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Gastroesophageal reflux disease (GERD) is a common disease in the western world. Usually it occurs with typical symptoms like heartburn and regurgitation, but almost every third GERD-patient presents with extraesophageal symptoms and diseases in which a causal relation with GERD is discussed. The extraesophageal symptoms possibly associated with GERD are chronic cough, bronchial asthma, sleep disturbances including obstructive sleep apnea, hoarseness, dental erosions, non-cardiac chest pain and idiopathic pulmonary fibrosis. This article gives an overview of the reflux-associated diseases of the airways as well as the proposed pathomechanisms and therapeutic options.

Background: Videofluoroscopy has gained high significance for the evaluation of deglutition disorders. Imaging alone cannot clarify whether the subjective symptom is represented morphologically or whether it is the substrate of a functional disorder., Method: The videofluoroscopies of 101 patients with dysphagia (n = 55) and globus pharyngitis (n = 46) were evaluated. Morphologic abnormalities were registered as well as sequential movement patterns. These data were compared with clinical and endoscopic findings., Results: In 87% of the dysphagia and 74% of the globus patients videofluoroscopy revealed pathologic findings. Functional disorders were seen significantly more often than morphologic abnormalities. Highest incidence was found for cricopharyngeal dyskinesia (42%). Hypopharyngeal pouches and degeneration signs of the cervical spine with bolus impression less than 40% are common but functionally not important. Additional esophago-gastroduodenoscopy was pathological in 83% in the dysphagia group and 96% in the globus group., Conclusion: Videofluoroscopy is indispensable for the differential diagnosis of dysphagia and globus sensation, especially for the detection of functional disorders in the pharyngoesophageal segment thus documenting the dynamic aspect of deglutition. Videofluoroscopy should be completed by a gastroenterologic examination in order to improve diagnosis.

Background: In a German multicenter questionnaire, answered by 89 departments, we had examined the strategies to prevent or to treat the acute morbidity of the skin and mucosa associated to radiation therapy. In this work, the recommendations from the literature are compared to the results of the questionnaire., Methods: An extensive research on common data information systems (Medline, Cancerlit, DIMDI and others) was performed. The criteria included the organ related morbidity and therapeutic strategies for its reduction. The obtained data were compared to the results from the questionnaire., Results: The study data found by the research often demonstrate small patient numbers and little convincing results. However, as in the questionnaire, the joint principle seems to be the reduction of acute inflammatory tissue reaction by evasion of bacterial and mycotic overgrowth and reduction of exo- and endogenous toxins., Conclusions: Further studies with more convincing results are required.

We report on two latex-allergic subjects who developed local hypersensitivity reactions after their lung compliance was measured by an oesophagus balloon catheter. Protein and allergen analyses of this catheter showed values of 85 and 9.8 micrograms per gram rubber. It is concluded that latex-allergic subjects should not undergo examinations with latex allergen-containing catheters. To our knowledge, this is the first report on allergic reactions caused by latex balloons of an oesophagus catheter.

We present four cases of esophageal rupture (three iatrogenic, one Boerhaave syndrome) to demonstrate the difficulty in diagnosis and therapy. The current literature is discussed and conclusions are drawn as regards the modus operandi. All our patients were operated on. The site of esophageal rupture was always closed with a primary suture and substantial irrigation and drainage were performed. In two cases the suture line was in addition covered with fibrin glue or by an omentum flap, respectively. All patients survived and recovered was unremarkable. Our own results and a subsequent analysis of literature allow the following conclusions. At an early stage of esophageal rupture surgical intervention is indicated. The method of choice is primary closure of the rupture site by suture, possibly combined with a muscle or omentum flap. In cases of delayed diagnosis with advanced mediastinitis, suture of the rupture site should also be striven for. Additional coverage is advisable in these cases. Resection procedures with or without reconstruction should be done only in exceptional cases before of the high surgical risk.

Together with three of our own observations of intramural rupture (IRO) or hematoma (IHO) of the esophagus, we have analyzed 91 case reports from the literature. Precipitating factors were identified in 63% of all patients. Most frequently potentially traumatic events such as vomiting (22%) or instrumentation (17%) preceded IRO/IHO. In 21% there were disturbances of hemostasis, either alone (15%) or in addition to a traumatic event (6%). 37% of IRO/IHO were spontaneous. In 35% the typical clinical triad of acute retrosternal pain, odynophagia or dysphagia and hematemesis was complete; in 46% only two out of three symptoms were present. IRO/IHO was managed conservatively in 84% of the patients, whereas 9% required surgery for complications. 7% were operated on without a precise indication. One patient died following surgery for endoscopic perforation. The rare syndrome of IRO/IHO must be considered in patients with acute retrosternal pain. Treatment is primarily conservative and the prognosis is excellent.

1966, 1967, and 1971 we published the good results with the "Transsectionsligature" of bleeding esophageal varices. The bleeding segment is nearly in all cases the angiomusculare strech closure segment in the terminal portion. In the last 27 patients we used the fundektomie of the stomach together with a splenektomie to stop the bleeding. Fundektomie abolished ulcusdisposition and splenektomie diminished the development of anaemia. Encephalopathy does not occur after these operations. All patients with a healthy liver remained alive. Cirrhotic patients come to death through their poor liver function. The selection of patients is the remaining problem.

Ingestion of 5 g guar gum (Glucotard) led to complete obstruction of the distal oesophagus in a 63-year-old diabetic. A daily intake of 5 g guar gum t.i.d. with 250 ml of water had been tolerated without problems for half a year. Intake of a sufficient amount of water, as well as an undisturbed oesophageal function, are absolutely essential for the ingestion of guar gum. Since alcohol can influence the process of swelling and the consistency of the bolus, simultaneous intake of alcohol and guar gum should be strictly avoided.

Clinical findings, symptoms and predisposing factors were studied in 43 patients with oesophageal candidiasis, 40 patients with peptic oesophagitis and 40 normal controls. Oesophageal candidiasis was confirmed cytologically. 2.4% of patients who had undergone gastroscopy had oesophageal candidiasis; only three of them had simultaneous candidiasis of the oral cavity. Cardiac failure, oesophageal varices, hiatus hernia and gastric ulcer were common associated disorders. 42% of patients with candidal oesophagitis were symptom-free. Most common symptoms were vomiting, retrosternal and epigastric pain. Peptic oesophagitis was more frequently associated with symptoms. Predisposing factors were present in 88% of cases of oesophageal candidiasis: alcoholism, hepatic cirrhosis, diabetes mellitus, malignant tumours and other wasting diseases. 18 patients had had treatment with cimetidine; they included all 13 patients whose candidiasis was first detected at check endoscopy.

Gastrointestinal manifestations of collagen diseases are frequent. In progressive systemic sclerosis esophageal involvement is found in 60% of cases and is thus the main gastrointestinal complication. Atrophy of the smooth muscle and fibrotic degeneration of the distal esophagus result in progressive motility disorders which may cause severe reflux esophagitis with typical consequences, such as stenosis and strictures. Manometry and cinematography are basic diagnostic procedures. Esophagoscopy and long-term pH-monitoring are most useful for evaluating the degree of esophageal involvement. The severity of sclerodermatous motility disorders should be classified according to a modification of the Garrett scale, which is particularly recommended for determining the further prognosis and therapeutic approach. Esophageal involvement of grades I and II should be treated conservatively, whereas grade III is a clear indication for surgical therapy. The original Nissen type of fundoplication or distal gastric resection with Roux-en-Y anastonosis are the methods of choice.

This paper deals with the morphological findings in the hypopharynx-esophageal region of two patients following laryngectomy. In these patients we found a median-sagittal infolding, situated above the ventral aspect of the hypopharynx-esophageal region. This infolding was due to the surgical closure of the ventral wall of the esophagus, following laryngectomy. Histological examination revealed a hernia-like prolapse of the tunica mücosa, m. mucosae and tela submucosa with numerous proliferated macrophages and blood vessels, but no lymphatics. These macrophages are concerned with the removal of an edema, which, however, is only imperfectly removed and finally turns out into a fibrous tissue. The functional meaning of this infolding is not yet clear, but it seems intimately related to the altered function of the hypopharynx-esophageal region following laryngectomy.

Spontaneous transmural rupture of the esophagus (Boerhaave's syndrome) is a life-threatening emergency. Prompt diagnosis is essential to a better prognosis, successful operative outcome and patient survival. The chest roentgenogram and the contrast esophagograms to follow are the most helpful diagnostic tests. The clinical manifestations are variable and may be misleading and thus delay accurate recognition. In our case report the major clinical features and radiological signs of Boerhaave's syndrome are described. The pathogenesis, characteristic clinical symptoms and the signs and radiological evaluation are reviewed.

Disturbances of the oesophageal function in dogs and cats lead to the clinical symptoms of dysphagia. An oesophageal dilatation of various degree can result from this and can be categorized as primary, i.e. idiopathic form, or secondary form, if its cause is known. This present study of our own patient population gives a survey of the symptomatology, diagnostic measures, incidence, pathogenesis, and therapy of oesophageal dilatation.

Two of our own patients with Boerhave's syndrome are reported. A disturbance of the vomiting process with abrupt increase of pressure in the esophageal lumen combined with a circumscribed constitutional weakness of the esophageal wall appears to be the decisive factor in the etiology of atraumatic complete esophageal rupture. The clinical picture is characterized by vomiting and painful sensations in the abdomen and thorax in addition to subsequent acute epigastric symptomatology. A water-soluble contrast medium is very useful in the radiological diagnosis. Thoracotomy with suture and drainage is recommended as the treatment of choice. Operative treatment treatment has a mortality of 38% compared with more than 60% with drainage alone.

"Spontaneous" rupture of the oesophagus is rare and happens after a marked rapid rise in intraluminal oesophageal pressure (massive vomiting, asthma etc.). As is known from the literature, forceful swallowing alone may produce spontaneous perforation in the case of damage to the mucosa or muscular layer of the oesophagus. Boerhaave's syndrome associated with rare diffuse idiopathic muscular hypertrophy of the lower oesophagus has been described in only three cases in the literature.

Belching and severe vomiting may lead in association with gastro-oesophageal prolapse to a variety of lesions within the gastro-oesophageal junction. Incarceration of the prolapse, diffuse hemorrhage from the prolapsed mucosa, longitudinal lacerations (Mallory-Weiss syndrome), intramural hematoma and spontaneous rupture (Boerhaave syndrome) are the most common complications. Based on 4 cases of incomplete rupture of the oesophagus we would like to draw attention to a disorder with mediastinal emphysema or pneumopericardium following severe vomiting. It is postulated that air escapes from a mucosal tear in the terminal oesophagus into the mediastinum. Conservative treatment seems justified.

Functional disorders of the esophagus were evaluated in 24 patients 4 +/- 2 months after sclerotherapy following the first hemorrhage. The mean volume of polidocanol required per patient was 181 +/- 111 ml. 9 patients complained of dysphagia and/or reflux symptoms; strictures were found in two cases; 4 patients had esophagitis. Manometrically the lower esophageal sphincter was completely insufficient in 14 patients; only 7 patients still had a competent cardia. The first group had received significantly more polidocanol than the latter. Tubular motility was disturbed by nonpropulsive (18%) and repetitive (7%) contractions. By longterm-pH-metry the percentage of oesophageal reflux was elevated in all patients.

A patient is described who suffered from prolapse of the lower oesophageal mucosa in the presence of a Schatzki ring. There was variable dysphagia culminating in total aphagia. The clinical symptoms disappeared without any treatment once the patient had overcome several years of psychological stress. The radiological appearances gave rise to a discussion of the radiological anatomy of the terminal oesophagus with a Schatzki ring since numerous similar appearances illustrated in the literature have been interpreted as axial hiatus hernias. A comparison of manometric and radiological fingings has shown that a hernia did not exist. The advantages and errors inherent in diagnosing hernias with the help of the "three rings", as described by Hafter, are discussed. The mucosal prolapse during the stage of aphagia is demonstrated and compared with cases from the literature showing prolapse at the upper and lower vestibular margins. The mechanism leading to these appearances is discussed.