Case Personal Diabetic Ulcer

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    STATUS OF PATIENT :

    A.PATIENT IDENTITY

    Name : Mrs. E

    Age : 50 years

    Sex : Female

    Occupation : Housewife

    Religion : Moslem

    Address : Kedaung

    Ethnic : Javenese

    Date of admission : February 11, 2012

    Date of discharge : March 22, 2012

    B. ANAMNESIS

    Main complaint :

    Pain in the right foot

    Additional complaints : - Numbness in the right leg

    -Difficulty to walk-Weakness-Nausea-Vommitus-Harder to breath-Bad appetite

    History of present illness :

    Mrs. E , aged 50 years old has came to Arjawinangun hospital complained of pain in

    the right foot and numbness in the right leg, lower knee region. This complaints has been felt

    since a months ago and getting worst in this last 2weeks. Patient also said that on the right

    foot there is a large wound that swollen and suppurate and smells bad. Other than that patient

    also complained patients daily life activities were limited, as the patient had to use a

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    wheelchair to move because her difficulty to walk. She also feel harder to breath sometimes,

    weakness, nausea, and vomittus. Due to these the patient also hadbad appetite.Past medical history :

    Patientsuffers from diabetes mellitus type 2 for the last 2 years, and was on treatmentbut not regulary take medicine. She also suffers from hypertension in this last year and never

    takes medications.

    Family history of disease:

    There was no family history of this disease.

    C. PHYSICAL EXAMINATION

    General condition: Moderately ill appearance

    Consciousness: Compos mentis

    Vital sign : - Blood pressure: 120/80 mmHg

    -Pulse frequency: 80x/minute-Respiratory rate: 24x/minute-Temperature: 36.6 oC

    General Status

    Skin : Skin color is black, no jaundice, enough turgor

    Head : Symmetrical, normochepal, equitable distribution of hair, no deformity.

    Eyes : Conjunctiva anemis (- / -), sclera icteric (- / -), isokor 3 mm pupil,

    light reflex (+ / +) normal

    Nose : Deviation of the septum (-), discharge (-)

    Mouth : Lips are moist not dry and no cyanosis, tongue is not dirty

    Throat : Tonsil T1/T1, Pharynx not hypermic

    Ears : symmetrical, cerumen right-left (+)

    Neck : No deviated trahea, no palpable enlargement of lymph nodes.

    Thoracic : Inspection : Symmetrical form and movement in right and left hemithorax

    Palpation : tactile fremitus symmetrical right and left

    Percussion : sonor to the hemithorax

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    Auscultation: Pulmo: vesicular breath sound, Ronchi +/ +, wheezing - / -

    Cor: heart sound I / II regular, Murmur (-), Gallop (-)

    Abdomen : Inspection : Symmetrical, flat abdomen, no visible abdominal mass

    Palpation : No abdominal tenderness, no muscular defense, no crepitus

    palpated, liver and spleen are not palpable, no abdominal

    mass.

    Percussion : timpani in the entire quadrant of the abdomen.

    Auscultation : bowel sounds (+)

    Extremity: Warm acral, cyanosis - / -, edema - / -

    Localist Status

    Pedal regionInspection : Seen large wound in right pedal sized 5x8 cm, the skin looks hyperemic,

    pus (+).

    Palpation : Pain (+), edema (+), the temperature is warmer than surrounding.

    D. WORKUP- Complete blood test March 20 2012:

    -Haemoglobin :8,8 g/dl-Haematocrit :27,2 %-Leukocytes :15.200 /ul-Thrombocyte :203.000 /ul

    - Blood glucose level March 20 2012:241mg/dl

    - Kidney function March 20 2012:-Ureum : 53,3 mg/dl-Creatinine : 1,46 mg/dl-Uric acid : 2,24 mg/dl

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    E. WORKING DIAGNOSIS- Diabetic foot ulcer

    F. DIFFERENTIAL DIAGNOSIS- Arteriosclerosis obliteran- Chronic Venous Insufficiency

    G.MANAGEMENT- IVFD NaCl 20 drops/minutes- PRC transfusion 500 cc- Cefoperazone 2x 1amp- Tramadol 2x1 amp- Ranitidin 2x1 amp- Debridement and Necrotomy- Consult to Internist for Diabetes melitus type 2 management.

    H. PROGNOSIS

    Quo ad vitam : dubia

    Quo ad functionam : dubia

    http://emedicine.medscape.com/article/461449-overviewhttp://emedicine.medscape.com/article/461449-overview
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    DIABETIC ULCER

    Foot ulcers are a significant complication of diabetes mellitus and often precede

    lower-extremity amputation. The most frequent underlying etiologies are neuropathy, trauma,

    deformity, high plantar pressures, and peripheral arterial disease. Sharp debridement and

    management of underlying infection and ischemia are also critical in the care of foot ulcers.

    Prompt and aggressive treatment of diabetic foot ulcers can often prevent exacerbation of the

    problem and eliminate the potential for amputation. The aim of therapy should be early

    intervention to allow prompt healing of the lesion and prevent recurrence once it is healed.

    Multidisciplinary management programs that focus on prevention, education, regular foot

    examinations, aggressive intervention, and optimal use of therapeutic footwear have

    demonstrated significant reductions in the incidence of lower-extremity amputations.

    Examples of foot lesions. A, Necrobiosis lipoidica diabeticorum. B, Toe ulceration. C, Plantar ulcer beneath the head of the metatarsal

    bones. D, Combined ischemic and neuropathic ulceration; note dry blackish skin and dry gangrene of the little toe.

    Gangrene

    Diabetic gangrene is commonly seen in diabetic patients as a complication. Gangrene is

    a condition that involves the death and decay of tissue, usually in the extremities. There are

    three different types of gangrene: dry, wet or gas gangrene. Dry gangrene is the one that most

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    often affects people with diabetes. Reduced blood flow or lack of circulation resulting from

    diabetes, cardiovascular problems, and smoking are the most common causes. Bacterial

    infections can also lead to gangrene.

    Toes, feet, lower limbs and sometimes fingers can all become vulnerable to the

    conditions that may cause gangrene. Symptoms include numbness in the affected part and it

    will also be cold to the touch.

    Dry gangrene

    At first, the area will become reddened but it gradually progresses to a brownish color.

    The skin may appear waxy. In the final stage, the affected body part will look withered and

    black in color. Gangrene is treatable if the symptoms are recognized early, before the death of

    tissue occurs. After tissue dies, removal of the dead tissue or amputation is the usualtreatment

    Charcot foot

    A Charcot foot is one characterized by destroyed bones and sometimes fractures and

    dislocations in the foot or ankle (Figure 3). Oftentimes, the arch of the foot collapses and

    there is a prominent bone felt on the bottom of the foot in the arch. This often leads to an

    ulcer on the bottom of the foot. Sometimes the bone will be infected if there is an ulcer that

    leads to it. Charcot foot is a condition that is commonly misdiagnosed as bone infection and

    may be unnecessarily amputated. It is important to have an expert in Charcot foot review the

    case prior to consenting to amputation because in the right hands, many cases are

    salvageable.

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    An X-ray f a Charcot foot that is dislocated

    A. CLASSIFICATIONThe Wagner and University of Texas systems are the ones most frequently used for

    classification of foot ulcers, and the stage is indicative of prognosis.

    B. ETIOLOGYThe etiology of diabetic foot ulcers usually has many components. A recent

    multicenter studyattributed 63 percent of diabetic foot ulcers to the critical triad of peripheral

    sensory neuropathy, trauma, and deformity. Other factors in ulceration are ischemia, callus

    formation, and edema. Although infection is rarely implicated in the etiology of diabetic foot

    ulcers, the ulcers are susceptible to infection once the wound is present. Many of the risk

    factors for foot ulcer are also predisposing factors for amputation, because ulcers are primary

    causes leading to amputation.

    The etiologies of diabetic ulceration include neuropathy,arterial disease,

    ]pressure,

    and

    foot deformity. Diabetic peripheral neuropathy, present in 60% of diabetic persons and 80%

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    of diabetic persons with foot ulcers, confers the greatest risk of foot ulceration; microvascular

    disease and suboptimal glycemic control contribute.

    C.PATHOPHYSIOLOGYAtherosclerosis and peripheral neuropathy occur with increased frequency in persons with

    diabetes mellitus (DM).

    Diabetes related atherosclerosisOverall, people with diabetes mellitus (DM) have a higher incidence of

    atherosclerosis, thickening of capillary basement membranes, arteriolar hyalinosis, and

    endothelial proliferation. Calcification and thickening of the arterial media are also noted

    with higher frequency in the diabetic population, although whether these factors have any

    impact on the circulatory status is unclear.

    Significant atherosclerotic disease of the infrapopliteal segments is particularly

    common in the diabetic population. Underlying digital artery disease, when compounded

    by an infected ulcer in close proximity, may result in complete loss of digital collateralsand precipitate gangrene.

    Diabetic peripheral neuropathy

    The pathophysiology of diabetic peripheral neuropathy is multifactorial and is

    thought to result from vascular disease occluding the vasa nervorum; endothelial

    dysfunction; deficiency of myoinositol-altering myelin synthesis and diminishing sodium-

    potassium adenine triphosphatase (ATPase) activity; chronic hyperosmolarity, causing

    edema of nerve trunks; and effects of increased sorbitol and fructose.

    The result of loss of sensation in the foot is repetitive stress; unnoticed injuries and

    fractures; structural foot deformity, such as, metatarsal deformities, or Charcot foot.

    Unnoticed excessive heat or cold, pressure from a poorly fitting shoe, or damage from a

    blunt or sharp object inadvertently left in the shoe may cause blistering and ulceration.

    These factors, combined with poor arterial inflow, confer a high risk of limb loss on the

    patient with diabetes.

    http://emedicine.medscape.com/article/1950759-overviewhttp://emedicine.medscape.com/article/1950759-overview
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    Charcot deformity with mal perforans ulcer of plantar midfoot.

    D. EPIDEMIOLOGYDiabetic foot lesions are responsible for more hospitalizations than any other

    complication of diabetes. Among patients with diabetes, 15% develop a foot ulcer, and 12-

    24% of individuals with a foot ulcer require amputation. In fact, every year approximately

    5% of diabetics develop foot ulcers and 1% require amputation.

    Age DistributionDiabetes occurs in 3-6% of Americans. Of these, 10% have type 1 diabetes and are

    usually diagnosed when they are younger than 40 years. Diabetic neuropathy tends to

    occur about 10 years after the onset of diabetes, and, therefore, diabetic foot deformity and

    ulceration occur sometime thereafter.

    Prevalence by raceThe issue of diabetic foot disease is of particular concern in the Latino communities

    of the Eastern United States, in African Americans, and in Native Americans, who tend to

    have the highest prevalence of diabetes in the world.

    E. DIAGNOSISThe history should focus on symptoms indicative of possible peripheral neuropathy or

    peripheral arterial insufficiency.

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    SymptomsSymptoms of peripheral neuropathy:

    - Hypesthesia- Hyperesthesia- Paresthesia- Dysesthesia- Radicular pain- Anhydrosis

    Symptoms of peripheral arterial insufficiency

    Most people harboring atherosclerotic disease of the lower extremities are

    asymptomatic; others develop ischemic symptoms. Some patients attribute ambulatory

    difficulties to old age and are unaware of the existence of a potentially correctible

    problem.

    Patients who are symptomatic may present with intermittent claudication,

    ischemic pain at rest, nonhealing ulceration of the foot, or frank ischemia of the foot.

    Cramping or fatigue of major muscle groups in one or both lower extremities that

    is reproducible upon walking a specific distance suggests intermittent claudication. This

    symptom increases with ambulation until walking is no longer possible, and it is

    relieved by resting for several minutes. The onset of claudication may occur sooner

    with more rapid walking or walking uphill or up stairs.

    The claudication of infrainguinal occlusive disease typically involves the calf

    muscles. Discomfort, cramping, or weakness in the calves or feet is particularly

    common in the diabetic population because they tend to have tibioperoneal

    atherosclerotic occlusions. Rest pain is less common in the diabetic population.

    Physical Examination

    Physical examinationPhysical examination of the extremity having a diabetic ulcer can be divided into 3

    broad categories:

    - Examination of the ulcer and the general condition of the extremity- Assessment of the possibility of vascular insufficiency

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    - Assessment for the possibility of peripheral neuropathy

    Examination of extremity

    Diabetic ulcers tend to occur in the following areas:

    -Areas most subjected to weight bearing, such as the heel, plantar metatarsal headareas, the tips of the most prominent toes, and the tips of hammer.

    -Areas most subjected to stress, such as the dorsal portion of hammer toes

    Other physical findings include the following:

    -Hypertrophic calluses-Brittle nails-Hammer toes-Fissures

    Assessment of posible peripheral arterial insufficiency

    Physical examination discloses absent or diminished peripheral pulses below a

    certain level.

    Specifically, loss of the femoral pulse just below the inguinal ligament occurs

    with a proximal superficial femoral artery occlusion. Loss of the popliteal artery pulse

    suggests superficial femoral artery occlusion, typically in the adductor canal.Loss of

    pedal pulses is characteristic of disease of the distal popliteal artery or its trifurcation.

    Other findings suggestive of atherosclerotic disease include a bruit heard

    overlying the iliac or femoral arteries, skin atrophy, loss of pedal hair growth, cyanosis

    of the toes, ulceration or ischemic necrosis.

    Assesment of posible periphral neuropathy

    Signs of peripheral neuropathy include loss of vibratory and position sense, loss

    of deep tendon reflexes (especially loss of the ankle jerk), trophic ulceration, foot drop,

    muscle atrophy, and excessive callous formation, especially overlying pressure points

    such as the heel.

    The nylon monofilament test helps diagnose the presence of sensory neuropathy.

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    F.DIFFERENTIAL DIAGNOSIS- Atherosclerosis- Chronic Venous Insufficiency- Diabetic Foot Infections

    G.WORKUPPatient workup for diabetic ulcers includes blood tests, ankle-brachial index,

    radiography, computed tomography, magnetic resonance imaging, and angiography.

    Blood TestsA complete blood count should be done. Leukocytosis may signal plantar abscess

    or other associated infection. Wound healing is impaired by anemia. In the face of

    underlying arterial insufficiency, anemia may precipitate rest pain.

    Assessment of serum glucose, glycohemoglobin, and creatinine levels helps to

    determine the adequacy of acute and chronic glycemic control and the status of renal

    function.

    Plain RadiographyPlain radiographic studies of the diabetic foot may demonstrate demineralization and

    Charcot joint and occasionally may suggest the presence of osteomyelitis.

    http://emedicine.medscape.com/article/461449-overviewhttp://emedicine.medscape.com/article/461449-overviewhttp://emedicine.medscape.com/article/237378-overviewhttp://emedicine.medscape.com/article/237378-overviewhttp://emedicine.medscape.com/article/237378-overviewhttp://emedicine.medscape.com/article/461449-overview
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    Computed Tomography and Magnetic Resonance ImagingComputed tomography (CT) scanning or magnetic resonance imaging (MRI) is indicated

    if a plantar abscess is suspected but not clear on physical examination.

    Conventional AngiographyIf vascular or endovascular surgical treatment is contemplated, angiography is needed to

    delineate the extent and significance of atherosclerotic disease.

    H. MANAGEMENTThe management of diabetic foot ulcers requires offloading the wound by using

    appropriate therapeutic footwear,daily saline or similar dressings to provide a moist wound

    environment, debridement when necessary, antibiotic therapy if osteomyelitis or cellulitis is

    present,optimal control of blood glucose, and evaluation and correction of peripheral arterial

    insufficiency.

    Wound and Foot CareThe basic principle of topical wound management is to provide a moist, but not wet,

    wound bed.

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    Wound coverage

    After debridement, apply a moist sodium chloride dressing or isotonic sodium

    chloride gel or a hydroactive paste. Optimal wound coverage requires wet-to-damp

    dressings, which support autolytic debridement, absorb exudate, and protect surrounding

    healthy skin. A polyvinyl film dressing that is semipermeable to oxygen and moisture and

    impermeable to bacteria is a good choice for wounds that are neither very dry nor highly

    exudative. Wound coverage recommendations for some other wound conditions are as

    follows:

    - Dry wounds: Hydrocolloid dressings- Exudative wounds: Absorptive dressings, such as calcium alginates- Very exudative wounds: Impregnated gauze dressings or hydrofiber dressings- Infected wounds: For infected superficial wounds, use Silvadene- Wounds covered by dry eschar: Simply protecting the wound until the eschar dries and

    separates may be the best management. Painting the eschar with povidone iodine is

    beneficial.

    - Fragile periwound skin: Hydrogel sheets and nonadhesive forms.

    Other topical preparations that occasionally may be useful in the management of

    diabetic foot ulcers are as follows:

    - Platelet-derived growth factors (PDGF): Topical recombinant human PDGF has abeneficial effect in promoting wound healing.

    - Collagen debridement

    Treatment of Charcot foot

    Charcot foot is treated initially with immobilization using special shoes or braces but

    eventually may require podiatric surgery such as ostectomy and arthrodesis.

    Surgical care

    Surgeon will consider debridement, revisional surgery on bony architecture, vascular

    reconstruction, and options for soft tissue coverage

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    DebridementSurgical management is indicated for debridement of nonviable and infected

    tissue from the ulceration, removal of excess callus, curettage of underlying

    osteomyelitic bone, skin grafting, and revascularization. The wound usually requires an

    initial surgical debridement and probing to determine the depth and involvement of

    bone or joint structures. Visible or palpable bone implies an 85% chance of

    osteomyelitis.

    Revisional surgerySuch intervention includes resection of metatarsal heads or ostectomy may be

    required to remove pressure points.

    Vascular reconstructionIndications for vascular surgery of a reconstructible arterial lesion include continous

    pain at rest or at night, foot ulcers that difficult to heal, and impending or existing

    gangrene.

    I. PREVENTION Daily foot inspection Gentle soap and water cleansing Application of skin moisturizer Inspection of the shoes to ensure good support, fit, and comfort. Minor wounds require prompt medical evaluation and treatment. Prophylactic podiatric surgery to correct high-risk foot deformities may be indicated. Avoid hot soaks, heating pads, and irritating topical agents.

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    Rooh-Ul-Muqim, Samson Griffin, Mukhtar Ahmed. Evaluation and Managementof Diabetic Foot According to Wagners Classification a Study of 100 Cases. On

    http://www.ayubmed.edu.pk/JAMC/PAST/15-3/rooh.htm

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