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Thread: Hypertrophic Pyloric Stenosis Images - Pediatric cases

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    Default Hypertrophic Pyloric Stenosis Images - Pediatric cases

    Practice Essentials
    Hypertrophic pyloric stenosis (HPS) causes a functional gastric outlet obstruction as a result of hypertrophy and hyperplasia of the muscular layers of the pylorus. In infants, HPS is the most common cause of gastric outlet obstruction and the most common surgical cause of vomiting.

    Essential update: Early azithromycin exposure may increase the risk of infantile pyloric stenosis
    In a retrospective study of pediatric data from the US military health system (MHS) spanning 11 years, investigators found that administering oral azithromycin to infants in the first 2 weeks of life increased their risk of developing HPS by more than 7 fold (P < 0.001); when azithromycin was given at ages 15-42 days, the risk of developing HPS was more than 2 fold (P =0.028).There were no cases of HPS among infants exposed to azithromycin between ages 43 and 90 days.Further studies have reported this association along with an increased risk of developing infantile hypertrophic pyloric stenosis following the ingestion of erythromycin and azithromycin, especially in the first 14 days of life. Based on these reports, monitoring for HPS in infants receiving erythromycin, azithromycin, or prostaglandin infusion during the first few weeks of life is recommended.

    Diagnosis
    Serum electrolytes should be measured to document adequacy of fluid resuscitation and correction of electrolyte imbalances before surgical repair. The classic biochemical abnormality in HPS is hypochloremic, hypokalemic metabolic alkalosis.

    Management
    Surgical repair of HPS is fairly straightforward and without many complications. However, properly preparing the infant is vitally important.

    Pathophysiology
    HPS occurs secondary to hypertrophy and hyperplasia of the muscular layers of the pylorus, which cause a functional gastric outlet obstruction. Diffuse hypertrophy and hyperplasia of the smooth muscle of the antrum of the stomach and pylorus proper narrow the channel, which then can become easily obstructed. The antral region is elongated and thickened to as much as twice its normal size. In response to outflow obstruction and vigorous peristalsis, stomach musculature becomes uniformly hypertrophied and dilated. Gastritis may occur after prolonged stasis. Hematemesis is occasionally noted. The patient may become dehydrated as a result of vomiting and develop marked hypochloremic alkalosis.

    Researchers have investigated the cause of this muscle hypertrophy for several decades. Many believe the problem is induced by the pyloric musculature failing to relax. Results of studies of pyloric muscle innervation are inconclusive, possibly showing a tendency toward fewer or more immature ganglion cells in affected individuals.
    Hypertrophic Pyloric Stenosis Images Pediatric attachment.php?s=793e652919d480e8b961b95024abf019&attachmentid=308&d=1435790203

    No definitive cause for hypertrophic pyloric stenosis has been found. However, various environmental and hereditary factors have been implicated. Suspected environmental factors include infantile hypergastrinemia, abnormalities in the myenteric plexus innervation, cow's milk protein allergy, and exposure to macrolide antibiotics. Hereditary factors may also play a role; hypertrophic pyloric stenosis occurs in as many as 7% of infants of affected parents. The etiology is probably multifactorial, with both genetic and environmental factors contributing. Recognition that hypertrophic pyloric stenosis is an acquired disorder and not a congenital disorder is increasing. Recently, genetic studies have identified susceptibility loci for infantile HPS and molecular studies have concluded that smooth muscle cells are not properly innervated in infantile HPS.

    Researchers who identified a cholesterol-related genetic locus associated with risk for infantile HPS have also demonstrated that low serum lipids are a risk factor for this disorder. In a genome-wide association study, Feenstra and colleagues found that the single-nucleotide polymorphism (SNP) most strongly associated with risk for HPS was rs12721025 on the long arm of chromosome . In a follow-up study, the researchers compared levels of total cholesterol, low-density lipoprotein, high-density lipoprotein, and triglycerides in plasma obtained prospectively from 46 HPS cases and 189 control patients. Mean total cholesterol levels for cases and controls were 65.2 mg/dL and 75.2 mg/dL, respectively. The risk for IHPS was inversely and significantly associated with total cholesterol level, with an odds ratio of 0.77 per 10 mg/dL.

    United States
    Pyloric stenosis is the most common cause of gastric outlet obstruction in infants. It is also the most common surgical cause of vomiting in infants. The prevalence of hypertrophic pyloric stenosis ranges from 1.5-4 cases per 1000 live births among whites, although it is less prevalent among blacks and Asian Americans.

    Mortality/Morbidity
    Operative therapy for hypertrophic pyloric stenosis has remained unchanged for nearly 100 years. Outcomes have improved through advances in early diagnosis, preoperative resuscitation, operative anesthetics, and nutritional management. Mortality may rarely result from late diagnosis, resulting in dehydration and shock. Mortality is also rare after pyloromyotomy.
    Hypertrophic Pyloric Stenosis Images Pediatric attachment.php?s=793e652919d480e8b961b95024abf019&attachmentid=309&d=1435790232

    Race
    Reported prevalence of hypertrophic pyloric stenosis among whites ranges from 1.5-4 cases 1000 live births; hypertrophic pyloric stenosis is less prevalent among blacks, Asians, and Hispanics.

    Sex
    Pyloric stenosis has a well-known predilection for occurring more often in males than in females, with reported ratios ranging from 2:1 to 5:1. First-born male children are believed to have the highest risk of developing hypertrophic pyloric stenosis.

    Age
    Newborns typically develop signs of gastric outlet obstruction at 3-4 weeks. Cases of hypertrophic pyloric stenosis have been documented from the first week of life to 3 months. Approximately 95% of infantile hypertrophic pyloric stenosis cases are diagnosed in those aged 3-12 weeks. Premature infants generally develop symptoms later than full-term infants, which may lead to a delay in diagnosis.

    Consultations
    Early consultation with a surgeon familiar with neonatal care is warranted because treatment is essentially surgical. Early consults facilitate decisions for diagnostic studies, fluid resuscitation, and scheduling the operative procedure. This is especially important if the child requires transfer to another facility for surgical care. The American Pediatric Surgical Association offers guidelines for appropriate consultation and transfer of small infants. Good outcome has been shown to depend on the quality of preoperative correction of fluid and electrolyte abnormalities, availability of a pediatric anesthetist, and training level of the surgeon.

    ٌReferences:
    http://emedicine.medscape.com/articl...9-treatment#d8











    Last edited by Medical Photos; 09-01-2015 at 07:21 PM.

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    Default Hypertrophic Pyloric Stenosis Images Pediatric cases

    Are there any pediatric urological surgery coders out there? Im looking to pick your brains and network. I find CPT has not kept up with the changing times and its hard to find codes for what the surgeons are doing.

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    Best work - it's highly paid hobby.

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