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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric ulceration after fundoplication for gastroesophageal reflux is relatively uncommon, occurring in 1% to 3% of cases. During the period 1974 to 1979, approximately 100 modified Belsey fundoplications were performed at McMaster University Medical Centre. In four patients gastric ulceration developed after the surgery. In all cases the ulcers were located in the proximal stomach, an unusual site. Published reports of gastric ulceration after fundoplication were reviewed, special attention being given to the cause. The authors conclude that local ischemia and mechanical trauma are important in the development of ulceration, which can occur as early as one week after fundoplication. The detection of ulcers requires awareness of the condition and special attention to the symptoms. Because the gastric anatomy is altered by the fundal wrap, the area can be visualized more easily by double-contrast barium studies than by endoscopy.
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PMID:Gastric ulceration after fundoplication. 173 87

Nissen's fundal plication is acknowledged as the most effective procedure to suppress gastroesophageal reflux. It entails some morbidity (dysphagia, gas bloat syndrome), in which obstruction is the least frequently evoked but most severe risk. We report about 6 cases (4 children and 2 adults). The 4 children had been operated 3 times during the first few months of life, and their reflux was secondary to the cure of atresia of the esophagus in 2 cases, and caused severe apneas in 1 case, a former premature infant. In three cases, the obstruction was complicated within a few hours by intestinal ischemia causing death. In one case, the emergent insertion of a gastric tube allowed the decompression of the digestive tract and second surgery; the obstruction recurred 2 months later, with no postoperative complications. Two adults (aged 64 and 66) presented with gastric perforation 7 days and 9 months after fundal pliction; one of them died. These cases show how serious these obstructions are (4 deaths/6 cases). The emergent measure in such cases consists of inserting a gastric tube, although which may be impossible (1 case). The patients and their parents must be informed of this risk of complication and of its expressions. Prevention is based on a strictly submesocolic surgical approach, without any exposure of the small bowel.
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PMID:[Intestinal obstruction after Nissen's fundo-plication]. 180 60

We studied 30 patients. 20 were males and 10 females. Mean age was 48 year old. Esophageal disease was not present neither gastro-esophageal reflux. Biopsy was taken between 24 hours and 25 days after nasogastric tube (NG) was put into place. Endoscopic findings were: hyperemic mucosa, submucosal hemorrhage, clots, erosions and ulcers near Esophago-gastric junction. Intraepithelial edema, vessel congestion, polymorphonuclear infiltration, fibrin thrombosis of submucosal vessels, ischemia, epithelial regeneration and ulcer were common histologic findings. All endoscopic and histologic alterations were related to the length of time of NG tube contact with the esophageal mucosa. We concluded that NG tube damages the esophageal mucosa by two mechanisms: a) Local irritation that favors b) gastric reflux by decreasing lower esophageal sphincter pressure.
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PMID:[Effect of nasogastric tube on esophageal mucosa]. 184 45

Angina-like chest pain, caused by alterations of esophageal function, is an increasingly common occurrence confronting cardiologists: advances in pathogenetic knowledge and in diagnostic possibilities in this field have in fact shed light on the prevalence of esophageal angina, which is present in approximately 60% of patients with angiographically intact coronaries (11% of anginal patients overall). Classically, esophageal chest pain is attributed to alterations of motility or to mucosal disease (pathologic gastro-esophageal reflux of the acid, mixed or alkaline type): this last cause prevails quantitatively. Little is known of the nociceptive mechanisms triggered by these alterations: as far as mucous disease is concerned, activation of the chemosensitive receptors has been postulated, while esophageal mechanoreceptors may be activated, in the course of a motor disorder, by distension of the wall. A recently proposed additional mechanism consists in the induction of parietal esophageal ischemia by chemical or mechanical injury: it is a fascinating and potentially resolvable mechanism, which however requires further investigation. Moreover, elements of psychological nature are also involved in the genesis of esophageal pain. A diagnosis of esophageal angina, heavily conditioned by obvious considerations of prognostic order, must necessarily aim for "certainty". Prolonged monitoring of the endoluminal pH and the adoption of provocative tests, in the course of pH monitoring and manometry, play an important role in achieving this aim (ergometric test, distension induced with a balloon, edrophonium, electrostimulation, seem most effective). A promising outlook is supported by the recent introduction of prolonged manometry. Finally, diagnostic attitude must necessarily abandon its limited specialistic horizon to consider the patient's profile in its entirety.
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PMID:[Esophageal angina]. 206 70

Antireflux operations are now commonly performed for severe gastroesophageal reflux with life-threatening presentations like recurrent aspiration pneumonia and apnea. We report a child who presented 2 years after Nissen fundoplication with jejunal volvulus resulting in massive gastric dilatation, gastric rupture, pneumoretroperitoneum, pneumomediastinum, and severely compromised circulation to the lower extremities. Because of the intense intraabdominal pressure from the gastric dilatation, there was severe ischemia of the pancreas, duodenum, small bowel, colon, and gallbladder. We suggest that gastrointestinal symptoms in a child who has had Nissen fundoplication should be promptly evaluated to avoid delay in recognition of acute gastric dilatation and to prevent a fatal outcome.
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PMID:Visceral ischemia secondary to gastric dilatation: a rare complication of Nissen fundoplication. 368 27

Portal hypertension is defined as an increase of the portal venous pressure over 20 cm H2O or 7 mm Hg, respectively. It may be induced by different types of portal venous stenosis or obstruction, primarily by cirrhosis and fibrosis of the liver and, less frequent by posthepatic disorders such as the Budd-Chiari-syndrome or congestive heart failure. Portal hypertension is followed by ectasia and phlebosclerosis of the portal vein, by splenomegaly, ascites and by various types of collateral circulation. Among these, oesophageal varices, are most important since they often lead to acute upper gastrointestinal haemorrhage, the major complication of portal hypertension. Bleeding from oesophaeal varices is essentially based on atrophy of the squamous epithelium, caused by ischemia from local hypoxia and venous stasis. Portal hypertension and the frequently compromised blood clotting mechanism due to reduced synthesis of clotting factors in the liver aggravate the bleeding. Atrophy of the esophageal mucosa presents an area of decreased resistance likely to ulcerate with easy erosion of the varices--usually lying very superficially--; with mechanical irritation by food or peptic erosion from gastroesophageal reflux being frequent inducers of hemorrhage.
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PMID:[Pathologic-anatomic reflections on portal hypertension (author's transl)]. 624 21

Transabdominal fundoplication is an effective operation for control of gastroesophageal reflux in the majority of patients. The operation is, however, associated with several sell-documented early and late complications. Recently, a few reports have appeared describing benign gastric ulceration (GU) occurring from one month to several years postplication. The etiology of GU in this setting is unknown, but preexisting delayed gastric emptying, pyloric incompetence, faulty wrap construction, local ischemia, and trauma to the vagus nerves have been incriminated. During a recent seven-year period, five cases of GU have occurred among a series of 158 patients who underwent fundoplication. The cases are cited in detail, and the recent literature is reviewed. Discussion is addressed to the various proposed factors and combination of factors thought to contribute to GU. Suggestions are included for the preoperative evaluation of patients with gastroesophageal reflux as an aid to intraoperative management. As trauma to the vagus nerves has been frequently mentioned as a contributing factor to postplication ulcer, an operative technique is described in which the vagus nerves are isolated and protected from the fundic wrap.
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PMID:Gastric ulceration after fundic wrapping. Vagal nerve entrapment, a possible causative factor. 707 54

Although most patients with gastroesophageal reflux disease (GERD) present with the classic symptoms of heartburn and acid regurgitation, many complain of atypical chest pain suggestive of cardiac disease. Once cardiac ischemia has been excluded, it is important to consider GERD because this may be established as the cause of pain in 10% to 50% of such patients. If GERD is suspected or documented, vigorous antireflux treatment, preferably with proton pump inhibitory therapy, is indicated.
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PMID:Management of complicated gastroesophageal reflux disease: atypical chest pain. 934 86

Diabetic gastropathy is a term that encompasses a number of neuromuscular dysfunctions of the stomach, including abnormalities of gastric contractility, tone, and myoelectrical activity in patients with diabetes. These abnormalities range from tachygastrias to antral hypomotility and frank gastroparesis. Diabetic gastropathies may be acutely produced during hyperglycemia. Symptoms of chronic diabetic gastropathy include chronic nausea, vague epigastric discomfort, postprandial fullness, early satiety, and vomiting. Because these symptoms are nonspecific, other disorders such as mechanical obstruction of the gastrointestinal tract, gastroesophageal reflux disease, cholecystitis, pancreatitis, mesenteric ischemia, and drug effects should be considered. Neuromuscular abnormalities of the stomach may be assessed noninvasively with gastric emptying tests, electrogastrography, and ultrasound. Gastrokinetic agents such as metoclopramide, cisapride, domperidone, and erythromycin increase fundic or antral contractions and/or eradicate gastric dysrhythmias. Diet and glucose control also are important in the management of diabetic gastropathy. As the pathophysiology of diabetic gastropathy is better understood, more specific and improved treatments will evolve.
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PMID:Diabetic gastropathy: gastric neuromuscular dysfunction in diabetes mellitus: a review of symptoms, pathophysiology, and treatment. 1038 75

Hypertension is a significant and prevalent risk factor for the development of cardiovascular disease and target organ damage. The urgency of treatment of high blood pressure depends on the level of blood pressure elevation and the presence of coexistent risk factors for cardiovascular disease. Likewise, the level to which blood pressure is reduced is not restricted to the definition of high blood pressure but instead depends on the underlying disease. Diabetes and renal insufficiency, for example, require blood pressure goals below those that are traditionally defined. In the absence of contraindications, beta-blockers and diuretics are still recommended as first-line agents for treatment of uncomplicated hypertension. Calcium channel antagonists also may reduce mortality. In patients with diabetes, ACE inhibitors are effective first-line agents in type 1 and type 2 diabetic patients who are hypertensive or have microalbuminuria. ACE inhibitors may be beneficial in patients with nondiabetic renal insufficiency as well. Calcium channel antagonists may have some effect in retarding progression of diabetic nephropathy although a recent trial found a higher incidence of death as a secondary endpoint in hypertensive diabetic patients who were treated with calcium channel antagonists. Beta-blockers seem to be safe and well tolerated in patients with mild to moderate intermittent claudication, although patients with rest pain or limb ischemia have not been studied. Beta-blockers should not be used in patients with asthma. Dihydropyridine calcium channel antagonists are the preferred treatment of hypertension in patients with Raynaud's but should be avoided in patients with severe gastroesophageal reflux disease. NSAIDs, particularly piroxicam and indomethacin, raise mean blood pressure by approximately 5 mm Hg, enough to consider a change of either NSAID or antihypertensive to one that is not as affected by NSAIDs. Cyclosporine A can induce hypertension by its vasoconstrictive effects, particularly on the kidney. Calcium channel antagonists may antagonize this vasoconstriction while allowing the clinician to reduce the dose of cyclosporine A required to achieve its immunosuppressive effect.
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PMID:Evaluation and treatment of hypertension. 1046 27


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