P2A353: Encephalopathy: An Unusual Presentation of MRSA Osteomyelitis and Sepsis

Introduction: Sepsis-associated encephalopathy (SAE) is diffuse brain dysfunction that occurs secondary to an infection not directly in the CNS and is an unusual presentation of sepsis. We present a case of SAE caused by methicillin-resistant Staphylococcus aureus (MRSA) osteomyelitis and sepsis.

Case Description: A 15-year-old female volleyball player presented with 2 days of fatigability that progressed to decreased alertness and monosyllabic speech. Within the week of presentation patient was treated for left lower extremity tendonitis. On admission, patient was febrile and tachycardic. Physical examination remarkable for an obtunded female and mild edema of left knee. Laboratory investigations showed: leukocytosis, anemia, thrombocytopenia, hyponatremia, elevated creatinine, transaminitis, raised creatinine kinase and inflammatory markers. Knee radiograph was normal. Chest radiograph had findings suggestive of embolic phenomenon and venous Doppler ultrasound of left lower extremity showed non-occlusive thrombus in the left common femoral vein. Imaging of the brain and neck along with cerebrospinal fluid studies, video EEG and echocardiogram with bubble study were normal. MRI of the lower extremity demonstrated left distal femur osteomyelitis with subperiosteal abscess and surrounding myositis (Fig. 1). Blood culture and tissue sample from incision and drainage grew MRSA. The patient was treated with ceftaroline and clindamycin. Lovenox was administered to treat the deep vein thrombosis. The patient was managed in the pediatric intensive care unit for septic shock with SAE and subsequently discharged to inpatient rehabilitation.
The patient was discharged home after a 1-month hospital course to complete 6-weeks of IV antibiotics with continued outpatient rehabilitation due to impairment in cognitive perceptual skills.

Discussion: SAE is an unusual diagnosis in children. It manifests with alteration in mental status that ranges in severity from confusion to coma without an alternative underlying explanation beyond sepsis. It is hypothesized that inflammatory cytokines contribute to microscopic brain injury, impaired blood-brain barrier, mitochondrial dysfunction and altered neurotransmission and cerebral metabolism. The treatment is supportive as for any patient with sepsis, with a focus on maintaining end–organ perfusion, oxygenation and timely reversal of shock. In this case the patient presented with encephalopathy prior to the onset of fever. Evaluation excluded: primary CNS infection, endocarditis, paradoxical embolism, seizure, ingestion and Macrophage Activation Syndrome which was considered due to the marked hyperinflammatory state. Elevated muscle enzyme raised suspicion for necrotizing fasciitis, a surgical emergency, leading to urgent MRI which established the presence of osteomyelitis with subperiosteal abscess. Rapid source control was achieved through surgical drainage which along with early rehabilitation may have contributed to a favorable patient outcome.

Conclusion: SAE though uncommon may be the first sign of evolving sepsis. Serious bacterial infection is a differential diagnosis to be considered in any patient presenting with altered mental status. The management focuses on treatment of infection, supportive care and rehabilitation.