Hematogenous Osteomyelitis

my project for 7th semester of MBBS.

1. Hematogenous osteomyelitis Clinical surgery Submitted by- Anubhuti Dave

2. definition Osteomyelitis is inflammation of the bone and bone marrow generally caused by a bacterial infection. The most common form in childhood is acute hematogenous osteomyelitis (AHO), which is infection of the bone of less than two weeks duration spread hematogenously .

3. epidemiology Frequency United States The exact frequency is unknown as osteomyelitis is not a reportable disease. International Chronic osteomyelitis is frequently reported in developing countries where medical and surgical treatment modalities are not commonly accessible. Mortality/Morbidity As noted in recent studies, patients may develop deep vein thrombosis and fractures.  [1, 2, 3, 4] Race Few studies have commented on race differences. Sex A preponderance in males is observed in all age groups. Factors related to increased incidence in males may include increased trauma due to risk-taking behavior or other physical activities that predispose to bone injury. Age One half of cases occur in preschool-aged children.

4. etiology Acute hematogenous osteomyelitis typically arises in the metaphysis of long tubular bones, with approximately twothirds of all cases involving the femur, tibia or humerus . While a variety of bacterial pathogens may be involved, Staphylococcus aureus is the pre-eminent pathogen and is responsible for 70–90% of acute hematogenous osteomyelitis infections in children. Other etiological agents, in no particular order, include Streptococcus pyogenes, Streptococcus pneumoniae, Group B streptococci, coagulasenegative staphylococci, Kingella kingae , enteric Gram-negative bacilli and anaerobic bacteria.

5. pathophysiology Young children primarily experience acute hematogenous osteomyelitis due to the rich vascular supply in their growing bones. Circulating organisms tend to start the infection in the metaphyseal ends of the long bones because of the sluggish circulation in the metaphyseal capillary loops. The presence of vascular connections between the metaphysis and the epiphysis make infants particularly prone to  arthritis  of the adjacent joint. Involvement of the shoulder joint or hip joint is also noted when the intracapsular metaphyseal end of the humerus or femoral is infected. If untreated, infection can also spread to the subperiosteal space after traversing the cortex.

6. pathogenesis In the metaphysis, nutrient arteries branch into non-anastomosing capillaries under the physis  make a sharp loop before entering venous sinusoids draining into the marrow ( Hair-pin Ends) Blood flow, sluggish and provides an ideal environment for bacterial seeding Relative paucity of phagocytic cells in this area

7. Pathogenesis- In neonates and young infants Transphyseal blood vessels connect the metaphysis and epiphysis commonly pus from the metaphysis enters the joint space Result in abnormal growth and bone or joint deformity Joint involvement takes place when the metaphysis is intra- articular as in hip, ankle, shoulder, and elbow joint or when sub-periosteal pus ruptures into the joint space

8. Pathogenesis- In child >18 months age Spread through the cortex. Porous metaphyseal cortex provides easy assess for the exit of exuate or pus Elevates the periosteum (thick periosteum loosly adherent to the cortex) Subperiosteal pus collection(further impairing blood supply to the cortex and metaphysis) Enough periosteal destruction → soft tissue abcess .

9. Pathogenesis …In later childhood and adolescence The growth plate closes, hematogenous osteomyelitis more often begins in the diaphysis and can spread to the entire intramedullary canal. Closed plate is relatively resistant to spread of infection. The periosteum becomes more adherent, favoring pus to decompress through the periosteum The fluid formed seeks the path of least resistance from the metaphysis

10. Clinical Features… Signs and symptoms Older infants and children are more likely to have fever, pain, and localizing signs such as edema, erythema, and warmth With involvement of the lower extremities, limp or refusal to walk Careful Physical examination may reveal focal bony tenderness.

11. Diagnosis Children with acute bone pain and systemic signs of sepsis should be considered to have acute hematogenous Osteomyelitis until proved otherwise . Diagnosis may be established if a patient fulfills two of the following criteria: Bone aspiration yield pus Bacterial culture of bone or blood positive Presence of the classical s/s of acute osteomyelitis Radiographic changes typical for osteomyelitis.

12. LABORATORY FINDINGS No specific laboratory tests. Elevations in peripheral WBC, ESR, and CRP – ESR-Nonspecific acute phase reactant Increased 48-72 hrs Increased in 90% of cases Not affected by antibiotic tx CRP- Increased in 98% of cases Blood culture- Positive in 30-50% Decreased with antibiotic 48 hours to get most organisms

13. Radiology Plain x-ray Sensitivity 43-75% Specificity 75-83% Soft tissue swelling 48hrs Periosteal reaction 5-7days Osteolysis 7-14 days of infection(need 30-50% bone loss) Magnetic Resonance Imaging (MRI) Computed Tomography (CT) Radionuclide Study

14. Bone Aspiration A bacteriologic diagnosis is made by culturing the involved bone or pus, once a clinical diagnosis of acute osteomyelitis is established. Useful to determine whether an abscess is present. The organism detection rate is increased to 75% to 80% by aspiration of the affected bone K. kingae may need to be identified by polymerase chain reaction Also useful in determining the future course of therapy of the child

15. treatment Antibiotics In NEONATES -I.V antibiotics Oxacillin or nafcillin (150 – 200 mg/kg/24 hrs in q6h IV) + BSA like Cephotaxime (150-225 mg/kg/24  hr divided q8h IV) provide coverage for the S. aureus, group B streptococcus, and gram-negative bacilli. If MRSA suspected  vancomycin is substituted for nafcillin In Neonate with Central Line , the possibility of nosocomial bacteria ( Pseudomonas ) or fungi (Candida) In older infants and children, the principal pathogens - S. aureus and streptococcus . Adjust according to culture reports.

16. IV to Oral Changing antibiotics from the IV route to oral administration when a patient's condition clearly has improved and the child is afebrile for ≥48-72  hr , may be considered. β-lactam drugs for susceptible staphylococcal or streptococcal infection  cephalexin Oral clindamycin in clindamycin-susceptible CA-MRSA or for patients who are seriously allergic or cannot tolerate β-lactam antibiotics.

17. Indication of Surgical Treatment Abscess collection ( Sub-periosteal , soft tissue, or intramedullary) Patient is not responding to appropriate antibiotic therapy after a negative bone aspiration (If a child with acute hematogenous osteomyelitis does not show symptomatic improvement with decrease in swelling and tenderness after 36-48 hrs of appropriate antibiotic treatment, the bone should be aspirated again and consideration given to surgical drainage) In subacute Osteomyelitis when debridement is necessary (granulation tissue within the cavity even though no pus) Radiographic lesion, sequestrum

18. prognosis Improvement in signs and symptoms is rapid when timely intervened. Failure to improve or worsening by 72  hr requires review of antibiotic therapy, the need for surgical intervention, or the correctness of the diagnosis. Recurrence of disease and development of chronic infection after treatment occur in <10% of patients.