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There’s More Where That Came From
ANSWER
The correct answer is pityriasis rosea (choice “d”).
Virtually all patients with this condition believe that they have a terrible case of “ringworm” (ie, fungal infection; choice “a”)—an opinion all too often corroborated by the medical provider unacquainted with pityriasis rosea. The two can be difficult to distinguish, but the “herald” patch, oval shape, odd color, and fine scale all serve to confirm the diagnosis. When necessary, a KOH prep or biopsy can be done.
Psoriasis (choice “b”) can manifest acutely, but it is distinctly salmon-pink under coarse, white scale that affects the palms, nails (with pits), and scalp. Psoriasis lesions are round (rather than oval), with coarser scale and without a herald patch.
The lack of antecedent sores and denial of sexual contact ruled out secondary syphilis (choice “c”). Patients with secondary syphilis often present with low-grade fever, malaise, and palmar scaly papules—all of which were missing in this case. Syphilis serology (rapid plasma reagin) can be easily obtained if doubt persists.
DISCUSSION
Pityriasis rosea (PR) is a papulosquamous eruption that is common in younger populations. About 40% of affected patients present with a large scaly lesion, which is followed by the appearance of multiple smaller oval lesions within days. In most cases, PR is fairly easy to diagnose: the lesion’s oval shape, pinkish-brown color, centripetal fine scale, herald patch, and adherence to skin tension lines are all characteristic findings.
Though the exact organism has not been identified, PR is almost certainly viral in origin. Like many viral exanthems, occurrence tends to peak in the spring and fall. There are also indications that the body builds immunity to the infection, since recurrence outside the acute phase is rare.
Treatment options are unsatisfactory, though exposure to UV sources appears to help. Patients must be informed that their condition will, unfortunately, last for at least six to nine weeks, during which crops of lesions will come and go.
ANSWER
The correct answer is pityriasis rosea (choice “d”).
Virtually all patients with this condition believe that they have a terrible case of “ringworm” (ie, fungal infection; choice “a”)—an opinion all too often corroborated by the medical provider unacquainted with pityriasis rosea. The two can be difficult to distinguish, but the “herald” patch, oval shape, odd color, and fine scale all serve to confirm the diagnosis. When necessary, a KOH prep or biopsy can be done.
Psoriasis (choice “b”) can manifest acutely, but it is distinctly salmon-pink under coarse, white scale that affects the palms, nails (with pits), and scalp. Psoriasis lesions are round (rather than oval), with coarser scale and without a herald patch.
The lack of antecedent sores and denial of sexual contact ruled out secondary syphilis (choice “c”). Patients with secondary syphilis often present with low-grade fever, malaise, and palmar scaly papules—all of which were missing in this case. Syphilis serology (rapid plasma reagin) can be easily obtained if doubt persists.
DISCUSSION
Pityriasis rosea (PR) is a papulosquamous eruption that is common in younger populations. About 40% of affected patients present with a large scaly lesion, which is followed by the appearance of multiple smaller oval lesions within days. In most cases, PR is fairly easy to diagnose: the lesion’s oval shape, pinkish-brown color, centripetal fine scale, herald patch, and adherence to skin tension lines are all characteristic findings.
Though the exact organism has not been identified, PR is almost certainly viral in origin. Like many viral exanthems, occurrence tends to peak in the spring and fall. There are also indications that the body builds immunity to the infection, since recurrence outside the acute phase is rare.
Treatment options are unsatisfactory, though exposure to UV sources appears to help. Patients must be informed that their condition will, unfortunately, last for at least six to nine weeks, during which crops of lesions will come and go.
ANSWER
The correct answer is pityriasis rosea (choice “d”).
Virtually all patients with this condition believe that they have a terrible case of “ringworm” (ie, fungal infection; choice “a”)—an opinion all too often corroborated by the medical provider unacquainted with pityriasis rosea. The two can be difficult to distinguish, but the “herald” patch, oval shape, odd color, and fine scale all serve to confirm the diagnosis. When necessary, a KOH prep or biopsy can be done.
Psoriasis (choice “b”) can manifest acutely, but it is distinctly salmon-pink under coarse, white scale that affects the palms, nails (with pits), and scalp. Psoriasis lesions are round (rather than oval), with coarser scale and without a herald patch.
The lack of antecedent sores and denial of sexual contact ruled out secondary syphilis (choice “c”). Patients with secondary syphilis often present with low-grade fever, malaise, and palmar scaly papules—all of which were missing in this case. Syphilis serology (rapid plasma reagin) can be easily obtained if doubt persists.
DISCUSSION
Pityriasis rosea (PR) is a papulosquamous eruption that is common in younger populations. About 40% of affected patients present with a large scaly lesion, which is followed by the appearance of multiple smaller oval lesions within days. In most cases, PR is fairly easy to diagnose: the lesion’s oval shape, pinkish-brown color, centripetal fine scale, herald patch, and adherence to skin tension lines are all characteristic findings.
Though the exact organism has not been identified, PR is almost certainly viral in origin. Like many viral exanthems, occurrence tends to peak in the spring and fall. There are also indications that the body builds immunity to the infection, since recurrence outside the acute phase is rare.
Treatment options are unsatisfactory, though exposure to UV sources appears to help. Patients must be informed that their condition will, unfortunately, last for at least six to nine weeks, during which crops of lesions will come and go.
About 10 days ago, an asymptomatic, scaly lesion arose overnight on this 21-year-old man’s upper left chest, near the anterior deltoid area. Within the past week, multiple scaly lesions—much smaller than the original—have appeared on his trunk and arms.
The patient claims to be in good health otherwise, denying fever, malaise, or myalgia. He denies sexual contact of any kind in the past two months. There is no personal or family history of skin disease or atopy.
On exam, the patient looks his stated age, is afebrile, and is in no acute distress. On his chest is an oval, pinkish brown, papulosquamous lesion with very fine, sparse scaling in the center. The long axis of the lesion parallels local skin tension lines.
About 20 additional lesions are observed elsewhere, primarily on the truncal skin, sparing the upper neck, face, and palms. All are oval, with the same odd color and scale, and follow skin tension lines. The patient’s elbows, knees, scalp, and nails are unaffected, as are the areas around and below the waist.
Obtaining cystatin-C levels useful in chronic kidney disease
SAN FRANCISCO – Routine lab tests for estimating the average glomerular filtration rate (GFR) are too imprecise, according to Michael G. Shlipak, MD.
“If you study 100 patients, the average GFR based on creatinine is going to be pretty close to estimated GFR,” Dr. Shlipak said at the UCSF Annual Advances in Internal Medicine meeting. “But with individual patients, the average GFR is going to be plus or minus 30%, which is a lot. If the estimated GFR is 70 mL/min per 1.73 m2, the real GFR could be between 50 and 90 mL/min per 1.73 m2; so that’s a wide range.”
“The main appeal of the Cockcroft-Gault equation is that you can almost do it in your head, so that’s a real positive,” said Dr. Shlipak, who is also scientific director of the Kidney Health Research Collaborative at the University of California, San Francisco, and professor of internal medicine, epidemiology, and biostatistics at UCSF Medical Center. “The main disadvantage is that it’s really a terrible equation. The Cockcroft-Gault equation is clearly inadequate, as it is standardized to creatinine clearance and very inaccurate, so it should no longer be used. The MDRD and the CKD-EPI are newer equations that are at least validated to real GFR and not creatinine clearance. In our system, the pharmacy uses the Cockcroft-Gault equation, and the lab gives us the MDRD GFR equation, so it’s quite confusing.”
Dr. Shlipak described using estimated GFR in clinical decision making as “better than using just creatinine, because it integrates demographic characteristics, which are determinants in part of the creatinine production, which is what determines how much creatinine is in the blood before it gets filtered. The equations make us think of GFR and kidney function instead of just the lab value.”
The downsides of using GFRs, he added, include the fact that they are mostly validated in younger patients with kidney disease, they rely on the assumption that demographic characteristics alone can define muscle mass, they were only developed in whites and blacks, and estimated GFR can be interpreted only as “suggested GFR.”
A blood test of kidney function known as cystatin C has been shown to be an alternative, better marker of creatinine, compared with GFR, and is supported by the Kidney Disease: Improving Global Outcomes CKD work group’s 2012 clinical practice guidelines for the evaluation and management of CKD. “Because cystatin C is not related to muscle mass, age, sex, and race, it has major advantages over creatinine,” Dr. Shlipak said. “It is a reliable, standardized, and automated measure that is available for clinical use.”
He and his associates conducted a meta-analysis comparing cystatin C and creatinine in determining prognosis for patients with baseline kidney disease. They included 16 studies involving 90,750 patients and compared associations of estimated GFR (eGFR) as measured with creatinine, cystatin C, and both creatinine and cystatin C with mortality risk; they also determined proportions reclassified by cystatin C in each subgroup of eGFR using creatinine and by the effect on risk associations (N Engl J Med. 2013 Sep 5; 369[10]:932-43).
In the general-population cohorts, the prevalence of an eGFR of less than 60 mL/min per 1.73 m2 of body surface area was higher with the cystatin C–based eGFR than with the creatinine-based eGFR (13.7% vs. 9.7%). Across all eGFR categories, the reclassification of the eGFR to a higher value with the measurement of cystatin C, compared with creatinine, was associated with a reduced risk of all three study outcomes. Reclassification to a lower eGFR was associated with an increased risk.
“When we looked at the threshold for where risk begins, traditionally we’ve said it starts when the GFR declines below 60 mL/min per 1.73 m2,” Dr. Shlipak explained. “That’s exactly what we found with creatinine. But with cystatin C, the threshold of risk was at 88 mL/min per 1.73 m2.
“So, from 88 mL/min per 1.73 m2 downward, every incremental reduction in GFR is associated with higher mortality and cardiovascular risk,” he added. “So cystatin C opens this new window of between 60 and 90 mL/min per 1.73 m2 to start measuring relative declines in kidney function. If you combine creatinine and cystatin C together in an equation, you get a similar estimate. Many advocate that the combined CKD-EPI creatinine-cystatin C equation is the best way to measure GFR.”
Dr. Shlipak reported that he is on the scientific advisory boards of TAI Diagnostics and Cricket Health.
SAN FRANCISCO – Routine lab tests for estimating the average glomerular filtration rate (GFR) are too imprecise, according to Michael G. Shlipak, MD.
“If you study 100 patients, the average GFR based on creatinine is going to be pretty close to estimated GFR,” Dr. Shlipak said at the UCSF Annual Advances in Internal Medicine meeting. “But with individual patients, the average GFR is going to be plus or minus 30%, which is a lot. If the estimated GFR is 70 mL/min per 1.73 m2, the real GFR could be between 50 and 90 mL/min per 1.73 m2; so that’s a wide range.”
“The main appeal of the Cockcroft-Gault equation is that you can almost do it in your head, so that’s a real positive,” said Dr. Shlipak, who is also scientific director of the Kidney Health Research Collaborative at the University of California, San Francisco, and professor of internal medicine, epidemiology, and biostatistics at UCSF Medical Center. “The main disadvantage is that it’s really a terrible equation. The Cockcroft-Gault equation is clearly inadequate, as it is standardized to creatinine clearance and very inaccurate, so it should no longer be used. The MDRD and the CKD-EPI are newer equations that are at least validated to real GFR and not creatinine clearance. In our system, the pharmacy uses the Cockcroft-Gault equation, and the lab gives us the MDRD GFR equation, so it’s quite confusing.”
Dr. Shlipak described using estimated GFR in clinical decision making as “better than using just creatinine, because it integrates demographic characteristics, which are determinants in part of the creatinine production, which is what determines how much creatinine is in the blood before it gets filtered. The equations make us think of GFR and kidney function instead of just the lab value.”
The downsides of using GFRs, he added, include the fact that they are mostly validated in younger patients with kidney disease, they rely on the assumption that demographic characteristics alone can define muscle mass, they were only developed in whites and blacks, and estimated GFR can be interpreted only as “suggested GFR.”
A blood test of kidney function known as cystatin C has been shown to be an alternative, better marker of creatinine, compared with GFR, and is supported by the Kidney Disease: Improving Global Outcomes CKD work group’s 2012 clinical practice guidelines for the evaluation and management of CKD. “Because cystatin C is not related to muscle mass, age, sex, and race, it has major advantages over creatinine,” Dr. Shlipak said. “It is a reliable, standardized, and automated measure that is available for clinical use.”
He and his associates conducted a meta-analysis comparing cystatin C and creatinine in determining prognosis for patients with baseline kidney disease. They included 16 studies involving 90,750 patients and compared associations of estimated GFR (eGFR) as measured with creatinine, cystatin C, and both creatinine and cystatin C with mortality risk; they also determined proportions reclassified by cystatin C in each subgroup of eGFR using creatinine and by the effect on risk associations (N Engl J Med. 2013 Sep 5; 369[10]:932-43).
In the general-population cohorts, the prevalence of an eGFR of less than 60 mL/min per 1.73 m2 of body surface area was higher with the cystatin C–based eGFR than with the creatinine-based eGFR (13.7% vs. 9.7%). Across all eGFR categories, the reclassification of the eGFR to a higher value with the measurement of cystatin C, compared with creatinine, was associated with a reduced risk of all three study outcomes. Reclassification to a lower eGFR was associated with an increased risk.
“When we looked at the threshold for where risk begins, traditionally we’ve said it starts when the GFR declines below 60 mL/min per 1.73 m2,” Dr. Shlipak explained. “That’s exactly what we found with creatinine. But with cystatin C, the threshold of risk was at 88 mL/min per 1.73 m2.
“So, from 88 mL/min per 1.73 m2 downward, every incremental reduction in GFR is associated with higher mortality and cardiovascular risk,” he added. “So cystatin C opens this new window of between 60 and 90 mL/min per 1.73 m2 to start measuring relative declines in kidney function. If you combine creatinine and cystatin C together in an equation, you get a similar estimate. Many advocate that the combined CKD-EPI creatinine-cystatin C equation is the best way to measure GFR.”
Dr. Shlipak reported that he is on the scientific advisory boards of TAI Diagnostics and Cricket Health.
SAN FRANCISCO – Routine lab tests for estimating the average glomerular filtration rate (GFR) are too imprecise, according to Michael G. Shlipak, MD.
“If you study 100 patients, the average GFR based on creatinine is going to be pretty close to estimated GFR,” Dr. Shlipak said at the UCSF Annual Advances in Internal Medicine meeting. “But with individual patients, the average GFR is going to be plus or minus 30%, which is a lot. If the estimated GFR is 70 mL/min per 1.73 m2, the real GFR could be between 50 and 90 mL/min per 1.73 m2; so that’s a wide range.”
“The main appeal of the Cockcroft-Gault equation is that you can almost do it in your head, so that’s a real positive,” said Dr. Shlipak, who is also scientific director of the Kidney Health Research Collaborative at the University of California, San Francisco, and professor of internal medicine, epidemiology, and biostatistics at UCSF Medical Center. “The main disadvantage is that it’s really a terrible equation. The Cockcroft-Gault equation is clearly inadequate, as it is standardized to creatinine clearance and very inaccurate, so it should no longer be used. The MDRD and the CKD-EPI are newer equations that are at least validated to real GFR and not creatinine clearance. In our system, the pharmacy uses the Cockcroft-Gault equation, and the lab gives us the MDRD GFR equation, so it’s quite confusing.”
Dr. Shlipak described using estimated GFR in clinical decision making as “better than using just creatinine, because it integrates demographic characteristics, which are determinants in part of the creatinine production, which is what determines how much creatinine is in the blood before it gets filtered. The equations make us think of GFR and kidney function instead of just the lab value.”
The downsides of using GFRs, he added, include the fact that they are mostly validated in younger patients with kidney disease, they rely on the assumption that demographic characteristics alone can define muscle mass, they were only developed in whites and blacks, and estimated GFR can be interpreted only as “suggested GFR.”
A blood test of kidney function known as cystatin C has been shown to be an alternative, better marker of creatinine, compared with GFR, and is supported by the Kidney Disease: Improving Global Outcomes CKD work group’s 2012 clinical practice guidelines for the evaluation and management of CKD. “Because cystatin C is not related to muscle mass, age, sex, and race, it has major advantages over creatinine,” Dr. Shlipak said. “It is a reliable, standardized, and automated measure that is available for clinical use.”
He and his associates conducted a meta-analysis comparing cystatin C and creatinine in determining prognosis for patients with baseline kidney disease. They included 16 studies involving 90,750 patients and compared associations of estimated GFR (eGFR) as measured with creatinine, cystatin C, and both creatinine and cystatin C with mortality risk; they also determined proportions reclassified by cystatin C in each subgroup of eGFR using creatinine and by the effect on risk associations (N Engl J Med. 2013 Sep 5; 369[10]:932-43).
In the general-population cohorts, the prevalence of an eGFR of less than 60 mL/min per 1.73 m2 of body surface area was higher with the cystatin C–based eGFR than with the creatinine-based eGFR (13.7% vs. 9.7%). Across all eGFR categories, the reclassification of the eGFR to a higher value with the measurement of cystatin C, compared with creatinine, was associated with a reduced risk of all three study outcomes. Reclassification to a lower eGFR was associated with an increased risk.
“When we looked at the threshold for where risk begins, traditionally we’ve said it starts when the GFR declines below 60 mL/min per 1.73 m2,” Dr. Shlipak explained. “That’s exactly what we found with creatinine. But with cystatin C, the threshold of risk was at 88 mL/min per 1.73 m2.
“So, from 88 mL/min per 1.73 m2 downward, every incremental reduction in GFR is associated with higher mortality and cardiovascular risk,” he added. “So cystatin C opens this new window of between 60 and 90 mL/min per 1.73 m2 to start measuring relative declines in kidney function. If you combine creatinine and cystatin C together in an equation, you get a similar estimate. Many advocate that the combined CKD-EPI creatinine-cystatin C equation is the best way to measure GFR.”
Dr. Shlipak reported that he is on the scientific advisory boards of TAI Diagnostics and Cricket Health.
AT THE ANNUAL ADVANCES IN INTERNAL MEDICINE
Chronic Epilepsy Linked to Cognitive Deficits
Patients in their 50s who have chronic epilepsy seem to have cognitive deficits that may be linked to metabolic, inflammatory, and vascular abnormalities, according to a clinical study that included 40 patients with chronic localized epilepsy and 152 controls.
- To reach that conclusion, researchers conducted neuropsychological assessment, clinical examination, and blood testing to evaluate patients’ vascular status.
- The evaluation included systolic and diastolic blood pressure, body mass index (BMI), high density lipoprotein, homocysteine levels, and inflammatory markers including high-sensitivity C-reactive protein (hs-CRP), and interleukin-6.
- The metabolic assessment included measurement of insulin resistance by means of glucose levels and homeostatic model assessment of insulin resistance (HOMA-IR).
- Patients with epilepsy had impaired cognitive factor scores across the board.
- These patients also had abnormal BMI, hs-CRP, fasting glucose, and HOMA-IR.
- There was also a link between higher HOMA-IR and poor immediate memory and visuospatial ability.
- Elevated hs-CRP was associated with poorer visuospatial and verbal abilities.
Hermann BP, Sager MA, Koscik RL, Young K, Nakamura K. Vascular, inflammatory, and metabolic factors associated with cognition in aging persons with chronic epilepsy. [Published online ahead of print Sept 4, 2017]. Epilepsia.
Patients in their 50s who have chronic epilepsy seem to have cognitive deficits that may be linked to metabolic, inflammatory, and vascular abnormalities, according to a clinical study that included 40 patients with chronic localized epilepsy and 152 controls.
- To reach that conclusion, researchers conducted neuropsychological assessment, clinical examination, and blood testing to evaluate patients’ vascular status.
- The evaluation included systolic and diastolic blood pressure, body mass index (BMI), high density lipoprotein, homocysteine levels, and inflammatory markers including high-sensitivity C-reactive protein (hs-CRP), and interleukin-6.
- The metabolic assessment included measurement of insulin resistance by means of glucose levels and homeostatic model assessment of insulin resistance (HOMA-IR).
- Patients with epilepsy had impaired cognitive factor scores across the board.
- These patients also had abnormal BMI, hs-CRP, fasting glucose, and HOMA-IR.
- There was also a link between higher HOMA-IR and poor immediate memory and visuospatial ability.
- Elevated hs-CRP was associated with poorer visuospatial and verbal abilities.
Hermann BP, Sager MA, Koscik RL, Young K, Nakamura K. Vascular, inflammatory, and metabolic factors associated with cognition in aging persons with chronic epilepsy. [Published online ahead of print Sept 4, 2017]. Epilepsia.
Patients in their 50s who have chronic epilepsy seem to have cognitive deficits that may be linked to metabolic, inflammatory, and vascular abnormalities, according to a clinical study that included 40 patients with chronic localized epilepsy and 152 controls.
- To reach that conclusion, researchers conducted neuropsychological assessment, clinical examination, and blood testing to evaluate patients’ vascular status.
- The evaluation included systolic and diastolic blood pressure, body mass index (BMI), high density lipoprotein, homocysteine levels, and inflammatory markers including high-sensitivity C-reactive protein (hs-CRP), and interleukin-6.
- The metabolic assessment included measurement of insulin resistance by means of glucose levels and homeostatic model assessment of insulin resistance (HOMA-IR).
- Patients with epilepsy had impaired cognitive factor scores across the board.
- These patients also had abnormal BMI, hs-CRP, fasting glucose, and HOMA-IR.
- There was also a link between higher HOMA-IR and poor immediate memory and visuospatial ability.
- Elevated hs-CRP was associated with poorer visuospatial and verbal abilities.
Hermann BP, Sager MA, Koscik RL, Young K, Nakamura K. Vascular, inflammatory, and metabolic factors associated with cognition in aging persons with chronic epilepsy. [Published online ahead of print Sept 4, 2017]. Epilepsia.
SUDEP More Likely to Happen During Sleep
Patients who have seizures at night are more likely to die suddenly from epilepsy, according to a recent study that compared seizures occurring while patients were awake to those who experienced them during sleep.
- Researchers point out that patients with epilepsy are 20 times more likely to experience sudden death, compared with the general public.
- The most frequent risk factor for these deaths is uncontrolled seizures.
- Researchers tracked respiratory parameters, comparing adults with epilepsy during wake and sleep periods.
- Sleep-related seizures were linked to lower oxygen saturation when compared with wakeful seizures, and this association remained significant during the ictal and postictal periods.
- Sleep-related seizures were also associated with greater drops in saturation.
- Postseizure EEG suppression occurred more often after sleep-related seizures as well.
- Researchers concluded that sudden unexpected death in epilepsy (SUDEP) is more likely to happen during sleep and that it is linked to more severe and longer occurrences of hypoxemia.
Latreille V, Abdennadher M, Dworetzky BA, et al. Nocturnal seizures are associated with more severe hypoxemia and increased risk of postictal generalized EEG suppression. Epilepsia. 2017;58(9):e127-e131.
Patients who have seizures at night are more likely to die suddenly from epilepsy, according to a recent study that compared seizures occurring while patients were awake to those who experienced them during sleep.
- Researchers point out that patients with epilepsy are 20 times more likely to experience sudden death, compared with the general public.
- The most frequent risk factor for these deaths is uncontrolled seizures.
- Researchers tracked respiratory parameters, comparing adults with epilepsy during wake and sleep periods.
- Sleep-related seizures were linked to lower oxygen saturation when compared with wakeful seizures, and this association remained significant during the ictal and postictal periods.
- Sleep-related seizures were also associated with greater drops in saturation.
- Postseizure EEG suppression occurred more often after sleep-related seizures as well.
- Researchers concluded that sudden unexpected death in epilepsy (SUDEP) is more likely to happen during sleep and that it is linked to more severe and longer occurrences of hypoxemia.
Latreille V, Abdennadher M, Dworetzky BA, et al. Nocturnal seizures are associated with more severe hypoxemia and increased risk of postictal generalized EEG suppression. Epilepsia. 2017;58(9):e127-e131.
Patients who have seizures at night are more likely to die suddenly from epilepsy, according to a recent study that compared seizures occurring while patients were awake to those who experienced them during sleep.
- Researchers point out that patients with epilepsy are 20 times more likely to experience sudden death, compared with the general public.
- The most frequent risk factor for these deaths is uncontrolled seizures.
- Researchers tracked respiratory parameters, comparing adults with epilepsy during wake and sleep periods.
- Sleep-related seizures were linked to lower oxygen saturation when compared with wakeful seizures, and this association remained significant during the ictal and postictal periods.
- Sleep-related seizures were also associated with greater drops in saturation.
- Postseizure EEG suppression occurred more often after sleep-related seizures as well.
- Researchers concluded that sudden unexpected death in epilepsy (SUDEP) is more likely to happen during sleep and that it is linked to more severe and longer occurrences of hypoxemia.
Latreille V, Abdennadher M, Dworetzky BA, et al. Nocturnal seizures are associated with more severe hypoxemia and increased risk of postictal generalized EEG suppression. Epilepsia. 2017;58(9):e127-e131.
Anion Gap May Help Separate Psychogenic Seizure from Epilepsy
An anion gap above 10, measured in the first 2 hours after a seizure, may help clinicians in the emergency department distinguish between psychogenic nonepileptic seizures (PNES) and generalized convulsive epileptic seizures (ES), according to an analysis of more than 1300 patients at a tertiary care center. Details of the analysis include the following:
- Investigators looked at anion gap, bicarbonate, and Denver Seizure Scores and found 27 patients with PNES and 27 with ES, using clinical signs and symptoms in conjunction with EEGs.
- Multivariate logistic regression helped detect a link between an anion gap above 10 and seizure type but also found that sensitivity and negative predictive value dropped off dramatically when samples were drawn more than 2 hours after the event.
- Anion gap values above 10 yielded a sensitivity of 81.8% and specificity of 100% when measured within 2 hours of the seizure.
Li Y, Matzka L, Maranda L, Weber D. Anion gap can differentiate between psychogenic and epileptic seizures in the emergency setting. Epilepsia. 2017;58(9):e132-e135.
An anion gap above 10, measured in the first 2 hours after a seizure, may help clinicians in the emergency department distinguish between psychogenic nonepileptic seizures (PNES) and generalized convulsive epileptic seizures (ES), according to an analysis of more than 1300 patients at a tertiary care center. Details of the analysis include the following:
- Investigators looked at anion gap, bicarbonate, and Denver Seizure Scores and found 27 patients with PNES and 27 with ES, using clinical signs and symptoms in conjunction with EEGs.
- Multivariate logistic regression helped detect a link between an anion gap above 10 and seizure type but also found that sensitivity and negative predictive value dropped off dramatically when samples were drawn more than 2 hours after the event.
- Anion gap values above 10 yielded a sensitivity of 81.8% and specificity of 100% when measured within 2 hours of the seizure.
Li Y, Matzka L, Maranda L, Weber D. Anion gap can differentiate between psychogenic and epileptic seizures in the emergency setting. Epilepsia. 2017;58(9):e132-e135.
An anion gap above 10, measured in the first 2 hours after a seizure, may help clinicians in the emergency department distinguish between psychogenic nonepileptic seizures (PNES) and generalized convulsive epileptic seizures (ES), according to an analysis of more than 1300 patients at a tertiary care center. Details of the analysis include the following:
- Investigators looked at anion gap, bicarbonate, and Denver Seizure Scores and found 27 patients with PNES and 27 with ES, using clinical signs and symptoms in conjunction with EEGs.
- Multivariate logistic regression helped detect a link between an anion gap above 10 and seizure type but also found that sensitivity and negative predictive value dropped off dramatically when samples were drawn more than 2 hours after the event.
- Anion gap values above 10 yielded a sensitivity of 81.8% and specificity of 100% when measured within 2 hours of the seizure.
Li Y, Matzka L, Maranda L, Weber D. Anion gap can differentiate between psychogenic and epileptic seizures in the emergency setting. Epilepsia. 2017;58(9):e132-e135.
AWARD-7: Dulaglutide benefits patients with diabetic renal disease
LISBON – Patients with type 2 diabetes mellitus who also have moderate-to-severe chronic kidney disease (CKD) may be as effectively treated with the glucagonlike peptide–1 receptor agonist dulaglutide (Trulicity) as insulin glargine, the results of an international study showed.
Although comparable effects on glycemic control were seen, patients who received dulaglutide rather than insulin glargine in conjunction with prandial insulin lispro (Humalog) exhibited greater weight loss, had fewer episodes of hypoglycemia, and experienced beneficial effects on two important renal parameters.
The adverse event profile of dulaglutide was typical of that seen with GLP-1 receptor antagonism, noted Dr. Tuttle, who is the executive director of Providence Medical Research Center, Providence Sacred Heart Medical Center in Spokane, Washington, and clinical professor of medicine in the nephrology division at the University of Washington in Seattle.
In Europe, the use of dulaglutide in patients with severely reduced kidney function is not currently recommended, and monitoring is required in the United States in those with gastrointestinal side effects.
AWARD-7 was a randomized, open-label parallel-arm study comparing once-weekly dulaglutide (0.75 mg or 1.5 mg) with insulin glargine plus prandial insulin lispro in 576 subjects who had T2DM and stage 3-4 chronic kidney disease. The aim of the trial was to show noninferiority of the dulaglutide regimen to the insulin glargine regimen.
The trial was open label because the dose of insulin glargine had to be regulated, Dr. Tuttle explained, but the dose of dulaglutide given was blinded. The dose of insulin glargine was targeted to fasting plasma glucose to achieve a value between 5.6 mmol/L and 8.3 mmol/L. The dose of insulin lispro was also adjusted to target preprandial plasma glucose between 6.7 mmol/L and 10.0 mmol/L.
Patients were included if they had a glycated hemoglobin (HbA1c) level of at least 7.5% but less than or equal to 10.5% (at least 57 but less than or equal to 91 mmol/mol) and an eGFR less than 60 but greater than or equal to 15 mL/min per 1.73 m2 at screening.
Approximately 45% of dulaglutide- and 52% of glargine-treated subjects were women; the average age of participants was 65 years, with an average duration of diabetes of around 18 years. The mean HbA1c level at study entry was 8.6% (70.5 mmol/mol), with around half of participants having a HbA1c above 8.5% (69.4 mmol/mol) at entry.
The majority of patients included had an eGFR of less than 45 mL/min per 1.73 m2, and about 30% of patients had stage 4 CKD (eGFR at least 15 but less than 30 mL/min per 1.73 m2), about 45% had macroalbuminuria, and a third or more had microalbuminuria.
The primary endpoint was change in HbA1c from baseline to week 26, and this was comparable for both dulaglutide (at around –1.1% to –1.2%) and insulin glargine (around –1.1%). The effects were maintained at 52 weeks, Dr. Tuttle said, adding that similar percentages (approximately 70% or more) of patients in the groups achieved a target HbA1c of less than 8.0 (64 mmol/mol) at 26 and at 52 weeks. Similar results were seen when the more conventional target of less than 7% (less than 52 mmol/mol) was used, with around 30% of patients achieving this target at 26 and at 52 weeks.
As for weight change, the insulin-treated patients gained about 1 kg in weight over the full course of the study while a dose-dependent decrease in weight of about 2-3 kg was seen with dulaglutide treatment.
“Rates of hypoglycemia were consistently lower in the dulaglutide groups [than in the glargine group],” Dr. Tuttle said, noting “the lowest rates of hypoglycemia were actually seen with the highest dose of dulaglutide.”
The rate of total hypoglycemia (less than or equal to 3.9 mmol/mol) in the 1.5-mg and 0.75-mg dulaglutide groups was 50% and 59.8% of patients, respectively, versus almost 75% of the glargine-treated patients. Rates for documented symptomatic (40.5%, 48.1%, 63.4%), nocturnal (20.5%, 23.8%, 47.9%), and severe (0%, 2.6%, 6.7%) hypoglycemia followed a similar pattern.
“Albuminuria was reduced in all study groups, but there were greater reductions in the patients receiving dulaglutide at 26 weeks,” Dr. Tuttle said. The mean change in UACR from baseline to week 26 was –27.7 for the 1.5-mg dose of dulaglutide, –26.7 for the 0.75-mg dose, and –16.4 for insulin glargine.
The expected rate of eGFR decline at week 26 was also lower with dulaglutide 1.5 mg and 0.75 mg than with glargine, at a respective –0.8%, –3.3%, and –7.7% or –0.1, –0.4, and –1.9 mL/min per 1.73 m2.
“In patients at this stage of CKD, we expect about a 4- to 5-mL per minute loss, so they are right on target or as expected in the insulin group, but this was essentially extinguished in the dulaglutide groups, where there was no significant loss in eGFR during the 26-week time period,” said Dr. Tuttle.
The only difference in side effect profiles between the dulaglutide groups and the glargine group was a higher rate of gastrointestinal side effects. Nausea was seen in 19.8%, 14.2%, and 4.6% of patients given the dulaglutide 1.5 mg, dulaglutide 0.75 mg, and glargine, respectively, with vomiting reported by 13.5%, 8.4%, and 4.6%.
Eli Lilly funded the study. Dr. Tuttle disclosed acting as a consultant on therapies for diabetic kidney disease for Eli Lilly, Boehringer Ingelheim, Gilead, and AstraZeneca.
This article was updated September 28, 2017.
LISBON – Patients with type 2 diabetes mellitus who also have moderate-to-severe chronic kidney disease (CKD) may be as effectively treated with the glucagonlike peptide–1 receptor agonist dulaglutide (Trulicity) as insulin glargine, the results of an international study showed.
Although comparable effects on glycemic control were seen, patients who received dulaglutide rather than insulin glargine in conjunction with prandial insulin lispro (Humalog) exhibited greater weight loss, had fewer episodes of hypoglycemia, and experienced beneficial effects on two important renal parameters.
The adverse event profile of dulaglutide was typical of that seen with GLP-1 receptor antagonism, noted Dr. Tuttle, who is the executive director of Providence Medical Research Center, Providence Sacred Heart Medical Center in Spokane, Washington, and clinical professor of medicine in the nephrology division at the University of Washington in Seattle.
In Europe, the use of dulaglutide in patients with severely reduced kidney function is not currently recommended, and monitoring is required in the United States in those with gastrointestinal side effects.
AWARD-7 was a randomized, open-label parallel-arm study comparing once-weekly dulaglutide (0.75 mg or 1.5 mg) with insulin glargine plus prandial insulin lispro in 576 subjects who had T2DM and stage 3-4 chronic kidney disease. The aim of the trial was to show noninferiority of the dulaglutide regimen to the insulin glargine regimen.
The trial was open label because the dose of insulin glargine had to be regulated, Dr. Tuttle explained, but the dose of dulaglutide given was blinded. The dose of insulin glargine was targeted to fasting plasma glucose to achieve a value between 5.6 mmol/L and 8.3 mmol/L. The dose of insulin lispro was also adjusted to target preprandial plasma glucose between 6.7 mmol/L and 10.0 mmol/L.
Patients were included if they had a glycated hemoglobin (HbA1c) level of at least 7.5% but less than or equal to 10.5% (at least 57 but less than or equal to 91 mmol/mol) and an eGFR less than 60 but greater than or equal to 15 mL/min per 1.73 m2 at screening.
Approximately 45% of dulaglutide- and 52% of glargine-treated subjects were women; the average age of participants was 65 years, with an average duration of diabetes of around 18 years. The mean HbA1c level at study entry was 8.6% (70.5 mmol/mol), with around half of participants having a HbA1c above 8.5% (69.4 mmol/mol) at entry.
The majority of patients included had an eGFR of less than 45 mL/min per 1.73 m2, and about 30% of patients had stage 4 CKD (eGFR at least 15 but less than 30 mL/min per 1.73 m2), about 45% had macroalbuminuria, and a third or more had microalbuminuria.
The primary endpoint was change in HbA1c from baseline to week 26, and this was comparable for both dulaglutide (at around –1.1% to –1.2%) and insulin glargine (around –1.1%). The effects were maintained at 52 weeks, Dr. Tuttle said, adding that similar percentages (approximately 70% or more) of patients in the groups achieved a target HbA1c of less than 8.0 (64 mmol/mol) at 26 and at 52 weeks. Similar results were seen when the more conventional target of less than 7% (less than 52 mmol/mol) was used, with around 30% of patients achieving this target at 26 and at 52 weeks.
As for weight change, the insulin-treated patients gained about 1 kg in weight over the full course of the study while a dose-dependent decrease in weight of about 2-3 kg was seen with dulaglutide treatment.
“Rates of hypoglycemia were consistently lower in the dulaglutide groups [than in the glargine group],” Dr. Tuttle said, noting “the lowest rates of hypoglycemia were actually seen with the highest dose of dulaglutide.”
The rate of total hypoglycemia (less than or equal to 3.9 mmol/mol) in the 1.5-mg and 0.75-mg dulaglutide groups was 50% and 59.8% of patients, respectively, versus almost 75% of the glargine-treated patients. Rates for documented symptomatic (40.5%, 48.1%, 63.4%), nocturnal (20.5%, 23.8%, 47.9%), and severe (0%, 2.6%, 6.7%) hypoglycemia followed a similar pattern.
“Albuminuria was reduced in all study groups, but there were greater reductions in the patients receiving dulaglutide at 26 weeks,” Dr. Tuttle said. The mean change in UACR from baseline to week 26 was –27.7 for the 1.5-mg dose of dulaglutide, –26.7 for the 0.75-mg dose, and –16.4 for insulin glargine.
The expected rate of eGFR decline at week 26 was also lower with dulaglutide 1.5 mg and 0.75 mg than with glargine, at a respective –0.8%, –3.3%, and –7.7% or –0.1, –0.4, and –1.9 mL/min per 1.73 m2.
“In patients at this stage of CKD, we expect about a 4- to 5-mL per minute loss, so they are right on target or as expected in the insulin group, but this was essentially extinguished in the dulaglutide groups, where there was no significant loss in eGFR during the 26-week time period,” said Dr. Tuttle.
The only difference in side effect profiles between the dulaglutide groups and the glargine group was a higher rate of gastrointestinal side effects. Nausea was seen in 19.8%, 14.2%, and 4.6% of patients given the dulaglutide 1.5 mg, dulaglutide 0.75 mg, and glargine, respectively, with vomiting reported by 13.5%, 8.4%, and 4.6%.
Eli Lilly funded the study. Dr. Tuttle disclosed acting as a consultant on therapies for diabetic kidney disease for Eli Lilly, Boehringer Ingelheim, Gilead, and AstraZeneca.
This article was updated September 28, 2017.
LISBON – Patients with type 2 diabetes mellitus who also have moderate-to-severe chronic kidney disease (CKD) may be as effectively treated with the glucagonlike peptide–1 receptor agonist dulaglutide (Trulicity) as insulin glargine, the results of an international study showed.
Although comparable effects on glycemic control were seen, patients who received dulaglutide rather than insulin glargine in conjunction with prandial insulin lispro (Humalog) exhibited greater weight loss, had fewer episodes of hypoglycemia, and experienced beneficial effects on two important renal parameters.
The adverse event profile of dulaglutide was typical of that seen with GLP-1 receptor antagonism, noted Dr. Tuttle, who is the executive director of Providence Medical Research Center, Providence Sacred Heart Medical Center in Spokane, Washington, and clinical professor of medicine in the nephrology division at the University of Washington in Seattle.
In Europe, the use of dulaglutide in patients with severely reduced kidney function is not currently recommended, and monitoring is required in the United States in those with gastrointestinal side effects.
AWARD-7 was a randomized, open-label parallel-arm study comparing once-weekly dulaglutide (0.75 mg or 1.5 mg) with insulin glargine plus prandial insulin lispro in 576 subjects who had T2DM and stage 3-4 chronic kidney disease. The aim of the trial was to show noninferiority of the dulaglutide regimen to the insulin glargine regimen.
The trial was open label because the dose of insulin glargine had to be regulated, Dr. Tuttle explained, but the dose of dulaglutide given was blinded. The dose of insulin glargine was targeted to fasting plasma glucose to achieve a value between 5.6 mmol/L and 8.3 mmol/L. The dose of insulin lispro was also adjusted to target preprandial plasma glucose between 6.7 mmol/L and 10.0 mmol/L.
Patients were included if they had a glycated hemoglobin (HbA1c) level of at least 7.5% but less than or equal to 10.5% (at least 57 but less than or equal to 91 mmol/mol) and an eGFR less than 60 but greater than or equal to 15 mL/min per 1.73 m2 at screening.
Approximately 45% of dulaglutide- and 52% of glargine-treated subjects were women; the average age of participants was 65 years, with an average duration of diabetes of around 18 years. The mean HbA1c level at study entry was 8.6% (70.5 mmol/mol), with around half of participants having a HbA1c above 8.5% (69.4 mmol/mol) at entry.
The majority of patients included had an eGFR of less than 45 mL/min per 1.73 m2, and about 30% of patients had stage 4 CKD (eGFR at least 15 but less than 30 mL/min per 1.73 m2), about 45% had macroalbuminuria, and a third or more had microalbuminuria.
The primary endpoint was change in HbA1c from baseline to week 26, and this was comparable for both dulaglutide (at around –1.1% to –1.2%) and insulin glargine (around –1.1%). The effects were maintained at 52 weeks, Dr. Tuttle said, adding that similar percentages (approximately 70% or more) of patients in the groups achieved a target HbA1c of less than 8.0 (64 mmol/mol) at 26 and at 52 weeks. Similar results were seen when the more conventional target of less than 7% (less than 52 mmol/mol) was used, with around 30% of patients achieving this target at 26 and at 52 weeks.
As for weight change, the insulin-treated patients gained about 1 kg in weight over the full course of the study while a dose-dependent decrease in weight of about 2-3 kg was seen with dulaglutide treatment.
“Rates of hypoglycemia were consistently lower in the dulaglutide groups [than in the glargine group],” Dr. Tuttle said, noting “the lowest rates of hypoglycemia were actually seen with the highest dose of dulaglutide.”
The rate of total hypoglycemia (less than or equal to 3.9 mmol/mol) in the 1.5-mg and 0.75-mg dulaglutide groups was 50% and 59.8% of patients, respectively, versus almost 75% of the glargine-treated patients. Rates for documented symptomatic (40.5%, 48.1%, 63.4%), nocturnal (20.5%, 23.8%, 47.9%), and severe (0%, 2.6%, 6.7%) hypoglycemia followed a similar pattern.
“Albuminuria was reduced in all study groups, but there were greater reductions in the patients receiving dulaglutide at 26 weeks,” Dr. Tuttle said. The mean change in UACR from baseline to week 26 was –27.7 for the 1.5-mg dose of dulaglutide, –26.7 for the 0.75-mg dose, and –16.4 for insulin glargine.
The expected rate of eGFR decline at week 26 was also lower with dulaglutide 1.5 mg and 0.75 mg than with glargine, at a respective –0.8%, –3.3%, and –7.7% or –0.1, –0.4, and –1.9 mL/min per 1.73 m2.
“In patients at this stage of CKD, we expect about a 4- to 5-mL per minute loss, so they are right on target or as expected in the insulin group, but this was essentially extinguished in the dulaglutide groups, where there was no significant loss in eGFR during the 26-week time period,” said Dr. Tuttle.
The only difference in side effect profiles between the dulaglutide groups and the glargine group was a higher rate of gastrointestinal side effects. Nausea was seen in 19.8%, 14.2%, and 4.6% of patients given the dulaglutide 1.5 mg, dulaglutide 0.75 mg, and glargine, respectively, with vomiting reported by 13.5%, 8.4%, and 4.6%.
Eli Lilly funded the study. Dr. Tuttle disclosed acting as a consultant on therapies for diabetic kidney disease for Eli Lilly, Boehringer Ingelheim, Gilead, and AstraZeneca.
This article was updated September 28, 2017.
AT EASD 2017
Key clinical point: Dulaglutide had more beneficial effects on renal parameters than insulin glargine in patients with type 2 diabetes and moderate-to-severe chronic kidney disease.
Major finding: The primary endpoint of change in HbA1c level from baseline to week 26 was comparable for both dulaglutide and insulin glargine.
Data source: A randomized, open-label parallel-arm study comparing once-weekly dulaglutide (0.75 or 1.5 mg) or insulin glargine plus prandial insulin lispro in 576 subjects with type 2 diabetes mellitus and stage 3–4 CKD.
Disclosures: Eli Lilly funded the study. The presenting author has been a consultant on therapies for diabetic kidney disease for Eli Lilly, Boehringer Ingelheim, Gilead, and AstraZeneca.
Letter: Working together to empower our next generation of leaders
Editor:
Dr. Nasim Afsar’s article of June 2, 2017 (“A case for building our leadership skills”) calls for the integration of leadership skills into medical training, and we at the University of Colorado wholeheartedly agree. There are several institutions around the country that are already addressing this problem head on, and we write this letter to highlight a few educational programs we’ve created that demonstrate the power of arming our trainees with this skill set. Furthermore, we wish to encourage collaboration between educators and institutions that are engaged in similar work in the hopes of moving this field forward.
Here at the University of Colorado, a team of Hospital Medicine faculty has created a number of programs to address the leadership education gap in learners at the undergraduate medical education,1 graduate medical education,2 and fellowship levels – creating a pipeline for developing leaders in hospital medicine. These programs include an immersive medical student elective, a dedicated leadership track in the Internal Medicine Residency Program, and a fellowship program in Hospital Medicine focused on Quality Improvement and Health Systems Leadership. Our goal in each of these programs to equip trainees across the spectrum of medical education with the knowledge, attitudes, and skills needed to lead high-functioning teams.
In our 5-year experience with our leadership training pipeline, we’ve learned a few important lessons. First, medical trainees are rarely exposed to the leadership skill set elsewhere in medical training, and are eager to learn new approaches to common problems that they encounter on a daily basis: How do I negotiate with a colleague? How can I motivate team members to change behavior to accomplish a goal? How can I use data to support requests for resources?
Secondly, trainees who are exposed to leadership concepts and who are given the opportunity to practice them through challenging project work in the live system routinely make meaningful changes to the health system. Our trainees have revamped our process of managing interhospital transfers, have decreased rates of inappropriate antibiotic usage, and have enhanced the patient experience in our stroke units. Further, our recent graduates have positioned themselves as leaders in health systems. Our graduates are leading a QI program at a major academic center, being promoted to educational leadership roles such as assistant program director within a residency training program, directing process improvement in a developing country, and leading the operations unit of a large physician group.
As Dr. Afsar highlights, there is much work to be done to better equip trainees with the skill set to lead. We strongly encourage other training programs to develop strategies to teach leadership and create forums for trainees to practice their burgeoning skill set. In addition to responding to Dr. Afsar’s call to develop programs, we should form collaborative working groups through our regional and national organizations to develop comprehensive leadership programs for medical trainees at all levels. Collaborating to empower the next generation of providers is critical to our future as hospitalists as we continue to take the lead in improving and shaping our health care systems.
Tyler Anstett, DO
Manuel Diaz, MD
Emily Gottenborg, MD
University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colo.
References
1. Sweigart JR, Tad-Y D, Kneeland P, Williams MV, Glasheen JJ. Hospital Medicine Resident Training Tracks: Developing the Hospital Medicine Pipeline. J Hosp Med. 2017 Mar;12(3):173-176. doi: 10.12788/jhm.2703.
2. Tad-y D, Price L, Cumbler E, Levin D, Wald H, Glasheen J. An experiential quality improvement curriculum for the inpatient setting – part 1: design phase of a QI project. MedEdPORTAL Publications. 2014;10:9841. http://doi.org/10.15766/mep_2374-8265.9841.
Editor:
Dr. Nasim Afsar’s article of June 2, 2017 (“A case for building our leadership skills”) calls for the integration of leadership skills into medical training, and we at the University of Colorado wholeheartedly agree. There are several institutions around the country that are already addressing this problem head on, and we write this letter to highlight a few educational programs we’ve created that demonstrate the power of arming our trainees with this skill set. Furthermore, we wish to encourage collaboration between educators and institutions that are engaged in similar work in the hopes of moving this field forward.
Here at the University of Colorado, a team of Hospital Medicine faculty has created a number of programs to address the leadership education gap in learners at the undergraduate medical education,1 graduate medical education,2 and fellowship levels – creating a pipeline for developing leaders in hospital medicine. These programs include an immersive medical student elective, a dedicated leadership track in the Internal Medicine Residency Program, and a fellowship program in Hospital Medicine focused on Quality Improvement and Health Systems Leadership. Our goal in each of these programs to equip trainees across the spectrum of medical education with the knowledge, attitudes, and skills needed to lead high-functioning teams.
In our 5-year experience with our leadership training pipeline, we’ve learned a few important lessons. First, medical trainees are rarely exposed to the leadership skill set elsewhere in medical training, and are eager to learn new approaches to common problems that they encounter on a daily basis: How do I negotiate with a colleague? How can I motivate team members to change behavior to accomplish a goal? How can I use data to support requests for resources?
Secondly, trainees who are exposed to leadership concepts and who are given the opportunity to practice them through challenging project work in the live system routinely make meaningful changes to the health system. Our trainees have revamped our process of managing interhospital transfers, have decreased rates of inappropriate antibiotic usage, and have enhanced the patient experience in our stroke units. Further, our recent graduates have positioned themselves as leaders in health systems. Our graduates are leading a QI program at a major academic center, being promoted to educational leadership roles such as assistant program director within a residency training program, directing process improvement in a developing country, and leading the operations unit of a large physician group.
As Dr. Afsar highlights, there is much work to be done to better equip trainees with the skill set to lead. We strongly encourage other training programs to develop strategies to teach leadership and create forums for trainees to practice their burgeoning skill set. In addition to responding to Dr. Afsar’s call to develop programs, we should form collaborative working groups through our regional and national organizations to develop comprehensive leadership programs for medical trainees at all levels. Collaborating to empower the next generation of providers is critical to our future as hospitalists as we continue to take the lead in improving and shaping our health care systems.
Tyler Anstett, DO
Manuel Diaz, MD
Emily Gottenborg, MD
University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colo.
References
1. Sweigart JR, Tad-Y D, Kneeland P, Williams MV, Glasheen JJ. Hospital Medicine Resident Training Tracks: Developing the Hospital Medicine Pipeline. J Hosp Med. 2017 Mar;12(3):173-176. doi: 10.12788/jhm.2703.
2. Tad-y D, Price L, Cumbler E, Levin D, Wald H, Glasheen J. An experiential quality improvement curriculum for the inpatient setting – part 1: design phase of a QI project. MedEdPORTAL Publications. 2014;10:9841. http://doi.org/10.15766/mep_2374-8265.9841.
Editor:
Dr. Nasim Afsar’s article of June 2, 2017 (“A case for building our leadership skills”) calls for the integration of leadership skills into medical training, and we at the University of Colorado wholeheartedly agree. There are several institutions around the country that are already addressing this problem head on, and we write this letter to highlight a few educational programs we’ve created that demonstrate the power of arming our trainees with this skill set. Furthermore, we wish to encourage collaboration between educators and institutions that are engaged in similar work in the hopes of moving this field forward.
Here at the University of Colorado, a team of Hospital Medicine faculty has created a number of programs to address the leadership education gap in learners at the undergraduate medical education,1 graduate medical education,2 and fellowship levels – creating a pipeline for developing leaders in hospital medicine. These programs include an immersive medical student elective, a dedicated leadership track in the Internal Medicine Residency Program, and a fellowship program in Hospital Medicine focused on Quality Improvement and Health Systems Leadership. Our goal in each of these programs to equip trainees across the spectrum of medical education with the knowledge, attitudes, and skills needed to lead high-functioning teams.
In our 5-year experience with our leadership training pipeline, we’ve learned a few important lessons. First, medical trainees are rarely exposed to the leadership skill set elsewhere in medical training, and are eager to learn new approaches to common problems that they encounter on a daily basis: How do I negotiate with a colleague? How can I motivate team members to change behavior to accomplish a goal? How can I use data to support requests for resources?
Secondly, trainees who are exposed to leadership concepts and who are given the opportunity to practice them through challenging project work in the live system routinely make meaningful changes to the health system. Our trainees have revamped our process of managing interhospital transfers, have decreased rates of inappropriate antibiotic usage, and have enhanced the patient experience in our stroke units. Further, our recent graduates have positioned themselves as leaders in health systems. Our graduates are leading a QI program at a major academic center, being promoted to educational leadership roles such as assistant program director within a residency training program, directing process improvement in a developing country, and leading the operations unit of a large physician group.
As Dr. Afsar highlights, there is much work to be done to better equip trainees with the skill set to lead. We strongly encourage other training programs to develop strategies to teach leadership and create forums for trainees to practice their burgeoning skill set. In addition to responding to Dr. Afsar’s call to develop programs, we should form collaborative working groups through our regional and national organizations to develop comprehensive leadership programs for medical trainees at all levels. Collaborating to empower the next generation of providers is critical to our future as hospitalists as we continue to take the lead in improving and shaping our health care systems.
Tyler Anstett, DO
Manuel Diaz, MD
Emily Gottenborg, MD
University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colo.
References
1. Sweigart JR, Tad-Y D, Kneeland P, Williams MV, Glasheen JJ. Hospital Medicine Resident Training Tracks: Developing the Hospital Medicine Pipeline. J Hosp Med. 2017 Mar;12(3):173-176. doi: 10.12788/jhm.2703.
2. Tad-y D, Price L, Cumbler E, Levin D, Wald H, Glasheen J. An experiential quality improvement curriculum for the inpatient setting – part 1: design phase of a QI project. MedEdPORTAL Publications. 2014;10:9841. http://doi.org/10.15766/mep_2374-8265.9841.
ICD-10-CM code changes: What's new for 2018
The list of new and revised International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) codes has been published, with changes becoming effective on October 1, 2017. This year, you can look forward to minimal code changes for gynecologic conditions. The biggest change in this category is the addition of codes that describe a lump in the breast according to which breast and the location on the breast, as well as the addition of a code for prophylactic removal of the fallopian tubes. The codes related to obstetrics will have more extensive changes. You will find revisions to the codes for ectopic pregnancy, a new set of codes for addressing an abnormal fetal heart rate during the antepartum period, and, most welcome of all, an expansion of the single code for antenatal testing to 17 very specific codes.
Gynecologic code changes
The single code N63, Unspecified lump in breast, has been expanded to include codes for both the right and the left breast. Code N63 therefore will be considered invalid after October 1, 2018. Expanded codes include:
- N63.0, Unspecified lump in unspecified breast
- N63.1, Unspecified lump in the right breast
- N63.10, Unspecified lump in the right breast, unspecified quadrant
- N63.11, Unspecified lump in the right breast, upper outer quadrant
- N63.12, Unspecified lump in the right breast, upper inner quadrant
- N63.13, Unspecified lump in the right breast, lower outer quadrant
- N63.14, Unspecified lump in the right breast, lower inner quadrant
- N63.2, Unspecified lump in the left breast
- N63.20, Unspecified lump in the left breast, unspecified quadrant
- N63.21, Unspecified lump in the left breast, upper outer quadrant
- N63.22, Unspecified lump in the left breast, upper inner quadrant
- N63.23, Unspecified lump in the left breast, lower outer quadrant
- N63.24, Unspecified lump in the left breast, lower inner quadrant
- N63.3, Unspecified lump in axillary tail
- N63.31, Unspecified lump in axillary tail of the right breast
- N63.32, Unspecified lump in axillary tail of the left breast
- N63.4, Unspecified lump in breast, subareolar
- N63.41, Unspecified lump in right breast, subareolar
- N63.42, Unspecified lump in left breast, subareolar
Other changes to gynecologic codes
There has been a minor change to the description for code Z31.5, Encounter for genetic counseling. It now is described as "Encounter for procreative genetic counseling."
The code Z40.02, Encounter for prophylactic removal of ovary(s), now refers to one or more ovaries without distinction of right or left, and a new code has been added for removal of the fallopian tube(s), Z40.03, Encounter for prophylactic removal of fallopian tube(s).
The inclusion term "endometriosis of the thorax" has been added to code N80.8, Other endometriosis.
The inclusion term "premenstrual dysphoric disorder" has been deleted from code N94.3, Premenstrual tension syndrome. If the patient has been diagnosed with this condition, the code F32.81, Premenstrual dysphoric disorder, should be reported, as this is considered a mental health issue.
The "excludes 1" note under code Z87.41, Personal history of dysplasia of the female genital tract, has been revised. The codes for personal history of intraepithelial neoplasia III that may not be reported with this code are Z86.001 and Z86.008.
Obstetric code changes
The ectopic pregnancy codes have been revised to include references to the right or left structure affected, which means the codes change from 5 digits to 6 digits in length, and the codes O00.10, O00.11, O00.20, and O00.21 will no longer be valid.
- O00.1, Tubal pregnancy
- O00.10, Tubal pregnancy without intrauterine pregnancy
- O00.101, Right tubal pregnancy without intrauterine pregnancy
- O00.102, Left tubal pregnancy without intrauterine pregnancy
- O00.109, Unspecified tubal pregnancy without intrauterine pregnancy
- O00.11, Tubal pregnancy with intrauterine pregnancy
- O00.111, Right tubal pregnancy with intrauterine pregnancy
- O00.112, Left tubal pregnancy with intrauterine pregnancy
- O00.119, Unspecified tubal pregnancy with intrauterine pregnancy
- O00.10, Tubal pregnancy without intrauterine pregnancy
- O00.2, Ovarian pregnancy
- O00.20, Ovarian pregnancy without intrauterine pregnancy
- O00.201, Right ovarian pregnancy without intrauterine pregnancy
- O00.202, Left ovarian pregnancy without intrauterine pregnancy
- O00.209, Unspecified ovarian pregnancy without intrauterine pregnancy
- O00.21, Ovarian pregnancy with intrauterine pregnancy
- O00.211, Right ovarian pregnancy with intrauterine pregnancy
- O00.212, Left ovarian pregnancy with intrauterine pregnancy
- O00.219, Unspecified ovarian pregnancy with intrauterine pregnancy
- O00.20, Ovarian pregnancy without intrauterine pregnancy
New codes for fetal heart rate abnormalities
New codes have been added to report a fetal heart rate or rhythm abnormality during the antepartum period. Until now, there only has been a code that addresses this issue during labor and delivery, O76, Abnormality in fetal heart rate and rhythm complicating labor and delivery.
- O36.83, Maternal care for abnormalities of the fetal heart rate or rhythm
- O36.831, Maternal care for abnormalities of the fetal heart rate or rhythm, first trimester
- O36.832, Maternal care for abnormalities of the fetal heart rate or rhythm, second trimester
- O36.833, Maternal care for abnormalities of the fetal heart rate or rhythm, third trimester
- O36.839, Maternal care for abnormalities of the fetal heart rate or rhythm, unspecified trimester
Several codes redefined
ICD-10 has corrected an "excludes" note error for the code O99.1, Other diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism complicating pregnancy, childbirth, and the puerperium. In 2017, any hemorrhage with coagulation defects defined in code category O45.- or codes O46.0-, O67.0, or O72.3 could be reported with O99.1. This set of codes has now been redefined as an "excludes 1" note, which means that they may not be reported with O99.1 since they are considered inclusive.
More specific codes added for antenatal screening
Great news for those awaiting a more specific code for antenatal screening: The code Z36 has been expanded to more closely match the codes that were available in ICD-9-CM, but it goes beyond the basic list in that codes have been added for things like nonvisualization of anatomic structures on a previous scan and screening for cervical length and fetal lung maturity. Be sure to pay attention to the excludes notes and other inclusive terms.
- Z36, Encounter for antenatal screening of mother (Screening is the testing for disease or disease precursors in asymptomatic individuals so that early detection and treatment can be provided for those who test positive for the disease.)
Includes: Encounter for placental sample (taken vaginally)
Excludes 2: O28.-, Abnormal findings on antenatal screening of mother
- Z36.5, Encounter for antenatal screening for isoimmunization
- Z36.4, Encounter for antenatal screening for fetal growth retardation
Intrauterine growth restriction (IUGR)/small-for-dates - Z36.3, Encounter for antenatal screening for malformations
Screening for a suspected anomaly - Z36.2, Encounter for other antenatal screening follow-up
Nonvisualized anatomy on a previous scan - Z36.1, Encounter for antenatal screening for raised alpha-fetoprotein level
Encounter for antenatal screening for elevated maternal serum alpha-fetoprotein level - Z36.0, Encounter for antenatal screening for chromosomal anomalies
- Z36.81, Encounter for antenatal screening for hydrops fetalis
- Z36.8A, Encounter for antenatal screening for other genetic defects
- Z36.89, Encounter for other specified antenatal screening
- Z36.88, Encounter for antenatal screening for fetal macrosomia
Screening for large-for-dates - Z36.87, Encounter for antenatal screening for uncertain dates
- Z36.86, Encounter for antenatal screening for cervical length
Screening for risk of preterm labor - Z36.85, Encounter for antenatal screening for Streptococcus B
- Z36.84, Encounter for antenatal screening for fetal lung maturity
- Z36.83, Encounter for fetal screening for congenital cardiac abnormalities
- Z36.82, Encounter for antenatal screening for nuchal translucency
- Z36.81, Encounter for antenatal screening for hydrops fetalis
- Z36.9, Encounter for antenatal screening, unspecified
Code changes for abortion and complications
The code range for use with Z3A, weeks of gestation, has changed from O00-O9A to O09-O9A to reflect the guideline change last year to remove the requirement to use this code with any code that describes pregnancy with an abortive outcome (codes O00-O08).
In addition, if a patient has retained products of conception (POC) after either a spontaneous or elective abortion, report the "without complication" code for the retained POC (O03.4, Incomplete spontaneous abortion without complication, or O07.4, Failed attempted termination of pregnancy without complication). If any other complication occurred in addition to the retained POC, use the code for that particular complication and not O03.4 or O07.4.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Ms. Witt is an independent coding and documentation consultant and former program manager, department of coding and nomenclature, American Congress of Obstetricians and Gynecologists.
The author reports no financial relationships relevant to this article.
Ms. Witt is an independent coding and documentation consultant and former program manager, department of coding and nomenclature, American Congress of Obstetricians and Gynecologists.
The author reports no financial relationships relevant to this article.
Ms. Witt is an independent coding and documentation consultant and former program manager, department of coding and nomenclature, American Congress of Obstetricians and Gynecologists.
The author reports no financial relationships relevant to this article.
The list of new and revised International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) codes has been published, with changes becoming effective on October 1, 2017. This year, you can look forward to minimal code changes for gynecologic conditions. The biggest change in this category is the addition of codes that describe a lump in the breast according to which breast and the location on the breast, as well as the addition of a code for prophylactic removal of the fallopian tubes. The codes related to obstetrics will have more extensive changes. You will find revisions to the codes for ectopic pregnancy, a new set of codes for addressing an abnormal fetal heart rate during the antepartum period, and, most welcome of all, an expansion of the single code for antenatal testing to 17 very specific codes.
Gynecologic code changes
The single code N63, Unspecified lump in breast, has been expanded to include codes for both the right and the left breast. Code N63 therefore will be considered invalid after October 1, 2018. Expanded codes include:
- N63.0, Unspecified lump in unspecified breast
- N63.1, Unspecified lump in the right breast
- N63.10, Unspecified lump in the right breast, unspecified quadrant
- N63.11, Unspecified lump in the right breast, upper outer quadrant
- N63.12, Unspecified lump in the right breast, upper inner quadrant
- N63.13, Unspecified lump in the right breast, lower outer quadrant
- N63.14, Unspecified lump in the right breast, lower inner quadrant
- N63.2, Unspecified lump in the left breast
- N63.20, Unspecified lump in the left breast, unspecified quadrant
- N63.21, Unspecified lump in the left breast, upper outer quadrant
- N63.22, Unspecified lump in the left breast, upper inner quadrant
- N63.23, Unspecified lump in the left breast, lower outer quadrant
- N63.24, Unspecified lump in the left breast, lower inner quadrant
- N63.3, Unspecified lump in axillary tail
- N63.31, Unspecified lump in axillary tail of the right breast
- N63.32, Unspecified lump in axillary tail of the left breast
- N63.4, Unspecified lump in breast, subareolar
- N63.41, Unspecified lump in right breast, subareolar
- N63.42, Unspecified lump in left breast, subareolar
Other changes to gynecologic codes
There has been a minor change to the description for code Z31.5, Encounter for genetic counseling. It now is described as "Encounter for procreative genetic counseling."
The code Z40.02, Encounter for prophylactic removal of ovary(s), now refers to one or more ovaries without distinction of right or left, and a new code has been added for removal of the fallopian tube(s), Z40.03, Encounter for prophylactic removal of fallopian tube(s).
The inclusion term "endometriosis of the thorax" has been added to code N80.8, Other endometriosis.
The inclusion term "premenstrual dysphoric disorder" has been deleted from code N94.3, Premenstrual tension syndrome. If the patient has been diagnosed with this condition, the code F32.81, Premenstrual dysphoric disorder, should be reported, as this is considered a mental health issue.
The "excludes 1" note under code Z87.41, Personal history of dysplasia of the female genital tract, has been revised. The codes for personal history of intraepithelial neoplasia III that may not be reported with this code are Z86.001 and Z86.008.
Obstetric code changes
The ectopic pregnancy codes have been revised to include references to the right or left structure affected, which means the codes change from 5 digits to 6 digits in length, and the codes O00.10, O00.11, O00.20, and O00.21 will no longer be valid.
- O00.1, Tubal pregnancy
- O00.10, Tubal pregnancy without intrauterine pregnancy
- O00.101, Right tubal pregnancy without intrauterine pregnancy
- O00.102, Left tubal pregnancy without intrauterine pregnancy
- O00.109, Unspecified tubal pregnancy without intrauterine pregnancy
- O00.11, Tubal pregnancy with intrauterine pregnancy
- O00.111, Right tubal pregnancy with intrauterine pregnancy
- O00.112, Left tubal pregnancy with intrauterine pregnancy
- O00.119, Unspecified tubal pregnancy with intrauterine pregnancy
- O00.10, Tubal pregnancy without intrauterine pregnancy
- O00.2, Ovarian pregnancy
- O00.20, Ovarian pregnancy without intrauterine pregnancy
- O00.201, Right ovarian pregnancy without intrauterine pregnancy
- O00.202, Left ovarian pregnancy without intrauterine pregnancy
- O00.209, Unspecified ovarian pregnancy without intrauterine pregnancy
- O00.21, Ovarian pregnancy with intrauterine pregnancy
- O00.211, Right ovarian pregnancy with intrauterine pregnancy
- O00.212, Left ovarian pregnancy with intrauterine pregnancy
- O00.219, Unspecified ovarian pregnancy with intrauterine pregnancy
- O00.20, Ovarian pregnancy without intrauterine pregnancy
New codes for fetal heart rate abnormalities
New codes have been added to report a fetal heart rate or rhythm abnormality during the antepartum period. Until now, there only has been a code that addresses this issue during labor and delivery, O76, Abnormality in fetal heart rate and rhythm complicating labor and delivery.
- O36.83, Maternal care for abnormalities of the fetal heart rate or rhythm
- O36.831, Maternal care for abnormalities of the fetal heart rate or rhythm, first trimester
- O36.832, Maternal care for abnormalities of the fetal heart rate or rhythm, second trimester
- O36.833, Maternal care for abnormalities of the fetal heart rate or rhythm, third trimester
- O36.839, Maternal care for abnormalities of the fetal heart rate or rhythm, unspecified trimester
Several codes redefined
ICD-10 has corrected an "excludes" note error for the code O99.1, Other diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism complicating pregnancy, childbirth, and the puerperium. In 2017, any hemorrhage with coagulation defects defined in code category O45.- or codes O46.0-, O67.0, or O72.3 could be reported with O99.1. This set of codes has now been redefined as an "excludes 1" note, which means that they may not be reported with O99.1 since they are considered inclusive.
More specific codes added for antenatal screening
Great news for those awaiting a more specific code for antenatal screening: The code Z36 has been expanded to more closely match the codes that were available in ICD-9-CM, but it goes beyond the basic list in that codes have been added for things like nonvisualization of anatomic structures on a previous scan and screening for cervical length and fetal lung maturity. Be sure to pay attention to the excludes notes and other inclusive terms.
- Z36, Encounter for antenatal screening of mother (Screening is the testing for disease or disease precursors in asymptomatic individuals so that early detection and treatment can be provided for those who test positive for the disease.)
Includes: Encounter for placental sample (taken vaginally)
Excludes 2: O28.-, Abnormal findings on antenatal screening of mother
- Z36.5, Encounter for antenatal screening for isoimmunization
- Z36.4, Encounter for antenatal screening for fetal growth retardation
Intrauterine growth restriction (IUGR)/small-for-dates - Z36.3, Encounter for antenatal screening for malformations
Screening for a suspected anomaly - Z36.2, Encounter for other antenatal screening follow-up
Nonvisualized anatomy on a previous scan - Z36.1, Encounter for antenatal screening for raised alpha-fetoprotein level
Encounter for antenatal screening for elevated maternal serum alpha-fetoprotein level - Z36.0, Encounter for antenatal screening for chromosomal anomalies
- Z36.81, Encounter for antenatal screening for hydrops fetalis
- Z36.8A, Encounter for antenatal screening for other genetic defects
- Z36.89, Encounter for other specified antenatal screening
- Z36.88, Encounter for antenatal screening for fetal macrosomia
Screening for large-for-dates - Z36.87, Encounter for antenatal screening for uncertain dates
- Z36.86, Encounter for antenatal screening for cervical length
Screening for risk of preterm labor - Z36.85, Encounter for antenatal screening for Streptococcus B
- Z36.84, Encounter for antenatal screening for fetal lung maturity
- Z36.83, Encounter for fetal screening for congenital cardiac abnormalities
- Z36.82, Encounter for antenatal screening for nuchal translucency
- Z36.81, Encounter for antenatal screening for hydrops fetalis
- Z36.9, Encounter for antenatal screening, unspecified
Code changes for abortion and complications
The code range for use with Z3A, weeks of gestation, has changed from O00-O9A to O09-O9A to reflect the guideline change last year to remove the requirement to use this code with any code that describes pregnancy with an abortive outcome (codes O00-O08).
In addition, if a patient has retained products of conception (POC) after either a spontaneous or elective abortion, report the "without complication" code for the retained POC (O03.4, Incomplete spontaneous abortion without complication, or O07.4, Failed attempted termination of pregnancy without complication). If any other complication occurred in addition to the retained POC, use the code for that particular complication and not O03.4 or O07.4.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
The list of new and revised International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) codes has been published, with changes becoming effective on October 1, 2017. This year, you can look forward to minimal code changes for gynecologic conditions. The biggest change in this category is the addition of codes that describe a lump in the breast according to which breast and the location on the breast, as well as the addition of a code for prophylactic removal of the fallopian tubes. The codes related to obstetrics will have more extensive changes. You will find revisions to the codes for ectopic pregnancy, a new set of codes for addressing an abnormal fetal heart rate during the antepartum period, and, most welcome of all, an expansion of the single code for antenatal testing to 17 very specific codes.
Gynecologic code changes
The single code N63, Unspecified lump in breast, has been expanded to include codes for both the right and the left breast. Code N63 therefore will be considered invalid after October 1, 2018. Expanded codes include:
- N63.0, Unspecified lump in unspecified breast
- N63.1, Unspecified lump in the right breast
- N63.10, Unspecified lump in the right breast, unspecified quadrant
- N63.11, Unspecified lump in the right breast, upper outer quadrant
- N63.12, Unspecified lump in the right breast, upper inner quadrant
- N63.13, Unspecified lump in the right breast, lower outer quadrant
- N63.14, Unspecified lump in the right breast, lower inner quadrant
- N63.2, Unspecified lump in the left breast
- N63.20, Unspecified lump in the left breast, unspecified quadrant
- N63.21, Unspecified lump in the left breast, upper outer quadrant
- N63.22, Unspecified lump in the left breast, upper inner quadrant
- N63.23, Unspecified lump in the left breast, lower outer quadrant
- N63.24, Unspecified lump in the left breast, lower inner quadrant
- N63.3, Unspecified lump in axillary tail
- N63.31, Unspecified lump in axillary tail of the right breast
- N63.32, Unspecified lump in axillary tail of the left breast
- N63.4, Unspecified lump in breast, subareolar
- N63.41, Unspecified lump in right breast, subareolar
- N63.42, Unspecified lump in left breast, subareolar
Other changes to gynecologic codes
There has been a minor change to the description for code Z31.5, Encounter for genetic counseling. It now is described as "Encounter for procreative genetic counseling."
The code Z40.02, Encounter for prophylactic removal of ovary(s), now refers to one or more ovaries without distinction of right or left, and a new code has been added for removal of the fallopian tube(s), Z40.03, Encounter for prophylactic removal of fallopian tube(s).
The inclusion term "endometriosis of the thorax" has been added to code N80.8, Other endometriosis.
The inclusion term "premenstrual dysphoric disorder" has been deleted from code N94.3, Premenstrual tension syndrome. If the patient has been diagnosed with this condition, the code F32.81, Premenstrual dysphoric disorder, should be reported, as this is considered a mental health issue.
The "excludes 1" note under code Z87.41, Personal history of dysplasia of the female genital tract, has been revised. The codes for personal history of intraepithelial neoplasia III that may not be reported with this code are Z86.001 and Z86.008.
Obstetric code changes
The ectopic pregnancy codes have been revised to include references to the right or left structure affected, which means the codes change from 5 digits to 6 digits in length, and the codes O00.10, O00.11, O00.20, and O00.21 will no longer be valid.
- O00.1, Tubal pregnancy
- O00.10, Tubal pregnancy without intrauterine pregnancy
- O00.101, Right tubal pregnancy without intrauterine pregnancy
- O00.102, Left tubal pregnancy without intrauterine pregnancy
- O00.109, Unspecified tubal pregnancy without intrauterine pregnancy
- O00.11, Tubal pregnancy with intrauterine pregnancy
- O00.111, Right tubal pregnancy with intrauterine pregnancy
- O00.112, Left tubal pregnancy with intrauterine pregnancy
- O00.119, Unspecified tubal pregnancy with intrauterine pregnancy
- O00.10, Tubal pregnancy without intrauterine pregnancy
- O00.2, Ovarian pregnancy
- O00.20, Ovarian pregnancy without intrauterine pregnancy
- O00.201, Right ovarian pregnancy without intrauterine pregnancy
- O00.202, Left ovarian pregnancy without intrauterine pregnancy
- O00.209, Unspecified ovarian pregnancy without intrauterine pregnancy
- O00.21, Ovarian pregnancy with intrauterine pregnancy
- O00.211, Right ovarian pregnancy with intrauterine pregnancy
- O00.212, Left ovarian pregnancy with intrauterine pregnancy
- O00.219, Unspecified ovarian pregnancy with intrauterine pregnancy
- O00.20, Ovarian pregnancy without intrauterine pregnancy
New codes for fetal heart rate abnormalities
New codes have been added to report a fetal heart rate or rhythm abnormality during the antepartum period. Until now, there only has been a code that addresses this issue during labor and delivery, O76, Abnormality in fetal heart rate and rhythm complicating labor and delivery.
- O36.83, Maternal care for abnormalities of the fetal heart rate or rhythm
- O36.831, Maternal care for abnormalities of the fetal heart rate or rhythm, first trimester
- O36.832, Maternal care for abnormalities of the fetal heart rate or rhythm, second trimester
- O36.833, Maternal care for abnormalities of the fetal heart rate or rhythm, third trimester
- O36.839, Maternal care for abnormalities of the fetal heart rate or rhythm, unspecified trimester
Several codes redefined
ICD-10 has corrected an "excludes" note error for the code O99.1, Other diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism complicating pregnancy, childbirth, and the puerperium. In 2017, any hemorrhage with coagulation defects defined in code category O45.- or codes O46.0-, O67.0, or O72.3 could be reported with O99.1. This set of codes has now been redefined as an "excludes 1" note, which means that they may not be reported with O99.1 since they are considered inclusive.
More specific codes added for antenatal screening
Great news for those awaiting a more specific code for antenatal screening: The code Z36 has been expanded to more closely match the codes that were available in ICD-9-CM, but it goes beyond the basic list in that codes have been added for things like nonvisualization of anatomic structures on a previous scan and screening for cervical length and fetal lung maturity. Be sure to pay attention to the excludes notes and other inclusive terms.
- Z36, Encounter for antenatal screening of mother (Screening is the testing for disease or disease precursors in asymptomatic individuals so that early detection and treatment can be provided for those who test positive for the disease.)
Includes: Encounter for placental sample (taken vaginally)
Excludes 2: O28.-, Abnormal findings on antenatal screening of mother
- Z36.5, Encounter for antenatal screening for isoimmunization
- Z36.4, Encounter for antenatal screening for fetal growth retardation
Intrauterine growth restriction (IUGR)/small-for-dates - Z36.3, Encounter for antenatal screening for malformations
Screening for a suspected anomaly - Z36.2, Encounter for other antenatal screening follow-up
Nonvisualized anatomy on a previous scan - Z36.1, Encounter for antenatal screening for raised alpha-fetoprotein level
Encounter for antenatal screening for elevated maternal serum alpha-fetoprotein level - Z36.0, Encounter for antenatal screening for chromosomal anomalies
- Z36.81, Encounter for antenatal screening for hydrops fetalis
- Z36.8A, Encounter for antenatal screening for other genetic defects
- Z36.89, Encounter for other specified antenatal screening
- Z36.88, Encounter for antenatal screening for fetal macrosomia
Screening for large-for-dates - Z36.87, Encounter for antenatal screening for uncertain dates
- Z36.86, Encounter for antenatal screening for cervical length
Screening for risk of preterm labor - Z36.85, Encounter for antenatal screening for Streptococcus B
- Z36.84, Encounter for antenatal screening for fetal lung maturity
- Z36.83, Encounter for fetal screening for congenital cardiac abnormalities
- Z36.82, Encounter for antenatal screening for nuchal translucency
- Z36.81, Encounter for antenatal screening for hydrops fetalis
- Z36.9, Encounter for antenatal screening, unspecified
Code changes for abortion and complications
The code range for use with Z3A, weeks of gestation, has changed from O00-O9A to O09-O9A to reflect the guideline change last year to remove the requirement to use this code with any code that describes pregnancy with an abortive outcome (codes O00-O08).
In addition, if a patient has retained products of conception (POC) after either a spontaneous or elective abortion, report the "without complication" code for the retained POC (O03.4, Incomplete spontaneous abortion without complication, or O07.4, Failed attempted termination of pregnancy without complication). If any other complication occurred in addition to the retained POC, use the code for that particular complication and not O03.4 or O07.4.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Bezlotoxumab may lower risk of C. difficile readmissions
Clostridium difficile infection (CDI) patients treated with bezlotoxumab were less likely to be readmitted for recurring symptoms within 30 days of discharge, according to a phase 3 trial funded by Merck.
Recurrent CDI is a burden on both patients and providers, increasing health risks with each recurrence and eating through hospital resources, according to Vimalanand S. Prabhu, PhD, associate principal scientist for Merck.
In a randomized, double-blind, placebo-controlled, study of 1,050 CDI patients, a total of 27 (5%) of 530 of those given bezlotoxumab were re-hospitalized 30 days after discharge, compared with 58 (11%) of 520 patients in the placebo group (Clin Infect Dis. 2017 Aug 11. doi. 10.1093/cid/cix523).
Patients were gathered from 322 sites across 30 countries between November 2011 and May 2015.
When measuring CDI-related readmissions, the investigators found use of bezlotoxumab reduced rCDI hospitalizations by 6%, and by approximately 8% in high-risk patients, such as those over 65 years old or with severe CDI.
Bezlotoxumab works by binding to CDI toxin B, a primary cause of CDI symptoms, according to Dr. Prabhu and fellow investigators. The researchers suggested that bezlotoxumab could be a prevailing factor in fighting the rate of CDI infections, which accounted for 29,000 deaths in 2011 (N Engl J Med. 2015 Jun 11;372[24]:2368-9).
Investigators acknowledged that patients admitted for the study may be healthier than the real-world CDI population.
All investigators reported some financial involvement, whether being a full-time employee or acting as a consultant, for Merck, which funded the study. Individually, investigators reported financial ties to similar medical companies, such as Pfizer and AstraZeneca.
AGA offers patient education materials on C. diff that can help your patients better understand the infection. Learn more at http://www.gastro.org/patient-care/conditions-diseases/clostridium-difficile-infection.
[email protected]
On Twitter @eaztweets
Clostridium difficile infection (CDI) patients treated with bezlotoxumab were less likely to be readmitted for recurring symptoms within 30 days of discharge, according to a phase 3 trial funded by Merck.
Recurrent CDI is a burden on both patients and providers, increasing health risks with each recurrence and eating through hospital resources, according to Vimalanand S. Prabhu, PhD, associate principal scientist for Merck.
In a randomized, double-blind, placebo-controlled, study of 1,050 CDI patients, a total of 27 (5%) of 530 of those given bezlotoxumab were re-hospitalized 30 days after discharge, compared with 58 (11%) of 520 patients in the placebo group (Clin Infect Dis. 2017 Aug 11. doi. 10.1093/cid/cix523).
Patients were gathered from 322 sites across 30 countries between November 2011 and May 2015.
When measuring CDI-related readmissions, the investigators found use of bezlotoxumab reduced rCDI hospitalizations by 6%, and by approximately 8% in high-risk patients, such as those over 65 years old or with severe CDI.
Bezlotoxumab works by binding to CDI toxin B, a primary cause of CDI symptoms, according to Dr. Prabhu and fellow investigators. The researchers suggested that bezlotoxumab could be a prevailing factor in fighting the rate of CDI infections, which accounted for 29,000 deaths in 2011 (N Engl J Med. 2015 Jun 11;372[24]:2368-9).
Investigators acknowledged that patients admitted for the study may be healthier than the real-world CDI population.
All investigators reported some financial involvement, whether being a full-time employee or acting as a consultant, for Merck, which funded the study. Individually, investigators reported financial ties to similar medical companies, such as Pfizer and AstraZeneca.
AGA offers patient education materials on C. diff that can help your patients better understand the infection. Learn more at http://www.gastro.org/patient-care/conditions-diseases/clostridium-difficile-infection.
[email protected]
On Twitter @eaztweets
Clostridium difficile infection (CDI) patients treated with bezlotoxumab were less likely to be readmitted for recurring symptoms within 30 days of discharge, according to a phase 3 trial funded by Merck.
Recurrent CDI is a burden on both patients and providers, increasing health risks with each recurrence and eating through hospital resources, according to Vimalanand S. Prabhu, PhD, associate principal scientist for Merck.
In a randomized, double-blind, placebo-controlled, study of 1,050 CDI patients, a total of 27 (5%) of 530 of those given bezlotoxumab were re-hospitalized 30 days after discharge, compared with 58 (11%) of 520 patients in the placebo group (Clin Infect Dis. 2017 Aug 11. doi. 10.1093/cid/cix523).
Patients were gathered from 322 sites across 30 countries between November 2011 and May 2015.
When measuring CDI-related readmissions, the investigators found use of bezlotoxumab reduced rCDI hospitalizations by 6%, and by approximately 8% in high-risk patients, such as those over 65 years old or with severe CDI.
Bezlotoxumab works by binding to CDI toxin B, a primary cause of CDI symptoms, according to Dr. Prabhu and fellow investigators. The researchers suggested that bezlotoxumab could be a prevailing factor in fighting the rate of CDI infections, which accounted for 29,000 deaths in 2011 (N Engl J Med. 2015 Jun 11;372[24]:2368-9).
Investigators acknowledged that patients admitted for the study may be healthier than the real-world CDI population.
All investigators reported some financial involvement, whether being a full-time employee or acting as a consultant, for Merck, which funded the study. Individually, investigators reported financial ties to similar medical companies, such as Pfizer and AstraZeneca.
AGA offers patient education materials on C. diff that can help your patients better understand the infection. Learn more at http://www.gastro.org/patient-care/conditions-diseases/clostridium-difficile-infection.
[email protected]
On Twitter @eaztweets
FROM CLINICAL INFECTIOUS DISEASES
Diabetes infusion sets under voluntary recall
Medtronic announced Sept. 11 that it has started to inform patients worldwide of a voluntary recall of specific lots of infusion sets used with all models of Medtronic insulin pumps.
The recall is for a certain discontinued component in these infusion sets and does not include insulin pumps or glucose sensors. According to recent reports from patients and root-cause analysis, the vent membrane in the recalled infusion sets may be susceptible to being blocked by fluid during the process of priming/fill-tubing. This can lead to potential over-delivery of insulin shortly after an infusion set change and may cause hypoglycemia.
Current manufactured infusion sets include a design update of this component that Medtronic believes reduces the risk of insulin over-delivery after an infusion set change. Medtronic said they are working with patients on recalled infusion sets with the discontinued component to replace the recalled sets with new infusion sets containing the updated component at no cost.
“Our priority is to work with our patients to mitigate risk to patient safety. While we have shipped a significant number of the new and enhanced sets since April, we are committed to replacing recalled infusion sets for all patients,” said Francine Kaufman, MD, chief medical officer of the Diabetes Group at Medtronic in a press release. “Our Medtronic Diabetes team will work as quickly as possible to complete all exchanges to the new and enhanced set and fully support our customers throughout this process.”
Read the full press release on the Food and Drug Administration’s website.
Medtronic announced Sept. 11 that it has started to inform patients worldwide of a voluntary recall of specific lots of infusion sets used with all models of Medtronic insulin pumps.
The recall is for a certain discontinued component in these infusion sets and does not include insulin pumps or glucose sensors. According to recent reports from patients and root-cause analysis, the vent membrane in the recalled infusion sets may be susceptible to being blocked by fluid during the process of priming/fill-tubing. This can lead to potential over-delivery of insulin shortly after an infusion set change and may cause hypoglycemia.
Current manufactured infusion sets include a design update of this component that Medtronic believes reduces the risk of insulin over-delivery after an infusion set change. Medtronic said they are working with patients on recalled infusion sets with the discontinued component to replace the recalled sets with new infusion sets containing the updated component at no cost.
“Our priority is to work with our patients to mitigate risk to patient safety. While we have shipped a significant number of the new and enhanced sets since April, we are committed to replacing recalled infusion sets for all patients,” said Francine Kaufman, MD, chief medical officer of the Diabetes Group at Medtronic in a press release. “Our Medtronic Diabetes team will work as quickly as possible to complete all exchanges to the new and enhanced set and fully support our customers throughout this process.”
Read the full press release on the Food and Drug Administration’s website.
Medtronic announced Sept. 11 that it has started to inform patients worldwide of a voluntary recall of specific lots of infusion sets used with all models of Medtronic insulin pumps.
The recall is for a certain discontinued component in these infusion sets and does not include insulin pumps or glucose sensors. According to recent reports from patients and root-cause analysis, the vent membrane in the recalled infusion sets may be susceptible to being blocked by fluid during the process of priming/fill-tubing. This can lead to potential over-delivery of insulin shortly after an infusion set change and may cause hypoglycemia.
Current manufactured infusion sets include a design update of this component that Medtronic believes reduces the risk of insulin over-delivery after an infusion set change. Medtronic said they are working with patients on recalled infusion sets with the discontinued component to replace the recalled sets with new infusion sets containing the updated component at no cost.
“Our priority is to work with our patients to mitigate risk to patient safety. While we have shipped a significant number of the new and enhanced sets since April, we are committed to replacing recalled infusion sets for all patients,” said Francine Kaufman, MD, chief medical officer of the Diabetes Group at Medtronic in a press release. “Our Medtronic Diabetes team will work as quickly as possible to complete all exchanges to the new and enhanced set and fully support our customers throughout this process.”
Read the full press release on the Food and Drug Administration’s website.