• LecturehallDiabetic Pedal Osteomyelitis - Concepts and Controversies Part 1
  • Lecture Transcript
  • TAPE STARTS – [00:00]

    Marlena Jbara: Diabetic pedal osteomyelitis concept and controversies part 1. My name is Marlena Jbara. I am a bone and joint radiologist from Staten Island University Hospital at Northwell Health and it is my pleasure to speak with you today. Disclosures: I or related party have no financial relationships to disclose. Learning objectives: This lectures will review the current epidemiologic trends and implications related to care and imaging of the diabetic foot. The current Infectious Disease Society of America and American College of Radiology guidelines will be reviewed with imaging findings of x-ray, MRI and PET-MRI in patients inflicted with a diabetic foot. We will review the epidemiology and pathophysiology of the diabetic foot. Review international and national guidelines with respect to imaging of the diabetic foot, review pertinent imaging findings and pitfalls of diabetic foot pathology with regards to x-ray, MRI and PET-MRI. I would like to take a special moment to thank many of the collaborators who have helped make this project come to life. First Kristina Wertheimer, assistant podiatric residency coordinator at Northwell Staten Island University Hospital, Naveed Mazda [phonetic] PGY-3 from Touro College of Osteopathic Medicine and Richie Pentore [phonetic] from E-Present. Thank you for your collaboration on this educational project. Outline: In this module, we will discuss the epidemiology, pathophysiology with regards to the diabetic foot.


    We will review clinical guidelines including the Infectious Disease Society of America and the international working group on the diabetic foot as well as international clinical guidelines from the National Health Service. We will look at the update on the role of imaging to be able to evaluate whether the foot is infected or not and look at that with x-rays. In the second part, we will go further to look at our update on the role of imaging including MRI, nuclear medicine with future imaging pathways. We will sort this statistics and review the American College of Radiology appropriateness criteria. Diabetes is expensive. It is currently estimated that the total cost of diagnosed diabetes was 263 billion in 2013. The breakdown in 2012 is that 176 billion was spent on the medical hospital inpatient care of diabetes with greater than 75 billion reserved for the surgical care of the diabetic foot. There was 69 billion in the cost of reduced productivity where people didn't return to work. And what worries them is that this number has almost doubled since 2002 where diabetes cost 132 billion. And we can see from this chart on the right that the health expenditure due to diabetes in 2013 cost an enormous fortune with North America leading the utility of these resources.


    Diabetes is common. It's the seventh leading cause of death. So the US population in 2018 is 326 million and the prevalence those that are diagnosed and undiagnosed diabetes in the United States all ages 2015, the total was 30.3 million or 9.4% of the US population. Diagnosed diabetes was 23 million and undiagnosed diabetes was 7.2 million or 24%. The incidence in 2015 was that 1.5 million newly diagnosed cases came yearly and this has tripled since the 80s. And as you can see from this chart on the right, new cases of diagnosed diabetes among US adults are on the rise since 1980. As per world statistics, approximately 422 million people are affected in 2014 and this is a nice chart, which looks at the expenditure versus the prevalence. The top 25 countries afflicted with diabetes in 2010 versus spending an international dollars clearly puts the United States ahead of the pack and it's far way back but India and China are also major consumers of countries inflicted with diabetes. The number of people with diabetes in 2013 and as you can see on this global map, there is far greater predilection to have diabetes if you are coming from India at 138 million for the Western Pacific affliction. In terms of amputations, the trend is declining. We have fewer toe, below-knee, trans-metatarsal and above-knee amputations than we saw in the late 90s.


    Let's turn to the diabetic foot. The diabetic foot represents a mixture of pathologies including peripheral vascular disease, Charcot neuroarthropathy, foot ulceration, osteomyelitis, and limb amputation. And as you can see from this x-ray and clinical picture on the right, what we are pointing to are the soft tissue ulcerations that provide a pathway ingressed towards the bone with poor healing potential resulting in osteomyelitis. So ulcers and osteomyelitis, a bone is infected from a direct contiguous spread from the skin to ulcer and we can see from this schematic on the right where you begin with a soft callus, which turns to an adventitial bursa, which then blisters to the skin surface and then provides an ingress of an infection, so from the skin surface bacteria can spread directly to the bone. And you can see this correlated with clinical pictures of the plantar aspect of the foot where you can see the development of a soft tissue ulcer. And then lastly at the bottom left, you can see on the x-ray the soft tissue ulceration denoted by the curved blue arrow at the plantar aspect of cuboid. Fast facts about ulcers: Diabetic neuropathy is present in more than 50% of patients greater than 60 years and increases the risk of foot ulceration by sevenfold. If you have an ulcer, you likely also have nephropathy, retinopathy, ischemic heart disease and strokes.


    Diabetes accounts for the majority of non-traumatic amputations. The incidents can be decreased with the multidisciplinary approach and this chart on the right provides a framework for diabetic foot service, which places the gatekeeper or the podiatrist at the center of the chart where he receives patient admission through the ER or hospital referral or from the primary care physician. The podiatrist then can guide the consultants including the many dia-pathologist, infectious disease, cardiologist, radiologist and ancillary services to defining the current state of the patient's diabetic foot or soft tissue ulcer. The pathophysiology of the diabetic foot and diabetic neuropathy essentially comes through three pathways, sensory, motor and autonomic. In the sensory pathway, demyelination of the nerves occurs through over-glycosylation. The presence of too much circulating sugar affects the axonal transmission through a nerve and resultant impaired sensory perception of pain, temperature, vibration and touch. This can create injury with mechanical, thermal and chemical insults affecting a foot that is insensate. Furthermore, the motor system is affected also through demyelination through small muscle atrophy. This imbalance of the flexor and extensor muscles resulting in toe clawing, prominent metatarsal heads, altered gait, callus and foot ulcer. Lastly, the autonomic pathways are affected; decreasing sweating, dry scaly skin, fissures resulting in infection.


    Also you have arterial venous shunting, decreased cell nutrition, decreased capillary pressure, edema and poor healing all resulting in the presence of a foot ulcer, which provide an ingress for bacteria to infect the bone. The pathophysiology of diabetic mellitus can also be extrapolated beyond neuropathy to trauma of an insensate foot and superimposed vascular disease. All of these inciting insults will decrease nutrient capillary blood flow to a neuropathic insensate foot resulting in diabetic foot ulceration and placing the patient at risk for amputation. Is the foot infected or not? Assessment of ulcer disease. So in the Wagner classification system, we can assess the size and depth of the ulcer where the grade 0 through 5 increases depending on whether the ulcer is superficial, deeper or contains gangrene. Moving on the University of Texas Classification adds infection and ischemia but doesn't adequately define the terms. So we have stages A through D defined by whether or not there is the presence of an ulcer, clinically whether it's infected, whether or not there is ischemia and of course whether it's infected and ischemic. The international working group on the diabetic foot provides a research driven ulcer classification called PEDIS with P standing for perfusion, E for extent, D for depth, I for infection and S for sensation with grading of 1 through 4 depending on whether or not there is perfusion, a larger size, depth of tissue loss, infection and sensation.


    And lastly, the international working group of the diabetic foot is available to you online and you can see the PEDIS grade 1 can be extrapolated to an Infectious Disease Society of North America infection severity being uninfected where PEDIS grade 4 where there is a local infection with signs of systemic inflammatory response. The idea says infection severity would be severe. The bottom line is that the larger your ulcer. In fact, JAMA quotes an article that if it's greater than 2 cm and greater than 3 mm in depth, it's associated with 92% specificity that that wound contains osteomyelitis. Using the probe to bone, there is a 66% sensitivity and 85% specificity that there is ulcer driven osteomyelitis. And in ESR greater than 70 has a 100% specificity but only 28% sensitivity. In 2012, the Infectious Disease Society of America created the clinical practice updated guideline for the diagnosis and treatment of the diabetic foot infections. In the presence of a longstanding or deep ulcer with elevated levels of inflammatory markers, the next test you would like to perform is probe to bone. And as you can see on this exam on the left, this clinical photograph, a probe to bone test takes a steely driven needle into the base of the bone and will test [indecipherable] [14:06] whether or not the bone is positive for infection.


    Sampling the bone is best done using a curettage method, scraping the base of the ulcer or bone. We no longer ask to swab or even to aspirate as swabs grow colonizers and don't grow the tough anaerobes that you could be missing to develop treatment. The Gold Standard would be a bone biopsy where you would be able to isolate the infection and causative organism from a bone culture and here is a clinical picture on the right performing a bone biopsy with a steely needle. Bone biopsy, how good is it? Well, there are limits to the cultures and that there are false negatives. Sampling errors, pretreatment on prior antibiotics, failure to isolate fastidious organisms and false positives. Colonizers are common and not necessarily virulent. Histopathology limits, there can be false negative sampling errors and false positives, presence of non-infectious inflammatory agents such as gout or inflammatory arthritis. The Infectious Disease Society of America provides evidence-based imaging recommendations. All patients with suspicion of a diabetic foot need an x-ray and there is strong evidence for this. MRI is reserved for those in need of additional imaging and it's more sensitive and specific for soft tissue abscess or deep tissue infection.


    For the National Health Service, there are guidelines created for imaging a suspected diabetic foot infection and they also agree to obtain plain x-rays to rule out osteomyelitis, Charcot or foreign body. They do not base osteomyelitis on x-rays alone, but if the initial x-ray does not confirm osteomyelitis they use MRI. They no longer use bone scan instead and these are updated guidelines as you can see under diabetic foot problems, prevention and management updated August 26, 2015. X-rays, so what's there to see? Well, you can see an erosion or break in the cortex, subcortical lucency, sclerosis with or without erosion, sequestrum, which would be the dense infected bone, the involucrum, which surrounds sequestrum, cloaca, which is a track from the sequestrum to cortex. You could see gas, soft tissue ulcer, foreign bodies. You could see the presence of Charcot, gout or arthritis, vascular calcifications and it can be used to target the field of view for MRI. Evaluating the x-ray ranges from subtle findings where you see periostitis in this example and erosion with a breaking cortex, subcortical lucency and the ulcer at the dorsal tip of this phalanx. And they range to the complex. Patients often have multiple amputations and comparison to prior x-rays is essential.


    In this example here, you can see multiple forefoot amputations with a recurrent soft tissue ulcer and persistent erosion at the hallux proximal phalangeal stump. Further looking for the ulcer, we can see at the medical hallux MTP joint, we have a soft tissue ulcer where we can see a break in the cortex with an adjacent erosion indicative of osteomyelitis. Other findings we can see subcortical lucency, ulcers and erosion. Here on this exaggerated example on the right, we see a large soft tissue ulcer adjacent to the hallux proximal phalanx with osseous erosions along the proximal phalanx and base of distal phalanx consistent with osteomyelitis. The ghost sign or eraser sign, which I placed this picture of an eraser to show the eraser of the cortex indicating underlying erosion and osteomyelitis. Osteomyelitis can be acute versus chronic or acute-on-chronic and what we are looking for here is that there are active lucencies and the erosions indicating active osteomyelitis. In chronic forms of osteomyelitis, there is a resultant sclerotic appearance where you have neuropathic change plus osteomyelitis plus erosion. So what's there to see? In this example, we are noticing a sequestrum, which is the sclerotic irregular dense infected central portion of this bone surrounded by fluffy periosteal new bone formation surrounding the sequestrum called the involucrum.


    Further the cloaca, which we will form will be the track, which takes the sequestrum to the cortex. Necrotizing infection, gangrene, we can see multiple subchondral and periarticular lucencies indicating gangrenous infection dissecting through the soft tissues. Furthermore, necrotizing infection can be seen with these lucencies overlying the hallux distal phalanx in this patient who has soft tissue loss and ulcers. Let's turn to Charcot arthropathy, which was described by Jean Martin in 1868. This is a severe progressive arthropathy and the etiology is still largely unknown. There is an increase blood flow initially, which resulted in osteopenic with sclerotic repair from imbalances and osteoclastic and blastic activity. Unperceived trauma to the insensate foot result in repetitive micro-trauma, progressive destruction with attempts to repair and it's initially described syphilis. The theories of its etiology range from neurovascular to neuro-traumatic. Pathophysiology of Charcot: Similar to the pathophysiology of the diabetic foot, again three pathways are affected, sensory, motor and autonomic. The sensory and motor pathways result from demyelination from over-glycosylation. There is impaired sensory perception of pain, temperature, vibration and touch with injuries related to mechanical, thermal and chemical disturbances.


    Demyelination occurs through small muscle atrophy with imbalance in musculature and changes in biomechanics. Autonomic, we have decreased sweating, fissures, and decreased healing with additional arterial venous shunting resulting in decreased capillary pressures and poor wound healing. The pathophysiology of Charcot results in the famous six D's; dislocation, debris, disorganization, destruction, increased density and distention of the joint. You can see in this example of Charcot, the dislocation, debris, disorganization, destruction, density and joint distention noted by this medial dislocation of the talus. There is navicular fragmentation, sclerosis, disorganization, debris and joint distention. Chronic example of Charcot neuroarthropathy can be seen here with vast remodeling, fusion, disorganization, debris and sclerosis. Also note the rocker bottom deformity on the lateral x-ray with resultant soft tissue ulcer, plantar to cuboid. Dr. Frykberg characterized the locations of Charcot, which would be a useful piece of information to differentiate from osteomyelitis and we can see that greater than 75% of Charcot involves the Chopart, Lisfranc and MTP joints with additional areas involving the calcaneus and tibiotalar joint totaling less than 15%.


    Of course, the pressure points of Codman's triangle will be your initial point of pressure under the first and fifth MTP joints and at the level of the heel. Charcot and necrotizing infection are not exclusive. In this example here, we can see Charcot midfoot neuroarthropathy with adjacent subcutaneous locules of gas consistent with necrotizing infection. And of course, comparison to prior films are essential as relapse and recurrence are the rule in osteomyelitis that can be seen here in this patient with multiple forefoot to midfoot amputations. There is now recurrent erosion at what remains of the cuneiform base. Charcot and septic arthritis, here is an example of superimposed erosions at the tibiotalar joint in previously Charcot patient where there was sclerosis there. So again comparison to prior films is essential. The downside of x-rays is that it requires 30% to 50% of bone loss to appreciate demineralization and that takes approximately 2 to 3 weeks to reveal, so there is a delay in diagnosis. And at best, the sensitivity of x-ray will range between 43% to 75% while the specificity will range from 75% to 83%.


    In summary, we have reviewed the epidemiology of the diabetic foot demonstrating how expensive the disease and common with incidents on the rise. We have reviewed the pathophysiology of the diabetic foot including the complex interplay between motor, sensory and autonomic systems and the dysfunction that results. We have reviewed the clinical guidelines to ulcer grading adding to the PEDIS ulcer grading for evaluation for perfusion. And lastly, we have looked at an update on the role of imaging. We have sorted the stats with regards to the utility of x-ray and reviewed x-ray findings of osteomyelitis including the ulcer, erosion, subcortical lucency and presence of gas. I thank you for your time and attention.

    TAPE ENDS - [27:04]