Acute Osteomyelitis

38,496 views 28 slides May 30, 2018
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About This Presentation

Student Seminar Presentation under supervision of orthopedic specialist. Reference as mentioned in the slides.


Slide Content

ACUTE OSTEOMYELITIS INFECTION OF BONE AND BONE MARROW

INTRODUCTION Infection of bone and bone marrow Can progress to osteonecrosis , bone destruction and septic arthritis Bimodal age distribution: Children under 5 years old Adults over 50 years of age Risk factors: Recent trauma or surgery Immunocompromised patients I llicit IV drug use Poor vascular supply Systemic conditions such as diabetes and sickle cells Peripheral neuropathy

CLASSIFICATION Acute within 2 weeks Subacute 2 – 6 weeks Chronic after 6 weeks Incidence of infection increases with increase in grade of open fracture: Type I – II : 2% Type III : 10 – 50% based on duration , mechanism, and host response DURATION

CLASSIFICATION Hematogenous Originated or transported by blood Etiology of 20% of osteomyelitis Vertebrae most common site; and metaphysis of long bone S. aureus is most common organism Contiguous factor Associated with previous surgery, trauma, wounds or poor vascularity Can be bacterial (most common), mycobacterial or fungal in nature Direct inoculation Penetrating injuries Surgical contamination based on duration, mechanism , and host response MECHANISM

CLASSIFICATION based on duration, mechanism, and host response HOST RESPONSE SYSTEMIC LOCAL Malnutrition Vascular compromise Renal failure, hepatic failure Chronic lymphodema Diabetes Extensive scarring Autoimmune disease Radiation fibrosis Malignancy Neuropathy Extreme age Immunosuppression drugs Immunodeficiency Smoking

CIERNY-MADER STAGING Medullary OM Infection confined to medullary cavity Superficial OM Contiguous type of infection. Confined to surface of bone Localized OM Full-thickness cortical sequestration which can easily be removed surgically Diffuse OM Loss of bone stability, even after surgical debridement ANATOMIC PHYSIOLOGIC Stage I: Medullary A. Host, good systemic defense and local vascularity Stage II: Superficial B. Host, good systemic and local compromise Stage III: Localized C. Host, non-candidate for surgery with treatment more problematic than disease process Stage IV: Diffuse

ORGANISM OSTEOMYELITIS ORGANISM TABLE AGE GROUP MOST COMMON ORGANISMS Newborns   (younger than 4 mo ) S. Aureus Enterobacter species Group A & B streptococcus species Children  (aged 4 mo to 4 y) S. Aureus Group A streptococcus species  Kingella kingae Enterobacter species Children, adolescents  (aged 4 y to adult) S. Aureus (80%) Group A streptococcus species  H. Influenzae Enterobacter species Adult S. Aureus  Occasionally Enterobacter or  Streptococcus species Sickle Cell Anemia  Patients S. Aureus is typically most common But Salmonella species is pathognomonic

ACUTE OSTEOMYELITIS Mainly a disease of children Occurs after an episode of bacteremia Trauma may determine the site of infection Possibly by causing small haematoma of fluid collection in the bone Most common organism in both children and adult is Staphyloccocus aureus (70%)

PATHOPHYSIOLOGY Affects metaphyseal region of long bones; femur (27%), tibia (22%), fibula (5%) more than upper extremity Bacteremia is the common event in childhood, consequence of other infections such as otitis media, pharyngitis and sinusitis Its presumed that bacteria gain access to metaphyseal location via nutrient arteries.

PATHOPHYSIOLOGY Staphylococcus aureus : Surface antigen plays key role in bacterial adherence to type 1 collagen and endotoxins that suppress local immune response Glycocalyx : may form around bacteria and enhance adherence to other bacteria and metallic implants

PATHOPHYSIOLOGY CAUSES OF METAPHYSEAL OSTEOMYLITIS Hair pin bend vessels Increased vascularity causes pooling of blood also called as “lake of blood” Immature cells in metaphysis due to high cell turnover Relative lack of phagocytosis Presence of degenerative cartilage cells End arteries in metaphysis Prone for trauma Single endothelial lining in metaphyseal arteries

PATHOPHYSIOLOGY CASCADE OF EVENTS

PATHOPHYSIOLOGY CASCADE OF EVENTS

PATHOPHYSIOLOGY SECOND ROUTE OF SPREAD OF INFECTION THIRD ROUTE OF SPREAD OF INFECTION

PATHOPHYSIOLOGY

CLINICAL FEATURE infant , children and adult INFANT Failure to thrive Metaphyseal tenderness, restricted joint movement CHILDREN Fever (high grade) Child refuse to use limb ( pseudoparalysis ) Local redness, swelling, warmth, odema

CLINICAL FEATURE infant, children and adult ADULT Commonest site is thoracolumbar spine History of urological procedure Followed by mild fever and backache Local tenderness

PHYSICAL EXAMINATION Ill looking Increase temperature and pulse Limb is held still Local redness, swelling and warmth Tenderness at near one of the larger joint Restricted joint movement – pseudoparalysis Edema Lymphadenopathy

INVESTIGATIONS A physical examination may shows bone tenderness and possibly swelling and redness Tests may include: Blood cultures Bone biopsy Bone scan Bone x-ray Full blood count C-reactive protein (CRP) Erythrocyte sedimentation rate (ESR) MRI of the bone Needle aspiration of the area around affected bone

INVESTIGATION BLOOD & FLUID Leukocytosis Elevated CRP & ESR Anti-staphylococcal antibody titre may be elevated Positive fluid or tissue aspiration Blood culture at the peak of fever may yield the causative organism X-RAY Earliest abnormality detected after first week of the onset of symptom Extra cortical outline (periosteal new bone formation at metaphysis)

INVESTIGATION ULTRASONOGRAPHY May detect a sub-periosteal collection of fluid in the early stages But it cannot distinguish between hematoma or pus BONE SCAN (RADIONUCLIDE SCANNING) Technetium – 99 Increased activity in both perfusion and bone phase Highly sensitive investigation even in the very early stages

INVESTIGATION MAGNETIC RESONANCE IMAGING (MRI) Helpful in cases of doubtful diagnosis Best method of demonstrating bone marrow inflammation

MANAGEMENT

TREATMENT Supportive treatment for pain and dehydration Analgesic IV fluid Splintage for comfort and prevent joint contracture Antibiotic therapy Bactericidal drugs are important to: Stop the spread of infection to healthy bone Control acute flares Oral therapy followed by IV route for 10 – 14 days Antibiotics used in treating OM : Amoxicillin Ciprofloxacin plus clindamycin Levofloxacin plus clindamycin Antibiotics is continued for another 6 weeks (min) but usually more than 6 months

TREATMENT Surgical drainage If antibiotics are given early (within first 48 hours) it is often unnecessary But if clinical features do not improve within 36 hours of starting treatment, or even earlier and there is sign of deep pus, drainage is required Debridement of infected tissues WHEN ANTIBIOTICS CAN BE STOPPED? CLINICALLY : Signs of healing, reduction of pain, no fever, can walk, no discharging sinus INFLAMMATORY PARAMETERS : normalizes SERIAL X-RAY : bone healing, no new OM changes

TREATMENT ALGORITHM OF CIERNY – MADER STAGES 3&4 LONG BONE OSTEOMYELITIS

DIFFERENTIAL DIAGNOSIS Rheumatic fever Gradual, poly-joint swelling Ewing’s sarcoma Radiological signs Acute suppurative arthritis Muscle spasm more marked, limited movements, effusions Cellulitis No intense pain Erysipelas Raised red margin

COMPLICATIONS Epiphyseal damage and altered bone growth Suppurative arthritis Metastatic infection Pathological fracture Chronic osteomyelitis