SNOWMASS, COLO. – As William T. Abraham, MD, speaks to colleagues around the country about heart failure therapy, he has noticed that the first-in-class drug ivabradine remains below the radar of most physicians.

“I’ve found that this is an agent that very few people know about, even though it’s been FDA [Food and Drug Administration] approved for about 3 years. It’s used fairly extensively in Europe because that’s where the pivotal SHIFT trial was done, but not very much in the United States,” according to Dr. Abraham, professor of medicine, physiology, and cell biology and director of the division of cardiovascular medicine at Ohio State University in Columbus.

That’s likely to change as word spreads about the May 2016 update of the American College of Cardiology/American Heart Association Guideline for the Management of Heart Failure. The update incorporated evidence-based recommendations on the use of two important new heart failure medications: ivabradine (Corlanor), which received a moderate class IIa recommendation, meaning the drug “should be considered,” and sacubitril/valsartan (Entresto), which received the strongest class I recommendation.

In the right patients, these two oral medications improve heart failure morbidity and mortality significantly beyond what’s achievable with what has been the gold standard, guideline-directed medical therapy. Dr. Abraham described how to get started using the two medications at the Annual Cardiovascular Conference at Snowmass.

Ivabradine

Ivabradine is a selective inhibitor of the sinoatrial pacemaker modulating I(f) current. It acts by slowing the sinus rate without reducing myocardial contractility.

“This agent does one thing and one thing alone: It lowers heart rate,” the cardiologist explained.

And that, he added, was sufficient to significantly reduce the risks of death due to heart failure and recurrent hospitalization for worsening heart failure in the pivotal SHIFT trial.

SHIFT included 6,505 patients with moderate to severe heart failure with reduced left ventricular ejection fraction (LVEF) and a resting heart rate above 70 bpm despite background guideline-directed medical therapy. Participants were randomized double blind to ivabradine titrated to a maximum of 7.5 mg twice daily or placebo and followed for a median of about 23 months. The rate of death due to heart failure was 3% with ivabradine and 5% with placebo, for a statistically significant 26% relative risk reduction favoring ivabradine.

But the drug’s main benefit was in reducing recurrent hospitalizations for heart failure, an endpoint of particular interest to health policy officials given that heart failure hospitalizations chew up a substantial proportion of the Medicare budget. Ivabradine reduced first hospitalizations for heart failure during the study period by 25%, second hospitalizations by 34%, and third hospitalizations by 29% (Eur Heart J. 2012 Nov;33[22]:2813-20).

The ACC/AHA guideline update stresses the importance of reserving ivabradine for heart failure patients whose resting heart rate exceeds 70 bpm, despite being on their maximum tolerated dose of a beta-blocker, Dr. Abraham noted.

Ivabradine is contraindicated in the setting of acute decompensated heart failure, severe liver disease, or hypotension, in patients on any of the numerous agents that strongly inhibit the enzyme cytochrome P450 3A4, and in those who have sick sinus syndrome, have sinoatrial block, or are pacemaker dependent.

Sacubitril/valsartan

Sacubitril inhibits neprilysin, an enzyme that blocks the action of endogenous vasoactive peptides including bradykinin, substance P, and natriuretic peptides, all of which counter important maladaptive mechanisms in heart failure. Sacubitril has been combined with the angiotensin receptor blocker valsartan to form the first-in-class angiotensin receptor neprilysin inhibitor, or ARNI, formerly known as LCZ696 and now marketed as Entresto.

In the pivotal double-blind PARADIGM-HF trial, 8,442 patients with heart failure with reduced ejection fraction were randomized to the ARNI at 200 mg b.i.d. or to enalapril at 10 mg b.i.d. on top of background guideline-directed medical therapy. The trial was stopped early because of evidence of overwhelming benefit: a 20% relative risk reduction in cardiovascular death and a 21% decrease in the risk of heart failure hospitalizations in the sacubitril/valsartan group, as well as significant reductions in heart failure symptoms and physical limitations (N Engl J Med. 2014 Sep 11;371[11]:993-1004).

The updated heart failure guidelines strongly recommend that patients with heart failure should be treated with either an ACE inhibitor, an angiotensin receptor blocker, or an ARNI. Further, patients who remain symptomatic on an ACE inhibitor or angiotensin receptor blocker should be switched to an ARNI; that’s a class Ib recommendation based upon the results of PARADIGM-HF.

In getting started using the ARNI, Dr. Abraham said it’s important to understand as background the selective nature of the PARADIGM-HF study design. During the single-blind run-in period of 5-8 weeks, roughly 10% of patients dropped out because they couldn’t tolerate enalapril at 10 mg b.i.d., and a similar percentage dropped out during the ARNI run-in. Thus, patients who couldn’t tolerate a low dose of an ACE inhibitor weren’t in the study. And patients capable of tolerating guideline-recommended full-dose ACE inhibitor therapy were not specifically sought for participation.

“So there are some unanswered questions about the ARNI. If you’re just getting started with this compound in treating your heart failure patients, my own feeling is you should maybe aim for the type of patient that was included in this trial: patients who could tolerate a moderate dose of an ACE inhibitor and had generally good blood pressure. That’s a great way to begin to get experience with this agent in heart failure,” the cardiologist advised.

He reported serving as a consultant to Abbott Vascular, Medtronic, Novartis, and St. Jude Medical.

[email protected]

SNOWMASS, COLO. – As William T. Abraham, MD, speaks to colleagues around the country about heart failure therapy, he has noticed that the first-in-class drug ivabradine remains below the radar of most physicians.

“I’ve found that this is an agent that very few people know about, even though it’s been FDA [Food and Drug Administration] approved for about 3 years. It’s used fairly extensively in Europe because that’s where the pivotal SHIFT trial was done, but not very much in the United States,” according to Dr. Abraham, professor of medicine, physiology, and cell biology and director of the division of cardiovascular medicine at Ohio State University in Columbus.

That’s likely to change as word spreads about the May 2016 update of the American College of Cardiology/American Heart Association Guideline for the Management of Heart Failure. The update incorporated evidence-based recommendations on the use of two important new heart failure medications: ivabradine (Corlanor), which received a moderate class IIa recommendation, meaning the drug “should be considered,” and sacubitril/valsartan (Entresto), which received the strongest class I recommendation.

In the right patients, these two oral medications improve heart failure morbidity and mortality significantly beyond what’s achievable with what has been the gold standard, guideline-directed medical therapy. Dr. Abraham described how to get started using the two medications at the Annual Cardiovascular Conference at Snowmass.

Ivabradine

Ivabradine is a selective inhibitor of the sinoatrial pacemaker modulating I(f) current. It acts by slowing the sinus rate without reducing myocardial contractility.

“This agent does one thing and one thing alone: It lowers heart rate,” the cardiologist explained.

And that, he added, was sufficient to significantly reduce the risks of death due to heart failure and recurrent hospitalization for worsening heart failure in the pivotal SHIFT trial.

SHIFT included 6,505 patients with moderate to severe heart failure with reduced left ventricular ejection fraction (LVEF) and a resting heart rate above 70 bpm despite background guideline-directed medical therapy. Participants were randomized double blind to ivabradine titrated to a maximum of 7.5 mg twice daily or placebo and followed for a median of about 23 months. The rate of death due to heart failure was 3% with ivabradine and 5% with placebo, for a statistically significant 26% relative risk reduction favoring ivabradine.

But the drug’s main benefit was in reducing recurrent hospitalizations for heart failure, an endpoint of particular interest to health policy officials given that heart failure hospitalizations chew up a substantial proportion of the Medicare budget. Ivabradine reduced first hospitalizations for heart failure during the study period by 25%, second hospitalizations by 34%, and third hospitalizations by 29% (Eur Heart J. 2012 Nov;33[22]:2813-20).

The ACC/AHA guideline update stresses the importance of reserving ivabradine for heart failure patients whose resting heart rate exceeds 70 bpm, despite being on their maximum tolerated dose of a beta-blocker, Dr. Abraham noted.

Ivabradine is contraindicated in the setting of acute decompensated heart failure, severe liver disease, or hypotension, in patients on any of the numerous agents that strongly inhibit the enzyme cytochrome P450 3A4, and in those who have sick sinus syndrome, have sinoatrial block, or are pacemaker dependent.

Sacubitril/valsartan

Sacubitril inhibits neprilysin, an enzyme that blocks the action of endogenous vasoactive peptides including bradykinin, substance P, and natriuretic peptides, all of which counter important maladaptive mechanisms in heart failure. Sacubitril has been combined with the angiotensin receptor blocker valsartan to form the first-in-class angiotensin receptor neprilysin inhibitor, or ARNI, formerly known as LCZ696 and now marketed as Entresto.

In the pivotal double-blind PARADIGM-HF trial, 8,442 patients with heart failure with reduced ejection fraction were randomized to the ARNI at 200 mg b.i.d. or to enalapril at 10 mg b.i.d. on top of background guideline-directed medical therapy. The trial was stopped early because of evidence of overwhelming benefit: a 20% relative risk reduction in cardiovascular death and a 21% decrease in the risk of heart failure hospitalizations in the sacubitril/valsartan group, as well as significant reductions in heart failure symptoms and physical limitations (N Engl J Med. 2014 Sep 11;371[11]:993-1004).

The updated heart failure guidelines strongly recommend that patients with heart failure should be treated with either an ACE inhibitor, an angiotensin receptor blocker, or an ARNI. Further, patients who remain symptomatic on an ACE inhibitor or angiotensin receptor blocker should be switched to an ARNI; that’s a class Ib recommendation based upon the results of PARADIGM-HF.

In getting started using the ARNI, Dr. Abraham said it’s important to understand as background the selective nature of the PARADIGM-HF study design. During the single-blind run-in period of 5-8 weeks, roughly 10% of patients dropped out because they couldn’t tolerate enalapril at 10 mg b.i.d., and a similar percentage dropped out during the ARNI run-in. Thus, patients who couldn’t tolerate a low dose of an ACE inhibitor weren’t in the study. And patients capable of tolerating guideline-recommended full-dose ACE inhibitor therapy were not specifically sought for participation.

“So there are some unanswered questions about the ARNI. If you’re just getting started with this compound in treating your heart failure patients, my own feeling is you should maybe aim for the type of patient that was included in this trial: patients who could tolerate a moderate dose of an ACE inhibitor and had generally good blood pressure. That’s a great way to begin to get experience with this agent in heart failure,” the cardiologist advised.

He reported serving as a consultant to Abbott Vascular, Medtronic, Novartis, and St. Jude Medical.

[email protected]

SNOWMASS, COLO. – As William T. Abraham, MD, speaks to colleagues around the country about heart failure therapy, he has noticed that the first-in-class drug ivabradine remains below the radar of most physicians.

“I’ve found that this is an agent that very few people know about, even though it’s been FDA [Food and Drug Administration] approved for about 3 years. It’s used fairly extensively in Europe because that’s where the pivotal SHIFT trial was done, but not very much in the United States,” according to Dr. Abraham, professor of medicine, physiology, and cell biology and director of the division of cardiovascular medicine at Ohio State University in Columbus.

That’s likely to change as word spreads about the May 2016 update of the American College of Cardiology/American Heart Association Guideline for the Management of Heart Failure. The update incorporated evidence-based recommendations on the use of two important new heart failure medications: ivabradine (Corlanor), which received a moderate class IIa recommendation, meaning the drug “should be considered,” and sacubitril/valsartan (Entresto), which received the strongest class I recommendation.

In the right patients, these two oral medications improve heart failure morbidity and mortality significantly beyond what’s achievable with what has been the gold standard, guideline-directed medical therapy. Dr. Abraham described how to get started using the two medications at the Annual Cardiovascular Conference at Snowmass.

Ivabradine

Ivabradine is a selective inhibitor of the sinoatrial pacemaker modulating I(f) current. It acts by slowing the sinus rate without reducing myocardial contractility.

“This agent does one thing and one thing alone: It lowers heart rate,” the cardiologist explained.

And that, he added, was sufficient to significantly reduce the risks of death due to heart failure and recurrent hospitalization for worsening heart failure in the pivotal SHIFT trial.

SHIFT included 6,505 patients with moderate to severe heart failure with reduced left ventricular ejection fraction (LVEF) and a resting heart rate above 70 bpm despite background guideline-directed medical therapy. Participants were randomized double blind to ivabradine titrated to a maximum of 7.5 mg twice daily or placebo and followed for a median of about 23 months. The rate of death due to heart failure was 3% with ivabradine and 5% with placebo, for a statistically significant 26% relative risk reduction favoring ivabradine.

But the drug’s main benefit was in reducing recurrent hospitalizations for heart failure, an endpoint of particular interest to health policy officials given that heart failure hospitalizations chew up a substantial proportion of the Medicare budget. Ivabradine reduced first hospitalizations for heart failure during the study period by 25%, second hospitalizations by 34%, and third hospitalizations by 29% (Eur Heart J. 2012 Nov;33[22]:2813-20).

The ACC/AHA guideline update stresses the importance of reserving ivabradine for heart failure patients whose resting heart rate exceeds 70 bpm, despite being on their maximum tolerated dose of a beta-blocker, Dr. Abraham noted.

Ivabradine is contraindicated in the setting of acute decompensated heart failure, severe liver disease, or hypotension, in patients on any of the numerous agents that strongly inhibit the enzyme cytochrome P450 3A4, and in those who have sick sinus syndrome, have sinoatrial block, or are pacemaker dependent.

Sacubitril/valsartan

Sacubitril inhibits neprilysin, an enzyme that blocks the action of endogenous vasoactive peptides including bradykinin, substance P, and natriuretic peptides, all of which counter important maladaptive mechanisms in heart failure. Sacubitril has been combined with the angiotensin receptor blocker valsartan to form the first-in-class angiotensin receptor neprilysin inhibitor, or ARNI, formerly known as LCZ696 and now marketed as Entresto.

In the pivotal double-blind PARADIGM-HF trial, 8,442 patients with heart failure with reduced ejection fraction were randomized to the ARNI at 200 mg b.i.d. or to enalapril at 10 mg b.i.d. on top of background guideline-directed medical therapy. The trial was stopped early because of evidence of overwhelming benefit: a 20% relative risk reduction in cardiovascular death and a 21% decrease in the risk of heart failure hospitalizations in the sacubitril/valsartan group, as well as significant reductions in heart failure symptoms and physical limitations (N Engl J Med. 2014 Sep 11;371[11]:993-1004).

The updated heart failure guidelines strongly recommend that patients with heart failure should be treated with either an ACE inhibitor, an angiotensin receptor blocker, or an ARNI. Further, patients who remain symptomatic on an ACE inhibitor or angiotensin receptor blocker should be switched to an ARNI; that’s a class Ib recommendation based upon the results of PARADIGM-HF.

In getting started using the ARNI, Dr. Abraham said it’s important to understand as background the selective nature of the PARADIGM-HF study design. During the single-blind run-in period of 5-8 weeks, roughly 10% of patients dropped out because they couldn’t tolerate enalapril at 10 mg b.i.d., and a similar percentage dropped out during the ARNI run-in. Thus, patients who couldn’t tolerate a low dose of an ACE inhibitor weren’t in the study. And patients capable of tolerating guideline-recommended full-dose ACE inhibitor therapy were not specifically sought for participation.

“So there are some unanswered questions about the ARNI. If you’re just getting started with this compound in treating your heart failure patients, my own feeling is you should maybe aim for the type of patient that was included in this trial: patients who could tolerate a moderate dose of an ACE inhibitor and had generally good blood pressure. That’s a great way to begin to get experience with this agent in heart failure,” the cardiologist advised.

He reported serving as a consultant to Abbott Vascular, Medtronic, Novartis, and St. Jude Medical.

[email protected]

There is history around every corner in Boston. This vibrant city is rich with art, music, and dance institutions, theatre and cultural attractions, distinguished dining and nightlife venues, world-class shopping and championship sports teams that attract millions of visitors each year.

The city’s downtown neighborhoods, each with its own personality, offer endless unique experiences, and Boston’s proximity to other must-see sites all around New England make it one of the country’s most diverse and exciting locales.Each of the city’s neighborhoods has a remarkably different style and tone. From the Back Bay’s cosmopolitan streets and ornate Victorian townhouses to the aromas spilling into the narrow and jumbled 17th-century streets of Boston’s North End to the spirited and funky neighborhood squares of Cambridge – all within easy distance from one another.Boston is “America’s Walking City.” Even though it is one of the largest cities in the country, its accessibility is unparalleled. And while sightseeing on foot is easy, Boston also has an excellent public transportation system to help you get around.

Boston is also known as the mecca of medicine. Boston is home to some of the most prestigious hospitals and medical schools, physicians, and medical scientists in the world. Thoralf M. Sundt, III, MD, and the AATS Centennial Committee have organized an engaging social program for the AATS Centennial.

Tour 1: ITALIAN GASTRONOMY NORTH END MARKET TOUR
Sunday, April 30, 2017
10:30 a.m.– 1:15 p.m.
Cost: $95 per person

Marcio Silva/Thinkstock

Tour 2: A VISIT TO THE ISABELLA STEWART GARDNER MUSEUM
Monday, May 1, 2017
12:15 p.m. – 2:45 p.m.
Cost: $85 per person

Victorgrigas/ Wikimedia Commons

Tour 3: BEACON HILL CIRCLE “BEHIND THE BRAHMIN DOORS”
Tuesday, May 2, 2017
9:15 a.m. – 11:45 a.m.
Cost: $110 per person

LUNAMARINA/Thinkstock

There is history around every corner in Boston. This vibrant city is rich with art, music, and dance institutions, theatre and cultural attractions, distinguished dining and nightlife venues, world-class shopping and championship sports teams that attract millions of visitors each year.

The city’s downtown neighborhoods, each with its own personality, offer endless unique experiences, and Boston’s proximity to other must-see sites all around New England make it one of the country’s most diverse and exciting locales.Each of the city’s neighborhoods has a remarkably different style and tone. From the Back Bay’s cosmopolitan streets and ornate Victorian townhouses to the aromas spilling into the narrow and jumbled 17th-century streets of Boston’s North End to the spirited and funky neighborhood squares of Cambridge – all within easy distance from one another.Boston is “America’s Walking City.” Even though it is one of the largest cities in the country, its accessibility is unparalleled. And while sightseeing on foot is easy, Boston also has an excellent public transportation system to help you get around.

Boston is also known as the mecca of medicine. Boston is home to some of the most prestigious hospitals and medical schools, physicians, and medical scientists in the world. Thoralf M. Sundt, III, MD, and the AATS Centennial Committee have organized an engaging social program for the AATS Centennial.

Tour 1: ITALIAN GASTRONOMY NORTH END MARKET TOUR
Sunday, April 30, 2017
10:30 a.m.– 1:15 p.m.
Cost: $95 per person

Marcio Silva/Thinkstock

Tour 2: A VISIT TO THE ISABELLA STEWART GARDNER MUSEUM
Monday, May 1, 2017
12:15 p.m. – 2:45 p.m.
Cost: $85 per person

Victorgrigas/ Wikimedia Commons

Tour 3: BEACON HILL CIRCLE “BEHIND THE BRAHMIN DOORS”
Tuesday, May 2, 2017
9:15 a.m. – 11:45 a.m.
Cost: $110 per person

LUNAMARINA/Thinkstock

There is history around every corner in Boston. This vibrant city is rich with art, music, and dance institutions, theatre and cultural attractions, distinguished dining and nightlife venues, world-class shopping and championship sports teams that attract millions of visitors each year.

The city’s downtown neighborhoods, each with its own personality, offer endless unique experiences, and Boston’s proximity to other must-see sites all around New England make it one of the country’s most diverse and exciting locales.Each of the city’s neighborhoods has a remarkably different style and tone. From the Back Bay’s cosmopolitan streets and ornate Victorian townhouses to the aromas spilling into the narrow and jumbled 17th-century streets of Boston’s North End to the spirited and funky neighborhood squares of Cambridge – all within easy distance from one another.Boston is “America’s Walking City.” Even though it is one of the largest cities in the country, its accessibility is unparalleled. And while sightseeing on foot is easy, Boston also has an excellent public transportation system to help you get around.

Boston is also known as the mecca of medicine. Boston is home to some of the most prestigious hospitals and medical schools, physicians, and medical scientists in the world. Thoralf M. Sundt, III, MD, and the AATS Centennial Committee have organized an engaging social program for the AATS Centennial.

Tour 1: ITALIAN GASTRONOMY NORTH END MARKET TOUR
Sunday, April 30, 2017
10:30 a.m.– 1:15 p.m.
Cost: $95 per person

Marcio Silva/Thinkstock

Tour 2: A VISIT TO THE ISABELLA STEWART GARDNER MUSEUM
Monday, May 1, 2017
12:15 p.m. – 2:45 p.m.
Cost: $85 per person

Victorgrigas/ Wikimedia Commons

Tour 3: BEACON HILL CIRCLE “BEHIND THE BRAHMIN DOORS”
Tuesday, May 2, 2017
9:15 a.m. – 11:45 a.m.
Cost: $110 per person

LUNAMARINA/Thinkstock

ORLANDO – Infusions of banked multivirus-specific T lymphocytes were associated with complete or partial responses in 93% of 42 patients who had undergone hematopoietic cell transplants and had drug-refractory viral illnesses. Further, these patients experienced minimal new or reactivated graft-versus-host disease (GVHD).

Viral infections cause nearly 40% of deaths after alternative donor hematopoietic cell transfer (HCT), Ifigeneia Tzannou, MD, said at the combined annual meetings of the Center for International Blood & Marrow Transplant Research and the American Society of Blood and Marrow Transplantation. Banked, “off-the-shelf” donor virus-resistant T cells can be an alternative to antiviral drugs, which are far from universally effective and may have serious side effects.

Kari Oakes/Frontline Medical News

[email protected]

On Twitter @karioakes

ORLANDO – Infusions of banked multivirus-specific T lymphocytes were associated with complete or partial responses in 93% of 42 patients who had undergone hematopoietic cell transplants and had drug-refractory viral illnesses. Further, these patients experienced minimal new or reactivated graft-versus-host disease (GVHD).

Viral infections cause nearly 40% of deaths after alternative donor hematopoietic cell transfer (HCT), Ifigeneia Tzannou, MD, said at the combined annual meetings of the Center for International Blood & Marrow Transplant Research and the American Society of Blood and Marrow Transplantation. Banked, “off-the-shelf” donor virus-resistant T cells can be an alternative to antiviral drugs, which are far from universally effective and may have serious side effects.

Kari Oakes/Frontline Medical News

[email protected]

On Twitter @karioakes

ORLANDO – Infusions of banked multivirus-specific T lymphocytes were associated with complete or partial responses in 93% of 42 patients who had undergone hematopoietic cell transplants and had drug-refractory viral illnesses. Further, these patients experienced minimal new or reactivated graft-versus-host disease (GVHD).

Viral infections cause nearly 40% of deaths after alternative donor hematopoietic cell transfer (HCT), Ifigeneia Tzannou, MD, said at the combined annual meetings of the Center for International Blood & Marrow Transplant Research and the American Society of Blood and Marrow Transplantation. Banked, “off-the-shelf” donor virus-resistant T cells can be an alternative to antiviral drugs, which are far from universally effective and may have serious side effects.

Kari Oakes/Frontline Medical News

[email protected]

On Twitter @karioakes

Cutaneous Larva Migrans 

Cutaneous larva migrans (CLM) is caused by the larval migration of animal hookworms. Ancylostoma braziliense, Ancylostoma ceylanicum, and Ancylostoma caninum are the species most commonly associated with the disease. The hookworm is endemic to tropical and subtropical climates in areas such as Africa, Southeast Asia, South America, and the southeastern United States.¹ Although cats and dogs are most commonly affected, humans can be infected if they are exposed to sand or soil containing hookworm larvae, often due to contamination from animal feces.² Cutaneous larva migrans is characterized by pruritic erythematous papules and linear or serpiginous, reddish brown, elevated tracks most commonly appearing on the feet, buttocks, thighs, and lower legs; however, lesions can appear anywhere. In human hosts, the larvae travel in the epidermis and are unable to invade the dermis; it is speculated that they lack the collagenase enzymes required to penetrate the basement membrane before invading the dermis.² 

On histopathology, there typically are small cavities in the epidermis corresponding to the track of the larvae.³ There often is a spongiotic dermatitis with a mixed inflammatory infiltrate following the larvae with scattered eosinophils. The migrating larvae may be up to 1 mm in size and have bilateral double alae, or winglike projections, on the side of the body (Figure 1).⁴ The larvae are difficult to find on histopathology because they often travel beyond the areas that demonstrate clinical findings. The diagnosis of CLM is mostly clinical, but if a biopsy is performed, the specimen should be taken ahead of the track. 

Disseminated strongyloidiasis is caused by Strongyloides stercoralis. When filariform larvae migrate out of the intestinal tract into the skin, they can cause an urticarial rash and serpiginous patterns on the skin that can move 5 to 15 cm per hour, a clinical condition known as larva currens. In immunocompromised individuals, there can be hyperinfection with diffuse petechial thumbprint purpura seen clinically, which characteristically radiate from the periumbilical area.¹ On pathology, there may be numerous larvae found between the dermal collagen bundles, measuring 9 to 15 µm in diameter. Rarely, they also can be found in small blood vessels.³ They often are accompanied by extravasated red blood cells in the tissues (Figure 2).

Myiasis represents the largest pathogen in the differential diagnosis for CLM. In myiasis, fly larvae will infest human tissue, usually by forming a small cavity in the dermis or subcutaneous tissue. The larvae are visible to the human eye and can be up to several centimeters in length. In the skin, the histology of myiasis usually is accompanied by a heavy mixed inflammatory cell infiltrate with many eosinophils. Fragments of the larvae are seen encased by a thick chitinous cuticle with widely spaced spines or pigmented setae (Figure 3) on the surface of the cuticle.⁵ Layers of striated muscle and internal organs may be seen beneath the cuticle.³

Onchocerciasis, or river blindness, is a parasitic disease caused by Onchocerca volvulus that is most often seen in sub-Saharan Africa. It may cause the skin finding of an onchocercoma, a subcutaneous nodule made up of Onchocerca nematodes. However, when the filaria disseminate, it may cause onchocerciasis with cutaneous findings of an eczematous dermatitis with itching and lichenification.¹ In onchocercal dermatitis, microfilariae may be found in the dermis and there may be a mild dermal chronic inflammatory infiltrate with eosinophils.³ These microfilariae are smaller than Strongyloides larvae (Figure 4).

Sarcoptes scabiei are mites that are pathologically found limited to the stratum corneum. There often is a spongiotic dermatitis as the mite travels with an accompanying mixed cell inflammatory infiltrate with many eosinophils. One or more mites may be seen with or without eggs and excreta or scybala (Figure 5). Pink pigtails may be seen connected to the stratum corneum, representing egg fragments or casings left behind after the mite hatches.³ The female mite measures up to 0.4 mm in length.³

Cutaneous Larva Migrans 

Cutaneous larva migrans (CLM) is caused by the larval migration of animal hookworms. Ancylostoma braziliense, Ancylostoma ceylanicum, and Ancylostoma caninum are the species most commonly associated with the disease. The hookworm is endemic to tropical and subtropical climates in areas such as Africa, Southeast Asia, South America, and the southeastern United States.¹ Although cats and dogs are most commonly affected, humans can be infected if they are exposed to sand or soil containing hookworm larvae, often due to contamination from animal feces.² Cutaneous larva migrans is characterized by pruritic erythematous papules and linear or serpiginous, reddish brown, elevated tracks most commonly appearing on the feet, buttocks, thighs, and lower legs; however, lesions can appear anywhere. In human hosts, the larvae travel in the epidermis and are unable to invade the dermis; it is speculated that they lack the collagenase enzymes required to penetrate the basement membrane before invading the dermis.² 

On histopathology, there typically are small cavities in the epidermis corresponding to the track of the larvae.³ There often is a spongiotic dermatitis with a mixed inflammatory infiltrate following the larvae with scattered eosinophils. The migrating larvae may be up to 1 mm in size and have bilateral double alae, or winglike projections, on the side of the body (Figure 1).⁴ The larvae are difficult to find on histopathology because they often travel beyond the areas that demonstrate clinical findings. The diagnosis of CLM is mostly clinical, but if a biopsy is performed, the specimen should be taken ahead of the track. 

Disseminated strongyloidiasis is caused by Strongyloides stercoralis. When filariform larvae migrate out of the intestinal tract into the skin, they can cause an urticarial rash and serpiginous patterns on the skin that can move 5 to 15 cm per hour, a clinical condition known as larva currens. In immunocompromised individuals, there can be hyperinfection with diffuse petechial thumbprint purpura seen clinically, which characteristically radiate from the periumbilical area.¹ On pathology, there may be numerous larvae found between the dermal collagen bundles, measuring 9 to 15 µm in diameter. Rarely, they also can be found in small blood vessels.³ They often are accompanied by extravasated red blood cells in the tissues (Figure 2).

Myiasis represents the largest pathogen in the differential diagnosis for CLM. In myiasis, fly larvae will infest human tissue, usually by forming a small cavity in the dermis or subcutaneous tissue. The larvae are visible to the human eye and can be up to several centimeters in length. In the skin, the histology of myiasis usually is accompanied by a heavy mixed inflammatory cell infiltrate with many eosinophils. Fragments of the larvae are seen encased by a thick chitinous cuticle with widely spaced spines or pigmented setae (Figure 3) on the surface of the cuticle.⁵ Layers of striated muscle and internal organs may be seen beneath the cuticle.³

Onchocerciasis, or river blindness, is a parasitic disease caused by Onchocerca volvulus that is most often seen in sub-Saharan Africa. It may cause the skin finding of an onchocercoma, a subcutaneous nodule made up of Onchocerca nematodes. However, when the filaria disseminate, it may cause onchocerciasis with cutaneous findings of an eczematous dermatitis with itching and lichenification.¹ In onchocercal dermatitis, microfilariae may be found in the dermis and there may be a mild dermal chronic inflammatory infiltrate with eosinophils.³ These microfilariae are smaller than Strongyloides larvae (Figure 4).

Sarcoptes scabiei are mites that are pathologically found limited to the stratum corneum. There often is a spongiotic dermatitis as the mite travels with an accompanying mixed cell inflammatory infiltrate with many eosinophils. One or more mites may be seen with or without eggs and excreta or scybala (Figure 5). Pink pigtails may be seen connected to the stratum corneum, representing egg fragments or casings left behind after the mite hatches.³ The female mite measures up to 0.4 mm in length.³

Cutaneous Larva Migrans 

Cutaneous larva migrans (CLM) is caused by the larval migration of animal hookworms. Ancylostoma braziliense, Ancylostoma ceylanicum, and Ancylostoma caninum are the species most commonly associated with the disease. The hookworm is endemic to tropical and subtropical climates in areas such as Africa, Southeast Asia, South America, and the southeastern United States.¹ Although cats and dogs are most commonly affected, humans can be infected if they are exposed to sand or soil containing hookworm larvae, often due to contamination from animal feces.² Cutaneous larva migrans is characterized by pruritic erythematous papules and linear or serpiginous, reddish brown, elevated tracks most commonly appearing on the feet, buttocks, thighs, and lower legs; however, lesions can appear anywhere. In human hosts, the larvae travel in the epidermis and are unable to invade the dermis; it is speculated that they lack the collagenase enzymes required to penetrate the basement membrane before invading the dermis.² 

On histopathology, there typically are small cavities in the epidermis corresponding to the track of the larvae.³ There often is a spongiotic dermatitis with a mixed inflammatory infiltrate following the larvae with scattered eosinophils. The migrating larvae may be up to 1 mm in size and have bilateral double alae, or winglike projections, on the side of the body (Figure 1).⁴ The larvae are difficult to find on histopathology because they often travel beyond the areas that demonstrate clinical findings. The diagnosis of CLM is mostly clinical, but if a biopsy is performed, the specimen should be taken ahead of the track. 

Disseminated strongyloidiasis is caused by Strongyloides stercoralis. When filariform larvae migrate out of the intestinal tract into the skin, they can cause an urticarial rash and serpiginous patterns on the skin that can move 5 to 15 cm per hour, a clinical condition known as larva currens. In immunocompromised individuals, there can be hyperinfection with diffuse petechial thumbprint purpura seen clinically, which characteristically radiate from the periumbilical area.¹ On pathology, there may be numerous larvae found between the dermal collagen bundles, measuring 9 to 15 µm in diameter. Rarely, they also can be found in small blood vessels.³ They often are accompanied by extravasated red blood cells in the tissues (Figure 2).

Myiasis represents the largest pathogen in the differential diagnosis for CLM. In myiasis, fly larvae will infest human tissue, usually by forming a small cavity in the dermis or subcutaneous tissue. The larvae are visible to the human eye and can be up to several centimeters in length. In the skin, the histology of myiasis usually is accompanied by a heavy mixed inflammatory cell infiltrate with many eosinophils. Fragments of the larvae are seen encased by a thick chitinous cuticle with widely spaced spines or pigmented setae (Figure 3) on the surface of the cuticle.⁵ Layers of striated muscle and internal organs may be seen beneath the cuticle.³

Onchocerciasis, or river blindness, is a parasitic disease caused by Onchocerca volvulus that is most often seen in sub-Saharan Africa. It may cause the skin finding of an onchocercoma, a subcutaneous nodule made up of Onchocerca nematodes. However, when the filaria disseminate, it may cause onchocerciasis with cutaneous findings of an eczematous dermatitis with itching and lichenification.¹ In onchocercal dermatitis, microfilariae may be found in the dermis and there may be a mild dermal chronic inflammatory infiltrate with eosinophils.³ These microfilariae are smaller than Strongyloides larvae (Figure 4).

Sarcoptes scabiei are mites that are pathologically found limited to the stratum corneum. There often is a spongiotic dermatitis as the mite travels with an accompanying mixed cell inflammatory infiltrate with many eosinophils. One or more mites may be seen with or without eggs and excreta or scybala (Figure 5). Pink pigtails may be seen connected to the stratum corneum, representing egg fragments or casings left behind after the mite hatches.³ The female mite measures up to 0.4 mm in length.³

The Diagnosis: Cutaneous Mastocytoma

Physical examination revealed a 58×51-mm hyperpigmented plaque with central pink coloration and scale on the right side of the back as well as a 39×33-mm pink plaque with a hyperpigmented border on the left side of the flank (Figure 1). At follow-up 2 weeks later, the patient's parents reported that blisters formed within both of the plaques. The blisters ruptured a few hours after forming and drained clear fluid with scant blood. Both plaques contained erosions from the ruptured bullae but remained the same size with no surrounding erythema or warmth. A 4-mm punch biopsy was performed of intact skin from the back lesion (Figure 2A). Histologic examination revealed a cellular infiltrate of monotonous bland cells that completely filled the dermis without epidermal involvement, along with occasional intermixed eosinophils. The morphology of these infiltrating cells was compatible with mast cells confirmed by strongly positive Leder staining (Figure 2B).

Mastocytosis encompasses a rare group of disorders characterized by abnormal mast cell accumulation or mast cell mediator release in various tissues. These disorders can be classified as either systemic mastocytosis with mast cell infiltration into bone marrow or other extracutaneous organs, or cutaneous mastocytosis with disease limited to the skin.¹ Mutations involving activation of the c-Kit receptor in stimulating mast cell growth and development have been implicated in both systemic and cutaneous forms of the disease.^2,3

Cutaneous mastocytosis is most often diagnosed in childhood and typically is characterized by spontaneous regression before puberty in a majority of cases.^1,4 Under the World Health Organization classification system, cutaneous mastocytosis can be further subdivided into 3 disorders (listed in order of most to least common): urticaria pigmentosa (also known as maculopapular cutaneous mastocytosis) with typical, plaque, and nodular forms; cutaneous mastocytoma (as seen in this patient); and diffuse cutaneous mastocytosis.⁵ Compared to the widespread distribution of small macules and papules in urticaria pigmentosa, the cutaneous mastocytoma subtype presents with 1 to 6 brown to orange-yellow plaques or nodules measuring more than 1 cm in diameter. Cutaneous mastocytoma typically presents in infancy and is located most commonly on the trunk and extremities, though it may be found on the face or scalp. The plaques of mastocytoma often have well-defined margins, and these lesions may become bullous or demonstrate Darier sign of urtication and erythema on physical stimulation. Patients most commonly experience pruritus from mast cell degranulation and rarely exhibit systemic symptoms of mast cell mediator release; however, generalized flushing, hypotension, headaches, and gastrointestinal symptoms may occur, particularly if the lesion is vigorously rubbed.^6,7 Conditions in the differential include aplasia cutis congenita, connective tissue nevus, epidermal nevus, and epidermolysis bullosa. They should not elicit a blister if rubbed, except for epidermolysis bullosa, which can easily be differentiated based on histology.

The workup for cutaneous mastocytosis in the pediatric population may include a biopsy of lesional skin, though in many cases the characteristic cutaneous manifestations are sufficient to make a diagnosis. Histologically, biopsy results often reveal abundant diffuse dermal infiltration of mast cells, which are characterized by their large pink granular cytoplasm and round dense central nuclei. In pediatric patients, mast cells typically are restricted to the dermis, and there is a low risk for hematologic abnormalities, thereby precluding the need for bone marrow examination in the absence of organomegaly or notable peripheral blood abnormalities such as severe cytopenia.^5,6

Management of cutaneous mastocytosis consists of avoidance of mast cell degranulation triggers and symptomatic treatment of histamine release. Triggers include certain medications (eg, narcotic analgesics, aspirin, nonsteroidal anti-inflammatory drugs, iodinated contrast agents, antibiotics, muscle relaxants), mechanical irritation, insect stings, spicy foods, stress, or extreme temperature changes.⁸ Symptomatic treatment can be achieved through topical corticosteroid or oral antihistamine use. Along with decreasing pruritus, topical corticosteroids also may be helpful in decreasing time to spontaneous resolution and healing.⁷ The patient in this case was treated with desonide ointment 0.05% daily to both lesions as well as mupirocin ointment 2% as needed for erosions. These treatments helped reduce the patient's symptoms, but her lesions persisted over a follow-up period of 4 months.

The Diagnosis: Cutaneous Mastocytoma

Physical examination revealed a 58×51-mm hyperpigmented plaque with central pink coloration and scale on the right side of the back as well as a 39×33-mm pink plaque with a hyperpigmented border on the left side of the flank (Figure 1). At follow-up 2 weeks later, the patient's parents reported that blisters formed within both of the plaques. The blisters ruptured a few hours after forming and drained clear fluid with scant blood. Both plaques contained erosions from the ruptured bullae but remained the same size with no surrounding erythema or warmth. A 4-mm punch biopsy was performed of intact skin from the back lesion (Figure 2A). Histologic examination revealed a cellular infiltrate of monotonous bland cells that completely filled the dermis without epidermal involvement, along with occasional intermixed eosinophils. The morphology of these infiltrating cells was compatible with mast cells confirmed by strongly positive Leder staining (Figure 2B).

Mastocytosis encompasses a rare group of disorders characterized by abnormal mast cell accumulation or mast cell mediator release in various tissues. These disorders can be classified as either systemic mastocytosis with mast cell infiltration into bone marrow or other extracutaneous organs, or cutaneous mastocytosis with disease limited to the skin.¹ Mutations involving activation of the c-Kit receptor in stimulating mast cell growth and development have been implicated in both systemic and cutaneous forms of the disease.^2,3

Cutaneous mastocytosis is most often diagnosed in childhood and typically is characterized by spontaneous regression before puberty in a majority of cases.^1,4 Under the World Health Organization classification system, cutaneous mastocytosis can be further subdivided into 3 disorders (listed in order of most to least common): urticaria pigmentosa (also known as maculopapular cutaneous mastocytosis) with typical, plaque, and nodular forms; cutaneous mastocytoma (as seen in this patient); and diffuse cutaneous mastocytosis.⁵ Compared to the widespread distribution of small macules and papules in urticaria pigmentosa, the cutaneous mastocytoma subtype presents with 1 to 6 brown to orange-yellow plaques or nodules measuring more than 1 cm in diameter. Cutaneous mastocytoma typically presents in infancy and is located most commonly on the trunk and extremities, though it may be found on the face or scalp. The plaques of mastocytoma often have well-defined margins, and these lesions may become bullous or demonstrate Darier sign of urtication and erythema on physical stimulation. Patients most commonly experience pruritus from mast cell degranulation and rarely exhibit systemic symptoms of mast cell mediator release; however, generalized flushing, hypotension, headaches, and gastrointestinal symptoms may occur, particularly if the lesion is vigorously rubbed.^6,7 Conditions in the differential include aplasia cutis congenita, connective tissue nevus, epidermal nevus, and epidermolysis bullosa. They should not elicit a blister if rubbed, except for epidermolysis bullosa, which can easily be differentiated based on histology.

The workup for cutaneous mastocytosis in the pediatric population may include a biopsy of lesional skin, though in many cases the characteristic cutaneous manifestations are sufficient to make a diagnosis. Histologically, biopsy results often reveal abundant diffuse dermal infiltration of mast cells, which are characterized by their large pink granular cytoplasm and round dense central nuclei. In pediatric patients, mast cells typically are restricted to the dermis, and there is a low risk for hematologic abnormalities, thereby precluding the need for bone marrow examination in the absence of organomegaly or notable peripheral blood abnormalities such as severe cytopenia.^5,6

Management of cutaneous mastocytosis consists of avoidance of mast cell degranulation triggers and symptomatic treatment of histamine release. Triggers include certain medications (eg, narcotic analgesics, aspirin, nonsteroidal anti-inflammatory drugs, iodinated contrast agents, antibiotics, muscle relaxants), mechanical irritation, insect stings, spicy foods, stress, or extreme temperature changes.⁸ Symptomatic treatment can be achieved through topical corticosteroid or oral antihistamine use. Along with decreasing pruritus, topical corticosteroids also may be helpful in decreasing time to spontaneous resolution and healing.⁷ The patient in this case was treated with desonide ointment 0.05% daily to both lesions as well as mupirocin ointment 2% as needed for erosions. These treatments helped reduce the patient's symptoms, but her lesions persisted over a follow-up period of 4 months.

The Diagnosis: Cutaneous Mastocytoma

Physical examination revealed a 58×51-mm hyperpigmented plaque with central pink coloration and scale on the right side of the back as well as a 39×33-mm pink plaque with a hyperpigmented border on the left side of the flank (Figure 1). At follow-up 2 weeks later, the patient's parents reported that blisters formed within both of the plaques. The blisters ruptured a few hours after forming and drained clear fluid with scant blood. Both plaques contained erosions from the ruptured bullae but remained the same size with no surrounding erythema or warmth. A 4-mm punch biopsy was performed of intact skin from the back lesion (Figure 2A). Histologic examination revealed a cellular infiltrate of monotonous bland cells that completely filled the dermis without epidermal involvement, along with occasional intermixed eosinophils. The morphology of these infiltrating cells was compatible with mast cells confirmed by strongly positive Leder staining (Figure 2B).

Mastocytosis encompasses a rare group of disorders characterized by abnormal mast cell accumulation or mast cell mediator release in various tissues. These disorders can be classified as either systemic mastocytosis with mast cell infiltration into bone marrow or other extracutaneous organs, or cutaneous mastocytosis with disease limited to the skin.¹ Mutations involving activation of the c-Kit receptor in stimulating mast cell growth and development have been implicated in both systemic and cutaneous forms of the disease.^2,3

Cutaneous mastocytosis is most often diagnosed in childhood and typically is characterized by spontaneous regression before puberty in a majority of cases.^1,4 Under the World Health Organization classification system, cutaneous mastocytosis can be further subdivided into 3 disorders (listed in order of most to least common): urticaria pigmentosa (also known as maculopapular cutaneous mastocytosis) with typical, plaque, and nodular forms; cutaneous mastocytoma (as seen in this patient); and diffuse cutaneous mastocytosis.⁵ Compared to the widespread distribution of small macules and papules in urticaria pigmentosa, the cutaneous mastocytoma subtype presents with 1 to 6 brown to orange-yellow plaques or nodules measuring more than 1 cm in diameter. Cutaneous mastocytoma typically presents in infancy and is located most commonly on the trunk and extremities, though it may be found on the face or scalp. The plaques of mastocytoma often have well-defined margins, and these lesions may become bullous or demonstrate Darier sign of urtication and erythema on physical stimulation. Patients most commonly experience pruritus from mast cell degranulation and rarely exhibit systemic symptoms of mast cell mediator release; however, generalized flushing, hypotension, headaches, and gastrointestinal symptoms may occur, particularly if the lesion is vigorously rubbed.^6,7 Conditions in the differential include aplasia cutis congenita, connective tissue nevus, epidermal nevus, and epidermolysis bullosa. They should not elicit a blister if rubbed, except for epidermolysis bullosa, which can easily be differentiated based on histology.

The workup for cutaneous mastocytosis in the pediatric population may include a biopsy of lesional skin, though in many cases the characteristic cutaneous manifestations are sufficient to make a diagnosis. Histologically, biopsy results often reveal abundant diffuse dermal infiltration of mast cells, which are characterized by their large pink granular cytoplasm and round dense central nuclei. In pediatric patients, mast cells typically are restricted to the dermis, and there is a low risk for hematologic abnormalities, thereby precluding the need for bone marrow examination in the absence of organomegaly or notable peripheral blood abnormalities such as severe cytopenia.^5,6

Management of cutaneous mastocytosis consists of avoidance of mast cell degranulation triggers and symptomatic treatment of histamine release. Triggers include certain medications (eg, narcotic analgesics, aspirin, nonsteroidal anti-inflammatory drugs, iodinated contrast agents, antibiotics, muscle relaxants), mechanical irritation, insect stings, spicy foods, stress, or extreme temperature changes.⁸ Symptomatic treatment can be achieved through topical corticosteroid or oral antihistamine use. Along with decreasing pruritus, topical corticosteroids also may be helpful in decreasing time to spontaneous resolution and healing.⁷ The patient in this case was treated with desonide ointment 0.05% daily to both lesions as well as mupirocin ointment 2% as needed for erosions. These treatments helped reduce the patient's symptoms, but her lesions persisted over a follow-up period of 4 months.

Take-Home Points

• Importance of on-field management.
• Preseason drilling of spinal injury management.
• Early and rapid intervention.
• Possible benefit of moderate systemic hypothermia as treatment for acute cervical injury.

In 2010, we reported the case of a professional American football player who sustained a complete cervical spinal cord injury (SCI) while tackling an opposing player.¹ He received prompt medical and surgical care based on then-current recommendations, but was also treated with systemic hypothermia soon after his injury. Although systemic hypothermia had been used in the management of other neurologic injuries at that time, it had not been used in humans with acute SCI, except as described in 2 case reports.^2,3 However, Dietrich⁴ described early emerging animal data on the efficacy of systemic hypothermia for acute SCI. We now provide a clinical update on our patient, who provided written informed consent for print and electronic publication of this case report.

Case Report

During a National Football League game, the player sustained a C3–C4 fracture-dislocation after a helmet-to-helmet hit on an opposing player. He fell face down on the ground and did not move. The team’s physician and trainer rushed to the player’s side, immediately assessed him, and initiated the emergency spinal resuscitation protocol.

As per protocol, the assigned team leader took charge of managing the player’s head to maintain in-line traction with the helmet in place until the head was secured in place on a backboard designed to accommodate the helmet.

Conclusion

At the time this player was injured, use of systemic hypothermia with standard therapy for acute SCI was unique and controversial. Since then, smaller randomized human studies have described the tolerable safety profile, efficacy, and potential benefits of this intervention in acute SCI in humans.^8-10 Now, modest systemic hypothermia can be one of many tools considered in the treatment of acute SCI. Before it can become the standard of care, however, additional larger prospective randomized studies need to be completed.

Am J Orthop. 2017;46(2):E79-E82. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Importance of on-field management.
• Preseason drilling of spinal injury management.
• Early and rapid intervention.
• Possible benefit of moderate systemic hypothermia as treatment for acute cervical injury.

In 2010, we reported the case of a professional American football player who sustained a complete cervical spinal cord injury (SCI) while tackling an opposing player.¹ He received prompt medical and surgical care based on then-current recommendations, but was also treated with systemic hypothermia soon after his injury. Although systemic hypothermia had been used in the management of other neurologic injuries at that time, it had not been used in humans with acute SCI, except as described in 2 case reports.^2,3 However, Dietrich⁴ described early emerging animal data on the efficacy of systemic hypothermia for acute SCI. We now provide a clinical update on our patient, who provided written informed consent for print and electronic publication of this case report.

Case Report

During a National Football League game, the player sustained a C3–C4 fracture-dislocation after a helmet-to-helmet hit on an opposing player. He fell face down on the ground and did not move. The team’s physician and trainer rushed to the player’s side, immediately assessed him, and initiated the emergency spinal resuscitation protocol.

As per protocol, the assigned team leader took charge of managing the player’s head to maintain in-line traction with the helmet in place until the head was secured in place on a backboard designed to accommodate the helmet.

Conclusion

At the time this player was injured, use of systemic hypothermia with standard therapy for acute SCI was unique and controversial. Since then, smaller randomized human studies have described the tolerable safety profile, efficacy, and potential benefits of this intervention in acute SCI in humans.^8-10 Now, modest systemic hypothermia can be one of many tools considered in the treatment of acute SCI. Before it can become the standard of care, however, additional larger prospective randomized studies need to be completed.

Am J Orthop. 2017;46(2):E79-E82. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Importance of on-field management.
• Preseason drilling of spinal injury management.
• Early and rapid intervention.
• Possible benefit of moderate systemic hypothermia as treatment for acute cervical injury.

In 2010, we reported the case of a professional American football player who sustained a complete cervical spinal cord injury (SCI) while tackling an opposing player.¹ He received prompt medical and surgical care based on then-current recommendations, but was also treated with systemic hypothermia soon after his injury. Although systemic hypothermia had been used in the management of other neurologic injuries at that time, it had not been used in humans with acute SCI, except as described in 2 case reports.^2,3 However, Dietrich⁴ described early emerging animal data on the efficacy of systemic hypothermia for acute SCI. We now provide a clinical update on our patient, who provided written informed consent for print and electronic publication of this case report.

Case Report

During a National Football League game, the player sustained a C3–C4 fracture-dislocation after a helmet-to-helmet hit on an opposing player. He fell face down on the ground and did not move. The team’s physician and trainer rushed to the player’s side, immediately assessed him, and initiated the emergency spinal resuscitation protocol.

As per protocol, the assigned team leader took charge of managing the player’s head to maintain in-line traction with the helmet in place until the head was secured in place on a backboard designed to accommodate the helmet.

Conclusion

At the time this player was injured, use of systemic hypothermia with standard therapy for acute SCI was unique and controversial. Since then, smaller randomized human studies have described the tolerable safety profile, efficacy, and potential benefits of this intervention in acute SCI in humans.^8-10 Now, modest systemic hypothermia can be one of many tools considered in the treatment of acute SCI. Before it can become the standard of care, however, additional larger prospective randomized studies need to be completed.

Am J Orthop. 2017;46(2):E79-E82. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Involuntary treatment is an everyday event in the emergency department and on the inpatient unit, but, for both patients and advocates, it remains the most distressing and controversial aspect of psychiatric care. We all value medical autonomy, and, even when people may be too ill to make decisions about their own care, the issue of whether to force treatment gets sticky. On the other hand, the decision not to force someone to get care when they are very sick has its own risks and distresses, and sometimes groups clash.

If you don’t believe me, check outside the convention center during the upcoming American Psychiatric Association’s annual meeting in San Diego this May. Every year, there are protesters: antipsychiatry groups who feel our treatments offer more harm than good. For those who believe the field is sullied by the pharmaceutical companies and that the treatments are harmful, forcing those treatments upon people is all the more egregious. Most years, protesters come from the Church of Scientology and MindFreedom International to make their feelings known. The pitch of the protests varies, as does the length of time they stay, but, some years, there are marchers, megaphones, and jumbotrons.

To learn more about the latest book by Dr. Miller and Dr. Hanson, “Committed: The Battle Over Involuntary Psychiatric Care,” visit https://jhupbooks.press.jhu.edu/content/committed.

Involuntary treatment is an everyday event in the emergency department and on the inpatient unit, but, for both patients and advocates, it remains the most distressing and controversial aspect of psychiatric care. We all value medical autonomy, and, even when people may be too ill to make decisions about their own care, the issue of whether to force treatment gets sticky. On the other hand, the decision not to force someone to get care when they are very sick has its own risks and distresses, and sometimes groups clash.

If you don’t believe me, check outside the convention center during the upcoming American Psychiatric Association’s annual meeting in San Diego this May. Every year, there are protesters: antipsychiatry groups who feel our treatments offer more harm than good. For those who believe the field is sullied by the pharmaceutical companies and that the treatments are harmful, forcing those treatments upon people is all the more egregious. Most years, protesters come from the Church of Scientology and MindFreedom International to make their feelings known. The pitch of the protests varies, as does the length of time they stay, but, some years, there are marchers, megaphones, and jumbotrons.

To learn more about the latest book by Dr. Miller and Dr. Hanson, “Committed: The Battle Over Involuntary Psychiatric Care,” visit https://jhupbooks.press.jhu.edu/content/committed.

Involuntary treatment is an everyday event in the emergency department and on the inpatient unit, but, for both patients and advocates, it remains the most distressing and controversial aspect of psychiatric care. We all value medical autonomy, and, even when people may be too ill to make decisions about their own care, the issue of whether to force treatment gets sticky. On the other hand, the decision not to force someone to get care when they are very sick has its own risks and distresses, and sometimes groups clash.

If you don’t believe me, check outside the convention center during the upcoming American Psychiatric Association’s annual meeting in San Diego this May. Every year, there are protesters: antipsychiatry groups who feel our treatments offer more harm than good. For those who believe the field is sullied by the pharmaceutical companies and that the treatments are harmful, forcing those treatments upon people is all the more egregious. Most years, protesters come from the Church of Scientology and MindFreedom International to make their feelings known. The pitch of the protests varies, as does the length of time they stay, but, some years, there are marchers, megaphones, and jumbotrons.

To learn more about the latest book by Dr. Miller and Dr. Hanson, “Committed: The Battle Over Involuntary Psychiatric Care,” visit https://jhupbooks.press.jhu.edu/content/committed.

Ivan Misner once spent one week on Necker Island – the tony 74-acre island in the British Virgin Islands that is entirely owned by billionaire Sir Richard Branson – because he met a guy at a convention.

And Misner is really good at networking.

“I stayed in touch with the person, and when there was an opportunity, I got invited to this incredible ethics program on Necker where I had a chance to meet Sir Richard. It all comes from building relationships with people,” said Misner, founder and chairman of BNI (Business Network International), a 32-year-old global business networking platform based in Charlotte, N.C., that has led CNN to call him “the father of modern networking.”

Ivan Misner once spent one week on Necker Island – the tony 74-acre island in the British Virgin Islands that is entirely owned by billionaire Sir Richard Branson – because he met a guy at a convention.

And Misner is really good at networking.

“I stayed in touch with the person, and when there was an opportunity, I got invited to this incredible ethics program on Necker where I had a chance to meet Sir Richard. It all comes from building relationships with people,” said Misner, founder and chairman of BNI (Business Network International), a 32-year-old global business networking platform based in Charlotte, N.C., that has led CNN to call him “the father of modern networking.”

Ivan Misner once spent one week on Necker Island – the tony 74-acre island in the British Virgin Islands that is entirely owned by billionaire Sir Richard Branson – because he met a guy at a convention.

And Misner is really good at networking.

“I stayed in touch with the person, and when there was an opportunity, I got invited to this incredible ethics program on Necker where I had a chance to meet Sir Richard. It all comes from building relationships with people,” said Misner, founder and chairman of BNI (Business Network International), a 32-year-old global business networking platform based in Charlotte, N.C., that has led CNN to call him “the father of modern networking.”

You have decided it is time to move on from your current hospital or medical group position and transition into a new role. While this decision is exciting and well-earned after years of hard work, it is critical that you make a plan and take specific steps to ensure that the transition is seamless.

The steps below are recommendations to make this process smoother.
 

Step 1: Determine how you are leaving the practice and your proposed timeline

Before anything else, you should decide how you are leaving your practice. Are you leaving the practice of medicine altogether, or are you simply leaving your current position for a different position elsewhere? This distinction will dictate what steps are necessary. Timing is also critical when leaving a practice, as it will dictate what steps should be taken and when. Having specific but realistic goals is imperative. Select a goal date for leaving the practice, but be aware that this goal may need to be adjusted.

Step 2: Create your team of advisers

Whether you are leaving your current practice or transitioning to a different position, it is extremely important to have the right individuals on your team. You should consider enlisting an attorney, a financial adviser, and an accountant to help facilitate the process. Enlisting lawyers with certain areas of expertise, such as in the areas of employment restrictive covenants, health care, or tax, may also be extremely beneficial and helpful throughout the process.

Step 3: Review your current employment agreement

It is quite likely that at the onset of your current employment arrangement, you signed an employment agreement with your hospital or group. You will want to carefully review this agreement, as it may contain provisions that can affect the steps you should take before you leave your current practice and work elsewhere. These provisions include the following:

a) Noncompetition provisions

It is critical to determine whether or not there are any restrictive covenants in your employment agreement that limit where you can work after you transition from your current practice into a new role. Restrictive covenants include noncompetition and nonsolicitation provisions, and prohibit employees from working at certain places or in certain geographic areas after they leave their current place of employment. Rules surrounding restrictive covenants vary from state to state. If there are restrictive covenants in your agreement, be sure to understand the scope of the covenant, including the geographic and temporal scope, as well as the types of medicine you are prohibited from practicing. If the covenants seem too broad or unnecessarily restrictive, consult with an attorney, as overly broad or unduly burdensome covenants are often unenforceable. However, a state-by-state analysis is required.

b) Notice and termination provisions

It is important to review whether or not there are any notice requirements in your employment agreement, which may require you to notify your employer in advance of a departure. Make sure to comply with the time requirements in the notice provision to avoid a breach of the agreement. It is also critical to determine whether terminating an agreement early will result in any termination penalties. At times, employers will impose a penalty if an employee prematurely terminates a working relationship. Understanding the penalties associated with terminating your agreement will allow you to decide whether you want to cancel the agreement and pay the penalty or push back your timeline until the end of the agreement’s term to avoid termination fees.

Step 4: Licensure obligations

macrovector/Thinkstock

Further, if your practice bills Medicare, you will want to file certain forms with Medicare to show that you are either changing your practice location or leaving medicine. For example, if you are leaving the hospital or group to practice elsewhere, you will need to fill out forms in order for your old group to submit claims and receive payments for Medicare services you provided while you were still part of that group. Furthermore, you will need to file reassignment forms to allow your new practice to bill on your behalf. Understanding which forms to complete can be confusing, so enlisting the help of a healthcare attorney may be worthwhile.
 

Step 5: Discuss your transition with your insurance representative

Even after you leave your current practice, you may be exposed to litigation for services you provided while you were employed or otherwise retained by such practice. To ensure that you are protected, discuss your insurance policy with your insurance representative. Review whether your insurance policy is “occurrence” or “claims-made.” If you have an occurrence policy, you are protected from covered incidents that occur during the policy period, regardless if your policy is still in existence. Claims-made policies only provide coverage for claims where both the incident and the claim occur during the policy period. For example, if you cancel your policy on March 1, and are sued on April 1 for an incident that allegedly occurred on Feb. 1, your claims-made insurance policy will not protect you. Therefore, it is important to analyze your policies to determine if tail insurance is needed.

There are a number of other issues you will want to address before you leave your practice, including financial responsibilities and medical record and privacy obligations. To ensure that you leave your practice properly, you should contact an experienced lawyer who can help you navigate this process.
 

Steven M. Harris is a nationally recognized health care attorney and a member of the law firm McDonald Hopkins LLC in Chicago. Write to him at [email protected].

You have decided it is time to move on from your current hospital or medical group position and transition into a new role. While this decision is exciting and well-earned after years of hard work, it is critical that you make a plan and take specific steps to ensure that the transition is seamless.

The steps below are recommendations to make this process smoother.
 

Step 1: Determine how you are leaving the practice and your proposed timeline

Before anything else, you should decide how you are leaving your practice. Are you leaving the practice of medicine altogether, or are you simply leaving your current position for a different position elsewhere? This distinction will dictate what steps are necessary. Timing is also critical when leaving a practice, as it will dictate what steps should be taken and when. Having specific but realistic goals is imperative. Select a goal date for leaving the practice, but be aware that this goal may need to be adjusted.

Step 2: Create your team of advisers

Whether you are leaving your current practice or transitioning to a different position, it is extremely important to have the right individuals on your team. You should consider enlisting an attorney, a financial adviser, and an accountant to help facilitate the process. Enlisting lawyers with certain areas of expertise, such as in the areas of employment restrictive covenants, health care, or tax, may also be extremely beneficial and helpful throughout the process.

Step 3: Review your current employment agreement

It is quite likely that at the onset of your current employment arrangement, you signed an employment agreement with your hospital or group. You will want to carefully review this agreement, as it may contain provisions that can affect the steps you should take before you leave your current practice and work elsewhere. These provisions include the following:

a) Noncompetition provisions

It is critical to determine whether or not there are any restrictive covenants in your employment agreement that limit where you can work after you transition from your current practice into a new role. Restrictive covenants include noncompetition and nonsolicitation provisions, and prohibit employees from working at certain places or in certain geographic areas after they leave their current place of employment. Rules surrounding restrictive covenants vary from state to state. If there are restrictive covenants in your agreement, be sure to understand the scope of the covenant, including the geographic and temporal scope, as well as the types of medicine you are prohibited from practicing. If the covenants seem too broad or unnecessarily restrictive, consult with an attorney, as overly broad or unduly burdensome covenants are often unenforceable. However, a state-by-state analysis is required.

b) Notice and termination provisions

It is important to review whether or not there are any notice requirements in your employment agreement, which may require you to notify your employer in advance of a departure. Make sure to comply with the time requirements in the notice provision to avoid a breach of the agreement. It is also critical to determine whether terminating an agreement early will result in any termination penalties. At times, employers will impose a penalty if an employee prematurely terminates a working relationship. Understanding the penalties associated with terminating your agreement will allow you to decide whether you want to cancel the agreement and pay the penalty or push back your timeline until the end of the agreement’s term to avoid termination fees.

Step 4: Licensure obligations

macrovector/Thinkstock

Further, if your practice bills Medicare, you will want to file certain forms with Medicare to show that you are either changing your practice location or leaving medicine. For example, if you are leaving the hospital or group to practice elsewhere, you will need to fill out forms in order for your old group to submit claims and receive payments for Medicare services you provided while you were still part of that group. Furthermore, you will need to file reassignment forms to allow your new practice to bill on your behalf. Understanding which forms to complete can be confusing, so enlisting the help of a healthcare attorney may be worthwhile.
 

Step 5: Discuss your transition with your insurance representative

Even after you leave your current practice, you may be exposed to litigation for services you provided while you were employed or otherwise retained by such practice. To ensure that you are protected, discuss your insurance policy with your insurance representative. Review whether your insurance policy is “occurrence” or “claims-made.” If you have an occurrence policy, you are protected from covered incidents that occur during the policy period, regardless if your policy is still in existence. Claims-made policies only provide coverage for claims where both the incident and the claim occur during the policy period. For example, if you cancel your policy on March 1, and are sued on April 1 for an incident that allegedly occurred on Feb. 1, your claims-made insurance policy will not protect you. Therefore, it is important to analyze your policies to determine if tail insurance is needed.

There are a number of other issues you will want to address before you leave your practice, including financial responsibilities and medical record and privacy obligations. To ensure that you leave your practice properly, you should contact an experienced lawyer who can help you navigate this process.
 

Steven M. Harris is a nationally recognized health care attorney and a member of the law firm McDonald Hopkins LLC in Chicago. Write to him at [email protected].

You have decided it is time to move on from your current hospital or medical group position and transition into a new role. While this decision is exciting and well-earned after years of hard work, it is critical that you make a plan and take specific steps to ensure that the transition is seamless.

The steps below are recommendations to make this process smoother.
 

Step 1: Determine how you are leaving the practice and your proposed timeline

Before anything else, you should decide how you are leaving your practice. Are you leaving the practice of medicine altogether, or are you simply leaving your current position for a different position elsewhere? This distinction will dictate what steps are necessary. Timing is also critical when leaving a practice, as it will dictate what steps should be taken and when. Having specific but realistic goals is imperative. Select a goal date for leaving the practice, but be aware that this goal may need to be adjusted.

Step 2: Create your team of advisers

Whether you are leaving your current practice or transitioning to a different position, it is extremely important to have the right individuals on your team. You should consider enlisting an attorney, a financial adviser, and an accountant to help facilitate the process. Enlisting lawyers with certain areas of expertise, such as in the areas of employment restrictive covenants, health care, or tax, may also be extremely beneficial and helpful throughout the process.

Step 3: Review your current employment agreement

It is quite likely that at the onset of your current employment arrangement, you signed an employment agreement with your hospital or group. You will want to carefully review this agreement, as it may contain provisions that can affect the steps you should take before you leave your current practice and work elsewhere. These provisions include the following:

a) Noncompetition provisions

It is critical to determine whether or not there are any restrictive covenants in your employment agreement that limit where you can work after you transition from your current practice into a new role. Restrictive covenants include noncompetition and nonsolicitation provisions, and prohibit employees from working at certain places or in certain geographic areas after they leave their current place of employment. Rules surrounding restrictive covenants vary from state to state. If there are restrictive covenants in your agreement, be sure to understand the scope of the covenant, including the geographic and temporal scope, as well as the types of medicine you are prohibited from practicing. If the covenants seem too broad or unnecessarily restrictive, consult with an attorney, as overly broad or unduly burdensome covenants are often unenforceable. However, a state-by-state analysis is required.

b) Notice and termination provisions

It is important to review whether or not there are any notice requirements in your employment agreement, which may require you to notify your employer in advance of a departure. Make sure to comply with the time requirements in the notice provision to avoid a breach of the agreement. It is also critical to determine whether terminating an agreement early will result in any termination penalties. At times, employers will impose a penalty if an employee prematurely terminates a working relationship. Understanding the penalties associated with terminating your agreement will allow you to decide whether you want to cancel the agreement and pay the penalty or push back your timeline until the end of the agreement’s term to avoid termination fees.

Step 4: Licensure obligations

macrovector/Thinkstock

Further, if your practice bills Medicare, you will want to file certain forms with Medicare to show that you are either changing your practice location or leaving medicine. For example, if you are leaving the hospital or group to practice elsewhere, you will need to fill out forms in order for your old group to submit claims and receive payments for Medicare services you provided while you were still part of that group. Furthermore, you will need to file reassignment forms to allow your new practice to bill on your behalf. Understanding which forms to complete can be confusing, so enlisting the help of a healthcare attorney may be worthwhile.
 

Step 5: Discuss your transition with your insurance representative

Even after you leave your current practice, you may be exposed to litigation for services you provided while you were employed or otherwise retained by such practice. To ensure that you are protected, discuss your insurance policy with your insurance representative. Review whether your insurance policy is “occurrence” or “claims-made.” If you have an occurrence policy, you are protected from covered incidents that occur during the policy period, regardless if your policy is still in existence. Claims-made policies only provide coverage for claims where both the incident and the claim occur during the policy period. For example, if you cancel your policy on March 1, and are sued on April 1 for an incident that allegedly occurred on Feb. 1, your claims-made insurance policy will not protect you. Therefore, it is important to analyze your policies to determine if tail insurance is needed.

There are a number of other issues you will want to address before you leave your practice, including financial responsibilities and medical record and privacy obligations. To ensure that you leave your practice properly, you should contact an experienced lawyer who can help you navigate this process.
 

Steven M. Harris is a nationally recognized health care attorney and a member of the law firm McDonald Hopkins LLC in Chicago. Write to him at [email protected].

We are in the midst of a revolution in genome editing. Science now exists in “AC,” or after CRISPR. Able to speedily and efficiently make genomic cuts with surgical precision, CRISPR/Cas9 is used almost ubiquitously now in the scientific community to study and alter DNA across fields ranging from medicine to agriculture to zoology. The possibilities of the biological and therapeutic implications are seemingly endless, as are the important ethical implications of their impact. Likely because of the latter, CRISPR technology has made its way from publications like Science and Nature into the lay public domains of Newsweek and NBC News.

In fact, CRISPR technology made its way into one of my favorite podcasts, WNYC’s “Radio Lab” in June 2015¹. The episode was entitled “Antibodies Part 1,” perhaps assuming that other technologies would also be discussed later although that has never happened. Actually, in an update early this year, the podcast jokingly addressed never moving on to “Part 2,” then followed with an update on how far CRISPR technology has progressed. Putting aside the technological advances and the early clinical applications, as well as the immense ethical considerations, CRISPR technology faces a new controversy, not one from a white coat but rather from a black robe.

References:

1. Radio Lab

2. CommonHealth blog

3. Jinek M, et al., A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity. Science. 2012 Aug 17;337(6096):816-21.

4. Le Cong et al., Multiplex genome engineering using CRISPR/Cas Systems. Science. 2013 Feb 15;339(6121):819-23. Multiplex genome engineering using CRISPR/Cas Systems.

Science. 2017 Feb 15: Round one of CRISPR patent legal battle goes to the Broad Institute.

StreetInsider.com: CRISPR Therapeutics (CRSP) says EPO to grant CRISPR/Cas gene editing patent.
 

[email protected]

On Twitter @thedoctorisvin
 

Dr. Viny is with the Memorial Sloan-Kettering Cancer Center, N.Y., where he is a clinical instructor, is on the staff of the leukemia service, and is a clinical researcher in the Ross Levine Lab. Contact Dr. Viny at [email protected].

We are in the midst of a revolution in genome editing. Science now exists in “AC,” or after CRISPR. Able to speedily and efficiently make genomic cuts with surgical precision, CRISPR/Cas9 is used almost ubiquitously now in the scientific community to study and alter DNA across fields ranging from medicine to agriculture to zoology. The possibilities of the biological and therapeutic implications are seemingly endless, as are the important ethical implications of their impact. Likely because of the latter, CRISPR technology has made its way from publications like Science and Nature into the lay public domains of Newsweek and NBC News.

In fact, CRISPR technology made its way into one of my favorite podcasts, WNYC’s “Radio Lab” in June 2015¹. The episode was entitled “Antibodies Part 1,” perhaps assuming that other technologies would also be discussed later although that has never happened. Actually, in an update early this year, the podcast jokingly addressed never moving on to “Part 2,” then followed with an update on how far CRISPR technology has progressed. Putting aside the technological advances and the early clinical applications, as well as the immense ethical considerations, CRISPR technology faces a new controversy, not one from a white coat but rather from a black robe.

References:

1. Radio Lab

2. CommonHealth blog

3. Jinek M, et al., A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity. Science. 2012 Aug 17;337(6096):816-21.

4. Le Cong et al., Multiplex genome engineering using CRISPR/Cas Systems. Science. 2013 Feb 15;339(6121):819-23. Multiplex genome engineering using CRISPR/Cas Systems.

Science. 2017 Feb 15: Round one of CRISPR patent legal battle goes to the Broad Institute.

StreetInsider.com: CRISPR Therapeutics (CRSP) says EPO to grant CRISPR/Cas gene editing patent.
 

[email protected]

On Twitter @thedoctorisvin
 

Dr. Viny is with the Memorial Sloan-Kettering Cancer Center, N.Y., where he is a clinical instructor, is on the staff of the leukemia service, and is a clinical researcher in the Ross Levine Lab. Contact Dr. Viny at [email protected].

We are in the midst of a revolution in genome editing. Science now exists in “AC,” or after CRISPR. Able to speedily and efficiently make genomic cuts with surgical precision, CRISPR/Cas9 is used almost ubiquitously now in the scientific community to study and alter DNA across fields ranging from medicine to agriculture to zoology. The possibilities of the biological and therapeutic implications are seemingly endless, as are the important ethical implications of their impact. Likely because of the latter, CRISPR technology has made its way from publications like Science and Nature into the lay public domains of Newsweek and NBC News.

In fact, CRISPR technology made its way into one of my favorite podcasts, WNYC’s “Radio Lab” in June 2015¹. The episode was entitled “Antibodies Part 1,” perhaps assuming that other technologies would also be discussed later although that has never happened. Actually, in an update early this year, the podcast jokingly addressed never moving on to “Part 2,” then followed with an update on how far CRISPR technology has progressed. Putting aside the technological advances and the early clinical applications, as well as the immense ethical considerations, CRISPR technology faces a new controversy, not one from a white coat but rather from a black robe.

References:

1. Radio Lab

2. CommonHealth blog

3. Jinek M, et al., A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity. Science. 2012 Aug 17;337(6096):816-21.

4. Le Cong et al., Multiplex genome engineering using CRISPR/Cas Systems. Science. 2013 Feb 15;339(6121):819-23. Multiplex genome engineering using CRISPR/Cas Systems.

Science. 2017 Feb 15: Round one of CRISPR patent legal battle goes to the Broad Institute.

StreetInsider.com: CRISPR Therapeutics (CRSP) says EPO to grant CRISPR/Cas gene editing patent.
 

[email protected]

On Twitter @thedoctorisvin
 

Dr. Viny is with the Memorial Sloan-Kettering Cancer Center, N.Y., where he is a clinical instructor, is on the staff of the leukemia service, and is a clinical researcher in the Ross Levine Lab. Contact Dr. Viny at [email protected].