Congratulations to our colleagues Nelson and coworkers and our long-time SALSAmigo, Oxford’s finest, Prof. BA Lipsky– for this superb work.
Abstract
Objective: To determine the extent of agreement and patterns of disagreement between wound swab and tissue samples in patients with an infected diabetic foot ulcer (DFU). Design: Multi-centre, prospective, cross-sectional study. Setting: Primary and secondary care foot ulcer/diabetic outpatient clinics and hospital wards across England. Participants: Inclusion criteria: Consenting patients aged ≥18 years; diabetes mellitus; suspected infected DFU. Exclusion criteria: Clinically inappropriate to take either sample. Interventions: Wound swab obtained using Levine’s technique; tissue samples collected using a sterile dermal curette or scalpel. Outcome measures: Co-primary: Reported presence, and number, of pathogens per sample; prevalence of resistance to antimicrobials among likely pathogens. Secondary: Recommended change in antibiotic therapy based on blinded clinical review; adverse events; and, sampling costs. Results: 400 consenting patients (79% male) from 25 centres. Most prevalent reported pathogens were Staphylococcus aureus (43.8%), Streptococcus (16.7%), and other aerobic gram-positive cocci (70.6%). At least one potential pathogen was reported from 70.1% of wound swab and 86.1% of tissue samples. Pathogen results differed between sampling method in 58% of patients, with more pathogens and fewer contaminants reported from tissues. The majority of pathogens were reported significantly more frequently in tissue than wound swab samples (p<0.01); with equal disagreement for Staphylococcus aureus and Pseudomonas aeruginosa. Blinded clinicians more often recommended a change in antibiotic regimen based on tissue compared with wound swab results (increase of 8.9%, 95% CI:2.65,15.3%). Ulcer pain and bleeding occurred more often after tissue collection versus wound swabs (pain: 9.3%,1.3%; bleeding: 6.8%,1.5%, respectively). Conclusion: Reports of tissue samples more frequently identified pathogens, and less frequently identified non-pathogens compared with wound swab samples. Blinded clinicians more often recommended changes in antibiotic therapy based on tissue compared with wound swab specimens. Further research is needed to determine the effect of the additional information provided by tissue samples. Study Registration: NRES Ref:11/YH/0078;UKCRN ID:10440;ISRCTN:52608451
in diabetic foot ulcers, in principle, there is no pathogen apart from excess sugar. The only useful treatment is debridement of both feet, knee-length toes for several months. Not with a scalpel but, a chemical that can give the skin all its elasticity and total sensitivity. that’s allall
be caraful what you define as an infected diabetic wound. If one obtains a tissue bx and does quantitative bacteriology on the tissue removed and the count is greater that 1×10-5th bacteria then by definition it is an infected wound. ( strep and a few other bacteria break this rule) A very innocent looking diabetic wound may be infected and clinical recognition is only made by probing the wound. Although the data is not clear yet, my bets are that ultrasound will be a helpful diagnostic tool in those lesions that are deep. Look back a good 20 or 30 years at the papers of Robson, Heggers and Krizek and be enlightened. Nice thoughtful study from the Oxford group. To answer the comment made about “sugar”–one can have neuropathy caused in part by lack of glucose control but the neuropathy may remain after good control of glucose is maintained so it is not an answer that can come from the present glucose level. One can have great glucose control and an ulcer from neuropathy or other promoting factors.
If he were still alive today, Louis Pasteur would tell us: Do not serching anymore. There are no significant pathogenic bacteria in the DFU . You’re wasting your time. Look at Walter’s experiences for curing it
1482/5000
Yes it’s true, you can have excellent glycemic control and an ulcer can not heal. It’s normal. It all depends on the aging of our ulcer. Once the ulcer is present and the skin of the leg is sclerotic, hyperkeratinized, our ulcer will continue to advance, even if the glucose is well regulated. Because the keratinocyte that arrives on the ulcer space took a few hours to migrate from the base to the cornea and did not have time to have the differentiation to get keratohyaline. Arrived in the wound, they are empty and they are extremely hard insoluble and do not leave their place to the new production that has had time to make the difference. And it is the crust that, from time to time, one can see with the eyes on the skin. At this moment the hole formed by the ulcer becomes an exit opening for which it must remain open for several reasons. Then each crust will open again with each new hyperglicemia and each call of the wound for a new arrige of massive proliferation of keratinocytes.or each pressure when one walks .. your ulcer becomes chronic … Yes, there is high bacterial presence but, the presence of the wound comes before the presence of bacteria, and controlled bacteria does not mean that the ulcer will be cured. All studies say and experience shows us. Bacteria are not significant pathogens for BFU cures