Editor,—The recent paper by Godbole et al is an interesting addition to the debate over the value of clinical examination versus ultrasound scanning in the diagnosis of infantile hypertrophic pyloric stenosis.1 Pyloric stenosis can often be diagnosed reliably on the basis of history and examination alone, with ultrasound imaging used only as an adjunct. In less certain cases, where history is strongly suggestive but examination is negative, ultrasound can be crucial. We describe a patient in whom an unusual incidental secondary diagnosis obscured the primary diagnosis and ultrasound confirmed both quickly and simply.

A 6 week old boy was seen in clinic with a two week history of vomiting and weight loss. The vomiting occurred 10–20 minutes after a bottle feed, without bile staining, and the parents described it as ‘like a fountain’ rather than projectile. After vomiting he would settle until the next feed was due. His birth weight was 3995 g, at 4 weeks he reached 4400 g, but had fallen to 4200 g when seen. He was the first child of healthy parents, though the father was said to have had problems with vomiting as a baby which settled without treatment. On examination he was an unhappy, wizened child. He was tachycardic at 160/min, all peripheral pulses were normal, heart sounds were thought to be normal, and there was no evidence of cardiac failure. No gut peristalsis was seen and palpation shortly after a feed did not reveal a pyloric tumour even though the child vomited. The differential diagnosis was between gastro-oesophageal reflux and pyloric stenosis. The ultrasound reported a dilated stomach with a thickened pylorus on the left side. The liver was also on the left side with the heart on the right and a right sided descending aorta. In the light of this the abdomen was re-examined after a feed with palpation in the left hypochondrial region rather than the right. A typical pyloric mass was found. An echocardiogram was done before surgery. This showed all connections were present, in a mirror image inversion. The inferior vena cava was on the left and the aorta was on the right. Uneventful pyloromyotomy (Ramstedt’s procedure) was performed two days later after correction of his biochemical status and he went home four days after that. At the first follow up three weeks after surgery, all vomiting had stopped and he had gained 740 g.

Pyloric stenosis has an incidence of 2–4/1000 live births,2 though this figure rises if a parent was affected, especially for firstborn males of an affected mother, for reasons unknown. Dextrocardia with situs inversus has an incidence of 0.09/1000 live births.3 There are no previous reported cases of the occurrence of these two conditions together. It is likely that their concurrence in this boy is simply a random association and does not imply a genetic linkage. In this case the situs inversus obscured the clinical diagnosis of pyloric stenosis and ultrasound was decisive.