الفهرس 
Anattomy off tthe FootOnly 14 pages are availabe for public view
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Abstract
The development of lower extremity ulcers is a well-known potential complication for patients with diabetes. The number of people with diabetes worldwide was estimated at 131 million in 2000; it is projected to increase to 366 million by 2030.
Previous studies have indicated that diabetic patients have up to a 25% lifetime risk of developing a foot ulcer. The annual incidence of diabetic foot ulcers is ~ 3%, and the reported incidence in U.S. and U.K. studies ranges as high as 10%.
Once an ulcer has developed, there is an increased risk of wound progression that may ultimately lead to amputation; diabetic ulceration has been shown to precede amputation in up to 85% of cases.
At least 40% of amputations in diabetic patients can be prevented with a team approach to wound care. The purpose of this review is to describe the causes of lower-extremity ulceration in diabetic patients and to identify common methods of classification and treatment to aid primary care providers in determining appropriate treatment approaches for their patients.
Diabetic foot ulcers result from the simultaneous action of multiple contributing causes. The major underlying causes are noted to be peripheral neuropathy and ischemia from peripheral vascular disease .Evidenced by the numerous pathophysiologic pathways .
loss of protective sensation and concomitant foot deformity, is the leading event precipitating foot ulceration in persons with diabetes. development of a callus, blister, and ulcer.
other common mechanism of ulceration involves prolonged repetitive moderate stress. This normally occurs on the sole of the foot and is related to prominent metatarsal heads, atrophied or anteriorly displaced fat pads, structural deformity of the lower extremity, and prolonged walking. Rigid deformities such as hallux valgus, hallux rigidus, hammertoe, Charcot arthropathy, and limited range of motion of the ankle (equinus), subtalar, and MTP joints have been linked to the development of diabetic foot ulcers.
Diabetic Foot Ulcers Classified by Wagner Ulcer Classification System and by University of Texas Wound Classification System .
Neuropathy in diabetic patients is manifested in the motor, autonomic, and sensory components of the nervous system. 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.
Peripheral arterial disease is a contributing factor to the development of foot ulcers in up to 50% of cases.
Immune system dysfunction It is the third major factor, which predisposes the diabetic patient to infection.
In general, a better regulation of the DM leads to an improvement of these cellular functions. Furthermore, some microorganisms become more virulent in a high glucose environment .
Foot infections may be described in terms of severity, extent of involvement, clinical appearance, location, and etiology .Simply classified into two categories: non-limb-threatening and limb-threatening infections .
The evaluation of the diabetic foot involves careful assimilation of:
-medical and foot history.
-Physical Examination : thorough lower extremity examination at least once annually, Patients with complaints require more frequent detailed evaluations .
-Laboratory tests
-Imaging Studies
-Neurological assessment
-Structural assessment
-Diagnosis of diabetic Charcot foot (neuropathic osteoarthropathy) .
-Ulcer Assessment.
-Vascular assessment
-Osteomyelitis assessment
Treatment Includes :
1-Conservative Treatment:
prevention through Education ,Foot care ,Screening of foot at risk ,Proper foot wear selection .
Multidisciplinary care team is effective in reducing the occurrence and recurrence of diabetic foot complications, including ulceration and amputation .
Management of comorbidities
Wound bed preparation.
Management of diabetic foot infection
Management of acute diabetic charcot foot
2-Adjunctive treatments:
Pressure relief and Off-Loading
Growth factors
Bioengineered skin substitutes
Stem cells
Hyperbaric oxygen
Negative - pressure wound therapy
Monochromatic Infrared Energy
Laser Biostimulation in Wound Healing
3-Surgical treatment :
a)Management of ischemia :
b)Surgical intervention and procedures:
Surgery include :
-Surgical debridement
-Forefoot Procedures:
First Ray.
Lesser Digit.
Lesser Metatarsal Procedures:
Lesser Metatarsal Osteotomy.
Lesser Metatarsal Head Resection with Ulcer Excision.
Pan-metatarsal Head Resection.
-Midfoot Procedures:
Ostectomy.
Exostectomy with Fasciocutanous Flap.
-Rearfoot Procedures.
c) Plastic and Reconstructive Surgery.
-Plantar Forefoot:
Toe Fillet Flap.
Toe Neurovascular Island Flap.
V-Y Plantar Flap.
The Distal Medial Plantar Artery Flap.
-Plantar Midfoot:
Superficial ulcers on the medial non-weight bearing treated using skin grafts .
Ulcers on the lateral weight-bearing region treated by techniques used to cover forefoot.
-Plantar Hindfoot:
Heel Pad Rotation with or Without Calcanectomy.
Medial Plantar Artery Flap.
Muscle Flaps.
Distally Based (Reversed) Sural Artery.
d)Amputation
-Forefoot Amputations:
Ray Amputation.
Single Toe Amputations.
The Remaining Toe.
Transmetatarsal amputation.
-Midfoot Amputations:
Lisfranc’s amputation.
Chopart’s amputation.
-Hindfoot Amputation(Syme’s amputation).
-Transtibial or Below Knee Amputation.
-Through knee amputation.
-Transfemoral or Above Knee Amputation
e)Rehabilitation