INFECTIONS AND DIABETES DR.AWADH AL-ANAZI Asst.Professor Consultant, infeciouse diseases Department...
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![Page 1: INFECTIONS AND DIABETES DR.AWADH AL-ANAZI Asst.Professor Consultant, infeciouse diseases Department of medicine King Khaled Hospital College of medicine.](https://reader035.fdocuments.in/reader035/viewer/2022062716/56649de95503460f94ae4b8d/html5/thumbnails/1.jpg)
INFECTIONS AND DIABETES
DR.AWADH AL-ANAZI
Asst.Professor
Consultant, infeciouse diseases
Department of medicine
King Khaled Hospital
College of medicine
King Saud University
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DIABETES & INFECTIONS
• Diabetics subject to same infections as non-diabetics
• Diabetic patients more susceptible to infection
• Infections in Diabetics more severe & difficult to treat
• Certain infections in Diabetics require more Hospitalisation
days than other Diabetic complications
• In U.S.A. > 60% Major Amputations as complication of D.M.
• Thus importance of Diabetic Foot to ALL H.C.W.
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• Few Infectious conditions exceptionally much more prevalent in Diabetics:
* Malignant otitis exterma
* Mucormycosis
• Other infections appear more common in Diabetics:
* Pyelonephritis
* Emphysematous cholangitis
• Infections indirectly due to Diabetic complications
* cystitis & upper U.T.I. In patients with neurogenic
bladder
* various forms of gangrene of cellulitis in patients with
L.L. vascular disease and Diab neuropathy.
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PATHOPHYSIOLOGY
1. Systemic Factors
• Diabetic more susceptible to infection --- not definite
• But once infected, more severe & difficult to treat
* Diabetic immune defenses have functional defects
• Decreased lymphocytes response
• Decreased lymphocytes glucose metabolism
• Defective PMN : Phagocytosis intracellular killing
• Chemotaxis & adherence
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• All diabetic patients with acidosis have defective
phagocytes & cell killing functions.
• Poor glycemic control assoc. with increased infections
incidence in diabetics.
• Other Factors contributing to infection in Diab.
* Blood hypercoagulability
* RBC & Plts. Changes
* connective tissue changes due to glycosylation
of glycogen.
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2. ISCHEMIA
• Most Diab. Patients elderly, obese, with long Hx DM-2.
•Smoking more in diabetics with diabetic foot.
•Vascular Dis: HTN, Hyperlipidemia, CAD, CVA, more
severe in patients with D.F.
3. PERIPHERAL NEUROPATHY
• Loss of protective pain sensations
• Repeated injuries to insensitive limb
• 80% D.F. patients have peripheral neuropathy
• Charcot’s joints & diabetic osteopathy
• Neuropathic ulcerations
• Other sources: superficial fungal infections, improper nail trimming
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MICROBIOLOGY
1. Mild non-limb-threatening infection
* 50% monomicrobial
* S.aureus more than 50%
* aerobic streptoccoi
* GNB
* anaerobes
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2. Severe-Limb-Threatening infections
* usually polymicrobial
* some studies quoted 5 species per pts.
* Asoc. With advanced vascular disease
* Deep tissue culture, avoiding surface
contamination, usu, Yield mixed aerobe and
anaerobe cultures
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Limb-threatening Infection: Aerobes:
a) S.Aureus & CNS:
• Most common aerobic isolates.
• Found in two third of patients with single organism isolated.
b)Streptococci and enterococci : 20 %
• CNS, enterococci, corynebacterium:
• These may be contaminant unless
* isolated in pure cultures
* OR pts. Not responding to Abx Not directed to them
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c) Enterobacteriaceae : 24 – 27%
* proteus, Enterobacter
* E.Coli, pseudomonas
* klebsiella, Acinetobacter
* Morganella morganii
GNB
•Anaerobes:
• 40 – 80% pts. With severe or advanced disease
• USU Yielding 4 organism or more on culture
•Growth density higher than aerobes
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CLINICAL MANIFESTATIONS:
1) Non-Limb-threatening Infections:
* Superficial infection
* Lack systemic toxicity
* Minimal cellulitis (< 2 cm. Extension from portal of
entry)
* Ulcer-if present-doesnot penetrate fully thru skin
* No bone or joint involvement
* No underlying ischemia
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2) Limb-threatening infections:
* Extensive cellulitis (> 2 cm.)
* Lymphangitis
* Full-thickness ulcers
* Frequent bone & joint infections
* Ischemia + gangrene
* Fever +
* Deep plantar abscesses
* Bacteremia + hematogenous spreading infections
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3) Local Signs
a) Infection
• Prognosis affected by anatomic location + proximal infection
• Along metatarsals Lower limb salvage
• At heel higher mortality.
• Above knee
• Most Lower Limb infections begin as perforating ulcer
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Infection signaled by:
* wormth
* redness
* swelling & purulent exudate
* Tenderness minimal (?)
Gas in soft tissues:
* by crepitus or X rays
* USU mixed infections – GNB & anaerobes
* foul odour (tissue necrosis & anaerobic infect)
* gangrene + (Infection or Ischemia)
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•Look for osteomyelitis & deep tissue destruction
•Unroof all encrusted areas, so that :-
* wound can be inspected carefully
* you can assess extent of :
- Deep tissue involvement
- Bone & joint involvement
•Importance of obtaining Deep tissue culture / bone
•22% osteomyelitis diagnosed clinically
•68% silent osteomyelitis by bone Bx & culture
(JAMA : 266: 1246, 1991)
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b) Vascular disease
* Intermittent claudication
* pulse – bruit
* shiny skin, reduced hair, nail growth
* collapsed veins
* use of doppler study
c) Neuropathy
* loss of protective pain sensation
* L.L. & forefoot more affected
* Assess pain, Temp., touch, propioception & DTR
* Nylon monofilament test
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4) Systemic S/Sx
•USU late & indicate severe infection
•Uncontrolled hyperglycemia – only reliable Sx.
•Fever in case of pus containment
•36% of patients with limb-threatening sepsis have temp. more than 37.8.c on Adm. Day.
(infec. Dis. Clin.North Am. 9 : 143.1995)
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DIAGNOSIS:
1) Leukocytosis
• Minimal / absent even with severe infection
• 53% of patients with limb threatening infection have WBC more than 10,000 / mm3
(Inf. Dis. N. Am (: 143,1995)
2) ESR
3) Blood culture
• Positive 10-15% but should be done in All patients
• Higher yields in febrile patients
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4) Wound or tissue cultures
• Obtain deep tissue cultures
• Avoid contact with surface ulcer and draining lession
• Thus growing contaminant organisms avoided
** Ulcer swab 62% as correlated with
** Needle aspirate 69% result of deep tissue
** Ulcer base curretage 75% obtained at amputation
(Rev. Infect Dis 6 *Suupl 1) S171, 1984)
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5) Obtain both aerobic & anaerobi culture before ABX
a) Debridement : Cult deep tissue including bone
: Asp & Bx unexposed bone not advised
b) Direct ulcer culture
• Clean ulcer carefully with betadine
• Allow to dry
• Remove with alcohol
• Remove overlying eschar
• Insert swab through ulcer opening to obtain deep culture
• Place in anaerobic transport needia,send quickly to lab.
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c) Indirect culture of ulcer base
• Clean skin adjacent to ulcer with betadine
• Insert needle thru intact skin, aiming at ulcer base
• Aspirate material from ulcer base
• You may inject sterile saline then aspirate and culture
d) Aspirate bullae or fluctuant collections
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6) Gram stain
• Usu. Not helpful (revealing mixed flora)
• However finding GP rods despite lacking inflam. response may indicate clostridial infection
• This may rapidly progressive
7) Radiographs – osteomyelitis vs Diab. osteopathy
• Sinugram
• Indium labelled leulocytes – most sensitive for ocult osteomyelitis
• CT Scan and MRI
• Probing base of ulcer to detect bone
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MANAGEMENT
Integrated multidisciplinary approach, involving
internists/ diabetologist
surgeons / orthopedics / constructive
Podiatrician, ID Physicians
Early surgical and infectious disease consultation
Essential
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MEDICAL TREATMENT
Antibiotics: Mainstay, recommended in presence of:
• Surrounding cellulitis When Abx choice
• Foul smelling lesion based on adequate
• Fever culture, no single ABx
• Deep tissue infection regimen being superior.
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EMPERIC ABX
• Necessary pending culture results
• Give full doses because poor penetration at infection site
• Avoid nephrotoxic ABX whenever possible
• Pts w/ advanced vascular disease need special attention to assure adequate dose at infection site
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a) Non limb threatening infections
• Direct ABX at commonly offending microorganism (staph. & strep)
• Outpation: clindamycin or cephalexin for 2 wks.
• Pts w/ superficial ulcer w/ cellulitis requiring Hosp Administration and parenteral ABX
-- cefazolin Modify according
-- cefoxitin or Amp salbactam to culture results
-- ticarcillin + BLI, tazocin or others
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b) Severe limb threatening infections
• Offending organism usu. polymicrobial
• Thus broad spectrum ABX use
• In the past: “Triple ABX” Amp + genta + metronidasole / clinda
• Authorities prefer avoiding AMG except when treating resistant pathogens
• ABX options include: Tazocin (piperacillin – tazobactam) ceftriaxone + clinda / Metronidazote.
• Enterococci: when isolated from deep culture, it maybe the offending agent esp. if no response to initial emperic therapy. Thus: choose ABX active against these microbes.
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c) Life threatening infections
• Use broad spectrum ABX, better those active against enterococci till culture result obtained
• Use imipenem or combination regim
• AMG active against GNB, can be used with broad spectrum ABX pending culture results nephrotoxicity minimal w/ short course
• In nosocomial infection remember MRSA, thus vancomycin use till culture reported
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ABX adjustment according to deep culture results
a) Pt responding clinically while ABX used not active against specific isolate from deep culture. What to do?
• Continue same eperic ABX started with
• Isolated pathogen may just be coloniser
• This isolate needs no directed ABX
b) Bacteria isolated resistant to current ABX and pt not responding clinically
• Extend ABX regime to cover isolated pathogens
• In seriously infected pts. Use of broad spectrum ABX that appear unnecessary maybe unavoidable
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Duration of Antibiotic Therapy
• Optimal duration not well established
• Osteomyelitis: 6-12 wks, esp if infected bone not removed
• Infection limited to soft tissue: 10-14 days IV if pt responding well, use p.o. therapy to complete 2 wks
• Non limb threatening
- 2 wks po therapy aimed at acute cellulitis
- continued ulcer care depends on local wound care and further ABX unnecessary
- foot infec. w/ secondary bacteremia usu. Staph or bacteroides spp. (prolonged ABX required.
- prolonged ABX course + I & D may spare amputation, but early surgical intervention usu. Needed to = control sepsis
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Emperic ABX for Diabetic Foot Infection
• Non-limb threatening infection
- Oral Regimen
* cephalexin
* Clindamycin
* Dicloxacillin
* Amoxicillin – Clavulanate (Augmention)
- Parenteral Regimen
* Cefazolin
* Oxacillin or nafcillin
* Clindamycin
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* Life Threatening Infection
• Parenteral Regimen
* Imipenem – Cilastin
* Vancomycin + metronidazole + aztreonam
* Amp salbactam + AMB
* Tazocin + AMG
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PREVENTION
An ounce of prevention is worth a pound of care
Diabetic foot infection better prevented than treated
* regular feet exam neuropathy, vasculopathy
* Pt education
*** smoking, daily self exam of feet, extreme temp, early medical advice, no barefoot, proper
footwear,
wt. Control, foot skin lubrication
* Early intervention, eg. Surgical, revascularization, etc
* Treat superficial infections early (eg. nail infections and paronychia)