PYLORIC STENOSIS Decreased frequency and volume of stools11.

Is the narrowing of the pyloric sphincter at the outlet of the stomach ETIOLOGY: uk PATHOPHYSIOLOGY:1. The pylorus narrows2. This leads to obstruction of the pyloric sphincter CLINICAL MANIFESTATIONS:1. No abnormal signs in the first weeks after birth2. Regurgitation or non-projectile vomiting3. Vomiting increases in frequency and force4. No signs of anorexia5. Promote adequate hydration4. No evidence of pain6. Prevent aspiration5. Weight loss7. Provide post-operative care6. Upper abdominal distention8. Provide family teaching Palpable mass9. Visible gastric peristaltic wave10. Signs of malnutrition and dehydration LABORATORY STUDIES:1. UTZ and upper-GI study2. ABG3. Electrolyte studies4. CBC NURSING MANAGEMENT1. Monitor feeding pattern and association between feedings and vomiting2. Assess the amount, character and frequency of vomitus3.

SURGICAL HISTORY PYLORIC STENOSIS 1. CHIEF COMPLAINT Pyloric stenosis 2. HPI 3. ROS 4. SYMPTOMS Nonbilious vomiting Regurgitation Emesis Poor weight gain Weight loss Marasmus Decreased urinary output Lethargy Shock Jaundice 5. HISTORY FAMILY HISTORY SOCIAL HISTORY PASTMEDICAL HISTORY CHRONIC CONDITIONS 6. ALLERGIES 7. PHYSICAL EXAMINATION Firm, nontender, and mobile hard pylorus that is 1-2 cm in diameter, described as an "olive," may be present in the right upper quadrant at the lateral edge of the rectus abdominus muscle. Gastric peristalsis just prior to emesis as the peristaltic waves tries to overcome the obstruction. Depressed fontanelles Dry mucous membranes Decreased tearing Poor skin turgor Lethargy 8. SPECIFIC DATA LIKE GRADING ETC 9. TESTS TO BE ORDERED CBP Serum Electrolytes Serum pH

BUN Serum Creatinine levels Bilirubin level Ultrasonography CT scan Upper GI endoscopy 10.ASSESSMENT /PLAN

Correct fluid loss, electrolytes, and acid-base imbalance with crystalloid fluid Patient should on nothing by mouth The Ramstedt pyloromyotomy 11.EDUCATION 12.MEDICATION 13.FOLLOW-UP

What Is Pyloric Stenosis? Pyloric stenosis is the narrowing of part of the stomach (the pylorus) that leads into the small intestines. This narrowing occurs because the muscle around the pylorus has grown too large. Most babies with pyloric stenosis begin to vomit during the second to third week of life. Babies begin with "spitting up" that turns into forceful projectile vomiting. The vomiting occurs after feeding. Sometimes, in formula-fed infants, different kinds of formula are tried without any change noted.

Diagram of normal stomach and pylorus. Note the crosssection showing normal pyloric opening. Diagram of stomach with pyloric stenosis. Note the crosssection showing how the pyloric opening is very narrowed. Diagram of stomach after repair of pyloric stenosis. Note (in the

crosssection) how an incision has been made in the muscle, enlarging the pylorus and relieving the obstruction . How is pyloric stenosis diagnosed? The diagnosis of pyloric stenosis is made when an infant has a history of progressive forceful vomiting. The pyloric valve (opening at the bottom of the stomach that regulates the stomach emptying) becomes bigger over time and blocks the stomach from emptying. The baby begins to lose weight, and may become dehydrated. Dehydrated means the baby is not keeping enough fluid in his body. The baby may show signs of being sleepy or not be as active as usual. The baby may not have had a wet diaper in several hours and the soft spot on the top of his head may be sunken. A physical exam by the doctor sometimes shows an enlarged pyloric valve. You may hear the doctor say that it feels like an olive because thats the way it feels in shape and firmness. Sometimes it is hard to examine the baby if he has a stomach full of breast milk/formula or air and it is necessary to place a small nasogastric (NG) tube. The NG tube is a small plastic

tube that goes through the infants nose or mouth into their stomach. It helps the stomach empty by draining air or anything else that may be in it. The doctor may do tests to determine if the baby has pyloric stenosis. One test is a barium study or upper GI. This test involves the baby drinking a small amount of barium (a white, chalky liquid) that shows up easily on an X-ray picture. This test can tell the doctor if the baby has pyloric stenosis or another condition called gastroesophageal reflux (GER). GER is when the contents of the stomach come back up the esophagus. Another test that may be done is an abdominal ultrasound. This test involves a metal wand that is moved over the babys stomach. The metal wand is able to take pictures using sound waves. It is a common test used in pregnancy to look at the baby and does not harm the baby. How is pyloric stenosis treated? If a diagnosis of pyloric stenosis is made, the baby will have some blood work done to check for dehydration. A catheter will be placed into the vein (IV) to replace fluids that the baby needs. The baby may go to surgery that day or the following day. It is very important that the baby not drink anything until after surgery. The operation is called a pyloromyotomy (pie-lore-oh-my-ottoe-me). This operation spreads open the muscle around the pyloric valve of the stomach. The incision is about 1 inch long either right around the belly button or on the right hand side of the abdomen. Stitches that dissolve are used, so they wont have to be removed later.

Feedings will start slowly . Your nurse will tell you when to start. The amount of breast milk or formula will be limited at first and will be increased with each feed. A few episodes of vomiting shortly after surgery are not uncommon but resolve quickly. Most babies can be discharged home 1-2 days after surgery and have no long term problems.

Vertical Pyloromyotomy scar (large) 30 hrs post-op in a 1 month-old baby

Horizontal Pyloromyotomy scar 10 days post-op in a 1 month-old baby Infantile pyloric stenosis is typically managed with surgery; very few cases are mild enough to be treated medically. [edit] Prior to surgery and surgery alternatives

The danger of pyloric stenosis comes from the dehydration and electrolyte disturbance rather than the underlying problem itself. Therefore, the baby must be initially stabilized by correcting the dehydration and hypochloremic alkalosis with IV fluids. This can usually be accomplished in about 2448 hours. Intravenous and oral atropine may be used to treat pyloric stenosis. It has a success rate of 85-89% compared to nearly 100% for pyloromyotomy, however it requires prolonged hospitalization, skilled nursing and careful follow up during treatment.[7] It might be an alternative to surgery in children who have contraindications for anesthesia or surgery. [edit] Surgery The definitive treatment of pyloric stenosis is with surgical pyloromyotomy known as Ramstedt's procedure (dividing the muscle of the pylorus to open up the gastric outlet). This is a relatively straightforward surgery that can possibly be done through a single incision (usually 34 cm long) or laparoscopically (through several tiny incisions), depending on the surgeon's experience and preference.[8] Today, the laparoscopic technique has largely supplanted the traditional open repairs which involved either a tiny circular incision around the navel or the Ramstedt procedure. Compared to the older open techniques, the complication rate is equivalent, except for a markedly lower risk of wound infection.[9] This is now considered the standard of care at the majority of Children Hospitals across the US, although some surgeons still perform the open technique. Following repair, the small 3mm incisions are hard to see. The vertical incision, pictured and listed above, is no longer usually required. Though many incisions have been horizontal in the past years.

Once the stomach can empty into the duodenum, feeding can commence. Some vomiting may be expected during the first days after surgery as the gastro-intestinal tract settles. Very occasionally the myotomy was incomplete and projectile vomiting continues, requiring repeat surgery. But the condition generally has no long term side-effects or impact on the child's future Mortality/Morbidity Death from infantile hypertrophic pyloric stenosis is rare and unexpected. The Race Infantile hypertrophic pyloric stenosis is more common in whites than Hispanics, blacks, or Asians. The incidence is 2.4 per 1000 live births in whites, 1.8 in Hispanics, 0.7 in blacks, and 0.6 in Asians. It is also less common amongst children of mixed race parents. Sex Infantile hypertrophic pyloric stenosis has a male-to-female predominance of 4:1, with 30% of patients with infantile hypertrophic pyloric stenosis being first-born males. Age reported mortality rate is very low and usually results from delays in diagnosis with eventual dehydration and shock. The usual age of presentation is approximately 3 weeks of life (1-18 wk). Approximately 95% of infantile hypertrophic pyloric stenosis cases are diagnosed in those aged 3-12 weeks. Infantile hypertrophic pyloric stenosis is rare in premature infants. In addition, premature infants have a delayed diagnosis secondary to low birth weight and atypical presentation. History
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Classically, the infant with pyloric stenosis has nonbilious vomiting or regurgitation, which may become projectile (in as many as 70% of cases),

after which the infant is still hungry.[4] Emesis may be intermittent or occur after each feeding. The emesis may become brown or coffee color due to blood secondary to gastritis or a MalloryWeiss tear at the gastroesophageal junction. The infant begins to show signs of dehydration and malnutrition, such as poor weight gain, weight loss, marasmus, decreased urinary output, lethargy, and shock. The infant may develop jaundice, which is corrected upon correction of the disease. In as many as 60-80% of the infants with infantile hypertrophic pyloric stenosis (IHPS), a firm, nontender, and mobile hard pylorus that is 1-2 cm in diameter, described as an "olive," may be present in the right upper quadrant at the lateral edge of the rectus

abdominus muscle. This is best palpated after the infant has vomited and when calm, or when the gastric contents have been removed via nasogastric tube. Clinicians may also observe gastric peristalsis just prior to emesis as the peristaltic waves try to overcome the obstruction. Signs of dehydration include depressed fontanelles, dry mucous membranes, decreased tearing, poor skin turgor, and lethargy. The classic signs of infantile hypertrophic pyloric stenosis are becoming less common. The mean age of presentation is getting significantly younger, and infants are not developing the physical signs or electrolyte abnormalities they were 20 years ago. Additionally, the availability of diagnostic imaging is allowing clinicians to make this diagnosis before other

clinical manifestations appear

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Marasmus is a form of severe protein-energy malnutrition characterized by energy deficiency. A child with marasmus looks emaciated. Body weight may be reduced to less than 80% of the average weight that corresponds to the height .[citation needed] Marasmus occurrence increases prior to age 1, whereas kwashiorkor occurrence increases after 18 months. It can be distinguished from kwashiorkor in that kwashiorkor is protein