Urology Surgery

Haematuria

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Definition

the presence of blood in the urine.

Macroscopic (gross) haematuria: the patient has seen blood.

Microscopic or dipstick haematuria: blood identified by urine microscopy or by dipstick testing, either in association with other urological symptoms (symptomatic microscopic haematuria) or during a routine medical examination (e.g. for insurance purposes) (asymptomatic microscopic haematuria).

Microscopic haematuria has been variably defined as 3 or more, 5 or more, or 10 or more red blood cells (RBCs) per high-power field.

Urine dipsticks test for heme (i.e. they test for the presence of haemoglobin and myoglobin in urine). Heme catalyses the oxidation of orthotolidine by an organic peroxidase, producing a blue coloured compound. Dipsticks are capable of detecting the presence of haemoglobin from 1 or 2 RBCs.

False +ve urine dipstick: occurs in the presence of myoglobinuria, bacterial peroxidases, povidone, hypochlorite.
False -ve urine dipstick (rare): occurs in the presence of reducing agents (e.g. ascorbic acid prevents the oxidation of orthotolidine).

Is microscopic or dipstick haematuria abnormal?

A few RBCs can be found in the urine of normal people. The upper limit of normal for RBC excretion is 1 million per 24h (as seen in healthy medical students). In healthy male soldiers undergoing yearly urine examination over a 12-yr period, 40% had microscopic haematuria on at least 1 occasion and 15% on 2 or more occasions. Transient microscopic haematuria may occur following rigorous exercise, sexual intercourse, or from menstrual contamination.

The fact that the presence of RBCs in the urine is normal explains why a substantial proportion of patients with microscopic and dipstick haematuria, and even macroscopic haematuria will have normal haematuria investigations (i.e. no abnormality is found). No abnormality is found in approximately 50% of subjects with macroscopic haematuria and 70% with microscopic haematuria, despite full conventional urological investigation (urine cytology, cystoscopy, renal ultrasonography, and IVU).

Causes and Investigation

Urological causes of haematuria

Cancer: bladder (TCC, SCC), kidney (adenocarcinoma), renal pelvis and ureter (TCC), prostate
Stones: kidney, ureteric, bladder
Infection: bacterial, mycobacterial (TB), parasitic (schistosomiasis), infective urethritis
Inflammation: cyclophosphamide cystitis, interstitial cystitis
Trauma: kidney, bladder, urethra (e.g. traumatic catheterization), pelvic fracture causing urethral rupture
Renal cystic disease (e.g. medullary sponge kidney)
Other urological causes: BPH (the large, vascular prostate), loin pain haematuria syndrome, vascular malformations
Nephrological causes of haematuria tend to occur in children or young adults and include, commonly, IgA nephropathy, postinfectious glomerulonephritis; less commonly, membranoproliferative glomerulonephritis, HenochSchÃnlein purpura, vasculitis, Alport's syndrome, thin basement membrane disease, Fabry's disease, etc.
Other medicalâ€™ causes of haematuria include coagulation disordersâ€”congenital (e.g. haemophilia), anticoagulation therapy (e.g. warfarin); sickle cell trait or disease; renal papillary necrosis; vascular disease (e.g. emboli to the kidney cause infarction and haematuria).
Nephrological causes are more likely in the following situations: children and young adults; proteinuria; red blood cell casts.

Urological investigation of haematuria

Conventional urological investigation involves urine culture (where, on the basis of associated cystitissymptoms urinary infection is suspected), urine cytology, cystoscopy, renal ultrasonography, and IVU.

Diagnostic cystoscopy

Nowadays this is carried out using a flexible, fibreoptic cystoscope, unless radiological investigation demonstrates a bladder cancer, in which case one may forego the flexible cystoscopy and proceed immediately to rigid cystoscopy and biopsy under anaesthetic (transurethral resection of bladder tumourTURBT).

Should cystoscopy be performed in patients with asymptomatic microscopic haematuria?

The AUA's Best Practice Policy on Asymptomatic Microscopic Hematuria recommends cystoscopy in all high-risk patients (high risk for development of TCC) with microscopic haematuria (see risk factors below). In asymptomatic, low-risk patients <40>

If no cause for haematuria is found (microscopic or macroscopic) is further investigation necessary?

Some say yes, quoting studies that show serious disease can be identified in a small number of patients where, in addition, retrograde ureterography, endoscopic examination of the ureters and renal pelvis (ureteroscopy), contrast CT, and renal angiography were done. Others say no, citing the absence of development of overt urological cancer during 24 year follow-up in patients originally presenting with microscopic or macroscopic haematuria (though without further investigations).³

When urine cytology, cystoscopy, renal US, and IVU are all normal, we perform CT scanning of the kidneys and ureters and retrograde ureterography in:

patients at high risk for TCC^*
where microscopic or dipstick haematuria persists at 3 months
where macroscopic haematuria persists

General principles of management of patients

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Communication skills
Communication is the imparting of knowledge and understanding. Good communication is crucial for the surgeon in his or her daily interaction with patients. The nature of any interaction between surgeon and patient will depend very much on the context of the â€˜interviewâ€™, whether you know the patient already, and on the quantity and type of information that needs to be imparted. As a general rule the basis of good communication requires the following:

Introduction
Give your name, explain who you are, greet the patient/relative appropriately (e.g. handshake), check you are talking to the correct person.

Establish the purpose of the interview
Explain the purpose of the interview from the patient's perspective and yours, and the desired outcome of the interview.

Establish the patient's baseline knowledge and understanding
Use open questions, let the patient talk and confirm what they know.

Listen actively
Make it clear to the patient that they have your undivided attentionâ€”that you are focusing on them. This involves appropriate body language (eye contact don't look out of the window!).

Pick up on and respond to cues
The patient/relative may offer verbal or non-verbal indications about their thoughts or feelings.

Elicit the patient's main concern(s)
What you think should be the patient's main concerns may not be. Try to find out exactly what the patient is worried about.

Chunks and checks
Give information in small quantities and check that this has been understood. A good way of doing this is to ask the patient to explain what they think you have said.

Show empathy
Let the patient know you understand their feelings.

Be non-judgemental
Don't express your personal views or beliefs.

Alternate control of the interview between the patient and yourself
Allow the patient to take the lead where appropriate.

Signpost changes in direction
State clearly when you move onto a new subject.

Avoid the use of jargon
Use language the patient will understand rather than medical terminology.

Body language
Use body language that shows the patient that you are interested in their problem and that you understand what they are going through. Respect cultural differences; in some cultures eye contact is regarded as a sign of aggression.

Summarize and indicate the next steps
Summarize what you understand to be the patient's problem, and what the next steps are going to be.

Documentation and notekeeping

Royal College of Surgeons' guidelines state that each clinical history sheet should include the patient's name, date of birth, and record number. Each entry should be timed, dated, and signed and your name and position (e.g. SHO for senior house officer or SPR for specialist registrar) should be clearly written in capital letters below each entry. You should also document which other medical staff were present with you on ward rounds or when seeing a patient (e.g. ward roundSPR (Mr X)/SHO/HO).
Contemporaneous notekeeping is an important part of good clinical practice. Medical notes document the patient's problems, the investigations they have undergone, the diagnosis, and the treatment and its outcome. The notes also provide a channel of communication between doctors and nurses on the ward and between different medical teams. In order for this communication to be effective and safe, medical notes must be clearly written. They will also be scrutinized in cases of complaint and litigation. Failure to keep accurate, meaningful notes, which are timed, dated, and signed, with your name written in capital letters below, exposes you to the potential for criticism in such cases. The standard of notekeeping is seen as an indirect measure of the standard of care you have given your patients. Sloppy notes can be construed as evidence of sloppy care, quite apart from the fact that such notes do not allow you to provide evidence of your actions! Unfortunately, the defence of not having sufficient time to write the notes is not an adequate one, and the courts will regard absence of documentation of your actions as indicating that you did not do what you said you did.
Do not write anything which might later be construed as a personal comment about a patient or colleague (e.g. do not comment on an individual's character or manner). Do not make jokes in the patient's notes. Such comments are unlikely to be helpful and may cause you embarrassment in the future when you are asked to interpret them.
Try to make the notes relevant to the situation, So, for example, in a patient with suspected bleeding, a record of blood pressure and pulse rate is important, but a record of a detailed neurological history and examination is less relevant (unless, for example, a neurological basis for the patient's problem is suspected).
The results of investigations should be clearly documented in the notes, preferably in red ink, with a note of the time and date when the investigation was performed.
Avoid the use of abbreviations. In particular, always write LEFT or RIGHT, in capital letters, rather than Lt/Rt or L/R. A handwritten L can sometimes be mistaken for an R and vice versa.
Operation notes. We include the following information on operation notes:

patient name, number, and date of birth
date of operation
surgeon, assistants
patient position (e.g. supine, prone, lithotomy, LloydDavies)
type of DVT prophylaxis (AKTEDS, Flowtrons, heparin, etc.)
type, time of administration, and doses of antibiotic prophylaxis
presence of image intensifier, if appropriate
type and size of endoscopes used
your signature and your name in capitals
post-op instructions and follow-up, if appropriate

If a consultant is supervising you, but is not scrubbed, you must clearly state that the consultant (named) was in attendance

Patient safety in surgical practice
The aviation, nuclear, and petrochemical industries are termed high reliability organizations (HROs) because they have adopted a variety of core safety principles that have enabled them to achieve safety success, despite operating in high-risk environments. Surgeons can learn much from HROs and can adopt some of these safety principles in surgical practice, in order to improve safety in the non-technical aspects of care.
Foremost amongst the safety principles of HROs are:

Teamworking
Use of standard operating procedures (SOPs): day-to-day tasks are carried out according to a set of rules and in a way which is standardized across the organization.
Cross-checking: members of the team check that a procedure, drug, or action has been done or administered by verbalizing that action to another team member. This is most familiar when aircraft cabin crew are asked by the pilot to check that the doors of the plane are locked shut (doors to cross-check) and crew members cross to the opposite door to confirm this has been done. In surgical practice an example of cross-checking could be antibiotic given?, confirmed by a specific reply such as240mg IV gentamicin givenâ.
Regular audit and feedback of audit data: performance data (both good and bad) is collected regularly and crucially team members are notified (e.g. in audit meetings) of where they are performing well or badly.
Establishment of variable hierarchies: development of a working environment where junior staff are encouraged to speak up if they believe an error is about to occur, without fear of criticism.
Cyclical training: frequent and regular training sessions to reinforce safe practice methods.

CLINICAL DECISION-MAKING - URINALYSIS

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URINALYSIS

The urinalysis is a fundamental test that should be performed in all urologic patients. Although, in many instances, a simple dipstick urinalysis will provide the necessary information, a complete urinalysis includes both chemical and microscopic analyses.

Collection of Urinary Specimens Males

In the male patient, a midstream urine sample is obtained. The uncircumcised male should retract the foreskin, cleanse the glans penis with antiseptic solution, and continue to retract the foreskin during voiding. The male patient begins urinating into the toilet, and then places a wide-mouth sterile container under his penis to collect a midstream sample. This avoids contamination of the urine specimen with skin and urethral organisms.

In men with chronic UTIs, four aliquots of urine are obtained. These aliquots have been designated Voided Bladder 1, Voided Bladder 2, Expressed Prostatic Secretions, and Voided Bladder 3 (VB1, VB2, EPS, and VB3). The VB1 is the initial 5 to 10 mL of urine voided, whereas the VB2 is the midstream urine. The EPS is the secretions obtained after gentle prostatic massage, and the VB3 specimen is the initial 2 to 3 mL of urine obtained after prostatic massage. The value of these cultures for localization of UTIs is that the VB1 sample represents urethral flora; the VB2, bladder flora; and the EPS and VB3 samples, prostatic flora. The VB3 sample is particularly helpful when there is little or no prostatic fluid obtained by massage. To better obtain prostatic secretions, patients should be instructed to attempt to void during prostatic massage and to avoid tightening the anal sphincter and pelvic floor muscles. The four-part urine sample is particularly useful in evaluating men with suspected bacterial prostatitis ( Meares and Stamey, 1968 ).

Females

In the female, it is more difficult to obtain a clean-catch midstream specimen. The female patient should cleanse the vulva, separate the labia, and collect a midstream specimen as described for the male patient. If infection is suspected, however, the midstream specimen is unreliable and should never be sent for culture and sensitivity. To evaluate for a possible infection in a female, a catheterized urine sample should always be obtained.

Neonates and Infants

The usual way to obtain a urine sample in a neonate or infant is to place a sterile plastic bag with an adhesive collar over the infant's genitalia. Obviously, however, these devices may not be able to distinguish contamination from true UTI. Whenever possible, all urine samples should be examined within 1 hour of collection and plated for culture and sensitivity if indicated. If urine is allowed to stand at room temperature for longer periods of time, bacterial overgrowth may occur, the pH may change, and red and white blood cell casts may disintegrate. If it is not possible to examine the urine promptly, it should be refrigerated at 5°C.

Physical Examination of Urine

The physical examination of the urine includes an evaluation of color, turbidity, specific gravity and osmolality, and pH.

Color

The normal pale yellow color of urine is due to the presence of the pigment urochrome. Urine color varies most commonly because of concentration, but many foods, medications, metabolic products, and infection may produce abnormal urine color. This is important, because many patients will seek consultation primarily because of a change in their urine color. Thus, it is important for the urologist to be aware of the common causes of abnormal urine color, and these are listed in Table 3-3 .

Table 3-3 -- Common Causes of Abnormal Urine Color

Colorless	Very dilute urine
Colorless	Overhydration
Cloudy/milky	Phosphaturia
	Pyuria
	Chyluria
Red	Hematuria
	Hemoglobinuria/myoglobinuria
	Anthrocyanin in beets and blackberries
	Chronic lead and mercury poisoning
	Phenolphthalein (in bowel evacuants)
	Phenothiazines (e.g., Compazine)
	Rifampin
Orange	Dehydration
	Phenazopyridine (Pyridium)
	Sulfasalazine (Azulfidine)
Yellow	Normal
	Phenacetin
	Riboflavin
Green-blue	Biliverdin
	Indicanuria (tryptophan indole metabolites)
	Amitriptyline (Elavil)
	Indigo carmine
	Methylene blue
	Phenois (e.g., IV cimetidine [Tagamet],
	IV promethazine [Phenergan])
	Resorcinol
	Triamterene (Dyrenium)
Brown	Urobilinogen
	Porphyria
	Aloe, fava beans, and rhubarb
	Chloroquine and primaquine
	Furazolidone (Furoxone)
	Metronidazole (Flagyl)
	Nitrofurantoin (Furadantin)
Brown-black	Alcaptonuria (homogentisic acid)
	Hemorrhage
	Melanin
	Tyrosinosis (hydroxyphenylpyruvic acid)
	Cascara, senna (laxatives)
	Methocarbamol (Robaxin)
	Methyldopa (Aldomet)
	Sorbitol

From Hanno PM, Wein AJ: A Clinical Manual of Urology. Norwalk, CT, Appleton-Century-Crofts, 1987, p 67.

Turbidity

Freshly voided urine is clear. Cloudy urine is most commonly due to phosphaturia, a benign process in which excess phosphate crystals precipitate in an alkaline urine. Phosphaturia is intermittent and usually occurs after meals or ingestion of a large quantity of milk. Patients are otherwise asymptomatic. The diagnosis of phosphaturia can be accomplished either by acidifying the urine with acetic acid, which will result in immediate clearing, or by performing a microscopic analysis, which will reveal large amounts of amorphous phosphate crystals.

Pyuria, usually associated with a UTI, is another common cause of cloudy urine. The large numbers of white blood cells cause the urine to become turbid. Pyuria is readily distinguished from phosphaturia either by smelling the urine (infected urine has a characteristic pungent odor) or by microscopic examination, which readily distinguishes amorphous phosphate crystals from leukocytes.

Rare causes of cloudy urine include chyluria (in which there is an abnormal communication between the lymphatic system and the urinary tract resulting in lymph fluid being mixed with urine), lipiduria, hyperoxaluria, and hyperuricosuria.

Specific Gravity and Osmolality

Specific gravity of urine is easily determined from a urinary dipstick and usually varies from 1.001 to 1.035. Specific gravity usually reflects the patient's state of hydration but may also be affected by abnormal renal function, the amount of material dissolved in the urine, and a variety of other causes mentioned later. A specific gravity less than 1.008 is regarded as dilute, and a specific gravity greater than 1.020 is considered concentrated. A fixed specific gravity of 1.010 is a sign of renal insufficiency, either acute or chronic.

In general, specific gravity reflects the state of hydration but also affords some idea of renal concentrating ability. Conditions that decrease specific gravity include (1) increased fluid intake, (2) diuretics, (3) decreased renal concentrating ability, and (4) diabetes insipidus. Conditions that increase specific gravity include (1) decreased fluid intake; (2) dehydration owing to fever, sweating, vomiting, and diarrhea; (3) diabetes mellitus (glucosuria); and (4) inappropriate secretion of antidiuretic hormone. Specific gravity will also be increased above 1.035 after intravenous injection of iodinated contrast and in patients taking dextran.

Osmolality is a measure of the amount of material dissolved in the urine and usually varies between 50 and 1200 mOsm/L. Urine osmolality most commonly varies with hydration, and the same factors that affect specific gravity will also affect osmolality. Urine osmolality is a better indicator of renal function, but it cannot be measured from a dipstick and must be determined using standard laboratory techniques.

Urinary pH is measured with a dipstick test strip that incorporates two colorimetric indicators, methyl red and bromothymol blue, which yield clearly distinguishable colors over the pH range from 5 to 9. Urinary pH may vary from 4.5 to 8; the average pH varies between 5.5 and 6.5. A urinary pH between 4.5 and 5.5 is considered acidic, whereas a pH between 6.5 and 8 is considered alkaline.

In general, the urinary pH reflects the pH in the serum. In patients with metabolic or respiratory acidosis, the urine is usually acidic; conversely, in patients with metabolic or respiratory alkalosis, the urine is alkaline. Renal tubular acidosis (RTA) presents an exception to this rule. In patients with both type I and II RTA, the serum is acidemic, but the urine is alkalotic because of continued loss of bicarbonate in the urine. In severe metabolic acidosis in type II RTA, the urine may become acidic; but in type I RTA, the urine is always alkaline, even with severe metabolic acidosis ( Morris and Ives, 1991 ). Urinary pH determination is used to establish the diagnosis of RTA; inability to acidify the urine below a pH of 5.5 after administration of an acid load is diagnostic of RTA.

Urine pH determinations are also useful in the diagnosis and treatment of UTIs and urinary calculus disease. In patients with a presumed UTI, an alkaline urine with a pH greater than 7.5 suggests infection with a urea-splitting organism, most commonly Proteus. Urease-producing bacteria convert ammonia to ammonium ions, markedly elevating the urinary pH and causing precipitation of calcium magnesium ammonium phosphate crystals. The massive amount of crystallization may result in staghorn calculi.

Urinary pH is usually acidic in patients with uric acid and cystine lithiasis. Alkalinization of the urine is an important feature of therapy in both of these conditions, and frequent monitoring of urinary pH is necessary to ascertain adequacy of therapy.

Chemical Examination of Urine Urine Dipsticks

Urine dipsticks provide a quick and inexpensive method for detecting abnormal substances within the urine. Dipsticks are short, plastic strips with small marker pads that are impregnated with different chemical reagents that react with abnormal substances in the urine to produce a colorimetric change. The abnormal substances commonly tested for with a dipstick include (1) blood, (2) protein, (3) glucose, (4) ketones, (5) urobilinogen and bilirubin, and (6) white blood cells.

Substances listed in Table 3-3 that produce an abnormal urine color may interfere with appropriate color development on the dipstick. In our experience, this most commonly occurs in patients taking phenazopyridine (Pyridium) for a UTI. Phenazopyridine turns the urine bright orange and makes dipstick evaluation of the urine unreliable.

Appropriate technique must be used to obtain an accurate dipstick determination. The reagent areas on the dipstick must be completely immersed in a fresh uncentrifuged urine specimen and then must be withdrawn immediately to prevent dissolution of the reagents into the urine. As the dipstick is removed from the urine specimen container, the edge of the dipstick is drawn along the rim of the container to remove excess urine. The dipstick should be held horizontally until the appropriate time for reading and then compared with the color chart. Excess urine on the dipstick or holding the dipstick in a vertical position will allow mixing of chemicals from adjacent reagent pads on the dipstick, resulting in a faulty diagnosis. False-negative results for glucose and bilirubin may be seen in the presence of elevated ascorbic acid concentrations in the urine. However, increased levels of ascorbic acid in the urine do not interfere with dipstick testing for hematuria. Highly buffered alkaline urine may cause falsely low readings for specific gravity and may lead to false-positive results for urinary protein. Other common causes of false results with dipstick testing are outdated test strips and exposure of the sticks, leading to damage to the reagents. In general, when the sticks are damaged, there will be color changes on the pads before their immersion in urine. If such color changes are noted, results with the dipstick may be inaccurate.

Hematuria

Normal urine should contain less than three red blood cells per HPF. A positive dipstick for blood in the urine indicates either hematuria, hemoglobinuria, or myoglobinuria. The chemical detection of blood in the urine is based on the peroxidase-like activity of hemoglobin. When in contact with an organic peroxidase substrate, hemoglobin catalyzes the reaction and causes subsequent oxidation of a chromogen indicator, which changes color according to the degree and amount of oxidation. The degree of color change is directly related to the amount of hemoglobin present in the urine specimen. Dipsticks frequently demonstrate both colored dots and field color change. If present, free hemoglobin and myoglobin in the urine are absorbed into the reagent pad and catalyze the reaction within the test paper, thereby producing a field change effect in color. Intact erythrocytes in the urine undergo hemolysis when they come in contact with the reagent test pad, and the localized free hemoglobin on the pad produces a corresponding dot of color change. Obviously, the greater the number of intact erythrocytes in the urine specimen, the greater the number of dots that will appear on the test paper, and a coalescence of the dots occurs when there are more than 250 erythrocytes/mL.

Hematuria can be distinguished from hemoglobinuria and myoglobinuria by microscopic examination of the centrifuged urine; the presence of a large number of erythrocytes establishes the diagnosis of hematuria. If erythrocytes are absent, examination of the serum will distinguish hemoglobinuria and myoglobinuria. A sample of blood is obtained and centrifuged. In hemoglobinuria, the supernatant will be pink. This is because free hemoglobin in the serum binds to haptoglobin, which is water insoluble and has a high molecular weight. This complex remains in the serum, causing a pink color. Free hemoglobin will appear in the urine only when all of the haptoglobin-binding sites have been saturated. In myoglobinuria, the myoglobin released from muscle is of low molecular weight and water soluble. It does not bind to haptoglobin and is therefore excreted immediately into the urine. Therefore, in myoglobinuria the serum remains clear.

The sensitivity of urinary dipsticks in identifying hematuria, defined as greater than 3 erythrocytes/HPF of centrifuged sediment examined microscopically, is over 90%. Conversely, the specificity of the dipstick for hematuria compared with microscopy is somewhat lower, reflecting a higher false-positive rate with the dipstick ( Shaw et al, 1985 ).

False-positive dipstick readings most often are due to contamination of the urine specimen with menstrual blood. Dehydration with resultant urine of high specific gravity can also yield false-positive results owing to the increased concentration of erythrocytes and hemoglobin. The normal individual excretes about 1000 erythrocytes/mL of urine, with the upper limits of normal varying from 5000 to 8000 erythrocytes/mL ( Kincaid-Smith, 1982 ). Therefore, examining urine of high specific gravity, such as the first morning voided specimen, increases the likelihood of a false-positive result. In addition to dehydration, another cause of false-positive results is exercise, which can increase the number of erythrocytes in the urine.

The efficacy of hematuria screening using the dipstick to identify patients with significant urologic disease is somewhat controversial. Studies in children and young adults have shown a very low rate of significant disease ( Woolhandler et al, 1989 ). In older adults, one study from the Mayo Clinic of 2000 patients with asymptomatic hematuria showed that only 0.5% had a urologic malignancy and only 1.8% developed other serious urologic diseases within 3 years after identification of the hematuria ( Mohr et al, 1986 ). Conversely, investigators at the University of Wisconsin found that 26% of adults who had at least one positive dipstick reading for hematuria were subsequently found to have significant urologic pathology ( Messing et al, 1987 ). Obviously, the age of the population, the completeness of the subsequent urologic evaluation, and the definition of significant disease all influence the disease rate in the group of patients with asymptomatic hematuria identified by dipstick screening. It is important to remember that, before proceeding to more complicated studies, the dipstick result should be confirmed with a microscopic examination of the centrifuged urinary sediment.

Differential Diagnosis and Evaluation of Hematuria.

Hematuria may reflect either significant nephrologic or urologic disease. Hematuria of nephrologic origin is frequently associated with casts in the urine and almost always associated with significant proteinuria. Even significant hematuria of urologic origin will not elevate the protein concentration in the urine into the 100 to 300 mg/dL or 2+ to 3+ range on dipstick, and proteinuria of this magnitude almost always indicates glomerular or tubulointerstitial renal disease.

Morphologic evaluation of erythrocytes in the centrifuged urinary sediment also helps localize their site of origin. Erythrocytes arising from glomerular disease are typically dysmorphic and show a wide range of morphologic alterations. Conversely, erythrocytes arising from tubulointerstitial renal disease and of urologic origin have a uniformly round shape; these erythrocytes may or may not retain their hemoglobin (“ghost cells”), but the individual cell shape is consistently round. In individuals without significant pathology with minimal amounts of hematuria, the erythrocytes are characteristically dysmorphic but the number of cells observed is far fewer than that observed in patients with nephrologic disease. Erythrocyte morphology is more easily determined using phase contrast microscopy, but with practice this can be accomplished using a conventional light microscope ( Schramek et al, 1989 ).

Glomerular Hematuria.

Glomerular hematuria is suggested by the presence of dysmorphic erythrocytes, red blood cell casts, and proteinuria. Of those patients with glomerulonephritis proven by renal biopsy, however, about 20% will have hematuria alone without red blood cell casts or proteinuria ( Fassett et al, 1982 ).

The glomerular disorders associated with hematuria are listed in Table 3-4 . Further evaluation of patients with glomerular hematuria should begin with a thorough history. Hematuria in children and young adults, usually males, associated with low-grade fever and an erythematous rash suggests a diagnosis of immunoglobulin A (IgA) nephropathy (Berger's disease). A family history of renal disease and deafness suggests familial nephritis or Alport's syndrome. Hemoptysis and abnormal bleeding associated with microcytic anemia are characteristic of Goodpasture's syndrome, and the presence of a rash and arthritis suggest systemic lupus erythematosus. Finally, poststreptococcal glomerulonephritis should be suspected in a child with a recent streptococcal upper respiratory tract or skin infection.

Table 3-4 -- Glomerular Disorders in Patients with Glomerular Hematuria

Disorder	Patients
IgA nephropathy (Berger's disease)	30
Mesangioproliferative GN	14
Focal segmental proliferative GN	13
Familial nephritis (e.g., Alport's syndrome)	11
Membranous GN	7
Mesangiocapillary GN	6
Focal segmental sclerosis	4
Unclassifiable	4
Systemic lupus erythematosus	3
Postinfectious GN	2
Subacute bacterial endocarditis	2
Others	4
Total	100

Adapted from Fassett RG, Horgan BA, Mathew TH: Detection of glomerular bleeding by phase-contrast microscopy. Lancet 1982;1:1432.

GN, glomerulonephritis; IgA, immunoglobulin A.

Further laboratory evaluation should include measurement of serum creatinine, creatinine clearance, and, when proteinuria in the urine is 2+ or greater, a 24-hour urine protein determination. Although these tests will quantitate the specific degree of renal dysfunction, further tests are usually required to establish the specific diagnosis and particularly to determine whether the disease is due to an immune or a nonimmune etiology. Frequently, a renal biopsy is necessary to establish the precise diagnosis, and biopsies are particularly important if the result will influence subsequent treatment of the patient. Renal biopsies are extremely informative when examined by an experienced pathologist using light, immunofluorescent, and electron microscopy.

An algorithm for the evaluation of glomerular hematuria is provided in Figure 3-6 .



Figure 3-6 Evaluation of glomerular hematuria (dysmorphic erythrocytes, erythrocyte casts, and proteinuria). ANA, antinuclear antibody; ASO, antistreptolysin O; Ig, immunoglobulin.

IgA Nephropathy (Berger's Disease).

IgA nephropathy, or Berger's disease, is the most common cause of glomerular hematuria, accounting for about 30% of cases ( Fassett et al, 1982 ). Therefore, it is described in greater detail in this section. IgA nephropathy occurs most commonly in children and young adults, with a male predominance ( Berger and Hinglais, 1968 ). Patients typically present with hematuria after an upper respiratory tract infection or exercise. Hematuria may be associated with a low-grade fever or rash, but most patients have no associated systemic symptoms. Gross hematuria occurs intermittently, but microscopic hematuria is a constant finding in some patients. The disease is chronic, but the prognosis in most patients is excellent. Renal function remains normal in the majority, but about 25% will subsequently develop renal insufficiency. An older age at onset, initial abnormal renal function, consistent proteinuria, and hypertension are indicators of a poor prognosis ( D'Amico, 1988 ).

The pathologic findings in Berger's disease are limited to either focal glomeruli or lobular segments of a glomerulus. The changes are proliferative and usually confined to mesangial cells ( Berger and Hinglais, 1968 ). Renal biopsy reveals deposits of IgA, IgG, and β_1c-globulin, although IgA and IgG mesangial deposits are found in other forms of glomerulonephritis as well. The role of IgA in the disease remains uncertain, although the deposits may trigger an inflammatory reaction within the glomerulus ( van den Wall Bake et al, 1989 ). Because gross hematuria frequently follows an upper respiratory tract infection, a viral etiology has been suspected but not established. The frequent association between hematuria and exercise in this condition remains unexplained.

The clinical presentation of IgA glomerulonephritis is alarming and similar to certain systemic diseases, including Schönlein-Henoch purpura, systemic lupus erythematosus, bacterial endocarditis, and Goodpasture's syndrome. Therefore, a careful clinical and laboratory evaluation is indicated to establish the correct diagnosis. The presence of red blood cell casts establishes the glomerular origin of the hematuria. In the absence of casts, a urologic evaluation is indicated to exclude the urinary tract as a source of bleeding and to confirm that the hematuria is arising from both kidneys. The diagnosis of IgA nephropathy is confirmed by renal biopsy demonstrating the classic deposits of immunoglobulins in mesangial cells, as described previously. Once the diagnosis has been established, repeat evaluations for hematuria are generally not indicated. Although there is no effective treatment for this condition, renal function remains stable in most patients and there are no other known long-term complications.

Nonglomerular Hematuria Medical.

Except for renal tumors, nonglomerular hematuria of renal origin is secondary to either tubulointerstitial, renovascular, or systemic disorders. The urinalysis in nonglomerular hematuria is distinguished from that of glomerular hematuria by the presence of circular erythrocytes and the absence of erythrocyte casts. Like glomerular hematuria, nonglomerular hematuria of renal origin is frequently associated with significant proteinuria, which distinguishes these nephrologic diseases from urologic diseases in which the degree of proteinuria is usually minimal, even with heavy bleeding.

As with glomerular hematuria, a careful history frequently helps establish the diagnosis. A family history of hematuria or bleeding tendency suggests the diagnosis of a blood dyscrasia, which should be investigated further. A family history of urolithiasis associated with intermittent hematuria may indicate stone disease, which should be investigated with serum and urine measurements of calcium and uric acid. A family history of renal cystic disease should prompt further radiologic evaluation for medullary sponge kidney and adult polycystic kidney disease. Papillary necrosis as a cause of hematuria should be considered in diabetics, African Americans (secondary to sickle cell disease or trait), and suspected analgesic abusers.

Medications may induce hematuria, particularly anticoagulants. Anticoagulation at normal therapeutic levels, however, does not predispose patients to hematuria. In one study, the prevalence of hematuria was 3.2% in anticoagulated patients versus 4.8% in a control group. Urologic disease was identified in 81% of patients with more than one episode of microscopic hematuria, and the cause of hematuria did not vary between groups ( Culclasure et al, 1994 ). Thus, anticoagulant therapy per se does not appear to increase the risk of hematuria unless the patient is excessively anticoagulated.

Exercise-induced hematuria is being observed with increasing frequency. It typically occurs in long-distance runners (>10 km), is usually noted at the conclusion of the run, and rapidly disappears with rest. The hematuria may be of renal or bladder origin. An increased number of dysmorphic erythrocytes have been noted in some patients, suggesting a glomerular origin. Exercise-induced hematuria may be the first sign of underlying glomerular disease such as IgA nephropathy. Conversely, cystoscopy in patients with exercise-induced hematuria frequently reveals punctate hemorrhagic lesions in the bladder, suggesting that the hematuria is of bladder origin.

Vascular disease may also result in nonglomerular hematuria. Renal artery embolism and thrombosis, arteriovenous fistulas, and renal vein thrombosis may all result in hematuria. Physical examination may reveal severe hypertension, a flank or abdominal bruit, or atrial fibrillation. In such patients, further evaluation for renal vascular disease should be undertaken.

An algorithm for the evaluation of nonglomerular hematuria is provided in Figure 3-7 .



Figure 3-7 Evaluation of nonglomerular renal hematuria (circular erythrocytes, no erythrocyte casts, and proteinuria). CT, computed tomography; IgA, immunoglobulin A; IVU, intravenous urography; PT, prothrombin time; PTT, partial thromboplastin time; R/O, rule out.

Surgical.

Nonglomerular hematuria or essential hematuria includes primarily urologic rather than nephrologic diseases. Common causes of essential hematuria include urologic tumors, stones, and UTIs.

The urinalysis in both nonglomerular medical and surgical hematuria is similar in that both are characterized by circular erythrocytes and the absence of erythrocyte casts. Essential hematuria is suggested, however, by the absence of significant proteinuria usually found in nonglomerular hematuria of renal parenchymal origin. It should be remembered, however, that proteinuria is not always present in glomerular or nonglomerular renal disease.

The American Urological Association (AUA) Best Practice Policy Panel on Microscopic Hematuria has formulated practice recommendations for the detection and evaluation of asymptomatic microscopic hematuria (Grossfeld et al, 2001a, 2001b [16] [17]). The panel concluded that, due to the lack of specificity of urinary dipstick examination, as well as the risk and expense of evaluation, patients with a positive dipstick test should only undergo complete evaluation for hematuria if this is confirmed by the finding of 3 or more RBC/HPF on subsequent microscopic evaluation. The mainstays of evaluation, according to the panel, are voided urinary cytology, cystoscopy, and urinary tract imaging using ultrasonography, CT, and/or intravenous urography (IVU). The use of these tests in an individual patient should be based in most cases on the relative risk of significant urinary tract pathology.

An algorithm for the evaluation of essential hematuria is provided in Figure 3-8 .



Figure 3-8 Evaluation of essential hematuria (circular erythrocytes, no erythrocyte casts, no significant proteinuria). CT, computed tomography; IVU, intravenous urography; R/O, rule out.

Proteinuria

Although healthy adults excrete 80 to 150 mg of protein in the urine daily, the qualitative detection of proteinuria in the urinalysis should raise the suspicion of underlying renal disease. Proteinuria may be the first indication of renovascular, glomerular, or tubulointerstitial renal disease, or it may represent the overflow of abnormal proteins into the urine in conditions such as multiple myeloma. Proteinuria also can occur secondary to nonrenal disorders and in response to various physiologic conditions such as strenuous exercise.

The protein concentration in the urine obviously depends on the state of hydration, but it seldom exceeds 20 mg/dL. In patients with dilute urine, however, significant proteinuria may be present at concentrations less than 20 mg/dL. Normally, urine protein is about 30% albumin, 30% serum globulins, and 40% tissue proteins, of which the major component is Tamm-Horsfall protein. This profile may be altered by conditions that affect glomerular filtration, tubular reabsorption, or excretion of urine protein, and determination of the urine protein profile by such techniques as protein electrophoresis may help determine the etiology of proteinuria.

Pathophysiology.

Most causes of proteinuria can be categorized into one of three categories: glomerular, tubular, or overflow. Glomerular proteinuria is the most common type of proteinuria and results from increased glomerular capillary permeability to protein, especially albumin. Glomerular proteinuria occurs in any of the primary glomerular diseases such as IgA nephropathy or in glomerulopathy associated with systemic illness such as diabetes mellitus. Glomerular disease should be suspected when the 24-hour urine protein excretion exceeds 1 g and is almost certain to exist when the total protein excretion exceeds 3 g.

Tubular proteinuria results from failure to reabsorb normally filtered proteins of low molecular weight such as immunoglobulins. In tubular proteinuria, the 24-hour urine protein loss seldom exceeds 2 to 3 g and the excreted proteins are of low molecular weight rather than albumin. Disorders that lead to tubular proteinuria are commonly associated with other defects of proximal tubular function, such as glucosuria, aminoaciduria, phosphaturia, and uricosuria (Fanconi's syndrome).

Overflow proteinuria occurs in the absence of any underlying renal disease and is due to an increased plasma concentration of abnormal immunoglobulins and other low-molecular-weight proteins. The increased serum levels of abnormal proteins result in excess glomerular filtration that exceeds tubular reabsorptive capacity. The most common cause of overflow proteinuria is multiple myeloma, in which large amounts of immunoglobulin light chains are produced and appear in the urine (Bence Jones protein).

Detection.

Qualitative detection of abnormal proteinuria is most easily accomplished with a dipstick impregnated with tetrabromophenol blue dye. The color of the dye changes in response to a pH shift related to the protein content of the urine, mainly albumin, leading to the development of a blue color. Because the background of the dipstick is yellow, various shades of green will develop, and the darker the green, the greater the concentration of protein in the urine. The minimal detectable protein concentration by this method is 20 to 30 mg/dL. False-negative results can occur in alkaline urine, dilute urine, or when the primary protein present is not albumin. Nephrotic range proteinuria in excess of 1 g/24 hr, however, is seldom missed on qualitative screening. Precipitation of urinary proteins with strong acids such as 3% sulfosalicylic acid will detect proteinuria at concentrations as low as 15 mg/dL and is more sensitive at detecting other proteins as well as albumin. Patients whose urine is negative on dipstick but strongly positive with sulfosalicylic acid should be suspected of having multiple myeloma, and the urine should be tested further for Bence Jones protein.

If qualitative testing reveals proteinuria, this should be quantitated with a 24-hour urinary collection. Further qualitative assessment of abnormal urinary proteins can be accomplished by either protein electrophoresis or immunoassay for specific proteins. Protein electrophoresis is particularly helpful in distinguishing glomerular from tubular proteinuria. In glomerular proteinuria, albumin makes up about 70% of the total protein excreted, whereas in tubular proteinuria, the major proteins excreted are immunoglobulins with albumin making up only 10% to 20%. Immunoassay is the method of choice for detecting specific proteins such as Bence Jones protein in multiple myeloma.

Evaluation.

Proteinuria should first be classified by its timing into transient, intermittent, or persistent. Transient proteinuria occurs commonly, especially in the pediatric population, and usually resolves spontaneously within a few days ( Wagner et al, 1968 ). It may result from fever, exercise, or emotional stress. In older patients, transient proteinuria may be due to congestive heart failure. If a nonrenal cause is identified and a subsequent urinalysis is negative, no further evaluation is necessary. Obviously, if proteinuria persists, it should be evaluated further.

Proteinuria may also occur intermittently, and this is frequently related to postural change ( Robinson, 1985 ). Proteinuria that occurs only in the upright position is a frequent cause of mild, intermittent proteinuria in young males. Total daily protein excretion seldom exceeds 1 g, and urinary protein excretion returns to normal when the patient is recumbent. Orthostatic proteinuria is thought to be secondary to increased pressure on the renal vein while standing. It resolves spontaneously in about 50% of patients and is not associated with any morbidity. Therefore, if renal function is normal in patients with orthostatic proteinuria, no further evaluation is indicated.

Persistent proteinuria requires further evaluation, and most cases have a glomerular etiology. A quantitative measurement of urinary protein should be obtained through a 24-hour urine collection, and a qualitative evaluation should be obtained to determine the major proteins excreted. The findings of greater than 2 g of protein excreted per 24 hours, of which the major components are high-molecular-weight proteins such as albumin, establishes the diagnosis of glomerular proteinuria. Glomerular proteinuria is the most common cause of abnormal proteinuria, especially in patients presenting with persistent proteinuria. If glomerular proteinuria is associated with hematuria characterized by dysmorphic erythrocytes and erythrocyte casts, the patient should be evaluated as outlined previously for glomerular hematuria (see Fig. 3-6 ). Patients with glomerular proteinuria who have no or little associated hematuria should be evaluated for other conditions, of which the most common is diabetes mellitus. Other possibilities include amyloidosis and arteriolar nephrosclerosis.

In patients in whom total protein excretion is 300 to 2000 mg/day, of which the major components are low-molecular-weight globulins, further qualitative evaluation with immunoelectrophoresis is indicated. This will determine whether the excess proteins are normal or abnormal. Identification of normal proteins establishes a diagnosis of tubular proteinuria, and further evaluation for a specific cause of tubular dysfunction is indicated.

If qualitative evaluation reveals abnormal proteins in the urine, this establishes a diagnosis of overflow proteinuria. Further evaluation should be directed to identify the specific protein abnormality. The finding of large quantities of light-chain immunoglobulins or Bence Jones protein establishes a diagnosis of multiple myeloma. Similarly, the finding of large amounts of hemoglobin or myoglobin establishes the diagnosis of hemoglobinuria or myoglobinuria.

An algorithm for the evaluation of proteinuria is provided in Figure 3-9 .



Figure 3-9 Evaluation of proteinuria.

Glucose and Ketones

Urine testing for glucose and ketones is useful in screening patients for diabetes mellitus. Normally, almost all the glucose filtered by the glomeruli is reabsorbed in the proximal tubules. Although very small amounts of glucose may normally be excreted in the urine, these amounts are not clinically significant and are below the level of detectability with the dipstick. If, however, the amount of glucose filtered exceeds the capacity of tubular reabsorption, glucose will be excreted in the urine and detected on the dipstick. This so-called renal threshold corresponds to a serum glucose of about 180 mg/dL; above this level, glucose will be detected in the urine.

Glucose detection with the urinary dipstick is based on a double sequential enzymatic reaction yielding a colorimetric change. In the first reaction, glucose in the urine reacts with glucose oxidase on the dipstick to form gluconic acid and hydrogen peroxide. In the second reaction, hydrogen peroxide reacts with peroxidase, causing oxidation of the chromogen on the dipstick, producing a color change. This doubleoxidative reaction is specific for glucose, and there is no cross-reactivity with other sugars. The dipstick test becomes less sensitive as the urine increases in specific gravity and temperature.

Ketones are not normally found in the urine but will appear when the carbohydrate supplies in the body are depleted and body fat breakdown occurs. This happens most commonly in diabetic ketoacidosis but may also occur during pregnancy and after periods of starvation or rapid weight reduction. Ketones excreted include acetoacetic acid, acetone, and β-hydroxybutyric acid. With abnormal fat breakdown, ketones will appear in the urine before the serum.

Dipstick testing for ketones involves a colorimetric reaction: sodium nitroprusside on the dipstick reacts with acetoacetic acid to produce a purple color. Dipstick testing will identify acetoacetic acid at concentrations of 5 to 10 mg/dL but will not detect acetone or β-hydroxybutyric acid. Obviously, a dipstick that tests positively for glucose should also be tested for ketones, and diabetes mellitus is suggested. False-positive results, however, can occur in very acidic urine of high specific gravity, in abnormally colored urine, and in urine containing levodopa metabolites, 2-mercaptoethane sulfonate sodium, and other sulfhydryl-containing compounds ( Csako, 1987 ).

Bilirubin and Urobilinogen

Normal urine contains no bilirubin and only very small amounts of urobilinogen. There are two types of bilirubin, direct (conjugated) and indirect. Direct bilirubin is made in the hepatocyte, where bilirubin is conjugated with glucuronic acid. Conjugated bilirubin has a low molecular weight, is water soluble, and normally passes from the liver into the small intestine through the bile ducts, where it is converted to urobilinogen. Therefore, conjugated bilirubin does not appear in the urine except in pathologic conditions in which there is intrinsic hepatic disease or obstruction of the bile ducts.

Indirect bilirubin is of high molecular weight and bound in the serum to albumin. It is water insoluble and, therefore, does not appear in the urine even in pathologic conditions.

Urobilinogen is the end product of conjugated bilirubin metabolism. Conjugated bilirubin passes through the bile ducts, where it is metabolized by normal intestinal bacteria to urobilinogen. Normally, about 50% of the urobilinogen is excreted in the stool and 50% reabsorbed into the enterohepatic circulation. A small amount of absorbed urobilinogen, about 1 to 4 mg/day, will escape hepatic uptake and be excreted in the urine. Hemolysis and hepatocellular diseases that lead to increased bile pigments can result in increased urinary urobilinogen. Conversely, obstruction of the bile duct or antibiotic usage that alters intestinal flora, thereby interfering with the conversion of conjugated bilirubin to urobilinogen, will decrease urobilinogen levels in the urine. In these conditions, obviously, serum levels of conjugated bilirubin rise.

There are different dipstick reagents and methods to test for both bilirubin and urobilinogen, but the basic physiologic principle involves the binding of bilirubin or urobilinogen to a diazonium salt to produce a colorimetric reaction. False-negative results can occur in the presence of ascorbic acid, which decreases the sensitivity for detection of bilirubin. False-positive results can occur in the presence of phenazopyridine because it colors the urine orange and, similar to the colorimetric reaction for bilirubin, turns red in an acid medium.

Leukocyte Esterase and Nitrite Tests

Leukocyte esterase activity indicates the presence of white blood cells in the urine. The presence of nitrites in the urine is strongly suggestive of bacteriuria. Thus, both of these tests have been used to screen patients for UTIs. Although these tests may have application in nonurologic medical practice, the most accurate method to diagnose infection is by microscopic examination of the urinary sediment to identify pyuria and subsequent urine culture. All urologists should be capable of performing and interpreting the microscopic examination of the urinary sediment. Therefore, leukocyte esterase and nitrite testing are less important in a urologic practice. For purposes of completion, however, both techniques are described briefly herein.

Leukocyte esterase and nitrite testing are performed using the Chemstrip LN dipstick. Leukocyte esterase is produced by neutrophils and catalyzes the hydrolysis of an indoxyl carbonic acid ester to indoxyl ( Gillenwater, 1981 ). The indoxyl formed oxidizes a diazonium salt chromogen on the dipstick to produce a color change. It is recommended that leukocyte esterase testing be done 5 minutes after the dipstick is immersed in the urine to allow adequate incubation ( Shaw et al, 1985 ). The sensitivity of this test subsequently decreases with time because of lysis of the leukocytes. Leukocyte esterase testing may also be negative in the presence of infection, because not all patients with bacteriuria will have significant pyuria. Therefore, if one uses leukocyte esterase testing to screen patients for UTI, it should always be done in conjunction with nitrite testing for bacteriuria ( Pels et al, 1989 ).

Other causes of false-negative results with leukocyte esterase testing include increased urinary specific gravity, glycosuria, presence of urobilinogen, medications that alter urine color, and ingestion of large amounts of ascorbic acid. The major cause of false-positive leukocyte esterase tests is specimen contamination.

Nitrites are not normally found in the urine, but many species of gram-negative bacteria can convert nitrates to nitrites. Nitrites can readily be detected in the urine because they react with the reagents on the dipstick and undergo diazotization to form a red azo dye. The specificity of the nitrite dipstick for detecting bacteriuria is over 90% ( Pels et al, 1989 ). The sensitivity of the test, however, is considerably less, varying from 35% to 85%. The nitrite test is less accurate in urine specimens containing fewer than 10⁵ organisms/mL ( Kellog et al, 1987 ). As with leukocyte esterase testing, the major cause of false-positive nitrite testing is contamination.

It remains controversial whether dipstick testing for leukocyte esterase and nitrites can replace microscopy in screening for significant UTIs. This issue is less important to urologists, who usually have access to a microscope and who should be trained and encouraged to examine the urinary sediment. A protocol combining the visual appearance of the urine with leukocyte esterase and nitrite testing has been proposed ( Fig. 3-10 ) that reportedly detects 95% of infected urine specimens and decreases the need for microscopy by as much as 30% ( Flanagan et al, 1989 ). Other studies, however, have shown that dipstick testing is not an adequate replacement for microscopy ( Propp et al, 1989 ). In summary, it has not been demonstrated conclusively that dipstick testing for UTI can replace microscopic examination of the urinary sediment. In our personal experience, we always examine the urinary sediment whenever we suspect a UTI and subsequently culture the urine when pyuria is identified.



Figure 3-10 Protocol for determining the need for urine sediment microscopy in an asymptomatic population. (From Flanagan PG, Rooney PG, Davies EA, Stout RW: Evaluation of four screening tests for bacteriuria in elderly people. Lancet 1989;1:1117. © by The Lancet Ltd., 1989.)

Urinary Sediment Obtaining and Preparing the Specimen

A clean-catch midstream urine specimen should be obtained. As described earlier, uncircumcised men should retract the prepuce and cleanse the glans penis before voiding. It is more difficult to obtain a reliable clean-catch specimen in females because of contamination with introital leukocytes and bacteria. If there is any suspicion of a UTI in a female, a catheterized urine sample should be obtained for culture and sensitivity.

If possible, the first morning urine specimen is the specimen of choice and should be examined within 1 hour. A standard procedure for preparation of the urine for microscopic examination has been described ( Cushner and Copley, 1989 ). Ten to 15 milliliters of urine should be centrifuged for 5 minutes at 3000 rpm. The supernatant is then poured off, and the sediment is resuspended in the centrifuge tube by gently tapping the bottom of the tube. Although the remaining small amount of fluid can be poured onto a microscope slide, this usually results in excess fluid on the slide. It is better to use a small pipette to withdraw the residual fluid from the centrifuge tube and to place it directly on the microscope slide. This usually results in an ideal volume of between 0.01 and 0.02 mL of fluid deposited on the slide. The slide is then covered with a coverslip. The edge of the coverslip should be placed on the slide first to allow the drop of fluid to ascend onto the coverslip by capillary action. The coverslip is then gently placed over the drop of fluid, and this technique allows for most of the air between the drop of fluid and the coverslip to be expelled. If one simply drops the coverslip over the urine, the urine will disperse over the slide and there will be a considerable number of air bubbles that may distort the subsequent microscopic examination.

Microscopy Technique

Microscopic analysis of the urinary sediment should be performed with both low-power (×100 magnification) and high-power (×400 magnification) lenses. The use of an oil immersion lens for higher magnification is seldom, if ever, necessary. Under low power, the entire area under the cover-slip should be scanned. Particular attention should be given to the edges of the coverslip, where casts and other elements tend to be concentrated. Low-power magnification is sufficient to identify erythrocytes, leukocytes, casts, cystine crystals, oval fat macrophages, and parasites such as Trichomonas vaginalis and Schistosoma hematobium.

High-power magnification is necessary to distinguish circular from dysmorphic erythrocytes, to identify other types of crystals, and, particularly, to identify bacteria and yeast. In summary, the urinary sediment should be examined microscopically for (1) cells, (2) casts, (3) crystals, (4) bacteria, (5) yeast, and (6) parasites.

Cells

Erythrocyte morphology may be determined under high-power magnification. Although phase contrast microscopy has been used for this purpose, circular (nonglomerular) erythrocytes can generally be distinguished from dysmorphic (glomerular) erythrocytes under routine brightfield high-power magnification (Figs. 3-11 to 3-15 [11] [12] [13] [14] [15]). This is facilitated by adjusting the microscope condenser to its lowest aperture, thus reducing the intensity of background light. This allows one to see fine detail not evident otherwise and also creates the effect of phase microscopy because cell membranes and other sedimentary components stand out against the darkened background.



Figure 3-15 Dysmorphic red blood cells from a patient with Wegener's granulomatosis. A, Brightfield illumination. B, Phase illumination. Note irregular deposits of dense cytoplasmic material around the cell membrane.



Figure 3-14 Red blood cells from a patient with Berger's disease. Note variations in membranes characteristic of dysmorphic red blood cells.



Figure 3-13 Red blood cells from a patient with interstitial cystitis. Cells were collected at cystoscopy.



Figure 3-12 Red blood cells from a patient with a bladder tumor.



Figure 3-11 Red blood cells, both smoothly rounded and mildly crenated, typical of epithelial erythrocytes.

Circular erythrocytes generally have an even distribution of hemoglobin with either a round or a crenated contour, whereas dysmorphic erythrocytes are irregularly shaped with minimal hemoglobin and irregular distribution of cytoplasm. Automated techniques for performing microscopic analysis to distinguish the two types of erythrocytes have been investigated but have not yet been accepted into general urologic practice and are probably unnecessary. In one study using a standard Coulter counter, microscopic analysis was found to be 97% accurate in differentiating between the two types of erythrocytes ( Sayer et al, 1990 ). Erythrocytes may be confused with yeast or fat droplets ( Fig. 3-16 ). Erythrocytes can be distinguished, however, because yeast will show budding and oil droplets are highly refractile.



Figure 3-16 Candida albicans. Budding forms surrounded by leukocytes.

Leukocytes can generally be identified under low power and definitively diagnosed under high-power magnification (Figs. 3-17 and 3-18 [17] [18]; see also Fig. 3-16 ). It is normal to find 1 or 2 leukocytes/HPF in men and up to 5/HPF in women in whom the urine sample may be contaminated with vaginal secretions. A greater number of leukocytes generally indicates infection or inflammation in the urinary tract. It may be possible to distinguish old leukocytes, which have a characteristic small and wrinkled appearance and which are commonly found in the vaginal secretions of normal women, from fresh leukocytes, which are generally indicative of urinary tract pathology. Fresh leukocytes are generally larger and rounder, and, when the specific gravity is less than 1.019, the granules in the cytoplasm demonstrate glitter-like movement, so-called glitter cells.



Figure 3-18 Fresh “glitter cells” with erythrocytes in background.



Figure 3-17 Old leukocytes. Staghorn calculi with Proteus infection.

Epithelial cells are commonly observed in the urinary sediment. Squamous cells are frequently detected in female urine specimens and are derived from the lower portion of the urethra, the trigone of postpubertal females, and the vagina. Squamous epithelial cells are large, have a central small nucleus about the size of an erythrocyte, and have an irregular cytoplasm with fine granularity.

Transitional epithelial cells may arise from the remainder of the urinary tract ( Fig. 3-19 ). Transitional cells are smaller than squamous cells, have a larger nucleus, and demonstrate prominent cytoplasmic granules near the nucleus. Malignant transitional cells have altered nuclear size and morphology and can be identified with either routine Papanicolaou staining or automated flow cytometry.



Figure 3-19 Transitional epithelial cells from bladder lavage.

Renal tubular cells are the least commonly observed epithelial cells in the urine but are most significant, because their presence in the urine is always indicative of renal pathology. Renal tubular cells may be difficult to distinguish from leukocytes, but they are slightly larger.

Casts

A cast is a protein coagulum that is formed in the renal tubule and traps any tubular luminal contents within the matrix. Tamm-Horsfall mucoprotein is the basic matrix of all renal casts; it originates from tubular epithelial cells and is always present in the urine. When the casts contain only mucoproteins, they are called hyaline casts and may not have any pathologic significance. Hyaline casts may be seen in the urine after exercise or heat exposure but may also be observed in pyelonephritis or chronic renal disease.

Red blood cell casts contain entrapped erythrocytes and are diagnostic of glomerular bleeding, most likely secondary to glomerulonephritis (Figs. 3-20 and 3-21 [20] [21]). White blood cell casts are observed in acute glomerulonephritis, acute pyelonephritis, and acute tubulointerstitial nephritis. Casts with other cellular elements, usually sloughed renal tubular epithelial cells, are indicative of nonspecific renal damage ( Fig. 3-22 ). Granular and waxy casts result from further degeneration of cellular elements. Fatty casts are seen in nephrotic syndrome, lipiduria, and hypothyroidism.



Figure 3-21 Red blood cell cast.



Figure 3-20 Red blood cell cast. A, Low-power view demonstrates distinct border of hyaline matrix. B, High-power view demonstrates the sharply defined red blood cell membranes (arrow). Berger's disease.



Figure 3-22 Cellular cast. Cells entrapped in a hyaline matrix.

Crystals

Identification of crystals in the urine is particularly important in patients with stone disease, because it may help determine the etiology ( Fig. 3-23 ). Although other types of crystals may be seen in normal patients, the identification of cystine crystals establishes the diagnosis of cystinuria. Crystals precipitated in acidic urine include calcium oxalate, uric acid, and cystine. Crystals precipitated in an alkaline urine include calcium phosphate and triple-phosphate (struvite) crystals. Cholesterol crystals are rarely seen in the urine and are not related to urinary pH. They occur in lipiduria and remain in droplet form.



Figure 3-23 Urinary crystals. A, Cystine. B, Calcium oxalate. C, Uric acid. D, Triple phosphate (struvite).

Bacteria

Normal urine should not contain bacteria; and in a fresh uncontaminated specimen, the finding of bacteria is indicative of a UTI. Because each HPF views between 1/20,000 and 1/50,000 mL, each bacterium seen per HPF signifies a bacterial count of more than 20,000/mL. Therefore, 5 bacteria/HPF reflects colony counts of about 100,000/mL. This is the standard concentration used to establish the diagnosis of a UTI in a clean-catch specimen. This level should apply only to women, however, in whom a clean-catch specimen is frequently contaminated. The finding of any bacteria in a properly collected midstream specimen from a male should be further evaluated with a urine culture.

Under high power, it is possible to distinguish various bacteria. Gram-negative rods have a characteristic bacillary shape ( Fig. 3-24 ), whereas streptococci can be identified by their characteristic beaded chains (Figs. 3-25 and 3-26 [25] [26]) and staphylococci can be identified when the organisms are found in clumps ( Fig. 3-27 ).



Figure 3-24 Gram-negative bacilli. Phase microscopy of Escherichia coli.



Figure 3-26 Streptococcal urinary tract infection (Gram's stain).



Figure 3-25 Streptococcal urinary tract infection with typical chain formation (arrow).



Figure 3-27 Staphylococcus aureus in typical clumps (arrow).

Yeast

The most common yeast cells found in urine are Candida albicans. The biconcave oval shape of yeast can be confused with erythrocytes and calcium oxalate crystals, but yeasts can be distinguished by their characteristic budding and hyphae (see Fig. 3-16 ). Yeasts are most commonly seen in the urine of patients with diabetes mellitus or as contaminants in women with vaginal candidiasis.

Parasites

Trichomonas vaginalis is a frequent cause of vaginitis in women and occasionally of urethritis in men. Trichomonads can be readily identified in a clean-catch specimen under low power ( Fig. 3-28 ). Trichomonads are large cells with rapidly moving flagella that quickly propel the organism across the microscopic field.



Figure 3-28 Trichomonad with ovoid shape and motile flagella.

Schistosoma hematobium is a urinary tract pathogen that is not found in the United States but is extremely common in countries of the Middle East and North Africa. Examination of the urine shows the characteristic parasitic ova with a terminal spike.

Expressed Prostatic Secretions

Although not strictly a component of the urinary sediment, the expressed prostatic secretions should be examined in any man suspected of having prostatitis. Normal prostatic fluid should contain few, if any, leukocytes, and the presence of a larger number or clumps of leukocytes is indicative of prostatitis. Oval fat macrophages are found in postinfection prostatic fluid (Figs. 3-29 and 3-30 [29] [30]). Normal prostatic fluid contains numerous secretory granules that resemble but can be distinguished from leukocytes under high power because they do not have nuclei.



Figure 3-30 Oval fat microphage, high-power view. Note the fine secretory granules in the prostatic fluid.



Figure 3-29 Oval fat macrophage. A, High-power view showing doubly refractile fat particles (arrow). B, Phase microscopy of the same specimen (arrow).

CLINICAL DECISION-MAKING - PHYSICAL EXAMINATION

2008-08-12T06:01:00.000-07:00

PHYSICAL EXAMINATION

KEY POINTS: EVALUATION OF THE UROLOGIC PATIENT

	▪	The urologist can undertake the initial evaluation and establish a diagnosis for almost all patients with diseases of the GU system.
	▪	A complete history and appropriate physical examination is critical in the assessment of urologic patients.
	▪	A complete urinalysis including chemical and microscopic analyses should be performed because this may provide important information critical to the diagnosis and treatment of urologic patients.

A complete and thorough physical examination is an essential component of the evaluation of patients who present with urologic disease. Although it is tempting to become dependent on results of laboratory and radiologic tests, the physical examination often simplifies the process and allows the urologist to select the most appropriate diagnostic studies. Along with the history, the physical examination remains a key component of the diagnostic evaluation and should be performed conscientiously.

General Observations

The visual inspection of the patient provides a general overview. The skin should be inspected for evidence of jaundice or pallor. The nutritional status of the patient should be noted. Cachexia is a frequent sign of malignancy, and obesity may be a sign of underlying endocrinologic abnormalities. In this instance, one should search for the presence of truncal obesity, a “buffalo hump,” and abdominal skin striae, which are stigmata of hyperadrenocorticism. In contrast, debility and hyperpigmentation may be signs of hypoadrenocorticism. Gynecomastia may be a sign of endocrinologic disease as well as a possible indicator of alcoholism or previous hormonal therapy for prostate cancer. Edema of the genitalia and lower extremities may be associated with cardiac decompensation, renal failure, nephrotic syndrome, or pelvic and/or retroperitoneal lymphatic obstruction. Supraclavicular lymphadenopathy may be seen with any GU neoplasm, most commonly prostate and testis cancer; inguinal lymphadenopathy may occur secondary to carcinoma of the penis or urethra.

Kidneys

The kidneys are fist-sized organs located high in the retroperitoneum bilaterally. In the adult, the kidneys are normally difficult to palpate because of their position under the diaphragm and ribs with abundant musculature both anteriorly and posteriorly. Because of the position of the liver, the right kidney is somewhat lower than the left. In children and thin women, it may be possible to palpate the lower pole of the right kidney with deep inspiration. However, it is usually not possible to palpate either kidney in men, and the left kidney is almost always impalpable unless it is abnormally enlarged.

The best way to palpate the kidneys is with the patient in the supine position. The kidney is lifted from behind with one hand in the costovertebral angle ( Fig. 3-1 ). On deep inspiration, the examiner's hand is advanced firmly into the anterior abdomen just below the costal margin. At the point of maximal inspiration, the kidney may be felt as it moves downward with the diaphragm. With each inspiration, the examiner's hand may be advanced deeper into the abdomen. Once again, it is more difficult to palpate kidneys in men because the kidneys tend to move downward less with inspiration and because they are surrounded with thicker muscular layers. In children, it is easier to palpate the kidneys because of decreased body thickness. In neonates, the kidneys can be felt quite easily by palpating the flank between the thumb anteriorly and the fingers over the costovertebral angle posteriorly.



Figure 3-1 Bimanual examination of the kidney. (From Judge RD, Zuidema GD, Fitzgerald FT [eds]: Clinical Diagnosis, 5th ed. Boston, Little, Brown, 1989, p 370.)

Transillumination of the kidneys may be helpful in children younger than 1 year of age with a palpable flank mass. Such masses frequently are of renal origin. A flashlight or fiberoptic light source is positioned posteriorly against the costovertebral angle. Fluid-filled masses such as cysts or hydronephrosis produce a dull reddish glow in the anterior abdomen. Solid masses such as tumors do not transilluminate. Other diagnostic maneuvers that may be helpful in examining the kidneys are percussion and auscultation. Although renal inflammation may cause pain that is poorly localized, percussion of the costovertebral angle posteriorly more often localizes the pain and tenderness more accurately. Percussion should be done gently, because in a patient with significant renal inflammation this may be quite painful. Auscultation of the upper abdomen during deep inspiration may occasionally reveal a systolic bruit associated with renal artery stenosis or an aneurysm. A bruit may also be detected in association with a large renal arteriovenous fistula.

Every patient with flank pain should also be examined for possible nerve root irritation. The ribs should be palpated carefully to rule out a bone spur or other skeletal abnormality and to determine the point of maximal tenderness. Unlike renal pain, radiculitis usually causes hyperesthesia of the overlying skin innervated by the irritated peripheral nerve. This hypersensitivity can be elicited with a pin or by pinching the skin and fat overlying the involved area. Finally, the pain experienced during the pre-eruptive phase of herpes zoster involving any of the segments between T11 and L2 may also simulate pain of renal origin.

Abnormal Findings.

The most common abnormality detected on examination of the kidneys is a mass. In adult patients, particularly those who are obese, renal masses may be difficult to palpate unless these masses are very large. In most cases, palpable renal masses are either benign cysts or malignant renal tumors, and this distinction generally cannot be made based on physical examination. In children, renal masses are frequently easier to palpate than in adults and may be either cystic (multicystic kidney, polycystic kidney, hydronephrosis) or malignant (Wilms' tumor, neuroblastoma). In neonates and younger children, the distinction between cystic, benign, and solid malignant masses can often be made by transillumination.

Bladder

A normal bladder in the adult cannot be palpated or percussed until there is at least 150 mL of urine in it. At a volume of about 500 mL, the distended bladder becomes visible in thin patients as a lower midline abdominal mass.

Percussion is better than palpation for diagnosing a distended bladder. The examiner begins by percussing immediately above the symphysis pubis and continuing cephalad until there is a change in pitch from dull to resonant. Alternatively, it may be possible in thin patients and in children to palpate the bladder by lifting the lumbar spine with one hand and pressing the other hand into the midline of the lower abdomen.

A careful bimanual examination, best done with the patient under anesthesia, is invaluable in assessing the regional extent of a bladder tumor or other pelvic mass. The bladder is palpated between the abdomen and the vagina in the female ( Fig. 3-2 ) or the rectum in the male ( Fig. 3-3 ). In addition to defining areas of induration, the bimanual examination allows the examiner to assess the mobility of the bladder; such information cannot be obtained by radiologic techniques such as CT and MRI, which convey static images.



Figure 3-2 Bimanual examination of the bladder in the female. (From Swartz MH: Textbook of Physical Diagnosis. Philadelphia, WB Saunders, 1989, p 405.)



Figure 3-3 Bimanual examination of the bladder in the male. (From Judge RD, Zuidema GD, Fitzgerald FT [eds]: Clinical Diagnosis, 5th ed. Boston, Little, Brown, 1989, p 376.)

Abnormal Findings.

The most common palpable abnormality involving the urinary bladder is a full bladder resulting from overdistention. This may occur in men with bladder outlet or urethral obstruction due to BPH or urethral stricture disease. In addition, a variety of neurologic conditions may lead to poor bladder emptying in men or women. Large bladder tumors or calculi may also be palpable in some patients, particularly on bimanual examination under anesthesia. Tenderness over the suprapubic area may indicate cystitis.

Penis

If the patient has not been circumcised, the foreskin should be retracted to examine for tumor or balanoposthitis (inflammation of the prepuce and glans penis). Most penile cancers occur in uncircumcised men and arise on the prepuce or glans penis. Therefore, in a patient with a bloody penile discharge in whom the foreskin cannot be withdrawn, a dorsal slit or circumcision must be performed to adequately evaluate the glans penis and urethra.

The position of the urethral meatus should be noted. It may be located proximal to the tip of the glans on the ventral surface (hypospadias) or, much less commonly, on the dorsal surface (epispadias). The penile skin should be examined for the presence of superficial vesicles compatible with herpes simplex and for ulcers that may indicate either venereal infection or tumor. The presence of venereal warts (condylomata acuminata), which appear as irregular, papillary, velvety lesions on the male genitalia, should also be noted.

The urethral meatus should be separated between the thumb and the forefinger to inspect for neoplastic or inflammatory lesions within the fossa navicularis. The dorsal shaft of the penis should be palpated for the presence of fibrotic plaques or ridges typical of Peyronie's disease. Tenderness along the ventral aspect of the penis is suggestive of periurethritis, often secondary to a urethral stricture.

Abnormal Findings Phimosis.

Phimosis is a condition in which the foreskin cannot be retracted behind the glans penis. In males younger than 4 years old it is normal for the foreskin to be unretractable; in older boys and adults, however, the foreskin usually can be easily withdrawn to the corona ( Oster, 1968 ). Phimosis is usually not painful, but it may produce urinary obstruction with ballooning of the foreskin and may lead to chronic inflammation and carcinoma.

Paraphimosis.

Paraphimosis is a condition in which the foreskin has been retracted and left behind the glans penis, constricting the glans and causing painful vascular engorgement and edema. Paraphimosis is often iatrogenic and frequently occurs after a well-meaning health care professional has examined the penis or inserted a urethral catheter and forgotten to replace the foreskin in its natural position. Paraphimosis can result in marked swelling of the glans penis such that the foreskin can no longer be drawn forward, necessitating an emergency dorsal slit or circumcision.

Peyronie's Disease.

Peyronie's disease is a common condition that results in fibrosis of the tunica albuginea, the elastic membrane that surrounds each corpus cavernosum, producing curvature of the penis during erection. Peyronie's disease may be difficult to diagnose in the flaccid state; however, the patient's history of curvature with erection establishes the diagnosis. Physical examination reveals fibrous plaques or ridges along the shaft of the penis. Peyronie's disease can be alarming to patients who may fear it represents malignancy. They should be reassured that this is always a benign condition that may resolve or stabilize spontaneously without treatment.

Priapism.

Priapism is a prolonged painful erection that is not related to sexual activity. It occurs most commonly in patients with sickle cell disease but can also occur in those with advanced malignancy, coagulation disorders, and pulmonary disease and in many patients without an obvious etiology. The patient usually presents with a painful, spontaneous erection of several hours' duration. Physical examination reveals the penis to be rigid and mildly tender; the glans penis, however, is usually flaccid.

Hypospadias.

Hypospadias is a congenital abnormality in which the urethral meatus is positioned either along the ventral shaft of the penis or on the scrotum or perineum instead of being located at the tip of the penis. This is a relatively common condition, occurring in about 1 in 300 live male births ( Avellan, 1975 ). In the more common, less severe forms of hypospadias, the urethra is located at or distal to the corona of the penis; these conditions frequently do not necessitate treatment except for cosmetic purposes. The less common but more severe forms of hypospadias, in which the meatus is located on the penile shaft or in the perineum, may interfere with normal urination in the usual male standing position and may, in adult life, interfere with fertility, because the semen is deposited in the distal vagina rather than at the cervix. Such cases are best corrected early in childhood to avoid social embarrassment and psychological trauma. Neonates with hypospadias and bilateral cryptorchidism (undescended testes) should be evaluated for the possibility of intersex, of which the most common cause is adrenogenital syndrome.

Carcinoma.

Carcinoma of the penis usually presents as a velvety, raised lesion arising on the glans penis or inner surface of the prepuce. Alternatively, it may present as an ulcerative lesion. Carcinoma of the penis occurs almost exclusively in uncircumcised men. It is more common in underdeveloped nations where there is poor hygiene. Penile carcinoma is most commonly a squamous cell tumor and is frequently associated with palpable inguinal lymphadenopathy.

Scrotum and Contents

The scrotum is a loose sac containing the testes and spermatic cord structures. The scrotal wall is made up of skin and an underlying thin muscular layer. The testes are normally oval, firm, and smooth; in adults, they measure about 6 cm in length and 4 cm in width. They are suspended in the scrotum, with the right testis normally anterior to the left. The epididymis lies posterior to the testis and is palpable as a distinct ridge of tissue. The vas deferens can be palpated above each testis and feels like a piece of heavy twine.

The scrotum should be examined for dermatologic abnormalities. Because the scrotum, unlike the penis, contains both hair and sweat glands, it is a frequent site of local infection and sebaceous cysts. Hair follicles can become infected and may present as small pustules on the surface of the scrotum. These usually resolve spontaneously, but they can give rise to more significant infection, particularly in patients with reduced immunity and in those with diabetes. Patients often become concerned about these lesions, mistaking them for testicular tumors.

The testes should be palpated gently between the finger tips of both hands. The testes normally have a firm, rubbery consistency with a smooth surface. Abnormally small testes suggest hypogonadism or an endocrinopathy such as Klinefelter's disease. A firm or hard area within the testis should be considered a malignant tumor until proved otherwise. The epididymis should be palpable as a ridge posterior to each testis. Masses in the epididymis (spermatocele, cyst, epididymitis) are almost always benign.

To examine for a hernia, the physician's index finger should be inserted gently into the scrotum and invaginated into the external inguinal ring ( Fig. 3-4 ). The scrotum should be invaginated in front of the testis, and care should be taken not to elevate the testis itself, which is quite painful. Once the external ring has been located, the physician should place the fingertips of his or her other hand over the internal inguinal ring and ask the patient to bear down (Valsalva's maneuver). A hernia will be felt as a distinct bulge that descends against the tip of the index finger in the external inguinal ring as the patient bears down. Although it may be possible to distinguish a direct inguinal hernia arising through the floor of the inguinal canal from an indirect inguinal hernia prolapsing through the internal inguinal ring, this is seldom possible and of little clinical significance because the surgical approach is essentially identical for both conditions.



Figure 3-4 Examination of the inguinal canal. (From Swartz MH: Textbook of Physical Diagnosis. Philadelphia, WB Saunders, 1989, p 376.)

The spermatic cord is also examined with the patient in the standing position. A varicocele is a dilated, tortuous spermatic vein that becomes more obvious as the patient performs a Valsalva maneuver. The epididymis can again be palpated as a ridge of tissue running longitudinally, posterior to each testis. The testis should be palpated again between the fingers of both hands, once again taking care not to exert any pressure on the testis itself so as to avoid pain.

Transillumination is helpful in determining whether scrotal masses are solid (tumor) or cystic (hydrocele, spermatocele). A small flashlight or fiberoptic light cord is placed behind the mass. A cystic mass transilluminates easily, whereas light is not transmitted through a solid tumor.

Abnormal Findings Testicular Cancer.

The most common physical finding in the testis is a mass. A useful guideline is that most masses arising from the testis are malignant, whereas almost all masses arising from the spermatic cord structures are benign. Thus, it is very important to distinguish the testis and epididymis during the physical examination. Testicular tumors usually present as painless, firm, irregular masses on the surface of the testis. They are usually discovered incidentally by the patient when showering or during self-examination. Testicular tumors can be readily distinguished from benign masses arising from the spermatic cord by transillumination and scrotal ultrasound.

Torsion.

Torsion is the twisting of the testis on the spermatic cord, resulting in strangulation of the blood supply and infarction of the testis. Torsion occurs most commonly between the ages of 12 and 20 years, although it does occur less frequently during the first year of life. The patient usually presents with the sudden onset of pain and swelling of the involved testis. The pain may radiate into the groin and lower abdomen; thus, it may be confused with appendicitis unless the physician examines the genitalia carefully. On physical examination, it is difficult to distinguish the testis from the epididymis because of localized swelling. For this reason, the condition is frequently misdiagnosed as epididymitis. Age is the most useful criterion in distinguishing torsion from epididymitis, because torsion usually occurs around puberty whereas epididymitis more often occurs in sexually active males, usually after age 20 years.

Hydrocele.

A hydrocele is a collection of fluid between the tunica vaginalis and the testis. The patient presents with progressive swelling and local discomfort on the involved side of the scrotum. Physical examination reveals smooth, symmetrical enlargement of one side of the scrotum in which it is very difficult to feel the testis. The diagnosis is made by transillumination of the scrotum. However, because about 10% of testicular tumors present as an associated reactive hydrocele, it is important to be sure that the hydrocele transilluminates completely and, if there is any doubt, to confirm the diagnosis with a subsequent scrotal ultrasound.

Varicocele.

A varicocele is an enlarged, tortuous spermatic vein above the testis that almost always occurs on the left side. The patient presents with a soft mass or swelling above the testis noted when he stands or strains. This has been described as a “bag of worms.” Varicoceles typically decrease in size and may disappear when the patient is supine. Patients with the sudden onset of a varicocele, a right-sided varicocele, or a varicocele that does not reduce in size in the supine position should be suspected of having a retroperitoneal neoplasm with obstruction of the spermatic vein where it enters either the renal vein on the left or the inferior vena cava on the right. Such patients should undergo ultrasonography or CT to rule out malignancy before receiving treatment for the varicocele.

Rectal and Prostate Examination in the Male

Digital rectal examination (DRE) should be performed in every male after age 40 years and in men of any age who present for urologic evaluation. Prostate cancer is the second most common cause of male cancer deaths after age 55 years and the most common cause of cancer deaths in men older than 70 years. Many prostate cancers can be detected in an early curable stage by DRE, and about 25% of colorectal cancers can be detected by DRE in combination with a stool guaiac test.

DRE should be performed at the end of the physical examination. It is done best with the patient standing and bent over the examining table or with the patient in the knee-chest position. In the standing position, the patient should stand with his thighs close to the examining table. The feet should be about 18 inches apart, with the knees flexed slightly. The patient should bend at the waist 90 degrees until his chest is resting on his forearms. The physician should give the patient adequate time to get in the proper position and relax as much as possible. A few reassuring words before the examination are helpful. The physician should place a glove on the examining hand and should lubricate the index finger thoroughly.

Before performing the DRE, the physician should place the palm of his other hand against the patient's lower abdomen. This provides subtle reassurance to the patient by allowing the physician to make gentle contact with the patient before touching the anus. It also allows the physician to steady the patient and provide gentle counterpressure if the patient tries to move away as the DRE is being performed. The DRE itself begins by separating the buttocks and inspecting the anus for pathology, usually hemorrhoids, but, occasionally, an anal carcinoma or melanoma may be detected. The gloved, lubricated index finger is then inserted gently into the anus. Only one phalanx should be inserted initially to give the anus time to relax and to easily accommodate the finger. Estimation of anal sphincter tone is of great importance; a flaccid or spastic anal sphincter suggests similar changes in the urinary sphincter and may be a clue to the diagnosis of neurogenic disease. If the physician waits only a few seconds, the anal sphincter will normally relax to the degree that the finger can be advanced to the knuckle without causing pain. The index finger then sweeps over the prostate; the entire posterior surface of the gland can usually be examined if the patient is in the proper position. Normally, the prostate is about the size of a chestnut and has a consistency similar to that of the contracted thenar eminence of the thumb (with the thumb opposed to the little finger).

The index finger is extended as far as possible into the rectum, and the entire circumference is examined to detect an early rectal carcinoma. The index finger is then withdrawn gently, and the stool on the glove is transferred to a guaiac-impregnated (Hemoccult) card for determination of occult blood. Although there may be a significant incidence of false-positive and false-negative results associated with fecal occult blood testing, particularly without dietary and drug restrictions, the guaiac test is simple and inexpensive and may lead to the detection of significant gastrointestinal abnormalities ( Bond, 1999 ). Adequate tissues, soap, and towels should be available for the patient to cleanse himself after the examination. The physician should then leave the room and allow the patient adequate time to wash and dress before concluding the consultation.

Abnormal Findings Acute Prostatitis.

Acute prostatitis most commonly occurs in sexually active men between the ages of 20 and 40 years. Symptoms include fever, malaise, perineal and rectal discomfort, urinary frequency, urgency, dysuria, and sometimes urinary retention. When acute prostatitis is suspected, rectal examination should be performed carefully. Examination reveals the prostate to be warm, tender, and sometimes fluctuant or boggy in consistency. A localized fluctuant, tender region within the prostate may indicate a prostatic abscess for which surgical drainage is required. The prostate should never be massaged for secretions in men with acute prostatitis. Massage of the acutely infected prostate is not only unnecessary but also extremely uncomfortable for the patient. In addition, massage may disseminate bacteria through the vas deferens, causing secondary epididymitis or, more significantly, may disseminate bacteria into the bloodstream, producing gram-negative septicemia.

Benign Prostatic Hyperplasia.

The physical findings in BPH are usually limited to the prostate. In BPH, the prostate remains rubbery in consistency, but may be variably enlarged from normal chestnut size to the size of a lemon, or, occasionally, even as large as an orange. There is only a general correlation between prostatic size and degree of symptoms.

Because BPH affects almost all men older than age 50 years, the finding of an enlarged prostate on physical examination is not a reason per se to initiate further urologic evaluation. The severity of the disease and the need for treatment are best determined by the patient's symptoms as well as the results of further urologic testing, such as measurement of a urinary flow rate and postvoid residual urine.

Carcinoma of the Prostate.

Prostate cancer usually arises in the posterior peripheral region of the prostate and, therefore, is frequently palpable in its early stages on rectal examination. On physical examination, prostatic carcinomas are palpable as firm, indurated nodules or regions within the prostate. These areas of induration are characterized by having a woodlike consistency. As prostatic carcinomas progress, the entire gland becomes firmer than usual. Eventually, these tumors may progress beyond the capsule of the prostate, extending cephalad into the seminal vesicles and laterally toward the pelvic side wall.

It should be emphasized that men with early, localized carcinoma of the prostate are almost always asymptomatic. Therefore, a patient should never be allowed to dissuade the urologist from performing a rectal examination simply because he is asymptomatic. Urinary obstructive symptoms and skeletal pain are symptoms of advanced, incurable disease.

Detection of early prostatic carcinoma on rectal examination takes practice and has been greatly facilitated by the discovery of PSA. An elevated PSA value should raise the suspicion of prostatic carcinoma, regardless of the findings on rectal examination. Conversely, a normal PSA test does not exclude the possibility of early prostate cancer, and, in fact, 30% of men with early prostate cancer will have a normal serum PSA test ( Partin et al, 1993 ).

A prostatic biopsy should be performed for any palpable lesion within the prostate. In one study, the detection rate of prostate cancer was 18% among men with an abnormal DRE and a PSA less than 4.0 ng/mL ( Crawford et al, 1999 ). In contrast, 56% of men with palpable abnormalities and a PSA greater than 4.0 ng/mL were found to have malignancy. Other causes of prostatic induration besides cancer include calculi (which are typically harder than tumors), inflammation, fibrous BPH, and infarction. Biopsies are now done easily using topical anesthesia under transrectal ultrasound guidance. There is no excuse for delaying a prostatic biopsy in an otherwise healthy younger man with either an abnormal DRE or an elevated PSA level. It serves no purpose to have the patient return in 6 months for a repeat examination to see whether the nodule has changed, because prostate cancers usually grow very slowly; the fact that a nodule does not change appreciably with time is of no clinical significance.

Pelvic Examination in the Female

Male urologists should always perform the female pelvic examination with a female nurse or other health care professional present. The patient should be allowed to undress in privacy and be fully draped for the procedure before the physician enters the room. The examination itself should be performed in standard lithotomy position with the patient's legs abducted. Initially, the external genitalia and introitus should be examined, with particular attention paid to atrophic changes, erosions, ulcers, discharge, or warts, all of which may cause dysuria and pelvic discomfort. The urethral meatus should be inspected for caruncles, mucosal hyperplasia, cysts, and mucosal prolapse. The patient is then asked to perform a Valsalva maneuver and is carefully examined for a cystocele (prolapse of the bladder) or rectocele (prolapse of the rectum). The patient is then asked to cough, which may precipitate stress urinary incontinence. Palpation of the urethra is done to detect induration, which may be a sign of chronic inflammation or malignancy. Palpation may also disclose a urethral diverticulum, and palpation of a diverticulum may cause a purulent discharge from the urethra. Bimanual examination of the bladder, uterus, and adnexa should then be performed with two fingers in the vagina and the other hand on the lower abdomen (see Fig. 3-3 ). Any abnormality of the pelvic organs should be evaluated further with a pelvic ultrasound or CT scan.

Abnormal Findings.

A careful bimanual examination of the female pelvis may reveal a variety of abnormalities of the uterus, ovaries, and cervix, including benign and malignant masses and inflammatory lesions. Various forms of pelvic prolapse, such as cystocele, rectocele, and enterocele, may also be detected. Inspection of the urethral meatus and vaginal introitus may also be helpful in identifying condylomata, urethral lesions, and other abnormalities.

Neurologic Examination

There are a variety of clinical situations in which the neurologic examination may be helpful in evaluating urologic patients. In some cases, the level of neurologic abnormalities can be localized by the pattern of sensory deficit noted during physical examination using a dermatome map ( Fig. 3-5 ). Sensory deficits in the penis, labia, scrotum, vagina, and perianal area generally indicate damage or injury to sacral roots or nerves. In addition to sensory examination, testing of reflexes in the genital area may also be performed. The most important of these is the bulbocavernosus reflex (BCR), which is a reflex contraction of the striated muscle of the pelvic floor that occurs in response to a variety of stimuli in the perineum or genitalia. This reflex is most commonly tested by placing a finger in the rectum and then squeezing the glans penis or clitoris. If a Foley catheter is in place, the BCR can also be elicited by gently pulling on the catheter. If the BCR is intact, tightening of the anal sphincter should be felt and/or observed. The BCR tests the integrity of the spinal cord mediated reflex arc involving S2-S4 and may be absent in the presence of sacral cord or peripheral nerve abnormalities.



Figure 3-5 Sensory dermatome maps used to help localize the level of neurologic deficit.

The cremasteric reflex can be elicited by lightly stroking the superior and medial thigh in a downward direction. The normal response in males is contraction of the cremasteric muscle that results in immediate elevation of the ipsilateral scrotum and testis. There is limited clinical utility for testing superficial reflexes such as the cremasteric when investigating neurologic dysfunction. However, there may be a role for testing this reflex when assessing patients with suspected testicular torsion or epididymitis. Finally, an overly active cremasteric reflex in children can lead to the mistaken diagnosis of an undescended testis in some cases.

CLINICAL DECISION-MAKING - History

2008-08-12T05:57:00.001-07:00

Urologists have a unique and interesting position in medicine. Their patients encompass all age groups, including prenatal, pediatric, adolescent, adult, and geriatric. Because there is no medical subspecialist with similar interests, the urologist has the ability to make the initial evaluation and diagnosis and to provide medical and surgical therapy for all diseases of the genitourinary (GU) system. Historically, the diagnostic armamentarium has included urinalysis, endoscopy, and intravenous pyelography. Recent advances in ultrasonography, computed tomography (CT), magnetic resonance imaging (MRI), and endourology have expanded our diagnostic capabilities. Despite these advances, however, the basic approach to the patient is still dependent on taking a complete history, executing a thorough physical examination, and performing a urinalysis. These basics dictate and guide the subsequent diagnostic evaluation.

HISTORY Overview

The medical history is the cornerstone of the evaluation of the urologic patient, and a well-taken history will frequently elucidate the probable diagnosis. However, many pitfalls can inhibit the urologist from obtaining an accurate history. The patient may be unable to describe or communicate symptoms because of anxiety, language barrier, or educational background. Therefore, the urologist must be a detective and lead the patient through detailed and appropriate questioning to obtain accurate information. There are practical considerations in the art of history taking that can help to alleviate some of these difficulties. In the initial meeting, an attempt should be made to help the patient feel comfortable. During this time, the physician should project a calm, caring, and competent image that can help foster two-way communication. Impaired hearing, mental capacity, and facility with English can be assessed promptly. These difficulties are frequently overcome by having a family member present during the interview or, alternatively, by having an interpreter present.

Patients need to have sufficient time to express their problems and the reasons for seeking urologic care; the physician, however, should focus the discussion to make it as productive and informative as possible. Direct questioning can then proceed logically. The physician needs to listen carefully without distractions to obtain and interpret the clinical information provided by the patient. A complete history can be divided into the chief complaint and history of the present illness, the patient's past medical history, and a family history. Each segment can provide significant positive and negative findings that will contribute to the overall evaluation and treatment of the patient.

Chief Complaint and Present Illness

Most urologic patients identify their symptoms as arising from the urinary tract and frequently present to the urologist for the initial evaluation. For this reason, the urologist frequently has the opportunity to act as both the primary physician and the specialist. The chief complaint must be clearly defined because it provides the initial information and clues to begin formulating the differential diagnosis. Most importantly, the chief complaint is a constant reminder to the urologist as to why the patient initially sought care. This issue must be addressed even if subsequent evaluation reveals a more serious or significant condition that requires more urgent attention. In our personal experience, a young woman presented with a chief complaint of recurrent urinary tract infections (UTIs). In the course of her evaluation, she was found to have a right adrenal mass. We subsequently focused on this problem and performed a right adrenalectomy for a benign cortical adenoma. We forgot about the woman's original symptoms until she presented for her subsequent postoperative examination. She reminded us of her original symptoms at that time, and subsequent evaluation revealed that she had a nylon suture that had eroded into the anterior wall of her bladder from a previous abdominal vesicourethropexy performed 2 years earlier for stress urinary incontinence. Her UTIs resolved after surgical removal of the suture.

In obtaining the history of the present illness, the duration, severity, chronicity, periodicity, and degree of disability are important considerations. The patient's symptoms need to be clarified for details and quantified for severity. Listed next are a variety of typical initial complaints. Specific questions that focus the differential diagnosis are provided.

Pain

Pain arising from the GU tract may be quite severe and is usually associated with either urinary tract obstruction or inflammation. Urinary calculi cause severe pain when they obstruct the upper urinary tract. Conversely, large, nonobstructing stones may be totally asymptomatic. Thus, a 2-mm-diameter stone lodged at the ureterovesical junction may cause excruciating pain whereas a large staghorn calculus in the renal pelvis or a bladder stone may be totally asymptomatic. Urinary retention from prostatic obstruction is also quite painful, but the diagnosis is usually obvious to the patient.

Inflammation of the GU tract is most severe when it involves the parenchyma of a GU organ. This is due to edema and distention of the capsule surrounding the organ. Thus, pyelonephritis, prostatitis, and epididymitis are typically quite painful. Inflammation of the mucosa of a hollow viscus such as the bladder or urethra usually produces discomfort, but the pain is not nearly as severe.

Tumors in the GU tract usually do not cause pain unless they produce obstruction or extend beyond the primary organ to involve adjacent nerves. Thus, pain associated with GU malignancies is usually a late manifestation and a sign of advanced disease.

Renal Pain.

Pain of renal origin is usually located in the ipsilateral costovertebral angle just lateral to the sacrospinalis muscle and beneath the 12th rib. Pain is usually caused by acute distention of the renal capsule, generally from inflammation or obstruction. The pain may radiate across the flank anteriorly toward the upper abdomen and umbilicus and may be referred to the testis or labium. A corollary to this observation is that renal or retroperitoneal disease should be considered in the differential diagnosis of any man who complains of testicular discomfort but has a normal scrotal examination. Pain due to inflammation is usually steady, whereas pain due to obstruction fluctuates in intensity. Thus, the pain produced by ureteral obstruction is typically colicky in nature and intensifies with ureteral peristalsis, at which time the pressure in the renal pelvis rises as the ureter contracts in an attempt to force urine past the point of obstruction.

Pain of renal origin may be associated with gastrointestinal symptoms because of reflex stimulation of the celiac ganglion and because of the proximity of adjacent organs (liver, pancreas, duodenum, gallbladder, and colon). Thus, renal pain may be confused with pain of intraperitoneal origin; it can usually be distinguished, however, by a careful history and physical examination. Pain that is due to a perforated duodenal ulcer or pancreatitis may radiate into the back, but the site of greatest pain and tenderness is in the epigastrium. Pain of intraperitoneal origin is seldom colicky, as with obstructive renal pain. Furthermore, pain of intraperitoneal origin frequently radiates into the shoulder because of irritation of the diaphragm and phrenic nerve; this does not occur with renal pain. Typically, patients with intraperitoneal pathology prefer to lie motionless to minimize pain, whereas patients with renal pain usually are more comfortable moving around and holding the flank.

Renal pain may also be confused with pain resulting from irritation of the costal nerves, most commonly T10-T12. Such pain has a similar distribution from the costovertebral angle across the flank toward the umbilicus. However, the pain is not colicky in nature. Furthermore, the intensity of radicular pain may be altered by changing position; this is not the case with renal pain.

Ureteral Pain.

Ureteral pain is usually acute and secondary to obstruction. The pain results from acute distention of the ureter and by hyperperistalsis and spasm of the smooth muscle of the ureter as it attempts to relieve the obstruction, usually produced by a stone or blood clot. The site of ureteral obstruction can often be determined by the location of the referred pain. With obstruction of the midureter, pain on the right side is referred to the right lower quadrant of the abdomen (McBurney's point) and thus may simulate appendicitis; pain on the left side is referred over the left lower quadrant and resembles diverticulitis. Also, the pain may be referred to the scrotum in the male or the labium in the female. Lower ureteral obstruction frequently produces symptoms of vesical irritability, including frequency, urgency, and suprapubic discomfort that may radiate along the urethra in men to the tip of the penis. Often, by taking a careful history, the astute clinician can predict the location of the obstruction. Ureteral pathology that arises slowly or produces only mild obstruction rarely causes pain. Therefore, ureteral tumors and stones that cause minimal obstruction are seldom painful.

Vesical Pain.

Vesical pain is usually produced either by overdistention of the bladder as a result of acute urinary retention or by inflammation. Constant suprapubic pain that is unrelated to urinary retention is seldom of urologic origin. Furthermore, patients with slowly progressive urinary obstruction and bladder distention (e.g., diabetics with a flaccid neurogenic bladder) frequently have no pain at all despite residual urine volumes over I L.

Inflammatory conditions of the bladder usually produce intermittent suprapubic discomfort. Thus, the pain in conditions such as bacterial cystitis or interstitial cystitis is usually most severe when the bladder is full and is relieved at least partially by voiding. Patients with cystitis sometimes experience sharp, stabbing suprapubic pain at the end of micturition, and this is termed strangury. Furthermore, patients with cystitis frequently experience pain referred to the distal urethra that is associated with irritative voiding symptoms such as urinary frequency and dysuria.

Prostatic Pain.

Prostatic pain is usually secondary to inflammation with secondary edema and distention of the prostatic capsule. Pain of prostatic origin is poorly localized, and the patient may complain of lower abdominal, inguinal, perineal, lumbosacral, and/or rectal pain. Prostatic pain is frequently associated with irritative urinary symptoms such as frequency and dysuria, and, in severe cases, marked prostatic edema may produce acute urinary retention.

Penile Pain.

Pain in the flaccid penis is usually secondary to inflammation in the bladder or urethra, with referred pain that is experienced maximally at the urethral meatus. Alternatively, penile pain may be produced by paraphimosis, a condition in which the uncircumcised penile foreskin is trapped behind the glans penis, resulting in venous obstruction and painful engorgement of the glans penis (see later). Pain in the erect penis is usually due to Peyronie's disease or priapism (see later).

Testicular Pain.

Scrotal pain may be either primary or referred. Primary pain arises from within the scrotum and is usually secondary to acute epididymitis or torsion of the testis or testicular appendices. Because of the edema and pain associated with both acute epididymitis and testicular torsion, it is frequently difficult to distinguish these two conditions. Alternatively, scrotal pain may result from inflammation of the scrotal wall itself. This may result from a simple infected hair follicle or sebaceous cyst, but it may also be secondary to Fournier's gangrene, a severe, necrotizing infection arising in the scrotum that can rapidly progress and be fatal unless promptly recognized and treated.

Chronic scrotal pain is usually related to noninflammatory conditions such as a hydrocele or a varicocele, and the pain is generally characterized as a dull, heavy sensation that does not radiate. Because the testes arise embryologically in close proximity to the kidneys, pain arising in the kidneys or retroperitoneum may be referred to the testes. Similarly, the dull pain associated with an inguinal hernia may be referred to the scrotum.

Hematuria

Hematuria is the presence of blood in the urine; greater than three red blood cells per high-power microscopic field (HPF) is significant. Patients with gross hematuria are usually frightened by the sudden onset of blood in the urine and frequently present to the emergency department for evaluation, fearing that they may be bleeding excessively. Hematuria of any degree should never be ignored and, in adults, should be regarded as a symptom of urologic malignancy until proved otherwise. In evaluating hematuria, several questions should always be asked, and the answers will enable the urologist to target the subsequent diagnostic evaluation efficiently:

		Is the hematuria gross or microscopic?
		At what time during urination does the hematuria occur (beginning or end of stream or during entire stream)?
		Is the hematuria associated with pain?
		Is the patient passing clots?
		If the patient is passing clots, do the clots have a specific shape?

Gross versus Microscopic Hematuria.

The significance of gross versus microscopic hematuria is simply that the chances of identifying significant pathology increase with the degree of hematuria. Thus, it is uncommon for patients with gross hematuria not to have identifiable underlying pathology whereas it is quite common for patients with minimal degrees of microscopic hematuria to have a negative urologic evaluation.

Timing of Hematuria.

The timing of hematuria during urination frequently indicates the site of origin. Initial hematuria usually arises from the urethra; it occurs least commonly and is usually secondary to inflammation. Total hematuria is most common and indicates that the bleeding is most likely coming from the bladder or upper urinary tracts. Terminal hematuria occurs at the end of micturition and is usually secondary to inflammation in the area of the bladder neck or prostatic urethra. It occurs at the end of micturition as the bladder neck contracts, squeezing out the last amount of urine.

Association with Pain.

Hematuria, although frightening, is usually not painful unless it is associated with inflammation or obstruction. Thus, patients with cystitis and secondary hematuria may experience painful urinary irritative symptoms but the pain is usually not worsened with passage of clots. More commonly, pain in association with hematuria usually results from upper urinary tract hematuria with obstruction of the ureters with clots. Passage of these clots may be associated with severe, colicky flank pain similar to that produced by a ureteral calculus, and this helps identify the source of the hematuria.

Presence of Clots.

The presence of clots usually indicates a more significant degree of hematuria, and, accordingly, the probability of identifying significant urologic pathology increases.

Shape of Clots.

Usually, if the patient is passing clots, they are amorphous and of bladder or prostatic urethral origin. However, the presence of vermiform (wormlike) clots, particularly if associated with flank pain, identifies the hematuria as coming from the upper urinary tract with formation of vermiform clots within the ureter.

It cannot be emphasized strongly enough that hematuria, particularly in the adult, should be regarded as a symptom of malignancy until proved otherwise and demands immediate urologic examination. In a patient who presents with gross hematuria, cystoscopy should be performed as soon as possible, because frequently the source of bleeding can be readily identified. Cystoscopy will determine whether the hematuria is coming from the urethra, bladder, or upper urinary tract. In patients with gross hematuria secondary to an upper tract source, it is very easy to see the jet of red urine pulsing from the involved ureteral orifice.

Although inflammatory conditions may result in hematuria, all patients with hematuria, except perhaps young women with acute bacterial hemorrhagic cystitis, should undergo urologic evaluation. Older women and men who present with hematuria and irritative voiding symptoms may have cystitis secondary to infection arising in a necrotic bladder tumor or, more commonly, flat carcinoma in situ of the bladder. The most common cause of gross hematuria in a patient older than age 50 years is bladder cancer.

Lower Urinary Tract Symptoms Irritative Symptoms.

Frequency is one of the most common urologic symptoms. The normal adult voids five or six times per day, with a volume of approximately 300 mL with each void. Urinary frequency is due either to increased urinary output (polyuria) or to decreased bladder capacity. If voiding is noted to occur in large amounts frequently, the patient has polyuria and should be evaluated for diabetes mellitus, diabetes insipidus, or excessive fluid ingestion. Causes of decreased bladder capacity include bladder outlet obstruction with decreased compliance, increased residual urine, and/or decreased functional capacity due to irritation; neurogenic bladder with increased sensitivity and decreased compliance; pressure from extrinsic sources; or anxiety. By separating irritative from obstructive symptoms, the astute clinician should be able to arrive at a proper differential diagnosis.

Nocturia is nocturnal frequency. Normally, adults arise no more than twice at night to void. As with frequency, nocturia may be secondary to increased urine output or decreased bladder capacity. Frequency during the day without nocturia is usually of psychogenic origin and related to anxiety. Nocturia without frequency may occur in the patient with congestive heart failure and peripheral edema in whom the intravascular volume and urine output increase when the patient is supine. Renal concentrating ability decreases with age; therefore, urine production in the geriatric patient is increased at night, when renal blood flow is increased as a result of recumbency. In general, nocturia may be attributed to nocturnal polyuria (nocturnal urine overproduction) and/or diminished nocturnal bladder capacity ( Weiss and Blaivas, 2000 ). Nocturia may also occur in people who drink large amounts of liquid in the evening, particularly caffeinated and alcoholic beverages, which have strong diuretic effects. In the absence of these factors, nocturia signifies a problem with bladder function secondary to urinary outlet obstruction and/or decreased bladder compliance.

Dysuria is painful urination that is usually caused by inflammation. This pain is usually not felt over the bladder but is commonly referred to the urethral meatus. Pain occurring at the start of urination may indicate urethral pathology, whereas pain occurring at the end of micturition (strangury) is usually of bladder origin. Dysuria is frequently accompanied by frequency and urgency.

Obstructive Symptoms.

Decreased force of urination is usually secondary to bladder outlet obstruction and commonly results from benign prostatic hyperplasia (BPH) or a urethral stricture. In fact, except for severe degrees of obstruction, most patients are unaware of a change in the force and caliber of their urinary stream. These changes usually occur gradually and go generally unrecognized by most patients. The other obstructive symptoms noted later are more commonly recognized and are usually secondary to bladder outlet obstruction in men due to either BPH or a urethral stricture.

Urinary hesitancy refers to a delay in the start of micturition. Normally, urination begins within a second after relaxing the urinary sphincter, but it may be delayed in men with bladder outlet obstruction.

Intermittency refers to involuntary start-stopping of the urinary stream. It most commonly results from prostatic obstruction with intermittent occlusion of the urinary stream by the lateral prostatic lobes.

Postvoid dribbling refers to the terminal release of drops of urine at the end of micturition. This is secondary to a small amount of residual urine in either the bulbar or the prostatic urethra that is normally “milked back” into the bladder at the end of micturition ( Stephenson and Farrar, 1977 ). In men with bladder outlet obstruction, this urine escapes into the bulbar urethra and leaks out at the end of micturition. Men frequently will attempt to avoid wetting their clothing by shaking the penis at the end of micturition. In fact, this is ineffective, and the problem is more readily solved by manual compression of the bulbar urethra in the perineum and blotting the urethral meatus with a tissue. Postvoid dribbling is often an early symptom of urethral obstruction related to BPH, but, in itself, seldom necessitates any further treatment.

Straining refers to the use of abdominal musculature to urinate. Normally, it is unnecessary for a man to perform a Valsalva maneuver except at the end of urination. Increased straining during micturition is a symptom of bladder outlet obstruction.

It is important for the urologist to distinguish irritative from obstructive lower urinary tract symptoms. This most frequently occurs in evaluating men with BPH. Although BPH is primarily obstructive, it produces changes in bladder compliance that result in increased irritative symptoms. In fact, men with BPH more commonly present with irritative than obstructive symptoms, and the most common presenting symptom is nocturia. The urologist must be careful not to attribute irritative symptoms to BPH unless there is documented evidence of obstruction. In general, lower urinary tract symptoms are nonspecific and may occur secondary to a wide variety of neurologic conditions as well as to prostatic enlargement ( Lepor and Machi, 1993 ). In this regard, two important examples are mentioned. Patients with high-grade flat carcinoma in situ of the bladder may present with urinary irritative symptoms. The urologist should be particularly aware of the diagnosis of carcinoma in situ in men who present with irritative symptoms, a history of cigarette smoking, and microscopic hematuria. In our personal experience, we cared for a 54-year-old man who presented with this history and was treated for BPH for 2 years before the diagnosis of bladder cancer was established. Once the correct diagnosis was made, the patient had developed muscle-invasive disease and required a cystectomy for cure.

The second important example is irritative symptoms resulting from neurologic disease, such as cerebrovascular accidents, diabetes mellitus, and Parkinson's disease. Most neurologic diseases encountered by the urologist are upper motor neuron in etiology and result in a loss of cortical inhibition of voiding with resultant decreased bladder compliance and irritative voiding symptoms. The urologist must be extremely careful to rule out underlying neurologic disease before performing surgery to relieve bladder outlet obstruction. Such surgery not only may fail to relieve the patient's irritative symptoms but also may result in permanent urinary incontinence.

Since its introduction in 1992, the American Urological Association (AUA) symptom index has been widely used and validated as an important means of assessing men with lower urinary tract symptoms ( Barry et al, 1992 ). The original AUA symptom score is based on the answers to seven questions concerning frequency, nocturia, weak urinary stream, hesitancy, intermittency, incomplete bladder emptying, and urgency. The International Prostate Symptom Score (I-PSS) includes these seven questions, as well as a global quality of life question ( Table 3-1 ). The total symptom score ranges from 0 to 35 with scores of 0 to 7, 8 to 19, and 20 to 35 indicating mild, moderate, and severe lower urinary tract symptoms, respectively. The I-PSS is a helpful tool both in the clinical management of men with lower urinary tract symptoms and in research studies regarding the medical and surgical treatment of men with voiding dysfunction.

Table 3-1 -- International Prostate Symptom Score

Patient's Name	Not At All	Less Than 1 Time in 5	Less Than Half the Time	About Half the Time	More Than Half the Time	Almost Always
Date of Birth Date Completed
1. Incomplete emptying
Over the past month, how often have you had a sensation of not emptying your bladder completely after you finished urinating?	0	1	2	3	4	5
2. Frequency
Over the past month, how often have you had to urinate again less than two hours after you finished urinating?	0	1	2	3	4	5
3. Intermittency
Over the past month, how often have you found you stopped and started again several times when you urinated?	0	1	2	3	4	5
4. Urgency
Over the past month, how often have you found it difficult to postpone urination?	0	1	2	3	4	5
5. Weak stream
Over the past month, how often have you had a weak urinary stream?	0	1	2	3	4	5
6. Straining
Over the past month, how often have you had to push or strain to begin urination?	0	1	2	3	4	5

	None	1 Time	2 Times	3 Times	4 Times	5 Times or More
7. Nocturia
Over the past month, how many times did you most typically get up to urinate from the time you went to bed at night until the time you got up in the morning?	0	1	2	3	4	5
*Total I-PSS Score*
Quality of Life Due to Urinary Symptoms	Delighted	Pleased	Mostly Satisfied	Mixed—About Equally Satisfied and Dissatisfied	Mostly Dissatisfied	Unhappy	Terrible
If you were to spend the rest of your life with your urinary condition just the way it is now, how would you feel about that?	0	1	2	3	4	5	6

From Cockett ATK, Aso Y, Denis L, et al: The Second International Consultation on Benign Prostatic Hyperplasia (BPH). In Cockett ATK, Aso Y, Chatelain C, et al (eds): The Second International Consultation on Benign Prostatic Hyperplasia (BPH). Pairs, Scientific Communication International, 1994, p 553.

There are limitations to the use of symptom indices, and it is important for the physician to discuss the patient's responses with him. It has been demonstrated that a grade 6 reading level is necessary to understand the I-PSS, and some patients with neurologic disorders and dementia may also have difficulty completing the symptom score ( MacDiarmid et al, 1998 ). In addition, the symptom score, as well as the obstructive and irritative voiding symptoms, is nonspecific, and the symptoms may be caused by a variety of conditions other than BPH. Similar symptom scores have been demonstrated to be present in age-matched men and women between 55 and 79 years of age ( Lepor and Machi, 1993 ). Despite these limitations, the I-PSS is a simple adjunct in assessing men with lower urinary tract symptoms and may be used in the initial evaluation of men with lower urinary tract symptoms as well as in the assessment of treatment response.

Incontinence.

Urinary incontinence is the involuntary loss of urine. A careful history of the incontinent patient will often determine the etiology. Urinary incontinence can be subdivided into four categories.

Continuous Incontinence.

Continuous incontinence is most commonly due to a urinary tract fistula that bypasses the urethral sphincter. The most common type of fistula that results in urinary incontinence is a vesicovaginal fistula usually secondary to gynecologic surgery, radiation, or obstetric trauma. Less commonly, ureterovaginal fistulas may occur from similar causes.

A second major cause of continuous incontinence is an ectopic ureter that enters either the urethra or the female genital tract. An ectopic ureter usually drains a small, dysplastic upper pole segment of kidney, and the amount of urinary leakage may be quite small. Such patients may void most of their urine normally but have a continuous amount of small urinary leakage that may be misdiagnosed for many years as a chronic vaginal discharge. In our experience, we cared for a 30-year-old woman—who had been misdiagnosed with enuresis in childhood and as having a chronic vaginal discharge in adult life—whose urinary leakage was totally corrected by surgical removal of the dysplastic, upper pole segment of her right kidney. Ectopic ureters never produce urinary incontinence in males because they always enter the bladder neck or prostatic urethra proximal to the external urethral sphincter.

Stress Incontinence.

Stress incontinence refers to the sudden leakage of urine with coughing, sneezing, exercise, or other activities that increase intra-abdominal pressure. During these activities, intra-abdominal pressure rises transiently above urethral resistance, resulting in a sudden, usually small amount of urinary leakage. Stress incontinence is most common in women after childbearing or menopause and is related to a loss of anterior vaginal support and weakening of pelvic tissues. Stress incontinence is also observed in men after prostatic surgery, most commonly radical prostatectomy, in which there may be injury to the external urethral sphincter. Stress urinary incontinence is difficult to manage pharmacologically, and patients with significant stress incontinence are usually best treated surgically.

Urgency Incontinence.

Urgency incontinence is the precipitous loss of urine preceded by a strong urge to void. This symptom is commonly observed in patients with cystitis, neurogenic bladder, and advanced bladder outlet obstruction with secondary loss of bladder compliance. It is important to distinguish urgency incontinence from stress incontinence for two reasons. First, urgency incontinence may result from a secondary underlying pathologic process, which should be identified; treatment of this primary problem, such as infection or bladder outlet obstruction, may result in resolution of urgency incontinence. Second, patients with urgency incontinence usually are not amenable to surgical correction but, rather, are more appropriately treated with pharmacologic agents that increase bladder compliance and/or increase urethral resistance.

Overflow Urinary Incontinence.

Overflow urinary incontinence, often called paradoxical incontinence, is secondary to advanced urinary retention and high residual urine volumes. In these patients, the bladder is chronically distended and never empties completely. Urine may dribble out in small amounts as the bladder overflows. This is particularly likely to occur at night when the patient is less likely to inhibit urinary leakage. Overflow incontinence has been termed paradoxical incontinence because it can often be cured by relief of bladder outlet obstruction. It is, however, often difficult to make the diagnosis of overflow incontinence by history and physical examination alone, particularly in the obese patient, in whom percussion of the distended bladder may be difficult. Overflow incontinence usually develops over a considerable length of time, and patients may be totally unaware of incomplete bladder emptying. Thus, any patient with significant incontinence should undergo measurement of postvoid residual urine.

Enuresis.

Enuresis refers to urinary incontinence that occurs during sleep. It occurs normally in children up to 3 years of age but persists in about 15% of children at age 5 and about 1% of children at age 15 ( Forsythe and Redmond, 1974 ). Enuresis must be distinguished from continuous incontinence, which occurs in the day as well as night and which, in a young girl, usually indicates the presence of an ectopic ureter. All children older than age 6 years with enuresis should undergo a urologic evaluation, although the vast majority will be found to have no significant urologic abnormality.

Sexual Dysfunction

Male sexual dysfunction is frequently used synonymously with impotence or erectile dysfunction, although impotence refers specifically to the inability to achieve and maintain an erection adequate for intercourse. Patients presenting with “impotence” should be questioned carefully to rule out other male sexual disorders, including loss of libido, absence of emission, absence of orgasm, and, most commonly, premature ejaculation. Obviously, it is important to identify the precise problem before proceeding with further evaluation and treatment.

Loss of Libido.

Because androgens have a major influence on sexual desire, a decrease in libido may indicate androgen deficiency arising from either pituitary or testicular dysfunction. This can be evaluated directly by measurement of serum testosterone that, if abnormal, should be further evaluated by measurement of serum gonadotropins and prolactin. Because the amount of testosterone required to maintain libido is usually less than that required for full stimulation of the prostate and seminal vesicles, patients with hypogonadism may also note decreased or absent ejaculation. Conversely, if semen volume is normal, it is unlikely that endocrine factors are responsible for loss of libido. A decrease in libido may also result from depression and a variety of medical illnesses that affect general health and well-being.

Impotence.

Impotence refers specifically to the inability to achieve and maintain an erection sufficient for intercourse. A careful history will often determine whether the problem is primarily psychogenic or organic. In men with psychogenic impotence, the condition frequently develops rather quickly secondary to a precipitating event such as marital stress or change or loss of a sexual partner. In men with organic impotence, the condition usually develops more insidiously and frequently can be linked to advancing age or other underlying risk factors.

In evaluating men with impotence, it is important to determine whether the problem exists in all situations. Many men who report impotence may not be able to have intercourse with one partner but will with another. Similarly, it is important to determine whether men are able to achieve normal erections with alternative forms of sexual stimulation (e.g., masturbation, erotic videos). Finally, the patient should be asked whether he ever notes nocturnal or early morning erections. In general, patients who are able to achieve adequate erections in some situations but not others have primarily psychogenic rather than organic impotence.

Failure to Ejaculate.

Anejaculation may result from several causes: (1) androgen deficiency, (2) sympathetic denervation, (3) pharmacologic agents, and (4) bladder neck and prostatic surgery. Androgen deficiency results in decreased secretions from the prostate and seminal vesicles causing a reduction or loss of seminal volume. Sympathectomy or extensive retroperitoneal surgery, most notably retroperitoneal lymphadenectomy for testicular cancer, may interfere with autonomic innervation of the prostate and seminal vesicles, resulting in absence of smooth muscle contraction and absence of seminal emission at time of orgasm. Pharmacologic agents, particularly α-adrenergic antagonists, may interfere with bladder neck closure at time of orgasm and result in retrograde ejaculation. Similarly, previous bladder neck or prostatic urethral surgery, most commonly transurethral resection of the prostate, may interfere with bladder neck closure, resulting in retrograde ejaculation. Finally, retrograde ejaculation may develop spontaneously in diabetic men.

Patients who complain of absence of ejaculation should be questioned regarding loss of libido or other symptoms of androgen deficiency, present medications, diabetes, and previous surgery. A careful history will usually determine the cause of this problem.

Absence of Orgasm.

Anorgasmia is usually psychogenic or caused by certain medications used to treat psychiatric diseases. Sometimes, however, anorgasmia may be due to decreased penile sensation owing to impaired pudendal nerve function. Most commonly, this occurs in diabetics with peripheral neuropathy. Men who experience anorgasmia in association with decreased penile sensation should undergo vibratory testing of the penis and further neurologic evaluation as indicated.

Premature Ejaculation.

Men who complain of premature ejaculation should be questioned carefully because this is obviously a very subjective symptom. It is common for men to ejaculate within 2 minutes after initiation of intercourse, and many men who complain of premature ejaculation in actuality have normal sexual function with abnormal sexual expectations. However, there are men with true premature ejaculation who reach orgasm within less than 1 minute after initiation of intercourse. This problem is almost always psychogenic and best treated by a clinical psychologist or psychiatrist who specializes in treatment of this problem and other psychological aspects of male sexual dysfunction. With counseling and appropriate modifications in sexual technique, this problem can usually be overcome. Alternatively, treatment with serotonin reuptake inhibitors, such as sertraline and fluoxetine, have been demonstrated to be helpful in men with premature ejaculation ( Murat Basar et al, 1999 ).

Hematospermia

Hematospermia refers to the presence of blood in the seminal fluid. It almost always results from nonspecific inflammation of the prostate and/or seminal vesicles and resolves spontaneously, usually within several weeks. It frequently occurs after a prolonged period of sexual abstinence, and we have observed it several times in men whose wives are in the final weeks of pregnancy. Patients with hematospermia that persists beyond several weeks should undergo further urologic evaluation, because, rarely, an underlying etiology will be identified. A genital and rectal examination should be done to exclude the presence of tuberculosis, a prostate-specific antigen (PSA) and a rectal examination done to exclude prostatic carcinoma, and a urinary cytology done to exclude the possibility of transitional cell carcinoma of the prostate. It should be emphasized, however, that hematospermia almost always resolves spontaneously and rarely is associated with any significant urologic pathology.

Pneumaturia

Pneumaturia is the passage of gas in the urine. In patients who have not recently had urinary tract instrumentation or a urethral catheter placed, this is almost always due to a fistula between the intestine and the bladder. Common causes include diverticulitis, carcinoma of the sigmoid colon, and regional enteritis (Crohn's disease). In rare instances, patients with diabetes mellitus may have gas-forming infections, with carbon dioxide formation from the fermentation of high concentrations of sugar in the urine.

Urethral Discharge

Urethral discharge is the most common symptom of venereal infection. A purulent discharge that is thick, profuse, and yellow to gray is typical of gonococcal urethritis; the discharge in patients with nonspecific urethritis is usually scant and watery. A bloody discharge is suggestive of carcinoma of the urethra.

Fever and Chills

Fever and chills may occur with infection anywhere in the GU tract but are most commonly observed in patients with pyelonephritis, prostatitis, or epididymitis. When associated with urinary obstruction, fever and chills may portend septicemia and necessitate emergency treatment to relieve obstruction.

Medical History

The past medical history is extremely important because it frequently provides clues to the patient's current diagnosis. The past medical history should be obtained in an orderly and sequential manner.

Previous Medical Illnesses with Urologic Sequelae

There are obviously many diseases that may affect the GU system, and it is important to listen and record the patient's previous medical illnesses. Patients with diabetes mellitus frequently develop autonomic dysfunction that may result in impaired urinary and sexual function. A previous history of tuberculosis may be important in a patient presenting with impaired renal function, ureteral obstruction, or chronic, unexplained UTIs. Patients with hypertension have an increased risk of sexual dysfunction because they are more likely to have peripheral vascular disease and because many of the medications that are used to treat hypertension frequently cause impotence. Patients with neurologic diseases such as multiple sclerosis are also more likely to develop urinary and sexual dysfunction. In fact, 5% of patients with previously undiagnosed multiple sclerosis present with urinary symptoms as the first manifestation of the disease ( Blaivas and Kaplan, 1988 ). As mentioned earlier, in men with bladder outlet obstruction, it is important to be aware of preexisting neurologic conditions. Surgical treatment of bladder outlet obstruction in the presence of detrusor hyperreflexia may result in increased urinary incontinence postoperatively. Finally, patients with sickle cell anemia are prone to a number of urologic conditions, including papillary necrosis and erectile dysfunction secondary to recurrent priapism. There are obviously many other diseases with urologic sequelae, and it is important for the urologist to take a careful history in this regard.

Family History

It is similarly important to obtain a detailed family history because many diseases are genetic and/or familial. Examples of genetic diseases include adult polycystic kidney disease, tuberous sclerosis, von Hippel-Lindau disease, renal tubular acidosis, and cystinuria; these are but a few common and well-recognized examples.

In addition to these diseases of known genetic predisposition, there are other conditions in which the precise pattern of inheritance has not been elucidated but that clearly have a familial tendency. It is well known that individuals with a family history of urolithiasis are at increased risk for stone formation. More recently, it has been recognized that 8% to 10% of men with prostate cancer have a familial form of the disease that tends to develop about a decade earlier than the more common type of prostate cancer ( Bratt, 2000 ). There are other familial conditions that are mentioned elsewhere in the text, but suffice it to state again that obtaining a careful history of previous illnesses and a family history of urologic disease can be extremely valuable in establishing the correct diagnosis.

Medications

It is similarly important to obtain an accurate and complete list of present medications because many drugs interfere with urinary and sexual function. For example, most of the antihypertensive medications interfere with erectile function, and changing antihypertensive medications can sometimes improve sexual function. Similarly, many of the psychotropic agents interfere with emission and orgasm. In our own recent experience, we cared for a man who presented with anorgasmia. He had been to several physicians without improvement in this problem. When we obtained his past medical history, he mentioned that he had been taking a psychotropic agent for transient depression for several years, and his anorgasmia resolved when this no longer needed medication was discontinued. The list of medications affecting urinary and sexual function is exhaustive, but, once again, each medication should be recorded and its side effects investigated to be sure that the patient's problem is not drug related. A listing of common medications that may cause urologic side effects is presented in Table 3-2 .

Table 3-2 -- Drugs Associated with Urologic Side Effects

Urologic Side Effects

Class of Drugs

Specific Examples

Decreased libido

Antihypertensives

Hydrochlorothiazide

Erectile dysfunction

Propranolol

Psychotropic drugs

Benzodiazepines

Ejaculatory dysfunction

		α-Adrenergic antagonists
		Psychotropic drugs

		Prazosin
		Tamsulosin
		α-Methyldopa
		Phenothiazines
		Antidepressants

Priapism

		Antipsychotics
		Antidepressants
		Antihypertensives

		Phenothiazines
		Trazodone
		Hydralazine
		Prazosin

Decreased spermatogenesis

		Chemotherapeutic agents
		Drugs with abuse potential
		Drugs affecting endocrine function

		Alkylating agents
		Marijuana
		Alcohol
		Nicotine
		Antiandrogens
		Prostaglandins

Incontinence or impaired voiding

		Direct smooth muscle stimulants
		Others
		Smooth muscle relaxants
		Striated muscle relaxants

		Histamine
		Vasopressin
		Furosemide
		Valproic acid
		Diazepam
		Baclofen

Urinary retention or obstructive voiding symptoms

		Anticholinergic agents or musculotropic relaxants
		Calcium channel blockers
		Antiparkinsonian drugs
		α-Adrenergic agonists
		Antihistamines

		Oxybutynin
		Diazepam
		Flavoxate
		Nifedipine
		Carbidopa
		Levodopa
		Pseudoephedrine
		Phenylephrine
		Loratadine
		Diphenhydramine

Acute renal failure

		Antimicrobials
		Chemotherapeutic drugs
		Others

		Aminoglycosides
		Penicillins
		Cephalosporins
		Amphotericin
		Cisplatin
		Nonsteroidal anti-inflammatory drugs
		Phenytoin

Gynecomastia

		Antihypertensives
		Cardiac drugs
		Gastrointestinal drugs
		Psychotropic drugs
		Tricyclic antidepressants

		Verapamil
		Digoxin
		Cimetidine
		Metoclopramide
		Phenothiazines
		Amitriptyline
		Imipramine

Previous Surgical Procedures

It is important to be aware of previous operations, particularly in a patient in whom surgery is intended. Obviously, previous operations may make subsequent ones more difficult. If the previous surgery was in a similar anatomic region, it is worthwhile to try to obtain the previous operative report. In our own experience, this small additional effort has been rewarded on numerous occasions by providing a clear explanation of the patient's previous surgery that greatly simplified the subsequent operation. In general, it is worthwhile obtaining as much information as possible before any intended surgery because most surprises that occur in the operating room are unhappy ones.

Smoking and Alcohol Use

Cigarette smoking and consumption of alcohol are clearly linked to a number of urologic conditions. Cigarette smoking is associated with an increased risk of urothelial carcinoma, most notably bladder cancer, and it is also associated with increased peripheral vascular disease and erectile dysfunction. Chronic alcoholism may result in autonomic and peripheral neuropathy with resultant impaired urinary and sexual function. Chronic alcoholism may also impair hepatic metabolism of estrogens, resulting in decreased serum testosterone, testicular atrophy, and decreased libido.

In addition to the direct urologic effects of cigarette smoking and alcohol consumption, patients who are actively smoking or drinking at the time of surgery are at increased risk for perioperative complications. Smokers are at increased risk for both pulmonary and cardiac complications. If possible, they should discontinue smoking at least 8 weeks before surgery to optimize their pulmonary function ( Warner et al, 1989 ). If they are unable to do this, they should at least quit smoking for 48 hours before surgery, because this will result in a significant improvement in cardiovascular function. Similarly, chronic alcoholics are at increased risk for hepatic toxicity and subsequent coagulation problems postoperatively. Furthermore, alcoholics who continue drinking up to the time of surgery may experience acute alcohol withdrawal during the postoperative period that can be life threatening. Prophylactic administration of lorazepam (Ativan) greatly reduces the potential risk of this significant complication.

Allergies

Finally, medicinal allergies should be questioned because, obviously, these medications should be avoided in future treatment of the patient. All medicinal allergies should be marked boldly on the front of the patient's chart to avoid potential complications from inadvertent exposure to the same medications.

In summary, a careful and thorough medical history, including the chief complaint and history of present illness, past medical history, and family history, should be obtained in every patient. Unfortunately, time constraints often make it difficult for the physician to spend the necessary time to obtain a full history. A reasonable substitute is to have a trained nurse or other health professional see the patient first. By using a standard history form, much of the information discussed previously can be obtained in a preliminary interview. It then remains for the urologist to only fill in the blanks, have the patient elaborate on potentially relevant aspects of the past medical history, and then perform a complete physical examination.

PERINEUM

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The perineum lies between the pubis, thighs, and buttocks and is limited superiorly by the levator ani. Viewed from below, the symphysis pubis, ischial tuberosities, and coccyx outline the diamond shape of the perineum; the inferior ischiopubic rami and sacrotuberous ligaments form its bony and ligamentous walls (Figs. 2-35 and 2-36 [35] [36]). A line drawn through the ischial tuberosities divides the perineum into an anal and a urogenital triangle.



Figure 2-35 Male perineum. (From Anson BJ, McVay CB: Surgical anatomy, 6th ed. Philadelphia, WB Saunders, 1984, p 893.)

Anal Triangle

At the apex of the prostate, the rectum turns approximately 90 degrees posteriorly and inferiorly to become the anus (see Figs. 2-10 and 2-30 [10] [30]). It traverses 4 cm to reach the skin near the center of the anal triangle. The subcutaneous fat that surrounds the anus is continuous with that of the urogenital triangle, buttocks, and medial thigh. Laterally, the fat fills the ischiorectal fossa, a space bounded by the levator ani medially, and obturator internus, and the sacrotuberous ligament laterally (see Fig. 2-14 ). Anteriorly, this space extends into a recess above the urogenital diaphragm; posteriorly, it is continuous with the intermediate stratum of the pelvis through the sciatic foramina. Through this continuity, infections may travel between the perineum and the pelvic cavity.

The anal sphincter is divided into internal and external components. The internal sphincter represents a thickening of the inner circular smooth muscle layer of the rectum. The outer longitudinal smooth muscle thins beyond the rectourethralis and blends with the external sphincter, although a few fibers insert in the skin around the anus (corrugator cutis ani) to give it a puckered appearance. The external sphincter surrounds the internal sphincter and is divided into subcutaneous, superficial, and deep portions. The subcutaneous part attaches to the perineal body by collagenous and muscular fibers that are thickest superficially and referred to as the central tendon of the perineum. The superficial sphincter attaches to the perineal body and coccyx. At the posterior inflection of the rectum, the deep sphincter blends with the puborectalis sling of levator ani. At this level, a firm band may be felt on rectal examination and corresponds to the internal and external sphincter. Division of this muscular band results in fecal incontinence. The prostate may be accessed anterior to the sphincter, by dividing the central tendon and sphincteric attachments to the perineum (Young's procedure) or by following the anterior rectal wall beneath the external anal sphincter (Belt's procedure).

Male Urogenital Triangle

The entire urogenital triangle is bridged by the urogenital diaphragm. The scrotum is dependent from the anterior aspect of the urogenital triangle; in the posterior aspect, skin and subcutaneous fat overlie Colles' fascia. The perineal membrane and the posterior and lateral attachments of Colles' fascia limit a potential space known as the superficial pouch (see Figs. 2-3, 2-14, and 2-36 [3] [14] [36]). In this space, the three erectile bodies of the penis have their bony and fascial attachments (the root of the penis). The paired corpora cavernosa attach to the inferior ischiopubic rami and perineal membrane and are surrounded by the ischiocavernosus muscles. The corpus spongiosum dilates as the bulb of the penis and is fixed to the center of the perineal membrane. It is encompassed by the bulbospongiosus muscles that arise from the perineal body and from a central tendinous raphe and pass around the bulb to attach to the perineal membrane and dorsum of the penis. Contraction of the ischiocavernosus and bulbospongiosus muscles compresses the erectile bodies and potentiates penile erection. The transversus perinei muscles (superficial and deep) run along the posterior edge of the perineal membrane and are thought to stabilize the perineal body. Deep to the perineal membrane rests the striated urethral sphincter (discussed earlier).

Blood supply to the anal and urogenital triangles is derived largely from the internal pudendal vessels ( Fig. 2-37 ). After entering the perineum through the lesser sciatic foramen, the artery runs in a fascial sheath on the medial aspect of obturator internus, the pudendal canal (of Alcock). Early in its course, it gives off three or four inferior rectal branches to the anus. Its perineal branch pierces Colles' fascia to supply the muscles of the superficial pouch and continues anteriorly to supply the back of the scrotum. The internal pudendal terminates as the common penile artery (to be discussed).



Figure 2-37 Male perineum, illustrating the internal pudendal artery and its branches on the left and the pudendal nerve and its branches on the right.

The internal pudendal veins communicate freely with the dorsal vein complex by piercing the levator ani. These communicating vessels enter the pelvic venous plexus on the lateral surface of the prostate and are a common, often unexpected, source of bleeding during apical dissection of the prostate. The inferior rectal veins anastomose with the middle and superior rectal veins and produce an important connection between the portal and the systemic circulation. Obstruction of the portal or systemic venous system may cause shunting of collateral venous drainage through the portal system, manifested by hemorrhoids.

The pudendal nerve follows the vessels in their course through the perineum (see Fig. 2-37 ). Its first branch, the dorsal nerve of the penis, travels ventral to the main pudendal trunk in Alcock's canal. Several inferior rectal branches supply the external sphincter muscle and provide sensation to perianal skin. The perineal branches follow the perineal artery into the superficial pouch to supply the ischiocavernosus, bulbospongiosus, and transversus perinei muscles. A few of these branches continue anteriorly to supply sensation to the posterior scrotum. Additional perineal branches pass deep to the perineal membrane to supply the levator ani and striated urethral sphincter.

Penis

As discussed, the root of the penis is fixed to the perineum within the superficial pouch. The corpora cavernosa join beneath the pubis (penile hilum) to form the major portion of the body of the penis. They are separated by a septum that becomes pectiniform distally, so that their vascular spaces freely communicate. They are enclosed by the tough tunica albuginea, which is predominantly collagenous ( Fig. 2-38 ). Its outer longitudinal and inner circular fibers form an undulating meshwork when the penis is flaccid and appear tightly stretched with erection ( Goldstein et al, 1982 ). Smooth muscle bundles traverse the erectile bodies to form the endothelium-lined cavernous sinuses. These sinuses give the erectile tissue a spongy appearance on gross examination.



Figure 2-38 Cross section of the penis, demonstrating the relationship between the corporal bodies, penile fascia, vessels, and nerves. (From Devine CJ Jr, Angermeier KW: Anatomy of the penis and male perineum. AUA Update Series 1994;13:10-23.)

Distal to the bulb, the corpus spongiosum tapers and runs on the underside (ventrum) of the corpora cavernosa and then expands to cap them as the glans penis. The corona separates the base of the glans from the shaft of the penis. The spongiosum is traversed throughout its length by the anterior urethra, which begins at the perineal membrane (see Fig. 2-27 ). The anterior urethra is dilated in its bulbar and glanular segments (fossa navicularis) and narrowest at the external meatus. Proximally, it is lined by stratified and pseudostratified columnar epithelium, distally by stratified squamous epithelium. The mucus-secreting glands (of Littre) may be seen as small outpouchings of the mucosa.

Buck's fascia surrounds both cavernosal bodies dorsally and splits to surround the spongiosum ventrally (see Fig. 2-38 ). Elastic and collagenous fibers from the rectus sheath blend with and surround Buck's fascia as the fundiform ligament of the penis. Deeper fibers from the pubis form the suspensory ligament of the penis. In the perineum, Buck's fascia fuses with the tunica albuginea deep to the muscles of the erectile bodies ( Uhlenhuth et al, 1949 ). Distally, it fuses with the base of the glans at the corona. Bleeding from a tear in the corporal bodies (e.g., penile fracture) is usually contained within Buck's fascia, and ecchymosis is limited to the penile shaft.

The skin of the penile shaft is highly elastic and without appendages (hair or glandular elements), except for the smegma-producing glands at the base of the corona. It is devoid of fat and quite mobile because of the loose attachment of its dartos backing to Buck's fascia. Distally, it folds over the glans as the foreskin and attaches firmly below the corona. Its blood supply is independent of the erectile bodies and is derived from the external pudendal branches of the femoral vessels (see Fig. 2-4 ). These vessels enter the base of the penis to run longitudinally in the dartos fascia as a richly anastomotic network. Thus, penile skin may be mobilized on a vascular pedicle as the ideal tissue for urethral reconstruction. The skin of the glans is immobile as a result of its direct attachment to the underlying thin tunica albuginea.

The common penile artery continues in Alcock's canal, above the perineal membrane, and terminates in three branches to supply the erectile bodies ( Fig. 2-39 ). The bulbourethral artery penetrates the perineal membrane to enter the spongiosum from above at its posterolateral border. This large, short artery can be difficult to isolate and control during urethrectomy. It supplies the urethra, spongiosum, and glans. The cavernosal artery pierces the corporal body in the penile hilum to near the center of its erectile tissue. It gives off straight and helicine arteries that ramify to supply the cavernous sinuses. The dorsal artery of the penis passes between the crus penis and the pubis to reach the dorsal surface of the corporal bodies. It runs between the dorsal vein and the dorsal penile nerve and with them attaches to the underside of Buck's fascia (see Fig. 2-41 ). As it courses to the glans, it gives off cavernous branches and circumferential branches to the spongiosum and urethra. The rich blood supply to the spongiosum allows safe division of the urethra during stricture repair ( Devine and Angermeier, 1994 ).



Figure 2-39 Arterial supply of the penis.

The surgeon contemplating penile revascularization must be aware that the penile arteries are highly variable in their branching, courses, and anastomoses ( Bare et al, 1994 ). It is not uncommon for a single cavernosal artery to supply both corporal bodies or to be absent altogether. Alternatively, an accessory pudendal artery may supplement or completely replace branches of the common penile artery ( Fig. 2-40 ). This artery usually arises from the obturator or inferior vesical arteries and runs anterolateral to or within the prostate to reach the penis in the company of the dorsal vein. This artery has been identified in 7 of 10 cadaveric specimens ( Breza et al, 1989 ) and noted at 4% of radical prostatectomies ( Polascik and Walsh, 1995 ); its resection at prostatectomy may adversely affect postoperative potency ( Droupy et al, 1999 ).

At the base of the glans, several venous channels coalesce to form the dorsal vein of the penis, which runs in a groove between the corporal bodies and drains into the preprostatic plexus ( Fig. 2-41 ). The circumflex veins originate in the spongiosum and pass around the cavernosa to meet the deep dorsal vein perpendicularly. They are present only in the distal two thirds of the penile shaft and number 3 to 10. Intermediary venules form from the cavernous sinuses to drain into a subtunical capillary plexus. These plexuses give rise to emissary veins, which commonly follow an oblique path between the layers of the tunica and drain into the circumflex veins dorsolaterally. Emissary veins in the proximal third of the penis join on the dorsomedial surface of the cavernous bodies to form two to five cavernous veins. At the hilum of the penis, these vessels pass between the crura and the bulb, receiving branches from each, and join the internal pudendal veins. Valves are found in the emissary, cavernosal, and deep dorsal veins and may thwart attempts to revascularize the penis by arteriovenous anastomosis ( Sohn, 1994 ).

The dorsal nerves provide sensory innervation to the penis. These nerves follow the course of the dorsal arteries and richly supply the glans (see Fig. 2-41 ). Small branches from the perineal nerve supply the ventrum of the penis near the urethra as far as the glans distally ( Uchio et al, 1999 ). These nerves must be anesthetized when performing a penile block to numb the ventrum of the penis. The route of the cavernous nerves has been described. After piercing the corporal bodies, they ramify in the erectile tissue to supply sympathetic and parasympathetic innervation from the pelvic plexus. Tonic sympathetic tone inhibits erection. Parasympathetic nerves release acetylcholine, nitric oxide, and vasoactive intestinal polypeptide, which cause the cavernosal smooth muscle and arterial relaxation necessary for erection ( Burnett, 1995 ). It is thought that during erection, the subtunical venules are occluded by being compressed against the nondistensible tunica albuginea. Insufficient venous occlusion, particularly in vessels draining into the deep dorsal and cavernosal veins, is thought to cause vasculogenic impotence.

Scrotum

The scrotal skin is pigmented, hair bearing, devoid of fat, and rich in sebaceous and sweat glands. It varies from loose and shiny to highly folded with transverse rugae, depending on the tone of its underlying smooth muscle. A midline raphe runs from the urethral meatus to the anus and represents the line of fusion of the genital tubercles. Deep to this raphe, the scrotum is separated into two compartments by a septum.

The dartos layer of smooth muscle is continuous with Colles', Scarpa's, and the dartos fascia of the penis (see Figs. 2-3 and 2-36 [3] [36]). The testes are suspended by their cords in the scrotal compartments. As the testes descend, they acquire coverings from the layers of the abdominal wall, known as the spermatic fascia, that form part of the scrotal wall ( Fig. 2-42 ). The external spermatic fascia derives from the external oblique fascia and remains firmly attached to the borders of the external ring. The cremasteric muscle and fascia arise from the internal oblique muscle and attach laterally to the inguinal ligament and iliopsoas fascia and medially to the pubic tubercle. The internal spermatic fascia is a continuation of the transversalis fascia. The parietal and visceral tunica vaginalis surround the testis with a mesothelium-lined pouch and are derived from the peritoneum. They are continuous at the posterolateral border of the testis at its mesentery, where it is fixed to the scrotal wall. The testis is also fixed at its lower pole by the gubernaculum. Occasionally, the mesentery and gubernaculum may be deficient, leaving the testis unfixed (bell-clapper deformity) and predisposing to torsion of the cord.



Figure 2-42 Scrotum and its layers. (From Pansky B: Review of Gross Anatomy, 6th ed. New York, McGraw-Hill, 1987, p 483.)

The anterior wall of the scrotum is supplied by the external pudendal vessels and the ilioinguinal and genitofemoral nerves (see Fig. 2-4 ). The anterior vessels and nerves typically run parallel to the rugae and do not cross the raphe; thus, transverse or midline raphe scrotal incisions are most appropriate. The back of the scrotum is supplied by the posterior scrotal branches of the perineal vessels and nerves (see Fig. 2-37 ). In addition, the posterior femoral cutaneous nerve (S3) gives a perineal branch to supply the scrotum and perineum (see Fig. 2-8 ). In accordance with their origin, the spermatic fasciae have a blood supply (cremasteric, vasal, testicular) separate from that of the scrotal wall. Fournier's gangrene usually does not involve these structures, and they may be spared during débridement.

Perineal Lymphatics

The penis, scrotum, and perineum drain into the inguinal lymph nodes. These nodes may be divided into superficial and deep groups, which are separated by the deep fascia of the thigh (fascia lata). In relation to the external pudendal, superficial inferior epigastric, and superficial circumflex iliac vessels, the superficial nodes lie at the saphenofemoral junction. At the saphenous opening (fossa ovalis) in the fascia lata, the greater saphenous vein joins the femoral vein, and the superficial nodes communicate with the deep group. Most of the deep inguinal nodes lie medial to the femoral vein and send their efferents through the femoral ring (beneath the inguinal ligament) to the external iliac and obturator nodes. Just outside the femoral ring, a large node (Cloquet's or Rosenmuller's node) is consistently present.

The scrotal lymphatics do not cross the median raphe and drain into the ipsilateral superficial inguinal lymph nodes. Lymphatics from the shaft of the penis converge on the dorsum and then ramify to both sides of the groin. Those of the glans pass deep to Buck's fascia dorsally and drain to superficial and deep groups in both sides of the groin. Direct lymphatic channels from the glans to the pelvic nodes, which bypass the inguinal nodes, have been proposed by anatomists; however, clinical studies have not confirmed their existence. Other studies have suggested that all penile lymphatic drainage passes through “sentinel nodes,” which lie medial to the superficial inferior epigastric veins. Clinical studies have also called this speculation into question ( Catalona, 1988 ). The perineal skin and fasciae drain into superficial nodes; the structures of the superficial pouch likely drain into the superficial and deep groups.

Testes

The testes are 4 to 5 cm long, 3 cm wide, and 2.5 cm deep and have a volume of 30 mL. They are enclosed in a tough capsule comprising (1) the visceral tunica vaginalis; (2) tunica albuginea, with collagenous and smooth muscle elements; and (3) the tunica vasculosa. The epididymis attaches to the posterolateral aspect of the testis. Beneath it, the tunica albuginea projects inward to form the mediastinum testis, the point at which vessels and ducts traverse the testicular capsule ( Fig. 2-43 ). Septa radiate from the mediastinum to attach to the inner surface of the tunica albuginea to form 200 to 300 cone-shaped lobules, each of which contains one or more convoluted seminiferous tubules. Each tubule is U-shaped and has a stretched length of nearly 1 m. Interstitial (Leydig) cells lie in the loose tissue surrounding the tubules and are responsible for testosterone production. Toward the apices of the lobules, the seminiferous tubules become straight (tubuli recti) and enter the mediastinum testis to form an anastomosing network of tubules lined by flattened epithelium. This network, known as the rete testis, forms 12 to 20 efferent ductules and passes into the largest portion of the epididymis, the caput. Here, the efferent ductules enlarge, become more convoluted, and form conical lobules. The duct from each lobule drains into a single epididymal duct, which winds approximately 6 m within the fibrous sheath of the epididymis to form its body and tail. As the duct approaches the tail, it thickens and straightens to become the vas deferens.

The spermatic cord is composed of the vas deferens, testicular vessels, and spermatic fasciae. As discussed in Chapter 1 , Surgical Anatomy of the Retroperitoneum, Kidneys, and Ureters, the testicular arteries arise from the aorta and travel in the intermediate stratum of the retroperitoneum to reach the internal inguinal ring. Lateral to the internal inguinal ring, the attachments of the intermediate stratum form the lateral spermatic fascia. These attachments may be taken down at orchidopexy to gain cord length. At the internal ring, the vessels are joined by the genital branch of the genitofemoral nerve, the ilioinguinal nerve, the cremasteric artery, and the vas deferens and its artery.

In its course to the testis, the testicular artery branches into an internal artery and an inferior testicular artery and into a capital artery to the head of the epididymis ( Fig. 2-44 ). The level of this branching varies and has been noted to occur within the inguinal canal in 31% to 88% of cases ( Beck et al, 1992 ; Jarow et al, 1992 ). When performing an inguinal varicocelectomy, the surgeon must remember that there may be two or three arterial branches at this level ( Hopps et al, 2003 ). A rich arterial anastomosis occurs at the head of the epididymis, between the testicular and the capital arteries, and at the tail between the testicular, the epididymal, the cremasteric, and the vasal arteries (see Fig. 2-44 ). The testicular arteries enter the mediastinum and ramify in the tunica vasculosa, principally in the anterior, medial, and lateral portions of the lower pole and the anterior segment of the upper pole ( Fig. 2-45 ). Thus, placement of a traction suture through the lower pole tunica albuginea risks damaging these important superficial vessels and devascularizing the testis ( Jarow, 1991 ). Testicular biopsy should be carried out in the medial or lateral surface of the upper pole, where the risk of vascular injury is minimal.



Figure 2-45 Distribution of subtunical testicular arteries compiled from 27 right and 26 left vascular casts. The highest density of subtunical arteries is found at the anterior upper pole and the entire lower pole. Lateral (L) and medial (M) sides of the upper pole are relatively free of arterial branches. (From Jarow JP: Clinical significance of intratesticular anatomy. J Urol 1991;145:777-779.)

The testicular veins form several highly anastomotic channels that surround the testicular artery as the pampiniform plexus. This arrangement allows countercurrent heat exchange, which cools the blood in the testicular artery. At the level of the inguinal canal, the veins join to form two or three channels and then a single vein that drains into the inferior vena cava on the right and the renal vein on the left. The testicular veins may anastomose with the external pudendal, cremasteric, and vasal veins ( Fig. 2-46 ). These connections can allow varicoceles to recur after ablative procedures. Testicular lymphatic vessels drain to the para-aortic and interaortocaval nodes as detailed in Chapter 1 , Surgical Anatomy of the Retroperitoneum, Kidneys, and Ureters.



Figure 2-46 Venous drainage of the testis and epididymis. Note connections between the pampiniform plexus and the saphenous, internal iliac, and external iliac veins.

Visceral innervation to the testis and epididymis travels by two routes. A portion arises in the renal and aortic plexuses and travels with the gonadal vessels. Additional gonadal afferent and efferent nerves course from the pelvic plexus in association with the vas deferens ( Rauchenwald et al, 1995 ). Intractable orchialgia may respond to anesthesia of the pelvic plexus ( Zorn et al, 1994 ). Intriguingly, some afferent and efferent nerves cross over to the contralateral pelvic plexus ( Taguchi et al, 1999 ). This neural cross-communication may explain how pathologic processes in one testis (e.g., tumor or varicocele) may affect the function of the contralateral testis. The genital branch of the genitofemoral nerve supplies sensation to the parietal and visceral tunica vaginalis and the overlying scrotum.

KEY POINTS: LOWER URINARY TRACT AND MALE GENITALIA

	▪	The pelvic cavity is divided into the false pelvis superiorly, and the true pelvis, inferiorly, wherein lie all of the pelvic organs.
	▪	The bony prominences and ligaments of the pelvis and lower abdomen will orient the surgeon during physical examination and in the operating room.
	▪	The pelvic floor is closed off by the levator ani and urogenital diaphragm, and the muscles and fasciae of the pelvic floor provide critical support for the pelvic organs.
	▪	The rectum, bladder, prostate, seminal vesicles, uterus, vagina, penis, and clitoris receive blood supply from the anterior trunk of the internal iliac artery and innervation from the pelvic autonomic plexus.
	▪	The urethra, vagina, and anus exit through the perineum in association with the external genitalia.
	▪	Detailed knowledge of the relationships of the pelvic organs to each other and the bones and muscles of the pelvis, as well as the locations of the blood supply and innervation of all pelvic and perineal structures, is critical for safely performing all pelvic operations.

Female Urogenital Triangle

The vestibule of the vagina runs vertically throughout the length of the urogenital triangle. The labia majora form its lateral sides and fuse anteriorly as the hood of the clitoris. The subcutaneous fat pad of the mons pubis continues posteriorly in the labia majora to frame the vestibule. The labial fat pads receive blood supply from the external pudendal vessels and may be raised on these vessels as a rotational flap for repair of vesicovaginal or urethrovaginal fistulas ( Fig. 2-47 ). The urethra enters the vestibule between the clitoris and the vagina.



Figure 2-47 Arteries and nerves of the female perineum. (From Doherty MG: Clinical anatomy of the pelvis. In Copeland LJ [ed]: Textbook of Gynecology. Philadelphia, WB Saunders, 1993, p 51.)

The structure of the superficial pouch is similar to that of the male ( Fig. 2-48 ). The crura of the clitoris attach to the inferior ischiopubic rami, surrounded by the ischiocavernosus muscles, and converge to form the body of the clitoris. The vestibular bulbs lie to either side of the vaginal vestibule, covered by the bulbospongiosus muscles. As homologues of the penile bulb, they are composed of erectile tissue and meet anteriorly to form the glans of the clitoris. The vestibular glands are deep to the vestibular bulbs but, unlike the bulbourethral glands in the male, are superficial to the perineal membrane. Their ducts travel 2 cm to open in the vaginal vestibule on the posteromedial sides of the labia minora. The perineal membrane, pierced in its center by the vagina, is less well developed than that of the male. The innervation, blood supply, and lymphatic drainage of the external genitalia and superficial pouch are similar to those described in the male.



Figure 2-48 Female superficial perineal pouch. On the left side, the muscles have been removed to show the vestibular bulb and Bartholin's gland. (From Williams PL, Warwick R: Gray's Anatomy, 35th British ed. Philadelphia, WB Saunders, 1973, p 1364.)

PELVIC VISCERA

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Rectum

The rectum begins with the disappearance of the sigmoid mesentery opposite the third sacral vertebra. Peritoneum continues anteriorly over the upper two thirds of the rectum as the rectovesical pouch in males and as the rectouterine pouch (of Douglas) in females ( Fig. 2-23 ; see also Fig. 2-11 ). This peritoneal pouch extends inferiorly to the seminal vesicles or to the posterior fornix of the vagina. Inferior to this pouch, the anterior rectum is related to its fascial continuation (the rectogenital or Denonvilliers' fascia) down to the level of the striated urethral sphincter (see Figs. 2-3, 2-23, and 2-33 [3] [23] [33]). The rectum describes a gentle curve on the sacrum, coccyx, and levator plate (see Fig. 2-21 ) and receives innervation from the laterally placed pelvic autonomic plexus and blood supply from the superior (from inferior mesenteric), middle (from internal iliac), and inferior (from internal pudendal) rectal arteries.



Figure 2-23 Sagittal section through the prostatic and membranous urethra, demonstrating the midline relations of the pelvic structures. (From Hinman F Jr: Atlas of Urosurgical Anatomy. Philadelphia, WB Saunders, 1993, p 356.)



Figure 2-33 Median sagittal section of the female pelvis, showing the potential spaces between the pelvic organs. The posterior two thirds of the vagina lie nearly horizontal and rest with the uterine cervix on the rectum, which is in turn supported by the posterior portion of levator ani (the levator plate, not shown). RVS, rectovaginal space, the anterior wall is formed by the rectovaginal (Denonvilliers') fascia; SVSe, supravaginal septum, the fusion between the bladder and cervix; VCS, vesicocervical space; VVS, vesicovaginal space. (From Nichols DH, Randall CL: Vaginal Surgery, 3rd ed. Baltimore, Williams & Wilkins, 1989, p 34.)

The rectal wall is composed of an inner layer of circular smooth muscle and a virtually continuous sheet of outer longitudinal smooth muscle derived from the tenia of the colon. In its lowest part, the rectum dilates to form the rectal ampulla. At the most inferior portion of the ampulla, anterior fibers of the longitudinal muscle leave the rectum to join Denonvilliers' fascia and the posterior striated urethral sphincter in the apex of the perineal body ( Brooks et al, 2002 ). When approached from below, these fibers, the rectourethralis muscle, are 2 to 10 mm thick and must be divided to gain access to the prostate (see Fig. 2-36 ). The apices of the prostate and ampulla are in close proximity, and rectal injuries during radical prostatectomy commonly occur at this location. As the rectourethralis is given off, the rectum makes a right-angle turn posteroinferiorly to exit the pelvis at the anal canal (see Fig. 2-10 ). The anatomy of the anal canal is considered with the perineum.



Figure 2-36 Muscles and superficial fasciae of the male perineum. (From Hinman F Jr: Atlas of Urosurgical Anatomy. Philadelphia, WB Saunders, 1993, p 219.)

Pelvic Ureter

The ureter is divided into abdominal and pelvic portions by the common iliac artery. The structure of the ureter and its abdominal course are reviewed in Chapter 1 , Surgical Anatomy of the Retroperitoneum, Kidneys, and Ureters. Intraoperatively, the ureter is identified by its peristaltic waves and is readily found anterior to the bifurcation of the common iliac artery. At ureteroscopy, pulsations of this artery can be seen in the posterior ureteral wall. The ovarian vessels (infundibulopelvic ligament) cross the iliac vessels anterior and lateral to the ureter, and dissection of the ovarian vessels at the pelvic brim is a common cause of ureteral injury (see Fig. 2-13 ) ( Daly and Higgins, 1988 ). Pyeloureterography discloses a narrowing of the ureter at the iliac vessels, and ureteral calculi frequently become lodged at this location. Because the ureter and iliac vessels rest on the arcuate line, the ureter is subject to compression and obstruction by the gravid uterus and by masses within the true pelvis.

The ureters come within 5 cm of each other as they cross the iliac vessels. On entering the pelvis, they diverge widely along the pelvic side walls toward the ischial spines. The ureter travels on the anterior surface of the internal iliac vessels and is related laterally to the branches of the anterior trunk. Near the ischial spine, the ureter turns anteriorly and medially to reach the bladder. In males, the anteromedial surface of the ureter is covered by peritoneum, and the ureter is embedded in retroperitoneal connective tissue, which varies in thickness (see Fig. 2-13 ). As the ureter courses medially, it is crossed anteriorly by the vas deferens and runs with the inferior vesical arteries, veins, and nerves in the lateral vesical ligaments. Viewed from the peritoneal side, the ureter is just lateral and deep to the rectogenital fold. In females, the ureter first runs posterior to the ovary and then turns medially to run deep to the base of the broad ligament before entering a loose connective tissue tunnel through the substance of the cardinal ligament (see Fig. 2-13 ). As in the male, the ureter can be found slightly lateral and deep to the rectouterine folds of peritoneum. It is crossed anteriorly by the uterine artery and is therefore subject to injury during hysterectomy. As it passes in front of the vagina, it crosses 1.5 cm anterior and lateral to the uterine cervix. The ureter may be injured at this level during hysterectomy, resulting in a ureterovaginal fistula. The ureter courses 1 to 4 cm on the anterior vaginal wall to reach the bladder. Occasionally, a stone lodged in the distal ureter can be palpated through the anterior vaginal wall. The intramural ureter is discussed in the section on the bladder.

The pelvic ureter receives abundant blood supply from the common iliac artery and most branches of the internal iliac artery. The inferior vesical and uterine arteries usually supply the ureter with its largest pelvic branches. Blood supply to the pelvic ureter enters laterally; thus, the pelvic peritoneum should be incised only medial to the ureter. Intramural vessels of the ureter run within the adventitia and generally follow one of two patterns. In approximately 75% of specimens, longitudinal vessels run the length of the ureter and are formed by anastomoses of segmental ureteral vessels. In the remaining ureters, the vessels form a fine interconnecting mesh (plexiform) with less collateral flow ( Shafik, 1972 ). The pelvic ureter appears to have a high preponderance of plexiform vessels, which render it more susceptible to ischemia and less suitable for ureteroureterotomy ( Hinman, 1993 ). Lymphatic drainage of the pelvic ureter is to the external, internal, and common iliac nodes. Pathologic enlargement of the common and internal iliac nodes can encroach on and obstruct the ureter.

The pelvic ureter has rich adrenergic and cholinergic autonomic innervation derived from the pelvic plexus. The functional significance of this innervation is unclear, inasmuch as the ureter continues to contract peristaltically after denervation. Afferent neural fibers travel through the pelvic plexus and account for the visceral quality of referred pain from ureteral irritation or acute obstruction.

Bladder Anatomic Relationships

When filled, the bladder has a capacity of approximately 500 mL and assumes an ovoid shape. The empty bladder is tetrahedral and is described as having a superior surface with an apex at the urachus, two inferolateral surfaces, and a posteroinferior surface or base with the bladder neck at the lowest point (see Fig. 2-23 ).

The urachus anchors the bladder to the anterior abdominal wall (see Fig. 2-8 ). There is a relative paucity of bladder wall muscle at the point of attachment of the urachus, predisposing to formation of diverticula. The urachus is composed of longitudinal smooth muscle bundles derived from the bladder wall. Near the umbilicus, it becomes more fibrous and usually fuses with one of the obliterated umbilical arteries. Urachal vessels run longitudinally, and the ends of the urachus must be ligated when it is divided. An epithelium-lined lumen usually persists throughout life and uncommonly gives rise to aggressive urachal adenocarcinomas ( Begg, 1930 ). In rare instances, luminal continuity with the bladder serves as a bacterial reservoir or results in an umbilical urinary fistula.

The superior surface of the bladder is covered by peritoneum. Anteriorly, the peritoneum sweeps gently onto the anterior abdominal wall (see Fig. 2-13 ). With distention, the bladder rises out of the true pelvis and separates the peritoneum from the anterior abdominal wall. It is therefore possible to perform a suprapubic cystostomy without risking entry into the peritoneal cavity. Posteriorly, the peritoneum passes to the level of the seminal vesicles and meets the peritoneum on the anterior rectum to form the rectovesical space.

Anteroinferiorly and laterally, the bladder is cushioned from the pelvic side wall by retropubic and perivesical fat and loose connective tissue. This potential space (of Retzius) may be entered anteriorly by dividing the transversalis fascia and provides access to the pelvic viscera as far posteriorly as the iliac vessels and ureters (see Fig. 2-11 ). The bladder base is related to the seminal vesicles, ampullae of the vas deferentia, and terminal ureter. The bladder neck, located at the internal urethral meatus, rests 3 to 4 cm behind the midpoint of the symphysis pubis. It is firmly fixed by the pelvic fasciae (see earlier discussion) and by its continuity with the prostate; its position changes little with varying conditions of the bladder and rectum.

In the female, the peritoneum on the superior surface of the bladder is reflected over the uterus to form the vesicouterine pouch and then continues posteriorly over the uterus as the rectouterine pouch (see Fig. 2-13 ). The vagina and uterus intervene between the bladder and the rectum, so that the base of the bladder and urethra rest on the anterior vaginal wall. Because the anterior vaginal wall is firmly attached laterally to the levator ani, contraction of the pelvic diaphragm (e.g., during increases in intra-abdominal pressure) elevates the bladder neck and draws it anteriorly. In many women with stress incontinence, the bladder neck drops below the pubic symphysis. In infants, the true pelvis is shallow and the bladder neck is level with the upper border of the symphysis. The bladder is a true intra-abdominal organ that can project above the umbilicus when full. By puberty, the bladder has migrated to the confines of the deepened true pelvis.

Structure

The internal surface of the bladder is lined with transitional epithelium, which appears smooth when the bladder is full but contracts into numerous folds when the bladder empties. This urothelium is usually six cells thick and rests on a thin basement membrane. Deep to this, the lamina propria forms a relatively thick layer of fibroelastic connective tissue that allows considerable distention. This layer is traversed by numerous blood vessels and contains smooth muscle fibers collected into a poorly defined muscularis mucosa. Beneath this layer lies the smooth muscle of the bladder wall. The relatively large muscle fibers form branching, interlacing bundles loosely arranged into inner longitudinal, middle circular, and outer longitudinal layers ( Fig. 2-24 ). However, in the upper aspect of the bladder, these layers are clearly not separable, and any one fiber can travel between each of the layers, change orientation, and branch into longitudinal and circular fibers. This meshwork of detrusor muscle is ideally suited for emptying the spherical bladder.



Figure 2-24 Dissection of the male bladder. 11, Posterior outer longitudinal detrusor, which forms the backing of the ureters (folded back); 11a, posterolateral portion of the outer longitudinal muscle forming a loop around the anterior bladder neck; 4′, 12, and 18, middle circular layer backing the trigone; 23 and 23a, lateral pedicle of the prostate. (From Uhlenhuth E: Problems in the Anatomy of the Pelvis. Philadelphia, JB Lippincott, 1953, p 187.)

Near the bladder neck, the detrusor muscle is clearly separable into the three layers described earlier. Here, the smooth muscle is morphologically and pharmacologically distinct from the remainder of the bladder, because the large-diameter muscle fascicles are replaced by much finer fibers. The structure of the bladder neck appears to differ between men and women. In men, radially oriented inner longitudinal fibers pass through the internal meatus to become continuous with the inner longitudinal layer of smooth muscle in the urethra.

The middle layer forms a circular preprostatic sphincter that is responsible for continence at the level of the bladder neck ( Fig. 2-25 ). The bladder wall posterior to the internal urethral meatus and the anterior fibromuscular stroma of the prostate form a continuous ringlike structure at the bladder neck ( Brooks et al, 1998 ). The fact that perfect continence can be maintained in men in whom the striated urethral sphincter is destroyed attests to the efficacy of this sphincter ( Waterhouse et al, 1973 ). This muscle is richly innervated by adrenergic fibers, which, when stimulated, produce closure of the bladder neck ( Uhlenhuth, 1953 ). Damage to the sympathetic nerves to the bladder, as a result of diabetes mellitus or retroperitoneal lymph node dissection for testis cancer, can cause retrograde ejaculation.



Figure 2-25 Structure of the male bladder neck and trigone. A, Anterior view reveals that the trigone narrows below the ureteral orifices and then widens at the bladder neck to become continuous with the anterior fibromuscular stroma of the prostate. B, Lateral projection shows that the trigone and anterior fibromuscular stroma are in continuity. The trigone thickens near the bladder neck as it meets the anterior fibromuscular stroma. C, Oblique view shows this structure at the bladder neck, where it forms the internal urethral sphincter. (From Brooks JD, Chao W-M, Kerr J: Male pelvic anatomy reconstructed from the Visible Human data set. J Urol 1998;159:868-872.)

The outer longitudinal fibers are thickest posteriorly at the bladder base. In the midline, they insert into the apex of the trigone and intermix with the smooth muscle of the prostate to provide a strong trigonal backing. Laterally, the fibers from this posterior sheet pass anteriorly and fuse to form a loop around the bladder neck (see Fig. 2-24 ). This loop is thought to participate in continence at the bladder neck. On the lateral and anterior surfaces of the bladder, the longitudinal fibers are not as well developed. Some anterior fibers course forward to join the puboprostatic ligaments in men and the pubourethral ligaments in women. These fibers contribute smooth muscle to these supports and are speculated to contribute to bladder neck opening during micturition ( DeLancey, 1989 ).

At the female bladder neck, the inner longitudinal fibers converge radially to pass downward as the inner longitudinal layer of the urethra, as described earlier. The middle circular layer does not appear to be as robust as that of the male, and several authors have denied its existence altogether (Gosling, 1979, 1985 [22] [23]; Williams et al, 1989 ). Whereas several other investigators have noted an anterior loop of external longitudinal muscle (see Fig. 2-32 ), the authors just cited deny the existence of this structure as well. They maintain instead that the external fibers pass obliquely and longitudinally down the urethra to participate in forming the inner longitudinal layer of smooth muscle. Regardless, the female bladder neck differs strikingly from the male in possessing little adrenergic innervation. In addition, its sphincteric function is limited; in 50% of continent women, urine enters the proximal urethra during a cough ( Versi et al, 1986 ).



Figure 2-32 Female bladder and striated urethral sphincter. a, Diagram of striated urethral sphincter showing disposition of the muscle fibers. 1, The proximal third of the sphincter encircles the urethra entirely. 2, The middle bundles surround the urethra in front and pass off the lateral sides to blend with the vaginal wall (compressor urethrae). 3, The distal portion surrounds the urethra and vagina together and has been called the urethrovaginal sphincter. The bulbocavernosus also acts as a sphincter around the vaginal vestibule. b, Urethral sphincter in its entirety. The relationship of the pelvic viscera is shown. Interlacing detrusor fibers are also demonstrated. c, Posterolateral outer longitudinal detrusor muscle looping anterior to the bladder neck. Inner longitudinal smooth muscle fibers run the length of the urethra, deep to the striated sphincter. d, Cross section of the urethra, showing thick, highly vascularized lamina propria and folded mucosa, which act as a urethral seal. Longitudinal smooth muscle surrounds the lamina propria. (From the Brödel Archives, Johns Hopkins School of Medicine, Baltimore.)

Ureterovesical Junction and the Trigone

As the ureter approaches the bladder, its spirally oriented mural smooth muscle fibers become longitudinal. Two to 3 cm from the bladder, a fibromuscular sheath (of Waldeyer) extends longitudinally over the ureter and follows it to the trigone ( Tanagho, 1992 ). The ureter pierces the bladder wall obliquely, travels 1.5 to 2 cm, and terminates at the ureteral orifice ( Fig. 2-26 ). As it passes through a hiatus in the detrusor (intramural ureter), it is compressed and narrows considerably. This is a common site in which ureteral stones become impacted. The intravesical portion of the ureter lies immediately beneath the bladder urothelium and therefore is quite pliant; it is backed by a strong plate of detrusor muscle. With bladder filling, this arrangement is thought to result in passive occlusion of the ureter, like a flap valve. Indeed, reflux does not occur in fresh cadavers when the bladder is filled ( Thomson et al, 1994 ). Vesicoureteral reflux is thought to result from insufficient submucosal ureteral length and poor detrusor backing. Chronic increases in intravesical pressure resulting from bladder outlet obstruction can cause herniation of the bladder mucosa through the weakest point of the hiatus above the ureter and produce a “Hutch diverticulum” and reflux ( Hutch et al, 1961 ).



Figure 2-26 Normal ureterovesical junction and trigone. A, Section of the bladder wall perpendicular to the ureteral hiatus shows the oblique passage of the ureter through the detrusor and also shows the submucosal ureter with its detrusor backing. Waldeyer's sheath surrounds the prevesical ureter and extends inward to become the deep trigone. B, Waldeyer's sheath continues in the bladder as the deep trigone, which is fixed at the bladder neck. Smooth muscle of the ureter forms the superficial trigone and is anchored at the verumontanum. (From Tanagho EA, Pugh RC: The anatomy and function of the ureterovesical junction. Br J Urol 1963;35:151-165.)

The triangle of smooth urothelium between the two ureteral orifices and the internal urethral meatus is referred to as the trigone of the bladder (see Fig. 2-26 ). The fine longitudinal smooth muscle fibers from the vesical side of the ureters pass to either side of their respective orifices to join the lateral and posterior ureteral wall fibers and fan out over the base of the bladder. Fibers from each ureter meet to form a triangular sheet of muscle that extends from the two ureteral orifices to the internal urethral meatus. The edges of this muscular sheet are thickened between the ureteral orifices (the interureteric crest or Mercier's bar) and between the ureters and the internal urethral meatus (Bell's muscle).

The muscle of trigone forms three distinct layers: (1) a superficial layer, derived from the longitudinal muscle of the ureter, which extends down the urethra to insert at the verumontanum; (2) a deep layer, which continues from Waldeyer's sheath and inserts at the bladder neck; and (3) a detrusor layer, formed by the outer longitudinal and middle circular smooth muscle layers of the bladder wall. Through its continuity with the ureter, the superficial trigonal muscle anchors the ureter to the bladder. During ureteral reimplantation, this muscle is tented up and divided to gain access to the space between Waldeyer's sheath and the ureter. In this space, only loose fibrous and muscular connections are found. This anatomic arrangement helps prevent reflux during bladder filling by fixing and applying tension to the ureteral orifice. As the bladder fills, its lateral wall telescopes outward on the ureter, thereby increasing intravesical ureteral length ( Hutch et al, 1961 ).

The urothelium overlying the muscular trigone is usually only three cells thick and adheres strongly to the underlying muscle by a dense lamina propria. During filling and emptying of the bladder, this mucosal surface remains smooth.

Bladder Circulation

In addition to the vesical branches, the bladder may be supplied by any adjacent artery arising from the internal iliac artery. For convenience, surgeons refer to the vesical blood supply as the lateral and posterior pedicles, which, when the bladder is approached from the rectovesical space, are lateral and posteromedial to the ureters, respectively. These pedicles are the lateral and posterior vesical ligaments in the male and part of cardinal and uterosacral ligaments in the female (see Fig. 2-13 ). The veins of the bladder coalesce into the vesicle plexus and drain into the internal iliac vein. Lymphatics from the lamina propria and muscularis drain to channels on the bladder surface, which run with the superficial vessels within the thin visceral fascia. Small paravesical lymph nodes can be found along the superficial channels. The bulk of the lymphatic drainage passes to the external iliac lymph nodes (see Fig. 2-18 ). Some anterior and lateral drainage may go through the obturator and internal iliac nodes, whereas portions of the bladder base and trigone may drain into the internal and common iliac groups.

Bladder Innervation

Autonomic efferent fibers from the anterior portion of the pelvic plexus (the vesical plexus) pass up the lateral and posterior ligaments to innervate the bladder. The bladder wall is richly supplied with parasympathetic cholinergic nerve endings and has abundant postganglionic cell bodies. Sparse sympathetic innervation of the bladder has been proposed to mediate detrusor relaxation but probably lacks functional significance. A separate nonadrenergic, noncholinergic (NANC) component of the autonomic nervous system participates in activating the detrusor, although the neurotransmitter has not been identified ( Burnett, 1995 ). As mentioned, the male bladder neck receives abundant sympathetic innervation and expresses α-adrenergic receptors. The female bladder neck has little adrenergic innervation. Nitric oxide synthase–containing neurons have been identified in the detrusor, particularly at the bladder neck, where they may facilitate relaxation during micturition. The trigonal muscle is innervated by adrenergic and nitric oxide synthase–containing neurons. Like the bladder neck, it relaxes during micturition. Afferent innervation from the bladder travels with both sympathetic (via the hypogastric nerves) and parasympathetic nerves to reach cell bodies in the dorsal root ganglia located at thoracolumbar and sacral levels. As a consequence, presacral neurectomy (division of the hypogastric nerves) is ineffective in relieving bladder pain.

Prostate Anatomic Relationships

The normal prostate weighs 18 g; measures 3 cm in length, 4 cm in width, and 2 cm in depth; and is traversed by the prostatic urethra (see Fig. 2-23 ). Although ovoid, the prostate is referred to as having anterior, posterior, and lateral surfaces, with a narrowed apex inferiorly and a broad base superiorly that is contiguous with the base of the bladder. It is enclosed by a capsule composed of collagen, elastin, and abundant smooth muscle. Posteriorly and laterally, this capsule has an average thickness of 0.5 mm, although it may be partially transgressed by normal glands. Microscopic bands of smooth muscle extend from the posterior surface of the capsule to fuse with Denonvilliers' fascia. Loose areolar tissue defines a thin plane between Denonvilliers' fascia and the rectum. On the anterior and anterolateral surfaces of the prostate, the capsule blends with the visceral continuation of endopelvic fascia. Toward the apex, the puboprostatic ligaments extend anteriorly to fix the prostate to the pubic bone (see Fig. 2-40 ). The superficial branch of the dorsal vein lies outside this fascia in the retropubic fat and pierces it to drain into the dorsal vein complex.

Laterally, the prostate is cradled by the pubococcygeal portion of levator ani and is directly related to its overlying endopelvic fascia (see Figs. 2-8 and 2-10 [8] [10]). Below the juncture of the parietal and visceral endopelvic fascia (arcus tendineus fascia pelvis), the pelvic fascia and prostate capsule separate and the space between them is filled by fatty areolar tissue and the lateral divisions of the dorsal vein complex. During a radical retropubic prostatectomy, the endopelvic fascia should be divided lateral to the arcus tendineus fascia pelvis to avoid injury to the venous complex. In the process, the endopelvic fascia overlying the levator ani is actually peeled off the muscle and displaced medially with the prostate. Although this is truly a parietal endopelvic fascia, it is commonly referred to as the “lateral prostatic fascia” ( Myers, 1994 ). As mentioned earlier, the cavernosal nerves run posterolateral to the prostate in the substance of the parietal pelvic fascia (lateral prostatic fascia). Thus, to preserve these nerves, this fascia must be incised lateral to the prostate and anterior to the neurovascular bundle ( Walsh et al, 1983 ).

The apex of the prostate is continuous with the striated urethral sphincter (see Fig. 2-30 ). Histologically, normal prostatic glands can be found to extend into the striated muscle with no intervening fibromuscular stroma or “capsule.” At the base of the prostate, outer longitudinal fibers of the detrusor fuse and blend with the fibromuscular tissue of the capsule. As mentioned, the middle circular and inner longitudinal muscles extend down the prostatic urethra as a preprostatic sphincter. As with the apex, no true capsule separates the prostate from the bladder. In surgically resected prostate carcinomas, this peculiar anatomic arrangement can make interpretation of these margins difficult and has led some pathologists to propose that the prostate does not possess a true capsule ( Epstein, 1989 ).

Structure

The prostate is composed of approximately 70% glandular elements and 30% fibromuscular stroma. The stroma is continuous with capsule and is composed of collagen and abundant smooth muscle. It encircles and invests the glands of the prostate and contracts during ejaculation to express prostatic secretions into the urethra.

The urethra runs the length of the prostate and is usually closest to its anterior surface. It is lined by transitional epithelium, which may extend into the prostatic ducts. The urothelium is surrounded by an inner longitudinal and an outer circular layer of smooth muscle. A urethral crest projects inward from the posterior midline, runs the length of the prostatic urethra, and disappears at the striated sphincter ( Fig. 2-27 ). To either side of this crest, a groove is formed (prostatic sinuses) into which all glandular elements drain ( McNeal, 1972 ). At its midpoint, the urethra turns approximately 35 degrees anteriorly, but this angulation can vary from 0 to 90 degrees (see Figs. 2-23, 2-25, and 2-28 [23] [25] [28]). This angle divides the prostatic urethra into proximal (preprostatic) and distal (prostatic) segments that are functionally and anatomically discrete (McNeal, 1972, 1988 [35] [36]). In the proximal segment, the circular smooth muscle is thickened to form the involuntary internal urethral (preprostatic) sphincter described earlier. Small periurethral glands, lacking periglandular smooth muscle, extend between the fibers of the longitudinal smooth muscle to be enclosed by the preprostatic sphincter. Although these glands constitute less than 1% of the secretory elements of the prostate, they can contribute significantly to prostatic volume in older men as one of the sites of origin of benign prostatic hyperplasia.



Figure 2-27 Posterior wall of the male urethra. (From Anson BJ, McVay CB: Surgical Anatomy, 6th ed. Philadelphia, WB Saunders, 1984, p 833.)



Figure 2-28 Zonal anatomy of the prostate as described by J. E. McNeal (Am J Surg Pathol 1988;12:619-633). The transition zone surrounds the urethra proximal to the ejaculatory ducts. The central zone surrounds the ejaculatory ducts and projects under the bladder base. The peripheral zone constitutes the bulk of the apical, posterior, and lateral aspects of the prostate. The anterior fibromuscular stroma extends from the bladder neck to the striated urethral sphincter.

Beyond to the urethral angle, all major glandular elements of the prostate open into the prostatic urethra. The urethral crest widens and protrudes from the posterior wall as the verumontanum (see Fig. 2-27 ). The small slitlike orifice of the prostatic utricle is found at the apex of the verumontanum and may be visualized cystoscopically. The utricle is a 6-mm müllerian remnant in the form of a small sac that projects upward and backward into the substance of the prostate. In males with ambiguous genitalia, it may form a large diverticulum that protrudes from the posterior side of the prostate. To either side of the utricular orifice, the two small openings of the ejaculatory ducts may be found. The ejaculatory ducts form at the juncture of the vas deferens and seminal vesicles and enter the prostate base where it fuses with the bladder. They course nearly 2 cm through the prostate in line with the distal prostatic urethra and are surrounded by circular smooth muscle ( Fig. 2-28 ; see also Figs. 2-23 and 2-25 [23] [25]).

In general, the glands of the prostate are tubuloalveolar with relatively simple branching and are lined with simple cuboidal or columnar epithelium. Scattered neuroendocrine cells, of unknown function, are found between the secretory cells. Beneath the epithelial cells, flattened basal cells line each acinus and are believed to be stem cells for the secretory epithelium. Each acinus is surrounded by a thin layer of stromal smooth muscle and connective tissue.

The glandular elements of the prostate have been divided into discrete zones, distinguished by the location of their ducts in the urethra, by their differing pathologic lesions, and, in some cases, by their embryologic origin (see Fig. 2-28 ). These zones can be demonstrated clearly with transrectal ultrasonography. At the angle dividing the preprostatic and prostatic urethra, the ducts of the transition zone arise and pass beneath the preprostatic sphincter to travel on its lateral and posterior sides. Normally, the transition zone accounts for 5% to 10% of the glandular tissue of the prostate. A discrete fibromuscular band of tissue separates the transition zone from the remaining glandular compartments and may be visualized at transrectal ultrasonography of the prostate. The transition zone commonly gives rise to benign prostatic hypertrophy, which expands to compress the fibromuscular band into a surgical capsule seen at enucleation of an adenoma. It is estimated that 20% of adenocarcinomas of the prostate originate in this zone.

The ducts of the central zone arise circumferentially around the openings of the ejaculatory ducts. This zone constitutes 25% of the glandular tissue of the prostate and expands in a cone shape around the ejaculatory ducts to the base of the bladder. The glands are structurally and immunohistochemically distinct from the remaining prostatic glands (which branch directly from the urogenital sinus), which has led to the suggestion that they are of wolffian origin ( McNeal, 1988 ). In keeping with this suggestion, only 1% to 5% of adenocarcinomas arise in the central zone, although it may be infiltrated by cancers from adjacent zones.

The peripheral zone makes up the bulk of the prostatic glandular tissue (70%) and covers the posterior and lateral aspects of the gland. Its ducts drain into the prostatic sinus along the entire length of the (postsphincteric) prostatic urethra. Seventy percent of prostatic cancers arise in this zone, and it is the zone most commonly affected by chronic prostatitis.

Up to one third of the prostatic mass may be attributed to the nonglandular anterior fibromuscular stroma. This region normally extends from the bladder neck to the striated sphincter, although considerable portions of it may be replaced by glandular tissue in adenomatous enlargement of the prostate. It is directly continuous with the prostatic capsule, anterior visceral fascia, and anterior portion of the preprostatic sphincter and is composed of elastin, collagen, and smooth and striated muscle. It is rarely invaded by carcinoma.

Clinically, the prostate is often spoken of as having two lateral lobes, separated by a central sulcus that is palpable on rectal examination, and a middle lobe, which may project into the bladder in older men. These lobes do not correspond to histologically defined structures in the normal prostate but are usually related to pathologic enlargement of the transition zone laterally and the periurethral glands centrally.

Vascular Supply

Most commonly, the arterial supply to the prostate arises from the inferior vesical artery. As it approaches the gland, the artery (often several) divides into two main branches ( Fig. 2-29 ). The urethral arteries penetrate the prostatovesical junction posterolaterally and travel inward, perpendicular to the urethra. They approach the bladder neck in the 1- to 5-o'clock and 7- to 11-o'clock positions, with the largest branches located posteriorly. They then turn caudally, parallel to the urethra, to supply it, the periurethral glands, and the transition zone. Thus, in benign prostatic hypertrophy, these arteries provide the principal blood supply of the adenoma ( Flocks, 1937 ). When these glands are resected or enucleated, the most significant bleeding is commonly encountered at the bladder neck, particularly at the 4- and 8-o'clock positions.



Figure 2-29 Arterial supply of the prostate. (Adapted from Flocks RH: The arterial distribution within the prostate gland: Its role in transurethral prostatic resection. J Urol 1937;37:524-548.)

The capsular artery is the second main branch of the prostatic artery. This artery gives off a few small branches that pass anteriorly to ramify on the prostatic capsule. The bulk of this artery runs posterolateral to the prostate with the cavernous nerves (neurovascular bundles) and ends at the pelvic diaphragm. The capsular branches pierce the prostate at right angles and follow the reticular bands of stroma to supply the glandular tissues. Venous drainage of the prostate is abundant through the periprostatic plexus (see Fig. 2-17 ).

Lymphatic drainage is primarily to the obturator and internal iliac nodes (see Fig. 2-18 ). A small portion of drainage may initially pass through the presacral group, or less commonly, the external iliac nodes.

Nerve Supply

Sympathetic and parasympathetic innervation from the pelvic plexus travels to the prostate through the cavernous nerves. Nerves follow branches of the capsular artery to ramify in the glandular and stromal elements. Parasympathetic nerves end at the acini and promote secretion; sympathetic fibers cause contraction of the smooth muscle of the capsule and stroma. α-Adrenergic blockade diminishes prostate stromal and preprostatic sphincter tone and improves urinary flow rates in men affected with benign prostatic hypertrophy; this emphasizes that this disease affects both the stroma and the epithelium. Peptidergic and nitric oxide synthase–containing neurons also have been found in the prostate and may affect smooth muscle relaxation ( Burnett, 1995 ). Afferent neurons from the prostate travel through the pelvic plexuses to pelvic and thoracolumbar spinal centers. A prostatic block may be achieved by instilling local anesthetic into the pelvic plexuses.

Membranous Urethra

In its course from the apex of the prostate to the perineal membrane, the membranous urethra spans on average 2 to 2.5 cm (range, 1.2 to 5 cm) ( Myers, 1991 ). It is surrounded by the striated (external) urethral sphincter, which is often incorrectly depicted as a flat sheet of muscle sandwiched between two layers of fascia. The striated sphincter is actually signet ring–shaped, broad at its base and narrowing as it passes through the urogenital hiatus of the levator ani to meet the apex of the prostate ( Fig. 2-30 ; see also Figs. 2-10 and 2-23 [10] [23]). In utero, this muscle forms a vertically oriented tube that extends from the perineal membrane to the bladder neck ( Oelrich, 1980 ). As the prostate grows, posterior and lateral portions of this muscle atrophy, although transverse fibers persist on the entire anterior prostate through adulthood. At the apex of the prostate, circular fibers surround the urethra, and they thin posteriorly to insert into a fibrous raphe. Distally, the fibers do not meet posteriorly; rather, they acquire an ω shape as they fan out laterally over the perineal membrane. Throughout its length, the posterior portion of the striated sphincter inserts into the perineal body. When the sphincter contracts, the walls of the urethra are pulled posteriorly toward the perineal body ( Strasser et al, 1998 ). In contrast to the levator ani, the sphincter consists only of fine, type I (slow-twitch) fibers, rich in acid-stable myosin adenosine triphosphatase, which appear designed for tonic contraction. The myofibrils are surrounded by abundant connective tissue that blends with adjacent supporting structures.

The striated sphincter is related anteriorly to the dorsal vein complex (which may invade its anterior portion with age) and laterally to the levator ani. Connective tissue from deep within the lateral and anterior walls inserts into the puboprostatic ligaments posteriorly and into the suspensory ligament of the penis anteriorly to form a sling of fibrous tissue that suspends the urethra from the pubis ( Steiner, 1994 ). A similar suspensory mechanism is found in the female urethra (see later discussion and Fig. 2-34 ). Two bulbourethral glands lie superior to the perineal membrane and are invested in the broad base of sphincter muscle. During sexual excitement, these glands secrete clear mucus into the bulbous urethra.



Figure 2-34 Urethral suspensory mechanism. The pubourethral ligament (P.U.L.) is composed of an anterior portion (suspensory ligament of the clitoris), a posterior portion (pubourethral ligament of endopelvic fascia), and an intermediate portion that bridges the other two. U.G.D., urogenital diaphragm; V, vagina; U, urethra. (From Milley PS, Nichols DH: The relationship between the pubo-urethral ligaments and the urogenital diaphragm in the human female. Anat Rec 1971;170:281-283.)

The striated sphincter corresponds to the location of peak urethral closing pressure and is responsible for continence after prostatectomy. Components involved in generating this closing pressure are (1) the pseudostratified columnar epithelium, which contracts into radial folds as it meets to occlude the lumen; (2) the submucosa, which is rich with blood vessels and soft connective tissue and contributes to urethral sealing ( Raz et al, 1972 ); (3) the longitudinal and circular urethral smooth muscle (intrinsic component of the external sphincter); (4) the striated sphincter; and (5) the pubourethral component of the levator ani.

Gross dissection and retrograde axonal tracing techniques have confirmed that the striated sphincter is supplied by the pudendal nerve ( Tanagho et al, 1982 ). However, urologists have long been puzzled as to why pudendal nerve sectioning does not ablate sphincter activity. Lawson (1974) and Zvara and colleagues (1994) identified a second source of somatic innervation to the sphincter: a branch of the sacral plexus that runs on the pelvic surface of the levator ani (see Fig. 2-20 ). Injury to this nerve at radical prostatectomy may contribute to postoperative urinary incontinence ( Hollabaugh et al, 1997 ). Autonomic innervation to the intrinsic smooth muscle of the membranous urethra is likely given by the cavernous nerves as they pass nearby, although dividing these nerves does not appear to affect urinary continence significantly ( Steiner et al, 1991 ). Afferent fibers from the striated sphincter have not been defined but are sure to have interesting and important functional roles, because this muscle lacks proprioceptive muscle spindles ( Gosling et al, 1981 ).

Vas Deferens and Seminal Vesicle

As it arises from the tail of the epididymis, the vas (ductus) deferens is somewhat tortuous for 2 to 3 cm (see Fig. 2-43 ). It runs posterior to the vessels of the cord and through the inguinal canal and emerges in the pelvis lateral to the inferior epigastric vessels (see Fig. 2-7 ). At the internal ring, it diverges from the testicular vessels and passes medial to all structures of the pelvic side wall to reach the base of the prostate posteriorly (see Figs. 2-7, 2-13, and 2-15 [7] [13] [15]). The terminal vas is dilated and tortuous (ampulla) and is capable of storing spermatozoa. The vas has a thick wall of outer longitudinal and inner circular smooth muscle and is lined by pseudostratified columnar epithelium with nonmotile stereocilia.



Figure 2-43 Testis and epididymis. A, One to three seminiferous tubules fill each compartment and drain into the rete testis in the mediastinum. Twelve to 20 efferent ductules become convoluted in the head of the epididymis and drain into a single coiled duct of the epididymis. The vas is convoluted in its first portion. B, Cross section of the testis, showing the mediastinum and septations continuous with the tunica albuginea. The parietal and visceral tunica vaginalis are confluent where the vessels and nerves enter the posterior aspect of the testis.

The seminal vesicle is a lateral outpouching of the vas, approximately 5 cm long, with a capacity of 3 to 4 mL (see Figs. 2-8 and 2-28 [8] [28]). Despite its name, it does not store sperm but contributes the largest portion of fluid to the ejaculate. The seminal vesicle comprises a single coiled tube with several outpouchings that is lined by columnar epithelium with goblet cells. The tube is encased in a thin layer of smooth muscle and is held in its coiled configuration by a loose adventitia.

The seminal vesicle and ampulla of the vas lie posterior to the bladder. The ureter enters the bladder medial to the tip of the seminal vesicle. As they join to form the ejaculatory duct, their smooth muscle coats fuse with the prostatic capsule at its base. Denonvilliers' fascia or, occasionally, the rectovesical pouch of peritoneum separates these structures from the rectum (see Fig. 2-23 ). Unless involved by a pathologic process, these structures are not palpable on rectal examination.

The blood supply for both structures comes from the vesiculodeferential artery, a branch of the superior vesical artery. This artery supplies the vas throughout its length and then passes onto the anterior surface of the seminal vesicle near its tip. Additional arterial supply may come from the inferior vesical artery. The pelvic vas and seminal vesicle drain into the pelvic venous plexus. Lymphatic drainage passes to the external and internal iliac nodes (see Fig. 2-18 ). Innervation arises from the pelvic plexus, with major excitatory efferents contributed by the (sympathetic) hypogastric nerves ( Kolbeck and Steers, 1993 ).

Female Pelvic Viscera

The uterus measures 8 × 6 × 4 cm in a normal woman and is composed largely of dense smooth muscle ( Fig. 2-31 ). It has a narrowed neck, the cervix, that opens through the anterior vaginal wall and a broad corpus that is capped by the rounded fundus. As discussed earlier, it lies in front of the rectum and over the dome of bladder; its impression may be appreciated cystoscopically (Figs. 2-32 and 2-33 [32] [33]). The fallopian tubes extend laterally from the junction of the corpus and fundus and are draped by leaves of peritoneum called the broad ligaments (see Figs. 2-13 and 2-31 [13] [31]). As they extend to the pelvic side walls, the fallopian tubes angle up and backward to open posteromedially. The tubes are divided into four segments: uterine, isthmus, ampulla, and infundibulum, which is crowned by the fimbriae. The ovary rests posterior to the elbow of the tube and is supported by its own peritoneal fold, the mesovarium. The ureter may be found directly posterior to the ovary, covered by pelvic peritoneum. The infundibulopelvic ligament, mentioned earlier, suspends the ovary and lateral fallopian tube from the pelvic side wall and transmits the ovarian vessels to both structures. The round ligament of the ovary passes medially through the broad ligament to fix the ovary to the lateral wall of the uterus. Beneath its point of attachment, the round ligament of the uterus passes laterally, in the leaves of the broad ligament, to exit through to inguinal canal and attach to the labial fat pad (see Figs. 2-13 and 2-31 [13] [31]).

The uterine artery crosses in front of the ureter and runs in the broad and cardinal ligaments to supply the proximal vagina, uterus, and medial two thirds of the fallopian tube (see Fig. 2-31 ). It is joined by a rich plexus of uterine veins that freely connect with the ovarian veins. Nerves from the pelvic plexus travel to the female pelvic viscera through the cardinal and uterosacral ligaments in the company of the vessels; thus, after hysterectomy, the bladder may become neurogenic.

The vagina extends inward from the vestibule at a 45-degree angle and then turns horizontal over the levator plate (see Fig. 2-33 ). It is lined by rugate nonkeratinized squamous epithelium backed by a thick, well-vascularized lamina propria. It is surrounded by a smooth muscle coat of inner circular and stronger external longitudinal layers. In cross section, the vagina is H shaped ( Fig. 2-34 ) as a result of firm attachments of its anterior wall to the levator ani at the arcus tendineus fascia pelvis and of its posterior wall to the rectovaginal septum. The anterior vaginal wall is pierced by the cervix proximally. The shallow fossae around the cervix are referred to as the anterior, lateral, and posterior fornices. Because the apex of the vagina is covered with the peritoneum of the rectouterine pouch, the peritoneal cavity may be accessed through the posterior fornix (see Fig. 2-33 ).

Immediately in front of the cervix, the base of the bladder rests on the vaginal wall. Smooth muscle fibers tether the posterior bladder wall and base to the uterine cervix and vagina (see Fig. 2-33 ). Division of these fibers yields posterior access to the vesicovaginal space. This space extends distally to the proximal third of the urethra (where the urethra and vagina fuse) and is limited to each side by the lateral ligaments of the bladder. It may be accessed transvaginally through incision of the anterior vaginal wall in front of the cervix. Incision of the anterior vaginal wall to either side of the urethra leads into the retropubic space (see Fig. 2-12 ). The tough leaves of visceral endopelvic fascia are felt medially and should be included in all transvaginal urethral suspension procedures ( Mostwin, 1991 ).

The vagina is separated from the rectum by the rectovaginal septum (see Fig. 2-33 ), and rectoceles result from a loss of integrity of this septum. Deep to this septum lies a second potential space, the rectovaginal space. The bowel may herniate into this space to form an enterocele. On its lateral surfaces, the vagina is related to the levator ani. Near the vestibule, fibers of the levator ani blend and fuse with the vaginal muscularis. The vaginal vessels and nerves lie on the anterolateral surface of the vagina deep to arcus tendineus fascia pelvis.

Female Urethra

On average, the female urethra traverses 4 cm from the bladder neck to the vaginal vestibule. Its lining changes gradually from transitional to nonkeratinized stratified squamous epithelium. Many small mucous glands open into the urethra and can give rise to urethral diverticula. Distally, these glands group together on either side of the urethra (Skene's glands) and empty through two small ducts to either side of the external urethral meatus. A thick, richly vascular submucosa supports the urethral epithelium and glands (see Fig. 2-32 ). Together, the mucosa and submucosa form a cushion that contributes significantly to urethral closure pressure ( Raz et al, 1972 ). These layers are estrogen dependent; at menopause they may atrophy, resulting in stress incontinence. A relatively thick layer of inner longitudinal smooth muscle continues from the bladder to the external meatus to insert into periurethral fatty and fibrous tissue. In contrast to the male proximal urethra, no circular smooth muscle sphincter can be identified. A rather thin layer of circular smooth muscle envelops the longitudinal fibers throughout the length of the urethra. It is thought that the longitudinal smooth muscle of the urethra contracts coordinately with the detrusor during micturition to shorten and widen the urethra ( Gosling, 1979 ).

The striated urethral sphincter invests the distal two thirds of the female urethra ( Oelrich, 1983 ). It is composed exclusively of delicate type I (slow-twitch) fibers surrounded by abundant collagen. Proximally, it forms a complete ring around the urethra that corresponds to the zone of highest urethral closure pressure (see Fig. 2-32 ). Farther down the urethra, the fibers do not meet posteriorly but continue off the lateral sides of the urethra onto the anterior and lateral walls of the vagina. Contraction of these fibers (the compressor urethrae) closes the urethra against the fixed anterior vaginal wall. Near the vestibule, the fibers completely surround the urethra and vagina to form a urethrovaginal sphincter. Contraction of this muscle group, along with bulbospongiosus, tightens the urogenital hiatus.

The suspensory ligament of the clitoris (anterior urethral ligament) and the pubourethral ligaments (posterior urethral ligaments) form a sling that suspends the urethra beneath the pubis (see Figs. 2-12 and 2-34 [12] [34]) ( Zacharin, 1963 ). The striated urethral sphincter receives dual somatic innervation, like that in the male, from the pudendal and pelvic somatic nerves ( Borirakchanyavat et al, 1997 ). Little sympathetic innervation is found in the female urethra. Parasympathetic cholinergic fibers are found throughout the smooth muscle. Somatic and autonomic nerves to the urethra travel on the lateral walls of the vagina near the urethra. During transvaginal incontinence surgery, the anterior vaginal wall should be incised laterally to avoid these nerves and prevent type III urinary incontinence ( Ball et al, 1997 ).

Female Pelvic Support

The pelvic muscles and fasciae cooperate to prevent prolapse of the urogenital organs through the hiatus. Three functional supportive elements are recognized: (1) the pubovisceral and perineal muscles, which form a sphincter around the urogenital hiatus (see Fig. 2-32 ); (2) the levator plate, which acts as a horizontal shelf beneath the bladder, uterine cervix, posterior vagina, and rectum (see Fig. 2-33 ); and (3) the cardinal and uterosacral ligaments, which anchor the pelvic viscera over the levator plate ( Zacharin, 1985 ; Mostwin, 1991 ; DeLancey, 1993 ). The pelvic muscles contract tonically to counteract gravitational forces. In response to stress, the levator ani contracts, closing the urogenital hiatus and increasing the anteroposterior length of the levator plate. Increased intra-abdominal pressure forces the pelvic viscera downward against a fixed levator plate, closing the vagina like a flap valve.

Pelvic and perineal muscles play the greatest role in pelvic support. Damage to the perineal body during parturition destroys the urogenital sphincter, enlarges the urogenital hiatus, and erodes the levator plate. Aging and birth trauma partially denervate and weaken the levator ani ( Snooks et al, 1985 ). With loss of muscular support, intra-abdominal forces impinge directly on the pelvic fasciae; over time, these either tear or stretch. Procedures to correct pelvic prolapse or urinary incontinence that rely solely on these fasciae may be successful initially but do not fare well over time ( Trockman et al, 1995 ). Repair of a single pelvic defect—a cystocele for instance—may unmask another (e.g., enterocele, rectocele); therefore, successful repair of pelvic prolapse must address all components of anatomic support ( Zacharin, 1985 ; DeLancey, 1993 ).

PELVIC INNERVATION

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Lumbosacral Plexus

The lumbosacral plexus and its rami are well illustrated in Chapter 1 , Surgical Anatomy of the Retroperitoneum, Kidneys, and Ureters; only the pelvic courses of its nerves are reviewed here (see Figs. 2-6 and 2-12 [6] [12] and Table 2-2 ). The iliohypogastric nerve (L1) travels between, and supplies, the internal oblique and the transversus muscles and pierces the internal and external oblique muscles 3 cm above the external inguinal ring to supply sensation over the lower anterior abdomen and pubis (see Fig. 2-4 ). The ilioinguinal nerve (L1) passes through the internal oblique muscle to enter the inguinal canal laterally. It travels anterior to the cord and exits the external ring to provide sensation to the mons pubis and anterior scrotum or labia majora (see Figs. 2-4 and 2-6 [4] [6]). The genitofemoral nerve (L1, L2) pierces the psoas muscle to reach its anterior surface in the retroperitoneum and then travels to the pelvis and splits into genital and femoral branches. The latter supplies sensation over the anterior thigh below the inguinal ligament. The genital branch follows the cord through the inguinal canal, supplies the cremaster muscle, and supplies sensation to the anterior scrotum.

Table 2-2 -- Somatic Nerves of the Lower Abdomen and Pelvis

Nerve Name	Origin	Supplies
Iliohypogastric	L1	Motor supply to internal oblique, transversus muscles, sensation over lower anterior abdominal wall
Ilioinguinal	L1	Sensation over anterior pubis (mons) and anterior scrotum or labia
Genitofemoral	L1, L2	Genital branch: motor supply to cremaster muscle, sensation to anterior scrotum; femoral branch: sensation to anterior thigh
Femoral	L2, L3, L4	Motor supply to extensors of the knee, sensation to anterior thigh
Obturator	L2, L3, L4	Motor supply to adductors of the thigh, sensation to medial thigh
Lumbosacral trunk	L4, L5	Joins the sacral nerves to form the lumbosacral plexus that supplies motor and sensory innervation to the lower extremities
Posterior femoral cutaneous	S2, S3	Sensation to perineum, posterior scrotum, and posterior thigh
Pudendal	S2, S3, S4	Motor to levator ani, muscles of the urogenital diaphragm, anal and striated urethral sphincter, sensation to the perineum, scrotum, and penis
Pelvic somatic efferents	S2, S3, S4	Motor supply to levator ani and striated urethral sphincter
Nervi erigentes	S2, S3, S4	Parasympathetic fibers from the sacral cord supply the pelvic viscera

For most of its pelvic course, the femoral nerve (L2, L3, L4) travels within the substance of the psoas muscle and then exits its lateral side to pass under the inguinal ligament ( Fig. 2-19 ). It supplies sensation to the anterior thigh and motor innervation to the extensors of the knee. During a psoas hitch, sutures should be placed in the direction of the nerve (and the psoas muscle fibers) to avoid nerve damage or entrapment. Retractor blades must not rest on the psoas muscle because they can produce a femoral nerve palsy, a potentially dangerous setback after pelvic surgery. The lateral femoral cutaneous nerve (L2, L3) may be seen lateral to the psoas in the iliacus fascia.



Figure 2-19 Femoral nerve as it relates to the psoas muscle. Retractor blades may compress this nerve to produce a femoral nerve palsy. (From Burnett AL, Brendler CB: Femoral neuropathy following major pelvic surgery: Etiology and prevention. J Urol 1994;151:163-165.)

The obturator nerve (L2, L3, L4) emerges in the true pelvis from beneath the psoas muscle, lateral to the internal iliac vessels, and passes through the obturator fossa to the obturator canal. In the fossa, it is lateral and superior to the obturator vessels and surrounded by the obturator and internal iliac lymph nodes. Damage to this nerve during pelvic lymphadenectomy weakens the adductors of the thigh.

The lumbosacral trunk (L4, L5) passes into the true pelvis behind the psoas and unites with the ventral rami of the sacral segmental nerves to form the sacral plexus. This plexus lies on the pelvic surface of the piriformis deep to the endopelvic fascia and posterior to the internal iliac vessels (see Fig. 2-15 ). It leaves the pelvis through the greater sciatic foramen immediately posterior to the sacrospinous ligament (where it may be injured during sacrospinous culposuspension) and supplies motor and sensory innervation to the posterior thigh and lower leg. An exaggerated lithotomy position may stretch this nerve or place pressure on its peroneal branch at the fibular head to produce footdrop. Pelvic and perineal branches of the sacral plexus include (1) the posterior femoral cutaneous nerve (S2, S3), which, after passing through the greater sciatic foramen, gives an anterior sensory branch to the perineum and posterior scrotum (see Fig. 2-8 ); (2) the pudendal nerve (S2, S3, S4), which follows the internal pudendal artery to the perineum (to be discussed); (3) the nervi erigentes (S2, S3, S4) to the autonomic plexus; and (4) pelvic somatic efferent nerves from the ventral rami of S2, S3, and S4 ( Fig. 2-20 ). These last nerves travel on the pelvic surface of the levator ani in close association with the rectum and prostate and are separated from the pelvic autonomic plexus by the endopelvic fascia. They supply the levator ani and extend anteriorly to the striated urethral sphincter ( Lawson, 1974 ; Zvara et al, 1994 ).



Figure 2-20 Pelvic floor somatic efferent nerves extending anteriorly on the pelvic surface of the levator ani to supply this muscle and the striated urethral sphincter. (From Lawson JON: Pelvic anatomy: Pelvic floor muscles. Ann R Coll Surg Engl 1974;54:244-252.)

Pelvic Autonomic Plexus

The presynaptic sympathetic cell bodies that project to the pelvic autonomic plexus reside in the lateral column of gray matter in the last three thoracic and first two lumbar segments of the spinal cord. They reach the pelvic plexus by two pathways: (1) The superior hypogastric plexus is formed by sympathetic fibers from the celiac plexus and the first four lumbar splanchnic nerves ( Fig. 2-21 ). Anterior to the bifurcation of the aorta, it divides into two hypogastric nerves that enter the pelvis medial to the internal iliac vessels, anterior to the sacrum, and deep to the endopelvic fascia. (2) The pelvic continuations of the sympathetic trunks pass deep to the common iliac vessels and medial to the sacral foramina and fuse in front of the coccyx at the ganglion impar (see Fig. 2-21 ). Each chain comprises four to five ganglia that send branches anterolaterally to participate in the formation of the pelvic plexus.



Figure 2-21 Sympathetic and parasympathetic contributions to the pelvic autonomic nervous plexus. (From Drake RL, Vogl W, Mitchell AWM: Gray's Anatomy for Students. Philadelphia, Elsevier, 2005.)

Presynaptic parasympathetic innervation arises from the intermediolateral cell column of the sacral cord. Fibers emerge from the second, third, and fourth sacral spinal nerves as the pelvic splanchnic nerves (nervi erigentes) to join the hypogastric nerves and branches from the sacral sympathetic ganglia to form the inferior hypogastric (pelvic) plexus (see Fig. 2-21 ). Some pelvic parasympathetic efferent fibers travel up the hypogastric nerves to the inferior mesenteric plexus, where they provide parasympathetic innervation to the descending and sigmoid colon.

The pelvic plexus is rectangular and is 4 to 5 cm long, and its midpoint is at the tips of the seminal vesicles ( Schlegel and Walsh, 1987 ). It is oriented in the sagittal plane on either side of the rectum and pierced by the numerous vessels going to and from the rectum, bladder, seminal vesicles, and prostate ( Fig. 2-22 ). Division of these vessels (the so-called lateral pedicles of the bladder and prostate) risks injury to the pelvic plexus with attendant postoperative impotence ( Walsh and Donker, 1982 ; Walsh et al, 1983 ). The right and left components of the pelvic plexus communicate behind the rectum and anterior and posterior to the vesical neck. Branches of the pelvic plexus follow pelvic blood vessels to reach the pelvic viscera, although nerves to the ureter may join it directly as it passes nearby. Visceral afferent and efferent nerves travel on the vas deferens to reach the testis and epididymis (see later discussion).



Figure 2-22 Lateral view showing the left pelvic autonomic nervous plexus and its relation to the pelvic viscera. Bl, bladder; Ur, ureter. (From Schlegel PN, Walsh PC: Neuroanatomical approach to radical cystoprostatectomy with preservation of sexual function. J Urol 1987;138:1402-1406.)

The most caudal portion of the pelvic plexus gives rise to the innervation of the prostate and the important cavernosal nerves ( Walsh and Donker, 1982 ). After passing the tips of the seminal vesicles, these nerves lie within leaves of the lateral endopelvic fascia near its juncture with, but outside, Denonvilliers' fascia ( Lepor et al, 1985 ). They travel at the posterolateral border of the prostate on the surface of the rectum and are lateral to the prostatic capsular arteries and veins (see Fig. 2-22 ). Because the nerves are composed of multiple fibers not visible on gross inspection, these vessels serve as a surgical landmark for the course of these nerves (the neurovascular bundle of Walsh). During radical prostatectomy, the nerves are most vulnerable at the apex of the prostate, where they closely approach the prostatic capsule at the 5- and 7-o'clock positions. On reaching the membranous urethra, the nerves divide into superficial branches, which travel on the lateral surface of the striated urethral sphincter at 3- and 9-o'clock positions, and deep fibers, which penetrate the substance of this muscle and send twigs to the bulbourethral glands. As the nerves reach the hilum of the penis, they join to form one to three discrete bundles, related to the urethra at 1- and 11-o'clock positions, superficial to the cavernous veins, and dorsomedial to the cavernous arteries (see Fig. 2-41 ) ( Lue et al, 1984 ; Breza et al, 1989 ). With the arteries, they pierce the corpora cavernosa to supply the erectile tissue (see later discussion). Small fibers also join the dorsal nerves of the penis as they course distally. In the female, the nerves to vestibular bodies and corpora cavernosa of the clitoris travel between the anterior vaginal wall and the bladder in association with the lateral venous plexuses.



Figure 2-41 Dorsal penile arteries, veins, and nerves. (From Hinman F Jr: Atlas of Urosurgical Anatomy. Philadelphia, WB Saunders, 1993, p 445.)

PELVIC CIRCULATION

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Arterial Supply

Major arteries of the pelvis are summarized in Table 2-1 . At the bifurcation of the aorta, the middle sacral artery arises posteriorly and travels on the pelvic surface of the sacrum to supply branches to the sacral foramina and the rectum. The common iliac arteries arise at the level of the fourth lumbar vertebra, run anterior and lateral to their accompanying veins, and bifurcate into the external and internal iliac arteries at the SI joint ( Fig. 2-15 ). The external iliac artery follows the medial border of the iliopsoas muscle along the arcuate line and leaves the pelvis beneath the inguinal ligament as the femoral artery ( Fig. 2-16 ). Its inferior epigastric artery is given off proximal to the inguinal ligament and ascends medial to the internal inguinal ring to supply the rectus muscle and overlying skin. Because the rectus is richly collateralized from above and laterally, the inferior epigastric arteries may be ligated with impunity. A rectus myocutaneous flap based on this artery has been used to correct major pelvic and perineal tissue defects. Near its origin, the inferior epigastric artery sends a deep circumflex iliac branch laterally and a pubic branch medially. Both vessels travel on the iliopubic tract and may be injured during inguinal hernia repair. Its cremasteric branch joins the spermatic cord at the internal inguinal ring and forms a distal anastomosis with the testicular artery (see Fig. 2-44 ). In 25% of people, an accessory obturator artery arises from the inferior epigastric artery and runs medial to the femoral vein to reach the obturator canal. This vessel must be avoided during obturator lymph node dissection.

Table 2-1 -- Arteries of the Pelvis

Artery Name	Origin	Supplies
Middle sacral	Aorta	Sacral nerves and sacrum
External Iliac Branches
Inferior epigastric	External iliac	Rectus abdominis muscle and overlying skin and fascia
Deep circumflex iliac	Inferior epigastric	Inguinal ligament and surrounding structures laterally
Pubic	Inferior epigastric	Inguinal ligament and surrounding structures medially
Cremasteric	Inferior epigastric	Vas deferens and testis
Internal Iliac Branches
Superior gluteal	Posterior trunk	Gluteus muscles and overlying skin
Ascending lumbar	Posterior trunk	Psoas and quadratus lumborum muscles and adjacent structures
Lateral sacral	Posterior trunk	Sacral nerves and sacrum
Superior vesical	Anterior trunk	Bladder, ureter, vas deferens, and seminal vesicle
Middle rectal	Anterior trunk	Rectum, ureter, and bladder
Inferior vesicle	Anterior trunk	Bladder, seminal vesicle, prostate, ureter, and the neurovascular bundle
Uterine	Anterior trunk	Uterus, bladder, and ureter
Internal pudendal	Anterior trunk	Rectum, perineum, and external genitalia
Obturator	Anterior trunk	Adductor muscles of the leg and overlying skin
Inferior gluteal	Anterior trunk	Gluteus muscles and overlying skin



Figure 2-15 Right internal and external iliac arteries. The ureter and vas deferens pass medial to the vessels. (From Clemente CD: Gray's Anatomy, 30th American ed. Philadelphia, Lea & Febiger, 1985, p 750.)



Figure 2-16 Right obturator fossa, showing the iliac vessels and obturator nerve. (From Skinner DG: Pelvic lymphadenectomy. In Glenn JF [ed]: Urological Surgery, 2nd ed. New York, Harper & Row, 1975, p 591.)



Figure 2-44 Collateral arterial circulation to the testis. (From Hinman F Jr: Atlas of Urosurgical Anatomy. Philadelphia, WB Saunders, 1993, p 497.)

The internal iliac (hypogastric) artery descends in front of the SI joint and divides into an anterior and a posterior trunk (see Fig. 2-15 ). The posterior trunk gives rise to three parietal branches: (1) the superior gluteal, which exits the greater sciatic foramen; (2) the ascending lumbar, which supplies the posterior abdominal wall; and (3) the lateral sacral, which passes medially to join the middle sacral branches at the sciatic foramina.

The anterior trunk gives off seven parietal and visceral branches: (1) The superior vesical artery arises from the proximal portion of the obliterated umbilical artery and gives off a vesiculodeferential branch to the seminal vesicles and vas deferens. The artery of the vas deferens travels the length of the vas to meet the cremasteric and testicular arteries distally (see Fig. 2-44 ). Because of these anastomoses, the testicular artery may be sacrificed without compromising the viability of the testis. (2) The middle rectal artery gives small branches to the seminal vesicles and prostate and anastomoses with the inferior and superior rectal arteries in the rectal wall. (3) The inferior vesical branches supply the lower ureter, the bladder base, the prostate, and the seminal vesicles. In the female, they supply the ureter, the bladder base, and the vagina. (4) The uterine artery passes above and in front of the ureter (“water flows under the bridge”) to ascend the lateral wall of the uterus and meet the ovarian artery in the lateral portion of the fallopian tube (see Figs. 2-13 and 2-31 [13] [31]). The ureter is vulnerable during division of the uterine pedicles. (5) The internal pudendal artery leaves the pelvic cavity through the greater sciatic foramen, passes around the sacrospinous ligament, and enters the lesser sciatic foramen to gain access to the perineum. Its perineal course is discussed later. (6) The obturator artery, variable in origin, travels through the obturator fossa medial and inferior to the obturator nerve and passes through its canal to supply the adductors of the thigh (see Fig. 2-16 ). (7) The inferior gluteal artery travels through the greater sciatic foramen to supply the buttock and thigh.



Figure 2-31 Female internal genitalia, from behind. The ureter passes beneath the uterine artery. (From Hinman F Jr: Atlas of Urosurgical Anatomy. Philadelphia, WB Saunders, 1993, p 402.)

The internal iliac artery can be ligated to control severe pelvic hemorrhage. Ligation decreases the pulse pressure, allowing hemostasis to occur more readily. Internal iliac blood flow does not stop but reverses its direction because of critical anastomoses (lumbar segmentals to iliolumbar; median sacral to lateral sacral; and superior rectal and middle rectal). Bilateral ligation almost invariably produces vasculogenic impotence.

Venous Supply

The dorsal vein of the penis passes between the inferior pubic arch and the striated urinary sphincter to reach the pelvis, where it trifurcates into a central superficial branch and two lateral plexuses ( Reiner and Walsh, 1979 ) ( Fig. 2-17 ). To minimize blood loss at radical retropubic prostatectomy, the dorsal vein complex is best divided distally, before its ramification. Part of this complex runs within the anterior and lateral wall of the striated sphincter; thus, care must be taken not to injure the sphincter when securing hemostasis. The superficial branch pierces the visceral endopelvic fascia between the puboprostatic ligaments and drains the retropubic fat, the anterior bladder, and the anterior prostate (see Figs. 2-17 and 2-40 [17] [40]).



Figure 2-17 Pelvic venous plexus. A, Trifurcation of the dorsal vein of the penis, viewed from the retropubic space. The relationship of the venous branches to the puboprostatic ligaments is shown. B, Lateral view of the pelvic venous plexus after removal of the lateral pelvic fascia. Normally these structures are difficult to see because they are embedded in pelvic fascia. (From Reiner WG, Walsh PC: An anatomical approach to the surgical management of the dorsal vein and Santorini's plexus during radical retropubic surgery. J Urol 1979;121:198-200.)

The lateral plexuses sweep down the sides of the prostate, receiving drainage from it and the rectum, and communicate with the vesical plexuses on the lower part of the bladder. Three to five inferior vesical veins emerge from the vesical plexus laterally and drain into the internal iliac vein. In the female, the dorsal vein of the clitoris bifurcates to empty into the laterally placed vaginal plexuses. These connect with the vesical, uterine, ovarian, and rectal plexuses and drain into the internal iliac veins. Connections between the pelvic plexuses, the emissary veins of the pelvic bones, and the vertebral plexus have been proposed to be routes for the dissemination of infection or tumor from the pelvic viscera to the axial and pelvic skeleton ( Batson, 1940 ).

The internal iliac vein is joined by tributaries corresponding to the branches of the internal iliac artery and ascends medial and posterior to the artery. This vein is relatively thin walled and at risk for injury during dissection of the artery or the nearby pelvic ureter. The external iliac vein travels medial and inferior to its artery and joins the internal iliac vein behind the internal iliac artery. In half the patients, one or more accessory obturator veins drain into the underside of the external iliac vein and can be easily torn during lymphadenectomy (see Fig. 2-16 ).

Pelvic Lymphatics

The pelvic lymph nodes can be difficult to appreciate on gross examination because they are embedded in the fatty and fibrous tissue of the intermediate stratum. Three major lymph node groups are associated with the pelvic vessels ( Fig. 2-18 ). A substantial portion of pelvic visceral lymphatic drainage passes through the internal iliac nodes and their tributaries: the presacral, obturator, and internal pudendal nodes. The external iliac nodes lie lateral, anterior, and medial to the vessels and drain the anterior abdominal wall, urachus, bladder, and, in part, internal genitalia. The external genitalia and perineum drain into the superficial and deep inguinal nodes (see later discussion). The inguinal nodes communicate directly with the internal and external iliac chains. The common iliac nodes receive efferent vessels from the external and internal iliac nodes and the pelvic ureter and drain into the lateral aortic nodes.



Figure 2-18 Lymphatic drainage of the male pelvis, perineum, and external genitalia.