NSG6435 Final EXAM 2023 WITH COMPLETE VERIFIED SOLUTIONS

GER uncomplicated recurrent spitting & vomiting in healthy infants that resolves spontaneously GERD : is present when reflux causes secondary symptoms or complications GERD Test UGI when anatomic etiologies of recurrent vomiting are considered, but should not be considered to be a test for GER and GERD pharmacotherapy •There is no sufficient evidence to support the use of prokinetic agents for GERD Rx •Medications are usually not recommended unless pathologic GER has been demonstrated EOE •Occurs in all ages, most frequently ♂ •Initial presentation feeding dysfunction & vague nonspecific S/S GERD -abd. pain, vomiting & regurgitation •History -Personal & FMH atopy, asthma, dysphagia, heartburn, feeding dysfunction, or food impaction -Young children- lengthy chewing, long mealtimes, washing food down w liquids & avoiding highly textured foods -Adolescents - solid food dysphagia, acute & recurrent food impactions •Suspect EoE when S/S unresponsive to Rx Most common complications: esophageal food impaction and stricture EOE treatment -Fluticasone BID puffed in the mouth and swallow, do not rinse mouth for 30 minutes H. Pylori treatment -: 7-10 days Amoxil + clarithromycin + PPI. Be aware of abx. resistance to biaxin, if so consider metronidazole, imidazole levofloxacin •Sequential Rx for Biaxin resistance: Amoxil + PPI x5 days, then Biaxin+Flagyl+PPI x 5 days Intussusception treatment •Reduction should not be attempted if signs of strangulated bowel, perforation or toxicity present -surgery is required. Acute appendicitis •Incidence of perforation high (40%) esp. younger kids (2 y/o) -pain is poorly localized & S/S are nonspecific-high fever perforation very high Acute appendicitis PE -Peri-umbilical pain at palpation, initially -+ McBurney's point tenderness -+ Rovsing's sign: palpation LLQ ↑ pain in RLQ -+ Psoas sign: passively extending thigh of pt. lying on side w knees extended (or flexing thigh at the hip) ↑ pain -+ Obturator sign: while child lies on back with hip & knee flexed at 90 degrees , examiner rotates the hip by moving the patient's ankle away from the patient's body while allowing the knee to move only inward. This is flexion and internal rotation of the hip. -+ Reboundness: not always reliable & very painful for child Celiac Disease, who to test? •Screening is recommended for patients with suggestive symptoms, and also for children in groups at ↑risk for having the disease, regardless of symptoms. •**Screening of asymptomatic patients who do not have risk factors is not generally recommended. ** •North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) recommend serologic screening to be performed in children with the classic clinical features and high-risk groups, provided they are on a gluten-containing diet CD clinical presentation •Classic clinical features of patients with celiac disease include symptoms of malabsorption such as diarrhea, steatorrhea, and weight loss. •Other GI symptoms may include abdominal pain, flatulence, abdominal distension, and paradoxical constipation •Many patients with celiac disease have non-gastrointestinal manifestations, in addition to or instead of GI symptoms. •The most specific non-gastrointestinal manifestation is dermatitis herpetiformis CD Diagnostics Most valuable test is for immunoglobulin A (IgA) antibodies against tissue transglutaminase (tTG-IgA), -Testing should be performed while on a gluten-containing diet. -Individuals previously started on a gluten-free diet without prior testing should resume a diet containing ideally at least 3 g gluten/day (equivalent to about one slice of bread daily) for at least 6- weeks before undergoing antibody testing, although the duration and amount of gluten required for diagnostic accuracy has not been fully clarified •Antiendomysial antibodies (EMA) is as accurate as tTG-IgA, yet is more expensive and somewhat dependent on operator interpretation. -EMA is typically used as a second-line test, to clarify the diagnosis in patients with equivocal results of tTG-IgA, including asymptomatic members of a high-risk group -EMA is an immunofluorescence test for IgA antibodies to endomysium, a structure of the smooth muscle connective tissue •Deamidated gliadin peptide (DGP) also has good diagnostic accuracy and may be particularly useful for young children; this is a second-generation antigliadin antibody test. •Standard (first-generation) IgA or immunoglobulin G (IgG) antigliadin antibodies are considerably less reliable and are not recommended. •Tests of antireticulin antibodies have reasonably high specificity, but lower sensitivity, and are no longer commonly used. Congenital Aganglionic Megacolon:Hirschsprung Disease •Failure to pass meconium stool within 24-48hours after birth •Ominous signs: fever, lethargy, bloody diarrhea Ecopresis •Consistency of stools will vary from normal to pellet like stools to liquid Mild Constipation •DO NOT GIVE MINERAL OIL TO NONAMBULATORY PEDS OR BED-BOUND OR GER Hx Acute watery diarrhea •the main danger is dehydration Dehydration management •Supportive treatment •Replacement of fluid & electrolytes deficits -ORT with Pedialyte is best; can continue breastfeeding -CLD or hypocaloric (diluted formula) diet for more than 48hrs IS NOT ADVISABLE •Early initiation of refeeding is recommended •BRAT diet initially- controversial •Lactose-free diet associated with shorter period of diarrhea but is not critical to successful recovery in healthy infants •Reduced-fat during recovery may ↓ N/V •Antibiotics only for culture proven bacterial/parasitic infection. •Antidiarrheal medications (kaolin-pectin combo) are ineffective & in some circumstance can be dangerous (particularly loperamide, tincture of opium, diphenoxylate with atropine) •Bismuth subsalicylate preparations may reduce stool volume but are not critical to recovery and are NOT RECOMMENDED due to salicylate component & risk of Reye syndrome •Close surveillance/observation: refer to be admitted if mod. or severe rehydration not responding to ORT •Parental reassurance Chronic Diarrhea diarrhea 14 days Abdominal pain treatment -REASSURANCE, REASSURANCE, REASSURANCE... REASSURANCE... Acute Abdomen •Timely & accurate Dx critical Food protein-induced enterocolitis syndrome (FPIES) •a non-immunoglobulin E (IgE)-mediated gastrointestinal food hypersensitivity •Presents as profuse, repetitive vomiting, sometimes with diarrhea, leading to dehydration and lethargy in the acute setting, or chronic, watery diarrhea with intermittent vomiting, leading to weight loss, failure to thrive, dehydration, and metabolic derangements in a chronic form •Primarily affects infants. •Most commonly caused by cow's milk (CM) or soy protein, although other foods can be triggers •Is a clinical diagnosis -Based on constellation of typical clinical symptoms with clinical improvement following withdrawal of the suspected causal protein; AND exclusion of other etiologies; PLUS an oral food challenge (OFC) FPIES management •Elimination of the offending food from the diet -A casein hydrolysate-based (hypoallergenic) formula is recommended in the infant with cow's milk (CM) FPIES if breastfeeding is not possible or the infant is exclusively formula fed due to frequent concomitant CM and soy FPIES. -In the rare case of FPIES in the nursing infant, the mother should completely eliminate the triggering food(s) from her diet. -Infants presenting with chronic symptoms due to CM or soy usually improve within 3 to 10 days of switching to a casein hydrolysate-based formula with or without temporary intravenous fluids -~10 -20% may require an amino acid-based formula Emergency treatment plan for acute episodes due to accidental exposures Food introduction •Ages and Stages -8-months of age or when developmentally appropriate: •High-iron foods -Offer soft-cooked and bite-and-dissolve textures from approximately 8 months of age or as tolerated by infant •Lower risk: Lamb, fortified quinoa cereal, millet •Moderate risk: Beef, fortified grits and corn cereal, wheat (whole wheat and fortified), fortified barley cereal •Higher risk: Fortified, infant rice and oat cereals -12 months of age or when developmentally appropriate: •Offer modified tolerated foods from the family table: chopped meats, soft cooked vegetables, grains, and fruits -Lower risk: Tree nuts and seed butters* (sesame, sunflower, etc) -Moderate risk: Peanut, other legumes (other than green pea and green bean) -Higher risk: Milk, soy, poultry, egg, fish GU disorder eval •Most reliable single indicator of glomerular function is serum creatinine UA with dipstick •Leukocyte Esterase and nitrite dipsticks are not reliable in children younger than 3 y/o. UTI •E.coli-pathogenic agent in 75% to 90% of all childhood UTIs •Streptococcus is the most common pathogen in NB, not after 1 month of life UTI diagnosis •Gold standard for diagnosis of uti is the culture of properly collected urine •Catheterization or suprapubic aspiration is the preferred method of urine collection for dipstick, microscopic examination, and culture of the urine in infants and young children who are not toilet-trained. A clean-voided specimen is the preferred method of collection in toilet-trained children. UTI diagnostic •Urinalysis-presence of urinary leukocyte esterase , nitrate and blood suggestive of UTI but NOT diagnostic •Urine culture mandatory for accurate diagnosis-technique for specimen collection depends on age and developmental status of child, severity of condition and urgency of need for unequivocal results •Per AAP recommendations catheterization or suprapubic collection is necessary to avoid contaminated samples UTI imaging •AAP AAP recommends RBUS for all infants and children 2 - 24 months following their first1st febrile UTI •Timing of RBUS •as soon as possible during the acute phase of illness to identify complications (eg, renal or perirenal abscess, pyonephrosis) in infants and young children with unusually severe illness or failure to improve as expected after initiation of antimicrobial therapy. •after the acute phase (to reduce the risk of false positive results secondary to renal inflammation during the acute episode) in infants and young children who respond as expected to appropriate antimicrobial therapy. •voiding cystourethrogram (VCUG) is the test of choice to establish the presence and degree of VUR. •VUR is the retrograde passage of urine from the bladder into the upper urinary tract. •It is an important risk factor for renal scarring (~25 - 30 % of children, 0 - 18 years with a first UTI have VUR •AAP and NICE guidelines: Do not use DMSA in the routine evaluation of children with first1st UTI. UTI management 50% of E. coli are resistant to amoxicillin or ampicillin •Cephalosporins to consider as 1st -line Rx •Amoxicillin and ampicillin are not routinely recommended for empiric therapy because of the high rate of resistance of E. coli. Hematuria •initial step in the evaluation of patients with red urine is to establish whether or not the urine discoloration is due to blood or another substance. •In patients with gross hematuria, the color change does not necessarily reflect the degree of blood loss, since as little as 1 mL of blood per liter of urine can induce a visible color change. Hematuria etiology •The most commonly identified etiologies for gross hematuria in children include UTI, irritation of the meatus or perineum, and trauma. Hematuria eval •initial hematuria (onset of urination) usually suggests urethral bleeding •Continuous bleeding throughout urination may occur from bleeding in the bladder, ureter or kidneys •terminal bleeding (at the end of urination) is indicative of bladder disease. •symptomatic-Renal ultrasonography is the preferred modality in children. asymptomatic-•Cystoscopy is rarely indicated for hematuria in children. Proteinuria evaluation •Transient proteinuria is the most common cause. •It can be induced by a variety of factors including fever, exercise, stress, seizures, and hypovolemia. •Persistent proteinuria should be more fully evaluated for underlying renal disease. Symptomatic proteinuria •major manifestations of nephrotic syndrome are heavy proteinuria (protein excretion 1000 mg/m2 per day or spot urine Pr/Cr ratio 1), edema, serum albumin 2.5 g/dL, and hypercholesterolemia. Testicular torsion •Surgical emergency due to the risk of gonadal loss : urgent surgery -if detected within 4 hrs. of symptoms onset, salvage rate is 100%; within 12 hrs. falls to 20%; after 24 hrs infarction is the rule AKI •Hallmark of early AKI is oliguria with subsequent variable rise in serum creatinine & BUN Nephrotic syndrome •caused by renal diseases that ↑ permeability across the glomerular filtration barrier. •classically characterized by 4 clinical features, but the 1st 2 are used diagnostically because the last two may not be seen in all patients: •Nephrotic range proteinuria − Urinary protein excretion greater than 50 mg/kg per day •Hypoalbuminemia − Serum albumin concentration less than 3 g/dL (30 g/L) •Edema •Hyperlipidemia Primary nephrotic syndrome •refers to nephrotic syndrome in the absence of an identifiable systemic disease. Within this category are patients with idiopathic nephrotic syndrome, who have no glomerular inflammation on renal biopsy, and patients with primary glomerulonephritis, who have an active sediment and glomerular inflammation on renal biopsy. Secondary Nephrotic syndrome refers to nephrotic syndrome in the presence of an identifiable systemic disease. Congenital and infantile nephrotic syndrome •occur in children less than one year of age and can be either secondary (mostly due to infection) or primary. Two-thirds of nephrotic syndrome cases that occur during the first year of life and as many as 85 percent of cases that occur during the first three months of life have a genetic basis and a poor outcome Nephrotic syndrome diagnosis •The diagnosis of nephrotic syndrome is made by the presence of 2 defining characteristics: •Urinary protein excretion greater than 50 mg/kg per day •Hypoalbuminemia •Although edema is generally the presenting sign of nephrotic syndrome, the diagnosis is confirmed by the presence of nephrotic range proteinuria and hypoalbuminemia Nephrotic syndrome eval •First morning void to measure urinary protein to creatinine ratio •Renal biopsy for children ≥12 years of age Nephrotic syndrome initial treatment Prednisone 2 mg/kg per day x6 wks., followed by alternate-day prednisone of 1.5 mg/kg for Add'L 6 weeks. Nephrotic syndrome relapse •Prednisone 2 mg/kg per day until the urine protein tests are negative or trace for 3-consecutive days, followed by alternate-day prednisone of 1.5 mg/kg x 4-Weeks. Nephrotic syndrome freq relapses •Prednisone 2 mg/kg per day until the urine protein tests are negative or trace for 3-consecutive days, followed by alternate-day prednisone of 1.5 mg/kg x4-weeks, which is then tapered over 2-months to 0.5 mg/kg every other day. •Steroid-dependent disease Nephrotic syndrome •Prednisone remains the preferred therapy in the absence of significant steroid toxicity.