Chapter 44 NURSING ASSESSMENT: urinary system

Written by Vicki Y. Johnson

Adapted by Ann Bonner

LEARNING OBJECTIVES

KEY TERMS

costovertebral angle (CVA)

creatinine

cystometrogram

cystoscopy

glomerular filtration rate (GFR)

glomerulus

intravenous pyelogram (IVP)

nephron

renal arteriogram

renal biopsy

retrograde pyelogram

urinalysis

Structure and function of the urinary system

‘Bones can break, muscles can atrophy, glands can loaf, even the brain can go to sleep without immediate danger to survival. But should the kidneys fail … neither bone, muscle, gland, nor brain could carry on.’1 This statement underlines the importance of our kidneys to our lives. Adequate functioning of the kidneys is essential to the maintenance of a healthy body. If there is complete kidney failure and treatment is not given, death is inevitable.

The upper urinary system consists of two kidneys and two ureters. The lower urinary system consists of a urinary bladder and a urethra (see Fig 44-1). Urine is formed in the kidneys, drains through the ureters to be stored in the bladder and then passes from the body through the urethra.

The kidneys are the principal organs of the urinary system. The primary functions of the kidneys are to: (1) regulate the volume and composition of extracellular fluid (ECF); and (2) excrete waste products from the body. The kidneys also function to control blood pressure, produce erythropoietin, activate vitamin D and regulate acid–base balance.

KIDNEYS

Macrostructure

The paired kidneys are bean-shaped organs located retroperitoneally (behind the peritoneum) on either side of the vertebral column at about the level of the twelfth thoracic (T12) vertebra to the third lumbar (L3) vertebra. Each kidney weighs between 115 and 175 g and is about 12 cm long. The right kidney, with the liver above it, is lower than the left. The right kidney is at the level of the twelfth rib. An adrenal gland lies on top of each kidney.

Each kidney is surrounded by a considerable amount of fat and connective tissue that serves to support and maintain its position. The surface of the kidney is covered by a thin, smooth layer of fibrous membrane called the capsule. These structures protect the kidney and serve as a shock absorber should the kidney be subjected to a sudden force from a blunt object striking the abdomen or back. The hilus on the medial side of the kidney serves as the entry site for the renal artery and nerves, as well as the exit site for the renal vein and ureter.

The parenchyma (actual tissue) of the kidney can be visualised on a longitudinal section of the kidney (see Fig 44-2). The outer layer is termed the cortex and the inner layer the medulla. The medulla consists of a number of pyramids. The apices of these pyramids are called papillae, through which urine passes to enter the calyces. The minor calyces widen and merge to form the major calyces, which form a funnel-shaped sac called the renal pelvis. The minor and major calyces transport urine to the renal pelvis in preparation for transportation to the bladder via the ureter. The pelvis of the kidney can store a small volume of urine (3–5 mL).

Blood supply

A blood supply of about 1200 mL per minute, which is 20–25% of the cardiac output, flows to the two kidneys. Blood reaches the kidneys via the renal artery, which arises from the aorta and enters the kidney through the hilus. The renal artery divides into secondary branches and then into still smaller branches, each of which eventually forms an afferent arteriole. The afferent arteriole divides into a capillary network termed the glomerulus, which is a tuft of up to 50 capillaries (see Fig 44-3). The capillaries of the glomerulus eventually unite in the efferent arteriole. This efferent arteriole splits to form a capillary network called the peritubular capillaries, which, as the name suggests, surround the tubular system. All peritubular capillaries drain into the venous system; the renal vein empties into the inferior vena cava.

Physiology of urine formation

The process of urine formation is extremely complex. It represents the outcome of a multi-step process of filtration, reabsorption, secretion and excretion of water, electrolytes and metabolic waste products. Although urine formation is the result of this process, the primary function of the kidneys is to filter the blood and maintain the body’s internal homeostasis.2

Glomerular function

Urine formation begins at the glomerulus, where blood is filtered. The glomerulus is a semipermeable membrane that allows filtration (see Fig 44-3). The hydrostatic pressure of the blood within the glomerular capillaries causes a portion of blood to be filtered across the semipermeable membrane into the Bowman’s capsule, where the filtered portion of the blood called the glomerular filtrate begins to pass down to the tubule. Filtration is more rapid in the glomerulus than in ordinary tissue capillaries because of the porosity of the glomerular membrane. The ultrafiltrate is similar in composition to blood except that it lacks blood cells, platelets and large plasma proteins. Under normal conditions the capillary pores are too small to allow the loss of these large blood components. In many renal diseases capillary permeability is increased, which permits plasma proteins and blood cells to pass into the urine.

The amount of blood filtered each minute by the glomeruli is expressed as the glomerular filtration rate (GFR). The normal GFR is about 125 mL/min. However, on average, only 1 mL/min is excreted as urine because most glomerular filtrate is reabsorbed by the peritubular capillary network before it reaches the end of the collecting duct.

Tubular function

The glomerular membrane is a selective filtration membrane that filters primarily by size, so it is adapted for the reabsorption of essential materials and the excretion of non-essential ones (see Table 44-1). The tubules and collecting ducts carry out these functions by means of reabsorption and secretion. Reabsorption is the passage of a substance from the lumen of the tubules through the tubule cells and into the capillaries. This process involves both active and passive transport. Tubular secretion is the passage of a substance from the capillaries through the tubular cells into the lumen of the tubule. Reabsorption and secretion occur along the entire length of the tubule, causing numerous changes in composition of the glomerular filtrate as it moves through the tubules.

TABLE 44-1 Functions of the segments of the nephron

Component Function
Glomerulus Selective filtration
Proximal tubule Reabsorption of 80% of electrolytes and water; reabsorption of all glucose and amino acids; reabsorption of HCO3; secretion of H+ and creatinine
Loop of Henle Reabsorption of Na+ and Cl in ascending limb; reabsorption of water in descending loop; concentration of filtrate
Distal tubule Secretion of K+, H+, ammonia; reabsorption of water (regulated by ADH); reabsorption of HCO3; regulation of Ca2+ and PO43– by parathyroid hormone; regulation of Na+ and K+ by aldosterone
Collecting duct Reabsorption of water (ADH required)

ADH, antidiuretic hormone; Ca2+, calcium; CI , chloride; H+, hydrogen; HCO3, bicarbonate; K+, potassium; na+, sodium; PO43–, phosphate.

In the proximal convoluted tubule, about 80% of the electrolytes are reabsorbed. Normally, all the glucose, amino acids and small proteins are reabsorbed. Although most reabsorption occurs by active transport, hydrogen ions (H+) and creatinine are secreted into the filtrate.

As reabsorption continues in the loop of Henle, water is conserved, which is important for concentrating the filtrate. The descending loop is permeable to water and moderately permeable to sodium, urea and other solutes. In the ascending limb, chloride ions (Cl) are actively reabsorbed, followed by passive reabsorption of sodium ions (Na+). About 25% of the filtered sodium is reabsorbed in the ascending limb.

Two important functions of the distal convoluted tubules are final regulation of water balance and acid–base balance. Antidiuretic hormone (ADH), which is released by the posterior pituitary gland, is required for water reabsorption. The stimuli for ADH release are increased serum osmolality and decreased blood volume. ADH makes the distal convoluted tubules and the collecting ducts permeable to water, allowing water to be reabsorbed into the peritubular capillaries and eventually returned to the circulation. In the absence of ADH, the tubules are essentially impermeable to water, thus any water in the tubules leaves the body as urine. Decreases in plasma osmolality are detected in the anterior hypothalamus by osmoreceptors. Osmoreceptors send neural input to other hypothalamic cells called superoptic nuclei cells. Superoptic nuclei cells have axonal extensions, which terminate in the posterior pituitary gland, that inhibit secretion of ADH. Decreases in blood pressure (decreased plasma volume) and increases in plasma osmolality cause diminished firing of baroreceptors and stimulation of ADH secretion (decreased blood pressure + increased plasma osmolality → decreased baroreceptor firing + increased ADH secretion). Aldosterone (released from the adrenal cortex) acts on the distal tubule to cause reabsorption of Na+ and water. In exchange for Na+, potassium ions (K+) are excreted. The secretion of aldosterone is influenced by both circulating blood volume and plasma concentrations of Na+ and K+.

Acid–base regulation involves reabsorbing and conserving most of the bicarbonate (HCO3) and secreting excess H+. The distal tubule functions in different ways to maintain the pH of ECF within a range of 7.35 to 7.45 (see Ch 16 for explanations about acid–base balance.)

Atrial natriuretic peptide (ANP) is a hormone secreted from cells in the right atrium in response to atrial distension due to an increase in plasma volume. ANP acts on the kidneys to increase sodium excretion. At the same time ANP inhibits renin, ADH and the action of angiotensin II on the adrenal glands, thereby suppressing aldosterone secretion. These combined effects of ANP result in the production of a large volume of dilute urine. Furthermore, secretion of ANP causes relaxation of the afferent arteriole, thus increasing the GFR.3

The renal tubules are also involved in calcium balance. Parathyroid hormone (PTH) is released from the parathyroid gland in response to low serum calcium levels. PTH maintains serum calcium levels by causing increased tubular reabsorption of calcium ions (Ca2+) and decreased tubular reabsorption of phosphate ions (PO42−). In renal disease, the effects of PTH may have a major effect on bone metabolism.

The basic function of nephrons is to clean or clear blood plasma of unnecessary substances. After the glomerulus has filtered the blood, the tubules select the unwanted from the wanted portions of tubular fluid. The necessary portions are returned to the blood and the unnecessary portions pass into urine.

Other functions of the kidneys

In addition to their function in regulating the volume and composition of the ECF, the kidneys also have other vital functions, including the production of erythropoietin, the activation of vitamin D, the production and secretion of renin, and prostaglandin (PG) synthesis.

Erythropoietin is produced and released in response to hypoxia and decreased renal blood flow. Erythropoietin stimulates the production of red blood cells (RBCs) in the bone marrow. A deficiency of erythropoietin occurs in renal failure, leading to anaemia.

Vitamin D is a hormone that can be obtained in the diet or synthesised by the action of ultraviolet radiation on cholesterol in the skin. These forms of vitamin D are inactive and require two more steps to become metabolically active. The first step occurs in the liver and the second step in the kidneys. Active vitamin D is essential for the absorption of calcium from the gastrointestinal (GI) tract. The patient with renal failure has a deficiency of the active metabolite of vitamin D and manifests problems of altered calcium and phosphate balance (see Ch 46).

Renin is important in the regulation of blood pressure. It is produced and secreted by juxtaglomerular cells of the kidneys (see Fig 44-4) and released into the bloodstream in response to decreased arterial blood pressure (decreased renal perfusion), renal ischaemia, ECF depletion, increased noradrenaline and increased urinary Na+ concentration. Renin catalyses the splitting of the plasma protein angiotensinogen (from the liver) into angiotensin I, which is subsequently converted to angiotensin II by angiotensin-converting enzyme (ACE), which is made in the lungs. ACE is located on the luminal surface of all blood vessels, with especially high levels in the vessels of the lungs. Angiotensin II stimulates the release of aldosterone from the adrenal cortex, which causes Na+ and water retention, leading to an increased ECF volume. Angiotensin II also causes increased peripheral vasoconstriction. Release of renin is suppressed by factors opposite to those that cause release. The elevation in blood pressure brought about by the increase in ECF and vasoconstriction and the increase in plasma sodium inhibit further renin release. Excessive renin production caused by impaired renal perfusion may be a contributing factor in the aetiology of hypertension.

PGs are synthesised by most body tissues from the precursor, arachidonic acid, in response to appropriate stimuli. PGs are involved in the regulation of cell function and host defences, and primarily exert their influence on cells or tissues that are close to the site where they are synthesised.

In the kidneys, PG synthesis (primarily PGE2 and PGI2) occurs mainly in the medulla. These PGs have a vasodilating action, thus increasing renal blood flow and promoting Na+ excretion. They counteract the vasoconstrictor effect of substances such as angiotensin and noradrenaline. Renal PGs may have a systemic effect in lowering blood pressure by decreasing systemic vascular resistance.4

The significance of renal PGs is related to the role of the kidneys in causing hypertension. In renal failure with a loss of functioning tissue, these renal vasodilator factors are also lost. This may be one factor that contributes to the common finding of hypertension in renal failure (see Ch 46).

URETERS

The ureters are tubes approximately 25–35 cm long and 0.2–0.8 cm in diameter that carry urine from the renal pelvis to the bladder (see Fig 44-1). The narrow area at which point each ureter joins the renal pelvis is termed the pelvoureteric junction (PUJ). After coursing down along the psoas muscle, the ureters cross over the pelvic brim and iliac artery and insert, at oblique angles, into either side of the bladder base at the vesicoureteric junction (VUJ). The ureteral lumen is narrowest at these junctions; consequently, they are often the sites of urinary stone (calculi) obstruction. Because the lumen of the ureter is narrow, it can be easily obstructed internally (e.g. urinary calculi) or externally (e.g. tumours, adhesions, inflammation).

Sympathetic and parasympathetic nerves, along with the vascular supply, surround the mucosal lining of the ureter. Circular and longitudinal smooth muscle fibres are arranged in a mesh-like outer layer and contract to promote the peristaltic one-way flow of urine. These muscle contractions can be affected by distension and neurological, endocrine and pharmacological factors. Stimulation of these nerves during passage of a stone or clot may cause acute, severe pain termed renal colic.

Because the renal pelvis holds only 3–5 mL of urine, kidney damage can result from a backflow of more than that amount of urine. The VUJ relies on the ureter’s angle of bladder penetration and muscle fibre attachments with the bladder to prevent the backflow of urine (reflux) and ascending infection. The distal ureter entering the bladder has more longitudinal muscle fibres than the upper ureter. This segment enters the bladder laterally at its base, courses along obliquely through the bladder wall for about 1.5 cm and intermingles with muscle fibres of the bladder base. Circular and longitudinal bladder muscle fibres adjacent to the embedded ureter help secure it. When bladder pressure rises (e.g. during voiding or coughing), muscle fibres that the ureter shares with the bladder base contract first to help promote ureteral lumen closure. The bladder then contracts against its base to further close the VUJ and prevent urine from moving back through the junction.

BLADDER

The urinary bladder is a distensible organ positioned behind the symphysis pubis and anterior to the vagina and rectum (see Fig 44-5). Its primary functions are to serve as a reservoir for urine and to help the body eliminate waste products. Normal adult urine output is approximately 1500 mL per day, which varies with food and fluid intake. The volume of urine produced at night is less than half of that formed during the day because of hormonal influences (e.g. ADH). This diurnal pattern of urination is normal. Typically, an individual will urinate five or six times during the day and occasionally at night.

The triangular area formed by the two ureteral openings and the bladder neck at the base of the bladder is termed the trigone. It is affixed to the pelvis by many ligaments and does not change its shape during bladder filling or emptying. The bladder muscle, termed the detrusor, is composed of layers of intertwined smooth muscle fibres and is capable of considerable distension during bladder filling and contraction during emptying.5 It is attached to the abdominal wall by an umbilical ligament, termed the urachus. As a result of this attachment, as the bladder fills, it rises towards the umbilicus. The dome, anterior and lateral aspects of the bladder expand and contract. When the bladder is empty, it appears as multiple folds within the pelvis.

On average, 200–250 mL of urine in the bladder causes moderate distension and the urge to urinate. When the quantity of urine reaches approximately 400–600 mL, the person feels uncomfortable. Bladder capacity varies with the individual, usually ranging from 600 mL to 1000 mL. Evacuation of urine is termed urination, micturition or voiding.6

The bladder has the same mucosal lining as that of the renal pelvis, ureter and bladder neck. It is lined by transitional cell epithelium or urothelium and is unique to the urinary tract. Transitional cell epithelium is resistant to absorption of urine. Therefore, urinary wastes produced by the kidneys do not leak out of the urinary system after they leave the kidneys. Microscopically, transitional cell epithelium is several cells deep. These cells stretch out in the bladder to only a few cells deep to accommodate filling. As the bladder empties, the urothelium resumes its multicellular layer formation.

Transitional cell tumours that occur in one section of the urinary tract can easily metastasise to other urinary tract areas given that the mucosal lining throughout the urinary tract is the same. Malignant cells may move down from upper urinary tract tumours and embed in the bladder, or a large bladder tumour can invade the ureter. Tumour recurrence within the bladder is common. Intact urothelium also has phagocytic properties, although the exact mechanism is unknown.

URETHRA

The urethra is a small muscular tube that leads from the bladder neck to the external meatus. The primary function of the urethra is to serve as a conduit for urine from the bladder neck to outside the body during voiding.

The urothelium and submucosal layers are the same as that of the bladder. Smooth muscle fibres extend from the bladder neck down into the urethra and are further supported by circular smooth muscle fibres around the urethra. Special C-shaped striated muscle fibres (the rhabdosphincter, or external sphincter) surround a portion of the urethra and voluntarily contract and prevent leaking when bladder pressure increases.

The female urethra is only 3–5 cm long and lies behind the symphysis pubis but anterior to the vagina (see Fig 44-1, C). The rhabdosphincter encircles the middle third of the urethra. The shortness of the urethra is a contributing factor to the increased incidence of urinary tract infections in women.

The male urethra, which is about 20–25 cm long, originates at the bladder neck and extends the length of the penis (see Fig 44-1, B). It can be seen as three parts. The prostatic urethra extends from the bladder neck through the prostate to the urogenital diaphragm. The membranous urethra passes through the urogenital diaphragm. The rhabdosphincter encircles this portion. Because of the concentrated muscular support, this short portion is not as expandable; consequently, stricture formation in this area after instrumentation is common. The penile urethra continues through the corpus spongiosum, a cavernous penile body, from the urogenital diaphragm to a distal dilated area, the fossa navicularis, before terminating at the meatus.

URETHROVESICAL UNIT FUNCTION

Together, the bladder, urethra and pelvic floor muscles form what is called the urethrovesical unit. Normal voluntary control of this unit is defined as continence. Various areas of the brain send stimulating and inhibiting impulses to the thoracolumbar (T11– L2) and sacral (S2– 4) areas of the spinal cord to control voiding. Distension of the bladder stimulates stretch receptors within the bladder wall. Impulses are transmitted to the sacral spinal cord and then to the brain, causing a desire to urinate. If the time to void is not appropriate, inhibitor impulses in the brain are stimulated and transmitted back through the thoracolumbar and sacral nerves innervating the bladder. In a coordinated fashion, the detrusor accommodates to the pressure (does not contract) while the sphincter and pelvic floor muscles tighten (contract) to resist bladder pressure. If voiding is appropriate, cerebral inhibition is voluntarily suppressed and impulses are transmitted via the spinal cord for the bladder neck, sphincter and pelvic floor muscles to relax and for the bladder to contract. The sphincter closes and the detrusor muscle relaxes when the bladder is empty.

Gerontological considerations: the effects of ageing on the urinary system

Anatomical changes in the ageing kidney include a 20–30% decrease in size and weight between the ages of 30 and 90 years. By the seventh decade of life, 30–50% of glomeruli have lost their function. Atherosclerosis has been found to accelerate the decrease of renal size with age. Despite these changes, older individuals maintain body fluid homeostasis unless they encounter diseases or other physiological stressors.7

Physiological changes in the ageing kidney include decreased renal blood flow, due in part to atherosclerosis, resulting in a decreased GFR. Alterations in hormone levels, including ADH, aldosterone and ANP, result in decreased urinary concentrating ability and alterations in the excretion of water, sodium, potassium and acid. Under normal conditions, the ageing kidney is able to maintain homeostasis. However, after abrupt changes in blood volume, acid load or other insults, the kidney may not be able to function effectively because much of its renal reserve has been lost.7

Physiological changes also occur in the ageing bladder and urethra.8 The female urethra, bladder, vagina and pelvic floor undergo a loss of elasticity, vascularity and structure. Periurethral striated muscle fibres and muscles supporting the bladder relax. Consequently, older women are more prone to urethral irritation and urethral and bladder infections. Although urinary incontinence in older women has long been associated with diminished oestrogen levels, recent research has found that the incidence of incontinence is higher in menopausal women who use hormone replacement therapy. These findings may promote changes in therapy for postmenopausal urinary incontinence.9

The prostate enlarges as men age and because it surrounds the proximal urethra, increasing prostate size may affect urinary patterns, causing hesitancy, retention, slow stream and bladder infections.

Constipation, a complaint often expressed by the elderly, can also affect urination. Partial urethral obstruction may occur because of the rectum’s close proximity to the urethra.

Age-related changes in the urinary system and differences in assessment findings are presented in Table 44-2.

Any disease or trauma that affects the function of the brain, spinal cord or nerves that directly innervate the bladder, bladder neck, external sphincter or pelvic floor can affect bladder function. These conditions include diabetes mellitus, multiple sclerosis, paraplegia and quadriplegia. Drugs affecting nerve transmission also can affect bladder function.

Assessment of the urinary system

While the majority of urinary-related problems that patients experience are mild, the consequences of serious disease can be profound. The nurse therefore needs to carefully assess all patients who visit the healthcare provider for advice.

SUBJECTIVE DATA

Important health information

Three aspects of the patient’s current and past health history need to be considered when assessing the patient’s presenting symptoms.

Medications

An assessment of the patient’s current and past use of medications is important. This should include over-the-counter drugs, as well as prescription medications and herbs. Drugs affect the urinary tract in several ways. Many drugs are known to be nephrotoxic (see Table 44-3). Certain drugs may alter the quantity and character of urine output (e.g. diuretics). A number of drugs change the colour of urine, such as rifampicin, nitrofurantoin and doxorubicin (which makes the urine red). Anticoagulants may cause haematuria. Many antidepressants, calcium channel blockers, antihistamines and drugs used for neurological and musculoskeletal disorders affect the ability of the bladder or sphincter to contract or relax normally.

Health perception–health management pattern

The nurse should ask about the patient’s general health, particularly when disease affecting the kidneys is suspected. Responses such as ‘I feel tired all the time’, changes in weight or appetite, excessive thirst, fluid retention and complaints of headache, pruritus or blurred vision may be related to abnormal kidney function. Similarly, an elderly patient may report malaise and non-localised abdominal discomfort as the only symptoms of a urinary tract infection.8

It is important to take an occupational history because exposure to certain chemicals can affect the kidneys and urinary tract system. Phenol and ethylene glycol are examples of nephrotoxic chemicals. Aromatic amines and certain organic chemicals may increase the risk of bladder cancers. Textile workers, painters, hairdressers and industrial workers have a high incidence of bladder tumours. A higher risk for urinary calculi is seen in professional chefs and others working in hot environments, as well as in taxi drivers who often try to minimise their fluid intake to avoid too many ‘toilet stops’.10

Obtain a smoking history. Cigarette smoking is a major factor in the risk for bladder cancer.11 Tumours occur more frequently in cigarette smokers than in non-smokers.

Places where a patient has lived may be important information to obtain. For example, living in a hot, dry climate may increase the risk of developing urinary calculi, and a person who has lived in the Middle East or Africa may have acquired certain parasites that can cause cystitis or bladder cancer.

A family history of certain renal or urological problems increases the likelihood of similar problems occurring in the patient. The nurse should ask about family members who have had any of the diseases referred to in the past health history, as well as polycystic renal disease and congenital urinary tract abnormalities, such as Alport syndrome (congenital nephritis).

Elimination pattern

Questions about urine elimination patterns are the cornerstone of the health history in the patient with a lower urinary tract disorder. This line of inquiry begins with a question of how the patient manages urine elimination. The majority of patients eliminate urine by spontaneous voiding, and they should be asked about daytime (diurnal) voiding frequency and the frequency of nocturia. Pelvic organ prolapse, particularly advanced anterior vaginal prolapse, may cause suprapubic pressure, frequency, urgency and incontinence secondary to urinary retention. Patients should be queried about additional troublesome lower urinary tract symptoms, including urgency, incontinence or urinary retention. Box 44-1 lists some of the common clinical manifestations of urinary tract disorders. Changes in the colour and appearance of urine are often significant and should be evaluated. If blood is visible in the urine, the nurse should determine whether it occurs at the beginning, during or at the end of urination.

Bowel function should also be investigated. Problems with faecal incontinence may signal neurological causes for bladder problems because of shared nerve pathways. Constipation and faecal impaction can partially obstruct the urethra, causing inadequate bladder emptying, overflow incontinence and infection.

The nurse should determine the patient’s method of handling a urinary problem. For example, the patient may already be using a catheter or collection device. Sometimes a patient has to assume a particular position to urinate or to perform such manoeuvres as pressing on the lower abdomen (Credé method), straining (Valsalva manoeuvre) or stretching the rectum to empty the bladder.

OBJECTIVE DATA

Physical examination

The physical examination consists of four stages, each of which is outlined below.

Auscultation

The bell of the stethoscope may be used to auscultate over both CVAs and in the upper abdominal quadrants. With this technique, the abdominal aorta and renal arteries are auscultated for a bruit (an abnormal murmur), which indicates impaired blood flow to the kidneys. Arteriovenous fistula and grafts should also be auscultated with a stethoscope to determine the presence of a bruit, which indicates the vascular access is patent. Bladder ultrasound, if available, can be used to verify urine volume.

Box 44-2 shows how to record the normal physical assessment findings of the urinary system. Table 44-5 presents common assessment abnormalities of the urinary system. Normally, assessment findings may vary in the older adult. Table 44-2 describes the age-related changes in the urinary system and differences in assessment findings.

TABLE 44-5

Urinary system

COMMON ASSESSMENT ABNORMALITIES

Finding Description Possible aetiology and significance
Anuria Technically no urination (24-h urine output <100 mL) Acute kidney injury, end-stage kidney disease, bilateral ureteral obstruction
Burning on urination Stinging pain in urethral area Urethral irritation, urinary tract infection
Dysuria Painful or difficult urination Sign of urinary tract infection and interstitial cystitis and wide variety of pathological conditions
Enuresis Involuntary nocturnal urinating Symptomatic of lower urinary tract disorder
Frequency Increased incidence of urinating Acutely inflamed bladder, retention with overflow, excess fluid intake
Haematuria Blood in the urine Cancer of genitourinary tract, blood dyscrasias, renal disease, urinary tract infection, stones in kidney or ureter, medications (anticoagulants)
Hesitancy Delay or difficulty in initiating urination Partial urethral obstruction
Incontinence Inability to voluntarily control discharge of urine neurogenic bladder, bladder infection, injury to external sphincter
Nocturia Frequency of urination at night Renal disease with impaired concentrating ability, bladder obstruction, heart failure, diabetes mellitus, finding after kidney transplant
Oliguria Diminished amount of urine in a given time (24-h urine output of 100–400 mL) Severe dehydration, shock, transfusion reaction, acute kidney injury, kidney disease, end-stage kidney disease
Pain Presence over suprapubic area (related to bladder), urethral pain (irritation of bladder neck), flank (CVA) pain Infection, urinary retention, foreign body in urinary tract, urethritis, pyelonephritis, renal colic or stones
Pneumaturia Passage of urine containing gas Fistula connections between bowel and bladder, gas-forming urinary tract infections
Polyuria Large volume of urine in a given time Diabetes mellitus, diabetes insipidus, chronic kidney disease, diuretics, excess fluid intake
Retention Inability to urinate even though bladder contains excessive amount of urine Finding after pelvic surgery, childbirth, catheter removal; urethral stricture or obstruction; neurogenic bladder; postanaesthesia
Stress incontinence Involuntary urination with increased pressure (sneezing or coughing) Weakness of sphincter control

BPH, benign prostatic hyperplasia; CVA, costovertebral angle; GFR, glomerular filtration rate; WBCs, white blood cells.

Diagnostic studies

Diagnostic studies are important in locating and understanding problems of the urinary system.Table 44-6 lists the diagnostic studies that are common for the urinary system; select studies are described in more detail in the following text. The accuracy of these diagnostic studies is influenced by: (1) adherence to the proper procedures; and (2) the cooperation of the patient in terms of fluid restriction, urine specimen collection, study preparation procedures, ability to remain positioned on the examination table and following other instructions.

TABLE 44-6 Urinary system

DIAGNOSTIC STUDIES

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BPH, benign prostatic hyperplasia; FBC, full blood count; GFR, glomerular filtration rate; GI, gastrointestinal; IV, intravenous; NBM, nil by mouth; WBC, white blood cell.

* N-acetylcysteine (Mucomyst), a renal vasodilator and antioxidant, is sometimes administered to reduce the incidence of contrast-induced nephropathy; can be given by oral or intravenous route. Source: Kshirsagar AV, Poole C, Mottl A et al. N-acetylcysteine for the prevention of radiocontrast nephropathy: a meta-analysis of prospective controlled trials. J Am Soc nephrol 2004; 15(3):761–769.

When a patient has diagnostic studies on consecutive days, it is important to prevent dehydration. It is common to have the patient nil by mouth (NBM) after midnight, spend all morning in the X-ray department, be too tired to eat, sleep all afternoon and be NBM after midnight again because of studies scheduled for the next day. Severe dehydration, especially in a diabetic, debilitated or older patient, may lead to acute kidney injury. The nurse is responsible for ensuring that a patient undergoing diagnostic studies is properly hydrated and given adequate nourishment between studies. The nurse should also check with the patient’s doctor regarding the insulin dose for the diabetic patient who is NBM.

Urinary system

CLINICAL PRACTICE

Use this checklist to ensure the key assessment steps have been done.

Subjective  
Ask the patient about any of the following and note responses.  
Painful urination Y N
Changes in colour of urine (blood, cloudy) Y N
Change in characteristics of urination (diminished, excessive) Y N
Problems with frequent night time urination (nocturia) Y N
Objective: diagnostic  
Check the following laboratory results for critical values.  
Serum urea
Serum creatinine
Urinalysis
Urine culture and sensitivity
Objective: physical examination  
Inspect  
Abdomen
Urinary meatus for inflammation or discharge
Palpate  
Abdomen for bladder distension, masses or tenderness
Percuss  
Costovertebral angle for tenderness
Auscultate  
Renal arteries for bruits

URINE STUDIES

Urinalysis

Urinalysis (see Tables 44-6 and 44-7) is one of the first studies completed to evaluate disorders of the urinary tract. Results from the urinalysis may indicate possible abnormalities, suggest the need for further studies or provide evidence of progression in a previously diagnosed disorder.12

For a routine urinalysis, a specimen may be collected at any time of the day. However, it is best to obtain the first specimen urinated in the morning. This concentrated specimen is more likely to contain abnormal constituents if they are present in the urine. The specimen should be examined within 1 hour of urinating. If it is not, bacteria multiply rapidly, red blood cells haemolyse, casts (moulds of renal tubules) disintegrate and the urine becomes alkaline as a result of urea-splitting bacteria. If it is not possible to send the specimen to the laboratory immediately, it should be refrigerated. However, to obtain the best results, the nurse should coordinate specimen collection with routine laboratory hours.

Multiple reagent strips (also called urine dipsticks) are commonly used by laboratories and in outpatient settings to provide chemical analysis of urine along with a microscopic interpretation. The results of a urinalysis usually include a description of the appearance, specific gravity (mass and density), pH, glucose, ketones and protein in the urine, and a microscopic examination of urine sediment for white blood cells, red blood cells, crystals and casts (see Table 44-7).

BLOOD CHEMISTRY

Blood chemistry (biochemistry) studies measuring electrolytes, creatinine, urea and uric acid are commonly used to detect the kidney’s functional ability to maintain normal homeostasis. Since 2005 all pathology services in Australia and New Zealand have introduced automatic GFR reporting for adults having serum creatinine measurements. This calculates an estimated GFR (eGFR) using the patient’s age and sex as well as the creatinine measurements. eGFR is best viewed as a screening tool; decreased eGFR levels should direct closer attention to the patient’s kidney health.12

RADIOLOGICAL STUDIES

Many radiological studies require the use of a bowel preparation the evening before the study to clear the lower GI tract of faeces and flatus. Because the kidneys lie in a retroperitoneal location, the contents of the colon may obstruct visualisation of the urinary tract. If the bowel preparation fails to adequately evacuate the lower tract, the study may be unsuccessful and have to be rescheduled. Commonly used bowel preparations include enemas, castor oil, magnesium citrate and bisacodyl tablets or suppositories. Some bowel preparations, such as magnesium citrate, are contraindicated in patients with renal failure. Magnesium cannot be excreted by patients with renal failure (see Ch 46).

Renal arteriogram

The purpose of a renal arteriogram (angiogram) is to visualise the renal blood vessels. The findings of an arteriogram can assist in diagnosing renal artery stenosis (see Fig 44-8), additional or missing renal blood vessels and renovascular hypertension, and in differentiating between a renal cyst and a renal tumour. Renal arteriograms are also included in the diagnostic examination of a potential renal transplant donor.

The patient is given a local anaesthetic at the site of catheter insertion. A catheter is usually inserted into the femoral artery and passed up the aorta to the level of the renal arteries (see Fig 44-9). Contrast medium is then injected to outline the renal blood supply and X-rays are taken. The patient may experience a transient warm feeling along the course of the blood vessel when the contrast material is injected. As with all contrast studies, possible iodine and shellfish allergies should be determined before the study.

After the catheter is removed, a pressure dressing is placed over the femoral injection site. It is important to observe the site for bleeding. Bed rest is usually prescribed with the affected leg straight. Peripheral pulses in the involved leg should be taken at least every 30–60 minutes to detect occlusion of blood flow caused by a thrombus. Complications that may result from a renal arteriogram include thrombus, embolus, local inflammation and haematoma. The patient with baseline renal insufficiency may experience a decrease in renal function secondary to the nephrotoxic contrast material, so adequate postprocedure hydration (often intravenous) and administration of N-acetylcysteine are required.

RENAL RADIONUCLIDE IMAGING

Renal biopsy

The purpose of a renal biopsy is to determine the nature and extent of renal disease. This information can be used in establishing a diagnosis or following the progression of renal disease. Biopsy material can be obtained through an open biopsy or a closed percutaneous needle biopsy. A percutaneous needle biopsy is more commonly done—an open biopsy is rarely performed because it requires a surgical procedure with anaesthesia.

Absolute contraindications to a percutaneous renal biopsy are bleeding disorders, the presence of a single kidney and uncontrolled hypertension. Relative contraindications include suspected renal infection, hydronephrosis and possible vascular lesions. The patient who is going to have a biopsy done should not be taking aspirin or warfarin before the procedure.

The procedure consists of having the patient lie prone with a pillow or sandbag to elevate the abdomen and kidneys. The position of the kidney is marked on the body using CT, IVP or ultrasound guidance. Local anaesthesia is used and a biopsy needle is inserted into the kidney just below the twelfth rib. Patients are instructed to hold their breath while the biopsy specimen is being taken.

After the procedure, a pressure dressing is applied and the patient is kept prone for 30–60 minutes. Following the procedure vital signs should be taken every 5–10 minutes during the first hour and then with decreasing frequency if no problems are noted. The biopsy site should be inspected frequently for bleeding. Serial urine specimens should be assessed for gross and microscopic haematuria. A dipstick can be used to test for bleeding, even when haematuria is not obvious. The healthcare provider may order all urine to be sent for laboratory analysis to detect possible haematuria. The patient should be assessed for flank pain, hypotension, decreasing haematocrit and temperature elevation, as well as being observed for chills, urinary frequency and dysuria. Most biopsies are carried out as a day-only procedure and patients are discharged after 8 hours if there are no complications.

Complications of a renal biopsy include renal haemorrhage, haematoma and infection. Even if no complications occur, the patient should be instructed to avoid lifting heavy objects for 5–7 days. The patient should be instructed not to take any anticoagulant drugs until permission is given by the doctor who performed the biopsy.

ENDOSCOPY

Cystoscopy

The main purpose of cystoscopy is to inspect the interior of the bladder with a tubular lighted scope called a cystoscope (see Fig 44-10). Cystoscopes can be used to insert ureteral catheters, remove calculi, obtain biopsy specimens of bladder lesions and treat bleeding lesions. In most cases, bladder disorders can be determined by cystoscopic examination.

Cystoscopy is usually done in a cystoscopy room in the X-ray department, in a urology clinic or in the operating room. Most of the pain associated with cystoscopy results from spasms and contractions of the bladder and sphincter. Getting the patient to relax and breathe deeply may alleviate some of the bladder and sphincter spasms. A local anaesthetic is instilled into the urethra before scope insertion. During the examination, saline solution is instilled slowly to distend the bladder. This allows better visualisation but causes an urge to urinate.

After the procedure the patient can expect to have some burning on urination, blood-tinged urine and urinary frequency from the irritation of scope insertion and manipulation. The nurse should observe for bright-red bleeding, which is not normal. After the procedure the nurse is responsible for keeping the patient well hydrated, administering mild analgesics, providing sitz baths and applying heat to decrease the patient’s discomfort. Complications that may result from cystoscopy include urinary retention, urinary tract haemorrhage, bladder infection and perforation of the bladder.

URODYNAMICS

Urodynamics is a set of tests that are designed to measure urinary tract function.14 Urodynamic tests study the storage of urine within the bladder and the flow of urine through the urinary tract to the outside of the body. A combination of techniques may be used to provide a detailed assessment of urinary function (see Table 44-6).

Review questions

1. A renal stone in the pelvis of the kidney will alter the function of the kidney by interfering with:

2. A patient with renal disease has oliguria and a creatinine clearance rate of 40 mL per minute. The nurse recognises that these findings most directly reflect abnormal function of:

3. The nurse identifies a risk for urinary calculi in a patient who relates a past health history that includes:

4. Normal changes associated with ageing of the urinary system that the nurse expects to find include:

5. During physical assessment of the urinary system, the nurse:

6. Normal findings expected by the nurse on physical assessment of the urinary system include:

7. An important nursing responsibility after an intravenous pyelogram is to:

8. On reading the urinalysis results of a dehydrated patient, the nurse would expect to find:

References

1 Smith HW. Fish to philosopher. Boston: Little, Brown, 1953. (Classic)

2 Paton KT, Thibodeau GA. Anatomy and physiology, 7th edn. St Louis: Mosby, 2010.

3 Prowle JR, Ishikawa K, May VN, Bellomo R. Renal plasma flow and glomerular filtration rate during acute kidney injury in man. Renal Failure. 2010;32(3):349–355.

4 Ponnuchamy B, Khalil RA. Cellular mediators of renal vascular dysfunction in hypertension. Am J Physiol Regul Integr Comp Physiol. 2009;296(4):R1001–R1018.

5 Corton MM. Anatomy of pelvic floor dysfunction. Obst Gyn Clin North Am. 2009;36(3):401–419.

6 Fitzgerald MP, Mueller E. Physiology of the lower urinary tract. Clin Obst Gynecol. 2004;47(1):18–27.

7 Sun X, Chen Y, Chen X, Wang J, Xi C, Lin S, Liu X. Change of glomerular filtrate in healthy adults with aging. Nephrol. 2009;14:506–513.

8 Lerma EV. Anatomic and physiologic changes of the aging kidney. Clin Geri Med. 2009;25(3):325–329.

9 Archer DF. Efficacy and tolerability of local estrogen therapy for urogenital atrophy. Menopause. 2010;17(1):194–203.

10 Johri N, Cooper B, Robertson W, Choong S, Rickards D, Unwin R. An update and practical guide to renal stone management. Nephron Clin Pract. 2010;116:c159–c171.

11 CancerhelpUK. Bladder cancer risks and causes. Available at www.cancerhelp.org.uk/type/bladder-cancer/about/bladder-cancer-risks-and-causes. accessed 28 December 2010.

12 Jones GR, Mathew T, Johnson D, Peake M. Implementation of the routine reporting of eGFR in Australia and New Zealand. Scand J Clin Lab Invest. 2008;241:23–29.

13 Wu X. Urinalysis: a review of methods and procedures. Crit Care Nurs Clin North Am. 2010;22(1):121–128.

14 Robertson TM, Hamlin AS. Urodynamics. Crit Care Nurs Clinics North Am. 2010;22(1):109–120.

Resources

See Chapters 45 and 46.

 

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See the Evolve site for more great resources at http://evolve.elsevier.com/AU/Brown/medsurg/