Diabetic foot laboratory findings: Difference between revisions
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==Laboratory Findings== | ==Laboratory Findings== | ||
*Even in deeply [[infection|infected]] [[ulcers]] laboratory measures such as [[White blood cells|WBC]], [[Erythrocyte sedimentation rate|ESR]] and [[C-reactive protein|CRP]] might be normal.<ref name="LepäntaloApelqvist2011">{{cite journal|last1=Lepäntalo|first1=M.|last2=Apelqvist|first2=J.|last3=Setacci|first3=C.|last4=Ricco|first4=J.-B.|last5=de Donato|first5=G.|last6=Becker|first6=F.|last7=Robert-Ebadi|first7=H.|last8=Cao|first8=P.|last9=Eckstein|first9=H.H.|last10=De Rango|first10=P.|last11=Diehm|first11=N.|last12=Schmidli|first12=J.|last13=Teraa|first13=M.|last14=Moll|first14=F.L.|last15=Dick|first15=F.|last16=Davies|first16=A.H.|title=Chapter V: Diabetic Foot|journal=European Journal of Vascular and Endovascular Surgery|volume=42|year=2011|pages=S60–S74|issn=10785884|doi=10.1016/S1078-5884(11)60012-9}}</ref> | *Even in deeply [[infection|infected]] [[ulcers]] laboratory measures such as [[White blood cells|WBC]], [[Erythrocyte sedimentation rate|ESR]] and [[C-reactive protein|CRP]] might be normal. Nevertheless elevated measures demonstrate [[infection]].<ref name="LepäntaloApelqvist2011">{{cite journal|last1=Lepäntalo|first1=M.|last2=Apelqvist|first2=J.|last3=Setacci|first3=C.|last4=Ricco|first4=J.-B.|last5=de Donato|first5=G.|last6=Becker|first6=F.|last7=Robert-Ebadi|first7=H.|last8=Cao|first8=P.|last9=Eckstein|first9=H.H.|last10=De Rango|first10=P.|last11=Diehm|first11=N.|last12=Schmidli|first12=J.|last13=Teraa|first13=M.|last14=Moll|first14=F.L.|last15=Dick|first15=F.|last16=Davies|first16=A.H.|title=Chapter V: Diabetic Foot|journal=European Journal of Vascular and Endovascular Surgery|volume=42|year=2011|pages=S60–S74|issn=10785884|doi=10.1016/S1078-5884(11)60012-9}}</ref> | ||
*Presence of [[infection]] in [[diabetic foot|diabetic ulcers]] can worsen the [[Diabetes management|glycemic control]].<ref name="Lipsky2004">{{cite journal|last1=Lipsky|first1=Benjamin A.|title=A report from the international consensus on diagnosing and treating the infected diabetic foot|journal=Diabetes/Metabolism Research and Reviews|volume=20|issue=S1|year=2004|pages=S68–S77|issn=1520-7552|doi=10.1002/dmrr.453}}</ref> | *Presence of [[infection]] in [[diabetic foot|diabetic ulcers]] can worsen the [[Diabetes management|glycemic control]].<ref name="Lipsky2004">{{cite journal|last1=Lipsky|first1=Benjamin A.|title=A report from the international consensus on diagnosing and treating the infected diabetic foot|journal=Diabetes/Metabolism Research and Reviews|volume=20|issue=S1|year=2004|pages=S68–S77|issn=1520-7552|doi=10.1002/dmrr.453}}</ref> | ||
*For detection of main responsible [[microorganisms]] [[biopsy]], [[curettage]] or aspiration a tissue sample is recommended. | *For detection of main responsible [[microorganisms]] [[biopsy]], [[curettage]] or aspiration a tissue sample is recommended. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Anahita Deylamsalehi, M.D.[2]
Overview
Laboratory Findings
- Even in deeply infected ulcers laboratory measures such as WBC, ESR and CRP might be normal. Nevertheless elevated measures demonstrate infection.[1]
- Presence of infection in diabetic ulcers can worsen the glycemic control.[2]
- For detection of main responsible microorganisms biopsy, curettage or aspiration a tissue sample is recommended.
References
- ↑ Lepäntalo, M.; Apelqvist, J.; Setacci, C.; Ricco, J.-B.; de Donato, G.; Becker, F.; Robert-Ebadi, H.; Cao, P.; Eckstein, H.H.; De Rango, P.; Diehm, N.; Schmidli, J.; Teraa, M.; Moll, F.L.; Dick, F.; Davies, A.H. (2011). "Chapter V: Diabetic Foot". European Journal of Vascular and Endovascular Surgery. 42: S60–S74. doi:10.1016/S1078-5884(11)60012-9. ISSN 1078-5884.
- ↑ Lipsky, Benjamin A. (2004). "A report from the international consensus on diagnosing and treating the infected diabetic foot". Diabetes/Metabolism Research and Reviews. 20 (S1): S68–S77. doi:10.1002/dmrr.453. ISSN 1520-7552.