musculoskeletal infections in diabetes mellitus
TRANSCRIPT
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Muscu loske le ta l
In fec t ion s in D ia bete s :
an ove r v iew
Bhaskar Borgohain
MS,DNB,Fellow (Arthroplasty).
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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 tomanagement ”
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The Definition: American Diabetic Association
Signs 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).
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BASIC FACTSDiabetics are predisposed to infections
Infection may be just the tip of the
icebergCommon infections: Diabetic foot with
infection, Cellulitis, Pyomyositis
Almost exclusive: Necrotizing fasciitis
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EXCLUSIVE INFECTIONS IN D.M.Necrotizing fasciitis,
Malignant Otitis media
Rhino-Cerebral Mucormycosis
High rates of morbidity and mortality
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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!
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SKIN & SOFT TISSUE INFECTIONS
"Diabetic Foot Complex”
Cellulitis
Pyomyositis
Necrotizing fasciitis
Mucocutaneous Candida infections
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Musculoskeletal infection Commonly encountered in Known diabetic
Can take many forms, depending on the
involvement of the tissue involved: soft-tissuelayers, bones, and joints.
Infection: Superficial cellulitis, Pyomyositis
(Deep), Soft-tissue abscess, Necrotizing or
nonnecrotizing fasciitis, Osteomyelitis, or Septic arthritis.
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WHY ONLY IN D.M. : IMMUNE
DYSFUNCTION
Depressed Neutrophil
function
Poor Adherence toendothelium
Poor Chemotaxis &
Phagocytosis
Depressed C.M.I.?
Compromized
bactericidal oxidation
system
Normal response to
vaccination !
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WOUND HEALINGAnabolic hormone
Entry of glucose
Entry of amino acids
Collagen synthesis
Wound healing
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PREDISPOSING FACTORS
Hyperglycemia
Statistically Significant Risk: > 250mg%
Diabetic Microangiopathy
Neurovasculopathy
Sensory Neuropathy
Atherosclerostic Vascular Disease
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OTHER RISK FACTORS Persistent edema
PVD (unrelated)
Tinea Dry skin
Past history of cellulitis
Smoking
IVDU Malnutrition
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WHY FOOT IS INVOLVEDDistal-most part of the body
Gloves and Stocking Neuropathy
Distal Vasculopathy
Unrecognized Injury
Weight bearing areaEdema tends to stay
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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
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PATHOPHYSIOLOGY Loss of protective
sensation (LOPS) Unrecognized
trauma Motor : Paralysis of
the intrinsic musclesof the feet
Foot Deformities
Uneven distribution
of body weight
Abnormalbiomechanics
Abnormal Plantar
Pressure
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INTRINSIC MUSCLE INVOLVEMENT &
OSTEOLYSIS
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ABNORMAL PLANTAR PRESSURE IN
FORCE PLATE ANALYSIS
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DEFORMITIES: EFFECTS
Main precursors of abnormal
biomechanics
Foot Deformities: Hammer & Claw toesRocker bottom abnormality of the sole
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NEUROPATHY
Autonomic Dysfunction: Decreased
sweating Dry Skin
Scaling skin susceptible to fungal & other superficial infections.
Nearly 44% of patients may have
paresthesia.Unrecognized trauma
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VASCULOPATHY
Add to the insult
Microangiopathy
P.V.D.Atherosclerosis
Smoking
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RBC DEFORMABILITY
“The presence of diabetes mellitus seems
to affect the already compromised RBCdeformability of septic patients, probablyleading to serious microcirculatoryfunctional impairments in septic diabetic
patients.” J. infect , May 2008
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MALPERFORANS ULCERS
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EXAMINATION: DETAIL
Sense Of Vibration
Joint Position Sense
> 10 Years Of D.M. Retinal Changes
Alcohol
Smoking
Previous H/O Ulcer/Cellulitis
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FOOT INFECTIONS
The most common soft tissue infection
Diabetic Neurovasculopathy pivotal
Diabetic foot ulcers: The most commongateways to foot infection.
> 50% ulcers get infected at some stage
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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 theinfection in ischemic
tissues
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FOOT ULCERS
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.
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ANTIBIOTICS IN INFECTION
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THE BACTERIOLOGY
Staphylococcus aureus = 56%
Group A streptococci (GAS)
Group B streptococci.
Wound > 1 month: Gram negative aerobes
(Pseudomonas) & anaerobes-Bacteroides fragilis &
Enterococci
Anaerobes only 5%.
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PARADOX
Because a person who has diabetes
may not feel foot pain or discomfort,
problems can remain undetected untilfever or other signs of systemic infection
appear.
As a result, even minor injuries heal
more slowly & likely to result in serious
health problems.
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NECROTIZING FASCIITIS (N.F.)
Definition: A deep-seated, life-threatening infection of subcutaneoustissue with progressive destruction of fascia, fat & muscles.
Diabetes/ Alcoholics/ IVDU Infection spreads rapidly along fascial
planes and through venous & lymphaticchannels.
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Necrotizing fasciitis
High risk: Patient with peripheral vascular disease & diabetes mellitus
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BACTERIOLOGY OF N.F.
Anaerobes with >1 facultative aerobes90%
Associated with GAS + S aureus 10%Recent Study: Necrotizing fasciitis
caused by CA-MRSACurrent or past IVDU represented 43%
of patients21% patients with D.M.
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CLINICAL FEATURES: N.F.
Pain out of proportion to skin findings
Anesthesia of overlying skin.
Violaceous discoloration of the skin thatevolves into vesicles and bullae
Crepitus is felt in half of the cases.
In the later stages: toxic, shock & multi-organ failure
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TREATMENT
Broad-spectrum intravenous antibiotics
Immediate aggressive surgical
debridementGood glycemic control
Serial debridement
Initial isolation is recommended ICU set up
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NECROTIZING FASCIITIS:
EPILOGUE
Untreated, it is universally fatal;
Even if recognized early mortality is high
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PYOMYOSITIS
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.
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Pyomyositis
S aureus common
Common in Tropic rare in temperate
Portal of entry oft unknownRisk factors: Collagen vascular disease
& Low immunity.
Infection localized unless strains -TSStoxin 1 OR enterotoxins
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D/D of Pyomyositis
Necrotic fasciitis
Focal inflammatory myositis
Vascular events-DVT, muscle infarctTrauma
Tumor
Diabetic amyotrophy
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PYOMYOSITIS
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TUBERCULOSIS IN DM
Relapse of T.B. After years
ATT is better now
Good resultsVigilance needed
12-18 months of ATT
INH-Neuropathy, Ethambutol -eye
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Role of CT and MRI in infections
Essential for defining the extent of soft-tissue and bone involvement.
Deep locations and Critical areasCT shows bony destruction wellCT: guide therapy toward emergency
surgical débridement in necrotizing
fasciitis /percutaneous drainage inabscess
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INVESTIGATIONS IN INFECTIONS
Routine
ESR, CRP
S. Albumin Bl. Sugar
Plain X-ray
USG
S. Creatinine
S. CPK
S. AlkalinePhosphate
Doppler
Biopsy
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KEY ISSUES IN MANAGEMENT
Emphasis: Intensify glycemic control --
Acute infection is a high stress state
Antimicrobial therapy Insulin may become an absolute necessity
Co morbid factors
Debridement
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SUMMARY
Infection in DM is just the tip of the iceberg-
look 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
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Epilogue
“ As the virulence of pathogens wax &
wane, as antibiotic resistance
progresses and as host responsivenesschanges as a result of
immunocompromising diseases, we will
forever be challenged to describe novel
clinical presentations, new etiologies and innovative treatments”
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