You are on page 1of 57

Musculoskeletal

Infections in Diabetes:
an over view

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

 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).
BASIC FACTS
 Diabetics 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.
 Necrotizing fasciitis,
 Malignant Otitis media

 Rhino-Cerebral Mucormycosis

 High rates of morbidity and mortality


EFFECT OF INFECTION IN D.M.
 May precipitate  Severity &
metabolic Complications: Long
derangements hospital stay
 Infection-related
 Metabolic
mortality risk
derangements may
 Mortality risk mediated
facilitate infection
by Cardiovascular
 Morbidity disease in Adults!
SKIN & SOFT TISSUE INFECTIONS

 "Diabetic Foot Complex”


 Cellulitis
 Pyomyositis
 Necrotizing fasciitis
 Mucocutaneous Candida infections
Musculoskeletal infection
 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  Depressed C.M.I.?


function  Compromized
 Poor Adherence to bactericidal oxidation
endothelium system
 Poor Chemotaxis &  Normal response to
Phagocytosis vaccination !
WOUND HEALING
 Anabolic hormone
 Entry of glucose

 Entry of amino acids

 Collagen synthesis

 Wound healing
PREDISPOSING FACTORS
 Hyperglycemia

 Statistically
Significant Risk: > 250mg%
 Diabetic Microangiopathy

 Neurovasculopathy

 Sensory Neuropathy

 Atherosclerostic Vascular Disease


OTHER RISK FACTORS
 Persistent edema  Past history of cellulitis
 PVD (unrelated)  Smoking
 Tinea  IVDU
 Dry skin  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

 Distal-most 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  Neuropathy decreases


process: symmetrical perception of infection
distal neuropathy
 Inability to perceive:
 All: Sensory, Motor & Light touch, Pressure &
Autonomic nerves Pain
PATHOPHYSIOLOGY
 Loss of protective  Uneven distribution
sensation (LOPS) of body weight
 Unrecognized  Abnormal
trauma biomechanics
 Motor : Paralysis of
the intrinsic muscles
 Abnormal Plantar
of the feet Pressure
 Foot Deformities
ARCHES OF FOOT
INTRINSIC MUSCLE INVOLVEMENT &
OSTEOLYSIS
NEUROPATHY
ABNORMAL PLANTAR PRESSURE IN
FORCE PLATE ANALYSIS
DEFORMITIES: EFFECTS
 Main precursors of abnormal
biomechanics
 Foot Deformities: Hammer & Claw toes

 Rocker bottom abnormality of the sole


NEUROPATHY
 Autonomic 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,  Aggressive deforming


Distension, Destruction & arthritis
Deformity & Debris
(Pathologic fractures)  Joint Position senses
 Repeated Micro- and macro-
trauma to the articular  The Role of inflammatory
surfaces of the tarsal & MT. Cytokines
 Important D/D of Infection
 Bisphosphonates: Reduce
osteoclastic resorption.
VASCULOPATHY
 Add to the insult
 Microangiopathy

 P.V.D.

 Atherosclerosis

 Smoking
VASCULOPATHY: EFFECTS
 Major cause of death:  PVD: More prevalent &
US data Younger age.
 Risk of myocardial  Additional risk factors:
infarction & stroke: 3-4 Hypertension,
times Hyperlipidemia,
 Accelerated Smoking & Family
atherosclerosis  Cumulative damage
RBC DEFORMABILITY

“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
 Specific 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
BIOMECHANICS
 Diabetic 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
MALPERFORANS ULCERS
 The plantar  Barefoot walking or
malperforans ulcers in Constricting shoes:
the high pressure
exacerbates abnormal
areas
biomechanics leading
 Heel, 1st & 5th MT
to ulceration.
heads: Common
expression of the
 Therapeutic shoes:
pathologic processes. lower plantar pressure
 Can their use alone
prevent ulceration?
MALPERFORANS ULCERS
EXAMINATION: DETAIL
 Sense Of Vibration  Alcohol
 Joint Position Sense  Smoking
 > 10 Years Of D.M.  Previous H/O Ulcer/
 Retinal Changes Cellulitis
FOOT INFECTIONS
 The 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  Portal of entry: small
trauma abrasions resulting from
 Progression to Cellulitis, trauma, fungal infection or
Soft tissue necrosis & indolent ulcers
extension into bone.  Concomitant neuropathy
 Serious complications: decreases perception of
osteomyelitis, amputation infection
& death.  Co-existing vascular
insufficiency - spread of the
infection in ischemic
tissues
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.
ANTIBIOTICS IN INFECTION
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%.
PARADOX
 Because 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.)
 Definition: A deep-seated, life-
threatening 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.
Necrotizing fasciitis

High risk: Patient with peripheral vascular disease & diabetes mellitus
BACTERIOLOGY OF N.F.
 Anaerobes with >1 facultative aerobes
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.
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 & multi-


organ failure
TESTS
 Elevated muscle enzymes: Serum
creatinine phosphokinase may be
markedly elevated.
 Soft tissue gas on Radiograph or CT.

 MRI: Decision making


TREATMENT

 Broad-spectrum intravenous antibiotics


 Immediate aggressive surgical
debridement
 Good glycemic control

 Serial debridement

 Initial isolation is recommended

 ICU set up
NECROTIZING FASCIITIS:
EPILOGUE
 Untreated, it is universally fatal;
 Even if recognized early mortality is high
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.
Pyomyositis
S 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  Pure PVD
 Charcot’s  DVT
Arthropathy  Tuberculosis
 Diabetic amyotrophy
D/D of Pyomyositis

 Necrotic fasciitis
 Focal inflammatory myositis

 Vascular events-DVT, muscle infarct

 Trauma

 Tumor

 Diabetic amyotrophy
PYOMYOSITIS
MUSCULOSKELETAL

TUBERCULOSIS IN DM

 Relapse 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
 Essential for defining the extent of soft-
tissue 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  S. Creatinine
 ESR, CRP  S. CPK
 S. Albumin  S. Alkaline
 Bl. Sugar Phosphate
 Plain X-ray  Doppler
 USG  Biopsy
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
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
Epilogue
“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

THANK YOU

You might also like