Food refusal in toddlers with chronic diseases.

Feeding refusal in children means a lack of appetite and falls under the rubric of feeding disorders. The factors that affect appetite in infants and children are poorly understood, although the control center for appetite clearly resides in the hunger and satiety centers in the hypothalamus. Hunger results from the integration of a variety of sensory inputs (taste, smell, and vision), limbic and cortical modulators (mood or affect), and visceral feedback (nociceptive stimuli, gastric volume and distention, substrates, and hormonal effects). Feeding disorders may affect normal children as well as those with medical or developmental problems. The estimated prevalence of feeding disorders in the pediatric population ranges from 25–35% in normal children, to 33–90% in children who suffer from developmental delay (1–3). Inability to feed interferes with normal childhood psychosocial development. To provide appropriate and effective therapy, we must understand the underlying pathophysiology of feeding disorders. In this issue of the Journal of Pediatric Gastroenterology and Nutrition, Zangen et al. investigate motility and gastric sensory activity in 14 children with a lifelong history of food aversion and retching or vomiting and they describe a multidisciplinary treatment program for these patients. They were able to delineate upper gastrointestinal (GI) motor and/or sensory disorders in all 14 children, and they demonstrated improvement in symptoms, quality of life, or advancement toward oral feeding in most patients. All 14 patients had a long history of food refusal associated with retching or vomiting, which had persisted even after maximal medical therapy (cisapride, H2 antagonists, and proton pump inhibitors) followed by surgery. In fact, all 14 children had received one fundoplication, and one had received two. Three children were affected by chronic medical illnesses, while the other 11 had cerebral palsy. The causes of food refusal in these children are obviously multifactorial. They include motility disorders in children with chronic illness, malnutrition and its effects on GI motility, and dysphoric caretaker-child interactions at mealtime. Even the permanent structural and functional changes that occur with fundoplication may contribute to the persistence of symptoms. Fundoplication is widely accepted as the treatment of choice for children who fail medical management of gastroesophageal reflux (GER) associated diseases (4). However, the incidence of persistent or worsening symptoms after antireflux surgery is as high as 50% in some series (5–6) Post-fundoplication problems are more common in certain categories of children, such as those with neurologic diseases, or a more generalized GI motility disorder (7). These children have challenging physiologic problems that make it difficult for any intervention to be successful. Several reports describe diffuse GI motility abnormalities after fundoplication in children with neurologic impairment. Although motility is not usually evaluated preoperatively, many experts believe that abnormal motility is present before surgery and not caused by it. In these patients, fundoplication merely worsens other aspects of the motility disorder. Gut motor function depends on the coordinated contractions of smooth muscle cells, controlled by the central nervous system (CNS), but more immediately, by the enteric nervous system (ENS). The ENS consists of approximately 100 million neurons organized throughout the GI tract into myenteric and submucosal ganglionated plexi. These plexi discharge both inhibitory and excitatory impulses that play essential roles in the production of the migrating motor complex (MMC) and peristaltic waves. Also present in the ENS are the interstitial cells of Cajal, thought to serve as pacemakers. The ENS mediates afferent activity as well: visceral sensation travels along A-delta fibers (which respond to short, sharp stimuli) and polymodal unmyelinated C fibers (which respond to more prolonged stimuli). The latter nerves mediate pain as well as the autonomic and emotional responses that are commonly noted in patients with functional GI diseases (8). Received May 16, 2003; accepted May 26, 2003. Address correspondence to: Annamaria Staiano, Dept of Pediatrics, University Federico II, Via S. Pansini, 5, 80131 NaplesItaly (e-mail: staiano@unina.it). Journal of Pediatric Gastroenterology and Nutrition 37:225–227 © September 2003 Lippincott Williams & Wilkins, Inc., Philadelphia