Renal and Urinary Systems

The urinary system—the structures of which precisely maintain the internal chemical environment of the body—perform various excretory, regulatory, and secretory
functions.

Function: to maintain the body’s state of homeostasis by regulating fluid and electrolytes, removing wastes, and providing hormones involved in red blood cell
production, bone metabolism, and control of blood pressure

Renal Anatomy

The kidneys are a pair of brownish-red structures located

retroperitoneally on the posteriorwall of the abdomen from
the 12th thoracic vertebra to the 3rd lumbar vertebra in the
adult. An adult kidney weighs 120 to 170 g (about 4.5 oz)
and is 12 cm (about 4.5 inches) long, 6 cm wide, and 2.5 cm
thick.

Normal adult kidney

cross section of adult kidney

Two regions are seen: an outer part, called the cortex, and an inner part, called the medulla. The medulla can be further subdivided into an outer medulla,
which is closer to the cortex, and an inner medulla, which is farther from the cortex.

The human kidney is organized into a series of lobes, usually 8 to 10 in number. Each lobe consists of a pyramid of medullary tissue. The tip of the
medullary pyramid forms a renal papilla. Each renal papilla drains its urine into a minor calyx, The minor calices unite to form a major calyx, and the urine then
flows into the renal pelvis.

The Nephron Is the Basic Unit of Renal Structure and Function

Each human kidney contains about one million nephrons each of which consists of a renal corpuscle and a renal tubule. The renal corpuscle consists of a
tuft of capillaries, the glomerulus, surrounded by Bowman's capsule. The renal tubule is divided into several segments. The part of the tubule nearest the glomerulus
is the proximal tubule. This is subdivided into a proximal convoluted tubule and proximal straight tubule. The straight portion heads toward the medulla, away
from the surface of the kidney. The loop of Henle includes the proximal straight tubule, thin limb, and thick ascending limb. Connecting tubules connect the next
segment, the short distal convoluted tubule, to the collecting duct system. Several nephrons drain into a cortical collecting duct, which passes into an outer
medullary collecting duct. In the inner medulla, inner medullary collecting ducts unite to form large papillary ducts.
Functions of the Kidneys
• Urine formation through filtration, reabsorption, and excretion.
• Excretion of waste products
• Regulation of electrolytes
• Regulation of acid-base balance
• Control of blood pressure
• Renal Clearance
• Regulation of red blood cell production
• Synthesis of vitamin D to active form
• Secretion of prostaglandins
• Regulates calcium and phosphorus balance
• Activates growth hormone

Ureters
• Are long fibromascular tubes that connect each kidney to the bladder
• It originates at the lower portion of the renal pnelvis and terminated in the trigone of the bladder wall.
• It’s lining is made up of urothelium that prevents reabsoption of urine
 • It has 3 narrowed areas of the ureters: the uretheropelvic junction, the urethral segment near the sacroiliac junction and the ureterovesical junction
• These 3 areas of the ureters have propensity for obstruction by calculi or stricture

Urinary Bladder
• It is muscular hallow sac located just behind the pubic bone
• The capacity of adult bladder is about 300 to 500 ml.
• The bladder is characterized by its hallow area called vesicle which has 2 inlets (the uretra) and one outlets the (the urethra)
• The bladder neck is called urethrovesical junction is responsible for efflux of urine
• It has internal sphinter.it helps to maintain incontinence.

• The Urethra It arises from the vase of the bladder

• In the male, it passes the penis, the prostate gland which lies below the bladder neck, surrounds the urethra posteriorly and laterally
• In the female, it opens just anterior to the vagina
--------------------------------------

Clinical manifestation of Urinary Dysfunction

Changes in micturation (voiding)

A. Hematuria (red blood cells in the urine)

1.Hematuria is considered a serious sign that requires evaluation
2.Color of bloody urine dependent on pH of urine and amount of blood present.
a. Acid urine is dark and smoky color
b. Alkaline urine is red in color
3.Hematuria may due to systemic cause such as blood dyscrasias,
Anticoagulant theraphy, neoplasm, trauma, extreme exercise
4.Painless hematuria may indicate neoplasm in the urinary tract
5. Hematuria from renal colic ( stone in the kidney)
6. Bloody spotting reveals bleeding from the urethra, bladder neoplasm.
7. Hematuria also seen in renal tuberculosis, polycystic disease of the kidney
Acute pyelonephritis, Trombosis and involving renal artery and vein
B. Protenuria (Albuminuria)
1. Normal urine does not contain significant quantities
2. Protenuria is characteristically seen in all form of acute and chronic renal disease (more of glumerulonephritis than pyelonephritis
a. The protein is mainly albumin but globulin is also present
b. Albumin and globulin escape through damage glomerular capillaries in a grater amount than can be reabsorbed by the tubules, or
damage tubules fails to reabsorbed amount filtered
3. Protenuria occurs in systemic disease where there varying degrees of renal
Anoxia, as in cardiac decompensation , diabetic glomerulosclerosis.
4. Mild protienuria may occur from other sources- Urethritis, prostatitis,
Cystitis
C. Dysuria (painful or difficult voiding)- seen in wide variety of pathologic condition
D. Frequency – voiding occurs more often than usual, when compared with the patient usual pattern (or with a generally accepted norm of once every 3-6
hours)
1. Determine if habits governing fluid intake have been altered
2. Increase in frequency can result in variety of conditions such as infection and disease of urinary tract, metabolic disease, medication (diuretics)
E. Urgency (strong desire to urinate- due to inflammatory lesion in the bladder,
prostate, or urethra, acute bacterial infection and chronic urethrotrigonitis in women
F. Burning upon urination- seen in urethral irritation or bladder infection
G. Other Changes
1. Strangury (slow and painful urination) only small amounts of urine is
Voided; blood staining may be noted- seen in severe cystitis
2. Hesitancy (undue delay and difficulty in initiating voiding) may indicate
Compression of urethra, outlet obstruction, nuerogenic bladder.
3. Nocturia (excessive urination at night)- it suggest decreasing renal
Concentrating ability or heart failure, diabetes mellitus, poor bladder emptying.
4. Urinary incontinence (involuntary loss of urine) may be due to injury to
External urinary sphincter acquired nuerogenic disease, nuerogenic disease
5. Stress incontinence (intermittent leakage of urine due to sudden strain) due
Weakness of sphincteric mechanism
6. Polyuria (large volume of urine voided in a given time)- demonstrated in
Diabetes mellitus, diabetes insipidus, chronic renal disease, diuretics.
7. Oliguria (small volume of urine; output between 100 to 500ml./24 hours)-
May result from acute renal failure, shock, dehydration, fluid-ion imbalance
8. Anuria ( absence of urine in the bladder ; output less than 50 ml./ in 24 hours indicates severe renal dysfunction requiring immediate medical
intervention.
9. Enuresis (involuntary voiding during sleep) may be physiologic at age of 3 years; thereafter may be functional or symptomatic of obstructive
disease( usually the urinary tract)
10. Pnuematuria (passage of gas during voiding) Cause by fistulos connection between the bladder and bowel, rectosigmoid cancer, regional ileitis,
sigmoid deverticulitis, and gas forming urinary tract infection
Urinary Tract pain
1. Genitourinary pain is not always present in renal disease, but generally seen in more
Acute conditions
2. Pain of renal disease is cause by sudden distension of the renal capsule; severity is
Related to how quickly the distension developed
3. Kidney pain- may be felt as a dull ache in costovertebral angle ; may spread to
 umbilicus.
4. Urethral pain – felt in the back and radiates to the abdomen, upper thighs, or labia
5. Flank pain (side area between the ribs and iluim )- radiates to lower abdomen or epigastrium and is often associated with nausea , vomiting, and paralytic ilues;
most commonly secondary to a renal lesion.
6. Bladder pain (low abdominal pain or suprapubic area) may be due bladder infection or over distended bladder.
7. Urethral pain from irritation of bladder neck , from foreign body in the canal , or from urethritis due to infection or trauma.
8. Pain in scrotal area from inflammatory swelling of epipidymis or testicle, or torsion of the testicle.
9. Testicular pain due to injury, mumps orchitis, torsion of spermatic cord.
10. Perineal or rectal discomfort from acute prostitis, prostatic abscess.
11. Back leg pain from cancer of prostate with metastases of pelvic bone
12. Pain in glands penis is usually from prostatitis; penile shaft pain is from urethral problems.

Related Gastrointestinal Symptoms

1. Gastrointestinal symptoms related to urologic conditions include nausea, vomiting
Abdominal discomfort, paralytic ileus, and gastrointestinal hemorrhage with uremia.
2. Occur with urologic conditions because the gastrointestinal and urinary tracts have
common autonomic and sensory innervations and because of renointestinal reflexes.

Assessment of Urologic Function

History and physical Assessment

Health History
Seek the following information related to urinary and renal function:
1. What is the patient chief concern? Why is he seeking help?
2. What is (are) the Patient’s present and past occupation(s)?(look for occupational hazard related to the urinary tract- contact with chemicals, plastics, pitch,
tar, rubber.
3. What is the patient history?
4. What is the past history, especially in the relation to urinary problems?
5. Is there any family history of renal disease
6. What childhood diseases did the patient have
7. Is there history of urinary infection
8. Did enuresis continue beyond age (past 3 years old
9. Are there any voiding disorder?
10. Is there pain present?
11. Has patient has fever? Chills? passage of stone?
12. Any history of genital lesion or history of STD.
13. Does the patient have diabetes mellitus? Hypertension? Allergies?
14. Does the patient is receiving any prescription or OTC ?

Diagnostic Test

Radiological Techniques
A. Plain film- of the abdomen or KUB (Kidneys, ureters, bladders)
1. Delineates size, shape of the kidneys
2. Reveals any deviation, Such as stone, Hydronephrosis, cysts, tumors.

B. Computed Tomography- provides a cross- sectional view of kidney and urinary tract to detect presence and extent of urologic disease.
C. Magnetic Resonance Imaging ( MRI)
1. Relies on magnets and computers to produce images.
2. In urology, provides excellent images of soft tissue.

H. Renal Angiography-visualization of renal arterial supply

1. A special needle is used to pierce the femoral artery (or axillary artery) and a
Catheter is threadend through the femoral and iliac arteries into the aorta or
Renal artery.
2.Contrast medium is injected to opacity the renal arterial supply.
3. Angiography evaluates blood flow dynamics, demonstrate abnormal
Vasculature , and differentiates renal cysts from renal tumors.
I. Radionuclide Imaging
1.Radiopharmaceutical ( 99 Tc- labeled compound or (131 I-hippurate) are
Injected intravenously.
2.Studies obtained with a scintillation camera placed posterior to the kidney with
The patient in supine position , prone or sitting position.
3. The resultant image (Scan) indicates the distribution of pharmaceutical with in
The kidneys.
4.The Tc scan provides information provides information about the kidney unctio
Perfusion and is useful when renal function is poor.
5. The hippurate scan provides information about the kidney function.
J. Ultrasound ( ultrasonic scan) uses sound waves that passed into the body. Organ
In the urinary system create ultrasonic images.
• Abnormalities such as masses, malformations or obstruction can be identified

ENDOUROLOGY (UROLOGIC ENDOSCOPIC EXMINATION)

A. Cystoscopic Examination is a method of direct visualization of the urethra , prostatic urethra , and bladder by means of a cystoscople that is inserted through the
urethra into the bladder. It has optical lens that provides view of the bladder
 B. Renal and urethral brush biopsy- after cystocopy, introduction of catheter dollowed by a biopsy brush, which is passed to the catheter, suspected lesion is brush
back and to obtain cells and surface tissue for histologic diagnosis.
C. Renal Endoscopy, Nephroscopy Intoduction of fibroptic scope into the renal pelvis during renal operation (pyelotomy) or percutaneous to view interior of the
renal pelvis, removed calculi, biopsy of small lesion, and diagnose renal hematuria and selected renal tumors.

NEEDLE BIOPSY OF THE KIDNEY

• It is performed by percutaneous needle biopsy through renal tissue or by open biopsy through a small flank incision.
• It is useful in evaluating renal disease and securing specimen for electron and immunoflorescent microscopy.

URINE EXAMINATION
Amount
1. 1200-1500ml/24 HRS. ; Less than 500ml is considered oliguria
2. Day volume 2-3 times more than night volume

Appearance
1. Normal is clear.
2. Turbid (cloudy) urine is not always pathologic. Normal urine may developed turbidity on refrigeration or by standing room temperature; bacteria ferment
quickly at room temerature
3. Abnormally cloudy urine- due to pus, blood, epithelial cells, bacteria, fat, colloidal partical, phosphate and urates.

Odor
1. Normal –Faint aromatic odor
2. Characteristic odors produced by ingestion of asparagus or thymol.
3. Cloudy urine with ammonia in odor- urea splitting bacteria such as proteus, causing urinary tract infection
4. Offensive odor- bacterial action in presence of pus

Color
1. Color shows degree of concentration and depends on amount voided.
2. Normal urine is clear, yellow amber because of the pigment urochrome.
3. Color varies with specific gravity
a. Dilute urine is straw colored.
b. Concentrated urine is highly colored; a sign of insufficient fluid intake
4. Abnormal colored urine
a. Turbid or smoky colored –may be from hematuria, spermatozoa, prostatic fluid, fat droplets, chyle
b. Red or Red-brown- due to blood pigments, porhyria, transfusion reaction, bleeding in the urogenetal tract, some drugs
c. Yellow brown or green-brown- may reveal obstructive lesion of bile duct system, or obstructive jaundice
d. Dark-brown or black- due to malignant melanoma, leukemia.

Reaction (pH)
1. Reflects the ability of kidney to maintain normal hydrogen ion concentration in plasma and extracellular fluid; indicates the acidity or ackalinity of urine.
2. The pH should be measured in fresh urine, since the breakdown of urine to ammonia causes urine to become alkaline.
3. Normal pH is around 6(acid); may normally vary from 4.6 to 7.5
4. Urine acidity or alkalinity has relatively little clinical significance unless the patient is on special diet or therapeutic program or is being treated for renal
calculus disease.
5. Alkaline urine is often cloudy because of phosphate crystals.

Specific gravity
1. Reflects the kidney’s ability to concentrate or dilute urine; may reflect degree of hydration or dehydration
2. Normal specific gravity ranges from 1.005- 1025
3. Specific gravity is fixed at 1.010 in chronic renal failure.
4. In a person eating normal diet , inability to concentrate or dilute urine indicates disease.

Osmolality
1. Osmolality is an indication of the amount of osmotically active particles in urine( specifically, it is the number of particles per volume of water).
2. The unit of osmotic mesure is the osmole
Average Values:
Females: 300- 1090 mOsm./Kg
Males:390-1090 mOsm./kg

Renal function tests

1. Renal concentration test
2. Creatinine clearance
3. Serum creatinine
4. Serum urea nitrogen
Tests the ability to concentrate solutes in the urine.
Provides a reasonable approximation of rate of glomerular filtration.
Balance between production and filtration by renal glomerulus.
Most sensitive test of renal function.
Serves as index of renal excretory capacity.
Urea is the nitrogenous end-product of protein metabolism.

5. Microalbumin Test for development of proteinuria; >30 mcg/mg creatinine predicts early
nephropathy.
6. Urine casts Mucoproteins and other substances present in renal inflammation.
Red cell casts present in glomerulonephritis.
Fatty casts in nephrotic syndrome.
White cell casts in pyelonephritis.
COMMON HEALTH PROBLEM

Congenital Disorder
Patent Urachus
 Patent urachus: A birth defect involving the urachus, a canal connecting the bladder of the fetus with the allantois, a
structure that contributes to the formation of the umbilical cord. The lumen (inside) of the urachus is normally obliterated during
embryonic development, transforming the urachus into a solid cord, a functionless remnant.

Pathology
Failure for the lumen of the urachus to be filled in leaves a patent (open) urachus. The telltale sign is leakage of urine
through the umbilicus. A patent urachus needs to be surgically removed.
Sign and symptoms
The presenting symptoms and signs included pyuria, fever, lower abdominal pain and palpable abdominal mass. Persistent drainage within umbilicus,
omphalitis.

During fetal development the urachus is a tube that connects the bladder to the umbilicus. After birth, the urachus normally closes and becomes a ligament.
If the urachus remains open, surgery is recommended so that bacteria or infection cannot be introduced into the bladder

Patent urachus repair

Patent urachus repair is surgery to repair a bladder defect. Children who have this surgery will receive general anesthesia
(asleep and pain-free). The surgeon will make an incision (cut) in the lower belly. Next the surgeon will locate the urachal tube and
remove it. The bladder opening will be repaired, and the incision will be closed.
The surgery can also be done with a laparoscope, an instrument that has a tiny camera and light on the end.
• The surgeon will make three small incisions in the child’s belly. The surgeon will insert the laparoscope through one of these incisions and other tools
through the other cuts.
• The surgeon uses the tools to remove the urachal tube and close off the bladder and area where the tube connects to the umbilicus. This surgery can be done
in children as young as 6 months.

While the infant is deep asleep and pain-free (using general anesthesia), an incision is made in the lower abdomen, below the
umbilicus.

The outcome is usually excellent. The infant can be fed normally and should recover rapidly. A few days of hospitalization is all that is
usually required.

Horseshoe kidney
Horseshoe kidney, also known as renal fusion, is a congenital disorder affecting about 1 in 400 people. In this disorder,
the patient's kidneys fuse together to form a horseshoe-shape during development in the womb.
Fusion abnormalities of the kidney can be categorized into two groups: horseshoe kidney and crossed fused ectopia. The
horseshoe kidney is the most common renal fusion anomaly.
 Horseshoe kidney

Crossed fuse

Signs and symptoms

About one-third of children will have no symptoms. One-third of individuals with horseshoe kidney will have another
anomaly or other complication involving the cardiovascular, nervous, or genitourinary system. Symptoms will vary depending
upon which body system is involved. The symptoms of horseshoe kidney may resemble other conditions or medical problems.
Always consult your child's physician for a diagnosis.
Associated conditions
1. Kidney Obstruction - abnormal placement of ureter
2. Kidney Infections - associated with vesicoureteral reflux
3. Kidney Stones - slow urine flow and kidney obstruction may lead to kidney stones
4. Kidney Cancer increased risk of renal cancer, especially Wilms' tumor, transitional cell carcinoma, and carcinoid tumor

Laboratory Studies
• Urinalysis with urine culture
• Serum chemistry with creatinine

Imaging Studies
• Intravenous pyelography (IVP)
• CT scanning (CT scanning of the abdomen and pelvis, with and without intravenous contrast) is the best initial radiologic study to determine anatomy and
relative renal function.

Medical Therapy
The horseshoe kidney is susceptible to medical renal disease. These diseases, if present, are treated as indicated. A
metabolic evaluation should be performed because metabolic causes for kidney stone disease are no less common in the patient
with horseshoe kidney than in the general population with kidney stone disease. Any identified metabolic abnormality should be
treated. Metabolic evaluation includes a 24-hour stone risk assessment and serum studies, including calcium, uric acid, and
phosphorous.

Surgical Therapy
Surgical treatment is based on the disease process and standard surgical indications. The anomalous vascular supply to the
kidney should be kept at the forefront of the surgeon's mind when planning the surgical approach. Generally, the midline abdominal
incision provides access to both sides of the horseshoe kidney and vessels.

Phimosis
Phimosis (fī-mō'sĭs,), from the Greek phimos ("muzzle")), is a condition where, in men, the male foreskin cannot be fully retracted from the head of the
penis. The term may also refer to clitoral phimosis in women, whereby the clitoral hood cannot be retracted, limiting exposure of the glans clitoris

Pathological phimosis (as opposed to the natural non-retractability of the foreskin) in childhood is rare and the causes are varied. Some cases may arise
from balanitis (inflammation of the glans penis), perhaps due in turn to inappropriate efforts to separate and retract an infant foreskin. include: scarring caused by
forcible retraction of the foreskin, masturbation practices that differed from the usual pulling down of the foreskin that mimics sexual intercourse.
Symptoms of Phimosis
The foreskin may be red, swollen, and tender.

Treatment of phimosis
1. Non surgical methods include: Application of topical steroid cream for 4-6 weeks to the narrow part of the foreskin,
Stretching of the foreskin can be accomplished manually
2. Circumcision is generally advised when the inflammation clears.
3. Preputioplasty, in which a limited dorsal slit with transverse closure is made along the constricting band of skin
aim of increasing the diameter of the preputial ring but without excising the prepuce (foreskin).

Hypospadias
Hypospadias is a malposition of the urethral opening that may be associated with other urogenital tract abnormalities. It is a rare congenital defect, more
common in males than in females.

Pathophysiology and Etiology

• Possibly caused by decreased testosterone production in early gestation.
• In males, the urethra opens on the ventral aspect of the penis, anywhere along the shaft of the penis, and may deflect the penis downward (chordee).
• In females, the urethra opens into the vagina (rare).
• Undescended testicle, hydrocele, or inguinal hernia may be associated.
• There is an increased chance for incidence with future male children.

Clinical Manifestations
• Inability to void with penis in normal elevated position.
• In females, urine dribbling from vagina.

Diagnostic Evaluation
• Usually not difficult to diagnose because of visual anomaly. Assess glans penis for possible hypospadias before circumcision.
• Severe cases require genotypic/phenotypic sex determination, chromosomal, and hormonal studies.
• Renal ultrasound, IVP, voiding cystourethrography to determine associated defects.

Treatment
Surgical reconstruction before age 1 and before circumcision because foreskin is essential for most repairs.

Complications
Severe forms interfere with reproductive ability.

Epispadias
Epispadias (also called bladder exstrophy) is a congenital defect of males in which the urethra opens on the upper surface (dorsum) of the penis. The
corresponding defect in females is a fissure in the upper wall of the urethra and is quite rare.
Description
In males with epispadias, the urethra opens on the superior surface or upper side of the penis. In females with epispadias, there is a crack or fissure in the
wall of the urethra and out of the body through an opening in the skin above the clitoris.

Treatment
Surgery is the treatment of choice for epispadias. In females, repair of epispadias may require multiple surgical procedures. Urinary continence and cosmetic
appearance are the usual primary considerations.

Prognosis
Most males and female with simple hypospadias and epispadias can lead normal lives with a penis that appears and functions in a normal manner including
conceiving and bearing children.
CRYPTORCHIDISM (UNDESCENDED TESTICLE)
Cryptorchidism refers to the failure of one or both testes to descend through the inguinal canal to the normal position in the scrotum. It is more common in
premature infants and is the most common surgical problem in pediatric urology.

Pathophysiology and Etiology

• Possibly caused by delayed descent, prevention of descent by mechanical lesion, or endocrine disorder (rare).
• Testicular and ductal development are abnormal. It is unclear whether this is because of congenital dysplasia or because of underdevelopment.
• Degeneration of the sperm-forming cells occurs after puberty because of the higher temperatures of the abdomen, compared with normal location in the
scrotum.

Clinical Manifestations
Testicle nonpalpable within the scrotum.

Diagnostic Evaluation
• Ultrasonography may reveal undescended testicle, but not as reliable as physical examination.
• Serum testosterone measurements may be decreased.

Treatment
• Orchiopexy surgery to achieve permanent fixation of the testis in the scrotum. Surgery should be performed between ages 6 and 15 months to prevent
damage to the tissues and to lessen emotional concerns related to body image.
• Plastic surgery in patients with one testicle.
• Administration of human chorionic gonadotropin has produced descent of the testicles in some children. Testicles may have descended spontaneously in
many of these cases.

Complications
• Testicular torsion
• Associated hernias
• Emotional disturbances
• Significant increase in sterility and malignancy later in life

Nursing Assessment
• Obtain history from prenatal and birth record, family, and child.
• Assess feeding and crying patterns, indicating potential obstruction or abdominal pain.
• Assess urinary elimination pattern to determine degree of disorder.
• Assess for associated congenital defects.
• Assess for failure to thrive.
• Determine family's response to body image changes. Expect anxieties regarding sterility and homosexuality and perceptions of the child as defective or
inadequate.
• Measure and record vital signs, height, weight, abdominal girth, and compare with previous measurements, if available. Renal insufficiency may alter
growth. Fever may be indicative of infection.
• Visually and manually inspect genitalia and record abnormalities (eg, if bladder mucosa is visible, describe signs of irritation).
• Palpate abdomen; note masses.
• Obtain urine for culture and sensitivity. Note color, amount, odor, degree of cloudiness.
• Review results of all laboratory and diagnostic procedures.
Nursing Diagnoses
• Deficient Knowledge related to surgery
 • Impaired Urinary Elimination related to the condition and surgical intervention
• Disturbed Body Image related to appearance of genitalia
• Risk for Infection related to surgical incision and drainage tubes
• Risk for Deficient Fluid Volume related to surgical losses
• Acute Pain related to surgical incision and drainage tubes

Nursing Interventions
Promoting Understanding of Surgical Treatment
• Determine the child's expectation regarding illness and hospitalization through discussion and play therapy.
• Explain the anatomy and physiology of the urinary system in terms the child can understand.
o Use a body outline appropriate for the age of the child.
o Explain how the child differs from the normal. Relate defect to symptoms whenever possible.
• Explain all diagnostic tests before their occurrence. These may include urinalysis, 24-hour urine collections, I.V. and retrograde pyelography, angiography,
and cystoscopy. Descriptions should include such information as:
o Preparation required (fasting, enemas.)
o Location of the testâ €”operating room, radiology department.
o Appearance and attire of personnel.
o Positioning.
o Anesthesia.
o Pain or discomfort.
o Expectations after the procedure(diet, rest, urine collections.)
• Determine the child's understanding of the procedure.
o Ask simple, direct questions.
o Allow child to perform the procedure on a doll or to demonstrate it on a diagram.
• Explain the surgical procedure, including the following:
o Preparation required -fasting, enemas.
o Description of the operating room, including the appearance of the personnel.
o Anesthesia.
o Postoperative appearance -urinary drainage tubing and collection devices, appearance of urine, sutures, bandages, I.V. infusion.
• Determine the child's understanding of surgery and reinforce teaching when necessary.
• Emphasize additional points:
o The child is in no way to blame for illness.
o No other part of the body will be operated on.
Promoting Normal Urine Output
• Monitor daily intake and output.
• Encourage adequate fluids and monitor daily weights.
• Care for all catheters and urinary tubes according to facility policy. Maintain appropriate position of tubes.
• Observe and record amount and appearance of urinary drainage, occurrence of bladder spasms, symptoms of urinary or incisional infection.
Providing Emotional Support Regarding Body Image
• Continue reassurance about appearance of genitalia.
• Maintain discussions regarding reactions. This may need to be done with patient and family alone as well as a family unit.
• Discuss plans for interim period from initial surgery until secondary or reconstructive procedures can be performed.
• Initiate independence of care.
• Focus on activities the child can perform and accomplish.
Preventing Infection
• Administer antibiotics and I.V. fluids as ordered.
• Maintain patency of catheters. Provide catheter care as directed.
• Administer wound care using aseptic technique. Inspect incision for drainage or signs of infection.
Maintaining Fluid Volume
• Administer fluids as ordered.
• Monitor vital signs for hypotension or tachycardia.
• Assess patient's skin turgor and mucous membranes for signs of dehydration.
• Measure and record accurate intake and output.
Promoting Comfort
• Administer analgesics as ordered and according to assessment of complaints of pain, restlessness, crying, or withdrawal.
• Administer antispasmodics as ordered for bladder spasm.
• Provide distraction and comfort measures.
Family Education and Health Maintenance
• Advise the family about follow-up appointments, additional surgeries, or procedures.
• Teach care of incision, signs of infection.
• Advise on avoidance of straddle toys for 6 weeks to promote healing.
• Encourage good nutrition to promote healing and to prevent infection.
Evaluation: Expected Outcomes
• Child and family verbalize understanding of surgery
• Clear urine draining via catheter
• Child and family verbalize relief that defects can be surgically repaired and reconstructed
• Incision without drainage or signs of infection
• Vital signs stable; urine output adequate
• Decreased crying and increased restful periods and sleep noted

Hydrocele
Hydrocele is a fluid-filled sack along the spermatic cord within the scrotum. Hydrocele is an accumulation of clear fluid in
the tunica vaginalis, the most internal of membranes containing a testicle.
A primary hydrocele causes a painless enlargement in the scrotum on the affected side and is thought to be due to the
defective absorption of fluid secreted between the two layers of the tunica vaginalis (investing membrane).
A secondary hydrocele is secondary to either inflammation or a neoplasm in the testis.

Alternative Names
Processus vaginalis; Patent processus vaginalis

Causes
Hydroceles are common in newborn infants. During normal development, the testicles descend down a tube from the abdomen into the scrotum. Hydroceles
result when this tube fails to close. Fluid drains from the abdomen through the open tube. The fluid builds up in the scrotum, where it becomes trapped. This causes the
scrotum to become swollen, a hydrocele may be associated with an inguinal hernia.

Hydroceles may also be caused by inflammation or injury of the testicle or epididymis, or by fluid or blood blockage within the spermatic cord. This type of
hydrocele is more common in older men.

Symptoms
The main symptom is a painless, swollen testicle , which feels like a water balloon. A hydrocele may occur on one or both sides. . Large hydroceles cause
discomfort because of their size. As the fluid of a hydrocele is transparent, light shone through a hydrocelic region will be visible from the other side.
Diagnostic test
Physical examination and ultrasound for confirmation.

Treatment
Hydrocelectomy, is often performed to correct a hydrocele. Aspiration may be the best alternative for people who have certain surgical risks but recurrence
rates are high. Sclerotherapy, (thickening or hardening) medications may be injected after aspiration to close off the opening may increase success rates

Complication related to hydrocele surgery may include:

• Blood clots
• Infection
• Injury to the scrotal tissue or structures

Complication related to aspiration and sclerosing may include:

• Infection
• Fibrosis
• Mild-to-moderate pain in the scrotal area

Nursing Intervention
1. Monitor for complications
a. Formation of hematoma in the loose tissue of scrotum
b. Scrotal edema – due to dissection and manipulation
2. Apply ice pack intermmitently to reduce pain.
3. Apply scrotal support for comfort.
Varicocele
Varicocele is an abnormal enlargement of the vein (pampiniform venous plexus) that is in the scrotum draining the testicles. Varicoceles usually occur in
the veins on the upper portion of the left testicle in adults
The testicular blood vessels originate in the abdomen and course down through the inguinal canal as part of the
spermatic cord on their way to the testis. Up-ward flow of blood in the veins is ensured by small one-way valves that prevent
backflow. Defective valves, or compression of the vein by a nearby structure, can cause dilatation of the veins near the testis,
leading to the formation of a varicocele.

Idiopathic varicocele occurs when the valves within the veins along the spermatic cord don't work properly. This
results in backflow of blood into the pampiniform plexus and causes increased pressures, ultimately leading to damage to the
testicular tissue. 98% of idiopathic varicoceles occur on the left side, apparently because the left testicular vein runs vertically
up to the renal vein. They are most frequently diagnosed when a patient is 15–25 years of age

Secondary varicocele is due to compression of the venous drainage of the testicle. A pelvic or abdominal malignancy is a definite concern when a
varicocele is newly diagnosed in a patient older than 40 years of age. The most common cause is hypernephroma then retroprotiniem
adhsion.
Symptoms
• Dragging-like or aching pain within scrotum.
• Feeling of heaviness in the testicle(s)
• Atrophy (shrinking) of the testicle(s)
• Visible or palpable (able to be felt) enlarged vein, likened to feeling a bag of worms.
• Infertility. Although no formal correlation has been established linking Infertility with varicocele, many suggest that the increased temperature within the
testes is the main cause in cases found with infertility

Diagnosis
1. Palpation of the scrotum - non-tender, twisted mass along the spermatic cord is felt.
2. Ultrasound - show dilatation of the vessels of the pampiniform plexus to greater than 2 mm.
3. Doppler ultrasound is a technique of measuring the speed at which blood is flowing in a vessel.

Treatment
Varicocelectomy – (the surgical correction of a varicocele) corrected surgically by ligating the external spermatic vein at the inguinal area (groin),
retroperitoneal (abdominal), and infrainguinal/subinguinal (below the groin).

Nursing Intervention
1. An ice pack may be applied to the scrotum for the first few hours after surgery to relieve edema.
2. The patient then wears a scrotal supporter for comfort.
3. Adviced patient of the following:
a. Notify surgeon if he bleed from operative site.
b. Avoid driving or heavy labor or activity until permitted by the doctor.

Possible complications after surgery

4. hematoma (bleeding into tissues)
 5. infection
6. injury to the artery that supplies the testicle and scrotal tissue or structures.

Prognosis
Varicocele is usually harmless except in cases of infertility. If surgery is required because of infertility or testicular
atrophy, the outlook is usually excellent. Removal of varicocele can lead to normal testicular temperatures and an increased sperm
production. An inguinal hernia can sometimes be misdiagnosed as a varicocele by an untrained eye.

Exstrophy of the Bladder

Exstrophy of the bladder is part of a spectrum of anomalies that involve the urogenital tract, the musculoskeletal system and, occasionally, the intestinal
tract. These occur in approximately 1 in 30,000 to 50,000 deliveries, with the male-to-female ratio 3:1. Hypospadias is an anomaly of the urethra only.
• Results from failure of the abdominal wall and its underlying structures to fuse in utero during the third to fourth week of gestation.
• In classic exstrophy (about 60% of bladder anomalies), the posterior bladder wall is externalized and lies open on the lower part of the abdomen with an
epispadial urethra, allowing constant passage of urine to the outside.
• Epispadias may occur without exstrophy (about 30% of bladder anomalies); the bladder remains an internal organ, but the urethra is laid open, possibly with
a split glans penis and the meatus located proximally..

Clinical Manifestations
• Urine dribbles constantly.
• Infection and ulceration of the bladder mucosa may occur.
• Genitalia may be ambiguous.
• Affected children may walk with a waddling or an unsteady gait.

Diagnostic Evaluation
• Inspection is the most important tool in evaluation. The obvious anomaly may involve multiple systems.
• Diagnostic procedures, such as radiography, ultrasound, cytoscopic examination, urodynamic testing, and IVP determine extent of the anomaly.

Management
• Surgical closure of bladder within first 24 to 48 hours of life.
• Complete correction by school age by means of staged reconstructive and orthopedic surgery.
• Urinary diversion should be rare.

Complications
• Skin excoriation, infection
• Trauma to bladder mucosa

Nursing Assessment
• Assess for growth and development during reconstruction.
• Assess the family for coping ability.

Nursing Diagnoses
• Impaired Urinary Elimination related to anatomical defect
• Risk for Injury related to complications of surgery

Nursing Interventions
Facilitating Urine Output Preoperatively
• Protect the bladder area from trauma and infection.
o Keep the infant in an Isolette to avoid irritation from clothing and blankets. Position on back or side.
o Humidity to exposed bladder using hood: may cover area with wet gauze, when out of Isolette, for feeding.
o Change bed linen frequently to maintain skin integrity.
• Observe the infant closely for signs of infection.
• Involve other members of the health care team for parental support because of the psychosocial implications of a child who has special needs.
• Assist the parents in dealing with their emotional reactions regarding the child's defect.
 • Prepare child and parents for the proposed surgery

Providing Postoperative Care to Prevent Complications

• Provide care for the ureteral and urethral catheters. Observe and record the amount of urinary drainage, catheter positions, and bladder spasms.
• Care for the child, who is placed in a body cast for several weeks or in a traction system
• Provide care and instruction for an ileal conduit as necessary
• Observe for complications.
o Urinary or incisional infections
o Fistulae in the suprapubic or penile incisions
• Recommend long-term support for children and families to help them deal with such fears as appearance of genitalia, potential inability to reproduce,
rejection by peers, and sexual function. Ongoing discussion groups for parents and children may be helpful.
• Teach the parents how to care for the child at home and make appropriate referrals.

Family Education and Health Maintenance

• Provide community nursing referral as needed to support family and make sure that family understands the importance of follow up with the various
specialists.
• Act as a liaison as necessary to coordinate care.
Evaluation: Expected Outcomes
• No skin breakdown or infection
• Incision healing well without fistula

Renal Agenesis
Renal agenesis is a medical condition in which one (unilateral) or both (bilateral) kidneys fail to develop in the fetus and are absent at birth.
Unilateral renal agenesis much more common, but is not usually of any major health consequence, as long as the other kidney is healthy. Adults with
unilateral renal agenesis have considerably higher chances of hypertension (high blood pressure). People with this condition are advised to approach contact sports with
caution.
Bilateral renal agenesis is the uncommon and serious failure of both a fetus' kidneys to develop during gestation, and is one causative agent of Potter
sequence. This absence of kidneys causes oligohydramnios, a deficiency of amniotic fluid in a pregnant woman. The condition more common in infants (male) born
to one or more parents with a malformed or absent kidney.

Prognosis
In the absence of kidney injury or disease, unilateral renal agenesis usually lead normal healthy lives. Bilateral renal agenesis has a very poor prognosis. It is
usually fatal in the first few days of life. The usual cause of death is respiratory failure and acute renal failure during the neonatal period.

o Preparation required (fasting, enemas.)

o Location of the testâ €”operating room, radiology department.
o Appearance and attire of personnel.
o Positioning.
o Anesthesia.
o Pain or discomfort.
o Expectations after the procedure(diet, rest, urine collections.)
• Determine the child's understanding of the procedure.
o Ask simple, direct questions.
o Allow child to perform the procedure on a doll or to demonstrate it on a diagram.
• Explain the surgical procedure, including the following:
o Preparation required -fasting, enemas.
o Description of the operating room, including the appearance of the personnel.
o Anesthesia.
o Postoperative appearance -urinary drainage tubing and collection devices, appearance of urine, sutures, bandages, I.V. infusion.
• Determine the child's understanding of surgery and reinforce teaching when necessary.
• Emphasize additional points:
o The child is in no way to blame for illness.
o No other part of the body will be operated on.
Promoting Normal Urine Output
• Monitor daily intake and output.
• Encourage adequate fluids and monitor daily weights.
• Care for all catheters and urinary tubes according to facility policy. Maintain appropriate position of tubes.
• Observe and record amount and appearance of urinary drainage, occurrence of bladder spasms, symptoms of urinary or incisional infection.
Providing Emotional Support Regarding Body Image
• Continue reassurance about appearance of genitalia.
• Maintain discussions regarding reactions. This may need to be done with patient and family alone as well as a family unit.
• Discuss plans for interim period from initial surgery until secondary or reconstructive procedures can be performed.
• Initiate independence of care.
• Focus on activities the child can perform and accomplish.
Preventing Infection
 • Administer antibiotics and I.V. fluids as ordered.
• Maintain patency of catheters. Provide catheter care as directed.
• Administer wound care using aseptic technique. Inspect incision for drainage or signs of infection.
Maintaining Fluid Volume
• Administer fluids as ordered.
• Monitor vital signs for hypotension or tachycardia.
• Assess patient's skin turgor and mucous membranes for signs of dehydration.
• Measure and record accurate intake and output.
Promoting Comfort
• Administer analgesics as ordered and according to assessment of complaints of pain, restlessness, crying, or withdrawal.
• Administer antispasmodics as ordered for bladder spasm.
• Provide distraction and comfort measures.
Family Education and Health Maintenance
• Advise the family about follow-up appointments, additional surgeries, or procedures.
• Teach care of incision, signs of infection.
• Advise on avoidance of straddle toys for 6 weeks to promote healing.
• Encourage good nutrition to promote healing and to prevent infection.

Evaluation: Expected Outcomes

• Child and family verbalize understanding of surgery
• Clear urine draining via catheter
• Child and family verbalize relief that defects can be surgically repaired and reconstructed
• Incision without drainage or signs of infection
• Vital signs stable; urine output adequate
• Decreased crying and increased restful periods and sleep noted

FLUIDS AND ELECTROLYTES

THE BODY FLUIDS

 A solution of solvent and solutes
 Our body is made up of fluids and solids
 About 50-60% of the body weight is WATER
 Note that 1 kg body weight= 1 liter of water
 The body has two major compartments:
1 Intracellular
2. Extracellular
FLUID BALANCE
 A solution of solvent and solutes
 Our body is made up of fluids and solids
 About 50-60% of the body weight is WATER
 Note that 1 kg body weight= 1 liter of water
 The body has two major compartments:
1 Intracellular
2. Extracellular

THE PROPORTION OF BODY FLUIDS

Intracellular fluid
40% Interstitial
15%
 Intravascular
5%

Transcellular
1-2%

INTRACELLULAR FLUID

 Found inside the cell surrounded by a membrane.

 This is compartment with the highest percentage
of water in adults.

THE EXTRACELLULAR FLUIDS

 Fluid found outside the cells

1. INTERSTITIAL FLUID
¬ Found in between the cells
2. INTRAVASCULAR FLUID
¬ Found inside the blood vessels and lymphatic vessels
3. TRANSCELLULAR FLUID
¬ Found inside body cavities like pleura, peritoneum, CSF

FLUID BALANCE

TOTAL BODY WATER (AS PERCENTAGE OF BODY WEIGHT) IN RELATION TO AGE AND SEX

AGE MALE FEMALE

Under 18 65% 55%

18-40 60% 50%
40-60 50-60% 40-50%
Over 60 50% 40%

INTRACELLULAR FLUID COMPARTMENT

 Includes all the water and electrolytes inside the cells of the body.
 Approximately 63% of the total body water is contained within cell membranes.
 Contains high concentrations of potassium, phosphate, magnesium and sulfate ions, along with most of the proteins in the body.

EXAMPLE: How much water is in the intracellular fluid compartment of a 25-year old male patient who weighs 60 kg?

Step #1: Compute the total body water (TBW) based on age and sex.

TBW = (60 kg) (0.6)

= 36 kg ◊ weight of water
= 36 liters ◊ volume of water

Step #2: Compute for the intracellular fluid volume (usually 63% of the total body water is intracellular fluid)
ICF = (36 liters) (0.63)
= 22.7 liters

EXTRACELLULAR FLUID COMPARTMENT

 Includes all the fluid outside the cells: interstitial fluid, plasma, lymph, secretions of glands, fluid within subcompartments separated by epithelial
membranes.
 Constitutes approximately 37% of the total body water.
 Contains high concentrations of sodium, chloride and bicarbonate.
 One-third of the ECF is in plasma.

EXAMPLE: How much water is in the circulatory system of a 32-year old female patient who weighs 52 kg?

Step #1: Compute for the total body water based on age and sex.
TBW = (52 kg) (0.5)
= 26 kg ◊ weight of water
= 26 liters ◊ volume of water

Step #2: Compute for the extracellular fluid volume (usually 37% of the total body water).
ECF = (26 liters) (0.37)
= 9.6 liters
 Step #3: Compute for the plasma volume.
Plasma = (9.6 liters)/3
= 3.2 liters

FLUID DYNAMICS

The movement of fluids (solutes and solvents) in the body compartment

 Diffusion
 Osmosis
 Filtration
 Active transport

THE CONCEPT OF TONICITY

 This is the concentration of solutes in a solution.

 A solution with high solute concentration is considered as HYPERTONIC.
 A solution with low solute concentration is considered as HYPOTONIC.
 A solution having the same tonicity as that of body fluid or plasma is considered ISOTONIC.

HELPFUL HINTS

 In a HYPERTONIC solution, fluid will go out from the cell, the cell will shrink.
 In a HYPOTONIC solution, fluid will enter the cell, the cell will swell.
 In an ISOTONIC solution, there will be no movement of fluid.

DIFFUSION

 The movement of SOLUTES or particles in a solution from a higher concentration to a lower concentration.
 If a sugar is placed in plain water, the glucose molecules will dissolve and diffuse distribute in the solution.

OSMOSIS

 The force that draws water or solvent from a less concentrated solution into a more concentrated solution through a semi-permeable membrane.
 The pressure that draws water inside the vessel which is more concentrated is called Osmotic pressure.
 A special type of osmotic pressure is exerted by the proteins in the plasma. It is called ONCOTIC PRESSSURE.

FILTRATION

 The movement of both solute and solvent by hydrostatic pressure, ie, from an area of a higher pressure to an area of a lower pressure.
 An example of this process is urine formation.
 Increased hydrostatic pressure is one mechanism producing edema.

ACTIVE TRANSORT

 This is the movement of solutes across a membrane from a lower concentration to a higher concentration with utilization of energy.
 Example is the Sodium-Potassium pump- a primarily active transport process.

SERUM OSMOLALITY

 Reflects the amount of solute particles in a solution and is a measure of the concentration of a given solution.
 Can be calculated using the formula:
Osmserum = 2 (Na) + BUN + glucose
Normal value = 285 – 295 mosm/kg

 Sodium is the most active determinant of serum osmolality and is therefore actively moved across membranes to ensure normal osmolality.

NORMAL VALUES AND MASS CONVERSION

FACTORS

Normal Plasma Mass Conversion

Values

Sodium 135 – 145 meq/L 23 mg = 1 meq

(Na+)

Potassium 3.5 – 5.0 meq/L 39 mg = 1 meq

(K+)
 Chloride 98 – 107 meq/L 35 mg = 1 meq
(Cl-)

Bicarbona 22 – 26 meq/L 61 mg = 1 meq

te (HCO3-)

Calcium 8.5 – 10.5 mg/dL 40 mg = 1 mmol

(Ca2+)

Phosphoru 2.5 – 4.5 mg/dL 31 mg = 1 mmol

s

Magnesiu 1.8 – 3.0 mg/dL 24 mg = 1 mmol

m (Mg2+)

Osmolality 285 – 295 -

mosm/kg
265 - 305
mosm/kg

THE CATIONS

• Sodium
• Potassium
• Magnesium
• Calcium

SODIUM

 The MOST ABUNDANT cation in the ECF

 Normal range is 135-145 mEq/L
 Major contributor of plasma osmolarity

FUNCTIONS

 1. participates in the Na-K pump

 2. assists in maintaining blood volume
 3. assists in nerve transmission and muscle contraction
 Aldosterone◊ increases sodium retention

 ANF◊ increases sodium excretion

 Dominant extracellular ion.
 About 90 to 95% of the osmotic pressure of the extracellular fluid results from sodium ions and the negative ions associated with them.
 Recommended dietary intake is less than 2.5 grams per day.
 Kidneys provide the major route by which the excess sodium ions are excreted.
 In the presence of aldosterone, the reabsorption of sodium ions in the loop of Henle is very efficient. When aldosterone is absent, the reabsorption of
sodium in the nephron is greatly reduced and the amount of sodium lost in the urine increases.
 Also excreted from the body through the sweat mechanism.
 Primary mechanisms that regulate the sodium ion concentration in the extracellular fluid:
 Changes in the blood pressure
 Changes in the osmolality of the extracellular fluid

POTASSIUM

 MOST ABUNDANT cation in the ICF

 Normal range is 3.5-5.0 mEq/L
 Major electrolyte maintaining ICVF balance

FUNCTIONS
 1. maintains ICF Osmolality
  2. nerve conduction and muscle contraction
 3. metabolism of carbohydrates, fats and proteins
 Aldosterone promotes renal excretion of K+
 Acidosis promotes exchange of K+ for H+ in the cell
 Electrically excitable tissue such as muscle and nerves are highly sensitive to slight changes in extracellular potassium concentration.
 The ECF concentration of potassium must be maintained within a narrow range for tissues to function normally.
 Aldosterone also plays a major role in regulating the concentration of potassium ions in the ECF.

 Circulatory system shock resulting from plasma loss, dehydration, and tissue damage causes extracellular potassium ions to become more concentrated than
normal. In response, aldosterone secretion increases and causes potassium secretion to increase.

CALCIUM

 Majority of calcium is in the bones and teeth

 Normal serum range 8.5-10 mg/dL

FUNCTIONS
 1. formation and mineralization of bones/teeth
 2. muscular contraction and relaxation
 3. cardiac function
 4. blood clotting
 5. enzyme activation

Regulation:
 GIT◊ absorbs Ca+ in the intestine with the help of Vit. D

 Kidney◊ Ca+ is filtered in the glomerulus and reabsorbed

in the tubules
 PTH◊ increases Ca+ by bone resorption, Ca+ retention
and activation of Vitamin D
 Calcitonin◊ released when Ca+ is high, it decreases Ca+
by excretion in the kidney
 Extracellular concentration of calcium ions is maintained within a narrow range.
 Increases and decreases in ECF concentration of calcium ions have dramatic effects on the electrical properties of excitable tissues.
 Parathyroid hormone (PTH) secreted by the parathyroid glands increases extracellular calcium levels.
 Calcitonin is secreted by the thyroid gland.
 It reduces blood levels of calcium when they are too high.

MAGNESIUM

 Second to K+ in the ICF

 Normal range is 1.3-2.1 mEq/L

FUNCTIONS
 1. intracellular production and utilization of ATP
 2. protein and DNA synthesis
 3. neuromuscular irritability

THE ANIONS

 CHLORIDE
 PHOSPHATES
 BICARBONATES

CHLORIDE

 The MAJOR Anion in the ECF

 Normal range is 95-108 mEq/L

FUNCTIONS
 1. major component of gastric juice aside from H+
 2. together with Na+, regulates plasma osmolality
 3. participates in the chloride shift
 4. acts as chemical buffer

PHOSPHATES
  The MAJOR Anion in the ICF
 Normal range is 2.5-4.5 mg/L

FUNCTIONS
 1. component of bones
 2. needed to generate ATP
 3. components of DNA and RNA
 PTH◊ decreases PO4 in blood by renal excretion

 Calcitonin◊ increases renal excretion of PO4

BICARBONATES

 Present both in ICF and ECF

 Normal range- 22-26 mEq/L

FUNCTION
 1. regulates acid-base balance
 2. component of the bicarbonate-carbonic acid
buffer system

PHOSPHATE AND SULFATE

 Phosphate and sulfate are reabsorbed by active transport in the kidneys.

 Rate of reabsorption is slow, so that if the concentration of these ions in the filtrate exceeds the ability of the nephron to reabsorb them, the excess is excreted
in the urine.

REGULATION OF BODY FLUID BALANCE

1. The Kidney

 Regulates primarily fluid output by urine formation

 Releases RENIN
 Regulates sodium and water balance

2. Endocrine regulation

 Regulates primarily fluid intake by thirst mechanism

 ADH◊ increase water reabsorption on collecting duct

 Aldosterone◊ increases Sodium retention in the distal nephron

 ANF◊ Promotes Sodium excretion and inhibits thirst mechanism

3. Gastro-intestinal regulation

 The GIT digests food and absorbs water

 Only about 200 ml of water is excreted in the fecal material per day

THE ELECTROLYTES

 Electrolytes are charged ions capable of conducting electricity and are solutes in all compartments.
 ANIONS are Negatively charged ions: Bicarbonate, chloride, PO4-
 CATIONS are positively charged ions: Sodium, Potassium, magnesium, calcium.

HELPFUL PNEMONICS

 PI-SO
 Potassium is inside
 Phosphate is inside
 Sodium is outside
 Chloride is outside

REGULATION OF ELECTROLYTE BALANCE

1. Renal regulation
 Occurs by the process of glomerular filtration, tubular reabsorption and tubular secretion.
 Urine formation
  If there is little water in the body, it is conserved.
 If there is water excess, it will be eliminated.

2. Endocrinal regulation
 Hormones play a role in electrolyte regulation
 Aldosterone◊ promotes Sodium retention and Potassium excretion

 ANF◊ promotes Sodium excretion

 Parathormone◊ promotes Calcium retention and Phosphate excretion

 Calcitonin◊ promotes Calcium excretion and Phosphate excretion

FLUID AND ELECTROLYTE MANAGEMENT

GENERAL MANAGEMENT OF FLUIDS

Sources of fluids:
Fluid Input
1. Exogenous sources
 Fluid intake- water from foodstuffs
 IVF
 Medications
 Blood products

2. Endogenous sources
 By products of metabolism
 Secretions

FLUID LOSSES
Routes of Fluid output
 Urine
 Fecal losses
 Sweat
 Insensible losses though the skin and lungs as
water vapor

MAINTENANCE THERAPY

MINIMUM WATER REQUIREMENTS

 Can be estimated from the sum of the urine output necessary to excrete the daily solute load (500 mL per day if the urine concentrating ability is normal)
plus the insensible water losses from the skin and respiratory system (500 to 1000 mL per day), minus the amount of water produced from endogenous
metabolism (300 mL per day)
 Two to three liters of water are needed to produce a urine volume of 1 to 1.5 liters daily.

Fluid / Electrolyte Replacement:

Insensible Water Losses

 Usually average 500 to 1000 mL daily, and depend on respiratory rate, ambient temperature, humidity and body temperature.
 Water losses increase by 100 ml daily for each degree of body temperature over 37°C.
 Fluid losses from sweating can vary enormously and depend on physical activity and body and ambient temperature.
 Mechanical ventilation accentuate losses from the respiratory tract.

Maintenance Therapy:

Minimum Water Requirements

 Weighing the patient daily is the best means of assessing net gain or loss of fluid, since the gastrointestinal, renal and insensible fluid losses of the
hospitalized patient are unpredictable.

ECF VOLUME DEPLETION

 Occurs with losses of both sodium and water.

 The character of the fluid loss will dictate the clinical picture. If the loss is isotonic, the osmolality is unaffected and intracellular volume will change
minimally.
 Loss of hypotonic fluid will lead to an increase in serum or plasma osmolality.
 Manifestations of ECF volume depletion depend on the magnitude and on serum osmolality.
 Symptoms:
 Anorexia
 Nausea
  Vomiting
 Apathy
COMMONLY USED PARENTERAL SOLUTIONS  Weakness
 Orthostatic lightheadedness
IV Osmolality Glucose Sodium Chloride  Syncope
Solutions (mosm/kg) (g/liter) (meq/liter) (meq/liter)
 Weight loss is an important sign and provides an estimate of the magnitude of
the volume deficit.
5% D/W 252 50 - -  Other physical findings:
 Orthostatic hypotension
10% 505 100 - -  Poor skin turgor
D/W
 Sunken eyes
50% 2525 500 - -  Absence of axillary sweat
D/W  Oliguria
0.45% 154 - 77 77  Tachycardia
NaCl  Shock and coma (severe volume depletion)
 Causes of ECF volume depletion:
0.9% 308 - 154 154  Gastrointestinal losses
NaCl
 Diuretics
3% 1026 - 513 513  Renal or adrenal disease
NaCl  Blood loss
Ringer’s 282 - 130 109  Sequestration of fluid
lactate
TREATMENT:
5% 294 50 147 147
D/NR  Should be directed at restoration of the ECF volume with solutions containing
the lost water and electrolytes.
5% 290 50 77 77  Daily assessment of weight, ongoing fluid losses and serum electrolyte
D/NM concentrations.
 Mild degrees of volume depletion can be corrected orally.
 More severe deficits accompanied by circulatory compromise should be treated initially through intravenous isotonic fluid replacement until hemodynamic
stability has been restored. One to two liters of fluid should be given over the first hour.
 Further therapy should be guided by the symptoms and signs.

PARENTERAL SOLUTIONS

ECF VOLUME EXCESS

Manifestations:

• Weight gain is the most sensitive and consistent sign of ECF volume excess.
• Edema is usually not apparent until 2 to 4 kg of fluid have been retained.
• Dyspnea
• Tachycardia
• Jugular venous distention
• Hepatojugular reflux
• Rales on pulmonary auscultation

Causes:

• Heart, liver or renal failure

• Excessive renal sodium and water retention
• Unnecessary salt administration

TREATMENT:

 Must address not only the ECF volume excess but also the underlying pathologic process.
  Treatment of the nephrotic syndrome and the cardiovascular volume overload associated with renal failure.
 Treatment of heart failure and cirrhosis.

FLUID AND ELECTROLYTE MANAGEMENT

SODIUM

 The primary extracellular cation.

 Always accompanies water in the extracellular fluid compartment.

Hyponatremia

 Defined as serum concentration less than 135 meq/L.

 Most common electrolyte abnormality observed in a general hospitalized population.
 Initial approach is the determination of serum osmolality.

TREATMENT

• Hypertonic (3%) saline with furosemide is indicated for symptomatic hyponatremic patients.

• For asymptomatic patients, approach includes water restriction, isotonic saline infusion and administration of
demeclocycline.

HYPERNATREMIA

 Serum sodium > 145 meq/L

 Develops from excess water loss, frequently accompanied by an impaired thirst mechanism.

TREATMENT:

 Directed toward correcting the cause of the fluid loss and replacing water and, as needed, electrolytes.
 Calculation of water deficit:
 When calculating fluid replacement, both the deficit and the maintenance requirement should be added to each 24-hour replacement regimen.
 Calculation of water deficit (cont’d)
Water deficit =

current TBW x ([Na] – 140)

140
where [Na] is the measured serum sodium and TBW is the total body water (as percentage of the total body weight based on age and sex.

FLUID AND ELECTROLYTE MANAGEMENT

POTASSIUM

Hypokalemia

 A total body deficit of about 350 meq occurs for each 1 meq/L decrement in serum potassium concentration.
 Changes in blood pH and hormones (insulin, aldosterone, and β-adrenergic agonists) independently affect serum potassium levels.
Clinical Findings:

 Symptoms and Signs:

 Muscular weakness
 Fatigue
 Muscle cramps
 Constipation or ileus
 Flaccid paralysis, hyporeflexia, and rhabdomyolysis

 Laboratory Findings:
 Decreased amplitude and broadening of the T waves
 Prominent U waves
 Depressed ST segments
 T wave inversion
 Atrioventricular block (1st, 2nd, 3rd degree AV blocks)
 Cardiac arrest

Note: Hypokalemia also increases the likelihood of digitalis toxicity

TREAT MENT

 Safest way is with oral potassium.

 Intravenous replacement is indicated for patients with severe hypokalemia.
 If serum potassium is > 2.5 meq/L, and there are ECG abnormalities, potassium can be given at a rate of 10 meq/L/hr in concentration that should never
exceed 80 meq/L.
 For severe deficiency, potassium may be given through a intravenous cutdown.
 Occasionally, hypokalemia may be refractory to potassium replacement. Magnesium deficiency may make potassium correction more difficult.
Concomitant magnesium repletion avoids this problem.

Hyperkalemia

 Many are spurious or associated with acidosis

 Common practice of repeatedly clenching and unclenching the fist during venipuncture may raise the potassium concentration by 1-2 meq/L by causing local
release of potassium from forearm muscles.

CAUSES OF HYPERKALEMIA

1.SPURIOUS
• Leakage from erythrocytes if separation of serum from clot is delayed.

• Thrombocytosis

• Marked leukocytosis

• Repeated fist clenching during phlebotomy

• Specimen drawn from arm with infusion

2.DECREASED EXCRETION
• Renal failure, acute and chronic

• Severe oliguria

• Renal secretory defects

• Adrenocortical insufficiency

• Hyporeninemic hypoaldosteronism

• Spironolactone, Triamterene, ACE-I, Trimethoprim, NSAIDs

3.SHIFT FROM TISSUES

• Burns, rhabdomyolysis, hemolysis

• Metabolic acidosis
 • Hyperosmolality

• Insulin deficiency

• Hyperkalemic periodic paralysis

• Succinylcholine, arginine, digitalis toxicity, beta-adrenergic blockers

4.EXCESSIVE INTAKE
Over treatment, orally or parenterally
CLINICAL FINDINGS
ϖ Weakness and flaccid paralysis

ϖ Abdominal distention and diarrhea

ϖ ECG is not a sensitive method, but if abnormalities are present, the most common findings are:

¬ Peaked T waves

¬ ST segment elevation

¬ Tachyarrhythmia / supraventricular tachycardia

¬ Ventricular tachycardia

¬ Ventricular fibrillation

¬ Cardiac arrest

TREATMENT
 Confirm that the elevated level of serum potassium is genuine.

 Measure plasma potassium.

 Withholding of potassium.

 Giving cation exchange resins by mouth or enema: polystyrene sulfate, 40-80 g/day in divided doses.

 Emergent treatment is indicated if cardiac toxicity or muscular paralysis is present, or if hyperkalemia is severe (> 6.5-7 meq/L) even in the absence of ECG
changes.

 Insulin plus 10-50% glucose may be employed to deposit potassium with glycogen in the liver.

 Calcium may be given intravenously as an antagonist ion.

 Stimulate transcellular shifts by giving beta-adrenergic agonist drugs.

 Sodium bicarbonate as an emergency measure.

 Hemodialysis or peritoneal dialysis.

FLUID ELECTROLYTE MANAGEMENT

CALCIUM
 Constitute 2% of body weight, but only 1% of the total body calcium is in solution in body fluid.

 In plasma, calcium is present as a non-diffusible complex with protein (33%); as a diffusible but undissociated complex with anions like citrate, bicarbonate,
and phosphate (12%); and as ionized calcium (55%).

 Normal total plasma (or serum) calcium concentration is 8.5 to 10.5 mg/dL.

 It is the ionized calcium that is necessary for muscle contraction and nerve function (normal: 4.7 to 5.3 mg/dL).

Hypocalcemia
 Seen commonly in critically ill patients due to acquired defects in parathyroid-vitamin D axis.

 Results occasionally in hypotension which responds to calcium replacement therapy.

CAUSES OF HYOCALCEMIA
1.DECREASED INTAKE OR ABSORPTION
ϖ Malabsorption

ϖ Small bowel bypass, short bowel

ϖ Vitamin D deficit

2.INCREASED IONS
ϖ Alcoholism

ϖ Chronic renal insufficiency

ϖ Diuretic therapy (furosemide or bumetanide)

3.ENDOCRINE DISEASES
ϖ True and pseudohypoparathyroidism

ϖ Calcitonin hypersecretion

4.PHYSIOLOGIC CAUSES
ϖ Alkalosis and decreased response to vit. D

ϖ Decreased serum albumin

ϖ Hyperphosphatemia

ϖ Aminoglycosides, loop diuretics, foscarnet

CLINICAL FINDINGS
Symptoms and Signs:
ϑ Extensive spasm of skeletal muscle causing cramps and tetany

ϑ Laryngospasm with stridor

ϑ Convulsions with paresthesias of the lips and extremities

ϑ Abdominal pain

ϑ Chvostek’s sign

ϑ Trousseau’s sign

Laboratory Findings
¬ Low serum calcium

¬ Elevated serum phosphorus

¬ Low serum magnesium

¬ Prolonged QT interval on the ECG

TREATMENT
ϑ Severe symptomatic hypocalcemia:

 In the presence of tetany, arrhythmias or seizures, calcium gluconate 10% is administered intravenously for 10-15
minutes or via calcium infusion.

 10-15 mg of calcium per kilogram body weight, or 6-8 10-ml vials of 10% calcium gluconate (558-744 mg of calcium) is
added to 1 liter of D5W and infused over 4 to 6 hours.

ϑ Asymptomatic hypocalcemia:
  Oral calcium and vitamin D preparations

 Calcium carbonate is well tolerated and inexpensive.

Hypercalcemia
CAUSES OF HYPERCALCEMIA
1.INCREASED INTAKE OR ABSORPTION
ϖ Milk-alkali syndrome

ϖ Vitamin D or vitamin A excess

2. ENDOCRINE DISORDERS
ϖ Primary and secondary hyperparathyroidism

ϖ Acromegaly

ϖ Adrenal insufficiency

3. NEOPLASTIC DISEASES
ϑ Tumors producing PTH-related proteins

ϑ Metastases to bone

ϑ Lymphoproliferative disease

ϑ Secretion of prostaglandins and osteolytic factors

4. MISCELLANEOUS CAUSES
ϑ Thiazide diuretics and renal transplant complications

ϑ Sarcoidosis and Paget’s disease of the bone

ϑ Hypophosphatasia, immobilization, iatrogenic

Clinical Findings
ϑ Symptoms and Signs:

¬ Polyuria and constipation

¬ Stupor, coma and azotemia

¬ Ventricular extrasystoles and idioventricular rhythm

ϑ Laboratory Findings:

¬ Significant elevation of serum calcium

¬ Serum phosphorus may or may not be elevated

¬ Shortened QT interval on the ECG

TREATMENT
 Renal excretion of calcium is promoted by giving saline with furosemide.

 Treatment of underlying condition.

FLUID AND ELECTROLYTE MANAGEMENT

MAGNESIUM
 About 50% of total body magnesium exists in the insoluble state in bone.

 Only 5% is present as extracellular cation; the remaining 45% is contained in cells as intracellular cation.

 Normal plasma concentration is 1.5-2.5 meq/L, with about one-third bound to protein and two-thirds existing as free cation.

 Excretion is via the kidney.

Hypomagnesemia
 Nearly half of hospitalized patients have unrecognized hypomagnesemia.

 In critically ill patients, arrhythmias and sudden death may be complications.

CAUSES OF HYOMAGNESEMIA
1. DIMINISHED ABSORPTION OR INTAKE
¬ Malabsorption, chronic diarrhea, laxative abuse

¬ Prolonged gastrointestinal suction

¬ Small bowel bypass, malnutrition

¬ Alcoholism, parenteral alimentation

2. INCREASED LOSS
 DKA, diuretic therapy, diarrhea

 Hyperaldosteronism, Bartter’s syndrome

 Hypercalciuria

 Renal magnesium wasting

3. UNEXPLAINED
ϑ Hyperparathyroidism

ϑ Postparathyroidectomy

ϑ Vitamin D therapy

ϑ Aminoglycoside antibiotics, cisplatin, amphotericin B

CLINICAL FINDINGS
 Symptoms and Signs:

 Weakness

 Muscle cramps

 CNS hyperexcitability with tremors

 Athetoid movements

 Jerking, nystagmus

 Positive Babinski response

 Hypertension, tachycardia and ventricular arrhythmias

 Confusion and disorientation

LABORATORY FINDINGS
 Decreased serum magnesium levels

 Hypocalcemia and hypokalemia

 Prolonged QT interval on the ECG

 Lengthening of the ST segment on the ECG

TREATMENT
 Use of IVF containing magnesium as chloride or sulfate, 240-1200 mg/day (10-50 mmol/day) during the period of severe deficit, followed by 120 mg/day (5
mmol/day) for maintenance.

 MgSO4 may also be given intramuscularly in a dosage of 200-800 mg/day (8-33 mmol/day) in four divided doses.

 Serum levels must be monitored.

Hypermagnesemia
 Almost always the result of renal insufficiency and the inability to excrete what has been taken in from food or drugs, especially antacids and laxatives.

 Potentially life-threatening as it impairs both central nervous system and muscular function.

CLINICAL FINDINGS
 Symptoms and Signs:

 Muscle weakness

 Mental obtundation and confusion

 Hypotension

 Respiratory muscle paralysis or cardiac arrest

 Laboratory Findings:

 Elevated serum magnesium, BUN, creatinine, K

 Decreased serum calcium

 Increased PR interval on the ECG

 Broadened QRS complex with elevated T waves

TREATMENT
 Alleviating renal insufficiency

 Administration of calcium

 Hemodialysis or peritoneal dialysis

FLUID AND ELECTROLYTE MANAGEMENT

ACID BASE DISTURBANCES
Arterial Blood Gases
 Regulation of pH is accomplished by:

 Kidneys

 Lungs

 Buffer systems

 Information obtained from the arterial blood gas measurements:

 pH

 Partial pressure of carbon dioxide (pCO2)

 Partial pressure of oxygen (pO2)

 HCO3 level

 Oxygen saturation (O2Sat)

NORMAL VALUES
 pH = 7.35 – 7.45
  pCO2 = 35 – 45 mmHg

 pO2 = 80 – 100 mmHg

 HCO3 = 22 – 26 meqs/L

 O2Sat > 95%

Steps in obtaining an ABG specimen:

ϑ Check the bleeding parameters of the patient.

Prepare the following:

 Glass syringe

 Heparin (1,000 units/mL)

 Alcohol

 Cotton balls (soaked with alcohol AND dry)

 Container with ice water

ϑ Aspirate 1 mL of heparin using a glass syringe

ϑ Coat the inner surface of the syringe with heparin, taking care to pull and push the plunger to make sure
heparin evenly coats the syringe.

ϑ Expel the excess heparin from the syringe.

ϑ Palpate for the radial pulse.

ϑ With the needle directed at a slight angle from the vertical, and pointed cephalad, gradually puncture the site
and wait for arterial blood to rush in.

ϑ After obtaining the specimen, secure the needle and place the syringe with the specimen in ice water.

ϑ Apply direct pressure on the puncture site for at least one minute, or until bleeding stops using a dry sterile
cotton ball.

ϑ Send the specimen directly to the laboratory.

ϑ A sample is allowed to stand for a maximum of two hours only.

ACID BASE CONCEPTS

Acid- substance that can donate or release hydrogen ions
 Carbonic acid, Hydrochloric acid

Base- substance that can accept hydrogen ions

 Bicarbonate

Buffer- substance that can accept or donate hydrogen

 Hemoglobin buffer

 Bicarbonate : carbonic acid buffer

 Phosphate buffer

Acid- substance that can donate or release hydrogen ions

 Carbonic acid, Hydrochloric acid

Base- substance that can accept hydrogen ions

 Bicarbonate

Buffer- substance that can accept or donate hydrogen

 Hemoglobin buffer
  Bicarbonate : carbonic acid buffer

 Phosphate buffer

HELPFUL HINTS
 Carbon dioxide is considered to be ACID because of its relationship with carbonic acid

 pH measures the degree of acidity and alkalinity. It is inversely related to Hydrogen. Normal ph 7.35-7.45

 Decreased pH- ACIDIC-increased Hydrogen—pH below 7.35

 Increased pH- ALKALOSIS-decreased hydrogen—pH above 7.45

REMEMBER
 a high hydrogen◊ acidic◊ pH is low

 a low hydrogen◊ alkalosis◊ pH is high

 a high CO2◊ may mean acidic

 a low CO2◊ may mean alkalosis

DYNAMICS OF ACIDS AND BASES

 Acids and bases are constantly produced in the body.

 They must be constantly regulated.

 CO2 and HCO3 are crucial in the balance.

 A ratio of 20:1 is maintained (HCO3:H2CO3)

 Respiratory and renal system are active in regulation.

WAYS TO BALANCE ACID AND BASES

Excretion
 Acid can be excreted, and Hydrogen can be excreted in ACIDOTIC condition.

 Bicarbonate can be excreted in ALKALOTIC condition.

Production
 Bicarbonate can be produced in ACIDOTIC condition.

 Hydrogen can be produced in ALKALOTIC condition.

The respiratory system compensates for metabolic problems

 CO2 (acid) can be exhaled from the body

to normalize the pH in ACIDOSIS.

 CO2 (acid) can be retained in the body to

normalize the pH in ALKALOSIS.

The kidney can compensate for problems in therespiratory system
 The Kidney reabsorbs and generates Bicarbonate

(alkaline) in ACIDOSIS.
 The Kidney can excrete H+ excess (Acidosis) to

normalize the pH in ACIDOSIS.

 The kidney can excrete bicarbonate (alkali) in

conditions of ALKALOSIS.
 The kidney can retain H+ (acid) in conditions of ALKALOSIS.

Chemical buffers can also participate in the balance of acid-base

 1. Carbonic acid- bicarbonate buffer
  2. Phosphate buffer

 3. protein buffer- ICF and hemoglobin

The action is immediate but very limited

PRIMARY GLOMRULAR DISEASES

GLOMEROLUNEPHRITIS
• It is defined as inflammation of capillary loops of the glomeruli.
• It is classified as acute , rapidly progressive, or chronic glumerolunephritis
• Acute streptococcal glomerulonephritis is the most common
• Rapidly progressive glomerulonephritis may be idiopathic or secondary to an active infection or secondary to an infection or multisystem
disease with greater incidence in males than females
• Chronic glomerulonephritis is the end stage of glumerular disorder

Causes
• Acute systemic disease such as SLE or Primary glumerular disease.
• Beta-hemolytic infection of the phyarnx or skin is the most common pricipatory factor.
• Staphylococal or viral infection can also lead to post infection of glomerulonephritis.

Pathophysiology
In Acute Glumerulonephritis
• The circulating antigen-antibody immune complexes are formed and trapped in the glomerular membrane
• This release vasoactive substance and inflammatory mediators
• Resulting to edema, and allowing plasma protein and blood cells escape the urine
• The rennin –angiotensin- aldosterone system is distrupted which could lead to hypertension.

Pathophysiology
In Rapidly Progressive Glomerulonephritis
• The glumerular cells proliforate with macrophages forming cresent- shaped lesion that obstruct the bowman’s capsule resulting in decrease
GFR.
Phatophysiology
In chronic glumerulonephritis
• It involves slow destruction of the glomeruli with impaired renal function
• The kidney decrease in size eventually all nephrons are destroyed

Sign and Symtoms

A. Acute glumerulonephritis; hematuria, protenuria, salt and water retention, red blood cell cast, hypertension, azotemia, fatigue, anorexia,
nausea, and vomiting and headache.
B. In Rapidly Progressive Glomerulonephrits; weakness ,nausea, vomiting, flulike symptoms, oliguria, abdominal or flank pain
C. Chronic Glomerulonephritis; often unrecognized until renal failure is evident.

Nursing Assessment
• Include Vital sign
• Weigh and presence of edema
• Measure Intake and output
• Sign of infection
• Client knowledge

Diagnostic test
Throat or skin cultures, Antistreptolysin (Aso) titer, Sedimentration rate, anti nuclear antibody test, BUN, createnine, Electrolytes, urinalysis, X-rays
studies, Kidney scan biopsy.

Nursing management
Treatment is symptomatic
1. Medication ( treating symptoms since no cure exist)
a. Immunosuppressive theraphy- to decrease risk of end stage of renal disease , cytoxan, Immuran , Leukoran
b. Glucocorticoids- to reduce remission of nephrotic syndromes
c. ACE- Inhibitors and non-steroidal anti-inflamatory drugs that decrease protein loss.
d. Antibiotics- like penicillin
e. Antihypertensive

2. Educate the client and family regarding disease process

3. Instruct the prescribed medication and sideeffects
4. Instruct regarding activity level and diet restriction

Nephrotic syndrome
Nephrotic syndrome is a primary glomerular disease characterized by the following:
• Marked increase in protein in the urine (proteinuria)
• Decrease in albumin in the blood (hypoalbuminemia)
• Edema
• High serum cholesterol and low-density lipoproteins (hyperlipidemia)

Physiology/Pathophysiology
 Damaged glomerular capillary membrane

Loss of plasma protein (albumin)

Stimulates synthesis of lipoproteins Hypoalbuminemia

Hyperlipidemia Decreased oncotic pressure

Generalized edema
(fluid moves from vascular space to extracellular fluid)

Activation of renin–angiotensin system

Sodium retention

Edema

Clinical Manifestations
1. Edema is typically the presenting symptom (soft and pitting) usually first apparent around the eyes (periorbital), in dependent areas (sacrum, ankles, and
hands), and in the abdomen (ascites).
2. Other symptoms, including malaise, headache, irritability, and fatigue, are common
3. Profound weight gain caused by edema; the child may actually double normal weight.
4. Decreased urine output during the edematous phase urine appears concentrated and frothy.
5. GI disturbances, including vomiting, diarrhea, and anorexia caused by edema of intestinal mucosa.

Diagnostic Evaluation
• Urinalysis:
o Protein usually 2+ or greater
o Blood - absent or transient
• 24-hour urine protein frequently greater than 2 g/m2 per day.
• Blood:
o Total protein reduced
o Albumin less than 2 g/dL
o Cholesterol—greater than 200 mg/dL with edema
• Renal biopsy is indicated if patient is steroid resistant (has failed to achieve remission after 28 days of steroid therapy).
• Anti-C1q antibodies are the most reliable markers for assessing disease activity in lupus nephritis

Complications
• Infections: (due to a deficient immune response)
o Peritonitis, most commonly caused by Streptococcus pneumoniae, but may also be caused by Escherichia coli and Haemophilus influenzae
o Gram-negative septicemia
o Staphylococcal cellulitis
• Thrombosis/ thromboembolism (especially of the renal vein)
• Hyperlipidemia
• Acute renal failure (due to hypovolemia)
• accelerated atherosclerosis (due to hyperlipidemia).

Medical Managements
1. Steroid Therapy - Prednisone is usually the drug of choice help to reduce salt retention and potassium
loss and is the least expensive
2. Immunosuppressants or Antineoplastic agents
o Cyclosporin A (Neoral, Sandimmune)
o Tacrolimus (Prograf)
o Cyclophosphamide (Cytoxan, Neosar)
3. I.V. Albumin 25% - To shift fluid from interstitial space into the vascular system for temporary treatment
to relieve edema
4. Diuretic agents
5. Angiotensin-converting enzyme (ACE) inhibitors
6. Low-sodium, liberal-potassium diet to enhance the sodium/potassium pump mechanism
 7. Protein intake should be about 0.8 g/kg/day, with emphasis on high biologic proteins (dairy products, eggs,
meats), and the diet should be low in saturated fats

Nursing Diagnoses
• Excess Fluid Volume related to fluid accumulation in tissues
• Risk for Infection related to urinary loss of proteins and chronic steroid use
• Imbalanced Nutrition: Less Than Body Requirements related to loss of proteins through urine and anorexia
• Interrupted Family Processes related to childhood illness

Nursing Interventions
Administer corticosteroids as recommended by the health care provider.
o Observe for adverse effects and complications of therapy such as Cushing's syndrome increased body hair (hirsutism), rounding of the face
(moon face), abdominal distention, striae, increased appetite with weight gain, cataracts, and aggravation of adolescent acne.
o Stress that these physical changes are not harmful or permanent and that they will disappear after the steroid treatment is stopped.
Administer immunosuppressive drugs as prescribed.
o Make sure that patient and parents understand the desired and adverse effects of therapy.
o Observe for complications of therapy, such as decreased white blood cell (WBC) count, increased susceptibility to infection, hair loss or
increased hair growth (hirsutism), gingival hyperplasia, hemorrhagic cystitis.

Administer diuretics as prescribed.

o Be aware of those diuretics that may cause potassium depletion.
o Offer foods high in potassium, such as orange juice, bananas, and dried fruits (eg, raisins, apricots).
o Administer supplemental potassium chloride as ordered and if the urine output is adequate.
Encourage activity as tolerated.
Restrict fluids as ordered (usually only during the extreme edematous phases).
o Restriction is carefully calculated at frequent intervals, based on the urine output of the previous day plus estimated insensible losses.
o Offer small amounts of fluids spaced at regular intervals throughout the day and evening. Use a cup of appropriate size for the amount of fluid
being offered.
o Measure fluids accurately in graduated containers. Do not estimate fluid intake or output.
o Place a sign on the child's bed to make sure that no urine is accidentally discarded and that all intake is recorded.
o Determine total intake and output every 8 hours. In children who are not toilet trained, a fairly accurate record of output can be obtained by
weighing diapers before and after voiding.
o Record other causes of fluid loss, such as the number of stools per day, perspiration.
• Assist with abdominal paracentesis; this may be required because of marked ascites. During the procedure, fluid is withdrawn from the peritoneal cavity
to relieve pressure symptoms and respiratory distress.
• Restrict sodium as ordered (usually done while the child is proteinuric). A starting point is 2 to 3 g/day.
o Use a low-sodium menu when ordering meals from the hospital.
o Assist family in making food choices that are low in sodium.
o Foods that should be limited include cured, salted, canned, or smoked meats; processed cheese; regular canned or frozen soups and
bouillon cubes; salted crackers and other snack foods..
DRUG ALERT
Administer cyclophosphamide in the morning, with large volumes of fluid, to prevent concentration of the drug in the urine and increased
susceptibility to cystitis.
Preventing Infection
• Monitor complete blood count for decreased WBC count and neutropenia.
• Closely observe the child who takes corticosteroids for signs of infection. Be aware that fever and other symptoms may be masked.
• Provide meticulous skin care to the edematous areas of the body.
o Bathe the child frequently and apply powder. Areas of concern are moist parts of the body and edematous male genitalia. Support the scrotum
with a cotton pad held in place by a T-binder, if necessary, for the child's comfort.
o Position the child so that edematous skin surfaces are not in contact. Place a pillow between the child's legs when lying on side.
o Elevate the child's head to reduce edema.
• If possible, avoid invasive procedures, such as femoral venipunctures and I.M. injections, to decrease the chance of introducing pathogens. Venipuncture of
the lower extremities may also predispose the child to thromboembolism because of the hypovolemia, stasis, and increased plasma concentration of clotting
factors.
• Educate parents regarding signs and symptoms of possible infections.
Enhancing Nutritional Status
• Assess nutritional intake, growth, and development as appropriate for age.
• Provide a diet low in sodium, fat, and sugar. Place a sign on the child's bed that indicates dietary restrictions, so that everyone will be aware of special
needs.
• Provide food choices that appeal to the child and that are easy to eat according to stage of development.
• Provide nutritional supplements as needed.
Providing Emotional Support
• Encourage frequent visiting and allow as much parental participation in the child's care as possible. Hospitalization, if necessary, is usually brief.
• Allow the child as much activity as tolerated.
 o Balance periods of rest, recreation, and quiet activities during the convalescent phase.
o Allow the child to eat meals with family or other children.
• Encourage the child and family to verbalize fears, frustrations, and questions.
o Be aware that young children frequently fear abandonment by their parents.
o Allow parents to express frustrations regarding the uncertainties associated with the cause of the disease, the clinical course, and prognosis.
o Explain the difference between nephritis and nephrosis if parents have questions.
• Help the child adjust to changes in body image, such as cushingoid appearance, by explaining changes ahead of time.
• Discuss the problems of discipline with the parents. Encourage them to set consistent limits and reasonable expectations of their child's behavior.
• Suggest parents get involved with a support group for families of children with chronic illnesses, as needed.
Family Education and Health Maintenance
• Prepare the family for home management of the child's care plan.
o Have the dietitian discuss special diets with the parents.
o Teach the parents about the child's medication the desired effects and the potential adverse effects.
o Demonstrate urine testing for protein.
o Initiate a community health nursing referral if necessary for reassessment and reinforcement of teaching.
• Encourage continued medical follow-up visits.
• Emphasize the necessity of taking medication according to the prescribed schedule and for an extended time. Discuss complications encountered with
steroid therapy.
• Teach prevention and recognition of signs and symptoms of infection.
• Advise family on activity restrictions necessary.
• Teach signs and symptoms of relapse (proteinuria on urine dipstick at home, increased edema, decreased urine output) and whom and when to call with
questions.
• Teach signs and symptoms of fluid imbalances (excess or dehydration).

Evaluation: Expected Outcomes

• Decreased edema and ascites; adequate urine output
• Exhibits no signs of infection
• Family verbalizes and follows dietary restrictions as demonstrated by appropriate weight gain/loss
• Family verbalizes concerns regarding child's illness as demonstrated by open communication with staff and other family members

NEPHROTIC SYNDROME
Nephrotic syndrome is a clinical disorder characterized by mark increase of protein in the urine.
Decrease in the albumin in the blood (hypoalbumiemia) , edema, and excess cholesterol in the blood (hypercholesteriolnemia)
These occur as consequence of excessive leakage of plasma proteins into the urine because of increased permeability of the glomerular capillary
membrane.

Etiology
(Seen in condition that seriously damage the glumerular capillary membrane)
1. Chronic Glomerulonephritis
2. Diabetes mellitus with intercapillary glomerulosclerosis
3. Amyloidosis of kidney
4. Renal Vein thrombosis
5. SLE
6. Secondary to malignancy

Clinical manifestation
1. Insdious onset of edema, easily pitting edema
2. Mark proteinura- leading to depletion of body protein
3. Hypercholesterolemia- may lead to accelerated atherosclerosis

Diagnostic Evaluation
1. Renal function test
2. Needle biopsy of the kidney- for histologic examination of renal tissue to confirm diagnosis
3. Serum electrolytes evaluations(protein, albumin, etc.)
4. Triglycerides profile –to evaluate degree of hyperlipidemia.
5. Urinary test may show microscopic hematuria, urinary cast, other abnormalities.

Management
1. Treatment of causative glomerular disease.
2. General management of edema
a. Sodium and fluid restriction
b. Diuretics if renal insufficiency is not severe
c. Steroids (prednisone) to reduce edema and protenuria

Nursing intervention
1. Monitor for complication- Thrombolitic complications: renal vein thrombosis, pulmonary embolism, coronary artery thrombosis, cerebral artery
thrombosis
2. Bed rest for a few days to help mobilize edema:however , some ambulation is necessary to reduce risk of thrombolytic complication
3. Encourage patient to follow the proposed dietary plan to counteract hyporotenemia.
 a. High protein diet to replenished wasted tissue and restore body protein
b. Mild to moderate sodium restriction to control severe edema
c. Control fluid intake as prescribed.
4. Monitor weigh and blood pressure – to follow rate of diuresis and determine that
Hypotension is not developing
5. Monitor for infection- Though to be loss of serum immunoglobulin in the urine

NEPHROSCLEROSIS
• Nephrosclerosis in the renal arteries is most often due to prolonged hypertension and diabetes, both of which can cause decrease blood flow
to the kidney and patchy necrosis of the renal parenchyma
• Over time, fibrosis occurs and glomeruli are destroyed
• Nephrosclerosis is the major cause of ESRD secondary to many disorder.

Pathophysiology
• There are two forms of nephrosclerosis:malignant (accelerated) and benign.
• Malignant nephrosclerosis is associated with malignant hypertension
• It is usually occur in young adult, and men is affected twice as often as woman.
• Without dialysis more than half of patient die with uremia in a few years.
• Benign Nephrosclerosis is usually found in older adults associated with atherosclerotis and hypertension

Assessment and Diagnostic Finding

• Symtoms are rarely in the disease, even though the urine contains protein and occasional cast
• Renal insufficiency and associated signs and symptoms occur late in the disease

Medical Management
• ACE Inhibitor for hypertension, alone or in combination reduces the incidence.

RENAL FAILURE
• It is a condition when the kidneys cannot remove the body metabolic wastes or performed their regulatory functions.
• The substances normally iliminated in the urine accumulate in the body fluids as a result of impaired renal excretion, leading to distruption in
endocrine and metabolic function as well as fluid, electrolyte, and acid-base disturbances.
• Renal failure is systemic disease and is final common pathways of many different kidney and renal diseases.

ACUTE RENAL FAILURE

• It is defined as rapid decrease in renal function
• It is generally recognize by a fall of urinary output and increase in BUN and/ or creatinine : oliguria is common but high output failure is
possible
• The most common cause of ARF is Ischemia and Nephrotoxin
• A fall of blood pressure or volume can cause ischemia of the kidneys
• The exposure of renal tissue is great when nephrotoxin are present in the blood
• ARF may be iatrogenic causes such as Nephrotoxin Radiologic contrast dye, and surgical shock.

Pathophysiology
1. Ischemia is the primary cause of ARF: if followed to continue longer than two hours ischemia leads to irreversible damage to the tubles with
patchy necrosis resulting to
a. decrease in GFR
b. activation of Renin- angiotensin system occurs
c. Tubular obstruction is cause by debries.

2, Nephrotoxin destroy tubular cells allowing fo the increase permeability cause by

Necrosis.
Phases of Acute renal Infection
1. Initiation Phase-
• begins with the onset of event causing tubular necrosis
• This phase ends when tubular injury occur

2. Maintainace Phase
• Begins with in hours of initiation phase and typically last 1 to 2 weeks
• It is characterized by persistent reduction of GFR and tubular necrosis.

3. Recovery Phase
• Begins when the GFR and tubular function have recovered
• Renal Function improves the first 5- 25 days up to 1 year

ASSESSMENT
• Changes in the urine output: Sudden weigh gain, head ache, nausea and vomiting, increase in BP, changes in LOC, Uremic smell (halitosis),
dry and itchy skin, increase BUN and decrease HCT and Hgb.
 • Fluid in excess –dyspnea, tachycardia, distended, neck veins, edema,crackles
• Hayperkalemia is the most dangerous imbalance in ARF because it has effect in the cardiac activity.
• Hyponatrimia- has an effect of water rather than a true lack of sodium.
• Hyperphosphatemia (phosphate is not excreted)

Nursing Care
• Daily weight, Vital sign, CVP monitoring
• Fluid and diuretics as ordered
• Diet high in CHO, Low Protien, low potassium, and low sodium diet
• Assist patient for dialysis, it may be required.

CHRONIC RENAL FAILURE (CRF)

• CRF- is defined as progressive inability over months to years of the kidney to respond changes in the body fluids and electrolytes composition
with an inability of the kidney to produce sufficient urine.
• GFR is less than 20% of normal- 125 ml./ min./1.73 meter squared
• Createnine is greater than 5 mg / dl
Pathophysiology
• The renal function declines as gradual loss of the entire nephron units and the renal mass is reduced leading to progressive detriation of
glomerular filtration, tubular secretion and reabsorption, eventually. The kidney are enable to excrete metabolic waste and regulate fluid and
electrolytes balance and uremia developes adversely affects every system of the body.

S/S – Clinical Manifestation

• Cardiovascular manifestation-(hypertension, heart failure, pulmonary edema
• Dermatologic manifestation (severe pruritus)
• Nuerologic manifestation (altered LOC)

Stages of chronic renal failure

• Stages of chronic kidney disease is based on GFR

Stage 1- increase or equal to 90 ml/ min/ 1.73 meter squared

Stage 2- GFR with 60-89 ml/ min/ 1.73 meter squared- mid decrease in GFR.
Stage 3- 30-59 ml/min/ 1.73 meter squared – moderate decrease in GFR
Stage 4- 15- 29 ml/ min/ 1.73 meter squared- Severe decrease in GFR
Stage 5- 15 ml/min/1.73 metred squared – Kidney failure

Nursing assessment
• Vital sign, I and O, edema, daily weigh , measurement of abdominal girth, fluid and dietary restriction, LOC.

Diagnostic Test
• BUN elevated, Createnine elevated,
• Electrolytes: decrease sodium, Increase Potassium, increase phosphate, decrease calcium
• CBC- severe anemia, thrombocytopenia.
• Urinalysis: Fixed specific gravity, protein, Blood cells, cast, urine C/S, createnine clearance
• ABG:metabolic acidosis, UZ, Kidney biopsy

NURSING MANAGEMENT
• MONITOR I and O
• Maintan fluid and dietary restriction (limit Na and protein, high CHO)
• Initiate Pharmacologic therapy( Ca and phosphorous binder are administer with food)
• Admister hypertensive and cardiovascular agent as ordered
• Administer antisiezure agent as ordered ( diazepam, phnytoin)
• Dietary supplement of iron may be given
• Patient education about dialysis is needed

DIALYSIS
• Process of removing fluid and uremic waste products from the body when the kidney are incapable

Complications;
• Atherosclorotic cardiovascular disease- leading cause of death
• Dialysis disequilibrium- more common in acute renal failure or when BUN is very high( increase of 150mg/di) it results from cerebral fluid
shift(headache, nausea and vomiting, restlessness, decrease level of conciousness and seizures)

Diet Restriction
• Protien(1.2- 1.3 g/kg/day)
• Soduim (2-3 g/day)
• Fluid daily output plus 500ml/day

HEMODIALYSIS
• The removal of fluid and uremic waste products from the blood
• Principles: diffusion, osmosis and ultrafiltaion
• Dialyzer- “artificial kidney” a hallow fiber device with thousand of tiny cellophane tubules and acts as semipermeable membrane that filters at
rate of 300-500 ml/min
• Dialysate- asolution composed of all important electrolytes in their ideal extracellular concentration.
• Diffusion- toxins and waste in the blood are removed from an area of higher concentration in the blood to an area of lower concentration.
• Osmosis- Excess water is removed from area of higher solute concentration(blood) to an area of lowr concentration (dialysate)
 • Ultrafiltration- water moves from high pressure to an area of lower pressure by applying a suctioning force to the dialysis membrane.

Vascular access for Hemodialysis

• Vascular access devices (immediate acess through subclavian, internal jugular and femoral vein it can used for no longer than 3 weeks.
• Arteriovenous Fistula- permanent acess, usually in the forearm by joining an artery to a vein, allow 14 days for healing.
• Arteriovenous Graft- subscutaneously interposing a biologic, semibiologic, or synthetic graft material between an artery and vein.

Peritoneal Dialysis
• The peritoneal membrane that covers the abdominal organs and lines the abdominal wall serves as the semi permeable membrane.
• The drenaige fluid is normally colorless or straw colored and should not be cloudy
Complications:
• Peritonitis- most commonly it is characterized by the cloudy dialysate, drainage, diffuse abdominal pain and rebound tenderness.
• Leakage
• Bleeding

KIDNEY TRANSPLANTATION
• Has become the treatment of choice of ESRD.
• Patients choice for kidney transplantation is to avoid high cost of dialysis and wish to live normal life.
• Involves transplanting a kidney from living donor or deceased donor to the recipient who has ESRD
• Kidney transplant from well- matched living donors who are related to patient (those compatible ABO and HLA antigens) are slightly
compatible than those from cadaver donors

Preoperative Management
• Goals include bringing the patient’s metabolic state levels as close to normal as possible.
• Making sure that patient is free from infection

Procedure
Renal transplantation
1. the diseases kidney may be removed and the renal artery and vein tied off.
2. The transplanted kidney is placed in the iliac fossa
3. The renal artery old donated kidney is sutered to the iliac artery, and the renal vein is sutured to iliac vein.
4. The urether of donated kidney is sutured to the paitient urether

Post operative management

• The goal of care is to maintain homeostasis until transplanted kidney is functioning well

Medical Management
• The survival transplanted kidneys depends on the ability to block the body’s immune response to transplanted kidney’s
• The body’s should overcome or minimize body defense mechanism.
• Immunosuppresive agents are prescribe example are cyclosporine,neoral, prograft,cellcept sre used to prevent rejection.

MANAGEMENT OF PATIENT WITH URINARY DISORDER

Urinary Tract Infections (UTIs)

• The second most common reason for seeking health care
• A common site of nosocomial infection
• Lower UTIs
– Cystitis
– Prostatitis
– Urethritis
• Upper UTIs
-Pyelonephritis: acute and chronic = vesicoureteral reflux, renal disease, trauma, or pregnancy. Chronic pyelonephritis may result in scarred, atrophic, and
nonfunctioning kidneys
– Interstitial nephritis,
– Renal abscess and perirenal abscess

Factors Contributing to UTI

• Function of glycosaminoglycan (GAG) -Glycosaminoglycan (GAG) - a hydrophilic protein
• Urethrovesical reflux
• Ureterovesical Reflux
• Uropathogenic bacteria (Escherichia coli)
• Shorter urethra in women
• Poor voiding habits
• In men, obstructive abnormalities

Urethrovesical Reflux (coughing, sneezing, or straining) (and

Ureterovesical Reflux (refers to the backward flow of urine from the bladder into one or both ureters)
Bladder Infection With
Long-Term Catherization (Pseudomonas, Enterococcus, Proteus, Klebsiella, Staphylococcus species. )

Nursing Process—Assessment of the Patient With a UTI

• Symptoms include pain and burning upon urination; frequency; nocturia; incontinence; suprapubic, pelvic, or back pain; hematuria; or change in urine or
urinary pattern
• About half of patients are asymptomatic
• Assess voiding patterns, association of symptoms with sexual intercourse, contraceptive practices, and personal hygiene
• Gerontologic considerations
50% of females have asymptomatic bacteriuria, structural abnormalities and neurogenic bladder secondary to strokes or autonomic neuropathy of diabetes
may prevent complete emptying of the bladder
In the absence of estrogen, postmenopausal women are susceptible to colonization and increased adherence of bacteria to the vagina and urethra.
The most common cause of recurrent UTI in the elderly male patient is chronic bacterial prostatitis. confusion, dementia, or bowel or bladder
incontinence.
• Assess urine, urinalysis, and urine cultures
• Other diagnostic tests. Multistrip dipstick testing for WBCs, known as the leukocyte esterase
test, and nitrite testing (Griess nitrate reduction test) are
common

Nursing Process—Diagnosis of the Patient With a UTI

• Acute pain
• Deficient knowledge

Collaborative Problems/Potential Complications

• Sepsis
• Renal failure

Nursing Process—Planning the Care of the Patient With a UTI

• Major goals include relief of pain and discomfort, increased knowledge of preventive measures and treatment modalities, and absence of complications

Interventions
• Prevention: avoid indwelling catheters; exercise proper care of catheters
• Exercise correct personal hygiene
• Take medications as prescribed: antibiotics, analgesics, and antispasmodics
• Apply heat to the perineum to relieve pain and spasm
• Increase fluid intake
• Avoid urinary tract irritants such as coffee, tea, citrus, spices, cola, and alcohol
• Frequent voiding
• Encourage plenty of fluids to promote urinary output
• Decrease the entry of microorganisms into the bladder during intercourse.

Urinary Incontinence
• An underdiagnosed and under reported problem that can significantly impact the quality of life and decrease independence and may lead to compromise of
the upper urinary system
• Urinary incontinence is not a normal consequence of aging

Types of Urinary Incontinence

• Stress – sudden increase in intra-abdominal pressure (affects women had vaginal deliveries, for men had radical prostatectomy
• Urge – strong urge to void that cannot be suppressed
• Reflex - absence of normal sensations usually associated with voiding. (spinal cord injury)
• Overflow – overdistention results from the bladder’s inability to empty normally, despite frequent urine loss.
• Functional - difficult for the patient to identify the need to void (Alzheimer’s dementia)
• Iatrogenic – involuntary loss of urine due to extrinsic medical factors, predominantly medications
• Mixed incontinence – is usually a combination of stress and urge incontinence.

Patient Teaching
• Behavioral therapies first choice to decrease or eliminate urinary incontinence.
A. Fluid Management
B. Voiding Frequency
Timed voiding, Prompted voiding, Habit retraining, Bladder retraining
C. Pelvic Muscle Exercise
• Management takes time (provide encouragement and support)
• Develop and use a voiding log or diary
• Medication teaching related to pharmacologic therapy Anticholinergic agents (oxybutynin [Ditropan], dicyclomine [Antispas]) inhibit bladder contraction).
Estrogen decreases obstruction to urine flow by restoring the mucosal, vascular, and muscular integrity of the urethra.
• Strategies for promoting continence.

ENURESIS
A. Description
1. Refers to a condition in which the child is unable to control bladder function even
though the child has reached an age at which control of voiding is expected
2. By age 5, most children are aware of bladder fullness and are able to control
Voiding

B. Primary nocturnal enuresis

1. Bed-wetting in a child who has never been dry for extended periods
2. Common in children, and most children will eventually outgrow bed-wetting
without therapeutic intervention
3. The child is not able to sense a full bladder and does not awaken to void
4. The child may have delayed maturation of the central nervous system (CNS)

C. Secondary or acquired enuresis

1. The onset of wetting after a period of established urinary continence
2. Mat occur during nighttime sleep (nocturnal), only during the waking hours
(diurnal), or during both times of the day
3. The child may complain of dysuria, urgency, or frequency
4. The child should be assessed for urinary tract infections

D. Assessment
1. Normal voiding pattern
2. History of bed-wetting with no extended period of dryness in a child older
Than age 5 year
E. Implementation
1. Obtain urinalysis and urine culture as prescribed to rule out infection or
existing disorder
2. Assist the family with identifying a treatment plan that will best fit their needs
3. Limit fluid intake at night, and encourage the child to void just before going to
Bed
4. Involve the child in caring for the wet sheets and changing the bed, to assist the
child to take ownership of the problem
5. Provide reward systems as appropriate for the child
6. Incorporate behavioral conditioning techniques
7. Encourage follow-up to determine the effectiveness of the treatment

NEPHROBLASTOMA (WILM’S TUMOR)

A. Description
1. A tumor of the kidney that may present unilaterally and localized or
Bilaterally, sometimes with metastasis to other organs
2. The peak incidence is at 3 years of age
3. Its occurrence is associated with a genetic inheritance and with several
congenital anomalies
4. Therapeutic management includes a combined treatment of surgery
(partial to total nephrectomy) and chemotherapy with or without radiation,
depending on the clinical stage and histologic pattern
 B. Assessment
1. Swelling or mass within the abdomen (mass is characteristically fir, confined to one side, and deep within the flank)
2. Abdominal pain
3. Urinary retention and/or hematuria
4. Anemia (secondary to hemorrhage within the tumor)
5. Pallor, anorexia, lethargy (occurs as a result of anemia)
6. Hypertension (caused by secretion of excess amounts of renin by the tumor)
7. Weight loss and fever
8. Symptoms of lung involvement, such as dyspnea, shortness of breath, and pain in the chest, if metastasis has occurred

C. Implementation preoperatively
1. Monitor vital signs, particularly blood pressure
2. Place a sign at the bedside: “Do Not Palpate Abdomen”
3. Avoid palpation of the abdomen
4. Measure abdominal girth

D. Implementation postoperatively
1. Monitor temperature and blood pressure closely
2. Monitor for signs of hemorrhage and infection
3. Maintain I&O and urine output closely
4. Monitor for abdominal distention, bowel sounds, and other signs of GI activity, because of the risk for intestinal obstruction

Urinary Retention
• Inability of the bladder to empty completely
• Residual urine: amount of urine left in the bladder after voiding
• Causes include age (50 to 100 mL in adults older than age 60 due to decreased detrusor muscle activity), diabetes, prostate enlargement, pregnancy,
neurologic disorders, and medications
• Assessment
• • What was the time of the last voiding, and how much urine was excreted?
• • Is the patient voiding small amounts of urine frequently?
• • Is the patient dribbling urine?
• • Does the patient complain of pain or discomfort in the lower abdomen?
• • Is the pelvic area rounded and swollen?
• • Does percussion of the suprapubic region elicit dullness?
• • Are other indicators of urinary retention present, such as restlessness and agitation?
• • Does a postvoid bladder ultrasound test reveal residual urine?
• Nursing measures to promote voiding
1. providing privacy, ensuring an environment and a position conducive to voiding
2. catheterization is used to prevent overdistention of the bladder
3. Modifying the home environment

Urolithiasis and Nephrolithiasis

• Calculi (stones) in the urinary tract or kidney
• Pathophysiology
• Causes: may be unknown
• substances prevent crystallization in the urine, such as citrate, magnesium, nephrocalcin, and uropontin.
• substances cause crystallization calcium oxalate, calcium phosphate, and uric acid
• stones tend to occur more often in dehydrated patients factors favor the formation of stones, including infection,urinary stasis, and periods of immobility
• Increased calcium concentrations in blood and urine promote precipitation of calcium and formation of stones

Manifestations
– Depend upon location and presence of obstruction or infection
– Pain and hematuria
Diagnosis:
x-ray, ultrasonography, blood chemistries, and stone analysis; strain all urine and save stones

Nursing Diagnosis
Based on the assessment data, the nursing diagnoses in the patient with renal stones may include the following:
• Acute pain related to inflammation, obstruction, and abrasion of the urinary tract
• Deficient knowledge regarding prevention of recurrence of renal stones

Management
1. Analgesics
2. Increase fluid intake
3. Nutritional therapy
4. Ureteroscopy, extracorporeal shock wave lithotripsy (ESWL), or endourologic (percutaneous) stone removal.
5. Percutaneous nephrolithotomy is used to treat larger stones
 6. Chemolysis, stone dissolution using infusions of chemical solutions (eg, alkylating agents, acidifying agents) for the purpose
of dissolving the stone,

Patient Teaching
• Signs and symptoms to report
• Follow-up care
• Urine pH monitoring
• Measures to prevent recurrent stones
• Importance of fluid intake
• Dietary teaching
• Medication teaching as needed

Urethral stricture
Urethral stricture is an abnormal narrowing of the tube that carries urine out of the body from the bladder (urethra). Urethral stricture is caused by
injury or disease such as urinary tract infections or other forms of urethritis.

Signs/ Symptoms
- pain during urination
- inability to fully empty the bladder.
- Increased frequency of Micturation
- Acute or Chronic Retention of Urine
- Urinary intermittency
Causes
Inflammation
Scar tissue from surgery, disease, or injury.
Enlarging tumor near the urethra
Other risks include:
• A history of sexually transmitted disease (STD)
• Any instrument inserted into the urethra (such as a catheter or cystoscope)
• Benign prostatic hyperplasia (BPH)
• Injury or trauma to the pelvic area
• Repeated episodes of urethritis

Complications
• Urinary retention
• Urethral diverticulum
• Periurethral abscess
• Urethral fistula
• Bilateral hydronephrosis
• Urinary infections
• Urinary calculus
• Hernia, haemorrhoids or Rectal prolapse from straining

Diagnosis
• Urethroscopy
• Urethrography
Treatment
1. An open urethroplasty may be done for longer strictures.
2. Suprapubic catheter may be placed as an emergency treatment.
3. The urethra may be widened (dilated) during cystoscopy

Prognosis
Treatment usually results in an excellent outcome. However, repeated therapies may be needed to remove the scar tissue.