Explanation:

Intussusception is telescoping of one portion of the intestine into an adjacent segment, causing intestinal obstruction and sometimes intestinal ischemia.
The initial symptoms are recurrent colicky abdominal pain that occurs after 15 to 20 min, often with vomiting. The child appears relatively well between episodes. Later, as intestinal ischemia develops, pain become steady, the child becomes lethargic and mucosal hemorrhage causes heme-positive stool on rectal examination and sometimes spontaneous passage of a “currant jelly” stool. A palpable abdominal mass, described as sausage-shaped, is sometimes present.
Biliary colic is unlikely to be present in this young child.

Explanation:

Hypertrophic pyloric stenosis can cause almost complete gastric outlet obstruction. Symptoms develop between 2 and 6 weeks of life. Projectile vomiting (without bile) occurs shortly after eating. Until dehydration sets in, the child feeds avidly and otherwise appears well, unlike many of those with vomiting due to systemic illness. Diagnosis is by abdominal ultrasonography showing increased thickness of the pylorus (typically to = 4 mm; normal, < 2 mm). The classic electrolyte pattern of an infant with pyloric stenosis is that of hypochloremic, hypokalemic, metabolic alkalosis. Initial treatment is directed at hydration and correcting electrolyte abnormalities. Definitive treatment is a longitudinal pyloromyotomy, which leaves the mucosa intact and separates the incised muscle fibers.

Explanation:

The girl in this clinical vignette has pseudomembranous colitis, which is caused by the toxins produced by clostridium difficile. The colon is colonized by C difficile after eradication of the normal microflora by a course of antibodies. Virtually all antibiotics, including metronidazole and vancomycin, have been implicated in the pathogenesis of pseudomembranous colitis. Patients usually present with watery or bloody diarrhea, tenesmus, fever, and abdominal pain. Symptoms typically occur 7- 10 days after initiation of the antibiotic; in rare cases, pseudomembranous colitis can occur up to 6 weeks after antibiotic initiation. On sigmoidoscopy or colonoscopy, the disease is characterized by an accumulation of an inflammatory exudates, the “pseudomembrane” over the mucosa. Assay for C difficile toxins is useful in diagnosing pseudomembranous colitis. An alternative is to perform stool cultures for C. difficile. Oral metronidazole is the treatment of choice.

Explanation:

Hypernatremia is plasma Na concentration > 145 mEq/L caused by a deficit of water relative to solute. A major symptom is thirst; other clinical manifestations are primarily neurologic (due to an osmotic shift of water out of cells), including confusion, neuromuscular excitability, seizures, and coma. Diagnosis is by measuring serum Na. Treatment is usually controlled water replacement with 5% dextrose/0.3% to 0.45% saline solution IV in volumes equal to the calculated fluid deficit, given over 2 to 3 days to avoid a rapid fall in serum osmolality, which would cause rapid movement of water into cells and potentially lead to cerebral edema. The goal of treatment is to decrease serum Na by about 10 mEq/day.

Explanation:

Ulcerative colitis is a chronic disease in which the large intestine becomes inflamed and ulcerated (pitted or eroded), leading to flare-ups (bouts or attacks) of bloody diarrhea, abdominal cramps, and fever. The Long-term risk of colon cancer is increased. Ulcerative colitis may start at any age but usually begins between the ages of 15 and 30. A small group of people have their first attack between the ages of 50 and 70. The symptoms of ulcerative colitis occur in flare-ups. A flare-up may be sudden and severe, producing violent diarrhea (typically bloody), high fever, abdominal pain, and peritonitis (inflammation of the lining of the abdominal cavity). During such flare-ups, the person is profoundly ill. More often, a flare-up begins gradually, and the person has an urgency to have a bowel movement defecate), mild cramps in the lower abdomen, and visible blood and mucus in the stool. A flare-up can last days or weeks and can recur at any time.
If that disease extends farther up the large intestine, the stool is loose: and the person may have as many as l0 to 20 bowel movements a day often, the person has severe abdominal cramps and distressing, painful spasms that accompany the urge to defecate. There is no relief at night. The stool may be watery and contain pus, blood, and mucus. Frequently, the stool consists almost entirely of blood and pus. The person clam may have a fever and a poor appetite and may lose weight

Explanation:

Celiac disease is characterized by inflammatiun of the upper small intestine in response to dietary gluten. The endomysial antibody test has led to improvements in the diagnosis of celiac disease.
Minimal or atypical symptoms occur in many patients, especially those presenting with the disease in adulthood. Severe symptoms are most common in young children. A fulminant form, characterized by diarrhea, failure to thrive, abdominal distention and vomiting, occurs in children younger thang two years of age. The median age at the time of diagnosis in children is four years, and loss of appetite is a common symptom. Formerly, the classic diagnostic approach was to obtain a series of intestinal biopsies: before treatment, after dietary withdrawal of gluten and, finally, following a challenge with gluten. Such a series of biopsies is now rarely performed.
The development of the serum endomysial antibody test has changed the method of diagnosis. Some authorities now consider a positive endomysial antibody test plus clinical improvement following withdrawal of gluten sufficient evidence for the diagnosis of celiac disease.

Explanation:

Intussusception is telescoping of one portion of the intestine (intussusception) into an adjacent segment (Intussusception), causing intestinal ischemia. Intussusception generally occurs between ages 3 months and 3 years, with 65% of cases occurring before age 1. It is the most common cause of intestinal obstruction in this age group, in whom it is usually idiopathic. In older children, there may be a “lead point.” i.e., a mass or other intestinal abnormality that triggers the telescoping; examples include polyps, lymphoma, Meckel´s diverticulum, and Henoch-Schonlein purpura. Cystic fibrosis is also a risk factor. The telescoping segments obstruct the intestine and ultimately impair blood flow, causing ischemia, gangrene, and perforation. The initial symptoms are recurrent colicky abdominal pain that occurs every 15 to 20 min, often with vomiting. The child appears relatively well between episodes. Later, as intestinal ischemia develops, pain become steady, the child becomes lethargic, and mucosal hemorrhage causes heme-positive stool on rectal examination and sometimes spontaneous passage of a “currant jelly” (blood mixed with mucus) stool. A palpable abdominal mass, described as sausage-shaped, is sometimes present not seen in volvulus which occurs in adults

Explanation:

Gastroesophageal reflux is a common cause of wheezing in infants. At 5 months of age, most infants no longer spit up several times a day, and this is a major clue that the wheezing may be from the reflux. Also there is no family history of asthma and the wheezing is not recurrent infections and failure to thrive than with intermittent wheezing.

Explanation:

Question Explanation:

A diaphragmatic hernia is a birth defect, which is an abnormality that occurs before birth as a fetus is forming in the mother´s uterus. An opening is present in the diaphragm (the muscle that separates the chest cavity from the abdominal cavity). With this type of birth defect, some of the organs that are normally found in the abdomen move up into the chest cavity through this abnormal opening. Respiratory distress usually develops shortly after the baby is born because of ineffective movement of the diaphragm and crowding of the lung tissue, which causes collapse. The reason why this occurs is not known. Symptoms include severe breathing difficulty, bluish coloration of the skin duo to lack of oxygen, fast breathing (tachypnea) asymmetry of the chest wall and fast heart rate (tachycardia).
Examination of the infant shows: chest movements asymmetric with breathing, breath sounds absent on the affected side and bowel sounds heard in the chest. A chest x-ray may show abdominal organs in chest cavity.

Explanation:

It is important to differentiate whether the patient´s abdominal pain is due to an underlying organic, psychogenic, or functional cause. A full history must be taken to determine the nature and characteristics of the pain and any associated symptoms. The initial interview should be performed with the entire family together; however, the patient and parents should then be interviewed separately. At this point, the physician may be able to discern if the abdominal pain is a manifestation of a stress in the home or school environment. The patient may also be more forthcoming when interviewed alone, and may verbalize any fears or complaints more easily.

Explanation:

Rectal prolapse occurs in 20% of patients with cystic fibrosis who are aged 6 months to 3 years. The appropriate intervention at this point is to order a sweat chloride test to see if this child has cystic fibrosis.

Explanation:

The most common symptom is painless rectal bleeding. Other warning signs include polyps protruding in the rectum; slipping of one part of the intestine into another; or malnutrition.
A juvenile polyp is a growth that projects from the lining of the intestine and originates in the tissues supporting that lining. It does not arise from the colonocytes (colonic lining cells) themselves but from the tissues underneath the lining cells. It is not neoplastic but hamartomatous. A hamartoma is a growth that arises from normal tissues. It is self-limiting and benign. Juvenile polyps can be solitary or multiple.
Juvenile polyps occur in children, they typically outgrow their blood supply and autoamputate some time during or after puberty. Treatment is required only for uncontrollable bleeding or intussusception.

Explanation:

Niacin overdose may cause anaphylaxis due to histamine release; also, cholestatic jaundice, cutaneous vasodilation, and cardiac arrhythmias may arise. Although thiamin toxicity is very rare, the potential adverse effects include an anaphylactic response and/or respiratory depression. There are no significant toxicities associated with biotin overdose. Vitamin A toxicity may cause pseudotumor cerebri, or retching associated with a rise in intracranial pressure. Finally, vitamin C overdose may cause a decrease in copper absorption or a rise in the excretion of oxalic acid

Explanation:

Meckel´s diverticulum is a common congenital anomaly that occurs when there is a persistence of the omphalomesenteric or vitelline duct. This duct initially connects the primitive gut to the yolk sac. Meckel´s diverticulum is usually found in the distal ileum within 12 inches of the ileocecal valve. It may contain heterotopic rests of gastric mucosa or pancreatic tissue. Technetium 99m pertechnetate scanning is used to locate ectopic gastric mucosa. The bladder is not a site of heterotopic rests of gastric mucosa. The duodenum is an important site of gastric heterotopia, but the basic pH of the secretions in the duodenum tends to keep the heterotopia from causing peptic ulceration. The esophagus can have gastric heterotopia but this, is fairly uncommon and only rarely causes ulceration.
The gallbladder is a rare site of gastric heterotopia.

Explanation:

This patient has ulcerative colitis and will most likely have elevated titers of p-ANCA. Ulcerative colitis is an inflammatory bowel disease that involves only the colon. Presentation can be insidious or fulminant, but typically includes bloody diarrhea with mucus. Abdominal pain and tenesmus may also be present. Ninety percent of the cases have mild to moderate disease. These patients have fewer than six stools per day, no fever, and no anemia. Moderate disease presents with greater than six stools per day, fever, anemia, and hypoalbuminemia. Severe, fulminant disease courses with severe anemia, high fever, leukocytosis, and tachycardia. Symptoms should be present or at least 3 to 4 weeks. The sedimentation rate may be elevated or normal. Antineutrophil cytoplasmic antibody with a perinuclear staining pattern (p-ANCA) has been shown to be positive in 50 to 90% of patients. Endoscopy with biopsy is helpful, particularly in mild disease. No skip lesions are seen. The mucosa is friable and bleeds easily. Diffuse superficial ulcerations are seen. Therapy is also aimed at symptom relief. Aminosalicylates and sulfasalazine are commonly used. Steroids, orally or as enemas, are beneficial. Surgical treatment is total colectomy. The chance of requiring total colectomy is directly related to severity of disease at presentation.-Patients with ulcerative colitis are at higher risk of developing colon cancer.
Infectious colitis and Crohn disease are the main differential diagnosis.
Antineutrophil cytoplasmic antibody with a cytoplasmic (central) staining pattern (c-ANCA) is highly associated with Wegener granulomatosis and less commonly with Churg-Strauss syndrome, both a severe form of vasculitis.
Antinuclear antibodies are commonly elevated in connective tissue diseases, such as reticular erythematous mucinosis, lupus erythematosus, dermatomyositis, or mixed connective tissue disease. They are not elevated in ulcerative colitis.
Anti-Ro antibodies are a marker of subacute cutaneous lupus erythematosus and neonatal lupus erythematous, especially when associated with congenital heart block. They are not elevated in ulcerative colitis. Anti-Smith antibodies are considered specific for systemic lupus erythematosus and are not detected in patients with ulcerative colitis.
Anti-gliadin antibodies are for celiac disease that usually manifests earlier and unlikely to give bloody diarrhea. The question does not give hint about gluten diet.

Explanation:

Dehydration results from a total body loss of water and sodium. Acute infectious gastroenteritis is among the most common causes of dehydration in infants and young children. Mild and moderate dehydration may be managed at home with oral rehydration. Therapy, even if the child continues intermittent vomiting.
Hospitalizing the child would become necessary if the child was severely dehydrated or if he or she was not able to tolerate anything by mouth. Making the child NPO would be incorrect, because the child should be encouraged to take sips of water, even if IV fluids were being administered.
Once the child is able to tolerate oral rehydration better, there is no need to restrict the diet or continue a clear liquid diet. In fact, the child should be encouraged to eat whatever he or she usually enjoys eating.

Explanation:

Mesenteric lymphadenitis is an inflammation of the lymph nodes on the wall of the mesentery (the covering of the intestines). If is often a childhood illness, though occasionally seen in adults. It is a very co mon cause of abdominal pain in children, mimicking appendicitis, and often difficult to differentiate from appendicitis. It is estimated that 1 in 5 children diagnosed with appendicitis actually have mesenteric lymphadenitis.
The main symptom is abdominal pain. This is often located in the right lower abdomen or right iliac fossa. It is a colicky abdominal pain which just resolves momentarily without any intervention. The sufferer, usually a child, may be completely pain free between attacks. Characteristically, the pain moves from one spot to the other on the abdomen, in keeping with the movement of the bowel loops in the abdominal cavity.
Asking the child to turn to the left side will demonstrate this shift as the area of pain and tenderness will move along with the bowel to the left.
In appendicitis, the pain may initially start around the umbilicus, then moves over to the right iliac fossa. Once it settles there, it does not move around any longer.

Explanation:

Hypertrophic pyloric stenosis can cause almost complete gastric outlet obstruction.

Symptoms develop between 2 and 6 weeks of life Projectile vomiting (without bile) occurs shortly after eating. Until dehydration sets in, the child feeds avidly and otherwise appears well, unlike many of those with vomiting due to systemic illness. Diagnosis is by abdominal ultrasonography showing increased thickness of the pylorus (typically to ≥ 4 mm; normal, < 2 mm). The classic electrolyte pattern of an infant with pyloric stenosis is that of hypochloremic, hypokalemic, metabolic alkalosis.
Initial treatment is directed at hydration and correcting electrolyte abnormalities. Definitive treatment is a longitudinal pyloromyotomy, which leaves the mucosa intact and separates the incised muscle fibers.

Explanation:

Hypertrophic pyloric stenosis is the most likely diagnosis in this case. If it is allowed to progress untreated, there may be signs of malnutrition, constipation, oliguria and profound hypchloremic metabolic alkalosis. The latter is a characteristic sign of pyloric obstruction. As the child vomits chloride and hydrogen-rich gastric contents, hypochloremic alkalosis sets in. Pneumonia is not a common problem with pylori stenosis, as it can be with congenital tracheoesophageal fistulae for example. After feeding, there may be a visible peristaltic wave that progresses across the abdomen. However, since the point of obstruction is proximal to the small and large intestines and affected infants lose weight, the abdomen is usually flat rather than distended, especially in the malnourished infant. Currant jelly stool is a common clinical manifestation of intussusception. Mild jaundice with elevated indirect bilirubin is seen in about 5% of infants with pyloric stenosis, but is not a characteristic sign

Explanation:

Gastroesophageal reflux (GER) is a functional process occurring in a healthy infant. It is common and self-limited, and represents a physiologic process of ´spitting up´. GER occurs in the absence of poor weight gain, irritability, cough, pain, or anemia. The majority of infants with GER are thriving. It is important to consider other systemic disorders, and rule them out when appropriate possible causes of spitting up include pyloric stenosis, infections (e.g., gastrointestinal, genitourinary), and metabolic disorders. It is not necessary to perform a diagnostic evaluation prior to starting drug therapy unless a structural defect is highly suspected. GER in infants is usually self limited and resolves by 1 year of age.

Explanation:

Necrotizing enterocolitis is an acquired disease, primarily of preterm or sick neonates, characterized by mucosal or even deeper intestinal necrosis.
Signs and symptoms include feeding intolerance, lethargy, temperature instability, ileus, bloating, bilious emesis, hematochezia, reducing substances in the stool, apnea, and sometimes signs of sepsis.
In infants who develop NEC, 3 intestinal factors are usually present: a preceding ischemic insult, bacterial colonization, and intraluminal substrate (ie, enteral feedings).
Etiology is believed that an ischemic insult damages the intestinal lining, leading to increased intestinal permeability and leaving the intestine susceptible to bacterial invasion. Once feedings are begun, ample substrate is present for proliferation of luminal bacteria, which can penetrate the damaged intestinal wall, producing hydrogen gas. The gas may collect within the intestinal wall (pneumatosis intestinalis) or enter the portal veins; Diagnosis is clinical and is confirmed by imaging studies. Treatment is primarily supportive and includes nasogastric suction, parenteral fluids, TPN, antibiotics, isolation in cases of infection, and, often, surgery.

Explanation:

Rotavirus is a common and contagious virus that causes vomiting and diarrhea. Rotavirus is one of the most common causes of diarrhea in children. Although hardly any children die from rotavirus, worldwide the virus causes over 600,000 deaths a year, mostly in developing countries. Infection is spread mainly by swallowing material contaminated by the virus. Adults can become infected, but serious illness is rare.
Symptoms begin with fever and vomiting, followed by watery diarrhea, which typically lasts 5 to 7 days. If fluid losses are not replaced, dehydration develops. Dehydration makes the child weak and listless, with a dry mouth and rapid pulse

Explanation:

This case presentation is fairly typical for intussusception, the “telescoping” of a portion of the intestine into itself with obstruction and crampy pain it generally occurs between the ages of 6 months and 24 months. A sausage-shaped mass is often palpable as a result of the ileum being trapped within the colon. The presence of bloody mucus supports the diagnosis.
Pyloric stenosis generally occurs in the first 4-6 weeks of life (although it can occur as late as the fifth month) with a striking first-born male predominance. Emesis is the most prominent feature of pyloric stenosis; it is usually painless, and there are no bloody stools. The small pyloric mass, which feels like an olive, may be palpable at the margin of the right rectus muscle. The onset is more insidious than with intussuscpetion. Duodenal atresia presents shortly after birth with vomiting and a “double-bubble” on radiograph, indicating a gas-filled stomach and proximal duodenum. A Meckel´s diverticulum may rarely be found at the lead point of an intussusception, but it usually presents as a cause of recurrent abdominal pain in later life. Gastroschisis is an antenatal evisceration through a small paraumbilical defect that is present at birth.

Explanation:

Her clinical picture most resembles that of a hiatal hernia.

Explanation:

In a choledochal cyst the common bile duct of the biliary tree is structurally abnormal, probably from the time of birth. Usually by the age of 2 or 3 years the bile begins to collect in the duct. It forms a sack or cyst which then presses on the bile duct and may prevent bile from reaching the intestine. Bile can back up into the liver and the patient becomes jaundiced (yellow).
The classic symptoms of abdominal mass, pain and jaundice is rarely seen during childhood. Some children may not show symptoms for years. In some patients, the cyst can be felt by the doctor examining the abdomen. Blood studies such as a serum amylase and liver function tests may be drawn during acute episodes of pain. In most patients the diagnosis can be confirmed by using Ultrasound pictures or by injecting a radioactive substance and performing a CT scan which gives an “image” of the abnormal duct. The abnormal bile duct is removed and a piece of intestine is used to replace it. In most cases, surgery permanently corrects the disease.

Explanation:

Toddler´s diarrhea also known as chronic nonspecific diarrhea of childhood, this is a perplexing condition for parents and doctors alike. It is defined as a diarrhea that lasts for more than two weeks, usually consists of 5-10 watery stools per day (often with undigested food particles in the stool, in a child between about 6 months to 4 or 5 years old, who is growing and developing normally and otherwise seems healthy, there is no detectable medical cause for the diarrhea such as infection, food malabsorption or allergy. The child´s diet must be evaluated. Fluid intake may play a factor. Studies have shown a link between excessive fluid consumption and toddler´s diarrhea, as well as high carbohydrate, low fat diets. Excess fruit juice intake-especially apple juice-is often the cause of mysterious diarrhea (apple juice contains sorbitol, the “active ingredient” in prunes). If the child is being given any natural remedies or health foods, these need to be mentioned to the doctor and probably stopped to see if there is an improvement in the diarrhea. Treatment is mostly dietary manipulation. Carbohydrates, especially fruit juices, are reduced and fat increased to 35-40% of the total calories. High fiber foods such as beans, fruit, breads, and cereals should be encouraged. Antidiarrheal medications are probably ok for very short periods of worsening symptoms, but should not be used for very long, or very often.

Explanation:

Salmonella gastroenteritis is diagnosed by isolating the organism from stool or another infected site. In bacteremic and focal forms, blood cultures are positive, but stool cultures are generally negative. In stool specimens stained with methylene blue, WBCs are often seen, indicating inflammatory colitis.
Salmonella gastroenteritis is treated symptomatically with oral or IV fluids. Antibiotics do not hasten resolution, may prolong excretion of the organism, and are unwarranted in uncomplicated cases. However, in elderly nursing home residents, infants, and patients with HIV infection, increased mortality dictates treatment with antibiotics. Antibiotic resistance is more common with nontyphoidal Salmonella than with S. typhi. Trimethoprim-sulfamethoxazole (TMP-SMX) for children and ciprofloxacin for adults.

Explanation:

Gilbert´s syndrome is decreased uridine diphosphate (UDP) gluconryl transferase activity, which produces a mild UCB. Ward Romano syndrome is a prolonged QT syndrome leading to severe and fatal arrhythmias. Crigler Najjar syndrome, Type I, is an absence of UDP gluconryl transferase activity and is usually fatal in infancy. Dubin Johnson and Rotors syndromes are defects in transport of conjugate bilirubin out of the hepatocyte. Dubin Johnson´s differs from Rotor´s in that the hepatocytes are pigmented in Dubin Johnson´s and not in Rotor´s.

Explanation:

This infant is suffering from Hirschsprung disease (HD), or congenital aganglionic megacolon. HD is 5 times more common in boys. It is characterized by migratory arrest of neuro blasts within the intestine, resulting in congenital absence of ganglion cells in either part of or the entire wall of the colon, thus causing ineffective peristalsis. In most cases, the aganglionic segment is limited to the rectosigmoid colon. The common clinical outcomes are incomplete distal intestinal obstruction or enterocolitis in neonates (manifested by abdominal distension and bilious or feculent vomiting) and chronic constipation in an older child. There might also be a history of delayed passage of meconium (i.e., after 48 hours of life). HD may be recognized early in life or it may go undetected for many years if only a short segment of the colon is involved. The cardinal symptom is constipation. Rectal examination may lead to explosive expulsion of stool and flatus, with relief of abdominal distension. Anorectal manometry is helpful as a screening test because a clearly normal study demonstrating relaxation of the internal anal sphincter with distension of the rectum excludes the diagnosis of HD. Megacolon proximal to the aganglionic segment might be visible on barium enema. Diagnosis is confirmed with full-thickness biopsy of the rectal mucosa. Treatment requires initial surgical decompression with colostomy. Once the colon is decompressed to normal caliber and the child is old enough, a definitive pull-through procedure can be performed. Barium enema may also be used to contribute to diagnosis, but anorectal manometry should be performed before barium enema, as a normal manometric study (relaxed sphincter with distended rectum) rules out the diagnosis of HD. If the manometric study is abnormal, a barium enema can be done to support the suspected diagnosis of HD. In HD, barium enema shows a transition zone of caliber change (usually in the rectosigmoid area).
Plain films show distended proximal colon (the normal portion) and “normal-looking” distal colon, which is the aganglionic part. This test has characteristic findings but cannot provide definitive diagnosis. Before obtaining a biopsy, an abdominal radiograph may be done, because it can be easily done and may show signs suggestive of obstruction (i.e., decreased or absent air in the rectum and dilated bowel loops proximal to the aganglionic region). Prescribing laxatives and dietary change is the treatment for functional constipation, which is the most common type of constipation in children. However, the diagnosis requires exclusion of organic causes. Functional constipation can generally be diagnosed on the basis of the history and physical examination, both of which should be normal except for stool retention. The present patient has abdominal distension and a past medical history of delayed passage of meconium, which points toward an organic cause and necessitates further workup.
Sweat chloride test is the best initial test if cystic fibrosis (CF) is suspected. Meconium ileus, if present (19-20% of present with CF), is pathognomonic of the diagnosis of CF. But the present patient only had delayed passage of meconium after 2 days. This is not meconium ileum, which presents with the features of small-intestinal obstruction (vomiting, abdominal distension, and failure to pass meconium). Moreover, CF would be suspected if the patient had persistent pulmonary infection or signs of pancreatic insufficiency. In CF, chronic diarrhea (steatorrhea) is more common than constipation.

Explanation:

The child described in the question has an infection with anal pinworms, Enterobius vermicularis, which is common in daycare and schools. The main symptom is typically anal pruritus. The scotch-tape test is done at night, when the adult pinworms actually come out to the external anal area. The organism is identified microscopically, and treatment is with a single dose of mebendazole, followed by a second dose 2 weeks later. Usually family members are also affected and therefore must be treated if symptomatic. Pinworm may not produce eosinophilia. Albendazole may also be used to treat pinworms; however, mebendazole is the first line of therapy in children. Ivermectin and ketoconazole have no role in pinworm treatment. Praziquantel is indicated in the treatment of some tapeworm infections, but not for pinworm infection. Metronidazole is used in Amebiasis and is not related to Pinworm infections.

Explanation:

This child is in distress, with nausea, vomiting, abdominal cramps, diarrhea, and breathlessness (high respiratory rate). Pupillary constriction is a helpful clue because only a few toxins can cause miosis, such as opioids and organophosphates. The lower motor neuron signs of weakness, absent reflexes, and fasciculations point toward a diagnosis of organophosphate poisoning, which inhibits acetylcholinesterase, resulting in an accumulation of acetylcholine. This results in cholinergic excess at muscarinic sites (salivation, arrhythmia, bronchoconstriction) and peripheral nicotinic sites (weakness and muscle fasciculations).
Pralidoxime activates acetylcholinesterase, reversing both, the muscarinic and nicotinic effects of organophosphates.
Atropine can be used in the treatment of OPC poisoning, but it competes with acetylcholine only at muscarinic receptors and thus will not reverse the nicotinic effects (muscle weakness and fasciculations) of organophosphates.
Botulism antitoxin is used in the treatment of botulism, which manifests acutely with descending paralysis, cranial nerve deficits, and hyporeflexia.
Dimercaprol is used in the treatment of lead poisoning, which can cause abdominal pain, nausea, and vomiting, but the neuropathy is chronic. Lead poisoning does not explain the miosis.
Plasmapheresis is used in the treatment of Guillain-Barre syndrome, which presents with acute ascending paralysis and areflexia.
It does not present with miosis.

Explanation:

This patient has intussusception, which occurs when a portion of the gastrointestinal tract slips or telescopes into the portion just distal to it. Most intussusceptions are ileocolic, and most have no known cause. Intussusception usually occurs in children 5 to 24 months of age. It characteristically presents with episodes of distress and crying interspersed with quiet periods of normal behavior and playing. Acute onset of cramping, colicky abdominal pain is the hallmark of intussusception. Patients may have vomiting. As the obstruction progresses, the patient may develop fever and lethargy.
More than 50% of children will pass stool mixed with mucus and blood, the “currant-jelly” stool. The classic currant-jelly stool is a late finding. Passing a stool may temporarily relieve pain. Sometimes a sausage-like mass may be palpable in the right upper abdomen. However, approximately one-third of patients do not pass blood or mucus or develop an abdominal mess. Usually the abdomen is soil and nontender, but with advanced intussusception there may be signs of peritonitis. If the obstruction becomes complete, there is abdominal distension and shock may ensue. An air contrast enema is diagnostic and therapeutic and is the treatment of choice for symptoms of less than 48 hours duration. Ultrasound is also helpful in establishing the diagnosis.
Intussusception is an emergency and should be reduced as quickly as possible. Hydrostatic reduction is successful approximately 50% of the ´time for symptoms lasting longer than 48 hours, and 75 to 80% for symptoms lasting less than 48 hours. Hydrostatic reduction should not be done in the face of prolonged intussusception, peritonitis, or perforation. Surgery is recommended in those cases or after failure of hydrostatic reduction. Untreated intussusception is almost uniformly fatal.
Immediate surgical reduction is not indicated in a patient who has had symptoms for less than 48 hours and does not have signs of intestinal necrosis or shock. A hydrostatic reduction (i.e., barium enema) should be attempted first.
Laparoscopy is emerging as a treatment modality and its use will most certainly grow as familiarly with the technique increases. It is, however, not yet the First line of treatment for intussusception.
Manual reduction can be attempted during surgical intervention before resecting the affected bowel. This should be performed only if hydrostatic reduction has failed and there are no signs of ischemic necrosis of the affected bowel segment Observation in expectation of spontaneous resolution is not indicated, as untreated intussusception is almost universally fetal.

Explanation:

This baby presented with a severe form of necrotizing enterocolitis (NEC), which requires surgical resection of the necrotic bowel and reanastomosis after 6 weeks. Necrotizing enterocolitis is the most common acquired emergency in newborn infants.
It is more com on in premature infants, with mortality rates as high as 50% in infants weighing <1500 g. The pathogenesis is multifactorial, with an immature gastrointestinal tract, mucosal injury, and n immature immune system said to be the major contributors. Because early presentation of NEC can be subtle, one must have high index of suspicion of any infant with signs of feeding intolerance and abdominal signs and symptoms. Indications for surgery include perforation (free air present on left lateral decubitus or free air under the diaphragm), Fixed dilated loops of bowel seen on serial abdominal x-rays, abdominal wall cellulitis, and progressive clinical deterioration.
Abdominal decompression electrolyte repletion and serial abdominal exams are needed in the management of mild NEC without perforation. Because this infant has manifested unstable vitals signs, abdominal cellulitis, and a perforated bowel wall, he must undergo immediate surgery to resect the necrotic bowel.
Broad-spectrum antibiotics with anaerobic coverage is appropriate in cases of NEC because there is a risk of sepsis. However, the most appropriate management step in this severe case of NEC is immediate surgical resection. Continuing to give enteral feeds in a baby with developing NEC worsens the disease and is not recommended.
Parenteral nutrition is given following surgery for approximately 10-14 days to rest the bowel. It is not the most appropriate initial step in the care of an acute abdomen.

Explanation:

This patient has Crohn´s disease. Crohn´s disease can have an insidious or fulminant presentation and may have multiple extraintestinal manifestations. Patients may have persistent fever of unknown origin, arthritis, mouth ulcers, skin manifestations, (erythema nodosum), weight loss, malaise, and growth retardation.
Abdominal pain is cramping in nature and diarrhea may at times be bloody. Perianal disease is very common, including abscesses and fistulas. Crohn´s disease can occur anywhere along the gastrointestinal tract. Diagnosis may take years, owing to the nonspecific symptoms. The sedimentation rate is often elevated,-as is the platelet count. Plain abdominal films may show partial small bowel obstruction. Upper gastrointestinal with small bowel follow-through can show thickened folds with narrowing of the gastrointestinal tract (string sign). Skip lesions may be seen when there are normal areas between the affected segments. Fistulas are common. Colonoscopy and biopsy may be helpful in establishing the diagnosis. Characteristically, there is transmural extension of the inflammation. Granulomas are found only in 30% of, cases. Treatment is aimed at relief of symptoms and includes steroids, aminosalicylates (including enemas), azathioprine and metronidazole for fistulas, cyclosporine, tacrolimus, and tumor necrosis factor alpha.
Antibiotics are commonly used because it is difficult to rule out an infectious process. Hyperalimentation provides calories for appropriate growth and resting the bowel. Surgical management is reserved for failure of medical management fistula formation, intestinal obstruction, and growth failure. Gastrointestinal obstruction requiring surgery; malabsorption, anemia, weight loss, and growth failure are all complications.
A good response to systemic steroids is seen in Crohn´s disease and ulcerative colitis and cannot serve as a diagnostic criterion for either of the diseases.
Involvement of the colon does not help in distinguishing between Crohn´s disease, which may affect any segment of the gastrointestinal tract, and ulcerative colitis, which affects only the colon and rectum.
Rectal bleeding and rectal disease are much more prominent and common in ulcerative colitis, but also may be seen in Crohn´s disease.

Explanation:

The patient has a 3-day history of diarrhea that has resulted in severe dehydration. This is clinically apparent in that he is lethargic, tachycardic, hypotensive, and hypernatremic. The type of dehydration is defined by his serum sodium concentration. A sodium >150 mEq/L constitutes hypernatremic or hypertonic dehydration.
This implies a greater loss of free water. In isotonic or isonatremic dehydration, there is proportional loss of water and sodium; this is defined by a serum sodium between 130 and 150 mEq/L. Hyponatremic or hypotonic dehydration means that there is a relatively greater loss of sodium than water, and it is defined by a serum sodium <130 mEq/L.
Regardless of the type of dehydration, for moderate to severe dehydration the first step should be rapid correction of the shock state, i.e., correction of the abnormal hemodynamic variables. In this case, we want to see the blood pressure increase and the heart rate decrease. Therefore, we give one or more fluid boluses of 20 mL/kg of either normal saline or Ringer lactate. Each bolus is given over 20 to 30 minutes and the patient is reevaluated. Another bolus is given and the patient is reevaluated; these two steps are repeated until the hemodynamic response is attained. After this, fluid therapy is then given per the type of dehydration.
The first calculation to make is maintenance therapy. This is the fluid that the patient needs simply to sustain daily normal metabolic activity. Maintenance therapy is always divided equally over 24 hours.
With hypernatremic dehydration, we must correct the serum sodium slowly because a rapid lowering of high sodium may lead to significant fluid shifts, causing cerebral edema. Therefore, hypernatremic dehydration is corrected over 48 hours. First calculate the total deficit and the free water deficit. The free water deficit represents the extra free water that was lost to account for the increase in serum sodium. In addition to the 24-hour maintenance, the entire solute deficit (the remainder of the deficit that contains electrolytes after the free water deficit has been subtracted) and one-half of the free water deficits are given over the first 24 hours. During the next 24 hours, the maintenance is then given with the other half of the free water deficit. This method allows complete rehydration with a slow decrease of the serum sodium.
The maintenance is certainly given equally over 24 hours, but not the deficit (choice C) is the method of correction of either isonatremic or hyponatremic dehydration. It allows for more rapid correction than in hypernatremic dehydration. As stated, the maintenance is given equally as usual, but half of the calculated deficit is given over the first 8 hours and the remainder over the next 16 hours. The correction, therefore, is made over 24 hours.
Other choices are incorrect because they do not represent any accepted mode of fluid therapy.

Explanation:

Infant with Malrotation and midgut volvulus often present in the first week of life with symptoms of bilious vomiting and bowel obstruction. Both duodenal and Jejunoileal atresia most commonly present within the first 24 hours of life. Vomiting associated with pyloric stenosis is always non-bilious, and the diagnosis is most commonly made after the first week of life. Necrotizing enterocolitis may also be associated with bilious vomiting, but typically occurs at 10-12 days of life and is accompanied by abdominal distension and visible and/or palpable loops of bowel. The statement “does not pull the knees to the chest and does not show dyspnea” preferentially rules out intussusception and bile stained vomiting is also a better indicator of volvulus.

Explanation:

In Hirschsprung´s disease (congenital megacolon), a section of the large intestine is missing the nerve network that controls the intestine´s rhythmic contractions. Symptoms of intestinal obstruction occur. The large intestine depends on a network of nerves within its walls to synchronize rhythmic contractions and move digested material toward the anus, where the material is expelled as feces. In Hirschsprung´s disease, the affected section of intestine cannot contract normally.
At the time of birth, newborns should pass a dark green fecal material (meconium). Delayed passage of meconium raises the suspicion of » Hirschsprung´s disease. Later in infancy, children with Hirschsprung´s disease can have symptoms that suggest intestinal obstruction, bile- stained vomit, a swollen abdomen, and refusal to eat. If only a small section of the intestine is affected, a child may have milder symptoms and may not be diagnosed until later in childhood. These children may have ribbon like stools and a swollen abdomen: they often fail to gain weight. In rare cases constipation is the only symptom.
Rectal biopsy and measurement of the pressure inside the rectum (manometry) are the only tests that can reliably be used to diagnose Hirschsprung´s disease. A barium enema may also be performed. During a barium enema, the doctor instills barium and air into the child´s rectum and then takes x-rays.

Explanation:

Ulcerative colitis is a chronic disease in which the large intestine becomes inflamed and ulcerated (pitted or eroded), leading to flare-ups (bouts or attacks) of bloody diarrhea, abdominal cramps, and fever. The Long-term risk of colon cancer is increased. Ulcerative colitis may start at any age but usually begins between the ages of 15 and 30. A small group of people have their first attack between the ages of 50 and 70. The symptoms of ulcerative colitis occur in flare-ups. A flare-up may be sudden and severe, producing violent diarrhea (typically bloody), high fever, abdominal pain, and peritonitis (inflammation of the lining of the abdominal cavity). During such flare-ups, the person is profoundly ill. More often, a flare-up begins gradually, and the person has an urgency to have a bowel movement defecate), mild cramps in the lower abdomen, and visible blood and mucus in the stool. A flare-up can last days or weeks and can recur at any time.
If that disease extends farther up the large intestine, the stool is loose: and the person may have as many as l0 to 20 bowel movements a day often, the person has severe abdominal cramps and distressing, painful spasms that accompany the urge to defecate. There is no relief at night. The stool may be watery and contain pus, blood, and mucus. Frequently, the stool consists almost entirely of blood and pus. The person clam may have a fever and a poor appetite and may lose weight.

Explanation:

Celiac disease is characterized by inflammatiun of the upper small intestine in response to dietary gluten. The endomysial antibody test has led to improvements in the diagnosis of celiac disease.
Minimal or atypical symptoms occur in many patients, especially those presenting with the disease in adulthood. Severe symptoms are most common in young children. A fulminant form, characterized by diarrhea, failure to thrive, abdominal distention and vomiting, occurs in children younger thang two years of age. The median age at the time of diagnosis in children is four years, and loss of appetite is a common symptom. Formerly, the classic diagnostic approach was to obtain a series of intestinal biopsies: before treatment, after dietary withdrawal of gluten and, finally, following a challenge with gluten. Such a series of biopsies is now rarely performed.
The development of the serum endomysial antibody test has changed the method of diagnosis. Some authorities now consider a positive endomysial antibody test plus clinical improvement following withdrawal of gluten sufficient evidence for the diagnosis of celiac disease.

Explanation:

Mesenteric lymphadenitis is an inflammation of the lymph nodes on the wall of the mesentery (the covering of the intestines). If is often a childhood illness, though occasionally seen in adults. It is a very co mon cause of abdominal pain in children, mimicking appendicitis, and often difficult to differentiate from appendicitis. It is estimated that 1 in 5 children diagnosed with appendicitis actually have mesenteric lymphadenitis.
The main symptom is abdominal pain. This is often located in the right lower abdomen or right iliac fossa. It is a colicky abdominal pain which just resolves momentarily without any intervention. The sufferer, usually a child, may be completely pain free between attacks. Characteristically, the pain moves from one spot to the other on the abdomen, in keeping with the movement of the bowel loops in the abdominal cavity.
Asking the child to turn to the left side will demonstrate this shift as the area of pain and tenderness will move along with the bowel to the left.
In appendicitis, the pain may initially start around the umbilicus, then moves over to the right iliac fossa. Once it settles there, it does not move around any longer.

Explanation:

Gastroesophageal reflux (GER) occurs when stomach contents reflux, or back up, into the esophagus during or after a meal. The esophagus is the tube that connects the mouth to the stomach. A ring of muscle at the bottom of the esophagus opens and closes to allow food to enter the stomach. This ring of muscle is called the lower esophageal sphincter (LES). The LES normally opens to release gas after meals. With infants, when the LES opens, stomach contents often reflux into the esophagus and out the mouth, resulting in regurgitation, or spitting up, and vomiting. GER can also occur when babies cough, cry, or strain. GER is common in healthy infants. More than half of all babies experience reflux in the first 3 months of life, but most stop spitting up between the ages of 12 to 24´months. Only a small number of infants have severe symptoms.

Explanation:

The “double bubble” sign is pathognomonic for duodenal atresia, which is a congenital anomaly associated with Bonn Syndrome. Two large gas collections, one in the stomach and one in the proximal duodenum are the only radiographic lucencies visible in the GI tract. The hallmark of duodenal obstruction is bilious vomiting without abdominal distention. Children with Down syndrome can also have esophageal atresia, imperforate anus, endocardial cushion defects and hypotonia.

Explanation:

Hypertrophic pyloric stenosis may cause almost complete gastric outlet obstruction. It is more common in males by a 4:1 ratio. The exact etiology is uncertain, but a genetic component is likely because siblings and offspring of affected people are at increased risk.
Symptoms develop between 2 and 6 weeks of life. Projectile vomiting (without bile) occurs shortly after eating. Until dehydiation sets in, the child feeds avidly and otherwise appears well, unlike many of those with vomiting due to systemic illness. Gastric peristaltic waves may be visible, crossing the epigastrium from left to right. A discrete, 2- to 3-cm, firm, movable olive-like pyloric mass is sometimes palpable deep in the right side of the epigastrium. With progression of illness, the child fails to gain weight, and signs of dehydration appear.
Diagnosis is by abdominal ultrasonography showing increased thickness of the pylorus (typically to Z 4 mm; normal, < 2 mm). The classic electrolyte pattern of an infant with pyloric stenosis is that of hypochloremic, hypokalemic metabolic alkalosis.

Explanation:

Rectal prolapse occurs in 20% of patients with cystic fibrosis who are aged 6 months to 3 years. The appropriate intervention when encountering a child with rectal prolapse is to order a sweat chloride test to see if the child has cystic fibrosis

Explanation:

In Hirschsprung´s disease (congenital megacolon), a section of the large intestine is missing the nerve network that controls the intestine´s rhythmic contractions.
At the time of birth, newborns should pass a dark green fecal material (meconium). Delayed passage of meconium raises the suspicion of Hirschsprung´s disease. Later in infancy, children with Hirschsprung´s disease can have symptoms that-suggest intestinal obstruction, bile- stained vomit, a swollen abdomen, and refusal to eat. Rectal biopsy and measurement of the pressure inside the rectum (manometry) are the only tests that can reliably be used to diagnose Hirschsprung´s disease. A barium enema may also be performed. During a barium enema, the doctor instills barium and air into the child´s rectum and then takes x-rays.

Explanation:

Dehydration is significant depletion of body water and, to Varying degrees, electrolytes. Symptoms and signs include thirst, lethargy, dry mucosa, decreased urine output, and, as the degree of dehydration progresses, tachycardia, hypotension, and shock. Diagnosis is based on history and physical examination. Treatment is with oral or IV replacement of fluid and electrolytes.
The most accurate method with acute dehydration is change in body weight; all short-term weight loss > 1%/day is presumed to represent fluid deficit. However, this method depends on knowing a precise, recent pre-illness weight.

Explanation:

Vitamin E toxicity may cause a necrotizing enterocolitis and hepatitis in children. Vitamin K toxicity, although uncommon, may cause vomiting and hemolysis, as well as albuminuria and hemoglobinuria. Vitamin D toxicity is associated with hypercalcemia, as well as constipation, and sometimes nephrocalcinosis. Pantothenic acid toxicity is associated with diarrhea. Pyridoxine toxicity, while very rare, is associated with peripheral sensory neuropathy.

Explanation:

Pantothenic acid toxicity is associated with diarrhea. Vitamin E toxicity may cause a necrotizing enterocolitis and hepatitis in children. Vitamin K toxicity, although uncommon, may cause vomiting and hemolysis, as well as albuminuria and hemoglobinuria. Vitamin D toxicity is associated with hypercalcemia, as well as constipation, and sometimes nephrocalcinosis. Pyridoxine toxicity, while very rare, is associated with peripheral sensory neuropathy

Explanation:

The disease is necrotizing enterocolitis which is a common cause of gastrointestinal emergency in premature and low birth weight infants. Typically, the infants are bottle fed and develop severe abdominal distress in the first week of life. Contributing factors include intestinal ischemia, poor neonatal immune response, and microbial agents. Both the small and large bowel may be affected. Necrotizing enterocolitis maybe complicated by intestinal gangrene, gastrointestinal bleeding intestinal perforation, and sepsis. Survivors of severe necrotizing enterocolitis may have had significant lengths of bowel surgically removed and later suffer from malabsorption and stricture formation. Histologically the appearance varies with disease stage but typically shows varying degrees of necrosis (transmural it perforation has occurred), inflammation, hemorrhage, and edema. A pseudomembrane composed of coagulated fibrin, neutrophils, and cellular debris may overlie the mucosa. Inflammatory polyps can be seen following reepithelialization of ulcers, typically in ulcerative colitis which would not be seen in the first week of life. Multiple diverticula are seen in diverticulosis, which does not usually develop before middle age. Neoplastic (precancerous) polyps, even in familial syndromes with a high colonic cancer rate would not be expected to cause an acute abdominal emergency in a neonate. A thickened collagenous band between surface epithelial cells and the lamina propria is seen with episodic watery diarrhea, usually in adults.

Explanation:

Pancreatitis is not always an easy diagnosis. The history of this boy is particularly suspect even with a normal serum amylase. Nearly one-third of all patients with acute pancreatitis have a normal serum amylase. An abdominal ultrasound may be useful in revealing an enlarged pancreas.
This young man is unlikely to have Fitz-Hugh-Curtis syndrome. Classically, Fitz-Hugh-Curtis syndrome is an extrapelvic manifestation of pelvic inflammatory disease in sexually active women. It is a perihepatitis consisting of adhesions between the liver capsule and the diaphragm or the anterior peritoneal surface. It was originally thought to be caused solely by Neisseria gonorrhoeae but recent studies have shown that Chlamydia trachomatis and other organisms may also be etiologies. The Fitz-Hugh-Curtis syndrome has rarely been reported in men, so sexual history should be obtained in this case.
Intussusception is not high on the list of differential diagnoses. The typical age for intussusception is in infancy, especially 6 to 12 months of age. This young man has persistent abdominal pain with fever, making this an unlikely diagnosis.
Wilms tumor is also unlikely in this case scenario. Wilms tumor usually occurs in early childhood, age 2 or 3 years. Although Wilms tumor is more prevalent in males, the usual presenting signs include an asymptomatic abdominal mass and hematuria.
Pyelonephritis typically presents with high fever, chills, and back pain. Although a urinalysis should be performed in this young man, the symptoms of midepigastric pain suggest an upper gastrointestinal problem, not pyelonephritis.
Viral hepatitis will not give a back pain, neutrophilia and also; jaundice, bilirubin levels or LFTs are not mentioned

Explanation:

The clue to this patient´s condition is the recent advancement of a honey- containing formula. Clostridium botulinum spores that are commonly found in honey germinate in the infant is gastrointestinal tract and produce the characteristic toxin. Infants younger than 1 year of age t should not be placed on a diet with honey.

Explanation:

Staphylococcal fool poising results from eating food contaminated with toxins produced by certain types of staphylococci, resulting in diarrhea and vomiting.
The staphylococci bacteria grow in food, in which they produce their toxins. Thus, staphylococcal food poisoning does not result from ingesting the bacteria but rather from ingesting the toxins that are already present in the contaminated food.
Typical contaminated foods include custard, cream filled pastry, milk, processed meats, and fish. The risk of an outbreak is high when food handlers with skin infections contaminate foods that are undercooked or left at room temperature.
Symptoms usually begin abruptly with severe nausea and vomiting starting about 2 to 8 hours after the contaminated food is eaten. Other symptoms may include abdominal cramping, diarrhea, and sometimes headache and fever severe fluid and electrolyte loss may cause weakness and very low blood pressure (shock). Symptoms usually last less than 12 hours, and recovery is usually complete.

Explanation:

Infant feeding difficulties can be categorized based on the timing of symptom onset. Causes of early feeding difficulties include annular pancreas and tracheoesophageal fistula; and they present in the first few days of life. Late feeding difficulties include congenital pyloric stenosis, which manifests in the first few weeks of life. This lesion is an annular pancreas, which is a rare pancreatic malformation in which the pancreatic head encircles the second part of the duodenum, potentially causing obstruction. An increase in thickness of the muscular part of the gastric wall can cause congenital pyloric stenosis. Physical examination commonly reveals a palpable mass. The time course for symptom development is typically between two and three weeks, as opposed to annular pancreas which presents with early feeding difficulty. Atresia of the duodenum itself can occur, but would not cause the appearance of a mass surrounding the duodenum. In hiatal hernia, the upper portion of the stomach protrudes through the diaphragm into the thoracic cavity it is much more common in older people. Tracheoesophageal fistula can occur, but would usually present with copious salivation, choking, or cyanosis with feeding.

Explanation:

The patient described in the vignette had a recent gallstone removed endoscopically. Generally, such patients can be followed clinically, and repeat laboratory studies are not necessary if the patient is asymptomatic. This girl´s bilirubin concentration is mildly elevated, which is not uncommon after recent episode of obstructive jaundice. Repeat measurement in 2 weeks can determine whether the hyperbilirubinemia has resolved.
Autoimmune hepatitis and viral hepatitis are both rather unlikely in the face of completely normal transaminase levels. For a patient who has persistent biliary sludge, oral administration of synthetic bile acid ursodeoxycholic acid may help facilitate biliary flow and promote sludge dissolution. Cholic acid is generally not used for that purpose.
Repeat ERCP is not necessary at this time, although it should be considered if there is evidence of another retained stone.

Explanation:

A Mallow-Weiss tear occurs in the lower esophagus after forceful retching with or without vomiting. In most cases, the bleeding is painless and resolves once the insulting incident (i.e., retching or vomiting) resolves.
Esophageal varices cause bright-red bleeding in vomit, which is the most common presenting symptom of portal hypertension. Other signs of portal hypertension (e.g., splenomegaly hepatomegaly, ascites) should be present.
Esophagitis in children is most often associated with gastroesophageal reflux disease. The patient will usually complain of chest and abdominal pain, with history of frequent regurgitation.
Gastritis in children is usually associated with abdominal pain. It rarely is associated with fever, and sometimes causes vomiting with bright-red blood.
Peptic ulcer disease has symptoms of mainly nocturnal abdominal pain. Vomiting is present in only 10% of cases, and only 5% have hematemesis.

Explanation:

The infant described here has steatorrhea, as evidenced by poorly formed and bulky stools and poor weight gain.
Detailed family history and physical examination are also useful in evaluation of fat malabsorption syndrome. The most useful test for the present infant is fecal fat quantification. When a malabsorption syndrome is confirmed, a sweat chloride test is indicated to evaluate for the possibility of cystic fibrosis. One of the most important reasons for steatorrhea in newborns is bile acid deficiency. Bile acids are very important in normal absorption of fat which constitutes a major portion of an infant´s calorie intake. Unfortunately, the bile acid pool in neonates is very small when compared with that in adults.
In addition, neonates often lose an excessive amount of bile acids in their stools. This results in physiologic steatorrhea because of poor absorption of fat. Preterm infants, like the one described here, have an even smaller bile acid pool and are more likely to have steatorrhea because of poor fat absorption. This will result in poor weight gain.
The solution to this problem is to substitute medium-chain triglycerides (MCTs) in the formula for long-chain triglycerides (LCTs) because, unlike LCTs, MCTs do not require bile acids for absorption.
Adding pancreatic enzymes offers no help in this case because the problem is not a lack of pancreatic enzymes. If the child ” had presented with meconium ileus alter birth, a possibility of cystic fibrosis could be suspected in which pancreatic enzyme deficiency causes malabsorption.
Changing to a lactose-free formula will not correct the steatorrhea Lactose-free formula is given to children who have lactose intolerance, which presents with vomiting and abdominal pain after ingestion of milk.
Increasing the volume per feeding without substituting MCTs for LCTs will only worsen the steatorrhea.
In steatorrhea, fat-soluble vitamins such as A and E are lost in the stool. However, supplementing vitamins A and E cannot correct the steatorrhea.

Explanation:

This infant has Hirschsprung disease, or congenital aganglionic bowel disease. It is five times more common in. boys than in girls. It results from congenital absence of ganglion cells in either part of or the entire wall of the colon, resulting in a state of chronic contraction. In most cases, the aganglionic segment is limited to the rectosigmoid colon. In very rare cases, part of or the entire small bowel can be aganglionic as well. Bilious or feculent vomiting, abdominal distention, and constipation are the classic clinical signs. There might also be a history of failure to pass meconium in the first 48 hours of life. If only a short segment of the colon is involved, Hirschsprung disease might not be evident until in childhood or adolescence. Megacolon proximal to the aganglionic segment might be visible on barium enema. The diagnosis is confirmed with the demonstration of an aganglionic segment of the bowel on punch biopsy.
Duodenal atresia usually presents with vomiting. A “double bubble” sign is seen on abdominal radiography. Thirty to forty percent of cases are associated with Down syndrome.
Intussusception is certainly in the differential diagnosis of vomiting and abdominal distention. In this case, however, the history of failure to pass meconium in the newborn period and failure to thrive is much more suggestive of Hirschsprung disease.
Intussusception occurs when one segment of the bowel telescopes into another segment just distal to it the most common site of intussusception is the ileocolic junction.
Malrotation is usually caused by the presence of a volvulus, which presents with sudden onset of bilious vomiting, abdominal distention, rectal hemorrhage, peritonitis, and shock. It is a surgical emergency.
Pyloric stenosis usually presents with projectile vomiting in the first 2 or 3 weeks of life. On examination, an olive-shaped mass is usually palpable in the epigastric area. It is caused by hypertrophy and hyperplasia of the antrum of the stomach, resulting in obstruction. It occurs in 1 of 50 boys and in 1 of 750 girls.

Explanation:

Explanation:

Diarrhea and vomiting in children is most often caused by viral gastroenteritis-and results in a proportional loss of water and sodium. The patient is therefore isonatremic hypovolemic, or even hyponatremic hypovolemic. This can be confirmed by the signs of dehydration the patient is displaying: lethargy, sunken fontanelle, increased capillary refill time, decreased urine output, tear production, and skin turgor, and tachycardia. Hypotension would typically be a late finding, indicating decompensated hypovolemic shock. The resulting hyponatremia would present low serum osmolality low serum sodium, low urine sodium and a very high urine osmolality (e.g., the urine would be very concentrated). None of the other choices reflect this scenario.
A low serum sodium with low osmolarity, and high urine sodium with high osmolality should alert the clinician to a lack of appropriate sodium-preserving renal mechanisms. This combination of laboratory studies is seen in the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Explanation:

Most bleeding in Meckel´s diverticulum is secondary to heterotrophic gastric mucosa, causing acid-induced ileal ulceration. Heliobacter pylori has not been shown to be an etiologic agent. Intussusception fairly common in patients with Meckel´s diverticulum but is not a frequent cause of bleeding. Arteriovenous malformation is not a major complication of Meckel´s diverticulum.