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1

formula intolerance

  • Signs of formula intolerance:

    • Diarrhea, vomiting

    • Blood or mucus in stool

    • Pulls legs up towards abdomen in pain

    • Difficulty gaining weight

    • Switching formulas should stop issues

  • Milk protein allergy: can cause vomiting, blood in stools, hives, irritability, wheezing, cough, congestion, reflux

    • Must use hydrolyzed formulas

    • Can do stool sample to test

    • If breastfeeding, mother must avoid all milk products & soy

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gastroesophageal reflex

  • Occurs when gastric contents reflux back up into esophagus, making esophageal mucosa vulnerable to injury from gastric acid

    • Smaller stomach, shorter esophagus, and immature esophageal sphincter muscle = contributes to increased symptoms in infants

  • GERD = tissue damage from GER

  • Risk factors: prematurity, neurological impairments, asthma, Cystic Fibrosis, cerebral palsy

  • Peak incidence occurs at 4 months old

    • About 40% of infants experience GER

  • Must differentiate between GERD / GER

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GER expected findings

  • Infants: spitting up or forceful vomiting, irritability, excessive crying, blood in vomit, arching of back, stiffening – colicky baby

    • Failure to thrive

    • Apnea (ALTE/BRUE) or other Respiratory problems (choking with feedings, cough)

  • Children: heartburn, abdominal pain, difficulty swallowing, chronic cough, noncardiac chest pain

  • If inflammation left untreated, scarring and strictures may form

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GER management

  • None: if gaining weight & happy

  • Nursing Care:

    • Small, frequent meals

    • Avoidance of foods that worsen reflux

    • Elevate head after meals

  • Avoid foods that worsen reflux: caffeine, citrus, peppermint, spicy or fried foods

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GER meds

  • PPI: omeprazole (Prilosec), lansoprazole (prevacid)

    • Most effective when given 30 mins before breakfast

    • Need to take for several days before improvement

  • H2 receptor antagonists (cimetidine, ranitidine (zantact), famotidine (Pepcid)

    • Helps to reduce gastric secretions, may stimulate some increase in esophageal sphincter tone

  • Thickened feedings (usually rice cereal or oat cereal)

  • Feeding tubes: if unable to gain weight

  • If aspiration risk: will need duodenal or jejunal feeding tube (G or J tube) or surgery (Nissen Fundoplication)

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GER Nissen Fundoplication

  • Operation done to tighten the outlet of the esophagus as it empties into the stomach

  • Wraps fundus of stomach around the distal esophagus

  • Necessary for children who have complications related to aspiration or for those who have persistent symptoms that are not relieved by medication

  • Appropriate for patients with loss of tone over time

  • With or without G-tube

  • Diet after surgery should start slow with clears, then soft foods

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NG tube or OG

cannot support self short term

preterm and unable to expend energy

status post heart surg

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gastric tube

surgical placed

  • long term nutritional support

  • need for continuous feedings

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nutrition

enteral feedings are preferred

parenteral only used if bowel is not an option

  • requires central line

  • caustic to liver over time

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acute gastroenteritis

An inflammation of the stomach and intestines

Most common causes: viruses, bacteria (food poisoning), and intestinal parasites

  • Viruses: usually cause of mild gastro; Norwalk-like virus (norovirus), adenoviruses, enterovirus and rotaviruses

  • Bacteria: usually produce high fevers, severe GI symptoms, and dehydration; campylobacter, salmonella, E. Coli (sicker, more severe), watch out for dehydration

  • Parasites: Giardia lamblia

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acute gastroenteritis signs

  • vomiting

  • diarrhea

  • generalized abdominal pain

  • fever

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acute gastroenteritis education

  • Decrease spread (make sure to wash hands, especially after diaper changes wash toys)

  • Maintain hydration, small amounts more frequently

  • Watch for signs of dehydration

  • Treatment depends on cause

    • Virus: self-limiting,, comfort care

    • Bacteria: antibiotic depending on cause

    • Parasite: Giardia treat with metronidazole (Flagyl)

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dehydration levels

  • Mild: behavior, mucous membranes, anterior fontanel, pulse, and blood pressure within expected findings

    • Possible slight thirst

  • Moderate: pulse slightly increased, dry mucous membranes, decreased tears, normal to sunken anterior fontanel on infants

    • Cap refill 2-4 seconds

    • Possible thirst and irritability

  • Severe: tachycardia present, orthostatic blood pressure can progress to shock, dry mucous membranes, no tearing, sunken eyeballs, sunken anterior fontanel

    • Cap refill > 4 seconds

    • Oliguria or anuria

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dehydration nursing actions

  • Oral rehydration FIRST for mild-moderate dehydration

  • If unable to drink enough to correct fluid losses, will need IV

  • Assess cap refill, monitor vital signs, monitor weight, maintain accurate I&O

  • start with pedialyte for young children and gatorade in older children

  • give 10-15 mLs every 15 minutes

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pyloric stenosis

  • Pyloric sphincter= ring of smooth muscle between the stomach and the duodenum

  • Thickened pyloric sphincter creates narrowing & obstruction

  • As stomach continues to try to push food through, peristalsis becomes so powerful that food is ejected into the esophagus and out of the mouth = projectile vomiting

  • More common in first born males

  • Most common at age 3 weeks

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pyloric stenosis signs

  • Failed formula changes

  • Projectile vomiting

  • Dehydrated

  • Constant hunger

  • Fluid electrolyte imbalance

  • Risk for metabolic alkalosis

  • On exam, olive shaped mass in RUQ

  • constant hunger because milk is not making its  way through

  • hyperkalemia

  • metabolic alkalosis because of all the vomiting

  • pyloric sphincter is so hard

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pyloric stenosis management

  • Need an ultrasound to confirm

  • Need to correct fluid and electrolyte imbalance

    • *at risk for hypokalemia & metabolic alkalosis*

  • Need surgery

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pyloric stenosis nursing considerations

  • Need fluid support prior to surgery

  • NPO prior to surgery

    • 4-6 hours postop can start clear liquids like pedialyte

    • 24 hours can go to formula or breastmilk

  • Pain management

  • Slow feeding protocol after surgery

  • Anticipatory guidance about setbacks

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Hirschsprung’s Disease

Aka Congenital aganglionic megacolon

  • Stools have ribbon pattern

  • Congenital condition in which the nerve cells of the myenteric plexus are absent in the distal bowel & rectum

    • Is a sustained sympathetic stimulation (cannot relax)

    • Decreased enteric nerve stimulation (loses motility)

    • Results in decreased motility & mechanical obstruction

    • Rectal internal sphincter cannot relax

    • Absence of parasympathetic ganglion cells in end of large intestine near rectum

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Hirschsprung’s Disease diagnosis

  • rectal biopsy to confirm absence of ganglion cells

  • X-ray: with contrast, will see dilated portions of colon

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Hirschsprung’s Disease risk factors

male gender, genetics, trisomy 21

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Hirschsprung’s Infant presentation

  • will not pass meconium

  • will see vomiting

  • can either be bile stained or of fecal material

  • will see abdominal distension, constipation

  • anorexia and poor feeding

  • may see temporary relief with enema

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Hirschsprung’s Older Children presentation

  • History of constipation since birth

  • Distension of abdomen

  • Thin abdominal wall with observable peristaltic movement

  • Stool appears ribbon like, fluid like, or in pellet form

  • Failure to grow; will see loss of subcutaneous fat

    • Child may appear malnourished or have stunted growth

    • Anemia

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Hirschsprung (SARCASM)

  • Sigmoid colon

  • Absence of movement

  • Ribbon shaped stool & Rectal biopsy for diagnosis

  • Congenital / will see constipation

  • Abdominal obstruction / abnormal feeding

  • Syndrome (common in those with Down Syndrome)

  • Meconium (infant will not pass in first 24 hours)

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Hirschsprung management

  • Surgery to remove aganglionic bowel

  • “pull through” normal section pulled through colon and attached to anus

  • If very ill, surgery will be done in two steps; will have temporary ostomy while gut heals

  • High protein, high calorie, low fiber diet

  • May need TPN in some cases

  • Monitor for signs of enterocolitis

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Hirschsprung compl.

  • Hirschsprung’s associated enterocolitis = inflammation and obstruction of intestines

  • Occurs in about 20% of neonates with Hirschsprung

  • Perforation of obstructed bowel

Presenting symptoms:

  • Foul smelling diarrhea either with or without blood

  • Fevers

  • Abdominal distension

  • Lethargy

  • Poor feeding

LIFE THREATENING – can lead to toxic megacolon and perforation of bowel

  • Can lead to sepsis if not treated urgently

  • Need antibiotics, fluid resuscitation, and decompression of obstructed bowel

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Intussusception

  • Telescoping of bowel on itself

  • Results in lymphatic and venous obstruction leading to edema

    • With progression/ no treatment, ischemia and increased mucus into \n intestine will occur

  • Most common in those 3 months to 6 years

    • More concerning if patient older

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Intussusception signs

  • Sudden, excruciating pain (drawing knees up to chest)

  • Currant jelly stools

  • Palpable abdominal mass (sausage shaped)

  • May see vomiting, fever, distended abdomen

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Intussusception treatment

  • Air enema

  • surgery

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The extreme: Short Bowel Syndrome

  • Aka “short gut”

  • Loss of so much bowel, can’t be nourished enterally

    • NEC

    • Intussusception

    • Hirschsprung

    • Gastroschisis

  • Will be TPN dependent

    • Will need central line

    • Liver burden

    • Failure to Thrive

  • Often have severe diarrhea due to accelerated intestinal transit, gastric acid hypersecretion, intestinal bacterial overgrowth, malabsorption of fats

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Short Bowel Syndrome signs/compl.

  • Watch for signs of dehydration & electrolyte imbalances

    • May see diarrhea, greasy, foul-smelling stools

    • Fatigue

    • Weight loss

    • Malnutrition (can’t absorb everything because it moves through GI tract so rapidly)

  • Must monitor intake & output and weight

  • Complications:

    • Central line infections & sepsis

    • Chronic renal failure

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Biliary Atresia

Complete or partial obstruction of the bile ducts inside or outside the liver

Congenital condition, ducts do not develop normally

  • Bile flow from liver to gallbladder is blocked → liver damage → cirrhosis of liver

    • Bile can’t flow so it backs up into the liver

  • Early diagnosis = key to prevent or slow liver damage

    • Will see increased AST, ALT, bili

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Biliary Atresia diag./treatment

  • scan (hepatobiliary iminodiacetic acid scan) to see if bile ducts / gallbladder are working properly; liver biopsy

  • Kasai procedure = only effective treatment

    • Removes biliary tree and adds new to drain bile

  • Hidascan to see flow of bili

  • Need liver transplant

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Biliary Atresia signs

Initially asymptomatic, then start with jaundice; as bili continues to rise will se distension and hepatomegaly

  • jaundice at 3-4 weeks

  • Distended abdomen

  • Dark urine (due to increased bili)

  • Pale or clay colored stools (due to bile pigments)

  • Slow or no weight gain

  • Bruising, bleeding, intense itching as it progresses

  • Failure to thrive is common

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constipation

A SYMPTOM NOT A DISEASE

A decrease in bowel movement frequency or increase in stool hardness for at least 2 weeks

Often associated with painful bowel movements, blood streaked or retained stool, abdominal pain, lack of appetite or stool incontinence

  • Trouble for more than 2 weeks

  • A triangle of frequency, consistency, ease

  • Frequency alone is not criterion

  • can be in kids just starting school because they don’t want to go or are scared to go

  • can lead to encopresis: leakage of stool around hard stool

*need to evaluate condition further if patient develops vomiting, abdominal distension, pain or evidence of growth failure; need to make sure there is nothing else going on

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cause of constipation

  • Structural causes:

    • hirschsprung's or other strictures

  • Systemic causes:

    • hypothyroidism, chronic lead poisoning,

    • can be side effect of medications: antiepileptic, opioids, iron

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constipation treatment

  • Need to both restore normal bowel function & stooling pattern

  • First line: miralax

    • Osmotic laxative – draws water into stool

    • Usually takes 1-2 days for effect

    • Can cause incontinence, abdominal pain, nausea, bloating

  • Can also use:

    • Docusate sodium (senna): stimulant – acts as a local irritant in the colon, stimulating peristalsis

      • Can cause diaper rash, do not use in those <1 year old

    • Magnesium hydroxide: laxative – causes osmotic gradient leading to laxative effect (aggressive)

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diarrhea

  • Abnormal transport of fluid and electrolytes across intestinal mucosa

  • A sudden increase in frequency and change in consistency of stool

  • Major cause of illness under age 5

  • Can be mild to severe, acute or chronic

  • Chronic if more than 14 days

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causes of diarrhea

  • Viral, bacterial, parasitic

  • Associated with other infections such as URI, UTI

  • Dietary

  • Medicine-related

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viral diarrhea

  • Most common cause of diarrhea in children <5 y/o

  • Fever

  • Onset of watery stools

  • Diarrhea for 5-7 days, vomiting for about 2 days

  • Transmission = fecal oral

  • Example: Rotavirus

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parasitic diarrhea

Enterobius Vermicularis

  • Perianal itching, sleeplessness, restless

  • Ingested or inhaled eggs hatch in upper intestines and mature then migrate out of intestine & lay eggs

Giardia lamblia

  • Children < 5 = Diarrhea, vomiting, anorexia

  • Older children: abdominal cramps, malodorous, pale, greasy stools

  • Transmitted person to person, food or animals

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bacterial diarrhea

  • Length of symptoms depends on source

  • Can be transmitted through undercooked meats, person to person, from pets, contaminated water

  • Examples: Yersinia, e. coli, salmonella, clostridium difficile, clostridium botulinum, shigella, norovirus, staph

  • More severe, higher fevers, worse symptoms

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nursing care for diarrhea

  • Obtain child’s weight at same time each day

  • Avoid rectal temps

  • Initiate IV fluids as ordered if needed

  • Administer antibiotics as prescribed (for Shigella, C. Diff, G. lamblia)

  • Avoid antibiotics with Salmonella and E. Coli

  • Avoid antimotility agents with E. Coli, Salmonella, Shigella

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diarrhea education

  • Child should stay home from school/ daycare during incubation period

  • Diet changes needed

    • Avoid fruit juices, stick to BRAT diet

  • Frequent skin care to avoid skin breakdown

  • Avoid antimotility agents because we want them to poop it out

  • To prevent spread of infection:

    • Clean toys and child care areas thoroughly

    • Hand hygiene after toileting and after changing diapers

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appendicitis

  • Inflammation of the vermiform appendix caused from an obstruction of the lumen of the appendix

    • Causes of obstruction: fecalith, stenosis, parasitic infection, tumor

    • Mucus continues to be secreted and bacteria grows causing increased pressure

      • impaired perfusion

  • Average age of presentation=10 years old

  • If untreated, can become gangrenous & ruptures

    • Rupture can occur within first 48 hours of complaint

    • More likely to rupture in younger children when not suspected

    • Can lead to sepsis and shock

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appendicitis signs

  • Vague midline pain that moves to RLQ and intensifies

  • Vomiting, diarrhea

  • Fevers

  • anorexia

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appendicitis exam findings

  • Rebound tenderness

  • Rigid abdomen

  • Guarding

  • Rovsing: palpation on the left lower quadrant of the abdomen results in pain in the right lower quadrant (at McBurney’s point)

  • Obturator: pain during internal rotation of right hip

  • Psoas:  pain at extension of right hip

  • Enemas, heat packs, and laxatives can’t be given

  • Morphine, toradol, antibiotics: most common treatment/plan

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appendicitis diag.

  • Labs:

    • Electrolytes

    • Increased WBC

    • Urine

  • Imaging:

    • US versus CT

      • ultrasound first to avoid CT

      • can look for swelling

      • cannot be officially diagnosed without CT

  • Shift to left: increase in WBC

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Nursing care pre and post appendectomy

Pre Appy

  • Monitor for signs of sepsis including increased heart rate and respiratory rate, fever, decreased bp

  • Watch for sudden relief of pain

  • Pain relief

  • Promote comfort

  • Administer antibiotics

  • NPO

Post Appy

  • Pain management

  • Semi-fowlers

  • Wound care (can either be laparoscopic or open)

  • NG tube for decompression

  • IV antibiotics

  • Prevention of complications

  • Wound infection

  • Line infection

  • UTI

  • Abscess

  • Pneumonia

  • Get up first day to get everything moving

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Appendectomy complication

peritonitis (inflammation in the peritoneal cavity)

Signs:

  • fever

  • sudden relief of pain after perforation followed by diffuse increase in pain

  • irritability

  • rigid abdomen

  • pallor

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Failure to thrive

Weight for age that is less than the 5th percentile on multiple occasions or weight deceleration

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failure to thrive clinical manifestations

  • Poor weight gain

  • Vomiting, food refusal, food fixation

  • Irritability

  • Nonorganic causes: food restriction, food rituals, poor appetite

  • organic causes: vomiting, diarrhea

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failure to thrive diag.

  • Height, weight, BMI

  • Feeding assessment (quality of food, ability to chew / swallow, 24 hour diet recall)

  • BMP, vit d, lead, zinc, iron

  • Albumin (with severe FTT)

  • CBC, ESR, electrolytes

  • Stool studies

  • Sweat chloride test

  • TSH

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celiac disease

  • Gluten sensitive enteropathy

  • An autoimmune reaction to gluten that leads to intestinal inflammation, atrophy, and malabsorption

  • Gluten= protein found in wheat, rye, barley

  • Chronic, irreversible disease

  • In early onset, fat absorption is impaired, leading to excretion of large amounts of fat in the stool

  • As it progresses, there is a malabsorption of proteins, carbs, and fat-soluble vitamins

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celiac disease diag.

  • transglutaminase IgA – if positive a biopsy of small intestine is done to evaluate intestinal mucosa damage

    • Should also get CBC, ferritin levels, iron levels – at risk for iron deficiency anemia

  • official diagnosis: get piece of intestine via colonoscopy

  • can do bloodwork to see if colonoscopy is necessary - but very expensive

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celiac disease assessment findings

  • Weight loss

  • Diarrhea

  • Vomiting

  • Foul-smelling stools

  • Delayed growth and development

  • Can get dermatitis herpetiformis (blistering, pruritic skin rash on elbows, knees, buttocks

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celiac disease severe form

  • Iron deficiency anemia

  • Vit b 12 deficiency

  • Osteopenia / osteoporosis r/t calcium malabsorption

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defects of GU

  • Hypospadias

  • Epispadias

  • Cryptorchidism

  • Phimosis

  • Testicular torsion

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hypospadias

  • birth defect

  • urethral opening located on the underside rather than tip of penis

  • Several degrees

  • If not treated can lead to problems later in life

    • Usually need surgical correction to restore proper flow

    • Avoid circumcision, because foreskin is used for surgical

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epispadias

  • rare birth defect at the opening of the urethra; the urethra

  • does not develop into full tube & the urine exits body from abnormal location

  • Male: widened pubic symphysis; urethra opening on the dorsal surface

  • Female: wide urethra

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cryptorchidism

one or both of the tests fail to descend from the abdomen into the scrotum

  • Cause of this is unknown

  • Undescended testicles that are left untreated can be a later cause of infertility

  • higher risk of testicular cancer, testicular torsion, and developing hernias

  • Testes should drop by 3-9 months of age; if they do not surgery will be done at about 12 months of age (orchiopexy)

  • Need to make sure patient still having good urine output

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Phimosis

foreskin is too tight to be pulled back over the head of thepenis

  • can be normal in babies and toddlers

  • older children it can be result of a skin condition that has caused scarring

  • redness, irritation, dysuria, or bleeding, would need further testing to determine cause

  • Treatment not needed in younger children who do not have complications or signs of infection

  • Immediate treatment will be needed in cases where it causes issues

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Testicular torsion

Occurs when a testicle rotates, twisting the spermatic cord that brings blood to the scrotum

  • Most common between ages 12-18

  • Presentation: most common = sudden, severe pain on one side of scrotum

    • Later, can be swelling and erythema

    • May have nausea / vomiting

  • No specific cause that precedes testicular torsion, found that sometimes an injury to the area has been associated with torsion

  • Considered a medical emergency

Treatment

  • immediate surgery needed, if blood not restored within 6 hours, may need to remove testicle

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GU lab numbers

Urine consists of what our body “doesn’t need”

  • Expected urinary output = 1ml/kg/hrr

  • Normal creatinine: 0.6 – 1.2 mg/dL

    • If increased = decreased function of kidney

  • BUN: normal 6- 20 mg/dL

    • Measures the urea (which is breakdown of protein in the liver)

    • If kidneys not working properly, will not be able to remove urea, so will see increased BUN

  • GFR: rate of blood flow through the kidneys

    • Tells us how well the glomerulus is filtering

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Vesico-ureteral reflux

  • Condition in which urine flows backward from the bladder to one or both ureters & sometimes the kidneys

  • Most common in infants or young children

  • Graded 1-5

  • May not have sx, may have UTI

  • Child more likely to have other problems such as urinary

    • incontinence, bedwetting, urinary retention

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causes of vesico-ureteral reflux

  • Primary: born with abnormal ureter

    • Valve between ureter and bladder does not close well

  • Secondary: may have blockage or narrowing in bladder neck or urethra

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Vesico-ureteral reflux imaging

  • Ultrasound

  • Voiding cystourethrogram

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acute glomerulonephritis

  • inflammation of glomeruli, which is part of the nephron that is vital infiltration

  • Usually glomerulus is not permeable to RBCs or protein, but with acute

  • glomerulonephritis it will leak RBC & protein

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cause of acute glomerulonephritis

  • Post strep infection; usually occurs about 14 days after infection of skin or throat

  • Common in ages 2-10 years old

  • Immune system creates antigen-antibody complexes to help fight bacteria can collect in glomeruli and cause congestion & inflammation which leads to leakage of RBCs & protein

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acute glomerulonephritis signs

  • Cloudy, tea-colored urine

  • Decreased urine output

  • Hematuria, proteinuria

  • Irritability

  • Ill appearance

  • Lethargy

  • Periorbital edema

  • Facial edema worse in the morning, then spreads to extremities and abdomen throughout the day

  • Low grade fever

  • Mild – severe hypertension

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acute glomerulonephritis HAD STREP

H – hypertension

A – ASO = anti-streptolysin titer +

D – Decreased GFR = low urinary output

S – Swelling in face, legs, edema mild, worse in morning

T – Tea colored urine

R – Recent strep infection

E – Elevated BUN & creatinine

P – Proteinuria

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acute glomerulonephritis lab

  • Urinalysis

    • Will have RBCs & proteinuria

    • Tea colored urine

  • Renal function tests

    • Increased BUN & creatinine

    • Decreased GFR

  • antistreptolysin O titier

  • CMP:

    • Potassium:

    • Sodium:

  • Throat culture

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acute glomerulonephritis nursing care

  • Those with normal bp can be managed at home

  • Need to monitor bp

  • Administer diuretics and antihypertensives

  • as needed *need to make sure renal status

  • is sufficient first

  • Monitor fluid status: need to watch their intake and output

  • Monitor electrolytes

  • Limit sodium

  • Limit fluid restriction

  • May need to limit potassium if they have decreased urinary output

  • Relapse not as common, but need to monitor for future strep infections

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nephrotic syndrome

Alterations in the glomerular membrane allows proteins (especially albumin) to pass into the urine, resulting in decreased blood osmotic pressure – this can then lead to proteinuria, hyperlipidemia, and edema

  • Main type of protein lost = albumin

    • Can also lose proteins such as immunoglobulins & proteins that help decrease clot formation

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nephrotic syndrome types

Primary: aka minimal change disease

  • Cause is unknown, but it can have several causes such as metabolic, biochemical or a physiochemical disturbance in the membrane of the glomeruli

  • Most common in ages 2-5 years old

  • Will do biopsy and see changes under electron microscope

Secondary: occurs after or is associated with glomeruli damage due to a known cause such as from lupus, diabetes, heart failure

Congenital: an inherited disorder

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nephrotic syndrome signs

  • weight gain over period of days / weeks

  • Periorbital and facial edema – decreases throughout the day

  • Ascites

  • Edema to lower extremities and genitalia

  • Muehrcke lines

  • Decreased urine output

  • Foamy, frothy, dark yellow urine

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nephrotic syndrome lab tests

  • 24 hour urine – up to >3 g of protein per day

  • Bloodwork:

    • Albumin:

    • Hgb, hct, platelets:

    • GFR:

    • Calcium:

    • Sodium:

    • hyperlipidemia

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nephrotic syndrome diag.

Kidney biopsy

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nephrotic syndrome nursing care

  • Monitor fluid status and swelling

    • Administer albumin & steroids to help decrease swelling

  • Watch for signs of infection, especially at edematous areas

  • Assess for signs of blood clots such as DVTs or Pes

  • Diet: limit sodium, fluids, fats

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nephrotic syndrome meds

corticosteroids: prednisone

  • high dose for 4-6 wk followed by lower dose q other day for 2-5 mon with taper, administer with meals

diuretic: furosemide

  • decrease excess fluid

  • encourage foods high in potassium

plasma expanders: albumin 25%

  • helps to increase plasma volume and decrease edema

immunosuppressants: cyclophosphamide

  • administered if not tolerate prednisone

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Hemolytic Uremic Syndrome

acute disease, caused by breakdown of RBCs that clog kidneys

  • One of the main causes of acute renal failure in early childhood

  • characterized by acute renal failure, hemolytic anemia (breakdown of RBCs), and thrombocytopenia (low platelets)

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Hemolytic Uremic Syndrome risk factors

Peak incidence 6 months – 4 years old

Diarrhea (+) HUS

  • 90% of cases

  • caused by ingestion of shiga toxin producing E. Coli

Diarrhea (-) HUS

  • can be due to non-enteric infections or disturbances in the complement system, malignancies, or genetic disorders

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Hemolytic Uremic Syndrome expected findings

  • Occurs after prodromal period of diarrhea and vomiting

  • Loss of appetite

  • Lethargy

  • Hallucinations

  • Pallor

  • Bruising, purpura, or rectal bleeding

  • Anuric and hypertensive in severe form

  • Urinary output can be reduced or increased

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Hemolytic Uremic Syndrome lab tests

  • CBC

  • Reticulocyte count

  • Urine

  • BUN and creatinine

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Hemolytic Uremic Syndrome nursing care

  • Monitor intake and output

  • Daily weights

  • Treat hypertension as needed

  • Monitor CNS for seizure activity and stupor

  • Seizure precautions as needed

  • Blood transfusion with packed RBCs for severe anemia

  • For child who is anuric for 24 hours or having oliguria with uremia or hypertension and seizures, may need hemodialysis, peritoneal dialysis, or continuous hemofiltration

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Hemolytic Uremic Syndrome education

  • Avoid undercooked meat, especially ground beef

  • Avoid unpasteurized apple juice and unwashed raw vegetables

  • Avoid public pools

  • Do NOT use antimotility agents for diarrhea

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Hemolytic Uremic Syndrome management

Support with antihypertensives, blood transfusions if needed, hemodialysis

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Acute Renal Failure

  • Sudden decrease in renal function

  • Kidneys no longer able to excrete waste material, concentrate urine, and conserve electrolytes as they should

  • Causes are pre-renal, intrinsic, or post-renal; most common cause is pre-renal

  • Can be reversible

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Acute Renal Failure risk factors

Pre-renal

  • dehydration secondary to diarrheal disease or persistent vomiting

  • surgical shock and trauma

  • accidental poisoning

  • prolonged anesthesia

Intrinsic

  • damage to glomeruli

  • tubules

  • renal vasculature from disease or nephrotoxicity

Post-renal

  • obstruction of urinary system

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cause of Acute Renal Failure

pre-renal

  • before kidney

  • decreases the amount of blood going to the kidney & kidney will be deprived of nutrients

  • lead to intrarenal injury where nephrons inside the kidney become damaged

  • Cardiac issue: if damage to the heart muscle, there will be a decreased cardiac output and decreased output to kidneys

    • Ex: MI

    • massive bleeding will lead to decreased blood volume

    • Dehydration from excessive vomiting or diarrhea

    • Burns that deplete system of fluids

Intrinsic/ intra-renal

  • damage to glomeruli, tubules, or renal vasculature, so damage to kidney itself

    • decreased ability to filter the blood

    • Can be caused by infection such as glomerulonephritis

    • Can be caused by nephrotoxic drugs such as NSAIDs, antibiotics, chemo therapy, or contrast dye

    • Can be caused by injury to the kidney

post-renal

  • extend all the way to urethra

    • Prevents urine from draining out of the system à increased pressure in kidneys

    • Causes: renal calculi, enlarged prostate, neuro injury such as stroke (bladder does not empty properly)

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stages of acute renal failure

initiation

oliguric

diuresis

recovery

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Initiation

  • starts from cause to kidney and ends when the signs and symptoms start to appear

  • Can be hours to days

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Oliguric

some patients skip this stage and enter directly into diuresis stage

  • Lasts 1-2 weeks, the longer this stage the higher the risk for end stage renal disease

  • Urine output decreased because glomerulus has a decreased ability to filter blood

__Signs & symptom__s:

  • Increased BUN & creatinine, azotemia (buildup of nitrogenous products)

  • May see neuro changes, sluggish, tired, and can have itching due to built up waste

  • edema

Lab changes:

  • Hyperkalemia

  • Metabolic acidosis, pH <7.35

  • Hyponatremia

  • Increased phosphate, decreased calcium

  • Urine: concentrated, specific gravity >1.020

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diuresis

  • nephrons on their way to recovery

  • During this stage, kidneys can filter blood but cannot yet concentrate urine

  • Lasts 1-3 weeks

Signs & lab changes:

  • GFR starting to improve

  • Patient will be more alert and oriented

  • Will be voiding a lot due to osmotic diuresis

  • Risk for dehydration, hypotension

  • Hypokalemia

  • <1.020 specific gravity

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recovery

starts when GFR returns to normal

  • Urinary output= normal

  • BUN & Creatinine = stabilized

  • Can take a year or more depending on amount of damage done, and their age

  • Some patients never make it to this stage and will develop chronic kidney disease

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Expected Findings with Acute Renal Failure

  • Oliguria

  • Abrupt diuresis: with return to normal urine volumes

  • Edema

  • Drowsiness

  • Cardiac arrhythmia (from hyperkalemia- irregular, weak pulse, abdominal cramps, weakness)

  • Seizures (from hyponatremia or hypocalcemia – tetany)

  • Tachypnea (from metabolic acidosis)

  • CNS manifestations (from continued oliguria)

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Labs and Diagnostic tests with Acute Renal Failure

  • Electrolytes: hyperkalemia, hyponatremia, hypocalcemia

  • Metabolic acidosis

  • Anemia

  • Elevated BUN & creatinine

  • ECG for cardiac arrhythmias

  • MRI to evaluate kidney function

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Nursing Care of Acute Renal Failure

  • Treat underlying cause

  • Admit to PICU

  • Strict I&O

  • Daily weights

  • Provide replacement IV fluids SLOWLY

  • Maintain urinary catheterization

  • Implement seizure precautions if indicated

  • Assess for infection

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acute renal failure meds

  • Mannitol & furosemide

  • Calcium gluconate

  • Glucose and insulin IV

  • Antihypertensives

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chronic renal failure

  • Begins when diseased kidney can no longer maintain normal chemical structure of body fluids under normal conditions

  • Extensive irreversible damage to nephrons

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