Ulerythema Ophryogenes: Updates and Insights

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Consensus Recommendations From the American Acne & Rosacea Society on the Management of Rosacea, Part 4: A Status Report on Physical Modalities and Devices

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Chondroid Syringoma

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What's Eating You? Turkey Mite and Lone Star Tick (Amblyomma americanum)

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Polymer could improve blood cryopreservation

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Scientists have found that a common polymer can help red blood cells (RBCs) survive storage at freezing temperatures, and it may offer benefits over current methods of cryopreservation.

The polymer, polyvinyl alcohol, mimics antifreeze properties found in cold-acclimatized fish, such as arctic cod.

And experiments revealed that using polyvinyl alcohol in blood cryopreservation can inhibit the growth of ice crystals, which damage RBCs and make them unusable.

Matthew Gibson, PhD, of the University of Warwick in the UK, and his colleagues conducted these experiments and reported the results in Nature Communications.

“We know that certain types of fish survive perfectly well in sub-zero sea temperatures without their blood freezing,” Dr Gibson said. “We used this as a starting point to search for synthetic substances which reflect what nature already does so well.”

“On closer examination, it turns out that polyvinyl alcohol, which is actually a derivative of wood glue, mimics the properties of the antifreeze proteins found in these kinds of fish.”

So Dr Gibson and his colleagues decided to see how polyvinyl alcohol fared in blood cryopreservation.

The team tested RBCs from sheep and humans and found that polyvinyl alcohol could inhibit ice crystal growth, even when used at concentrations as low as 0.01wt%.

The polymer was most effective at 0.1wt%, which allowed for 40% RBC recovery. Higher concentrations of polyvinyl alcohol did reduce the growth of ice crystals, but the benefits were counteracted by the secondary effects of ice shaping, which can pierce cell membranes.

The researchers noted that the current method of cryopreservation typically requires more than 20wt% of organic solvents to prevent ice formation. And the solvents must be removed before the blood can be used.

“Polyvinyl alcohol has 3 things in its favor when applied to freezing blood,” Dr Gibson said. “Firstly, it reduces the growth of ice crystals during thawing. Secondly, it reduces the need for organic solvents, and, crucially, it reduces the time between defrosting and having transfusion-ready blood by eliminating the need to remove solvent.”

Dr Gibson pointed out that, although polyvinyl alcohol appears to be a promising option for cryopreservation, additional research is needed. But if the polymer proves effective in subsequent studies, it could be used on other cell types as well.

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Bags of blood for transfusion

Credit: UAB Hospital

Scientists have found that a common polymer can help red blood cells (RBCs) survive storage at freezing temperatures, and it may offer benefits over current methods of cryopreservation.

The polymer, polyvinyl alcohol, mimics antifreeze properties found in cold-acclimatized fish, such as arctic cod.

And experiments revealed that using polyvinyl alcohol in blood cryopreservation can inhibit the growth of ice crystals, which damage RBCs and make them unusable.

Matthew Gibson, PhD, of the University of Warwick in the UK, and his colleagues conducted these experiments and reported the results in Nature Communications.

“We know that certain types of fish survive perfectly well in sub-zero sea temperatures without their blood freezing,” Dr Gibson said. “We used this as a starting point to search for synthetic substances which reflect what nature already does so well.”

“On closer examination, it turns out that polyvinyl alcohol, which is actually a derivative of wood glue, mimics the properties of the antifreeze proteins found in these kinds of fish.”

So Dr Gibson and his colleagues decided to see how polyvinyl alcohol fared in blood cryopreservation.

The team tested RBCs from sheep and humans and found that polyvinyl alcohol could inhibit ice crystal growth, even when used at concentrations as low as 0.01wt%.

The polymer was most effective at 0.1wt%, which allowed for 40% RBC recovery. Higher concentrations of polyvinyl alcohol did reduce the growth of ice crystals, but the benefits were counteracted by the secondary effects of ice shaping, which can pierce cell membranes.

The researchers noted that the current method of cryopreservation typically requires more than 20wt% of organic solvents to prevent ice formation. And the solvents must be removed before the blood can be used.

“Polyvinyl alcohol has 3 things in its favor when applied to freezing blood,” Dr Gibson said. “Firstly, it reduces the growth of ice crystals during thawing. Secondly, it reduces the need for organic solvents, and, crucially, it reduces the time between defrosting and having transfusion-ready blood by eliminating the need to remove solvent.”

Dr Gibson pointed out that, although polyvinyl alcohol appears to be a promising option for cryopreservation, additional research is needed. But if the polymer proves effective in subsequent studies, it could be used on other cell types as well.

Bags of blood for transfusion

Credit: UAB Hospital

Scientists have found that a common polymer can help red blood cells (RBCs) survive storage at freezing temperatures, and it may offer benefits over current methods of cryopreservation.

The polymer, polyvinyl alcohol, mimics antifreeze properties found in cold-acclimatized fish, such as arctic cod.

And experiments revealed that using polyvinyl alcohol in blood cryopreservation can inhibit the growth of ice crystals, which damage RBCs and make them unusable.

Matthew Gibson, PhD, of the University of Warwick in the UK, and his colleagues conducted these experiments and reported the results in Nature Communications.

“We know that certain types of fish survive perfectly well in sub-zero sea temperatures without their blood freezing,” Dr Gibson said. “We used this as a starting point to search for synthetic substances which reflect what nature already does so well.”

“On closer examination, it turns out that polyvinyl alcohol, which is actually a derivative of wood glue, mimics the properties of the antifreeze proteins found in these kinds of fish.”

So Dr Gibson and his colleagues decided to see how polyvinyl alcohol fared in blood cryopreservation.

The team tested RBCs from sheep and humans and found that polyvinyl alcohol could inhibit ice crystal growth, even when used at concentrations as low as 0.01wt%.

The polymer was most effective at 0.1wt%, which allowed for 40% RBC recovery. Higher concentrations of polyvinyl alcohol did reduce the growth of ice crystals, but the benefits were counteracted by the secondary effects of ice shaping, which can pierce cell membranes.

The researchers noted that the current method of cryopreservation typically requires more than 20wt% of organic solvents to prevent ice formation. And the solvents must be removed before the blood can be used.

“Polyvinyl alcohol has 3 things in its favor when applied to freezing blood,” Dr Gibson said. “Firstly, it reduces the growth of ice crystals during thawing. Secondly, it reduces the need for organic solvents, and, crucially, it reduces the time between defrosting and having transfusion-ready blood by eliminating the need to remove solvent.”

Dr Gibson pointed out that, although polyvinyl alcohol appears to be a promising option for cryopreservation, additional research is needed. But if the polymer proves effective in subsequent studies, it could be used on other cell types as well.

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ASCO explains how ACA impacts trial participation

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Credit: Rhoda Baer

The Affordable Care Act (ACA) includes provisions that may make it easier for US cancer patients to participate in clinical trials.

But this aspect of the law has not received much attention and is not well understood, according to the American Society of Clinical Oncology (ASCO).

So the organization has created educational materials for providers and patients that explain ACA coverage as it relates to clinical trials.

“ASCO and other groups fought long and hard for this law requiring insurers nationwide to cover the routine costs of care for individuals participating in clinical trials,” said ASCO President Clifford A. Hudis, MD, FACP.

“Healthcare providers, financial counselors, and others involved in helping patients need to understand the law’s provisions so that their patients can benefit and we can make scientific progress.”

The law, which is effective for health plans newly issued or renewed after January 1, 2014, prohibits health plans or insurance issuers from:

  • Denying participation of beneficiaries in clinical trials
  • Denying or limiting coverage of routine patient care costs, subject to the plan’s out-of-network coverage policy
  • Discriminating against the individual on the basis of participation in a trial.

The federal government has not yet issued regulations to guide implementation of the law. While much of the statutory language is clear, in the absence of federal guidance, payers will likely vary on the legal interpretation of each element of the provision.

Therefore, understanding the provisions can help patients and their healthcare providers seek the best available treatment options, which may include participation in a clinical trial.

Provider materials are available on ASCO’s Clinical Trials Coverage web page at www.ASCO.org/ClinicalTrialsCoverage.

Patient materials available on Cancer.Net include a detailed article explaining health insurance coverage of clinical trials at www.cancer.net/clinicaltrials and a fact sheet that provides an overview of the ACA provision at www.cancer.net/factsheets.

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Doctor consults with a cancer

patient and her father

Credit: Rhoda Baer

The Affordable Care Act (ACA) includes provisions that may make it easier for US cancer patients to participate in clinical trials.

But this aspect of the law has not received much attention and is not well understood, according to the American Society of Clinical Oncology (ASCO).

So the organization has created educational materials for providers and patients that explain ACA coverage as it relates to clinical trials.

“ASCO and other groups fought long and hard for this law requiring insurers nationwide to cover the routine costs of care for individuals participating in clinical trials,” said ASCO President Clifford A. Hudis, MD, FACP.

“Healthcare providers, financial counselors, and others involved in helping patients need to understand the law’s provisions so that their patients can benefit and we can make scientific progress.”

The law, which is effective for health plans newly issued or renewed after January 1, 2014, prohibits health plans or insurance issuers from:

  • Denying participation of beneficiaries in clinical trials
  • Denying or limiting coverage of routine patient care costs, subject to the plan’s out-of-network coverage policy
  • Discriminating against the individual on the basis of participation in a trial.

The federal government has not yet issued regulations to guide implementation of the law. While much of the statutory language is clear, in the absence of federal guidance, payers will likely vary on the legal interpretation of each element of the provision.

Therefore, understanding the provisions can help patients and their healthcare providers seek the best available treatment options, which may include participation in a clinical trial.

Provider materials are available on ASCO’s Clinical Trials Coverage web page at www.ASCO.org/ClinicalTrialsCoverage.

Patient materials available on Cancer.Net include a detailed article explaining health insurance coverage of clinical trials at www.cancer.net/clinicaltrials and a fact sheet that provides an overview of the ACA provision at www.cancer.net/factsheets.

Doctor consults with a cancer

patient and her father

Credit: Rhoda Baer

The Affordable Care Act (ACA) includes provisions that may make it easier for US cancer patients to participate in clinical trials.

But this aspect of the law has not received much attention and is not well understood, according to the American Society of Clinical Oncology (ASCO).

So the organization has created educational materials for providers and patients that explain ACA coverage as it relates to clinical trials.

“ASCO and other groups fought long and hard for this law requiring insurers nationwide to cover the routine costs of care for individuals participating in clinical trials,” said ASCO President Clifford A. Hudis, MD, FACP.

“Healthcare providers, financial counselors, and others involved in helping patients need to understand the law’s provisions so that their patients can benefit and we can make scientific progress.”

The law, which is effective for health plans newly issued or renewed after January 1, 2014, prohibits health plans or insurance issuers from:

  • Denying participation of beneficiaries in clinical trials
  • Denying or limiting coverage of routine patient care costs, subject to the plan’s out-of-network coverage policy
  • Discriminating against the individual on the basis of participation in a trial.

The federal government has not yet issued regulations to guide implementation of the law. While much of the statutory language is clear, in the absence of federal guidance, payers will likely vary on the legal interpretation of each element of the provision.

Therefore, understanding the provisions can help patients and their healthcare providers seek the best available treatment options, which may include participation in a clinical trial.

Provider materials are available on ASCO’s Clinical Trials Coverage web page at www.ASCO.org/ClinicalTrialsCoverage.

Patient materials available on Cancer.Net include a detailed article explaining health insurance coverage of clinical trials at www.cancer.net/clinicaltrials and a fact sheet that provides an overview of the ACA provision at www.cancer.net/factsheets.

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Affluence seems to affect CML survival in the UK

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Affluence seems to affect CML survival in the UK

Doctor evaluating a patient

Credit: CDC

Results of population-based research suggest that financial status may affect survival in patients with chronic myeloid leukemia (CML) living in the UK.

The study showed that, despite equal access to the same clinical care and treatment, survival rates were significantly lower for patients living in more deprived areas.

The researchers said this difference might be explained by lower rates of treatment compliance in the less affluent population.

“These findings highlight the importance of conducting comprehensive, population-based studies to examine treatment pathways across the entire patient population, rather than solely concentrating on findings from clinical trials,” said study author Alexandra Smith, PhD, of the University of York in the UK.

She and her colleagues recounted their findings in BMJ Open.

The team analyzed data from 242 patients who were diagnosed with CML from September 2004 to August 2011. Ninety-seven percent of patients had chronic-phase disease at presentation, and 86% were Ph-positive.

Fifty-five percent of patients were younger than 60 at diagnosis, and 60% were male. Fifty-nine percent lived in deprivation quintiles 1 to 3, and 41% lived in the less affluent quintiles 4 and 5.

Ninety-seven percent of patients received treatment with tyrosine kinase inhibitors (TKIs)—94% imatinib and the rest dasatinib. Three percent of patients were not treated with TKIs due to death, relocation, refusal, a more serious competing comorbidity, or the use of supportive care alone.

Factors affecting survival

The minimum follow-up was 1.5 years, and the maximum was 8.5 years. The overall 5-year survival was 79%. And the relative survival, which took into account the background mortality in the general population, was 89%.

The relative survival curves did not differ significantly between the 2 age groups. Five-year relative survival was 90% for patients younger than 60 and 87% for those older than 60.

Gender also had little impact on relative survival. The 5-year rates were 90% for men and 89% for women.

However, relative survival differed significantly according to affluence. The 5-year relative survival was 95% for the most affluent patients (quintiles 1 to 3) and 80% for the least affluent (quintiles 4 and 5).

Although 41% of all patients lived in the less affluent areas, this group accounted for about 60% of the deaths.

The researchers said this finding could not be attributed to biological features of disease or access to therapy. But they believe a lack of treatment compliance could be the cause.

“We suspect a major factor is that we are not supporting patients sufficiently to allow them to be fully compliant with a treatment that needs to be taken every day to be effective,” said Russell Patmore, MD, of Castle Hill Hospital in the UK.

“We would encourage all teams treating patients with CML to use these findings to focus their resource where it is likely to be most beneficial. This includes helping patients to manage their CML by explaining fully the importance of daily treatment and providing easy access to ongoing support.”

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Doctor evaluating a patient

Credit: CDC

Results of population-based research suggest that financial status may affect survival in patients with chronic myeloid leukemia (CML) living in the UK.

The study showed that, despite equal access to the same clinical care and treatment, survival rates were significantly lower for patients living in more deprived areas.

The researchers said this difference might be explained by lower rates of treatment compliance in the less affluent population.

“These findings highlight the importance of conducting comprehensive, population-based studies to examine treatment pathways across the entire patient population, rather than solely concentrating on findings from clinical trials,” said study author Alexandra Smith, PhD, of the University of York in the UK.

She and her colleagues recounted their findings in BMJ Open.

The team analyzed data from 242 patients who were diagnosed with CML from September 2004 to August 2011. Ninety-seven percent of patients had chronic-phase disease at presentation, and 86% were Ph-positive.

Fifty-five percent of patients were younger than 60 at diagnosis, and 60% were male. Fifty-nine percent lived in deprivation quintiles 1 to 3, and 41% lived in the less affluent quintiles 4 and 5.

Ninety-seven percent of patients received treatment with tyrosine kinase inhibitors (TKIs)—94% imatinib and the rest dasatinib. Three percent of patients were not treated with TKIs due to death, relocation, refusal, a more serious competing comorbidity, or the use of supportive care alone.

Factors affecting survival

The minimum follow-up was 1.5 years, and the maximum was 8.5 years. The overall 5-year survival was 79%. And the relative survival, which took into account the background mortality in the general population, was 89%.

The relative survival curves did not differ significantly between the 2 age groups. Five-year relative survival was 90% for patients younger than 60 and 87% for those older than 60.

Gender also had little impact on relative survival. The 5-year rates were 90% for men and 89% for women.

However, relative survival differed significantly according to affluence. The 5-year relative survival was 95% for the most affluent patients (quintiles 1 to 3) and 80% for the least affluent (quintiles 4 and 5).

Although 41% of all patients lived in the less affluent areas, this group accounted for about 60% of the deaths.

The researchers said this finding could not be attributed to biological features of disease or access to therapy. But they believe a lack of treatment compliance could be the cause.

“We suspect a major factor is that we are not supporting patients sufficiently to allow them to be fully compliant with a treatment that needs to be taken every day to be effective,” said Russell Patmore, MD, of Castle Hill Hospital in the UK.

“We would encourage all teams treating patients with CML to use these findings to focus their resource where it is likely to be most beneficial. This includes helping patients to manage their CML by explaining fully the importance of daily treatment and providing easy access to ongoing support.”

Doctor evaluating a patient

Credit: CDC

Results of population-based research suggest that financial status may affect survival in patients with chronic myeloid leukemia (CML) living in the UK.

The study showed that, despite equal access to the same clinical care and treatment, survival rates were significantly lower for patients living in more deprived areas.

The researchers said this difference might be explained by lower rates of treatment compliance in the less affluent population.

“These findings highlight the importance of conducting comprehensive, population-based studies to examine treatment pathways across the entire patient population, rather than solely concentrating on findings from clinical trials,” said study author Alexandra Smith, PhD, of the University of York in the UK.

She and her colleagues recounted their findings in BMJ Open.

The team analyzed data from 242 patients who were diagnosed with CML from September 2004 to August 2011. Ninety-seven percent of patients had chronic-phase disease at presentation, and 86% were Ph-positive.

Fifty-five percent of patients were younger than 60 at diagnosis, and 60% were male. Fifty-nine percent lived in deprivation quintiles 1 to 3, and 41% lived in the less affluent quintiles 4 and 5.

Ninety-seven percent of patients received treatment with tyrosine kinase inhibitors (TKIs)—94% imatinib and the rest dasatinib. Three percent of patients were not treated with TKIs due to death, relocation, refusal, a more serious competing comorbidity, or the use of supportive care alone.

Factors affecting survival

The minimum follow-up was 1.5 years, and the maximum was 8.5 years. The overall 5-year survival was 79%. And the relative survival, which took into account the background mortality in the general population, was 89%.

The relative survival curves did not differ significantly between the 2 age groups. Five-year relative survival was 90% for patients younger than 60 and 87% for those older than 60.

Gender also had little impact on relative survival. The 5-year rates were 90% for men and 89% for women.

However, relative survival differed significantly according to affluence. The 5-year relative survival was 95% for the most affluent patients (quintiles 1 to 3) and 80% for the least affluent (quintiles 4 and 5).

Although 41% of all patients lived in the less affluent areas, this group accounted for about 60% of the deaths.

The researchers said this finding could not be attributed to biological features of disease or access to therapy. But they believe a lack of treatment compliance could be the cause.

“We suspect a major factor is that we are not supporting patients sufficiently to allow them to be fully compliant with a treatment that needs to be taken every day to be effective,” said Russell Patmore, MD, of Castle Hill Hospital in the UK.

“We would encourage all teams treating patients with CML to use these findings to focus their resource where it is likely to be most beneficial. This includes helping patients to manage their CML by explaining fully the importance of daily treatment and providing easy access to ongoing support.”

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Drug gets breakthrough designation for SAA

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The US Food and Drug Administration (FDA) has granted breakthrough therapy designation for the thrombopoietin receptor agonist eltrombopag (Promacta/Revolade) to treat patients with severe aplastic anemia (SAA) who have had an insufficient response to immunosuppressive therapy (IST).

Eltrombopag is not approved in this setting anywhere in the world, and there are no approved therapies for SAA patients who are unresponsive to initial IST.

Of those patients who are unresponsive to initial IST, approximately 40% die from infection or bleeding within 5 years of their diagnosis.

Breakthrough therapy designation is the newest of the FDA’s programs aimed at accelerating the development and review of drugs for serious or life-threatening conditions. A drug receives the designation when preliminary clinical evidence suggests it may offer substantial improvement over available therapies on at least one clinically significant endpoint.

Eltrombopag was granted breakthrough designation based on results from an open-label, phase 2 study in 43 heavily pretreated SAA patients with an insufficient response to IST. Updated results of this trial were published in December (Desmond et al, Blood 2013).

Patients received varying doses of eltrombopag to improve blood counts. At 3 to 4 months of follow-up, the overall response rate was 40% (17/43), which included 1 tri-lineage and 5 bi-lineage responses.

Most of the 17 patients who remained on eltrombopag in an extension study continued to show improvement, but 3 lost their response. Ultimately, 7 patients had significant increases in neutrophil, red cell, and platelet counts.

Five patients who experienced robust near-normalization of blood counts discontinued the drug and maintained stable counts a median of 13 months after discontinuation (range, 1-15).

Eight patients, including 2 who responded, developed new cytogenetic abnormalities while on eltrombopag. But none have evolved to acute myeloid leukemia to date.

The only dose-limiting toxicity was reversible transaminitis. Two patients had reversible transaminitis related to treatment, and both required dose interruption.

There were no thrombotic events while patients were on treatment, but 1 responding patient developed deep-vein thrombosis 14 months after treatment discontinuation.

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red blood cells

Red blood cells

The US Food and Drug Administration (FDA) has granted breakthrough therapy designation for the thrombopoietin receptor agonist eltrombopag (Promacta/Revolade) to treat patients with severe aplastic anemia (SAA) who have had an insufficient response to immunosuppressive therapy (IST).

Eltrombopag is not approved in this setting anywhere in the world, and there are no approved therapies for SAA patients who are unresponsive to initial IST.

Of those patients who are unresponsive to initial IST, approximately 40% die from infection or bleeding within 5 years of their diagnosis.

Breakthrough therapy designation is the newest of the FDA’s programs aimed at accelerating the development and review of drugs for serious or life-threatening conditions. A drug receives the designation when preliminary clinical evidence suggests it may offer substantial improvement over available therapies on at least one clinically significant endpoint.

Eltrombopag was granted breakthrough designation based on results from an open-label, phase 2 study in 43 heavily pretreated SAA patients with an insufficient response to IST. Updated results of this trial were published in December (Desmond et al, Blood 2013).

Patients received varying doses of eltrombopag to improve blood counts. At 3 to 4 months of follow-up, the overall response rate was 40% (17/43), which included 1 tri-lineage and 5 bi-lineage responses.

Most of the 17 patients who remained on eltrombopag in an extension study continued to show improvement, but 3 lost their response. Ultimately, 7 patients had significant increases in neutrophil, red cell, and platelet counts.

Five patients who experienced robust near-normalization of blood counts discontinued the drug and maintained stable counts a median of 13 months after discontinuation (range, 1-15).

Eight patients, including 2 who responded, developed new cytogenetic abnormalities while on eltrombopag. But none have evolved to acute myeloid leukemia to date.

The only dose-limiting toxicity was reversible transaminitis. Two patients had reversible transaminitis related to treatment, and both required dose interruption.

There were no thrombotic events while patients were on treatment, but 1 responding patient developed deep-vein thrombosis 14 months after treatment discontinuation.

red blood cells

Red blood cells

The US Food and Drug Administration (FDA) has granted breakthrough therapy designation for the thrombopoietin receptor agonist eltrombopag (Promacta/Revolade) to treat patients with severe aplastic anemia (SAA) who have had an insufficient response to immunosuppressive therapy (IST).

Eltrombopag is not approved in this setting anywhere in the world, and there are no approved therapies for SAA patients who are unresponsive to initial IST.

Of those patients who are unresponsive to initial IST, approximately 40% die from infection or bleeding within 5 years of their diagnosis.

Breakthrough therapy designation is the newest of the FDA’s programs aimed at accelerating the development and review of drugs for serious or life-threatening conditions. A drug receives the designation when preliminary clinical evidence suggests it may offer substantial improvement over available therapies on at least one clinically significant endpoint.

Eltrombopag was granted breakthrough designation based on results from an open-label, phase 2 study in 43 heavily pretreated SAA patients with an insufficient response to IST. Updated results of this trial were published in December (Desmond et al, Blood 2013).

Patients received varying doses of eltrombopag to improve blood counts. At 3 to 4 months of follow-up, the overall response rate was 40% (17/43), which included 1 tri-lineage and 5 bi-lineage responses.

Most of the 17 patients who remained on eltrombopag in an extension study continued to show improvement, but 3 lost their response. Ultimately, 7 patients had significant increases in neutrophil, red cell, and platelet counts.

Five patients who experienced robust near-normalization of blood counts discontinued the drug and maintained stable counts a median of 13 months after discontinuation (range, 1-15).

Eight patients, including 2 who responded, developed new cytogenetic abnormalities while on eltrombopag. But none have evolved to acute myeloid leukemia to date.

The only dose-limiting toxicity was reversible transaminitis. Two patients had reversible transaminitis related to treatment, and both required dose interruption.

There were no thrombotic events while patients were on treatment, but 1 responding patient developed deep-vein thrombosis 14 months after treatment discontinuation.

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VTE Codes in Academic Medical Centers

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Incidence of hospital‐acquired venous thromboembolic codes in medical patients hospitalized in academic medical centers

Pulmonary embolism (PE) and deep venous thrombosis (DVT), historically referred to together as venous thromboembolism (VTE), are common, treatable, sometimes fatal, and potentially preventable medical problems.[1] Such thromboses can both precipitate a hospitalization as well as complicate it (either during or soon after discharge). Preventing such thrombosis as a complication of medical care has become a national imperative. Landmark studies such as Prophylaxis in Medical Patients With Enoxaparin (MEDENOX)[2] and Prospective Evaluation of Dalteparin Efficacy for Prevention of VTE in Immobilized Patients Trial (PREVENT)[3] demonstrated both a high incidence of thrombosis in a hospitalized high‐risk medical population (15% and 5% in the 2 trials' placebo arms, respectively) as well as significant relative risk reduction through venous thromboembolism pharmacoprophylaxis (VTEP)63% and 45%, respectively. The Joint Commission,[4] the Society of Hospital Medicine,[5] and the American College of Chest Physicians[6, 7] have thus all strived to ensure the appropriate provision of VTEP in order to reduce the morbidity and mortality associated with thrombosis in hospitalized patients, including those on medical services.

Ideally, the global success of these efforts would be assessed by measuring the rate of hospital‐associated VTE (potentially including superficial venous thrombosis [SVT], which, like upper‐extremity deep venous thrombosis [UE‐DVT], is commonly a central venous catheter [CVC]‐associated, or peripherally inserted central catheter [PICC]‐associated, complication)thrombosis acquired and diagnosed during either the index hospitalization (hospital‐acquired, or HA‐VTE/SVT) or up to 30 days postdischarge. Unfortunately, postdischarge VTE/SVT is difficult to measure because patients developing it may not present to the original hospital, or at all (eg, if they do not seek care, are treated as outpatients, or, in the most extreme case, die at home). In this context, despite being far less comprehensive, HA‐VTE/SVT is a useful subset of hospital‐associated VTE/SVT, for several reasons. First, the Centers for Medicare & Medicaid Services (CMS) have mandated hospitals to qualify all medical diagnoses as present‐on‐admission (POA = Y) or not (POA = N) since 2008, such that all medical diagnoses coded POA = N can be considered hospital acquired.[8] Second, refinements made to the International Classification of Diseases, 9th Revision (ICD‐9) codes now allow differentiation of UE‐DVT and SVT from lower‐extremity (LE) DVT/PE, whereas the former were sometimes obscured by nonspecific coding.[9] Third, recent studies have shown that medical diagnoses administratively coded as HA‐VTE/SVT correlated well with HA‐VTE/SVT ascertained through chart review.[9, 10] Finally, previous work has estimated that approximately half of all hospital‐associated VTE are HA‐VTE and the other half are postdischarge VTE.[11] Thus, HA‐VTE, though comprising only approximately half of all hospital‐associated VTE, is often used as a surrogate for measuring the success of ongoing VTE prevention programs.[12]

Our study aimed to assess the incidence of HA‐VTE plus HA‐SVT in the era of mandatory POA coding and newer ICD‐9 codes for VTE.

METHODS

Setting and Cases

We conducted a retrospective analysis of discharges from the 83 academic medical centers belonging to the UHC (formerly, the University HealthSystem Consortium, https://www.uhc.edu)[13] between October 1, 2009 and March 31, 2011. UHC collects demographic, clinical, and billing data from these centers including medical diagnoses and procedures coded using the ICD‐9‐Clinical Modification (ICD‐9‐CM), a POA indicator for each diagnosis; UHC also collects data on medication use. This study was approved by the institutional review board at the University of California Davis.

Patients in our analysis were age 18 years and discharged with a medical medical severity diagnostic‐related group (MS‐DRG) code, hospitalized for 48 hours, and did not have a surgical or obstetric MS‐DRG code (except when assigned a surgical MS‐DRG code solely due to insertion of an inferior vena cava filter, with no other major procedures performed). Cases excluded discharges with a principal diagnosis of acute VTE/SVT (defined here as including PE, LE‐DVT, UE‐DVT, SVT, chronic VTE, and thrombosis not otherwise specified), as coding guidelines prohibit assigning a HA‐VTE as the principal diagnosis for the index hospitalization.[14]

Hospital‐Acquired Venous Thromboembolism or Superficial Venous Thrombosis

Cases were classified as having a HA‐VTE/SVT if there was 1 VTE/SVT coded in a secondary diagnosis position (other diagnosis) with a corresponding POA indicator equal to either N (not POA) or U (documentation insufficient to clarify whether VTE was POA or not). This usage corresponds to CMS guidelines and reimbursement policies for hospital‐acquired conditions.[15] Among cases with 1 HA‐VTE (or SVT), we assigned 1 HA‐VTE diagnosis using a hierarchy based on the highest level of clinical importance: first, PE; then LE‐DVT; then UE‐DVT; then SVT; then chronic VTE; then, finally, unspecified VTE. We subsequently excluded cases with primarily chronic VTE from our analysis because these were likely miscodes (ie, it is unclear how a chronic VTE could not be POA) and there were only 30 such cases. Cases with HA‐PE or HA‐LE DVT were analyzed separately as an important subset of HA‐VTE (plus SVT), because HA‐PE/LE‐DVT is both life‐threatening and theoretically preventable with VTEP.

Severity of Illness and Other Measures of Comorbidity

For each case we used proprietary software (3M Health Information Systems, Murray UT) to classify severity of illness (SOI). The SOI scale, based on physiologic derangement and organ system loss of function,[16] has 4 levels: minor, major, severe, and extreme. Defined within specific disease groups (All Patient Refined DRGs), it is often compared across diseases as well.[17] We also assessed whether patients had a cancer diagnosis, spent time in the intensive care unit (ICU), and died in the hospital.

Central Venous Catheter Use in Patients With Upper‐Extremity Deep Venous Thrombosis or Superficial Venous Thrombosis

Because UE‐DVT and SVT are frequently associated with a CVC or PICC, we assessed central venous catheterization among patients with an UE‐DVT or SVT of the cephalic, basilic, or antecubital veins using diagnosis codes for complications related to dialysis devices, implants, and grafts.

Pharmacologic Thromboprophylaxis

Pharmacy records of the subset of HA‐VTE/SVT cases with PE or LE‐DVT were analyzed to determine if VTEP was administered on hospital day 1 or 2, as per Joint Commission performance requirements.[4] Medications that met criteria as VTEP included unfractionated heparin, 5000 IU, given 2 or 3 a day; enoxaparin, 40 mg, given daily; dalteparin, 2500 or 5000 IU, given daily; fondaparinux, 2.5 mg, given daily; and warfarin. We could not reliably determine if VTEP was used throughout the entire hospitalization, or whether mechanical prophylaxis was used at all.

Statistical Analysis

This was a descriptive analysis to determine the incidence of HA‐VTE/SVT and describe the demographic and clinical characteristics of this population. We calculated means and standard deviations (SD) for continuous variables and proportions for binary variables (including HA‐VTE/SVT incidence). All comparisons between populations were performed as either 2‐tailed t tests or 2 analyses. All analysis was conducted using SAS software, version 9.2 (SAS Institute, Inc., Cary, NC).

RESULTS

For the 18‐month period between October 1, 2009, and March 31, 2011, across 83 UHC hospitals, there were 2,525,068 cases. Among these, 12,847 (0.51%) had 1 HA‐VTE/SVT coded. As per the clinical importance hierarchy described above, 2449 (19.1%) cases had at least a PE coded; 3848 (30%) had at least a LE‐DVT (but not a PE) coded; 2893 (22.5%) had at least an UE‐DVT coded; 3248 (25.3%) had at least an SVT coded; 30 had at least a chronic VTE coded; and 379 had at least a VTE coded with no specified location. Of those with SVT, 192 (5.8%) were LE‐SVT codes, whereas the rest were SVT/thrombophlebitis of the upper extremities or not otherwise specified. There were 11,882 (92.5%) hospitalizations with a single HA‐VTE/SVT code and an additional 965 (7.5%) with multiple codes, for a total of 13,749 HA‐VTE/SVT events (see Supporting Information, Table S1, in the online version of this article for more specific data for the individual ICD‐9 codes used to specify HA‐VTE events).

Compared with those who did not develop any HA‐VTE/SVT, patients with HA‐PE/LE‐DVT were more likely to be Caucasian (65% vs 58%, P < 0.001) and were older (age 62 vs 48 years, P < 0.001) and sicker (79.9% vs 44.9% with a severe or extreme SOI, P < 0.001). They also were more likely to have cancer, have longer lengths of stay, be more likely to stay in the ICU, and die in the hospital (P < 0.001 for all comparisons; Table 1).

Patients With No HA‐VTE Code and Patients With a HA‐PE/LE‐DVT Code (ICD‐9‐CM)
CharacteristicNo HA‐VTE, n = 2,512,221HA‐PE/LE DVT, n = 6,297aP Valueb
  • NOTE: Data are presented as n (%) or mean SD. Abbreviations: API, Asian or Pacific Islander; HA‐PE/LE DVT, hospital‐acquired pulmonary embolism or lower‐extremity deep venous thrombosis; HA‐VTE, hospital‐acquired venous thromboembolism; ICD‐9‐CM, International Classification of Diseases, Ninth Revision, Clinical Modification; ICU, intensive care unit; LMWH, low‐molecular‐weight heparin; SD, standard deviation; SOI, severity of illness.

  • The first 2 columns, no HA‐VTE and HA‐PE/LE DVT, were compared as noted in the third column. Data on upper‐extremity or superficial thrombosis are not shown in this table.

  • For all variables except age and length of stay, P values are calculated by 2; for age and length of stay, P value is calculated by rank‐sum test.

  • Prophylaxis with LMWH, fondaparinux, unfractionated heparin, or warfarin on the first or second day of hospitalization. Prophylaxis was not estimated in the population that did not develop a HA‐VTE.

Proportion of hospitalizations, %99.490.25 
Age, y48.2 27.162.5 20.0<0.001
Female sex1,347,219 (53.6)3,104 (49.3)<0.001
Race  <0.001
Caucasian1,455,215 (57.9)3,963 (64.7) 
Black600,991 (23.9)1,425 (23.3) 
Hispanic206,553 (8.2)263 (4.3) 
API59,560 (2.4)88 (1.4) 
Other189,902 (7.6)389 (6.4) 
Admission SOI  <0.001
Minor461,411 (18.4)181 (2.9) 
Major922,734 (36.7)1,081 (17.2) 
Severe880,542 (35.1)2,975 (47.2) 
Extreme247,244 (9.8)2,060 (32.7) 
Unknown290 (0.01)0 (0.0) 
Had an active diagnosis of cancer331,705 (13.2)2,162 (34.3)<0.001
Length of stay, d7.31 9.3118.7 19.5<0.001
Spent time in the ICU441,412 (17.6)3,011 (47.8)<0.001
Died in hospital57,954 (2.3)1,036 (16.5)<0.001
Received prophylaxiscc3,454 (54.9)c

Among cases with a code for UE‐DVT (22.5% of all patients with HA‐VTE), 74% were noted to also have a code for a CVC, as did 60% of cases with a HA‐SVT of the antecubital, basilic, or cephalic veins (71% of SVT events; see Supporting Information, Table S1, in the online version of this article).

Of those with HA‐PE/LE‐DVT, 54.9% received pharmacologic prophylaxis on hospital day 1 or 2 (mostly with low‐molecular‐weight heparin or unfractionated heparin).

DISCUSSION

In this study of medical patients admitted to academic medical centers throughout the United States, we found that HA‐VTE/SVT was coded in approximately 0.51% of discharges, and the incidence of HA‐PE/LE‐DVT was 0.25%. Patients with a HA‐PE/LE‐DVT code were, in general, older and sicker than those who did not develop VTE. We further found that close to half of all HA‐VTE/SVT occurred in the upper extremity, with the majority of these occurring in patients who had CVCs. Finally, the majority of patients diagnosed with HA‐PE/LE‐DVT were started on VTEP on the first or second hospital day.

The overall incidence of HA‐VTE/SVT we discovered corresponds well to other studies, even those with disparate populations. A single‐institution study found a HA‐VTE/SVT incidence of approximately 0.6% among hospitalized patients on medical and nonmedical services.[12] The study by Barba found a rate of 0.93%,[18] whereas the study by Lederle found a rate of approximately 1%.[19] Spyropolous found an HA‐VTE incidence of 0.55%.[11] Rothberg found a lower rate of 0.25% in his risk‐stratification study, though in the pre‐POA and preupdated code era.[20] Our findings extend and provide context for, in a much larger population, the results of these prior studies, and represent the first national examination of HA‐VTE/SVT in the setting of numerous quality‐improvement and other efforts to reduce hospital‐associated VTE.

The incidence of HA‐VTE/SVT codes we observed likely underestimates the incidence of hospital‐associated VTE/SVT by a factor of approximately 4, for 2 reasons. First, although VTE/SVT codes with a POA flag set to No are truly hospital‐acquired events on chart review approximately 75% of the time, and thus overestimate HA‐VTE/SVT, 25% of POA = Yes codes are actually HA‐VTE/SVT events on chart review, and therefore lead to underestimation of HA‐VTE/SVT.[9] Because VTE/SVT codes with a POA flag set to Yes outnumber those flagged No by 3 or 4 to 1, events mis‐flagged Yes contribute a much greater number of undercounted HA‐VTE/SVT, elevating the actual HA‐VTE/SVT event rate by a factor of approximately 2. Second, HA‐VTE events do not include hospital‐associated VTE events that are diagnosed after the index hospitalization. In the Spyropolous study, 45% of hospital‐associated VTE events occurred after discharge, so translating HA‐VTE/SVT events to hospital‐associated VTE/SVT events would again involve multiplying by a factor of 2.[11] Thus, the overall incidence of hospital‐associated VTE/SVT events in our sample may have been approximately 2% (0.51% 4), and the overall incidence of hospital‐associated PE or LE‐DVT events may have been approximately 1%, though there may be significant variation around these estimates given that individual institutions were themselves quite variable in their POA flag accuracy in our study.[9] There is additionally the possibility that hospitals may have deliberately left some VTE/SVT uncoded, but in the absence of financial incentives to do so for anything other than postsurgical VTE, and in the presence of penalties from CMS for undercoding, we believe this to be unlikely, at least at present.

Despite these upward extrapolations, the estimated incidence of hospital‐associated VTE/SVT in our study may seem low compared with that reported in the MEDENOX[2] and PREVENT studies.[3] Much of this discrepancy vanishes on closer examination. In the large randomized trials, patients were uniformly and routinely assessed for LE‐DVT using vascular ultrasound; in contrast, in our population of hospitalizations patients may have only had diagnostic studies done for signs or symptoms. Clinically apparent hospital‐associated VTE is less common than all hospital‐associated VTE, as it was even in PREVENT,[3] and increased surveillance may even be partially driving increased hospital‐associated VTE/SVT at some hospitals.[21] Our findings suggest that success or failure in preventing administratively coded, clinically apparent HA LE‐VTE/PE should be judged, broadly, against numbers in the range established in our study (eg, 0.25%), not the 5% or 15% of chart‐abstracted, aggressively ascertained (and sometimes clinically silent) hospital‐associated VTE in the large randomized controlled trials. That is, 0.25% is not an achievement, but rather the average, expected value.

Almost 25% of the observed HA‐VTE/SVTs coded were UE‐DVT, with roughly 75% of these being likely related to central venous catheterization (including those peripherally inserted). An additional 1/5 were upper‐extremity SVT of the antecubital, cephalic, and basilic veins, with the majority of these (60%) also listed as catheter‐related. Such thrombosis is best prevented by decreased use of central catheters or perhaps by using smaller‐caliber catheters.[22] It is unclear if VTEP can prevent such clots, though in cancer patients at least one recent trial seems promising.[23]

We found that patients with a coded HA‐PE/LE‐DVT were remarkably different from those not developing HA‐VTE/SVT. Patients with HA‐PE or HA‐LE‐DVT were older, sicker, more likely to have cancer, significantly more likely to spend time in the ICU, and much more likely to die in the hospital; risk factors for HA‐VTE overlap significantly with risk factors for death in the hospital. A small majority (55%) of patients in the HA‐PE/LE‐DVT group had actually received VTEP on at least day 1 or 2 of hospitalization. It may be the case that the dose of VTEP was insufficient to suppress clot formation in these patients, or that HA‐PE/LE‐DVT in patients with this degree of comorbidity is difficult to prevent.

There are a number of limitations to our study. We analyzed administrative codes, which underestimate hospital‐associated VTE/SVT events as noted above. This was a descriptive study, cross‐sectional across each hospitalization, and we were unable to draw any causal inference for differences in HA‐VTE/SVT incidence that might exist between subpopulations. We estimated VTEP from medication usage in just the first 2 days of hospitalization; we could not assess mechanical prophylaxis in this dataset; and we did not have any VTEP data for the first 2 days of hospitalization on the patients who did not develop a HA‐VTE/SVT, which made it impossible to compare the 2 populations on this measure. For those who did not receive VTEP, we were unable to obtain data regarding possible contraindications to VTEP, such as ongoing gastrointestinal or intracerebral hemorrhage. Additionally, our data are based on academic hospitals only and may not generalize to nonacademic settings. Extrapolating from HA‐VTE/SVT to hospital‐associated VTE/SVT may not be possible due to heterogeneity of clotting events and perhaps variability in whether patients would return to the hospital for all of them (eg, superficial or UE VTE may not result in readmission). Finally, it is unclear whether a switch to ICD Tenth Revision (ICD‐10) codes will impact our measured baseline in the coming year. The strengths of our analysis included stratification by type of HA‐VTE/SVT and our ability to assess the incidence of HA‐VTE/SVT in a large national population, and the provision of a baseline for VTE incidenceeasily usable by any individual hospital, network, or researcher with access to administrative datagoing forward.

In conclusion, among patients hospitalized in academic medical centers, HA‐VTE/SVT was coded in approximately 0.51% of patients with a medical illness staying >2 days, with approximately half of the events due to HA‐PE/LE‐DVT. Patients who developed HA‐PE/LE‐DVT were more acutely ill than those who did not, and VTE developed despite 55% of these patients receiving VTEP on day 1 or 2. Hospitals can reasonably treat the 0.25% figure as the baseline around which to assess their own performance in preventing HA‐PE/LE‐DVT, and can measure their own performance using administrative data. Further research is needed to determine how best to achieve further reductions in HA‐VTE/SVT through risk stratification and/or through other interventions.

Disclosures

Nothing to report.

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References
  1. Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ;American College of Chest Physicians AntithromboticTherapy and Prevention of Thrombosis Panel. Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence‐Based Clinical Practice Guidelines [published corrections appear in Chest. 2012;141(4):1129 and 2012;142(6):1698]. Chest. 2012;141(2 suppl):7S–47S.
  2. Samama MM, Cohen AT, Darmon JY, et al;Prophylaxis in Medical Patients with Enoxaparin Study Group. A comparison of enoxaparin with placebo for the prevention of venous thromboembolism in acutely ill medical patients. N Engl J Med. 1999;341(11):793800.
  3. Leizorovicz A, Cohen AT, Turpie AG, Olsson CG, Vaitkus PT, Goldhaber SZ. Randomized, placebo‐controlled trial of dalteparin for the prevention of venous thromboembolism in acutely ill medical patients. Circulation. 2004;110(7):874879.
  4. The Joint Commission.Specifications Manual for National Hospital Inpatient Quality Measures. Available at: http://www.jointcommission.org/specifications_manual_for_national_hospital_inpatient_quality_measures.aspx. Accessed July 18, 2012.
  5. Maynard G, Stein J. Preventing Hospital‐Acquired Venous Thromboembolism: A Guide for Effective Quality Improvement. Prepared by the Society of Hospital Medicine. Rockville, MD: Agency for Healthcare Research and Quality; AHRQ Publication No. 08‐0075.
  6. Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126(3 suppl):338S400S.
  7. Kahn SR, Lim W, Dunn AS, et al. Prevention of VTE in nonsurgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence‐Based Clinical Practice Guidelines. Chest. 2012;141(2 suppl):e195Se226S.
  8. Centers for Medicare 46(6 part 1):19461962.
  9. Spyropoulos AC, Anderson FA, Fitzgerald G, et al. Predictive and associative models to identify hospitalized medical patients at risk for VTE. Chest. 2011;140(3):706714.
  10. Khanna R, Vittinghoff E, Maselli J, Auerbach A. Unintended consequences of a standard admission order set on venous thromboembolism prophylaxis and patient outcomes. J Gen Intern Med. 2012;27(3):318324.
  11. United Health Consortium Website. Available at: https://www.uhc.edu. Accessed March 8, 2012.
  12. ICD‐9‐CM Official Guidelines for Coding and Reporting. Available at: http://www.cdc.gov/nchs/data/icd9/icdguide10.pdf. Published 2010. Accessed June 4, 2013.
  13. Centers for Medicare 27(5):587612.
  14. Overview of Disease Severity Measures Disseminated with the Nationwide Inpatient Sample (NIS) and Kids' Inpatient Database (KID). Available at: http://www.hcup‐us.ahrq.gov/db/nation/nis/OverviewofSeveritySystems.pdf. Published December 9, 2005. Accessed June 4, 2013.
  15. Barba R, Zapatero A, Losa JE, et al. Venous thromboembolism in acutely ill hospitalized medical patients. Thromb Res. 2010;126(4):276279.
  16. Lederle FA, Zylla D, MacDonald R, Wilt TJ. Venous thromboembolism prophylaxis in hospitalized medical patients and those with stroke: a background review for an American College of Physicians Clinical Practice Guideline. Ann Intern Med. 2011;155(9):602615.
  17. Rothberg MB, Lindenauer PK, Lahti M, Pekow PS, Selker HP. Risk factor model to predict venous thromboembolism in hospitalized medical patients. J Hosp Med. 2011;6(4):202209.
  18. Bilimoria KY, Chung J, Ju MH, et al. Evaluation of surveillance bias and the validity of the venous thromboembolism quality measure. JAMA. 2013;310(14):14821489.
  19. Evans RS, Sharp JH, Linford LH, et al. Reduction of peripherally inserted central catheter‐associated DVT. Chest. 2013;143(3):627633.
  20. Lavau‐Denes S, Lacroix P, Maubon A, et al. Prophylaxis of catheter‐related deep vein thrombosis in cancer patients with low‐dose warfarin, low molecular weight heparin, or control: a randomized, controlled, phase III study. Cancer Chemother Pharmacol. 2013;72(1):6573.
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Pulmonary embolism (PE) and deep venous thrombosis (DVT), historically referred to together as venous thromboembolism (VTE), are common, treatable, sometimes fatal, and potentially preventable medical problems.[1] Such thromboses can both precipitate a hospitalization as well as complicate it (either during or soon after discharge). Preventing such thrombosis as a complication of medical care has become a national imperative. Landmark studies such as Prophylaxis in Medical Patients With Enoxaparin (MEDENOX)[2] and Prospective Evaluation of Dalteparin Efficacy for Prevention of VTE in Immobilized Patients Trial (PREVENT)[3] demonstrated both a high incidence of thrombosis in a hospitalized high‐risk medical population (15% and 5% in the 2 trials' placebo arms, respectively) as well as significant relative risk reduction through venous thromboembolism pharmacoprophylaxis (VTEP)63% and 45%, respectively. The Joint Commission,[4] the Society of Hospital Medicine,[5] and the American College of Chest Physicians[6, 7] have thus all strived to ensure the appropriate provision of VTEP in order to reduce the morbidity and mortality associated with thrombosis in hospitalized patients, including those on medical services.

Ideally, the global success of these efforts would be assessed by measuring the rate of hospital‐associated VTE (potentially including superficial venous thrombosis [SVT], which, like upper‐extremity deep venous thrombosis [UE‐DVT], is commonly a central venous catheter [CVC]‐associated, or peripherally inserted central catheter [PICC]‐associated, complication)thrombosis acquired and diagnosed during either the index hospitalization (hospital‐acquired, or HA‐VTE/SVT) or up to 30 days postdischarge. Unfortunately, postdischarge VTE/SVT is difficult to measure because patients developing it may not present to the original hospital, or at all (eg, if they do not seek care, are treated as outpatients, or, in the most extreme case, die at home). In this context, despite being far less comprehensive, HA‐VTE/SVT is a useful subset of hospital‐associated VTE/SVT, for several reasons. First, the Centers for Medicare & Medicaid Services (CMS) have mandated hospitals to qualify all medical diagnoses as present‐on‐admission (POA = Y) or not (POA = N) since 2008, such that all medical diagnoses coded POA = N can be considered hospital acquired.[8] Second, refinements made to the International Classification of Diseases, 9th Revision (ICD‐9) codes now allow differentiation of UE‐DVT and SVT from lower‐extremity (LE) DVT/PE, whereas the former were sometimes obscured by nonspecific coding.[9] Third, recent studies have shown that medical diagnoses administratively coded as HA‐VTE/SVT correlated well with HA‐VTE/SVT ascertained through chart review.[9, 10] Finally, previous work has estimated that approximately half of all hospital‐associated VTE are HA‐VTE and the other half are postdischarge VTE.[11] Thus, HA‐VTE, though comprising only approximately half of all hospital‐associated VTE, is often used as a surrogate for measuring the success of ongoing VTE prevention programs.[12]

Our study aimed to assess the incidence of HA‐VTE plus HA‐SVT in the era of mandatory POA coding and newer ICD‐9 codes for VTE.

METHODS

Setting and Cases

We conducted a retrospective analysis of discharges from the 83 academic medical centers belonging to the UHC (formerly, the University HealthSystem Consortium, https://www.uhc.edu)[13] between October 1, 2009 and March 31, 2011. UHC collects demographic, clinical, and billing data from these centers including medical diagnoses and procedures coded using the ICD‐9‐Clinical Modification (ICD‐9‐CM), a POA indicator for each diagnosis; UHC also collects data on medication use. This study was approved by the institutional review board at the University of California Davis.

Patients in our analysis were age 18 years and discharged with a medical medical severity diagnostic‐related group (MS‐DRG) code, hospitalized for 48 hours, and did not have a surgical or obstetric MS‐DRG code (except when assigned a surgical MS‐DRG code solely due to insertion of an inferior vena cava filter, with no other major procedures performed). Cases excluded discharges with a principal diagnosis of acute VTE/SVT (defined here as including PE, LE‐DVT, UE‐DVT, SVT, chronic VTE, and thrombosis not otherwise specified), as coding guidelines prohibit assigning a HA‐VTE as the principal diagnosis for the index hospitalization.[14]

Hospital‐Acquired Venous Thromboembolism or Superficial Venous Thrombosis

Cases were classified as having a HA‐VTE/SVT if there was 1 VTE/SVT coded in a secondary diagnosis position (other diagnosis) with a corresponding POA indicator equal to either N (not POA) or U (documentation insufficient to clarify whether VTE was POA or not). This usage corresponds to CMS guidelines and reimbursement policies for hospital‐acquired conditions.[15] Among cases with 1 HA‐VTE (or SVT), we assigned 1 HA‐VTE diagnosis using a hierarchy based on the highest level of clinical importance: first, PE; then LE‐DVT; then UE‐DVT; then SVT; then chronic VTE; then, finally, unspecified VTE. We subsequently excluded cases with primarily chronic VTE from our analysis because these were likely miscodes (ie, it is unclear how a chronic VTE could not be POA) and there were only 30 such cases. Cases with HA‐PE or HA‐LE DVT were analyzed separately as an important subset of HA‐VTE (plus SVT), because HA‐PE/LE‐DVT is both life‐threatening and theoretically preventable with VTEP.

Severity of Illness and Other Measures of Comorbidity

For each case we used proprietary software (3M Health Information Systems, Murray UT) to classify severity of illness (SOI). The SOI scale, based on physiologic derangement and organ system loss of function,[16] has 4 levels: minor, major, severe, and extreme. Defined within specific disease groups (All Patient Refined DRGs), it is often compared across diseases as well.[17] We also assessed whether patients had a cancer diagnosis, spent time in the intensive care unit (ICU), and died in the hospital.

Central Venous Catheter Use in Patients With Upper‐Extremity Deep Venous Thrombosis or Superficial Venous Thrombosis

Because UE‐DVT and SVT are frequently associated with a CVC or PICC, we assessed central venous catheterization among patients with an UE‐DVT or SVT of the cephalic, basilic, or antecubital veins using diagnosis codes for complications related to dialysis devices, implants, and grafts.

Pharmacologic Thromboprophylaxis

Pharmacy records of the subset of HA‐VTE/SVT cases with PE or LE‐DVT were analyzed to determine if VTEP was administered on hospital day 1 or 2, as per Joint Commission performance requirements.[4] Medications that met criteria as VTEP included unfractionated heparin, 5000 IU, given 2 or 3 a day; enoxaparin, 40 mg, given daily; dalteparin, 2500 or 5000 IU, given daily; fondaparinux, 2.5 mg, given daily; and warfarin. We could not reliably determine if VTEP was used throughout the entire hospitalization, or whether mechanical prophylaxis was used at all.

Statistical Analysis

This was a descriptive analysis to determine the incidence of HA‐VTE/SVT and describe the demographic and clinical characteristics of this population. We calculated means and standard deviations (SD) for continuous variables and proportions for binary variables (including HA‐VTE/SVT incidence). All comparisons between populations were performed as either 2‐tailed t tests or 2 analyses. All analysis was conducted using SAS software, version 9.2 (SAS Institute, Inc., Cary, NC).

RESULTS

For the 18‐month period between October 1, 2009, and March 31, 2011, across 83 UHC hospitals, there were 2,525,068 cases. Among these, 12,847 (0.51%) had 1 HA‐VTE/SVT coded. As per the clinical importance hierarchy described above, 2449 (19.1%) cases had at least a PE coded; 3848 (30%) had at least a LE‐DVT (but not a PE) coded; 2893 (22.5%) had at least an UE‐DVT coded; 3248 (25.3%) had at least an SVT coded; 30 had at least a chronic VTE coded; and 379 had at least a VTE coded with no specified location. Of those with SVT, 192 (5.8%) were LE‐SVT codes, whereas the rest were SVT/thrombophlebitis of the upper extremities or not otherwise specified. There were 11,882 (92.5%) hospitalizations with a single HA‐VTE/SVT code and an additional 965 (7.5%) with multiple codes, for a total of 13,749 HA‐VTE/SVT events (see Supporting Information, Table S1, in the online version of this article for more specific data for the individual ICD‐9 codes used to specify HA‐VTE events).

Compared with those who did not develop any HA‐VTE/SVT, patients with HA‐PE/LE‐DVT were more likely to be Caucasian (65% vs 58%, P < 0.001) and were older (age 62 vs 48 years, P < 0.001) and sicker (79.9% vs 44.9% with a severe or extreme SOI, P < 0.001). They also were more likely to have cancer, have longer lengths of stay, be more likely to stay in the ICU, and die in the hospital (P < 0.001 for all comparisons; Table 1).

Patients With No HA‐VTE Code and Patients With a HA‐PE/LE‐DVT Code (ICD‐9‐CM)
CharacteristicNo HA‐VTE, n = 2,512,221HA‐PE/LE DVT, n = 6,297aP Valueb
  • NOTE: Data are presented as n (%) or mean SD. Abbreviations: API, Asian or Pacific Islander; HA‐PE/LE DVT, hospital‐acquired pulmonary embolism or lower‐extremity deep venous thrombosis; HA‐VTE, hospital‐acquired venous thromboembolism; ICD‐9‐CM, International Classification of Diseases, Ninth Revision, Clinical Modification; ICU, intensive care unit; LMWH, low‐molecular‐weight heparin; SD, standard deviation; SOI, severity of illness.

  • The first 2 columns, no HA‐VTE and HA‐PE/LE DVT, were compared as noted in the third column. Data on upper‐extremity or superficial thrombosis are not shown in this table.

  • For all variables except age and length of stay, P values are calculated by 2; for age and length of stay, P value is calculated by rank‐sum test.

  • Prophylaxis with LMWH, fondaparinux, unfractionated heparin, or warfarin on the first or second day of hospitalization. Prophylaxis was not estimated in the population that did not develop a HA‐VTE.

Proportion of hospitalizations, %99.490.25 
Age, y48.2 27.162.5 20.0<0.001
Female sex1,347,219 (53.6)3,104 (49.3)<0.001
Race  <0.001
Caucasian1,455,215 (57.9)3,963 (64.7) 
Black600,991 (23.9)1,425 (23.3) 
Hispanic206,553 (8.2)263 (4.3) 
API59,560 (2.4)88 (1.4) 
Other189,902 (7.6)389 (6.4) 
Admission SOI  <0.001
Minor461,411 (18.4)181 (2.9) 
Major922,734 (36.7)1,081 (17.2) 
Severe880,542 (35.1)2,975 (47.2) 
Extreme247,244 (9.8)2,060 (32.7) 
Unknown290 (0.01)0 (0.0) 
Had an active diagnosis of cancer331,705 (13.2)2,162 (34.3)<0.001
Length of stay, d7.31 9.3118.7 19.5<0.001
Spent time in the ICU441,412 (17.6)3,011 (47.8)<0.001
Died in hospital57,954 (2.3)1,036 (16.5)<0.001
Received prophylaxiscc3,454 (54.9)c

Among cases with a code for UE‐DVT (22.5% of all patients with HA‐VTE), 74% were noted to also have a code for a CVC, as did 60% of cases with a HA‐SVT of the antecubital, basilic, or cephalic veins (71% of SVT events; see Supporting Information, Table S1, in the online version of this article).

Of those with HA‐PE/LE‐DVT, 54.9% received pharmacologic prophylaxis on hospital day 1 or 2 (mostly with low‐molecular‐weight heparin or unfractionated heparin).

DISCUSSION

In this study of medical patients admitted to academic medical centers throughout the United States, we found that HA‐VTE/SVT was coded in approximately 0.51% of discharges, and the incidence of HA‐PE/LE‐DVT was 0.25%. Patients with a HA‐PE/LE‐DVT code were, in general, older and sicker than those who did not develop VTE. We further found that close to half of all HA‐VTE/SVT occurred in the upper extremity, with the majority of these occurring in patients who had CVCs. Finally, the majority of patients diagnosed with HA‐PE/LE‐DVT were started on VTEP on the first or second hospital day.

The overall incidence of HA‐VTE/SVT we discovered corresponds well to other studies, even those with disparate populations. A single‐institution study found a HA‐VTE/SVT incidence of approximately 0.6% among hospitalized patients on medical and nonmedical services.[12] The study by Barba found a rate of 0.93%,[18] whereas the study by Lederle found a rate of approximately 1%.[19] Spyropolous found an HA‐VTE incidence of 0.55%.[11] Rothberg found a lower rate of 0.25% in his risk‐stratification study, though in the pre‐POA and preupdated code era.[20] Our findings extend and provide context for, in a much larger population, the results of these prior studies, and represent the first national examination of HA‐VTE/SVT in the setting of numerous quality‐improvement and other efforts to reduce hospital‐associated VTE.

The incidence of HA‐VTE/SVT codes we observed likely underestimates the incidence of hospital‐associated VTE/SVT by a factor of approximately 4, for 2 reasons. First, although VTE/SVT codes with a POA flag set to No are truly hospital‐acquired events on chart review approximately 75% of the time, and thus overestimate HA‐VTE/SVT, 25% of POA = Yes codes are actually HA‐VTE/SVT events on chart review, and therefore lead to underestimation of HA‐VTE/SVT.[9] Because VTE/SVT codes with a POA flag set to Yes outnumber those flagged No by 3 or 4 to 1, events mis‐flagged Yes contribute a much greater number of undercounted HA‐VTE/SVT, elevating the actual HA‐VTE/SVT event rate by a factor of approximately 2. Second, HA‐VTE events do not include hospital‐associated VTE events that are diagnosed after the index hospitalization. In the Spyropolous study, 45% of hospital‐associated VTE events occurred after discharge, so translating HA‐VTE/SVT events to hospital‐associated VTE/SVT events would again involve multiplying by a factor of 2.[11] Thus, the overall incidence of hospital‐associated VTE/SVT events in our sample may have been approximately 2% (0.51% 4), and the overall incidence of hospital‐associated PE or LE‐DVT events may have been approximately 1%, though there may be significant variation around these estimates given that individual institutions were themselves quite variable in their POA flag accuracy in our study.[9] There is additionally the possibility that hospitals may have deliberately left some VTE/SVT uncoded, but in the absence of financial incentives to do so for anything other than postsurgical VTE, and in the presence of penalties from CMS for undercoding, we believe this to be unlikely, at least at present.

Despite these upward extrapolations, the estimated incidence of hospital‐associated VTE/SVT in our study may seem low compared with that reported in the MEDENOX[2] and PREVENT studies.[3] Much of this discrepancy vanishes on closer examination. In the large randomized trials, patients were uniformly and routinely assessed for LE‐DVT using vascular ultrasound; in contrast, in our population of hospitalizations patients may have only had diagnostic studies done for signs or symptoms. Clinically apparent hospital‐associated VTE is less common than all hospital‐associated VTE, as it was even in PREVENT,[3] and increased surveillance may even be partially driving increased hospital‐associated VTE/SVT at some hospitals.[21] Our findings suggest that success or failure in preventing administratively coded, clinically apparent HA LE‐VTE/PE should be judged, broadly, against numbers in the range established in our study (eg, 0.25%), not the 5% or 15% of chart‐abstracted, aggressively ascertained (and sometimes clinically silent) hospital‐associated VTE in the large randomized controlled trials. That is, 0.25% is not an achievement, but rather the average, expected value.

Almost 25% of the observed HA‐VTE/SVTs coded were UE‐DVT, with roughly 75% of these being likely related to central venous catheterization (including those peripherally inserted). An additional 1/5 were upper‐extremity SVT of the antecubital, cephalic, and basilic veins, with the majority of these (60%) also listed as catheter‐related. Such thrombosis is best prevented by decreased use of central catheters or perhaps by using smaller‐caliber catheters.[22] It is unclear if VTEP can prevent such clots, though in cancer patients at least one recent trial seems promising.[23]

We found that patients with a coded HA‐PE/LE‐DVT were remarkably different from those not developing HA‐VTE/SVT. Patients with HA‐PE or HA‐LE‐DVT were older, sicker, more likely to have cancer, significantly more likely to spend time in the ICU, and much more likely to die in the hospital; risk factors for HA‐VTE overlap significantly with risk factors for death in the hospital. A small majority (55%) of patients in the HA‐PE/LE‐DVT group had actually received VTEP on at least day 1 or 2 of hospitalization. It may be the case that the dose of VTEP was insufficient to suppress clot formation in these patients, or that HA‐PE/LE‐DVT in patients with this degree of comorbidity is difficult to prevent.

There are a number of limitations to our study. We analyzed administrative codes, which underestimate hospital‐associated VTE/SVT events as noted above. This was a descriptive study, cross‐sectional across each hospitalization, and we were unable to draw any causal inference for differences in HA‐VTE/SVT incidence that might exist between subpopulations. We estimated VTEP from medication usage in just the first 2 days of hospitalization; we could not assess mechanical prophylaxis in this dataset; and we did not have any VTEP data for the first 2 days of hospitalization on the patients who did not develop a HA‐VTE/SVT, which made it impossible to compare the 2 populations on this measure. For those who did not receive VTEP, we were unable to obtain data regarding possible contraindications to VTEP, such as ongoing gastrointestinal or intracerebral hemorrhage. Additionally, our data are based on academic hospitals only and may not generalize to nonacademic settings. Extrapolating from HA‐VTE/SVT to hospital‐associated VTE/SVT may not be possible due to heterogeneity of clotting events and perhaps variability in whether patients would return to the hospital for all of them (eg, superficial or UE VTE may not result in readmission). Finally, it is unclear whether a switch to ICD Tenth Revision (ICD‐10) codes will impact our measured baseline in the coming year. The strengths of our analysis included stratification by type of HA‐VTE/SVT and our ability to assess the incidence of HA‐VTE/SVT in a large national population, and the provision of a baseline for VTE incidenceeasily usable by any individual hospital, network, or researcher with access to administrative datagoing forward.

In conclusion, among patients hospitalized in academic medical centers, HA‐VTE/SVT was coded in approximately 0.51% of patients with a medical illness staying >2 days, with approximately half of the events due to HA‐PE/LE‐DVT. Patients who developed HA‐PE/LE‐DVT were more acutely ill than those who did not, and VTE developed despite 55% of these patients receiving VTEP on day 1 or 2. Hospitals can reasonably treat the 0.25% figure as the baseline around which to assess their own performance in preventing HA‐PE/LE‐DVT, and can measure their own performance using administrative data. Further research is needed to determine how best to achieve further reductions in HA‐VTE/SVT through risk stratification and/or through other interventions.

Disclosures

Nothing to report.

Pulmonary embolism (PE) and deep venous thrombosis (DVT), historically referred to together as venous thromboembolism (VTE), are common, treatable, sometimes fatal, and potentially preventable medical problems.[1] Such thromboses can both precipitate a hospitalization as well as complicate it (either during or soon after discharge). Preventing such thrombosis as a complication of medical care has become a national imperative. Landmark studies such as Prophylaxis in Medical Patients With Enoxaparin (MEDENOX)[2] and Prospective Evaluation of Dalteparin Efficacy for Prevention of VTE in Immobilized Patients Trial (PREVENT)[3] demonstrated both a high incidence of thrombosis in a hospitalized high‐risk medical population (15% and 5% in the 2 trials' placebo arms, respectively) as well as significant relative risk reduction through venous thromboembolism pharmacoprophylaxis (VTEP)63% and 45%, respectively. The Joint Commission,[4] the Society of Hospital Medicine,[5] and the American College of Chest Physicians[6, 7] have thus all strived to ensure the appropriate provision of VTEP in order to reduce the morbidity and mortality associated with thrombosis in hospitalized patients, including those on medical services.

Ideally, the global success of these efforts would be assessed by measuring the rate of hospital‐associated VTE (potentially including superficial venous thrombosis [SVT], which, like upper‐extremity deep venous thrombosis [UE‐DVT], is commonly a central venous catheter [CVC]‐associated, or peripherally inserted central catheter [PICC]‐associated, complication)thrombosis acquired and diagnosed during either the index hospitalization (hospital‐acquired, or HA‐VTE/SVT) or up to 30 days postdischarge. Unfortunately, postdischarge VTE/SVT is difficult to measure because patients developing it may not present to the original hospital, or at all (eg, if they do not seek care, are treated as outpatients, or, in the most extreme case, die at home). In this context, despite being far less comprehensive, HA‐VTE/SVT is a useful subset of hospital‐associated VTE/SVT, for several reasons. First, the Centers for Medicare & Medicaid Services (CMS) have mandated hospitals to qualify all medical diagnoses as present‐on‐admission (POA = Y) or not (POA = N) since 2008, such that all medical diagnoses coded POA = N can be considered hospital acquired.[8] Second, refinements made to the International Classification of Diseases, 9th Revision (ICD‐9) codes now allow differentiation of UE‐DVT and SVT from lower‐extremity (LE) DVT/PE, whereas the former were sometimes obscured by nonspecific coding.[9] Third, recent studies have shown that medical diagnoses administratively coded as HA‐VTE/SVT correlated well with HA‐VTE/SVT ascertained through chart review.[9, 10] Finally, previous work has estimated that approximately half of all hospital‐associated VTE are HA‐VTE and the other half are postdischarge VTE.[11] Thus, HA‐VTE, though comprising only approximately half of all hospital‐associated VTE, is often used as a surrogate for measuring the success of ongoing VTE prevention programs.[12]

Our study aimed to assess the incidence of HA‐VTE plus HA‐SVT in the era of mandatory POA coding and newer ICD‐9 codes for VTE.

METHODS

Setting and Cases

We conducted a retrospective analysis of discharges from the 83 academic medical centers belonging to the UHC (formerly, the University HealthSystem Consortium, https://www.uhc.edu)[13] between October 1, 2009 and March 31, 2011. UHC collects demographic, clinical, and billing data from these centers including medical diagnoses and procedures coded using the ICD‐9‐Clinical Modification (ICD‐9‐CM), a POA indicator for each diagnosis; UHC also collects data on medication use. This study was approved by the institutional review board at the University of California Davis.

Patients in our analysis were age 18 years and discharged with a medical medical severity diagnostic‐related group (MS‐DRG) code, hospitalized for 48 hours, and did not have a surgical or obstetric MS‐DRG code (except when assigned a surgical MS‐DRG code solely due to insertion of an inferior vena cava filter, with no other major procedures performed). Cases excluded discharges with a principal diagnosis of acute VTE/SVT (defined here as including PE, LE‐DVT, UE‐DVT, SVT, chronic VTE, and thrombosis not otherwise specified), as coding guidelines prohibit assigning a HA‐VTE as the principal diagnosis for the index hospitalization.[14]

Hospital‐Acquired Venous Thromboembolism or Superficial Venous Thrombosis

Cases were classified as having a HA‐VTE/SVT if there was 1 VTE/SVT coded in a secondary diagnosis position (other diagnosis) with a corresponding POA indicator equal to either N (not POA) or U (documentation insufficient to clarify whether VTE was POA or not). This usage corresponds to CMS guidelines and reimbursement policies for hospital‐acquired conditions.[15] Among cases with 1 HA‐VTE (or SVT), we assigned 1 HA‐VTE diagnosis using a hierarchy based on the highest level of clinical importance: first, PE; then LE‐DVT; then UE‐DVT; then SVT; then chronic VTE; then, finally, unspecified VTE. We subsequently excluded cases with primarily chronic VTE from our analysis because these were likely miscodes (ie, it is unclear how a chronic VTE could not be POA) and there were only 30 such cases. Cases with HA‐PE or HA‐LE DVT were analyzed separately as an important subset of HA‐VTE (plus SVT), because HA‐PE/LE‐DVT is both life‐threatening and theoretically preventable with VTEP.

Severity of Illness and Other Measures of Comorbidity

For each case we used proprietary software (3M Health Information Systems, Murray UT) to classify severity of illness (SOI). The SOI scale, based on physiologic derangement and organ system loss of function,[16] has 4 levels: minor, major, severe, and extreme. Defined within specific disease groups (All Patient Refined DRGs), it is often compared across diseases as well.[17] We also assessed whether patients had a cancer diagnosis, spent time in the intensive care unit (ICU), and died in the hospital.

Central Venous Catheter Use in Patients With Upper‐Extremity Deep Venous Thrombosis or Superficial Venous Thrombosis

Because UE‐DVT and SVT are frequently associated with a CVC or PICC, we assessed central venous catheterization among patients with an UE‐DVT or SVT of the cephalic, basilic, or antecubital veins using diagnosis codes for complications related to dialysis devices, implants, and grafts.

Pharmacologic Thromboprophylaxis

Pharmacy records of the subset of HA‐VTE/SVT cases with PE or LE‐DVT were analyzed to determine if VTEP was administered on hospital day 1 or 2, as per Joint Commission performance requirements.[4] Medications that met criteria as VTEP included unfractionated heparin, 5000 IU, given 2 or 3 a day; enoxaparin, 40 mg, given daily; dalteparin, 2500 or 5000 IU, given daily; fondaparinux, 2.5 mg, given daily; and warfarin. We could not reliably determine if VTEP was used throughout the entire hospitalization, or whether mechanical prophylaxis was used at all.

Statistical Analysis

This was a descriptive analysis to determine the incidence of HA‐VTE/SVT and describe the demographic and clinical characteristics of this population. We calculated means and standard deviations (SD) for continuous variables and proportions for binary variables (including HA‐VTE/SVT incidence). All comparisons between populations were performed as either 2‐tailed t tests or 2 analyses. All analysis was conducted using SAS software, version 9.2 (SAS Institute, Inc., Cary, NC).

RESULTS

For the 18‐month period between October 1, 2009, and March 31, 2011, across 83 UHC hospitals, there were 2,525,068 cases. Among these, 12,847 (0.51%) had 1 HA‐VTE/SVT coded. As per the clinical importance hierarchy described above, 2449 (19.1%) cases had at least a PE coded; 3848 (30%) had at least a LE‐DVT (but not a PE) coded; 2893 (22.5%) had at least an UE‐DVT coded; 3248 (25.3%) had at least an SVT coded; 30 had at least a chronic VTE coded; and 379 had at least a VTE coded with no specified location. Of those with SVT, 192 (5.8%) were LE‐SVT codes, whereas the rest were SVT/thrombophlebitis of the upper extremities or not otherwise specified. There were 11,882 (92.5%) hospitalizations with a single HA‐VTE/SVT code and an additional 965 (7.5%) with multiple codes, for a total of 13,749 HA‐VTE/SVT events (see Supporting Information, Table S1, in the online version of this article for more specific data for the individual ICD‐9 codes used to specify HA‐VTE events).

Compared with those who did not develop any HA‐VTE/SVT, patients with HA‐PE/LE‐DVT were more likely to be Caucasian (65% vs 58%, P < 0.001) and were older (age 62 vs 48 years, P < 0.001) and sicker (79.9% vs 44.9% with a severe or extreme SOI, P < 0.001). They also were more likely to have cancer, have longer lengths of stay, be more likely to stay in the ICU, and die in the hospital (P < 0.001 for all comparisons; Table 1).

Patients With No HA‐VTE Code and Patients With a HA‐PE/LE‐DVT Code (ICD‐9‐CM)
CharacteristicNo HA‐VTE, n = 2,512,221HA‐PE/LE DVT, n = 6,297aP Valueb
  • NOTE: Data are presented as n (%) or mean SD. Abbreviations: API, Asian or Pacific Islander; HA‐PE/LE DVT, hospital‐acquired pulmonary embolism or lower‐extremity deep venous thrombosis; HA‐VTE, hospital‐acquired venous thromboembolism; ICD‐9‐CM, International Classification of Diseases, Ninth Revision, Clinical Modification; ICU, intensive care unit; LMWH, low‐molecular‐weight heparin; SD, standard deviation; SOI, severity of illness.

  • The first 2 columns, no HA‐VTE and HA‐PE/LE DVT, were compared as noted in the third column. Data on upper‐extremity or superficial thrombosis are not shown in this table.

  • For all variables except age and length of stay, P values are calculated by 2; for age and length of stay, P value is calculated by rank‐sum test.

  • Prophylaxis with LMWH, fondaparinux, unfractionated heparin, or warfarin on the first or second day of hospitalization. Prophylaxis was not estimated in the population that did not develop a HA‐VTE.

Proportion of hospitalizations, %99.490.25 
Age, y48.2 27.162.5 20.0<0.001
Female sex1,347,219 (53.6)3,104 (49.3)<0.001
Race  <0.001
Caucasian1,455,215 (57.9)3,963 (64.7) 
Black600,991 (23.9)1,425 (23.3) 
Hispanic206,553 (8.2)263 (4.3) 
API59,560 (2.4)88 (1.4) 
Other189,902 (7.6)389 (6.4) 
Admission SOI  <0.001
Minor461,411 (18.4)181 (2.9) 
Major922,734 (36.7)1,081 (17.2) 
Severe880,542 (35.1)2,975 (47.2) 
Extreme247,244 (9.8)2,060 (32.7) 
Unknown290 (0.01)0 (0.0) 
Had an active diagnosis of cancer331,705 (13.2)2,162 (34.3)<0.001
Length of stay, d7.31 9.3118.7 19.5<0.001
Spent time in the ICU441,412 (17.6)3,011 (47.8)<0.001
Died in hospital57,954 (2.3)1,036 (16.5)<0.001
Received prophylaxiscc3,454 (54.9)c

Among cases with a code for UE‐DVT (22.5% of all patients with HA‐VTE), 74% were noted to also have a code for a CVC, as did 60% of cases with a HA‐SVT of the antecubital, basilic, or cephalic veins (71% of SVT events; see Supporting Information, Table S1, in the online version of this article).

Of those with HA‐PE/LE‐DVT, 54.9% received pharmacologic prophylaxis on hospital day 1 or 2 (mostly with low‐molecular‐weight heparin or unfractionated heparin).

DISCUSSION

In this study of medical patients admitted to academic medical centers throughout the United States, we found that HA‐VTE/SVT was coded in approximately 0.51% of discharges, and the incidence of HA‐PE/LE‐DVT was 0.25%. Patients with a HA‐PE/LE‐DVT code were, in general, older and sicker than those who did not develop VTE. We further found that close to half of all HA‐VTE/SVT occurred in the upper extremity, with the majority of these occurring in patients who had CVCs. Finally, the majority of patients diagnosed with HA‐PE/LE‐DVT were started on VTEP on the first or second hospital day.

The overall incidence of HA‐VTE/SVT we discovered corresponds well to other studies, even those with disparate populations. A single‐institution study found a HA‐VTE/SVT incidence of approximately 0.6% among hospitalized patients on medical and nonmedical services.[12] The study by Barba found a rate of 0.93%,[18] whereas the study by Lederle found a rate of approximately 1%.[19] Spyropolous found an HA‐VTE incidence of 0.55%.[11] Rothberg found a lower rate of 0.25% in his risk‐stratification study, though in the pre‐POA and preupdated code era.[20] Our findings extend and provide context for, in a much larger population, the results of these prior studies, and represent the first national examination of HA‐VTE/SVT in the setting of numerous quality‐improvement and other efforts to reduce hospital‐associated VTE.

The incidence of HA‐VTE/SVT codes we observed likely underestimates the incidence of hospital‐associated VTE/SVT by a factor of approximately 4, for 2 reasons. First, although VTE/SVT codes with a POA flag set to No are truly hospital‐acquired events on chart review approximately 75% of the time, and thus overestimate HA‐VTE/SVT, 25% of POA = Yes codes are actually HA‐VTE/SVT events on chart review, and therefore lead to underestimation of HA‐VTE/SVT.[9] Because VTE/SVT codes with a POA flag set to Yes outnumber those flagged No by 3 or 4 to 1, events mis‐flagged Yes contribute a much greater number of undercounted HA‐VTE/SVT, elevating the actual HA‐VTE/SVT event rate by a factor of approximately 2. Second, HA‐VTE events do not include hospital‐associated VTE events that are diagnosed after the index hospitalization. In the Spyropolous study, 45% of hospital‐associated VTE events occurred after discharge, so translating HA‐VTE/SVT events to hospital‐associated VTE/SVT events would again involve multiplying by a factor of 2.[11] Thus, the overall incidence of hospital‐associated VTE/SVT events in our sample may have been approximately 2% (0.51% 4), and the overall incidence of hospital‐associated PE or LE‐DVT events may have been approximately 1%, though there may be significant variation around these estimates given that individual institutions were themselves quite variable in their POA flag accuracy in our study.[9] There is additionally the possibility that hospitals may have deliberately left some VTE/SVT uncoded, but in the absence of financial incentives to do so for anything other than postsurgical VTE, and in the presence of penalties from CMS for undercoding, we believe this to be unlikely, at least at present.

Despite these upward extrapolations, the estimated incidence of hospital‐associated VTE/SVT in our study may seem low compared with that reported in the MEDENOX[2] and PREVENT studies.[3] Much of this discrepancy vanishes on closer examination. In the large randomized trials, patients were uniformly and routinely assessed for LE‐DVT using vascular ultrasound; in contrast, in our population of hospitalizations patients may have only had diagnostic studies done for signs or symptoms. Clinically apparent hospital‐associated VTE is less common than all hospital‐associated VTE, as it was even in PREVENT,[3] and increased surveillance may even be partially driving increased hospital‐associated VTE/SVT at some hospitals.[21] Our findings suggest that success or failure in preventing administratively coded, clinically apparent HA LE‐VTE/PE should be judged, broadly, against numbers in the range established in our study (eg, 0.25%), not the 5% or 15% of chart‐abstracted, aggressively ascertained (and sometimes clinically silent) hospital‐associated VTE in the large randomized controlled trials. That is, 0.25% is not an achievement, but rather the average, expected value.

Almost 25% of the observed HA‐VTE/SVTs coded were UE‐DVT, with roughly 75% of these being likely related to central venous catheterization (including those peripherally inserted). An additional 1/5 were upper‐extremity SVT of the antecubital, cephalic, and basilic veins, with the majority of these (60%) also listed as catheter‐related. Such thrombosis is best prevented by decreased use of central catheters or perhaps by using smaller‐caliber catheters.[22] It is unclear if VTEP can prevent such clots, though in cancer patients at least one recent trial seems promising.[23]

We found that patients with a coded HA‐PE/LE‐DVT were remarkably different from those not developing HA‐VTE/SVT. Patients with HA‐PE or HA‐LE‐DVT were older, sicker, more likely to have cancer, significantly more likely to spend time in the ICU, and much more likely to die in the hospital; risk factors for HA‐VTE overlap significantly with risk factors for death in the hospital. A small majority (55%) of patients in the HA‐PE/LE‐DVT group had actually received VTEP on at least day 1 or 2 of hospitalization. It may be the case that the dose of VTEP was insufficient to suppress clot formation in these patients, or that HA‐PE/LE‐DVT in patients with this degree of comorbidity is difficult to prevent.

There are a number of limitations to our study. We analyzed administrative codes, which underestimate hospital‐associated VTE/SVT events as noted above. This was a descriptive study, cross‐sectional across each hospitalization, and we were unable to draw any causal inference for differences in HA‐VTE/SVT incidence that might exist between subpopulations. We estimated VTEP from medication usage in just the first 2 days of hospitalization; we could not assess mechanical prophylaxis in this dataset; and we did not have any VTEP data for the first 2 days of hospitalization on the patients who did not develop a HA‐VTE/SVT, which made it impossible to compare the 2 populations on this measure. For those who did not receive VTEP, we were unable to obtain data regarding possible contraindications to VTEP, such as ongoing gastrointestinal or intracerebral hemorrhage. Additionally, our data are based on academic hospitals only and may not generalize to nonacademic settings. Extrapolating from HA‐VTE/SVT to hospital‐associated VTE/SVT may not be possible due to heterogeneity of clotting events and perhaps variability in whether patients would return to the hospital for all of them (eg, superficial or UE VTE may not result in readmission). Finally, it is unclear whether a switch to ICD Tenth Revision (ICD‐10) codes will impact our measured baseline in the coming year. The strengths of our analysis included stratification by type of HA‐VTE/SVT and our ability to assess the incidence of HA‐VTE/SVT in a large national population, and the provision of a baseline for VTE incidenceeasily usable by any individual hospital, network, or researcher with access to administrative datagoing forward.

In conclusion, among patients hospitalized in academic medical centers, HA‐VTE/SVT was coded in approximately 0.51% of patients with a medical illness staying >2 days, with approximately half of the events due to HA‐PE/LE‐DVT. Patients who developed HA‐PE/LE‐DVT were more acutely ill than those who did not, and VTE developed despite 55% of these patients receiving VTEP on day 1 or 2. Hospitals can reasonably treat the 0.25% figure as the baseline around which to assess their own performance in preventing HA‐PE/LE‐DVT, and can measure their own performance using administrative data. Further research is needed to determine how best to achieve further reductions in HA‐VTE/SVT through risk stratification and/or through other interventions.

Disclosures

Nothing to report.

References
  1. Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ;American College of Chest Physicians AntithromboticTherapy and Prevention of Thrombosis Panel. Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence‐Based Clinical Practice Guidelines [published corrections appear in Chest. 2012;141(4):1129 and 2012;142(6):1698]. Chest. 2012;141(2 suppl):7S–47S.
  2. Samama MM, Cohen AT, Darmon JY, et al;Prophylaxis in Medical Patients with Enoxaparin Study Group. A comparison of enoxaparin with placebo for the prevention of venous thromboembolism in acutely ill medical patients. N Engl J Med. 1999;341(11):793800.
  3. Leizorovicz A, Cohen AT, Turpie AG, Olsson CG, Vaitkus PT, Goldhaber SZ. Randomized, placebo‐controlled trial of dalteparin for the prevention of venous thromboembolism in acutely ill medical patients. Circulation. 2004;110(7):874879.
  4. The Joint Commission.Specifications Manual for National Hospital Inpatient Quality Measures. Available at: http://www.jointcommission.org/specifications_manual_for_national_hospital_inpatient_quality_measures.aspx. Accessed July 18, 2012.
  5. Maynard G, Stein J. Preventing Hospital‐Acquired Venous Thromboembolism: A Guide for Effective Quality Improvement. Prepared by the Society of Hospital Medicine. Rockville, MD: Agency for Healthcare Research and Quality; AHRQ Publication No. 08‐0075.
  6. Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126(3 suppl):338S400S.
  7. Kahn SR, Lim W, Dunn AS, et al. Prevention of VTE in nonsurgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence‐Based Clinical Practice Guidelines. Chest. 2012;141(2 suppl):e195Se226S.
  8. Centers for Medicare 46(6 part 1):19461962.
  9. Spyropoulos AC, Anderson FA, Fitzgerald G, et al. Predictive and associative models to identify hospitalized medical patients at risk for VTE. Chest. 2011;140(3):706714.
  10. Khanna R, Vittinghoff E, Maselli J, Auerbach A. Unintended consequences of a standard admission order set on venous thromboembolism prophylaxis and patient outcomes. J Gen Intern Med. 2012;27(3):318324.
  11. United Health Consortium Website. Available at: https://www.uhc.edu. Accessed March 8, 2012.
  12. ICD‐9‐CM Official Guidelines for Coding and Reporting. Available at: http://www.cdc.gov/nchs/data/icd9/icdguide10.pdf. Published 2010. Accessed June 4, 2013.
  13. Centers for Medicare 27(5):587612.
  14. Overview of Disease Severity Measures Disseminated with the Nationwide Inpatient Sample (NIS) and Kids' Inpatient Database (KID). Available at: http://www.hcup‐us.ahrq.gov/db/nation/nis/OverviewofSeveritySystems.pdf. Published December 9, 2005. Accessed June 4, 2013.
  15. Barba R, Zapatero A, Losa JE, et al. Venous thromboembolism in acutely ill hospitalized medical patients. Thromb Res. 2010;126(4):276279.
  16. Lederle FA, Zylla D, MacDonald R, Wilt TJ. Venous thromboembolism prophylaxis in hospitalized medical patients and those with stroke: a background review for an American College of Physicians Clinical Practice Guideline. Ann Intern Med. 2011;155(9):602615.
  17. Rothberg MB, Lindenauer PK, Lahti M, Pekow PS, Selker HP. Risk factor model to predict venous thromboembolism in hospitalized medical patients. J Hosp Med. 2011;6(4):202209.
  18. Bilimoria KY, Chung J, Ju MH, et al. Evaluation of surveillance bias and the validity of the venous thromboembolism quality measure. JAMA. 2013;310(14):14821489.
  19. Evans RS, Sharp JH, Linford LH, et al. Reduction of peripherally inserted central catheter‐associated DVT. Chest. 2013;143(3):627633.
  20. Lavau‐Denes S, Lacroix P, Maubon A, et al. Prophylaxis of catheter‐related deep vein thrombosis in cancer patients with low‐dose warfarin, low molecular weight heparin, or control: a randomized, controlled, phase III study. Cancer Chemother Pharmacol. 2013;72(1):6573.
References
  1. Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ;American College of Chest Physicians AntithromboticTherapy and Prevention of Thrombosis Panel. Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence‐Based Clinical Practice Guidelines [published corrections appear in Chest. 2012;141(4):1129 and 2012;142(6):1698]. Chest. 2012;141(2 suppl):7S–47S.
  2. Samama MM, Cohen AT, Darmon JY, et al;Prophylaxis in Medical Patients with Enoxaparin Study Group. A comparison of enoxaparin with placebo for the prevention of venous thromboembolism in acutely ill medical patients. N Engl J Med. 1999;341(11):793800.
  3. Leizorovicz A, Cohen AT, Turpie AG, Olsson CG, Vaitkus PT, Goldhaber SZ. Randomized, placebo‐controlled trial of dalteparin for the prevention of venous thromboembolism in acutely ill medical patients. Circulation. 2004;110(7):874879.
  4. The Joint Commission.Specifications Manual for National Hospital Inpatient Quality Measures. Available at: http://www.jointcommission.org/specifications_manual_for_national_hospital_inpatient_quality_measures.aspx. Accessed July 18, 2012.
  5. Maynard G, Stein J. Preventing Hospital‐Acquired Venous Thromboembolism: A Guide for Effective Quality Improvement. Prepared by the Society of Hospital Medicine. Rockville, MD: Agency for Healthcare Research and Quality; AHRQ Publication No. 08‐0075.
  6. Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126(3 suppl):338S400S.
  7. Kahn SR, Lim W, Dunn AS, et al. Prevention of VTE in nonsurgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence‐Based Clinical Practice Guidelines. Chest. 2012;141(2 suppl):e195Se226S.
  8. Centers for Medicare 46(6 part 1):19461962.
  9. Spyropoulos AC, Anderson FA, Fitzgerald G, et al. Predictive and associative models to identify hospitalized medical patients at risk for VTE. Chest. 2011;140(3):706714.
  10. Khanna R, Vittinghoff E, Maselli J, Auerbach A. Unintended consequences of a standard admission order set on venous thromboembolism prophylaxis and patient outcomes. J Gen Intern Med. 2012;27(3):318324.
  11. United Health Consortium Website. Available at: https://www.uhc.edu. Accessed March 8, 2012.
  12. ICD‐9‐CM Official Guidelines for Coding and Reporting. Available at: http://www.cdc.gov/nchs/data/icd9/icdguide10.pdf. Published 2010. Accessed June 4, 2013.
  13. Centers for Medicare 27(5):587612.
  14. Overview of Disease Severity Measures Disseminated with the Nationwide Inpatient Sample (NIS) and Kids' Inpatient Database (KID). Available at: http://www.hcup‐us.ahrq.gov/db/nation/nis/OverviewofSeveritySystems.pdf. Published December 9, 2005. Accessed June 4, 2013.
  15. Barba R, Zapatero A, Losa JE, et al. Venous thromboembolism in acutely ill hospitalized medical patients. Thromb Res. 2010;126(4):276279.
  16. Lederle FA, Zylla D, MacDonald R, Wilt TJ. Venous thromboembolism prophylaxis in hospitalized medical patients and those with stroke: a background review for an American College of Physicians Clinical Practice Guideline. Ann Intern Med. 2011;155(9):602615.
  17. Rothberg MB, Lindenauer PK, Lahti M, Pekow PS, Selker HP. Risk factor model to predict venous thromboembolism in hospitalized medical patients. J Hosp Med. 2011;6(4):202209.
  18. Bilimoria KY, Chung J, Ju MH, et al. Evaluation of surveillance bias and the validity of the venous thromboembolism quality measure. JAMA. 2013;310(14):14821489.
  19. Evans RS, Sharp JH, Linford LH, et al. Reduction of peripherally inserted central catheter‐associated DVT. Chest. 2013;143(3):627633.
  20. Lavau‐Denes S, Lacroix P, Maubon A, et al. Prophylaxis of catheter‐related deep vein thrombosis in cancer patients with low‐dose warfarin, low molecular weight heparin, or control: a randomized, controlled, phase III study. Cancer Chemother Pharmacol. 2013;72(1):6573.
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Journal of Hospital Medicine - 9(4)
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Journal of Hospital Medicine - 9(4)
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Incidence of hospital‐acquired venous thromboembolic codes in medical patients hospitalized in academic medical centers
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Incidence of hospital‐acquired venous thromboembolic codes in medical patients hospitalized in academic medical centers
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Address for correspondence and reprint requests: Raman Khanna, MD, MAS, Assistant Clinical Professor of Medicine, University of California San Francisco, Department of Medicine, Division of Hospital Medicine, 533 Parnassus, U136, San Francisco, CA; Telephone: 415‐476‐4806; Fax: 415‐514‐2094; E‐mail: [email protected].
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ED Care Within 30 Days of Discharge

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Factors contributing to emergency department care within 30 days of hospital discharge and potential ways to prevent it: Differences in perspectives of patients, caregivers, and emergency physicians

Reducing hospital admissions within 30 days of inpatient discharge is the focus of numerous policies, incentives, and payment models, led by the Centers for Medicare & Medicaid Services.[1] Accordingly, care‐transition programs have been developed and are found to be effective in reducing hospital readmissions.[2, 3] Interestingly, emergency department (ED) visits have not been included in this definition of readmission, no programs have focused specifically on reducing ED visits,[4] and some have even increased ED visits.[5]

The prevalence and costs associated with ED care within 30 days of hospital discharge are not insignificant. Up to 24% of discharged patients present to the ED within 30 days, among whom only 50% are readmitted.[6] ED care alone accounts for nearly 40% of all costs in the acute postdischarge period.[7] This is in addition to the costs associated with readmissions from the ED, which are the result of disposition decisions made by ED clinicians.

To begin to build effective care‐transition programs to reduce ED visits after inpatient discharge, greater understanding is needed on what factors influence the utilization of the ED and what potential interventions could have prevented them. Studies from inpatient populations have been successful in eliciting these factors through stakeholder interviews.[8, 9, 10] In fact, the American College of Physicians and Society of Hospital Medicine emphasize involvement of the patient and family members in plans of care.[11] No prior studies have used stakeholders to inform care‐transition models for patients who return to the ED within 30 days of inpatient discharge.

Therefore, the primary objective of this study was to collect various stakeholder perspectives to improve the understanding of factors associated with ED visits within 30 days of hospital discharge and identify potentially useful interventions to prevent them. We hypothesized that there would be significant discordances between patients, their caregivers, and emergency physicians. Findings from this study could inform an expanded framework for understanding the complexity of care needs after hospital discharge and suggest interventions to improve health outcomes and to reduce healthcare costs.

METHODS

Setting

The study took place in the ED of a 525‐bed urban teaching hospital in Pittsburgh, Pennsylvania, with 55,000 annual ED visits and 26,137 hospital admissions per year. Overall demographics of patients presenting to this ED in 2012 were 82% white, 17% black, and 0.3% Asian. The institutional review board of the University of Pittsburgh approved this study.

Participants

Patients were eligible to participate if they: (1) had the capacity to complete an interview, as determined by the attending emergency physician based on their exam; and (2) presented to the ED within 30 days of a prior discharge from any affiliate hospital. Eligible participants were identified by a trained research associate (J.H.) on the day of the ED visit by screening the electronic medical record. We excluded 2 patients from analysis who had both been to the ED prior to a readmission and had already completed the survey in the last 30 days. Caregivers were eligible to participate if they: (1) were in the ED at the time of patient evaluation, and (2) were identified by participating patients. ED physicians were eligible to participate if they had seen and evaluated the enrolled patient and were the attending staff physician. Eligible caregivers and physicians underwent separate informed consent.

Development of Survey Instrument

A collaborative team of physicians and hospital administrators used a defined conceptual framework,[9] literature search, and pilot administration to construct a survey to elucidate factors potentially contributing to ED visits within 30 days of hospital discharge and interventions that could have potentially prevented the ED visit. All participants (patients, caregivers, and physicians) were asked to complete the following questions: (1) In your opinion, is your/the patient's ED visit today directly related to your/their last hospitalization? (2) In your opinion, did any of the following contribute to your/the patient's ED visit today? (3) In your opinion, which of the following could have prevented your/the patient's ED visit today? For questions 2 and 3, participants were asked to mark any and all prespecified options that apply, including none of the above. Participants were also given an other choice, which allowed them to provide open‐ended answers. Across participant categories, the surveys differed only in the demographic questions. For patients, we asked questions regarding age, sex, race, highest education, relationship status, living situation, access to mobile communication, and chief complaint. For caregivers, we asked questions regarding age, relationship to patient, and frequency of patient contact. For physicians, we asked for sex and years of experience practicing emergency medicine. Prior to administration, the survey was pretested with 10 patients and revised to improve reliability and comprehensibility.

Survey Administration

Participants were screened and enrolled during 5‐ to 10‐hour blocks that were chosen by the research associate. Sampling was balanced between weekdays and weekends and between daytime and evening hours. The research associate typically took 5 minutes to conduct the survey in person with each participant and recorded all responses directly into an electronic file. The research associate made every effort to conduct all surveys in a private area without others present to reduce reporting biases.

Analysis

Participant descriptor and response profiles for perceived factors contributing to ED visits and interventions to potentially prevent them were first visually examined and described. Summary statistics were calculated and displayed as number (percentage) for categorical data or mean (standard deviation [SD]) for continuous data. For each individual item, patient‐physician and patient‐caregiver dyads were considered concordant if they both agreed on either the presence or absence of a given factor. To quantify dyad concordance, we calculated weighted statistics for concordance in each individual item and the agreement rate for concordance in each individual item.[12] To determine the relative additional contribution of caregivers and physicians, we calculated and displayed the percentage of factors identified by caregivers and physicians when the patient did not identify them. All data were analyzed using Stata 10.0 (StataCorp, College Station, TX).

RESULTS

Participant Characteristics

We surveyed 135 patients who had been discharged from the hospital within the last 30 days (Table 1). The number of days since discharge ranged from 1 to 30, with a mean of 12 (SD 9) days. Forty‐four percent of cases presented to the ED within 7 days of the last discharge. Patients represented a wide age range from 18 to 96 years, with 61% under 65 years of age. Around a third (31%) were black, and 44% had no college education. Most (65%) were not currently married, the majority lived in the community (93%), and 63% live with at least 1 other person. Frequent ED chief complaints included chest pain or shortness of breath (24%), musculoskeletal pain (20%), and weakness (13%). To achieve 135 patient‐physician dyads, we surveyed 22 unique emergency physicians, with each individual physician completing between 1 and 17 surveys and the median completion of 5 surveys. The mean number of years in practice was 12 (SD 9). We also surveyed 49 unique patient caregivers, who were between 20 and 86 years of age (mean age, 52 years [SD 14]). Eighty‐eight percent of caregivers were family members, 8% friends, and 4% paid caregivers. The majority (63%) of caregivers lived with the patient and spent a mean of 11 hours (SD 7) per day with them.

Study Participant Characteristics
Participant CharacteristicsValue
  • NOTE: All data are presented as number (%) unless otherwise specified. Abbreviations: GED, General Education Development test; SD, standard deviation.

Patient characteristic, N=135 
Age, y, mean (SD)59 (18)
Sex, female74 (55)
Race 
Black41 (31)
White92 (69)
Asian1 (1)
Highest education 
Less than high school17 (13)
High school or GED41 (31)
At least some college75 (56)
Relationship 
Married47 (35)
Single58 (43)
Separated/widowed29 (21)
Living situation 
Alone40 (30)
With 1 other49 (36)
With multiple family members37 (27)
Nursing home/assisted living9 (7)
Access to communication, personal mobile phone110 (81)
Chief complaint 
Chest pain/shortness of breath32 (24)
Musculoskeletal pain27 (20
Weakness18 (13)
Abdominal pain/nausea/vomiting14 (10)
Postoperative complaint12 (9)
Headache5 (4)
Other27 (20)
Caregiver characteristic, N=49 
Age, y, mean (SD)52 (13)
Relationship to patient 
Family member43 (88)
Friend4 (8)
Paid caregiver2 (4)
Frequency of patient contact 
Lives with patient31 (63)
Waking hours per day with patient, mean (SD)11 (7)
Physician characteristic, N=22 
Sex 
Female7 (30)
Male15 (70)
Years practicing emergency medicine, mean (SD)11 (9)

Factors Contributing to Need for Acute Care Within 30 Days of Hospital Discharge

Overall, 89% of patients, 87% of emergency physicians, and 96% of caregivers identified at least 1 factor contributing to the return ED visit (Table 2). Patient‐physician concordances in factors contributing to early ED care were generally poor, with weighted statistics ranging from 0.02 to 0.33 and agreement rates ranging from 59% to 93%. Patient‐caregiver concordances in factors contributing to early ED care were generally better, with weighted statistics ranging from 0.05 to 0.68 and agreement rates ranging from 78% to 96%.

Stakeholder Perceptions and Concordances of Factors Contributing to Early Acute Care Visit and Potential Ways to Prevent It
 Patient Report, N=135Physician Report, N=135Caregiver Report, N=49Patient‐Physician ConcordancePatient Caregiver Concordance
n%n%n% Agreement % Agreement %
  • NOTE: data represents the weighted kappa statistic.

Factors contributing to early acute care
Issues related to prior hospitalization9268886536730.33700.5178
Progression of chronic disease or medical condition5641604422450.15590.5880
Missed doses or not taking prescribed medications9775240.34930.392
Not enough support at home751511240.02850.0590
Fall or unsteadiness when walking12964480.05880.6596
Side effects of current medication2619547140.21830.6890
Potential ways to prevent early acute care visit
Improved discharge care instructions13101713360.09790.4692
Review of medications1310755100.08850.5582
Home health visits972116240.19840.0394
Follow‐up appointment with primary care doctor14102921000.0874  
Follow‐up appointment with specialist10728215100.05750.3388

Both physicians and caregivers identified factors contributing to ED visits when patients did not (Table 3). Specifically, they identified issues related to prior hospitalization contributing to the ED visit between 42% and 45% of the time when patients did not. Physicians identified progression of chronic disease or medical condition 38% of the time when the patient did not, compared to caregivers, who identified it 23% of the time patients did not. Physicians also indicated that not enough support at home as contributing to ED visits 11% of the time patents did not, compared to a 4% increase when caregivers were asked. Other reasons were reported through free text by 20% of patients, 16% of emergency physicians, and 22% of caregivers. Across all stakeholders, around one‐third (27%31%) of these other factors related to postoperative complications, and 27% to 44% related to the perception of being discharged too early.

Factors and Potential Ways to Prevent Early Acute Care Identified by Physicians and Caregivers When Not Identified by Patients
 If Patient Did Not Report
Physician ReportCaregiver Report
  • NOTE: Frequencies and percentages are reported as n (%).

Factors contributing to early acute care  
Issues related to prior hospitalization18 (42)9 (45)
Progression of disease or medical condition30 (38)7 (23)
Missed doses or not taking prescribed medications4 (3)1 (2)
Not enough support at home14 (11)2 (4)
Fall or unsteadiness when walking5 (4)2 (4)
Side effects of current medication1 (1)0
Potential ways to prevent early acute care visit  
Improved discharge care instructions16 (13)1 (2)
Review of medications7 (6)2 (5)
Home health visits17 (13)2 (4)
Follow‐up appointment with primary care doctor25 (21)0
Follow‐up appointment with specialist25 (20)3 (7)

Potential Ways to Prevent Early Acute Care Within 30 Days of Hospital Discharge

Overall, 56% of patients, 55% of emergency physicians, and 49% of caregivers selected at least 1 intervention that could have potentially prevented the ED visit. However, no single intervention was identified by more than one‐fifth of participants (Table 2). Around 10% of patients identified either improved discharge instructions, review of medications, and follow‐up care with primary care provider as potential ways to prevent ED visits. Physicians identified both follow‐up with a primary care provider and specialist around 21% of the time as potential preventive interventions. Patient‐physician concordances in potential ways to prevent ED care were extremely poor, with weighted statistics ranging from 0.08 to 0.19 and agreement rates ranging from 74% to 85%. Patient‐caregiver concordances in potential ways to prevent ED care again were generally better, with weighted statistics ranging from 0.03 to 0.55 and agreement rates ranging from 82% to 94%.

Other potential interventions were reported by 16% of patients, 10% of emergency physicians, and 10% of caregivers. From patients, other interventions related to staying in the hospital longer on last admission and better medication instructions from last admission. Other interventions reported by physicians included home physical therapy, improved primary care provision, and more home support. Physicians, but not caregivers, more frequently identified potentially useful interventions when patients did not (Table 3). Other interventions reported by caregivers included staying in the hospital longer, improved patient activity, and better medications.

DISCUSSION

Several findings from this study can improve the understanding of what factors influence the utilization of the ED soon after inpatient discharge and what interventions could potentially prevent them. Consistent with our hypothesis, there are significant discordances between patients, their caregivers, and emergency physicians. Additionally, emergency physicians and caregivers were able to identify factors and potential opportunities for prevention a significant, albeit variable, amount of time the patients did not. Perhaps not surprisingly, we found that across stakeholders, the majority of ED visits are perceived as related to issues from the prior hospitalization or progression of chronic disease or medical condition. Of some concern, we found that less than half of patients, physicians, and caregivers could identify an intervention to potentially prevent the ED visit.

The large discordances between patients' and physicians' perceptions in our study were similar to those found in prior studies from primary care.[13, 14, 15] No prior study has examined discordances in emergency care or regarding perceptions about care‐transition difficulties. Feigenbaum et al.[10] interviewed patients, caregivers, and physicians to create composite definitions of potentially preventable readmissions. They did not, however, look at how these perceptions differ or describe the relative contribution of individual stakeholders to overall definitions. The discordances between patient and emergency physician perceptions may be due to a couple of potential causes. First, emergency physicians may have greater access to medical history data than patients, allowing them to develop more objective assessments. This is supported by our finding that physicians identified factors when patients did not. Second, patients may understand certain care‐transition difficulties that physicians do not elicit from history taking. This may be especially apparent in the emergency setting, where physicians are time limited and do not have established care relationships with patients.

The moderate agreement between patient and caregiver perceptions are similar to a couple of studies examining perceived quality of life among patients.[16, 17] These discordances can be due to a couple of potential causes. First, caregivers may witness deficits or transition difficulties that the patient may not. This may be particularly true for caregivers who are providing substantial support in managing the patient's healthcare or for patients with cognitive impairment. Second, caregivers may not know the patient history well enough to know what specific issues affect the patient. This would be likely when caregivers do not live with patients or serve a central role in caregiving.

The overwhelming perception that the majority of ED visits are related to issues from the prior hospitalization or progression of chronic disease or medical condition suggests that, by and large, acute care needs soon after hospital discharges are not new unrelated medical issues, and thus theoretically could be predicted and prevented. This is consistent with prior prediction models showing that chronic medical comorbidities have strong associations with hospital readmission.[18, 19] It also supports probing care issues with patients prior to hospital discharge.[20]

The finding that less than half of patients, physicians, or caregivers could identify an intervention to potentially prevent the ED visit echoes prior research, indicating that only a minority of readmissions may be truly preventable,[21] and suggests that there may not be obvious needs that can be addressed to prevent acute care visits. An alternative interpretation is that the healthcare system does not currently have a suitable alternative to meet the perceived needs of patients. Despite this, patients occasionally perceived that better discharge instructions, review of medications, and sooner follow‐up appointments with a primary care doctor could have potentially prevented their ED visit. This is consistent with numerous prior studies and supports better transition‐of‐care programs.

Our study had a small sample size, which results in wide confidence intervals on all point estimates of percentages, limiting the precision of our findings. No medical charts were reviewed to determine the medical reasons for the index admission, the prior course of care, or subsequent hospital course after emergency care, limiting our ability to link perceptions with actual past hospital experiences or compare differences in perceptions by subsequent readmission. Another limitation is a lack of generalizability of our findings to other patients, hospitals, or regions. Our patient population was largely white and English speaking only for participation in this study. Also, our hospital ED admits an average of 48% of patients, which is higher than most hospitals. We enrolled a convenience sample as opposed to a consecutive sample of patients due to limitations in research associate staffing, potentially biasing our sample. We attempted to minimize this bias by scheduling shifts across days and time periods. We did not systematically collect the number of patients or caregivers who refused participation, but believe that it was less than 5% of those approached. Other limitations include possible reporting biases associated with in‐person interviews, which we attempted to minimize by conducting all surveys in private.

SUMMARY

Identifying needs in patients who utilize the ED soon after being discharged from inpatient care is essential for planning appropriate care‐transition interventions. Our findings suggest that multiple stakeholders may be necessary to fully elicit targets for effective care‐transition programs.

 

Disclosure: Nothing to report.

Files
References
  1. Medicare Payment Advisory Commission. Payment policy for inpatient readmissions. In: Report to the congress: promoting greater efficiency in Medicare. Available at: http://www.medpac.gov/chapters/Jun07_Ch05.pdf. Accessed February 9, 2010.
  2. Jack BW, Chetty VK, Anthony D, et al. A reengineered hospital discharge program to decrease rehospitalization: a randomized trial. Ann Intern Med. 2009;150(3):178187.
  3. Hasan O, Meltzer DO, Shaykevich SA, et al. Hospital readmission in general medicine patients: a prediction model. J Gen Intern Med. 2010;25(3):211219.
  4. Rennke S, Nguyen OK, Shoeb MH, Magan Y, Wachter RM, Ranji SR. Hospital‐initiated transitional care interventions as a patient safety strategy: a systematic review. Ann Intern Med. 2013;158(5 pt 2):433440.
  5. Benbassat J, Taragin M. Hospital readmissions as a measure of quality of health care: advantages and limitations. Arch Intern Med. 2000;160(8):10741081.
  6. Rising KL, White LF, Fernandez WG, Boutwell AE. Emergency department visits after hospital discharge: a missing part of the equation. Ann Emerg Med. 2013;62(2):145150.
  7. Vashi AA, Fox JP, Carr BG, et al. Use of hospital‐based acute care among patients recently discharged from the hospital. JAMA. 2013;309(4):364371.
  8. Soler RS, Juvinya Canal D, Noguer CB, Poch CG, Brugada Motge N, Del Mar Garcia Gil M. Continuity of care and monitoring pain after discharge: patient perspective. J Adv Nurs. 2010;66(1):4048.
  9. Kangovi S, Grande D, Meehan P, Mitra N, Shannon R, Long JA. Perceptions of readmitted patients on the transition from hospital to home. J Hosp Med. 2012;7(9):709712.
  10. Feigenbaum P, Neuwirth E, Trowbridge L, et al. Factors contributing to all‐cause 30‐day readmissions: a structured case series across 18 hospitals. Med Care. 2012;50(7):599605.
  11. Snow V, Beck D, Budnitz T, et al. Transition of care consensus policy statement, American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatric Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine. J Gen Intern Med. 2009;24(8):971976.
  12. Cicchetti DV, Feinstein AR. J Clin Epidemiol. 1990;43(6):551558.
  13. Starfield B, Steinwachs D, Morris I, Bause G, Siebert S, Westin C. Patient‐doctor agreement about problems needing follow‐up visit. JAMA. 1979;242(4):344346.
  14. Britt H, Harris M, Driver B, Bridges‐Webb C, O'Toole B, Neary S. Reasons for encounter and diagnosed health problems: convergence between doctors and patients. Fam Pract. 1992;9(2):191194.
  15. Greene MG, Adelman RD, Charon R, Friedmann E. Concordance between physicians and their older and younger patients in the primary care medical encounter. Gerontologist. 1989;29(6):808813.
  16. Giovannetti ER, Reider L, Wolff JL, et al. Do older patients and their family caregivers agree about the quality of chronic illness care? Int J Qual Health Care. 2013;25(5):515524.
  17. Tamim H, McCusker J, Dendukuri N. Proxy reporting of quality of life using the EQ‐5D. Med Care. 2002;40(12):11861195.
  18. Kangovi S, Grande D. Hospital readmissions—not just a measure of quality. JAMA. 2011;306(16):17961797.
  19. Allaudeen N, Vidyarthi A, Maselli J, Auerbach A. Redefining readmission risk factors for general medicine patients. J Hosp Med. 2011;6(2):5460.
  20. Moore C, McGinn T, Halm E. Tying up loose ends: discharging patients with unresolved medical issues. Arch Intern Med. 2007;167(12):13051311.
  21. Donze J, Aujesky D, Williams D, Schnipper JL. Potentially avoidable 30‐day hospital readmissions in medical patients: derivation and validation of a prediction model. JAMA Intern Med. 2013;173(8):632638.
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Reducing hospital admissions within 30 days of inpatient discharge is the focus of numerous policies, incentives, and payment models, led by the Centers for Medicare & Medicaid Services.[1] Accordingly, care‐transition programs have been developed and are found to be effective in reducing hospital readmissions.[2, 3] Interestingly, emergency department (ED) visits have not been included in this definition of readmission, no programs have focused specifically on reducing ED visits,[4] and some have even increased ED visits.[5]

The prevalence and costs associated with ED care within 30 days of hospital discharge are not insignificant. Up to 24% of discharged patients present to the ED within 30 days, among whom only 50% are readmitted.[6] ED care alone accounts for nearly 40% of all costs in the acute postdischarge period.[7] This is in addition to the costs associated with readmissions from the ED, which are the result of disposition decisions made by ED clinicians.

To begin to build effective care‐transition programs to reduce ED visits after inpatient discharge, greater understanding is needed on what factors influence the utilization of the ED and what potential interventions could have prevented them. Studies from inpatient populations have been successful in eliciting these factors through stakeholder interviews.[8, 9, 10] In fact, the American College of Physicians and Society of Hospital Medicine emphasize involvement of the patient and family members in plans of care.[11] No prior studies have used stakeholders to inform care‐transition models for patients who return to the ED within 30 days of inpatient discharge.

Therefore, the primary objective of this study was to collect various stakeholder perspectives to improve the understanding of factors associated with ED visits within 30 days of hospital discharge and identify potentially useful interventions to prevent them. We hypothesized that there would be significant discordances between patients, their caregivers, and emergency physicians. Findings from this study could inform an expanded framework for understanding the complexity of care needs after hospital discharge and suggest interventions to improve health outcomes and to reduce healthcare costs.

METHODS

Setting

The study took place in the ED of a 525‐bed urban teaching hospital in Pittsburgh, Pennsylvania, with 55,000 annual ED visits and 26,137 hospital admissions per year. Overall demographics of patients presenting to this ED in 2012 were 82% white, 17% black, and 0.3% Asian. The institutional review board of the University of Pittsburgh approved this study.

Participants

Patients were eligible to participate if they: (1) had the capacity to complete an interview, as determined by the attending emergency physician based on their exam; and (2) presented to the ED within 30 days of a prior discharge from any affiliate hospital. Eligible participants were identified by a trained research associate (J.H.) on the day of the ED visit by screening the electronic medical record. We excluded 2 patients from analysis who had both been to the ED prior to a readmission and had already completed the survey in the last 30 days. Caregivers were eligible to participate if they: (1) were in the ED at the time of patient evaluation, and (2) were identified by participating patients. ED physicians were eligible to participate if they had seen and evaluated the enrolled patient and were the attending staff physician. Eligible caregivers and physicians underwent separate informed consent.

Development of Survey Instrument

A collaborative team of physicians and hospital administrators used a defined conceptual framework,[9] literature search, and pilot administration to construct a survey to elucidate factors potentially contributing to ED visits within 30 days of hospital discharge and interventions that could have potentially prevented the ED visit. All participants (patients, caregivers, and physicians) were asked to complete the following questions: (1) In your opinion, is your/the patient's ED visit today directly related to your/their last hospitalization? (2) In your opinion, did any of the following contribute to your/the patient's ED visit today? (3) In your opinion, which of the following could have prevented your/the patient's ED visit today? For questions 2 and 3, participants were asked to mark any and all prespecified options that apply, including none of the above. Participants were also given an other choice, which allowed them to provide open‐ended answers. Across participant categories, the surveys differed only in the demographic questions. For patients, we asked questions regarding age, sex, race, highest education, relationship status, living situation, access to mobile communication, and chief complaint. For caregivers, we asked questions regarding age, relationship to patient, and frequency of patient contact. For physicians, we asked for sex and years of experience practicing emergency medicine. Prior to administration, the survey was pretested with 10 patients and revised to improve reliability and comprehensibility.

Survey Administration

Participants were screened and enrolled during 5‐ to 10‐hour blocks that were chosen by the research associate. Sampling was balanced between weekdays and weekends and between daytime and evening hours. The research associate typically took 5 minutes to conduct the survey in person with each participant and recorded all responses directly into an electronic file. The research associate made every effort to conduct all surveys in a private area without others present to reduce reporting biases.

Analysis

Participant descriptor and response profiles for perceived factors contributing to ED visits and interventions to potentially prevent them were first visually examined and described. Summary statistics were calculated and displayed as number (percentage) for categorical data or mean (standard deviation [SD]) for continuous data. For each individual item, patient‐physician and patient‐caregiver dyads were considered concordant if they both agreed on either the presence or absence of a given factor. To quantify dyad concordance, we calculated weighted statistics for concordance in each individual item and the agreement rate for concordance in each individual item.[12] To determine the relative additional contribution of caregivers and physicians, we calculated and displayed the percentage of factors identified by caregivers and physicians when the patient did not identify them. All data were analyzed using Stata 10.0 (StataCorp, College Station, TX).

RESULTS

Participant Characteristics

We surveyed 135 patients who had been discharged from the hospital within the last 30 days (Table 1). The number of days since discharge ranged from 1 to 30, with a mean of 12 (SD 9) days. Forty‐four percent of cases presented to the ED within 7 days of the last discharge. Patients represented a wide age range from 18 to 96 years, with 61% under 65 years of age. Around a third (31%) were black, and 44% had no college education. Most (65%) were not currently married, the majority lived in the community (93%), and 63% live with at least 1 other person. Frequent ED chief complaints included chest pain or shortness of breath (24%), musculoskeletal pain (20%), and weakness (13%). To achieve 135 patient‐physician dyads, we surveyed 22 unique emergency physicians, with each individual physician completing between 1 and 17 surveys and the median completion of 5 surveys. The mean number of years in practice was 12 (SD 9). We also surveyed 49 unique patient caregivers, who were between 20 and 86 years of age (mean age, 52 years [SD 14]). Eighty‐eight percent of caregivers were family members, 8% friends, and 4% paid caregivers. The majority (63%) of caregivers lived with the patient and spent a mean of 11 hours (SD 7) per day with them.

Study Participant Characteristics
Participant CharacteristicsValue
  • NOTE: All data are presented as number (%) unless otherwise specified. Abbreviations: GED, General Education Development test; SD, standard deviation.

Patient characteristic, N=135 
Age, y, mean (SD)59 (18)
Sex, female74 (55)
Race 
Black41 (31)
White92 (69)
Asian1 (1)
Highest education 
Less than high school17 (13)
High school or GED41 (31)
At least some college75 (56)
Relationship 
Married47 (35)
Single58 (43)
Separated/widowed29 (21)
Living situation 
Alone40 (30)
With 1 other49 (36)
With multiple family members37 (27)
Nursing home/assisted living9 (7)
Access to communication, personal mobile phone110 (81)
Chief complaint 
Chest pain/shortness of breath32 (24)
Musculoskeletal pain27 (20
Weakness18 (13)
Abdominal pain/nausea/vomiting14 (10)
Postoperative complaint12 (9)
Headache5 (4)
Other27 (20)
Caregiver characteristic, N=49 
Age, y, mean (SD)52 (13)
Relationship to patient 
Family member43 (88)
Friend4 (8)
Paid caregiver2 (4)
Frequency of patient contact 
Lives with patient31 (63)
Waking hours per day with patient, mean (SD)11 (7)
Physician characteristic, N=22 
Sex 
Female7 (30)
Male15 (70)
Years practicing emergency medicine, mean (SD)11 (9)

Factors Contributing to Need for Acute Care Within 30 Days of Hospital Discharge

Overall, 89% of patients, 87% of emergency physicians, and 96% of caregivers identified at least 1 factor contributing to the return ED visit (Table 2). Patient‐physician concordances in factors contributing to early ED care were generally poor, with weighted statistics ranging from 0.02 to 0.33 and agreement rates ranging from 59% to 93%. Patient‐caregiver concordances in factors contributing to early ED care were generally better, with weighted statistics ranging from 0.05 to 0.68 and agreement rates ranging from 78% to 96%.

Stakeholder Perceptions and Concordances of Factors Contributing to Early Acute Care Visit and Potential Ways to Prevent It
 Patient Report, N=135Physician Report, N=135Caregiver Report, N=49Patient‐Physician ConcordancePatient Caregiver Concordance
n%n%n% Agreement % Agreement %
  • NOTE: data represents the weighted kappa statistic.

Factors contributing to early acute care
Issues related to prior hospitalization9268886536730.33700.5178
Progression of chronic disease or medical condition5641604422450.15590.5880
Missed doses or not taking prescribed medications9775240.34930.392
Not enough support at home751511240.02850.0590
Fall or unsteadiness when walking12964480.05880.6596
Side effects of current medication2619547140.21830.6890
Potential ways to prevent early acute care visit
Improved discharge care instructions13101713360.09790.4692
Review of medications1310755100.08850.5582
Home health visits972116240.19840.0394
Follow‐up appointment with primary care doctor14102921000.0874  
Follow‐up appointment with specialist10728215100.05750.3388

Both physicians and caregivers identified factors contributing to ED visits when patients did not (Table 3). Specifically, they identified issues related to prior hospitalization contributing to the ED visit between 42% and 45% of the time when patients did not. Physicians identified progression of chronic disease or medical condition 38% of the time when the patient did not, compared to caregivers, who identified it 23% of the time patients did not. Physicians also indicated that not enough support at home as contributing to ED visits 11% of the time patents did not, compared to a 4% increase when caregivers were asked. Other reasons were reported through free text by 20% of patients, 16% of emergency physicians, and 22% of caregivers. Across all stakeholders, around one‐third (27%31%) of these other factors related to postoperative complications, and 27% to 44% related to the perception of being discharged too early.

Factors and Potential Ways to Prevent Early Acute Care Identified by Physicians and Caregivers When Not Identified by Patients
 If Patient Did Not Report
Physician ReportCaregiver Report
  • NOTE: Frequencies and percentages are reported as n (%).

Factors contributing to early acute care  
Issues related to prior hospitalization18 (42)9 (45)
Progression of disease or medical condition30 (38)7 (23)
Missed doses or not taking prescribed medications4 (3)1 (2)
Not enough support at home14 (11)2 (4)
Fall or unsteadiness when walking5 (4)2 (4)
Side effects of current medication1 (1)0
Potential ways to prevent early acute care visit  
Improved discharge care instructions16 (13)1 (2)
Review of medications7 (6)2 (5)
Home health visits17 (13)2 (4)
Follow‐up appointment with primary care doctor25 (21)0
Follow‐up appointment with specialist25 (20)3 (7)

Potential Ways to Prevent Early Acute Care Within 30 Days of Hospital Discharge

Overall, 56% of patients, 55% of emergency physicians, and 49% of caregivers selected at least 1 intervention that could have potentially prevented the ED visit. However, no single intervention was identified by more than one‐fifth of participants (Table 2). Around 10% of patients identified either improved discharge instructions, review of medications, and follow‐up care with primary care provider as potential ways to prevent ED visits. Physicians identified both follow‐up with a primary care provider and specialist around 21% of the time as potential preventive interventions. Patient‐physician concordances in potential ways to prevent ED care were extremely poor, with weighted statistics ranging from 0.08 to 0.19 and agreement rates ranging from 74% to 85%. Patient‐caregiver concordances in potential ways to prevent ED care again were generally better, with weighted statistics ranging from 0.03 to 0.55 and agreement rates ranging from 82% to 94%.

Other potential interventions were reported by 16% of patients, 10% of emergency physicians, and 10% of caregivers. From patients, other interventions related to staying in the hospital longer on last admission and better medication instructions from last admission. Other interventions reported by physicians included home physical therapy, improved primary care provision, and more home support. Physicians, but not caregivers, more frequently identified potentially useful interventions when patients did not (Table 3). Other interventions reported by caregivers included staying in the hospital longer, improved patient activity, and better medications.

DISCUSSION

Several findings from this study can improve the understanding of what factors influence the utilization of the ED soon after inpatient discharge and what interventions could potentially prevent them. Consistent with our hypothesis, there are significant discordances between patients, their caregivers, and emergency physicians. Additionally, emergency physicians and caregivers were able to identify factors and potential opportunities for prevention a significant, albeit variable, amount of time the patients did not. Perhaps not surprisingly, we found that across stakeholders, the majority of ED visits are perceived as related to issues from the prior hospitalization or progression of chronic disease or medical condition. Of some concern, we found that less than half of patients, physicians, and caregivers could identify an intervention to potentially prevent the ED visit.

The large discordances between patients' and physicians' perceptions in our study were similar to those found in prior studies from primary care.[13, 14, 15] No prior study has examined discordances in emergency care or regarding perceptions about care‐transition difficulties. Feigenbaum et al.[10] interviewed patients, caregivers, and physicians to create composite definitions of potentially preventable readmissions. They did not, however, look at how these perceptions differ or describe the relative contribution of individual stakeholders to overall definitions. The discordances between patient and emergency physician perceptions may be due to a couple of potential causes. First, emergency physicians may have greater access to medical history data than patients, allowing them to develop more objective assessments. This is supported by our finding that physicians identified factors when patients did not. Second, patients may understand certain care‐transition difficulties that physicians do not elicit from history taking. This may be especially apparent in the emergency setting, where physicians are time limited and do not have established care relationships with patients.

The moderate agreement between patient and caregiver perceptions are similar to a couple of studies examining perceived quality of life among patients.[16, 17] These discordances can be due to a couple of potential causes. First, caregivers may witness deficits or transition difficulties that the patient may not. This may be particularly true for caregivers who are providing substantial support in managing the patient's healthcare or for patients with cognitive impairment. Second, caregivers may not know the patient history well enough to know what specific issues affect the patient. This would be likely when caregivers do not live with patients or serve a central role in caregiving.

The overwhelming perception that the majority of ED visits are related to issues from the prior hospitalization or progression of chronic disease or medical condition suggests that, by and large, acute care needs soon after hospital discharges are not new unrelated medical issues, and thus theoretically could be predicted and prevented. This is consistent with prior prediction models showing that chronic medical comorbidities have strong associations with hospital readmission.[18, 19] It also supports probing care issues with patients prior to hospital discharge.[20]

The finding that less than half of patients, physicians, or caregivers could identify an intervention to potentially prevent the ED visit echoes prior research, indicating that only a minority of readmissions may be truly preventable,[21] and suggests that there may not be obvious needs that can be addressed to prevent acute care visits. An alternative interpretation is that the healthcare system does not currently have a suitable alternative to meet the perceived needs of patients. Despite this, patients occasionally perceived that better discharge instructions, review of medications, and sooner follow‐up appointments with a primary care doctor could have potentially prevented their ED visit. This is consistent with numerous prior studies and supports better transition‐of‐care programs.

Our study had a small sample size, which results in wide confidence intervals on all point estimates of percentages, limiting the precision of our findings. No medical charts were reviewed to determine the medical reasons for the index admission, the prior course of care, or subsequent hospital course after emergency care, limiting our ability to link perceptions with actual past hospital experiences or compare differences in perceptions by subsequent readmission. Another limitation is a lack of generalizability of our findings to other patients, hospitals, or regions. Our patient population was largely white and English speaking only for participation in this study. Also, our hospital ED admits an average of 48% of patients, which is higher than most hospitals. We enrolled a convenience sample as opposed to a consecutive sample of patients due to limitations in research associate staffing, potentially biasing our sample. We attempted to minimize this bias by scheduling shifts across days and time periods. We did not systematically collect the number of patients or caregivers who refused participation, but believe that it was less than 5% of those approached. Other limitations include possible reporting biases associated with in‐person interviews, which we attempted to minimize by conducting all surveys in private.

SUMMARY

Identifying needs in patients who utilize the ED soon after being discharged from inpatient care is essential for planning appropriate care‐transition interventions. Our findings suggest that multiple stakeholders may be necessary to fully elicit targets for effective care‐transition programs.

 

Disclosure: Nothing to report.

Reducing hospital admissions within 30 days of inpatient discharge is the focus of numerous policies, incentives, and payment models, led by the Centers for Medicare & Medicaid Services.[1] Accordingly, care‐transition programs have been developed and are found to be effective in reducing hospital readmissions.[2, 3] Interestingly, emergency department (ED) visits have not been included in this definition of readmission, no programs have focused specifically on reducing ED visits,[4] and some have even increased ED visits.[5]

The prevalence and costs associated with ED care within 30 days of hospital discharge are not insignificant. Up to 24% of discharged patients present to the ED within 30 days, among whom only 50% are readmitted.[6] ED care alone accounts for nearly 40% of all costs in the acute postdischarge period.[7] This is in addition to the costs associated with readmissions from the ED, which are the result of disposition decisions made by ED clinicians.

To begin to build effective care‐transition programs to reduce ED visits after inpatient discharge, greater understanding is needed on what factors influence the utilization of the ED and what potential interventions could have prevented them. Studies from inpatient populations have been successful in eliciting these factors through stakeholder interviews.[8, 9, 10] In fact, the American College of Physicians and Society of Hospital Medicine emphasize involvement of the patient and family members in plans of care.[11] No prior studies have used stakeholders to inform care‐transition models for patients who return to the ED within 30 days of inpatient discharge.

Therefore, the primary objective of this study was to collect various stakeholder perspectives to improve the understanding of factors associated with ED visits within 30 days of hospital discharge and identify potentially useful interventions to prevent them. We hypothesized that there would be significant discordances between patients, their caregivers, and emergency physicians. Findings from this study could inform an expanded framework for understanding the complexity of care needs after hospital discharge and suggest interventions to improve health outcomes and to reduce healthcare costs.

METHODS

Setting

The study took place in the ED of a 525‐bed urban teaching hospital in Pittsburgh, Pennsylvania, with 55,000 annual ED visits and 26,137 hospital admissions per year. Overall demographics of patients presenting to this ED in 2012 were 82% white, 17% black, and 0.3% Asian. The institutional review board of the University of Pittsburgh approved this study.

Participants

Patients were eligible to participate if they: (1) had the capacity to complete an interview, as determined by the attending emergency physician based on their exam; and (2) presented to the ED within 30 days of a prior discharge from any affiliate hospital. Eligible participants were identified by a trained research associate (J.H.) on the day of the ED visit by screening the electronic medical record. We excluded 2 patients from analysis who had both been to the ED prior to a readmission and had already completed the survey in the last 30 days. Caregivers were eligible to participate if they: (1) were in the ED at the time of patient evaluation, and (2) were identified by participating patients. ED physicians were eligible to participate if they had seen and evaluated the enrolled patient and were the attending staff physician. Eligible caregivers and physicians underwent separate informed consent.

Development of Survey Instrument

A collaborative team of physicians and hospital administrators used a defined conceptual framework,[9] literature search, and pilot administration to construct a survey to elucidate factors potentially contributing to ED visits within 30 days of hospital discharge and interventions that could have potentially prevented the ED visit. All participants (patients, caregivers, and physicians) were asked to complete the following questions: (1) In your opinion, is your/the patient's ED visit today directly related to your/their last hospitalization? (2) In your opinion, did any of the following contribute to your/the patient's ED visit today? (3) In your opinion, which of the following could have prevented your/the patient's ED visit today? For questions 2 and 3, participants were asked to mark any and all prespecified options that apply, including none of the above. Participants were also given an other choice, which allowed them to provide open‐ended answers. Across participant categories, the surveys differed only in the demographic questions. For patients, we asked questions regarding age, sex, race, highest education, relationship status, living situation, access to mobile communication, and chief complaint. For caregivers, we asked questions regarding age, relationship to patient, and frequency of patient contact. For physicians, we asked for sex and years of experience practicing emergency medicine. Prior to administration, the survey was pretested with 10 patients and revised to improve reliability and comprehensibility.

Survey Administration

Participants were screened and enrolled during 5‐ to 10‐hour blocks that were chosen by the research associate. Sampling was balanced between weekdays and weekends and between daytime and evening hours. The research associate typically took 5 minutes to conduct the survey in person with each participant and recorded all responses directly into an electronic file. The research associate made every effort to conduct all surveys in a private area without others present to reduce reporting biases.

Analysis

Participant descriptor and response profiles for perceived factors contributing to ED visits and interventions to potentially prevent them were first visually examined and described. Summary statistics were calculated and displayed as number (percentage) for categorical data or mean (standard deviation [SD]) for continuous data. For each individual item, patient‐physician and patient‐caregiver dyads were considered concordant if they both agreed on either the presence or absence of a given factor. To quantify dyad concordance, we calculated weighted statistics for concordance in each individual item and the agreement rate for concordance in each individual item.[12] To determine the relative additional contribution of caregivers and physicians, we calculated and displayed the percentage of factors identified by caregivers and physicians when the patient did not identify them. All data were analyzed using Stata 10.0 (StataCorp, College Station, TX).

RESULTS

Participant Characteristics

We surveyed 135 patients who had been discharged from the hospital within the last 30 days (Table 1). The number of days since discharge ranged from 1 to 30, with a mean of 12 (SD 9) days. Forty‐four percent of cases presented to the ED within 7 days of the last discharge. Patients represented a wide age range from 18 to 96 years, with 61% under 65 years of age. Around a third (31%) were black, and 44% had no college education. Most (65%) were not currently married, the majority lived in the community (93%), and 63% live with at least 1 other person. Frequent ED chief complaints included chest pain or shortness of breath (24%), musculoskeletal pain (20%), and weakness (13%). To achieve 135 patient‐physician dyads, we surveyed 22 unique emergency physicians, with each individual physician completing between 1 and 17 surveys and the median completion of 5 surveys. The mean number of years in practice was 12 (SD 9). We also surveyed 49 unique patient caregivers, who were between 20 and 86 years of age (mean age, 52 years [SD 14]). Eighty‐eight percent of caregivers were family members, 8% friends, and 4% paid caregivers. The majority (63%) of caregivers lived with the patient and spent a mean of 11 hours (SD 7) per day with them.

Study Participant Characteristics
Participant CharacteristicsValue
  • NOTE: All data are presented as number (%) unless otherwise specified. Abbreviations: GED, General Education Development test; SD, standard deviation.

Patient characteristic, N=135 
Age, y, mean (SD)59 (18)
Sex, female74 (55)
Race 
Black41 (31)
White92 (69)
Asian1 (1)
Highest education 
Less than high school17 (13)
High school or GED41 (31)
At least some college75 (56)
Relationship 
Married47 (35)
Single58 (43)
Separated/widowed29 (21)
Living situation 
Alone40 (30)
With 1 other49 (36)
With multiple family members37 (27)
Nursing home/assisted living9 (7)
Access to communication, personal mobile phone110 (81)
Chief complaint 
Chest pain/shortness of breath32 (24)
Musculoskeletal pain27 (20
Weakness18 (13)
Abdominal pain/nausea/vomiting14 (10)
Postoperative complaint12 (9)
Headache5 (4)
Other27 (20)
Caregiver characteristic, N=49 
Age, y, mean (SD)52 (13)
Relationship to patient 
Family member43 (88)
Friend4 (8)
Paid caregiver2 (4)
Frequency of patient contact 
Lives with patient31 (63)
Waking hours per day with patient, mean (SD)11 (7)
Physician characteristic, N=22 
Sex 
Female7 (30)
Male15 (70)
Years practicing emergency medicine, mean (SD)11 (9)

Factors Contributing to Need for Acute Care Within 30 Days of Hospital Discharge

Overall, 89% of patients, 87% of emergency physicians, and 96% of caregivers identified at least 1 factor contributing to the return ED visit (Table 2). Patient‐physician concordances in factors contributing to early ED care were generally poor, with weighted statistics ranging from 0.02 to 0.33 and agreement rates ranging from 59% to 93%. Patient‐caregiver concordances in factors contributing to early ED care were generally better, with weighted statistics ranging from 0.05 to 0.68 and agreement rates ranging from 78% to 96%.

Stakeholder Perceptions and Concordances of Factors Contributing to Early Acute Care Visit and Potential Ways to Prevent It
 Patient Report, N=135Physician Report, N=135Caregiver Report, N=49Patient‐Physician ConcordancePatient Caregiver Concordance
n%n%n% Agreement % Agreement %
  • NOTE: data represents the weighted kappa statistic.

Factors contributing to early acute care
Issues related to prior hospitalization9268886536730.33700.5178
Progression of chronic disease or medical condition5641604422450.15590.5880
Missed doses or not taking prescribed medications9775240.34930.392
Not enough support at home751511240.02850.0590
Fall or unsteadiness when walking12964480.05880.6596
Side effects of current medication2619547140.21830.6890
Potential ways to prevent early acute care visit
Improved discharge care instructions13101713360.09790.4692
Review of medications1310755100.08850.5582
Home health visits972116240.19840.0394
Follow‐up appointment with primary care doctor14102921000.0874  
Follow‐up appointment with specialist10728215100.05750.3388

Both physicians and caregivers identified factors contributing to ED visits when patients did not (Table 3). Specifically, they identified issues related to prior hospitalization contributing to the ED visit between 42% and 45% of the time when patients did not. Physicians identified progression of chronic disease or medical condition 38% of the time when the patient did not, compared to caregivers, who identified it 23% of the time patients did not. Physicians also indicated that not enough support at home as contributing to ED visits 11% of the time patents did not, compared to a 4% increase when caregivers were asked. Other reasons were reported through free text by 20% of patients, 16% of emergency physicians, and 22% of caregivers. Across all stakeholders, around one‐third (27%31%) of these other factors related to postoperative complications, and 27% to 44% related to the perception of being discharged too early.

Factors and Potential Ways to Prevent Early Acute Care Identified by Physicians and Caregivers When Not Identified by Patients
 If Patient Did Not Report
Physician ReportCaregiver Report
  • NOTE: Frequencies and percentages are reported as n (%).

Factors contributing to early acute care  
Issues related to prior hospitalization18 (42)9 (45)
Progression of disease or medical condition30 (38)7 (23)
Missed doses or not taking prescribed medications4 (3)1 (2)
Not enough support at home14 (11)2 (4)
Fall or unsteadiness when walking5 (4)2 (4)
Side effects of current medication1 (1)0
Potential ways to prevent early acute care visit  
Improved discharge care instructions16 (13)1 (2)
Review of medications7 (6)2 (5)
Home health visits17 (13)2 (4)
Follow‐up appointment with primary care doctor25 (21)0
Follow‐up appointment with specialist25 (20)3 (7)

Potential Ways to Prevent Early Acute Care Within 30 Days of Hospital Discharge

Overall, 56% of patients, 55% of emergency physicians, and 49% of caregivers selected at least 1 intervention that could have potentially prevented the ED visit. However, no single intervention was identified by more than one‐fifth of participants (Table 2). Around 10% of patients identified either improved discharge instructions, review of medications, and follow‐up care with primary care provider as potential ways to prevent ED visits. Physicians identified both follow‐up with a primary care provider and specialist around 21% of the time as potential preventive interventions. Patient‐physician concordances in potential ways to prevent ED care were extremely poor, with weighted statistics ranging from 0.08 to 0.19 and agreement rates ranging from 74% to 85%. Patient‐caregiver concordances in potential ways to prevent ED care again were generally better, with weighted statistics ranging from 0.03 to 0.55 and agreement rates ranging from 82% to 94%.

Other potential interventions were reported by 16% of patients, 10% of emergency physicians, and 10% of caregivers. From patients, other interventions related to staying in the hospital longer on last admission and better medication instructions from last admission. Other interventions reported by physicians included home physical therapy, improved primary care provision, and more home support. Physicians, but not caregivers, more frequently identified potentially useful interventions when patients did not (Table 3). Other interventions reported by caregivers included staying in the hospital longer, improved patient activity, and better medications.

DISCUSSION

Several findings from this study can improve the understanding of what factors influence the utilization of the ED soon after inpatient discharge and what interventions could potentially prevent them. Consistent with our hypothesis, there are significant discordances between patients, their caregivers, and emergency physicians. Additionally, emergency physicians and caregivers were able to identify factors and potential opportunities for prevention a significant, albeit variable, amount of time the patients did not. Perhaps not surprisingly, we found that across stakeholders, the majority of ED visits are perceived as related to issues from the prior hospitalization or progression of chronic disease or medical condition. Of some concern, we found that less than half of patients, physicians, and caregivers could identify an intervention to potentially prevent the ED visit.

The large discordances between patients' and physicians' perceptions in our study were similar to those found in prior studies from primary care.[13, 14, 15] No prior study has examined discordances in emergency care or regarding perceptions about care‐transition difficulties. Feigenbaum et al.[10] interviewed patients, caregivers, and physicians to create composite definitions of potentially preventable readmissions. They did not, however, look at how these perceptions differ or describe the relative contribution of individual stakeholders to overall definitions. The discordances between patient and emergency physician perceptions may be due to a couple of potential causes. First, emergency physicians may have greater access to medical history data than patients, allowing them to develop more objective assessments. This is supported by our finding that physicians identified factors when patients did not. Second, patients may understand certain care‐transition difficulties that physicians do not elicit from history taking. This may be especially apparent in the emergency setting, where physicians are time limited and do not have established care relationships with patients.

The moderate agreement between patient and caregiver perceptions are similar to a couple of studies examining perceived quality of life among patients.[16, 17] These discordances can be due to a couple of potential causes. First, caregivers may witness deficits or transition difficulties that the patient may not. This may be particularly true for caregivers who are providing substantial support in managing the patient's healthcare or for patients with cognitive impairment. Second, caregivers may not know the patient history well enough to know what specific issues affect the patient. This would be likely when caregivers do not live with patients or serve a central role in caregiving.

The overwhelming perception that the majority of ED visits are related to issues from the prior hospitalization or progression of chronic disease or medical condition suggests that, by and large, acute care needs soon after hospital discharges are not new unrelated medical issues, and thus theoretically could be predicted and prevented. This is consistent with prior prediction models showing that chronic medical comorbidities have strong associations with hospital readmission.[18, 19] It also supports probing care issues with patients prior to hospital discharge.[20]

The finding that less than half of patients, physicians, or caregivers could identify an intervention to potentially prevent the ED visit echoes prior research, indicating that only a minority of readmissions may be truly preventable,[21] and suggests that there may not be obvious needs that can be addressed to prevent acute care visits. An alternative interpretation is that the healthcare system does not currently have a suitable alternative to meet the perceived needs of patients. Despite this, patients occasionally perceived that better discharge instructions, review of medications, and sooner follow‐up appointments with a primary care doctor could have potentially prevented their ED visit. This is consistent with numerous prior studies and supports better transition‐of‐care programs.

Our study had a small sample size, which results in wide confidence intervals on all point estimates of percentages, limiting the precision of our findings. No medical charts were reviewed to determine the medical reasons for the index admission, the prior course of care, or subsequent hospital course after emergency care, limiting our ability to link perceptions with actual past hospital experiences or compare differences in perceptions by subsequent readmission. Another limitation is a lack of generalizability of our findings to other patients, hospitals, or regions. Our patient population was largely white and English speaking only for participation in this study. Also, our hospital ED admits an average of 48% of patients, which is higher than most hospitals. We enrolled a convenience sample as opposed to a consecutive sample of patients due to limitations in research associate staffing, potentially biasing our sample. We attempted to minimize this bias by scheduling shifts across days and time periods. We did not systematically collect the number of patients or caregivers who refused participation, but believe that it was less than 5% of those approached. Other limitations include possible reporting biases associated with in‐person interviews, which we attempted to minimize by conducting all surveys in private.

SUMMARY

Identifying needs in patients who utilize the ED soon after being discharged from inpatient care is essential for planning appropriate care‐transition interventions. Our findings suggest that multiple stakeholders may be necessary to fully elicit targets for effective care‐transition programs.

 

Disclosure: Nothing to report.

References
  1. Medicare Payment Advisory Commission. Payment policy for inpatient readmissions. In: Report to the congress: promoting greater efficiency in Medicare. Available at: http://www.medpac.gov/chapters/Jun07_Ch05.pdf. Accessed February 9, 2010.
  2. Jack BW, Chetty VK, Anthony D, et al. A reengineered hospital discharge program to decrease rehospitalization: a randomized trial. Ann Intern Med. 2009;150(3):178187.
  3. Hasan O, Meltzer DO, Shaykevich SA, et al. Hospital readmission in general medicine patients: a prediction model. J Gen Intern Med. 2010;25(3):211219.
  4. Rennke S, Nguyen OK, Shoeb MH, Magan Y, Wachter RM, Ranji SR. Hospital‐initiated transitional care interventions as a patient safety strategy: a systematic review. Ann Intern Med. 2013;158(5 pt 2):433440.
  5. Benbassat J, Taragin M. Hospital readmissions as a measure of quality of health care: advantages and limitations. Arch Intern Med. 2000;160(8):10741081.
  6. Rising KL, White LF, Fernandez WG, Boutwell AE. Emergency department visits after hospital discharge: a missing part of the equation. Ann Emerg Med. 2013;62(2):145150.
  7. Vashi AA, Fox JP, Carr BG, et al. Use of hospital‐based acute care among patients recently discharged from the hospital. JAMA. 2013;309(4):364371.
  8. Soler RS, Juvinya Canal D, Noguer CB, Poch CG, Brugada Motge N, Del Mar Garcia Gil M. Continuity of care and monitoring pain after discharge: patient perspective. J Adv Nurs. 2010;66(1):4048.
  9. Kangovi S, Grande D, Meehan P, Mitra N, Shannon R, Long JA. Perceptions of readmitted patients on the transition from hospital to home. J Hosp Med. 2012;7(9):709712.
  10. Feigenbaum P, Neuwirth E, Trowbridge L, et al. Factors contributing to all‐cause 30‐day readmissions: a structured case series across 18 hospitals. Med Care. 2012;50(7):599605.
  11. Snow V, Beck D, Budnitz T, et al. Transition of care consensus policy statement, American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatric Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine. J Gen Intern Med. 2009;24(8):971976.
  12. Cicchetti DV, Feinstein AR. J Clin Epidemiol. 1990;43(6):551558.
  13. Starfield B, Steinwachs D, Morris I, Bause G, Siebert S, Westin C. Patient‐doctor agreement about problems needing follow‐up visit. JAMA. 1979;242(4):344346.
  14. Britt H, Harris M, Driver B, Bridges‐Webb C, O'Toole B, Neary S. Reasons for encounter and diagnosed health problems: convergence between doctors and patients. Fam Pract. 1992;9(2):191194.
  15. Greene MG, Adelman RD, Charon R, Friedmann E. Concordance between physicians and their older and younger patients in the primary care medical encounter. Gerontologist. 1989;29(6):808813.
  16. Giovannetti ER, Reider L, Wolff JL, et al. Do older patients and their family caregivers agree about the quality of chronic illness care? Int J Qual Health Care. 2013;25(5):515524.
  17. Tamim H, McCusker J, Dendukuri N. Proxy reporting of quality of life using the EQ‐5D. Med Care. 2002;40(12):11861195.
  18. Kangovi S, Grande D. Hospital readmissions—not just a measure of quality. JAMA. 2011;306(16):17961797.
  19. Allaudeen N, Vidyarthi A, Maselli J, Auerbach A. Redefining readmission risk factors for general medicine patients. J Hosp Med. 2011;6(2):5460.
  20. Moore C, McGinn T, Halm E. Tying up loose ends: discharging patients with unresolved medical issues. Arch Intern Med. 2007;167(12):13051311.
  21. Donze J, Aujesky D, Williams D, Schnipper JL. Potentially avoidable 30‐day hospital readmissions in medical patients: derivation and validation of a prediction model. JAMA Intern Med. 2013;173(8):632638.
References
  1. Medicare Payment Advisory Commission. Payment policy for inpatient readmissions. In: Report to the congress: promoting greater efficiency in Medicare. Available at: http://www.medpac.gov/chapters/Jun07_Ch05.pdf. Accessed February 9, 2010.
  2. Jack BW, Chetty VK, Anthony D, et al. A reengineered hospital discharge program to decrease rehospitalization: a randomized trial. Ann Intern Med. 2009;150(3):178187.
  3. Hasan O, Meltzer DO, Shaykevich SA, et al. Hospital readmission in general medicine patients: a prediction model. J Gen Intern Med. 2010;25(3):211219.
  4. Rennke S, Nguyen OK, Shoeb MH, Magan Y, Wachter RM, Ranji SR. Hospital‐initiated transitional care interventions as a patient safety strategy: a systematic review. Ann Intern Med. 2013;158(5 pt 2):433440.
  5. Benbassat J, Taragin M. Hospital readmissions as a measure of quality of health care: advantages and limitations. Arch Intern Med. 2000;160(8):10741081.
  6. Rising KL, White LF, Fernandez WG, Boutwell AE. Emergency department visits after hospital discharge: a missing part of the equation. Ann Emerg Med. 2013;62(2):145150.
  7. Vashi AA, Fox JP, Carr BG, et al. Use of hospital‐based acute care among patients recently discharged from the hospital. JAMA. 2013;309(4):364371.
  8. Soler RS, Juvinya Canal D, Noguer CB, Poch CG, Brugada Motge N, Del Mar Garcia Gil M. Continuity of care and monitoring pain after discharge: patient perspective. J Adv Nurs. 2010;66(1):4048.
  9. Kangovi S, Grande D, Meehan P, Mitra N, Shannon R, Long JA. Perceptions of readmitted patients on the transition from hospital to home. J Hosp Med. 2012;7(9):709712.
  10. Feigenbaum P, Neuwirth E, Trowbridge L, et al. Factors contributing to all‐cause 30‐day readmissions: a structured case series across 18 hospitals. Med Care. 2012;50(7):599605.
  11. Snow V, Beck D, Budnitz T, et al. Transition of care consensus policy statement, American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatric Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine. J Gen Intern Med. 2009;24(8):971976.
  12. Cicchetti DV, Feinstein AR. J Clin Epidemiol. 1990;43(6):551558.
  13. Starfield B, Steinwachs D, Morris I, Bause G, Siebert S, Westin C. Patient‐doctor agreement about problems needing follow‐up visit. JAMA. 1979;242(4):344346.
  14. Britt H, Harris M, Driver B, Bridges‐Webb C, O'Toole B, Neary S. Reasons for encounter and diagnosed health problems: convergence between doctors and patients. Fam Pract. 1992;9(2):191194.
  15. Greene MG, Adelman RD, Charon R, Friedmann E. Concordance between physicians and their older and younger patients in the primary care medical encounter. Gerontologist. 1989;29(6):808813.
  16. Giovannetti ER, Reider L, Wolff JL, et al. Do older patients and their family caregivers agree about the quality of chronic illness care? Int J Qual Health Care. 2013;25(5):515524.
  17. Tamim H, McCusker J, Dendukuri N. Proxy reporting of quality of life using the EQ‐5D. Med Care. 2002;40(12):11861195.
  18. Kangovi S, Grande D. Hospital readmissions—not just a measure of quality. JAMA. 2011;306(16):17961797.
  19. Allaudeen N, Vidyarthi A, Maselli J, Auerbach A. Redefining readmission risk factors for general medicine patients. J Hosp Med. 2011;6(2):5460.
  20. Moore C, McGinn T, Halm E. Tying up loose ends: discharging patients with unresolved medical issues. Arch Intern Med. 2007;167(12):13051311.
  21. Donze J, Aujesky D, Williams D, Schnipper JL. Potentially avoidable 30‐day hospital readmissions in medical patients: derivation and validation of a prediction model. JAMA Intern Med. 2013;173(8):632638.
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Journal of Hospital Medicine - 9(5)
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Journal of Hospital Medicine - 9(5)
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315-319
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Factors contributing to emergency department care within 30 days of hospital discharge and potential ways to prevent it: Differences in perspectives of patients, caregivers, and emergency physicians
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Factors contributing to emergency department care within 30 days of hospital discharge and potential ways to prevent it: Differences in perspectives of patients, caregivers, and emergency physicians
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Address for correspondence and reprint requests: Brian Suffoletto, MD, Department of Emergency Medicine, University of Pittsburgh, Iroquois Building, Suite 400A, 3600 Forbes Ave., Pittsburgh, PA 15261; Telephone: 412–901‐6892; Fax: 412–647‐6669; E‐mail: [email protected]
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