Transcript HALL PASSES

Renal
Pediatric
Learning Objectives
•
•
•
•
•
•
Review the normal structure and function of the genitourinary system
Formulate a plan of care for the child with an obstructive disorder.
Discuss the preoperative preparation of the child and parents when the
child has a structural defect of the genitourinary tract.
Compare the child with minimal-change nephrotic syndrome and the child
with acute glomerulonephritis in terms of clinical manifestations and
nursing care.
Contrast the causes, complications, and management of acute and
chronic renal failure.
Outline a nursing care plan for a child with the following conditions
including a teaching plan for home care.
–
–
–
–
–
–
Glomerulonephritis
Polycystic Kidney
Hypospadias
Nephrotic Syndrome
Enuresis
HUS
Renal- Pediatric Anatomical Differences
– Kidneys
• Glomerular filtration rate is approximately half of an
adult
• Most renal growth occurs during the first 5 years of
life
• Bladder capacity – nerve development
• Lack of fat padding
– Normal urine output:
• Infants 2 mL / kg / hr
• Children 0.5 mL / kg / hr
• Adolescents 40-80 mL/ hr
Renal Nursing Care Plans
Nursing Diagnosis
•Fluid volume deficit r/t loss
of fluid through abnormal
routes
•Fluid volume excess r/t
compromised regulatory
mechanism
•Risk for impaired skin
integrity r/t renal failure
•Risk of infection r/t
medication immune
suppressant
Interventions
• Assess weight
• Assess input and output
• Assess for signs and
symptoms of
complications
• Provide appropriate diet
with choices for ages
• Bundle care
• Infection control
Hypospadias and epispadias (dorsal surface)
• Pathophysiology
• Collaborative Care
– Congenital anomalies
– Diagnosis with
ultrasound/physical
– Abnormal location of
exam
the urethral meatus in
males
– Do not circumcise
– Mild – slightly off
• Nursing Care
center
– Preoperative teaching
– Severe – on the
– Postoperative
scrotum require
• Risk of infection
surgical correction
• Stent or catheter
• Fluid intake
• I/O
– Kinks
• Antibiotics
Glomerulonephritis
• Age
– 3 to 10 years
• Pathophysiology
– Group A beta-hemolytic
streptococci
– Inflammation of the
gomerulus
– Obstruction
– Decreased filtration rate
• Symptoms
–
–
–
–
Fever
HA
Dark urine
Periorbital edema
• Complications
–
–
–
–
–
Hypertension
Cardiac enlargement
Liver enlargement
Orthopnea
Pulmonary Edema
• Patient Care
– Diet
• No added Salt
• low protein
– Medications
• Antihypertensive
• Diuretics
• Antibiotics?
– Position
• Semi-fowlers
Nephrotic Syndrome
• Pathophysiology
– After a glomerular disease or
other disorders
– Spill protein in urine
• Ages
– 2-3 years
• Symptoms
–
–
–
–
–
–
–
–
Hypoproteinemia
Hypoalbuminemia
hyperlipidemia
Massive edema
Poor renal perfusion
Hypotension
Fatigue
Anorexia
• Patient Care
– Infection control
– Medication
• Corticosteroids
• Lasix,
• Cytoxin
– Diet
• Low sodium (edema)
• Regular (remission)
– Fluid restriction
• Because of edema
– Skin care
• Turn frequently
– Position
• Semi-fowlers
Polycystic Kidney
•Pathophysiology
–Genetic disorder
•Autosomal recessive
•Dominant
•Liver abnormalities common
–Cyst sacs form enlarge and become fibrosis as the child
grows
–Reduced kidney function
•Signs/Symptoms
–Potter facies
–HTN
–Normal or little urine output
–Polyuria and polydypsia
–Respiratory distress
–Anorexia
Polycystic Kidney
•Nursing Care
–Preparing child for
procedures
–Infection
–Weight
–Intake/output
–Skin care
–Avoid contact sports
Enuresis
•
Nocturnal enuresis versus Diurnal enuresis
– Primary enuresis
– Intermittent enuresis
– Secondary enuresis
•
Look for causes
– Neurologic, congenital structural disorders, illness, stress, abuse
– Small capacity
– Vasopressin abnormality = produce more urine at night
•
Diagnostic Tests
– History
– Urine analysis/culture
•
• Specific gravity concerns
• Glucosuria
Treatment
–
–
–
–
–
Medications: Desmopressin acetate (DDAVP), Oxygutynin, Imipramine
Fluid intake program
Timed voiding
Enuresis alarms
Reward system
HUS
• Pathophysiology
– Acute renal disease
– Escherichia coli (often linked)
• Shigella, Samonella, Yersinia, and Campylobacter
– Damages the lining of the glomerular arterials –
swelling of the endothelia
– 1 to 2 weeks prior to HUS – gastroenteritis, URI
or UTI
• Signs/Symptoms
– Prodromal stage: URI, Fever, Irritable,
Lymphadenopath, Skin rash, Edema, Abdominal
pain, nausea, vomiting, and bloody diarrhea
– Acute stage: Hemolytic anemia, HTN, Pallor,
purpura, Neurologic involvement, Renal failure
HUS
Organism
produces a
verotoxin
Damages the lining
of the glomerular
arterioles
Endothelial
cells swell
Hemolysis,
hemolytic anemia
RBC’s damaged
passing through
occulusion
Clotting mechanisms
deposit fibrin in the
renal arterioles and
capillaries
Platelets cluster at the
damage =
thrombocytopenia
Acute tubular
necrosis
HUS - Treatment
•
Diet:
– Fluid restriction
– High calorie, high carbohydrate diet – low protein, sodium,
potassium and phosphorus.
•
• Enteral feedings as needed
Medications:
–
–
–
–
–
–
•
Calcium gluconate, calcium chloride
Aluminum hydroxide gel to bind to phosphorus
Kayexalate to remove excess potassium
Antihypertensive agents
Insulin as needed
Antibiotics? Not often
Dialysis
– Peritoneal dialysis
•
Transfusion
– RBC’s
– Platelets