Clinical question: On what aspects of VTE management in cancer patients are there consensus among the major guideline panels?

Background: VTE is a common and serious complication of cancer. Patients might be hypercoagulable due to prothrombotic mediators released or mediated by tumor cells, chemotherapeutic agents, debility, central venous catheters, hospitalizations, or surgical procedures. The optimal management often is problematic due to uncertain benefit and risk of bleeding.

Study design: Review of major guideline statements.

Synopsis: The authors examined five VTE guidelines of American and European cancer societies. Each guideline was reviewed to determine the main recommendations and whether there was consensus on key aspects of anticoagulant management.

The study authors concluded that consensus was reached on most key recommendations:

• VTE prophylaxis in hospitalized medical patients. All five guidelines recommend the use of prophylaxis, though some guidelines recommend anticoagulant prophylaxis for all inpatients in the absence of contraindications and some recommend limiting prophylaxis to immobilized patients. All five recommend the use of either unfractionated heparin, low-molecular-weight heparin (LMWH), or fondaparinux.
• VTE prevention in cancer patients undergoing surgery. All five guidelines recommend anticoagulant prophylaxis in the absence of contraindications and extending prophylaxis approximately four weeks after major surgery.
• VTE prophylaxis in cancer patients with central venous catheters. Not recommended.
• VTE prophylaxis in ambulatory cancer patients without central venous catheters. Recommended only for multiple myeloma patients receiving a thalidomide-lenalidomide regimen.
• Long-term treatment of acute VTE in cancer patients. All five guidelines recommend initial treatment with LMWH for at least three to six months, followed by indefinite treatment with LMWH or a vitamin K antagonist.

Bottom line: Major guideline panels agree on key aspects of VTE management for cancer patients, including the use of prophylaxis for hospitalized medical and surgical patients and the use of long-term LMWH treatment for cancer patients with acute VTE.

Citation: Khorana AA, Streiff MB, Farge D, et al. Venous thromboembolism prophylaxis and treatment in cancer: a consensus statement of major guidelines panels and call to action. J Clin Oncol. 2009; 27(29):4919-4926.

Clinical question: On what aspects of VTE management in cancer patients are there consensus among the major guideline panels?

Background: VTE is a common and serious complication of cancer. Patients might be hypercoagulable due to prothrombotic mediators released or mediated by tumor cells, chemotherapeutic agents, debility, central venous catheters, hospitalizations, or surgical procedures. The optimal management often is problematic due to uncertain benefit and risk of bleeding.

Study design: Review of major guideline statements.

Synopsis: The authors examined five VTE guidelines of American and European cancer societies. Each guideline was reviewed to determine the main recommendations and whether there was consensus on key aspects of anticoagulant management.

The study authors concluded that consensus was reached on most key recommendations:

• VTE prophylaxis in hospitalized medical patients. All five guidelines recommend the use of prophylaxis, though some guidelines recommend anticoagulant prophylaxis for all inpatients in the absence of contraindications and some recommend limiting prophylaxis to immobilized patients. All five recommend the use of either unfractionated heparin, low-molecular-weight heparin (LMWH), or fondaparinux.
• VTE prevention in cancer patients undergoing surgery. All five guidelines recommend anticoagulant prophylaxis in the absence of contraindications and extending prophylaxis approximately four weeks after major surgery.
• VTE prophylaxis in cancer patients with central venous catheters. Not recommended.
• VTE prophylaxis in ambulatory cancer patients without central venous catheters. Recommended only for multiple myeloma patients receiving a thalidomide-lenalidomide regimen.
• Long-term treatment of acute VTE in cancer patients. All five guidelines recommend initial treatment with LMWH for at least three to six months, followed by indefinite treatment with LMWH or a vitamin K antagonist.

Bottom line: Major guideline panels agree on key aspects of VTE management for cancer patients, including the use of prophylaxis for hospitalized medical and surgical patients and the use of long-term LMWH treatment for cancer patients with acute VTE.

Citation: Khorana AA, Streiff MB, Farge D, et al. Venous thromboembolism prophylaxis and treatment in cancer: a consensus statement of major guidelines panels and call to action. J Clin Oncol. 2009; 27(29):4919-4926.

Clinical question: On what aspects of VTE management in cancer patients are there consensus among the major guideline panels?

Background: VTE is a common and serious complication of cancer. Patients might be hypercoagulable due to prothrombotic mediators released or mediated by tumor cells, chemotherapeutic agents, debility, central venous catheters, hospitalizations, or surgical procedures. The optimal management often is problematic due to uncertain benefit and risk of bleeding.

Study design: Review of major guideline statements.

Synopsis: The authors examined five VTE guidelines of American and European cancer societies. Each guideline was reviewed to determine the main recommendations and whether there was consensus on key aspects of anticoagulant management.

The study authors concluded that consensus was reached on most key recommendations:

• VTE prophylaxis in hospitalized medical patients. All five guidelines recommend the use of prophylaxis, though some guidelines recommend anticoagulant prophylaxis for all inpatients in the absence of contraindications and some recommend limiting prophylaxis to immobilized patients. All five recommend the use of either unfractionated heparin, low-molecular-weight heparin (LMWH), or fondaparinux.
• VTE prevention in cancer patients undergoing surgery. All five guidelines recommend anticoagulant prophylaxis in the absence of contraindications and extending prophylaxis approximately four weeks after major surgery.
• VTE prophylaxis in cancer patients with central venous catheters. Not recommended.
• VTE prophylaxis in ambulatory cancer patients without central venous catheters. Recommended only for multiple myeloma patients receiving a thalidomide-lenalidomide regimen.
• Long-term treatment of acute VTE in cancer patients. All five guidelines recommend initial treatment with LMWH for at least three to six months, followed by indefinite treatment with LMWH or a vitamin K antagonist.

Bottom line: Major guideline panels agree on key aspects of VTE management for cancer patients, including the use of prophylaxis for hospitalized medical and surgical patients and the use of long-term LMWH treatment for cancer patients with acute VTE.

Citation: Khorana AA, Streiff MB, Farge D, et al. Venous thromboembolism prophylaxis and treatment in cancer: a consensus statement of major guidelines panels and call to action. J Clin Oncol. 2009; 27(29):4919-4926.

Clinical question: What is the relationship between acute DVT and pulmonary embolism (PE) in trauma patients?

Background: Major trauma is associated with an increased risk of acute DVT and PE. It is assumed that the majority of PEs arise from DVTs in the lower extremities. Definitive evidence demonstrating that PEs form in situ rather than embolize from leg veins could impact indications for inferior vena cava filters.

Study design: Retrospective chart review.

Setting: Academic Level 1 trauma center in Boston.

Synopsis: The medical records of 247 trauma patients with suspected PE who underwent CT angiography of the lungs and simultaneous CT venography of the pelvis and lower extremities from January 2004 to December 2007 were reviewed. High-risk patients also underwent weekly screening with duplex ultrasonagraphy of the legs.

PE was diagnosed in 46 patients (19%) and DVT in 18 patients (7%). Anticoagulant prophylaxis had been administered to 96% and 78% of the patients with PE and DVT, respectively. PE was diagnosed a median of 5.5 days after admission (range 0-40 days) and the majority (61%) were in segmental or subsegmental branches, rather than in the main or lobar pulmonary arteries (39%). Only seven of the 46 patients (15%) diagnosed with PE also had a pelvic or lower-extremity DVT on simultaneous imaging with CT venography.

Bottom line: Trauma patients with PE often do not have a DVT at the time of diagnosis, though it remains unknown whether this is due to in-situ pulmonary thrombosis or complete embolization from the lower extremities.

Citation: Velmahos GC, Spaniolas K, Tabbara M, et al. Pulmonary embolism and deep venous thrombosis in trauma: are they related? Arch Surg. 2009;144:928-932.

Clinical question: What is the relationship between acute DVT and pulmonary embolism (PE) in trauma patients?

Background: Major trauma is associated with an increased risk of acute DVT and PE. It is assumed that the majority of PEs arise from DVTs in the lower extremities. Definitive evidence demonstrating that PEs form in situ rather than embolize from leg veins could impact indications for inferior vena cava filters.

Study design: Retrospective chart review.

Setting: Academic Level 1 trauma center in Boston.

Synopsis: The medical records of 247 trauma patients with suspected PE who underwent CT angiography of the lungs and simultaneous CT venography of the pelvis and lower extremities from January 2004 to December 2007 were reviewed. High-risk patients also underwent weekly screening with duplex ultrasonagraphy of the legs.

PE was diagnosed in 46 patients (19%) and DVT in 18 patients (7%). Anticoagulant prophylaxis had been administered to 96% and 78% of the patients with PE and DVT, respectively. PE was diagnosed a median of 5.5 days after admission (range 0-40 days) and the majority (61%) were in segmental or subsegmental branches, rather than in the main or lobar pulmonary arteries (39%). Only seven of the 46 patients (15%) diagnosed with PE also had a pelvic or lower-extremity DVT on simultaneous imaging with CT venography.

Bottom line: Trauma patients with PE often do not have a DVT at the time of diagnosis, though it remains unknown whether this is due to in-situ pulmonary thrombosis or complete embolization from the lower extremities.

Citation: Velmahos GC, Spaniolas K, Tabbara M, et al. Pulmonary embolism and deep venous thrombosis in trauma: are they related? Arch Surg. 2009;144:928-932.

Clinical question: What is the relationship between acute DVT and pulmonary embolism (PE) in trauma patients?

Background: Major trauma is associated with an increased risk of acute DVT and PE. It is assumed that the majority of PEs arise from DVTs in the lower extremities. Definitive evidence demonstrating that PEs form in situ rather than embolize from leg veins could impact indications for inferior vena cava filters.

Study design: Retrospective chart review.

Setting: Academic Level 1 trauma center in Boston.

Synopsis: The medical records of 247 trauma patients with suspected PE who underwent CT angiography of the lungs and simultaneous CT venography of the pelvis and lower extremities from January 2004 to December 2007 were reviewed. High-risk patients also underwent weekly screening with duplex ultrasonagraphy of the legs.

PE was diagnosed in 46 patients (19%) and DVT in 18 patients (7%). Anticoagulant prophylaxis had been administered to 96% and 78% of the patients with PE and DVT, respectively. PE was diagnosed a median of 5.5 days after admission (range 0-40 days) and the majority (61%) were in segmental or subsegmental branches, rather than in the main or lobar pulmonary arteries (39%). Only seven of the 46 patients (15%) diagnosed with PE also had a pelvic or lower-extremity DVT on simultaneous imaging with CT venography.

Bottom line: Trauma patients with PE often do not have a DVT at the time of diagnosis, though it remains unknown whether this is due to in-situ pulmonary thrombosis or complete embolization from the lower extremities.

Citation: Velmahos GC, Spaniolas K, Tabbara M, et al. Pulmonary embolism and deep venous thrombosis in trauma: are they related? Arch Surg. 2009;144:928-932.

Q) I have heard about a gene that causes high blood pressure. Did I hear that right? Is testing for this gene available now?

African-Americans have a higher risk for chronic kidney disease (CKD), including end-stage renal disease (ESRD; defined as kidney failure requiring dialysis or transplant), than any other racial or ethnic group in the United States.¹ Previously, this has been attributed to poorly controlled hypertension and diabetes, as well as socioeconomic factors such as limited access to health care.

Research now shows that autosomal recessive genetic variations on chromosome 22q, the gene that encodes apolipoprotein-1 (APOL1; an HDL protein), promote hypertension. This subsequently increases the risk for and progression of CKD in black patients (who have up to 29x higher risk than white patients without this genetic variation).²

The APOL1 gene has two alleles. Having at least one of them provides resistance to Trypanosoma brucei, the cause of “sleeping sickness” transmitted by the tsetse fly, but increases risk for CKD and ESRD (see Table 1).^2,3 Black patients descending from the southern and western portions of Africa are most likely to have two alleles, putting them at the highest risk for hypertension and associated CKD.

Foster et al reported that black patients with two altered alleles had a 31% higher risk for CKD and ESRD, compared with individuals with hypertension-induced nephrosclerosis who had zero to one altered alleles.⁴ Nondiabetic black patients with CKD who have two altered alleles are at highest risk for focal segmental glomerulosclerosis, HIV nephropathy, and CKD attributable to hypertension.² The African-American Study of Kidney Disease and Hypertension found that black patients with hypertension controlled by ACE inhibitors had slower progression of CKD, regardless of allele variation.⁵ Currently, there is no treatment for this genetic alteration.⁴

One could posit that black patients undergoing renal transplant would have a higher risk for renal failure in the transplanted kidney due to APOL1-related hypertension, compared to nonblack renal transplant recipients. Additionally, a donor kidney with an altered APOL1 gene may have a higher risk for failure.⁶

Genotyping for APOL1 (CPT code: 81479) is available in select laboratories at a cost of approximately $400.⁷ For a family that has a member affected by kidney failure at a young age, knowing whether the APOL1 gene is carried in the family would allow early aggressive hypertension management to help prevent a lifetime of severe CKD.

Susan E. Brown, MS, ARNP,
ACNP-BC, CCRN
Great River Nephrology,
West Burlington, Iowa

REFERENCES

1.  United States Renal Data System. Annual data report: atlas of chronic kidney disease and end-stage renal disease in the United States (2012). www.usrds.org/2012/view/v1_01.aspx. Accessed October 19, 2014.

2.  Kopp JB, Nelson GW, Sampath K, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy.
J Am Soc Nephrol. 2011;22(11):2129-2137.

3.  Parsa A, Kao L, Xie D, et al; AASK and CRIC Study Investigators. APOL1 risk variants, race and progression of chronic kidney disease.
N Engl J Med. 2013;369:2183-2196.

4.  Foster MC, Coresh J, Fornage M, et al. APOL1 variants associate with increased risk of CKD among African Americans. J Am Soc Nephrol. 2013;24(9):1484-1491.

5.  Lipkowitz MS, Freedman BI, Langefeld CD, et al; AASK Investigators. Apolipoprotein L1 gene variants associate with hypertension-attributed nephropathy and the rate of kidney function decline in African Americans. Kidney Int. 2013;83(1):114–120.

6.  Reeves-Daniel AM, DePalma JA, Bleyer AJ, et al. The APOL1 gene and allograft survival after kidney transplantation. Am J Transplant. 2011;11(5):1025-1030.

7.  Partners Healthcare Personalized Medicine. Order APOL1 genotyping test for non-diabetic nephropathy kidney disease. http://personalizedmedicine.partners.org/Laboratory-For-Molecular-Medicine/Ordering/Kidney-Disease/APOL1-Gene-Sequencing.aspx. Accessed October 19, 2014.

8.  Grovas A, Fremgen A, Rauck A, et al. The National Cancer Data Base report on patterns of childhood cancers in the United States. Cancer. 1997;80(12):2321-2332.

9.  Johns Hopkins Medicine. Wilm’s tumor. www.hopkinsmedicine.org/kimmel_cancer_center/centers/pediatric_oncology/cancer_types/wilms_tumor.html. Accessed October 19, 2014.

10.  Dome JS, Huff V. Wilms tumor overview. In: Pagon RA, Adam MP, Ardinger HH, et al (eds). GeneReviews® [Internet]. Seattle, WA: University of Washington, Seattle; 1993-2014. www.ncbi.nlm.nih.gov/books/NBK1294/. Accessed October 19, 2014.

11.  Urbach A, Yermalovich A, Zhang J, et al. Lin28 sustains early renal progenitors and induces Wilms tumor. Genes & Dev. 2014;28:971-982.

12.  Fernandez C, Geller JI, Ehrlich PF, et al. Renal tumors. In: Pizzo P, Poplack D (eds). Principles and Practice of Pediatric Oncology. 6th ed, St Louis, MO: Lippincott Williams & Wilkins. 2011; 861.

13.  Metzger ML, Dome JS. Current therapy for Wilms’ tumor. Oncologist. 2005;10(10):815-826.

Q) I have heard about a gene that causes high blood pressure. Did I hear that right? Is testing for this gene available now?

African-Americans have a higher risk for chronic kidney disease (CKD), including end-stage renal disease (ESRD; defined as kidney failure requiring dialysis or transplant), than any other racial or ethnic group in the United States.¹ Previously, this has been attributed to poorly controlled hypertension and diabetes, as well as socioeconomic factors such as limited access to health care.

Research now shows that autosomal recessive genetic variations on chromosome 22q, the gene that encodes apolipoprotein-1 (APOL1; an HDL protein), promote hypertension. This subsequently increases the risk for and progression of CKD in black patients (who have up to 29x higher risk than white patients without this genetic variation).²

The APOL1 gene has two alleles. Having at least one of them provides resistance to Trypanosoma brucei, the cause of “sleeping sickness” transmitted by the tsetse fly, but increases risk for CKD and ESRD (see Table 1).^2,3 Black patients descending from the southern and western portions of Africa are most likely to have two alleles, putting them at the highest risk for hypertension and associated CKD.

Foster et al reported that black patients with two altered alleles had a 31% higher risk for CKD and ESRD, compared with individuals with hypertension-induced nephrosclerosis who had zero to one altered alleles.⁴ Nondiabetic black patients with CKD who have two altered alleles are at highest risk for focal segmental glomerulosclerosis, HIV nephropathy, and CKD attributable to hypertension.² The African-American Study of Kidney Disease and Hypertension found that black patients with hypertension controlled by ACE inhibitors had slower progression of CKD, regardless of allele variation.⁵ Currently, there is no treatment for this genetic alteration.⁴

One could posit that black patients undergoing renal transplant would have a higher risk for renal failure in the transplanted kidney due to APOL1-related hypertension, compared to nonblack renal transplant recipients. Additionally, a donor kidney with an altered APOL1 gene may have a higher risk for failure.⁶

Genotyping for APOL1 (CPT code: 81479) is available in select laboratories at a cost of approximately $400.⁷ For a family that has a member affected by kidney failure at a young age, knowing whether the APOL1 gene is carried in the family would allow early aggressive hypertension management to help prevent a lifetime of severe CKD.

Susan E. Brown, MS, ARNP,
ACNP-BC, CCRN
Great River Nephrology,
West Burlington, Iowa

REFERENCES

1.  United States Renal Data System. Annual data report: atlas of chronic kidney disease and end-stage renal disease in the United States (2012). www.usrds.org/2012/view/v1_01.aspx. Accessed October 19, 2014.

2.  Kopp JB, Nelson GW, Sampath K, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy.
J Am Soc Nephrol. 2011;22(11):2129-2137.

3.  Parsa A, Kao L, Xie D, et al; AASK and CRIC Study Investigators. APOL1 risk variants, race and progression of chronic kidney disease.
N Engl J Med. 2013;369:2183-2196.

4.  Foster MC, Coresh J, Fornage M, et al. APOL1 variants associate with increased risk of CKD among African Americans. J Am Soc Nephrol. 2013;24(9):1484-1491.

5.  Lipkowitz MS, Freedman BI, Langefeld CD, et al; AASK Investigators. Apolipoprotein L1 gene variants associate with hypertension-attributed nephropathy and the rate of kidney function decline in African Americans. Kidney Int. 2013;83(1):114–120.

6.  Reeves-Daniel AM, DePalma JA, Bleyer AJ, et al. The APOL1 gene and allograft survival after kidney transplantation. Am J Transplant. 2011;11(5):1025-1030.

7.  Partners Healthcare Personalized Medicine. Order APOL1 genotyping test for non-diabetic nephropathy kidney disease. http://personalizedmedicine.partners.org/Laboratory-For-Molecular-Medicine/Ordering/Kidney-Disease/APOL1-Gene-Sequencing.aspx. Accessed October 19, 2014.

8.  Grovas A, Fremgen A, Rauck A, et al. The National Cancer Data Base report on patterns of childhood cancers in the United States. Cancer. 1997;80(12):2321-2332.

9.  Johns Hopkins Medicine. Wilm’s tumor. www.hopkinsmedicine.org/kimmel_cancer_center/centers/pediatric_oncology/cancer_types/wilms_tumor.html. Accessed October 19, 2014.

10.  Dome JS, Huff V. Wilms tumor overview. In: Pagon RA, Adam MP, Ardinger HH, et al (eds). GeneReviews® [Internet]. Seattle, WA: University of Washington, Seattle; 1993-2014. www.ncbi.nlm.nih.gov/books/NBK1294/. Accessed October 19, 2014.

11.  Urbach A, Yermalovich A, Zhang J, et al. Lin28 sustains early renal progenitors and induces Wilms tumor. Genes & Dev. 2014;28:971-982.

12.  Fernandez C, Geller JI, Ehrlich PF, et al. Renal tumors. In: Pizzo P, Poplack D (eds). Principles and Practice of Pediatric Oncology. 6th ed, St Louis, MO: Lippincott Williams & Wilkins. 2011; 861.

13.  Metzger ML, Dome JS. Current therapy for Wilms’ tumor. Oncologist. 2005;10(10):815-826.

Q) I have heard about a gene that causes high blood pressure. Did I hear that right? Is testing for this gene available now?

African-Americans have a higher risk for chronic kidney disease (CKD), including end-stage renal disease (ESRD; defined as kidney failure requiring dialysis or transplant), than any other racial or ethnic group in the United States.¹ Previously, this has been attributed to poorly controlled hypertension and diabetes, as well as socioeconomic factors such as limited access to health care.

Research now shows that autosomal recessive genetic variations on chromosome 22q, the gene that encodes apolipoprotein-1 (APOL1; an HDL protein), promote hypertension. This subsequently increases the risk for and progression of CKD in black patients (who have up to 29x higher risk than white patients without this genetic variation).²

The APOL1 gene has two alleles. Having at least one of them provides resistance to Trypanosoma brucei, the cause of “sleeping sickness” transmitted by the tsetse fly, but increases risk for CKD and ESRD (see Table 1).^2,3 Black patients descending from the southern and western portions of Africa are most likely to have two alleles, putting them at the highest risk for hypertension and associated CKD.

Foster et al reported that black patients with two altered alleles had a 31% higher risk for CKD and ESRD, compared with individuals with hypertension-induced nephrosclerosis who had zero to one altered alleles.⁴ Nondiabetic black patients with CKD who have two altered alleles are at highest risk for focal segmental glomerulosclerosis, HIV nephropathy, and CKD attributable to hypertension.² The African-American Study of Kidney Disease and Hypertension found that black patients with hypertension controlled by ACE inhibitors had slower progression of CKD, regardless of allele variation.⁵ Currently, there is no treatment for this genetic alteration.⁴

One could posit that black patients undergoing renal transplant would have a higher risk for renal failure in the transplanted kidney due to APOL1-related hypertension, compared to nonblack renal transplant recipients. Additionally, a donor kidney with an altered APOL1 gene may have a higher risk for failure.⁶

Genotyping for APOL1 (CPT code: 81479) is available in select laboratories at a cost of approximately $400.⁷ For a family that has a member affected by kidney failure at a young age, knowing whether the APOL1 gene is carried in the family would allow early aggressive hypertension management to help prevent a lifetime of severe CKD.

Susan E. Brown, MS, ARNP,
ACNP-BC, CCRN
Great River Nephrology,
West Burlington, Iowa

REFERENCES

1.  United States Renal Data System. Annual data report: atlas of chronic kidney disease and end-stage renal disease in the United States (2012). www.usrds.org/2012/view/v1_01.aspx. Accessed October 19, 2014.

2.  Kopp JB, Nelson GW, Sampath K, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy.
J Am Soc Nephrol. 2011;22(11):2129-2137.

3.  Parsa A, Kao L, Xie D, et al; AASK and CRIC Study Investigators. APOL1 risk variants, race and progression of chronic kidney disease.
N Engl J Med. 2013;369:2183-2196.

4.  Foster MC, Coresh J, Fornage M, et al. APOL1 variants associate with increased risk of CKD among African Americans. J Am Soc Nephrol. 2013;24(9):1484-1491.

5.  Lipkowitz MS, Freedman BI, Langefeld CD, et al; AASK Investigators. Apolipoprotein L1 gene variants associate with hypertension-attributed nephropathy and the rate of kidney function decline in African Americans. Kidney Int. 2013;83(1):114–120.

6.  Reeves-Daniel AM, DePalma JA, Bleyer AJ, et al. The APOL1 gene and allograft survival after kidney transplantation. Am J Transplant. 2011;11(5):1025-1030.

7.  Partners Healthcare Personalized Medicine. Order APOL1 genotyping test for non-diabetic nephropathy kidney disease. http://personalizedmedicine.partners.org/Laboratory-For-Molecular-Medicine/Ordering/Kidney-Disease/APOL1-Gene-Sequencing.aspx. Accessed October 19, 2014.

8.  Grovas A, Fremgen A, Rauck A, et al. The National Cancer Data Base report on patterns of childhood cancers in the United States. Cancer. 1997;80(12):2321-2332.

9.  Johns Hopkins Medicine. Wilm’s tumor. www.hopkinsmedicine.org/kimmel_cancer_center/centers/pediatric_oncology/cancer_types/wilms_tumor.html. Accessed October 19, 2014.

10.  Dome JS, Huff V. Wilms tumor overview. In: Pagon RA, Adam MP, Ardinger HH, et al (eds). GeneReviews® [Internet]. Seattle, WA: University of Washington, Seattle; 1993-2014. www.ncbi.nlm.nih.gov/books/NBK1294/. Accessed October 19, 2014.

11.  Urbach A, Yermalovich A, Zhang J, et al. Lin28 sustains early renal progenitors and induces Wilms tumor. Genes & Dev. 2014;28:971-982.

12.  Fernandez C, Geller JI, Ehrlich PF, et al. Renal tumors. In: Pizzo P, Poplack D (eds). Principles and Practice of Pediatric Oncology. 6th ed, St Louis, MO: Lippincott Williams & Wilkins. 2011; 861.

13.  Metzger ML, Dome JS. Current therapy for Wilms’ tumor. Oncologist. 2005;10(10):815-826.

Clinical question: Using available data, what is the estimated cost savings of eliminating adverse events and avoiding redundant tests?

Background: Reimbursement schemes are changing such that hospitals are reimbursed less for some adverse events. This financial disincentive is expected to spark interest in improved patient safety. The authors sought to model the cost savings generated by eliminating redundant testing and adverse events from literature-based estimates.

Study design: Development of conceptual model to identify common or costly adverse events, redundant tests, and simulated costs.

Setting: Literature review, expert opinion, data from safety organizations and epidemiologic studies, and patient data from the 2004 National Inpatient Data Sample.

Synopsis: The conceptual model identified 5.7 million adverse events in U.S. hospitals, of which 3 million were considered preventable. The most common events included hospital-acquired infections (82% preventable), adverse drug events (26%), falls (33%), and iatrogenic thromboembolic events (62%). The calculated cost savings totaled $16.6 billion (5.5% of total inpatient costs) for adverse events and $8.2 billion for the elimination of redundant tests. When looking at hospital subtypes, the greatest savings would come from major teaching hospitals.

This study is limited by its use of published and heterogeneous data spanning a 15-year period. The authors did not include events for which there was no epidemiologic or cost data. As hospital-care changes and technology is adopted, it is uncertain how this changes the costs, prevalence, and the preventable nature of these events. The model was not consistently able to identifying high- and low-risk patients. For instance, in some models, all patients were considered at risk for events.

Bottom line: Based on a conceptual model of 2004 hospitalized patients, eliminating preventable adverse events could have saved $16.6 billion, while eliminating redundant tests could have saved another $8 billion.

Citation: Jha AK, Chan DC, Ridgway AB, Franz C, Bates DW. Improving safety and eliminating redundant tests: cutting costs in U.S. hospitals. Health Aff (Millwood). 2009;28(5):1475-1484.

Clinical question: Using available data, what is the estimated cost savings of eliminating adverse events and avoiding redundant tests?

Background: Reimbursement schemes are changing such that hospitals are reimbursed less for some adverse events. This financial disincentive is expected to spark interest in improved patient safety. The authors sought to model the cost savings generated by eliminating redundant testing and adverse events from literature-based estimates.

Study design: Development of conceptual model to identify common or costly adverse events, redundant tests, and simulated costs.

Setting: Literature review, expert opinion, data from safety organizations and epidemiologic studies, and patient data from the 2004 National Inpatient Data Sample.

Synopsis: The conceptual model identified 5.7 million adverse events in U.S. hospitals, of which 3 million were considered preventable. The most common events included hospital-acquired infections (82% preventable), adverse drug events (26%), falls (33%), and iatrogenic thromboembolic events (62%). The calculated cost savings totaled $16.6 billion (5.5% of total inpatient costs) for adverse events and $8.2 billion for the elimination of redundant tests. When looking at hospital subtypes, the greatest savings would come from major teaching hospitals.

This study is limited by its use of published and heterogeneous data spanning a 15-year period. The authors did not include events for which there was no epidemiologic or cost data. As hospital-care changes and technology is adopted, it is uncertain how this changes the costs, prevalence, and the preventable nature of these events. The model was not consistently able to identifying high- and low-risk patients. For instance, in some models, all patients were considered at risk for events.

Bottom line: Based on a conceptual model of 2004 hospitalized patients, eliminating preventable adverse events could have saved $16.6 billion, while eliminating redundant tests could have saved another $8 billion.

Citation: Jha AK, Chan DC, Ridgway AB, Franz C, Bates DW. Improving safety and eliminating redundant tests: cutting costs in U.S. hospitals. Health Aff (Millwood). 2009;28(5):1475-1484.

Clinical question: Using available data, what is the estimated cost savings of eliminating adverse events and avoiding redundant tests?

Background: Reimbursement schemes are changing such that hospitals are reimbursed less for some adverse events. This financial disincentive is expected to spark interest in improved patient safety. The authors sought to model the cost savings generated by eliminating redundant testing and adverse events from literature-based estimates.

Study design: Development of conceptual model to identify common or costly adverse events, redundant tests, and simulated costs.

Setting: Literature review, expert opinion, data from safety organizations and epidemiologic studies, and patient data from the 2004 National Inpatient Data Sample.

Synopsis: The conceptual model identified 5.7 million adverse events in U.S. hospitals, of which 3 million were considered preventable. The most common events included hospital-acquired infections (82% preventable), adverse drug events (26%), falls (33%), and iatrogenic thromboembolic events (62%). The calculated cost savings totaled $16.6 billion (5.5% of total inpatient costs) for adverse events and $8.2 billion for the elimination of redundant tests. When looking at hospital subtypes, the greatest savings would come from major teaching hospitals.

This study is limited by its use of published and heterogeneous data spanning a 15-year period. The authors did not include events for which there was no epidemiologic or cost data. As hospital-care changes and technology is adopted, it is uncertain how this changes the costs, prevalence, and the preventable nature of these events. The model was not consistently able to identifying high- and low-risk patients. For instance, in some models, all patients were considered at risk for events.

Bottom line: Based on a conceptual model of 2004 hospitalized patients, eliminating preventable adverse events could have saved $16.6 billion, while eliminating redundant tests could have saved another $8 billion.

Citation: Jha AK, Chan DC, Ridgway AB, Franz C, Bates DW. Improving safety and eliminating redundant tests: cutting costs in U.S. hospitals. Health Aff (Millwood). 2009;28(5):1475-1484.

Q) In school, they always emphasized the abdominal exam to rule out Wilms tumors. Are Wilms tumors still with us? Has treatment and evaluation changed?

Wilms tumor is a renal cancer found most commonly in children younger than 9 and represents approximately 7% of all malignancies in children.^8,9 It can occur in one or both kidneys, with earlier diagnosis noted with bilateral involvement. Risk is highest among non-Hispanic white persons and African-Americans and lowest among Asians.⁸

Wilms tumor develops due to a genetic mutation in the WT1 gene located on the 11p13 chromosome. Defects are also noted on the 11p15 chromosome and the p53 tumor suppressor gene.¹⁰ Urbach et al recently identified a relationship between the LIN28 gene and Wilms tumor.¹¹ Tumors develop when embryonic renal cells that should cease growing at the time of birth continue to grow in the postnatal period. Wilms tumor can be familial or sporadic. It can also be associated with various congenital anomalies manifested within various syndromes (see Table 2), as well as isolated genitourinary abnormalities, especially in boys.¹⁰

Most children present with a palpable, smooth, firm, generally painless mass in the abdomen; those who have bilateral renal involvement usually present earlier than those with unilateral involvement. Palpation of the abdomen during examination, if vigorous, can result in rupture of the renal capsule and tumor spillage. Additional symptoms include hematuria, fever, and hypertension. Referral to pediatric oncology is imperative.¹²

Definitive diagnosis is made by histologic evaluation following biopsy or surgical excision.¹³ Other possible diagnostic tests include but are not limited to abdominal ultrasound or CT; chest CT (to rule out metastatic lung disease); urinalysis (to evaluate for hematuria and proteinuria); liver function studies (to evaluate for hepatic involvement); and laboratory studies to measure coagulation, serum calcium, blood urea nitrogen, creatinine, and complete blood count.

Histologic examination for staging (I-V) occurs following surgical excision of the tumor. There are two staging systems available: the National Wilms Tumor Study, based on postoperative tumor evaluation, and the International Society of Pediatric Oncology, based on postchemotherapy evaluation.¹³

Treatment options include surgical excision (including complete nephrectomy of the affected kidney), chemotherapy based on tumor staging, and internal and/or external radiation therapy.¹³

Susan E. Brown, MS, ARNP,
ACNP-BC, CCRN
Great River Nephrology,
West Burlington, Iowa

REFERENCES

1.  United States Renal Data System. Annual data report: atlas of chronic kidney disease and end-stage renal disease in the United States (2012). www.usrds.org/2012/view/v1_01.aspx. Accessed October 19, 2014.

2.  Kopp JB, Nelson GW, Sampath K, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy.
J Am Soc Nephrol. 2011;22(11):2129-2137.

3.  Parsa A, Kao L, Xie D, et al; AASK and CRIC Study Investigators. APOL1 risk variants, race and progression of chronic kidney disease.
N Engl J Med. 2013;369:2183-2196.

4.  Foster MC, Coresh J, Fornage M, et al. APOL1 variants associate with increased risk of CKD among African Americans. J Am Soc Nephrol. 2013;24(9):1484-1491.

5.  Lipkowitz MS, Freedman BI, Langefeld CD, et al; AASK Investigators. Apolipoprotein L1 gene variants associate with hypertension-attributed nephropathy and the rate of kidney function decline in African Americans. Kidney Int. 2013;83(1):114–120.

6.  Reeves-Daniel AM, DePalma JA, Bleyer AJ, et al. The APOL1 gene and allograft survival after kidney transplantation. Am J Transplant. 2011;11(5):1025-1030.

7.  Partners Healthcare Personalized Medicine. Order APOL1 genotyping test for non-diabetic nephropathy kidney disease. http://personal izedmedicine.partners.org/Laboratory-For-Molecular-Medicine/Ordering/Kidney-Dis ease/APOL1-Gene-Sequencing.aspx. Accessed October 19, 2014.

8.  Grovas A, Fremgen A, Rauck A, et al. The National Cancer Data Base report on patterns of childhood cancers in the United States. Cancer. 1997;80(12):2321-2332.

9.  Johns Hopkins Medicine. Wilm’s tumor. www.hopkinsmedicine.org/kimmel_cancer_center/centers/pediatric_oncology/cancer_types/wilms_tumor.html. Accessed October 19, 2014.

10.  Dome JS, Huff V. Wilms tumor overview. In: Pagon RA, Adam MP, Ardinger HH, et al (eds). GeneReviews® [Internet]. Seattle, WA: University of Washington, Seattle; 1993-2014. www.ncbi.nlm.nih.gov/books/NBK1294/. Accessed October 19, 2014.

11.  Urbach A, Yermalovich A, Zhang J, et al. Lin28 sustains early renal progenitors and induces Wilms tumor. Genes & Dev. 2014;28:971-982.

12.  Fernandez C, Geller JI, Ehrlich PF, et al. Renal tumors. In: Pizzo P, Poplack D (eds). Principles and Practice of Pediatric Oncology. 6th ed, St Louis, MO: Lippincott Williams & Wilkins. 2011; 861.

13.  Metzger ML, Dome JS. Current therapy for Wilms’ tumor. Oncologist. 2005;10(10):815-826.

Q) In school, they always emphasized the abdominal exam to rule out Wilms tumors. Are Wilms tumors still with us? Has treatment and evaluation changed?

Wilms tumor is a renal cancer found most commonly in children younger than 9 and represents approximately 7% of all malignancies in children.^8,9 It can occur in one or both kidneys, with earlier diagnosis noted with bilateral involvement. Risk is highest among non-Hispanic white persons and African-Americans and lowest among Asians.⁸

Wilms tumor develops due to a genetic mutation in the WT1 gene located on the 11p13 chromosome. Defects are also noted on the 11p15 chromosome and the p53 tumor suppressor gene.¹⁰ Urbach et al recently identified a relationship between the LIN28 gene and Wilms tumor.¹¹ Tumors develop when embryonic renal cells that should cease growing at the time of birth continue to grow in the postnatal period. Wilms tumor can be familial or sporadic. It can also be associated with various congenital anomalies manifested within various syndromes (see Table 2), as well as isolated genitourinary abnormalities, especially in boys.¹⁰

Most children present with a palpable, smooth, firm, generally painless mass in the abdomen; those who have bilateral renal involvement usually present earlier than those with unilateral involvement. Palpation of the abdomen during examination, if vigorous, can result in rupture of the renal capsule and tumor spillage. Additional symptoms include hematuria, fever, and hypertension. Referral to pediatric oncology is imperative.¹²

Definitive diagnosis is made by histologic evaluation following biopsy or surgical excision.¹³ Other possible diagnostic tests include but are not limited to abdominal ultrasound or CT; chest CT (to rule out metastatic lung disease); urinalysis (to evaluate for hematuria and proteinuria); liver function studies (to evaluate for hepatic involvement); and laboratory studies to measure coagulation, serum calcium, blood urea nitrogen, creatinine, and complete blood count.

Histologic examination for staging (I-V) occurs following surgical excision of the tumor. There are two staging systems available: the National Wilms Tumor Study, based on postoperative tumor evaluation, and the International Society of Pediatric Oncology, based on postchemotherapy evaluation.¹³

Treatment options include surgical excision (including complete nephrectomy of the affected kidney), chemotherapy based on tumor staging, and internal and/or external radiation therapy.¹³

Susan E. Brown, MS, ARNP,
ACNP-BC, CCRN
Great River Nephrology,
West Burlington, Iowa

REFERENCES

1.  United States Renal Data System. Annual data report: atlas of chronic kidney disease and end-stage renal disease in the United States (2012). www.usrds.org/2012/view/v1_01.aspx. Accessed October 19, 2014.

2.  Kopp JB, Nelson GW, Sampath K, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy.
J Am Soc Nephrol. 2011;22(11):2129-2137.

3.  Parsa A, Kao L, Xie D, et al; AASK and CRIC Study Investigators. APOL1 risk variants, race and progression of chronic kidney disease.
N Engl J Med. 2013;369:2183-2196.

4.  Foster MC, Coresh J, Fornage M, et al. APOL1 variants associate with increased risk of CKD among African Americans. J Am Soc Nephrol. 2013;24(9):1484-1491.

5.  Lipkowitz MS, Freedman BI, Langefeld CD, et al; AASK Investigators. Apolipoprotein L1 gene variants associate with hypertension-attributed nephropathy and the rate of kidney function decline in African Americans. Kidney Int. 2013;83(1):114–120.

6.  Reeves-Daniel AM, DePalma JA, Bleyer AJ, et al. The APOL1 gene and allograft survival after kidney transplantation. Am J Transplant. 2011;11(5):1025-1030.

7.  Partners Healthcare Personalized Medicine. Order APOL1 genotyping test for non-diabetic nephropathy kidney disease. http://personal izedmedicine.partners.org/Laboratory-For-Molecular-Medicine/Ordering/Kidney-Dis ease/APOL1-Gene-Sequencing.aspx. Accessed October 19, 2014.

8.  Grovas A, Fremgen A, Rauck A, et al. The National Cancer Data Base report on patterns of childhood cancers in the United States. Cancer. 1997;80(12):2321-2332.

9.  Johns Hopkins Medicine. Wilm’s tumor. www.hopkinsmedicine.org/kimmel_cancer_center/centers/pediatric_oncology/cancer_types/wilms_tumor.html. Accessed October 19, 2014.

10.  Dome JS, Huff V. Wilms tumor overview. In: Pagon RA, Adam MP, Ardinger HH, et al (eds). GeneReviews® [Internet]. Seattle, WA: University of Washington, Seattle; 1993-2014. www.ncbi.nlm.nih.gov/books/NBK1294/. Accessed October 19, 2014.

11.  Urbach A, Yermalovich A, Zhang J, et al. Lin28 sustains early renal progenitors and induces Wilms tumor. Genes & Dev. 2014;28:971-982.

12.  Fernandez C, Geller JI, Ehrlich PF, et al. Renal tumors. In: Pizzo P, Poplack D (eds). Principles and Practice of Pediatric Oncology. 6th ed, St Louis, MO: Lippincott Williams & Wilkins. 2011; 861.

13.  Metzger ML, Dome JS. Current therapy for Wilms’ tumor. Oncologist. 2005;10(10):815-826.

Q) In school, they always emphasized the abdominal exam to rule out Wilms tumors. Are Wilms tumors still with us? Has treatment and evaluation changed?

Wilms tumor is a renal cancer found most commonly in children younger than 9 and represents approximately 7% of all malignancies in children.^8,9 It can occur in one or both kidneys, with earlier diagnosis noted with bilateral involvement. Risk is highest among non-Hispanic white persons and African-Americans and lowest among Asians.⁸

Wilms tumor develops due to a genetic mutation in the WT1 gene located on the 11p13 chromosome. Defects are also noted on the 11p15 chromosome and the p53 tumor suppressor gene.¹⁰ Urbach et al recently identified a relationship between the LIN28 gene and Wilms tumor.¹¹ Tumors develop when embryonic renal cells that should cease growing at the time of birth continue to grow in the postnatal period. Wilms tumor can be familial or sporadic. It can also be associated with various congenital anomalies manifested within various syndromes (see Table 2), as well as isolated genitourinary abnormalities, especially in boys.¹⁰

Most children present with a palpable, smooth, firm, generally painless mass in the abdomen; those who have bilateral renal involvement usually present earlier than those with unilateral involvement. Palpation of the abdomen during examination, if vigorous, can result in rupture of the renal capsule and tumor spillage. Additional symptoms include hematuria, fever, and hypertension. Referral to pediatric oncology is imperative.¹²

Definitive diagnosis is made by histologic evaluation following biopsy or surgical excision.¹³ Other possible diagnostic tests include but are not limited to abdominal ultrasound or CT; chest CT (to rule out metastatic lung disease); urinalysis (to evaluate for hematuria and proteinuria); liver function studies (to evaluate for hepatic involvement); and laboratory studies to measure coagulation, serum calcium, blood urea nitrogen, creatinine, and complete blood count.

Histologic examination for staging (I-V) occurs following surgical excision of the tumor. There are two staging systems available: the National Wilms Tumor Study, based on postoperative tumor evaluation, and the International Society of Pediatric Oncology, based on postchemotherapy evaluation.¹³

Treatment options include surgical excision (including complete nephrectomy of the affected kidney), chemotherapy based on tumor staging, and internal and/or external radiation therapy.¹³

Susan E. Brown, MS, ARNP,
ACNP-BC, CCRN
Great River Nephrology,
West Burlington, Iowa

REFERENCES

1.  United States Renal Data System. Annual data report: atlas of chronic kidney disease and end-stage renal disease in the United States (2012). www.usrds.org/2012/view/v1_01.aspx. Accessed October 19, 2014.

2.  Kopp JB, Nelson GW, Sampath K, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy.
J Am Soc Nephrol. 2011;22(11):2129-2137.

3.  Parsa A, Kao L, Xie D, et al; AASK and CRIC Study Investigators. APOL1 risk variants, race and progression of chronic kidney disease.
N Engl J Med. 2013;369:2183-2196.

4.  Foster MC, Coresh J, Fornage M, et al. APOL1 variants associate with increased risk of CKD among African Americans. J Am Soc Nephrol. 2013;24(9):1484-1491.

5.  Lipkowitz MS, Freedman BI, Langefeld CD, et al; AASK Investigators. Apolipoprotein L1 gene variants associate with hypertension-attributed nephropathy and the rate of kidney function decline in African Americans. Kidney Int. 2013;83(1):114–120.

6.  Reeves-Daniel AM, DePalma JA, Bleyer AJ, et al. The APOL1 gene and allograft survival after kidney transplantation. Am J Transplant. 2011;11(5):1025-1030.

7.  Partners Healthcare Personalized Medicine. Order APOL1 genotyping test for non-diabetic nephropathy kidney disease. http://personal izedmedicine.partners.org/Laboratory-For-Molecular-Medicine/Ordering/Kidney-Dis ease/APOL1-Gene-Sequencing.aspx. Accessed October 19, 2014.

8.  Grovas A, Fremgen A, Rauck A, et al. The National Cancer Data Base report on patterns of childhood cancers in the United States. Cancer. 1997;80(12):2321-2332.

9.  Johns Hopkins Medicine. Wilm’s tumor. www.hopkinsmedicine.org/kimmel_cancer_center/centers/pediatric_oncology/cancer_types/wilms_tumor.html. Accessed October 19, 2014.

10.  Dome JS, Huff V. Wilms tumor overview. In: Pagon RA, Adam MP, Ardinger HH, et al (eds). GeneReviews® [Internet]. Seattle, WA: University of Washington, Seattle; 1993-2014. www.ncbi.nlm.nih.gov/books/NBK1294/. Accessed October 19, 2014.

11.  Urbach A, Yermalovich A, Zhang J, et al. Lin28 sustains early renal progenitors and induces Wilms tumor. Genes & Dev. 2014;28:971-982.

12.  Fernandez C, Geller JI, Ehrlich PF, et al. Renal tumors. In: Pizzo P, Poplack D (eds). Principles and Practice of Pediatric Oncology. 6th ed, St Louis, MO: Lippincott Williams & Wilkins. 2011; 861.

13.  Metzger ML, Dome JS. Current therapy for Wilms’ tumor. Oncologist. 2005;10(10):815-826.

Clinical question: Does the use of 80% oxygen perioperatively in abdominal surgery decrease the frequency of surgical-site infection within 14 days without increasing the rate of pulmonary complications?

Background: Low oxygen tension in wounds can negatively impact immune response and healing. Increasing inspiratory oxygen fraction during the perioperative period translates into higher wound oxygen tension. However, the benefit of increased oxygen fraction therapy in abdominal surgery healing and complications is not clear, nor is the frequency of pulmonary complications.

Study design: Patient- and observer-blinded clinical trial.

Setting: Fourteen Danish hospitals from October 2006 to October 2008.

Synopsis: Patients were randomized to receive a fraction of inspired oxygen (FIO₂) of 0.80 or 0.30. The primary outcome—surgical-site infection in the superficial or deep wound or intra-abdominal cavity within 14 days of surgery—was defined using Centers for Disease Control and Prevention (CDC) criteria. Secondary outcomes included pulmonary complications within 14 days (pneumonia, atelectasis, or respiratory failure), 30-day mortality, duration of post-op course, ICU stay within 14 days post-op, and any abdominal operation within 14 days. The 1,386 patients were enrolled in the intention-to-treat analysis.

Infection occurred in 19.1% of patients given 0.80 FIO2 and in 20.1% of patients given 0.30 FIO2; odds ratio of 0.94 (95% CI 0.72 to 1.22; P=0.64). Numbers of pulmonary complications were not significantly different between the groups.

This trial included acute and nonacute laparotomies with followup for adverse outcomes. Study limitations included the inability to ensure that both groups received timely antibiotics and prevention for hypothermia. Of patients in the 30% FIO2 group, 7.3% required higher oxygen administration. Additionally, infection might have been underestimated in 11.3% of patients who were not followed up on between days 13 and 30.

Bottom line: High oxygen concentration administered during and after laparotomy did not lead to fewer surgical site infections, nor did it significantly increase the frequency of pulmonary complications or death.

Citation: Meyhoff CS, Wetterslev J, Jorgensen LN, et al. Effect of high perioperative oxygen fraction on surgical site infection and pulmonary complications after abdominal surgery: the PROXI randomized clinical trial. JAMA. 2009;302(14):1543-1550.

Clinical question: Does the use of 80% oxygen perioperatively in abdominal surgery decrease the frequency of surgical-site infection within 14 days without increasing the rate of pulmonary complications?

Background: Low oxygen tension in wounds can negatively impact immune response and healing. Increasing inspiratory oxygen fraction during the perioperative period translates into higher wound oxygen tension. However, the benefit of increased oxygen fraction therapy in abdominal surgery healing and complications is not clear, nor is the frequency of pulmonary complications.

Study design: Patient- and observer-blinded clinical trial.

Setting: Fourteen Danish hospitals from October 2006 to October 2008.

Synopsis: Patients were randomized to receive a fraction of inspired oxygen (FIO₂) of 0.80 or 0.30. The primary outcome—surgical-site infection in the superficial or deep wound or intra-abdominal cavity within 14 days of surgery—was defined using Centers for Disease Control and Prevention (CDC) criteria. Secondary outcomes included pulmonary complications within 14 days (pneumonia, atelectasis, or respiratory failure), 30-day mortality, duration of post-op course, ICU stay within 14 days post-op, and any abdominal operation within 14 days. The 1,386 patients were enrolled in the intention-to-treat analysis.

Infection occurred in 19.1% of patients given 0.80 FIO2 and in 20.1% of patients given 0.30 FIO2; odds ratio of 0.94 (95% CI 0.72 to 1.22; P=0.64). Numbers of pulmonary complications were not significantly different between the groups.

This trial included acute and nonacute laparotomies with followup for adverse outcomes. Study limitations included the inability to ensure that both groups received timely antibiotics and prevention for hypothermia. Of patients in the 30% FIO2 group, 7.3% required higher oxygen administration. Additionally, infection might have been underestimated in 11.3% of patients who were not followed up on between days 13 and 30.

Bottom line: High oxygen concentration administered during and after laparotomy did not lead to fewer surgical site infections, nor did it significantly increase the frequency of pulmonary complications or death.

Citation: Meyhoff CS, Wetterslev J, Jorgensen LN, et al. Effect of high perioperative oxygen fraction on surgical site infection and pulmonary complications after abdominal surgery: the PROXI randomized clinical trial. JAMA. 2009;302(14):1543-1550.

Clinical question: Does the use of 80% oxygen perioperatively in abdominal surgery decrease the frequency of surgical-site infection within 14 days without increasing the rate of pulmonary complications?

Background: Low oxygen tension in wounds can negatively impact immune response and healing. Increasing inspiratory oxygen fraction during the perioperative period translates into higher wound oxygen tension. However, the benefit of increased oxygen fraction therapy in abdominal surgery healing and complications is not clear, nor is the frequency of pulmonary complications.

Study design: Patient- and observer-blinded clinical trial.

Setting: Fourteen Danish hospitals from October 2006 to October 2008.

Synopsis: Patients were randomized to receive a fraction of inspired oxygen (FIO₂) of 0.80 or 0.30. The primary outcome—surgical-site infection in the superficial or deep wound or intra-abdominal cavity within 14 days of surgery—was defined using Centers for Disease Control and Prevention (CDC) criteria. Secondary outcomes included pulmonary complications within 14 days (pneumonia, atelectasis, or respiratory failure), 30-day mortality, duration of post-op course, ICU stay within 14 days post-op, and any abdominal operation within 14 days. The 1,386 patients were enrolled in the intention-to-treat analysis.

Infection occurred in 19.1% of patients given 0.80 FIO2 and in 20.1% of patients given 0.30 FIO2; odds ratio of 0.94 (95% CI 0.72 to 1.22; P=0.64). Numbers of pulmonary complications were not significantly different between the groups.

This trial included acute and nonacute laparotomies with followup for adverse outcomes. Study limitations included the inability to ensure that both groups received timely antibiotics and prevention for hypothermia. Of patients in the 30% FIO2 group, 7.3% required higher oxygen administration. Additionally, infection might have been underestimated in 11.3% of patients who were not followed up on between days 13 and 30.

Bottom line: High oxygen concentration administered during and after laparotomy did not lead to fewer surgical site infections, nor did it significantly increase the frequency of pulmonary complications or death.

Citation: Meyhoff CS, Wetterslev J, Jorgensen LN, et al. Effect of high perioperative oxygen fraction on surgical site infection and pulmonary complications after abdominal surgery: the PROXI randomized clinical trial. JAMA. 2009;302(14):1543-1550.

By Mark Shen, MD

Reviewed by Pediatric Editor Mark Shen, MD, medical director of hospital medicine at Dell Children’s Medical Center, Austin, Texas.

Clinical question: Is a short course (less than four weeks) of antibiotics effective for the treatment of acute osteomyelitis and septic arthritis?

Background: The optimal duration of treatment for acute bone and joint infections in children has not been assessed adequately in prospectively designed trials. Historically, intravenous (IV) antibiotics in four- to six-week durations have been recommended, although the evidence for this practice is limited. There is widespread variation in both the route of administration (oral vs. IV) and duration of this treatment.

Study design: Prospective cohort study.

Setting: Two children’s hospitals in Australia.

Synopsis: Seventy children ages 17 and under who presented to two tertiary-care children’s hospitals with osteomyelitis or septic arthritis were enrolled. Primary surgical drainage was performed for patients with septic arthritis. Intravenous antibiotics were administered for at least three days, and until clinical symptoms improved and the C-reactive protein levels had stabilized. Patients then were transitioned to oral antibiotics and discharged to complete a minimum of three weeks of therapy.

Fifty-nine percent of patients were converted to oral antibiotics by day three, 86% by day five of therapy. Based on clinical and hematologic assessment, 83% of patients had oral antibiotics stopped at the three-week followup and remained well through the 12-month follow-up period.

This study essentially involved prospective data collection for a cohort of children receiving standardized care. Although the results suggest that a majority of children can be treated with a three-week course of oral antibiotics, the results would have been further strengthened by an explicit protocol with well-defined criteria for the oral to IV transition and cessation of antibiotic therapy. Additional limitations include pathogens and antibiotic choices that might not be applicable to North American populations.

Bottom line: After initial intravenous therapy, a three-week course of oral antibiotics can be effective for acute osteomyelitis and septic arthritis in children.

Citation: Jagodzinski NA, Kanwar R, Graham K, Bache CE. Prospective evaluation of a shortened regimen of treatment for acute osteomyelitis and septic arthritis in children. J Pediatr Orthop. 2009;29(5):518-525.

By Mark Shen, MD

Reviewed by Pediatric Editor Mark Shen, MD, medical director of hospital medicine at Dell Children’s Medical Center, Austin, Texas.

Clinical question: Is a short course (less than four weeks) of antibiotics effective for the treatment of acute osteomyelitis and septic arthritis?

Background: The optimal duration of treatment for acute bone and joint infections in children has not been assessed adequately in prospectively designed trials. Historically, intravenous (IV) antibiotics in four- to six-week durations have been recommended, although the evidence for this practice is limited. There is widespread variation in both the route of administration (oral vs. IV) and duration of this treatment.

Study design: Prospective cohort study.

Setting: Two children’s hospitals in Australia.

Synopsis: Seventy children ages 17 and under who presented to two tertiary-care children’s hospitals with osteomyelitis or septic arthritis were enrolled. Primary surgical drainage was performed for patients with septic arthritis. Intravenous antibiotics were administered for at least three days, and until clinical symptoms improved and the C-reactive protein levels had stabilized. Patients then were transitioned to oral antibiotics and discharged to complete a minimum of three weeks of therapy.

Fifty-nine percent of patients were converted to oral antibiotics by day three, 86% by day five of therapy. Based on clinical and hematologic assessment, 83% of patients had oral antibiotics stopped at the three-week followup and remained well through the 12-month follow-up period.

This study essentially involved prospective data collection for a cohort of children receiving standardized care. Although the results suggest that a majority of children can be treated with a three-week course of oral antibiotics, the results would have been further strengthened by an explicit protocol with well-defined criteria for the oral to IV transition and cessation of antibiotic therapy. Additional limitations include pathogens and antibiotic choices that might not be applicable to North American populations.

Bottom line: After initial intravenous therapy, a three-week course of oral antibiotics can be effective for acute osteomyelitis and septic arthritis in children.

Citation: Jagodzinski NA, Kanwar R, Graham K, Bache CE. Prospective evaluation of a shortened regimen of treatment for acute osteomyelitis and septic arthritis in children. J Pediatr Orthop. 2009;29(5):518-525.

By Mark Shen, MD

Reviewed by Pediatric Editor Mark Shen, MD, medical director of hospital medicine at Dell Children’s Medical Center, Austin, Texas.

Clinical question: Is a short course (less than four weeks) of antibiotics effective for the treatment of acute osteomyelitis and septic arthritis?

Background: The optimal duration of treatment for acute bone and joint infections in children has not been assessed adequately in prospectively designed trials. Historically, intravenous (IV) antibiotics in four- to six-week durations have been recommended, although the evidence for this practice is limited. There is widespread variation in both the route of administration (oral vs. IV) and duration of this treatment.

Study design: Prospective cohort study.

Setting: Two children’s hospitals in Australia.

Synopsis: Seventy children ages 17 and under who presented to two tertiary-care children’s hospitals with osteomyelitis or septic arthritis were enrolled. Primary surgical drainage was performed for patients with septic arthritis. Intravenous antibiotics were administered for at least three days, and until clinical symptoms improved and the C-reactive protein levels had stabilized. Patients then were transitioned to oral antibiotics and discharged to complete a minimum of three weeks of therapy.

Fifty-nine percent of patients were converted to oral antibiotics by day three, 86% by day five of therapy. Based on clinical and hematologic assessment, 83% of patients had oral antibiotics stopped at the three-week followup and remained well through the 12-month follow-up period.

This study essentially involved prospective data collection for a cohort of children receiving standardized care. Although the results suggest that a majority of children can be treated with a three-week course of oral antibiotics, the results would have been further strengthened by an explicit protocol with well-defined criteria for the oral to IV transition and cessation of antibiotic therapy. Additional limitations include pathogens and antibiotic choices that might not be applicable to North American populations.

Bottom line: After initial intravenous therapy, a three-week course of oral antibiotics can be effective for acute osteomyelitis and septic arthritis in children.

Citation: Jagodzinski NA, Kanwar R, Graham K, Bache CE. Prospective evaluation of a shortened regimen of treatment for acute osteomyelitis and septic arthritis in children. J Pediatr Orthop. 2009;29(5):518-525.

Clinical question: Do on-screen, computer-based clinical reminders improve adherence to target processes of care or clinical outcomes?

Background: Gaps between practice guidelines and routine care are caused, in part, by the inability of clinicians to access or recall information at the point of care. Although automated reminder systems offer the promise of “just in time” recommendations, studies of electronic reminders have demonstrated mixed results.

Study design: Literature review and meta-analysis.

Setting: Multiple databases and information repositories, including MEDLINE, EMBASE, and CINAHL.

Synopsis: The authors conducted a literature search to identify randomized and quasi-randomized controlled trials measuring the effect of computer-based reminders on process measures or clinical outcomes. To avoid statistical challenges inherent in unit-of-analysis errors, the authors reported median improvement in process adherence or median change in clinical endpoints.

Out of a pool of 2,036 citations, 28 studies detailing 32 comparative analyses were included. Across the 28 studies, reminders resulted in a median improvement in target process adherence of 4.2% (3.3% for prescribing behavior, 2.8% for test ordering). Eight comparisons reported dichotomous clinical endpoints and collectively showed a median absolute improvement of 2.5%.

The greatest contribution to measured treatment effects came from large academic centers with well-established electronic health records and robust informatics departments. No characteristics of the reminder system or the clinical context were associated with the magnitude of impact. A potential limitation in reporting median effects across studies is that all studies were given equal weight.

Bottom line: Electronic reminders appear to have a small, positive effect on clinician adherence to recommended processes, although it is uncertain what contextual or design features are responsible for the greatest treatment effect.

Citation: Shojania K, Jennings A, Mayhew A, Ramsay CR, Eccles MP, Grimshaw J. The effects of on-screen, point of care computer reminders on processes and outcomes of care. Cochrane Database Syst Rev. 2009(3):CD001096. TH

Clinical question: Do on-screen, computer-based clinical reminders improve adherence to target processes of care or clinical outcomes?

Background: Gaps between practice guidelines and routine care are caused, in part, by the inability of clinicians to access or recall information at the point of care. Although automated reminder systems offer the promise of “just in time” recommendations, studies of electronic reminders have demonstrated mixed results.

Study design: Literature review and meta-analysis.

Setting: Multiple databases and information repositories, including MEDLINE, EMBASE, and CINAHL.

Synopsis: The authors conducted a literature search to identify randomized and quasi-randomized controlled trials measuring the effect of computer-based reminders on process measures or clinical outcomes. To avoid statistical challenges inherent in unit-of-analysis errors, the authors reported median improvement in process adherence or median change in clinical endpoints.

Out of a pool of 2,036 citations, 28 studies detailing 32 comparative analyses were included. Across the 28 studies, reminders resulted in a median improvement in target process adherence of 4.2% (3.3% for prescribing behavior, 2.8% for test ordering). Eight comparisons reported dichotomous clinical endpoints and collectively showed a median absolute improvement of 2.5%.

The greatest contribution to measured treatment effects came from large academic centers with well-established electronic health records and robust informatics departments. No characteristics of the reminder system or the clinical context were associated with the magnitude of impact. A potential limitation in reporting median effects across studies is that all studies were given equal weight.

Bottom line: Electronic reminders appear to have a small, positive effect on clinician adherence to recommended processes, although it is uncertain what contextual or design features are responsible for the greatest treatment effect.

Citation: Shojania K, Jennings A, Mayhew A, Ramsay CR, Eccles MP, Grimshaw J. The effects of on-screen, point of care computer reminders on processes and outcomes of care. Cochrane Database Syst Rev. 2009(3):CD001096. TH

Clinical question: Do on-screen, computer-based clinical reminders improve adherence to target processes of care or clinical outcomes?

Background: Gaps between practice guidelines and routine care are caused, in part, by the inability of clinicians to access or recall information at the point of care. Although automated reminder systems offer the promise of “just in time” recommendations, studies of electronic reminders have demonstrated mixed results.

Study design: Literature review and meta-analysis.

Setting: Multiple databases and information repositories, including MEDLINE, EMBASE, and CINAHL.

Synopsis: The authors conducted a literature search to identify randomized and quasi-randomized controlled trials measuring the effect of computer-based reminders on process measures or clinical outcomes. To avoid statistical challenges inherent in unit-of-analysis errors, the authors reported median improvement in process adherence or median change in clinical endpoints.

Out of a pool of 2,036 citations, 28 studies detailing 32 comparative analyses were included. Across the 28 studies, reminders resulted in a median improvement in target process adherence of 4.2% (3.3% for prescribing behavior, 2.8% for test ordering). Eight comparisons reported dichotomous clinical endpoints and collectively showed a median absolute improvement of 2.5%.

The greatest contribution to measured treatment effects came from large academic centers with well-established electronic health records and robust informatics departments. No characteristics of the reminder system or the clinical context were associated with the magnitude of impact. A potential limitation in reporting median effects across studies is that all studies were given equal weight.

Bottom line: Electronic reminders appear to have a small, positive effect on clinician adherence to recommended processes, although it is uncertain what contextual or design features are responsible for the greatest treatment effect.

Citation: Shojania K, Jennings A, Mayhew A, Ramsay CR, Eccles MP, Grimshaw J. The effects of on-screen, point of care computer reminders on processes and outcomes of care. Cochrane Database Syst Rev. 2009(3):CD001096. TH

Clinical question: Does the inclusion of a medication adherence counseling session during a hospital discharge reconciliation process reduce discrepancies in the final medication regimen?

Background: Inadvertent medication prescribing errors are an important cause of preventable adverse drug events and commonly occur at transitions of care. Although medication reconciliation processes can identify errors, the best strategies for implementation remain unclear.

Study design: Prospective, observational cohort.

Setting: A 550-bed teaching hospital in the Netherlands.

Synopsis: Of 437 patients admitted to a pulmonary ward and screened for eligibility, 267 were included in the analysis. A pharmacy specialist reviewed all available community prescription records, inpatient documentation, and discharge medication lists in an effort to identify discrepancies. Potential errors were discussed with the prescriber. Then, the pharmacy specialist interviewed the patient and provided additional counseling. Any new discrepancies were discussed with the prescriber. All questions raised by the pharmacist were recorded, as were all subsequent prescriber interventions.

The primary outcome measure was the number of interventions made as a result of pharmacy review. A total of 940 questions were asked. At least one intervention was recorded for 87% of patients before counseling (mean 2.7 interventions/patient) and for 97% of patients after (mean 5.3 interventions/patient). Discrepancies were addressed for 63.7% of patients before counseling and 72.5% after. Pharmacotherapy was optimized for 67.2% of patients before counseling and 76.3% after.

Bottom line: Patient engagement in the medication reconciliation process incrementally improves the quality of the history and helps identify clinically meaningful discrepancies at the time of hospital discharge.

Citation: Karapinar-Carkit F, Borgsteede S, Zoer J, Smit HJ, Egberts AC, van den Bemt P. Effect of medication reconciliation with and without patient counseling on the number of pharmaceutical interventions among patients discharged from the hospital. Ann Pharmacother. 2009;43(6):1001-1010.

Clinical question: Does the inclusion of a medication adherence counseling session during a hospital discharge reconciliation process reduce discrepancies in the final medication regimen?

Background: Inadvertent medication prescribing errors are an important cause of preventable adverse drug events and commonly occur at transitions of care. Although medication reconciliation processes can identify errors, the best strategies for implementation remain unclear.

Study design: Prospective, observational cohort.

Setting: A 550-bed teaching hospital in the Netherlands.

Synopsis: Of 437 patients admitted to a pulmonary ward and screened for eligibility, 267 were included in the analysis. A pharmacy specialist reviewed all available community prescription records, inpatient documentation, and discharge medication lists in an effort to identify discrepancies. Potential errors were discussed with the prescriber. Then, the pharmacy specialist interviewed the patient and provided additional counseling. Any new discrepancies were discussed with the prescriber. All questions raised by the pharmacist were recorded, as were all subsequent prescriber interventions.

The primary outcome measure was the number of interventions made as a result of pharmacy review. A total of 940 questions were asked. At least one intervention was recorded for 87% of patients before counseling (mean 2.7 interventions/patient) and for 97% of patients after (mean 5.3 interventions/patient). Discrepancies were addressed for 63.7% of patients before counseling and 72.5% after. Pharmacotherapy was optimized for 67.2% of patients before counseling and 76.3% after.

Bottom line: Patient engagement in the medication reconciliation process incrementally improves the quality of the history and helps identify clinically meaningful discrepancies at the time of hospital discharge.

Citation: Karapinar-Carkit F, Borgsteede S, Zoer J, Smit HJ, Egberts AC, van den Bemt P. Effect of medication reconciliation with and without patient counseling on the number of pharmaceutical interventions among patients discharged from the hospital. Ann Pharmacother. 2009;43(6):1001-1010.

Clinical question: Does the inclusion of a medication adherence counseling session during a hospital discharge reconciliation process reduce discrepancies in the final medication regimen?

Background: Inadvertent medication prescribing errors are an important cause of preventable adverse drug events and commonly occur at transitions of care. Although medication reconciliation processes can identify errors, the best strategies for implementation remain unclear.

Study design: Prospective, observational cohort.

Setting: A 550-bed teaching hospital in the Netherlands.

Synopsis: Of 437 patients admitted to a pulmonary ward and screened for eligibility, 267 were included in the analysis. A pharmacy specialist reviewed all available community prescription records, inpatient documentation, and discharge medication lists in an effort to identify discrepancies. Potential errors were discussed with the prescriber. Then, the pharmacy specialist interviewed the patient and provided additional counseling. Any new discrepancies were discussed with the prescriber. All questions raised by the pharmacist were recorded, as were all subsequent prescriber interventions.

The primary outcome measure was the number of interventions made as a result of pharmacy review. A total of 940 questions were asked. At least one intervention was recorded for 87% of patients before counseling (mean 2.7 interventions/patient) and for 97% of patients after (mean 5.3 interventions/patient). Discrepancies were addressed for 63.7% of patients before counseling and 72.5% after. Pharmacotherapy was optimized for 67.2% of patients before counseling and 76.3% after.

Bottom line: Patient engagement in the medication reconciliation process incrementally improves the quality of the history and helps identify clinically meaningful discrepancies at the time of hospital discharge.

Citation: Karapinar-Carkit F, Borgsteede S, Zoer J, Smit HJ, Egberts AC, van den Bemt P. Effect of medication reconciliation with and without patient counseling on the number of pharmaceutical interventions among patients discharged from the hospital. Ann Pharmacother. 2009;43(6):1001-1010.

Clinical question: In patients with symptoms consistent with pulmonary embolism (PE), can evaluation with a clinical risk assessment tool and D-dimer assay identify patients who do not require CT angiography to exclude PE?

Background: D-dimer is a highly sensitive but nonspecific marker of VTE, and studies suggest that VTE can be ruled out without further imaging in patients with low clinical probability of disease and a negative D-dimer test. Nevertheless, this practice has not been adopted uniformly, and CT angiography (CTA) overuse continues.

Study design: Prospective registry cohort.

Setting: A 550-bed community teaching hospital in Chicago.

Synopsis: Consecutive patients presenting to the ED with symptoms suggestive of PE were evaluated with 1) revised Geneva score; 2) D-dimer assay; and 3) CTA. Among the 627 patients who underwent all three components of the evaluation, 44.8% were identified as low probability for PE by revised Geneva score, 52.6% as intermediate probability, and 2.6% as high probability. The overall prevalence of PE (using CTA as the gold standard) was very low (4.5%); just 2.1% of low-risk, 5.2% of intermediate-risk, and 31.2% of high-risk patients were ultimately found to have PE on CTA.

Using a cutoff of 1.2 mg/L, the D-dimer assay accurately detected all low- to intermediate-probability patients with PE (sensitivity and negative predictive value of 100%). One patient in the high probability group did have a PE, even though the patient had a D-dimer value <1.2 mg/L (sensitivity and NPV both 80%). Had diagnostic testing stopped after a negative D-dimer result in the low- to intermediate-probability patients, 172 CTAs (27%) would have been avoided.

Bottom line: In a low-prevalence cohort, no pulmonary emboli were identified by CTA in any patient with a low to intermediate clinical risk assessment and a negative quantitative D-dimer assay result.

Citation: Gupta RT, Kakarla RK, Kirshenbaum KJ, Tapson VF. D-dimers and efficacy of clinical risk estimation algorithms: sensitivity in evaluation of acute pulmonary embolism. AJR Am J Roentgenol. 2009;193(2):425-430.

Clinical question: In patients with symptoms consistent with pulmonary embolism (PE), can evaluation with a clinical risk assessment tool and D-dimer assay identify patients who do not require CT angiography to exclude PE?

Background: D-dimer is a highly sensitive but nonspecific marker of VTE, and studies suggest that VTE can be ruled out without further imaging in patients with low clinical probability of disease and a negative D-dimer test. Nevertheless, this practice has not been adopted uniformly, and CT angiography (CTA) overuse continues.

Study design: Prospective registry cohort.

Setting: A 550-bed community teaching hospital in Chicago.

Synopsis: Consecutive patients presenting to the ED with symptoms suggestive of PE were evaluated with 1) revised Geneva score; 2) D-dimer assay; and 3) CTA. Among the 627 patients who underwent all three components of the evaluation, 44.8% were identified as low probability for PE by revised Geneva score, 52.6% as intermediate probability, and 2.6% as high probability. The overall prevalence of PE (using CTA as the gold standard) was very low (4.5%); just 2.1% of low-risk, 5.2% of intermediate-risk, and 31.2% of high-risk patients were ultimately found to have PE on CTA.

Using a cutoff of 1.2 mg/L, the D-dimer assay accurately detected all low- to intermediate-probability patients with PE (sensitivity and negative predictive value of 100%). One patient in the high probability group did have a PE, even though the patient had a D-dimer value <1.2 mg/L (sensitivity and NPV both 80%). Had diagnostic testing stopped after a negative D-dimer result in the low- to intermediate-probability patients, 172 CTAs (27%) would have been avoided.

Bottom line: In a low-prevalence cohort, no pulmonary emboli were identified by CTA in any patient with a low to intermediate clinical risk assessment and a negative quantitative D-dimer assay result.

Citation: Gupta RT, Kakarla RK, Kirshenbaum KJ, Tapson VF. D-dimers and efficacy of clinical risk estimation algorithms: sensitivity in evaluation of acute pulmonary embolism. AJR Am J Roentgenol. 2009;193(2):425-430.

Clinical question: In patients with symptoms consistent with pulmonary embolism (PE), can evaluation with a clinical risk assessment tool and D-dimer assay identify patients who do not require CT angiography to exclude PE?

Background: D-dimer is a highly sensitive but nonspecific marker of VTE, and studies suggest that VTE can be ruled out without further imaging in patients with low clinical probability of disease and a negative D-dimer test. Nevertheless, this practice has not been adopted uniformly, and CT angiography (CTA) overuse continues.

Study design: Prospective registry cohort.

Setting: A 550-bed community teaching hospital in Chicago.

Synopsis: Consecutive patients presenting to the ED with symptoms suggestive of PE were evaluated with 1) revised Geneva score; 2) D-dimer assay; and 3) CTA. Among the 627 patients who underwent all three components of the evaluation, 44.8% were identified as low probability for PE by revised Geneva score, 52.6% as intermediate probability, and 2.6% as high probability. The overall prevalence of PE (using CTA as the gold standard) was very low (4.5%); just 2.1% of low-risk, 5.2% of intermediate-risk, and 31.2% of high-risk patients were ultimately found to have PE on CTA.

Using a cutoff of 1.2 mg/L, the D-dimer assay accurately detected all low- to intermediate-probability patients with PE (sensitivity and negative predictive value of 100%). One patient in the high probability group did have a PE, even though the patient had a D-dimer value <1.2 mg/L (sensitivity and NPV both 80%). Had diagnostic testing stopped after a negative D-dimer result in the low- to intermediate-probability patients, 172 CTAs (27%) would have been avoided.

Bottom line: In a low-prevalence cohort, no pulmonary emboli were identified by CTA in any patient with a low to intermediate clinical risk assessment and a negative quantitative D-dimer assay result.

Citation: Gupta RT, Kakarla RK, Kirshenbaum KJ, Tapson VF. D-dimers and efficacy of clinical risk estimation algorithms: sensitivity in evaluation of acute pulmonary embolism. AJR Am J Roentgenol. 2009;193(2):425-430.