Hey, that foot looks like it is infected. There are multiple, sometime simultaneous, flavors of the diabetic foot infection (mmmmmmmmm diabetic foot):
To diagnose osteomyelitis, the only good test is a probe in the hands of a doctor looking for soft bone; x-rays, CT's, and WBC scans are almost always a waste of time to make the diagnosis, as both the false positive and negative rates are too high; they can be helpful in determining the extent of disease. Needle biopsies are not reliable (PubMed).
If you feel you must do a radiographic study for osteomyelitis, the best bet is to go straight to an MRI (PubMed).
To quote from a meta analysis (PubMed):
"Exposed bone or probe-to-bone test had a sensitivity of 0.60 and a specificity of 0.91. Plain radiography had a sensitivity of 0.54 and a specificity of 0.68. MRI had a sensitivity of 0.90 and a specificity of 0.79. Bone scan was found to have a sensitivity of 0.81 and a specificity of 0.28. Leukocyte scan was found to have a sensitivity of 0.74 and a specificity of 0.68. The diagnostic odds ratios for clinical examination, radiography, MRI, bone scan, and leukocyte scan were 49.45, 2.84, 24.36, 2.10, and 10.07, respectively.The presence of exposed bone or a positive probe-to-bone test result is moderately predictive of osteomyelitis. MRI is the most accurate imaging test for diagnosis of osteomyelitis".
"Pooled sensitivity and specificity for the probe to bone test was 0.87 (95% confidence interval [CI], .75-.93) and 0.83 (95% CI, .65-.93), respectively. " (Pubmed)
Is it Charcot? Lets compare and contrast: Charcot is uncommon, occurs in the midfoot and requires good blood flow. Osteomyelitis is common, occurs in forefoot over the metatarsal heads and is ischemic/pressure.
Having a foot and diabetes; the worse the vasculopathy, neuropathy and diabetic control, the more likely the infection.
Cultures under represent the number of organisms by a factor of 5 compared to using molecular techniques; there are always anaerobes, although their pathogenicity is uncertain (Review).
Different versions of this disease as follows
- Ulcer: ulcers are not infected, although it can serve as a source of infection. It you culture a clinically uninfected ulcer, you can grow anything; consider the ulcer an extension of the rectum. And culturing an ulcer when there is a soft tissue infection of the foot or leg is like culturing the rectum for sore throat. Sure, they are connected anatomically, but the utility of the culture is questionable.
Same. For non-necrotizing/dead meat infections diabetics have the same causal bacteria as non-diabetics for their cellulitis: Strep and Staph. (PubMed). Unless they have a necrotizing fasciitis all they need is cefazolin.
- Fetid foot: a dead foot on the end of a leg: can grow anything.
- Rapidly progressive cellulitis/fasciitis/myositis with sepsis and poorly controlled sugars i.e. mixed synergistic necrotizing fasciitis: gram negative rods PLUS streptococci PLUS anaerobes OR Group A Streptococci OR methicillin resistant S. aureus.
- Osteomyelitis: Anything. Biopsy is both diagnostic and therapeutic. There may be many more organisms in the bone than be grown (Pubmed), but I wonder the clinical relevance as they are all susceptible to debridmement.
Heres my opinion:
Surgery. If there are anaerobes and gram negative bacilli, that means dead tissue and that means aggressive debridement. Most dead tissue, while it grows bacteria, is not infected.
Here is a surprise (at least to me). After successful treatment diabetic foor infections tend to recur (not a surprise) but the prior treatment doesn't lead to subsequent infections from resistant organisms (PubMed). That is a surprise.
If mixed synergistic necrotizing fasciitis: third generation cephalosporins PLUS metronidazole OR carbapenems OR quinolone PLUS metronidazole ORpiperacillin/tazobactam ALL SELECTIONS +/- aminoglycosides if septic.
The treatment of diabetic foot osteomyelitis is removal of the dead bone, which should be definitive therapy. If there is infection left behind, they need further debridement, not further antibiotics. Conservative treatment of the diabetic foot osteomyelitis (medical not surgical) means that they are more likely to lose the whole foot later. I treat osteomyelitis for 24-48 hours after debridement with IV then send them home on po or nothing; the surgery should have cured the infection and unlike some quantum effects, antibiotics do not work at a distance (i.e. treat the infection in the pathology lab).
Hyperbaric oxygen? I was once asked what I thought of hyperbaric and I said the data was of variable quality except for the bends and most served to enrich the hyperbaric chamber owners. Why? I am the new director of the hyperbaric chamber he replied. When someone asks a question on a controversial topic, ask why before answering. What to you think of Morgellons? Chronic Lyme? etc. That being said, the better studies suggest it is NOT helpful (PubMed).
Antibiotics without debridement is the definition of futility. Look it up; it's in the OED.
Duration of therapy? Cure, however you define it. Usually debridement equals cure, but if infected bone cannot always be removed 12 to 6 weeks of therapy may be curative. The guidelines say 12 weeks, although a study with small numbers suggests 6 may suffice (PubMed).
An ounce of prevention is worth a pound of cure. At least until the economic meltdown of 09. After than an ounce of prevention was worth 9 lbs of cure, so everyone defaulted in their prevention loan and there were a lot of foreclosures.
Every visit the diabetic should be reminded about good foot care.
A big hole in the foot is bad. Diabetic foot ulcers markedly increase the risk for a variety of severe invasive infections in the next year, especially with MRSA (PubMed).
Much to my surprise, recurrent infections do not usually breed increasingly resistant flora (PubMed).>
The worst thing for a diabetic is new shoes; they lead to blister to ulcer to infection to osteomyelitis to amputation. The next worse thing is sandals; they allow pebbles in.