Manifestations of Endocrine Disease

Fig. 1

Schematic diagram showing orderly progression of neuroarthropathic changes across the midfoot [1]. Type 1. Changes limited to medial three tarsometatarsal joints and adjacent inter-cuneiform joints. Type 2. Additional involvement of the 4th tarsometatarsal joint. Type 3. Additional involvement of the cuneiform-navicular joints. Type 4. Additional involvement of the 5th tarsometatarsal and peri-cuboid joints. Type 4 (lateral) is relatively greater involvement of cuboid than navicular bone. Type 5. Additional involvement of the hindfoot

Much less commonly, hindfoot or ankle neuroarthropathy may develop de novo in the absence of midfoot disease. Similarly forefoot disease may develop de novo and tends to be atrophic in type with bony reabsorption and ‘penciling’ of the phalanges.

Charcot’ neuroarthropathy sometimes needs to be differentiated from osteomyelitis and septic arthritis. Osteomyelitis is uncommon in the absence of cutaneous ulceration since it usually occurs secondary to soft tissue infection.

Helpful imaging features to distinguishing between neuroarthropathy and osteomyelitis are as follows:

1.

Charcot’s neuroarthropathy is joint centered while osteomyelitis commonly involves the non-articular segments of bone. An inflammatory response not centred on the joint is indicative of osteomyelitis.
2.

Charcot’s arthropathy has got a classic pattern of progression in the midfoot (Fig. 1) [1]. If this pattern is not followed then one should strongly consider osteomyelitis. If for example, one sees cuboid destruction in the absence of arthropathy on the medial aspect of the tarsus, then this would strongly favour osteomyelitis.
3.

Continuity of any inflammation with cutaneous ulceration favours osteomyelitis. Osteomyelitis usually occurs at pressure sites prone to soft tissue injury and ulceration such as the first and fifth metatarsophalangeal joints, distal phalanx of the big toe, the posterior aspect of the calcaneum, or the base of the midfoot with ‘rocker bottom deformity’ consequent on end-stage Charcot’s neuroarthropathy.
4.

Soft tissue fluid collections on ultrasound, CT or MRI examination favour infection. These collections may be aspirated under image guidance.
5.

Severe localised osteolysis or progressive osteolysis favours osteomyelitis. Review of any prior imaging studies is helpful.
6.

Identification of osseous or soft tissue sinus tracts on CT or MRI is also indicative of osteomyelitis.
7.

Positive indium-111 labelled leucocyte scintigraphy scan favours osteomyelitis.
8.

18-F flourodeoxy glucose positron emission tomography-computed tomography (PET-CT) imaging is more specific than three-phase bone scintigraphy and also probably more specific than indium-111 labelled leucocyte scintigraphy though has not been directly compared with the latter in the diabetic foot [2–4].

Diabetes mellitus is also associated with an increased prevalence of musculoskeletal manifestations related to increased tissue fibrosis. These include:

Diabetic cheiroarthropathy (cheiros = hand in Greek) is a quite common complication said to effect at least 10% with both insulin-dependent and non-insulin-dependent diabetes. It is marked by hand stiffness (hence also known as ‘stiff hand syndrome’ or ‘limited joint mobility syndrome”) and mainly affects persons with poorly controlled diabetes, particularly if a smoker. It is characterised by thick, waxy skin on the dorsum of the fingers and hands with flexion contractures of the metacarpophalangeal and interphalangeal joints [5]. Skin changes in the absence of joint problems can be found. Arterial calcification is a quite common accompaniment.

Clinically it can be similar to scleroderma though the absence of Raynaud’s phenomen, calcinosis, cutaneous telangiectasia, dermal atrophy, and autoantibodies allows distinction between diabetic cheiroarthropathy and scleroderma.

Although common in diabetes mellitus, diabetic cheiroarthropathy is not often encountered in radiology departments as it is a clinical diagnosis that does not require imaging confirmation. The classic clinical signs are the ‘prayer sign’ and ‘table top sign’ when the patient is not able to extend the fingers fully in a prayer position or to lie the fingers flat on the table top (Fig. 2) [5].

Fig. 2

Prayer sign were the fingers are held in slight palmar flexion limiting the ability to hold the fingers in a prayer position

Dupuytren’s disease affects 1% of patients with diabetes mellitus. In the early stages of Dupuytren’s disease, contracture may be present and palmar nodular thickening may be the only clinical manifestation without finger contraction. Ultrasound can help at this early stage of the diagnosis when the clinical signs are not clear-cut. Peripheral hypoxia results in increased free radicles which stimulate fibroblasts [5].

Trigger Finger

A similar aetiology lies behind the development of trigger finger. Trigger finger results from thickening of the A1 pulley usually with restricted movement of the underlying flexor digitorum tendons. The normal thickness of the A1 pulley measured at 10 or 2 o’clock is <0.5 mm (Fig. 3). Trigger finger is said to affect 5% of patients with diabetes mellitus. It usually affects the ring and middle fingers as well as the thumb. In routine clinical patients, if more than three fingers are affected, then diabetes mellitus should be actively excluded [5].

Fig. 3

Transverse ultrasound of the middle finger metatarsophalangeal region in a patient with clinically apparent trigger finger. The A1 pulley (arrows) is markedly thickened (1.2 mm) as shown by the electronic calipers at the 2 o’clock position. Normal thickness of the A1 pulley is <0.5 mm. This is consistent with trigger finger

A condition closely related to trigger finger is deQuervain’s disease. This is associated with thickening of the extensor retinaculum of the first compartment extensor tendons. It is particularly common in postpartum women (‘babies thumb’) though in this context is not usually associated with diabetes mellitus.

Carpal Tunnel Syndrome

Carpal tunnel syndrome also occurs with increased frequency in diabetes mellitus though it is not clear whether this association is due to increased fibrosis of the transverse retinaculum and/or the coexistence of obesity and diabetes mellitus. Carpal tunnel syndrome is diagnosed clinically supported by nerve conduction tests or ultrasound examination. Ultrasound examination is almost as sensitive as nerve conduction test for confirming carpal tunnel syndrome. Various ultrasound parameters are used. In our department, a cross-sectional area of the median nerve just proximal to the tunnel inlet, at the tunnel inlet, at the tunnel outlet, or just distal to the tunnel outlet of >14 mm² is considered diagnostic of carpal tunnel syndrome. A CSA of <10 mm² at all of these locations is considered normal. If any measurement is >10 mm² but <14 mm², this is considered suggestive of but not diagnostic [6]. Different MRI criteria can also be applied to diagnose carpal tunnel syndrome.

Adhesive capsulitis affects about 10% of patients with diabetes mellitus compared to about 2% of control subjects [5]. Adhesive capsulitis is characterised by limitation of shoulder movement. During the initial inflammatory stage, the disease is very painful, especially during movement and when lying on the affected shoulder. Later, during the fibrotic stage, the pain subsides and limitation of movement, particularly external rotation, becomes the predominant feature. Finally, slow progressive improvement in the degree of shoulder movement occurs until complete resolution. The entire process, from initiation to resolution, lasts about 3–4 years.

Histologically there is synovitis and capsular proliferation of fibroblasts. MRI is an excellent modality to determine the existence of, severity of and type of (inflammatory or fibrotic) adhesive capsulitis. Synovial/capsular thickening can be seen in the subcoracoid recess, along the coracohumeral ligament, in the rotator cuff interval, along the glenohumeral ligaments, and at the axillary recess particularly the anterior limb of the inferior glenohumeral ligament.

Adhesive capsulitis seems to develop earlier in diabetic patients and non-diabetic patient i.e. before the age of 40 years of age. It seems to be associated with the duration but not with the type of diabetes.

Other Manifestations of Diabetes Mellitus

Diabetic Muscle Infarction

This is a relatively uncommon condition usually seen in end-stage diabetes mellitus and therefore in association with nephropathy, retinopathy, neuropathy and arteriopathy. It presents as painful muscle swelling. Onset is both acute and severe. The thigh muscles are most commonly affected followed by the gluteal and calf muscles. Creatinine kinase levels may be slightly elevated. It may present clinically as a soft tissue sarcoma. On imaging, one usually sees an area of nodular fibrotic-type swelling thickening in the centre of the muscle with surrounding muscle oedema. Both the ultrasound and MRI appearances are quite characteristic allowing the diagnosis to be made with confidence in the appropriate clinical setting and with no need for percutaneous biopsy [7]. Classically, ultrasound shows no surrounding hyperaemia in the early stages followed by progressive hyperaemia as repair occurs. Similarly, on MRI examination, one sees an area of muscle haemorrhage/oedema with peripheral hyper-perfusion (Fig. 4a–c). The lesion tends to become progressively smaller and more nodular/fibrotic in nature with healing. It is associated with a poor overall prognosis in that patient’s usually succumb to the other manifestations of diabetes within 1–2 years of developing diabetic muscle infarction [7].

Fig. 4

Typical appearances of diabetic muscle infarction (a) T1-weighted axial MR image of the calf showing T1 hyperintensity within lateral belly gastrocnemius muscle (arrow) as a result of intramuscular haemorrhage. (b) T2-weighted fat-suppressed axial images at the same level as Fig. 4a, showing marked oedema within lateral belly gastrocnemius muscle (arrow). (c) T1-weighted fat-suppressed axial image post-contrast at the same level showing marked enhancement within lateral belly of the gastrocnemius muscle (arrow)

Diffuse idiopathic skeletal hyperostosis (DISH) with flowing intervertebral ossification is also more common in diabetes mellitus. The definition of DISH requires the presence of flowing ossification between four adjoining vertebral bodies. DISH results from ossification of the anterior longitudinal ligament. DISH mainly affects the thoracic spine though can also affect the lumbar and cervical spine. The reason for the association between DISH and diabetes mellitus is unknown. It may have a vascular aetiology. It may also be related to obesity and hence the association with diabetes. Growth hormone levels and inflammatory-like growth factor I (IGFI) are increased in patient with DISH. This may stimulate soft tissue ossification through osteoblastic proliferation and/or activation.

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