Esophageal perforation after placement of wireless Bravo pH probe.
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Biomedical subjects
Publications and source records attributed to Noel R Fajardo.
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Functional dyspepsia (FD) refers to unexplained pain or discomfort in the upper abdomen and is commonly seen in gastroenterology practice. The underlying pathophysiologic mechanisms associated with FD are unclear, although traditionally, delayed gastric emptying, visceral hypersensitivity to acid or mechanical distention, and impaired gastric accommodation have been implicated as putative physiologic disturbances. It also remains uncertain whether FD and irritable bowel syndrome are different presentations of the same disorder. Recent data on pathophysiologic mechanisms of FD have focused on postprandial motor disturbances (accelerated gastric emptying, antral-fundic incoordination, and abnormal phasic contractions), alterations of neurohormonal mechanisms in response to a meal, and previous acute infection. Pharmacologic therapies for FD may be guided by these novel mechanisms, as current available therapeutic options are limited. Novel prokinetics and gastric accommodation modulators, visceral analgesics, and agents targeting the neurohormonal response to food ingestion are the next therapeutic frontiers in FD. This review summarizes traditional knowledge and more recent advances in the pathophysiology of FD and potential therapeutic opportunities.
OBJECTIVES: In persons with spinal cord injury (SCI), several studies have shown that large bowel transit is decreased at the level of the left colon and rectum, and that postprandial colonic response to food is absent. To define these parameters further, the effects of food on colonic motility in persons with SCI were studied and compared to those of spinally intact (SI) individuals. METHODS: The study was conducted in eight subjects with SCI (four paraplegic and four quadriplegic) and six age-matched SI subjects. After routine bowel preparation, colonoscopy was performed with the proximal end of a solid state pressure transducer catheter (four sensors each separated by 10 cm) tethered to the splenic flexure using endoclips (Olympus). The subjects were then allowed to carry out their usual daily activities. Two phases were compared: 1 h before breakfast, designated as the "resting phase," and 1 h during breakfast, designated as the "food-ingestion phase." RESULTS: Baseline colonic activity of the SCI group was significantly less than in SI subjects. During meals, the motility index, mean amplitude of the waves, percent activity, and number of waves was significantly less in the SCI group. In both the SI and SCI groups, a postprandial colonic response was observed. However, in the SCI group, the response was seen only in the descending colon and not in the rectosigmoid region. CONCLUSIONS: SCI decreases colonic motility, and this alteration may relate to difficulty with evacuation. The postprandial colonic response in SCI is present but is suboptimal and confined to the descending colon.
Difficulty with evacuation (DWE) is common in individuals with spinal cord injury (SCI). Numerous studies have concluded that constipation, impaction, and incontinence cause significant morbidity and, collectively, constitute an important quality-of-life issue in individuals with SCI. Colonic motor activity was assessed using a solid-state manometry probe. We report here that colonic pressure activity is depressed during sleep compared to that observed in able-bodied controls. In addition, pressure activity was decreased during sleep compared to pre-sleep and post-sleep. We suspect that this may contribute to delayed colon transit time after SCI. In addition, since contraction of the abdominal wall musculature plays a role in normal defecation, we assessed whether an abdominal belt with implanted electrodes would improve DWE. In this respect, we demonstrated that neuromuscular stimulation of the abdominal wall improves a number of indices of defecatory function, including time to first stool and total bowel care time.