Chronic Osteomyelitis

Classification of Chronic Osteomyelitis

Osteomyelitis can also be classified (according to the mechanism of infection/pathogenesis), as exogenous or haematogenous.
The most commonly used classification system of chronic osteomyelitis in adults is the Cierny–Mader classification.
It includes prognostic factors & delineates treatment for each clinical stage as per the anatomical type and physiological class of the host, providing guidelines for the successful management of osteomyelitis that correlate to the clinical and biologic response to therapy.
Cierny–Mader Classification System

Table1

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Anatomic type
Type	Characteristic
I	Medullary Osteomyelitis
II	Superficial Osteomyelitis
III	Localized Osteomyelitis
IV	Diffused Osteomyelitis
Physiological Class
Host	Characteristic
A	-Good immune system & delivery
B	-Compromised locally (BL) or systemically (BS)
C	-Requires suppressive or no treatment; Minimal disability; Treatment worse than disease; Not a surgical candidate
Factors affecting Physiological class
Systemic Factors(S)	Local Factors(L)
Malnutrition Renal or Hepatic Failure Diabetes mellitus Chronic hypoxia Immune disease Extremes of age Immunosuppression Immune deficiency Tobacco abuse Alcohol abuse Malignancy	Chronic Lymphoedema Venous stasis Major vessel compromise Arteritis Extensive scarring Radiation fibrosis Small-vessel disease Neuropathy

Etiopathogenesis

Exogenous(contiguous contamination)

-Direct inoculation of pathogens into the bone(by trauma) & by surgical trauma (CRIF/ORIF of fractures): Most Common
-From chronic overlying open wounds
-From contiguous soft tissue infections.

Haematogenous

-Seeding of pathogen(s) into the bone through the systemic circulation(predominately in paediatric patients)
-From a distal site of infection usually involving vertebral bodies & adjacent intervertebral discs (in adults)

Others

-Vascular/Neurological insufficiency, e.g. pt with DM (soft tissue infection spreads to bone, like in diabetic foot)

Pathogens

–Monomicrobic (in haematogenous osteomyelitis) vs Polymicrobic (in Contiguous infection osteomyelitis)
–Staphylococcus aureus (most common in adults)
–Staphylococcus epidermidis, Pseudomonas aeruginosa, Serratia marcescens and Escherichia coli
-Mycobacterial and fungal infections (uncommon, usually associated with immunodeficiency).

Predisposing factors

-history of trauma,
-open fractures
-surgery
-the presence of implants(formation of biofilm)

-Other factors:
diabetes,
peripheral vascular disease,
malnutrition,
hypotension,
chronic steroid use,
malignancy,
alcoholism,
smoking,
systemic/local immunocompromise,
IV drug use,
decubitus ulcers.

Pathology

Chronic osteomyelitis- a progressive inflammatory process characterized by bone destruction and sequestrum formation.

-the introduction of pathogen(s) into the bone/bone marrow cavity
-adherence to membrane proteins(e.g. fibronectin or collagen receptors) establishing an infection
-attacking various host cells & degrading the extracellular matrix
-formation of a relatively impermeable polysaccharide/protein matrix- the biofilm

( ~surrounded by the biofilm, the pathogens present with an altered phenotype with regards to growth, gene expression & protein production that protects them from the host’s defence mechanisms & the systemic effect of antibiotics. They can remain in quiscent state for long periods of time & can cause flare-ups many years after the initial inoculation. )

-The inflammatory factors produced by the pathogens & by the host’s leucocytes, & the compression and obliteration of the vascular network around the involved area, causes tissue necrosis & bone destruction
-Avascular necrosed tissue/dead bone called the sequestrum– an ideal harbour for bacteria around which reactive hyperaemia & increased osteoclastic activity results in localised bone loss & osteoporosis
-simultaneously, osteoblastic activity causes periosteal new bone formation- the involucrum.

Clinical features

Non-specific, a variety of features from no skin lesions to open wounds over fractured bones.
Symptoms:
-Chronic pain,
-chills, low grade fever & general malaise
Signs:
-erythema of the affected bone area, swelling & bone tenderness,
-impaired wound healing, tissue necrosis, increased drainage/persistent sinus tracts,

In neglected cases-a history of cyclical pain increasing in severity, associated with fever which subside when pus breaks out through the fistula.

In diabetic patients-differentiation of signs of osteomyelitis from soft tissue infection is difficult.

Imaging Studies

-help in the characterisation differential diagnosis of osteomyelitis

• Plain Radiography
  -may differentiate osteomyelitis from other pathologies such as fractures & malignancies (primary or metastatic)
  -EARLY SIGNS(as early as 10 to 21 days after the bone infection): soft tissue swelling, periosteal reaction, loss of definition, loss of bone density & osteolysis,(may not be detectable until there is a loss of 30% to 50% of the bone mineral content)
  -LATE SIGNS: increased bone resorption, sequestra formation, & new bone formation in the periosteum or endosteum(involucrum)
• CT Scan shows-
  -details imaging of sequesra & intra-osseous fistula;
  -periosteal reaction & bone-marrow involvement
• MRI
  -assessment of bone-marrow & soft tissues
  -to differentiate bone from soft tissue infections
  -as an adjunct in estimating the margins required for the debridement, or to assess the response to therapy
• Routine bone scintigraphy & Leucocyte scintigraphy- limited specificity & false-positive results
• PET(Positron emission tomography)– highest sensitivity & specitivity, but costlier & not easily available.
• Ultrasonography (US)- may be used at the early stages for detecting purulent collections within the soft tissues.

Lab Investigations

They lack specificity & are supportive only.
–⭡ed CRP & ESR
-Leukocytosis & elevated α-1 acid glycoprotein levels

–Culture & Sensitivity: the presence of +ve microbial cultures from bone tissue taken from areas of bone necrosis is essential. The sample must not be from superficial wounds/fistulae, as there is risk of contamination & inclusion of non-pathogenic micro-organisms that colonise the wound.
-In patient with implant-related osteomyelitis, if samples taken from up to 5 sites around the implant increases the diagnostic yield.

–Histopathology Examination: for additional information like presence of large amount of Neutrophils & positive special staining showing presence of pathogens even before culture.

Management of Osteomyelitis

-depends on many factors such as duration & severity of symptoms, local tissue status, the presence of medical comorbidities, etc.

–Goal of treatment -to eliminate the inflammatory process by removing all the pathogens & the necrosed/dead tissue, & to promote healing by providing the mechanical & biological support.

-a combination of treatment with antibiotics, surgical debridement & management of the dead space

• Antibiotics
  – Empiric antibiotic therapy after obtaining the culture samples
  -a duration of 4-6 weeks of antibiotic therapy is recommended which can vary from case to case.
  -The antibiotic regime should be modified according to the results of the cultures and sensitivities.
  -In polymicrobial cases/in case of prosthetic infections, a combination of antibiotics is recommended to cover all pathogens & to reduce the recurrence rate.
  –Local delivery of high doses of antibiotics as polymethylmethacrylate (PMMA) beads, calcium sulfate beads(rapid release of high concentrations of antibiotics, biodegradable), hydroxyapatite-ceramic beads & polylactide-polyglycolide co-polymer implants.
• Surgical treatment
  -is the keystone of the treatment of chronic osteomyelitis.
  -includes an adequate surgical debridement with removal of all pathogens along with their biofilms & sequestra (dead bone) reaching down to healthy & viable tissue- paprika sign.
  -local soft tissue debridement & reconstruction
  -saucerization
  -if medullary canal involved, debridement with the reamer-irrigator-aspirator (RIA) technique & insertion of an antibiotic-impregnated intramedullary cement rod.
  -samples of removed tissues should be sent for pathological examination & Culture-sensitivity examination.
  –Amputation, in some cases, e.g. in some diabetes cases
• Management of dead space
  -Antibiotic-impregnated cement spacers & antibiotic beads are used in cases of two-stage procedures, temporarily filling the dead space until reconstruction is performed.
  -use of induced membrane (Masquelet) technique
  -Ilizarov (circular) external fixation device & bone transport
  -use of Local flaps (muscle flaps, pedicled muscle flaps, myocutaneous flaps & osseous flaps)
  -use of Vascularised free flaps
  -recent use of bioactive glass, along with antibiotic therapy, a safe & effective bone substitute in the presence of infection.
  (Bioactive glass a synthetic, biocompatible material with osteoconductive, angiogenic & antimicrobial properties, resulting in its integration into bone and soft tissues, a potentially useful adjunct in the management of dead space)

Complications

-Abscess formation
-sinus tracts formation & extension to adjacent structures
-persistence of infection
-Malignant transformation into squamous cell carcinoma, Marjolin’s ulcer.

Please see this article for details:
Chronic osteomyelitis: what the surgeon needs to know
by Michalis Panteli and Peter V. Giannoudis