Anatomy of foot Pathogenesis of diabetic foot

1. Surgical Anatomy and
Pathogenesis of Diabetic
foot
A. Bharath

2. Surgical Anatomy of Foot
• Skin
• Subcutaneous tissues
• Muscles of foot
• Bones - Arches of foot
• Blood and nerve supply

3. Skin
• Skin of sole is thick, Dermis is richly vascular
• Bound to subcutaneous tissue firmly
• Devoid of any hair follicles, sebaceous glands or apocrine sweat
glands
• Merkel cells are present, which act as pressure sensing mechano-
receptors

4. • Skin over dorsum of foot is relatively thin
• Loosely bound to underlying tissue
• Has hair follicles and sebaceous glands

5. Subcutaneous tissues
• Subcutaneous fat in foot is specialised for weight bearing
• Particularly over heel and heads of metatarsals
• The thickness of the subcutaneous tissue of heel can be 2 cm
• Fibrous septa are oriented in spiral fashion through the subcutaneous
tissue
• These septa form precise system of chambers that hold the heel fat
over the calcaneum

6. • Normal heel fat pads tend to broadly disperse weight-bearing forces
• The septal walls of atrophic heels tend to be fragmented and wider
than normal
• Atrophic heel fat pads tend to have more concentrated peak pressure
distribution
• Higher percentages of unsaturated fatty acids and lower percentages
of saturated fatty acids are found in normal heel fat than other bodily
fatty tissues.
• The increased unsaturated fatty acid ratio decreases triglyceride
viscosity and enhances biomechanical efficiency for weight
distribution

7. • Fat under metatarsal heads is called submetatarsal cushion
• Held in place by longitudinal fibrous bands which arch under the fat
to hold it in place
• Also helps to cushion the neurovascular bundles in between
metatarsals
• Fat of non weight bearing areas of foot is similar to that of rest of the
body

8. Plantar aponeurosis / fascia
• Thickened deep fascia of sole
• Attached proximally to calcaneum
• Distally splints into 5 slips and attached to metatarsal heads
• Relatively avascular structure
• Acts as support for foot arches

9. Mucles of foot
• Both intrinsic and extrinsic muscles are present
• Muscles over dorsum can be classified into superficial and deep
planes
• Muscles of plantar aspect are arranged in 4 layers
• Tendons, Blood vessels and nerves from eg enter sole from medial
aspect of calcaneum behind medial malleolus

10. Layer 1 -
Abductor hallucis,
Flexor digitorum brevis,
Abductor digiti minimi

11. Neurovascular plane -
Posterior tibial artery branches and
tibial nerve branches
Layer 2 -
Flexor digitorum longus,
Flexor hallucis longus,
Lumbricals,
Accessory flexor digitorm

12. Layer 3 -
Flexor hallucis brevis,
Adductor hallucis,
Flexor digiti minimi brevis

13. Layer 4 -
Plantar interossei and
tendons of Tibialis
posterior,
Peroneus longus

14. Dorsum of foot
Superficial -
Extensor digitorum longus,
Extensor hallucis longs,
Extensor digitorum brevis

15. Neurovascular plane -
Dorsalis pedis artery and Deep
peroneal nerve branches
Deep - Dorsal interossei

16. Cutaneous Nerve supply
Superficial
peroneal nerve

17. Bones of foot
• Tarsals - Calcaneum, Talus, Navicular, Cuboid, 3 cuneiforms
• Metatarsals - 5
• Phalanges
• Total of 26 bones that articulate in 29 joints

18. Bones of foot

19. Arches of foot
Longitudinal arches
•Medial
•Lateral
Transverse arches
•Anterior
•Posterior

20. Medial longitudinal arch
• Its summit is at the superior articular surface of the talus
• Its two extremities are the tuberosity on the plantar surface of the
calcaneus posteriorly and the heads of the first, second, and third
metatarsal bones anteriorly
• Its weakest part is the joint between the talus and navicular
• This portion is braced by the spring ligament, and is supported
inferiorly by the tendon of the Tibialis posterior, which is spread out
in a fanshaped insertion and prevents undue tension of the ligament

21. Lateral longitudinal arch
• Summit is superior surface of calcaneum
• Two extremities are formed by lateral border of calcaneum and
lateral 2 metatarsals with cuboid
• Lower and stiffer compared to medial arch
• Built for weight bearing

22. Supports to arches

23. Functions of arches of foot
• Helps in distribution of body weight
• Acts as shock absorber
• Elasticity helps in recoil of joints to normal position to prevent wear
• Concavities help in tissue expansion

24. Diabetic foot
• IWGDF defines Diabetic foot as
Infection, ulceration or destruction of tissues of the foot
associated with neuropathy and/or peripheral artery disease in the
lower extremity of people with diabetes

25. • Diabetic foot is a dreaded complication of diabetis manifesting in 15%
of diabetics all over the world
• In India it is estimated that around 40,000 amputations are done in a
year; 3/4th of which are due to diabetic foot infection
• Not only morbidity due to loss of limb, diabetic foot is a great
financial burden both directly and indirectly
• Duration of diabetis, poor control, atherosclerosis, trauma and
smoking are well established risk factors for developing diabetic foot

26. In India, there is relatively higher prevalence and late presentation
compared to west.
•low socioeconomic status
•barefoot walking,
•illiteracy,
•ignorance about diabetic foot care
•belief in the alternative systems of medicine

27. Pathogenesis
• Diabetic foot ulcers result from the simultaneous actions of multiple
contributing causes
• Diabetic foot is characterized by a classical triad of
•neuropathy,
•ischemia, and
•infection.

28. Diabetic Neuropathy
• More than 60% of diabetic foot ulcers are the result of underlying
neuropathy
• One of the more commonly described mechanisms of action is the
polyol pathway
• Additional nerve dysfunction follows from glycosylation of nerve cell
proteins
• Manifests as Sensory, Motor and Autonomic neuropathy

29. Polyol pathway
NO synthase
Decreased
Myoinositol uptake

30. UDP-GlcNAc : uridine
diphosphate-N-acetylhexosamine

31. Protein kinase C
• Hyperglycemia and reduced myoinositol increase activation of
protein kinase C
• Protein Kinase C regulates
•BM synthesis
•SMC contractility
•Vascular permeablity

32. A Unifying hypothesis
• In 2004 Brownlee proposed that all these mechanisms seem to reflect
a single hyperglycemia induced process of overproduction of
superoxide by mitochondrial electron transport chain
• It also helps explain phenomenon of Metabolic memory

33. Sensory Neuropathy
• The loss of sensation as a part of peripheral neuropathy exacerbates
the development of ulcerations.
• As trauma occurs at the affected site, patients are unable to detect
the insult to their lower extremities.
• As a result, many wounds go unnoticed and progressively worsen as
the affected area is continuously subjected to repetitive pressure and
shear forces from ambulation and weight bearing

34. Motor Neuropathy
• Damage to the innervations of the intrinsic foot muscles leads to an
imbalance between flexion and extension of the affected foot.
• This produces anatomic foot deformities that create abnormal bony
prominences and pressure points, which gradually cause skin
breakdown and ulceration

37. Autonomic Neuropathy
• Damage to autonomic nerves impairs sweat gland function
• the foot loses it's ability to moisturize skin,
• This leads to the skin becoming dry, scaly and cracks easily under
pressure
• This ultimately leads to development of epidermal cracks and skin
breakdown

38. Charcots arthropathy
• Progressive degeneration of a weight bearing joint, marked by bony
destruction, bone resorption, and eventual deformity
• Diabetes mellitus, together with neuropathy, is currently considered
the main cause
• Two main theories
• The neurotraumatic theory
• The neurovascular theory

39. Neurotraumatic theory
•Sensory neuropathy leading to loss of peripheral sensation and motor
neuropathy leading to deformities of foot result in repetitive
microtrauma to the joint
•Usually goes unnoticed by the patient
•Inflammatory response leads to defective new bone formation
increasing unnatural pressure in joint leading to further trauma

40. Neurovascular theory
•Autonomic neuropathy results in loss of tone in blood vessels leading
to hyperemia
•Increased expression of NF-KB results in increased Osteoclastic activity
•Together result in increased bone resorption and weakening of bone
structure

41. Eichenholtz classification.
Stage Radiographic finding Clinical finding
development Osteopenia, osseous
fragmentation, joint subluxation or
dislocation
Swelling, erythema, warmth,
ligamentous laxity
coalescence Absorption of debris, sclerosis,
fusion of larger fragments
Decreased warmth, decreased
swelling, decreased erythema
reconstruction Consolidation of deformity, fibrous
ankylosis, rounding and smoothing
of bone fragments
Absence of warmth, absence of
swelling, absence of erythema,
fixed deformity

42. Sanders and Frykberg classification
Type Localization
•I Metatarsophalangeal and interphalangeal joints
•II Tarsometatarsal articulations (Lisfranc)
•III Midtarsal joint line (Chopart)
•IV Ankle joint and subtalar joint
•V Calcaneus

44. Vasculopathy
• Peripheral arterial disease (PAD) is a contributing factor to the
development of foot ulcers in up to 50% of cases.
• Macroangiopathy presents as atherosclerosis of major blood vessels
of lower limb
• It commonly affects the tibial and peroneal arteries of the calf
• Other vessels effected are Bifurcation sites of Aorto-ilac, superficial
femoral and popliteal arteries

45. • Microangiopathy manifests as thickening of basement membrane
leading to tissue hypoxia (including peripheral nerves)
• Endothelial cell dysfunction and smooth cell abnormalities develop in
peripheral arteries as a consequence of the persistent hyperglycemic
state.
• There is a resultant decrease in endothelium-derived vasodilators
leading to constriction.
• Further, the hyperglycemia in diabetes is associated with an increase
in thromboxane A2, (vasoconstrictor and platelet aggregator), which
leads to an increased risk for plasma hypercoagulability

46. Blue toe syndrome
• Usually seen in elderly men
• Present with painful, discoloured toe with palpable peripheral pulses
• Due to cholesterol or atheroembolism of distal arteries
• Can occur spontaneously / post procedural / anti coagulant therapy
• Is a sign of more wide spread atherosclerosis and embolic potential

47. • Immune dysregulation secondary to hyperglycemia
• Decreased leukocyte phagocytosis
• increased t cell apoptosis
• Neutrophil function abnormalities
• Increased seusceptiblity to infections
• Impaired wound healing

48. Infections
• Infections are common in diabetic foot ulcers because of multiple
contributing factors
• Poor wound healing
• Continued trauma
• Ischemia
• Deformity

49. • Infections are always polymicrobial
• MC organism isolated is staph aureus
• Other organisms like Peudomonas, Klebsiella, enterococci are also
found
• Anaerobes like peptostreptococci are also not uncommon
• Hospital stay increases the risk of infection with more resistant
organisms

51. Thank You