Pediatric Genitourinary Dysfunction

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GU Abnormalities

Back 1

must be fixed early on for psychosocial reasons – preferably by the age of 3

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Inguinal Hernia

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needs to be surgically fixed, if not then the bowel could get stuck and get incarcerated and cut off the blood supply (strangulate) and that part of the bowel could die

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Phimosis

Back 3

when the foreskin can’t be pulled back because it’s stuck from adhesions, just clean with soap and water, should eventually be able to be pulled back, if they can’t pull back by age 5 need circumcisions

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Hypospadias

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urethral opening is on the ventral side of the penis, must be fixed by age of 3 for body image and fertility issues

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Epispadias

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urethral opening is on the top side of the penis, must be surgically corrected by 3 for body image purposes and infertility

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Chryptorchidism

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the absence of one or both testes from the scrotum

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Exstrophy of the bladder

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(bladder on the outside of the body)

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most common organism to cause UTI’s

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E. coli

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Most common ages for UTI's

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Under age of 1 boys are more likely to get a UTI, after a year it’s more of a female issue

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Urinary Tract Infection

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Lower urinary tract Upper urinary tract – kidneys are involved (pyelonephritis) Symptoms of infection – sometimes flank pain, but often little to no symptoms, may have foul smelling urine, fever, vomiting, diarrhea, older children may have incontinence, must consider diabetes if child begins urinating more frequently

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Urinary Tract Infection Anatomic Factors

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Urethral length and closure – if muscle at end of urethra doesn’t close all the way urine can leak and not empty fully (urinary stasis) Circumcision Other Factors – wiping methods Urinary stasis – primary cause of UTI’s Constipation – stool pressing on urethra may prevent urine from coming out Vesicoureteral Reflux Urine chemistry – bacteria grows better if urine is alkaline

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Urinary Tract Infection Urinalysis

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Obtaining the specimen ‘Bag the bag’ – don’t use, likely to get a false positive Culture and Sensitivity (C & S) – positive if over 50k-100k organisms, increasing resistance to antibiotics Treatment Further Testing – a girl who has 2 ATI’s by age of 5 to check for hydronephrosis or other anatomical problems, or a boy by the age of 1 needs further testing for anatomical problems

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Prevention of UTIs

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Voiding schedule – double voiding or placing girls backwards on toilets also helps Wiping Scratching between legs (pinworms for example) Toilet sitting Control of constipation Liberal fluid intake Underwear (cotton)

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Enuresis

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bed wetting after age 5, if parent wet the bed there is an increased chance that the child will, medication is DDAVP (desmopressin) can be used for bed wetting and increases ADH, bedwetting alarms, Types Treatment Consequences

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Vesicoureteral Reflux-VUR

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‘Abnormal retrograde flow of bladder urine into the ureters from the bladder.’ – urine flows backwards Bacteria flows up from the bladder to the kidneys risking pyelonephritis. VUR with sterile urine is not a problem (hydronephrosis). VUR with UTI is the #1 cause of renal scarring in children and causes kidney malfunction. It may occur with the first urinary tract infection.
Voiding Cystourethrogram
VCUG Vesicoureteral reflux
Treatment & Prevention-VUR Primary goal – prevention
Low grade VUR Antibiotics – give at night because urine is there longer Urine cultures VCUG
High grade VUR – surgical correction, re-implant ureters

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Glomerular Diseases

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Glomerulus – structures in the kidney that filter blood to make urine Nephrotic Syndrome- high protein and low salt diet for prevention Acute Glomerulonephritis (AGN) – almost always the result of having a strep infection

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Nephrotic Syndrome
Minimal-Change Nephrotic Syndrome

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– minimal change in the kidneys MCNS Most common type of nephrotic syndrome in children Pathogenesis of NS is not understood Glomeruli impermeable to protein; become permeable to protein (albumin) so when proteins go into the urine there is too much protein in the urine and not enough in the blood Albumin and immunoglobulins leak through the basement membrane of glomeruli Into the urine-Hyperalbuminuria Out of the serum-Hypoalbuminemia

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Nephrotic Syndrome Manifestations

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Hyperalbuminuria Hypoalbuminemia Causes fluid shift from plasma from bloodstream to: Interstitial spaces causing edema Body cavities causing ascites Decreased blood volume; Na and water retained Hyperlipidemia Liver increases synthesis of lipoprotein to correct hypoalbuminemia

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Nephrotic Syndrome-Diagnosis

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Previously well child aged 2-8-years Slowly worsening edema Decreased urine output of dark, ‘frothy’ urine Hyperalbuminuria Hypoalbuminemia Hyperlipidemia Normal glomerular filtration rate (function)

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Nephrotic Syndrome
Management Goals

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Decrease urinary excretion of protein Decrease fluid retention and blood pressure Prevent infection Promoting adequate nutrition Minimize complications of treatment

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Nephrotic Syndrome-Management Corticosteroids

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Stimulate remission and protein excretion Monitor closely for side effects Relapse – first sign of relapse is protein in the urine so parents should dip stick once a week 2/3 will relapse, but in 80%, prognosis favorable

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Nephrotic Syndrome-Management medications

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Immunosuppressants Diuretics furosemide (Lasix) Plasma protein Albumin – frequent vital signs, will help restore the fluid volume Antihypertensives

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Nephrotic Syndrome-Management and Nursing Interventions

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Protein rich diet (1-2g/kg/d) Strict I/O, salt and fluid restriction Daily weights and abdominal girth Daily urine protein measurements Assessment for edema Vitals to identify shock every 4-6 hours, infection, high blood pressure

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Nephrotic Syndrome-Education

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Medication Correct dosing and side effects Corticosteroids Antihypertensives Relapse Urine Blood pressure Timing – can happen after live vaccines, infections
Flu vaccinations

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Acute Glomerulonephritis (AGN)

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Inflammation of the glomerular capillaries Usually postinfectious Acute Post Streptococcal Glomerulonephritis (APSGN) Other risk factors – 6-8 years old because that’s when they start school and strep starts being a risk, high protein/sodium diets, nephrotoxic medications (gentamycin, tetracycline, NSAIDS) especially if given to a dehydrated child

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Acute Post Streptococcal

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Glomerulonephritis (APSGN) After impetigo or pharyngitis with group A -hemolytic streptococcal infection Glomerulonephritis occurs ~10-21 days after infection Rarely does it occur more than once, more common in boys

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Acute Glomerulonephritis Pathophysiology

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Immune complex disease Filtered from plasma through the kidneys Form deposits in basement membrane Glomeruli are infiltrated with leukocytes Cause occlusion of the capillaries Decreases glomerular filtration rate Increased Na and water retention causes edema Untreated can lead to acute renal failure

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Acute Glomerulonephritis Clinical Symptoms

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Healthy with abrupt onset Symptoms of fluid overload Shortness of breath, dyspnea Basilar rales Edema Acute hypertension Decreased urine output Headache, encephalopathy, seizures can occur

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Acute Glomerulonephritis Symptoms

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Gross hematuria Tea colored urine without bacteria, just blood Decreased urine output Proteinuria 3-4+, increased BUN and creatnine Azotemia – nitrogenous waste in the blood From impaired glomerular filtration Increased BUN and creatnine

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Acute Glomerulonephritis
Diagnosis

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Positive strep test
Rising ASO titer Antistreptolysin-O Circulating serum antibodies to strep Indicates a current infection
Low serum complement (C3) Rising C3 indicates improving disease Usually normalize by 8 weeks

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AGN Nursing Interventions

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Fluid and salt restriction Restricted potassium because kidneys are filtering it out Strict I/O Vital signs q 4-6 hours Daily weights, monitor for high blood pressure Antibiotics – only if there is an infection to prevent spread of strep to the child’s family