Peds Unit 1 GI

olanjones's version from 2017-02-02 05:35


Question Answer
Dehydration (based on pre-illness wt)s/s Change in LOC- Drowsy, lethargic, irritable, Tachycardia, Low BP, Sunken fontanel/eyes, Absent tears, Cool extremities/mottling, Weight loss, Change in electrolytes
Mild5% wt loss or 50 ml/kg
Moderate10% wt loss or 50-90 ml/kg
Severe15% wt loss 100 ml/kg
Isotonic130-150 Na+: normal/isotonic
Hypotonic<130 Na+: no free water to kids under a year
Hypertonic>150 Na+: seizures. Neuro sx. Causes: sweating, ketoacidosis, malnutrition, neglect, diabetes insipidus
Mild/moderate dehydration txoral rehydration therapy. 2-3 ml q 2-3 min or 10 ml q 5min (Rehydration can be repeated 3x)
Severe dehydration txIV fluid resusc. Isotonic solution NS or LR
Daily Maintenance Fluid RequirementsChild’s wt in KILOGRAMS and broken down into 3 separate ranges to allow for proper calculation of daily fluid requirement:
100 mL/kg for first 10 kg body wt (0-10kg),
1000 mL + 50 mL/kg for second 10 kg body wt (11-20kg)
1500 + 20 mL/kg for remaining body wt (>20kg)
Divide total amount by 25 hours (NOT 24) to obtain rate in mL per hour
Acid/BaseCO2 role in acid-base chemistry: respiratory acid
HCO3 role in acid-base chemistry: metabolic buffer/base made by kidneys and excreted in stool
CPT1 deficiencyDextrose with AKNatives. Need glucose source. RF for seizures.

Diarrhea & Vomiting

Question Answer
Diarrhea (losing buffer)HCO3; more acid or metabolic acidosis (Cause: metabolic), base comes out of butt
Eti DiarrheaMost pathogens spread by fecal/oral - contaminated food/water, person to person, poor hygiene, nutritional deficiency, and poor sanitation
Acute DiarrheaUsually self-limiting, Lasts < 14 days, Usually no tx required unless dehydration occurs
Chronic DiarrheaLasts > 14 days, May be r/t allergies, malabsorption, IBD
Diarrhea Interventionsrehydration (oral is preferred), rotavirus vaccination
Vomiting (losing acid)metabolic alkalosis, ARFing acid
Eti Vomitinggi and non gi causes (most common eti in infants = overfeeding)
Complications of vomitingdehydration, metabolic alkalosis, aspiration pneumonia
BOLO VomitingBile in vomit, Large amounts of blood: bad sign, notify provider
Vomiting, labs to getGet BMP: C6, electrolyte, fluid balance indicators, etc
Interventions vomitingzofran, phenergan (infiltration of IV high risk), if vomiting sever, withhold feeding, speech therapist help w/ select appropriate nipple. Positioning,

Cleft lip & palate

Question Answer
Cleft Lip and/or PalateMay appear separately or together, May be an isolated anomaly or occur with other congenital defects
Sx Correction of Cleft LipDone at 10 weeks, once child reaches 10 pounds, Done early to promote better seal for nipple feeding. Post-op: Protect suture line, minimize crying (pain meds, holding), Elbow/cuff restraints (no-nos)
Sx Correction of Cleft PalateDone at 10 months. Post-Op: Nothing sharp in mouth! No utensils, straws, or hard/jagged foods. Use open cup, syringe feed, No sucking (keep sutures intact)
Complications with Cleft Lip/PalateFeeding problems- Unable to suck successfully, Excess air intake, Speech development, Teeth may be impacted or missing, Parent/infant attachment may be affected (watch for after sx as well)


Question Answer
AssessmentNeonate not stooling 1-2 days of life - abd distension, feeding intolerance w/ bilious vomiting, constip.
Hirschsprung DiseaseCongenital megacolon: No ganglionic cells = no peristalsis - mechanical obstruction from inadequate motility, May be acute, life-threatening, or chronic
HD InterventionTx surgical, rectal biopsy, enemas
Preop enema to clear bowel. High cal, high prot diet
Surgical prepbowel prep NG: go lytely, abx, rectal irrig, parent/child educ: colostomy
IntussusceptionAnti-slinky “telescoping” of intestine. May present sudden onset, draw knees up, bilious vomiting.
Intussusception Dx&TxBarium enema - Reextends telescoped areas. “Currant jelly stools” (late sign)
IncidenceMore common in males, Has been associated with Down syndrome
Intussusception Most common cause of acute intestinal obstruction in children less than 5 years

Pyloric Stenosis/GERD

Question Answer
Pyloric StenosisHypertrophy of pyloric canal muscle causing obstruction. Partial obstruction → inflammation and edema → Complete obstruction → forceful projectile vomiting → dehydration and electrolyte imbalance.
S/S pyloric stenosisOlive sized mass RUQ, may see peristalsis. Projectile vomiting 30-60 min post feed. Infant remains hungry, irritable, ↓wt.
Pyloric Stenosis Dxultrasound, Serum electrolytes – metabolic alkalosis (prolonged vomiting)
Pyloric Stenosis Tx pyloromyotomy – surgical release of pyloric muscle to relieve obstruction. Feedings usually begun 4-6 hours post-op. Infants usually go home the next day – may continue to have emesis/GER
Gastroesophageal Reflux (GER)transfer of gastric contents into the esophagus (Common in infants – resolves by 6 to 12 mo)
Gastroesophageal Reflux Disease (GERD)gastric contents reflux into the esophagus/oropharynx & cause symptoms/tissue damage
GERD Symptomspoor weight gain/failure to thrive (may desat when feeding), esophagitis, dysphagia, bleeding, and/or respiratory symptoms. Often seen in children with asthma, cystic fibrosis, neurologic disorders
GERD Dxbarium swallow, upper GI series, esophageal pH Probe monitoring
Treatment of GERD Mild - Infants Burp every 1 -2 ounces, Hold upright for 30-60 minutes after feeds, Raise head of crib 30 degrees, thicken formula with rice cereal
GERD Treatment Mild – Children(similar to adults tx) Avoid caffeine, citrus, tomatoes, peppermint, and spicy/fried foods, Weight loss, Elevate HOB
GERD Treatment Mod-severeAntacids, H2 receptor blockers (e.g., zantac), or Proton Pump Inhibitors (e.g., prevacid), Nissen Fundoplication
RF & Complix GERDRF: prematurity, BPD, CP; Complix: apspiraiton pneumonia, FTT

Esophageal atresia /Tracheoestophageal fistula

Question Answer
Esophageal Atresia & Tracheoesophageal FistulaFailed separation of the esophagus and trachea by the 4th week of gestation, Foregut fails to develop into two parallel tubes (esophagus and trachea), Esophagus ends in blind pouch (EA) or develops as a pouch connected to the trachea (TEF), Many different variations of this can occur
EA & TEF may occur asseparate entities or in combination
EA & TEF Cause unknown (hx of maternal polyhydramnios is noted)
Clinical manifestationsexcessive salivation & drooling, the 3 C’s (coughing, choking, & cyanosis), apnea, increased respiratory distress after feeding & abdominal distention (If EA or TEF is suspected keep NPO)
TEF Diagnosis of EA/TEF based onclinical manifestations and is usually made after first feeding; Can dx with NG, confirmation determined by X-ray
TEF Pre-opNPO, IVF, elevate HOB, continuous suction of mouth and upper pouch. Priority is to maintain a patent airway!
TEF Surgical interventionThoracotomy w/ division & ligation, and an end-to-side anastomosis of esophagus. May have gastrostomy during healing


Question Answer
Celiac Diseasesensitivity gluten found in wheat, 2nd leading cause of malabsorption syndrome, Appears 6-18 mos
CD 4 characteristicsSteatorrhea (fatty, foul, frothy, bulky stools), General malnutrition, Abdominal Distention, Secondary vitamin deficiencies
CD Interventions-GF diet (eliminate of wheat, rye, barley, oats), subs corn, rice, millet
-Vits: multi, folic acid, IRON
-Avoid high fiber during flares
AppendicitisSeasonal (may be assoc with virus). Can be ruptured or intact
Appy S/SPain in RLQ. BOLO Rebound tenderness, Board like rigid abdomen →peritonitis! Pain that suddenly relieved, then diffuse pain →ruptured! NO HEAT, can potentiate rupture
Appy Txused to be primarily surgical but now some tx w/ABX/TPN/bowel rest
Appy post-opTreat as a post op pt. TCDB! Ambulate! SemiFowlers, NG, intermittent suction, check every hour, Tx Pain

Hyperbilirubinemia/Biliary Atresia

Question Answer
Two causes of hyperbilirubinemianeonatal jaundice, Biliary atresia (Eti: Polycythemia)
Hyperbilirubinemia Two typesUnconjugated/indirect: bilirubin elevation before liver, caused by inc. RBC bkdn. Conjugated/direct: bilirubin elevation caused by liver disease (cirrohsis, hepatitis, meds, blockage of bile duct)
Hyperbilirubinemia TxBili light - 12-15 cm from light, Check bili meter to see if it's working. Teaching: Not waking up, not eating → Call ED or PCP!
Neonatal jaundice1st 24 hrs/at 1 week → pathologic. Look at nose, conjunctiva to check color, When drawing blood for bilirubin, turn lights bili lights down. Can get hot, check temp freq. make sure eating and pooping. Cord blood → check Rh incompatibility
Biliary AtresiaDestructive, idiopathic, inflammatory process that leads to fibrosis and obliteration of the biliary tree, Absence or closure of the hepatic or common bile ducts → blocks bile flow from liver to duodenum → inflammation and fibrotic changes. Without treatment is fatal (usu by age 2)
BA S/SItching, pale stool, hepatomegaly, FTT, can’t absorb Vit ADEK
BA Dxhistory, exam, labs (↑bilirubin, alkaline phosphatase, and prothrombin time)
BA most common symptomJaundice, Light-colored stools (white, tan, or gray), Dark urine, Enlarged liver and abdominal distention, Liver biopsy confirms diagnosis
BA Early intervention is KEY to survival, Surgery to correct obstruction (Kasai)- buys time until you get transplant, Segment of intestine is anastomosed to the resected porta hepatis (liver) to attempt bile drainage

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