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Transcript of InfectionsDM 1999
8/13/2019 InfectionsDM 1999
http://slidepdf.com/reader/full/infectionsdm-1999 1/33
Diploma in Medicine
Endocrinology Unit
Dr. Kimberly Oman
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“Poorly characterized defects in hostimmunity ... make them more susceptible tocertain types of infections including bacterial
infections of the skin and soft tissue” (CID1997;25:1318) Impaired wound healing in diabetics (ibid) Decreased cell mediated immunity (Mandell
1990 p. 129) Decreased neutrophil chemotaxis and
phagocytosis (Mandell p. 145)
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Mild diabetic decompensation
Does not seem to be deleterious to the phagocyticsystem
Severe diabetic decompensation
Poor chemotaxis, ingestion and killing by PMNs (?Partly due to hyperosmolar state)
Staphylococcus aureus in diabetes mellitus (Mandell - 1990 p.1496)
Increased nasopharyngeal colonization of diabetic
patients on insulin ? Increased frequency of infection More likely to be severe and protracted
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Crepitant soft tissue wounds (p. 809): non-
clostridial anaerobic cellulitis, necrotizingfasciitis, synergistic necrotizing cellulitis (“Gas gangrene”) Fornier’s gangrene (necrotizing fasciitis of the
male genitals) - “if the abdominal wall
becomes involved in an obese patient withdiabetes, the process can spread like wildfire”(p. 810)
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Candida vaginitis (p. 1946) Chronic or persistent bacterial pneumonia (p.
566) Infectious arthritis (p. 912) Rhinocerebral mucormycosis (DM esp.
acidosis, leukemia, renal transplant) : facial
pain, headache, involvement of orbit & brain-treat with radicaldebridement (p.1964) ? Cryptococcosis (fungal meningitis,
pneumonia) p. 1982
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Clinical presentation Unwell Minimal or no localizing signs Often confused +/- fever Often high white count
Respond to cloxacillin and gentamicin May do poorly if antibiotics withheld
Not uncommon in Fiji but not described in theliterature
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Ischemia
Arterial insufficiency in 60% with non-healing
ulcers and 46% with major amputations Infection
Superficial fungal infections leading to
maceration or broken skin
Increased nasal and skin colonization with
Staphylococcus aureus
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Peripheral neuropathy present in over 80% ofdiabetics with foot lesions
Sensory neuropathy Unperceived injury
Motor neuropathy: Gait disturbances, foot deformities (such as claw
toe) Autonomic neuropathy Interference with sweating can lead to dry,
cracked skin
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Good glycemic control No smoking
Early detection of loss of protective sensation Vibration
Monofilament testing
Regular foot inspection by clinicians Education in foot care and proper footwear
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Wash and dry your feet thoroughly every day,
especially between the toes Inspect your feet daily for blister, skin breaks
and infection Apply cream to the skin Cut your toenails carefully Wear well-fitting shoes that don’t rub or hurt
your feet or cause blisters Don’t go barefoot
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Seek medical care if you have an infection or
skin breakdown on your feet. Tell patients that preventing foot problems
and treating foot problems early can preventamputations
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Most common Unperceived, excessive and repetitive pressure on
plantar bony prominences such as metatarsalheads
Others Foot deformities (elevated focal pressure) Small foreign bodies in footwear Pressure necrosis from poorly fitting footwear Puncture wounds Pacific Islands: going barefoot
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History
Prior ulceration Prior surgery involving the metatarsal bones
Physical findings
Callus or hemorrhagic callus Blister or macerated skin Limited hallux dorsiflexion (<30 degrees)
Prominent metatarsal heads inadequately coveredwith soft tissue Other plantar bony prominences
Radiographic findings: Charcot’s fracture
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No apparent infection
(No signs of inflammation or drainage or evidenceof osteomyelitis on plain xray)
Mild infection Superficial, < 2 cm of cellulitis
No serious ischemia
No bone or joint involvement
Patient reliable, good home support
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Limb-threatening infections Full-thickness ulcer
>2 cm of cellulitis with or without lymphangitis
Bone or joint involvement
Systemic toxicity
Serious ischemia
Patient unreliable or poor home support Major problem: determining if osteomyelitis
is present
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Often difficult / problematic
Early osteomyelitis Similar to soft tissue infection
No changes on radiographs
Hard to distinguish on xray from diabeticosteopathy (Charcot’s changes)
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History: Ulcer present for more than one week Previous osteomyelitis
History of other foot complications secondary toperipheral neuropathy
Physical exam: Many are not febrile Increased risk if ulcer over bony prominence
Larger or deeper ulcer Bone visible or can be touched with a sterile blunt
probe
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Laboratory tests ESR
▪ >70 mm/hr: 100% have osteomyelitis
▪ >40 mm/hr: 12x risk of osteomyelitis WBC, other tests not helpful
Radiography Findings: focal osteopenia; lucencies in cortex or
medullary bone bony abnormalities not present on plain films for 10-20
days Overseas: bone scans / gallium scans / indium labeled
leukocytes / MRI
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Bone culture Sensitivity 95% / Specificity 99% Surgical approach OR Percutaneous through uninfected tissue
Laboratory studies Gram stain and culture Histopathology
Not always done due to expense Some skip if osteomyelitis highly likely Consider for suspected unusual organisms
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Similar for soft tissue infection and osteomyelitis Soft tissue cultures often grow different organisms
from bone cultures in the same patient Most infections are polymicrobial
Average: 2.2 pathogens in osteomyelitis, twice that in
soft tissue infections Staphylococcus aureus most common
Other gram +: Streptococcus spp., Enterococcus spp.
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Gram negative bacilli
Enterobacteriaceae; Pseudomonas (puncturewound especially with rubber-soled shoes; soaking
feet) Anaerobes
Relatively frequent in serious soft tissue infections Less common in osteomyelitis
More frequent in long-standing infections,infections not eradicated by previous antibiotics ornecrotic tissue / foul odor
? Role of Staph epi and Corynebacterium spp.
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Guided by soft tissue or bone cultures Some treat all organisms cultured, others do
not Less serious: anti-Staphylococcal cover is
often sufficient More serious: Staphylococcal, gram negative
and anaerobe cover
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Traditional: 4 - 6 weeks IV antibiotics
Basis: animal models and anecdotes No reliable data on:
Duration of antibiotic therapy When to switch to oral agents
Approach (CID 1997;25:1310)
Consider bone biopsy for culture and histopathology
Remove entire section of infected bone plus 2 weeks ofantibiotics
OR 4-6 weeks of culture-guided antibiotic therapywithout bony resection
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Approach (NEJM 1994;13:854) Traditional 4 - 6 week IV therapy OR Remove entire section of infected bone plus 2 - 3
weeks of antibiotics - at least one week IV (longer fortarsal or calcaneal bone which must be removedpiecemeal)
Also mentioned (CID and NEJM) 10 - 12 weeks antibiotics without surgical debridement Chronic suppression without cure can be a valid
approach
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Probe to bone? - Osteomyelitis Suggestive xray? - Osteomyelitis
Unclear? (Too early for xray changes?) Treat as for soft tissue infection (culture-directed)
for 2 weeks
Repeat xray in 2 weeks to look for osteomyelitis
Soft tissue infections: beware gas gangreneand necrotizing soft tissue infections
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Mild to moderate infections (not defined) Metronidazole 400mg po 8/24 PLUS
Flucloxacillin 500mg po 6/24 Severe infections
metronidazole 400mg po 8/24 PLUS cloxacillin 1-2g IV 6/24 PLUS
Gentamicin 80mg IV 8/24 (adjust as needed) Alternative
metronidazole 400mg po 8/24 PLUS cephalothin 1-2 gm IV 4/24
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Change to oral therapy when infection isunder control
Duration of treatment depends on response Adjust therapy based on culture results
Surgical debridement is often necessary Surgical advice should be sought (often not
necessary in mild cases) Proper dressings and wound care very
important
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Clindamycin (old antibiotic) po/IV
Staphylococcus aureus, other gram positives,
anaerobes, excellent in necrotizing Streptococcalor anaerobic infections
Fluoroquinolones (Ciprofloxacin)
Staphylococcus aureus & gram negatives
Not anaerobes
Newer quinolones cover other gram positives (but
not Ciprofloxacin)
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B-lactam / B-lactamase combinations po/IV: gramnegative, S. aureus, anaerobes
Amoxicillin - clavulanate - po Ampicillin - sulbactam - IV Ticarcillin - clavulanate - IV Piperacillin - tazobactam - IV
Cefoxitin or cefotetan (2nd generation cephalosporins) -
IV S. aureus, anaerobes, gram “-” with holes
Carbapenems (imipenem / meropenem) - IV
gram negative, S. aureus, anaerobes
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Debridement of infected tissue (“diabetics donot tolerate undrained suppuration”)
Remove infected bone if possible (ie. digitalor ray amputation) When to amputate? Revascularization procedures if needed
(overseas)
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2-year mortality rate:
35-50%
1-3 year cumulative amputation rate:
40%
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High morbidity and mortality Often hard to distinguish soft tissue infection
from osteomyelitis Little data on optimal duration of treatment Little data on IV vs. oral antibiotics
Many valid approaches Therefore best treatment is still uncertain
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Caputo GM, Cavanagh PR, Ulbrecht JS,Gibbons GW, Karchmer AW. Assessment andmanagement of foot disease in patients withdiabetes. N Engl J Med 1994;331:854-60.
Lipsky BA. Osteomyelitis of the foot indiabetic patients. Clin Infect Dis1997;25:1318-26.
MandellGL, Douglas RG, Bennett JE eds.Principles of Infectious Diseases 3rd Edition.Churchill Livingstone: New York; 1990.