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DIABETIC RELATED INFECTION AND MANAGEMENT
Complications of Diabetes Mellitus
Acute Chronic
1. Diabetic Ketoacidosis
2. Hyperosmolar Nonketotic Coma
3. Hypoglycemia
1. Microangiopathy-Stroke-IHD-Peripheral Vascular Disease
2. Macroangiopathy-Diabetic retinopathy-Diabetic nephropathy-Diabetic neuropathy
3. Diabetic foot
Pathogenesis of Chronic Complication
1. Formation of Advanced Glycation End products(AGEs)
2. Activation of Protein Kinase C (PKC)
3. Intracellular hyperglycemia with disturbance of polyol pathway
Formation of Advanced Glycation End Products (AGEs)
Intracellular glucose-derived dicarbonyl precursors
+ (Non enzymatic reaction)
Amino group (intracellular & extracellular protein)
AGEs
Effects of glycosylation
Extracellular matrix protein
Circulating plasma protein
Cross-links between polypeptide(Eg.
Collagen)
Trap non-glycosylated plasma and interstitial protein
Trapping LDL at vessel wall accelerates
atherogenesis
Binds to AGE receptors on endothelial cells, mesangial cells &
macrophages
•Release cytokines & GF
•Increase vascular permeability
•Induce procoagulant activity
•Enhance ECM synthesis
Trapping albumin at BM thickens BM in diabetic
glomerulopathy
Activation of Protein Kinase CIntracellular hyperglycaemia
Stimulates de novo synthesis for diacylglycerol (DAG)
Activates PKC
Downstream effects:•Production of vascular endothelial growth factor •Increased vasoconstriction•increased deposition of extracellular matrix and basement membrane material•Production of plasminogen activator inhibitor •Production of proinflammatory cytokines
Polyol pathway
Glucose Sorbitol Fructose
NADPH + HNADPH + H++ NADP+
NAD+ NADH + H+
Aldosereductase
Polyoldehydrogenase
Disturbance in polyol pathwayHyperglycemia
increase IC glucose
(eg: nerves, lens, kidney, blood vessels)
metabolize by aldose reductase
sorbitol (polyol)
Fructose
Accumulated sorbitol & fructoseAccumulated sorbitol & fructose
Increase IC osmolarityIncrease IC osmolarity
Influx of waterInflux of water
Osmotic cell injury Osmotic cell injury
NADPH used up during polyol pathway
Decreased GSH (Reduced glutathione)
Cells susceptible to oxidative stress
Oxidative cell injury
Risk factor
• Diabetic foot ulcer is a combination of peripheral vascular disease (PVD), peripheral neuropathy (PNP), immunocompromised and infection.
• Other factors have been identified such as repetitive stress and pressure on insensitive feet, poor glycaemic control and others
Peripheral neuropathy 1. Chronic sensorimotor neuropathy• Sensory component - onset is insidious and
cause reduce or loss of sensation to vibration, painful and thermal stimuli.
• Severe case, proprioception may be affected and patient develop sensory ataxia.
• Motor component – atrophy of small intrinsic muscle of foot and cause unopposed pulling of extensor and flexor tendon resulting in clawing of toe and prominence of metatarsal head
• This lead to abnormal pressure point, which in an insensitive foot ultimately predispose to diabetic foot ulcer
Peripheral neuropathy
2. Autonomic neuropathy• Decrease sweat production dry foot
crack and fissure formation serve as nidus for infection and ulceration
• Increase arteriovenous shunting and raised venous pressure
• Impaired cutenous hyperaemic respond to injury
• Impaired vasoregulatory respond to changes in temperature.
Peripheral vascular disease
• DM increase risk of atheroslerosis• Reduce lower limb transcutenous oxygen tension and
reduce large vessel perfusion • This will cause delayed wound healing and development
of gangrene.• Diabetic patient also have an increase risk of
coagulability and thrombosis role in impairment of tissue perfusion and difficulty in delivering antibiotic
• Lazy lymphocyte syndrome – leukocyte function is impaired in uncontrolled diabetic
• Abnormality in migration, phagocytosis, intracelullar killing and chemotaxis and this is likely to interfere with healing process of diabetic foot.
Biomechanical factor
• Non-enzymatic glycosylation of collagen results in stiffening of connective tissue surrounding the joints leading to limited joint mobility.
• This causes increased plantar pressure during normal gait.
• Callus is known to contribute to high plantar foot pressure acting as an extrinsic source of stress and is highly predictive of subsequent ulceration.
Infection
• DM impaired tissue perfusion and lazy leukocyte syndrome cause delayed wound healing.
• Gram positive cocci – Stap. aureus, Strep. spp, Corynebacterium spp.
• Gram negative rod – E. coli, proteus species
Somatic neuropathy
•Reduce pain
•Diminished proprioception
•Clawing of toes
Autonomic neuropathy
•Absent sweating
•Dry skin fissure
•Altered blood flow regulation
•Distended foot veins
•Charcot neuroarthropathy
Peripheral vascular disease
•Claudication: rest pain
•Cold extremities
•Reduced foot pulses
Increase foot pressure
Callus formation Foot ischaemia
Foot ulceration
Gangrene
Infection
Amputation
Connective tissue change
•Limited joint mobility
•Orthopaedic disorder
SOFT TISSUE INFECTION
Factor that affect host respond
Systemic factor• Malnutrition• Renal and hepatic failure• Diabetes mellitus• Cancer • Immunosuppressive
therapy• Chronic hypoxia• Immune deficiency• Extremes of age• Alcohol abuse• Active cigarette abuse
Local factor• Major vessel compromise• Chronic lymphoedema• Arteritis• Extensive scarring• Radiation fibrosis• Small vessel disease• Venous stasis• Insensate region
Folliculitis• Infection of hair follicles
• Risk factor
- exfoliation of skin
- damage hair follicle (shaving, use of loofan sponge)
• Stap aureus or Stap epidermidis
Furuncle
• Skin disease caused by inflammation of hair follicle, thus resulting in the localized accumulation of pus and dead tissue.
• Common bacteria infection:
* stap aureus
* stap epidermidis
Carbuncle
• Collection of multiple furuncle characterize by red, hot, painful nodule that often drains pus through multiple openings of the skin.
• Usually extends into the deeper layers of the skin -- the subcutaneous fat.
• tend to occur in areas with thicker skin like the nape of the neck, the back, or the thighs.
Cellulitis • Acute spreading inflammation involving the
epidermis, dermis and subcutenous fat• Often occurs where the skin has previously been
broken: cracks in the skin, cuts, blisters, burns, insect bites, surgical wounds, or sites of IV cathether insertion
• Can be caused by normal skin flora or by exogenous bacteria
• Crepitant anaerobic cellulitis appears as a necrotic soft tissue infection with abundant connective tissue gas. Characterize by gradual onset, absence of muscle involvement, lack of marked systemic toxicity.
Causative Agents
Commonly caused by group A streptococci especially Streptococcus pyogenes
Occasionally streptococci from other Lancefield groups such as B, C and G can also cause cellulitis
Majority of celulitis (facial cellulitis) in childhood are caused by Staphylocuccus aureus, less commonly by Haemophilus influenzae type b, but they rarely cause cellulitis in adult.
Necrotizing Fasciitis• Is an infection of subcutaneous tissue and fascia
characterized by progressive necrosis.• Rare infection with high mortality (30 – 40 %)• Clinical menifestation include necrosis of the superficial and
often deep fascia.• Types of necrotizing fasciitis
# type 1-polymicrobial form (Mixed infection of anaerobic and aerobic bacteria)# type 2-monomicrobial form
• Aerobic organism especially Strep. pyogenes, Stap. aureus and members of E. coli, Enterobacteriaceae
• Anaerobes organism is Peptostreptococcus, Bacteroides, Fusobacterium
Clinical features• Initially begins as cellulitis which advances slowly -
redness, oedema, pain, very tender and warm • Over the next 2- 4 days, skin changing from red to purple
to pathognomonic gray- blue with ill- defined patches• Haamorrhagic bullae may develop• Necrosis of superficial fascia and ‘dishwater pus’
discharge• Meanwhile, systemic toxicity develops- high grade fever
with chill and malaise, tarchycardia,generalised toxicity septic shock
• *As infection spreading along the fascia, intensity of pain is in excess given external skin lesion.
• * woody hard feel of the subcutaneous tissue while in erysipelas or cellulits is yielding (give way to pressure)
Diagnose NF
• Failure to respond to initial antibiotic therapy
• Little improvement even on therapy
• Woody- hard feel of subcutaneous tissue extending beyond the skin involvement
• Systemic toxicity often with altered mental status
NF at presentation rapid progression seen after 24hours
Gas gangrene• Terrifying condition is produce by Clostridial infection
primarily of muscle tissue.• Clostridial species:
*clostridium perfringens 90%*clostridium novyi 4%*clostridium septicum 2%*clostridium histolyticum
• Gram positive bacilli, anaerobic organism that can survive and multiply only in tissue with low oxygen tension eg. dirty wound with dead muscle, area of major trauma or surgery or as complication of thermal burns
• Immunocompromised, diabetic, or malignant disease are at greater risk
• Toxins produce by the organism destroy the cell wall and rapidly lead to tissue necrosis.
Gas gangrene
• Clinical features appear with in 24hours of the injury
• Pain and swelling around the wound• Crepitus ( gas in tissue)• Brownish discharge, exudate describe as having
a “sweet mousy odour”• Little or no pyrexia• Pulse rate increase• Patient becomes toxaemic
Diagnose GG• Diagnosed mainly on a clinical basis• Step 1 - Expect the onset of gas gangrene to be sudden and
dramatic. There will be a pale to brownish red inflammation at the site of the infection with very painful swelling. Gas may be felt under the skin when the swollen area is pressed and the infection can expand quickly enough to be seen. Blisters may form with brown-red fluid and have a bad-smelling discharge.
• Step 2 - Use the extreme pain of the infection to distinguish gas gangrene from cellitus. This is due to the muscles not getting enough oxygen.
• Step 3 - Observe systemic symptoms of gas gangrene such as moderate to high fever and sweating. The skin may be initially pale with cold extremities, but then become yellow as blood cells break down. The patient can develop hypotension, rapid heart rate, kidney failure, coma and death if left untreated.
• Step 4 - Perform routine laboratory tests to indicate gas gangrene. Conduct a gram stain of infected fluid to see gram-positive bacteria. A CT scan, MRI or X-ray may show gas in the tissue.
• Step 5 - Confirm the diagnosis by growing a culture of cloistridium from infected fluid or tissue.
• Plain X-ray often shows gas in the subcutaneous tissue and fascial plains
MANAGEMENT
PREVENTION IS BATTER THAN CURE
Management of diabetic foot ulcer
1. Regular inspection and examination
2. Investigation
3. Treatment
Examination-inspection
• ischemic or neuropathy ulcer
• infected ulcer or not
• Discharge
• Sign of osteomylitis
• Sign of charcot joint
Wagner Ulcer Classification System
• Grade 0 - No open lesions; at risk• Grade 1 - Superficial diabetic ulcer (partial or full
thickness) • Grade 2 - Ulcer extension to ligament, tendon, joint
capsule, or deep fascia without abscess or osteomyelitis• Grade 3 - Deep ulcer with abscess, osteomyelitis, or joint
sepsis• Grade 4 - Gangrene localized to portion of forefoot or
heel • Grade 5 - Extensive gangrenous involvement of the
entire foot
Ischaemia VS Neuropathy
Ischaemia Neuropathy
Symptoms Claudication
Rest pain
Usually painless
Or painful neuropathy
Inspection Dependent rubor
Trophic changes
High arch + clawing of toes
Present or No trophic changes
Palpation Cold
Pulseless
Warm
Bounding pulses
Ulceration Painful
Heels and toes
Painless
Plantar
Ischemic foot ulcer
Dorsum of 2nd toe shows ischaemic lesion.Whitish color on the tipd/t ischaemia
Neuropathic foot ulcer
Ulcer on the 1st metatarsal head.Health granulation tissue on its bed.Callus formation on its surrounding ulcer lesion.
Mixed etiology (Neuro-ischemic) ulcer
Gangrene
Death of tissue usually in considerable massGenerally d/t loss of vascular supply& followed by bacterial infection
Investigation
1. Random blood sugar
2. FBC
3. Deep swab from ulcer base for culture and sensitivity
4. Plain radiograph of foot and ankle
6. Neurological investigation Two-point discrimination monofilament test vibration perception are used toassess
peripheral sensory neuropathy
Investigation
6. Vascular investigation:- Ankle- brachial systolic index
- >1.0 normal- <0.9 some degree of arterial obstruction- <0.3 suggests imminent necrosis
Toe systolic pressure- <40mmHg
Transcutenous PO2 level- <30mmHg
Doppler ultrasound
Treatment• Primary goal obtain wound closure
prevent limb loss
prevent ulceration and recurrence
maintain quality of life and
prevent further complication• Management of DFU is largely determined by
severity, vascularity and present of infection• Proper treatment of diabetic foot ulcers can lower
the incidence of lower limb amputations
Treatment for DFU
• Principle of treatment-Debridement of necrotic tissue-Wound care-Reduction of plantar pressure (off-loading) (eg. total non-weight bearing,total contact cast, foot cast or boots)-Treatment of infection-Vascular management of ischaemia (vascular reconstruction surgery )-Medical management of co morbidities-Surgical management to reduce or remove bony prominences and improve soft tissue cover-Reduce risk of recurrence
Debridement
• removal of all non-viable tissues and slough from the ulcer.
• Diabetic foot ulcers should be frequently and thoroughly debrided of necrotic tissues to enhance healing process
Wound care
• Moist wound environment bandaged to protect it from trauma and local contamination
• To facilitate the healing process
• Type of dressing depend on size, depth, location and wound surface
• Normal saline are use for standard wound care
Surgical Management of DFU
• Chronic foot ulcers are usually associated with areas of increased peak pressure where off loading and wound care techniques are not effective
• Then it treated surgically to reduce high-pressure areas or to redistribute pressure evenly so as to affect ulcer healing.
• All infected bones and tissues are to be removed and amputation done for gangrenous parts until viable bones and tissues are attained to allow optimum function of the remaining foot.
• The wounds are packed with antiseptic dressing and periodically assessed during wound care.
• use of local flaps, split skin grafts or full thickness grafts may be required (act as secondary wound healing)
Surgical treatment • Surgery on infected site includes debridement of wounds,
incision & drainage of abscesses,necrotising fascitis and amputations of gangrenous tissues
• Repeated procedures may be necessary to control infection • Indications for amputation: ( 3D – dead, dangerous,
damned nuisance)Minor amputations:* As part of open debridement* Chronic neuropathic ulcer – if too much tissue loss to save digit* Ischaemia – after infection is controlled and limb is revascularisedMajor amputations:* Extensive tissue loss* Unreconstructable ischaemia* Failed revascularisation* Charcot’s of ankle with instability
Treatment for DFU + infection
Principle of treatment • Surgical treatment• Wound care• Antibiotic treatment• Hyperglycemia control• Correct electrolytes• Optimize comorbidities• Frequent reassessment of response to treatment• If infection subsides but ulcer persists, follow
principles of diabetic ulcer treatment• Prevention
Antibiotic 1) Empirical antibiotics
I. Benzylpenicillin or ampicillin – Streptococcus sp.II. Oxacillin, nafcillin or 1st generation cephalosporin (eg. cefazolin) –
Staphylococcus sp.III. Quinolone + aminoglycoside (gentamycin) – Pseudomonas sp.IV. Methicillin-resistant Staphylococcus aureus – vancomycin or cotri-
moxazole
2) Clostridial species are sensitive to a combination of penicillin G and clindamycin
3) Duration of antibiotic treatment * 1-2 weeks course for mild to moderate infections * more than 2 weeks for more serious infections * 6 - 8weeks for osteomyelitis * If all infected bone is removed,a shorter course (1-2 weeks) of antibiotics, as for soft tissue infection, maybe adequate
Depth Classification
Definition Treatment
0At-risk foot, no ulceration
Patient education, accommodative footwear, regular clinical examination
1Superficial ulceration, not infected
Offloading with total contact cast (TCC), walking brace, or special footwear
2Deep ulceration exposing tendons or joints
Surgical debridement, wound care, offloading, culture-specific antibiotics
3Extensive ulceration or abscess
Debridement or partial amputation, offloading, culture-specific antibiotics
Ischemia Classification
A Not ischemic
BIschemia without gangrene
Noninvasive vascular testing, vascular consultation if symptomatic
CPartial (forefoot) gangrene
Vascular consultation
D Complete foot gangreneMajor extremity amputation, vascular consultation
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