peds GI and renal

formula intolerance

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

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

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

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

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)

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

NG tube or OG

cannot support self short term

preterm and unable to expend energy

status post heart surg

gastric tube

surgical placed

• long term nutritional support

• need for continuous feedings

nutrition

enteral feedings are preferred

parenteral only used if bowel is not an option

• requires central line

• caustic to liver over time

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

acute gastroenteritis signs

• vomiting

• diarrhea

• generalized abdominal pain

• fever

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)

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

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

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

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

pyloric stenosis management

• Need an ultrasound to confirm

• Need to correct fluid and electrolyte imbalance

  • *at risk for hypokalemia & metabolic alkalosis*

• Need surgery

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

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

Hirschsprung’s Disease diagnosis

• rectal biopsy to confirm absence of ganglion cells

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

Hirschsprung’s Disease risk factors

male gender, genetics, trisomy 21

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

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

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)

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

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

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

Intussusception signs

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

• Currant jelly stools

• Palpable abdominal mass (sausage shaped)

• May see vomiting, fever, distended abdomen

Intussusception treatment

• Air enema

• surgery

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

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

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

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

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

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

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

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)

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

causes of diarrhea

• Viral, bacterial, parasitic

• Associated with other infections such as URI, UTI

• Dietary

• Medicine-related

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

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

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

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

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

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

appendicitis signs

• Vague midline pain that moves to RLQ and intensifies

• Vomiting, diarrhea

• Fevers

• anorexia

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

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

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

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

Failure to thrive

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

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

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

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

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

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

celiac disease severe form

• Iron deficiency anemia

• Vit b 12 deficiency

• Osteopenia / osteoporosis r/t calcium malabsorption

defects of GU

• Hypospadias

• Epispadias

• Cryptorchidism

• Phimosis

• Testicular torsion

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

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

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

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

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

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

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

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

Vesico-ureteral reflux imaging

• Ultrasound

• Voiding cystourethrogram

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

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

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

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

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

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

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

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

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

nephrotic syndrome lab tests

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

• Bloodwork:

  • Albumin:

  • Hgb, hct, platelets:

  • GFR:

  • Calcium:

  • Sodium:

  • hyperlipidemia

nephrotic syndrome diag.

Kidney biopsy

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

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

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)

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

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

Hemolytic Uremic Syndrome lab tests

• CBC

• Reticulocyte count

• Urine

• BUN and creatinine

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

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

Hemolytic Uremic Syndrome management

Support with antihypertensives, blood transfusions if needed, hemodialysis

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

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

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)

stages of acute renal failure

initiation

oliguric

diuresis

recovery

Initiation

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

• Can be hours to days

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

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

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

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)

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

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

acute renal failure meds

• Mannitol & furosemide

• Calcium gluconate

• Glucose and insulin IV

• Antihypertensives

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