Published online before print October 2, 2003, 10.1148/radiol.2292021303
(Radiology 2003;229:389-393.)
© RSNA, 2003
Hypertrophic Pyloric Stenosis in Infants: US Evaluation of Vascularity of the Pyloric Canal1
Marta Hernanz-Schulman, MD,
Yuwei Zhu, MD, MS,
Sharon M. Stein, MD,
Richard M. Heller, MD and
L. Allison Bethel, RD, MS, RTR, BS
1 From the Departments of Radiology (M.H.S., S.M.S., R.M.H., L.A.B.) and Pediatrics (Y.Z.), Vanderbilt University Medical Center, MCN D-1120, 21st Ave and Garland St, Nashville, TN 37232. Received October 9, 2002; revision requested December 26; final revision received April 4, 2003; accepted May 19. Address correspondence to M.H.S. (e-mail: marta.schulman@vanderbilt.edu).
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ABSTRACT
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PURPOSE: To determine if there is increased flow to the pylorus in infants with hypertrophic pyloric stenosis (HPS) and, if so, whether the flow is localized to the muscle layer, mucosal layer, or both.
MATERIALS AND METHODS: Seventy-five infants examined for clinical suspicion of HPS were prospectively recruited for the study. Color scale was standardized at 4.2–4.4 cm/sec. Color Doppler flow at ultrasonography (US) was graded as follows: Grade 1 meant no signal; grade 2, two to five flow signals; and grade 3, extensive or continuous flow. Flow to the muscle or mucosal layer was documented and confirmed with spectral analysis. Infants without HPS served as control patients. Descriptive analyses were conducted to assess the demographic data and US results. Significance was assessed with 
2 or t tests. P < .05 was considered to indicate a significant difference.
RESULTS: HPS was present in 41 infants with a mean age of 5 weeks ± 2.0 (SD). Their mean flow grade was 2.80 ± 0.4 in muscle and 2.88 ± 0.4 in mucosa. HPS was not present in 34 infants with a mean age of 5.9 weeks ± 4.5. Their mean flow grade was 1.26 ± 0.5 in muscle and 1.15 ± 0.5 in mucosa (P < .001). There was no significant difference in flow grades when the dimensions of the pyloric muscle and mucosa were compared. There was no significant difference in age between the HPS and control patient groups.
CONCLUSION: Increased flow accompanies and may conceivably represent an integral component of the changes that occur with infantile HPS.
© RSNA, 2003
Index terms: Pylorus, stenosis, 724.1431 • Stomach, abnormalities, 724.1431 • Stomach, US, 724.12981, 724.12983, 724.12989 • Ultrasound (US), Doppler studies, 724.12981, 724.12983, 724.12989
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INTRODUCTION
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Infantile hypertrophic pyloric stenosis (IHPS) is a condition in which the antropyloric portion of the stomach becomes abnormally thickened, resulting in obstruction to gastric emptying. IHPS occurs in patients aged 2–10 weeks and is the most common surgical condition in infants (1), with a frequency of approximately two to four cases per thousand births (2). Despite the frequency of this condition, it was not recognized until the late 19th century, when the detailed description of two fatal cases was reported by Hirschsprung in 1887 and published 1 year later (3). Since that time, great progress has been made in the diagnosis and treatment of IHPS, yet its etiology remains unknown.
Many characteristics of IHPS are intriguing. The abnormality consists of thickening of the antropyloric portion of the stomach and crowding of redundant and edematous mucosa within the lumen; these anomalies cause obstruction to the passage of gastric contents (4,5). Despite Hirschsprung’s mistaken assumption that this abnormality is congenital, IHPS develops in the first few weeks of postnatal life. The thickened muscle has been shown to be depleted of inhibitory peptides such as vasoactive intestinal polypeptide; of synaptic vesicles, presynaptic terminals, and neural cell adhesion molecules; of markers for enteric glia; of interstitial cells of Cajal, and of nitric oxide synthase activity at the messenger RNA level, with increases in insulin-like and platelet-derived growth factors (1). Yet, the surgical treatment, developed by Ramstedt in 1912 (6) and consisting of surgical splitting of the muscle along its long axis, is curative. Within 2–5 months after theprocedure the muscle involutes and the pylorus reverts to its normal appearance (7,8). As early as 4 months after surgery, assays for nerve growth factor, interstitial cells of Cajal, and nitric oxide synthase activity revert to normal (7).
It is therefore reasonable to hypothesize that postnatal feeding leads to a chain or cycle of reversible events that results in mucosal edema and muscle hypertrophy and that these phenomena may be accompanied by an increase in the normal blood flow (9) to the muscle and the submucosal plexus of the antropyloric region. Thus, the purpose of our study was to determine if there is increased flow to the pylorus in patients with pyloric stenosis and, if so, whether the flow is localized to the muscle layer, mucosal layer, or both.
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MATERIALS AND METHODS
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Patients and Imaging
This prospective study involved 75 consecutive infants with nonbilious vomiting who were referred for ultrasonography (US) because of clinical suspicion of IHPS. Infants who did not have IHPS served as control patients. There were 49 boys and 26 girls with a mean age of 5 weeks ± 3.4 (SD). The presence of IHPS was confirmed surgically; the absence of IHPS was determined by reviewing the medical records. Institutional review board approval was granted for the study, and informed consent was obtained from the parent or legal guardian.
The infants were examined with US, performed with Sequoia (Acuson, Mountain View, Calif) or ATL 5000 (Advanced Technology Laboratory, Bothell, Wash) units, in a standard fashion in the longitudinal and transverse planes with a linear transducer operating at a 7–10-MHz frequency. All examinations were performed by an author (M.H.S., S.M.S., or L.A.B.) and under the direct supervision of an author (M.H.S., S.M.S., or R.M.H.). The thicknesses of the pyloric muscle and the mucosa were measured with electronic calipers as part of the routine US examination in infants with pyloric stenosis. Muscle thickness was measured on both longitudinal and transverse sections of the pylorus; mucosal thickness was measured on transverse sections.
The pylorus was subsequently evaluated with color Doppler US, with the color scale set at 4.2–4.4 cm/sec. The presence of color signal in the muscle layer or mucosal layer was documented, and the number of signals (ie, degree of flow) was graded on a three-point scale: Grade 1 meant no flow signal; grade 2, two to five signals (ie, moderate flow); and grade 3, extensive or continuous flow. Flow was confirmed with Doppler spectrum analysis. The US images obtained in patients who underwent more than one examination prior to the diagnosis of pyloric stenosis were evaluated in the same manner.
Statistical Analysis
Descriptive analyses of age and sex data and of US results were performed. The frequencies of each sex in the IHPS and control groups were compared by using the 2 test in a two-by-two contingency table format. The Fisher exact test was used to analyze the mucosal flow data for the female infants, because all of them had the same mucosal flow grade. For further statistical analysis of the IHPS group data, high flow was defined as grade 3 and low flow as any grade lower than 3. The t test was used to compare mean age and mean muscle and mucosal flow grades between the two patient groups and to compare mean muscle and mucosal thicknesses between patients with high and those with low flow grades. Analyses were performed by using computer software (SPSS version 11.0.1; SPSS, Chicago, Ill). Two-tailed P values less than .05 were considered to indicate a significant difference. Patients who underwent more than one US examination were counted only once, and only the last, presurgical examination data were considered in the analyses.
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RESULTS
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IHPS was present in 41 infants, who had a mean age of 5 weeks ± 2.0 (SD). There were 31 boys and 10 girls in this group. Thirty-four infants did not have IHPS and served as control patients; their mean age was 5.9 weeks ± 4.5. There were 18 boys and 16 girls in this group. Although the infants in the IHPS group were somewhat younger than those in the control group, the mean age was not significantly different between the two groups. There were significantly more boys than girls in the IHPS group (31 [76%] of 41 patients, P = .04); therefore, sex was controlled in further analyses.
In the IHPS group, the mean grade of flow in the muscle layer was 2.80 ± 0.4 and in the mucosal layer 2.88 ± 0.4 (Table 1, Fig 1). In the control group, the mean grade of flow in the muscle layer was 1.26 ± 0.5 and in the mucosal layer 1.15 ± 0.5 (Table 1, Fig 2). The difference in muscle and mucosal flow grade between the IHPS and control groups was highly significant (P < .001). The mean grades of flow to the muscle and the mucosa remained significantly different between the IHPS and control groups after stratification by sex (Table 1).
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Figure 1a. Doppler US findings in patients with IHPS. (a) Longitudinal image shows markedly increased flow to hypertrophied pylorus in 4-week-old girl. Solid arrows point to muscle layer. Open arrow points to mucosal flow. (b) Transverse image obtained in 5-week-old girl. Note the collar of increased flow in the submucosal plexus, branching into the luminal mucosa and adjacent muscle layer (arrows). (c) Longitudinal image of hypertrophied pylorus in 3-week-old boy with typical IHPS. Note the increased flow to the mucosa within the canal, protruding into the adjacent fluid-filled antrum (A). Straight arrows outline the adjacent thickened muscle. Curved arrow points to base of duodenal bulb. (d) Longitudinal image of hypertrophied pylorus in 5-week-old boy with typical IHPS. Note the markedly increased flow to the mucosal layer, which is detailed in the spectral tracing at the bottom of the image. A = antrum. (e) Longitudinal image of hypertrophied pylorus in 2-week-old boy with IHPS. Note the markedly increased flow to the muscle layer, which is detailed in the spectral tracing at the bottom of the image. D = duodenal bulb. (f) Longitudinal image of atypical pylorus in 5-week-old boy with IHPS. Although there is detectable flow, it is less visible than that in most other patients with IHPS. Arrows point to muscle layer. (g) Transverse image of pylorus in same patient as in f, with similar findings. Arrows point to muscle layer.
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Figure 1b. Doppler US findings in patients with IHPS. (a) Longitudinal image shows markedly increased flow to hypertrophied pylorus in 4-week-old girl. Solid arrows point to muscle layer. Open arrow points to mucosal flow. (b) Transverse image obtained in 5-week-old girl. Note the collar of increased flow in the submucosal plexus, branching into the luminal mucosa and adjacent muscle layer (arrows). (c) Longitudinal image of hypertrophied pylorus in 3-week-old boy with typical IHPS. Note the increased flow to the mucosa within the canal, protruding into the adjacent fluid-filled antrum (A). Straight arrows outline the adjacent thickened muscle. Curved arrow points to base of duodenal bulb. (d) Longitudinal image of hypertrophied pylorus in 5-week-old boy with typical IHPS. Note the markedly increased flow to the mucosal layer, which is detailed in the spectral tracing at the bottom of the image. A = antrum. (e) Longitudinal image of hypertrophied pylorus in 2-week-old boy with IHPS. Note the markedly increased flow to the muscle layer, which is detailed in the spectral tracing at the bottom of the image. D = duodenal bulb. (f) Longitudinal image of atypical pylorus in 5-week-old boy with IHPS. Although there is detectable flow, it is less visible than that in most other patients with IHPS. Arrows point to muscle layer. (g) Transverse image of pylorus in same patient as in f, with similar findings. Arrows point to muscle layer.
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Figure 1c. Doppler US findings in patients with IHPS. (a) Longitudinal image shows markedly increased flow to hypertrophied pylorus in 4-week-old girl. Solid arrows point to muscle layer. Open arrow points to mucosal flow. (b) Transverse image obtained in 5-week-old girl. Note the collar of increased flow in the submucosal plexus, branching into the luminal mucosa and adjacent muscle layer (arrows). (c) Longitudinal image of hypertrophied pylorus in 3-week-old boy with typical IHPS. Note the increased flow to the mucosa within the canal, protruding into the adjacent fluid-filled antrum (A). Straight arrows outline the adjacent thickened muscle. Curved arrow points to base of duodenal bulb. (d) Longitudinal image of hypertrophied pylorus in 5-week-old boy with typical IHPS. Note the markedly increased flow to the mucosal layer, which is detailed in the spectral tracing at the bottom of the image. A = antrum. (e) Longitudinal image of hypertrophied pylorus in 2-week-old boy with IHPS. Note the markedly increased flow to the muscle layer, which is detailed in the spectral tracing at the bottom of the image. D = duodenal bulb. (f) Longitudinal image of atypical pylorus in 5-week-old boy with IHPS. Although there is detectable flow, it is less visible than that in most other patients with IHPS. Arrows point to muscle layer. (g) Transverse image of pylorus in same patient as in f, with similar findings. Arrows point to muscle layer.
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Figure 1d. Doppler US findings in patients with IHPS. (a) Longitudinal image shows markedly increased flow to hypertrophied pylorus in 4-week-old girl. Solid arrows point to muscle layer. Open arrow points to mucosal flow. (b) Transverse image obtained in 5-week-old girl. Note the collar of increased flow in the submucosal plexus, branching into the luminal mucosa and adjacent muscle layer (arrows). (c) Longitudinal image of hypertrophied pylorus in 3-week-old boy with typical IHPS. Note the increased flow to the mucosa within the canal, protruding into the adjacent fluid-filled antrum (A). Straight arrows outline the adjacent thickened muscle. Curved arrow points to base of duodenal bulb. (d) Longitudinal image of hypertrophied pylorus in 5-week-old boy with typical IHPS. Note the markedly increased flow to the mucosal layer, which is detailed in the spectral tracing at the bottom of the image. A = antrum. (e) Longitudinal image of hypertrophied pylorus in 2-week-old boy with IHPS. Note the markedly increased flow to the muscle layer, which is detailed in the spectral tracing at the bottom of the image. D = duodenal bulb. (f) Longitudinal image of atypical pylorus in 5-week-old boy with IHPS. Although there is detectable flow, it is less visible than that in most other patients with IHPS. Arrows point to muscle layer. (g) Transverse image of pylorus in same patient as in f, with similar findings. Arrows point to muscle layer.
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Figure 1e. Doppler US findings in patients with IHPS. (a) Longitudinal image shows markedly increased flow to hypertrophied pylorus in 4-week-old girl. Solid arrows point to muscle layer. Open arrow points to mucosal flow. (b) Transverse image obtained in 5-week-old girl. Note the collar of increased flow in the submucosal plexus, branching into the luminal mucosa and adjacent muscle layer (arrows). (c) Longitudinal image of hypertrophied pylorus in 3-week-old boy with typical IHPS. Note the increased flow to the mucosa within the canal, protruding into the adjacent fluid-filled antrum (A). Straight arrows outline the adjacent thickened muscle. Curved arrow points to base of duodenal bulb. (d) Longitudinal image of hypertrophied pylorus in 5-week-old boy with typical IHPS. Note the markedly increased flow to the mucosal layer, which is detailed in the spectral tracing at the bottom of the image. A = antrum. (e) Longitudinal image of hypertrophied pylorus in 2-week-old boy with IHPS. Note the markedly increased flow to the muscle layer, which is detailed in the spectral tracing at the bottom of the image. D = duodenal bulb. (f) Longitudinal image of atypical pylorus in 5-week-old boy with IHPS. Although there is detectable flow, it is less visible than that in most other patients with IHPS. Arrows point to muscle layer. (g) Transverse image of pylorus in same patient as in f, with similar findings. Arrows point to muscle layer.
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Figure 1f. Doppler US findings in patients with IHPS. (a) Longitudinal image shows markedly increased flow to hypertrophied pylorus in 4-week-old girl. Solid arrows point to muscle layer. Open arrow points to mucosal flow. (b) Transverse image obtained in 5-week-old girl. Note the collar of increased flow in the submucosal plexus, branching into the luminal mucosa and adjacent muscle layer (arrows). (c) Longitudinal image of hypertrophied pylorus in 3-week-old boy with typical IHPS. Note the increased flow to the mucosa within the canal, protruding into the adjacent fluid-filled antrum (A). Straight arrows outline the adjacent thickened muscle. Curved arrow points to base of duodenal bulb. (d) Longitudinal image of hypertrophied pylorus in 5-week-old boy with typical IHPS. Note the markedly increased flow to the mucosal layer, which is detailed in the spectral tracing at the bottom of the image. A = antrum. (e) Longitudinal image of hypertrophied pylorus in 2-week-old boy with IHPS. Note the markedly increased flow to the muscle layer, which is detailed in the spectral tracing at the bottom of the image. D = duodenal bulb. (f) Longitudinal image of atypical pylorus in 5-week-old boy with IHPS. Although there is detectable flow, it is less visible than that in most other patients with IHPS. Arrows point to muscle layer. (g) Transverse image of pylorus in same patient as in f, with similar findings. Arrows point to muscle layer.
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Figure 1g. Doppler US findings in patients with IHPS. (a) Longitudinal image shows markedly increased flow to hypertrophied pylorus in 4-week-old girl. Solid arrows point to muscle layer. Open arrow points to mucosal flow. (b) Transverse image obtained in 5-week-old girl. Note the collar of increased flow in the submucosal plexus, branching into the luminal mucosa and adjacent muscle layer (arrows). (c) Longitudinal image of hypertrophied pylorus in 3-week-old boy with typical IHPS. Note the increased flow to the mucosa within the canal, protruding into the adjacent fluid-filled antrum (A). Straight arrows outline the adjacent thickened muscle. Curved arrow points to base of duodenal bulb. (d) Longitudinal image of hypertrophied pylorus in 5-week-old boy with typical IHPS. Note the markedly increased flow to the mucosal layer, which is detailed in the spectral tracing at the bottom of the image. A = antrum. (e) Longitudinal image of hypertrophied pylorus in 2-week-old boy with IHPS. Note the markedly increased flow to the muscle layer, which is detailed in the spectral tracing at the bottom of the image. D = duodenal bulb. (f) Longitudinal image of atypical pylorus in 5-week-old boy with IHPS. Although there is detectable flow, it is less visible than that in most other patients with IHPS. Arrows point to muscle layer. (g) Transverse image of pylorus in same patient as in f, with similar findings. Arrows point to muscle layer.
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Figure 2a. Doppler US findings in patients without IHPS (control patients). A = antrum, D = duodenal bulb. Longitudinal images obtained in (a) a 2-month-old boy, (b) a 3-month-old boy, and (c) an 8-week-old girl show no detectable flow. Antropyloric canal is closed in a and open in b and c. (d) Longitudinal image obtained in 10-day-old girl shows atypical high flow in the open antropyloric canal. There is visible flow to the dorsal portion of the muscle layer.
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Figure 2b. Doppler US findings in patients without IHPS (control patients). A = antrum, D = duodenal bulb. Longitudinal images obtained in (a) a 2-month-old boy, (b) a 3-month-old boy, and (c) an 8-week-old girl show no detectable flow. Antropyloric canal is closed in a and open in b and c. (d) Longitudinal image obtained in 10-day-old girl shows atypical high flow in the open antropyloric canal. There is visible flow to the dorsal portion of the muscle layer.
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Figure 2c. Doppler US findings in patients without IHPS (control patients). A = antrum, D = duodenal bulb. Longitudinal images obtained in (a) a 2-month-old boy, (b) a 3-month-old boy, and (c) an 8-week-old girl show no detectable flow. Antropyloric canal is closed in a and open in b and c. (d) Longitudinal image obtained in 10-day-old girl shows atypical high flow in the open antropyloric canal. There is visible flow to the dorsal portion of the muscle layer.
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Figure 2d. Doppler US findings in patients without IHPS (control patients). A = antrum, D = duodenal bulb. Longitudinal images obtained in (a) a 2-month-old boy, (b) a 3-month-old boy, and (c) an 8-week-old girl show no detectable flow. Antropyloric canal is closed in a and open in b and c. (d) Longitudinal image obtained in 10-day-old girl shows atypical high flow in the open antropyloric canal. There is visible flow to the dorsal portion of the muscle layer.
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With stratification of the patients with IHPS into high-flow (grade 3.00) and low-flow (grade < 3.00) groups, we identified 29 infants in the high-flow group (mean flow grade of 3.00 for both muscle and mucosa by definition) and 12 infants in the low-flow group (mean flow grades, 2.33 for muscle and 2.58 for mucosa). Comparison of muscle and mucosal thickness between these two groups yielded no significant difference, with or without stratification by sex (Table 2). Comparison of patient sex between the high- and low-flow groups also yielded no significant difference.
Only one patient underwent more than one US examination. This male patient was in the IHPS group and is of special interest. This infant had a family history of IHPS in an older male sibling; consequently his symptoms generated a high index of clinical suspicion, which led to an early request for US imaging on the basis of clinical grounds alone. Therefore, this patient was imaged with US three times during the development of IHPS: at ages 2, 5, and 6 weeks. As stated previously, this infant’s data were counted only once, and only his last examination results were considered in the group analyses. However, this patient’s findings from preceding examinations are of interest. When this infant was aged 2 weeks, the muscle was 2.8-mm thick and the mucosa 4.0-mm thick, and because opening of the pyloric canal could be seen in real time, a diagnosis of IHPS was not made; the flow grade was 2 for the muscle and 3 for the mucosa. At age 5 weeks, the muscle was 3.0-mm thick and the mucosa 3.8-mm thick, the flow grade was 3 for both the muscle and the mucosa, and opening of the pyloric canal was again visible in real time. At age 6 weeks, the muscle was 3.5-mm thick and the mucosa 5.0-mm thick; the flow grade was 3 for both the muscle and the mucosa. IHPS was confirmed surgically after the third US examination.
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DISCUSSION
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Although there is a familial predisposition for the development of IHPS, no clear picture has emerged regarding either the exact genetic mechanism involved or the postnatal events that lead to the complete evolution and clinical presentation of this abnormality. Untreated, IHPS leads to dehydration, emaciation, and often death. Surgery is curative and results in the return of the muscle to its normal state within 2–4 months (7,8).
Several theories to explain the development of IHPS have been proposed. Most current theories are focused on the innervation of the abnormally thickened antropyloric musculature; a multiplicity of associated abnormalities in the innervation of the muscle have been identified and documented (1). However, these associated findings alone do not explain the permanent and relatively rapid resolution of the anatomic abnormalities once the obstruction has been surgically relieved. Intravenous therapy with atropine for approximately 1 week followed by oral therapy for several weeks can lead to cessation of vomiting and eventual return—within several months—of the pylorus to a normal state (10). These findings suggest that uninhibited muscle contractions are one of the major contributors to the clinical symptoms of IHPS. The results further indicate a wide range of effective doses, which the authors ascribe in part to possibly compromised blood flow to the affected muscle. Our study results indicate, in contrast, that this blood flow is increased in patients with IHPS.
Another theory suggests that some infants may be born with an increased parietal cell mass (11). This mass, in turn, leads to gastric hypersecretion, repeated pyloric contraction, and delayed emptying and thus creates the setting for a cycle of obstruction and hypersecretion that culminates in IHPS.
To our knowledge, the blood flow to the antropyloric area in patients with IHPS has not been previously evaluated. However, Doppler US enables the assessment of blood flow to the antropyloric canal in vivo and represents a new method of studying this common and enigmatic condition. Our study findings indicate that there is a significant increase in the vascularity of the antropyloric canal in infants with IHPS; the increased blood flow occurs in both muscle and mucosal layers and is not dependent on either the magnitude of these components or the sex of the patient. It seems unlikely that this phenomenon is a precipitating event. Rather, it is much more likely that this increased vascularity is a mediator in the chain of events that occurs in predisposed patients and that leads to the morphologic changes of IHPS; the presence of increased flow in both muscle and mucosal layers strongly suggests that both layers are implicated in the evolution of IHPS.
One question remains unanswered: What is the timing of the increased flow with respect to the inception and evolution of IHPS? If one were to assume that muscle thickness is a progressive continuum, then the lack of a significant difference between muscle thickness and flow grade in patients with hypertrophic pyloric stenosis would suggest that the vascularity to the pylorus is not a time-dependent phenomenon. The exact time that the abnormality develops is very difficult to determine on medical history–based clinical grounds, however. Many infants with IHPS have 
spitting-up
episodes for variable periods, and the transition to forceful vomiting is difficult to identify with precision. Because this determination is imprecise, we chose not to consider the onset of symptoms in our current investigation.
In one patient in this study, a progressive increase in muscle and mucosal thickness with increased flow to both components, but primarily to the mucosal layer, and concomitant progression of pyloric relaxation failure and clinical symptoms was observed during the period of IHPS evolution. However, no valid inferences can be drawn from the single patient who was observed during the development of IHPS, and the observations made are anecdotal at this point.
One of the limitations of this study is the fact that the control group consisted of infants who were vomiting and was therefore not a strictly healthy group. Although the majority of these patients probably had uncomplicated reflux, it is possible that some of them had gastritis or other similar abnormalities, which may explain why there was some increased flow in a minority of these patients. Nevertheless, there was a highly significant difference in the degree of flow between the IHPS and non-IHPS patient groups, with the majority of infants without IHPS demonstrating no detectable flow during Doppler US examination.
In summary, the multiple abnormalities documented within the hypertrophied pylorus in infants with hypertrophic pyloric stenosis develop soon after the postnatal inception of feeding. These abnormalities are reversible, and relief of obstruction by means of longitudinal division of the muscle results in a permanent cure and relatively rapid reversal of the abnormal anatomic and histochemical parameters to normal states. Our study findings indicate that increased blood flow accompanies and may be required to induce the morphologic changes that occur in the antropyloric muscle and mucosa of infants during the development of IHPS.
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FOOTNOTES
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Abbreviation: IHPS = infantile hypertrophic pyloric stenosis
Author contributions: Guarantor of integrity of entire study, M.H.S.; study concepts, all authors; study design, M.H.S.; literature research, M.H.S.; clinical studies, M.H.S., R.M.H., S.M.S., L.A.B.; experimental studies, M.H.S., R.M.H., S.M.S., L.A.B.; data acquisition, M.H.S., S.M.S., L.A.B.; data analysis/interpretation, M.H.S., Y.Z.; statistical analysis, Y.Z.; manuscript preparation, definition of intellectual content, and editing, M.H.S.; manuscript revision/review, M.H.S., R.M.H., S.M.S., Y.Z.; manuscript final version approval, all authors
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REFERENCES
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B. P. Wood
What is the Pathology of Pyloric Stenosis?
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March 1, 2004;
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ABSTRACT
INTRODUCTION
