exam 2 - nutrition Flashcards

(47 cards)

1
Q

s notes

A

know when to start introducing which foods

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

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2
Q

-growth trajectory- if pt is born at 5lbs what should they be at 1mo, 6mo, 1yr

A

1 month: should be 1.5 lbs heavier
double at 6 months (10 lbs)
triple at 12 months (15 lbs)

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3
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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4
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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5
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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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
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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14
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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15
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

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16
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

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17
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

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18
Q

undernutrition: risk factors

A

-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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19
Q

undernutrition: assessment

A

-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)

20
Q

undernutrition: Tx

A

-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

21
Q

overwt and obesity

A

-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)

22
Q

overwt and obesity: RF, dx, and tx

A

-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

23
Q

GERD *

A

-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

24
Q

GERD dx and tx *

A

-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

👶 INFANTS
✅ Physiologic Reflux (VERY common)
Due to:

Short esophagus

Small stomach capacity

Frequent feeds

Supine position

Symptoms:

Effortless or forceful spit-up, especially post-feeds

No distress, no poor weight gain

Course:

Resolves by 12–18 months

No treatment needed except reassurance

⚠️ When Reflux Becomes GERD (Pathologic)
RED FLAGS:

Sign Suggests GERD or complications
Failure to thrive (FTT) Poor weight gain
Pain behaviors Arching, crying, irritability
Feeding refusal Due to discomfort
GI bleeding Hematemesis, anemia
Respiratory sx Cough, wheeze, apnea, stridor
Sandifer syndrome Dystonic posturing after feeds (reflux-related)

🧒 OLDER CHILDREN
Symptoms:
Heartburn

Regurgitation into mouth

Dysphagia

Chest or epigastric pain

Risk factors:
Asthma, CF

Neurologic impairment (spasticity, developmental delay)

Hiatal hernia

Esophageal surgeries (e.g., repaired TEF)

🔬 Complications of GERD
Esophagitis

Esophageal stricture

Barrett’s esophagus (rare in peds)

Respiratory symptoms (recurrent pneumonia, chronic cough)

🛠️ Management Overview
Step Details
Reassurance If healthy infant with normal weight gain
Positioning Upright after feeds; avoid supine feeding
Thickened feeds Rice cereal or thickened formula
Trial acid suppression H2 blocker (ranitidine*) or PPI if concerning GERD
Refer to GI If poor growth, severe symptoms, bleeding

Note: Ranitidine withdrawn in many places — PPIs often used if needed

🔒 TL;DR
Infant reflux is normal unless there are red flags (FTT, pain, feeding issues, bleeding)

Older kids = classic GERD symptoms (heartburn, dysphagia)

GERD can cause esophagitis or respiratory issues

Treat based on severity and impact on nutrition or quality of life

25
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
26
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)
27
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
28
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
29
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
30
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 ## Footnote intargetssusception
31
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
32
umbilical hernia *** test
-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 *****
33
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
34
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
35
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
36
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
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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
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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)
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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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constipation: *** - 2-3days no BM, no distention -> ____________ -5-7 days no BM, mass, distention -> _____
- 2-3 days no BM, no distention = dietary mod: add prunes, pear juice, fruits/veggies (miralax maybe) -5-7 days no BM, mass, distention -> cleanout: suppository, enema, disimpaction - manual removal
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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