MODULE COMPETENCE
• Thismodule is designed to enable the learner:
• Promote health.
• Prevent illiness.
• Manage and rehabilitate patients suffering from renal and genitourinary conditions.
3.
MODULE OUTCOMES
By theend of the module the learner
should;
1.Perform assessment of the renal system,
2.Manage disorders of the renal system using
the nursing process .
3.Manage disorders of the ureters,urinary
bladder and ureters using the nursing process.
4.
MODULE CONTENT
• Overviewof the renal system, anatomical view,functions of the renal system,assessment
of the the renal system, lab tests,
• General signs and symptoms of the GUD.
• Disorders of the kidney
• Acute glomerulonephritis, Renal caliculi,pyelonephritis,Nephrotic syndrome,TB of the
kidney,prostate cancer,Renal trauma,renal tumours,Hydronephrosis,Acute Renal failure,
(AKI),Chronic Kidney Disease(CKD),End stage Renal
Disease( ESRD)Dialysis(hemodialysis,peritoneal dialysis),Renal transplant.
5.
• Disorders ofureters,urinary bladder and urethra:
• Cystitis,urinary incontinence,urinary reflux,urinary retention,urinary bladder
caliculi,bladder neoplasm,neurologic
bladder,fistulae,diverticuli,urethritis,ureteritis,urethral caliculi,tumours(ureters,bladder
and urethra),trauma(ureters,bladder and urethra),urethral strictures,testicular
torsion,benign prostate hypertrophy,carcinoma of the prostate,congenital
disorders(hypospadias,epispadias,phimosis,paraphimosis,balanitis)
11.
ANATOMICAL REVIEW OFTHE RENAL
SYSTEM
• Urinary systems-kidneys, ureters, bladder and urethra.
• Kidneys- are bean-shaped, brownish-red structures located retroperitoneal (behind and outside the peritoneal
cavity.
• -Adrenal gland is situated on top of each kidney.
• - The renal parenchyma is divided into two (cortex and medulla).
• -The Medulla contains loops of henle, and collecting ducts.
• -Each kidney contains 8-18 pyramids which drain into 2-3 major calices that open to the renal pelvis.
• -The kidney is supplied by renal artery and drained by renal vein (branches of abdominal aorta and inferior
vena cava).
12.
Nephrons
• Each kidneyhas 1 million nephrons located at the parenchyma responsible for initial formation of urine.
• Two type (cortical nephrons located in the outermost part of cortex-80-85% and juxtamedullary nephrons located
deeper in cortex-15-20% (distinguished by long loops of henle surrounded by long capillary loops called vasa recta.
• Afferent and efferent blood vessels are enclosed in an epithelial structure called bowmans capsule then proximal
tubule, loop of henle, distal tubule and either cortical or medullary collecting duct.
• Renin is produced by macula densa cells at the distal tubules.
13.
Ureters, bladder andurethra
• Ureters are long fibro-muscular tubes connecting each kidney to the bladder (24-30cm long.)
• have three narrow areas: Ureteropelvic junction, the ureteral segment near the sacroiliac joint and the
ureterovesical junction all prone to obstruction by kidney stones.
Urinary bladder
• Muscular hollow sack located behind the pubic bone,
• Its vesicle contains two inlets and one outlet.
• Contains four layer: FROM OUTSIDE: adventitia (made of connective tissues), smooth muscle layer known as
detrusor, sub mucosal layer of loose connective tissue and mucosal lining (innermost layer).
14.
Urinary badder ctd
•Bladder neck contains involuntary smooth muscles that form part of urethral sphincter.
• In male the prostate gland lies just below the bladder neck, surrounds the urethra
posteriorly and laterally.
15.
Urethra
• Arises frombase of bladder, passes through the penis in males and in females it opens just anterior
to the vagina.
Urine formation
• Formed in three steps: glomerular filtration, tubular re absorption and tubular secretion.
• Substances filtered by glomerular, reabsorbed by tubules and excreted in urine include: sodium,
chloride, bicarbonate, potassium, glucose, urea, creatinine and uric acid.
• NB: amino acids and glucose are filtered at the glomerulars and reabsorbed so that neither is
excrete in urine
16.
Renin angiotensin pathway
•Decrease in renal perfusion pressure or to kidney tubules due to e.g. hemorrhage, heart
failure, cirrhosis, loop diuretic and reduced salt intake__________ angiotensinogen from the
liver converted by renin to angiotensinogen 1 which changes to angiotensinogen 11 by
action of angiotensin converting enzyme from the lungs.
• -It’s a powerful vasoconstrictor which increases pressure by: vasoconstriction, increased
myocardial contractility and prostaglandin release :increase circulating volume by:
aldosterone release, sodium and water reabsorption, potassium excretion and ADH release.
17.
FUNCTIONS OF THERENAL SYSTEM
KIDNEYS
• Regulation of acid base balance in two ways. Reabsorbing and returning to the body’s circulation any bicarbonate from the urinary filtrate or
excretion of acid in urine
• Help regulate blood pressure; when the vasa recta ( specialized vessels of the kidney) detect a decrease in blood pressure, specialized juxtaglomerular
cells called delta cells, near the afferent arteriole, distal tubule and afferent arteriole secrete the hormone renin which convert angiotensinogen to
angiotensin 1, which is then converted to angiotensin 11 the most powerful vasoconstrictor; which causes blood pressure to increase. The adrenal
cortex secretes aldosterone in response to stimulation by the pituitary gland which occurs in response to poor perfusion or increasing serum
osmolality resulting in increase in blood pressure. When the vasa recta recognizes the increase in blood pressure, renin secretion stops.
• Regulation of red blood production; when the kidneys detect a decrease in the oxygen tension in the renal blood flow, they release erythropoietin
18.
• Vitamin Dsynthesis; the kidneys are responsible for the final conversion of inactive vitamin D to its active form
1,25-dihydroxycholecalciferol.
20.
KIDNEY CONT……
• Excretionof the waste products; the kidneys eliminate body’s metabolic waste products, creatinine,phosphates, sulfates,
urea and uric acid.
• Secretion of prostaglandins; the kidney also produces prostaglandin E and prostacyclin, which have a vasolidilatory
effect and are important in maintaining renal blood flow.
• Regulation of electrolyte and water balance; when the kidneys are functioning well, the volume of electrolytes excreted
per day is equal to the amount ingested. The regulation of sodium volume excreted depend on aldosterone, a hormone
synthesized and released from the adrenal cortex.
• Urine formation in three steps;
• 1. glomerular filtration, tubular reabsorption, and tubular secretion.
21.
2. The ureterstransport urine from the kidneys to the urinary bladder.
3. The urinary bladder stores urine.
4. The urethra discharges urine from the body.
22.
ASSESMENT OF THERENAL SYSTEM
History taking
Presenting complains or the reason for seeking health care, onset of the problem and its effect on the patient’s quality
of life
Location, characteristics and duration of pain and its relationship to voiding , factors precipitating and factors relieving
symptoms
History of urinary tract infection including past treatment
Previous renal or urinary diagnostic tests, use of indwelling catheter
Dysuria and when during voiding ( i.e. Irritation or at termination of voiding)
Hesitancy, straining, urinary incontinence
Hematuria, Pyuria, nocturia
Renal calculi, passage of stones or gravel in urine
23.
• Female patients;ask for vaginal infection, discharge irritation
• History of anuria, or other renal problem presence of genital lessions or sexually
transmitted infections
• Any prescription over the counter
24.
COMMON SYMPTOMS
• Pain;genitourinary pain is caused by distension of some portion of the urinary tract as a result of
obstructed urine flow or inflammation and swelling of tissues.
• Changes in voiding; frequency, urgency, dysuria, hesitancy, incontinence, enuresis, polyuria, oliguria,
anuria, hematuria.
• Gastrointestinal symptoms; associated with urologic conditions because of shared autonomic and
sensory innervation and renoinstetinal reflexes. Nausea, vomiting, diarrhoea, abdominal discomfort,
and abdominal distention.
• Unexplained anaemia; shortness of breath, exercise intolerance, pallor.
25.
Past medical history
•Previous health problem or disease history of hospitalization for UTI, etc.
• Previous renal or urinary diagnosis tests or use of indwelling catheter.
• Dysuria, hesitancy, straining or pain during or after voiding.
• Childhood diseases, urethral invasion procedure.
• History of blood transfusion.
• Medication history.
• Occupation history.
26.
Family and socialhistory
• Family history of vascular or cardiovascular disorders.
• History of Diabetes Mellitus and hypertension(leading causes of CKD).
• Occupation history –plastic tar and mercury processing.
• History of alcoholism and substance abuse.
Obstetric history for female
• History of traumatic delivery etc. number and type of delivery, use of forceps, vaginal infections,
discharge or irritation.
27.
PHYSICAL EXAMINATION
Head totoe examination with emphasis on abdomen, suprapubic region, genitalia, lower back, and lower
extremities
INSPECTION
• Inspect the Skin for pallor, yellow-gray, excoriations, changes in turgor, bruises, texture (e.g. rough, dry
skin)
• Assess decreased level of consciousness which might be a sign of end stage renal disease.
• Asses mouth for stomatitis and ammonia breath.
• Inspect the face & extremities for generalized edema, peripheral edema, bladder distention, masses, and enlarged
kidney.
• Inspect abdominal contour for midline mass in lower abdomen (may indicate urinary retention) or unilateral mass.
28.
• Weight: weightgain for edema, weight loss & muscle wasting in renal failure.
• Asses the general state of health for fatigue, lethargy, & diminished alertness
29.
PALPATION
• Palpate thekidneys; place one hand under the patients back with fingers under the ribs
• Place the other one anterior to the kidney with finger above the umbilicus
• Palpate as patient inhales
• Tenderness at the 12th
rib with vertebra indicates renal dysfunction
Normal findings
• No cost vertebral angle tenderness, non palpable kidney and bladder, no palpable mass
30.
PERCUSSION
• Tenderness inthe flank may be detected by fist percussion.
• If tenderness & pain are present, indicate a kidney infection or polycystic kidney disease.
• Percuss for urine residue after voiding.
• Dullness shows incomplete bladder emptying
AUSCULTATION
• Lung sounds to rule out pulmonary edema secondary to fluid retention
• The abdominal aorta & renal arteries are auscultated for a bruit, which indicates impaired blood flow to the
kidneys ( renal artery stenosis)
31.
For men
• Performdigital rectal examination; feel the growth for men 40 years and above- routine annually
• Collect prostate specific antigen (PSA) prior examination. Otherwise will be increased.
Women
• Examine vulva and urethra. Check for herniation. Urethrocele, cervix prolapse, rectocele. Check for urine
leakage.
32.
LABORATORY TESTS
URINALYSIS
• Doneto check for Color, odor, and turbidity, Pale- DM, severe head injury, Yellow/ milky- infection, Red- fresh
bleeding, Orange/ deep amber- fever, dehydration, bile, nitrofurantoin
• Specific gravity, measures the kidney’s ability to concentrate urine. Measured by multiple-test dipstick (most common
method), refractometer-instrument used in the lab, urinometer (least accurate method).
• Cold specimens produce a false high reading.
• Factors that interfere with an accurate reading include;
• radiopaque contrast agents,
• glucose &
• Proteins.
33.
• A decreasein SG (less conc. urine) occurs with
• increased fluid intake,
• diuretic administration,
• Diabetes insipidus.
• An increase SG (more conc. Urine) occurs with
• insufficient fluid intake,
• decreased renal perfusion, or
• The presence of high ADH.
• Normal 1.003 to 1.030 in relation to wt. in distilled water
34.
• PH- UrinePH- Normal 4.6 to 8.
• Acidic- DM, dehydration, starvation.
• Alkaline- UTI, salicylate poisoning.
• Proteins.
• Glomerular diseases, malignancy, collagen disease, diabetes, PET, hypothyroidism, exposure to heavy metals
• Glucose- high blood sugar. Renal threshold is 180 mg/dl.
• Ketones; diabetes ketoacidosis.
• RBCs; normal 2-3 / field- if more acute infection, renal calculi and neoplasms
• Osmolality
• Accurate way of measuring kidneys capability to dilute and concentrate urine
• Normal for urine 50-1200
35.
URINE CULTURE ANDSENSITIVITY
• Identifies the presence of microorganisms & determines the specific prescription that will
treat the existing microorganisms. It determine the strain and concentration
• Note that urine from a client who forced fluids may be too dilute to provide a positive
culture
36.
RENAL FUNCTION TESTS
•Evaluates the severity of kidney disease and assess the status of the patients kidney function. Include serum urea and nitrogen and creatinine clearance in 24hrs
BLOOD UREA AND NITROGEN
• Measures the amount of nitrogen in the blood that comes from the waste product urea.
• Urea is made in the liver when protein is broken down and removed from the body via the renal system.
• BUN is done to evaluate kidney damage, to determine effectiveness of dialysis.
• Elevated BUN can be due to urinary tract obstruction, dehydration, shock, severe burns and use of certain medication
Creatinine clearance test
• Evaluates how well the kidneys remove creatinine from the blood
• The urine specimen for the creatinine clearance is usually collected for 24 hours
Uric acid test
• A 24hour urine collection sample is tested to diagnose gout and kidney disease
37.
OTHER LAB STUDIES
Serumosmolarity- potassium levels will be high
• Calcium levels – low in kidney disease, helps in conversion of vit D to its active form
• Phosphorus level- elevates as phosphorus is retained in the body due to low calcium
levels
• Magnesium levels- Mg is an antagonist of Ca thus levels are elevated
38.
TISSUE STUDIES
• Renalbiopsy; an invasive procedure used to determine histological diagnosis and severity of the disease
process
• Can be done using a needle puncture or surgical incision
RADIOLOGICAL STUDIES
• KUB; (kidney ureter and bladder studies) x-ray to show size, shape and position of kidney, bladder and ureters
• Renal ultrasonography
• Retrograde pyelogram- catheters are advanced through the ureters into the pelvis by a cystoscopy. A contrast
agent is then inserted
39.
• Cystography- acatheter is inserted into the bladder
• Renal angiography/arteriography- provides an image of the renal arteries. The femoral vein is pierced
with a needle and a catheter is advanced up through the femoral and iliac arteries into the aorta and then
the renal artery. A contrast agent is then injected to opacify
• Intravenous pyelography- intravenous injection of contrast media. Then a series of radiological films are
obtained
• Urethrography- Visualizes the urinary tract to assess urine flow through the urethra. A urethral catheter
is inserted and a contrast agent instilled into the bladder when the patient feels like voiding, the catheter
is removed then the patient allowed to void. Mostly done when urethral trauma is suspected
40.
GENERAL SIGNS ANDSYMPTOMS OF GENITO-URINARY
DISORDERS
• Fever, weight loss and malaise are common
• Changes in micturition
• Frequent micturition- may be due to injury to the bladder mucosa, infection, foreign bodies or tumor. These
produce a functional decrease due to pain which results from mild stretching of the bladder
• Urgency of micturition- strong desire to urinate. Involuntary urination may occur if voiding is not immediate.
Voiding is usually in small amount of volume. The desire to urinate is almost constant until the voiding process.
• Dysuria- difficulty voiding. Suggest irritation or inflammation of bladder neck or urethra or bacterial infection
• Nocturia- excessive urination at night may come as a result of decreased renal concentrating ability, renal disease
and diabetes mellitus. May also come as a result of excessive intake of fluids in the late evening or poor bladder
training
41.
• Enuresis –bed wetting at night be physiological during the first 2-3years but later it can be due to
delayed neuromuscular maturation. Can also come as a result of distal urethral stenosis in girls. And
posterior urethral valves in boys. Neurogenic bladder can also be a possible cause.
• Hesitancy- un-due delay and difficulty in initiating micturition/ voiding straining and decrease in
force and caliber of urinary system. This may be as a result of : symptoms of obstruction distal to the
bladder, prostatic obstruction in men, urethral stricture and congenital urethral stricture in a child
• Incontinence- loss of urine without warning. As a result of atrophy of bladder, epispadiasis,
prostatectomy, childbirth, congenital and acquired neurogenic and bladder dysfunction.
•
42.
Changes in urinaryoutput
• Polyuria- urine output of above 2500 mls daily found in diabetes mellitus
• Oliguria- urine output of below 500mls daily as a result of decreased renal perfusion
• Anuria- urine output below 100mls per day which may be a result of anemia of anaphylactic shock.
Changes in urine appearance
• Hematuria- blood in urine or not noticeable depending on the amount of blood. This as a result of renal
vesicle or prostatic disease tumor of bladder or kidney stones in the bladder
• Pyuria- pus in urine. Presence of white of white blood cells in urine, color changes to cloudy due to
infection, cystitis, pyelonephritis, urethritis and tuberculosis of the kidney
43.
• Pain- feltin the flank or at the back between the 12th rib and the iliac crest/radiation to the epigastrium. Tenderness
over the kidney pain is intermittent but doesn’t completely remit between pains of colic could be due to chronic
cystitis.
• Retention of urine- this causes agonizing pain on the supra-pubic area.
• Edema- caused by excessive water and sodium retention in the extracellular surface as a result of abnormal renal
excretion, abnormal cardiac or renal disease
• Hypertension- This is due to increased renin production or secretion from obstructed side
• Skin may show pallor suggestive of anemia, excoriations suggesting pruritus infection.
• On palpation kidney bladder or prostate gland may be enlarged
•
44.
ACUTE GLOMERULOEPHRITIS
• Def.Acute glomerulonephritis is the inflammation of the glomerular capillary which causes the kidneys to malfunction.
• It comprise a specific set of renal diseases in which immunologic mechanism trigger inflammation and proliferation of
glomerular tissue that can result in damage to the basement membrane or capillary endothelium.
• It occurs secondary to acute respiratory system infection with group A beta hemolytic streptococcal infection of the throat
• Other infections that may cause glomerulonephritis are hepatitis B, Epstein Barr virus, mumps, varicella zoster viruses,
HIV
• It is also called Acute Nephritis, Glomerulonephritis and Post-Streptococcal Glomerulonephritis
• Predominantly affects children from ages 2 to 12
• Incubation period is 2 to 3 weeks
• Antigen- antibodycomplexes are deposited on the walls of the capillaries and activate the
inflammatory response
• Macrophages attempt to remove the complexes and in the process they release lysosomes
which damage the basement membrane of the capillaries
• When this happens, there is swelling and proliferation of endothelial cells. This leads to
increased permeability of the capillaries and leakage of proteins, red cells and other cells
• If inflammation continues, the basement membrane thickens followed by increased proteinuria.
As the glomeruli heal they become fibrosed and form tufts making the kidney look nodular
48.
Classical signs andsymptoms
• Hematuria: dark brown or smoky urine
• Oliguria: urine output is < 400 ml/day
• Edema: starts in the eye lids and face then the lower and upper limbs then becomes
generalized; may be migratory
• Hypertension: usually mild to moderate
• Proteinuria due to impaired permeability
49.
Other Signs andsymptoms
• Fever
• Headache
• Malaise
• Flank pains
• Anorexia
• Nausea and vomiting
• High blood pressure
• Pallor due to edema and/or anemia
• Confusion
• Lethargy
50.
Diagnosis
• Base linemeasurements:
• ↑ Urea
• ↑ Creatinine
• Urinalysis :
Urine microscopy (red cell cast)
Proteinuria
• Blood urea- moderately high in oliguric phase otherwise normal
• Throat and skin swab for culture
• Physical examination- enlarged kidneys, edema, congested lungs
51.
Complications
• Hypertensive encephalopathy,heart failure and acute pulmonary edema may occur in
severe cases
• Acute renal necrosis due to injury of capillary or capillary thrombosis
• Heart failure
• Pulmonary edema
• End stage renal failure
52.
MEDICAL MANAGEMENT
• Consistof mainly treating symptoms, attempting to preserve kidney function and prompt treatment of
complications
• Antibiotics- penicillin if streptococcal infection is suspected
• Corticosteroid and immunosuppressant prescribed for patients with rapidly progressive acute
glomerulonephritis
• Loop diuretic to remove excess fluids and edema e.g. iv Lasix
• Antihypertensive to treat hypertension e.g. calcium blockers and vasodilators
• Nutrition- restrict dietary protein when renal insufficiency and nitrogen retention develops. Restrict
sodium to control hypertension and edema and to prevent heart failure
53.
NURSING MANAGEMENT
• Mostuncomplicated cases are managed as outpatients
• In hospital setting, nutritional care is given. Carbohydrates are given liberally to provide energy and reduce
protein catabolism
• Give fluids according to the patients fluids losses –(urine output, lung losses, skin losses) and daily body
weight
• Patient education on fluid and diet restrictions
• Educate on signs of renal failure- fatigue, nausea, vomiting, reduced urine output
• Educate on importance of follow up evaluations of BP, urinalysis, BUN and serum creatinine levels
54.
CHRONIC GLOMERULONEPHRITIS
• Nearlyall forms of acute glomerulonephritis have a tendency to progress to chronic
glomerulonephritis.
• The progression from acute glomerulonephritis to chronic glomerulonephritis is variable results in
hardening of the renal arteries (nephrosclerosis) due to hypertension or secondary to diseases like
systemic lupus erythematosus
• Whereas complete recovery of renal function is the rule for patients with post streptococcal
glomerulonephritis, several other glomerulonephritis, such as immunoglobulin A (IgA)
nephropathy, often have a relatively benign course and many do not progress to ESRD
55.
Pathogenesis
• Reduction innephron mass from the initial injury reduces the GFR.
• This reduction leads to hypertrophy and hyperfiltration of the remaining nephrons and to the
initiation of intraglomerular hypertension.
• These changes occur in order to increase the GFR of the remaining nephrons, thus
minimizing the functional consequences of nephron loss.
• The changes, however, are ultimately detrimental because they lead to glomerulosclerosis
and further nephron loss.
56.
Pathophysiology
• Following repeatedepisodes of AGN, HTN nephrosclerosis, hyperlipidemia, chronic
tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis, results in
hardening of the renal arteries and the kidneys are reduced to as little as one fifth normal
size. Cortex shrinks to a layer 1-2mm thicker
• Bands of scar tissue distort the remaining cortex making kidney surface rough and irregular.
• Numerous glomeruli and their tubules become scarred and branches of renal artery are
thickened leading to ESRD
57.
Clinical manifestation
• Uremia-specificfindings irritability, headache dizziness
• Edemas
• Increased nocturia
• Hypertension
• Jugular venous distension (if severe volume overload is present)
• Pulmonary rales (if pulmonary edema is present)
• Pericardial friction rub in pericarditis
• Tenderness in the epigastric region or blood in the stool (possible indicators for uremic gastritis or enteropathy)
• Decreased sensation and asterixis (indicators for advanced uremia)
58.
Diagnosis
• Urinalysis- fixedspecific gravity 1.010, proteinuria, urinary casts
• Serum chemistry
• Serum creatinine and urea nitrogen levels are elevated.
• Impaired excretion of potassium, free water, and acid results in hyperkalemia, hyponatremia, and low serum bicarbonate levels, respectively.
• Impaired vitamin D-3 production results in hypocalcaemia, hyperphosphatemia, and high levels of parathyroid hormone.
• Low serum albumin levels may be present if uremia interferes with nutrition or if the patient is nephrotic
• FHG anaemia, Hypoalbuminemia
• Renal ultrasonogram
• Obtain a renal ultrasonogram to determine renal size, to assess for the presence of both kidneys, and to exclude structural lesions that may be responsible for
azotemia.
• Small kidneys often indicate an irreversible process.
• Kidney biopsy
• Chest X-RAY – cardiac enlargement and pulmonary edema
• CT Scan and MRI- decreased size of renal cortex
59.
Treatment
• High-dose corticosteroids;cyclophosphamide ± plasma exchange/ renal transplantation. Prognosis: Poor if initial serum creatinine
>600µmol/L The target pressure for patients with proteinuria greater than 1 g/d is less than 125/75 mm Hg; for patients with
proteinuria less than 1 g/d, the target pressure is less than 130/80 mm Hg.
• Angiotensin-converting enzyme inhibitors (ACEIs)
• angiotensin II receptor blockers (ARBs)
• Combination therapy with ACEIs and ARBs.
• Diuretics are often required because of decreased free-water clearance, and high doses may be required to control edema and hypertension
when the GFR falls to less than 25 mL/min.
• Beta-blockers, calcium channel blockers, central alpha-2 agonists (e.g., clonidine), alpha-1 antagonists, and direct vasodilators
(e.g., minoxidil, nitrates) may be used to achieve the target pressure
60.
• Renal osteodystrophycan be managed early by replacing vitamin D and by administering phosphate binders.
• Seek and treat nonuremic causes of anemia, such as iron deficiency, before instituting therapy with
erythropoietin.
• Discuss options for renal replacement therapy (e.g., hemodialysis, peritoneal dialysis, renal transplantation).
• Treat hyperlipidemia (if present)
• Expose patients to educational programs for early rehabilitation from dialysis or transplantation.
• Nutrition- protein of high biologic value, plenty carbohydrates to provide adequate calories and spare proteins
61.
NURSING MANAGEMENT
• Observefor common fluid and electrolyte imbalance
• Explain diet and fluid restrictions to ensure cooperation
• Emotional support to patient and family to allay anxiety
• Monitor BP regularly
• Health education to the family on the prescribed treatment plan- instruct patient on follow-up
evaluation i.e. BP, urinalysis for protein and casts, BUN, and serum creatinine levels
• If long-term dialysis is required, teach patient and family on procedure, how to care for access
sites and dietary restrictions
62.
RENAL CALCULI
• Def.:These are hard stone-like masses that form anywhere in urinary tract and can cause pain,
bleeding, obstruction of urinary flow or infection
• OR They are crystalline structures made up of materials of kidney excretion in urine which
include: calcium salts, uric acid or magnesium ammonium phosphate
• Lithiasis means stones formation. When stone forms in the kidney it is known as nephrolithiasis
and if it forms elsewhere in the urinary tract e.g. the bladder it is called urolythiasis
• Calculi is a mass of precipitated material derived from mineral salts and acids
• About 75% of renal stones are calcium based ( Ca oxalate, phosphate, uric acid or Mg phosphate)
63.
Predisposing factors
• Age;common between the 3rd
-5th
decade of life
• Personal family history of urinal calculi
• Dehydration with resultant increased urine concentration
• Excessive dietary intake of calcium leads to hypercalce-urea precipitate calcium oxalate
• Gout and leukemia predispose to uric acid calculi from its side
• Urinary stasis or repeated infections
• Urethral twist or kink
• Anatomic derangements e.g. polycystic kidney disease, chronic strictures
• Medications- antacids, vit D, laxatives, high dose of aspirin
• Vitamin deficiency
• Tumors of either abdominal or pelvic organs pressing on the ureter preventing free flow of urine
64.
Clinical features
• Tendernessand dull ache in the loins on back worse on movement
• Ureteric renal colic characterized by an excruciating pain in the flank that spreads across the abdomen
• Manifestations of UTI including chills and fever
• Manifestations as result of obstructed urine flow with resulting distension and tissue trauma caused by passage of rough edged
crystalline stone.
• The severity of pain often causes a sympathetic response with associated nausea, vomiting, pallor and cool clammy skin.
• A small stone may be passed in urine
• Trauma may cause gross hematuria
• Diarrhoea and abdominal discomfort due to proximity of kidney and GIT
65.
Pathophysiology
• When theconcentration of an insoluble salt in the urine is very high i.e. when the urine is supersaturated, crystals
may form which disperse and are eliminated because the bonds holding them together are weak.
• However the nucleus of crystals may develop stable bonds to form a stone. More often crystals form around an
organic matrix or mucoprotein nucleus to become a stone.
• The stimulus required to initiate crystallization in supersaturated urine may be minimal. Ingesting a meal high in
soluble salt or decreased fluid intake as occurs during sleep allows the concentration to increase to the point
where precipitation occurs and stones are formed and grow.
• When fluid intake is adequate, no stone growth occurs. The acidity or alkalinity of urine and presence or absence
of calculus inhibiting compounds also affect lithiasis.
66.
•
LOCATION OF STONES
•Stones in renal pelvis
• Intense deep ache costovertical region
• Hematuria and pyuria
• Pain that radiates anteriorly and downward toward the bladder in females and toward testes in male
• Acute pain, nausea, vomiting costovertical area tenderness (renal colic)
67.
Ureteral stones
• Stonesin the ureters. Presents with Acute excruciating, colicky, wavelike pain, radiating down the thigh to the
genitalia.
• Frequent desire to void but little urine passed; usually contain blood because of the abrasive action of the stones
Bladder stones
• Symptoms of irritation associated with urinary tract infection and hematuria
• Urinary retention if stones obstruct bladder neck
• Possible urosepsis if infection is present with stone
68.
Types of kidneystones
• Calcium stones (common 75-80%)- composed of calcium phosphate. They are generally associated
with high concentration of calcium in the blood or urine.
• Uric acid stones-develop when the urine concentration of uric acid is high. They are more common
in men and we are associated with gout due to accumulation of uric acid in joints.
• Sturvite-they are associated with UTI caused by urea producing bacteria such as proteus. These
stones can grow to become very large filling the renal pelvis and calyces.
• Cystirie stones-are rare associated with a genetic defect in renal absorption of cysteine ( an amino
acid).
69.
Nursing diagnosis
• Deficientknowledge regarding prevention of recurrence of renal stones
• Acute pain related to inflammation, obstruction and abrasion of the urinary tract
• Altered urinary elimination related to presence of calculi
• Risk of infection related to obstruction of the urinary tract by calculi
• ETC
70.
NURSING INTERVENTION
• Analgesiato relieve pain
• Encourage assumption of comfortable position
• Prevent infection and obstruction; monitor fluid intake and output
• Monitor voiding of patients
• Encourage increased intake of fluid to prevent dehydration & increase hydrostatic pressure that aids in
elimination of stones
• Ambulation may help move the stones through the urinary tract
• Strain the urine on a gauze to detect uric acid stones that may crumble or blood clots
• Instruct patient to report any decrease in urine volume, bloody or cloudy urine
71.
• Monitor vitalsigns closely to detect early signs of infection because UTI may be treated
with appropriate antibiotics before efforts are made to dissolve the stone
• Health education about causes of kidney stones, predisposing factors and
recommendations to prevent occurrence
• Importance of high fluid intake, change of lifestyle
• Reassurance to control anxiety
•
72.
Dietary management
• Increasedfluid intake which prevents the stone forming salts from becoming concentrated enough to
precipitate
• For calcium stones, dietary calcium and Vit D enriched foods are limited which inhibits the absorption of
calcium from the GIT
• Limit phosphorus and oxalate in diet if patient has calcium stones
• Clients with uric acid stones requires a diet low in purines like organs meat
• Recommend patient to take a diet rich in urine alkalinizing foods
73.
Surgery
• Treatment ofexisting calculi depends on the location of the stone, the extend of obstruction, renal function or
absence of UTI and clients general state of health
• In general the stone is removed if it is causing :severe obstruction, infection, unrelieved pain and serious
bleeding
• Lithotripsy – using sound or shock waves to crash the stone is the preferred treatment for urinary calculi
• Nephrectomy. This is the removal of kidney if its non-functional secondary to infection or hydronephrosis
• Pyelolithotomy- removal of stones from renal pelvis
• Chemolysis- stone dilution using infusions of chemical solution e.g. alkylating agents to dissolve the stone
74.
Complications
• -Obstruction- stonescan obstruct urinary system at any point
• -Hydronephrosis- kidneys continue to produce urine causing pressure
• -Infection- urine stasis associated with partial or complete obstruction increases the risk of urinary tract infections
Prevention
• -Diuretics reduce new stone formation
• -Taking large amount of water
• -Avoid oxalate rich foods like spinach, nuts, pepper and tea
• -Low diet in meat, fish and poultry for they increase level of uric acid
75.
PYELONEPHRITIS
PYELONEPHRITIS
• Is theinflammation of the renal pelvis, tubules and interstitial cells of one or both kidneys caused by bacterial infections
• Bacteria reach the kidney from the bladder or spread from systemic sources reaching the kidneys through the
bloodstream
• Mostly caused by Escherichia coli that ascends the urinary tract , klebsiella sp, and Proteus sp
• Most common in females than in males because-
The female urethra is short
Close proximity of the urethral opening to the anus
Pregnancy due to kinking of the ureters causing stasis and reflux of urine
76.
Classification ; acuteand chronic
• Acute pyelonephritis is characterized by;
Enlarged kidney with interstitial infiltration and inflammation, abscess in renal capsule,
atrophy and destruction of tubules
The patient is acutely ill with chills, fever, leukocytosis, bacteuria and pyuria, low back
pain
77.
Pathophysiology
• Infection spreadsfrom the renal pelvis to the cortex. The pelvis, calyces and medulla of the kidney are primarily
affected with white blood cells infiltration and inflammation. The kidney becomes grossly edematous and
localized abscesses may develop on the cortical surface of the kidney.
78.
Signs and symptoms
•Chills and fever
• General malaise
• Dysuria , frequency and urgency in urination
• Anorexia nausea and vomiting
• Urine contains proteins, numerous pus cells, bacteria and some blood
• Urine is cloudy and usually has an unpleasant smell i.e. fishy odor associated with infection of E. coli
• Flank pain
• Hematuria
• Pyuria
79.
Systemic signs
• Patientfeels ill with general body malaise
• Pyrexia and hyperpyrexia
• Sweating rigors, chills nausea and vomiting
• Conversion in children
• Abdominal rigidity in severe cases
• The body shows leukocytosis (excess white blood cells)
80.
Diagnostic tests
• Labtests
• Urinalysis to asses for Pyuria and blood cells in the urine showing high bacterial count
• Gram stain of urine done to identify the infecting organism
• Urine for culture and sensitivity tests to identify the infecting organism and most effective antibiotic
• White blood cell count (in FHG) to detect leukocytosis
81.
Confirmatory tests
• Intravenouspyelography to evaluate the structure and excretory function of kidneys, ureters and bladder.
• Voiding cystourethrography- involves instilling contrast media into bladder then using x-rays to asses it and
urethra when voiding
• Cystoscopy- directly visualize the bladder through a cystoscope
Radiological exam
• Ultrasound or CT Scan to rule out or locate obstruction
•
82.
Management
• Treat thepredisposing
• Ensure complete bed rest in acute phase
• Give appropriate antibiotics after isolating the micro-organism penicillins and cephalosporins
• Nitrofurantoin 50-100mg 6 hourly for seven days (acts as a microbial antiseptic in patients with renal diseases)
• Antiemetic’s i.e. plasil 10 mg once daily for one week
• Analgesics and antipyretics for relief of pain and temperature because stress response and delay healing
• Sodium bicarbonate (citrate) 3gm to keep the urine alkaline
83.
Nursing care
• Completebed rest since during rest slow rate in urine formation
• Vital signs four hourly when patient is in acute stage
• Monitor general appearance of the patient, excretion, urine colour, deposit/ smell or you instruct the patient to do it
• Observe the effects of drugs
• Maintain fluid balance chart (to monitor renal functions)
• Regular testing of the urine
• Since warmth relaxes muscles relieving spasms and increases local blood supply
84.
• Apply warmcompresses at the affected site to relieve pain
• Lie patient on the non-affected side to ease pressure off ureters
• Provide psychological and spiritual care
• Increase fluid intake unless contraindicated to dilute urine
• Discuss the need to avoid voluntary urinary retention and emptying the bladder every three-four hours
• Encourage patients to maintain generous fluid intake during hot whether
• Instruct women to cleanse the peritoneal area from front to back after voiding and defecating
• Teach clients to void before and after sexual intercourse to flush out bacteria introduced into the urethra and
bladder
85.
Prevention
• Provide instructionson the following topics:
• Risk factors four urinary tract infection or minimize these factors
• Earlier manifestation of UTI and importance of seeking early medical intervention
• Maintain optimal immune system functions by attending to physiological and psychological stressors.
• The importance of completing the prescribed treatment and keeping follow up appointment
Complications
• Chronic pyelonephritis
• Hypertension
86.
Chronic pyelonephritis
• Def.: This is a long standing urinary tract infections which affect one or more kidneys
occurring with repeated bouts of acute pyelonephritis. It may continue progress to chronic
renal failure.
• Predisposing factor- Acute pyelonephritis
87.
SIGNS AND SYMPTOMS
Usuallyhas no signs of unless an acute exacerbation
• Fatigue
• Headache
• Poor appetite
• Polyuria
• Excessive thirst
• Weight loss
• Persistent recurring infections may produce scarring of the kidney resulting in kidney failure
88.
Diagnosis
• Intravenous urogram
•Urine culture and sensitivity
• Creatinine levels are elevated
• Blood urea nitrogen
• Creatinine clearance test
Management
• Admit patientand have complete bed rest
• Maintain strict input and output chart
• Administer intravenous fluid and maintain strict input output
• Administer antibiotics nitrofuratoin is used to suppress bacterial growth
• Nutrition care. Give balanced diet, small frequent meals and monitor weight
• Take diet low in salt and proteins
• Transfuse in case of anemia
• Take urine for C/S
91.
• If obstructionhave surgery done
• Discharge patient on treatment
• Advice to seek medical care in care of relapse, observe hygiene and comply with
medication and regular bladder emptying
92.
NURSING DIAGNOSIS
• Painrelated to inflammation of the kidney as evidenced by….
• Altered nutrition less than body requirements related to loss of appetite
• Altered body fluid and electrolyte balance related to excessive urination
• Knowledge deficit related to disease process
93.
NEPHROTIC SYNDROME
• It’sa non specific kidney disorder characterized by proteinuria, edema, hyperlipidemia and Hypoalbuminemia
• Hyperlipidemia is due to decrease plasma protein levels, the body respond by increasing lipoprotein breakdown which enters blood
circulation
• The syndrome is apparent in any condition that seriously damages the glomerular capillary membrane
• Causes
• Primary causes. It means the disease originates from the kidneys. They include;
• Hereditary nephropathy
• Focal glomerulosclerosis
• Membranous nephropathy
• Minimal change nephropathy
•
95.
Secondary causes. Includesrenal manifestation of systemic general illness. Includes;
• Diabetes mellitus
• Viral infection e.g. hepatitis B, hepatitis C, Human Immunodeficiency Virus.
• Amyloidosis
• Chronic glomerulonephritis
• Systemic lupus erythematosus
• Renal vein thrombosis
96.
PATHOPHYSIOLOGY
• Damage occursto glomerular capillary membrane, increasing its permeability to plasma
proteins- majorly albumin. Proteins are lost through urine(proteinuria). Loss of albumin
leads to Hypoalbuminemia. Hypoalbuminemia results in decreased oncotic pressure
hence fluid shift from vascular compartment into interstitial space(hypovolemia and
generalized edema. Hypovolemia stimulates activation of renin angiotensin system,
causing sodium retention with resultant edema.
• Loss of plasma proteins also stimulates synthesis of lipoproteins leading to
hyperlipidemia
97.
Clinical features
• Edemaparticularly of the eyes ankle and feet
• Proteinuria
• Fatigue
• Weight gain
• ascites
• Loss of appetite
• headache
98.
Nursing assessment
• Assesedema when performing physical examination of a child with nephrotic syndrome.
• Weight daily and record the abdominal measurements to serve as a baseline.
• Vital signs more so blood pressure
• Skin - inspect skin for pallor irritation and breakdown
99.
• Nursing diagnosis
•Excessive fluid volume related to fluid accumulation in tissues.
• Fatigue related to edema.
• Risk of imbalanced nutrition less than body requirement related to anorexia.
• Risk for impaired skin integrity.
100.
Nursing care goals
•Relieve edema
• Improve nutritional status
• Maintain skin integrity
• Conserving energy
• Preventing infection
101.
Nursing intervention
• Nursepatient in Fowlers position
• Administer medication, assess patient’s response and adverse reaction
• Monitor diet
• Check patient’s urine protein- frothy appearance
• Skin care- to combat edema and pressure areas; pressure reducing mattress, turning and moving.
• Encourage activity and exercises, provide anti embolism stockings
• Family reassurance and support especially during aute phase
• Monitoring fluid intake and output. Accurately monitor and document intake and output, weigh the patient daily,
• Improve nutritional intake, offer appealing and nutritious diet in small servings
• Promoting skin integrity, inspect all skin surfaces regularly for breakdown, turn and position 2 hourly
• Promoting energy conservation. Bed rest is common in edema stages, balance the activity with rest period and encourage rest when fatigued
• Preventing infection. Protect the patient from anyone with infection, and strict medical asepsis essentials and observe for any early signs of infection
102.
• Improve nutritionalintake, offer appealing and nutritious diet in small servings
• Promoting skin integrity, inspect all skin surfaces regularly for breakdown, turn and position
2 hourly
• Promoting energy conservation. Bed rest is common in edema stages, balance the activity
with rest period and encourage rest when fatigued
• Preventing infection. Protect the patient from anyone with infection, and strict medical
asepsis essentials and observe for any early signs of infection
103.
• Improve nutritionalintake, offer appealing and nutritious diet in small servings
• Promoting skin integrity, inspect all skin surfaces regularly for breakdown, turn and
position 2 hourly
• Promoting energy conservation. Bed rest is common in edema stages, balance the activity
with rest period and encourage rest when fatigued
• Preventing infection. Protect the patient from anyone with infection, and strict medical
asepsis essentials and observe for any early signs of infection
104.
TUBERCULOSIS OF THEKIDNEYS
• Def: It is a secondary infection caused by pulmonary tuberculosis
• Etiology- Mycobacterium Tuberculosis
105.
• Pathophysiology
It occursafter tuberculosis invades the kidney. Early in the disease, renal cortex or
medulla is affected. Tissue damage is progressive and eventually the renal cortex can
rupture into the renal pelvis and infection can spread via mucosa of the remainder of the
urinary tract. If infection involved ureters, structures can develop complicating the
infection by causing and obstruction. In addition, blood supply will also be affected due
to redestruction of kidney tissues by masses of tubercles, initially collateral circulation
will become insufficient and the kidney become
106.
Clinical features
• Theyare mild and include:
• -unexplained weight loss
• - Loss of appetite (anorexia)
• - Fever
• - Hematuria may be present
• - General body malaise may be present
• - Pyuria
107.
Diagnosis
• ESR iselevated
• Urine sample for mycobacterium tuberculosis
• Intravenous urogram
• Cystoscopy since it can advance and affect the bladder
• Kidney biopsy
108.
Management
• Anti-TB medicationsregime
• Medications typically used include isoniazid, rifampicin and ethambutol and pyrazinamide
• If the spread of infection has caused structural damage, a nephrectomy or urinary diversion may be necessary
• Nursing care e.g. pain management, education regarding medication regime to continue with medication after
symptoms subside
• Educating the patient, family and community regarding the risk factors and prevention of TB
• Advice the patient on condom use during sexual intercourse to avoid spread
• Patients with affected penis or urethra should abstain from sex during medication.
• Re-start the treatment in-case of relapse
PROSTATE CANCER
• Prostaticcancer is the most common cancer in men.
• Its common in older me of more than 65 years.
• Prostate tumors are more prevalent in entire genitourinary system
• It has no warning signs, once the tumor causes prostate gland to swell, or spread to other
areas, symptoms appear
111.
RENAL TRAUMA
• Renaltrauma is injury to the kidney caused by an outside force
• The kidneys are protected by the rib cage and musculature of the back posteriorly and by
a cushion of abdominal wall and viscera anteriorly
• As long as about one third of one kidney remains functional, survival is possible
112.
Types of renaltrauma
1. Blunt injury
• Damaged caused by impact from an object that doesn’t break the skin
• Causes include; Rapid deceleration (e.g. motor vehicle, crash, fall from tall building),
Direct blow to the flank (e.g. pedestrian struck, sports injury)
• More common than penetrating trauma and accounts for 80%-90% of all renal injury).
Normally minor and self-limiting
113.
Classification of blunttrauma
• Contusion –bruises or hemorrhage under the renal capsule and collecting system though the
capsule is intact.
• Minor lacerations –superficial disruption of the cortex, renal medulla and collecting system
are not involved.
• Major lacerations – parenchymal disruption extends into the cortex and medulla possible
involving the collecting ducts.
• Vascular injury –tears into the renal arteries and veins
114.
• Penetrating injury
•Usually results from gunshot wounds and stabbings
• More severe and most likely require surgical management
• Causes
• Pelvic fractures
• Road traffic accidents
• Small internal laceration’s of the kidney
• Penetrating or perforating wound
• Pelvic surgery
• Blunt crashing injuries
• Radiation therapy
2
There are threetypes of management
1. Active resuscitative management
2. Conservative management
3. Surgical intervention
Active resuscitative management
• Treatment of shock if present
• Control bleeding
• Maintain whole blood pressure and establish urinary flow
• Observe vital signs four hourly
• Save all urine and send to laboratory for investigations
• Record time of voiding and volume
• Monitor patients or signs of oliguria or hemorrhage
• Detect the presence of hematuria
• Palpate areas around the lower ribs, upper lumbar vertebrae, flank and abdomen for palpable mass and tenderness
• Outline the area of original mass with a marking pencil
117.
Conservative management
Indicated inminor injuries
• Complete bed rest
• Administer intravenous fluids
• Antimicrobial drugs to prevent infection
• Meticulous observation and evaluation of patient for the first few days
• Monitor vital signs to detect evidence
Surgical exploration/ intervention
• Removal or repair of the affected kidney, urethra or bladder
• Urethra
• Pre and post-operative care
• Educate the patient on home health care
• Ensure follow up
•
118.
Complications
• Early complications
•Re-bleeding
• Fistula formation
• Sepsis
• Urine extra-vasation
• Sepsis
• Later complications
• Hypertension
• Stone formation
• Urethral strictures
• Impotence more in men
• Infection
• Cystitis
• Loss of renal function
• Urine incontinence
HYDRONEPHROSIS
• Def.: Isdistension (dilation) of the kidney with urine, caused by backward pressure on
the kidney when the flow of urine is obstructed.
• If the obstruction is in the urethra or bladder, the back pressure affects both kidneys but if
the obstruction is in one of the ureters because of a stone or kink, only one kidney is
damaged
• Partial or intermittent obstruction may be caused by a renal stone that has formed in the
renal pelvis but has moved into ureters and blocked it. Obstruction may be due to tumor
pressing on the ureters
122.
Pathophysiology
• Following obstructionof urine flow since it flow out of the kidney a extremely low
pressure, urine backs up in the small tubes of the kidney and the central collecting area
(renal pelvis), distending the kidney and putting pressure on its delicate tissues
• The pressure from prolonged and severe hydronephrosis ultimately damages tissue so that
kidney function is gradually lost.
Causes
• Ureteropelvic junctionobstruction (an obstruction located at the junction of the ureter and renal
pelvis.
• The causes include:
• Structural abnormalities e.g. insertion of ureter into the renal pelvis is too high
• Kinking in this junction resulting from a kidney shifting downwards
• Stones in the renal pelvis
• Compression of the ureter by fibrous bands, an abnormally located artery or vein or tumor
125.
Causes
• Ureteropelvic junctionobstruction (an obstruction located at the junction of the ureter and renal
pelvis.
• The causes include:
• Structural abnormalities e.g. insertion of ureter into the renal pelvis is too high
• Kinking in this junction resulting from a kidney shifting downwards
• Stones in the renal pelvis
• Compression of the ureter by fibrous bands, an abnormally located artery or vein or tumor
126.
• Obstruction belowthe junction of the ureter and renal pelvis or from backflow of urine from the bladder
Causes include
• Stones in the ureter
• Tumors in or near the ureter
• Narrowing of the ureter from birth defect, an injury, an infection, radiation or surgery
• Disorders of the muscles or nerves in the ureter or bladder
• Formation of fibrous tissues in or around the ureter resulting from surgery, X-ray or drugs
• Ureterocele (bulging of the lower end of a ureter into the bladder)
• Cancers of the bladder, cervix, ureters, prostate, or other pelvic organs
• Obstruction that prevents urine from prostate enlargement, inflammation or cancer
• Backflow of urine from the bladder resulting from a birth defect or an injury
• Severe urinary tract infection temporary preventing the ureter from contracting
128.
• Occasionally hydronephrosisoccurs during pregnancy if the enlarging uterus compresses the ureters. Hormonal changes during
pregnancy may aggravate the muscular contractions of ureters that normally move urine to the bladder
• NB this type of hydronephrosis usually ends when the pregnancy ends, although the renal pelvis and ureters may remain somewhat
distended afterward
Signs and symptoms
• Excruciating, intermittent pain in the flank on the affected side
• Attack of dull, aching discomfort in the flank on the affected side
• Urinary tract infections
• Discomfort in the area of the bladder
• Blood test shows high urea levels
• Intestinal symptoms e.g. nausea
129.
Treatment
• Treat urinarytract infection and kidney failure promptly
• In acute hydronephrosis, urine that has accumulated above the obstruction in the kidney is drained as soon as possible by use of a
needle inserted through the skin
• A catheter may also be inserted to the renal pelvis to temporarily drain the urine if pain is severe
• Chronic hydronephrosis is corrected by treating the cause and by relieving the urinary obstruction
• A narrow or abdominal section of the ureter may be surgically removed and the cut ends joined together.
• If the junction of the ureters and bladder is obstructed, the ureters can be surgically detached the attached to a different part of the
bladder.
• If the urethra is obstructed, treatment can include drugs such as hormone therapy for prostate cancer, surgery or enlargement of the
urethra with dilators.
RENAL FAILURE
• Renalfailure describes the inability of the kidneys to remove metabolic waste products and regulate fluids,
electrolytes and the pH
• The substances normally eliminated in the urine accumulate in the body fluids as a result of impaired renal
excretion
• There are two types- acute and chronic
Acute Renal Failure
• Is a reversible clinical syndrome characterized by a rapid decline in renal function with progressive azotemia (an
accumulation of nitrogenous waste products such as Blood Urea Nitrogen (BUN) and increasing levels of
creatinine). Acute renal failure is associated with a decrease in urinary output to less than 400ml per day
• The kidney fails to excrete nitrogenous waste and to maintain fluid and electrolyte homeostasis
132.
CAUSES OF ACUTERENAL FAILURE
Pre-renal-factors outside the kidneys that reduce renal blood flow. Results from impaired blood flow to the kidney
causing hypoperfusion of the kidney and reduced glomerular filtration.
The kidney has an auto regulatory mechanism for maintaining renal blood flow by constricting the efferent
arterioles. This slows down renal blood flow from the glomerulus increasing hydrostatic pressure and promoting
glomerular filtration. Failure of this mechanism leads to acute renal failure They are the most common causes and
accounts for 70% of all the cases, they include:
1. Volume depletion states; hemorrhage, gastrointestinal loses (NGT sunction, vomiting, diarrhoea), renal loses
( diuretics)
2. Impaired cardiac efficiency; myocardial infarction, heart failure, cardiogenic shock, dysarrhythmias
3. Vasodilation; sepsis, anaphylaxis, antihypertensives or other drugs that causes vasodilation
133.
INTRARENAL
Direct renal damageto the renal tissue (parenchyma) or changes that result in the malfunction of the
nephrons. Intra-renal causes account for approximately 25% of all the cases. Acute tubular necrosis results
from nephrotoxic agents(30%) and ischaemia due to decreased perfusion(50%) Examples include:
• Nephrotoxic substances, for example aminoglycosides, antibiotics, heavy metals
• Prolonged renal ischaemia resulting from myoglobinuria(trauma, crush injuries, burns), hemoglobinuria (
transfusion reaction, hemolytic anaemia)
• Infectious processes; acute pyelonephritis, acute glomerulonephritis
• Trauma
• Solvents and chemicals; ethylene glycol, carbontetrachloride, arsenic
134.
POST RENAL
Mechanical obstructionof urinary outflow. As the flow of urine is blocked, urine backs up into the renal pelvis
resulting in renal failure. The obstruction leads to stasis of urine all the way to the renal pelvis, accumulation of urine
in the renal pelvis creates tension in the kidney. Post renal causes account for less than 5% of the cases.
The most common causes are:
• Benign prostatic hyperplasia
• Renal calculi
• Strictures
• Blood clots
• Tumors; bladder, prostate, cervix
• Post-surgical or traumatic interruption or retroperitoneal fibrosis
135.
PATHOPHYSIOLOGY OF A.R.F
Renalvasoconstriction:
• Hypovolemia and decreased renal blood flow reducing oxygen and nutrient supply to the kidneys.
This causes ischemia leading to damage. The auto regulation mechanism of kidneys maintains
blood flow. However, when systolic BP is less than 70mmhg, the mechanism fails resulting in
ischemia which is worsened by the renin angiotensin mechanism.
• Ischemia leads to necrosis of cells of the renal tubules. The cells sloughs off and block the renal
tubules
• Nephrotoxic substances kill the cells leading to sloughing off and blocking the tubules- most
affected is the loop of henle
136.
THE PHASES OFA.R.F
There are three phases:
• Onset
• Oliguric Phase
• Diuretic Phase
• Recovery Phase
Onset/ initiation. This is the initial phase of injury to the kidney and reversal or prevention of kidney
dysfunction
is possible. Begins when the kidney function is affected by the disease. It begins with the initial insult and
ends when oliguria develops
137.
OLIGURIC PHASE
• Urineis less than 400ml/day.
• Is accompanied by a rise in serum concentration of the elements (urea, creatinine, uric acid and
intracellular cations potassium and magnesium).
• The patient is acutely ill and the phase lasts approximately 10 - 14 days.
• In this phase, uremic symptoms first appear and life threatening conditions such as hyperkalemia develops
• There is a non Oliguric form where the patient has reduced renal function with increasing nitrogen
retention, yet they excrete normal amount of urine (2L/24hrs). This occurs after exposure of the patient to
nephrotoxic agents
• The longer this phase, the worse the prognosis
138.
DIURETIC PHASE
• Patientexperiences a gradual increase in daily urinary output which may be greater
than 2000ml/day, but about one to three litres per day.
• Despite the urinary output rising, the nephrons are still not fully functional.
• The kidneys have also recovered their ability to excrete wastes but not to concentrate
urine
• Patients should be observed closely for signs of dehydration during this phase. If
dehydration occurs, the uremic symptoms are likely to increase
139.
RECOVERY PERIOD
• Thephase begins when the glomerular filtrate rate rises and the blood urea nitrogen
and serum creatinine levels start to stabilise and then decrease. It signals
improvement of renal function. The phase lasts 3 - 12 months.
140.
CLINICAL FEATURES
Depend onaffected system
Has a rapid onset which results from retention of fluids metabolic wastes and the inability to regulate electrolytes.
The patient is acutely ill and may suffer from acidosis, anaemia, fluid and electrolytes imbalances, fluid overload or deficit
and gastrointestinal distress.
• Hyperkalemia due to decreased potassium excretion
• Oliguria (urine output of less than 400ml per day) or anuria (urine output of less than 100ml/day
• Increased BUN(azotemia) i.e. there is increased protein catabolism which leads to increased urea, creatinine and uric acid
levels in blood. This manifests as anorexia, vomiting, diarrhoea, hiccups, headache, drowsiness, muscle twitching and
convulsions
• Ventricular fibrillation due to increased impulse conduction muscles secondary to hyperkalemia. It can lead to asystole
141.
CLINICAL PRESENTATIONS
Pre renalIntrarenal Post renal
BUN Increased increased increased
Urine output reduced Often decreased Decreased
Creatinine Increased Increased Increased
Urine sodium Decreased to <20
mEq/L
Increased > 40
mEq/L
Often decreased to
<20mEq/L
Urine osmolality Increased normal varies
Urine specific gravity increased Normal/ low varies
142.
MANAGEMENT
• The objectiveis to restore normal chemical balance and prevent complications until repair of renal tissue and restoration of renal
functioning can occur.
• Management includes maintaining fluid balance, avoiding fluid excesses or possibly performing dialysis
• The underlying cause is identified and treated
• Maintenance of fluid balance is based on daily weight, measurement of central venous pressure, serum and urine concentration, fluid
losses, BP and clinical status of the patient
• Fluid excesses can be detected by dyspnea, tachycardia, distended neck veins, crackles in the lungs, and generalized edema
• Mannitol, frusemide or ethacrynic acid may be prescribed to initiate diuresis and prevent complications
• Adequate blood flow to the kidneys may be restored by IV fluids or transfusion of blood products
• If ARF is due to hypovolemia secondary to hypoproteinemia, albumin infusion is given
• Dialysis may be initiated to prevent serious complications e.g. hyperkalemia, severe metabolic acidosis, pericarditis and pulmonary edema
143.
NUTRITION THERAPY
• Proteinsand potassium are restricted to help reduce the accumulation of electrolytes and
metabolic wastes.-bananas, citrus fruits, juices, coffee
• Fluid and sodium are restricted during the Oliguric phase to decrease fluid overload.
• Dietary supplements, for example multivitamin and iron supplements
• Weigh patient daily
• High carbohydrate meals to meet caloric needs so that-protein spared for healing and growth
• In diuretic phase may give high protein and high caloric diet
144.
DRUG THERAPY
Drug Therapy
•Digoxin to increase stroke volume.
• Antihypertensive to reduce the elevated blood pressure.
• Stool softeners may be given to prevent constipation and excessive straining.
• Phosphate binding agents- aluminium hydroxide( reduce phosphate absorption from GIT)
145.
DIALYSIS
Preferably hemodialysis iscommonly indicated in :
Volumes overload resulting in congestive heart failure
Pulmonary edema
Potassium levels greater than 6.0mmoL
Metabolic acidosis (serum bicarbonate level less than 15mml/L
BUN level greater than 120gm/dl 43 mMol/L
Significant change in mental status
Pericarditis
146.
HYPERKALEMIA MANAGEMENT
• Cationexchange resins(sodium polysterene sulfonate:kayexalate)- exchange sodium for K+ in
GIT. Administer with sorbitol to induce diarrhoea
• IV 50% dextrose
• Insulin
• Dialysis
• Calcium gluconate
NB: they help to shift K+ into cells
Albuterol sulfate
147.
NURSING MANAGEMENT
ASSESMENT
• Assesspatient medical history for any factors that may lead to renal failure
• Assess for signs of fluid overload
• Assess urologic function i.e. Fluid intake and output. Oliguria or concentrated urine
• Establish basal body weight and vital signs for reference
148.
NURSING DIAGNOSIS
• Alteredbreathing pattern related to metabolic acidosis as evidenced by increased respirations
• Altered nutrition less than body requirements related to nausea and vomiting….
• Anxiety related to unknown outcome of disease process
• Knowledge deficit on the cause of the disease and treatment regimen
• Risk of impaired skin integrity related to edema
• High risk of infection related to lowered immunity
INTERVENTIONS
• Monitor patient’sserum electrolyte levels and physical indicators of complications
• Parenteral solutions and oral intake should be carefully selected according to the patients fluid and electrolyte status
• Monitor patient’s cardiac function and musculoskeletal status closely for signs of hyperkalemia
• Monitor fluid status by paying close attention to fluid intake, urine output, edema, distention of jugular veins,
alterations in heart and breath sounds and increased difficulty in breathing
• Accurate daily weighing
• For adequate nutrition, provide a high carbohydrate, low protein food in Oliguric phase, but increase protein in
diuresis phase
151.
• Assist patientto turn, cough and take deep breathing exercise frequently to prevent lung
atelectasis and respiratory tract infections
• Maintain bedrest to reduce exertion of metabolic rate
• Maintain asepsis with invasive lines and catheters to minimize the risk of infection
• Avoid indwelling catheters wherever possible due to high risk of infections
• Frequent turning, keeping skin clean and well moisturized to prevent skin breakdown
• Give patient and family psychological support
152.
CHRONIC RENAL FAILURE
Thisis the progressive irreversible destruction of the nephrons in both kidneys. The destruction progresses and
the nephrons are destroyed and replaced by non-functional scar tissue. The body is unable to maintain metabolic
and fluid and electrolytes balance leading to azotemia or uremia
Causes
1. Systemic diseases; diabetes, hypertension, chronic glomerulonephritis, chronic pyelonephritis, SLE,
2. Obstruction of urinary system
3. Hereditary lesions; polycystic kidney disease
4. Vascular disorders
5. Medication or nephrotoxic agents e.g. lead
153.
PATHOPHYSIOLOGY
• Following thedeterioration and loss of nephrons, the sum total of renal function progressively reduces too
especially if the underlying systemic disease e.g DM is not well controlled consequently the GFR falls as serum
creatinine reduces too along with continued accumulation of nitrogenous wastes.
• The remaining nephrones hypertrophy as they are required to filter a large load of solutes nevertheless the kidney
continues losing its ability to concentrate urine adequately. In attempt to continue excreting solutes, a large volume
of dilute urine is passed making the patient susceptible to fluid depletion.
• On the other hand the tubules gradually lose the ability to reabsorb electrolytes; this initially leads to salt wasting in
which urine contains large amounts of sodium enhancing polyuria further. As the number of functioning nephrones
keeps declining further along with GFR, the body is unable to get rid of water, salts and nitrogenous waste. By the
time GFR is less than 20ml/min, the body is severely uremic which has far reaching effects to all body systems
154.
STAGES OF CRFBASED ON GFR( NORMAL
125ML/MIN/1.73M2
Stage 1 Kidney damage with normal
or ↑ GFR
GFR ≥ 90 ml/min/1.73 m2
Stage 2 Kidney damage with mild ↓
GFR
GFR 60-89
Stage 3 Moderate ↓ GFR GFR 30-59
Stage 4 Severe ↓ GFR GFR 15-29
Stage 5 Kidney failure GFR <15 (or dialysis)
155.
CLINICAL FEATURES
Every bodysystem is involved. The clinical manifestations are as a result of retained substances
which include urea creatinine, hormones, electrolytes and water, imbalance of fluids and
electrolytes.
Manifestations may include: Uremia, anaemia, acidosis.
• Fluid and sodium are either abnormally retained or excreted.
• Urinary volume may be increased, normal or decreased.
• Hypertension is common due to increase in total body water and sodium.
156.
CV- most commoncause of death in ESRD Dermatologic manifestation
HTN( water and Na+ retention and
activation of RAAS), HF, pulmonary edema,
pericarditis (uremic toxin irritation), pitting
edema (feet, hands, sacrum, periorbital),
engorged neck veins, pericardial effusion,
hyperkalemia, hyperlipidemia
Severe pruritis/itching
Uremic frost( deposit of urea cryatals on the
skin-grey bronze skin)
Dry flaking skin
Ecchymosis
Purpura
Thin brittle nails
Coarse thinning hair
157.
Git Neurologic examination
Anorexia,nausea, vomiting and hiccups
Uremic fetor(urine odour breath, ammonia
odour)
Metallic taste
Mouth ulcerations
Constipation
Bleeding from GIT
Inability to concertrate, loss of conscious,
muscle twitching, agitation, confusion,
seizures, tremors
Peripheral neuropathy
Restless leg syndrome and burning feet
Asterixis
Complain of severe pain and discomfort
DIAGNOSIS
Based on:
• History.
•Symptoms.
• GFR – the amount of plasma filtered through the glomerular per unit time
• Laboratory studies - serum creatinine and creatinine clearance. A rise in serum creatinine and a fall in creatinine clearance
indicates renal failure. Serum creatinine is the more sensitive indicator of renal failureBlood gas analysis –metabolic acidosis
(inability to excrete ammonia(NH3-) and to reabsorb bicarbonates(HCO3)
• CBC – low Hb and RBC (inadequate erythropoietin, reduced lifespan of RBC, nutritional imbalance)
• Electrolyte monitoring- increased K+ and phosphate ions, low calcium (an increase in serum phosphate lead to a decrease calcium
levels)
Reduced Ca+ leads to calcium release from bone hence renal osteodystrophy
161.
MANAGEMENT
The focus ison conservative management which is directed toward:
• Preserving existing renal function
• Treating the symptoms
• Preventing complications
• Providing for the patient's comfort
All factors that contribute to ESRD and are reversible are identified and treated
162.
DRUG THERAPY
Avoid non-steroidalanti-inflamanatory drugs since they block synthesis of prostaglandin in the
kidney that promote vasodilatation and thereby reducing blood supply to the kidney.
• Acute hyperkalaemia is treated by (IV) glucose and IV 10% calcium gluconate, dialysis
• Hypertension - treatment consists of:
Sodium and fluid restriction
Antihypertensive, for example beta blockers like nicardipine, nifedipine; inotropic agents
such as digoxin and dobutamine
Diuretic therapy
163.
• Calcium supplimentsand phosphorus binders
Eg calcium carbonate, calcium acetate,(adminster with food), avoid magnesium based antacids to prevent
magnesium toxicity
Antiseizure agents
Phenytoin and diazepam, monitor for twitching, headache, delirium etc, raise side rails
• Anaemia - iron supplements and folic acid,Transfusion (severe anaemia), erythropoietin administration
• Gastrointestinal symptoms, for example nausea is treated with antacids, antiemetics, dietary control of
nitrogenous wastes and maintenance of fluid and electrolyte balance
164.
NUTRITION THERAPY
• Restrictproteins - administer only 20g of high quality protein to prevent accumulation of
nitrogenous waste products.
• Restriction of sodium and potassium (depend on the degree of oedema and hypertension.)
• Fluid restriction - depend on daily urine output but up to 500-600 ml more than the previous
day’s 24-hr urine output
• Phosphate intake is reduced to less than 1000mg/day.
• Adequate caloric intake
• Supplement vitamins as patient loses water soluble vitamins durinf=g dialysis
165.
PROMOTION OF PATIENTSCOMFORT
• The patients are prone to muscle cramping, pruritus, headaches, ocular irritation, insomnia and
fatigue.
• The primary treatment involves control of the electrolyte imbalance.
• Treatment of pruritus is aimed at decreasing the phosphorus.
• Local and systemic agents may be administered to decrease the itching.
• Ocular irritation is as a result of calcium deposits and treatment is aimed at decreasing the plasma
phosphate levels.
• Insomnia and fatigue are due to uremia and are treated by decreasing metabolic wastes and providing
psychological support.
166.
NURSING CARE OFA PATIENT WITH CHRONIC
RENAL FAILURE
1. Excess fluid volume related to decreased urine output, dietary excesses and retention of sodium and water as evidenced by…..
• Goal; maintenance of ideal bodyweight without excess fluid
Intervention
• Assess fluid status through;
Daily weight
Input and output balance
Skin turgor and presence of edema
Distention of neck veins
BP, pulse rate and rhythm
Explain to the patient and family rationale for fluid restriction to ensure cooperation
Assist patient to cope with the discomfort resulting from fluid restriction e.g. water gargles
Provide and encourage oral hygiene to decrease dryness of the oral mucosa membrane
167.
2. imbalance nutritionless than body requirements related to anorexia, nausea, vomiting, dietary restriction and altered oral mucosa membrane
as evidenced by….
Goal; maintenance of adequate nutrition intake
Interventions
• Assess nutritional status through
Weight changes
Lab values- serum electrolytes, BUN, creatinine, protein, iron
• Assess patient dietary patterns
Diet history
Calorie count
Food preferences
168.
• Assess factorscontributing to altered nutritional intake
Anorexia, nausea and vomiting
Unpalatable diet
Depression
Lack of understanding of dietary restriction
Stomatitis
• Promote intake of high biologic value protein foods
• Encourage high caloric, low protein, low sodium, and low potassium snacks between meals
• Explain rationale for dietary restriction
• Provide written list of foods allowed and suggestions for improving their taste
• Daily weighing
169.
3. knowledge deficitregarding condition and treatment
Interventions
• Assess knowledge on cause, consequences, and treatment of renal failure
• Explain condition and its management
• Provide oral and written information about renal function, failure, fluid and dietary
restrictions, medication and follow up
170.
4. activity intolerancerelated to fatigue, anaemia, retention of waste products and dialysis
procedure
Interventions
• Assess factors contributing to activity intolerance, fatigue, anaemia, fluid and electrolyte
imbalance
• Promote independence in self care activities as tolerated
• Alternate activity with rest
DIALYSIS
Dialysis is theprocess of artificial removal of fluid and uremic waste products from the body when the kidneys
cannot do so
It is used to treat patients with edema that does not respond to other treatment, hepatic coma, hyperkalemia,
hypercalcemia, hypertension and uremia
The are three methods
Hemodialysis
Peritoneal dialysis
Continuous renal replacement therapy
The need for dialysis can be acute or chronic
173.
Indications for acutedialysis
• High increasing level of serum potassium
• Fluid overload/impending pulmonary edema
• Increasing acidosis
• Pericarditis
• Severe confusion
• Poisoning/toxins/ medication overload
174.
Indications for chronic/maintenancedialysis
ESRD- main indication when it presents with;
• Presence of uremic signs and symptoms(nausea, vomiting, severe anorexia, increasing lethargy,
mental confusion)
• Hyperkalemia
• Fluid overload not reponding to diuretics and fluid restriction
• General lack of well being
NB; an urgent indication for dialysis in patient with chronic renal failure is pericardial friction
rub
175.
• Patients withno renal functions can be maintained on dialysis for years
• Dialysis is initiated when the patient cannot maintain a reasonable lifestyle with conservative management
Principles of dialysis
Diffusion
Osmosis
Ultra filtration
Diffusion
• Toxins and waste in the blood are removed by diffusion from an area of higher concentration in the blood to an
area of lower concentration in the dialysate
176.
Osmosis
• Movement ofsolvent such as water across a semipermeable membrane from areas of less
solute to areas of high concentration of solute
Ultrafiltration
• Movement of fluid across a semipermeable membrane from a high pressure area to a low
pressure area
• It is more efficient in removal of water than osmosis. Negative pressure is created against a
dialysis membrane to draw water from the blood
177.
HEMODIALYSIS
• Hemodialysis isthe most common method used to treat advanced and permanent kidney failure
• It is used for;
Patients who are acutely ill and require short term dialysis of days to weeks
Patients with ESRD who require long term or permanent therapy
Objectives
To extract toxic nitrogenous substances from blood
To remove excess water
178.
Components of hemodialysisinclude
• Dialyser
• Clot and bubble trap
• Blood pump
• BP monitor
• Dialysate flow system
• Blood lines
• Heparin pump
179.
Dialyser
• They arehollow filters devices containing thousands of tiny cellophane tubules that act as
semipermeable membranes, replacing the glomeruli and tubules
• The blood flows through the tubules while a solution (dialysate) circulates around. The exchange of
waste products from the blood to dialysate occurs through a semipermeable membrane of tubules
• Because of cost, dialysers are reused in some centres upon sterilization
Blood lines
• Are plastic synthetic tubules which take blood from the patient attached with A.V fistula and dialyser
180.
Blood pump
• Createsa sunction force that circulates blood through hemodialyser
Heparin pump
• In blood that come in contact with synthetic material, clotting is likely. To prevent this blood is injected with heparin mixed
with normal saline to ensure it doesn’t clot in the blood lines
Clot and bubble trap
• Trap and prevent embolising the patient with air or blood clot
• It filters blood and allow any air to escape
Dialysate flow system
• System of pump which takes the dialysate through the dialyser in a counter current version
183.
PRINCIPLES OF HEMODIALYSIS
•Diffusion- toxins and wastes are removed by diffusion (highly concentrated in blood than
dialysate. Dializer has a sem-ipermeable membrane that prevents diffusion of RBCs and
proteins(large molecules)
• Osmosis-removal of excess water. Blood has a high solute concentration, dialysate has
low solute concentration
• Ultrafiltration- removal of water from the area of high pressure(blood) to the area of low
pressure(dialysate). Accomplished by applying negative pressure or a suctioning force to
the dialysis membrane
184.
VASCULAR ACCESS
• Accessto the patient vascular system must be established to allow blood to be removed,
cleaned and returned to the patients vascular system
Several types of access available are
Use of large veins
Use of fistula
Use of grafts
185.
Use of largeveins
• Used in immediate access to the patients circulation for acute hemodialysis and is achieved by
inserting a double lumen catheter into subclavian, internal jugular and femoral vein. It involves risk
of hematoma formation
• While not in use it is heparinized to prevent blood from clotting and is covered with a sterile dressing
• The catheter is removed when nolonger needed e.g. if patient condition improves or another type of
access has been established
• Double lumen, cuffed catheters may be also inserted into the internal jugular vein of the patients
requiring a central venous catheter for dialysis
• These catheters are used for long term access
186.
Arteriovenous fistula
• Preferredmethod for permanent access
• It is created surgically usually in the forearm by anastomosing an artery to the vein either side to side or end to side
• Needles are inserted into the vessel to obtain blood flow adequate to pass through the dialyser
• The arterial segment of the fistula is used for arterial flow to the dialyser and the venous segment for reinfusion of
the dialysed blood
• The fistula should be allowed at least 14 days to mature (allow healing and dilatation of the venous segment)
• Needle of gauge 14-16 are used for taking blood from the patient and back
• The patient is encouraged to take exercise to increase the size of the vessel
187.
Arteriovenous graft
Surgical Placingof a graft (biological, semi biological or synthetic) between artery and
vein( tube joining artery and vein)
• Usually a graft is created when the patients vessels are not suitable for creation of a
fistula e.g. those with compromised vascular system as in DM
• Infections and thrombosis are the most common complicatins of Arteriovenous graft
188.
NURSING MANAGEMENT
• Constantmonitoring of the patient, dialyzer and dialysate to rule out clotting, air
embolism, excess ultrafiltration( hypotension, cramping, vomiting), blood leaks,
contamination and vascular complications
• Patient education
• Care of vascular access-patency; avoid use of the hand for BP,blood collection, tight
dressing, restraints or jewellery; check fro ‘ bruit and thrill’ 8 hrly(if absent suspect
blockage and clotting) assess symptoms of infection(redness, swelling, drainage, fever
chills) change dressings as indicated)
189.
Pharmacological
Avoid antihypertensives ondialysis day
Withhold once a day drugs until dialysis is done
Nutritional fluid therapy
Goals-
• Minimize uremic syndromes and fluid and electrolyte imbalances
• Maintain good nutritional status with adequate proteins, calorie, vitamin and minerals
• Enable patient eat palatable and enjoyable diet
190.
• Restrict dietaryprotein to 1.2-1.3 g/kg/day. Use proteins of high biologic value with
essential amino acids such as eggs, meat, poultry and fish
• Restrict sodium to 2-3 g/day
• Fluid restriction to equal amount lost +500ml/day
• Potassium restriction
Psychological management- anxiety, counseling, psychotherapy
191.
COMPLICATION OF HEMODIALYSIS
•Disturbance of lipid metabolism- hypertriglyceridemia which is accentuated by hemodialysis causing atherosclerosis
leading to heart failure, coronary heart disease and angina pain
• Gastric ulcers and other GI problems resulting from the physiologic stress of chronic illness and medication
• Disturbed calcium metabolism leads to bone pain and fractures( renal osteodystrophy
• Sleep disturbance in 85% of patients undergoing hemodialysis
• Blood loss if blood lines separate or dialysis needle dislodge
• Air embolism- rare but can occur if air enters the vascular system
• Dialysis disequilibrium due to rapid fluid shift from the cerebral fluid and its characterized by headache, nausea, vomiting,
restlessness, decreased level of consciousness and seizures
• Dysarrhythmias due to electrolyte and PH changes or from removal of antiarrhythmic medication during dialysis
192.
PERITONEAL DIALYSIS
• Involvesusing peritoneum as a filter. Like kidneys, peritoneum has thousands of tiny blood vessels making it useful as a
filtering device
Goals
• To remove toxic substances and metabolic wastes
• To re establish normal fluid and electrolyte balance
Indications
Patients with renal failure unable or unwilling to undergo hemolysis or renal transplant
Patients susceptible to rapid fluid and electrolyte, and metabolic changes that occur with hemodialysis
Patients at risk of adverse effects of systemic heparin
In peritoneal dialysis, the peritoneum that covers the abdominal organs serves as a semipermeable membrane
193.
MECHANISM OF PERITONEALDIALYSIS
• Involves insertion of a catheter into peritoneal cavity and then dialysate introduction. As
blood moves through peritoneum, waste products and excess fluid are moved from blood
into dialysis fluid. The fluid is then drained from the cavity. The process last for about
30-40 minutes and is repeated 4 times a day. It may also be done overnight. It takes
36-48 hours to achieve what hemodialysis accomplishes in 6-8 hours
195.
PREPARATION
• Explain tothe patient, obtain baseline studies( weight, electrolyte levels etc.)
• Encourage the patient to empty bladder and bowel to reduce the risk of injury
• Assess the level of anxiety and provide support
• Assemble equipments
• Establish concentration of dialysate, heparin may be added to prevent fibrin formation
• Get broad spectrum antibiotics to prevent infection
• Prepare patient for insertion of peritoneal catheter
196.
EXCHANGE CYCLE
• Consistsof infusion, dwelling and drainage
Infusion : 2-3 litres of dialysate infused by gravity into peritoneal cavity in about 5-10
seconds
Dwell : allows diffusion of molecules. It peaks at 5-10 minutes of dwell
Drainage : unclamp the tube, allow drainage by gravity. Fluid is colourless or straw-
coloured and should not be cloudy. Blood drainage may be seen in the first few
exchanges after insertion.
197.
• The entireexchange takes 30-45 minutes. The cycle may be repeated severally depending
on patient’s physical status and acuity of illness
• Excess water is removed by use of hypertonic dialysate such as high dextrose solutions
Complications
Acute complications
Peritonitis- caused by gram positive bacteria( S. aureus and S. epidermidis) and gram
negative (Pseudomonas aeruginosa, E. coli and Klebsiella
198.
Peritonitis is characterizedby;
• Cloudy dialysate drainage
• Diffuse abdominal pain
• Rebound tenderness
• Hypotension and shock
Managed by rapid infusions and addition of antibiotics( cephalosporins and aminoglycosides) in dialysate
• Leakage
• bleeding
199.
LONG-TERM COMPLICATIONS
• Hypertriglyceridemia
•Sub-optimal blood pressure
• Abdominal hernia- incisional, inguinal, umbilical, diaphragmatic, due high abdominal
pressure
• Low back pain and anorexia
200.
APPROACHES TO PERITONEALDIALYSIS
. Acute intermittent peritoneal dialysis- has various cycle exchanges
• Indications – uremic signs, fluid overload, acidosis, hyperkalemia
• Mnx- use strict aseptic technique, monitor: weight vital signs, in/output, lab values,
patients condition. Record each exchange- dialysate conc., drugs added, exchange
volume, dwell time, fluid lost or gained. Evaluate fluid status
• Monitor drainage- secure drainage system, turn patient from side to side, raise the head
of the bed, inspect kinks, closed clamps and air lock
201.
NURSING MANAGEMENT DURING
DIALYSIS
•Protecting vascular access
• Avoid rapid/ excessive IV infusion to prevent pulmonary edema
• Monitor signs of uremia
• Monitor cardiac and respiratory values to detect complications-crackles, dyspnea,
hypotension, pericarditis( sub sternal chest pain, low grade fever, pericardial friction rub,
pulsus paradoxus- reduction in BP more than 10mmHg during inspiration
202.
• Control electrolytelevels and diet
• Management of pain and discomfort- antihistamines, analgesics, keep skin clean and nails
short
• Monitor BP and prevent infections
• Catheter site care- 3-4 times a week during showering or daily, exit site should not be
submerged in bath water
• Psychological support
CYSTITIS
• Def; inflammationof the bladder.
• Causes.
• UTI.
• Certain drugs or radiation therapy.
• Longtime catheter use,
• Complication of another illiness e,g diabetes.
205.
SYMPTOMS
• Persistent urgeto urinate.
• Pain or burning sensation on urination.
• Passing small frequent amounts of urine.
• Haematuria.
• Cloudy or smelly urine.
• Pelvic discomfort.
• Low grade fever.
206.
TYPES OF CYSTITIS
•bacterial cystitis.-when bacteria enters the urinary tract thru the urethra and begin to
multiply.e.g E.coli.
• Non infectious
• Interstial cystitis,drug related cystitis,(chemotherapy),radiation,foreign body cystitis,
(catheter),chemical cystitis(spray,spermicide,)associated with other conditions-kidney
stones, DM.
RISK FACTORS.
• Sexuallyactive.
• Use of certain types of birth control.
• Pregnancy-hormonal changes may increase risk of bladder infection.
• Having gone thru meni=opause due to changes in hormones.
• Interference with flow of urine-kidney stones.
• Changes in immune system.
• Longterm use of catheters.
NURSING MANAGEMENT
• Hygiene.
•Increase fluid intake.
• Patterns of voiding.
• Check on characteristics of urine,colour,odour.
• Pain relieve.
211.
PREVENTION
• Take plentyof fluids.
• Urinate frequently.
• Wipe from front to back.
• Take showers instead of bath tubs.
• Gently wash skin around genitals.
• Empty bladder ASAP after sex.
• Avoid using deodorant sprays or hygiene products in the genital area.
URINARY INCONTINENCE
• Itis defined as involuntary or uncontrolled loss of urine from the bladder sufficient to cause a social or hygienic
problem
• Urinary incontinence (UI) affects well over 13 million people in USA. Estimated costs in excess of $15 billion annually.
Most women do not seek help for incontinence
• Because of social embarrassment
• Be unaware that help is available
• Incontinence is part of the “normal” aging process is no longer acceptable
• The advances in modern medicine during the last 80 years have increased the life expectancy of women well into the
eighth and ninth decades
• We are caring for patients longer and better than ever, enabling women to enjoy longer and more productive lifetimes
Types of incontinence
•Stress urinary incontinence (SUI)
• Urge incontinence
• Mixed incontinence
• Overflow incontinence
• Extra urethral sources of urine
Stress urinary incontinence
• Loss of urine that occurs with increased abdominal pressure, such as coughing or straining
• Result of loss of anatomic support of the urethrovesical junction or urethra
• It most commonly occurs following pelvic floor muscle and nerve damage that resulted from childbearing
217.
Urge incontinence
• Isdefined by the symptom of urine loss that occurs when the patient experiences urgency, or a strong desire to void
• Is often accompanied by symptoms of urinary frequency, urgency, and nocturia .
Mixed incontinence
• Occurs when both stress and detrusor instability occur simultaneously
• Patients may present with symptoms of both types of incontinence
Overflow incontinence
• Occurs because of underactivity of the detrusor muscle
• Be associated with retention of urine
• The bladder does not empty completely, and “dribbling” of urine occurs
218.
Extra urethral sourcesof urine incontinence
• Include genitourinary fistulas
• Be congenital or follow pelvic surgery or radiation
• These typically cause continuous leaking of urine
Diagnosis
• History
• Physical examination
• Intravenous pyelogram
• Cystoscopy
219.
History taking
• Adetailed history is essential and should include:
• a. Urinary symptoms, including the presence of voiding frequency, nocturia, urgency, precipitating events, and frequency of
loss. A voiding diary allows the patient to document voiding frequency and incontinence episodes during a specific period
• b. Previous urologic surgery
• c. Obstetric history, including parity, birth weights, and mode of delivery
• d. CNS or spinal cord disorders
• e. Use of medications, including diuretics, antihypertensive, caffeine, alcohol, anticholinergic, decongestants, nicotine, and
psychotropics
• f. Presence of other medical disorders (e.g., hypertension or hematuria)
220.
Physical examination maydetect:
• a. Exacerbating conditions, such as chronic obstructive pulmonary disease, obesity, or intra-abdominal mass
• b. Hypermobility of the urethra
• c. Neurologic disorder
Diagnostic tests
• a. A midstream urine specimen. -- midstream urine specimen. Be collected for urinalysis or culture and sensitivity. Infection may
aggravate urinary incontinence
• b. Post void residual urine volume post residual urine volume should be measured (by ultrasound or catheterization) after the patient
has voided. Typically, the post void residual urine volume is less than 50 to 100 ml
• Cystoscopy is performed in some patients to examine the bladder and urethral mucosa for abnormalities such as diverticula or
neoplasms
221.
Therapy depends onthe underlying diagnosis.
• Treatment of exacerbating factors
• Pelvic muscle rehabilitation
• Pessaries are useful conservative therapies for Stress Urinary Incontinence
• Drug therapy-co adrenergics ,anti cholinergics.
• Surgery
• Treatment of exacerbating factors may improve Stress Urinary Incontinence- excess weight, chronic cough and constipation
• Pelvic muscle rehabilitation -- be helpful for SUI using Kegel exercises, Biofeedback and Electrical stimulation
• Drug treatment
• a. α-Adrenergic stimulating agents increase smooth muscle contraction in the urethral sphincter and may decrease SUI symptoms
• b. Estrogens improve irritative bladder symptoms such as urgency and dysuria in postmenopausal women but do not significantly improve urinary
leakage.
222.
• c. Anticholinergicsto inhibit bladder contraction e.g. oxybutynine
Surgery is extremely effective in the treatment of SUI.
• a. Injection of bulking agents around the urethra
• b. Retropubic urethropexy
• c. Transvaginal needle procedures
• d. Sub urethral sling procedures
• e. Chronic catherization
URINARY REFLUX
• Itis the abnormal flow of urine from the bladder back to the ureters that connect the
kidneys to the bladder
• Causes
• Primary vesicoureteral reflux due to defect in the valve that prevents urine from flowing
backwards from bladder to ureters
• Secondary vesicoureteral reflux from failure of the bladder to empty properly due to
blockage or failure of the bladder muscle or damage to the nerves that control normal
bladder emptying
225.
• Risk factors
•Bladder and bowel dysfunction
• Age common in infants and children upto age 2
• Family history
• Urinary tract infection
• Complications
• Kidney scarring due to untreated UTIs
• Hypertension due to build up of wastes that can raise blood pressure
• Kidney failure due to scarring
226.
• Signs andsymptoms
• A strong persistent urge to urinate
• A burning sensation when urinating
• The need to pass small amounts of urine frequently
• Cloudy urine
• Fevers
• Pain on the flank or abdomen
• Irritability
• Bed wetting
• Diagnosis
• Voiding cystourethrogram
• Radionuclide cystogram
• Abdominal ultrasound
227.
Nursing diagnosis
• Acutepain
• Anxiety
• Risk of infection
• Deficient knowledge
Medical management
• Administer long-term suppressive antibiotics e.g. nitrofurantoin
• Anticholinergic – bladder relaxant to control detrusor over activity e.g. oxybutynin
• Correct underlying voiding dysfunction
• Conduct follow up radiologic studies
• Bladder and bowel training
228.
• Surgical management
•Ureteral reimplantation / ureteroneocystomy to correct primary reflux
• Endoscopic treatment – using a cystoscope, inject a biocompatible bulking agent under
the intravesical portion of ureter to elevate ureteral orifice and distal ureter to prevent
regurgitation of urine
229.
ACUTE AND CHRONICURINE RETENTION
• Urine retention is the inability to voluntarily void urine. The body’s failure to effectively and
completely empty the bladder
• Categories of urine retention
• Obstructive caused by benign prostatic hyperplasia. Strictures. Bladder calculi, Faecal Impaction.
Phimosis / paraphimosis, Benign/malignant pelvic masses, Meatal Stenosis Organ prolapse e.g.:
cystocele, rectocele, uterine prolapse. Pelvic mass – gynae malignancy. Uterine fibroid / ovarian
cyst. Retroverted impacted gravid uterus and Foreign bodies
• Infectious & Inflammatory Prostatitis caused by Prostatic abscess, Cystitis, Acute vulvovaginitis,
Bilharzia, Herpes simplex virus
230.
• Pharmacologic relatedto side effects of medications e.g. anesthetic drugs, antihypertensives and
antispasmodics Drugs with anticholingeric properties e.g.: tricyclic antidepressants (amitriptyline),
Opioids, Sympathomimetic drugs e.g.: oral decongestants containing Ephedrine ( Sudafed),
NSAIDs ,Antiparkinsonian agents (levodopa), Antipsychotics (chlorpromazine), Muscle relaxants
(Baclofen
• Neurologic causes by autonomic and peripheral nerve disorders, Diabetes mellitus, Guillain-Barre
syndrome and radical pelvic surgery. Brain disorders (CVA, MS, Tumour, Parkinson’s disease,
concussion) spinal cord disorders (Haematoma / abscess / tumour, Cauda equine, spina bifida occulta)
• Other causes include Post-op complications, Pregnancy-associated retention, Trauma e.g.: penile fracture
or laceration, Idiopathic detrusor failure, Pain or fear of pain
231.
Presentation of acuteurine retention
• Sudden inability to pass urine
• Suprapubic pain which typically causes spasm
• Patient is acutely distressed
• Often longer history of bladder outflow symptoms
• Bladder is visible, tender and palpable and distended
232.
Presentation of chronicurine retention
• Completely different – maybe painless
• Incomplete emptying
• Often nocturnal enuresis
• Large bladder? Uremic? Anaemic? Fluid overloaded
• Large residual volume
• Bladder drainage may cause haematuria
• Urine frequency, hesitancy, and urgency
233.
Management of acuteurine retention
• Decompression by Catheterisation if U&E’S and Creatinine normal, patient is Systemically well
• Discharge Home with catheter
• Do Follow-up plan
Management of chronic urine retention
• Admit for observation including fluid balance chart
• Check renal function and decompress by catheterization
• Image upper tracts
• Manage post obstructive diuresis
234.
Nursing assessment
• Assesthe quantity, frequency and character of urine, e.g. color, odor, and specific gravity.
• Review previous pattern of voiding
• Allow patient to keep a record of the amount and time of each void
• Asses vital signs and change in level of consciousness
• Monitor urinalysis and blood for urea, creatinine and nitrogen
• Promote fluids if not contraindicated, around 1500ml/day
• Place patient in upright position to facilitate successful voiding
• Encourage the patient to void at least every 4 hours
• Decompress bladder moderately to produce pressure on pelvic arteries and cause venous pooling
• Catheterize and measure residual urine
• Keep catheter patent and maintain drainage tubing kink free
• Instruct patient to observe the signs and symptoms of urinary tract infection
235.
• Complications
• BilateralHydronephrosis
• Renal Impairment
• Infections
• Stones
• Urethral catheterization
• Check for sepsis prior to catheterisation
• Ensure correct catheter selection
• Always use an aseptic procedure
• Never force catheter against resistance
• Never inflate balloon in urethra
• Know your limitations
• Always record details and residual volume
236.
Complications of urethralcatherization
• Infection
• Irritation / Erosion
• Injury
• Removal difficulties- non deflation
• Pain or discomfort
• Catheter expulsion
• Infected peri-urethral glands causing abscess/fistula
• Reduced bladder capacity
• Reduced mobility
Benefits of urinary catherization
• Continence
• Preserves renal function
• May reinstate social independence
• Prevents high pressure bladder
•
BLADDER NEOPLASM-CA BLADDER
•Of all malignant tumours of urinary tract, 90% are transitional cell carcinomas, 5-8% are
squamous cell carcinorma, 1-2% are adenorcacinoma while less than 1% are sarcomas
• Malignant tumors of the bladder are the most common tumors within the urinary system
Cancer of the bladder is most common between the ages of 50 and 70 years and it is four
times as common in men as in women
239.
TYPES OF BLADDERCANCER
Three types :
• Transitional cell carcinoma. most common (90% )
• Squamous cell carcinoma.
• Adenocarcinoma - common in individual with chronic recurrent bladder stones,
chronic lower urinary tract infections and in patients who have indwelling catheters
for long periods.
Most cancers arise at the base of the bladder and involve ureteral orifices and bladder
neck
240.
The tumours canbe identified as being papillary or non-papillary lesions.
• Papillary- superficial/ non invasive and grow outward from the mucosa, most common
(70%)
• Non-papillary tumours – invasive solid growths that tend to extent deep into the
bladder wall, are fatal and likely to metastasize
241.
Stages
• The carcinomaspreads by first invading the submucosa and muscularis layer of the bladder. It leaves the bladder and spread to lymph nodes, liver,
lungs, bones
• It also spread locally to invade the prostate, uterus, vagina, rectum, and intestines
• It has the following stages ( Jewett- Marshall- Strong system)
Stage 0- carcinoma insitu limited to mucosa
Stage A- superficial tumor extends submucosa
Stage B1- involves superficial muscles layer
Stage B2- involves deep muscle layer
Stage C- involves the serosa of the bladder
Stage D1- involves pelvic organs and lymph nodes
Stage D2- beyond the pelvis (distant metastasis)
242.
CLINICAL MANIFESTATION
Painless haematuria(most common symptom) and may be a gross or microscopic finding.
This can occur with each voiding or intermittently.
• Irritative voiding symptoms such as dysuria, frequency and urgency
• It may metastasize to cause pelvic pain, bone pain, unexplained weight loss, leg swelling
• Obstruction in voiding
243.
Diagnosis
based on symptoms,history and diagnostic tests which may include:
• Urine specimen is taken for cytology to determine the presence of neoplastic cells. (urine
cytology)
• Radiological studies - intravenous pyelogram, ultrasound, Computed Tomography (CT)
scan or Magnetic Resonance Imaging (MRI).
• Cystoscopy with biopsy
244.
MANAGEMENT
The type oftreatment initiated depends on the form of tumour and the stages of the disease.
Surgical Treatment of Papillary or Superficial Bladder Cancer
1. Transurethral resection of bladder tumour (TURBT)/fulguration(cauterization)
• The tumour is excised by a blade inserted through the cystoscope, the remaining
portions of the tumour are cauterised then followed by chemotherapy. Is the initial and
most common treatment for superficial bladder cancer. The urinary tract is assessed for
any recurrence of cancerous lesions every three to six months after the operation.
245.
2. Open loopresection: used for the control of bleeding for large superficial tumours
and for multiple lesions which require segmental resection of the bladder
(segmental cystectomy).
3. Incase of invasive or multifocal tumor, a simple or radical cystectomy is performed
4. Radical cystectomy in men involves removal of the bladder, prostate and seminal vesicles while in
women it involves removal of bladder, lower ureter, uterus, fallopian tubes, ovaries, anterior
vagina and urethra. It may involve removal of pelvic lymph nodes
5. Removal of bladder requires urinary diversions. Urinary diversions are means of diverting the
urinary stream from the bladder so that it exits through new route and opening in the skin.(stoma)
246.
SURGICAL TREATMENT OFNON-PAPILLARY
OR MUSCLE - INVASIVE BLADDER CANCER
6. Segmental or partial cystectomy:
Is done if there is a tumour in the bladder that in not accessible to treatment by
transurethral resection. The objective is to only remove that portion of the bladder
affected without injuring the ureters, bladder neck or prostate.
.
247.
RADIATION THERAPY
• Radiationtherapy is used with cystectomy or as the primary therapy when the cancer
is inoperable.
• Sometimes radio therapy is combined with systemic chemotherapy preoperatively or
to treat distant metastases. Hydrostatic therapy may be used if the patient has gross
haematuria after radiotherapy.
• Examples of chemotherapies are methotrexate, 5-fluoral uracil, vinblastin, doxorubicin
and cisplatin
248.
Post-operative Management
• Patientis instructed to drink large amounts of fluids each day
• Monitor intake output chart
• Administer analgesics and stool softeners if necessary
• Health education on patient's condition and follow up care
250.
NEUROLOGICNEUROGENIC BLADDER
• Def.:A neurogenic bladder is the loss of normal bladder function caused by damage to part of the nervous system
• It may result from a disease, an injury or a birth defect affecting the brain, spinal cord or nerves leading to the bladder, its outlet or both
• Under active- it is unable to contract (non contractile) and unable to empty well
• Over active (spastic) - emptying by uncontrolled reflexes
• Causes
• Under active bladder usually results from interruption of local nerves supplying the bladder
• Birth defects e.g. spina bifida or myelomeningocele affecting the spinal cord
• Over active bladder usually results from an interruption of normal control of the bladder by the spinal cord and brain
• Another common cause is an injury or disorder e.g. multiple sclerosis affecting the spinal cord which may also result in legs paralysis
or arms
251.
Symptoms
• Under activebladder
• It doesn’t empty
• Un-painful enlargement because it has little or no local nerve supply
• It may remain large but constantly leaking small amount of urine
• Bladder infection may occur because the pool of residual urine provides the condition that encourages bacterial growth
• Stones may occur following permanent placement of a catheter due to chronic bladder infection
• Overactive bladder
• It fills and empty without control and with varying degrees of warning (controls involuntarily)
• There may be damage of the kidney because of the pressure and backflow of urine from the bladder up through the ureters
252.
Diagnosis
• Physical examination
•X-ray imaging using radio-opaque substance injected through a vein
• Ultra sound scanning imaging
• Cystoscopy to look into the bladder
• Cytsometrography (it measures pressure within the bladder and urethra by connecting it to a meter)
Treatment
• When a underactive bladder is caused by a neurologic injury, a catheter may be inserted through urethra to drain it continuously
• Insert the catheter immediately to prevent muscle damage from overstretching and to prevent bladder infection
• Intermittent self catheterization is preferred whereby the patient uses a catheter that he can insert and remove to drain the bladder
• People who have overactive bladder may need a catheter if spasms of the bladder outlet prevent the bladder from emptying completely
• For quantriplegic males who can’t catheterize themselves, the sphincter muscle may have to be cut to allow emptying and an external collecting device can be worn
253.
• Electric stimulationmay be applied to the bladder, the nerves that control the bladder or spinal cord to induce
the bladder to contract
• Anticholinergic drugs may be used to relax the bladder and thus improve control of an overactive bladder
• Surgery to divert the urine to an external opening (ostomy) made in the abdominal wall or to increase the
bladder size is sometimes recommended
• Kidney function is monitored closely and kidney infection treated promptly
• Drinking at least eight glasses of fluids daily is recommended
• A paralyzed person position is changed frequently and others are encouraged to walk as soon as possible
254.
FISTULAE
• Def.: Isan abnormal passage between two cavities or between a cavity and the surface or
between a cavity and the surface of the body that result in communication between one
body part and another hollow organ or the skin
• Fistula patients require a coordinated, interdisciplinary, care including nurses, dietician,
social worker, pharmacist, surgeon and physician
255.
• Sites ofUrine Leakage through the Vagina
• Vesico vaginal fistula i.e. from bladder
• Uretero vaginal fistula i.e. from ureter
• Urethro vaginal fistula i.e. from urethra
•
• Vesico vaginal fistula
• It’s an abnormal opening between the bladder and the vagina which might result from prolonged pressure in neglected
obstructed labor
• The genital tract fistula may occur between the vagina or uterus and any adjacent organ that the most frequent concentrated
fistula are between vagina and bladder
256.
Pathophysiology
• During obstructedlabor the prolonged pressure at baby’s head against the mothers pelvis cuts off blood to soft tissue surrounding the bladder and vagina
• The injured tissue rots away/ sloughing leaving a hole or fistula
• The obstruction can occur if woman’s pelvis is too small (contracted pelvis). If baby’s head is too big compared to women pelvis called cephalopelvic
disproportion (CPD)
Causes
• Obstetric injury
• Surgical trauma during hysterectomy
• Radiation in cervical Cancer
• Direct trauma e.g. penetrating injuries of the anterior wall
• Anterior episiotomy or tear
• Congenital malformation
257.
Predisposing factors
• Earlypregnancy
• Lack of education
• Low status of woman in the society
• Gender discrimination
• Culture and tradition which encourage early marriage
• Limited access to medical services
Signs and symptoms
• Urine leak into vagina
• Vaginal and vulva tissue become excoriated
• Chronic UTI
• Experiences wetness and a sensation or feeling unclean
• Vaginal fistula produces severely distressing psychosocial problems
• Disruption of social activities
• Client become withdraw
• Seek medical attention late or feel embarrassed
258.
Diagnosis
• Methylene dyetest is done in-case of vesico-vaginal fistula
• Introduction of dye is also done in recto-vaginal fistula
• X-ray is done after introducing a dye
• Pelvic ultrasound can confirm the diagnosis
• Management urinary fistula
• For small lesions:
• Bladder catheter
• Wait for spontaneous closure
• For larger lesions:
• Wait until “healed”
• Then close from below or above
• 3-layered closure
• Management of recto-vaginal fistula
259.
• May requirea diversionary colostomy
• Must treat the underlying problem when there is inflammatory disease or cancer
• May also require anal sphincter repair
260.
DIVERTICULI
DIVERTICULI
• Def.: Bladderdiverticulum, an out pouching of the mucosa through the muscular wall of the
bladder, is a multifactorial disease process that can be either acquired or congenital.
Signs and symptoms
• Although small diverticuli are usually asymptomatic, a large diverticulum may result in
hematuria, urinary tract infection, acute abdomen due to its rupture, acute urinary retention,
or neoplasm formation.
261.
Diagnosis
• CT scanabdomen and pelvis (confirmatory)
• Pelvic ultra sound
• Full hemogram
• IV contrast to look for possible ischaemia
•
• The congenital form of bladder diverticuli usually manifests in children younger than ten years old and is thought to be due to weakness of the
ureterovesical junction or a posterior urethral valve [3]. In the former instance, weakness of the junction allows out pouching to occur, and, in the latter
instance, increased intravesical pressure leads to wall stress and mucosal out pouching.
• The acquired form generally occurs in males over the age of 60, and diverticuli are often located along the lateral bladder walls [3, 4]. Similar to the
mechanism in children with posterior urethral valves, it is thought that intravesical pressure increases from other underlying pathology, such as prostatic
disease or neurologic processes
262.
Management
• The patientis admitted to the hospital (surgical ward)
• Patient is given IV antibiotics and analgesics to control pain, with a Urology Consult.
• The patient is scheduled for cystoscopy, surgical removal of the pouch and stone removal if any.
• Pre and post-operative management is done as for the other patients
Complications
• Intra diverticular transitional cell carcinoma 1-10%
• Bladder stones
• Bladder rupture
.
263.
URETHRITIS
• Urethra infection(urethritis)
IT is inflammation of urethra primarily caused by STIs. It is the most frequent STD syndrome in men
Inflammation of the urethra due to chemical irritation, trauma. Post traumatic urethritis can occur with
interminent catheterization or instrumentation of the urethra. Bubble bath and sitz bath are common urethral
irritants. Infection can also be caused by spermicidal agents
Classification
Can be specific or non-specific.
Specific- Gonococci and non gonocccal organisms cause urethritis
Non-specific- no particular micro-organisms are implicated.
264.
CAUSES
• Gonococcal –N. gonorrhea, usually accompanied by C. trachomatis
• Non gonococcal-
C. trachomatis (most common), Trichomonas vaginalis, HPV, Herpes simplex virus, CMV,
Adenovirus, Mycoplasma genitalium, Ureaplasma urealyticum, Enteric bacteria (mouth,
anus and vagina)
265.
CLINICAL MANIFESTATION
Incubation period;
•Gonorrhea – 2-6 days after exposure, characterized by purulent discharge
• Non gonococcal- 1-5 weeks after infection with its peak being 2 weeks, characterized by
clear or mucoid discharge
• General symptoms- dysuria, itching/burning near urethral opening, blood in semen or
urine, urgency, abdominal pain, fever, chills
266.
Diagnosis
• History takingand physical examination, urinalysis, vaginal/urethral swab for gram
staining, leukocyte esterase test
• Offer HIV and syphilis testing
Management
Use syndromic management of urethral discharge
267.
• Gonorrhea andChlamydia-
Ceftriaxone 250mg IM stat PLUS either Azithromycin 1g PO start OR Doxycycline 100mg PO BD X 7/7
Gonorrhea – one of the following;
• Acqueous procaine penicillin 4.8 mu PLUS Amoxyclav1tab PLUS probenecid 1g PO half an hour
before penicillin
• Norfloxacin 500 PO start
• Ceftriaxone 250 mg IM stat
• Kanamycin 2g IM stat
268.
• Non gonocccal
Chlamydia– tetracycline 500mg QID 7/7 OR Doxycycline 200mg stat then 100 mg 7/7 and
Erythromycin 500mg PO QID 7/7
If the symptoms are not resolved consider
Re-infection, poor compliance, doxycycline resistant M. genitalium, T. vaginalis or U.
urealyticum
TREAT with; Metronidazole 2g PO stat OR Tinidazole 1g PO stat
269.
Points to note
•Offer HIV and syphilis testing
• Avoid sexual intercourse till recovery
• Emphasize on Dose completion
• Treat the partner
• Consider 4 Cs- counselling, compliance, condoms, contact tracing
Complications
• Urethral abscess, urethral stricture, prostatitis, cystitis, epididymitis and orchitis
• Septicaemia, arthritis, meningitis, endocarditis
RENAL TUMOURS
• Renaltumour may arise from the renal capsule, parenchyma, connective tissue or fatty tissues.
Most of the renal cancers are adenocarcinoma ( from epithelial tissue) accounting 85%
• Occur as twice as many as in men as women
• It may metastatize to lungs, bone, liver brain and contralateral kidney
• 25% are metastatized at the time of diagnosis
Clinical manifestation
No symptoms but a palpable abdominal mass is discovered on routine diagnosis
273.
• Other triadof symptoms include;
Painless haematuria
Dull pain due to compression ureters
Mass in the flank
Colicky pain may occur if clot/mass of tumor cells passes down ureter
Symptoms of metastasis include unexplained weight loss, weakness, anemia
MANAGEMENT
Goal – toeradicate tumour before metastasis
Surgical management
• Radical nephrectomy – preferred treatment if the tumor can be removed. It includes removal of the kidney and
tumor, adrenal gland, fascia fat and lymph nodes. Radiation or chemotherapy may be used along with surgery
• Partial nephrectomy- done for patients with bilateral tumors or cancers of a single functioning kidney. It is also
called nephron sparing surgery. It involves removal of a part of the kidney without affecting the adrenal gland
• Renal artery embolization- done for patients with metaplastic renal carcinomas. The renal artery or tumor
vessel may be occluded to impede blood supply to the tumor and this kills the tumor cells
276.
Medical management
The goalis to eradicate the tumor before metastasis
• Pharmacotherapy- chemotherapeutic agents following surgical removal depending on the
stage of the tumor e.g. vinblastine
• Radiation therapy- as an adjunct with chemotherapy and surgery
277.
Nursing management
• Giveemotional support because client may be anxious about surgery post op renal function and possible recurrence of disease
• Post op the patient usually has catheters and drains in place to maintain urinary tract to drain urine and to permit accurate
measurement of urine output
• The patient experiences pain and muscle soreness secondary to the procedure and thus require frequent analgesia and other
coping mechanism
• Frequent assistance in turning, deep breathing and coughing are encouraged to prevent atelectasis and other pulmonary
complications
• Provide family support for patient to cope with diagnosis and prognosis
• Patient education on the care of incision site, activity restriction, signs of complication e.g. wound drainage, fever, hematuria,
disease process and treatment plan, importance of follow up
278.
CANCER OF THEBLADDER
• Of all malignant tumours of urinary tract, 90% are transitional cell carcinomas, 5-8% are
squamous cell carcinorma, 1-2% are adenorcacinoma while less than 1% are sarcomas
• Malignant tumors of the bladder are the most common tumors within the urinary system
Cancer of the bladder is most common between the ages of 50 and 70 years and it is four
times as common in men as in women
279.
TYPES OF BLADDERCANCER
Three types :
• Transitional cell carcinoma. most common (90% )
• Squamous cell carcinoma.
• Adenocarcinoma - common in individual with chronic recurrent bladder stones,
chronic lower urinary tract infections and in patients who have indwelling catheters
for long periods.
Most cancers arise at the base of the bladder and involve ureteral orifices and bladder
neck
280.
The tumours canbe identified as being papillary or non-papillary lesions.
• Papillary- superficial/ non invasive and grow outward from the mucosa, most common
(70%)
• Non-papillary tumours – invasive solid growths that tend to extent deep into the
bladder wall, are fatal and likely to metastasize
281.
Stages
• The carcinomaspreads by first invading the submucosa and muscularis layer of the bladder. It leaves the bladder and spread to lymph nodes, liver,
lungs, bones
• It also spread locally to invade the prostate, uterus, vagina, rectum, and intestines
• It has the following stages ( Jewett- Marshall- Strong system)
Stage 0- carcinoma insitu limited to mucosa
Stage A- superficial tumor extends submucosa
Stage B1- involves superficial muscles layer
Stage B2- involves deep muscle layer
Stage C- involves the serosa of the bladder
Stage D1- involves pelvic organs and lymph nodes
Stage D2- beyond the pelvis (distant metastasis)
282.
CLINICAL MANIFESTATION
Painless haematuria(most common symptom) and may be a gross or microscopic finding.
This can occur with each voiding or intermittently.
• Irritative voiding symptoms such as dysuria, frequency and urgency
• It may metastasize to cause pelvic pain, bone pain, unexplained weight loss, leg swelling
• Obstruction in voiding
283.
Diagnosis
based on symptoms,history and diagnostic tests which may include:
• Urine specimen is taken for cytology to determine the presence of neoplastic cells. (urine
cytology)
• Radiological studies - intravenous pyelogram, ultrasound, Computed Tomography (CT)
scan or Magnetic Resonance Imaging (MRI).
• Cystoscopy with biopsy
284.
MANAGEMENT
The type oftreatment initiated depends on the form of tumour and the stages of the disease.
Surgical Treatment of Papillary or Superficial Bladder Cancer
1. Transurethral resection of bladder tumour (TURBT)/fulguration(cauterization)
• The tumour is excised by a blade inserted through the cystoscope, the remaining
portions of the tumour are cauterised then followed by chemotherapy. Is the initial and
most common treatment for superficial bladder cancer. The urinary tract is assessed for
any recurrence of cancerous lesions every three to six months after the operation.
285.
2. Open loopresection: used for the control of bleeding for large superficial tumours
and for multiple lesions which require segmental resection of the bladder
(segmental cystectomy).
3. Incase of invasive or multifocal tumor, a simple or radical cystectomy is performed
4. Radical cystectomy in men involves removal of the bladder, prostate and seminal vesicles while in
women it involves removal of bladder, lower ureter, uterus, fallopian tubes, ovaries, anterior
vagina and urethra. It may involve removal of pelvic lymph nodes
5. Removal of bladder requires urinary diversions. Urinary diversions are means of diverting the
urinary stream from the bladder so that it exits through new route and opening in the skin.(stoma)
286.
• Surgical Treatmentof Non-papillary or Muscle - Invasive Bladder Cancer.
. Segmental or partial cystectomy:
Is done if there is a tumour in the bladder that in not accessible to treatment by
transurethral resection. The objective is to only remove that portion of the bladder
affected without injuring the ureters, bladder neck or prostate.
.
287.
RADIATION THERAPY
• Radiationtherapy is used with cystectomy or as the primary therapy when the cancer
is inoperable.
• Sometimes radio therapy is combined with systemic chemotherapy preoperatively or
to treat distant metastases. Hydrostatic therapy may be used if the patient has gross
haematuria after radiotherapy.
• Examples of chemotherapies are methotrexate, 5-fluoral uracil, vinblastin, doxorubicin
and cisplatin
288.
Post-operative Management
• Patientis instructed to drink large amounts of fluids each day
• Monitor intake output chart
• Administer analgesics and stool softeners if necessary
• Health education on patient's condition and follow up care
289.
TRAUMA
URETERAL TRAUMA
Caused bypenetrating trauma and unintentional injury during surgery, trauma to the ureters, and gunshots
• Signs and symptoms
• Flank pain
• Fever and sepsis
• Urinoma
• Costovertebral angle tenderness
• Fistula – ureterovaginal or ureterocutanous
• Diagnosis
• Intravenous urography
• History taking and physical examination
290.
Treatment
• Surgical repairwith placement of stent to divert urine away from the anastomoses
• Percutaneous nephrostomy with delayed repair as needed in patients when stent replacement is unsuccessful or not possible
• Complications following repair
• Urinary leakage from anastomoses manifested by urinoma, abscess, or peritonitis.
• Strictures
• Hydronephrosis
• Sepsis
• Fistula formation
• Pain
• Renal function loss
291.
BLADDER TRAUMA
• Injuryto the bladder due to pelvic fracture, multiple trauma or blow to the lower
abdomen when bladder if full
• Blunt trauma result in contusion evident as an ecchymosis – a large discolored bruise
resulting from escape of blood into the tissues and involving a segment of the bladder
wall
• Penetrating injury (a tear) is damage caused by something piercing through the bladder
292.
Causes
• Blunt traumafrom a blow, kick
• Penetrating injury from gunshots and stabbing
• Obstetric trauma from prolonged labour or difficult forceps delivery
• Gynecological trauma during vaginal or abdominal hysterectomy
• Urologic trauma during bladder biopsy, transurethral resection of bladder tumor
• Orthopedic trauma during internal fixation of pelvic fractures
293.
Signs and symptoms
•Hard to start urinating
• Weak urine stream
• Painful urination
• Fever
• Severe back pains
• Urine leak from bladder via vagina when vagina trauma is involved
294.
Diagnosis
• Placing acatheter into the bladder and taking series of x-rays
• History taking and physical examination
Management
• Urinary catheterization
• Surgical exploration to assess involvement of other organs
• Closure of bladder defects performed in a two layer fashion using absorbable sutures
295.
Complications of bladdertrauma
• Hemorrhage
• Sepsis
• Shock
• Wound dehiscence
• Pelvic abscess
• Urinary tract infection
• Low bladder capacity
• Urinary urgency
• Extravasation of blood into the tissues
296.
URETHRAL TRAUMA
• Occurswith blunt trauma to the lower abdomen or pelvic region.
• Many patients have associated pelvic fractures
• Trauma to anterior urethra due to straddle injuries due to sharp blow to the perineum while trauma to the posterior urethra
results from a severe injury.
• Urethral injuries can also result from objects piercing the sex organs or pelvis
Triad of symptoms include
• Blood in the urinary meatus
• Inability to void
• Distended bladder
297.
Other symptoms include
•Swelling and inflammation
• Infection
• Pain in the belly
• Not being able to pass urine
• Blood in the urine
Diagnosis
• An x-ray is done after squirting a special dye into the urethra
• History and physical examination
298.
Management
• Catheterization throughthe urethra into the bladder.
• Supra pubic catheter in severe injuries for bladder drainage and subsequent delayed
repair.
• Endoscopic realignment using combined transurethral and percutaneous transvesical
approach
299.
URETHRAL STRICTURE
• Def.:Is a condition in which a section of the urethra is narrowed. Narrowing of the lumen of the stricture as a result of
scar tissue and contraction caused by urethral injury
• Is the narrowing of the urethra, and can occur at any section of the urethra, however there are common sites where
stricture are found resulting in difficulties in passing urine. It can occur congenitally or from a scar along the urethra
• Causes
• Trauma, injury, damage of the urethra are common caused by surgical instrumentation (transurethral surgery),
indwelling catheters, cystoscopy and automobile accidents
• Radiotherapy treatment may cause damage to urethra
• Infection including STIs e.g. gonorrhea or chlamydia
• Cancer in the urethra
300.
Signs and symptoms
•Reduced urine flow and straining to pass urine
• Spraying of urine or a double stream
• Dribbling of urine after the main flow has finished
• Needing to pass urine more than usual
• Urinary tract infections
• Hyperdistended bladder
• Pain when passing urine
• Blood in urine or semen
301.
Diagnosis
• Physical examto show enlarged distended bladder, redness on the underside of the penis, discharge
from the urethra
• Cystoscopy to identify presence of a stricture
• Urethroscopy to identify length and exact location of stricture
• Flow test to determine flow rate of urine
• X-ray to determine length and severity of stricture IV urography
•
302.
Treatment Objectives
• Toimprove flow of urine
• To ease symptoms
• To prevent possible complications
Urethral dilatation done under anesthesia to stretch and widen the stricture without causing scarring using metal sounds or bougies
If the stricture prevent catheter passage, a bougie is used to search for an opening. It is then left in place to allow urine drainage. The opening is then
dilated using a larger sound
• Urethrotomy to see where stricture is, under general anesthesia
• Urethroplasty – a short stricture is cut out and the two ends of urethra stitched together
• Intermittent self-dilatation to reduce risk of urethral stricture from recurring
• Sometimes suprapubic cystotomy must be performed
303.
Complications
• Bladder stonesdue to chronic slowing of urinary flow or infections
• Abscess above the stricture causing further damage to the urethra
• Bladder, kidney and prostate infections
• Cancer of the urethra due to longstanding stricture
BENIGN PROSTATE HYPERTROPHY
•Benign prostatic hypertrophy(enlarged prostate) is a non-malignant increase in size of the
prostate gland primarily by proliferation of smooth muscle and epithelial cells within
the prostate.
• It is common in men over 40 years of age. 90% occur 80 yrs and above.
• It may be symptomatic(clinical BPH) or asymptomatic (histologic BPH)
• It is a hormone dependent condition hence does not occur in castrated men.
• Normally, the prostate increases in size with passing age between 31 and 50 yrs. It doubles
in size in every 4.5 yrs but this rate decreases subsequently.
306.
Advanced age
Obesity-
a) Promotescellular proliferation and increases sympathetic tone through increased insulin and leptin levels,
activates renin aldosterone angiotensin system(RAAS)
b) Formation of androgens
NB- BMI and waist circumference exhibit a linear relationship with prostate volume
Diet –
• Heavy alcohol consumption and cigarret smoking
• High polyunsaturated fats, fatty acids, beef products and high plasma glucose
307.
PATHOPHYSIOLOGY
• STATIC COMPONENT
EnlargedProstate compresses the prostatic and vesical neck urethra causing obstruction and hence incomplete
emptying of the bladder and urinary retention. As a result, a gradual dilation of ureters (hydroureter) and kidneys
(hydronephrosis) car occur. The urinary stream flow becomes weaker. Incontinence, frequency and nocturia are
common
• Urinary stasis can cause UTI
• DYNAMIC COMPONENT
Prostatic stromal smooth muscle cells which is controlled by adrenergic stimulation can become hyperactive
and constrict the prostatic urethra. This can be secondary to drugs such as TCA antidepressants,
anticholinergics and narcotics
308.
CLINICAL MANIFESTATION
• Urinaryhesitancy
• Increased frequency
• Interruption of urinary stream and dribbling after urination
• Sensation of incomplete emptying
• Abdominal straining with urination may lead to micturation syncope
• Urinary urgency
• Decreased volume and force of the urinary stream
• Acute urinary retention
• Recurrent UTI
• Others- fatique, anorexia, nausea, vomiting, epigastric discomfort
309.
DIAGNOSIS
• Physical examination-abdominal palpation(palpable bladder), DRE(large, rubbery non
tender prostate gland), respiratory and cardiac ass.
• Urinalysis
• Blood – U/E, creatinine, CBC, PSA levels
• Imaging – if there urinary obstruction, abdominal U/S and Intravenous Urography
• Cystoscopy, urine flow rate
310.
MANAGEMENT
• If minimalsymptoms- watchful waiting( reassurance, education, monitoring)
• Acute obstruction- catheterization
• Pharmacology –
Alpha adrenergic blockers-reduces the tone of the neck of the bladder and
prostate(terazosin, doxazosin, tamulosin, alfuzosin, prazosin)
Hormonal manipulation- antiandrogens (finasteride, dutasteride) they prevent conversion of
testosterone to dihydrotesterone. However they can cause gynecomastia, erectyle
dysfunction, reduce libido, ejaculation disorder
311.
Surgical intervention- indicatedin:
• Large prostate, failure to respond to medical therapy, acute urinary retention, recurrent gross hematuria,
renal insufficiency due to obstruction.
Prostatectomy
Transurethral resectionof prostate( TURP)- standard procedure
Transurethral incision of prostate (TUIP)- prostate less than 30g
Transurethral needle ablation (TUNA)
Transurethral vaporization of prostate(TUVP) prostate more than 75g, bladder stones, bladder diverticulum
312.
Post operatively; vitalobservations, monitoring the patency of the urinary catheters,
input-output monitoring and change of dressings, education on perineal exercises to
regain bladder control encourage increased fluid intake of at least 3,000ml per day.
A catheter is required until bleeding stops.
Urethral stricture, retrograde ejaculation and erectile dysfunction may occur
• Urinary antiseptics and antibiotics are given to prevent urinary tract infections eg
Nalidixic acid and nitrofurantoin.
PROSTATE CANCER
• Prostaticcancer is the most common cancer in men.
• Its common in older men of more than 65 years.
• Prostate tumors are more prevalent in entire genitourinary system
• It has no warning signs, once the tumor causes prostate gland to swell, or spread to other
areas, symptoms appear
315.
• It canspread to bones, lymph nodes and lungs
• As it progresses, there is anaemia, with metastases to other organs.
• Mainly weight loss, easy fatigability, urinary obstruction, nocturia, and frequent urinary
tract infections are manifested.
• The assessment of the patient involves rectal examination, enzyme studies and other
investigations involving blood and electrolytes
316.
PREDISPOSING FACTORS
• Advancingage-80% occur above 65 years
• Family history- father,brother
• Diet –excessive red meat that has lots of fat,excessive dairy products with high fats, meat
cooked at a high temperature produces cancer causes substances that affect prostate
• BRCA2 mutation
• Hormones – testosterone speeds up growth
• Metals,sedentary life, occupation(welders, battery manufactures, rubber workers
317.
• Factors thatlowers the risks of prostate cancer
• Diet – tomato sauce, vegetables such as broccoli, cauliflower, cabbage, beta carotene
• Drugs – aspirin, finasteride, cholesterol lowering drugs, beta blockers, anti-inflammaory
drugs
Symptoms
Early stages rarely produces symptoms
Late stage produces symptoms similar to those of benign prostatic hypertrophy
318.
• Symptoms
• Itcan metastasize to bones and lymph nodes causing;
• backache, hip pain, anaemia, weakness, weight loss, nausea, perineal and rectal
discomfort, oliguria
They may be the first indications of prostate cancer
319.
SYMPTOMS
• It canmetastasize to bones and lymph nodes causing;
• backache, hip pain, anaemia, weakness, weight loss, nausea, perineal and rectal
discomfort, oliguria
They may be the first indications of prostate cancer
320.
DIAGNOSIS
• Digital RectalExamination- normal prostate gland is 20g(the fingers breadth represents
about 15-20g), firm but not hard, smooth without nodules, median sulcus should be
clearly defined. Cancerous prostate has lumpy areas
• Blood test-
Prostate specific antigen(PSA) levels. It is a protein produced by prostate gland. It indicate
the presence of prostate tissue and not necessarily malignancy. It is a tumour marker and
its level in blood is proportional to total prostatic mass
321.
• PSA cutoff value is 20. normal values per age include;
50-59=3.0
60-69=4.0
70 and above= more than 5
High levels of PSA indicate enlarged or infected or malignant prostate
Confirmatory tests
Examination of prostate cells under microscope after biopsy
Transrectal ultrasound(TRUS) for patients with abnormal PSA levels and DRE findings. Can even detect non palpable cancers
Medical and family history
Other tests include bone scans, excretory urography, renal function tests CT scan of pelvis
322.
CANCER STAGING
Stage 1Not felt on DRE, localized within prostate, Gleason
less 6, PSA Less 10
Stage 2 Not spread to nearby lymph nodes, Gleason 7 or less,
PSA less/equal to 20
Stage 3 Spread outside prostate to seminal vesicles, but not
lymph nodes, any Gleason score and PSA level
Stge 4 Spread to other tissues( urethral sphincter, rectum,
bladder, wall of pelvis) any Gleason score and PSA
levels
323.
MANAGEMENT
. Surgery- prostatectomy
•Radical prostatectomy( removal of prostate, seminal vesicles, tips of vas deferens,
surrounding fat, nerves and blood vessels). Leads to impotence
Surgical approaches
1. Transurethral resection of prostate(TURP) often associated with TUR syndrome. The
syndrome is caused by rapid absorption of solution used to irrigate surgical site.
Symptoms-lethargy, confusion, hypotesion, headache, collapse, tachycardia, seizures,
muscle spasms. Rarely causes ED
324.
2. Suprapubic prostatectomy(abdominal incision)
3. Perineal prostatectomy- when other options fail. Useful for open biopsy
4. Retropubic prostatectomy- lower abdomen with no bladder entry- large glands located
high in pelvis
5. Transurethral incision of prostate(TUIP)-for small glands and BPH
6. Laparoscopic radical prostatectomy – with visualization
325.
Surgical complications
• Sexualdysfunction( ED due destruction of pudental nerves, retrograde ejaculation, impotence)
• Haemorrhage
• Bladder infections
• Urinary and fecal incontinence
Other treatment measures
2. External radiation therapy(teletherapy) and internal radiation therapy(brachytherapy)
3. Chemotherapy- paclitaxel and docetaxel, high dose ketoconazole
Drugs can cause;
•Thromboembolism, pulmonary embolism, myocardial infarction and stroke (DES)
• Reduced libido, gynecomastia, reduced sperm count, difficulty in achieving organism (estrogen)
Nursing management
1. To address anxiety, reduce stress, improve ability to cope- provide and clarify information about cancer,
social services, support groups, and community agencies available
2. To improve pattern of urination
• Assess pattern of urination and signs of retention
• Catheterize , encourage voiding, adminster anticholinergs, prepare for surgery
328.
To improve abilityto resume/ enjoy modified sexual function
• Determine effect of cancer, explain effects of cancer treatment on sexual function, involve
partner
4.To relieve pain
• Evaluate pain, avoid activities that aggravate pain, avoid injuries, analgesics
5. Monitor for complications such as haemorrhage.
329.
PROSTATECTOMY MANAGEMENT
• Postoperatively-irrigation of the bladder, close observation, antibiotics and wound care.
Explain to patients that female sexual characteristics may develop as a result of estrogen
therapy
• Chemotherapy and radiotherapy may be attempted. Provide general nursing care related
to chemotherapy such as infection prevention and treatment of anaemia.
Education on the populations at risk and frequent checkups for men from the age of 40
years must be shared with the community.
330.
• These arecongenital anomalies of urethra opening. In hypospadias, urethra opening is a
groove on the underside of the penis. In epispadias, its on the dorsum of the penis
Risk factors
• Family history, maternal age over 40 years, exposure to smoking and chemicals,
cryptorchidism
Development of the penis occurs between 9-12 weeks of pregnancy
331.
HYPOSPADIA AND EPISPADIA
•These are congenital anomalies of urethra opening. In hypospadias, urethra opening is a
groove on the underside of the penis. In epispadias, its on the dorsum of the penis
Risk factors
• Family history, maternal age over 40 years, exposure to smoking and chemicals,
cryptorchidism
Development of the penis occurs between 9-12 weeks of pregnancy
332.
Epispadias
• It alsoaffect external genitalia, urethra, bladder and large intestines. It is associated with bladder
exstrophy( bladder inside out and sticks through abdominal wall)
• It affects both men and women, but more common in males
Boys/males
• Penis is typically broad, short and curved towards abdomen (dorsal chordee)
• Penis attached to pelvic bones which are widely separated resulting in a penis that is pulled back towards the
body
• Meatus is located at the top of the penis hence it is split and opened forming a gutter
333.
Epispadias
Classification in malesis based on location
• Glannular – on glans
• Penile – shaft
• Penopubic –near pubic bone
Problems associated with epispadias in males
• Impaired sexual function
• UTIs
• Urinary incontinence
• Retrograde ejaculation(infertility) –failure of bladder neck to close during ejaculation
334.
EPISPADIA CTD
• NB-the position of the bladder predicts the degree to which the bladder can store urine.
The closer the meatus to the top base of the penis, the more likely the bladder will
not hold urine
• The bones of the pelvis do not come together in front, hence the bladder neck cannot
close completely and the result is leakage of urine
• Hence, penopubic and penile epispadias present with stress incontinence
335.
EPISPADIA CTD
Girls -Rare
• The opening is between clitoris (double clitoris), labia and belly area. Pubic bones are
separated hence clitoris does not fuse during development.
• Bladder neck is almost always affected therefore they have stress incontinence
UTIs are common esp in exstrophy epispadias. Female lack risks of infertility because the
rest of reproductive system is normal
336.
EPISPADIA CTD
Management
• Goals
•Maximize penile length and function by correcting dorsal bend and chordee
• Create functionality and cosmetically acceptable external genitalia
• Establish urinary continence and preserve fertility
Surgical management
Cantwell technique-
Partial disassembly of the penis and placement of urethra in normal position
337.
EPISPADIA CTD
Mitchell technique
Completedisassembly of penis into two corpora cavernosa and
corpus spongiosum and then re assembling so that urethra is
positioned correctly. It has lower complication rate and facilitate
bladder repair.
338.
HYPOSPADIA
• 80% occurnear head, but may also occur at the mid shaft or below the scrotum
• It occurs in mainly in boys in which 8% have undescended testis
Clinically
• Downward curve of the penis(chordee)
• Hooded penis because only the top half of the penis is covered by the foreskin
• Abnormal spraying during urination
339.
• Surgery –suitable between 3-18 months but possible at any age
• Aim – create normal straight penis with urinary channel that ends at the tip of the head of the penis
Involves four steps
• Straightening the shaft
• Creating urinary channel
• Positioning urethra
• Circumcising/ reconstruction
After surgery
• Small catheter is left insitu for urine drainage
• Bladder antispasmodics may be given
Complications
• Scarring
• Urinary channel- skin fistula