Emergency Medicine

A 55-year-old man with type 2 diabetes mellitus, hypertension, anemia, and ulcerative colitis presented to the emergency department with an ulcer on his left leg (Figure 1). He said the lesion had started as a “large pimple” that ruptured one night while he was sleeping and then became drastically worse over the past week. He said the lesion was painful and was “oozing blood.”

On examination, the lesion was 7 cm by 6.5 cm, with fibrinous, necrotic tissue, purulence, and a violaceous tint at the borders. The patient’s body temperature was 100.5°F (38.1°C) and the white blood cell count was 8.1 x 10⁹/L (reference range 4.0–11.0).

Based on the patient’s medical history, the lesion was initially diagnosed as an infected diabetic ulcer. He was admitted to the hospital and intravenous (IV) vancomycin and clindamycin were started. During this time, the lesion expanded in size, and a second lesion appeared on the right anterior thigh, in similar fashion to how the original lesion had started. The original lesion expanded to 8 cm by 8.5 cm by hospital day 2. The patient continued to have episodes of low-grade fever without leukocytosis.

Cultures of blood and tissue from the lesions were negative, ruling out bacterial infection. Magnetic resonance imaging of the left tibia was negative for osteomyelitis. Punch biopsy of the ulcer border was done on day 3 to evaluate for pyoderma gangrenosum.

On hospital day 5, the patient developed acute kidney injury, with a creatinine increase to 2.17 mg/dL over 24 hours from a baseline value of 0.82 mg/dL. The IV antibiotics were discontinued, and IV fluid hydration was started. At this time, diabetic ulcer secondary to infection and osteomyelitis were ruled out. The lesions were diagnosed as pyoderma gangrenosum.

The patient was started on prednisone 30 mg twice daily. After 2 days, the low-grade fevers resolved, both lesions began to heal, and his creatinine level returned to baseline (Figure 2). He was discharged on hospital day 10. The prednisone was tapered over 1 month, with wet-to-dry dressing changes for wound care.

After discharge, he remained adherent to his steroid regimen. At a follow-up visit to his dermatologist, the ulcers had fully closed, and the skin had begun to heal. Results of the punch biopsy study came back 2 days after the patient was discharged and further confirmed the diagnosis, with a mixed lymphocytic composition composed primarily of neutrophils.

APPROACH TO DIAGNOSIS

Pyoderma gangrenosum is rare, with an incidence of 3 to 10 cases per million people per year.¹ It is a rapidly progressive ulcerative condition typically associated with inflammatory bowel disease.² Despite its name, the condition involves neither gangrene nor infection. The ulcer typically appears on the legs and is rapidly growing, painful, and purulent, with tissue necrosis and a violaceous border.³

Pyoderma gangrenosum is often misdiagnosed as infective ulcer and inappropriately treated with antibiotics.² It can also be mistreated with surgical debridement, which can result in severe complications such as pathergy.¹

The differential diagnosis includes diabetic ulcer, peripheral vascular disease, vasculitis, bacterial infection, osteomyelitis, and malignancy. Because it presents as an open, necrotic ulcer, ruling out infection is a top priority.³ However, an initial workup to rule out infection or other conditions can delay diagnosis and treatment,¹ and treatment with broad-spectrum antibiotics poses the risk of nephrotoxicity and new complications during the hospital stay.

Diagnosis requires meeting 2 major criteria—ie, presence of the characteristic ulcerous lesion, and exclusion of other causes of skin ulceration—and at least 2 minor criteria including histologic confirmation of neutrophil infiltrate at the ulcer border, the presence of a systemic disease associated with pyoderma gangrenosum, and a rapid response to steroid treatment.^4,5

Our patient was at high risk for an infected diabetic ulcer. After infection was ruled out, clinical suspicion for pyoderma gangrenosum was high, given the patient’s presentation and his history of ulcerative colitis.

TREATMENT

Treatment of pyoderma gangrenosum begins with systemic corticosteroids, as was done in this patient. Additional measures depend on whether the disease is localized or extensive and can include wound care, topical treatments, immunosuppressants, and immunomodulators.¹

A 55-year-old man with type 2 diabetes mellitus, hypertension, anemia, and ulcerative colitis presented to the emergency department with an ulcer on his left leg (Figure 1). He said the lesion had started as a “large pimple” that ruptured one night while he was sleeping and then became drastically worse over the past week. He said the lesion was painful and was “oozing blood.”

On examination, the lesion was 7 cm by 6.5 cm, with fibrinous, necrotic tissue, purulence, and a violaceous tint at the borders. The patient’s body temperature was 100.5°F (38.1°C) and the white blood cell count was 8.1 x 10⁹/L (reference range 4.0–11.0).

Based on the patient’s medical history, the lesion was initially diagnosed as an infected diabetic ulcer. He was admitted to the hospital and intravenous (IV) vancomycin and clindamycin were started. During this time, the lesion expanded in size, and a second lesion appeared on the right anterior thigh, in similar fashion to how the original lesion had started. The original lesion expanded to 8 cm by 8.5 cm by hospital day 2. The patient continued to have episodes of low-grade fever without leukocytosis.

Cultures of blood and tissue from the lesions were negative, ruling out bacterial infection. Magnetic resonance imaging of the left tibia was negative for osteomyelitis. Punch biopsy of the ulcer border was done on day 3 to evaluate for pyoderma gangrenosum.

On hospital day 5, the patient developed acute kidney injury, with a creatinine increase to 2.17 mg/dL over 24 hours from a baseline value of 0.82 mg/dL. The IV antibiotics were discontinued, and IV fluid hydration was started. At this time, diabetic ulcer secondary to infection and osteomyelitis were ruled out. The lesions were diagnosed as pyoderma gangrenosum.

The patient was started on prednisone 30 mg twice daily. After 2 days, the low-grade fevers resolved, both lesions began to heal, and his creatinine level returned to baseline (Figure 2). He was discharged on hospital day 10. The prednisone was tapered over 1 month, with wet-to-dry dressing changes for wound care.

After discharge, he remained adherent to his steroid regimen. At a follow-up visit to his dermatologist, the ulcers had fully closed, and the skin had begun to heal. Results of the punch biopsy study came back 2 days after the patient was discharged and further confirmed the diagnosis, with a mixed lymphocytic composition composed primarily of neutrophils.

APPROACH TO DIAGNOSIS

Pyoderma gangrenosum is rare, with an incidence of 3 to 10 cases per million people per year.¹ It is a rapidly progressive ulcerative condition typically associated with inflammatory bowel disease.² Despite its name, the condition involves neither gangrene nor infection. The ulcer typically appears on the legs and is rapidly growing, painful, and purulent, with tissue necrosis and a violaceous border.³

Pyoderma gangrenosum is often misdiagnosed as infective ulcer and inappropriately treated with antibiotics.² It can also be mistreated with surgical debridement, which can result in severe complications such as pathergy.¹

The differential diagnosis includes diabetic ulcer, peripheral vascular disease, vasculitis, bacterial infection, osteomyelitis, and malignancy. Because it presents as an open, necrotic ulcer, ruling out infection is a top priority.³ However, an initial workup to rule out infection or other conditions can delay diagnosis and treatment,¹ and treatment with broad-spectrum antibiotics poses the risk of nephrotoxicity and new complications during the hospital stay.

Diagnosis requires meeting 2 major criteria—ie, presence of the characteristic ulcerous lesion, and exclusion of other causes of skin ulceration—and at least 2 minor criteria including histologic confirmation of neutrophil infiltrate at the ulcer border, the presence of a systemic disease associated with pyoderma gangrenosum, and a rapid response to steroid treatment.^4,5

Our patient was at high risk for an infected diabetic ulcer. After infection was ruled out, clinical suspicion for pyoderma gangrenosum was high, given the patient’s presentation and his history of ulcerative colitis.

TREATMENT

Treatment of pyoderma gangrenosum begins with systemic corticosteroids, as was done in this patient. Additional measures depend on whether the disease is localized or extensive and can include wound care, topical treatments, immunosuppressants, and immunomodulators.¹

A 55-year-old man with type 2 diabetes mellitus, hypertension, anemia, and ulcerative colitis presented to the emergency department with an ulcer on his left leg (Figure 1). He said the lesion had started as a “large pimple” that ruptured one night while he was sleeping and then became drastically worse over the past week. He said the lesion was painful and was “oozing blood.”

On examination, the lesion was 7 cm by 6.5 cm, with fibrinous, necrotic tissue, purulence, and a violaceous tint at the borders. The patient’s body temperature was 100.5°F (38.1°C) and the white blood cell count was 8.1 x 10⁹/L (reference range 4.0–11.0).

Based on the patient’s medical history, the lesion was initially diagnosed as an infected diabetic ulcer. He was admitted to the hospital and intravenous (IV) vancomycin and clindamycin were started. During this time, the lesion expanded in size, and a second lesion appeared on the right anterior thigh, in similar fashion to how the original lesion had started. The original lesion expanded to 8 cm by 8.5 cm by hospital day 2. The patient continued to have episodes of low-grade fever without leukocytosis.

Cultures of blood and tissue from the lesions were negative, ruling out bacterial infection. Magnetic resonance imaging of the left tibia was negative for osteomyelitis. Punch biopsy of the ulcer border was done on day 3 to evaluate for pyoderma gangrenosum.

On hospital day 5, the patient developed acute kidney injury, with a creatinine increase to 2.17 mg/dL over 24 hours from a baseline value of 0.82 mg/dL. The IV antibiotics were discontinued, and IV fluid hydration was started. At this time, diabetic ulcer secondary to infection and osteomyelitis were ruled out. The lesions were diagnosed as pyoderma gangrenosum.

The patient was started on prednisone 30 mg twice daily. After 2 days, the low-grade fevers resolved, both lesions began to heal, and his creatinine level returned to baseline (Figure 2). He was discharged on hospital day 10. The prednisone was tapered over 1 month, with wet-to-dry dressing changes for wound care.

After discharge, he remained adherent to his steroid regimen. At a follow-up visit to his dermatologist, the ulcers had fully closed, and the skin had begun to heal. Results of the punch biopsy study came back 2 days after the patient was discharged and further confirmed the diagnosis, with a mixed lymphocytic composition composed primarily of neutrophils.

APPROACH TO DIAGNOSIS

Pyoderma gangrenosum is rare, with an incidence of 3 to 10 cases per million people per year.¹ It is a rapidly progressive ulcerative condition typically associated with inflammatory bowel disease.² Despite its name, the condition involves neither gangrene nor infection. The ulcer typically appears on the legs and is rapidly growing, painful, and purulent, with tissue necrosis and a violaceous border.³

Pyoderma gangrenosum is often misdiagnosed as infective ulcer and inappropriately treated with antibiotics.² It can also be mistreated with surgical debridement, which can result in severe complications such as pathergy.¹

The differential diagnosis includes diabetic ulcer, peripheral vascular disease, vasculitis, bacterial infection, osteomyelitis, and malignancy. Because it presents as an open, necrotic ulcer, ruling out infection is a top priority.³ However, an initial workup to rule out infection or other conditions can delay diagnosis and treatment,¹ and treatment with broad-spectrum antibiotics poses the risk of nephrotoxicity and new complications during the hospital stay.

Diagnosis requires meeting 2 major criteria—ie, presence of the characteristic ulcerous lesion, and exclusion of other causes of skin ulceration—and at least 2 minor criteria including histologic confirmation of neutrophil infiltrate at the ulcer border, the presence of a systemic disease associated with pyoderma gangrenosum, and a rapid response to steroid treatment.^4,5

Our patient was at high risk for an infected diabetic ulcer. After infection was ruled out, clinical suspicion for pyoderma gangrenosum was high, given the patient’s presentation and his history of ulcerative colitis.

TREATMENT

Treatment of pyoderma gangrenosum begins with systemic corticosteroids, as was done in this patient. Additional measures depend on whether the disease is localized or extensive and can include wound care, topical treatments, immunosuppressants, and immunomodulators.¹

I have been ruminating about the Bai et al article on independent billing in the emergency department (ED) for weeks.¹ I keep wondering why the data analysis seems so off base. Don’t get me wrong: The data gathered from Medicare is what it is—but a key piece of information is not present in the pure numbers input to the Medicare database.

So, I continued to probe this study with my colleagues. To a person, their comments supported that the intent of the study is unclear. The authors posit their objective to be an examination of the “involvement of NPs and PAs” in emergency services, using billing data. But to use billing data as a measure of “involvement” does not tell the whole story.

Independence in billing does not mean that the care NPs and PAs are providing is “beyond their scope of practice.” Moreover, the billing does not capture whether, or to what extent, physician consultation or assistance was involved. If the NP or PA dictated the chart, then they are by default the “only” (independent) provider. However, billing independently does not mean a physician (or other provider) was not consulted about the plan of care. 

Case in point: Years ago, I had a young woman present to the ED with a sore throat. Her presenting complaint was a symptom of a peritonsillar abscess. So I phoned an ENT colleague (a physician) and asked him about the best treatment and follow-up in this case. Did he make a note in or sign the chart? No. Was I the only provider of record? Yes. Was that care “independent,” if you only look at the billing (done by a coder, for the record)? Yes. 

Admittedly, Bai and colleagues do add in their conclusion that “independence in billing … does not necessarily indicate [NPs’/PAs’] independence in care delivery.”1 And they do note that the true challenge in the ED is determining how best to “blend” the expertise of the three professions (MD, NP, and PA) to provide efficient and cost-effective care.

However, throughout the article, there is an underpinning of inference that NPs and PAs are potentially practicing beyond their scope. Their comment that the increase in billing for NP and PA services results in a “reduction of the proportion of emergency physicians” speaks volumes.¹ Perhaps there is more concern here about ED physician job security than about independent billing!

Regardless of the intention by Bai et al—and acknowledging that the analysis they presented is somewhat interesting—I see two missed opportunities to “actionalize” the data.² One is to use the information to identify whether a problem with billing exists (ie, is there upcharging as a result of more details contained within the electronic health record?). The second is to use the data to investigate innovative ways to improve access to care across the continuum. Essentially, how do we use the results of any data analysis in a way that can be useful? That is the real challenge. 

Continue to: The biggest conclusion I've drawn...

The biggest conclusion I’ve drawn from my exploration of these study findings? The opportunity to investigate the competencies of all ED providers, with the goal of improving access and controlling costs, is there. And as the NPs and PAs providing the care, we should undertake the next research study or data analysis and not leave the research on us to other professions!

I’d love to hear your thoughts on the Bai et al study or any aspect of this 4-part discussion! Drop me a line at NPEditor@mdege.com.

I have been ruminating about the Bai et al article on independent billing in the emergency department (ED) for weeks.¹ I keep wondering why the data analysis seems so off base. Don’t get me wrong: The data gathered from Medicare is what it is—but a key piece of information is not present in the pure numbers input to the Medicare database.

So, I continued to probe this study with my colleagues. To a person, their comments supported that the intent of the study is unclear. The authors posit their objective to be an examination of the “involvement of NPs and PAs” in emergency services, using billing data. But to use billing data as a measure of “involvement” does not tell the whole story.

Independence in billing does not mean that the care NPs and PAs are providing is “beyond their scope of practice.” Moreover, the billing does not capture whether, or to what extent, physician consultation or assistance was involved. If the NP or PA dictated the chart, then they are by default the “only” (independent) provider. However, billing independently does not mean a physician (or other provider) was not consulted about the plan of care. 

Case in point: Years ago, I had a young woman present to the ED with a sore throat. Her presenting complaint was a symptom of a peritonsillar abscess. So I phoned an ENT colleague (a physician) and asked him about the best treatment and follow-up in this case. Did he make a note in or sign the chart? No. Was I the only provider of record? Yes. Was that care “independent,” if you only look at the billing (done by a coder, for the record)? Yes. 

Admittedly, Bai and colleagues do add in their conclusion that “independence in billing … does not necessarily indicate [NPs’/PAs’] independence in care delivery.”1 And they do note that the true challenge in the ED is determining how best to “blend” the expertise of the three professions (MD, NP, and PA) to provide efficient and cost-effective care.

However, throughout the article, there is an underpinning of inference that NPs and PAs are potentially practicing beyond their scope. Their comment that the increase in billing for NP and PA services results in a “reduction of the proportion of emergency physicians” speaks volumes.¹ Perhaps there is more concern here about ED physician job security than about independent billing!

Regardless of the intention by Bai et al—and acknowledging that the analysis they presented is somewhat interesting—I see two missed opportunities to “actionalize” the data.² One is to use the information to identify whether a problem with billing exists (ie, is there upcharging as a result of more details contained within the electronic health record?). The second is to use the data to investigate innovative ways to improve access to care across the continuum. Essentially, how do we use the results of any data analysis in a way that can be useful? That is the real challenge. 

Continue to: The biggest conclusion I've drawn...

The biggest conclusion I’ve drawn from my exploration of these study findings? The opportunity to investigate the competencies of all ED providers, with the goal of improving access and controlling costs, is there. And as the NPs and PAs providing the care, we should undertake the next research study or data analysis and not leave the research on us to other professions!

I’d love to hear your thoughts on the Bai et al study or any aspect of this 4-part discussion! Drop me a line at NPEditor@mdege.com.

I have been ruminating about the Bai et al article on independent billing in the emergency department (ED) for weeks.¹ I keep wondering why the data analysis seems so off base. Don’t get me wrong: The data gathered from Medicare is what it is—but a key piece of information is not present in the pure numbers input to the Medicare database.

So, I continued to probe this study with my colleagues. To a person, their comments supported that the intent of the study is unclear. The authors posit their objective to be an examination of the “involvement of NPs and PAs” in emergency services, using billing data. But to use billing data as a measure of “involvement” does not tell the whole story.

Independence in billing does not mean that the care NPs and PAs are providing is “beyond their scope of practice.” Moreover, the billing does not capture whether, or to what extent, physician consultation or assistance was involved. If the NP or PA dictated the chart, then they are by default the “only” (independent) provider. However, billing independently does not mean a physician (or other provider) was not consulted about the plan of care. 

Case in point: Years ago, I had a young woman present to the ED with a sore throat. Her presenting complaint was a symptom of a peritonsillar abscess. So I phoned an ENT colleague (a physician) and asked him about the best treatment and follow-up in this case. Did he make a note in or sign the chart? No. Was I the only provider of record? Yes. Was that care “independent,” if you only look at the billing (done by a coder, for the record)? Yes. 

Admittedly, Bai and colleagues do add in their conclusion that “independence in billing … does not necessarily indicate [NPs’/PAs’] independence in care delivery.”1 And they do note that the true challenge in the ED is determining how best to “blend” the expertise of the three professions (MD, NP, and PA) to provide efficient and cost-effective care.

However, throughout the article, there is an underpinning of inference that NPs and PAs are potentially practicing beyond their scope. Their comment that the increase in billing for NP and PA services results in a “reduction of the proportion of emergency physicians” speaks volumes.¹ Perhaps there is more concern here about ED physician job security than about independent billing!

Regardless of the intention by Bai et al—and acknowledging that the analysis they presented is somewhat interesting—I see two missed opportunities to “actionalize” the data.² One is to use the information to identify whether a problem with billing exists (ie, is there upcharging as a result of more details contained within the electronic health record?). The second is to use the data to investigate innovative ways to improve access to care across the continuum. Essentially, how do we use the results of any data analysis in a way that can be useful? That is the real challenge. 

Continue to: The biggest conclusion I've drawn...

The biggest conclusion I’ve drawn from my exploration of these study findings? The opportunity to investigate the competencies of all ED providers, with the goal of improving access and controlling costs, is there. And as the NPs and PAs providing the care, we should undertake the next research study or data analysis and not leave the research on us to other professions!

I’d love to hear your thoughts on the Bai et al study or any aspect of this 4-part discussion! Drop me a line at NPEditor@mdege.com.

Diagnostic error is the most common allegation against pediatricians when sued by patients and their families, a study finds.

Investigators with The Doctors Company, a national medical liability insurer, examined 1,215 closed claims involving children from the company’s database between 2008 and 2017. Results showed that diagnostic mistakes, including delayed diagnosis, incorrect diagnosis, and failure to diagnose, were the most common accusations among claims that involved children ages 1 through 17. Poor medical treatment was the second most common allegation for claims that involved children aged 1-9, while surgical treatment-related error was the second most frequent accusation for children ages 10-17.

Pediatricians, orthopedic surgeons, and emergency medicine physicians were the most frequently named specialists in claims associated with children older than 1 month. Obstetricians were most frequently defendants in claims involving neonates. For these cases, errors during labor and delivery care were the most common complaints.

Of the 1,215 claims, obstetricians were named in 24% of the cases and pediatricians were named in 15% of the cases. The majority of claims were filed against physicians in the first 3 years following the medical incident alleged, according to the study, published by The Doctors Company.

The average patient payment in each case was $630,456, and the average expense to defend each claim was $157,502, according to the analysis. Claims that involved neonates had the highest average payment ($936,843) and the highest defense costs ($187,117), while claims involving children aged 10-17 years had the lowest average payment ($386,849) and cost the least to defend ($129,816).

For cases involving neonates, the type of therapy selected during labor and delivery and how it was managed were the most common factors contributing to the alleged injury, according to the analysis.

The most frequent factors contributing to patient harm for other age groups involved patient assessment issues and communication problems between the patient/family and the physician. Inadequate patient assessments were closely linked to incorrect diagnoses, while incomplete communication between patients/family members and providers impacted clinicians’ ability to make correct diagnoses, according to the study.

This analysis “shows that pediatric malpractice lawsuits impact nearly every area of medicine,” William F. Getman, MD, a pediatrician in Austin, Tex., said in an interview. “I was surprised to see that the most common age of a patient in a malpractice lawsuit was less than 1 month old. This age group also sustained the most severe injuries and had the highest indemnity paid.”

The study offers several key takeaways, including the importance of identifying system weaknesses in your medical practice and evaluating if improvements are needed, according to Darrell Ranum, vice president for patient safety and risk management for The Doctors Company.

agallegos@mdedge.com

SOURCE: Ranum, D. The Doctor’s Advocate. First Quarter 2019.

Diagnostic error is the most common allegation against pediatricians when sued by patients and their families, a study finds.

Investigators with The Doctors Company, a national medical liability insurer, examined 1,215 closed claims involving children from the company’s database between 2008 and 2017. Results showed that diagnostic mistakes, including delayed diagnosis, incorrect diagnosis, and failure to diagnose, were the most common accusations among claims that involved children ages 1 through 17. Poor medical treatment was the second most common allegation for claims that involved children aged 1-9, while surgical treatment-related error was the second most frequent accusation for children ages 10-17.

Pediatricians, orthopedic surgeons, and emergency medicine physicians were the most frequently named specialists in claims associated with children older than 1 month. Obstetricians were most frequently defendants in claims involving neonates. For these cases, errors during labor and delivery care were the most common complaints.

Of the 1,215 claims, obstetricians were named in 24% of the cases and pediatricians were named in 15% of the cases. The majority of claims were filed against physicians in the first 3 years following the medical incident alleged, according to the study, published by The Doctors Company.

The average patient payment in each case was $630,456, and the average expense to defend each claim was $157,502, according to the analysis. Claims that involved neonates had the highest average payment ($936,843) and the highest defense costs ($187,117), while claims involving children aged 10-17 years had the lowest average payment ($386,849) and cost the least to defend ($129,816).

For cases involving neonates, the type of therapy selected during labor and delivery and how it was managed were the most common factors contributing to the alleged injury, according to the analysis.

The most frequent factors contributing to patient harm for other age groups involved patient assessment issues and communication problems between the patient/family and the physician. Inadequate patient assessments were closely linked to incorrect diagnoses, while incomplete communication between patients/family members and providers impacted clinicians’ ability to make correct diagnoses, according to the study.

This analysis “shows that pediatric malpractice lawsuits impact nearly every area of medicine,” William F. Getman, MD, a pediatrician in Austin, Tex., said in an interview. “I was surprised to see that the most common age of a patient in a malpractice lawsuit was less than 1 month old. This age group also sustained the most severe injuries and had the highest indemnity paid.”

The study offers several key takeaways, including the importance of identifying system weaknesses in your medical practice and evaluating if improvements are needed, according to Darrell Ranum, vice president for patient safety and risk management for The Doctors Company.

agallegos@mdedge.com

SOURCE: Ranum, D. The Doctor’s Advocate. First Quarter 2019.

Diagnostic error is the most common allegation against pediatricians when sued by patients and their families, a study finds.

Investigators with The Doctors Company, a national medical liability insurer, examined 1,215 closed claims involving children from the company’s database between 2008 and 2017. Results showed that diagnostic mistakes, including delayed diagnosis, incorrect diagnosis, and failure to diagnose, were the most common accusations among claims that involved children ages 1 through 17. Poor medical treatment was the second most common allegation for claims that involved children aged 1-9, while surgical treatment-related error was the second most frequent accusation for children ages 10-17.

Pediatricians, orthopedic surgeons, and emergency medicine physicians were the most frequently named specialists in claims associated with children older than 1 month. Obstetricians were most frequently defendants in claims involving neonates. For these cases, errors during labor and delivery care were the most common complaints.

Of the 1,215 claims, obstetricians were named in 24% of the cases and pediatricians were named in 15% of the cases. The majority of claims were filed against physicians in the first 3 years following the medical incident alleged, according to the study, published by The Doctors Company.

The average patient payment in each case was $630,456, and the average expense to defend each claim was $157,502, according to the analysis. Claims that involved neonates had the highest average payment ($936,843) and the highest defense costs ($187,117), while claims involving children aged 10-17 years had the lowest average payment ($386,849) and cost the least to defend ($129,816).

For cases involving neonates, the type of therapy selected during labor and delivery and how it was managed were the most common factors contributing to the alleged injury, according to the analysis.

The most frequent factors contributing to patient harm for other age groups involved patient assessment issues and communication problems between the patient/family and the physician. Inadequate patient assessments were closely linked to incorrect diagnoses, while incomplete communication between patients/family members and providers impacted clinicians’ ability to make correct diagnoses, according to the study.

This analysis “shows that pediatric malpractice lawsuits impact nearly every area of medicine,” William F. Getman, MD, a pediatrician in Austin, Tex., said in an interview. “I was surprised to see that the most common age of a patient in a malpractice lawsuit was less than 1 month old. This age group also sustained the most severe injuries and had the highest indemnity paid.”

The study offers several key takeaways, including the importance of identifying system weaknesses in your medical practice and evaluating if improvements are needed, according to Darrell Ranum, vice president for patient safety and risk management for The Doctors Company.

agallegos@mdedge.com

SOURCE: Ranum, D. The Doctor’s Advocate. First Quarter 2019.

The Food and Drug Administration on April 19 approved the first generic naloxone hydrochloride nasal spray (Narcan) as treatment for stopping or reversing an opioid overdose.

“In the wake of the opioid crisis, a number of efforts are underway to make this emergency overdose reversal treatment more readily available and more accessible,” said Douglas Throckmorton, MD, deputy center director for regulatory programs in the FDA’s Center for Drug Evaluation and Research, in a press release. “In addition to this approval of the first generic naloxone nasal spray, moving forward, we will prioritize our review of generic drug applications for naloxone.”

The agency said the naloxone nasal spray does not need assembly and can be used by anyone, regardless of medical training. The drug is administered by spraying naloxone into one nostril while a patient is lying on his or her back and can be repeated. If the spray is administered quickly after the overdose begins, the effect of the opioid will be countered, often within minutes. However, patients should still seek immediate medical attention.

The FDA cautioned that, when used on a patient with an opioid dependence, naloxone can cause severe opioid withdrawal, characterized by symptoms such as body aches, diarrhea, tachycardia, fever, runny nose, sneezing, goose bumps, sweating, yawning, nausea or vomiting, nervousness, restlessness or irritability, shivering or trembling, abdominal cramps, weakness, and increased blood pressure.

Find the full press release on the FDA website.

lfranki@mdedge.com

The Food and Drug Administration on April 19 approved the first generic naloxone hydrochloride nasal spray (Narcan) as treatment for stopping or reversing an opioid overdose.

“In the wake of the opioid crisis, a number of efforts are underway to make this emergency overdose reversal treatment more readily available and more accessible,” said Douglas Throckmorton, MD, deputy center director for regulatory programs in the FDA’s Center for Drug Evaluation and Research, in a press release. “In addition to this approval of the first generic naloxone nasal spray, moving forward, we will prioritize our review of generic drug applications for naloxone.”

The agency said the naloxone nasal spray does not need assembly and can be used by anyone, regardless of medical training. The drug is administered by spraying naloxone into one nostril while a patient is lying on his or her back and can be repeated. If the spray is administered quickly after the overdose begins, the effect of the opioid will be countered, often within minutes. However, patients should still seek immediate medical attention.

The FDA cautioned that, when used on a patient with an opioid dependence, naloxone can cause severe opioid withdrawal, characterized by symptoms such as body aches, diarrhea, tachycardia, fever, runny nose, sneezing, goose bumps, sweating, yawning, nausea or vomiting, nervousness, restlessness or irritability, shivering or trembling, abdominal cramps, weakness, and increased blood pressure.

Find the full press release on the FDA website.

lfranki@mdedge.com

The Food and Drug Administration on April 19 approved the first generic naloxone hydrochloride nasal spray (Narcan) as treatment for stopping or reversing an opioid overdose.

“In the wake of the opioid crisis, a number of efforts are underway to make this emergency overdose reversal treatment more readily available and more accessible,” said Douglas Throckmorton, MD, deputy center director for regulatory programs in the FDA’s Center for Drug Evaluation and Research, in a press release. “In addition to this approval of the first generic naloxone nasal spray, moving forward, we will prioritize our review of generic drug applications for naloxone.”

The agency said the naloxone nasal spray does not need assembly and can be used by anyone, regardless of medical training. The drug is administered by spraying naloxone into one nostril while a patient is lying on his or her back and can be repeated. If the spray is administered quickly after the overdose begins, the effect of the opioid will be countered, often within minutes. However, patients should still seek immediate medical attention.

The FDA cautioned that, when used on a patient with an opioid dependence, naloxone can cause severe opioid withdrawal, characterized by symptoms such as body aches, diarrhea, tachycardia, fever, runny nose, sneezing, goose bumps, sweating, yawning, nausea or vomiting, nervousness, restlessness or irritability, shivering or trembling, abdominal cramps, weakness, and increased blood pressure.

Find the full press release on the FDA website.

lfranki@mdedge.com

Nurse practitioners (and PAs, I would submit) have been the most researched group of health care professionals since the inception of the role. Much of that research has focused on evaluating our contributions to primary care. Numerous studies of NP performance in various settings have concluded that we perform as well as physicians with respect to patient outcomes, proper diagnosis, management of specific medical conditions, and patient satisfaction.¹

Over the past 10 years, however, the interest in our roles has shifted from the primary care arena to the emergency department (ED). Even before the introduction of the Affordable Care Act (ACA), two-thirds of all EDs utilized NPs and PAs.² The ACA increased the number of Americans with insurance coverage, resulting in a greater demand for health care services—including ED utilization. Faced with an already strained system, hospital administrators looked for a solution and found one: hiring NPs and PAs to augment the clinician workforce.

This decision to (increasingly) employ NPs and PAs in ED settings was based on a desire to reduce wait times, increase throughput, improve access to care, and control costs. For the most part, these goals have been achieved. A systematic review of the impact of NPs in the ED on quality of care and patient satisfaction demonstrated a reduction in wait times.³ Moreover, in a national survey that included a review of the types of visits made to the ED, NPs and PAs were comparable to MDs in terms of reasons for care, diagnosis, and treatment.⁴

Given these results, I again ask: What was the intent of the research by Bai et al?⁵ Surely proper and prompt care is the goal of every ED provider. So the decision to examine only the billing is confounding.

Are the authors suggesting that hospital administrators prefer employing NPs and PAs over MDs? Are we replacing physicians in certain areas or filling voids where the physician workforce is inadequate to meet the community demands? Maybe yes to both. But, if the goal is to improve access, then we should focus on meeting the needs and on the quality of the care, not on who bills for it.

My cynical self says the goal of Bai et al was to establish that NPs and PAs are taking the jobs of ED physicians, and we must be stopped! Am I tilting at windmills with this train of thought? Next week, we’ll conclude our examination and draw our own conclusions! You can join the conversation by writing to NPEditor@mdedge.com.

Nurse practitioners (and PAs, I would submit) have been the most researched group of health care professionals since the inception of the role. Much of that research has focused on evaluating our contributions to primary care. Numerous studies of NP performance in various settings have concluded that we perform as well as physicians with respect to patient outcomes, proper diagnosis, management of specific medical conditions, and patient satisfaction.¹

Over the past 10 years, however, the interest in our roles has shifted from the primary care arena to the emergency department (ED). Even before the introduction of the Affordable Care Act (ACA), two-thirds of all EDs utilized NPs and PAs.² The ACA increased the number of Americans with insurance coverage, resulting in a greater demand for health care services—including ED utilization. Faced with an already strained system, hospital administrators looked for a solution and found one: hiring NPs and PAs to augment the clinician workforce.

This decision to (increasingly) employ NPs and PAs in ED settings was based on a desire to reduce wait times, increase throughput, improve access to care, and control costs. For the most part, these goals have been achieved. A systematic review of the impact of NPs in the ED on quality of care and patient satisfaction demonstrated a reduction in wait times.³ Moreover, in a national survey that included a review of the types of visits made to the ED, NPs and PAs were comparable to MDs in terms of reasons for care, diagnosis, and treatment.⁴

Given these results, I again ask: What was the intent of the research by Bai et al?⁵ Surely proper and prompt care is the goal of every ED provider. So the decision to examine only the billing is confounding.

Are the authors suggesting that hospital administrators prefer employing NPs and PAs over MDs? Are we replacing physicians in certain areas or filling voids where the physician workforce is inadequate to meet the community demands? Maybe yes to both. But, if the goal is to improve access, then we should focus on meeting the needs and on the quality of the care, not on who bills for it.

My cynical self says the goal of Bai et al was to establish that NPs and PAs are taking the jobs of ED physicians, and we must be stopped! Am I tilting at windmills with this train of thought? Next week, we’ll conclude our examination and draw our own conclusions! You can join the conversation by writing to NPEditor@mdedge.com.

Nurse practitioners (and PAs, I would submit) have been the most researched group of health care professionals since the inception of the role. Much of that research has focused on evaluating our contributions to primary care. Numerous studies of NP performance in various settings have concluded that we perform as well as physicians with respect to patient outcomes, proper diagnosis, management of specific medical conditions, and patient satisfaction.¹

Over the past 10 years, however, the interest in our roles has shifted from the primary care arena to the emergency department (ED). Even before the introduction of the Affordable Care Act (ACA), two-thirds of all EDs utilized NPs and PAs.² The ACA increased the number of Americans with insurance coverage, resulting in a greater demand for health care services—including ED utilization. Faced with an already strained system, hospital administrators looked for a solution and found one: hiring NPs and PAs to augment the clinician workforce.

This decision to (increasingly) employ NPs and PAs in ED settings was based on a desire to reduce wait times, increase throughput, improve access to care, and control costs. For the most part, these goals have been achieved. A systematic review of the impact of NPs in the ED on quality of care and patient satisfaction demonstrated a reduction in wait times.³ Moreover, in a national survey that included a review of the types of visits made to the ED, NPs and PAs were comparable to MDs in terms of reasons for care, diagnosis, and treatment.⁴

Given these results, I again ask: What was the intent of the research by Bai et al?⁵ Surely proper and prompt care is the goal of every ED provider. So the decision to examine only the billing is confounding.

Are the authors suggesting that hospital administrators prefer employing NPs and PAs over MDs? Are we replacing physicians in certain areas or filling voids where the physician workforce is inadequate to meet the community demands? Maybe yes to both. But, if the goal is to improve access, then we should focus on meeting the needs and on the quality of the care, not on who bills for it.

My cynical self says the goal of Bai et al was to establish that NPs and PAs are taking the jobs of ED physicians, and we must be stopped! Am I tilting at windmills with this train of thought? Next week, we’ll conclude our examination and draw our own conclusions! You can join the conversation by writing to NPEditor@mdedge.com.

In an attempt to understand the data presented by Bai et al regarding independent billing by NPs and PAs in the emergency department (ED), I reached out to several colleagues to get their take on the study.¹ Four of them are ED providers (2 MDs, 1 NP, 1 PA), and another is an experienced data analyst. In short, the analysis was analyzed!

Each member of my “expert panel” had similar comments and concerns, particularly regarding billing versus providing care. These are two different animals, or—as I often say—Bai and colleagues were comparing “oranges and shoes.” Several colleagues questioned the purpose of the article: What were the authors really trying to say?

Both MDs noted the absence of comments related to any consultation between the NP/PA and the ED physician during the patient encounter. They also pointed out the sheer volume of patients in EDs, resulting in the increasing popularity and utilization of NP/PAs to provide timely care to patients in need.

More than one of us initially wondered whether there could be potential “overbilling.” With the implementation of electronic health records (EHRs), the average charge per patient has increased. Maybe the EHR, now so common in EDs, more accurately captures the amount of time the provider spends caring for the patient and allows for more detailed documentation of the visit. This might result in a prima facie higher level of billing without necessarily representing the acuity of the presenting complaint.

One fact not presented in the Bai article is that, in many instances, providers (whether MDs, NPs, or PAs) do not complete the bills submitted to the insurance companies. In many EDs, medical coders extract the patient encounter data from the medical record. The reality is, the acuity of the patient is being decided by the person who is coding the visit—not the provider. And thus, it is potentially flawed thinking to rely on billing data alone to assess an increase in the acuity of patients seen by NPs and PAs in the ED.

Since we know (through data!) that there are more NPs and PAs providing care in EDs across the country, it follows logically that there will be more bills submitted in our names. This leads me to wonder: What was the motivation for Bai and colleagues to perform this study? What point are they actually trying to make?

Stay tuned ... There’s more to say next week! (In the meantime, you can share your thoughts by writing to me at NPEditor@mdedge.com.)

In an attempt to understand the data presented by Bai et al regarding independent billing by NPs and PAs in the emergency department (ED), I reached out to several colleagues to get their take on the study.¹ Four of them are ED providers (2 MDs, 1 NP, 1 PA), and another is an experienced data analyst. In short, the analysis was analyzed!

Each member of my “expert panel” had similar comments and concerns, particularly regarding billing versus providing care. These are two different animals, or—as I often say—Bai and colleagues were comparing “oranges and shoes.” Several colleagues questioned the purpose of the article: What were the authors really trying to say?

Both MDs noted the absence of comments related to any consultation between the NP/PA and the ED physician during the patient encounter. They also pointed out the sheer volume of patients in EDs, resulting in the increasing popularity and utilization of NP/PAs to provide timely care to patients in need.

More than one of us initially wondered whether there could be potential “overbilling.” With the implementation of electronic health records (EHRs), the average charge per patient has increased. Maybe the EHR, now so common in EDs, more accurately captures the amount of time the provider spends caring for the patient and allows for more detailed documentation of the visit. This might result in a prima facie higher level of billing without necessarily representing the acuity of the presenting complaint.

One fact not presented in the Bai article is that, in many instances, providers (whether MDs, NPs, or PAs) do not complete the bills submitted to the insurance companies. In many EDs, medical coders extract the patient encounter data from the medical record. The reality is, the acuity of the patient is being decided by the person who is coding the visit—not the provider. And thus, it is potentially flawed thinking to rely on billing data alone to assess an increase in the acuity of patients seen by NPs and PAs in the ED.

Since we know (through data!) that there are more NPs and PAs providing care in EDs across the country, it follows logically that there will be more bills submitted in our names. This leads me to wonder: What was the motivation for Bai and colleagues to perform this study? What point are they actually trying to make?

Stay tuned ... There’s more to say next week! (In the meantime, you can share your thoughts by writing to me at NPEditor@mdedge.com.)

In an attempt to understand the data presented by Bai et al regarding independent billing by NPs and PAs in the emergency department (ED), I reached out to several colleagues to get their take on the study.¹ Four of them are ED providers (2 MDs, 1 NP, 1 PA), and another is an experienced data analyst. In short, the analysis was analyzed!

Each member of my “expert panel” had similar comments and concerns, particularly regarding billing versus providing care. These are two different animals, or—as I often say—Bai and colleagues were comparing “oranges and shoes.” Several colleagues questioned the purpose of the article: What were the authors really trying to say?

Both MDs noted the absence of comments related to any consultation between the NP/PA and the ED physician during the patient encounter. They also pointed out the sheer volume of patients in EDs, resulting in the increasing popularity and utilization of NP/PAs to provide timely care to patients in need.

More than one of us initially wondered whether there could be potential “overbilling.” With the implementation of electronic health records (EHRs), the average charge per patient has increased. Maybe the EHR, now so common in EDs, more accurately captures the amount of time the provider spends caring for the patient and allows for more detailed documentation of the visit. This might result in a prima facie higher level of billing without necessarily representing the acuity of the presenting complaint.

One fact not presented in the Bai article is that, in many instances, providers (whether MDs, NPs, or PAs) do not complete the bills submitted to the insurance companies. In many EDs, medical coders extract the patient encounter data from the medical record. The reality is, the acuity of the patient is being decided by the person who is coding the visit—not the provider. And thus, it is potentially flawed thinking to rely on billing data alone to assess an increase in the acuity of patients seen by NPs and PAs in the ED.

Since we know (through data!) that there are more NPs and PAs providing care in EDs across the country, it follows logically that there will be more bills submitted in our names. This leads me to wonder: What was the motivation for Bai and colleagues to perform this study? What point are they actually trying to make?

Stay tuned ... There’s more to say next week! (In the meantime, you can share your thoughts by writing to me at NPEditor@mdedge.com.)

Recently, my colleague Randy D. Danielsen, PhD, DFAAPA, PA-C Emeritus, shared a study from the American Journal of Emergency Medicine that focused on “the involvement of NPs and PAs who billed independently” in emergency departments (EDs).¹ In casual conversation, several of us agreed the findings didn’t “pass the sniff test,” so I decided to do some investigating.

The context: Data from 2006-2009 indicate that in two-thirds of all EDs, NPs and PAs are involved in the care of 13.7% of all patients.² Further analysis of Medicare Public Use Files from 2014 reveal that of 58,641 unique emergency medicine clinicians, 14,360 (24.5%) are advanced practice providers.³ All interesting statistics.

The American Journal of Emergency Medicine article, however, gave me (and several colleagues) pause. In it, the authors presented their analysis of Medicare provider utilization and payment data from 2012-2016.¹ The researchers documented billing increases of 65% for NPs and 35% for PAs.

But what stopped me in my tracks was that the researchers emphasized an increase—from 18% to 24%—in NP/PA treatment of patients with the highest severity illness or injury (CPT code 99285).¹ I discussed this finding with ED-based colleagues, and they too questioned its accuracy.

In fact, the more we parsed this study, the more questions we had … and the higher our eyebrows raised. What were the researchers examining and drawing conclusions on— independent billing by NPs and PAs, or independent practice? These are two very different measures. Were the authors in fact grousing about the increase in NP/PA providers in EDs? 

There is a paucity of research on billing by NPs and PAs, and the discussion surrounding this particular study will undoubtedly prompt additional questions. Over the next 3 weeks, we invite you to join us on Thursdays as we continue our examination of this data—and encourage you to share your thoughts with us along the way!

Recently, my colleague Randy D. Danielsen, PhD, DFAAPA, PA-C Emeritus, shared a study from the American Journal of Emergency Medicine that focused on “the involvement of NPs and PAs who billed independently” in emergency departments (EDs).¹ In casual conversation, several of us agreed the findings didn’t “pass the sniff test,” so I decided to do some investigating.

The context: Data from 2006-2009 indicate that in two-thirds of all EDs, NPs and PAs are involved in the care of 13.7% of all patients.² Further analysis of Medicare Public Use Files from 2014 reveal that of 58,641 unique emergency medicine clinicians, 14,360 (24.5%) are advanced practice providers.³ All interesting statistics.

The American Journal of Emergency Medicine article, however, gave me (and several colleagues) pause. In it, the authors presented their analysis of Medicare provider utilization and payment data from 2012-2016.¹ The researchers documented billing increases of 65% for NPs and 35% for PAs.

But what stopped me in my tracks was that the researchers emphasized an increase—from 18% to 24%—in NP/PA treatment of patients with the highest severity illness or injury (CPT code 99285).¹ I discussed this finding with ED-based colleagues, and they too questioned its accuracy.

In fact, the more we parsed this study, the more questions we had … and the higher our eyebrows raised. What were the researchers examining and drawing conclusions on— independent billing by NPs and PAs, or independent practice? These are two very different measures. Were the authors in fact grousing about the increase in NP/PA providers in EDs? 

There is a paucity of research on billing by NPs and PAs, and the discussion surrounding this particular study will undoubtedly prompt additional questions. Over the next 3 weeks, we invite you to join us on Thursdays as we continue our examination of this data—and encourage you to share your thoughts with us along the way!

Recently, my colleague Randy D. Danielsen, PhD, DFAAPA, PA-C Emeritus, shared a study from the American Journal of Emergency Medicine that focused on “the involvement of NPs and PAs who billed independently” in emergency departments (EDs).¹ In casual conversation, several of us agreed the findings didn’t “pass the sniff test,” so I decided to do some investigating.

The context: Data from 2006-2009 indicate that in two-thirds of all EDs, NPs and PAs are involved in the care of 13.7% of all patients.² Further analysis of Medicare Public Use Files from 2014 reveal that of 58,641 unique emergency medicine clinicians, 14,360 (24.5%) are advanced practice providers.³ All interesting statistics.

The American Journal of Emergency Medicine article, however, gave me (and several colleagues) pause. In it, the authors presented their analysis of Medicare provider utilization and payment data from 2012-2016.¹ The researchers documented billing increases of 65% for NPs and 35% for PAs.

But what stopped me in my tracks was that the researchers emphasized an increase—from 18% to 24%—in NP/PA treatment of patients with the highest severity illness or injury (CPT code 99285).¹ I discussed this finding with ED-based colleagues, and they too questioned its accuracy.

In fact, the more we parsed this study, the more questions we had … and the higher our eyebrows raised. What were the researchers examining and drawing conclusions on— independent billing by NPs and PAs, or independent practice? These are two very different measures. Were the authors in fact grousing about the increase in NP/PA providers in EDs? 

There is a paucity of research on billing by NPs and PAs, and the discussion surrounding this particular study will undoubtedly prompt additional questions. Over the next 3 weeks, we invite you to join us on Thursdays as we continue our examination of this data—and encourage you to share your thoughts with us along the way!

WASHINGTON – Of patients with ST-elevation MI (STEMI) complicated by cardiogenic shock, 13% are readmitted within 30 days and remain in hospital for an average of 6 days, according to an analysis from the National Readmission Database presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

“About one in four of the readmissions was for heart failure,” reported Karan Sud, MD, a cardiology resident at the Mount Sinai St. Luke’s West Hospital, New York.

Despite gains in acute survival among STEMI patients in cardiogenic shock, little attention has been paid to the risk of readmissions, according to Dr. Sud. According to data collected from the National Readmissions Database for 2010-2014, these rates are high enough to deserve attention, he said.
 

“Our goal is now to develop a scoring system based on our predictive model to identify patients at the index admission who are at risk for readmission,” Dr. Sud reported. On the basis of these predictors, it might be possible to implement strategies to optimize management and improve access to care.

In the years studied, there were 94,991 patients with STEMI and cardiogenic shock captured in the National Readmissions Database, of whom 43,205 survived and were followed for readmission. Of the 5,503 readmissions within 30 days, 12% were considered unplanned.

Half of the readmissions were for noncardiovascular causes, including sepsis, respiratory failure, and major bleeding. Of those related to cardiovascular disease, about half, or nearly 25% of the total, were for heart failure.

The predictors of readmission included female sex, age older than 75 years, average length of stay longer than 10 days, and more than three comorbidities, such as diabetes or chronic kidney disease, according to Dr. Sud.

“Those sent home from the index admission were more likely than those discharged to an extended care facility to be readmitted,” he added. He also noted that lower socioeconomic status was a risk factor for readmission, a phenomenon that he attributed to access issues regarding follow-up care.

“We are now conducting a prospective study to look at readmissions at 6 months,” reported Dr. Sud, who believes that efforts to understand the risk of readmission following STEMI complicated by cardiogenic shock might uncover opportunities for better management.

WASHINGTON – Of patients with ST-elevation MI (STEMI) complicated by cardiogenic shock, 13% are readmitted within 30 days and remain in hospital for an average of 6 days, according to an analysis from the National Readmission Database presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

“About one in four of the readmissions was for heart failure,” reported Karan Sud, MD, a cardiology resident at the Mount Sinai St. Luke’s West Hospital, New York.

Despite gains in acute survival among STEMI patients in cardiogenic shock, little attention has been paid to the risk of readmissions, according to Dr. Sud. According to data collected from the National Readmissions Database for 2010-2014, these rates are high enough to deserve attention, he said.
 

“Our goal is now to develop a scoring system based on our predictive model to identify patients at the index admission who are at risk for readmission,” Dr. Sud reported. On the basis of these predictors, it might be possible to implement strategies to optimize management and improve access to care.

In the years studied, there were 94,991 patients with STEMI and cardiogenic shock captured in the National Readmissions Database, of whom 43,205 survived and were followed for readmission. Of the 5,503 readmissions within 30 days, 12% were considered unplanned.

Half of the readmissions were for noncardiovascular causes, including sepsis, respiratory failure, and major bleeding. Of those related to cardiovascular disease, about half, or nearly 25% of the total, were for heart failure.

The predictors of readmission included female sex, age older than 75 years, average length of stay longer than 10 days, and more than three comorbidities, such as diabetes or chronic kidney disease, according to Dr. Sud.

“Those sent home from the index admission were more likely than those discharged to an extended care facility to be readmitted,” he added. He also noted that lower socioeconomic status was a risk factor for readmission, a phenomenon that he attributed to access issues regarding follow-up care.

“We are now conducting a prospective study to look at readmissions at 6 months,” reported Dr. Sud, who believes that efforts to understand the risk of readmission following STEMI complicated by cardiogenic shock might uncover opportunities for better management.

WASHINGTON – Of patients with ST-elevation MI (STEMI) complicated by cardiogenic shock, 13% are readmitted within 30 days and remain in hospital for an average of 6 days, according to an analysis from the National Readmission Database presented at CRT 2019 sponsored by MedStar Heart & Vascular Institute.

“About one in four of the readmissions was for heart failure,” reported Karan Sud, MD, a cardiology resident at the Mount Sinai St. Luke’s West Hospital, New York.

Despite gains in acute survival among STEMI patients in cardiogenic shock, little attention has been paid to the risk of readmissions, according to Dr. Sud. According to data collected from the National Readmissions Database for 2010-2014, these rates are high enough to deserve attention, he said.
 

“Our goal is now to develop a scoring system based on our predictive model to identify patients at the index admission who are at risk for readmission,” Dr. Sud reported. On the basis of these predictors, it might be possible to implement strategies to optimize management and improve access to care.

In the years studied, there were 94,991 patients with STEMI and cardiogenic shock captured in the National Readmissions Database, of whom 43,205 survived and were followed for readmission. Of the 5,503 readmissions within 30 days, 12% were considered unplanned.

Half of the readmissions were for noncardiovascular causes, including sepsis, respiratory failure, and major bleeding. Of those related to cardiovascular disease, about half, or nearly 25% of the total, were for heart failure.

The predictors of readmission included female sex, age older than 75 years, average length of stay longer than 10 days, and more than three comorbidities, such as diabetes or chronic kidney disease, according to Dr. Sud.

“Those sent home from the index admission were more likely than those discharged to an extended care facility to be readmitted,” he added. He also noted that lower socioeconomic status was a risk factor for readmission, a phenomenon that he attributed to access issues regarding follow-up care.

“We are now conducting a prospective study to look at readmissions at 6 months,” reported Dr. Sud, who believes that efforts to understand the risk of readmission following STEMI complicated by cardiogenic shock might uncover opportunities for better management.

A 12-lead electrocardiogram (Figure 1) showed ST-segment elevation of more than 2 mm in leads V₂, V₃, V₄, and V₅, with no reciprocal changes.

Based on the classic angiographic appearance and the absence of atherosclerotic disease in other coronary arteries, type 2 spontaneous coronary artery dissection (SCAD) was diagnosed.

CORONARY ARTERY WALL SEPARATION

SCAD is defined as a nontraumatic, noniatrogenic intramural hemorrhage leading to separation of the coronary arterial wall and the formation of a false lumen. The separation can occur between any of the coronary artery wall layers and may or may not involve an intimal tear. The bleeding may result in an intramural hematoma and possible narrowing of the arterial lumen. Depending on the severity of narrowing, blood supply to the myocardium could be compromised, resulting in symptoms of ischemia.¹

SCAD usually involves a single coronary artery, although multiple coronary artery involvement has been reported.²

CASE CONTINUED: MANAGEMENT

The patient recovered completely and was discharged home with plans to return for outpatient imaging for fibromuscular dysplasia.

SCAD appears to be a rare cause of acute coronary syndrome, but it is likely underdiagnosed and is becoming increasingly recognized worldwide. Typically, it affects women younger than 50, with women in general outnumbering men 9 to 1.³ Overall, SCAD causes up to 4% of acute myocardial infarctions, but in women age 50 or younger, it is responsible for 24% to 35% of acute myocardial infarctions, and the proportion is even higher in pregnant women.⁴

Not just pregnancy-associated    

SCAD was previously thought to be mainly idiopathic and mostly affecting women peripartum. Current understanding paints a different picture: pregnancy-associated SCAD does not account for the majority of cases. That said, SCAD is the most common cause of myocardial infarction peripartum, with the third trimester and early postpartum period being the times of highest risk.⁵ SCAD development at those times is believed to be related to hormonal changes causing weakening of coronary artery walls.⁶

Weakening of the coronary artery wall also may occur in the setting of fibromuscular dysplasia, connective tissue disease, recurrent pregnancies, systemic inflammatory disease, hormonal therapy, and other disease states that cause arteriopathy. Exposure to a stressor in a patient with underlying risk factors can lead to either an intimal tear or rupture of the vasa vasorum, with subsequent formation of intramural hemorrhage and eventually SCAD.⁷ Stressors can be emotional or physical and can include labor and delivery, intense physical exercise, the Valsalva maneuver, and drug abuse.⁸

Presentation is variable

SCAD presentation depends on the degree of flow limitation and extent of the dissection. Presentation can range from asymptomatic to sudden cardiac death and can include signs and symptoms of acute coronary syndrome caused by ST-segment elevation or non-ST-segment elevation myocardial infarction.

DIAGNOSIS BY ANGIOGRAPHY    

SCAD can be diagnosed by coronary angiography. There are 3 angiographic types:

Type 1 (about 25% of SCAD cases) has typical contrast dye staining of the arterial wall and multiple radiolucent luminal abnormalities, with or without dye hang-up.

Type 2 (about 70%) has diffuse, smooth narrowing of the coronary artery, with the left anterior descending artery the most frequently affected.⁸

Type 3 (about 5%) mimics atherosclerosis, with focal or tubular stenosis.⁹

Types 1 and 2 are usually easy to recognize. To diagnose type 2, intravenous nitroglycerin should first be administered to rule out coronary spasm.

Type 3 SCAD is more challenging to diagnose because its appearance on angiography is similar to that of atherosclerosis. For equivocal findings in any type, but especially in type 3, intravascular ultrasonography or optical coherence tomography can help.¹⁰ Optical coherence tomography is preferred because of superior image resolution, although ultrasonography offers better tissue penetration.¹¹ 

MANAGE MOST CASES CONSERVATIVELY

Management algorithms for SCAD are available.^8,12

The initial and most critical step is to make the correct diagnosis. Although the presentation of acute coronary syndrome caused by SCAD is often identical to that of atherosclerosis, the conditions have different pathophysiologies and thus require different management. Theoretically, systemic anticoagulation may worsen an intramural hemorrhage.

First-line therapy for most patients with SCAD is conservative management and close inpatient monitoring for 3 to 5 days.¹³ More aggressive management is indicated for any of the following:

• Left main or severe proximal 2-vessel dissection
• Hemodynamic instability
• Ongoing ischemic symptoms.

In a prospective cohort of 168 patients, 134 (80%) were initially treated conservatively; of those, in-hospital myocardial infarction recurred in 4.5%, a major cardiac event occurred within 2 years in 17%, and SCAD recurred in 13%.⁸

Observational data on patients with SCAD who had repeat angiography weeks to months after the initial event has shown that lesions heal in 70% to 97% of patients.¹²

WHEN TO CONSIDER AGGRESSIVE MANAGEMENT

Under the circumstances listed above, revascularization with PCI or coronary artery bypass grafting (CABG) should be considered, with choice of procedure determined by feasibility, technical considerations, and local expertise.

The American Heart Association recommendations are as follows¹²:     

• For left main or severe proximal 2-vessel dissection in clinically stable patients, consider CABG
• For active ischemia or hemodynamic instability, consider PCI if feasible or perform urgent CABG.

A few series have shown that the prognosis with conservative management or CABG is better than with PCI.^8,13,14 The success rate for revascularization with PCI is only about 60% because of challenges including risk of inducing iatrogenic dissection, passing the wire into the false lumen and worsening a dissection, and propagating an intramural hematoma with stenting and further compromising coronary blood flow. In addition, dissection tends to extend into distal arteries that are difficult to stent. There is also the risk of stent malapposition after resorption of the intramural hematoma, causing late stent thrombosis.⁷ 

SCREEN FOR OTHER VASCULAR PROBLEMS

Imaging of the renal, iliac, and cerebral vasculature is recommended for all patients with SCAD.¹² Screening for fibromuscular dysplasia can be done with angiography, computed tomographic angiography (CTA), or magnetic resonance angiography (MRA).¹² 

Multifocal fibromuscular dysplasia in extracoronary arteries occurs with SCAD in 25% to 86% of cases. In a single-center series of 115 patients with confirmed SCAD who underwent CTA from 2010 to 2014, extracoronary vascular abnormalities were found in 66%, with fibromuscular dysplasia being the most common type (45%).¹⁵ In another single-center study, 327 patients with SCAD were prospectively followed from 2012 to 2016 with screening for cerebrovascular, renal, and iliac fibromuscular dysplasia using CTA or catheter angiography. Fibromuscular dysplasia was found in 63%, and intracranial aneurysm was found in 14% of patients with fibromuscular dysplasia.⁹ 

SCAD can also be associated with connective tissue disorders such as Ehlers-Danlos syndrome type IV and Marfan syndrome.^16,17

LONG-TERM MANAGEMENT

Patients with SCAD should start long-term aspirin and 1 year of clopidogrel. Statins are indicated for patients with hyperlipidemia^8,18 but otherwise offer no clear benefit for SCAD alone. If there are no contraindications, a beta-adrenergic blocker should be considered, especially if left ventricular dysfunction or arrhythmias are present. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers should also be considered with concomitant left ventricular dysfunction. Antianginal therapy can be used for post-SCAD chest pain syndromes.¹²

Repeat angiography is recommended only to evaluate recurrent symptoms, to confirm an unclear initial diagnosis, to assess for atherosclerosis-related stenosis, or to evaluate high-risk anatomy, eg, involvement of the left main coronary artery.¹²

Genetic testing is reserved for patients with a high clinical suspicion of connective tissue disease or systemic arteriopathy.¹⁹

A 12-lead electrocardiogram (Figure 1) showed ST-segment elevation of more than 2 mm in leads V₂, V₃, V₄, and V₅, with no reciprocal changes.

Based on the classic angiographic appearance and the absence of atherosclerotic disease in other coronary arteries, type 2 spontaneous coronary artery dissection (SCAD) was diagnosed.

CORONARY ARTERY WALL SEPARATION

SCAD is defined as a nontraumatic, noniatrogenic intramural hemorrhage leading to separation of the coronary arterial wall and the formation of a false lumen. The separation can occur between any of the coronary artery wall layers and may or may not involve an intimal tear. The bleeding may result in an intramural hematoma and possible narrowing of the arterial lumen. Depending on the severity of narrowing, blood supply to the myocardium could be compromised, resulting in symptoms of ischemia.¹

SCAD usually involves a single coronary artery, although multiple coronary artery involvement has been reported.²

CASE CONTINUED: MANAGEMENT

The patient recovered completely and was discharged home with plans to return for outpatient imaging for fibromuscular dysplasia.

SCAD appears to be a rare cause of acute coronary syndrome, but it is likely underdiagnosed and is becoming increasingly recognized worldwide. Typically, it affects women younger than 50, with women in general outnumbering men 9 to 1.³ Overall, SCAD causes up to 4% of acute myocardial infarctions, but in women age 50 or younger, it is responsible for 24% to 35% of acute myocardial infarctions, and the proportion is even higher in pregnant women.⁴

Not just pregnancy-associated    

SCAD was previously thought to be mainly idiopathic and mostly affecting women peripartum. Current understanding paints a different picture: pregnancy-associated SCAD does not account for the majority of cases. That said, SCAD is the most common cause of myocardial infarction peripartum, with the third trimester and early postpartum period being the times of highest risk.⁵ SCAD development at those times is believed to be related to hormonal changes causing weakening of coronary artery walls.⁶

Weakening of the coronary artery wall also may occur in the setting of fibromuscular dysplasia, connective tissue disease, recurrent pregnancies, systemic inflammatory disease, hormonal therapy, and other disease states that cause arteriopathy. Exposure to a stressor in a patient with underlying risk factors can lead to either an intimal tear or rupture of the vasa vasorum, with subsequent formation of intramural hemorrhage and eventually SCAD.⁷ Stressors can be emotional or physical and can include labor and delivery, intense physical exercise, the Valsalva maneuver, and drug abuse.⁸

Presentation is variable

SCAD presentation depends on the degree of flow limitation and extent of the dissection. Presentation can range from asymptomatic to sudden cardiac death and can include signs and symptoms of acute coronary syndrome caused by ST-segment elevation or non-ST-segment elevation myocardial infarction.

DIAGNOSIS BY ANGIOGRAPHY    

SCAD can be diagnosed by coronary angiography. There are 3 angiographic types:

Type 1 (about 25% of SCAD cases) has typical contrast dye staining of the arterial wall and multiple radiolucent luminal abnormalities, with or without dye hang-up.

Type 2 (about 70%) has diffuse, smooth narrowing of the coronary artery, with the left anterior descending artery the most frequently affected.⁸

Type 3 (about 5%) mimics atherosclerosis, with focal or tubular stenosis.⁹

Types 1 and 2 are usually easy to recognize. To diagnose type 2, intravenous nitroglycerin should first be administered to rule out coronary spasm.

Type 3 SCAD is more challenging to diagnose because its appearance on angiography is similar to that of atherosclerosis. For equivocal findings in any type, but especially in type 3, intravascular ultrasonography or optical coherence tomography can help.¹⁰ Optical coherence tomography is preferred because of superior image resolution, although ultrasonography offers better tissue penetration.¹¹ 

MANAGE MOST CASES CONSERVATIVELY

Management algorithms for SCAD are available.^8,12

The initial and most critical step is to make the correct diagnosis. Although the presentation of acute coronary syndrome caused by SCAD is often identical to that of atherosclerosis, the conditions have different pathophysiologies and thus require different management. Theoretically, systemic anticoagulation may worsen an intramural hemorrhage.

First-line therapy for most patients with SCAD is conservative management and close inpatient monitoring for 3 to 5 days.¹³ More aggressive management is indicated for any of the following:

• Left main or severe proximal 2-vessel dissection
• Hemodynamic instability
• Ongoing ischemic symptoms.

In a prospective cohort of 168 patients, 134 (80%) were initially treated conservatively; of those, in-hospital myocardial infarction recurred in 4.5%, a major cardiac event occurred within 2 years in 17%, and SCAD recurred in 13%.⁸

Observational data on patients with SCAD who had repeat angiography weeks to months after the initial event has shown that lesions heal in 70% to 97% of patients.¹²

WHEN TO CONSIDER AGGRESSIVE MANAGEMENT

Under the circumstances listed above, revascularization with PCI or coronary artery bypass grafting (CABG) should be considered, with choice of procedure determined by feasibility, technical considerations, and local expertise.

The American Heart Association recommendations are as follows¹²:     

• For left main or severe proximal 2-vessel dissection in clinically stable patients, consider CABG
• For active ischemia or hemodynamic instability, consider PCI if feasible or perform urgent CABG.

A few series have shown that the prognosis with conservative management or CABG is better than with PCI.^8,13,14 The success rate for revascularization with PCI is only about 60% because of challenges including risk of inducing iatrogenic dissection, passing the wire into the false lumen and worsening a dissection, and propagating an intramural hematoma with stenting and further compromising coronary blood flow. In addition, dissection tends to extend into distal arteries that are difficult to stent. There is also the risk of stent malapposition after resorption of the intramural hematoma, causing late stent thrombosis.⁷ 

SCREEN FOR OTHER VASCULAR PROBLEMS

Imaging of the renal, iliac, and cerebral vasculature is recommended for all patients with SCAD.¹² Screening for fibromuscular dysplasia can be done with angiography, computed tomographic angiography (CTA), or magnetic resonance angiography (MRA).¹² 

Multifocal fibromuscular dysplasia in extracoronary arteries occurs with SCAD in 25% to 86% of cases. In a single-center series of 115 patients with confirmed SCAD who underwent CTA from 2010 to 2014, extracoronary vascular abnormalities were found in 66%, with fibromuscular dysplasia being the most common type (45%).¹⁵ In another single-center study, 327 patients with SCAD were prospectively followed from 2012 to 2016 with screening for cerebrovascular, renal, and iliac fibromuscular dysplasia using CTA or catheter angiography. Fibromuscular dysplasia was found in 63%, and intracranial aneurysm was found in 14% of patients with fibromuscular dysplasia.⁹ 

SCAD can also be associated with connective tissue disorders such as Ehlers-Danlos syndrome type IV and Marfan syndrome.^16,17

LONG-TERM MANAGEMENT

Patients with SCAD should start long-term aspirin and 1 year of clopidogrel. Statins are indicated for patients with hyperlipidemia^8,18 but otherwise offer no clear benefit for SCAD alone. If there are no contraindications, a beta-adrenergic blocker should be considered, especially if left ventricular dysfunction or arrhythmias are present. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers should also be considered with concomitant left ventricular dysfunction. Antianginal therapy can be used for post-SCAD chest pain syndromes.¹²

Repeat angiography is recommended only to evaluate recurrent symptoms, to confirm an unclear initial diagnosis, to assess for atherosclerosis-related stenosis, or to evaluate high-risk anatomy, eg, involvement of the left main coronary artery.¹²

Genetic testing is reserved for patients with a high clinical suspicion of connective tissue disease or systemic arteriopathy.¹⁹

A 12-lead electrocardiogram (Figure 1) showed ST-segment elevation of more than 2 mm in leads V₂, V₃, V₄, and V₅, with no reciprocal changes.

Based on the classic angiographic appearance and the absence of atherosclerotic disease in other coronary arteries, type 2 spontaneous coronary artery dissection (SCAD) was diagnosed.

CORONARY ARTERY WALL SEPARATION

SCAD is defined as a nontraumatic, noniatrogenic intramural hemorrhage leading to separation of the coronary arterial wall and the formation of a false lumen. The separation can occur between any of the coronary artery wall layers and may or may not involve an intimal tear. The bleeding may result in an intramural hematoma and possible narrowing of the arterial lumen. Depending on the severity of narrowing, blood supply to the myocardium could be compromised, resulting in symptoms of ischemia.¹

SCAD usually involves a single coronary artery, although multiple coronary artery involvement has been reported.²

CASE CONTINUED: MANAGEMENT

The patient recovered completely and was discharged home with plans to return for outpatient imaging for fibromuscular dysplasia.

SCAD appears to be a rare cause of acute coronary syndrome, but it is likely underdiagnosed and is becoming increasingly recognized worldwide. Typically, it affects women younger than 50, with women in general outnumbering men 9 to 1.³ Overall, SCAD causes up to 4% of acute myocardial infarctions, but in women age 50 or younger, it is responsible for 24% to 35% of acute myocardial infarctions, and the proportion is even higher in pregnant women.⁴

Not just pregnancy-associated    

SCAD was previously thought to be mainly idiopathic and mostly affecting women peripartum. Current understanding paints a different picture: pregnancy-associated SCAD does not account for the majority of cases. That said, SCAD is the most common cause of myocardial infarction peripartum, with the third trimester and early postpartum period being the times of highest risk.⁵ SCAD development at those times is believed to be related to hormonal changes causing weakening of coronary artery walls.⁶

Weakening of the coronary artery wall also may occur in the setting of fibromuscular dysplasia, connective tissue disease, recurrent pregnancies, systemic inflammatory disease, hormonal therapy, and other disease states that cause arteriopathy. Exposure to a stressor in a patient with underlying risk factors can lead to either an intimal tear or rupture of the vasa vasorum, with subsequent formation of intramural hemorrhage and eventually SCAD.⁷ Stressors can be emotional or physical and can include labor and delivery, intense physical exercise, the Valsalva maneuver, and drug abuse.⁸

Presentation is variable

SCAD presentation depends on the degree of flow limitation and extent of the dissection. Presentation can range from asymptomatic to sudden cardiac death and can include signs and symptoms of acute coronary syndrome caused by ST-segment elevation or non-ST-segment elevation myocardial infarction.

DIAGNOSIS BY ANGIOGRAPHY    

SCAD can be diagnosed by coronary angiography. There are 3 angiographic types:

Type 1 (about 25% of SCAD cases) has typical contrast dye staining of the arterial wall and multiple radiolucent luminal abnormalities, with or without dye hang-up.

Type 2 (about 70%) has diffuse, smooth narrowing of the coronary artery, with the left anterior descending artery the most frequently affected.⁸

Type 3 (about 5%) mimics atherosclerosis, with focal or tubular stenosis.⁹

Types 1 and 2 are usually easy to recognize. To diagnose type 2, intravenous nitroglycerin should first be administered to rule out coronary spasm.

Type 3 SCAD is more challenging to diagnose because its appearance on angiography is similar to that of atherosclerosis. For equivocal findings in any type, but especially in type 3, intravascular ultrasonography or optical coherence tomography can help.¹⁰ Optical coherence tomography is preferred because of superior image resolution, although ultrasonography offers better tissue penetration.¹¹ 

MANAGE MOST CASES CONSERVATIVELY

Management algorithms for SCAD are available.^8,12

The initial and most critical step is to make the correct diagnosis. Although the presentation of acute coronary syndrome caused by SCAD is often identical to that of atherosclerosis, the conditions have different pathophysiologies and thus require different management. Theoretically, systemic anticoagulation may worsen an intramural hemorrhage.

First-line therapy for most patients with SCAD is conservative management and close inpatient monitoring for 3 to 5 days.¹³ More aggressive management is indicated for any of the following:

• Left main or severe proximal 2-vessel dissection
• Hemodynamic instability
• Ongoing ischemic symptoms.

In a prospective cohort of 168 patients, 134 (80%) were initially treated conservatively; of those, in-hospital myocardial infarction recurred in 4.5%, a major cardiac event occurred within 2 years in 17%, and SCAD recurred in 13%.⁸

Observational data on patients with SCAD who had repeat angiography weeks to months after the initial event has shown that lesions heal in 70% to 97% of patients.¹²

WHEN TO CONSIDER AGGRESSIVE MANAGEMENT

Under the circumstances listed above, revascularization with PCI or coronary artery bypass grafting (CABG) should be considered, with choice of procedure determined by feasibility, technical considerations, and local expertise.

The American Heart Association recommendations are as follows¹²:     

• For left main or severe proximal 2-vessel dissection in clinically stable patients, consider CABG
• For active ischemia or hemodynamic instability, consider PCI if feasible or perform urgent CABG.

A few series have shown that the prognosis with conservative management or CABG is better than with PCI.^8,13,14 The success rate for revascularization with PCI is only about 60% because of challenges including risk of inducing iatrogenic dissection, passing the wire into the false lumen and worsening a dissection, and propagating an intramural hematoma with stenting and further compromising coronary blood flow. In addition, dissection tends to extend into distal arteries that are difficult to stent. There is also the risk of stent malapposition after resorption of the intramural hematoma, causing late stent thrombosis.⁷ 

SCREEN FOR OTHER VASCULAR PROBLEMS

Imaging of the renal, iliac, and cerebral vasculature is recommended for all patients with SCAD.¹² Screening for fibromuscular dysplasia can be done with angiography, computed tomographic angiography (CTA), or magnetic resonance angiography (MRA).¹² 

Multifocal fibromuscular dysplasia in extracoronary arteries occurs with SCAD in 25% to 86% of cases. In a single-center series of 115 patients with confirmed SCAD who underwent CTA from 2010 to 2014, extracoronary vascular abnormalities were found in 66%, with fibromuscular dysplasia being the most common type (45%).¹⁵ In another single-center study, 327 patients with SCAD were prospectively followed from 2012 to 2016 with screening for cerebrovascular, renal, and iliac fibromuscular dysplasia using CTA or catheter angiography. Fibromuscular dysplasia was found in 63%, and intracranial aneurysm was found in 14% of patients with fibromuscular dysplasia.⁹ 

SCAD can also be associated with connective tissue disorders such as Ehlers-Danlos syndrome type IV and Marfan syndrome.^16,17

LONG-TERM MANAGEMENT

Patients with SCAD should start long-term aspirin and 1 year of clopidogrel. Statins are indicated for patients with hyperlipidemia^8,18 but otherwise offer no clear benefit for SCAD alone. If there are no contraindications, a beta-adrenergic blocker should be considered, especially if left ventricular dysfunction or arrhythmias are present. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers should also be considered with concomitant left ventricular dysfunction. Antianginal therapy can be used for post-SCAD chest pain syndromes.¹²

Repeat angiography is recommended only to evaluate recurrent symptoms, to confirm an unclear initial diagnosis, to assess for atherosclerosis-related stenosis, or to evaluate high-risk anatomy, eg, involvement of the left main coronary artery.¹²

Genetic testing is reserved for patients with a high clinical suspicion of connective tissue disease or systemic arteriopathy.¹⁹

A 40-year-old man with type 1 diabetes mellitus and recurrent renal calculi presented to the emergency department with nausea, vomiting, and abdominal pain for the past day. He had been checking his blood glucose level regularly, and it had usually been within the normal range until 2 or 3 days previously, when he stopped taking his insulin because he ran out and could not afford to buy more.

He said he initially vomited clear mucus but then had 2 episodes of black vomit. His abdominal pain was diffuse but more intense in his flanks. He said he had never had nausea or vomiting before this episode.

In the emergency department, his heart rate was 136 beats per minute and respiratory rate 24 breaths per minute. He appeared to be in mild distress, and physical examination revealed a distended abdomen, decreased bowel sounds on auscultation, tympanic sound elicited by percussion, and diffuse abdominal tenderness to palpation without rebound tenderness or rigidity. His blood glucose level was 993 mg/dL, and his anion gap was 36 mmol/L.

The patient was treated with hydration, insulin, and a nasogastric tube to relieve the pressure. The following day, his symptoms had significantly improved, his abdomen was less distended, his bowel sounds had returned, and his plasma glucose levels were in the normal range. The nasogastric tube was removed after he started to have bowel movements; he was given liquids by mouth and eventually solid food. Since his condition had significantly improved and he had started to have bowel movements, no follow-up imaging was done. The next day, he was symptom-free, his laboratory values were normal, and he was discharged home.

GASTROPARESIS

Gastroparesis is defined by delayed gastric emptying in the absence of a mechanical obstruction, with symptoms of nausea, vomiting, bloating, and abdominal pain. Most commonly it is idiopathic or caused by long-standing uncontrolled diabetes.

Diabetic gastroparesis is thought to result from impaired neural control of gastric function. Damage to the pacemaker interstitial cells of Cajal and underlying smooth muscle may be contributing factors.¹ It is usually chronic, with a mean duration of symptoms of 26.5 months.² However, acute gastroparesis can occur after an acute elevation in the plasma glucose concentration, which can affect gastric sensory and motor function³ via relaxation of the proximal stomach, decrease in antral pressure waves, and increase in pyloric pressure waves.⁴

Patients with diabetic ketoacidosis often present with symptoms similar to those of gastroparesis, including nausea, vomiting, and abdominal pain.⁵ But acute gastroparesis can coexist with diabetic ketoacidosis, as in our patient, and the gastroparesis can go undiagnosed, since imaging studies are not routinely done for diabetic ketoacidosis unless there is another reason—as in our patient.         

More study is needed to answer questions on long-term outcomes for patients presenting with acute gastroparesis: Do they develop chronic gastroparesis? And is there is a correlation with progression of neuropathy?

The diagnosis usually requires a high level of suspicion in patients with nausea, vomiting, fullness, abdominal pain, and bloating; exclusion of gastric outlet obstruction by a mass or antral stenosis; and evidence of delayed gastric emptying. Gastric outlet obstruction can be ruled out by endoscopy, abdominal CT, or magnetic resonance enterography. Delayed gastric emptying can be quantified with scintigraphy and endoscopy. In our patient, gastroparesis was diagnosed on the basis of the clinical symptoms and CT findings.

Treatment is usually directed at symptoms, with better glycemic control and dietary modification for moderate cases, and prokinetics and a gastrostomy tube for severe cases.

TAKE-HOME POINTS

• Gastroparesis is usually chronic but can present acutely with acute severe hyperglycemia.
• Gastrointestinal tract motor function is affected by plasma glucose levels and can change over brief intervals.
• Diabetic ketoacidosis symptoms can mask acute gastroparesis, as imaging studies are not routinely done.
• Acute gastroparesis can be diagnosed clinically along with abdominal CT or endoscopy to rule out gastric outlet obstruction.
• Acute gastroparesis caused by diabetic ketoacidosis can resolve promptly with tight control of plasma glucose levels, anion gap closing, and nasogastric tube placement.

A 40-year-old man with type 1 diabetes mellitus and recurrent renal calculi presented to the emergency department with nausea, vomiting, and abdominal pain for the past day. He had been checking his blood glucose level regularly, and it had usually been within the normal range until 2 or 3 days previously, when he stopped taking his insulin because he ran out and could not afford to buy more.

He said he initially vomited clear mucus but then had 2 episodes of black vomit. His abdominal pain was diffuse but more intense in his flanks. He said he had never had nausea or vomiting before this episode.

In the emergency department, his heart rate was 136 beats per minute and respiratory rate 24 breaths per minute. He appeared to be in mild distress, and physical examination revealed a distended abdomen, decreased bowel sounds on auscultation, tympanic sound elicited by percussion, and diffuse abdominal tenderness to palpation without rebound tenderness or rigidity. His blood glucose level was 993 mg/dL, and his anion gap was 36 mmol/L.

The patient was treated with hydration, insulin, and a nasogastric tube to relieve the pressure. The following day, his symptoms had significantly improved, his abdomen was less distended, his bowel sounds had returned, and his plasma glucose levels were in the normal range. The nasogastric tube was removed after he started to have bowel movements; he was given liquids by mouth and eventually solid food. Since his condition had significantly improved and he had started to have bowel movements, no follow-up imaging was done. The next day, he was symptom-free, his laboratory values were normal, and he was discharged home.

GASTROPARESIS

Gastroparesis is defined by delayed gastric emptying in the absence of a mechanical obstruction, with symptoms of nausea, vomiting, bloating, and abdominal pain. Most commonly it is idiopathic or caused by long-standing uncontrolled diabetes.

Diabetic gastroparesis is thought to result from impaired neural control of gastric function. Damage to the pacemaker interstitial cells of Cajal and underlying smooth muscle may be contributing factors.¹ It is usually chronic, with a mean duration of symptoms of 26.5 months.² However, acute gastroparesis can occur after an acute elevation in the plasma glucose concentration, which can affect gastric sensory and motor function³ via relaxation of the proximal stomach, decrease in antral pressure waves, and increase in pyloric pressure waves.⁴

Patients with diabetic ketoacidosis often present with symptoms similar to those of gastroparesis, including nausea, vomiting, and abdominal pain.⁵ But acute gastroparesis can coexist with diabetic ketoacidosis, as in our patient, and the gastroparesis can go undiagnosed, since imaging studies are not routinely done for diabetic ketoacidosis unless there is another reason—as in our patient.         

More study is needed to answer questions on long-term outcomes for patients presenting with acute gastroparesis: Do they develop chronic gastroparesis? And is there is a correlation with progression of neuropathy?

The diagnosis usually requires a high level of suspicion in patients with nausea, vomiting, fullness, abdominal pain, and bloating; exclusion of gastric outlet obstruction by a mass or antral stenosis; and evidence of delayed gastric emptying. Gastric outlet obstruction can be ruled out by endoscopy, abdominal CT, or magnetic resonance enterography. Delayed gastric emptying can be quantified with scintigraphy and endoscopy. In our patient, gastroparesis was diagnosed on the basis of the clinical symptoms and CT findings.

Treatment is usually directed at symptoms, with better glycemic control and dietary modification for moderate cases, and prokinetics and a gastrostomy tube for severe cases.

TAKE-HOME POINTS

• Gastroparesis is usually chronic but can present acutely with acute severe hyperglycemia.
• Gastrointestinal tract motor function is affected by plasma glucose levels and can change over brief intervals.
• Diabetic ketoacidosis symptoms can mask acute gastroparesis, as imaging studies are not routinely done.
• Acute gastroparesis can be diagnosed clinically along with abdominal CT or endoscopy to rule out gastric outlet obstruction.
• Acute gastroparesis caused by diabetic ketoacidosis can resolve promptly with tight control of plasma glucose levels, anion gap closing, and nasogastric tube placement.

A 40-year-old man with type 1 diabetes mellitus and recurrent renal calculi presented to the emergency department with nausea, vomiting, and abdominal pain for the past day. He had been checking his blood glucose level regularly, and it had usually been within the normal range until 2 or 3 days previously, when he stopped taking his insulin because he ran out and could not afford to buy more.

He said he initially vomited clear mucus but then had 2 episodes of black vomit. His abdominal pain was diffuse but more intense in his flanks. He said he had never had nausea or vomiting before this episode.

In the emergency department, his heart rate was 136 beats per minute and respiratory rate 24 breaths per minute. He appeared to be in mild distress, and physical examination revealed a distended abdomen, decreased bowel sounds on auscultation, tympanic sound elicited by percussion, and diffuse abdominal tenderness to palpation without rebound tenderness or rigidity. His blood glucose level was 993 mg/dL, and his anion gap was 36 mmol/L.

The patient was treated with hydration, insulin, and a nasogastric tube to relieve the pressure. The following day, his symptoms had significantly improved, his abdomen was less distended, his bowel sounds had returned, and his plasma glucose levels were in the normal range. The nasogastric tube was removed after he started to have bowel movements; he was given liquids by mouth and eventually solid food. Since his condition had significantly improved and he had started to have bowel movements, no follow-up imaging was done. The next day, he was symptom-free, his laboratory values were normal, and he was discharged home.

GASTROPARESIS

Gastroparesis is defined by delayed gastric emptying in the absence of a mechanical obstruction, with symptoms of nausea, vomiting, bloating, and abdominal pain. Most commonly it is idiopathic or caused by long-standing uncontrolled diabetes.

Diabetic gastroparesis is thought to result from impaired neural control of gastric function. Damage to the pacemaker interstitial cells of Cajal and underlying smooth muscle may be contributing factors.¹ It is usually chronic, with a mean duration of symptoms of 26.5 months.² However, acute gastroparesis can occur after an acute elevation in the plasma glucose concentration, which can affect gastric sensory and motor function³ via relaxation of the proximal stomach, decrease in antral pressure waves, and increase in pyloric pressure waves.⁴

Patients with diabetic ketoacidosis often present with symptoms similar to those of gastroparesis, including nausea, vomiting, and abdominal pain.⁵ But acute gastroparesis can coexist with diabetic ketoacidosis, as in our patient, and the gastroparesis can go undiagnosed, since imaging studies are not routinely done for diabetic ketoacidosis unless there is another reason—as in our patient.         

More study is needed to answer questions on long-term outcomes for patients presenting with acute gastroparesis: Do they develop chronic gastroparesis? And is there is a correlation with progression of neuropathy?

The diagnosis usually requires a high level of suspicion in patients with nausea, vomiting, fullness, abdominal pain, and bloating; exclusion of gastric outlet obstruction by a mass or antral stenosis; and evidence of delayed gastric emptying. Gastric outlet obstruction can be ruled out by endoscopy, abdominal CT, or magnetic resonance enterography. Delayed gastric emptying can be quantified with scintigraphy and endoscopy. In our patient, gastroparesis was diagnosed on the basis of the clinical symptoms and CT findings.

Treatment is usually directed at symptoms, with better glycemic control and dietary modification for moderate cases, and prokinetics and a gastrostomy tube for severe cases.

TAKE-HOME POINTS

• Gastroparesis is usually chronic but can present acutely with acute severe hyperglycemia.
• Gastrointestinal tract motor function is affected by plasma glucose levels and can change over brief intervals.
• Diabetic ketoacidosis symptoms can mask acute gastroparesis, as imaging studies are not routinely done.
• Acute gastroparesis can be diagnosed clinically along with abdominal CT or endoscopy to rule out gastric outlet obstruction.
• Acute gastroparesis caused by diabetic ketoacidosis can resolve promptly with tight control of plasma glucose levels, anion gap closing, and nasogastric tube placement.