1.genitourinary

8/2/2019 1.Genitourinary

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Alteration in Genitourinary System

Pediatric Nursing

Nur. 352Dr. Manal Kassab


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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 plasmaglobulin to form erythropoietin which in turn stimulateserythropoiesis in the bone marrow

Renin: secreted in response to reduced blood volume, decreasedblood pressure or increased secretion of catecholamines (releasedadrenal glands, stress). It stimulates the production of theangiotensins, 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) filtratingunits for water and solutes

All are enclosed by a double

walled chamber called Bowmans

capsule


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With renal disease

Impaired glomerular and tubular function:metabolic waste products (creatinine, urea,

uric acid) rather being excreted are retainedin the blood.

Urea is formed from the breakdown of aminoacids by the liver

Creatinine: Due to breakdown of creatininekinase (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 thirdof the urethra, which is usually colonized

with bacteria)


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Urinary Tract Infection

Infection in the upper (Ureters, renal pelvis, calycesand renal parenchyma)

or lower parts (Urethra & Bladder)

Females 10-30x risk of males

Culture & Sensitivity

E. coli and other gram negative enteric-

organisms (most occur normally or

pathogenically in intestines)80% of cases


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Anatomic and Physical Factors

Shorter urethra in females

26 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 evaluatedfor UTI

Cleancatch 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)

Pyelonephritis

(kidneys):

GI disorders

Feeding problems

FTT

Fever

Diaper rashes

Foul or strong

urine odor

Pain in urination

(dysuria)

Frequency

(polyuria)

Burning

Hematuria

Mild abdominal

pain

Enuresis

Symptoms are

more acute

High fever

Flank or

abdominal pain

Vomiting

Malaise

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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

Cleancatch urine after 72 h to assesseffectiveness

For recurrent UTI, a prophylactic antibioticsfor 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 agewhen a child should be expected to haveattained bladder control (usually by age of 4

years for night control)

Occur approximately 5- 7 years of age

Enuresis is primarily an alteration ofneuromuscular 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 developmentin children up to 3 years.

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Types

Primary: if bladder training was neverachieved.

Secondary or acquired: if control wasestablished 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 drugthat 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 ofurine from the bladder back into the ureters duringmicturition (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. 22


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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 thewomb.

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 bladderthat leads to swelling of the ureter.

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Grade I: urine refluxes part-way up the ureter

Grade II: urine refluxes all the way up theureter

Degree of reflux from bladder into upper genitourinary tract


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Grade III: urine refluxes all the way up the ureter withdilatation of the ureter and calyces(part of the kidney whereurine collects)

Grade IV: urine refluxes all the way up the ureter withmarked 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 acontrast material which is injected into bladder

It shows urethra, bladder, presence & grade of reflux.


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Dysuria

Urinary frequency and urgency

Urine retention

Cloudy, dark or blood-tinged urine

Urinalysis: increased RBCs

Voiding cystourethrogram (VCUG): structural

abnormalities

Findings


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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 - prophylacticantibiotics, routine urine cultures

Postop: drainage tubes, analgesics


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Acute Glomerulonephritis (AGN)

Glomerulonephritis is a kidneycondition that involves damage to theglomeruli (tiny structures within the

kidney that filter blood)

Other name: Acute poststreptococcalGlomerulonephritis

It is an immune complex disease afterinfection with nephritogenicstreptococcus (APSGN) (Group A +ve)(immune-mediated post-streptococcal sequelae)

Common in early school age,uncommon in children < 2 ears35


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Acute Glomerulonephritis (AGN)

A reduction in glomerular filtration rate

(GFR) of plasma occurs leading to

accumulation of water and retention ofsodium

Increased plasma and interstitial fluid volumecause

circulatory congestion

edema 36


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What causes post-infxs GN???

Bacteria

Strep

Pseudomonas Proteus

Treponema

Parasites

Plasmodium Trichinella

Fungi

Coccidio

Viral

Hep B and C

Varicella Echovirus 10

Coxsackie

EBV, CMV

Measles

Mumps

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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, andabdomen

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)


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Urine analysis test to look for blood, protein,bacteria, and other evidence of kidney damage in theurine

Blood tests: KFT, BUN, creatinine, ESR, Hgb

+ Antistreptolysin O (Serum ASO)is an antibody found inhuman blood produced upon an infection by Group A Streptococcusbacteria.

Proteinuria

hypoalbuminemia

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Diagnosis


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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.41


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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 anddecreased activity

Altered nutrition: less than body requirements r/tfluid and diet restrictions

Anxiety r/t hospitalization, knowledge deficit ofdisease

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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 44


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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 thekidneys, particularly the basement membrane of the glomerulus.

This immediately causes abnormal excretion of protein especiallyalbumin in urine

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Nephrotic Syndrome

95% iodiopathic especially primary type(unknown)

Reduced serum albumin decreases thecolloidal osmotic pressure in thecapillaries fluid accumulates in theinterstitial spaces and body cavities

The shift of fluid from plasma to theinterstitial spaces reduces the vascularfluid volume(hypovolemia) stimulaterenin-angiotension system & secretionofADH (regulates blood pressure and water)

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The renin-angiotensin system (RAS) or the renin-

angiotensin-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 ofangiotensin 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 48

Therenin-angiotensin system (RAS)


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3 Forms of Nephrotic Syndrome

Primary - Minimal Change Nephrotic Syndrome (MCNS)

Idiopathic Viral URTI may precede 4-8 days (precipitatingfactor)

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

Diuretics also used to reduce swelling (helping the childurinate)

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)

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 whichsubsides 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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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 ESR56


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Management

Goals

Reduce urinary protein excretion

Maintain a protein-free urine

Reduce tissue fluid retention/ control of

edema

Prevent infectionMinimize complications

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General measures

Bed rest during edema

Antibiotics with infections

Diet: restricted salt during massive edema, highprotein diet

Corticosteroids (steroids): prednisone ( it chancefor infection as immunity are weaken)

Immunosuppressant (do not administerimmunization)

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 andtubular function, resulting in the failure ofthe 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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Azotemiais 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 tract63


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Pathophysiology

Severe reduction in the glomerular filtrationrate,

an elevated blood urea nitrogen level,

decreased tubular reabsorption of sodium fromthe proximal tubule.

Increase concentration of sodium in the distaltubule which causes stimulation of the renin-angiotensin mechanism

P th h i l


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Pathophysiology

The local action of angiotensin causes

vasoconstriction of afferent arteriole

which further reduces glomerularfiltration and prevents urinary losses of

sodium.

There is a significant reduction in renalblood flow & ischemia then nephrons

destruction

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Acute renal failure:


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common clinical features

azotemia

circulatory congestion/ hypervolemia

electrolytes abnormalities:

K+ (arrhythmia) phosphate

Na+ (seizures) calcium metabolic acidosis kidneys are not removing enough acid whichleads to (tachypnea)

Signs of hyperkalemia:

ECG abnormalities, bradycardia, serum potassium level > 7mEq/L

A t l f il


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hypertension

oliguria: output < 1ml/kg/hr

Anuria: no urinary output in 24 hours

Nausea, Vomiting

Drowsiness

Edema

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common clinical features


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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 (preventmalnutrition)

limit protein intake to control increases in BUN

minimize potassium and phosphorus intake

limit fluid intake

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If adequate caloric intake can not be achieveddue to fluid limitations, some form of dialysisshould 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 thediseased kidneys can no longer maintain the normal

chemical structure of body fluids under normal

conditions.73

CRF/ Pathophysiology


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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 & vascularcongestion

Hyperkalemia

Metabolic acidosis: inability of the kidney to excretemetabolic acids

Anemia: production of erthropoietin, bleedingtendency Calcium () & phosphorus () disturbances bonedemineralization & impaired growth

The final stage of chronic renal failure, end-stage renal

disease (ESRD) is irreversible. 74


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Management

Calcium and Vitamin D, phosphorus intake(decrease protein & milk diet)

Antihypertensives

Diuretics

Bicarbonate to correct the acidosis

Antiepileptics

Treatment with dialysis or transplantation isrequired when the GFR decreased below 10% -15 %of normal

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Treatment of CRF

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Peritoneal Dialysis:

Abdominal cavity actsas 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

FeverSwelling and tenderness over

graft area

Decreased urine outputElevated blood pressure

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H di /E i di


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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)

Undescended testes can be categorized further


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Undescended testes can be categorized further

according to location:

Abdominal: Proximal to the internal inguinal

ring

Canalicular: Between the internal andexternal 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. 87


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Anorchia is the complete absence of a

testis. Anorchia is suspected whenever one

or both testes cannot be palpated in thepatient with cryptorchidism.

Retractile testes can be found at any levelwithin 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 thescrotum

By 1 year of age, undescended testes willdescend spontaneously in approximately75% of cases

A trial of hormone therapy with luteinizingreleasing hormone (nasal spray) and humanchorionic gonadotropin (injection) may beattempted

surgical treatment is the preferred

management (orchidopexy).


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Surgical repair is done to:

prevent damage to the undescended testicle byexposure to the higher degree of body heat in theundescended location, thus maintaining future

fertility decrease the incidence oftumor formation,

which is higher in undescended testicles

avoid trauma and torsion (rotation)

prevent the cosmetic and psychologic handicapof 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 andurine.

Observation of the wound for complications

Activity restriction

The family is counselled regarding the prognosis.

In most cases the family can be reassured of normalfunction in adulthood.

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