exam 2 - nutrition Flashcards

1
Q

know when to start introducing which foods

A

-honey >12mo
-6mo- cereal -> fruit/veg -> meat

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2
Q

lactate deficiency

A
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3
Q

new foods every 3-4 days

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4
Q

corkscrew sign, target sign, double double

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5
Q

intussiception -> US

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6
Q

umbilical hernia!! -> observe

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7
Q

not testing on chronic diarrhea

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8
Q

dont need to know rome criteria or bristol

A
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9
Q

miralax is go to

A
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10
Q

breast feeding

A

-provides optimal nutrition during early months
-Formulas resemble breast milk, but cannot replicate nutritional/immune composition of human milk
-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)

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11
Q

breast feeding techniques

A

-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)

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12
Q

common problems in breast feeding

A

-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?!

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13
Q

breast feeding: maternal drug use

A

-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”

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14
Q

formula feeding

A

-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)

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15
Q

complementary feeding

A

-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

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16
Q

nutrition for ages 2yrs+

A

-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

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17
Q

malabsorption syndromes: lactose intolerance

A

-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

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18
Q

malabsorption syndromes: cows milk protein intolerance

A

-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

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19
Q

malabsorption syndromes: celiac ds

A

-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)

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20
Q

vitamin deficiencies: vitamin A

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)

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21
Q

niacin (B3) deficiency

A

-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)

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22
Q

vitamin C deficiency

A

-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

23
Q

vitamin D deficiency

A

-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

24
Q

undernutrition

A

-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

25
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
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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)
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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
28
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)
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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
30
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
31
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
32
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
33
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)
34
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
35
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
36
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
37
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
38
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
39
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
40
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
41
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
42
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
43
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
44
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
45
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)
46
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
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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
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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
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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)
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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
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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
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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
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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 s