diabetic foot infections & osteomyelitis - cb

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Foot pain case Christopher Betts

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Page 1: Diabetic Foot Infections & Osteomyelitis - cb

Foot pain case

Christopher Betts

Page 2: Diabetic Foot Infections & Osteomyelitis - cb

HPI

• 44 yo CM with h/o uncontrolled DM and diabetic neuropathy presents with 1 month of progressive bilateral foot ulcers. Patient stated that initially it started as dry peeling skin under both feet but he began habitually picking at it until they became open wounds.

• Patient does not recall stepping on sharp objects in home or walking outdoors barefoot. Denies any recall of recent bug bites. Pain and swelling associated with the ulcerations in feet which are localized over the soles of both feet with radiation up to level of midshins.

Page 3: Diabetic Foot Infections & Osteomyelitis - cb

HPI

• Patient went to GHS ER at the end of the second week of symptoms and he was discharged with 10 days of Bactrim DS and Keflex. The ulcers continued to progress with no real improvement and the patient returned after the 10 days of abx to the GHS ER, there he was re-prescribed 10 additional days of Bactrim DS and Keflex.

Page 4: Diabetic Foot Infections & Osteomyelitis - cb

Rx:

• Ativan 1 mg bid prn• Lisinopril 5 mg po qd• Metoprolol 50mg po bid• ASA 81mg po qd• Nitroglycerin 0.4mg

q5min prn CP• Novolog 70/30 mix, 40U

in am and 35U in pm, bid

• Neurontin 600mg po tid• Norco 325-7.5 mg po

q6h prn • Keflex 500mg po tid x

10 days• Bactrim DS 800mg-

160mg po bid x 10 days

Page 5: Diabetic Foot Infections & Osteomyelitis - cb

PMHx, PSHx, FMHx, SHx

• PMHx: severe CAD s/p multiple stents, uncontrolled DM, diabetic neuropathy, HTN, +MRSA, Anxiety, Depression, HLD, OCD

• PSHx: R cubital tunnel syndrome, I&D of R nares and facial abscess, Appendectomy

• FMHx: CAD, DM II, father passed away of heart disease.

• SHx: No alcohol or drug use. Positive tobacco use for years; currently 18-20 cigarettes per day.

Page 6: Diabetic Foot Infections & Osteomyelitis - cb

ROS

• (+) for ulcers over soles b/l, taut skin changes, leg edema, claudication, UE and LE paresthesia/ numbness/ tingling/ and burning sensation, poor erection ability

• (-) for fevers, chills, night sweats, appetite changes, N/V, abd pain, myalgia, dyspnea, cough or sputum

Page 7: Diabetic Foot Infections & Osteomyelitis - cb

PE

• General: in NAD, malodorous of tobacco smoke

• Heart: S1, S2 present; RRR w/o m/r/g• Lungs: CTAB• Abd: soft, non-tender

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PE• Neuro: poor pin-prick and light touch from ankles, to feet, to

soles and toes. Poor position sense over toes. Gait w/ limp d/t pain in feet.

• Skin: severely dry skin over feet, major scaling and ulceration of skin over soles to feet; global swelling w/ blanching erythema

• Extremities: non-pitting edema from the level of middle shin to feet b/l, +1 pulses over dorsalis pedis and post tib.

• Feet: multiple ulcers over sole of feet w/ surrounding scaling. Two large ulcers over first MTP joint of each foot; both of these w/ exposed subcutaneous tissue. No drainage or bleeding. Calluses present w/maceration and cracking

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Diagnostic tests

• HgbA1c = 12.1%• Other tests??

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A/P

• Diabetic Foot Infection– Increase Novolog 70/30 mix to 45U in am and 40U in

pm– Started Metformin 500mg po bid – Discontinued Bactrim DS and Keflex– Started Doxycycline 100mg PO bid x 7 days– Advised patient to soaking feet in very warm water

daily and gently wipe off sores after soaking. – 1 week follow up (further d/w smoking cessation and

Rx for orthotics).

Page 11: Diabetic Foot Infections & Osteomyelitis - cb

Diabetic Foot Infections

• Infections that involve the soft tissue or bone below the malleoli.

• Most occur in a site of skin trauma or ulceration.

• Estimated lifetime risk of a diabetic developing a foot ulcer is 15% to 25%.

• Predisposing risk factors: peripheral neuropathy, PAD, and impaired immunity.

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Diabetic Foot Infections

• More than one-half of non-traumatic lower extremity amputations are related to diabetic foot infections and 85% of all LE amputations in diabetics are preceded by an ulcer.

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Pathogenesis

• Hyperglycemia, sensory and autonomic neuropathy, and peripheral arterial disease all contribute to the pathogenesis of LE infections in diabetics.

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Pathogens

• Most common pathogens involved are Aerobic Gm(+) cocci (i.e. Staph species)

• MRSA is present in 10-32% of diabetic infections and a/w higher rates of treatment failure in patients with diabetic foot infection.

• Moderate to severe infections and wounds that were previously treated are often polymicrobial including Gm(-) bacilli.

• Anaerobic pathogens are commonly present in necrotic wounds and infections of the ischemic foot.

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Diagnosis

• It is a clinical diagnosis based on two classic findings of inflammation and purulence.

• Evaluation should involve a thorough assessment of the wound, the limb, and the patient's overall health.

• Local signs of an infection include redness, warmth, induration or swelling, pain or tenderness, and purulent secretions.

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Diagnosis

• Neuropathy can be detected with a simple neurologic exam of the LE involving the use of a 10-g monofilament, to test sensation, or a composite score such as a modified neurodisability score.

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Neuropathy Disability Score in Patients with Diabetes.

Boulton AJ et al. N Engl J Med 2004;351:48-55.

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Diagnosis

• Callus formation and a plantar site of ulceration also suggest neuropathy as a major contributory cause. A combination of lack of sensation, limited joint mobility, autonomic dysfunction rseulting in dry skin and repetitive high pressure may lead to callus formation.

• The relative risk of ulcer development at an area of high pressure (i.e. the metatarsal heads, as compared with the mid-foot) is 4.7, and that of an ulcer developing at a site of callus is 11.0.

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Diagnosis

• Failure of a wound to heal in spite of proper treatment, and the presence of non-purulent discharge, malodor, and necrotic or friable tissue also suggest infection.

• Cultures of superficial swabs are discouraged because these often yield contaminants.

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Classification

• IDSA and International Working Group on the Diabetic Foot classify diabetic wounds as uninfected or infected, with mild, moderate, and severe grades of infection.

• This classification was found to reliably predict the need for hospitalization and limb amputation.

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Classification

• No systemic or local signs or infection = 1 (uninfected)

• Local signs of infection involving only the skin or subcutaneous tissue; any erythema >0.5cm but <2cm around wound = 2 (mild infection)

• As above but erythema >2cm, or involving deeper structures = 3 (moderate infection)

• Any of the above PLUS signs of SIRS = 4 (severe infection)

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Classification

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ULCER TYPE GENERAL CHARACTERISTICS PATHOPHYSIOLOGY CLINICAL FEATURES TREATMENT OPTIONSVenous Most common type;

women affected more than men; often occurs in older persons

Venous hypertension Shallow, painful ulcer located over bony prominences, particularly the gaiter area (over medial malleolus); granulation tissue and fibrin present

Leg elevation, compression therapy, aspirin, pentoxifylline (Trental), surgical management

Associated findings include edema, venous dermatitis, varicosities, and lipodermatosclerosis

Arterial Associated with cardiac or cerebrovascular disease; patients may present with claudication, impotence, pain in distal foot; concomitant with venous disease in up to 25 percent of cases

Tissue ischemia Ulcers are commonly deep, located over bony prominences, round or punched out with sharply demarcated borders; yellow base or necrosis; exposure of tendons. Associated findings include abnormal pedal pulses, cool limbs, femoral bruit and prolonged venous filling time

Revascularization, antiplatelet medications, management of risk factors

Neuropathic Most common cause of foot ulcers, usually from diabetes mellitus

Trauma, prolonged pressure

Usually occurs on plantar aspect of feet in patients with diabetes, neurologic disorders, or Hansen disease

Off-loading of pressure, topical growth factors; tissue-engineered skin

Pressure Usually occurs in patients with limited mobility

Tissue ischemia and necrosis secondary to prolonged pressure

Located over bony prominences; risk factors include excessive moisture and altered mental status

Off-loading of pressure; reduction of excessive moisture, sheer, and friction; adequate nutrition

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Diabetic Foot Osteomyelitis

• Definitive diagnostic method: bone Bx w/ histopathology c/w bond infection or positive Cx

• Most accurate diagnostic imaging study: MRI• Test w/ high sensitivity and specificity in

outpatient: Probe-to-Bone test• The ability to obtain bone biopsy with

histopathology is not widely available to physicians, thus they must rely on a combination of clinical, radiographic, and laboratory findings.

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Diabetic Foot Osteomyelitis

• Infection of bone is a serious complication in a diabetic foot infection.

• Increased risk of treatment failure and LE amputation.

• Present in up to 20% of mild and moderate diabetic ulcer infections.

• Present in up to 50-60% of severe diabetic ulcer infections.

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Diagnosis

• A diabetic foot osteomyelitis should be suspected if the foot ulcer...– Is large (>2cm) or deep (>3mm)– Overlays a bony prominence– Is chronic and refractory to wound care– With a visible bone or palpable bone with probing.

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Diagnostic Imaging

• Plain radiography has limited sensitivity for diabetic foot osteomyelitis especially in the early stages of the condition. This is because it takes weeks for bone infection to become radiographically present. Depending on the timing of plain radiography and the severity of infection when the radiograph is done, sensitivity ranges from 28% to 75%.

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Diagnostic Imaging

• Triple phase technetium-99m methylene diphosphonate bone scan is more sensitive than plain radiography, with a sensitivity of about 90% but it has a much lower specificity (46%).

• MRI is the most accurate imaging study in the diagnosis of osteomyelitis (90% sensitive and 80% specific); it may be of limited value in differentiating osteomyelitis from acute Charcot neuroarthopathy.

Page 29: Diabetic Foot Infections & Osteomyelitis - cb

Probe-to-bone testing

• Probe-to-bone (attempting to reach exposed bone with a metal probe) testing is an inexpensive diagnostic tool used to support the dx of osteomyelitis and should be performed after debridement of devitalized and necrotic tissue.

• A positive result meant touching a hard or gritty bone surface; this increases the likelihood of osteo in patients with high pretest probability. A negative result in a patient with low pretest probability makes osteo unlikely but not excluded from diagnosis.

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Probe-to-Bone study

• A study of outpatients w/ diabetic foot ulcers found probe-to-bone testing to be 87% sensitive and 91% specific for osteo.

• Negative result on probe-to-bone makes osteomyelitis unlikely but does not exclude the dx.

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Laboratory diagnostics• Leukocytosis and elevated erythrocyte sed rate increase the

risk of a diabetic foot infection but their absence does not rule it out.

• In one multicenter study, investigators found that more than one-half of patients admitted with acute diabetic foot infection had a normal leukocyte count, and 83.7% had a normal neutrophil count.

• The absence of leukocytosis, left shift, or elevation of acute phase reactants still does not exclude infection.

• Erythrocyte sedimentation rate and C-reactive protein are helpful biochemical markers to monitor therapeutic response.

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Treatment

• The management of a diabetic foot infection is based on the extent and severity of the infection. There is no single superior antibiotic for all infections and selection is on a case-by-case basis.

• In general, mild infections should be treated with 1-2 weeks of oral abx in the outpatient setting; coverage for aerobic gram positive pathogens

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Treatment

• Selected patients with moderate infections and all patients with severe infections require hospitalization to receive parenteral abx with broad-spectrum coverage, surgical consultation, and additional evaluation.

• In general, duration of abx coverage for moderate to severe soft tissue infection should be for 2-3 weeks.

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Treatment

• Selected patients include those with poor glycemic control or PAD, and patients unable to adhere to a treatment plan which includes abx tx, appropriate wound care, pressure off-loading, and return for close follow up.

• Surgical interventions may include I&D, extensive debridement of necrotic and devitalized tissue, resection, amputation, and revascularization.

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Treatment

• In diabetic foot osteomyelitis, the abx duration is traditionally prolonged, but if the surgical intervention includes removal of the infected bone, the duration may be a shorter course.

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Treatment

• The National Institute for Health and Clinical Excellence guidelines on the inpatient management of diabetic foot problems recommend that each hospital have a care pathway carried out by a multidisciplinary team.

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Treatment

• A recent systematic review of several randomized controlled and cohort studies by the International Working Group on the Diabetic Foot comparing different antibiotic regimens showed there was no one superior regimen, route of administration, or duration of treatment for diabetic foot infections. IDSA also reached the same conclusion.

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Treatment

• Subsequent Abx choices depend on – Extent of infection– Cx results and abx sensitivities– Clinical response to initial therapy. – Local abx resistance patterns– Presence of MDR organisms– Renal and hepatic impairments of the patient– Allergies and immunosuppression– Patient compliance– Cost of treatment

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Role of PAD

• An independent risk factor for diabetic foot infections and the most important predictor of the outcome of diabetic foot ulceration.

• PAD is present in up to 40% of patients with diabetic foot infections.

• Risks of amputation and five-year mortality rate after amputation remain high.

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Role of PAD

• Evaluation of the vascular supply is critical in the treatment of diabetic foot infection. Examination should include color and temperature of the skin, palpation of the peripheral pulses, and signs of arterial insufficiency, including skin and nail atrophy.

• ABI < 0.9 indicates occlusive arterial disease and <0.5 is c/w significant PAD.

• Doppler exam may be warranted. CT angiography and MRA are most useful in patients who are candidates for revascularization.

Page 43: Diabetic Foot Infections & Osteomyelitis - cb

Prevention

• All diabetics should undergo a systematic foot examination at least once a year, and more frequently if risk factors for diabetic foot ulcers exist.

• Appropriate preventive measures include patient education about proper foot care, glycemic and blood pressure control, smoking cessation, use of prescription foot wear, intensive podiatric care, and evaluation for surgical interventions if indicated.

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Key Recommendations for practice• Diagnosis of diabetic foot infection is based on the

presence of at least two classic findings of inflammation or purulence.

• MRI is the most accurate imaging study in early osteomyelitis.

• Surgical debridement and drainage of deep tissue abscesses and infections should be performed in a timely manner.

• All patients with diabetes should undergo a systematic foot examination at least once a year, and more frequently if risk factors for diabetic foot ulcers exist.

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Questions.

• References:– Diabetic Foot Infections, Fassil W. Gemechu – Amer

Fam Phys 2013 Vol. 88, Number 3– Neuropathic Diabetic Foot Ulcers, Boulton, Andrew –

NEJM 2004; 351:48-55– Clinical Manifestations, diagnosis, and management of

diabetic infections of the lower extremities, Weintrob, Amy C – Up To Date, last updated Sep 30 2013

– Diagnosis and Treatment of Venous Ulcers, Collins, Lauren – Amer Fam Phys 2010 Apr 15;81(8):989-996