjusted to produce less food? Will this mean there is more food for the those experiencing “food insecurity”? I doubt it. Most food insecurity seems to be a problem of distribution and inequality, not supply.

Physicians now caution patients taking GLP-1 agonists to eat a healthy and balanced diet. When the drugs are more commonly available, will this caution be heeded by the majority? Will we see a population that may no longer be obese but nonetheless malnourished because of bad choices?

And, finally, in a similar vein, will previously obese individuals suddenly or gradually begin to be more physically active once the appetite blunting medicines have helped them lose weight? Here, I have my doubts. Of course, some leaner individuals begin to take advantage of their new body morphology. But, I fear that old sedentary habits will die very slowly for most, and not at all for many. We have built a vehicle-centric society in which being physically active requires making a conscious effort. Electronic devices and sedentary entertainment options are not going to disappear just because a significant percentage of the population is no longer obese.

So there you have it. I suspect that I am correct about which way some of the winds are blowing as the obesity becomes moves into its treatable “disease” phase. But, as always, I haven’t a clue which way the tide is running.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

I am not planning on having a headstone on my grave, or even having a grave for that matter. However, if my heirs decide to ignore my wishes and opt for some pithy observation chiseled into a tastefully sized granite block, I suspect they might choose “He always knew which way the wind was blowing ... but wasn’t so sure about the tides.” Which aptly describes both my navigational deficiencies they have observed here over my six decades on the Maine coast as well as my general inability to predict the future. Nonetheless, I am going to throw caution to the wind and take this opportunity to ponder where obesity in this country will go over the next couple of decades.

In March of last year the London-based World Obesity Federation published its World Obesity Atlas. In the summary the authors predict that based on current trends “obesity will cost the global economy of US $4 trillion of potential income in 2035, nearly 3% of current global domestic product (GDP).” They envision the “rising prevalence of obesity to be steepest among children and adolescents rising from 10% to 20% of the world’s boys during the period 2029 to 2035, and rising fro 8% to 18% of the world’s girls.”

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

These dire predictions assume no significant measures to reverse this trajectory such as universal health coverage. Nor do the authors attempt to predict the effect of the growing use of GLP-1 agonists. This omission is surprising and somewhat refreshing given the fact that the project was funded by an unrestricted grant from Novo Nordisk, a major producer of one of these drugs.

Unfortunately, I think it is unlikely that over the next couple of decades any large countries who do not already have a functioning universal health care system will find the political will to develop one capable of reversing the trend toward obesity. Certainly, I don’t see it in the cards for this country.

On the other hand, I can foresee the availability and ease of administration for GLP-1 agonists and similar drugs improving over the near term. However, the cost and availability will continue to widen the separation between the haves and the have-nots, both globally and within each country. This will mean that the countries and population subgroups that already experience the bulk of the economic and health consequences of obesity will continue to shoulder an outsized burden of this “disease.”

It is unclear how much this widening of the fat-getting-fatter dynamic will add to the global and national political unrest that already seems to be tracking the effects of climate change. However, I can’t imaging it is going to be a calming or uniting force.

Narrowing our focus from an international to an individual resource-rich country such as the United States, let’s consider what the significant growth in availability and affordability of GLP-1 agonist drugs will mean. There will certainly be short-term improvements in the morbidity and mortality of some of the obesity related diseases. However, for other conditions it may take longer than two decades for us to notice an effect. While it is tempting to consider these declines as a financial boon for the country that already spends a high percentage of its GDP on healthcare. However, as the well-known Saturday Night Live pundit Roseanne Roseannadanna often observed, ”it’s always something ... if it’s not one thing it’s another.” There may be other non-obesity conditions that surge to fill the gap, leaving us still with a substantial financial burden for healthcare.

Patients taking GLP-1 agonists lose weight because they feel full and eat less food. While currently the number of patients taking these drugs is relatively small, the effect on this country’s food consumption is too small to calculate. However, let’s assume that 20 years from now half of the obese patients are taking appetite blunting medication. Using today’s statistics this means that 50 million adults will be eating significantly less food. Will the agriculturists have gradually adjusted to produce less food? Will this mean there is more food for the those experiencing “food insecurity”? I doubt it. Most food insecurity seems to be a problem of distribution and inequality, not supply.

Physicians now caution patients taking GLP-1 agonists to eat a healthy and balanced diet. When the drugs are more commonly available, will this caution be heeded by the majority? Will we see a population that may no longer be obese but nonetheless malnourished because of bad choices?

And, finally, in a similar vein, will previously obese individuals suddenly or gradually begin to be more physically active once the appetite blunting medicines have helped them lose weight? Here, I have my doubts. Of course, some leaner individuals begin to take advantage of their new body morphology. But, I fear that old sedentary habits will die very slowly for most, and not at all for many. We have built a vehicle-centric society in which being physically active requires making a conscious effort. Electronic devices and sedentary entertainment options are not going to disappear just because a significant percentage of the population is no longer obese.

So there you have it. I suspect that I am correct about which way some of the winds are blowing as the obesity becomes moves into its treatable “disease” phase. But, as always, I haven’t a clue which way the tide is running.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.

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Reducing Unnecessary Antibiotics for Conjunctivitis

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Changed
Tue, 07/02/2024 - 11:17

 

TOPLINE:

More than two thirds of children with conjunctivitis received antibiotics within a day of their initial ambulatory care visit; however, follow-up visits and new antibiotic dispensations were rare regardless of treatment, suggesting that not receiving antibiotics may not lead to additional health care use.

METHODOLOGY:

  • Researchers evaluated the frequency of topical antibiotic treatment and its association with subsequent health care use among commercially insured children with acute infectious conjunctivitis in the United States.
  • This cohort study analyzed data from the 2021 MarketScan Commercial Claims and Encounters Database, including 44,793 children with conjunctivitis (median age, 5 years; 47% girls) and ambulatory care encounters.
  • The primary exposure was a topical antibiotic prescription dispensed within 1 day of an ambulatory care visit, with outcomes assessed 2-14 days after the visit.
  • The primary outcomes were ambulatory care revisits for conjunctivitis and same-day dispensation of a new topical antibiotic, and secondary outcomes included emergency department revisits and hospitalizations.

TAKEAWAY:

  • Topical antibiotics were dispensed within a day of an ambulatory care visit in 69% of the cases; however, they were less frequently dispensed following visits to eye clinics (34%), for children aged 6-11 years (66%), and for those with viral conjunctivitis (28%).
  • Ambulatory care revisits for conjunctivitis within 2 weeks occurred in only 3.2% of children who had received antibiotics (adjusted odds ratio [aOR], 1.11; 95% CI, 0.99-1.25).
  • Similarly, revisits with same-day dispensation of a new antibiotic were also rare (1.4%), with no significant association between antibiotic treatment and revisits (aOR, 1.10; 95% CI, 0.92-1.33).
  • Hospitalizations for conjunctivitis occurred in 0.03% of cases, and emergency department revisits occurred in 0.12%, with no differences between children who received antibiotics and those who did not.

IN PRACTICE:

“Given that antibiotics may not be associated with improved outcomes or change in subsequent health care use and are associated with adverse effects and antibiotic resistance, efforts to reduce overtreatment of acute infectious conjunctivitis are warranted,” the authors wrote.

SOURCE:

The study was led by Daniel J. Shapiro, MD, MPH, of the Department of Emergency Medicine at the University of California, San Francisco, and published online on June 27, 2024, in JAMA Ophthalmology.

LIMITATIONS:

The major limitations of the study included the inability to distinguish scheduled visits from unscheduled revisits, incomplete clinical data such as rare complications of conjunctivitis, and the inability to confirm the accuracy of the coded diagnosis of infectious conjunctivitis, especially in children who did not receive a thorough eye examination.

DISCLOSURES:

This study did not declare receiving funding from any sources. One author reported receiving grants from several sources outside the submitted work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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TOPLINE:

More than two thirds of children with conjunctivitis received antibiotics within a day of their initial ambulatory care visit; however, follow-up visits and new antibiotic dispensations were rare regardless of treatment, suggesting that not receiving antibiotics may not lead to additional health care use.

METHODOLOGY:

  • Researchers evaluated the frequency of topical antibiotic treatment and its association with subsequent health care use among commercially insured children with acute infectious conjunctivitis in the United States.
  • This cohort study analyzed data from the 2021 MarketScan Commercial Claims and Encounters Database, including 44,793 children with conjunctivitis (median age, 5 years; 47% girls) and ambulatory care encounters.
  • The primary exposure was a topical antibiotic prescription dispensed within 1 day of an ambulatory care visit, with outcomes assessed 2-14 days after the visit.
  • The primary outcomes were ambulatory care revisits for conjunctivitis and same-day dispensation of a new topical antibiotic, and secondary outcomes included emergency department revisits and hospitalizations.

TAKEAWAY:

  • Topical antibiotics were dispensed within a day of an ambulatory care visit in 69% of the cases; however, they were less frequently dispensed following visits to eye clinics (34%), for children aged 6-11 years (66%), and for those with viral conjunctivitis (28%).
  • Ambulatory care revisits for conjunctivitis within 2 weeks occurred in only 3.2% of children who had received antibiotics (adjusted odds ratio [aOR], 1.11; 95% CI, 0.99-1.25).
  • Similarly, revisits with same-day dispensation of a new antibiotic were also rare (1.4%), with no significant association between antibiotic treatment and revisits (aOR, 1.10; 95% CI, 0.92-1.33).
  • Hospitalizations for conjunctivitis occurred in 0.03% of cases, and emergency department revisits occurred in 0.12%, with no differences between children who received antibiotics and those who did not.

IN PRACTICE:

“Given that antibiotics may not be associated with improved outcomes or change in subsequent health care use and are associated with adverse effects and antibiotic resistance, efforts to reduce overtreatment of acute infectious conjunctivitis are warranted,” the authors wrote.

SOURCE:

The study was led by Daniel J. Shapiro, MD, MPH, of the Department of Emergency Medicine at the University of California, San Francisco, and published online on June 27, 2024, in JAMA Ophthalmology.

LIMITATIONS:

The major limitations of the study included the inability to distinguish scheduled visits from unscheduled revisits, incomplete clinical data such as rare complications of conjunctivitis, and the inability to confirm the accuracy of the coded diagnosis of infectious conjunctivitis, especially in children who did not receive a thorough eye examination.

DISCLOSURES:

This study did not declare receiving funding from any sources. One author reported receiving grants from several sources outside the submitted work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

 

TOPLINE:

More than two thirds of children with conjunctivitis received antibiotics within a day of their initial ambulatory care visit; however, follow-up visits and new antibiotic dispensations were rare regardless of treatment, suggesting that not receiving antibiotics may not lead to additional health care use.

METHODOLOGY:

  • Researchers evaluated the frequency of topical antibiotic treatment and its association with subsequent health care use among commercially insured children with acute infectious conjunctivitis in the United States.
  • This cohort study analyzed data from the 2021 MarketScan Commercial Claims and Encounters Database, including 44,793 children with conjunctivitis (median age, 5 years; 47% girls) and ambulatory care encounters.
  • The primary exposure was a topical antibiotic prescription dispensed within 1 day of an ambulatory care visit, with outcomes assessed 2-14 days after the visit.
  • The primary outcomes were ambulatory care revisits for conjunctivitis and same-day dispensation of a new topical antibiotic, and secondary outcomes included emergency department revisits and hospitalizations.

TAKEAWAY:

  • Topical antibiotics were dispensed within a day of an ambulatory care visit in 69% of the cases; however, they were less frequently dispensed following visits to eye clinics (34%), for children aged 6-11 years (66%), and for those with viral conjunctivitis (28%).
  • Ambulatory care revisits for conjunctivitis within 2 weeks occurred in only 3.2% of children who had received antibiotics (adjusted odds ratio [aOR], 1.11; 95% CI, 0.99-1.25).
  • Similarly, revisits with same-day dispensation of a new antibiotic were also rare (1.4%), with no significant association between antibiotic treatment and revisits (aOR, 1.10; 95% CI, 0.92-1.33).
  • Hospitalizations for conjunctivitis occurred in 0.03% of cases, and emergency department revisits occurred in 0.12%, with no differences between children who received antibiotics and those who did not.

IN PRACTICE:

“Given that antibiotics may not be associated with improved outcomes or change in subsequent health care use and are associated with adverse effects and antibiotic resistance, efforts to reduce overtreatment of acute infectious conjunctivitis are warranted,” the authors wrote.

SOURCE:

The study was led by Daniel J. Shapiro, MD, MPH, of the Department of Emergency Medicine at the University of California, San Francisco, and published online on June 27, 2024, in JAMA Ophthalmology.

LIMITATIONS:

The major limitations of the study included the inability to distinguish scheduled visits from unscheduled revisits, incomplete clinical data such as rare complications of conjunctivitis, and the inability to confirm the accuracy of the coded diagnosis of infectious conjunctivitis, especially in children who did not receive a thorough eye examination.

DISCLOSURES:

This study did not declare receiving funding from any sources. One author reported receiving grants from several sources outside the submitted work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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Exercise Plus GLP-1 RAs Upped Weight Loss, Bone Retention

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Changed
Tue, 07/02/2024 - 11:11

 

TOPLINE:

People with obesity who exercise while taking glucagon-like peptide 1 receptor agonists (GLP-1 RAs; liraglutide) showed increased weight loss and preserved bone health, according to a study published in JAMA Network Open.

METHODOLOGY:

  • Patients were placed on an initial diet that consisted of no more than 800 calories per day for 8 weeks. Those who lost at least 5% of their starting weight were then placed into a 1-year program.
  • Participants included 195 adults aged between 18 and 65 years with obesity and no diabetes, 64% of whom were women.
  • They were split into four groups of interventions: Exercise only (48 patients), liraglutide only (49 patients), a combination of both (49 participants), and placebo (49 participants), for a 1-year period.
  • Patients received liraglutide or volume-matched placebo as daily injections starting at 0.6 mg/d with a weekly increase until 3 mg/d was reached; exercise entailed 30-minute sessions for 4 days a week.
  • Researchers studied bone health at each patient’s hip, spine, and forearm after they lost weight, by measuring bone mineral density (BMD).

TAKEAWAY:

  • The overall average change in weight loss over the course of 52 weeks was 7.03 kg in the placebo group, 11.19 kg in the exercise group, 13.74 kg in the liraglutide group, and 16.88 kg in the combination group.
  • After the initial low-calorie diet-induced weight loss, the placebo group regained weight, the exercise and liraglutide groups maintained weight loss, and the combination group lost additional weight.
  • BMD did not change in the combination group in comparison to the placebo group at the hip (mean change, −0.006 g/cm2; 95% CI, −0.017 to 0.004 g/cm2; P = .24) or spine (−0.010 g/cm2; 95% CI, −0.025 to 0.005 g/cm2; P = .20).
  • BMD of the spine in the liraglutide group decreased in comparison to the exercise group (mean change, −0.016 g/cm2; 95% CI, −0.032 to −0.001 g/cm2; P = .04) and the placebo group, in addition to decreases in the hip.

IN PRACTICE:

“Our results show that the combination of exercise and GLP-1 RA was the most effective weight loss strategy while preserving bone health,” study authors wrote.

SOURCE:

The study was led by Simon Birk Kjær Jensen, PhD, of the Department of Biomedical Sciences and Faculty of Health and Medical Sciences at the University of Copenhagen in Denmark, and published on June 25 in JAMA Network Open.

LIMITATIONS:

The study only included adults aged between 18 and 65 years without other chronic diseases and may not apply to patients who are older or have diabetes. The study sample was diverse but was conducted in Denmark, with a population of generally similar ancestry.

DISCLOSURES:

One study author reported serving on advisory boards for AstraZeneca, Boehringer Ingelheim, Bayer, and Amgen, among others. Other authors reported various financial interests, including grants, personal fees, and salaries, from Amgen, Novo Nordisk, and Abbott Lab, among others.

A version of this article first appeared on Medscape.com.

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TOPLINE:

People with obesity who exercise while taking glucagon-like peptide 1 receptor agonists (GLP-1 RAs; liraglutide) showed increased weight loss and preserved bone health, according to a study published in JAMA Network Open.

METHODOLOGY:

  • Patients were placed on an initial diet that consisted of no more than 800 calories per day for 8 weeks. Those who lost at least 5% of their starting weight were then placed into a 1-year program.
  • Participants included 195 adults aged between 18 and 65 years with obesity and no diabetes, 64% of whom were women.
  • They were split into four groups of interventions: Exercise only (48 patients), liraglutide only (49 patients), a combination of both (49 participants), and placebo (49 participants), for a 1-year period.
  • Patients received liraglutide or volume-matched placebo as daily injections starting at 0.6 mg/d with a weekly increase until 3 mg/d was reached; exercise entailed 30-minute sessions for 4 days a week.
  • Researchers studied bone health at each patient’s hip, spine, and forearm after they lost weight, by measuring bone mineral density (BMD).

TAKEAWAY:

  • The overall average change in weight loss over the course of 52 weeks was 7.03 kg in the placebo group, 11.19 kg in the exercise group, 13.74 kg in the liraglutide group, and 16.88 kg in the combination group.
  • After the initial low-calorie diet-induced weight loss, the placebo group regained weight, the exercise and liraglutide groups maintained weight loss, and the combination group lost additional weight.
  • BMD did not change in the combination group in comparison to the placebo group at the hip (mean change, −0.006 g/cm2; 95% CI, −0.017 to 0.004 g/cm2; P = .24) or spine (−0.010 g/cm2; 95% CI, −0.025 to 0.005 g/cm2; P = .20).
  • BMD of the spine in the liraglutide group decreased in comparison to the exercise group (mean change, −0.016 g/cm2; 95% CI, −0.032 to −0.001 g/cm2; P = .04) and the placebo group, in addition to decreases in the hip.

IN PRACTICE:

“Our results show that the combination of exercise and GLP-1 RA was the most effective weight loss strategy while preserving bone health,” study authors wrote.

SOURCE:

The study was led by Simon Birk Kjær Jensen, PhD, of the Department of Biomedical Sciences and Faculty of Health and Medical Sciences at the University of Copenhagen in Denmark, and published on June 25 in JAMA Network Open.

LIMITATIONS:

The study only included adults aged between 18 and 65 years without other chronic diseases and may not apply to patients who are older or have diabetes. The study sample was diverse but was conducted in Denmark, with a population of generally similar ancestry.

DISCLOSURES:

One study author reported serving on advisory boards for AstraZeneca, Boehringer Ingelheim, Bayer, and Amgen, among others. Other authors reported various financial interests, including grants, personal fees, and salaries, from Amgen, Novo Nordisk, and Abbott Lab, among others.

A version of this article first appeared on Medscape.com.

 

TOPLINE:

People with obesity who exercise while taking glucagon-like peptide 1 receptor agonists (GLP-1 RAs; liraglutide) showed increased weight loss and preserved bone health, according to a study published in JAMA Network Open.

METHODOLOGY:

  • Patients were placed on an initial diet that consisted of no more than 800 calories per day for 8 weeks. Those who lost at least 5% of their starting weight were then placed into a 1-year program.
  • Participants included 195 adults aged between 18 and 65 years with obesity and no diabetes, 64% of whom were women.
  • They were split into four groups of interventions: Exercise only (48 patients), liraglutide only (49 patients), a combination of both (49 participants), and placebo (49 participants), for a 1-year period.
  • Patients received liraglutide or volume-matched placebo as daily injections starting at 0.6 mg/d with a weekly increase until 3 mg/d was reached; exercise entailed 30-minute sessions for 4 days a week.
  • Researchers studied bone health at each patient’s hip, spine, and forearm after they lost weight, by measuring bone mineral density (BMD).

TAKEAWAY:

  • The overall average change in weight loss over the course of 52 weeks was 7.03 kg in the placebo group, 11.19 kg in the exercise group, 13.74 kg in the liraglutide group, and 16.88 kg in the combination group.
  • After the initial low-calorie diet-induced weight loss, the placebo group regained weight, the exercise and liraglutide groups maintained weight loss, and the combination group lost additional weight.
  • BMD did not change in the combination group in comparison to the placebo group at the hip (mean change, −0.006 g/cm2; 95% CI, −0.017 to 0.004 g/cm2; P = .24) or spine (−0.010 g/cm2; 95% CI, −0.025 to 0.005 g/cm2; P = .20).
  • BMD of the spine in the liraglutide group decreased in comparison to the exercise group (mean change, −0.016 g/cm2; 95% CI, −0.032 to −0.001 g/cm2; P = .04) and the placebo group, in addition to decreases in the hip.

IN PRACTICE:

“Our results show that the combination of exercise and GLP-1 RA was the most effective weight loss strategy while preserving bone health,” study authors wrote.

SOURCE:

The study was led by Simon Birk Kjær Jensen, PhD, of the Department of Biomedical Sciences and Faculty of Health and Medical Sciences at the University of Copenhagen in Denmark, and published on June 25 in JAMA Network Open.

LIMITATIONS:

The study only included adults aged between 18 and 65 years without other chronic diseases and may not apply to patients who are older or have diabetes. The study sample was diverse but was conducted in Denmark, with a population of generally similar ancestry.

DISCLOSURES:

One study author reported serving on advisory boards for AstraZeneca, Boehringer Ingelheim, Bayer, and Amgen, among others. Other authors reported various financial interests, including grants, personal fees, and salaries, from Amgen, Novo Nordisk, and Abbott Lab, among others.

A version of this article first appeared on Medscape.com.

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Does Semaglutide Reduce Inflammation?

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Tue, 07/02/2024 - 11:06

— The anti-obesity drug semaglutide is associated with significant reductions in the inflammatory marker high-sensitivity C-reactive protein (CRP), even in patients who do not lose substantial amounts of weight with the drug, according to data from the SELECT clinical trial.

The research, presented at the European Atherosclerosis Society 2024, involved over 17,600 patients with overweight or obesity and had established cardiovascular disease but not diabetes.

Those given semaglutide experienced a 38% reduction in high-sensitivity CRP levels compared with placebo regardless of baseline body mass index, statin use, cholesterol levels, and other measures.

“Weight loss was associated with greater high-sensitivity CRP reduction in both treatment groups,” said study presenter Jorge Plutzky, MD, director of Preventive Cardiology at Brigham and Women’s Hospital, Boston, but “with increased high-sensitivity CRP reductions in those receiving semaglutide.”

The drug also “significantly reduced high-sensitivity CRP early,” he said, “prior to major weight loss and in those who did not lose significant amounts of weight.” The reductions reached approximately 12% at 4 weeks and around 20% at 8 weeks, when the weight loss “was still quite modest,” at 2% and 3% of body weight, respectively. Even among patients who achieved weight loss of less than 2% body weight, semaglutide was associated with a reduction in high-sensitivity CRP levels.

In the SELECT trial, semaglutide also resulted in a consistent reduction of around 20% vs placebo in major adverse cardiovascular events such as cardiovascular mortality, nonfatal myocardial infarction, or nonfatal stroke.

But Naveed Sattar, MD, PhD, professor of cardiometabolic medicine at the University of Glasgow, Scotland, said in an interview that body weight “is probably the major driver” of CRP levels in the population, accounting for between 20% and 30% of the variation.

Dr. Sattar, who was not involved in the study, said that because drugs like semaglutide lower weight but also have anti-inflammatory effects, the question becomes: “Could the anti-inflammatory effects be part of the mechanisms by which these drugs affect the risk of major adverse cardiovascular events?”
 

Reducing Cardiovascular Events

The current analysis, however, cannot answer the question, he said. “All it tells us is about associations.”

“What we do know is semaglutide, predominantly by lowering weight, is lowering CRP levels and equally, we know that when you lose weight, you improve blood pressure, you improve lipids, and you reduce the risk of diabetes,” he said.

Dr. Sattar also took issue with the researchers’ conclusion that the high-sensitivity CRP reductions seen in SELECT occurred prior to major weight loss because the “pattern of CRP reduction and weight reduction is almost identical.”

Dr. Sattar also pointed out in a recent editorial that the drug appears to have a direct effect on blood vessels and the heart, which may lead to improvements in systemic inflammation. Consequently, he said, any assertion that semaglutide is genuinely anti-inflammatory is, at this stage, “speculation.”

Dr. Plutzky said that “systemic, chronic inflammation is implicated as a potential mechanism and therapeutic target in atherosclerosis and major adverse cardiovascular events, as well as obesity,” and high-sensitivity CRP levels are an “established biomarker of inflammation and have been shown to predict cardiovascular risk.”

However, the relationship between high-sensitivity CRP, responses to glucagon-like peptide 1 receptor agonists like semaglutide, and cardiovascular outcomes in obesity “remains incompletely understood,” said Dr. Plutzky.
 

A version of this article appeared on Medscape.com.

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— The anti-obesity drug semaglutide is associated with significant reductions in the inflammatory marker high-sensitivity C-reactive protein (CRP), even in patients who do not lose substantial amounts of weight with the drug, according to data from the SELECT clinical trial.

The research, presented at the European Atherosclerosis Society 2024, involved over 17,600 patients with overweight or obesity and had established cardiovascular disease but not diabetes.

Those given semaglutide experienced a 38% reduction in high-sensitivity CRP levels compared with placebo regardless of baseline body mass index, statin use, cholesterol levels, and other measures.

“Weight loss was associated with greater high-sensitivity CRP reduction in both treatment groups,” said study presenter Jorge Plutzky, MD, director of Preventive Cardiology at Brigham and Women’s Hospital, Boston, but “with increased high-sensitivity CRP reductions in those receiving semaglutide.”

The drug also “significantly reduced high-sensitivity CRP early,” he said, “prior to major weight loss and in those who did not lose significant amounts of weight.” The reductions reached approximately 12% at 4 weeks and around 20% at 8 weeks, when the weight loss “was still quite modest,” at 2% and 3% of body weight, respectively. Even among patients who achieved weight loss of less than 2% body weight, semaglutide was associated with a reduction in high-sensitivity CRP levels.

In the SELECT trial, semaglutide also resulted in a consistent reduction of around 20% vs placebo in major adverse cardiovascular events such as cardiovascular mortality, nonfatal myocardial infarction, or nonfatal stroke.

But Naveed Sattar, MD, PhD, professor of cardiometabolic medicine at the University of Glasgow, Scotland, said in an interview that body weight “is probably the major driver” of CRP levels in the population, accounting for between 20% and 30% of the variation.

Dr. Sattar, who was not involved in the study, said that because drugs like semaglutide lower weight but also have anti-inflammatory effects, the question becomes: “Could the anti-inflammatory effects be part of the mechanisms by which these drugs affect the risk of major adverse cardiovascular events?”
 

Reducing Cardiovascular Events

The current analysis, however, cannot answer the question, he said. “All it tells us is about associations.”

“What we do know is semaglutide, predominantly by lowering weight, is lowering CRP levels and equally, we know that when you lose weight, you improve blood pressure, you improve lipids, and you reduce the risk of diabetes,” he said.

Dr. Sattar also took issue with the researchers’ conclusion that the high-sensitivity CRP reductions seen in SELECT occurred prior to major weight loss because the “pattern of CRP reduction and weight reduction is almost identical.”

Dr. Sattar also pointed out in a recent editorial that the drug appears to have a direct effect on blood vessels and the heart, which may lead to improvements in systemic inflammation. Consequently, he said, any assertion that semaglutide is genuinely anti-inflammatory is, at this stage, “speculation.”

Dr. Plutzky said that “systemic, chronic inflammation is implicated as a potential mechanism and therapeutic target in atherosclerosis and major adverse cardiovascular events, as well as obesity,” and high-sensitivity CRP levels are an “established biomarker of inflammation and have been shown to predict cardiovascular risk.”

However, the relationship between high-sensitivity CRP, responses to glucagon-like peptide 1 receptor agonists like semaglutide, and cardiovascular outcomes in obesity “remains incompletely understood,” said Dr. Plutzky.
 

A version of this article appeared on Medscape.com.

— The anti-obesity drug semaglutide is associated with significant reductions in the inflammatory marker high-sensitivity C-reactive protein (CRP), even in patients who do not lose substantial amounts of weight with the drug, according to data from the SELECT clinical trial.

The research, presented at the European Atherosclerosis Society 2024, involved over 17,600 patients with overweight or obesity and had established cardiovascular disease but not diabetes.

Those given semaglutide experienced a 38% reduction in high-sensitivity CRP levels compared with placebo regardless of baseline body mass index, statin use, cholesterol levels, and other measures.

“Weight loss was associated with greater high-sensitivity CRP reduction in both treatment groups,” said study presenter Jorge Plutzky, MD, director of Preventive Cardiology at Brigham and Women’s Hospital, Boston, but “with increased high-sensitivity CRP reductions in those receiving semaglutide.”

The drug also “significantly reduced high-sensitivity CRP early,” he said, “prior to major weight loss and in those who did not lose significant amounts of weight.” The reductions reached approximately 12% at 4 weeks and around 20% at 8 weeks, when the weight loss “was still quite modest,” at 2% and 3% of body weight, respectively. Even among patients who achieved weight loss of less than 2% body weight, semaglutide was associated with a reduction in high-sensitivity CRP levels.

In the SELECT trial, semaglutide also resulted in a consistent reduction of around 20% vs placebo in major adverse cardiovascular events such as cardiovascular mortality, nonfatal myocardial infarction, or nonfatal stroke.

But Naveed Sattar, MD, PhD, professor of cardiometabolic medicine at the University of Glasgow, Scotland, said in an interview that body weight “is probably the major driver” of CRP levels in the population, accounting for between 20% and 30% of the variation.

Dr. Sattar, who was not involved in the study, said that because drugs like semaglutide lower weight but also have anti-inflammatory effects, the question becomes: “Could the anti-inflammatory effects be part of the mechanisms by which these drugs affect the risk of major adverse cardiovascular events?”
 

Reducing Cardiovascular Events

The current analysis, however, cannot answer the question, he said. “All it tells us is about associations.”

“What we do know is semaglutide, predominantly by lowering weight, is lowering CRP levels and equally, we know that when you lose weight, you improve blood pressure, you improve lipids, and you reduce the risk of diabetes,” he said.

Dr. Sattar also took issue with the researchers’ conclusion that the high-sensitivity CRP reductions seen in SELECT occurred prior to major weight loss because the “pattern of CRP reduction and weight reduction is almost identical.”

Dr. Sattar also pointed out in a recent editorial that the drug appears to have a direct effect on blood vessels and the heart, which may lead to improvements in systemic inflammation. Consequently, he said, any assertion that semaglutide is genuinely anti-inflammatory is, at this stage, “speculation.”

Dr. Plutzky said that “systemic, chronic inflammation is implicated as a potential mechanism and therapeutic target in atherosclerosis and major adverse cardiovascular events, as well as obesity,” and high-sensitivity CRP levels are an “established biomarker of inflammation and have been shown to predict cardiovascular risk.”

However, the relationship between high-sensitivity CRP, responses to glucagon-like peptide 1 receptor agonists like semaglutide, and cardiovascular outcomes in obesity “remains incompletely understood,” said Dr. Plutzky.
 

A version of this article appeared on Medscape.com.

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Diagnostic yield reporting of bronchoscopic peripheral pulmonary nodule biopsies: A call for standardization

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Tue, 07/02/2024 - 15:20

THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Interventional Procedures Section

More than 1.5 million Americans are diagnosed with an incidental CT scan-detected lung nodule annually. Advanced bronchoscopy, as a diagnostic tool for evaluation of these nodules, has evolved rapidly, incorporating a range of techniques and tools beyond CT scan-guided biopsies to assess peripheral lesions. The primary goal is to provide patients with accurate benign or malignant diagnoses. However, accurately determining the effectiveness of innovative technologies in providing a diagnosis remains challenging, in part due to limitations in study design and outcome reporting, along with the scarcity of comparative and randomized controlled studies.1,2 Current literature shows significant variability in diagnostic yield definition, lacking generalizability.

CHEST
Dr. Irene Riestra Guiance

To address this issue, an official research statement by the American Thoracic Society and CHEST defines the diagnostic yield as “the proportion of all individuals undergoing the diagnostic procedure under evaluation in whom a specific malignant or benign diagnosis is established.”3 To achieve this measure, the numerator includes all patients with lung nodules in whom the result of a diagnostic procedure establishes a specific benign or malignant diagnosis that is readily sufficient to inform patient care without additional diagnostic workup, and the denominator should include all patients in whom the procedure was attempted or performed. This standardized definition is crucial for ensuring consistency across studies, allowing for comparison or pooling of results, enhancing the reliability of diagnostic yield data, and informing clinical decisions.

CHEST
Dr. Samira Shojaee


The adoption of standardized outcome definitions is essential to critically evaluate modern, minimally invasive procedures for peripheral lung nodules diagnosis and to guide patient-centered care while minimizing the downstream effects of nondiagnostic biopsies. Clear, transparent, and consistent reporting will enable physicians to choose the most appropriate diagnostic tools, improve patient outcomes by reducing unnecessary procedures, and expedite accurate diagnoses. This initiative is a crucial first step toward creating high-quality studies that can inform technology implementation decisions and promote equitable health care.


References

1. Tanner NT, Yarmus L, Chen A, et al. Standard bronchoscopy with fluoroscopy vs thin bronchoscopy and radial endobronchial ultrasound for biopsy of pulmonary lesions: a multicenter, prospective, randomized trial. Chest. 2018;154(5):1035-1043.

2. Ost DE, Ernst A, Lei X, et al. Diagnostic yield and complications of bronchoscopy for peripheral lung lesions. Results of the AQuIRE Registry. Am J Resp Crit Care Med. 2016;193(1):68-77.

3. Gonzalez AV, Silvestri GA, Korevaar DA, et al. Assessment of advanced diagnostic bronchoscopy outcomes for peripheral lung lesions: a Delphi consensus definition of diagnostic yield and recommendations for patient-centered study designs. An official American Thoracic Society/American College of Chest Physicians research statement. Am J Respir Crit Care Med. 2024;209(6):634-646.

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THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Interventional Procedures Section

More than 1.5 million Americans are diagnosed with an incidental CT scan-detected lung nodule annually. Advanced bronchoscopy, as a diagnostic tool for evaluation of these nodules, has evolved rapidly, incorporating a range of techniques and tools beyond CT scan-guided biopsies to assess peripheral lesions. The primary goal is to provide patients with accurate benign or malignant diagnoses. However, accurately determining the effectiveness of innovative technologies in providing a diagnosis remains challenging, in part due to limitations in study design and outcome reporting, along with the scarcity of comparative and randomized controlled studies.1,2 Current literature shows significant variability in diagnostic yield definition, lacking generalizability.

CHEST
Dr. Irene Riestra Guiance

To address this issue, an official research statement by the American Thoracic Society and CHEST defines the diagnostic yield as “the proportion of all individuals undergoing the diagnostic procedure under evaluation in whom a specific malignant or benign diagnosis is established.”3 To achieve this measure, the numerator includes all patients with lung nodules in whom the result of a diagnostic procedure establishes a specific benign or malignant diagnosis that is readily sufficient to inform patient care without additional diagnostic workup, and the denominator should include all patients in whom the procedure was attempted or performed. This standardized definition is crucial for ensuring consistency across studies, allowing for comparison or pooling of results, enhancing the reliability of diagnostic yield data, and informing clinical decisions.

CHEST
Dr. Samira Shojaee


The adoption of standardized outcome definitions is essential to critically evaluate modern, minimally invasive procedures for peripheral lung nodules diagnosis and to guide patient-centered care while minimizing the downstream effects of nondiagnostic biopsies. Clear, transparent, and consistent reporting will enable physicians to choose the most appropriate diagnostic tools, improve patient outcomes by reducing unnecessary procedures, and expedite accurate diagnoses. This initiative is a crucial first step toward creating high-quality studies that can inform technology implementation decisions and promote equitable health care.


References

1. Tanner NT, Yarmus L, Chen A, et al. Standard bronchoscopy with fluoroscopy vs thin bronchoscopy and radial endobronchial ultrasound for biopsy of pulmonary lesions: a multicenter, prospective, randomized trial. Chest. 2018;154(5):1035-1043.

2. Ost DE, Ernst A, Lei X, et al. Diagnostic yield and complications of bronchoscopy for peripheral lung lesions. Results of the AQuIRE Registry. Am J Resp Crit Care Med. 2016;193(1):68-77.

3. Gonzalez AV, Silvestri GA, Korevaar DA, et al. Assessment of advanced diagnostic bronchoscopy outcomes for peripheral lung lesions: a Delphi consensus definition of diagnostic yield and recommendations for patient-centered study designs. An official American Thoracic Society/American College of Chest Physicians research statement. Am J Respir Crit Care Med. 2024;209(6):634-646.

THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Interventional Procedures Section

More than 1.5 million Americans are diagnosed with an incidental CT scan-detected lung nodule annually. Advanced bronchoscopy, as a diagnostic tool for evaluation of these nodules, has evolved rapidly, incorporating a range of techniques and tools beyond CT scan-guided biopsies to assess peripheral lesions. The primary goal is to provide patients with accurate benign or malignant diagnoses. However, accurately determining the effectiveness of innovative technologies in providing a diagnosis remains challenging, in part due to limitations in study design and outcome reporting, along with the scarcity of comparative and randomized controlled studies.1,2 Current literature shows significant variability in diagnostic yield definition, lacking generalizability.

CHEST
Dr. Irene Riestra Guiance

To address this issue, an official research statement by the American Thoracic Society and CHEST defines the diagnostic yield as “the proportion of all individuals undergoing the diagnostic procedure under evaluation in whom a specific malignant or benign diagnosis is established.”3 To achieve this measure, the numerator includes all patients with lung nodules in whom the result of a diagnostic procedure establishes a specific benign or malignant diagnosis that is readily sufficient to inform patient care without additional diagnostic workup, and the denominator should include all patients in whom the procedure was attempted or performed. This standardized definition is crucial for ensuring consistency across studies, allowing for comparison or pooling of results, enhancing the reliability of diagnostic yield data, and informing clinical decisions.

CHEST
Dr. Samira Shojaee


The adoption of standardized outcome definitions is essential to critically evaluate modern, minimally invasive procedures for peripheral lung nodules diagnosis and to guide patient-centered care while minimizing the downstream effects of nondiagnostic biopsies. Clear, transparent, and consistent reporting will enable physicians to choose the most appropriate diagnostic tools, improve patient outcomes by reducing unnecessary procedures, and expedite accurate diagnoses. This initiative is a crucial first step toward creating high-quality studies that can inform technology implementation decisions and promote equitable health care.


References

1. Tanner NT, Yarmus L, Chen A, et al. Standard bronchoscopy with fluoroscopy vs thin bronchoscopy and radial endobronchial ultrasound for biopsy of pulmonary lesions: a multicenter, prospective, randomized trial. Chest. 2018;154(5):1035-1043.

2. Ost DE, Ernst A, Lei X, et al. Diagnostic yield and complications of bronchoscopy for peripheral lung lesions. Results of the AQuIRE Registry. Am J Resp Crit Care Med. 2016;193(1):68-77.

3. Gonzalez AV, Silvestri GA, Korevaar DA, et al. Assessment of advanced diagnostic bronchoscopy outcomes for peripheral lung lesions: a Delphi consensus definition of diagnostic yield and recommendations for patient-centered study designs. An official American Thoracic Society/American College of Chest Physicians research statement. Am J Respir Crit Care Med. 2024;209(6):634-646.

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Post–intensive care syndrome and insomnia

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Changed
Tue, 07/02/2024 - 15:22

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.1 We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.2 Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST
Dr. Leela Krishna Teja Boppana

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.3 When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST
Dr. Mariam Louis


Since the American Academy of Sleep Medicine (AASM) 2021 clinical practice guideline on behavioral and psychological treatments for chronic insomnia, which made a strong recommendation for CBT-I, we continue to face barriers to incorporating CBT-I into our own clinical practice.4 This is due to limited access to CBT-I psychotherapists and patients’ lack of knowledge or treatment beliefs, among other reasons. However, there are numerous digital CBT-I platforms that patients can freely access from their mobile phone and are listed in the AASM article, “Digital cognitive behavioral therapy for insomnia: Platforms and characteristics,” which can help with treatment of insomnia.

For patients who are seen in post-ICU clinics, the first step in treating insomnia is discussing good sleep hygiene, providing resources for CBT-I (digital or in person), and treating coexistent psychiatric conditions.

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

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SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.1 We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.2 Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST
Dr. Leela Krishna Teja Boppana

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.3 When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST
Dr. Mariam Louis


Since the American Academy of Sleep Medicine (AASM) 2021 clinical practice guideline on behavioral and psychological treatments for chronic insomnia, which made a strong recommendation for CBT-I, we continue to face barriers to incorporating CBT-I into our own clinical practice.4 This is due to limited access to CBT-I psychotherapists and patients’ lack of knowledge or treatment beliefs, among other reasons. However, there are numerous digital CBT-I platforms that patients can freely access from their mobile phone and are listed in the AASM article, “Digital cognitive behavioral therapy for insomnia: Platforms and characteristics,” which can help with treatment of insomnia.

For patients who are seen in post-ICU clinics, the first step in treating insomnia is discussing good sleep hygiene, providing resources for CBT-I (digital or in person), and treating coexistent psychiatric conditions.

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.1 We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.2 Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST
Dr. Leela Krishna Teja Boppana

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.3 When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST
Dr. Mariam Louis


Since the American Academy of Sleep Medicine (AASM) 2021 clinical practice guideline on behavioral and psychological treatments for chronic insomnia, which made a strong recommendation for CBT-I, we continue to face barriers to incorporating CBT-I into our own clinical practice.4 This is due to limited access to CBT-I psychotherapists and patients’ lack of knowledge or treatment beliefs, among other reasons. However, there are numerous digital CBT-I platforms that patients can freely access from their mobile phone and are listed in the AASM article, “Digital cognitive behavioral therapy for insomnia: Platforms and characteristics,” which can help with treatment of insomnia.

For patients who are seen in post-ICU clinics, the first step in treating insomnia is discussing good sleep hygiene, providing resources for CBT-I (digital or in person), and treating coexistent psychiatric conditions.

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

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Short telomere length and immunosuppression: Updates in nonidiopathic pulmonary fibrosis, interstitial lung disease

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Tue, 07/02/2024 - 15:25

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Interstitial Lung Disease Section

Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.

CHEST
Dr. Mamta Chhabria

Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).

CHEST
Dr. Ryan D. Boente


Data in patients with non-IPF ILD (which is arguably more difficult to diagnose and manage) were lacking until a recent retrospective cohort study of patients from five centers across the US demonstrated that immunosuppressant exposure in patients with age-adjusted telomere length <10th percentile was associated with a reduced 2-year transplant-free survival in fibrotic hypersensitivity pneumonitis and unclassifiable ILD subgroups.1 This study was underpowered to detect associations in the connective tissue disease-ILD group. Interestingly, authors noted that immunosuppressant exposure was not associated with lung function decline in the short telomere group, suggesting that worse outcomes may be attributable to unmasking extrapulmonary manifestations of short telomeres, such as bone marrow failure and impaired adaptive immunity. Studies like these are essential to guide decision-making in the age of personalized medicine and underscore the necessity for prospective studies to validate these findings.

References

1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.

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DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Interstitial Lung Disease Section

Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.

CHEST
Dr. Mamta Chhabria

Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).

CHEST
Dr. Ryan D. Boente


Data in patients with non-IPF ILD (which is arguably more difficult to diagnose and manage) were lacking until a recent retrospective cohort study of patients from five centers across the US demonstrated that immunosuppressant exposure in patients with age-adjusted telomere length <10th percentile was associated with a reduced 2-year transplant-free survival in fibrotic hypersensitivity pneumonitis and unclassifiable ILD subgroups.1 This study was underpowered to detect associations in the connective tissue disease-ILD group. Interestingly, authors noted that immunosuppressant exposure was not associated with lung function decline in the short telomere group, suggesting that worse outcomes may be attributable to unmasking extrapulmonary manifestations of short telomeres, such as bone marrow failure and impaired adaptive immunity. Studies like these are essential to guide decision-making in the age of personalized medicine and underscore the necessity for prospective studies to validate these findings.

References

1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Interstitial Lung Disease Section

Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.

CHEST
Dr. Mamta Chhabria

Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).

CHEST
Dr. Ryan D. Boente


Data in patients with non-IPF ILD (which is arguably more difficult to diagnose and manage) were lacking until a recent retrospective cohort study of patients from five centers across the US demonstrated that immunosuppressant exposure in patients with age-adjusted telomere length <10th percentile was associated with a reduced 2-year transplant-free survival in fibrotic hypersensitivity pneumonitis and unclassifiable ILD subgroups.1 This study was underpowered to detect associations in the connective tissue disease-ILD group. Interestingly, authors noted that immunosuppressant exposure was not associated with lung function decline in the short telomere group, suggesting that worse outcomes may be attributable to unmasking extrapulmonary manifestations of short telomeres, such as bone marrow failure and impaired adaptive immunity. Studies like these are essential to guide decision-making in the age of personalized medicine and underscore the necessity for prospective studies to validate these findings.

References

1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.

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Expanding recommendations for RSV vaccination

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Changed
Tue, 07/02/2024 - 15:23

AIRWAYS DISORDERS NETWORK

Asthma and COPD Section

Respiratory syncytial virus (RSV) has been increasingly recognized as a prevalent cause of lower respiratory tract infection (LRTI) among adults in the United States. The risk of hospitalization and mortality from RSV-associated respiratory failure is higher in those with chronic lung disease. In adults aged 65 years or older, RSV has shown to cause up to 160,000 hospitalizations and 10,000 deaths annually.

CHEST
Dr. Melanie Krongold

In 2023, the US Food and Drug Administration approved the adjuvanted RSVPreF3 vaccine (Arexvy, GSK) and the bivalent RSVPreF vaccine (Abrysvo, Pfizer). Both vaccines have been shown to significantly reduce the risk of developing RSV LRTI and are currently recommended for single-dose administration in adults 60 years or older—irrespective of comorbidities.

RSV has been well established as a major cause of LRTI and morbidity among infants. Maternal vaccination with RSVPreF in patients who are pregnant is suggested between 32 0/7 and 36 6/7 weeks of gestation if the date of delivery falls during RSV season to prevent severe illness in young infants in their first months of life. At present, there are no data supporting vaccine administration to patients who are pregnant delivering outside of the RSV season.

CHEST
Dr. Megan Conroy


What about the rest of the patients? A phase 3b clinical trial to assess the safety and immunogenicity of the RSVPreF3 vaccine in individuals 18 to 49 years of age at increased risk for RSV LRTI, including those with chronic respiratory diseases, is currently underway with projected completion in April 2025 (clinical trials.gov; ID NCT06389487). Additional studies examining safety and immunogenicity combining RSV vaccines with PCV20, influenza, COVID, or Tdap vaccines are also underway. These outcomes will be significant for future recommendations to further lower the risk of developing LRTI, hospitalization, and death among patients less than the age of 60 with chronic lung diseases.


Resources

1. Melgar M, Britton A, Roper LE, et al. Use of respiratory syncytial virus vaccines in older adults: recommendations of the Advisory Committee on Immunization Practices - United States, 2023. MMWR Morb Mortal Wkly Rep. 2023;72(29):793-801.

2. Healthcare Providers: RSV Vaccination for Adults 60 Years of Age and Over. Centers for Disease Control and Prevention. Updated March 1, 2024. https://www.cdc.gov/vaccines/vpd/rsv/hcp/older-adults.html

3. Ault KA, Hughes BL, Riley LE. Maternal Respiratory Syncytial Virus Vaccination. The American College of Obstetricians and Gynecologists. Updated December 11, 2023. https://www.acog.org/clinical/clinical-guidance/practice-advisory/articles/2023/09/maternal-respiratory-syncytial-virus-vaccination

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AIRWAYS DISORDERS NETWORK

Asthma and COPD Section

Respiratory syncytial virus (RSV) has been increasingly recognized as a prevalent cause of lower respiratory tract infection (LRTI) among adults in the United States. The risk of hospitalization and mortality from RSV-associated respiratory failure is higher in those with chronic lung disease. In adults aged 65 years or older, RSV has shown to cause up to 160,000 hospitalizations and 10,000 deaths annually.

CHEST
Dr. Melanie Krongold

In 2023, the US Food and Drug Administration approved the adjuvanted RSVPreF3 vaccine (Arexvy, GSK) and the bivalent RSVPreF vaccine (Abrysvo, Pfizer). Both vaccines have been shown to significantly reduce the risk of developing RSV LRTI and are currently recommended for single-dose administration in adults 60 years or older—irrespective of comorbidities.

RSV has been well established as a major cause of LRTI and morbidity among infants. Maternal vaccination with RSVPreF in patients who are pregnant is suggested between 32 0/7 and 36 6/7 weeks of gestation if the date of delivery falls during RSV season to prevent severe illness in young infants in their first months of life. At present, there are no data supporting vaccine administration to patients who are pregnant delivering outside of the RSV season.

CHEST
Dr. Megan Conroy


What about the rest of the patients? A phase 3b clinical trial to assess the safety and immunogenicity of the RSVPreF3 vaccine in individuals 18 to 49 years of age at increased risk for RSV LRTI, including those with chronic respiratory diseases, is currently underway with projected completion in April 2025 (clinical trials.gov; ID NCT06389487). Additional studies examining safety and immunogenicity combining RSV vaccines with PCV20, influenza, COVID, or Tdap vaccines are also underway. These outcomes will be significant for future recommendations to further lower the risk of developing LRTI, hospitalization, and death among patients less than the age of 60 with chronic lung diseases.


Resources

1. Melgar M, Britton A, Roper LE, et al. Use of respiratory syncytial virus vaccines in older adults: recommendations of the Advisory Committee on Immunization Practices - United States, 2023. MMWR Morb Mortal Wkly Rep. 2023;72(29):793-801.

2. Healthcare Providers: RSV Vaccination for Adults 60 Years of Age and Over. Centers for Disease Control and Prevention. Updated March 1, 2024. https://www.cdc.gov/vaccines/vpd/rsv/hcp/older-adults.html

3. Ault KA, Hughes BL, Riley LE. Maternal Respiratory Syncytial Virus Vaccination. The American College of Obstetricians and Gynecologists. Updated December 11, 2023. https://www.acog.org/clinical/clinical-guidance/practice-advisory/articles/2023/09/maternal-respiratory-syncytial-virus-vaccination

AIRWAYS DISORDERS NETWORK

Asthma and COPD Section

Respiratory syncytial virus (RSV) has been increasingly recognized as a prevalent cause of lower respiratory tract infection (LRTI) among adults in the United States. The risk of hospitalization and mortality from RSV-associated respiratory failure is higher in those with chronic lung disease. In adults aged 65 years or older, RSV has shown to cause up to 160,000 hospitalizations and 10,000 deaths annually.

CHEST
Dr. Melanie Krongold

In 2023, the US Food and Drug Administration approved the adjuvanted RSVPreF3 vaccine (Arexvy, GSK) and the bivalent RSVPreF vaccine (Abrysvo, Pfizer). Both vaccines have been shown to significantly reduce the risk of developing RSV LRTI and are currently recommended for single-dose administration in adults 60 years or older—irrespective of comorbidities.

RSV has been well established as a major cause of LRTI and morbidity among infants. Maternal vaccination with RSVPreF in patients who are pregnant is suggested between 32 0/7 and 36 6/7 weeks of gestation if the date of delivery falls during RSV season to prevent severe illness in young infants in their first months of life. At present, there are no data supporting vaccine administration to patients who are pregnant delivering outside of the RSV season.

CHEST
Dr. Megan Conroy


What about the rest of the patients? A phase 3b clinical trial to assess the safety and immunogenicity of the RSVPreF3 vaccine in individuals 18 to 49 years of age at increased risk for RSV LRTI, including those with chronic respiratory diseases, is currently underway with projected completion in April 2025 (clinical trials.gov; ID NCT06389487). Additional studies examining safety and immunogenicity combining RSV vaccines with PCV20, influenza, COVID, or Tdap vaccines are also underway. These outcomes will be significant for future recommendations to further lower the risk of developing LRTI, hospitalization, and death among patients less than the age of 60 with chronic lung diseases.


Resources

1. Melgar M, Britton A, Roper LE, et al. Use of respiratory syncytial virus vaccines in older adults: recommendations of the Advisory Committee on Immunization Practices - United States, 2023. MMWR Morb Mortal Wkly Rep. 2023;72(29):793-801.

2. Healthcare Providers: RSV Vaccination for Adults 60 Years of Age and Over. Centers for Disease Control and Prevention. Updated March 1, 2024. https://www.cdc.gov/vaccines/vpd/rsv/hcp/older-adults.html

3. Ault KA, Hughes BL, Riley LE. Maternal Respiratory Syncytial Virus Vaccination. The American College of Obstetricians and Gynecologists. Updated December 11, 2023. https://www.acog.org/clinical/clinical-guidance/practice-advisory/articles/2023/09/maternal-respiratory-syncytial-virus-vaccination

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Bringing trainee wellness to the forefront

Article Type
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Tue, 07/02/2024 - 15:16

Researching the impact of reflection in medical training

Before the spread of COVID-19, and increasingly during the pandemic, Ilana Krumm, MD, noticed a burgeoning focus on wellness for trainees and how to combat burnout in the medical space.

But Dr. Krumm also noticed that most of the existing programs focused on the individual level, rather than the system level. The onus was on the trainees to manage their wellness and burnout.

“I wanted to look at something that could be instituted at a systems level as opposed to putting all the burden of this wellness on the resident, as someone who already has a huge burden of work, stress, and time constraints as they try to learn their discipline,” Dr. Krumm said. “Asking them to meditate on their own time seemed very impractical.”

CHEST
Dr. Ilana Krumm


Eager to research this idea, Dr. Krumm applied for the CHEST Research Grant in Medical Education.

“The fact that CHEST is willing to support medical education research is really important for all those trying to better the educational environment. Although there’s a movement toward more support for medical education research and more recognition of its value, I think the fact that CHEST has already done so has helped advance the field and the support for the field as a whole,” Dr. Krumm said.

With the support of a CHEST medical education research grant, and under the mentorship of Rosemary Adamson, MBBS, Dr. Krumm began studying how incorporating a system-level program called Reflection Rounds could help trainees alleviate burnout.

“Having the support from a reputable institution like CHEST inherently gave the work that I was doing value,” Dr. Krumm said. “It gave folks an understanding that this research in medical education has importance.”

Dr. Krumm’s project focused on the monthly Reflection Rounds between the ICU, palliative care, and chaplaincy staff that were held at the Seattle VA Medical Center, where residents could discuss the challenges of caring for critically ill patients during a protected time. While similar interventions around death and dying have been shown to help residents reduce burnout in medical intensive care rotations, it was unknown which aspects of these sessions would be most effective.

Participant interviews were conducted before and after the residents’ monthly sessions to understand the impact these sessions had on wellness and burnout levels.

“With the grant funding from CHEST, our team was able to purchase the recording equipment, transcription, and software necessary to complete a thorough qualitative research project, which greatly accelerated the project timeline,” she said.

Through these interviews, Dr. Krumm’s team identified three key themes that shed light on the impact of Reflection Rounds.
 

1. Cultural precedent

Participants were encouraged to participate as little or as much as they wanted during the session. Despite some residents being less vocal during these discussions, every resident agreed that this type of session set an important cultural precedent in their program and acknowledged the value of a program that encouraged space for decompression and reflection.

2. Shared experiences

During this project, many residents experienced an increased sense of isolation, as COVID-19 precautions were stricter in the ICU. Having this protected time together allowed residents to discover their shared experiences and find comfort in them while feeling supported.

“A lot of residents commented that it was nice to know that others were going through this as well or that they were also finding this particular instance difficult,” Dr. Krumm said.
 

3. Ritual

At the opening of each hour-long session, participants were invited to light a candle and say aloud or think to themselves the name of a patient they had lost, had a hard time with, or cared for during their time in the ICU.

“Every single person pointed to that moment as meaningful and impactful,” Dr. Krumm said.

This ritual gave the residents time to center and have a common focus with their peers to think about patient stories that they were carrying with them.

“Maybe just incorporating a small moment like that, a point of reflection, could potentially have a big impact on the weight we carry as providers who care for [patients who are] critically ill,” Dr. Krumm said. “What I’ve learned from this project will make me a better leader in the ICU, not only in taking care of critically ill individuals but also in taking care of the team doing that work.”

Dr. Krumm credits the CHEST grant funding and subsequent research project with helping her join a highly competitive fellowship program at the University of California San Francisco, where she can continue to conduct research in the field of medical education.

“I am working closely with medical education faculty and peers to design new research studies and further establish myself in the field of medical education, leading to my ultimate goal of becoming a program director at a strong med-ed-focused program.”

This article was adapted from the Spring 2024 online issue of CHEST Advocates. For the full article—and to engage with the other content from this issue—visit chestnet.org/chest-advocates.

Support CHEST grants like this

Through clinical research grants, CHEST assists in acquiring vital data and clinically important results that can advance medical care. You can help support projects like this by making a gift to CHEST.

MAKE A GIFT » | LEARN ABOUT CHEST PHILANTHROPY »

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Researching the impact of reflection in medical training

Researching the impact of reflection in medical training

Before the spread of COVID-19, and increasingly during the pandemic, Ilana Krumm, MD, noticed a burgeoning focus on wellness for trainees and how to combat burnout in the medical space.

But Dr. Krumm also noticed that most of the existing programs focused on the individual level, rather than the system level. The onus was on the trainees to manage their wellness and burnout.

“I wanted to look at something that could be instituted at a systems level as opposed to putting all the burden of this wellness on the resident, as someone who already has a huge burden of work, stress, and time constraints as they try to learn their discipline,” Dr. Krumm said. “Asking them to meditate on their own time seemed very impractical.”

CHEST
Dr. Ilana Krumm


Eager to research this idea, Dr. Krumm applied for the CHEST Research Grant in Medical Education.

“The fact that CHEST is willing to support medical education research is really important for all those trying to better the educational environment. Although there’s a movement toward more support for medical education research and more recognition of its value, I think the fact that CHEST has already done so has helped advance the field and the support for the field as a whole,” Dr. Krumm said.

With the support of a CHEST medical education research grant, and under the mentorship of Rosemary Adamson, MBBS, Dr. Krumm began studying how incorporating a system-level program called Reflection Rounds could help trainees alleviate burnout.

“Having the support from a reputable institution like CHEST inherently gave the work that I was doing value,” Dr. Krumm said. “It gave folks an understanding that this research in medical education has importance.”

Dr. Krumm’s project focused on the monthly Reflection Rounds between the ICU, palliative care, and chaplaincy staff that were held at the Seattle VA Medical Center, where residents could discuss the challenges of caring for critically ill patients during a protected time. While similar interventions around death and dying have been shown to help residents reduce burnout in medical intensive care rotations, it was unknown which aspects of these sessions would be most effective.

Participant interviews were conducted before and after the residents’ monthly sessions to understand the impact these sessions had on wellness and burnout levels.

“With the grant funding from CHEST, our team was able to purchase the recording equipment, transcription, and software necessary to complete a thorough qualitative research project, which greatly accelerated the project timeline,” she said.

Through these interviews, Dr. Krumm’s team identified three key themes that shed light on the impact of Reflection Rounds.
 

1. Cultural precedent

Participants were encouraged to participate as little or as much as they wanted during the session. Despite some residents being less vocal during these discussions, every resident agreed that this type of session set an important cultural precedent in their program and acknowledged the value of a program that encouraged space for decompression and reflection.

2. Shared experiences

During this project, many residents experienced an increased sense of isolation, as COVID-19 precautions were stricter in the ICU. Having this protected time together allowed residents to discover their shared experiences and find comfort in them while feeling supported.

“A lot of residents commented that it was nice to know that others were going through this as well or that they were also finding this particular instance difficult,” Dr. Krumm said.
 

3. Ritual

At the opening of each hour-long session, participants were invited to light a candle and say aloud or think to themselves the name of a patient they had lost, had a hard time with, or cared for during their time in the ICU.

“Every single person pointed to that moment as meaningful and impactful,” Dr. Krumm said.

This ritual gave the residents time to center and have a common focus with their peers to think about patient stories that they were carrying with them.

“Maybe just incorporating a small moment like that, a point of reflection, could potentially have a big impact on the weight we carry as providers who care for [patients who are] critically ill,” Dr. Krumm said. “What I’ve learned from this project will make me a better leader in the ICU, not only in taking care of critically ill individuals but also in taking care of the team doing that work.”

Dr. Krumm credits the CHEST grant funding and subsequent research project with helping her join a highly competitive fellowship program at the University of California San Francisco, where she can continue to conduct research in the field of medical education.

“I am working closely with medical education faculty and peers to design new research studies and further establish myself in the field of medical education, leading to my ultimate goal of becoming a program director at a strong med-ed-focused program.”

This article was adapted from the Spring 2024 online issue of CHEST Advocates. For the full article—and to engage with the other content from this issue—visit chestnet.org/chest-advocates.

Support CHEST grants like this

Through clinical research grants, CHEST assists in acquiring vital data and clinically important results that can advance medical care. You can help support projects like this by making a gift to CHEST.

MAKE A GIFT » | LEARN ABOUT CHEST PHILANTHROPY »

Before the spread of COVID-19, and increasingly during the pandemic, Ilana Krumm, MD, noticed a burgeoning focus on wellness for trainees and how to combat burnout in the medical space.

But Dr. Krumm also noticed that most of the existing programs focused on the individual level, rather than the system level. The onus was on the trainees to manage their wellness and burnout.

“I wanted to look at something that could be instituted at a systems level as opposed to putting all the burden of this wellness on the resident, as someone who already has a huge burden of work, stress, and time constraints as they try to learn their discipline,” Dr. Krumm said. “Asking them to meditate on their own time seemed very impractical.”

CHEST
Dr. Ilana Krumm


Eager to research this idea, Dr. Krumm applied for the CHEST Research Grant in Medical Education.

“The fact that CHEST is willing to support medical education research is really important for all those trying to better the educational environment. Although there’s a movement toward more support for medical education research and more recognition of its value, I think the fact that CHEST has already done so has helped advance the field and the support for the field as a whole,” Dr. Krumm said.

With the support of a CHEST medical education research grant, and under the mentorship of Rosemary Adamson, MBBS, Dr. Krumm began studying how incorporating a system-level program called Reflection Rounds could help trainees alleviate burnout.

“Having the support from a reputable institution like CHEST inherently gave the work that I was doing value,” Dr. Krumm said. “It gave folks an understanding that this research in medical education has importance.”

Dr. Krumm’s project focused on the monthly Reflection Rounds between the ICU, palliative care, and chaplaincy staff that were held at the Seattle VA Medical Center, where residents could discuss the challenges of caring for critically ill patients during a protected time. While similar interventions around death and dying have been shown to help residents reduce burnout in medical intensive care rotations, it was unknown which aspects of these sessions would be most effective.

Participant interviews were conducted before and after the residents’ monthly sessions to understand the impact these sessions had on wellness and burnout levels.

“With the grant funding from CHEST, our team was able to purchase the recording equipment, transcription, and software necessary to complete a thorough qualitative research project, which greatly accelerated the project timeline,” she said.

Through these interviews, Dr. Krumm’s team identified three key themes that shed light on the impact of Reflection Rounds.
 

1. Cultural precedent

Participants were encouraged to participate as little or as much as they wanted during the session. Despite some residents being less vocal during these discussions, every resident agreed that this type of session set an important cultural precedent in their program and acknowledged the value of a program that encouraged space for decompression and reflection.

2. Shared experiences

During this project, many residents experienced an increased sense of isolation, as COVID-19 precautions were stricter in the ICU. Having this protected time together allowed residents to discover their shared experiences and find comfort in them while feeling supported.

“A lot of residents commented that it was nice to know that others were going through this as well or that they were also finding this particular instance difficult,” Dr. Krumm said.
 

3. Ritual

At the opening of each hour-long session, participants were invited to light a candle and say aloud or think to themselves the name of a patient they had lost, had a hard time with, or cared for during their time in the ICU.

“Every single person pointed to that moment as meaningful and impactful,” Dr. Krumm said.

This ritual gave the residents time to center and have a common focus with their peers to think about patient stories that they were carrying with them.

“Maybe just incorporating a small moment like that, a point of reflection, could potentially have a big impact on the weight we carry as providers who care for [patients who are] critically ill,” Dr. Krumm said. “What I’ve learned from this project will make me a better leader in the ICU, not only in taking care of critically ill individuals but also in taking care of the team doing that work.”

Dr. Krumm credits the CHEST grant funding and subsequent research project with helping her join a highly competitive fellowship program at the University of California San Francisco, where she can continue to conduct research in the field of medical education.

“I am working closely with medical education faculty and peers to design new research studies and further establish myself in the field of medical education, leading to my ultimate goal of becoming a program director at a strong med-ed-focused program.”

This article was adapted from the Spring 2024 online issue of CHEST Advocates. For the full article—and to engage with the other content from this issue—visit chestnet.org/chest-advocates.

Support CHEST grants like this

Through clinical research grants, CHEST assists in acquiring vital data and clinically important results that can advance medical care. You can help support projects like this by making a gift to CHEST.

MAKE A GIFT » | LEARN ABOUT CHEST PHILANTHROPY »

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