Musculoskeletal Infections in Diabetes Mellitus

8/14/2019 Musculoskeletal Infections in Diabetes Mellitus

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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).

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 ”

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 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

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-tissuelayers, 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 toendothelium

Poor Chemotaxis &

Phagocytosis

Depressed C.M.I.?

Compromized

bactericidal oxidation

system

Normal response to

vaccination !

WOUND HEALINGAnabolic 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

WHY FOOT IS INVOLVEDDistal-most part of the body

Gloves and Stocking Neuropathy

Distal Vasculopathy

Unrecognized Injury

Weight bearing areaEdema tends to stay

PATHOPHYSIOLOGY OF DIABETIC

Main pathologic

process: symmetrical

distal neuropathy

All: Sensory, Motor &

Autonomic nerves

Neuropathy decreases

perception of infection

Inability to perceive:

Light touch, Pressure &

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

INTRINSIC MUSCLE INVOLVEMENT &

OSTEOLYSIS

ABNORMAL PLANTAR PRESSURE IN

FORCE PLATE ANALYSIS

DEFORMITIES: EFFECTS

Main precursors of abnormal

biomechanics

Foot Deformities: Hammer & Claw toesRocker 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

VASCULOPATHY

Add to the insult

Microangiopathy

P.V.D.Atherosclerosis

Smoking

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

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 commongateways 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 theinfection 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 untilfever 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 subcutaneoustissue with progressive destruction of fascia, fat & muscles.

Diabetes/ Alcoholics/ IVDU Infection spreads rapidly along fascial

planes and through venous & lymphaticchannels.

Necrotizing fasciitis

High risk: Patient with peripheral vascular disease & diabetes mellitus

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.

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

TREATMENT

Broad-spectrum intravenous antibiotics

Immediate aggressive surgical

debridementGood 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 unknownRisk factors: Collagen vascular disease

& Low immunity.

Infection localized unless strains -TSStoxin 1 OR enterotoxins

D/D of Pyomyositis

Necrotic fasciitis

Focal inflammatory myositis

Vascular events-DVT, muscle infarctTrauma

Diabetic amyotrophy

PYOMYOSITIS

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

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

INVESTIGATIONS IN INFECTIONS

Routine

ESR, CRP

S. Albumin Bl. Sugar

Plain X-ray

S. Creatinine

S. CPK

S. AlkalinePhosphate

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 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 responsivenesschanges 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

Musculoskeletal Infections in Diabetes Mellitus

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