Diabetic foot infection: Difference between revisions
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==Diagnosis == | ==Diagnosis == | ||
*Determine presence/extent of infection and likelihood of OM/fasciitis | *Determine presence/extent of infection and likelihood of OM/fasciitis | ||
*Consider Charcot arthropathy (diabetic neuropathic osteoarthropathy) | *Consider Charcot arthropathy (diabetic neuropathic osteoarthropathy) | ||
**commonly missed diagnosis | |||
**requires different management (total contact cast, NWB) | |||
*DM foot ulcer infection presumed if: | *DM foot ulcer infection presumed if: | ||
**2 or more of following: erythema, warmth, tenderness, or swelling | **2 or more of following: erythema, warmth, tenderness, or swelling | ||
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===Imaging === | ===Imaging === | ||
*X-rays to detect soft tissue gas, | *X-rays to detect soft tissue gas, foreign body, OM, or structural foot deformities | ||
**OM x-ray changes occur late in | **OM: x-ray changes occur late in disease, negative xrays do not exclude | ||
*MRI to eval for OM (not usually done in ED) | *MRI to eval for OM (not usually done in ED) | ||
Revision as of 02:03, 13 July 2016
Background
- 1st key factor is to assess extent and depth of ulcer (typically more extensive than they appear)
- Ulcer depth is important predictor of healing rate, osteomyelitis (OM) & risk of amputation.
- Failure of ulcer to heal by 50% or more after 1 month of treatment is a strong predictor that the ulcer is unlikely to heal after 3 mos.
- 75% of patients have polymicrobial infection, usu 70% are gram positive
- Severe limb/life threatening infection are more likely to involve gram negative aerobic & anaerobic bacteria as well.
- MRSA is increasing in frequency
- 50% or more of patients with SEVERE diabetic foot infections will have no systemic signs and symptoms of infection (i.e. fever, tachycardia, leukocytosis, left shift)
- Recurrence of amputation is 50-70% over 3-5 yrs. Overall, 50-80% will heal w/in 6 mos with optimal care.
- DM ulcers usually occur at areas of increased pressure (sole of foot) or friction
- Venous ulcers usually present above malleoli with irregular borders
- Arterial ulcers usually found on the toes or shins, with pale, "punched-out" borders (typically painful)
Clinical Features
HPI
- Ask about recent trauma
- Duration of current lesions
- Associated systemic symptoms
- Prior treatments
Physical Exam
- Determine ulcer location, dimensions, depth, and appearance
- Note hair and nail growth, determine vascular status (palpate DP, PT, and popliteal pulse)
- Probe ulceration site, note involvement of bone, joint, tendon, or sinus tract formation
- Use sterile probe, if hit bone chance of OM 90% higher
Differential Diagnosis
Foot diagnoses
Acute
- Foot and toe fractures
- Subtalar dislocation
- Metatarsophalangeal joint sprain (turf toe)
- Acute arterial ischemia
- Calcaneal bursitis
Subacute/Chronic
- Diabetic foot infection
- Peripheral artery disease
- Plantar fasciitis
- Trench foot
- Ingrown toenail
- Paronychia
- Tinea pedis
- Morton's neuroma
- Diabetic neuropathy
Hyperglycemia
Diabetic Emergencies
- Diabetic ketoacidosis (DKA)
- Diabetic ketoacidosis (peds)
- Hyperosmolar hyperglycemic state (HHS)
- Nonketotic hyperglycemia
- Euglycemic DKA (SGLT-2 inhibitors, pregnancy, fasting)
Diabetes Mellitus (New or Known)
- Type 1 diabetes mellitus (new-onset or uncontrolled)
- Type 2 diabetes mellitus (new-onset or uncontrolled)
- Medication noncompliance or insulin pump malfunction
- Gestational diabetes
- Latent autoimmune diabetes of adults (LADA)
Medication/Drug-Induced
- Corticosteroids (most common drug-induced cause)
- Thiazide diuretics
- Atypical antipsychotics (olanzapine, clozapine, quetiapine)
- Beta-blockers (especially non-selective)
- Phenytoin
- Tacrolimus, cyclosporine (transplant patients)
- Protease inhibitors (HIV antiretrovirals)
- Catecholamines (epinephrine, norepinephrine infusions)
- SGLT-2 inhibitors (paradoxical DKA with euglycemia)
- Total parenteral nutrition (TPN)
- Dextrose-containing IV fluids (iatrogenic)
- Niacin
- Pentamidine (initially hyperglycemia, then hypoglycemia from beta-cell destruction)
Physiologic Stress Response
- Sepsis / critical illness (stress hyperglycemia — very common in the ED)
- Trauma / major surgery / burns
- Acute coronary syndrome / myocardial infarction
- Stroke (especially hemorrhagic)
- Pancreatitis (both a cause and consequence)
- Shock (any etiology)
- Pain (catecholamine surge)
- Seizure (postictal)
- Physiologic stress alone rarely causes glucose >200 mg/dL in non-diabetics; glucose >200 in a "stress response" should prompt evaluation for undiagnosed diabetes or prediabetes
Endocrine
- Cushing syndrome / Cushing disease (cortisol excess)
- Pheochromocytoma (catecholamine excess)
- Hyperthyroidism / thyroid storm
- Acromegaly (growth hormone excess)
- Glucagonoma (rare)
- Somatostatinoma (rare)
Pancreatic
- Pancreatitis (acute or chronic — destruction of islet cells)
- Pancreatic malignancy (adenocarcinoma, neuroendocrine tumors)
- Post-pancreatectomy
- Cystic fibrosis-related diabetes
- Hemochromatosis (iron deposition in pancreas — "bronze diabetes")
Toxic/Overdose
- Iron toxicity (hepatic injury → impaired glucose regulation)
- Salicylate toxicity (can cause both hyper- and hypoglycemia)
- Sympathomimetic toxicity (cocaine, methamphetamine)
- Calcium channel blocker toxicity (impairs insulin secretion)
- Carbon monoxide toxicity (stress response)
Other
- Renal failure (chronic kidney disease, acute kidney injury — impaired insulin clearance AND insulin resistance)
- Cirrhosis / hepatic failure (impaired glycogenolysis regulation)
- Pregnancy (gestational diabetes, steroid administration for fetal lung maturity)
- Parenteral nutrition (TPN, dextrose-containing fluids)
- Post-transplant diabetes (immunosuppressants)
Complications of Diabetes (Not Causes of Hyperglycemia)
These are associated conditions that may be present alongside hyperglycemia but do not themselves cause elevated glucose:
- Diabetic foot infection
- Diabetic peripheral neuropathy
- Cerebral edema in DKA
- Diabetic retinopathy
- Diabetic nephropathy
Diagnosis
- Determine presence/extent of infection and likelihood of OM/fasciitis
- Consider Charcot arthropathy (diabetic neuropathic osteoarthropathy)
- commonly missed diagnosis
- requires different management (total contact cast, NWB)
- DM foot ulcer infection presumed if:
- 2 or more of following: erythema, warmth, tenderness, or swelling
- OR if pus coming from ulcer site or nearby sinus tract
- Severe DM foot infection if:
- Abnormal vital signs
- Rim of erythema surrounding ulcer or ulcer >2 cm in diameter
- Lymphangitic streaking or signs of fasciitis (crepitus, skip lesions, severe TTP, bullae), or if probe reaches bone/joint/tendon
- Obtain ABI on all patients with: nonpalpable DP/PT, claudication sx, ischemic foot pain
- Call vascular if:
- ABI <0.4 (severe obstruction)
- ABI 0.4-0.69 (mod obstruction)
- Call vascular if:
Imaging
- X-rays to detect soft tissue gas, foreign body, OM, or structural foot deformities
- OM: x-ray changes occur late in disease, negative xrays do not exclude
- MRI to eval for OM (not usually done in ED)
Labs
- Chem 10, CBC, Coags, A1c, consider ESR/CRP (useful for monitoring response to Rx)
- ESR >40 incr chance of OM 12 fold, an ESR >70 makes dx nearly certain.
Likelihood of OM
- Factors that increase likelihood of OM:
- Visible bone or probe to bone
- Ulcer >2cm in size
- ESR >70
- Ulcer duration >2 weeks
Management
Noninfected chronic wounds[1]
- Prophylactic antibiotics not indcated
- For clinically uninfected wounds, do not collect a specimen for culture
- Moist dressing to allow for healing and proper footwear to prevent worsening abrasions
Infected Wounds[1]
- Obtain specimens for culture prior tostarting empiric antibiotic therapy. However cultures may be unnecessary for a mild infection in a patients who have not recently received antibiotic therapy.
- Coverage is targeted at MSSA + Strep)
- Strict non-weight bearing, tight glycemic control, meticulous wound care
Severe infection[1]
- Admit with surgical consult
- Empiric therapy directed at Pseudomonas aeruginosa is NOT necessary except for patients with risk factors for true infection with this organism
- MRSA coverage in a patient with a prior history of MRSA infection
Antibiotics
Associated organisms include Staphylococcus, Streptococcus, Enterococcus, Enterobacteriaceae, Proteus, Bacteroides, and Pseudomonas, and Klebsiella
Superficial Mild Infections
- Clindamycin 450mg PO q8hrs daily x 14 days OR
- TMP/SMX 2DS tabs PO q12hrs daily x 14 days OR
- Doxycycline 100mg PO q12hrs daily x 14 days
Prior antibiotic treatment or moderate infections
- Amoxicillin/Clavulanate 875/125mg PO q12hrs + TMP/SMX 2DS tabs PO q12hrs daily x 14 days OR
- Clindamycin 450mg PO q8hrs + Ciprofloxacin 750mg PO q12hrs x 14 days
Inpatient Treatment
- Vancomycin 15-20mg/kg IV q12hrs plus
- Ampicillin/Sulbactam 3g IV q6hrs OR
- Piperacillin/Tazobactam 4.5g IV q8hrs OR
- Ticarcillin/Clavulanate 3.1g IV q8hrs OR
- Imipenem 500mg IV q6hrs OR
- Metronidazole 500mg IV q8hrs PLUS
- Cefepime 2g IV q12hrs OR
- Ciprofloxacin 400mg IV q12hrs OR
- Aztreonam 2g IV q8hrs
