Alteration in Genitourinary System

Pediatric Nursing Nur. 352 Dr. Manal Kassab

The Kidneys
1. Regulate blood volume and blood pressure:
by adjusting volume of water lost in urine releasing erythropoietin and renin
Erythropoietin stimulating factor (ESF): which acts on a plasma globulin to form erythropoietin which in turn stimulates erythropoiesis in the bone marrow Renin: secreted in response to reduced blood volume, decreased blood pressure or increased secretion of catecholamines (released adrenal glands, stress). It stimulates the production of the angiotensins, which produce arteriolar constriction and elevation in blood pressure.
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2. Regulate plasma ion concentrations:

sodium, potassium, and chloride ions (by controlling quantities lost in urine)

3. Help stabilize blood pH:

by controlling loss of hydrogen ions and bicarbonate ions in urine
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Structural and functional unit

Nephron: composed of
Tubules Arterioles Venules Capillaries (glomerulus) filtrating
units for water and solutes

All are enclosed by a double walled chamber called Bowmans capsule

With renal disease

Impaired glomerular and tubular function: metabolic waste products (creatinine, urea, uric acid) rather being excreted are retained in the blood.
Urea is formed from the breakdown of amino acids by the liver Creatinine: Due to breakdown of creatinine kinase (important in muscle contraction)
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GU Disorders and Defects

Urinary Tract Infection (UTI) Vesicoureteral Reflux Hypospadias/ Epispadias Nephrotic Syndrome Acute Glomerular Nephritis Renal failure
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Urinary Tract Infection

UTI is applied to the presence of significant numbers of microorganisms anywhere within the urinary tract (except the distal one third of the urethra, which is usually colonized with bacteria)

Urinary Tract Infection

Infection in the upper (Ureters, renal pelvis, calyces
and renal parenchyma)

or lower parts (Urethra & Bladder) Females 10-30x risk of males Culture & Sensitivity E. coli and other gram negative entericorganisms (most occur normally or pathogenically in intestines) 80% of cases
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Anatomic and Physical Factors

Shorter urethra in females 2 6 years of age Uncircumcised males Incomplete bladder emptying (reflux, stenosis)
Altered urine and bladder chemistry/ sterility: Adequate fluid intake promote urine sterility Use of cranberry juice increased urine acidity and so prevent UTI
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Anatomic and Physical Factors

Extrinsic factors: Indicates Further need for teaching of Patient Bladder neck obstruction: pregnancy, chronic constipation, tight clothing/ diapers Altered N. flora: antimicrobial agents Catheters Poor hygiene, use of bubble bath, hot tubs
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Assessment
Any child with fever should be evaluated for UTI Clean catch urine for culture & sensitivity With UTI, urine is positive for proteinuria due to bacterial growth Hematuria due to mucosal irritation Increase WBC Urine pH is more alkaline (>7)
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Manifestation
Newborn: Older children Cystitis (infection of bladder) Mild abdominal pain Enuresis Pyelonephritis (kidneys): Symptoms are more acute High fever Flank or abdominal pain Vomiting Malaise
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GI disorders Feeding problems FTT Fever Diaper rashes Foul or strong urine odor

Pain in urination (dysuria) Frequency (polyuria) Burning Hematuria

Clinical Manifestations of Urinary Tract Infection

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Management
10 days antibiotics (beta-lactamGram+) (penicillins, sulfonamide, cephalosporins, tetracyclines) Mild analgesics/ antipyretics Increase fluid intake: flush out infection Clean catch urine after 72 h to assess effectiveness For recurrent UTI, a prophylactic antibiotics for 6 months
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Nursing considerations
Identify child with UTI Education regarding prevention & treatment Instruct parents to observe for clues that suggest UTI:
Incontinence in a toilet-trained child Strong-smelling urine Frequency or urgency
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Enuresis
Involuntary passage of urine past the age when a child should be expected to have attained bladder control (usually by age of 4 years for night control) Occur approximately 5- 7 years of age Enuresis is primarily an alteration of neuromuscular bladder functioning The symptoms may be influenced by emotional factors (birth of a sibling).

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Enuresis
No clear etiology.

Predictive factors are: Longer duration of sleep in infancy. Positive family history. Slower rate of physical development in children up to 3 years.
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Types
Primary: if bladder training was never achieved. Secondary or acquired: if control was established but has now been lost. Nocturnal: occur at night (most common type) Diurnal: occur during the day. Both.
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ASSESSMENT FINDINGS
Associated findings: complete physical and psychological evaluation to role out UTI, neurologic disorders, DM.etc Manifestations:
Nocturnal bed-wetting Urinary urgency & frequency, dysuria, and restlessness
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Management
Attempts to correct stress factors if any. Limit fluids after dinner. Drug therapy (Tofranil): anticholinergic drug
that inhibits urination, given an hour before bed.

Bladder stretching exercises. Motivational therapy/ positive reinforcement (recording the dry nights). Punishment is contraindicated.

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Vesicoureteral Reflux (VUR)

Vesicoureteral reflux (VUR) is the abnormal flow of urine from the bladder back into the ureters during micturition (urination) until next void Lead to infection (provides a place for bacteria to grow)

Cause: Defective bladder valve Incorrect placement of ureters

Valve defect either from birth repeated UTIs.
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Types of VUR
Primary reflux:
Child is born with congenital anomaly affects the ureterovesical junction The ureter did not grow long enough during the child's development in the womb. The valve doesn't close properly, so urine backs up (refluxes) from the bladder to the ureters, and eventually to the kidneys.

This type of VUR can get better or disappear as the child gets older.
The ureter gets longer as the child grows, and the function of the valve improves
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Types of VUR
Secondary reflux: 1. Acquired condition, UTI, neuropathic bladder dysfunction (CNS/Peripheral nerves) 2. Blockage anywhere in the urinary system whcih caused by an infection in the bladder that leads to swelling of the ureter.
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Degree of reflux from bladder into upper genitourinary tract

Grade I: urine refluxes part-way up the ureter Grade II: urine refluxes all the way up the ureter
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 Grade III: urine refluxes all the way up the ureter with dilatation of the ureter and calyces (part of the kidney where
urine collects)

Grade IV: urine refluxes all the way up the ureter with marked dilatation of the ureter and calyces Grade V: massive reflux of urine up the ureter with marked dilatation of the ureter and calyces

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Radiological Tests
Renal/Bladder Ultrasound

is an x-ray examination of the bladder and lower urinary tract that uses a special form of x-ray called fluoroscopy and a contrast material which is injected into bladder It shows urethra, bladder, presence & grade of reflux.
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Findings
Dysuria Urinary frequency and urgency Urine retention Cloudy, dark or blood-tinged urine Urinalysis: increased RBCs Voiding cystourethrogram (VCUG): structural abnormalities
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Management
Spontaneous resolution over time 20-30% 80% probability of remission/ reduction may occur in grades I and II reflux when managed medically Continuous low-dose antibacterial therapy to prevent the infection from moving into the kidneys Frequent urine cultures Surgical correction for grades IV & V Grade III is managed conservatively unless there are complications
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Indication for surgery

Significant anatomic abnormalities Recurrent UTIs High grades of VUR Non-compliance with medical therapy Intolerance to antibiotics VUR after puberty in females
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Nursing Diagnoses
High risk for injury related to possibility of kidney damage from chronic infection (pyelonephritis) Anxiety related to unfamiliar procedures Altered family processes related to illness of a child

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Nursing Interventions
Administration of antibiotics Education Prevention
Perineal hygiene Complete bladder emptying Frequent voiding

Conservative management - prophylactic antibiotics, routine urine cultures Postop: drainage tubes, analgesics
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Acute Glomerulonephritis (AGN)

Glomerulonephritis is a kidney condition that involves damage to the glomeruli (tiny structures within the kidney that filter blood)
Other name: Acute poststreptococcal Glomerulonephritis

It is an immune complex disease after infection with nephritogenic streptococcus (APSGN) (Group A +ve)
(immune-mediated post-streptococcal sequelae)

Common in early school age, uncommon in children < 2years

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Acute Glomerulonephritis (AGN)

A reduction in glomerular filtration rate (GFR) of plasma occurs leading to accumulation of water and retention of sodium Increased plasma and interstitial fluid volume cause circulatory congestion
edema
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What causes post-infxs GN???

Bacteria
Strep Pseudomonas Proteus Treponema

Viral
Hep B and C Varicella Echovirus 10 Coxsackie EBV, CMV Measles Mumps

Parasites
Plasmodium Trichinella

Fungi
Coccidio

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morning, especially in the face, feet, hands, and abdomen

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Symptoms of GN
Macroscopic hematuria (50%)
Tea or cola colored (hematuria) Foamy appearance of urine

Oliguria/ anuria common

Fluid overload
Edema in the morning, especially in the face, feet, hands, and abdomen
Periorbital, rarely severe Weight gain (remission--Weight loss within 1 lb of the preillness weight)

HTN (60-70%)
drowsiness, vomiting, vision changes, convulsions (encephalopathy) Inspiratory crackles (pulmonary edema) . Life threatening Abdomen, flank tenderness common Anorexia Presence of RBC casts in urine (glomerular injury)

Diagnosis
Urine analysis test to look for blood, protein, bacteria, and other evidence of kidney damage in the urine Blood tests: KFT, BUN, creatinine, ESR, Hgb + Antistreptolysin O (Serum ASO) is an antibody found in
human blood produced upon an infection by Group A Streptococcus bacteria.

Proteinuria hypoalbuminemia
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Treatment
Usually resolves spontaneously
Course of disease is 1-2 weeks

Antibiotics Antihypertensive Diuretics to reduce fluid retention Medications to suppress the immune system Treat the other symptoms (supportive)
HTN, oliguria, pulmonary overload, etc.
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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
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Nursing Interventions
General measures:
No added salt diet Fluid restriction Cut down on protein in the diet. Q4h BP Daily weights I&O No bed rest but restrict competitive activity
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Prognosis
> 90% recover from their illness The assoc HTN etc can be fatal
is bad when the course is prolonged as it leads to Acute renal failure Hyperkalemia Nephrotic syndrome Chronic glomerulonephritis Chronic renal failure End-stage renal disease Hypertension Congestive heart failure or pulmonary edema

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Nephrotic Syndrome
Nephrotic syndrome is a group of symptoms including: protein in the urine, low blood protein levels, high cholesterol levels, high triglyceride levels, and swelling

Nephrotic syndrome is caused by various disorders that damage the kidneys, particularly the basement membrane of the glomerulus. This immediately causes abnormal excretion of protein especially albumin in urine
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Nephrotic Syndrome
95% iodiopathic especially primary type (unknown)
Reduced serum albumin decreases the colloidal osmotic pressure in the capillaries fluid accumulates in the interstitial spaces and body cavities

The shift of fluid from plasma to the interstitial spaces reduces the vascular fluid volume (hypovolemia) stimulate renin-angiotension system & secretion of ADH (regulates blood pressure and water)

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The renin-angiotensin system (RAS)

The renin-angiotensin system (RAS) or the reninangiotensin-aldosterone system (RAAS) is a hormone system that regulates BP and H2O balance. When blood volume is low, the kidneys secrete renin. Renin stimulates the production of angiotensin I, which is then converted to angiotensin II. Angiotensin II causes blood vessels to constrict, resulting in increased BP. Also it stimulates secretion of the hormone aldosterone from the adrenal cortex Aldosterone causes the tubules of the kidneys to increase the reabsorption of Na+ and H2O into the blood which increases volume of fluid in the body, and increases BP

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3 Forms of Nephrotic Syndrome

Primary - Minimal Change Nephrotic Syndrome (MCNS) Idiopathic Viral URTI may precede 4-8 days (precipitating factor) 80% of all cases Good prognosis Diagnostic finding is present of Proteinuria

Secondary: glomerular damage occurs secondary to another disorder (e.g D.M)

Congenital: autosomal recessive gene, does not respond to usual therapy (high mortality)
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Large amounts of protein are lost through the urine as a result of an increased permeability of the glomerular basement membrane.

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Minimal Change NS
The condition is called minimal change disease because children with this form of the nephrotic syndrome have normal or nearly normal biopsies Tx by prednisone (belongs to a class of corticosteroids) which stops the movement of protein from the blood into the urine (Remission----Urine is 0 to trace for protein for 5 to 7 days)

Diuretics also used to reduce swelling (helping the child urinate)

Cytotoxic (alkylating agent) is the 2nd chocie if 1st option drug doesn't work (8 to 12 weeks)
It affects growth and action of some cells that cause swelling

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Manifestations
Progressive weight gain Puffiness of face, periorbital at morning which subsides during the day when swelling of abdomen, scrotum & lower extremities is more prominent Respiratory difficulty (pleural effusion) Skin pallor, shiny, breakdown Edema of intestinal mucosa cause diarrhea, loss of appetite, poor intestinal absorption Decrease urine volume/ dark, frothy Normal or slightly decreased BP Irritable, easily fatigued
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Puffiness of face/ generalized edema

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Older child with nephrotic syndrome

Pitting peripheral edema

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Ascites

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Diagnostic evaluation
Marked proteinuria Minimal hematuria; few RBC Increase serum cholesterol: > 450- to 1500mg/dl (as a result of hypprotenemia) Reduce serum protein: albumin < 2 g/dl Increase specific gravity (SG) measures kidney's
ability to concentrate or dilute urine

Elevated ESR
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Management
Goals
Reduce urinary protein excretion Maintain a protein-free urine Reduce tissue fluid retention/ control of edema Prevent infection Minimize complications
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 General measures
Bed rest during edema Antibiotics with infections Diet: restricted salt during massive edema, high protein diet Corticosteroids (steroids): prednisone ( it chance
for infection as immunity are weaken)

Immunosuppressant (do not administer immunization) Albumin (plasma expander) and lasix
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Nursing Diagnosis
Fluid volume excess related to fluid accumulation in tissues Goal: Will exhibit no or minimal evidence of fluid accumulation Interventions: Assess I & O Assess changes in edema Measure abd girth Assess edema around eyes / & dependent areas Weigh daily note degree of pitting Test urine for specific gravity and albumin (hyperalbuminuria ) Administer corticosteroids (to reduce excretions of urinary protein) Administer diuretics (relieve edema) Limit fluids as indicated Change the child's position who is edematous Expected outcome : no or minimal evidence of fluid accumulation
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Acute Renal
Failure
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Acute Renal Failure:

definition
ARF is an abrupt decline in glomerular and tubular function, resulting in the failure of the kidneys to Excrete nitrogenous waste products Maintain fluid & electrolyte homeostasis
Unlike adults, most children do regain normal kidney function after acute renal failure.
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Azotemia is the accumulation of nitrogenous waste within the blood Uremia is a more advanced condition in which retention of nitrogenous products produces toxic symptoms.

Azotemia is a consistent feature of acute renal failure (ARF)

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Etiology
Causes are classified into: 1. Prerenal (hypoperfusion)
decreased perfusion without cellular injury renal tubular and glomerular functions are intact reversible if underlying cause is corrected

2.Intrarenal (intrinsic) Classified according primary site of injury/inflamation: tubular, interstitium, vessels, glomerulus (Escherichia coli) 3. Postrenal (obstructive) urinary tract
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Pathophysiology
Severe reduction in the glomerular filtration rate,
an elevated blood urea nitrogen level, decreased tubular reabsorption of sodium from the proximal tubule. Increase concentration of sodium in the distal tubule which causes stimulation of the reninangiotensin mechanism
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Pathophysiology
The local action of angiotensin causes vasoconstriction of afferent arteriole which further reduces glomerular filtration and prevents urinary losses of sodium. There is a significant reduction in renal blood flow & ischemia then nephrons destruction
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Acute renal failure: common clinical features

azotemia

circulatory congestion/ hypervolemia

electrolytes abnormalities:

K+ (arrhythmia)
Na+ (seizures)

phosphate
calcium

metabolic acidosis kidneys are not removing enough acid which leads to (tachypnea)

Signs of hyperkalemia:
ECG abnormalities, bradycardia, serum potassium level > 7mEq/L
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Acute renal failure: common clinical features

hypertension oliguria: output < 1ml/kg/hr Anuria: no urinary output in 24 hours Nausea, Vomiting Drowsiness Edema
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Prevention
recognize patients at risk (postoperative states, cardiac surgery, septic shock, dehydration) prevent progression from prerenal to renal phase
preserve renal perfusion
isovolemia, cardiac output, normal blood pressure avoid nephrotoxins (aminoglycosides, diuretics, blockers, vasodilator agents, NSAIDS)
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Management
treat the underlying disease Management of the complications Provision of supportive therapy strictly monitor intake and output (weight, urine output, insensible losses, IVF) monitor serum electrolytes adjust medication dosages according to GFR
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Nutrition
provide adequate caloric intake (prevent
malnutrition)

limit protein intake to control increases in BUN minimize potassium and phosphorus intake limit fluid intake
If adequate caloric intake can not be achieved due to fluid limitations, some form of dialysis should be considered
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ARF Nursing Interventions

Vital signs Strict I & O, daily weights Fluid restriction Monitor electrolytes Minimize risk of infection Provide comfort and stability
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Chronic Renal
Failure
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Chronic Renal Failure

The kidneys are able to maintain the chemical composition of fluids within normal limits until more than 50% of functional renal capacity is destroyed by disease or injury. Final stage------------- End-stage renal disease (ESRD) Chronic renal failure or insufficiency begins when the diseased kidneys can no longer maintain the normal chemical structure of body fluids under normal conditions.
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CRF/ Pathophysiology Uremia

Retention of waste products
Water & Na+ retention: nephrons are unable to maintain
sodium & water balance under stress edema & vascular congestion

Hyperkalemia Metabolic acidosis: inability of the kidney to excrete metabolic acids Anemia: production of erthropoietin, bleeding tendency Calcium () & phosphorus () disturbances bone demineralization & impaired growth The final stage of chronic renal failure, end-stage renal disease (ESRD) is irreversible. 74

Management
Calcium and Vitamin D, phosphorus intake (decrease protein & milk diet) Antihypertensives Diuretics Bicarbonate to correct the acidosis Antiepileptics Treatment with dialysis or transplantation is required when the GFR decreased below 10% -15 % of normal
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Treatment of CRF

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Peritoneal Dialysis:
Abdominal cavity acts as a semipermeable membrane Dwell time Cycles of draining & refilling (exchange).

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Treatment of CRF
Hemodialysis: reserved for ESRF
May be used acutely for conditions such as:
Severe metabolic acidosis Accidental poisoning Hypernatremia Hyperkalemia Acute RF

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Treatment of CRF
Kidney Transplantation LRD living related donor CAD cadaver donor

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Renal Transplantation
Watch for
Fever Swelling and tenderness over graft area Decreased urine output Elevated blood pressure
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Hypospadias/Epispadias
It is a birth defect of the urethra in the male that involves an abnormally placed urinary meatus (the opening, or male external urethral orifice) Instead of opening at the tip of the penis glans, a hypospadic urethra opens anywhere along a line Location of the urinary meatus behind the glans penis or anywhere on the penile shaft
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Hypospadias/Epispadias
Circumcision delayed: save the foreskin for repair Surgical correction any time between 8-12 months and before toilet training.
To enable voiding in standing position Improve physical appearance Sexual adequacy
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Nursing Considerations
Assess for birth defects Maintain body image Preparation for operation Care for indwelling catheter Avoid tub bath, rough activities Antibacterial ointment Increase fluid intake
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Cryptorchidism (Crptorchism)
Is failure of one or both testes to descend normally through the inguinal canal into the scrotum. can be a result of
(1) undescended (cryptorchid) testes, (2) retractile testes, or (3) anorchia (absence of testes)
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Undescended testes can be categorized further according to location:

Abdominal: Proximal to the internal inguinal ring Canalicular: Between the internal and external inguinal rings Ectopic: outside the normal pathways of descent between the abdominal cavity and the scrotum
For the infant's comfort, the infant should be examined in a warm room with the examiner's hands warmed. Testes can retract into the inguinal canal if the infant is upset or cold.

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 Anorchia is the complete absence of a testis. Anorchia is suspected whenever one or both testes cannot be palpated in the patient with cryptorchidism. Retractile testes can be found at any level within the path of testicular descent, but they are most commonly identified in the groin

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Risk Factors
Prematurity Low birth weight Twins Hormonal abnormalities (fetus) Toxic exposures in the mother Mother younger than 20 or older than 35 years A family history of undescended testes
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Therapeutic management:
Retractile testis can be manipulated into the scrotum By 1 year of age, undescended testes will descend spontaneously in approximately 75% of cases A trial of hormone therapy with luteinizing releasing hormone (nasal spray) and human chorionic gonadotropin (injection) may be attempted surgical treatment is the preferred management (orchidopexy). 90

Surgical repair is done to:

prevent damage to the undescended testicle by exposure to the higher degree of body heat in the undescended location, thus maintaining future fertility decrease the incidence of tumor formation, which is higher in undescended testicles avoid trauma and torsion (rotation) prevent the cosmetic and psychologic handicap of an empty scrotum
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Postoperative care:
Prevention of infection Home care including pain control. Infection is prevented by
Carefully cleansing the operative site of stool and urine. Observation of the wound for complications Activity restriction The family is counselled regarding the prognosis. In most cases the family can be reassured of normal function in adulthood.
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