Bone and Soft-Tissue Disorders
= multisystem disorder
Prevalence: 26 million (= 8.3% of population) in USA in 2010
Path: macro- and microvascular disease; neuropathy; increased susceptibility to infection
Sequelae: neuropathy, nephropathy, retinopathy
- Genitourinary diabetes mellitus
- Spinal disorders in diabetes
- Dialysis-associated spondyloarthropathy
- Pyogenic spondylodiskitis
- Neuropathic spine
- Musculoskeletal diabetes
Diabetic neuropathy: 35% during lifetime
Neuropathic Joint of Diabetic Foot
= most common site of neuropathic joint in diabetes
Pathophysiology:
- repetitive stress on insensitive foot → bone + joint disruption, valgus / varus deformity, joint instability → joint degeneration, subluxation, joint destruction
Prevalence: 5% of diabetic patients
Age: most commonly during 5th–7th decade
- grossly deformed usually painfree foot
Location: Lisfranc joint (60%), metatarsophalangeal joint (30%), tibiotalar joint (10%)
NUC:
- labeled WBC accumulation in noninfected joint due to
- ↑cytokine activity → conversion of yellow into red marrow (not due to infection)
- fracture → conversion of yellow into red marrow
Diabetic Foot Ulcer (mal perforans)
= focal skin interruption with elevated margins and associated soft-tissue defect
Cause: breakdown of callus / minor skin trauma (eg, toenail cutting)
Prevalence: 5% of US population
Lifetime risk among diabetics: 25%
Location:
- typical sites: beneath heads of 1st + 5th metatarsal bones, tip of 1st toe, calcaneus, malleoli
- additional sites due to neuropathic foot deformity: cuboid, midfoot (from arch collapse), dorsum of claw toe, heel
- poor healing ← vascular disease
- ESR >70 mm/h (highly specific, 28% sensitive)
- bone contact during probing of ulcer (89% PPV, 56% NPV)
MR (in >90% of diabetic osteomyelitis):
- interruption of cutaneous signal (low PPV; higher PPV if ulcer >2 cm2 and >3 mm deep)= ulcer:
- with low SI on T1WI + high SI on T2WI + intense peripheral enhancement (= granulation tissue)
- reticulation of fat (of high T2 + intermediate T1 signal intensity) in area of soft-tissue swelling:
- WITHOUT enhancement = edema
- WITH enhancement = cellulitis
- focal ill-defined vaguely enhancing soft-tissue mass effect of low SI on T1WI + intermediate to high SI on T2WI replacing subcutaneous fat (= phlegmon)
- focal fluid signal intensity with rimlike enhancement (= abscess)
- sharply demarcated nonenhancing area of devitalized tissue ± peripheral enhancement = dry gangrene:
- + multiple small foci of gas distributed along fascial planes displaying blooming artifact on T2 and GRE images = wet gangrene
- thin linear soft-tissue signal with “tram-track” pattern of enhancing margins (high on T2WI) = sinus tract
Diabetic Osteomyelitis of Foot
Pathophysiology: pressure points → callus → ulceration → soft-tissue infection → osteomyelitis
X-ray (lags behind by 10–20 days):
- Repeat radiographs after 2–4 weeks!
- bone destruction
- periostitis
- soft-tissue gas
NUC (80% accuracy for labeled leukocytes)
MR (modality of choice; 90% sensitive, 83% specific):
- primary osseous signs:
- low marrow SI on T1WI + high marrow SI on T2WI (= bone marrow edema immediately adjacent to a soft-tissue infection / ulcer)
DDx: reactive osteitis (hyperintense on T2WI but NOT hypointense on T1WI) ← adjacent cortical (not medullary) / soft-tissue infection - marrow enhancement = infected viable tissue
◊ Estimated GFR should be >30 mL/min before administering contrast medium! - ± cortical interruption / destruction
- low marrow SI on T1WI + high marrow SI on T2WI (= bone marrow edema immediately adjacent to a soft-tissue infection / ulcer)
- secondary osseous signs:
- periostitis = linear edema / enhancement along outer cortical margin
- low-SI line (= calcified periosteum) separated from bone by high-SI layer (= fluid)
- secondary soft-tissue signs (in >90%):
- redistribution of fat away from planta of foot
- skin callus = focal infiltration / mass within subcutaneous fat:
- low SI on T1WI + enhancement
- low to intermediate SI on T2WI
- ± adventitial bursitis = thin flat fluid collection over osseous prominence with preserved surrounding fat (DDx to abscess)
Location: same as for ulcers - tracking of ulcer / sinus track down to bone
Cx:
- Devitalized tissue without infection
- focal often triangular sharply demarcated nonenhancing area of variable SI:
- central tissue of usually high SI on T2WI + enhancing marginal zone = dry gangrene
- multiple small foci of gas distributed along fascial planes displaying blooming artifact on T2WI + gradient-echo images = wet gangrene
- focal often triangular sharply demarcated nonenhancing area of variable SI:
- Bone infarct / necrosis
- sharply demarcated nonenhancing marrow
- Spread of infection to foot compartments: tendon (tenosynovitis), joint (= septic arthritis), bone (= osteomyelitis)
Prognosis: 39–80% mortality rate at 5 years after diabetes-related amputation of lower extremity
DDx: Neuropathic osteoarthropathy (dislocation, disorganizaton, debris, destruction, density preserved, mildly symptomatic, joint effusion, multiple joints involved, marrow edema, periarticular enhancement; more common in ankle / Lisfranc / Chopart joints)
Diabetic Muscle Ischemia
= DIABETIC MUSCLE INFARCTION / MYONECROSIS
Predisposed: long-standing poorly controlled diabetes
Path: fibrinous occlusion of arterioles + capillaries; muscle fiber necrosis + edema
Location: thigh, calf
Site: multiple noncontiguous foci of muscle involvement
- abrupt onset of severe pain + swelling
- palpable painful mass; NO leukocytosis / fever!
MRI:
- muscle enlargement
- edema of muscle + fascia
- muscle enhancement + central nonenhancing region
Rx: glycemic control, analgesics, antiplatelet therapy
Prognosis: typically self-limited disorder responding to conservative therapy
DDx: infectious / inflammatory myositis, deep vein thrombosis, compartment syndrome
Diabetic Infectious Myositis
Cause: hematogenous spread of bacteria ← immune dysfunction in diabetic patients
- fever + leukocytosis with left shift, bacteremia
- smooth-walled intramuscular abscess
- rimlike enhancement
Rx: antibiotics, drainage
Diabetic Inflammatory Myositis
Cause: dermatomyositis, polymyositis, inclusion body myositis
- insidious gradually progressive proximal muscle weakness
Location: muscles in pelvis + thigh
- bilateral symmetric edema
Dx: MRI-directed biopsy of affected muscle
Diabetic Muscle Denervation
Location: intrinsic muscles of foot (usually)
- peripheral nerve distribution (!)
- Subacute
- subacute T2 signal hyperintensity of affected muscle
- maintained normal SI on T1WI
- Chronic
- reduced bulk + fatty infiltration of muscle on T1WI
DDx: diabetic muscle ischemia (fascial edema)
Diabetic Neuropathic (Charcot) Osteoarthropathy 
Frequency: 1.4% of diabetics
Cause: repetitive trauma to insensate joint + autonomic dysfunction of blood flow
Pathophysiology: bone hyperemia → bone resorption → bone weakening; localized inflammation → bone destruction → joint subluxation → dislocation → foot deformity
Location: tarsometatarsal, subtalar, intertarsal, ankle joints
Eichenholtz classification:
- stage 1: osteopenia, periarticular fragmentation, fracture, joint laxity with subluxation, capsular distension
- swollen erythematous foot
- stage 2: absorption of bone debris, osseous fusion / osteosclerosis
- reduction in redness + warmth
- stage 3: reconstruction + remodeling ± ankylosis of bone fragments, fixed rocker-bottom deformity
- absence of inflammation
NUC:
- positive findings on blood-flow + blood-pool + delayed phase of 3-phase bone scan
- combined leukocyte-bone marrow scintigraphy (procedure of choice) to separate from superimposed infection
MRI:
- acute
- extensive soft-tissue edema
- multiple foci of bone marrow + subchondral edema
- enhancement far into medullary cavity
- periarticular enhancement
- subchondral cysts, articular erosions, joint effusion
- chronic
- less inflammation + less enhancement
- low marrow signal intensity (bone sclerosis)
- bone debris, intraarticular bodies, ankylosis
- joint subluxation + dislocation ← subchondral collapse
Cx: ulcers of midfoot → cuboid osteomyelitis