Peritonitis following percutaneous gastrostomy tube insertions in children.

BACKGROUND: Percutaneous retrograde gastrostomy has a high success rate, low morbidity, and can be performed under different levels of sedation or local anesthesia in children. Despite its favourable safety profile, major complications can occur. Few studies have examined peritonitis following percutaneous retrograde gastrostomy in children. OBJECTIVE: To identify potential risk factors and variables influencing the development and early diagnosis of peritonitis following percutaneous retrograde gastrostomy. MATERIALS AND METHODS: We conducted a retrospective case-control study of children who developed peritonitis within 7 days of percutaneous retrograde gastrostomy between 2003 and 2012. From the 1,504 patients who underwent percutaneous retrograde gastrostomy, patients who developed peritonitis (group 1) were matched by closest date of procedure to those without peritonitis (group 2). Peritonitis was defined according to recognized clinical criteria. Demographic, clinical, procedural, management and outcomes data were collected. RESULTS: Thirty-eight of 1,504 children (2.5%; 95% confidence interval, 1.8-3.5) who underwent percutaneous retrograde gastrostomy developed peritonitis ≤7 days post procedure (group 1). Fever (89%), irritability (63%) and abdominal pain (55%) occurred on presentation of peritonitis. Group 1 patients were all treated with antibiotics; 41% underwent additional interventions: tube readjustments (8%), aspiration of pneumoperitoneum (23%), laparotomy (10%) and intensive care unit admission (10%). In group 1, enteral feeds started on average 3 days later and patients were discharged 5 days later than patients in group 2. There were two deaths not directly related to peritonitis. Neither age, gender, weight, underlying diagnoses nor operator was identified as a risk factor. CONCLUSION: Peritonitis following percutaneous retrograde gastrostomy in children occurs in approximately 2.5% of cases. No risk factors for its development were identified. Medical management is usually sufficient for a good outcome. Patients with peritonitis are delayed starting feeds and have a hospital stay that is an average of 5 days longer than those without.

Modulation of the carotid body sensory discharge by NO: an up-dated hypothesis.

The carotid body (CB) is a peripheral chemoreceptor organ that initiates compensatory reflex responses so as to maintain gas homeostasis. Stimuli such as low oxygen (hypoxia) and high CO(2)/H(+) (acid hypercapnia) cause an increase in 'afferent' sensory discharge that is relayed via the carotid sinus nerve (CSN) to the brainstem, resulting in corrective changes in ventilation. A parallel autonomic pathway has been recognized for >40 years as the source of 'efferent' inhibition of the CB sensory discharge and, more recently, nitric oxide (NO) has been identified as the key mediator. This review will examine our current understanding of the role of nNOS-positive autonomic neurons, embedded in 'paraganglia' within the glossopharyngeal (GPN) and CSN nerves, in mediating efferent CB chemoreceptor inhibition. We highlight recent data linking the actions of hypoxia, ACh and ATP to NO synthesis/release from GPN neurons. Finally, we consider the novel hypothesis that pannexin-1 channels present in GPN neurons may play a role in NO signaling during hypoxia.