Pyloric stenosis: evolution from pylorospasm?

Abstract

Over a 10-year period, we have performed pyloromyotomy on 260 infants with hypertrophic pyloric stenosis (HPS), 10 of whom had a history suggestive of pyloric stenosis but initially had neither the physical nor radiological findings to confirm the diagnosis. All 10 demonstrated pylorospasm on upper gastrointestinal series (UGIS), were treated medically without improvement, and subsequently developed classic HPS confirmed by repeat UGIS. Age at diagnosis ranged from 3 to 16 weeks (mean 8 weeks). Vomiting was progressively more projectile and severe from the onset until diagnosis and operation, with a duration of 5-5 0 days (mean 24 days). In 9 of the 10 patients a second UGIS demonstrated the diagnostic signs of HPS in 8 and suggested an antral web in the 9th. The interval between the two UGIS ranged from 2 to 46 days (mean 13 days). The 10th patient had a palpable hypertrophic pyloric muscle 9 days after the first UGIS and was operated upon without a follow-up UGIS. All 10 patients had classic HPS at operation. We conclude that although most infants with pylorospasm on UGIS improve with medical management, a small but significant number go on to develop HPS. Awareness of this variant of pyloric stenosis and appropriate follow-up UGIS will help to avoid undue delay in correctly diagnosing infants with persistent non-bilious vomiting.

The Progressive Development of Pyloric Stenosis: A Role for Repeat Ultrasound

“…This large prospective series effectively confirms the postulate that pyloric stenosis is a dynamic process rather than a fixed congenital lesion [11]. Pylorospasm evolving to pyloric stenosis has been previously reported and suggests that while an obstructive hypertrophy may not be present until a few weeks of life, the pyloric musculature may have a congenital defect predisposing to spasm and subsequent hypertrophy [9,15]. The nonoperative approach for pyloric stenosis, popularized in Asia, demonstrates a natural resolution of the disease [1,5,6,16].…”

Treatment With Pamidronate for Osteoporosis Complicating Long‐term Intestinal Failure

“…Vitamin D dose was between 200 and 400 IU depending on oral intake and 25-OH vitamin D blood levels. The calorie-tonitrogen ratio was higher than 150 as recommended (5,6).…”

Late-onset primary gastric outlet obstruction—an unusual cause of growth retardation

“…On the other hand, transient relaxation of the sphincter to permit the forward passage of food is accomplished by activation of inhibitory motor neurons [6][7][8]. High-amplitude contractions in gastroduodenal junction uncoordinated with antral contractions are partially responsible for pylorospasm leading to IHPS [9][10][11]. Nitric oxide synthase deficiency leading to lack of locally available nitric oxide may cause failure of muscular relaxation and neuromuscular incoordination at pylorus [4,6,12].…”