Nutrition Flashcards
know when to start introducing which foods
-honey >12mo
-6mo- cereal -> fruit/veg -> meat
lactate deficiency
new foods every 3-4 days
corkscrew sign, target sign, double double
intussiception -> US
umbilical hernia!! -> observe
not testing on chronic diarrhea
dont need to know rome criteria or bristol
miralax is go to
breast feeding
-provides optimal nutrition for normal infant during early months of life
-Formulas resemble breast milk, but cannot replicate nutritional/immune composition of human milk
-WHO and AAP recommend exclusive breast-feeding for first 6 months with continued breast-feeding along with appropriate complementary foods through the first 2 years of life
-Immunologic factors provide protection against GI infections and URIs, fosters maternal-child bond
-Absolute CI (rare):
-Active tuberculosis (in mother) and galactosemia (in the infant)
-Breast-feeding is associated with maternal-to-child transmission of HIV, but risk is influenced by duration/pattern of breast-feeding and maternal factors (immunologic status and presence of mastitis)
-Use of ART and exclusive breast-feeding is promoted (if available)
breast feeding techniques
-Baby-Friendly Hospital Initiative (BFHI) is a global initiative that assists hospitals in giving mothers information, confidence, and skills necessary to successfully initiate and continue breast-feeding
-Initiated as soon as both mother and baby are stable after delivery (30-60 minutes)
-Correct positioning and technique are necessary to ensure effective nipple stimulation and breast emptying within minimal nipple discomfort
-While sitting, infant held at height of breast and turned to face mother
-Mother’s arms supporting infant held tightly at sides, bringing baby in line with breast
-Breast supported by lower fingers of free hand, nipple compressed between thumb and index fingers to make it more protractile
-Nipple/areola inserted when baby opens mouth
-Duration- 5 mins per breast at each feeding the 1st day, 10 mins per breast 2nd day, and 10-15 mins per side thereafter; mean feeding frequency 8-12 times daily (post-partum)
-Adequacy of milk intake assessed by voiding and stooling
-Well-hydrated infant: Voids 6-8 times a day (soaked diaper, colorless), by 5-7 days, loose yellow stools should be passed QID
-MCC of poor early weight gain in breast-fed infants is poorly managed mammary engorgement, which rapidly decreases milk supply
-Results from long intervals between feeding, improper suckling, nondemanding infant, sore nipples, maternal/infant illness, nursing from only one breast, and latching difficulties
-Weight loss should not exceed 7% (after birth) and birthweight should be regained by 10 days
-Telephone follow-up between discharge and 3-5 days of age, then 2 weeks of age (when milk secretions become copious – avoids engorgement)
common problems in breast feeding
-Nipple tenderness requires attention to positioning and correct latch-on
-Nursing for shorter times, beginning feedings on less sore side, air drying nipples after nursing, use of lanolin cream
-Severe pain/cracking: Improper latch
-Temporary pumping may be needed
-Mastitis: Flu-like symptoms with breast tenderness, firmness, and erythema
-Tx: Abx x 10 days (B-lactamase organism coverage), analgesics, breast pumping
-Remember breast-milk and breast-feeding jaundice?!
breast feeding: maternal drug use
-Factors determining effect: Route of administration, dosage, molecular weight, pH, and protein binding
-Absolute CI: Radioactive compounds, antimetabolites, lithium, and certain antithyroid drugs
-Mother should be advised against use of alcohol, nicotine, caffeine, and/or “street drugs”
formula feeding
-Majority of commercial formulas are cow’s milk based and most have added iron
-Carbohydrate in standard formulas is generally lactose (though lactose-free, cow’s milk-based formulas are available)
-Caloric density is 20 kcal/ounce, similar to human milk
Manufacturers have begun to examine the benefits of adding variety of nutrients and biologic factors to infant formula (to better mimic composition/quality of breast milk)
-Soy-based formulas for newborns with cow’s milk allergies (Similac, Enfamil)
-Hypoallergenic formulas (cow’s milk and soy milk intolerant) for infants who cannot tolerate regular formulas (Similac Alimentum, Enfamil Nutramigen)
-Proteins broken down to basic components > easier to digest
-Special formulas for premature, LBW babies
-Formula-fed babies at higher risk for obesity later in childhood (may be related to better caloric self-regulation by newborns/infants who are breast-fed)
complementary feeding
-introduction of solid foods in normal infants at approximately 6 months of age
Fortified cereals, fruits, vegetables, and meats should complement breast milk diet
-Meats are an important source of iron and zinc (inadequate to meet an infant’s needs in human milk by 6 months)
-Pureed meats may be introduced early
-Single-ingredient foods introduced one at a time at 3- to 4-day intervals before a new food group is given to assess for allergy intolerance
-For infants with severe eczema or egg allergy, but without evidence of active peanut sensitization by skin prick test or peanut IgE, introduction of 6-7 g/week of peanut protein served as a puree recommended at 4-6 months to reduce risk of peanut allergy
-Fruit juice is unnecessary – if given, should be in a cup, not bottle and less than 4 oz/day
-Whole cow’s milk can be introduced after the first year of life
nutrition for ages 2yrs+
-3 regular meals/day (promoting variety)
-Fat less than 35% of total calories, carbohydrates 45-65% of calories, high fiber diet (whole grains)
-Consumption of lean cuts of meat, poultry, fish; skim/low-fat milk (endorsed by AAP with history of obesity/heart disease); vegetable oils; fruits/veggies
-Limitation of grazing/sodium intake
-Lifestyle counseling: Maintenance of healthy BMI, regular physical activity, limiting sedentary behaviors, avoidance of smoking
malabsorption syndromes: lactose intolerance
-Non-immune intolerance to carbohydrates due to deficiency in an enzyme/transporter or due to excess consumption overloading a functional transporter (small bowel epithelial membrane)
-Non-absorbed molecules cause osmotic diarrhea and are fermented in the gut producing gas
-Clinical manifestations include abdominal distention, bloating, flatulence, abdominal discomfort, nausea, and watery diarrhea
-Stools are liquid, frothy, and acidic
-Diagnostic tests are breath tests, genetic tests, and disaccharide activity assays on mucosal bx specimens
-Symptoms resolve with dietary avoidance or with enzyme supplementation
-Disaccharidase Deficiency
-Sucrose and lactose require hydrolysis by intestinal brush border disaccharidases for absorption
-Primary deficiency: Permanent disaccharide intolerance, absence of intestinal injury, frequent family history
-Lactase Deficiency
-Genetic/familial lactase deficiency presents after 5 years of age
-Transient or secondary lactase deficiency caused by mucosal injury (AGI) resolves within a few weeks
malabsorption syndromes: cows milk protein intolerance
-Non-allergic food sensitivity, M > F, young infants with family history of atopy
-Healthy, well-appearing infant fed with formula/breast milk with cow’s milk protein, develops flecks of blood in stool/loose, mucoid, blood-streaked stools
-Removal of cow’s milk protein is treatment
-If symptoms mild and infant thriving, no treatment may be needed
malabsorption syndromes: celiac ds
-Immune-mediated enteropathy triggered by gluten (protein in wheat, rye, and barley)
-GI: Chronic diarrhea, abdominal distention, irritability, anorexia, vomiting, poor weight gain
-Non-GI: Delayed puberty/short stature, delayed menarche
-Consider in children with IDA, decreased bone mineral density, elevated LFTs, arthritis, epilepsy with cerebral calcifications, or intensely pruritic rash
-Labs:
-Screening (> 2 years of age): Serum IgA and TTG IgA
-< 2 years: Deamidated gliadin peptide IgG sent as well
-Stools may have partially digested fats/acidic
-IDA common
-Up to 30-70% of patients estimated to be unresponsive to HB vaccine before treatment with gluten-free diet
-!Bx findings: Duodenal patchy villous atrophy with increased intraepithelial lymphocytes
-Tx:
-Strict dietary gluten restriction for life
-Improvement after 6-12 months of treatment (Ab titers ~ 12 months to normalize)
vitamin deficiencies: vitamin A
-Basic constituent of vitamin A group is retinol
-Ingested plant carotene or animal tissue retinol esters release retinol after hydrolysis by pancreatic and intestinal enzymes
-Eye: Retinol is metabolized to form rhodopsin
-Action of light on rhodopsin is the first step of the visual process
-Deficiency appears as a group of ocular signs termed xerophthalmia
-Night blindness, followed by xerosis of conjunctiva and cornea
-Clinical/subclinical signs: Immunodeficiency (measles)
niacin (B3) deficiency
-Involved in fat synthesis, intracellular respiratory metabolism, and glycolysis
-Content of tryptophan must be considered (converted to niacin)
-Pellagra (niacin deficiency): Weakness, lassitude, dermatitis, photosensitivity, inflammation of mucous membranes, V/D, dysphagia, dementia (severe cases)
vitamin C deficiency
-Principal forms are ascorbic acid and dehydroascorbic acid
-Scurvy: Irritability, bone tenderness/swelling, pseudoparalysis of legs
-Progression: Subperiosteal hemorrhage, bleeding gums/petechiae, hyperkeratosis of hair follicles, mental changes, anemia, decreased iron absorption, abnormal folate metabolism
vitamin D deficiency
-Cholecalciferol (D3) and ergocalciferol (D2) require further activation to become active
-Clothing, lack of sunlight, and skin pigmentation decrease generation of vitamin D in epidermis and dermis
-Vitamin D deficiency appears as rickets in children and as osteomalacia in postpubertal adolescents
-RICKETS:
-Failure of mineralization -> soft zones of bone -> compression/lateral bulging or flaring of ends of bones
-Sx- MC < 2yo
-Craniotabes: Thinning of outer table of skull (when compressed > feels like ping-pong ball)
-Enlargement of costochondral junction (rachitic rosary) and thickening of wrists and ankles
-Enlarged anterior fontanelle
-Scoliosis, exaggerated lordosis, bow-legs/knock knees, greenstick fractures
-DX: Based on hX and poor intake of vitamin D/little UV exposure
-Serum calcium low-normal, phosphorus reduced, alkaline phosphatase activity increased
-Best measure is level of 25(OH)D
-Radiographic changes:
-Distal ulna/radius: Widening, concave cupping, frayed/poorly demarcated ends
undernutrition
-Multifactorial in origin; successful treatment depends on accurate identification and management of causative factors
-Failure to thrive: Growth faltering in infants and young children whose weight curve has fallen by 2 major percentiles from previously established rate of growth, or whose weight falls below the 5th percentile
-Differences in wt gain noticeable after 6mo
-Acute loss of weight/failure to gain weight at expected rate
-Wasting: Reduced weight for height
-Stunting: Reduced height for age (chronic malnutrition)
-Mild pediatric malnutrition: Decreased wt, normal ht and head circumference
-Severe acute malnutrition: severe wasting called marasmus (< 3 SD wt for ht) and Kwashiorkor (edematous malnutrition)
-Kwashiorkor: Significant protein deprivation
undernutrition: risk factors
-MCC is inadequate dietary intake
-Young infants: Weak, uncoordinated suck; CHD, laryngomalacia
-Inappropriate formula mixing
-Dietary beliefs
-Dietary restriction based on suspicion of food allergies/intolerances
-Deficiencies of iron/zinc in older breast-fed infants (diet low in meats/fortified foods)/toddlers not taking fortified formula/dietary sources
-Substitution of milk alternatives (rice, hemp, almond, unfortified soy) for infant formula
undernutrition: assessment
-Measurements: Weight for age, length/height for age, head circumference, weight for length, BMI, percent ideal body weight
-Downward crossing of growth percentiles: Acute malnutrition
-Linear growth stunting: Chronic malnutrition
-Hx: Diet intake/feeding patterns, PMHx, birth/developmental history, family history, social history, ROS
-PE: Skin (rash), mouth, eyes, nails, and hair for signs of micronutrient and protein deficiencies; neurologic exam (loss of deep tendon reflexes, abnormal strength, and tone)
-Labs: Low yield in dx
-Screening: CMP, CBC, iron panel/ferritin, TFTs (for stunting), serology for celiac disease (short stature/linear growth faltering)
undernutrition: Tx
-Dietary counseling for children/families
-Fat/protein food sources
-Structured meal times, with family members
-Correction of micronutrient deficiencies
-Refeeding syndrome may occur with rehab of patients with severe a acute malnutrition
-Monitor for hypophosphatemia, hypokalemia, hypomagnesemia, and hyperglycemia x 3-4 days
-Intake should be increased slowly to avoid metabolic instability
overwt and obesity
-2018- 19.3% of 2-9yo in U.S. have obesity and 6.1% have severe obesity (higher rates among minority and economically disadvantaged)
-Increasing prevalence of childhood obesity if related to a complex combination of socioeconomic, epigenetic, and biological factors
-Childhood obesity is associated with significant comorbidities
-Cardiovascular, endocrine (dyslipidemia, insulin resistance, and T2DM), orthopedic, pulmonary (OSA), mental health problems
-BMI is standard measure of obesity
-BMI between 85th and 95th percentile for age/sex = overweight
-BMI > 95th percentile = obesity
-BMI > 99th percentile = severe obesity (classes II and III)
-Children < 2yo: Wt for length > 95th percentile = overweight and warrants further assessment (energy intake, feeding behaviors)
overwt and obesity: RF, dx, and tx
-RF: Family hx (especially both parents), consumption of sugar-sweetened beverages, lack of family meals, large portion sizes, foods prepared outside of home, excess screen time, poor sleep, lack of activity
-Dx:
-Measurements: Height, weight, BMI + plotting on age- and sex-appropriate growth charts (evaluate for upward crossing of BMI percentiles)
-Hx: Diet and activity patterns, family history, ROS
-PE: BP, distribution of adiposity, markers of comorbidities (acanthosis nigricans, hirsutism, hepatomegaly, orthopedic abnormalities), and physical stigmata of genetic syndromes
-Labs: Onset at age 10 or at onset of puberty
-Overweight (with family hx of HD risk factors) or obesity: Fasting lipid profile, fasting glucose, and/or hemoglobin A1C, ALT
-Severe obesity (Early onset, 2-5 years): Genetic testing
-Tx:
-Uncomplicated obesity: Achieve healthy eating and activity patterns (not necessarily to achieve ideal body weight)
-Wt goals range from weight maintenance to up to 1 pound/month weight loss for < 12 years and up to 2 pounds/week for > 12 years
-Motivational interviewing with patient and families
-Limited screen time for children younger than 2 years, max of 2 hours/day for older children
-Staged approach:
-Prevention plus: Counseling on problem areas
-Structured weight management: More specific and structured dietary pattern – meal planning, exercise prescription, and behavior change goals
-Comprehensive multidisciplinary: Increases structure of therapeutic interventions and support, employs multidisciplinary team, and weekly group meetings
-Tertiary care intervention: Unsuccessful at other levels with severe obesity; intensive behavior therapy, specialized diets, medications, and surgery
-Medications: Orlistat (lipase inhibitor) approved for pts > 12 yo
-Bariatric surgery for select, closely monitored patients
GERD
-Reflux of gastric contents into the esophagus during spontaneous relaxations of the lower esophageal sphincter
-INFANTS:
-common in young infants and physiologic
-RF: Small stomach capacity, frequent large-volume feedings, short esophageal length, supine positioning, slow swallowing response to refluxed material
-MC sx -> frequent, postprandial regurgitation (effortless to forceful)
-Usually benign and resolves by 12-18mo
-FTT, food refusal, pain behavior, GI bleeding, upper/lower airway sx, or Sandifer syndrome indicate GERD (reflux causing secondary complications)
-OLDER KIDS:
-Regurgitation into mouth, heartburn, and dysphagia
-Secondary complications (GERD): Esophagitis
-Risk: Asthma, CF, developmental delay/spasticity, hiatal hernia (HH), repaired esophageal atresia-tracheoesophageal fistulas
GERD dx and tx
-H&P should help differentiate infants with benign, recurrent vomiting (GER) from those with red flags for GERD
-Warning signs that warrant further investigation: Bilious emesis, GI bleeding, vomiting > 6mo onset, FTT, diarrhea, fever, hepatosplenomegaly, abdominal tenderness/distension, or neurologic changes
-Upper GI series when anatomic etiologies of recurrent vomiting are considered
-Older children: Trial of acid-suppressant therapy may be dx and tx -> Referral to specialist if no improvement
-Esophagoscopy and mucosal bx for eval of mucosal injury 2ndary to GERD (Barrett esophagus, stricture, erosive esophagitis) or other disease like EoE
-Intraluminal esophageal pH monitoring (probe) and combined multiple impedance and pH monitoring (impedance probe) to quantify reflux
-Tx:
-Spontaneous resolution in 85% of affected infants by 12 months of age (erect posture and solid feedings)
-Reduction via small feedings at frequent intervals and by thickening feedings with rice cereal (2-3 tsp/ounce of formula – 4-6 months)
-Older infants/children: Acid suppression for suspected esophageal/extraesophageal complications of reflux
-Histamine-receptor antagonists or proton pump inhibitors (x 8-12 weeks)
-Older children: Intermittent use of acid blockers versus chronic acid suppression
-Antireflux surgery (Nissen fundoplication) for pts who:
-Fail medical therapy
-Depend on persistent, aggressive medical therapy
-Have sx and are nonadherent to medical therapy
-Have persistent, severe respiratory/life-threatening complications of GERD
foreign body ingestion
-Majority (80-90%) of FBs pass spontaneously, with only 10-20% requiring endoscopic or surgical management
-MC sx: Dysphagia, odynophagia, drooling, regurgitation, and chest or abdominal pain
-Coins are MC FBI in children -> lodge in narrowed areas
-Initial evaluation: Plain radiographs
-Contrast esophagram for suspected, retained, nonradiopaque EFBs
-US, high-definition radiographs, and CT have utility in early and accurate diagnosis of FBI
-Most removed from esophagus/stomach via flexible endoscopy (within 24 hours of ingestion)
-Smooth FBs in stomach monitored for several weeks, if asymptomatic
-Should remove double-sided sharp objects, fish bones, wooden toothpicks, and objects longer than 5 cm (unable to pass ligament of Treitz)
-Multiple magnets/single magnet + metallic object should be removed due to risk of fistula or erosion of mucosal tissue trapped between adherent FBs
-Esophageal button batteries should be removed emergently (gastric injury/perforation within 2 hours of ingestion)
-Lavage solutions (polyethylene glycol) may promote passage of smooth FBs lodged in intestine
pyloric stenosis
-Postnatal pyloric muscular hypertrophy with gastric outlet obstruction
-Incidence of 1-8/1000 births with 4:1 male predominance
-Projectile postprandial vomiting between 2 and 4 weeks of age (as late as 12 weeks)
-Vomitus rarely bilious, but may be blood-streaked
-Infants usually hungry and nurse avidly
-Upper abdomen may be distended after feedings, and prominent gastric peristaltic waves from L to R may be seen
-Oval mass, 5-15 mm in longest dimension palpable in the RUQ of abdomen (only present in 13.6% of patients)
pyloric stenosis dx and tx
-Labs:
-Hypochloremic alkalosis with potassium depletion
-Dehydration: Elevated hemoglobin/hematocrit
-Imaging:
-US shows a hypoechoic muscle ring > 4 mm thickness with hyperdense center and pyloric channel length > 15 mm
-Barium upper GI series: Retention of contrast in stomach and a long narrow pyloric channel with a double track of barium
-Tx:
Pyloromyotomy – Incision down the mucosa along the pyloric length
Treatment of dehydration/electrolyte imbalance prior
duodenal obstruction/atresia
-Obstruction is either intrinsic or extrinsic
-Extrinsic: Congenital peritoneal bands associated with intestinal malrotation, annular pancreas, or duodenal duplication
-Intrinsic: Congenital atresia, stenosis, mucosal webs
-Imaging:
-Prenatal ultrasound versus postnatal abdominal plain films: Presence of a “double-bubble” – distention of the stomach and proximal duodenum
-Absence of distal intestinal gas suggests atresia
-Barium enema may be usual in determining atresia
-Duodenal Atresia:
-Maternal polyhydramnios
-Bilious emesis and epigastric distention within several hours of birth
-Pre-term birth and Down syndrome associations
-Tx:
Surgical intervention – Duodenoduodenostomy to bypass atresia
Good prognosis, mortality risk due to associated anomalies other than duodenal obstruction
intestinal malrotation
-Bowel from ligament of Treitz to mid-transverse colon rotates around narrow mesenteric root (from incomplete rotation during development) and occludes the SMA (volvulus)
-Malrotation with volvulus accounts for 10% of neonatal intestinal obstructions
-First 3 weeks of life: Bilious emesis or overt SBO
-Later signs: Intermittent intestinal obstruction, malabsorption, protein-losing enteropathy, or diarrhea
-Older children: Chronic GI symptoms of N/V/D, abdominal pain, dyspepsia, bloating, and early satiety
-Imaging:
-Upper GI series is gold standard: Duodenojejunal junction and the jejunum on the R side of the spine; “corkscrew sign” from twisted configuration of proximal small bowel loops
-Barium enema: Mobile cecum in midline, RUQ, or left abdomen
-US/CT scan: “Whirlpool sign” denoting midgut volvulus
-Tx:
-Surgical intervention – Ladd procedure: Duodenum mobilized, short mesenteric root extended, and bowel fixed in a more normal distribution
-Midgut volvulus is a surgical emergency (bowel necrosis from occlusion of the SMA)
-Guarded prognosis if perforation, peritonitis, or extensive intestinal necrosis is present
intussusception
-one segment of intestine telescopes into another
-Can occur anywhere along the small and large bowel and usually starts proximal to the ileocecal valve and extends for varying distances into the colon
-MCC of intestinal obstruction in 1st 2 years of life and 3x more common in males
-Sx related to obstruction and ischemia are due to swelling, hemorrhage, vascular compromise, and necrosis of intussuscepted ileum
-Primary causes include SB polyp, Meckel diverticulum, omphalomesenteric remnant, duplication, lymphoma, lipoma, parasites, FB, and viral enteritis with hypertrophy of Peyer patches (MC)
-In children > 6yo, lymphoma is the MCC
-Previously healthy 3-12mo develops recurring paroxysms of abdominal pain with screaming and drawing up of knees
-Vomiting and diarrhea occur (90% of cases)
-Bloody bowel movements with mucus (“currant jelly stools”) appear within first 12 hours
-May be febrile, lethargic between episodes
-Abdomen tender/distended
Sausage-shaped mass may be palpated, upper mid abdomen
-Dx/Tx
-Abdominal US is 98-100% sensitive for diagnosis – “Target sign”
-Barium enema and air enema are diagnostic and therapeutic
-Not if ischemic damage to intestine is suspected > perforation
-Surgery for identifying lead point
inguinal hernia
-Occur at any age, MC indirect, more frequent in boys (9:1)
-Painless inguinal swelling
-Partial obstruction > severe pain
-Rarely, bowel becomes trapped in the hernia and complete intestinal obstruction occurs
-Gangrene of hernia contents or testis may occur
-In girls, hernia may prolapse into the hernia sac presenting as a mass below the inguinal ligament
-History of inguinal fullness associated with coughing or long periods of standing, or presence of firm, globular, and tender swelling sometimes associated with vomiting and abdominal distention
-Tx:
-Incarceration of inguinal hernia: Manual reduction
-CI if present > 12 hours or if blood stools noted
-Surgery if hernia has incarcerated in past
umbilical hernia
-Occur MC in full-term, African American infants
-Most regress spontaneously if fascial defect has a diameter of < 1 cm
-Asymptomatic UHs are managed expectantly with no intervention until 4-5 years, after which they are usually treated surgically
meckel diverticulum
-MC form of omphalomesenteric duct remnant
-Complications 3x more common in males and 50% occur in first 2 years of life
-40-60% of pts have painless episodes of maroon or melanotic rectal bleeding
-Bleeding due to ileal ulcers adjacent to the diverticulum caused by acid secreted by heterotopic gastric tissue (may cause shock and anemia)
-Intestinal obstruction in 25% of symptomatic patients -> Ileocolonic intussusception
-Imaging:
-Dx is made with a Meckel scan
-Technetium-99m-pertechnetate take up by heterotopic gastric mucosa in the diverticulum and outlines diverticulum on a nuclear scan
-Tx: Surgical with good prognosis
acute appendicitis
-MC indication for emergency abdominal surgery in childhood
-Frequency increases with age and peaks between 15 and 30 years
-Obstruction of appendix by fecalith (25%) is a common predisposing factor
-Incidence of perforation is high in childhood (40%) – pain poorly localized and nonspecific
-Low grade fever and periumbilical abdominal discomfort, becoming localized to RLQ with signs of peritoneal irritation
-Anorexia, vomiting, constipation, and diarrhea can also occur
-Serial examinations are important
-Labs:
-WBCs seldom > 15K/uL
-Pyuria, fecal leukocytes, guaiac + stool sometimes present
-Combo of elevated CRP and leukocytosis has been reported to have PPV of 92%
-Imaging:
-Radio-opaque fecalith in 2/3 of cases of ruptured appendix
-US: Noncompressible, thickened appendix in 93% of cases
-Abdominal CT after rectal instillation of contrast may be dx
-Tx:
-Exploratory laparotomy or laparoscopy when diagnosis cannot be ruled out
-Post-operative antibiotics for patients with gangrenous or perforated appendix
-< 1 % mortality rate during childhood, despite high rate of perforation
congenital aganglionic megacolon/hirschsprung ds
-1 in 5,000 live births, 4x greater in males
-MC chromosomal abnormality associated is Down syndrome
-Results from an absence of ganglion cells in the mucosal and muscular layers of the colon
-Absence of ganglion cells results in failure of the colon muscle to relax
-Aganglionic segments have normal or slightly narrowed caliber with dilation of the normal colon proximally
-Mucosa of the dilated colonic segment may become thin and inflamed > diarrhea, bleeding, and protein loss
congenital aganglionic megacolon/hirschsprung ds presentation
-Failure of newborn to pass meconium (within first 24 hours of life), followed by vomiting, abdominal distention, and reluctance to feeds
-Enterocolitis manifested by fever, dehydration, and explosive diarrhea in 50% of affected newborns
-May lead to inflammatory and ischemic changes in the colon, with perforation and sepsis
-Later infancy: Alternating obstipation and diarrhea predominate
-Older children: Constipation alone
-Other symptoms may include foul-smelling or ribbon-like stools, distended abdomen, intermittent bouts of abdominal obstruction, hypoproteinemia, and FTT
-DRE: Anal canal/rectum devoid of fecal material despite obvious retained stool on abdominal examination/radiograph
vomiting
-Presenting sign of many pediatric conditions
-MCC in childhood is viral gastroenteritis
-Others: Obstruction, acute/chronic inflammation of GI tract; CNS inflammation, increased ICP, or mass effect; metabolic derangements associated with inborn errors of metabolism, sepsis, drug intoxication
-Tx:
-Control of vomiting with medication is rarely necessary in acute gastroenteritis, but may relieve N/V and decrease need for IV fluids and/or hospitalization
-Antihistamines/anticholinergics for motion sickness
-5-HT3-receptor antagonists (ondansetron, granisetron)
-Benzodiazepines, corticosteroids, and substituted benzamides: CTX
-Butyrophenones (droperidol, haloperidol): Intractable vomiting in acute gastritis, CTX, post-op
acute diarrhea
-Viruses MCC in developing and developed countries
-Rotavirus (developing) and Norovirus (developed) are MC, followed by enteric adenovirus, and Astrovirus
-Affects small intestine, causing voluminous, watery diarrhea without leukocytes or blood
-!Norovirus: Mainly vomiting (also diarrhea) with short duration of symptoms (1-2 days)
acute diarrhea: rotavirus
-In U.S., primary affects infants between 3 and 15 months of age, peaks in winter, transmitted via fecal-oral route and survives for hours and hands/days on environmental surfaces
-Incubation period of 1-3 days
-Vomiting is first symptom (80-90%), followed by low-grade fever and watery diarrhea within 24 hours (diarrhea lasts x 4-8 days)
-Detected in feces using EIA or latex agglutination
-Other lab findings: Normal WBC count, electrolyte abnormalities with dehydration, metabolic acidosis (bicarbonate loss), ketosis, lactic acidosis (severe cases)
-Treatment is supportive
-Replacement of fluid and electrolyte deficits/ongoing losses via ORT/IVT
-ORT solutions appropriate in most cases (not clear liquids or dilute formulas > 48 hours)
-Intestinal lactase levels may be decreased (short course of lactose-free diet)
-Reduced fat intake may decrease N/V
-No anti-diarrheal medications indicated
chronic diarrhea (low yield)
-Gradual or sudden increase in the number or volume of stools to more than 15 g/kg/day combined with increased fluidity should raise suspicion
-Antibiotic Therapy
-Eradication of normal gut flora and overgrowth of other organisms
-Prevention: Use of probiotics to restore intestinal microbial balance
-Treatment: Symptoms resolve with discontinuation of antibiotic
-Extraintestinal Infections
-UTIs/URIs: Abx treatment, toxins released by infecting organisms, local irritation of rectum (bladder infection)
-Malnutrition
-Decreased bile acid synthesis, decreased pancreatic enzyme output, decreased disaccharidase activity, altered motility, changes intestinal flora
-Severely malnourished: Higher risk of enteric infections due to decreased immunity
-Protein-calorie malnutrition may result in villous atrophy/malabsorption
-Diet/Medications
-Deficiency of pancreatic amylase (after starchy foods), fruit juices, intestinal irritants (spices/fiber), histamine-containing/releasing foods (citrus, tomatoes, fermented cheeses, red wines, tuna, mahi mahi)
-Laxative abuse
-Allergic Diarrhea
-Cow’s milk protein allergy
-Food protein-induced enterocolitis syndrome (FPIES)
-Systemic allergic reaction occurring during infancy: Large-volume diarrhea, acidosis, and shock (common food products (milk/soy))
-Anaphylactic reactions- Vomiting, diarrhea, pallor, hypotension -> RAST/skin testing positive
chronic diarrhea: chronic nonspecific diarrhea, immunologic, other
-Chronic Nonspecific Diarrhea (Toddler’s diarrhea):
-MCC of loose stools in otherwise thriving children
-Healthy, thriving child aged 6-20 months who has 3-6 loose stools per day during waking hours (without blood)
-Syndrome resolves spontaneously by 3.5 years of age or after potty training
-Loperamide for symptomatic relief, if dietary changes/restrictions fail
-Immunologic: Immune deficiency states (IgA/T-cell abnormalities), autoimmune enteropathy (immune deficient, chronic infection)
-Other causes
-MC in immunocompetent: Giardia lamblia, Entamoeba histolytica, Salmonella, Yersinia
-Bacterial overgrowth in those with SBS, CTX, or anatomic abnormalities
-Pancreatic insufficiency with CF, tumors, hyperthyroidism, IBS
dehydration
-MCC in kids is vomiting/diarrhea
-Children at greater risk of hypovolemia
-Higher frequencies of gastroenteritis
-Higher surface area to volume ratio/insensible volume losses
-Unable to communicate fluid needs
-Classified by % of total body water lost (mild, moderate, severe)
-Vitals (including orthostatic BP)
-Urinalysis: Elevated SG, ketonuria; BMP (electrolyte abnormalities); serum bicarbonate (metabolic acidosis); BUN (elevated with hypovolemia)
-Tx:
-Mild-Moderate: ORT (Pedialyte/Gatorade), BRAT diet (diarrhea)
-Typically, 1 mL/kg every 5-10 minutes or 0.5 ounces every 5-10 minutes (higher aliquots for dehydration may be used)
-Ondansetron if needed to tolerate ORT (for vomiting)
-Severe: IV fluids
-Initial bolus of 20 mL/kg normal saline over 20-30 minutes
-½ fluid deficit over first 8 hours, second ½ over next 16 hours
-FD = % dehydration x weight (kg)
functional constipation/encopresis
-Infrequent BMs, passage of hard stools, difficult passage of large-diameter stool, and soiling (Rome Criteria/Bristol stool charts are very helpful in arriving at diagnosis)
-Approximately 30% of U.S. children affected by constipation with peak prevalence in preschool child age group
->90% of cases are functional – no identifiable causative organic condition
-Key features are occurrence after infancy, presence of stool-withholding behavior, absence of red flags, and episodic passage of large-diameter stools
-Red flags: Poor growth, weight loss, FTT, emesis, abdominal distention and bloating, perianal disease, blood in stool, abnormal urinary stream, history of delayed passage of meconium
-!Encopresis: Intentional or involuntary passage of feces into clothing in children with a developmental age of 4 years or more
-Leakage of stool due to underlying constipation or fecal impaction
functional constipation/encopresis: etiology
-3 periods in child development during which children are prone to developing functional constipation
-Introduction of solids (> 6 months), toilet training (2-3 years of age), start of school (3-5 years of age)
-Etiology of both functional constipation and soiling includes diet, slow GI transit time, and chronic withholding of bowl movements
-95% of children referred to a subspecialist for encopresis have no underlying pathologic condition
-Diet: Well-balanced diet of fruits/vegetables with an age-appropriate level of fiber is recommended for all children
-Little evidence that adding extra fiber is helpful to those with significant constipation
-Withholding Behaviors
-May begin to delay defecation due to history of pain
-Stool accumulates in rectum and becomes harder/larger, causing even more pain when eventually passed
-Parental attempts at early toilet training and coercion to potty train can lead to stool holding behavior with significant sequelae
functional constipation/encopresis: sx and tx
-Uncontrolled defection (encopresis), painful defecation, impaction, and withholding
-Stool impaction felt on abdominal exam (firm packed stool in rectum)
-Evaluation of anal placement and neurologic exam (for spinal cord abnormalities)
-Imaging not required – may help to demonstrate degree of stool load to parents
-Tx:
-Tx begins first with education and demystification for the child and parent
-Involves combination of behavioral training and use of stool-softening therapy, with possible addition of laxative therapy
-Next steps include adequate colonic cleanout/disimpaction
-Behavioral training: Timed toilet-sitting sessions at scheduled frequencies, praise/positive reinforcement
-Successful cleanout > maintenance phase: Promotes regular stool production and prevents re-impactions
-Dietary changes – Sorbitol juices (prune, pear, apple)
-Maintenance medications
enterobiasis (pinworms)
-Caused by Enterobius vermicularis
-Males live in colon; females deposit eggs on the perineal area, primarily at night, causing intense pruritis
-Scratching contaminates fingers and allows transmission back to host or to contacts through fecal-oral spread
-Intense, localized pruritis or the anus and vulva
-Can migrate (lumen of appendix, bowel wall, peritoneal cavity, urethra, bladder, vagina)
-Dx:
-Pressing a piece of transparent tape on the child’s anus in the morning prior to bathing > placing it on a drop of xylene on a slide > ova visible
-Parents may visualize adult worms in the perianal region at nighttime
-Tx:
-All household members treated at the same time to prevent reinfections
-Pyrantel pamoate, given as a single dose
-Albendazole in a single dose
-Ivermectin -> Therapy typically repeated in 2 weeks to target new hatchlings
