The incidence of malignant melanoma has been rising in the United States, especially among non-Hispanic white men and women. Death rates have increased for those aged 65 years or older, and incidence rates have increased for all age groups.¹ It is a serious public health issue.

Given the unique biology of melanoma, metastatic disease can present in a variety of ways. In most cases, the lymph nodes and lungs are involved.² The incidence of brain metastases is 10%-40%, however the percentage may be even higher based on reported incidence of autopsy reports.³ The most common forms of metastatic melanoma to the spine are vertebral and intramedullary.⁴ Specifically, leptomeningeal involvement can be found in 20% of patients in clinical studies and 44%-70% in autopsy series of patients with central nervous system (CNS) metastatic disease.⁵ Despite its incidence, leptomeningeal disease (LMD) from melanoma is rarely discussed in the literature and the diagnosis may be difficult. Even rarer is the documented presentation of intramedullary spinal cord metastases, or “drop metastases.”⁶ In our review of the literature, we found no published case reports to date of drop metastases from melanoma causing cauda equina syndrome.

The prognosis of patients with metastatic melanoma with brain metastases is very poor, with a median overall survival of about 4 months reported in several studies.^7-9 Prognosis is even worse for patients with leptomeningeal involvement, and median survival without therapy is about 4-6 weeks.¹⁰ A combination of intrathecal and systemic chemotherapy can be used to treat LMD.¹¹

Case presentation and summary

This is the case of a 56-year-old man with history of metastatic melanoma that had been initially diagnosed about 4 years before the current case presentation. Original sites of disease were a supraclavicular lymph node and solitary liver metastasis, both of which were resected. The patient then developed biopsy-proven lung involvement that required left and right wedge resections. Mutation testing for BRAF V600E and BRAF V600K was sent and not detected. Therefore the patient did not receive any BRAF-targeted therapies. Subsequently, recurrent metastatic disease to the brain with 2 dominant lesions in the cerebellum and the occiput as well as numerous small lesions at the gray-white matter junction was identified (Figure 1 and Figure 2).

The patient received whole-brain radiation (30 Gy in 10 fractions of 3 Gy each). There was no evidence of disease in his spine at that time. About 2 weeks after completing whole-brain radiation, the patient presented to the hospital with left lower extremity weakness, urinary retention, bowel incontinence, saddle anesthesia, and malaise. The symptoms had begun after he had finished whole-brain radiation and weakness progressed to the point at which he need a cane to be able to walk. A physical examination was significant for hyporreflexia, decreased strength and sensitivity on left lower extremity, saddle anesthesia, and lumbar spinal tenderness to palpation. The results of magnetic-resonance imaging (MRI) of the spine revealed multiple soft-tissue nodules extending from the conus medullaris throughout the cauda equina, consistent with intramedullary metastases, as well as concomitant leptomeningeal involvement (Figure 3).

Conclusions

Although metastatic melanoma to the brain is not uncommon, leptomeningeal and intramedullary drop metastases are an infrequent presentation. Even more rare are intramedullary drop metastasis that are significant enough to cause cauda equina syndrome, as with our patient. The incidence of LMD has increased over the years and may continue to increase, likely because of the improved overall survival and a prolonged control of extracranial disease with newly approved systemic therapeutic drugs, such as molecularly targeted therapy and immunotherapy.¹² Intramedullary metastases are extremely rare, but reported incidence has seemed to be increasing due to detection with MRI. Currently there are fewer than 100 case reports of intramedullary spinal cord metastasis.⁶ In one retrospective study, 40 patients with intramedullary metastatic disease secondary to systemic cancer were identified during 1980-1993.⁶ About half of those cases were from lung cancer, the second most common was breast cancer.

CNS involvement by melanoma can have debilitating complications and confers a poor prognosis. In another retrospective study, several patient characteristics were found to be associated with significantly shorter survival in patients with known brain metastases, including presence of neurologic symptoms and leptomeningeal involvement.³

Malignant cells can reach the CSF by several routes: direct extension, hematogenous, venous access, venous drainage from bone marrow and cranial and peripheral nerves. Once the tumor has reached the CSF, it can seed any portion of the nervous system that has contact with the CSF and become entangled among the cauda equine.¹³

Given the rarity of leptomeningeal and intramedullary involvement of melanoma, there are no standard treatment guidelines. Treatment for LMD usually consists of intrathecal and systemic chemotherapy. Commonly used intrathecal agents are methotrexate, liposomal cytarabine, and thiopeta.¹¹ The goals of treatment are to improve or stabilize neurologic status of the patient and ideally prolong survival. The choice of agent for intrathecal chemotherapy is guided by the primary tumor, however, there is no strong evidence to choose one agent over the other.^12,14 Methotrexate or cytarabine are generally recommended in the National Comprehensive Cancer Network (NCCN) guidelines. Targeted therapy toward the primary tumor is occasionally used for treatment of LMD, for example rituximab can be given intrathecally for lymphoma,¹⁵ and trastuzumab has been given intrathecally for breast cancer.¹⁶ No intrathecal targeted agents are currently available for melanoma. Administration of intrathecal chemotherapy is given via lumbar puncture or Ommaya reservoir. Induction intrathecal chemotherapy is recommended by NCCN to be given for 4-6 weeks. The schedule of administration varies based on the agent used. Most systemic chemotherapy has poor CSF penetration, which is the basis behind using chemotherapy intrathecally in these patients.¹⁴ However, novel therapies for melanoma, such as ipilimumab, have shown activity in the CNS, and it is not known if intrathecal chemotherapy will continue to play role in the management of LMD.¹⁷

Systemic therapy for metastatic melanoma has changed with the development of novel agents, which have shown better efficacy than traditional chemotherapy. The recommendation for first-line systemic therapy of metastatic unresectable melanoma is based on several factors: BRAF mutation status, tempo of disease, and presence or absence of cancer-related symptoms. Immunotherapy for metastatic melanoma that is unresectable includes anti-programmed cell death protein-1 (PD-1) monotherapy (nivolumab or pembrolizumab) or combination therapy with nivolumab plus ipilimumab. Targeted therapy is preferred in cases with an identified BRAF mutation. Combination therapy with dabrafenib plus trametinib or with vemurafenib plus cobimetinib is recommended. Single-agent therapy may also be used with dabrafenib or vemurafenib.¹⁸

Ipilimumab is a monoclonal antibody that blocks cytotoxic T-lymphocyte antigen-4 to potentiate an anti-tumor T-cell response that was approved in 2011 by the US Food and Drug Administration for the treatment of melanoma. A randomized, phase 3 clinical trial showed an increase in overall survival in patients with unresectable metastatic disease who had received previous treatment.¹⁹ Before that, no therapy had been shown to improve overall survival in patients with metastatic melanoma. Patients with CNS metastases were included in this study.¹⁹

The activity of ipilimumab specifically in patients with brain metastasis was further studied in a phase 2 trial that enrolled 72 patients, 1 cohort with symptomatic brain metastases and the other cohort with asymptomatic brain metastases.²⁰ After 12 weeks of therapy, response was assessed by modified World Health Organization criteria for disease control (complete response plus partial response plus stable disease). In all, 18% of patients with asymptomatic brain metastasis achieved disease control, compared with 10% of patients with symptomatic brain metastases. When the brain alone was assessed, 24% of asymptomatic patients and 10% of symptomatic patients achieved disease control. No unexpected toxic effects occurred during the study. Anti-PD1 therapy such as nivolumab, which has shown durable responses in metastatic melanoma, has no published results specifically in patients with active brain metastases.

Of the BRAF-targeted therapy, dabrafenib and vemurafenib have also been studied in patients with brain metastases. For darafenib, 172 patients with BRAF-mutated metastatic melanoma were included in a phase 2 clinical trial that showed an intracranial response of 39% in previously untreated patients and 31% in patients whose brain metastases had progressed after previous local treatment.²¹ Vemurafenib has also shown intracranial response in a phase 2 clinical trial.²²

The role of the aforementioned therapies in patients with metastatic melanoma with CNS disease should not be overlooked because these patients are typically excluded from clinical trials. As already noted, agents such as ipilimumab and the dabrafenib–vemurafenib combination have been studied in patients with brain metastases and have shown disease control, but more studies are needed to truly assess whether there is an improvement in overall survival and whether that will change treatment guidelines. Although patients with parenchymal brain metastases were included in these studies, it is not clear how patients with LMD and intramedullary spinal cord metastases, such as our patient, would be affected. It is also not clear whether intrathecal chemotherapy will continue to play a role in management of metastatic melanoma with LMD, especially if these newer agents have CNS activity in addition to controlling extracranial disease. Although rarely documented, leptomeningeal and intramedullary metastatic disease will likely become increasingly recognized as patients with cancer live longer and diagnostic studies improve. These initial studies showing intracranial disease control show compelling evidence to continue enrolling patients with active CNS disease in clinical trials.

The incidence of malignant melanoma has been rising in the United States, especially among non-Hispanic white men and women. Death rates have increased for those aged 65 years or older, and incidence rates have increased for all age groups.¹ It is a serious public health issue.

Given the unique biology of melanoma, metastatic disease can present in a variety of ways. In most cases, the lymph nodes and lungs are involved.² The incidence of brain metastases is 10%-40%, however the percentage may be even higher based on reported incidence of autopsy reports.³ The most common forms of metastatic melanoma to the spine are vertebral and intramedullary.⁴ Specifically, leptomeningeal involvement can be found in 20% of patients in clinical studies and 44%-70% in autopsy series of patients with central nervous system (CNS) metastatic disease.⁵ Despite its incidence, leptomeningeal disease (LMD) from melanoma is rarely discussed in the literature and the diagnosis may be difficult. Even rarer is the documented presentation of intramedullary spinal cord metastases, or “drop metastases.”⁶ In our review of the literature, we found no published case reports to date of drop metastases from melanoma causing cauda equina syndrome.

The prognosis of patients with metastatic melanoma with brain metastases is very poor, with a median overall survival of about 4 months reported in several studies.^7-9 Prognosis is even worse for patients with leptomeningeal involvement, and median survival without therapy is about 4-6 weeks.¹⁰ A combination of intrathecal and systemic chemotherapy can be used to treat LMD.¹¹

Case presentation and summary

This is the case of a 56-year-old man with history of metastatic melanoma that had been initially diagnosed about 4 years before the current case presentation. Original sites of disease were a supraclavicular lymph node and solitary liver metastasis, both of which were resected. The patient then developed biopsy-proven lung involvement that required left and right wedge resections. Mutation testing for BRAF V600E and BRAF V600K was sent and not detected. Therefore the patient did not receive any BRAF-targeted therapies. Subsequently, recurrent metastatic disease to the brain with 2 dominant lesions in the cerebellum and the occiput as well as numerous small lesions at the gray-white matter junction was identified (Figure 1 and Figure 2).

The patient received whole-brain radiation (30 Gy in 10 fractions of 3 Gy each). There was no evidence of disease in his spine at that time. About 2 weeks after completing whole-brain radiation, the patient presented to the hospital with left lower extremity weakness, urinary retention, bowel incontinence, saddle anesthesia, and malaise. The symptoms had begun after he had finished whole-brain radiation and weakness progressed to the point at which he need a cane to be able to walk. A physical examination was significant for hyporreflexia, decreased strength and sensitivity on left lower extremity, saddle anesthesia, and lumbar spinal tenderness to palpation. The results of magnetic-resonance imaging (MRI) of the spine revealed multiple soft-tissue nodules extending from the conus medullaris throughout the cauda equina, consistent with intramedullary metastases, as well as concomitant leptomeningeal involvement (Figure 3).

Conclusions

Although metastatic melanoma to the brain is not uncommon, leptomeningeal and intramedullary drop metastases are an infrequent presentation. Even more rare are intramedullary drop metastasis that are significant enough to cause cauda equina syndrome, as with our patient. The incidence of LMD has increased over the years and may continue to increase, likely because of the improved overall survival and a prolonged control of extracranial disease with newly approved systemic therapeutic drugs, such as molecularly targeted therapy and immunotherapy.¹² Intramedullary metastases are extremely rare, but reported incidence has seemed to be increasing due to detection with MRI. Currently there are fewer than 100 case reports of intramedullary spinal cord metastasis.⁶ In one retrospective study, 40 patients with intramedullary metastatic disease secondary to systemic cancer were identified during 1980-1993.⁶ About half of those cases were from lung cancer, the second most common was breast cancer.

CNS involvement by melanoma can have debilitating complications and confers a poor prognosis. In another retrospective study, several patient characteristics were found to be associated with significantly shorter survival in patients with known brain metastases, including presence of neurologic symptoms and leptomeningeal involvement.³

Malignant cells can reach the CSF by several routes: direct extension, hematogenous, venous access, venous drainage from bone marrow and cranial and peripheral nerves. Once the tumor has reached the CSF, it can seed any portion of the nervous system that has contact with the CSF and become entangled among the cauda equine.¹³

Given the rarity of leptomeningeal and intramedullary involvement of melanoma, there are no standard treatment guidelines. Treatment for LMD usually consists of intrathecal and systemic chemotherapy. Commonly used intrathecal agents are methotrexate, liposomal cytarabine, and thiopeta.¹¹ The goals of treatment are to improve or stabilize neurologic status of the patient and ideally prolong survival. The choice of agent for intrathecal chemotherapy is guided by the primary tumor, however, there is no strong evidence to choose one agent over the other.^12,14 Methotrexate or cytarabine are generally recommended in the National Comprehensive Cancer Network (NCCN) guidelines. Targeted therapy toward the primary tumor is occasionally used for treatment of LMD, for example rituximab can be given intrathecally for lymphoma,¹⁵ and trastuzumab has been given intrathecally for breast cancer.¹⁶ No intrathecal targeted agents are currently available for melanoma. Administration of intrathecal chemotherapy is given via lumbar puncture or Ommaya reservoir. Induction intrathecal chemotherapy is recommended by NCCN to be given for 4-6 weeks. The schedule of administration varies based on the agent used. Most systemic chemotherapy has poor CSF penetration, which is the basis behind using chemotherapy intrathecally in these patients.¹⁴ However, novel therapies for melanoma, such as ipilimumab, have shown activity in the CNS, and it is not known if intrathecal chemotherapy will continue to play role in the management of LMD.¹⁷

Systemic therapy for metastatic melanoma has changed with the development of novel agents, which have shown better efficacy than traditional chemotherapy. The recommendation for first-line systemic therapy of metastatic unresectable melanoma is based on several factors: BRAF mutation status, tempo of disease, and presence or absence of cancer-related symptoms. Immunotherapy for metastatic melanoma that is unresectable includes anti-programmed cell death protein-1 (PD-1) monotherapy (nivolumab or pembrolizumab) or combination therapy with nivolumab plus ipilimumab. Targeted therapy is preferred in cases with an identified BRAF mutation. Combination therapy with dabrafenib plus trametinib or with vemurafenib plus cobimetinib is recommended. Single-agent therapy may also be used with dabrafenib or vemurafenib.¹⁸

Ipilimumab is a monoclonal antibody that blocks cytotoxic T-lymphocyte antigen-4 to potentiate an anti-tumor T-cell response that was approved in 2011 by the US Food and Drug Administration for the treatment of melanoma. A randomized, phase 3 clinical trial showed an increase in overall survival in patients with unresectable metastatic disease who had received previous treatment.¹⁹ Before that, no therapy had been shown to improve overall survival in patients with metastatic melanoma. Patients with CNS metastases were included in this study.¹⁹

The activity of ipilimumab specifically in patients with brain metastasis was further studied in a phase 2 trial that enrolled 72 patients, 1 cohort with symptomatic brain metastases and the other cohort with asymptomatic brain metastases.²⁰ After 12 weeks of therapy, response was assessed by modified World Health Organization criteria for disease control (complete response plus partial response plus stable disease). In all, 18% of patients with asymptomatic brain metastasis achieved disease control, compared with 10% of patients with symptomatic brain metastases. When the brain alone was assessed, 24% of asymptomatic patients and 10% of symptomatic patients achieved disease control. No unexpected toxic effects occurred during the study. Anti-PD1 therapy such as nivolumab, which has shown durable responses in metastatic melanoma, has no published results specifically in patients with active brain metastases.

Of the BRAF-targeted therapy, dabrafenib and vemurafenib have also been studied in patients with brain metastases. For darafenib, 172 patients with BRAF-mutated metastatic melanoma were included in a phase 2 clinical trial that showed an intracranial response of 39% in previously untreated patients and 31% in patients whose brain metastases had progressed after previous local treatment.²¹ Vemurafenib has also shown intracranial response in a phase 2 clinical trial.²²

The role of the aforementioned therapies in patients with metastatic melanoma with CNS disease should not be overlooked because these patients are typically excluded from clinical trials. As already noted, agents such as ipilimumab and the dabrafenib–vemurafenib combination have been studied in patients with brain metastases and have shown disease control, but more studies are needed to truly assess whether there is an improvement in overall survival and whether that will change treatment guidelines. Although patients with parenchymal brain metastases were included in these studies, it is not clear how patients with LMD and intramedullary spinal cord metastases, such as our patient, would be affected. It is also not clear whether intrathecal chemotherapy will continue to play a role in management of metastatic melanoma with LMD, especially if these newer agents have CNS activity in addition to controlling extracranial disease. Although rarely documented, leptomeningeal and intramedullary metastatic disease will likely become increasingly recognized as patients with cancer live longer and diagnostic studies improve. These initial studies showing intracranial disease control show compelling evidence to continue enrolling patients with active CNS disease in clinical trials.

The incidence of malignant melanoma has been rising in the United States, especially among non-Hispanic white men and women. Death rates have increased for those aged 65 years or older, and incidence rates have increased for all age groups.¹ It is a serious public health issue.

Given the unique biology of melanoma, metastatic disease can present in a variety of ways. In most cases, the lymph nodes and lungs are involved.² The incidence of brain metastases is 10%-40%, however the percentage may be even higher based on reported incidence of autopsy reports.³ The most common forms of metastatic melanoma to the spine are vertebral and intramedullary.⁴ Specifically, leptomeningeal involvement can be found in 20% of patients in clinical studies and 44%-70% in autopsy series of patients with central nervous system (CNS) metastatic disease.⁵ Despite its incidence, leptomeningeal disease (LMD) from melanoma is rarely discussed in the literature and the diagnosis may be difficult. Even rarer is the documented presentation of intramedullary spinal cord metastases, or “drop metastases.”⁶ In our review of the literature, we found no published case reports to date of drop metastases from melanoma causing cauda equina syndrome.

The prognosis of patients with metastatic melanoma with brain metastases is very poor, with a median overall survival of about 4 months reported in several studies.^7-9 Prognosis is even worse for patients with leptomeningeal involvement, and median survival without therapy is about 4-6 weeks.¹⁰ A combination of intrathecal and systemic chemotherapy can be used to treat LMD.¹¹

Case presentation and summary

This is the case of a 56-year-old man with history of metastatic melanoma that had been initially diagnosed about 4 years before the current case presentation. Original sites of disease were a supraclavicular lymph node and solitary liver metastasis, both of which were resected. The patient then developed biopsy-proven lung involvement that required left and right wedge resections. Mutation testing for BRAF V600E and BRAF V600K was sent and not detected. Therefore the patient did not receive any BRAF-targeted therapies. Subsequently, recurrent metastatic disease to the brain with 2 dominant lesions in the cerebellum and the occiput as well as numerous small lesions at the gray-white matter junction was identified (Figure 1 and Figure 2).

The patient received whole-brain radiation (30 Gy in 10 fractions of 3 Gy each). There was no evidence of disease in his spine at that time. About 2 weeks after completing whole-brain radiation, the patient presented to the hospital with left lower extremity weakness, urinary retention, bowel incontinence, saddle anesthesia, and malaise. The symptoms had begun after he had finished whole-brain radiation and weakness progressed to the point at which he need a cane to be able to walk. A physical examination was significant for hyporreflexia, decreased strength and sensitivity on left lower extremity, saddle anesthesia, and lumbar spinal tenderness to palpation. The results of magnetic-resonance imaging (MRI) of the spine revealed multiple soft-tissue nodules extending from the conus medullaris throughout the cauda equina, consistent with intramedullary metastases, as well as concomitant leptomeningeal involvement (Figure 3).

Conclusions

Although metastatic melanoma to the brain is not uncommon, leptomeningeal and intramedullary drop metastases are an infrequent presentation. Even more rare are intramedullary drop metastasis that are significant enough to cause cauda equina syndrome, as with our patient. The incidence of LMD has increased over the years and may continue to increase, likely because of the improved overall survival and a prolonged control of extracranial disease with newly approved systemic therapeutic drugs, such as molecularly targeted therapy and immunotherapy.¹² Intramedullary metastases are extremely rare, but reported incidence has seemed to be increasing due to detection with MRI. Currently there are fewer than 100 case reports of intramedullary spinal cord metastasis.⁶ In one retrospective study, 40 patients with intramedullary metastatic disease secondary to systemic cancer were identified during 1980-1993.⁶ About half of those cases were from lung cancer, the second most common was breast cancer.

CNS involvement by melanoma can have debilitating complications and confers a poor prognosis. In another retrospective study, several patient characteristics were found to be associated with significantly shorter survival in patients with known brain metastases, including presence of neurologic symptoms and leptomeningeal involvement.³

Malignant cells can reach the CSF by several routes: direct extension, hematogenous, venous access, venous drainage from bone marrow and cranial and peripheral nerves. Once the tumor has reached the CSF, it can seed any portion of the nervous system that has contact with the CSF and become entangled among the cauda equine.¹³

Given the rarity of leptomeningeal and intramedullary involvement of melanoma, there are no standard treatment guidelines. Treatment for LMD usually consists of intrathecal and systemic chemotherapy. Commonly used intrathecal agents are methotrexate, liposomal cytarabine, and thiopeta.¹¹ The goals of treatment are to improve or stabilize neurologic status of the patient and ideally prolong survival. The choice of agent for intrathecal chemotherapy is guided by the primary tumor, however, there is no strong evidence to choose one agent over the other.^12,14 Methotrexate or cytarabine are generally recommended in the National Comprehensive Cancer Network (NCCN) guidelines. Targeted therapy toward the primary tumor is occasionally used for treatment of LMD, for example rituximab can be given intrathecally for lymphoma,¹⁵ and trastuzumab has been given intrathecally for breast cancer.¹⁶ No intrathecal targeted agents are currently available for melanoma. Administration of intrathecal chemotherapy is given via lumbar puncture or Ommaya reservoir. Induction intrathecal chemotherapy is recommended by NCCN to be given for 4-6 weeks. The schedule of administration varies based on the agent used. Most systemic chemotherapy has poor CSF penetration, which is the basis behind using chemotherapy intrathecally in these patients.¹⁴ However, novel therapies for melanoma, such as ipilimumab, have shown activity in the CNS, and it is not known if intrathecal chemotherapy will continue to play role in the management of LMD.¹⁷

Systemic therapy for metastatic melanoma has changed with the development of novel agents, which have shown better efficacy than traditional chemotherapy. The recommendation for first-line systemic therapy of metastatic unresectable melanoma is based on several factors: BRAF mutation status, tempo of disease, and presence or absence of cancer-related symptoms. Immunotherapy for metastatic melanoma that is unresectable includes anti-programmed cell death protein-1 (PD-1) monotherapy (nivolumab or pembrolizumab) or combination therapy with nivolumab plus ipilimumab. Targeted therapy is preferred in cases with an identified BRAF mutation. Combination therapy with dabrafenib plus trametinib or with vemurafenib plus cobimetinib is recommended. Single-agent therapy may also be used with dabrafenib or vemurafenib.¹⁸

Ipilimumab is a monoclonal antibody that blocks cytotoxic T-lymphocyte antigen-4 to potentiate an anti-tumor T-cell response that was approved in 2011 by the US Food and Drug Administration for the treatment of melanoma. A randomized, phase 3 clinical trial showed an increase in overall survival in patients with unresectable metastatic disease who had received previous treatment.¹⁹ Before that, no therapy had been shown to improve overall survival in patients with metastatic melanoma. Patients with CNS metastases were included in this study.¹⁹

The activity of ipilimumab specifically in patients with brain metastasis was further studied in a phase 2 trial that enrolled 72 patients, 1 cohort with symptomatic brain metastases and the other cohort with asymptomatic brain metastases.²⁰ After 12 weeks of therapy, response was assessed by modified World Health Organization criteria for disease control (complete response plus partial response plus stable disease). In all, 18% of patients with asymptomatic brain metastasis achieved disease control, compared with 10% of patients with symptomatic brain metastases. When the brain alone was assessed, 24% of asymptomatic patients and 10% of symptomatic patients achieved disease control. No unexpected toxic effects occurred during the study. Anti-PD1 therapy such as nivolumab, which has shown durable responses in metastatic melanoma, has no published results specifically in patients with active brain metastases.

Of the BRAF-targeted therapy, dabrafenib and vemurafenib have also been studied in patients with brain metastases. For darafenib, 172 patients with BRAF-mutated metastatic melanoma were included in a phase 2 clinical trial that showed an intracranial response of 39% in previously untreated patients and 31% in patients whose brain metastases had progressed after previous local treatment.²¹ Vemurafenib has also shown intracranial response in a phase 2 clinical trial.²²

The role of the aforementioned therapies in patients with metastatic melanoma with CNS disease should not be overlooked because these patients are typically excluded from clinical trials. As already noted, agents such as ipilimumab and the dabrafenib–vemurafenib combination have been studied in patients with brain metastases and have shown disease control, but more studies are needed to truly assess whether there is an improvement in overall survival and whether that will change treatment guidelines. Although patients with parenchymal brain metastases were included in these studies, it is not clear how patients with LMD and intramedullary spinal cord metastases, such as our patient, would be affected. It is also not clear whether intrathecal chemotherapy will continue to play a role in management of metastatic melanoma with LMD, especially if these newer agents have CNS activity in addition to controlling extracranial disease. Although rarely documented, leptomeningeal and intramedullary metastatic disease will likely become increasingly recognized as patients with cancer live longer and diagnostic studies improve. These initial studies showing intracranial disease control show compelling evidence to continue enrolling patients with active CNS disease in clinical trials.

The several-week duration of this 14-year-old boy’s rash is worrisome to him and his family, despite a lack of other symptoms. Located on his right axilla, the rash was previously diagnosed as “yeast infection” but was unaffected by topical anti-yeast medications (nystatin and clotrimazole creams) and oral fluconazole.

A serious family crisis preceded the appearance of the rash: The parents lost custody of their children, who were then placed under the care of grandparents in another state. The boy lost his family and friends and had to start again in a new school.

EXAMINATION
Additional rashes are present on his face, in and behind his ears, and on focal areas of his genitals. They are all orangish red with faintly scaly surfaces. The scale on his face, ears, and genitals is coarser than that of his axilla, but it is the same salmon-pink. Focal areas of his brows and scalp are also involved.

What is the diagnosis?

Non-dermatology providers often incorrectly diagnose axillary rashes as yeast infections, or seborrhea on the face as fungal infection, simply for lack of a complete differential. The truth is, yeast infections of the skin are unusual. The differential should include psoriasis or eczema, as well as sebopsoriasis (an overlap condition with signs of both seborrhea and psoriasis).

The “trick” to diagnosing seborrhea is to recognize that it is incredibly common (affecting around 30% of the Caucasian population), is often inherited, and can affect multiple sites. When it is seen in one area, corroboration can be sought by locating typical changes elsewhere.

Although there is no cure, control is obtained through use of topical anti-yeast creams (eg, ketoconazole) combined with a mild topical steroid (eg, 2.5% hydrocortisone). Using ketoconazole 2% shampoo for the scalp and other affected areas can be helpful as well. Use of nystatin, however, has long been replaced by more effective alternatives.

With a bit of luck, the patient’s stress will diminish over time, which should be a big help in resolving this problem.

TAKE-HOME LEARNING POINTS

• Seborrhea, or seborrheic dermatitis, is extremely common among those of northern European descent and can affect not only the scalp, but also the face, ears, chest, axillae, and genitals.
• The rash is usually orangish pink and slightly scaly, unless it’s in the axillae, where moisture and friction preclude the formation of significant scale.
• Seborrhea is often misdiagnosed as yeast infection, but the latter is quite unusual on the skin.
• The differential should include psoriasis, eczema, and sebopsoriasis (an overlap condition with signs of both seborrhea and psoriasis).

The several-week duration of this 14-year-old boy’s rash is worrisome to him and his family, despite a lack of other symptoms. Located on his right axilla, the rash was previously diagnosed as “yeast infection” but was unaffected by topical anti-yeast medications (nystatin and clotrimazole creams) and oral fluconazole.

A serious family crisis preceded the appearance of the rash: The parents lost custody of their children, who were then placed under the care of grandparents in another state. The boy lost his family and friends and had to start again in a new school.

EXAMINATION
Additional rashes are present on his face, in and behind his ears, and on focal areas of his genitals. They are all orangish red with faintly scaly surfaces. The scale on his face, ears, and genitals is coarser than that of his axilla, but it is the same salmon-pink. Focal areas of his brows and scalp are also involved.

What is the diagnosis?

Non-dermatology providers often incorrectly diagnose axillary rashes as yeast infections, or seborrhea on the face as fungal infection, simply for lack of a complete differential. The truth is, yeast infections of the skin are unusual. The differential should include psoriasis or eczema, as well as sebopsoriasis (an overlap condition with signs of both seborrhea and psoriasis).

The “trick” to diagnosing seborrhea is to recognize that it is incredibly common (affecting around 30% of the Caucasian population), is often inherited, and can affect multiple sites. When it is seen in one area, corroboration can be sought by locating typical changes elsewhere.

Although there is no cure, control is obtained through use of topical anti-yeast creams (eg, ketoconazole) combined with a mild topical steroid (eg, 2.5% hydrocortisone). Using ketoconazole 2% shampoo for the scalp and other affected areas can be helpful as well. Use of nystatin, however, has long been replaced by more effective alternatives.

With a bit of luck, the patient’s stress will diminish over time, which should be a big help in resolving this problem.

TAKE-HOME LEARNING POINTS

• Seborrhea, or seborrheic dermatitis, is extremely common among those of northern European descent and can affect not only the scalp, but also the face, ears, chest, axillae, and genitals.
• The rash is usually orangish pink and slightly scaly, unless it’s in the axillae, where moisture and friction preclude the formation of significant scale.
• Seborrhea is often misdiagnosed as yeast infection, but the latter is quite unusual on the skin.
• The differential should include psoriasis, eczema, and sebopsoriasis (an overlap condition with signs of both seborrhea and psoriasis).

The several-week duration of this 14-year-old boy’s rash is worrisome to him and his family, despite a lack of other symptoms. Located on his right axilla, the rash was previously diagnosed as “yeast infection” but was unaffected by topical anti-yeast medications (nystatin and clotrimazole creams) and oral fluconazole.

A serious family crisis preceded the appearance of the rash: The parents lost custody of their children, who were then placed under the care of grandparents in another state. The boy lost his family and friends and had to start again in a new school.

EXAMINATION
Additional rashes are present on his face, in and behind his ears, and on focal areas of his genitals. They are all orangish red with faintly scaly surfaces. The scale on his face, ears, and genitals is coarser than that of his axilla, but it is the same salmon-pink. Focal areas of his brows and scalp are also involved.

What is the diagnosis?

Non-dermatology providers often incorrectly diagnose axillary rashes as yeast infections, or seborrhea on the face as fungal infection, simply for lack of a complete differential. The truth is, yeast infections of the skin are unusual. The differential should include psoriasis or eczema, as well as sebopsoriasis (an overlap condition with signs of both seborrhea and psoriasis).

The “trick” to diagnosing seborrhea is to recognize that it is incredibly common (affecting around 30% of the Caucasian population), is often inherited, and can affect multiple sites. When it is seen in one area, corroboration can be sought by locating typical changes elsewhere.

Although there is no cure, control is obtained through use of topical anti-yeast creams (eg, ketoconazole) combined with a mild topical steroid (eg, 2.5% hydrocortisone). Using ketoconazole 2% shampoo for the scalp and other affected areas can be helpful as well. Use of nystatin, however, has long been replaced by more effective alternatives.

With a bit of luck, the patient’s stress will diminish over time, which should be a big help in resolving this problem.

TAKE-HOME LEARNING POINTS

• Seborrhea, or seborrheic dermatitis, is extremely common among those of northern European descent and can affect not only the scalp, but also the face, ears, chest, axillae, and genitals.
• The rash is usually orangish pink and slightly scaly, unless it’s in the axillae, where moisture and friction preclude the formation of significant scale.
• Seborrhea is often misdiagnosed as yeast infection, but the latter is quite unusual on the skin.
• The differential should include psoriasis, eczema, and sebopsoriasis (an overlap condition with signs of both seborrhea and psoriasis).

The Diagnosis: Lichen Aureus

The clinicopathological findings were diagnostic of lichen aureus (LA). Microscopic examination revealed a relatively sparse, superficial, perivascular and interstitial lymphohistiocytic infiltrate with scattered siderophages in the upper dermis. Extravasation of red blood cells also was noted (Figure 1). An immunohistochemical stain for Melan-A highlighted a normal number and distribution of single melanocytes at the dermoepidermal junction with no evidence of pagetoid scatter. A Perls Prussian blue stain for iron demonstrated abundant hemosiderin in the dermis (Figure 2).

Pigmented purpuric dermatosis (PPD) describes a group of cutaneous lesions that are characterized by petechiae and pigmentary changes. These lesions most commonly present on the lower limbs; however, other sites have been reported.1 This group includes several major clinical forms such as Schamberg disease, LA, purpura annularis telangiectodes of Majocchi, eczematidlike purpura of Doucas and Kapetanakis, and lichenoid PPD of Gougerot and Blum. Lesions typically demonstrate a striking golden brown color clinically and by definition occur in the absence of platelet defects or vasculitis.¹

Factors implicated in the pathogenesis of pigmented purpura include gravitational dependency, venous stasis, infection, and drugs.² It is suggested that cellular immunity may play a role in the development of the disease based on the presence of CD4⁺ T lymphocytes in the infiltrate and the expression of HLA-DR by these lymphocytes and the keratinocytes.³ Lichen aureus differs in that it relates to increased intravascular pressure from an incompetent valve in an underlying perforating vein.⁴

Lichen aureus, also referred to as lichen purpuricus, is one major variant of PPD. The name reflects both the characteristic golden brown color and the histopathologic pattern of inflammation.¹ Lichen aureus usually presents as a unilateral, asymptomatic, confined single lesion located mainly on the leg,¹ though it can develop at other sites or as a localized group of lesions. Extensive lesions have been reported⁵ and cases with a segmental distribution have been described.⁶ In contrast, Schamberg disease demonstrates pinhead-sized reddish lesions giving the characteristic cayenne pepper pigmentation. These lesions coalesce to form thumbprint patches that progress proximally.¹ Majocchi purpura is annular and telangiectatic, while lichenoid purpura of Gougerot and Blum presents with flat-topped, polygonal, violaceous papules that turn brown over time.

Some authors have championed a role for dermoscopy in diagnosis of LA.⁷ By dermoscopy, LA demonstrates a diffuse copper background reflecting the lymphohistiocytic dermal infiltrate, red dots and globules representing the extravasated red blood cells and the dilated swollen vessels, and grey dots that reflect the hemosiderin present in the dermis.⁸

Histologically, LA demonstrates a superficial perivascular infiltrate composed mainly of CD4⁺ lymphocytes surrounding the superficial capillaries. Over time, red cell extravasation leads to the formation of hemosiderin-laden macrophages, which can be highlighted with Perls Prussian blue stain. A bandlike infiltrate with thin strands of collagen separating it from the epidermis also may be noted.⁹

An important consideration in the differential diagnosis of PPD is mycosis fungoides (MF). Mycosis fungoides is a cutaneous T-cell lymphoma that clinically presents as a single or multiple hypopigmented or hyperpigmented patches or as erythematous scaly lesions in the patch or plaque stage. These lesions eventually may evolve into tumor stage.¹⁰ Mycosis fungoides may mimic PPD clinically and/or histopathologically, and rarely PPD also may precede MF.¹¹ Involvement of the trunk, especially the lower abdomen and buttock region, favors a diagnosis of MF. Typically, histopathologic examination of MF demonstrates an epidermotropic lymphocytic infiltrate composed of atypical cerebriform lymphocytes overlying papillary dermal fibrosis. Although classic MF would be difficult to confuse with PPD, the atrophic lichenoid pattern of MF may show remarkable overlap with PPD.¹² Such cases require clinicopathologic correlation, immunophenotyping of the epidermotropic lymphocytes, and occasionally T-cell clonality studies.

Lichen aureus is a chronic persistent disease unless the underlying incompetent perforator vessel is ligated. Various treatments have been used for other forms of pigmented purpura including topical corticosteroids, topical tacrolimus, systemic vasodilators such as prostacyclin and pentoxifylline, and phototherapy.¹ Clinical follow-up is recommended for lesions that show some clinical or histopathological overlap with MF. Additional biopsies also may prove useful in establishing a definitive diagnosis in ambiguous cases.

The Diagnosis: Lichen Aureus

The clinicopathological findings were diagnostic of lichen aureus (LA). Microscopic examination revealed a relatively sparse, superficial, perivascular and interstitial lymphohistiocytic infiltrate with scattered siderophages in the upper dermis. Extravasation of red blood cells also was noted (Figure 1). An immunohistochemical stain for Melan-A highlighted a normal number and distribution of single melanocytes at the dermoepidermal junction with no evidence of pagetoid scatter. A Perls Prussian blue stain for iron demonstrated abundant hemosiderin in the dermis (Figure 2).

Pigmented purpuric dermatosis (PPD) describes a group of cutaneous lesions that are characterized by petechiae and pigmentary changes. These lesions most commonly present on the lower limbs; however, other sites have been reported.1 This group includes several major clinical forms such as Schamberg disease, LA, purpura annularis telangiectodes of Majocchi, eczematidlike purpura of Doucas and Kapetanakis, and lichenoid PPD of Gougerot and Blum. Lesions typically demonstrate a striking golden brown color clinically and by definition occur in the absence of platelet defects or vasculitis.¹

Factors implicated in the pathogenesis of pigmented purpura include gravitational dependency, venous stasis, infection, and drugs.² It is suggested that cellular immunity may play a role in the development of the disease based on the presence of CD4⁺ T lymphocytes in the infiltrate and the expression of HLA-DR by these lymphocytes and the keratinocytes.³ Lichen aureus differs in that it relates to increased intravascular pressure from an incompetent valve in an underlying perforating vein.⁴

Lichen aureus, also referred to as lichen purpuricus, is one major variant of PPD. The name reflects both the characteristic golden brown color and the histopathologic pattern of inflammation.¹ Lichen aureus usually presents as a unilateral, asymptomatic, confined single lesion located mainly on the leg,¹ though it can develop at other sites or as a localized group of lesions. Extensive lesions have been reported⁵ and cases with a segmental distribution have been described.⁶ In contrast, Schamberg disease demonstrates pinhead-sized reddish lesions giving the characteristic cayenne pepper pigmentation. These lesions coalesce to form thumbprint patches that progress proximally.¹ Majocchi purpura is annular and telangiectatic, while lichenoid purpura of Gougerot and Blum presents with flat-topped, polygonal, violaceous papules that turn brown over time.

Some authors have championed a role for dermoscopy in diagnosis of LA.⁷ By dermoscopy, LA demonstrates a diffuse copper background reflecting the lymphohistiocytic dermal infiltrate, red dots and globules representing the extravasated red blood cells and the dilated swollen vessels, and grey dots that reflect the hemosiderin present in the dermis.⁸

Histologically, LA demonstrates a superficial perivascular infiltrate composed mainly of CD4⁺ lymphocytes surrounding the superficial capillaries. Over time, red cell extravasation leads to the formation of hemosiderin-laden macrophages, which can be highlighted with Perls Prussian blue stain. A bandlike infiltrate with thin strands of collagen separating it from the epidermis also may be noted.⁹

An important consideration in the differential diagnosis of PPD is mycosis fungoides (MF). Mycosis fungoides is a cutaneous T-cell lymphoma that clinically presents as a single or multiple hypopigmented or hyperpigmented patches or as erythematous scaly lesions in the patch or plaque stage. These lesions eventually may evolve into tumor stage.¹⁰ Mycosis fungoides may mimic PPD clinically and/or histopathologically, and rarely PPD also may precede MF.¹¹ Involvement of the trunk, especially the lower abdomen and buttock region, favors a diagnosis of MF. Typically, histopathologic examination of MF demonstrates an epidermotropic lymphocytic infiltrate composed of atypical cerebriform lymphocytes overlying papillary dermal fibrosis. Although classic MF would be difficult to confuse with PPD, the atrophic lichenoid pattern of MF may show remarkable overlap with PPD.¹² Such cases require clinicopathologic correlation, immunophenotyping of the epidermotropic lymphocytes, and occasionally T-cell clonality studies.

Lichen aureus is a chronic persistent disease unless the underlying incompetent perforator vessel is ligated. Various treatments have been used for other forms of pigmented purpura including topical corticosteroids, topical tacrolimus, systemic vasodilators such as prostacyclin and pentoxifylline, and phototherapy.¹ Clinical follow-up is recommended for lesions that show some clinical or histopathological overlap with MF. Additional biopsies also may prove useful in establishing a definitive diagnosis in ambiguous cases.

The Diagnosis: Lichen Aureus

The clinicopathological findings were diagnostic of lichen aureus (LA). Microscopic examination revealed a relatively sparse, superficial, perivascular and interstitial lymphohistiocytic infiltrate with scattered siderophages in the upper dermis. Extravasation of red blood cells also was noted (Figure 1). An immunohistochemical stain for Melan-A highlighted a normal number and distribution of single melanocytes at the dermoepidermal junction with no evidence of pagetoid scatter. A Perls Prussian blue stain for iron demonstrated abundant hemosiderin in the dermis (Figure 2).

Pigmented purpuric dermatosis (PPD) describes a group of cutaneous lesions that are characterized by petechiae and pigmentary changes. These lesions most commonly present on the lower limbs; however, other sites have been reported.1 This group includes several major clinical forms such as Schamberg disease, LA, purpura annularis telangiectodes of Majocchi, eczematidlike purpura of Doucas and Kapetanakis, and lichenoid PPD of Gougerot and Blum. Lesions typically demonstrate a striking golden brown color clinically and by definition occur in the absence of platelet defects or vasculitis.¹

Factors implicated in the pathogenesis of pigmented purpura include gravitational dependency, venous stasis, infection, and drugs.² It is suggested that cellular immunity may play a role in the development of the disease based on the presence of CD4⁺ T lymphocytes in the infiltrate and the expression of HLA-DR by these lymphocytes and the keratinocytes.³ Lichen aureus differs in that it relates to increased intravascular pressure from an incompetent valve in an underlying perforating vein.⁴

Lichen aureus, also referred to as lichen purpuricus, is one major variant of PPD. The name reflects both the characteristic golden brown color and the histopathologic pattern of inflammation.¹ Lichen aureus usually presents as a unilateral, asymptomatic, confined single lesion located mainly on the leg,¹ though it can develop at other sites or as a localized group of lesions. Extensive lesions have been reported⁵ and cases with a segmental distribution have been described.⁶ In contrast, Schamberg disease demonstrates pinhead-sized reddish lesions giving the characteristic cayenne pepper pigmentation. These lesions coalesce to form thumbprint patches that progress proximally.¹ Majocchi purpura is annular and telangiectatic, while lichenoid purpura of Gougerot and Blum presents with flat-topped, polygonal, violaceous papules that turn brown over time.

Some authors have championed a role for dermoscopy in diagnosis of LA.⁷ By dermoscopy, LA demonstrates a diffuse copper background reflecting the lymphohistiocytic dermal infiltrate, red dots and globules representing the extravasated red blood cells and the dilated swollen vessels, and grey dots that reflect the hemosiderin present in the dermis.⁸

Histologically, LA demonstrates a superficial perivascular infiltrate composed mainly of CD4⁺ lymphocytes surrounding the superficial capillaries. Over time, red cell extravasation leads to the formation of hemosiderin-laden macrophages, which can be highlighted with Perls Prussian blue stain. A bandlike infiltrate with thin strands of collagen separating it from the epidermis also may be noted.⁹

An important consideration in the differential diagnosis of PPD is mycosis fungoides (MF). Mycosis fungoides is a cutaneous T-cell lymphoma that clinically presents as a single or multiple hypopigmented or hyperpigmented patches or as erythematous scaly lesions in the patch or plaque stage. These lesions eventually may evolve into tumor stage.¹⁰ Mycosis fungoides may mimic PPD clinically and/or histopathologically, and rarely PPD also may precede MF.¹¹ Involvement of the trunk, especially the lower abdomen and buttock region, favors a diagnosis of MF. Typically, histopathologic examination of MF demonstrates an epidermotropic lymphocytic infiltrate composed of atypical cerebriform lymphocytes overlying papillary dermal fibrosis. Although classic MF would be difficult to confuse with PPD, the atrophic lichenoid pattern of MF may show remarkable overlap with PPD.¹² Such cases require clinicopathologic correlation, immunophenotyping of the epidermotropic lymphocytes, and occasionally T-cell clonality studies.

Lichen aureus is a chronic persistent disease unless the underlying incompetent perforator vessel is ligated. Various treatments have been used for other forms of pigmented purpura including topical corticosteroids, topical tacrolimus, systemic vasodilators such as prostacyclin and pentoxifylline, and phototherapy.¹ Clinical follow-up is recommended for lesions that show some clinical or histopathological overlap with MF. Additional biopsies also may prove useful in establishing a definitive diagnosis in ambiguous cases.

Hospital readmissions are frequent, harmful, and costly. Consider the fact that 18% of Medicare patients can expect to be readmitted within 30 days at a cost of more than $17 billion.¹ Recent changes in health care policy aimed at reducing readmission have substantially increased attention to this major health care issue.²

The Affordable Care Act has mandated that the Centers for Medicare & Medicaid Services reduce payment to hospitals with higher-than-expected 30-day readmissions, with its Hospital Readmissions Reduction Program. This has driven rapid growth in the study of patients rehospitalized within 30 days of discharge.³ So what are some strategies that have either been proven to reduce readmissions or show promise in doing so?

FY 2017 IPPS Final Rule HRRP Supplemental Data File. Courtesy of Advisory Board.

An ounce of prevention

In studying inpatient and outpatient physicians’ perspectives regarding factors contributing to readmission,⁴ Shoshana Herzig, MD, MPH, assistant professor of medicine, Harvard Medical School, and director of Hospital Medicine Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, and her colleagues identified some potential preventive strategies.

The most commonly endorsed strategy to prevent readmissions by both primary care physicians and hospitalists surveyed involved improving self-management plans at discharge. “This refers to actions such as providing patient-centered discharge instructions (that is, making sure they are written in language that patients can understand) or asking transition coaches to help facilitate a successful transition,” Dr. Herzig said. “This finding is consistent with the fact that the factor most commonly identified as contributing to readmissions was insufficient patient understanding or ability to self-manage. Combined, these findings suggest that strategies to enhance patient understanding of their illness, care plan, and what to expect after hospital discharge, are likely to be important components of successful readmission reduction programs.”

monkeybusinessimages/Thinkstock

Interviewing patients regarding readmissions

After involved clinicians and independent physician reviewers performed extensive case reviews of more than 700 readmitted patients,⁶ Ashley Busuttil, MD, FHM, associate section chief, Hospital Medicine, University of California, Los Angeles Department of Medicine; and executive medical director, Medicine Services, UCLA Department of Medicine, and Erin Dowling, MD, assistant clinical professor, General Internal Medicine, Hospitalist Services, UCLA Medical Center, Santa Monica, Calif., and their colleagues were unable to identify which readmissions could have easily been prevented, and found that readmission causality varied extensively.

Employing the HOSPITAL score

In another effort to reduce hospital readmissions, Jacques Donzé, MD, MSc, associate physician, Bern University Hospital, Switzerland, and research associate, Brigham and Women’s Hospital, Boston, and his colleagues used the HOSPITAL score to identify patients at high risk of 30-day potentially avoidable readmission.

To most efficiently reduce hospital readmissions, hospitals need to target complex and intensive discharge interventions for patients at high risk of potentially avoidable readmission who are more likely to benefit.² “However, prior research indicates that clinical health care providers are not able to accurately identify which patients are at high risk for readmission,” Dr. Donzé said.

Karen Appold is a medical writer in Pennsylvania.

Using hospitalist reflections as a means to reduce readmissions

Readmission studies and the development of readmission scoring systems and prediction tools rely on data from a large number of patients, typically extracted from administrative databases.

To complement this data, Deanne Kashiwagi, MD, consultant, Hospital Internal Medicine, Mayo Clinic, Rochester, Minn., and her colleagues asked hospitalists to reflect upon the readmissions of patients for whom they cared to add insight into the culture of patient care transitions within the health system.

“We felt there was some value in considering these nuances of the local care environment, which may not be represented in studies drawing from large databases, as potential targets for readmission efforts,” she said.

References

1. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360(14):1418-28.

2. Donzé JD, Williams MV, Robinson EJ, et al. International validity of the HOSPITAL Score to predict 30-day potentially avoidable hospital readmissions. JAMA Intern Med. 2016 Apr;176(4):496-502.

3. Kashiwagi DT, Burton MC, Hakim FA, et al. Reflective practice: a tool for readmission reduction. Am J Med Qual. 2016 May;31(3):265-71.

4. Herzig SJ, Schnipper JL, Doctoroff L, et al. Physician perspectives on factors contributing to readmissions and potential prevention strategies: a multicenter survey. J Gen Intern Med. 2016 Nov;31(11):1287-93. Epub 2016 Jun 9.

5. Allaudeen N, Schnipper JL, Orav EJ, et al. Inability of providers to predict unplanned readmissions. J Gen Intern Med. 2011 Jul;26(7):771-6.

6. Busuttil A, Howard-Anderson J, Dowling EP, et al. Building a comprehensive patient-centered readmission reduction program [abstract]. J Hosp Med. 2016;11(suppl 1).

7. Rana V, Thapa B, Saini SC, et al. Self-reflection as a tool to increase hospitalist participation in readmission quality improvement. Qual Manag Health Care. 2016 Oct/Dec;25(4):219-24.

Hospital readmissions are frequent, harmful, and costly. Consider the fact that 18% of Medicare patients can expect to be readmitted within 30 days at a cost of more than $17 billion.¹ Recent changes in health care policy aimed at reducing readmission have substantially increased attention to this major health care issue.²

The Affordable Care Act has mandated that the Centers for Medicare & Medicaid Services reduce payment to hospitals with higher-than-expected 30-day readmissions, with its Hospital Readmissions Reduction Program. This has driven rapid growth in the study of patients rehospitalized within 30 days of discharge.³ So what are some strategies that have either been proven to reduce readmissions or show promise in doing so?

FY 2017 IPPS Final Rule HRRP Supplemental Data File. Courtesy of Advisory Board.

An ounce of prevention

In studying inpatient and outpatient physicians’ perspectives regarding factors contributing to readmission,⁴ Shoshana Herzig, MD, MPH, assistant professor of medicine, Harvard Medical School, and director of Hospital Medicine Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, and her colleagues identified some potential preventive strategies.

The most commonly endorsed strategy to prevent readmissions by both primary care physicians and hospitalists surveyed involved improving self-management plans at discharge. “This refers to actions such as providing patient-centered discharge instructions (that is, making sure they are written in language that patients can understand) or asking transition coaches to help facilitate a successful transition,” Dr. Herzig said. “This finding is consistent with the fact that the factor most commonly identified as contributing to readmissions was insufficient patient understanding or ability to self-manage. Combined, these findings suggest that strategies to enhance patient understanding of their illness, care plan, and what to expect after hospital discharge, are likely to be important components of successful readmission reduction programs.”

monkeybusinessimages/Thinkstock

Interviewing patients regarding readmissions

After involved clinicians and independent physician reviewers performed extensive case reviews of more than 700 readmitted patients,⁶ Ashley Busuttil, MD, FHM, associate section chief, Hospital Medicine, University of California, Los Angeles Department of Medicine; and executive medical director, Medicine Services, UCLA Department of Medicine, and Erin Dowling, MD, assistant clinical professor, General Internal Medicine, Hospitalist Services, UCLA Medical Center, Santa Monica, Calif., and their colleagues were unable to identify which readmissions could have easily been prevented, and found that readmission causality varied extensively.

Employing the HOSPITAL score

In another effort to reduce hospital readmissions, Jacques Donzé, MD, MSc, associate physician, Bern University Hospital, Switzerland, and research associate, Brigham and Women’s Hospital, Boston, and his colleagues used the HOSPITAL score to identify patients at high risk of 30-day potentially avoidable readmission.

To most efficiently reduce hospital readmissions, hospitals need to target complex and intensive discharge interventions for patients at high risk of potentially avoidable readmission who are more likely to benefit.² “However, prior research indicates that clinical health care providers are not able to accurately identify which patients are at high risk for readmission,” Dr. Donzé said.

Karen Appold is a medical writer in Pennsylvania.

Using hospitalist reflections as a means to reduce readmissions

Readmission studies and the development of readmission scoring systems and prediction tools rely on data from a large number of patients, typically extracted from administrative databases.

To complement this data, Deanne Kashiwagi, MD, consultant, Hospital Internal Medicine, Mayo Clinic, Rochester, Minn., and her colleagues asked hospitalists to reflect upon the readmissions of patients for whom they cared to add insight into the culture of patient care transitions within the health system.

“We felt there was some value in considering these nuances of the local care environment, which may not be represented in studies drawing from large databases, as potential targets for readmission efforts,” she said.

References

1. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360(14):1418-28.

2. Donzé JD, Williams MV, Robinson EJ, et al. International validity of the HOSPITAL Score to predict 30-day potentially avoidable hospital readmissions. JAMA Intern Med. 2016 Apr;176(4):496-502.

3. Kashiwagi DT, Burton MC, Hakim FA, et al. Reflective practice: a tool for readmission reduction. Am J Med Qual. 2016 May;31(3):265-71.

4. Herzig SJ, Schnipper JL, Doctoroff L, et al. Physician perspectives on factors contributing to readmissions and potential prevention strategies: a multicenter survey. J Gen Intern Med. 2016 Nov;31(11):1287-93. Epub 2016 Jun 9.

5. Allaudeen N, Schnipper JL, Orav EJ, et al. Inability of providers to predict unplanned readmissions. J Gen Intern Med. 2011 Jul;26(7):771-6.

6. Busuttil A, Howard-Anderson J, Dowling EP, et al. Building a comprehensive patient-centered readmission reduction program [abstract]. J Hosp Med. 2016;11(suppl 1).

7. Rana V, Thapa B, Saini SC, et al. Self-reflection as a tool to increase hospitalist participation in readmission quality improvement. Qual Manag Health Care. 2016 Oct/Dec;25(4):219-24.

Hospital readmissions are frequent, harmful, and costly. Consider the fact that 18% of Medicare patients can expect to be readmitted within 30 days at a cost of more than $17 billion.¹ Recent changes in health care policy aimed at reducing readmission have substantially increased attention to this major health care issue.²

The Affordable Care Act has mandated that the Centers for Medicare & Medicaid Services reduce payment to hospitals with higher-than-expected 30-day readmissions, with its Hospital Readmissions Reduction Program. This has driven rapid growth in the study of patients rehospitalized within 30 days of discharge.³ So what are some strategies that have either been proven to reduce readmissions or show promise in doing so?

FY 2017 IPPS Final Rule HRRP Supplemental Data File. Courtesy of Advisory Board.

An ounce of prevention

In studying inpatient and outpatient physicians’ perspectives regarding factors contributing to readmission,⁴ Shoshana Herzig, MD, MPH, assistant professor of medicine, Harvard Medical School, and director of Hospital Medicine Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, and her colleagues identified some potential preventive strategies.

The most commonly endorsed strategy to prevent readmissions by both primary care physicians and hospitalists surveyed involved improving self-management plans at discharge. “This refers to actions such as providing patient-centered discharge instructions (that is, making sure they are written in language that patients can understand) or asking transition coaches to help facilitate a successful transition,” Dr. Herzig said. “This finding is consistent with the fact that the factor most commonly identified as contributing to readmissions was insufficient patient understanding or ability to self-manage. Combined, these findings suggest that strategies to enhance patient understanding of their illness, care plan, and what to expect after hospital discharge, are likely to be important components of successful readmission reduction programs.”

monkeybusinessimages/Thinkstock

Interviewing patients regarding readmissions

After involved clinicians and independent physician reviewers performed extensive case reviews of more than 700 readmitted patients,⁶ Ashley Busuttil, MD, FHM, associate section chief, Hospital Medicine, University of California, Los Angeles Department of Medicine; and executive medical director, Medicine Services, UCLA Department of Medicine, and Erin Dowling, MD, assistant clinical professor, General Internal Medicine, Hospitalist Services, UCLA Medical Center, Santa Monica, Calif., and their colleagues were unable to identify which readmissions could have easily been prevented, and found that readmission causality varied extensively.

Employing the HOSPITAL score

In another effort to reduce hospital readmissions, Jacques Donzé, MD, MSc, associate physician, Bern University Hospital, Switzerland, and research associate, Brigham and Women’s Hospital, Boston, and his colleagues used the HOSPITAL score to identify patients at high risk of 30-day potentially avoidable readmission.

To most efficiently reduce hospital readmissions, hospitals need to target complex and intensive discharge interventions for patients at high risk of potentially avoidable readmission who are more likely to benefit.² “However, prior research indicates that clinical health care providers are not able to accurately identify which patients are at high risk for readmission,” Dr. Donzé said.

Karen Appold is a medical writer in Pennsylvania.

Using hospitalist reflections as a means to reduce readmissions

Readmission studies and the development of readmission scoring systems and prediction tools rely on data from a large number of patients, typically extracted from administrative databases.

To complement this data, Deanne Kashiwagi, MD, consultant, Hospital Internal Medicine, Mayo Clinic, Rochester, Minn., and her colleagues asked hospitalists to reflect upon the readmissions of patients for whom they cared to add insight into the culture of patient care transitions within the health system.

“We felt there was some value in considering these nuances of the local care environment, which may not be represented in studies drawing from large databases, as potential targets for readmission efforts,” she said.

References

1. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360(14):1418-28.

2. Donzé JD, Williams MV, Robinson EJ, et al. International validity of the HOSPITAL Score to predict 30-day potentially avoidable hospital readmissions. JAMA Intern Med. 2016 Apr;176(4):496-502.

3. Kashiwagi DT, Burton MC, Hakim FA, et al. Reflective practice: a tool for readmission reduction. Am J Med Qual. 2016 May;31(3):265-71.

4. Herzig SJ, Schnipper JL, Doctoroff L, et al. Physician perspectives on factors contributing to readmissions and potential prevention strategies: a multicenter survey. J Gen Intern Med. 2016 Nov;31(11):1287-93. Epub 2016 Jun 9.

5. Allaudeen N, Schnipper JL, Orav EJ, et al. Inability of providers to predict unplanned readmissions. J Gen Intern Med. 2011 Jul;26(7):771-6.

6. Busuttil A, Howard-Anderson J, Dowling EP, et al. Building a comprehensive patient-centered readmission reduction program [abstract]. J Hosp Med. 2016;11(suppl 1).

7. Rana V, Thapa B, Saini SC, et al. Self-reflection as a tool to increase hospitalist participation in readmission quality improvement. Qual Manag Health Care. 2016 Oct/Dec;25(4):219-24.

Compared with starting patients with hepatocellular carcinoma on a standard dose of sorafenib, reducing the starting dose was associated with reduced treatment costs, yet did not reduce overall survival, a large retrospective analysis showed.

“Our data suggest that the initiation of sorafenib at a reduced dosage may be a safe and reasonable strategy for some patients with HCC,” researchers led by Kim A. Reiss, MD, wrote in the Journal of Oncology.

Dr. Reiss, of the Philadelphia-based Perelman Center for Advanced Medicine, and her associates analyzed data from 4,903 patients with HCC who were prescribed sorafenib at 128 Veterans Health Administration hospitals between January 2006 and April 2015. They used Cox regression analysis to examine the impact of the drug’s starting dose on patient outcomes and cost. The primary endpoint was overall survival of patients who were prescribed a standard starting dose of sorafenib at 800 mg/d, compared with a starting dose of less than 800 mg/d.

The mean age of patients was 62 years, 99% were male, and 61% where white. In an unmatched and unadjusted analysis, the researchers found that compared with patients who received a standard starting dose of sorafenib, those who received a reduced starting dose had more Barcelona Clinic Liver Cancer stage D disease (P less than .001), higher Model for End-Stage Liver Disease Sodium scores (P less than .001), higher Child-Turcotte-Pugh scores (P less than .001), higher Cirrhosis Comorbidity Index scores (P=.01), and a lower overall survival (a median of 200 vs. 233 days, respectively; HR 1.10). However, after propensity score matching and adjustment for potential confounders, the difference in overall survival between the two treatment groups dropped below the noninferiority margin (P less than .001), the investigators reported (J Clin Oncol. 2017 Sept 5 doi.org/10.1200/JCO.2017.73.8245).

In addition, patients who received a reduced starting dose of sorafenib had a significantly lower total cost of the medication ($5,636 vs. $8,661; P less than .001) and were less likely to stop taking sorafenib because of GI effects (8.7% vs. 10.8%; P = .047).

The study was supported by unrestricted research funds from Bayer HealthCare Pharmaceuticals and the VA HIV, Hepatitis, and Related Conditions Programs in the Office of Specialty Care Services. One of the authors, Ronac Mamtani, MD, is supported by National Institutes of Health/National Cancer Institute grant K23CA18718.

[email protected]

Compared with starting patients with hepatocellular carcinoma on a standard dose of sorafenib, reducing the starting dose was associated with reduced treatment costs, yet did not reduce overall survival, a large retrospective analysis showed.

“Our data suggest that the initiation of sorafenib at a reduced dosage may be a safe and reasonable strategy for some patients with HCC,” researchers led by Kim A. Reiss, MD, wrote in the Journal of Oncology.

Dr. Reiss, of the Philadelphia-based Perelman Center for Advanced Medicine, and her associates analyzed data from 4,903 patients with HCC who were prescribed sorafenib at 128 Veterans Health Administration hospitals between January 2006 and April 2015. They used Cox regression analysis to examine the impact of the drug’s starting dose on patient outcomes and cost. The primary endpoint was overall survival of patients who were prescribed a standard starting dose of sorafenib at 800 mg/d, compared with a starting dose of less than 800 mg/d.

The mean age of patients was 62 years, 99% were male, and 61% where white. In an unmatched and unadjusted analysis, the researchers found that compared with patients who received a standard starting dose of sorafenib, those who received a reduced starting dose had more Barcelona Clinic Liver Cancer stage D disease (P less than .001), higher Model for End-Stage Liver Disease Sodium scores (P less than .001), higher Child-Turcotte-Pugh scores (P less than .001), higher Cirrhosis Comorbidity Index scores (P=.01), and a lower overall survival (a median of 200 vs. 233 days, respectively; HR 1.10). However, after propensity score matching and adjustment for potential confounders, the difference in overall survival between the two treatment groups dropped below the noninferiority margin (P less than .001), the investigators reported (J Clin Oncol. 2017 Sept 5 doi.org/10.1200/JCO.2017.73.8245).

In addition, patients who received a reduced starting dose of sorafenib had a significantly lower total cost of the medication ($5,636 vs. $8,661; P less than .001) and were less likely to stop taking sorafenib because of GI effects (8.7% vs. 10.8%; P = .047).

The study was supported by unrestricted research funds from Bayer HealthCare Pharmaceuticals and the VA HIV, Hepatitis, and Related Conditions Programs in the Office of Specialty Care Services. One of the authors, Ronac Mamtani, MD, is supported by National Institutes of Health/National Cancer Institute grant K23CA18718.

[email protected]

Compared with starting patients with hepatocellular carcinoma on a standard dose of sorafenib, reducing the starting dose was associated with reduced treatment costs, yet did not reduce overall survival, a large retrospective analysis showed.

“Our data suggest that the initiation of sorafenib at a reduced dosage may be a safe and reasonable strategy for some patients with HCC,” researchers led by Kim A. Reiss, MD, wrote in the Journal of Oncology.

Dr. Reiss, of the Philadelphia-based Perelman Center for Advanced Medicine, and her associates analyzed data from 4,903 patients with HCC who were prescribed sorafenib at 128 Veterans Health Administration hospitals between January 2006 and April 2015. They used Cox regression analysis to examine the impact of the drug’s starting dose on patient outcomes and cost. The primary endpoint was overall survival of patients who were prescribed a standard starting dose of sorafenib at 800 mg/d, compared with a starting dose of less than 800 mg/d.

The mean age of patients was 62 years, 99% were male, and 61% where white. In an unmatched and unadjusted analysis, the researchers found that compared with patients who received a standard starting dose of sorafenib, those who received a reduced starting dose had more Barcelona Clinic Liver Cancer stage D disease (P less than .001), higher Model for End-Stage Liver Disease Sodium scores (P less than .001), higher Child-Turcotte-Pugh scores (P less than .001), higher Cirrhosis Comorbidity Index scores (P=.01), and a lower overall survival (a median of 200 vs. 233 days, respectively; HR 1.10). However, after propensity score matching and adjustment for potential confounders, the difference in overall survival between the two treatment groups dropped below the noninferiority margin (P less than .001), the investigators reported (J Clin Oncol. 2017 Sept 5 doi.org/10.1200/JCO.2017.73.8245).

In addition, patients who received a reduced starting dose of sorafenib had a significantly lower total cost of the medication ($5,636 vs. $8,661; P less than .001) and were less likely to stop taking sorafenib because of GI effects (8.7% vs. 10.8%; P = .047).

The study was supported by unrestricted research funds from Bayer HealthCare Pharmaceuticals and the VA HIV, Hepatitis, and Related Conditions Programs in the Office of Specialty Care Services. One of the authors, Ronac Mamtani, MD, is supported by National Institutes of Health/National Cancer Institute grant K23CA18718.

[email protected]

As Irma, the most powerful Atlantic hurricane in recorded history, approaches south Florida, the state’s Department of Health is moving quickly to prepare.

Once Gov. Rick Scott (R) declared a state of emergency in all 67 counties Sept. 4, the department swung into action.

“Florida has a robust emergency operation system and once activated, Florida Department of Health is the lead for State Emergency Function 8 or ESF-8. Hospital evacuations, special needs sheltering, and other tasks are coordinated through that function,” Mara Gambineri, communications director for the department, said in an interview. “We have plans in place and exercise those frequently to prepare for these situations.”

[email protected]

On Twitter @eaztweets

As Irma, the most powerful Atlantic hurricane in recorded history, approaches south Florida, the state’s Department of Health is moving quickly to prepare.

Once Gov. Rick Scott (R) declared a state of emergency in all 67 counties Sept. 4, the department swung into action.

“Florida has a robust emergency operation system and once activated, Florida Department of Health is the lead for State Emergency Function 8 or ESF-8. Hospital evacuations, special needs sheltering, and other tasks are coordinated through that function,” Mara Gambineri, communications director for the department, said in an interview. “We have plans in place and exercise those frequently to prepare for these situations.”

[email protected]

On Twitter @eaztweets

As Irma, the most powerful Atlantic hurricane in recorded history, approaches south Florida, the state’s Department of Health is moving quickly to prepare.

Once Gov. Rick Scott (R) declared a state of emergency in all 67 counties Sept. 4, the department swung into action.

“Florida has a robust emergency operation system and once activated, Florida Department of Health is the lead for State Emergency Function 8 or ESF-8. Hospital evacuations, special needs sheltering, and other tasks are coordinated through that function,” Mara Gambineri, communications director for the department, said in an interview. “We have plans in place and exercise those frequently to prepare for these situations.”

[email protected]

On Twitter @eaztweets

Clues are emerging that Staphylococcus species may be contributors to acne vulgaris, according to a new study that examined changes in the skin microbiota of acne patients undergoing topical treatment.

Comparing topical antibiotic treatment for acne with a novel cosmetic formulation, Brigitte Dreno, MD, PhD, and her colleagues found that normal skin had fewer surface staphylococci than did skin with comedones or papulopustular eruptions (P = .004 for comedones; P = .003 for papules and pustules). Further, the number of staphylococci increased as acne severity increased (P less than .05 for the increase seen between scores of GEA-2 and GEA-3 on the Global Acne Severity Scale).

These results were seen in a split-face study of 26 adults with mild to moderate acne (GEA-2 and GEA-3) that compared a topical 4% erythromycin gel to a “dermocosmetic” containing lipohydroxy, linoleic, and salicylic acids, niacinamide, piroctone olamine, a ceramide, and water from a thermal spring. Each patient used each product on half of his or her face for 28 consecutive days while avoiding use of other skin care products or topical medications during the study period (Exp Dermatol. 2017;26[9]:798-803; doi: 10.1111/exd.13296).

Patients’ acne severity was assessed at days 0, 14, and 28 using the GEA scale, together with a count of inflammatory and noninflammatory lesions. The mean GEA grade for patients at enrollment was 2.4. For each patient, skin microbiota samples were obtained from an area with comedones, an area with papulopustular lesions, and an unaffected area.

Dr. Dreno, professor of dermatology at University Hospital, Nantes, France, and her coauthors noted that the range of bacterial diversity was similar on all the facial areas sampled.

After 28 days of treatment, the antibiotic-treated facial skin had significantly less Actinobacteria species, including corynebacteria and propionibacteria. However, the effect on Staphylococci was limited, “potentially confirming the increased resistance of the bacterium to macrolides,” they wrote.

Facial skin treated with the cosmetic, by contrast, had fewer Actinobacteria and fewer Staphylococcus species by the end of the study period, though staphylococci remained the predominant organisms after treatment. Patients saw a significant reduction in both inflammatory and noninflammatory lesions during the study period (P less than .05), with no significant difference between antibiotic- and cosmetic-treated skin.

The authors said that previous studies have shown that propionibacteria are common commensal organisms, representing up to 30% of the bacteria on healthy skin. For the individuals enrolled in the study, though, propionibacteria made up just 2% of the bacteria on the surface of both healthy skin and skin with acne.

Staphylococci, and S. epidermidis in particular, may use fermentation as a defense against other organisms in the skin microbiota. Since staphylococci are aerobic and facultative anaerobic species, they flourish on the skin surface. Propionibacterium acnes, by contrast, is anaerobic, and primarily inhabits the sebaceous follicle.

The complex interplay of skin microbiota contribute to acne and other dermatologic pathology in ways that are just beginning to be understood. “Even though the association between P. acnes and acne vulgaris is well established, very few studies have investigated the entire facial skin microbiota of patients with acne,” wrote Dr. Dreno and her coauthors.

One of the six study authors are employees of L’Oreal; two are employees of La Roche–Posay Dermatological Laboratory, which funded the study and produced the cosmetic product used by the researchers.

[email protected]

On Twitter @karioakes

Clues are emerging that Staphylococcus species may be contributors to acne vulgaris, according to a new study that examined changes in the skin microbiota of acne patients undergoing topical treatment.

Comparing topical antibiotic treatment for acne with a novel cosmetic formulation, Brigitte Dreno, MD, PhD, and her colleagues found that normal skin had fewer surface staphylococci than did skin with comedones or papulopustular eruptions (P = .004 for comedones; P = .003 for papules and pustules). Further, the number of staphylococci increased as acne severity increased (P less than .05 for the increase seen between scores of GEA-2 and GEA-3 on the Global Acne Severity Scale).

These results were seen in a split-face study of 26 adults with mild to moderate acne (GEA-2 and GEA-3) that compared a topical 4% erythromycin gel to a “dermocosmetic” containing lipohydroxy, linoleic, and salicylic acids, niacinamide, piroctone olamine, a ceramide, and water from a thermal spring. Each patient used each product on half of his or her face for 28 consecutive days while avoiding use of other skin care products or topical medications during the study period (Exp Dermatol. 2017;26[9]:798-803; doi: 10.1111/exd.13296).

Patients’ acne severity was assessed at days 0, 14, and 28 using the GEA scale, together with a count of inflammatory and noninflammatory lesions. The mean GEA grade for patients at enrollment was 2.4. For each patient, skin microbiota samples were obtained from an area with comedones, an area with papulopustular lesions, and an unaffected area.

Dr. Dreno, professor of dermatology at University Hospital, Nantes, France, and her coauthors noted that the range of bacterial diversity was similar on all the facial areas sampled.

After 28 days of treatment, the antibiotic-treated facial skin had significantly less Actinobacteria species, including corynebacteria and propionibacteria. However, the effect on Staphylococci was limited, “potentially confirming the increased resistance of the bacterium to macrolides,” they wrote.

Facial skin treated with the cosmetic, by contrast, had fewer Actinobacteria and fewer Staphylococcus species by the end of the study period, though staphylococci remained the predominant organisms after treatment. Patients saw a significant reduction in both inflammatory and noninflammatory lesions during the study period (P less than .05), with no significant difference between antibiotic- and cosmetic-treated skin.

The authors said that previous studies have shown that propionibacteria are common commensal organisms, representing up to 30% of the bacteria on healthy skin. For the individuals enrolled in the study, though, propionibacteria made up just 2% of the bacteria on the surface of both healthy skin and skin with acne.

Staphylococci, and S. epidermidis in particular, may use fermentation as a defense against other organisms in the skin microbiota. Since staphylococci are aerobic and facultative anaerobic species, they flourish on the skin surface. Propionibacterium acnes, by contrast, is anaerobic, and primarily inhabits the sebaceous follicle.

The complex interplay of skin microbiota contribute to acne and other dermatologic pathology in ways that are just beginning to be understood. “Even though the association between P. acnes and acne vulgaris is well established, very few studies have investigated the entire facial skin microbiota of patients with acne,” wrote Dr. Dreno and her coauthors.

One of the six study authors are employees of L’Oreal; two are employees of La Roche–Posay Dermatological Laboratory, which funded the study and produced the cosmetic product used by the researchers.

[email protected]

On Twitter @karioakes

Clues are emerging that Staphylococcus species may be contributors to acne vulgaris, according to a new study that examined changes in the skin microbiota of acne patients undergoing topical treatment.

Comparing topical antibiotic treatment for acne with a novel cosmetic formulation, Brigitte Dreno, MD, PhD, and her colleagues found that normal skin had fewer surface staphylococci than did skin with comedones or papulopustular eruptions (P = .004 for comedones; P = .003 for papules and pustules). Further, the number of staphylococci increased as acne severity increased (P less than .05 for the increase seen between scores of GEA-2 and GEA-3 on the Global Acne Severity Scale).

These results were seen in a split-face study of 26 adults with mild to moderate acne (GEA-2 and GEA-3) that compared a topical 4% erythromycin gel to a “dermocosmetic” containing lipohydroxy, linoleic, and salicylic acids, niacinamide, piroctone olamine, a ceramide, and water from a thermal spring. Each patient used each product on half of his or her face for 28 consecutive days while avoiding use of other skin care products or topical medications during the study period (Exp Dermatol. 2017;26[9]:798-803; doi: 10.1111/exd.13296).

Patients’ acne severity was assessed at days 0, 14, and 28 using the GEA scale, together with a count of inflammatory and noninflammatory lesions. The mean GEA grade for patients at enrollment was 2.4. For each patient, skin microbiota samples were obtained from an area with comedones, an area with papulopustular lesions, and an unaffected area.

Dr. Dreno, professor of dermatology at University Hospital, Nantes, France, and her coauthors noted that the range of bacterial diversity was similar on all the facial areas sampled.

After 28 days of treatment, the antibiotic-treated facial skin had significantly less Actinobacteria species, including corynebacteria and propionibacteria. However, the effect on Staphylococci was limited, “potentially confirming the increased resistance of the bacterium to macrolides,” they wrote.

Facial skin treated with the cosmetic, by contrast, had fewer Actinobacteria and fewer Staphylococcus species by the end of the study period, though staphylococci remained the predominant organisms after treatment. Patients saw a significant reduction in both inflammatory and noninflammatory lesions during the study period (P less than .05), with no significant difference between antibiotic- and cosmetic-treated skin.

The authors said that previous studies have shown that propionibacteria are common commensal organisms, representing up to 30% of the bacteria on healthy skin. For the individuals enrolled in the study, though, propionibacteria made up just 2% of the bacteria on the surface of both healthy skin and skin with acne.

Staphylococci, and S. epidermidis in particular, may use fermentation as a defense against other organisms in the skin microbiota. Since staphylococci are aerobic and facultative anaerobic species, they flourish on the skin surface. Propionibacterium acnes, by contrast, is anaerobic, and primarily inhabits the sebaceous follicle.

The complex interplay of skin microbiota contribute to acne and other dermatologic pathology in ways that are just beginning to be understood. “Even though the association between P. acnes and acne vulgaris is well established, very few studies have investigated the entire facial skin microbiota of patients with acne,” wrote Dr. Dreno and her coauthors.

One of the six study authors are employees of L’Oreal; two are employees of La Roche–Posay Dermatological Laboratory, which funded the study and produced the cosmetic product used by the researchers.

[email protected]

On Twitter @karioakes

Over the last 5 years, I’ve periodically devoted this column to providing updates to the Hospital Value-Based Purchasing program. HVBP launched in 2013 as a 5-year mixed upside/downside incentive program with mandatory participation for all U.S. acute care hospitals (critical access, acute inpatient rehabilitation, and long-term acute care hospitals are exempt). The program initially included process and patient experience measures. It later added measures for mortality, efficiency, and patient safety.

For the 2017 version of HVBP, the measures are allocated as follows: eight for patient experience, seven for patient safety (1 of which is a roll up of 11 claims-based measures), three for process, and three for mortality. HVBP uses a budget-neutral funding approach with some winners and some losers but overall net zero spending on the program. It initially put hospitals at risk for 1% of their Medicare inpatient payments (in 2013), with a progressive increase to 2% by this year. HVBP has used a complex approach to determining incentives and penalties, rewarding either improvement or achievement, depending on the baseline performance of the hospital.

Dr. Whitcomb is chief medical officer at Remedy Partners in Darien, Conn., and a cofounder and past president of SHM.

References

1. Ryan AM, Burgess JF, Pesko MF, Borden WB, Dimick JB. “The early effects of Medicare’s mandatory hospital pay-for-performance program” Health Serv Res. 2015;50:81-97.

2. Figueroa JF, Tsugawa Y, Zheng J, Orav EJ, Jha AK. “Association between the Value-Based Purchasing pay for performance program and patient mortality in US hospitals: observational study” BMJ. 2016;353:i2214.

3. Ryan AM, Krinsky S, Maurer KA, Dimick JB. “Changes in Hospital Quality Associated with Hospital Value-Based Purchasing” N Engl J Med. 2017;376:2358-66.

Over the last 5 years, I’ve periodically devoted this column to providing updates to the Hospital Value-Based Purchasing program. HVBP launched in 2013 as a 5-year mixed upside/downside incentive program with mandatory participation for all U.S. acute care hospitals (critical access, acute inpatient rehabilitation, and long-term acute care hospitals are exempt). The program initially included process and patient experience measures. It later added measures for mortality, efficiency, and patient safety.

For the 2017 version of HVBP, the measures are allocated as follows: eight for patient experience, seven for patient safety (1 of which is a roll up of 11 claims-based measures), three for process, and three for mortality. HVBP uses a budget-neutral funding approach with some winners and some losers but overall net zero spending on the program. It initially put hospitals at risk for 1% of their Medicare inpatient payments (in 2013), with a progressive increase to 2% by this year. HVBP has used a complex approach to determining incentives and penalties, rewarding either improvement or achievement, depending on the baseline performance of the hospital.

Dr. Whitcomb is chief medical officer at Remedy Partners in Darien, Conn., and a cofounder and past president of SHM.

References

1. Ryan AM, Burgess JF, Pesko MF, Borden WB, Dimick JB. “The early effects of Medicare’s mandatory hospital pay-for-performance program” Health Serv Res. 2015;50:81-97.

2. Figueroa JF, Tsugawa Y, Zheng J, Orav EJ, Jha AK. “Association between the Value-Based Purchasing pay for performance program and patient mortality in US hospitals: observational study” BMJ. 2016;353:i2214.

3. Ryan AM, Krinsky S, Maurer KA, Dimick JB. “Changes in Hospital Quality Associated with Hospital Value-Based Purchasing” N Engl J Med. 2017;376:2358-66.

Over the last 5 years, I’ve periodically devoted this column to providing updates to the Hospital Value-Based Purchasing program. HVBP launched in 2013 as a 5-year mixed upside/downside incentive program with mandatory participation for all U.S. acute care hospitals (critical access, acute inpatient rehabilitation, and long-term acute care hospitals are exempt). The program initially included process and patient experience measures. It later added measures for mortality, efficiency, and patient safety.

For the 2017 version of HVBP, the measures are allocated as follows: eight for patient experience, seven for patient safety (1 of which is a roll up of 11 claims-based measures), three for process, and three for mortality. HVBP uses a budget-neutral funding approach with some winners and some losers but overall net zero spending on the program. It initially put hospitals at risk for 1% of their Medicare inpatient payments (in 2013), with a progressive increase to 2% by this year. HVBP has used a complex approach to determining incentives and penalties, rewarding either improvement or achievement, depending on the baseline performance of the hospital.

Dr. Whitcomb is chief medical officer at Remedy Partners in Darien, Conn., and a cofounder and past president of SHM.

References

1. Ryan AM, Burgess JF, Pesko MF, Borden WB, Dimick JB. “The early effects of Medicare’s mandatory hospital pay-for-performance program” Health Serv Res. 2015;50:81-97.

2. Figueroa JF, Tsugawa Y, Zheng J, Orav EJ, Jha AK. “Association between the Value-Based Purchasing pay for performance program and patient mortality in US hospitals: observational study” BMJ. 2016;353:i2214.

3. Ryan AM, Krinsky S, Maurer KA, Dimick JB. “Changes in Hospital Quality Associated with Hospital Value-Based Purchasing” N Engl J Med. 2017;376:2358-66.

NASHVILLE, TENN. – When newborns withdrawing from opioids stay with their mothers after delivery instead of going to the NICU, they are far less likely to receive morphine and other drugs and leave the hospital days sooner; they also are more likely to go home with their mother, a meta-analysis showed.

The analysis likely is the first to pool results from studies of rooming-in for infants with neonatal abstinence syndrome (NAS). A strong case has been building in the literature for several years that newborns do better with rooming-in, instead of the traditional approach for NAS – NICU housing and opioid dosing based on a symptom checklist.

M. Alexander Otto/Frontline Medical News

[email protected]

NASHVILLE, TENN. – When newborns withdrawing from opioids stay with their mothers after delivery instead of going to the NICU, they are far less likely to receive morphine and other drugs and leave the hospital days sooner; they also are more likely to go home with their mother, a meta-analysis showed.

The analysis likely is the first to pool results from studies of rooming-in for infants with neonatal abstinence syndrome (NAS). A strong case has been building in the literature for several years that newborns do better with rooming-in, instead of the traditional approach for NAS – NICU housing and opioid dosing based on a symptom checklist.

M. Alexander Otto/Frontline Medical News

[email protected]

NASHVILLE, TENN. – When newborns withdrawing from opioids stay with their mothers after delivery instead of going to the NICU, they are far less likely to receive morphine and other drugs and leave the hospital days sooner; they also are more likely to go home with their mother, a meta-analysis showed.

The analysis likely is the first to pool results from studies of rooming-in for infants with neonatal abstinence syndrome (NAS). A strong case has been building in the literature for several years that newborns do better with rooming-in, instead of the traditional approach for NAS – NICU housing and opioid dosing based on a symptom checklist.

M. Alexander Otto/Frontline Medical News

[email protected]

BARCELONA – The time is right for a placebo-controlled, randomized trial of ivabradine in patients with heart failure with reduced ejection fraction who are unwilling or unable to take a beta-blocker as recommended in the guidelines, John G.F. Cleland, MD, asserted at the annual congress of the European Society of Cardiology.

He cited as the rationale for such a study a new post-hoc analysis of data from the SHIFT trial showing that ivabradine (Corlanor) significantly reduced both cardiovascular and all-cause mortality, as well as hospitalizations for heart failure, in the subset of study participants who weren’t on beta-blocker therapy.

Bruce Jancin/Frontline Medical News

[email protected]

BARCELONA – The time is right for a placebo-controlled, randomized trial of ivabradine in patients with heart failure with reduced ejection fraction who are unwilling or unable to take a beta-blocker as recommended in the guidelines, John G.F. Cleland, MD, asserted at the annual congress of the European Society of Cardiology.

He cited as the rationale for such a study a new post-hoc analysis of data from the SHIFT trial showing that ivabradine (Corlanor) significantly reduced both cardiovascular and all-cause mortality, as well as hospitalizations for heart failure, in the subset of study participants who weren’t on beta-blocker therapy.

Bruce Jancin/Frontline Medical News

[email protected]

BARCELONA – The time is right for a placebo-controlled, randomized trial of ivabradine in patients with heart failure with reduced ejection fraction who are unwilling or unable to take a beta-blocker as recommended in the guidelines, John G.F. Cleland, MD, asserted at the annual congress of the European Society of Cardiology.

He cited as the rationale for such a study a new post-hoc analysis of data from the SHIFT trial showing that ivabradine (Corlanor) significantly reduced both cardiovascular and all-cause mortality, as well as hospitalizations for heart failure, in the subset of study participants who weren’t on beta-blocker therapy.

Bruce Jancin/Frontline Medical News

[email protected]