It is becoming recognised that weakness of the valve mechanism between oesophagus and stomach is a not infrequent cause of vomiting in infancy and early childhood (1, 2). This gastro-oesophageal incompetence allows abnormal reflux of stomach contents into the gullet, a process facilitated by the horizontal posture and fluid diet of infancy. In 1947, Neuhauser and Berenberg described in babies the condition of cardio-oesophageal relaxation or “chalasia,” in which the cardia is normally situated but wide and patulous, permitting easy reflux (3–5). More frequent than this condition, in our experience with children, is the so-called “short oesophagus,” with a small proportion of the stomach situated above the diaphragm. At The Children's Hospital in Birmingham (England), the annual incidence of hypertrophic pyloric stenosis is about 90 cases. In one year we see about 18 infants under twelve months of age, as well as a number in the older age groups, in whom vomiting is associated with a minor degree of partial thoracic stomach. Thus the condition is of considerable importance. The present paper is based on a study of 115 cases. Pathology The normal valve mechanism between the oesophagus and the stomach may be considered as a triple entity (6–10). One component is the “pinchcock” of the muscular right crus of the diaphragm, which largely constitutes the oesophageal hiatus. Possibly more important is the normal obliquity of insertion of the oesophagus into the stomach. This angle is maintained by the oblique fibres of the stomach wall, looped around the cardiac incisura, and by the sling-like action of the right crus, an action which Allison (10) compares to that of the pubo-rectalis muscle in controlling defaecation. The third and perhaps weakest element is the sphincteric action inherent in the lower end of the oesophagus itself; although there is no anatomical sphincter to be detected here, there is evidence that a functional sphincter exists. In the condition of “short oesophagus” and partial thoracic stomach, the oesophagus has a normal direct course but terminates above the diaphragm by entering the apex of a small loculus of the thoracic stomach. The proportion of the stomach that lies above the diaphragm is variable; in all of the present series of cases it has been estimated at under 15 per cent and often very much less. (More gross herniations are relatively uncommon; they are less apt to produce symptoms due to gastro-oesophageal incompetence and may conceivably have a different aetiology.) The diaphragmatic hiatus is wider than usual and, as a result, the “pinch-cock” action of the right crus is less effective than in the normal individual. Moreover, the direct entry of the oesophagus into the apex of the thoracic stomach means that the second valvular element, the obliquity of insertion, is lost. Only the weak sphincteric action of the oesophagus remains (Fig. 1).