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Damian McNamara is a journalist for Medscape Medical News and MDedge. He worked full-time for MDedge as the Miami Bureau covering a dozen medical specialties during 2001-2012, then as a freelancer for Medscape and MDedge, before being hired on staff by Medscape in 2018. Now the two companies are one. He uses what he learned in school – Damian has a BS in chemistry and an MS in science, health and environmental reporting/journalism. He works out of a home office in Miami, with a 100-pound chocolate lab known to snore under his desk during work hours.
Metabolic Syndrome Tied to Poor SFA Intervention Outcomes
NAPLES, FLA. – Presence of metabolic syndrome is a risk factor for poor outcomes during superficial femoral artery interventions, according to a retrospective database study.
Although approximately half of patients with peripheral artery disease also have metabolic syndrome, its impact on peripheral interventions is not unknown, Dr. Christopher J. Smolock said at the annual meeting of the Southern Association for Vascular Surgery.
To find out more, Dr. Smolock and his associates reviewed a database of 870 patients who underwent endovascular treatment for symptomatic superficial femoral artery (SFA) disease. In this study, 46% of patients met criteria for metabolic syndrome, the average age was 67 years, and 64% were men.
A total 1,006 limbs of these patients were treated between 1999 and 2009 at the DeBakey Heart and Vascular Center at the Methodist Hospital in Houston. The researchers compared patient factors at presentation and outcomes between patients without metabolic syndrome (542 treated limbs) and patients with the syndrome (464 treated limbs).
Limbs in the metabolic syndrome group were significantly more likely to come from women (44% vs. 31%), to come from patients with critical ischemia symptoms of pain at rest and tissue loss (54% vs. 38%), and to feature more advanced SFA lesions (51% vs. 31%), compared with limbs in the group without metabolic syndrome.
Claudication was a presentation for 46% of the limbs in the group with metabolic syndrome versus 62% of limbs in the non–metabolic syndrome group.
The investigators compared 30-day mortality and morbidity between these groups. In addition, they assessed the 5-year rates for primary and secondary patency; freedom from recurrent symptoms; and limb salvage. "We wanted to look at metabolic syndrome’s effect on these outcomes," said Dr. Smolock of the DeBakey Heart and Vascular Center.
"This addresses the important topic of outcomes with SFA interventions in those with metabolic syndrome," said study discussant Dr. Scott L. Stevens. "Of note, mortality was not increased among those with metabolic syndrome." Dr. Stevens is a vascular surgeon at the University of Tennessee Medical Center in Knoxville.
There was no significant difference in 30-day mortality: 0.2% in the metabolic syndrome group and the 1.3% in the nonsyndrome group.
A lower percentage of the metabolic syndrome group, 67% vs. 73%, experienced freedom from recurrent symptoms over 5 years.
"Primary patency decreased as well significantly over 5 years in those with metabolic syndrome," Dr. Smolock said. The study revealed 56% of the metabolic syndrome group had 5-year primary patency, compared with 66% in unaffected group; 71% vs. 78% had assisted primary patency; and 71% vs. 78% had secondary patency. Secondary patency decreased also, but there was no significant difference between groups, he added.
Because critical ischemia more often affected the group with metabolic syndrome, the rate of limb amputation was higher in this group (22% versus 13% of the unaffected group at 5 years).
Dr. Stevens asked why the metabolic group experienced significantly higher morbidity but not mortality, compared with the unaffected group. This might be because the mortality figures were calculated for only the first 30 days and not over the 5 years, Dr. Smolock said. In addition, the low 30-day mortality "could speak to this being a local procedure, not [one] done under general anesthesia." He added, "I hope some of that has to do with our risk-reduction strategies preoperatively."
"What changes have you made in your practice to reduce risk factors in those patients with metabolic syndrome?" Dr. Stevens asked.
"Our beta blocker, statin, and aspirin use were not at levels we wanted," Dr. Smolock replied. So use of these agents is now prescribed for all patients without a contraindication, he said.
Dr. Stevens also asked if metabolic syndrome might just be a surrogate for patients with smaller arteries and/or more plaque. "I don’t think this is because of small or poor targets," Dr. Smolock said. "The SVS [Society for Vascular Surgery] runoff score was equal between the groups. Diabetes is a risk in and of itself for small or poor targets, but it’s not something we could see anatomically."
Metabolic syndrome was defined in this study using the National Heart, Lung and Blood Institute/American Heart Association criteria. Therefore, patients had to have three or more of the following: systolic blood pressure of 130 mm Hg or greater/diastolic blood pressure of 85 mm Hg or greater; triglycerides of 150 mg/dL or greater; HDL cholesterol of 50 mg/dL or lower for women or 40 mg/dL or lower for men; fasting blood glucose of 110 mg/dL or greater; or body mass index of 30 kg/m2 or greater.
Dr. Smolock said that he had no relevant disclosures.
NAPLES, FLA. – Presence of metabolic syndrome is a risk factor for poor outcomes during superficial femoral artery interventions, according to a retrospective database study.
Although approximately half of patients with peripheral artery disease also have metabolic syndrome, its impact on peripheral interventions is not unknown, Dr. Christopher J. Smolock said at the annual meeting of the Southern Association for Vascular Surgery.
To find out more, Dr. Smolock and his associates reviewed a database of 870 patients who underwent endovascular treatment for symptomatic superficial femoral artery (SFA) disease. In this study, 46% of patients met criteria for metabolic syndrome, the average age was 67 years, and 64% were men.
A total 1,006 limbs of these patients were treated between 1999 and 2009 at the DeBakey Heart and Vascular Center at the Methodist Hospital in Houston. The researchers compared patient factors at presentation and outcomes between patients without metabolic syndrome (542 treated limbs) and patients with the syndrome (464 treated limbs).
Limbs in the metabolic syndrome group were significantly more likely to come from women (44% vs. 31%), to come from patients with critical ischemia symptoms of pain at rest and tissue loss (54% vs. 38%), and to feature more advanced SFA lesions (51% vs. 31%), compared with limbs in the group without metabolic syndrome.
Claudication was a presentation for 46% of the limbs in the group with metabolic syndrome versus 62% of limbs in the non–metabolic syndrome group.
The investigators compared 30-day mortality and morbidity between these groups. In addition, they assessed the 5-year rates for primary and secondary patency; freedom from recurrent symptoms; and limb salvage. "We wanted to look at metabolic syndrome’s effect on these outcomes," said Dr. Smolock of the DeBakey Heart and Vascular Center.
"This addresses the important topic of outcomes with SFA interventions in those with metabolic syndrome," said study discussant Dr. Scott L. Stevens. "Of note, mortality was not increased among those with metabolic syndrome." Dr. Stevens is a vascular surgeon at the University of Tennessee Medical Center in Knoxville.
There was no significant difference in 30-day mortality: 0.2% in the metabolic syndrome group and the 1.3% in the nonsyndrome group.
A lower percentage of the metabolic syndrome group, 67% vs. 73%, experienced freedom from recurrent symptoms over 5 years.
"Primary patency decreased as well significantly over 5 years in those with metabolic syndrome," Dr. Smolock said. The study revealed 56% of the metabolic syndrome group had 5-year primary patency, compared with 66% in unaffected group; 71% vs. 78% had assisted primary patency; and 71% vs. 78% had secondary patency. Secondary patency decreased also, but there was no significant difference between groups, he added.
Because critical ischemia more often affected the group with metabolic syndrome, the rate of limb amputation was higher in this group (22% versus 13% of the unaffected group at 5 years).
Dr. Stevens asked why the metabolic group experienced significantly higher morbidity but not mortality, compared with the unaffected group. This might be because the mortality figures were calculated for only the first 30 days and not over the 5 years, Dr. Smolock said. In addition, the low 30-day mortality "could speak to this being a local procedure, not [one] done under general anesthesia." He added, "I hope some of that has to do with our risk-reduction strategies preoperatively."
"What changes have you made in your practice to reduce risk factors in those patients with metabolic syndrome?" Dr. Stevens asked.
"Our beta blocker, statin, and aspirin use were not at levels we wanted," Dr. Smolock replied. So use of these agents is now prescribed for all patients without a contraindication, he said.
Dr. Stevens also asked if metabolic syndrome might just be a surrogate for patients with smaller arteries and/or more plaque. "I don’t think this is because of small or poor targets," Dr. Smolock said. "The SVS [Society for Vascular Surgery] runoff score was equal between the groups. Diabetes is a risk in and of itself for small or poor targets, but it’s not something we could see anatomically."
Metabolic syndrome was defined in this study using the National Heart, Lung and Blood Institute/American Heart Association criteria. Therefore, patients had to have three or more of the following: systolic blood pressure of 130 mm Hg or greater/diastolic blood pressure of 85 mm Hg or greater; triglycerides of 150 mg/dL or greater; HDL cholesterol of 50 mg/dL or lower for women or 40 mg/dL or lower for men; fasting blood glucose of 110 mg/dL or greater; or body mass index of 30 kg/m2 or greater.
Dr. Smolock said that he had no relevant disclosures.
NAPLES, FLA. – Presence of metabolic syndrome is a risk factor for poor outcomes during superficial femoral artery interventions, according to a retrospective database study.
Although approximately half of patients with peripheral artery disease also have metabolic syndrome, its impact on peripheral interventions is not unknown, Dr. Christopher J. Smolock said at the annual meeting of the Southern Association for Vascular Surgery.
To find out more, Dr. Smolock and his associates reviewed a database of 870 patients who underwent endovascular treatment for symptomatic superficial femoral artery (SFA) disease. In this study, 46% of patients met criteria for metabolic syndrome, the average age was 67 years, and 64% were men.
A total 1,006 limbs of these patients were treated between 1999 and 2009 at the DeBakey Heart and Vascular Center at the Methodist Hospital in Houston. The researchers compared patient factors at presentation and outcomes between patients without metabolic syndrome (542 treated limbs) and patients with the syndrome (464 treated limbs).
Limbs in the metabolic syndrome group were significantly more likely to come from women (44% vs. 31%), to come from patients with critical ischemia symptoms of pain at rest and tissue loss (54% vs. 38%), and to feature more advanced SFA lesions (51% vs. 31%), compared with limbs in the group without metabolic syndrome.
Claudication was a presentation for 46% of the limbs in the group with metabolic syndrome versus 62% of limbs in the non–metabolic syndrome group.
The investigators compared 30-day mortality and morbidity between these groups. In addition, they assessed the 5-year rates for primary and secondary patency; freedom from recurrent symptoms; and limb salvage. "We wanted to look at metabolic syndrome’s effect on these outcomes," said Dr. Smolock of the DeBakey Heart and Vascular Center.
"This addresses the important topic of outcomes with SFA interventions in those with metabolic syndrome," said study discussant Dr. Scott L. Stevens. "Of note, mortality was not increased among those with metabolic syndrome." Dr. Stevens is a vascular surgeon at the University of Tennessee Medical Center in Knoxville.
There was no significant difference in 30-day mortality: 0.2% in the metabolic syndrome group and the 1.3% in the nonsyndrome group.
A lower percentage of the metabolic syndrome group, 67% vs. 73%, experienced freedom from recurrent symptoms over 5 years.
"Primary patency decreased as well significantly over 5 years in those with metabolic syndrome," Dr. Smolock said. The study revealed 56% of the metabolic syndrome group had 5-year primary patency, compared with 66% in unaffected group; 71% vs. 78% had assisted primary patency; and 71% vs. 78% had secondary patency. Secondary patency decreased also, but there was no significant difference between groups, he added.
Because critical ischemia more often affected the group with metabolic syndrome, the rate of limb amputation was higher in this group (22% versus 13% of the unaffected group at 5 years).
Dr. Stevens asked why the metabolic group experienced significantly higher morbidity but not mortality, compared with the unaffected group. This might be because the mortality figures were calculated for only the first 30 days and not over the 5 years, Dr. Smolock said. In addition, the low 30-day mortality "could speak to this being a local procedure, not [one] done under general anesthesia." He added, "I hope some of that has to do with our risk-reduction strategies preoperatively."
"What changes have you made in your practice to reduce risk factors in those patients with metabolic syndrome?" Dr. Stevens asked.
"Our beta blocker, statin, and aspirin use were not at levels we wanted," Dr. Smolock replied. So use of these agents is now prescribed for all patients without a contraindication, he said.
Dr. Stevens also asked if metabolic syndrome might just be a surrogate for patients with smaller arteries and/or more plaque. "I don’t think this is because of small or poor targets," Dr. Smolock said. "The SVS [Society for Vascular Surgery] runoff score was equal between the groups. Diabetes is a risk in and of itself for small or poor targets, but it’s not something we could see anatomically."
Metabolic syndrome was defined in this study using the National Heart, Lung and Blood Institute/American Heart Association criteria. Therefore, patients had to have three or more of the following: systolic blood pressure of 130 mm Hg or greater/diastolic blood pressure of 85 mm Hg or greater; triglycerides of 150 mg/dL or greater; HDL cholesterol of 50 mg/dL or lower for women or 40 mg/dL or lower for men; fasting blood glucose of 110 mg/dL or greater; or body mass index of 30 kg/m2 or greater.
Dr. Smolock said that he had no relevant disclosures.
FROM THE ANNUAL MEETING OF THE SOUTHERN ASSOCIATION FOR VASCULAR SURGERY
Selective Lumbar Spinal Drainage Counters Ischemia After TEVAR
NAPLES, FLA. – Selective lumbar spinal drainage is worthwhile to reduce adverse neurologic outcomes for patients who develop symptoms of spinal cord ischemia after thoracic aortic endograft repair, according to a retrospective study.
Although surgeons who perform open aortic repair commonly employ perioperative lumbar spinal drainage, there is no consensus regarding drain placement for spinal cord ischemia (SCI) that is associated with thoracic endovascular aorta repair (TEVAR), Charles J. Keith said at the annual meeting of the Southern Association for Vascular Surgery.
Mr. Keith, a medical student at the University of Alabama at Birmingham, and his associates reviewed 10 years of experience at their institution to compare outcomes between drained and nondrained patients. Of 266 TEVAR interventions in 239 patients, of whom 167 (70%) were men, between January 2000 and June 2010, 16 (7% of cases) developed SCI within 30 days.
History of stroke, infrarenal pathology, and a longer aortic coverage in centimeters were significant risk factors for SCI in this patient population, Mr. Keith said. There were 147 interventions that involved aneurysms in the study, accounting for just more than half of the aortic pathology treated.
Left subclavian artery stent graft coverage was required in 80 interventions (30%), but it was not significantly associated with SCI.
Study discussant Dr. Peter H. Lin asked about routine or prophylactic drainage for patients with these risk factors. "Use of prophylactic drainage is supported by some, but we would have deployed an extra 105 unnecessary drains in this population," Mr. Keith replied. "There are risks associated with drainage, such as epidural hematoma, as was experienced by one of our patients."
Patients who developed SCI were three times more likely to die within 1 year, compared with non-SCI patients (odds ratio, 3.0).
Focus your efforts on complete symptom recovery after TEVAR and perform frequent neurologic assessments of high-risk patients, Mr. Keith said. These actions will minimize time to drain placement when indicated, improve symptom resolution, and increase 1-year survival.
In all, 10 of the 16 SCI cases were drained. There were no significant differences in terms of risk factors or demographics between drained and nondrained patients. Of the 10 drained cases, three patients experienced complete neurologic symptom resolution, four had partial resolution, and three had no resolution. Of the six patients who were not drained, four experienced complete resolution and two experienced no resolution.
Another aim of the study was to evaluate a drainage protocol adopted at their institution. Since 2007, all patients receive a neurologic evaluation post TEVAR. If they show any symptoms of neurologic deficit, their mean arterial pressure is increased to greater than 110 mm Hg, and the frequency of neurologic exams increases to hourly. Also, a lumbar drain is immediately placed if they have a major deficit and within 3 hours if minor symptoms persist postoperatively.
Although patients who experienced SCI after TEVAR had diminished outcomes, compared with non-SCI patients, the study supports the use of a spinal drainage protocol to improve neurologic outcomes in a select patient population, Mr. Keith said.
There are reports that support the use of steroids to reduce swelling and spinal cord edema, said Dr. Lin of the division of vascular and endovascular therapy at Baylor College of Medicine, Houston.
"Steroids are not included in our protocol, but it’s definitely something to consider," Mr. Keith said.
Dr. Lin asked if the study findings have changed the treatment approach at the University of Alabama. Mr. Keith deferred to Dr. William D. Jordan Jr., a coauthor of the study and moderator of this session at the meeting.
"We seek input from neurologic surgeons and anesthesia to help us place the drains in a more timely fashion," said Dr. Jordan, chief of vascular surgery at the University of Alabama.
A meeting attendee commented that that approach might work at the University of Alabama, but what if feedback from neurosurgery or anesthesia is not available in a timely fashion at another institution?
"In some places, they place a drain the night before in the ICU. If that works at your institution, fine," Dr. Jordan said.
Another attendee asked about the 3-hour window before drain placement. Dr. Jordan replied, "We are basically telling anesthesia: ‘We need these [patients] awake to make sure they are kicking their legs.’ That is why we chose 3 hours for recovery, but we can often tell within 1 hour if the [patient] is moving."
There is no consensus on measures to prevent SCI, Mr. Keith said. In addition to lumbar drainage, others report use of vasopressors to increase mean arterial pressure and predeployment aortic occlusion to detect diminished spinal cord evoked potentials.
Mr. Keith and Dr. Lin said that they had no relevant disclosures. Dr. Jordan had multiple disclosures, including being a consultant, speaker, and advisor for Abbott Vascular; an advisor for LeMaitre Vascular; a speaker and advisor for Medtronic; and a consultant and speaker for W.L. Gore.
NAPLES, FLA. – Selective lumbar spinal drainage is worthwhile to reduce adverse neurologic outcomes for patients who develop symptoms of spinal cord ischemia after thoracic aortic endograft repair, according to a retrospective study.
Although surgeons who perform open aortic repair commonly employ perioperative lumbar spinal drainage, there is no consensus regarding drain placement for spinal cord ischemia (SCI) that is associated with thoracic endovascular aorta repair (TEVAR), Charles J. Keith said at the annual meeting of the Southern Association for Vascular Surgery.
Mr. Keith, a medical student at the University of Alabama at Birmingham, and his associates reviewed 10 years of experience at their institution to compare outcomes between drained and nondrained patients. Of 266 TEVAR interventions in 239 patients, of whom 167 (70%) were men, between January 2000 and June 2010, 16 (7% of cases) developed SCI within 30 days.
History of stroke, infrarenal pathology, and a longer aortic coverage in centimeters were significant risk factors for SCI in this patient population, Mr. Keith said. There were 147 interventions that involved aneurysms in the study, accounting for just more than half of the aortic pathology treated.
Left subclavian artery stent graft coverage was required in 80 interventions (30%), but it was not significantly associated with SCI.
Study discussant Dr. Peter H. Lin asked about routine or prophylactic drainage for patients with these risk factors. "Use of prophylactic drainage is supported by some, but we would have deployed an extra 105 unnecessary drains in this population," Mr. Keith replied. "There are risks associated with drainage, such as epidural hematoma, as was experienced by one of our patients."
Patients who developed SCI were three times more likely to die within 1 year, compared with non-SCI patients (odds ratio, 3.0).
Focus your efforts on complete symptom recovery after TEVAR and perform frequent neurologic assessments of high-risk patients, Mr. Keith said. These actions will minimize time to drain placement when indicated, improve symptom resolution, and increase 1-year survival.
In all, 10 of the 16 SCI cases were drained. There were no significant differences in terms of risk factors or demographics between drained and nondrained patients. Of the 10 drained cases, three patients experienced complete neurologic symptom resolution, four had partial resolution, and three had no resolution. Of the six patients who were not drained, four experienced complete resolution and two experienced no resolution.
Another aim of the study was to evaluate a drainage protocol adopted at their institution. Since 2007, all patients receive a neurologic evaluation post TEVAR. If they show any symptoms of neurologic deficit, their mean arterial pressure is increased to greater than 110 mm Hg, and the frequency of neurologic exams increases to hourly. Also, a lumbar drain is immediately placed if they have a major deficit and within 3 hours if minor symptoms persist postoperatively.
Although patients who experienced SCI after TEVAR had diminished outcomes, compared with non-SCI patients, the study supports the use of a spinal drainage protocol to improve neurologic outcomes in a select patient population, Mr. Keith said.
There are reports that support the use of steroids to reduce swelling and spinal cord edema, said Dr. Lin of the division of vascular and endovascular therapy at Baylor College of Medicine, Houston.
"Steroids are not included in our protocol, but it’s definitely something to consider," Mr. Keith said.
Dr. Lin asked if the study findings have changed the treatment approach at the University of Alabama. Mr. Keith deferred to Dr. William D. Jordan Jr., a coauthor of the study and moderator of this session at the meeting.
"We seek input from neurologic surgeons and anesthesia to help us place the drains in a more timely fashion," said Dr. Jordan, chief of vascular surgery at the University of Alabama.
A meeting attendee commented that that approach might work at the University of Alabama, but what if feedback from neurosurgery or anesthesia is not available in a timely fashion at another institution?
"In some places, they place a drain the night before in the ICU. If that works at your institution, fine," Dr. Jordan said.
Another attendee asked about the 3-hour window before drain placement. Dr. Jordan replied, "We are basically telling anesthesia: ‘We need these [patients] awake to make sure they are kicking their legs.’ That is why we chose 3 hours for recovery, but we can often tell within 1 hour if the [patient] is moving."
There is no consensus on measures to prevent SCI, Mr. Keith said. In addition to lumbar drainage, others report use of vasopressors to increase mean arterial pressure and predeployment aortic occlusion to detect diminished spinal cord evoked potentials.
Mr. Keith and Dr. Lin said that they had no relevant disclosures. Dr. Jordan had multiple disclosures, including being a consultant, speaker, and advisor for Abbott Vascular; an advisor for LeMaitre Vascular; a speaker and advisor for Medtronic; and a consultant and speaker for W.L. Gore.
NAPLES, FLA. – Selective lumbar spinal drainage is worthwhile to reduce adverse neurologic outcomes for patients who develop symptoms of spinal cord ischemia after thoracic aortic endograft repair, according to a retrospective study.
Although surgeons who perform open aortic repair commonly employ perioperative lumbar spinal drainage, there is no consensus regarding drain placement for spinal cord ischemia (SCI) that is associated with thoracic endovascular aorta repair (TEVAR), Charles J. Keith said at the annual meeting of the Southern Association for Vascular Surgery.
Mr. Keith, a medical student at the University of Alabama at Birmingham, and his associates reviewed 10 years of experience at their institution to compare outcomes between drained and nondrained patients. Of 266 TEVAR interventions in 239 patients, of whom 167 (70%) were men, between January 2000 and June 2010, 16 (7% of cases) developed SCI within 30 days.
History of stroke, infrarenal pathology, and a longer aortic coverage in centimeters were significant risk factors for SCI in this patient population, Mr. Keith said. There were 147 interventions that involved aneurysms in the study, accounting for just more than half of the aortic pathology treated.
Left subclavian artery stent graft coverage was required in 80 interventions (30%), but it was not significantly associated with SCI.
Study discussant Dr. Peter H. Lin asked about routine or prophylactic drainage for patients with these risk factors. "Use of prophylactic drainage is supported by some, but we would have deployed an extra 105 unnecessary drains in this population," Mr. Keith replied. "There are risks associated with drainage, such as epidural hematoma, as was experienced by one of our patients."
Patients who developed SCI were three times more likely to die within 1 year, compared with non-SCI patients (odds ratio, 3.0).
Focus your efforts on complete symptom recovery after TEVAR and perform frequent neurologic assessments of high-risk patients, Mr. Keith said. These actions will minimize time to drain placement when indicated, improve symptom resolution, and increase 1-year survival.
In all, 10 of the 16 SCI cases were drained. There were no significant differences in terms of risk factors or demographics between drained and nondrained patients. Of the 10 drained cases, three patients experienced complete neurologic symptom resolution, four had partial resolution, and three had no resolution. Of the six patients who were not drained, four experienced complete resolution and two experienced no resolution.
Another aim of the study was to evaluate a drainage protocol adopted at their institution. Since 2007, all patients receive a neurologic evaluation post TEVAR. If they show any symptoms of neurologic deficit, their mean arterial pressure is increased to greater than 110 mm Hg, and the frequency of neurologic exams increases to hourly. Also, a lumbar drain is immediately placed if they have a major deficit and within 3 hours if minor symptoms persist postoperatively.
Although patients who experienced SCI after TEVAR had diminished outcomes, compared with non-SCI patients, the study supports the use of a spinal drainage protocol to improve neurologic outcomes in a select patient population, Mr. Keith said.
There are reports that support the use of steroids to reduce swelling and spinal cord edema, said Dr. Lin of the division of vascular and endovascular therapy at Baylor College of Medicine, Houston.
"Steroids are not included in our protocol, but it’s definitely something to consider," Mr. Keith said.
Dr. Lin asked if the study findings have changed the treatment approach at the University of Alabama. Mr. Keith deferred to Dr. William D. Jordan Jr., a coauthor of the study and moderator of this session at the meeting.
"We seek input from neurologic surgeons and anesthesia to help us place the drains in a more timely fashion," said Dr. Jordan, chief of vascular surgery at the University of Alabama.
A meeting attendee commented that that approach might work at the University of Alabama, but what if feedback from neurosurgery or anesthesia is not available in a timely fashion at another institution?
"In some places, they place a drain the night before in the ICU. If that works at your institution, fine," Dr. Jordan said.
Another attendee asked about the 3-hour window before drain placement. Dr. Jordan replied, "We are basically telling anesthesia: ‘We need these [patients] awake to make sure they are kicking their legs.’ That is why we chose 3 hours for recovery, but we can often tell within 1 hour if the [patient] is moving."
There is no consensus on measures to prevent SCI, Mr. Keith said. In addition to lumbar drainage, others report use of vasopressors to increase mean arterial pressure and predeployment aortic occlusion to detect diminished spinal cord evoked potentials.
Mr. Keith and Dr. Lin said that they had no relevant disclosures. Dr. Jordan had multiple disclosures, including being a consultant, speaker, and advisor for Abbott Vascular; an advisor for LeMaitre Vascular; a speaker and advisor for Medtronic; and a consultant and speaker for W.L. Gore.
FROM THE ANNUAL MEETING OF THE SOUTHERN ASSOCIATION FOR VASCULAR SURGERY
Endovascular Aortic Repair Aids Some With Marfan Syndrome
NAPLES, Fla. – Some people with Marfan syndrome benefit from endovascular aortic repair, according to a review of 16 patients who were treated at the University of Florida, Gainesville, between January 2000 and June 2010.
Most patients had a history of multiple interventions, which points to the complexity of Marfan syndrome and a need to follow patients closely over the long term, Dr. Alyson L. Waterman said at the annual meeting of the Southern Association for Vascular Surgery.
Dr. Waterman and her associates reviewed their experience with endovascular abdominal aorta repair (EVAR) and thoracic aorta repair (TEVAR) for Marfan syndrome patients at the University of Florida.
After a median of 8.3 months, seven patients had clinical and radiographic evidence of successful treatment. Another six patients were primary treatment failures (for example, they had a type I endovascular leak or persistent false lumen flow), and two patients had a secondary treatment failure (initial success, followed by proximal or distal aortic failure unrelated to the original intervention site). The remaining patient was lost to follow-up.
"Results are sobering but support [the concept that] some Marfan syndrome patients benefit from endovascular therapy," said Dr. Waterman of the department of surgery at the University of Florida, Gainesville.
The main causes of death in Marfan syndrome are aortic dissection and rupture, Dr. Waterman said. She pointed out that open surgery is still required for repair of the ascending aorta, but endovascular intervention is an option for descending thoracic and abdominal aorta repair for those with this connective-tissue disorder.
The 16 Marfan syndrome patients in the series underwent a total of 19 relevant procedures (1 EVAR, 15 TEVAR, and 3 combined procedures). The median patient age was 52 years. Three patients had a secondary TEVAR within 28 months of their index intervention.
In all, 15 of the patients had previous surgery (from 17 years to 1 week prior) of the ascending aorta or arch. Chronic dissection and/or aneurysmal dilation of the descending aorta were the indications for elective intervention in 13 patients. Two acute dissection/malperfusion cases and one anastomotic disruption early after an open surgery led to emergency intervention in three patients.
Four of the TEVAR procedures required adjunctive endovascular procedures (one subclavian artery embolization, one vertebral artery stent, one renal artery stent, and one celiac and superior mesenteric artery stent). All four EVAR procedures required complex adjunctive endovascular procedures involving visceral arteries.
Five patients died during follow-up. Two died perioperatively: the patient who underwent emergent TEVAR for anastomotic disruption, and a patient who required multivisceral revascularization in conjunction with a second TEVAR. Two patients died following discharge (a respiratory failure at 3 months, and a cardiac arrest at 4 months). The remaining patient died more than 6 years after EVAR from advanced age (84 years).
"This is clearly a group for whom treatment options are difficult at best," said study discussant Dr. Eric D. Endean of the University of Kentucky, Lexington.
All were deemed poor candidates for open surgery, and they had a history of an average of almost two previous aortic operations. Six (38%) were classified as primary treatment failures, all required open repair, and half died, Dr. Endean said. "Results are indeed sobering."
"As you point out, diagnosis of Marfan syndrome was based on clinical diagnosis," Dr. Endean said. He asked how confident Dr. Waterman is about the diagnoses in her series.
"That is one of the difficulties with Marfan syndrome; a lot is based on clinical diagnosis alone." Not all patients undergo genetic screening for the fibrillin-1 mutation, she said.
A small population that makes the study "essentially a case series" is a limitation, Dr. Waterman said.
"Open surgery still has a big role in replacement of these aortas because these aortas are not genetically normal." Dr. Waterman also said there is still a place for endovascular therapy and a need to identify which patients are likely to benefit. She added that the cardiologists at University of Florida also treat Marfan syndrome patients, and they have yet to look at these patient populations combined.
Dr. Waterman and Dr. Endean said that they had no relevant disclosures.
NAPLES, Fla. – Some people with Marfan syndrome benefit from endovascular aortic repair, according to a review of 16 patients who were treated at the University of Florida, Gainesville, between January 2000 and June 2010.
Most patients had a history of multiple interventions, which points to the complexity of Marfan syndrome and a need to follow patients closely over the long term, Dr. Alyson L. Waterman said at the annual meeting of the Southern Association for Vascular Surgery.
Dr. Waterman and her associates reviewed their experience with endovascular abdominal aorta repair (EVAR) and thoracic aorta repair (TEVAR) for Marfan syndrome patients at the University of Florida.
After a median of 8.3 months, seven patients had clinical and radiographic evidence of successful treatment. Another six patients were primary treatment failures (for example, they had a type I endovascular leak or persistent false lumen flow), and two patients had a secondary treatment failure (initial success, followed by proximal or distal aortic failure unrelated to the original intervention site). The remaining patient was lost to follow-up.
"Results are sobering but support [the concept that] some Marfan syndrome patients benefit from endovascular therapy," said Dr. Waterman of the department of surgery at the University of Florida, Gainesville.
The main causes of death in Marfan syndrome are aortic dissection and rupture, Dr. Waterman said. She pointed out that open surgery is still required for repair of the ascending aorta, but endovascular intervention is an option for descending thoracic and abdominal aorta repair for those with this connective-tissue disorder.
The 16 Marfan syndrome patients in the series underwent a total of 19 relevant procedures (1 EVAR, 15 TEVAR, and 3 combined procedures). The median patient age was 52 years. Three patients had a secondary TEVAR within 28 months of their index intervention.
In all, 15 of the patients had previous surgery (from 17 years to 1 week prior) of the ascending aorta or arch. Chronic dissection and/or aneurysmal dilation of the descending aorta were the indications for elective intervention in 13 patients. Two acute dissection/malperfusion cases and one anastomotic disruption early after an open surgery led to emergency intervention in three patients.
Four of the TEVAR procedures required adjunctive endovascular procedures (one subclavian artery embolization, one vertebral artery stent, one renal artery stent, and one celiac and superior mesenteric artery stent). All four EVAR procedures required complex adjunctive endovascular procedures involving visceral arteries.
Five patients died during follow-up. Two died perioperatively: the patient who underwent emergent TEVAR for anastomotic disruption, and a patient who required multivisceral revascularization in conjunction with a second TEVAR. Two patients died following discharge (a respiratory failure at 3 months, and a cardiac arrest at 4 months). The remaining patient died more than 6 years after EVAR from advanced age (84 years).
"This is clearly a group for whom treatment options are difficult at best," said study discussant Dr. Eric D. Endean of the University of Kentucky, Lexington.
All were deemed poor candidates for open surgery, and they had a history of an average of almost two previous aortic operations. Six (38%) were classified as primary treatment failures, all required open repair, and half died, Dr. Endean said. "Results are indeed sobering."
"As you point out, diagnosis of Marfan syndrome was based on clinical diagnosis," Dr. Endean said. He asked how confident Dr. Waterman is about the diagnoses in her series.
"That is one of the difficulties with Marfan syndrome; a lot is based on clinical diagnosis alone." Not all patients undergo genetic screening for the fibrillin-1 mutation, she said.
A small population that makes the study "essentially a case series" is a limitation, Dr. Waterman said.
"Open surgery still has a big role in replacement of these aortas because these aortas are not genetically normal." Dr. Waterman also said there is still a place for endovascular therapy and a need to identify which patients are likely to benefit. She added that the cardiologists at University of Florida also treat Marfan syndrome patients, and they have yet to look at these patient populations combined.
Dr. Waterman and Dr. Endean said that they had no relevant disclosures.
NAPLES, Fla. – Some people with Marfan syndrome benefit from endovascular aortic repair, according to a review of 16 patients who were treated at the University of Florida, Gainesville, between January 2000 and June 2010.
Most patients had a history of multiple interventions, which points to the complexity of Marfan syndrome and a need to follow patients closely over the long term, Dr. Alyson L. Waterman said at the annual meeting of the Southern Association for Vascular Surgery.
Dr. Waterman and her associates reviewed their experience with endovascular abdominal aorta repair (EVAR) and thoracic aorta repair (TEVAR) for Marfan syndrome patients at the University of Florida.
After a median of 8.3 months, seven patients had clinical and radiographic evidence of successful treatment. Another six patients were primary treatment failures (for example, they had a type I endovascular leak or persistent false lumen flow), and two patients had a secondary treatment failure (initial success, followed by proximal or distal aortic failure unrelated to the original intervention site). The remaining patient was lost to follow-up.
"Results are sobering but support [the concept that] some Marfan syndrome patients benefit from endovascular therapy," said Dr. Waterman of the department of surgery at the University of Florida, Gainesville.
The main causes of death in Marfan syndrome are aortic dissection and rupture, Dr. Waterman said. She pointed out that open surgery is still required for repair of the ascending aorta, but endovascular intervention is an option for descending thoracic and abdominal aorta repair for those with this connective-tissue disorder.
The 16 Marfan syndrome patients in the series underwent a total of 19 relevant procedures (1 EVAR, 15 TEVAR, and 3 combined procedures). The median patient age was 52 years. Three patients had a secondary TEVAR within 28 months of their index intervention.
In all, 15 of the patients had previous surgery (from 17 years to 1 week prior) of the ascending aorta or arch. Chronic dissection and/or aneurysmal dilation of the descending aorta were the indications for elective intervention in 13 patients. Two acute dissection/malperfusion cases and one anastomotic disruption early after an open surgery led to emergency intervention in three patients.
Four of the TEVAR procedures required adjunctive endovascular procedures (one subclavian artery embolization, one vertebral artery stent, one renal artery stent, and one celiac and superior mesenteric artery stent). All four EVAR procedures required complex adjunctive endovascular procedures involving visceral arteries.
Five patients died during follow-up. Two died perioperatively: the patient who underwent emergent TEVAR for anastomotic disruption, and a patient who required multivisceral revascularization in conjunction with a second TEVAR. Two patients died following discharge (a respiratory failure at 3 months, and a cardiac arrest at 4 months). The remaining patient died more than 6 years after EVAR from advanced age (84 years).
"This is clearly a group for whom treatment options are difficult at best," said study discussant Dr. Eric D. Endean of the University of Kentucky, Lexington.
All were deemed poor candidates for open surgery, and they had a history of an average of almost two previous aortic operations. Six (38%) were classified as primary treatment failures, all required open repair, and half died, Dr. Endean said. "Results are indeed sobering."
"As you point out, diagnosis of Marfan syndrome was based on clinical diagnosis," Dr. Endean said. He asked how confident Dr. Waterman is about the diagnoses in her series.
"That is one of the difficulties with Marfan syndrome; a lot is based on clinical diagnosis alone." Not all patients undergo genetic screening for the fibrillin-1 mutation, she said.
A small population that makes the study "essentially a case series" is a limitation, Dr. Waterman said.
"Open surgery still has a big role in replacement of these aortas because these aortas are not genetically normal." Dr. Waterman also said there is still a place for endovascular therapy and a need to identify which patients are likely to benefit. She added that the cardiologists at University of Florida also treat Marfan syndrome patients, and they have yet to look at these patient populations combined.
Dr. Waterman and Dr. Endean said that they had no relevant disclosures.
FROM THE ANNUAL MEETING OF THE SOUTHERN ASSOCIATION FOR VASCULAR SURGERY
Major Finding: In all, 7 of 16 patients with Marfan syndrome had successful endovascular treatment of their aortas.
Data Source: Review of endovascular repairs at the University of Florida, Gainesville, from 2000 to 2010.
Disclosures: Dr. Waterman and Dr. Endean said they had no relevant disclosures.
Endovascular Aortic Repair Aids Some With Marfan Syndrome
NAPLES, Fla. – Some people with Marfan syndrome benefit from endovascular aortic repair, according to a review of 16 patients who were treated at the University of Florida, Gainesville, between January 2000 and June 2010.
Most patients had a history of multiple interventions, which points to the complexity of Marfan syndrome and a need to follow patients closely over the long term, Dr. Alyson L. Waterman said at the annual meeting of the Southern Association for Vascular Surgery.
Dr. Waterman and her associates reviewed their experience with endovascular abdominal aorta repair (EVAR) and thoracic aorta repair (TEVAR) for Marfan syndrome patients at the University of Florida.
After a median of 8.3 months, seven patients had clinical and radiographic evidence of successful treatment. Another six patients were primary treatment failures (for example, they had a type I endovascular leak or persistent false lumen flow), and two patients had a secondary treatment failure (initial success, followed by proximal or distal aortic failure unrelated to the original intervention site). The remaining patient was lost to follow-up.
"Results are sobering but support [the concept that] some Marfan syndrome patients benefit from endovascular therapy," said Dr. Waterman of the department of surgery at the University of Florida, Gainesville.
The main causes of death in Marfan syndrome are aortic dissection and rupture, Dr. Waterman said. She pointed out that open surgery is still required for repair of the ascending aorta, but endovascular intervention is an option for descending thoracic and abdominal aorta repair for those with this connective-tissue disorder.
The 16 Marfan syndrome patients in the series underwent a total of 19 relevant procedures (1 EVAR, 15 TEVAR, and 3 combined procedures). The median patient age was 52 years. Three patients had a secondary TEVAR within 28 months of their index intervention.
In all, 15 of the patients had previous surgery (from 17 years to 1 week prior) of the ascending aorta or arch. Chronic dissection and/or aneurysmal dilation of the descending aorta were the indications for elective intervention in 13 patients. Two acute dissection/malperfusion cases and one anastomotic disruption early after an open surgery led to emergency intervention in three patients.
Four of the TEVAR procedures required adjunctive endovascular procedures (one subclavian artery embolization, one vertebral artery stent, one renal artery stent, and one celiac and superior mesenteric artery stent). All four EVAR procedures required complex adjunctive endovascular procedures involving visceral arteries.
Five patients died during follow-up. Two died perioperatively: the patient who underwent emergent TEVAR for anastomotic disruption, and a patient who required multivisceral revascularization in conjunction with a second TEVAR. Two patients died following discharge (a respiratory failure at 3 months, and a cardiac arrest at 4 months). The remaining patient died more than 6 years after EVAR from advanced age (84 years).
"This is clearly a group for whom treatment options are difficult at best," said study discussant Dr. Eric D. Endean of the University of Kentucky, Lexington.
All were deemed poor candidates for open surgery, and they had a history of an average of almost two previous aortic operations. Six (38%) were classified as primary treatment failures, all required open repair, and half died, Dr. Endean said. "Results are indeed sobering."
"As you point out, diagnosis of Marfan syndrome was based on clinical diagnosis," Dr. Endean said. He asked how confident Dr. Waterman is about the diagnoses in her series.
"That is one of the difficulties with Marfan syndrome; a lot is based on clinical diagnosis alone." Not all patients undergo genetic screening for the fibrillin-1 mutation, she said.
A small population that makes the study "essentially a case series" is a limitation, Dr. Waterman said.
"Open surgery still has a big role in replacement of these aortas because these aortas are not genetically normal." Dr. Waterman also said there is still a place for endovascular therapy and a need to identify which patients are likely to benefit. She added that the cardiologists at University of Florida also treat Marfan syndrome patients, and they have yet to look at these patient populations combined.
Dr. Waterman and Dr. Endean said that they had no relevant disclosures.
NAPLES, Fla. – Some people with Marfan syndrome benefit from endovascular aortic repair, according to a review of 16 patients who were treated at the University of Florida, Gainesville, between January 2000 and June 2010.
Most patients had a history of multiple interventions, which points to the complexity of Marfan syndrome and a need to follow patients closely over the long term, Dr. Alyson L. Waterman said at the annual meeting of the Southern Association for Vascular Surgery.
Dr. Waterman and her associates reviewed their experience with endovascular abdominal aorta repair (EVAR) and thoracic aorta repair (TEVAR) for Marfan syndrome patients at the University of Florida.
After a median of 8.3 months, seven patients had clinical and radiographic evidence of successful treatment. Another six patients were primary treatment failures (for example, they had a type I endovascular leak or persistent false lumen flow), and two patients had a secondary treatment failure (initial success, followed by proximal or distal aortic failure unrelated to the original intervention site). The remaining patient was lost to follow-up.
"Results are sobering but support [the concept that] some Marfan syndrome patients benefit from endovascular therapy," said Dr. Waterman of the department of surgery at the University of Florida, Gainesville.
The main causes of death in Marfan syndrome are aortic dissection and rupture, Dr. Waterman said. She pointed out that open surgery is still required for repair of the ascending aorta, but endovascular intervention is an option for descending thoracic and abdominal aorta repair for those with this connective-tissue disorder.
The 16 Marfan syndrome patients in the series underwent a total of 19 relevant procedures (1 EVAR, 15 TEVAR, and 3 combined procedures). The median patient age was 52 years. Three patients had a secondary TEVAR within 28 months of their index intervention.
In all, 15 of the patients had previous surgery (from 17 years to 1 week prior) of the ascending aorta or arch. Chronic dissection and/or aneurysmal dilation of the descending aorta were the indications for elective intervention in 13 patients. Two acute dissection/malperfusion cases and one anastomotic disruption early after an open surgery led to emergency intervention in three patients.
Four of the TEVAR procedures required adjunctive endovascular procedures (one subclavian artery embolization, one vertebral artery stent, one renal artery stent, and one celiac and superior mesenteric artery stent). All four EVAR procedures required complex adjunctive endovascular procedures involving visceral arteries.
Five patients died during follow-up. Two died perioperatively: the patient who underwent emergent TEVAR for anastomotic disruption, and a patient who required multivisceral revascularization in conjunction with a second TEVAR. Two patients died following discharge (a respiratory failure at 3 months, and a cardiac arrest at 4 months). The remaining patient died more than 6 years after EVAR from advanced age (84 years).
"This is clearly a group for whom treatment options are difficult at best," said study discussant Dr. Eric D. Endean of the University of Kentucky, Lexington.
All were deemed poor candidates for open surgery, and they had a history of an average of almost two previous aortic operations. Six (38%) were classified as primary treatment failures, all required open repair, and half died, Dr. Endean said. "Results are indeed sobering."
"As you point out, diagnosis of Marfan syndrome was based on clinical diagnosis," Dr. Endean said. He asked how confident Dr. Waterman is about the diagnoses in her series.
"That is one of the difficulties with Marfan syndrome; a lot is based on clinical diagnosis alone." Not all patients undergo genetic screening for the fibrillin-1 mutation, she said.
A small population that makes the study "essentially a case series" is a limitation, Dr. Waterman said.
"Open surgery still has a big role in replacement of these aortas because these aortas are not genetically normal." Dr. Waterman also said there is still a place for endovascular therapy and a need to identify which patients are likely to benefit. She added that the cardiologists at University of Florida also treat Marfan syndrome patients, and they have yet to look at these patient populations combined.
Dr. Waterman and Dr. Endean said that they had no relevant disclosures.
NAPLES, Fla. – Some people with Marfan syndrome benefit from endovascular aortic repair, according to a review of 16 patients who were treated at the University of Florida, Gainesville, between January 2000 and June 2010.
Most patients had a history of multiple interventions, which points to the complexity of Marfan syndrome and a need to follow patients closely over the long term, Dr. Alyson L. Waterman said at the annual meeting of the Southern Association for Vascular Surgery.
Dr. Waterman and her associates reviewed their experience with endovascular abdominal aorta repair (EVAR) and thoracic aorta repair (TEVAR) for Marfan syndrome patients at the University of Florida.
After a median of 8.3 months, seven patients had clinical and radiographic evidence of successful treatment. Another six patients were primary treatment failures (for example, they had a type I endovascular leak or persistent false lumen flow), and two patients had a secondary treatment failure (initial success, followed by proximal or distal aortic failure unrelated to the original intervention site). The remaining patient was lost to follow-up.
"Results are sobering but support [the concept that] some Marfan syndrome patients benefit from endovascular therapy," said Dr. Waterman of the department of surgery at the University of Florida, Gainesville.
The main causes of death in Marfan syndrome are aortic dissection and rupture, Dr. Waterman said. She pointed out that open surgery is still required for repair of the ascending aorta, but endovascular intervention is an option for descending thoracic and abdominal aorta repair for those with this connective-tissue disorder.
The 16 Marfan syndrome patients in the series underwent a total of 19 relevant procedures (1 EVAR, 15 TEVAR, and 3 combined procedures). The median patient age was 52 years. Three patients had a secondary TEVAR within 28 months of their index intervention.
In all, 15 of the patients had previous surgery (from 17 years to 1 week prior) of the ascending aorta or arch. Chronic dissection and/or aneurysmal dilation of the descending aorta were the indications for elective intervention in 13 patients. Two acute dissection/malperfusion cases and one anastomotic disruption early after an open surgery led to emergency intervention in three patients.
Four of the TEVAR procedures required adjunctive endovascular procedures (one subclavian artery embolization, one vertebral artery stent, one renal artery stent, and one celiac and superior mesenteric artery stent). All four EVAR procedures required complex adjunctive endovascular procedures involving visceral arteries.
Five patients died during follow-up. Two died perioperatively: the patient who underwent emergent TEVAR for anastomotic disruption, and a patient who required multivisceral revascularization in conjunction with a second TEVAR. Two patients died following discharge (a respiratory failure at 3 months, and a cardiac arrest at 4 months). The remaining patient died more than 6 years after EVAR from advanced age (84 years).
"This is clearly a group for whom treatment options are difficult at best," said study discussant Dr. Eric D. Endean of the University of Kentucky, Lexington.
All were deemed poor candidates for open surgery, and they had a history of an average of almost two previous aortic operations. Six (38%) were classified as primary treatment failures, all required open repair, and half died, Dr. Endean said. "Results are indeed sobering."
"As you point out, diagnosis of Marfan syndrome was based on clinical diagnosis," Dr. Endean said. He asked how confident Dr. Waterman is about the diagnoses in her series.
"That is one of the difficulties with Marfan syndrome; a lot is based on clinical diagnosis alone." Not all patients undergo genetic screening for the fibrillin-1 mutation, she said.
A small population that makes the study "essentially a case series" is a limitation, Dr. Waterman said.
"Open surgery still has a big role in replacement of these aortas because these aortas are not genetically normal." Dr. Waterman also said there is still a place for endovascular therapy and a need to identify which patients are likely to benefit. She added that the cardiologists at University of Florida also treat Marfan syndrome patients, and they have yet to look at these patient populations combined.
Dr. Waterman and Dr. Endean said that they had no relevant disclosures.
FROM THE ANNUAL MEETING OF THE SOUTHERN ASSOCIATION FOR VASCULAR SURGERY
ASG Score Clinically Valid for Endovascular Aneurysm Repair
NAPLES, FLA. – The Anatomic Severity Grade score is a clinically valid indicator of which patients about to undergo endovascular aneurysm repair are more likely to present technical challenges, such as a need for additional endovascular implants or adjunct maneuvers, according to a retrospective study.
Increased operating time, length of hospital stay, blood loss, use of contrast, number of adjunct maneuvers, and costs were each significantly higher among 52 patients with a higher Anatomic Severity Grade (ASG) score, compared with 58 others who scored lower.
Dr. Sadaf S. Ahanchi of Eastern Virginia Medical School, Norfolk, and her colleagues reviewed patient factors, early outcomes, and costs for all patients who underwent endovascular intervention at the medical school for an infrarenal abdominal aortic aneurysm between April 2009 and July 2010. Their aim was to assess how the ASG score translated clinically regarding endovascular aneurysm repair in this patient population.
In 2002, the Society for Vascular Surgery and the American Association for Vascular Surgery devised the scoring system to grade abdominal aortic aneurysms. The ASG score would be 0 in a patient with optimal anatomy and would range up to 44 in a patient with complex anatomy, Dr. Ahanchi said. In the current study, patients were classified into a low-score group (defined as an ASG score of less than 14 points) and a high-score group (a score of 14 points or higher). Each patient’s total ASG score was calculated preoperatively based on aortic neck, aneurysm, and iliac anatomic factors, such as diameter, length, angulation, and tortuosity, using three-dimensional imaging software from M2S Inc. in West Lebanon, N.H.
The ASG score "can be easily and rapidly calculated from CT images using 3-D imaging," Dr. Ahanchi said.
Mean procedure time was longer in the high-score group, at 210 minutes vs. 113 minutes in the low-score group. The amount of contrast used was greater (at 131 mL vs. 100 mL), and blood loss was greater in the high-score group, at 886 mL vs. 227 mL in the low-score group.
Half of the high-score patients required access adjunct maneuvers, compared with only 14% of the low-score patients. Endarterectomy, patch angioplasty, and percutaneous angioplasty were the most common access-site adjuncts. Intraoperative adjuncts were required by 80% of the high-score group vs. 54% of the others; these included distal limb extension, access-site management, and iliac artery occlusive disease management.
Total mean number of endograft implants used during the cases was four in the high-score group vs. three in the low-score group, a statistically significant difference.
No patient was converted to an open repair. Length of stay was an average 5 days in the high-score group vs. 2 days in the lower-score patients, Dr. Ahanchi said.
No patient died within the first 30 days. At a mean follow-up of 5 months, there were no endograft issues or aneurysm-related deaths. Two patients in the high-score group died of unrelated causes, Dr. Ahanchi said.
Total systemic morbidity – 35% in the high score group vs. 18% in the low score group – "trended toward significant and were mostly respiratory and wound complications."
The patients with high ASG scores accounted for a 55% increase in operating room supply costs and a 48% increase in hospital charges, compared with the low-scoring patients. Mean OR supply charges were $25,765 in the high-score group vs. $16,646 in the low-score group. Total mean hospital charges were $105,153 among the high-score patients vs. $70,956 for the low-score group.
More than 90% of patients in the study had an aneurysm greater than 5 cm. Mean patient age was 75 years, 78% were men, and 91% were asymptomatic. A majority (81%) was white, 17% were black, and 2% were "other." All patients were retrospectively identified using CPT codes. To limit confounding variables, the researchers included only patients who had a Talent or AneuRx brand endograft (Medtronic).
Dr. Ahanchi said she had no relevant disclosures.
NAPLES, FLA. – The Anatomic Severity Grade score is a clinically valid indicator of which patients about to undergo endovascular aneurysm repair are more likely to present technical challenges, such as a need for additional endovascular implants or adjunct maneuvers, according to a retrospective study.
Increased operating time, length of hospital stay, blood loss, use of contrast, number of adjunct maneuvers, and costs were each significantly higher among 52 patients with a higher Anatomic Severity Grade (ASG) score, compared with 58 others who scored lower.
Dr. Sadaf S. Ahanchi of Eastern Virginia Medical School, Norfolk, and her colleagues reviewed patient factors, early outcomes, and costs for all patients who underwent endovascular intervention at the medical school for an infrarenal abdominal aortic aneurysm between April 2009 and July 2010. Their aim was to assess how the ASG score translated clinically regarding endovascular aneurysm repair in this patient population.
In 2002, the Society for Vascular Surgery and the American Association for Vascular Surgery devised the scoring system to grade abdominal aortic aneurysms. The ASG score would be 0 in a patient with optimal anatomy and would range up to 44 in a patient with complex anatomy, Dr. Ahanchi said. In the current study, patients were classified into a low-score group (defined as an ASG score of less than 14 points) and a high-score group (a score of 14 points or higher). Each patient’s total ASG score was calculated preoperatively based on aortic neck, aneurysm, and iliac anatomic factors, such as diameter, length, angulation, and tortuosity, using three-dimensional imaging software from M2S Inc. in West Lebanon, N.H.
The ASG score "can be easily and rapidly calculated from CT images using 3-D imaging," Dr. Ahanchi said.
Mean procedure time was longer in the high-score group, at 210 minutes vs. 113 minutes in the low-score group. The amount of contrast used was greater (at 131 mL vs. 100 mL), and blood loss was greater in the high-score group, at 886 mL vs. 227 mL in the low-score group.
Half of the high-score patients required access adjunct maneuvers, compared with only 14% of the low-score patients. Endarterectomy, patch angioplasty, and percutaneous angioplasty were the most common access-site adjuncts. Intraoperative adjuncts were required by 80% of the high-score group vs. 54% of the others; these included distal limb extension, access-site management, and iliac artery occlusive disease management.
Total mean number of endograft implants used during the cases was four in the high-score group vs. three in the low-score group, a statistically significant difference.
No patient was converted to an open repair. Length of stay was an average 5 days in the high-score group vs. 2 days in the lower-score patients, Dr. Ahanchi said.
No patient died within the first 30 days. At a mean follow-up of 5 months, there were no endograft issues or aneurysm-related deaths. Two patients in the high-score group died of unrelated causes, Dr. Ahanchi said.
Total systemic morbidity – 35% in the high score group vs. 18% in the low score group – "trended toward significant and were mostly respiratory and wound complications."
The patients with high ASG scores accounted for a 55% increase in operating room supply costs and a 48% increase in hospital charges, compared with the low-scoring patients. Mean OR supply charges were $25,765 in the high-score group vs. $16,646 in the low-score group. Total mean hospital charges were $105,153 among the high-score patients vs. $70,956 for the low-score group.
More than 90% of patients in the study had an aneurysm greater than 5 cm. Mean patient age was 75 years, 78% were men, and 91% were asymptomatic. A majority (81%) was white, 17% were black, and 2% were "other." All patients were retrospectively identified using CPT codes. To limit confounding variables, the researchers included only patients who had a Talent or AneuRx brand endograft (Medtronic).
Dr. Ahanchi said she had no relevant disclosures.
NAPLES, FLA. – The Anatomic Severity Grade score is a clinically valid indicator of which patients about to undergo endovascular aneurysm repair are more likely to present technical challenges, such as a need for additional endovascular implants or adjunct maneuvers, according to a retrospective study.
Increased operating time, length of hospital stay, blood loss, use of contrast, number of adjunct maneuvers, and costs were each significantly higher among 52 patients with a higher Anatomic Severity Grade (ASG) score, compared with 58 others who scored lower.
Dr. Sadaf S. Ahanchi of Eastern Virginia Medical School, Norfolk, and her colleagues reviewed patient factors, early outcomes, and costs for all patients who underwent endovascular intervention at the medical school for an infrarenal abdominal aortic aneurysm between April 2009 and July 2010. Their aim was to assess how the ASG score translated clinically regarding endovascular aneurysm repair in this patient population.
In 2002, the Society for Vascular Surgery and the American Association for Vascular Surgery devised the scoring system to grade abdominal aortic aneurysms. The ASG score would be 0 in a patient with optimal anatomy and would range up to 44 in a patient with complex anatomy, Dr. Ahanchi said. In the current study, patients were classified into a low-score group (defined as an ASG score of less than 14 points) and a high-score group (a score of 14 points or higher). Each patient’s total ASG score was calculated preoperatively based on aortic neck, aneurysm, and iliac anatomic factors, such as diameter, length, angulation, and tortuosity, using three-dimensional imaging software from M2S Inc. in West Lebanon, N.H.
The ASG score "can be easily and rapidly calculated from CT images using 3-D imaging," Dr. Ahanchi said.
Mean procedure time was longer in the high-score group, at 210 minutes vs. 113 minutes in the low-score group. The amount of contrast used was greater (at 131 mL vs. 100 mL), and blood loss was greater in the high-score group, at 886 mL vs. 227 mL in the low-score group.
Half of the high-score patients required access adjunct maneuvers, compared with only 14% of the low-score patients. Endarterectomy, patch angioplasty, and percutaneous angioplasty were the most common access-site adjuncts. Intraoperative adjuncts were required by 80% of the high-score group vs. 54% of the others; these included distal limb extension, access-site management, and iliac artery occlusive disease management.
Total mean number of endograft implants used during the cases was four in the high-score group vs. three in the low-score group, a statistically significant difference.
No patient was converted to an open repair. Length of stay was an average 5 days in the high-score group vs. 2 days in the lower-score patients, Dr. Ahanchi said.
No patient died within the first 30 days. At a mean follow-up of 5 months, there were no endograft issues or aneurysm-related deaths. Two patients in the high-score group died of unrelated causes, Dr. Ahanchi said.
Total systemic morbidity – 35% in the high score group vs. 18% in the low score group – "trended toward significant and were mostly respiratory and wound complications."
The patients with high ASG scores accounted for a 55% increase in operating room supply costs and a 48% increase in hospital charges, compared with the low-scoring patients. Mean OR supply charges were $25,765 in the high-score group vs. $16,646 in the low-score group. Total mean hospital charges were $105,153 among the high-score patients vs. $70,956 for the low-score group.
More than 90% of patients in the study had an aneurysm greater than 5 cm. Mean patient age was 75 years, 78% were men, and 91% were asymptomatic. A majority (81%) was white, 17% were black, and 2% were "other." All patients were retrospectively identified using CPT codes. To limit confounding variables, the researchers included only patients who had a Talent or AneuRx brand endograft (Medtronic).
Dr. Ahanchi said she had no relevant disclosures.
Use Clinical Insight, Biopsies to Diagnose Causes of Hypopigmentation
NEW ORLEANS – When a patient presents with patches of lighter skin and you immediately go through the most likely clinical culprits in your head, don’t forget to include hypochromia in your differential diagnosis among the common hypopigmentation disorders, Dr. James J. Nordlund said.
Although most diagnoses will not be definitive without a biopsy, your clinical suspicions are essential to alert your pathologist to look for subtle signs that in some cases can make a big difference in clinical treatment and outcomes, Dr. Nordlund said.
Mycosis fungoides, progressive macular hypomelanosis, sarcoidosis, and pityriasis alba are true hypopigmentation disorders characterized by decreases in melanin in the skin. In contrast, hypochromia or patches of light- or white-colored skin, can throw you off until the pathology report reveals normal melanin levels.
"These are some of the problems I struggle with. They are common and I see them every day, and I certainly have some successes and failures," Dr. Nordlund said at the annual meeting of the American Society of Dermatology.
A misdiagnosis of hypopigmentation "is probably the biggest problem when we don’t get a great response in patients. You have to ask yourself if the condition is related to a melanin decrease," said Dr. Nordlund, professor of clinical dermatology at Wright State University in Dayton, Ohio.
Nevus anemicus is an example of hypochromia. This vascular anomaly often mimics hypopigmentation, Dr. Nordlund said. Scars also can cause hypochromia. A Wood’s lamp might reveal excessive collagen in the dermis and decreased vascularity with scar tissue. "It appears to be depigmentation but it’s not."
Mycosis fungoides, in contrast, is a true hypopigmentation disorder. The ultraviolet glow of a Wood’s lamp, however, will be insufficient for most diagnoses. The clinical presentation is vague, so a biopsy helps to identify this condition, Dr. Nordlund said. He performs longitudinal shave biopsies if there is any doubt.
"It’s important to keep hypopigmentation mycosis fungoides in mind as a cause of hypopigmentation on the trunk and extremities," Dr. Nordlund said. "Alert your pathologist to this possible diagnosis so they can look for the subtle signs."
Mycosis fungoides is more common in darker skin, affects both children and adults, and generally has a good prognosis. Treatment response generally is better with narrow-band ultraviolet B phototherapy or psoralen and ultraviolet A (PUVA) therapy than with topical steroids.
You also may see hypopigmentation in association with sarcoidosis, a granulomatous inflammation that most often presents as red, indurated nodules on the skin, although it can affect any or all organs. A punch biopsy can confirm if a lesion is sarcoid, Dr. Nordlund said. "You really cannot be sure except with histology."
A biopsy also helps to distinguish mycosis fungoides or sarcoidosis from a third hypopigmentation disorder called progressive macular hypomelanosis. Ill-defined macules typically begin on the back and spread, sparing the face, in darker-skinned patients. A meeting attendee asked if there are diagnostic studies for this condition. Dr. Nordlund said no. "I biopsy them, because I don’t think it’s distinguishable from mycosis fungoides or sarcoidosis. That is all I do, biopsy." Pathology generally reveals a mild-to-moderate deficiency of melanin.
This is "one disorder I see too often for my own desires. It’s hard to treat," Dr. Nordlund said. PUVA is an option, but the hypopigmentation can return after treatment is discontinued. Some researchers suggest the condition is a form of Pityrosporum (now called Malassezia) infection, he added. "Minocycline 100 mg with benzoyl peroxide – I’ve tried this off-label approach – and sometimes I get a response."
There also is an idiopathic form. In idiopathic guttate hypomelanosis, melanocytes usually are present but melanization is suppressed. The epidermis will appear normal to slightly atrophic. Pathogenesis might be genetic and/or due to exposure to sunlight, "but I can’t convince myself of the sunlight etiology," Dr. Nordlund said.
Also consider pityriasis alba, characterized by hypopigmentation with slight scaling but no pruritus, in your differential diagnosis. This condition is very common in children and young adults.
"From my own experience, UV light is not very helpful," Dr. Nordlund said. "Oftentimes the mistake is to use high-potency steroids, which also suppress melanin. You essentially turn off melanin production and don’t get a good response." Instead, he recommended long-term, mild steroid treatment with a product such as Desonide Lotion (available as a generic).
Tinea versicolor is a common infection that also causes hypopigmentation. The yeastlike Malassezia furfur fungus infects the stratum corneum. The condition is easily treated with topical or oral ketoconazole, Dr. Nordlund said, but complete response can take time. "Warn patients that hypopigmentation can persist for months."
Dr. Nordlund said that he had no relevant financial disclosures.
NEW ORLEANS – When a patient presents with patches of lighter skin and you immediately go through the most likely clinical culprits in your head, don’t forget to include hypochromia in your differential diagnosis among the common hypopigmentation disorders, Dr. James J. Nordlund said.
Although most diagnoses will not be definitive without a biopsy, your clinical suspicions are essential to alert your pathologist to look for subtle signs that in some cases can make a big difference in clinical treatment and outcomes, Dr. Nordlund said.
Mycosis fungoides, progressive macular hypomelanosis, sarcoidosis, and pityriasis alba are true hypopigmentation disorders characterized by decreases in melanin in the skin. In contrast, hypochromia or patches of light- or white-colored skin, can throw you off until the pathology report reveals normal melanin levels.
"These are some of the problems I struggle with. They are common and I see them every day, and I certainly have some successes and failures," Dr. Nordlund said at the annual meeting of the American Society of Dermatology.
A misdiagnosis of hypopigmentation "is probably the biggest problem when we don’t get a great response in patients. You have to ask yourself if the condition is related to a melanin decrease," said Dr. Nordlund, professor of clinical dermatology at Wright State University in Dayton, Ohio.
Nevus anemicus is an example of hypochromia. This vascular anomaly often mimics hypopigmentation, Dr. Nordlund said. Scars also can cause hypochromia. A Wood’s lamp might reveal excessive collagen in the dermis and decreased vascularity with scar tissue. "It appears to be depigmentation but it’s not."
Mycosis fungoides, in contrast, is a true hypopigmentation disorder. The ultraviolet glow of a Wood’s lamp, however, will be insufficient for most diagnoses. The clinical presentation is vague, so a biopsy helps to identify this condition, Dr. Nordlund said. He performs longitudinal shave biopsies if there is any doubt.
"It’s important to keep hypopigmentation mycosis fungoides in mind as a cause of hypopigmentation on the trunk and extremities," Dr. Nordlund said. "Alert your pathologist to this possible diagnosis so they can look for the subtle signs."
Mycosis fungoides is more common in darker skin, affects both children and adults, and generally has a good prognosis. Treatment response generally is better with narrow-band ultraviolet B phototherapy or psoralen and ultraviolet A (PUVA) therapy than with topical steroids.
You also may see hypopigmentation in association with sarcoidosis, a granulomatous inflammation that most often presents as red, indurated nodules on the skin, although it can affect any or all organs. A punch biopsy can confirm if a lesion is sarcoid, Dr. Nordlund said. "You really cannot be sure except with histology."
A biopsy also helps to distinguish mycosis fungoides or sarcoidosis from a third hypopigmentation disorder called progressive macular hypomelanosis. Ill-defined macules typically begin on the back and spread, sparing the face, in darker-skinned patients. A meeting attendee asked if there are diagnostic studies for this condition. Dr. Nordlund said no. "I biopsy them, because I don’t think it’s distinguishable from mycosis fungoides or sarcoidosis. That is all I do, biopsy." Pathology generally reveals a mild-to-moderate deficiency of melanin.
This is "one disorder I see too often for my own desires. It’s hard to treat," Dr. Nordlund said. PUVA is an option, but the hypopigmentation can return after treatment is discontinued. Some researchers suggest the condition is a form of Pityrosporum (now called Malassezia) infection, he added. "Minocycline 100 mg with benzoyl peroxide – I’ve tried this off-label approach – and sometimes I get a response."
There also is an idiopathic form. In idiopathic guttate hypomelanosis, melanocytes usually are present but melanization is suppressed. The epidermis will appear normal to slightly atrophic. Pathogenesis might be genetic and/or due to exposure to sunlight, "but I can’t convince myself of the sunlight etiology," Dr. Nordlund said.
Also consider pityriasis alba, characterized by hypopigmentation with slight scaling but no pruritus, in your differential diagnosis. This condition is very common in children and young adults.
"From my own experience, UV light is not very helpful," Dr. Nordlund said. "Oftentimes the mistake is to use high-potency steroids, which also suppress melanin. You essentially turn off melanin production and don’t get a good response." Instead, he recommended long-term, mild steroid treatment with a product such as Desonide Lotion (available as a generic).
Tinea versicolor is a common infection that also causes hypopigmentation. The yeastlike Malassezia furfur fungus infects the stratum corneum. The condition is easily treated with topical or oral ketoconazole, Dr. Nordlund said, but complete response can take time. "Warn patients that hypopigmentation can persist for months."
Dr. Nordlund said that he had no relevant financial disclosures.
NEW ORLEANS – When a patient presents with patches of lighter skin and you immediately go through the most likely clinical culprits in your head, don’t forget to include hypochromia in your differential diagnosis among the common hypopigmentation disorders, Dr. James J. Nordlund said.
Although most diagnoses will not be definitive without a biopsy, your clinical suspicions are essential to alert your pathologist to look for subtle signs that in some cases can make a big difference in clinical treatment and outcomes, Dr. Nordlund said.
Mycosis fungoides, progressive macular hypomelanosis, sarcoidosis, and pityriasis alba are true hypopigmentation disorders characterized by decreases in melanin in the skin. In contrast, hypochromia or patches of light- or white-colored skin, can throw you off until the pathology report reveals normal melanin levels.
"These are some of the problems I struggle with. They are common and I see them every day, and I certainly have some successes and failures," Dr. Nordlund said at the annual meeting of the American Society of Dermatology.
A misdiagnosis of hypopigmentation "is probably the biggest problem when we don’t get a great response in patients. You have to ask yourself if the condition is related to a melanin decrease," said Dr. Nordlund, professor of clinical dermatology at Wright State University in Dayton, Ohio.
Nevus anemicus is an example of hypochromia. This vascular anomaly often mimics hypopigmentation, Dr. Nordlund said. Scars also can cause hypochromia. A Wood’s lamp might reveal excessive collagen in the dermis and decreased vascularity with scar tissue. "It appears to be depigmentation but it’s not."
Mycosis fungoides, in contrast, is a true hypopigmentation disorder. The ultraviolet glow of a Wood’s lamp, however, will be insufficient for most diagnoses. The clinical presentation is vague, so a biopsy helps to identify this condition, Dr. Nordlund said. He performs longitudinal shave biopsies if there is any doubt.
"It’s important to keep hypopigmentation mycosis fungoides in mind as a cause of hypopigmentation on the trunk and extremities," Dr. Nordlund said. "Alert your pathologist to this possible diagnosis so they can look for the subtle signs."
Mycosis fungoides is more common in darker skin, affects both children and adults, and generally has a good prognosis. Treatment response generally is better with narrow-band ultraviolet B phototherapy or psoralen and ultraviolet A (PUVA) therapy than with topical steroids.
You also may see hypopigmentation in association with sarcoidosis, a granulomatous inflammation that most often presents as red, indurated nodules on the skin, although it can affect any or all organs. A punch biopsy can confirm if a lesion is sarcoid, Dr. Nordlund said. "You really cannot be sure except with histology."
A biopsy also helps to distinguish mycosis fungoides or sarcoidosis from a third hypopigmentation disorder called progressive macular hypomelanosis. Ill-defined macules typically begin on the back and spread, sparing the face, in darker-skinned patients. A meeting attendee asked if there are diagnostic studies for this condition. Dr. Nordlund said no. "I biopsy them, because I don’t think it’s distinguishable from mycosis fungoides or sarcoidosis. That is all I do, biopsy." Pathology generally reveals a mild-to-moderate deficiency of melanin.
This is "one disorder I see too often for my own desires. It’s hard to treat," Dr. Nordlund said. PUVA is an option, but the hypopigmentation can return after treatment is discontinued. Some researchers suggest the condition is a form of Pityrosporum (now called Malassezia) infection, he added. "Minocycline 100 mg with benzoyl peroxide – I’ve tried this off-label approach – and sometimes I get a response."
There also is an idiopathic form. In idiopathic guttate hypomelanosis, melanocytes usually are present but melanization is suppressed. The epidermis will appear normal to slightly atrophic. Pathogenesis might be genetic and/or due to exposure to sunlight, "but I can’t convince myself of the sunlight etiology," Dr. Nordlund said.
Also consider pityriasis alba, characterized by hypopigmentation with slight scaling but no pruritus, in your differential diagnosis. This condition is very common in children and young adults.
"From my own experience, UV light is not very helpful," Dr. Nordlund said. "Oftentimes the mistake is to use high-potency steroids, which also suppress melanin. You essentially turn off melanin production and don’t get a good response." Instead, he recommended long-term, mild steroid treatment with a product such as Desonide Lotion (available as a generic).
Tinea versicolor is a common infection that also causes hypopigmentation. The yeastlike Malassezia furfur fungus infects the stratum corneum. The condition is easily treated with topical or oral ketoconazole, Dr. Nordlund said, but complete response can take time. "Warn patients that hypopigmentation can persist for months."
Dr. Nordlund said that he had no relevant financial disclosures.
EXPERT ANALYSIS FROM THE ANNUAL MEETING OF THE AMERICAN ACADEMY OF DERMATOLOGY
AAD: Lasers for Pigmentary Disorders: Yes, No, and Maybe
NEW ORLEANS - Even if you don't use lasers in your day-to-day practice of dermatology, it's helpful to know the options and their limitations to prevent unnecessary referrals, Dr. Harvey Lui said.
"For those of you who do not use lasers, hopefully you can learn which things those of us who do lasers can help you with and things we cannot," Dr. Lui said at the annual meeting of the American Academy of Dermatology.
If the question is whether to use laser treatment for pigmentation disorders, the answers vary from yes to maybe to no.
As a general guide, the depth of the dyspigmentation makes the difference with lasers, so Dr. Lui addressed their use for epidermal, mixed epidermal-dermal, or dermal disorders.
Epidermal Dyspigmentation. Lentigines are the prototype epidermal pigmentation disorder. "Lasers are highly effective, relatively simple, [and work in] one to two treatments," Dr. Lui said. Although lasers are not the only treatment option (for example, there is cryotherapy), "I get more precise effects in my practice for darker-skinned patients."
Lasers are also useful to treat a seborrheic keratosis. The advantage with lasers is an ability to target each spot to be cleared, Dr. Lui said.
In contrast, a Becker's nevus does not respond very well to laser treatment, "even though pigmentation is right there in the epidermis just begging to be removed," said Dr. Lui, medical director of the Skin Care Centre and head of the department of dermatology and skin science at the University of British Columbia, Vancouver. "There was some initial excitement using fractional photothermolysis, but I don't think that has panned out over time."
Lasers are not ideal for an epidermal nevus either, Dr. Lui said, due to a higher recurrence rate. However, he added, "in a highly motivated patient, I might do a test spot first."
A high recurrence rate and an unpredictable response are reasons to avoid laser treatment for café au lait macules, Dr. Lui said. Smaller lesions tend to respond the best. He advised caution, because there can be some paradoxical darkening in these patients.
Mixed Epidermal-Dermal Dyspigmentation. Expect a variable response to lasers for melanocytic nevi. "The best response is with small, junctional nevi." Use the highest fluence possible, Dr. Lui advised. An unknown long-term risk and incomplete pigment removal that can lead to problematic lesions are considerations. "Tell the patient that if the pigment does not completely clear, we are going to cut it out. You don't want to leave them with a lesion that meets one of the ABCD criteria [that could develop into melanoma someday]," Dr. Lui said.
Congenital melanocytic nevi may respond to a normal-mode ruby laser, but again, the long-term risk is unknown.
Dr. Lui generally does not recommend lasers for melasma. "The bottom line is that melasma will reliably darken with lasers. You can bet on it." Initial excitement about fractional lasers did not pan out, he added.
Dr. Lui also cautioned against lasers for postinflammatory hyperpigmentation. "A laser usually generates more postinflammatory hyperpigmentation. It's just a vicious circle, so the bottom line is 'Don't go there.' " Instead, convince your patient to be patient. "The best treatment is often time, and it's the cheapest, too."
Dermal Dyspigmentation. Nevus of Ota and nevus of Ito, which are more common in Asian patients, feature an excellent responsiveness to laser treatment, Dr. Lui said. "These are life-transforming types of procedures you can do for patients. This is why I became a doctor."
Lasers also are appropriate for treatment of Hori's macules. These often look like lentigines, Dr. Lui said. To distinguish between the two types of lesions, look for a blue-gray color (as opposed to a brown color with lentigines) and lesions that appear smudgy rather than well delineated.
Lasers can be used to treat blue nevi, but caution is advised, Dr. Lui said.
Dr. Lui said that he had no relevant financial disclosures.
NEW ORLEANS - Even if you don't use lasers in your day-to-day practice of dermatology, it's helpful to know the options and their limitations to prevent unnecessary referrals, Dr. Harvey Lui said.
"For those of you who do not use lasers, hopefully you can learn which things those of us who do lasers can help you with and things we cannot," Dr. Lui said at the annual meeting of the American Academy of Dermatology.
If the question is whether to use laser treatment for pigmentation disorders, the answers vary from yes to maybe to no.
As a general guide, the depth of the dyspigmentation makes the difference with lasers, so Dr. Lui addressed their use for epidermal, mixed epidermal-dermal, or dermal disorders.
Epidermal Dyspigmentation. Lentigines are the prototype epidermal pigmentation disorder. "Lasers are highly effective, relatively simple, [and work in] one to two treatments," Dr. Lui said. Although lasers are not the only treatment option (for example, there is cryotherapy), "I get more precise effects in my practice for darker-skinned patients."
Lasers are also useful to treat a seborrheic keratosis. The advantage with lasers is an ability to target each spot to be cleared, Dr. Lui said.
In contrast, a Becker's nevus does not respond very well to laser treatment, "even though pigmentation is right there in the epidermis just begging to be removed," said Dr. Lui, medical director of the Skin Care Centre and head of the department of dermatology and skin science at the University of British Columbia, Vancouver. "There was some initial excitement using fractional photothermolysis, but I don't think that has panned out over time."
Lasers are not ideal for an epidermal nevus either, Dr. Lui said, due to a higher recurrence rate. However, he added, "in a highly motivated patient, I might do a test spot first."
A high recurrence rate and an unpredictable response are reasons to avoid laser treatment for café au lait macules, Dr. Lui said. Smaller lesions tend to respond the best. He advised caution, because there can be some paradoxical darkening in these patients.
Mixed Epidermal-Dermal Dyspigmentation. Expect a variable response to lasers for melanocytic nevi. "The best response is with small, junctional nevi." Use the highest fluence possible, Dr. Lui advised. An unknown long-term risk and incomplete pigment removal that can lead to problematic lesions are considerations. "Tell the patient that if the pigment does not completely clear, we are going to cut it out. You don't want to leave them with a lesion that meets one of the ABCD criteria [that could develop into melanoma someday]," Dr. Lui said.
Congenital melanocytic nevi may respond to a normal-mode ruby laser, but again, the long-term risk is unknown.
Dr. Lui generally does not recommend lasers for melasma. "The bottom line is that melasma will reliably darken with lasers. You can bet on it." Initial excitement about fractional lasers did not pan out, he added.
Dr. Lui also cautioned against lasers for postinflammatory hyperpigmentation. "A laser usually generates more postinflammatory hyperpigmentation. It's just a vicious circle, so the bottom line is 'Don't go there.' " Instead, convince your patient to be patient. "The best treatment is often time, and it's the cheapest, too."
Dermal Dyspigmentation. Nevus of Ota and nevus of Ito, which are more common in Asian patients, feature an excellent responsiveness to laser treatment, Dr. Lui said. "These are life-transforming types of procedures you can do for patients. This is why I became a doctor."
Lasers also are appropriate for treatment of Hori's macules. These often look like lentigines, Dr. Lui said. To distinguish between the two types of lesions, look for a blue-gray color (as opposed to a brown color with lentigines) and lesions that appear smudgy rather than well delineated.
Lasers can be used to treat blue nevi, but caution is advised, Dr. Lui said.
Dr. Lui said that he had no relevant financial disclosures.
NEW ORLEANS - Even if you don't use lasers in your day-to-day practice of dermatology, it's helpful to know the options and their limitations to prevent unnecessary referrals, Dr. Harvey Lui said.
"For those of you who do not use lasers, hopefully you can learn which things those of us who do lasers can help you with and things we cannot," Dr. Lui said at the annual meeting of the American Academy of Dermatology.
If the question is whether to use laser treatment for pigmentation disorders, the answers vary from yes to maybe to no.
As a general guide, the depth of the dyspigmentation makes the difference with lasers, so Dr. Lui addressed their use for epidermal, mixed epidermal-dermal, or dermal disorders.
Epidermal Dyspigmentation. Lentigines are the prototype epidermal pigmentation disorder. "Lasers are highly effective, relatively simple, [and work in] one to two treatments," Dr. Lui said. Although lasers are not the only treatment option (for example, there is cryotherapy), "I get more precise effects in my practice for darker-skinned patients."
Lasers are also useful to treat a seborrheic keratosis. The advantage with lasers is an ability to target each spot to be cleared, Dr. Lui said.
In contrast, a Becker's nevus does not respond very well to laser treatment, "even though pigmentation is right there in the epidermis just begging to be removed," said Dr. Lui, medical director of the Skin Care Centre and head of the department of dermatology and skin science at the University of British Columbia, Vancouver. "There was some initial excitement using fractional photothermolysis, but I don't think that has panned out over time."
Lasers are not ideal for an epidermal nevus either, Dr. Lui said, due to a higher recurrence rate. However, he added, "in a highly motivated patient, I might do a test spot first."
A high recurrence rate and an unpredictable response are reasons to avoid laser treatment for café au lait macules, Dr. Lui said. Smaller lesions tend to respond the best. He advised caution, because there can be some paradoxical darkening in these patients.
Mixed Epidermal-Dermal Dyspigmentation. Expect a variable response to lasers for melanocytic nevi. "The best response is with small, junctional nevi." Use the highest fluence possible, Dr. Lui advised. An unknown long-term risk and incomplete pigment removal that can lead to problematic lesions are considerations. "Tell the patient that if the pigment does not completely clear, we are going to cut it out. You don't want to leave them with a lesion that meets one of the ABCD criteria [that could develop into melanoma someday]," Dr. Lui said.
Congenital melanocytic nevi may respond to a normal-mode ruby laser, but again, the long-term risk is unknown.
Dr. Lui generally does not recommend lasers for melasma. "The bottom line is that melasma will reliably darken with lasers. You can bet on it." Initial excitement about fractional lasers did not pan out, he added.
Dr. Lui also cautioned against lasers for postinflammatory hyperpigmentation. "A laser usually generates more postinflammatory hyperpigmentation. It's just a vicious circle, so the bottom line is 'Don't go there.' " Instead, convince your patient to be patient. "The best treatment is often time, and it's the cheapest, too."
Dermal Dyspigmentation. Nevus of Ota and nevus of Ito, which are more common in Asian patients, feature an excellent responsiveness to laser treatment, Dr. Lui said. "These are life-transforming types of procedures you can do for patients. This is why I became a doctor."
Lasers also are appropriate for treatment of Hori's macules. These often look like lentigines, Dr. Lui said. To distinguish between the two types of lesions, look for a blue-gray color (as opposed to a brown color with lentigines) and lesions that appear smudgy rather than well delineated.
Lasers can be used to treat blue nevi, but caution is advised, Dr. Lui said.
Dr. Lui said that he had no relevant financial disclosures.
EXPERT ANALYSIS FROM THE ANNUAL MEETING OF THE AMERICAN ACADEMY OF DERMATOLOGY
Should You Use Lasers for Pigmentary Disorders: Yes, No, and Maybe
NEW ORLEANS – Even if you don’t use lasers in your day-to-day practice of dermatology, it’s helpful to know the options and their limitations to prevent unnecessary referrals, Dr. Harvey Lui said.
"For those of you who do not use lasers, hopefully you can learn which things those of us who do lasers can help you with and things we cannot," Dr. Lui said at the annual meeting of the American Academy of Dermatology.
If the question is whether to use laser treatment for pigmentation disorders, the answers vary from yes to maybe to no.
As a general guide, the depth of the dyspigmentation makes the difference with lasers, so Dr. Lui addressed their use for epidermal, mixed epidermal-dermal, or dermal disorders.
Epidermal Dyspigmentation. Lentigines are the prototype epidermal pigmentation disorder. "Lasers are highly effective, relatively simple, [and work in] one to two treatments," Dr. Lui said. Although lasers are not the only treatment option (for example, there is cryotherapy), "I get more precise effects in my practice for darker-skinned patients."
Lasers are also useful to treat a seborrheic keratosis. The advantage with lasers is an ability to target each spot to be cleared, Dr. Lui said.
In contrast, a Becker’s nevus does not respond very well to laser treatment, "even though pigmentation is right there in the epidermis just begging to be removed," said Dr. Lui, medical director of the Skin Care Centre and head of the department of dermatology and skin science at the University of British Columbia, Vancouver. "There was some initial excitement using fractional photothermolysis, but I don’t think that has panned out over time."
Lasers are not ideal for an epidermal nevus either, Dr. Lui said, due to a higher recurrence rate. However, he added, "in a highly motivated patient, I might do a test spot first."
A high recurrence rate and an unpredictable response are reasons to avoid laser treatment for café au lait macules, Dr. Lui said. Smaller lesions tend to respond the best. He advised caution, because there can be some paradoxical darkening in these patients.
Mixed Epidermal-Dermal Dyspigmentation. Expect a variable response to lasers for melanocytic nevi. "The best response is with small, junctional nevi." Use the highest fluence possible, Dr. Lui advised. An unknown long-term risk and incomplete pigment removal that can lead to problematic lesions are considerations. "Tell the patient that if the pigment does not completely clear, we are going to cut it out. You don’t want to leave them with a lesion that meets one of the ABCD criteria [that could develop into melanoma someday]," Dr. Lui said.
Congenital melanocytic nevi may respond to a normal-mode ruby laser, but again, the long-term risk is unknown.
Dr. Lui generally does not recommend lasers for melasma. "The bottom line is that melasma will reliably darken with lasers. You can bet on it." Initial excitement about fractional lasers did not pan out, he added.
Dr. Lui also cautioned against lasers for postinflammatory hyperpigmentation. "A laser usually generates more postinflammatory hyperpigmentation. It’s just a vicious circle, so the bottom line is ‘Don’t go there.’ " Instead, convince your patient to be patient. "The best treatment is often time, and it’s the cheapest, too."
Dermal Dyspigmentation. Nevus of Ota and nevus of Ito, which are more common in Asian patients, feature an excellent responsiveness to laser treatment, Dr. Lui said. "These are life-transforming types of procedures you can do for patients. This is why I became a doctor."
Lasers also are appropriate for treatment of Hori’s macules. These often look like lentigines, Dr. Lui said. To distinguish between the two types of lesions, look for a blue-gray color (as opposed to a brown color with lentigines) and lesions that appear smudgy rather than well delineated.
Lasers can be used to treat blue nevi, but caution is advised, Dr. Lui said.
Dr. Lui said that he had no relevant financial disclosures.
NEW ORLEANS – Even if you don’t use lasers in your day-to-day practice of dermatology, it’s helpful to know the options and their limitations to prevent unnecessary referrals, Dr. Harvey Lui said.
"For those of you who do not use lasers, hopefully you can learn which things those of us who do lasers can help you with and things we cannot," Dr. Lui said at the annual meeting of the American Academy of Dermatology.
If the question is whether to use laser treatment for pigmentation disorders, the answers vary from yes to maybe to no.
As a general guide, the depth of the dyspigmentation makes the difference with lasers, so Dr. Lui addressed their use for epidermal, mixed epidermal-dermal, or dermal disorders.
Epidermal Dyspigmentation. Lentigines are the prototype epidermal pigmentation disorder. "Lasers are highly effective, relatively simple, [and work in] one to two treatments," Dr. Lui said. Although lasers are not the only treatment option (for example, there is cryotherapy), "I get more precise effects in my practice for darker-skinned patients."
Lasers are also useful to treat a seborrheic keratosis. The advantage with lasers is an ability to target each spot to be cleared, Dr. Lui said.
In contrast, a Becker’s nevus does not respond very well to laser treatment, "even though pigmentation is right there in the epidermis just begging to be removed," said Dr. Lui, medical director of the Skin Care Centre and head of the department of dermatology and skin science at the University of British Columbia, Vancouver. "There was some initial excitement using fractional photothermolysis, but I don’t think that has panned out over time."
Lasers are not ideal for an epidermal nevus either, Dr. Lui said, due to a higher recurrence rate. However, he added, "in a highly motivated patient, I might do a test spot first."
A high recurrence rate and an unpredictable response are reasons to avoid laser treatment for café au lait macules, Dr. Lui said. Smaller lesions tend to respond the best. He advised caution, because there can be some paradoxical darkening in these patients.
Mixed Epidermal-Dermal Dyspigmentation. Expect a variable response to lasers for melanocytic nevi. "The best response is with small, junctional nevi." Use the highest fluence possible, Dr. Lui advised. An unknown long-term risk and incomplete pigment removal that can lead to problematic lesions are considerations. "Tell the patient that if the pigment does not completely clear, we are going to cut it out. You don’t want to leave them with a lesion that meets one of the ABCD criteria [that could develop into melanoma someday]," Dr. Lui said.
Congenital melanocytic nevi may respond to a normal-mode ruby laser, but again, the long-term risk is unknown.
Dr. Lui generally does not recommend lasers for melasma. "The bottom line is that melasma will reliably darken with lasers. You can bet on it." Initial excitement about fractional lasers did not pan out, he added.
Dr. Lui also cautioned against lasers for postinflammatory hyperpigmentation. "A laser usually generates more postinflammatory hyperpigmentation. It’s just a vicious circle, so the bottom line is ‘Don’t go there.’ " Instead, convince your patient to be patient. "The best treatment is often time, and it’s the cheapest, too."
Dermal Dyspigmentation. Nevus of Ota and nevus of Ito, which are more common in Asian patients, feature an excellent responsiveness to laser treatment, Dr. Lui said. "These are life-transforming types of procedures you can do for patients. This is why I became a doctor."
Lasers also are appropriate for treatment of Hori’s macules. These often look like lentigines, Dr. Lui said. To distinguish between the two types of lesions, look for a blue-gray color (as opposed to a brown color with lentigines) and lesions that appear smudgy rather than well delineated.
Lasers can be used to treat blue nevi, but caution is advised, Dr. Lui said.
Dr. Lui said that he had no relevant financial disclosures.
NEW ORLEANS – Even if you don’t use lasers in your day-to-day practice of dermatology, it’s helpful to know the options and their limitations to prevent unnecessary referrals, Dr. Harvey Lui said.
"For those of you who do not use lasers, hopefully you can learn which things those of us who do lasers can help you with and things we cannot," Dr. Lui said at the annual meeting of the American Academy of Dermatology.
If the question is whether to use laser treatment for pigmentation disorders, the answers vary from yes to maybe to no.
As a general guide, the depth of the dyspigmentation makes the difference with lasers, so Dr. Lui addressed their use for epidermal, mixed epidermal-dermal, or dermal disorders.
Epidermal Dyspigmentation. Lentigines are the prototype epidermal pigmentation disorder. "Lasers are highly effective, relatively simple, [and work in] one to two treatments," Dr. Lui said. Although lasers are not the only treatment option (for example, there is cryotherapy), "I get more precise effects in my practice for darker-skinned patients."
Lasers are also useful to treat a seborrheic keratosis. The advantage with lasers is an ability to target each spot to be cleared, Dr. Lui said.
In contrast, a Becker’s nevus does not respond very well to laser treatment, "even though pigmentation is right there in the epidermis just begging to be removed," said Dr. Lui, medical director of the Skin Care Centre and head of the department of dermatology and skin science at the University of British Columbia, Vancouver. "There was some initial excitement using fractional photothermolysis, but I don’t think that has panned out over time."
Lasers are not ideal for an epidermal nevus either, Dr. Lui said, due to a higher recurrence rate. However, he added, "in a highly motivated patient, I might do a test spot first."
A high recurrence rate and an unpredictable response are reasons to avoid laser treatment for café au lait macules, Dr. Lui said. Smaller lesions tend to respond the best. He advised caution, because there can be some paradoxical darkening in these patients.
Mixed Epidermal-Dermal Dyspigmentation. Expect a variable response to lasers for melanocytic nevi. "The best response is with small, junctional nevi." Use the highest fluence possible, Dr. Lui advised. An unknown long-term risk and incomplete pigment removal that can lead to problematic lesions are considerations. "Tell the patient that if the pigment does not completely clear, we are going to cut it out. You don’t want to leave them with a lesion that meets one of the ABCD criteria [that could develop into melanoma someday]," Dr. Lui said.
Congenital melanocytic nevi may respond to a normal-mode ruby laser, but again, the long-term risk is unknown.
Dr. Lui generally does not recommend lasers for melasma. "The bottom line is that melasma will reliably darken with lasers. You can bet on it." Initial excitement about fractional lasers did not pan out, he added.
Dr. Lui also cautioned against lasers for postinflammatory hyperpigmentation. "A laser usually generates more postinflammatory hyperpigmentation. It’s just a vicious circle, so the bottom line is ‘Don’t go there.’ " Instead, convince your patient to be patient. "The best treatment is often time, and it’s the cheapest, too."
Dermal Dyspigmentation. Nevus of Ota and nevus of Ito, which are more common in Asian patients, feature an excellent responsiveness to laser treatment, Dr. Lui said. "These are life-transforming types of procedures you can do for patients. This is why I became a doctor."
Lasers also are appropriate for treatment of Hori’s macules. These often look like lentigines, Dr. Lui said. To distinguish between the two types of lesions, look for a blue-gray color (as opposed to a brown color with lentigines) and lesions that appear smudgy rather than well delineated.
Lasers can be used to treat blue nevi, but caution is advised, Dr. Lui said.
Dr. Lui said that he had no relevant financial disclosures.
EXPERT ANALYSIS FROM THE ANNUAL MEETING OF THE AMERICAN ACADEMY OF DERMATOLOGY
AAD: Toxic Epidermal Necrolysis Supportive Care Saves Lives
NEW ORLEANS – Their presentation can be alarming, even for dermatologists accustomed to seeing all kinds of adverse skin manifestations. Widespread necrosis, skin detachment, erythema, large bullae, and more are seen in patients with the life-threatening drug eruption, toxic epidermal necrolysis.
Medical management with intravenous immunoglobulin and a focus on supportive care save lives at the University of Miami, a toxic epidermal necrolysis (TEN) referral center.
"The survival rate is extremely low for this set of patients," Dr. Carlos A. Ricotti said at the annual meeting of the American Academy of Dermatology. But "the outcome at the University of Miami is very good. We see these patients, and we have a good understanding they are going to leave the hospital well."
Medical management is swift and comprehensive. "Assume there will be fluid loss, possible infection, impaired thermal regulation, altered immunity, and increased energy expenditure," Dr. Ricotti said. "Each of these has to be addressed."
In addition, despite a clinical appearance similar to that of burns, recognize that patients with TEN differ from burn patients in important ways, said Dr. Ricotti, who is on the dermatology staff at the University of Miami Hospital. TEN patients typically feature less edema, minimal vascular damage, and less damage to regenerative tissue, leading to faster re-epithelialization, compared with burn patients. "The rate of healing is much faster."
The hospital’s dermatologic medical management of TEN begins with withdrawal of offending medication. Because patients present with a burning sensation, pain control is essential to achieve comfort and to decrease their movement during recovery.
Think in terms of "acute skin failure" when providing supportive care, Dr. Ricotti said. Consider medical ICU or a burn unit admission; an air mattress with pressure ulcer prophylaxis; nonstick sheets and heating blankets; and maintenance of room temperature at 30° C.
"We don’t do debridement," Dr. Ricotti said. Pathology reveals that the entire dermis is not necrotic. The remaining viable tissue can act as a natural biologic dressing that may retake as a graft. "This speeds re-epithelialization ... and we believe this speeds recovery of the patient."
By day 6-10 of admission, most of the skin erosions re-epithelialize (as opposed to second-degree burns, which can take 14 days or longer). Because of this rapid tissue regeneration, patients require high caloric intake, which can include total parenteral nutrition or feeding via a nasogastric tube.
Strict fluid monitoring is essential, Dr. Ricotti said. "We feel very strongly about [fluid management]. We feel this plays an important role in our excellent outcomes." They typically administer IV fluids with half normal saline and 20 mEq KCl. Fluids in and out are monitored with a urine output goal of 40-80 mL/hr.
"We know that in TEN, there is potential for alveolar/epithelial barrier alteration due to the systemic nature of the disease," Dr. Ricotti said. "Our working hypothesis is that by decreasing fluid overload, we can minimize pulmonary involvement and improve outcomes." He recommended reading the results of a prospective clinical trial for more insight into the management of pulmonary complications (Intensive Care Med. 1997;23:1237-44).
Not only is intravenous immunoglobulin (IVIG) therapy important, the total dose makes a difference, Dr. Ricotti said. Survival increases significantly with each 1-g/kg increase in IVIG dose (odds ratio 4.2), according to a review article (Expert Rev. Dermatol. 2007;2:299-303).
A typical IVIG protocol at the hospital is 1 g/kg per day for 4 days, Dr. Ricotti said in response to a meeting attendee’s question. "The higher the dosage, the better the outcome." Although IVIG is essential, so is treatment at a center of excellence with special expertise in treating patients with drug eruptions.
TEN know-how also is important, he said, because "with its low incidence, it’s difficult to perform large, multicenter prospective trials."
Infections can occur. Cutaneous infection, pneumonia, and subsequent life-threatening sepsis are well-recognized complications of TEN. However, "we refrain from using empiric antibiotic therapy," Dr. Ricotti said.
They do routinely provide anticoagulation prophylaxis with heparin to prevent deep vein thrombosis, gastrointestinal prophylaxis with proton pump inhibitors, and eye care with tobramycin and dexamethasone.
TEN is relatively rare, with an estimated incidence of 1 person per million per year. Even so, "we see drug eruptions all the time in inpatient units," Dr. Ricotti said.
In addition to TEN (classified as "with spots" or "without spots" by extent of skin involvement), other drug eruptions include erythema multiforme major, Stevens-Johnson syndrome (SJS), and patients who have an overlap of SJS and TEN. Consider staphylococcal scalded skin syndrome and TEN with drug hypersensitivity syndrome in your differential diagnosis, he added.
Dr. Ricotti said he had no relevant disclosures.
NEW ORLEANS – Their presentation can be alarming, even for dermatologists accustomed to seeing all kinds of adverse skin manifestations. Widespread necrosis, skin detachment, erythema, large bullae, and more are seen in patients with the life-threatening drug eruption, toxic epidermal necrolysis.
Medical management with intravenous immunoglobulin and a focus on supportive care save lives at the University of Miami, a toxic epidermal necrolysis (TEN) referral center.
"The survival rate is extremely low for this set of patients," Dr. Carlos A. Ricotti said at the annual meeting of the American Academy of Dermatology. But "the outcome at the University of Miami is very good. We see these patients, and we have a good understanding they are going to leave the hospital well."
Medical management is swift and comprehensive. "Assume there will be fluid loss, possible infection, impaired thermal regulation, altered immunity, and increased energy expenditure," Dr. Ricotti said. "Each of these has to be addressed."
In addition, despite a clinical appearance similar to that of burns, recognize that patients with TEN differ from burn patients in important ways, said Dr. Ricotti, who is on the dermatology staff at the University of Miami Hospital. TEN patients typically feature less edema, minimal vascular damage, and less damage to regenerative tissue, leading to faster re-epithelialization, compared with burn patients. "The rate of healing is much faster."
The hospital’s dermatologic medical management of TEN begins with withdrawal of offending medication. Because patients present with a burning sensation, pain control is essential to achieve comfort and to decrease their movement during recovery.
Think in terms of "acute skin failure" when providing supportive care, Dr. Ricotti said. Consider medical ICU or a burn unit admission; an air mattress with pressure ulcer prophylaxis; nonstick sheets and heating blankets; and maintenance of room temperature at 30° C.
"We don’t do debridement," Dr. Ricotti said. Pathology reveals that the entire dermis is not necrotic. The remaining viable tissue can act as a natural biologic dressing that may retake as a graft. "This speeds re-epithelialization ... and we believe this speeds recovery of the patient."
By day 6-10 of admission, most of the skin erosions re-epithelialize (as opposed to second-degree burns, which can take 14 days or longer). Because of this rapid tissue regeneration, patients require high caloric intake, which can include total parenteral nutrition or feeding via a nasogastric tube.
Strict fluid monitoring is essential, Dr. Ricotti said. "We feel very strongly about [fluid management]. We feel this plays an important role in our excellent outcomes." They typically administer IV fluids with half normal saline and 20 mEq KCl. Fluids in and out are monitored with a urine output goal of 40-80 mL/hr.
"We know that in TEN, there is potential for alveolar/epithelial barrier alteration due to the systemic nature of the disease," Dr. Ricotti said. "Our working hypothesis is that by decreasing fluid overload, we can minimize pulmonary involvement and improve outcomes." He recommended reading the results of a prospective clinical trial for more insight into the management of pulmonary complications (Intensive Care Med. 1997;23:1237-44).
Not only is intravenous immunoglobulin (IVIG) therapy important, the total dose makes a difference, Dr. Ricotti said. Survival increases significantly with each 1-g/kg increase in IVIG dose (odds ratio 4.2), according to a review article (Expert Rev. Dermatol. 2007;2:299-303).
A typical IVIG protocol at the hospital is 1 g/kg per day for 4 days, Dr. Ricotti said in response to a meeting attendee’s question. "The higher the dosage, the better the outcome." Although IVIG is essential, so is treatment at a center of excellence with special expertise in treating patients with drug eruptions.
TEN know-how also is important, he said, because "with its low incidence, it’s difficult to perform large, multicenter prospective trials."
Infections can occur. Cutaneous infection, pneumonia, and subsequent life-threatening sepsis are well-recognized complications of TEN. However, "we refrain from using empiric antibiotic therapy," Dr. Ricotti said.
They do routinely provide anticoagulation prophylaxis with heparin to prevent deep vein thrombosis, gastrointestinal prophylaxis with proton pump inhibitors, and eye care with tobramycin and dexamethasone.
TEN is relatively rare, with an estimated incidence of 1 person per million per year. Even so, "we see drug eruptions all the time in inpatient units," Dr. Ricotti said.
In addition to TEN (classified as "with spots" or "without spots" by extent of skin involvement), other drug eruptions include erythema multiforme major, Stevens-Johnson syndrome (SJS), and patients who have an overlap of SJS and TEN. Consider staphylococcal scalded skin syndrome and TEN with drug hypersensitivity syndrome in your differential diagnosis, he added.
Dr. Ricotti said he had no relevant disclosures.
NEW ORLEANS – Their presentation can be alarming, even for dermatologists accustomed to seeing all kinds of adverse skin manifestations. Widespread necrosis, skin detachment, erythema, large bullae, and more are seen in patients with the life-threatening drug eruption, toxic epidermal necrolysis.
Medical management with intravenous immunoglobulin and a focus on supportive care save lives at the University of Miami, a toxic epidermal necrolysis (TEN) referral center.
"The survival rate is extremely low for this set of patients," Dr. Carlos A. Ricotti said at the annual meeting of the American Academy of Dermatology. But "the outcome at the University of Miami is very good. We see these patients, and we have a good understanding they are going to leave the hospital well."
Medical management is swift and comprehensive. "Assume there will be fluid loss, possible infection, impaired thermal regulation, altered immunity, and increased energy expenditure," Dr. Ricotti said. "Each of these has to be addressed."
In addition, despite a clinical appearance similar to that of burns, recognize that patients with TEN differ from burn patients in important ways, said Dr. Ricotti, who is on the dermatology staff at the University of Miami Hospital. TEN patients typically feature less edema, minimal vascular damage, and less damage to regenerative tissue, leading to faster re-epithelialization, compared with burn patients. "The rate of healing is much faster."
The hospital’s dermatologic medical management of TEN begins with withdrawal of offending medication. Because patients present with a burning sensation, pain control is essential to achieve comfort and to decrease their movement during recovery.
Think in terms of "acute skin failure" when providing supportive care, Dr. Ricotti said. Consider medical ICU or a burn unit admission; an air mattress with pressure ulcer prophylaxis; nonstick sheets and heating blankets; and maintenance of room temperature at 30° C.
"We don’t do debridement," Dr. Ricotti said. Pathology reveals that the entire dermis is not necrotic. The remaining viable tissue can act as a natural biologic dressing that may retake as a graft. "This speeds re-epithelialization ... and we believe this speeds recovery of the patient."
By day 6-10 of admission, most of the skin erosions re-epithelialize (as opposed to second-degree burns, which can take 14 days or longer). Because of this rapid tissue regeneration, patients require high caloric intake, which can include total parenteral nutrition or feeding via a nasogastric tube.
Strict fluid monitoring is essential, Dr. Ricotti said. "We feel very strongly about [fluid management]. We feel this plays an important role in our excellent outcomes." They typically administer IV fluids with half normal saline and 20 mEq KCl. Fluids in and out are monitored with a urine output goal of 40-80 mL/hr.
"We know that in TEN, there is potential for alveolar/epithelial barrier alteration due to the systemic nature of the disease," Dr. Ricotti said. "Our working hypothesis is that by decreasing fluid overload, we can minimize pulmonary involvement and improve outcomes." He recommended reading the results of a prospective clinical trial for more insight into the management of pulmonary complications (Intensive Care Med. 1997;23:1237-44).
Not only is intravenous immunoglobulin (IVIG) therapy important, the total dose makes a difference, Dr. Ricotti said. Survival increases significantly with each 1-g/kg increase in IVIG dose (odds ratio 4.2), according to a review article (Expert Rev. Dermatol. 2007;2:299-303).
A typical IVIG protocol at the hospital is 1 g/kg per day for 4 days, Dr. Ricotti said in response to a meeting attendee’s question. "The higher the dosage, the better the outcome." Although IVIG is essential, so is treatment at a center of excellence with special expertise in treating patients with drug eruptions.
TEN know-how also is important, he said, because "with its low incidence, it’s difficult to perform large, multicenter prospective trials."
Infections can occur. Cutaneous infection, pneumonia, and subsequent life-threatening sepsis are well-recognized complications of TEN. However, "we refrain from using empiric antibiotic therapy," Dr. Ricotti said.
They do routinely provide anticoagulation prophylaxis with heparin to prevent deep vein thrombosis, gastrointestinal prophylaxis with proton pump inhibitors, and eye care with tobramycin and dexamethasone.
TEN is relatively rare, with an estimated incidence of 1 person per million per year. Even so, "we see drug eruptions all the time in inpatient units," Dr. Ricotti said.
In addition to TEN (classified as "with spots" or "without spots" by extent of skin involvement), other drug eruptions include erythema multiforme major, Stevens-Johnson syndrome (SJS), and patients who have an overlap of SJS and TEN. Consider staphylococcal scalded skin syndrome and TEN with drug hypersensitivity syndrome in your differential diagnosis, he added.
Dr. Ricotti said he had no relevant disclosures.
EXPERT ANALYSIS FROM THE ANNUAL MEETING OF THE AMERICAN ACADEMY OF DERMATOLOGY
AAD: TEN Responds to IVIG Therapy, Supportive Care
NEW ORLEANS - Their presentation can be alarming, even for dermatologists accustomed to seeing all kinds of adverse skin manifestations. Widespread necrosis, skin detachment, erythema, large bullae, and more are seen in patients with the life-threatening drug eruption, toxic epidermal necrolysis.
Medical management with intravenous immunoglobulin and a focus on supportive care save lives at the University of Miami, a toxic epidermal necrolysis (TEN) referral center.
"The survival rate is extremely low for this set of patients," Dr. Carlos A. Ricotti said at the annual meeting of the American Academy of Dermatology. But "the outcome at the University of Miami is very good. We see these patients, and we have a good understanding they are going to leave the hospital well."
Medical management is swift and comprehensive. "Assume there will be fluid loss, possible infection, impaired thermal regulation, altered immunity, and increased energy expenditure," Dr. Ricotti said. "Each of these has to be addressed."
In addition, despite a clinical appearance similar to that of burns, recognize that patients with TEN differ from burn patients in important ways, said Dr. Ricotti, who is on the dermatology staff at the University of Miami Hospital. TEN patients typically feature less edema, minimal vascular damage, and less damage to regenerative tissue, leading to faster re-epithelialization, compared with burn patients. "The rate of healing is much faster."
The hospital's dermatologic medical management of TEN begins with withdrawal of offending medication. Because patients present with a burning sensation, pain control is essential to achieve comfort and to decrease their movement during recovery.
Think in terms of "acute skin failure" when providing supportive care, Dr. Ricotti said. Consider medical ICU or a burn unit admission; an air mattress with pressure ulcer prophylaxis; nonstick sheets and heating blankets; and maintenance of room temperature at 30° C.
"We don't do debridement," Dr. Ricotti said. Pathology reveals that the entire dermis is not necrotic. The remaining viable tissue can act as a natural biologic dressing that may retake as a graft. "This speeds re-epithelialization ... and we believe this speeds recovery of the patient."
By day 6-10 of admission, most of the skin erosions re-epithelialize (as opposed to second-degree burns, which can take 14 days or longer). Because of this rapid tissue regeneration, patients require high caloric intake, which can include total parenteral nutrition or feeding via a nasogastric tube.
Strict fluid monitoring is essential, Dr. Ricotti said. "We feel very strongly about [fluid management]. We feel this plays an important role in our excellent outcomes." They typically administer IV fluids with half normal saline and 20 mEq KCl. Fluids in and out are monitored with a urine output goal of 40-80 mL/hr.
"We know that in TEN, there is potential for alveolar/epithelial barrier alteration due to the systemic nature of the disease," Dr. Ricotti said. "Our working hypothesis is that by decreasing fluid overload, we can minimize pulmonary involvement and improve outcomes." He recommended reading the results of a prospective clinical trial for more insight into the management of pulmonary complications (Intensive Care Med. 1997;23:1237-44).
Not only is intravenous immunoglobulin (IVIG) therapy important, the total dose makes a difference, Dr. Ricotti said. Survival increases significantly with each 1-g/kg increase in IVIG dose (odds ratio 4.2), according to a review article (Expert Rev. Dermatol. 2007;2:299-303).
A typical IVIG protocol at the hospital is 1 g/kg per day for 4 days, Dr. Ricotti said in response to a meeting attendee’s question. "The higher the dosage, the better the outcome." Although IVIG is essential, so is treatment at a center of excellence with special expertise in treating patients with drug eruptions.
TEN know-how also is important, he said, because "with its low incidence, it's difficult to perform large, multicenter prospective trials."
Infections can occur. Cutaneous infection, pneumonia, and subsequent life-threatening sepsis are well-recognized complications of TEN. However, "we refrain from using empiric antibiotic therapy," Dr. Ricotti said.
They do routinely provide anticoagulation prophylaxis with heparin to prevent deep vein thrombosis, gastrointestinal prophylaxis with proton pump inhibitors, and eye care with tobramycin and dexamethasone.
TEN is relatively rare, with an estimated incidence of 1 person per million per year. Even so, "we see drug eruptions all the time in inpatient units," Dr. Ricotti said.
In addition to TEN (classified as "with spots" or "without spots" by extent of skin involvement), other drug eruptions include erythema multiforme major, Stevens-Johnson syndrome (SJS), and patients who have an overlap of SJS and TEN. Consider staphylococcal scalded skin syndrome and TEN with drug hypersensitivity syndrome in your differential diagnosis, he added.
Dr. Ricotti said he had no relevant disclosures.
NEW ORLEANS - Their presentation can be alarming, even for dermatologists accustomed to seeing all kinds of adverse skin manifestations. Widespread necrosis, skin detachment, erythema, large bullae, and more are seen in patients with the life-threatening drug eruption, toxic epidermal necrolysis.
Medical management with intravenous immunoglobulin and a focus on supportive care save lives at the University of Miami, a toxic epidermal necrolysis (TEN) referral center.
"The survival rate is extremely low for this set of patients," Dr. Carlos A. Ricotti said at the annual meeting of the American Academy of Dermatology. But "the outcome at the University of Miami is very good. We see these patients, and we have a good understanding they are going to leave the hospital well."
Medical management is swift and comprehensive. "Assume there will be fluid loss, possible infection, impaired thermal regulation, altered immunity, and increased energy expenditure," Dr. Ricotti said. "Each of these has to be addressed."
In addition, despite a clinical appearance similar to that of burns, recognize that patients with TEN differ from burn patients in important ways, said Dr. Ricotti, who is on the dermatology staff at the University of Miami Hospital. TEN patients typically feature less edema, minimal vascular damage, and less damage to regenerative tissue, leading to faster re-epithelialization, compared with burn patients. "The rate of healing is much faster."
The hospital's dermatologic medical management of TEN begins with withdrawal of offending medication. Because patients present with a burning sensation, pain control is essential to achieve comfort and to decrease their movement during recovery.
Think in terms of "acute skin failure" when providing supportive care, Dr. Ricotti said. Consider medical ICU or a burn unit admission; an air mattress with pressure ulcer prophylaxis; nonstick sheets and heating blankets; and maintenance of room temperature at 30° C.
"We don't do debridement," Dr. Ricotti said. Pathology reveals that the entire dermis is not necrotic. The remaining viable tissue can act as a natural biologic dressing that may retake as a graft. "This speeds re-epithelialization ... and we believe this speeds recovery of the patient."
By day 6-10 of admission, most of the skin erosions re-epithelialize (as opposed to second-degree burns, which can take 14 days or longer). Because of this rapid tissue regeneration, patients require high caloric intake, which can include total parenteral nutrition or feeding via a nasogastric tube.
Strict fluid monitoring is essential, Dr. Ricotti said. "We feel very strongly about [fluid management]. We feel this plays an important role in our excellent outcomes." They typically administer IV fluids with half normal saline and 20 mEq KCl. Fluids in and out are monitored with a urine output goal of 40-80 mL/hr.
"We know that in TEN, there is potential for alveolar/epithelial barrier alteration due to the systemic nature of the disease," Dr. Ricotti said. "Our working hypothesis is that by decreasing fluid overload, we can minimize pulmonary involvement and improve outcomes." He recommended reading the results of a prospective clinical trial for more insight into the management of pulmonary complications (Intensive Care Med. 1997;23:1237-44).
Not only is intravenous immunoglobulin (IVIG) therapy important, the total dose makes a difference, Dr. Ricotti said. Survival increases significantly with each 1-g/kg increase in IVIG dose (odds ratio 4.2), according to a review article (Expert Rev. Dermatol. 2007;2:299-303).
A typical IVIG protocol at the hospital is 1 g/kg per day for 4 days, Dr. Ricotti said in response to a meeting attendee’s question. "The higher the dosage, the better the outcome." Although IVIG is essential, so is treatment at a center of excellence with special expertise in treating patients with drug eruptions.
TEN know-how also is important, he said, because "with its low incidence, it's difficult to perform large, multicenter prospective trials."
Infections can occur. Cutaneous infection, pneumonia, and subsequent life-threatening sepsis are well-recognized complications of TEN. However, "we refrain from using empiric antibiotic therapy," Dr. Ricotti said.
They do routinely provide anticoagulation prophylaxis with heparin to prevent deep vein thrombosis, gastrointestinal prophylaxis with proton pump inhibitors, and eye care with tobramycin and dexamethasone.
TEN is relatively rare, with an estimated incidence of 1 person per million per year. Even so, "we see drug eruptions all the time in inpatient units," Dr. Ricotti said.
In addition to TEN (classified as "with spots" or "without spots" by extent of skin involvement), other drug eruptions include erythema multiforme major, Stevens-Johnson syndrome (SJS), and patients who have an overlap of SJS and TEN. Consider staphylococcal scalded skin syndrome and TEN with drug hypersensitivity syndrome in your differential diagnosis, he added.
Dr. Ricotti said he had no relevant disclosures.
NEW ORLEANS - Their presentation can be alarming, even for dermatologists accustomed to seeing all kinds of adverse skin manifestations. Widespread necrosis, skin detachment, erythema, large bullae, and more are seen in patients with the life-threatening drug eruption, toxic epidermal necrolysis.
Medical management with intravenous immunoglobulin and a focus on supportive care save lives at the University of Miami, a toxic epidermal necrolysis (TEN) referral center.
"The survival rate is extremely low for this set of patients," Dr. Carlos A. Ricotti said at the annual meeting of the American Academy of Dermatology. But "the outcome at the University of Miami is very good. We see these patients, and we have a good understanding they are going to leave the hospital well."
Medical management is swift and comprehensive. "Assume there will be fluid loss, possible infection, impaired thermal regulation, altered immunity, and increased energy expenditure," Dr. Ricotti said. "Each of these has to be addressed."
In addition, despite a clinical appearance similar to that of burns, recognize that patients with TEN differ from burn patients in important ways, said Dr. Ricotti, who is on the dermatology staff at the University of Miami Hospital. TEN patients typically feature less edema, minimal vascular damage, and less damage to regenerative tissue, leading to faster re-epithelialization, compared with burn patients. "The rate of healing is much faster."
The hospital's dermatologic medical management of TEN begins with withdrawal of offending medication. Because patients present with a burning sensation, pain control is essential to achieve comfort and to decrease their movement during recovery.
Think in terms of "acute skin failure" when providing supportive care, Dr. Ricotti said. Consider medical ICU or a burn unit admission; an air mattress with pressure ulcer prophylaxis; nonstick sheets and heating blankets; and maintenance of room temperature at 30° C.
"We don't do debridement," Dr. Ricotti said. Pathology reveals that the entire dermis is not necrotic. The remaining viable tissue can act as a natural biologic dressing that may retake as a graft. "This speeds re-epithelialization ... and we believe this speeds recovery of the patient."
By day 6-10 of admission, most of the skin erosions re-epithelialize (as opposed to second-degree burns, which can take 14 days or longer). Because of this rapid tissue regeneration, patients require high caloric intake, which can include total parenteral nutrition or feeding via a nasogastric tube.
Strict fluid monitoring is essential, Dr. Ricotti said. "We feel very strongly about [fluid management]. We feel this plays an important role in our excellent outcomes." They typically administer IV fluids with half normal saline and 20 mEq KCl. Fluids in and out are monitored with a urine output goal of 40-80 mL/hr.
"We know that in TEN, there is potential for alveolar/epithelial barrier alteration due to the systemic nature of the disease," Dr. Ricotti said. "Our working hypothesis is that by decreasing fluid overload, we can minimize pulmonary involvement and improve outcomes." He recommended reading the results of a prospective clinical trial for more insight into the management of pulmonary complications (Intensive Care Med. 1997;23:1237-44).
Not only is intravenous immunoglobulin (IVIG) therapy important, the total dose makes a difference, Dr. Ricotti said. Survival increases significantly with each 1-g/kg increase in IVIG dose (odds ratio 4.2), according to a review article (Expert Rev. Dermatol. 2007;2:299-303).
A typical IVIG protocol at the hospital is 1 g/kg per day for 4 days, Dr. Ricotti said in response to a meeting attendee’s question. "The higher the dosage, the better the outcome." Although IVIG is essential, so is treatment at a center of excellence with special expertise in treating patients with drug eruptions.
TEN know-how also is important, he said, because "with its low incidence, it's difficult to perform large, multicenter prospective trials."
Infections can occur. Cutaneous infection, pneumonia, and subsequent life-threatening sepsis are well-recognized complications of TEN. However, "we refrain from using empiric antibiotic therapy," Dr. Ricotti said.
They do routinely provide anticoagulation prophylaxis with heparin to prevent deep vein thrombosis, gastrointestinal prophylaxis with proton pump inhibitors, and eye care with tobramycin and dexamethasone.
TEN is relatively rare, with an estimated incidence of 1 person per million per year. Even so, "we see drug eruptions all the time in inpatient units," Dr. Ricotti said.
In addition to TEN (classified as "with spots" or "without spots" by extent of skin involvement), other drug eruptions include erythema multiforme major, Stevens-Johnson syndrome (SJS), and patients who have an overlap of SJS and TEN. Consider staphylococcal scalded skin syndrome and TEN with drug hypersensitivity syndrome in your differential diagnosis, he added.
Dr. Ricotti said he had no relevant disclosures.
EXPERT ANALYSIS FROM THE ANNUAL MEETING OF THE AMERICAN ACADEMY OF DERMATOLOGY