MDedge Dermatology

On this occasion of writing our last of a decade of tech columns, we want to take the time to emphasize that our collective excitement about medical technology should never eclipse the reason for which it is created: to facilitate high-quality care.

Indeed, science and technology provide opportunities to improve outcomes in ways not even imagined 100 years ago, yet we must acknowledge that technology also threatens to erect barriers between us and our patients. We can be easily tempted to confuse new care delivery tools with the actual care itself.

Courtesy Dr. Christopher Notte

Threats to the physician-patient relationship

Medical history provides many examples of how our zeal to innovate can have untoward consequences to the physician-patient relationship.

In the late 1800s, for example, to convey a sense of science, purity of intent, and trust, the medical community began wearing white coats. Those white coats have been discussed as creating emotional distance between physicians and their patients.¹

Even when we in the medical community are slow and reluctant to change, the external forces propelling us forward often seem unstoppable; kinetic aspirations to innovate electronic information systems and new applications seem suddenly to revolutionize care delivery when we least expect it. The rapidity of change in technology can sometimes be dizzying but can at the same time can occur so swiftly we don’t even notice it.

After René Laennec invented the stethoscope in the early 1800s, clinicians no longer needed to physically lean in and place an ear directly onto patients to hear their hearts beating. This created a distance from patients that was still lamented 50 years later, when a professor of medicine is reported to have said, “he that hath ears to hear, let him use his ears and not a stethoscope.” Still, while the stethoscope has literally distanced us from patients, it is such an important tool that we no longer think about this distancing. We have adapted over time to remain close to our patients, to sincerely listen to their thoughts and reassure them that we hear them without the need to feel our ears on their chests.

Francis Peabody, the eminent Harvard physician, wrote an essay in 1927 titled, “The Care of the Patient.” At the end of the first paragraph, he states: “The most common criticism made at present by older practitioners is that young graduates ... are too “scientific” and do not know how to take care of patients.” He goes on to say that “one of the essential qualities of the clinician is interest in humanity, for the secret of the care of the patient is in caring for the patient.”²

We agree with Dr. Peabody. As we embrace science and technology that can change health outcomes, our patients’ needs to feel understood and cared for will not diminish. Instead, that need will continue to be an important aspect of our struggle and joy in providing holistic, humane, competent care into the future.

Twenty-first century physicians have access to an ever-growing trove of data, yet our ability to truly know our patients seems somehow less accessible. Home health devices have begun to provide a flow of information about parameters, ranging from continuous glucose readings to home blood pressures, weights, and inspiratory flow readings. These data can provide much more accurate insight into patients than what we can glean from one point in time during an office visit. Yet we need to remember that behind the data are people with dreams and desires, not just table entries in an electronic health record.

In 1923, the German philosopher Martin Buber published the book for which he is best known, “I and Thou.” In that book, Mr. Buber says that there are two ways we can approach relationships: “I-Thou” or “I-It.” In I-It relationships, we view the other person as an “it” to be used to accomplish a purpose, or to be experienced without his or her full involvement. In an I-Thou relationship, we appreciate the other people for all their complexity, in their full humanness. We must consciously remind ourselves amid the rush of technology that there are real people behind those data. We must acknowledge and approach each person as a unique individual who has dreams, goals, fears, and wishes that may be different from ours but to which we can still relate.

‘From the Beating End of the Stethoscope’

John Ciardi, an American poet, said the following in a poem titled, “Lines From the Beating End of the Stethoscope”:

I speak, as I say, the patient’s point of view.

But, given time, doctors are patients, too.

And there’s our bond: beyond anatomy,

Or in it, through it, to the mystery

Medicine takes the pulse of and lets go

Forever unexplained. It’s art, we know,

Not science at the heart. Doctor be whole,

I won’t insist the patient is a soul,

But he’s a something, possibly laughable,

Or possibly sublime, but not quite graphable.

Not quite containable on a bed chart.

Where science touches man it turns to art.³

This poem is a reminder of the subtle needs of patients during their encounters with doctors, especially around many of the most important decisions and events in their lives. Patients’ needs are varied, complex, difficult to discern, and not able to be fully explained or understood through math and science.

Einstein warned us that the modern age would be characterized by a perfection of means and a confusion of goals.⁴ As clinicians, we should strive to clarify and align our goals with those of our patients, providing care that is real, compassionate, and personal, not just an optimized means to achieve standardized metrics. While technology can assist us in this pursuit, we’ll need be careful that our enchantment with innovation does not cloud our actual goal: truly caring for our patients.
 

Dr. Notte is a family physician and chief medical officer of Abington (Pa.) Hospital–Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health. They have no conflicts related to the content of this piece.

References

1. Jones VA. The white coat: Why not follow suit? JAMA. 1999;281(5):478. doi: 10.1001/jama.281.5.478-JMS0203-5-1

2. Peabody, Francis (1927). “The care of the patient.” JAMA. 88(12):877-82. doi: 10.1001/jama.1927.02680380001001.

3. Ciardi, John. Lines from the Beating End of the Stethoscope. Saturday Review, Nov. 18, 1968.

4. Albert Einstein, Out of My Later Years, 1950.

On this occasion of writing our last of a decade of tech columns, we want to take the time to emphasize that our collective excitement about medical technology should never eclipse the reason for which it is created: to facilitate high-quality care.

Indeed, science and technology provide opportunities to improve outcomes in ways not even imagined 100 years ago, yet we must acknowledge that technology also threatens to erect barriers between us and our patients. We can be easily tempted to confuse new care delivery tools with the actual care itself.

Courtesy Dr. Christopher Notte

Threats to the physician-patient relationship

Medical history provides many examples of how our zeal to innovate can have untoward consequences to the physician-patient relationship.

In the late 1800s, for example, to convey a sense of science, purity of intent, and trust, the medical community began wearing white coats. Those white coats have been discussed as creating emotional distance between physicians and their patients.¹

Even when we in the medical community are slow and reluctant to change, the external forces propelling us forward often seem unstoppable; kinetic aspirations to innovate electronic information systems and new applications seem suddenly to revolutionize care delivery when we least expect it. The rapidity of change in technology can sometimes be dizzying but can at the same time can occur so swiftly we don’t even notice it.

After René Laennec invented the stethoscope in the early 1800s, clinicians no longer needed to physically lean in and place an ear directly onto patients to hear their hearts beating. This created a distance from patients that was still lamented 50 years later, when a professor of medicine is reported to have said, “he that hath ears to hear, let him use his ears and not a stethoscope.” Still, while the stethoscope has literally distanced us from patients, it is such an important tool that we no longer think about this distancing. We have adapted over time to remain close to our patients, to sincerely listen to their thoughts and reassure them that we hear them without the need to feel our ears on their chests.

Francis Peabody, the eminent Harvard physician, wrote an essay in 1927 titled, “The Care of the Patient.” At the end of the first paragraph, he states: “The most common criticism made at present by older practitioners is that young graduates ... are too “scientific” and do not know how to take care of patients.” He goes on to say that “one of the essential qualities of the clinician is interest in humanity, for the secret of the care of the patient is in caring for the patient.”²

We agree with Dr. Peabody. As we embrace science and technology that can change health outcomes, our patients’ needs to feel understood and cared for will not diminish. Instead, that need will continue to be an important aspect of our struggle and joy in providing holistic, humane, competent care into the future.

Twenty-first century physicians have access to an ever-growing trove of data, yet our ability to truly know our patients seems somehow less accessible. Home health devices have begun to provide a flow of information about parameters, ranging from continuous glucose readings to home blood pressures, weights, and inspiratory flow readings. These data can provide much more accurate insight into patients than what we can glean from one point in time during an office visit. Yet we need to remember that behind the data are people with dreams and desires, not just table entries in an electronic health record.

In 1923, the German philosopher Martin Buber published the book for which he is best known, “I and Thou.” In that book, Mr. Buber says that there are two ways we can approach relationships: “I-Thou” or “I-It.” In I-It relationships, we view the other person as an “it” to be used to accomplish a purpose, or to be experienced without his or her full involvement. In an I-Thou relationship, we appreciate the other people for all their complexity, in their full humanness. We must consciously remind ourselves amid the rush of technology that there are real people behind those data. We must acknowledge and approach each person as a unique individual who has dreams, goals, fears, and wishes that may be different from ours but to which we can still relate.

‘From the Beating End of the Stethoscope’

John Ciardi, an American poet, said the following in a poem titled, “Lines From the Beating End of the Stethoscope”:

I speak, as I say, the patient’s point of view.

But, given time, doctors are patients, too.

And there’s our bond: beyond anatomy,

Or in it, through it, to the mystery

Medicine takes the pulse of and lets go

Forever unexplained. It’s art, we know,

Not science at the heart. Doctor be whole,

I won’t insist the patient is a soul,

But he’s a something, possibly laughable,

Or possibly sublime, but not quite graphable.

Not quite containable on a bed chart.

Where science touches man it turns to art.³

This poem is a reminder of the subtle needs of patients during their encounters with doctors, especially around many of the most important decisions and events in their lives. Patients’ needs are varied, complex, difficult to discern, and not able to be fully explained or understood through math and science.

Einstein warned us that the modern age would be characterized by a perfection of means and a confusion of goals.⁴ As clinicians, we should strive to clarify and align our goals with those of our patients, providing care that is real, compassionate, and personal, not just an optimized means to achieve standardized metrics. While technology can assist us in this pursuit, we’ll need be careful that our enchantment with innovation does not cloud our actual goal: truly caring for our patients.
 

Dr. Notte is a family physician and chief medical officer of Abington (Pa.) Hospital–Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health. They have no conflicts related to the content of this piece.

References

1. Jones VA. The white coat: Why not follow suit? JAMA. 1999;281(5):478. doi: 10.1001/jama.281.5.478-JMS0203-5-1

2. Peabody, Francis (1927). “The care of the patient.” JAMA. 88(12):877-82. doi: 10.1001/jama.1927.02680380001001.

3. Ciardi, John. Lines from the Beating End of the Stethoscope. Saturday Review, Nov. 18, 1968.

4. Albert Einstein, Out of My Later Years, 1950.

On this occasion of writing our last of a decade of tech columns, we want to take the time to emphasize that our collective excitement about medical technology should never eclipse the reason for which it is created: to facilitate high-quality care.

Indeed, science and technology provide opportunities to improve outcomes in ways not even imagined 100 years ago, yet we must acknowledge that technology also threatens to erect barriers between us and our patients. We can be easily tempted to confuse new care delivery tools with the actual care itself.

Courtesy Dr. Christopher Notte

Threats to the physician-patient relationship

Medical history provides many examples of how our zeal to innovate can have untoward consequences to the physician-patient relationship.

In the late 1800s, for example, to convey a sense of science, purity of intent, and trust, the medical community began wearing white coats. Those white coats have been discussed as creating emotional distance between physicians and their patients.¹

Even when we in the medical community are slow and reluctant to change, the external forces propelling us forward often seem unstoppable; kinetic aspirations to innovate electronic information systems and new applications seem suddenly to revolutionize care delivery when we least expect it. The rapidity of change in technology can sometimes be dizzying but can at the same time can occur so swiftly we don’t even notice it.

After René Laennec invented the stethoscope in the early 1800s, clinicians no longer needed to physically lean in and place an ear directly onto patients to hear their hearts beating. This created a distance from patients that was still lamented 50 years later, when a professor of medicine is reported to have said, “he that hath ears to hear, let him use his ears and not a stethoscope.” Still, while the stethoscope has literally distanced us from patients, it is such an important tool that we no longer think about this distancing. We have adapted over time to remain close to our patients, to sincerely listen to their thoughts and reassure them that we hear them without the need to feel our ears on their chests.

Francis Peabody, the eminent Harvard physician, wrote an essay in 1927 titled, “The Care of the Patient.” At the end of the first paragraph, he states: “The most common criticism made at present by older practitioners is that young graduates ... are too “scientific” and do not know how to take care of patients.” He goes on to say that “one of the essential qualities of the clinician is interest in humanity, for the secret of the care of the patient is in caring for the patient.”²

We agree with Dr. Peabody. As we embrace science and technology that can change health outcomes, our patients’ needs to feel understood and cared for will not diminish. Instead, that need will continue to be an important aspect of our struggle and joy in providing holistic, humane, competent care into the future.

Twenty-first century physicians have access to an ever-growing trove of data, yet our ability to truly know our patients seems somehow less accessible. Home health devices have begun to provide a flow of information about parameters, ranging from continuous glucose readings to home blood pressures, weights, and inspiratory flow readings. These data can provide much more accurate insight into patients than what we can glean from one point in time during an office visit. Yet we need to remember that behind the data are people with dreams and desires, not just table entries in an electronic health record.

In 1923, the German philosopher Martin Buber published the book for which he is best known, “I and Thou.” In that book, Mr. Buber says that there are two ways we can approach relationships: “I-Thou” or “I-It.” In I-It relationships, we view the other person as an “it” to be used to accomplish a purpose, or to be experienced without his or her full involvement. In an I-Thou relationship, we appreciate the other people for all their complexity, in their full humanness. We must consciously remind ourselves amid the rush of technology that there are real people behind those data. We must acknowledge and approach each person as a unique individual who has dreams, goals, fears, and wishes that may be different from ours but to which we can still relate.

‘From the Beating End of the Stethoscope’

John Ciardi, an American poet, said the following in a poem titled, “Lines From the Beating End of the Stethoscope”:

I speak, as I say, the patient’s point of view.

But, given time, doctors are patients, too.

And there’s our bond: beyond anatomy,

Or in it, through it, to the mystery

Medicine takes the pulse of and lets go

Forever unexplained. It’s art, we know,

Not science at the heart. Doctor be whole,

I won’t insist the patient is a soul,

But he’s a something, possibly laughable,

Or possibly sublime, but not quite graphable.

Not quite containable on a bed chart.

Where science touches man it turns to art.³

This poem is a reminder of the subtle needs of patients during their encounters with doctors, especially around many of the most important decisions and events in their lives. Patients’ needs are varied, complex, difficult to discern, and not able to be fully explained or understood through math and science.

Einstein warned us that the modern age would be characterized by a perfection of means and a confusion of goals.⁴ As clinicians, we should strive to clarify and align our goals with those of our patients, providing care that is real, compassionate, and personal, not just an optimized means to achieve standardized metrics. While technology can assist us in this pursuit, we’ll need be careful that our enchantment with innovation does not cloud our actual goal: truly caring for our patients.
 

Dr. Notte is a family physician and chief medical officer of Abington (Pa.) Hospital–Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health. They have no conflicts related to the content of this piece.

References

1. Jones VA. The white coat: Why not follow suit? JAMA. 1999;281(5):478. doi: 10.1001/jama.281.5.478-JMS0203-5-1

2. Peabody, Francis (1927). “The care of the patient.” JAMA. 88(12):877-82. doi: 10.1001/jama.1927.02680380001001.

3. Ciardi, John. Lines from the Beating End of the Stethoscope. Saturday Review, Nov. 18, 1968.

4. Albert Einstein, Out of My Later Years, 1950.

To the Editor:

There is emerging evidence of skin findings in patients with COVID-19, including perniolike changes of the toes as well as urticarial and vesicular eruptions.¹ Magro et al² reported 3 cases of livedoid and purpuric skin eruptions in critically ill COVID-19 patients with evidence of thrombotic vasculopathy on skin biopsy, including a 32-year-old man with striking buttocks retiform purpura. Histopathologic analysis revealed thrombotic vasculopathy and pressure-induced ischemic necrosis. Since that patient was first evaluated (March 2020), we identified 6 more cases of critically ill COVID-19 patients from a single academic hospital in New York City with essentially identical clinical findings. Herein, we report those 6 cases of critically ill and intubated patients with COVID-19 who developed retiform purpura on the buttocks only, approximately 11 to 21 days after onset of COVID-19 symptoms.

We provided consultation for 5 men and 1 woman (age range, 42–78 years) who were critically ill with COVID-19 and developed retiform purpura on the buttocks (Figures 1 and 2). All had an elevated D-dimer concentration: 2 patients, >700 ng/mL; 2 patients, >2000 ng/mL; 2 patients, >6000 ng/mL (reference, 229 ng/mL). Three patients experienced a peak D-dimer concentration on the day retiform purpura was reported.

Further evidence of coagulopathy in these patients included 1 patient with a newly diagnosed left popliteal deep vein thrombosis and 1 patient with a known history of protein C deficiency and deep vein thromboses. Five patients were receiving anticoagulation on the day the skin changes were documented; anticoagulation was contraindicated in the sixth patient because of oropharyngeal bleeding. Anticoagulation was continued at the treatment dosage (enoxaparin 80 mg twice daily) in 3 patients, and in 2 patients receiving a prophylactic dose (enoxaparin 40 mg daily), anticoagulation was escalated to treatment dose due to rising D-dimer levels and newly diagnosed retiform purpura. Skin biopsy was deferred for all patients due to positional and ventilatory restrictions. At that point in their care, 3 patients remained admitted on medicine floors, 2 were in the intensive care unit, and 1 had died.

Although the differential diagnosis for retiform purpura is broad and should be fully considered in any patient with this finding, based on the elevated D-dimer concentration, critical illness secondary to COVID-19, and striking similarity to earlier reported case of buttocks retiform purpura with thrombotic vasculopathy and pressure injury noted histopathologically,² we suspect the buttocks retiform purpura in our 6 cases also represent a combination of cutaneous thrombosis and pressure injury. In addition to acral livedoid eruptions (also reported by Magro and colleagues²), we suspect that this cutaneous manifestation might be associated with a hypercoagulable state in some patients, especially in the setting of a rising D-dimer concentration. One study found that 31% of 184 patients with severe COVID-19 had thrombotic complications,³ a clinical picture that portends a poor prognosis.⁴

COVID-19 patients presenting with retiform purpura should be fully evaluated based on the broad differential for this morphology. We present 6 cases of buttocks retiform purpura in critically ill COVID-19 patients—all with strikingly similar morphologic findings, an elevated D-dimer concentration, and critical illness due to COVID-19—to alert clinicians to this constellation of findings and propose that this cutaneous manifestation could indicate an associated hypercoaguable state and should prompt a hematology consultation. Additionally, biopsy of this skin finding should be considered, especially if biopsy results might serve to guide management; however, obtaining a biopsy specimen can be technically difficult because of ventilatory requirements.

Given the magnitude of the COVID-19 pandemic and the propensity of these patients to experience thrombotic events, recognition of this skin finding in COVID-19 is important and might allow timely intervention.

To the Editor:

There is emerging evidence of skin findings in patients with COVID-19, including perniolike changes of the toes as well as urticarial and vesicular eruptions.¹ Magro et al² reported 3 cases of livedoid and purpuric skin eruptions in critically ill COVID-19 patients with evidence of thrombotic vasculopathy on skin biopsy, including a 32-year-old man with striking buttocks retiform purpura. Histopathologic analysis revealed thrombotic vasculopathy and pressure-induced ischemic necrosis. Since that patient was first evaluated (March 2020), we identified 6 more cases of critically ill COVID-19 patients from a single academic hospital in New York City with essentially identical clinical findings. Herein, we report those 6 cases of critically ill and intubated patients with COVID-19 who developed retiform purpura on the buttocks only, approximately 11 to 21 days after onset of COVID-19 symptoms.

We provided consultation for 5 men and 1 woman (age range, 42–78 years) who were critically ill with COVID-19 and developed retiform purpura on the buttocks (Figures 1 and 2). All had an elevated D-dimer concentration: 2 patients, >700 ng/mL; 2 patients, >2000 ng/mL; 2 patients, >6000 ng/mL (reference, 229 ng/mL). Three patients experienced a peak D-dimer concentration on the day retiform purpura was reported.

Further evidence of coagulopathy in these patients included 1 patient with a newly diagnosed left popliteal deep vein thrombosis and 1 patient with a known history of protein C deficiency and deep vein thromboses. Five patients were receiving anticoagulation on the day the skin changes were documented; anticoagulation was contraindicated in the sixth patient because of oropharyngeal bleeding. Anticoagulation was continued at the treatment dosage (enoxaparin 80 mg twice daily) in 3 patients, and in 2 patients receiving a prophylactic dose (enoxaparin 40 mg daily), anticoagulation was escalated to treatment dose due to rising D-dimer levels and newly diagnosed retiform purpura. Skin biopsy was deferred for all patients due to positional and ventilatory restrictions. At that point in their care, 3 patients remained admitted on medicine floors, 2 were in the intensive care unit, and 1 had died.

Although the differential diagnosis for retiform purpura is broad and should be fully considered in any patient with this finding, based on the elevated D-dimer concentration, critical illness secondary to COVID-19, and striking similarity to earlier reported case of buttocks retiform purpura with thrombotic vasculopathy and pressure injury noted histopathologically,² we suspect the buttocks retiform purpura in our 6 cases also represent a combination of cutaneous thrombosis and pressure injury. In addition to acral livedoid eruptions (also reported by Magro and colleagues²), we suspect that this cutaneous manifestation might be associated with a hypercoagulable state in some patients, especially in the setting of a rising D-dimer concentration. One study found that 31% of 184 patients with severe COVID-19 had thrombotic complications,³ a clinical picture that portends a poor prognosis.⁴

COVID-19 patients presenting with retiform purpura should be fully evaluated based on the broad differential for this morphology. We present 6 cases of buttocks retiform purpura in critically ill COVID-19 patients—all with strikingly similar morphologic findings, an elevated D-dimer concentration, and critical illness due to COVID-19—to alert clinicians to this constellation of findings and propose that this cutaneous manifestation could indicate an associated hypercoaguable state and should prompt a hematology consultation. Additionally, biopsy of this skin finding should be considered, especially if biopsy results might serve to guide management; however, obtaining a biopsy specimen can be technically difficult because of ventilatory requirements.

Given the magnitude of the COVID-19 pandemic and the propensity of these patients to experience thrombotic events, recognition of this skin finding in COVID-19 is important and might allow timely intervention.

To the Editor:

There is emerging evidence of skin findings in patients with COVID-19, including perniolike changes of the toes as well as urticarial and vesicular eruptions.¹ Magro et al² reported 3 cases of livedoid and purpuric skin eruptions in critically ill COVID-19 patients with evidence of thrombotic vasculopathy on skin biopsy, including a 32-year-old man with striking buttocks retiform purpura. Histopathologic analysis revealed thrombotic vasculopathy and pressure-induced ischemic necrosis. Since that patient was first evaluated (March 2020), we identified 6 more cases of critically ill COVID-19 patients from a single academic hospital in New York City with essentially identical clinical findings. Herein, we report those 6 cases of critically ill and intubated patients with COVID-19 who developed retiform purpura on the buttocks only, approximately 11 to 21 days after onset of COVID-19 symptoms.

We provided consultation for 5 men and 1 woman (age range, 42–78 years) who were critically ill with COVID-19 and developed retiform purpura on the buttocks (Figures 1 and 2). All had an elevated D-dimer concentration: 2 patients, >700 ng/mL; 2 patients, >2000 ng/mL; 2 patients, >6000 ng/mL (reference, 229 ng/mL). Three patients experienced a peak D-dimer concentration on the day retiform purpura was reported.

Further evidence of coagulopathy in these patients included 1 patient with a newly diagnosed left popliteal deep vein thrombosis and 1 patient with a known history of protein C deficiency and deep vein thromboses. Five patients were receiving anticoagulation on the day the skin changes were documented; anticoagulation was contraindicated in the sixth patient because of oropharyngeal bleeding. Anticoagulation was continued at the treatment dosage (enoxaparin 80 mg twice daily) in 3 patients, and in 2 patients receiving a prophylactic dose (enoxaparin 40 mg daily), anticoagulation was escalated to treatment dose due to rising D-dimer levels and newly diagnosed retiform purpura. Skin biopsy was deferred for all patients due to positional and ventilatory restrictions. At that point in their care, 3 patients remained admitted on medicine floors, 2 were in the intensive care unit, and 1 had died.

Although the differential diagnosis for retiform purpura is broad and should be fully considered in any patient with this finding, based on the elevated D-dimer concentration, critical illness secondary to COVID-19, and striking similarity to earlier reported case of buttocks retiform purpura with thrombotic vasculopathy and pressure injury noted histopathologically,² we suspect the buttocks retiform purpura in our 6 cases also represent a combination of cutaneous thrombosis and pressure injury. In addition to acral livedoid eruptions (also reported by Magro and colleagues²), we suspect that this cutaneous manifestation might be associated with a hypercoagulable state in some patients, especially in the setting of a rising D-dimer concentration. One study found that 31% of 184 patients with severe COVID-19 had thrombotic complications,³ a clinical picture that portends a poor prognosis.⁴

COVID-19 patients presenting with retiform purpura should be fully evaluated based on the broad differential for this morphology. We present 6 cases of buttocks retiform purpura in critically ill COVID-19 patients—all with strikingly similar morphologic findings, an elevated D-dimer concentration, and critical illness due to COVID-19—to alert clinicians to this constellation of findings and propose that this cutaneous manifestation could indicate an associated hypercoaguable state and should prompt a hematology consultation. Additionally, biopsy of this skin finding should be considered, especially if biopsy results might serve to guide management; however, obtaining a biopsy specimen can be technically difficult because of ventilatory requirements.

Given the magnitude of the COVID-19 pandemic and the propensity of these patients to experience thrombotic events, recognition of this skin finding in COVID-19 is important and might allow timely intervention.

To the Editor:

A 56-year-old man with a history of opioid abuse and splenectomy decades prior due to a motor vehicle accident was brought to an outside emergency department with confusion, slurred speech, and difficulty breathing. Over the next few days, he became febrile and hypotensive, requiring vasopressors. Clinical laboratory testing revealed a urine drug screen positive for opioids and a low platelet count in the setting of a rapidly evolving retiform purpuric rash.

The patient was transferred to our institution 6 days after initial presentation with primary diagnoses of septic shock with multiorgan failure and disseminated intravascular coagulation (DIC). Blood cultures were positive for gram-negative rods. After several days of broad-spectrum antibiotics and supportive care, cultures were reported as positive for Capnocytophaga canimorsus. Upon further questioning, the patient’s wife reported that the couple had a new puppy and that the patient often allowed the dog to bite him playfully and lick abrasions on his hands and legs. He had not received medical treatment for any of the dog’s bites.

On initial examination at the time of transfer, the patient’s skin was remarkable for diffuse areas of stellate and retiform purpura with dusky centers and necrosis of the nasal tip and earlobes. Both hands were purpuric, with necrosis of the fingertips (Figure 1A). The flank was marked by large areas of full-thickness sloughing of the skin (Figure 1B). The lower extremities were edematous, with some areas of stellate purpura and numerous large bullae that drained straw-colored fluid (Figure 1C). Lower extremity pulses were found with Doppler ultrasonography.

Given the presence of rapidly developing retiform purpura in the clinical context of severe sepsis, purpura fulminans (PF) was the primary consideration in the differential diagnosis. Levamisole-induced necrosis syndrome also was considered because of necrosis of the ears and nose as well as the history of substance use; however, the patient was not known to have a history of cocaine abuse, and a test of antineutrophil cytoplasmic antibody was negative.

A punch biopsy of the abdomen revealed intravascular thrombi with epidermal and sweat gland necrosis, consistent with PF (Figure 2). Gram, Giemsa, and Gomori methenamine-silver stains were negative for organisms. Tissue culture remained negative. Repeat blood cultures demonstrated Candida parapsilosis fungemia. Respiratory culture was positive for budding yeast.

The patient was treated with antimicrobials, intravenous argatroban, and subcutaneous heparin. Purpura and bullae on the trunk slowly resolved with systemic therapy and wound care with petrolatum and nonadherent dressings. However, lesions on the nasal tip, all fingers of both hands, and several toes evolved into dry gangrene. The hospital course was complicated by renal failure requiring continuous renal replacement therapy; respiratory failure requiring ventilator support; and elevated levels of liver enzymes, consistent with involvement of the hepatic microvasculature.

The patient was in the medical intensive care unit at our institution for 2 weeks and was transferred to a burn center for specialized wound care. At transfer, he was still on a ventilator and receiving continuous renal replacement therapy. Subsequently, the patient required a left above-the-knee amputation, right below-the-knee amputation, and amputation of several digits of the upper extremities. In the months after the amputations, he required multiple stump revisions and experienced surgical site infections that complicated healing.

Purpura fulminans is an uncommon syndrome characterized by intravascular thrombosis and hemorrhagic infarction of the skin. The condition commonly is associated with septic shock, causing vascular collapse and DIC. It often develops rapidly.

Because of associated high mortality, it is important to differentiate PF from other causes of cutaneous retiform purpura, including other causes of thrombosis and large vessel vasculitis. Leading causes of PF include infection and hereditary or acquired deficiency of protein C, protein S, or antithrombin III. Regardless of cause, biopsy results demonstrate vascular thrombosis out of proportion to vasculitis. The mortality rate is 42% to 50%. The incidence of postinfectious sepsis sequelae in PF is higher than in survivors of sepsis only, especially amputation.^1-3 Most patients do not die from complications of sepsis but from sequelae of the hypercoagulable and prothrombotic state associated with PF.⁴ Hemorrhagic infarction can affect the kidneys, brain, lungs, heart, eyes, and adrenal glands (ie, necrosis, namely Waterhouse-Friderichsen syndrome).⁵

The most common infectious cause of PF is sepsis secondary to Neisseria meningitidis, with as many as 25% of infected patients developing PF.⁶Streptococcus pneumoniae is another common cause. Other important causative organisms include Streptococcus pyogenes; Staphylococcus aureus (in the setting of intravenous substance use); Klebsiella oxytoca; Klebsiella aerogenes; rickettsial organisms; and viruses, including cytomegalovirus and varicella-zoster virus.^2,7-13 Two earlier cases associated with Capnocytophaga were characterized by concomitant renal failure, metabolic acidosis, hemolytic anemia, and DIC.¹⁴

It is estimated that Capnocytophaga causes 11% to 46% of all cases of sepsis¹⁵; sepsis resulting from Capnocytophaga has extremely poor outcomes, with mortality reaching as high as 60%. The organism is part of the normal oral flora of cats and dogs, and a bite (less often, a scratch) is the cause of most Capnocytophaga infections. The clinical spectrum of C canimorsus infection associated with dog saliva exposure more commonly includes cellulitis at or around the site of inoculation, meningitis, and endocarditis.¹⁶

Although patients affected by PF can be young and healthy, several risk factors for PF have been identified^2,6,16: asplenia, an immunocompromised state, systemic corticosteroid use, cirrhosis, and alcoholism. Asplenic patients have been shown to be particularly susceptible to systemic Capnocytophaga infection; when bitten by a dog, they should be treated with prophylactic antibiotics to cover Capnocytophaga.¹⁷ Immunocompetent patients rarely develop severe infection with Capnocytophaga.^16,18,19 The complement system in particular is critically important in defending against C canimorsus.²⁰

The underlying pathophysiology of acute infectious PF is multifactorial, encompassing increased expression of procoagulant tissue factor by monocytes and endothelial cells in the presence of bacterial pathogens. Dysfunction of protein C, an anticoagulant component of the coagulation cascade, often is cited as a crucial derangement leading to the development of a prothrombotic state in acute infectious PF.²¹ Serum protein S and antithrombin deficiency also can play a role.²² Specific in vitro examination of C canimorsus has revealed a protease that catalyzes N-terminal cleavage of procoagulant factor X, resulting in loss of function.¹⁵

Retiform purpura is a hallmark feature of PF, often beginning as nonblanching erythema with localized edema and petechiae before evolving into the characteristic stellate lesions with hemorrhagic bullae and subsequent necrosis.²³ Pathologic examination reveals microthrombi involving arterioles and smaller vessels.²⁴ There typically is laboratory evidence of DIC in PF, including elevated prothrombin time and partial thromboplastin time, thrombocytopenia, elevated D-dimer, and a decreased fibrinogen level.^6,23

Capnocytophaga bacteria are challenging to grow on standard culture media. Optimal media for growth include 5% sheep’s blood and chocolate agar.¹⁶ Polymerase chain reaction can identify Capnocytophaga; in cases in which blood culture does not produce growth, 16S ribosomal RNA gene sequencing of tissue from skin biopsy has identified the pathogen.²⁵

Some Capnocytophaga isolates have been shown to produce beta-lactamase; individual strains can be resistant to penicillins, cephalosporins, and imipenem.²⁶ Factors associated with an increased risk for death include decreased leukocyte and platelet counts and an increased level of arterial lactate.²⁷

Empiric antibiotic therapy for Capnocytophaga sepsis should include a beta-lactam and beta-lactamase inhibitor, such as piperacillin-tazobactam. Management of DIC can include therapeutic heparin or low-molecular-weight heparin and prophylactic platelet transfusion to maintain a pre-established value.^28-30 Debridement should be conservative; it is important to wait for definite delineation between viable and necrotic tissue,³¹ which might take several months.³² Human skin allografts, in addition to artificial skin, are utilized as supplemental therapy for more rapid wound closure after removal of necrotic tissue.^33,34 Hyperoxygenated fatty acids have been noted to aid in more rapid wound healing in infants with PF.³⁵

Fresh frozen plasma is one method to replace missing factors, but it contains little protein C.³⁶ Outcomes with recombinant human activated protein C (drotrecogin alfa) are mixed, and studies have shown no benefit in reducing the risk for death.^37,38 Protein C concentrate has shown therapeutic benefit in some case reports and small retrospective studies.⁴ In one case report, protein C concentrate and heparin were utilized in combination with antithrombin III.²¹

Hyperbaric O₂ might be of benefit when initiated within 5 days after onset of PF. However, hyperbaric O₂ does carry risk; O₂ toxicity, barotrauma, and barriers to timely resuscitation when the patient is inside the pressurized chamber can occur.²

There is a single report of successful use of the vasodilator iloprost for meningococcal PF without need for surgical intervention; the team also utilized topical nitroglycerin patches on the fingers to avoid digital amputation.³⁹ Epoprostenol, tissue plasminogen activator, and antithrombin have been utilized in cases of extensive PF. Fibrinolytic therapy might have some utility, but only in a setting of malignancy-associated DIC.⁴⁰

Treatment of acute infectious PF lacks a high level of evidence. Options include replacement of anticoagulant factors, anticoagulant therapy, hyperbaric O₂, topical and systemic vasodilators, and, in the setting of underlying cancer, fibrinolytics. Even with therapy, prognosis is guarded.

To the Editor:

A 56-year-old man with a history of opioid abuse and splenectomy decades prior due to a motor vehicle accident was brought to an outside emergency department with confusion, slurred speech, and difficulty breathing. Over the next few days, he became febrile and hypotensive, requiring vasopressors. Clinical laboratory testing revealed a urine drug screen positive for opioids and a low platelet count in the setting of a rapidly evolving retiform purpuric rash.

The patient was transferred to our institution 6 days after initial presentation with primary diagnoses of septic shock with multiorgan failure and disseminated intravascular coagulation (DIC). Blood cultures were positive for gram-negative rods. After several days of broad-spectrum antibiotics and supportive care, cultures were reported as positive for Capnocytophaga canimorsus. Upon further questioning, the patient’s wife reported that the couple had a new puppy and that the patient often allowed the dog to bite him playfully and lick abrasions on his hands and legs. He had not received medical treatment for any of the dog’s bites.

On initial examination at the time of transfer, the patient’s skin was remarkable for diffuse areas of stellate and retiform purpura with dusky centers and necrosis of the nasal tip and earlobes. Both hands were purpuric, with necrosis of the fingertips (Figure 1A). The flank was marked by large areas of full-thickness sloughing of the skin (Figure 1B). The lower extremities were edematous, with some areas of stellate purpura and numerous large bullae that drained straw-colored fluid (Figure 1C). Lower extremity pulses were found with Doppler ultrasonography.

Given the presence of rapidly developing retiform purpura in the clinical context of severe sepsis, purpura fulminans (PF) was the primary consideration in the differential diagnosis. Levamisole-induced necrosis syndrome also was considered because of necrosis of the ears and nose as well as the history of substance use; however, the patient was not known to have a history of cocaine abuse, and a test of antineutrophil cytoplasmic antibody was negative.

A punch biopsy of the abdomen revealed intravascular thrombi with epidermal and sweat gland necrosis, consistent with PF (Figure 2). Gram, Giemsa, and Gomori methenamine-silver stains were negative for organisms. Tissue culture remained negative. Repeat blood cultures demonstrated Candida parapsilosis fungemia. Respiratory culture was positive for budding yeast.

The patient was treated with antimicrobials, intravenous argatroban, and subcutaneous heparin. Purpura and bullae on the trunk slowly resolved with systemic therapy and wound care with petrolatum and nonadherent dressings. However, lesions on the nasal tip, all fingers of both hands, and several toes evolved into dry gangrene. The hospital course was complicated by renal failure requiring continuous renal replacement therapy; respiratory failure requiring ventilator support; and elevated levels of liver enzymes, consistent with involvement of the hepatic microvasculature.

The patient was in the medical intensive care unit at our institution for 2 weeks and was transferred to a burn center for specialized wound care. At transfer, he was still on a ventilator and receiving continuous renal replacement therapy. Subsequently, the patient required a left above-the-knee amputation, right below-the-knee amputation, and amputation of several digits of the upper extremities. In the months after the amputations, he required multiple stump revisions and experienced surgical site infections that complicated healing.

Purpura fulminans is an uncommon syndrome characterized by intravascular thrombosis and hemorrhagic infarction of the skin. The condition commonly is associated with septic shock, causing vascular collapse and DIC. It often develops rapidly.

Because of associated high mortality, it is important to differentiate PF from other causes of cutaneous retiform purpura, including other causes of thrombosis and large vessel vasculitis. Leading causes of PF include infection and hereditary or acquired deficiency of protein C, protein S, or antithrombin III. Regardless of cause, biopsy results demonstrate vascular thrombosis out of proportion to vasculitis. The mortality rate is 42% to 50%. The incidence of postinfectious sepsis sequelae in PF is higher than in survivors of sepsis only, especially amputation.^1-3 Most patients do not die from complications of sepsis but from sequelae of the hypercoagulable and prothrombotic state associated with PF.⁴ Hemorrhagic infarction can affect the kidneys, brain, lungs, heart, eyes, and adrenal glands (ie, necrosis, namely Waterhouse-Friderichsen syndrome).⁵

The most common infectious cause of PF is sepsis secondary to Neisseria meningitidis, with as many as 25% of infected patients developing PF.⁶Streptococcus pneumoniae is another common cause. Other important causative organisms include Streptococcus pyogenes; Staphylococcus aureus (in the setting of intravenous substance use); Klebsiella oxytoca; Klebsiella aerogenes; rickettsial organisms; and viruses, including cytomegalovirus and varicella-zoster virus.^2,7-13 Two earlier cases associated with Capnocytophaga were characterized by concomitant renal failure, metabolic acidosis, hemolytic anemia, and DIC.¹⁴

It is estimated that Capnocytophaga causes 11% to 46% of all cases of sepsis¹⁵; sepsis resulting from Capnocytophaga has extremely poor outcomes, with mortality reaching as high as 60%. The organism is part of the normal oral flora of cats and dogs, and a bite (less often, a scratch) is the cause of most Capnocytophaga infections. The clinical spectrum of C canimorsus infection associated with dog saliva exposure more commonly includes cellulitis at or around the site of inoculation, meningitis, and endocarditis.¹⁶

Although patients affected by PF can be young and healthy, several risk factors for PF have been identified^2,6,16: asplenia, an immunocompromised state, systemic corticosteroid use, cirrhosis, and alcoholism. Asplenic patients have been shown to be particularly susceptible to systemic Capnocytophaga infection; when bitten by a dog, they should be treated with prophylactic antibiotics to cover Capnocytophaga.¹⁷ Immunocompetent patients rarely develop severe infection with Capnocytophaga.^16,18,19 The complement system in particular is critically important in defending against C canimorsus.²⁰

The underlying pathophysiology of acute infectious PF is multifactorial, encompassing increased expression of procoagulant tissue factor by monocytes and endothelial cells in the presence of bacterial pathogens. Dysfunction of protein C, an anticoagulant component of the coagulation cascade, often is cited as a crucial derangement leading to the development of a prothrombotic state in acute infectious PF.²¹ Serum protein S and antithrombin deficiency also can play a role.²² Specific in vitro examination of C canimorsus has revealed a protease that catalyzes N-terminal cleavage of procoagulant factor X, resulting in loss of function.¹⁵

Retiform purpura is a hallmark feature of PF, often beginning as nonblanching erythema with localized edema and petechiae before evolving into the characteristic stellate lesions with hemorrhagic bullae and subsequent necrosis.²³ Pathologic examination reveals microthrombi involving arterioles and smaller vessels.²⁴ There typically is laboratory evidence of DIC in PF, including elevated prothrombin time and partial thromboplastin time, thrombocytopenia, elevated D-dimer, and a decreased fibrinogen level.^6,23

Capnocytophaga bacteria are challenging to grow on standard culture media. Optimal media for growth include 5% sheep’s blood and chocolate agar.¹⁶ Polymerase chain reaction can identify Capnocytophaga; in cases in which blood culture does not produce growth, 16S ribosomal RNA gene sequencing of tissue from skin biopsy has identified the pathogen.²⁵

Some Capnocytophaga isolates have been shown to produce beta-lactamase; individual strains can be resistant to penicillins, cephalosporins, and imipenem.²⁶ Factors associated with an increased risk for death include decreased leukocyte and platelet counts and an increased level of arterial lactate.²⁷

Empiric antibiotic therapy for Capnocytophaga sepsis should include a beta-lactam and beta-lactamase inhibitor, such as piperacillin-tazobactam. Management of DIC can include therapeutic heparin or low-molecular-weight heparin and prophylactic platelet transfusion to maintain a pre-established value.^28-30 Debridement should be conservative; it is important to wait for definite delineation between viable and necrotic tissue,³¹ which might take several months.³² Human skin allografts, in addition to artificial skin, are utilized as supplemental therapy for more rapid wound closure after removal of necrotic tissue.^33,34 Hyperoxygenated fatty acids have been noted to aid in more rapid wound healing in infants with PF.³⁵

Fresh frozen plasma is one method to replace missing factors, but it contains little protein C.³⁶ Outcomes with recombinant human activated protein C (drotrecogin alfa) are mixed, and studies have shown no benefit in reducing the risk for death.^37,38 Protein C concentrate has shown therapeutic benefit in some case reports and small retrospective studies.⁴ In one case report, protein C concentrate and heparin were utilized in combination with antithrombin III.²¹

Hyperbaric O₂ might be of benefit when initiated within 5 days after onset of PF. However, hyperbaric O₂ does carry risk; O₂ toxicity, barotrauma, and barriers to timely resuscitation when the patient is inside the pressurized chamber can occur.²

There is a single report of successful use of the vasodilator iloprost for meningococcal PF without need for surgical intervention; the team also utilized topical nitroglycerin patches on the fingers to avoid digital amputation.³⁹ Epoprostenol, tissue plasminogen activator, and antithrombin have been utilized in cases of extensive PF. Fibrinolytic therapy might have some utility, but only in a setting of malignancy-associated DIC.⁴⁰

Treatment of acute infectious PF lacks a high level of evidence. Options include replacement of anticoagulant factors, anticoagulant therapy, hyperbaric O₂, topical and systemic vasodilators, and, in the setting of underlying cancer, fibrinolytics. Even with therapy, prognosis is guarded.

To the Editor:

A 56-year-old man with a history of opioid abuse and splenectomy decades prior due to a motor vehicle accident was brought to an outside emergency department with confusion, slurred speech, and difficulty breathing. Over the next few days, he became febrile and hypotensive, requiring vasopressors. Clinical laboratory testing revealed a urine drug screen positive for opioids and a low platelet count in the setting of a rapidly evolving retiform purpuric rash.

The patient was transferred to our institution 6 days after initial presentation with primary diagnoses of septic shock with multiorgan failure and disseminated intravascular coagulation (DIC). Blood cultures were positive for gram-negative rods. After several days of broad-spectrum antibiotics and supportive care, cultures were reported as positive for Capnocytophaga canimorsus. Upon further questioning, the patient’s wife reported that the couple had a new puppy and that the patient often allowed the dog to bite him playfully and lick abrasions on his hands and legs. He had not received medical treatment for any of the dog’s bites.

On initial examination at the time of transfer, the patient’s skin was remarkable for diffuse areas of stellate and retiform purpura with dusky centers and necrosis of the nasal tip and earlobes. Both hands were purpuric, with necrosis of the fingertips (Figure 1A). The flank was marked by large areas of full-thickness sloughing of the skin (Figure 1B). The lower extremities were edematous, with some areas of stellate purpura and numerous large bullae that drained straw-colored fluid (Figure 1C). Lower extremity pulses were found with Doppler ultrasonography.

Given the presence of rapidly developing retiform purpura in the clinical context of severe sepsis, purpura fulminans (PF) was the primary consideration in the differential diagnosis. Levamisole-induced necrosis syndrome also was considered because of necrosis of the ears and nose as well as the history of substance use; however, the patient was not known to have a history of cocaine abuse, and a test of antineutrophil cytoplasmic antibody was negative.

A punch biopsy of the abdomen revealed intravascular thrombi with epidermal and sweat gland necrosis, consistent with PF (Figure 2). Gram, Giemsa, and Gomori methenamine-silver stains were negative for organisms. Tissue culture remained negative. Repeat blood cultures demonstrated Candida parapsilosis fungemia. Respiratory culture was positive for budding yeast.

The patient was treated with antimicrobials, intravenous argatroban, and subcutaneous heparin. Purpura and bullae on the trunk slowly resolved with systemic therapy and wound care with petrolatum and nonadherent dressings. However, lesions on the nasal tip, all fingers of both hands, and several toes evolved into dry gangrene. The hospital course was complicated by renal failure requiring continuous renal replacement therapy; respiratory failure requiring ventilator support; and elevated levels of liver enzymes, consistent with involvement of the hepatic microvasculature.

The patient was in the medical intensive care unit at our institution for 2 weeks and was transferred to a burn center for specialized wound care. At transfer, he was still on a ventilator and receiving continuous renal replacement therapy. Subsequently, the patient required a left above-the-knee amputation, right below-the-knee amputation, and amputation of several digits of the upper extremities. In the months after the amputations, he required multiple stump revisions and experienced surgical site infections that complicated healing.

Purpura fulminans is an uncommon syndrome characterized by intravascular thrombosis and hemorrhagic infarction of the skin. The condition commonly is associated with septic shock, causing vascular collapse and DIC. It often develops rapidly.

Because of associated high mortality, it is important to differentiate PF from other causes of cutaneous retiform purpura, including other causes of thrombosis and large vessel vasculitis. Leading causes of PF include infection and hereditary or acquired deficiency of protein C, protein S, or antithrombin III. Regardless of cause, biopsy results demonstrate vascular thrombosis out of proportion to vasculitis. The mortality rate is 42% to 50%. The incidence of postinfectious sepsis sequelae in PF is higher than in survivors of sepsis only, especially amputation.^1-3 Most patients do not die from complications of sepsis but from sequelae of the hypercoagulable and prothrombotic state associated with PF.⁴ Hemorrhagic infarction can affect the kidneys, brain, lungs, heart, eyes, and adrenal glands (ie, necrosis, namely Waterhouse-Friderichsen syndrome).⁵

The most common infectious cause of PF is sepsis secondary to Neisseria meningitidis, with as many as 25% of infected patients developing PF.⁶Streptococcus pneumoniae is another common cause. Other important causative organisms include Streptococcus pyogenes; Staphylococcus aureus (in the setting of intravenous substance use); Klebsiella oxytoca; Klebsiella aerogenes; rickettsial organisms; and viruses, including cytomegalovirus and varicella-zoster virus.^2,7-13 Two earlier cases associated with Capnocytophaga were characterized by concomitant renal failure, metabolic acidosis, hemolytic anemia, and DIC.¹⁴

It is estimated that Capnocytophaga causes 11% to 46% of all cases of sepsis¹⁵; sepsis resulting from Capnocytophaga has extremely poor outcomes, with mortality reaching as high as 60%. The organism is part of the normal oral flora of cats and dogs, and a bite (less often, a scratch) is the cause of most Capnocytophaga infections. The clinical spectrum of C canimorsus infection associated with dog saliva exposure more commonly includes cellulitis at or around the site of inoculation, meningitis, and endocarditis.¹⁶

Although patients affected by PF can be young and healthy, several risk factors for PF have been identified^2,6,16: asplenia, an immunocompromised state, systemic corticosteroid use, cirrhosis, and alcoholism. Asplenic patients have been shown to be particularly susceptible to systemic Capnocytophaga infection; when bitten by a dog, they should be treated with prophylactic antibiotics to cover Capnocytophaga.¹⁷ Immunocompetent patients rarely develop severe infection with Capnocytophaga.^16,18,19 The complement system in particular is critically important in defending against C canimorsus.²⁰

The underlying pathophysiology of acute infectious PF is multifactorial, encompassing increased expression of procoagulant tissue factor by monocytes and endothelial cells in the presence of bacterial pathogens. Dysfunction of protein C, an anticoagulant component of the coagulation cascade, often is cited as a crucial derangement leading to the development of a prothrombotic state in acute infectious PF.²¹ Serum protein S and antithrombin deficiency also can play a role.²² Specific in vitro examination of C canimorsus has revealed a protease that catalyzes N-terminal cleavage of procoagulant factor X, resulting in loss of function.¹⁵

Retiform purpura is a hallmark feature of PF, often beginning as nonblanching erythema with localized edema and petechiae before evolving into the characteristic stellate lesions with hemorrhagic bullae and subsequent necrosis.²³ Pathologic examination reveals microthrombi involving arterioles and smaller vessels.²⁴ There typically is laboratory evidence of DIC in PF, including elevated prothrombin time and partial thromboplastin time, thrombocytopenia, elevated D-dimer, and a decreased fibrinogen level.^6,23

Capnocytophaga bacteria are challenging to grow on standard culture media. Optimal media for growth include 5% sheep’s blood and chocolate agar.¹⁶ Polymerase chain reaction can identify Capnocytophaga; in cases in which blood culture does not produce growth, 16S ribosomal RNA gene sequencing of tissue from skin biopsy has identified the pathogen.²⁵

Some Capnocytophaga isolates have been shown to produce beta-lactamase; individual strains can be resistant to penicillins, cephalosporins, and imipenem.²⁶ Factors associated with an increased risk for death include decreased leukocyte and platelet counts and an increased level of arterial lactate.²⁷

Empiric antibiotic therapy for Capnocytophaga sepsis should include a beta-lactam and beta-lactamase inhibitor, such as piperacillin-tazobactam. Management of DIC can include therapeutic heparin or low-molecular-weight heparin and prophylactic platelet transfusion to maintain a pre-established value.^28-30 Debridement should be conservative; it is important to wait for definite delineation between viable and necrotic tissue,³¹ which might take several months.³² Human skin allografts, in addition to artificial skin, are utilized as supplemental therapy for more rapid wound closure after removal of necrotic tissue.^33,34 Hyperoxygenated fatty acids have been noted to aid in more rapid wound healing in infants with PF.³⁵

Fresh frozen plasma is one method to replace missing factors, but it contains little protein C.³⁶ Outcomes with recombinant human activated protein C (drotrecogin alfa) are mixed, and studies have shown no benefit in reducing the risk for death.^37,38 Protein C concentrate has shown therapeutic benefit in some case reports and small retrospective studies.⁴ In one case report, protein C concentrate and heparin were utilized in combination with antithrombin III.²¹

Hyperbaric O₂ might be of benefit when initiated within 5 days after onset of PF. However, hyperbaric O₂ does carry risk; O₂ toxicity, barotrauma, and barriers to timely resuscitation when the patient is inside the pressurized chamber can occur.²

There is a single report of successful use of the vasodilator iloprost for meningococcal PF without need for surgical intervention; the team also utilized topical nitroglycerin patches on the fingers to avoid digital amputation.³⁹ Epoprostenol, tissue plasminogen activator, and antithrombin have been utilized in cases of extensive PF. Fibrinolytic therapy might have some utility, but only in a setting of malignancy-associated DIC.⁴⁰

Treatment of acute infectious PF lacks a high level of evidence. Options include replacement of anticoagulant factors, anticoagulant therapy, hyperbaric O₂, topical and systemic vasodilators, and, in the setting of underlying cancer, fibrinolytics. Even with therapy, prognosis is guarded.

To the Editor:

Purpura fulminans (PF) is an acute, life-threatening condition characterized by intravascular thrombosis and hemorrhagic necrosis of the skin. It classically presents as retiform purpura with branched or angular purpuric lesions. Purpura fulminans often occurs in the setting of disseminated intravascular coagulation, secondary to sepsis, trauma, malignancy, autoimmune disease, and congenital or acquired protein C or S deficiency, among other abnormalities.¹ Rapid identification and treatment of the underlying cause are mainstays of management. We report a case of PF secondary to Vibrio vulnificus infection and highlight the importance of timely consideration of this etiologic agent due to the high mortality rate and specific treatment required.

A 58-year-old man with liver cirrhosis and hepatitis B virus presented with pain, swelling, and localized erythema affecting both legs as well as a fever. He reported vomiting blood and an episode of bloody diarrhea over the preceding 24 hours. He denied exposure to sick contacts or a history of autoimmune disease. At initial presentation to the emergency department, physical examination revealed few scattered, sharply demarcated, erythematous to violaceous patches that rapidly progressed overnight to hemorrhagic bullae and widespread retiform purpuric patches on both legs (Figure 1). As the patient’s skin condition worsened, he had a blood pressure of 80/50 mm Hg and a pulse rate of 110/min. Serum analysis was notable for mild leukocytosis (10.74×10⁹/L [reference range, 4.8–10.8×10⁹/L), thrombocytopenia (39×10⁹/L [reference range, 150–450×10⁹/L]), and decreased C3 (25 mg/dL [reference range, 81–157 mg/dL]) and C4 (8 mg/dL [reference range, 13–39 mg/dL]). Laboratory findings also were remarkable for prothrombin time (23.3 seconds [reference range, 8.8–12.3 seconds]), partial thromboplastin time (52.5 seconds [reference range, 23.6–35.8 seconds]), and international normalized ratio (2.01 [reference range, 0.8–1.13]). Aspartate transaminase (237 U/L [reference range, 11–39 U/L]) and alanine transaminase (80 U/L [reference range, 11–35 U/L]) were elevated, while antineutrophil cytoplasmic antibodies, serum immunoglobulin, and cryoglobulins were unremarkable. Punch biopsies of the left thigh were performed, and histopathology revealed small vessel thrombosis and ischemic changes consistent with PF (Figure 2). Vancomycin, clindamycin, cefepime injection, and piperacillin-tazobactam were administered intravenously for empiric broad-spectrum sepsis coverage. Within hours, the patient experienced refractory septic shock with disseminated intravascular coagulation and died from pulmonary embolism and subsequent cardiac arrest. Tissue and blood cultures grew V vulnificus.

Vibrio vulnificus is a gram-negative bacillus and a rare cause of primary septicemia following consumption of shellfish, especially oysters. Wounds exposed to saltwater or brackish water contaminated with the microorganism can produce soft-tissue infections. Individuals with chronic liver disease are at greater risk for V vulnificus infection.² The clinical presentation of V vulnificus includes early cellulitislike patches, late purpura with hemorrhagic bullae, and rapidly progressing shock.³

Mortality rates from V vulnificus infection are high.⁴ Therefore, it is recommended to presumptively diagnose V vulnificus septicemia in any individual at risk for infection who presents with the characteristic history in the setting of hypotension, fever, or septic shock. It is crucial for providers to be aware that broad-spectrum antibiotics commonly used for sepsis are inadequate for the treatment of V vulnificus. Immediate treatment with tetracycline (minocycline or doxycycline) and a third-generation cephalosporin (cefotaxime or ceftriaxone injection) or in combination with ciprofloxacin has been proven effective.^4,5

Vibrio vulnificus rarely is described in the literature as inducing PF. In one previously reported case, the patient was otherwise healthy and managed to recover following antibiotic therapy and wound debridement,⁶ whereas in another case the patient had undiagnosed liver cirrhosis and died from the infection.^6,7 In the latter case, the patient presented to the emergency department in a coma. Our patient did not have the clinical signs of sepsis upon initial presentation to the emergency department. It is possible the infection rapidly progressed because of his underlying liver disease. Genotyping analysis of V vulnificus has shown that strains with low pathogenicity can cause primary septicemia in humans.⁷

Our case reinforces the need to quickly recognize V vulnificus as a rare underlying cause of PF and administer the appropriate treatment.

To the Editor:

Purpura fulminans (PF) is an acute, life-threatening condition characterized by intravascular thrombosis and hemorrhagic necrosis of the skin. It classically presents as retiform purpura with branched or angular purpuric lesions. Purpura fulminans often occurs in the setting of disseminated intravascular coagulation, secondary to sepsis, trauma, malignancy, autoimmune disease, and congenital or acquired protein C or S deficiency, among other abnormalities.¹ Rapid identification and treatment of the underlying cause are mainstays of management. We report a case of PF secondary to Vibrio vulnificus infection and highlight the importance of timely consideration of this etiologic agent due to the high mortality rate and specific treatment required.

A 58-year-old man with liver cirrhosis and hepatitis B virus presented with pain, swelling, and localized erythema affecting both legs as well as a fever. He reported vomiting blood and an episode of bloody diarrhea over the preceding 24 hours. He denied exposure to sick contacts or a history of autoimmune disease. At initial presentation to the emergency department, physical examination revealed few scattered, sharply demarcated, erythematous to violaceous patches that rapidly progressed overnight to hemorrhagic bullae and widespread retiform purpuric patches on both legs (Figure 1). As the patient’s skin condition worsened, he had a blood pressure of 80/50 mm Hg and a pulse rate of 110/min. Serum analysis was notable for mild leukocytosis (10.74×10⁹/L [reference range, 4.8–10.8×10⁹/L), thrombocytopenia (39×10⁹/L [reference range, 150–450×10⁹/L]), and decreased C3 (25 mg/dL [reference range, 81–157 mg/dL]) and C4 (8 mg/dL [reference range, 13–39 mg/dL]). Laboratory findings also were remarkable for prothrombin time (23.3 seconds [reference range, 8.8–12.3 seconds]), partial thromboplastin time (52.5 seconds [reference range, 23.6–35.8 seconds]), and international normalized ratio (2.01 [reference range, 0.8–1.13]). Aspartate transaminase (237 U/L [reference range, 11–39 U/L]) and alanine transaminase (80 U/L [reference range, 11–35 U/L]) were elevated, while antineutrophil cytoplasmic antibodies, serum immunoglobulin, and cryoglobulins were unremarkable. Punch biopsies of the left thigh were performed, and histopathology revealed small vessel thrombosis and ischemic changes consistent with PF (Figure 2). Vancomycin, clindamycin, cefepime injection, and piperacillin-tazobactam were administered intravenously for empiric broad-spectrum sepsis coverage. Within hours, the patient experienced refractory septic shock with disseminated intravascular coagulation and died from pulmonary embolism and subsequent cardiac arrest. Tissue and blood cultures grew V vulnificus.

Vibrio vulnificus is a gram-negative bacillus and a rare cause of primary septicemia following consumption of shellfish, especially oysters. Wounds exposed to saltwater or brackish water contaminated with the microorganism can produce soft-tissue infections. Individuals with chronic liver disease are at greater risk for V vulnificus infection.² The clinical presentation of V vulnificus includes early cellulitislike patches, late purpura with hemorrhagic bullae, and rapidly progressing shock.³

Mortality rates from V vulnificus infection are high.⁴ Therefore, it is recommended to presumptively diagnose V vulnificus septicemia in any individual at risk for infection who presents with the characteristic history in the setting of hypotension, fever, or septic shock. It is crucial for providers to be aware that broad-spectrum antibiotics commonly used for sepsis are inadequate for the treatment of V vulnificus. Immediate treatment with tetracycline (minocycline or doxycycline) and a third-generation cephalosporin (cefotaxime or ceftriaxone injection) or in combination with ciprofloxacin has been proven effective.^4,5

Vibrio vulnificus rarely is described in the literature as inducing PF. In one previously reported case, the patient was otherwise healthy and managed to recover following antibiotic therapy and wound debridement,⁶ whereas in another case the patient had undiagnosed liver cirrhosis and died from the infection.^6,7 In the latter case, the patient presented to the emergency department in a coma. Our patient did not have the clinical signs of sepsis upon initial presentation to the emergency department. It is possible the infection rapidly progressed because of his underlying liver disease. Genotyping analysis of V vulnificus has shown that strains with low pathogenicity can cause primary septicemia in humans.⁷

Our case reinforces the need to quickly recognize V vulnificus as a rare underlying cause of PF and administer the appropriate treatment.

To the Editor:

Purpura fulminans (PF) is an acute, life-threatening condition characterized by intravascular thrombosis and hemorrhagic necrosis of the skin. It classically presents as retiform purpura with branched or angular purpuric lesions. Purpura fulminans often occurs in the setting of disseminated intravascular coagulation, secondary to sepsis, trauma, malignancy, autoimmune disease, and congenital or acquired protein C or S deficiency, among other abnormalities.¹ Rapid identification and treatment of the underlying cause are mainstays of management. We report a case of PF secondary to Vibrio vulnificus infection and highlight the importance of timely consideration of this etiologic agent due to the high mortality rate and specific treatment required.

A 58-year-old man with liver cirrhosis and hepatitis B virus presented with pain, swelling, and localized erythema affecting both legs as well as a fever. He reported vomiting blood and an episode of bloody diarrhea over the preceding 24 hours. He denied exposure to sick contacts or a history of autoimmune disease. At initial presentation to the emergency department, physical examination revealed few scattered, sharply demarcated, erythematous to violaceous patches that rapidly progressed overnight to hemorrhagic bullae and widespread retiform purpuric patches on both legs (Figure 1). As the patient’s skin condition worsened, he had a blood pressure of 80/50 mm Hg and a pulse rate of 110/min. Serum analysis was notable for mild leukocytosis (10.74×10⁹/L [reference range, 4.8–10.8×10⁹/L), thrombocytopenia (39×10⁹/L [reference range, 150–450×10⁹/L]), and decreased C3 (25 mg/dL [reference range, 81–157 mg/dL]) and C4 (8 mg/dL [reference range, 13–39 mg/dL]). Laboratory findings also were remarkable for prothrombin time (23.3 seconds [reference range, 8.8–12.3 seconds]), partial thromboplastin time (52.5 seconds [reference range, 23.6–35.8 seconds]), and international normalized ratio (2.01 [reference range, 0.8–1.13]). Aspartate transaminase (237 U/L [reference range, 11–39 U/L]) and alanine transaminase (80 U/L [reference range, 11–35 U/L]) were elevated, while antineutrophil cytoplasmic antibodies, serum immunoglobulin, and cryoglobulins were unremarkable. Punch biopsies of the left thigh were performed, and histopathology revealed small vessel thrombosis and ischemic changes consistent with PF (Figure 2). Vancomycin, clindamycin, cefepime injection, and piperacillin-tazobactam were administered intravenously for empiric broad-spectrum sepsis coverage. Within hours, the patient experienced refractory septic shock with disseminated intravascular coagulation and died from pulmonary embolism and subsequent cardiac arrest. Tissue and blood cultures grew V vulnificus.

Vibrio vulnificus is a gram-negative bacillus and a rare cause of primary septicemia following consumption of shellfish, especially oysters. Wounds exposed to saltwater or brackish water contaminated with the microorganism can produce soft-tissue infections. Individuals with chronic liver disease are at greater risk for V vulnificus infection.² The clinical presentation of V vulnificus includes early cellulitislike patches, late purpura with hemorrhagic bullae, and rapidly progressing shock.³

Mortality rates from V vulnificus infection are high.⁴ Therefore, it is recommended to presumptively diagnose V vulnificus septicemia in any individual at risk for infection who presents with the characteristic history in the setting of hypotension, fever, or septic shock. It is crucial for providers to be aware that broad-spectrum antibiotics commonly used for sepsis are inadequate for the treatment of V vulnificus. Immediate treatment with tetracycline (minocycline or doxycycline) and a third-generation cephalosporin (cefotaxime or ceftriaxone injection) or in combination with ciprofloxacin has been proven effective.^4,5

Vibrio vulnificus rarely is described in the literature as inducing PF. In one previously reported case, the patient was otherwise healthy and managed to recover following antibiotic therapy and wound debridement,⁶ whereas in another case the patient had undiagnosed liver cirrhosis and died from the infection.^6,7 In the latter case, the patient presented to the emergency department in a coma. Our patient did not have the clinical signs of sepsis upon initial presentation to the emergency department. It is possible the infection rapidly progressed because of his underlying liver disease. Genotyping analysis of V vulnificus has shown that strains with low pathogenicity can cause primary septicemia in humans.⁷

Our case reinforces the need to quickly recognize V vulnificus as a rare underlying cause of PF and administer the appropriate treatment.

For years, it has been strongly suspected that malignant melanoma is underreported in the United States. I have audited my melanoma cases (biopsies and excisions sent to me) and discovered that of the 240 cases confirmed over the past 5 years, only 41 were reported to the Ohio state health department and are in that database. That amounts to 199 unreported cases – nearly 83% of the total.

This raises the question as to who is responsible for reporting these cases. Dermatology is unique in that our pathology specimens are not routinely passed through a hospital pathology laboratory. The big difference in reporting is that hospital labs have trained data registrars to report all reportable cancers to state health departments. Therefore, in my case, only patients sent to a hospital-based surgeon for sentinel node biopsies or exceptionally large excisions get reported. When I have spoken about this to my dermatology lab and biopsying physicians, the discussion rapidly turns into a finger pointing game of who is responsible. No one, except perhaps the dermatologist who did the biopsy, has all the data.

Unfortunately, these cases are tedious and time consuming to report. Despite state laws requiring reporting, even with penalties for nonreporters, many small dermatology practices do not report these cases and expect their dermatopathology labs to do so, but the labs expect the biopsying dermatologist to report the cases. This is a classic case of an unfunded mandate since small dermatology practices do not have the time or resources for reporting.

I have worked with the Ohio Department of Health to remove any unnecessary data fields and they have managed to reduce the reporting fields (to 59!). This is the minimum amount required to be included in the National Cancer Institute’s SEER (Surveillance, Epidemiology, and End Results) database. Many of these fields are not applicable to thin melanomas and after reviewing the 1-hour online training course, each patient can be entered (once the necessary data are collected) in about 15 minutes. This is still a formidable task for small offices, which cannot be blamed for ducking and hoping someone else reports.

While there is controversy regarding the relevance of thin melanomas to overall survival, more accurate reporting can only bolster either argument.
 

A solution to underreporting

I believe we have developed a unique solution to this conundrum. Our office is partnering with the local melanoma support group (Melanoma Know More) to train volunteers to help with the data collection and reporting of these thin melanomas. We have also discovered that the local community college has students who are majoring in pathology data registry reporting and are happy to gain a little experience before graduating.

We eventually hope to become a clearinghouse for the entire state of Ohio. The state health department has agreed not to apply punitive measures to physicians who are new reporters. It is our plan to obtain melanoma pathology reports, run these past the state database, identify unreported cases, and obtain further data as needed from the biopsying physicians, and then complete the reporting.

I think dermatologic oncologists in every state should view this as an opportunity for a significant quality improvement project, and as a terrific service to the general dermatology community.

The ramifications of more comprehensive reporting of melanomas are great. I would expect more attention to the disease by researchers, and much more clout with state and national legislators. Think about increased funding for melanoma research, allowing sunscreen use for school children, sunshades for playgrounds, and more responsible tanning bed restrictions.

Now, I must inform you that this is my last column, but I plan to continue writing. Over the past 6 years, I have been able to cover a wide range of topics ranging from human trafficking and the American Medical Association, to the many problems faced by small practices. I have enjoyed myself hugely. To quote Douglas Adams, from The Hitchhiker’s Guide to the Galaxy, “So long and thanks for all the fish!” Keep in touch at [email protected].
 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].

For years, it has been strongly suspected that malignant melanoma is underreported in the United States. I have audited my melanoma cases (biopsies and excisions sent to me) and discovered that of the 240 cases confirmed over the past 5 years, only 41 were reported to the Ohio state health department and are in that database. That amounts to 199 unreported cases – nearly 83% of the total.

This raises the question as to who is responsible for reporting these cases. Dermatology is unique in that our pathology specimens are not routinely passed through a hospital pathology laboratory. The big difference in reporting is that hospital labs have trained data registrars to report all reportable cancers to state health departments. Therefore, in my case, only patients sent to a hospital-based surgeon for sentinel node biopsies or exceptionally large excisions get reported. When I have spoken about this to my dermatology lab and biopsying physicians, the discussion rapidly turns into a finger pointing game of who is responsible. No one, except perhaps the dermatologist who did the biopsy, has all the data.

Unfortunately, these cases are tedious and time consuming to report. Despite state laws requiring reporting, even with penalties for nonreporters, many small dermatology practices do not report these cases and expect their dermatopathology labs to do so, but the labs expect the biopsying dermatologist to report the cases. This is a classic case of an unfunded mandate since small dermatology practices do not have the time or resources for reporting.

I have worked with the Ohio Department of Health to remove any unnecessary data fields and they have managed to reduce the reporting fields (to 59!). This is the minimum amount required to be included in the National Cancer Institute’s SEER (Surveillance, Epidemiology, and End Results) database. Many of these fields are not applicable to thin melanomas and after reviewing the 1-hour online training course, each patient can be entered (once the necessary data are collected) in about 15 minutes. This is still a formidable task for small offices, which cannot be blamed for ducking and hoping someone else reports.

While there is controversy regarding the relevance of thin melanomas to overall survival, more accurate reporting can only bolster either argument.
 

A solution to underreporting

I believe we have developed a unique solution to this conundrum. Our office is partnering with the local melanoma support group (Melanoma Know More) to train volunteers to help with the data collection and reporting of these thin melanomas. We have also discovered that the local community college has students who are majoring in pathology data registry reporting and are happy to gain a little experience before graduating.

We eventually hope to become a clearinghouse for the entire state of Ohio. The state health department has agreed not to apply punitive measures to physicians who are new reporters. It is our plan to obtain melanoma pathology reports, run these past the state database, identify unreported cases, and obtain further data as needed from the biopsying physicians, and then complete the reporting.

I think dermatologic oncologists in every state should view this as an opportunity for a significant quality improvement project, and as a terrific service to the general dermatology community.

The ramifications of more comprehensive reporting of melanomas are great. I would expect more attention to the disease by researchers, and much more clout with state and national legislators. Think about increased funding for melanoma research, allowing sunscreen use for school children, sunshades for playgrounds, and more responsible tanning bed restrictions.

Now, I must inform you that this is my last column, but I plan to continue writing. Over the past 6 years, I have been able to cover a wide range of topics ranging from human trafficking and the American Medical Association, to the many problems faced by small practices. I have enjoyed myself hugely. To quote Douglas Adams, from The Hitchhiker’s Guide to the Galaxy, “So long and thanks for all the fish!” Keep in touch at [email protected].
 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].

For years, it has been strongly suspected that malignant melanoma is underreported in the United States. I have audited my melanoma cases (biopsies and excisions sent to me) and discovered that of the 240 cases confirmed over the past 5 years, only 41 were reported to the Ohio state health department and are in that database. That amounts to 199 unreported cases – nearly 83% of the total.

This raises the question as to who is responsible for reporting these cases. Dermatology is unique in that our pathology specimens are not routinely passed through a hospital pathology laboratory. The big difference in reporting is that hospital labs have trained data registrars to report all reportable cancers to state health departments. Therefore, in my case, only patients sent to a hospital-based surgeon for sentinel node biopsies or exceptionally large excisions get reported. When I have spoken about this to my dermatology lab and biopsying physicians, the discussion rapidly turns into a finger pointing game of who is responsible. No one, except perhaps the dermatologist who did the biopsy, has all the data.

Unfortunately, these cases are tedious and time consuming to report. Despite state laws requiring reporting, even with penalties for nonreporters, many small dermatology practices do not report these cases and expect their dermatopathology labs to do so, but the labs expect the biopsying dermatologist to report the cases. This is a classic case of an unfunded mandate since small dermatology practices do not have the time or resources for reporting.

I have worked with the Ohio Department of Health to remove any unnecessary data fields and they have managed to reduce the reporting fields (to 59!). This is the minimum amount required to be included in the National Cancer Institute’s SEER (Surveillance, Epidemiology, and End Results) database. Many of these fields are not applicable to thin melanomas and after reviewing the 1-hour online training course, each patient can be entered (once the necessary data are collected) in about 15 minutes. This is still a formidable task for small offices, which cannot be blamed for ducking and hoping someone else reports.

While there is controversy regarding the relevance of thin melanomas to overall survival, more accurate reporting can only bolster either argument.
 

A solution to underreporting

I believe we have developed a unique solution to this conundrum. Our office is partnering with the local melanoma support group (Melanoma Know More) to train volunteers to help with the data collection and reporting of these thin melanomas. We have also discovered that the local community college has students who are majoring in pathology data registry reporting and are happy to gain a little experience before graduating.

We eventually hope to become a clearinghouse for the entire state of Ohio. The state health department has agreed not to apply punitive measures to physicians who are new reporters. It is our plan to obtain melanoma pathology reports, run these past the state database, identify unreported cases, and obtain further data as needed from the biopsying physicians, and then complete the reporting.

I think dermatologic oncologists in every state should view this as an opportunity for a significant quality improvement project, and as a terrific service to the general dermatology community.

The ramifications of more comprehensive reporting of melanomas are great. I would expect more attention to the disease by researchers, and much more clout with state and national legislators. Think about increased funding for melanoma research, allowing sunscreen use for school children, sunshades for playgrounds, and more responsible tanning bed restrictions.

Now, I must inform you that this is my last column, but I plan to continue writing. Over the past 6 years, I have been able to cover a wide range of topics ranging from human trafficking and the American Medical Association, to the many problems faced by small practices. I have enjoyed myself hugely. To quote Douglas Adams, from The Hitchhiker’s Guide to the Galaxy, “So long and thanks for all the fish!” Keep in touch at [email protected].
 

Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].

Deer, COVID, how?

Usually humans cannot get close enough to a deer to really be face-to-face, so it’s easy to question how on Earth deer are contracting COVID-19. Well, stranger things have happened, and honestly, we’ve just stopped questioning most of them.

petemeade/PxHere

Exhibit A comes to us from a Penn State University study: Eighty percent of deer sampled in Iowa in December 2020 and January 2021 – as part of the state’s chronic wasting disease surveillance program – were found to be positive for COVID-19.

A statement from the university said that “white-tailed deer may be a reservoir for the virus to continually circulate and raise concerns about the emergence of new strains that may prove a threat to wildlife and, possibly, to humans.” The investigators also suggested that deer probably caught the virus from humans and then transmitted it to other deer.

If you or someone you know is a hunter or a white-tailed deer, it’s best to proceed with caution. There’s no evidence that COVID-19 has jumped from deer to humans, but hunters should wear masks and gloves while working with deer, worrying not just about the deer’s face, but also … you know, the gastrointestinal parts, Robert Salata, MD, of University Hospitals Cleveland Medical Center, told Syracuse.com. It also shouldn’t be too risky to eat venison, he said, just make sure the meat is cooked thoroughly.

The more you know!
 

The neurological super powers of grandma are real

What is it about grandmothers that makes them seem almost magical at times? They somehow always know how you feel. And they can almost always tell when something is wrong. They also seem to be the biggest ally a child will have against his or her parents.

Mark Edward Atkinson/Tracey Lee

So what makes these super matriarchs? The answer is in the brain.

Apparently there’s a function in the brains of grandmothers geared toward “emotional empathy.” James Rilling, PhD, of Emory University, lead author of a recent study focused on looking at the brain function of grandmothers, suggested that they’re neurologically tapped into feeling how their grandchildren feel: “If their grandchild is smiling, they’re feeling the child’s joy. And if their grandchild is crying, they’re feeling the child’s pain and distress.”

And then there’s the cute factor. Never underestimate a child’s ability to manipulate his or her grandmother’s brain.

So how do the researchers know this? Functional MRI showed more brain activity in the parts of the brain that deal with emotional empathy and movement in the participating grandmas when shown pictures of their grandchildren. Images of their own adult children lit up areas more associated with cognitive empathy. So less emotional and more mental/logical understanding.

Kids, don’t tell Mom about the secret midnight snacks with grandma. She wouldn’t get it.

Then there’s the grandmother hypothesis, which suggests that women tend to live longer to provide some kind of evolutionary benefit to their children and grandchildren. Evidence also exists that children with positive engagement from their grandmothers tend to have better social and academic outcomes, behavior, and physical health.

A lot of credit on how children turn out, of course, goes to parents, but more can be said about grandmas. Don’t let the age and freshly baked cookies fool you. They have neurologic superpowers within.
 

Brain cleanup on aisle 5

You’ve got your local grocery store down. You know the ins and outs; you know where everything is. Last week you did your trip in record time. This week, however, you have to stop at a different store. Same chain, but a different location. You stroll in, confidently walk toward the first aisle for your fruits and veggies, and ... it’s all ice cream. Oops.

Max Pixel

There’s a lot we don’t understand about the brain, including how it remembers familiar environments to avoid confusion. Or why it fails to do so, as with our grocery store example. However, thanks to a study from the University of Arizona, we may have an answer.

For the experiment, a group of participants watched a video tour of three virtual cities. Those cities were very similar, being laid out in basically identical fashion. Stores could be found in the same places, but the identity of those stores varied. Some stores were in all three cities, some were in two, and some were unique. Participants were asked to memorize the layouts, and those who got things more than 80% correct ran through the test again, only this time their brain activity was monitored through MRI.

In general, brain activity was similar for the participants; after all, they were recalling similar environments. However, when asked about stores that appeared in multiple cities, brain activity varied dramatically. This indicated to the researchers that the brain was recalling shared stores as if they were more dissimilar than two completely disparate and unique stores, a concept often known to brain scientists as “repulsion.” It also indicates that the memories regarding shared environments are stored in the prefrontal cortex, not the hippocampus, which typically handles memory.

The researchers plan to apply this information to questions about diseases such as Alzheimer’s, so the next time you get turned around in a weirdly unfamiliar grocery store, just think: “It’s okay, I’m helping to solve a terrible brain disease.”
 

The real endgame: Friction is the winner

Spoiler alert! If you haven’t seen “Avengers: Infinity War” yet, we’re about to ruin it for you.

Georgia Tech

For those still with us, here’s the spoiler: Thanos would not have been able to snap his fingers while wearing the Infinity Gauntlet.

Saad Bhamla, PhD, of Georgia Tech University’s school of chemical and biomolecular engineering, had been studying powerful and ultrafast motions in living organisms along with several colleagues before the movie came out in 2018, and when they saw the finger-snapping scene it got them wondering.

Being scientists of course, they had no choice. They got out their high-speed imaging equipment, automated image processing software, and dynamic force sensors and analyzed finger snaps, paying close attention to friction by covering fingers with “different materials, including metallic thimbles to simulate the effects of trying to snap while wearing a metallic gauntlet, much like Thanos,” according to a statement on Eurekalert.

With finger snaps, it’s all about the rotational velocity. The angular acceleration involved is the fastest ever measured in a human, with a professional baseball pitcher’s throwing arm a distant second.

Dr. Bhamla’s reaction to their work explains why scientists are the ones doing science. “When I first saw the data, I jumped out of my chair,” he said in the written statement.

Rotational velocities dropped dramatically when the friction-reducing thimbles were used, so there was no snap. Which means that billions and billions of fictional lives could have been saved if the filmmakers had just talked to the right scientist.

That scientist, clearly, is Dr. Bhamla, who said that “this is the only scientific project in my lab in which we could snap our fingers and get data.”

Deer, COVID, how?

Usually humans cannot get close enough to a deer to really be face-to-face, so it’s easy to question how on Earth deer are contracting COVID-19. Well, stranger things have happened, and honestly, we’ve just stopped questioning most of them.

petemeade/PxHere

Exhibit A comes to us from a Penn State University study: Eighty percent of deer sampled in Iowa in December 2020 and January 2021 – as part of the state’s chronic wasting disease surveillance program – were found to be positive for COVID-19.

A statement from the university said that “white-tailed deer may be a reservoir for the virus to continually circulate and raise concerns about the emergence of new strains that may prove a threat to wildlife and, possibly, to humans.” The investigators also suggested that deer probably caught the virus from humans and then transmitted it to other deer.

If you or someone you know is a hunter or a white-tailed deer, it’s best to proceed with caution. There’s no evidence that COVID-19 has jumped from deer to humans, but hunters should wear masks and gloves while working with deer, worrying not just about the deer’s face, but also … you know, the gastrointestinal parts, Robert Salata, MD, of University Hospitals Cleveland Medical Center, told Syracuse.com. It also shouldn’t be too risky to eat venison, he said, just make sure the meat is cooked thoroughly.

The more you know!
 

The neurological super powers of grandma are real

What is it about grandmothers that makes them seem almost magical at times? They somehow always know how you feel. And they can almost always tell when something is wrong. They also seem to be the biggest ally a child will have against his or her parents.

Mark Edward Atkinson/Tracey Lee

So what makes these super matriarchs? The answer is in the brain.

Apparently there’s a function in the brains of grandmothers geared toward “emotional empathy.” James Rilling, PhD, of Emory University, lead author of a recent study focused on looking at the brain function of grandmothers, suggested that they’re neurologically tapped into feeling how their grandchildren feel: “If their grandchild is smiling, they’re feeling the child’s joy. And if their grandchild is crying, they’re feeling the child’s pain and distress.”

And then there’s the cute factor. Never underestimate a child’s ability to manipulate his or her grandmother’s brain.

So how do the researchers know this? Functional MRI showed more brain activity in the parts of the brain that deal with emotional empathy and movement in the participating grandmas when shown pictures of their grandchildren. Images of their own adult children lit up areas more associated with cognitive empathy. So less emotional and more mental/logical understanding.

Kids, don’t tell Mom about the secret midnight snacks with grandma. She wouldn’t get it.

Then there’s the grandmother hypothesis, which suggests that women tend to live longer to provide some kind of evolutionary benefit to their children and grandchildren. Evidence also exists that children with positive engagement from their grandmothers tend to have better social and academic outcomes, behavior, and physical health.

A lot of credit on how children turn out, of course, goes to parents, but more can be said about grandmas. Don’t let the age and freshly baked cookies fool you. They have neurologic superpowers within.
 

Brain cleanup on aisle 5

You’ve got your local grocery store down. You know the ins and outs; you know where everything is. Last week you did your trip in record time. This week, however, you have to stop at a different store. Same chain, but a different location. You stroll in, confidently walk toward the first aisle for your fruits and veggies, and ... it’s all ice cream. Oops.

Max Pixel

There’s a lot we don’t understand about the brain, including how it remembers familiar environments to avoid confusion. Or why it fails to do so, as with our grocery store example. However, thanks to a study from the University of Arizona, we may have an answer.

For the experiment, a group of participants watched a video tour of three virtual cities. Those cities were very similar, being laid out in basically identical fashion. Stores could be found in the same places, but the identity of those stores varied. Some stores were in all three cities, some were in two, and some were unique. Participants were asked to memorize the layouts, and those who got things more than 80% correct ran through the test again, only this time their brain activity was monitored through MRI.

In general, brain activity was similar for the participants; after all, they were recalling similar environments. However, when asked about stores that appeared in multiple cities, brain activity varied dramatically. This indicated to the researchers that the brain was recalling shared stores as if they were more dissimilar than two completely disparate and unique stores, a concept often known to brain scientists as “repulsion.” It also indicates that the memories regarding shared environments are stored in the prefrontal cortex, not the hippocampus, which typically handles memory.

The researchers plan to apply this information to questions about diseases such as Alzheimer’s, so the next time you get turned around in a weirdly unfamiliar grocery store, just think: “It’s okay, I’m helping to solve a terrible brain disease.”
 

The real endgame: Friction is the winner

Spoiler alert! If you haven’t seen “Avengers: Infinity War” yet, we’re about to ruin it for you.

Georgia Tech

For those still with us, here’s the spoiler: Thanos would not have been able to snap his fingers while wearing the Infinity Gauntlet.

Saad Bhamla, PhD, of Georgia Tech University’s school of chemical and biomolecular engineering, had been studying powerful and ultrafast motions in living organisms along with several colleagues before the movie came out in 2018, and when they saw the finger-snapping scene it got them wondering.

Being scientists of course, they had no choice. They got out their high-speed imaging equipment, automated image processing software, and dynamic force sensors and analyzed finger snaps, paying close attention to friction by covering fingers with “different materials, including metallic thimbles to simulate the effects of trying to snap while wearing a metallic gauntlet, much like Thanos,” according to a statement on Eurekalert.

With finger snaps, it’s all about the rotational velocity. The angular acceleration involved is the fastest ever measured in a human, with a professional baseball pitcher’s throwing arm a distant second.

Dr. Bhamla’s reaction to their work explains why scientists are the ones doing science. “When I first saw the data, I jumped out of my chair,” he said in the written statement.

Rotational velocities dropped dramatically when the friction-reducing thimbles were used, so there was no snap. Which means that billions and billions of fictional lives could have been saved if the filmmakers had just talked to the right scientist.

That scientist, clearly, is Dr. Bhamla, who said that “this is the only scientific project in my lab in which we could snap our fingers and get data.”

Deer, COVID, how?

Usually humans cannot get close enough to a deer to really be face-to-face, so it’s easy to question how on Earth deer are contracting COVID-19. Well, stranger things have happened, and honestly, we’ve just stopped questioning most of them.

petemeade/PxHere

Exhibit A comes to us from a Penn State University study: Eighty percent of deer sampled in Iowa in December 2020 and January 2021 – as part of the state’s chronic wasting disease surveillance program – were found to be positive for COVID-19.

A statement from the university said that “white-tailed deer may be a reservoir for the virus to continually circulate and raise concerns about the emergence of new strains that may prove a threat to wildlife and, possibly, to humans.” The investigators also suggested that deer probably caught the virus from humans and then transmitted it to other deer.

If you or someone you know is a hunter or a white-tailed deer, it’s best to proceed with caution. There’s no evidence that COVID-19 has jumped from deer to humans, but hunters should wear masks and gloves while working with deer, worrying not just about the deer’s face, but also … you know, the gastrointestinal parts, Robert Salata, MD, of University Hospitals Cleveland Medical Center, told Syracuse.com. It also shouldn’t be too risky to eat venison, he said, just make sure the meat is cooked thoroughly.

The more you know!
 

The neurological super powers of grandma are real

What is it about grandmothers that makes them seem almost magical at times? They somehow always know how you feel. And they can almost always tell when something is wrong. They also seem to be the biggest ally a child will have against his or her parents.

Mark Edward Atkinson/Tracey Lee

So what makes these super matriarchs? The answer is in the brain.

Apparently there’s a function in the brains of grandmothers geared toward “emotional empathy.” James Rilling, PhD, of Emory University, lead author of a recent study focused on looking at the brain function of grandmothers, suggested that they’re neurologically tapped into feeling how their grandchildren feel: “If their grandchild is smiling, they’re feeling the child’s joy. And if their grandchild is crying, they’re feeling the child’s pain and distress.”

And then there’s the cute factor. Never underestimate a child’s ability to manipulate his or her grandmother’s brain.

So how do the researchers know this? Functional MRI showed more brain activity in the parts of the brain that deal with emotional empathy and movement in the participating grandmas when shown pictures of their grandchildren. Images of their own adult children lit up areas more associated with cognitive empathy. So less emotional and more mental/logical understanding.

Kids, don’t tell Mom about the secret midnight snacks with grandma. She wouldn’t get it.

Then there’s the grandmother hypothesis, which suggests that women tend to live longer to provide some kind of evolutionary benefit to their children and grandchildren. Evidence also exists that children with positive engagement from their grandmothers tend to have better social and academic outcomes, behavior, and physical health.

A lot of credit on how children turn out, of course, goes to parents, but more can be said about grandmas. Don’t let the age and freshly baked cookies fool you. They have neurologic superpowers within.
 

Brain cleanup on aisle 5

You’ve got your local grocery store down. You know the ins and outs; you know where everything is. Last week you did your trip in record time. This week, however, you have to stop at a different store. Same chain, but a different location. You stroll in, confidently walk toward the first aisle for your fruits and veggies, and ... it’s all ice cream. Oops.

Max Pixel

There’s a lot we don’t understand about the brain, including how it remembers familiar environments to avoid confusion. Or why it fails to do so, as with our grocery store example. However, thanks to a study from the University of Arizona, we may have an answer.

For the experiment, a group of participants watched a video tour of three virtual cities. Those cities were very similar, being laid out in basically identical fashion. Stores could be found in the same places, but the identity of those stores varied. Some stores were in all three cities, some were in two, and some were unique. Participants were asked to memorize the layouts, and those who got things more than 80% correct ran through the test again, only this time their brain activity was monitored through MRI.

In general, brain activity was similar for the participants; after all, they were recalling similar environments. However, when asked about stores that appeared in multiple cities, brain activity varied dramatically. This indicated to the researchers that the brain was recalling shared stores as if they were more dissimilar than two completely disparate and unique stores, a concept often known to brain scientists as “repulsion.” It also indicates that the memories regarding shared environments are stored in the prefrontal cortex, not the hippocampus, which typically handles memory.

The researchers plan to apply this information to questions about diseases such as Alzheimer’s, so the next time you get turned around in a weirdly unfamiliar grocery store, just think: “It’s okay, I’m helping to solve a terrible brain disease.”
 

The real endgame: Friction is the winner

Spoiler alert! If you haven’t seen “Avengers: Infinity War” yet, we’re about to ruin it for you.

Georgia Tech

For those still with us, here’s the spoiler: Thanos would not have been able to snap his fingers while wearing the Infinity Gauntlet.

Saad Bhamla, PhD, of Georgia Tech University’s school of chemical and biomolecular engineering, had been studying powerful and ultrafast motions in living organisms along with several colleagues before the movie came out in 2018, and when they saw the finger-snapping scene it got them wondering.

Being scientists of course, they had no choice. They got out their high-speed imaging equipment, automated image processing software, and dynamic force sensors and analyzed finger snaps, paying close attention to friction by covering fingers with “different materials, including metallic thimbles to simulate the effects of trying to snap while wearing a metallic gauntlet, much like Thanos,” according to a statement on Eurekalert.

With finger snaps, it’s all about the rotational velocity. The angular acceleration involved is the fastest ever measured in a human, with a professional baseball pitcher’s throwing arm a distant second.

Dr. Bhamla’s reaction to their work explains why scientists are the ones doing science. “When I first saw the data, I jumped out of my chair,” he said in the written statement.

Rotational velocities dropped dramatically when the friction-reducing thimbles were used, so there was no snap. Which means that billions and billions of fictional lives could have been saved if the filmmakers had just talked to the right scientist.

That scientist, clearly, is Dr. Bhamla, who said that “this is the only scientific project in my lab in which we could snap our fingers and get data.”

Medications may cause a variety of cutaneous reactions. The most common type of reaction is an exanthematous (morbilliform or scarlatiniform) drug reaction. Reactions can occur anytime from within the first 2 weeks of treatment up to 10 days after the treatment has been discontinued. If a drug is rechallenged, eruptions may occur sooner. Pruritus is commonly seen. Clinically, erythematous papules and macules present symmetrically on the trunk and upper extremities and then become more generalized. A low-grade fever may be present.

Courtesy Dr. Donna Bilu Martin

Antibiotics are the most common causes of exanthematous drug eruptions. Penicillins and trimethoprim-sulfamethoxazole are common offenders. Cephalosporins, anticonvulsants, and allopurinol may also induce a reaction. As this condition is diagnosed clinically, skin biopsy is often not necessary. Histology is nonspecific and shows a mild perivascular lymphocytic infiltrate and few epidermal necrotic keratinocytes.

In drug reaction with eosinophilia and systemic symptoms (DRESS), symptoms present 2-6 weeks after the offending medication has been started. The cutaneous rash appears similar to an exanthematous drug eruption; however, lesions will also present on the face, and facial edema may occur. Fever is often present. Laboratory findings include a marked peripheral blood hypereosinophilia. Elevated liver function tests may be seen. Viruses such as Epstein-Barr virus, enteroviruses, adenovirus, early HIV, human herpesvirus 6, and parvovirus B19 have a similar clinical appearance to an exanthematous drug eruption. A mild eosinophilia, as seen in a drug eruption, helps to distinguish between a drug eruption and viral exanthem. In Stevens-Johnson Syndrome, mucosal membranes are involved and skin is often painful or appears dusky.

Treatment of exanthematous drug eruptions is largely supportive. Discontinuing the drug will help speed resolution and topical steroids may alleviate pruritus.

This case and photo were submitted by Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

1. Bolognia J et al. “Dermatology” (St. Louis: Mosby/Elsevier, 2008).

2. James W et al. “Andrews’ Diseases of the Skin,” 13th ed. (Philadelphia: Saunders Elsevier, 2006).

Medications may cause a variety of cutaneous reactions. The most common type of reaction is an exanthematous (morbilliform or scarlatiniform) drug reaction. Reactions can occur anytime from within the first 2 weeks of treatment up to 10 days after the treatment has been discontinued. If a drug is rechallenged, eruptions may occur sooner. Pruritus is commonly seen. Clinically, erythematous papules and macules present symmetrically on the trunk and upper extremities and then become more generalized. A low-grade fever may be present.

Courtesy Dr. Donna Bilu Martin

Antibiotics are the most common causes of exanthematous drug eruptions. Penicillins and trimethoprim-sulfamethoxazole are common offenders. Cephalosporins, anticonvulsants, and allopurinol may also induce a reaction. As this condition is diagnosed clinically, skin biopsy is often not necessary. Histology is nonspecific and shows a mild perivascular lymphocytic infiltrate and few epidermal necrotic keratinocytes.

In drug reaction with eosinophilia and systemic symptoms (DRESS), symptoms present 2-6 weeks after the offending medication has been started. The cutaneous rash appears similar to an exanthematous drug eruption; however, lesions will also present on the face, and facial edema may occur. Fever is often present. Laboratory findings include a marked peripheral blood hypereosinophilia. Elevated liver function tests may be seen. Viruses such as Epstein-Barr virus, enteroviruses, adenovirus, early HIV, human herpesvirus 6, and parvovirus B19 have a similar clinical appearance to an exanthematous drug eruption. A mild eosinophilia, as seen in a drug eruption, helps to distinguish between a drug eruption and viral exanthem. In Stevens-Johnson Syndrome, mucosal membranes are involved and skin is often painful or appears dusky.

Treatment of exanthematous drug eruptions is largely supportive. Discontinuing the drug will help speed resolution and topical steroids may alleviate pruritus.

This case and photo were submitted by Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

1. Bolognia J et al. “Dermatology” (St. Louis: Mosby/Elsevier, 2008).

2. James W et al. “Andrews’ Diseases of the Skin,” 13th ed. (Philadelphia: Saunders Elsevier, 2006).

Medications may cause a variety of cutaneous reactions. The most common type of reaction is an exanthematous (morbilliform or scarlatiniform) drug reaction. Reactions can occur anytime from within the first 2 weeks of treatment up to 10 days after the treatment has been discontinued. If a drug is rechallenged, eruptions may occur sooner. Pruritus is commonly seen. Clinically, erythematous papules and macules present symmetrically on the trunk and upper extremities and then become more generalized. A low-grade fever may be present.

Courtesy Dr. Donna Bilu Martin

Antibiotics are the most common causes of exanthematous drug eruptions. Penicillins and trimethoprim-sulfamethoxazole are common offenders. Cephalosporins, anticonvulsants, and allopurinol may also induce a reaction. As this condition is diagnosed clinically, skin biopsy is often not necessary. Histology is nonspecific and shows a mild perivascular lymphocytic infiltrate and few epidermal necrotic keratinocytes.

In drug reaction with eosinophilia and systemic symptoms (DRESS), symptoms present 2-6 weeks after the offending medication has been started. The cutaneous rash appears similar to an exanthematous drug eruption; however, lesions will also present on the face, and facial edema may occur. Fever is often present. Laboratory findings include a marked peripheral blood hypereosinophilia. Elevated liver function tests may be seen. Viruses such as Epstein-Barr virus, enteroviruses, adenovirus, early HIV, human herpesvirus 6, and parvovirus B19 have a similar clinical appearance to an exanthematous drug eruption. A mild eosinophilia, as seen in a drug eruption, helps to distinguish between a drug eruption and viral exanthem. In Stevens-Johnson Syndrome, mucosal membranes are involved and skin is often painful or appears dusky.

Treatment of exanthematous drug eruptions is largely supportive. Discontinuing the drug will help speed resolution and topical steroids may alleviate pruritus.

This case and photo were submitted by Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

References

1. Bolognia J et al. “Dermatology” (St. Louis: Mosby/Elsevier, 2008).

2. James W et al. “Andrews’ Diseases of the Skin,” 13th ed. (Philadelphia: Saunders Elsevier, 2006).

Read More

Read More

Read More

“When 900-years-old you reach, look as good you will not.” –Yoda

I’ve been on a roll lately: 100, 94, 90, 97, 94. These aren’t grades or even what I scratched on my scorecard for 18 holes (that’s more like 112), but rather patients I’ve seen.

Our oldest-old have been in COVID-19 protection for the last couple of years and only now feel safe to come out again. Many have skin cancers. Some of them have many. I’m grateful that for all their health problems, basal cell carcinomas at least I can cure. And while I treat them, I get the benefit of hearing directly from our elders. I love asking them for general life advice. Here are a few things I learned.

From a 94-year-old woman who was just discharged from the hospital for sepsis: First, sepsis can sneak up from behind and jump you when you’re 94. She was sitting in a waiting room for a routine exam when she passed out and woke up in the ICU. She made it home and is back on her feet, literally. When I asked her how she made it though, she was very matter of fact. Trust that the doctors know what’s right. Trust that someone will tell you what to do next. Trust that you know your own body and what you can and cannot do. Ask for help, then simply trust it will all work out. It usually does.

From a 97-year-old fighter pilot who fought in the Korean War: Let regrets drop away and live to fight another day. He’s had multiple marriages, built and lost companies, been fired and fired at, and made some doozy mistakes, some that caused considerable pain and collateral damage. But each day is new and requires your best. He has lived long enough to love dozens of grandkids and give away more than what most people ever make. His bottom line, if you worry and fret and regret, you’ll make even more mistakes ahead. Look ahead, the ground never comes up from behind you.

From a 94-year-old whose son was killed in a car accident nearly 60 years ago: You can be both happy and sad. When she retold the story of how the police knocked on her door with the news that her son was dead, she started to cry. Even 60 years isn’t long enough to blunt such pain. She still thinks of him often and to this day sometimes finds it difficult to believe he’s gone. Such pain never leaves you. But she is still a happy person with countless joys and is still having such fun. If you live long enough, both will likely be true.

From a 90-year old who still played tennis: “Just one and one.” That is, one beer and one shot, every day. No more. No less. I daren’t say I recommend this one; however, it might also be the social aspect of drinking that matters. He also advised to be free with friendships. You’ll have many people come in and out of your life; be open to new ones all the time. Also sometimes let your friends win.

From a 100-year-old, I asked how he managed to get through the Great Depression, WWII, civil unrest of the 1950s, and the Vietnam War. His reply? “To be honest, I’ve never seen anything quite like this before.”

When there’s time, consider asking for advice from those elders who happen to have an appointment with you. Bring you wisdom, they will.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

“When 900-years-old you reach, look as good you will not.” –Yoda

I’ve been on a roll lately: 100, 94, 90, 97, 94. These aren’t grades or even what I scratched on my scorecard for 18 holes (that’s more like 112), but rather patients I’ve seen.

Our oldest-old have been in COVID-19 protection for the last couple of years and only now feel safe to come out again. Many have skin cancers. Some of them have many. I’m grateful that for all their health problems, basal cell carcinomas at least I can cure. And while I treat them, I get the benefit of hearing directly from our elders. I love asking them for general life advice. Here are a few things I learned.

From a 94-year-old woman who was just discharged from the hospital for sepsis: First, sepsis can sneak up from behind and jump you when you’re 94. She was sitting in a waiting room for a routine exam when she passed out and woke up in the ICU. She made it home and is back on her feet, literally. When I asked her how she made it though, she was very matter of fact. Trust that the doctors know what’s right. Trust that someone will tell you what to do next. Trust that you know your own body and what you can and cannot do. Ask for help, then simply trust it will all work out. It usually does.

From a 97-year-old fighter pilot who fought in the Korean War: Let regrets drop away and live to fight another day. He’s had multiple marriages, built and lost companies, been fired and fired at, and made some doozy mistakes, some that caused considerable pain and collateral damage. But each day is new and requires your best. He has lived long enough to love dozens of grandkids and give away more than what most people ever make. His bottom line, if you worry and fret and regret, you’ll make even more mistakes ahead. Look ahead, the ground never comes up from behind you.

From a 94-year-old whose son was killed in a car accident nearly 60 years ago: You can be both happy and sad. When she retold the story of how the police knocked on her door with the news that her son was dead, she started to cry. Even 60 years isn’t long enough to blunt such pain. She still thinks of him often and to this day sometimes finds it difficult to believe he’s gone. Such pain never leaves you. But she is still a happy person with countless joys and is still having such fun. If you live long enough, both will likely be true.

From a 90-year old who still played tennis: “Just one and one.” That is, one beer and one shot, every day. No more. No less. I daren’t say I recommend this one; however, it might also be the social aspect of drinking that matters. He also advised to be free with friendships. You’ll have many people come in and out of your life; be open to new ones all the time. Also sometimes let your friends win.

From a 100-year-old, I asked how he managed to get through the Great Depression, WWII, civil unrest of the 1950s, and the Vietnam War. His reply? “To be honest, I’ve never seen anything quite like this before.”

When there’s time, consider asking for advice from those elders who happen to have an appointment with you. Bring you wisdom, they will.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

“When 900-years-old you reach, look as good you will not.” –Yoda

I’ve been on a roll lately: 100, 94, 90, 97, 94. These aren’t grades or even what I scratched on my scorecard for 18 holes (that’s more like 112), but rather patients I’ve seen.

Our oldest-old have been in COVID-19 protection for the last couple of years and only now feel safe to come out again. Many have skin cancers. Some of them have many. I’m grateful that for all their health problems, basal cell carcinomas at least I can cure. And while I treat them, I get the benefit of hearing directly from our elders. I love asking them for general life advice. Here are a few things I learned.

From a 94-year-old woman who was just discharged from the hospital for sepsis: First, sepsis can sneak up from behind and jump you when you’re 94. She was sitting in a waiting room for a routine exam when she passed out and woke up in the ICU. She made it home and is back on her feet, literally. When I asked her how she made it though, she was very matter of fact. Trust that the doctors know what’s right. Trust that someone will tell you what to do next. Trust that you know your own body and what you can and cannot do. Ask for help, then simply trust it will all work out. It usually does.

From a 97-year-old fighter pilot who fought in the Korean War: Let regrets drop away and live to fight another day. He’s had multiple marriages, built and lost companies, been fired and fired at, and made some doozy mistakes, some that caused considerable pain and collateral damage. But each day is new and requires your best. He has lived long enough to love dozens of grandkids and give away more than what most people ever make. His bottom line, if you worry and fret and regret, you’ll make even more mistakes ahead. Look ahead, the ground never comes up from behind you.

From a 94-year-old whose son was killed in a car accident nearly 60 years ago: You can be both happy and sad. When she retold the story of how the police knocked on her door with the news that her son was dead, she started to cry. Even 60 years isn’t long enough to blunt such pain. She still thinks of him often and to this day sometimes finds it difficult to believe he’s gone. Such pain never leaves you. But she is still a happy person with countless joys and is still having such fun. If you live long enough, both will likely be true.

From a 90-year old who still played tennis: “Just one and one.” That is, one beer and one shot, every day. No more. No less. I daren’t say I recommend this one; however, it might also be the social aspect of drinking that matters. He also advised to be free with friendships. You’ll have many people come in and out of your life; be open to new ones all the time. Also sometimes let your friends win.

From a 100-year-old, I asked how he managed to get through the Great Depression, WWII, civil unrest of the 1950s, and the Vietnam War. His reply? “To be honest, I’ve never seen anything quite like this before.”

When there’s time, consider asking for advice from those elders who happen to have an appointment with you. Bring you wisdom, they will.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

Adding a single cycle of rituximab to belimumab (Benlysta) did not improve disease control for patients with systemic lupus erythematosus (SLE) in comparison with belimumab alone in a phase 3, randomized, controlled trial.

Among patients with SLE who were randomly assigned to receive belimumab with either rituximab, placebo, or standard care, there were no statistically significant differences between the rituximab and placebo arms for the primary endpoint of the proportion of patients with disease control at week 52 or in the secondary endpoints of clinical remission at week 64 or disease control at week 104, Cynthia Aranow, MD, reported in a late-breaking poster session presented during the virtual annual meeting of the American College of Rheumatology.

“Using a new, clinically meaningful endpoint underscores the efficacy of belimumab for disease control, with some patients maintaining disease control with considerable reductions in steroids, and no immunosuppressants,” said Dr. Aranow, a rheumatologist specializing in SLE and RA in New York and director of the Clinical Autoimmunity Center of Excellence at Feinstein Institutes for Medical Research, Manhasset, N.Y.

Use of the combination of belimumab and rituximab was, however, associated with significant improvement over belimumab and placebo in several secondary efficacy endpoints.

Investigators in the randomized, controlled trial, dubbed BLISS-BELIEVE, had previously published a rationale for sequential therapy with belimumab, a human monoclonal antibody that binds to soluble B-lymphocyte stimulator, and rituximab, a B-cell–depleting anti-CD20 monoclonal antibody.

“These biologics, which operate through complementary mechanisms, might result in an enhanced depletion of circulating and tissue-resident autoreactive B lymphocytes when administered together. Thus, belimumab and rituximab combination may be a highly effective treatment of SLE,” they wrote in an article published in 2019 in BMJ Open.
 

Three-arm trial

The investigators screened 396 patients, of whom 292 were randomly assigned in a 1:2:1 ratio to receive either subcutaneous belimumab 200 mg/wk plus intravenous placebo at weeks 4 and 6 (BEL/PBO, 72 patients), belimumab plus IV rituximab 1,000 mg at weeks 4 and 6 (BEL/RTX, 144 patients), or open-label belimumab plus standard therapy. Patients were allowed to continue taking antimalarial and nonsteroidal anti-inflammatory drugs throughout the study.

The primary disease-control endpoint was defined as a Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) score of 2 or less, achieved without other immunosuppression, equivalent to that achieved with prednisone 5 mg/day or less.

As noted before, there were no significant differences between the BEL/RTX and BEL/PBO arms in either disease control at week 52 or in the secondary endpoints of clinical remission at week 64 (SLEDAI-2K score, 0) or in the proportion of patients with disease control at week 104.

However, use of BEL/RTX was associated with a significantly longer duration of disease control through 52 weeks than was BEL/PBO (mean, 105.4 days vs. 60.1 days; P = .0188) and with a large SLEDAI-2K mean change from baseline at week 104 (–7.2 vs 5.1; P = .0033).

In addition, there was a trend toward a shift in proteinuria from baseline high (>0.5 g/24 h) to normal in the BEL/RTX group at week 52 and a significantly greater shift at week 104 (P = .0085).

The overall adverse event profiles were generally consistent with those of the individual agents, although serious infections and infestations occurred more frequently with BEL/RTX than BEL/PBO.
 

Further analyses planned to look for subgroups that benefit

In a poster discussion session, Akshat Khanna, PhD, of Newtown, Pa., a consultant with Effimed Life Sciences Research, asked Dr. Aranow about the rationale for giving rituximab and belimumab concurrently and noted that, in the BEAT-LUPUS and CALIBRATE trials, anti-CD20 agents were given first, followed by belimumab, to prevent activation of humoral immunity.

“The two B-cell agents were given sequentially. Belimumab was given first to maximize the effect of peripheral B-cell depletion and [was] then continued after rituximab to suppress the elevation [of B-lymphocyte stimulator] that occurs after rituximab monotherapy. We used this approach (instead of that used in CALIBRATE and BEAT LUPUS), as we thought this might be more efficacious,” she explained.

When asked whether there were subgroups of patients who might still benefit from the combination, compared with belimumab alone, Dr. Aranow replied: “There may be individual patients in which it might be considered. Further analyses of the data are ongoing/planned.”

The study was supported by GlaxoSmithKline. Dr. Aranow has received grant/research support from GlaxoSmithKline and has consulted for Bristol-Myers Squibb. Dr. Khanna has disclosed no relevant financial relationships.

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

Adding a single cycle of rituximab to belimumab (Benlysta) did not improve disease control for patients with systemic lupus erythematosus (SLE) in comparison with belimumab alone in a phase 3, randomized, controlled trial.

Among patients with SLE who were randomly assigned to receive belimumab with either rituximab, placebo, or standard care, there were no statistically significant differences between the rituximab and placebo arms for the primary endpoint of the proportion of patients with disease control at week 52 or in the secondary endpoints of clinical remission at week 64 or disease control at week 104, Cynthia Aranow, MD, reported in a late-breaking poster session presented during the virtual annual meeting of the American College of Rheumatology.

“Using a new, clinically meaningful endpoint underscores the efficacy of belimumab for disease control, with some patients maintaining disease control with considerable reductions in steroids, and no immunosuppressants,” said Dr. Aranow, a rheumatologist specializing in SLE and RA in New York and director of the Clinical Autoimmunity Center of Excellence at Feinstein Institutes for Medical Research, Manhasset, N.Y.

Use of the combination of belimumab and rituximab was, however, associated with significant improvement over belimumab and placebo in several secondary efficacy endpoints.

Investigators in the randomized, controlled trial, dubbed BLISS-BELIEVE, had previously published a rationale for sequential therapy with belimumab, a human monoclonal antibody that binds to soluble B-lymphocyte stimulator, and rituximab, a B-cell–depleting anti-CD20 monoclonal antibody.

“These biologics, which operate through complementary mechanisms, might result in an enhanced depletion of circulating and tissue-resident autoreactive B lymphocytes when administered together. Thus, belimumab and rituximab combination may be a highly effective treatment of SLE,” they wrote in an article published in 2019 in BMJ Open.
 

Three-arm trial

The investigators screened 396 patients, of whom 292 were randomly assigned in a 1:2:1 ratio to receive either subcutaneous belimumab 200 mg/wk plus intravenous placebo at weeks 4 and 6 (BEL/PBO, 72 patients), belimumab plus IV rituximab 1,000 mg at weeks 4 and 6 (BEL/RTX, 144 patients), or open-label belimumab plus standard therapy. Patients were allowed to continue taking antimalarial and nonsteroidal anti-inflammatory drugs throughout the study.

The primary disease-control endpoint was defined as a Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) score of 2 or less, achieved without other immunosuppression, equivalent to that achieved with prednisone 5 mg/day or less.

As noted before, there were no significant differences between the BEL/RTX and BEL/PBO arms in either disease control at week 52 or in the secondary endpoints of clinical remission at week 64 (SLEDAI-2K score, 0) or in the proportion of patients with disease control at week 104.

However, use of BEL/RTX was associated with a significantly longer duration of disease control through 52 weeks than was BEL/PBO (mean, 105.4 days vs. 60.1 days; P = .0188) and with a large SLEDAI-2K mean change from baseline at week 104 (–7.2 vs 5.1; P = .0033).

In addition, there was a trend toward a shift in proteinuria from baseline high (>0.5 g/24 h) to normal in the BEL/RTX group at week 52 and a significantly greater shift at week 104 (P = .0085).

The overall adverse event profiles were generally consistent with those of the individual agents, although serious infections and infestations occurred more frequently with BEL/RTX than BEL/PBO.
 

Further analyses planned to look for subgroups that benefit

In a poster discussion session, Akshat Khanna, PhD, of Newtown, Pa., a consultant with Effimed Life Sciences Research, asked Dr. Aranow about the rationale for giving rituximab and belimumab concurrently and noted that, in the BEAT-LUPUS and CALIBRATE trials, anti-CD20 agents were given first, followed by belimumab, to prevent activation of humoral immunity.

“The two B-cell agents were given sequentially. Belimumab was given first to maximize the effect of peripheral B-cell depletion and [was] then continued after rituximab to suppress the elevation [of B-lymphocyte stimulator] that occurs after rituximab monotherapy. We used this approach (instead of that used in CALIBRATE and BEAT LUPUS), as we thought this might be more efficacious,” she explained.

When asked whether there were subgroups of patients who might still benefit from the combination, compared with belimumab alone, Dr. Aranow replied: “There may be individual patients in which it might be considered. Further analyses of the data are ongoing/planned.”

The study was supported by GlaxoSmithKline. Dr. Aranow has received grant/research support from GlaxoSmithKline and has consulted for Bristol-Myers Squibb. Dr. Khanna has disclosed no relevant financial relationships.

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

Adding a single cycle of rituximab to belimumab (Benlysta) did not improve disease control for patients with systemic lupus erythematosus (SLE) in comparison with belimumab alone in a phase 3, randomized, controlled trial.

Among patients with SLE who were randomly assigned to receive belimumab with either rituximab, placebo, or standard care, there were no statistically significant differences between the rituximab and placebo arms for the primary endpoint of the proportion of patients with disease control at week 52 or in the secondary endpoints of clinical remission at week 64 or disease control at week 104, Cynthia Aranow, MD, reported in a late-breaking poster session presented during the virtual annual meeting of the American College of Rheumatology.

“Using a new, clinically meaningful endpoint underscores the efficacy of belimumab for disease control, with some patients maintaining disease control with considerable reductions in steroids, and no immunosuppressants,” said Dr. Aranow, a rheumatologist specializing in SLE and RA in New York and director of the Clinical Autoimmunity Center of Excellence at Feinstein Institutes for Medical Research, Manhasset, N.Y.

Use of the combination of belimumab and rituximab was, however, associated with significant improvement over belimumab and placebo in several secondary efficacy endpoints.

Investigators in the randomized, controlled trial, dubbed BLISS-BELIEVE, had previously published a rationale for sequential therapy with belimumab, a human monoclonal antibody that binds to soluble B-lymphocyte stimulator, and rituximab, a B-cell–depleting anti-CD20 monoclonal antibody.

“These biologics, which operate through complementary mechanisms, might result in an enhanced depletion of circulating and tissue-resident autoreactive B lymphocytes when administered together. Thus, belimumab and rituximab combination may be a highly effective treatment of SLE,” they wrote in an article published in 2019 in BMJ Open.
 

Three-arm trial

The investigators screened 396 patients, of whom 292 were randomly assigned in a 1:2:1 ratio to receive either subcutaneous belimumab 200 mg/wk plus intravenous placebo at weeks 4 and 6 (BEL/PBO, 72 patients), belimumab plus IV rituximab 1,000 mg at weeks 4 and 6 (BEL/RTX, 144 patients), or open-label belimumab plus standard therapy. Patients were allowed to continue taking antimalarial and nonsteroidal anti-inflammatory drugs throughout the study.

The primary disease-control endpoint was defined as a Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) score of 2 or less, achieved without other immunosuppression, equivalent to that achieved with prednisone 5 mg/day or less.

As noted before, there were no significant differences between the BEL/RTX and BEL/PBO arms in either disease control at week 52 or in the secondary endpoints of clinical remission at week 64 (SLEDAI-2K score, 0) or in the proportion of patients with disease control at week 104.

However, use of BEL/RTX was associated with a significantly longer duration of disease control through 52 weeks than was BEL/PBO (mean, 105.4 days vs. 60.1 days; P = .0188) and with a large SLEDAI-2K mean change from baseline at week 104 (–7.2 vs 5.1; P = .0033).

In addition, there was a trend toward a shift in proteinuria from baseline high (>0.5 g/24 h) to normal in the BEL/RTX group at week 52 and a significantly greater shift at week 104 (P = .0085).

The overall adverse event profiles were generally consistent with those of the individual agents, although serious infections and infestations occurred more frequently with BEL/RTX than BEL/PBO.
 

Further analyses planned to look for subgroups that benefit

In a poster discussion session, Akshat Khanna, PhD, of Newtown, Pa., a consultant with Effimed Life Sciences Research, asked Dr. Aranow about the rationale for giving rituximab and belimumab concurrently and noted that, in the BEAT-LUPUS and CALIBRATE trials, anti-CD20 agents were given first, followed by belimumab, to prevent activation of humoral immunity.

“The two B-cell agents were given sequentially. Belimumab was given first to maximize the effect of peripheral B-cell depletion and [was] then continued after rituximab to suppress the elevation [of B-lymphocyte stimulator] that occurs after rituximab monotherapy. We used this approach (instead of that used in CALIBRATE and BEAT LUPUS), as we thought this might be more efficacious,” she explained.

When asked whether there were subgroups of patients who might still benefit from the combination, compared with belimumab alone, Dr. Aranow replied: “There may be individual patients in which it might be considered. Further analyses of the data are ongoing/planned.”

The study was supported by GlaxoSmithKline. Dr. Aranow has received grant/research support from GlaxoSmithKline and has consulted for Bristol-Myers Squibb. Dr. Khanna has disclosed no relevant financial relationships.

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