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A diabetic patient with wound on foot

A patient presents with an ulcer that progresses to gangrene.

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A diabetic patient with wound on foot

  1. 1. A Diabetic Patient with wound on foot A Presentation by: Abdullah Mohammad 2014-001
  2. 2. Case Mr. XYZ is a 50 year old gentleman who presented to the OPD clinic with chief complaint of lesion on the right foot and swelling for one week. HOPC: Mr. XYZ who is a known case of type 2 diabetes mellitus for the last 18 years was in his usual state of health 1 week back when he noticed a lesion on his right foot. He doesn’t know when the lesion actually appeared. At first he did not bother with it and thought it is just a result of some trauma but for the last 1 day he has also noticed redness and swelling around the lesion which brought him to the clinic today. It does not interfere with his walking. There is no history of fever, rigors or chills. There is no history of trauma. ROS: Unremarkable Past Medical Hx: On insulin for the control of his blood sugar. He monitors it occasionally and it is not properly controlled. He does not complain of decrease in vision or frothy urine. There are no other co-morbids Past Surgical Hx: Nil Social Hx: He smokes 1-2 cigarettes per day for the last 10 years. There are no other addictions
  3. 3. Physical Examination • Vital signs are stable. • On inspection of the right foot a purulent ulcer was present on the 5th metatarsal head with about 1 cm induration and erythema around the ulcer. The ulcer had a punched out edge. There was no visible deformity of the foot. The color and hair distribution of the rest of the foot was normal. On palpation of the ulcer, it was warm as compared to the surrounding skin and non-tender to touch. It measured 0.5 cm in length, 1 cm in width and 3 mm in depth. The base of the ulcer was pink and granulating surrounded by callus. There was no visible or palpable bone with probing. Peripheral pulses were Palpable. Light touch, vibration, and monofilament pressure perception was greatly diminished. Deep tendon reflexes were normal. There was no inguinal lymphadenopathy. • Examination of the left foot was unremarkable
  4. 4. Investigations • CBC • Fasting Blood Sugar • Gram Stain and Culture of the discharge from the ulcer • XRAY / MRI foot • Arterial Duplex scanning • Angiography if required
  5. 5. Results • CBC revealed total WBC of 7000, Hb of 13.5 gm/dl, MCV of 85 and Plt count of 210,000 • Fasting blood sugar was 180 mg/dl • Culture of the discharge grew Staphylococcus Aureus sensitive to vancomycin, linezolid and ceftazidime • XRAY of the foot showed no evidence of osteomyelitis • Arterial Duplex scanning revealed good flow in all the peripheral pulses
  6. 6. Treatment • Foot ulcers in diabetes require multidisciplinary assessment, usually by diabetes specialists and surgeons. • Treatment consists of • Appropriate bandages • Antibiotics (against staphylococcus, streptococcus and anaerobe strains) • Debridement, • Arterial revascularisation • Platelet-rich fibrin therapies.
  7. 7. Typical features of Diabetic foot ulcer according to etiology Feature Neuropathic Ischemic Neuroischemic Sensation Sensory loss Painless Painful Degree of sensory loss and painless Callus/necrosis Callus present and often thick Necrosis common Minimal callus Prone to necrosis Wound bed Pink and granulating, surrounded by callus Pale and sloughy with poor granulation Poor granulation Foot temperature and pulses Warm with pulses present Cool with absent pulses Cool with absent pulses Other Dry skin and fissuring Delayed healing High risk of infection Typical location Weight bearing areas of the foot such as metatarsal heads, the heel and over the dorsum of clawed toes Tips of toes, nail edges and between the toes and lateral borders of the foot Margins of the foot and toes
  10. 10. Assessment of a Diabetic Foot Ulcer • Examination of the ulcer • Testing for loss of sensation. 10g Semmes-Weinstein monofilament and standard 128Hz tuning fork are simple and effective screening tool • Testing for vascular status. This can be done by palpation of the peripheral pulses, Duplex ultrasound, Angiography • Identifying infection and taking culture • Full blood count, electrolytes, inflammatory markers (ESR, CRP) • Assessing bone involvement (Using XRAY or MRI) • Inspecting feet for deformities
  11. 11. Monofilament for pressure sensation (pinprick sense) • Place a 10g nylon Semmes-Weinstein monofilament at a right angle to the skin • Apply pressure until the monofilament buckles, indicating that a specific pressure has been applied. • Inability to perceive the 10g of force applied by the monofilament is associated with clinically significant large fibre neuropathy and an increased risk of ulceration (sensitivity of 66 to 91%) • Test 4 plantar sites on the forefoot (great toe and the base of 1st, 3rd and 5th metatarsals ) to identify 90% of patients with an insensate foot. Monofilament test
  12. 12. Assessment Infected Ulcers • Assessing foot ulcers for the presence of infection is vital. All open wounds are likely to get colonised with microorganisms, such as Staphylococcus aureus, and not necessarily infected. Therefore, the presence of infection needs to be defined clinically rather than microbiologically. An infected ulcer Signs suggesting infection include; 1. purulent secretions 2. presence of friable tissue 3. undermined edges 4. foul odour
  13. 13. Assessment Structural Abnormalities and Deformities • Structural abnormalities and deformities lead to bony prominences which are associated with high mechanical pressure on the overlying skin. • This results in ulceration, particularly in the absence of a protective pain sensation and when shoes are unsuitable. • Ideally, the deformity should be recognised early and accommodated in properly fitting shoes before ulceration occurs. • Common abnormalities / deformities include: i. Callus ii. Bunion iii. Hammer toes iv. Claw toes v. Charcot foot vi. Nail deformities • Note: It is vital to inspect the patients shoes as part of the assessment! Callus on plantar surface Bunion on the medial border of the foot
  14. 14. Claw toes Charcot foot deformity Nail deformity Assessment - Some Common Foot Deformities
  15. 15. Classification of Diabetic Foot Ulcers • Several foot ulcer classifications have been proposed although none is universally accepted. • The simplest classification is based on the underlying pathogenesis: neuropathic, ischaemic or neuroischemic. • It is vital to carefully monitor the progress of an ulcer once one has developed. • The University of Texas system shown on the next slide can be used to predict outcome by grading wound depth and presence of infection and/or ischemia. However there is no measure of neuropathy.
  16. 16. Ulcer Grade ( depth ) 0 I. II. III. Ulcer stage A Pre / postulcerative lesion completely epethelialised Superficial lesion, not involving tendon, capsule or bone Wound penetrating to tendon or capsule Wound penetrating to bone or joint B Pre / postulcerative lesion with Infection Superficial lesion, not involving tendon, capsule or bone with Infection Wound penetrating to tendon or capsule with Infection Wound penetrating to bone or joint with Infection C Pre / postulcerative lesion with ishaemia Superficial lesion, not involving tendon, capsule or bone with ischaemia Wound penetrating to tendon or capsule with ishaemia Wound penetrating to bone or joint with ishaemia D Pre /postulcerative lesion with infection and ishaemia Superficial lesion, not involving tendon, capsule or bone with infection and ischaemia Wound penetrating to tendon or capsule with infection and ischemia Wound penetrating to bone or joint with infection and ischemia University of Texas system for classification of ulcers
  17. 17. WAGNER CLASSIFICATION FOR DIABETIC FOOT LESIONS • Grade 0 – No open lesion(callus may be present) • Grade 1 – Superficial Ulcer • Grade 2 – Deep Ulcer to Tendon, Capsule or Bone • Grade 3 – Deep Ulcer with abscess, osteomyelitis, joint sepsis • Grade 4 – Localized gangrene • Grade 5 – Gangrene of entire foot Non Surgical Management Surgical and Medical Management
  18. 18. Managing a Diabetic Foot Ulcer • General Principles of Therapy: 1. Stabilize the patient • Restoration of fluid and electrolyte balance • Correction of hyperglycemia, hyperosmolarity, acidosis, and azotemia • Treat other exacerbating factors Note – improving glycemic control may aid in eradicating the infection and healing the wound • Cardiovascular risk factors such as smoking, dyslipidaemia and hypertension should be addressed to reduce risks of Peripheral Vascular Disease, acute coronary syndrome and chronic renal failure • Education of patients on proper foot care and on the importance of seeking medical advice early is very important • Ensure an adequate blood supply • Local wound care (tissue debridement, inflammation and infection control, moisture balance)
  19. 19. • Choose an antibiotic regimen • Severe infection: • start broad spectrum IV abx (ensure Gram Positive Coverage, gram negative and anaerobic coverage) • Mild-Moderate infection: • Relatively narrow spectrum only covering aerobic Gram Positive Coverage • No evidence for anti-anaerobic therapy • Oral therapy with highly bioavailable agents is appropriate • Mildly infected open wounds with minimal cellulitis: • Limited data support the use of topical antimicrobial therapy (B-I)
  20. 20. • “It’s an ulcer..what now!?”-Don’t panic, be methodical. • Treatment of diabetic foot ulcers largely depends on the underlying causes: ischaemia, neuropathy or a combination of both. Treatment approaches for ischaemia include: Ischaemic necrosis of a toe and an extensive plantar ulcer Medical: reduce cardiovascular risk factors Surgical: revascularisation to achieve timely and durable wound healing is sometimes necessary. Patients with supra-inguinal (aorta- iliac) disease may be amenable to angioplasty (+/- stenting), with good long-term results being achieved at a low risk. Open bypass surgery may be considered for those patients who do not have an endovascular option.
  21. 21. • The best method is some form of cast. • If not available, temporary ready-made shoes with a plastozote insole such as Drushoe can off-load the site of ulceration. Alternatively, weight-relief shoes and felt pads may also be used. • Other weight-relieving measures such as the use of crutches, wheelchairs and zimmer frames should be encouraged. • Heeled ulcers also need off-loading by foam wedges, heel protector splints or rings. The common site for a neuropathic ulcer The key to treatment here is to redistribute plantar pressure.
  22. 22. • “These cast things sound useful...what are they?” • Various casts are available and all aim to relieve plantar pressure. Their use is governed by local experience and expertise • Air cast (walking brace) • A bivalved cast with the halves joined together with Velcro strapping. The cast is lined with 4 air cells which can be inflated with a hand pump to ensure a close fit. The cast can be removed easily by patients to check their ulcers and before going to bed. • Scotch cast boot • A simple, removable boot made of stockinette, soffban bandage, felt and fibreglass tape. • Total contact cast • It is a close-fitting plaster of paris and fibreglass cast applied over minimum padding. It is very efficient method of redistributing plantar pressure, and should be reserved for plantar ulcers that have not responded to other casting treatments. An air cast A scotch cast boot
  23. 23. Casts should be removed every week for wound inspection and then renewed. Cast problems to be aware of: • Iatrogenic lesions (rubs, pressure sores, infections) which often go undetected • Cast are often heavy and uncomfortable and reduce the patient’s mobilty • Patients may not drive a car in a cast • The leg may develop immobilisation osteoporosis • Danger of fracture and the development of a Charcot foot when coming out of a cast if patient walks too far too soon • A few patients develop a cast phobia and will not wear them
  24. 24. • “What can we do to treat the ulcer?” • In both isacheamic and neuropathic ulcers, treatment is based on debridement of the wound and dressing application. Debridement is the removal of necrotic and dead tissue in order to enhance healing. Debridement is undertaken to: • Remove callus in neuropathic foot to lower plantar pressure • Assess the true dimension of the ulcer • Drain exudate and remove dead tissue to render infection less likely • Take a deep swab for culture • Encourage healing and restore a chronic wound to an acute wound Forcep and a scalpel is the usual technique by cutting away of all slough and non- viable tissue.
  25. 25. ) • The larvae of the green bottle fly (which feed on dead flesh) are sometimes used to debride ulcers, especially in the ischaemic foot. Only sterile maggots obtained from a medical maggot farm should be used! • Maggots produce a mixture of proteolytic enzymes that breakdown slough and necrotic tissue which they ingest as a source of nutrients. During this process, they also ingest and kill bacteria including antibiotic resistant strains. • As a result of their wound cleansing activity, the application of maggots has been found to reduce wound odour, and it has also been reported that their presence within a wound stimulates the formation of granulation tissue. • Contra-indications to maggot therapy: • Free range maggots should not be introduced into wounds that communicate with the body cavity or any internal organ • They should not be applied to wounds that have a tendency to bleed easily or contain exposed large blood vessels • They should not be applied to patients with clotting disorders, or individuals receiving anticoagulant therapy unless under constant medical supervision in a health facility.
  26. 26. • Maggots are available in 2 forms. 1. ‘Free Range’ maggots • applied directly to the wound • roam freely over the surface seeking out areas of slough or necrotic tissue • generally left on wound for a maximum of 3 days. 2. BioFOAM Dressing • Maggots enclosed in net pouches containing pieces of hydrophilic polyurethane foam • dressing is placed directly upon the wound surface • BioFOAM Dressing can be left for up to 5 days then the wound is reassessed. BioFOAM dressing with maggots inside
  27. 27. Management - Wound Dressings • A sterile, non-adherent dressing should cover all open diabetic foot lesions to protect them from trauma, absorb exudate, reduce infection and promote healing. • Dressings should be lifted every day to ensure that problems or complications are detected quickly, especially in patients who lack nociception. • Additional approaches include • Skin graft: •A split-skin graft may be harvested and applied to the ulcer to speeds healing of the ulcer which if has a clean granulating wound bed •Vacuum-Assisted closure (VAC) pump: •This is an innovative measure to close diabetic foot wounds. It applies gentle negative pressure to the ulcer via a tube and foam sponge which are applied to the ulcer over a dressing and sealed in place with a plastic film to create a vacuum. Exudate from the wound is sucked along the tube to a disposable collecting chamber. The negative pressure improves the vascularity and stimulates granulation of the wound.
  28. 28. “Are there any new interesting aids for wound healing?” –Yes, three here;  Hyperbaric oxygen therapy: Poor tissue oxygenation with diabetic microangiopathy reduces wound healing. Therefore hyperbaric oxygen therapy (HBOT) would theoretically aid in faster wound healing, there is however little evidence for this at present.  Growth factor therapy: Recombinant platelet derived growth factor (PDGF) was the first growth factor approved by the Food and Drug Administration (FDA) for the treatment of lower extremity diabetic neuropathic ulcers that extend into the subcutaneous tissue and have adequate blood supply. PDGF, applied as a gel , theoretically acts to enhance granulation tissue formation and facilitate epithelialisation . It may be useful in small, low-grade so may have a role in chronic neuropathic ulcers that are refractory to conventional therapy but there is no evidence to support this theory.  Bioengineered human dermis transplantation: Dermagraft is a cultured human dermis produced by seeding dermal fibroblasts on a biodegradable scaffold. After culture, a living dermal tissue is created which can later support the formation of an epidermis. Furthermore, dermatograft can generate growth factors, cytokines, matrix proteins and glycosaminoglycan, thus aiding the healing process. There have been a limited number of trials have confirmed the efficacy of dermagraft in healing chronic ulcers in a significantly shorter time.
  29. 29. • “And when the bone gets infected?” • Lastly, treating underlying osteomyelitis is an important therapeutic challenge. Presence of osteomyelitis warrants long-term treatment of at least 4 – 6 weeks duration with antibiotics that penetrate well into bone such as fluoroquinolones, clindamycin or fusidic acid. • Surgical ressection still remains the most definitive treatment for osteomyelitis especially for patients not responding to antibiotics. Treating Charcot’s neuro-osteoarthropathy “Charcot foot” refers to bone and joint destruction that occurs in the neuropathic foot or rarely just the toe. It can be divided into three phases: •Acute onset; •Bony destruction / deformity; •Stabilistion; 1. Acute onset Characterised by unilateral erythema and oedema and the foot is at least 2˚C hotter than the contralateral foot. About 30% of patients may complain of pain or discomfort which is rarely severe. X-ray may be normal, but a technnetium methylene diphosphonate bone scan will detect early evidence of bony destruction. An infected ulcer draining pus
  30. 30. • Patients awaiting bone scan should be treated as if the diagnosis has been confirmed; • Initially the foot is off-loaded and immobilised in a non-weight-bearing cast to prevent deformity. After 1 month, a total-contact cast is applied and the patient may mobilise for brief period. However, the patient is given crutches and encouraged to keep walking to a minimum. • If given early, these measures can prevent bony destruction. Bisphosphonates are potent inhibitors of osteoclast activation and may also be used in this phase. • 2. Bony destruction • Clinical signs are swelling, warmth, a temperature 2˚C greater than the contralateral foot and deformities • X-ray reveals fragmentation, fracture, new bone formation, subluxation & dislocation. • The aim of treatment is immobilisation until there is no X-ray evidence of continuing bone destruction and the foot temperature is within 2˚C of contra lateral foot. A photo showing a charcot foot with an ulcer on the sole
  31. 31. • 3. Stabilisation The foot is no longer warm and red. There may still be oedema but the difference in skin temperature between the feet is less than 2˚C. the X-ray shows fracture healing, sclerosis and bone remodelling. The patient can now progress from a total-contact cast to an orthotic walker. Cautious rehabilitation should be the rule, beginning with a few short steps in a new footwear. Regular reduction of callus can prevent ulceration. During the acute stage, charcot foot’s foot may be misdiagnosed as;  Cellulitis  Osteomyelitis  Deep vein thrombosis  Inflammatory arthropathy Therefore a high index of suspicion is very important at this stage!
  32. 32. Gangrene • Gangrene is a serious condition that arises when a considerable mass of body tissue dies (necrosis). The primary cause of gangrene in a diabetic patient is reduced blood supply to the affected tissues which results in cell death. • There are different types of gangrenes i.e. wet gangrene, dry gangrene, gas gangrene • Necrosis in chronic ischemia may be patchy and localized if there is a developed collateral circulation. Such necrosis is usually confined to toes or a limited part of the forefoot. The necrotic area slowly becomes hard, black and mummified (dry gangrene) and may eventually separate spontaneously from the viable tissue. However, there is always a risk that the necrotic area can become infected. The tissue then becomes ulcerated and the infection and gangrene spread proximally. This wet gangrene requires urgent treatment often with a combination of revascularization and amputation. • Treatment options include debridement, amputation, antibiotics, vascular surgery, maggot therapy or hyperbaric oxygen therappy
  33. 33. Amputation • Indications for amputation are: 1. If revascularization is technically impossible 2. If there is substantial tissue necrosis and functionally useless foot or spreading infection is present 3. A non healing ulcer that is accompanied by a higher burden of disease than would result from amputation. 4. Ischemic rest pain that cannot be managed by analgesics or revascularization 5. As part of debridement (minor amputation) 6. Spreading cellulitis
  34. 34. Level of Amputation Two principles guide the level of amputation 1. The amputation must be made through healthy tissue. If not, there is a high risk of wound breakdown and chronic ulceration, requiring further amputation at a higher level. When amputation is for (uncorrected) peripheral ischemia, it is almost always necessary to amputate at mid-tibial level or above to ensure healing 2. The choice of amputation level must take into account the fitting of a prosthetic limb. For this purpose, the mid-tibia (below-knee) and lower femoral levels (above-knee) are preferred. If the knee joint can be saved, the functional success of a prosthesis is much better.
  35. 35. Types of Amputation • Minor This involves simple amputation at the base of the digit or ‘ray’ amputations where, e.g. in the foot, the metatarsal head and tendons are removed. Occasionally for ischemia of all toes, transmetatarsal amputation may be undertaken. • Major 1. Below Knee amputation: This provides the patient with the best chance of mobilizing with a prosthesis. This is suitable in diabetics with a palpable popliteal pulse. The standard tibial stump is 8-12 cm long 2. Above Knee amputation: This is a common amputation in patients with arteriosclerosis. The stump of the femur is 25 cm long measured from the greater trochanter
  36. 36. Postoperative care • Pain relief • Care of the good limb: This involves physiotherapy. It is important to avoid pressure ulcers by nursing on air bed • Physiotherapy: Build up muscle power and coordination. Start as soon as the patient is comfortable and continue in gymnasium. The aim is to prevent contractures and ensure rapid mobilization with prosthesis • Prosthesis: Measure patient as soon as stump shrinks and volume of stump is stable
  37. 37. Complications • Early: These include hemorrhage, hematoma, abscess, gas gangrene, wound dehiscence, ischemic flaps and fat embolism • Late: These include pain, sinus formation, osteomyelitis, phantom limb and ulceration of the skin (pressure from prosthesis or continuing ischemia)