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Chapter 23 (page 107)
In a larger series of cases Blumhagen and Noble (l983) followed the normal hypoechoic
muscle layer of the proximal stomach distally to the gastric outlet. Where the thickness
of the muscle layer of the distal antrum and pylorus was 4.0 mm or more, a confident
diagnosis of IHPS could be made. (The thickness varied from 3.0 mm to 6.0 mm in
IHPS, being approximately 4.5 mm in the majority of cases). It was stated that at
sonography the hypertrophied antral and pyloric circular musculature formed a thick,
rounded cylinder having the appearance of a hypoechoic ring in cross section, and an
ellipse with an echogenic core in sections parallel to the long axis. The best safeguard
against making a false positive sonographic diagnosis is to identify the continuity of the
thickened pyloric muscular layer with that of the remainder of the stomach, and to
measure its thickness, rather than to measure the diameter of the mass, as advocated by
previous authors.
Khamapirad and Athey (l983) obtained transverse and longitudinal sonographic images
in l8 babies between the ages of one and 6 weeks with IHPS. A constant finding was a
hypoechoic mass greater than 1.0 cm in diameter and containing a round or stellate
central echogenic area. (The diameter of the mass ranged from 1.2 cm to 2.2 cm, with an
average of l.7 cm). This was considered to be one of the main criteria for the diagnosis,
the other being the ability to demonstrate a continuation of the hypoechoic mass with the
gastric "antrum".
Graif et al. (l984) considered previous sonographic measurements in IHPS to have been
inconclusive, especially in borderline cases. In order to increase the diagnostic accuracy
of the modality other parameters and features of the hypertrophied muscle were
evaluated, using a high resolution real-time unit with a 10 MHz transducer. In 22 infants
with IHPS between the ages of 2 and 10 weeks the following measurements were
obtained (mean and standard deviations were given respectively): the transverse
diameter of the pylorus was 13.4 ± 1.6mm, the single wall thickness 4.5 ±
0.9 mm, and the mean pyloric length was 84 percent longer than that of normals. It was
noted that high resolution, high frequency real-time scanning also showed the pressure
effects of the hypertrophied muscle on the adjacent "antrum" by direct vision, confirming
the fact that the concave indentations were caused by the muscle mass.
(Comment: In radiology hypertrophy of the muscular wall is inferred from
the configuration of intraluminal barium).
Wilson and Vanhoutte (l984) held that the true pyloric muscle length was the most
important criterion for the diagnosis of IHPS. This was obtained by rotating the
transducer from a short axis image of the pylorus until a maximum long axis was
produced. In 16 proven cases of IHPS the true pyloric muscle length ranged from 2.0 to
2.6 cm. In 17 normal controls the range varied from 12.0 mm to 15.0 mm. It was felt
that measurements of the true pyloric muscle length approached more closely the
established radiological criterion of an elongated pyloric muscle and that it defined the
anatomic abnormality seen at surgery more clearly. It was concluded that a true pyloric
muscle length of 2.0 cm or more was a reliable sonographic sign of IHPS.
Stunden et al. (l986) achieved 100 percent accuracy in the ultrasound diagnosis of IHPS
in 112 cases. Criteria used included measurements of the pyloric diameter, muscle
thickness, canal length, real-time observation of the function of the pylorus and gastric
peristalsis. Statistics showed that canal length was the only factor which could
discriminate precisely between a normal and an hypertrophied pylorus. The overall
diameter of the ring in IHPS was usually more than 11.0 mm (normal 11.0 mm or less)
and the thickness of the muscle layer in the wall more than 2.5 mm (normal less than 2.5
mm). The canal length in IHPS was more than 16mm (normal less than 15 mm). When
viewing the hypertrophied pylorus in real-time, relaxation of the canal did not occur, little
fluid passed through it and gastric peristalsis was increased.
Carver et al. (l988) pointed out that in most of the previous publications where normal
and abnormal ranges for length, breadth and muscle thickness were determined, there was
often an overlap between the normal and abnormal ranges for all three measurements.
By using a 7.5 MHz real-time sector scanner they estimated pyloric muscle volume and
correlated this with body weight. In 21 babies with surgically confirmed IHPS, the
pyloric muscle index was obtained by dividing the pyloric muscle volume in cubic
centimeters by the body weight in kilograms. If this index was less than 0.4 the pylorus
was normal, and if more than 0.4 the diagnosis of IHPS could be made with confidence.
In many instances Bowen (l988) was unable to identify the normal pyloric muscles with 5
MHz mechanical sector transducers; the normal pyloric muscle was much easier to
demonstrate with computed sonography using a 5 MHz linear transducer. Normally
pyloric dimensions might vary during real-time ultrasonic scanning, probably related to
peristaltic contractions involving the pyloric muscle itself; the contracted gastric antrum
might simulate an elongated pyloric channel of IHPS.
Meuwissen and Sloof (l932, l934) were of the opinion that the condition was entirely due
to spasm of the pyloric muscle, causing a permanent contraction. This might or might
not be associated with muscular hypertrophy.
Torgersen (l942) thought the simplest explanation would be that the circular musculature
of the canalis egestorius had developed disproportionately strongly in comparison with
the longitudinal musculature. During foetal life the circular musculature was laid down
earlier and reached considerable thickness before the longitudinal layer was differentiated
(Chap. 3). It seemed possible that regressive changes in the powerful circular
musculature, which normally occurred at or near birth, had not taken place. Torgersen
(l949) later also pointed out that the pyloric sulcus had an asymmetrical position in
relation to the axis of the transverse part of the stomach, being closer to the angulus on
the lesser curvature side. In IHPS genetic causes might lead to excessive asymmetry with
consequent hypertrophy of the musculature of the canalis (i.e. the sphincteric cylinder).
Meeker and De Nicola (l948) described IHPS in a newborn infant; it had caused gastric
outlet obstruction on the 2nd day of life and required operation on the 4th day. The
etiology was unclear, and the question was whether muscular hypertrophy had preceded
or followed pylorospasm. As the condition appeared to be congenital in their case, it was
thought that it had occurred too early in life for spasm to have caused hypertrophy.
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