Africa
Define Charcot arthropathy of the foot.
It is the loss of sensation to a joint.
**AKA diabetic neuroarthropathy AKA diabetic osteoarthropathy
Pop Quiz: what is the prevalence of diabetes around the world?
(10% type 1, 90% type 2)
Pop quiz: without looking at your case, what did the patient present with in this case?
Look at case afterwards.
Describe the epidemiology of CA.
Low incidence in general diabetic population.
**But results may vary because data is from specialty centers that treat more severe cases of diabetes, and diagnostic criteria for neuroarthropathy vary between series.
Random Question: do you have any experience with diabetic patients who have developed Charcot Arthropathy?
Thank you for sharing :)
What is Diabetes Mellitus?
Diabetes mellitus refers to a group of diseases that affect how the body uses blood sugar (glucose).
What are the lab findings for a case of Charcot Arthropathy with no signs of infections?
When there is no infection, WBC count = normal & synovial fluid should be sterile, with no crystals or organisms on microscopy and no growth on culture.
Pop Quiz: when are the signs/symptoms most severe for patient's with Charcot Arthropathy?
*Hint: either morning or night...
Often worse at night.
Explore Dr. Jones’ use of elevating the foot to diagnose CA.
...
Compare before and after imaging for healing of Charcot Arthropathy.
Refer to case and if anyone has an extra picture.
Why did they call it Charcot... who/what is Charcot?
The condition was named after French neurologist Jean-Martin Charcot.
Prototype of this disorder was described by Charcot in relation to tabes dorsalis (another condition).
Identify the clinical presentations and risk factors of Charcot arthropathy.
collapsed arch, sudden onset of unilateral warmth, redness, and edema over the foot or ankle, often with a hx of minor trauma.
Justify the diagnostic tool used presented to diagnose Charcot arthropathy:
CBC
CRP
ESR
Explore the relationship between Diabetes Mellitus and Charcot Arthropathy.
DM may lead to the development of CA: trauma to neuropathic foot --> exaggerated local inflammatory response --> proinflammatory cytokines (NFKB & IL-1beta; increase activation of RANK-L and increases TFs NFKB).
Relate the radiograph findings to the pathophysiology of Charcot Arthropathy.
Early acute disease: plain film radiographic changes may be mild or nonspecific, showing only soft tissue swelling, loss of joint space, or osteopenia.
Later stages: bone resorption may predominate in the forefoot, leading to osteolysis of phalanges and to a variety of further changes, including partial or complete disappearance of the metatarsal heads or “pencil-pointing” of phalangeal and metatarsal shafts. Osseous fragmentation, sclerosis, new bone formation, subluxation, and dislocation are more likely to occur in the midfoot and hindfoot.
**Stress fractures, which may be difficult to diagnose, can complicate the neuroarthropathy. An uncomplicated stress fracture not apparent on a plain radiograph can be located by MRI or nuclear scintigraphy and can often be confirmed by MRI or serial radiography. However, both MRI and scintigraphy may show nonspecific abnormalities in the diabetic neuropathic foot, and delay in diagnosis may occur if one waits for the characteristic radiologic changes to become apparent.
Justify Dr. Jones’ use of the patient portal for communication.
Pop Quiz: What is the prognosis of a patient with Charcot Arthropathy.
Early presentation and confirmation of the diagnosis, with rapid offloading of the foot, are the most important factors in ensuring a good outcome.
In patients who present later in disease, joint disorganization is often severe and irreversible. This may result in foot ulceration, with secondary infection leading to the risk of amputation.
Relate the pertinent positive physical exam findings to the pathophysiology of Charcot Arthropathy.
Present with case.
List potential differential diagnosis of Charcot Arthropathy.
In early stage it’s often confused as cellulitis.
Other DDx: Osteomyelitis, septic arthritis, gout, osteoarthritis, inflammatory arthritis, and idiopathic inflammatory diseases; and complex regional pain syndrome may also occur in setting of diabetes neuropathy.
Define the Semmes-Weinstein monofilament test and pulse grading.
Normal light touch.
Diminished light touch (with retention of two point discrimination).
Diminished protective sensation (difficulty with manual dexterity and abnormal two point discrimination).
Loss of protective sensation (markedly decreased stereognosis and manual dexterity).
Loss of deep protective sensation (as above plus a risk of injury).
Identify the management of Charcot Arthropathy.
-Immobilization: treatment with casting is used to offload the affected foot. This should be continued until resolution of the redness and swelling occurs, skin temperature reduces to within one to two degrees of that of the unaffected foot, and there is improvement in radiologic signs, if present (eg, resolving resorptive changes, resorption of osseous debris, and evidence of repair).
-Total Contact Cast: recommended time is 3-25 months depending on severity.
-Knee walker: can use knee walker, crutches, or wheelchair depending on severity of illness and/or lifestyle of patient.
Explore the clinical sequelae of Charcot Arthropathy.
-Loss of toe/foot, sharp drops in blood pressure, digestive problems, sexual dysfunction, increased sweating, *hypoglycemia unawareness
Differentiate the possible types of Charcot Arthropathy.
Pop Quiz: list the treatment plan for a patient with Charcot Arthropathy.
*Hint: if you were the patient's doctor how would you explain this to your patient?
-Earlier stages: avoid weight-bearing and the use of casting to offload the affected foot.
-Gradual progression to normal weight-bearing with prescription footwear and close management as acute and subacute inflammatory changes resolve and bony fragments coalesce.
-When offloading is ineffective, and chronic disease and joint injury is present, referral to an orthopedic surgeon to evaluate the potential risks and benefits of surgical intervention in the individual patient.
Outline the pathophysiology of Charcot Arthropathy.
Trauma to the neuropathic foot may trigger an exaggerated local inflammatory response, mediated by proinflammatory cytokines (eg, tumor necrosis factor-alpha and interleukin [IL]-1 beta), resulting in the osteoarthropathy. A possible cytokine-associated effect is suggested by the finding of enhanced osteoclastic activity in surgical specimens from patients with neuropathic arthropathy [5]. Other laboratory studies suggested that both receptor activator of nuclear factor (NF) kappa B (RANK) Ligand (RANKL)-dependent and -independent pathways may be involved in the increased bone resorption seen in this condition [6]. Subsequent work showed increased serum concentrations of proinflammatory cytokines tumor necrosis factor (TNF)-alpha and IL-6, correlating with raised bone turnover markers, at the presentation of acute neuropathic arthropathy. Regardless of the initiating mechanism, an initial resorptive phase may occur in the development of a neuropathic joint, which is then followed by a hypertrophic repair phase.