[Esophageal rupture with aortic-esophageal fistula due to ingestion of foil packaged drugs]. / Oesofagusruptuur met aorto-oesofageale fistel door ingestie van medicatieverpakking.

A 78-year-old man was admitted because of haematemesis. A week before, the patient was admitted for prostate resection. During that admission he ingested an analgesic tablet complete with foil packaging. Since then, he suffered from dysphagia. Endoscopic examination revealed the foil packaging, but during the procedure massive bleeding in the oesophagus occurred. Despite initial haemodynamic stabilisation, fatal bleeding occurred a short while later. Post mortem examination revealed an aortic-oesophageal fistula which was ascribed to the foil packaging. One other oesophageal rupture was thought to be due to the packaging and a third rupture was ascribed to the inserted Sengstaken-Blakemore tube. Ingestion of a foil packaging warrants active medical intervention, as is stated elsewhere in the literature.

Small intestinal motor abnormalities in patients with functional dyspepsia demonstrated by ambulatory manometry.

AIMS/METHODS: In 30 patients with functional dyspepsia and in 20 healthy volunteers, ambulatory duodenojejunal manometry was performed to examine the interdigestive and postprandial small intestinal motility patterns in relation to symptoms. RESULTS: In the fasting state, the number of migrating motor complex cycles mean (SEM) was significantly lower in patients, especially in patients with dysmotility-like dyspepsia, than in control subjects (3.8 (0.4), 2.6 (0.5), and 5.3 (0.7) cycles, respectively; p < 0.05), due to a longer duration of phase II. Non-propagated and retrogradely propagated phase III activity was more prevalent in patients than in control subjects (48% v 15%; p = 0.020). During phase II and after dinner no differences were found in contraction incidence, mean amplitude or motility index. However, 1 1/2 hours after completing breakfast the motility index was higher in patients at all three recording levels (p < 0.05). Burst activity was more prevalent in patients than in control subjects (22% v 6% of the subjects; p = 0.003). In 41% of the patients the symptom index was > 75%. CONCLUSIONS: These results suggest that small intestinal motor abnormalities, especially during fasting, participate in the pathogenesis of symptoms in patients with functional dyspepsia. Ambulatory manometry of the small intestine is a valuable tool to demonstrate these abnormalities in outpatients pursuing their daily activities.

Gastric myoelectrical activity and gastrointestinal motility in patients with functional dyspepsia.

The aim of our study was to examine the prevalence of gastric myoelectrical disturbances in relation to gastrointestinal motility abnormalities in patients with functional dyspepsia, using simultaneous electrogastrography and antroduodenojejunal manometry. We carried out electrogastrography in 20 patients with functional dyspepsia and in 20 healthy volunteers. In 10 of these patients and in 10 of the volunteers antroduodenojejunal manometry was performed simultaneously. Apart from a higher postprandial power content of the 3 cycles per minute (cpm) component in the patients (1263 +/- 317 and 393 +/- 101 microV2, respectively; P = 0.016), no differences in the electrogastrographic variables were found between the groups. In the manometric part of the study, postprandial antral hypoactivity was not a prominent finding. Instead, small intestinal hyperactivity was found in the dyspeptic patients, with both a higher frequency and amplitude of the contractions (P < 0.05). This hyperactivity often consisted of bursts, which were significantly more frequent in patients than in control subjects (total duration of burst activity 25.6 +/- 6.4 and 6.0 +/- 1.7 min, respectively; P = 0.013). A positive correlation was found between the frequency of the gastric electrical control activity and the antral contraction frequency (P = 0.006), between the power content of the electrographic signal and the antral contraction amplitude (P = 0.025), and between the postprandial/fasting electrographic power ratio and the antral motility index (P = 0.007). In conclusion, gastric myoelectrical activity is minimally disturbed in patients with functional dyspepsia. Motor abnormalities, especially small intestinal hyperactivity, are more likely to play a prominent role in the genesis of dyspeptic symptoms.

Role of electrogastrography and gastric impedance measurements in evaluation of gastric emptying and motility.

Electrogastrography records electrical potential variations brought about by myoelectrical activity of the stomach. Abnormal myoelectrical rhythms such as tachygastrias may also be detected. Electrogastrography provides little information on gastric motility and emptying. Impedance epigastrography is a technique that uses changes in epigastric impedance to evaluate gastric emptying of large-volume liquid meals. The results are inferior to those of tomographic impedance imaging. Phasic antral contractions may lead to phasic impedance changes recorded with nonimaging techniques and a phasic signal recorded with high-speed electrical impedance tomography. However, the relationship between phasic contractions and phasic variations in impedance do not appear consistent enough to allow clinical application of the technique.

Gastric myoelectrical activity in patients with type I diabetes mellitus and autonomic neuropathy.

In patients with diabetes mellitus and gastroparesis, dysrhythmias of gastric myoelectrical activity, especially tachygastrias, are thought to be involved in the pathogenesis of dyspeptic symptoms. Using surface electrogastrography we studied the prevalence of these abnormalities, and their relationships to dyspeptic symptoms and the extent of cardiac autonomic neuropathy in 30 euglycemic patients with type I diabetes mellitus and 12 controls. Neither in the fasting nor in the postprandial state were differences in mean frequency of gastric electrical control activity and its variability found between patients and controls. In the fasting state, the power content of the 3 cpm component in the power spectrum of the electrogastrogram was even higher in patients than in controls (P = 0.049). In the fasting state, second harmonics of the 3 cpm fundamental gastric signal were seen more often in patients than in controls (P = 0.03). In patients with symptoms during the study, no second harmonics were found after the meal. The postprandial/fasting power ratio was decreased in patients with symptoms during the study as compared to patients without symptoms and controls (P < 0.05). The incidence of dysrhythmias, such as tachygastrias and bradygastrias, was not higher in patients than in controls (17% and 8%, respectively). No correlation was found between electrogastrographic parameters and the severity of autonomic neuropathy or dyspeptic symptoms scored before the study. In conclusion, this study has shown that patients with type I diabetes mellitus and autonomic neuropathy studied under euglycemic conditions do not have grossly disturbed myoelectrical activity, except when symptomatic during the study.

Relationships between dyspeptic symptoms and gastrointestinal motility in patients with type 1 (insulin-dependent) diabetes mellitus.

Reports on motor abnormalities in Type 1 (insulin-dependent) diabetes mellitus are inconsistent. In 20 Type 1 diabetic patients and in 11 control subjects antroduodenojejunal manometry was performed under euglycaemic conditions in order to examine the prevalence of gastric and small intestinal motor abnormalities in relation to dyspeptic symptoms and the degree of cardiac autonomic neuropathy. In diabetic patients compared to control subjects phase III (regular, high-amplitude contractile activity at maximal frequency) involved the gastric antrum less often (12 vs 35%, p < 0.05), the duration of phase I (motor quiescence) was shorter (6 +/- 1 vs 21 +/- 4 min, p < 0.002) and in phase II (irregular motor activity) the frequency of duodenal and jejunal contractions was higher. After a meal the duration of the fed state was shorter in diabetic patients with symptoms during the study than in diabetic patients without symptoms and than in control subjects (57 +/- 27 vs 157 +/- 11 and 140 +/- 13 min, p < 0.02). Postprandial antral hypomotility was seen in diabetic patients with symptoms only in the first 30 min after the meal. One hour after the meal the frequency of duodenal and jejunal contractions was again higher in diabetic patients. In diabetic patients compared to control subjects more burst activity (clusters of non-propagated high-amplitude contractile activity at maximal frequency) was seen (7.9 +/- 1.6 vs 0.8 +/- 0.5% of the total time of study, p < 0.002). No correlation was found between manometric parameters and the degree of cardiac autonomic neuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

[Ranitidine therapeutically effective in functional dyspepsia with reflux-like symptoms]. / Ranitidine vooral werkzaam bij functionele dyspepsie met klachten passend bij refluxziekten.

OBJECTIVE: To investigate the effect of ranitidine in patients with functional dyspepsia according to different subgroups. SETTING: University Hospital Utrecht, department of gastroenterology. DESIGN: Prospective double blind cross-over study. METHOD: Thirty patients with chronic upper abdominal symptoms were included, without somatic cause was found at gastroscopy (no Helicobacter pylori), ultrasonography and blood tests. The mean symptom score of: nausea, vomiting, retrosternal pain, epigastric pain, heartburn, bloating, belching, and early satiety was > or = 2. The patients recorded severity and frequency of the symptoms in a diary. The same diary was used to score the symptoms during treatment with ranitidine (2 dd 150 mg) or placebo, each for 2 weeks with a wash out period of 3 days. 29 patients scored correctly. RESULTS: 13 (43%) patients had dysmotility-like dyspepsia, 5 (17%) reflux-like dyspepsia, and 11 (40%) non-specific dyspepsia (i.e. a combination of dysmotility-like, reflux-like or ulcer-like symptoms). Ranitidine significantly improved the severity of heartburn after two weeks of treatment, as compared to placebo (p = 0.035), notably in the patients with reflux-like dyspepsia. Because of a carry-over effect analysis of the symptoms 'belching' and 'early satiety' was not possible. CONCLUSION: Within the group of patients with functional dyspepsia a subgroup of reflux-like dyspepsia patients can be identified that responds well to ranitidine.

Pathophysiology and treatment of functional dyspepsia.

Functional dyspepsia (or 'non-ulcer') is usually defined as chronic or intermittent upper abdominal symptoms for which no organic cause can be found. Division of functional dyspepsia into subgroups such as reflux-like, ulcer-like, dysmotility-like and non-specific dyspepsia has been proposed, but lacks a scientific basis. Gastric acid hypersecretion, Helicobacter pylori-associated gastritis, gastric and small intestinal motor disorders, psychological and neurohormonal factors all might play a role in the pathogenesis. The heterogeneity of the underlying abnormalities makes it unlikely that one single treatment modality will ever be beneficial to all patients. In general practice, a therapeutic trial, with either a prokinetic or an acid secretion inhibiting drug, is usually carried out before diagnostic procedures are performed to exclude organic abnormalities. In the choice of the initial therapy, some guidance can be derived from the prominent symptoms. In a study in 30 H. pylori-negative patients with functional dyspepsia ranitidine (150 mg bid) significantly reduced the severity of heartburn. The effect was most pronounced in patients of the reflux-like subgroup.