Endocrine System and Hormones PDF

Endocrine System and Hormones – Endocrine System: controls cellular activity through release of hormones – Glands of the endocrine system include: – Hormones have specific controlling effects on the cells in the body anterior parathyroid...

Endocrine System and Hormones – Endocrine System: controls cellular activity through release of hormones – Glands of the endocrine system include: – Hormones have specific controlling effects on the cells in the body anterior parathyroid pituitary adrenal hypothalamus pancreas posterior ovaries & testes pituitary thyroid Disorders of the Pituitary Function – Normal Physiology – Different Disorders anterior pituitary secretes growth hormone, TSH, ACTH, FSH, LH, prolactin, MSH, ß- growth – hormone related endorphins ADH- related  diabetes insipidus posterior pituitary secretes ADH and oxytocin  SIADH precocious puberty Growth Hormone Deficiency – often idiopathic, but may be caused by tumor growth – Treatment interference w/ production or release of growth hormone growth hormone therapy (somatropin)  subq injections daily – Manifestations  optimum dosing achieved at bedtime short stature but proportional height & weight  therapy ends when epiphyseal plates close or when growth is < 1 in./yr and bone  below 3rd percentile age of 14 in girls and 16 in boys delayed epiphyseal closure encourage child’s devl. and self-esteem retarded bone age proportional to height at risk for teasing premature aging common in later life increased insulin sensitivity – Diagnostics  decreased IGF-1  child fast the night before test growth hormone stimulation test  1. NPO & limited activity 10-12 hrs. prior to test.  2. Draw baseline blood sample 0600 & 0800  3. Administer med. that triggers release of growth nnhormone.  4. Obtain blood sample every 30 min. for a 3- hr. nnperiod. skeletal maturity x-ray  general skeletal survey if < 3 yrs.  hands & wrists of older children Hyperpituitarism – growth hormone excess – Treatment excessive secretion of growth hormone inc. growth rate surg. removal of tumor or pituitary gland commonly caused by pituitary adenoma (tumor)  may need lifelong pituitary hormone replacement if gland is removed increased GH and IGF-q levels, MRI radiation therapy, radioactive implants meds: somatostatin receptor, receptor ligands, dopamine agonists, GH receptor agonists Precocious Puberty – secondary sexual characteristic before 8 yrs. in girls, 9 yrs. in boys – early release of gonadotropin-releasing hormone – usually idiopathic, could be from tutor – early growth spurt ending early & resulting in short stature – monthly injections of Lupron depot – GnRH implant for 1-2 yrs. – mental age congruent w/ chronologic age Diabetes Insipidus – disorder of posterior pituitary gland, unable to concentrate urine in kidneys – Treatment: desmopressin acetate (DDAVP) – central results from inadequate production of ADH acts as hormone replacement and dec. urine output careful monitoring intake/output, electrolytes (prevent hyperkalemia, – nephrogenic results from ineffective action of ADH in kidneys hyponatremia) – known causes include, tumors, trauma, infection, surgery daily weights – Manifestations avoid intake of excessive fluid polyuria, polydipsia (1st sign freq. enuresis)  won’t be able to excrete excess water w/ DDAVP dehydration, hypernatremia inform school to ensure child has unrestricted access to restroom  urine can’t be concentrated, no matter how dehydrated child is needs to wear medical alert ID  dehydration ep. leads to diagnosis infants show irritability, lethargy, vomiting, poor feeding, failure to thrive, constipation test urine osmolality (decreased), specific gravity of urine (increased) look for causes such as tumors w. CT, MRI fluid deprivation test: monitor UOP and UA when fluids withheld Syndrome of Inappropriate Antidiuretic Hormone (SIADH) – excessive ADH, caused by CNS infections, brain tumors, brain trauma – Treatment – failure of feedback mechanisms causes excessive water reabsorption despite low fluid restriction serum osmolality diuretics demeclocycline to block action of ADH – Manifestations hypertonic saline for hyponatremic encephalopathy causes water intoxication and hyponatremia  crackles in lungs – daily weights  weight gain – monitor for signs of electrolyte imbalance  decreased urine output – refer family to registered dietician to assist in identifying hidden sources of water &  N/V, stomach cramps fluids  weakness, confusion, seizures, personality changes hyponatremic encephalopathy: cerebral edema d/t low sodium level labs show high urine osmolality, high urine specific gravity Congenital Hypothyroidism. Lymphocytic Thyroiditis (Hashimoto) – causes: underdeveloped thyroid, iodine deficiency – most common cause of juvenile hypothyroidism – most common preventable cause of cognitive impairment – occurs most freq. < 6 yrs., peak incidence during adolescence early diagnosis and tx. essential – manifestations – manifestations enlarged thyroid gland “quiet and good” baby tracheal compression prolonged jaundice possible hyperthyroidism constipation – diagnostics umbilical hernia TSH levels elevated – diagnostics T4/T3 decreased newborn screening – management – management thyroid hormone replacement lifelong thyroid hormone replacement therapy  Synthroid, Levothyroid – educate parents on sign of overdose Hyperthyroidism – a.k.a. Graves’ disease (autoimmune disorder) – Treatment most common etiology for children thyroidectomy – Manifestations antithyroid drugs hyperactivity of sympathetic nervous system ablation w/ radioiodine  tachycardia, hypertension – needs to wear medical alert ID enlarged, nontender thyroid gland (goiter) – child easily fatigued & need scheduled rest periods at home/school prominent, bulging eyes (exophthalmos) – quiet, unstimulating env. conducive to rest nervousness, hyperactivity – teach family of the need for lifelong thyroid hormone replacement after gland removed voracious appetite w/ weight loss emotional liability, moodiness – monitor for thyrotoxicosis “thyroid storm” heat intolerance Thyrotoxicosis (a.k.a. Thyroid Storm) – occurs d/t sudden release of thyroid hormone – treatment – manifestations antithyroid drugs, beta blockers severe irritability and restlessness – darkened, low stimulation environment vomiting/diarrhea hyperthermia HTN severe tachycardia delirium > coma > death Adrenal Insufficiency (Addison Disease) – caused by genetic disorder – adrenal crisis caused by stressors – chronic manifestations infection, surgery, trauma, vomiting, diarrhea neuro symptoms early: inc. irritability, headache, weakness, N/V, diarrhea pigment changes shock like state: weak/rapid pulse, hypotension, shallow respirations, GI symptoms cold/clammy skin, cyanosis, circulatory collapse circulatory symptoms treat w/ fluids, IV glucose, IV hydrocortisone hypoglycemia – avoid crisis by increasing doses during periods of stress – Diagnostic: ACTH stimulation admin. triple strength dose steroid (hydrocortisone) q6-8 hrs. while stressor present always keep injectable hydrocortisone available Cushing Syndrome – group of systems results from excess blood levels of glucocorticoid hormones (esp. cortisol) – diagnostic evaluation 24 hr. urine level, 17 hydroxy corticoids and 17 ketosteroids serum cortisol level, urine free cortisol cortisone suppression test imaging to rule our tumor – management bilateral adrenalectomy of tumor gradual withdrawal of steroid therapy if exogenous Pheochromocytoma – tumor in adrenal gland characterized by secretion of catecholamines – treatment – manifestations surgical removal of tumor HTN – curative surgical removal of all tumors may trigger release of epinephrine and tachycardia norepinephrine leading to pheochromocytoma crisis headache HTN, tachycardia: treat w/ alpha-adrenergic blocking agents decreased GI activity 24 hr. urine collection post-op for several days to measure catecholamines increased metabolism – DON’T PALPATE MASS – diagnostics CT/MRI 24 hr. urinary levels of catecholamines Diabetes Mellitus Type 1 – autoimmune destruction of pancreatic cells that – diagnosis – management produce insulin based on presence of classic symptoms (3 P’s) and insulin given as 2 or more inj./day or as continuous symptomatic when 90% of cells destroyed one of the following plasma glucose levels SQ infusion via pump – insulin helps transport glucose into cells  HGBA1C > 6.5% self-monitoring of blood glucose  fasting blood sugar > 126 after 8 hrs.  maintain range of 80-120 mg/dl – glycosuria once blood is over 180 mg/dl, pulls water  2 hr. plasma glucose > 200 during oral glucose meals and snacks eaten in accordance to peak with it, causing polyuria tolerance test insulin action – present w/ polyuria, polydipsia, polyphagia, weight  random plasma glucose > 200 exercise encouraged loss, enuresis, fatigue if sick, check BG and urine ketones q3hrs often present in DKA at first diagnosis  notify PCP of vomiting.>1x, BG >240 mg/dl, urine ketones elevated children can help w/ care at roughly 6-8 yrs.  testing BG, keeping records, etc. adolescents can manage self-care, desires to be like peers can interfere w/ tx adherence self-mgmt. is the eventual goal utilize dietician, nurse educator, social worker puberty may be delayed w/ inadequate control children may use condition to get what they want teach parents to check for ketones in urine Diabetic Ketoacidosis – prim. in children w/ type 1 DM who miss insulin doses, – possible symptoms – treatment administer insulin incorrectly or experience a stressor, or hyperglycemia dehydration isotonic IV fluid boluses at first diagnosis symp. kussmual resp. IV reg. insulin at 0.1 un/kg/hr. drip – fat broken down to create energy, ketones then released N/V acetone breath  avoid dec. glucose faster than 100 mg/dl/hr. d/t into body causing acidosis tachycardia risk of cerebral edema – late signs  maintenance IV fluids w/ glucose and potassium – criteria altered LOC irregular when BG 250-300 to maintain BG 120-240 blood glucose > 300 mg/dl hypotension respirations monitor for cardiac arrhythmias serum or urine ketones electrolyte widening pulse monitor mental status for signs of cerebral edema pH < 7.3, bicarb < 15 meQ/L imbalances pressure assess dehydration arrhythmias inappropriate intake and output measurements pupillary changes slowing of HR assess for hypoglycemia and hypokalemia Diabetes Mellitus Type 2 – insulin resistance developed over time – management – often do not have an acute onset focus is on prevention assess any child w/ BMI > 85th percentile for signs of insulin resistance – risk factors  acanthosis nigricans obesity  hypertension low levels of physical activity  dyslipidemia intake of high-energy foods  family hx of DM2 low socioeconomic status customize strategies to fit child to try to promote exercise and dec. sedentary ethnicity activity time family hx – increasingly occurring in younger children Nutritional Needs of Infants – fluid req. high – breastfeeding – bottle feeding & formula – weaning dec. ability to concentrate urine exclusive feeding for 6 mo. commercial iron-fortified formula relinquishing the breast or bottle for a inc. basal metabolic rate (BMR) continue through 12 mo. total amt. of ingested formula levels cup inc. surface area to mass ratio iron supplement if still exclusively off at about 32 oz./day by 6 mo. offer cup at 8-9 mo. – human milk is most desirable complete breastfed after 4 mo. cow’s milk not app. for < 12 mo. infant usually becomes less diet for first 6 months advantages propping bottle discouraged interested in milk  excellent nutritional balance nighttime feeding is usually last to – no add. fluids req. during first 4 months  promotion of GI function be discontinued – vit. d supp. starting at first few days of  fosters immune defense never let a child take a bottle of milk life to prevent rickets  psychologic & economic to bed advantages no sweet liquids (juice) at bedtime Introduction of Complementary Foods – recommended to start introducing at 6 mo. – spoon feeding – human milk or formula is still the primary source of nutrition to 12 mo. infants often push away and appear dissatisfied initially food pushed out should be scooped up and refed – signs that baby is ready will start to open mouth in anticipation. or kept closed if disliked interest in solid foods push food to back of tongue extrusion reflex has disappeared small spoon w/ short handle well-developed and voluntary head control 1-2 tsp food initially and gradually inc. swallowing more coordinated – avoid hot dogs, hard veggies, candy, chunks of peanut butter, and supervise at all times Nutritional Needs – Toddlers – Preschoolers – School-Age Children – Adolescents 3 meals and 2 snacks/day picky eaters, but more willing to develop taste for variety of foods > 2000 cal/day, up to 3000 cals. for  1 tbsp/ yr for serving size sample diff. foods by 5 yrs. easy to fill up on empty calories boys, even more if playing sports 24-48 oz milk/day, low-fat after 2 yrs.  esp. if they helped prepare it teach children to prepare their own many opportunities to choose physiologic anorexia at 18 mo. food jags common nutritious meals unhealthy foods become picky eaters w/ strong taste assess intake over 102 wk. period, not avoid using food as reward  excessive fast food common preferences daily avoid skipping meals and eating fast skipping breakfast freq. ritualism 5x/day of fruits and veggies food frequently milk usually passed over in favor of prefer using their fingers limit 100% fruit juice to 4-6oz./day soft drinks can use spoon at 18 mo. encouraged to make healthy food encourage self-feed & simple selections choices emphasize physical activity  eats at table w/others & only at specified times imitate others  if parent refuses food, they will brush teeth after each meal no eating/drinking while playing/lying down Failure to Thrive (FTT) – inadequate growth from an inability to obtain or use – manifestations – management calories req. for growth growth failure > less than 5th percentile goal is reversing cause of the growth failure – diagnosis based on growth parameters in persistent developmental delays provide sufficient cal.to support “catch up” growth deviation undernutrition  2-3x avg. weight gain for age apathy, withdraen behavior food intake record – causes no fear of strangers high calorie formulas ( 24kcal/oz) inadequate caloric intake avoidance of eye contact assess weight, head circumference, length/height inadequate absorption “radar gaze” educate parents increased metabolism stiff or flaccid fruit juice restricted until adequate weight gain defective utilization minimal smiling achieved – poverty greatest risk factor Obesity Phenylketonuria – BMI most accurate for screening (> 95th percentile) – inborn error of metabolism as an autosomal trait – influencing factors – deficiency of hepatic enzyme phenylalanine hydroxylases, converts phenylalanine to tyrosine community – screening required by law, done shortly after first feeding: Guthrie blood test institutional physical inactivity (screen time) – phenylalanine accumulates in the blood, disrupts cellular process of myelination & protein synthesis causes psychologic irreversible brain damage and severe intellectual ability – best management is preventative – symptoms – diet, behavior modification growth failure musty odor to urine – pharm. agents (orlistat) freq. vomiting microcephaly irritability – excellent prognosis w/ low – phenylalanine diet Galactosemia Celiac Disease – deficiency of liver enzyme that converts galactose to – autoimmune disorder triggered by ingestion of gluten r/t villous atrophy in small intestine glucose, metabolites collects in body and damages organs – symptoms appear when gluten introduced between 1-5 yrs. – if dx not made at birth, death w/in 1 mo. w/o tx impaired fat absorption behavioral changes – early signs: poor sucking, poor weight gain, vomiting, impaired nutrient absorption celiac crisis diarrhea – diagnosis – late signs: ascites, sepsis, lethargy, seizures, coma serologic blood test for tissue transglutaminase & antiendomysial antibodies  if positive, f/u w/ upper GI endoscopy w/ biopsy – newborn screening – treatment – lactose and galactose free diet for life total exclusion of gluten soy protein formula supplementation must learn how to avoid meds. w/ lactose fillers symptoms may take weeks to improve read food labels intestinal villi take 6 mo. to recover Food Allergy Food Reactions – adverse immunologic reaction to food – food intolerance – peanuts most common followed by milk then shellfish not IgE-mediated sweating indigestion rhinitis – diagnostics: double-blind placebo-controlled food challenged, skin prick test, flatulence serum IgE – food allergy – avoid foods causing allergies IgE-mediated anaphylaxis – prevention includes rapid onset swelling of lips, mouth, uvula exclusive breastfeeding until 4-6 mo. introduce high-allergy food soon after low-allergy foods Enteral Therapy Total Parenteral Nutrition – reasons – intravenous nutritional support weakness of throat and mouth – requires a central venous catheter and IV tubing w/ filter neoplasm – reasons immune dysfunction congenital malformation of GI tract acute states of recovery brain injury – nasogastric tube, gastric or jejunal tube severe burns bone marrow transplant pts. sepsis Diarrhea – acute: < 14 days, often caused by infectious agent in GI tract such as Rota virus – Management – chronic: > 14 days, often caused by chronic conditions such as IBD oral rehydration therapy or IV rehydration avoid sugary and caffeinated drinks – host pathogens spread via contaminated food/water or person to person early reintroduction of a normal diet – risk factors teach caregivers to monitor for signs of dehydration lack of clean water skin care of diaper region poor hygiene no rectal temperatures  nutritional deficiency freq. hand washing and washing of soiled linens/clothes poor sanitation – Rotavirus: incubation period of 48 hrs. manifestations  fever  vomiting followed by onset of watery stools  watery stools persist for 5-7 days Constipation Encopresis – alteration in freq., consistency, or ease of passing stool – abnormal elimination pattern characterized by recurrent soiling or passage of stool – < 3 stools/wk for children > 4 yrs. at inappropriate times – can be functional or r/t organic cause – retention of stool in lower bowel and rectum, dilation of lower bowel, incompetence of inner sphincter – infants: transition from breast milk to cow’s milk – loose stool can leak around hard stool – children: r/t environmental. changes or normal development – may lose urge to defecate, develop incontinence – management increase fluids – bowel training increase physical activity bowel training increase high-fiber foods medications  glycerin suppository  polyethylene glycol (PEG)  docusate  lactulose disimpaction Vomiting – common, self-limiting – green bilious vomiting > bowel obstruction – identify and treat cause, prevent complications – oral rehydration or IV therapy – anti- emetic (ondansetron) – gradual return to regular dier – monitor for electrolyte imbalances – rinse mouth or brush teeth after vomiting Hirschsprung Disease – congenital absence of ganglion cells in wall of a segment of rectum and colon, prevents – diagnosis peristalsis, inadequate motility causes obstruction in the intestine hx abdominal xray showing – accounts for ¼ of all neonatal intestinal obstructions rectal biopsy for ganglion cells distend bowel, dilated contrast edema bowel loops – more common in males – repair – clinical manifestations remove aganglionic portion may need to treat enterocolitis bilious vomiting may require colostomy failure to pass meconium w/in first 24-48 hrs. after birth failure to thrive – management abdominal distension foster infant-parent bonding constipation low fiber, high calorie, high-protein diet ribbonlike, foul-smelling stools bowel preparation pre-op; saline enemas measure abdominal circumference  can leave paper tape under patient to reduce stress monitor for return of GI function Gastroesophageal Reflux – GER: transfer of gastric contents into the esophagus – management – GERD: symptoms or tissue damage that results from GER no therapy for thriving infant w/ no respiratory complications avoidance of foods that exacerbate reflux – peak incidence at 4 mo. thickened feeds, upright positioning – resolves spontaneously for most infants by 1 yr.  enlarged nipple opening – inappropriate relaxation of lower esophageal sphincter H2- receptor antagonists or PPIs – manifestations fundoplication for those w/ severe complications spitting up, regurgitation, recurrent vomiting excessive crying, irritability, arching of back, stiffening poor weight gain feeding refusal respiratory problems Colic – abdominal pain/cramping manifested by loud crying and drawing legs up to abdomen – management – symptoms worse in late afternoon/evening rule out organic causes assess feeding process as demonstrated by parent – self-limiting, usually resolves by 12-16 wks. antispasmodics, antihistamines, antiflatulents – potential causes reassure parents they are not to blame for infants discomfort feeding too rapidly improper feeding technique disappears spontaneously by 3-4 mo., by can last longer overfeeding emotional stress/tension between at risk for shaken baby syndrome swallowing excessive air parent/infant Appendicitis – inflammation of appendix – diagnostics – management – most common cause of emergency abdominal surgery in childhood NPO status immediately antibiotics preop w/ IV fluids start IV and draw labs maintain NPO status – peak incidence at 12-18 yrs.  elevated WBC no laxatives or enemas – perforation occurs in up to 82% of children < 5 yrs.  elevated neutrophils monitor for bowel function post-op likely d/t inability to verbalize symptoms  elevated CRP scheduled analgesics – cause is obstruction of appendiceal lumen  electrolytes if appendix ruptured: RLQ pain McBurney pt.: 2/3 distance along imaging  IV antibiotics and fluid fever line between umbilicus and  appendix ultrasound  NGT to suction vomiting (following pain anterosuperior iliac spine  CT w/ contrast  drain may be present post op onset) symptom relief – perforation > peritonitis  morphine and ondansetron – sudden relief of pain usually means appendix has perforated right-side lying position Meckel’s Diverticulum – omphalomesenteric duct fails to atrophy, leaving outpouching of ileum near the ileocecal valve pouch contains gastric contents, causing ulceration clinical manifestations appear by age 2 GI bleeding, obstruction, bloody stool, irritability, fatigue, abdominal pain/distention, N/V – most common GI malformation – diagnosis made by labs and imaging Meckel scan imaging test of choice – treatment is surgical removal of diverticulum and involved bowel Pyloric Stenosis – etiology unknown, various associations – manifestations – diagnostics – hypertrophy of the circular pylorus muscle projectile vomiting and visible peristalsis ultrasound to determine diameter  non-bilious, possibly blood tinged blood tests to measure dehydration, electrolytes – stenosis occurs between stomach and hungry, irritable, few stools NPO immediately, start IV fluids duodenum dehydrated NGT if vomiting continues – can occur as young as 1 wk. and as late as 5 metabolic alkalosis intake and output mo. peristaltic waves may be observed fixed by laparoscopic pyloromyotomy olive-sized mass in RUQ  good prognosis, discharged w/in 24 hrs. after advanced diet – management IV fluid rehydration, NPO NGT for gastric decompression if vomiting still present clear liquids resumed in small increments 4-6 hrs post op formula 24 hrs. postop post op vomiting normal for first 24-48 hrs. scheduled analgesics monitor operative site for infection Intussusception – portion of intestine prolapses & invaginates (telescopes) into another – diagnosis and tx – more common in males and those 3 mo. to 6 yrs. ultrasound pneumoenema (gas enema) or ultrasound- guided hydrostatic enema to – 65% occur before 1 yr. reduce – generally idiopathic surgery if unsuccessful – ileocecal valve most common site – may need NG tube for gastric decompression – can lead to edema, necrosis, perforation, sepsis – maintain NPO – manifestations – passage of normal brown stool indicates spontaneous reduction abrupt onset abdominal pain screaming w/ drawing knees to chest during episodes of pain bilious vomiting intermittent periods of comfort palpable abdominal mass (sausage-shaped) stools become red and resemble currant jelly due to mix of blood and mucus Volvulus – twisting of the intestine which may disrupt blood flow – often associated w/ congenital malrotation, which occurs in 1 of 500 births – manifestations bilious vomiting bloody stools distended, firm abdomen dehydration irritability – emergency surgery required to prevent necrosis, or to remove necrotic tissue to prevent further necrosis possible short bowel syndrome and ostomy placement after operation Necrotizing Enterocolitis – inflammatory disease caused by ischemia or hypoxemia producing vascular compromise – diagnostics of bowel mucosa and necrotic patches that interfere w/ digestion diagnosed by abdominal XR – most common in premature infants  sausage shaped dilation of intestine  characteristic “soapsuds” appearance of intestinal wall d/t air inflation – symptoms usually start 2nd wk. of life management distended (often shiny) abdomen, bloody stools, gastric retention, localized abdominal  d/c oral feedings > TPN wall erythema, bilious test  NGT suction – if untreated, progresses to sepsis  IV antibiotics  surgical resection Biliary Atresia – unknown etiology – diagnosis – extrahepatic bile duct fails to develop or are closed, leading to cholestasis, cirrhosis, portal history, physical exam hypertension, end-stage liver disease, and eventually death if not treated by 3 yrs. labs  bilirubin, CBC, liver function tests – leading reason for liver transplant in children percutaneous liver biopsy suggesting biliary atresia – newborn initially asymptomatic exploratory and intraoperative cholangiography to confirm diagnosis – bile blockage causes inflammation in the liver, lack of bile in duodenum interferes w/ – treatment digestion of fat-soluble vitamins surgery to correct obstruction, Kasai procedure – manifestations  many still need liver transplant eventually starts = 2-3 wks. after birth IV antibiotics and 1-2 yrs. of PO antibiotics to prevent cholangitis jaundice persisting > 2 wks of age supplementation of vitamins ADEK, IM vitamin K prior to invasive procedures dark urine breastfed or given special formula gray stools enteral feedings hepatomegaly Cleft Lip and Palate – maxillary process fails to fuse properly – apparent from birth – union of upper lip completed by week 7 gestation, secondary palate fusion at 5-12 wks. – cleft lip repair at 2-3 mo. gestation, hard and soft palates completed by 1 st trimester. – cleft palate repair before 12 mo. – folate intake may help prevention protects formation of tooth buds allows more normal speech pattern development – soft elbow restraints used postop to protect incision – may affect feeding, may need longer nipples w/ enlarged holes Esophageal Atresia and Tracheoesophageal Fistula – failure if esophagus to develop as a continuous passage – diagnosis – failure of trachea and esophagus to separate into distinct structures may be detected in utero through prenatal ultrasound tube inserted into esophagus to check for resistance – can occur separately or in combination  if resistance met, CXR or abdomen XR to confirm – manifestations may need hospitalization and G-tube until repair excessive salivation and drooling  primary: connect two ends of esophagus and ligate fistula frothy saliva  delayed primary: G-tube placed, fistula ligated, esophagus ends classic signs connected once length adequate  cyanosis  choking  coughing fluid returns through infant’s nose and mouth during feeding