Diabetic foot


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Diabetic foot

  1. 1. Pathophysiology and Management of diabetic Foot Dr Vijaya Lakshmi. L DNB General Surgery 06-10-2010
  2. 2. Introduction • Principles of etiology, treatment and prevention established by pioneer work of Paul Brand • One of the commonest complications • Major limb amputation – end point of foot lesions in diabetes • Classical triad – Neuropathy, Ischemia, Infection • Advanced diabetic foot is like prothrombotic stage
  3. 3. Epidemiology 1. Foot Ulcers • 15% of all diabetic individuals during their life time • 85% of amputations are preceded by diabetic foot ulcers • Most important risk factors are – Peripheral sensory neuropathy followed by PVD • The proportions of neuropathic 54%, neuroischemic 34%, purely ischemic 10% in diabetics
  4. 4. Epidemiology • 2. PVD • Asians ( 3-6% ) Western ( 25-45%) • Prevalence increases with advancing age , increased duration of diabetes • 3. Lower Extremity Amputation • Rates increase with advanced age. Higher in males than females • Approx 50% of amputees undergo second or contralateral amputation (leg) within 1-3 yrs
  5. 5. Epidemiology • In western pts – mortality, contra limb amputation, AKA is higher mainly because of older age, generalized atherosclerosis and multi-system involvement • In west most common indication for major limb amputation is neuro-ischemic foot while in India it is neuropathic foot with secondary infection mainly because of incorrect or delayed treatment
  6. 6. Classification I Into 3 types Neuropathic Foot – Neuropathy dominates. Fissures, bullae, neuropathic joints and edema, digital necrosis. Neuroischemic Foot – Occlusive vascular disease main factor while neuropathy is present. Rest pain, foot margin ulceration, digital necrosis and gangrene. Non neuroischemic foot – No significant neuropathy or ischemia. Secondary to trauma. Infected because of uncontrolled, often undetected diabetes
  7. 7. Classification • II. Wagner’s Classification ( Grading ) Specific for neuropathic foot & secondary infection • Grade 0 - No ulceration in a high risk foot • Grade 1 - Superficial ulceration • Grade 2 - Deep ulceration up to tendon, ligament, deep fascia, bone or joint • Grade 3 - Osteomyelitis or deep abscess • Grade 4 - Localized gangrene • Grade 5 - Extensive gangrene requiring major amputation
  8. 8. Risk Factors 1. Smoking 2. Hypertension 3. Hyperlipidaemia 4. Insulin resistance with compensatory hyperinsulinaemia 5. Severity and duration of diabetes 6. Age 7. Genetic predisposition
  9. 9. Pathogenesis 1. Neuropathy -Chronic sensitomotor peripheral neuropathy is most common long term complication -Components of peripheral neuropathy are sensory neuropathy, motor neuropathy, autonomic neuropathy. -Loss of sensation -> trauma -> ulceration -Loss of proprioception -> foot deformities -> ulceration -Sympathetic dysfunction -> infection
  10. 10. Pathogenesis - Neuropathy -The atrophy of intrinsic muscle of foot predominantly plantar flexors of toes alters flexor/extensor balance at MPJ-claw toes and prominent metatarsal heads (due to pushing forward of fibro-fatty metatarsal cushions) -Footshape alter- increases plantar pressure -Majority of wounds-occur from continuous pressure -Callus acts as foreign body & increases plantar pressure exacerbating the problem
  11. 11. Neuropathy autonomic sensory motor reduced vascular painless bone muscle sweating effects trauma changes atrophy dry skin charcot joint deformity infection ulcer callus abnormal pressure points
  12. 12. Pathogenesis - Neuropathy • Walking briskly-progressive hyperemia over points of maximum stress • Thermography outlines temperature contrast of progressive inflammation from such a process • Insensitive feet-hyperemia at old scars site • In shoe foot prints-points of persistent and maximum stress on feet
  13. 13. Pathogenesis - Neuropathy • Classical peripheral neuropathy – bilateral and symmetrical • Sensory component predominates – subjective pain & paraesthesia, objective examination blunting sensation of pain & temperature “The painful painless leg” • Sensory disturbance-distal portion lower extremities eventually progressing to stock and glove distribution • Involvement of sensory & motor fibers impairs light touch & proprioception
  14. 14. Foot ulcer vs. Neuropathy C fiber dysfunction Large fiber dysfunction loss of pain & warm loss of vibration & thermal perception position sensation wasted interossei equinus hammer toes warm feet dry scaly feet osteopenia decreased blood flow increased blood flow
  15. 15. Pathogenesis - Neuropathy Neuropathy assessed by clinical examination, conduction studies, tuning fork, pin prick tester, nylon monofilament, tendon hammer Biothesiometer measure vibration perception threshold (VPT) VPT >25 V-severe neuropathy & foot at risk 10-g nylon monofilament also documents VPT
  16. 16. Foot tests • Pin prick test – use a disposable instrument e.g. a disposable pin • Light touch – use a consistent method, ideally a cotton wisp • Vibration test – use 128 Hz tuning fork, initially on the big toe • Pressure perception - 10g monofilament absence of sensation in the foot • Ankle reflex – compare it with knee reflex
  17. 17. Pathogenesis 2. Biochemical aspect - The non - enzymatic glycosylation of collagen leads to thickening and cross linkage of collagen bundles, stiffness of ligaments - restrictions in the range of motions of the joints of foot particularly in sub talar joint and ankle leading to increased plantar pressure and alters mechanism of walking • Limited joint mobility also occurs in hands
  18. 18. Pathogenesis 3. Biomechanics - Commonest sites of ulceration-in forefoot - Ulcers occur at sites of high pressure on either plantar or dorsal surface - Ulcers caused by undue bony prominences, ill fitting footwear and toe deformities - Foot deformities result from atrophy of intrinsic muscles of foot
  19. 19. Pathogenesis - Biomechanics • Altered foot architecture, loss of flexibility and free joint movements – relatively rigid and unstable foot with altered weight bearing pressure areas • Bony prominences push forward the fibro- fatty shock absorbing pads exposing condyles of metatarsal heads • Combination of risk factors & neuropathy increase plantar pressure on forefoot & hallux, significantly increasing risk of foot ulceration
  20. 20. Pathogenesis - Biomechanics • Semi quantitative estimation of plantar pressure – ink pad on which patient’s foot leaves an impression in different shades. Quite specific, not very sensitive • Bare foot measurements – pts walk onto platform, information from single foot contact collected • In-shoe measurements – matrix of transducers manufactured into thin pliable insole placed in shoe in direct contact with foot, information from multiple steps
  21. 21. Pathogenesis - Biomechanics -Normal peak plantar pressures 50-300 KPa -Pressures lowest on mid foot region, highest on heel, heads of first 3 metatarsals and hallux -In diabetes peak plantar pressure- increased 2-3 folds -Elevated plantar pressure major factor in pathogenesis of plantar ulcer -In-shoe measurements refine footwear prescription by defining exact degree of pressure relief at high risk areas
  22. 22. Pathogenesis 4. Haemorrheology - Macro vessel haemorrheology constituted by Hct, plasma viscosity, platelet activity and RBC aggregation - Micro vessel haemorrheology involves RBC and WBC deformability - All these components are altered in diabetics, accentuating ischaemic process due to structural changes in large and small blood vessels
  23. 23. Pathogenesis 5. Infection - Frequent and severe infections in diabetics due to vascular insufficiency - In presence of infection increased blood supply cannot be met. Skin breaks down and tissue necrosis – nidus for organisms - Bacteroids commonest - Soft tissue gas formation by coliform group (aerobic/anaerobic G –ve rods), streptococci, staphylococci
  24. 24. Pathogenesis - Infection -Non healing ulcer over bony prominence – suspect osteomyelitis. It should be differentiated from diabetic osteopathy occurring as a result of denervation -Radiological hallmark of diabetic osteopathy “ peppermint stick sign “ – pointed distal metatarsal -Diabetic osteopathy distribution multifocal & bilateral. Associated with normal WBC count & ESR
  25. 25. Pathogenesis 6. Peripheral vascular disease -Bilateral pathology, multi-segmental, predilection for vessels below popliteal artery -collateral vessels are involved in diabetes -Gangrene occur in patchy areas of foot & toes -Present with intermittent claudication, nocturnal pain and rest pain
  26. 26. Features of ischemic foot • Thin atrophic feet, thickened nails, sparse hair • Painful lesions: dry gangrene confined to toe or heel, or extensive or superinfected • Cold feet that become pale on elevation & cyanosed on depression • Weak/absent peripheral pulses • Slow venous filling • Vascular investigation – ischemia • Normally/slightly reduced reflexes or sensation
  27. 27. Features of neuropathic foot • Disproportion between lesions and absence of pain • Keratosis, cracks, ulcers & plantar ulcers • Deformity of foot & toes, amyotrophy • Loss of sense of touch, pain, vibration & tendon reflexes • Warm dry feet, venous congestion, edema • Pulses present, no evidence of ischemia on investigation
  28. 28. Pathogenesis - PVD • Ankle-toe pressures, ankle-brachial systolic pressure ratio (ischaemic index), pattern of flow – indices for assessment • Normal ankles-brachial systolic BP is >1.0 and values <0.6 - significant arterial stenosis • Doppler USG pulse wave in peripheral vessels • Ankle pressure <70 mmHg– poor healing, >100 mmHg good prognosis • Toe pressure <20 mmHg- increased failure of distal amputation, >40 mmHg good prognosis
  29. 29. Foot ulcer risk factors • Risk factor Neuropathy • Screening method Clinical examination, pressure & vibration perception threshold • Abnormal result/risk of foot ulceration Absent ankle reflexes or sensory loss, insensitivity to 10g monofilament on plantar surface Vibration >25 V at the greater toe
  30. 30. Foot ulcers risk factors • Risk factor PVD , previous foot lesion • Screening method Clinical examination, doppler pressures, history • Abnormal result/risk of foot ulceration Less than 2/4 palpable foot/ankle pulses Systolic ankle pressure<90% of brachial pressure History of ulcer or amputation
  31. 31. Pathogenesis - PVD • Sophisticated techniques like skin blood flow calculated from xenon-133 clearance, a micro-invasive procedure & transcutaneous oxymetry • Cutaneous blood flow of >2.6ml/100g/min associated with good healing • However above indices cannot predict healing accurately because state of local wound dominates the outcome • Neuropathy is starter, Vasculopathy is chaser, Infection is perpetuator
  32. 32. Clinical evaluation 1. History The inciting event may be cutting a toenail, soaking the foot in a warm bath, or applying a heating pad. The duration of the ulcer- long-standing, nonhealing ulcer is strongly suggestive of ischemia heal with some further treatment, whether it be offloading of weight-bearing areas, treatment of infection, or correction of arterial insufficiency.
  33. 33. Clinical evaluation -history History of intermittent healing & relapse - possibility of underlying untreated infection (recurrent osteomyelitis) or uncorrected architectural abnormality (bony/varus deformity). Type and duration of treatments for the current problem - patient with an ischemic ulceration may have completed several different antibiotics courses without success. It is also helpful to know which treatments were not previously offered to the patient and to look critically at why they were not offered.
  34. 34. Clinical evaluation -history Inquiries - previous foot and limb problems, ulcers on the same foot that healed spontaneously, duration of healing, foot surgery on that side. History of previous leg revascularization (including percutaneous therapies) clue to underlying arterial insufficiency. Predilection for mirror image-atherosclerotic occlusive disease, the contralateral leg must be considered as well. Other cardiovascular risk factors, such as cigarette smoking and hyperlipidemia, must also be taken into account
  35. 35. Clinical evaluation -history The patient should be asked about worsening hyperglycemia, recent blood glucose control, and higher insulin requirements. As a consequence of the microvascular and neuropathic abnormalities, classic symptoms of infection (e.g., chills and pain) are often absent, and hyperglycemia is often the sole presenting symptom of undrained infection. Faced with ongoing infection and hyperglycemia, the surgeon should strongly suspect impending ketoacidosis or NKHOC, with symptoms of weakness, confusion, and altered mental status
  36. 36. Clinical evaluation -history Patients with a diabetic foot often need some type of operative intervention - history should include comprehensive assessment of overall health status to stratify perioperative risk e.g. previous cardiac events (MI/revascularization) and current cardiac status help determine whether perioperative cardiac monitoring or preoperative cardiac testing is indicated Similarly, in patient with infection & ischemia, h/o worsening renal function or need for hemodialysis determine choice & dosage of antibiotics & plan for contrast
  37. 37. Clinical evaluation 2. Physical examination Fever and tachycardia- suggestive of deep or undrained infection, with hypotension being a late manifestation of ongoing sepsis. However, that these signs may be absent in diabetic patients with impending or progressive infection.
  38. 38. Clinical evaluation-Physical examination Evaluation of the diabetic foot ulcer should include suspicion of infection and a thorough search for it. In a patient with cellulitis, the entire foot, including the web spaces and the nail beds, should be examined for any potential portals of entry, such as a puncture wound or an interdigital ulcer. Encrusted and heavily calloused areas over the ulceration should be unroofed and the wound thoroughly inspected to determine the extent of involvement.
  39. 39. Clinical evaluation-Physical examination A benign-appearing dry gangrenous eschar often hides an undrained infectious collection Cultures should be taken from the base of the ulcer; superficial swabs may yield only colonizing organisms Purulent discharge, crepitus, tenderness, erythema, and sinus formation indicate infection. With more advanced and deep infection, edema may be present as a result of elevated pressures within one or more of the plantar compartments.If left untreated,it may spread proximally along tendon sheaths to involve ankle or calf.
  40. 40. Clinical evaluation-Physical examination Close inspection of the ulcer and the use of a sterile probe confirms the presence of osteomyelitis. If bone is detected with gentle probing, osteomyelitis is presumed present. Neuropathy should be assessed by 10g monofilament; inability to feel the monofilament correlates with an increased risk of foot ulceration. Advanced sensorimotor neuropathy leads to claw foot or Charcot degeneration -> abnormal pressure points on the plantar
  41. 41. Clinical evaluation-Physical examination Physical examination must include a systematic approach to the assessment of arterial insufficiency. Simple inspection of the leg, foot & ulcer, provides suggestive clues e.g. distal ulceration on the tip of a digit, ulceration unassociated with an exostosis or a weight-bearing area, and gangrene are consistent with underlying ischemia The presence of multiple ulcerations or gangrenous areas on foot, absence of granulation tissue, lack of bleeding with
  42. 42. Clinical evaluation-Physical examination Other signs- pallor with elevation, fissures (particularly at the heel), absence of hair growth, poor skin condition and hyperkeratosis should be noted The pulse examination, including of foot pulses, is the most important component of the physical examination. Absence of a palpable pulse indicates ischemia.
  43. 43. Clinical evaluation-Physical examination The femoral pulse - palpated midway between the ASIS and the pubic tubercle, just below the inguinal ligament. The popliteal pulse - palpated with both hands and with the knee flexed no more than 15°. The dorsalis pedis is located between the first and second metatarsal bones, just lateral to the extensor hallucis longus tendon, and its pulse is palpated with the pads of the fingers as the hand is partially wrapped around the foot . If the pulse cannot be palpated, the fingers may be moved a few millimeters in each direction
  44. 44. Clinical evaluation-Physical examination posterior tibial artery is located in the hollow curve just behind the medial malleolus, approximately halfway between the malleolus and the Achilles tendon. The examiner's hand should be contralateral to the examined foot (i.e the right hand should be used to palpate the left foot, and vice versa), so that the curvature of the hand naturally follows the contours of the ankle
  45. 45. Assessment of clinical findings Once the clinical evaluation is complete, the next step is to assess the findings from the history and the physical examination This assessment is made at the bedside, focusing on three main concerns: 1. The presence and severity of infection – first priority in management of diabetic foot 2. The salvageability of the limb 3. The presence of ischemia.
  46. 46. Infection Infection in diabetic foot range from minimal superficial infection to fulminant sepsis with extensive necrosis tissue destruction The microbiology varies according to the depth and severity of the infection and the nature of the patient's environment - hospitalized or outpatient. Mild localized and superficial ulcerations, particularly in outpatients, are usually caused by aerobic gram-positive cocci - Staph aureus and streptococci.
  47. 47. Infection Deeper ulcers and generalized limb- threatening infections are usually polymicrobial. Gram-positive cocci, gram- negative bacilli - E coli, Klebsiella, Enterobacter aerogenes, Proteus mirabilis, and Pseudomonas aeruginosa, and anaerobes - Bacteroides fragilis and peptostreptococci. Enterococci may also be isolated from the wound, notably in hospitalized patients; in the absence of other cultured virulent organisms, they should probably be considered pathogenic.
  48. 48. Infection Currently, S. aureus (MRSA), are playing a growing role in the development of skin and soft tissue infections. Traditionally arising in patients who had previously been hospitalized and those who had previously received antibiotic therapy Awareness of increasing prevalence of resistant organisms is critical for management In a compliant patient with a small ulcer and no evidence of deep space involvement or systemic infection, treatment may be delivered on an outpatient basis.
  49. 49. Infection A dual-antibiotic regimen (pending culture results) typically consisting of a cephalosporin or a betalactam antibiotic (for activity against staphylococci and streptococci) and vancomycin (for activity against MRSA). A dual regimen consisting of fluoroquinolone and linezolid is an alternative that also provides adequate coverage. In addition, the patient is instructed to offload weight from the involved extremity and is taught appropriate methods for changing wound dressings. Frequent
  50. 50. Infection A more common presentation - patient with ulceration/gangrene with deep infection affecting tendon/bone and systemic involvement - immediate hospitalization indicated, bed rest, elevation of the foot, correction of any systemic abnormalities, and broad-spectrum I.V. antibiotic therapy (which may be focused more tightly once culture results are complete). Because the clinical findings of impending sepsis may be subtle, these patients should undergo a complete laboratory workup to detect and correct electrolyte
  51. 51. Infection The choice of antibiotics and duration of therapy are dependent on the extent of the infection. For patients with deep/chronic recurrent ulcers, typically polymicrobial, or limb or life-threatening infections, appropriate empirical antibiotic options include (1) vancomycin + betalactam antibiotic with a betalactamase inhibitor (e.g., piperacillin-tazobactam) (2) Vancomycin + metronidazole plus a
  52. 52. Infection In the absence of osteomyelitis, antibiotics should be continued until the wound appears clean and all surrounding cellulitis has resolved typically, 10 to 14 days If osteomyelitis is present, treatment should include both surgical debridement and a prolonged (4-6 week) course of antibiotic therapy (though the course may be abbreviated if the entire infected bone has been removed, as with digital or transmetatarsal amputation)
  53. 53. Infection Heel lesions often present with some degree of calcaneal destruction & determination of osteomyelitis may be made by clinical examination either alone or in conjunction with other radiographic tests MRI. In the presence of an abscess/deep space infection, immediate I &D of all infected tissue planes is mandatory. Incisions should be chosen with an eye to the normal anatomy of the foot (including the various compartments) and the need for subsequent secondary (foot salvage) procedures. Drainage should be complete, with incisions placed for dependent drainage, and all necrotic tissue debrided.
  54. 54. Infection Drainage incisions on the dorsum of the foot should be avoided. Abscesses in the medial, central, or lateral compartment should be drained via longitudinal incisions made in the direction of the neurovascular bundle and extending the entire length of the abscess. The medial and central compartments are drained through a medial incision, and the lateral compartment is drained through a lateral incision; both of these incisions are made just above the plantar surface of the forefoot
  55. 55. Infection Web space infections may be drained similarly through the plantar aspect of the foot. A patient with an ongoing undrained infection may present with an unsalvageable foot and fulminant sepsis. Such patients should undergo prompt open (guillotine) below-the-knee amputation This type of amputation is usually performed at the ankle level, with the aim of removing the septic source while allowing for revision and closure at a later date.
  56. 56. Infection Administration of I.V. antibiotics, correction of electrolyte abnormalities, continuous cardiac monitoring are essential throughout treatment Once debrided,wound inspection and management are essential. Ongoing necrosis should raise the possibility of undrained infection or untreated ischemia, in which case further debridement and treatment may be necessary. Avoidance of weight-bearing should be continued.
  57. 57. Medical stabilization Hyperglycemia is almost always seen when infection is present; it should be gradually corrected. Serum concentrations of electrolytes, magnesium, and creatinine Dehydration is common in hyperglycemic patients and should be corrected A urinary catheter is mandatory to help guide the response to fluid therapy; in unstable patients Continuous cardiac monitoring is essential in patients with the hyperglycemic hyperosmolar syndrome or ketoacidosis.
  58. 58. Salvageability of limb Determined largely on the patient's functional status and the degree of foot destruction. For example, primary limb amputation may be considered in a nonambulatory, bedridden patient or in a patient with severe Charcot degeneration, for whom no further reconstructive foot surgery is possible Assessment of limb salvageability carried out simultaneously with treatment of infection because appropriate drainage and antibiotics can dramatically change the appearance and viability of the foot. If limb salvage not possible, BKA or AKA done
  59. 59. Ischaemia Patients who might benefit from testing for ischaemia include • Those with absent foot pulses • Who have a superficial ulcer with evidence of healing or a previous history of a healed foot ulcer • Those without any foot lesions who are scheduled to undergo elective foot surgery. Segmental Doppler waveforms and pulsed volume recordings are unaffected by medial calcification
  60. 60. Ischaemia • Regional transcutaneous oximetry measurements are also unaffected by medial calcinosis, and this modality appears to be reliable for predicting ulcer healing and amputation levels • However, measurements are actually higher in patients with diabetics possibly because of the effects of arteriovenous shunting
  61. 61. Ischaemia In evident ischemia, arteriography of the entire lower extremity should be performed. For a complete assessment, the arteriogram should include the foot vessels in both lateral and anterior views
  62. 62. Management 1. Revascularization • approaches include endovascular techniques (angioplasty and stenting) • Bypass grafting (with autogenous or prosthetic grafts) • Combination of the two. • In patients with isolated iliac artery stenoses, angioplasty may be effective by itself, but in patients with multilevel disease, it may have to be combined with an infrainguinal bypass
  63. 63. Revascularization Arterial bypass grafting is required for restoration of the foot pulse Proximal bypass to either the popliteal, tibial, peroneal arteries may restore foot pulses Restoration of pulsatile flow to the foot may be accomplished with autogenous vein bypass grafts to the paramalleolar or inframalleolar arteries (e.g., the dorsalis pedis) The vein graft can be prepared as an in situ graft, a reversed graft, or a nonreversed
  64. 64. Management 2. Wound care Wounds should be kept moist - wet dressings Chemical enzymatic debriding agents Growth factors Hyperbaric oxygen therapy Hyperglycemia and malnutrition correction
  65. 65. Management 3. Secondary foot procedures Goals (1) to remove infected bone (if present) (2) to restore functional stability, (3) to reduce risk of subsequent ulceration In the forefoot- digital, ray, or transmetatarsal amputation performed, depending on the location of the ulcer.
  66. 66. Secondary foot procedures Bony deformities corrected with hallux arthroplasty, metatarsal head resection, metatarsal osteotomy, or sesamoidectomy Ulceration on a previous transmetatarsal amputation may be the result of an equinovarus deformity (from disrupted tendons and a decrease in calcaneal inclination). Treated with revision of the transmetatarsal amputation (perhaps in conjunction with ulcer excision) and biomechanical correction (e.g., Achilles tendon lengthening or, in more severe cases, posterior tibial tendon release).
  67. 67. Secondary foot procedures In heel lesions dry eschars with no evidence of deep infection/abscess treated with offloading alone in the fully revascularized foot. In patients with chronic ulceration or osteomyelitis, partial calcanectomy may be considered. adjunctive studies such as MRI Given the relatively fixed nature of the heel, either secondary healing or some type of flap coverage is usually indicated
  68. 68. 3. Preventive foot care patient education, focusing on general hygiene, daily inspection of the feet. To avoid walking barefoot, employing heat pads, wearing thong sandals
  69. 69. Foot wear prescription • Outsole – should be tough to prevent penetrating injuries, serrated, heel should be 5 cm • Shoe size – length of shoe should allow 1.25 cm b/w end of shoe & longest toe & widest at 1st MTP joint • Countor • Shoes with laces – adjustability needed for edema and deformities
  70. 70. Foot wear prescription • Shoe depth – extra depth to allow dorsal deformities & removable insoles • Toe box – rounded & high toe box to accommodate dorsal deformity • Uppers – soft inner lining to prevent bunions • Insoles - cushioning & allow distribution of plantar pressures
  71. 71. s
  72. 72. Lateral radiograph of an ankle with a destructive arthritis caused by a neuropathic condition
  73. 73. Thank you