**4. Differential diagnoses**

fracture should be considered [10]. Sternal OM is extremely rare, but has been reported [11]. Neonates are most vulnerable to multifocal infection [12, 13]. **Pathophysiology.** Osteomyelitis in neonates is usually due to hematogenous spread of bacterial infections or less frequently to direct inoculation as a result of a trauma or puncture wounds or surgery, infected cephalo‐ hematoma [14–16]. In preterm infants, direct injection of bacteria can result from heel or veni‐ puncture and artery or vein umbilical catheterization. Indirect contamination from a nearby infection, for example, cellulitis is also possible. Premature rupture of membranes, transpla‐ cental infection, and urinary tract infections has been described as risk factors too [17, 18]. A few cases of neonatal Gram‐negative germ osteoarthritis have been reported, associated with a vesico‐ureteral reflux (VUR) or hydronephrosis by the same microorganism [19, 20]. The most susceptible areas to haematogenous seeding of infection are metaphyseal of long bones, in particular the areas adjacent to the cartilaginous growth plate (physis) that is highly vascu‐ larized with slow intravascular flow. Abscess can result from the passage of bacteria through gaps from the sinusoidal veins to the capillaries into the tissue, where they are provided an ideal environment to grow. These abscesses frequently rupture into the joint [21]. Acute hae‐ matogenous OM and septic arthritis of the adjacent joint coexist in up to 76% of all cases as a result of a unique vascular anatomy characterized by the presence of vascular connections between the metaphysis and the epiphysis, particularly before the appearance of a secondary ossification center. Involvement of the shoulder or hip joints is noted when the intracapsular

metaphyseal end of the humerus or femoral are involved from infection.

Asymmetric movement of extremities, irritability and poor feeding may be often the early and unspecific findings of OM [9, 22]. Common symptoms include bone pain, swelling, red‐ ness, guarding and failure to move the affected body part (pseudoparalysis). Fever may or may not be present because of an immature immune system. It is important to ascertain joint involvement through the detection of pseudoparalysis and pain during passive movements and signs of local inflammation [22]. Dierig et al. [23] reported a newborn with combined OM and suppurative arthritis caused by *Streptococcus pyogenes* giving rise to right brachial plexus palsy. Acute haematogenous OM is usually defined acute if the signs or symptoms are pres‐ ent for less than 14 days, and subacute if signs or symptoms are present for more than 14 days.

The causative agents of OM reflect those of neonatal sepsis, which vary from country to coun‐ try and in many cases remain unknown. The most common pathogen is *Staphylococcus aureus*, found in 70–90% of culture positive cases [24, 25]. Other pathogens include *Streptococcus* mainly group B (*Streptococcus agalactiae*) and Gram‐negative enteric bacteria (*Escherichia coli and Klebsiella pneumoni*a) *Pseudomonas aeruginosa* [26, 27]. Multi‐drug resistant *S. aureus*

**2. Symptoms**

98 Selected Topics in Neonatal Care

In neonates, acute forms predominate [1].

**3. Causative microorganisms**

Differential diagnosis may be difficult and cellulitis, septic arthritis, subcutaneous abscess, fractures, and bone tumors should be taken into account. CNS disease (cerebral hemorrhage), trauma, scurvy, and child abuse are to be considered in the case of pseudoparalysis. Allagui et al. [29] described a case of acute OM of the clavicle in a 30‐day‐old newborn, with clinical symptoms simulating obstetric brachial plexus palsy. Laboratory tests are necessary to con‐ firm a clinical diagnosis of OM. Neonates with OM may have a normal leukocyte count that is elevated in only half of the patients with or without thrombocytosis. The C‐reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are almost always elevated (except in small bone infections). It is important to obtain blood, bone, or joint aspirate cultures if necessary, to identify the causative organism, before any antibiotics are given. Because OM usually is a consequence of sepsis, hence lumbar puncture should be considered. Any potential source of infection should be examined, including intravascular catheter tips. Serum procalcitonin may be used as a sensitive and specific marker in the diagnosis of acute OM [30] more suitable as an aid for rule‐in diagnosis rather than for exclusion. Its diagnostic performance is better for a lower cut‐off value compared to a conventional cut‐off of 0.5 ng/ml which is specific but less sensitive [31]. A bone biopsy is advisable if the patient does not respond to the standard therapy.
