1. The Child with Genitourinary Alterations
N422-Pediatrics
Feb 2001
Linda Heath

2. Pediatric Differences
Kidney begins to reach adult functioning about 1 year of age
Infants cannot concentrate urine as efficiently as older children and adults

4. Review Genitourinary System
Maintain fluid & electrolyte balance through glomerular filtration, tubular reabsorption, and secretion
Hormonal functions
Produces renin in glomerulus—regulates BP
Produces Erythropoietin—stimulates RBC production in bone marrow
Metabolized Vitamin D—to active form which is important in calcium metabolism

6. Medications commonly used for GU Disorders
Diuril
Produces diuresis
Tofranil
Treatment of nocturnal enuresis
Lasix
Treat edema
Ditropan
Antispasmodic.Relieves symptoms of bladder contractions
Epoeitn
Stimulates RBC production.
Cyclosporine
Used with corticosteroids to prevent rejection of transplanted organs

7. Common Tests CT scan Cystocopy IVP KUB Renal Arteriogram Renal Biopsy
BUN (Increases in renal insufficiency)
Creatinine
Serum Osmolality
Urinalysis
Specific Gravity pH
Protein
Glucose
Ketones
WBCs, RBCs
Bacteria
CT scan
Cystocopy
IVP
KUB
Renal Arteriogram
Renal Biopsy
Renogram
Renal Ultrasound
VCUG

8. Urinary Tract Infections
Cystitis
Pyelonephritis
Incidence
Assessment
Evaluation
Treatment
Prevention

10. Vesicoureteral Reflux (VUR)
Backflow or reflux of urine from the bladder into the ureters and possibly to the kidney
Urine returns to bladder after voiding
UTI (urinary tract infection) is the most common clinical manifestation
VCUG, renal scan
Graded I – V
Low dose prophylactic antibiotic therapy

11. Classification of Reflux

12. Glomerulonephritis Hematuria Proteinuria Edema Injury in glomerulus
Follows bacterial or viral infection (Strept)
Hematuria
Proteinuria
Edema
Renal insufficiency
S&S of fluid overload

13. Pathophys of Glomerulonephritis

14. Nsg Dx: Glomerulonephritis
Fluid volume excess r/t decreased U.O.
Risk for activity intolerance r/t fatigue
Risk for impaired skin integrity r/t edema and decreased activity
Altered nutrition: less than body requirements r/t fluid and diet restrictions
Anxiety r/t hospitalization, knowledge deficit of disease

15. Nephrotic Syndrome Primary Proteinuria Hypoalbuminemia Edema Secondary
Most common
Disorder within glomerulus
Proteinuria
Hypoalbuminemia
Edema
Secondary
Hepatitis
SLE
Heavy metal poisoning
Cancer

16. Pathophys of Nephrotic Syndrome

17. Nephrotic Syndrome Edema
Noted in periorbital spaces and dependent areas of the body
Child may awaken with facial edema, as the day progresses, edema becomes less noticeable

18. Nsg Dx: Nephrotic Syndrome
Risk for impaired skin integrity r/t edema and decreased circulation
Risk for infections r/t urinary loss of gammaglobulins
Risk for fluid volume deficit (intravascular) r/t proteinuria, edema, and effects of diuretics
Fluid volume excess r/t decreased excretion of Na and water retention
Anxiety (parental) r/t caring for child with chronic disease and hospitalization

19. Comparison Nephrotic Syndrome & Glomerulonephritis
3-4+ Proteinuria
Microscopic Hematuria
Low Serum Albumin
Neg ASO & streptozyme
Normotensive
Electrolytes normal
Glomerulonephritis
0-2+ Proteinuria
Hematuria
Normal Serum Albumin
Positive ASO & strepto
Frequently hypertensive
Na (low), K (elevated)

20. Enuresis
Unable to control bladder function although reached an age at which control of voiding is expected
“Nocturnal Enuresis”—Bed wetting
Most will eventually outgrow with therapeutic intervention

21. Pathophys and etiology of Enuresis
Control of urination is r/t maturation of CNS
By 5 years, most are aware of bladder fullness and can control voiding
Daytime first with nighttime dryness later
Girls seems to master before boys
Children with primary enuresis may have delayed maturations of this part of CNS. They are not able to “sense” bladder fullness and do not awaken to void

22. Nsg Dx: Enuresis
Situational low self-esteem r/t bedwetting or urinary incontinence
Impaired social interaction r/t bedwetting or urinary incontinence
Ineffective family coping: compromised r/t negative social stigma and increased laundry load

23. Cryptorchidism Undescended or “hidden” testicle
One or both testes fail to descend through inguinal canal into the scrotal sac
Inguinal hernias are commonly associated with this
Most infants with cryptorchidism will have spontaneous descent of their testes during the first year of life; Surgical intervention after that

24. Pathophys of Cryptorchidism
Fetal development: testes descend from the abdomen during 7th – 9th month gestation
Failure to descend unknown
?abnormality of testis itself
?insufficient hormonal stimulation for the normal descent process
Sperm production is decreased in undescended testis and increased risk of developing a malignancy when child receives adulthood

25. Nsg Dx: Crytorchidism
Knowledge deficit (parental) r/t cause and management of cryptorchidism
Anxiety r/t possible decreased fertility and increased risk of testicular malignancy

26. Hypospadius Congenital anomaly
Actual opening of the urethral meatus is “below” the normal placement on the glans of the penis
Goal of surgery: to make urinary & sexual function as normal as possible and improve appearance of penis

27. Pathophys of Hypospadias
Incomplete development of urethra in utero
Exact cause unknown (? R/T genetic, environmental and hormonal influences)
Displacement of urethral meatus does not usually interfere with urinary continence
Stenosis of opening can occur causing problems with partial obstruction of outflowing urine. This might result in hydronephrosis or UTIs
Ventral placement of urethral opening might interfere with fertility in the mature male, if left uncorrected

28. Nsg Dx: Hypospadius
Knowledge deficit (parental) r/t diagnosis, surgical correction, & post-op care
Risk of infection r/t indwelling catheter
Impaired physical mobility r/t surgical procedure of penis

29. Bladder Extrophy Congenital anomaly
Extrusion of bladder to the outside of the body through defect in lower abdominal wall
May be associated with genital anomalies or defects of anus

30. Pathophys of Bladder Exstrophy
Result of inappropriate growth during embryonic development
Degree of deformity depends on when the disruption occurs during fetal development. The earlier in development the more severe the deformity
Most infants with bladder exstrophy have normal kidneys but may be at risk for kidney damage due to VUR and bladder dysfunction, which may occur after surgical reconstruction

31. Nsg Dx: Bladder Exstrophy
Impaired tissue integrity r/t exposed bladder mucosa
Knowledge deficit (parental) r/t diagnosis and anomaly
Risk for Infection r/t anatomical defect, surgical procedures, and probable abnormal bladder function
Body image disturbance r/t physical appearance of lower abdomen and genitalia

32. Acute Renal Failure Sudden severe loss of kidney function
Kidneys can no longer filter waste products, regulate fluid volume, nor maintain chemical balance
Uncommon in the pediatric patient
Most children with ARF regain renal function

33. Pathophys of ARF Prerenal ARF Intrarenal ARF Postrenal ARF
Decreased perfusion of kidney
Decreased blood flow and ischemia cause cell swelling, cell injury, and poss cell death
Causes: dehydration, perinatal asphyxia, hypotension, septic shock, hemorrhagic shock, and renal artery obstruction
Intrarenal ARF
Actual damage to kidney tissue
Causes: aminoglycosides, contrast dye, obstruction, HUS, glomerulonephritis, pyelonephritis
Postrenal ARF
Obstruction of urine outflow causing decreased renal function due to pressure within kidney
Causes: obstruction problems within kidney, neurogenic bladder, stones, tumor, edema

34. Dialysis

35. Chronic Renal Failure ESRD & Kidney transplant

36. Nsg Dx: ARF Fluid volume excess r/t kidney dysfunction
Risk for infection r/t invasive procedures and fluid overload
Altered family process r/t child hospitalized with serious disorder
Altered nutrition: less than body requirements r/t anorexia and decreased intake due to restrictions
Knowledge deficit r/t disease process, therapy, and prognosis

37. Hemolytic Uremic Syndrome (HUS)
Anemia
Thrombocytopenia
Acute renal failure
E.coli 0157:H7

38. Pathophys of HUS Prodrome of GI symptoms E. coli 0157:H7
Bacteria grow and multiply in intestines
Bacteria produce toxin that damages the endothelial cells of capillary walls leading to inflammation. Significant in renal glomeruli
Occlusion of glomeruli decreases filtration and results in ARF
Vascular process of HUS can affect any organ
Anemia results damaged RBC as they pass through occluded vessels and are removed from circulation by spleen
Thrombocytopenia occurs because the platelets get trapped within the small vessels