Bhadra Hamal Orthopaedic Resident NAMS, Bir Hospital

DIABETES IN ORTHOPAEDICS-DIABETIC FOOT

Diabetes mellitus- refers to a group of common metabolic

disorders that share the phenotype of hyperglycemia

Diagnosed by symptoms of diabetes and a two hour plasma glucose >11.1mmol/l (200mg/dl)and a fasting glucose>7.0mmol/l (126mg/dl)(WHO criteria)

Complications of diabetes

 Retinopathy(nonproliferative/proliferative)     

Macular edema   Neuropathy     Sensory

and motor (mono- and polyneuropathy)     

Autonomic   Nephropathy Angiopathy:    Coronary artery disease    Peripheral arterial

disease    Cerebrovascular disease

Gastrointestinal (gastroparesis, diarrhea)   

Genitourinary (uropathy/sexual dysfunction)   

Dermatologic Infections   Cataracts    Glaucoma    Periodontal disease MUSCULOSKELETAL

DIABETIC FOOT

Ancient Egyptian prostheses of big toe

Lancet 2000;356:2176-79

Risk factors for Diabetic foot

NEUROPATHY

VASCULOPATHY

IMMUNOPATHY

NEUROPATHY

Different metabolic pathways activated by excess glucose- reactive oxygen species(ROS) ie, nitric oxide, hydrogen peroxide, advanced glycosylation end products such as HbA1c

ROS cause damage by causing nerve ischemia affecting protein and cell lipids and injuring nuclear material leading to increased apoptosis

Advanced glycosylation end products, by binding cellular receptors decrease the cells ability to detoxify itself

Nerve myelinization can be affected, along with injury to nerve ion channel which decrease conduction velocity

Microvascular disease also damage nerves

When large sensory fibres are affected protective sensation can be lost

Small fibres afferent neuropathy can lead to increased pain generation

Motor neuropathy can cause claw toes –ulcerations over bony prominences

When sympathetic nervous system is affected ,skin becomes dry and scaly-cracks in skin-invasion by bacteria

VASCULOPATHY

Advanced glycosylation end products can damage vascular endothelium leading to microthrombosis and capillary obstruction,also increase LDL which cause atherosclerosis

Vascular tone loss due to Reactive oxygen species(ROS)

IMMUNOPATHY

Defects in leucocyte response to infection ie,problems with chemotaxis, adherence,

impaired fibroblast proliferation, phagocytosis,and intracellular killing

Impaired growth factor 80% increased risk of cellulitis Four fold risk of osteomyelitis Double risk of sepsis and death from infection

DELAYED BONE HEALING

Collagen synthesis is decreased Biomechanical strength of fracture callus

is lower in diabetics Decreased cellular proliferation at

fracture site and decreased mechanical stiffness

DIABETIC ULCER

PATHOPHYSIOLOGY Sensory neuropathy- loss of sensation Motor neuropathy- claw toes bony

prominences make skin vulnerable to breakdown

Achillies contracture-(due to disorganisation of tendon fibres and calcification within tendon) increased forefoot pressure forefoot ulceration

Peripheral arterial disease- ischemia

Wagner classification

Grade 0- skin at risk

Grade 1- superficial ulcer

Grade 2- exposed tendon and deep structures

Grade 3-deep ulcer with abscess or osteomyelitis

Grade 4-partial gangrene

Grade 5- more extensive gangrene

TREATMENT

NONOPERATIVE TOTAL CONTACT CASTING (TCC) is the standard of

care because it reduces plantar loads better than a well molded shoe cast

GOAL of total contact casting is the relief of pressure by distributing stresses over a large surface area

TOTAL CONTACT CASTING

Removable diabetic boots

TREATMENT

Negative pressure wound treatment with vacuum assisted closure

Hyperbaric oxygen treatment overall healing rate 76% compared with 48%

without the use of it

Extracorporeal shockwave treatment helpful for healing of chronic ulcer

Antibiotic treatment-if infected deep culture obtained after debridement; superficial

swab often yield contaminants

TREATMENT

OPERATIVE Indications for urgent surgical

intervention -necrotising infections -gangrene -deep abscess-Incision and drainage with thorough

debridement-Complete excision of infected bone

TREATMENT

Osteomyelitis of metatarsal head -metatarsal head resection If osteomyelitis involve more than

metatarsal head -ray resection Osteomyelitis of calcaneum secondary to

ulcer -partial calcanectomy Achilles lenghtening -to decrese plantar pressure

CHARCOT ARTHROPATHY

HISTORY Prof Jean-Martin Charcot (1825-1893) French Neurologist and

professor of anatomical pathology

First described in

patient with Tabes dorsalis

CHARCOT ARTHROPATHY

Diabetes – most common cause Others - syphilis, syringomyelia, alcoholism,

stroke, congenital insensitivity to pain, spinal cord or peripheral nerve injury, and spina bifida

Loss of autonomic control of the vasculature High resting blood flow Osteopenia, combined with somatosensory loss of pain and proprioception multiple small mechanical insults unrecognized by the patient which set the stage for bony dissolution and loss of structural integrity, followed by a collapse deformity

Clinical Features

Foot swelling Redness Numbness Pain – not a chief complaint (if present,

less than expected) CRT – usually normal Infected charcot’s joint – warm & red

Radiographs Early neuropathic arthropathy – joint

widening and stress fractures Progressive and late stages – further

destruction and multiple joint involvement are seen.

Technetium bone scan is positive

CLASSIFICATION-EICHENHOLTZ“I CAN HOLDS”

Stage 0: No radiographic changes, marked warmth and swelling after injury

Stage 1: Fragmentation. Erythema, warmth and swelling of the extremity, with subluxation/dislocation of joints and bony debris and fragmentation of subchondral bone.

Stage 2: Coalescence. Decreased erythema, warmth and swelling of the extremity, with absorption of fine debris, new bone formation, and coalescence of larger

fragments.

Stage 3: Consolidation. Resolution of swelling; however, residual deformity is present, with remodeling of bone seen on radiographs.

Anatomical classification-BRODSKY

Type 1: Involvement of the tarsometatarsal joints.

Type 2: Involvement of the Chopart and subtalar joints. Type 3A: involvement of the ankle

Type 3B: involvement of the calcaneus

Type 4 :involvement of multiple regions

Type 5: involvement of forefoot

TREATMENT

NONOPERATIVE- Orthotics: custom-molded orthotics

that accommodate the deformity, resist progression

-Total contact casting with protected weight bearing

DRUGSBisphosphonate -may reduce bone turnover in charcot arthropathy and help with pain reliefCalcitonin decrease bone turnover

OPERATIVE -surgery required for approx

25% patients with charcots arthropathy

GOAL -Deformity correction and

stabilisation to create/maintain a braceable, infection free foot and ankle

TREATMENT

EXOSTECTOMY-remove bony prominences causing ulceration. It should be done only if it doesn’t lead to further instability

ARTHRODESIS-indicated for deformity correction and for instability

AMPUTATION- last resort

REFERENCES

Campbell’s operative orthopaedics-12th edition

Apley’s System of Orthopaedics and Fractures- 9th edition

Review of orthopaedics ,Miller-6th edition

Internet