Objective: To report an outbreak of Burkholderia (B.) cepacia related to contaminated surface cleaner in the pediatric ward of a tertiary hospital in Turkey. Methods: This study retrospectively reported the outbreak occurred between January 16, 2018 and January 23, 2018. Twelve immunocompetent patients who developed a bloodstream infection a few days after the hospitalization and who were positive for B. cepacia were included. Environmental samples were collected from various areas in the hospital to find the source of the outbreak. Results: All patients had clinical and biochemical evidence of sepsis. None of the patients had an underlying disease or had a central venous catheter as a risk factor. B. cepacia was isolated from the samples taken from the surface cleaners. The antibiotic susceptibilities of B. cepacia isolates were identical in the surface cleaners with the isolates from the patients' blood cultures. The outbreak was controlled after removing the surface cleaners from use. None of the infected patients died during the outbreak. Conclusions: Nosocomial B. cepacia outbreak may occur in immunocompetent children as well. Rapid identification of the outbreak, defining the source and taking appropriate measures to control the outbreak are the key points in the management.

Intracranial hypotension is a clinical syndrome characterized by orthostatic headache and low cerebrospinal fluid pressure. Noninvasive management is the usual first line treatment. Epidural blood patch is the treatment of choice if noninvasive treatments are ineffective. Cases with rebound intracranial hypertension after epidural blood patch treatment have been reported in the medical literature previously. We report here three patients with rebound intracranial hypertension who were treated noninvasively for intracranial hypotension. This phenomenon has not been reported previously. The underlying cause of intracranial hypotension was epidural anesthesia in the first, lumbar disc surgery in the second patient, and idiopathic in the third patient. They had been treated either with bed rest or with medical treatment not requiring epidural blood patch. After a short remission the patients were seen with a different headache pattern. They all had papilledema on examination. Automated perimetry revealed bilateral blind spot enlargement in Patient 1 and peripheral constriction in Patient 2. Cranial MRI and MRV in all three patients were normal. All the patients recovered very quickly with acetazolamide 1.5 or 2gm/day. In conclusion, rebound intracranial hypertension should be kept in mind in patients with intracranial hypotension who developed changes in the headache pattern, had new symptoms of nausea, vomiting, blurred or double vision during follow-up. Rebound intracranial hypertension can develop after conservative treatment of intracranial hypotension.