1. Hematogenous osteomyelitis is a bacterial infection of the bone that most commonly affects the metaphysis of long bones in children. Staphylococcus aureus is the primary cause in 70-90% of cases. 2. Infection typically begins in the vascular metaphyseal region of bones and can spread to the joint space in young children. Symptoms include fever, bone pain, and local swelling. Diagnosis involves blood tests, imaging, and bone aspiration to confirm bacteria. 3. Treatment involves IV antibiotics targeting S. aureus for 2-4 weeks, followed by oral antibiotics if the child improves. Surgery to drain abscesses may be needed

1. HEMATOGENOUS
OSTEOMYELITIS
CLINICAL SURGERY
SUBMITTED BY- ANUBHUTI DAVE

4. 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.

5. 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.

6. 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.

7. 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.

8. 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

9. 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

10. 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.

11. 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

12. 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.

13. 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:
1. Bone aspiration yield pus
2. Bacterial culture of bone or blood positive
3. Presence of the classical s/s of acute osteomyelitis
4. Radiographic changes typical for osteomyelitis.

14. 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

15. 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

16. 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

17. 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.

18. 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.

19. 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

20. 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.