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 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

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 function Poor Adherence to endothelium Poor Chemotaxis & Phagocytosis

Depressed C.M.I.?  Compromized bactericidal oxidation system  Normal response to 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  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
 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 process: symmetrical distal neuropathy All: Sensory, Motor & Autonomic nerves

Neuropathy decreases perception of infection Inability to perceive: Light touch, Pressure & Pain

 

PATHOPHYSIOLOGY
  

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

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, 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.

VASCULOPATHY
 Add

to the insult  Microangiopathy  P.V.D.  Atherosclerosis  Smoking

VASCULOPATHY: EFFECTS

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

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 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?

MALPERFORANS ULCERS

EXAMINATION: DETAIL
   

Sense Of Vibration Joint Position Sense > 10 Years Of D.M. Retinal Changes

  

Alcohol Smoking Previous H/O Ulcer/ 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 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

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, 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.

Necrotizing fasciitis

High risk: Patient with peripheral vascular disease & diabetes mellitus

BACTERIOLOGY OF N.F.
 Anaerobes

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

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 Charcot’s Arthropathy Diabetic amyotrophy

  

Pure PVD DVT Tuberculosis

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 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
 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 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

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”

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