This action might not be possible to undo. Are you sure you want to continue?
Bhaskar Borgohain MS,DNB,Fellow (Arthroplasty).
AMERICAN DIABETIC ASSOCIATION
“The world is currently experiencing an epidemic of Diabetes Mellitus, particularly Type II or Adult onset. The need is to understand this disease in great detail. Precision in diagnosis and prevention of complication is the key to management ”
The Definition: American Diabetic Association
and symptoms of Glycosuria or a Random blood glucose > 200mg% (11.1mmol/dL ) A fasting blood glucose > 126mg% (7mmol/dL ) on two occasions or 2 Hr Blood Glucose after oral 75gm load of Glucose 200mg% (11.1mmol/dL).
are predisposed to infections Infection may be just the tip of the iceberg Common infections: Diabetic foot with infection, Cellulitis, Pyomyositis Almost exclusive: Necrotizing fasciitis
EXCLUSIVE INFECTIONS IN D.M.
fasciitis, Malignant Otitis media Rhino-Cerebral Mucormycosis High rates of morbidity and mortality
EFFECT OF INFECTION IN D.M.
May precipitate metabolic derangements Metabolic derangements may facilitate infection Morbidity
Severity & Complications: Long hospital stay Infection-related mortality risk Mortality risk mediated by Cardiovascular disease in Adults!
SKIN & SOFT TISSUE INFECTIONS
"Diabetic Foot Complex” Cellulitis Pyomyositis Necrotizing fasciitis Mucocutaneous Candida infections
Commonly encountered in Known diabetic Can take many forms, depending on the involvement of the tissue involved: soft-tissue layers, bones, and joints. Infection: Superficial cellulitis, Pyomyositis (Deep), Soft-tissue abscess, Necrotizing or nonnecrotizing fasciitis, Osteomyelitis, or Septic arthritis.
WHY ONLY IN D.M. : IMMUNE DYSFUNCTION
Depressed Neutrophil function Poor Adherence to endothelium Poor Chemotaxis & Phagocytosis
Depressed C.M.I.? Compromized bactericidal oxidation system Normal response to vaccination !
hormone Entry of glucose Entry of amino acids Collagen synthesis Wound healing
Significant Risk: > 250mg% Diabetic Microangiopathy Neurovasculopathy Sensory Neuropathy Atherosclerostic Vascular Disease
OTHER RISK FACTORS
Persistent edema PVD (unrelated) Tinea Dry skin
Past history of cellulitis Smoking IVDU Malnutrition
WHAT IS DIABETIC FOOT INFECTION
Diabetic foot infections are infections that can develop in the skin, muscles, or bones of the foot as a result of nerve damage & poor circulation that is associated with diabetes
WHY FOOT IS INVOLVED
part of the body Gloves and Stocking Neuropathy Distal Vasculopathy Unrecognized Injury Weight bearing area Edema tends to stay
PATHOPHYSIOLOGY OF DIABETIC FOOT
Main pathologic process: symmetrical distal neuropathy All: Sensory, Motor & Autonomic nerves
Neuropathy decreases perception of infection Inability to perceive: Light touch, Pressure & Pain
Loss of protective sensation (LOPS) Unrecognized trauma Motor : Paralysis of the intrinsic muscles of the feet Foot Deformities
Uneven distribution of body weight Abnormal biomechanics Abnormal Plantar Pressure
ARCHES OF FOOT
INTRINSIC MUSCLE INVOLVEMENT & OSTEOLYSIS
ABNORMAL PLANTAR PRESSURE IN FORCE PLATE ANALYSIS
precursors of abnormal biomechanics Foot Deformities: Hammer & Claw toes Rocker bottom abnormality of the sole
Dysfunction: Decreased sweating Dry Skin Scaling skin susceptible to fungal & other superficial infections. Nearly 44% of patients may have paresthesia. Unrecognized trauma
NEUROPATHIC OSTEOARTHROPATHY (CHARCOT’S FOOT)
The 5 D’s- Dislocation, Distension, Destruction & Deformity & Debris (Pathologic fractures) Repeated Micro- and macrotrauma to the articular surfaces of the tarsal & MT. Important D/D of Infection
Aggressive deforming arthritis Joint Position senses The Role of inflammatory Cytokines Bisphosphonates: Reduce osteoclastic resorption.
to the insult Microangiopathy P.V.D. Atherosclerosis Smoking
Major cause of death: US data Risk of myocardial infarction & stroke: 3-4 times Accelerated atherosclerosis
PVD: More prevalent & Younger age. Additional risk factors: Hypertension, Hyperlipidemia, Smoking & Family Cumulative damage
“The presence of diabetes mellitus seems to affect the already compromised RBC deformability of septic patients, probably leading to serious microcirculatory functional impairments in septic diabetic patients.” J. infect, May 2008
PVD in DM
pattern of infrapopliteal disease requiring more distal bypass A pattern of medial calcification in vessels Noninvasive identification of insufficiency may be difficult. Ischemia: Suspect if non-healing ulcer Surgical revascularization: But required in 20-25% only
neuropathy with LOPS & foot deformities Result: abnormal plantar pressures Abnormal plantar pressures: the final common pathway Development of typical malperforans ulcer Most ulcers: Sole of foot
The plantar malperforans ulcers in the high pressure areas Heel, 1st & 5th MT heads: Common expression of the pathologic processes.
Barefoot walking or Constricting shoes: exacerbates abnormal biomechanics leading to ulceration. Therapeutic shoes: lower plantar pressure Can their use alone prevent ulceration?
Sense Of Vibration Joint Position Sense > 10 Years Of D.M. Retinal Changes
Alcohol Smoking Previous H/O Ulcer/ Cellulitis
most common soft tissue infection Diabetic Neurovasculopathy pivotal Diabetic foot ulcers: The most common gateways to foot infection. > 50% ulcers get infected at some stage
FOOT INFECTION IN DM
Begins after a minor trauma Progression to Cellulitis, Soft tissue necrosis & extension into bone. Serious complications: osteomyelitis, amputation & death.
Portal of entry: small abrasions resulting from trauma, fungal infection or indolent ulcers Concomitant neuropathy decreases perception of infection Co-existing vascular insufficiency - spread of the infection in ischemic tissues
The most common gateway to foot infection Exploration the ulcer: Crucial to determine the depth of the ulcer Presence of palpable bone: Strongly S/O Osteomyelitis Important: Determine presence of sinus tracts Obtain a culture.
ANTIBIOTICS IN INFECTION
aureus = 56% Group A streptococci (GAS) Group B streptococci. Wound > 1 month: Gram negative aerobes (Pseudomonas) & anaerobes-Bacteroides fragilis & Enterococci Anaerobes only 5%.
a person who has diabetes may not feel foot pain or discomfort, problems can remain undetected until fever or other signs of systemic infection appear. As a result, even minor injuries heal more slowly & likely to result in serious health problems.
NECROTIZING FASCIITIS (N.F.)
A deep-seated, lifethreatening infection of subcutaneous tissue with progressive destruction of fascia, fat & muscles. Diabetes/ Alcoholics/ IVDU Infection spreads rapidly along fascial planes and through venous & lymphatic channels.
High risk: Patient with peripheral vascular disease & diabetes mellitus
BACTERIOLOGY OF N.F.
90% Associated with GAS + S aureus 10% Recent Study: Necrotizing fasciitis caused by CA-MRSA Current or past IVDU represented 43% of patients 21% patients with D.M.
with >1 facultative aerobes
CLINICAL FEATURES: N.F.
Pain out of proportion to skin findings Anesthesia of overlying skin. Violaceous discoloration of the skin that evolves into vesicles and bullae Crepitus is felt in half of the cases. In the later stages: toxic, shock & multiorgan failure
muscle enzymes: Serum creatinine phosphokinase may be markedly elevated. Soft tissue gas on Radiograph or CT. MRI: Decision making
intravenous antibiotics Immediate aggressive surgical debridement Good glycemic control Serial debridement Initial isolation is recommended ICU set up
NECROTIZING FASCIITIS: EPILOGUE
it is universally fatal; Even if recognized early mortality is high
Deep infection of the skeletal muscles. Infection deep: No erythema or warmth; But tenderness & swelling Thigh quadriceps , glutei muscles, iliopsoas: common. If S pyogenes: Primary Streptococcal Necrotizing Myositis, severe systemic toxicity. Frequent bacteremia, shock, and organ failure.
aureus common Common in Tropic rare in temperate Portal of entry oft unknown Risk factors: Collagen vascular disease & Low immunity. Infection localized unless strains -TSS toxin 1 OR enterotoxins
DIFF.DIAGNOSIS OF INFECTION
Aseptic myonecrosis Charcot’s Arthropathy Diabetic amyotrophy
Pure PVD DVT Tuberculosis
D/D of Pyomyositis
fasciitis Focal inflammatory myositis Vascular events-DVT, muscle infarct Trauma Tumor Diabetic amyotrophy
MUSCULOSKELETAL TUBERCULOSIS IN DM
of T.B. After years ATT is better now Good results Vigilance needed 12-18 months of ATT INH-Neuropathy, Ethambutol -eye
Role of CT and MRI in infections
for defining the extent of softtissue and bone involvement. Deep locations and Critical areas CT shows bony destruction well CT: guide therapy toward emergency surgical débridement in necrotizing fasciitis /percutaneous drainage in abscess
INVESTIGATIONS IN INFECTIONS
Routine ESR, CRP S. Albumin Bl. Sugar Plain X-ray USG
S. Creatinine S. CPK S. Alkaline Phosphate Doppler Biopsy
KEY ISSUES IN MANAGEMENT
Intensify glycemic control - Acute infection is a high stress state Antimicrobial therapy Insulin may become an absolute necessity Co morbid factors Debridement
Infection in DM is just the tip of the iceberglook beyond the infection! Clinical & lab features may be misleading High index of suspicion on clinical evaluation Glycemic control is as important as antimicrobials and selective debridement Co-morbid conditions must be addressed
“As the virulence of pathogens wax & wane, as antibiotic resistance progresses and as host responsiveness changes as a result of immunocompromising diseases, we will forever be challenged to describe novel clinical presentations, new etiologies and innovative treatments”
BEST IS BEST
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue reading from where you left off, or restart the preview.